It is a procedure in which a patient
receives a blood product through an
intravenous line.
1. Whole blood
2. Packed cell
3. Platelet
4. Fresh frozen plasma
5. Cryoprecipitate
6. Protein solution
7. Factor concentrate
8. granulocyte concentration
Major trauma with massive blood loss adults->20% children->10% of their
blood volume.
Major operative procedures minimum acceptable Hb 10g% & Hct 35%
Preoperatively in cases of chronic anemia requiring surgery.
Postoperatively if patient becomes severely anemic.
Following severe burn.
In septicemia.
Severe hemorrhage from pathological lesion like
cancer, GIT lesions.
Patients with bleeding disorder. Hemophilia, thrombocytopenia, liver disease.
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Each person has one of the following blood Before a blood transfusion, a
types: A, B, AB, or O. technician tests the patient's
O can be given to anyone but can only blood to find out what blood type
receive O. they have (that is, A, B, AB, or O
AB can receive any type but can only be and Rh positive or Rh negative).
given to AB.
Some patients may have allergic reactions even
Also, every person's blood is either
when the blood given does work with their own
Rh-positive or Rh-negative.
The blood used in a transfusion must be blood type.
compatible with the patient's blood type.
Type O blood is called the universal donor
People with type AB blood are called
universal recipients
People with Rh-positive blood can get
Rh-positive or Rh-negative blood. But
people with Rh-negative blood should
get only Rh-negative blood.
Blood banks collect, test, and store
blood.
ADMINISTERING BLOOD
Blood transfusions take place in either a doctor's office or a hospital. They can be
done at the patient's home, but this is less common.
A needle is used to insert an intravenous (IV) line into a blood vessel. Through this
line, the blood is transfused. the procedure usually takes one to four hours. The time
depends on how much blood is needed, which blood product is given, and whether the
patient's body can safely receive blood quickly or not.
During the blood transfusion, a nurse carefully watches the patient, especially for
the first 15 minutes. This is when bad reactions are most likely to occur.
After a blood transfusion, vital signs are checked (such as temperature, blood
pressure, respiration rate, and heart rate)
Follow-up blood tests may be necessary to show how the body is reacting to the
transfusion.
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TYPES OF REACTIONS
1.HEMOLYTIC REACTION
CAUSE CLINICAL SIGNS NURSING INTERVENTIONS
incompatibility Chills, fever, headache, 1. Discontinue the transfusion
between client’s backache, dyspnea, immediately. NOTE: when the
blood and donor’s cyanosis, chest pain, transfusion is discontinued, use new
blood tachycardia, tubing for the normal saline
hypotension infusion.
2. Notify primary care provider
immediately.
3. Monitor vital signs.
4. Monitor fluid intake and output.
5. Send the remaining blood, bag,
filter, tubing, a sample of the
client’s blood, and a urine sample to
the laboratory.
2.FEBRILE REACTION:
CAUSE CLINICAL SIGNS NURSING INTERVENTIONS
sensitivity of the Fever, chills, warm 1. Discontinue the
client’s and flushed skin, transfusion immediately.
blood to white headache, 2. Give antipyretics as ordered.
blood anxiety, muscle pain 3. Notify the primary
cells, platelets, or care provider.
plasma 4. Keep the vein open with a normal
proteins saline infusion.
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3.ALLERGIC REACTION (MILD)
CLINICAL SIGNS NURSING INTERVENTIONS
Flushing, itching, 1. Stop or slow the transfusion,
urticaria, bronchial depending on agency protocol.
wheezing 2. Notify the primary care provider.
3. Administer antihistamines as
ordered.
4.ALLERGIC REACTION (SEVERE)
CLINICAL SIGNS NURSING INTERVENTIONS
Dyspnea, chest pain, 1. Stop the transfusion.
circulatory collapse, 2. Keep the vein open with a normal
cardiac arrest saline solution.
3. Notify the primary care provider
immediately.
4. Monitor vital signs. Administer CPR if
needed.
5. Administer medications or oxygen as
ordered.
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5.CIRCULATORY OVERLOAD
CAUSE CLINICAL SIGNS NURSING INTERVENTIONS
blood administered Cough, dyspnea, 1. Place the client upright, with feet
faster than the crackles (rales), dependent.
circulation can distended neck veins, 2. Stop or slow the transfusion.
accommodate tachycardia, 3. Notify the primary care provider.
hypertension 4. Administer diuretics or oxygen as
ordered.
6.SEPSIS
CAUSE CLINICAL SIGNS NURSING INTERVENTIONS
Contaminated blood High fever, chills, 1. Stop the transfusion.
administration. vomiting, diarrhea, 2. Keep the vein open with a normal
hypotension saline solution infusion.
3. Notify the primary care provider.
4. Administer IV fluids, Antibiotics.
5. Obtain a blood specimen from
the client for culture. 6. Send the
remaining blood and tubing to the
laboratory
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BLOOD PRODUCTS
PACKED RED BLOOD CELLS FRESH FROZEN PLASMA
(PRBCS) (FFP)
Most common type of Plasma is the liquid component of blood;
blood product for transfusion it has proteins called clotting factors
Used to increase the oxygen-carrying Expands blood volume and provides
capacity of blood clotting factors. Contains no RBCs 1 unit
Help the body get rid of carbon dioxide of FFP = increases level of any clotting
and other waste products factor by 2-3%
1 unit of PRBCs =
raises hematocrit by 2-
3% ALBUMIN AND PLASMA PROTEIN
FRACTION
Blood volume expander Provides
PLATELETS plasma protein
Also known as thrombocytes
Tiny cell structures necessary in
blood clotting process
CLOTTING FACTORS AND
Replaces platelets in clients with CRYOPRECIPITATE
A portion of plasma containing certain
bleeding disorders, or platelet
specific clotting factors
deficiency
Used for clients with clotting factor
1 unit = increases the average adult
deficiencies
client’s platelet count by about
Contains Fibrinogen
5,000 platelets/microliter
AUTOLOGOUS RED BLOOD
WHOLE BLOOD CELLS
Not commonly used except for extreme Used for blood replacement following
cases of acute hemorrhage planned elective surgery
Replaces blood volume and all blood Must be donated 4-5 weeks prior to
products surgery
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THE NURSING PROCESS
''ADPIE''
1.Assessment
Gather information & review
Verify the information collected is clear & accurate
2. Diagnosis
Interpret the information collected
Identify & prioritize the problem through a nursing
diagnosis
3. Planning
Set goals to solve the problem
Prioritize the outcomes of care
4. Implementation
Reaching those goals through performing the
nursing action
"Implementing" the goals set above in the planning
stage
5. Evaluation
Determine the outcome of the goals
Evaluate the patient compliance
Document client's response to pain
Modify & assess for needed changes
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ABBREVIATIONS
ABD Abdomen
A.B.G Arterial blood gas
ADL Activities of daily living
A.C Before meals
A&O Alert & Oriented
BP Blood pressure
DC Discontinue
H&H Hemoglobin & Hematocrit
DNR Do not resuscitate
ICU Intensive care unit
I&O Intake & output
IM Intramuscular
IV Intravenous
NGT Nasogastric tube
NPO Nothing by mouth
CPR Cardiopulmonary
PPE Resuscitation
Personal Protective
Equipment
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ABBREVIATIONS
DX Diagnosis
ECG Electrocardiogram
Fx Fracture
h.s At bedtime
HOB Head of bed
HOH Hard of hearing
H&P History & physical
HR Heart rate
PO By mouth
P.R.N As needed
ROM Range of motion
S&S Signs & Symptoms
STAT Immediately
U/A Urinalysis
VS Vital Signs
PERRLA Pupils equal, round,
reactive to light &
accomodation
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NURSING ETHICS & LAW
PATIENT RIGHTS HIPAA
Privacy The Health Insurance
Considerate & respectful care Portability &
Be informed Accountability Act
Know the names & roles of the Patient's records are
persons who are involved in care private & they have the
Consent or refuse a treatment right to ensure the
Have an advance directive medical information is
Obtain their own medical not shared without
records & results permission
All health care
professionals must
inform the patient how
their health information
is used.
The patient has the right
to obtain a copy of their
personal health
information
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ETHICAL PRINCIPLES respect for an individual's right to make
AUTONOMY
their own decision
NONMALEFICENCE obligation to do & cause no harm to others
BENEFICENCE duty to do good to others
JUSTICE distribution of benefits & services fairly
VERACITY obligation to tell the truth
FIDELITY following through with a promise
TYPES OF CONSENT
Admission Agreement Surgical Consent
Immunization Consent Research Consent
Blood Transfusion Special Consent
Treatment cannot be done without the patient's consent.
In case of emergency when a patient cannot give consent, consent is
implied through emergency laws.
Those under 18 (minors), consent must be obtained from a parent or
legal guardian.
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Take note!
Before signing the consent, the pt must be informed
of the ff risks & benefits of
surgery, treatments, procedures, & plan of care in
layman's terms so the pt
understands clearly what is being done.
MANIPULATION NCP
Promote 3C's
Cooperation
Compromise
Collaboration
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ROLES AND FUNCTION
OF A NURSE
Change agent Caregiver
identifies a vision and As a caregiver, a nurse
rationale for the change and is provides hands-on care to
a role model for nurses and patients in a variety of settings.
other health care personnel. This includes physical needs,
which can range from total
Leader care (doing everything for
A nurse leader oversees a someone) to helping a patient
team of nurses, making with illness prevention.
decisions and directing
patient care initiatives. They
Communicator
have advanced clinical As a communicator, the nurse
knowledge and are focused understands that effective
on improving patient health communication techniques
outcomes can help improve the
healthcare environment.
Manager Barriers to effective
esponsible for managing human communication can inhibit
and financial resources; the healing proces
ensuring patient and staff
satisfaction; maintaining a safe
environment for staff, patients,
and visitors; ensuring standards
and quality of care are
maintained; and aligning the
unit's goals with the hospital's
strategic goals
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Teacher Case Manager
Nurse educators inspire, teach, A nurse case manager develops,
and mentor the next generation implements, and reviews
of nurses, leading the way to the healthcare plans for patients
future of patient care that are geriatric, recovering
from serious injuries, or dealing
Client advocate with chronic illnesses.
A nurse advocate is a nurse who Researcher
works on behalf of patients to
maintain quality of care and identify research questions,
protect patients' rights. design and conduct scientific
studies, collect and analyze data
Counselor and report their findings
the nurse may represent the
client's needs and wishes to
other health professionals, such
as relaying the client's wishes
for information to the
physician.
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GLASGOW COMA SCALE
Behaviour Response
4. Spontaneously
3. To speech
2. To pain
Eye opening response 1.No response
5. Oriented in time, person and place
4. Confused
3. Inappropriate words
2. Incomprehensible sounds
Verbal response 1. No response
6. Obeys command
5. Moves to localised pain
4. Flex to witthdraw from pain
3. Abnormal flexion
Motor response 2. Abnormal extension
1. No response
MASLOW'S HIERARCHY OF BASIC NEEDS
the realization of one's best qualities +
drive to reach their full potential
Self-respect and independence
Affection, feeling loved, relationship
Physical + emotional safety
air, food, water, shelter, sleep and
temperature regulation
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LABORATORY AND DIAGNOSTIC EXAMINATIONS
Urine Specimen
1.Clean-Catch mid-stream urine
-specimen for routine urinalysis, culture and sensitivity test
Best time to collect is in the morning, first voided urine
Provide sterile container
Do perineal care before collection of the urine
Discard the first flow of urine
Label the specimen properly
Send the specimen immediately to the laboratory
Document the time of specimen collection and transport to the lab.
Document the appearance, odor, and usual characteristics of the specimen
2. 24-hour urine specimen
Discard the first voided urine
Collect all specimens thereafter until the following day
Soak the specimen in a container with ice
Add preservative as ordered according to hospital policy
3. Second-Voided urine
Discard the first urine
Give the patient a glass of water to drink
After few minutes, ask the patient to void
4. Catheterized urine specimen
Clamp the catheter for 30 min to 1 hour to allow urine to accumulate in the
bladder and adequate specimen can be collected.
Clamping the drainage tube and emptying the urine into a container are
contraindicated after a genitourinary surgery
Stool Specimen
1.Fecalysis
to assess gross appearance of stool and presence of ova or parasite
Stool Specimen
Secure a sterile specimen container
Ask the pt. to defecate into a clean, dry bed pan or a portable commode
Instruct client not to contaminate the specimen with urine or toilet
paper (urine inhibits bacterial growth and paper towel contain bismuth
which interfere with the test result.
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2. Stool culture and sensitivity test
To assess specific etiologic agent causing gastroenteritis and bacterial
sensitivity to various antibiotics.
3. Fecal Occult blood test
Are valuable test for detecting occult blood (hidden) which may be
present in colo-rectal cancer, detecting melena stool
Hematest – (an Orthotolidin reagent tablet)
Hemoccult slide– (filter paper impregnated with guaiac)
Both test produces blue reaction id occult blood lost exceeds 5 ml in 24 hours.
Colocare – a newer test, requires no smear
Instructions
Advise client to avoid ingestion of red meat for 3 days
Patient is advice on a high residue diet
Avoid dark food and bismuth compound
If client is on iron therapy, inform the MD
Make sure the stool in not contaminated with urine, soap solution or toilet paper
Test sample from several portion of the stool.
VENIPUNCTURE
Never collect a venous sample from the arm or a leg that is already being
use d for I.V therapy or blood administration because it mat affect the
result.
Never collect venous sample from an infectious site because it may
introduce pathogens into the vascular system
Never collect blood from an edematous area, AV shunt, site of previous
hematoma, or vascular injury.
Don’t wipe off the povidine-iodine with alcohol because alcohol cancels the
effect of povidine iodine.
If the patient has a clotting disorder or is receiving anticoagulant coagulant
therapy, maintain
pressure on the site for at least 5 min after withdrawing the needle.
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Arterial puncture for ABG test
Before arterial puncture, perform Allen’s test first. If the patient is receiving oxygen,
make sure that the patient’s therapy has been underway for at least 15 min before
collecting arterial sample Be sure to indicate on the laboratory request slip the amount
and type of oxygen therapy the patient is having. If the patient has just received a
nebulizer treatment, wait about 20 minutes before collecting the sample.
Blood Specimen
No fasting for the following tests:
CBC, Hgb, Hct, clotting studies, enzyme studies, serum electrolytes
Fasting is required:
FBS, BUN, Creatinine, serum lipid (cholesterol, triglyceride)
Sputum Specimen
1.Gross appearance of the 3. Acid-Fast Bacilli
sputum To assess presence of active
Collect early in the morning
pulmonary tuberculosis
Use sterile container
Collect sputum in three consecutive
Rinse the mount with plain water before
mornings
collection of the specimen
Instruct the patient to hack-up sputum
2. Sputum culture and 4. Cytologic sputum exam
sensitivity test To assess for presence of abnormal
Use sterile container or cancer cells.
Collect specimen before the first
dose of antibiotic
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BLOOD COMPONENTS
Antigen
Proteins that elicit immune response
Identifies the cell
Plasma Antibodies
Protects body from “invaders” (think
ANTI) Opposite of the type of antigen
that is found on the RBC
Blood Plasma
Components 55%
RBC's
45%
Rh factor
Has Rh on surface Can receive
Does not have Rh Can receive
on surface
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LAB VALUE MEMORY TRICKS
Electrolytes
Potassium: 3.5-5.0 mEq/L Magnesium: 1.5 - 2.5
You buy 3-5 bananas MAGnifying glass
at a time. uou see 15 - 25
bigger than normal
Chloride: 98-106 mEq/L Phosphorus: 2.5-4.5
Think of a chlorinated pool that you PHOR: 4
want to go in when its SUPER HOT: 95- US:2(me+you=2)
105°F *dont forget the 5
Calcium: 9-11 mg/dL Sodium 135-145
CALL 911 *commit to memory!
COMPLETE BLOOD COUNT (CDC)
Hemoglobin Female
Female: 12-16 g/dL 12 x 3 = 36
Male: 13 - 18 g/dL 16 x 3 = 48
To remember HCT,
Hematocrit Male
multiply Hgb by 3
Female: 36% 0 48% 12 x 3 = 36
Male: 39% - 54% 16 x 3 = 48
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BASAL METABOLIC PANEL (BMP)
BUN: 7- 20 mg/dL Creatinine: 0.6-1.2 mg/dL
Think of hamburger BUNs.. This is the same value as
Hamburgers can cost anywhere LITHIUM's therapeutic range
from $7- $20 dollars (0.6 - 12 mmol/L)
Lithium is excreted almost
solely by the kidneys.
And creatinine is a value that
tests how well your
kidneys filter
BLOOD TRANSFUSION
ADVANTAGES OF BLOOD COMPONENT THERAPY
Avoids the risk of sensitizing the patients to other blood components.
Provides optimal therapeutic benefit while reducing risk of volume overload.
Increases availability of needed blood products to larger population.
Principles of blood transfusion therapy
1.Whole blood transfusion
Indicated only for patients who need both increased oxygen- carrying capacity
and restoration of blood volume when there is no time to prepare or obtain
the specific blood components needed.
2. Packed RBCs
Should be transfused over 2 to 3 hours; if patient cannot tolerate volume over a
maximum of 4 hours, it may be necessary for the blood bank to divide a unit into
smaller volumes, providing proper refrigeration of remaining blood until needed.
One unit of packed red cells should raise hemoglobin approximately 1%, hemactocrit
3%.
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3. Platelets
Administer as rapidly as tolerated (usually 4 units every 30 to 60 minutes).
Each unit of platelets should raise the recipient’s platelet count by 6000 to
10,000/mm3: however, poor incremental increases occur with alloimmunization
from previous transfusions, bleeding, fever, infection, autoimmune
destruction, and hypertension.
4. Granulocytes
May be beneficial in selected population of infected, severely granulocytopenic
patients (less than 500/mm3) not responding to antibiotic therapy and who are
expected to experienced prolonged suppressed granulocyte production
5. Plasma
Because plasma carries a risk of hepatitis equal to that of whole blood, if only
volume expansion is required, other colloids (e.g., albumin) or electrolyte
solutions (e.g., Ringer’s lactate) are preferred. Fresh frozen plasma should be
administered as rapidly as tolerated because coagulation factors become unstable
after thawing.
6. Albumin
Indicated to expand to blood volume of patients in hypovolemic shock and to
elevate level of circulating albumin in patients with hypoalbuminemia. The large
protein molecule is a major contributor to plasma oncotic pressure.
7. Cryoprecipitate
Indicated for treatment of hemophilia A, Von Willebrand’s disease, disseminated
intravascular coagulation (DIC), and uremic bleeding.
8. Factor IX concentrate
Indicated for treatment of hemophilia B; carries a high risk of hepatitis
because it requires pooling from many donors
9. Factor VIII concentrate
Indicated for treatment of hemophilia A; heat-treated product decreases the
risk of hepatitis and HIV transmission
10. Prothrombin complex
Indicated in congenital or acquired deficiencies of these factors.
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ADMINISTRATION OF THE TRANSFUSION
Insert and IV line using an 18-19-gauge IV needle
Run it with normal saline (keep vein open rate)
Use the largest catheter part available
Begin the transfusion slowly
a. The first 15 min "MOST CRITICAL"
, monitor the patient for S/S of
any transfusion reaction.
b. Vital signs are monitored every 30 mins to 1 hour.
c. After 15 mins, the flow can be increased unless transfusion
reaction occurred.
5. Document the client's tolerance to the administration of blood
product.
TRANSFUSION REACTION
Is an adverse reaction that happens as a result of receiving blood transfusion
Immediate chills, diaphoresis, aches, chest pain, rash, hives, itching,
transfusion reaction swelling rapid, thready pulse, dyspnea, cough or wheezing
Circulatory overload Rise in venous pressure, Dyspnea, Crackles or rales,
Septicemia Distended neck vein, Cough, Elevated BP
Iron overload Rapid onset of chills, Vomiting, Marked Hypotension,
High fever
Vomiting, Diarrhea, Hypotension, Altered hematologic
values
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NURSING ACTIONS TO A TRANSFUSION REACTION
Stop the infusion
Change the IV tubing down to the IV site
Keep the IV open w/ normal saline
Notify the HCP and blood bank
Do not leave the client alone (monitor vs & continue
to assess the patient
FACTS ABOUT BLOOD TRANSFUSION
Administered by the RN
Only Normal Saline (NS) can be used in conjunction with blood
Type & screen and a cross match are good for 72 hours
30 minutes - from the time you received it from the blood bank to the
time you infuse
4 hours - All blood must be transfused
STOP the transfusion if you suspect transfusion reaction
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LABORATORY VALUES
- BUN: 5-20 mg/dL - Erythrocytes (RBC): 4.5-5.0 million/L
- Creatinine: 0.6-1.3 mg/dL - Leucocytes (WBC): 4,500-11,000
- Creatinine clearance: 90-130 ml/min cells/mm3 (Neutropenia
- Total cholesterol: 140-199 mg/dL <1000/mm3/ Severe neutropenia:
- HDL: 30-70 mg/dL <500/mm3)
- LDL: <130 mg/dL - Neutrophils: 1800-7800 cells/mm3
- Triglycerides: <200 mg/dL - Lymphocytes: 1000-4800 cells/mm3
- Protein: 6-8 g/dL - Potassium: 3.5-5.0 mEq/L
- Albumin: 3.4-5 g/dL - Sodium: 135-145 mEq/L
- Chloride: 98-107 mEq/L
- Alanine aminotransferase (ALT): 10-40 units/L
- Phosphate: 2.5-4.5 mg/dL
- Aspartate aminotransferase (AST): 10-30 units/L
- Magnesium: 1.6-2.6 mg/dL
- Total Bilirubin: <1.5 mg/dL
- Phosphorus: 2.7-4.5 mg/dL
- Uric acid: 3.5—7.5 mg/dL
- Calcium: 8.6-10 mg/dL
- CPK: 21-232 U/L
- Digoxin: 0.8—2.0 ng/ml
- Glucose: 70-110 mg/dL
- Lithium: 0.8—1.5 mEq/L
- Hemoglobin A1c:
- Phenytoin: 10—20 mcg/dL
4%-5.9%: nondiabetic - Theophylline (Aminophylline): 10—20
<7%: good diabetic control mcg/dL
7% to 8%: fair diabetic control
>8%: poor diabetic control
- Hemoglobin:
Female: 12-15 g/dL
Male: 14-16.5 g/dL
- Hematocrit:
Female: 35%-47%
Male: 42%-52%
- Platelets: 150,000-400,000 cells/mm3
- aPTT: 20-36 sec, depending on testing method
Therapeutic (Heparin): 46-70 seconds
- Prothrombin time (PT): 9.5-11.8 sec
- International Normalized Ratio (INR):2-3: standard
warfarin therapy
3-4.5: high-dose warfarin therapy
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ABG VALUES &
EVALUATION
HYPERKALEMIA
- pH: 7.35—7.45
- HCO3: 24—26 mEq/L Causes:
- CO2: 35—45 mEq/L “The body CARED too much about potassium”
- PaO2: 80%—100% Cellular movement of K from intracellular to
- SaO2: >95% extracellular (burns, tissue damages, acidosis).
Adrenal insufficiency with Addison’s Disease.
Renal failure. Excessive K intake. Drugs (K-
sparing like spironolactone, triamterene, ACE
inhibitors, NSAIDS).
Signs & Symptoms (MURDER):
Muscle weakness. Urine production little or none
(renal failure).
Respiratory failure. Decreased cardiac
HYPOKALEMIA contractility (weak pulse, low BP).
Early signs of muscle twitches/cramp…
Causes: Late profound weakness, flaccidity. Rhythm
“Your body is trying to DITCH potassium” changes.
Drugs (laxatives, diuretics, corticosteroids)
HYPOCALCEMIA
Inadequate consumption of K (NPO, anorexia).
Too much water intake (dilutes the K).
Cushing’s syndrome (the adrenal glands Causes (LOW CALCIUM):
produce excessive amounts of aldosterone). Low parathyroid hormone due (any neck
Heavy fluid loss (NG suction, vomiting, diarrhea, surgery: check the Ca level). Oral intake
wound drainage, excessive diaphoresis). inadequate (alcoholism, bulimia etc.). Wound
drainage (especially GI system). Celiac’s &
Crohn’s disease (malabsorption of Ca). Acute
Signs & Symptoms:
pancreatitis. Low vitamin D levels. Chronic
Everything is going to be SLOW and LOW.
kidney issues (excessive excretion). Increased
- Weak pulses (irregular and thread).
phosphorus levels in the blood. Using certain
- Orthostatic hypotension.
medications (Ma supplements, laxatives, loop
- Shallow respirations with diminished breath
diuretics, Ca binder drugs). Mobility issues
sounds.
- Confusion and weakness.
Signs & Symptoms (CRAMPS):
- Flaccid paralysis.
Confusion.
- Decrease deep tendon reflexes.
Reflexes: hyperactive.
- Decreased bowel sounds.
Arrhythmias.
Muscle spasms in calves or feet, tetany, seizures.
Positive Trousseau’s (happens before Chvostek’s
sign and tetany).
Signs of Chvostek’s.
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HYPERCALCEMIA HYPONATREMIA
Causes (HIGH CAL): Causes (NO Na):
Hyperparathyroidism (++ Ca released in Na excretion increased (renal
the blood). problems, NG suction, vomiting,
Increased intake of Ca. diuretics, sweating, diarrhea,
Glucocorticoids (suppresses Ca secretion of aldosterone).
absorption). Overload of fluid (congestive heart
Hyperthyroidism. failure, hypotonic fluids
Calcium excretion decreased (Diuretics, infusions, renal failure).
renal failure, bone cancer). Na intake low (low salt diets or NPO).
Adrenal insufficiency (Addison’s disease). Antidiuretic hormone over secretion
Lithium usage (affects the parathyroid (SIADH).
gland).
Signs & Symptoms (SALT LOSS):
Signs & Symptoms: Seizures & Stupor.
“The body is too WEAK” Abdominal cramping, Attitude changes
Weakness of muscles (profound). (confusion).
EKG changes. Lethargic.
Absent reflexes & minded (disorientated), Tendon reflexes diminished, Trouble
Abdominal concentrating (confused).
distention from constipation. Loss of urine and appetite.
Kidney stone formation. Orthostatic hypotension, Overactive bowel
sounds.
HYPERNATREMIA Shallow respirations (due to skeletal
muscle weakness).
Causes (HIGH SALT): Spasms of muscles.
Hyperventilation, Hypercortisolism
(Cushing’s syndrome).
Increased intake of sodium (oral or IV).
GI feeding (tube) without adequate water
supplements.
Hypertonic solutions. Sodium excretion
decreased and corticosteroids.
Aldosterone insufficiency.
Loss of fluids, infection (fever),
diaphoresis, diarrhea, and diabetes
insipidus). Thirst impairment.
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HYPERNATREMIA HYPOPHOSPHATEMIA
Signs & Symptoms: Causes (Low PHOSPHATE):
“No FRIED foods for you!” Pharmacy (aluminum hydroxide-based
Fever, Flushed skin. or magnesium-based
Restless, Really agitated. antacids cause malabsorption in the GI
Increased fluid retention. system).
Edema, Extremely confused. Hyperparathyroidism (there is an over
Decreased urine output, Dry mouth/skin. secretion of PTH which
causes phosphate to not be reabsorbed).
Oncogenic osteomalacia.
HYPOPHOSPHATEMIA Syndrome of Refeeding: causes
Signs & Symptoms (BROKEN): electrolytes and fluid problems
Breathing problems (due to muscle due to malnutrition or starvation (watch
weakness). for per os after TPN).
Rhabdomyolysis (tea-colored urine, Pulmonary issues such as respiratory
muscle weakness/pain), alkalosis.
Reflexes (deep tendon) decreased. Hyperglycemia. Alcoholism. Thermal
Osteomalacia (softening of the bones) Burns. Electrolyte imbalances:
fractures and decreased hypercalcemia, hypomagnesemia,
bone density (alteration in bone shape), hypokalemia.
cardiac Output
decreased.
Kills immune system with immune
HYPERPHOSPHATEMIA
suppression and decreases Causes (PHOS-HI):
platelet aggregation. Phospho-soda overuse: phosphate
Extreme weakness, Ecchymosis. containing laxatives or
Neuro status changes (irritability, enemas (Sodium Phosphate/Fleets enema).
confusion, seizures). Hypoparathyroidism.
Overuse of vitamin D.
HYPERPHOSPHATEMIA Syndrome of Tumor Lysis.
rHabdomyolysis.
Signs & Symptoms (CRAMPS): Insufficiency of kidneys (renal failure is
Confusion. the main cause).
Reflexes hyperactive.
Anorexia.
Muscle spasms in calves or feet, tetany,
seizures.
Positive Trousseau’s Signs, Pruritus.
Signs of Chvostek.
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HYPOMAGNESEMIA HYPERMAGNESEMIA
Causes (LOW MAG): Causes (MAG)*:
Limited intake of Mg (starvation). Magnesium containing antacids and
Other electrolyte issues (hypokalemia, laxatives.
hypocalcemia). Addison’s disease (adrenal
Wasting Magnesium kidneys (loop and insufficiency).
thiazide diuretics; Glomerular filtration insufficiency
cyclosporine). (<30mL/min).
Malabsorption issues (Crohn’s and celiac *Hypermagnesemia is less common than
diseases, “-prazole” hypomagnesemia. It
drugs, diarrhea/vomiting). typically happens when trying to
Alcohol (stimulates the kidneys to correct hypomagnesemia with
excreted Mg). magnesium sulfate IV infusion.
Glycemic issues (diabetic ketoacidosis,
insulin administration).
Signs & Symptoms (LETHARGIC)*:
*Happens in severe hypermagnesemia,
Signs & Symptoms (TWITCHING): mild one is
Trousseau’s (positive due to asymptomatic.
hypocalcemia). Lethargy (profound).
Weak respirations. EKG changes (prolonged PR & QR
Irritability. interval and widened QRS
Torsades de pointes, Tetany (seizures). complex).
Cardiac changes, Chvostek’s sign. Tendon reflexes absent or grossly
Hypertension, Hyperreflexia. diminished.
Involuntary movements. Hypotension.
Nausea. Arrhythmias (bradycardia, heart
GI issues (decreased bowel sounds and blocks).
mobility). Respiratory arrest.
GI issues (nausea, vomiting).
Impaired breathing (due to skeletal
weakness).
Cardiac arrest.
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THERAPEUTIC DIETS
- Acute renal disease: protein-restricted, high-calorie, fluid ->
controlled, Na and K controlled.
- Addison’s disease: high sodium, low potassium.
- ADHD and bipolar: high-calorie and provide finger foods.
- Anemia: high protein/iron/vitamins.
- Atherosclerosis: low saturated fats.
- Burns: high protein, high caloric, -> Vitamin C.
- Cancer: high-calorie, high-protein.
- Celiac disease: gluten-free (no BROW: wheat, oats, rye,
barley).
- Cholecystitis/Cholelithiasis: low fat liquids, powder
supplements high in protein/carb into skim milk; avoid fried
foods, pork, cheese, alcohol.
- After surgery may need low fat diet for several weeks.
- Low fat, high carb/protein.
- Chronic renal disease: protein-restricted, low-sodium, fluid -->
restricted, potassium-restricted, phosphorus-restricted.
- Cirrhosis (stable): normal protein.
- Cirrhosis with hepatic insufficiency: restrict protein, fluids,
and sodium.
- Constipation: high-fiber, increased fluids.
- COPD: soft, high-calorie, low-carbohydrate, high-fat, small
frequent feedings.
- Cushing’s disease: low sodium, high potassium.
- Cystic fibrosis: increase in fluids; pancreatic enzyme
replacement before or with meals; high protein, high calorie in
advanced stages.
- Diarrhea: liquid, low-fiber, regular, fluid and electrolyte
replacement.
- Diverticular disease: high-fiber, avoid seeds.
- Dumping syndrome (rapid passage of food: diaphoresis,
diarrhea, hypotension): restrict fluids w/ meals, drink 1h
before or 1h after; eat in recumbent position, lie down 20-30
min after eating; small frequent meals; low-carb/low-fiber.
- Gallbladder disease: low-fat, calorie-restricted.
- Gastritis: low-fiber, bland diet.
- Gout: low purine (no fish and organ meats).
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- Hypertension, heart failure, CAD: low-sodium, calorie->restricted, fat-controlled.
- Kidney stones: increased fluid intake, calcium-controlled,
low-oxalate.
- Meniere’s: low sodium, avoid caffeine, nicotine and alcohol.
- Nephrotic syndrome: sodium-restricted, high-calorie, high protein, potassium-restricted.
- Obesity/Overweight: calorie-restricted, high-fiber .
- Ostomy: high calorie/protein/carb; low residue before
surgery.
- Ileostomy: low residue diet, no meats, corn, nuts.
- Colostomy: diet not restricted after 6 weeks.
- Pancreatitis: low-fat, regular, small frequent feedings; tube
feeding or total parenteral nutrition.
- Peptic ulcer: bland diet.
- Pernicious anemia: Vitamin B12.
- IM B12 shot (25-100 g), followed by 500-1000 g shot
every 1-2 months or cyanocobalamin nasal spray.
- Phenylketonuria (PKU): special milk substitutes for infants,
low protein for children.
- Pheochromocytoma: increase calories, vitamins and minerals
intake; avoid coffee, tea, cola, tyramine foods.
- Sickle cell anemia: increase fluids to maintain hydration since
sickling increases when patients become dehydrated.
- Stroke: mechanical soft, regular, or tube-feeding.
- Underweight: high-calorie, high protein.
- Ulcerative colitis & Crohn’s disease: high protein/calorie; low
fat/fiber.
- Ulcers: 3 meals/day, avoid Tº extremes, avoid
caffeine/alcohol/milk&cream.
- Postoperative: Vit B12 parenteral for life and iron
supplements.
- Vomiting: fluid and electrolyte replacement.
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COMMON SIGNS AND SYMPTOMS
- Pulmonary tuberculosis: low-grade afternoon fever.
- Pneumonia: rust-colored sputum.
- Asthma: wheezing on expiration.
- Emphysema: barrel chest.
- Pernicious anemia: red beefy tongue.
- Cholera: rice-watery stool and wrinkled hands from
dehydration.
- Malaria: stepladder like fever with chills.
- Typhoid: rose spots in the abdomen.
- Dengue: fever, rash, and headache; positive Herman’s sign.
- Diphtheria: pseudo membrane formation.
- Measles: Koplik’s spots (clustered white lesions on buccal
mucosa).
- Systemic lupus erythematosus: butterfly rash.
- Leprosy: leonine facies (thickened folded facial skin).
- Appendicitis: rebound tenderness at McBurney’s point;
Rovsing’s sign (palpation of LLQ elicits pain in RLQ); psoas sign
(pain from flexing the thigh to the hip).
- Meningitis: Kernig’s sign (stiffness of hamstrings causing
inability to straighten the leg when the hip is flexed to 90º);
Brudzinski’s sign (forced flexion of the neck elicits a reflex
flexion of the hips).
- Tetany: hypocalcemia; positive Trousseau’s and Chvostek
sign.
- Tetanus: Risus sardonicus or rictus grin.
- Pancreatitis: Cullen’s sign (ecchymosis of the umbilicus); Grey
Turner’s sign (bruising of the flank).
- Pyloric stenosis: olive like mass.
- Patent ductus arteriosus: washing machine-like murmur.
- Addison’s disease: bronze-like skin pigmentation.
- Cushing’s syndrome: moon face appearance and buffalo
hump.
- Graves’ disease (hyperthyroidism): Exophthalmos.
- Intussusception: sausage-shaped mass.
- Multiple sclerosis: Charcot’s triad: nystagmus, intention
tremor, and dysarthria.
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- Myasthenia gravis: descending muscle weakness, ptosis.
- Guillain-Barre syndrome: ascending muscle weakness.
- Deep vein thrombosis: Homan’s sign.
- Angina: crushing, stabbing pain relieved by nitroglycerin
(NTG).
- Myocardial Infarction: crushing, stabbing pain radiating to left
shoulder, neck, and arms; unrelieved by NTG.
- Cytomegalovirus infection: owl’s eye appearance of cells
(huge nucleus in cells).
- Retinal detachment: flashes of light, shadow with curtain
across vision.
- Basilar skull fracture: raccoon eyes (periorbital ecchymosis)
and Battle’s sign (mastoid ecchymosis).
- Buerger’s disease: intermittent claudication (pain at buttocks
or legs from poor circulation resulting in impaired walking).
- Diabetic ketoacidosis: acetone breathe.
- Pre-eclampsia: proteinuria, hypertension, edema.
- Diabetes mellitus: polydipsia, polyphagia, polyuria.
- Hirschsprung’s Disease (Toxic Megacolon): ribbon-like stool.
- Herpes Simplex Type II: painful vesicles on genitalia.
- Genital Warts: warts 1-2 mm in diameter.
- Syphilis: painless chancres.
- Chancroid: painful chancres.
- Gonorrhea: green, creamy discharges and painful urination.
- Chlamydia: milky discharge and painful urination.
- Candidiasis: white cheesy odorless vaginal discharges.
- Trichomoniasis: yellow, itchy, frothy, and foul-smelling vaginal
discharges.
- Pulmonary edema: pink, frothy sputum, tachypnea, use of
accessory muscles, crackles, anxiety/restlessness (Tx:
furosemide).
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MEDICATION MISCELLANEOUS
HIGH ALERT MEDICATIONS NARROW THERAPEUTIC RANGE DRUGS
- Insulin. - Gentamicin.
- Opiates and narcotics. - Vancomycin.
- Injectable potassium chloride (or - Warfarin.
phosphate) concentrate. - Lithium.
- IV coagulants (heparin). - Digoxin.
- Sodium chloride solutions >0.9%. - Theophylline.
- Methotrexate.
- Phenytoin.
- Insulin.
- Ciclosporin.
*Rifampicin: causes red-orange tears and urine.
*Ethambutol: causes problems with vision, liver problem.
*Isoniazid: can cause peripheral neuritis; take vitamin B6 to
counter.
MONOAMINE OXIDASE INHIBITORS (MAOI’s):
- Tyramine-rich foods may cause severe hypertension in
patients who take MAOI’s.
- Tyramine-rich foods include: aged cheese, chicken liver,
avocados, bananas, meat tenderizer, salami, bologna, Chianti
wine, and beer.
PYRIDIUM:
- Urinary tract analgesic and spasmolytic
- Not an anti-infective
- Turns urine bright orange.
NITROGLYCERINE PATCH is administered up to three times
with intervals of five minutes.
MORPHINE:
- Contraindicated in pancreatitis because it causes spasms of
the Sphincter of Oddi.
- Meperidine (Demerol) should be given.
CLOZAPINE:
- A significant associated toxic risk is blood dyscrasia.
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MEDICATION MISCELLANEOUS
DIGOXIN:
- Assess pulses for a full minute, if less than 60 bpm hold dose.
- Check digitalis and potassium levels.
HALOPERIDOL ADVERSE EFFECTS:
ALUMINUM HYDROXIDE:
- Drowsiness.
- Treatment of GERD and kidney stones.
- Insomnia.
- WOF: constipation.
- Weakness.
- Headache
- Extrapyramidal symptoms: akathisia, tardive dyskinesia,
dystonia.
HYDROXYZINE:
- Treatment of anxiety and itching.
- WOF: dry mouth.
MIDAZOLAM:
- Given for conscious sedation.
- WOF: respiratory depression and hypotension.
AMIODARONE
- Take missed dose any time in the day or skip it entirely.
- Do not take double dose.
- WOF: diaphoresis, dyspnea, lethargy.
WARFARIN (COUMADIN)
- Stress importance of complying with prescribed dosage and
follow-up appointments.
- WOF: signs of bleeding, diarrhea, fever, rash.
METHYLPHENIDATE (RITALIN)
- Treatment of ADHD.
- Assess for heart related side-effects and report immediately.
- Child may need a drug holiday because the drug stunts
growth.
DOPAMINE
- Treatment of hypotension, shock and low cardiac output.
- Monitor ECG for arrhythmias and blood pressure.
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LAB VALUES
Complete Blood Count Vital Signs Coagulation (COAGs)
RBC Blood Pressure
PT 11 - 15 seconds
Systolic 120 mmHg
WBC 5,000 – 10,000 PTT 60 – 70 seconds
Diastolic 80 mmHg
Hemoglobin (Hgb) Respiration 12 - 20/min APTT 30 – 45 seconds
Hematocrit (Hct) Temperature 97.8 - 99F >1.5 – 2.0 *Higher for
prosthetic valve
Pulse OX 95 - 100%
Platelet 150,000 – 400,000 D-Dimer <0.5
Heart Rate 60 - 100BPM
Arterial Blood Gas (ABGs) Lipid Panel Basal Metabolic Panel (BMP)
PH 7.35 - 7.45 Total Cholesterol <200 mg/dL Potassium 3.5 - 5.0 mEq/L
Creatinine 0.6 - 1.5 mg/dL
PaCO2 35 - 45 mm Hg Tryglyceride <150 mg/dL
BUN 6 - 23 mg/dL
HCO3 22 - 26 mEq/L LDL <100 mg/dL Bad Cholesterol Total Protein 6.2 - 8.2 g/dL
O2 sat 96 – 100%
HDL >60 mg/dL Good Cholesterol Specific Gravity 1.010 – 1.030
PaO2 85 - 100 mm Hg
Amylase (AMS) 60 – 120
BE -2 to +2 mmol/L
Renal Liver Function Test (LFT) Pancreas
Calcium 8 - 11 mg/dL
ALT 4 - 36 Amylase 30 -110 U/L
Magnesium 1.5 - 2.5 mg/dL ALP 30 - 120 Lipase 0 -150 U/L
Phosphorus 2.2 - 4.8 mg/dL Albumin 3.5 - 5
Chloride 96 - 112 mEq/L Bilirubin 0.3 - 1.0
GFR 90 - 120 mL/min Ammonia (serum) 80 - 100
70 - 110 mg/dL
(diuresis greater than AST 0 - 35
or equal to 180 mg/dL)
HbA1c Cardiac
Troponin I: <0.1 ng/mL
NON-DIABETIC 4 - 5.6%
Troponin T: <0.3 ng/mL
PRE-DIABETIC 5.7 - 6.4%
Creatine Kinase: 30 - 170
DIABETIC >6.5% Myoglobin: 28 - 72 (M) 25 - 58 (E)
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LAB VALUES
Neurological Values Endocrine Values Cerebral Spinal Fluid
Cerebral Perfusion Pressure 17- Hydroxycorticosteroid Appearance Clear
70 - 90 mm Hg (17-OHCS) >4 mg/day
Glucose 40 - 85 mg/dL
5 - 15 mm Hg or Adrenocorticotrophic Osmolality 290 - 298 mOsm/L
Intracranial Pressure Hormone (ACTH) 20-100 pg/ml
5 - 10 cm H2O
Prolactin (PRL) 0-14 ng/ml 70 - 180 mm/H2O
Serum Alpha Fetoprotein Protein 15 - 45 mg/dL
(AFP) 0-44 ng/ml Total cell count 0 - 5 cells
Cl
You Can Call It As
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CARDIAC STUDY GUIDE WITH
VISUAL REFERENCE
LOCATION
•The heart is located in the thoracic cavity
• Posterior to the sternum
• Superior to the diaphragm
• Between the lungs
• The tip of the heart is called the ‘apex
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ANATOMY
The heart has:
3 layers
• pericardium
• endocardium
• myocardium
4 chambers
• 2 atrium
• 2 ventricles
4 valves
• Mitral
• Aortic
• Tricuspid
• Pulmonary
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FUNCTION
The heart pumps oxygen and nutrient
rich blood to the organs, tissues and
cells of the body, and eliminates waste products
Blood is carried from the heart to the organs through
arteries, arterioles and capillaries
Blood returns to the heart through venules and veins
LAYERS OF THE HEART
PERICARDIUM:
The heart is surrounded by a fibro serous
sac called the pericardium
The function of the pericardium is:
• To limit cardiac distension and restrict
excessive movement
• To protect and lubricate
The pericardium is composed of:
• Visceral pericardium
• Parietal pericardium
• Pericardial cavity
ENDOCARDIUM:
• Innermost/deepest layer of the heart
• Lines the heart chambers and the valves
• Smooth thin lining to reduce friction of
blood flow through the chambers
• Cardiac conduction system located in this
layer
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MYOCARDIUM:
• Middle, thickest layer
of the heart
• Contains the muscle fibres
which are responsible for
pumping
• Contraction of this layer
allows blood to be pumped
through to the blood vessels
HEART IS DIVIDED INTO FOUR CHAMBERS:
A: Right Atrium
V: Right Ventricle
A: Left Atrium
V: Left Ventricle
The upper chambers are: The lower chambers are:
• The atria • The ventricles
- Right - Right
- Left - Left
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THE RIGHT ATRIUM: LOWER CHAMBERS
Receives deoxygenated blood from The right ventricle:
the body through the: Receives de-oxygenated blood
• superior vena cava (head and as the right atrium contracts
The left ventricle:
upper body)
Receives oxygenated blood
• inferior vena cava (legs and lower as the left atrium
torso) contracts
THE CARDIOVASCULAR SYSTEM
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The Cardiovascular System consists of the: Pulmonary circulation and the heart
• Heart The inferior and superior vena cava carry oxygen depleted
• Lungs blood to the relaxed right atrium of
the heart
• Blood vessels
The right atrium contracts and blood travels through the
it includes: tricuspid valve into the relaxed right
• Pulmonary circulation ventricle
• Systemic circulation The right ventricle contracts, the blood is pumped through
Pulmonary circulation is: the pulmonary valve into the
The carriage of oxygen-depleted blood away pulmonary artery to the lungs
from the heart to the lungs via the pulmonary as exchange occurs in the lungs
artery o2 is released and oxygen is absorbed
The return of oxygen-rich blood to the heart
via the pulmonary vein Systemic circulation
Systemic circulation is:
• The carriage of oxygen-rich blood
away from the heart to the body
• The return of oxygen-depleted blood
back to the heart
Systemic circulation and the heart
• Oxygen rich blood travels from the lungs via the
pulmonary veins to the left atrium
• The left atrium contracts, and blood flows through
the mitral valve into the relaxed left ventricle
• The strong left ventricle contracts and pumps oxygen
rich blood through the aortic valve into the aorta
• The aorta carries blood to the organs of the body
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CARDIAC DISORDERS
Angina
Angina:
A type of chest pain caused by reduced blood flow to the heart. Angina is
a symptom of coronary artery disease.It feels like squeezing, pressure,
heaviness, tightness or pain in the chest. It can be sudden or recur over time.
Depending on severity, it can be treated by lifestyle changes, medication,
angioplasty or surgery.
UNSTABLE ANGINA & NON–ST ELEVATION MYOCARDIAL INFARCTION
Unstable angina (UA) and non–ST elevation myocardial infarction (NSTEMI) are clinical syndromes
characterized by myocardial ischemia without electrocardiographic ST elevation.Both syndromes are caused by
plaque rupture and associated nonocclusive thrombus.
Although UA and NSTEMI have a similar underlying pathophysiology, they differ in the degree of ischemia.
Although UA is not associated with a clinically detectable cardiac enzyme (creatine kinase myocardial
band, myoglobin, or troponin) leak, there can be electrocardiographic (EKG) changes consistent with ischemia.
In contrast, NSTEMI is characterized by a gradual rise and fall in biomarkers for myocardial necrosis
associated with anginal-like symptoms.
Thrombi in UA/NSTEMI are platelet rich and usually nonocclusive. In contrast, occluding thrombi are characteristic
of acute STEMI and typically comprised of fibrin and red blood cells.
• The disrupted plaque and associated thrombus reduces myocardial blood flow and impairs oxygen delivery to
cardiac myocytes. However, microembolization of platelet aggregates also occlude small arteriolar and capillary beds,
thus furthering ischemia. Indeed, microembolization is thought to be necessary to induce frank myocardial necrosis
and the parallel release of biomarkers (creatine phosphokinase [CPK] and troponins)
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The classic symptoms of UA/NSTEMI are characterized
by poorly localizing chest or arm discomfort described as pressure-like or tightening. The discomfort typically
radiates to the jaw and arms.
Symptoms may be precipitated by emotional or physical exertion or may occur spontaneously at rest.
• Often the clinical presentation is atypical, especially
in the elderly (age >65), in women and in patients
with comorbid conditions (diabetes mellitus).
• Atypical symptoms of UA/NSTEMI include the following:
Epigastric pain
Unexplained fatigue
Dyspnea (at rest or with exertion)
Confusion
Nausea
Diaphoresis
• Certain clinical features are considered characteristic of Unstable Angina. These include:
.. Rest angina (particularly if prolonged or associated with transient ST changes),
..New onset angina after minimal exertion,
.. Changes in the frequency of angina
• Features considered not characteristic, but often confused, with myocardial ischemia include the following:
-Pleuritic stabbing pain worse with respiration.
-Lower or midabdominal pain.
-Point tenderness, especially over the apex.
-Pain reproduced with chest wall palpation.
-Constant pain lasting for hours (especially in the absence of ST changes)
-Fleeting pain lasting only seconds.
-Pain radiating to the lower extremities.
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TREATMENT
• The treatment of ACS is designed to decrease cardiacmyocardial oxygen demand and increase oxygen
delivery (eg, coronary flow).
OXYGEN
• Oxygen should be administered to patients with arterial saturations less than 90%.
NITROGLYCERINE
• Nitroglycerine dilates the venous bed, decreasing preload and thus myocardial oxygen demand.
• It also dilates the arterial bed (although it is much less potent) and reduces afterload (thus reducing oxygen
consumption).
• Promotes collateral flow by dilating precapillary sphincters of the coronary microvasculature.
• Dilates normal and atherosclerotic epicardial coronary arteries redistributing flow to ischemic areas of myocardium.
• Initially, 0.4 mg is administered sublingually to patients with ischemia. This dose may be repeated as needed for the
symptoms and signs of ischemia.
• If pain is not relieved with sublingual nitroglycerine, intravenous (IV) nitroglycerine should be administered at a rate
of 10 µg/min and increased by 5 to 10 µg/min every 3 to 5 minutes until relief of symptoms. Although 200 µg/min is
commonly considered the maximal dose, higher doses can be safely administered provided that the patients blood
pressure remains stable.
• The blood pressure must be monitored closely. A systolic blood pressure of >110 mm Hg should be maintained.
Large abrupt decreases in blood pressure should be avoided as they may aggravate cardiac ischemia or precipitate a
cerebrovascular event.
• Tolerance to nitroglycerine develops within 24 hours and generally necessitates an increase in dosage.
• After 12 to 24 hours of symptom control, the nitroglycerine is weaned and changed to an oral preparation
MORPHINE SULFATE
• Because morphine sulfate has analgesic, anxiolytic &vasodilatory effects, it decreases myocardial oxygen
demand.
• Administered in doses of 1 to 5 mg intravenously
• Must monitor closely for hypotension and respiratorydepression.
• Intravenous doses of naloxone 0.4 to 2.2 mg will antagonize
morphine’s effects.
β-BLOCKERS
• β-Blockers reduce blood pressure, heart rate, and contractility, decreasing myocardial oxygen demand.
• Considerable evidence supports the use of β-blockers in the management of all forms of coronary artery disease.
• Intravenous administration is recommended with protracted ischemia eg, metoprolol 5 mg intravenously every 5
minutes for three doses, then 25 to 50 mg by mouth every 6 hours.
• Bronchospasm, hypotension, and bradycardia can occur. Esmolol has a very short half-life and may prove especially
useful in patients with comorbid conditions that could be worsened by β-blocker therapy (COPD)..
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TREATMENT
CALCIUM CHANNEL ANTAGONISTS
• Calcium channel antagonists decrease myocardial oxygen demand and theoretically limit the extent and severity of
myocardial necrosis.
• Calcium channel antagonists have been used to control ischemia and treat hypertension in ACS. However, the
American College of Cardiology/American Heart Association (ACC/AHA) guidelines on NSTEMI (and STEMI),
emphasized that no calcium channel blocker has been shown to reduce mortality in acute MI and that in certain
patients they may be harmful.
• Short-acting dihydropyridine agents (nifedipine) are contraindicated in ACS in the absence of a β-blocker.Verapamil
and diltiazem are contraindicated in patients with significant left ventricular dysfunction, eg, ejections fraction <45%
because of their negative inotropic effect. In general, calcium channel blockers should only be used in patients in
whom β-blockers are contraindicated.
ANGIOTENSIN-CONVERTING
ENZYME INHIBITORS
• Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce mortality in patients with
an acute MI with ischemic left ventricular dysfunction as well as in nonischemic cardiomyopathy.
• The HOPE and EUROPA trials demonstrated beneficial effects of ACE inhibitors in diabetic patients or patients with
preexisting CAD and at least one additional risk factor but without left ventricular dysfunction.
Accordingly, most patients discharged after undergoing management for UA/NSTEMI will be treated with an ACE
inhibitor.
• The ACC/AHA also recommends the administration of ACE inhibitors in all postmyocardial infarct patients with left
ventricular dysfunction, diabetes mellitus, and hypertension not controlled by β-blockers.
ASPIRIN
• In multiple clinical trials, aspirin has demonstrated significant benefits in patients with coronary artery disease.
• Aspirin should be administered as soon as possible in all cases of suspected ACS (eg, in the emergency department
and continued daily).
• If the patient has not been receiving aspirin as an outpatient, 160 to 325 mg (chewed to maximize absorption) is
recommended, followed by a dose of 81 mg daily.
UNFRACTIONATED HEPARIN AND LOW-MOLECULAR-WEIGHT HEPARIN
• Heparin accelerates the action of circulating antithrombin III, which is a proteolytic enzyme that inactivates
thrombin as well as factor IXa and Xa. Heparin should be used in combination with aspirin in all patients presenting
with UA or NSTEMI.
• The usual dose of unfractionated heparin is 60 to 70 U/kg (maximum 5000 U) as a bolus with an infusion of 12 to 15
U/kg/min. The partial thromboplastin time (PTT) should be maintained between 1.5 to 2.5 times control. The optimal
length of treatment is not known, but most trials using unfractionated heparin (UFH) lasted 2 to 5 days.
• Low-molecular-weight heparin (LMWH) activates factor Xa. The anticoagulant effect of LMWH is more predictable
than with UFH, therefore PTT monitoring is not necessary.
• In a pooled study of clinical trials comparing UFH to LMWH, patients on LMWH experienced a lower 30-day event
rate without a significant increase in bleeding. This was especially evident in patients managed conservatively (eg, not
taken directly to the catheterization laboratory). Importantly, the SYNERGY trial demonstrated a statistically
significant risk of bleeding in patients who were switched from UFH to LMWH and vice versa.
• Serial complete blood counts and platelet counts should be obtained daily during heparin administration. Mild to
significant thrombocytopenia may occur with heparin; and autoimmune-induced thrombocytopenia (HIT) with
thrombosis is a rare but catastrophic complication. If a patient has a history of heparin-induced thrombocytopenia,
a direct thrombin inhibitor such as hirudin can be used. Hirudin is administered as a 0.4 mg/g IV bolus
over 15 to 20 seconds followed by a continuous infusion of 0.15 mg/kg/h. The PTT should be maintained
between 1.5 to 2.5 times control
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HYPERTENSION
In any person persistent rise of blood pressure above the
arbitrary level of 140/90 mm of Hg is known as hypertension .
CAUSES OF HYPERTENSION
A. Primary or essential hypertension or
idiopathic (80-90 %) ;
B. Secondary (10-20%)
1. Renal cause—
i. Acute glomerulonephritis
ii. Chronic glomerulonephritis
iii.Chronic pyelonephritis
iv. Polycystic diseases of the kidney
v. Renal artery stenosis
vi. Hydronephrosis
VII. Any other diseases which affect the
kidney e.g.,S.L.E.
2.Endocrine causes
i. Cushing syndrome
ii. Primary aldosteronism (Conn’s
syndrome)
iii. Phaeochromocytoma
iv. Thyrotoxicosis MECHANISM OF HYPERTENSION
v. Myxoedema Blood pressure= Cardiac output × peripheral resistance. Four
3. Metabolic causes— factors control blood pressure by the above formula :
i. Diabetes mellitus 1. Baro-reflex
ii. Toxaemia of pregnency 2. Blood volume
iii. Chronic gout 3. Renin angiotensis mechanism
iv. Atherosclerosis 4. Vascular autoregulation
4. Drugs—
i. Contraceptive pill INVESTIGATION OF HYPERTENSION
ii. Steroid 1. Urine: Routine examination for album,in, RBC and
5.Congenital –coarctation of aorta pus cell may present.
6. Blood diseases like polycythaemia 2.Xray chest
rubra vera 3. Blood urea, serum creatinine, serum electrolyte and
7. Psychogenic serum cholesterol
4. E.C.G
5. E.T.T.
6. Angiogram
7.Echocardiogram
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CLINICAL FEATURES OF HYPERTENSION
SYMPTOMS:
A. Cerebral
i. Headache at the occipital region particularly in the
TREATMENT
1. General treatment;
morning. i. If obese reduction of weight
ii. Dizziness ii. Restricted salt intake
iii. Insomnia iii. Stop smoking
iv. Irritability iv. Moderate exercise daily
v. vomiting v. Avoid anxiety and tension
vi. Fatiguability vi. If diabetic control the diseases
vii. Personality change and lack of concentration v. Disciplined life
B. cardiac 2. Treatment by drugs ;
i. Angina pectoris or chest pain Three types of drugs are used in treating
ii. Shortness of breathing which
iii. Symptoms of right and left ventricular failure (tachycardia, hypertension which are as follows
facial oedema) i. Diuretics (thiazide, frusemide)
C. Vascular ii. Adrenergic blocking drugs (methyldopa,
i. Bleeding from unexpected site propanolol)
ii. Cerebro vascular attack iii. Vasidilators (hydrazine, prozocin)
D. Ocular- i. Blurring of vision ii. Scotoma Malignant Hypertension:
E. Renal 1. Hypertensive
i. Increased nocturnal frequency of urine encephalopathy
ii.Diuresis 2. Brain haemmorhage.
iii. Symptoms of renal failure (leg oedema) Duration of treatment: Life long
iv. Uraemia
SIGN:
1. Pulse: Rate may be slow
2. Blood pressure above 140/90 in adult
3. Enlargement of the heart
4. Flame shaped hemorrhage and papilloedema in the eye
(fundoscopic examination)
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ACUTE CORONARY SYNDROME
Acute coronary syndrome is a term used to describe a range of conditions associated with sudden, reduced
blood flow to the heart. • It is almost always associated with rupture of an atherosclerotic plaque and partial
or complete thrombosis of the infarct-related artery. • ACS leads to myocardial ischemia and eventually
necrosis which results in compromised cardiac functioning
TYPES
UNSTABLE ANGINA
• Non Occlusive Thrombus
• Normal ECG
• No Cardiac Enzymes
NON ST ELEVATION MYOCARDIAL
INFRACTION
• Partial Coronary Artery Occlusion
• Partial Thickness Necrosis (+ Ti, CKMB)
• ST depression/ T wave Inversion
ST ELEVATION MYOCARDIAL
INFRACTION
• Complete Ischemia
• Full Thickness Necrosis ( ++ Ti, CK MB)
• ST Elevation
PATHOPHYSIOLOGY
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CLINICAL MANIFESTATIONS
• Chest Pain, Pressure or Heaviness
• Palpitations
• Pain Radiating to Neck, Jaw, Left Arm, Back and Epigastric Region
• Syncope
• Shortness of Breath
• Nausea and Vomiting
• Diaphoresis and Decreased Exercise Tolerance
INVESTIGATIONS
ECG CARDIAC MARKERS CXR
• Pulmonary edema
• ST Depression, Elevation; T wave • CK-MB • Cardiomegaly
Inversion, Arrhythmias, LBBB • Troponin I • Pneumonia
• Thoracic aneurysm
ECHO BLOOD TEST
• Reduced Ejection fraction • Leukocytosis
• Ventricular Wall abnormalities • Elevated ESR/CRP
• Complications ( MR, LV Rupture) • Hyperglycemia
MANAGEMENT
Immediate Therapy : In Hospital Within 12 hrs
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MANAGEMENT PERCUTANEOUS CORONARY INTERVENTION
• Immediate emergency reperfusion therapy has no
demonstrable benefit in patients with non-ST segment
elevation MI and thrombolytic therapy may be harmful.
• In ST segment elevation acute coronary syndrome;
Immediate reperfusion therapy restores coronary artery
patency, preserves left ventricular function and improves survival.
• Primary PCI is more effective than thrombolysis for the
treatment of acute MI. Death, non-fatal re-infarction and
stroke are reduced from 14% with thrombolytic therapy
to 8% with primary PCI
MANAGEMENT LONG TERM THERAPY
SECONDARY PREVENTION Others
LIFESTYLE drug therapy • Rehabilitation
modification • Antiplatelet
therapy (aspirin • Implantable
• Diet (weight
control, lipid lowering
and/or clopidogrel) cardiac
• β-blocker
Mediterranean • ACE inhibitor/ARB
defibrillator
diet) • Statin
• Cessation of • Additional
smoking therapy for control
of diabetes and
• Regular exercise
hypertension
• Mineralocorticoid
receptor
antagonist
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HEART FAILURE
• Structural or functional CD
• impairs the blood filling/ejecting ability
of ventricles
• inability to maintain the metabolic needs
of the body
CAUSES
CLASSIFICATIONS
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ACUTE VS CHRONIC
Acute Chronic SYMPTOMS
• Fatigue
• Develops rapidly • Long term
• Activity decrease
• Can be immediately life • More insidious
• Cough (especially supine)
threatening • Associated with the heart
• Edema
• Dramatic drop in cardiac output undergoing adaptive
• Shortness of breath
• May be new (e.g. acute MI, responses (e.g. dilation,
sepsis) or an exacerbation hypetrophy) to a
of chronic disease precipitating cause
PATHOPHYSIOLOGY
Compensatory mechanism:
1. Hemodynamic alterations
2. Neurohormonal responses (SNS, RAAS,
Vasopressin)
3. Ventricular dilation
4. Ventricular hypertrophy
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ECG
Frank-Starling Mechanism
• The ability of the heart to change its force of
contraction and therefore stroke volume in
response to changes in venous return. ECG findings are not diagnostic, but:
• In heart failure, there is a compensatory • Old MI or recent MI
increase in venous return which is augmented • Arrhythmia
by neurohormonal mechanisms. • Some forms of tachycardia related
• Due to increase in venous return, there is a cardiomyopathies
temporary increase in stroke volume. • LBBB
Diagnostic Studies APPROACH TO THE PATIENT WITH HF
• X-ray (Kerley B lines)
• ECG
• Echocardiography (EF)
• Laboratory data (cardiac enzymes, BNP, serum
chemistries ,liver function studies ,thyroid
function studies and complete blood count)
• Stress testing (exercise or medicine)
• Cardiac catheterization- determine heart
pressures ( inc.PAW )
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BURNS NURSING STUDY GUIDE
BURNS
WOUNDS CAUSED BY EXPOSURE TO:
1. excessive heat
2. Chemicals
3. fire/steam
4. radiation
5. electricit
Results in 10-20 thousand deaths annually
Survival best at ages 15-45
Children, elderly, and diabetics
Survival best burns cover less than 20% of TBA
TYPES OF BURNS
THERMAL
Exposure to flame or a hot object
CHEMICAL
Exposure to acid, alkali or organic substances
ELECTRICAL
Result from the conversion of electrical energy into heat.
Extent of injury depends on the type of current, the pathway of flow, local tissue resistance,
and duration of contact
RADIATION
Result from radiant energy being transferred to the body resulting in production of
cellular toxins
BURN WOUND ASSESSMENT
Classified according to depth of injury and extent of body surface area involved
Burn wounds differentiated depending on the level of dermis and subcutaneous
tissue involved
1. superficial (first-degree)
2. deep (second-degree)
3. full thickness (third and fourth degree)
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CALCULATION OF BURNED BODY
SURFACE AREA
TOTAL BODY SURFACE AREA (TBSA)
Superficial burns are not involved in the calculation
Lund and Browder Chart is the most accurate because it adjusts for age
Rule of nines divides the body – adequate for initial assessment for adult
burns
LUND BROWDER CHART USED FOR DETERMINING BSA
Parkland Formula for fluid
replacement following loss
due to thermal burns:
4ml/kg / % burn of Ringer’s
Lactate / Hartmann’s Solution
(or 0.9% Saline)
½ given over first 8hrs (from
time of injury) then ½ given
over subsequent 16hrs
In children 4.5% albumin should
be used as the burn
replacement fluid for this
period of 16hrs
AREA AGE 0 1 5 10 15 ADULT
A = ½ of Head 9½ 8½ 6½ 5½ 4½ 3½
B = ½ of one Thigh 2¾ 3¼ 4 4½ 4½ 4¾
C = ½ of one Leg 2½ 2½ 2¾ 3 3¼ 3½
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RULES OF NINES
Head & Neck = 9%
Each upper extremity (Arms) = 9%
Each lower extremity (Legs) = 18%
Anterior trunk= 18%
Posterior trunk = 18%
Genitalia (perineum) = 1%
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VASCULAR CHANGES RESULTING
FROM BURN INJURIES
Circulatory disruption occurs at the burn
site immediately after a burn injury
Blood flow decreases or cease due to
occluded blood vessels
Damaged macrophages within the tissues
release chemicals that cause constriction
of vessel
Blood vessel thrombosis may occur
causing necrosis
Macrophage: A type of white blood that ingests (takes in) foreign
material. Macrophages are key players in the immune response to foreign
invaders such as infectious microorganisms.
FLUID SHIFT FLUID
Occurs after initial vasoconstriction, then
dilation
Blood vessels dilate and leak fluid into
REMOBILIZATION
the interstitial space Occurs after 24 hours
Known as third spacing or capillary leak Capillary leak stops
syndrome See diuretic stage where edema fluid
Causes decreased blood volume and blood shifts from the interstitial spaces into the
pressure vascular space
Occurs within the first 12 hours after the Blood volume increases leading to
burn and can continue to up to 36 hours increased renal blood flow and diuresis
Body weight returns to normal
FLUID IMBALANCES
Occur as a result of fluid shift and cell
damage
Hypovolemia
Metabolic acidosis
Hyperkalemia
Hyponatremia
Hemoconcentration (elevated blood
osmolarity, hematocrit/hemoglobin) due to
dehydration
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PHASES OF BURN INJURIES
Emergent (24-48 hrs)
Acute
Rehabilitative
EMERGENT PHASE CLINICAL
MANIFESTATIONS
*Immediate problem is fluid loss, edema,
reduced blood flow (fluid and electrolyte
shifts)
Goals: Clients with major burn injuries and with
1. secure airway inhalation injury are at risk for respiratory
2. support circulation by fluid problems
replacement Inhalation injuries are present in 20% to 50%
3. keep the client comfortable with of the clients admitted to burn centers
analgesics Assess the respiratory system by inspecting
4. prevent infection through wound care the mouth, nose, and pharynx
5. maintain body temperature Burns of the lips, face, ears, neck, eyelids,
6. provide emotional support eyebrows, and eyelashes are strong indicators
Knowledge of circumstances surrounding the that an inhalation injury may be present
burn injury Change in respiratory pattern may indicate a
Obtain client’s pre-burn weight (dry weight) to pulmonary injury.
calculate fluid rates The client may: become progressively hoarse,
Calculations based on weight obtained after develop a brassy cough, drool or have
fluid replacement is started are not accurate difficulty swallowing, produce expiratory
because of water-induced weight gain sounds that include audible wheezes, crowing,
Height is important in determining body and stridor
surface area (BSA) which is used to calculate Upper airway edema and inhalation injury are
nutritional most common in the trachea and mainstem
needs bronchi
Know client’s health history because the Auscultate these areas for wheezes
physiologic stress seen with a burn can make a If wheezes disappear, this indicates impending
latent disease process develop symptoms airway obstruction and demands immediate
intubation.
CLINICAL
MANIFESTATIONS
Cardiovascular will begin immediately which can include shock (Shock is a
common cause of death in the emergent phase in clients with serious injuries)
Obtain a baseline EKG
Monitor for edema, measure central and peripheral pulses, blood pressure,
capillary refill and pulse oximetry
Changes in renal function are related to decreased renal blood flow
Urine is usually highly concentrated and has a high specific gravity
Urine output is decreased during the first
24 hours of the emergent phase
Fluid resuscitation is provided at the rate
needed to maintain adult urine output at 30 to 50- mL/hr.
Measure BUN, creat and NA levels
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SKIN ASSESSMENT
Sympathetic stimulation during the
emergent phase causes reduced GI
motility and paralytic ileus
Assess the skin to determine the size and Auscultate the abdomen to assess bowel
depth of burn injury sounds which may be reduced
The size of the injury is first estimated in
comparison to the total body surface area Monitor for n/v and abdominal distention
(TBSA). For example, a burn that Clients with burns of 25% TBSA or who
involves 40% of the TBSA is a 40% burn are intubated generally require a NG tube
Use the rule of nines for clients whose inserted to prevent aspiration and
weights are in normal proportion to their heights removal of gastric secretions
IV FLUID THERAPY
Infusion of IV fluids is needed to maintain sufficient
blood volume for normal CO NURSING DIAGNOSIS
IN THE EMERGENT
Clients with burns involving 15% to 20% of the TBSA
require IV fluid
Purpose is to prevent shock by maintaining adequate
PHASE
circulating blood fluid volume
Severe burn requires large fluid loads in a short time
to maintain blood flow to vital organs
Fluid replacement formulas are calculated from the Decreased CO
time of injury and not from the time of arrival at the Deficient fluid volume r/t active fluid
hospital volume loss
Diuretics should not be given to increase urine output. Ineffective Tissue perfusion
Change the amount and rate of fluid administration. Ineffective breathing pattern
Diuretics do not increase CO; they actually decrease
circulating volume and CO by pulling fluid from the
circulating blood volume to enhance diuresis
Protenate or 5% albumin in isotonic
ACUTE PHASE OF
saline (1/2
given in first 8 hr; ½ given in next 16 hr)
BURN INJURY
LR (Lactate Ringer) without dextrose
(1/2 given
in first 8 hr; ½ given in next 16 hr)
• Lasts until wound closure is complete Crystalloid (hypertonic saline) adjust to
• Care is directed toward continued assessment and maintain
maintenance of the cardiovascular and respiratory urine output at 30 mL/hr
system Crystalloid only (lactated ringers)
• Pneumonia is a concern which can result in
respiratory
failure requiring mechanical ventilation
• Infection (Topical antibiotics – Silvadene)
• Tetanus toxoid
• Weight daily without dressings or splints and
compare
to pre-burn weight
• A 2% loss of body weight indicates a mild deficit
• A 10% or greater weight loss requires modification
of calorie intake
• Monitor for signs of infection
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LOCAL AND SYSTEMIC SIGNS
OF INFECTION- GRAM NEGATIVE BACTERIA
Pseudomonas, Proteus
May led to septic shock
Conversion of a partial-thickness injury to a full-thickness injury
Ulceration of health skin at the burn site
Erythematous, nodular lesions in uninvolved skin
Excessive burn wound drainage
Odor
Sloughing of grafts
Altered level of consciousness
Changes in vital signs
Oliguria
GI dysfunction such as diarrhea, vomiting
Metabolic acidosis
LAB VALUES
Na – hyponatremia or Hypernatremia
K – Hyperkalemia or Hypokalemia
WBC – 10,000-20,000
NURSING DIAGOSIS IN THE ACUTE PHASE
Impaired skin integrity
Risk for infection
Imbalanced nutrition
Impaired physical mobility
Disturbed body image
PLANNING AND IMPLEMENTATION
Nonsurgical management: removal of exudates
and necrotic tissue, cleaning the area,
stimulating granulation and revascularization
and applying dressings. Debridement may be
needed
DRESSING THE BURN WOUND
After burn wounds are cleaned and debrided,
topical antibiotics are reapplied to prevent infection
Standard wound dressings are multiple layers of
gauze applied over the topical agents on the burn wound
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REHABILITATIVE PHASE OF BURN INJURY
Started at the time of admission
Technically begins with wound closure
and ends when the client returns to the
highest possible level of functioning
Provide psychosocial support
Assess home environment, financial
resources, medical equipment, prosthetic rehab
Health teaching should include symptoms
of infection, drugs regimens, f/u
appointments, comfort measures to reduce pruritus
DIET
Initially NPO
Begin oral fluids after bowel sounds return
Do not give ice chips or free water lead to
electrolyte imbalance DEBRIDEMENT
High protein, high calorie Done with forceps and curved scissor or
through hydrotherapy (application of water for
GOALS treatment)
Only loose eschar removed
Prevent complications (contractures) Blisters are left alone to serve as a protector
Vital signs hourly – controversial
Assess respiratory function
Tetanus booster
Anti-infective SKIN GRAFTS
Analgesics Done during the acute phase
No aspirin Used for full-thickness and deep partial
Strict surgical asepsis thickness wounds
Turn q2h to prevent contractures
Emotional support
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CANCER NURSING
Cancer (medical term: malignant neoplasm) is a class of diseases in which a
group of cell display uncontrolled growth through division beyond normal limits,
invasion that intrudes upon and destroys adjacent tissues, and sometimes
metastasis, which spreads the cells to other locations in the body via lymph or
blood. These three malignant properties of cancers differentiate them from
benign tumors, which are self-limited, and do not invade or metastasize.
• Cancers are primarily an environmental disease with 90-95% of cases due to
lifestyle and environmental factors and 5-10% due to heredity.1. Common
environmental factors leading to cancer death include:
• tobacco:- (25-30%),diet and obesity:- (30-35%),infections:- (15-20%),
radiation, stress, lack of physical activity, and environmental pollutants.[1]These
environmental factors cause abnormalities in the genetic material of cells.
Genetic abnormalities found in cancer typically affect two general classes of
genes oncogene sand tumor suppressor genes.
• Definitive diagnosis requires the examination of a biopsy specimen, although
the initial indication of malignancy can be symptomatic or radiographic. Most
cancers can be treated and this may include chemotherapy and radiotherapy
and/or surgery. The prognosis is most influenced by the type of cancer and the
extent of disease. While cancer can affect people of all ages the risk typically
increasing with age.[3] In 2004 cancer caused about 13% of all human deaths
[4] (7.6 million).
CLASSIFICATION
Cancers are classified by the type of cell that resembles the
tumor and, therefore, the tissue presumed to be the origin of the
tumor. These are the histology and the location, respectively.
Examples of general categories include:
• Carcinoma: Malignant tumors derived from epithelial cells. This group
represents the most common cancers, including the common forms of
breast, prostate, lung and colon cancer.
• Sarcoma: Malignant tumors derived from connective tissue, or
mesenchymal cells.
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• Lymphoma and leukemia: Malignancies derived from hematopoietic
(blood-forming) cells
• Germ cell tumor: Tumors derived from totipotent cells. In adults most
often found in the testicle and ovary; in fetuses, babies, and young
children most often found on the body midline, particularly at the tip of the
tailbone; in horses most often found at the poll (base of the skull).
• Blasti tumor or blastoma: A tumor (usually malignant) which resembles
an immature or embryonic tissue. Many of these tumors are most
common in children.
SIGNS AND SYMPTOMS
ROUGHLY, CANCER SYMPTOMS CAN BE DIVIDED INTO THREE GROUPS:
• Local symptoms: unusual lumps or swelling (tumor), hemorrhage
(bleeding), pain and/or ulceration. Compression of surrounding tissues
may cause symptoms such as jaundice (yellowing the eyes and skin).
• Symptoms of metastasis (spreading): enlarged lymph nodes, cough and
hemoptysis, hepatomegaly (enlarged liver), bone pain, fracture of
affected bones and neurological symptoms. Although advanced cancer
may cause pain, it is often not the first symptom.
• Systemic symptoms: weight loss, poor appetite, fatigue and cachexia
(wasting), excessive sweating (night sweats), anemia and specific
paraneoplastic phenomena, i.e. specific conditions that are due to an
active cancer, such as thrombosis or hormonal changes.
TYPES OF CANCER
LEUKEMIA
SYMPTOMS
Symptoms are often nonspecific, but some patients have experienced:
Tiredness ,Fevers,Profuse sweating at night,Unexplained weight loss
Shortness of breath,Dizziness,Infections,Easy bruising or bleeding
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DIAGNOSIS
How is acute lymphoblastic leukemia diagnosed? A significant number of leukemia cells
in the blood, bone marrow and other biopsy materials must be apparent before we can
accurately determine a diagnosis of acute lymphoblastic leukemia.
Immunophenotyping, a test performed using a sample of tissue or blood, is performed to
diagnose the type of leukemia. Cytogenetics testing—in which chromosomal
abnormalities are identified—and molecular profiling are also routinely performed. The
results of these tests form an essential part of the diagnosis and care plan for our
patients. Your care team will explain the steps involved in each diagnostic test and
answer questions that you may have about how a diagnosis is determined.
TREATMENT
Acute lymphoblastic leukemia treatment at the CTRC The following treatments are offered to
patients: Induction chemotherapy: Chemotherapy that is designed to rid the body of all visible
evidence of leukemiaConsolidation chemotherapy: Chemotherapy designed to get rid of microscopic
clones of leukemia after a patient appears to be in remission from induction therapy Maintenance
chemotherapy: Chemotherapy given in specific doses over a prolonged period of time to help ensure
that the leukemia remains in remission Survivorship care: Our patients are provided with long-term
surveillance and regular follow-up visits are planned to provide the best long-term survivorship care.
Follow-up and surveillance: An important part of the follow-up and surveillance for acute
lymphoblastic leukemia is Minimal Residual Disease (MRD) detection using techniques designed to
detect leukemia clones that cannot be detected by conventional methods
ACUTE MYELOID LEUKEMIA
SYMPTOMS
Tiredness, Fevers,Shortness of breath,Dizziness,Infections, Easy bruising or
bleeding Some patients may have neurological symptoms, such as
headache, double vision and signs of nerve injury.
DIAGNOSIS
How is acute myeloid leukemia diagnosed? Because leukemia cells are found in blood
and bone marrow, blood work and other tests must be performed to properly diagnose
this disease. Specialized tests that define the immunological origin of the leukemia cells,
called immunophenotyping, and tests that define the genetic basis of this leukemia,
called cytogenetics and molecular profiling, are routinely performed and form an
essential part of the diagnosis and care of patients with acute myeloid leukemia
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TREATMENT
Discuss treatment options, which may include: Induction chemotherapy and consolidation
chemotherapy: After your treatment team observes signs that you appear to be in remission after
induction chemotherapy treatment, consolidation chemotherapy may be recommended to assure
there are no microscopic clones of leukemia still in your body. Maintenance chemotherapy: Selected
patients with certain types of acute myeloid leukemia may receive chemotherapy given in specific
doses over a prolonged period of time to suppress the recurrence of leukemia and to prevent new
leukemia clones from emerging. Stem cell transplantation: Stem cell transplantation may be
identified by your treatment team as the best option based on your diagnosis. Our goal at the CTRC
is to provide seamless care between the leukemia treatment team and the stem cell transplant
team, so you can expect good communication between your doctors if this treatment. Survivorship
care: Our patients are provided with long-term surveillance and regular follow-up visits are planned
to provide the best long-term survivorship care
CHRONIC MYELOID LEUKEMIA
SYMPTOMS
Some patients with this disease, especially those who are in what is known as the chronic phase,
may not feel any symptoms and the diagnosis is made based on abnormal blood counts on routine
blood tests. The typical symptoms of chronic myeloid leukemia are often nonspecific, and may
include tiredness, abdominal discomfort, feeling full after a small meal, fevers, shortness of breath,
and easy bruising or bleeding. If you have what is known as the accelerated phase of chronic
myeloid leukemia, or the blast crisis phase, your symptoms may be similar to those of someone with
acute leukemia, meaning that you are seriously ill and your disease will likely require more
aggressive treatment.
DIAGNOSIS
How is chronic myeloid leukemia diagnosed? A tissue or blood sample showing the
Philadelphia Chromosome and its molecular signature (referred to as bcr-abl) in the
blood or bone marrow and other biopsy materials will confirm a chronic myeloid
leukemia diagnosis. Doctors will also look for other signs of the disease in your blood or
tissue and will conduct tests to determine the type and severity of your disease
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TREATMENT
CHRONIC MYELOID LEUKEMIA
Primary treatment: Medications taken by mouth called tyrosine kinase inhibitors are the
treatment of choice for this disease. Most patients are treated with imatinib, nilotinib, or
dasatanib. This chemotherapy is designed to eradicate all evidence of leukemia and to result
in a remission known as a molecular remission, meaning that test results will no longer show
evidence of the Philadelphia chromosome and the bcr-abl proteins in the blood and bone marrow.
FOLLOW-UP CHEMOTHERAPY:
You’ll be monitored after treatment concludes and you’ll be asked
to submit to a specific set of blood and bone marrow on a set schedule of three months, six
months, one year and beyond. Your treatment team will look at your test results to confirm: a
normal blood count, disappearance of the Philadelphia chromosome and undetectable bcr-abl.
You doctor may pursue further treatment depending on the results of your periodic tests.
Chemotherapy for accelerated or blast phase leukemia: Treatment is more aggressive for
accelerated or blast phase leukemia and your care team may opt to treat your disease in the
same way they would attack acute leukemia in another patient.
Stem cell transplantation: In some cases, stem cell transplantation is identified as the most
viable treatment option. If that’s the case based on your diagnosis, Treatment team will work
closely with your transplant team throughout the process.
Survivorship care: Our patients are provided with long-term surveillance and regular follow-up visits
are planned to provide the best long-term survivorship care
CHRONIC LYMPHOCYTIC LEUKEMIA
SYMPTOMS
Chronic lymphocytic leukemia is often found after an abnormal blood count is discovered during a
routine blood test. This is the first step in a determining that someone has the disease. Symptoms of
this type of leukemia are often nonspecific and may include fever, profuse sweating at night and
unexplained weight loss. Tiredness, abdominal discomfort, swollen lymph nodes and feeling full after
a small meal can sometimes be clues that lead to a diagnosis of this disease. As a result of the
weakened immune system associated with chronic lymphocytic leukemia, you may be susceptible to
serious infections.
DIAGNOSIS
How is chronic lymphocytic leukemia diagnosed? Lab tests, including an analysis of your
blood, will reveal an excess of small lymphocytes if you have chronic lymphocytic
leukemia. Other tests of your blood, bone marrow and other tissue will help doctors
determine the type and severity of your disease.
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TREATMENT
Primary treatment: Some patients do not need immediate treatment because
leukemia progress may be slow and stable. You won’t feel a certain symptom or take
a certain test to determine when treatment will begin. You treatment team will
communicate with you to determine when it makes sense to start treating your
disease. Your treatment may include specific types of chemotherapy and
immunotherapy using antibodies designed to attack the leukemic lymphocytes in the
hopes that your cancer will go into remission.
Stem cell transplantation: If your diagnosis determines that you have high-risk
chronic lymphocytic leukemia, you may be referred to a stem cell transplantation
team. The team works closely with transplant teams. We understand how important
communication is at every stage of your treatment.
Clinical trial-based treatment: Partnership with the National Cancer Institute, is
testing the addition of newer drugs like ibrutinib, along with rituximab, versus
standard treatments in a clinical trial called a Phase III or randomized clinical trial
(RCT).
Survivorship care: Our patients are provided with long-term surveillance and regular
follow-up visits are planned to provide the best long-term survivorship care.
BLADDER CANCER
Cancer that forms in tissues of the bladder (the
organ that stores urine). Most bladder cancers are
transitional cell carcinomas (cancer that begins in
cells that normally make up the inner lining of the
bladder). Other types include squamous cell
carcinoma (cancer that begins in thin, flat cells)
and adenocarcinoma (cancer that begins in cells
that make and release mucus and other fluids).
The cells that form squamous cell carcinoma and
adenocarcinoma develop in the inner lining of the
bladder
SYMPTOMS
Finding blood in your urine (which may make the urine look rusty or darker red)
-- Feeling an urgent need to empty your bladder
-- Having to empty your bladder more often than you used to
Feeling the need to empty your bladder without results
-- Needing to strain (bear down) when you empty your bladder
-- Feeling pain when you empty your bladder
These symptoms may be caused by bladder cancer or by other health problems, such as an
infection. People with these symptoms should tell their doctor so that problems can be diagnosed
and treated as early as possible. National Cancer Insititute
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DIAGNOSIS
How is bladder cancer diagnosed? The diagnosis of bladder cancer requires
confirmation, usually by an insertion of a scope into the bladder (cystoscopy) and biopsy
of suspicious areas. While initial biopsies may be performed in a doctor’s office, a more
detailed biopsy may need to be done with a cystoscopy under anesthesia. Some
patients may need removal of the tumor or portions of the tumor through the same
scope. This is called transurethral resection of bladder tumor or TURBT. Other tests
include blood tests, CT scans and other scans will be performed to determine extent of
disease, a process also called staging. The stage of the cancer determines the ideal
primary treatment. The stage of the cancer determines how we’ll approach your
treatment.
TREATMENT
Acute lymphoblastic leukemia treatment at the CTRC The following treatments are offered to
patients: Induction chemotherapy: Chemotherapy that is designed to rid the body of all visible
evidence of leukemiaConsolidation chemotherapy: Chemotherapy designed to get rid of
microscopic clones of leukemia after a patient appears to be in remission from induction therapy
Maintenance chemotherapy: Chemotherapy given in specific doses over a prolonged period of time
to help ensure that the leukemia remains in remission Survivorship care: Our patients are provided
with long-term surveillance and regular follow-up visits are planned to provide the best long-term
survivorship care. Follow-up and surveillance: An important part of the follow-up and surveillance
for acute lymphoblastic leukemia is Minimal Residual Disease (MRD) detection using techniques
designed to detect leukemia clones that cannot be detected by conventional methods
BREAST CANCER
STATISTICS
1 in 8 women will be diagnosed in their lifetime
1 in 1000 men will be diagnosed in their lifetime (Primarily after the age of
60)
Median age at DX = 61
Approx. 39,000 deaths annually in the US
Approx. 254,000 new cases annually in the US
NORMAL / CANCER CELL COMPARRISON
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NORMAL
FEMALE
BREAST
SYMPTOMS
Early stage is often asymtomatic Lump in the breast or armpit
Change in size, shape or feeling of the nipple or surrounding breast
tissue Discharge from the nipple
TREATMENT
Lumpectomy Mastectomy Chemotherapy Radiation HPT
– Hormone Replacement Therapy
RISK FACTORS
AGE & GENDER
Most advanced cases of breast cancer are diagnosed in women over age 50
FAMILY HISTORY
Family history of breast, ovarian, uterine or colon cancer indicates a 20-30% increased likelihood
to develop the disease
MENSTRUAL CYCLES
Women who have their first menstrual cycle before the age of 12, or begin menapause after the age
of 55, have been found to have an increased risk of developing breast cancer.
GENETICS
BRCA 1 and BRCA 2 genetic defects increase a woman’s chance of developing breast cancer by up
to 80%
CHILDBIRTH
OBESITY
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LUNG CANCER
Most lethal of all cancer’s worldwide
One in ten patients with this disease
will survive the following five years
SYMPTOMS
A chronic cough
Worsening breathless
Weight loss
Excessive faigue
DIAGNOSIS
How is lung cancer diagnosed? Diagnose lung cancer using a combination of CT scans and a
biopsy usually performed by radiologists, lung specialists or thoracic surgeons. We handle
biopsy specimens with great care to determine specific markers, called biomarkers, for
molecular profiling. Other tests—including blood tests, PET/CT scans and other scans—to
determine extent of disease, a process also called staging. The location, type of cancer and
other features help us determine the ideal primary treatment for your cancer.
TREATMENT
Surgery: For patients with early stage, non-small cell lung cancer, surgery provides the best
chance for cure. Radiation therapy: This is an important part of treatment for many patients with
lung cancer. Techniques include brachytherapy, stereotactic body radiation therapy (SBRT) and
standard external beam radiation therapy. Some lung cancer patients need chemotherapy along
with radiation therapy, called chemoradiation. Chemotherapy: We have a variety of
chemotherapy options available for select patients. The choice of chemotherapy treatment
depends on the type of lung cancer. Advanced stage disease and recurrent disease: Lung cancer
team partners with the National Cancer Institute on unique new groundbreaking clinical trials
designed to advance the efficient development of targeted therapy for lung cancer, such as the
Lung Master Protocol (called Lung-MAP).
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LIVER CANCER
SYMPTOMS
Symptoms Abdominal pain, Distention of the abdomen, Nausea, Vomiting, Unexplained
weight loss, Jaundice .
DIAGNOSIS
Live Cancer Symptoms Abdominal pain, Distention of the abdomen, Nausea, Vomiting,
Unexplained weight loss, Jaundice . Diagnosis How is liver cancer diagnosed? Liver cancer
can be a silent cancer. Tests are necessary to confirm diagnosis. Blood tests can show tumor
markers such as alpha feto-protein (AFP) or other liver function tests. Ultrasounds and other
scans also may be used. CT or MRI scans and other imaging tests will be reviewed and
interpreted by expert radiology staff in partnership with Liver Cancer team. Biopsy: This
may be necessary for select patients. Tests, including blood tests, CT scans and other
imaging scans, will be performed to determine extent of disease. This is called staging. The
stage of the cancer and the assessment of liver function determines the ideal primary
treatment.
TREATMENTS
Our liver cancer experts will discuss treatment options at one appointment: Surgery: The cancer
is removed by a team that includes liver transplant surgeons and other surgeons who
specialize in liver cancer surgery. Radiology or image-guided treatments: Radiofrequency
ablation, chemo embolization and use of radioactive isotopes are placed directly into the liver
cancer by interventional radiology doctors who specialize in liver cancer treatments. Radiation
therapy: Techniques that are specific to liver cancer are available. Chemotherapy: Standard
chemotherapy options are used with some patients. Clinical trial-based new treatment: Options
will be discussed and treatments will be tailored to each patient’s needs. Survivorship care: Our
patients are provided with long-term surveillance and regular follow-up visits are planned to
provide the best long-term survivorship care. Causes/Risk Factors Risk factors for liver cancer
include: Hepatitis B virus infection, Hepatitis C virus infection, Related liver disease Chronic liver
disorders: These may also predispose a person to liver cancer. Screening programs for early
detection may be recommended for specific
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OVARIAN CANCER
SYMPTOMS
Non-specific pelvic discomfort Bloating Abdominal pain Urinary symptoms
that are frequent Feeling full after eating Loss of appetite
DIAGNOSIS
How is ovarian cancer diagnosed? For patients with specific symptoms consistent with ovarian
cancer, or when a pelvic mass that warrants evaluation is found during a gynecological
examination, tests such as a pelvic ultrasound examination, CT scan, and a blood test—a tumor-
marker, called CA-125—will confirm a diagnosis. Routine screening tests such as blood tests,
ultrasounds, or scans are not recommended for healthy women without risk factors.
TREATMENTS
Surgery (total abdominal hysterectomy and bilateral salpingoophorectomy): The uterus and the
ovaries are removed and surgeons carefully review your abdominal and pelvic organs during
surgery in search of signs that the disease has spread. The treatment team attempts to remove
as much of the cancer as possible through surgery. Chemotherapy after surgery: Most, but not
all, ovarian cancer patients will need chemotherapy after surgery. Survivorship care: Ovarian
cancer patients long after their treatments are done with surveillance and regular follow-up visits
to provide the best long-term survivorship care.
CAUSES/RISK
Women who have never been pregnant and women who have had their first pregnancy at or
after the age of 35 appear to be at higher risk of the disease. About 5 percent of ovarian cancer
cases may be caused by genetic conditions, such as BRCA1 and BRCA2 mutations.
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PROSTATE CANCER
SYMPTOMS
Prostate cancer almost never causes symptoms until it has spread. A
man may have an early or even a very late prostate cancer and not
know it until the cancer has spread. Unfortunately, once this has occurred,
prostate cancer is usually not curable. However, there are treatments to
slow prostate cancer’s spread.
TREATMENTS
A minimum of four treatment options should be offered to the patient: Surgery (radical
prostatectomy): The prostate gland is removed. Radiation therapy with external beam: A high-
dose X-rays or other types of rays may be used after surgery to prevent the tumor from
returning. Radiation therapy with implanted radioactive seeds: Doses of radioactive material are
placed near the cancer cells or placed directly within the tumor. This is known as brachytherapy.
Active surveillance: Watchful monitoring of the cancer using regular checkups, blood tests and
periodic prostate biopsies to determine if the tumor is growing or becoming more aggressive.
Survivorship care: Our patients are provided with long-term surveillance and regular follow-up
visits are planned to provide the best long-term survivorship care. Physicians have extensive
experience in all four forms of treatment of prostate cancer. Patients treated take advantage of
many years of experience in caring for individuals with prostate cancer by physicians who
oftentimes conducted the clinical studies that set the standard-of-care for physicians around the
world
DIAGNOSIS
How is prostate cancer diagnosed? Physicians have recommended regular physicals for men
older than 50 to find the cancer early, treat it and prevent problems or death from the disease.
These physicals include: Digital Rectal Examination: A physician inserts a gloved finger into the
patient’s rectum and feels the prostate, seeking any firm areas (called nodules) that might
indicate the presence of cancer.Prostate Specific Antigen (PSA) test: A blood test that looks at the
levels of prostate specific antigen, which is used in conjunction with other information to determine
the possibility of prostate cancer. Prostate Cancer Risk Calculator: Scientists and physicians
developed the Prostate Cancer Risk Calculator . The Prostate Cancer Risk Calculator combines the
following six factors: Age, Race/ethnicity, PSA, Rectal examination findings (normal or
abnormal)Family history of prostate cancer (yes or no), History of a prior negative prostate biopsy
(yes or no)
An important aspect of the calculator is that it not only estimates the risk of prostate cancer but
also estimates the risk of aggressive prostate cancer — one that spreads more quickly and has a
higher risk of causing death
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HEMATOLOGY
• The hematologic or hematopoietic system includes the blood, blood vessels,
and blood forming organs ( bone marrow, spleen, liver, lymph nodes, and
thymus gland).
• Major function of blood is to carry necessary materials ( oxygen, nutrients )
to cells and to remove CO2 system and metabolic waste products.
• It also plays a role in hormone transport, inflammatory and immune
responses, temperature regulation, fluid-electrolyte balance, and acid-base
balance.
THREE BROAD FUNCTIONS OF BLOOD
1.Transportation
• Respiratory – transport of gases by the RBC
• Nutritive – transport of digested nutrients from the GIT to the different cells of the body
• Excretory – transport of metabolic wastes to the kidneys and excreted as urine
2.Regulation
• Hormones and other molecules that help regulate metabolism are also carried in the blood
• Thermoregulation
• Protection
• Blood clotting
• Leukocytes
COMPONENTS OF THE BLOOD
1. Plasma
2. Formed Elements
• Erythrocytes or RBC
• Leukocytes or WBC
• Thrombocytes or Platelets
BLOOD
• Average volume is 5 – 6 liters or approximately 6 quarts
• pH is 7.35 – 7.45
• Arterial blood is usually bright red in color compared to venous blood
which has a darker color, due primarily to the large concentration of
oxyhemoglobin found in arterial blood
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a.) Plasma - fluid portion of the blood
Contains :
proteins / albumin fibrinogen
clotting factors electrolytes
waste products nutrients
b.) Cellular Components
1. Leukocytes (WBC)
2. Erythrocyte (RBC)
3. Thrombocyte (Platelets)
Hematopoiesis– occurs in the bone marrow ( pelvis, ribs, vertebrae and sternum.
Extramedullary Hematopoiesis- the liver and the spleen produces blood cells
PLASMA
• The liquid part of the blood approximately 90% water
• Also contains nutrients, ions (salts, primarily Na), respiratory gases,
hormones, plasma proteins, antibodies and various wastes and products of
cellular metabolism
• PLASMA PROTEINS – the most abundant solutes in the plasma
–Three Types
1.Albumin
2.Globulin
3.Fibrinogen
FORMED ELEMENTS OF THE BLOOD
ERYTHROCYTES
• Also called Red Blood Cells or RBC’s
• Function primarily to ferry Oxygen in the blood to all cells in the body
• Also transports Carbon dioxide out of the body
• Lifespan of 120 days only
• Hemoglobin in the RBC binds with the Oxygen as it is transported in the blood
• Female : 12 – 16 g/100ml
• Male : 13 – 18 g/100ml
• Normal RBC count: about 4 – 6 million/mm³
• Hematocrit (HCT) – percentage of RBC per given volume of blood and
is an important indicator of the Oxygen-carrying capacity of the blood
• Female : 37 – 48%
• Male : 45 – 52%
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LEUKOCYTES
• Also called White Blood Cells or WBC’s
• Average value : 4,000 – 11,000 / mm³
• Protects the body against any damage
• Are able to slip in and out of the blood vessels by ameboid fashion – in a
process called diapedesis
• When mobilized, the body speeds up production which usually indicates
the presence of infection in the body
• Leukocytosis – total WBC count above 11,000 / mm³
• Leukopenia – an abnormally low WBC count
TYPES: CELLS OF THE IMMUNE SYSTEM
1.Granulocytes • Lymphocytes
–Neutrophils -Basophils –Lymphocytes are created in the bone marrow and migrate to the Thymus
–Eosinophils where they mature
2.Agranulocytes –After becoming immunocompetent, the B & T cells transfer to the lymph
–Lymphocytes -Monocytes nodes & spleen
TYPES :
• Killer T Cells – binds to the surface of invading cells, disrupt the cell
membrane & destroy it by altering it’s environment
• Helper T cells – helps to stimulate the B Cells to mature into Plasma
Cells which synthetize & secrete immunoglobulins (Antibodies)
• Suppressor T Cells – Reduces the Humoral response
CELLULAR (CELL-MEDIATED) IMMUNE
RESPONSE
TYPES • T – Cells
1.B lymphocytes or B cells – produces antibodies to • Responds directly to antigens
incapacitate the • Will destroy target cells thru secretions of Lymphokines
antigen and Perforin (
2.T lymphocytes or T Cells – attacks antigens directly “Kiss of Death”) which is inserted to the cell membrane,
• Macrophages shortly after that,
• Literally means “Big Eaters” the target cell ruptures
• Arise from monocytes formed in the bone marrow • They have a:
• Major role : to engulf foreign particles • License to KILL
• License to HELP
• License to Suppress
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CELL TYPE NORMAL VALUES THROMBOCYTES
RBC 4-6 million • Also called Platelets
WBC 4,000-11,000 • Average value : 250,000 – 450,000 / mm³
Neutrophils 3000-7000 • Lives for about 5 – 10 days
60-70% od WBC • Important in blood clotting
Eosinophils 100-400
1-4% of WBC
Basophils 20-50
0-2 of WBC
Lymphocytes 1500-3000
20-45 of WBC
Monocytes 100-700
2-8%of WBC
Platelets 150,000-450,000
HUMORAL (ANTIBODY-MEDIATED) IMMUNE RESPONSE
B Cells
–Matures into Plasma Cells responsible for Antibody production
–5 Classes of Immunoglobulins (MADGE) :
–Immunoglobulin M (IgM)
• 1st immunoglobulin produced in an immune response present in plasma,
too big to cross membrane barriers
– Immunoglobulin A (IgA)
• Sound in body secretions like saliva, tears, mucus, bile, milk & colostrum
– Immunoglobulin D (IgD)
• Present only in the plasma & is always attached to the B Cell
–Immunoglobilin G (IgG)
• 80% of circulating antibodies
• Can cross the placenta and provide passive immunity
• Present in all body fluids
–Immunoglobulin E (IgE)
• Responsible for Allergic & hypersensitivity reactions
• Stimulates Mast cells & Basophils to release Histamine which mediates
inflammation & the allergic response
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HEMATOPOIESIS (BLOOD CELL FORMATION)
• Occurs in the Red Bone Marrow, chiefly in flat bones like Skull, ribs,
pelvis, sternum and proximal epiphyses of the humerus and femur
• Erythropoiesis – RBC production, is a very active process
• RBC are continuously being destroyed by the liver & spleen
• RBC’s have a lifespan of 120 days
• As RBC’s are destroyed, iron is recycled to the bone marrow for use in
the formation of new RBC’s
• Erythropoietin – secreted by the kidneys & released when blood levels of
Oxygen begins to decline for any reason; which stimulates the Red Bone
Marrow to produce more RBC’s
ERYTHROCYTES
> destruction
- mature cells removed chiefly by spleen & liver
* BILIRUBIN = byproduct of Hgb released when RBC’s destroyed
* IRON = freed from Hgb during bilirubin formation
= transported to bone marrow via
TRANSFERIN & reclaimed for new Hgb production
ERYTHROPOIESIS- RBC production Plasma Clotting Factors
Requirements : I Fibrinogen
a. Erythropoietin II Prothrombin
b. Iron III Tissue Thromboplastin
c. Folic Acid IV Calcium
d. Vitamin B6, Vitamin B12 V Proacelerin
e. Vitamin C VII Proconvertin
`` Liver and Spleen- Graveyard of the RBC VIII Antihemophilic Factor
Hemostasis (Blood Clotting) IX Christmas Factor
X Stuart – Prower Factor
XI Plasma Thromboplastin Antecedent
XII Hageman Factor
XIII Fibrin Stabilizing Factor
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ANEMIA
• Conditions in which the number of RBC’s or amount of hemoglobin is
lower than normal leads to hypoxia and ischemia
CLASSIFICATIONS OF ANEMIA ACCORDING TO ETIOLOGY
BLOODING HYPOPROLIFERATIVE HEMOLYTIC
Resulting from RBC Loss Low RBC production Increase RBC destruction
Accidents/trauma Iron deficiency Enlarged spleen
Surgery Vit B12 deficiency Sickle Cell
Childbirth Folic acid deficiency Thalassemia
Ruptured Blood Vessel Vit C deficiency G6PD
Menorrhagia Chronic disease Drug-induced
Aspistaxia Low erythropoietin
Hemorrhoids Cancer
GI Bleeding
Cancer
IRON DEFICIENCY ANEMIA
• most common type of anemia
•Iron stores are depleted, resulting in a decreased supply of iron for the
manufacture of hemoglobin in RBC’s
Commonly results from blood loss, increased metabolic demands, syndromes of
gastrointestinal malabsorption, and dietary inadequacy
• cause : inadequate absorption or excessive loss of iron
• Bleeding – principal cause in adults
• Vegetarian diets
• Vitamin C – increases iron absorption
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ASSESSMENT FINDINGS
-fatigue, dyspnea, palpitatations & dizziness, pallor, brittle hair & nails, pica,
glossitis, cheilosis, koilonychia
Mild cases – asymptomatic
NURSING INTERVENTIONS
1. Identify the cause
2. Monitor S/Sx of bleeding – stool, urine and GI contents
3. Provide rest
4. Give iron preparations ( 6 – 12 months )
-Ferrous Sulfate, Gluconate , Fumarate
a. always give after meals or snacks
b. dilute liquid preps and give thru straw
c. give with orange juice (Vitamin C enhances
absorption)
d. warn clients the stool will become black and can cause constipation
5. For clients with poor absorption or continuous blood loss Cheilosis
-IM or IV of Iron Dextran Laboratory findings :
a. Use 1 needle to withdraw and another for injection RBC’s are small / microcytic and pale
b. Use z-track method • ↓ hemoglobin & hematocrit
c. don’t massage but encourage ambulation • ↓serum iron & ferritin
d. usually, deep IM at buttocks
6. Give dietary teaching – liver, meats, nuts, egg yolk, shellfish, legumes,
etc.
7. Increase intake of roughage and fluids to prevent constipation.
PERNICIOUS ANEMIA
• Vitamin B12 Deficiency Anemia
• caused by inadequate Vit. B12 intake or deficiency in intrinsic factor Vit.
B12 combines with intrinsic factor so it can be absorbed in the ileum into
the bloodstream
• the result is abnormally large erythrocytes and hypochlorhydria ( a
deficiency of hydrochloric acid in gastric secretions).
• Lack of intrinsic factor is caused by gastric mucosal atrophy (possibly due to
heredity, prolonged iron deficiency, or an autoimmune disorder), can also
result in client who have had a total gastrectomy
• Usually occurs in men and women over age 50, with an increase in blue eyed
persons.
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Assessment : Lab Results
Anemia- symptoms are: -Decrease RBC
•Fatigue, weakness • dyspnea -Decreased free Hydrochloric acid
•Palpitations & dizziness • paresthesias -Large RBC / Megaloblast
•Pallor • wt. loss -Positive Schilling Test– definitive test for Pernicious
•Confusion anemia
↓
• intellectual function - used to detect lack of intrinsic factor
•Sore tongue
NURSING INTERVENTIONS
1. Drug Therapy
a. Vit. B12 injections monthly for life
b. Iron Preparations
c. Folic Acid
2. Transfusion therapy
3. Bed rest
4. Mouth care
5. Dietary teaching
6. Teach about importance of lifelong Vitamin B12
therapy
HEMOLYTIC ANEMIAS
• ↑ rate of RBC destruction
• short life span of RBC
• G6PD
• Sickle cell anemia
• Thalassemia
• DIC
• Transfussion incompatibilities
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SICKLE CELL ANEMIA
• Most common inherited disease among black Americans.
• Also found in Arabian, Mediterranean and Caribbean descent
• Hgb S ( abnormal hemoglobin ), which has reduced oxygen carrying
capacity, replaces all or part of the hemoglobin in the RBC’s.
• Life span is 6-20 days instead of 120, causing hemolytic anemia.
• Death often occurs in early adulthood due to occlusion or infection.
• During decreased O2 tension, lowered pH, dehydration and severe
infections, RBC’s change from round to sickle or crescent shape
• Sickled cells don’t slide thru vessels as normal RBC’s do, causing
clumping, thrombosis, arterial obstruction, increased blood viscosity,
hemolysis and eventual tissue ischemia and necrosis
ASSESSMENT
• Signs and symptoms of anemia – pallor, weakness
• Hepatospleenomegaly
• Dactylitis (Symmetric swelling of the hands and feet) – called hand-foot
syndrome
• Other problems :
– CVA
– MI
– Growth retardation – initial manifestation
– Decreased fertility
– Priapism
– Recurrent severe infections
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MEDICAL MANAGEMENT
A. Drug therapy
> analgesic/narcotics to control pain
• Avoid meperidine (Demerol) due increased risk of seizures in children
> antibiotics to control infection.
B. Blood transfusions
C. Hydration:oral and IV
D. Bed rest
E. Surgery: splenectomy
INTERVENTIONS
• Administer O2 & Blood Transfusion as Rx
• Maintain adequate hydration
• Avoid tight clothing that could impair circulation.
• Keep wounds clean and dry.
• Provide bed rest to decrease energy expenditure and oxygen use.
• Encourage patient to eat foods high in calories, CHON, with folic acid
supplementation.
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THALASSEMIA
What is thalassemia?
Genetic blood disorder resulting in a mutation or
deletion of the genes.
Normal hemoglobin is composed of 2 alpha and 2
beta globins
2 types of thalassemia:
alpha and beta.
Hemolytic anemia: Thalassemia
• Decrease in hb level, small red blood
THALASSEMIA cells, anemia and destructions of red
• which are characterized by reduced or blood cell (hemolysis).
absent synthesis of one or more globin • Abnormal globulin chain in hemoglobin.
chain type. • It is alpha and beta
• The imbalance of globin chain synthesis, • Thalassemia major is characterized by
which result leads to ineffective severe anemia, hemolysis, and ineffective
erythropoiesis. It need blood transfusion
erythropoiesis and a shortened red cell
for proper child growth and development.
lifespan.
Hemolytic anemia: Thalassemia
• Organ dysfunction result from iron
overload so chelation therapy is needed.
• Chelation therapy is a medical procedure
that involves the administration of
chelating agents to remove heavy metals
from the body.
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HEMOLYTIC ANEMIA: G6PD • Clinical manifestation: asymptomatic then
• Deficiency in the gene within red blood cell pallor, jaundice, hemoglubinuria, increase retics
which protect its stability. increase
• Assessment and diagnostic finding:
• It happens when RBCs is stressed by screening test of G6PD
medication (they should carry identification card • Medical management: stop causing
with them) or curtain substance (Naftalin, medication, transfusion in severe cases,
Henna, beans • Nursing management: educate patient
and give him/her list of medication to be
avoided, genetic counseling may be
needed.
Identify different bleeding disorders, clinical manifestation, assessment and diagnostic findings,
medical and nursing management
1. THROMPOCYTOPENIA
2. HEMOPHILIA
THROMPOCYTOPENIA
• Is low platelet level from decreased production,
increased destruction and increase consumption
of platelets. table 33-4
• Clinical manifestation: bleeding, petechiae, • Nursing management: chart 33-8 pg 938
nasal bleeding or after surgery, Aspirin ,,,,,,,, to prevent complication and control
• Assessment and diagnostic finding: bone bleeding.
marrow aspiration, peripheral smear test
• Medical management: platelets
transfusion, splenectomy
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HEMOPHILIA
• Nursing management: prevent unnecessary
trauma, safety at home and workplace, avoid
• Two types: hemophilia A ( deficiency medication interfere with platelet aggregation
factor VIII and B (deficiency factor IX) e.g: aspirin, NSAIDs, herbs and alcohol. Dental
hygiene to prevent bleeding from dental
extraction, no injections, carrying Identification
• Clinical manifestation: hemorrhage after card everywhere, use cold compress for pain,
minimal trauma to knees, elbow, wrists, genetic testing and premarital counseling for
pain, hematoma males to prevent its occurrence for future
generation
• Medical management: before fresh
frozen plasma now factor VIII and factor IX
replacement, some medication is found
useful in these case to raise the factor.
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IMMUNOLOGY
It the branch of bio medical science that
covers the study of all the cells of immune
system. It deals with the physiological
function of both health and disease.
The immunity is derived from Latin word
(IMMUNITAS) which means exemption
from performing public service and charge.
TYPES OF IMMUNITY
1)Classical Immunology
2)Clinical Immunology
3)Developmental Immunology
4)Diagnostic Immunology
5)Cancer Immunology
6)Reproductive Immunology
Clinical Immunology:-
It deals with the study of disease caused by disorder of immune system i.e. malignant growth and
allograft (transplant rejection).
Classical Immunology:-
It lies in the field of epidemiology and medicine Deals with the relation of body system pathogens
and immunity.
Diagnostic Immunology:-
It deals with specificity of the bond between antigen and antibody and their interaction.
Cancer Immunology:-
It deals with interaction between the cancerous cells and the immune system
including tumors that may be benign or malignant.
Reproductive Immunology:-
It deals with the study of reproductive process including fetus acceptance, fertility
problems and premature deliveries.
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IMMUNITY
State of having efficient biological defenses to avoid the infection or
disease & other unwanted biological invasions. Basically it the capability of
the body to resist the harmful microbes from entering.
NATURAL IMMUNITY:-
It is innate (in born) naturally present in a
person at the time of birth.
It is further divided into two types
ACTIVE:-
It is induced when a person exposed to a live pathogen then its body induces a primary immune
response which is stored in a immunological memory
PASSIVE:-
It is induced in new born babies when they drink the mothers milk because mothers milk
naturally contains antibodies or antibodies may transfer through placenta to the fetus. It is
short lived immunity
FIRST LINE OF DEFENSE:-
1)The aim of the first line of defense is to
stop microbe to entering in the body
2)The skin and the mucous membrane act
as a physical to stop their entering.
3)If there is wounded or cut then the clot
of blood prevent the entry of microbes
4)The surface body of The skin , digestive
system and nose covered by the microbes
known as GERNAL BODY FLORA. They protect
us from invading of harmful microbes.
5)The respiratory track and the nose is lined
with the sticky fluid called as MUCUS. Along
with mucus CILIA is also present both of these
trap the dust particles and they move out by
sneeze or cough reflex
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SECOND LINE OF DEFENSE:-
1)If the microbes some how manage to gain entry in
body then the second line of defense will be activate.
2)It is non specific as it can encounter any type of
microbe.
3)When microbe gain entry then our immune system
send PHAGOCYTES that engulf these microbes and
digest them by digestive enzymes.
4)This process of engulfing microbes or other solid
particles is called PHAGOCYTOSIS.
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ANTIBODIES/ IMMUNOGLOBULIN'S:-
A protein that is produce by B
lymphocytes in response to the
presence of an antigen is called
ANTIBODY.
Antibody is gamma globulin in nature so
its is also called immnoglobulin(Ig).
Immunoglobulin's forms 20% of plasma
protein.
ANTIBODY TYPE FUNCTION
IgA Found in saliva, tears, mucus, breast milk and intestinal fluid,
IgA protects against ingested and inhaled pathogens.
This antibody is found on the surface of your B cells. Though
IgD its exact function is unclear, experts think that IgD supports
B cell maturation and activation.
Found mainly in the skin, lungs and mucus membranes, IgE
antibodies cause your mast cells (a type of white blood cell)
IgE to release histamine and other chemicals into your
bloodstream. IgE antibodies are helpful for fighting off
allergic reactions.
This is the most common antibody, making up approximately
IgG 70% to 75% of all immunoglobulins in your body. It’s found
mainly in blood and tissue fluids. IgG antibodies help protect
your body from viral and bacterial infections.
Found in your blood and lymph system, IgM antibodies act as
IgM the first line of defense against infections. They also play a
large role in immune regulation.
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MECHANISM OF ACTION OF ANTIBODIES
THERE ARE TWO METHODS AS FOLLOW:
1)DIRECT METHOD.
2)COMPLEMENT SYSTEM.
1)DIRECT METHOD:-
Agglutination:-
The foreign bodies like RBC’s or bacteria with
antigens on their surface are held together in a clump by antibodies.
Precipitation:-
The soluble antigens like (Tetanus) toxins are
converted into insoluble forms and the precipitated.
Neutralization:-
The antibodies covers the site of antigenic products.
Lysis:-
It is done by the most potent antibodies.
These antibodies rupture the cell membrane of the organisms and destroy them.
COMPLEMENT SYSTEM:-
The indirect action of the antibodies are
stronger than the direct action and play a vital role in defense mechanism.
Complement system enhances the various activities during the fight against
organisms.
It is the system of plasma enzymes represented by number
(C1,C2……C9).Including three subunits of
C1(C1q,C1r,C1s)
ANTIGEN
Those substance that induce specific immune reactions in body Or a foreign
substance that induces the formation of antibodies.
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ROLE OF APC:-
The invading foreign organisms either engulfed
by macrophages through phagocytoses .Latter
the antigens from these organisms is digested
into small peptide products move towards the
surface of APC and bind with Human leukocyte
Antigen (HLA).
HLA is genetic matter present in the molecule
of class II major histocompatibility complex
(MHC)which is situated on the surface of APC..
CELLULAR IMMUNE RESPONSE /CELL
MEDIATED RESPONSE:
Cellular immune response kills the cells of the
body that have been effected with virus or
cancerous. In this response Tc (cytoxic T cells)
play vial role .Tc contain a molecule called as
perforin.This molecule pokes hole in the
target cell and kills them
HUMORAL IMMUNE RESPONSE:-
In this response the immune triggers specific B cells to
proliferate and to secrete large amount of specific
antibodies. These antibodies combat a particular virus or
microorganisms and kill them.
The Helper T cells (Th cells) play a
vital role in immune system. They do this
by forming a series of mediators called as
Lymphokines
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IMMUNE DEFICIENCY DISEASE:-
IT IS THE GROUP OF DISEASE IN WHICH SOME
COMPONENTS OF IMMUNE SYSTEM IS
MISSING OR DEFECTIVE. NORMALLY THE
DEFENSE MECHANISM THAT DEFEND OUR
BODY IS FAIL TO PROTECT US AND THE
ORGANISM OF EVEN LOW VIRULENCE PRODUCES
SEVERE EFFECT.
THE ORGANISM WHICH TAKE ADVANTAGE OF
DEFECTIVE IMMUNE SYSTEM ARE CALLED
OPPORTUNISTS
ACQUIRED IMMUNE DEFICIENCY DISEASE:
ITS IS OCCURS BY SOME ORGANISM. ITS MOST
COMMON TYPE IS (AIDS)ACQUIRE IMMUNE
DEFICIENCY SYNDROME.
AIDS IS BASICALLY THE INFECTIOUS DISEASE THAT IS
CAUSE BY HUMAN IMMUNE DEFICIENCY VIRUS
(HIV).
A PERSON IS DIAGNOSED WITH AIDS WHEN THE
CD4 (CLUSTER OF DIFFERENTIATION 4 A
GLYCOPROTEIN FOUND ON THE SURFACE OF IMMUNE
CELLS) COUNT IS BELOW 200 CELLS PER MILIMETER
BLOOD.
INFECTION OCCURS WHEN A GLYCOPROTEIN SYMPTOMS:-
FROM HIV BINDS TO THE SURFACE RECEPTOR OF 1)Fatigue.
T LYMPHOCYTES ,MONOCYTES,MACROPHAGES 2)Loss of Weight.
AND LEADING TO THE DESTRUCTION OF THESE 3)Night sweats.
CELLS. IT CAUSES THE DECREASE IN THE 4)Oral and Vaginal ulcers.
PROGRESSIVENESS OF IMMUNE FUNCTION AND Mode of transmission:-
RESULTING IN OPPORTUNIST INFECTION OF 1)Contaminated blood transfusion.
VARIOUS TYPES. THE COMMON OPPORTUNIST 2)Contaminated needles.
INFECTION WHICH KILL THE PATIENT ARE 3)From mother to fetus during pregnancy and
1)PNEUMONIA breast feeding.
2)MALIGNANT SKIN CANCER 5)Unsafe vaginal sexual intercourse.
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Auto Immune Disease:-
COMMON AUTOIMMUNE DISEASE:-
A condition in which the immune system
mistakenly attacks body’s own cells & tissues.
1)INSULIN DEPENDENT DIABETES
Tolerance:- MELLITUS(IDDM)
Usually the antigen induces the immune 2)HASHIMOTOS THYRODITIS
response in the body. The condition in the 3)GRAVES DISEASE
immune system fails to give response to an
antigen is called Tolerance.
This is true with respect to the body’s own
ALLERGY:-
antigen called as Self Antigen or Auto The term allergy means
antigens . Hypersensitivity.
Normally the body has a tolerance against the Allergy is the abnormal immune
self antigen however in some occasions the response to a chemical or physical
tolerance fails. Such a state is called is agent.
autoimmunity and the T lymphocytes or the Allergens:-
production of the autoantiboies from Any physical or chemical agent that
lymphocytes.Tc cells of the immune system produces the manifestation of allergy
attacks the body’s normal cells whose surface is called Allergens.
contain the self antigen. 1)During the first exposure to an allergen, the
Thus the autoimmune disease occurs when immune doesn't normally produce any
body normal tolerance decrease and the reaction in the body.
immune system fails to recognize the body’s 2)Sensitization to the allergens is required.
own tissues as “self” 3)So the subsequent exposure to allergens is
required to cause a variety of inflammatory
IDDM:-
responses. These inflammatory responses are
It is very common in childhood and it is due to Human
called Allergic Reactions or Immunological
Leukocyte Antigen (HLA).
Hypersensitivity Reactions.
Common Causes:-
Common Allergic conditions are:-
1)Development of islets cell
1)Food Allergy.
autoantibody against Beta cells in the islets of
2)Bronchial Asthma.
langerhans in pancreas.
Common Allergens:-
2)Development of autoantibody against insulin.
1)Contact (chemical substance)
3)Activation of T cells against Islets.
2)Inhalation (pollen)
2)Hashimotos Thyroditis:-
3)Ingestion (food)
It is common in late middle-age women.
4)Injection (drug
The auto antibodies impair the activity of thyroid
follicles leading to the hypothyroidism.
3)Graves Disease:-
In some cases the auto antibodies stimulate the
(TSH) receptors leading to
the hypothyroidism.
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NEUROLOGY VISUAL GUIDE Neurology is the branch of medicine that
deals with diseases of the nervous system.
CENTRAL NERVOUS SYSTEM
INTRACRANIAL CEREBRUM
PART Two cerebral hemispheres
Connected to:
CEREBRUM 1. each other by corpus
callosum
BRAIN STEM 2. brain stem by cerebral
peduncles
CEREBELLUM
SPINAL PART
SPINAL CORD & CEREBELLUM
CAUDA EQUINA
• Behind the brain stem
• Formed of : medline vermis
two cerebellar hemispheres
• Composed of :
outer grey matter and inner
White matter
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Frontal Parietal
Lobe Lobe
Temporal Occipital
Lobe Lobe
CONTAINS: CEREBELLAR
PEDUNCLES
• CN 3,4 in midbrain
• CN 5,6,7,8 in pons
• CN 9,10,11,12 in medulla -Superior peduncle connects
cerebellum with midbrain.
-Middle peduncle connects
cerebellum with pons.
-Inferior peduncle connects
cerebellum with medulla
oblongata
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CRANIAL NERVES
OLFACTORY NERVE
Smell
OPTIC NERVE
Visual
Acuity
OCULOMOTOR NERVE
Eye movement
TRIGEMINAL NERVE
Facial
TROCHLEAR NERVE Sensation
Vertical Eye
movement
ABDUCENT NERVE
Lateral Eye
movement
TRIGEMINAL NERVE
Facial
Expression
VESTIBULOCOCHLEAR
NERVE
Hearing
Balance GLOSSOPHARYNGEAL
NERVE
Swallowing,
gagging
HYPOGLOSSAL NERVE
Tongue
Movement
VAGUS NERVE
Gas, reflux,
cough, sensation,
digestion
Sensory cranial nerves: contain only afferent (sensory) fibers
Ⅰ
– Olfactory nerve
Ⅱ
– Optic nerve
– ⅧVestibulocochlear nerve
• Motor cranial nerves: contain only efferent (motor) fibers
– ⅢOculomotor nerve
– ⅣTrochlear nerve
Ⅵ
– Abducent nerve
– ⅪAccessory nerve
– ⅫHypoglossal nerve
• Mixed nerves: contain both sensory and motor fibers
Ⅴ
– Trigeminal nerve,
– ⅦFacial nerve,
– ⅨGlossopharyngeal nerve
Ⅹ
– Vagus nerve
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CERVICAL
SPINE
THORACIC • Inside spinal canal
SPINE •
•
•
End at lower border of L1
The lowest 3 segments = Conus
The above 4 segments = Epiconus
• Inner grey matter and outer white matter
LUMBAR
SPINE
SACRUM
COCCYXE
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STROKES
• Acute severe manifestations of cerebrovascular disease
Hemorrhage
Ischemic
Cholesterol
plaque build
Blood lot up
blocks artery
ETIOLOGY RISK
Hypertension
A. Ischaemic stroke
- Lacunar infarct
- Carotid circulation obstruction High BP
- Vertebrobasilar obstruction
B. Hemorrhagic stroke
- Spontaneous intracerebral hemorrhage
- Subarachnoid hemorrhage
Cardiac
- Intra cranial aneurysm abnormalities
- Arteriovenous malformation LVH, Dilatation
Obesity Diabetes
Glucose
intolerance Elevated
Smoking blood
lipids
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RENAL NURSING
Lateral to vertebral
column high on body
wall, under floating ribs
in retro-peritoneal position
SECTIONAL ANATOMY
Cortex: outer layer, light reddish
brow, granular appearance (due
to many capillaries)
Medulla: darker striped
appearance (due to tubules)
Subdivided into distinct renal
pyramids, terminating with a
papilla. Separated by renal
columns from the cortex
URINE COLLECTION
Ducts within each renal papilla release urine into:
MINOR CALYX
MAJOR CALYX
RENAL PELVIS
URETER
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FUNCTIONS OF URINARY SYSTEM (KIDNEYS)
Regulate various properties of the blood.
Ionic composition
PH
Volume
Pressure Produce hormones
Excrete waste products & foreign substances.
FUNCTIONAL UNIT: TWO TYPES OF NEPHRONS
NEPHRON • Cortical nephrons (85%)
shorter, mostly in cortex of
● Renal corpuscle: kidney,
– Glomerulus • Juxtamedullary nephrons
– Bowman’s capsule (15%), "juxta-next-to" the
• Tubular passageways with medulla - responsive to ADH,
associated blood vessels: can concentrate urine
– Proximal Convoluted Tubule
– Loop Of Henle
– Distal Convoluted Tubule
– Collecting Duct
ANATOMY OF URINARY BLADDER
Hollow muscular organ
Internal folds - rugae - permit expansion (max. holding capacity ~ 1L)
Area at base delineated by openings of ureters and urethra -
without muscle
Consist of…
1. Transitional epithelium
2. Detrusor muscle – smooth muscle
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TRANSITIONAL EPITHELIUM
from renal pelvis to neck of urethra.
URETHRA
Muscular tube
2 types
1)External urethral sphincters – voluntary skeletal
muscle spincter
2)Internal urethral sphincter-involuntery smooth
muscle spincter
Female - short – from base of bladder to vestibule
Male
1. prostatic urethra
2. membranous urethra
3. penile (spongy) urethra
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HORMONAL
CONTROL OF
KIDNEY
FUNCTION
ABNORMAL
CONSTITUTES OF
URINE
Glucose- when present in urine Albuminuria- nonpathological conditions
condition called glycosuria excessive exertion, pregnancy, overabundant
(nonpathological) [glucose not normally protein intake-- leads to physiologic albuminuria
found in urine] Pathological condition- kidney trauma due to
Indicative of: blows, heavy metals, bacterial toxin
• Excessive carbohydrate intake Ketone bodies- normal in urine but in small amts
• Stress Ketonuria- find during starvation, using fat stores
• Diabetes mellitus Ketonuria is couples w/a finding of glycosuria-- which
Albumin-abnormal in urine; it’s a very large is usually diagnosed as diabetes mellitus
molecule, too large to pass through glomerular RBC-hematuria
membrane > abnormal increase in permeability Hemoglobin
of membrane Hemoglobinuria- due to fragmentation or hemolysis of
RBC; conditions: hemolytic anemia, transfusion
reaction, burns or renal disease
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BILE PIGMENTS
Bilirubinuria (bile pigment in urine)- liver pathology such as
hepatitis or cirrhosis
WBC
Pyuria- urinary tract infection; indicates inflammation of
urinary tract
Casts- hardened cell fragments, cylindrical, flushed out of
urinary tract
WBC casts- pyelonephritus
RBC casts- glomerulonephritus
Fatty casts- renal damage
RENAL FAILURE
SYMPTOMS OF KIDNEY FAILURE
The symptoms that occur in both acute and chronic kidney failure
include:
Edema: Reduced excretory function leads to water retention in
the body tissues, giving rise to puffiness. Face, hands and
legs (especially feet and ankles) swell up owing to such fluid
buildup.
Vomiting and diarrhea: Accumulation of excessive amounts of
urea and other wastes in blood, leads to nausea and
vomiting. In individuals with chronic kidney failure, vomiting
generally occurs in the morning, whereas those with acute
renal failure experience frequent episodes of vomiting within
a period of 2-3 days. It is often accompanied with diarrhea.
Dehydration: The excessive loss of fluids through vomiting and
diarrhea, leads to dehydration and excessive thirst.
Breathing difficulty: The inability to get rid of excess fluids may
lead to fluid accumulation in the lungs, thereby causing
shortness of breath. Also, the oxygen-carrying capacity of
blood reduces due to increased blood toxicity, leading to
heavy breathing.
Bloody stools: In extreme cases, kidney failure may lead to
gastric or intestinal bleeding. This is indicated by the
presence of blood in stools. Black or tarry stools indicate
bleeding in the upper gastrointestinal tract
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NEUROLOGICAL AND NEUROMUSCULAR SYMPTOMS: URINARY SYMPTOMS:
Renal failure leads to an increase Depending on the exact cause and
in the phosphate levels of blood, physiological abnormality, either a
which affects the function of reduction or an increase in the urine output
peripheral nerves as well as the and frequency occurs. The prominent
neuromuscular functions. This urinary signs and symptoms of renal failure
causes: are:
• Muscle pain • Oliguria/Hyperuria
• Muscle spasticity • Excessive urination at night
• Confusion • Painful urination
• Irritability • Urine discoloration
• Depression • Blood in urine
• Mood swings • High amounts of protein in the urine
• Disorientation
• Numbness and tingling in the limbs
SYMPTOMS OF KIDNEY FAILURE
Other symptoms: The above health issues collectively lead to the following symptoms.
• Easy bruising
• Breath odor
• Fatigue
• Easy tiring
ACUTE KIDNEY INJURY (AKI)
Previously known as acute renal failure ( ARF), is rapidly progressive
loss of renal functions. A condition in which the kidneys are unable to remove
accumulated metabolism from the blood, leading to altered
fluid, electrolyte and acid-base balance.
AKI has an abrupt onset and with propmt intervention is often reversible; if left
untreated it leads to permanent renal damage.
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CHRONIC KIDNEY DISEASE (CKD)
• CKD ; a spectrum of different pathophysiologic
processes associated with abnormal kidney function,
and a progressive decline in glomerular filtration rate
(GFR).
• chronic renal failure applies to the process of
continuing significant irreversible reduction in
nephron number, and typically corresponds to CKD
stages 3–5.
• End-stage renal disease; a stage of CKD where the
accumulation of toxins, fluid, and electrolytes
normally excreted by the kidneys results in the
uremic syndrome.
STAGES OF CHRONIC RENAL DISEASE
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RISK FACTORS FOR CKD
• hypertension
• diabetes mellitus
• autoimmune disease such as SLE, vasculitis
• older age
• African ancestry
• family history of renal disease
• previous episode of acute renal failure & the presence
of proteinuria
• structural abnormalities of the urinary tract.
• Congenital; Polycystic kidney disease, Alport’s
syndrome.
• Glomerular diseases eg IgA nephropathy
• Renal artery stenosis
PATHOPHYSIOLOGY OF CKD
2 mechanisms;
- Initiating mechanisms specific to the underlying
etiology (e.g., immune complexes and mediators
of inflammation or toxin exposure)
- A set of progressive mechanisms, involving
hyperfiltration and hypertrophy of the
remaining viable nephrons, eventually sclerosis
& dropout of the remaining nephrons.
• The responses to reduction in nephron number
are mediated by vasoactive hormones,
cytokines, and growth factors.
CLINICAL PRESENTATION
NB: Uraemia refers to clinical symptoms & signs • Nocturia
of RF due to loss of the excretory, metabolic • tiredness or breathlessness
and endocrine functions of the kidney. • Weakness
• asymptomatic until GFR falls below 30 • Kussmaul's breathing
ml/minute • anorexia and nausea
• may present as a raised blood urea and • hiccoughs
creatinine found during routine examination, • pruritus
often accompanied by HTN, proteinuria or • vomiting
anaemia. • muscular twitching
• fits,
Tireddrowsiness and
of bad grades? coma
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PHYSICAL EXAMINATION
• Wasted • Ecchymoses
• Yellow complexion • Increased RR & depth
• Pallor • P. neuropathy
• Features of cardiac • Absent reflexes
tamponade • Reduced sensation
• Brown line • Paraesthesias
pigmentation of nails
• Restless legs
• Excoriations
DIAGNOSIS AND MANAGEMENT
• Proper history(causes/risk factors, symptoms,
complications)
• Physical examination If diagnosis is not known
• Immunoglobulins and protein electrophoresis
• INVESTIGATIONS
• Urinary Bence Jones protein
- CBC
• Complement
- Urinalysis; protein
• ANA: and dsDNA if ANA is positive
- RFTs
• ENA: if a connective tissue disorder is suspected
- LFTs (albumin) • Rheumatoid factor
- Calcium and phosphate levels • ANCA: in all possible inflammatory renal disease
- PTH • Anti-GBM: in all possible inflammatory renal
- Hepatitis(B & C) and HIV serology disease
- Others tailored to underlying cause • Imaging
- Renal U/S ( kidneys, symmetry, size, renal masses,
TREATMENT evidence of obstruction)
• Identify the underlying renal disease , by
- Renal artery imaging: if renovascular disease is
history, examination, testing of biochemistry,
immunology, radiology and biopsy suspected… doppler U/S
• Look for reversible factors which are making - Voiding cystogram; reflux nephropathy
renal function worse
• Attempt to prevent further renal damage.
- Radiographic contrast imaging not recommended
• Attempt to limit the adverse effects of the loss - Chest X-ray; heart size, pulmonary oedema
of renal function. - ECG; if > 40 years or there are risk factors for cardiac
• Institute renal replacement therapy (dialysis,
transplantation
disease
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Renal Calculi
UROLITHIASIS(RENAL STONES)
The stone formation within the kidney or collecting system is called
Urolithiasis
Urolithiasis calculus formation at any level in the urinary collecting system
• kidney (nephrolithiasis),
• ureter (ureterolithiasis),
• bladder (cystolithiasis),
COMMON STONES:
OXALATE (CALCIUM OXALATE)
PHOSPHATE
URIC ACID / URATE
CYSTINE
UN-COMMON
XANTHINE STONES – (Autosomal Recessive . Def of Xanthine
Oxidase leading to Xanthinuria)
DIHYDROXY ADENINE STONE – ( Def. of enzyme adenine phospo
ribosyl transferase )
SlLICATE STONES – Rare in humans ( excess intake of Antacid with
Mg Trisilicate. Mostly in cattle due to ingestion of Sand )
MATRIX - Infection by Proteus - Radiolucent (all calculi have some amt
( 3%) of matrix but matrix calculus has 65% Matrix content in calculi)
Types of stones
Calcium oxalate stones:
Most common type (70%) containing calcium oxalate or calcium
oxalate mixed with calcium phosphate
Triple phosphate stones:
(15%) composed of magnesium ammonium phosphate
Urate stones:
About (10%) copmmposed of uric acid
Cystine stones: (1-2%) made up cystine
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PATHOGENESIS
Calcium oxalate stones
Hypercalcemia:
About (10%) of patients have hypercalcemia due to hyperparattyroidism,
or vitamin D intoxication etc.
Hypercalciuria:
About (55%) have hypercalciuria without hypercalcemia (idipathic
hypercalciuria). Probably it results from hyperabsorption from calcium
from intestine or impairment in renal tubular reabsorption of calcium
Idiopathic:
In about 20% patients,stone formation occurs without either
hypercalcemia or hypercalciuria
Triple phosphate stones:
The magnesium ammonium phosphate (struvite) stones usually follow
the infection by urea splitting bacteria(proteus and stayphlococcus)
which convert urea to ammonia,producing urine alkaline in which
magnesium ammonium phosphate salts precipitate to form stone.
• Urate stones:
Composed by Uric acid
Caused by high intake of protein diet and gout
Cystine stones:
They are associated with genetically determined defect in the renal
transport of cystine aminoacid.
Common sites of stone formation
•Renal pelvis
• Calyces
•Urinary bladder
PREDISPOSING FACTORS
Metabolic factors: Stasis:
• Hypercalciuria Obstruction to urine flow encourages salt
• Hyperphosphaturia precipitation
• Oxaluria Urinary pH:Uric acid and oxalate stones form in
• Uric acid excess an acidic urine,while
Dehydration: the phophate stones develop in an alkaline
Causing increased urinary urine
concentration Renal disease:
Renal infections(producing urine alkaline)
Renal Tumors (producing renal stasis)
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COPMLICATIONS CLINICAL FEATURES
• Pyelonephritis • Gross hematuria
• Acute urinary retension • Nausea and vomiting
• Recurrent chances of infection • Frequent or painful urination
• Dull pain when stone remains in kidney
• Renal failure
• Episode of flank pain radiating to
• Pyonephrosis
the groin when small stones pass
Acute obstruction of ureter--- into the ureters
severe colic
Flank pain referred to genitalia
Nausea, vomiting
Microhematuria
Chronic stone distends to be
associated with large or multiple
stones
can be little or no pain
may have impaired renal function,
anemia, weight loss etc.
concomitant infection more likely
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GLOMERULONEPHRITIS
It is acute nephritic syndrome: the sudden onset of gross hematuria, edema, hypertension, and
renal insufficiency. Most common cause of gross hematuria in children next is IgA
nephropathy
ETIOLOGY AND EPIDEMIOLOGY
Acute poststreptococcal glomerulonephritis follows infection of the throat or skin with certain
“nephritogenic” strains of group A b-hemolytic streptococci.
In cold weather, poststreptococcal glomerulonephritis commonly follows streptococcal
pharyngitis,
In warm weather glomerulonephritis follows streptococcal skin infections.
PATHOLOGY
Kidneys - symmetrically enlarged.
Light microscopy - all glomeruli appear enlarged
diffuse mesangial cell proliferation
Polymorphonuclear leukocytes are common in glomeruli
Crescents and interstitial inflammation may be seen in severe cases.
Immunofluorescence microscopy - deposits of immunoglobulin and complement on the
glomerular basement membranes (GBMs) and in the mesangium.
Electron microscopy - electron-dense deposits are observed on the epithelial side of the GBM
PATHOGENESIS
depression in the serum complement (C3) level suggest that poststreptococcal
glomerulonephritis is mediated by immune complexes,
complement activation is primarily through the alternative (immune complex activated)
pathway
CLINICAL MANIFESTATIONS
rare before the age of 3 yr.
Onset 1–2 wk after an antecedent streptococcal infection.
asymptomatic microscopic hematuria with normal renal function
acute renal failure.
Depending on the severity of renal involvement,
edema, hypertension, oliguria.
Encephalopathy or heart failure due to hypertension or both
The edema is usually a result of salt and water retention, nephrotic syndrome may also occur.
Nonspecific symptoms such as malaise, lethargy, abdominal or flank pain, and fever are
common.
The acute phase generally resolves within 2 mo after onset, but urinary abnormalities may
persist for more than 1 yr
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DIAGNOSIS
Urine - red blood cells (RBCs),
with RBC casts and proteinuria +, ++
Blood - Polymorphonuclear leukocytosis
Normochromic anemia due to hemodilution and low-grade hemolysis.
The serum C3 level is usually reduced.
Renal function tests –Urea and creatinine
Throat culture may be positive
Elevated antibody titer to streptococcal antigen(s) - ASO titer may not rise after streptococcal
skin infections.
Best single antibody titer to measure is that to the deoxyribonuclease (DNase) B antigen. An
alternative is the Streptozyme test -a slide agglutination procedure - detects antibodies to
streptolysin O, DNase B, hyaluronidase, streptokinase, and nicotinamide-adenine
dinucleotidase.
Rrenal biopsy ordinarily is indicated. To exclude systemic lupus erythematosus and an acute
exacerbation of chronic glomerulonephritis.
DD - Acute glomerulonephritis may also follow infection with coagulase-positive and -negative
staphylococci, Streptococcus pneumoniae, gram-negative bacteria, and certain fungal,
rickettsial, and viral diseases.
Bacterial endocarditis may also produce a hypocomplementemic glomerulonephritis with renal
failure.
COMPLICATIONS - Are due to ARF
volume overload
heart failure
hypertension
Hyperkalemia
Hyperphosphatemia
hypocalcemia
acidosis
seizures
uremia
PREVENTION
Systemic antibiotic therapy of streptococcal throat and skin infections does not eliminate
the risk of glomerulonephritis.
Family members of patients with acute glomerulonephritis should be cultured for group A
b-hemolytic streptococci and treated if culture positive.
PROGNOSIS
Complete recovery occurs in more than 95% of children with acute post streptococcal
glomerulonephritis.
Acute phase may be severe and lead to chronic renal insufficiency.
Appropriate management of the acute renal or cardiac failure and hypertension can avoid
mortality in the acute stage.
Recurrences are extremely rare. Hence no penicillin prophylaxis like Rheumatic fever
Compiled by Dr.N.S.Mani,Assistant Professor in Paediatrics,Medical College,Trichur.
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TREATMENT
Management is that of acute renal failure
10-day course of systemic antibiotic therapy, with penicillin therapy may be given but it does
not change the natural history of glomerulonephritis.
Bed rest if there is complication
Antihypertensive medications (diuretics, Angiotensin-converting enzyme inhibitors) are
indicated to treat hypertension and to avoid hypertensive complications.
THE NEPHROTIC SYNDROME
The nephrotic syndrome is clinical complex charactrised by number of reanal and external
features, the most prominent are
-Albumin Decrease
-Hypercoagulability
-Edema
-Lipiduria
-Proteinuria of >3.5g/day
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GLOMERULAR PROTEINURIA
When the components of the filtration barrier are disrupted leads to protein
loss and worsens renal function
COMPLICATIONS:
-Albumin edema
-Transferin anemia
-Vit-S binding globulin
Hypocalcemia>convulsions
HYPOALBUMINEA AND HYPERLIPIDEMIA
Due to urinary loss of albumin, Liver tries to compensate this protein loss
by increasing the synthesis of albumin as well as other molicule like VLDL
and LDL contributing to development of Hperlipidemia.
EDEMA
It is due to a combination of a decrease in
oncotic pressure from the
Hypoalbuminaemia
as well a primary renal sodium retention
in the collecting tubules.
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ANTIBIOTICS FOR NEPHROTIC SYNDROME
Nephrotic Syndrome is associated with immune complexes depositing in the kidneys when
get fever, cold or infection, excessive immune complexes come into being and deposit in the
kidneys, triggering the relapse of nephrotic syndrome.
-Antibiotics can kill the bacteria invading into the body so as to reduce their damage to body.
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RESPIRATORY DISORDERS BEST FOR NURSES
PNEUMONIA
Acute inflammatory process of the alveolar spaces
→ lung consolidation → exudate [alveoli]
CLASSIFICATION
CAP: most common; occurs in the community or 48
H before hospitalization
S. pneumoniae, H. influenza, M. pneumoniae
Nosocomial: onset of S/S is 48-72 H post
hospitalization
P. aeruginosa, S. pneumoniae, K. pneumoniae
Aspiration pneumonia
S. pneumoniae, H. influenza, S. pneumoniae,
gastric contents
PNEUMOCYSTIS CARINII PNEUMONIA
Opportunistic infection
Often related to HIV
& other immunocompromised conditions
CLINICAL MANIFESTATIONS
Increasing SOB
Nonproductive cough
Low-grade fever
TREATMENT
Cotrimoxazole
Pentamidine
MANAGEMENT
Increase OFI 3-4 L/day. HOME CARE
Administer O2. RECOGNIZE S/SX OF INFECTION.
Assess respiratory status. AVOID EXPOSURE TO PEOPLE WITH INFECTIONS.
Monitor VS, I/O, lab studies, & pulse ox INCREASE OFI AT 3 L/DAY.
Monitor & record color, consistency,
& amount of sputum
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TYPES
Bacterial pneumonia
Lobar [Strep] – constant dry, hacking cough,
pleuritic pain, watery to rust-colored sputum
Bronchopneumonia [Strep/Staph] – due to
aspiration, productive cough w/ yellow or green
sputum
Alveolar pneumonia [viral] – scanty sputum
Atypical pneumonia [rickettsial] – “walking”, non
Productive cough
CLINICAL MANIFESTATIONS
Cough
Chills
Dyspnea
Elevated temperature
Crackles
Rhonchi
Pleural friction rub
Sputum production
Rusty, green, or bloody: pneumococcal
Yellow-green: BPN
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CHRONIC OBSTRUCTIVE PULMONARY DISEASE
BRONCHITIS Chronic Smoking, RTI, Pollutants
EMPHYSEMA Bronchitis Mucosal edema
Excessive Inflammation
bronchial Bradykinin, Histamine, PGs
CAUSES mucus Fluid/Cellular Exudation
Hypersecretion of mucus
Congenital weakness production
Persistent Cough
Respiratory irritants: smoke, polluted air, Chronic or
chemical irritants recurrent
Respiratory tract infections productive
Genetic predisposition cough
Smoking, heredity, Emphysema
aging process Destruction of elastin
Loss of elastic recoil alters alveolar walls
Disequilibrium between & narrows airways
elastase & antielastase Enlargement
Overdistention of alveoli of air spaces distal
CO2 retention to terminal bronchioles
Hypoxia leads to coalesced alveoli
Respiratory acidosis & air trapping
EMPHYSEMA CHRONIC BRONCHITIS
No cyanosis (Pink) R-sided Heart Failure Cyanosis (Blue)
Thin appearance Pulmonary HPN Edematous
Exertional dyspnea Spontaneous Exertional dyspnea
Ineffective cough pneumothorax Recurrent cough w/
Barrel chest Sputum production
Pursed-lip breathing Digital clubbing
Prolonged expiration ↑Respiratory rate
Use of accessory muscles Use of accessory muscles
R-sided Heart Failure
Cor pulmonale
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BRONCHIECTASIS
MANAGEMENT
Rest: O2 demand of tissues Destruction of bronchial
Fluid intake: 3 L/day mucosa with fibrous scar
Diet: calorie, CHON, CHO, vit. C
Low-flow O2 therapy: 1-3 LPM tissue formation
Breathing exercises [pursed-lip]
Avoid cigarette smoking, alcohol, pollutants
CPT: postural drainage percussion vibration Loss of resilience
Bronchial hygiene measures: steam, aerosol,
medimist inhalation
& airway dilation causes
Pharmacotherapy: Antitussives, bronchodilators, pooling of secretions
antihistamine, steroids, antimicrobials
Obstruction of airflow
Bronchiectasis is an uncommon disease, most often secondary to an infectious process, that results in the abnormal and
permanent distortion of one or more of the conducting bronchi or airways.
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ASTHMA
ALLERGY (Extrinsic)
INFLAMMATION (Intrinsic)
Histamine,
Bradykinin, Bronchospasm Narrowing of AWs work
PG, Serotonin, Mucosal edema of Breathing
Leukotrienes Hypersecretion of mucus
Hypoventilation Exhaustion Respiratory effort
Hypoxia & Respiratory
Air trapping
Acidosis
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CLINICAL MANAGEMENT
Manifestations Pharmacotherapy
Orthopnea Beta agonists [Epinephrine,
Restlessness Terbutaline]
Dyspnea, tachypnea Methylxanthines
Tachycardia [Aminophylline]
Nasal flaring Corticosteroids
Retractions Anticholinergics [Atropine]
Cough Mast cell inhibitors [Cromolyn]
Chest tightness Oxygen via nasal cannula
Cold clammy skin Fluids to 3L/day
Wheezing Breathing exercises
Cyanosis Metered dose inhaler
ACUTE RESPIRATORY DISTRESS SYNDROME
CLINICAL SYNDROME OF RESPIRATORY INSUFFICIENCY
Damaged capillary membranes
Interstitial edema
Intraalveolar hemorrhage
Hypoxemia
CAUSES
Viral pneumonia
Fat emboli
Sepsis
Decreased surfactant production
CLINICAL DIAGNOSTICS AGENTS MANAGEMENT
Manifestations ABGs: Intubation & mechanical
Dyspnea Respiratory acidosis, ventilation using PEEP
hypoxemia Pharmacotherapy
Tachypnea
CXR: Antibiotics
Crackles Analgesics
interstitial edema
Rhonchi Steroids
Anxiety Neuromuscular blocking
Breath sounds Diagnostics agents
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CHEST PHYSIOTHERAPY
Postural drainage Percussion Vibration
NURSING CARE
Perform before or 3-4 hrs after meal
Bronchodilators 15-20 mins before
Remove all tight clothing
Percuss on area approx 3mins during I & E
Vibrate on area during E
Assist pt in coughing & positioning
Provide good oral hygiene
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PULMONARY TUBERCULOSIS
Airborne, infectious, communicable
Acute or chronic
Mycobacterium tuberculosis
CLINICAL MANIFESTATIONS
Fatigue, malaise
Anorexia, weight loss
Night sweats
Late afternoon low-grade fever
Productive chronic cough
Hemoptysis (advanced)
DIAGNOSTICS MANAGEMENT
Mantoux test TB medications [6-12 mos]
Read after 48-72 H
INH, RIF, (6 mos);
[>10 mm induration]
PZA, ethambutol, streptomycin
Chest x-ray
Calcified lesions (2 mos)
Sputum exam Pt non-infectious 2-3wks of Tx
Acid-fast bacillus 9 mos continuous therapy
RIF: discoloration ; hepatotoxic
INH: peripheral neuropathy (B6), liver function test (AST, ALT)
PZA: thrombocytopenia, hyperurecemia → ↑ OFI
ETHAMBUTOL: optic neuritis
STREPTOMYCIN: hepatotoxic, nephrotoxic, ototoxic, given IM
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PLEURAL EFFUSION & PNEUMOTHORAX
CAUSES MANAGEMENT CLINICAL MANIFESTATIONS
Trauma High-Fowler’s Sudden sharp chest pain
Pain relief Shortness of breath (SOB)
Thoracic surgery
Restlessness/anxiety
Positive pressure O2 therapy
Tachycardia, tachypnea
ventilation Chest tube insertion Diminished/absent BS
Thoracentesis Thoracentesis Chest asymmetry
CVP line insertion Chest x-ray Tracheal deviation
Emphysema ABGs towards unaffected side
Tympany
Monitor for shock
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PULMONARY EMBOLISM
Undissolved substance in pulmonary vasculature
obstructs blood flow
Types: Fat, Air, Thrombus
CAUSES
Flat or long bone fractures
Thrombophlebitis
Venous stasis
CLINICAL MANIFESTATIONS
Dyspnea, tachypnea, crackles
MANAGEMENT
DIAGNOSTICS Intubation & mechanical ventilation
ABGs
Anticoagulants
Respiratory alkalosis, hypoxemia
Thrombolytics
Lung Scan
Assess for (+) Homan’s sign
Pulmonary circulation & blood flow
obstruction Monitor PT & PTT
Angiography WOF S/S of excessive anticoagulation
Location of embolus
Filling defect of pulmonary artery
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BRONCHOGENIC CARCINOMA
Primary pulmonary tumors arising from bronchial
epithelium; metastasis primarily by direct extension,
via the circulatory or the lymphatic systems
INCIDENCE
Men > 40 years; 1 out of 10 heavy smokers
Right lung > Left lung
ETIOLOGY
Inhaled carcinogens
[cigarette smoke, asbestos, nickel, iron oxides]
Pre-existing pulmonary DO [COPD, TB
CLINICAL MANIFESTATIONS DIAGNOSTICS
Persistent cough CXR
[productive, blood-tinged] Presence of tumor;
Chest pain, dyspnea metastasis
Unilateral wheezing Sputum for cytology
Friction rub Malignant cells
Fatigue, anorexia Thoracentesis
Nausea & vomiting Pleural fluid
Pallor with malignant cells
MANAGEMENT
Depends on cell type, stage of disease, Provide support & guidance to client
and condition of the patient Relief/control of pain and nausea
Radiation therapy Meds as ordered, monitor effects
Chemotherapy
Surgery
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NCLEX RN NOTES
DO NOT DELEGATE (PACET):
- Planning;
TIPS: - Assessment (initial);
- Deal with patients rather than with
- Collaboration;
machines.
- AVOID: never, always, must, “why?”, “I - Evaluation;
understand”.
- Teaching.
- If 2 opposites (e.g. hyper-/hypo-), one is
correct.
- Do not leave the patient alone.
- Choose physical over psychological.
--UAP’s cannot be delegated: “EAT”,
- IDK the answer: pick the one with the
medication & unstable patients.
most information.
ABC (except in emergencies, distress
--LPN’s cannot be delegated anything
situations & CPR)
related with blood and are assigned the
Assessment vs. Implementation
most stable patients.
Acute vs. Chronic
Stable vs. Unstable
Expected vs. Unexpected
Real vs. Potential
Odd man out
1 TSP = 5 ML 1 PINT = 2 CUPS (16 OZ)
1 TBSP = 3 TSP (15 ML) 1 QUART = 2 PINTS (32 OZ)
1 OZ = 30 ML 1 GR (GRAIN) = 60 MG
1 CUP = 8 OZ 1 KG = 2,2 LBS
1 G = 1 ML (DIAPERS) ºF = (ºC X 1,8) + 32
TEMPERATURE NORMAL RANGE: 98,6ºF ±1 (37ºC ±0,5)
MAP: (SYSTOLIC + 2XDYASTOLIC)/3
NORMAL: 70-105 MMHG (>60 MMHG)
CVP: 2-8 MMHG (CVP CAN INDICATE RIGHT VENTRICULAR FAILURE OR
FLUID VOLUME OVERLOAD)
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ETHICS & LEGAL
ISSUES
- Veracity is truth and is an essential
component of a CULTURAL
therapeutic relationship between a
CONSIDERATION
health care provider and his
patient. 1. African Americans
- Beneficence is the duty to do no - Higher incidence of high blood pressure and
harm and the duty to do obesity;
- High incidence of lactose intolerance.
good. There’s an obligation in patient
2. Arab Americans
care to do no harm and
- May remain silent about STIs, substance abuse,
an equal obligation to assist the
and mental illness;
patient. - After death, the family may want to prepare
- Nonmaleficence is the duty to do the body and autopsy is discouraged unless
no harm. required by law;
- Tort: litigation in which one person - Use same-sex family members as interpreters.
asserts that an injury 3. Asian Americans
(physical, emotional or financial) - Believe in the yin/yang “hot-cold” theory of
occurred as a consequence of illness;
another’s actions or failure to act. - Sodium intake is generally high because of
- Negligence: harm that results salted and dried foods;
- Usually refuse organ donation;
because a person didn’t act
- May nod without necessarily understanding.
reasonably.
4. Latino Americans
- Malpractice: professional
- Family members are typically involved in all
negligence. aspects of decision making such as terminal
- Slander: character attacked and illness;
uttered in the presence of others. - May see no reason to submit to mammograms
- Assault: act in which there is a or vaccinations.
threat or attempt to do bodily harm. 5. Native Americans
- Battery: unauthorized physical - Diet may be deficient in vitamin D and calcium
contact because many suffer from lactose intolerance or
don’t drink milk;
- Obesity and diabetes are major health
concerns.
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RELIGIOUS
CONSIDERATIONS
- Jehovah’s Witness: no blood
products should be used.
- Hindu: no beef or items containing
gelatin.
- Jewish: special dietary restrictions,
TRACTIONS
use of kosher foods. - Buck’s traction: knee immobility
- Adventists: no pork nor alcohol and - Russell traction: femur or lower leg
sometimes no meat. - Dunlap traction: skeletal or skin
- Muslims: no pork nor alcohol; people - Bryant’s traction: children <3y, <35 lbs with
with chronic illnesses and women that femur fracture.
are pregnant, breast-feeding or
menstruating don’t fast during INFANT’S
Ramadan.
DEVELOPMENT:
ORDER OF 2-3 months: turns head side to side
4-5 months: grasps, switch & roll
ASSESSMENT: 6-7 months: sit at 6 and waves bye-bye
8-9 months: stands straight at eight
Inspection 10-11 months: belly to butt (phrase has 10 letters)
Palpation 12-13 months: twelve and up, drink from a cup
Percussion
Auscultation
ERIKSON’S STAGES
OF PSYCHOSOCIAL
ABO BLOOD TYPE DEVELOPMENT
COMPATIBILITY:
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LABORATORY VALUES
- BUN: 5-20 mg/dL - Erythrocytes (RBC): 4.5-5.0 million/L
- Creatinine: 0.6-1.3 mg/dL - Leucocytes (WBC): 4,500-11,000
- Creatinine clearance: 90-130 ml/min cells/mm3 (Neutropenia
- Total cholesterol: 140-199 mg/dL <1000/mm3/ Severe neutropenia:
- HDL: 30-70 mg/dL <500/mm3)
- LDL: <130 mg/dL - Neutrophils: 1800-7800 cells/mm3
- Triglycerides: <200 mg/dL - Lymphocytes: 1000-4800 cells/mm3
- Protein: 6-8 g/dL - Potassium: 3.5-5.0 mEq/L
- Albumin: 3.4-5 g/dL - Sodium: 135-145 mEq/L
- Chloride: 98-107 mEq/L
- Alanine aminotransferase (ALT): 10-40 units/L
- Phosphate: 2.5-4.5 mg/dL
- Aspartate aminotransferase (AST): 10-30 units/L
- Magnesium: 1.6-2.6 mg/dL
- Total Bilirubin: <1.5 mg/dL
- Phosphorus: 2.7-4.5 mg/dL
- Uric acid: 3.5—7.5 mg/dL
- Calcium: 8.6-10 mg/dL
- CPK: 21-232 U/L
- Digoxin: 0.8—2.0 ng/ml
- Glucose: 70-110 mg/dL
- Lithium: 0.8—1.5 mEq/L
- Hemoglobin A1c:
- Phenytoin: 10—20 mcg/dL
4%-5.9%: nondiabetic - Theophylline (Aminophylline): 10—20
<7%: good diabetic control mcg/dL
7% to 8%: fair diabetic control
>8%: poor diabetic control
- Hemoglobin:
Female: 12-15 g/dL
Male: 14-16.5 g/dL
- Hematocrit:
Female: 35%-47%
Male: 42%-52%
- Platelets: 150,000-400,000 cells/mm3
- aPTT: 20-36 sec, depending on testing method
Therapeutic (Heparin): 46-70 seconds
- Prothrombin time (PT): 9.5-11.8 sec
- International Normalized Ratio (INR):2-3: standard
warfarin therapy
3-4.5: high-dose warfarin therapy
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ABG VALUES &
EVALUATION
HYPERKALEMIA
- pH: 7.35—7.45
- HCO3: 24—26 mEq/L Causes:
- CO2: 35—45 mEq/L “The body CARED too much about potassium”
- PaO2: 80%—100% Cellular movement of K from intracellular to
- SaO2: >95% extracellular (burns, tissue damages, acidosis).
Adrenal insufficiency with Addison’s Disease.
Renal failure. Excessive K intake. Drugs (K-
sparing like spironolactone, triamterene, ACE
inhibitors, NSAIDS).
Signs & Symptoms (MURDER):
Muscle weakness. Urine production little or none
(renal failure).
Respiratory failure. Decreased cardiac
HYPOKALEMIA contractility (weak pulse, low BP).
Early signs of muscle twitches/cramp…
Causes: Late profound weakness, flaccidity. Rhythm
“Your body is trying to DITCH potassium” changes.
Drugs (laxatives, diuretics, corticosteroids)
Inadequate consumption of K (NPO, anorexia).
Too much water intake (dilutes the K).
HYPOCALCEMIA
Cushing’s syndrome (the adrenal glands Causes (LOW CALCIUM):
produce excessive amounts of aldosterone). Low parathyroid hormone due (any neck
Heavy fluid loss (NG suction, vomiting, diarrhea, surgery: check the Ca level). Oral intake
wound drainage, excessive diaphoresis). inadequate (alcoholism, bulimia etc.). Wound
drainage (especially GI system). Celiac’s &
Crohn’s disease (malabsorption of Ca). Acute
Signs & Symptoms:
pancreatitis. Low vitamin D levels. Chronic
Everything is going to be SLOW and LOW.
kidney issues (excessive excretion). Increased
- Weak pulses (irregular and thread).
phosphorus levels in the blood. Using certain
- Orthostatic hypotension.
medications (Ma supplements, laxatives, loop
- Shallow respirations with diminished breath
diuretics, Ca binder drugs). Mobility issues
sounds.
- Confusion and weakness.
Signs & Symptoms (CRAMPS):
- Flaccid paralysis.
Confusion.
- Decrease deep tendon reflexes.
Reflexes: hyperactive.
- Decreased bowel sounds.
Arrhythmias.
Muscle spasms in calves or feet, tetany, seizures.
Positive Trousseau’s (happens before Chvostek’s
sign and tetany).
Signs of Chvostek’s.
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HYPERCALCEMIA HYPONATREMIA
Causes (HIGH CAL): Causes (NO Na):
Hyperparathyroidism (++ Ca released in Na excretion increased (renal
the blood). problems, NG suction, vomiting,
Increased intake of Ca. diuretics, sweating, diarrhea,
Glucocorticoids (suppresses Ca secretion of aldosterone).
absorption). Overload of fluid (congestive heart
Hyperthyroidism. failure, hypotonic fluids
Calcium excretion decreased (Diuretics, infusions, renal failure).
renal failure, bone cancer). Na intake low (low salt diets or NPO).
Adrenal insufficiency (Addison’s disease). Antidiuretic hormone over secretion
Lithium usage (affects the parathyroid (SIADH).
gland).
Signs & Symptoms (SALT LOSS):
Signs & Symptoms: Seizures & Stupor.
“The body is too WEAK” Abdominal cramping, Attitude changes
Weakness of muscles (profound). (confusion).
EKG changes. Lethargic.
Absent reflexes & minded (disorientated), Tendon reflexes diminished, Trouble
Abdominal concentrating (confused).
distention from constipation. Loss of urine and appetite.
Kidney stone formation. Orthostatic hypotension, Overactive bowel
sounds.
HYPERNATREMIA Shallow respirations (due to skeletal
muscle weakness).
Causes (HIGH SALT): Spasms of muscles.
Hyperventilation, Hypercortisolism
(Cushing’s syndrome).
Increased intake of sodium (oral or IV).
GI feeding (tube) without adequate water
supplements.
Hypertonic solutions. Sodium excretion
decreased and corticosteroids.
Aldosterone insufficiency.
Loss of fluids, infection (fever),
diaphoresis, diarrhea, and diabetes
insipidus). Thirst impairment.
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HYPERNATREMIA HYPOPHOSPHATEMIA
Signs & Symptoms: Causes (Low PHOSPHATE):
“No FRIED foods for you!” Pharmacy (aluminum hydroxide-based
Fever, Flushed skin. or magnesium-based
Restless, Really agitated. antacids cause malabsorption in the GI
Increased fluid retention. system).
Edema, Extremely confused. Hyperparathyroidism (there is an over
Decreased urine output, Dry mouth/skin. secretion of PTH which
causes phosphate to not be reabsorbed).
HYPOPHOSPHATEMIA Oncogenic osteomalacia.
Syndrome of Refeeding: causes
Signs & Symptoms (BROKEN): electrolytes and fluid problems
Breathing problems (due to muscle due to malnutrition or starvation (watch
weakness). for per os after TPN).
Rhabdomyolysis (tea-colored urine, Pulmonary issues such as respiratory
muscle weakness/pain), alkalosis.
Reflexes (deep tendon) decreased. Hyperglycemia. Alcoholism. Thermal
Osteomalacia (softening of the bones) Burns. Electrolyte imbalances:
fractures and decreased hypercalcemia, hypomagnesemia,
bone density (alteration in bone shape), hypokalemia.
cardiac Output
decreased. HYPERPHOSPHATEMIA
Kills immune system with immune
suppression and decreases Causes (PHOS-HI):
platelet aggregation. Phospho-soda overuse: phosphate
Extreme weakness, Ecchymosis. containing laxatives or
Neuro status changes (irritability, enemas (Sodium Phosphate/Fleets enema).
confusion, seizures). Hypoparathyroidism.
Overuse of vitamin D.
HYPERPHOSPHATEMIA Syndrome of Tumor Lysis.
rHabdomyolysis.
Signs & Symptoms (CRAMPS): Insufficiency of kidneys (renal failure is
Confusion. the main cause).
Reflexes hyperactive.
Anorexia.
Muscle spasms in calves or feet, tetany,
seizures.
Positive Trousseau’s Signs, Pruritus.
Signs of Chvostek.
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HYPOMAGNESEMIA HYPERMAGNESEMIA
Causes (LOW MAG): Causes (MAG)*:
Limited intake of Mg (starvation). Magnesium containing antacids and
Other electrolyte issues (hypokalemia, laxatives.
hypocalcemia). Addison’s disease (adrenal
Wasting Magnesium kidneys (loop and insufficiency).
thiazide diuretics; Glomerular filtration insufficiency
cyclosporine). (<30mL/min).
Malabsorption issues (Crohn’s and celiac *Hypermagnesemia is less common than
diseases, “-prazole” hypomagnesemia. It
drugs, diarrhea/vomiting). typically happens when trying to
Alcohol (stimulates the kidneys to correct hypomagnesemia with
excreted Mg). magnesium sulfate IV infusion.
Glycemic issues (diabetic ketoacidosis,
insulin administration).
Signs & Symptoms (LETHARGIC)*:
*Happens in severe hypermagnesemia,
Signs & Symptoms (TWITCHING): mild one is
Trousseau’s (positive due to asymptomatic.
hypocalcemia). Lethargy (profound).
Weak respirations. EKG changes (prolonged PR & QR
Irritability. interval and widened QRS
Torsades de pointes, Tetany (seizures). complex).
Cardiac changes, Chvostek’s sign. Tendon reflexes absent or grossly
Hypertension, Hyperreflexia. diminished.
Involuntary movements. Hypotension.
Nausea. Arrhythmias (bradycardia, heart
GI issues (decreased bowel sounds and blocks).
mobility). Respiratory arrest.
GI issues (nausea, vomiting).
Impaired breathing (due to skeletal
weakness).
Cardiac arrest.
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FOOD SOURCES OF WATER-SOLUBLE VITAMINS
- Folic acid: green leafy vegetables, liver, beef and fish,
legumes, grapefruit and oranges.
- Niacin: meats, poultry, fish, beans, peanuts, grains.
- Vitamin B1 (thiamine): pork, nuts, whole-grain cereals,
legumes.
- Vitamin B2 (riboflavin): milk, lean meats, fish, grains.
- Vitamin B6 (pyridoxine): yeast, corn, meat, poultry, fish.
- Vitamin B12 (cobalamin): meat, liver.
- Vitamin C (ascorbic acid): citrus fruits, tomatoes, broccoli,
cabbage.
FOOD SOURCES OF FAT-SOLUBLE VITAMINS
- Vitamin A: liver, egg yolk, whole milk, green or orange
vegetables, fruits.
- Vitamin D: fortified milk, fish oils, cereals.
- Vitamin E: vegetable oils, green leafy vegetables, cereals,
apricots, apples, peaches.
- Vitamin K: green leafy vegetables, cauliflower, cabbage.
FOOD SOURCES OF MINERALS
- Calcium: broccoli, carrots, cheese, collard greens, green
beans, milk, rhubarb, spinach, tofu, yogurt.
- Chloride: salt.
- Iron: bread and cereals, dark green vegetables, dried fruits,
egg yolk, legumes, liver, meats.
- Magnesium: avocado, canned white tuna, cauliflower, cooked
rolled oats, green leafy vegetables, milk, peanut butter, peas,
pork, beef, chicken, potatoes, raisins, yogurt.
- Phosphorus: fish, nuts, organ meats, pork, beef, chicken,
whole-grain bread and cereals.
- Potassium: avocado, banana, cantaloupe, carrots, fish,
mushrooms, oranges, pork, beef, veal, potatoes, raisins,
spinach, strawberries, tomatoes.
- Sodium: American cheese, bacon, butter, canned food,
cottage cheese, cured pork, hot dogs, ketchup, milk, mustard,
processed food, soy sauce, table salt, white and whole-wheat
bread.
- Zinc: eggs, leafy vegetables, meats, protein-rich foods.
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EXPECTED DATE OF
DELIVERY (EDD)
1st day of the last menstrual period
Naegele’s rule: + 7 days
- 3 months TORCH INFECTIONS
e.g. Sep 13th – Sep 20th – Jun 20th Toxoplasmosis
Other (Hepatitis, Syphilis, HIV)
PREGNANCY OUTCOME – GTPAL Rubella
G – gravidity Cytomegalovirus
T – term births Herpes simplex
P – preterm births
A – abortions or miscarriages
L – current living children
They cause the
- It is administered (IM route) at 28 weeks of gestation and worst damage
again within 72 hours after delivery. during the 1st
- It should also be administered within 72 hours after potential
t r i m e ster
or actual exposure to Rh+ blood and must be given with each
subsequent exposure to Rh+ blood.
Folic acid should be started 3 months before the woman
becomes pregnant; it decreases the incidence of neural tube
defects.
Warfarin is teratogenic (especially in the 1st trimester).
Heparin is not.
PREDISPOSING CONDITIONS FOR
DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)
- Abruptio placentae
- Amniotic fluid embolism DRUGS USED TO STOP PRETERM LABOR: TOCOLYTICS
- Gestational hypertension “It’s not my time”
- Intrauterine fetal death Indomethacin (NSAID)
- Liver disease Nifedipine (Calcium channel blocker)
- Sepsis
Magnesium sulfate
Terbutaline
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STAGES OF LABOR
1st stage: Cervical dilation
- Begins with onset of regular FETAL ACELERATIONS
PLACENTA PREVIA
contractions and ends with AND DECELERATIONS
- Painless bright red
complete dilation. Variable decelerations
vaginal bleeding.
- Latent (0-3cm)/Active (4- Early decelerations
- Soft uterus.
7cm)/Transitional (8-10cm) Accelerations
- Vaginal exams are
2nd stage: Expulsion Late accelerations
contraindicated.
- Begins with complete dilation and Cord compression
ABRUPTIO PLACENTAE
ends with delivery of fetus. Head compression
- Dark red vaginal
3rd stage: Placental Okay!
bleeding.
- Begins immediately after fetus is Placental insufficiency
- Uterine pain and/or
born and ends when the tenderness.
placenta is delivered. - Uterine rigidity.
4th stage: maternal homeostatic
stabilization
- Begins after the delivery of the
placenta and continues for 1-4
hours after delivery.
NORMAL POSTPARTUM VITAL SIGNS
- Temperature: may increase to 100.4ºF during the first 24h
FETAL HEART RATE:
postpartum because of dehydrating effects of labor. Any higher
120-160bpm (variability 6-
elevation may be causes by infection and must be reported.
10bpm)
- Heart rate: may decrease to 50bpm (normal puerperal
CONTRACTIONS: 2-5
bradycardia); >100bpm may indicate excessive blood loss or
minutes apart with duration
infection.
of <90
- Blood pressure: should be normal; suspect hypovolemia if it
seconds and intensity of
decreases.
<100 mmHg.
- Respiratory rate: rarely changes; if it increases significantly,
AVA: the umbilical cord has
suspect pulmonary embolism, uterine atony or hemorrhage.
2 arteries and 1 vein.
ANTIBIOTICS CONTRAINDICATED
APGAR DURING PREGNANCY (MCATO)
Metronidazole* -> hepatic failure
Appearance Chloramphenicol -> gray baby syndrome
Pulse Aminoglycosides -> ototoxicity
Grimace Tetracyclines -> teeth discoloration & liver
Activity failure
Respiration Others -> Nitrofurantoin, Quinolones &
sulfonamides
*relatively contraindicated
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STOP
- This is the treatment for Score interventions:
maternal hypotension after an 8-10: no intervention required expect to
epidural anesthesia: support newborn’s
1. Stop oxytocin if infusing. spontaneous efforts.
2. Turn the client on the left side. 4-7: stimulate; rub newborn’s back;
3. Administer oxygen. administer oxygen, rescore
4. If hypovolemia is present, push at specific intervals.
IV fluids. 0-3: requires full resuscitation; rescore at
PREGNANCY CATEGORY OF specific intervals.
DRUGS
- Category A: No risk in FONTANELS
controlled human studies - Anterior: closes between 12-18 months of age.
- Category B: No risk in other - Posterior: closes between birth-2/3 months of age.
studies.
- Category C: Risk not ruled out. SIGNS OF A POSSIBLE HEART DEFECT
- Category D: Positive evidence of (CORBIN)
risk. Color: bluish skin or extremities.
- Category X: Contraindicated in O2: low pulse oximetry percentage.
Pregnancy. Rhythm: abnormal heart rate.
- Category N: Not yet classified. Breathing: heavy or labored.
Increase in sweat, especially on the forehead.
IMMUNIZATIONS Nursing: trouble feeding and breathing at the
SCHEDULE same time or
poor appetite
SAFETY PRINCIPLES REGARDING TOYS
- No small toys for children under age 4 y/o.
- No metal (dycast) toys if O2 is in use (sparks).
- Beware of fomites (they harbor bacteria -
stuffed animal is a
fomite).
- For a child -> 9 months, do not pick any of the
answers with the
words: build, make, construct, sort, stack.
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POSITIONING PATIENTS
- Asthma: orthopneic position where patient is sitting up and
bent forward with arms supported on a table or chair arms.
- Post bronchoscopy: flat on bed with head hyperextended.
- Cerebral aneurysm: high Fowler’s.
- Hemorrhagic stroke: HOB elevated 30º to reduce ICP and
facilitate venous drainage.
- Ischemic stroke: HOB flat.
- Cardiac catheterization: keep site extended.
- Epistaxis: lean forward.
- Above knee amputation: elevate for first 24h on pillow,
position on prone daily for hip extension.
- Below knee amputation: foot of bed elevated for first 24h,
position prone daily for hip extension.
- Tube feeding for patients with decreased LOC: position
patient on right side to promote emptying of the stomach with
HOB elevated to prevent aspiration.
- Air/Pulmonary embolism: turn patient to left side and lower
HOB.
- Postural drainage: lung segment to be drained should be in
the uppermost position to allow gravity to work.
- Post lumbar puncture: patient should lie flat in supine to
prevent headache and leaking of CSF.
- Continuous Bladder Irrigation (CBI): catheter should be taped
to thigh so legs should be kept straight.
- After myringotomy: position on the side of affected ear after
surgery (allows drainage of secretion).
- Post cataract surgery: patient will sleep on unaffected side
with a night shield for 1-4 weeks.
- Detached retina: area of detachment should be in the
dependent position.
- Post thyroidectomy: low or semi- Fowler’s, support head,
neck and shoulders.
- Thoracentesis: sitting on the side of the bed and leaning over
the table (during procedure); affected side up (after
procedure).
- Spina bifida: position infant on prone so that sac does not
rupture.
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POSITIONING PATIENTS
- Buck’s traction: elevate foot of bed for counter-traction.
- Post total hip replacement: don’t sleep on operated side,
don’t flex hip more than 45-60º and don’t elevate HOB more
than 45º; maintain hip abduction by separating thighs with
pillows.
- Prolapsed umbilical cord: knee-chest position or
Trendelenburg.
- Cleft-lip: position on back or in infant seat to prevent trauma
to the suture line; while feeding, hold in upright position.
- Cleft-palate: prone.
- Hemorrhoidectomy: assist to lateral position.
- Hiatal hernia: upright position.
- Preventing Dumping syndrome: eat in reclining position, lie
down after meals for 20-30min (also restrict fluids during
meals, low fiber diet, and small frequent meals).
- Enema administration: position patient in left-side lying (Sim’s
position) with knees flexed.
- Post supratentorial surgery (incision behind hairline): elevate
HOB 30-45º.
- Post infratentorial surgery (incision at nape of neck): position
patient flat and lateral on either side.
- Increased ICP: high Fowler’s.
- Laminectomy: back as straight as possible; log roll to move
and sand bag on sides.
- Spinal cord injury: immobilize on spine board, with head in
neutral position; immobilize head with padded C-collar,
maintain traction and alignment of head manually; log roll
patient and do not allow patient to twist or bend.
- Liver biopsy: right side lying with pillow or small towel under
puncture site for at least 3h.
- Paracentesis: flat on bed or sitting.
- Intestinal tubes: place patient on right side to facilitate
passage into duodenum.
- Nasogastric tubes: elevate HOB 30º to prevent aspiration.
Maintain elevation for continuous feeding or 1h after
intermittent feedings.
- Pelvic exam: lithotomy position.
- Rectal exam: knee-chest position, Sim’s, or dorsal recumbent.
- During internal radiation: patient should be on bed rest while
implant is in place.
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THERAPEUTIC DIETS
- Acute renal disease: protein-restricted, high-calorie, fluid ->
controlled, Na and K controlled.
- Addison’s disease: high sodium, low potassium.
- ADHD and bipolar: high-calorie and provide finger foods.
- Anemia: high protein/iron/vitamins.
- Atherosclerosis: low saturated fats.
- Burns: high protein, high caloric, -> Vitamin C.
- Cancer: high-calorie, high-protein.
- Celiac disease: gluten-free (no BROW: wheat, oats, rye,
barley).
- Cholecystitis/Cholelithiasis: low fat liquids, powder
supplements high in protein/carb into skim milk; avoid fried
foods, pork, cheese, alcohol.
- After surgery may need low fat diet for several weeks.
- Low fat, high carb/protein.
- Chronic renal disease: protein-restricted, low-sodium, fluid -->
restricted, potassium-restricted, phosphorus-restricted.
- Cirrhosis (stable): normal protein.
- Cirrhosis with hepatic insufficiency: restrict protein, fluids,
and sodium.
- Constipation: high-fiber, increased fluids.
- COPD: soft, high-calorie, low-carbohydrate, high-fat, small
frequent feedings.
- Cushing’s disease: low sodium, high potassium.
- Cystic fibrosis: increase in fluids; pancreatic enzyme
replacement before or with meals; high protein, high calorie in
advanced stages.
- Diarrhea: liquid, low-fiber, regular, fluid and electrolyte
replacement.
- Diverticular disease: high-fiber, avoid seeds.
- Dumping syndrome (rapid passage of food: diaphoresis,
diarrhea, hypotension): restrict fluids w/ meals, drink 1h
before or 1h after; eat in recumbent position, lie down 20-30
min after eating; small frequent meals; low-carb/low-fiber.
- Gallbladder disease: low-fat, calorie-restricted.
- Gastritis: low-fiber, bland diet.
- Gout: low purine (no fish and organ meats).
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- Hypertension, heart failure, CAD: low-sodium, calorie->restricted, fat-controlled.
- Kidney stones: increased fluid intake, calcium-controlled,
low-oxalate.
- Meniere’s: low sodium, avoid caffeine, nicotine and alcohol.
- Nephrotic syndrome: sodium-restricted, high-calorie, high protein, potassium-restricted.
- Obesity/Overweight: calorie-restricted, high-fiber .
- Ostomy: high calorie/protein/carb; low residue before
surgery.
- Ileostomy: low residue diet, no meats, corn, nuts.
- Colostomy: diet not restricted after 6 weeks.
- Pancreatitis: low-fat, regular, small frequent feedings; tube
feeding or total parenteral nutrition.
- Peptic ulcer: bland diet.
- Pernicious anemia: Vitamin B12.
- IM B12 shot (25-100 g), followed by 500-1000 g shot
every 1-2 months or cyanocobalamin nasal spray.
- Phenylketonuria (PKU): special milk substitutes for infants,
low protein for children.
- Pheochromocytoma: increase calories, vitamins and minerals
intake; avoid coffee, tea, cola, tyramine foods.
- Sickle cell anemia: increase fluids to maintain hydration since
sickling increases when patients become dehydrated.
- Stroke: mechanical soft, regular, or tube-feeding.
- Underweight: high-calorie, high protein.
- Ulcerative colitis & Crohn’s disease: high protein/calorie; low
fat/fiber.
- Ulcers: 3 meals/day, avoid Tº extremes, avoid
caffeine/alcohol/milk&cream.
- Postoperative: Vit B12 parenteral for life and iron
supplements.
- Vomiting: fluid and electrolyte replacement.
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TOP NCLEX HERBS
Garlic: lowers blood pressure and cholesterol levels.
- Interacts with aspirin and warfarin.
Ginkgo Biloba: improves memory.
- Thins the blood (don’t take with aspirin or warfarin).
- Do not take with history of seizures.
Echinacea: immune-boosting function
- Can cause liver toxicity in renal patients.
- Not effective with HIV.
Ginger: Relieves nausea and vomiting.
- Do not take if history of deep venous thrombosis.
- Interacts with blood thinners.
Black Cohosh: treats menopausal symptoms.
- Contraindicated in pregnancy (causes premature labor).
Kava Kava: treats insomnia and muscle pain.
- It’s associated with liver illnesses.
Saw Palmetto: used for prostate health.
- No specific patient teaching.
* If it starts with G, it thins the blood. Do not give with
warfarin, aspirin and heparin.
COMMON ANTIDOTES
Warfarin........................................................... Vitamin K
Benzodiazepines............................................ Flumanezil
Heparin ...............................................Protamine Sulfate
Opioids............................................................. Naloxone
Anticholinergics....................................... Physostigmine
Beta Blockers....................................................Glucagon
Methotrexate .......................... Folinic Acid (Leucovorin)
Tricyclic antidepressants................ Sodium Bicarbonate
Digoxin..........................Digoxin Immune Fab (Digiband)
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COMMON SIGNS AND
SYMPTOMS
- Pulmonary tuberculosis: low-grade afternoon fever.
- Pneumonia: rust-colored sputum.
- Asthma: wheezing on expiration.
- Emphysema: barrel chest.
- Pernicious anemia: red beefy tongue.
- Cholera: rice-watery stool and wrinkled hands from
dehydration.
- Malaria: stepladder like fever with chills.
- Typhoid: rose spots in the abdomen.
- Dengue: fever, rash, and headache; positive Herman’s sign.
- Diphtheria: pseudo membrane formation.
- Measles: Koplik’s spots (clustered white lesions on buccal
mucosa).
- Systemic lupus erythematosus: butterfly rash.
- Leprosy: leonine facies (thickened folded facial skin).
- Appendicitis: rebound tenderness at McBurney’s point;
Rovsing’s sign (palpation of LLQ elicits pain in RLQ); psoas sign
(pain from flexing the thigh to the hip).
- Meningitis: Kernig’s sign (stiffness of hamstrings causing
inability to straighten the leg when the hip is flexed to 90º);
Brudzinski’s sign (forced flexion of the neck elicits a reflex
flexion of the hips).
- Tetany: hypocalcemia; positive Trousseau’s and Chvostek
sign.
- Tetanus: Risus sardonicus or rictus grin.
- Pancreatitis: Cullen’s sign (ecchymosis of the umbilicus); Grey
Turner’s sign (bruising of the flank).
- Pyloric stenosis: olive like mass.
- Patent ductus arteriosus: washing machine-like murmur.
- Addison’s disease: bronze-like skin pigmentation.
- Cushing’s syndrome: moon face appearance and buffalo
hump.
- Graves’ disease (hyperthyroidism): Exophthalmos.
- Intussusception: sausage-shaped mass.
- Multiple sclerosis: Charcot’s triad: nystagmus, intention
tremor, and dysarthria.
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- Myasthenia gravis: descending muscle weakness, ptosis.
- Guillain-Barre syndrome: ascending muscle weakness.
- Deep vein thrombosis: Homan’s sign.
- Angina: crushing, stabbing pain relieved by nitroglycerin
(NTG).
- Myocardial Infarction: crushing, stabbing pain radiating to left
shoulder, neck, and arms; unrelieved by NTG.
- Cytomegalovirus infection: owl’s eye appearance of cells
(huge nucleus in cells).
- Retinal detachment: flashes of light, shadow with curtain
across vision.
- Basilar skull fracture: raccoon eyes (periorbital ecchymosis)
and Battle’s sign (mastoid ecchymosis).
- Buerger’s disease: intermittent claudication (pain at buttocks
or legs from poor circulation resulting in impaired walking).
- Diabetic ketoacidosis: acetone breathe.
- Pre-eclampsia: proteinuria, hypertension, edema.
- Diabetes mellitus: polydipsia, polyphagia, polyuria.
- Hirschsprung’s Disease (Toxic Megacolon): ribbon-like stool.
- Herpes Simplex Type II: painful vesicles on genitalia.
- Genital Warts: warts 1-2 mm in diameter.
- Syphilis: painless chancres.
- Chancroid: painful chancres.
- Gonorrhea: green, creamy discharges and painful urination.
- Chlamydia: milky discharge and painful urination.
- Candidiasis: white cheesy odorless vaginal discharges.
- Trichomoniasis: yellow, itchy, frothy, and foul-smelling vaginal
discharges.
- Pulmonary edema: pink, frothy sputum, tachypnea, use of
accessory muscles, crackles, anxiety/restlessness (Tx:
furosemide).
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MEDICATION MISCELLANEOUS
HIGH ALERT MEDICATIONS NARROW THERAPEUTIC RANGE DRUGS
- Insulin. - Gentamicin.
- Opiates and narcotics. - Vancomycin.
- Injectable potassium chloride (or - Warfarin.
phosphate) concentrate. - Lithium.
- IV coagulants (heparin). - Digoxin.
- Sodium chloride solutions >0.9%. - Theophylline.
- Methotrexate.
TUBERCULOSIS DRUGS (RIPE): - Phenytoin.
Rifampicin - Insulin.
Isoniazid - Ciclosporin.
Pyrazinamide
Ethambutol
*Rifampicin: causes red-orange tears and urine.
*Ethambutol: causes problems with vision, liver problem.
*Isoniazid: can cause peripheral neuritis; take vitamin B6 to
counter.
MONOAMINE OXIDASE INHIBITORS (MAOI’s):
- Tyramine-rich foods may cause severe hypertension in
patients who take MAOI’s.
- Tyramine-rich foods include: aged cheese, chicken liver,
avocados, bananas, meat tenderizer, salami, bologna, Chianti
wine, and beer.
PYRIDIUM:
- Urinary tract analgesic and spasmolytic
- Not an anti-infective
- Turns urine bright orange.
NITROGLYCERINE PATCH is administered up to three times
with intervals of five minutes.
MORPHINE:
- Contraindicated in pancreatitis because it causes spasms of
the Sphincter of Oddi.
- Meperidine (Demerol) should be given.
CLOZAPINE:
- A significant associated toxic risk is blood dyscrasia.
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MEDICATION MISCELLANEOUS
DIGOXIN:
- Assess pulses for a full minute, if less than 60 bpm hold dose.
- Check digitalis and potassium levels.
HALOPERIDOL ADVERSE EFFECTS:
ALUMINUM HYDROXIDE:
- Drowsiness.
- Treatment of GERD and kidney stones.
- Insomnia.
- WOF: constipation.
- Weakness.
- Headache
- Extrapyramidal symptoms: akathisia, tardive dyskinesia,
dystonia.
HYDROXYZINE:
- Treatment of anxiety and itching.
- WOF: dry mouth.
MIDAZOLAM:
- Given for conscious sedation.
- WOF: respiratory depression and hypotension.
AMIODARONE
- Take missed dose any time in the day or skip it entirely.
- Do not take double dose.
- WOF: diaphoresis, dyspnea, lethargy.
WARFARIN (COUMADIN)
- Stress importance of complying with prescribed dosage and
follow-up appointments.
- WOF: signs of bleeding, diarrhea, fever, rash.
METHYLPHENIDATE (RITALIN)
- Treatment of ADHD.
- Assess for heart related side-effects and report immediately.
- Child may need a drug holiday because the drug stunts
growth.
DOPAMINE
- Treatment of hypotension, shock and low cardiac output.
- Monitor ECG for arrhythmias and blood pressure.
PHENYTOIN
- Enteral feedings: stop the feeding 1-2h before and after the
administration of the phenytoin because the enteral feedings
decrease its absorption.
- Flush with 30-50ml of NaCl before and after the
administration of phenytoin.
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NURSING PROCESS
It is a systematic, rational method of planning and
providing individualized nursing care.
THE NURSING PROCESS PURPOSE OF NURSING PROCESS
Is the underlying scheme that provides order To identify a client’s health status and actual
and direction to nursing care. or potential health care problems or needs. To
It is the essence of professional nursing establish plans to meet the identified needs.
practice. It was developed as a specific method for
It has been conceptualized as a systematic applying a scientific approach or a problem
series of independent nursing actions directed solving approach to nursing practice.
toward promoting an optimum level of wellness
for the client.
It is cyclical; the components follow a logical
sequence, but more than one component may be
involved at any one time.
STEPS IN NURSING PROCESS
A DELICIOUS PIE
A SSESSMENT
D IAGNOSIS
P LANNING
I MPLEMENTATION
E VALUATION
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ASSESSMENT
To establish baseline information on the client.
To determine the client’s normal function.
To determine the client’s risk for diagnosis function.
To determine presence or absence of diagnosis function.
To determine client’s strengths.
To provide data for the diagnostic phase.
TYPES OF ASSESSMENT
INITIAL ASSESSMENT FOCUS ASSESSMENT
Initial identification of normal function, status determine of a specific problem
functional status and collection of data identified during previous assessment.
concerning actual and potential
dysfunction.
TIME-LAPSED
EMERGENCY ASSESSMENT
REASSESSMENT:
During emergency situation to identify any Several months after initial
life threatening situation. assessment. To compare the client’s
Eg: Rapid assessment of an individual’s current health status with the data
airway, breathing status, and circulation previously obtained.
during a cardiac arrest.
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CLINICAL SKILLS USED IN ASSESSMENT
OBSERVATION INTERVIEWING PHYSICAL EXAMINATION
INSPECTION
Act of noticing client cues.
PERCUSSION
*looking, watching, examining, Interaction AUSCULTATION
scrutinizing, surveying, scanning,
appraising. and INTUITION
Defined as insights,
*uses different senses: vision,
smell, hearing, touch. communication. instincts or clinical
experiences to
make judgment about
client care.
STAGES OF AN INTERVIEW
The opening or introduction
The body or development
The closing
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EXAMINATION ORGANIZATION OF DATA
The physical examination The nurse uses a format that organizes
is a systematic data collection method to the assessment data systematically. This is
detect health problems. To conduct the often referred to as nursing health history or
examination, the nurse uses techniques of nursing assessment form.
inspection, palpation, percussion and
auscultation.
VALIDATION OF DATA DOCUMENTATION OF DATA
The information gathered during the To complete the assessment phase,
assessment is “double-checked” or the nurse records client data. Accurate
verified documentation is essential and should
to confirm that it is accurate and include all data collected about the client’s
complete. health status.
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DIAGNOSIS
Diagnosis is the second phase of the
nursing process. In this phase, nurses use
critical thinking skills to interpret
assessment
data to identify client problems.
North American Nursing Diagnosis
Association (NANDA) define or refine
nursing diagnosis.
STATUS OF THE NURSING CLASSIFICATION OF
DIAGNOSIS NURSING DIAGNOSIS
The status of nursing diagnosis are actual,
health promotion and risk.
HIGH PRIORITY
Life threatening and requires
An actual diagnosis is a client problem immediate attention.
that is present at the time of the nursing MEDIUM PRIORITY
assessment. Resulting to unhealthy
A health promotion diagnosis
consequences.
relates to clients’ preparedness
to improve their
LOW PRIORITY
Can be resolve with minimal
health condition.
interventions.
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CHARACTERISTICS OF OUTCOME CRITERIA
S PECIFIC
MEASURABLE
WILLINGNESS TO CARE
A TTAINABLE HEART OF THE
NURSING PROCESS
Keep the focus on
what is best for the R EALISTIC •KNOWLEDGE
T IME FRAME
•SKILLS
patient.
- manual, intellectual,
• Respect the beliefs
interpersonal.
values of others.
•CARING
• Stay involved.
• Maintain a healthy
PLANNING
Involves determining
beforehand the strategies or
course of actions to be taken
before implementation of
nursing care.
To be effective, involve the
client and his family in planning
IMPLEMENTATION
Putting nursing care plan into ACTION!
To help client attain goals and achieve optimal
level of health.
Requires: Knowledge, Technical skills,
Communication skills, Therapeutic Use of Self.
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EVALUATION
IS ASSESSING THE CLIENT’S RESPONSE
TO NURSING INTERVENTIONS.
COMPARING THE RESPONSE TO
PREDETERMINED STANDARDS OR
OUTCOME CRITERIA.
FOUR POSSIBLE JUDGMENTS:
• The goal was completely met.
• The goal was partially met.
• The goal was completely unmet.
• New problems or nursing diagnoses have developed
CHARACTERISTICS OF NURSING PROCESS
Problem-oriented.
• Goal oriented.
• Orderly, planned, step by step.
(systematic)
• Open to new information.
• Interpersonal.
• Permits creativity.
• Cyclical.
• Universal.
BENEFITS OF THE NURSING PROCESS: FOR THE CLIENT BENEFITS OF THE NURSING PROCESS: FOR THE NURSE
• CONSISTENT AND SYSTEMATIC
• QUALITY CLIENT CARE NURSING EDUCATION.
• CONTINUITY OF CARE • JOB SATISFACTION.
• PARTICIPATION BY • PROFESSIONAL GROWTH.
CLIENTS IN THEIR • AVOIDANCE OF LEGAL ACTION.
HEALTH CARE • MEETING PROFESSIONAL NURSING
STANDARDS.
• MEETING STANDARDS OF
ACCREDITED HOSPITALS.
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PHARMACOKINETICS
COMMONLY USED PHARMACOKINETIC
PROCESSES OF PHARMACOKINETICS
PARAMETER
(i) Absorption (i) Bio-availability
(ii) Distribution (ii) Volume of distribution
(iii) Metabolism (iii) Half-Life
(Bio-transformation) (iv) Clearance
(iv) Elimination
All the processes of Pharmacokinetics involve the passage of the drug across the cell Mb.
Cell Mb: Consists of a bilayer of Amphipathic lipids with the hydrocarbon chains oriented inward to the
center of the bilayer to form a continuous hydrophobic phase and their hydrophilic head is oriented
outward.
Drugs cross the membrane either by passive processes or by mechanism involving active participation of
components of the Mb.
A. PASSIVE TRANSPORT B. ACTIVE TRANSPORT
(i) Simple diffusion-most common- (i) Facilitated diffusion e.g BI2, folic acid
usually lipid soluble drug. e.g (ii) Drug transporters
Propranolol, Diazepam,
Thiopentone Na….. Facilitated transport: Describes a
(ii) Paracellular transport. carrier-mediated transport process in
which there is no input of
energy.
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ABSORPTION
It is the movement of a drug from its site of administration into the
central compartment and the extent
to which this occurs.
FACTORS AFFECTING ABSORPTION
A. PHARMACEUTICAL FACTORS (EXTRINSIC FACTORS)
-DRUG RELATED FACTORS
1. Physical state of the drug: Drug given in aqueous/ liquid dosage are more rapidly
absorbed. e.g colloids are slowly absorbed(dextran, albumin), compared to crystalloid
(saline, glucose).
2. Water/Lipid solubility
Drug given in aqueous solution mix more readily with the aqueous phase of the
absorbing the surface than when given in solution.
Aqueous solution more easily absorbed.
3. Particle size
Solid dosage forms containing smaller particles-microfine crystals are better absorbed
from the gut. e.g Aspirin , Warfarin ,Griseofulvin.
Solid dosage containing larger particles are little absorbed e.g Neomycin.
4. Ionisation of the drug
Non-ionised drugs are better absorbed from the GIT, e.g Aspirin in stomach and
morphine in intestine.
5. Disintegration-time of the drug
It is the time taken for solid dosage form (e.g tablet) of a drug to break down into finer
particles in the gut completely. Longer the disintegration time, the slower will be the
rate of absorption.
6. Dissolution-Time of a drug
Time taken for a solid dosage form e.g tablet to go into the solution form in the gut after
it has disintegrated. Shorter dissolution time, higher will be the rate of absorption.
7. Enteric-coated tablet
They are made-enteric coated by means of cellulose/Phthalate.
They resist disintegration & dissolution by gastric juice, but permits disintegration
& dissolution in alkaline medium of the gut.
They have prolonged action- e.g S.R Tablet-Prolonged action.
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B. HUMAN FACTORS/OTHER FACTORS
1. Concentration of the drug
Passive diffusion depends on the concentration gradient. Higher concentration of the drug, faster
will be the rate of absorption.
2. Area of the absorbing surface
Larger the surface area, more is theabsorption.
3. Vascularity of the absorbing surface
The higher the blood flow, the more and faster is the absorption.
4. Route of absorption
(FACTORS AFFECTING ABSORPTION FROM ORAL ROUTE)
1. Epithelial lining of GIT is lipoidal; lipid soluble drug are better absorbed.
2. Acid labile drug e.g Insulin is destroyed by this route
3. Ionised drug e.g basic drug-Morphine are better absorbed in duodenum.
4. Presence of food in the stomach (other drugs)
In general food in stomach retards absorption e.g Rifampicin, Ampicicillin, Iron, Isonicinil.
Rifampicin is best given on empty stomach.
Fatty food increases the absorption of:
Ribavirin
Albendazole /Mebendazole
Effavirenz
Atovaquone
Vitamin C increases absorption of Iron.
Phytates /oxalates decreases absorption of iron
Iron & Tetracycline (tetracycline chelates iron)
Phenytoin &sucralfate (sucralfate decreases the absorption of phenytoin).
6. Rate of absorption increases with increasing rate of gastric emptying. Pregnancy delays gastric
emptying: decreases absorption by oral route.
Migraine also cause gastro-paresis
PCM + Metoclopramide
Rabeprazole + Domperidone in Gastroparesis
7. Pathological state
→
CCF Mucosal oedema delays absorption
→
GIT Malabsorption
B. Parenteral :Intramuscular / subcutaneous Route
Heat / muscular exercise / massage causes vasodilation and hence increases the
absorption of the drug.
Vasoconstrictors e.g Epinephrine decrease absorption and prolonged duration action of
such drug in local site Lignocaine + Epinephrine.
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C. TOPICAL
Inflamed, Denuded areas has increased vascularity such that absorption of the given drug
increases drastically to such an extent that toxicity can easily occurs.
Contact time of the site of absorption: If a drug moves through the GIT very quickly as in severe
diarrhea, it will not be absorbed.
→ →
N.B: Anything that delays the transport of drug from stomach Intestine delays rate of
absorption. e,gDicyclomine
BIO-AVAILABILITY
It is defined as the fraction of the drug dose that reaches the systemic circulation in unchanged
form after pre-systemic elimination and is available for action.
Relative Bio-availability= Amount of Drug absorption
Amount of drug administered by any route
Bio-availability Incomplete Bio-availability may be due to
IV route : 100% (i) Incomplete absorption
Oral: 0- 100% (ii) First-pass metabolism
Absolute Bio-availability is calculated by
AUC after oral dose x 100
AUC after IV dose
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FACTORS MODIFYING / AFFECTING BIO-AVAILABILITY
(i) Route of administration
(ii) Presence of food / Drug in GIT
(iii) Effect of Pre-systemic elimination
(iv)Entero-hepatic recycling
(vi) Drug distribution / Plasma protein binding
(vi) Pharmaceutical factors. e.g ( Physical& chemical properties of the drug
Dosage form, particle size ,Disintegration / Dissolution).
ENTERO-HEPATIC RECYCLING (EHR)
It is the process of re-circulation of drugs whereby the
drug enters the liver from intestine by portal vein
and back to the intestine via Bile-duct.
β-Glucoronidase is needed for entero-hepatic recycling
to occur. Hydrolysis is needed such that
reabsorption can occur.
EXAMPLE OF DRUGS UNDERGOING EHR
All NSAIDs except Nabumetone (PCM, Indomethacin /Diclofenac)
Opioids: Morphine, Buprenorphin, Methadone..
Diazepam, OCP, Amoxycillin, Ampicillin, Sulfonamides, Tamoxifen, Digoxin.
Endogeneous subs: Vit D3, Oestrogen, Progesterone, Vit B12, Thyroxine.
SIGNIFICANCE
1. Help in prolongation of action of the drug but however decreases its potency.
2. Certain drugs inhibit EHC and are useful in the treatment of toxicities of drugs that are capable
of undergoing entero-hepatic recycling.
e.g Activated charcoal
Anion exchange resin for Digoxin
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DRUG DISTRIBUTION
It refers to the reversible transfer of a drug between the blood and the extravascular fluids
and Tissues of the body (e.g fat, muscle & brain tissue).
DISTRIBUTION IS A PASSIVE PROCESS:
The driving force is the concentration gradient between blood and the tissues.
The process occurs by the diffusion of free drug until equilibrium is established.
Distribution of a drug is not uniform throughout the body because different tissues receive the drug
from plasma at different rates and to different extents.
Following absorption or systemic administration into the blood stream, a drug distributes into
interstitial and intracellular fluids.
FIRST DISTRIBUTION PHASE SECOND DISTRIBUTION PHASE
May require minutes to several hours before the
Initially well perfused organ-Liver
concentration of the drug in tissues is in
/Heart / Kidney /Brain receive the blood.
equilibrium with that of blood.
Involves larger fraction of the body
Delivery to less well-perfused organ e.g Adipose
tissue,muscles, Skin.
APPARENT VOLUME OF DISTRIBUTION, VD
It is the volume that would accommodate all the drug in the body if the concentration
throughout was
same as in plasma i.e the body was behaving as a single homogeneous compartment.
Amount of drug in body
Vd =
Conc of drug in blood /Plasma
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REDISTRIBUTION
Highly lipid soluble drugs when given by IV or inhalational route
initially gets distributed to
organs of high blood flow such as brain /heart /Kidney.
If site of action of the drug was in one of those highly perfused
organ; the onset of action will be
very rapid (e.g thiopental –IV GA)
Later less vascular but more bulky tissues (muscles /fat) take up the
drug & plasma
concentration falls and the drug is withdrawn from these sites.
In the above case, redistribution leads to terminate of action of the
drug.
N.B: Greater the lipid solubility of the drug, faster is its rate of
redistribution. However, when the same
drug is given repeatedly /continuously over longer periods , the low
perfusion, high capacity sites gets
progressively filled up & the drug becomes longer acting.
Example
Nitrazepam sedative action lasting 6-8 hrs initially but after
prolonged use the t1/2 becomes 30 hours.
The real volume of distribution has physiological meaning and is
related to body water (total 42L).
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FACTORS AFFECTING DISTRIBUTION OF DRUG
1. TISSUE PERMEABILITY OF THE DRUGS
Lipid solubility & transmembrane pH gradient.
PKa of the drug. ( especially for drugs that are weak acids
/bases)
Molecular wt
Partition coefficient
Physiological barriers to diffusion of the drugs
Ionisation (Unionized drug promotes more easily)
2. RELATIVE BINDING TO PLASMA PROTEIN.
Limit concentration of the free drug
N.B: Drugs that are extensively bound to PPB are largely restricted to the vascular compartment
Therefore they have a low volume of distribution.
e.g Warfarin 99% PPB
Vd: 9.8 L/70kg
3. SEQUESTRATION IN TISSUES.
Vd of such drugs are much more than the total body water or even body
mass.
Morphine: 230L/70kg
Digoxin: 500L/70kg
Chloroquine: 13000L/70kg
4. PRESENCE OF SPECIFIC TISSUE TRANSPORTERS
e.g P-gP Organ / Tissue size and perfusion rate
5. PATHOLOGICAL STATES
CCF / Cirrhosis /anaemia / Obesity Alternate of
distribution of water Permeability of Mb altered
6. Drug-interaction /Pregnancy
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CLINICAL SIGNIFICANCE
1. Drugs with very high volume of distribution have much
higher concentration in extravascular
tissue than in vascular compartment. Therefore, they are
not homogenously distributed.
Drugs with small volume of distribution are
homogeneously distribution.
2. In case of Poisoning with drugs low Vd, in general
Haemodialysis can be of use e.g these
drugs are confined to the vascular compartment.
N.B: Drugs that remain confined in
(i) Blood /Plasma : small Vd 5-10 L
(II) Drugs going beyond vasc comp (e.g tissue) Vd =10-20L
(iii) Drugs sequestered in tissues, Vd 500-50,000L
When Vd exceeds total body water (<42L), it means that there is sequestration of the drug in tissues.
PLASMA PROTEIN BINDING
Many drugs circulate in the blood stream bound to
Plasma Protein. The binding is usually reversible. Covalent
binding with reactive drugs such as alkylating agent
occurs occasionally
Albumin-major carrier for acidic drugs.
Examples of drugs that bind to albumin:
NSAIDs
Warfarin
Barbiturates
Benzodiazepines
Sulfonamides
α -1 acid Glycoprotein binds basic drugs
Examples of drugs that bind to α -1 acid Glycoprotein:
β-Blockers
Imipramine
Verapamil
Methadone
Non specific binding to other plasma Proteins occurs to a much smaller extent. e.g certain drugs bind to
proteins that function as specific hormone carrier protein. E.g Thyroid hormone-Thyroxine binding
globulin.
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KINETICS OF PROTEIN DRUG BINDING
The kinetics of reversible drug-protein binding for a protein
with one simple binding site can be
described by the low of mass action:
Protein + Drug Drug Protein complex.
The function of total drugs in Plasma that is bound is determined by:
(i) Drug concentration
(ii) Affinity for the binding sites
(iii) Number of binding sites
Therefore Plasma Protein binding is non-linear & saturable process.
(iv) Disease related factors:
e.g Hypoalbuminaemia secondary to liver disease / Nephrolic syndrome decrease PPB and
increases the unbound fraction.
↑
Condition leading to Acute Phase response: Cancer /Crohn’s Disease /MI leads to
an increase in α1 –Acid glycoprotein and enhanced binding of basic drugs.
(v) Drug-Drug interaction.
IMPLICATION OF PPB
1. Highly Plasma protein bound drugs are largely restricted to the vascular compartment, therefore
they have a low Vd.
2. Bound fraction is not available for action
Acts as drug reservoir
They are in equilibrium with free drug in Plasma and dissociate when conc of the water
is reduced.
3. Makes the drug longer acting.
Not available for metabolism /excrete unless they are actively extracted by liver /kidney tubules.
Limits the drug Glomeruler filtration
N.B: PPB generally does not limit renal tubular secretion / biotransformation as when the
free drug concentration decreases, dissociation will occur.
4. One drug can bind to many sites of albumin molecule and also more than one drug can bind to
the same drug.
5. Drug-Drug interaction.
Drugs having higher affinity will displace the one with lower affinity. If the drug is having high
affinity for different sites-no interaction occurs.
Acidic drug will not displace basic drug
Important displacement Reactions:
Salicylates with Sulfonylureas
Phenytoin with Warfarin
Aspirin & Warfarin
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TISSUE BINDING
Many drugs accumulates in tissues at high concentration rather than ECF
e.g Quinacrine-Liver
Chloroquine-Relina
Iodine-thyroid
Thiopentone-Adipose tissue
Tetracycline –Bone / teeth
Tissue binding occurs through cellular constituent such as:
Protein
Phospholipids ------- generally reversible
Nuclear protein
It serves as reservoir and prolongs the duration of action of the drug.
Consequence: Such as accumulation of drug & tissue Binding – local toxicity
e.g
Chloroquine –retinopathy
Gentamicin—ototoxicity /Nephotoxicity.
CNS & CEREBROSPINAL FLUID
Distribution of drugs into CNS from Blood is unique.
Brain capillary endothelial cells have continuous tight junction, therefore drug penetration into the brain
depends on transcellular rather than paracellular transport.
This unique characteristic of brain capillary endothetial cells & capillary cells constitute the Blood Brain
Barrier.
→
At choroid Plexus Blood-CSF barrier
(epithelial cells joined by height junctions rather than endothelial cells)
N.B: Only lipid-soluble drugs are able to penetrate and have action on CNS.
Other mechanism to prevent entry drugs in brain.
(i) Efflux transporters P-gP, organic anion transporter Polypeptide ( OATP) control the drug.
(ii) Enzymatic BBB
MAO, Cholinesterase and other enzymes
Prevent entry of cathecholines, 5HT ,ACH to enter the brain in their active form.
Blood Brain Barrier is deficient at CTZ ( floor of 4th ventricle)
(Even Lipid insoluble drugs are emetics)
N.B: Inflammation of meninges or brain increase permeability of these barriers.
Significance:
Important for designing drugs e.g 2nd generate Anti-histaminics
Less sedating as less lipid solution.
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PLACENTAL TRANSFER OF DRUGS.
General determinants in drug transfer across the placenta.
(i) Lipid solubility
(ii) Extent of Plasma protein binding
(iii) Degree of ionisation of weak acids or bases
Fetal plasma is slightly more acidic than that of the mother ( PH 7.0-7.2 v/s 7.4)
Therefore iron trapping of basic drugs occurs.
Here also, P-Gp + other export transporters are present which limit the exposure of the
fetus to potentially dangerous agents.
N.B: Placental barrier is not an absolute barrier. The fetus is to some extent exposed to
all drugs taken by the mother.
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DRUG METABOLISM
Drugs are most often eliminated by bio-transformation/ and or excreted into urine or bile. Liver is the
major site of drug metabolism; Other tissues involves the kidney, intestine, lung.
Half –life
Plasma half life
It is the time taken for the plasma concentration of a drug to fall to one half of its value during
elimination (during a constant infusion)
T1/2 = ln 2 x Vd
CL
Note:
Most drugs have an alpha T1/2 and remain in plasma; due to distribution.
Some drugs have beta- T1/2: they have 2 T1/2; one in plasma and one in tissues; due to elimination.
Examples of half-life of some drugs: In first T1/2: 50% of drug is
Adenosine: 10 seconds eliminated
Esmolol: 10 minutes In second T1/2: 75% of drug is
Aspirin: 15 minutes eliminated
Digoxin: 4 hours In third T1/2: 87.5% of drug is
Digitoxin: 40 hours eliminated
Amiodarone: 100 days In fourth T1/2: 93.75% of drug is
eliminated
In fifth T1/2: 97% of drug is
eliminated
Thus almost complete elimination
occurs in about 4-5 T1/2
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FACTORS AFFECTING T1/2
1. Clearance
2. Volume of distribution
3. Plasma-protein binding
4. Types of elimination kinetics (zero/first order)
5. Pathological states
6. Active metabolites
7. Entero-hepatic recycling.
CLINICAL SIGNIFICANCE OF KNOWING THE PLASMA T1/2
1. Duration of action of the drug can be determined.
2. Effective dose and dosage schedule can be planned more easily.
3. Time to reach steady state concentration and time for complete elimination of the drug from
the body can be calculated.
CLINICAL SITUATION WHERE PLASMA T1/2 IS INCREASED
1. Decrease renal plasma flow eg CCF, cardigenic shock, haemorrhage
2. Increase volume of distribution
3. Decreased excretion of the drug, eg renal disease.
4. Decrease metabolism of the drug, eg cirrhosis.
Biological T1/2
It is the time in which the pharmacological effect of a drug or its active metabolite is reduced to half.
It is applicable to drugs whose effects persists long after the drug has been eliminated.
Eg anti-cancer drugs.
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PHARMACOLOGY STUDY GUIDE
Pharmacology – Study of the biological effects of chemicals
Pharmacotherapeutics – Clinical pharmacology involving drugs use to
treat, prevent, or diagnose a disease
NURSING PROCESS AND MEDICATION ADMINISTRATION
1. Assessment
Allergies
Pattern of health care
Understanding of the disease process
Financial support
2. Physical Assessment
Age and weight
Social support at home
Chronic condition
3. Diagnostic test, Laboratory test
4. Medication History
Prescriptions
OTCS
Herbals
Response to medications
NURSING DIAGNOSIS
Human response to illness
Drug therapy may only be a
part of the total picture
Drug therapy is incorporated
in the total picture
PLANNING
1. identify possible intractions
2. client and family education
3. gather equipment, review procedures,
safety
measures, timing and frequency of drugs
4. storage of drugs
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IMPLEMENTATION
1. Maximizing therapeutic effects
2. Minimizing adverse effects
3. SIX rights of medication administration
EVALUATION
Monitor the patient response to drug therapy expected outcome
Unexpected outcome
THE 5 RIGHTS OF MEDICATION ADMINISTRATION
Right drug
Right dose
Right time
Right route
Right patient
SIX ELEMENTS OF A DRUG ORDER
Name of the patient
Date order is written
Name of medication
Dosage which includes size, frequency
and number of doses
Route of delivery
Name and signature of the prescriber
DRUG NAMES
1. Chemical Name
Describe the chemical structure
and composition
2. Generic Name
Non propriety name given by
USANC
3.Brand Name
Registered trademark
EXAMPLES
Chemical Name
Propionic acid
Generic Name
Ibuprofen
Brand Name
Motrin
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SAFETY AND EFFICACY
1. Always verify the Five Rights .
a. the right medications
b. the right client
c. the right dosage
d. the right form, route and technique
e. the right time
2. Chart drug administration only after its been given, never before.
3. Never leave the medication on cart or tray unattended.
4. Chart observed therapeutic and adverse effects accurately and
fully.
5. Check history for allergies and potential drug interactions
before
administering a newly ordered drug.
6. Inform the prescribing physician of any observed adverse effects;
if
cannot be
located, inform the nursing supervisor
7. Question drug orders that are unclear, that appear to contain
errors, or that have potential to harm.
8. Take the following actions if an error occurs :
a. immediately notify the nursing supervisor, the prescribing
physician, and the pharmacist.
b. assess the client’s condition and provide any necessary care.
9. For postpartum women, advice to take drugs after breastfeeding
ADMINISTRATION OF DRUGS :
ROUTES AND NURSING CONSIDERATIONS:
1. ENTERAL – ORAL, SUBLINGUAL, RECTAL, GASTRIC TUBES
- CAPSULATED PILL, SUSTAINED RELEASE AND ENTERIC COATED SHOULD NOT BE
CRUSHED.
2. PARENTERAL – IV, IM, SQ, ID, IT, IA, EPIDURAL.
- VASTUS LATERALIS (SAFEST SITE FOR IM)
3. TOPICAL – SKIN, INHALANTS, MUCUS MEMBRANE.
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MAJOR ROUTES OF ADMINISTRATION
ORAL ADMINISTRATION OF MEDICATIONS
ADVANTAGES
CONVENIENT
INEXPENSIVE TO ADMINISTER
DISADVANTAGES:
ABSORPTION VARIES FROM PERSON TO
PERSON
ORAL MEDS MAY IRRITATE GI TRACT
CLIENT MUST COOPERATE
ABSORPTION: TWO GATES OF ABSORPTION
GASTROINTESTINAL TRACT
CAPILLARY WALLS
MOST OF AN ORAL DOSE IS ABSORBED IN THE
SMALL INTESTINE
RATE AND DEGREE OF ABSORPTION DEPENDS ON
PH OF STOMACH CONTENTS
FOOD IN STOMACH
GASTRIC EMPTYING TIME
COATING ON MEDICATION PREPARATION
TOPICAL MEDICATIONS(SKIN, NOSE, EYE, EAR,
VAGINA, RECTUM)
CLASSIFICATIONS OF DRUGS
CENTRAL AND AUTONOMIC SYSTEM DRUGS
CHOLINERGIC AGENTS (PARASYMPATHOMEMITICS)
Prototype
- synthetic acetylcholine, pilocarpine,
carbachol, bethanecol
(Urocholine),
edrophonium (Tensilon), neostigmine
(Prostigmine),
pyridostigmine (Mestinon)
Mechanism of action
- stimulates cholinergic receptors by
mimicking acetylcholine or inhibition of
enzyme cholinesterase.
Indications
- glaucoma, urine retention, Myasthenia
Gravis - antidote to neuromuscular blocking
agents : tricyclic antidepressants and atropine
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Adverse effects
- blurring of vision, miosis - increase in
salivation, intestinal cramps -
bronchoconstriction, wheezing, DOB -
hypotension and bradycardia
Nursing considerations
1. Warn & monitor clients of the side effects.
2. Have atropine available for use as antidote.
CHOLINERGIC BLOCKING AGENTS
(PARASYMPATHOLYTICS,
ANTICHOLINERGICS)
Prototype
- atropine, scopalamine (Triptone),
dicyclomine (Bentyl), propantheline (ProBanthine).
Mechanism of action
- block the binding of acetylcholine in the
receptors of parasympathetic nerves.
e- use preoperatively to dry up secretions. -
treat spasticity of GI or urinary tract. - use for
treatment of bradycardia, asthma,
parkinsonism. - use for antidote in
organophosphate poisoning.
Indications
Adverse effects
- dry mouth , dilatation of pupils, tachycardia
- urinary retention, ileus, heat stroke
Nursing considerations
1. Keep client’s in cool environment.
2. Watch out for signs of heatstroke and
dehydration.
3. Encourage clients to increase fluid intake
and use of sugarless gum/candy for dry
mouth.
4. For GI spasticity, administer 30 minutes
before meals and at bed time.
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SKELETAL MUSCLE RELAXANTS AGENTS
ANTICONVULSANTS
Prototype
a. Hydantoins - phenytoin (Dilantin) b.
Barbiturates - phenobarbital ( Luminal) c.
Miscellaneous - carbamazepine (Tegretol),
diazepam, clorazepate (Tranxene), valproic
acid (Dapakene), ethosuximide (Zarontin).
Mechanism of action
- treat seizures by depressing abnormal
neuronal activity in motor cortex.
Adverse effects
- sedation & drowsiness, gingival hyperplasia
- diplopia, nystagmus, vertigo, dizziness -
thrombocytopenia, aplastic anemia
Nursing considerations
1. Advise female clients to use contraceptives. 2.
Inform clients taking phenytoin that harmless
urine discoloration is common. 3. Warn clients
with diabetes that hydantoins may increase blood
sugar level and that valproic acid may produce a
false positive result in urine ketone test. 4. Teach
clients receiving carbamazepine to identify
symptoms of bone marrow depressions. 5.
Reassure that barbiturates are not addictive at a
low dosage. 6. Avoid taking alcohol with
barbiturates. 7. Administer IV phenytoin slowly to
avoid cardiotoxicity. 8. Avoid mixing other drugs
in same syringe with phenytoin.
ANTIPARKINSONIAN AGENTS
Prototype
- amphetamines, methylphenidate (Ritalin)
Mechanism of action
- increase excitatory CNS neurotransmitter
activity and blocks inhibitory impulses.
Indications
- for obesity (amphetamines) - attention
deficit hyperactivity disorders - narcolepsy -
drug-induced respiratory depressions.
Adverse effects
- nervousness, insomnia, restlessness -
hypertension, tachycardia, headache -
anorexia, dry mouth.
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Nursing considerations
1. Should be given at morning.
2. Don’t stop amphetamine abruptly to avoid
withdrawal symptoms.
3. Monitor blood pressure and pulse.
4. Ice chips or sugarless gum for dry mouth.
5. Watch out for growth retardation in children
taking methylphenidate.
MENTAL HEALTH DRUGS
SEDATIVES, HYPNOTICS, AND ANXIOLYTICS
Prototype
a. Benzodiazepines - diazepam (Valium),
lorazipam (Ativan), alprazolam (Xanax),
flurazepam (Dalmane) b. Barbiturates -
amobarbital, phenobarbital, secobarbital c.
Miscellaneous - chloral hydrate (Noctec),
buspirone (Buspar), paraldehyde (Paral)
Mechanism of action
a. Benzodiazepines - increase the effect of
inhibitory neuro transmitter GABA (gammaamino butyric acid) b.
Barbiturates and
Miscellaneous agents - depress CNS
Indications
- induce sleep, sedate and calm clients
Adverse effects
- hangover-effect, dizziness, CNS depression -
respiratory depression, drug-dependence
Nursing considerations
1. Warn clients of injuries and falls.
2. Brief period of confusion and excitement upon
waking up is common with benzodiazepines.
3. Warn clients not to discontinue medications
abruptly without consulting a physician.
4. Avoid alcohol while taking these drugs.
5. Rotate and don’t shake the ampules of
barbiturates. Don’t mix with other drugs.
6. Warn female clients that diazepam is
associated with cleft lip.
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ANTIDEPRESSANTS AND MOOD DISORDER DRUGS
Prototype
a. Tricyclic antidepressants - amitriptyline (Elavil),
protriptyline (Vivactil), - imipramine (Tofranil),
desipramine b. MAO (monoamine oxidase
inhibitors ) - isocarboxazid (Marplan), phenelzine
(Nardil), tranylcypromine (Pernate) c. Secondgeneration
antidepressants - fluoxetine (Prozac),
trazodone (Desyrel) d. Lithium
Mechanism of action
-a. Tricyclic antidepressants - increase receptor
sensitivity to serotonin and/or norepinephrine. b.
MAO inhibitors - inhibit the enzyme MAO that
metabolize the neurotransmitters norepinephrine
and serotonin. c. Second – generation
antidepressants - inhibits the reuptake of
serotonin. d. Lithium - increase serotonin &
norepinephrine uptake
Adverse effects
- dry mouth, blurred vision, urine retention,
constipation (anticholinergic effects) -
orthostatic hypotension, insomnia -
hypertensive crisis (MAO) - dehydration
(Lithium).
Nursing considerations
1. Caution client to rise slowly to reduce the effects of
orthostatic hypotension.
2. Take antidepressant with food to enhance
absorption
3. Explain to client that full response may take several
weeks (2 weeks).
4. Assess client for constipation resulting from
tricyclic antidepressant use.
5. Client taking MAO inhibitors should avoid
tyramine-rich foods to avoid hypertensive crisis. -
aged cheese, sour cream, yogurt, beer, wine, chocolate,
soy sauce and yeast - pentholamine (Regintine) is the
drug of choice for hypertensive crisis.
Sedatives, Hypnotics, and Anxiolytics
6. Inform physician and withhold fluoxetine if
client develop rashes.
7. Take lithium with food to reduce GI effects
- > 1.5 mEq/L blood level may cause toxicity
manifested by:
confusion, lethargy, seizures,hyperreflexia.
- maintain salt and adequate fluid intake
- tremors may occur but it is temporary
- monitor white blood cell count (increase).
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ANTICONVULSANTS/ANTISEIZURE MEDICATIONS
Prototype
a. Hydantoins - phenytoin (Dilantin)
b. Barbiturates - phenobarbital ( Luminal)
Adverse effects
- sedation & drowsiness, gingival hyperplasia
- diplopia, nystagmus, vertigo, dizziness -
thrombocytopenia, aplastic anemia
Nursing considerations
1. Advise female clients to use contraceptives.
2. Inform clients taking phenytoin that harmless
urine discoloration is common.
3. Warn clients with diabetes that hydantoins
may increase blood sugar level.
4. Reassure that barbiturates are not addictive at
a low dosage.
5. Avoid taking alcohol with barbiturates.
6. Administer IV phenytoin slowly to avoid
cardiotoxicity.
7. Avoid mixing other drugs in same syringe with
phenytoin.
PAIN MANAGEMENT
LOCAL AND TOPICAL ANESTHETIC
Prototype
ocal : bupivacaine, lidocaine, tetracaine,
procaine, mepivacaine, prilocaine topical :
benzocaine, butacaine, dibucaine,lignocaine
Mechanism of action
- block transmission of impulses across nerve
cell membrane.
- cardiac dysrhythmias
Adverse effects
Nursing considerations
- lignocaine + prilocaine (EMLA cream) should
be applied topically 60 minutes before
procedure. - administer cautiously to the areas
of large broken skin. - observe for fetal
bradycardia in pregnant clients.
ANALGESICS
Prototype
a. Narcotic analgesics - codeine, meperidine
(Demerol) morphine, butorphanol (Stadol)
nalbuphine (Nubain) b. Non – narcotic
analgesic NSAIDs – aspirin (aminosalicylic
acid), mefenamic acid (Ponstan), ibuprofen
(Motrin), naproxen, ketoprofen (Orudis),
ketorolac. paracetamol and acetaminophen
(Tylenol)
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Mechanism of action
a. Narcotic analgesics - alter pain perception
by binding to opiod receptors in CNS.
b. Non narcotic analgesic - relieves pain and fever by
inhibiting the prostaglandin pathway.
CARDIOVASCULAR SYSTEM DRUGS
ANTIPLATELET MEDICATIONS
Prototype
aspirin, Dipyridamole (Persantin)
Clopidoigrel (Plavix), Ticlopidine
Mechanism of action
- inhibit the aggregation of platelet thereby
prolonging bleeding time.
Indications
- used in the prophylaxis of long-term
complication following M.I, coronary
revascularization, and thrombotic CVA.
Nursing considerations
- Monitor bleeding time ( NV = 1-9 mins) - Take
the medication with food.
CARDIAC GLYCOSIDES
Prototype
- digoxin (Lanoxin) and digitoxin
(Crystodigin)
Mechanism of action
- increase intracellular calcium, which causes
the heart muscle fibers to contract more
efficiently, producing positive inotropic &
negative chronotropic
- use for CHF, atrial tachycardia and
fibrillation
Nursing considerations
- Monitor for toxicity as evidence by : nausea,
vomiting, anorexia, halo vision, confusion,
bradycardia and heart blocks . - Do not
administer if pulse is less than 60 bpm. - Should
be caution in patient with hypothyroidism and
hypokalemia. - Antidote : Digi-bind - Phenytoin is
the drug of choice to manage digitalis-induced
arrhythmia.
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ANTI-ARRHYTHMIC DRUGS
Class I (block Na channels)
IA - quinidine, procainamide
IB - lidocaine
IC - flecainamide
Class II (Beta-blockers)
propanolol, esmolol
Class III (block K channels)
amiodarone, bretylium
Class IV (block Ca channels)
verapramil, diltiazem
Nursing considerations
1. Watch out for signs of CHF. 2. Have client
weigh themselves and report weight gain. 3.
Watch out for signs of lidocaine toxicity : -
confusion and restlessness
NITRATES
Prototype
- isosorbide dinitrate (Isordil) - nitroglycerine
(Deponit, Nitrostat)
Mechanism of action
- - produce vasodilatation including coronary
artery
Indications
- angina pectoris, MI, peripheral arterial
occlusive disease.
Adverse effects
- headache, orthostatic hypotension .
Nursing considerations
1. Transdermal patch - apply the patch to a
hairless area using a new patch and different site
each day. - remove the patch after 12-24 hours,
allowing 10-12 hours “patch free” each day to
prevent tolerance. 2. Sublingual medications : -
note the BP before giving the medication. - offer
sips of water before giving because dryness may
inhibit absorption. - one tablet for pain and
repeat every 5 mins. for a total of three doses; if
not relieved after 15 mins., seek medical help. -
stinging or burning sensation indicates that the
tablet is fresh. - instruct patient not to swallow
the pill - sustained release medications should be
swallowed and not to be crush. - protect the pills
from light.
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DIURETICS
- USUALLY GIVEN AT MORNING
CARBONIC ANHYDRASE INHIBITORS
- Acetazolimide (Diamox)
- increase Na+, K+, & HCO3 secretion, along
with it is H2O
- metabolic acidosis
OSMOTIC DIURETIC
- Mannitol
- Increase osmotic pressure of the glomerular
filtrate.
- hypotension
POTASSIUM SPARING DIURETICS
- Spironolactone (Aldactone)
- excrete Na and water but it reabsorb K
- hyperkalemia
RESPIRATORY DRUGS
GLUCOCORTICOIDS (CORTICOSTEROIDS)
Prototype
- dexamethasone, budesonide, fluticasone,
prednisone, beclomethasone.
Mechanism of action
- act as anti-inflammatory agents and reduce
edema of the airways, as well as pulmonary
edema.
Nursing considerations
- Take drugs at meal time or with food. - Eat
foods high in potassium, low in sodium. - Instruct
client to avoid individuals with RTI. - Instruct
client not to stop medication abruptly, it should
be tapered to prevent adrenal insufficiency -
Avoid taking NSAID while taking steroids. - Take
inhaled bronchodilators first before taking
inhaled steroids, and rinse mouth after using
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MAST CELL STABILIZERS
Prototype
cromolyn sodium (Intal)
Mechanism of action
- stabilize mast cells that release histamine
triggering asthmatic attacks.
Nursing considerations
- Should be given before asthmatic attacks. -
Administer oral capsule at least 30 mins before
meals for better absorption. - Drink a few sips of
water before & after inhalation to prevent cough
& unpleasant taste - Assess for lactose intolerance.
ANTI-HISTAMINES (H-1 BLOCKERS)
Prototype
- Astemizole (Hismanal), Loratidine
(Claritin), Brompheniramine (Dimetapp),
Diphenhydramine (Benadryl), Cetirizine
(Iterax), Celestamine (Tavist).
Mechanism of action
- decrease nasopharyngeal secretions and
decrease nasal itching by blocking histamine
in H1-receptor
Nursing considerations
- Administer with food and drink.
- Given IM via Z-track method or orally.
- Precautions in handling machine and driving
while taking these drugs.
- Ice chips or candy for dry mouth
Indications
- common colds, rhinitis, nausea and
vomiting, urticaria, allergies and as sleep
aid.
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ANTI-TUBERCULOSIS
Isoniazid
- should be given 1 hr before or 2 hrs after
meals because food may delay absorption. -
should be given at least 1 hr before antacids. -
instruct to notify physician for signs of
hepatoxicity (jaundice), and neurotoxicity
numbness of extremities. - administer with
Vitamin B6 to counteract the neurotoxic side
effects. - avoid alcohol.
Prototype
First line
- Isoniazid (INH)
- Rifampicin (Rifadin)
- Ethambutol
- Pyrazinamide
- Streptomycin
Second line
- Cycloserine
- Kanamycin
- Ethonamide
- Para-aminosalicylic acid
- active tuberculosis are treated with drug
combination for 6-9 mos.
- multidrug-resistant strain (MDR-TB) are medicated
for 1 year up to
2 years
- given before meal.
GI DRUGS
ANTACIDS
Prototype
- aluminum/magnesium compounds
(Maalox) - sodium bicarbonate (Alka-Seltzer)
- calcium carbonate (Tums) - magnesium
hydroxide (Milk of Magnesia).
Mechanism of action
- neutralize the stomach acidity.
Adverse effects
- metabolic alkalosis, stone formation -
electrolyte imbalance - diarrhea
(magnesium), constipation (aluminum).
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Nursing considerations
- Give 1 hr after meals.
- Avoid giving medications within 1-2 hrs of
antacid administration (decreases absorption).
- Take fluids to flush after intake of antacid
suspensions.
- Monitor for changes of bowel patterns.
HISTAMINE – 2 BLOCKERS
Prototype
- cimetidine (Tagamet), ranitidine (Zantac),
famotidine (Pepcid), nizatidine (Axid).
Mechanism of action
- blocks H2 receptors in the stomach,
reducing acid secretions.
Nursing considerations
- Given before or with meals
- Avoid giving other drugs with cimetidine -
Gynecomastia may developed with chronic use of
cimetidine.
PROTON – PUMP INHIBITORS (PPI)
Prototype
- omeprazole (Losec), Lansoprazole (Lanz),
pantoprazole (Pantoloc).
Mechanism of action
- inhibit the proton H+ to combine with Cl-to form hydrochloric acid.
Nursing considerations
- Given before meals preferably at morning.
ANTI-DIARRHEAL AGENTS
Prototype
- diphenoxylate (Lomotil), loperamide
(Imodium), kaolin/pectin mixture
(Kaopectate).
Mechanism of action
- decrease stomach motility and peristalsis.
Nursing considerations
- Monitor for rebound constipation.
- Be cautious taking if with infectious diarrhea.
- Monitor atropine toxicity with diphenoxylate.
- Clay, white or pale stool is common with
kaopectate.
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ENDOCRINE SYSTEM DRUGS
PROTON – PUMP INHIBITORS (PPI)
Prototype
-- Proloid (thryroglobulin ) - Synthroid
(levothyroxine) - Cytomel ( liothyronine).
Mechanism of action
- function as natural or synthetic hormones.
Nursing considerations
- Taken in the morning. - Caution with coronary
artery disease. - Monitor for signs of
hyperthyroidism and refer for decreasing the
dose
PARATHYROID AGENTS
Prototype
a. calcitonin (Calcimar), etidronate
(Didronel), b. calcitrol (Rocaltrol), calcifediol
(Calcedrol)
Mechanism of action
a. reduce bone resorption b. promotes
calcium absorption
Nursing considerations
- Monitor signs of calcium imbalance - Report for
bone pains. - Remain sitting upright after taking
etidronate.
INSULIN
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PROTON – PUMP INHIBITORS (PPI)
Prototype
- conjugated estrogen (Premarin), estrone
(Bestrone), estradiol (Estrace),
diethylstilbestrol (DES).
Indications
- prostate cancer, contraceptions - estrogen
replacement
Nursing considerations
1. Mix estrogen or progestins prior to IM
administration by rolling vials between palms.
2. Monitor blood pressure
3. Teach patient how to perform BSE.
4. Regular follow-up examination is required to
detect associated risk of acquiring CA
ESTROGENS AND
PROGESTINS
Adverse effects
estrogen - endometrial CA, gallbladder
disease, HPN, migraine, breast tenderness
progesterone - altered menstrual flow, risk of
thrombo embolism
INFECTION TREATMENT DRUGS
ANTIBACTERIAL AGENTS
1. Cell wall inhibitors
a. penicillins - pen G, amoxicillin, cloxacillin
b. cephalosphorins
- cephalexin, cefaclor
c. glycopeptide - vancomycin
2. Protein synthesis inhibitors
a. aminoglycosides - amikacin, gentamycin
b. macrolide - erythromycins, roxithromycin
c. lincosamides - clindamycins
d. chloramphenicol, tetracyclines
3. Antimetabolites
- blocks folic acid synthesis a. Sulfonamides -
cotrimoxazole
4. DNA synthesis inhibitors
a. quinolones - ciprofloxacin, ofloxacin
b. metronidazole
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Adverse effects Antiviral Agents
1. Aminoglycoside - nephrotoxicity & ototoxicity Prototype
2. Sulfonamides - Steven-Johnson’s syndrome,
- acyclovir (Zovirax), ganciclovir (Cytovene),
photosynsetivity
vidarabine (Vira-A), amantidine (Symmetrel),
3. Quinolones - insomnia
ribavirin (Virazole), zidovidine (Retrovir).
4. Tetracyclines - bone problems
5. Chloramphenicol - Gray syndrome, bone marrow Mechanism of actions
depression - inhibits virus specific enzymes involve in DNA
6. Erythromycin - hepatitis synthesis. They only control the growth of virus
but it does not cure.
Nursing considerations
1. Collect appropriate specimen for C & S before Adverse effects
starting antibiotics. - granulocytopenia, thrombocytopenia, nausea,
2. Check client’s history of allergies. nervousness, headache, nephrotoxicity.
3. Avoid administering erythromycin and quinolones
with food. Nursing considerations
4. Pregnant precautions. - Pregnant and breastfeeding precautions.
5. Report for diarrhea - pseudomembranous colitis - Administer IV antivirals to avoid crystallization in
(clindamycin) renal tubules.
6. Monitor adverse effects. - Give ribavirin only with aerosol generator.
- Monitor CBC and creatinine level.
- Refer for signs of bleeding.
- Take amantidine after meals.
ANTIPARASITIC AGENTS
Prototype ANTIHELMINTIC
a. Antimalarial - chlroquine, mefloquine, Prototype
primaquine, quinine, pyrimethamine - mebendazole (Vermox), thiabendazole,
b. Antiamebiasis - metronidazole (Flagyl), niclosamide (Niclocide), piperazine (Antepar),
iodoquinol, furozolidone (Furoxone). praziquantel (Biltricide).
Mechanism of actions Mechanism of actions
a. antimalarial – alters protozoal DNA, depleting
- paralyze larva and adult helmints by acting on
folates, & reducing nucleic acid production b.
parasite microtubules.
antiamoeba – block protein synthesis.
Adverse effects
Nursing considerations - GI upset, urinary odor (thiabendazole) -
1. Administer anti-malarial drugs with food. headache, dizziness, fatigue
2. Take seizure precautions while administering
antimalarial drugs. Nursing considerations
3. Refer cinchonism during quinine treatment: -
tinnitus, headache, vertigo, fever, and visual changes. 1. Treat all the family members for nematodes
4. Inform clients that iodoquinol falsify thyroid infection to prevent recurrence.
function test for up to 6 months. 2. Praziquantel must swallowed rapidly because of its
bitter taste to avoid gagging.
3. Other antihelmintics should be chewed.
ANTI-NEOPLASTIC DRUGS
General considerations
- kills or inhibit the reproduction of neoplasmic cells but as
well as
normal cells.
- it could be cell cycle phase specific or cell cycle non-
specific.
- preferably given through IV route.
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Prototype
1. Alkylating Agents
- inhibits cell production by causing cross linking of
DNA
a. Busulfan – hyperuricemia
b. Chlorambucil – gonadal suppression
c. Cisplatin – ototoxicity and nephrotoxicity
d. Cyclophosphamide – hemorrhagic cystitis.
2. Antitumor Antibiotic Agents
- interfere in DNA and RNA synthesis
a. Plicamycin – affects bleeding time
b. Doxurubicin – cardiotoxicity
c. Bleomycin – pulmonary toxicity.
3. Antimetabolites
- replace normal proteins required for DNA synthesis
by inhibiting
the S phase
a. Cytarabine – hepatotoxicity
b. 5-flourouracil – phototoxicity reaction and
cerebellar
dysfunctions
c. 6-marcaptopurine – hyperuricemia
d. Methotrexate – photosensitivity
- given with leucoverin to lessen its toxicity.
4. Mitotic Inhibitors (Vinca Alkaloids)
- prevent mitosis acting on the M phase causing cell
death
a. Vincristine sulfate – neurotoxicity, numbness
5. Hormonal Medications and Enzymes
- block the normal hormones in hormone sensitive
tumors
a. Tamoxifen citrate – visual problems
– elevate cholesterol & triglycerides level
b. Diethylstilbestrol – impotence and gynecomastia
in men.
Side Effects
- Stomatitis - bland diet, avoid strong mouthwash -
soft tooth brush, ice chips
- Diarrhea, nausea and vomiting - anti-emetic,
replace fluids and electrolytes
- Alopecia - reassure that it is temporary -
encourage o wear wigs, hats and head scarf
- Skin pigmentation - inform that it is only
temporary
- Tumor lysis syndrome - hyperuricemia &
hyperkalemia - force fluids
- Infection - notify physician if WBC is <2000/mm3
- monitor for signs of infection - reverse isolation -
low bacteria diet
- Anemia - iron, B-12, folic acid rich food - provide
rest periods
- Bleeding - avoid NSAIDs - minimize invasive
procedures - use soft toothbrush and electric
razor
- menstrual changes - reassure that menstruation
will resume.
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ANEMIA RELATED DRUGS
Prototype Prototype
hydroxocobalamin (Hydro-Crysti 12) ferrous sulfate (Feosol) Ep
Prototype: hydroxocobalamin (Hydro-Crysti 12) - given Mechanism of actions
IM everyday for 5 to 10 days, then once a month for
↑
life - used in states of demand or dietary deficiency
- elevate the serum iron concentration
Indications
Mechanism of actions
- folic acid and vitamin B12 : for cell growth and - treatment of iron deficiency anemias - adjunctive
division, and production of strong stroma in RBCs therapy in patients receiving epoetin alfa
- Vitamin B12: maintenance of the myelin sheath in Adverse effects
nerve tissue - direct GI irritation
Indications - with increasing serum levels, iron can be CNS
- replacement therapy for dietary deficiencies - toxic, causing coma and death
replacement in high-demand states (such as - parenteral iron: severe anaphylactic reactions,
pregnancy and lactation) local irritation, staining of the tissues, phlebitis
- treat megaloblastic anemia Nursing considerations
- folic acid: rescue drug for cells exposed to some
- confirm chronic, renal failure before drug
toxic chemotherapeutic agents administration
Adverse effects - give epoetin alfa 3 times a week, IV or SQ
- pain and discomfort at injection sites - do not mix with any other drug solution
- nasal irritation with the use of nasal sprays - monitor access lines for clotting
- arrange for hematocrit reading before drug
Nursing considerations administration
- confirm the nature of megaloblastic anemia - evaluate iron stores before and during therapy
- give both types of drugs in pernicious anemia - maintain seizure precautions on standy
- parenteral Vitamin B12 must be given IM each day for
5 to 10 days, then once a month for life
- arrange for nutritional consultation
- monitor for hypersensitivity reactions Prototype
- arrange for hematocrit and hemoglobin hydroxocobalamin (Hydro-Crysti 12)
measurements before and during therapy Prototype: hydroxocobalamin (Hydro-Crysti 12) - given IM
everyday for 5 to 10 days, then once a month for life - used
↑
in states of demand or dietary deficiency
Mechanism of actions
- folic acid and vitamin B12 : for cell growth and
division, and production of strong stroma in RBCs
- Vitamin B12: maintenance of the myelin sheath in
nerve tissue
Indications
- replacement therapy for dietary deficiencies -
replacement in high-demand states (such as
pregnancy and lactation)
- treat megaloblastic anemia
- folic acid: rescue drug for cells exposed to some
toxic chemotherapeutic agents
Nursing considerations
- confirm the nature of megaloblastic anemia
- give both types of drugs in pernicious anemia
- parenteral Vitamin B12 must be given IM each day for
5 to 10 days, then once a month for life
- arrange for nutritional consultation
- monitor for hypersensitivity reactions
- arrange for hematocrit and hemoglobin
measurements before and during therapy
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