LIBRAN JN

0967-008-6734
Digestive Tract
*mouth  digestion starts
1. mechanical
~ mastication (chewing) BOLUS
2. chemical
~ with the aid of ptyalin
*esophagus
*gastrum  “stomach”
 digestion continues (2-4 hrs)
1. mechanical
~ gastrokinesis
2. chemical
~ Pepsinogen
~ HCl (hydrochloric acid)

*** Intrinsic Factor

- for intestinal absorption of Vit B12
*intestine
- small intestine
> duodenum  digestion continues
 no absorption yet
> jejunum  absorption of nutrients
> ileum  ‘’
- large intestine (colon)
***absorption of water
- rectum and anus
Acid – Pepsin Related Disorders
 associated with hyperchlorhydria or achlorhydria
(hyperacidity) (absence of HCl)
 2 disorders:
* GERD
* PUD
GERD
 Gastro-esophageal Reflux Disease
 Problem:
~ regurgitation / backflow of gastric contents into
esophagus
 factors:
*diet
- fatty, carbonated (soda/cola) , caffeinated
*increased intra-abdominal pressure
- pregnancy
- obesity
*incompetent LES (lower esophageal sphincter)
- smoking, alcohol
*pyloric stenosis
* hiatal hernia
- protrusion of stomach into the diaphragmatic
hiatus
 S/Sx:
#1 pyrosis  heartburn
esophagitis  inflam of esophageal mucosa
*dysphagia  “difficult”
*odynophagia  “painful”
dyspepsia  indigestion
*bloating / abdominal distention
*N/V
*sour “eructation”
~ belching / burping
PUD – Peptic Ulcer Dse

Problem:
lesion (wound) or excavation (crater) on the
mucosa of duodenum or stomach

Types:
*Gastric U.  located in the stomach
 (+) epigastric pain
- aggravated by food intake
- felt 30 min – 1 hour after meal
- relieved by vomiting
*risk: metabolic alkalosis
*Duodenal U.  located in the duodenum
 (+) epigastric pain
- relieved by food intake
- felt 2 – 3 hours after meal
 Factors:

#1 P ylori infection
*Helicobacter pylori
 Test: Urea Breath Test
E xcessive eating
*fatty
*carbonated
*caffeinated
P ositive family history
*Blood Type O
S tress
I ntake or use of:
*alcohol
*cigarette
 decreases Bicarbonate (acid neutralizer)
N SAID
Management
A lcohol avoidance
N o smoking
T hree balanced-meal a day (PUD)
* small frequent meals (GERD)
A dvice on diet
* acute pain
- Bland Diet
* active bleeding
- NPO
C affeinated / carbonated / fatty / spicy X
I dentify PERFORATION
* risk: PERITONITIS
- fever
- leukocytosis
- abdominal pain
- abdominal rigidity (board-like abdomen)
D rugs  CHAPPPA
Cytoprotective
 coats the mucosa
*Sucralfate (Carafate)
*Misoprostol (Cytotec)
Histamine 2 Antagonist
 reduces acid production
*Ranitidine (Zantac)
*Cimetidine (Tagamet)
~ S/E: gynecomastia
Antacid
 neutralizes acid
* Al – Hydroxide (Amphogel)
S/E: constipation
* Mg – Hydroxide (Milk of Magnesia)
S/E: diarrhea
* Al – Mg Hydroxide (Maalox, Mylanta)
* Sodium Biarbonate + Sodium Alginate (Gaviscon)
* Calcium Carbonate (Tums)
Proton Pump Inhibitor (PPI)
 stops acid production
* Omeprazole (Prilosec, Risek, Omepron)
* Esomeprazole (Nexium)

Prokinetic / Gastrokinetic
 accelerates gastric emptying
* Domperidone (Motilium)
Pepto – Bismol
 inhibits the growth of H. pylori
* Bismuth Salt

Antibiotic
 kills H. pylori
* Tetracycline
Surgeries:
 Pyloromyotomy
* for pyloric stenosis
 Nissen Fundoplication (“gastric wrap”)
* for hiatal hernia
Surgeries:
 Vagotomy
* for intractable hyperacidity
Surgeries:
 Partial Gastrectomy
* Gastroduodenostomy (Billroth I)
* Gastrojejunostomy (Billroth II)
*** complications:
*Dumping Syndrome
- rapid emptying of gastric contents into the
intestine
- S/Sx: diarrhea, dehydration, dizziness,
diaphoresis, digital (finger) tremors
- Mng’t:
* Small, frequent meals
* Low CHO, High CHON diet
* Avoid liquids with meals
* Rest on recumbent position or
left side after meal.
*Pernicious Anemia
- faulty maturation of RBC due to lack of
intrinsic factor
- Dx:
Schilling’s Test
- Vit B12 absorption test
- Mng’t:
Vit B12 Supplement
- IM
- monthly
- lifetime
APPENDICITIS
 inflam of appendix
*location:
- RLQ @ McBurney’s Point
- 2/3 from umbilicus to Right ASIS
(anterior-superior-iliac-spine)
causes:
- fecalith #1
>> tiny (minute) and hard mass of stool
- obstruction by a tumor
A norexia
P ain
 initial: epigastric
 acute: localized @ RLQ
NOTE: Classic Signs of Appendicitis
*Blumberg - rebound tenderness @ RLQ
*Rovsing - paradoxical pain @ RLQ when LLQ
is palpated
*Psoas - RLQ pain when R thigh is flexed backward
P erforation
 “rupture”
 can happen 24 hours from the onset of pain
 risk:
* Peritonitis > Sepsis > Septic Shock
E levated temp (fever)
N/V
D x Test
 CT scan
 Sonogram (ultrasound)
I ncreased WBC (leukocytosis)
X pain w/o intervention
 initial sign of rupture
 followed by abdominal distension (rigid, boardlike)
and increasing pain
Mng’t:
* NPO
* if in pain:
- let client assume comfortable position
* if (+) S/Sx of rupture
- elevate the HOB
> to prevent sub-diaphragmatic abscess
*avoid:
- warm compress
 causes dilation  rupture
- enema / laxative (cathartic)
 increases peristalsis  rupture
- analgesic (if Ap. is not yet diagnosed)
 masks rupture
*IVF therapy
*prophylactic antibiotic
*surgery
 Appendectomy
 Exploratory Laparotomy
Sphincter of Oddi
LIVER
location:
* Right subcostal area on top of R. kidney (RUQ)
 highly vascular organ
***Heart
 Aorta
 Splanchnic Arteries
*Celiac Artery
- to stomach, esophagus, liver, spleen
*Sup. Mesenteric A.
*Inf. Mesenteric A.
***Heart
 Aorta
 Splanchnic Arteries
*Celiac Artery
- to stomach, esophagus, liver, spleen
*Sup. Mesenteric A.
intestines
*Inf. Mesenteric A.
*Drainage:
Portal Venous Circulation
~ enters into the liver

hepatic vein

IVC
(inferior vena cava)

HEART
FUNCTIONS OF LIVER

A lbumin
B ile
C oagulation
D extrose
E xcretion
F errum (iron)
G lutathione
ALBUMIN SYNTHESIS
 a plasma protein
 function:
* regulator of “colloid osmotic pressure”
- oncotic pressure
- “pulling” force of blood

Note: “ hydrostatic pressure”

- “pushing” force of blood against
vessel wall
BILE SYNTHESIS
* Hemolysis (RBC destruction)
~ end product: biliverdin

unconjugated bilirubin (fat-soluble)

LIVER = “conjugation” happens

conjugated bilirubin (water-soluble)

“stercobilin”
~ excreted thru STOOL
“urobilin”
~ re-absorbed in the intestine back to
bloodstream and excreted thru URINE
C oagulation
 synthesis of clotting factors
~ needed for platelet activation
D extrose (sugar) storage
 glucose to glycogen
- stored in liver
E xcretion of nitrogenous wastes
 source: CHON
***CHON
 amino acid
 ammonia (toxic)
*excreted directly thru stool
*goes to LIVER
~ ammonia  urea
*excreted thru urine
(kidney)
F e (iron) storage
 For hemoglobin synthesis

Glutathione synthesis
 Anti-oxidant
HEPATIC CIRRHOSIS
“fibrosis” / “scarring” of liver
TYPES
*Laennec’s
 chronic alcoholism
*Post-necrotic
 viral infection of liver
***Hepatitis B (Serum Hepatitis)
*Biliary
 obstruction of the biliary tract (ex. Biliary Atresia)
*Cardiac
 Right Sided H.F.
Tests:
* Liver Function Test
~ALT (SGPT) #1
~AST (SGOT)
~Bilirubin
* Serum Cholesterol
* Bleeding Time: 1.5 – 9.5 minutes
* CBC
* Hepa B Profile Test
PROBLEMS IN LIVER CIRRHOSIS
J aundice
A norexia
U RQ pain radiating to the back
N/V
D efective coagulation  “bleeding tendency”
I tchiness (pruritus)
C hange in the characteristics of:
*urine: dark-colored
*stool: ~ gray / clay (acholic)
~ fatty/greasy, bulky, floating (steatorrhea)
E levated bilirubin and WBC
*Anemia
 low RBC count (hypoxia, fatigue, weakness, palpitation)
 mng’t:
*Iron Supplement
 parenteral: use Z track
- prevents leakage of med into
subQ tissue  “staining”
 oral ~ tablet
~ liquid
Note:
* can cause dark stool & constipation
(increase OFI)
*Hormonal Imbalance
* ↑ SHBG (sex hormone binding globulin)
* ↓ testosterone
* ↑ estrogen
 gynecomastia
 telangiectasia - “spider veins”
*Ascites
~ problem: fluid accumulation in the peritoneal cavity
~ causes:
* portal hypertension
* hypoalbuminemia
~ low oncotic pressure
~ mng’t:
- position: high Fowler’s
- diet: low Na
- daily monitoring  weight & abddominal girth
- diuretic  Spironolactone (Aldactone)
- paracentesis  consent
 position: sitting
 before aspiration: client should void
 monitor & report: hypo-tachy-tachy
 after: apply pressure
*Portal Hypertension
sign: “varicosities”  abnormally dilated veins
~rectal: Hemorrhoid
Hot Sitz Bath
*Portal Hypertension
sign: “varicosities”  abnormally dilated veins
~rectal: Hemorrhoid
~abddominal wall: Caput Medusae
*Portal Hypertension
sign: “varicosities”  abnormally dilated veins
~rectal: Hemorrhoid
~abddominal wall: Caput Medusae
~esophagus: Esophageal Varix
*risk: rupture  bleeding
~ Pitressin (Vasopressin)
*constriction of splanchnic
arteries.
Sengstaken – Blakemore Tube (SB Tube)
 “balloon tamponade”
 bedside: scissors
***CHON
 amino acid
 ammonia (toxic)
*excreted directly thru stool
*goes to LIVER
~ ammonia  urea
*excreted thru urine
(kidney)
HEPATIC ENCEPHALOPATHY
Problem: deterioration of neuro function due to
elevated serum ammonia
S/Sx:
M ental status change  confusion
I rritability
N somnia
D isorientation
T remors of hand/s
 “flapping” <ASTERIXIS>
O dor of breath
 “ammonia” / “fetid” <FETOR HEPATICUS>
X deep tendon reflex
I nability to perform simple tasks
 handwriting / drawing
C oma
S eizure
 Mng’t:
M onitor the serum ammonia level
E ncourage
 Low CHON, High CHO
* to prevent ketosis
N euro assessment  GCS
T ake daily record of handwriting / drawing
A dministration of drug
* Lactulose
- osmotic laxative
- to promote excretion of ammonia thru stool
- take with empty stomach
- can be mixed with water, juice or milk
- monitor: LOC and bowel movement (2-3x a day)
*Neomycin
 macrolide antibiotic
 has low absorption rate in the intestine
 kills ammonia-producing bacteria in the
intestine
L ast option
* Dialysis
Sphincter of Oddi
GALLBLADDER
location: RUQ
function: storage of bile
disorders:
*Cholecystitis ~ inflam of GB
( > 90% of cases has bilestone )
*Cholangitis ~ inflam of bile duct
*Cholelithiasis ~ bilestone in the GB
*Choledocholithiasis ~ bilestone in the CBD
(common bile duct)
Factors:
F emale
F air
F at
F atty diet
F requent weight change
F ertile  estro
F orty y/o and up
F amilial tendency
F oreigner  Native Americans
Dx:
* Ultrasound
*ERCP – Endoscopic Retrograde Cholangio Pancreatography
~ direct visualization of biliary tract
~ invasive: use of side-viewing endoscope
~ procedure: NPO post-midnight
Consent
Sedation
Anesthesia
(+) contrast medium
Fluoroscopy
S/Sx:
J aundice
A norexia
U RQ pain radiating to the back (Murphy’s Sign)
N/V
D efective coagulation  “bleeding tendency”
I tchiness (pruritus)
C hange in the characteristics of:
*urine: dark-colored
*stool: ~ gray / clay (acholic)
~ fatty/greasy, bulky, floating (steatorrhea)
E levation of serum bilirubin, WBC
 WHO Ladder of Pain

Mild  1-3
 Rx:
>> NSAIDs
- Ibuprofen
- Naproxen
- Paracetamol
Moderate  4-7
 Rx:
>> NSAIDs
>> Weak Opioids
- Codeine
- Tramadol
Severe  8-10
 Rx:
>> NSAIDs
>> Strong Opioids
- Morphine #1
- Hydromorphone
- Fentanyl
>> Note: Meperidine (Demerol)
- can be broken down
into metabolites that can
cross BBB  seizure!
Mng’t:
L ow fat diet
I ncrease the fiber intake
P ain mng’t #1
I ncrease the fluid intake
D issolve / fragment the stone
* apple juice
* Rx: Ursodiol
* ESWL (Extracorporeal Shock Wave Lithotripsy)
S urgery
* Cholecystectomy
Sphincter of Oddi
 ACUTE PANCREATITIS
 cause: Alcoholism
 increases production of pancreatic
digestive enzymes especially Amylase
 causes spasm and narrowing of
pancreatic duct
 problem: Autodigestion
 severe “self-digestion” can lead to
hemorrhagic pancreatitis
~ internal bleeding
 S/Sx:
A bdominal pain #1
A bdominal guarding
A norexia, N/V
A mylase ↑
A bnormal imaging test result
- ultrasound, CT scan, MRI
A ssess using ERCP
- endoscopic retrograde cholangio-
pancreatography
 management:
P ain management #1
 Morphine [narcotic]
- primary drug for acute and severe pain
 Meperidine [narcotic]
- breaks down into metabolites that can
cross BBB  Seizure
A nti-spasmodic
 Propantheline Bromide [Pro-Banthine]
 Hyoscine [Buscopan]
N PO  during acute attack
 to prevent further production of
pancreatic digestive enzyme
C heck body areas with ecchymosis
 peri-umbilical region [Cullen’s Sign]
 flank region [Turner’s Sign]
Note: signs of hemorrhagic pancreatitis
~ shock alert!!!
R est  reduces production of pancreatic
digestive enzymes
E ndocrine disturbance
 Hyperglycemia
- beta cells of Langerhans are also
damaged during autodigestion  insulin
A dministration of:
 Insulin - to reduce blood glucose level
 Cholecystokin (Pancreozymin)
- relaxes the Sphincter of Oddi and
pancreatic duct
S urgery
 Whipple Surgery
- Pancreaticoduodenectomy
KIDNEY/S
 2 bean-shaped organs
 located in the retroperitoneal area
A cid – base balance
 regulation of HCO3
- acid neutralizer
B P regulation
 production of renin
- regulation of RAAS
C alcium regulation
 conversion of cholecalciferol into calcitriol
- inactive Vit D - active Vit D
- precursor of calcium
D etoxification
 K excretes nitrogenous wastes
- urea, creatinine

E rythrocyte (RBC) production

 synthesis of erythropoietin
- stimulates erythropoiesis [RBC production]

F luid & electrolyte balance

 thru urine production
RENAL FAILURE (Kidney Failure)
 functional deterioration of kidneys
 types:
* AKI (ARF)
* CKD (CRF)
ACUTE KIDNEY INJURY
 “Acute Renal Failure”
onset:
- abrupt / sudden
- may develop in few hours to days
prognosis:
- potentially reversible
subtypes:
Pre-renal
 cause:
- decreased renal perfusion (blood flow to kidney)
examples:
- bleeding
- dehydration
- hypovolemic shock
Intra-renal / Renal / Intrinsic RF
cause:
- direct insult to kidney or nephron
examples:
- AGN (acute glomerulonephritis)
- BT reaction (hemolytic)
- nephrotoxic drugs
Post-renal
cause:
- obstruction in the flow of urine
 examples:
- BPH
- calculi
- neurogenic bladder (flaccid bladder)
Chronic Kidney Disease
“Chronic Renal Failure”
onset:
- gradual
- develops in several weeks – months
prognosis:
- irreversible
- leads to ESRD
- End-Stage Renal Disease
- renal functionality drops to <10 %
 causes of CKD:

Kidney infection
- recurrent pyelonephritis
Increased BP (HTN)
Diabetes
Nflammation of glomeruli
- glomerulonephritis
Enlarged prostate or kidney stone
Ynherited kidney disorder
- polycystic kidney disease
PROBLEMS IN RF:
1. Anemia
- low RBC
- Tx:
Human Recombinant Erythropoietin
~ ex: Epoeitin Alfa (Epogen)
~ subQ / IV , 3x a week
~ monitor: Hematocrit

Note:
~ Iron is added to help in Hgb synthesis
2. Hypervolemia
- fluid overload [ edema, weight gain, HPN ]
- due to oliguria  fluid retention
- Tx:
~ daily weight monitoring
~ low fluid
~ low Na
~ diuretic (K-wasting)
*** Furosemide (Lasix)
~ dialysis
3. Azotemia
~ accumulation of nitrogenous wastes
~ primary problem: “Uremia”
~ S/Sx:
Increased ICP
Anorexia
N/V
Muscle twitching
Uremic Frost (urea crystals on skin)
~ causes pruritus
~ Tx:
* low CHON
* high CHO
- prevents ketosis when low CHON is used
* colloidal oatmeal bath  relieves itchiness
* dialysis
4. Metabolic Acidosis
~ Tx:
* Na HCO3
* Dialysis
5. Electrolyte Imbalances
~ Hypocalcemia
* Calcium Carbonate (Tums)  antacid
* Calcium Gluconate  if tetanic
~ Hyperphosphatemia
* d/t inverse relation of phosphate to Ca
* phosphate binder
- Aluminum Hydroxide (Amphogel)  antacid
- Sevelamer (Renvela)
~ Hypernatremia
* low Na diet
* D5W
~ Hyperkalemia
 risk: cardiac arrhythmia / arrest
 mng’t:
* low K diet
- avoid fresh fruits/veg.
- no salt substitute (low Na / high K)
* Furosemide (Lasix)
- K – wasting diuretic
* Sorbitol (laxative)
- to achieve diarrhea-like effect
* Kayexalate [ cation exchange resin ]
- binds K in intestine
* Calcium Gluconate
- protects the heart from fatal arrhythmia
* Glucose + Insulin
* Dialysis
DIALYSIS
mechanical way of cleaning the blood
indications:
A cidosis
E lectrolyte imbalance
I ntoxication
O verload of fluid
U remia
 requirements:
*artificial kidney
- site of dialysis
*dialysate
- dialyzing solution (fluid containing balanced electrolytes)
*access to the circulation
 Processes in Dialysis
* Diffusion
- movement of solute (particles) from an area of
higher to lower solute concentration
* Osmosis
- movement of solvent (fluid) from an area of
higher to lower pressure
 HEMODIALYSIS PERITONEAL
DIALYSIS
DURATION 3 – 4 hours / session
FREQUENCY 3x / week
ARTIFICIAL K. dialyzer
DIALYSATE run by dialysis machine
ACCESS AV fistula / AV shunt

COMPLICATION Disequilibrium Syndrome

AV SHUNT
Care of AV Shunt / Fistula:
 avoid: BP taking / blood extraction / constrictive sleeves
 shunt care: sterile technique (surgical asepsis)
 prevent clotting: Heparin flush
 check patency
(+) bruit – auscultate
(+) thrill – palpate
 alert: exsanguination
- “fatal blood loss”
- due to dislodged lines
complications of HD:
* psychologic
 Reactive Depression
~ exogenous depression
* physiologic
 DDS (Dialysis Disequilibrium Syndrome)
~ prob: fluid shifting to cerebral tissues
 result: cerebral edema
~ cause: rapid dialysis rate
~ S/Sx: ↑ ICP, mental status change,
muscle twitching
~ mng’t: ↓ dialysis rate
 HEMODIALYSIS PERITONEAL
DIALYSIS
DURATION 3 – 4 hours / session 1 – 4 hours / session
FREQUENCY 3x / week based on status
ARTIFICIAL K. dialyzer peritoneal cavity
DIALYSATE run by dialysis machine via manual infusion
ACCESS AV fistula / AV shunt peritoneal catheter
(Tenckhoff Catheter)
COMPLICATION Disequilibrium Syndrome Peritonitis & Hyperglycemia
Dialysate Infusion in PD
 total duration: 1 – 4 hrs
1. infusion time
 administration of dialysate
 2 L w/in 5-10 min
 X cold dialysate
2. dwell time
 varies (depends on hemodynamic status)
3. drainage
 10-30 min
input output
2L 2L
2L 2.2L
2L 1.8L
 complication of PD:
* Peritonitis
* signs:
- cloudy drainage
- fever
- abdominal pain (diffused or vague)
- abdominal distention / rigidity
* risk : ileus paralyticus (paralytic ileus)
- absence of peristalsis
*Tx: Antibiotic Therapy (14 days)
* Hyperglycemia
* dialyzing solution contains glucose
* monitor BSL
Alert:
***before & after dialysis:
 weight
 VS
Kidney Transplant
best donor: twin
site of attachment of the new kidney: iliac fossa
position of donor: lateral
position of recipient: supine
risk: organ rejection
* S/Sx: fever, hypertension, oliguria, weight gain
* mng’t:
Immunosuppressant Therapy
*Cyclophosphamide (Cytoxan)
*Azathioprine (Imuran)
*Cyclosporine (Sand-Immune)
 Lifetime
 Pt is prone to infection >> Reverse Isolation!
UTI
 Urinary Tract Infection
 causes:
- Escherichia coli – most common
* normal flora of intestine
- Nosocomial (hospital-acquired)
- Urinary stasis
 “ascending infection”
Nephritis / Pyelonephritis
(pus)
Ureteritis

Cystitis
Urethritis
 S/Sx:
P ain
 dysuria
 suprapubic
 flank
A bnormal urinary pattern
 frequency
 hesistancy
 urgency
I ncreased temperature (fever)
N ote for sign of pyelonephritis
 (+) CVA tenderness
- “costovertebral angle”
- checked thru kidney punch
 Dx:
* CBC
* U/A
* Urine C&S
Mng’t:
A cidify the urine
 acid-ash: citrus, cranberry, prune, plum, protein-rich
B ubble bath X
C hange undergarments regularly
 cotton fabric
D rugs
 Quinolones: Ciprofloxacin
 Cephalosporin: Cefuroxime, Cefixime
E mpty bladder regularly
F luid intake
 at least 3L per day
G irl hygience
 “front to back”
H ealth education
 practice post-coital voiding
CALCULI
 “lithiasis” = stone
- Urolithiasis - urinary tract
- Ureterolithiasis - ureter
- Nephrolithiasis - kidney
- Cystolithiasis - bladder
causes:
* dehydration
* frequent UTI
 “struvite” stone
* diet-related:
 acidic stone
~cystine: protein-rich food
~purine: uric acid
 alkaline stone
~calcium: milk & dairy products
~oxalate: coffee, tea, chocolates,
green leafy vegetables
S/Sx:
R enal colic
 severe flank pain radiating to the groin
E levated
 RBC in urine (hematuria)
N/V
A bnormal urinary pattern
 frequency
 hesistancy
 urgency
L eukocytosis ( WBC)
Mng’t:
S train the urine
T ake plenty of fluid (at least 3L / day)
O bserve and report  hematuria
* for antibiotic treatment
N arcotic analgesic for pain  Morphine
E ncourage ambulation
E SWL
 extracorporeal shockwave lithotripsy
S urgery
 Percutaneous Nephrolithotomy
 Cystoscopy - alternative for small stones
BPH  Benign Prostatic Hyperplasia
 “enlarged prostate”
P athologic origin
 ↑ testosterone – converted into DHT
*Dihydrotestosterone
~stimulates prostatic cell growth
R isk factors
 matanda (aging)
 mataba (obesity)
 mamantika (high fat)
 manginginom (alcohol)
 maninigarilyo (smoking)
NOTE: Exact cause is unknown.
O nset
 > 40 y/o
S / Sx
 abnormal urinary pattern
- hesitancy / urgency / frequency / dribbling
 decreased and intermittent force of stream
 sensation of incomplete bladder emptying
 acute urinary retention
 recurrent UTI
T ests
 DRE (Digital Rectal Exam)
* findings: large, rubbery, non-tender
 Urinalysis
* to check hematuria and UTI
 PSA (Prostate Specific Antigen)
* tumor marker for Prostate Ca
A lert for complications
 hydroureter
 hydronephrosis
 azotemia (retention of nitrogenous wastes)
T reatment
 exercise & low fat diet
 emergency admission d/t inability to void
~ catheterization w/ stylet or metal catheter
 Rx: Finasteride (Proscar, Propecia)
~ inhibits conversion of testosterone into DHT
 Surgery:
*TURP ~ Trans Urethral Resection of Prostate
~ endoscopic surgery
~ (-) incision
~ expect pink-tinged urine post-op (24-48 hrs)
E ducate pt about sexual function after prostatectomy
 ED (erectile dysfunction) / impotence)
* Rx:
Sildenafil (Viagra)
Tadalafil (Cialis)
 Retrograde ejaculation
Continuous Bladder Irrigation
 AKA: “cystoclysis”
 process: inflow & outflow of solution
(saline) into and out of the bladder
 purpose:
- to maintain patency of
urinary catheter
 uses triple lumen catheter
 should be a closed system
- to reduce the risk of UTI
 flow rate: 40 – 60 drops / min or as ordered by MD
 LAYERS OF THE SKIN
* Epidermis
 outermost
 composed of dead cells
* Dermis
 middle layer
 contains blood vessels and nerves
* Hypodermis
 composed of fat / subQ / adipose
BURN
transfer of heat from a heat source to the body through
conduction or electromagnetic radiation.
can lead to disruption of the skin and fluid & electrolyte
imbalance.
 types:
* thermal
* chemical
* electrical
main problems in burn
* cellular lysis
- hyperkalemia  arrhythmia / arrest
* loss of skin barrier
- infection
* possible inhalation injury
- hypoxia
* increased capillary permeability
- plasma leakage  burn shock
* pain
UNIVERSAL ALGORITHM IN CASE OF FIRE
R escue
 evacuate clients / victims
A mbulatory
B ed-ridden
C ritically - ill
A larm
C onfine
 close the windows and doors
E xtiguish
PROPER USE OF FIRE EXTINGUISHER

P ull the pin

A im the nozzle to the base of fire

S queeze the lever

S weep the fire

 EMERGENCY RESPONSE
Primary Survey
 Focus: Stabilization of a client’s status
A irway
- anaphylaxis, airway burn, choking
B reathing
- chest injury, CO poisoning
C irculation
- hemorrhage, cardiac arrest / arrhythmia
D isability of nervous system
- head injury and SCI
Secondary Survey
 Focus: Completion of assessment data

A ssessment (head to toe)

B aseline data and history taking
C are of the wound
D iagnostic and laboratory testing
TBSA
Total Body Surface Area
used to estimate the extent of burn injury
methods of assessment:
* Lund and Browder
* Rule of Nines
* Palm Method
Lund and Browder
most precise / accurate
% corresponds to anatomic parts based on client’s age
ideally used for pediatric clients
Rule of Nines
* Head 9 %
* R. arm 9 %
* L. arm 9 %
* Anterior trunk 18 %
* Posterior trunk 18 %
* R. leg 18 %
* L. leg 18 %
* Genital 1 %
Palm Method
used for scattered burn injuries
note:
* size of the palm of patient = 1 %
Baxter Formula
aka: Parkland Formula
used to estimate the amount of IVF to be administered
in a burn client
formula:
4 mL x weight in kg x % TBSA
Note:
- computed amount should be
administered within 24 hours
- example:
A 50-kg patient sustained burn injury with 10% TBSA.
How much fluid is to be administered per hour on the
first 8 hours?

4 mL x 50 x 10 = 2000 mL

* 1st 8 hours: 50% = 1000 mL / 8 = 125 mL per hour

* 2nd 8 hours: 25% = 500 mL / 8 = 62.5 mL per hour
* 3rd 8 hours: 25% = 500 mL / 8 = 62.5 mL per hour
Characteristics 1st Degree (SPT) 2nd Degree (DPT) 3rd / 4th Degree (FT)
Layer - Epidermis - Epidermis - Epidermis, dermis
- Partial Dermis - Entire dermis - Adipose, muscle
Appearance -Red - Blisters - Brown, black or
- Dry - “Weeping” pale
- Minimal to no - Edematous - Leathery, dry
edema - Eschar
Sensation - Painful - Painful - Painless
- Soothed by - Sensitive to cold
cooling
Recovery - 1 week - 2-4 weeks - Non-specific
Wound Care in Burn
use hydrotherapy
water temp: 37.8 degree C
room temp: 26.6 – 29.4 degree C
duration: 20 – 30 minutes
frequency: at least daily
residue adhering to body: clear water spray
with blisters: do not prick / break
after: pat dry with towels
Infection Prevention
standard precaution
tetanus immunization
topical antibiotic
- Silvadene (Silver Sulfadiazene) - cream
- Sulfamylon (Mafenide Acetate) - cream
- Silver nitrate - aqueous solution
oral antibiotic
- Gentamycin (Garamycin)
- A/E: nephrotoxic
 Types of Skin Graft
* Autograft
 pt’s own skin
* thigh
* buttocks
 Types of Skin Graft
* Autograft
 pt’s own skin
* thigh
* buttocks
* Homograft [ Allograft ]
 cadaver
* Heterograft [ Xenograft ]
 animal
 TYPES OF WOUND HEALING

Primary Intention
 wound edges are “approximated”
>> closure is through the use of staples, stitches, glues,
or other forms of wound-closing processes
 e.g. surgical wound
Secondary Intention
 wound that cannot be stitched; has uneven surfaces
 wound healing relies on the body’s own healing
mechanisms
 e.g. bed sores
Tertiary Intention
 for wounds that need to delay the wound-closing
process
 e.g. temporary colostomy, fasciotomy
 Phases of Wound Healing

1. Hemostasis
 can last for two days
 vasoconstriction & coagulation

2. Inflammation
 can last for up to seven days
 inflammation, redness, edema, heat, and pain
 phagocytosis
3. Proliferation
 can last for four days to up to three weeks or more
 focuses on filling and covering the wound
 formation of granulation tissue

4. Remodeling
 also known as maturation phase
 can last for months or years
 collagen production continues to strengthen tissue
 scar tissue formation
CARBON MONOXIDE POISONING
 CO - colorless, odorless & tasteless gas
- a product of combustion
- has strong affinity to hemoglobin
 problem in CO poisoning:
- CO binds with Hgb = Carboxyhemoglobin
* Oxyhemoglobin
* Hypoxemia
* Hypoxia
- Cerebral Hypoxia!!!
 S/Sx:
* ICP
- LOC
- restlessness
- headache
- vomiting
- ataxia
- amnesia BRAIN DAMAGE
- visual disturbance
- psychotic features
 - skin color
* pallor, cyanosis, cherry red NOT
- pulse oximeter reading RELIABLE
* may show 100 % saturation reading

 Dx Test:
- Serum Carboxyhemoglobin Level
 management:
- carry the patient to fresh air immediately
* open all windows / doors if possible
- loosen tight clothings
- initiate CPR as necessary
- O2 therapy
* 100% using hyperbaric oxygen chamber
- assessment of neuro status
HEMORRHAGE
 “bleeding”
 problem:
* tissue perfusion

hypovolemic shock

MODS
(Multiple Organ Dysfunction Syndrome)
 S/Sx:
* hypotension
* tachycardia
* tachypnea
* delayed capillary refill time
* cold clammy skin
* oliguria
- late sign
- indicates decreased renal insufficiency  ARF
 management:
* stop the bleeding
- application of pressure
- immobilization
- elevation of affected extremity
- application of tourniquet
* fluid and blood replacement
 IVF
- plasma expanders, LR, NSS
 BT
- whole blood
* universal donor: O+
* universal recipient: AB+