Comprehensive Reviewer on Multiple Sclerosis (MS) 3.5.

Hormonal Factors

1. Introduction  Pregnancy: Some studies suggest that

pregnancy may influence the course of MS,
Multiple Sclerosis (MS) is a chronic, progressive, potentially due to hormonal changes.
autoimmune disease characterized by the
inflammation and subsequent destruction of the 4. Clinical Manifestations
myelin sheath surrounding nerve fibers in the
central nervous system (CNS). This demyelination The symptoms of MS can vary widely among individuals
disrupts communication between the brain and other and can be classified into four main clinical patterns:
parts of the body, leading to a variety of neurological
symptoms.
4.1. Clinical Patterns

2. Incidence
1. Relapsing-Remitting MS (RRMS):
Characterized by clearly defined episodes of
 Age of Onset: MS typically manifests between exacerbation followed by periods of remission.
the ages of 20 and 40.
 Gender Prevalence: Women are approximately 2. Primary Progressive MS (PPMS): Progressive
two to three times more likely to develop MS neurological decline from onset without distinct
than men (AANN, 2011). relapses or remissions.
 Ethnic Distribution: Caucasians, particularly 3. Secondary Progressive MS (SPMS): Follows
those of Northern European descent, have a an initial relapsing-remitting course, transitioning
higher incidence compared to other ethnic into a progressive decline.
groups, such as Hispanics, Blacks, and Asians. 4. Progressive-Relapsing MS (PRMS):
 Geographic Influence: MS is more prevalent in Progressive disease from the onset with
regions with colder climates, including parts of intermittent acute relapses.
North America and Europe.
4.2. Symptoms
3. Etiology and Risk Factors
Motor Symptoms:
While the precise etiology of MS remains unknown,
several contributing factors have been identified: o Weakness or paralysis of limbs, trunk,
or head
3.1. Genetic Factors o Muscle spasticity
o Diplopia (double vision) and scanning
 Family History: Individuals with a first-degree speech
relative with MS have a higher risk, indicating a
genetic predisposition. Sensory Symptoms:

3.2. Environmental Factors o Paresthesias (numbness, tingling)

o Patchy blindness (scotomas) and
 Geographic Location: Higher prevalence in blurred vision
northern latitudes suggests environmental and o Lhermitte's sign: An electric shock
climatic influences. sensation down the spine with neck
 Viral Infections: The Epstein-Barr virus has flexion
been implicated as a possible environmental o Vertigo, tinnitus, and hearing loss
trigger. o Chronic neuropathic pain
o Romberg’s sign (hands swaying when
3.3. Lifestyle Factors patient is standing with eyes closed and
feet together)
 Smoking: Tobacco use has been linked to an o Nystagmus
increased risk of developing MS.
 Obesity: Particularly during adolescence, Cerebellar Signs:
obesity is considered a risk factor.
o Ataxia (loss of coordination)
3.4. Autoimmune Associations o Dysarthria (slurred speech)
o Dysphagia (difficulty swallowing)
 Individuals with other autoimmune diseases
(e.g., thyroid disease, type 1 diabetes, and
Other problems
inflammatory bowel disease) may have an
elevated risk.
 Can’t hold urine : nocturia, overacting bladder
 Problems with contracting to void (retention)
 Bowel issues : constipation/diarrhea  Corticosteroid Therapy:
 Uthoff’s sign ( heat makes the sins and symptoms
worse) o Methylprednisolone (IV or orally) for
acute exacerbations.
5. Diagnostic Evaluation o Azathioprine and cyclophosphamide
may be used in severe cases.
Diagnosis of MS is complex and relies on a combination o WOF! Infection,
of clinical assessments and diagnostic tests: hyperglycemia,edema, neuro issues

5.1. Clinical Evaluation 7.2. Disease-Modifying Treatments

 Patient History: A comprehensive history of  Interferon Beta-1b (Betaseron): Subcutaneous

neurological symptoms and episodes of administration for RRMS, acting as an antiviral
dysfunction. and immunomodulator.
 Physical Examination: Neurological  Interferon Beta-1a (Avonex): For treating
assessment to identify deficits. relapsing forms of MS.
 WOF! Risk for infection because it decreases
5.2. Diagnostic Tests WBC, Hepatotoxicity, neuro issues, thyroid
issues
 Cerebrospinal Fluid (CSF) Analysis: Identifies  Glatiramer Acetate (Copaxone): Indicated for
the presence of oligoclonal bands or elevated RRMS, helps to modify disease progression.
IgG levels.
 Evoked Potentials: Measures electrical activity 7.3. Symptomatic Treatments
in response to stimuli, assessing nerve
conduction speed.  Bladder Dysfunction: Oxybutynin ( relaxes the
 Magnetic Resonance Imaging (MRI): The gold bladder muscle), bethanechol (helps in
standard for detecting demyelination, revealing emptying the bladder or contraction) or
lesions or plaques in the CNS. propantheline to manage urgency and
 Computed Tomography (CT) Scan: Less frequency.
detailed than MRI but may show areas of  Note : has anticholinergic effect
demyelination.  Constipation Management: Use of fiber
supplements like psyllium hydrophilic mucilloid
6. Surgical Management and suppositories.
 Note : promote hydration and patient may
In cases where conservative management options have experience gas and bloating
failed, surgical interventions may be considered:  Fatigue Management: Amantadine (antiviral
and antiparkinsonian) or modafinil to improve
energy levels.
6.1. Deep Brain Stimulation  Note : Monitor cardiac, mental, and GI status,
 Patient may experience Livedo reticularis: A
 Indication: For patients with severe tremors in unique side effect of amantadine, livedo
the limbs unresponsive to other treatments. reticularis (a mottled, purple skin
 Procedure: A device is implanted to stimulate discoloration, typically on the legs)
targeted areas of the brain, potentially reducing  Spasticity Management: Baclofen, diazepam,
tremors and improving motor function. or dantrolene for muscle stiffness.
 WOF! : Resiratory distress, orthostatic
6.2. Implantation of a Drug Catheter or Pump hypotension
 Tremor Control: Propranolol , Isoniazid or
 Indication: For patients experiencing severe clonazepam may help reduce tremors.
pain or spasticity.  Neuropathic Pain Management:
 Procedure: A catheter is placed in the lower Carbamazepine, phenytoin, or amitriptyline for
spinal area to deliver a constant flow of dysesthesias.
medication, such as baclofen, to alleviate
symptoms. 8. Nursing Management

7. Medical Management Nurses play a crucial role in the multidisciplinary

management of patients with MS. Below are relevant
There is currently no cure for MS; however, treatment nursing diagnoses, interventions, and rationales:
focuses on managing symptoms and modifying the
disease course: 8.1. Nursing Diagnosis: Impaired Urinary Elimination
Pattern

Related to: Bladder dysfunction as evidenced by low

7.1. Management of Acute Relapses output and acute pain.
  Interventions: o Consult with a doctor regarding the
need for splints to support affected
o Assess the skin for incontinence- areas.
associated dermatitis with each voiding.
o Maintain fluid intake of 2000 mL/day to Acute Glomerulonephritis
promote adequate urine output.
o Schedule toileting every 2 hours to Definition and Overview
manage urgency.
o Scan the bladder for post-void residual  Acute glomerulonephritis (AGN) is a common
volume. renal disease in children, primarily
o If PVR is more than 100 mL, then characterized by hematuria, which presents as
catheterize to prevent complications. red urine due to the presence of blood. It often
follows a streptococcal infection of the throat or
8.2. Nursing Diagnosis: Impaired Elimination Pattern skin, typically presenting one to three weeks
after the initial infection.
Related to: Immobility & demyelination as evidenced by
disturbed bowel movement. Epidemiology

 Interventions:  AGN is an immune-mediated inflammatory

disease of the renal glomeruli, particularly
o Assess for normal bowel movements to affecting the capillary loops.
monitor changes.  It is more prevalent in males than females and
o Administer suppositories as advised by commonly occurs in preschool and early school-
aged children, with a peak onset at ages 6 to 7
the physician to facilitate bowel
years.
evacuation.
 The condition is rare in children under two years
o Teach the client to consume a high-fiber
of age and accounts for approximately 2-4% of
diet and 2000 mL of fluid to promote
pediatric admissions and about 90% of renal
regularity.
diseases in childhood.

8.3. Nursing Diagnosis: Fatigue

Etiology

Related to: Increased energy needs as evidenced by

 The presumed cause of AGN is an antigen-
facial expression of client.
antibody reaction following an infection in the
body, most frequently associated with
 Interventions: nephritogenic strains of Group A beta-hemolytic
streptococcus (type 12).
o Keep the environment cool to minimize  Common initial infections include:
fatigue triggers.
o Provide mental support to encourage o Upper respiratory infections (e.g.,
emotional well-being. pharyngitis).
o Plan for rest periods during the day to o Skin infections.
manage energy levels.
o Facilitate sleep by reducing nighttime Clinical Feature
interruptions, noise, and light.
Urinary Symptoms:
8.4. Nursing Diagnosis: Impaired Physical Mobility
o Decreased urine output.
Related to: Weakness, contractures, spasticity, and o Presence of bloody or brown-colored
ataxia as evidenced by pain in muscles and verbal
urine.
experience.
Edema:
 Interventions:
o Generally mild, often manifesting as
o Assess the degree of muscle spasticity
periorbital edema (face/eyes), especially
to tailor interventions.
noticeable in the morning.
o Stretch muscles and perform range-of-
o May also present as rapid weight gain
motion exercises to maintain mobility.
and can be generalized, influenced by
o Administer anti-spasmotics as ordered
posture.
to relieve spasticity.
o Position the patient in neutral alignment
to prevent contractures.

Hypertension:
 o Observed in over 50% of cases, Outpatient Treatment: Patients with mild
typically mild but may present suddenly. oliguria and normal blood pressure may be
o Usually appears during the first four to managed with outpatient-based treatment.
five days of illness.
Monitoring:
Other Symptoms:
o Regular assessment of hematuria, urine
o Malaise, mild headache. output, signs of edema, hypertension,
o Gastrointestinal disturbances, such as and potential congestive heart failure.
anorexia and vomiting, often o Daily records of the patient’s general
accompanied by abdominal and loin condition, edema, weight, heart rate,
pain. respiratory rate, blood pressure, fluid
o Additional signs include pallor, intake, and urinary output.
irritability, lethargy, dysuria, and fever. o Frequent kidney function tests.

Diagnosis Bed Rest

Diagnosis is confirmed through a combination of  Indication: Bed rest is primarily recommended

history-taking, physical examination, and during the acute phase, especially if acute renal
laboratory tests: failure or complications are present.
 Positioning: In cases of congestive heart failure
Urine Examination: or hypertension, patients should be positioned
upright with oxygen support.
o Increased specific gravity and dark,
Dietary Management
"smoky" brown-colored urine with
reduced total volume in 24 hours.
o Mild to moderate or severe albuminuria.  Restrictions: Limit protein, salt, and fluid intake
o Microscopic examination reveals red during periods of oliguria or elevated blood urea
blood cells, white blood cells, pus cells, levels.
epithelial cells, and granular casts.  Allowed Foods: Carbohydrates can be
o Proteinuria (3+ to 4+). consumed freely to meet energy needs.
 Fluid Intake Calculation: Fluid allowance is
based on the previous day's urine output plus
Blood Examination: insensible losses.
 Daily Weight Monitoring: Important for tracking
o Increased levels of urea, creatinine, changes in edema and overall fluid balance.
erythrocyte sedimentation rate (ESR),  For pediatric patients, they should void =
antistreptolysin O (ASO) titer, and anti- 1ml/kg/hr
DNase B.  If low urinary output, monitor for hyperkalemia
o Decreased levels of hemoglobin, serum
complement, and albumin. Fluid Balance
o Hyponatremia and hyperkalemia may
occur in cases of persistent oliguria.  Regular Monitoring: Vital signs, body weight,
and intake-output records are essential for
Throat Swab Culture: detecting any complications.
 Sodium and Water Restriction: Advised when
o May reveal the presence of beta- urinary output is significantly low (<200-300
hemolytic streptococcus in some mL/day).
children.  Diuretics: Furosemide (Lasix) may be
administered for significant edema and fluid
Chest X-ray: overload.

o May show signs of pulmonary Blood Pressure Control

congestion.
 Hypertension Management: Blood pressure
should be checked every 4-6 hours.
Management
 Treatment Options: Mild hypertension can be
managed with loop diuretics; severe cases may
Hospitalization and Monitoring require antihypertensives like calcium channel
blockers, beta blockers, or ACE inhibitors.
Severe Cases: Patients with severe oliguria or
azotemia require hospitalization for intensive
monitoring and care.
Dialysis
  Indications: Required for patients with severe, o Phases:
prolonged oliguria or renal failure.
 Oliguric Phase: Lasts 5-10
Antibiotics days, characterized by edema
and low urine output.
 Penicillin: A 7-10 day course may be given to  Diuretic Phase: Begins with
eliminate streptococcal infection in the throat or increased urine output and
skin. decreased edema.

Medications Allergy (Hypersensitivity) and Anaphylaxis: A

Comprehensive Overview
 Antihypertensives: Nifedipine and atenolol for
hypertension control. What is an Allergy?
 Diuretics: To manage fluid overload.
 Magnesium Sulfate: Used to reduce cerebral  An allergy is an immune system response to a
edema in hypertensive encephalopathy. harmless substance known as an allergen (e.g.,
 Sedatives: Diazepam may be prescribed for pollen, dust, certain foods).
restlessness.  Mechanism: IgE antibodies bind to FCE
 Complications: Management of serious receptors on mast cells and basophils,
complications (e.g., congestive heart failure, leading to the release of granules with
hypertensive encephalopathy) may require inflammatory agents, causing an allergic
dopamine infusion, steroids, or respiratory response.
support.
Immune Hypersensitivity

 Hypersensitivity is an overly strong immune

Complications response, which can be immediate or delayed:

Hypertensive Encephalopathy o Immediate Hypersensitivity:

 Mediated by antibodies.
o Manifestations: Restlessness,  Includes:
convulsions, vomiting, headache, visual  Allergies (up to
disturbances. anaphylactic shock),
o Cause: Likely due to vasospasm and (Type I)
ischemia.  Antibody-mediated
o Duration: Usually self-limiting over 1-2 cytotoxicity, (Type II)
days as blood pressure decreases.  Sickness from immune
complex accumulation.
(Type III)
Congestive Heart Failure (CHF)
o Delayed Hypersensitivity (Type IV):

o Manifestations: Dyspnea, tachycardia,

 Mediated by T cells,
liver engorgement.
 Involves cytotoxic T
o Cause: Persistent hypertension,
lymphocytes (CTLs) and
hypervolemia, and vasoconstriction. macrophages.
o Duration: Subsides as blood pressure  Common in contact sensitivity
stabilizes. reactions.

Uremia (Rare) Types of Allergies

o Manifestations: Acidosis, drowsiness,  Food Allergies: Affect 4-6% of children and 4%

coma, muscle twitching, convulsions. of adults, commonly triggered by:

Anemia o Eggs, milk, peanuts, tree nuts, fish,

shellfish, wheat, and soy.
o Cause: Due to hypervolemia rather than
red blood cell loss in urine. Allergic Reaction Process

1. Exposure to allergen via inhalation, ingestion, or

skin contact.
2. Body produces IgE antibodies specific to the
allergen.
Renal Failure
 3. IgE binds to mast cells in areas like airways Symptoms of Anaphylaxis
and intestines.
4. When allergen re-exposure occurs, it binds IgE  Onset within 5-30 minutes after exposure:
on mast cells, causing release of chemicals like
histamine. o Red rash with hives, swollen throat,
5. Histamine triggers most allergy symptoms. wheezing, chest tightness, difficulty
breathing, hoarse voice,
Symptoms of Allergic Reactions o Vomiting, diarrhea, stomach
cramping,
o Paleness or flushing, difficulty
 Inhaled or Skin Allergens:
swallowing, and potential loss of
consciousness.
o Itchy, watery eyes, sneezing, runny
nose, rashes, fatigue, and hives.
Managing Anaphylaxis
 Food Allergies:
 Avoid Allergens: Key to prevention.
 Preparedness: Individuals at risk should carry
o Stomach cramps, vomiting, diarrhea. auto-injectable epinephrine and understand
how to use it in case of emergency.
 Insect Sting Allergies:
o Swelling, redness, pain. Introduction to Systemic Lupus Erythematosus
(SLE)
Allergy Diagnosis Systemic lupus erythematosus (SLE) is a chronic
autoimmune disorder that leads to inflammation and
 Allergy Testing helps identify specific damage across multiple organ systems. In SLE, the
allergens: immune system creates autoantibodies against self-
o Skin Testing: Provides quick results at antigens, leading to immune complex formation that
a lower cost. affects tissues throughout the body. This disorder
o Blood Testing: Involves a single needle predominantly affects women of childbearing age but
prick but is more expensive. can manifest in children, typically around puberty.
 Results are interpreted in the context of medical Notably, SLE is rare in those under nine and shows
history. equal gender distribution in younger patients,
contrasting with its female predominance in adults. The
prevalence of pediatric SLE is approximately 10–25
Allergy Treatment cases per 100,000 children.

1. Medications: Inflammation of :

o Decongestants and antihistamines for  Joints

symptoms like congestion, sneezing,  Lungs
and itching.  Heart
o Corticosteroids reduce inflammation in  Kidneys
the nose.  Brain

2. Immunotherapy: Also affects :

o Preventive treatment with gradually Skin and Blood system

increasing doses of the allergen to
reduce sensitivity. Historical Background
The term "lupus" is derived from the Latin word for wolf,
Anaphylaxis reflecting the wolf-like appearance of the facial rash
associated with the disease. In 1851, Dr. Cazenave
identified a facial rash in patients, which he termed
 Anaphylaxis is a severe, potentially life-
Discoid Lupus Erythematosus (DLE). In 1885, Sir
threatening allergic reaction.
William Osler expanded the disease's scope,
recognizing it as a systemic condition affecting multiple
o Commonly triggered by foods, insect organs, thus naming it Systemic Lupus Erythematosus
stings, medications, or latex. (SLE).

 Immediate Treatment: Requires epinephrine

injection (e.g., epi-pen) and emergency
medical attention.
  Gastrointestinal: Abdominal pain, nausea,
vomiting.
Types of Lupus  Dermatological: Alopecia, butterfly rash,
mucous membrane lesions, discoid (coin-like)
rash in the skin, photosensitivity, purpura,
Systemic Lupus Erythematosus (SLE)
Raynaud’s phenomenon (fingers turn lighter,
then darker and feels numb, occurs when cold),
1. The most commonly referred to form of urticaria, vasculitis.
lupus.  Hematologic: Anemia, leukopenia,
2. Affects multiple organ systems and can thrombocytopenia(avoid live vax),
range from mild to severe symptoms. antiphospholipid syndrome (increased clotting
3. Typically occurs between ages 15 and factor)
45 but can also affect children and older  Musculoskeletal: Arthralgia, arthritis, myositis.
adults.  Pulmonary: Pleurisy, pulmonary hypertension,
lung parenchymal involvement, pneumonia)
 Neuropsychiatric: Cranial neuropathies,
organic brain syndrome, peripheral
neuropathies, psychosis, seizures, transverse
Discoid Lupus Erythematosus (DLE) myelitis.
 Renal: Casts in urine, hematuria, nephrotic
1. A chronic skin condition characterized syndrome, proteinuria, hypertension, fluid
by red, raised rashes, often on the face retention
or scalp.  Reticuloendothelial: Hepatomegaly,
2. The rash may become thick, scaly, and lymphadenopathy, splenomegaly.
lead to scarring.
3. A small percentage of DLE cases may Pediatric SLE Manifestations
develop into SLE over time.
 Children with SLE often experience fever, rash,
Neonatal Lupus alopecia, arthritis, and renal involvement.
 Compared to adults, pediatric patients have a
higher incidence of malar rash, anemia,
1. A rare condition affecting newborns, leukopenia, and neurological or renal
likely caused by maternal complications.
autoantibodies (anti-Ro/SSA and anti-
La/SSB).
Primary signs of a flare : Fatigue, Lowgrade fever, Achy
2. Symptoms include skin rashes, liver joints, Rashes, Edema (legs & hands)
issues, and low blood counts, which
typically resolve within months.
3. Some infants may develop a permanent
heart condition affecting heart rhythm.
Etiology of Systemic Lupus Erythematosus
Drug-Induced Lupus
The exact cause of SLE is unknown. However, it is an
autoimmune disorder where the body’s immune system
1. SLE-like symptoms triggered by certain attacks its tissues, producing autoantibodies, particularly
medications. antinuclear antibodies (ANA). These autoantibodies
2. Symptoms usually resolve once the contribute to inflammation and damage in various
causative drug is discontinued. organs.
3. Organs such as the kidneys and brain
are rarely affected. Factors believed to play a role in SLE development
include:

 Genetic Predisposition: Although no specific

Clinical Features of SLE "lupus gene" has been identified, family studies
indicate that genetic factors contribute to the
disease.
SLE presents with a range of symptoms, which can vary
 Environmental Triggers: Sunlight, stress,
significantly among individuals. The disease also
medications, and infections (such as viruses)
exhibits episodic flare-ups, with patients experiencing
may contribute to SLE onset in genetically
active periods interspersed with remissions.
predisposed individuals.
 Hormonal Influences: Hormonal factors, given
Systemic Clinical Manifestations the female predominance in adults, may also
contribute to susceptibility.
 Cardiac: Endocarditis, myocarditis, pericarditis,
HF
 Constitutional: Fatigue, fever, weight loss.
 Chronic Cutaneous Lupus

1. Discoid rash (localized or generalized)

2. Hypertrophic (verrucous) lupus, Lupus
Diagnostic Criteria for SLE panniculitis
3. Mucosal lupus, Lupus erythematosus
The diagnosis of SLE is complex and typically based on tumidus, Chilblains lupus
a combination of clinical symptoms and laboratory 4. Discoid lupus/lichen planus overlap
findings.
Oral or Nasal Ulcers
American College of Rheumatology (ACR) Criteria
for SLE Diagnosis
The ACR has established criteria for SLE diagnosis, 1. Ulcers on palate, buccal mucosa, or
requiring the presence of at least four of the following tongue (excludes causes like infections,
symptoms, either concurrently or at different times: reactive arthritis, or acidic foods)

Nonscarring Alopecia
1. Malar Rash: Butterfly-shaped rash across
cheeks and nose.
2. Discoid Rash: Red, disk-shaped, raised 1. Diffuse hair thinning or fragility with
patches. visible broken hairs
3. Photosensitivity: Skin rash worsened by
sunlight exposure. Synovitis
4. Oral Ulcers: Ulcers within the mouth.
5. Arthritis: Joint pain and swelling in two or more 1. Swelling or effusion in ≥2 joints, or
joints, without bone destruction. tenderness with morning stiffness
6. Serositis: Inflammation of the lung or heart lasting ≥30 minutes
linings (pleuritis or pericarditis).
7. Kidney Disorder: Persistent protein or cellular Renal
casts in urine.
8. Neurological Disorder: Seizures or psychosis. 1. Urine protein-to-creatinine ratio
9. Blood Disorders: Anemia, leukopenia, indicating >500 mg/24 hours protein or
lymphopenia, or thrombocytopenia. presence of red blood cell casts
10. Immunologic Disorder: Presence of anti-DNA,
anti-Sm, or positive antiphospholipid antibodies. Serositis
11. Positive ANA Test: The most common
autoantibody associated with SLE. 1. Pleurisy or pericarditis lasting >1 day,
with symptoms like effusion, rubs, or
Systemic Lupus International Collaborating Clinics pain relieved by sitting forward
(SLICC) Classification Criteria
To diagnose SLE using the SLICC criteria: Neurologic Manifestations

 The patient must have at least four criteria (with 1. Seizures, psychosis, mononeuritis
one clinical and one immunologic), or a biopsy- multiplex, myelitis, peripheral or cranial
proven case of lupus nephritis with positive ANA neuropathy, or acute confusional state
or anti-dsDNA.
Hematologic Abnormalities
Clinical Criteria for Diagnosis
1. Hemolytic anemia, leukopenia
Acute Cutaneous Lupus (<4000/mm³), lymphopenia
(<1000/mm³), thrombocytopenia
1. Lupus malar rash (not malar discoid) (<100,000/mm³)
2. Bullous lupus, Toxic epidermal
necrolysis variant of SLE Immunologic Criteria
3. Maculopapular lupus rash,
Photosensitive lupus rash  Antibodies: Elevated ANA, Anti-dsDNA (>2-
4. Subacute cutaneous lupus: Psoriaform fold), Anti-Smith (Anti-Sm), antiphospholipid
or annular lesions resolving without antibodies
scarring  Complement Levels: Low complement (C3,
C4, or CH50)
 Direct Coombs Test: Positive in absence of
hemolytic anemia
Monitoring Parameters

During Clinic Visit NSAIDs

o Complete history and physical exam, o Symptom relief for fever, arthritis, mild
blood tests, CBC, creatinine serositis; high incidence of
measurement, and urinalysis hepatotoxicity in SLE patients

Laboratory Indicators of Flare Risk Sunscreen

o Decreased serum complement, o SPF ≥15 to prevent dermal/systemic

increased dsDNA, elevated ESR, flares from UV exposure
reduced hemoglobin, leukocyte, or
platelet counts, elevated CPK, and Potential Complications
microscopic hematuria or proteinuria
 Long-term organ dysfunction is found in ~88%
Treatment Goals of patients due to SLE or its treatment,
including:
1. Control Disease Manifestations
2. Maintain Quality of Life o Hypertension, growth retardation,
chronic pulmonary impairment, ocular
o Minimize exacerbations and prevent abnormalities, permanent renal
serious organ damage damage, neuropsychiatric symptoms,
musculoskeletal damage, and gonadal
impairment.
3. Prevent Adverse Drug Effects
 Pregnancy precautions : lupus needs to be in
Pharmacotherapy coontrol for at least 6 months before conceiving

Corticosteroids Comprehensive Review of Rheumatoid Arthritis (RA)

o Oral: Low-dose maintenance for mild Overview

cases, high-dose for severe
manifestations Rheumatoid arthritis (RA) is a chronic autoimmune
o Topical: For discoid lesions, especially disorder characterized by the immune system
on the face (use mild steroids to avoid mistakenly attacking the synovial membrane, leading to
atrophy) inflammation primarily in the joints. This condition can
o Parenteral: IV pulse therapy combined affect various tissues and organs throughout the body,
with immunosuppressants for severe but its most notable impact is on joint health.
SLE
Epidemiology
Hydroxychloroquine
 Prevalence: RA affects approximately 0.5% to
o Manages skin and joint manifestations, 1.0% of the population in the USA.
prevents flares, and aids as background  Gender Ratio: The disease is more prevalent in
treatment for nephritis females than males, with a ratio of 3:1.
o Doesn’t work immediately (takes a  Age of Onset: Although RA can affect
couple of months) individuals at any age, it typically manifests
o Take with food between the ages of 45 and 65, with some early
o Have regular eye check because of onset cases occurring in individuals aged 20 to
retinal damage 45 years. Approximately 75% of those
diagnosed are women.
Immunosuppressants
Risk Factors
o For severe CNS manifestations,
glomerulonephritis, thrombocytopenia, Several factors have been identified that may increase
and hemolytic anemia the likelihood of developing RA:
o Examples: Azathioprine, Belimumab,
Cyclophosphamide, IV Immune Globulin  Idiopathic: The exact cause is often unknown.
(IVIg), Methotrexate  Genetic Factors: A positive family history and
inherited tissue types related to major
histocompatibility complex (MHC) antigens may
play a role.
  Environmental Factors: Smoking, bacterial detailed visualization of joint and soft
and fungal infections, and specific viral tissue involvement.
infections, such as herpes simplex and Epstein-
Barr virus (EBV), are implicated. Blood Tests:
 Vitamin D Deficiency: Low levels of vitamin D
may contribute to the risk. o Rheumatoid Factor (RF): This specific
antibody may be present, but its
Clinical Manifestations absence does not rule out RA (known
as seronegative RA).
The symptoms of RA can vary but commonly include: o Anti-Citrullinated Protein Antibodies
(ACPAs): Highly specific for RA, with
Joint Symptoms: about 95% specificity.
o Other Tests:
o Swelling: Joints, particularly in the
hands, become swollen, red, and  Erythrocyte Sedimentation
tender. Rate (ESR): Measures
o Swan Neck Deformity: Characterized inflammation by assessing how
by hyperextension of the proximal quickly red blood cells settle in
interphalangeal joint while the distal joint a tube over an hour.
is flexed.  C-Reactive Protein (CRP):
o Mallet Finger: A simple flexion Indicates the presence of
deformity of the distal interphalangeal inflammation in the body.
joint, preventing extension.  Full Blood Count: Provides
o Z Deformity of the Thumb: Severe information about various blood
hyperextension of the interphalangeal cell types.
joint of the thumb.  Renal Function Tests: Assess
o Symmetrical Affected Joints: RA kidney health.
typically affects joints on both sides of  Liver Enzyme Tests: Evaluate
the body, known as polyarthritis. liver function.

Systemic Symptoms: Medical Management

o Fatigue Management of RA involves various pharmacological

and non-pharmacological strategies:
o Joint pain, tenderness, swelling,
redness, and warmth
o Joint stiffness, particularly in the Salicylates:
morning or after inactivity
o Loss of joint range of motion o Acetylated: Aspirin
o Limping and potential joint deformity o Nonacetylated:

Seven S  Choline magnesium trisalicylate

(Trilisate)
 Sunrise stiffness (usually lasts 30 mins)  Choline salicylate (Arthropan)
 Soft, tender feeling in joints
 Swelling in the joints (warm) Nonsteroidal Anti-inflammatory Drugs
 Symmetrical (NSAIDs):
 Synovium (iniflammed)
 Systemic (fever, fatigue, headaches,anemia due o Diclofenac (Voveran)
to decreased erythropoetin etc.) o Etodolac (Lodine)
 Stages ( Synovitis, Pannus, Ancylosis) o Flurbiprofen (Ansaid)
o Ibuprofen
Diagnostic Studies o Meclofenamate (Meclomen)
o Meloxicam
Several diagnostic tests are utilized to confirm the o Nabumetone (Relafen)
diagnosis of RA:
Disease-Modifying Antirheumatic Drugs
Imaging Studies: (DMARDs):

o X-Rays: Usually focused on the hands o Antimalarials:

and feet to identify joint damage.
o Magnetic Resonance Imaging (MRI)  Hydroxychloroquine
and Ultrasound: Used for more  Chloroquine
  Action: Anti-inflammatory, Rest the joints using splinting devices
inhibits lysosomal enzymes  Heat for Stiffness
 Cold for Pain and inflammation
o Gold-containing Compounds:

 Aurothioglucose (Solganol)
Physical exercise but do not overexert
 Gold sodium thiomalate
Supplementation for anemia
 Auranofin (Ridaura)
 Sulfasalazine (Azulfidine)
 Penicillamine (Cuprimine)
 Action: Inhibits T- and B-cell
activity, suppresses synovitis Type 1 Diabetes Mellitus (T1DM)
during active stages of
rheumatoid arthritis Overview

o Immunosuppressives: Type 1 Diabetes Mellitus (T1DM) is an autoimmune

disease characterized by the destruction of insulin-
 Methotrexate (Rheumatrex) producing beta cells in the pancreas. It leads to a
 Azathioprine (Imuran) lifelong dependency on insulin therapy for glucose
 Cyclophosphamide (Cytoxan) management, given the absolute deficiency of
 Action: Immune suppression, endogenous insulin. This condition often emerges in
affects DNA synthesis and other childhood or adolescence but can occur at any age.
cellular processes

o Corticosteroids:
Pathophysiology of Type 1 Diabetes
 Prednisone
 Prednisolone Autoimmune Response:
 Hydrocortisone
 Intra-articular injections
 Action: Anti-inflammatory and
1. T1DM is often triggered by
environmental factors (e.g., viral
analgesic; used for the shortest
infections) in genetically predisposed
duration at the lowest effective
individuals, leading to an autoimmune
dose to minimize adverse
attack against beta cells in the
effects
pancreas.
o Topical Analgesics:
2. T-cells (a type of white blood cell)
mistakenly attack and destroy
 Capsaicin (Zostrix)
pancreatic beta cells, which produce
insulin.
Surgical Management
Insulin Deficiency
For individuals with severe RA, surgical options may
include:
1. With most beta cells destroyed, the
pancreas cannot produce enough
 Arthroplasty: Joint replacement surgery,
insulin to transport glucose into cells,
commonly performed on the hip or knee.
resulting in hyperglycemia.
 Arthroscopy: A minimally invasive procedure
using a small lighted instrument to remove 2. Cells begin to starve for glucose, even
debris or inflamed tissue from a joint. with elevated blood glucose levels, as
 Carpal Tunnel Release: Alleviates pressure on they require insulin to absorb glucose.
the median nerve in the wrist.
 Cervical Spinal Fusion: Addresses severe Alternative Energy Source:
neck pain and nerve issues.
 Hand and Finger Surgeries: Correct joint 1. In response to this "starvation" at the
problems in the hand. cellular level, the body starts breaking
 Foot Surgery: Such as phalangeal head down fat stores and muscle protein,
resection. leading to ketone production as an
 Synovectomy: Removal of inflamed joint alternative fuel source.
tissue. 2. This ketone production, if excessive,
causes ketoacidosis (an accumulation
Nursing Management of acids in the blood), leading to
diabetic ketoacidosis (DKA).
For swollen and inflammed joints
 Insulin Therapy

Electrolyte Imbalance:  Types of Insulin:

1. Ketones and hyperglycemia cause o Rapid-acting (e.g., Lispro, Aspart):

dehydration and loss of electrolytes Onset within 15 minutes, peaks at 1-2
through osmotic diuresis, resulting in hours, lasts 3-5 hours. Used for
significant shifts in electrolyte levels, mealtime bolus dosing.
particularly potassium. o Short-acting (e.g., Regular insulin):
Onset in 30 minutes, peaks at 2-4
hours, lasts 5-8 hours.
o Intermediate-acting (e.g., NPH):
Provides coverage for about half the
Signs and Symptoms of Type 1 Diabetes
day or overnight.
o Long-acting (e.g., Glargine, Detemir):
1. Polyuria (frequent urination): Caused by Onset within 1-2 hours, no peak, lasts
osmotic diuresis from excess glucose in the 24 hours, providing basal insulin.
bloodstream.
2. Polydipsia (excessive thirst): Dehydration from  Insulin Regimens: Multiple daily injections
fluid loss leads to increased thirst. (MDI) or insulin pump therapy for tight glycemic
3. Polyphagia (increased hunger): Due to cellular control.
starvation for glucose.
4. Weight Loss: Breakdown of muscle and fat due Blood Glucose Monitoring
to lack of glucose uptake by cells.
5. Fatigue and Weakness: Inadequate glucose  Self-Monitoring of Blood Glucose (SMBG):
uptake leads to decreased energy levels. Essential before meals, at bedtime, and as
needed. Frequency is adjusted based on
Additional Symptoms of Diabetic Ketoacidosis (DKA) individual needs.
Include:  Continuous Glucose Monitoring (CGM): Real-
time data for high-risk patients, providing alerts
 Nausea, vomiting, abdominal pain. for hypo- and hyperglycemia trends.
 Fruity odor on the breath (acetone breath).
 Kussmaul respirations (deep, rapid breathing) to Diet and Nutrition
compensate for metabolic acidosis.
 Altered mental status, which may progress to  Carbohydrate Counting: Aligns insulin dose
coma if untreated. with carbohydrate intake, typically 1 unit of
rapid-acting insulin per 15 grams of carbs.
 Glycemic Index Awareness: Helps patients
choose foods that impact blood glucose more
gradually.
Diagnostic Criteria for Type 1 Diabetes
 Balanced Meals: Include high-fiber, low-fat
options and avoid sugary foods to stabilize
1. Fasting Blood Glucose ≥ 126 mg/dL (7 blood sugar levels.
mmol/L).
2. Random Blood Glucose ≥ 200 mg/dL (11.1 Exercise Management
mmol/L) with symptoms of hyperglycemia.
3. Hemoglobin A1c (HbA1c) ≥ 6.5% indicates  Exercise improves insulin sensitivity, but close
poor glycemic control over 2-3 months. monitoring of glucose levels is necessary to
4. Oral Glucose Tolerance Test (OGTT) ≥ 200 avoid hypoglycemia. Patients should bring quick
mg/dL at 2 hours (less commonly used in T1DM glucose sources (e.g., candy, juice) during
diagnosis). physical activities.
5. Autoantibody Testing:
Management of Acute Complications
o Presence of islet cell antibodies (ICA),
insulin autoantibodies (IAA), and  Hypoglycemia (blood glucose < 70 mg/dL):
glutamic acid decarboxylase (GAD) Treat with 15-20g of fast-acting carbs (e.g.,
antibodies confirm autoimmune glucose tablets, juice), recheck blood glucose
destruction. in 15 minutes.
 Diabetic Ketoacidosis (DKA): Requires
emergency care, including fluid replacement,
electrolyte correction, and continuous IV insulin
to reduce glucose and ketone production.
Medical Management of Type 1 Diabetes
 o Electrolyte Monitoring: Check
potassium levels regularly, as insulin
therapy can lead to hypokalemia.

Nursing Assessment and Interventions

Assessment

1. Vital Signs: Monitor for tachycardia,

hypotension (suggesting dehydration).
2. Blood Glucose Levels: Regular monitoring to Complications of Type 1 Diabetes
assess effectiveness of treatment.
3. Signs of Dehydration: Skin turgor, mucous Acute Complications
membranes, urine output.
4. Electrolytes and Acid-Base Balance: Monitor o Hypoglycemia: Symptoms include
potassium and bicarbonate levels, especially shakiness, sweating, confusion, and
in DKA. irritability. If untreated, can lead to
5. Weight Monitoring: Unintentional weight loss seizures or coma.
may indicate poor glycemic control. o Diabetic Ketoacidosis (DKA):
Symptoms include fruity breath odor,
deep breathing (Kussmaul respirations),
Interventions
nausea, vomiting, and abdominal pain.
Requires hospitalization.
Insulin Administration
Chronic Complications
o Educate on proper injection techniques,
rotating sites to prevent o Microvascular Complications:
lipodystrophy.
o Verify the correct insulin dose before
administration.  Retinopathy: Damage to retinal
blood vessels can lead to
blindness.
Prevention and Management of  Nephropathy: Progression to
Hypoglycemia: end-stage renal disease if
untreated. Regular monitoring
o Recognize early symptoms (shakiness, of urine microalbumin is critical.
sweating, confusion) and respond with  Neuropathy: Peripheral nerve
quick glucose intake. damage causing loss of
o Teach patients to carry fast-acting sensation, particularly in the
glucose and avoid skipping meals after feet, increasing the risk of injury
insulin administration. and infection.

Patient Education: o Macrovascular Complications:

o Diet and Carb Counting: Emphasize  Cardiovascular Disease:

balanced intake with an emphasis on Increased risk of heart attack
consistent carbohydrate management. and stroke.
o Exercise Precautions: Encourage  Peripheral Artery Disease:
exercise but educate on the importance Poor circulation leading to leg
of blood glucose monitoring and ulcers and increased
carrying quick-acting carbohydrates. amputation risk.
o Sick-Day Management: Teach patients
to check glucose more frequently and
continue insulin even if eating less.
Patient Education
Management of Diabetic Ketoacidosis (DKA):
Insulin Administration:
o IV Fluid Administration: Start with
isotonic saline to correct o Teach injection sites, rotation to prevent
dehydration. lipodystrophy, and correct timing for
o IV Insulin: Continuous infusion to mealtime insulin
reduce blood glucose levels gradually.
Blood Glucose Monitoring

o Emphasize regular monitoring and

maintaining a log to share with
healthcare providers.

Diet and Exercise:

o Explain carbohydrate counting, meal

planning, and the importance of physical
activity. Educate on preventing
hypoglycemia by checking glucose
before and after exercise.

Sick-Day Rules:

o Continue insulin as prescribed, even

with decreased food intake. Check
glucose more frequently, and test for
ketones in urine if glucose is high.

Foot Care:

o Daily inspection, proper hygiene, well-

fitting shoes, and no barefoot walking to
prevent foot injuries and infection.

Signs of Hypoglycemia and Hyperglycemia:

o Teach patients and family members to

recognize symptoms and know when to
seek emergency assistance.