Care of Clients with Immunologic Disorders

Immunologic Disorders
- Immunologic disorders, also known as immunological disorders or immune system disorders,
refer to a wide range of conditions where the immune system malfunctions. The immune system
is responsible for protecting the body from infections, diseases, and abnormal cells (like cancer
cells). When the immune system is not functioning properly, it can lead to various health
problems.

Examples of Immunologic disorders

1. Autoimmune Disorders: In autoimmune disorders, the immune system mistakenly targets and
attacks the body's own healthy cells, tissues, and organs. Examples include:
 Rheumatoid Arthritis: The immune system attacks the joints, causing pain, swelling, and
stiffness.
 Systemic Lupus Erythematosus (SLE): Affecting various body systems, SLE can lead to joint
pain, skin rashes, and organ damage.
 Type 1 Diabetes: The immune system destroys insulin-producing cells in the pancreas,
leading to high blood sugar levels.
2. Allergies: Allergic reactions occur when the immune system overreacts to harmless substances
(allergens) like pollen, pet dander, or certain foods. Common allergic conditions include hay fever,
asthma, and food allergies.
3. Immunodeficiency Disorders: These disorders weaken the immune system, making it less
effective at fighting off infections. Examples include:
 HIV/AIDS: The virus attacks the immune system, leaving the body vulnerable to various
infections and cancers.
 Common Variable Immunodeficiency (CVID): A group of disorders characterized by a
weakened immune system, leading to recurrent infections.
4. Hypersensitivity Reactions: These are exaggerated or inappropriate immune responses to
substances that are generally harmless. There are four types of hypersensitivity reactions, ranging
from immediate (Type I) to delayed (Type IV) reactions.

Multiple Sclerosis (MS)

- A degenerative disorder of the CNS that is characterized by demyelization of the neurons. It is a
chronic, progressive, and noncontagious disorder.
- It usually occurs between the ages of 20 and 50 years and consists of periods of remissions and
exacerbations.
- The causes are unknown, but the disease is thought to be the result of an autoimmune
response or viral infection.
- Precipitating factors include pregnancy, fatigue, stress, infection, and trauma.
- Electroencephalographic findings are abnormal.
- Assessment of a lumbar puncture indicates an increased gamma globulin level, but the serum
globulin level is normal

 Clinical Manifestations
Common symptoms include:
1. Fatigue and weakness
2. Numbness or tingling in the limbs
3. Difficulty with coordination and balance
4. Muscle spasms and stiffness
5. Problems with vision, such as blurred vision or double vision
6. Cognitive changes, including memory problems and difficulty concentrating
7. Bowel and bladder dysfunction
8. Sensory changes, like decreased sensitivity to touch or temperature

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 9. Depression and emotional changes
10. Pain often described as sharp or burning sensations.

 Assessment and Diagnostic Findings

Diagnosing MS can be challenging, as its symptoms can be similar to other neurological
conditions. A comprehensive assessment and diagnostic process may include:
1. Medical history and neurological examination to evaluate symptoms and physical signs.
2. Magnetic Resonance Imaging (MRI) to visualize brain and spinal cord lesions.
3. Lumbar puncture (spinal tap) to analyze cerebrospinal fluid for abnormalities and
immune system markers.
4. Evoked potential tests to measure electrical activity in the brain in response to stimuli.
5. Blood tests to rule out other conditions and check for certain markers associated with
MS.

 Different types of Multiple Sclerosis

1. Relapsing-Remitting Multiple Sclerosis (RRMS):
a. RRMS is the most common form of MS, affecting about 85% of people diagnosed
with the condition.
b. It is characterized by clearly defined episodes of new or increasing neurological
symptoms, known as relapses, followed by periods of partial or complete
recovery (remission).
c. In between relapses, there is usually a stable or improving condition.
2. Primary Progressive Multiple Sclerosis (PPMS):
a. PPMS accounts for about 10-15% of MS cases.
b. It is characterized by a gradual but steady progression of symptoms from the
onset, with no distinct relapses or remissions.
c. Unlike RRMS, PPMS typically does not have periods of stability or improvement.
3. Secondary Progressive Multiple Sclerosis (SPMS):
a. Many people with RRMS will eventually transition into a phase known as
secondary progressive MS.
b. In SPMS, there is a gradual worsening of the condition with or without occasional
relapses, minor recoveries, or plateaus in between.
4. Progressive-Relapsing Multiple Sclerosis (PRMS):
a. PRMS is a less common form, occurring in about 5% of MS cases.
b. It involves a steady progression of symptoms from the beginning, but with
occasional clear relapses that may or may not lead.

 Medical Management
o The primary goal of MS management is to control symptoms, slow disease progression, and
improve the patient's quality of life. Medical management involves
o Disease-modifying therapies (DMTs) reduce the frequency and severity of relapses and slow
disease progression.
o Corticosteroids (e.g., methylprednisolone) manage acute exacerbations (relapses) and
reduce inflammation.

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 o Medications to manage specific symptoms such as muscle relaxants for spasticity or
antidepressants for mood disturbances.
o Physical therapy, occupational therapy, and speech therapy to maintain function and
independence.
o Lifestyle modifications, including regular exercise, a balanced diet, and stress management.

 Pharmacologic Therapy
 Various pharmacological agents are used in the management of MS, including:
 Interferons (e.g., interferon beta-1a, interferon beta-1b) as disease-modifying
therapies.
 Fingolimod, dimethyl fumarate, teriflunomide, and other oral medications to modify
disease activity.
 Natalizumab and alemtuzumab as monoclonal antibodies targeting specific immune
responses.
 Symptomatic treatments such as muscle relaxants, antispasmodics, and
antidepressants for symptom relief.

 Nursing Management
o The client with multiple sclerosis should be aware of triggers that cause worsening of the
disease and avoid them where possible.
o Provide energy conservation measures during exacerbation.
o Protect the client from injury by providing safety measures.
o Place an eye patch on the eye for diplopia.
o Monitor for potential complications such as urinary tract infections, calculi, pressure ulcers,
respiratory tract infections, and contractures.
o Promote regular elimination by bladder and bowel training.
o Encourage independence.
o Assist the client to establish a regular exercise and rest program and to balance moderate
activity with rest periods.
o Assess the need for assistive devices and provide as needed.
o Initiate physical and speech therapy
o Instruct the client to avoid fatigue, stress, infection, overheating, and chilling.
o Instruct the client to increase fluid intake and eat a balanced diet, including low-fat, high-fiber
foods and foods high in potassium.
o Instruct the client in safety measures related to sensory loss, such as regulating the
temperature of bath water and avoiding heating pads.
o Instruct the client in safety measures related to motor loss, such as avoiding the use of
scatter rugs and using assistive devices.
o Instruct the client in the self-administration of prescribed medications.
o Anticholinergic agents are used for bladder spasticity and intravenous glucocorticoids for
acute flare-ups.

Diabetes
- A group of diseases characterized by hyperglycemia caused by defects in insulin secretion,
insulin action, or both
- Affects nearly 25.8 million people in the United States; one third of the cases are undiagnosed
- Prevalence is increasing
- Minority populations and older adults are disproportionately affected

 Classifications of Diabetes
o Type 1 diabetes

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 o Type 2 diabetes
o Latent autoimmune diabetes of adults (LADA)
o Gestational diabetes
o Diabetes associated with other conditions or syndromes

 Risk factors
a. Family history of diabetes (e.g., parents or siblings with diabetes)
b. Obesity (i.e., ≥20% over desired body weight or body mass index ≥30 kg/m2)
c. Race/ethnicity (e.g., African Americans, Hispanic Americans, Native Americans,
Asian Americans, Pacific Islanders)
d. Age equal to or greater than 45 years
e. Previously identified impaired fasting glucose or impaired glucose tolerance
f. Hypertension (≥140/90 mm Hg)
g. High-density lipoprotein (HDL) cholesterol level ≤35 mg/dL (0.90 mmol/L) and/or
triglyceride level ≥250 mg/dL (2.8 mmol/L)
h. History of gestational diabetes or delivery of a baby over 9 lb.

 Functions of Insulin
o Transports and metabolizes glucose for energy
o Stimulates storage of glucose in the liver and muscle as glycogen
o Signals the liver to stop the release of glucose
o Enhances storage of dietary fat in adipose tissue
o Accelerates transport of amino acids into cells
o Inhibits the breakdown of stored glucose, protein, and fat

 Type 1 Diabetes
- Insulin-producing beta cells in the pancreas are destroyed by a combination of genetic,
immunologic, and environmental factors
- Results in decreased insulin production, unchecked glucose production by the liver and
fasting hyperglycemia
- Affects 5% of adults with diabetes
 Clinical Manifestations
o Depends on the level of hyperglycemia
o “Three Ps”
 Polyuria
 Polydipsia
 Polyphagia
o Fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry skin, skin
lesions or wounds that are slow to heal, recurrent infections
o Type 1 may have sudden weight loss

 Types of Blood Glucose test

 Fasting blood sugar (FBS) measures blood glucose after you have not eaten for at least 8
hours. It is often the first test done to check for prediabetes and diabetes.
 Random blood sugar (RBS) measures blood glucose regardless of when you last ate.
Several random measurements may be taken throughout the day. Random testing is useful
because glucose levels in healthy people do not vary widely throughout the day. Blood
glucose levels that vary widely may mean a problem. This test is also called a casual blood
glucose test.
 A 2-hour postprandial blood sugar test measures blood sugar exactly 2 hours after you
start eating a meal. This test is most often done at home when you have diabetes. It can see
if you are taking the right amount of insulin with meals.
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  The hemoglobin A1c test and the oral glucose tolerance test (OGTT) are other tests
used to look at blood sugar levels. The A1c test can be used to estimate your average blood
sugar level over the past 2 to 3 months. The OGTT is commonly used to diagnose diabetes
that occurs during pregnancy (gestational diabetes).

 Criteria for the diagnosis of Diabetes

1. Symptoms of diabetes plus casual plasma glucose concentration equal to or greater than
200 mg/dL (11.1 mmol/L). Casual is defined as any time of day without regard to time
since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and
unexplained weight loss.

2. Fasting plasma glucose greater than or equal to 126 mg/dL (7.0 mmol/L). Fasting is
defined as no caloric intake for at least 8 hours.

3. Two-hour post load glucose equal to or greater than 200 mg/dL (11.1mmol/L) during an
oral glucose tolerance test. The test should be performed as described by the World
Health Organization, using a glucose load containing the equivalent of 75 g anhydrous
glucose dissolved in water.

4. A1C ≥6.5% (48 mmol/mol). In the absence of unequivocal hyperglycemia with acute
metabolic decompensation, these criteria should be confirmed by repeat testing on a
different day. The third measure is not recommended for routine clinical use.

 Medical Management of Diabetes

o Main goal is to normalize insulin activity and blood glucose levels to reduce the development
of complications.
o The ADA now recommends HgbA1c less than 7%
o Diabetes management has five components:
 Nutritional therapy
 Exercise
 Monitoring
 Pharmacologic therapy
 Education

 Dietary Management Goals

o Control of total caloric intake to attain or maintain a reasonable body weight
o Control of blood glucose levels
o Normalization of lipids and blood pressure to prevent heart disease

 Role of the Nurse

 Be knowledgeable about dietary management
 Communicate important information to the dietician or other management specialists
 Reinforce patient understanding
 Support dietary and lifestyle changes

 Meal Planning
o Consider food preferences, lifestyle, usual eating times, and cultural and ethnic background
o Review diet history and need for weight loss, gain, or maintenance
o Caloric requirements and calorie distribution throughout the day; exchange lists
 Carbohydrates: 50% to 60% carbohydrates; emphasize whole grains
 Fat: 30%, limiting saturated fats to 10% and <300 mg cholesterol
 Nonanimal sources of protein (e.g., legumes, whole grains) and increase fiber

 Glycemic Index
o Combining starchy foods with protein and fat slows absorption and glycemic response
o Raw or whole foods tend to have lower responses than cooked, chopped, or pureed foods
o Eat whole fruits rather than juices; this decreases glycemic response because of fiber
(slowing absorption)

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 o Adding food with sugars may produce lower response if eaten with foods that are more
slowly absorbed

 Other Dietary Concerns

 Alcohol
 Nutritive and nonnutritive sweeteners
 Misleading food labels
 Exercise
 Lowers blood sugar
 Aids in weight loss, easing stress, and maintaining a feeling of well-being
 Lowers cardiovascular risk

 General Considerations for Exercise in People with Diabetes

The nurse instructs the patient to:
a) Exercise three times each week with no more than 2 consecutive days without
exercise.
b) Perform resistance training twice a week if you have type 2 diabetes.
c) Exercise at the same time of day (preferably when blood glucose levels are at
their peak) and for the same duration each session.
d) Use proper footwear and, if appropriate, other protective equipment (i.e., helmets
for cycling).
e) Avoid trauma to the lower extremities, especially if you have numbness due to
peripheral neuropathy. Inspect feet daily after exercise.
f) Avoid exercise in extreme heat or cold.
g) Avoid exercise during periods of poor metabolic control.
h) Stretch for 10 to 15 minutes before exercising.

 General Considerations for Exercise in People with Diabetes

a. Exercise three times each week with no more than 2 consecutive days without exercise.
b. Perform resistance training twice a week if you have type 2 diabetes.
c. Exercise at the same time of day (preferably when blood glucose levels are at their peak)
and for the same duration each session.
d. Use proper footwear and, if appropriate, other protective equipment
e. (i.e., helmets for cycling).
f. Avoid trauma to the lower extremities, especially if you have
g. numbness due to peripheral neuropathy.
h. Inspect feet daily after exercise.
i. Avoid exercise in extreme heat or cold.
j. Avoid exercise during periods of poor metabolic control.
k. Stretch for 10 to 15 minutes before exercising.

 Exercise Precautions
 Exercise elevates blood sugar levels; insulin must be adjusted
 Insulin normally decreases with exercise; patients on exogenous insulin should eat a 15-g
carbohydrate snack before moderate exercise to prevent hypoglycemia
 Potential postexercise hypoglycemia
 Need to monitor blood glucose levels
 Gerontologic considerations

 Insulin Therapy
a. Blood glucose monitoring:
 Cornerstone of diabetes management
 Self-monitoring of blood glucose (SMBG) levels has dramatically altered diabetes
care
b. Categories of insulin
 Rapid acting
 Short acting: regular insulin
 Intermediate acting: NPH insulin
 Very long acting: “Peakless”

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  Categories of Insulin

 Complications of Insulin Therapy

a. Local allergic reactions
b. Systemic allergic reactions
c. Insulin lipodystrophy
d. Resistance to injected insulin
e. Morning hyperglycemia

 Methods of Insulin Delivery

 Traditional subcutaneous injections
 Insulin pens
 Jet injectors
 Insulin pumps
 Future: Implantable insulin pumps

 Educating Patients in Insulin Self-Management

 Use and action of insulin
 Symptoms of hypoglycemia and hyperglycemia
Required actions
 Blood glucose monitoring
 Self-injection of insulin
 Insulin pump use

Question #1
What category of insulin is rapid acting?
A. Humalog
B. Humalog R
C. Humulin N
D. Glargine (Lantus)

Answer to Question #1
A. Humalog
Aspart is a rapid-acting insulin, Humalog R is a short-acting insulin, Humulin N is an intermediate-acting
insulin, and Glargine (Lantus) is a very long-acting insulin

ACUTE GLOMERULONEPHRITIS (AGN)

- Inflammatory & degenerative disorder of the glomerulus

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 - Damage to both kidney from filtration of trapping of antibody-antigen complexes within the
glomeruli resulting to decrease glomerular filtration rate

 Types:
1. Acute post-streptococcal
 After 7 - 10 days after streptococcal throat infection
 Immune reaction to the presence of an infectious organism (group A beta hemolytic
streptococcus/GABHS)
2. Chronic Glomerulonephritis
 Hypertensive nephrosclerosis
 Heat failure
 Chronic renal failure

 Signs and Symptoms

o Pathognomonic sign: Periorbital edema
o Flank pain, costovertebral tenderness
o Headache, visual disturbance
o Fever, malaise, weakness, fatigue
o Anorexia
o Dyspnea (salt & water retention)
o Tachycardia, hypertension
o Oliguria
o Hematuria
o Proteinuria

 Assessment and Diagnostic Test

 Urinalysis
 Hematuria & proteinuria (MOST important indicator of glomerular injury)
 Casts
 Elevated BUN & creatinine
 Positive antibody response test for streptococcus
 Elevated Erythropoietin Sedimentation Rate
 Hyponatremia, hypophosphatemia
 Hyperkalemia

 Management
 Pharmacologic management
 Diuretics
 Antihypertensive
 Corticosteroids
 If residual streptococcal infection is suspected, penicillin is the agent of choice

 Nursing Management
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  Monitor VS, I & O daily weight & urine specific gravity
 Dietary restriction of sodium, fluid & protein
 Carbohydrates are given liberally to provide energy and reduce the catabolism of protein.
 Provide special skin care
 Provide for complication (renal failure, cardiac failure, hypertensive encephalopathy)
 Monitor urinalysis, BUN creatinine levels
 Promote rest & regular activity when hematuria & proteinuria resolve

Systemic Lupus Erythematosus (SLE)

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease where the body's immune system
mistakenly attacks healthy tissues, causing widespread inflammation and damage to various organs. SLE
can affect the skin, joints, kidneys, heart, lungs, brain, and blood vessels, leading to a wide range of
symptoms and complications. The disease is characterized by periods of flare-ups and remissions. SLE
predominantly affects women, particularly during their childbearing years.

Causes
The exact cause of SLE is unknown, but it is believed to result from a combination of genetic, hormonal,
environmental, and immunological factors.
1. Genetics: Certain genes increase susceptibility to SLE, particularly those involved in immune
regulation.
2. Hormonal Influence: SLE is more common in women, suggesting a role for estrogen. Many
women experience disease flare-ups during menstruation or pregnancy.
3. Environmental Triggers:
o Ultraviolet (UV) light exposure: Can trigger or exacerbate skin rashes.
o Infections: Certain viral or bacterial infections may trigger an abnormal immune response.
o Medications: Some drugs, such as hydralazine, procainamide, and certain antiepileptics,
can induce lupus-like symptoms.
o Stress: Both physical and emotional stress may contribute to disease flares.

Pathophysiology
SLE occurs when the immune system produces autoantibodies that target normal cells and tissues. These
autoantibodies form immune complexes (antigen-antibody complexes) that deposit in various organs,
triggering inflammation and tissue damage. The body's failure to clear these immune complexes and
apoptotic (dying) cells contributes to the chronic inflammatory process.
Common autoantibodies in SLE include:
 Anti-nuclear antibodies (ANA)
 Anti-dsDNA antibodies (specific for SLE)
 Anti-Smith (Anti-Sm) antibodies
 Antiphospholipid antibodies (can lead to clotting disorders)

Assessment
A comprehensive assessment for SLE includes gathering a detailed history, conducting a physical
examination, and performing diagnostic tests.
1. History Taking:
o Ask about fatigue, joint pain, skin rashes, hair loss, and fevers.
o Inquire about symptoms related to organ involvement, such as difficulty breathing (lungs),
swelling in the legs (kidneys), or neurological symptoms (brain).
o Family history of autoimmune diseases can suggest a genetic predisposition.
2. Physical Examination:
o Skin: Look for characteristic rashes, such as the malar rash (butterfly-shaped rash across
the cheeks and nose) or discoid rash (circular, red, scaly patches).
o Joints: Assess for swelling, pain, or stiffness, especially in the hands and wrists (symptoms
of polyarthritis).
o Kidneys: Check for signs of edema (swelling) in the extremities, which could indicate kidney
damage (lupus nephritis).
o Neurological Examination: Assess for signs of cognitive impairment, seizures, or
headaches.
Clinical Manifestations

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SLE can affect almost every organ system in the body, leading to a wide range of symptoms. The most
common manifestations include:
1. General Symptoms:
o Fatigue: One of the most common and debilitating symptoms.
o Fever: Often low-grade and associated with active disease flares.
o Weight loss or gain: Fluid retention or systemic inflammation can cause fluctuations in
weight.
2. Skin and Mucous Membranes:
o Malar rash (butterfly rash): A red, raised rash across the cheeks and nose.
o Discoid rash: Thick, scaly patches of skin that can cause scarring.
o Photosensitivity: Increased sensitivity to sunlight, resulting in skin rashes.
o Alopecia: Hair loss, often patchy.
o Oral or nasal ulcers: Painless sores inside the mouth or nose.
3. Musculoskeletal System:
o Polyarthritis: Inflammation of multiple joints, typically symmetrical and affecting the small
joints of the hands, wrists, and knees.
o Joint pain and stiffness: Often without significant swelling or deformity (unlike rheumatoid
arthritis).
4. Kidneys:
o Lupus nephritis: A severe complication that causes inflammation of the kidneys, leading to
proteinuria (protein in urine), hematuria (blood in urine), edema, and high blood pressure.
5. Cardiovascular System:
o Pericarditis: Inflammation of the lining around the heart, causing chest pain that worsens
with deep breathing.
o Myocarditis: Inflammation of the heart muscle.
o Increased risk of blood clots (due to antiphospholipid syndrome).
6. Lungs:
o Pleuritis: Inflammation of the lining of the lungs, causing sharp chest pain.
o Interstitial lung disease: Chronic inflammation leading to scarring and difficulty breathing.
7. Neurological System:
o Seizures, psychosis, and cognitive dysfunction: Can occur due to inflammation of the
brain or blood vessels.
o Headaches and mood changes.
8. Hematological System:
o Anemia, leukopenia (low white blood cell count), and thrombocytopenia (low platelet
count): Common blood abnormalities in SLE.
o Antiphospholipid syndrome (APS): A condition associated with SLE that leads to an
increased risk of blood clots, miscarriages, and strokes.

Diagnostics
Diagnosis of SLE is based on a combination of clinical findings and laboratory tests. The American
College of Rheumatology (ACR) has criteria that help guide diagnosis, but no single test can definitively
diagnose SLE.
1. Blood Tests:
o Antinuclear antibody (ANA) test: Positive in nearly all SLE patients but not specific to
lupus.
o Anti-dsDNA and Anti-Sm antibodies: Highly specific for SLE.
o Complement levels (C3, C4): Low complement levels are often associated with active
disease.
o Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP): Indicators of
inflammation but not specific to SLE.
2. Urinalysis:
o To detect proteinuria and hematuria, which are signs of lupus nephritis.
3. Imaging Studies:
o Chest X-rays or CT scans: To assess lung involvement (e.g., pleuritis, interstitial lung
disease).
o Echocardiogram: To evaluate for pericarditis or myocarditis.
4. Kidney Biopsy:

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 o May be performed if lupus nephritis is suspected to assess the degree of kidney damage
and guide treatment.
Medical Interventions
Treatment for SLE focuses on controlling symptoms, preventing flare-ups, and reducing organ damage.
The treatment plan is individualized based on the organs involved and disease severity.
1. Nonsteroidal Anti-inflammatory Drugs (NSAIDs):
o Used to relieve mild joint pain and inflammation. However, caution is needed in patients with
kidney or gastrointestinal issues.
2. Corticosteroids:
o Prednisone is commonly used during flares to suppress the immune system and reduce
inflammation. Dosage is adjusted based on disease activity.
o Topical corticosteroids may be used for skin rashes.
3. Antimalarial Drugs:
o Hydroxychloroquine (Plaquenil): A cornerstone in SLE management, especially for skin,
joint, and fatigue symptoms. It also reduces the risk of flares and helps prevent long-term
organ damage.
4. Immunosuppressive Drugs:
o Methotrexate, Azathioprine, Mycophenolate mofetil: Used in more severe cases,
particularly when there is kidney, lung, or neurological involvement.
o Cyclophosphamide: Used for life-threatening complications, such as severe lupus nephritis
or CNS lupus.
o Biologic agents: Belimumab (Benlysta) is an FDA-approved biologic therapy that targets
specific B-cells involved in the abnormal immune response in SLE.
5. Anticoagulants:
o For patients with antiphospholipid syndrome or a history of blood clots, anticoagulants
(e.g., warfarin, low-molecular-weight heparin) are used to prevent thrombotic events.

Nursing Interventions
Nursing care for patients with SLE focuses on managing symptoms, educating the patient, and monitoring
for complications.
1. Monitoring and Assessments:
o Regularly monitor for signs of disease flares (e.g., joint pain, skin rashes, fatigue) and organ
involvement (e.g., kidney function).
o Monitor laboratory results, especially kidney function tests (BUN, creatinine), urine output,
and blood counts (anemia, thrombocytopenia).
o Check for cardiovascular and respiratory symptoms, such as chest pain, dyspnea, or
peripheral edema.
2. Medication Administration:
o Administer prescribed immunosuppressive drugs, corticosteroids, and NSAIDs as ordered,
and monitor for side effects (e.g., infection risk, gastrointestinal issues).
o Ensure the patient is adherent to long-term therapies, such as hydroxychloroquine, to reduce
the frequency of flares.
3. Patient Education:
o Teach patients about the importance of avoiding sun exposure and using sunscreen to
prevent UV-triggered flares.
o Encourage regular medical check-ups and lab tests to monitor disease activity.
o Educate patients about recognizing early signs of a flare (fatigue, joint pain, rash) and when
to seek medical attention.
4. Nutrition and Lifestyle:
o Encourage a balanced diet rich in calcium and vitamin D, especially for patients on long-term
corticosteroid therapy, to prevent osteoporosis.
o Encourage stress management techniques and energy conservation strategies to help
manage fatigue.
5. Infection Control:
o Teach patients to recognize signs of infection and report them promptly, as
immunosuppressive therapy increases the risk of infection.
6. Emotional and Psychological Support:
o Provide emotional support and consider referrals to counseling services or lupus support
groups, as patients may experience depression, anxiety, or frustration due to chronic illness.

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Nursing Diagnoses
1. Chronic Pain related to joint inflammation and disease activity.
2. Fatigue related to chronic inflammatory response and autoimmune activity.
3. Impaired Skin Integrity related to skin lesions and rashes.
4. Risk for Infection related to immunosuppressive therapy.
5. Disturbed Body Image related to visible skin rashes, hair loss, and weight changes from
corticosteroid use.

Hashimoto's Thyroiditis

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis, is an autoimmune disorder where the
immune system attacks the thyroid gland. This leads to inflammation, gradual destruction of thyroid tissue,
and, over time, hypothyroidism (underactive thyroid), where the gland cannot produce enough thyroid
hormones. It is the most common cause of hypothyroidism in iodine-sufficient areas.

Causes
The exact cause of Hashimoto’s thyroiditis is not entirely understood, but it involves a combination of
genetic, environmental, and immunological factors. The immune system produces antibodies that
mistakenly target proteins in the thyroid gland, including:
 Thyroid peroxidase (TPO): An enzyme involved in the production of thyroid hormones.
 Thyroglobulin (TG): A protein produced by the thyroid gland, essential for thyroid hormone
synthesis.

Several risk factors include:

1. Genetics: A family history of thyroid disorders or other autoimmune diseases.
2. Gender: Women are much more likely to develop Hashimoto’s than men.
3. Age: Commonly occurs in middle-aged individuals but can affect younger people as well.
4. Other Autoimmune Conditions: Hashimoto's is often associated with other autoimmune diseases
like type 1 diabetes, rheumatoid arthritis, or celiac disease.
5. Environmental Triggers: Such as stress, radiation exposure, or excessive iodine intake, may
contribute to the onset of the disorder.

Pathophysiology
In Hashimoto's thyroiditis, immune cells (T lymphocytes) infiltrate the thyroid gland and release pro-
inflammatory cytokines. These immune attacks gradually damage thyroid cells, impairing the gland's ability
to synthesize and secrete thyroid hormones. Over time, this leads to thyroid atrophy and fibrosis, resulting
in hypothyroidism.

Assessment
The assessment of a patient with suspected Hashimoto's thyroiditis involves both clinical and laboratory
evaluation:
1. History Taking:
o Symptoms of Hypothyroidism: Fatigue, weight gain, cold intolerance, constipation, dry
skin, hair loss, and memory problems. Women may experience menstrual irregularities or
infertility.
o Family History: Ask about a history of thyroid disease or autoimmune conditions in family
members.
o Medications: Certain medications, such as lithium or amiodarone, may affect thyroid
function.
2. Physical Examination:
o Thyroid Gland: Palpate for enlargement (goiter), nodules, or tenderness. Over time, the
thyroid may feel firm or irregular in texture.
o Vital Signs: Check for bradycardia (slow heart rate) and low blood pressure.
o Skin and Hair: Examine for dry, rough skin and brittle hair, common in hypothyroidism.
o Reflexes: Delayed relaxation of deep tendon reflexes (e.g., Achilles reflex) is a sign of
hypothyroidism.
Clinical Manifestations
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Hashimoto’s thyroiditis often progresses slowly, and symptoms may not be obvious in the early stages.
Over time, the following clinical manifestations of hypothyroidism develop:
1. General Symptoms:
o Fatigue and lethargy
o Weight gain
o Sensitivity to cold
o Dry skin and brittle hair
o Constipation
o Puffy face and periorbital edema (swelling around the eyes)
2. Cardiovascular Symptoms:
o Bradycardia (slow heart rate)
o Hypotension (low blood pressure)
o Hyperlipidemia (elevated cholesterol levels)
3. Neurological Symptoms:
o Depression or mood changes
o Difficulty concentrating or memory impairment
o Slowed reflexes
4. Reproductive Symptoms:
o Irregular menstrual cycles or heavy periods (menorrhagia) in women
o Infertility or miscarriage
o Reduced libido
5. Goiter (Thyroid Enlargement):
o Early in the disease, the thyroid may be diffusely enlarged (goiter), which can cause a
feeling of fullness in the neck or difficulty swallowing.

Diagnostics
The diagnosis of Hashimoto’s thyroiditis involves blood tests and imaging studies:
1. Thyroid Function Tests:
o TSH (Thyroid-Stimulating Hormone): Elevated levels indicate hypothyroidism because the
pituitary produces more TSH in response to low thyroid hormone levels.
o Free T4 (Thyroxine): Low levels confirm hypothyroidism.
2. Antibody Testing:
o Anti-thyroid peroxidase (anti-TPO) antibodies: Elevated in most cases of Hashimoto’s.
o Anti-thyroglobulin (anti-TG) antibodies: May also be elevated, supporting the diagnosis.
3. Ultrasound of the Thyroid Gland:
o May show changes typical of Hashimoto’s thyroiditis, such as an irregularly shaped thyroid,
a heterogeneous texture, and sometimes small nodules or cysts.
4. Thyroid Biopsy (if necessary):
o Rarely used, but in some cases, a biopsy may be performed to exclude malignancy,
especially if nodules are present.

Medical Interventions
The primary treatment goal for Hashimoto's thyroiditis is to restore normal thyroid function and relieve
symptoms of hypothyroidism. The mainstay of treatment is thyroid hormone replacement.
1. Levothyroxine (T4 Replacement):
o This synthetic form of thyroxine is used to normalize thyroid hormone levels (TSH and free
T4) and manage hypothyroid symptoms.
o The dosage is based on the patient's weight, age, severity of hypothyroidism, and TSH
levels.
o Monitoring: Regular monitoring of TSH levels (every 6-12 weeks initially, then yearly) is
necessary to adjust the levothyroxine dose.
2. Symptomatic Management:
o Hyperlipidemia: Statins may be prescribed if hypothyroidism has led to elevated
cholesterol.
o Constipation: Dietary fiber, laxatives, or stool softeners may be used to alleviate
constipation.
o Depression: If mood disturbances are significant, antidepressants may be considered.
3. Surgical Intervention:

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 o Surgery is rarely needed in Hashimoto’s unless a large goiter is causing compression
symptoms (difficulty breathing or swallowing) or if there is suspicion of thyroid cancer.

Nursing Interventions
Nursing care focuses on education, symptom management, and monitoring for complications related to
hypothyroidism.
1. Medication Administration and Education:
o Educate the patient on taking levothyroxine on an empty stomach, typically 30 minutes to an
hour before breakfast, to improve absorption.
o Emphasize the importance of taking the medication consistently and not abruptly stopping it.
o Inform patients about potential interactions with other medications (e.g., calcium
supplements, iron, antacids) that can interfere with levothyroxine absorption.
2. Monitor for Hypothyroidism Symptoms:
o Regularly assess the patient for changes in energy levels, mood, weight, skin, and bowel
habits.
o Monitor vital signs, particularly heart rate and blood pressure.
3. Weight and Diet Management:
o Encourage a balanced diet with adequate fiber to prevent constipation.
o Monitor weight gain and advise on appropriate calorie intake if necessary.
4. Monitor for Signs of Myxedema:
o Myxedema is a severe form of hypothyroidism, marked by extreme fatigue, confusion,
hypothermia, and bradycardia. It can lead to a life-threatening condition called myxedema
coma. Watch for symptoms and provide urgent care if they develop.
5. Psychosocial Support:
o Depression and cognitive changes can be challenging for patients. Provide support, and
consider referrals to mental health services if necessary.
6. Patient Education:
o Teach the patient the importance of lifelong treatment and regular follow-up for thyroid
function monitoring.
o Educate about recognizing signs of worsening hypothyroidism or side effects from
levothyroxine (e.g., palpitations, nervousness).

Nursing Diagnoses
1. Activity Intolerance related to fatigue and lethargy.
2. Imbalanced Nutrition: More Than Body Requirements related to decreased metabolic rate and
weight gain.
3. Constipation related to slowed gastrointestinal motility.
4. Disturbed Thought Processes related to slowed mental function and hypothyroid effects on
cognition.

Rheumatoid Arthritis
- Rheumatoid arthritis is a chronic systemic inflammatory disease (immune complex
disorder); the cause may be related to a combination of environmental and genetic
factors.
- Rheumatoid arthritis leads to destruction of connective tissue and synovial membrane
within the joints.
- Rheumatoid arthritis weakens the joint, leading to dislocation and permanent deformity of
the joint.
- Pannus forms at the junction of synovial tissue and articular cartilage and projects into
the joint cavity, causing necrosis.
- Exacerbations of disease manifestations occur during periods of physical or emotional
stress and fatigue.
- Vasculitis can impede blood flow, leading to organ or organ system malfunction and
failure caused by tissue ischemia.

 Assessment
o Inflammation, tenderness, and stiffness of the joints

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 o Moderate to severe pain, with morning stiffness lasting longer than 30 minutes
o Joint deformities, muscle atrophy, and decreased range of motion in affected joints
o Spongy, soft feeling in the joints
o Low-grade temperature, fatigue, and weakness
o Anorexia, weight loss, and anemia
o Elevated ESR and positive rheumatoid factor
o Radiographic study showing joint deterioration
o Synovial tissue biopsy reveals inflammation.

 Swan neck Deformities

 Rheumatoid Arthritis
o Rheumatoid factor
 Blood test used to assist in diagnosing rheumatoid arthritis
 Reference interval: Negative or less than 60 IU/ mL
o Medications:
 Combination of pharmacological therapies includes NSAIDs, disease-modifying
antirheumatic drugs (DMARDs), and glucocorticoids

 Physical Mobility
a. Preserve joint function.
b. Provide range-of-motion exercises to maintain joint motion and muscle
strengthening.
c. Balance rest and activity.
d. Splints may be used during acute inflammation to prevent deformity.
e. Prevent flexion contractures.
f. Apply heat or cold therapy as prescribed to joints.
g. Apply paraffin baths and massage as prescribed.
h. Encourage consistency with exercise program.
i. Use joint-protecting devices.
j. Avoid weight bearing on inflamed joints

 Client Education for Rheumatoid Arthritis and Degenerative Joint Disease

a. Assist the client to identify and correct safety hazards in the home.
b. Instruct the client in the correct use of assistive or adaptive devices.
c. Instruct the client in energy conservation measures.
d. Review the prescribed exercise program.
e. Instruct the client to sit in a chair with a high, straight back.
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  Client Education for Rheumatoid Arthritis and Degenerative Joint Disease
a. Instruct the client to use only a small pillow when lying down.
b. Instruct the client in measures to protect the joints.
c. Instruct the client regarding the prescribed medications.
d. Stress the importance of follow-up visits with the primary health care provider.
 Self-care
1. Assess the need for assistive devices such as raised toilet seats, self-rising chairs,
wheelchairs, and scooters to facilitate mobility.
2. Work with an occupational therapist or PHCP to obtain assistive or adaptive devices.
3. Instruct the client in alternative strategies for providing activities of daily living.

 Fatigue
a.
Identify factors that may contribute to fatigue.
b.
Monitor for signs of anemia, and administer iron, folic acid, and vitamins as prescribed.
c.
Monitor for medication-related blood loss by testing the stool for occult blood.
d.
Instruct the client in measures to conserve energy, such as the pacing of activities and
obtaining assistance when possible.
 Disturbed body image
1. Assess the client’s reaction to the body change.
2. Encourage the client to verbalize feelings.
3. Assist the client with self-care activities and grooming.
4. Encourage the client to get dressed daily and to wear street clothes.

 Surgical Interventions
1. Synovectomy: Surgical removal of the synovia to help maintain joint function
2. Arthrodesis: Bony fusion of a joint to regain some mobility
3. Joint replacement (arthroplasty): Surgical replacement of diseased joints with artificial
joints; performed to restore motion to a joint and function to the muscles, ligaments, and
other soft tissue structures that control a joint

 Hypersensitivity Reactions
 Hypersensitivity reactions are exaggerated or inappropriate immune responses that can cause
damage to tissues and organs. They are classified into four types based on the immune mechanism
involved. Understanding these reactions is crucial for diagnosis and management since they can
range from mild allergies to life-threatening conditions.

Types of Hypersensitivity Reactions

1. Type I (Immediate Hypersensitivity)

This is an IgE-mediated allergic reaction, often called immediate hypersensitivity because the reaction
occurs within minutes of exposure to the antigen (allergen). Common examples include anaphylaxis, hay
fever, allergic asthma, and food allergies.
Causes
 Exposure to allergens such as pollen, animal dander, food (e.g., peanuts, shellfish), insect stings, or
medications (e.g., penicillin).
 IgE antibodies bind to mast cells and basophils, causing the release of histamine and other
inflammatory mediators when re-exposure to the antigen occurs.
Clinical Manifestations
 Mild reactions: Sneezing, itching, hives, runny nose (allergic rhinitis), or itchy/watery eyes.
 Severe reactions (anaphylaxis): Difficulty breathing, swelling of the face or throat (angioedema),
rapid drop in blood pressure (shock), urticaria (hives), wheezing, and possible loss of
consciousness.

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Diagnostics
 Skin Prick Test: Small amounts of allergen are applied to the skin to observe a local reaction.
 Serum IgE Testing: Measures specific IgE antibodies in the blood.
 Radioallergosorbent Test (RAST): Measures the level of IgE antibodies to specific allergens in the
blood.
Medical Interventions
 Mild reactions: Antihistamines (e.g., diphenhydramine), decongestants, and corticosteroids to
reduce symptoms.
 Severe reactions (Anaphylaxis):
o Epinephrine (adrenaline): Administered immediately via an autoinjector (e.g., EpiPen).
o IV fluids and oxygen: To maintain blood pressure and oxygenation.
o Corticosteroids and antihistamines: After epinephrine to prevent recurrence.
Nursing Interventions
1. Emergency Management:
o If anaphylaxis occurs, administer epinephrine and maintain the airway.
o Monitor vital signs and oxygen saturation closely.
2. Patient Education:
o Teach patients how to avoid known allergens.
o Ensure they know how to use an epinephrine autoinjector and carry it at all times.
3. Monitor for Recurrence:
o After initial treatment, anaphylaxis can recur (biphasic reaction), so observe the patient for
several hours post-exposure.
2. Type II (Cytotoxic Hypersensitivity)
This reaction involves IgG or IgM antibodies that bind to antigens on the surface of the body’s own cells,
leading to their destruction. Common examples include hemolytic anemia, Goodpasture’s syndrome,
and transfusion reactions.
Causes
 Drug reactions: Certain drugs (e.g., penicillin) can bind to red blood cells and become targets for
antibody-mediated destruction.
 Blood transfusions: Mismatched blood transfusions can lead to the destruction of red blood cells.
 Autoimmune disorders: In diseases like Goodpasture’s syndrome, antibodies attack the
basement membranes in the lungs and kidneys.
Clinical Manifestations
 Hemolytic anemia: Fatigue, pallor, jaundice, dark urine, and shortness of breath.
 Goodpasture’s syndrome: Hemoptysis (coughing up blood), shortness of breath, and blood in the
urine (hematuria).
 Transfusion reaction: Fever, chills, back pain, dark urine, and hypotension.
Diagnostics
 Direct Coombs Test: Detects antibodies bound to the surface of red blood cells.
 Indirect Coombs Test: Detects antibodies in the serum that are free and could bind to red blood
cells.
 Kidney and lung function tests (for Goodpasture’s syndrome) to assess damage.
Medical Interventions
 Corticosteroids: To suppress the immune response and reduce inflammation.
 Immunosuppressive agents: Such as cyclophosphamide for autoimmune conditions.
 Plasmapheresis: To remove circulating antibodies from the blood in severe cases like
Goodpasture’s syndrome.
 Blood transfusions or exchange transfusions: For severe anemia.
Nursing Interventions
1. Monitor for Hemolytic Anemia:
o Assess for signs of anemia (e.g., fatigue, pallor) and jaundice.
o Monitor lab values like hemoglobin, hematocrit, and bilirubin levels.

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 2. Ensure Compatibility for Blood Transfusions:
o Double-check blood type compatibility before transfusion.
o Monitor for any signs of transfusion reactions (e.g., fever, back pain) during and after the
transfusion.
3. Patient Education:
o Teach patients with autoimmune conditions the importance of adhering to
immunosuppressive therapy and regular follow-ups.
3. Type III (Immune Complex Hypersensitivity)
In type III hypersensitivity, immune complexes (antigen-antibody complexes) form in the bloodstream and
get deposited in tissues, leading to inflammation and tissue damage. Examples include systemic lupus
erythematosus (SLE), rheumatoid arthritis, and serum sickness.
Causes
 Autoimmune diseases: SLE and rheumatoid arthritis involve the formation of immune complexes
that deposit in various tissues, leading to chronic inflammation.
 Infections or vaccines: In some cases, the body’s immune response to an infection or vaccine can
lead to excess immune complex formation.
 Medications: Certain drugs can trigger immune complex formation, leading to serum sickness.
Clinical Manifestations
 Systemic lupus erythematosus (SLE): Symptoms vary, but can include fatigue, joint pain, a
butterfly-shaped facial rash, kidney damage (glomerulonephritis), and cardiovascular issues.
 Rheumatoid arthritis: Joint pain, swelling, and stiffness, particularly in the hands and feet.
 Serum sickness: Fever, rash, joint pain, and swollen lymph nodes.
Diagnostics
 Antinuclear antibody (ANA) test: Commonly used in diagnosing autoimmune diseases like SLE.
 Rheumatoid factor (RF) test: Helps diagnose rheumatoid arthritis.
 Complement levels: Low levels of complement proteins (C3, C4) can indicate immune complex
formation.
 Urinalysis: To check for kidney involvement in diseases like SLE (e.g., proteinuria).
Medical Interventions
 Corticosteroids: To reduce inflammation in conditions like SLE and rheumatoid arthritis.
 Immunosuppressive drugs: Such as methotrexate for rheumatoid arthritis and SLE.
 Nonsteroidal anti-inflammatory drugs (NSAIDs): For joint pain and inflammation.
 Plasmapheresis: May be used in severe cases to remove immune complexes.
Nursing Interventions
1. Monitor for Signs of Organ Involvement:
o For SLE, monitor renal function (urine output, blood pressure, and lab values) and watch for
signs of cardiovascular complications.
2. Pain Management:
o Administer NSAIDs and corticosteroids as prescribed.
o Encourage physical therapy to maintain joint mobility in rheumatoid arthritis.
3. Patient Education:
o Educate on recognizing signs of flare-ups (e.g., fever, rash, joint pain).
o Encourage regular monitoring of disease progression through lab tests and doctor visits.
4. Type IV (Delayed Hypersensitivity)
Type IV hypersensitivity is T-cell-mediated and involves a delayed immune response, typically taking 48-
72 hours to develop. This response does not involve antibodies but is cell-mediated. Common examples
include contact dermatitis, tuberculin skin reactions, and transplant rejection.
Causes
 Contact with allergens: Such as poison ivy, latex, or nickel, triggering contact dermatitis.
 Tuberculin skin test (PPD test): A localized skin reaction occurs in individuals previously exposed
to Mycobacterium tuberculosis.
 Chronic infections: Such as tuberculosis or fungal infections.

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  Transplant rejection: Involves T-cell-mediated destruction of transplanted organs.
Clinical Manifestations
 Contact dermatitis: Red, itchy rash that may blister or peel after exposure to an allergen.
 Tuberculin reaction: Red, raised, and hard area at the site of the skin test.
 Transplant rejection: Signs depend on the organ affected (e.g., decreased urine output in kidney
transplant rejection, jaundice in liver transplant rejection).
Diagnostics
 Patch testing: For contact dermatitis to identify allergens.
 Tuberculin skin test (PPD test): For tuberculosis diagnosis.
 Biopsy: Of affected tissues may be needed to diagnose chronic infections or transplant rejection.
Medical Interventions
 Corticosteroids: Topical steroids for contact dermatitis and systemic steroids for severe organ
rejection.
 Immunosuppressive drugs: Such as tacrolimus or cyclosporine for preventing organ transplant
rejection.
 Antibiotics or antifungals: For chronic infections like tuberculosis.
Nursing Interventions
1. Monitor for Signs of Rejection:
o In organ transplant patients, monitor for signs of organ dysfunction (e.g., reduced urine
output for kidney transplants).
2. Skin Care:
o In contact dermatitis, educate the patient to avoid known allergens and use appropriate
topical treatments (e.g., corticosteroids).
3. Infection Control:
o For tuberculosis, ensure patients adhere to prescribed antibiotic regimens and follow up with
regular testing.

 Psoriasis
Psoriasis is a chronic autoimmune skin condition characterized by an abnormally rapid turnover of skin
cells, leading to the buildup of thick, red, scaly patches, often with silver-white scales. It typically affects the
scalp, elbows, knees, and lower back, but it can occur anywhere on the body. Psoriasis can also affect nails
and joints, with some patients developing psoriatic arthritis.

 Causes
 The exact cause of psoriasis is unknown, but it is believed to involve a combination of
genetic and environmental factors that trigger an abnormal immune response. Key elements
include:

 Genetics: Many people with psoriasis have a family history of the condition.
 Immune System Dysfunction: T-cells (a type of white blood cell) mistakenly attack healthy
skin cells, triggering an accelerated skin cell production cycle.
 Environmental Triggers: Factors that can exacerbate or trigger psoriasis flare-ups include:
 Stress
 Skin injuries (e.g., cuts, burns)
 Infections (e.g., streptococcal throat infections)
 Cold weather
 Certain medications (e.g., lithium, beta-blockers)
 Smoking and heavy alcohol consumption

 Assessment
 Skin Examination:

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 o Location: Assess common areas affected by psoriasis, such as the scalp, elbows,
knees, and lower back. Look for red, inflamed patches covered with silvery-white
scales.
o Severity: Assess the extent of the lesions (e.g., localized vs. widespread).

Type of Psoriasis:
 Plaque Psoriasis: The most common form, presenting as raised, red patches covered
with scales.
 Guttate Psoriasis: Characterized by small, drop-shaped lesions.
 Inverse Psoriasis: Appears as red, smooth, and shiny patches, typically in body folds.
 Pustular Psoriasis: Includes pus-filled blisters (rare but severe).
 Nail Assessment:
o Look for signs of nail pitting, discoloration, or separation of the nail from the nail bed
(onycholysis), which are common in psoriasis patients.
 Joint Involvement:
o Screen for symptoms of psoriatic arthritis, such as joint pain, swelling, and stiffness,
particularly in the fingers, toes, and spine.

 Medical Interventions
o Topical Treatments:
 Corticosteroids: Reduce inflammation and slow cell turnover.
 Vitamin D analogs (e.g., Calcipotriene): Help regulate skin cell growth.
 Retinoids: Reduce scaling and skin cell production.
 Coal Tar and Salicylic Acid: Soften and reduce scales.
o Phototherapy (Light Therapy):
o UVB Phototherapy: Involves controlled exposure to ultraviolet light, which slows down
skin cell growth.
o PUVA (Psoralen + UVA): A combination of a drug called psoralen and exposure to UVA
light.

o Systemic Medications:
o Immunosuppressants (e.g., Methotrexate, Cyclosporine): Suppress the immune system
to control inflammation.
o Biologic Drugs (e.g., TNF inhibitors like Infliximab, Adalimumab): Target specific immune
system components to reduce inflammation.
o Oral Retinoids (e.g., Acitretin): Help to normalize skin cell growth.

Lifestyle Changes:
 Moisturizing: Regular moisturizing to prevent dryness and irritation.
 Dietary Adjustments: Maintaining a balanced diet, avoiding known triggers (e.g., alcohol, smoking),
and staying hydrated.

Nursing Interventions
o Patient Education:
o Teach the patient to avoid triggers such as stress and infections.
o Instruct on the proper use of prescribed medications and topical treatments.
o Encourage regular use of moisturizers to prevent skin dryness and cracking.

o Emotional Support:

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 o Help the patient cope with the psychological impact of psoriasis, as it can affect body image and
self-esteem.
o Offer resources for mental health support if needed (e.g., support groups, counseling).
o Skin Care:
o Monitor for signs of skin infections, especially in areas where skin is cracked or inflamed.
o Advise the patient to avoid scratching and use gentle, non-irritating soaps.

Ankylosing Spondylitis (AS)

Ankylosing spondylitis (AS) is a chronic inflammatory arthritis primarily affecting the spine and sacroiliac
joints, causing pain, stiffness, and progressive fusion of the vertebrae. It can also affect other joints and
organs, including the eyes (causing uveitis), lungs, and heart.

Causes
The exact cause of AS is unknown, but it is thought to involve genetic and environmental factors. Key
contributors include:
Genetics: The HLA-B27 gene is strongly associated with ankylosing spondylitis, though not all people with
the gene develop the disease.
Immune System Dysfunction: AS is considered an autoimmune disease, where the immune system attacks
the joints, especially those of the spine and pelvis.
Environmental Triggers: Infections and other unknown factors may trigger the onset of symptoms in
genetically susceptible individuals.

Assessment
Pain Assessment:
 Assess for chronic back pain and stiffness, particularly in the lower back and sacroiliac joints. The
pain is often worse in the morning or after periods of inactivity and improves with movement.
 Ask the patient about nocturnal back pain that may wake them up from sleep.
Posture and Mobility Assessment:
 Observe for signs of progressive spinal stiffness or loss of flexibility. Over time, this can lead to a
stooped posture or kyphosis (forward curvature of the spine).
 Perform Schober’s test to assess lumbar spine mobility.
Joint and Soft Tissue Involvement:
 Assess peripheral joints (e.g., hips, knees, shoulders) for pain, swelling, and limited range of
motion.
 Examine for enthesitis (inflammation of the sites where tendons and ligaments attach to bone),
especially in the heels and lower back.
Extra-Articular Manifestations:
 Eye Involvement: Screen for signs of uveitis (eye inflammation), which can cause eye redness,
pain, and blurred vision.
Chest and Lung Assessment:
 Ask about chest pain or difficulty breathing, as AS can cause reduced chest expansion due to
inflammation of the rib joints.
Cardiovascular Assessment:
 Monitor for any signs of aortic inflammation or conduction abnormalities.

Medical Interventions
 The goals of treatment for AS are to relieve pain, reduce inflammation, and prevent spinal deformity.
Management typically involves:
 Medications:
 Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): (e.g., Ibuprofen, Naproxen) reduce inflammation
and pain.

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  Tumor Necrosis Factor (TNF) Inhibitors: (e.g., Etanercept, Infliximab) block the inflammatory protein
TNF, slowing disease progression.
 Interleukin-17 (IL-17) Inhibitors: (e.g., Secukinumab) target other pathways of inflammation.
 Corticosteroids: Short-term use to manage flare-ups.
 Disease-Modifying Anti-Rheumatic Drugs (DMARDs): (e.g., Methotrexate, Sulfasalazine) for
peripheral joint involvement.

Physical Therapy:
 Helps maintain flexibility and posture through exercises that improve spinal mobility and strengthen
core muscles.
 Stretching exercises to reduce stiffness and maintain range of motion.

Surgical Intervention:
 Surgery may be considered in severe cases, particularly if spinal fusion or joint replacement (e.g.,
hips) is required due to advanced deformity.

Lifestyle Modifications:
 Posture Training: Maintaining good posture is crucial in preventing or reducing spinal deformity.
 Exercise: Regular low-impact exercise (e.g., swimming, yoga) is encouraged to maintain flexibility.
 Quit Smoking: Smoking worsens lung function and inflammation, and can accelerate disease
progression.

Nursing Interventions

Pain Management:
 Administer prescribed NSAIDs or biologics as ordered.
 Encourage the use of heat or cold therapy to relieve muscle and joint stiffness.
Promoting Mobility:
 Educate the patient on proper body mechanics and posture alignment to minimize spinal deformity.
 Encourage adherence to physical therapy exercises and routines.
Patient Education:
 Educate on the importance of regular physical activity to maintain joint mobility and flexibility.
 Instruct on the proper use of medications, including potential side effects and monitoring
requirements.
Monitor for Complications:
 Watch for signs of extra-articular complications, such as eye pain or blurred vision (uveitis),
shortness of breath (lung involvement), and chest pain (heart involvement).
 Ensure regular follow-up with healthcare providers to monitor disease progression and adjust
treatment as necessary.

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