NR 283 Exam 1

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Chamberlain University

NR-283: Pathophysiology

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NR283 Pathophysiology Study Guide for Exam 1

Chapter 1: Introduction to Pathology

1. Describe the cellular adaptations made in each of the following processes and their causative factors: atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia

Cellular adaptation refers to the ability of cells to adjust in response to environmental changes, stress, or injury. These adaptations can be beneficial or may signal the onset of disease if the stimulus is persistent or severe.

Table 1 below summarizes each type of cellular adaptation and its primary causes.

Adaptation Type	Description	Common Causes	Clinical Examples
Atrophy	Reduction in the size of cells, leading to decreased tissue mass.	Decreased functional demand, poor nutrition, loss of hormonal/neural stimulation, aging.	Muscle wasting in limb immobilization; brain atrophy in dementia.
Hypertrophy	Enlargement of individual cells, increasing tissue mass.	Increased functional demand, hormonal stimulation.	Myocardial hypertrophy from hypertension.
Hyperplasia	Increase in the number of cells, leading to tissue enlargement.	Hormonal stimulation, compensation after tissue loss, chronic irritation.	Endometrial hyperplasia; liver regeneration after partial hepatectomy.
Dysplasia	Abnormal variation in cell size, shape, and organization; often increased mitotic rate.	Chronic irritation, inflammation, precancerous changes.	Cervical dysplasia detected by Pap smear.
Metaplasia	Replacement of one mature cell type by another mature type better suited to stress.	Chronic irritation, vitamin A deficiency.	Replacement of ciliated columnar epithelium by stratified squamous epithelium in smokers.

These changes are often reversible if the causative factor is removed. However, dysplasia is considered premalignant and warrants close monitoring.

3. Identify the most common cause of cellular injury

The leading cause of cellular injury is ischemia—an inadequate supply of oxygenated blood to tissues due to obstructed blood flow. This results in hypoxia, impairing ATP production and cellular metabolism.

Other causes of cellular injury include:

• Physical agents: Extreme heat, cold, or radiation exposure.
• Mechanical trauma: Pressure, tearing, or crushing of tissue.
• Chemical agents: Toxins, drugs, pollutants.
• Biologic agents: Bacteria, viruses, parasites.
• Metabolic imbalances: Accumulation of abnormal metabolites.
• Nutritional deficiencies or electrolyte disturbances.

Ischemic injury can lead to rapid cell death if not reversed, particularly in high-metabolic-demand tissues such as the brain and heart.

4. Describe cellular injury caused by infection and inflammation

Infectious agents such as bacteria, viruses, and fungi can directly damage cells or trigger immune-mediated injury. Some pathogens activate pyroptosis, a programmed cell death pathway characterized by plasma membrane rupture and release of inflammatory mediators.

Inflammation accompanying infection results in:

• Increased vascular permeability.
• Swelling and pain due to fluid accumulation.
• Local tissue damage from enzymes and reactive oxygen species released by immune cells.

Prolonged or excessive inflammation can impair tissue function and promote chronic disease.

5. Describe the major mechanism of tissue damage caused by chemical injury

Chemical injury occurs when exogenous agents (from outside the body) or endogenous compounds (produced internally) disrupt cell function.

Mechanisms include:

• Altering cell membrane permeability, impairing transport of ions and nutrients.
• Generating free radicals, which damage proteins, lipids, and nucleic acids.
• Disrupting mitochondrial activity, reducing ATP production.

Examples:

• Carbon monoxide binding to hemoglobin (reducing oxygen transport).
• Acetaminophen overdose causing hepatocyte necrosis via toxic metabolite buildup.

6. Discuss the manifestations of the four major types of necrosis, and give examples of the tissue types affected by each type of necrosis

Necrosis is uncontrolled cell death due to injury, leading to inflammation and tissue destruction.

Type of Necrosis	Pathologic Process	Common Sites	Example Conditions
Liquefaction	Dead cells are digested by enzymes, forming a liquid mass.	Brain, abscess cavities.	Stroke, bacterial brain abscess.
Coagulative	Cell proteins denature; cell outlines remain temporarily intact.	Heart, kidney, adrenal glands.	Myocardial infarction.
Fat	Lipases break down fat into fatty acids, which bind calcium (saponification).	Breast, pancreas.	Acute pancreatitis.
Caseous	Combination of coagulative and liquefactive necrosis, producing a soft, cheese-like material.	Lungs, lymph nodes.	Tuberculosis with Ghon complex formation.

7. Discuss apoptosis

Apoptosis is a programmed cell death process essential for normal tissue development, immune regulation, and removal of damaged cells. Unlike necrosis, it does not cause inflammation.

Key features:

• Cell shrinkage and chromatin condensation.
• Formation of membrane-bound apoptotic bodies.
• Phagocytosis by neighboring cells or macrophages.

NR 283 Exam 1

Triggers include:

• DNA damage.
• Viral infections.
• Excessive or defective cell proliferation.
• Aging

Chapter 02: Fluids and Electrolytes, Acids and Bases

1. Discuss the two functional fluid compartments of the body

The body’s total water content is distributed into two main compartments:

1. Intracellular Fluid (ICF) Compartment
   • Found inside cells.
   • Accounts for roughly two-thirds of total body water and approximately 40% of total body weight.
   • Functions include maintaining cellular shape, enabling metabolic reactions, and stabilizing cell organelles.
2. Extracellular Fluid (ECF) Compartment
   • Located outside cells.
   • Comprises about one-third of total body water and includes:
     • Intravascular fluid – plasma and other components in blood vessels.
     • Interstitial fluid – fluid between cells.
     • Cerebrospinal fluid (CSF) – protects brain and spinal cord.
     • Transcellular fluids – specialized fluids in spaces such as the pericardial, pleural, and synovial cavities.

2. Discuss the ways water moves between plasma and interstitial fluid

Water moves between the vascular compartment (plasma) and the interstitial compartment through capillary membranes, driven by:

• Hydrostatic pressure – pushes fluid out of capillaries.
• Osmotic pressure – pulls fluid into capillaries due to solute concentration (mainly plasma proteins).

Process:

• Arteriolar end – Hydrostatic pressure exceeds osmotic pressure → fluid moves out into interstitial space.
• Venous end – Osmotic pressure exceeds hydrostatic pressure → fluid returns into capillaries.

3. Describe the causation, pathophysiologic process, and clinical manifestations of edema

Edema is an abnormal accumulation of fluid in the interstitial compartment. It may be localized or generalized.

Causes include:

1. Increased capillary hydrostatic pressure – often due to elevated blood pressure or increased blood volume.
2. Loss of plasma proteins (albumin) – reduces plasma osmotic pressure; can occur in malnutrition, liver disease, or nephrotic syndrome.
3. Obstruction of lymphatic drainage – prevents protein and fluid return to circulation.
4. Increased capillary permeability – due to inflammation, burns, or allergic reactions.

Clinical manifestations:

• Swelling (localized or generalized).
• Weight gain.
• Pale or reddened skin.
• Pulmonary congestion → cough, shortness of breath.
• Possible impaired wound healing due to poor oxygen delivery.

Table 2: Summary of Edema Causes and Effects

NR 283 Exam 1

Cause	Mechanism	Example Condition
↑ Hydrostatic pressure	Forces fluid out of capillaries	CHF, pregnancy
↓ Plasma proteins	Less osmotic pull back into capillaries	Liver failure, malnutrition
Lymphatic obstruction	Accumulated proteins & fluid	Tumor blocking lymph nodes
↑ Capillary permeability	Protein leakage → fluid retention in interstitial space	Burns, allergic reaction

4. Discuss the regulatory processes for sodium and water balance in the body, including the role of antidiuretic hormone, renin-angiotensin-aldosterone

Antidiuretic Hormone (ADH)

• Secreted by the posterior pituitary.
• Promotes water reabsorption from kidney tubules → reduces urine output.

Aldosterone

• Produced by adrenal cortex.
• Promotes sodium reabsorption and water retention, while increasing potassium excretion.

Renin-Angiotensin-Aldosterone System (RAAS)

1. Low BP/Na⁺ → kidneys release renin.
2. Renin converts angiotensinogen → angiotensin I.
3. ACE (lungs) converts angiotensin I → angiotensin II.
4. Angiotensin II causes vasoconstriction and stimulates aldosterone release.
5. Aldosterone increases Na⁺ and water retention → raises BP and volume.

5. Identify the basic causes and clinical manifestations of hypernatremia, hyponatremia, hyperkalemia, hypokalemia, hypocalcemia, and hypercalcemia

Table 3: Electrolyte Imbalances

Condition	Common Causes	Key Signs/Symptoms
Hypernatremia	Excess Na⁺ intake, water loss, diabetes insipidus	Thirst, dry mucosa, weakness, agitation, edema, ↑ BP
Hyponatremia	Excess fluid intake, diuretics, adrenal insufficiency	Nausea, cramps, confusion, seizures, ↓ BP
Hyperkalemia	Renal failure, tissue injury, K⁺-sparing diuretics	Arrhythmias, muscle weakness, paresthesia
Hypokalemia	Diuretics, vomiting, diarrhea, poor intake	Arrhythmias, constipation, muscle cramps
Hypercalcemia	Bone destruction, hyperparathyroidism, immobility	Lethargy, constipation, kidney stones, arrhythmias
Hypocalcemia	Hypoparathyroidism, vit. D deficiency, alkalosis	Tetany, muscle spasms, arrhythmias

6. Discuss the causes, clinical manifestations, complications of water deficit (hypovolemia)

Causes: Severe diarrhea, vomiting, hemorrhage, burns, excessive sweating, poor intake.

Pathophysiology: Fluid loss reduces circulating blood volume → decreased tissue perfusion → cellular hypoxia.

Symptoms:

• Thirst, dry mucous membranes.
• Weak pulse, hypotension.
• Weight loss.
• Dizziness, confusion.

Complications: Shock, organ failure.

7. Discuss the causes, clinical manifestations, complications of water excess (hypervolemia)

Causes: Kidney failure, excessive IV fluids, heart failure, excessive sodium intake.

Symptoms:

• Edema, weight gain.
• Hypertension, bounding pulse.
• Pulmonary congestion, dyspnea.

8. Explain the buffer systems that regulate acid-base balance in the body

The body’s pH is tightly maintained between 7.35 and 7.45 to ensure proper enzyme function and metabolic activity. This balance is regulated by buffer systems, respiratory control, and renal function.

Major buffer systems:

Buffer System	Components	Primary Action	Speed
Bicarbonate-Carbonic Acid	H₂CO₃ (carbonic acid) / NaHCO₃ (bicarbonate)	Neutralizes acids or bases; works with respiratory and renal systems	Seconds to minutes
Phosphate Buffer	NaH₂PO₄ / Na₂HPO₄	Important in intracellular and renal tubular fluids	Minutes
Protein Buffers	Hemoglobin, plasma proteins	Bind or release hydrogen ions	Immediate
Hemoglobin Buffer	Oxyhemoglobin and deoxyhemoglobin	Buffers acids in RBCs and assists CO₂ transport	Seconds

The bicarbonate buffer is the most important extracellular system, while proteins and phosphates dominate intracellular buffering.

9. Describe the compensatory mechanisms that occur in response to changes in blood pH

When blood pH deviates from the normal range:

1. Respiratory Compensation
   • If pH decreases (acidosis) → respiratory rate increases to blow off CO₂, reducing hydrogen ion concentration.
   • If pH increases (alkalosis) → respiratory rate decreases, retaining CO₂ to raise hydrogen ion concentration.
2. Renal Compensation
   • Kidneys excrete hydrogen ions and retain bicarbonate in acidosis.
   • Kidneys retain hydrogen ions and excrete bicarbonate in alkalosis.
   • Slower process (hours to days) but more effective for long-term regulation.

10. Discuss the causes, clinical manifestations, and compensations for respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis

Table 4: Acid-Base Imbalances

Disorder	Common Causes	Signs & Symptoms	Compensation
Respiratory Acidosis	Hypoventilation (COPD, drug overdose, airway obstruction) → CO₂ retention	Headache, confusion, drowsiness, ↑ PaCO₂	Kidneys retain HCO₃⁻, excrete H⁺
Respiratory Alkalosis	Hyperventilation (anxiety, high altitude, fever) → ↓ CO₂	Lightheadedness, tingling, seizures, ↓ PaCO₂	Kidneys excrete HCO₃⁻, retain H⁺
Metabolic Acidosis	DKA, renal failure, diarrhea (HCO₃⁻ loss)	Kussmaul respirations, weakness, ↓ HCO₃⁻	Lungs blow off CO₂; kidneys excrete H⁺
Metabolic Alkalosis	Vomiting, NG suction, diuretics	Irritability, muscle cramps, ↑ HCO₃⁻	Lungs retain CO₂; kidneys retain H⁺

11. Explain why older adults are more vulnerable to fluid and electrolyte imbalances

Older adults have:

• Decreased total body water → smaller fluid reserve.
• Reduced kidney function → impaired concentration/dilution ability.
• Blunted thirst sensation → reduced fluid intake.
• Chronic health conditions (e.g., heart failure, diabetes) that predispose to imbalances.
• Polypharmacy (diuretics, laxatives) increasing loss of fluids/electrolytes.

Chapter 05: Inflammation, Infection, and Skin Disorders

1. Pruritus

Definition: Pruritus refers to itching that may occur with allergic responses, chemical irritation (e.g., insect bites), or parasitic infestations (e.g., scabies).

Pathophysiology: Often caused by histamine release during a hypersensitivity reaction. Mild stimulation of pain receptors by irritants may also contribute.

Clinical Manifestations:

• Redness (erythema)
• Persistent itchiness
• Scratching may increase inflammation and lead to secondary infections by breaking the skin barrier, allowing microbial entry.

2. Forms of Dermatitis

Type	Cause	Key Signs & Symptoms	Treatment
Contact Dermatitis	Exposure to allergen (type IV cell-mediated hypersensitivity) or chemical/mechanical irritation	Localized pruritic and erythematous area; often with small vesicles	Remove irritant; topical glucocorticoids
Urticaria (Hives)	Type I hypersensitivity (often ingested allergens: shellfish, fruits, drugs)	Raised erythematous lesions, scattered or generalized; highly pruritic	Antihistamines; corticosteroids for severe cases
Atopic Dermatitis (Eczema)	Chronic allergic inflammation (type I hypersensitivity); elevated IgE and eosinophils	Children: moist, red vesicular lesions with crusts on face, neck, limbs, buttocks. Adults: dry, scaling, thickened (lichenified) patches	Identify & avoid triggers; topical glucocorticoids; antihistamines; moisturizers
Psoriasis	Chronic inflammatory disorder; abnormal T-cell activation and cytokine release	Red plaques with silvery scales; may involve face, scalp, elbows, knees; nail changes; joint stiffness	Topical glucocorticoids; tar preparations; methotrexate (severe); UV light
Pemphigus	Autoimmune disorder; antibodies disrupt cohesion between epidermal cells	Painful, non-pruritic blisters starting in mouth/scalp → spread to skin; possible airway involvement	Systemic glucocorticoids; immunosuppressants
Scleroderma	Cause unknown; collagen deposition → fibrosis & vascular narrowing	Hard, shiny, immovable skin; narrowed fingertips; facial tightening; Raynaud’s phenomenon; may affect internal organs	NSAIDs, corticosteroids, immunosuppressants; vasodilators for vascular disease

3. Selected Infections and Infestations

Table: Key Skin Disorders

Disorder	Etiology	Manifestations
Discoid Lupus Erythematosus	Autoimmune; chronic skin form of lupus	Red, inflamed patches with scaling/crusting, often on face, ears, scalp
Tinea (Ringworm)	Dermatophyte fungal infection	Circular red rings, itching/burning; types: capitis (scalp), pedis (feet), corporis (body), cruris (groin), unguium (nails)
Candidiasis	Candida albicans overgrowth (often after antibiotics)	Red, moist patches; possible white exudate
Herpes Zoster (Shingles)	Reactivated varicella-zoster virus	Pain along dermatome → vesicular rash; more severe in immunocompromised
Impetigo	S. aureus or streptococci	Vesicles → yellow-brown crusts; pruritus; contagious
Folliculitis	S. aureus infection of hair follicles	Red bumps or pustules; may follow ingrown hairs
Furuncle (Boil)	S. aureus deep infection of hair follicle	Painful, firm nodule with pus; risk of spreading
Cellulitis	S. aureus infection of dermis/subcutaneous tissue	Red, swollen, painful skin; often lower legs
Carbuncle	Cluster of interconnected furuncles	Large, draining abscess
Leprosy	Mycobacterium leprae	Skin, nerve, mucous membrane damage; possible limb loss
Acute Necrotizing Fasciitis	Mixed aerobic/anaerobic bacteria	Rapid tissue destruction, severe pain, systemic toxicity
HPV (Human Papillomavirus)	Viral infection	Warts (verrucae); genital warts (types 6 & 11)
Scabies	Sarcoptes scabiei mite	Intense itching, burrows in skin with eggs/larvae
Pediculosis (Lice)	Pediculus humanus	Itchy scalp/body; visible lice/nits

4. Skin Cancers

Keratoses (Benign Lesions)

• Seborrheic Keratoses: Basal cell proliferation; dark, elevated lesions on face/trunk.
• Actinic Keratoses: Sun-exposed skin; rough, scaly patches; may progress to squamous cell carcinoma.

Squamous Cell Carcinoma (SCC)

• Malignant epidermal tumor, often from sun exposure.
• Signs: Reddish, scaly lesion with irregular borders; may ulcerate.
• Early detection → good prognosis.

NR 283 Exam 1

Malignant Melanoma

• Arises from melanocytes; often from changing nevi (ABCDE signs: Asymmetry, Border irregularity, Color variation, Diameter >6 mm, Evolving).
• Rapid growth, early metastasis → poor prognosis if advanced.
• Tx: Surgical excision; chemo/radiation for spread.

Kaposi Sarcoma

• Vascular tumor linked to HHV-8; common in immunosuppressed (HIV/AIDS).
• Purplish macules → nodules; may involve skin and organs.
• Tx: Combination of chemo, radiation, surgery, biologic therapy.

NR 283 Exam 1