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Maximize your academic achievement with this comprehensive NUR 650 Advanced Pathophysiology Exam 2 Question Bank for the 2026/2027 academic year. Designed as an elite exam preparation workbook and study guide, this asset features over 100 high-yield practice questions accompanied by detailed explanations and evidence-based rationales. Mastery of core concepts is simplified with targeted coverage on cellular injury cascades, mechanisms of ATP depletion, reversible vs. irreversible cell injury, necrosis types (coagulative, liquefactive, caseous, fat, and gangrenous), cellular adaptations (atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia), and acute vs. chronic inflammation.NUR 650, Advanced Pathophysiology, NUR 650 Exam 2, Pathophysiology Question Bank, Pathophysiology Test Bank, Exam Preparation Workbook, Study Guide, Revision Guide, Practice Questions, Mock Exam Preparation, Comprehensive Review, High-Yield Concepts, Detailed Explanations, Final Exam Review, Midterm Review
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Exam Practice 100+ Questions & Answers with Rationales
Question 1
Correct Answer: B
Rationale: ATP depletion impairs the Na⁺/K⁺ATPase pump, which depends on ATP to maintain ion gradients. When the pump fails, sodium accumulates inside the cell, drawing in water and causing cell swelling. This is an early and reversible event in ischemic injury. Membrane rupture and caspase activation occur later or through different pathways.
Question 2
Correct Answer: B
Rationale: Lethal cell injury is associated with a marked rise in intracellular calcium. Calcium activates destructive enzymes including phospholipases, proteases, and endonucleases, which degrade membranes, proteins, and DNA. This calcium influx is a hallmark of irreversible injury. ATP synthesis falls rather than rises in lethal injury.
Question 3
Correct Answer: C
Rationale: Necrosis refers to the pathological death of cells or tissues within a living organism, typically resulting from external injury, ischemia, or infection. Apoptosis is programmed cell death and differs in mechanism and morphology. Atrophy is a
Cellular Injury
A. Immediate cell membrane rupture
B. Failure of the sodiumpotassium pump
C. Activation of apoptotic caspases
D. Increased oxidative phosphorylation
Cellular Injury
A. Decreased intracellular sodium
B. Increased intracellular calcium
C. Increased ATP synthesis
D. Decreased intracellular water
Cell Death
A. Apoptosis
B. Atrophy
C. Necrosis
D. Autolysis
reduction in cell size. Autolysis occurs after the organism has died.
Question 4
Correct Answer: C
Rationale: Failure of the Na⁺/K⁺ATPase pump during ischemia causes sodium to accumulate inside the cell. This increase in intracellular sodium raises osmotic pressure, drawing water into the cell and causing cellular swelling, also called hydropic change. Potassium leaks out of the cell rather than accumulating. Calcium also enters but through different mechanisms.
Question 5
Correct Answer: B
Rationale: Hypertrophy is an increase in the size of individual cells in response to increased workload or hormonal stimulation. Skeletal muscle enlargement from exercise is a classic physiological example. Hyperplasia involves an increase in cell number. Metaplasia is the replacement of one cell type with another. Dysplasia refers to disordered cell growth.
Question 6
Correct Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type by another, typically in response to chronic irritation. Cigarette smoke induces squamous metaplasia in bronchial epithelium. This adaptation protects against injury but removes normal mucociliary function. Dysplasia involves architectural disorganization and is considered preneoplastic.
Cellular Injury
A. Potassium
B. Chloride
C. Sodium
D. Magnesium
Cellular Adaptations
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Cellular Adaptations
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Atrophy
Correct Answer: C
Rationale: Liquefactive necrosis occurs when enzymatic digestion of dead cells produces a liquid viscous mass. This is most characteristic of brain infarcts and bacterial abscesses, where proteolytic enzymes from leukocytes or microorganisms liquefy the tissue. Myocardial infarction produces coagulative necrosis. Acute pancreatitis produces fat necrosis. Tuberculosis produces caseous necrosis.
Question 11
Correct Answer: B
Rationale: Free radicals are highly reactive molecules that cause cell injury by oxidizing lipids in cell membranes, crosslinking and inactivating proteins, and damaging DNA. This process is called oxidative stress. Antioxidants such as superoxide dismutase, catalase, and glutathione normally neutralize free radicals. Free radical injury plays a role in ischemiareperfusion injury, chemical toxicity, and aging.
Question 12
Correct Answer: B
Rationale: Cell swelling, also called hydropic change or cloudy swelling, is the earliest and most common manifestation of reversible cell injury. It results from failure of energydependent ion pumps, leading to sodium and water accumulation. Membrane blebbing is also seen early. Nuclear changes and lysosomal rupture are features of irreversible injury and cell death.
Question 13
A. Myocardial infarction
B. Acute pancreatitis
C. Bacterial brain abscess
D. Pulmonary tuberculosis
Cellular Injury
A. Direct inhibition of the sodiumpotassium ATPase
B. Oxidation of lipids, proteins, and nucleic acids
C. Activation of the complement cascade
D. Precipitation of intracellular proteins
Cellular Injury
A. Nuclear fragmentation
B. Membrane blebbing and cell swelling
C. Lysosomal rupture
D. Mitochondrial calcification
Inflammation
A. Pallor, pain, hypothermia, edema, and immobility
B. Redness, warmth, swelling, pain, and loss of function
C. Cyanosis, fever, hyperemia, rigidity, and bleeding
D. Erythema, pruritis, scaling, induration, and atrophy
Correct Answer: B
Rationale: The five cardinal signs of acute inflammation, described by Celsus and Virchow, are rubor (redness), calor (heat), tumor (swelling), dolor (pain), and functio laesa (loss of function). These result from vasodilation, increased vascular permeability, and leukocyte migration into tissues. They represent the body's response to injury or infection.
Question 14
Correct Answer: B
Rationale: Histamine is one of the first mediators released in acute inflammation, primarily from mast cells, basophils, and platelets. It causes vasodilation and increases vascular permeability by causing endothelial cell contraction, allowing plasma proteins and fluid to leak into tissues. Interleukin10 and TGFbeta are antiinflammatory. Interferongamma activates macrophages in chronic inflammation.
Question 15
Correct Answer: C
Rationale: Neutrophils are the first leukocytes to emigrate from the bloodstream into inflamed tissues, typically within 6 to 24 hours. They are the dominant cell in early acute inflammation and are responsible for phagocytosing bacteria and debris. Macrophages arrive later (24 to 48 hours) and predominate in chronic inflammation. Lymphocytes are central to adaptive immunity.
Question 16
Correct Answer: C
Inflammation
A. Interleukin
B. Histamine
C. Interferongamma
D. Transforming growth factorbeta
Inflammation
A. Macrophage
B. Lymphocyte
C. Neutrophil
D. Eosinophil
Inflammation
A. Neutrophils
B. Eosinophils
C. Macrophages and lymphocytes
D. Mast cells
driver of scar formation. TNFalpha and IL6 are proinflammatory cytokines. Interferongamma activates macrophages and inhibits fibrosis.
Question 20
Correct Answer: B
Rationale: An embolus is any intravascular mass, solid, liquid, or gas, carried in the bloodstream to a site distant from its origin. Most emboli arise from thrombi (thromboembolism). Common destinations include the pulmonary vasculature (from deep vein thrombosis) and the cerebral circulation (from cardiac thrombi). An infarct is the resulting area of ischemic necrosis, not the traveling mass itself.
Question 21
Correct Answer: B
Rationale: Cardiogenic shock results from failure of the heart to pump sufficient blood to meet the metabolic demands of the body. Common causes include massive myocardial infarction, severe arrhythmias, and endstage cardiomyopathy. It is characterized by low cardiac output, high systemic vascular resistance, and signs of endorgan hypoperfusion. Septic shock involves vasodilation; hypovolemic shock involves volume loss.
Question 22
Correct Answer: C
Rationale: An infarct is a localized area of ischemic necrosis caused by interruption of the blood supply to a tissue. The morphology depends on the tissue type and whether the infarct is pale (anemic) or red (hemorrhagic). Pale infarcts occur in solid organs with single blood supply. Red infarcts occur in tissues with dual circulation or after reperfusion.
Hemodynamic Disorders
A. Infarct
B. Embolus
C. Thrombus
D. Vegetation
Hemodynamic Disorders
A. Massive peripheral vasodilation leading to decreased systemic vascular resistance
B. Pump failure of the heart resulting in decreased cardiac output and tissue hypoperfusion
C. Absolute volume depletion due to hemorrhage or dehydration
D. Distributive failure due to systemic release of inflammatory mediators
Hemodynamic Disorders
A. Abscess
B. Granuloma
C. Infarct
D. Embolus
Question 23
Correct Answer: B
Rationale: Plasma oncotic pressure is maintained primarily by albumin. When albumin levels fall significantly, as in liver failure, nephrotic syndrome, or malnutrition, the oncotic pressure holding fluid within the vascular space decreases. Fluid leaks into the interstitium, causing edema. This is distinct from edema caused by increased hydrostatic pressure, which occurs in heart failure.
Question 24
Correct Answer: C
Rationale: The classic sequence of ischemic cell injury begins with ATP depletion, which inactivates the Na⁺/K⁺ATPase pump. Sodium accumulates intracellularly, drawing in water and causing cell swelling. Subsequently, calcium influx activates destructive enzymes (phospholipases, proteases, endonucleases), leading to irreversible injury and necrosis. Understanding this cascade is fundamental to pathophysiology.
Question 25
Correct Answer: B
Rationale: An adenoma is a benign tumor derived from glandular or epithelial tissue. Examples include colonic polyps and pituitary adenomas. Adenocarcinoma is the malignant counterpart arising from glandular epithelium. Lipoma is a benign tumor of adipose tissue and fibroma arises from fibrous connective tissue. The suffix "oma" generally denotes a benign neoplasm, while "carcinoma" or "sarcoma" denotes malignancy.
Question 26
Fluid and Electrolyte Disorders
A. Increased hydrostatic pressure in capillaries
B. Decreased oncotic pressure allowing fluid to leak into interstitium
C. Lymphatic obstruction preventing fluid drainage
D. Increased sodium reabsorption by the kidneys
Cellular Injury
A. Ca²⁺ influx → ATP depletion → Na⁺ accumulation → cell swelling
B. Membrane rupture → Na⁺ influx → ATP depletion → necrosis
C. ATP depletion → Na⁺/K⁺ pump failure → Na⁺ and water influx → cell swelling → Ca²⁺ influx → irreversible injury
D. Free radical formation → pump failure → apoptosis → coagulative necrosis
Neoplasia
A. Adenocarcinoma
B. Adenoma
C. Lipoma
D. Fibroma
Neoplasia
Correct Answer: D
Rationale: Type I hypersensitivity (immediate/anaphylactic) reactions are mediated by IgE antibodies. Upon first exposure to an antigen, IgE is produced and binds to mast cells and basophils. On reexposure, the antigen crosslinks IgE, triggering degranulation and release of histamine and other mediators. Examples include allergic rhinitis, asthma, and anaphylaxis. IgG mediates Type II and III reactions.
Question 30
Correct Answer: B
Rationale: Autoimmune diseases result from loss of selftolerance, in which the immune system fails to recognize selfantigens and mounts an immune response against the body's own tissues. Examples include rheumatoid arthritis, systemic lupus erythematosus, type 1 diabetes mellitus, and multiple sclerosis. The etiology involves genetic susceptibility and environmental triggers.
Question 31
Correct Answer: C
Rationale: T lymphocytes are the central mediators of cellmediated immunity. CD4+ T helper cells coordinate immune responses by releasing cytokines, while CD8+ cytotoxic T cells directly kill infected or malignant cells. Cellmediated immunity is critical for defense against intracellular pathogens, viruses, fungi, and tumor cells. B lymphocytes and plasma cells mediate humoral (antibodybased) immunity.
Question 32
Correct Answer: C
Immunity
A. A deficiency in innate immune function leading to recurrent infections
B. An immune response directed against the body's own tissues
C. A reaction to an exogenous antigen leading to inflammation
D. Loss of Bcell function resulting in decreased antibody production
Immunity
A. B lymphocytes
B. Plasma cells
C. T lymphocytes
D. Natural killer cells
Cellular Adaptations
A. Uterine enlargement during pregnancy
B. Liver regeneration after partial hepatectomy
C. Endometrial hyperplasia due to unopposed estrogen
D. Skeletal muscle hypertrophy from exercise
Rationale: Pathological hyperplasia results from excessive or inappropriate hormonal or growth factor stimulation. Endometrial hyperplasia caused by excess estrogen is a classic example and carries a risk of malignant transformation. Physiological hyperplasia includes uterine enlargement during pregnancy and liver regeneration after injury, which are normal, controlled responses. Skeletal muscle enlargement is hypertrophy, not hyperplasia.
Question 33
Correct Answer: C
Rationale: Mitochondria are the primary sites of ATP production through oxidative phosphorylation. During ischemia, oxygen deprivation halts mitochondrial respiration, rapidly depleting cellular ATP. Mitochondrial swelling and membrane dysfunction are among the earliest ultrastructural changes in cell injury. Loss of mitochondrial membrane potential is also a key trigger of apoptosis in the intrinsic pathway.
Question 34
Correct Answer: B
Rationale: Reversible cell injury refers to changes that can be corrected if the cause is eliminated before cell death occurs. Features include cell swelling, fatty change, and reduced ATP. Irreversible injury results in cell death, either by necrosis or apoptosis, and is characterized by severe membrane damage, massive calcium influx, and mitochondrial permeabilization. The distinction is clinically important in conditions such as myocardial ischemia.
Question 35
Correct Answer: B
Rationale: Apoptosis is programmed cell death characterized by cell shrinkage, chromatin condensation (pyknosis), nuclear fragmentation, and formation of apoptotic bodies that are phagocytosed without inflammation. In contrast, necrosis involves
Cellular Injury
A. Golgi apparatus
B. Endoplasmic reticulum
C. Mitochondria
D. Lysosomes
Cellular Injury
A. Reversible injury involves DNA fragmentation; irreversible injury involves cell swelling
B. Reversible injury can be corrected if the injurious stimulus is removed; irreversible injury leads to cell death
C. Reversible injury always leads to necrosis; irreversible injury leads to apoptosis
D. Reversible injury involves calcium influx; irreversible injury involves sodium influx
Cell Death
A. Triggers an inflammatory response and involves cell swelling
B. Involves cell shrinkage, chromatin condensation, and no inflammatory response
C. Is always pathological and caused by external injury
D. Results in plasma membrane disruption and release of intracellular contents
pulmonary embolism. Classic presentation includes sudden dyspnea, pleuritic chest pain, and hypoxia. This is a common and potentially fatal postoperative complication.
Question 39
Correct Answer: B
Rationale: In congestive heart failure, impaired cardiac pumping leads to increased venous hydrostatic pressure. This elevated pressure forces fluid from the capillaries into the interstitial space, resulting in dependent edema. The increased hydrostatic pressure overcomes the oncotic pressure keeping fluid within the vasculature. This is distinct from edema caused by low albumin or inflammatory mediators.
Question 40
Correct Answer: B
Rationale: Normal serum sodium ranges from 135 to 145 mEq/L. Hyponatremia is defined as a serum sodium below 135 mEq/L. It can result from water excess (dilutional), sodium deficit, or both. Symptoms range from mild nausea and headache to severe neurological manifestations including seizures and coma, depending on the severity and rate of decline.
Question 41
Correct Answer: B
Rationale: Ischemia refers to the deprivation of blood supply, resulting in deficient delivery of oxygen and nutrients to cells. This impairs mitochondrial respiration and ATP production. Ischemia is distinct from hypoxia, which involves only oxygen deprivation without loss of metabolite delivery and waste removal. Ischemia is more damaging than hypoxia alone because waste products also accumulate.
Fluid and Electrolyte Disorders
A. Decreased oncotic pressure due to hypoalbuminemia
B. Increased hydrostatic pressure due to venous congestion
C. Lymphatic obstruction from tumor invasion
D. Increased vascular permeability from inflammation
Fluid and Electrolyte Disorders
A. 145 mEq/L
B. 135 mEq/L
C. 125 mEq/L
D. 115 mEq/L
Cellular Injury
A. Direct toxinmediated disruption of the cell membrane
B. Deprivation of oxygen and nutrient supply to metabolically active tissue
C. Immunemediated destruction by cytotoxic T lymphocytes
D. Excessive accumulation of free radicals from reperfusion
Question 42
Correct Answer: B
Rationale: When blood flow is restored after ischemia, reperfusion injury occurs paradoxically. The sudden reintroduction of oxygen leads to a burst of reactive oxygen species (ROS) generation by mitochondria and xanthine oxidase. These ROS cause oxidative damage to cell membranes, proteins, and DNA. Neutrophilmediated injury also contributes. This explains why some damage occurs after rather than during the ischemic episode.
Question 43
Correct Answer: A
Rationale: Leukocyte emigration into tissues involves several steps: margination (accumulation along vessel walls), rolling, adhesion to endothelium via selectins and integrins, transmigration through vessel walls (diapedesis), and migration toward the injury site along a chemical gradient (chemotaxis). Opsonization enhances phagocytosis. The complete process is essential for delivering phagocytes to the site of infection or injury.
Question 44
Correct Answer: B
Rationale: Serous inflammation produces a watery, proteinpoor exudate, as seen in early blister formation or pleural effusion in viral infection. Fibrinous inflammation results from more severe injury causing greater vascular permeability, allowing fibrinogen to escape and polymerize into fibrin. Fibrinous pericarditis (breadandbutter pericarditis) is a classic example. Excessive fibrin may be organized by fibroblasts, leading to adhesions.
Question 45
Cellular Injury
A. Continued ATP depletion after blood flow is restored
B. Generation of reactive oxygen species when blood flow returns
C. Reactivation of the sodiumpotassium pump
D. Calcium efflux from the cell upon reperfusion
Inflammation
A. Diapedesis and chemotaxis
B. Opsonization
C. Phagocytosis
D. Margination
Inflammation
A. Fibrinous inflammation involves only serous membranes
B. Fibrinous inflammation features a large exudate rich in fibrin due to greater vascular permeability
C. Serous inflammation always leads to abscess formation
D. Fibrinous inflammation is exclusively caused by viral infections
Healing and Repair
Correct Answer: C
Rationale: Trisomy 21, or Down syndrome, results from the presence of three copies of chromosome 21 rather than the normal two. It is the most common chromosomal cause of intellectual disability. Features include characteristic facial features, cardiac defects, hypotonia, and increased risk of Alzheimer disease and leukemia. It most commonly results from nondisjunction during maternal meiosis.
Question 49
Correct Answer: B
Rationale: Autosomal dominant inheritance requires only one mutant allele for disease expression. Affected individuals have a 50% chance of passing the disorder to each offspring. There is typically vertical transmission across generations with no skipping of generations. Examples include Huntington disease, Marfan syndrome, and familial hypercholesterolemia. Autosomal recessive disorders require two copies of the mutant allele.
Question 50
Correct Answer: B
Rationale: Viruses cause cell injury through several mechanisms: direct cell lysis after intracellular replication, immunemediated destruction of infected cells, induction of apoptosis, inhibition of host cell protein synthesis, and in some cases, oncogenic transformation (e.g., HPV, EBV). Exotoxin production is a bacterial mechanism. Granuloma formation is characteristic of mycobacterial and fungal infections.
Question 51
B. Chromosome 18
C. Chromosome 21
D. Chromosome 22
Genetics
A. Only affected individuals with two copies of the mutant allele show disease
B. One mutant allele is sufficient to cause disease and the trait passes from one generation to the next
C. The gene is located on the X chromosome and primarily affects males
D. Both parents must be carriers for a child to be affected
Infectious Disease
A. Direct production of exotoxins that lyse host cell membranes
B. Intracellular replication leading to cell lysis, immunemediated damage, or transformation
C. Induction of granulomatous inflammation at the site of invasion
D. Activation of complement via the alternative pathway
Cell Death
A. Pulmonary infarction
B. Acute pancreatitis
C. Renal ischemia
D. Cerebral abscess
Correct Answer: B
Rationale: Fat necrosis occurs most classically in acute pancreatitis, where pancreatic lipases are released and digest peripancreatic adipose tissue. The resulting free fatty acids combine with calcium to form chalky white deposits (saponification). Fat necrosis also occurs in breast tissue after trauma. The gross appearance of white, chalky deposits on a background of adipose tissue is distinctive.
Question 52
Correct Answer: B
Rationale: Gangrenous necrosis is not a distinct morphological type but rather a clinical description. Dry gangrene refers to coagulative necrosis from ischemia, often affecting limbs. Wet gangrene occurs when bacterial infection is superimposed, adding liquefactive features. Gas gangrene is caused by Clostridium perfringens. Gangrene most commonly affects the lower extremities in diabetic patients and those with peripheral vascular disease.
Question 53
Correct Answer: B
Rationale: DIC is a serious acquired syndrome in which systemic activation of coagulation pathways leads to widespread formation of microthrombi throughout the vasculature, consuming clotting factors and platelets. This paradoxically results in simultaneous bleeding and thrombosis. Common triggers include sepsis, obstetric complications, massive trauma, and malignancy. It is a lifethreatening emergency requiring treatment of the underlying cause.
Question 54
Correct Answer: C
Cell Death
A. A specific morphological type of necrosis distinct from coagulative necrosis
B. A clinical term describing coagulative necrosis complicated by bacterial superinfection
C. A form of necrosis exclusive to the brain parenchyma
D. Necrosis caused by autoimmune destruction of tissue
Hemodynamic Disorders
A. A hereditary clotting disorder caused by factor VIII deficiency
B. A systemic activation of coagulation leading to widespread thrombosis and secondary hemorrhage
C. Localized venous thrombosis confined to the deep veins of the legs
D. An acquired platelet disorder causing isolated thrombocytopenia
Hemodynamic Disorders
A. Septic shock
B. Cardiogenic shock
C. Hypovolemic shock
D. Neurogenic shock
vitamin D activation. Hypoparathyroidism and vitamin D deficiency cause hypocalcemia. Renal failure typically causes hypocalcemia due to impaired vitamin D activation and phosphate retention.
Question 58
Correct Answer: C
Rationale: C5a is a powerful anaphylatoxin and chemotactic factor generated during complement activation. It recruits neutrophils and monocytes to the site of inflammation and activates them. C3b acts as an opsonin, enhancing phagocytosis. C1q initiates the classical complement pathway. Complement activation is a key amplifier of innate immune responses to infection and tissue injury.
Question 59
Correct Answer: B
Rationale: Prostaglandins are derived from arachidonic acid, which is released from cell membrane phospholipids by phospholipase A2. Arachidonic acid is then converted to prostaglandins by cyclooxygenase (COX) enzymes. Prostaglandins cause fever, pain sensitization, and vasodilation during inflammation. NSAIDs such as aspirin and ibuprofen inhibit COX enzymes, thereby reducing prostaglandin synthesis and inflammation.
Question 60
Correct Answer: C
Rationale: A keloid is an exuberant scar that extends beyond the original wound margins due to excessive collagen deposition by fibroblasts. It does not regress spontaneously and is more common in individuals with darker skin pigmentation. Hypertrophic scars also involve excess collagen but remain within wound boundaries and may regress. Contractures result from excessive wound contraction and are common after severe burns.
Inflammation
A. C1q
B. C3b
C. C5a
D. C4b
Inflammation
A. Cholesterol
B. Arachidonic acid
C. Phosphatidylcholine
D. Glycogen
Healing and Repair
A. Granuloma
B. Fibrosis
C. Keloid
D. Contracture
Question 61
Correct Answer: C
Rationale: Alphafetoprotein (AFP) is significantly elevated in most patients with hepatocellular carcinoma and is used both as a diagnostic marker and to monitor treatment response. PSA is used for prostate cancer. CEA is associated with colorectal cancer and other adenocarcinomas. CA125 is used for ovarian cancer surveillance. Tumor markers are not diagnostic alone but are useful in the appropriate clinical context.
Question 62
Correct Answer: B
Rationale: Carcinogenesis is a multistep process involving initiation (an irreversible mutagenic event), promotion (clonal expansion of initiated cells by nonmutagenic stimuli), and progression (accumulation of further genetic changes leading to malignancy and invasiveness). This model explains why cancer takes years to decades to develop and why multiple genetic hits are required. No single mutation is sufficient for malignant transformation.
Question 63
Correct Answer: B
Rationale: Type IV hypersensitivity is cellmediated and does not involve antibodies. Sensitized CD4+ T cells release cytokines upon reexposure to antigen, activating macrophages and causing tissue damage. The reaction peaks 48 to 72 hours after antigen contact, hence the term "delayed." Classic examples include the tuberculin skin test, contact dermatitis, and granulomatous reactions. Immediate hypersensitivity (Type I) involves IgE and occurs within minutes.
Question 64
Neoplasia
A. Prostatespecific antigen (PSA)
B. Carcinoembryonic antigen (CEA)
C. Alphafetoprotein (AFP)
D. CA
Neoplasia
A. Single mutation → immediate invasion → metastasis
B. Initiation → promotion → progression
C. Hyperplasia → atrophy → malignant transformation
D. Apoptosis → necrosis → mutagenesis
Immunity
A. Antibodymediated reaction occurring within minutes of antigen exposure
B. Tcellmediated reaction peaking 48 to 72 hours after antigen contact
C. Immune complex deposition in vessel walls and glomeruli
D. IgEmediated degranulation of mast cells
Immunity