Galen College of Nursing NSG 3850 / NSG3850 Pathophysiology II Exam 4 | Complete Questions & Answers | 100% Updated .

Galen College of Nursing NSG 3850 / NSG3850 Pathophysiology II Exam 4 | Complete Questions & Answers | 100% Updated . ### 1. Which mechanism represents the most common regulatory system controlling hormone production and secretion in the human endocrine system? A. Neural reflex arc B. Direct enzymatic cleavage C. Positive feedback mechanism D. Negative feedback mechanism ### 2. A nurse is reviewing pituitary hormones. Which pair of hormones is synthesized and stored in the posterior pituitary gland? A. Antidiuretic hormone (vasopressin) and Oxytocin B. Luteinizing hormone and FSH C. Growth hormone and Prolactin D. Thyroid stimulating hormone (TSH) and ACTH ### 3. Which thyroid hormones are secreted by the thyroid gland, and which specific cells synthesize calcitonin? A. T3 and T4 are secreted by follicular cells; Calcitonin is made by parafollicular cells (C cells). B. T3 and T4 are secreted by chief cells; Calcitonin is made by follicular cells. C. T3 and T4 are secreted by C cells; Calcitonin is made by colloid cells. D. T3, T4, and Calcitonin are all produced exclusively by thyroid follicular cells. ### 4. What is the primary pathophysiology underlying Hashimoto thyroiditis? A. Pituitary adenoma hypersecreting TSH leading to thyroid exhaustion. B. Bacterial infection of the thyroid follicles resulting in acute purulent thyroiditis. C. Autoimmune destruction of the thyroid gland, making it the most common cause of acquired hypothyroidism. D. Thyroid dysgenesis resulting in total congenital absence of thyroid tissue. ### 5. A patient is evaluated for hypothyroidism. Laboratory results indicate elevated TSH, decreased T3, decreased T4, and positive antithyroid antibodies. How should these findings be classified? A. Tertiary hypothyroidism B. Subclinical hyperthyroidism C. Secondary hypothyroidism D. Primary hypothyroidism ### 6. Which lab profile differentiates Secondary Hypothyroidism from Primary Hypothyroidism? A. Decreased TSH with elevated T3 and T4. B. Increased TSH with decreased T3 and T4. C. Decrease in all three parameters: TSH, T3, and T4. D. Elevated TSH and elevated T3 with normal T4. ### 7. Which clinical scenario is recognized as a cause of secondary hypothyroidism? A. Surgical excision of the thyroid gland B. Hashimoto thyroiditis autoimmune attack C. Severe head trauma or cranial neoplasms affecting hypothalamic-pituitary function D. Severe dietary iodine deficiency ### 8. A nurse assesses a client presenting with weakness, lethargy, cold intolerance, bradycardia, weight gain, and cool dry skin. Which endocrine disorder do these symptoms reflect? A. Hypothyroidism (hypometabolic state) B. Hyperparathyroidism C. Hyperthyroidism (hypermetabolic state) D. Cushing's disease ### 9. What life-threatening medical emergency is a direct complication of severe, unmanaged hypothyroidism? A. Thyroid storm B. Myxedema C. Addisonian crisis D. Scleroderma renal crisis ### 10. What triggers the release of Thyrotropin-Releasing Hormone (TRH) and TSH in the hypothalamic-pituitary-thyroid axis? A. ACTH hypersecretion directly activates the thyroid gland. B. Elevated serum calcium levels directly trigger hypothalamic TRH release. C. Decreased circulating levels of free T3 and T4 stimulate TRH from the hypothalamus, which stimulates TSH from the anterior pituitary. D. High levels of circulating T3 and T4 stimulate anterior pituitary TSH release. ### 11. Which form of hypothyroidism is present at birth due to thyroid dysgenesis? A. Subacute thyroiditis B. Congenital hypothyroidism C. Acquired hypothyroidism D. Secondary hypothyroidism ### 12. Which gastrointestinal clinical manifestation is consistently seen in patients with hypothyroidism? A. Esophageal dysmotility with dysphagia B. Diarrhea due to hypermotility C. Constipation due to decreased intestinal motility D. Frequent belching and epigastric burning ### 13. Why does a patient with severe iodine deficiency develop a goiter? A. Lack of iodine prevents T3/T4 synthesis, leading to persistent TSH stimulation and thyroid gland enlargement. B. Parathyroid hormone hypersecretion causes thyroid tissue swelling. C. Excess iodine accumulates inside follicular cells causing cellular hypertrophy. D. Autoantibodies stimulate TSH receptors causing hyperplasia. ### 14. A patient taking levothyroxine for hypothyroidism presents with dry cool skin, coarse hair, and a heart rate of 52 bpm. What does the nurse suspect? A. Acute hypoparathyroidism B. Graves disease exacerbation C. Development of thyroid storm D. Under-replacement of thyroid hormone medication ### 15. Which cardiac abnormality is characteristic of hypothyroidism? A. QT prolongation with tetany B. Atrial fibrillation C. Early tachycardia D. Bradycardia ### 16. What is the primary pathophysiological mechanism underlying Graves disease? A. Autoantibodies bind to and stimulate TSH receptors, producing excess T3 and T4. B. Pituitary adenoma hypersecreting ACTH. C. Follicular destruction causing sudden release of stored preformed hormones. D. Cellular resistance to T3 and T4 at the peripheral tissue level. ### 17. What laboratory pattern is characteristic of Graves disease? A. High T3 & T4 levels with low or undetectable TSH levels. B. Low T3 & T4 levels with markedly elevated TSH. C. Decreased TSH, decreased T3, and decreased T4. D. Elevated TSH with normal free T4. ### 18. Which clinical manifestation is UNIQUE and specific to Graves disease? A. Goiter B. Heat intolerance C. Tachycardia D. Exophthalmos (prominent eyes) ### 19. A patient presents with insomnia, tremors, restlessness, heat intolerance, weight loss despite increased appetite, and tachycardia. Which condition is indicated? A. Hypoparathyroidism B. Addison's disease C. Hyperthyroidism D. Hypothyroidism ### 20. In the early acute phase of Hashimoto thyroiditis, why might serum T3 and T4 levels be elevated? A. The pituitary gland secretes excessive ACTH. B. Destruction of thyroid follicular cells releases preformed stored T3 and T4 all at once. C. Autoantibodies permanently activate TSH receptors. D. Parafollicular C cells hypersecrete T3. ### 21. Which antithyroid medications are prescribed to inhibit thyroid hormone synthesis in hyperthyroidism? A. Levothyroxine and Liothyronine B. Hydrocortisone and Fludrocortisone C. Propylthiouracil (PTU) and Methimazole D. Furosemide and Spironolactone ### 22. Why are Beta-Blockers administered to a patient experiencing hyperthyroidism or thyroid storm? A. To control cardiovascular symptoms such as severe hypertension and tachycardia. B. To directly block pituitary release of TSH. C. To stimulate thyroid follicular cell re-uptake of iodine. D. To correct serum hypocalcemia and muscle tetany. ### 23. What life-threatening complication of hyperthyroidism manifests with extreme fever, severe tachycardia, hypertension, diaphoresis, and delirium? A. Thyroid Storm (Thyrotoxicosis) B. Myxedema coma C. Addisonian crisis D. Scleroderma renal crisis ### 24. Which therapeutic intervention is essential during the management of a Thyroid Storm? A. Fluid replacement, Beta-blockers, Antithyroid drugs (PTU/Methimazole), Iodine, and Antipyretics. B. Immediate administration of IV Calcium and Vitamin D. C. High-dose corticosteroid withdrawal. D. Morphine administration to relieve abdominal pain. ### 25. What skin and hair characteristics are typical of a patient with hyperthyroidism? A. Bronze hyperpigmented skin with striae B. Warm, silky skin and fine silky hair with diaphoresis C. Cool, dry, coarse skin with brittle hair D. Tightened, fibrotic skin with calcinosis ### 26. Which menstrual irregularity is commonly reported by female patients with hyperthyroidism? A. Polymenorrhea B. Amenorrhea C. Menorrhagia D. Dysmenorrhea ### 27. What is the role of Radioactive Iodine therapy in hyperthyroidism management? A. It stimulates parathyroid glands to increase calcium reabsorption. B. It neutralizes circulating antithyroid antibodies in serum. C. It binds to TSH receptors to prevent autoantibody binding. D. It selectively destroys hyperactive thyroid parenchymal cells to reduce hormone production. ### 28. An early cardiac clinical manifestation of hyperthyroidism is: A. Heart block B. Tachycardia C. Bradycardia D. Complete cardiac arrest ### 29. What intestinal clinical manifestation occurs in hyperthyroidism? A. Increased intestinal motility and weight loss despite increased appetite B. Severe constipation and abdominal distension C. Esophageal dysmotility D. Epigastric burning and gallstone colic ### 30. How do autoantibodies affect TSH receptors in Graves disease? A. They mimic TSH by binding to and continuously activating TSH receptors. B. They block TSH receptors and cause thyroid gland atrophy. C. They destroy TSH receptors leading to pituitary failure. D. They deposit antigen-antibody complexes in renal glomeruli. ### 31. What metabolic change directly triggers the parathyroid gland to secrete Parathyroid Hormone (PTH)? A. An elevation in serum calcium levels B. A decrease in serum calcium levels C. A drop in serum sodium levels D. An increase in serum potassium levels ### 32. Through which three target tissues does Parathyroid Hormone (PTH) act to elevate serum calcium? A. Bones, renal tubules, and intestine B. Hypothalamus, anterior pituitary, and gallbladder C. Thyroid gland, adrenal cortex, and liver D. Pancreas, spleen, and skeletal muscle ### 33. A patient following accidental surgical removal of the parathyroid glands during thyroidectomy develops hypoparathyroidism. Which lab findings are expected? A. Decreased PTH, decreased phosphate, and hypercalcemia B. Elevated PTH, elevated calcium, and low phosphate C. Elevated PTH, decreased phosphate, and hypercalcemia D. Decreased PTH, elevated phosphate, and hypocalcemia ### 34. Which clinical signs confirm increased neuromuscular irritability secondary to hypocalcemia? A. Positive Anti-HCV and Elevated AST/ALT ratio B. Positive Philadelphia chromosome and Bence Jones protein C. Positive Chvostek sign and positive Trousseau sign D. Malar rash and Swan neck deformity ### 35. Which electrocardiogram (ECG) alteration is a hallmark diagnostic feature of hypocalcemia in hypoparathyroidism? A. Prominent U waves B. Shortening of the ST segment C. Prolongation of the Q-T interval D. Widened QRS complex ### 36. Which symptoms reflect hypocalcemia in a patient with hypoparathyroidism? A. Truncal obesity, moon face, and striae B. Circumoral numbness, paresthesias, muscle cramps, tetany, and seizures C. Polyuria, dehydration, bradycardia, and kidney stones D. Hyperpigmentation, hyperkalemia, and severe hypotension ### 37. What is the primary medical treatment for hypoparathyroidism? A. Calcium and Vitamin D supplementation B. Hydrocortisone and Fludrocortisone C. Propylthiouracil and Beta-blockers D. Fluid replacement and loop diuretics ### 38. A patient presents with elevated serum PTH and hypercalcemia. Which renal complication is this patient at high risk for developing? A. Proteinuria B. Kidney stones (nephrolithiasis) C. Renal artery stenosis D. Glomerulonephritis ### 39. Which clinical manifestations are associated with severe hypercalcemia due to hyperparathyroidism? A. Hyperpigmentation, hypoglycemia, and hyperkalemia B. Circumoral numbness, muscle tetany, and QT prolongation C. Tremors, exophthalmos, and heat intolerance D. Polyuria, dehydration, bradycardia, heart block, and cardiac arrest ### 40. What is the initial conservative treatment for hyperparathyroidism to reduce serum calcium concentration? A. Vitamin D and Calcium administration B. Antithyroid medication C. Corticosteroid replacement therapy D. Fluid replacement and diuretics (in severe cases) ### 41. How does elevated serum calcium affect parathyroid hormone release in a healthy individual? A. It degrades circulating calcitonin. B. It triggers pituitary ACTH release. C. It suppresses PTH secretion via negative feedback. D. It stimulates excess PTH secretion. ### 42. Which clinical sign involves tapping the facial nerve to elicit facial muscle twitching? A. Chvostek sign B. Trousseau sign C. Brudzinski sign D. Kernig sign ### 43. How is Trousseau sign elicited during a physical examination? A. Dorsiflexing the foot elicits calf muscle pain. B. Flexing the neck causes involuntary hip flexion. C. Inflating a blood pressure cuff on the upper arm causes carpopedal spasm. D. Tapping the anterior cheek bone causes eyelid twitching. ### 44. Which electrolyte imbalance co-occurs with low serum calcium in hypoparathyroidism? A. Decreased serum phosphate B. Elevated serum phosphate (Hyperphosphatemia) C. Elevated serum sodium D. Decreased serum potassium ### 45. What is a common etiology of secondary hyperparathyroidism? A. Exogenous corticosteroid administration B. Chronic renal failure causing persistent hypocalcemia and hyperphosphatemia C. Pituitary adenoma hypersecreting TSH D. Autoimmune destruction of the thyroid gland ### 46. What three categories of steroid hormones are produced by the adrenal cortex? A. Insulin, Glucagon, and Somatostatin B. Epinephrine, Norepinephrine, and Dopamine C. Glucocorticoids (cortisol), Mineralocorticoids (aldosterone), and Androgens (DHEA) D. TSH, ACTH, and Growth Hormone ### 47. What is the sequence of the Hypothalamic-Pituitary-Adrenal (HPA) regulatory axis? A. Pituitary produces CRH - CRH stimulates adrenal cortex Cortisol - Cortisol stimulates hypothalamus. B. Adrenal cortex produces ACTH - ACTH stimulates hypothalamic CRH. C. Hypothalamus produces CRH - CRH stimulates anterior pituitary ACTH - ACTH stimulates adrenal cortex to produce hormones. D. Hypothalamus produces ACTH - ACTH stimulates pituitary CRH - CRH stimulates adrenal medulla. ### 48. A client with primary adrenal insufficiency (Addison's disease) presents with bronze hyperpigmentation of the skin. What causes this characteristic discoloration? A. Excessive cortisol deposition in sub-dermal tissues B. Elevated ACTH levels from the anterior pituitary gland stimulating melanocytes C. Bilirubin accumulation secondary to liver failure D. Deposition of Bence Jones proteins in skin capillaries ### 49. What electrolyte and metabolic pattern is characteristic of Addison's disease? A. Hypercalcemia, Hyperphosphatemia, and Hyperglycemia B. Hyperkalemia, Hyponatremia, Hypoglycemia, and Hypotension C. Hypocalcemia, Hypokalemia, and Malignant HTN D. Hypokalemia, Hypernatremia, Hyperglycemia, and Hypertension ### 50. What is the most common cause of Secondary Adrenal Cortical Insufficiency? A. Adrenal gland hemorrhage B. Tuberculosis infection of the adrenals C. Autoimmune adrenalitis D. Exogenous corticosteroid use (suppressing the HPA axis) ### 51. How does the ACTH Provocation Test confirm Primary Adrenal Insufficiency? A. Cortisol administration causes an immediate spike in serum potassium. B. CRH administration causes suppression of pituitary ACTH secretion. C. ACTH administration causes a rapid surge in serum cortisol above normal baseline. D. Exogenous ACTH is administered, but the adrenal cortex fails to produce cortisol 30-60 minutes later. ### 52. What is the most common cause of Primary Hypercortisolism (Cushing's Syndrome)? A. Adrenal cortical carcinoma B. Pituitary ACTH-secreting microadenoma C. Hypothalamic CRH hypersecretion D. Exogenous corticosteroid medication use ### 53. How do serum ACTH levels distinguish Primary Cushing's from Secondary Cushing's disease? A. Primary Cushing's has LOW ACTH levels; Secondary Cushing's has HIGH ACTH levels. B. Primary Cushing's has HIGH ACTH; Secondary Cushing's has LOW ACTH. C. Primary Cushing's features elevated CRH while secondary features elevated aldosterone. D. Both primary and secondary Cushing's have undetectable ACTH. ### 54. A patient presenting with truncal obesity, moon face, flushed cheeks, abdominal striae, hypertension, and hyperglycemia is displaying symptoms of: A. Hypothyroidism B. Cushing's disease (Hypercortisolism) C. Addison's disease D. Graves disease ### 55. Why does hypokalemia occur in Cushing's disease? A. ACTH directly binds to renal tubules to absorb potassium. B. High levels of cortisol exerting mineralocorticoid effects drive renal potassium excretion. C. Glucocorticoid deficiency inhibits renal absorption of potassium. D. Aldosterone deficiency causes renal potassium retention. ### 56. Which primary etiology can cause Addison's disease (Adrenal Cortical Insufficiency)? A. Long-term thyroid hormone ingestion B. Idiopathic autoimmune destruction, adrenal hemorrhage, TB infection, or trauma C. Adrenal adenomas hypersecreting aldosterone D. Anterior pituitary hyperfunction ### 57. Which lab finding is characteristic of Cushing's disease? A. Hyperglycemia and elevated serum Cortisol B. Hypoglycemia and decreased serum Cortisol C. Hyperkalemia and hyponatremia D. Hypocalcemia and elevated PHOS ### 58. What is the primary intervention for Cushing's syndrome caused by exogenous corticosteroid therapy? A. Immediate bilateral adrenalectomy B. Gradually taper and stop the corticosteroid medication. C. High-dose ACTH injections D. Lifetime hydrocortisone replacement ### 59. Why do patients with Addison's disease develop severe hypotension? A. ACTH suppression inhibits cardiac pacemaker cells. B. Excessive cortisol causes peripheral arterial vasodilation. C. High potassium levels stimulate excessive cardiac contractility. D. Deficiency of aldosterone causes renal sodium and water loss, leading to hypovolemia. ### 60. A patient diagnosed with Cushing's disease exhibits thin skin, easy bruising, and purple abdominal striae. What causes these skin changes? A. Excessive melanin synthesis triggered by high ACTH B. Subcutaneous calcium deposition from hyperparathyroidism C. Severe systemic vasculopathy from autoantibody immune complexes D. Protein catabolism and collagen breakdown driven by hypercortisolism ### 61. What is the primary feature that distinguishes malignant tumors from benign tumors? A. The rate of intracellular protein synthesis. B. The ability to secrete peptide hormones. C. The presence of a smooth fibrous capsule around the tumor. D. The propensity of malignant tumors to invade adjacent tissue and metastasize to distant sites. ### 62. Which tumor nomenclature suffix correctly indicates a benign tumor, and what are the notable exceptions? A. Suffix -CARCINOMA indicates benign; exceptions include fibroma and adenoma. B. Suffix -OMA indicates benign; exceptions include melanoma, lymphoma, hepatoma, and leukemia, which are all malignant. C. Suffix -SARCOMA indicates benign; exceptions include lipoma and osteoma. D. Suffix -OMA indicates malignant; exceptions include fibrosarcoma. ### 63. Which terms specifically denote malignant neoplasms derived from epithelial tissue and connective tissue, respectively? A. Sarcoma (epithelial) and Carcinoma (connective tissue) B. Carcinoma (epithelial) and Sarcoma (connective tissue) C. Adenoma (epithelial) and Fibroma (connective tissue) D. Melanoma (epithelial) and Lymphoma (connective tissue) ### 64. What are the four sequential steps required for cancer cell metastasis to occur? A. 1) Cytotoxic T-cell activation, 2) Histamine release, 3) Vasodilation, 4) Fibrosis. B. 1) Escape basement membrane, 2) Follow blood/lymph circulation, 3) Survival in circulation, 4) Tumor growth dependent on angiogenesis. C. 1) Gene mutation, 2) Apoptosis, 3) Phagocytosis, 4) Extravasation. D. 1) Encapsulation, 2) Hyperplasia, 3) Anaplasia, 4) Phagocytosis. ### 65. What critical process is required for a distant metastatic tumor colony to grow beyond a limited size? A. Encapsulation B. Apoptosis C. Angiogenesis (new blood vessel formation) D. Phagocytosis ### 66. How do malignant cancer cells differ fundamentally from normal host cells regarding growth control? A. They exhibit antisocial properties that ignore growth-controlling signals, proliferate excessively, and become immortal. B. They strictly respect contact inhibition signals from neighboring cells. C. They undergo rapid premature senescence and cell death. D. They depend completely on exogenous hormone stimulation to survive. ### 67. What is the defining distinction between benign and malignant tumors regarding host survival? A. Both benign and malignant tumors possess equal potential to cause distant metastasis. B. Benign always kills the host rapidly; Malignant never kills the host. C. Benign DOES NOT have the potential to kill host; Malignant DOES have the potential to kill the host if left untreated. D. Benign tumors lack cellular membranes, whereas malignant tumors are fully encapsulated. ### 68. What defines an autoimmune disease pathophysiology? A. Eosinophils undergo neoplastic transformation in bone marrow. B. The immune system completely fails to produce immunoglobulins. C. Self-cells are recognized as foreign non-self antigens and attacked by the host immune system. D. Exogenous bacterial toxins selectively destroy T-helper cells. ### 69. Patients with severe T-cell immunodeficiency disorders are uniquely susceptible to chronic infections caused by which opportunistic organisms? A. Candida albicans and Staphylococcus aureus B. Clostridium difficile and Giardia lamblia C. Streptococcus pneumoniae and Haemophilus influenzae D. Escherichia coli and Pseudomonas aeruginosa ### 70. Which environmental factors are recognized triggers capable of initiating or exacerbating autoimmune disorders in genetically susceptible individuals? A. Viral or bacterial infections, smoke, heavy metals, UV light, vaccines, and pharmaceutical agents B. Isotonic fluid administration and bed rest C. High-protein diets and physical exercise D. Hypovolemic shock and acute blood transfusion ### 71. Which category of immunodeficiency is present from birth due to genetic defects? A. Acquired immunodeficiency B. Secondary immunodeficiency C. Primary immunodeficiency D. Iatrogenic immunodeficiency ### 72. Which immunodeficiency is an example of an acquired immunodeficiency syndrome? A. Severe Combined Immunodeficiency (SCID) B. HIV / AIDS C. DiGeorge syndrome D. Agammaglobulinemia ### 73. Why do malignant tumor cells survive in blood circulation despite hemodynamic shear forces? A. They secrete high levels of calcitonin to neutralize lymphocytes. B. They transform into mature basophils while circulating. C. They aggregate with platelets and fibrin to evade immune surveillance and mechanical destruction. D. They shrink in size to match red blood cells. ### 74. Fibrosarcoma is classified as a: A. Benign tumor of glandular epithelium B. Malignant tumor of epithelial origin C. Malignant tumor of connective tissue origin D. Benign tumor of fibrous connective tissue ### 75. A benign tumor of fibrous tissue is named a: A. Fibroma B. Fibrosarcoma C. Adenocarcinoma D. Melanoma ### 76. Which antibody mediator drives Type I Hypersensitivity immediate allergic reactions? A. IgG antibodies B. IgE antibodies C. IgM antibodies D. IgA antibodies ### 77. Which immune mechanisms mediate Type II Hypersensitivity reactions? A. Immune-complex deposition in blood vessels B. Delayed T-cell mediated cell destruction C. IgE-mediated mast cell degranulation D. Tissue-specific, cytotoxic reactions mediated by IgM or IgG antibodies ### 78. Which clinical condition is a classic example of a Type II Cytotoxic Hypersensitivity reaction featuring drooping eyelids (ptosis) as a hallmark? A. Systemic Lupus Erythematosus B. Myasthenia Gravis C. Graves Disease D. Rheumatoid Arthritis ### 79. Which condition represents a Type II Hypersensitivity reaction classified under Type B in Unit 11? A. Glomerulonephritis B. Blood transfusion reaction C. Contact dermatitis D. Graves Disease ### 80. What is the etiology and typical timing of post-infectious Immune Complex Glomerulonephritis (Type III Hypersensitivity)? A. Occurs 10 to 14 days after an infection with Streptococcus or Staphylococcus. B. Occurs 6 months after receiving a live attenuated viral vaccine. C. Occurs 48 to 72 hours following a tuberculin skin injection. D. Occurs immediately within 15 minutes of exposure to plant oils. ### 81. Contact dermatitis resulting from plant oils (poison ivy), cosmetics, dyes, or adhesives is classified as which hypersensitivity type? A. Type I Immediate Hypersensitivity B. Type IVa Contact Hypersensitivity (delayed cell-mediated) C. Type III Immune Complex Hypersensitivity D. Type II Cytotoxic Hypersensitivity ### 82. When interpreting a Tuberculin (TB) skin test, at what time frame does the dermal induration peak, and what does a positive test indicate? A. Peaks in 24 hours; indicates complete immunity requiring no follow-up. B. Peaks in 7 days; indicates Type I anaphylactic sensitization. C. Peaks in 15 minutes; confirms active pulmonary TB destruction. D. Peaks in 48-72 hours; indicates a hypersensitivity reaction from prior TB exposure, latent TB, or past BCG vaccination. ### 83. What follow-up diagnostic procedures are MANDATORY following a positive TB skin test result? A. Immediate repeat skin test in 24 hours B. Skin biopsy of the forearm C. Chest X-ray and blood test D. Bone marrow aspiration ### 84. What are the three most common severe organ complications associated with Systemic Lupus Erythematosus (SLE)? A. 1) Sclerodactyly, 2) Raynaud's, 3) Calcinosis. B. 1) Splenomegaly, 2) Bone lesions, 3) Hypercalcemia. C. 1) Liver failure, 2) Gallstones, 3) Pancreatitis. D. 1) Cardiac (pericarditis, valvular, myocarditis w/ CHF), 2) Lungs (interstitial pneumonitis, PE, pulm HTN), 3) Renal (acute glomerulonephritis with proteinuria/hematuria). ### 85. A female patient presents with periods of exacerbation and remission, joint pain, and a classic malar 'butterfly' rash across her nose and cheeks. Which condition is suspected? A. Scleroderma B. Discoid Lupus Erythematosus C. Rheumatoid Arthritis D. Systemic Lupus Erythematosus (SLE) ### 86. How does Discoid Lupus Erythematosus differ from Systemic Lupus Erythematosus? A. Discoid Lupus causes progressive renal failure and pericarditis. B. Discoid Lupus affects ONLY the skin and is diagnosed via skin biopsy. C. Discoid Lupus is diagnosed via positive Bence Jones proteinuria. D. Discoid Lupus is twice as common in males than females. ### 87. What underlying joint pathology drives the escalation of structural damage in Rheumatoid Arthritis (RA)? A. Subcutaneous calcium deposits eroding the bone marrow. B. Escalating inflammatory response leads to accumulation of dense aggregates of immune cells, causing edema and proliferation of synovium. C. Uric acid crystal deposition causing acute synovial necrosis. D. Loss of articular cartilage due to wear and tear without inflammation. ### 88. Which characteristic hand and finger deformities are classic manifestations of chronic Rheumatoid Arthritis? A. Chvostek sign and Trousseau sign B. Swan neck deformity, Boutonniere deformity, and Ulnar deviation C. Sclerodactyly, Calcinosis, and Telangiectasia D. Heberden nodes and Bouchard nodes ### 89. What is the primary underlying vascular pathology in Scleroderma? A. Granulomatous destruction of portal triads. B. Malignant proliferation of mature plasma cells in bone marrow. C. IgE-mediated allergic inflammation of epidermal basement membranes. D. Vasculopathy and vascular injury in smooth muscle cells causing tissue ischemia, followed by diffuse tissue fibrosis. ### 90. What life-threatening emergency crisis can suddenly develop in a patient with Scleroderma? A. Thyroid storm B. Myxedema coma C. Scleroderma renal crisis (malignant hypertension and acute renal failure) D. Superior Vena Cava obstruction ### 91. What does the acronym CREST stand for in Limited Scleroderma? A. Carcinoma, Renal crisis, Erythema, Splenomegaly, Thrombocytopenia B. Calcium elevation, Rash, Esophagitis, Synovitis, Tremors C. Cardiac failure, Raynaud's, Embolism, Striae, Tachypnea D. Calcinosis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia ### 92. What conservative nursing and pharmacological interventions are indicated for managing Raynaud's phenomenon in Scleroderma? A. Apply ice packs to hands; administer Beta-blockers. B. Perform immediate surgical sympathectomy; administer heparin. C. Keep fingers and extremities warm; administer Calcium Channel Blockers if severe. D. Encourage cold water immersion; administer high-dose aspirin. ### 93. What bone marrow aspirate diagnostic finding is MANDATORY to confirm a diagnosis of Acute Myeloid Leukemia (AML)? A. Greater than 20% blast cell proliferation of underdeveloped cells B. Greater than 90% mature basophils with Philadelphia chromosome C. Presence of Reed-Sternberg giant cells D. Bence Jones proteins in marrow fluid ### 94. A patient with Acute Myeloid Leukemia (AML) experiences bone pain, anemia, and thrombocytopenia. What is the primary cause of frequent infections in these patients? A. Immune complex deposition in alveolar membranes B. Hyposecretion of adrenal glucocorticoids C. Direct destruction of CD4 T-cells by retroviral enzymes D. Proliferation of immature unfunctional blast cells crowding out normal functional WBCs ### 95. What genetic hallmark is diagnostic for Chronic Myeloid Leukemia (CML)? A. Philadelphia chromosome (Ph+ cell) B. Anti-HAV IgG antibody C. Bence Jones protein D. Reed-Sternberg cell ### 96. How do circulating granulocyte cells in Chronic Myeloid Leukemia (CML) differ from those in Acute Myeloid Leukemia (AML)? A. CML consists exclusively of immature T-cell blasts. B. CML cells are more MATURE granulocytes (basophils, neutrophils, eosinophils), whereas AML consists of immature blasts (20%). C. AML consists of fully mature plasma cells secreting IgG. D. CML granulocytes lack nuclear material entirely. ### 97. Why does Chronic Myeloid Leukemia (CML) carry a poor prognosis? A. CML does not respond well to traditional chemotherapy. B. CML rapidly causes acute scleroderma renal crisis. C. CML exclusively affects pediatric patients under 2 years. D. CML leads to immediate anaphylactic shock. ### 98. Acute Lymphoid Leukemia (ALL) is characterized as a: A. Highly proliferative rapid malignant disorder of B-cell lymphoid cell lineage. B. Benign hyperplasia of cervical lymph nodes. C. Slow insidious tumor of mature plasma cells. D. Non-malignant viral infection of monocytes. ### 99. Multiple Myeloma is a malignant transformation of which specific immune cell type? A. Monocytes and macrophages B. Immature T-helper CD4 cells C. Natural Killer (NK) cells D. Mature antibody-secreting B-lymphocytes called plasma cells ### 100. What pathognomonic urinalysis finding is 100% diagnostic for Multiple Myeloma? A. Glucosuria with high ketone levels B. Elevated HAV IgM antibodies C. Heavy proteinuria with hematuria and red cell casts D. Presence of Bence Jones proteins in the urine ### 101. Which clinical triad of manifestations is classic for Multiple Myeloma? A. Splenomegaly, Malar rash, and Drooping eyelids B. Bone lesions, Hypercalcemia, and Pathological fractures C. Truncal obesity, Moon face, and Striae D. Hyperpigmentation, Hyperkalemia, and Hypotension ### 102. What is the key microscopic diagnostic cell required to diagnose Hodgkin's Lymphoma? A. Reed-Sternberg cell B. C cell C. Mallory body D. Philadelphia chromosome ### 103. How does Hodgkin's Lymphoma typically present and spread clinically? A. Widespread bone marrow necrosis without lymph node involvement. B. Painful fixed ulcerating skin nodules that spread randomly. C. Rapid abdominal distension with ascites and jaundice. D. Painless, movable lymph node enlargement that progresses systematically in a predictable pattern. ### 104. How does Non-Hodgkin's Lymphoma differ from Hodgkin's Lymphoma regarding cell markers and prognosis? A. Hodgkin's lymphoma lacks lymph node involvement entirely. B. Non-Hodgkin's lacks Reed-Sternberg cells, can arise from B, T, or NK cells, and carries a worse prognosis. C. Non-Hodgkin's affects females exclusively and responds 100% to chemo. D. Non-Hodgkin's has Reed-Sternberg cells and carries a far better prognosis. ### 105. Which viral infection is strongly associated with the development of Burkitt Lymphoma (a form of Non-Hodgkin's Lymphoma)? A. Hepatitis C Virus (HCV) B. Human Immunodeficiency Virus (HIV) C. Cytomegalovirus (CMV) D. Epstein-Barr Virus (EBV) ### 106. Which oncological emergency associated with Non-Hodgkin's Lymphoma manifests with facial/neck swelling and engorged head/neck veins? A. Spinal cord compression B. Scleroderma renal crisis C. Thyroid storm D. Obstruction of the Superior Vena Cava (SVC Syndrome) ### 107. What is the most common cause of Hypercalcemia of Malignancy among hematologic cancers? A. Lymphoma B. Acute Myeloid Leukemia C. Chronic Persistent Hepatitis D. Discoid Lupus ### 108. Why is Human Immunodeficiency Virus (HIV) classified as a Retrovirus? A. It replicates exclusively outside host cells in serum. B. It utilizes double-stranded DNA to destroy host red blood cells. C. It directly converts host DNA into viral proteins without RNA. D. It carries single-stranded RNA and replicates backwards by converting RNA into DNA inside host cells. ### 109. What three essential enzymes are required for HIV to successfully replicate inside human host cells? A. Reverse Transcriptase, Integrase, and Protease B. Calcitonin, Renin, and Angiotensin C. Amylase, Lipase, and Trypsin D. AST, ALT, and Alkaline Phosphatase ### 110. Which primary immune cells are targeted and destroyed by HIV? A. B-cell plasma cells and Eosinophils B. CD8+ Cytotoxic T-cells and Neutrophils C. CD4+ T-helper lymphocytes and Macrophages D. Basophils and Erythrocytes ### 111. What is recognized as the major primary anatomical site of HIV replication in the body? A. Renal tubular epithelium B. Thyroid follicular lumen C. Gastrointestinal (GI) tract mucosal tissue D. Central nervous system ### 112. Which mode of transmission represents the MOST COMMON route of HIV spread? A. Contaminated food and water supplies B. Casual contact with urine or saliva C. Accidental hospital needle stick exposure D. Unprotected sexual contact ### 113. Can HIV be transmitted through contact with infected urine or saliva? A. Yes, saliva carries the highest viral load of HIV. B. Yes, but only if the recipient has high levels of IgE. C. No, there is NO transmission via urine or saliva. D. Yes, urine is the primary transmission route in hospitals. ### 114. What criteria confirm that an HIV-positive patient has converted to AIDS? A. Elevated HAV IgG antibodies with mild fever. B. Positive ELISA test alone regardless of CD4 count. C. Presence of Philadelphia chromosome in bone marrow. D. HIV positive status combined with a CD4+ count 200 cells/mcL OR the presence of an AIDS-defining opportunistic infection. ### 115. Which infections are classified as classic AIDS-defining opportunistic infections? A. Tuberculosis (TB), Pneumocystis jirovecii pneumonia (PCP), Oral Candidiasis, Kaposi Sarcoma, and PID. B. Myasthenia Gravis, SLE, and Rheumatoid Arthritis C. Hepatitis A, Acute Cholecystitis, and NASH D. Graves disease, Hashimoto thyroiditis, and Addison's ### 116. What is the primary pharmacological target of modern Antiretroviral (ARV) drugs in managing HIV? A. Stimulating thyroid follicular cell uptake of iodine B. Destroying circulating CD4+ helper T-cells C. Inhibiting the 3 viral enzymes (Reverse Transcriptase, Integrase, and Protease) D. Blocking parathyroid hormone receptors on bone ### 117. What diagnostic testing sequence is standard for confirming HIV infection? A. Anti-HCV RNA assay followed by liver biopsy. B. Screening with ELISA, confirmation with Western Blot, and monitoring CD4 count. C. ACTH provocation test followed by HIDA scan. D. Bone marrow aspiration followed by Bence Jones urinalysis. ### 118. Without antiretroviral treatment, approximately how long does it take for HIV to typically progress to AIDS? A. About 8 to 10 years B. 20 to 30 years C. 2 to 4 weeks D. 6 months ### 119. What is the MOST COMMON cause of death in patients diagnosed with AIDS? A. Acute liver failure from hepatitis A B. Severe hypocalcemic tetany C. Malignant scleroderma renal crisis D. Opportunistic infections (due to severe immune system depletion) ### 120. Which specific opportunistic pulmonary infection is recognized as the MOST COMMON infection in patients with HIV/AIDS? A. Mycoplasma pneumonia B. Pneumocystis jirovecii pneumonia (PCP) C. Legionella pneumonia D. Klebsiella pneumonia ### 121. What is the chief pathophysiological cause of cholesterol gallstone formation (Cholelithiasis)? A. Bacterial destruction of the sphincter of Oddi. B. Supersaturation of bile with cholesterol causing cholesterol crystal formation, nucleation, and gallbladder hypomotility (stasis). C. Hypersecretion of calcitonin by C cells. D. Excessive hepatic synthesis of conjugated bilirubin. ### 122. Which patient risk factors increase the probability of developing Cholelithiasis? A. Female gender (2:1 ratio), obesity, TPN diet, high cholesterol, spinal cord injury, rapid weight loss, pregnancy, and DM2. B. Male gender, underweight BMI 18, chronic alcohol abuse, and low fat intake. C. Young age 10 years, hyperthyroidism, and Addison's disease. D. T-cell immunodeficiency, acute AML, and hypoparathyroidism. ### 123. What is the chief complaint and pain pattern associated with Chronic Cholelithiasis? A. Intermittent biliary colic consisting of persistent epigastric or Right Upper Quadrant (RUQ) abdominal pain radiating to the back. B. Substernal chest pain radiating down the left arm. C. Severe periumbilical pain relieved by eating high-fat meals. D. Constant left lower quadrant pain radiating to the groin. ### 124. What precipitates an episode of biliary colic in a patient with gallstones? A. Administration of IV antipyretic therapy B. Strict adherence to a zero-carbohydrate fasting diet C. Ingestion of a high-fat meal or spontaneous onset occurring at night D. Strenuous physical exercise ### 125. What causes biliary colic during gallstone disease? A. Periodic transient obstruction of the cystic duct by a gallstone (or sphincter of Oddi spasm). B. Bacterial infection of portal triads. C. Permanent necrosis of centrilobular hepatocytes. D. Autoimmune destruction of pancreatic beta cells. ### 126. Why is Morphine CONTRAINDICATED for pain management in acute cholecystitis, and what medication is preferred? A. Morphine causes the Sphincter of Oddi to spasm and close; Dilaudid is preferred. B. Morphine causes severe acute hepatotoxicity; Acetaminophen is preferred. C. Morphine triggers thyroid storm; Propylthiouracil is preferred. D. Morphine worsens hypocalcemia; Calcium gluconate is preferred. ### 127. Which clinical and laboratory findings DISTINGUISH Acute Cholecystitis from uncomplicated Cholelithiasis? A. Nausea and vomiting B. Presence of gallstones on ultrasound C. Fever and Leukocytosis (elevated WBC) D. Epigastric pain radiating to back ### 128. Is overt Jaundice typically present in uncomplicated Acute Cholecystitis? A. Yes, jaundice occurs alongside bronze skin hyperpigmentation. B. No, jaundice is typically absent (only mild elevations in bilirubin occur). C. Yes, jaundice is caused by destruction of RBCs in the gallbladder. D. Yes, severe deep jaundice is mandatory for diagnosis. ### 129. What serious complication can arise from untreated Chronic Cholecystitis? A. Gallbladder wall scarring resulting in a calcified or 'porcelain' gallbladder, which carries a higher risk of gallbladder cancer. B. Acute scleroderma renal crisis C. Severe Addisonian crisis with hypoglycemia D. Development of Philadelphia chromosome CML ### 130. What is the primary cause of Acute Cholecystitis in over 90% of cases? A. Primary viral hepatitis A infection B. Autoimmune destruction of parafollicular C cells C. Direct trauma to the portal vein D. Gallstone obstruction of the cystic duct (Cholelithiasis) ### 131. What diagnostic imaging modalities are utilized to evaluate gallbladder inflammation and duct obstruction? A. ACTH provocation test and ECG B. Bone marrow aspiration and Urinalysis C. Chest X-ray and Western Blot D. Abdominal Ultrasound, HIDA scan, CT, MRCP, and ERCP ### 132. How does rapid weight loss or prolonged fasting promote gallstone formation? A. It destroys TSH receptors in the thyroid. B. It triggers autoantibody synthesis against RBCs. C. It increases hepatic cholesterol secretion into bile and promotes biliary stasis. D. It decreases serum calcium causing muscle tetany. ### 133. What is a characteristic symptom associated with chronic gallstone distress after eating? A. Circumoral numbness and QT prolongation B. Bronze hyperpigmentation and hypoglycemia C. Exophthalmos and fine tremors D. Fatty food intolerance, belching, flatus, and abdominal bloating ### 134. Which statement regarding Biliary Malignancy is accurate? A. It presents immediately with classic malar rash. B. It may remain completely asymptomatic until the disease reaches an advanced stage. C. It is exclusively caused by Type I IgE hypersensitivity. D. It is diagnosed via positive Bence Jones proteinuria. ### 135. Which symptom distinguishes chronic cholecystitis exacerbation from acute cholecystitis? A. Chronic cholecystitis is treated with morphine injections. B. Chronic cholecystitis may be completely asymptomatic between intermittent biliary colic attacks. C. Chronic cholecystitis always causes high fever 104°F. D. Acute cholecystitis lacks severe abdominal tenderness. ### 136. What are the four cardinal general clinical manifestations of advanced Liver Disease? A. Moon face, Truncal obesity, Striae, and Buffalo hump B. Exophthalmos, Goiter, Tremor, and Heat intolerance C. Swan neck deformity, Ulnar deviation, Tetany, and Chvostek sign D. Jaundice, Ascites, Edema, and Altered Mental Status (AMS) ### 137. Pathophysiologically, what causes Ascites in liver failure patients? A. Portal Hypertension and Hypoalbuminemia leading to fluid accumulation in the peritoneal cavity. B. Elevated PTH causing renal calcium reabsorption. C. Hypercortisolism causing subcutaneous fat accumulation. D. Hypersecretion of aldosterone causing pulmonary edema. ### 138. What is the major lethal complication resulting from Portal Hypertension in end-stage liver disease? A. Scleroderma renal crisis with malignant HTN. B. Osteosarcoma with pathological fractures. C. Rupture of esophageal varices causing uncontrolled gastrointestinal hemorrhage. D. Thyroid storm with extreme fever. ### 139. Which Hepatitis virus is transmitted via the fecal-oral route, causes ONLY acute infection, and is diagnosed by HAV IgM during acute disease? A. Hepatitis A (HAV) B. Hepatitis C (HCV) C. Hepatitis D (HDV) D. Hepatitis B (HBV) ### 140. How is Hepatitis B (HBV) transmitted, and what primary serological marker indicates acute HBV infection? A. Transmitted via plant oils; indicated by positive tuberculin skin test. B. Transmitted via sex, blood, and parenterally; acute infection is indicated by Hepatitis B surface antigen (HBsAg). C. Transmitted via fecal-oral contaminated water; indicated by HAV IgM. D. Transmitted via casual saliva contact; indicated by Bence Jones protein. ### 141. Which Hepatitis virus is a single-stranded RNA virus with a high mutation rate, most commonly spread via IV drug use and blood transfusions, leading to high rates of chronic liver disease? A. Hepatitis A (HAV) B. Hepatitis E (HEV) C. Hepatitis C (HCV) D. Hepatitis B (HBV) ### 142. Which Hepatitis virus is an incomplete organism that REQUIRES the presence of Hepatitis B (HBV) for viral replication? A. Hepatitis D (HDV / Delta) B. Hepatitis C (HCV) C. Hepatitis A (HAV) D. Hepatitis E (HEV) ### 143. Which Hepatitis virus causes ONLY acute infection spread via fecal-contaminated water and carries an exceptionally HIGH MORTALITY rate in pregnant women? A. Hepatitis D (HDV) B. Hepatitis E (HEV) C. Hepatitis C (HCV) D. Hepatitis B (HBV) ### 144. What microscopic cellular inclusion in centrilobular hepatocytes is pathognomonic for Alcoholic Hepatitis? A. Philadelphia chromosome B. Mallory bodies C. Bence Jones proteins D. Reed-Sternberg cells ### 145. What enzyme ratio pattern on liver function tests is characteristic of Alcoholic Hepatitis? A. Elevated TSH with suppressed T3/T4 B. Equal 1:1 ratio of AST and ALT below 10 U/L C. AST (SGOT) markedly greater than ALT (SGPT) D. ALT markedly greater than AST ### 146. Why do patients with severe alcoholic liver damage fail to clot normally after an injury? A. High bilirubin levels break down fibrinogen directly. B. High aldosterone causes rapid loss of serum calcium. C. Alcoholic liver disease destroys circulating blood platelets. D. The damaged liver cannot synthesize Vitamin K-dependent clotting factors. ### 147. What defines Non-Alcoholic Steatohepatitis (NASH)? A. Gallbladder perforation secondary to chronic stone irritation. B. Accumulation of fat in liver cells in individuals drinking 2 alcoholic drinks per day, associated with obesity (BMI 30), high cholesterol, and DM2. C. Autoimmune invasion of hepatic lobules following strep infection. D. Infiltration of mature basophils carrying the Philadelphia chromosome. ### 148. How does Chronic Persistent Hepatitis differ from Chronic Active Hepatitis? A. Chronic Active is self-limiting within 2 weeks requiring no intervention. B. Chronic Persistent involves low-grade inflammation of portal triads WITHOUT lobule destruction (needs no tx); Chronic Active extends into hepatic lobule causing destruction, jaundice, and ascites. C. Chronic Persistent is caused by HIV, while Chronic Active is caused by trauma. D. Chronic Persistent causes acute renal failure, while Chronic Active causes thyroid storm. ### 149. What anatomical and physiological changes occur in the liver due to aging (Geriatric Considerations)? A. Bilirubin metabolism becomes 100% more efficient. B. The liver stops producing Vitamin K completely at age 65. C. Liver size and hepatic blood flow decrease with age. D. Liver size and hepatic blood flow double by age 70. ### 150. What is the pharmacological consequence of age-related decreases in hepatic blood flow in geriatric patients? A. It causes rapid drug elimination requiring double dosage. B. It prevents all oral medications from being absorbed in GI tract. C. It increases the serum half-life of drugs metabolized by the liver, predisposing patients to drug toxicity. D. It neutralizes antithyroid medications completely.