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Test Bank For Advanced Physiology and Pathophysiology, 2nd Edition, By Nancy Tkacs, All Chapters 1-17 LATEST

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Test Bank For Advanced Physiology and Pathophysiology, 2nd Edition, By Nancy Tkacs, All Chapters 1-17 LATEST

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Test Bank For Advanced Physiology and Patho
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physiology, 2nd Edition, By Nancy Tkacs, All C nb nb nb nb nb nb nb




hapters 1-17 LATEST nb nb




Advanced Physiology and Pathophysiology, 2nd Edition
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Test Bank nb




Instructions: Select the single best answer for each question.
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Unit 1: Cellular and Molecular Foundations
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1. A 65-year-
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old patient with a history of atherosclerosis presents with stable angina. Which of the fol
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lowing best describes the primary mechanism of cellular injury in this patient's myocardi
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um?
A. Reversible cell injury due to increased intracellular calcium and ATP depletion.
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B. Irreversible cell injury characterized by karyolysis and coagulation necrosis.
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C. Cellular adaptation characterized by hypertrophy of cardiomyocytes without injury.
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D. Ischemic preconditioning that protects the myocardium from further injury.
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Correct Answer: A nb nb




Rationale: In stable angina, myocardial ischemia is temporary and reversible, leading to ATP de
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pletion, failure of the Na+/K+ pump, and increased intracellular calcium. While this can lead to
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cell death if prolonged, in stable angina the injury is typically reversible upon reperfusion (Opti
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on A). Option B describes irreversible injury, which is more typical of an MI. Option C is a long-
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term adaptation to pressure overload, not acute ischemia. Option D is a protective mechanism,
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not the primary mechanism of injury from the ischemia itself.
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2. A researcher is studying the effect of a novel drug on cellular apoptosis. The drug is f
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ound to activate the intrinsic (mitochondrial) pathway. Which of the following molecular
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events would the researcher most likely observe?
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A. Activation of death receptors (e.g., Fas) on the cell surface.
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B. Release of cytochrome c from the mitochondria into the cytosol.
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C. Activation of caspase-8 as the initiator caspase.
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D. A decrease in the ratio of Bax to Bcl-2 proteins.
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,Correct Answer: B nb nb




Rationale: The intrinsic pathway of apoptosis is initiated by mitochondrial stress, leading to inc
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reased mitochondrial permeability and the release of pro-
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apoptotic factors, including cytochrome c (Option B). Option A and C are characteristic of the e
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xtrinsic (death receptor) pathway. Option D is incorrect because an increase in the Bax/Bcl-
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2 ratio promotes apoptosis.
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3. A patient with chronic hypertension develops left ventricular hypertrophy. This is an e
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xample of which type of cellular adaptation?
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A. Metaplasia
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B. Dysplasia
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C. Hyperplasia
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D. Hypertrophy
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Correct Answer: D nb nb




Rationale: Hypertrophy is an increase in the size of cells in response to increased workload, lea
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ding to an increase in the size of the organ. The heart, being composed of terminally differenti
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ated muscle cells, responds to chronic pressure overload (hypertension) primarily through hype
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rtrophy of individual myocytes (Option D). Hyperplasia (Option C) is an increase in cell number.
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Metaplasia (Option A) and dysplasia (Option B) are changes in cell type or abnormal growth, re
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spectively.



Unit 2: The Immune System and Inflammation
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4. A 22-year-
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old patient presents with a fever, sore throat, and swollen cervical lymph nodes. A throa
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t swab is positive for Streptococcus pyogenes. What type of hypersensitivity reaction is re
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sponsible for the acute rheumatic fever that may develop weeks later if this infection is
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untreated?
A. Type I (IgE-mediated) hypersensitivity
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B. Type II (antibody-mediated) hypersensitivity
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C. Type III (immune complex-mediated) hypersensitivity
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D. Type IV (T-cell mediated) hypersensitivity
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Correct Answer: B nb nb




Rationale: Acute rheumatic fever is a classic example of a Type II hypersensitivity reaction. Anti
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bodies produced against the M-protein of S. pyogenes cross-
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react with similar antigens on host tissues, particularly in the heart, joints, and brain, leading to
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antibody-
mediated cell destruction and inflammation (Option B). Type I is anaphylactic (Option A), Type I
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,II involves circulating immune complexes (Option C), and Type IV is delayed-
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type hypersensitivity mediated by T-cells (Option D).
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5. A patient with Rheumatoid Arthritis is prescribed a TNF-
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alpha inhibitor. The mechanism of action of this drug is to block a pro-
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inflammatory cytokine. Which of the following cells is the primary source of TNF-
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alpha during the inflammatory response?
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A. Mast cells
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B. Macrophages
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C. B-lymphocytes
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D. Endothelial cells
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Correct Answer: B nb nb




Rationale: Macrophages are the primary source of pro-inflammatory cytokines, including TNF-
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alpha, IL-1, and IL- nb nb nb




6, during the acute inflammatory response (Option B). While mast cells release histamine and o
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ther mediators (Option A), and endothelial cells facilitate leukocyte adhesion, they are not the
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primary source of TNF-alpha. nb nb nb




6. A patient with a history of severe allergies is experiencing an anaphylactic reaction aft
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er eating peanuts. Which of the following mediators is most directly responsible for the
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severe bronchoconstriction and vasodilation seen in this condition?
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A. Histamine
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B. Tumor Necrosis Factor-alpha (TNF-α)
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C. Interferon-gamma (IFN-γ)
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D. Complement proteins C3a and C5a
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Correct Answer: A nb nb




Rationale: In a Type I hypersensitivity reaction (anaphylaxis), mast cell degranulation releases l
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arge quantities of histamine and other preformed mediators. Histamine is a potent vasodilator
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and bronchoconstrictor, responsible for the acute, life-threatening symptoms (Option A). TNF-
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α and IFN-γ are involved in chronic inflammation and T-
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cell responses. Complement anaphylatoxins (C3a, C5a) can also cause mast cell degranulation b
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ut are not the primary mediators of the initial response in a peanut allergy.
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Unit 3: Fluid, Electrolyte, and Acid-Base Balance
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7. A patient with congestive heart failure is prescribed furosemide, a loop diuretic. Whic
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h of the following acid-
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, base disturbances is this patient at the highest risk for developing?
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A. Metabolic acidosis
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B. Metabolic alkalosis
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C. Respiratory acidosis
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D. Respiratory alkalosis
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Correct Answer: B nb nb




Rationale: Loop diuretics like furosemide inhibit the Na+/K+/2Cl-
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cotransporter in the thick ascending limb of the loop of Henle. This leads to increased delivery
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bof sodium and water to the distal nephron, which promotes secretion of both K+ and H+ ions
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into the urine. The loss of hydrogen ions results in a metabolic alkalosis (Option B).
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8. A 70-year-
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old patient with chronic kidney disease (Stage 4) presents with fatigue, confusion, and d
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eep, rapid respirations (Kussmaul breathing). His arterial blood gas (ABG) results are: pH
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7.25, PaCO2 30 mmHg, HCO3-
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12 mEq/L. Which of the following best describes this patient's acid-base status?
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A. Uncompensated metabolic acidosis
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B. Compensated metabolic acidosis
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C. Uncompensated respiratory acidosis
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D. Compensated respiratory alkalosis
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Correct Answer: B nb nb




Rationale: The primary disturbance is a low pH (acidemia) and a low HCO3-
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(metabolic acidosis). The PaCO2 is below the normal range (35-
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45 mmHg), indicating a compensatory respiratory alkalosis (hyperventilation) in response to the
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metabolic acidosis. Since the pH is still below 7.35, the compensation is partial, but the conditi
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on is termed "compensated metabolic acidosis" (Option B). "Uncompensated" would mean the
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PaCO2 was normal. nb nb




9. A patient is admitted with severe vomiting over the past 3 days. Laboratory results re
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veal a serum potassium level of 2.8 mEq/L. Which of the following ECG changes would b
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e expected in this patient?
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A. Tall, peaked T-waves
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B. Prolonged PR interval and widened QRS complex
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C. Flattened T-waves and prominent U-waves
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D. Shortened QT interval
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Correct Answer: C nb nb




Rationale: Hypokalemia (low serum potassium) is characterized by ECG changes including ST-
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