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HSC 4558 Final Exam V2 | HSC 4558 Pathophysiology II | Actual Q&A with Rationale (HSC4558 Final Exam) | University of Central Florida

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HSC 4558 Final Exam V2 | HSC 4558 Pathophysiology II | Actual Q&A with Rationale (HSC4558 Final Exam) | University of Central Florida

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HSC 4558 Final Exam V2 | HSC 4558 Pathophysiology II | Actual Q&A
with Rationale (HSC4558 Final Exam) | University of Central Florida


1. A patient presents with polydipsia, polyuria, and a urine specific gravity of 1.002. Which
condition is most likely responsible for these symptoms?
A. Diabetes Insipidus

B. SIADH

C. Diabetes Mellitus Type 2

D. Cushing’s Syndrome

Answer: A
Explanation: Diabetes Insipidus is characterized by a deficiency of ADH or a lack of
response to it, leading to the inability to concentrate urine. This results in the excretion of
large volumes of dilute urine and excessive thirst to compensate for fluid loss. The low
specific gravity specifically indicates the lack of solute concentration in the urine.

2. Which of the following describes the pathophysiology of Graves’ disease?
A. Destruction of thyroid follicles by T-cells

B. Iodine deficiency leading to goiter

C. Pituitary adenoma secreting excess TSH

D. Production of thyroid-stimulating immunoglobulins (TSI) that mimic TSH
Answer: D
Explanation: Graves’ disease is an autoimmune disorder where antibodies known as TSI
bind to and activate TSH receptors on the thyroid gland. This stimulation leads to the
overproduction of thyroid hormones (T3 and T4) and enlargement of the gland. It is the
most common cause of hyperthyroidism in the United States.

3. What is the primary underlying mechanism of Type 1 Diabetes Mellitus?
A. Insulin resistance in peripheral tissues

B. Increased hepatic glucose production

C. Beta cell exhaustion due to obesity

D. Autoimmune destruction of pancreatic beta cells
Answer: D

,Explanation: Type 1 Diabetes Mellitus results from a T-cell mediated autoimmune attack
on the insulin-producing beta cells in the Islets of Langerhans. This leads to an absolute
insulin deficiency, requiring exogenous insulin for survival. It typically manifests in
childhood or adolescence but can occur at any age.

4. A patient with Chronic Kidney Disease (CKD) presents with anemia. What is the most likely
cause?
A. Inadequate production of erythropoietin

B. Iron deficiency due to poor diet

C. Chronic blood loss during dialysis

D. Vitamin B12 malabsorption

Answer: A
Explanation: The kidneys are responsible for secreting erythropoietin in response to
hypoxia, which stimulates red blood cell production in the bone marrow. As renal function
declines in CKD, the production of this hormone decreases significantly. This results in a
normocytic, normochromic anemia commonly seen in advanced stages of kidney disease.

5. Which process leads to the development of hepatic encephalopathy in patients with
cirrhosis?
A. Excessive bilirubin crossing the blood-brain barrier

B. Reduced oncotic pressure leading to cerebral edema

C. Accumulation of ammonia due to impaired urea cycle function

D. Hyponatremia causing neuronal shrinkage

Answer: C
Explanation: Hepatic encephalopathy occurs when the liver can no longer convert
ammonia, a byproduct of protein metabolism, into urea. High levels of ammonia cross the
blood-brain barrier and act as a neurotoxin to astrocytes. This leads to cognitive
impairment, altered consciousness, and characteristic signs like asterixis.

6. In the context of the Monro-Kellie hypothesis, what happens if there is an increase in the
volume of one intracranial component?
A. The skull expands to accommodate the volume

B. Blood flow to the brain increases automatically

C. Volumes of the other components must decrease to maintain pressure

D. The blood-brain barrier becomes more permeable
Answer: C

, Explanation: The Monro-Kellie hypothesis states that the cranial vault is a fixed volume
containing brain tissue, blood, and cerebrospinal fluid (CSF). If one increases, another must
decrease to keep intracranial pressure (ICP) stable. Failure of this compensatory
mechanism leads to a rapid rise in ICP and potential brain herniation.

7. What is the primary defect in Myasthenia Gravis?
A. Autoantibody destruction of acetylcholine receptors at the neuromuscular junction

B. Degeneration of lower motor neurons

C. Demyelination of peripheral nerves

D. Deficiency of dopamine in the basal ganglia

Answer: A
Explanation: Myasthenia Gravis is an autoimmune disorder where IgG antibodies block or
destroy nicotinic acetylcholine receptors at the postsynaptic membrane. This results in
impaired signal transmission, leading to progressive muscle weakness and fatigability.
Symptoms often improve with rest and the administration of anticholinesterase
medications.

8. A patient experiences a sudden onset of ‘the worst headache of my life’ and neck stiffness.
Which condition is most likely?
A. Ischemic stroke

B. Transient Ischemic Attack (TIA)

C. Migraine with aura

D. Subarachnoid hemorrhage

Answer: D
Explanation: A ‘thunderclap headache’ is the classic presentation of a subarachnoid
hemorrhage, often caused by a ruptured berry aneurysm. The blood enters the
subarachnoid space, causing meningeal irritation and increased intracranial pressure.
Immediate neurosurgical evaluation is required to prevent re-bleeding or permanent
damage.

9. Which characteristic distinguishes Crohn’s disease from Ulcerative Colitis?
A. Inflammation is limited to the mucosal layer

B. It presents with ‘skip lesions’ throughout the GI tract

C. It only involves the rectum and colon

D. Bloody diarrhea is the hallmark symptom
Answer: B

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