PORTAGE LEARNING
NURS 231 Pathophysiology
FINAL EXAM
Official Cumulative Final Assessment 2026/2027
100 75% One-Time Cert
QUESTIONS PASSING SCORE RECERTIFICATION
TABLE OF CONTENTS
Section 1 Cellular & Genetic Pathophysiology Q1-Q20
Section 2 Systemic Disorders (Cardiovascular & Respiratory) Q21-Q40
Section 3 Systemic Disorders (Renal, GI & Hepatic) Q41-Q60
Section 4 Endocrine & Reproductive Pathophysiology Q61-Q80
Section 5 Neurologic, Infectious & Immunologic Disorders Q81-Q100
Instructions: Select the single best answer for each question. This is the cumulative final exam for Portage Learning NURS 231
PORTAGE LEARNING NURS 231 PATHOPHYSIOLOGY FINAL EXAM - 2026/2027 | Passing Score: 75% | Page 1 of 52
, SECTION 1 | Cellular & Genetic Pathophysiology | Q1-Q20 | NURS 231 Final Exam 2026/2027
Q1 Question 1 of 100
A 34-year-old woman presents with progressive muscle weakness and exercise intolerance.
Muscle biopsy reveals ragged red fibers, and laboratory testing shows elevated lactate levels
at rest. Her maternal uncle died of cardiomyopathy at age 42. Genetic analysis is most likely
to reveal a mutation in which cellular structure?
A. Nuclear DNA encoding sarcomeric proteins
B. Lysosomal hydrolase genes on chromosome 7
C. Ribosomal RNA genes on chromosome 21
D. Mitochondrial DNA encoding electron transport chain components
Correct Answer: D
Rationale:
Ragged red fibers and elevated lactate are hallmarks of mitochondrial myopathy, caused by mutations in
mitochondrial DNA affecting oxidative phosphorylation. Nuclear DNA sarcomeric mutations cause
hypertrophic cardiomyopathy without ragged red fibers. Ribosomal and lysosomal gene mutations produce
different clinical syndromes.
Q2 Question 2 of 100
A 6-month-old infant is brought to the clinic with recurrent infections, failure to thrive, and
absent thymic shadow on chest radiograph. Genetic testing reveals a deletion on
chromosome 22q11.2. The underlying mechanism of this disorder involves abnormal
development of which embryonic structure?
A. Mesodermal cells forming the cardiac outflow tract
B. Endodermal cells forming the thyroid diverticulum
C. Neural crest cells migrating to the pharyngeal pouches
D. Ectodermal cells forming the neural tube
Correct Answer: C
Rationale:
DiGeorge syndrome (22q11.2 deletion) results from aberrant neural crest cell migration to the third and
fourth pharyngeal pouches, leading to thymic hypoplasia, parathyroid hypoplasia, and cardiac defects. The
other structures listed are affected secondarily or through different mechanisms.
PORTAGE LEARNING NURS 231 PATHOPHYSIOLOGY FINAL EXAM - 2026/2027 | Passing Score: 75% | Page 2 of 52
, SECTION 1 | Cellular & Genetic Pathophysiology | Q1-Q20 | NURS 231 Final Exam 2026/2027
Q3 Question 3 of 100
A 28-year-old man of Ashkenazi Jewish descent develops recurrent episodes of severe
abdominal pain, joint swelling, and fever that resolve after 2-3 days. His serum amyloid A
levels are markedly elevated during attacks. Genetic testing reveals a mutation in the MEFV
gene. This condition exemplifies which category of genetic disorder?
A. Autosomal dominant gain-of-function disorder
B. X-linked recessive disorder
C. Autosomal recessive autoinflammatory disorder
D. Mitochondrial inheritance disorder
Correct Answer: C
Rationale:
Familial Mediterranean fever, caused by MEFV mutations, is an autosomal recessive autoinflammatory
disorder characterized by recurrent episodes of serositis and fever. The MEFV gene encodes pyrin, and
loss-of-function leads to dysregulated inflammasome activity. It is not X-linked, dominant, or mitochondrial.
Q4 Question 4 of 100
A 45-year-old man with a long history of alcohol abuse presents with jaundice, ascites, and
asterixis. Laboratory studies reveal elevated AST and ALT with an AST-to-ALT ratio greater
than 2:1. At the cellular level, the primary mechanism of hepatocyte injury in this condition
involves which process?
A. Direct viral cytopathic effect on hepatocytes
B. Antibody-mediated complement lysis of bile ducts
C. Oxidative stress and acetaldehyde-protein adduct formation
D. Ischemic necrosis from portal vein thrombosis
Correct Answer: C
Rationale:
Alcoholic liver disease involves oxidative stress from cytochrome P450 2E1 induction and
acetaldehyde-protein adduct formation, leading to hepatocyte injury and stellate cell activation. The
AST:ALT ratio greater than 2 is characteristic. Viral, autoimmune, and ischemic mechanisms produce
different laboratory patterns.
PORTAGE LEARNING NURS 231 PATHOPHYSIOLOGY FINAL EXAM - 2026/2027 | Passing Score: 75% | Page 3 of 52
, SECTION 1 | Cellular & Genetic Pathophysiology | Q1-Q20 | NURS 231 Final Exam 2026/2027
Q5 Question 5 of 100
A 3-year-old boy is evaluated for developmental delay, self-mutilating behavior such as lip
biting, and hyperuricemia. His serum uric acid level is 12 mg/dL. The enzyme deficient in this
disorder normally catalyzes which reaction?
A. Conversion of hypoxanthine to inosine monophosphate
B. Conversion of guanine to guanosine monophosphate
C. Conversion of adenosine to inosine
D. Conversion of hypoxanthine to xanthine and xanthine to uric acid
Correct Answer: D
Rationale:
Lesch-Nyhan syndrome results from deficiency of hypoxanthine-guanine phosphoribosyltransferase
(HGPRT), which normally salvages hypoxanthine and guanine. Without HGPRT, the purine degradation
pathway is overactive, leading to excess uric acid production. HGPRT does not convert hypoxanthine to IMP
or adenosine to inosine.
Q6 Question 6 of 100
A 50-year-old woman presents with bilateral hearing loss and multiple cafe-au-lait spots on
her trunk. MRI reveals bilateral vestibular schwannomas. Her father had similar findings. The
tumor suppressor gene involved in this condition normally produces a protein that regulates
which cellular process?
A. Cell cycle progression by inhibiting Rho GTPase signaling
B. Apoptosis by activating caspase cascades
C. Cell cycle arrest by linking merlin to contact-dependent inhibition
D. DNA repair by facilitating nucleotide excision repair
Correct Answer: C
Rationale:
Neurofibromatosis type 2 involves mutations in the NF2 gene encoding merlin (schwannomin), which
regulates contact-dependent inhibition of proliferation by linking the actin cytoskeleton to cell surface
receptors. Merlin does not primarily regulate Rho signaling, caspases, or nucleotide excision repair.
PORTAGE LEARNING NURS 231 PATHOPHYSIOLOGY FINAL EXAM - 2026/2027 | Passing Score: 75% | Page 4 of 52