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NUR 5433 DIABETES EXAM LATEST 2026 UPDATE 100+ QUESTIONS AND DETAILED VERIFIED ANSWERS FROM ACTUAL EXAMS TEST GRADE A+

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NUR 5433 DIABETES EXAM LATEST 2026 UPDATE 100+ QUESTIONS AND DETAILED VERIFIED ANSWERS FROM ACTUAL EXAMS TEST GRADE A+

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NUR 5433 DIABETES EXAM LATEST 2026
UPDATE 100+ QUESTIONS AND DETAILED
VERIFIED ANSWERS FROM ACTUAL EXAMS
TEST GRADE A+

Pathophysiology & Etiology
1. Type 1 diabetes mellitus (T1DM) results primarily from:
A) Insulin resistance and compensatory hyperinsulinemia
B) Autoimmune destruction of pancreatic beta cells
C) Mutation of the insulin receptor gene on chromosome 19
D) Excessive glucagon secretion from alpha cells
Correct Answer: B
*Explanation: T1DM is characterized by cell-mediated autoimmune destruction of
pancreatic beta cells, leading to absolute insulin deficiency. Option A describes
Type 2 diabetes (T2DM). Option C is a rare cause of severe insulin resistance.
Option D contributes to hyperglycemia but is not the primary cause.*
2. Which autoantibody is most specific for predicting progression to Type 1
diabetes?
A) Anti-GAD65 (Glutamic Acid Decarboxylase)
B) Anti-thyroperoxidase
C) Anti-nuclear antibody (ANA)
D) Rheumatoid factor (RF)
Correct Answer: A
*Explanation: Anti-GAD65 antibodies are present in 70–80% of newly diagnosed
T1DM patients and appear years before clinical onset. Anti-thyroperoxidase
suggests autoimmune thyroid disease; ANA is for lupus; RF for rheumatoid
arthritis.*

,3. The "accelerator hypothesis" suggests that Type 1 diabetes is linked to:
A) Viral infections alone
B) Rapid weight loss in childhood
C) Increased beta-cell apoptosis due to insulin resistance and rapid growth
D) Exclusive genetic inheritance from the paternal line
Correct Answer: C
*Explanation: The accelerator hypothesis proposes that insulin resistance (from
obesity and rapid growth) accelerates beta-cell apoptosis in genetically susceptible
individuals, linking T1DM and T2DM mechanisms. Viral infections may trigger but
are not the sole factor.*
4. A 22-year-old presents with polyuria, polydipsia, and weight loss. BMI is 21.
Random glucose is 450 mg/dL. Which test best confirms autoimmune etiology?
A) C-peptide level
B) Hemoglobin A1c
C) Islet cell cytoplasmic antibodies (ICA)
D) Oral glucose tolerance test (OGTT)
Correct Answer: C
*Explanation: ICA positivity confirms autoimmune beta-cell destruction in T1DM.
C-peptide indicates endogenous insulin secretion (low in T1DM) but does not
confirm autoimmunity. A1c diagnoses diabetes but not type. OGTT assesses
glucose tolerance.*
5. Maturity-Onset Diabetes of the Young (MODY) is best characterized by:
A) Ketoacidosis at presentation in a toddler
B) Autosomal dominant inheritance and non-insulin-dependent diabetes before
age 25
C) Complete absence of C-peptide
D) Strong association with HLA-DR3/DR4 haplotypes
Correct Answer: B
*Explanation: MODY is monogenic diabetes with autosomal dominant inheritance,

,onset <25 years, and preserved beta-cell function (non-insulin-dependent).
Ketoacidosis suggests T1DM. HLA-DR3/DR4 associates with T1DM, not MODY.*
6. Which of the following genetic haplotypes confers the highest risk for Type 1
diabetes?
A) HLA-DQ2 and HLA-DQ8
B) HLA-B27
C) HLA-DR4 alone
D) CFTR gene mutation
Correct Answer: A
*Explanation: HLA-DQ2 and HLA-DQ8 (often linked with DR3 and DR4) account for
~40-50% of genetic risk for T1DM. HLA-B27 is for ankylosing spondylitis. CFTR
mutations cause cystic fibrosis-related diabetes.*
7. In Type 2 diabetes, the "ominous octet" describes:
A) Eight genetic mutations causing neonatal diabetes
B) Eight pathophysiologic defects including liver, muscle, adipocytes, pancreas,
gut, brain, kidney, and alpha cells
C) Eight diagnostic criteria for metabolic syndrome
D) Eight complications of uncontrolled diabetes
Correct Answer: B
Explanation: DeFronzo's ominous octet includes defects in muscle (insulin
resistance), liver (glucose overproduction), pancreas (beta-cell dysfunction),
adipocytes (lipolysis), gut (incretin effect), alpha cells (glucagon excess), kidney
(glucose reabsorption), and brain (neurotransmitter dysfunction).
8. A patient with long-standing T2DM on metformin and glipizide presents with
fasting glucose 280 mg/dL and elevated C-peptide. This indicates:
A) Absolute insulin deficiency requiring insulin
B) Significant insulin resistance with preserved secretion
C) Factitious hypoglycemia
D) MODY

, Correct Answer: B
Explanation: Elevated C-peptide with hyperglycemia confirms preserved
endogenous insulin secretion but with severe insulin resistance. Absolute
deficiency would show low C-peptide. Factitious hypoglycemia presents with low
glucose, not elevated.
9. Glucagon-like peptide-1 (GLP-1) is primarily secreted by:
A) Pancreatic alpha cells
B) Pancreatic beta cells
C) Intestinal L-cells
D) Hepatic sinusoidal endothelial cells
Correct Answer: C
*Explanation: GLP-1 is an incretin hormone secreted by intestinal L-cells in
response to nutrient ingestion, enhancing glucose-dependent insulin secretion.
Alpha cells secrete glucagon; beta cells secrete insulin; liver cells do not secrete
GLP-1.*
10. Which statement best describes the enteroinsular axis?
A) Neural signals from stomach to pancreas
B) Hormonal communication between gut and pancreatic islets regulating insulin
secretion
C) Renal tubular reabsorption of glucose
D) Hepatic gluconeogenesis regulation by cortisol
Correct Answer: B
*Explanation: The enteroinsular axis refers to gut-derived incretin hormones (GLP-
1, GIP) that enhance glucose-stimulated insulin secretion. Option A is vagal, not
primary. Options C and D are unrelated to gut-pancreas signaling.*
11. A 14-year-old presents with diabetic ketoacidosis (DKA), undetectable C-
peptide, and positive GAD antibodies. Which treatment is essential long-term?
A) Metformin
B) Multiple daily insulin injections or insulin pump

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