ATI Multisystem Disorders Practice Exam
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Question 1
A client with systemic lupus erythematosus (SLE) presents with new-
onset seizures and confusion. Which of the following is the most likely
underlying pathophysiological mechanism?
A) Deposition of immune complexes in the cerebral microvasculature
B) Acute bacterial meningitis secondary to immunosuppression
C) Rapidly progressive cerebral atrophy due to chronic corticosteroid
use
D) Ischemic stroke from antiphospholipid antibody-induced thrombosis
Answer: A) Deposition of immune complexes in the cerebral
microvasculature
Explanation: Neuropsychiatric SLE (NPSLE) is primarily driven by
immune-complex deposition and complement-mediated inflammation
in the cerebral vasculature, leading to endothelial dysfunction, blood-
brain barrier disruption, and neuronal injury. While antiphospholipid
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antibodies increase thrombotic risk (D), the acute onset of seizures and
confusion in active SLE more directly implicates immune-complex
vasculopathy. Bacterial meningitis (B) is less common without specific
risk factors, and corticosteroid-induced atrophy (C) is a chronic, not
acute, phenomenon.
Question 2
A 68-year-old male with type 2 diabetes mellitus and chronic kidney
disease stage 4 is admitted with hyperkalemia (serum K+ 6.8 mEq/L)
and peaked T waves. Which intervention should the nurse anticipate
administering first?
A) Intravenous calcium gluconate
B) Intravenous insulin with dextrose
C) Oral sodium polystyrene sulfonate
D) Intravenous sodium bicarbonate
Answer: A) Intravenous calcium gluconate
Explanation: In hyperkalemia with electrocardiographic changes
(peaked T waves), the priority is myocardial membrane stabilization to
prevent lethal arrhythmias. Calcium gluconate directly antagonizes the
effects of elevated potassium on cardiac myocyte excitability. Insulin
with dextrose (B) shifts potassium intracellularly but takes 15-30
minutes; sodium polystyrene sulfonate (C) is slower and removes
potassium via the gastrointestinal tract; sodium bicarbonate (D) is
effective primarily in metabolic acidosis, which may not be the
predominant driver here.
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Question 3
A patient with chronic obstructive pulmonary disease (COPD) and cor
pulmonale is receiving digoxin. Which assessment finding would most
strongly suggest digoxin toxicity?
A) Heart rate of 58 beats per minute
B) Anorexia and nausea
C) Visual disturbances such as yellow-green halos
D) Serum digoxin level of 1.8 ng/mL
Answer: C) Visual disturbances such as yellow-green halos
Explanation: Digoxin toxicity manifests with gastrointestinal (anorexia,
nausea), cardiac (bradyarrhythmias, ectopy), and neurologic/visual
symptoms. Xanthopsia (yellow-green halos) is a classic and highly
specific sign of toxicity. A heart rate of 58 (A) may be therapeutic in
COPD with cor pulmonale. Serum digoxin level of 1.8 ng/mL (D) is within
the therapeutic range (0.8–2.0 ng/mL), though toxicity can occur even
at therapeutic levels in renal impairment or electrolyte disturbances.
Question 4
A 55-year-old female with rheumatoid arthritis is started on
methotrexate. To minimize the risk of methotrexate-induced
hepatotoxicity and myelosuppression, which supplemental agent
should be co-administered?
A) Vitamin B12
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B) Folic acid
C) Vitamin C
D) Calcium carbonate
Answer: B) Folic acid
Explanation: Methotrexate is a folate antagonist; its inhibition of
dihydrofolate reductase leads to decreased synthesis of purines and
thymidylate, causing cytotoxicity. Supplemental folic acid (1–5 mg daily)
reduces the incidence of gastrointestinal side effects, hepatotoxicity,
and bone marrow suppression without significantly compromising
therapeutic efficacy. Vitamin B12 (A) is not the primary deficiency;
vitamin C and calcium (C, D) do not counteract methotrexate’s
mechanism.
Question 5
A client with acute pancreatitis is experiencing severe abdominal pain,
nausea, and vomiting. Which laboratory finding is most specific for the
diagnosis of acute pancreatitis?
A) Elevated serum amylase
B) Elevated serum lipase
C) Elevated serum bilirubin
D) Leukocytosis
Answer: B) Elevated serum lipase