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GRAND CANYON UNIVERSITY FINAL EXAM STUDY GUIDE
2025 LATEST UPDATE 100+ QUESTIONS AND CORRECT
DETAILED ANSWERS (VERIFIED ANSWERS) |GRADED A+
2 drugs that directly work on pathophysiological causes of gout - ANSWER:
allopurinol and febuxostat because they block the xanthine oxidase enzyme,
inhibiting formation of uric acid
What comorbid can occur with gout - ANSWER: renal calculi
what reduces inflammatory response in gout, reduces the pain in acute gout but
does not stop gout from developing into gouty arthritis - ANSWER: colchicine
Colchicine efficacy is affected by what - ANSWER: incidence of adverse effects
Urate lowering therapy can initiate an acute gouty attack, what do you give with
ULT drugs to decrease incidence of ULT induced gouty attacks? - ANSWER:
concomitant colchicine, NSAIDs or corticosteroids
what is agent of choice for individuals with gout and high serum urate levels with
underlying renal dysfunction, history of tophaceous gout or urinary caliculi? -
ANSWER: allopurinol
Acute gouty attacks treated preferentially with what? - ANSWER: NSAIDS
(indomethacin, ibuprofen, naproxen, sulindac)
NSAIDs can cause GI bleeding. What can you switch to to avoid? - ANSWER:
COX-2 inhibitor (celecoxib)
Pharmacokinetics - ANSWER: The process by which drugs are absorbed,
distributed within the body, metabolized, and excreted.
The route of administration with highest bioavailability - ANSWER: intravenous
steady state (SS) is reached in what time frame - ANSWER: 4-5 half lives of a
drug
zero order (non-linear) pharmacokinetics - ANSWER: drug is metabolized at a
constant rate per unit time
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Steps of drug development - ANSWER: phase 1 preclinical research with animal
testing
phase 2 human subjects for med safety
Phase 3 humans comparing drug to accepted meds or placebo
FDA review of results
post-marketing study
Angiotensin-converting enzyme (ACE) inhibitors MOA - ANSWER: lower blood
pressure by inhibiting the conversion of angiotensin I (an inactive enzyme) to
angiotensin II (a potent vasoconstrictor)
ACEIs ending - ANSWER: -pril
Important side effects of ACEIs (2) - ANSWER: cough, angioedema
ARBs end in? - ANSWER: -sartan
ARBs MOA - ANSWER: Block angiotensin-2 type 1 receptors (AT1 receptor)
Decrease BP via arteriolar and venous dilation
Block aldosterone secretion (decreased Na2+ and H2O retention)
Does NOT increase Bradykinin levels
Decrease diabetic nephrotoxicity
% of htn that are essential (primary) - ANSWER: 90%
nitrates are contraindicated for pts w/ - ANSWER: PDE-5 inhibitors (sildenafil and
vardenafil)
Alpha-1 adrenergic stimulation results in - ANSWER: vasoconstriction and
increased blood pressure
Alpha 1 adrenergic blockade results in - ANSWER: vasodilation and reduced
blood pressure
Beta 1 adrenergic stimulation by beta agonists results in - ANSWER: increased
heart rate, increased blood pressure, increased cardiac output
Beta blockers ending - ANSWER: -olol
GRAND CANYON UNIVERSITY FINAL EXAM STUDY GUIDE
2025 LATEST UPDATE 100+ QUESTIONS AND CORRECT
DETAILED ANSWERS (VERIFIED ANSWERS) |GRADED A+
2 drugs that directly work on pathophysiological causes of gout - ANSWER:
allopurinol and febuxostat because they block the xanthine oxidase enzyme,
inhibiting formation of uric acid
What comorbid can occur with gout - ANSWER: renal calculi
what reduces inflammatory response in gout, reduces the pain in acute gout but
does not stop gout from developing into gouty arthritis - ANSWER: colchicine
Colchicine efficacy is affected by what - ANSWER: incidence of adverse effects
Urate lowering therapy can initiate an acute gouty attack, what do you give with
ULT drugs to decrease incidence of ULT induced gouty attacks? - ANSWER:
concomitant colchicine, NSAIDs or corticosteroids
what is agent of choice for individuals with gout and high serum urate levels with
underlying renal dysfunction, history of tophaceous gout or urinary caliculi? -
ANSWER: allopurinol
Acute gouty attacks treated preferentially with what? - ANSWER: NSAIDS
(indomethacin, ibuprofen, naproxen, sulindac)
NSAIDs can cause GI bleeding. What can you switch to to avoid? - ANSWER:
COX-2 inhibitor (celecoxib)
Pharmacokinetics - ANSWER: The process by which drugs are absorbed,
distributed within the body, metabolized, and excreted.
The route of administration with highest bioavailability - ANSWER: intravenous
steady state (SS) is reached in what time frame - ANSWER: 4-5 half lives of a
drug
zero order (non-linear) pharmacokinetics - ANSWER: drug is metabolized at a
constant rate per unit time
, 2|Page
Steps of drug development - ANSWER: phase 1 preclinical research with animal
testing
phase 2 human subjects for med safety
Phase 3 humans comparing drug to accepted meds or placebo
FDA review of results
post-marketing study
Angiotensin-converting enzyme (ACE) inhibitors MOA - ANSWER: lower blood
pressure by inhibiting the conversion of angiotensin I (an inactive enzyme) to
angiotensin II (a potent vasoconstrictor)
ACEIs ending - ANSWER: -pril
Important side effects of ACEIs (2) - ANSWER: cough, angioedema
ARBs end in? - ANSWER: -sartan
ARBs MOA - ANSWER: Block angiotensin-2 type 1 receptors (AT1 receptor)
Decrease BP via arteriolar and venous dilation
Block aldosterone secretion (decreased Na2+ and H2O retention)
Does NOT increase Bradykinin levels
Decrease diabetic nephrotoxicity
% of htn that are essential (primary) - ANSWER: 90%
nitrates are contraindicated for pts w/ - ANSWER: PDE-5 inhibitors (sildenafil and
vardenafil)
Alpha-1 adrenergic stimulation results in - ANSWER: vasoconstriction and
increased blood pressure
Alpha 1 adrenergic blockade results in - ANSWER: vasodilation and reduced
blood pressure
Beta 1 adrenergic stimulation by beta agonists results in - ANSWER: increased
heart rate, increased blood pressure, increased cardiac output
Beta blockers ending - ANSWER: -olol
