Endocrine and metabolic drugs: Practice MCQs

60 practice questions with answers and explanations across 10 drug classes. All practice questions · Endocrine and metabolic drugs study guides · Download as flashcards (CSV)

Biguanides

Revise the Biguanides guide

  1. What is metformin's primary mechanism of lowering blood glucose?

    1. Stimulating pancreatic insulin secretion
    2. Reducing hepatic gluconeogenesis and improving peripheral insulin sensitivity
    3. Blocking intestinal disaccharidases
    4. Inhibiting renal glucose reabsorption
    Show answer

    Answer: B. Reducing hepatic gluconeogenesis and improving peripheral insulin sensitivity

    Metformin activates AMPK, which reduces hepatic glucose production and improves peripheral (mainly skeletal muscle) glucose uptake; it is not an insulin secretagogue.

  2. Below what eGFR is metformin absolutely contraindicated?

    1. 60 mL/min/1.73 m2
    2. 45 mL/min/1.73 m2
    3. 30 mL/min/1.73 m2
    4. 15 mL/min/1.73 m2
    Show answer

    Answer: C. 30 mL/min/1.73 m2

    The FDA label states metformin is contraindicated at eGFR below 30 mL/min/1.73 m2, and it is not recommended to be started at eGFR 30 to 45.

  3. What is the correct management of metformin around iodinated contrast imaging in an at-risk patient?

    1. Permanently discontinue metformin
    2. No action is needed regardless of renal function
    3. Discontinue at the time of or before the procedure and re-evaluate eGFR 48 hours later before restarting
    4. Double the metformin dose before the procedure
    Show answer

    Answer: C. Discontinue at the time of or before the procedure and re-evaluate eGFR 48 hours later before restarting

    The label directs a temporary hold around the procedure in patients with eGFR 30-60, liver disease, alcoholism, heart failure, or intra-arterial contrast, with renal re-evaluation 48 hours afterward.

  4. Which long-term deficiency is specifically monitored during metformin therapy?

    1. Vitamin D
    2. Vitamin B12
    3. Folate
    4. Iron
    Show answer

    Answer: B. Vitamin B12

    Metformin is associated with decreased vitamin B12 levels with long-term use, and the label recommends periodic hematologic and B12 monitoring.

  5. Why does the biguanide class carry a lactic acidosis boxed warning even though metformin's own risk is low?

    1. Because metformin caused a major lactic acidosis outbreak in trials
    2. Because the warning is a regulatory holdover from earlier biguanides, phenformin and buformin, that were withdrawn for this reason
    3. Because metformin is metabolized to a toxic lactate compound
    4. There is no lactic acidosis warning on metformin's label
    Show answer

    Answer: B. Because the warning is a regulatory holdover from earlier biguanides, phenformin and buformin, that were withdrawn for this reason

    Phenformin and buformin were withdrawn from most markets due to an unacceptable lactic acidosis rate; the mechanistic family resemblance is why the warning persists on metformin's label despite its own much lower reported risk.

  6. According to the ADA Standards of Care, what typically prompts early addition of an SGLT2 inhibitor or GLP-1 receptor agonist alongside metformin?

    1. Any elevation in HbA1c above target alone
    2. Presence of cardiovascular, renal, hepatic or obesity-related risk, independent of glycemic control
    3. Patient preference for injectable therapy only
    4. Metformin intolerance is required first
    Show answer

    Answer: B. Presence of cardiovascular, renal, hepatic or obesity-related risk, independent of glycemic control

    The ADA Standards of Care direct early addition of these classes based on cardiovascular, renal, hepatic or obesity risk rather than waiting for glycemic control alone to fail.

Bisphosphonates and bone agents

Revise the Bisphosphonates and bone agents guide

  1. What is the molecular target of nitrogen-containing bisphosphonates inside the osteoclast?

    1. RANKL
    2. Farnesyl pyrophosphate synthase in the mevalonate pathway
    3. The PTH type 1 receptor
    4. Carbonic anhydrase
    Show answer

    Answer: B. Farnesyl pyrophosphate synthase in the mevalonate pathway

    Nitrogen-containing bisphosphonates such as alendronate and zoledronic acid inhibit farnesyl pyrophosphate synthase, impairing the prenylation osteoclasts need for their cytoskeleton and driving them to apoptosis.

  2. Why must oral bisphosphonates be taken on an empty stomach with plain water and followed by remaining upright?

    1. To increase the drug's half-life
    2. Because oral bioavailability is extremely low and reduced further by food, other beverages or medication, and because of esophageal irritation risk
    3. Because the drug is destroyed by stomach acid otherwise
    4. To prevent hypocalcemia
    Show answer

    Answer: B. Because oral bioavailability is extremely low and reduced further by food, other beverages or medication, and because of esophageal irritation risk

    Oral bisphosphonate bioavailability is under 1% even under ideal fasting conditions and is reduced further by co-ingested food, drink or medication; remaining upright reduces esophageal reflux of the drug and the associated irritation risk.

  3. Which of the following is a labelled risk specifically of stopping denosumab, rather than of continuing it?

    1. Osteonecrosis of the jaw
    2. Rebound increase in bone turnover with increased vertebral fracture risk
    3. Acute-phase reaction
    4. Hypercalcemia
    Show answer

    Answer: B. Rebound increase in bone turnover with increased vertebral fracture risk

    Because denosumab's effect is not stored in bone the way a bisphosphonate's is, stopping it causes bone turnover to rebound, with an increased risk of vertebral fracture, including multiple vertebral fractures — the label calls for transitioning to another antiresorptive rather than simple discontinuation.

  4. What mechanistically distinguishes teriparatide and abaloparatide from the bisphosphonates and denosumab?

    1. They are given orally
    2. They are antiresorptive like the others but longer-acting
    3. They act as agonists at the PTH type 1 receptor and are anabolic, stimulating new bone formation rather than only slowing resorption
    4. They have no labelled long-term risks
    Show answer

    Answer: C. They act as agonists at the PTH type 1 receptor and are anabolic, stimulating new bone formation rather than only slowing resorption

    Teriparatide (PTH(1-34)) and abaloparatide (a PTHrP(1-34) analog) activate the PTH1 receptor on osteoblasts; given intermittently this favours new bone formation, the opposite direction from the antiresorptive bisphosphonates and denosumab.

  5. Zoledronic acid is contraindicated at what level of renal function?

    1. Creatinine clearance below 60 mL/min
    2. Creatinine clearance below 35 mL/min, or acute renal impairment
    3. Any degree of chronic kidney disease
    4. There is no renal contraindication
    Show answer

    Answer: B. Creatinine clearance below 35 mL/min, or acute renal impairment

    Reclast (zoledronic acid) is contraindicated in patients with creatinine clearance below 35 mL/min or evidence of acute renal impairment, reflecting its renal elimination pathway and reports of acute renal failure with the drug.

  6. What finding in animal studies led both teriparatide and abaloparatide to carry a two-year lifetime-use limitation?

    1. Hepatotoxicity in dogs
    2. Dose-dependent increases in osteosarcoma in rats
    3. Renal failure in primates
    4. QT prolongation in guinea pigs
    Show answer

    Answer: B. Dose-dependent increases in osteosarcoma in rats

    Both drugs caused a dose- and duration-dependent increase in osteosarcoma incidence in rats at exposures well above the human clinical dose, and it is unknown whether this translates to humans, which is why both labels cap lifetime use at two years.

Sex hormones and hormonal contraceptives

Revise the Sex hormones and hormonal contraceptives guide

  1. Which component of a combined hormonal contraceptive is primarily responsible for suppressing ovulation?

    1. Estrogen
    2. Progestin
    3. Neither hormone affects ovulation
    4. Only the placebo-week tablets
    Show answer

    Answer: B. Progestin

    The progestin component is primarily responsible for inhibiting gonadotropin release and preventing ovulation, while the estrogen component mainly stabilises the endometrium for predictable bleeding.

  2. The boxed warning restricting combined hormonal contraceptive use specifically applies to which group?

    1. Any woman with migraine
    2. Women over 35 years old who smoke
    3. All women over age 40
    4. Women using the method for more than 5 years
    Show answer

    Answer: B. Women over 35 years old who smoke

    The labelling contraindicates combined hormonal contraceptive use in women over 35 who smoke because of sharply increased serious cardiovascular event risk in that specific combination of age and smoking.

  3. What is the signature boxed-warning risk of depot medroxyprogesterone acetate that is not shared with combined oral contraceptives?

    1. Venous thromboembolism
    2. Loss of bone mineral density with prolonged use
    3. Endometrial cancer
    4. Virilization of a partner
    Show answer

    Answer: B. Loss of bone mineral density with prolonged use

    Depot medroxyprogesterone acetate's own boxed warning covers bone mineral density loss that increases with duration of use and may not be fully reversible, distinct from the estrogen-driven VTE warning on combined methods.

  4. Why is a progestin added to estrogen therapy for a postmenopausal woman with an intact uterus?

    1. To reduce hot flashes further
    2. To protect the endometrium from unopposed estrogen's proliferative effect and reduce endometrial cancer risk
    3. To reduce the estrogen dose needed
    4. It has no additional purpose beyond estrogen alone
    Show answer

    Answer: B. To protect the endometrium from unopposed estrogen's proliferative effect and reduce endometrial cancer risk

    Unopposed estrogen in a woman with a uterus raises endometrial cancer risk roughly two to twelve-fold; adding a progestin counteracts that proliferative effect, which is the reason combined menopausal hormone therapy exists as a distinct product from estrogen alone.

  5. According to the Women's Health Initiative findings referenced in the Prempro/Premphase label, which outcome was increased with combined estrogen-plus-progestin therapy?

    1. Only endometrial cancer
    2. Stroke, DVT, pulmonary embolism, myocardial infarction, invasive breast cancer, and probable dementia in women 65 and older
    3. Only bone fracture reduction
    4. No cardiovascular outcomes were affected
    Show answer

    Answer: B. Stroke, DVT, pulmonary embolism, myocardial infarction, invasive breast cancer, and probable dementia in women 65 and older

    The Women's Health Initiative estrogen-plus-progestin substudy found increased stroke, venous thromboembolism, myocardial infarction and invasive breast cancer, and the associated Memory Study found increased probable dementia in women 65 and older.

  6. What does the boxed warning on topical testosterone gel primarily address?

    1. Direct hepatotoxicity in the treated patient
    2. Virilization in a child or partner from secondary skin contact with an unwashed application site
    3. An increased risk of osteoporosis
    4. A drug interaction with hormonal contraceptives
    Show answer

    Answer: B. Virilization in a child or partner from secondary skin contact with an unwashed application site

    The boxed warning concerns virilization from secondary exposure — a child or partner who contacts an unwashed application site can absorb enough testosterone to show signs of androgen exposure themselves.

Systemic corticosteroids

Revise the Systemic corticosteroids guide

  1. What is the dominant molecular mechanism by which systemic corticosteroids suppress inflammation?

    1. Direct inhibition of cyclooxygenase enzyme activity
    2. Binding the intracellular glucocorticoid receptor and altering transcription of inflammatory genes
    3. Blocking histamine H1 receptors
    4. Inhibiting bacterial cell wall synthesis
    Show answer

    Answer: B. Binding the intracellular glucocorticoid receptor and altering transcription of inflammatory genes

    Corticosteroids bind the cytoplasmic glucocorticoid receptor; the hormone-receptor complex translocates to the nucleus and predominantly suppresses transcription of pro-inflammatory genes, which is the genomic mechanism responsible for most of the class's anti-inflammatory effect.

  2. What does the prednisone label say about stopping the drug after long-term therapy?

    1. It should be stopped abruptly to avoid dependency
    2. It should be withdrawn gradually rather than abruptly, to minimise drug-induced adrenocortical insufficiency
    3. No tapering is ever necessary regardless of dose or duration
    4. It can only be stopped by switching directly to dexamethasone
    Show answer

    Answer: B. It should be withdrawn gradually rather than abruptly, to minimise drug-induced adrenocortical insufficiency

    The label states that after long-term therapy, prednisone should be withdrawn gradually rather than abruptly, because gradual dose reduction minimises drug-induced secondary adrenocortical insufficiency.

  3. Which of the following statements about predicting HPA axis suppression is correct?

    1. High doses for less than one week never cause suppression
    2. Neither dose nor duration of corticosteroid therapy reliably predicts which patient develops clinically significant suppression
    3. Only IV corticosteroids can suppress the HPA axis
    4. Suppression always resolves within 48 hours of stopping the drug
    Show answer

    Answer: B. Neither dose nor duration of corticosteroid therapy reliably predicts which patient develops clinically significant suppression

    StatPearls specifically notes that duration and dosage of corticosteroid therapy are not reliable predictors of HPA suppression, and that suppression can persist for months after the drug is stopped.

  4. Why is dexamethasone often preferred over hydrocortisone when a high-potency glucocorticoid effect without fluid retention is needed, such as in cerebral edema?

    1. Dexamethasone has higher mineralocorticoid activity
    2. Dexamethasone has substantially higher glucocorticoid potency and negligible mineralocorticoid activity compared with hydrocortisone
    3. Dexamethasone cannot cross into the central nervous system
    4. Hydrocortisone is not absorbed orally
    Show answer

    Answer: B. Dexamethasone has substantially higher glucocorticoid potency and negligible mineralocorticoid activity compared with hydrocortisone

    Dexamethasone is roughly 25-30 times more potent than hydrocortisone on a glucocorticoid basis while having negligible mineralocorticoid activity, avoiding the sodium retention and edema that a mineralocorticoid-active agent like hydrocortisone would cause at an equivalent anti-inflammatory dose.

  5. Which adverse effect is specifically tied to the duration of corticosteroid therapy rather than appearing rapidly?

    1. Insomnia
    2. Osteoporosis
    3. Acute hyperglycemia
    4. Injection-site reaction
    Show answer

    Answer: B. Osteoporosis

    Osteoporosis develops with sustained glucocorticoid exposure — up to roughly 40% of patients on long-term therapy develop clinically significant bone loss — in contrast to effects such as insomnia or hyperglycemia, which can appear within days.

  6. Why is prednisolone sometimes used directly instead of prednisone in a patient with significant liver disease?

    1. Prednisolone has no adverse effects
    2. Prednisone is a prodrug requiring hepatic conversion to prednisolone, its active form, so impaired liver function can reduce its effect
    3. Prednisolone is not metabolised at all
    4. Prednisone cannot be given orally
    Show answer

    Answer: B. Prednisone is a prodrug requiring hepatic conversion to prednisolone, its active form, so impaired liver function can reduce its effect

    Prednisone must be converted hepatically to prednisolone to become active; in a patient with significant hepatic impairment that conversion may be reduced, so prednisolone is sometimes given directly instead.

Thyroid and antithyroid agents

Revise the Thyroid and antithyroid agents guide

  1. Why does levothyroxine's label direct separating its dose from calcium or iron supplements by at least 4 hours?

    1. Calcium and iron increase levothyroxine toxicity
    2. Calcium and iron reduce levothyroxine's oral absorption
    3. Levothyroxine reduces calcium and iron absorption instead
    4. There is no pharmacological interaction, only a taste conflict
    Show answer

    Answer: B. Calcium and iron reduce levothyroxine's oral absorption

    The label lists calcium and iron supplements among substances that reduce levothyroxine absorption, so dosing is separated by at least 4 hours to protect efficacy.

  2. Which thionamide is specifically preferred in the first trimester of pregnancy, and why?

    1. Methimazole, because it has no teratogenic risk at all
    2. Propylthiouracil, because its own teratogenic profile is judged less severe than methimazole's in that window
    3. Methimazole, because it crosses the placenta less readily
    4. Neither is used in pregnancy under any circumstances
    Show answer

    Answer: B. Propylthiouracil, because its own teratogenic profile is judged less severe than methimazole's in that window

    Methimazole carries a distinct first-trimester teratogenicity risk (including aplasia cutis and craniofacial anomalies), so propylthiouracil is specifically favoured in that trimester despite its own hepatotoxicity risk.

  3. What safety concern do methimazole and propylthiouracil share, and how are patients told to respond to it?

    1. Hearing loss; patients are told to get annual audiometry
    2. Agranulocytosis; patients are told to report fever or sore throat immediately
    3. Weight gain; patients are told to reduce caloric intake
    4. Photosensitivity; patients are told to avoid direct sunlight
    Show answer

    Answer: B. Agranulocytosis; patients are told to report fever or sore throat immediately

    Both thionamide labels warn of agranulocytosis and instruct patients to report fever or sore throat right away rather than waiting for a scheduled blood test, because onset can be abrupt.

  4. Why does propylthiouracil have a specific role in thyroid storm that methimazole does not share?

    1. It has a longer half-life than methimazole
    2. It additionally inhibits peripheral conversion of T4 to the more potent T3
    3. It is the only thionamide that can be given intravenously
    4. It works faster because it does not need to inhibit thyroid peroxidase
    Show answer

    Answer: B. It additionally inhibits peripheral conversion of T4 to the more potent T3

    Beyond its thyroidal TPO-inhibiting action shared with methimazole, propylthiouracil also blocks peripheral T4-to-T3 conversion, a second mechanism useful in the acute setting of thyroid storm.

  5. How soon after a levothyroxine dose change should TSH typically be rechecked in an adult?

    1. The next day
    2. After 1 week
    3. After 6 to 8 weeks
    4. TSH is never rechecked once a stable dose is found
    Show answer

    Answer: C. After 6 to 8 weeks

    Levothyroxine's label specifies rechecking TSH 6 to 8 weeks after a dosage change in adults, reflecting the drug's roughly week-long half-life and the time needed to reach a new steady state.

  6. What typically happens to thyroid function after radioactive iodine ablation for hyperthyroidism?

    1. Thyroid function usually normalises permanently without further treatment
    2. Most patients become hypothyroid and need lifelong levothyroxine replacement
    3. It has no lasting effect on thyroid hormone levels
    4. It converts hyperthyroidism into thyroid cancer in most patients
    Show answer

    Answer: B. Most patients become hypothyroid and need lifelong levothyroxine replacement

    Radioactive iodine gradually destroys thyroid tissue, and most patients subsequently become hypothyroid and require lifelong levothyroxine replacement — the same drug this page opens with.

Sulfonylureas

Revise the Sulfonylureas guide

  1. What is the immediate molecular target of a sulfonylurea on the pancreatic beta cell?

    1. The insulin receptor
    2. The SUR1 subunit of the ATP-sensitive potassium (KATP) channel
    3. GLUT2 glucose transporter
    4. AMP-activated protein kinase
    Show answer

    Answer: B. The SUR1 subunit of the ATP-sensitive potassium (KATP) channel

    Sulfonylureas bind SUR1, the regulatory subunit of the beta-cell KATP channel, closing it directly rather than through glucose metabolism.

  2. Why can sulfonylureas cause hypoglycemia in a way metformin cannot?

    1. Sulfonylureas are renally toxic
    2. Sulfonylureas trigger insulin release independent of the current blood glucose level, while metformin does not stimulate insulin secretion at all
    3. Metformin blocks insulin receptors
    4. Sulfonylureas increase glucagon secretion
    Show answer

    Answer: B. Sulfonylureas trigger insulin release independent of the current blood glucose level, while metformin does not stimulate insulin secretion at all

    Because sulfonylureas close the KATP channel directly rather than in response to glucose-driven ATP changes, insulin is released even when glucose is already normal or low — a mechanism metformin does not share.

  3. Which sulfonylurea carries the highest hypoglycemia risk and is specifically discouraged in elderly patients?

    1. Glipizide
    2. Glimepiride
    3. Glyburide
    4. All three carry identical risk
    Show answer

    Answer: C. Glyburide

    Glyburide's longer duration of action and active metabolites give it the highest hypoglycemia risk of the three, and it is specifically flagged for avoidance in elderly and renally impaired patients.

  4. The UGDP-derived cardiovascular mortality warning on sulfonylurea labels originated from a trial of which drug?

    1. Glyburide
    2. Tolbutamide
    3. Glimepiride
    4. Metformin
    Show answer

    Answer: B. Tolbutamide

    The University Group Diabetes Program studied tolbutamide, an older first-generation sulfonylurea, and its finding of increased cardiovascular mortality versus diet alone is now referenced on labels across the class.

  5. Why are sulfonylureas ineffective in type 1 diabetes?

    1. Type 1 diabetes patients metabolise the drug too quickly
    2. Sulfonylureas require functioning pancreatic beta cells to release insulin, and these are destroyed in type 1 diabetes
    3. Sulfonylureas are too weak for type 1 diabetes glucose levels
    4. They cause paradoxical hyperglycemia in type 1 diabetes
    Show answer

    Answer: B. Sulfonylureas require functioning pancreatic beta cells to release insulin, and these are destroyed in type 1 diabetes

    The KATP-channel mechanism only produces an effect if there is stored insulin in functioning beta cells to release, which is not the case once beta cells are destroyed in type 1 diabetes.

  6. Which adverse effect distinguishes the sulfonylurea class from metformin, SGLT2 inhibitors and GLP-1 receptor agonists?

    1. Lactic acidosis
    2. Weight gain
    3. Euglycemic ketoacidosis
    4. Genital mycotic infection
    Show answer

    Answer: B. Weight gain

    Weight gain is a recognised sulfonylurea class effect tied to the sustained rise in circulating insulin, in contrast to the weight-neutral or weight-reducing profile of the other classes listed.

SGLT2 inhibitors

Revise the SGLT2 inhibitors guide

  1. What transporter do SGLT2 inhibitors block, and where?

    1. GLUT4 in skeletal muscle
    2. SGLT2 in the early proximal renal tubule
    3. SGLT1 in the small intestine
    4. GLUT2 in the pancreatic beta cell
    Show answer

    Answer: B. SGLT2 in the early proximal renal tubule

    SGLT2, expressed in the early proximal renal tubule, is responsible for most filtered glucose reabsorption; blocking it produces glucosuria.

  2. What makes euglycemic diabetic ketoacidosis with SGLT2 inhibitors diagnostically tricky?

    1. It only occurs in type 1 diabetes
    2. Blood glucose at presentation can be below the level typically expected for DKA, sometimes under 250 mg/dL
    3. It never involves ketones
    4. It always presents with severe hyperglycemia first
    Show answer

    Answer: B. Blood glucose at presentation can be below the level typically expected for DKA, sometimes under 250 mg/dL

    Euglycemic DKA can present with a near-normal or only mildly elevated glucose, which can delay recognition if ketone assessment is gated on a high glucose reading.

  3. Which SGLT2 inhibitor's amputation signal led to a boxed warning that was later removed by the FDA?

    1. Empagliflozin
    2. Dapagliflozin
    3. Canagliflozin
    4. All three carried this boxed warning
    Show answer

    Answer: C. Canagliflozin

    Canagliflozin's CANVAS and CANVAS-R trials showed an increased lower-limb amputation rate, prompting a boxed warning that the FDA removed in 2020 as further data accumulated.

  4. Which indications for empagliflozin and dapagliflozin apply even in patients without type 2 diabetes?

    1. Genital mycotic infection prophylaxis
    2. Heart failure and chronic kidney disease
    3. Hypoglycemia prevention
    4. Weight-loss maintenance
    Show answer

    Answer: B. Heart failure and chronic kidney disease

    Both drugs carry heart-failure and CKD indications approved on the strength of outcomes trials conducted in populations including patients entirely without diabetes.

  5. How long before elective surgery should an SGLT2 inhibitor typically be withheld?

    1. No need to withhold
    2. At least 24 hours
    3. At least 3 days
    4. At least 3 weeks
    Show answer

    Answer: C. At least 3 days

    The labels direct withholding the drug for at least 3 days before elective surgery or a procedure involving prolonged fasting, reflecting euglycemic-DKA risk in that setting.

  6. What is the most common class-specific adverse effect of SGLT2 inhibitors?

    1. Lactic acidosis
    2. Genital mycotic infection
    3. Severe hypoglycemia
    4. Agranulocytosis
    Show answer

    Answer: B. Genital mycotic infection

    Genital mycotic infection is the most frequently reported class-specific adverse effect, reflecting the glucosuria the mechanism itself produces.

GLP-1 receptor agonists

Revise the GLP-1 receptor agonists guide

  1. Why is hypoglycemia uncommon when a GLP-1 receptor agonist is used alone?

    1. The drugs block glucose absorption in the gut
    2. Insulin secretion and glucagon suppression are glucose-dependent, so the effect fades as glucose normalizes
    3. The drugs have no effect on insulin at all
    4. They are metabolized before reaching the pancreas
    Show answer

    Answer: B. Insulin secretion and glucagon suppression are glucose-dependent, so the effect fades as glucose normalizes

    GLP-1 receptor agonists potentiate insulin secretion and suppress glucagon only when glucose is elevated, which is why hypoglycemia is uncommon on monotherapy but rises when combined with insulin or a sulfonylurea.

  2. Which GLP-1 receptor agonist is available as an oral tablet?

    1. Liraglutide
    2. Dulaglutide
    3. Semaglutide
    4. Exenatide
    Show answer

    Answer: C. Semaglutide

    Semaglutide is marketed as the oral tablet Rybelsus in addition to the injectable products Ozempic and Wegovy; it is the only class member with an oral formulation.

  3. What distinguishes tirzepatide's mechanism from the other drugs in this class?

    1. It is a sulfonylurea
    2. It activates the GIP receptor in addition to the GLP-1 receptor
    3. It has no incretin activity
    4. It works only in type 1 diabetes
    Show answer

    Answer: B. It activates the GIP receptor in addition to the GLP-1 receptor

    Tirzepatide is a dual GIP/GLP-1 receptor agonist, distinguishing it mechanistically from the GLP-1-only agents semaglutide, liraglutide, dulaglutide and exenatide.

  4. What is the basis of the thyroid C-cell tumor boxed warning shared by this class?

    1. Confirmed cases of medullary thyroid carcinoma in large human trials
    2. Dose-dependent thyroid C-cell tumors observed in rodent studies, with unknown human relevance
    3. Routine calcitonin monitoring showing elevated levels in most patients
    4. A single case report in one patient
    Show answer

    Answer: B. Dose-dependent thyroid C-cell tumors observed in rodent studies, with unknown human relevance

    The boxed warning is based on rodent data showing dose- and duration-dependent thyroid C-cell tumors; the label states human relevance is unknown, and routine calcitonin monitoring is not recommended.

  5. Which class member carries a specific caution against use in severe renal impairment or end-stage renal disease?

    1. Semaglutide
    2. Liraglutide
    3. Exenatide
    4. Dulaglutide
    Show answer

    Answer: C. Exenatide

    Exenatide has meaningful renal clearance and is not recommended in severe renal impairment or end-stage renal disease, a caution not shared by the other members reviewed here.

  6. Semaglutide and liraglutide are each marketed under a diabetes brand name and a separate weight-management brand name. Which pairing is correct?

    1. Ozempic for weight management, Wegovy for diabetes
    2. Victoza for weight management, Saxenda for diabetes
    3. Ozempic for diabetes, Wegovy for weight management; Victoza for diabetes, Saxenda for weight management
    4. Both drugs use the same brand name for both indications
    Show answer

    Answer: C. Ozempic for diabetes, Wegovy for weight management; Victoza for diabetes, Saxenda for weight management

    Ozempic (semaglutide) and Victoza (liraglutide) are the diabetes-indicated products; Wegovy (semaglutide) and Saxenda (liraglutide) are the higher-dose weight-management products.

DPP-4 inhibitors

Revise the DPP-4 inhibitors guide

  1. What is the core mechanistic difference between DPP-4 inhibitors and GLP-1 receptor agonists?

    1. DPP-4 inhibitors are injectable, GLP-1 receptor agonists are oral
    2. DPP-4 inhibitors block the enzyme that degrades the body's own incretins; GLP-1 receptor agonists directly activate the GLP-1 receptor with an external analog
    3. They have identical mechanisms with different names
    4. DPP-4 inhibitors cause more weight loss than GLP-1 receptor agonists
    Show answer

    Answer: B. DPP-4 inhibitors block the enzyme that degrades the body's own incretins; GLP-1 receptor agonists directly activate the GLP-1 receptor with an external analog

    DPP-4 inhibitors raise levels of the patient's own endogenous GLP-1 and GIP by blocking their degrading enzyme, while GLP-1 receptor agonists supply an external molecule that activates the GLP-1 receptor directly, producing a larger effect.

  2. Which DPP-4 inhibitor has a dedicated cardiovascular outcomes trial (SAVOR-TIMI 53) showing a higher rate of heart-failure hospitalization than placebo?

    1. Sitagliptin
    2. Linagliptin
    3. Saxagliptin
    4. None of the class
    Show answer

    Answer: C. Saxagliptin

    SAVOR-TIMI 53 studied saxagliptin specifically and found heart-failure hospitalization in 3.5% of the saxagliptin group versus 2.8% on placebo.

  3. Which DPP-4 inhibitor requires no dose adjustment for renal impairment of any severity?

    1. Sitagliptin
    2. Alogliptin
    3. Saxagliptin
    4. Linagliptin
    Show answer

    Answer: D. Linagliptin

    Linagliptin is eliminated predominantly through the enterohepatic/biliary route, so no dosage adjustment is recommended for renal impairment at any severity, unlike the other three members of the class.

  4. How does the DPP-4 inhibitor class compare with insulin and GLP-1 receptor agonists in HbA1c-lowering efficacy, per the ADA Standards of Care?

    1. DPP-4 inhibitors produce the largest HbA1c reductions
    2. DPP-4 inhibitors produce the smallest HbA1c reductions among major glucose-lowering classes
    3. All classes produce identical HbA1c reductions
    4. DPP-4 inhibitors cannot lower HbA1c at all
    Show answer

    Answer: B. DPP-4 inhibitors produce the smallest HbA1c reductions among major glucose-lowering classes

    The ADA Standards of Care describe insulin, select GLP-1 receptor agonists (particularly semaglutide) and tirzepatide as producing the largest HbA1c reductions, with DPP-4 inhibitors producing the smallest.

  5. What joint-related adverse effect is described across DPP-4 inhibitor labelling?

    1. Mild, self-limited myalgia only
    2. Severe and disabling arthralgia, with onset from one day to years after starting treatment
    3. Permanent joint destruction in all patients
    4. No joint-related effects have been reported
    Show answer

    Answer: B. Severe and disabling arthralgia, with onset from one day to years after starting treatment

    Linagliptin's and saxagliptin's labelling describe severe and disabling arthralgia as a recognised DPP-4 inhibitor class effect, with variable onset and symptom relief reported on discontinuation in some patients.

  6. Which DPP-4 inhibitor's label specifically names Stevens-Johnson syndrome among its serious hypersensitivity reactions?

    1. Linagliptin
    2. Sitagliptin
    3. Saxagliptin
    4. Alogliptin
    Show answer

    Answer: B. Sitagliptin

    Sitagliptin's label specifically names Stevens-Johnson syndrome, along with anaphylaxis and angioedema, among the serious hypersensitivity reactions that have occurred, typically within the first three months of treatment.

Insulins

Revise the Insulins guide

  1. What is the basis for classifying insulins into rapid, short, intermediate and long-acting categories?

    1. Different molecular targets for each category
    2. Pharmacokinetic differences in onset, peak and duration, since all insulins act on the same receptor
    3. Different routes of administration only
    4. Different indications for type 1 versus type 2 diabetes
    Show answer

    Answer: B. Pharmacokinetic differences in onset, peak and duration, since all insulins act on the same receptor

    Every insulin formulation activates the same insulin receptor; the rapid/short/intermediate/long-acting categories describe how quickly each formulation is absorbed and how long it lasts, not a different mechanism.

  2. Which insulin formulation is labelled for intravenous administration?

    1. Insulin lispro
    2. Insulin glargine
    3. Regular human insulin
    4. NPH insulin
    Show answer

    Answer: C. Regular human insulin

    Regular human insulin can be administered intravenously under close medical supervision with glucose and potassium monitoring; the rapid-acting analogs, glargine, degludec and NPH in the material reviewed here are subcutaneous-only.

  3. What must be done with NPH insulin before each dose, and why?

    1. Nothing, it is a clear ready-to-inject solution
    2. It must be gently rolled and inverted to resuspend the cloudy suspension evenly
    3. It must be diluted with saline
    4. It must be warmed to body temperature
    Show answer

    Answer: B. It must be gently rolled and inverted to resuspend the cloudy suspension evenly

    NPH is a protamine-containing cloudy suspension that settles between doses; the label instructs gently rolling and inverting the vial or pen, not shaking, to resuspend it evenly before each injection.

  4. What distinguishes insulin's contraindication profile from that of the oral glucose-lowering drug classes?

    1. Insulin has more absolute contraindications than oral agents
    2. Insulin has no absolute contraindication beyond hypersensitivity and active hypoglycemia, because dose is titrated to the individual
    3. Insulin cannot be used in renal impairment under any circumstances
    4. Insulin and oral agents have identical contraindication profiles
    Show answer

    Answer: B. Insulin has no absolute contraindication beyond hypersensitivity and active hypoglycemia, because dose is titrated to the individual

    Because insulin dose has no fixed ceiling and is adjusted to the individual patient's glucose response, it carries no absolute contraindication beyond hypersensitivity and active hypoglycemia in the material reviewed, unlike oral agents with fixed dosing and renal/hepatic thresholds.

  5. What is the basal-bolus concept in insulin therapy?

    1. Using only one type of insulin for all purposes
    2. Pairing a long-acting (basal) insulin for background coverage with a rapid- or short-acting (bolus) insulin dosed before meals
    3. Giving insulin only during acute illness
    4. Using premixed insulin exclusively
    Show answer

    Answer: B. Pairing a long-acting (basal) insulin for background coverage with a rapid- or short-acting (bolus) insulin dosed before meals

    A basal-bolus regimen combines a long-acting insulin that supplies steady background coverage with a rapid- or short-acting insulin dosed before meals to cover the glucose load from food, approximating normal pancreatic insulin secretion.

  6. Which long-acting insulin has the longest labelled duration of glucose-lowering effect?

    1. NPH
    2. Insulin glargine
    3. Insulin degludec
    4. Regular human insulin
    Show answer

    Answer: C. Insulin degludec

    Insulin degludec's labelled glucose-lowering effect persists for at least 42 hours after the final dose, with a roughly 25-hour half-life at steady state, longer than glargine's approximately 24-hour duration.