Pharm 1
Pharm 2
Pharm 3
Pharm 4
Pharm 5
100

A 24-year-old woman comes to the emergency department after a tonic-clonic seizure. Prior to the seizure, she had increasing lethargy and confusion for 1 day. She has type 2 diabetes mellitus (DM). She discontinued metformin 3 months ago because of lactic acidosis and started on another oral medication for her DM. On physical examination, she is groggy and cannot answer questions fluently.

Which of the following medications was most likely prescribed 3 months ago?

a. Acarbose

b. Exenatide

c. Glyburide

d. Rosiglitazone

e. Saxagliptin

C. Glyburide

This patient with type 2 DM presents with symptoms of fatigue and seizures that are typical of hypoglycemia. In this patient, the hypoglycemia is likely an adverse effect of her diabetes medication.


Step 2: Drug Adverse Effects


Sulfonylureas (eg, glipizide, glyburide) treat type 2 DM by increasing insulin secretion. Sulfonylureas block the adenosine triphosphate–sensitive potassium channels in β-cells, causing cell membrane depolarization and thus opening the voltage intracellular calcium channel, leading to calcium influx and triggering insulin release. The hypoglycemia in this patient is an adverse effect of increased insulin secretion caused by sulfonylureas. Compared to other forms of medications used to manage diabetes, sulfonylureas have the greatest risk for hypoglycemia. In addition, these drugs can cause weight gain.


The other choices are incorrect:

  • Saxagliptin and other gliptins can cause nausea and increased risk of heart failure.
  • Rosiglitazone, a type of thiazolidinedione, increases peripheral insulin sensitivity by upregulating the number of peroxisome proliferation-activated receptors. Adverse effects include weight gain, edema, increased fracture risk, and potential hepatotoxicity.
  • α-Glucosidase inhibitors such as acarbose work by decreasing intestinal absorption of carbohydrates. Flatulence and abdominal pain are frequent adverse effects of these drugs.
  • Exenatide is a glucagon-like peptide 1 agonist. These drugs cause gastrointestinal side effects.
100

A 68-year-old woman undergoes percutaneous balloon angioplasty after an acute ST-segment elevation myocardial infarction (STEMI). Medical history is significant for hypertension and severe chronic obstructive pulmonary disease. Following the angioplasty, she is started on a regimen that includes a medication that primarily acts by decreasing the slope of phase 4 in cardiac pacemaker cells.This patient was most likely prescribed which of the following drugs?

a. Labetalol 

b. Metoprolol 

c. Pindolol 

d. Propranolol 

e. Sotalol 

b. Metoprolol

 

Patients who have experienced a STEMI will likely be administered four types of medications that have proven to reduce morbidity and mortality in this population: an antiplatelet medication such as aspirin and/or clopidogrel, an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker, a statin, and a β-blocker. β-Blockers decrease sympathetic input to the heart and conductive system. By decreasing cAMP levels in sinoatrial (SA) nodal cells, β-blockers reduce the activity of the funny current (If), thus flattening the slope of phase 4 of the action potential in SA nodal cells and slowing heart rate.


Step 2: Drug Mechanism


β-Blockers may be cardioselective or nonselective. Because nonselective β-blockers act on β2-receptors on bronchial smooth muscle cells and favor contraction, they are contraindicated in patients with airway diseases, such as this patient with severe chronic obstructive pulmonary disease. Therefore only β1-blockers (cardioselective) should be used in patients with chronic obstructive pulmonary disease. These medications include atenolol, esmolol, metoprolol, and nebivolol. The β-blocker metoprolol is the only cardioselective β-blocker among the options listed, making it the preferred treatment in this case.


The other choices are incorrect:

  • Propranolol and pindolol are nonselective β-blockers.
  • Sotalol is a class III antiarrhythmic drug that blocks potassium channels and is a nonselective β-blocker.
  • Labetalol is a nonselective β-blocker with α1-blockade.
100

How do α1-receptor blockers reduce the urinary symptoms of benign prostatic hyperplasia?

α1-Receptor blockers dilate the urethra by preventing urethral, prostatic, and bladder neck smooth muscle contraction.

100

What are the major functions of β1-receptor activation? (p 239)

β1-receptor activation increases the following: heart rate and contractility, renin release from the kidneys, and lipolysis of adipose tissue.

100

A 63-year-old man is referred to long-term care after his first myocardial infarction. Is a β-blocker suggested or contraindicated for this patient? Why? (p 246)

How do β-blockers work in the setting of angina pectoris? (p 246)  

Suggested. After myocardial infarction, patients should receive β-blockers to decrease risk of mortality (long-term)

 They decrease heart rate and contractility, thereby reducing myocardial oxygen consumption

200

A 26-year-old man is receiving antimicrobial treatment for methicillin-resistant Staphylococcus aureus endocarditis. Shortly after the antibiotic is given as a bolus intravenously, he becomes severely flushed around the face and neck.Which of the following strategies would best avoid this adverse drug effect while effectively treating his disease?

a. Desensitization therapy 

b. Oral administration rather than intravenous 

c. Pretreatment with cortisone 

d. Pretreatment with ipratropium 

e. Slower infusion of the drug

E. slower infusion of the drug

Vancomycin is the drug of choice for patients with methicillin-resistant S aureus infections, including endocarditis.


Step 2: Drug Adverse Effects


This patient has vancomycin infusion reaction (formerly known as red man syndrome), given the description of flushing around the face and neck shortly after antibiotic infusion. This is a nonallergic reaction due to the release of histamine following the administration of vancomycin.


Step 3: Drug Adverse Effects:  Drug Infusion


Slower infusion of the drug, along with pretreatment with antihistamines, can decrease the incidence of vancomycin infusion reaction. In situations that threaten a patient’s life, slower infusion is not practical. Such patients need to be managed to secure airway, breathing, and circulation first. However, the general treatment includes antihistamines (H1 and H2-receptor blockers can offer protection). Prevention of infusion-related adverse events of vancomycin include premedication with diphenhydramine, and a decrease in infusion rates to less than 10 mg/min.


The other choices are incorrect:

  • Desensitization therapy plays an important role in the administration of essential drugs to patients with severe allergies.
  • Pretreatment with cortisone would not be indicated because steroids are typically used after anaphylactic drug reactions, not before. 
  • Oral administration rather than intravenous administration of vancomycin would not be effective in treating S aureus endocarditis because oral vancomycin is not effectively absorbed from the gastrointestinal tract.
  • Pretreatment with ipratropium would decrease airway smooth muscle contraction and is typically used in patients with chronic obstructive pulmonary disease.
200

A 60-year-old man comes to the clinic for evaluation of sudden-onset severe pain in his fingers and toes. He has a history of alcohol use disorder. Once his acute episode has been appropriately managed, he is prescribed a drug that reduces uric acid reabsorption in renal proximal tubule cells.Which of the following medications was most likely prescribed?

a. Allopurinol 

b. Anakinra 

c. Colchicine 

d. Cortisone 

e. Methotrexate 

f. Probenecid 

f. Probenecid

 

This patient likely has gout, based on the acute-onset severe pain in his fingers and toes and a history of alcohol use disorder. While the exact mechanism by which alcohol use disorder increases the risk of gout is unknown, it is thought that alcohol use disorder alters the amount of uric acid that is eliminated by the kidneys, and it is known that some types of alcohol contain purines that are metabolized into uric acid. Gout is associated with elevations in serum uric acid levels, which can lead to the formation of uric acid crystals. This can cause extremely painful inflammation, most commonly in the metatarsophalangeal joints.


Step 2: Drug Mechanism


This patient was most likely prescribed probenecid. Probenecid and sulfinpyrazone are useful in the treatment of gout because they inhibit uric acid reabsorption in the proximal convoluted tubule. Typically, organic anion transporters are responsible for reabsorbing uric acid from the renal filtrate in the proximal convoluted tubule. Probenecid has a higher affinity to these organic anion transporters than uric acid and therefore uric acid is not reabsorbed. In the presence of probenecid, urine will contain higher levels of uric acid, thereby explaining its role in preventing chronic gout. Probenecid, however, is not useful in the management of an acute gout flare because it does not have anti-inflammatory properties, nor does it remove urate deposits from joint spaces in an acute setting.


The other choices are incorrect:

  • Allopurinol is the treatment of choice for chronic gout, but works by blocking the enzyme xanthine oxidase, preventing the formation of uric acid from purines. Overall, this results in decreased uric acid concentrations in serum and urine.
  • Colchicine depolymerizes microtubules, limiting the inflammatory response to urate crystals.
  • A cortisone injection can reduce inflammation and pain in gout patients, and it is best used for acute episodes.
  • Anakinra is an interleukin-1 (IL-1) inhibitor used to treat acute episodes of gout and prevent such episodes. It works by blocking the action of IL-1.
  • Methotrexate is an immunosuppressive drug that is used for rheumatoid arthritis. It is contraindicated in gout because it can cause acute gouty attacks.


200


Which principle is most important in treating the severe hypertension of pheochromocytoma?

a. First block α1-receptors, then α2-receptors

b. First block α1-receptors, then β-receptors

c. First block α2-receptors, then α1-receptors

d. First block β-receptors, then α1-receptors





First block β-receptors, then α2-receptors 

b. First block α1-receptors, then β-receptors

The correct answer is first block α1-receptors, then β-receptors (B). Pheochromocytoma leads to a massive outpouring of catecholamines that stimulates all adrenergic receptors. It is important to first block α1-receptors, then β-receptors because blocking β-receptors first would lead to unopposed α1-receptor action with worsening of the already severe hypertension. The other options (A, C, D, and E) are not the correct sequence, and α2-receptor blockade is less important in treatment.

200

What is the major effect of β2-receptor activation on the body's vasculature? What is the effect on the respiratory system? (p 239)

Vasodilation; bronchodilation.

200

Which drugs must be avoided in patients with sulfa allergy? (p 253)

1. Sulfonamide antibiotics,

2.  sulfasalazine, 

3. probenecid, 

4. furosemide, 

5. acetazolamide, 

6. celecoxib, 

7. thiazides, and 

8. sulfonylureas

 (Remember: Scary Sulfa Pharm FACTS.)

300

A 46-year-old woman comes to her physician because she always feels thirsty, despite drinking large volumes of water; is urinating more often and in greater volume; and has dizziness upon standing. She has bipolar disorder and says she occasionally doubles her medication when she thinks she is entering a depressive phase. Which of the following set of findings is most likely present in this patient?

a. Hypernatremia, high urine sodium, and high urine osmolality 

b. Hypernatremia, low urine sodium, and high urine osmolality 

c. Hypernatremia, low urine sodium, and low urine osmolality 

d. Hyponatremia, high urine sodium, and high urine osmolality 

c. Hypernatremia, Low urine sodium, and low urine osmolality

This patient is taking medication for bipolar disorder and now presents with polydipsia, polyuria, and dizziness upon standing. Together, these symptoms suggest that she has nephrogenic diabetes insipidus (NDI) due to lithium. NDI is caused by unresponsiveness to ADH by the principal cells of the cortical collecting duct. NDI can be caused by lithium as well as chronic interstitial kidney diseases, urinary obstruction, and chronic hypokalemia or hypercalcemia. Twenty percent of patients taking lithium develop NDI.


Step 2: Disease Mechanism


NDI causes free water losses, causing large volumes of dilute urine. This leads to volume depletion, causing the kidney to retain sodium, and hypernatremia, reflecting the total body water depletion. Overall, this means the patient would have hypernatremia, low urine sodium, and low urine osmolality. She should be given normal saline (to correct volume depletion) and then free water (to correct the water deficit).


The other answers are incorrect:

  • Hyponatremia, low urine sodium, and low urine osmolality would be seen in primary polydipsia.
  • Hyponatremia, high urine sodium, and high urine osmolality would be seen in the syndrome of inappropriate secretion of ADH.
  • Hypernatremia, low urine sodium, and high urine osmolality would characterize nonrenal free water losses.
  • Hypernatremia, high urine sodium, and high urine osmolality would be seen with high salt intake.
  • Hyponatremia, low urine sodium, and high urine osmolality would indicate low arterial perfusion and high ADH levels with renal sodium retention. 
300

What are the main clinical uses of α1-agonists?

Inhaled α1-agonists (eg, phenylephrine) may be used to relieve nasal congestion. 

Systemic α1-agonists (eg, midodrine) may be used to treat orthostatic hypotension and reflex syncope.

300

A 46-year-old man with a medical history of hypertension that is being controlled by diet comes to clinic because of persistent nausea. He recently purchased a boat and experiences nausea and vomiting that begin soon after each trip is underway, especially when he is below deck. His evaluation is otherwise completely normal. The physician suspects the patient is experiencing simple motion sickness. Which of the following muscarinic antagonists would be most suitable for this patient? 

a. Atropine

b. Ipratropium

c. Oxybutynin

d. Scopolamine

e. Tropicamide 

d. Scopolamine

The correct answer is scopolamine (D). Scopolamine is available as a patch, allowing the drug to be absorbed into the systemic circulation to treat motion sickness. Atropine (A) has effects similar to those of scopolamine, but it is used primarily as a pre-anesthetic medication to reduce secretions and in the treatment of heart block or sinus bradycardia. Ipratropium (B) is used mainly as an inhaled medication in the treatment of asthma and COPD. Oxybutynin (C) is used in the treatment of detrusor overactivity or urge incontinence. Tropicamide (E) is used in eye-drop form to induce mydriasis prior to fundoscopic exams.

300

Name seven indirect agonists (anticholinesterases). (p 241)

1. Neostigmine, 

2. pyridostigmine, 

3. physostigmine, 

4. donepezil, 

5. rivastigmine, 

6. galantamine, and 

7. edrophonium

300

Which medications can cause pulmonary fibrosis? (p 252)

1. Bleomycin, 

2. amiodarone, 

3. methotrexate, 

4. nitrofurantoin, 

5. carmustine, and 

6. busulfan. 

400

A 58-year-old man comes to the physician because of fatigue, fever, and joint pain for the past several weeks. He has a history of systolic heart failure treated with enalapril, which was discontinued because of angioedema. The patient was switched to isosorbide and an antihypertensive agent. On physical examination today, his knees and hands are edematous and tender to palpation. Laboratory studies are notable for positive anti-histone antibodies and antinuclear antibodies.

Which of the following best describes the mechanism of action of the newly prescribed antihypertensive agent that was paired with isosorbide?

a. Blocks angiotensin II receptors 

b. Dilates arterioles 

c. Inhibits the Na+/K+/2Cl– contransporter 

d. Inhibits the distal tubule Na+/Cl– cotransporter 

e. Prevents the influx of calcium into cardiac and smooth muscle cell 

b. Dilates arterioles

 

This patient has arthritis, fever, and fatigue with positive antinuclear antibodies and anti-histone antibodies, suggesting drug-induced lupus erythematosus. This is an autoimmune disease with autoantibodies formed against certain drugs, most commonly procainamide (30% of patients) and hydralazine (5% to 10% of patients); minocycline, penicillamine, and anti-TNF agents such as etanercept are less common causes. Compared to systemic lupus erythematosus, patients are less likely to have skin, hematologic, or renal disease. Fever, arthritis, and pericardiac/pleural inflammation are the most common manifestations.


Step 2: Drug mechanism


Of the common medications that cause drug-induced lupus, hydralazine is most likely to have been prescribed to this patient. It is paired with nitrates as secondary therapy for systolic heart failure in patients who are resistant to angiotensin-converting enzyme inhibitors or cannot tolerate them. Hydralazine is a direct arteriolar dilator. It is only rarely used for hypertension.


The other choices are incorrect:

  • Calcium channel blockers prevent the influx of calcium into cardiac and smooth muscle cells and may cause adverse effects including peripheral edema, flushing, dizziness, and gingival hyperplasia.
  • Angiotensin-receptor blockers block angiotensin II receptors and may cause adverse effects including hyperkalemia and acute kidney injury.
  • Loop diuretics inhibit the Na+/K+/2Cl– cotransporter and may cause adverse effects such as ototoxicity, dehydration, and hypokalemia.
  • Thiazide diuretics inhibit the distal tubule Na+/Cl– cotransporter and may cause adverse effects including hypokalemia, hyperglycemia, hyponatremia, and hyperuricemia.
400

What are the main clinical uses of β2-agonists?

β2-Agonists are mainly used in the treatment of asthma attacks and the management of hyperkalemia.

400

What are the major effects of α1-receptor activation? (p 239)

α1-receptor activation increases vascular smooth muscle contraction, pupillary dilator muscle contraction (mydriasis), and intestinal and bladder sphincter muscle contraction

400

What are the clinical uses for nonspecific PDE inhibitors and PDE-5 inhibitors? (p 247)

Nonspecific PDE inhibitors are used to treat COPD and asthma (rarely) PDE-5 inhibitors are used to treat erectile dysfunction, pulmonary hypertension, and BPH.

400

Which medications can cause megaloblastic anemia? (p 251)

1. Hydroxyurea, 

2. phenytoin, 

3. methotrexate, and 

4. sulfa drugs.

500

A 45-year-old man comes to his primary care physician for an annual examination. He has type 2 diabetes mellitus for which he initially took metformin, but the drug was soon discontinued due to adverse effects. He was then started on another oral medication and is now experiencing flatulence and abdominal pain. On physical examination, he has decreased sensation in both lower extremities. Laboratory studies show hemoglobin A1c of 9%. Fingerstick glucose level is 220 mg/dL.

Which of the following drugs most likely caused the patient’s gastrointestinal symptoms?

a. Acarbose

b. Canagliflozin 

c. Meglitinide 

d. Sulfonylurea 

e. Thiazolidinediones 

This patient with a history of type 2 diabetes mellitus (DM) is experiencing flatulence and abdominal pain. Among the oral antidiabetic drugs, acarbose is the most likely drug to cause gastrointestinal (GI) symptoms such as flatulence, diarrhea, and abdominal pain.


Step 2: Drug Adverse Effects


α-Glucosidase inhibitors such as acarbose act by inhibiting the α-glucosidase enzyme, which is produced by the brush border cells of the small intestine and is responsible for conversion of polysaccharides to disaccharides and monosaccharides. This reduces the amount of carbohydrates absorbed from the intestine and hence causes GI upset and flatulence.


The other choices are incorrect:

  • Meglitinides are short-acting insulin secretagogues. They can cause hypoglycemia and are generally better tolerated.
  • Canagliflozin is an oral antidiabetic drug that acts by inhibiting filtered glucose reabsorption in the kidney. It can cause fractures, hyperkalemia, ketoacidosis, urinary tract infection, acute kidney injury, and volume depletion.
  • Sulfonylureas are insulin secretagogues. They can cause hypoglycemia.
  • Thiazolidinediones increase peripheral insulin sensitivity by upregulating the number of peroxisome proliferation–activated receptors. Adverse effects include weight gain, edema, and potential hepatotoxicity.
500

What is the effect of β2-blockade in the lungs?

In the lungs, β2-blockade results in constriction of the bronchioles.

500

What are the major functions of α2-receptor activation? (p 239)

α2-receptor activation decreases sympathetic (adrenergic) outflow, lipolysis, aqueous humor production, and insulin release, while increasing platelet aggregation.

500

What are the clinical applications of epinephrine? (p 243) 

What are the clinical applications of phenylephrine? (p 243)

What is the clinical application for albuterol? (p 243)

Epinephrine treats anaphylaxis, open-angle glaucoma, and asthma. 

Phenylephrine treats nasal congestion (rhinitis), hypotension (vasoconstrictor), dilates pupils, and counters ischemic priapism. 

 Albuterol treats acute asthma and COPD.

500

Which medications can cause a Parkinson-like syndrome? (p 252)

1. Antipsychotics, 

2. metoclopramide, and 

3. reserpine.