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Pharm_Part1 Flashcards

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USMLE® Step 1 flashcards
1
Q

“Fibrates” (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

A

Mechanism: Upregulate LPL → ↑TG clearance Toxicity: Myositis, hepatotoxicity (↑LFTs), cholesterol gallstones LDL↓; HDL↑; TG↓↓↓

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2
Q

“Monday disease” in industrial exposure of nitrate

A

Development of tolerance for the vasolilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness and headache on reexposure

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3
Q

5-fluorouracil (5-FU)

A

Mechanism: Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase → ↓ dTMP → ↓ DNA and ↓ protein synthesis Clinical use: Colon cancer and other solid tumors, basal cell carcinoma (topical). Synergy with MTX. Toxicity: 1. Myelosuppression, which is reversible with thymidine “rescue” 2. Photosensivity

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4
Q

6-mercaptopurine (6-MP)

A

Mechanism: Purine (thiol) analog → ↓ de novo purine synthesis. Activated by HGPRTase. Clinical use: Leukemias, lymphomas (not CLL or Hodgkin’s) Toxicity: Bone marrow, GI, liver. Metabolized by xanthine oxidase; thus ↑ toxicity with allopurinol.

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5
Q

6-thioguanine (6-TG)

A

Mechanism: Purine (thiol) analog → ↓ de novo purine synthesis. Activated by HGPRTase. Clinical use: Acute lymphoid leukemia Toxicity: Bone marrow depression, liver. Can be given with allopurinol.

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6
Q

Abciximab

A

Mechanism: Monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation Clinical use: Acute coronary syndromes, percutaneous transluminal coronary angioplasty Toxicity: Bleeding, thrombocytopenia

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7
Q

Alcohol toxicity

A

Page 246 of FA2011, focus on: Alcohol dehydrogenase - Fomepizole Acetaldehyde dehydrogenase - Disulfiram

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8
Q

Amiodarone

A

Has class I, II, III, and IV effects because it alters the lipid membrane

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9
Q

Amphetamine

A

Indirect sympathomimetics, indirect general agonist, releases stored catecholamines Clinical use: Narcolepsy, obesity, attention deficit disorder

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10
Q

Antacid Overuse

A
  1. Aluminum hydroxide - constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures 2. Magnesium hydroxide - diarrhea, hyporeflexia, hypotension, cardiac arrest 3. Calcium carbonate - hypercalcemia, rebound acid ↑ PS: Can also cause hypokalemia, can chelate and ↓ the effectiveness of other drugs (e.g., tetracycline)
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11
Q

Antacid use affecting the body

A

Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.

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12
Q

Antianginal therapy

A

Nitrates + β-blockers; β-blockers; Nitrates **Page 281 on FA2011, comparison in different components of drug effects

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13
Q

Antianginal therapy: Calcium channel blockers

A

Nifedipine is similar to nitrates in effect; Verapamil is similar to β-blockers in effect

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14
Q

Antiarrhythmics - Ca2+ channel blockers (Class IV)

A

Verapamil, diltiazem Mechanism: ↓ conduction velocity, ↑ ERP, ↑ PR interval. Used in prevention of nodal arrhythmias (e.g., SVT) Toxicity: Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

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15
Q

Antiarrhythmics - K+ channel blockers (Class III): Names + Mechanism

A

Sotalol, ibutilide, bretylium, dofetilide, amiodarone Mechanism: ↑AP duration, ↑ERP. Used when other antiarrhythmics fail. ↑QT interval.

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16
Q

Antiarrhythmics - Na+ channel blockers (Class IA): Names + Mechanism

A

Quinidine, Procainamide, Disopyramide ↑AP duration, ↑effective refractory period (ERP), ↑QT interval. Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia

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17
Q

Antiarrhythmics - Na+ channel blockers (Class IB): Names + Mechanism

A

Lidocaine, Mexiletine, Tocainide ↓AP duration. Preferentially affect ischemic or depolarized Purkinjie and ventricular tissue. Useful in acute ventricular arrhythmias (especially post-MI) and in digitalis-induced arrhythmias

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18
Q

Antiarrhythmics - Na+ channel blockers (Class IC): Names + Mechanism

A

Flecainide, Encainide, Propafenone No effect on AP duration. Useful in V-tachs that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrhythmias. For patients without structural abnormalities

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19
Q

Antiarrhythmics - β-blockers (Class II)

A

Mechanism: ↓cAMP, ↓Ca2+ currents. Suppress abnormal pacemakers by ↓ slope of phase 4. AV node particularly sensitive - ↑ PR interval. Esmolol very short acting. Clinical use: V-tach, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. Toxicity: Impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Treat overdose with glucagon.

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20
Q

Antiarrhythmics: Adenosine

A

↑K+ out of cells → hyperpolarizing the cell + ↓ Ica. Drug of choice in diagnosing / abolishing supraventricular tachycardia. Very short acting (~15s). Toxicity includes flushing, hypotension, chest pain. Effects blocked by theophylline

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21
Q

Antiarrhythmics: K+

A

Depresses ectopic pacemakers in hypokalemia (e.g., digoxin toxicity)

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22
Q

Antiarrhythmics: Mg2+

A

Effective in torsades de pointes and digoxin toxicity

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23
Q

Antibodies to avoid in pregnancy (8)

A

Sulfonamides - kernicterus Aminoglucosides - ototoxicity Fluoroquinolones - cartilage damage Metronidazole - mutagenesis Tetracyclines - discolored teeth, inhibition of bone growth Ribavirin (antiviral) - teratogenic Griseofulvin (antifungal) - teratogenic Chloramphenicol - “gray baby”

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24
Q

Antidote: Acetaminophen

A

N-acetylcysteine

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25
Q

Antidote: Acetylcholinesterase inhibitors, organophosphates

A

Atropine, pralidoxime

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26
Q

Antidote: Amphetamines (basic)

A

NH4Cl (acidify urine)

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27
Q

Antidote: Antimuscarinic, anticholinergic

A

Physostigmine salicylate

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28
Q

Antidote: Benzodiazepines

A

Flumazenil

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29
Q

Antidote: Carbon monoxide

A

100% O2, hyperbaric O2

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30
Q

Antidote: Cardiac glycosides - Digoxin

A

Slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+

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31
Q

Antidote: Copper, arsenic, gold

A

Penicillamine

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32
Q

Antidote: Cyanide

A

Nitrite, hydroxocobalamin, thiosulfate

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33
Q

Antidote: Digitalis

A

Stop digitalis, normalize K+, lidocaine, anti-dig Fab fragments, Mg2+

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34
Q

Antidote: Heparin

A

Protamine

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35
Q

Antidote: Iron

A

Deferoxamine

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36
Q

Antidote: Lead

A

CaEDTA, dimercaprol, succimer, penicillamine

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37
Q

Antidote: Mercury, arsenic, gold

A

Dimercaprol (BAL), succimer

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38
Q

Antidote: Methanol, ethylene glycol (antifreeze)

A

Ethanol, dialysis, fomepizole

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39
Q

Antidote: Methemoglobin

A

Methylene blue, vitamin C

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40
Q

Antidote: Opioids

A

Naloxone, naltrexone

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41
Q

Antidote: Salicylates

A

NaHCO3 (alkalinize urine), dialysis

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42
Q

Antidote: TCAs

A

NaHCO3 (plasma alkalinization)

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43
Q

Antidote: Theophylline

A

β-blocker

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44
Q

Antidote: tPA, streptokinase

A

Aminocaproic acid

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45
Q

Antidote: Warfarin

A

For reversal of warfarin overdose, give vitamin K. For rapid reversal of severe warfarin overdose, give fresh frozen plasma.

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46
Q

Antidote: Warfarin (Acute, chronic)

A

Acute: Fresh frozen plasma Chronic: Vitamin K

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47
Q

Antidote: β-blockers

A

Glucagon

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48
Q

Antifungal therapy: Amphotericin B

A

Mechanism: Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes Clinical use: Serious, systemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier. Toxicity: Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (“amphoterrible”). Hydration reduces nephrotoxicity. Liposomal amphotericin reduces toxicity.

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49
Q

Antifungal therapy: Azoles (Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole)

A

Mechanism: Inhibit fungal sterol (egosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to egosterol. Clinical use: Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients (because it can cross blood-brain barrier) and candidal infections of all types. Ketoconazole for Blastomyces, Coccidioides, Histoplasma, Candida albicans; hypercortisolism. Clotrimazole and micronazole for topical fungal infections. Toxicity: Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.

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50
Q

Antifungal therapy: Caspofungin

A

Mechanism: Inhibits cell wall synthesis by inhibiting synthesis of β-glucan Clincal use: Invasive aspergillosis Toxicity: GI upset, flushing

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51
Q

Antifungal therapy: Flucytosine

A

Mechanism: Inhibits DNA synthesis by conversion to 5-fluorouracil Clinical use: Used in systemic fungal infections (e.g., Candida, Cryptococcus) in combination with amphotericin B Toxicity: Nausea, vomiting, diarrhea, bone marrow suppression

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52
Q

Antifungal therapy: Griseofulvin

A

Mechanism: Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (e.g., nails) Clinical use: Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm) Toxicity: Teratogenic, carcinogenic, confusion, headaches, ↑P-450 and warfarin metabolism

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53
Q

Antifungal therapy: Nystatin

A

Mechanism: Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes. Topical form because too toxic for systemic use. Clinical use: “Swish and swallow” for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis

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54
Q

Antifungal therapy: Terbinafine

A

Mechanism: Inhibits the fungal enzyme squalene epoxidase Clinical use: Used to treat dermatophytoses (especially onychomycosis - fungal infection of finger or toe nails)

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55
Q

Antihypertensive therapy: CHF

A

Diuretics, ACE inhibitors / ARBs, β-blockers (compensated CHF), K+-sparing diuretics. PS: β-blockers are contraindicated in decompensated CHF

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56
Q

Antihypertensive therapy: Diabetes mellitus

A

ACE inhibitors / ARBs, calcium channel blockers, diuretics, β-blockers, α-blockers. PS: ACE inhibitors are protective against diabetic nephropathy

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57
Q

Antihypertensive therapy: Essential hypertension

A

Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers

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58
Q

Antiviral: Acyclovir

A

Mechanism: Monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination Clinical use: HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Toxicity: Generally well tolerated

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59
Q

Antiviral: Amantadine

A

Mechanism: Blocks viral penetration / uncoating (M2 protein). Also causes the release of dopamine from intact nerve terminals. Clinical use: Prophylaxis and treatment of influenza A only; Parkinson’s disease. Toxicity: Ataxia, dizziness, slurred speech

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60
Q

Antiviral: Famciclovir

A

Mechanism: Monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination Clinical use: HSV, VZV, EBV. Used for herpes zoster. No effect on latent forms of HSV and VZV. Toxicity: Generally well tolerated

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61
Q

Antiviral: Foscarnet

A

Mechanism: Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase. Clinical use: CMV retinitis in immunocomprimised patients when ganciclovir fails; acyclovir-resistant HSV. Toxicity: Nephrotoxicity

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62
Q

Antiviral: Ganciclovir

A

Mechanism: 5’-monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase. Clinical use: CMV, especially in immunocompromised patients. Toxicity: Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

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63
Q

Antiviral: Interferons

A

Mechanism: Glycoproteins synthesized by virus-infected cells block replication of both RNA and DNA viruses Clinical use: IFN-α - Chronic hepatitis B and C, Kaposi’s sarcoma. IFN-β - MS. IFN-γ - NADPH oxidase deficiency Toxicity: Neutropenia

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64
Q

Antiviral: Ribavirin

A

Mechanism: Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase Clinical use: RSV, chronic hepatitis C Toxicity: Hemolytic anemia. Severe teratogen

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65
Q

Antiviral: Rimantidine

A

A derivative with fewer CNS side effects of amantadine. Does not cross the blood-brain barrier.

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66
Q

Antiviral: Zanamivir, oseltamivir

A

Mechanism: Inhibit influenza neuraminidase, decreasing the release of progeny virus. Clinical use: Both influenza A and B.

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67
Q

Aspirin (ASA)

A

Mechanism: Acetylates and irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) to prevent conversion of arachidonic acid to thromboxane A2 (TxA2). ↑ bleeding time. No effect on PT, PTT. Clinical use: Antipyretic, analgesic, anti-inflammatory, antiplatelet drug. Toxicity: Gastric ulceration, bleeding, hyperventilation, Reye’s syndrome, tinnitus (CN VIII)

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68
Q

Azathioprine

A

Mechanism: Antimetabolite precursor of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes. Clinical use: Kidney transplantation, autoimmune disorders (including glomerulonephritis and hemolytic anemia) Toxicity: Bone marrow suppression. Active metabolite mercaptopurine is metabolized by xanthine oxidase; thus, toxic effects may be ↑ by allopurinol

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69
Q

Basic concepts on Autonomic drugs

A

P235-P242 of FA2011, very important!!!

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70
Q

Bethanechol

A

Direct cholinomimetic agents Clinical use: Postoperative and neurogenic ileus and urinary retention Action: Activates bowel and bladder smooth muscle; resistant to AChE

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71
Q

Biguanides (first name them)

A

Metformin Mechanism: Exact mechanism is unknown. ↓gluconeogenesis, ↑glycolysis, ↑peripheral glucose uptake (insulin sensitivity) Clinical use: Oral, can be used in patients without islet function. Toxicity: Most grave adverse effect is lactic acidosis

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72
Q

Bile acid resins

A

Mechanism: Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more Toxicity: Patients hate it - tastes bad and cause GI discomfort, ↓ absorption of fat-soluble vitamins. Cholesterol gallstones. LDL↓↓; HDL↑(slightly); TG↑(slightly)

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73
Q

Bile acid resins: Names

A

Cholestyramine, colestipol, colesevelam

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74
Q

Bismuth, sucralfate

A

Mechanism: Bind to ulcer base, providing physical protection, and allow HCO3- secretion to reestablish pH gradient in the mucous layer Clinical use: ↑ ulcer healing, traveler’s diarrhea

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75
Q

Bleomycin

A

Mechanism: Induces free radical formation, which causes breaks in DNA strands Clinical use: Testicular cancer, Hodgkin’s lymphoma Toxicity: Pulmonary fibrosis, skin changes. Minimal myelosuppression.

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76
Q

Busulfan

A

Mechanism: Alkylates DNA Clinical use: CML. Also used to ablate patient’s bone marrow before bone marrow transportation. Toxicity: Pulmonary fibrosis, hyperpigmentation

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77
Q

Calcium channel blockers: Names (a properties)

A

Nifedipine, verapamil, diltiazem Vascular smooth muscle - Nifedipine > diltiazem > verapamil Heart - Verapamil > diltiazem > nifedipine

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78
Q

Carbachol

A

Direct cholinomimetic agents Clinical use: Glaucoma, pupillary contraction, and relief of intraocular pressure Action: Carbon copy of acetylcholine

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79
Q

Cholesterol absorption blockers (ezetimibe)

A

Mechanism: Prevent cholesterol reabsorption at small intestine brush border Toxicity: Rare ↑ LFTs LDL↓↓; HDL-; TG-

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80
Q

Cholinesterase inhibitor poisoning

A

Often due to organophosphates, such as parathion, that irreversibly inhibit AchE. Causes Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, and Salivation Antidote - atropine + pralidoxime (regenerates active AchE)

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81
Q

Cisplatin / Carboplatin

A

Mechanism: Cross-link DNA Clinical use: Testicular, bladder, ovary, and lung carcinomas Toxicity: Nephrotoxicity and acoustic nerve damage

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82
Q

Clinical presentation: Sulfa allergy

A

May develop fever, pruritic rash, Steven-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria (hives). Symptoms range from mild to life-threatening.

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83
Q

Clinical use: Calcium channel blockers

A

Hypertension, angina, arrhythmias (not nifedipine), Prinzmetal’s angina, Raynaud’s syndrome.

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84
Q

Clinical use: Cardiac glycosides - Digoxin

A

CHF (↑ contractility); atrial fibrillation (↓ conduction at AV node and depression of SA node)

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85
Q

Clinical use: Glucocorticoids

A

Addison’s disease, inflammation, immune suppression, asthma

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86
Q

Clinical use: H2 blockers

A

Peptic ulcer, gastritis, mild esophageal reflux

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87
Q

Clinical use: Heparin

A

Immediate anticoagulation for pulmonary embolism, stroke, acute coronary syndrome, MI, DVT. Used during pregnancy (does not cross the placenta). Follow PTT.

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88
Q

Clinical use: Thrombolytics

A

Early MI, early ischemic stroke.

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89
Q

Clinical use: Warfarin (Coumadin)

A

Chronic anticoagulation. Not used in pregnant women (because warfarin, unlike heparin, can cross the placenta). Follow PT/INR values.

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90
Q

Clinical use: β-blockers

A

Hypertension: ↓cardiac output, ↓renin secretion (due to β-receptor blockade on JGA cells) Angina pectoris: ↓heart rate and contractility, resulting in ↓O2 consumption MI: β-blockers ↓mortality SVT (propranolol, esmolol): ↓AV conduction velocity (class II antiarrhythmic) CHF: Slows progression of chronic failure Glaucoma (timolol): ↓secretion of aqueous humor

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91
Q

Clopidogrel, ticlopidine

A

Mechanism: Inhibit platelet aggregation by irreversibly blocking ADP receptors, preventing glycoprotein IIb/IIIa from binding fibrinogen Clinical use: Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of thrombotic stroke. Toxicity: Neuropenia (ticlopidine)

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92
Q

Cocaine

A

Indirect sympathomimetics, indirect general agonist, uptake inhibitor Clinical use: Causes vasoconstriction and local anesthesia

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93
Q

Comparison between Heparin and Warfarin

A

P362 on FA2011, though personally do not think it to be needed if you understood the two drugs itself…

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94
Q

Contraindication: Antiarrhythmics - Na+ channel blockers (Class IC)

A

Post-MI

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95
Q

Contraindication: Biguanides (Metformin)

A

Renal failure

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96
Q

Contraindication: Hydralazine

A

in Angina / CAD

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97
Q

Contraindication: Metoclopramide

A

patients with small bowel obstruction

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98
Q

Contraindication: Misoprostol

A

in women of childbearing potential (abortifacient)

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99
Q

Contraindications: Pindolol, acebutolol

A

Angina, because they are partial β-agonists

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100
Q

Cyclophosphamide / Isosfamide

A

Mechanism: Covalently X-link (interstrand) DNA at guanine N-7. Require bioactivation by liver. Clinical use: Non-Hodgkin’s lymphoma, breast and ovarian carcinomas. Also immunosuppressants. Toxicity: Myelosuppression; hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolite)

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101
Q

Cyclosporine

A

Mechanism: Binds to cyclophilins. Complex blocks the differentiation and activation of T cells by inhibiting calcineurin, thus preventing the production of IL-2 and its receptor Clinical use: Suppresses organ rejection after transplantation; selected autoimmune disorders Toxicity: Predisposes patient to viral infections and lymphoma; nephrotoxic (preventable with mannitol diuresis)

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102
Q

Cytarabine (ara-C)

A

Mechanism: Pyrimidine analog → inhibition of DNA polymerase Clinical use: AML, ALL, high-grade non-Hodgkin’s lymphoma Toxicity: Leukopenia, thrombocytopenia, megaloblastic anemia

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103
Q

Daclizumab

A

Mechanism: Monoclonal antibody with high affinity for the IL-2 receptor on activated T cells

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104
Q

Dactinomycin (Actinomycin D)

A

Mechanism: Intercalates in DNA Clinical use: Wilm’s tumor, Ewing’s sarcoma, rhabdomyosarcoma. Used for childhood tumors. Toxicity: Myelosuppression

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105
Q

Demeclocycline

A

Mechanism: ADH antagonist (member of the tetracycline family) Clinical use: SIADH Toxicity: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

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106
Q

Dobutamine

A

Mechanism: β1 > β2, inotropic but not chronotropic Clinical use: Heart failure, cardiac stress testing

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107
Q

DOC: Hemorrhagic cystitis

A

Mesna, thiol group of mesna binds toxic metabolite causing hemorrhagic cystitis

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108
Q

Dopamine

A

Mechanism: D1 = D2 > β > α, inotropic and chronotropic Clinical use: Shock (↑ renal perfusion)

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109
Q

Doxorubicin (Adriamycin) / Daunorubicin

A

Mechanism: Generate free radicals. Noncovalently intercalate in DNA → breaks in DNA → ↓ replication. Clinical use: Hodgkin’s lymphomas, also for myelomas, sarcomas, and solid tumors (breast, ovary, lung) Toxicity: Cardiotoxicity, myelosuppression, and alopecia. Toxic to tissues with extravasation.

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110
Q

Drug ending category: -afil

A

Erectile dysfunction (Sildenafil)

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111
Q

Drug ending category: -ane

A

Inhalational general anesthetic (Halothane)

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112
Q

Drug ending category: -azepam

A

Benzodiazepine (Diazepam)

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113
Q

Drug ending category: -azine

A

Phenothiazine (neuroleptic, antiemetic) (Chlorpromazine)

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114
Q

Drug ending category: -azole

A

Antifungal (Ketoconazole)

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115
Q

Drug ending category: -barbital

A

Barbiturate (Phenobarbital)

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116
Q

Drug ending category: -caine

A

Local anesthetic (Lidocaine)

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117
Q

Drug ending category: -cillin

A

Penicillin (Methicillin)

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118
Q

Drug ending category: -cycline

A

Antibiotic, protein synthesis inhibitor (Tetracycline)

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119
Q

Drug ending category: -etine

A

SSRI (Fluoxetine)

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120
Q

Drug ending category: -ipramine

A

TCA (Imipramine)

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121
Q

Drug ending category: -navir

A

Protease inhibitor (Saquinavir)

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122
Q

Drug ending category: -olol

A

β antagonist (Propranolol)

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123
Q

Drug ending category: -operidol

A

Butyrophenone (neuroleptic) (Haloperidol)

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124
Q

Drug ending category: -oxin

A

Cardiac glycoside (inotropic agent) (Digoxin)

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125
Q

Drug ending category: -phylline

A

Methylxanthine (Theophylline)

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126
Q

Drug ending category: -pril

A

ACE inhibitor (Captopril)

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127
Q

Drug ending category: -terol

A

β2 agonist (Albuterol)

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128
Q

Drug ending category: -tidine

A

H2 antagonist (Cimetidine)

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129
Q

Drug ending category: -triptan

A

5-HT(1B/1D) agonist (migraine) (Sumatriptan)

130
Q

Drug ending category: -triptyline

A

TCA (Amitriptyline)

131
Q

Drug ending category: -tropin

A

Pituatory hormone (Somatotropin)

132
Q

Drug ending category: -zolam

A

Benzodiazepine (Alprazolam)

133
Q

Drug ending category: -zosin

A

α1 antagonist (Prazosin)

134
Q

Drug group: Amiodarone

A

Antiarrhythmics - K+ channel blockers (Class III)

135
Q

Drug group: Bertylium

A

Antiarrhythmics - K+ channel blockers (Class III)

136
Q

Drug group: Dofetilide

A

Antiarrhythmics - K+ channel blockers (Class III)

137
Q

Drug group: Ibutilide

A

Antiarrhythmics - K+ channel blockers (Class III)

138
Q

Drug group: Sotalol

A

Antiarrhythmics - K+ channel blockers (Class III)

139
Q

Drug reactions: Acute cholestatic hepatitis

A

Macrolides

140
Q

Drug reactions: Adrenocortical insufficienty

A

Glucocorticoid withdrawal (HPA suppression)

141
Q

Drug reactions: Agranulocytosis (6)

A

Clozapine, carbamazepine, colchicine, propylthiouracil, methimazole, dapsone

142
Q

Drug reactions: Aplastic anemia (5)

A

Chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole

143
Q

Drug reactions: Atropine-like side effects

A

TCAs

144
Q

Drug reactions: Cinchonism (2)

A

Quinidine, Quinine

145
Q

Drug reactions: Coronary vasospasm (2)

A

Cocaine, sumatriptan

146
Q

Drug reactions: Cough

A

ACE inhibitors (note: ARBs like losartan - no cough)

147
Q

Drug reactions: Cutaneous flushing (4)

A

VANC: Vancomycin, Adenosine, Niacin, Ca2+ channel blockers

148
Q

Drug reactions: Diabetes insipidus (2)

A

Lithium, demeclocycline

149
Q

Drug reactions: Dilated cardiomyopathy (2)

A

Doxorubicin (Adriamycin), daunorubicin

150
Q

Drug reactions: Direct Coombs-positive hemolytic anemia

A

Methyldopa

151
Q

Drug reactions: Disulfiram-like reaction (4)

A

Metronidazole, certain cephalosporins, procarbazine, 1st-generation sulfonylureas

152
Q

Drug reactions: Fanconi’s syndrome

A

Expired tetracycline

153
Q

Drug reactions: Focal to massive hepatic necrosis (4)

A

Halothane, valproic acid, acetaminophen, Amanita phalloides

154
Q

Drug reactions: Gingival hyperplasia

A

Phenytoin

155
Q

Drug reactions: Gout (2)

A

Furosemide, thiazides

156
Q

Drug reactions: Grey baby syndrome

A

Chloramphenicol

157
Q

Drug reactions: Gynecomastia (6)

A

Spironolactone, Digitalis, Cimetidine, chronic alcohol use, estrogens, Ketoconazole

158
Q

Drug reactions: Hemolysis in G6PD-deficient patients (6)

A

Hemolysis IS PAIN, Isoniazid (INH), Sulfonamides, Primaquine, Aspirin, Ibuprofen, Nitrofurantoin

159
Q

Drug reactions: Hemorrhagic cystitis (2)

A

Cyclophosphamide, ifosfamide (prevent by coadministering with mesna)

160
Q

Drug reactions: Hepatitis

A

INH

161
Q

Drug reactions: Hot flashes (2)

A

Tamoxifen, clomiphene

162
Q

Drug reactions: Hypothyroidism (2)

A

Lithium, amiodarone

163
Q

Drug reactions: Interstitial nephritis (3)

A

Methicillin, NSAIDs, furosemide

164
Q

Drug reactions: Megaloblastic anemia (3)

A

Phenytoin, Methotrexate, Sulfa drugs

165
Q

Drug reactions: Nephrotoxicity / neurotoxicity

A

Polymyxins

166
Q

Drug reactions: Nephrotoxicity / ototoxicity (4)

A

Aminoglycosides, vancomycin, loop diuretics, cisplatin

167
Q

Drug reactions: Osteoporosis (2)

A

Corticosteroids, heparin

168
Q

Drug reactions: Parkinson-like syndrome (4)

A

Haloperidol, chlorpromazine, reserpine, metoclopramide

169
Q

Drug reactions: Photosensitivity (3)

A

Sulfonamides, Amiodarone, Tetracycline

170
Q

Drug reactions: Pseudomembranous colitis (2)

A

Clindamycin, ampicillin

171
Q

Drug reactions: Pulmonary fibrosis

A

Bleomycin, Amiodarone, Busulfan (BLAB)

172
Q

Drug reactions: Rash (Steves-Johnson syndrome) (8)

A

Ethosuximide, lamotrigine, carbamazepine, phenobarbital, phenytoin, sulfa drugs, penicillin, allopurinol

173
Q

Drug reactions: Seizures (3)

A

Bupropion, imipenem / cilastatin, isoniazid

174
Q

Drug reactions: SLE-like syndrome (4)

A

Hydalazine, INH, Procainamide, Phenytoin

175
Q

Drug reactions: Tardive dyskinesia

A

Antipsychotics

176
Q

Drug reactions: Tendonitis, tendon rupture, and cartilage damage (kids)

A

Fluoroquinolones

177
Q

Drug reactions: Thrombotic complication

A

OCPs (e.g., estrogens and progestins)

178
Q

Drug reactions: Torsades de pointes (2)

A

Class III (sotalol), class IA (quinidine) antiarrhythmics

179
Q

Echothiophate

A

Indirect cholinomimetic agents Clinical use: Glaucoma Action: ↑endogenous ACh

180
Q

Edrophonium

A

Indirect cholinomimetic agents Clinical use: Diagnosis of myasthenia gravis (extremely short acting) Action: ↑endogenous ACh

181
Q

Ephedrine

A

Indirect sympathomimetics, indirect general agonist, releases stored catecholamines Clinical use: Nasal decongestion, urinary incontinence, hypotension

182
Q

Epinephrine

A

Mechanism: α & β, low doses selective for β1, high doses selective for α Clinical use: Anaphylaxis, glaucoma (open angle), asthma, hypotension

183
Q

Etoposide (VP-16) / Teniposide

A

Mechanism: Inhibits topoisomerase II → ↑ DNA degradation Clinical use: Small cell carcinoma of the lung and prostate, testicular carcinoma Toxicity: Myelosuppression, GI irritation, alopecia

184
Q

First generation Sulfonyureas (first name them)

A

Tolbutamide, Chlorpropamide Mechanism: Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx Clinical use: Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type I DM. Toxicity: Disulfiram-like effects

185
Q

Glitazones / thiazolidinediones (first name them)

A

Pioglitazone, Rosiglitazone (-glitazone) Mechanism: ↑ insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator. Clinical use: Used as monotherapy in type 2 DM or combined with above agents. Toxicity: Weight gain, edema. Hepatotoxicity, CV toxicity.

186
Q

GLP-1 analogs (first name them)

A

Exenatide Mechanism: ↑insulin, ↓glucagon release Clinical use: Type 2 DM Toxicity: Nausea, vomiting, pancreatitis

187
Q

Glucocorticoids: Names

A

Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone

188
Q

H2 blockers: Names

A

Cimetidine, ranitidine, famotidine, nizatidine (-tidine)

189
Q

Heparin-induced thrombocytopenia (HIT)

A

heparin binds to platelet factor IV, causing antibody production that binds to and activates platelets leading to their clearance and resulting in a thrombocytopenic, hypercoagulable state.

190
Q

Hexamethonium

A

Mechanism: Nicotinic antagonist Clinical use: Ganglionic blocker. Used in experimental models to prevent vagal reflex responses to changes in blood pressure - e.g., prevents reflex bradycardia caused by NE Toxicity: Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction.

191
Q

HIV therapy: Fusion inhibitors

A

Enfuvirtide Mechanism: Bind viral gp41 subunit; inhibit conformational change required for fusion with CD4 cells, blocking entry and replication. Used in patients with persistent viral replication despite antiretroviral therapy Toxicity: Hypersensitivity reactions, reactions at subcutaneous injection site, ↑ risk of bacterial pneumonia

192
Q

HIV therapy: Highly active antiretroviral therapy (HAART)

A

Initiated when patients present with AIDs-defining illness, low CD4-cell counts (<350 cells/mm^3), or high viral load. Regimen consists of 3 drugs to prevent resistance: [2 nucleoside reverse transcriptase inhibitors (NRTIs) + 1 protease inhibitor] OR [2 NRTIs + 1 non-nucleoside reverse transcriptase inhibitor (NNRTI-)]

193
Q

HIV therapy: NNRTIs

A

Nevirapine, Efavirenz, Delavirdine Mechanism: Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides. Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)

194
Q

HIV therapy: NRTIs

A

Zidovudine (ZDV), Didanosine (ddI), Zalcitabine (ddC), Stavudine (d4T) Mechanism: Competitively inhibit nucleotide binding to reverse transcriptase or terminate the DNA chain (lack a 3’-OH group). Must be phosphorylated by thymidine kinase to be active. ZDV is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission. Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (ZDV)

195
Q

HIV therapy: Protease inhibitors

A

Saquinvir, Ritonavir, Indinavir, Nelfinavir, Amprenavir (-navir) Mechanism: Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses Toxicity: Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy (Cushingoid), thrombocytopenia (indinavir)

196
Q

HMG-Coa reductase inhibitors (-statin)

A

Mechanism: Inhibit cholesterol percursor, mevalonate Toxicity: Hepatotoxicity (↑LFTs), rhabdomyolysis LDL↓↓↓; HDL↑; TG↓

197
Q

Hydralazine

A

Mechanism: ↑ cGMP → smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction. Clinical use: Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa. Frequently coadministered with a β-blocker to prevent reflex tachycardia. Toxicity: Compensatory tachycardia, fluid retention, nausea, headache, angina, Lupus-like syndrome.

198
Q

Hydroxyurea

A

Mechanism: Inhibits ribonucleotide reductase → ↓ DNA synthesis (S-phase specific) Clinical use: Melanoma, CML, sickle cell disease (↑ HbF) Toxicity: Bone marrow suppression, GI upset.

199
Q

Hypothalamic / pituitary drugs - Clinical use: ADH (desmopressin)

A

Pituitary (central, not nephrogenic) DI

200
Q

Hypothalamic / pituitary drugs - Clinical use: GH

A

GH deficiency, Turner syndrome

201
Q

Hypothalamic / pituitary drugs - Clinical use: Oxytocin

A

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

202
Q

Hypothalamic / pituitary drugs - Clinical use: Somatostatin (octreotide)

A

Acromegaly, carcinoid, gastrinoma, glucagonoma

203
Q

Imatinib (Gleevec)

A

Mechanism: Philadelphia chromosome bcr-abl tyrosine kinase inhibitor. Clinical use: CML, GI stromal tumors Toxicity: Fluid retention

204
Q

Infliximab

A

Mechanism: A monoclonal antibody to TNF, proinflammatory cytokine. Clincal use: Crohn’s disease, rheumatoid arthritis Toxicity: Respiratory infection (including reactivation of latent TB), fever, hypotension

205
Q

Insulin

A

Mechanism: Bind insulin receptor (tyrosine kinase activity). Liver - ↑glucose stored as glycogen. Muscle - ↑ glycogen and protein synthesis, K+ uptake. Fat - aids TG storage Clincal use: Type 1 DM, type 2 DM, gestational diabetes, life-threatening hyperkalemia, and stress-induced hyperglycemia. Toxicity: Hypoglycemia, hypersensitivity reaction (very rare)

206
Q

Isoproterenol

A

Mechanism: β1 = β2 (isolated to β) Clinical use: AV block (rare)

207
Q

Ketorolac

A

NSAID often used as an analgesic, indicated for short-term management of moderate to severe pain

208
Q

Lepirudin, bivalirudin

A

Hirudin derivatives; directly inhibit thrombin. Used as an alternative to heparin for anticoagulating patients with HIT

209
Q

Leucovorin

A

Folinic acid, rescue methotrexate (MTX) myelosuppression

210
Q

Levothyroxine, triiodothyronine

A

Mechanism: Thyroxine replacement Clinical use: Hypothyroidism, myxedema Toxicity: Tachycardia, heat intolerance, tremors, arrhythmias

211
Q

Low-molecular-weight-heparins (e.g., enoxaparin)

A

act more on Xa, have better bioavailability and 2-4 times longer half-life. Can be administered subcutaneously and without laboratory monitoring. Not easily reversible.

212
Q

Malignant hypertension treatment: Diazoxide

A

K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia (reduces insulin release)

213
Q

Malignant hypertension treatment: Fenoldopam

A

Dopamine D1 receptor agonist - relaxes renal vascular smooth muscle

214
Q

Malignant hypertension treatment: Nitroprusside

A

Short acting; ↑ cGMP via direct release of NO. Can cause cyanide toxicity (releases CN)

215
Q

Mechanism of resistance: Acyclovir, famciclovir

A

Lack of viral thymidine kinase

216
Q

Mechanism of resistance: Amantadine

A

Mutated M2 protein. 90% of all influenza A strains are resistant to amantadine, so not used.

217
Q

Mechanism of resistance: Foscarnet

A

Mutated DNA polymerase

218
Q

Mechanism of resistance: Ganciclovir

A

Mutated CMV DNA polymerase or lack of viral kinase

219
Q

Mechanism: Atropine

A

Eye: ↑pupil dilation, cycloplegia Airway: ↓secretion Stomach: ↓acid secretion Gut: ↓motility Bladder: ↓urgency in cystitis

220
Q

Mechanism: Calcium channel blockers

A

Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reducing muscle contractility.

221
Q

Mechanism: Cardiac glycosides - Digoxin

A

75% bioavailability, 20-40% protein bond, t1/2 = 40 hours, urinary excretion Directly inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. ↑[Ca2+]i → positive inotropy. Stimulates vagus nerve.

222
Q

Mechanism: Glucocorticoids

A

↓ the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2

223
Q

Mechanism: H2 blockers

A

Reversible block of histamine H2 receptors → ↓ H+ secretion by parietal cells

224
Q

Mechanism: Heparin

A

Cofactor for the activation of antithrombin, ↓ thrombin, and Xa. Short half life.

225
Q

Mechanism: Sorafenib

A

↓ serine / threonine kinase activity

226
Q

Mechanism: Thrombolytics

A

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. ↑ PT, ↑ PTT, no change in platelet count.

227
Q

Mechanism: Warfarin (Coumadin)

A

Interferes with normal synthesis and γ-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X and protein C and S. Metabolized by the cytochrome P-450 pathway. In laboratory essay, has effect on extrinsic pathway and ↑ PT. Long half-life.

228
Q

Metaproterenol (albuterol, sameterol, terbutaline)

A

Mechanism: Selective β2-agonists (β2>β1) Clinical use: MAST: Metaproterenol and Albuterol for acute asthma; Salmeterol for long-term treatment; Terbutaline to reduce premature uterine contractions

229
Q

Methacholine

A

Direct cholinomimetic agents Clinical use: Challenge test for diagnosis of asthma Action: Stimulates muscarinic receptors in airway when inhaled

230
Q

Methimazole

A

Mechanism: Inhibit organification of iodide and coupling of thyroid hormone synthesis. Clinical use: Hyperthyroidism Toxicity: Skin rash, agranulocytosis (rare), aplastic anemia, a possible teratogen.

231
Q

Methotrexate (MTX)

A

Mechanism: Folic acid analog that inhibits dihydrofolate reductase → ↓ dTMP → ↓ DNA and ↓ protein synthesis Clinical use: Cancers: Leukemias, lymphomas, choriocarcinoma, sarcomas. Non-neoplastic: Abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis Toxicity: 1. Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue” 2. Macrovesicular fatty change in liver 3. Mucositis 4. Teratogenic

232
Q

Metoclopramide

A

Mechanism: D2 receptor antagonist. ↑ resting tone, contractility, LES tone, motility. Does not influence colon transport time. Clinical use: Diabetic and post-surgery gastroparesis Toxicity: ↑ parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interaction with digoxin and diabetic agents.

233
Q

Mimetics (first name them)

A

Pramlintide Mechanism: ↓ glucagon Clinical use: Type 2 DM Toxicity: Hypoglycemia, nausea, diarrhea

234
Q

Misoprostol

A

Mechanism: A PGE1 analog. ↑ production and secretion of gastric mucous barrier. ↓ acid production. Clinical use: Prevention of NSAID-induced peptic ulcers; maintenance of a patent ductus arteriosus. Also used to induce labor. Toxicity: Diarrhea

235
Q

Muromonab-CD3 (OKT3)

A

Mechanism: Monoclonal antibody that binds to CD3 (epsilon chain) on the surface of T cells. Blocks cellular interaction with CD3 protein responsible for T-cell signal transduction. Clinical use: Immunosuppression after kidney transplantation. Toxicity: Cytokine release syndrome, hypersensitivity reaction

236
Q

Muscarinic antagonists (GI): Names

A

Pirenzepine, propantheline

237
Q

Muscarinic antagonists: Atropine, homatropine, tropicamide

A

Organ system: Eye Clinical use: Produces mydriasis and cycloplegia

238
Q

Muscarinic antagonists: Benztropine

A

Organ system: CNS Clinical use: Parkinson’s disease

239
Q

Muscarinic antagonists: Ipratropium

A

Organ system: Respiratory Clinical use: Asthma, COPD

240
Q

Muscarinic antagonists: Methscopolamine, pirenzepine, propantheline

A

Organ system: Gastrointestinal Clinical use: Peptic ulcer treatment

241
Q

Muscarinic antagonists: Oxybutynin, glycopyrrolate

A

Organ system: Genitourinary Clinical use: Reduce urgency in mild cystitis and reduce bladder spasms

242
Q

Muscarinic antagonists: Scopolamine

A

Organ system: CNS Clinical use: Motion sickness

243
Q

Neostigmine

A

Indirect cholinomimetic agents Clinical use: Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative) Action: ↑endogenous ACh; no CNS penetration

244
Q

Niacin

A

Mechanism: Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation Toxicity: Red, flushed face (↓ by aspirin in long-term use), hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbates gout) LDL↓↓; HDL↑↑; TG↓

245
Q

Nitroglycerin, isosorbide dinitrate

A

Mechanism: Vasodilate by releasing nitric oxide in smooth muscle, causing ↑ in cGMP and smooth muscle relaxation. Dilate veins&raquo_space; arteries. ↓ preload Clinical use: Angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer. Toxicity: Reflex tachycardia, hypotension, flushing, headache, “Monday disease”.

246
Q

Nitrosoureas (carmustine, lomustine, semustine, streptozocin)

A

Mechanism: Require bioactivator. Cross blood-brain barrier → CNS. Clinical use: Brain tumors (including glioblastoma multiforme) Toxicity: CNS toxicity (dizziness, ataxia)

247
Q

Nonselective α-blockers (2)

A

Phenoxybenzamine (irreversible), phentolamine (reversible) Clinical use: Pheochromocytoma (use before removing tumor, since high levels of released catecholamines will not be able to overcome blockage) Toxicity: Orthostatic hypotension, reflex tachycardia

248
Q

Norepinephrine

A

Mechanism: α > β Clinical use: Hypotension (but ↓ renal perfusion)

249
Q

Octreotide

A

Mechanism: Somatostatin analog Clinical use: Acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors. Toxicity: Nausea, cramps, steatorrhea

250
Q

Ondansetron

A

Mechanism: 5-HT3 antagonist. Powerful central-acting antiemetic. Clinical use: Control vomiting postoperatively and in patients undergoing cancer therapy. Toxicity: Headache, constipation

251
Q

P-450 Inducers (+)

A

Quinidine; Barbiturates; Phenytoin; Rifampin; Griseofulvin; Carbamazepine; Chronic alcohol use

252
Q

P-450 Inhibitors (-)

A

HIV protease inhibitors; Ketoconazole; Erythromycin; Sulfonamides; Isoniazid; Cimetidine; Grapefruit juice; Acute alcohol use

253
Q

Paclitaxel / Other -taxols

A

Mechanism: Hyperstabilize polymerized microtubules in M-phase so that mitotic spindle cannot break down (anaphase cannot occur) Clinical use: Ovarian and breast carcinomas Toxicity: Myelosuppression and hypersensitivity

254
Q

Phenylephrine

A

Mechanism: α1 > α2 Clinical use: Pupillary dilation, vasoconstriction, nasal decongestion

255
Q

Physostigmine

A

Indirect cholinomimetic agents Clinical use: Glaucoma (crosses blood-brain barrier → CNS) and atropine overdose Action: ↑endogenous ACh

256
Q

Pilocarpine

A

Direct cholinomimetic agents Clinical use: Potent stimulator of sweat, tears, saliva Action: Contracts ciliary muscle of eye (open angle), pupillary sphincter (narrow angle); resistant to AChE.

257
Q

Pirenzepine, propantheline

A

Mechanism: Block M1 receptors on ECL cells (↓ histamine secretion) and M3 receptors on parietal cells (↓ H+ secretion). Clinical use: Peptic ulcer (rarely used) Toxicity: Tachycardia, dry mouth, difficulty focusing eyes

258
Q

Prednisone

A

Mechanism: May trigger apoptosis. May even work on nondividing cells. Clinical use: Most commonly used glucocorticoid in cancer therapy. Used in CLL, Hodgkin’s lymphomas (part of the MOPP regimen). Also an immunosuppressant used in autoimmune diseases. Toxicity: Cushing-like symptoms; immunosuppression, catarcts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis

259
Q

Propylthiouracil

A

Mechanism: Inhibit organification of iodide and coupling of thyroid hormone synthesis, also ↓ peripheral conversion of T4 to T3. Clinical use: Hyperthyroidism Toxicity: Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity.

260
Q

Proton pump inhibitors

A

Omeprazole, lansoprazole (-prazole) Mechanism: Irreversibly inhibit H+/K+-ATPase in stomach parietal cells. Clinical use: Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome

261
Q

Pyridostigmine

A

Indirect cholinomimetic agents Clinical use: Myasthenia gravis (long acting); does not penetrate CNS Action: ↑endogenous ACh; ↑strength

262
Q

Raloxifene

A

Mechanisms: SERMs - receptor antagonists in breast and agonists in bone. Block the binding of estrogen to estrogen receptor positive cells. Clinical use: Breast cancer. Also useful to prevent osteoporosis. Toxicity: No ↑ in endomerial carcinoma because it is an endometrial antagonist

263
Q

Recombinant cytokines: Aldeleukin

A

interleukin-2 for Renal cell carcinoma, metastatic melanoma

264
Q

Recombinant cytokines: Erythropoietin (epoetin)

A

Anemias (especially in renal failure)

265
Q

Recombinant cytokines: Filgrastim

A

granulocyte colony-stimulating factor for Recovery of bone marrow

266
Q

Recombinant cytokines: Oprelvekin

A

interleukin-11 for Thrombocytopenia

267
Q

Recombinant cytokines: Sargramostim

A

granulocyte-macrophage colony-stimulating factor for Recovery of bone marrow

268
Q

Recombinant cytokines: Thrombopoietin

A

Thrombocytopenia

269
Q

Recombinant cytokines: α-interferon

A

Hepatitis B and C, Kaposi’s sarcoma, leukemias, malignant melanoma

270
Q

Recombinant cytokines: β-interferon

A

Multiple sclerosis

271
Q

Recombinant cytokines: γ-interferon

A

Chronic granulomatous disease

272
Q

Ritodrine

A

Mechanism: β2 Clincal use: Reduces premature uterine contractions

273
Q

Rituximab

A

Mechanism: Monoclonal antibody against CD20, which is found on most B-cell neoplasms. Clinical use: Non-Hodgkin’s lymphoma, rheumatoid arthritis (with methotrexate)

274
Q

Second generation Sulfonylureas (first name them)

A

Glyburide, Glimepiride, Glipizide Mechanism: Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx Clinical use: Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type I DM. Toxicity: Hypoglycemia

275
Q

Selective α1-blockers

A

Prazosin, terazosin, doxazosin (-zosin) Clinical use: Hypertension, urinary retention in BPH Toxicity: 1st-dose orthostatic hypotension, dizziness, headache

276
Q

Selective α2-blockers

A

Mirtazapine Clinical use: Depression Toxicity: Sedation, ↑serum cholesterol, ↑appetite

277
Q

Selectivity: Nonselective α- & β- antagonists

A

Carvedilol, labetalol

278
Q

Selectivity: Nonselective β antagonists (β1 = β2)

A

Propranolol, timolol, nadolol, pindolol (>N)

279
Q

Selectivity: Partial β agonists

A

Pindolol, Acebutolol

280
Q

Selectivity: Selective β1 antagonists (β1 > β2)

A

Acebutolol, Betaxolol, Esmolol (short acting), Atenolol, Metoprolol (<M)

281
Q

Sirolimus (rapamycin)

A

Mechanism: Inhibits mTOR. Inhibits T-cell proliferation in response to IL-2 Clinical use: Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids. Toxicity: Hyperlipidemia, thrombocytopenia, leukopenia

282
Q

Sulfa drugs

A

Celecoxib, furosemide, probenecid, thiazides, TMP-SMX, sulfasalazine, sulfonylureas, acetazolamide, sulfonamide antibiotics

283
Q

Sulfasalazine

A

Mechanism: A combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria. Clinical use: Ulcerative colitis, Crohn’s disease Toxicity: Malaise, nausea, sulfonamide toxicity, reversible oligospermia

284
Q

Sympathoplegics (2)

A

Clonidine, α-methyldopa Mechanism: Centrally acting α2-agonist, ↓central adrenergic outflow Clinical use: Hypertension, especially with renal disease (no ↓ in blood flow to kidney)

285
Q

Tacrolimus (FK506)

A

Mechanism: Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines. Clinical use: Potent immunosuppressive used in organ transplant recepients Toxicity: Significant - nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia

286
Q

Tamoxifen

A

Mechanisms: SERMs - receptor antagonists in breast and agonists in bone. Block the binding of estrogen to estrogen receptor positive cells. Clinical use: Breast cancer. Also useful to prevent osteoporosis. Toxicity: May ↑ the risk of endometrial carcinoma via partial agonist effects; “hot flashes”

287
Q

Therapeutic antibodies: Abciximab

A

Target: Glycoprotein IIb/IIIa Clinical use: Prevent cardiac ischemia in unstable angina and in patients treated with percutaneous coronary intervention

288
Q

Therapeutic antibodies: Adalimumab

A

Target: TNF-α Clinical use: Crohn’s disease, rheumatoid arthritis, psoriatic arthritis

289
Q

Therapeutic antibodies: Daclizumab

A

Target: IL-2 receptor Clinical use: Prevent acute rejection of renal transplant

290
Q

Therapeutic antibodies: Digoxin Immune Fab

A

Target: Digoxin Clinical use: Antidote for digoxin intoxication

291
Q

Therapeutic antibodies: Infliximab

A

Target: TNF-α Clinical use: Crohn’s disease, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis

292
Q

Therapeutic antibodies: Muromonab-CD3 (OKT3)

A

Target: CD3 Clinical use: Prevent acute transplant rejection

293
Q

Therapeutic antibodies: Rituximab

A

Target: CD20 Clinical use: B-cell non-Hodgkin’s lymphoma

294
Q

Therapeutic antibodies: Trastuzumab (Herceptin)

A

Target: erb-B2 Clinical use: HER-2 overexpressing breast cancer

295
Q

Thrombolytics: Names

A

Streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)

296
Q

Toxicity: Amiodarone

A

Pulmonary fibrosis, hepatotoxicity, hypothyroidism / hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF)

297
Q

Toxicity: Antiarrhythmics - Na+ channel blockers (Class IA)

A

thrombocytopenia; torsades de pointes due to ↑QT interval

298
Q

Toxicity: Antiarrhythmics - Na+ channel blockers (Class IB)

A

local anesthetic. CNS stimulation / depression, cardiovascular depression

299
Q

Toxicity: Antiarrhythmics - Na+ channel blockers (Class IC)

A

Proarrhythmic, especially post-MI. Significantly prolongs refractory period in AV node.

300
Q

Toxicity: Atropine

A

↑body temperature (due to sweating); rapid pulse; dry mouth; dry, flushed skin; cycloplegia; constipation; disorientation Can cause acute angle-closure glaucoma in elderly, urinary retention in men with prostatic hyperplasia, and hyperthermia in infants

301
Q

Toxicity: Bretylium

A

New arrhythmias, hypertension

302
Q

Toxicity: Calcium channel blockers

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation

303
Q

Toxicity: Cardiac glycosides - Digoxin

A

Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). ECG - ↑PR, ↓QT, scooping, T-wave inversion, arrhythmia, hyperkalemia Worsened renal failure (↓ excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase), quinidine (↓ digoxin clearance, displaces digoxin from tissue-binding sites)

304
Q

Toxicity: Cimetidine

A

a potent inhibitor of P-450, it also has antiandrogenic effects (prolactin release, gynecomastia, impotence, ↓ libido in males); can cross blood-brain barrier (confusion, dizziness, headaches) and placenta, ↓ renal excretion of creatinine

305
Q

Toxicity: Glucocorticoids

A

Iatrogenic Cushing’s syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic) Adrenal insufficiency when drug stopped after chronic use.

306
Q

Toxicity: Heparin

A

Bleeding thrombocytopenia (HIT), osteoporosis, drug-drug interactions. For rapid reversal (antidote), use protamine sulfate (positively charged molecule that binds negatively charged heparin)

307
Q

Toxicity: Ibutilide

A

Torsades de pointes

308
Q

Toxicity: Metoprolol

A

Dyslipidemia

309
Q

Toxicity: Procainamide

A

Reversible SLE-like syndrome

310
Q

Toxicity: Quinidine

A

chichonism - headache, tinnitus;

311
Q

Toxicity: Ranitidine

A

↓ renal excretion of creatinine

312
Q

Toxicity: Sotalol

A

torsades de pointes, excessive β block

313
Q

Toxicity: Thrombolytics

A

Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis

314
Q

Toxicity: Warfarin (Coumadin)

A

Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions.

315
Q

Toxicity: β-blockers

A

Impotence, exacerbation of asthma, cardiovascular adverse effects (bradycardia, AV block, CHF), CNS adverse effects (sedation, sleep alterations); use with caution in diabetics

316
Q

Trastuzumab (Herceptin)

A

Mechanism: Monoclonal antibody against HER-2 (erb-B2). Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity. Clinical use: Metastatic breast cancer Toxicity: Cardiotoxicity

317
Q

Triple therapy of H. pylori ulcers

A

Metronidazole, amoxicillin (or tetracycline), bismuth. Can also use PPI.

318
Q

Types of Insulin

A

Rapid-acting: Lispro, Aspart, Regular Intermediate: NPH Long-acting: Glargine, Detemir

319
Q

Vinblastine

A

Mechanism: Alkaloids that bind to tubulin in M-phase and block polymerization of microtubules so that mitotic spindle cannot form. Clinical use: Hodgkin’s lymphoma, Wilm’s tumor, choriocarcinoma. Toxicity: Myelosuppression

320
Q

Vincristine

A

Mechanism: Alkaloids that bind to tubulin in M-phase and block polymerization of microtubules so that mitotic spindle cannot form. Clinical use: Hodgkin’s lymphoma, Wilm’s tumor, choriocarcinoma. Toxicity: Neurotoxicity (areflexia, peripheral neuritis), paralytic ileus

321
Q

α-glucosidase inhibitors (first name them)

A

Acarbose, Miglitol Mechanism: Inhibit intestinal brush border α-glucosidases. Delayed sugar hydrolysis and glucose absorption lead to ↓ postprandial hyperglycemia Clinical use: Used as monotherapy in type 2 DM or in combination with above agents. Toxicity: GI disturbances

USMLE (12 decks)

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