Pharm_Part1 Flashcards
(321 cards)
1
Q
“Fibrates” (gemfibrozil, clofibrate, bezafibrate, fenofibrate)
A
Mechanism: Upregulate LPL → ↑TG clearance Toxicity: Myositis, hepatotoxicity (↑LFTs), cholesterol gallstones LDL↓; HDL↑; TG↓↓↓
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
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
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.
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.
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
7
Q
Alcohol toxicity
A
Page 246 of FA2011, focus on: Alcohol dehydrogenase - Fomepizole Acetaldehyde dehydrogenase - Disulfiram
8
Q
Amiodarone
A
Has class I, II, III, and IV effects because it alters the lipid membrane
9
Q
Amphetamine
A
Indirect sympathomimetics, indirect general agonist, releases stored catecholamines Clinical use: Narcolepsy, obesity, attention deficit disorder
10
Q
Antacid Overuse
A
- 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)
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.
12
Q
Antianginal therapy
A
Nitrates + β-blockers; β-blockers; Nitrates **Page 281 on FA2011, comparison in different components of drug effects
13
Q
Antianginal therapy: Calcium channel blockers
A
Nifedipine is similar to nitrates in effect; Verapamil is similar to β-blockers in effect
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)
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.
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
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
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
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.
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
21
Q
Antiarrhythmics: K+
A
Depresses ectopic pacemakers in hypokalemia (e.g., digoxin toxicity)
22
Q
Antiarrhythmics: Mg2+
A
Effective in torsades de pointes and digoxin toxicity
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”
24
Q
Antidote: Acetaminophen
A
N-acetylcysteine
25
Antidote: Acetylcholinesterase inhibitors, organophosphates
Atropine, pralidoxime
26
Antidote: Amphetamines (basic)
NH4Cl (acidify urine)
27
Antidote: Antimuscarinic, anticholinergic
Physostigmine salicylate
28
Antidote: Benzodiazepines
Flumazenil
29
Antidote: Carbon monoxide
100% O2, hyperbaric O2
30
Antidote: Cardiac glycosides - Digoxin
Slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+
31
Antidote: Copper, arsenic, gold
Penicillamine
32
Antidote: Cyanide
Nitrite, hydroxocobalamin, thiosulfate
33
Antidote: Digitalis
Stop digitalis, normalize K+, lidocaine, anti-dig Fab fragments, Mg2+
34
Antidote: Heparin
Protamine
35
Antidote: Iron
Deferoxamine
36
Antidote: Lead
CaEDTA, dimercaprol, succimer, penicillamine
37
Antidote: Mercury, arsenic, gold
Dimercaprol (BAL), succimer
38
Antidote: Methanol, ethylene glycol (antifreeze)
Ethanol, dialysis, fomepizole
39
Antidote: Methemoglobin
Methylene blue, vitamin C
40
Antidote: Opioids
Naloxone, naltrexone
41
Antidote: Salicylates
NaHCO3 (alkalinize urine), dialysis
42
Antidote: TCAs
NaHCO3 (plasma alkalinization)
43
Antidote: Theophylline
β-blocker
44
Antidote: tPA, streptokinase
Aminocaproic acid
45
Antidote: Warfarin
For reversal of warfarin overdose, give vitamin K. For rapid reversal of severe warfarin overdose, give fresh frozen plasma.
46
Antidote: Warfarin (Acute, chronic)
Acute: Fresh frozen plasma Chronic: Vitamin K
47
Antidote: β-blockers
Glucagon
48
Antifungal therapy: Amphotericin B
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.
49
Antifungal therapy: Azoles (Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole)
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.
50
Antifungal therapy: Caspofungin
Mechanism: Inhibits cell wall synthesis by inhibiting synthesis of β-glucan Clincal use: Invasive aspergillosis Toxicity: GI upset, flushing
51
Antifungal therapy: Flucytosine
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
52
Antifungal therapy: Griseofulvin
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
53
Antifungal therapy: Nystatin
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
54
Antifungal therapy: Terbinafine
Mechanism: Inhibits the fungal enzyme squalene epoxidase Clinical use: Used to treat dermatophytoses (especially onychomycosis - fungal infection of finger or toe nails)
55
Antihypertensive therapy: CHF
Diuretics, ACE inhibitors / ARBs, β-blockers (compensated CHF), K+-sparing diuretics. PS: β-blockers are contraindicated in decompensated CHF
56
Antihypertensive therapy: Diabetes mellitus
ACE inhibitors / ARBs, calcium channel blockers, diuretics, β-blockers, α-blockers. PS: ACE inhibitors are protective against diabetic nephropathy
57
Antihypertensive therapy: Essential hypertension
Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers
58
Antiviral: Acyclovir
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
59
Antiviral: Amantadine
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
60
Antiviral: Famciclovir
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
61
Antiviral: Foscarnet
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
62
Antiviral: Ganciclovir
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.
63
Antiviral: Interferons
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
64
Antiviral: Ribavirin
Mechanism: Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase Clinical use: RSV, chronic hepatitis C Toxicity: Hemolytic anemia. Severe teratogen
65
Antiviral: Rimantidine
A derivative with fewer CNS side effects of amantadine. Does not cross the blood-brain barrier.
66
Antiviral: Zanamivir, oseltamivir
Mechanism: Inhibit influenza neuraminidase, decreasing the release of progeny virus. Clinical use: Both influenza A and B.
67
Aspirin (ASA)
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)
68
Azathioprine
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
69
Basic concepts on Autonomic drugs
P235-P242 of FA2011, very important!!!
70
Bethanechol
Direct cholinomimetic agents Clinical use: Postoperative and neurogenic ileus and urinary retention Action: Activates bowel and bladder smooth muscle; resistant to AChE
71
Biguanides (first name them)
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
72
Bile acid resins
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)
73
Bile acid resins: Names
Cholestyramine, colestipol, colesevelam
74
Bismuth, sucralfate
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
75
Bleomycin
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.
76
Busulfan
Mechanism: Alkylates DNA Clinical use: CML. Also used to ablate patient's bone marrow before bone marrow transportation. Toxicity: Pulmonary fibrosis, hyperpigmentation
77
Calcium channel blockers: Names (a properties)
Nifedipine, verapamil, diltiazem Vascular smooth muscle - Nifedipine > diltiazem > verapamil Heart - Verapamil > diltiazem > nifedipine
78
Carbachol
Direct cholinomimetic agents Clinical use: Glaucoma, pupillary contraction, and relief of intraocular pressure Action: Carbon copy of acetylcholine
79
Cholesterol absorption blockers (ezetimibe)
Mechanism: Prevent cholesterol reabsorption at small intestine brush border Toxicity: Rare ↑ LFTs LDL↓↓; HDL-; TG-
80
Cholinesterase inhibitor poisoning
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)
81
Cisplatin / Carboplatin
Mechanism: Cross-link DNA Clinical use: Testicular, bladder, ovary, and lung carcinomas Toxicity: Nephrotoxicity and acoustic nerve damage
82
Clinical presentation: Sulfa allergy
May develop fever, pruritic rash, Steven-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria (hives). Symptoms range from mild to life-threatening.
83
Clinical use: Calcium channel blockers
Hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's syndrome.
84
Clinical use: Cardiac glycosides - Digoxin
CHF (↑ contractility); atrial fibrillation (↓ conduction at AV node and depression of SA node)
85
Clinical use: Glucocorticoids
Addison's disease, inflammation, immune suppression, asthma
86
Clinical use: H2 blockers
Peptic ulcer, gastritis, mild esophageal reflux
87
Clinical use: Heparin
Immediate anticoagulation for pulmonary embolism, stroke, acute coronary syndrome, MI, DVT. Used during pregnancy (does not cross the placenta). Follow PTT.
88
Clinical use: Thrombolytics
Early MI, early ischemic stroke.
89
Clinical use: Warfarin (Coumadin)
Chronic anticoagulation. Not used in pregnant women (because warfarin, unlike heparin, can cross the placenta). Follow PT/INR values.
90
Clinical use: β-blockers
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
91
Clopidogrel, ticlopidine
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)
92
Cocaine
Indirect sympathomimetics, indirect general agonist, uptake inhibitor Clinical use: Causes vasoconstriction and local anesthesia
93
Comparison between Heparin and Warfarin
P362 on FA2011, though personally do not think it to be needed if you understood the two drugs itself...
94
Contraindication: Antiarrhythmics - Na+ channel blockers (Class IC)
Post-MI
95
Contraindication: Biguanides (Metformin)
Renal failure
96
Contraindication: Hydralazine
in Angina / CAD
97
Contraindication: Metoclopramide
patients with small bowel obstruction
98
Contraindication: Misoprostol
in women of childbearing potential (abortifacient)
99
Contraindications: Pindolol, acebutolol
Angina, because they are partial β-agonists
100
Cyclophosphamide / Isosfamide
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)
101
Cyclosporine
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)
102
Cytarabine (ara-C)
Mechanism: Pyrimidine analog → inhibition of DNA polymerase Clinical use: AML, ALL, high-grade non-Hodgkin's lymphoma Toxicity: Leukopenia, thrombocytopenia, megaloblastic anemia
103
Daclizumab
Mechanism: Monoclonal antibody with high affinity for the IL-2 receptor on activated T cells
104
Dactinomycin (Actinomycin D)
Mechanism: Intercalates in DNA Clinical use: Wilm's tumor, Ewing's sarcoma, rhabdomyosarcoma. Used for childhood tumors. Toxicity: Myelosuppression
105
Demeclocycline
Mechanism: ADH antagonist (member of the tetracycline family) Clinical use: SIADH Toxicity: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth
106
Dobutamine
Mechanism: β1 > β2, inotropic but not chronotropic Clinical use: Heart failure, cardiac stress testing
107
DOC: Hemorrhagic cystitis
Mesna, thiol group of mesna binds toxic metabolite causing hemorrhagic cystitis
108
Dopamine
Mechanism: D1 = D2 > β > α, inotropic and chronotropic Clinical use: Shock (↑ renal perfusion)
109
Doxorubicin (Adriamycin) / Daunorubicin
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.
110
Drug ending category: -afil
Erectile dysfunction (Sildenafil)
111
Drug ending category: -ane
Inhalational general anesthetic (Halothane)
112
Drug ending category: -azepam
Benzodiazepine (Diazepam)
113
Drug ending category: -azine
Phenothiazine (neuroleptic, antiemetic) (Chlorpromazine)
114
Drug ending category: -azole
Antifungal (Ketoconazole)
115
Drug ending category: -barbital
Barbiturate (Phenobarbital)
116
Drug ending category: -caine
Local anesthetic (Lidocaine)
117
Drug ending category: -cillin
Penicillin (Methicillin)
118
Drug ending category: -cycline
Antibiotic, protein synthesis inhibitor (Tetracycline)
119
Drug ending category: -etine
SSRI (Fluoxetine)
120
Drug ending category: -ipramine
TCA (Imipramine)
121
Drug ending category: -navir
Protease inhibitor (Saquinavir)
122
Drug ending category: -olol
β antagonist (Propranolol)
123
Drug ending category: -operidol
Butyrophenone (neuroleptic) (Haloperidol)
124
Drug ending category: -oxin
Cardiac glycoside (inotropic agent) (Digoxin)
125
Drug ending category: -phylline
Methylxanthine (Theophylline)
126
Drug ending category: -pril
ACE inhibitor (Captopril)
127
Drug ending category: -terol
β2 agonist (Albuterol)
128
Drug ending category: -tidine
H2 antagonist (Cimetidine)
129
Drug ending category: -triptan
5-HT(1B/1D) agonist (migraine) (Sumatriptan)
130
Drug ending category: -triptyline
TCA (Amitriptyline)
131
Drug ending category: -tropin
Pituatory hormone (Somatotropin)
132
Drug ending category: -zolam
Benzodiazepine (Alprazolam)
133
Drug ending category: -zosin
α1 antagonist (Prazosin)
134
Drug group: Amiodarone
Antiarrhythmics - K+ channel blockers (Class III)
135
Drug group: Bertylium
Antiarrhythmics - K+ channel blockers (Class III)
136
Drug group: Dofetilide
Antiarrhythmics - K+ channel blockers (Class III)
137
Drug group: Ibutilide
Antiarrhythmics - K+ channel blockers (Class III)
138
Drug group: Sotalol
Antiarrhythmics - K+ channel blockers (Class III)
139
Drug reactions: Acute cholestatic hepatitis
Macrolides
140
Drug reactions: Adrenocortical insufficienty
Glucocorticoid withdrawal (HPA suppression)
141
Drug reactions: Agranulocytosis (6)
Clozapine, carbamazepine, colchicine, propylthiouracil, methimazole, dapsone
142
Drug reactions: Aplastic anemia (5)
Chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole
143
Drug reactions: Atropine-like side effects
TCAs
144
Drug reactions: Cinchonism (2)
Quinidine, Quinine
145
Drug reactions: Coronary vasospasm (2)
Cocaine, sumatriptan
146
Drug reactions: Cough
ACE inhibitors (note: ARBs like losartan - no cough)
147
Drug reactions: Cutaneous flushing (4)
VANC: Vancomycin, Adenosine, Niacin, Ca2+ channel blockers
148
Drug reactions: Diabetes insipidus (2)
Lithium, demeclocycline
149
Drug reactions: Dilated cardiomyopathy (2)
Doxorubicin (Adriamycin), daunorubicin
150
Drug reactions: Direct Coombs-positive hemolytic anemia
Methyldopa
151
Drug reactions: Disulfiram-like reaction (4)
Metronidazole, certain cephalosporins, procarbazine, 1st-generation sulfonylureas
152
Drug reactions: Fanconi's syndrome
Expired tetracycline
153
Drug reactions: Focal to massive hepatic necrosis (4)
Halothane, valproic acid, acetaminophen, Amanita phalloides
154
Drug reactions: Gingival hyperplasia
Phenytoin
155
Drug reactions: Gout (2)
Furosemide, thiazides
156
Drug reactions: Grey baby syndrome
Chloramphenicol
157
Drug reactions: Gynecomastia (6)
Spironolactone, Digitalis, Cimetidine, chronic alcohol use, estrogens, Ketoconazole
158
Drug reactions: Hemolysis in G6PD-deficient patients (6)
Hemolysis IS PAIN, Isoniazid (INH), Sulfonamides, Primaquine, Aspirin, Ibuprofen, Nitrofurantoin
159
Drug reactions: Hemorrhagic cystitis (2)
Cyclophosphamide, ifosfamide (prevent by coadministering with mesna)
160
Drug reactions: Hepatitis
INH
161
Drug reactions: Hot flashes (2)
Tamoxifen, clomiphene
162
Drug reactions: Hypothyroidism (2)
Lithium, amiodarone
163
Drug reactions: Interstitial nephritis (3)
Methicillin, NSAIDs, furosemide
164
Drug reactions: Megaloblastic anemia (3)
Phenytoin, Methotrexate, Sulfa drugs
165
Drug reactions: Nephrotoxicity / neurotoxicity
Polymyxins
166
Drug reactions: Nephrotoxicity / ototoxicity (4)
Aminoglycosides, vancomycin, loop diuretics, cisplatin
167
Drug reactions: Osteoporosis (2)
Corticosteroids, heparin
168
Drug reactions: Parkinson-like syndrome (4)
Haloperidol, chlorpromazine, reserpine, metoclopramide
169
Drug reactions: Photosensitivity (3)
Sulfonamides, Amiodarone, Tetracycline
170
Drug reactions: Pseudomembranous colitis (2)
Clindamycin, ampicillin
171
Drug reactions: Pulmonary fibrosis
Bleomycin, Amiodarone, Busulfan (BLAB)
172
Drug reactions: Rash (Steves-Johnson syndrome) (8)
Ethosuximide, lamotrigine, carbamazepine, phenobarbital, phenytoin, sulfa drugs, penicillin, allopurinol
173
Drug reactions: Seizures (3)
Bupropion, imipenem / cilastatin, isoniazid
174
Drug reactions: SLE-like syndrome (4)
Hydalazine, INH, Procainamide, Phenytoin
175
Drug reactions: Tardive dyskinesia
Antipsychotics
176
Drug reactions: Tendonitis, tendon rupture, and cartilage damage (kids)
Fluoroquinolones
177
Drug reactions: Thrombotic complication
OCPs (e.g., estrogens and progestins)
178
Drug reactions: Torsades de pointes (2)
Class III (sotalol), class IA (quinidine) antiarrhythmics
179
Echothiophate
Indirect cholinomimetic agents Clinical use: Glaucoma Action: ↑endogenous ACh
180
Edrophonium
Indirect cholinomimetic agents Clinical use: Diagnosis of myasthenia gravis (extremely short acting) Action: ↑endogenous ACh
181
Ephedrine
Indirect sympathomimetics, indirect general agonist, releases stored catecholamines Clinical use: Nasal decongestion, urinary incontinence, hypotension
182
Epinephrine
Mechanism: α & β, low doses selective for β1, high doses selective for α Clinical use: Anaphylaxis, glaucoma (open angle), asthma, hypotension
183
Etoposide (VP-16) / Teniposide
Mechanism: Inhibits topoisomerase II → ↑ DNA degradation Clinical use: Small cell carcinoma of the lung and prostate, testicular carcinoma Toxicity: Myelosuppression, GI irritation, alopecia
184
First generation Sulfonyureas (first name them)
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
Glitazones / thiazolidinediones (first name them)
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
GLP-1 analogs (first name them)
Exenatide Mechanism: ↑insulin, ↓glucagon release Clinical use: Type 2 DM Toxicity: Nausea, vomiting, pancreatitis
187
Glucocorticoids: Names
Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone
188
H2 blockers: Names
Cimetidine, ranitidine, famotidine, nizatidine (-tidine)
189
Heparin-induced thrombocytopenia (HIT)
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
Hexamethonium
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
HIV therapy: Fusion inhibitors
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
HIV therapy: Highly active antiretroviral therapy (HAART)
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
HIV therapy: NNRTIs
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
HIV therapy: NRTIs
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
HIV therapy: Protease inhibitors
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
HMG-Coa reductase inhibitors (-statin)
Mechanism: Inhibit cholesterol percursor, mevalonate Toxicity: Hepatotoxicity (↑LFTs), rhabdomyolysis LDL↓↓↓; HDL↑; TG↓
197
Hydralazine
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
Hydroxyurea
Mechanism: Inhibits ribonucleotide reductase → ↓ DNA synthesis (S-phase specific) Clinical use: Melanoma, CML, sickle cell disease (↑ HbF) Toxicity: Bone marrow suppression, GI upset.
199
Hypothalamic / pituitary drugs - Clinical use: ADH (desmopressin)
Pituitary (central, not nephrogenic) DI
200
Hypothalamic / pituitary drugs - Clinical use: GH
GH deficiency, Turner syndrome
201
Hypothalamic / pituitary drugs - Clinical use: Oxytocin
Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage
202
Hypothalamic / pituitary drugs - Clinical use: Somatostatin (octreotide)
Acromegaly, carcinoid, gastrinoma, glucagonoma
203
Imatinib (Gleevec)
Mechanism: Philadelphia chromosome bcr-abl tyrosine kinase inhibitor. Clinical use: CML, GI stromal tumors Toxicity: Fluid retention
204
Infliximab
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
Insulin
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
Isoproterenol
Mechanism: β1 = β2 (isolated to β) Clinical use: AV block (rare)
207
Ketorolac
NSAID often used as an analgesic, indicated for short-term management of moderate to severe pain
208
Lepirudin, bivalirudin
Hirudin derivatives; directly inhibit thrombin. Used as an alternative to heparin for anticoagulating patients with HIT
209
Leucovorin
Folinic acid, rescue methotrexate (MTX) myelosuppression
210
Levothyroxine, triiodothyronine
Mechanism: Thyroxine replacement Clinical use: Hypothyroidism, myxedema Toxicity: Tachycardia, heat intolerance, tremors, arrhythmias
211
Low-molecular-weight-heparins (e.g., enoxaparin)
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
Malignant hypertension treatment: Diazoxide
K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia (reduces insulin release)
213
Malignant hypertension treatment: Fenoldopam
Dopamine D1 receptor agonist - relaxes renal vascular smooth muscle
214
Malignant hypertension treatment: Nitroprusside
Short acting; ↑ cGMP via direct release of NO. Can cause cyanide toxicity (releases CN)
215
Mechanism of resistance: Acyclovir, famciclovir
Lack of viral thymidine kinase
216
Mechanism of resistance: Amantadine
Mutated M2 protein. 90% of all influenza A strains are resistant to amantadine, so not used.
217
Mechanism of resistance: Foscarnet
Mutated DNA polymerase
218
Mechanism of resistance: Ganciclovir
Mutated CMV DNA polymerase or lack of viral kinase
219
Mechanism: Atropine
Eye: ↑pupil dilation, cycloplegia Airway: ↓secretion Stomach: ↓acid secretion Gut: ↓motility Bladder: ↓urgency in cystitis
220
Mechanism: Calcium channel blockers
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reducing muscle contractility.
221
Mechanism: Cardiac glycosides - Digoxin
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
Mechanism: Glucocorticoids
↓ the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2
223
Mechanism: H2 blockers
Reversible block of histamine H2 receptors → ↓ H+ secretion by parietal cells
224
Mechanism: Heparin
Cofactor for the activation of antithrombin, ↓ thrombin, and Xa. Short half life.
225
Mechanism: Sorafenib
↓ serine / threonine kinase activity
226
Mechanism: Thrombolytics
Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. ↑ PT, ↑ PTT, no change in platelet count.
227
Mechanism: Warfarin (Coumadin)
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
Metaproterenol (albuterol, sameterol, terbutaline)
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
Methacholine
Direct cholinomimetic agents Clinical use: Challenge test for diagnosis of asthma Action: Stimulates muscarinic receptors in airway when inhaled
230
Methimazole
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
Methotrexate (MTX)
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
Metoclopramide
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
Mimetics (first name them)
Pramlintide Mechanism: ↓ glucagon Clinical use: Type 2 DM Toxicity: Hypoglycemia, nausea, diarrhea
234
Misoprostol
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
Muromonab-CD3 (OKT3)
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
Muscarinic antagonists (GI): Names
Pirenzepine, propantheline
237
Muscarinic antagonists: Atropine, homatropine, tropicamide
Organ system: Eye Clinical use: Produces mydriasis and cycloplegia
238
Muscarinic antagonists: Benztropine
Organ system: CNS Clinical use: Parkinson's disease
239
Muscarinic antagonists: Ipratropium
Organ system: Respiratory Clinical use: Asthma, COPD
240
Muscarinic antagonists: Methscopolamine, pirenzepine, propantheline
Organ system: Gastrointestinal Clinical use: Peptic ulcer treatment
241
Muscarinic antagonists: Oxybutynin, glycopyrrolate
Organ system: Genitourinary Clinical use: Reduce urgency in mild cystitis and reduce bladder spasms
242
Muscarinic antagonists: Scopolamine
Organ system: CNS Clinical use: Motion sickness
243
Neostigmine
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
Niacin
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
Nitroglycerin, isosorbide dinitrate
Mechanism: Vasodilate by releasing nitric oxide in smooth muscle, causing ↑ in cGMP and smooth muscle relaxation. Dilate veins >> arteries. ↓ preload Clinical use: Angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer. Toxicity: Reflex tachycardia, hypotension, flushing, headache, "Monday disease".
246
Nitrosoureas (carmustine, lomustine, semustine, streptozocin)
Mechanism: Require bioactivator. Cross blood-brain barrier → CNS. Clinical use: Brain tumors (including glioblastoma multiforme) Toxicity: CNS toxicity (dizziness, ataxia)
247
Nonselective α-blockers (2)
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
Norepinephrine
Mechanism: α > β Clinical use: Hypotension (but ↓ renal perfusion)
249
Octreotide
Mechanism: Somatostatin analog Clinical use: Acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors. Toxicity: Nausea, cramps, steatorrhea
250
Ondansetron
Mechanism: 5-HT3 antagonist. Powerful central-acting antiemetic. Clinical use: Control vomiting postoperatively and in patients undergoing cancer therapy. Toxicity: Headache, constipation
251
P-450 Inducers (+)
Quinidine; Barbiturates; Phenytoin; Rifampin; Griseofulvin; Carbamazepine; Chronic alcohol use
252
P-450 Inhibitors (-)
HIV protease inhibitors; Ketoconazole; Erythromycin; Sulfonamides; Isoniazid; Cimetidine; Grapefruit juice; Acute alcohol use
253
Paclitaxel / Other -taxols
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
Phenylephrine
Mechanism: α1 > α2 Clinical use: Pupillary dilation, vasoconstriction, nasal decongestion
255
Physostigmine
Indirect cholinomimetic agents Clinical use: Glaucoma (crosses blood-brain barrier → CNS) and atropine overdose Action: ↑endogenous ACh
256
Pilocarpine
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
Pirenzepine, propantheline
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
Prednisone
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
Propylthiouracil
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
Proton pump inhibitors
Omeprazole, lansoprazole (-prazole) Mechanism: Irreversibly inhibit H+/K+-ATPase in stomach parietal cells. Clinical use: Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome
261
Pyridostigmine
Indirect cholinomimetic agents Clinical use: Myasthenia gravis (long acting); does not penetrate CNS Action: ↑endogenous ACh; ↑strength
262
Raloxifene
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
Recombinant cytokines: Aldeleukin
interleukin-2 for Renal cell carcinoma, metastatic melanoma
264
Recombinant cytokines: Erythropoietin (epoetin)
Anemias (especially in renal failure)
265
Recombinant cytokines: Filgrastim
granulocyte colony-stimulating factor for Recovery of bone marrow
266
Recombinant cytokines: Oprelvekin
interleukin-11 for Thrombocytopenia
267
Recombinant cytokines: Sargramostim
granulocyte-macrophage colony-stimulating factor for Recovery of bone marrow
268
Recombinant cytokines: Thrombopoietin
Thrombocytopenia
269
Recombinant cytokines: α-interferon
Hepatitis B and C, Kaposi's sarcoma, leukemias, malignant melanoma
270
Recombinant cytokines: β-interferon
Multiple sclerosis
271
Recombinant cytokines: γ-interferon
Chronic granulomatous disease
272
Ritodrine
Mechanism: β2 Clincal use: Reduces premature uterine contractions
273
Rituximab
Mechanism: Monoclonal antibody against CD20, which is found on most B-cell neoplasms. Clinical use: Non-Hodgkin's lymphoma, rheumatoid arthritis (with methotrexate)
274
Second generation Sulfonylureas (first name them)
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
Selective α1-blockers
Prazosin, terazosin, doxazosin (-zosin) Clinical use: Hypertension, urinary retention in BPH Toxicity: 1st-dose orthostatic hypotension, dizziness, headache
276
Selective α2-blockers
Mirtazapine Clinical use: Depression Toxicity: Sedation, ↑serum cholesterol, ↑appetite
277
Selectivity: Nonselective α- & β- antagonists
Carvedilol, labetalol
278
Selectivity: Nonselective β antagonists (β1 = β2)
Propranolol, timolol, nadolol, pindolol (>N)
279
Selectivity: Partial β agonists
Pindolol, Acebutolol
280
Selectivity: Selective β1 antagonists (β1 > β2)
Acebutolol, Betaxolol, Esmolol (short acting), Atenolol, Metoprolol (
281
Sirolimus (rapamycin)
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
Sulfa drugs
Celecoxib, furosemide, probenecid, thiazides, TMP-SMX, sulfasalazine, sulfonylureas, acetazolamide, sulfonamide antibiotics
283
Sulfasalazine
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
Sympathoplegics (2)
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
Tacrolimus (FK506)
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
Tamoxifen
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
Therapeutic antibodies: Abciximab
Target: Glycoprotein IIb/IIIa Clinical use: Prevent cardiac ischemia in unstable angina and in patients treated with percutaneous coronary intervention
288
Therapeutic antibodies: Adalimumab
Target: TNF-α Clinical use: Crohn's disease, rheumatoid arthritis, psoriatic arthritis
289
Therapeutic antibodies: Daclizumab
Target: IL-2 receptor Clinical use: Prevent acute rejection of renal transplant
290
Therapeutic antibodies: Digoxin Immune Fab
Target: Digoxin Clinical use: Antidote for digoxin intoxication
291
Therapeutic antibodies: Infliximab
Target: TNF-α Clinical use: Crohn's disease, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis
292
Therapeutic antibodies: Muromonab-CD3 (OKT3)
Target: CD3 Clinical use: Prevent acute transplant rejection
293
Therapeutic antibodies: Rituximab
Target: CD20 Clinical use: B-cell non-Hodgkin's lymphoma
294
Therapeutic antibodies: Trastuzumab (Herceptin)
Target: erb-B2 Clinical use: HER-2 overexpressing breast cancer
295
Thrombolytics: Names
Streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)
296
Toxicity: Amiodarone
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
Toxicity: Antiarrhythmics - Na+ channel blockers (Class IA)
thrombocytopenia; torsades de pointes due to ↑QT interval
298
Toxicity: Antiarrhythmics - Na+ channel blockers (Class IB)
local anesthetic. CNS stimulation / depression, cardiovascular depression
299
Toxicity: Antiarrhythmics - Na+ channel blockers (Class IC)
Proarrhythmic, especially post-MI. Significantly prolongs refractory period in AV node.
300
Toxicity: Atropine
↑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
Toxicity: Bretylium
New arrhythmias, hypertension
302
Toxicity: Calcium channel blockers
Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation
303
Toxicity: Cardiac glycosides - Digoxin
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
Toxicity: Cimetidine
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
Toxicity: Glucocorticoids
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
Toxicity: Heparin
Bleeding thrombocytopenia (HIT), osteoporosis, drug-drug interactions. For rapid reversal (antidote), use protamine sulfate (positively charged molecule that binds negatively charged heparin)
307
Toxicity: Ibutilide
Torsades de pointes
308
Toxicity: Metoprolol
Dyslipidemia
309
Toxicity: Procainamide
Reversible SLE-like syndrome
310
Toxicity: Quinidine
chichonism - headache, tinnitus;
311
Toxicity: Ranitidine
↓ renal excretion of creatinine
312
Toxicity: Sotalol
torsades de pointes, excessive β block
313
Toxicity: Thrombolytics
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
Toxicity: Warfarin (Coumadin)
Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions.
315
Toxicity: β-blockers
Impotence, exacerbation of asthma, cardiovascular adverse effects (bradycardia, AV block, CHF), CNS adverse effects (sedation, sleep alterations); use with caution in diabetics
316
Trastuzumab (Herceptin)
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
Triple therapy of H. pylori ulcers
Metronidazole, amoxicillin (or tetracycline), bismuth. Can also use PPI.
318
Types of Insulin
Rapid-acting: Lispro, Aspart, Regular Intermediate: NPH Long-acting: Glargine, Detemir
319
Vinblastine
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
Vincristine
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
α-glucosidase inhibitors (first name them)
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
