Pharmacology Step 1 Part 2

Front 1

Bupropion (mechanism, use, toxicity)

Back 1

Increases NE and dopamine; used for smoking sensation, depression; seizures

Front 2

Mirtazapine (mechanism, use, toxicity)

Back 2

Alpha-2 antagonist, increases NE and serotonin release, and serotonin receptor agonist; used for depression; sedation, increased appetite with weight gain;

Front 3

Maprotiline (mechanism, use, toxicity)

Back 3

Blocks NE reuptake; used for depression; sedation, hypotension

Front 4

Trazodone (mechanism, use, toxicity)

Back 4

Inhibits serotonin uptake; used for insomnia; pripism

Front 5

Mannitol (mechanism, use, toxicity)

Back 5

Osmotic diuretic; used to treat drug overdose and increased ICP; pulmonary edema, CHF

Front 6

Acetazolamide (mechanism, use, toxicity)

Back 6

Carbonic anhydrase inhibitor; used for glaucoma, metabolic alklalosis; hyperchloremic metabolic acidosis, ammonia toxicity, sulfa allergy

Front 7

Furosemide (mechanism, use, toxicity)

Back 7

Inhibits NKCC channel, preventing urine concentration; used in hypertension, CHF, hypercalcemia; ototoxicity, hypokalemia, hypocalcemia, nephritis, gout, sulfa allergy

Front 8

Ethacrynic acid (mechanism, use, toxicity)

Back 8

Inhibits NKCC channel; used in patients with furosemide (sulfa) allergy; hyperuricemia

Front 9

Hydrochlorothiazide (mechanism, use, toxicity)

Back 9

Inhibits NaCl reabsorption in DCT and increases Ca reabsorption; hypertension and hypercalcinuria; hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

Front 10

Spironolactone, eplerenone (mechanism, use, toxicity)

Back 10

Aldosterone receptor antagonists; hyperaldosteronism, CHF, hypokalemia; hyperkalemia (arrhythmias), antiandrogen effects with spironolactone

Front 11

Triamterene, amiloride (mechanism, use, toxicity)

Back 11

Block sodium channels in cortical collecting duct; hyperaldosteronism, CHF

Front 12

Captopril, enalapril, lisinopril (mechanism, use, toxicity)

Back 12

ACE inhibitor, leads to reduced angiotensin II levels and decreases GFR; prevents heart remodeling, hypertension, CHF; cough, angioedema, transient creatinine increase, hyperkalemia

Front 13

Losartan, valsartan (mechanism, use, toxicity)

Back 13

Angiotensin II receptor antagonists; similar to ACE inhibitors, but do not cause cough due to normal metabolism of bradykinin

Front 14

Leuprolide (mechanism, use, toxicity)

Back 14

GnRH analog that acts as an agonist in pulsatile doses and an antagonist in continuous doses; used as an agonist for infertility and an antagonist for prostate cancer, fibroids, and precocious puberty; antiandrogenic

Front 15

Finasteride (mechanism, use, toxicity)

Back 15

5-alpha reductase inhibitor; used for BPH and male-pattern baldness

Front 16

Flutamide (mechanism, use, toxicity)

Back 16

Testosterone receptor antagonist; used in prostate cancer

Front 17

Ketoconazole (mechanism, use, toxicity)

Back 17

Inhibits 17,20-desmolase, stopping sex steroid synthesis; used to treat polycystic ovarian syndrome

Front 18

Clomiphene (mechanism, use, toxicity)

Back 18

Partial estrogen agonist in the hypothalamus, increases release of LH and FSH, stimulating ovulation; used for infertility and PCOS

Front 19

Tamoxifen (mechanism, use, toxicity)

Back 19

Estrogen receptor antagonist at the breast; used for breast cancer; partial agonist at the uterus, can cause endometrial hyperplasia

Front 20

Raloxifene (mechanism, use, toxicity)

Back 20

Estrogen receptor agonist at bone, inhibits osteoclast activity and stimulates osteoblast activity; used to treat osteoporosis

Front 21

Anastrozole, exemestane (mechanism, use, toxicity)

Back 21

Aromatase inhibitors; used in breast cancer

Front 22

Mifepristone (mechanism, use, toxicity)

Back 22

Progesterone receptor antagonist, given with misoprostol for abortion; abortifacient; bleeding, abdominal pain

Front 23

Terbutaline (mechanism, use, toxicity)

Back 23

Beta-2 agonist, inhibits uterine contractions

Front 24

Tamsulosin (mechanism, use, toxicity)

Back 24

Alpha-1 antagonist; used to treat BPH

Front 25

Sildenafil, vardenafil (mechanism, use, toxicity)

Back 25

Phosphodiesterase 5 inhibitors, causing inc. cGMP levels and smooth muscle relaxation; used in erectile dysfunction; impaired blue-green vision, contradindicated with nitrates

Front 26

Danazol (mechanism, use, toxicity)

Back 26

Partial androgen receptor agonist; used to treat endometriosis and hereditary angioedema; weight gain, acne, hirsutism, low HDL, hepatoxicity

Front 27

Treat methemoglobinemia with

Back 27

Methylene blue

Front 28

Diphenhydramine, dimenhydrinate, chlorpheniramine (mechanism, use, toxicity)

Back 28

(First generation) H1 antagonists; used in allergies, motion sickness, insomnia; sedation, antiadrenergic, antiserotonergic, and antimuscarinic effects due to CNS penetration

Front 29

Loratadine, fexofenadine, desloratadine, cetrizine (mechanism, use, toxicity)

Back 29

H1 antagonists, 2nd gen; used in allergies; less fatigue than 1st gen antihistamines due to decreased CNS penetration

Front 30

Albuterol (mechanism, use, toxicity)

Back 30

Short-acting beta-2 agonist; asthma

Front 31

Salmeterol, formoterol (mechanism, use, toxicity)

Back 31

Long-acting beta-2 agonist; asthma; tremor, arrhythmias

Front 32

Theophylline (mechanism, use, toxicity)

Back 32

Phosphodiesterase inhibitor, increases cAMP and causes bronchodilation; asthma; cardiotoxicity, neurotoxicity

Front 33

Ipratropium (mechanism, use, toxicity)

Back 33

Muscarinic antagonist, prevents bronchoconstriction; asthma and COPD

Front 34

Beclomethasone, fluticasone (mechanism, use, toxicity)

Back 34

Inhibit cytokine synthesis, reducing inflammation due to asthma; 1st line for chronic asthma

Front 35

Montelukast, zafirlukast (mechanism, use, toxicity)

Back 35

Leukotriene receptor antagonists; especially useful in aspirin-induced asthma

Front 36

Zileuton (mechanism, use, toxicity)

Back 36

Inhibits activity of 5-lipoxygenase, inhibiting leukotriene production; reduces inflammation

Front 37

Omalizumab (mechanism, use, toxicity)

Back 37

Anti-IgE antibody; used in refractory allergic asthma

Front 38

Guaifenesin (mechanism, use, toxicity)

Back 38

Thins respiratory secretions

Front 39

N-acetylcysteine (mechanism, use, toxicity)

Back 39

Loosens mucus plugs; used in CF patients and as an antidote to acetominaphen posioning

Front 40

Bosentan (mechanism, use, toxicity)

Back 40

Antagonizes endothelin-1 receptors, reducing vascular resistance in the pulmonary vessels; used in pulmonary hypertension

Front 41

Dextromethorphan (mechanism, use, toxicity)

Back 41

Antagonizes NMDA receptors, inhibiting coughing; produces opioid effects in large doses and carries mild abuse potential

Front 42

Pseudoephedrine, phenylephrine (mechanism, use, toxicity)

Back 42

Alpha-1 agonists that reduce edema and nasal congestion; rhinitis; hypertension, quick tolerance (recurrence of symptoms despite continued treatment)

Front 43

Difference in competitive vs noncompetitve inhibitors?

Back 43

competitive = decrease potency, noncompetitive = decrease efficacy.

Front 44

What is Km?

Back 44

Inverse relation of affinity of enzyme for its substrate.

Front 45

What is Vmax?

Back 45

Direct proportion to enzyme concentration

Front 46

What is bioavailability?

Back 46

Fraction of administered drug that reaches systemic circulation unchanged.

Front 47

Time to steady state depends on?

Back 47

depends on half-life. Does not depend on frequency or size of dose.

Front 48

What is rate of elimination in zero order kinetics?

Back 48

constant amount eliminated per time.

Front 49

Give three drugs that are zero order eliminated.

Back 49

PEA - phenytoin, Ethanol, Aspirin.

Front 50

What is the rate of elimination for first order kinetics?

Back 50

A constant FRACTION is eliminted, variable by concentration!

Front 51

How does ionization relate to urine pH?

Back 51

Ionzied species are trapped in urine and not resorbed. Neutral can be resorbed.

Front 52

How do you treat overdose of weak acid? Give drug examples.

Back 52

Treat with Bicarb to make neutral. Exp: phenobarbital, methotrexate, aspirin.

Front 53

How do you treat overdose of weak base? Give drug examples.

Back 53

Treat with ammonium chloride. exp: amphetamines.

Front 54

What is phase I drug metabolism? What pt. population loses this?

Back 54

Reduction, Oxidation, hydrolysis with CYP450. Often gives neutral products. Geriatrics lose this phase.

Front 55

What is phase II metaboloism? What population depend on this?

Back 55

Conjugation (Glucuronidation, Acetylation, and Sulfation.) Gives charged products. Geriatrics depend on this, old people have GAS.

Front 56

What is efficacy?

Back 56

maximal effect a drug can produce.

Front 57

What is potency?

Back 57

amount of drug needed for the same effect.

Front 58

What happends to efficacy when a partial agonist and full agonist are mixed?

Back 58

DECREASED efficacy. fight for same binding site, full agonist cant exert full effect.

Front 59

What is therapetuic index?

Back 59

LD50/ED50. Median lethal dose divded by median effective dose. Safer drugs have a higher TI.

Front 60

What is a therapeutic window?

Back 60

Minimum effective dose to minimum toxic dose. Think of it as range of use.

Front 61

What are the two types of Nicotonic receptors? What kind of messenger do they use?

Back 61

1. Nicotinic - Ligang gated Na/K channels. Two nicotinic types: Nm(NMJ) and Nn(autonomic ganglia. 2. Muscarinic - G-proteins. 5 types, M1-M5.

Front 62

Alpha-1 sympathetic receptor (G-protein class, major function)

Back 62

q, increase: vasc. smooth muscle contraction, pupillary dilator muscle contraction, intestinal and bladder sphincter contaction.

Front 63

Alpha-2 sympathetic receptor(G-protein class, major function)

Back 63

i, decrease: sympathetic outflow, insulin release, lipolysis. increase: platlet aggregation.

Front 64

Beta-1 sympathetic receptor(G-protein class, major function)

Back 64

s, increase: heart rate, contractilty, renin release, lipolysis

Front 65

Beta-2 sympathetic receptor(G-protein class, major function)

Back 65

s, vasodilation, brochodilation, increase: heart rate, contractility, lipolysis, insulin release, aqueous humor production. decrease: uterine tone, ciliary muscle tone.

Front 66

M-1 Parasymp receptor(G-protein class, major function)

Back 66

q, CNS, enteric nervouse system.

Front 67

M-2 Parasymp(G-protein class, major function)

Back 67

i, decease: heart rate, contractility of atria

Front 68

M-3 parasymp(G-protein class, major function)

Back 68

increase: exocrine gland secretion (tears, gastric, etc), gut peristalsis, bladder contraction, bronchoconstriction, pupillary spinchter contraction, cilliary muscle contraction.

Front 69

What receptor is responsible for miosis and accomodation?

Back 69

Parasympathetic M-3.

Front 70

What receptor is responsbile for mydriasis?

Back 70

Sympathetic Alpha-1.

Front 71

Dopamine D-1 receptor(G-protein class, major function)

Back 71

s, relaxes renal vascular smooth muscle

Front 72

Dopamine D-2 receptor(G-protein class, major function)

Back 72

i, modulates transmitter release especially in brain.

Front 73

Histamine H-1 receptor(G-protein class, major function)

Back 73

q, increase: mucus production, contraction of bronchioles, pruritus, pain.

Front 74

histamine H-2 receptor(G-protein class, major function)

Back 74

a, increase gastric acid secretion

Front 75

vasopression V-1 receptor(G-protein class, major function)

Back 75

q, increase: vascular smooth muscle contraction

Front 76

vasopression V-2 receptor(G-protein class, major function)

Back 76

s, increase water permeability and reabsorption in kidneys. (V2 found in 2 kidneys).

Front 77

Which receptors work via Gq -> Phospholipase C ->Pip2->DAG + IP3?

Back 77

H1,Alpha1,V1,M1,M3. (remember HAVe 1 M&M)

Front 78

DAG causes activation of what?

Back 78

Protein Kinase C.

Front 79

IP3 causes increase in what?

Back 79

Calcium -> smouth muscle contraction

Front 80

Which receptors work via Gi->Adenyly cyclase ->cAMP ->Protein Kinase A?

Back 80

M2, Alpha2, D2. (remember MAD 2's.)

Front 81

Which receptors work via Gs->adenylyate cyclase ->cAMP->Protein Kinase A?

Back 81

Beta1, Beta2, D1, H2,V2.

Front 82

What does protein kinase A do?

Back 82

increase calcium release in heart and blocks myosin light chain kinase.

Front 83

What are the two classes of cholinomimetics?

Back 83

1. direct agonsts 2. indirect agonists (anticholinesterases).

Front 84

Bethanechol(mechanism,use,toxicity)

Back 84

Direct cholinomimetic. Postop or neurogenic ileus, urinary retention. COPD+asthma exacerbation, peptic ulcers.

Front 85

Carbachol(mechanism,use,toxicity)

Back 85

Direct Cholinomimetic. Identical to Ach. Glaucoma, pupillary contraction, relief of IOP. COPD+asthma exacerbation, peptic ulcers.

Front 86

Pilocarpine(mechanism,use,toxicity)

Back 86

Direct Cholinomimetic. Stimulates tears, salvia, sweat. Open and closed-angle glaucoma.COPD+asthma exacerbation, peptic ulcers.

Front 87

methacholine(mechanism,use,toxicity)

Back 87

Direct Cholinomimetic. challenge test of asthma diagnosis. COPD+asthma exacerbation, peptic ulcers.

Front 88

Neostigmine(mechanism,use,toxicity)

Back 88

Indirect cholinomimetic agonist. NO cns penetration. Postop and neurogenic ileus, myasthenia gravis, reversal of NMJ block. COPD+asthma exacerbation, peptic ulcers.

Front 89

pyridostigmine(mechanism,use,toxicity)

Back 89

indirect cholinomimetic agonist. Long acting myasthenia gravis treatment. COPD+asthma exacerbation, peptic ulcers.

Front 90

edrophonium(mechanism,use,toxicity)

Back 90

indirect cholinomimetic agonist. Short acting, for myasthenia gravis diagnosis. COPD+asthma exacerbation, peptic ulcers.

Front 91

Physostigmine(mechanism,use,toxicity)

Back 91

indirect cholinomimetic agonist. for anti-cholinergic overdose, crosses BBB. COPD+asthma exacerbation, peptic ulcers.

Front 92

Donepezil(mechanism,use,toxicity)

Back 92

indirect cholinomimetic agonist. Alzheimers disease. COPD+asthma exacerbation, peptic ulcers.

Front 93

signs of cholinesterase inhibitor poisoning. treatment.

Back 93

DUMBBELSS (diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle +CNS, lacrimation, sweating, salvia.) tx: atropine + pralidoxime.

Front 94

Parathion(mechanism, treatment)

Back 94

Irreversible cholinesterase inhibitor, ACH overdose. Tx: atropine + pralidoxime.

Front 95

Atropine, homatropine, tropicamide (mechanism, use, toxicity).

Back 95

Muscarinic antagonist. produces mydriasis and cycloplegia. (Atropine also used for bradycardia). Causes hot as a hare, dry as bone, red as beet, blind as bat, mad as a hatter.

Front 96

Benztropine(mechanism,use,toxicity)

Back 96

Muscarinic antagoist. Parkinsons disease (park my benz). Can be used in haloperiodal O.D, whihc causes torticolliosis. Causes hot as a hare, dry as bone, red as a beet, blind as a bat, mad as a hatter.

Front 97

Scopolamine(mechanism,use,toxicity)

Back 97

Muscarinic antagonist. Motion sickness. causes hot as a hare, dry as a cone, red as a beet, blind as a bat, mad as a hatter.

Front 98

Ipratropium,tiotropium (mechanism, use, toxicity)

Back 98

Muscarinic antagonist. COPD, Asthma. Causes hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter.

Front 99

Oxybutynin(mechanism,use,toxicity)

Back 99

Muscarinic anatagonist. reduces urgency in mild cystitis and reduce bladder spasms. causes hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter.

Front 100

Glycopyrrolate(mechanism,use,toxicity)

Back 100

Muscarinic anatagonist. IP: given in preop to reduce airway secretions. oral:reduce drooling, peptic ulcer. Can cause hot as a hare, dry as a bone red as a beet, blind as a bat, mad as a hatter.

Front 101

Jimson Weed(mechanism, toxicity)

Back 101

muscarinic antagonist, causes gardner's pupil (mydriasis).

Front 102

Epinephrine(Mechanism, receptors bound, use, toxicity)

Back 102

Direct Sympathomemetic. A1,A2,B1,B2. Anaphylaxis, open angle glaucoma, asthma, hypotension.

Front 103

Norepinephine(Mechanism, receptors bound, use, toxicity)

Back 103

direct sympathomemetic. A1,A2, some B1. used in hypotension but it decrease renal perfusion.

Front 104

Isoproterenol(Mechanism, receptors bound, use, toxicity)

Back 104

Direct sympathomemetic. B1, B2. Used in Torsade de pointe and bradyarryhmia. Can cause tachycardia and worsen cardiac ischemia.

Front 105

dopamine(Mechanism, receptors bound, use, toxicity)

Back 105

Direct sympathomimetics. Receptors depend on dose. low = D1, med = D1,B2,B1, high = A1,A2,B1,B2,D1. Used in shock and heart failure (ionotropic and chronotropic).

Front 106

dobutamine(Mechanism, receptors bound, use, toxicity)

Back 106

Direct sympathomimetic. Mostly B1, little a1,a2,b2. Used in heart failure and cardiac stresstest (ionotrpic and chronotropic)

Front 107

Phenylephrine(Mechanism, receptors bound, use, toxicity)

Back 107

Direct sympathomimetic. A1, A2. Used in hypotension, to cause mydriasis, and rhinitis (decongestant).

Front 108

Albuterol, salmetrol, terbutaline (Mechanism, receptors bound, use, toxicity)

Back 108

Direct sympathomimetic. Mostly B2, some b1. Sal = long term ashtma or copd. Albuterol for short term asthma. Terbutaline for to reduce premture uterine contractions.

Front 109

Ritodrine(Mechanism, receptors bound, use, toxicity)

Back 109

Direct sympathomimetic. B2 only. Used to reduce premature uterine contractions.

Front 110

Amphetamine (mechanism, use)

Back 110

indirect sympathomimetic. Releases stored catecholamines. Used for narcolepsy, obesity, ADD.

Front 111

Epinephrine(Mechanism, use, toxicity)

Back 111

indirect sympathomimetic. Releases stored catecholamines. Used for nasal decongestion, urinary incontience, hypotension.

Front 112

Cocaine (mechanims, use).

Back 112

direct sympathomimetic. Reuptake inhibitor. Causes vasoconstriction and local anesthesia.

Front 113

Why must B-Blockers be avoided in suspected cocaine intoxication?

Back 113

mixing them can lead to unopposed A1 activation and extreme hypertenion.

Front 114

How does norepinephrine cause reflex bradycardia?

Back 114

stimulates A1>B2. Causes increased vasoconstrciton -> increased BP. This causes reflex bradycardia and slowing of HR.

Front 115

How does isoproterenol cause reflex tachycardia?

Back 115

Stimulates B2>A1. This cause vasodilation and dropping of BP. B1 is stimulated and causes tachycardia.

Front 116

Clonidine, alpha-methyldopa(Mechanism, receptors bound, use)

Back 116

Centrally acting alpha-2 agonists, this causes LESS peripheral sympathetic release.Used in hypertension, especially renal disease due to no increase in renal blood flow!

Front 117

Phenoxybenzamine(Mechanism, receptors bound, use, toxicity)

Back 117

IRREVERSIBLE nonslective alpha blocker. Used in pheochromosytoma BEFORE surgery! toxic: orhtostatic hypotension, reflec tachycardia.

Front 118

phentolamine(Mechanism, receptors bound, use, toxicity)

Back 118

REVERSBILE nonselective alpha blocker. give to patients on MAOI who each tyramine contraining foods.

Front 119

Prazosin, Terazosin, Doxazosin,Tamsulosin(Mechanism, receptors bound, use, toxicity)

Back 119

Alpha-1 blocker. Used in hypertension, urinary rentention in BPH. tox:orthostatic hypotension, dizziness, headache.

Front 120

Mirtazapine (mechanism, use, toxicity)

Back 120

Alpha-2 blocker. Used in depression. tox: sedation, hypercholesterolemia, increased apetite.

Front 121

Describe what occurs when you alpha-blockade epi vs. phenylephrine.

Back 121

Before blockade: Both epi and phen RAISES BP. After alpha blockade: only epi raises, no change in phenyl. Why: Epi has B binding, phenyl does NOT.

Front 122

Give 6 applications of Beta-blockers in general.

Back 122

Angina - decreases HR and contractility, decreasing oxygen use. MI - decrease mortality. SVT - decrease AV duction. Hypertension - decrease CO and renin secretion. CHF - slows progression. Glaucoma - decrease secretion of aqueous humor.

Front 123

give general toxicites of b-blockers

Back 123

impotence, asthma exacerbation, bradycardia, seizures, sedation, hides hypoglycemia.

Front 124

What are the B1 selective b-blockers? When are they useful?

Back 124

A BEAM. acebutolol, betaxolol, Esmolol, Atenolol, Metoprolol. Useful in comorbid pum. disease.

Front 125

What are the nonselective ( b1 = b2) b-blockers?

Back 125

Please Try Not Being Picky. Propranolol, Timolol, Nadolol, Pindolol. B = B-blocker.

Front 126

what are the nonselective a and b-antagonists?

Back 126

Carvedilol, labetalol.

Front 127

What are the partial B-agonists?

Back 127

Pindolol, Acebutolol.

Front 128

Give treatment for acetaminophen overdose.

Back 128

N-Acetylcysteine (replenishes glutathione).

Front 129

Give treatment for salicylates overdose.

Back 129

NaHCO3 (alkalinize urine)

Front 130

give treatment for amphetamines overdose

Back 130

NH4Cl (acidify urine)

Front 131

Give treatment for antimuscarinic and anticholinergic overdose.

Back 131

Phygostigmine and control the hyperhermia.

Front 132

Give treatment for b-blocker overdose

Back 132

Glucagon

Front 133

Give treatment for digitalis overdose

Back 133

(KLAM) normalize K, Lidocaine, Anti-dig fab fragments, Mg2

Front 134

give treatment for iron overdose.

Back 134

deFEroxamine, deFErasirox.