Pharm Flashcards

Question

Which one of the following drugs enters the target cell and acts on a nuclear receptor? A. Diazepam B. Epinephrine C. Insulin D. Prednisone E. Heparin

Answer 1

D. Diazepam, epinephrine, and insulin act at ion channel receptors, G-protein-linked receptors, and tyrosine kinase-linked receptors, res- pectively. These three receptor types are cell surface receptors. Thyroid hormone and steroid hormones or drugs, such as prednisone, act on Sample Exam Answer Key ▼ 411 nuclear receptors, accounting for much of their action. Heparin’s action is to stimulate antithrombin III in the plasma. Its action is extracellular.

Answer 2

A. All of the choices are oral hypoglycemic agents. | Only acarbose inhibits α-glucosidase.

Answer 3

D. Spironolactone, a potassium-sparing diuretic useful in treating edema and heart failure, is a competitive antagonist at the aldosterone receptor.

Answer 4

B. Aldosterone and fludrocortisone are selective mineralocorticosteroids. Hydrocortisone has sig- nificant mineralocorticoid and glucocorticoid activity. Dexamethasone has very little mineralo- corticoid activity.

Answer 5

B. Glucocorticoids characteristically stimulate glu- coneogenesis and lipolysis. Insulin has the oppo- site effects. The other hormones have minor or negligible effects.

Answer 6

C. Renal tubular acidosis, aminoaciduria, and hyperphosphaturia are some of the manife- stations of proximal tubule damage in Fanconi syndrome.

Answer 7

D. Of the choices given, only vancomycin is effec- tive against many methicillin-resistant Staphy- lococci. Various penicillins, macrolides, and clindamycin are ineffective.

Answer 8

C. Because it lacks a cell wall, Mycoplasma pneumo- niae is not sensitive to cell wall inhibitors such as penicillin V. The macrolides, such as clar- ithromycin, are ribosomal protein synthesis inhibitors that are effective against Mycoplasma pneumoniae. Streptococcus viridans, Strep- tococcus pneumoniae, and Streptococcus pyo- genes are gram-positive cocci. Leptotrichia buccalis is a gram-negative oral bacillus.

Answer 9

A. The short elimination half-time for penicillin V is due to rapid excretion of penicillin in the urine. About 90% of this renal excretion is a result of active tubular transport, a rapid and efficient process. (Very little metabolism of penicillin occurs.)

Answer 10

E. Amoxicillin, clarithromycin, and clindamycin are effective against some anaerobes but their spec- trum is not limited to anaerobic bacteria. Aminoglycosides are effective only against aer- obes. Metronidazole’s action requires a reduced environment. Its antibacterial spectrum is limited to anaerobes. Metronidazole is also effective against many parasites.

Answer 11

C. Only weak acids and weak bases are greatly affected in their distribution by changes in pH. Weak organic acids dissociate more from protons at higher pH, making a higher percent- age of their molecules charged. This traps them in that compartment.

Answer 12

A. Drug agonists have an intrinsic activity of greater than 0 and less than or equal to 1. This refers to the maximal effect attainable by the drug. Potency and receptor affinity are not directly related to intrinsic activity. The therapeutic index (TI) requires a quantal dose–response curve, unlike the other characteristics listed which require graded concentration–response curves. Drugs with the same intrinsic activity may vary a great deal in their aqueous solubility.

Answer 13

A. Inhibition of adenylyl cyclase through Gi , result- ing from stimulation of α2-adrenergic receptor, leads to a reduction in intracellular cAMP.

Answer 14

C. Circulating muscarinic cholinergic receptor agonists stimulate these receptors on endothelial cells, leading to release of nitric oxide and vasodilation.

Answer 15

B. Carbidopa is used to inhibit dopa decarboxylase. Its usefulness is based on reducing conversion of L-dopa to dopamine outside the central nervous system. Carbidopa does not penetrate the blood–brain barrier and therefore does not inter- fere with the beneficial effect of L-dopa in the brain, but prevents the adverse effects of dopa- mine in the periphery.

Answer 16

A. Bupivacaine has the highest lipid solubility of the drugs listed. This is the major chemical charac- teristic of the local anesthetic that determines duration of action. Procaine is the only ester given as a choice and is rarely used.

Answer 17

B. Nitrous oxide oxidizes the cobalt in vitamin B12, resulting in the inhibition of methionine synthase. Nitrous oxide has greater analgesic potency than other inhaled anesthetics (e.g., halothane, isoflu- rane). Ketamine is not inhaled; rather, it is injected. It also does not inhibit methionine syn- thase. The same is true for propofol.

Answer 18

C. Alpha adrenergic receptor stimulation accounts | for the vasoconstrictor effect of levonordefrin.

Answer 19

E. The recently described mild analgesic effect of dextromethorphan has been linked to N-methyl- D-aspartate (NMDA) receptor antagonism in the CNS.

Answer 20

D. Naloxone is a competitive antagonist at opioid | receptors.

Answer 21

C. Cyclooxygenase (COX) is a key enzyme in the synthesis of prostaglandins. Prostaglandins, including PGE2 and PGF2α, are important media- tors for such functions as pain, and are a product of COX. Aspirin inhibits both COX-1 and COX-2.

Answer 22

C. The use of oral ketorolac (an NSAID) is limited to | continue therapy after a parenteral dose.

Answer 23

E. Basophils and mast cells release histamine. However, the cell that responds to histamine stimulation at the H2 receptor is the parietal cell of the stomach. Stimulation of this receptor leads to proton release and a decrease in the pH of the stomach lumen. H2 histamine receptor blockers are used to reduce stomach acid.

Answer 24

A. Renin release from the kidney is enhanced by stimulation of the β1-adrenergic receptors in the juxtaglomerular cells. From the above list, only β blockers reduce renin release. Although angiotensin converting enzyme inhibitors and angiotensin II receptor blockers act on the renin-angiotensin system, they do not inhibit renin release. In fact, they tend to increase plasma renin.

Answer 25

C. Alpha adrenoceptor blockers, like phenoxyben- zamine, inhibit the vasoconstrictor effect of epi- nephrine but not the vasodilator effect of epinephrine. Therefore, the administration of alpha blockers results in epinephrine reversal. Propranolol would only block the vasodilator effect of epinephrine. Guanethidine and tyra- mine act largely at prejunctional sites and don’t block adrenergic receptors.

Answer 26

B. Enoxaparin is a low-molecular-weight heparin. It | activates antithrombin III and inhibits factor Xa.

Answer 27

D. The effect of glucocorticosteroids remaining in the mouth after inhalation is to make the oral cavity more susceptible to fungal infection. The mouth should be rinsed with water after inhala- tion use. Inhaled methacholine, unlike the other drugs listed, is not used therapeutically but, rather, is used to diagnose hyperactive airway.

Answer 28

E. Di- and trivalent cations, such as those found in oral antacids, chelate tetracyclines and prevent their absorption.

Answer 29

D. A decrease in glycogen breakdown is a classic effect of insulin. Epinephrine (by acting as an agonist at α1- and β2-adrenergic receptors), albuterol (by acting as an agonist at β2 -adrenergic receptors), and glucagon (by acting at glucagon receptors) all tend to increase glycogen. Parathyroid hormone has little effect on glycogenolysis.

Answer 30

B. Nitroglycerin is a nitrovasodilator. It produces nitric oxide, which activates guanylyl cyclase which, in turn, catalyzes the production of cGMP.

Answer 31

C. Clavulanic acid has very little antimicrobial activity. Its value in combination with certain penicillins is due to its ability to inhibit certain penicillinases. This protects the penicillin from bacterial enzyme attack. Transpeptidase is inhibited by β-lactams, such as penicillin. DNA gyrase is inhibited by the fluoroquinolones such as ciprofloxacin.

Answer 32

E. Transpeptidase is the enzyme that catalyzes the peptide crosslinking of peptidoglycan. Trans- peptidase, is inhibited by penicillins and ceph- alosporins.

Answer 33

E. Trimethoprim, by virtue of its inhibition of bacte- rial dihydrofolate reductase, acts synergistically with the sulfonamides.

Answer 34

D. Clindamycin is useful for some oral infections, including those involving Streptococcus viridans. Klebsiella pneumoniae and Pseudomonas aerug- inosa are gram-negative rods and not subject to clinical inhibition by clindamycin. Methicillin- resistant Staphylococci are insensitive to clinda- mycin and most traditional antistaphylococcal drugs. Candida albicans is a yeastlike fungus and is not inhibited by antibacterial drugs such as clindamycin.

Answer 35

E. The mammalian enzyme form of dihydrofolate reductase is the target for methotrexate. Bleo- mycin produces strand breaks in DNA. Cisplatin is an alkylating agent. Doxorubicin intercalates with DNA. 5-Fluorouracil, after undergoing activation, inhibits thymidylate synthase.

Answer 36

local anesthetics

Answer 37

procaine, tetracaine, cocaine

Answer 38

esters in plasma by esterases; amides (tertiary!) in liver

Answer 39

methemoglobinemia

Answer 40

prilocaine

Answer 41

myocardial depression, cardiovascular collapse, hypotensive shock

Answer 42

prevent generation of impulses; block Na transport

Answer 43

free base, non-ionized

Answer 44

inflammation --> lower pH --> less non-ionized form available to penetrate

Answer 45

one carpule is 1.8 mL 2% means 20 mg/mL so 20 x 1.6 = 36 mg in one 1.8 mL carpule

Answer 46

(a) Proccaine is the only ester listed -- all the rest are amides

Answer 47

(a) is the only | statement that is true

Answer 48

(ii) another ester vs. amide type identification question. Lidoccaine is an amide, thus other amides will be cross- allergenic - mepivacaine, prilocaine and dibucaine are the other amides listed. Procaine and tetracaine are esters and will not be cross-allergenic.

Answer 49

(c) procaine is an ester; esters are metabolized predominately by pseudocholinesterases in the plasma.

Answer 50

(c) esters are metabolized by plasma esterases - tetracaine is the only ester listed, all the rest are amides

Answer 51

(d) remember #9 above? see the word "mainly"? same question, but worded a little differently to throw you off. Again, procaine is an ester; esters are metabolized predominately by pseudocholinesterases in the plasma, but also to some extent by esters in the liver.

Answer 52

(c) the word "EXCEPT" should alert you that this is basically a true-false type question with 4 true statements and 1 false statement; you just have to figure out which one! In this case, you just have to remember that plasma cholinesterase levels are only important for the duration of action of ester-type LAs, not amides, which are metabolized in the liver. All the other statements are variables which affect duration of the block, but apply to both esters and amides.

Answer 53

(c) again, just another question that requires you to be able to pick out an ester or an amide from a list. Since procaine is an ester, only another ester LA would be cross-allergenic. In this list the only ester listed is tetracaine.

Answer 54

(d) According to textbooks, local anesthetics fall into the following classes in terms of duration of action: short: procaine; moderate: prilocaine, mepivacaine, lidocaine; long: bupivacaine, tetracaine, etidocaine. Statements (a), 3, and 4 would be true if the question was comparing mepivacaine to bupivacaine, which are structurally similar; but the comparison is to lidocaine. The only difference that applies is duration of action ((d)), bupivacaine is longer. (b) is wrong, both are amides.

Answer 55

(b) don't forget: esters in plasma; amides in liver

Answer 56

(b) this is an interaction I tested you on several times – now you know why! Propranolol interacts with lidocaine in two ways. By slowing down the heart via beta receptor blockade, blood delivery (and lidocaine) to the liver is reduced, thus lidocaine remains in the systemic circulation longer, and can potentially accumulate to toxic levels. Propranolol and lidocaine also compete for the same enzyme in the liver, thus metabolism of lidocaine can be reduced.

Answer 57

non-selective beta-blocker | slows down heart

Answer 58

(b) Answer is (b)- You should be able to recognize that all of these drugs are local anesthetics. Local anesthetics are of one of two types, either esters or amides. Ester types are subject to hydrolysis in the plasma and thus have short half lives. Amides are metabolized primarily in the liver and have longer half lives. Thus the biotransformation (e.g., metabolism; again, the rats are using a different word to confuse you, even though they are asking the same basic question) of an amide type local anesthetic would be the most altered in the presence of sever liver disease. The key word here is "least". Of the drugs listed, only procaine is an ester. The rest are amides.

Answer 59

(d) same as above but asked backwards. Methemoglobinemia may result from a toluidine metabolite of prilocaine, orthotoluidine.

Answer 60

prilocaine; metHbemia

Answer 61

(e) Most toxic reactions of a serious nature are related to excessive blood levels arising from inadvertent intravascular injection. Hypersensitivity reactions (options b & c) are rare, but excessive blood levels will induce toxic reactions like CNS stimulation in most everyone. This is a case where option (e) is the "best" answer, because it is more likely than the other alternatives, which might be true, but are not as likely (e.g, “most probable”) to happen.

Answer 62

(d) Initially LAs inhibit central inhibitory neurons, which results in CNS stimulation, which can proceed to convulsions. At higher doses, they inhibit both inhibitory and excitatory neurons, leading to a generalized state of CNS depression which can result in respiratory depression and death.

Answer 63

(c) same question as above just worded differently. The intra- arterial injection would result in the high plasma levels mentioned in the previous question.

Answer 64

(c) it is a sympathomimetic after all. All the other reactions are related to elevated lidocaine levels

Answer 65

(a) Grave’s disease is an autoimmune disease that causes hyperthyroidism – the resulting high levels of circulating thyroid hormone result in a hypermetabolic state with heightened sympathetic activity, which combined with injected epinephrine could result in a hypertensive crisis.

Answer 66

(d) Cardiovascular collapse is due to a direct action of the local anesthetic on the heart muscle itself (LA's in toxic doses depress membrane excitability and conduction velocity), thus (d) is the correct answer. All of the other alternatives are indirect ways to affect the heart.

Answer 67

(e) Of the options listed, this is the one that will kill the patient, which I guess makes it the most serious.

Answer 68

(a) All the listed local anesthetics except cocaine are vasodilators, especially ester-ctype drugs such as proccaine and the amide lidocaine. Cocaine is the only local anesthetic that predictably produces vasoconstriction. Cocaine is also the only local anesthetic to block the reuptake of NE into adrenergic neurons, and thus potentiate the NE that has been released from nerve endings

Answer 69

(a) see explanation above *NE potentiation)

Answer 70

(e) didn’t I make you memorize this? You should at keast remember Na+ ions are involved, which limits your choices to (c) and (e). (c) would increase or facilitate nervous impulse conduction, which is the opposite of what you want the local anesthetic to do, so pick (e).

Answer 71

(c) Answer is (c)- straight memorization- nerve impulses are generated by the influx of sodium resulting in depolarization. repolarization and inactivity occurs when potassium moves out. (sodium-potassium pump). LAs act by blocking Na+ movement.

Answer 72

(a) while some of the other alternatives sound plausible, think about the factoids you were taught about local anesthetics and variables that affect their action. An important one was the role of pH and ionization factors. Remember, the free base or nonionized form is the form that passes through membranes, yet once inside the neuron only the ionized form is effective. Inflamed tissue has a lower pH than normal tissue and will shift the equilibrium of the LA solution such that most of it remains ionized and thus unavailable to penetrate

Answer 73

(c) only options (b) and (c) are relevant here - the others have nothing to do with LA penetration into membranes. Membrane permeability is affected by whether or not the molecule is “charged” or ionized or not (e.g., unionized). Only the latter form passes readily through membranes. See, they’re asking the same thing they asked in the previous question, just coming at it from another angle. Remember the fact and you can cover the angles.

Answer 74

(c) the ratio of ionized to unionized forms is given by the formula log A/AH= pH-pKa. In this instance the difference between pH and pKa is 0. Thus lidocaine will exist as an equal mixture ( so (c) is correct). Most local anesthetics are weak bases with pKa ranging from 7.5 to 9.5. LA’s intended for injection are usually prepared in salt form by addition of HCl. They penetrate as the unionized form into the neuron where they re-equilibrate to both charged and uncharged forms inside the neuron - the positively charged ion blocks nerve conduction.

Answer 75

(b) - the theory goes that there is a size dependent critical length of anesthetic exposure necessary to block a given nerve. Small fibers will be blocked first because the anesthetic concentration to h critical length in a small fiber will be reached faster than the critical length in a larger fiber. You have to block three nodes of ranvier, and they are farther apart in larger fibers than they are in small diameter fibers.

Answer 76

(ii) if you knew the fact above about small nerves, then this question basically becomes a true false type thing, and (c) is the false statement. (a) and (d) make logical sense so you are stuck picking between (b) and (c). You have your pick of memorizing the small nerve thing or the myelinated nerve nodes of ranvier thing.

Answer 77

(d) 2% solution = 20 mg/ml X 1.8 ml = 36 mg lidocaine.

Answer 78

(d) 2% lidocaine = 20 mg/ml x 3 = 60 mg lidocaine | 1: 100,000 epi = 0.01 mg/ml x 3 = 0.03 mg epi

Answer 79

(c) 2% mepivacaine = 20 mg/ml, so 300 mg / 20 mg/ml = 15 ml

Answer 80

(d) 0.05% = 0.5 mg/ml . To give 30 mg, you have to give 30mg/0.5 mg/ml or 60 ml. 1 cartridge = 1.8 ml, thus 60ml /1.8ml = 33.3 cartridges. - first express the percentage of solution as a fraction of 100, then add the units gm/ml. 0.05% equals 0.5 or 1/2 gms per 100 ml. The cartridge is 1.8 ml which you can round off to almost 2 mls total. In this 2 ml you would have 1 gm of the local anesthetic. You need to give 30 gms, which would require 30 cartridges. The alternative that meets this answer is (d).

Answer 81

(d) the AHA limit is 0.04 mg, compared to 0.2 mg in the healthy patient. 1:200,000 equals 0.005 mg/ml or 0.009 per 1.8 ml carpule. 4 carpules would thus contain 0.036 mg, which is just below the 0.04 mg limit

Answer 82

1.8 mL /200,000 = 0.9 ug of epi in one carpule - 0.009 mg

Answer 83

G more susceptible to acid degradation, injected more often than peroral

Answer 84

ampicillin

Answer 85

ampicillin, cephalosporins

Answer 86

dicloxacillin

Answer 87

carbenicllin (extended spectrum)

Answer 88

NOT for joints anymore! unless complications, then refer to their surgeon - yes for infective endocarditis; prosthetic valves, hx of infective endocarditis, cardiac transplant; congenital heart defects

Answer 89

2g of amoxicillin (4 of 500mg) 1 hr before procedure | for kids: 50mg/hr before procedure

Answer 90

clindamycin 600 mg 1 hour PO (4 x 150mg) | kids 20 mg/kg

Answer 91

same dosages but 1/2 hr before procedure

Answer 92

restorative, intracanal endo, impressions

Answer 93

250-500mg, q6h for 7 days | kids 20-50 mg/kg, qid

Answer 94

150-300 mg, q8h for 7 days | kids 8-12 mg/kg tid or qid

Answer 95

500mg q8h for 7 days | kids 20-40

Answer 96

inhibit cell wall synthesis | bactericidal!

Answer 97

inhibit protein synthesis on ribosomes; static

Answer 98

bind to ergosterol, weaken cell wall (like Nystatin)

Answer 99

antifungal

Answer 100

compete with PABA in folic acid synthesis

Answer 101

sulfonamides

Answer 102

dermatitis, stomatitis, bronchoconstriction and cardiovascular collapse

Answer 103

GI upset and pseudomonas infection

Answer 104

clindamycin

Answer 105

broad spectrum, like tetracyclines

Answer 106

narrow, unlikely

Answer 107

chloramphenicol

Answer 108

aplastic anemia

Answer 109

erythromycin

Answer 110

cholestatic hepatitis

Answer 111

cancel each other: cidal vs static

Answer 112

pribenecid

Answer 113

antacids, dairy

Answer 114

can reduce effectiveness

Answer 115

ampicillin decrease the effectiveness of oral contraceptives due to suppression of normal Gl flora involved in the recycling of active steroids from bile conjugates, leading to more rapid excretion of the steroids from the body

Answer 116

seldane, digoxin

Answer 117

fluconazole, ketoconazole

Answer 118

systemic antifungals

Answer 119

c; Penicillin G is destroyed by acid in the stomach resulting in variable and irregular absorption. Penicillin V is acid stable and available for oral use. Penicillin G procaine is typically given intramuscularly in repository form, yielding a tissue depot from which the drug is absorbed over hours. In this form, it cannot be given IV or subcutaneously.

Answer 120

(c) again, just asking you to know something about the various forms of penicillin. Since in most cases you are going to use Pen VK orally, this question is an old one showing its age and probably not likely to appear anymore on board excams

Answer 121

(b) all of the other methods involve unacceptable risk. Once sensitized, even a small amount can cause an allergic response. Remember, it is not a dose-related response that won’t be problematic if you only inject a little bit.

Answer 122

CLINDAMYCIN IS BEST BUT b reason (b) is the right answer is that the spectrum of activity of erthromycin is very similar to penicillin. The others offer a much broader spectrum of coverage than we usually require; always use the drug with the narrowest spectrum possible that includes the microbe in question. Standards have now changed such that clindamycin is the drug of choice in this situation. But if they don’t include clindamycin, look for erythromycin, or for that matter Azithromycin

Answer 123

e that’s really the only use for dicloxacillin

Answer 124

(b) of those listed only (b) is penicillinase resistant. Ampicillin is an extended spectrum penicillin, and is not penicillinase resistant. Erythromycin shouldn’t be affected by penicillinases, since it isn’t a peniciilin, but it doesn’t work against staph for other reasons.

Answer 125

tetracycline

Answer 126

(e) tetracycline is bacteriostatic and would slow the rapid growth of the microbial population that a bactericidal drug such as penicillin needs to be effective, sine only when rapidly dividing are the cells making cell walls

Answer 127

(c) (a) streptomycin can damage the eighth nerve, affecting both balance and hearing, but is not associated with liver damage. (b) other than allergic reactions, penicillins are extremely safe, with no effect on the liver. (d) the cephalosporins are chemically related to the penicillins and share their relatively nontoxic nature. (e) amphotericin B, is an antifungal agent that produces such adverse side effects as nephrotoxicity and hypokalemia, but not liver toxicity. Thus (c) is the correct answer. Tetracyclines have been shown to be hepatotoxic following high doses in pregnant patients with a history of renal disease.

Answer 128

balance and hearing

Answer 129

renal + hypoKemia

Answer 130

c bc narrow

Answer 131

(c) The only 2 possibilities that produce GI upset are (c) and (e). As for producing colitis, (b) and (c) are associated with this adverse side effect. (c) is the only drug which does both, therefore it's the right answer.

Answer 132

Suprainfection b. Photosensitivity d. Discoloration of newly forming teeth e. Gastrointestinal symptoms (when administered orally)

Answer 133

(d) broad spectrum vs. narrow spectrum. Tetracyclines certainly have more side effects than penicillin, and are certainly one of the antibiotics to avoid during pregnancy.

Answer 134

(d) Answer is (d)- remember, tetracyclines are broad spectrum antibiotics effective against both gram-negative and gram- positive cocci and bacilli. Clindamycin has a spectrum of activity similar to erthyromycin and vancomycin, which is less than that of the tetracylines, mainly affecting gram-positive microorganisms. Ist generation cephalosporins are effective against both gram-negative and gram-positive organisms, but the third generation ones have increased activity against gram- negative but greatly decreased activity against gram-positive microorganisms.

Answer 135

Answer is (e)- Again, the important phrase in the question is not (Hey, just Wayne and Garth). Obviously the fact that you will remember about tetracylines is that they can discolor teeth in the fetus when taken by the mother during pregnancy. But don't circle that answer because (a) is also characteristic of tetracyclines (they are the most likely of all the antibiotics to cause superinfection), and is an annoying side effect in adults resulting from alteration of the oral, gastric and intestinal flora. The real answer is (e). Tetracyclines are not the drug of choice for prophylaxis against infective endocarditis. This is due to streptococcal infection. 15-20% of group A streptococci are resistant to tetracyclines, but none are resistant to penicillin or erythromycin. Recently a non-streptococcal induced subacute bacterial endocarditis has been identified, especially in juvenile periodontitis patients. The causative bacterium is not susceptible to penicillin or erythromycin. It may be necessary to treat predisposed patients with tetracycline for a few weeks, and then follow this with a course of penicillin or erythromycin. Remember that these drugs are antagonistic to each other and thus can't be used concurrently. Penicillin is a bactericidal drug which kills or destroys microorganisms by interfering with the synthesis or function of the cell wall, cell membrane or both. Thus it is most effective against bacteria that are multiplying. Tetracycline is a bacteriostatic antibiotic that acts by inhibiting the growth and multiplication of organisms by inhibiting protein synthesis by binding reversibly to the 30 S subunit of the bacterial ribosome. When the two types are given together, their effectiveness is negated or reduced.

Answer 136

Answer is (d)- penicillin is metabolized in the liver, but it rapidly disappears from the blood due to rapid clearance by the kidneys. 90% is excreted by tubular secretion. Thus patients with renal disease will show high blood levels of penicillin. Similarly, probenicid, a uricosuric agent (a drug which tends to enhance the excretion of uric acid by reducing renal tubular transport mechanisms), reduces the renal clearance of penicillins. And you wondered why we had those lectures on pharmacokinetics!

Answer 137

(b) remember the famous erythromycin –Seldane potentially lethal interaction, whereby erythromycin blocks the metabolism of Seldane to its antihistamine metabolite – it stays unmetabolized and causes cardiac arrthymias. Of course this question could have many other options listed, since erythromycin decreases the metabolism of so many other useful drugs, such as digoxin.

Answer 138

Cardioselective beta-blocker, HTN metoprolol too reduces cardiac output

Answer 139

non-selective beta-blocker, htn, angina, also paroxysmal tachy reduces cardiac output and renin release

Answer 140

Ace inhibitor, HTN also congestive heart failure

Answer 141

Loop diuretic, HTN

Answer 142

selective Alpha-1 - blocker, HTN inhibits NE release

Answer 143

Neuro inhibitor, severe HTN

Answer 144

Metaprolol, atenolol

Answer 145

Nitroglycerin, propranolol, Ca-channel blockers (verapamil)

Answer 146

Ca-channel blocker, angina | also supraventricular tachyarrhythmia, paroxysmal tachycardia, afib

Answer 147

ventricular arrhythmias

Answer 148

reverse digitalis induced arrhythmias

Answer 149

supraventricular tachyarrhythm, afib

Answer 150

afib, paroxysmal tachy | it's a glycoside

Answer 151

quinidine, verapamil

Answer 152

quinidine, verapamil, digoxin

Answer 153

verapamil, digoxin, propranolol

Answer 154

glycosides (digoxin, digitalis) and ACE inhibitors (captopril)

Answer 155

digitalis, digoxin -- congestive heart failure; | afib, paroxysmal tachy

Answer 156

quinidine: prolongs refractory period

Answer 157

lidocaine: decreases excitability

Answer 158

for afib: decreses rate of AV conduction for congestive heart failure: increase force of contraction (+ inotropic) --> inhibit Na/K ATPase --> increased Ca influx. reduce compensatory changes in CHF (heart size, rate, edema)

Answer 159

insufficient oxygen for myocardium

Answer 160

direct vasodilatory action on smooth muscla in coronary arteries --> increases oxygen supply

Answer 161

reduces oxygen demand -- reduces chronotropic response to epi and stress

Answer 162

decrease oxygen demand --> reduce afterload --> reduce peripheral resistance via vasodilation

Answer 163

blocks conversion of angiotensin 1 to 2 (latter is potent constrictor)

Answer 164

alpha 2 agonist, centrally reduces sympathetic outflow

Answer 165

alpha 2 agonist, centrally reduces sympathetic outflow

Answer 166

decrease the renal absorption of sodium, thus resulting in fluid loss and a reduction in blood volume. This decreases the work the heart has to pump. Also have weak dilatory action.

Answer 167

thiazides - chlorothiazide loop - furosemide K sparing - spironolactone

Answer 168

K sparing diuretic

Answer 169

(d) by elimination. Hypertension ((a)) is treated primarily with beta blockers such as propranolol. Angina is primarily treated with nitroglycerin, while digoxin (digitalis) is the drug of choice for congestive heart failure. Quinidine is classed as an antiarrthymic drug (Type I-blocks sodium channels). It reduces automaticity and responsiveness and increases refractoriness. It also has an antimuscarinic action preventing the bradycardia that follows vagal stimulation.

Answer 170

(b) arrhythmias are defined as any abnormality of the normal sinus rhythm of the heart due to disease or injury induced damage to the impulse conducting systems. They also result from the development of ectopic pacemakers or abnormal pacemaker rhythms. Drugs such as lidocaine are used to normalize these rhythms. Lidocaine, a local anesthetic, depresses cardiac excitability, answer (b). The refractory period of cardiac muscle is increased, thus slowing the heart down. All of the other alternatives given would exacerbate the arrhythmia.

Answer 171

(f) first off, how can you have an option (f)?! (a) is how diuretics lower BP, (b) is why they can cause hypokalemia, which is conveniently option (e), and hypokalemia can potentiate digitalis induced arrythmias option(c). Theyy apparently can also cause hyperglycemia, which would relate to option (d). How the heck are you supposed to remember all of this?

Answer 172

hyperglycemia

Answer 173

thiazide increases K excretio --> can exacerbte digitalis toxicity

Answer 174

(b) people with high BP are always told to reduce salt intake, since high sodium levels cause fluid retention which can increase BP, so ipso facto, reducing renal reabsorption of sodium makes BP go down

Answer 175

Answer is (d)- Remember, cardiac glycosides such as digoxin are used in the treatment of congestive heart failure, which is the failure of the heart to function adequately as a pump and thus maintain an adequate circulation. Cardiac glycosides are thought to act by altering calcium ion movement, with a desired effect of increasing the force of contraction of the myocardium (e.g. the inotropic effect). While several of the alternatives involve calcium, the way digoxin does it is via (d), inhibition of Na+, K+ ATPase, resulting in an increase of calcium ion influx into the cardiac cells, and a subsequent enhancement of the contractile mechanism. (a) is the way epinephrine works.

Answer 176

(a) All of these drugs are used to treat hypertension, but act by different mechanisms. (a), methyldopa, is the drug with central action- it alters CNS control of blood pressure by acting on cardioregulatory and vasomotor systems of the brain by stimulating alpha2 receptors in the brain stem. Clonidine is the usual drug that is involved in this particular question. (b) metropolol is a selectively blocks beta-1 receptors in the heart to reduce cardiac output. (c) hydralazine has a direct action on vascular smooth muscle to reduce hypertension via vasodilation. (d) propranolol blocks beta receptors in the heart, while (e) guanethidine prevents the release and causes depletion of catecholamines taken up into storage vesicles and is released like a false transmitter. It does not cross the blood- brain barrier.

Answer 177

(v) Answer is (v)- You should immediately recognize that propranolol is the prototypic beta-adrenergic receptor blocker, thus any answer with alternative a (i and ii) is wrong. Similarly, d is wrong as well-propranolol is a competitive beta- receptor blocker- it has no effect on NE release. Another drug used for hypertension, Clonidine, acts via this mechanism by stimulating alpha-2 autoreceptors. Thus ii, iii, and iv are wrong. This leaves (v) as the only possible right answer. Indeed, aside from blocking beta-1 receptors, blocking of renin release is thought to be the other mechanism whereby beta-blockers alter hypertension.

Answer 178

(d) Chlorthiazide is a diuretic which causes potassium loss or hypokalemia. This results in greater penetration of digitalis into the myocardium, and thus potential toxicity.

Answer 179

acetaminphen - no anti-inflammatory activity no GI upset is hepatotoxic

Answer 180

hypothalamus

Answer 181

(a) The first fact you must remember is that aspirin prevents platelet aggregation- this limits your choices to (a) and (b). They hope to confuse you by using prostacylin, but of course you know that this is wrong immediately, the right word is prostaglandin, as in (c), but you have already eliminated that choice because it doesn't mention prevention of platelet aggregation. Thus, even if you didn't remember that thromboxane A2 induces platelet aggregation, and aspirin blocks this action, you could get the answer by elimination. (d) is how heparin works, while (e) is how coumarin works.

Answer 182

(c) triamcinolone is a corticosteroid. Corticosteroids inhibit phospholipase A2, the enzymatic step that precedes prostaglandin synthetase. Diflunisal is a salicylate analgesic, like aspirin.

Answer 183

(a) you might be tempted to answer acetaminophen, because it doesn’t cause GI upset, but remember it is also not anti- inflammatory. The answer is ibuprofen.

Answer 184

(a) This is a straight drug identification question. Answers 2-5 are all non-steroidal antiinflammatory drugs which cause gastric irritation and bleeding due to their effects on prostaglandin synthesis in the mucosal wall of the gut. # , phenytoin, is an anti-convulsant-its major side effect that often appears as a question on boards is the production of gingival hyperplasia.

Answer 185

(e) note the difference in this question and #11 and 12. Ibuprofen was previously the answer to “shows reduced GI irritation”, but it does cause some, which you have to remember to answer #12 and this question. So aspirin and ibuprofen are out. Indomethacin is a very strong NSAID that causes lots of GI irritation, so much that use is limited in humans, so it is out. What about alocohol vs. acetaminophen. Well, you should really know that acetaminophen is usually the answer to these types of analgesics questions, but if you didn’t know that, perhaps may know that alcohol also causes GI irritation, so it is out.

Answer 186

(c) it only lowers your temperature if you have a fever,, taking aspirin does not have any effect on body temperature in the non-feverish patient, but high doses can cause all the other effects listed.

Answer 187

d Answer is (d)- (a) & (b) are the major side effects of aspirin (resulting from the inhibition of prostaglandin synthesis) for the majority of people, and one reason for the popularity of aspirin alternatives such as acetaminophen and ibuprofen, which produce these effects to a lesser extent. # 3 & 5 may also be seen following larger doses of aspirin. (d) is not seen with aspirin, but is a major therapeutic use of narcotic opiates such as codeine. I guess they are hoping that you will get the effects of codeine and aspirin mixed up, since the two are often compared and contrasted as moderate pain relievers.

Answer 188

(b) because it ain’t a salicylate, but the other statements are true

Answer 189

(c) Remember, acetaminophen (tylenol) is an aspirin alternative. Alternatives 1, 4, 5 are side effects of aspirin-type drugs. The popularity of acetaminophen as an aspirin alternative is because the incident of such effects with this drug is very low. However, because acetaminophen can undergo biotransformation to a toxic intermediate, hepatic and renal necrosis have been reported, especially after very high doses. (c), hepatic necrosis is the most prominent, especially when combined with alcohol consumption, since the alcohol induces the liver enzymes which make the hepatotoxic metabolites of acetaminophen

Answer 190

Answer is (c)- (a), 2, 4, and 5 are NSAIDS that reduce inflammation by reducing prostaglandin synthesis by blocking the activity of cyclooxygenase. Prednisone is a corticosteroid. Corticosteroids are potent nonspecific inhibitors of the inflammatory process, acting at a variety of point throughout the inflammatory process. Although they do reduce prostaglandin production as well, they do this by a mechanism other then blocking cyclooxygenase, probably by inhibiting the release of the fatty acid substrate for prostaglandin synthesis.

Answer 191

(c) acetaminophen is the best choice. Aspirin is contraindicated due to the potential for causing Reye’s syndrome. Ibuprofen is approved, but usually not the #1 choice. The others would be inappropriate as well.

Answer 192

(c) Diflunisal can be taken twice a day, the others three-four times a day is required.

Answer 193

(b) Again, the key word is least. Narcotics, in the form of paregoric (tincture of opium), and Lomotil (loperamide) are over the counter oral preparations for the treatment of diarrhea. Opiates act on receptors in the gut to produce constipation. Thus (b) is obviously wrong. All of the other answers are side effects of opiate administration.

Answer 194

(b) the only drugs that do this are opioids, and codeine and merperidine are the two opioids on the list. Of the two, codeine is much better at this than meperidine.

Answer 195

(a) They might reword the question in a way that asks you to | remember that the specific receptors are the mu receptors.

Answer 196

e opioids decrease the response of respiratory centers in the brainstem to the carbon dioxide tension of the blood, and also depresses pontine and medullary centers regulating respiratory frequency. Opioids do not cause oxygen apnea, ((a)), they can be convulsive, but not terminally so ((c)), they are stabilizing on the heart and some are actually used in open-heart surgery ((b)), and they do not cause circulatory collapse ((d)).

Answer 197

(e) This is an example of the type of question where the drug class is given. You are asked to not only identify a drug from the list as being from this class, but additionally that it has the properties that are given in the question that distinguish it from the other drugs of the class that are listed as alternatives. In this example, there is only one drug which meets this criterion. All are drugs which act via opiate receptors, but 3 are agonists ((a), (b), (d)), 1 is an antagonist only ((c)). (e) pentazocine is the only drug which has both types of action, and is the one drug left by the process of elimination.

Answer 198

(e) lot of memorization required here for a drug that isn’t used that much. I guess it was big news when these questions were written many years ago and they seemed hopeful, since statement (c) was true and was therapeutically an advantage, but it soon became apparent that (d) was also true

Answer 199

(a) nalorphine and pentazocine are mixed agonist-antagonists, levallorphan is an opioid agonist, as is propoxyphene

Answer 200

(d) This is an example of the kind of question that requires that you have memorized a fact about a particular drug, in this case the fact is (d). Methadone you will remember is not an antagonist like naloxone- it is a full agonist with analgesic properties, just like morphine. When taken orally it is not euphoric in addicts, but acts just like morphine to produce tolerance and physical dependence. Withdrawal is less severe than with morphine because methadone has a much longer half life. Facts 1, 2, and 3 would be met by an antagonist such as naloxone, or perhaps even a mixed agonist-antagonist such as pentazocine.

Answer 201

ganglionic ACh nicotine | end-organ ACh muscarinic

Answer 202

ganglionic ACh nicotine | end-organ usually adrenergic: except sweat glands ACh muscarinic

Answer 203

muscular ACh nicotine

Answer 204

(d) - (a) is wrong- botulinum toxin does this. (b) is wrong- hemicholinium works this way. (c) is wrong- ACh is broken down almost instantaneously, so it is almost impossible to enhance its destruction. (e) is wrong-these drugs don’t have any actions of their own, they just prevent ACh effects by blocking receptors: atropine and propantheline are postganglionic muscarinic receptor blockers-thus the answer is (d).

Answer 205

(b) – neostigmine is a cholinesterase inhibitor like physostigmine. These differ from the insecticides and nerve gases listed below in that they are reversible and can be used clinically; the latter are irreversible.

Answer 206

(3) drugs which potentiate cholinergic stimulation can do so by being either direct acting cholinergic agonists, acting on the cholinergic receptor, or by indirectly increasing the duration of action Ach by preventing its enzymatic degradation. Methacholine and pilocarpine are direct-acting cholinergic agonists, whereas neostigmine acts indirectly. Scopolamine is a muscarinic antagonist like atropine, and will reduce or block cholinergic action via direct receptor antagonism. Pralidoxime is a chemical antidote used to regenerate AchE after nerve gas or insecticide exposure.

Answer 207

(b) the action will be prolonged because neostigmine prevents its breakdown by AchE! Its action would be blocked by atropine or scopolamine

Answer 208

(e)a strange and amazing truth! Denerevated means the skeletal muscle is not receiving neural input, and thus stimulating a cholinergic neuron to release Ach which would then stimulate the NMJ can’t happen. But if you inject a drug which can stimulate the nicotinic receptors directly then you can see an effect on the muscle. Neostigmine is one of those anticholinesterases that can act like Ach at nicotinic receptors, in addition to prolonging the action of Ach itself by blocking the acetylcholinesterase that is trying to break the Ach down.

Answer 209

(e) What is needed is a skeletal muscle relaxant. This requires a drug that acts at the neuromuscular junction. Of those listed, only succinylcholine (e) is in this category. (a) atropine is a cholinergic (Muscarinic) receptor blocker, (b) epinephrine is an adrenergic agonist, and (c) diazepam is a benzodiazepine, and (d) is an anticholinesterase.

Answer 210

(c) salivation is typically considered to be a cholinergic response. Xerostomia is too little saliva and thus one could use a cholinergic agonist to stimulate more saliva secretion (assuming there is functional salivary gland tissue, which may not be the case in patients that have been subject to radiation therapy!) From the list, only neostigmine would produce a cholinergic effect, since it is an indirect acting cholinergic agonist. Of the others, atropine and scopolamine are cholinergic antagonists, and are actually used to reduce salivation, mecamylamine is a ganglionic blocker (not the action we desire, too non-specific, and a blocker at that!). Ephedrine is a mixed acting adrenergic agonist.

Answer 211

(3) you are probably thinking, who the hell ever heard of meprobamate and methantheline, or for that matter, chlorpromazine! Well, these are drugs that may have been useful in the olden days, but would be probably replace in this type of questions by more modern equivalents. But of course you should figure out that atropine (b), being the prototype anticholinergic drug has to be one of the answers. So option 5 has to bee incorrect, since it does not include atropine. Now only the most corrupt dentist would prescribe codeine to reduce salivation, so #4 should also be incorrect – that leaves 1, 2, or 3. So see, you didn’t even have to recognize that chlorpromazine is an antipsychotic drug. So what is meprobamate – if we can eliminate that one then we are down to only option 3 as a possible answer. Meprobamate happens to be an antianxiety, skeletal muscle relaxant drug sometimes used by dentists to treat muscle spasms associated with TMD – also has use for external sphincter spasticity – imagine! But it doesn’t seem to have anticholinergic activity that is significant enough to cause significant reduction of saliva. Methantheline, in contrast, is Banthine, a synthetic version of atropine! So option 3, atropine and methantheline are the drugs for this purpose.

Answer 212

(d) a ganglionic blocker, since it acts by preventing cACh from stimulating nicotinic receptors at the ganglia level will have both anticholinergic and antiadrenergic effects. Options a, b, c, and e are symptoms of cholinergic stimulation, and thus can’t be right. Option (d), the remaining answer, is an antiadrenergic effect, arising from decreases in sympathetic tone to the vasculature

Answer 213

(b) - Atropine and scopolamine are muscarinic cholinergic receptor blockers. Just knowing that eliminates all the alternatives except (b). But you should also remember that heart rate is kept under tight reflexive control: any sudden increase in HR usually stimulates baroreceptors to send a signal to the vagus nerve to stimulate the heart to slow it back down. This reflex is cholinergically mediated, and will be blocked by cholinergic blockers such as atropine. Even when given in the absence of higher than normal heart rate, atropine will block the normal cholinergic control over the heart, leaving the sympathetic system in charge with a resulting tachycardia.

Answer 214

(a) - The first thing you have to know is that a cholinomimetic drug is one that mimics the action of acetylcholine, the endogenous neurotransmitter in the parasympathetic or cholinergic nervous system. The acronym for remembering the effects of cholinergic stimulation is SLUD, or increased salivation, lacrimation, defecation, and urination. The heart is the exception in that activity or heart rate is decreased (bradycardia)- thus since the question asks for an effect which does not occur with cholinergic stimulation, that leaves (a) as the only possibility. Miosis, not mydriasis, occurs with cholinergic stimulation.

Answer 215

(d) because succinylcholine (SUX) is an agonist at nicotinic receptors, so the initial response is muscle stimulation. But the NMJ rapidly depolarizes due to the inability of the plasma cholinesterase to break down the SUX, which isjust two molecules of acetylcholine fused together – the other information has no relevance unless you’re just stuck thinking “gee, I know that SUX has something to do with autonomics but not sure exactly what!”

Answer 216

(d) organophosphates kill you from too much cholinergic stimulation (SLUD). Option (a) is from nicotinic receptor stimulation, (b) and (c) and (e) are also cholinergic stimulation. Option (d) is an atropine, anticholinergic type reaction and thus doesn’t fit the pattern of responses given.

Answer 217

(e) basically the same question as the preceding question, they just changed organophosphate insecticides to neostigmine. The difference is that neostigmine is a reversible anticholinesterase, whereas insecticides are irreversible. But again, the question just basically wants you to recognize two things – that neostigmine is an indirect acting cholinergic drug and then know what the symptoms of cholinergic stimulation are. But even if you didn’t know those facts you might be able to get if you remember that neostigmine is a drug that is used to reverse the skeletal muscle paralysis produced by drugs of the curare class – the non-depolarizing neuromuscular junction blockers

Answer 218

(2) glandular secretions are generally under cholinergic control, so sweating and salivation are greatly reduced by the anticholinergic drug atropine. So if you can’t salivate or sweat, you very possible will show what kind of symptoms? How about a burning dry mouth and hyperthemia? Nausea and vomiting are cholinergic overdose, as is orthostatic hypotension.

Answer 219

(a) just when you thought you could get by with the anti-SLUD strategy, they then expect you to remember that atropine overdose causes CNS excitation and tachycardia? Actually, that is one of the interesting diffs between atropine and scopolamine, and the reason that scopolamine is used for sedation, while atropine isn’t (b) and (e) are cholinergic stimulation I think, (c) is histamine produced, while I haven’t got a clue what “ptyalism” is – do you? But I do know that if atropine causes dry hot skin because it prevents sweating then (d) can’t be right!

Answer 220

(d) so ya gotta know scopolamine is anticholinergic, so ya need a cholinergic agonist, either direct or indirect to overcome its effects. The options in the list are c and (d). Acetylcholine won’t work because it gets broken down way to rapidly by acetylcholinesterase, and thus is useless to inject. Physostigmine will work since it is an indirect acetylcholinesterase.

Answer 221

(d) - while some of these are indeed associated with organophosphate toxicity, the immediate cause of death is due to (d), which results from the stimulation of nicotinic receptors at the neuromuscular junction resulting in paralysis of skeletal muscles.

Answer 222

(c) this is an except question, don’t miss that word! So looking at the list, we got the S (option d) and the L (option b) from SLUD, so we are left with (a), c, and (e) as possibles. (e) results from cholinergic stimulation of the NMJ, so that can’t be it. (a) or bradycardia, can occur from too much cholinergic stimulation of the heart (that’s why atropine is useful in surgery, to reverse the bradycardia that sometimes arises. So, by default, vasoconstriction is the exception we are looking for.

Answer 223

(c) that’s why it is long-acting in patient’s that have a deficiency in this enzyme

Answer 224

adrenergic blocker | inhibits NE reuptake, depletes NE

Answer 225

adrenoblocker, inhibits catecholamine release

Answer 226

adrenoblocker

Answer 227

cocaine, TCAs

Answer 228

amphetamine, ephedrine, tyramine

Answer 229

decrease in blood pressure bc beta-dilatio predominates

Answer 230

vasoconstriction, urinary retention, mydriasis

Answer 231

increased heart rat

Answer 232

broncho and vasodilation

Answer 233

vasodilation

Answer 234

decreased heart rate

Answer 235

bronchoconstriction

Answer 236

Parkinson's tx can enter brain carbidopa given to divert peripheral decarboxylase activity sympathomimetic toxicity: face twitches, mental disturbances, nausea vomiting, cardiac arrhythmias

Answer 237

inhibits catecholamine release

Answer 238

(e) see, didn’t I just tell you in the previous question that they could just change the drug and use some of the same definitions? But they are tricky, since they think you will speed reading the options, see “false” transmitter, and jump at option (d), and not read further to see that option (e) is the correct answer. Drugs like methyldopa and clonidine are the only centrally acting antihypertensives, reducing sympathetic outflow via alpha-1 agonist action.

Answer 239

(b) amphetamine is one of the many indirect-acting sympathomimetics. It acts by causing the release of neurotransmitter.Just as a review: cocaine: reuptake inhibition and release, TCA antidepressant:, reuptake inhibition, ephedrine:causes release but also acts at receptor itself, MAOIs: block NT degradation.

Answer 240

(c) this you just gotta memorize. Option (d) is true except for the fact that the imbalance is between dopamine and too much cholinergic activity, not norepinephrine. Since levodopa has dopa in its name, you could just narrow the question down to options (b) and (c). But you still have to know, Parkinson’s is due to a deficiency in dopamine. So the treatment is to restore DA levels.

Answer 241

(c) - The injection of a sympathomimetic (e.g. a drug that acts like NE) stimulates both alpha and beta-receptors. Alpha- receptor stimulation produces vasoconstriction, increased systolic and diastolic pressure and reflex tachycardia. Alpha and beta-receptor blockers can block these effects. the only alternative that lists both an alpha (prazosin) and beta (propranolol) blocker is (c). Atropine is a muscarinic (cholinergic ) receptor blocker that would accelerate the heart, the opposite effect that you want, thus (a) and 2 are wrong. Phenoxybenzamine is an alpha-blocker, but curare is a nicotinic receptor blocker, not beta receptor- thus (d) is wrong. As for # 5, amphetamine is an indirect acting sympathomimetic, not a blocker, thus (e) is wrong.

Answer 242

(a) reserpine causes depletion of NE from storage sites, thus it cannot be released by amphetamine. All of the others listed act postsynaptically. Since this drug is no longer used clinically, I would be very surprised if they asked such a question! Wait, I think I said that a few questions ago!

Answer 243

(ii) phentolamine is an alpha blocker, thus the epinephrine will stimulate beta receptors primarily, with the effects listed in option (ii): relaxation of bronchiolar smooth muscle (Beta-1), skeletal muscle vessel dilation (beta-2), and positiver chronotropic and inotropic action on the heart (b)

Answer 244

(iv)well, beta receptor stimulation means stimulation of beta-1 receptors in the cardiac muscle,which will increase systolic bP, and beta-2 stimulation which will dilate vessels going to the liver and skeletal muscle, producing a decrease in diastolic BP. Mydriasis or papillary dilation is also a beta receptor response, so c is also right. While you might be tempted by “cardiac acceleration”, none of the options including (b) work.

Answer 245

(b)all of the above are actions of epinephrine except bronchiolar constriction. Epinephrine would cause bronchodilation – that is why it is used to treat acute brochospasm. So option (b) has to be the exception, because it is just obviously wrong!

Answer 246

(a) epinephrine is a potent stimulator of both alpha and beta receptors. Injection of epi usually causes a rise in blood pressure due to 1) myocardial stimulation that increases ventricular contraction, 2) an increase in heart rate, and most important, 3) vasoconstriction due to alpha receptor stimulation. However, blood flow to skeletal muscles is increased due to powerful beta-2 receptor vasodilator action that is only partially counterbalanced by a vasoconstrictor action on the alpha receptors that are also present in the vascular bed. When given in the presence of an alpha blocker, beta-receptor mediated vasodilation is more pronounced, the total peripheral resistance is decreased and the mean blood pressure falls. This decrease in blood pressure is called "epinephrine reversal". The only alpha-blocker listed is prazosin, answer (a). Atropine is a cholinergic muscarinic receptor blocker, propranolol is a beta- blocker, neostigmine is a cholinesterase inhibitor, and isoproterenol is a predominately beta receptor agonist.

Answer 247

(a)- alternatives 2-4 all increase heart rate, while NE has no effect at muscarinic receptors (e), which are specific for cholinergic drugs.

Answer 248

(iii) Answer is (c)- Alpha-adrenergic agonists such as epinephrine produce vasoconstriction, which would accomplish both "b" and "e". # 3 is the only alternative that includes both b and e thus you don't have to know anything else. "a" and "c" are false. Vasoconstrictors are include in local anesthetic preparations to (1) prolong and increase the depth of anesthesia by retaining the anesthetic in the area injected, (2) reduce the toxic effect of the drug by delaying its absorption into the general circulation and (3) to render the area of injection less hemorrhagic.

Answer 249

(d) CPZ is a potent alpha blocker like prazosin.

Answer 250

(d) What is needed for bronchodilation is relaxation of bronchial smooth muscles. This is accomplished with beta2 receptor stimulation. Isoproterenol is the only drug listed with potent beta2 action. (a) stimulates alpha receptors in the CNS, (b) NE stimulates alpha and beta1 receptors more than beta2, (c) phenylephrine is an alpha receptor agonist, while (e) methoxamine is a vasoconstrictor that stimulates alpha receptors preferentially.

Answer 251

(iii) vasoconstriction is a result of stimulation of the smooth muscle of the peripheral vasculatire, which is an alpha-1 stimulatory action. Of the options, (a), (c) and (e) are alpha-1 agonists. Phentoalmine is a nonselective alpha blocker and thus would cause vasodilation. Propranolol is a non-specific beta- blocker.

Answer 252

(e) levodopa apparently overstimulates DA receptors in the basal ganglia and can cause visual and auditory hallucinations (option c), dyskinesia (option (a)), mood changes, depression and anxiety. It also can stimulate the emetic center, producing the effects given in (d). That leaves you with a choice between (b) and (e). Well, apparently, one of the first things you should know about levodopa therapy is that some people think that levodopa can sensitize the beta-1 receptors in the heart and this is a contraindication to using a local anesthetic containing epinephrine. So option (e) is all that is left to be the exception. How you are supposed to remember all this stuff about levodopa is way beyond me, but good luck!

Answer 253

(b) an asthmatic patient typically takes a drug that has bronchodilatory effects. For this action, you need a drug that is a beta-2 agonist (remember those charts?). Of the list, albuterol is the only beta-2 agonist listed. Phenylephrine is an alpha-1 agonist used for stuffy noses, pseudoephedrine might have distracted you, since it is a decongestant, prazosin and propranolol are antihypertensives.

Answer 254

(b) TI= LD50/ED50, never forget

Answer 255

(c) epinephrine acts as a physiologic antagonist. It nonspecifically antagonizes histamine by exerting its own distinct effects, for example, vasoconstriction, bronchodilation, and decreased GI motility. It does not reverse the effect of histamine by blocking at a specific receptor ((d)), as do antihistamines. It does not prevent the release of histamine as does a drug such as cromolyn ((a), by preventing mast cell degranulation). Answer (b) is not relevant, while (a) is the mechanism of action for cromolyn, which inhibits mast cell degranulation..

Answer 256

(b) epinephrine would stimulate alpha adrenergic receptors to produce vasoconstriction, whereas nitroglycerin relaxes vascular smooth muscle. Thus the two drugs would have opposing actions. However, the actions are produced by the drugs acting on different mechanisms; nitroglycerin does not act at alpha receptors as does epinephrine. If it did, the interaction would be competitive. In this case the interaction is via competing physiological effects.

Answer 257

(c) Idiosyncratic reactions are genetically determined abnormal responses to a drug. They are the most unpredictable in occurrence because the genetically-based difference responsible for such a reaction to a drug may not become evident until the drug is taken for the first time by the patient. Typically, the effect is one of abnormal sensitivity to a drug, such that a therapeutic effect is present at doses much lower than normally used, while the normal dose may result in a toxic reaction. An example is the response to succinylcholine in patients with atypical plasma cholinesterase. These patients don't metabolize succinylcholine at the same rate, and thus show a prolonged drug action and increased sensitivity to the drug. The other alternatives are typically related to the dose of the drug and because the majority of the population do not possess an atypical genetic basis for the response to the drug, the effects are predictable given the dose and knowledge of what the drug does.

Answer 258

intermitten porphyria

Answer 259

respiratory depression

Answer 260

(b) Barbiturates are problematic as anesthetics because they often induce excessive salivation and bronchial secretion, usually requiring the use of an anticholinergic drug to be administered to reduce these secretions. Thus (b) has to be the false statement.

Answer 261

(d) is correct- thiopental is the classic example always given of a drug whose duration of action is determined by redistribution away from its site of action in the brain to less well perfused tissues.

Answer 262

(iii) Answer is (c)- Barbiturates are not analgesics, thus any answer with "a" such as (a) can be eliminated.. "b" is true, thus the answer must contain "b" as one of the alternatives, thus (d) and (e) are eliminated.. "c" is also true, barbiturates are always classified according to duration of action (thiopental- ultra-short acting; phenobarbital-long-acting, etc.). This eliminates # 3 so the answer must be (b). Of course, you should have been able to rapidly eliminate answers (c), 4, and 5 because barbiturates cause death by respiratory depression, not cardiovascular depression.

Answer 263

(i) Answer is (a)- “d” is the absolute contraindication for barbiturate use, since these drugs stimulate the synthesis of enzymes involved in the synthesis of porphyrins and thus will aggravate this disease. Thus the answer must contain “d”, eliminating (c) and (d). Since both (a) and (b) differ only by alternative c, that is the second fact you must know. Barbiturates are not analgesics, but sedatives. When pain is present, they may even make the pain worse, resulting in arousal, rage and perhaps delirium in the patient. Thus, “c” would seem to be a pretty strong contraindication, making (a) the right answer.

Answer 264

(b) is correct. This is one of the adverse side effects of IV diazepam. None of the other alternatives apply.

Answer 265

(d) barbs can be lethal due to respiratory depression, so keep them breathing!

Answer 266

thrombophlebitis

Answer 267

(d) while all have sedative actions, and have their uses given the appropriate setting, benzodiazepines are by far the most popular now given their safety compared to the other agents. The most popular oral BDZs has been diazepam (Valium), but there is a trend recently to the ultrashort acting versions such as triazolam (Halcion).

Answer 268

BDZs in general are great for dental sedation precisely because they present less risk of respiratory depression in comparison to barbiturates and opioids. This is an advantage shared across all the BDZs, so if you know this you don’t really have to know anything else. The others are true advantages of midazolam vs. diazepam. Midazolam is water soluble, and thus does not need to be dissolved in propylene glycol like valium – it is the solvent that cause the thrombophlebitis seen with valium injections. Midazolam also is short acting compared to valium because it does not have active metabolites like valium. Because of the above factors, statement (d) is also true.

Answer 269

b naloxone, since this is used to reverse the effects of Opioids. Midazolam is a BDZ, aminophylline is a theophylline derivative, and physostigmine is a cholinesterase inhibitor.

Answer 270

blocking dopaminergic receptors

Answer 271

tardive dyskinesia from extrapyramidal stimulation | anticholinergic effects

Answer 272

antipsychotic 1st generation

Answer 273

2nd gen antipsychotic

Answer 274

less extrapyramidal side effects (like tardive dyskinesia) treat negative and positive symptoms dopaminergic + serotonin (%-HT) receptors halo = 1st; clozapine - 2nd

Answer 275

imipramine | amitriptyline

Answer 276

(i) You should immediately know that (a) has to be included as part of the answer, thus i or ii has to be right. If you also can dredge up from the recesses of your memory banks that antipsychotics are also effective antiemetics, and are often used clinically for this purpose, then you realize that (c) is wrong, thus limiting your answer to i.

Answer 277

(c) Answer is (c)- Chlorpromazine is the prototypic phenothiazine, an antipsychotic drug used in the treatment of schizophrenia. Other antipsychotic drugs used for this purpose are haloperidol and thioridazine. These drugs act via dopaminergic receptors.

Answer 278

e | all are seen – key word here is irreversible

Answer 279

(d) Tardive dyskinesia is an irreversible condition that consists of involuntary movement of skeletal muscles, a condition which may be seen following prolonged use of drugs. This is typically a dopaminergic mediated effect. The phenothiazine antipsychotics are the only drugs listed which act via dopamine. The others, such as tricyclics and MAO inhibitors affect adrenergic transmission, barbiturates act via GABA, as does alcohol.

Answer 280

(d) - Extrapyramidal side effects are the major side effects of antipsychotic medication and include Parkinson-like effects as well as tardive dyskinesia (from development of supersensitivity resulting from chronic blockade of dopamine receptors in basal ganglia)- abnormal rapid alternating movements of tongue and perioral areas, facial grimacing, etc. Phenothiazines are the only antipsychotic drugs listed.

Answer 281

(c) Answer is (c)- (c) should stand out immediately because this is almost always mentioned as a side effect of dilantin, which is not a phenothiazine, but an anti-convulsant. Phenothiazine derivatives are antipsychotic drugs such as haloperidol (Halcyon) or chlorpromazine used in the treatment of disorders such as schizophrenia. You should remember that the most troubling side effect of these drugs is the production of tardive dyskinesia and the parkinsonian-like extrapyramidal disorders. Thus # 5 is eliminated. As a rule these drugs have anticholinergic and anti-alpha-adrenergic side effects, which would eliminate xerostomia, and postural hypotension (due to an anti-adrenergic depressant effect on both vasomotor centers and the autonomic nervous system) as possible answers. Jaundice is a less frequent side effect than the extrapyramidal symptoms, and often results from an allergic reaction to these drugs. Thus the answer is (c).

Answer 282

c -- bc anticholinergic effects, dry

Answer 283

(e) a long winded way of saying reuptake blockers

Answer 284

(b) TCAs are strong anticholinergics, and atropine is the only anticholinergic drug listed

Answer 285

(v) Answer is (e)- Corticosteroids are antiinflammatory drugs used topically, orally and parenterally. However, they suppress the immune system of the body. They have been known to cause peptic ulcers, as well as mask the symptoms of an ulcer, and perforation and hemorrhage may result. Thus “d” has to be in the answer, eliminating (a). Because they are immunosuppressive, they would obvious make an AIDS patient, who already has a compromised immune system, worse. Similarly, latent tuberculosis could also be reactivated. Thus # 3 and (d) can be eliminated. Use of corticosteroids in inhalers for asthma, while advantageous in reducing the side effects resulting from systemic administration, has led to an increase in problems with Candidiasis, so “b” has to be in the answer. (e) is the only answer that meets all these requirements.

Answer 286

(d) Answer is (d)- Glucocorticoids such as hydrocortisone are classed as antiinflammatories, inhibiting every step of the inflammatory process.- thus (d) is the correct answer. The other alternatives are single steps along the pathway, that are handled by other drugs that are more selective than glucocorticoids.

Answer 287

(a) adrenal steroids, otherwise known as corticosteroids, | actually cause gastric ulcers! All the rest are therapeutic uses.

Answer 288

more soluble - need to give more

Answer 289

hepatotoxicity

Answer 290

1 - analgesia 2 - delirium 3 - surgical anesthesia 4 - medullary paralysis

Answer 291

(b) the rule is, the more insoluble the agent is, the faster the onset and offset of effect. That’s why nitrous oxide, which is very insoluble in blood works so fast and leaves the body so quickly once you stop administration.

Answer 292

(b) maybe cuz it’s the base of the brain? They will eventually depress medullary centers (Stage IV), patient will stop breathing and die. (c), (d), and (e) are desirable actions, (a) is stage II of anesthesia

Answer 293

Answer is (c)- this is the classic clinical use of atropine and one you should have committed to memory. Atropine does not induce muscular relaxation- that would be a neuromuscular junction blocker such as curare, thus (b) and (d) are wrong. #! might confuse you. Atropine is used to override vagal activity, but that is not the reason it is given before halothane.

Answer 294

H1: derm allergies (chlorpheniramine) preop antiemesis, sedation, anticholinergic (promethazone) parkinson sx control (diphenhydramine) H2: gastric secretion reduction, heartburn - cimetidine

Answer 295

H2 antihistamine, gastric secretion control, heartburn

Answer 296

H1: preop, sedation, antiemesis, anticholinergic

Answer 297

H1 antihistamine, derm allergies

Answer 298

H1 parkinson sx control

Answer 299

(c) meclizine is used for vertigo, the others for allergies

Answer 300

(a) Remember that Parkinsonism is a due to a deficiency of DA in the brain, and is currently treated with levodopa and carbidopa. However, prior to these, anticholinergic drugs were the first drugs found to be somewhat effective for treatment of this disease, in that cholinergic and dopaminergic tracts interact in the brain, and thus reducing cholinergic activity via anticholinergic drugs improves or enhances dopaminergic function, suggesting one is inhibitory to the other. Drugs with anticholinergic activity are often still the first drug tried. Antihistamine drugs such as diphenhydramine often have strong anticholinergic activity, which accounts for their effectiveness in drying nasal secretions associated with a cold. Therefore, the answer is (a). (e) is there to confuse you, but don't be. Diphenhydramine does not stimulate dopaminergic nerves in the basal ganglia. Adrenergic blockers ((c)) do see some use in the treatment of Parkinson's, but diphenhydramine has no adrenergic blocking activity. Diphenhydramine does have the actions given in (b) and (d), but these are not responsible for its efficacy in Parkinson's..

Answer 301

b H1 antihistamines are competitive histamine receptor blockers. Many students answer (e), but this is the mechanism of action of cromolyn. (c) also draws some answers, but is wrong-epinephrine is the physiological antagonist of histamine.

Answer 302

Answer is (b)- This is a memorization question. Carbamazepine, as well as phenytoin, are the main drugs used to treat trigeminal neuralgia. Clonazepam is a benzodiazepine, succinylcholine is a depolarizing neuromuscular blocking agent, while acetazolamine is an anticonvulsant like carbamazepine.

Answer 303

The answer is (b), Cardiac arrthymias are the main bad side effect of epinephrine as a vasoconstrictor. Epi stimulates both alpha and beta receptors. Beta receptors are found in the heart and stimulation of beta receptors increases heart rate, force of contraction, cardiac output and oxygen utilization. (a) is wrong, epi elevates blood glucose. (c) is wrong- beta stimulation in smooth muscle and bronchi causes bronchodilation, and is thus a drug of choice for acute asthmatic attacks. (d) is obviously wrong- a decrease in blood pressure would not result from adrenergic stimulation, increased blood pressure is the rule.

Answer 304

The answer is (d). Miosis ((a)) is a cholinergic effect typically observed with opiates. Cocaine doesn’t cause this kind of effect for example. (b), tolerance, is common to many drugs such as opiates, barbiturates and sedatives, but has not been clearly demonstrated for all abused drugs. (c), physical dependence, is usually thought to be true only for morphine, alcohol, caffeine, and perhaps cocaine.

Answer 305

Answer is (e)- Alcohol inhibits the CNS, thus eliminating (a), (b), and (c), leaving the choice between 4 and 5. Alcohol has been postulated to inhibit GABA effects, the major inhibitory transmitter in the CNS, especially in the cortex. Thus (e) is the answer.

Answer 306

Answer is (c)- memorization- alpha agonists decrease insulin release, beta agonists increase it. Thus because both of these are adrenergic stimulation, (a) can’t be the answer. (b)- muscarinic agonists increase insulin release, but this is not the mechanism of sulfonylureas. They cause insulin release by (c), and are the primary oral antidiabetic agents used therapeutically.

Answer 307

Answer is (e)- Dicoumarol is an oral anticoagulant. Thus the risk in an extraction is that the patient may bleed excessively, or that a serious interaction with a drug that you might require in your management of the patient, such as barbiturates or salicylates may occur. You may need to adjust the anticoagulant activity to within a safe range for surgical procedures. Since dicoumarol prevents blood clotting by preventing the conversion of Vitamin K to prothrombin, (e) is the only appropriate test.

Answer 308

Answer is (c)- 2 gm at 0 hr, at 4 hrs 1/2 from first injection is gone, leaving 1 gm in the body and you inject 2 more for a total after the second injection of 3. At the third dose, 1/2 of 3 is gone, leaving 1.5 gms, you inject 2 more for a total of 3.5 immediately after the third dose.

Answer 309

(a) (b) is wrong-Protamine is an antagonist of heparin, not dicoumarol. (c): phenylbutazone enhances the toxicity of warfarin by displacing it from plasma protein binding sites. (d): hyperbaric oxygen would be a useful treatment for carbon monoxide poisoning, not CO2

Answer 310

``` Answer is (d)- remember, diabetes medications can be organized into 3 groups based on their onset and duration of action: 1)fast-acting: insulin injection, 2) intermediate acting: Isophane insulin suspension, and 3) long acting: protamine zinc insulin suspension ```

Answer 311

answer is (a)- most people answer 3, confusing protein binding sites from active receptor sites where drugs exert their effects. Protein binding sites are just uptake sites that take up a drug and keep it from getting to its real receptor site of action. Some drugs are extensively protein bound, for example coumarin is 97% protein bound and only 3% is left to reach effective sites. Administration with another drug that is also extensively plasma protein bound will displace the drug that is already on these sites via competition, and thus effectively increase the level of drug that can now get to an active receptor site.

Answer 312

Answer is (e)- Addison's disease results from failure of the adrenal cortices to produce adrenocortical hormones such as aldosterone. Aldosterone is a mineralocorticoid that controls sodium retention and potassium excretion. Lack of aldosterone results in electrolyte imbalances, with the major problem being hyponatremia (sodium loss). Similar symptoms may also be seen when a patient is withdrawn from chronic adrenal steroid therapy. Due to depressed adrenal function, patients can't respond to stressful situations (such as dental procedures) adequately, and an adrenal crisis may occur. The recommended treatment is (e), 100 mg of hydrocortisone hemisuccinate. Of the other corticosteroids given, he dose given for prednisolone ((b)) is too low, while triamcinolone lacks any effects on sodium retention. NE and Epi would not be used in this situation- they might be used in a case of adrenal medulla insufficiency.

Answer 313

Answer is (b)- usually biotransformation results in a more water soluble, more readily excreted form of the parent drug. In most cases this inactivates the drug, but there are some exceptions which involve the formation of metabolites with activity (diazepam) or when an inactive prodrug is given (levodopa) which becomes active after the first step in the biotransformation pathway (DOPA) sometimes are asked in questions of this form.

Answer 314

``` Answer is (c)- Remember that local anesthetics are either esters or amides. All of the other alternatives diverge widely in their structures. ```

Answer 315

Answer is (c)- Remember, cimetidine or "Tagamet" is an H2 antihistamine are used therapeutically to inhibit gastric secretion ((c)) in cases of peptic ulcer. This is its only clinical use. You might see it in a question regarding drug metabolism- it is also a potent inhibitor of the mixed function oxidase drug metabolizing enzyme system in the liver. The other alternatives are to confuse you because you probably at least remember that it is an antihistamine, but you don't know the difference between H1 and H2 antihistamines.

Answer 316

d (a) & (b) are alkylating agents, (c) is an alkaloid derived from plants. (d) is a folate antagonist, which acts as an antimetabolite. Just for your future edification, most cancer chemotherapy drugs cause cell death by affecting the ability of cells to divide. The drugs thus inhibit one or more phases of the cell cycle or prevent a cell in Go (the nondividing phase) from entering into the cycle of cell division. Antimetabolites may act in 2 ways (1) by incorporation into a metabolic pathway and formation of a false metabolite which is nonfunctional or (2) by inhibition of the catalytic function of an enzyme or enzyme system. Methotrexate is an example of a cell cycle specific antimetabolite that inhibits DNA synthesis during the S phase. Vincristine acts during the mitotic phase

Answer 317

alkylating agentm anti-cancer

Answer 318

Answer is (b)- maintaining the concentration of Ca++ in extracellular fluid by regulating the deposition and mobilization of calcium from bone, absorption from the GI tract, excretion etc. is the main function of parathyroid hormone. Thyrocalcitonin is another name for calcitonin. They hope to confuse you because there is a correlation between calcitonin and calcium, except that calcium concentrations regulate the synthesis and release of calcitonin. Glucagon is a pancreatic hormone that stimulates glucose production, thyrotropin is there to confuse you with parathyroid hormone, and aldosterone regulates Na+ levels not Ca++.

Answer 319

Answer is (d)- scopolamine is a muscarinic receptor blocker similar to atropine, thus (a) is wrong. Levodopa has nothing to do with this question. To counteract a competitive muscarinic receptor block, you need to increase the levels of agonist, in this case acetylcholine. However, you can't give ACh because it is broken down almost instantaneously by acetylcholinesterase. The answer is to give a drug which knocks out the acetylcholinesterase, allowing endogenously released ACh to accumulate to overcome the action of scopolamine. The drug which will do this is physostigmine.

Answer 320

like atropine, anticholinergic

Answer 321

Answer is (c)- “a” can’t be right because exercise increases blood flow through muscles and thus improves absorption. Thus # 1 is wrong. “b” is obviously right for the same reason. “c” would also result in reduced blood flow so slower absorption would also be a problem. “d” is often used for prolonged and steady drug release so it also is true. The answer must thus be (c).

Answer 322

Answer is (e)- “Salicylism” is a mild toxic reaction to aspirin (acetylsalicylic acid), usually occurring after prolonged treatment with large doses. Nausea, tinnitus, vomiting and GI bleeding are all symptoms of salicylism. Other notable side effects of aspirin which result from ingestion of a single large dose are disturbances of acid-base imbalance (acidosis or alkalosis), fever, hypoglycemia. Remember, aspirin, is contraindicated in children suffering from influenza or chicken pox: aspirin has been implicated in the development of Renee’s syndrome.

Answer 323

Answer is (b)- This is a pure memorization question. All of these drugs are benzodiazepines, which typically have a long duration of action because they are converted to pharmacologically active metabolites with long half-lives. Oxazepam, midazolam, and lorazepam are exceptions that are not converted to active metabolites. The answer is thus (b).

Answer 324

Answer is (e)- The central actions of alcohol are depressant. Thus the choice of correct answer comes down to knowing which of the drugs listed is not a CNS depressant. Diazepam is a benzodiazepine, pentobarbital is a barbiturate. Both are sedating. Meperidine is an opiate, while chlorpromazine is a phenothiazine antipsychotic. Both of these classes of drugs are also typically sedating. The correct answer is (e), methylphenidate (Ritalin). Ritalin is an indirect acting sympathomimetic, and acts similar to amphetamine in the CNS- it is a stimulant.

Answer 325

Answer is (d)- Nalbuphine is a mixed agonist-antagonist that is analgesically equipotent with morphine (thus # 1 is ruled out). However, analgesia is produced by its agonistic effects at kappa opioid receptors. It has pronounced antagonistic effects at the mu receptor, and can be used clinically to reverse respiratory depression (by blocking mu receptors) without a loss of analgesic effects (by stimulating kappa receptors). Thus, # 2 is ruled out. # 4 is not likely. The mixed agonist-antagonists were designed to combine analgesia with enough antagonistic properties to prevent their abuse. Thus, # 3 is the right answer. Typically, these drugs can mimic the effect of morphine in a drug free patient, but antagonize opiate action in a dependent patient, thus precipitating withdrawal. Of this class of drugs, butorphanol is the exception- it will not precipitate withdrawal because it is only a weak mu antagonist.

Answer 326

Answer is (b)- Nonsynthetic reactions (phase I reactions) include the various transformations of molecular structure: oxidation, reduction, and hydrolysis; they represent the first stage of biotransformation. Synthetic (phase II) reactions consist of the conjugation of drugs or their metabolites with functional groups. Of the alternatives, (c) and (d) are conjugation reactions, and thus are wrong because they are synthetic reactions. Alternative (a) is tricky. It is made to sound like N-dealkylation, which is a nonsynthetic or phase I oxidative reaction. There is no reaction called N-alkylation. Thus (b), an oxidative phase I reaction is left as the right answer

Answer 327

(b) ventricular arrythmias are the life threatening ones, and lidocaine is particularly effective for this kind of arrhythmia when given parenterally in an emergency situation. It has a very rapid onset of action when given IV, which is obviously important in an emergency. The others all also have antiarrythmic action, mostly used for supraventricular tachyarrythmias

Answer 328

(b) the issue is obviously that the patient may bleed excessively, a situation that would cause problems during dental surgical procedures. Dentist should consult with the patient’s physician about stopping the Coumadin for a few days. Options (a) and (e) might be appropriate in an emergency situation, but that is not what we are dealing with here. Option (c) would take longer to reduce (PT) than just stopping the Coumadin. Finally, heparin is not a Coumadin antagonist, but an anticoagulant in its own right.

Answer 329

(b) the rule is ..04 mg of epi max in CV patients. The easiest way to figure this one out is to remember you shouldn’t give more than 2.2 carpules of xylocaine with 1:100,000 epi - your usual choice as a local anesthetic. Two carpules is 3.6 cc. This eliminates options (c) and (d), since they would be safe but not maximal. Since 1:50,000 is twice as concentrated as 1:100,000, 1 cc of 1:50,000 (option (a)) is the same as 2 cc of 1:100,000 so still not close to max, so (b) has to be the right answer. Of course, you could have just remembered, 1:100,000 equals .01 mg per cc, so 1:50,000 equals .02 mg per cc, so (b) would equal the max of .04 mg.

Answer 330

(a) memorize, memorize. Most are anticonvulsants, but diazepam is drug of choice. Chlorpromazine is an antipsychotic, not an anticonvulsant. Phenytoin, is an anticonvulsant, and is one of the answers to the question “which of the following causes gingival hyperplasia?” Don’t forget diazepam is also given for antianxiety and sedation.

Answer 331

(a) bradycardia is a reflexive slowed heart rate, controlled by vagal input to the heart, and is cholinergically mediated, which means you need a cholinergic receptor blocker to reduce the vagal effect. Atropine is the only drug listed which is a cholinergic agent. They threw in epinephrine as a tease, because if you knew bradycardia was cardiac slowing, you might be tempted to think epi, which usually speeds up the heart, would be the right answer- but you’ve got to block the vagal input, epi won’t work.

Answer 332

(a) nonionized forms of drugs cross membranes more readily and are highly lipid soluble, and tend to get stored in fat tissue from where they are only slowly released. Thus highly ionized drugs, which are less lipid soluble don’t get stored in fatty tissue and are subject to more rapid excretion.

Answer 333

(c) platelet aggregation is controlled by two factors, prostacyclin, which decreases it, and thromboxane, which enhances it. Low dose aspirin blocks the latter, so (c) is right, (a) is the mechanism of action of corticosteroid drugs, (d) is the mechanism of action of anticoagulant drugs like coumadin.

Answer 334

(d) for bronchodilation you want a potent beta-2 adrenergic receptor agonist- of the drugs listed (d) is the best. Isoproterenol is a non- specific beta agonist. Methoxamine and phenylephrine are alpha- 1 agonists, amphetamine is an indirect acting agonist that causes the release of norepinephrine, which is less potent at beta receptors than isoproterenol.

Answer 335

c Neuromuscular transmission requires the action of acetylcholine at the nicotinic receptors on the neuromuscular junction endplate. The two drugs used clinically to do this are curare and succinylcholine. Curare is a nicotinic receptor blocker, succinylcholine acts to overstimulate the receptor, thereby causing its subsequent depolarization of the neuron and a block of nuscle activity. (e) is how spider venoms and snake toxins work, not succinylcholine. (a) would enhance neuromuscular action, and is actually made use of clinically with myasthenia gravis patients. (d) isn’t possible.

Answer 336

(c) the only definition which covers all three drugs. (a) applies only to pentobarbital, (b) applies only to meperidine, and (d) applies only to diazepam.

Answer 337

b Buspirone is used to relieve anxiety – it is not a benzodiazepine like diazepam and alprazolam (BDZs may not be that sedating, but can cause impairment of psychomotor skills), and not a strong sedative like chloral hydrate

Answer 338

(c) vitamin K is stored in the liver – this is decreased by cirrhosis – the result is deficiencies in prothrombin dependent coagulation factors

Answer 339

(d) locals don’t have actions (a), (b), or (c)! Nervous patients, however, do salivate more.

Answer 340

(c) a sympathomimetic drug is going to potentially activate both alpha and beta receptors, so you would need a pairing of drugs which blocks those receptors. Prazosin, an alpha-1 blocker,, and propranolol, a non-specific beta-blocker, are the only pair that block both types sympathetic/adrenergic receptors. Atropine is a muscarinic blocker (anticholinergic), phenoxybenzamine is an alpha-blocker, but curare is neuromuscular junction blocker. Amphetamine is a sympathomimetic drug, not a blocker or sympatholytic drug. a

Answer 341

(d) because it will also cause the anticholinergic effect of | mydriasis, or papillary dilation

Answer 342

(b) memorize that list of opioid analgesic potencies. It would go propoxyphene< codeine< pentazocine< oxycodone

Answer 343

propoxyphene < codeine < pentazocine < oxycodone

Answer 344

(d) each one of these drugs has a side effect that they may use in the stem of this question, and give you the same list of drugs: the effects are polymixin- renal necrosis, chloramphenicol- bone marrow depression, amphotericin B –nephrotoxicity

Answer 345

bone marrow

Answer 346

rental necrosis

Answer 347

auditory nerve deafness | streptomycin too

Answer 348

(a) xerostomia is an anticholinergic effect. All the drugs listed except opioids are unfortunately strongly anticholinergic, in addition to their desired mechanism of action.

Answer 349

(d) BDZs are better than narcotics or barbiturates because they don’t cause anywhere near the problem with respiratory depression that those two do.. Phenothiazines have more side effects.

Answer 350

c “pure” competitive receptor antagonist – such a drug binds to a receptor with high affinity, but has no intrinsic activity. If it did it would be an agonist.

Answer 351

(a) why would you care which one is the least likely? Actually, because if it binds covalently, that is a non-reversible situation that can’t be overcome – you get a long-lasting drug effect that can only be overcome by making new receptors. Some antagonists work this way.

Answer 352

(a) easy – the only “transmitter” listed is acetylcholine. You don’t have to have any idea what the question is about (I don’t!) as long as you recognize that there is only one transmitter listed – the others kinda sound the same – cholinesterase is the enzyme that breaks acetylcholine down, acetylsalicylic acid is aspirin, have no idea what hydroxycholine is

Answer 353

(a) miconazole and amphotericin B you should recognize, I hope, as antifungals, so your choice is between (a) and (b). Novobiocin sounds like an antibiotic, which it actually is, so guess (a)

Answer 354

(c) mydriasis is papillary dilation, which is a hallmark effect of anticholinergic drugs, and why they are used in eye exams

Answer 355

c (a) is an alpha-1 blocker, (b) alpha-2 agonist that decreases sympathetic outfloe from CNS, (d) is a direct acting vasodilator, and (e) is a type I calcium channel blocker

Answer 356

(a) these are all opioid receptors – only mu and kappa are involved in analgesia, mu at the supraspinal level and kappa at the spinal level (the receptor that pentazocine (Talwin), the mixed acting agonist/antagonist acts on

Answer 357

a procaine, benzocaine and tetracaine are esters, lidocaine, prilocaine and mepivacaine are amides. Amides, unlike esters are not by rule cross-allergenic

Answer 358

e Actions a, c, and d are all clinically useful actions of the phenothiazines, which you might remember were discussed under the category of antipsychotic drugs. But wait- Promethazine (Phenergan) is used in dentistry as a sedative, often in combination with Demerol because it reduces the nausea associated with the use of the opioid and also potentiates its analgesic effect, allowing lower dose to be used, thus again reducing the potential for adverse side effects. Alpha adrenergic effects are an adverse side effect.

Answer 359

a cocaine is an indirect acting adrenergic agonist, acting by causing the release of adrenergic neurotransmitters as well as blocking their reuptake, thereby prolonging their activity. The other drugs listed are just local anesthetics that don’t have this action - they just block sodium influx into the neuron.

Answer 360

(d) Patients using corticosteroids for arthritis often develop ulcers because these drug block prostaglandin action in the stomach, thereby increasing acid secretion while decreasing the protective mucosal barrier of the stomach.

Answer 361

d the first three are all signs that the patient is getting too much nitrous.

Answer 362

(b) sedation does not decrease the local anesthetic requirement, the patient will still feel pain. Sedatives, with the exception of nitrous oxide, have no analgesic effect -barbiturate sedatives may make the patient more sensitive to pain.

Answer 363

(b) only benzodiazepines are actually classified as antianxiety drugs, although other drugs, such as opioids have antianxiety actions in addition to their other clinically useful actions. (b) lorazepam is the only BDZ listed. Methohexital is a barbiturate - these are classified as seatives. Haloperidol is an antipsychotic, pentazocine an opioid, and phenylpropanolamine is a decongestant used in cold medications.

Answer 364

2, 7, 9, 10, antociagulant proteins C and S

Answer 365

vit K reductase

Answer 366

anticoagulant | binds reversibly to anti-thrombin II, prevents conversion of fibrinogen to fibrin

Answer 367

inhibits vit K reductase

Answer 368

A - factor 8 | B - factor 9

Answer 369

INR (= 2.0-3.0)

Answer 370

Proceed with treatment because his INR is < 2.5 1 is normal (12 seconds) higher INR -- more bleeding, higher PT

Answer 371

2. 5 - Bleeding measurements: PTT 25-36 sec PT 5-7 sec platelets 150K-450K minimum platelets 50k bleeding time: less than 9 min INR: 1 do not treat with more than 3.5

Answer 372

b. Stop medication of 5 days (stop drug 5 days before, and resume the day after surgery)

Answer 373

Decrease K+ needed to synthesize factors II, VII, IX, X

Answer 374

C. fibrinogen to fibrin.

Answer 375

Coronary infarct

Answer 376

Myocardial infarction

Answer 377

give vitamin KKKKKKKKKK

Answer 378

- PT --> extrinsic system (Vit. K coagulation factors-2,7,9,10); used to test warfarin/Coumadin effectiveness, for liver damage, and Vit. K status PTT --> intrinsic system, iused to test Heparin

Answer 379

liver glucouronidation

Answer 380

b. bleeding time

Answer 381

coagulation necrosis.

Answer 382

bleeding time

Answer 383

platelet adherence Bleeding time = time required for blood to stop (2-6min normal) - Bleeding time is increased in disorders of platelet count, uremia, and ingestion of aspirin and other anti-inflammatory medication

Answer 384

none it affects plts and bleeding time

Answer 385

2-6 minutes

Answer 386

A. Coumarin (Coumadin®)

Answer 387

alter platelet function, inhibits platelet aggregation irreversibly

Answer 388

nhibits platelet aggregation | Given to patients allergic to aspirin àno ulcer side effect, given to patients with past ulcer history

Answer 389

PG decrease gastric acid and increase gastric mucous. Inhibiting PG will increase gastric acid and decrease mucosa. That's why people taking too much aspirin can get stomach bleeding cause more acidic and no protection

Answer 390

Arachidonic acid

Answer 391

Ginseng is an antiplatelet (interferes with coagulation – not given with aspirin). pt on warfarin, aspirin

Answer 392

ASPIRIN (not digitalis) | - Ginseng = antiplatelet

Answer 393

Warfarin, NSAIDS, and Aspirin

Answer 394

Aspirin | - Saw palmetto enhances anti-coagulants

Answer 395

b. Saw Palmetto

Answer 396

45 for males, 40 for females if lower, consult physician for extractions

Answer 397

c. Continue treatment | - Mosby’s states that normal INR of people on anticoagulants is 2.5-3.0.

Answer 398

Refer for INR

Answer 399

Fibrinolysis

Answer 400

glucose level over extended period

Answer 401

Hyperglycemia

Answer 402

bradycardia, mydriasis (pupil dilation), diaphoresis (sweating), mental confusion

Answer 403

administer glucose

Answer 404

alcohol risk factors for the development of hypoglycemia: exercise, alcohol, older age, renal dysfunction, infection, decreased intake of energy, and mental health issues, including dementia, depression, and psychiatric illnesses.

Answer 405

Diabetes type 1/hyperglycemic

Answer 406

Hyperglycemia

Answer 407

c) Blindness

Answer 408

blindness (retinopathy)

Answer 409

enhance insulin secretion (glyburide, glipizide, glimepiride)

Answer 410

produces less glucose in the liver (metformin)

Answer 411

slow carbohydrate digestion (acarbose, miglitol)

Answer 412

Rapid acting (5-15min); Short acting (30-60min); Intermediate (2-4h); Long acting (6-10h); Premixed (30-60min)

Answer 413

Diabetes - steroids can raise blood sugar & increase the need for more medication to control sugar levels. Diabetics on steroids may have to raise their insulin dose dramatically.

Answer 414

sulfonylurea & metformin

Answer 415

They do not have beta cells for insulin & Sulfonylureas MoA is to stimulate those cells

Answer 416

Stimulate insulin release from Beta cells in the pancreas

Answer 417

increase insulin PRODUCTION and SENSITIVITY by Beta cells stimulation by binding to ATP-dependent K channels - stimulating pancreatic insulin release by bind to ATP K+ channels & causing depolarization, which stimulates calcium ion influx & induces insulin secretion.

Answer 418

suppresses glucose production in liver (decreasing hepatic gluconeogenesis) à decreases glucagon levels) – bind to AMP protein kinase receptors

Answer 419

D. Action as direct receptor agonists for the insulin receptor

Answer 420

duration of action

Answer 421

d. Congestive heart failure

Answer 422

Orthopnea | - other symptoms: dyspnea, fatigue, paroxysmal nocturnal dyspnea, edema

Answer 423

Respiratory distress

Answer 424

Ventricular septal defects | - communications between the bottom chambers, structural heart defects

Answer 425

à congestive heart failure

Answer 426

Congestive heart failure

Answer 427

Pain that goes away with LA

Answer 428

Thrombosis

Answer 429

b. Unstable angina

Answer 430

Hypertension / CHF

Answer 431

congestive heart failure

Answer 432

Inhibit Na/K ATPase & Increase Na and Ca in cell to increases the refractory period.

Answer 433

increase influx more Ca

Answer 434

``` glycoside Increase Ionotropic (contractions) effect of the heart ```

Answer 435

Post myocardial infarction, Supraventricular arrhythmia | - digitalis/cardiac glycoside = common indications for use is for atrial fibrillation

Answer 436

Inhibits Na/K ATPase of cardiac cell membranes resulting in increase of Na concentration intracellularly, cardiac glycoside, increases intracellular Ca++

Answer 437

contraceptives and anti-virals (HIV), caution with bleeding

Answer 438

• Med consult with physician

Answer 439

Decreases repolarization rate, prolongs refractory period

Answer 440

- you can give Quinidine, Verapamil, and Digitalis for atrial and the side mechanism of Quinidine is it increases the refractory period

Answer 441

orthostatic hypotension and headache

Answer 442

patient should take nitroglycerin FALSE-give for | angina to prevent heart attacks.

Answer 443

Vasodilation of arteries à decreased BP à tachycardia - Nitroglycerin is a nitrovasodilator. It produces nitric oxide, which activates guanylyl cyclase which, in turn, catalyzes the production of ⬆ cGMP.

Answer 444

through blood vessels (dilate blood vessels)

Answer 445

relaxing and widening the blood vessels in the body, allowing more blood and oxygen to flow to the heart. Since the arteries are wider, it is easier for the heart to pump blood, so it does not require as much blood and oxygen.

Answer 446

natural reflex to the decrease in blood | pressure

Answer 447

b/c of increased blood flow caused increased blood flow to | kidney

Answer 448

Decreases nausea Hydralazine (Apresoline) is a direct-acting smooth muscle relaxant used to treat HTN by acting as a vasodilator primarily in arteries and arterioles to decrease peripheral resistance, thereby lowering blood pressure and decreasing afterload.

Answer 449

Propranolol

Answer 450

thiazide | those are diuretics

Answer 451

SV arrhythmias

Answer 452

Beta 2 receptor for | lungs, Beta 1 receptor for heart

Answer 453

Wheezing when exhaling | - Wheezing à exhale with high pitch

Answer 454

Asthma (induced by stress)

Answer 455

Asthma have problem breathing in (but wheeze when exhaling), COPD has problem exhaling

Answer 456

Hyperventilation

Answer 457

Hyperventilation

Answer 458

tachycardia and tachypnea (rapid breathing)

Answer 459

soft tissue emphysema (sudden painless swelling) | - Emphysema: constriction of air sacks

Answer 460

subcutaneous emphysema

Answer 461

Dyspnea, wheezing, cough, chest tightness. Air sacks are all destroyed (narrowing of distal airways)

Answer 462

laryngospasms

Answer 463

laryngospasm - blockage of UPPER resp. tract

Answer 464

bronchodilater, increase HR, | increase BP

Answer 465

prevent and treat wheezing, SOB (shortness of breath), and difficulty breathing caused by asthma, chronic bronchitis, emphysema, and other lung diseases. It relaxes and opens air passages in the lungs, making it easier to breathe.

Answer 466

albuterol- generic name is Salbutamol. It is a beta-2 agonist, which causes bronchodilation

Answer 467

Epinephrine

Answer 468

Aminophiline (bronchodilator)

Answer 469

Aspirin (NSAID) so NO NSAIDS for asthmatic patients

Answer 470

Albuterol, corticosteroids, aminophylline

Answer 471

corticosteroid

Answer 472

o Give oxygen

Answer 473

on her left - to avoid compression of inferior vena cava

Answer 474

Have pt lay on left side

Answer 475

Raise right hip up | - Baby crushing IVC so lay on left hip & raise right hip UP

Answer 476

Beware of compression to inferior vena ceva

Answer 477

Inferior Vena Cava

Answer 478

maintain airway

Answer 479

upright/standing

Answer 480

maint circulation so that the most vital organs are never hypoxic.

Answer 481

TRENDELENBURG POSITION SUPINE WITH FEET ELEVATED SLIGHTLY - The most common early sign of syncope is PALLOR (paleness).

Answer 482

Hydralazine (Apresoline) is a direct-acting smooth muscle relaxant used to treat HTN by acting as a vasodilator primarily in arteries and arterioles to decrease peripheral resistance, thereby lowering blood pressure and decreasing afterload.

Answer 483

Tendenberg

Answer 484

Decreased perfusion to tissue

Answer 485

transient loss of consciousness

Answer 486

Inhale ammonia to irritates es. trigeminal nerve sensory, 100% oxygen works except with hyperventilation syndrome

Answer 487

Hyperventilation syndrome

Answer 488

Due to vasoconstrictor injected into venous system.

Answer 489

consistent with a diagnosis of syncope.

Answer 490

blood pressure falls

Answer 491

blood pressure and heart rate rises

Answer 492

Hyperventilation Carpopedal spasms are severely painful cramps of the hand/feet muscles. - May be caused by low blood calcium levels or by tetanus.

Answer 493

Respiratory depression

Answer 494

Pregnant, myasthenia gravis, acute narrow glaucoma, COPD, emphysema

Answer 495

Phenytoin/ Dilantin

Answer 496

Valium / diazepam

Answer 497

grand mal seizures - Febrile seizures, which occur in young children & are provoked by fever, are the most common type of provoked seizures in childhood. Then, generalized tonic-clonic (grand mal)

Answer 498

Hydralazine (Apresoline) is a direct-acting smooth muscle relaxant used to treat HTN by acting as a vasodilator primarily in arteries and arterioles to decrease peripheral resistance, thereby lowering blood pressure and decreasing afterload.

Answer 499

Tendenberg

Answer 500

Decreased perfusion to tissue

Answer 501

transient loss of consciousness

Answer 502

Inhale ammonia to irritates es. trigeminal nerve sensory, 100% oxygen works except with hyperventilation syndrome

Answer 503

Hyperventilation syndrome

Answer 504

Due to vasoconstrictor injected into venous system.

Answer 505

consistent with a diagnosis of syncope.

Answer 506

blood pressure falls

Answer 507

blood pressure and heart rate rises

Answer 508

Hyperventilation Carpopedal spasms are severely painful cramps of the hand/feet muscles. - May be caused by low blood calcium levels or by tetanus.

Answer 509

Respiratory depression

Answer 510

Pregnant, myasthenia gravis, acute narrow glaucoma, COPD, emphysema

Answer 511

Phenytoin/ Dilantin

Answer 512

Valium / diazepam

Answer 513

grand mal seizures- Febrile seizures, which occur in young children & are provoked by fever, are the most common type of provoked seizures in childhood. Then, generalized tonic-clonic (grand mal)

Answer 514

A. Diazepam (Valium®)

Answer 515

Valium (diazapams) 5-10 mg IV / per minute

Answer 516

CONTRAINDICATIONS: Pregnant, myasthenia gravis, acute narrow glaucoma, COPD, emphysema

Answer 517

B. Diazepam

Answer 518

Ethosuximide - Only 2 drugs for absence seizures (petit mal): ethosuximide (Zarontin) – only treats petit mal- and valproic acid (Depakene, Depacon) – treats grand mal, petit, and myoclonic seizures.

Answer 519

c. Hyponantremia (low sodium)

Answer 520

a. Ethosuximide – petit mal seizures b. Diazepam - Status epilepticus c. Lasix (furosemide) – HTN loop diuretic

Answer 521

D. Less potential for respiratory depression - midazolam has a milder effect, but more long lasting

Answer 522

E. Hepatic biotransformation

Answer 523

D. Diazepam

Answer 524

A. It is recommended as an end-point. - The most frequently used signs for IV diazepam sedation are ptosis, (“the Verrill sign”), altered speech and blurred vision.

Answer 525

Diazepam (Valium ̈)

Answer 526

o LOT: Lorazepam, Oxazepam, Temazepam

Answer 527

triazolam, midazolam, and alprazolam à short sedative

Answer 528

Phenobarbital is used to treat certain types of seizures

Answer 529

these are for insomnia | reverse with flumazenil

Answer 530

Facilitates GABA receptor binding by Increasing the frequency of chloride channel opening.

Answer 531

Mechanism of action of on GABA receptors: increasing the frequency of chloride channels by benzodiazepines - Barbiturates increase the duration of chloride channel opening

Answer 532

GABA receptors

Answer 533

Xanax (alprazolam)

Answer 534

Anti-convulsant & sedative

Answer 535

cleft palate (teratogenic effect)

Answer 536

no effect as opposed to other benzos

Answer 537

voluntary muscles

Answer 538

Long acting one (like diazepam) | - Short to intermediate-acting benzodiazepines are preferred in the elderly (ex. oxazepam, temazepam, midazolam)

Answer 539

amnesia and little memory of the event.

Answer 540

Oxazepam | - LOT: Lorazepam, Oxazepam, Temazepam

Answer 541

Flumazenil | - Flumazenil: Benzodiazepine antagonist b/c competitive GABA receptor.

Answer 542

(versed = midazolam) Flumazenil C. Naloxone (for opioids) D. Disulfuriam (for alcoholics)

Answer 543

a) pregnancy

Answer 544

moderate doses ANTIANXIOLYTIC and high doses is SEDATIVE

Answer 545

Antipsychotic, part of withdrawal - Several anxiolytics & hypnotics have a rebound effect, which cause severe anxiety and insomnia worse than the original insomnia or anxiety disorder.

Answer 546

Thiopental

Answer 547

rapid-onset short ultra-acting barbiturate(IV) for general anesthesia

Answer 548

Ambien (sedative and makes patient sleep).

Answer 549

a. oxidation (occurs in the liver)

Answer 550

redistribution.

Answer 551

histidine | - Histidine decarboxylase (HDC) enzyme catalyzes the reaction that makes histamine from histidine w/ vitamin B6

Answer 552

1st generation anti-histamine - H1 blockers

Answer 553

Diphenhydramine (Benadryl)

Answer 554

Xerostomia (anti-cholinergic, anti-histamine, sedative)

Answer 555

Anticholinergic

Answer 556

Anti-histamine - antihistamine relieves itchy/watery eyes and itchy throat by blocking a substance (histamine) released by allergies. - anticholinergic dries up a runny nose & the fluid that runs down your throat causing itching/irritation.

Answer 557

H1 blocker 2nd generation - Allegra, Claritin (loratidine), Clarinex (Desloratidine) Certizine (Zyrtec) because they don’t cross BBB, poor CNS penetration

Answer 558

(2nd generation H1 blocker) Diphenylhydramine/ Benadryl (Most) chlorpheniramine (LEAST) Tripelennamine - Chlorphenamine, is a first-generation alkylamine antihistamine

Answer 559

Loratidine (Claritin)

Answer 560

second generation H1 blocker/antihistamine

Answer 561

loratadine

Answer 562

DIPHENHYDRAMINE (BENADRYL)

Answer 563

Competitive inhibition of histamine receptors

Answer 564

compete w/ histamine to bind at H1 receptor sites.

Answer 565

(causes CNS depression) | a. CNS increase

Answer 566

competitive inhibition of H1 receptors so block vasodilation, bronchoconstriction, and capillary permeability à Vasoconstriction, bronchodilation, and decrease capillary permeability

Answer 567

Cimetidine – decrease ulcers - Cimetidine (Tagamet) is a histamine H2 receptor antagonist that inhibits stomach acid production & is used as an antacid.

Answer 568

or gastric reflux or GERD (gastric esophageal reflux disease) - Cimetidine & Ranitidine

Answer 569

Dilate blood vessel & lower BP

Answer 570

• Promethazine

Answer 571

promethazine others AVOID

Answer 572

Meperidine (Pethidine, Demerol) - Can cause life-threatening hyperpyrexia reactions (fever)

Answer 573

severe head injury

Answer 574

pentazocine Pentazocine is a synthetically-prepared prototypical mixed agonist–antagonist narcotic (opioid analgesic) Another one is nalbuphine

Answer 575

pentozocaine

Answer 576

C. Sedation and ability to produce dependence

Answer 577

Allergy to Codeine/Oxycodone/Hydrocodone | - give Methadone or Meperidine or Tramadol instead (Group 3 synthetic)

Answer 578

tramadol, methadone, meperidine (demerol), propozyphene, fentanyl

Answer 579

meperidine (an exception)

Answer 580

Secobarbitol or pentobarbital (good for pre-op/anxious kids) - Ketamine is used in emergency situations (good anxiolytic and analgesic at low doses) - Meperidine should not be used in kids

Answer 581

Diuresis (opiates cause urinary retention)

Answer 582

constipation, respiratory depression, euphoria, miosis, coma

Answer 583

hypotension others are withdrawal

Answer 584

hypothermia | rest are withdrawal symptoms

Answer 585

Cold and Clammy skin

Answer 586

Respiratory depression

Answer 587

respiratory depression.

Answer 588

B. Pin-point pupils

Answer 589

constricted pupils and absent/slow breathing

Answer 590

brain, spinal cord and digestive GI tract.

Answer 591

brain, not on stomach receptors!

Answer 592

c. acting as Mu receptor agonists

Answer 593

for Opioid overdose. - Naloxone blocks or reverses the effects of opioid medication, including extreme drowsiness, slowed breathing, or loss of consciousness

Answer 594

(Oxycodone + aspirin)? all opiate antidote is Nalaxone.

Answer 595

No intrinsic activity, High affinity - Intrinsic activity (IA) or efficacy refers to the relative ability of a drug-receptor complex to produce a maximum functional response.

Answer 596

Binds to receptor but lacks intrinsic activity (doesn’t activate receptor)

Answer 597

Fentanyl | - Fentanyl = opioid analgesic given via transdermally patch

Answer 598

alleviate withdrawal from heroine (opiates). - Methadone for detoxification of opioid addicts, give to heroin addicts to decrease withdrawal symptoms - Methadone is a synthetic opioid, analgesic, antitussive, anti-addictive, acts on MU receptors so produces similar effects of opioids but without addictive qualities, receptor antagonist to glutamate. Long 1⁄2 life.

Answer 599

It’s a mixed agonist-antagonist which may | potentiate/increase withdrawal symptoms.

Answer 600

Medulla (bind to opioid receptors in CNS)

Answer 601

(stimulates medullary chemoreceptor trigger zone)

Answer 602

Chemotactic receptor zone (CRZ)

Answer 603

via central action (medulla)

Answer 604

analgesic, antitussive (suppress coughing), anti-diarrheal, anti-hypertensive, anxiolytic, anti-depressant, sedative and hypnotic properties. IT IS ADDICTIVE.

Answer 605

acetaminophen with aspirin - ALLERGY TO CODEINE: can prescribe another opioid from different class: Meperidine or fentanyl for moderate to severe pain or acetaminophen or NSAID for mild pain.

Answer 606

d. Acetaminophen + aspirin

Answer 607

Propoxyphene

Answer 608

use synthetic opioids (meperidine, tramadol) à Demerol (meperidine)

Answer 609

Tylenol #3 has codeine Naproxen

Answer 610

Tylenol #3 (acetaminophen & codeine)

Answer 611

(Tylenol #3)? Increase its activity & increase how long it’s around due to clearance

Answer 612

acetaminophen & hydrocodone works differently, and combining these effects makes it stronger - acetaminophen blocks the binding of protein w/ hydrocodone, so hydrocodone level higher in blood à stronger response - Narcotics work in brain (CNS) while NSAIDS/acetaminophen work in peripheral tissues (PNS) – 2 diff mechanisms complement each other for effective pain reduction

Answer 613

• Hydrocodone

Answer 614

Codeine, tetracycline, benzos - Codeine medication may be harmful to an unborn baby, and could cause breathing problems or addiction/withdrawal symptoms in a newborn.

Answer 615

headache due to increase intracranial pressure.

Answer 616

ABUSE POTENTIAL or dependency potential (addiction)

Answer 617

o Schedule II drugs cannot get a refill. A new prescription must be written!

Answer 618

oxycodone, codeine etc.

Answer 619

2: oxycodone + acetaminophen

Answer 620

2 | acetaminophen + hydrocodone

Answer 621

less than 15 milligrams of hydrocodone per dosage unit (Vicodin®)

Answer 622

less than 90 milligrams of codeine per dosage unit.

Answer 623

all acetaminophen with opioid except for one that was hydrocodone with ibuprofen (vicoprofen)

Answer 624

Aspirin and NSAIDs inhibit platelet cyclooxygenase, thereby blocking the formation of thromboxane A2. - Aspirin irreversibly blocks cyclooxygenase & it’s actions persist for circulating lifetime of platelet. - NSAIDS inhibit cyclooxygenase reversibly & duration of action depends on drug dose/serum levels/half-life.

Answer 625

celebrex, targets just COX-2 | all others both COX-1 and 2

Answer 626

N-acetylcysteine

Answer 627

NAC, N-acethylcysteine-liposome.

Answer 628

hepatotoxicity

Answer 629

Anti-pyretic and analgesic | - Difference: aspirin is anti-inflammatory, common: anti pyretic

Answer 630

Anti-pyretic and analgesic

Answer 631

acetaminophen

Answer 632

Reyes fever and adults, GI problems. If liver problems, give aspirin.

Answer 633

inhibits platelet aggregation

Answer 634

inactivate cyclooxygenase à decreased prostaglandin synthesis

Answer 635

stopping the local signal production and transduction

Answer 636

CELEBREX (Selective NSAID - Cox 2 inhibitor only) | - Cox 2 does not increase bleeding time and less platelet adhesion.

Answer 637

Celebrex (Celecoxib)

Answer 638

b) Is it necessary to stop? No c) For long will the platelets be inhibited? 5-7days - aspirin stays in body for 7 days.

Answer 639

Cyclo-ox pathway

Answer 640

Inhibits thromboxane A2, preventing platelet synthesis | - aspirin affects bleeding time

Answer 641

Take acetaminophen. DO NOT take ibuprofen.

Answer 642

b. Demerol - narcotic w/out aspirin pentazocine is with aspirin

Answer 643

• ceiling analgesia at 400mg

Answer 644

contraindication

Answer 645

Acidosis and increased bleeding time | - Causes acidosis since acetylsalicylic acid is aspirin. It’s an acid & 3g daily is a lot!

Answer 646

NSAID that inhibits prostaglandin synthesis (competitive non-selective cox inhibit).

Answer 647

acetaminophen - The other drugs are NSAIDS and they affect the kidney in a more negative way. This drug affects the liver and causes liver toxicity.

Answer 648

increases with use of NSAIDS or penicillin

Answer 649

Tylenol 325mg

Answer 650

- For pregnant- only give Tylenol- NOTHING WITH CODEINE

Answer 651

Tylenol | - Asthmatic only use Tylenol (not aspirin bc of hypervent)

Answer 652

Naproxen --- a nonselective COX | inhibitor—NSAID

Answer 653

DDI w/ aspirin antiplatelet activity

Answer 654

• Difluzole (vaginal candidiasis medication)

Answer 655

physiological antagonist of - Doesn’t act on same mechanism (epi = α vasoconstriction vs nitro = smooth muscle dilatator) but opposing action - Same mechanism = competive antagonist; physiological antagonist = competing physicological effects

Answer 656

Increase in polarity, more ionized and more water soluble - Whatever helps its excretion – polar and more water soluble

Answer 657

more ionized in plasma (more water soluble)

Answer 658

more ionic

Answer 659

All drugs or alcohol (Phenobarbitals) | - Excretion of acidic drugs is accelerated with sodium bicarbonate

Answer 660

Sodium bicarbonate

Answer 661

More water soluble and less lipid soluble.

Answer 662

enzymatic degradation in the liver prior to drug reaching its site of action

Answer 663

enterohepatic circulation, metabolism in liver

Pharm Flashcards

(928 cards)