Kaplan Comlex Pharmacology

Front 1

Which form of drug is water soluble: ionized or nonionized?

Back 1

water soluble=ionized

Front 2

Which form of drug is lipid soluble: ionized or nonionized?

Back 2

lipid soluble=nonionized

Front 3

Which form of drug can cross biomembranes: ionized or nonionized?

Back 3

nonionized

Front 4

Which form of drug is better renally excreted: ionized or nonionized?

Back 4

ionized (water soluble)

Front 5

Which form of drugs become "trapped" in the filtrate: ionized or nonionized?

Back 5

ionized (nonionized are secreted or reabsorbed)

Front 6

What does it mean to acidify urine?

Back 6

increase ionization of weak bases to increase renal elimination

Front 7

What does it mean to alkalinized urine?

Back 7

increase ionization of weak acids to increase renal elimination

Front 8

What is primarily used to acidify urine? What is primarily used to alkalinize urine?

Back 8

1. acidify=NH4Cl or cranberry juice
2. alkalinize=NaHCO3 or acetazolamide

Front 9

T of F: only free, unbound drug is filtered.

Back 9

true

Front 10

ASA is a typical weak acid with a pKa of 3. If pH<pKa, is ASA mostly ionized or nonionized?

Back 10

nonionized

Front 11

Quinidine is a typical weak base. In an acid environment, will most of quinidine be ionized or nonionized?

Back 11

ionized (a base can accept H+ ions, whereas an acid can donate H+ ions)

Front 12

What is the term for the measure of the fraction of a dose that reaches the systemic circulation?

Back 12

bioavailability

Front 13

What is the formula for bioavailability?

Back 13

f=AUC po/AUC iv

Front 14

What 2 factors must be present for bioequivalence between 2 drugs?

Back 14

same bioavailability and same rate of absorption

Front 15

If the rate of absorption of a drug increases, what happens to the Tmax and Cmax?

Back 15

T max decreases and Cmax increases

Front 16

What molecules help to distribute drugs from systemic circulation to organs and tissues?

Back 16

plasma proteins (e.g. albumin)

Front 17

The BBB is only permeable to _____-soluble drugs.

Back 17

lipid

Front 18

What is the formula for the Volume of Distribution (Vd)?

Back 18

Vd=dose/concentration at zero time

Front 19

For a 70 kg mane, what is the typical plasma volume? Blood volume? ECF volume? TBW volume?

Back 19

1. 3 L
2. 5 L
3. 12-14 L
4. 40-42 L

Front 20

If the Vd is low, will there be a low or high percentage of drug bount to plasma proteins?

Back 20

high

Front 21

In the examples on page 9, what 2 drugs can displace digoxin from tissue-binding sites?

Back 21

verapamil and quinidine

Front 22

Thiopental is an IV anesthetic that has a short duration of action despite having a long half-life. Why?

Back 22

it is distributed to the brain rapidly, but it also diffuses away rapidly, redistributing into other tissues

Front 23

What is another term for biotransformation?

Back 23

metabolism

Front 24

What is the main purpose for metabolism?

Back 24

ionize the drug for excretion

Front 25

What is significant about the metabolism of benzodiazepines?

Back 25

they metabolize to nordiazepam, which is an active metabolite

Front 26

Phase I microsomal metabolism involves what major enzyme system?

Back 26

Cytochrome P450 enzymes

Front 27

What are the two absolute requirements for P450's?

Back 27

molecular oxygen and NADPH

Front 28

Phase I nonmicrosomal metabolism involves what 3 methods?

Back 28

hydrolysis, monamine oxidases, and ETOH metabolism

Front 29

T or F: some patients lack the enzymes to metabolize succinylcholine.

Back 29

true

Front 30

Phase II metabolism is defined as what?

Back 30

conjugation with endogenous compounds

Front 31

What are the 4 methods of Phase II metabolism?

Back 31

glucuronidation, acetylation, sulfation, and glutathione conjugation

Front 32

What do monoamine oxidases metabolize?

Back 32

dopamine, norepinephrine, serotonin, and tyramine

Front 33

Which has reduced activity in neonates, Phase I or Phase II metabolism?

Back 33

Phase II

Front 34

What are the 3 drugs that can induce SLE?

Back 34

HIP drugs: hydralazine, procainamide, and isoniazid

Front 35

What are the general CYP450 inducers?

Back 35

anticonvulsants (barbiturates, phenytoin, carbemazepine), antibiotics (rifampin), chronic ETOH, and glucocorticoids

Front 36

What are the general CYP450 inhibitors?

Back 36

antiulcer meds (cimetidine, omeprazole), antibiotics (chloramphenicol, macrolides, ritonavir, ketoconazole), acute ETOH, grapefruit juice

Front 37

In zero order elimination, what happens?

Back 37

elimination rate is constant, half-life is variable

Front 38

In first order elimination, what happens?

Back 38

elimination rate is variable, half-life is constant (First=halF liFe)

Front 39

Most drugs follow first order elimination, what are 3 examples that are zero order elimination?

Back 39

ETOH, phenytoin, and salicylates

Front 40

What is the formula for rate of elimination?

Back 40

GFR + secretion - reabsorption

Front 41

Why is inulin clearance used to estimate GFR?

Back 41

it is not reabsorbed or secreted

Front 42

What is a normal GFR?

Back 42

120 mL/min

Front 43

The volume of blood cleared of drug per unit of time is the definition of what?

Back 43

clearance

Front 44

When does clearance=GFR?

Back 44

when there is no reabsorption, secretion, or plasma protein binding

Front 45

95% steady state is normally reached in how many half-lives?

Back 45

4-5

Front 46

How many half-lives are required to reach mathematical steady state?

Back 46

7

Front 47

90% of steady state is reached in how many half-lives?

Back 47

3.3

Front 48

What is the formula for loading dose?

Back 48

LD=Css x Vd

Front 49

If doses are given at each half-life, and MEC=Css, then the loading dose is what?

Back 49

2x the maintenance dose

Front 50

What is the formula for half-life?

Back 50

0.7/k (k=elimination constant)

Front 51

What is the formula for clearance?

Back 51

k x Vd (k=elimination constant)

Front 52

What is the formula for infusion rate?

Back 52

Cl x Css

Front 53

What is the formula for maintenance dose?

Back 53

Cl x Css x dosing interval

Front 54

What does k0 mean?

Back 54

infusion rate

Front 55

Pharmacokinetics or pharmacodynamics: which involves the actions of the drug on the body? Which involves the actions of the body on the drug?

Back 55

1. pharmacodynamics
2. pharmacokinetics

Front 56

T or F: affinity is directly related to the Kd of a drug.

Back 56

false-inversely related

Front 57

Pindolol and buspirone are examples of what kind of drugs?

Back 57

partial agonists

Front 58

Which will cause a parallel shift to the right in the D-R curve for agonists?

Back 58

competitive antagonists

Front 59

T or F: competitive antagonists can not be reversed by dose of the agonist drug.

Back 59

false

Front 60

Which will cause a nonparallel shift to the right in the D-R curve for agonists?

Back 60

noncompetitive antagonists

Front 61

Which will decrease efficacy of the agonist: competitive or noncompetitive antagonists?

Back 61

noncompetitive antagonists

Front 62

The median effective dose in 50% of the population is called what?

Back 62

ED50

Front 63

The median toxic dose of a drug that causes toxicity in 50% of the population is called what?

Back 63

TD50

Front 64

Briefly explain how intracellular receptors work.

Back 64

drug binds intracellular receptors, dimerizes drug-receptor complex, translocates to nucleus, leads to changes in gene expression

Front 65

What are some examples of drugs or hormones that work via intracellular receptors?

Back 65

thyroid hormones, steroids, and vitamin D

Front 66

Briefly explain how Gs/Gi protein coupling signaling works.

Back 66

Gs/Gi proteins are bound to AC, which converts ATP to cAMP, which activates pkA, which causes downstream phosphorylation

Front 67

Briefly explain how Gq protein coupling signaling works.

Back 67

Gq proteins are bound to phospholipase C, which releases IP3 and DAG, IP3 releases Ca++ from SR, DAG activates pkC, which causes downstream phosphorylation

Front 68

What receptors are influenced by Gs proteins (stimulatory)?

Back 68

beta-1, beta-2, and dopamine-1 subtype

Front 69

What receptors are influenced by Gi proteins (inhibitory)?

Back 69

M-2, alpha-2, dopamine-2 subtype

Front 70

What receptors are influenced by Gq proteins?

Back 70

M-1, M-3, alpha-1

Front 71

Briefly explain cyclic GMP and NO signaling.

Back 71

NO in endothelial cells diffuses into smooth muscle, activates guanylyl cyclase, increases cGMP, causes vasodilation

Front 72

What 2 endogenous compounds act via NO?

Back 72

bradykinin and histamine

Front 73

Transmembrane enzymes mediate the first steps in signaling by what two hormones?

Back 73

insulin and growth factors (EGF and PDGF)

Front 74

Briefly describe how transmembrane enzymes work.

Back 74

transmembrane enzymes bind to ligand, cause conformational changes, tyrosine kinase dimerizes and is activated, downstream phosphorlyation occurs

Front 75

What drugs are listed as category X?

Back 75

statins, OCP's, clomiphene, misoprostol, vitamin A, phenytoin, belladonic acid

Front 76

When can you use a category D drug on a pregnant patient?

Back 76

when the benefits to the mother outweight the detriments to the fetus

Front 77

What do category B drugs mean?

Back 77

either the drug is negative on animal studies and there are human studies; or the drug is positive on animal studies, but not in human studies

Front 78

What do category C drugs mean?

Back 78

no human studies and either a positive animal study or no animal studies

Front 79

T or F: category X drugs may be given to pregnant patients if the benefits outweigh the costs.

Back 79

false, these are absolutely contraindicated

Front 80

T or F: the ganglia of the PNS lies in the two paraventral chains adjacent to the vertebral column.

Back 80

false, the PNS ganglia are in the organs themselves

Front 81

When dopamine binds to D1 receptors, what happens in renal and mesenteric vascular beds?

Back 81

vasodilation

Front 82

What is the formula for BP?

Back 82

TPR x CO

Front 83

What specific receptors cause increased TPR? Decreased TPR?

Back 83

alpha-1-receptors; beta-2-receptors

Front 84

What drugs can block a reflex bradycardia? Reflex tachycardia?

Back 84

muscarinic antagonist; beta-1-antagonist

Front 85

T or F: hormonal feedback loop BP control is only affected by decreases in BP.

Back 85

true

Front 86

Pupil size is controlled by which receptors?

Back 86

M3 and alpha-1

Front 87

What happens during adrenergic stimulation of the pupillary muscles?

Back 87

adrenergic stimulation targets alpha-1 receptors in the radial eye muscle, causing it to contract, which then pulls the pupil open (mydriasis)

Front 88

What happens during muscarinic stimulation of the pupillary muscles?

Back 88

muscarinic stimulation targets M3 receptors in the sphincter eye muscle, causing it to contract, which then contracts the pupil (miosis)

Front 89

Why is an alpha-1-agonist preferred over a m-blocker to cause mydriasis?

Back 89

the alpha-1-agonist will cause pupil dilation only; they m-blocker will also cause cycloplegia (paralysis of accomodation), which is an unwanted side effect

Front 90

What is the effect of muscarinic drugs on lens accomodation? What muscle is affected?

Back 90

muscarinic drugs will cause accomodation to near vision, m-blockers will cause accomodation to far vision, which is cycloplegia; these act on the ciliary muscle of the eye

Front 91

Choline uptake into the presynaptic terminal is inhibited by what?

Back 91

hemicholinium

Front 92

Where does botulinum toxin cause its effects in the cholinergic neuron?

Back 92

it prevents ACh release from the presynaptic membrane

Front 93

What happens when ACh binds with a presynaptic ACh autoreceptor?

Back 93

it produces a negative feedback effect

Front 94

What are 6 reversible AChE inhibitors?

Back 94

edrophonium, physostigmine, neostigmine, pyridostigmine, donepezil, tacrine

Front 95

What are 3 irreversible AChE inhibitors?

Back 95

echothiophate, malathion, and parathion

Front 96

T or F: M-receptor agonists and antagonists are site specific.

Back 96

false

Front 97

Which M-receptors are found in the eye? What are the effects?

Back 97

M3; miosis and near vision accomodation

Front 98

Which M-receptors are found in the heart? What are the effects?

Back 98

M2; decrease HR and conduction velocity

Front 99

Which M-receptors are found in the lungs? What are the effects?

Back 99

M3; contraction and secretion

Front 100

Which M-receptors are found in the stomach? What are the effects?

Back 100

M3; increased motility (cramps)

Front 101

Which M-receptors are found in GI glands? What are the effects?

Back 101

M1; secretion

Front 102

Which M-receptors are found in the intestines? What is the effect?

Back 102

M3; contraction (diarrhea, incontinence)

Front 103

Which M-receptors are found in the bladder? What is the effect?

Back 103

M3; detrusor contraction, trigone relaxation (voiding, incontinence)

Front 104

Which M-receptors are found in sphincters? What is the effect?

Back 104

M3; relaxation except for LES, which will contract

Front 105

Which M-receptors are found in glands? What is the effect?

Back 105

M3; secretion (thermal sweating, salivation, lacrimation)

Front 106

Which M-receptors are found in blood vessels? What is the effect?

Back 106

M3; dilation (via NO)

Front 107

Which cholinergic receptors are Gq coupled? What is the sequence of events?

Back 107

M1 and M3; increased phospholipase C->increased IP3, DAG, Ca++

Front 108

Which cholinergic receptors are Gi coupled?

Back 108

M2; decreased AC->decreased cAMP

Front 109

Why is ACh not used clinically?

Back 109

broken down too quickly by AChE

Front 110

What are 3 direct-acting cholinomimetics?

Back 110

bethanechol, methacholine, and pilocarpine

Front 111

What is bethanechol used for clinically?

Back 111

postop ileus and urinary retention (causes voiding)

Front 112

What is methacholine used for clinically?

Back 112

diagnose bronchial hyperreactivity (response to low dose shows hyperreactive airway)

Front 113

What is pilocarpine used for clinically?

Back 113

glaucoma (causes miosis), xerostomia

Front 114

T or F: pilocarpine is broken down by AChE.

Back 114

false

Front 115

T or F: the reason bethanechol is used for ileus and urinary retention is because it has a long half-life because it is not broken down by AChE.

Back 115

true

Front 116

What does the tensilon test refer to? What is this drug and what are it's clinical uses?

Back 116

edrophonium (tensilon) is used to diagnose MG

Front 117

What is physostigmine used for clinically?

Back 117

glaucoma and antidote for atropine overdose

Front 118

What is neostigmine and pyridostigmine used for clinically?

Back 118

ileus, urinary retention, MG (long term), reversal of NM blockers

Front 119

What are donepezil and tacrine used for clinically?

Back 119

Alzheimer disease

Front 120

What is echothiophate used for clinically?

Back 120

glaucoma

Front 121

What does "DUMBBELSS" stand for?

Back 121

AChE inhibitor poisoning: diarrhea, urination, miosis, bradycardia, bronchoconstriction, excitation, lacrimation, salivation, and sweating

Front 122

What is used for symptom control in organophosphate poisoning (due to AChE toxicity)? What is the antidote?

Back 122

atropine is used for symptom control; 2-PAM is used to regenerate AChE and is the actual antidote

Front 123

How long do you have to give 2-PAM after organophosphate poisoning?

Back 123

2 hours (must break phosphate bonds before they become permanent)

Front 124

What will chronic toxicity of AChE inhibitors cause? What causes this?

Back 124

peripheral neuropathy; paraoxon/malaoxon metabolites

Front 125

What are 6 M blockers?

Back 125

atropine, tropicamide, ipratropium, scopolamine, benztropine, and trihexyphenidyl

Front 126

What is atropine used for clinically?

Back 126

antispasmodic, antisecretory (pre-op), AChE inhibitor OD, antidiarrheal, ophthalmology

Front 127

What is tropicamide used for clinically?

Back 127

ophthalmology (topical)

Front 128

What is ipratropium used for clinically?

Back 128

asthma and COPD

Front 129

What is scopolamine used for clinically?

Back 129

motion sickness, causes sedation and short-term memory loss

Front 130

What are benztropine and trihexyphenidyl used for clinically?

Back 130

parkinsonism; acute extrapyramidal symptoms from antipsychotics

Front 131

In tissues with dual innervation (SA/AV nodes, pupil, GI/GU muscles, sphincters), which is normally dominant: PNS or SNS?

Back 131

PNS

Front 132

What is the rate-limiting step of NE synthesis?

Back 132

tyrosine converts to DOPA via tyrosine hydroxylase

Front 133

T or F: MAO inactivates NE stored in presynaptic granules.

Back 133

false; it inactivates NE in the mobile pool

Front 134

What percent of NE is reuptaken to the presynaptic junction?

Back 134

60%

Front 135

If a drug exerts both beta and alpha effects, which is predominant in low doses? High doses?

Back 135

beta; alpha

Front 136

What causes rapid inactivation of NE accumulated in target cells?

Back 136

COMT

Front 137

Which adrenergic receptor acts as a negative feedback mechanism for presynaptic terminals?

Back 137

alpha-2

Front 138

Where are alpha-1 receptors located? Generally speaking, what is the overall action?

Back 138

eye (mydriasis), arterioles, veins, bladder trigone and sphincter (retention), male sex organs (ejaculation), liver (increased glycogenolysis), kidney (decreased renin); contraction

Front 139

Where are the alpha-2 receptors located? What is their action?

Back 139

prejunctional nerve terminals (decrease NE), platelets (aggregation), pancreas (decreased insulin)

Front 140

Where are the beta-1 receptors located? What is their action?

Back 140

heart (increased chronotropy, inotropy, and dromotropy (conduction velocity)) and kidneys (increased renin release)

Front 141

Where are the beta-2 receptors located? What is their action?

Back 141

blood vessels (vasodilation), uterus (relaxation), bronchioles (dilation), skeletal muscle (increased glycogenolysis), liver (increased glycogenolysis), pancreas (increased insulin)

Front 142

Where are D1 receptors located in the periphery? What is their effect?

Back 142

renal (increased RBF, GFR, and Na secretion), mesenteric and coronary vasculature (vasodilation)

Front 143

What is the mechanism for alpha-1 receptors? What is the signaling protein?

Back 143

Gq: increased phospholipase C->increased IP3, DAG, and Ca

Front 144

What is the mechanism for alpha-2 receptors? What is the signaling protein?

Back 144

Gi: decreased AC->decreased cAMP

Front 145

What is the mechanism for beta-1, beta-2, and D1 receptors? What is the signaling protein?

Back 145

Gs: increased AC->increased cAMP

Front 146

What are 2 alpha-1 agonists and what are they used for clinically?

Back 146

phenylephrine (nasal decongestant and mydriatic); methoxamine (paroxysmal atrial tachycardia)

Front 147

What are 2 alpha-2 agonists and what are they used for clinically?

Back 147

clonidine (binds alpha-2 receptor to decrease NE) and methyldopa (acts as false NT); both reduce HTN

Front 148

What are 2 non-selective beta agonists and what are they used for clinically?

Back 148

isoproterenol (B1=B2) used for bronchospasm, heart block, and bradyarrhythmias; and dobutamine (B1>B2) used for CHF

Front 149

What are 4 selective beta-2 agonists and what are they used for clinically?

Back 149

salmeterol, albuterol, and terbutaline (asthma); ritodrine (premature labor)

Front 150

Which adrenergic receptor has potential reflex bradycardia?

Back 150

alpha-1 receptors (either from alpha-1 agonists or high dose EPI)

Front 151

NE affects which receptors?

Back 151

alpha-1 and beta-1 (not beta-2)

Front 152

EPI affects which receptors at low dose? At high dose?

Back 152

low: beta-1 and beta-2; high: beta-1, beta-2, and alpha-1 (acts like NE)

Front 153

How do you differ EPI vs NE HTN?

Back 153

administer an alpha-1-blocker; this will block alpha-1 receptor mediated HTN; this will then uncover the hypotension caused by the beta-2 stimulation

Front 154

What is methylphenidate used for clinically? How does it work?

Back 154

narcolepsy and ADHD; central release of DA, NE, and 5HT

Front 155

Where does MAO-A work mainly? Where does MAO-B work mainly?

Back 155

A=anywhere (mostly liver); B=brain

Front 156

What will happen if a patient taking MAOI's has too much red wine or cheese?

Back 156

hypertensive crisis

Front 157

What are alpha-blockers used for clinically?

Back 157

HTN, pheochromocytoma (nonselective), and BPH (selective)

Front 158

What are the 2 major AE's of alpha receptor antagonists?

Back 158

reflex tachycardia and salt/water retention

Front 159

How are phentolamine and phenoxybenzamine the same? How are the different?

Back 159

both are nonselective alpha-blockers; phentolamine is a competitive inhibitor, phenoxybenzamine is a noncompetitive inhibitor

Front 160

What are 4 selective alpha-1 blockers?

Back 160

prazosin, doxazosin, terazosin, and tamsulosin

Front 161

What are 4 indirect acting adrenergic receptor activators?

Back 161

amphetamine, cocaine, ephedrine, tyramine

Front 162

What are 2 selective alpha-2 blockers and what are they used for clinically?

Back 162

yohimbine (postural hypotension and impotence) and mirtazapine (antidepressant)

Front 163

T or F: beta blockers will not mask the tachycardia typically seen in hypoglycemia.

Back 163

false, it will mask the tachycardia

Front 164

What are the effects of a beta-1 blockade?

Back 164

decreased HR/SV/CO, decreased renin, decreased aqueous humor production

Front 165

What are the effects of a beta-2 blockade?

Back 165

blocks glycogenolysis, gluconeogenesis, increases LDL's and TG's

Front 166

Which beta blocker is the only one that won't raise lipids?

Back 166

acebutolol

Front 167

What are the cardioselective beta-1 blockers?

Back 167

acebutolol, atenolol, and metoprolol

Front 168

What are the nonselective beta blockers?

Back 168

pindolol, propranolol, and timolol

Front 169

T or F: you must ween a patient off of beta-blockers.

Back 169

true, otherwise you might get cardiovascular rebound effects

Front 170

How are beta-blockers used clinically?

Back 170

angina, HTN, post-MI, antiarrhythmics, glaucoma, migraines, thyrotoxicosis, performance anxiety, essential tremor

Front 171

Which beta blockers are specifically antiarrhythmics?

Back 171

class II: propranolol, acebutolol, and esmolol

Front 172

Which beta blocker is specific to glaucoma treatment?

Back 172

timolol

Front 173

Which beta blocker is specific to essential tremor treatment?

Back 173

propranolol

Front 174

What are 3 symptoms of thyroid storm?

Back 174

anxiety, chest pain, tremors

Front 175

What are 2 combo alpha-1 and beta blockers? What are they used for clinically?

Back 175

labetalol and carvedilol; CHF

Front 176

What drug has combo of K+ channel and beta blocking activity? What is it used for clinically?

Back 176

sotalol; Class III antiarrhythmic

Front 177

Which is painless and results in progressive visual loss: open-angle or closed-angle glaucoma?

Back 177

open-angle (closed angle is emergent and painful)

Front 178

What is the main problem in open-angle glaucoma?

Back 178

decreased reabsorption of aqueous humor

Front 179

What is the main problem in closed-angle glaucoma?

Back 179

blockade of the canal of Schlemm

Front 180

What is the treatment for open-angle glaucoma?

Back 180

beta blockers (decrease fluid formation) and muscarinic agonists (improves drainage through canal of Schlemm)

Front 181

What is the treatment for closed-angle glaucoma?

Back 181

emergent treatment: cholinomimetics, carbonic anhydrase inhibitors, and mannitol; surgery is definitive treatment

Front 182

How does timolol work to treat glaucoma?

Back 182

blocks NE at ciliary epithelium to decrease aqueous humor production

Front 183

Which 2 beta blockers are used to treat glaucoma? How do they work?

Back 183

pilocarpine and echothiophate; m-receptor activation contracts ciliary muscle, opens flos through canal of Schlemm

Front 184

What occurs during phase 0 of the cardiac muscle/His-Purkinje system AP?

Back 184

fast Na channels open, Na influx causes depolarization

Front 185

What antiarrhythmics work to delay phase 0 of the cardiac muscle/His-Purkinje system AP?

Back 185

class I

Front 186

What occurs during phase 1 of the cardiac muscle/His-Purkinje system AP?

Back 186

fast Na channels close, K efflux and Cl influx

Front 187

What occurs during phase 2 of the cardiac muscle/His-Purkinje system AP?

Back 187

plateau phase, slow Ca influx is balanced by K efflux (delayed rectifier current)

Front 188

What occurs during phase 3 of the cardiac muscle/His-Purkinje system AP?

Back 188

repolarization, delayed rectifier K efflux increases, Ca influx stops

Front 189

What antiarrhythmics work to delay phase 3 of the cardiac muscle/His-Purkinje system AP?

Back 189

class III

Front 190

The slow Na current prolongs the duration of the cardiac muscle/His-Purkinje system AP. What phases does this affect?

Back 190

phases 0-3

Front 191

What occurs during phase 4 of the cardiac muscle/His-Purkinje system AP?

Back 191

return to resting membrane potential

Front 192

T or F: the more negative the resting potential, the slower the response.

Back 192

false, the more negative the resting potential, the faster the response

Front 193

What occurs during phase 0 of the nodal AP?

Back 193

Ca influx via L-type Ca channels

Front 194

What antiarrhythmics work on phase 0 of the nodal AP?

Back 194

class IV

Front 195

What occurs during phase 3 of the nodal AP?

Back 195

K efflux begins during phase 0, overcomes Ca influx, Ca channels close during phase 3

Front 196

What occurs during phase 4 of the nodal AP?

Back 196

inward Na I-sub-f and Ca currents, outward K current

Front 197

What antiarrhythmics work on phase 4 of the nodal AP?

Back 197

class II and IV

Front 198

Why is does the effective refractory period last into late stage 3 of the AP?

Back 198

Na channels are inactive and not in the ready state

Front 199

When is the relative refractory period usually present?

Back 199

phase 3 and phase 4

Front 200

The ERP/APD ratio should usually be what?

Back 200

0.85

Front 201

T or F: class I drugs are most active when Na channels are in the resting state.

Back 201

false, they are least active during this time

Front 202

Beta blockers are what class antiarrhythmics?

Back 202

class II

Front 203

Is cAMP proportionate or inversely proportionate to HR?

Back 203

proportionate (cAMP increases in beta-1 agonism, cAMP decreases in M2 agonism)

Front 204

Generally speaking, what are the classes of antiarrhythmics?

Back 204

Class 1: Na channel blockers, Class 2: beta blockers,
Class 3: K channel blockers
Class 4: Ca channel blockers

Front 205

Which Na channels do Class I antiarrhythmics block?

Back 205

fast Na channels

Front 206

What differs Class I antiarrhythmics?

Back 206

rate of recovery from blockade: IA intermediate, IB very fast, IC very slow

Front 207

What will Class IA antiarrhythmics increase?

Back 207

APD and ERP

Front 208

In addition to fast Na channels, Class IA antiarrhythmics will block what other channels?

Back 208

K channels

Front 209

What 2 drugs are Class IA antiarrhythmics?

Back 209

quinidine and procainamide

Front 210

What is quinidine used for clinically?

Back 210

many arrhythmias

Front 211

What are major AE's of quinidine?

Back 211

1. M2 blockade
2. alpha-1-blockade w/reflex tachycardia
3. cinchonism
4. prolonged QT interval

Front 212

What drug will have a major reaction with quinidine?

Back 212

digoxin (increases serum digoxin by displacing it from tissue binding sites)

Front 213

What makes procainamide better than quinidine for many arrythmias?

Back 213

less muscarinic and alpha blockade

Front 214

What are the major AE's of procainamide?

Back 214

SLE-like syndrome and prolonged QT interval

Front 215

What other Class IA antiarrhythmic is there besides procainamide and quinidine? Why is this not preferable?

Back 215

disopyramide (more antimuscarinic effects)

Front 216

What are 3 Class IB antiarrhythmics?

Back 216

lidocaine, mexiletine, and tocainide

Front 217

What tissues do Class IB antiarrhythmics work best on? What will they do to the APD and ERP?

Back 217

depolarized, ischemic tissue; decreased

Front 218

What arrhythmia will lidocaine not work on?

Back 218

a-fib or a-flutter (these are structural defects, not from ischemia)

Front 219

What is lidocaine used for clinically?

Back 219

1. post-MI
2. open-heart surgery
3. vtach/vfib

Front 220

Since lidocaine is the least cardiotoxic antiarrhythmic, what are the main AE's to worry about?

Back 220

1. CNS toxicity
2. must be given IV because of first pass metabolism

Front 221

What is the main difference between lidocaine and mexiletine/tocainide?

Back 221

mexiletine/tocainide are PO drugs

Front 222

What are 2 Class IC antiarrhythmics?

Back 222

flecainide and propafenone

Front 223

What would be the major indication for flecainide? When is it contraindicated?

Back 223

a-fib "pocket pill"; won't cause torsades; any cardiac structural abnormalities

Front 224

What Class III drugs are specifically mentioned in COMLEX?

Back 224

propranolol (nonselective); acebutolol and esmolol (cardioselective)

Front 225

When do you use beta-blockers as antiarrhythmics?

Back 225

1. post-MI
2. SVT's (esmolol for acute SVT's)

Front 226

What are 2 Class III antiarrhythmics? What portion of the AP does amiodarone work on?

Back 226

amiodarone and sotalol; phase 3 (blocks K, but also Na, Ca, alpha and beta)

Front 227

T or F: class III antiarrhythmics decrease APD and ERP.

Back 227

false

Front 228

What is the half-life of amiodarone?

Back 228

80 days

Front 229

What are 3 important AE's of amiodarone?

Back 229

1. pulmonary fibrosis
2. smurf skin
3. thyroid dysfunction

Front 230

T or F: amiodarone can not be used to treat HF.

Back 230

false, it is the only Class III antiarrhythmic that can be used to treat HF

Front 231

What is the advantage and disadvantage of using dronedarone instead of amiodarone?

Back 231

no thyroid problems, but can't be used in HF

Front 232

How do you treat torsades?

Back 232

1. correct hypokalemia
2. correct hypomagnesemia
3. discontinue any drugs causing it (class IA and III)
4. try to shorten APD with isoproterenol

Front 233

What does sotalol block? What is it used to treat?

Back 233

beta-1; life-threatening ventricular arrhythmias

Front 234

T or F: APD and ERP are increased with amiodarone.

Back 234

true

Front 235

What are the 2 Class IV antiarrhythmics?

Back 235

verapamil and diltiazem

Front 236

What phases of the AP do Class IV antiarrhythmics block?

Back 236

phase 0 and phase 4 (slows nodal activity)

Front 237

What are Class IV antiarrhythmics used for?

Back 237

supraventricular tachycardias

Front 238

What are the major AE's of Class IV antiarrhythmics?

Back 238

constipation (also dizziness, flushing, hypotension, AV block); has additive effect with beta blockers or digoxin

Front 239

Adenosine is DOC for what?

Back 239

paroxysmal supraventricular tachycardias and AV nodal arrhythmias

Front 240

What can be used to antagonize adenosine?

Back 240

theophylline

Front 241

How does adenosine work?

Back 241

binds to adenosine receptors, causes Gi-coupled decrease in cAMP

Front 242

What drugs can cause torsades?

Back 242

Class IA and III antiarrhythmics, TCA's, and antipsychotics

Front 243

What are the 2 alpha-2-agonists used in HTN?

Back 243

clonidine and methyldopa

Front 244

What alpha-2-agonist is used in HTN management in pregnancy?

Back 244

methyldopa

Front 245

Which alpha-2-agonist is used in opiate withdrawal?

Back 245

clonidine

Front 246

What drugs can decrease the antihypertensive effects of alpha-2-agonists?

Back 246

TCA's

Front 247

What are 3 AE's of alpha-2-agonists?

Back 247

1. positive coomb's (methlydopa)
2. CNS depression
3. edema

Front 248

What are 3 alpha-1-antagonists that can be used to treat mild HTN?

Back 248

prazosin, doxazosin, and terazosin

Front 249

What are 2 AE's of alpha-1-antagonists?

Back 249

first dose syncope and urinary incontinence (because it decreases tone of urinary sphincters)

Front 250

What is 1 advantage of using alpha-1-antagonists for mild HTN?

Back 250

raises HDL's, lowers LDL's

Front 251

What are some AE's of beta blockers?

Back 251

1. fatigue
2. sexual dysfunction
3. increased LDL's and TG's

Front 252

What are 2 drugs that act directly through NO?

Back 252

hydralazine and nitroprusside

Front 253

How do hydralazine and nitroprusside differ in their MOA's?

Back 253

hydralazine works by arteriolar vasodilation; nitroprusside works by arteriolar and venule vasodilation

Front 254

What are hydralazine and nitroprusside used for clinically?

Back 254

hypertensive urgency/emergency

Front 255

What are the major AE's of hydralazine?

Back 255

1. SLE-like syndrome
2. reflex tachycardia

Front 256

What is the major AE of nitroprusside?

Back 256

cyanide toxicity

Front 257

If cyanide toxicity occurs due to nitroprusside, what is the treatment?

Back 257

amyl nitrate/sodium nitrate will change hemoglobin to methemoglobin, which will outcompete cytochrome oxidase for CN binding; cyanomethemoglobin is formed; this is followed by sodium thiosulfate, which will convert cyanomethemoglobin to methemoglobin, and also creates thiocyanate (less toxic) instead of CN

Front 258

How does minoxidil work?

Back 258

opens K channels, hyperpolarizes smooth muscle, results in arteriolar vasodilation

Front 259

What is minoxidil used for clinically?

Back 259

1. hypertensive emergencies
2. severe HTN
3. baldness

Front 260

What is the sister drug of minoxidil?

Back 260

diazoxide

Front 261

What is the major AE of minoxidil? Diazoxide?

Back 261

1. hypertrichosis
2. hyperglycemia due to decreased insulin release
3. reflex tachycardia (both)

Front 262

How do CCB's work?

Back 262

block L-type Ca channels in heart and blood vessels, results in decreased intracellular Ca

Front 263

What are the 2 non-DHP's of the CCB's?

Back 263

verapamil and diltiazem

Front 264

What are the effects of CCB's?

Back 264

non-DHP's will decrease CO and TPR; DHP's will only decrease TPR

Front 265

What are CCB's used for clinically?

Back 265

1. HTN
2. angina
3. antiarrhythmics (non-DHP's)

Front 266

What are 2 AE's of DHP's?

Back 266

1. gingival hyperplasia
2. reflex tachycardia

Front 267

What is the major AE of verapamil?

Back 267

constipation (changes GI tone)

Front 268

What suffix indicates that a drug is a CCB (DHP)?

Back 268

-dipine

Front 269

In addition to converting angiotensin I to angiotensin II, what other function does ACE have?

Back 269

converting bradykinin to its inactive form

Front 270

How do ACEI's work?

Back 270

1. blocks ACE, which blocks formation of angiotensin II to prevent aldosterone secretion and vasoconstriction
2. blocks inactivation of bradykinin to allow vasodilation

Front 271

What suffix indicates that a drug is an ACEI?

Back 271

-pril

Front 272

What suffix indicates that a drug is an ARB?

Back 272

-sartan

Front 273

ACEI's block formation of angiotensin II. What do ARB's block?

Back 273

AT1 receptors

Front 274

T or F: ARB's will interfere with bradykinin, but ACEI's will not.

Back 274

false, the reverse is true

Front 275

What is the only renin inhibitor? What does it block?

Back 275

aliskerin; blocks renin, which blocks formation of antiotensin I

Front 276

What is the term for rapid swelling in the nose, mouth, throat, glottis, larynx, lips, and/or tongue?

Back 276

angioedema

Front 277

What are the 3 uses of ACEI's?

Back 277

1. mild/moderate HTN
2. protect against diabetic nephropathy
3. CHF

Front 278

What are 4 AE's or ACEI's?

Back 278

1. dry cough
2. hyperkalemia
3. acute renal failure
4. angioedema

Front 279

What are 2 contraindications to using ACEI's?

Back 279

1. pregnancy
2. bilateral renal artery stenosis

Front 280

What drugs are used in patients with HTN and angina?

Back 280

beta blockers and CCB's

Front 281

What drugs are used in patients with HTN and diabetes?

Back 281

ACEI's and ARB's

Front 282

What drugs are used in patients with HTN and CHF?

Back 282

ACEI's and ARB's

Front 283

What drugs are used in post-MI patients with HTN?

Back 283

beta blockers

Front 284

What drugs are used in patients with HTN and BPH?

Back 284

alpha blockers

Front 285

What drugs are used in patients with HTN and dyslipidemias?

Back 285

alpha blockers, CCB's, ACEI's, and ARB's

Front 286

What are the functions of endothelin and prostacyclin in PAH?

Back 286

endothelin causes vasoconstriction and proliferation of vessel walls; prostacyclin causes vasodilation of vessel walls and is anti-proliferative

Front 287

What 3 drugs are used to treat PAH?

Back 287

bosentan, epoprostenol, sildenafil, and CCB's

Front 288

Which drug used to treat PAH is an endothelin-A antagonist? Which is a prostacyclin analog? Which is a PDE-5 inhibitor?

Back 288

bosentan, epoprostenol, sildenafil

Front 289

What is the acute vasoreactivity test?

Back 289

only give CCB's to patients who initially respond to epoprostenol

Front 290

What are AE's from bosentan?

Back 290

vasodilatory AE's, elevated liver enzymes

Front 291

What are AE's from epoprostenol?

Back 291

jaw, leg, foot pain; thrombocytopenia, classic leukocytic vasculitis

Front 292

What is a very rare AE from sildenafil?

Back 292

nonarteritic ischemic optic neuropathy

Front 293

What is the only contraindication with bosentan?

Back 293

pregnancy

Front 294

What is the main focus of treatment in CHF?

Back 294

decrease cardiac remodeling

Front 295

If a person develops resistance to thiazides, what thiazide might still work?

Back 295

metolazone

Front 296

Which vasodilators are arteriolar? Venular? Both?

Back 296

1. CCB's, hydralazine, minoxidil
2. nitrates
3. the rest

Front 297

Digoxin does not help in CHF. What drugs do help in CHF?

Back 297

ACEI's, ARB's, carvedilol, and spironolactone

Front 298

Are inotropes more effective in acute or chronic CHF?

Back 298

acute CHF (but patient must be stable before you can use digoxin!)

Front 299

How does digoxin work?

Back 299

it inhibits the Na/K exchanger on the cardiac myocyte; this keeps more Na in the cell, which slows down the Na/Ca exchanger; this keeps more Ca in the cell, causing more forceful contraction

Front 300

What is an indirect effect of digoxin?

Back 300

inhibits Na/K exchanger on neurons, increasing vagal and sympathetic stimulation

Front 301

What are 4 important pharmacokinetic properties of digoxin?

Back 301

1. long half life
2. need high loading dose
3. caution in renal impairment
4. easily displaced by other drugs

Front 302

Digoxin can be used in supraventricular tachycardias except which one? What drugs can be used?

Back 302

WPW; class IA and III antiarrhythmics

Front 303

What is the relation between digoxin and extracellular K?

Back 303

hyperkalemia will impair digoxin efficacy; hypokalemia will improve digoxin efficacy

Front 304

T or F: digoxin is effective in treating acutely decompensated HF.

Back 304

false, only used when the patient is stabilized

Front 305

What are early signs of digoxin toxicity? Late signs?

Back 305

1. NVD, CNS symptoms
2. vasual halos

Front 306

Aside from digoxin toxicity symptoms, what is a big AE for digoxin?

Back 306

arrhythmias

Front 307

What is the treatment for digoxin toxicity?

Back 307

digibind, Fab antibodies to digoxin

Front 308

What are 4 drugs that interact with digoxin?

Back 308

1. diuretics
2. quinidine
3. verapamil
4. sympathomimetics

Front 309

What are the first line drugs for CHF?

Back 309

diuretics, ACEI's, and ARB's

Front 310

What benefit do spironolactone and ACEI's have in treating CHF?

Back 310

reduce remodeling

Front 311

Are metoprolol and carvedilol used in compensated or decompensated CHF?

Back 311

compensated

Front 312

What is nesiritide, how does it work, and what is it used for?

Back 312

1. recombinant BNP
2. binds natriuretic receptors, increases cGMP, vasodilates
3. acutely decompensated CHF

Front 313

How does dobutamine work in CHF?

Back 313

binds beta-1>beta-2>alpha receptors; results in increased contractility without increasing HR

Front 314

Dopamine can be used in CHF. How does it work?

Back 314

binds DA receptors to vasodilate renal vessels; higher doses will bind beta-1 receptors to increase contractility

Front 315

What are the 2 PDE inhibitors used for CHF?

Back 315

inamrinone and milrinone

Front 316

How does inamrinone work?

Back 316

increases cAMP to increase inotropy and decrease TPR

Front 317

What are the two kinds of angina and how do they differ?

Back 317

1. classic (stable) and variant (prinzmetal or vasospastic)
2. classic is from exertion, variant is from decreased coronary blood flow

Front 318

What 2 drug classes work well for vasospastic angina?

Back 318

nitrates and CCB's

Front 319

What 3 drug classes work well for classic angina?

Back 319

nitrates, CCB's, and BB's

Front 320

How do nitrates work?

Back 320

bind to endothelial cells, release NO, NO travels to smooth muscle cells, activates cGMP, leads to relaxation

Front 321

Nitroglycerine is used acutely, but what nitrate is used chronically?

Back 321

isosorbide

Front 322

How can you prevent tolerance from developing from using nitrates?

Back 322

give break every 12 hours

Front 323

What happens if you give more than 3 nitroglycerin tablets in 6-8 minutes?

Back 323

tachyphylaxis (short term tolerance)

Front 324

Which CCB is important for vasospastic angina?

Back 324

nifedipine

Front 325

What drugs are contraindicated in vasospastic angina?

Back 325

BB's

Front 326

What alpha and beta blocker can be used to treat stable angina?

Back 326

carvedilol

Front 327

How do theophyline, inamrinone, and sildenafil differ in their MOA's?

Back 327

sildenafil inhibits PDE from cGMP breakdown; the others inhibit PDE from cAMP breakdown

Front 328

Explain the loss of K with certain diuretics.

Back 328

Na reabsorption is blocked above the collecting ducts. Na load to collecting ducts is therefore high, resulting in gradient, allowing some Na to be reabsorbed. K efflux results.

Front 329

What diuretics will result in alkalosis due to loss of H ions? Why

Back 329

loops and thiazides; K efflux is accompanied by H efflux due to high Na gradient at collecting duct

Front 330

What can be given to patients to replace K loss with diuretics?

Back 330

orange juice and bananas

Front 331

Where does mannitol work? How does it work?

Back 331

thin descending loop; inhibits water reabsorption

Front 332

What is mannitol used for clinically?

Back 332

1. decreases IOP in glaucoma
2. decreases ICP
3. rhabdomyolysis

Front 333

How do CAI's work?

Back 333

decreases H formation in PCT, which prevents Na/H antiport, increases Na and HCO3 in lumen

Front 334

What are 2 CAI's?

Back 334

acetazolamide and dorzolamide

Front 335

What are CAI's used for clinically?

Back 335

glaucoma, acute mountain sickness, and metabolic alkalosis

Front 336

What are major AE's of CAI's?

Back 336

1. acidosis
2. hypokalemia
3. hyperchloremia
4. renal stones

Front 337

Acetazolamide must be avoided in patients with what hypersensitivity?

Back 337

sulfonamide

Front 338

Why does acetazolamide cause acidosis?

Back 338

loss of HCO3

Front 339

Patients with sulfonamide allergies must avoid what drugs?

Back 339

1. CAI's
2. loops (except ethacrynic acid)
3. thiazides
4. sulfa abx
5. celecoxib

Front 340

What 4 ions will be blocked in loop diuretics? Where does this take place?

Back 340

1. Ca, Mg, Na, Cl, and some K
2. Na-K-2Cl transporter in the loop of henle

Front 341

What are 6 uses of loops?

Back 341

1. CHF
2. HTN as adjunct
3. refractory edema
4. hypercalcemia
5. acute pulmonary edema
6. ARF

Front 342

What unusual AE will ethacrynic acid cause that furosemide won't cause?

Back 342

ototoxicity

Front 343

What drug interactions exist for loops?

Back 343

1. AG's (ototoxicity)
2. lithium (decreased clearance)
3. digoxin (increased toxicity)

Front 344

If a patient developed tophi from loops, why would this be?

Back 344

loops can cause hyperuricemia, precipitating gouty attacks

Front 345

What are 2 thiazides?

Back 345

hydrochlorothiazide and indapamide

Front 346

How do thiazides work?

Back 346

block Na/Cl transporter and increase Ca reabsorption in DCT

Front 347

What are 4 uses of thiazides?

Back 347

1. HTN
2. CHF as adjunct
3. renal stones
4. nephrogenic DI

Front 348

Loops and thiazides have mostly the same AE's. What AE's do thiazides have that loops don't?

Back 348

hyperglycemia, hyperlipidemia, and sexual dysfunction

Front 349

Why should you avoid using thiazides in patients with DM?

Back 349

causes hyperglycemia

Front 350

What are 2 Na channel blockers?

Back 350

triamterene and amiloride

Front 351

How do Na channel blockers work? What class do these fall under?

Back 351

blocks Na channel on collecting duct apical membrane; K-sparing diuretic

Front 352

What are Na channel blockers used for clinically?

Back 352

1. adjunct diuretic
2. amiloride used in lithium-induced DI

Front 353

What is an aldosterone-receptor antagonist? What class does this fall under?

Back 353

spironolactone; K-sparing diuretic

Front 354

How does spironolactone work?

Back 354

blocks mineralocorticoid receptors in principal cell of collecting duct

Front 355

What is spironolactone used for clinically?

Back 355

1. hyperaldosterone state
2. adjunct diuretic
3. female hirsutism
4. CHF

Front 356

If a patient is taking spironolactone and develops antiandrogenic symptoms, what should you do?

Back 356

switch to eplerenone

Front 357

What is the primary difference between chylomicrons and VLDL?

Back 357

chylomicrons transport TG's and cholesterol from the diet, lipoprotein lipase breaks these into FFA's to adipose tissue and glycerol to liver, chylomicron remnants transport dietary cholesterol to liver; VLDL does the same thing, but with endogenous TG's

Front 358

After lipoprotein lipase breaks TG's off of VLDL, and while the VLDL still carries cholesterol, what is it then called?

Back 358

IDL

Front 359

What are the 2 possible fates of IDL's?

Back 359

they can either bind to LDL receptors in the liver and be degraded, or they can be converted to LDL's

Front 360

What does LDL do?

Back 360

takes cholesterol to extrahepatic tissue

Front 361

What does HDL do that makes it special?

Back 361

activates lipoprotein lipase, picks up cholesterol from deteriorating membranes, and delivers it to the liver

Front 362

Statin drugs are what kind of inhibitors?

Back 362

HMG-CoA reductase; the rate limiting step in cholesterol formation in the liver

Front 363

What lipids do statins lower?

Back 363

LDL mostly, also lowers VLDL and consequently TG's

Front 364

What are the AE's of statins?

Back 364

myalgia, rhabdomyolysis, hepatotoxicity

Front 365

What drug will increase the incidence of rhabdomyolysis seen in statins?

Back 365

gemfibrozil

Front 366

Which statins are special in that they are not affected by CYP3A4 metabolism?

Back 366

fluvastatin, rosuvastatin, and pravastatin

Front 367

Most statins (except rosuvastatin and atorvastatin) should be taken when?

Back 367

at night

Front 368

What tests should be performed every 6 months when taking statins?

Back 368

LFT's

Front 369

What is the principle behind using bile acid sequestrants?

Back 369

must have cholesterol to make bile acids; 95% of biles acids are recycled; if you prevent them from being recycled, then you must use more cholesterol to make them

Front 370

What prefix do bile acid sequestrants have?

Back 370

chol- or col- (cholestyramine and colestipol)

Front 371

How do bile acid sequestrants work?

Back 371

bile acid exchanges a chloride ion with the bile acid sequestrant and binds it in the GI tract

Front 372

What are some AE's of bile acid sequestrants?

Back 372

malabsorption, raises TG's

Front 373

When are bile acid sequestrants contraindicated?

Back 373

hypertriglyceridemia

Front 374

When might you use a bile acid sequestrant?

Back 374

as an adjunct to statins

Front 375

What is lowered in bile acid sequestrants?

Back 375

LDLs

Front 376

How does niacin work?

Back 376

in order for a FFA and glycerol to make a TG, DGA2 must be present; niacin blocks DGA2; the result is decreased VLDL synthesis

Front 377

What does niacin do to lipids?

Back 377

decreases VLDL, TG's, and LDL; increases HDL

Front 378

What are 2 AE's of niacin?

Back 378

1. niacin flush
2. hepatotoxicity

Front 379

How does gemfibrozil work?

Back 379

activates PPAR-alpha, which activates lipoprotein lipase

Front 380

What does gemfibrozil do to lipids?

Back 380

decreases VLDL, TG's, and LDL's; increases HDL's

Front 381

When might you use gemfibrozil?

Back 381

hypertrigylceridemia

Front 382

What are 2 AE's of gemfibrozil?

Back 382

gallstones and myositis

Front 383

What drug is a cholesterol absorption inhibitor?

Back 383

ezetimibe

Front 384

What is ezetimibe used for clinically?

Back 384

adjunctive therapy to lower LDL's only

Front 385

What is orlistat used for clinically?

Back 385

weight loss

Front 386

How does orlistat work?

Back 386

inhibits pancreatic lipase, decreased TG breakdown

Front 387

What are 2 AE's of orlistat?

Back 387

oily stools and decreased lipid-soluble vitamin absorption

Front 388

How do BZ's work?

Back 388

they bind to BZ receptor on the GABA-A ionophore, causing GABA to bind to its site, causing Cl influx, causing hyperpolarization and thus inhibition

Front 389

Do BZ's increase the duration or frequency of Cl channel opening?

Back 389

BZ=frequency; Barbs=duration

Front 390

What is the antidote for BZ toxicity?

Back 390

flumazenil

Front 391

Which is better treated with BZ's: panic attacks or chronic GAD?

Back 391

panic attacks; GAD is better treated with SSRI's

Front 392

Which 3 BZ's don't get metabolized to active forms?

Back 392

"out the liver"=oxazepam, temazepam, and lorazepam

Front 393

T or F: BZ's have GABA mimetic activity at high doses.

Back 393

false, barbs and ETOH do though

Front 394

What are the 3 major uses for diazepam?

Back 394

preop sedation and status epilepticus (along with lorazepam); muscle relaxation

Front 395

Temazepam and oxazepam are used to treat what?

Back 395

sleep disorders

Front 396

Midazolam can be used for what?

Back 396

preop sedation and anesthesia

Front 397

What is phenobarbitol used for? Thiopental?

Back 397

seizures; induction of anesthesia

Front 398

Which BZ is best in elderly patients?

Back 398

lorazepam

Front 399

When are barbs contraindicated?

Back 399

porphyrias

Front 400

T or F: psychological and physical dependence occur with sedative-hypnotics.

Back 400

true (abuse liability of BZ's is less than ETOH or barbs)

Front 401

What do you give a pregnant patient who is seizing?

Back 401

phenobarbitol in low doses

Front 402

What BZ can you give to a pregnant patient?

Back 402

buspirone

Front 403

What drugs have an additive effect when given with BZ's?

Back 403

anesthetics, antihistamines, opiates, and BB's

Front 404

What are zolpidem and zaleplon?

Back 404

BZ-1 receptor agonists

Front 405

What are zolpidem and zaleplon used for clinically?

Back 405

sleep disorders

Front 406

How does buspirone work?

Back 406

partial 5HT-1A agonist

Front 407

What is buspirone used to treat? Is this sedating? How long does buspirone take to work?

Back 407

GAD; no; 1-2 weeks

Front 408

T or F: all alcohols cause metabolic alkalosis.

Back 408

false, they cause metabolic acidosis

Front 409

How does disulfiram work?

Back 409

inhibits acetaldehyde dehydrogenase, prevents acetaldehyde from being metabolized, which keeps the AE's in effect

Front 410

What are the symptoms of FAS?

Back 410

growth restriction, midfacial hypoplasia, microcephaly, CNS dysfunction, MR

Front 411

What is the end product of ethylene glycol metabolism?

Back 411

oxalic acid

Front 412

What is the end product of methanol metabolism?

Back 412

formic acid

Front 413

What are 3 major signs and symptoms of ethylene glycol toxicity?

Back 413

CNS depression, severe metabolic acidosis, and nephrotoxicity

Front 414

What are 3 major signs and symptoms of methanol toxicity?

Back 414

respiratory failure, anion gap metabolic acidosis, and ocular damage

Front 415

Methanol is found in what 2 items?

Back 415

wood alcohol and paint thinners

Front 416

What is the treatment for ethylene glycol and methanol poisoning?

Back 416

either fomepizole (inhibits alcohol dehydrogenase) or give regular alcohol

Front 417

What are signs and symptoms of Wernicke Korsikoff syndrome? What is deficient in this syndrome?

Back 417

ataxia, gout, metabolic acidosis, peripheral neuropathy; folic acid deficiency

Front 418

What 6 drugs can cause a disulfiram-like reaction?

Back 418

metronidazole, griseofulvin, cefamandole, cefoperazone, cefotetan, and chlorpropamide

Front 419

What does acetaldehyde cause in alcohol metabolism?

Back 419

1. N/V
2. HA
3. hypotension
4. inactivates folate
5. decreases thiamine availability

Front 420

What are 4 signs and symptoms of chronic alcoholism?

Back 420

1. hypoglycemia
2. fatty liver/lipemia
3. muscle wasting (poor diet)
4. gout (lactate competes with urate for excretion)

Front 421

What are 3 main signs and symptoms of alcohol toxicity?

Back 421

1. CNS depression
2. metabolic acidosis
3. acetaldehyde toxicity

Front 422

What is the end product of ETOH metabolism?

Back 422

acetic acid

Front 423

How do carbamazepine and phenytoin work?

Back 423

block Na influx, decreases axonal conduction

Front 424

How do lamotrigine and topiramate work?

Back 424

decreases excitatory effects of glutamic acid (topiramate blocks AMPA receptors)

Front 425

How do ethosuximide and valproic acid work?

Back 425

decrease Ca influx through type-T channels in thalamic neurons

Front 426

T or F: phenytoin can be used for any seizures.

Back 426

true

Front 427

What drugs are used to treat partial simple, partial complex, and general tonic-clonic seizures?

Back 427

valproic acid, phenytoin, and carbamazepine

Front 428

What drugs are used to treat general absence seizures?

Back 428

ethosuximide

Front 429

What drugs are used to treat status epilepticus?

Back 429

lorazepam, diazepam, phenytoin, or fosphenytoin

Front 430

What is the difference between a simple and complex partial seizure?

Back 430

simple would not have altered consciousness, complex would have altered consciousness

Front 431

Where do partial complex seizure focal EEG spikes originate?

Back 431

temporal lobe

Front 432

Which seizure has 3 spikes per second on EEG?

Back 432

absence

Front 433

How is phenytoin eliminated?

Back 433

zero order kinetics

Front 434

What are 3 major AE's of phenytoin?

Back 434

1. gingival hyperplasia
2. osteomalacia
3. megaloblastic anemia

Front 435

What drug is the DOC for trigeminal neuralgia?

Back 435

carbamazepine

Front 436

What are 2 major AE's of carbamazepine?

Back 436

osteomalacia and megaloblastic anemia

Front 437

How does valproic acid work?

Back 437

blocks T-type Ca channels, inhibits GABA transaminase

Front 438

In addition to seizures, what else is valproic acid used to treat?

Back 438

mania or bipolar disorders, migr

Front 439

Does valproic acid inhibit or induce cytochrome P450?

Back 439

inhibits

Front 440

What are the 3 big AE's of valproic acid?

Back 440

hepatotoxicity, thrombocytopenia, and pancreatitis

Front 441

T or F: valproic acid is teratogenic.

Back 441

true, causes spina bifida

Front 442

A female patient must be removed from anticonvulsants for how long before she can get pregnant?

Back 442

1 month

Front 443

Felbamate and lamotrigine are Na channel and glutamate receptor blockers. What is the major AE for lamotrigine?

Back 443

SJS

Front 444

How does gabapentin work?

Back 444

increased GABA effects

Front 445

In addition to seizures, how else is gabapentin used?

Back 445

neuropathic pain

Front 446

What is meant by the term MAC for anesthetics?

Back 446

concentration of inhaled anesthetic at which 50% of patients do not respond to surgical stimulus

Front 447

Which is correct: lower MAC=higher potency or higher MAC=higher potency?

Back 447

lower MAC=higher potency

Front 448

Which is correct: high blood-gas ratio=slow recovery and onset or low blood-gas ratio=slow recovery and onset?

Back 448

high blood-gas ratio=slow recovery and onset

Front 449

The more lipid soluble the anesthetic, the _____ the MAC and _____ the potency.

Back 449

lower; greater

Front 450

Which has a lower MAC, NO or halothane?

Back 450

halothane (0.8%)

Front 451

Which has a lower blood-gas ratio, NO or halothane?

Back 451

NO

Front 452

What are 2 characteristics associated with NO?

Back 452

diffusional hypoxia and spontaneous abortions

Front 453

What are 2 characteristics associated with halothane?

Back 453

malignant hyperthermia and arrhythmias

Front 454

What is the treatment for malignant hyperthermia?

Back 454

dantrolen

Front 455

Which is an indicator of anesthetic potency: MAC or blood gas-ratio? What about anesthetic speed of onset and recovery?

Back 455

potency is MAC; blood-gas ratio is speed of onset and recovery

Front 456

T or F: thiopental is a long-acting barb used in induction.

Back 456

false, it is short-acting

Front 457

What kind of drug is midazolam?

Back 457

BZ

Front 458

What is midazolam used for clinically?

Back 458

1. preop sedation
2. anterograde amnesia
3. induction
4. outpatient surgery

Front 459

What drug is known as "milk of amnesia?"

Back 459

propofol

Front 460

What is propofol used for clinically?

Back 460

induction and maintenance of anesthesia; antiemetic

Front 461

What is fentanyl used for clinically?

Back 461

induction and maintenance of anesthesia

Front 462

How does ketamine cause its effects?

Back 462

NMDA-receptor antagonist

Front 463

What are the 2 major AE's of ketamine?

Back 463

1. emergent delirium
2. hallucinations

Front 464

How do local anesthetics work?

Back 464

nonionized form of drug crosses membrane; ionized form blocks inactivated Na channel

Front 465

How do you differ ester anesthetics and amide anesthetics?

Back 465

esters have 1 "i"; amides have 2 "i"s

Front 466

Which is metablized by liver enzymes, esters or amides?

Back 466

amides; esters are metabolized by plasma enzymes

Front 467

Which nerve fibers are most sensitive to blockade?

Back 467

smallest diameter with highest firing rate

Front 468

What is the order for blockade of nerve fibers?

Back 468

B and C>A-delta>A-beta>A-gamma>A-alpha

Front 469

Where does tetrodotoxin come from? Saxitoxin?

Back 469

puffer fish; algae (red tide)

Front 470

How do tetrodotoxin and saxitoxin work?

Back 470

block activated Na channels to decrease Na influx

Front 471

Where does ciguatoxin come from? Batrachotoxin?

Back 471

exotic fish; frogs

Front 472

How do ciguatoxin and batrachotoxin work?

Back 472

bind activated Na channels, cause inactivation, prolong Na influx

Front 473

How does cocaine cause vasoconstriction?

Back 473

blocks NE reuptake

Front 474

What are the 2 AE's of local anesthetics?

Back 474

1. CV toxicity (amides)
2. neurotoxicity
3. allergies (esters via PABA)

Front 475

What are the 2 classes of skeletal muscle relaxants?

Back 475

nondepolarizing (competitive) and depolarizing (noncompetitive)

Front 476

Nicotinic receptors have how many subunits?

Back 476

5

Front 477

Generally speaking, how do skeletal muscle relaxants work (nondepolarizing)?

Back 477

nicotinic antagonism leads to progressive paralysis

Front 478

What is the prototype for the nondepolarizing skeletal muscle relaxants?

Back 478

D-tubocurarine

Front 479

T or F: nondepolarizing skeletal muscle relaxants have no effects on cardiac and smooth muscle.

Back 479

true

Front 480

T or F: nondepolarizing skeletal muscle relaxants have CNS effects.

Back 480

false

Front 481

How do you reverse nondepolarizing skeletal muscle relaxants?

Back 481

AChE inhibitors

Front 482

Name the 3 nondepolarizing skeletal muscle relaxants.

Back 482

D-tubocurarine, atracurium, and mivacurium

Front 483

What is the AE for atracurium?

Back 483

can be inactivated to laudanosine, which causes seizures

Front 484

How is mivacurium metabolized?

Back 484

plasma cholinesterases

Front 485

What is the only drug listed for depolarizing skeletal muscle relaxants?

Back 485

succinylcholine

Front 486

How does succinylcholine work?

Back 486

nicotinic agonist:
phase 1: depolarizes, fasciulates, prolonged depolarization, flaccid paralysis
phase 2: desensitization

Front 487

What effect do AChE inhibitors have on succinylcholine?

Back 487

increases phase 1, no effect on phase 2

Front 488

How is succinylcholine metabolized?

Back 488

plasma pseudocholinesterases

Front 489

What are 3 AE's of succinylcholine?

Back 489

1. atypical pseudocholinesterase (genetic disorder)
2. hyperkalemia
3. malignant hyperthermia

Front 490

Why does malignant hyperthermia occur?

Back 490

mutation in ryanadine receptors leads to Ca release from SR, causes extreme muscle rigidity and hyperthermia, HTN, acidosis, and hyperkalemia

Front 491

Through what receptors does baclofen work?

Back 491

GABA-B

Front 492

What are the 3 drugs that can cause malignant hyperthermia?

Back 492

succinylcholine, halothane, and tubocurarine

Front 493

How does dantrolene fix malignant hyperthermia?

Back 493

blocks Ca release from SR, decreases contractility

Front 494

What are 4 centrally acting skeletal muscle relaxants?

Back 494

1. BZ's
2. baclofen
3. carisoprodol
4. cyclobenzaprine

Front 495

What are 3 endogenous opiate peptides?

Back 495

endorphins, enkephalins, and dynorphins

Front 496

Which receptor is most important in opioid analgesics?

Back 496

mu (others are kappa and delta)

Front 497

How do opioid receptors work?

Back 497

opioids bind mu receptors, cause pre/postsynaptic inhibition through Gi coupling, decrease cAMP, which decreases Ca release and also opens K channels to cause hyperpolarization

Front 498

T or F: you should first give oxygen for morphine-caused respiratory depression.

Back 498

false, give naloxone first

Front 499

Does morphine constrict or relax circular muscles?

Back 499

constricts

Front 500

What happens to the GI, GU, biliary, and pupils from morphine?

Back 500

1. decreased peristalsis
2. urinary retention
3. increased pressure
4. miosis

Front 501

What triggers the NV from morphine?

Back 501

CTZ in area postrema

Front 502

Morphine is metabolized to what?

Back 502

morhpine-6-glucuronide (longest acting opioid)

Front 503

What is the classic triad of AE's from morphine?

Back 503

1. pinpoint pupils
2. respiratory depression
3. coma

Front 504

What is used to treat morphine-caused diarrhea?

Back 504

docusate

Front 505

What opioid can be given during pregnancy or labor/delivery?

Back 505

meperidine

Front 506

What are the contraindications for opioids?

Back 506

1. head injuries
2. pulmonary problems
3. hepatic/renal problems
4. adrenal/thyroid problems
5. pregnancy (not meperidine)

Front 507

What are the only effects that will not develop tolerance with opioids?

Back 507

miosis and constipation

Front 508

What are signs of opiate withdrawal?

Back 508

1. yawning
2. lacrimation, rhinorrhea, salivation
3. anxiety, sweating, goosebumps
4. muscle cramps, spasms, neuropathic pain

Front 509

Acute opioid toxicity requres supportive therapy and naloxone. What about withdrawal?

Back 509

supportive, methadone, and clonidine

Front 510

What are 2 opioid-related drugs, and what are they used for?

Back 510

1. loperamide: diarrhea
2. dextromethorphan: cough

Front 511

What happens if you give a partial agonist to a patient on a full agonist opioid?

Back 511

immediate withdrawal symptoms

Front 512

What is the difference between use of naloxone and use of naltrexone?

Back 512

1. naloxone-IV, reverses respiratory depression
2. naltrexone-PO, decreases ETOH craving and used in opioid addiction

Front 513

Which opioid can cause seizures? How?

Back 513

meperidine-metabolized to normeperidine, an SSRI which can cause seizures

Front 514

Which opioid is also antimuscarinic? How does this change symptoms?

Back 514

1. meperidine
2. no miosis, tachycardia, no GI/GU/gallbladder spasms

Front 515

What are 3 weak mu agonists and what are they used for?

Back 515

1. codeine: cough suppressant, analgesic, used w/NSAIDs
2. hydrocodone, oxycodone

Front 516

What are 3 mixed agonist opioids?

Back 516

nalbuphine, pentazocine, and buprenorphine

Front 517

What is the only opioid that is a kappa receptor agonist? What else is this drug?

Back 517

pentazocine; partial mu agonist

Front 518

What might pentazocine be used for?

Back 518

spinal analgesia

Front 519

What are the 4 major dopaminergic pathways?

Back 519

1. nigrostriatal tract
2. mesolimbic-mesocortical tracts
3. tuberoinfundibular
4. CTZ

Front 520

Briefly describe DA's effects on the nigrostriatal tract.

Back 520

substantia nigra projects to neostriatum and release DA, which inhibits GABA; loss of these neurons leads to extrapyramidal dysfunction

Front 521

Briefly describe DA's effects on the mesolimbic-mesocortical tracts.

Back 521

midbrain projects to cerebrocortical and limbic structures and releases DA, which affects pleasure and reward pathways

Front 522

Briefly describe DA's effects on the tuberoinfundibular pathway.

Back 522

hypothalamus projects to anterior pituitary and releases DA, which decreases prolactin

Front 523

Briefly describe DA's effects on the CTZ.

Back 523

activating DA receptors in the CTZ will increase vomiting

Front 524

Increased DA in the mesolimbic-mesocortical tract leads to what?

Back 524

reinforcement of behaviors

Front 525

Increased DA in the tuberoinfundibular pathway leads to what?

Back 525

decreased prolactin

Front 526

D1 receptors are coupled to what G protein? D2?

Back 526

D1=Gs
D2=Gi

Front 527

What are the D2 receptor subtypes and where are they located?

Back 527

D2A=nigrostriatum; D2B=mesolimbic

Front 528

What are 3 major signs and symptoms of PD? Will tremors increase or decrease with intention?

Back 528

1. bradykinesia, muscle rigidity, and resting "pill rolling" tremor
2. decrease

Front 529

What is the imbalance that occurs with PD?

Back 529

ACh and DA; ACh dominates because DA is decreased

Front 530

What are the 3 treatment goals in PD?

Back 530

1. antagoinize ACh
2. reduce DA loss
3. increase DA production

Front 531

Why is carbidopa always given with levodopa?

Back 531

it blocks aromatic amino acid decarboxylase; this enzyme normally converts levodopa to dopamine in the periphery; if you block peripheral conversion, more goes to brain

Front 532

Which form is BBB permeable: levodopa or dopamine?

Back 532

levodopa

Front 533

What are 3 important AE's for levodopa?

Back 533

1. "on-off" syndrome
2. psychosis
3. vomiting

Front 534

What drug is used to treat hyperprolactinemia?

Back 534

bromocriptine

Front 535

What are 2 COMT inhibitors used to treat PD?

Back 535

tolcapone and entacapone

Front 536

What does COMT do in the CNS?

Back 536

converts DA to 3-O-methyldopa, a partial agonist

Front 537

What is the major AE of COMT inhibitors?

Back 537

hepatotoxicity

Front 538

What are 2 MAOB inhibitors?

Back 538

selegiline and rasagiline

Front 539

T or F: levodopa and selegiline have the same AE's except that selegiline causes insomnia.

Back 539

true

Front 540

What are 3 DA receptor agonists?

Back 540

bromcriptine (ergot); pramipexole, and ropinorole (non-ergot)

Front 541

In addition to prolactinomas, what else can bromocriptine be used to treat?

Back 541

acromegaly

Front 542

Which DA receptor agonist may be neuroprotective and slow progression of PD?

Back 542

ropinorole

Front 543

What drugs will decrease ACh function in PD? Why?

Back 543

benztropine, trihexyphenidyl, and diphenhydramine; they are M-blockers specific to CNS

Front 544

What antiviral can be used to treat PD? How does it work?

Back 544

amantadine; M-blocker and increases DA function

Front 545

What is the important AE of amantadine?

Back 545

livedo reticularis

Front 546

What is the DA hypothesis in regards to schizophrenia?

Back 546

symptoms are caused by excessive DA activity in the mesolimbic system

Front 547

Name 4 typical antipsychotics.

Back 547

chlorpromazine, thioridazine, fluphenazine, and haloperidol

Front 548

Name 4 atypical antipsychotics.

Back 548

clozapine, olanzapine, risperidone, and aripiprazole

Front 549

T or F: all antipsychotics block D1 receptors.

Back 549

false, D2 receptors

Front 550

In addition to blocking D2 receptors, what other receptor blockade is useful in treating schizophrenia?

Back 550

5HT2 (serotonin)

Front 551

Which are stronger and blocking 5HT2 receptors: typical or atypical antipsychotics?

Back 551

atypicals are stronger at blocking non-D2 receptors

Front 552

What are 4 diseases that antipsychotic drugs can treat?

Back 552

1. schizophrenia
2. schizoaffective disorder
3. bipolar disorder
4. tourette syndrome

Front 553

What are 5 AE's of DA blockade?

Back 553

1. extrapyramidal symptoms
2. dysphoria
3. endocrine dysfunction
4. muscarinic blockade AE's
5. alpha blockade AE's

Front 554

What are the acute EPS?

Back 554

pseudoparkinsonism, dystonia, akathisia, fixed gaze with head turning

Front 555

What is the treatment for acute EPS?

Back 555

antimuscarinic drugs (benztropine and diphenhydramine)

Front 556

What are the chronic EPS?

Back 556

tardive dyskinesia (lateral jaw movement, tongue protrusion, lip smacking, fixed gaze)

Front 557

What is the treatment for chronic EPS?

Back 557

switch to atypical antipsychotics

Front 558

What are the endocrine dysfunction symptoms that can result from DA blockade?

Back 558

1. neuroleptic malignant syndrome (give dantrolene)
2. hyperprolactinemia
3. increased eating (weight gain)

Front 559

Typicals or atypicals: which causes alpha and muscarinic blockade symptoms?

Back 559

typicals

Front 560

What are AE's of thioridazine?

Back 560

cardiotoxicity (torsades) and retinal deposits

Front 561

What antipsychotic is most likely to cause neuroleptic malignant syndrome and tardive dyskinesia?

Back 561

haloperidol

Front 562

Which receptor blockade is associated with positive symptoms in psychosis? Negative symptoms?

Back 562

1. DA
2. 5HT2

Front 563

Why is risperidone not used in older patients?

Back 563

stroke risk

Front 564

What is unique about aripiprazole?

Back 564

partial D2 agonist as well as 5HT2 blockade

Front 565

Clozapine is the favored antipsychotic. What are 3 important AE's of clozapine?

Back 565

1. agranulocytosis (need weekly wbc count)
2. increased salivation
3. seizures

Front 566

What is the amine hypothesis of depression?

Back 566

deficiency of amine NT's like NE, 5HT, and DA causes depression

Front 567

What is the acute mechanism of antidepressants?

Back 567

increase NE and 5HT

Front 568

What are 2 MAOI's?

Back 568

phenelzine and tranylcypromine

Front 569

How do MAOI's work?

Back 569

block MAO-A and MAO-B, increase NE

Front 570

What happens if a patient on MAOI takes too much cheese, red wine, or avocado?

Back 570

hypertensive crisis because these foods have too much tyramine, which is a precursor of NE

Front 571

In addition to foods, what drugs can precipitate a hypertensive crisis in patients on MAOI's?

Back 571

TCA's, alpha-1-agonists, and levodopa

Front 572

What drugs interact with MAOI's to cause serotonin syndrome?

Back 572

SSRI's, TCA's, meperidine, and dextromethorphan

Front 573

What are signs and symptoms of serotonin syndrome?

Back 573

sweating, rigidity, myoclonus, hyperthermia, ANS instability, and seizures

Front 574

What drug is used almost exclusively to treat neuropathic pain?

Back 574

amitriptyline

Front 575

What are 3 TCA's?

Back 575

amitriptyline, imipramine, and clomipramine

Front 576

What is the MOA of TCA's?

Back 576

blockade of 5HT and NE reuptake

Front 577

If a patient were to switch from TCA's to MAOI's, how long must they "wash out"?

Back 577

2 weeks

Front 578

TCA's are used clinically for what?

Back 578

1. major depression
2. phobia and panic-anxiety
3. OCD
4. neuropathic pain
5. enuresis (anticholinergic effects in bladder)

Front 579

What are the AE's for TCA's?

Back 579

muscarinic and alpha blockade AE's

Front 580

What occurs in TCA toxicity?

Back 580

3 "c"s: coma, convulsions, cardiotoxicity

Front 581

In addition to their interactions with MAOI's and SSRI's, what other drugs will TCA's interfere with?

Back 581

alpha 2 agonists and guanethidine

Front 582

What are 3 SSRI's?

Back 582

fluoxetine, paroxetine, and sertraline

Front 583

What are SSRI's used to treat clinically?

Back 583

1. major depression
2. OCD
3. bulimia
4. anxiety disorders
5. PMDD

Front 584

What are AE's of SSRI's?

Back 584

1. anxiety
2. agitation
3. bruxism
4. sexual dysfunction
5. weight loss

Front 585

Trazodone is what kind of drug? What are it's AE's?

Back 585

1. antidepressant
2. arrhythmias and priapism

Front 586

Venlafaxine is what kind of drug? What is the advantage over SSRI's?

Back 586

1. SNRI's (nonselective serotonin reuptake inhibitor)
2. no ANS AE's

Front 587

How does bupropion work? What is it used for?

Back 587

1. DA reuptake blocker
2. smoking cessation

Front 588

What kind of drug is mirtazapine? What is the major AE?

Back 588

1. alpha-2-antagonist
2. weight gain

Front 589

What is the DOC in bipolar disorders?

Back 589

lithium

Front 590

How does lithium work?

Back 590

prevents recycling of inositol, decreases PIP2, decreases cAMP

Front 591

What are 5 major AE's of lithium?

Back 591

1. flu-like sx
2. tremor
3. seizures
4. hypothyroidism with goiter
5. nephrogenic DI

Front 592

In addition to lithium, what other 2 drugs can be used to treat bipolar disorder?

Back 592

valproate and lamotrigine

Front 593

Lithium is teratogenic. What drugs can be used in pregnancy to treat bipolar disorder?

Back 593

clonazepam and gabapentin

Front 594

What are 2 drugs used to treat ADHD?

Back 594

methylphenidate and atomoxetine

Front 595

What is the MOA for atomoxetine?

Back 595

selective NE reuptake inhibitor

Front 596

What is the MOA for cocaine?

Back 596

blocks DA, NE, and 5HT reuptake; local anesthetic from Na channel blockade

Front 597

What is the MOA for amphetamines?

Back 597

block NE and DA reuptake, releases amines from mobile pool, MAO inhibitors

Front 598

What urine metabolite is often tested in cocaine?

Back 598

benzoyl agonine

Front 599

Nicotine and barbiturates send noradrenergic transmission to what location? Where does it go from there?

Back 599

ventral tegmental area; nucleus accumbens (reward)

Front 600

How do you manage cocaine and amphetamine withdrawal?

Back 600

antidepressants

Front 601

How does PCP work?

Back 601

NMDA antagonist

Front 602

What drug causes horizontal and vertical nystagmus, paranoia, rhabdomyolysis, convulsions, and death?

Back 602

PCP

Front 603

T or F: inhaled drugs of abuse do not cause blindness.

Back 603

false

Front 604

MDMA is what street drug? How does it work?

Back 604

ecstasy; amphetamine like with strong 5HT pharmacology

Front 605

PCN is synergistic with what other drug? What other antibiotic antagonizes PCN?

Back 605

1. AG's
2. tets

Front 606

What drugs and classes work as bacterial cell-wall synthesis inhibitors?

Back 606

1. PCN
2. cephalosporins
3. imipenem/meropenem
4. aztreonam
5. vancomycin

Front 607

What drugs and classes work as bacterial protein synthesis inhibitors?

Back 607

1. AG's
2. chloramphenicol
3. macrolides
4. tets
5. streptogramins
6. linezolid

Front 608

What drugs and classes work as nucleic acid synthesis inhibitors?

Back 608

1. FQ's
2. rifampin

Front 609

What drugs and classes work as folic acid synthesis inhibitors?

Back 609

1. sulfas
2. trimethoprim
3. pyrimethamine

Front 610

What is the primary mechanism of resistance with PCN's and cephalosporins?

Back 610

beta-lactamase production; changes in PBP's; changes in porins

Front 611

What is the primary mechanism of resistance with AG's?

Back 611

formation of enzymes that inactivate drugs via conjugation reactions the transfer acetyl, phosphoryl, or adenylyl groups

Front 612

What is the primary mechanism of resistance with macrolides?

Back 612

formation of methyltransferases that alter drug binding sites of the 50S ribosomal subunit; active transport out of cells

Front 613

What is the primary mechanism of resistance with tets?

Back 613

increased activity of transport systems that "pump" drugs out of the cell

Front 614

What is the primary mechanism of resistance with sulfonamides?

Back 614

change in sensitivity to inhibition of target enzymes; increased formation of PABA; use of exogenous folic acid

Front 615

What is the primary mechanism of resistance to FQ's?

Back 615

change in sensitivity to inhibition of target enzymes; increased activity of transport systems that promote drug efflux

Front 616

What is the primary mechanism of resistance of chloramphenicol?

Back 616

formation of inactivating acetyltransferases

Front 617

What drug is responsible for "gray baby syndrome"?

Back 617

chloramphenicol

Front 618

How do PCN's work?

Back 618

bind to PBP's to inhibit transpeptidation and cross-linking, which are steps in cell wall synthesis

Front 619

What bugs can break the beta lactam ring?

Back 619

staphylococci

Front 620

What bug has resistance to PCN via structural change in PBP's?

Back 620

MRSA

Front 621

What bug has resistance to PCN via change in porin structure?

Back 621

pseudomonas

Front 622

What bugs are sensitive to PCN G and PCN V?

Back 622

1. streptococci
2. pneumococci
3. meningococci
4. treponema pallidum

Front 623

What bugs are sensitive to nafcillin, dicloxacillin, and oxacillin? (these are not sensitive to PCN G or PCN V due to beta-lactamase resistance)

Back 623

staphylococci (not MRSA)

Front 624

What bugs are sensitive to ampicillin and amoxicillin?

Back 624

HELPSS:
1. h. influenzae
2. e. coli
3. listeria
4. proteus
5. salmonella
6. shigella (ampicillin)

Front 625

AG's can be given with ampicillin or amoxicillin to treat what infection?

Back 625

enterococcal spp.

Front 626

What bugs are ticarcillin and piperacillin used to treat?

Back 626

1. everything PCN G treats (streptococci, meningococci, pneumococci, and t. pallidum)
2. everything nafcillin treats (staph spp.)
3. everything that ampicillin treats (h. influenzae, e. coli, listeria, proteus, salmonella, shigella)
4. pseudomonas, klebsiella, and serratia

Front 627

AG's can be given with ticarcillin and piperacillin to treat what infection?

Back 627

pseudomonas

Front 628

T or F: dose reduction of PCN's is needed with any renal dysfunction.

Back 628

false, only major renal dysfunction

Front 629

What PCN has a half-life of 2 weeks?

Back 629

benzathine PCN G

Front 630

What reaction may develop when treating syphilis with PCN's?

Back 630

Jarisch-Herxheimer (endotoxin-like reaction due to syphilis destruction: fever, chills, aches)

Front 631

What are the 2 1st Gen Cephs?

Back 631

cefazolin and cephalexin

Front 632

What bugs do 1st Gen Cephs treat?

Back 632

1. PCN G spectrum bugs
2. PEcK: proteus, e. coli, and klebsiella

Front 633

In addition to their specific spectrum of action, what are 1st Gen Cephs used for?

Back 633

surgical prophylaxis

Front 634

What are the 3 2nd Gen Cephs?

Back 634

cefotetan, cefaclor, and cefuroxime

Front 635

What bugs do 2nd Gen Cephs treat?

Back 635

1. PCN G spectrum bugs
2. HEN PEcK: h. influenzae, enterobacter, neisseria, proteus, e. coli, and klebsiella

Front 636

Which 2nd Gen Ceph enters the CNS?

Back 636

only cefuroxime

Front 637

What are the 3rd Gen Cephs?

Back 637

ceftriaxone, cefotaxime, cefdinir, and cefixime

Front 638

What bugs will 3rd Gen Cephs work against?

Back 638

1. pseudomonas
2. klebsiella
3. e. coli
4. proteus
5. serratia

Front 639

What bugs won't be killed by cephs?

Back 639

LAME: listeria, atypicals (chlamydia, mycoplasma), MRSA, and enterococci

Front 640

What is the only 4th Gen Ceph?

Back 640

cefepime

Front 641

What bugs will 4th Gen Cephs work against?

Back 641

same as 3rd Gen Ceph, but better against pseudomonas, s. aureus, s. pneumoniae, haemophilus, and neisseria

Front 642

What cephs are bile-excreted? Why is this important?

Back 642

1. cefoperazone and ceftriaxone
2. tx failure if taken with bile acid sequestrants

Front 643

If a person is allergic to PCN, can you give a ceph?

Back 643

not recommended because 5% of patients will have partial cross-allergenicity

Front 644

In addition to allergic reactions, what are the main 2 AE's with cephs?

Back 644

1. disulfiram-like reactions
2. hypoprothrombinemia

Front 645

The MOA of cephs and PCN's are the same. What other drugs fall into this category?

Back 645

1. imipenem and meropenem
2. aztreonam

Front 646

What bugs are imipenem and meropenem used to treat?

Back 646

1. (given empirically for severe, life-threatening infections)
2. enterobacter and pseudomonas

Front 647

What drug should always be given with imipenem? Why?

Back 647

1. cilastatin
2. inhibits metabolism by renal dehydropeptidase to increase half-life

Front 648

What are 3 important AE's for imipenem and meropenem?

Back 648

1. NVD
2. partial cross-allergenicity w/PCN=drug fever
3. CNS effects (seizures)

Front 649

What drug is the magic bullet for gram negatives?

Back 649

aztreonam

Front 650

What is the main bug aztreonam is used to treat?

Back 650

MDR pseudomonas

Front 651

T or F: aztreonam does not demonstrate cross-allergenicity to PCN's or cephs.

Back 651

true

Front 652

What are 3 beta-lactamase inhibitors?

Back 652

1. clavulinic acid
2. sulbactam
3. tazobactam

Front 653

How does vancomycin work?

Back 653

binds alanine-alanine pentapeptide to block transglycosylation reactions of chain building

Front 654

What bugs does vancomycin work against?

Back 654

1. MRSA
2. enterococci
3. c. difficile (2nd choice)

Front 655

What is the DOC for c. difficile?

Back 655

metronidazole

Front 656

What is the mechanism of resistance in VRE?

Back 656

change in target, terminal alanine is replaced by lactate

Front 657

What are 3 major AE's of vancomycin?

Back 657

1. "red man syndrome"
2. ototoxicity
3. nephrotoxicity

Front 658

What is the MOA for AG's?

Back 658

blocks initiation codon at the 30S site, leads to misreading of code

Front 659

How do AG's get into the bacteria?

Back 659

through porin channels via O2-dependent uptake (ineffective against anaerobes)

Front 660

What are 5 AG's?

Back 660

1. streptomycin
2. neomycin
3. gentamicin
4. tobramycin
5. amikacin

Front 661

AG's work mostly against what kind of bugs? Specifically?

Back 661

1. GNR's
2. enterococci (with PCN's)
3. pseudomonas (with extended-spectrum PCN or 3rd Gen Ceph)
4. bubonic plague and tularemia

Front 662

What are the 3 big AE's in AG's?

Back 662

1. nephrotoxicity
2. ototoxicity
3. NM blockade

Front 663

T or F: ototoxicity from AG's is not reversible.

Back 663

true

Front 664

What are the 5 tets?

Back 664

1. doxycycline
2. minocycline
3. tetracycline
4. tigecycline
5. demeclocycline

Front 665

How do tets work?

Back 665

blocks attachment of tRNA to acceptor site

Front 666

What bugs do tets work against?

Back 666

1. chlamydia
2. mycoplasma
3. h. pylori
4. rickettsia
5. b. burgdorferi
6. brucella
7. vibrio
8. plasmodium
9. b. anthracis
10. syphillis (2nd choice)

Front 667

Which tets are bile-excreted?

Back 667

doxycycline, minocycline, and tigecycline

Front 668

Which tet is used in meningococcal carriers?

Back 668

minocycline (gets into CSF)

Front 669

Which tet reaches higher concentrations in prostatic fluid and is used to treat prostatitis?

Back 669

doxycycline

Front 670

Which tet is used to treat SIADH because it blocks ADH receptor function in collecting ducts?

Back 670

demeclocycline

Front 671

T or F: tets are chelators.

Back 671

true; this will decrease their absorption

Front 672

Which tet is not affected by efflux pump resistance?

Back 672

tigecycline (also used for VRE, MRSA, and PRSP)

Front 673

Which tet causes vestibular reactions?

Back 673

minocycline

Front 674

Tets are the classic drugs that cause what AE?

Back 674

PC

Front 675

Fanconi syndrome results from what?

Back 675

using old or discarded tet meds

Front 676

Which classes of drugs work on the 30S subunit?

Back 676

AG's and tets

Front 677

What bugs will chloramphenicol work against?

Back 677

usually reserved for life-threatening infections: rickettsia, salmonella, b. fragilis, bacterial meningitis

Front 678

How does chloramphenicol work?

Back 678

inhibits activity of peptidyltransferase, prevents formation of peptide bond

Front 679

What are 3 major AE's of chloramphenicol?

Back 679

1. BMD
2. aplastic anemia
3. "gray baby syndrome"

Front 680

How does "gray baby syndrome" occur?

Back 680

neonates lack glucuronosyl transferase to metabolize drug, leads to NV and gray color

Front 681

What are the 3 macrolides?

Back 681

erythromycin, azithromycin, and clarithromycin

Front 682

How do macrolides work?

Back 682

inhibit translocation of peptidyl tRNA from acceptor to donor site

Front 683

What bugs do macrolides work against?

Back 683

1. same spectrum as PCN G
2. m. pneumoniae
3. chlamydia
4. b. pertussis
5. campylobacter
6. legionaire's
7. mycobacterium avium
8. diphtheria
9. h. pylori (clarithromycin)

Front 684

Which macrolide does not inhibit CYP3A4?

Back 684

azithromycin

Front 685

Which macrolide is safe in pregnancy?

Back 685

azithromycin

Front 686

Which macrolides are excreted in bile?

Back 686

erythromycin and clarithromycin

Front 687

What are the main 3 AE's in macrolides?

Back 687

1. GI distress due to motilin receptor stimulation
2. reversible deafness
3. cholestasis, jaundice (erythromycin estolate)

Front 688

How does clindamycin work?

Back 688

same as macrolides

Front 689

What bugs will clindamycin work against?

Back 689

1. anaerobic staph and strep
2. b. fragilis
3. c. perfringens

Front 690

Which ABX aren't used in pregnancy?

Back 690

1. AG's
2. macrolides (except azithromycin)
3. FQ's
4. sulfonamides
5. tets

Front 691

Clindamycin may help with what infections due to it's high concentration in this area?

Back 691

bone infections (osteomyelitis)

Front 692

What are the 2 big AE's of clindamycin?

Back 692

diarrhea and PC (classic)

Front 693

How does the quinupristin-dalfopristin drug combo work?

Back 693

quinupristin binds at same site as macrolides, then dalfopristin will interfere with polypeptide chain formation

Front 694

What does quinupristin-dalfopristin treat?

Back 694

1. VRE
2. VRSA
3. PRSP

Front 695

What are the 2 main AE's of quinupristin-dalfopristin?

Back 695

1. myalgias and arthralgias
2. CYP3A4 inhibitor

Front 696

How does linezolid work?

Back 696

blocks 30S and 50S from coming together-blocks initiation complex

Front 697

What does linezolid treat?

Back 697

1. VRE (both types)
2. VRSA
3. PRSP

Front 698

What are 2 AE's of linezolid?

Back 698

1. MAO inhibitor
2. BMD

Front 699

What drugs are called streptogramins?

Back 699

quinupristine and dalfopristin

Front 700

How does daptomycin work?

Back 700

binds to and forms pores in bacteria, leads to depolarization and cell death

Front 701

What does daptomycin treat?

Back 701

1. all gram positives
2. VRE (both types)
3. MRSA

Front 702

What are 2 AE's of daptomycin?

Back 702

1. myopathy
2. PC

Front 703

How do sulfonamides work?

Back 703

inhibit dihydropteroate synthetase, which inhibits folate synthesis (antimetabolite)

Front 704

What do sulfonamide-trimethoprim combos treat?

Back 704

1. uncomplicated UTI's
2. nocardiosis
3. toxoplasmosis
4. p. carinii
5. gram negatives (e. coli, salmonella, shigella, h. influenzae)
6. gram positives (staph and strep)

Front 705

What is sulfasalazine used to treat?

Back 705

UC or RA

Front 706

Which sulfonamide is used to treat bacterial conjunctivitis?

Back 706

sodium sulfacetamide

Front 707

How are sulfonamides metabolized?

Back 707

hepatic acetylation

Front 708

Why must sulfonamides be avoided in 3rd trimester?

Back 708

kernicterus can develop because of it's high plasma protein binding that displaces bilirubin from albumin

Front 709

How can you treat crystalluria that can develop in sulfonamide treatment due to lack of hydration?

Back 709

alkalinize urine

Front 710

How does trimethoprim work?

Back 710

inhibits DHFR, prevents folate synthesis (antimetabolite)

Front 711

What are the major AE's of trimethoprim-sulfonamides?

Back 711

1. rashes and SJS
2. phototoxicity
3. G6PD deficiency patients will have hemolysis
4. BMD
5. NV

Front 712

What are 4 FQ's?

Back 712

1. norfloxacin
2. ciprofloxacin
3. moxifloxacin
4. levofloxacin

Front 713

How do FQ's work?

Back 713

inhibits topoisomerases II and IV (II prevents overcoiling, IV separates replicated DNA); this prevents DNA synthesis

Front 714

What bugs do FQ's work against?

Back 714

1. pseudomonas (cipro)
2. neisseria
3. klebsiella
4. MSSA
5. chlamydia
6. shigella
7. salmonella
8. e. coli
9. campylobacter
10. legionella
11. mycoplasma
12. s. pneumo (levofloxacin)

Front 715

Which FQ is cleared hepatically?

Back 715

moxifloxacin

Front 716

T or F: antacids impair absorption of FQ's.

Back 716

true

Front 717

What are the major AE's of FQ's?

Back 717

1. NV
2. achilles tendon rupture
3. prolonged QT interval

Front 718

Why aren't FQ's used in kids?

Back 718

inhibits chondrogenesis

Front 719

What are 2 combos to treat h. pylori?

Back 719

1. BMT: bismuth, metronidazole, and tet
2. clarithromycin, amoxicillin, and omeprazole

Front 720

What drug is a urinary antiseptic?

Back 720

nitrofurantoin (3rd line for UTI's after sulfonamides and FQ's)

Front 721

What are 3 AE's of nitrofurantoin?

Back 721

1. brown urine
2. G6PD patients get hemolytic anemia
3. acute pneumonitis

Front 722

How does metronidazole work?

Back 722

inactive form taken up by parasite, electron is donated to drug to activate it, then it disrupts DNA and inhibits nucleic acid synthesis

Front 723

What bugs and worms does metronidazole work against?

Back 723

1. bacterioides, clostridium, and h. pylori
2. giardia, trichomonas, and entamoeba

Front 724

What are the main AE's of metronidazole?

Back 724

1. NVD
2. metallic taste
3. disulfiram-like effect

Front 725

How does isoniazid work?

Back 725

prodrug that converts via catalase from mycobacterium-inhibits mycolic acid synthesis

Front 726

Which anti-tubercular drug inhibits CYP3A4?

Back 726

isoniazid

Front 727

What are the main AE's of isoniazid?

Back 727

1. hepatitis
2. SLE-like syndrome
3. peripheral neuritis (always prescribe with vitamin B6 to prevent this)

Front 728

How does rifampin work?

Back 728

RNA polymerase inhibitor

Front 729

What are the 3 main AE's of rifampin?

Back 729

1. P450 inducer
2. red-orange urine
3. hepatitis

Front 730

What drug is used instead of rifampin in HIV patients?

Back 730

rifabutin

Front 731

What are the 2 main AE's of pyrazinamide?

Back 731

1. most hepatotoxic of antitubercular rx
2. hyperuricemia

Front 732

How does ethambutol work?

Back 732

inhibits arabinosyl transferases, which are necessary to cell wall synthesis

Front 733

What is the main AE in ethambutol?

Back 733

optic neuritis (also decreases red-green discrimination)

Front 734

Which anti-TB drug is not effective orally?

Back 734

streptomycin

Front 735

Which anti-TB drugs are hepatotoxic?

Back 735

RIP: rifampin, isoniazid, and pyrazinamide

Front 736

Which anti-TB drug is not bactericidal?

Back 736

ethambutol

Front 737

How do Amp B and nystatin work?

Back 737

bind ergosterol, form pores, cell becomes leaky and lyses

Front 738

Amp B can be given synergistically with what drug?

Back 738

flucytosine

Front 739

What are 2 major AE's of Amp B?

Back 739

1. nephrotoxicity
2. infusion-related cytokine storm

Front 740

How does flucytosine work?

Back 740

activated to 5-FU, will form 5-Fd-UMP, which inhibits thymidylate synthase, which inhibits thymine, which inhibits DNA synthesis

Front 741

What are 2 major AE's of flucytosine?

Back 741

1. BMD
2. NVD

Front 742

How does griseofulvin work?

Back 742

interferes with microtubule formation, disrupts mitotic spindle and prevents mitosis

Front 743

What does griseofulvin treat?

Back 743

tinea infections

Front 744

What are 4 AE's of griseofulvin?

Back 744

1. hepatotoxic
2. avoid in porphyrias
3. disulfiram-like reaction
4. P450 inducer

Front 745

How does terbinafine work?

Back 745

inhibits squalene metabolism, squaline is toxic to fungi

Front 746

What does terbinafine treat?

Back 746

DOC for tineas

Front 747

What drug will cause terbinafine clearance?

Back 747

rifampin

Front 748

What are the major AE's of terbinafine?

Back 748

1. hepatotoxic
2. neutropenia

Front 749

How do "azoles" work?

Back 749

inhibit 14-alpha-demethylase, a fungal P450 enzyme, which converts lanosterol to ergosterol

Front 750

Ketoconazole is used to treat what 3 non-fungal diseases?

Back 750

1. adrenal CA (decreases corticosteroids)
2. prostate CA (decreases testosterone)
3. Cushing's Syndrome (decreases glucocorticoids)

Front 751

Ketoconazole is used to treat what mostly?

Back 751

tineas and candidasis

Front 752

What decreases ketoconazole absorption? Increases?

Back 752

antacids lower absorption; food or cola

Front 753

Which "azole" is used to treat fungal meningitis?

Back 753

fluconazole (only "azole" that goes into CSF)

Front 754

Which azole is DOC for candidiasis and coccidiomycoses?

Back 754

fluconazole

Front 755

Which azole is DOC for blastomycoses and sporotrichoses?

Back 755

itraconazole

Front 756

What are the major AE's of all azoles?

Back 756

decreased steroid synthesis and hepatotoxicity

Front 757

Which antivirals work by blocking viral penetration/uncoating?

Back 757

amantadine, enfuvirtide

Front 758

Which antivirals work by inhibiting DNA polymerase?

Back 758

acyclovir, ganciclovir, and foscarnet

Front 759

Which antivirals work by inhibiting RNA polymerase?

Back 759

foscarnet, ribavirin

Front 760

Which antivirals work by inhibiting viral reverse transcriptase?

Back 760

zidovudine, didanosine, zalcitabine, lamivudine, stavudine, nevirapine, delavirdine, and efavirenz

Front 761

Which antivirals work by inhibiting viral aspartate protease?

Back 761

indinavir, ritonavir, saquinavir, nelfinavir

Front 762

Which antvirals work by inhibiting viral neuraminidase?

Back 762

zanamivir, oseltamivir

Front 763

What are 3 antiherpetics?

Back 763

acyclovir, ganciclovir, and foscarnet

Front 764

Which antiherpetic works on CMV?

Back 764

ganciclovir

Front 765

How does acyclovir work?

Back 765

phosphorylated by viral thymidine kinase to triphosphate form, inhibits viral DNA polymerase and terminates chain

Front 766

T or F: acyclovir helps with postherpetic neuralgia.

Back 766

false, only decreases acute neuritis, but no effect on postherpetic neuralgia

Front 767

What are 2 major AE's of IV acyclovir? How can this be avoided?

Back 767

1. crystalluria and neurotoxicity
2. hydration and slow infusion

Front 768

What are the main AE's in ganciclovir?

Back 768

1. BMD
2. mucositis
3. crystalluria
4. seizures

Front 769

What is foscarnet used to treat?

Back 769

acyclovir and ganciclovir-resistant herpes infections

Front 770

What are 2 major AE's of foscarnet?

Back 770

1. nephrotoxicity
2. hypocalcemia

Front 771

What is the MOA for zanamivir and oseltamivir?

Back 771

inhibit neuraminidase, less particles for virus spread

Front 772

What are zanamivir and oseltamivir used to treat?

Back 772

influenza A and B

Front 773

What are the main AE's of zanamivir and oseltamivir?

Back 773

1. NV (both)
2. zanamivir causes nasal and throat irritation and bronchospasm (not for COPD or asthma)

Front 774

Which drug is effective for prophylaxis and treatment, zanamivir or oseltamivir?

Back 774

oseltamivir

Front 775

What is the MOA for amantadine and rimantadine?

Back 775

prevents viral uncoating

Front 776

What are amantadine and rimantadine used to treat?

Back 776

1. influenza A
2. parkinsonism (amantadine)

Front 777

What are the main AE's of amantadine and rimantadine?

Back 777

1. CNS effects
2. atropine-like peripheral effects and livedo reticularis

Front 778

What is the MOA for ribavirin?

Back 778

inhibits IMP dehydrogenase, RNA polymerase, and end-capping of RNA

Front 779

What is ribavirin used to treat?

Back 779

1. HBV and HCV in combo with interferon-alpha
2. RSV

Front 780

What are the 3 main AE's of ribavirin?

Back 780

1. pulmonary problems
2. anemia
3. teratogenic

Front 781

T or F: whether you follow a NNRTI or PI regimen, you always add at least 2 NRTI's.

Back 781

true

Front 782

What are 5 NRTI's?

Back 782

1. lamivudine
2. zidovudine
3. stavudine
4. didanosine
5. zalcitabine

Front 783

What are 5 PI's?

Back 783

1. ritonavir
2. indinavir
3. amprenavir
4. nelfinavir
5. saquinavir

Front 784

What are 3 NNRTI's?

Back 784

1. delavirdine
2. nevirapine
3. efavirenz

Front 785

What is the 1 fusion inhibitor?

Back 785

enfuvirtide

Front 786

What is the 1 CCR5 co-receptor antagonist?

Back 786

maraviroc

Front 787

What is the 1 integrase inhibitor?

Back 787

raltegravir

Front 788

How do NRTI's work?

Back 788

phosphorylated to triphosphate that inhibits reverse transcriptase, also causes chain termination

Front 789

What are 2 black box warnings for NRTI's?

Back 789

lactic acidosis and hepatic steatosis

Front 790

What is the major AE for zidovudine?

Back 790

hematotoxicity

Front 791

What is the major AE for didanosine and zalcitabine?

Back 791

pancreatitis

Front 792

What is the least toxic NRTI? What is it also used to treat?

Back 792

lamivudine; also used in HBV

Front 793

Most NRTI's cause what?

Back 793

peripheral neuropathy

Front 794

How do NNRTI's work?

Back 794

bind directly to HIV reverse transcriptase, conformational change occurse, can't add nucleotides

Front 795

Which NNRTI is preferred? Which is safe for pregnancy?

Back 795

efavirenz; nevirapine

Front 796

NNRTI's have what major AE in general?

Back 796

P450 problems

Front 797

What are 2 major AE's in efavirenz?

Back 797

neuropsychiatric and teratogenic

Front 798

What are 2 major AE's in nevirapine?

Back 798

SJS/TEN and hepatitis

Front 799

How do PI's work?

Back 799

binds to a dipeptide inside of aspartate protease, the viral enzyme that cleaves precursor polypeptides in HIV buds to form proteins in mature virus core

Front 800

NRTI's should always be given with what other thing?

Back 800

folic acid

Front 801

What are 3 main AE's in PI's?

Back 801

1. hepatotoxicity
2. GI distress
3. disordered lipid metabolism
4. CYP3A4 inhibitors

Front 802

What is the MOA for enfuviritide?

Back 802

binds gp41 and inhibits fusion of HIV-1 to CD4 cells