Usmle Pharmacology

Front 1

amount of drug in body/_______ = Vd

Back 1

plasma drug concentration (note: Vd is Volume of Distribution)

Front 2

rate of elimination of drug/[plasma drug] = ?

Back 2

CL (Clearance)

Front 3

(.7)(Vd)/CL = ?

Back 3

T 1/2

Front 4

A drug infused at a constant rate reaches about 94% of steady state after _______ t 1/2s.

Back 4

4

Front 5

Dosage Calculations

Back 5

p. 288

Front 6

A loading dose is calculated using this formula.

Back 6

(Cp)(Vd)/F (note: Cp = target plasma concentration, and F = bioavailability)

Front 7

A maintenance dose is calculated using this formula.

Back 7

(Cp)(CL)/F

Front 8

Elimination of Drugs

Back 8

p. 288

Front 9

Rate of elimination is proportional to _______ ______ in 1st order elimination.

Back 9

drug concentration

Front 10

In the case of EtOH, which is elimated by _____ order elimination, a constant amount of drug is eliminated per unit time.

Back 10

zero

Front 11

Phase I vs. Phase II metabolism

Back 11

p. 289

Front 12

Phase ____ (I or II) reactions yield slightly polar metabolites that are often _____ (active or inactive)

Back 12

I, active

Front 13

Phase ____ (I or II) reactions yield very polar metabolites that are often _____ (active or inactive) and are excreted by the _______.

Back 13

II, inactive, kidney

Front 14

Phase II reactions are often of this type.

Back 14

conjugation

Front 15

Cytochrome P-450 is involved in _____ phase (I or II) reactions.

Back 15

I

Front 16

Drug Development

Back 16

p. 289

Front 17

A patent lasts for _____ years after filing for application.

Back 17

20

Front 18

How many phases are there in drug development?

Back 18

4

Front 19

Drugs are first tested in patients in phase _____ of clinical testing, pharmacokinetic safety is determined in phase ______ of clinical testing, double blind tests are done in phase ____ and post-market surveillance is done in phase _____.

Back 19

2,1,3,4

Front 20

Pharmacodynamics

Back 20

p. 289

Front 21

In a dose response curve, a competitive antagonist shifts the curve _____, while a non-competitive antagonist shifts the curve ______.

Back 21

right, down

Front 22

What pharmacologic relationship would determine the existence of spare receptors?

Back 22

EC50 < Kd

Front 23

What does it mean if EC50 and Kd are equal?

Back 23

The system does not have spare receptors

Front 24

A partial agonist acts on the same receptor system as a full agonist? T/F

Back 24

TRUE

Front 25

What's the main difference between a partial agonist and a full agonist?

Back 25

A partial agonist has a lower maximal efficacy.

Front 26

Is a partial agonist less potent than a full agonist?

Back 26

Not necessarily. It can be less, more or equally potent as a full agonist.

Front 27

Antimicrobial Tx -- Mechanism of Action

Back 27

p. 291

Front 28

The penicillin type drugs work by blocking ------ synthesis, specifically by inhibiting this molecule from cross-linking?

Back 28

blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.

Front 29

Which other drugs (aside from penicillin) have this same mechanism of action?

Back 29

Imipenem, aztreonam and cephalosporins

Front 30

Bacitracin, vancomycin and cycloserine block the synthesis of this molecule, preventing cell wall synthesis

Back 30

peptidoglycans

Front 31

These drugs block the 50s ribosomal subunit

Back 31

clindamycin, chloramphenicol, erythromycin, lincomycin, linezolid, streptogramins "Buy AT 30, CELL at 50"

Front 32

These drugs block the 30s ribosomal subunit

Back 32

Aminoglycosides and tetracyclines "Buy AT 30, CELL at 50"

Front 33

These drugs block nucleotide synthesis by interfering with the folate pathway

Back 33

Sulfonamides (e.g. Bactrim), trimethoprim

Front 34

These drugs block DNA topoisomerases

Back 34

Quinolones (e.g. Cipro)

Front 35

Which drug blocks mRNA synthesis

Back 35

rifampin

Front 36

Which are the bacteriacidal Abx

Back 36

Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole

Front 37

These drugs disrupt the bacterial/fungal cell membranes

Back 37

polymyxins

Front 38

These specific disrupt fungal cell membranes

Back 38

amphotericin B, nystatin, fluconazole/azoles (FAN the fungal cell membranes)

Front 39

What is the mechanism of action of Pentamidine

Back 39

Unknown

Front 40

Penicillin

Back 40

p. 291

Front 41

Which is the IV form and which is the oral form

Back 41

G = IV, V=oral

Front 42

Which of these is not a mechanism of penicillin action: (1) binds penicillin-binding protein, (2) blocks peptidoglycan synthesis, (3) blocks transpeptidase catalyzed cross-linking of cell wall and (4) activates autolytic enzymes

Back 42

Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and cycloserine do that

Front 43

T or F: penicillin is effective against gram pos and gram neg rods

Back 43

False: penicillin is used to treat common streptococci (but not staph), meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not used to treat gram neg rods.

Front 44

What should you watch out for when giving penicillin?

Back 44

Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia

Front 45

Methicillin, nafcillin, dicloxacillin

Back 45

p. 291

Front 46

These drugs are used mainly for what type of infection

Back 46

Staphlococcal infection (hence very narrow spectrum)

Front 47

T or F: these drugs have the same mechanism of action as penicillin

Back 47

TRUE

Front 48

Are these drugs penicillinase resistant? If so why?

Back 48

Bulkier R group makes these drugs resistant to penicillinase

Front 49

What should you watch out for when giving these drugs?

Back 49

Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase interstitial nephritis

Front 50

Ampicillin and amoxicillin

Back 50

p. 291

Front 51

T or F: these drugs have the same mechanism of action as penicillin

Back 51

TRUE

Front 52

Which has greater oral bioavailability?

Back 52

amOxicillin (O for Oral)

Front 53

What do you use these for?

Back 53

Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella)

Front 54

Can penicillinase effect these drugs efficacy?

Back 54

Yes, they are penicillinase sensitive

Front 55

Why not give these drugs with a penicillinase inhibitor. Name one.

Back 55

clavulanic acid

Front 56

What should you watch out for when giving these drugs?

Back 56

Hypersensitivity rxn (ampicillin rash), pseudomembranous colitis

Front 57

Carbenicillin, piperacillin, ticarcillin

Back 57

p. 292

Front 58

Why are these considered to have an extended spectrum?

Back 58

Because they are effective against pseudomonas and other gram neg rods (enterobacter and some species of klebsiella)

Front 59

What should you watch out for when giving these drugs?

Back 59

Hypersensitivity rxn

Front 60

Why does concomitant administration with clavulanic acid increase the efficacy of these drugs?

Back 60

Because they are penicillinase sensitive. (only piperacillin and ticarcillin)

Front 61

Cephalosporins

Back 61

p. 292

Front 62

What is the mechanism of action of Cephalosporins?

Back 62

inhibit cell wall synthesis

Front 63

How are they similar/different from penicillin?

Back 63

both have a beta-lactam ring structure but cephalosporins are less susceptible to penicillinases

Front 64

What are the main similarities/difference between 1st and 2nd generation cephalosporins?

Back 64

2nd gen has extensive gram neg coverage but weaker gram pos coverage

Front 65

1st gen covers what bugs?

Back 65

gram positives (staph and strep), Proteus mirabilis, E. coli, Klebsiella (PEcK)

Front 66

2nd gen covers what bugs?

Back 66

gram positives (staph and strep) though less so, H. influenzae, Enterobacter aerogenes, Neisseria, Proteus mirabilis, E. coli, Klebsiella (HEN PEcK)

Front 67

What can 3rd generation drugs do that 1st and 2nd generation can't?

Back 67

Cross the blood brain barrier

Front 68

What are some other benefits of 3rd gen?

Back 68

better activity against gram neg bugs resistant to beta-lactam drugs. Ceftazidime for Pseudomonas and ceftriaxone for N. gonorrhea

Front 69

What are the benefits of 4th gen (e.g. Cefipime)?

Back 69

increased activity against Pseudomonas, gram pos organisms and more beta-lactamase resistant (i.e. 4th gen combines 1st gen and 3rd gen characteristics into super drug)

Front 70

What drugs should you avoid taking with cephalosporins?

Back 70

Aminoglycosides (increases nephrotoxicity) and ethanol (causes a disulfiram-like rxn -- headache, nausea, flushing, hypotension)

Front 71

Aztreonam

Back 71

p. 292

Front 72

When would you use aztreonam?

Back 72

Only to treat Klebsiella, Pseudomonas and Serratia spp.

Front 73

Is it beta-lactamase resistant?

Back 73

Yes, this is one of the huge benefits of the drug, and it is not cross-reactive with PCN!

Front 74

Which population of pt. is this drug good for?

Back 74

The PCN-allergic patient that can't take aminoglycosides b/c of renal insufficiency

Front 75

Are there any toxicity issues with this drug?

Back 75

Not really. Generally well tolerated with occasional GI upset. Vertigo, Headache and rare hepatotoxicity have been reported.

Front 76

Imipenem/cilastatin

Back 76

p.293

Front 77

What is imipenem?

Back 77

broad spectrum beta-lactamase-resistant abx

Front 78

What do you always administer it with and why?

Back 78

cilastatin -- it decreases inactivation of imipenem in renal tubules

Front 79

What do you use it for?

Back 79

Gram pos cocci, gram neg rods and anaerobes (broad spectrum)

Front 80

What bug is it the drug of choice for?

Back 80

Enterobacter

Front 81

What are its side-effects

Back 81

GI distress, skin rash, seizures at high conc.

Front 82

Vancomycin

Back 82

p. 293

Front 83

Is it bactericidal or bacteriastatic and why?

Back 83

Bactericidal because it blocks cross linkage and elongation of peptidoglycan by binding D-ala D-ala protion of cell wall.

Front 84

How does resistance to Vanco occur?

Back 84

D-ala D-ala is replaced with D-ala D-lactate which vanco does not block

Front 85

What is it used for?

Back 85

Used for serious infection that is resistant to other drugs (e.g. gram pos multi-drug resistant organisms like S. aureus and C. difficile, methicillin resistant staph (MRSA))

Front 86

What are the important toxicities of vanco?

Back 86

generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis

Front 87

What can happen with rapid infusion of vanco?

Back 87

"Red man's" syndrome. Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate

Front 88

Protein Synthesis Inhibitors

Back 88

p. 293

Front 89

Which drugs target bacterial protein synthesis by blocking the 30S unit vs 50S unit?

Back 89

Buy AT 30, CELL at 50

Front 90

What does AT stand for?

Back 90

A = Aminoglycosides (streptomycin, gentamicin, tobramycin an damikacin. And T = Tetracyclines

Front 91

What does CELL stand for?

Back 91

C = Chloramphenicol, E= Erythromycin, L= Lincomycin and L= cLindamycin

Front 92

Which of the above are bactericidal?

Back 92

Only the aminoglycosides are, the rest are bacteriostatic

Front 93

Aminoglycosides

Back 93

p. 294

Front 94

Name some aminoglycosides?

Back 94

Gentamicin, neomycin, amikacin, tobramycin and streptomycin

Front 95

How do these drugs work?

Back 95

They inhibit formation of the initiation complex in mRNA translation

Front 96

Why are they ineffective against anaerobes?

Back 96

They require oxygen for uptake into bacteria

Front 97

When would you use aminoglycosides?

Back 97

against severe gram-negative rod infections

Front 98

What drugs can you use aminoglycosides with for synergy?

Back 98

the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -- the beta-lactam antibiotics). Presumably this allows the drug to get in with out reliance on oxygen transport

Front 99

What drug in this class is commonly used for bowel surgery?

Back 99

Neomycin

Front 100

What are the two major toxicities?

Back 100

Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides

Front 101

Tetracyclines

Back 101

p. 294

Front 102

Name some tetracylcines

Back 102

Tetracycline, doxycycline, demeclocycline, minocycline

Front 103

How does it work?

Back 103

Blocks t-RNA attachment to 30S subunit

Front 104

Which tetracycline can you use in patients with renal failure and why?

Back 104

Can use doxycycline because its elimination is fecal

Front 105

Should you take these drugs with a glass of milk?

Back 105

NO, because it intereferes with absorption in the gut as does antacids and iron-containing preparations

Front 106

What are tetracyclines used for?

Back 106

VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi, Rickettsia, tularemia

Front 107

What are the common toxicities

Back 107

GI distress, teeth discoloration, inhibition of bone growth in children, Fanconi's syndrome and photosensitivity

Front 108

Macrolides

Back 108

p. 294

Front 109

Name some macrolides?

Back 109

Erythromycin, azithromycin, clarithromycin

Front 110

How do these drugs work?

Back 110

inhibit protein synthesis

Front 111

What are they used for?

Back 111

URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.

Front 112

Pneumonic for macrolide use?

Back 112

Eryc's Nipple is at his Mid Clavicular Line (Eryc is brand name for erythromycin). Mycoplasm, Legionella, Chlamydia, Neisseria.

Front 113

What are the major toxicities?

Back 113

GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes

Front 114

What is the most common cause for non-compliance to macrolides?

Back 114

GI discomfort

Front 115

Chloramphenicol

Back 115

p. 294

Front 116

How does this drug work?

Back 116

inhibits 50S peptidyltransferase

Front 117

Main use?

Back 117

Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively b/c of toxicity

Front 118

What are the main toxicities?

Back 118

Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in premes b/c they lack UDP-glucoronyl transferase)

Front 119

Clindamycin

Back 119

p. 294

Front 120

How does it work?

Back 120

blocks peptide bond formation at 50S

Front 121

When do you use it?

Back 121

Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens)

Front 122

Toxicities?

Back 122

Pseudomembranous colitis, fever, diarrhea

Front 123

Sulfonamides

Back 123

p. 295

Front 124

Name some sulfonamides

Back 124

Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine

Front 125

How does it work?

Back 125

Inhibits bacterial folic acid synthesis from PABA by blocking dihydropteroate synthase.

Front 126

What are its uses?

Back 126

Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX for simple UTIs

Front 127

Toxicities?

Back 127

hypersensitivity rxn, hemolysis if G6PD deficient, nephorotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (e.g. warfarin)

Front 128

Trimethoprim

Back 128

p. 295

Front 129

How does it work?

Back 129

inhibits folic acid pathway by blocking dihydrofolate reductase which humans have as well

Front 130

What are its uses?

Back 130

used in combo with Sulfamethoxazole (TMP-SMX) causing a sequential block of folate synthesis. Used for recurrent UTIs, Shigella, Salmonella, and prophylaxis for PCP in AIDS patients

Front 131

Toxicities?

Back 131

Megaloblastic anemia, pancytopenia (may be alleviated with supplemental folinic acid)

Front 132

Fluoroquinolones

Back 132

p. 295

Front 133

What the most famous floroquinolone?

Back 133

Ciprfloxacin (treatment for Anthrax)

Front 134

How does it work?

Back 134

inhibits DNA gyrase (topoisomerase II)

Front 135

What are its uses?

Back 135

Gram neg rods or urinary and GI tract (incl. pseudomonas), Neisseria, some gram pos spp

Front 136

What population is contraindicated for use?

Back 136

pregnancy and children

Front 137

What are its toxicities?

Back 137

GI upset, superinfection, skin rashes, headache, dizziness and tendonitis and tendon rupture in adults. FluoroquinoLONES hurt attachment to BONES.

Front 138

Metronidazole

Back 138

p. 296

Front 139

How does it work?

Back 139

forms toxic metabolites in the bacteria. Bactericidal.

Front 140

What are its uses?

Back 140

anti-protozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (bacteroides, clostridium)

Front 141

What is the role of Metronidazole in H. pylori infection?

Back 141

Used as part of triple therapy: bismuth, amoxicillin and metronidazole

Front 142

Main toxicity?

Back 142

disulfiram-like (antabuse) reaction to alcohol and headache

Front 143

Which drug do you use to treat anaerobic infections above the diaphram and below the diaphram

Back 143

anaerobes above diaphram: Clindamycin, and anaerobes below diaphram: metronidazole

Front 144

Polymyxins

Back 144

p. 296

Front 145

How does it work?

Back 145

disrupts osmotic properties of bacteria, acts like a detergent

Front 146

What is it used for?

Back 146

resistant gram negative infections

Front 147

Toxicities?

Back 147

neurotoxicity, ATN

Front 148

Isoniazid

Back 148

p. 296

Front 149

How does it work?

Back 149

decreases synthesis of mycolic acid

Front 150

What is it used for?

Back 150

MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis against TB

Front 151

Toxicities?

Back 151

Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicitiy, drug induced SLE. INH, Injures Neurons and Hepatocytes

Front 152

What vitamin prevents neurotoxicity

Back 152

Vitamin B6 (pyridoxine)

Front 153

Why are toxicities particularly important to monitor in patients taking INH?

Back 153

INH half-lives are different in fast versus slow acetylators!

Front 154

Rifampin

Back 154

P. 296

Front 155

How does it work?

Back 155

inhibits DNA-dependent RNA polymerase

Front 156

What is it used for?

Back 156

MTB, meningococcal prophylaxis

Front 157

Toxicities?

Back 157

Minor hepatotoxicity and increases P-450

Front 158

How can it be used for leprosy?

Back 158

rifampin delays resistance to dapsone when used for leprosy

Front 159

What would happen if you used rifampin alone?

Back 159

get rapid resistance

Front 160

What does it do to bodily fluids?

Back 160

makes them red/orange in color

Front 161

What are the 4 R's of Rifampin

Back 161

RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body fluids, Resistance is rapid

Front 162

Anti-TB Drugs

Back 162

p. 296

Front 163

What are the anti-TB drugs?

Back 163

Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -- RESPIre

Front 164

What do you use for TB prophylaxis?

Back 164

INH

Front 165

What toxicity is common to all?

Back 165

hepatotoxicity

Front 166

arachadonic acid products

Back 166

pg 150

Front 167

name the enzyme that liberates AA from the cell membrane

Back 167

phospholipase A2

Front 168

what does the lipoxygenase pathway yield

Back 168

leukotrienes (L for Lipoxygenase and Leukotrienes)

Front 169

LTB4 is a____

Back 169

neutrophil chemotactic agent

Front 170

which leukotrienes are involved in bronchoconstriction, vasoconstriction, smooth muscle contraction, and increased vascular permeability

Back 170

LT C4, D4, E4 (SRS-A)

Front 171

what are the 3 products of the cyclooxygenase pathway?

Back 171

thromboxane, prostacyclin, prostaglandin

Front 172

what are the 2 functions of TxA2

Back 172

platelet aggregation, vasoconstricion

Front 173

what are the 2 functions of PGI2

Back 173

inhibition of platelet aggregation; vasodilation (Platelet Gathering Inhibitor)

Front 174

microtubule

Back 174

pg 150

Front 175

what are the shape and dimensions of a microtubule?

Back 175

cylindrical, 24 nm in diameter, variable length.

Front 176

what are the components of a microtubule

Back 176

polymerized dimers of alpha and beta tubulin (+2 GTPs per dimer)

Front 177

where are microtubules found

Back 177

cilia, flagella, mitotic spindles, neuronal axons (slow axoplasmic transport)

Front 178

antihelminthic drug that acts on microtubules

Back 178

mebendazole/thiabendazole

Front 179

anti breast cancer drug that acts on microtubules (prevent disassembly)

Back 179

taxol

Front 180

antifungal drug that acts on microtubules

Back 180

griseofluvin

Front 181

anti cancer drug that acts on microtubules (prevent assembly)

Back 181

vincristine/vinblastine

Front 182

anti gout drug that acts on microtubules

Back 182

cholchicine

Front 183

Resistance mechanisms for various antibiotics

Back 183

p297

Front 184

Most common resistance mechanism for penicillins / cephalosporins.

Back 184

Beta-lactamase cleavage of beta-lactam ring.

Front 185

Most common resistance mechanism for aminoglycosides.

Back 185

Modification via acetylation, adenylation, or phosphorylation.

Front 186

Most common resistance mechanism for vancomycin.

Back 186

Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.

Front 187

Most common resistance mechanism for Chlorampenicol.

Back 187

Modification via acetylation.

Front 188

Most common resistance mechanism for macrolides.

Back 188

Methylation of rRNA near erythromycin's ribosome-binding site.

Front 189

Most common resistance mechanism for tetracycline.

Back 189

Decrease uptake or increase transport out of cell.

Front 190

Most common resistance mechanism for sulfonamides.

Back 190

Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or increase PABA synthesis.

Front 192

Nonsurgical antimicrobial prophylaxis

Back 192

p297

Front 193

Drug of choice for meningococcal infection.

Back 193

Rifampin (drug of choice), minocycline.

Front 194

Drug of choice for gonorrhea.

Back 194

Cefriaxone.

Front 195

Drug of choice for syphilis.

Back 195

Benzathine penicillin G.

Front 196

Drug of choice for history of recurrent UTIs.

Back 196

TMP-SMX.

Front 197

Drug of choice for Pneumocystis carinii pneumonia.

Back 197

TMP-SMX (drug of choice), aerosolized pentamindine.

Front 199

Anti-fungal therapy

Back 199

p297

Front 200

Mechanism of action of the anti-fungal therapy polyenes.

Back 200

Form artificial pores in the cytoplasmic membrane.

Front 201

Mechanism of action of the anti-fungal therapies terbinafine and azoles.

Back 201

Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the conversion of lanosterol to ergosterol.

Front 202

Mechanism of action of the anti-fungal therapy flucytosine.

Back 202

Blocks the production of purines from the precurors.

Front 203

Mechanism of action of the anti-fungal therapy griseofulvin.

Back 203

Disrupts microtubles.

Front 205

Amphotericin B

Back 205

p298

Front 206

Mechanism of action of Amphotericin B.

Back 206

Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the fungal membrane by forming pores."

Front 207

Clinical uses of Amphotericin B.

Back 207

Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.

Front 208

Symptoms of Amphotericin B toxicity.

Back 208

Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").

Front 210

Nystatin

Back 210

p298

Front 211

Mechanism of action of Nystatin.

Back 211

Binds to ergosterol, disrupting fungal membranes.

Front 212

Clinical use of Nystatin.

Back 212

"Swish and swallow" for oral candidiasis (thrush).

Front 214

Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.

Back 214

p298

Front 215

Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.

Back 215

Inhibits fungal steroid (ergosterol) synthesis.

Front 216

Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.

Back 216

Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.

Front 217

Symptoms of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole toxicity.

Back 217

Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.

Front 219

Flucytosine

Back 219

p298

Front 220

Mechanism of action of Flucytosine.

Back 220

Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil.

Front 221

Clinical uses of Flucytosine.

Back 221

Used in sytemic fungal infections (e.g. Candida, Cryptococcus).

Front 222

Symptoms of Flucytosine toxicity.

Back 222

Nausea, vomitting, diarrhea, bone marrow suppression.

Front 224

Caspofungin

Back 224

p298

Front 225

Mechanism of action for Caspofungin.

Back 225

Inhibits cell wall synthesis.

Front 226

Clinical use of Caspofungin.

Back 226

Invasive aepergillosis.

Front 227

Symptoms of Caspofungin toxicity.

Back 227

GI upset, flushing.

Front 229

Terbinafine

Back 229

p298

Front 230

Mechanism of action of Terbinafine.

Back 230

Inhibits the fungal enzyme squalene epoxidase.

Front 231

Clinical use of Terbinafinel.

Back 231

Used to treat dermatophytoses (especially onychomycosis).

Front 233

Griseofulvin

Back 233

p298

Front 234

Mechanism of action of Griseofulvin.

Back 234

Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails).

Front 235

Clinical use of Griseofulvin.

Back 235

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).

Front 236

Symptoms of Griseofulvin toxicity.

Back 236

Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism.

Front 238

Antiviral chemotherapy

Back 238

p299

Front 239

Viral adsorption and penetration into the cell is blocked by ---------.

Back 239

Gama-globulins (non-specific).

Front 240

Uncoating of the virus after its penetration into the cell is blocked by --------.

Back 240

Amantadine (influenza A).

Front 241

Early viral protein synthesis is blocked by --------.

Back 241

Fomivirsen (CMV).

Front 242

Viral nuclei acid synthesis is blocked by --------.

Back 242

Purine, pyrimidine analogs; reverse transcriptase inhibitors.

Front 243

Late viral protein synthesis and processing is blocked by --------.

Back 243

Methimazole (variola); protease inhibitors.

Front 244

Packaging and assembly of new viron is blocked by --------.

Back 244

Rifampin (vaccinia).

Front 246

Amantadine

Back 246

p299

Front 247

Mechanism of action of Amantadine.

Back 247

Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."

Front 248

Clinical uses of Amantadine.

Back 248

Prophylaxis for influenza A; Parkinson's disease.

Front 249

Symptoms of Amantadine toxicity.

Back 249

Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.)

Front 250

Zanamivir

Back 250

p299

Front 251

Mechanism of action of Zanamivir.

Back 251

Inhibits influenza neuraminidase.

Front 252

Clinical use of Zanamivir.

Back 252

Both influenza A and B.

Front 254

Ribavirin

Back 254

p299

Front 255

Mechanism of action of Ribavirin.

Back 255

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.

Front 256

Clinical use of Ribavirin.

Back 256

RSV (respiratory syncytial virus).

Front 257

Symptoms of Ribavirin toxicity.

Back 257

Hemolytic anemia. Severe teratogen.

Front 259

Acyclovir

Back 259

p299

Front 260

Mechanism of aciton of Acyclovir.

Back 260

Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.

Front 261

Clinical use of Acyclovir.

Back 261

HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.

Front 262

Symptoms of Acyclovir toxicity.

Back 262

Delirium, tremor, nephrotoxicity.

Front 264

Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine)

Back 264

p300

Front 265

Mechanism of action of Ganciclovir.

Back 265

Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.

Front 266

Clinical use of Ganciclovir.

Back 266

CMV, especially in immunocompromised patients.

Front 267

Symptoms of Ganciclovir toxicity.

Back 267

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

Front 269

Foscarnet

Back 269

p300

Front 270

Mechanism of action of Foscarnet.

Back 270

Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."

Front 271

Clinical use of Foscarnet.

Back 271

CMV retinitis in immunocompromised patients when ganciclovir fails.

Front 272

Symptoms of Foscarnet toxicity.

Back 272

Nephrotoxicity.

Front 274

HIV therapy

Back 274

p300

Front 275

Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.

Back 275

Protease inhibitor.

Front 276

Mechanism of action of protease inhibitors.

Back 276

Inhibit assembly of new virus by blocking protease enzyme.

Front 277

Symptoms of protease inhibitor toxicity.

Back 277

GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir).

Front 279

Reverse transcriptase inhibitors:

Front 280

Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), and abacavir are examples of --------- reverse transcriptase inhibitors.

Back 280

Nucleoside.

Front 281

Nevirapine, delavirdine, and efavirenz are examples of --------- reverse transcriptase inhibitors.

Back 281

Non-nucleoside.

Front 282

Mechanism of action of reverse transcriptase inhibitors.

Back 282

Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of viral genome into host DNA.

Front 283

Symptoms of reverse transcriptase inhibitor toxicity.

Back 283

Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).

Front 284

Highly active antiretroviral therapy (HAART) generally entails combination therapy with ---------- and -----------.

Back 284

Protease inhibitors, reverse transcriptase inhibitors.

Front 285

When should HIV therapy be initiated?

Back 285

When patients have low CD4 counts (<500 cells/mm3) or high viral load.

Front 286

-------- is used during pregnancy to reduce risk of fetal transmission.

Back 286

AZT.

Front 288

Interferons

Back 288

p300

Front 289

Mechanism of action of Interferons.

Back 289

Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.

Front 290

Clinical use of Interferons.

Back 290

Chronic hepatitis B and C, Kaposi's sarcoma.

Front 291

Symptoms of Interferon toxicity.

Back 291

Neutropenia.

Front 293

Antiparasitic drugs

Back 293

p301

Front 294

Clinical uses of Ivermectin.

Back 294

Onchocerciasis "rIVER blindness treated with IVERmectin".

Front 295

Clinical uses of Mebendazole / thiabendazole.

Back 295

Nematode/roundworm (e.g., pinworm, whipworm) infections.

Front 296

Clinical uses of Pyrantel pamoate.

Back 296

Giant roundworm (Ascaris), hookworm (Necator/Ancylostoma), pinworm (Enterobius).

Front 297

Clinical uses of Praziquantel.

Back 297

Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis) and cysticercosis.

Front 298

Clinical uss of Niclosamide

Back 298

Cestode/tapeworm (e.g., Diphyllobothrium latum, Taenia species) infections except cysticercosis.

Front 299

Clinical uses of Pentavalent antimony.

Back 299

Leishmaniasis.

Front 300

Clinical uses of Chloroquine, quinine, mefloquine, atovaquone, proguanil.

Back 300

Malaria.

Front 301

Clinical uses of Primaquine.

Back 301

Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P.ovale).

Front 302

Clinical uses of Metronidazole.

Back 302

Giardiasis, amebic dysentery (Entamoeba histolytica), bacterial vaginitis (Gardnerella vaginalis), Trichomonas.

Front 303

Clinical uses of Pentamidine.

Back 303

Pneumocystis carinii pneumonia prophylaxis.

Front 304

Clinical uses of Nifurtimox.

Back 304

Chagas' disease, American trypanosomiasis (Trypanosoma cruzi).

Front 305

Clinical uses of Suramin.

Back 305

African trypanosomiasis (sleeping sickness).

Front 307

Pharmacology - CNS / Neurologic drugs

Back 307

p301

Front 308

Parasympathetic preganglionic neurons release the neurotransmitter -------- which act on -------- receptors.

Back 308

Ach, nicotinic.

Front 309

Sympathetic preganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.

Back 309

Ach, nicotinic.

Front 311

Autonomic drugs

Back 311

p302

Front 312

Cholinergic:

Front 313

Ach is synthesized from acetyl-CoA and choline by the enzyme ---------.

Back 313

Choline acetyltransferase.

Front 315

Noradrenergic:

Front 316

In the noradrenergic nerve terminal, tyrosine is hydroxylated to -------, which is decarboxylated to --------, which is finally hydroxylated to NE.

Back 316

DOPA, dopamine.

Front 317

The action of NE and DA is terminated by --------- and ----------.

Back 317

Reuptake, diffusion (different than for Ach).

Front 318

The drugs --------- and ---------- inhibit the reuptake of NE.

Back 318

Cocaine, TCA.

Front 319

Ach inhibits the release of NE from the noradrenergic nerve terminal by binding to --------- receptors.

Back 319

M1.

Front 321

Cholinomimetics

Back 321

p303

Front 322

Direct agonists:

Front 323

Clinical application and action of Carbachol and Pilocarpine.

Back 323

Glaucoma. / Activates ciliary muscle of eye (open angle), pupillary sphincter (narrow angle).

Front 325

Indirect agonists (anticholinesterases):

Front 326

Clinical application / action of Neostigmine.

Back 326

Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative). / Increase endogenous Ach.

Front 327

Clinical application / action of Pyridostigmine.

Back 327

Myasthenia gravis. / Increase Ach; increase strength.

Front 328

Clinical application / action of Physostigmine.

Back 328

Glaucoma (crosses blood-brain barrier) and atropine overdose. / Increase endogenous Ach.

Front 329

Clinical application / action of Echothiophate.

Back 329

Glaucoma. / Increase endogenous Ach.

Front 331

Symptoms of cholinesterase inhibitor poisoning.

Back 331

Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation (also abdominal cramping). "DUMBBELSS".

Front 332

Cholinesterase inhibitor poisoning may be caused by ---------.

Back 332

Parathion and other organophosphates.

Front 333

The cholinesterase regenerator ------- can be used as an antidote for cholinesterase inhibitor poisoning.

Back 333

Pralidoxime.

Front 334

Mechanism of action of Pralidoxime.

Back 334

Regenerates active cholinesterase, chemical antagonist, used to treat organophosphate exposure.

Front 336

Cholinoreceptor blockers:

Back 336

p303

Front 337

Clinical uses of the muscarinic antagonist Atropine.

Back 337

Dilate pupils, decrease acid secretion in peptic ulcer disease, decrease urgency in mild cystitis, decrease GI motility, reduce airway secretions, and treat organophosphate poisoning. "Blocks SLUD: Salivation, Lacrimation, Urination, Defecation."

Front 338

Side effects of Atropine.

Back 338

Increase body temp, rapid pulse, dry mouth, dry/flushed skin, disorientation, mydriasis with cycloplegia, and constipation. "Atropine parasympathetic block side effects: Blind as bat, Red as a beet, Mad as a hatter, Hot as a hare, Dry as a bone."

Front 340

Hexamethonium (ganglionic blocker) blocks -------- receptors.

Back 340

Nicotinic.

Front 341

antimuscarinic drugs

Back 341

p. 304

Front 342

"tropi" are anti-muscarinic

Back 342

while vacationing in the tropics you lie on a beach and your muscles waste away!

Front 343

benztropine is used to treat

Back 343

Parkinson's disease

Front 344

scopolamine is used to treat

Back 344

motion sickness

Front 345

scopolamine is an antimuscarinic that does not convert to the mnemonic!

Front 346

name 2 antimuscarinic drugs that act on the CNS

Back 346

benztropine, scopolamine

Front 347

name a muscarinic used to treat motion sickness

Back 347

scopolamine

Front 348

name a muscarinic used to treat Parkinson's disease

Back 348

benztropine

Front 349

mechanism of action of benztropine

Back 349

antimuscarinic

Front 350

mechanism of action of scopolamine

Back 350

antimuscarinic

Front 351

name three antimuscarinics that act on eye

Back 351

atropine, homatropine, tropicamide

Front 352

the action of atropine is ______

Back 352

produce mydriasis, cycloplegia

Front 353

mechanism of atropine is

Back 353

antimuscarinic

Front 354

the action of homatropine is ______

Back 354

produce mydriasis, cycloplegia

Front 355

mechanism of homatropine is

Back 355

antimuscarinic

Front 356

the action of tropicamide is

Back 356

produce mydriasis, cycloplegia

Front 357

mechanism of tropicamide is

Back 357

antimuscarinic

Front 358

ipatropium is used to treat

Back 358

asthma, COPD

Front 359

mechanism of ipatropium is

Back 359

antimuscarinic

Front 360

name an antimuscarinic used to treat asthma and COPD

Back 360

ipatropium

Front 362

neuromuscular blocking drugs

Back 362

p. 304

Front 363

neuromuscular blocking drugs are used for

Back 363

muscle paralysis in surgery or mechanical ventilation

Front 364

name a depolarising neurmuscular blocking drug

Back 364

succinylcholine

Front 365

name 6 nondepolarizing neuromuscular blocking drugs

Back 365

tubocurarine

Front 366

*mnemonic -- the "cur" drugs are nondepolarizing neuromuscular blocking agents

Back 366

atracurium

Back 367

mivacurium

Back 368

pancuronium

Back 369

vecuronium

Back 370

rapacuronium

Front 371

is succinylcholine depolarizing or nondepolarizing?

Back 371

depolarizing

Front 372

is tubocurarine depolarizing or nondepolarizing?

Back 372

nondepolarizing

Front 373

is atracurium depolarizing or nondepolarizing?

Back 373

nondepolarizing

Front 374

is mivacurium depolarizing or nondepolarizing?

Back 374

nondepolarizing

Front 375

is pancuronium depolarizing or nondepolarizing?

Back 375

nondepolarizing

Front 376

is vacuronium depolarizing or nondepolarizing?

Back 376

nondepolarizing

Front 377

is rapacuronium depolarizing or nondepolarizing?

Back 377

nondepolarizing

Front 378

what is tubocurarine used for

Back 378

nondepolarizing neuromuscular blockade

Front 379

what agents are used to reverse neuromuscular blockade by succinylcholine?

Back 379

cholinesterase inhibitors in phase II (ex -- neostigmine)

Front 380

what phase of succinylcholine neuomuscular bloackade is reversible?

Back 380

phase II (repolarized but blocked)

Front 381

what agents are used to reverse pahse I neuromuscular blockade by succinylcholine?

Back 381

phase I Succinylcholine neuromuscular blockade cannot be reversed

Front 382

what phase of succinylcholine neuomuscular bloackade is irreversible?

Back 382

phase I Succinylcholine neuromuscular blockade cannot be reversed

Front 383

what is atracurium used for

Back 383

nondepolarizing neuromuscular blockade

Front 384

what is the effect of cholinesterase inhibitors on succinylcholine neuromuscular blockade?

Back 384

phase I: cholinesterase inhibitors potentiates the blockade phase II: cholinesterase inhibitors reverse the blockade

Front 385

what cholinesterase inhibitor is used to reverse phase II of succinylcholine neuromuscular blockade?

Back 385

neostigmine

Front 386

what is mivacurium used for

Back 386

nondepolarizing neuromuscular blockade

Front 388

Dantrolene

Back 388

p. 304

Front 389

what is dantrolene used for

Back 389

treat malignant hyperthermia

Front 390

what causes malignant hyperthermia

Back 390

use inhalation anesthetics and succinylcholine together

Front 391

what inhalation anesthetic DOES NOT cause malignanat hyperthermia?

Back 391

N2O

Front 392

what is dantrolene used for

Back 392

neuroleptic malignant syndrome

Front 393

what is neuroleptic malignant syndrome

Back 393

a toxicity of antipsychotic drugs

Front 394

what drug is used to treat malignant hyperthermia

Back 394

dantrolene

Front 395

what is the mechanism of dantrolene

Back 395

prevents release of Ca++ from saarcoplasmic reticulum of skeletal muscle

Front 397

Sympathomimetics

Back 397

p. 305

Front 398

epinephrine, NE, isoproterenol, dopamine, and dobutamine are all________________

Back 398

catecholamines

Front 399

catecholamines are_____________________

Back 399

sympathomimetics

Front 400

name 5 catecholamines

Back 400

EPI, NE, Isoproterenol, dopamine, dobutamine

Front 401

what receptors does epinephrine act on?

Back 401

alpha-1, alpha-2, beta-1, beta-2 adrenergics

Front 402

what receptors does NE work on?

Back 402

alpha-1, alpha-2, beta-1 adrenergics

Front 403

what receptors does isoproterenol work on?

Back 403

beta-1 = beta-2 adrenergics

Front 404

what receptors does dopamine work on?

Back 404

D1 = D2, D1 and D2 more than beta, beta more than alpha

Front 405

what receptors does dobutamine work on?

Back 405

beta-1 > beta-2

Front 406

which catecholamines are agonists to alpha-adrenergic receptors

Back 406

EPI, NE > dopamine

Front 407

which catecholamines are agonists to beta-1 adrenergic receptors

Back 407

EPI, NE, Isoproterenol, dopamine, dobutamine

Front 408

which catecholamines are agonists to beta-2 adrenergic receptors

Back 408

EPI, isoproterenol, dopamine and dobutamine (less)

Front 409

what is epinephrine used to treat?

Back 409

anaphylaxis, open-angle glaucoma, asthma, hypotension

Front 410

what is norepinephrine used to treat?

Back 410

hypotension (but decreases renal perfusion)

Front 411

what is isoproterenol used to treat?

Back 411

AV block

Front 412

what is dopamine used to treat

Back 412

shock with renal failure, heart failure

Front 413

what is dobutamine used to treat

Back 413

shock, heart failure

Front 414

what catecholamine is used to treat anaphylaxis

Back 414

epinephrine ("EPI-pen")

Front 415

what catecholamines are used to treat hypotension

Back 415

EPI, NE

Front 416

what catecholamine is used to treat asthma

Back 416

epinephrine

Front 417

what catecholamine is used to treat AV block

Back 417

isoproterenol

Front 418

what catecholamines are used to treat shock

Back 418

doapmine, dobutamine

Front 419

what is the action of amphetamine

Back 419

indirect general adrenergic agonist, releases stored catecholamines

Front 420

what is the action of ephedrine

Back 420

indirect general adrenergic agonist, releases stored catecholamines

Front 421

what is amphetamine used to treat

Back 421

narcolepsy, obesity, attention deficit disorder

Front 422

what is ephedrine used to treat

Back 422

nasal decongestion, urinary incontinence, hypotension

Front 423

name three sympathomimetic drugs used to treat hypotension

Back 423

epinephrine, norepinephrin, ephedrine

Front 424

what is the action of phenylephrine

Back 424

adrenergic agonist, alpha-1 > alpha-2

Front 425

what is the action of albuterol

Back 425

adrenergic agonist, beta-2 >beta-1

Front 426

what is the action of terbutaline

Back 426

adrenergic agonist, beta-2 >beta-2

Front 427

what is phenylephrine used for?

Back 427

pupil dilator, vasoconstriction, nasal decongestion

Front 428

what sympathomimetics are used to treat nasal congestion

Back 428

ephedrine, phenylephrine

Front 429

what is the mechanism of cocaine

Back 429

indirect general adrenergic agonist, catecholamine uptake inhibitor

Front 430

what is the action of cocaine

Back 430

vasoconstriction, local anesthesia

Front 431

what is the mechanism of clonidine

Back 431

centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow

Front 432

what drug has the same mechanism as amphetamine

Back 432

ephedrine

Front 433

what is the mechanism of alpha-methyldopa

Back 433

centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow

Front 434

what drug has the same mechanism as clonidine

Back 434

alpha-methyldopa

Front 435

what are clonidine and alpha-methyldopa used to treat

Back 435

hypertension, especially in renal disease because they do not decreased blood flow to the kidney

Front 436

what sympathomimetic is used to treat urinary incontinence

Back 436

ephedrine

Front 437

what sympathomimetic is used to treat attention deficit disorder

Back 437

amphetamine

Front 438

what sympathomimetic is used to treat narcolepsy

Back 438

amphetamine

Front 440

alpha-blockers

Back 440

p. 306

Front 441

name a nonselective irreversible alpha blocker

Back 441

phenoxybenzamine

Front 442

name a nonselective reversible alpha blocker

Back 442

phentolamine

Front 443

what is the mechanism of phenoxybenzamine

Back 443

nonselective irreversible alpha blocker

Front 444

what is the mechanism of phentolamine

Back 444

nonselective reversible alpha blocker

Front 445

what are phenoxybenzamine and phentolamine used for

Back 445

pheochromocytoma

Front 446

what are the side effects of nonselective alpha blockers

Back 446

orthostatic hypotension, reflex tachycardia

Front 447

name 3 alpha-1 selective adrenergic blockers

Back 447

prazosin, terazosin, doxazosin

Front 448

what is the mechanism of prazosin

Back 448

alpha-1 selective adrenergic blocker

Front 449

what is the mechanism of terazosin

Back 449

alpha-1 selective adrenergic blocker

Front 450

what is the mechanism of doxazosin

Back 450

alpha-1 selective adrenergic blocker

Front 451

what are alpha-1 selective adrenergic alpha blockers used for

Back 451

hypertension, urinary retention in BPH

Front 452

what are the side effects of alpha-1 blockers

Back 452

orthostatic hypotension, dizziness, headache

Front 453

what is prazosin used for?

Back 453

hypertension, urinary retention in BPH

Front 454

what drugs have the same action as prazosin

Back 454

terazosin, doxazosin

Front 455

what are the side effects of terazosin?

Back 455

orthostatic hypotension, dizziness, headache

Front 456

what selective alpha blockers cause orthostatic hypotension

Back 456

phenoxybenzamine, phentolamine, terazosin, prazosin, doxazosin

Front 457

name an alpha-2 selective adrenergic blocker

Back 457

yohimbine

Front 458

what is yohimbine used for

Back 458

impotence (effectiveness controversial)

Front 459

what alpha blockers are used to treat pheochromocytoma

Back 459

phenoxybenzamine, phentolamine

Front 461

beta-blockers ("lol"s)

Back 461

p. 307

Front 462

name some beta-blockers

Back 462

propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol

Front 463

what is the mechanism of propanolol

Back 463

selective beta-adrenergic blocker

Front 464

what is the mechanism of metoprolol

Back 464

selective beta-adrenergic blocker

Front 465

what is the mechanism of esmolol

Back 465

selective beta-adrenergic blocker

Front 466

what is the mechanism of pindolol

Back 466

selective beta-adrenergic blocker

Front 467

what are beta-blockers used to treat

Back 467

hypertension, angina, MI, SVT, CHF, glaucoma

Front 468

how do beta blockers treat hypertension

Back 468

decrease cardiac output, decrease renin secretion

Front 469

how do beta blockers treat angina

Back 469

decrease heart rate, decrease cardiac contractility, decreased O2 consumption

Front 470

why are beta blockers used to treat MI

Back 470

decrease MI mortality

Front 471

which beta blockers are used to treat SVT

Back 471

propanolol, esmolol

Front 472

how do propanolol and esmolol treat SVT

Back 472

decrease AV conduction velocity

Front 473

how do beta blockers treat CHF

Back 473

slow progression of chronic failure

Front 474

which beta blocker is used to treat glaucoma

Back 474

timolol

Front 475

what is timolol used to treat glaucoma

Back 475

decrease secretion of aqueous humor

Front 476

what are the toxic effects of beta blockers

Back 476

impotence, exacerbation of asthma, caution in diabetes

Front 477

what are the cardiovascular toxic effects of beta blockers

Back 477

bradychardia, AV block, CHF

Front 478

what are the CNS adverse effects of beta blockers

Back 478

sedation, sleep alterations

Front 479

which beta blockers are beta-1 selective

Back 479

acebutolol, betaxolol, esmolol, atenolol, metaprolol (A BEAM of beta-1 blockers)

Front 480

which beta-1 blocker is short-acting

Back 480

esmolol

Front 481

which beta blockers are non-selective

Back 481

propanolol, timolol, pindolol, nadolol, labetalol

Front 482

which beta blocker also blocks alpha receptors

Back 482

labetalol (all others are spelled "olol")

Front 484

glaucoma drugs

Back 484

p. 307

Front 485

which alpha agonists are used to treat glaucoma

Back 485

epinephrine, brimonidine

Front 486

which beta blockers are used to treat glaucoma

Back 486

timolol, betxolol, carteolol

Front 487

which cholinomimetics are used to treat glaucoma

Back 487

pilocarpine, carbachol, physostigmine, echothiophate

Front 488

which diuretics are used to treat glaucoma

Back 488

acetazolamide, dorzolamide, brinzolamide

Front 489

which prostaglandin is used to treat glaucoma

Back 489

latanoprost

Front 490

what classes of drugs are used to treat glaucoma

Back 490

alpha agonists, beta blockers, cholinomimetics, diuretics, prostaglandins (*mnemonic -- treating glaucoma is easy as ABCD)

Front 491

what is the effect of epinephrine in glaucoma

Back 491

increase outflow of aqueous humor

Front 492

what are the side effects of epinephrine treatment in glaucoma

Back 492

mydriasis, stinging

Front 493

what glaucoma should epinephrine NOT be used for

Back 493

closed-angle glaucoma

Front 494

what is the effect of brimonidine in glaucoma

Back 494

decreased aqueous humor synthesis

Front 495

what are the side effects of brimonidine treatment in glaucoma

Back 495

no pupillary or vision changes

Front 496

what is the effect of beta-blocker treatment in glaucoma

Back 496

decrease aqueous humor secretion

Front 497

what are the side effects of beta blocker treatment in glauzoma

Back 497

no pupillary or vision changes

Front 498

what is the effect of cholinomimetics in glaucoma

Back 498

ciliary muscle contraction, opening of trabecular meshwork, increase outflow of aqueous humor

Front 499

what are the side effects of cholinomimetics in glaucoma

Back 499

miosis, cyclospasm

Front 500

what is the effect of diuretic treatment in glaucoma

Back 500

inhibition of carbonic anhydrase --> decrease HCO3 secretion --> decrease aqueous humor secretion

Front 501

what are the side effects of diuretics in glaucoma

Back 501

no pupillary or vision changes

Front 502

what is the effect of prostaglandin (latanoprost) treatment in glaucoma

Back 502

increase outflow of aqueous humor

Front 503

what is the side effect of prostaglandin treatment in glaucoma

Back 503

darkens color of iris (browning)

Front 504

which drugs used to treat glaucoma increase outflow of aqueous humor

Back 504

cholinomimetics, prostaglandin, epinephrine

Front 505

can you use epinephrine in closed-angle glaucoma

Back 505

NO

Front 506

brimonidine is used to treat what eye disease

Back 506

glaucoma

Front 507

what kind of drug is latanoprost

Back 507

prostaglandin

Front 508

latanoprost is used to treat what eye disease

Back 508

glaucoma

Front 509

which glaucoma drugs decrease aqueous secretion

Back 509

beta blockers, diuretics

Front 510

L-dopa/carbidopa

Back 510

p. 307

Front 511

what does L-dopa stand for

Back 511

levodopa

Front 512

what is the mechanism of action of L-dopa/carbidopa

Back 512

increase dopamine level in brain

Front 513

what is L-dopa/carbidopa used to treat

Back 513

Parkinson's disease

Front 514

how is L-dopa different from dopamine

Back 514

L-dopa can cross the blood-brain barrier, dopamine cannot

Front 515

what happens to L-dopa after it crosses the BBB

Back 515

converted to dopamine by dopa decarboxylase

Front 516

what enzyme convertes L-dopa to dopamine

Back 516

dopa decarboxylase

Front 517

what is the function of carbidopa

Back 517

peripheral decarboxylase inhibitor

Front 518

why is carbidopa given with L-dopa

Back 518

increase L-dopa availability in CNS by inhibiting decarboxylase in periphery, also limits peripheral side effects

Front 519

what are the side effects of L-dopa.carbidopa treatment

Back 519

arrhythmias, dyskinesias

Front 520

why do patients taking L-dopa get arrhythmias

Back 520

peripheral effects of dopamine

Front 521

why do patients taking L-dopa get dyskinesias

Back 521

excess dopamine stimulation in CNS

Front 523

Parkinson's disease drugs

Back 523

p.308

Front 524

what drugs are used to treat Parkinson's disease

Back 524

dopamine agonists, MAO inhibitors, antimuscarinics

Front 525

specifically, which drugs are used to treat Parkinson's

Back 525

Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics (BALSA)

Front 526

which dopamine agosts are used to treat Parkinson's

Back 526

L-dopa/carbidopa, bromocriptine, pramipexole, ropinirole, amantadine

Front 527

what is the action of bromocriptine in Parkinson's

Back 527

ergot alkaloid, partial dopamine agonist

Front 528

what is the action of amantadine in Parkinson's

Back 528

enhances dopamine release

Front 529

what MAOI is used to treat Parkinson's

Back 529

selegiline

Front 530

what is the mechanism of selegiline

Back 530

selective MAO type B inhibitor

Front 531

what antimuscarinic is used to treat Parkinson's

Back 531

benztropine

Front 532

what is the effect of benztropine in Parkinson's

Back 532

improves tremor, rigidity, little effect on bradykinesia

Front 534

Sumatriptan

Back 534

p. 308

Front 535

what is sumatriptan used for

Back 535

acute migraine, cluster headache attacks

Front 536

what is the mechanism of sumatriptan

Back 536

5-HT1D agonist

Front 537

what is the half life of sumatriptan

Back 537

less than 2 hours

Front 538

what are the side effects of sumatriptan

Back 538

chest discomfort, mild tingling

Front 539

what are the contraindications for sumatriptan

Back 539

patients with CAD or Prinzmetal's angina

Front 541

Epilepsy drugs

Back 541

p. 308

Front 542

which drugs are used for simple and complex partial seizures

Back 542

phenytoin, carbamazapine, lamotrigine, gabapentin, topiramate, phenobarbital

Front 543

what types of seizures is phenytoin indicated for

Back 543

simple and complex partial, tonic-clonic, status epilepticus

Front 544

what types of seizures is carbamazepine indicated for

Back 544

simple and complex partial, tonic-clonic

Front 545

what types of seizures is lamotrigine indicated for

Back 545

simple and complex partial, tonic-clonic

Front 546

what types of seizures is gabapentin indicated for

Back 546

simple and complex partial, tonic-clonic

Front 547

what types of seizures is topiramate indicated for

Back 547

simple and complex partial

Front 548

what types of seizures is phenobarbital indicated for

Back 548

simple and complex partial, tonic-clonic

Front 549

what drugs can be used for tonic-clonic seizures

Back 549

phenytoin, carbamazapine, lamotrigine, gabapentin, phenobarbital, valproate

Front 550

what drugs can be used for absence seizures

Back 550

valproate, ethosuximide

Front 551

what drugs can be used for status epilepticus

Back 551

phenytoin, benzodiazapines (diazepam, lorazepam)

Front 552

what types of seizure is valproate indicated for

Back 552

tonic-clonic, absence

Front 553

what types of seizure is ethosuximide inidcated for

Back 553

absence

Front 554

what type of seizure are benzodiazepines indicated for

Back 554

status epilepticus

Front 555

other than anti-seizure, what else is phenytoin used for

Back 555

class 1B anti-arrhythmic

Front 556

how should a patient taking carbamazepine be followed

Back 556

monitor LFT's weekly

Front 557

which seizure drugs have adjunct use

Back 557

gabapentin, topiramate

Front 558

which seizure drug is safest in pregnant women

Back 558

phenobarbital

Front 559

which seizure drug is used in Crigler-Najjar II

Back 559

phenobarbital

Front 560

what are the advantages of phenobarbital

Back 560

can be used in pregnant women, Crigler Najjar II

Front 562

Epilepsy drug toxicities

Back 562

p. 309

Front 563

what are the side effects of benzodiazepines

Back 563

sedation, tolerance, dependence

Front 564

what are the side effects of carbamazepine

Back 564

diplopia, ataxia, CYP induction, blood dyscrasias, liver toxicity

Front 565

what are the side effects of ethosuximide

Back 565

GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome

Front 566

what are the side effects of phenobarbital

Back 566

sedation, CYP induction, tolerance, dependence

Front 567

what are the side effects of phenytoin

Back 567

nystagmus, diplopia, ataxia, sedation, ginigival hyperplasia, hirsutism, anemias, teratogenic

Front 568

what are the side effects of valproate

Back 568

GI distress, rare by fatal hepatotoxicity, neural tube defects (spina bifida)

Front 569

what are the side effects of lamotrigine

Back 569

life-threatening rash, Stevens-Johnson syndrome

Front 570

what are the side effects of gabapentin

Back 570

sedation, movement disorders

Front 571

what are the side effects of topiramate

Back 571

sedation, mental dulling, kidney stones, weight loss

Front 572

which anti-epileptic drug is teratogenic

Back 572

phenytoin

Front 573

which anti-epileptic drug can cause dependence

Back 573

benzodiazepines, phenobarbital

Front 574

which anti-epileptic drug can cause neural tube defects

Back 574

valproate

Front 575

which anti-epileptic drugs can cause GI distress

Back 575

valproate, ethosuximide

Front 576

it is necessary to check LFT's with which anti-epileptic drugs

Back 576

carbamazepine, valproate

Front 577

which anti-epileptic drugs cause CYP induction

Back 577

phenobarbital, carbamazepine

Front 578

which anti-epileptic drugs can cause blood problems

Back 578

carbamazepine, phenytoin

Front 579

which anti-epileptic drugs can cause Stevens-Johnson syndrome

Back 579

lamotrigine, ethosuximide

Front 580

which anti-epileptic drugs can cause diplopia

Back 580

carbamazepine, phenytoin

Front 582

Phenytoin

Back 582

p. 309

Front 583

what is the mechanism of phenytoin action

Back 583

use-dependent blockade of Na+ channels

Front 584

what is the clinical application of phenytoin

Back 584

grand mal seizures

Front 585

what are the toxicities of phenytoin

Back 585

nystagmus, ataxia, diplopia, lethargy

Front 586

what are the chronic toxicities of phenytoin

Back 586

gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia, malignant hyperthermia (rare)

Front 587

should pregnant women take phenytoin

Back 587

NO -- teratogenic

Front 588

why does phenytoin cause megaloblastic anemia

Back 588

causes decreased vitamin B-12

Front 590

Barbiturates

Back 590

p. 309

Front 591

name 4 barbiturates

Back 591

phenobarbital, pentobarbital, thiopental, secobarbital

Front 592

what is the mechanism of barbiturate action

Back 592

increase duration of Cl channel opening --> decreased neuron firing --> facilitate GABA-A action

Front 593

how do barbiturates facilitate GABA-A action

Back 593

increase duration of Cl channel opening which decreases neuron firing (Barbidurate increases duration

Front 594

is barbiturate action on the CNS stimulatory or inhibitory

Back 594

inhibitory

Front 595

what is the clinical application of barbiturates

Back 595

sedative for anxiety, seizures, insomnia, anesthesia induction (thiopental)

Front 596

which barbiturate is used for anesthesia induction

Back 596

thiopental

Front 597

what are the side effects of barbiturates

Back 597

dependence, additive CNS depression effects with alcohol, respiratory or CV depression (death), drug interactions due to CYP induction

Front 598

what should you find out before giving a patient barbiturates

Back 598

what other medications they take, because of CYP induction and many drug interactions

Front 599

what happens if you give barbiturates to a patient in alcohol-induced coma or DT's

Back 599

they might DIE!! Because of additive effect of barbiturates and alcohol --> respiratory depression

Front 600

when are barbiturates contra-indicated

Back 600

porphyria

Front 601

can barbiturates cause dependence

Back 601

YES

Front 602

My friend Barb was very anxious so her doctor gave her barbiturates to increase the duration of the time she could speak in public without freaking out and having a seizure. She became so dependent on it that she recommended it to her friend Portia who couldn't take it because of porphyria. One day Barb drank too much alcohol and took her barbiturates and never woke up! THE END

Back 602

clinical pharmacology made ridiculous. Period

Front 604

Benzodiazepines

Back 604

p. 309

Front 605

name a bunch of benzodiazepines

Back 605

diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide (all have ZZZ in them)

Front 606

what is the mechanism of benzodiazepines

Back 606

increase frequency of Cl channel opening --> facilitate GABA-A action (Frenzodiazepines increase frequency)

Front 607

which GABA receptors are facilitated by barbiturates and bezodiazepines

Back 607

GABA-A

Front 608

what are the clinical applications of benzodiazepines

Back 608

anxiety, spasticity, status epilepticus (diazepam), detoxification (alcohol withdrawal, DT's)

Front 609

which benzodiazepine can be used for status epilepticus

Back 609

diazepam

Front 610

what drugs can be used to treat alcohol withdrawal

Back 610

benzodiazepines

Front 611

which benzodiazepines are short-acting

Back 611

TOM thumb: Triazolam, Oxazepam, Midazolam

Front 612

what are the toxic effects of benzos

Back 612

dependence, additive CNS depression effects with alcohol

Front 613

how are benzos better than barbiturates

Back 613

less respiratory depression and coma risk

Front 614

how do you treat benzo overdose

Back 614

flumazenil

Front 615

what is flumzenil used for

Back 615

benzo overdose

Front 616

how does flumazenil work

Back 616

competitive antagonist at GABA receptor

Front 617

can a patient become benzodiazepine dependent

Back 617

YES

Front 618

are barbiturates or benzodiazepines used for alcohol withdrawal

Back 618

benzodiazepines

Front 620

Antipsychotics (neuroleptics)

Back 620

p. 310

Front 621

what is another name for antipsychotics

Back 621

neuroleptics

Front 622

name 4 antipsychotic drugs

Back 622

thioridazine, haloperidol, fluphenazine, chlorpromazine

Front 623

how do you keep benzos straight from antipsychotics

Back 623

Benzos help 3rd year Jon Kazam be less anxious around patients: Shazam Kazam! Without antipsychotics patients talk like a crazy 'zine (well, not perfect, but I'm working on it)

Front 624

what is the mechanism of most antipsychotics

Back 624

block dopamine D2 receptors

Front 625

what is the clinical application of antipsychotics

Back 625

schizophrenia, psychosis

Front 626

what are the side effects of antipsychotics

Back 626

extrapyramidal side effects (EPS), sedation, endocrine, muscarinic blockade, alpha blockade, histamine blockade

Front 627

what is a long-term effect of antipsychotic use

Back 627

tardive dyskinesia

Front 628

what is neuroleptic malignant syndrome

Back 628

a side effect of antipsychotics; rigidity, autonomic instability, hyperpyrexia

Front 629

how do you treat neuroleptic malignant syndrome

Back 629

dantrolene, dopamine agonists

Front 630

what is tardive dyskinesia

Back 630

side effect of neuroleptics; stereotypic oral-facial movements, may be due to dopamine receptor sensitization

Front 631

what is the "rule of 4" with EPS side effects from antipsychotic drugs

Back 631

evolution of EPS side effects: 4 hours -- acite dystonia, 4 days -- akinesia, 4 weeks -- akasthesia, 4 months -- tardvie dyskinesia

Front 632

is tardvie dyskinesia reversible

Back 632

often irreversible

Front 633

what is fluphenazine used for

Back 633

schizophrenia, psychosis

Front 635

Atypical antipsychotics

Back 635

p. 310

Front 636

name 3 atypical antipsychotics

Back 636

clozapine, olanzapine, risperidone

Front 637

what type of antipsychotic is clozapine

Back 637

atypical

Front 638

what type of antipsychotic is olanzapine

Back 638

atypical

Front 639

what type of antipsychotic is risperidone

Back 639

atypical

Front 640

what is the mechanism of atypical antipsychotics

Back 640

block 5-HT2 and dopamine receptors

Front 641

what is the mechanism of clozapine

Back 641

block 5-HT2 and dopamine receptors

Front 642

what is the mechanism of olanzapine

Back 642

block 5-HT2 and dopamine receptors

Front 643

what is the mechanism of risperidone

Back 643

block 5-HT2 and dopamine receptors

Front 644

what is the clinical application of clozapine

Back 644

schizophrenia positive and negative symptoms

Front 645

what is the clinical application of olanzapine

Back 645

schizophrenia positive and negative symptoms, OCD, anxiety disorder, depression

Front 646

what is the clinical application of risperidone

Back 646

schizophrenia positive and negative symptoms

Front 647

how are atypical antipsychotics different from classic ones

Back 647

atypicals treat positive and negative symptoms of schizophrenia, fewer extrapyramidal and anticholinergic side effects than classic antipsychotics

Front 648

which antipsychotics should be used to treat positive and negative symptoms of schizophrenia

Back 648

atypical ones -- clozapine, olanzapine, risperidone

Front 649

which antipsychotics should be used for fewer side effects

Back 649

atypical ones -- clozapine, olanzapine, risperidone

Front 650

what is a potential toxicity of clozapine

Back 650

agranulocytosis

Front 651

which antipsychotic drug can cause agranulocytosis

Back 651

clozapine

Front 652

what test must be done weekly on patients taking clozapine

Back 652

WBC count because of potential agranulocytosis

Front 654

Lithium

Back 654

p. 310

Front 655

what is the mechanism of action of lithium

Back 655

unknown; may be related to inhibition of phosphoinositol cascade

Front 656

what is the clinical application of lithium

Back 656

mood stabilizer for bipolar disorder

Front 657

how does lithium help people with bipolar disorder

Back 657

prevents relapse and acute manic episodes

Front 658

what are the side effects of lithium

Back 658

tremor, hypothyroidism, polyuria, teratogenic

Front 659

is it OK for women taking lithium to get pregnant

Back 659

NO -- teratogenic

Front 660

what does lithium cause polyuria

Back 660

ADH antagonist --> nephrogenic diabetes insipidus

Front 661

Antidepressants

Back 661

pg 311

Front 662

What do the following drugs inhibit: 1. MAO inhibitors, 2. Desipramine/maprotilline, 3. Mirtazapine and 4. Fluoxetine/trazodone?

Back 662

1. MAO 2. NE reuptake 3. Alpha 2-R 4. 5HT reuptake

Front 663

All of the above actions are ------synaptic

Back 663

PRE

Front 664

List the Tricyclic Antidepressants

Back 664

pg 311 Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin

Front 665

What are the three C's of their toxicity?

Back 665

Convulsions, Coma, Cardiotoxicity (arrythmias). Also respiratory depression, hypyrexia.

Front 666

How about toxicity in the eldery?

Back 666

confusion and hallucinations due to anticholinergic SE

Front 667

What is the mechanism of TCA?

Back 667

block reuptake of NE and 5HT

Front 668

What is the clinical uses of TCAs?

Back 668

Endogenous depresion. Bed wetting - imipramine. OCD- clomipramine.

Front 669

How are tertiary TCA's different than secondary in terms of side effects?

Back 669

Amitriptyline (tertiary) has more anti-cholinergic effects than do secondary (nortriptyline). Desipramine is the least sedating.

Front 670

what are the SE of TCAs?

Back 670

sedation, alpha blocking effects, atropine-like anti cholinergic side effects (tachycardia, urinary retention)

Front 671

Fluoxetine, sertraline, paroxetine, citalopram are what class of drugs?

Back 671

pg 311 SSRI's for endogenous depression

Front 672

How long does it take an anti-depressant to have an effect?

Back 672

2-3weeks

Front 673

How does the toxicity differ fromTCA's and what are they?

Back 673

Fewer than TCA's. CNS stimulation - anxiety, insomnia, tremor, anorexia, nausea, and vomiting.

Front 674

What toxicity happens with SSRI's and MAO inhibitors given together?

Back 674

Seratonin Syndrome! Hyperthermia, muscle rigidity, cardiovascular collapse

Front 675

What are heterocyclics?

Back 675

pg 312 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used major depression.

Front 676

Examples of heterocyclics?

Back 676

trazodone, buproprion, venlafaxine, mirtazapine, maprotiline

Front 677

Which one is used for smoking cessation?

Back 677

Buproprion. Mechanism not known. Toxicity - stimulant effects, dry mouth, aggrevation of pyschosis

Front 678

Which one used in GAD?

Back 678

Venlafaxine - inhibits 5HT and DA reuptake. Toxicity - stimulant effects

Front 679

which one blocks NE reuptake

Back 679

maprotiline

Front 680

Which one increases release of NE and 5HT via alpha 2 antagonism?

Back 680

mirtazapine. Also potent 5HT Rantagonist. Toxicity - sedation, increase serum cholesterol, increase appetite

Front 681

What is trazodone and it' SE?

Back 681

primarily inhibits seratonin reuptake. Toxicity - sedation, nausea, priapism, postural hypotension

Front 682

Give 2 examples of MAO

Back 682

pg 312 phenelzine. Tranylcypromine

Front 683

Mechanism and Clinical Uses?

Back 683

non selevtive MAO inhibition. Atypical antidepressant, anxiety, hypochondriasis

Front 684

What is the toxicity with tyramine ingestion (in foods) and meperidine?

Back 684

Hypertensive crisis

Front 685

Other toxicities?

Back 685

CNS stimulation, contraindicated with SSRI's or B-agonists

Front 686

What is the mechanims of selgiline (deprenyl)?

Back 686

pg 312 Selectively inhibits MAO-B, increasing DA

Front 687

what is the clinical use and toxicity?

Back 687

adjunctive agent to L-dopa for Parkinsons. May enhance adverse effects of L-dopa

Front 688

Analgesics/ Anesthetics

Back 688

pg 312

Front 689

General principles

Back 689

pg 312

Front 690

What is the significance of drugs with decreased solubility in blood?

Back 690

rapid induction and recovery times . Ie. N20

Front 691

What is the significance of drugs with increased solubility in blood?

Back 691

increased potency = I/ MAC. Ie. Halothane

Front 692

Inhaled Anesthetics

Back 692

pg 312

Front 693

list them

Back 693

halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide

Front 694

What is good about lower solubility?

Back 694

the quicker the anesthetic response, and the quicker the recovery

Front 695

What are these drug's effects?

Back 695

myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow

Front 696

What toxicity mactches the following drugs 1. Halothane 2. Methoxyflurane 3. Enflurane 4. Rare

Back 696

1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4. Malignant hyperthermia

Front 697

IV anesthetics

Back 697

pg313

Front 698

What do barbituates, benzodiazepines, arylcyclohexylamines and narcotic analgesics have in common?

Back 698

they are IV anesthetics

Front 699

What the pharmacokinetics and uses of thiopental?

Back 699

high lipid solubility, rapid entry into brain. Used for induction of anesthesia for short surgical procedures. Terminated by redistribution from brain. Decreased cerebral blood flow

Front 700

Give an example of a benzo and what is this class's shortcoming?

Back 700

midazolam used for endoscopy. Used with gaseous anesthetics and narcotics. May cause severe post-op respiratory depressio and amnesia

Front 701

What does Ketamine (PCP analog and an arylcyclohexylamine) do?

Back 701

dissociative anesthetic. Cardiovascular stimulant. Causes disorientation, hallucination, bad dreams. Increases cerebral blood flow.

Front 702

How are narcotic analgesics used? Examples?

Back 702

Morphone and fentanyl are used with CNS depressant during general anesthesia.

Front 703

What is the advantage of propofol

Back 703

used for rapid anesthesia induction and short procedures. Less post-op nausea than thiopental

Front 704

Local anesthetics

Back 704

pg 313

Front 705

Name some esters?

Back 705

procaine, cocaine, tetracaine,

Front 706

Name some amides?

Back 706

lidocaine, bupivacaine, (amides have two I's in name!)

Front 707

What is the mechanism and clinical use?

Back 707

bind receptor and block Na channels. Tertiary amine local anesthetics penetrate membrane in uncharge form, then bind charged form. Use for minor surgical procedures, spinal anesthesia.

Front 708

How do you decide to use ester or amides?

Back 708

if allergic to esters, give amides

Front 709

what is the toxicity

Back 709

CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, arrhythmias (cocaine)

Front 710

In infected ________ tissue, anesthetics are charged and cannot penetrate membrane. Therefore, ______ anesthetics are needed.

Back 710

acidic; more

Front 711

What is the order of nerve blockade for size and myelination? Which factor predominates?

Back 711

small diameter> large diameter. Myelinated fibers> unmyelinated fibers. Size factor predominates

Front 712

what is the order of loss of sensation?

Back 712

pain first, then temp, then touch, then pressure

Front 713

Why would you give these drugs with vasoconstrictors?

Back 713

to enhance local action

Front 714

Opiod analgesics

Back 714

pg 313

Front 715

List as many as you can.

Back 715

morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan

Front 716

Mechanism: They act as _____ for opiod receptors to modulate synaptic transmission

Back 716

agonists

Front 717

which drugs act at the mu, delta, kappa receptors?

Back 717

morphine enkephalin, dynorphin

Front 718

Clinical use?

Back 718

pain, cough supression (dex), diarrhea (loperamide), acute pulmonary edema, methadone maintenance programs

Front 719

What are the major toxicities?

Back 719

addiction, respiratory depression, constipation, miosis, additive CNS depression wth other drugs

Front 720

Tolerance does not develop to __________and ______

Back 720

miosis and constipation

Front 721

How would you treat toxicity?

Back 721

naloxone, naltrexone (opiod R antagonist)

Front 722

Other NSAIDS

Back 722

pg 313

Front 723

List three NSAIDS?

Back 723

ibuprofen, naproxen, indomethacin

Front 724

What is their mechanism?

Back 724

reversibly inhibit COX 1 and 2. Blocks PG synthesis

Front 725

What is their clinical use (3As)?

Back 725

Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.

Front 726

What are common toxicities?

Back 726

renal damage, aplastic anemia, GI distress, ulcers

Front 727

COX 2 Inhibitors

Back 727

pg 314

Front 728

Where is cox2 found?

Back 728

in inflammatory cells and mediates inflammation and pain

Front 729

Why is cox2 inhibition better than cox1?

Back 729

cox1 helps to maintain gastric mucosa, thus, should not have the corrosive effects of other NSAIDs on the GI lining (less incidence of ulcers and bleeding)

Front 730

Clinical Use?

Back 730

RA and osteoarthritis

Front 731

Acetaminophen

Back 731

pg 314

Front 732

What is its mechanism and where does it work?

Back 732

reversibly inhibits cox, mostly in CNS. Inactivated peripherally.

Front 733

What are its 2 As?

Back 733

antipyretic, analgesic but NOT anti-inflammatory.

Front 734

Overdose effects?

Back 734

hepatic necrosis, acetaminophen metabolites depletes glutathine and forms toxic tissue adducts in the liver

Front 735

cardiovascular therapy

Back 735

pg 314

Front 736

Changes in CO affect two major pathways?

Back 736

1. Carotid sinus firing, sympa discharge 2. Renal blood flow, renin-ang pathway

Front 737

What is the effect of the following drugs: 1. Positive inotropic drugs 2. Beta blockers 3. Ace inhibitors 4. AII antagonists 5. Vasodilators and 6. Diuretics

Back 737

1. Increases cardiac output. 2. Inhibit renin release. 3. Inhibit ACE 4. Inhibits effects of AngII including increasing the preload, increasing the afterload and remodelling. 5. Decrease the preload and afterload. 6. Decrease the preload and afterload

Front 738

antihypertensive drugs

Back 738

pg 315

Front 739

What are the adverse effects of these two diueretics: hydrochlorothiazide, loop diuretics

Back 739

1. Hypokalemia, hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia 2. Hypokalemia, met alk, hypotension, ototoxicity

Front 740

These are wahat class of drugs: clonidine, methyldopa, ganglionic blockers, reserpine, guanethidine, prazosin, beta blockers?

Back 740

sympathoplegics

Front 741

Adverse effects of clonidine?

Back 741

dry mouth, sedation, severe rebound HTN

Front 742

Adverse effects of methyldopa?

Back 742

sedation, positive coombs test

Front 743

Adverse effects of ganglionic blockers?

Back 743

orthostatic HTN, blurred vision, constitpation, sexual dysfuncction

Front 744

Adverse effects of reserpine?

Back 744

sedation, depression, nasal stuffiness, diarrhea

Front 745

adverse effects of beta blockers?

Back 745

impotence, asthma, cardiovascular, cns

Front 746

Adverse effects of guanethidine?

Back 746

orthostatic and exercise Hypotension, sex dysfxn, diarrhea

Front 747

Adverse effects of prazosin?

Back 747

1st dose orthostatic hypotension, dizzy, headache

Front 748

The following are what class: hydralazine, minoxidil, nifedipine, verapamil, nitroprusside

Back 748

vasodilators

Front 749

which one causes lupus like syndrome? Other toxicities?

Back 749

hydralazine, nausea, headache, reflex tachycardia, angina, salt retention

Front 750

adverse effets of minoxidil?

Back 750

hypertrichosis (hair growth - think Rogaine with minoxidil!), pericardial effusion, reflex tachycardia, angina, salt retention

Front 751

Side effects of nifedipine, verapamil?

Back 751

dizziness, flushing, constipation, nausea

Front 752

which one causes cynide toxicity?

Back 752

nitroprusside

Front 753

Adverse effects of ACE-I Captorpil? Think CAPTOPRIL

Back 753

C: cough, A: angioedema, P: proteinuria, T: taste changes, O: hypOtension, P: pregnancy problems like fetal renal damage, R: rash, I: increased renin, L: lower angiotensin. Also hyperkalemia.

Front 754

Losartan is a ----------- R-Inhibitor? With ____-toxicity and ____kalemia

Back 754

angiotensin II, fetal renal, hyper

Front 755

Hydralizine

Back 755

pg 315

Front 756

Which two anti-htn drugs do you use with B blockers to prevent reflex tachycardia, diuretic to block salt retention?

Back 756

hydralizine, minoxidil

Front 757

What is hydralizine's mechanims and clinical use?

Back 757

increase cGMP --> smooth muscle relaxation. Vasodilates arteries > veins. Reduces afterload. Used for severe HTN or CHF

Front 758

Calcium channel blockers, name three

Back 758

pg. 315 - nifedipine, verapamil, diltiazem

Front 759

Mechanism: block _____ chanels of cardiac and smooth muscles to reduce contractility

Back 759

voltage dependednt L type Ca

Front 760

Rank their effects on vascular smooth muscle ad on the heart.

Back 760

smooth muscle nifed> diltia > verapamil heart: vera> diltia> nifedepine

Front 761

What is the calcium channel blockers use?

Back 761

HTN, angina, arrythmias (not nifedipine)

Front 762

ACE -I, name three

Back 762

pg 316 - captopril, enalapril, lisinopril

Front 763

Mechanim considering bradykinin and renin release?

Back 763

reduce lvels of ang II, prevent inactivation of bradykinin, renin release is increased to to loss of feedback inhibition

Front 764

what is the clinical use of these?

Back 764

HTN, CHF, diabetic renal disease

Front 765

Diuretics- site of action

Back 765

pg 316

Front 766

What is the site of action of 1. Acetazolamide, 2. Osmotic agents, 3. Loop agents, 4. Thiazides, 5. Potassium sparing, 6. ADH antagonists

Back 766

1. PCT 2. PCT, thin desc limb, CD 3. Thick ascending limb 4. Distal conv tubule 5. DCT a bit later 6. CD in inner medulla

Front 767

How does mannitol an osmotic diuretic work?

Back 767

increase tubular fluid osmolarity, producing increased urine flow

Front 768

what is the use and toxicity?

Back 768

Use: shock, drug overdose, decrease intracranial pressure. Toxicity - pulmonary edema, dehydration. Contraindicated in anuria, CHF

Front 769

Acetazolamide

Back 769

pg 317

Front 770

Is a ______inhibitor. Causes ______diuresis and _____ in total body HC03 stores.

Back 770

Carbonic anhydrase, self-limited NaHCO3, reduction.

Front 771

What electrolye disturbace does it treat? Does it cause?

Back 771

treats met alk, causes in toxicity hyperchloremic met acidosis. ACIDazolamide caues ACIDosis.

Front 772

Other toxicity?

Back 772

neuropathy, NH3 toxicity, sulfa allergy

Front 773

uses?

Back 773

glaucoma, urinary alk, met alk, altitude sickeness

Front 774

Furosemide

Back 774

pg 317

Front 775

This sulfonamide loop diuretic inhibits _______cotransport

Back 775

NA, K, 2CL

Front 776

Furosemide also works by?

Back 776

abolishes hypertonicit y of medulla, prevent concentration of urine. Increase Caexcertion. Loops Lose calcium

Front 777

The three uses for this loop diuretic?

Back 777

edematous states, htn, hypercalcemia

Front 778

Toxicity using the OH DANG?

Back 778

ototoxicity, hypokalemia, dehydration, allergy, nephritis interstitial, gout

Front 779

Ethacrynic Acid

Back 779

pg 317

Front 780

How is this drug different from furosemide? And how does that affect its use?

Back 780

Although both have the same action, ethacrynic is a phenoxyacetic acid derivative not a sulfonamide. Therefore use this drug when you are allergic to sulfa.

Front 781

What drug can be used to treat acute gout?

Back 781

ethacrynic acid

Front 782

Hydrochlorothiazide

Back 782

p.318

Front 783

Hydrochlorothiazide is a thiazide diuretic that inhibits the reabsorption of ----- in the ---- tubule

Back 783

NaCl; early distal tubule

Front 784

Does hydrochlorothiazide increase or decrease the excretion of calcium ion?

Back 784

decrease

Front 785

A toxic dose of hydrochlorathiazide will do what to the blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid, calcium

Back 785

hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)

Front 786

K+-sparing diuretics

Back 786

p.318

Front 787

Spironolactone is a competitive antagonist to the --- receptor in the ---- tubule

Back 787

aldosterone; cortical collecting tubule

Front 788

Name two K+-sparing diuretics that block Na+ channels in the cortical collecting duct

Back 788

Triamterine and amiloride

Front 789

Besides causing hyperkalemia, a toxic dose of spironolactone will cause this endocrine effect

Back 789

Gynecomastia (antiandrogen effect)

Front 790

Name three K+-sparing diuretics

Back 790

Spironolactone, Triamterene, Amiloride (The K+ STAys.)

Front 791

Diuretics: electrolye exchange

Back 791

p.318

Front 792

Diuretics are classified as carbonic anhydrase inhibitors, loop diuretics, thiazides, and K+-sparing diuretics. Which of these causes in increase in urine NaCl?

Back 792

All of them!

Front 793

Which types of diuretucs increase urine K+?

Back 793

All except K+-sparing diuretics. Carbonic anhydrase inhibitors, loop diuretics, thiazides.

Front 794

Do carbonic anhydrase inhibitors increase or decrease blood pH?

Back 794

Decrease, cause acidosis

Front 795

Do K+-sparing diuretics cause acidosis or alkalosis?

Back 795

Acidosis, decreases pH

Front 796

Do loop diuretics cause acidosis or alkalosis?

Back 796

Alkalosis, increases pH

Front 797

Do thiazide diuretics cause an increase or decrease in blood pH?

Back 797

Increase, cause alkalosis

Front 798

Do loop diuretics increase or decrease levels of urine calcium ion?

Back 798

Increase

Front 799

Do thiazide diuretics increase or decrease levels of urine calcium ion?

Back 799

Decrease

Front 800

Antianginal therapy

Back 800

p.319

Front 801

Name four determinants of the level of myocardial oxygen consumption

Back 801

There are five: end diastolic volume, blood pressure, heart rate, contractility, ejection time

Front 802

Do nitrates affect preload or afterload?

Back 802

preload

Front 803

Do Beta-blockers affect preload or afterload?

Back 803

afterload

Front 804

What is the effect of nitrates on: diastolic volume, blood pressure, contractility, heart rate, ejection time?

Back 804

decrease EDV, decrease BP, increase contractility (reflex response), increase HR (reflex response), decrease ejection time

Front 805

What is the effect of Beta-blockers on: diastolic volume, blood pressure, contractility, heart rate, ejection time?

Back 805

increase EDV, decrease BP, decrease contractility, decreased HR, increase ejection time

Front 806

The effects of using nitrates and Beta-blockers together will: a) decrease myocardial oxygen demands by the same amount as using either alone, b) decrease myocardial oxygen demands by an amount greater than if each were used alone, or c) have no effect on myocardial oxygen demand

Back 806

b) Decrease myocardial oxygen demands by an amount greater that if each were used alone

Front 807

Nifedipine blocks -- channels

Back 807

calcium

Front 808

In its effects on myocardial oxygen consumption, is Nifedipine similar to Nitrates or B-blockers?

Back 808

Nitrates (Nifedipine is similar to Nitrates)

Front 809

In its effects on myocardial oxygen consumption, is Verapamil similar to Nitrates or B-blockers?

Back 809

B-blockers

Front 810

Nitroglycerine, isosorbide dinitrate

Back 810

p.319

Front 811

Dose nitroglycerin dilate arteries or veins more?

Back 811

Veins>>arteries

Front 812

Does nitroglycerin increase or decrease cGMP in smooth muscle?

Back 812

Increase

Front 813

In industrial exposure to nitroglycerine, weekend withdrawal is characterized by which three symptoms?

Back 813

Tachycardia, dizziness , and headache ("Monday disease")

Front 814

Toxic dosage of nitroglycerine causes which three symptoms?

Back 814

Tachycardia, hypotension, headache

Front 815

Cardiac drugs: sites of action

Back 815

p.320

Front 816

Digitalis has its action on which cell membrane transporter?

Back 816

Na/K ATPase

Front 817

Ryanodine has its action on which channel?

Back 817

Calcium release channel in the sarcoplasmic receptor

Front 818

Calcium enters cardiac cells through which channel?

Back 818

Voltage-gated calcium channel

Front 819

Cytoplasmic calcium concentrations in cardiac cells can be decreased by sequestering calcium in the sarcoplasmic reticulum. Calcium enters the SR through which transporter?

Back 819

Calcium pump in the wall of the SR

Front 820

Calcium channel blockers have their effect on which calcium transporters?

Back 820

Voltage-gated calcium channel

Front 821

Cardiac Glycosides

Back 821

p.320

Front 822

What is digoxin's effect on the intracellular Na+ level?

Back 822

Increase

Front 823

What is digoxin's effect on the intracellular calcium level?

Back 823

Increase

Front 824

Name two ECG changes ellicited by digoxin administration

Back 824

There are 4: increase PR, decrease QT, scooping of ST segment, T-wave inversion

Front 825

Name three symptoms of digoxin toxicity

Back 825

Nausea, vomiting, diarrhea, blurry vision, arrhythmia

Front 826

Which potentiates the effects of digoxin- hypo- or hyperkalemia?

Back 826

hypokalemia

Front 827

Antiarrhythmics- Na+ channel blockers (classI)

Back 827

p.321

Front 828

Which phase of the cardiac action potential do antiarrhythmics decrease the slope of?

Back 828

Phase 4 depolarization

Front 829

What type of antiarrhythmic is Amiodarone?

Back 829

Class 1A (Class 1A includes Quinidine, Amiodarone, Procainamide, Disopyramide, "Queen Amy Proclaims Diso's pyramid."

Front 830

Do class 1A antiarrhythmics increase or decrease the effective refractory period, AP duration, and QT interval?

Back 830

Increase ERP, increase AP duration, increase QT interval

Front 831

What do class 1B antiarrhythmics do to the AP duration?

Back 831

Decrease AP duration

Front 832

What type of antiarrhythmic is mexiletine?

Back 832

Class 1B (includes Lidocaine, mexiletine, tocainide)

Front 833

What type of antiarrhythmic is encainide?

Back 833

Class IC (includes flecainide, encainide, propafenone)

Front 834

What effect do class 1C antiarrhythmics have on the AP duration?

Back 834

No effect!

Front 835

Antiarrhythmics- Beta-blockers (classII)

Back 835

p. 322

Front 836

What does esmolol do to the cAMP in cardiac cells?

Back 836

decreases cAMP (a beta-blocker)

Front 837

What does atenolol do the calcium currents in cardiac cells?

Back 837

decreases calcium current (beta-blocker)

Front 838

Timolol decreases the slope of which phase of the cardiac AP cycle?

Back 838

Phase 4 (a beta-blocker)

Front 839

What does propanolol do the the PR interval?

Back 839

Increases interval (beta-blocker)

Front 840

Is esmolol a short- or long-acting beta blocker?

Back 840

short-acting

Front 841

Antiarrhythmics- K+ channel blockers (class III)

Back 841

p. 322

Front 842

Does amiodarone increase or decrease AP duration?

Back 842

Increase (K+ channel blocker)

Front 843

Does sotalol increase or decrease the effective refractory period?

Back 843

Increase (K+ channel blocker)

Front 844

Does bretylium increase or decrease the QT interval?

Back 844

Increase (K+ channel blocker)

Front 845

Name a symptom of sotalol toxicity.

Back 845

Torsades de pointes (K+ channel blocker)

Front 846

Name three of the symptoms of amiodarone toxicity.

Back 846

Pulmonary fibrosis, corneal deposits, hepatoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, bradychardia, heart block, CHF, hypothyroidism/hyperthyroidism. (Therefore, should check PFTs, LFTs, and TFTs)

Front 847

Antiarrhythmics- Ca2+ channel blockers (class IV)

Back 847

p. 323

Front 848

Does verapamil increase or decrease the conduction velocity of the AV nodal cells?

Back 848

Decrease (calcium channel blocker)

Front 849

How does diltiazem affect the effective refractory period and the PR interval?

Back 849

Increases ERP, increases PR (calcium channel blocker)

Front 850

Other antiarrhythmics

Back 850

p. 323

Front 851

Name a potential use of Mg+ to treat arrhythmias.

Back 851

To treat torsades de pointes and digoxin toxicity

Front 852

Name a potential use of K+ to treat arrhythmias.

Back 852

Depress ectopic pacemakers, especially in digoxin toxicity

Front 853

Name a use of adenosine in treating arrhythmias.

Back 853

To diagnose and abolish AV nodal arrhythmias.

Front 854

Lipid-lowering agents

Back 854

p. 324

Front 855

What is the effect of cholestyramine on the serum triglyceride level?

Back 855

Slight increase (cholestyramine is a bile acid resin)

Front 856

What is the effect of colestipol on HDL?

Back 856

No effect! (colestipol is a bile acid resin)

Front 857

What is the effect of lovastatin on HDL?

Back 857

Increase (lovastatin is an HMG-CoA reductase inhibitor)

Front 858

Name 2 side effects of pravastatin.

Back 858

Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase inhibitor)

Front 859

What is the effect of Niacin on HDL?

Back 859

Increase

Front 860

What are the side effects of clofibrate?

Back 860

Incease LFTs and cause myositis (Clofibrate is a "Fibrate")

Front 861

Which increases HDL most: simvastatin, niacin, or gemfibrozil?

Back 861

Niacin

Front 862

Which decreases triglyceride level most: colestipol, Atorvastatin, niacin, or bezafibrate?

Back 862

Bezafibrate

Front 863

What is the main effect of ezetimibe?

Back 863

decrease serum LDL (a cholesterol absorption inhibitor)

Front 864

Gemfibrozil increases the activity of which enzyme?

Back 864

Lipoprotein lipase (which converts VLDL to IDL)

Front 865

Arachidonic acid products

Back 865

p.325

Front 866

What enzyme breaks down membrane lipid into arachidonic acid?

Back 866

Phospholipase A2

Front 867

What two enzymes are responsible for the production of Hydroperoxides (HPETEs) and Endoperoxidases, respectively from arachidonate?

Back 867

Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases

Front 868

What major class of products do HPETEs give rise to?

Back 868

Leukotrienes

Front 869

What are the 3 major products of Endoperoxidases?

Back 869

Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA)

Front 870

In general what effect do leukotrienes have on bronchial tone?

Back 870

Leukotrienes in general increase bronchial tone

Front 871

In the arachodonic acid pathway, what two enzymes do corticosteroids block?

Back 871

Phospholipase A2, COX-2

Front 872

NSAIDs, Acetaminophen and COX-2 inhibitors block which arachadonic acid pathway enzymes

Back 872

NSAIDs-non-selectively block COX-1 and COX-2, acetaminophen doesn't block COX-1 or COX-2, but instead it may block COX-3 in found in the brain, COX-2 inhibitors block COX-2

Front 873

What are the 4 major effects of Prostacyclin

Back 873

decrease platelet aggregation, decrease vascular tone, decrease bronchial tone, decrease uterine tone

Front 874

What are the 3 major effects of Prostaglandins

Back 874

increased uterine tone, decrease vascular tone, decrease bronchial tone

Front 875

What are the 3 major effects of Thromboxane

Back 875

increase platelet aggregation, increase vascular tone, increase bronchial tone

Front 876

Zileuton is a ________ pathway inhibitor?

Back 876

Lipoxygenase

Front 877

Zariflukast is associated with what enzymes?

Back 877

Lekukotrienes

Front 879

Asthma drugs

Back 879

p 326

Front 880

Bronchodilation is mediated by what molecule

Back 880

cAMP

Front 881

Bronchoconstriction is mediated by _________ and ___________

Back 881

Ach and adenosine

Front 882

How many asthma drug categories are there?

Back 882

7- (1) nonspecific B-agonists, (2) B2 agonists, (3) Methylxanthines, (4) muscarinic antagonist, (5) cromolyn, (6) corticosteroids, (7) Antileukotrienes

Front 883

What is the only nonspecific B-agonist drug and what are its effects?

Back 883

Isoprotenerol-relaxes bronchial smooth muscle (B2) and tachycardia (B1) (adverse effect).

Front 884

What are the two B2 selective agonist asthma drugs?

Back 884

Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol

Front 885

What are the indications for Albuterol and Salmetrol, respectively?

Back 885

Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for prophylaxis

Front 886

what are the notable adverse effects of B2 agonist?

Back 886

arythmias and tremor

Front 887

B2-agonists activate this enzyme in bronchial smooth muscle that leads to an increase in ________ = bronchodilation

Back 887

B2 agonists activate adenylate cyclase and increase conversion of ATP to cAMP

Front 888

What are the likely mechanism of action theophylline?

Back 888

bronchodialation by inhibition phosphodiesterase (PDE), decreasing cAMP hydrolysis and antagnonizing adenosine action

Front 889

Why is usage of theophylline limited?

Back 889

limited b/c narrow therapeutic index (cardiotoxicity, neurotxicity)

Front 890

What kind of drug is Ipratropium?

Back 890

muscarinic antagonist

Front 891

How does mechanism of action of Ipratropium?

Back 891

competitive block of muscarinic receptors= prevention of bronchoconstriction

Front 892

cromolyn works by inhibiting the release of _______ from ______ cell?

Back 892

prevents release of medicators from mast cells

Front 893

Cromolyn is mainly used for the ______ of athsma and it is not indicated for _______ treatment of athsma?

Back 893

Used only for prophylaxis, not effective during acute episode. Also, toxicity rare

Front 894

__________and ________ are two major corticosteroids used for treatment of what kind of asthma?

Back 894

Beclomethasone and prednisone are 1st line therapy for chronic asthma

Front 895

What is the mechanism of action of corticosteroids?

Back 895

inhibits the synthesis of virtually of cytokines-->inactivates NF-KB, the transcription factor that induces the production of TNF-a, amonth other inflammatory agents.

Front 896

Zileuton blocks the conversion of _______ to ________.

Back 896

zileuton is a 5-lipoxygenase pathway inhibitior. Blocks the conversion of arachidonic acti to leukotrienes

Front 897

Zafirlukast works by_______ ________ ________

Back 897

bloking leukotriene receptors

Front 898

What the most basic asthma treatment strategy?

Back 898

avoidance of exposure to antingen (dust, pollen, etc)

Front 899

After exposure to antigen crosslinks IgE on mast cells. This is prevented by the following drugs: _________ and ________

Back 899

cromolyn and steroids

Front 900

Following allergen exposure mediators are released (ex. _______ and _________). This triggers an ______ asthmatic response characterized by ________ and may be treated with the following 3 asthmatic drug categories to treat the symptoms.

Back 900

examples of mediators are leukotrienes and histamine. Following allergen exposure an early asthmatic response characterized by bronchoconstriction that can be treated with B-agonsists, methylxanthines, and muscarinic antagonists.

Front 901

Also, mediators elicit a ________ response is which leads to bronchial __________ and is treated with __________.

Back 901

mediators elicit a late response and this leads to bronchial hyperactivity. This is best treated with steroids.

Front 903

GI therapy

Back 903

p. 327

Front 904

the following questions are from the diagram at the top of the page

Front 905

_____ cells are predominatly found in the antrum and _________ cells are predominatly found in the fundus.

Back 905

Gastrin cells are predominant in the antrum and parietal cells are predominant in the fundus.

Front 906

What are the 3 main stimuli of acid secretion?

Back 906

Ach, histamine, gastrin

Front 907

Gastrin stimulates the ECL cells to secrete histamine that stimulates ______ cells. Gastrin also activate the ______ cells to increase expression of _______ that increases ______secretion.

Back 907

Gastrin stimulates the ECL cells to secrese histamine that stimulates parietal cells. Parietal cells are also activated by gastrin to increase the expression of the H,K ATPase that increases acid secretion.

Front 908

This type of drug acts by inhibiting M1 and M3 receptors on ECL cells and Parietal cells, respectively.

Back 908

muscarinic antagonists block M1 receptors in ECL cells and M3 receptors in parietal cells.

Front 909

This type of drug inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the _____ receptor.

Back 909

H2 blocker inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the parietal H2 receptor.

Front 910

The most direct way of inhibiting acid secretion is by using this type of drug which acts on this enzyme.

Back 910

the most direct way of inhibiting acid secretion is by using proton pump blockers which inhibit the H,K ATPase on parietal cells.

Front 911

____________ acts by binding to the ulcer and increasing its healing. It may interfere with drug absorption in the stomach.

Back 911

sucralfate binds to the ulcer base and provides physical protection. It allows HCO3- secretion to reestablish pH gradient in the mucus layer.

Front 912

What hormone binds ECL cells and decreases acid secretion?

Back 912

somatostatin

Front 913

These type of drugs used to decrease pH in the stomach.

Back 913

antacids….duh….jk. (I was instructed to make a question of every word)

Front 914

questions not from the diagram

Front 915

____________, ___________, ___________, and ___________ are examples of H2 blockers and they act by (reversibly/irreversibly)

Back 915

cimetedine, ranitidine, famotidine, nizatidine reversilbly block H2 receptors.

Front 916

This H2 blocker is the only one that has many side effects which include potent inhibition of ______, _____ effects, and _____ renal excretion of creatinine.

Back 916

cimetedine is a potent inhibitor of P450, it has antiandrogenic effect and decrease renal excretion of creatinine. Other H2 blockers are relatively free of these effects.

Front 917

_________ and _________ (reversibly/irreversibly) inhibit the H/K ATPase in the stomach _______cells.

Back 917

Omeprazole and Iansoprazole irreversibly inhibit the H/K ATPase in stomach parietal cells

Front 918

Proton pump inhibitors are indicated for peptic ulcer, ________, _______, and _________ syndrome

Back 918

peptic ulcer, gastritis, esophageal reflux, and Zollinger-Ellison syndrome

Front 919

T/F: Bismuth and sucralfate allow HCO3- secretion.

Back 919

True: bismuth and sucralfate bind to ulcer base and provide physical protection, and allow HCO3- secretion to reestablish pH gradient in the mucus layer=increased ulcer healing

Front 920

T/F: misoprostol is a PGE2 analog and increases the production and secretion of gastric mucous barrier.

Back 920

False: misoprostol is a PGE1 analog and it increases the production and secretion of gastric mucous barrier.

Front 921

What are the 3 indications for misoprosol?

Back 921

prevention of NSAID-induced peptic ulcers, maintains a PDA and used to induce labor

Front 922

In what population is misoprostol contraindicated?

Back 922

women of childbearing potential (abortifacient). It also casues diarrhea

Front 923

Infliximab is ___________ against ______.

Back 923

monoclonal antibody to TNFa

Front 924

The clinical indication for Infliximab is:

Back 924

Crohn's, along with fistula healing

Front 925

T/F: Infliximab can cause respiratory infection, fever, hypotension

Back 925

TRUE

Front 927

GI Drugs (cont.)

Back 927

p. 328

Front 928

This drug offers both anitbacterial action and anti-inflamatory effects. It is used for 2 inflammatory GI diseases ______ and _______.

Back 928

sulfasalazine: combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory effects). It is used for Ulcerative colitis and remission of Crohn's.

Front 929

T/F: Side effects of the above include: malaise, sulfonamide toxicity, neutropenia

Back 929

false: side effects: malaise, nausea, sulfonamide toxicity

Front 930

___________ is a powerful central-acting antiemetic. It acts by antagonizing the______ receptor.

Back 930

Ondansetron: is a powerful antiemetic. Think: you will not vomit with ondansetron, so you can go on dancing.

Front 931

T/F used to treat vomiting preoperatively and for cancer chemo therapy pts.

Back 931

False: it is used to treat vomiting postoperatively.

Front 932

Headache and __________ are side effects

Back 932

constipation (can't vomit or poop)

Front 933

Antacid overuse can affect:_________, __________, or ______ excretion of other drugs by altering ______ and ______ pH or by delaying gastric _________.

Back 933

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

Front 934

Constipation and (hypo/hyper) phosphatemia is seen with overuse of ________________

Back 934

aluminum hydroxide - Aluminimum amt. of feces

Front 935

Magnesium hydroxide overuse = ___________

Back 935

diarhea; Mg = Must go to the bathroom

Front 936

Calicium carbonate= hypercalcemia and (increase/decreased) acid

Back 936

causes hypercalcemia and increased acid.

Front 937

T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2

Back 937

False! hypokalemia

Front 939

Hematologic Drugs

Back 939

p328

Front 941

heparin

Front 942

Catalyzes activation of ____________, decreases ________ and __________. It has a ____t1/2. check PTT

Back 942

catalyzes the activation of antithrombin III, decreases thrombin and Xa. It has a short t1/2

Front 943

It is used for immediated anticoagulation for pulmonary embolism,_______, _______, MI, and ________. Follow PTT

Back 943

used for pulmonary embolism, stroke, angina, MI, and DVT.

Front 944

T/F: Is used during pregnancy

Back 944

true: it is used during pregnancy because it does not cross the placenta.

Front 945

It can cause bleeding,___________, and drug-drug interactions.

Back 945

thrombocytopenia

Front 946

___________ is used for rapid reversal of heparization (it is a _______ charged molecule that binds the ________ charged heparin)

Back 946

protamine sulfate is used for rapid reversal of heparinization (it is a positively charged molecule that binds the negatively charged heparin).

Front 947

Newer________________ (enoxaparin) act more on _____, have better bioavailability and 2-4 times longer t1/2. Can be administered subcut and (with/without) lab monitoring.

Back 947

lower-molecular-weight heparins (enoxaparin) act more on Xa, have better bioavailabitlity and 2-4 times longer half-life. Can be adm. Subcut and without lab monitoring.

Front 949

warfirin (coumandin)

Back 949

p. 328

Front 950

Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent factors ___, ___, ___, and ___, also, ___ and ___ via ______ antagonism.

Back 950

Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, protein C and S via vitamin K antagonism.

Front 951

t1/2 (short/long)

Back 951

long

Front 952

Used for _______ anticoagulation. Follow PT

Back 952

WEPT - Warfirin affects the Extrinsic pathway and prolongs PT

Front 953

T/F: is used during pregnacy

Back 953

False! (warfarin, unlike heparin, can cross the placenta).

Front 954

Toxicity: bleeding, _________, drug-drug interactions

Back 954

teratogenic

Front 956

heparin vs. warfarin

Back 956

p. 329

Front 957

Heparin is a (large/small) _____charged acicid polymer while Warfarin is (large/small) (charged/neutral) molecule

Back 957

Heparin is a large negatively charged acidic polymer while Warfarin is a small neutral charged lipid-soluble molecule

Front 958

T/F: Heparin is given orally while warfarin is given SC/IV

Back 958

False! Heparin is given IV/SC and warfarin is give oral

Front 959

Site of action: heparin _________, warfarin ______

Back 959

heparin's site of action is the blood; warfarin's site of action is the liver (synthesises clotting factors)

Front 960

Onset of action of _________ is slow; the onset of action of ______ is rapid

Back 960

onset of action of heparin is rapid (secs) and the onset of action of warfarin is slow, limitd by t1/2 of normal clotting factors.

Front 961

Warfarin works by imparing the synthesis of _______ dependent factors __, ___, ___, and ___ also _____, and ____; heparin activates _____, ____ and ___

Back 961

Warfarin works by imparing the synthesis of vitamin K dependent factors II, VII, IX, and X also protein S and protein C; heparin activates ATIII, Iia (thrombin) and Xa.

Front 962

Heparin 's duration of action is (acute/chronic); warfarin's duration of action is (actue/chronic)

Back 962

Heparin's duration of action is actute and warfarin's duration of action is chronic.

Front 963

Tx of acute OD: Heparin = _________; warfarin=______

Back 963

Tx of heparin OD is protamine sulfate; Tx of warfarin= IV vit. K and fresh frozen plasma.

Front 964

Warfarin is monitored by _________ while Heparin is monitored by ___________.

Back 964

Warfrin is monitored by PT (extrinsic pathway) (WEPT) and heparin is monitored by PTT (intrinsic pathway)

Front 966

Thrombolytics

Back 966

p. 329

Front 967

questions from diagram at bottom of page

Front 968

plasmin is the major ___________ enzyme. It breaks down both _______ and _______

Back 968

fibrinolytic enzyme. It accelerates breaks down of both fribin and fibrinogen yielding fibrin splip products and degradation products, respectively.

Front 969

Fibrinogen is converted to fibrin by _________

Back 969

thrombin

Front 970

tPA and urokinase promote the converson of ______ to ________ thereby increasing fibrinolysis.

Back 970

plasminogen to plasmin

Front 971

Various stimuli activate a blood proactivator to a blood activator that promotes conversion of _________ to blank thereby increasing fibrinolysis

Back 971

plasminogen to plasmin

Front 972

Streptokinase and anistreplase both activate and Activator that increases convesion of plasminogen to plasmin.

Front 973

Aminocaproic acid:____________ fibrinolysis.

Back 973

inhibits fibrinolysis by inhibition of plasminogen conversion to plasmin.

Front 974

4 examples of thrombolytics include: ________, _________, _____________, and ___________

Back 974

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

Front 975

work by directly or indirectly aiding the conversion of ___________ to __________, which cleaves ______ and ________ clots. tPA specifically coverts _______________ to plasmin

Back 975

Directly or indirectly aid conversion of plaminogen to plasmin, which cleaves thrombin and fribrin clots. It is claimed that tPA specifically coverts fribrin-bound plasminogen to plasmin.

Front 976

T/F: clinical use is for DVTs

Back 976

False: used for early MI

Front 977

pts. receiving this medication are at most risk for: ______

Back 977

bleeding

Front 979

Hematologic Drugs

Back 979

p. 330

Front 981

mechanism of antiplatelet interaction

Front 982

questions from diagram at top of page

Front 983

When a break in the endothelium occurs _________ and _________ are exposed.

Back 983

collagen and vWF

Front 984

Platelets are activated by binding to the above macromolecules. The two structures expressed by the platelets involved in this process are __________ and _________ and they bind to _________ and __________, repectively

Back 984

Platelets bind to collagen and vWF. The two structures expressed by platelets that are involved in this process are GP 1a and GP 1b. GP 1a and GP 1b bind to collagen and vWF, respectively.

Front 985

After platelet activation _________ is expressed on their surface. What is the role of this structure?

Back 985

after platelets are activated they express GP IIb/IIIa. This molecule is important in platlelet-platelet aggregation.

Front 986

_________ and _________ interaction is needed in order for platelet aggregation to occur.

Back 986

GP IIb/IIIa and fribinogen

Front 987

5-HT, _______, and ________ are molecules that play a role in the glycoprotein expression of activated platelets.

Back 987

5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein expression of activated platelets.

Front 988

Aspirin acts by inhibiting production of ________ that in turn inhibits glycoprotein expression in activated platelets.

Back 988

TxA2

Front 989

ADP production is inhibited by the drug _________.

Back 989

ticlopidine

Front 990

This antibody drug targets the _______ on platelets.

Back 990

Abciximab

Front 992

Copidogrel, ticlopidine

Back 992

p. 330

Front 993

T/F: inhibits platele aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen

Back 993

TRUE

Front 994

It is used for ______ ________ syndrome, coronary _______, and it has been shown to decrease the incidence or recurrence of___ ____.

Back 994

it is used for acute coronary syndrome, coronary stenting. Decreases incidence or recurrence of thrombotic stroke

Front 995

Ticlopidine is associated with_________ as a side effect.

Back 995

Ticlopidine causes neutropenia and it is reserved for those who cannot tolerate aspirin.

Front 997

Abciximab

Back 997

p. 330

Front 998

This drug binds to __________ on activated platelets.

Back 998

gp IIb/Iia

Front 999

It is used for ___________ and ________ _________ ___________ ___________

Back 999

acute coronary syndromes and percutanous transluminal coronary angioplasty

Front 1000

toxiciites are _______ and ________

Back 1000

bleeding and thrombocytopenia

Front 1001

Aspirin

Back 1001

p 330

Front 1002

It ________ and (reversibly/irreversibly) inhibits COX1 and COX2 to prevent the conversion of _______ to prostaglandins.

Back 1002

acetilates and irreversably inhibits COX-1 and COX-2

Front 1003

T/F: aspirin has an effect of PT, PTT

Back 1003

false it has no effect

Front 1004

What are the 4 A's of aspirin and NSAIDS in general

Back 1004

Antipyretic, Analgesic, Anti-inflam, antiplatelet

Front 1005

Important toxicities include _________, bleeding, hyperventilation, __________- in children, and CN ____ toxicity

Back 1005

gastric ulceration, bleeding, hyperventilation, Reyes syndrome and tinnitus (CNVIII).

Front 1006

Endocrine Drugs

Back 1006

pg 332

Front 1007

Hydrocortisone, prednisone, triamcinolone, dexamtasone, bleclomethasone are examples of what kind of drugs?

Back 1007

Glucocorticoid

Front 1008

Glucocorticoids decrease the production of ___ and ____

Back 1008

Leukotrienes and prostanglandins

Front 1009

To treat Addison's disease, inflammation, immune suppression, asthma, use ____

Back 1009

Glucocorticoids

Front 1010

An important side-effect of Glucocortioid usage is ____

Back 1010

Iatrogenic Cushing's Syndrome

Front 1011

Buffalo hump, moon facies, truncal obesity, muscles wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers characterize what syndrome?

Back 1011

Cushing's Syndrome

Front 1013

Reproductive Drugs

Back 1013

pg 332

Front 1014

Which two drugs inhibit cGMP phosphodiesterase, leading to smooth muscle relaxation in the corpus cavernosum and penile erection?

Back 1014

Sildenafil and Verdenafil --they fill the penis

Front 1015

What class of drugs are used tto treat erectile dysfunction

Back 1015

cGMP Inhibitors

Front 1016

CGMP inibitors taken with ____have a high risk of liofe-threeatening hypotension

Back 1016

nitrates

Front 1017

Which drugs is a partial agonist of estrogen recpetors in the pituitary gland, stimulating increase in LH and FSH, which stimulates ovulation to treat infertility

Back 1017

clomiphene

Front 1018

Clomiphene's side effects include:

Back 1018

Hotflashes, ovarian enlargment, multiple simultaneous pregnancies, visual disturbances

Front 1019

What abortifacient is a competitite inhibitor of preogestins at progesterone recpetor and may lead to heavy menstrual-like bleeding?

Back 1019

Mifepristone (RU486)

Front 1020

The advantage of this drug is that it is reliable, decreases incidence of ectopic pregnancy, decreases risk of pelvic infections, and regulates menses; however it also puts you in a hypercoagulable stat and may increase your trigylcerides, weight, and blood pressure

Back 1020

Oral Contracpetices - syntheitc progestins/estrogen

Front 1022

Rheumatologic Drugs

Back 1022

pg 333

Front 1023

____is converted to uric acid which leads to gout

Back 1023

Xanthine (converted from excess purines)

Front 1024

This drug depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation, and used to treat acute gout

Back 1024

Colchicine

Front 1025

This drugs inhibits reabsorption of uric acid and used to treat chronic gout

Back 1025

Probenecid

Front 1026

This drug is used to treat chronic gout, but also inhbits secretion of penicillin

Back 1026

Probenecid

Front 1027

This drugs inhibits xanthine oxidase decreasing the conversion fo xanthine to uric acid

Back 1027

Allopurinol

Front 1029

Oncologic Drugs

Back 1029

pg 333-336

Front 1030

What are the cell cycle specific oncologic drugs

Back 1030

antimetabolites, plant alkaloids, stroid hormones, bleomycin, paclitaxel, etoposide

Front 1031

What are the cell cycle Nonspecific oncologic drugs?

Back 1031

alkylating agents and antibiotics

Front 1032

____is an S-phase-specific anti-metabolite that is an folic acid analog that inhibits dihydrofolate reducate decreasing dTMP(thymidine and purines) and decreaing DNA/prtein synthesis.

Back 1032

Methotrexate

Front 1033

____is an S-phase-specific anti-metabolite that is a pyrmidine analog which complexed to folic acid, inhibiting thymidylate synthase, decreasing dTMP and decreasing DNA/protein synthesis

Back 1033

5-Fluorouracil (5-FU)

Front 1034

Myelosuppression by methotrxate is reversible with ____

Back 1034

leucovorin (folinic acid) rescue

Front 1035

Which drug blocks purine synthesis and is used to treat leukemias, lymphomas (not CLL or Hodgkins)

Back 1035

6-mercaptopurine (6-MP)

Front 1036

Which drug alkylates DNA and is used to treat CML?

Back 1036

Busulfan

Front 1037

Which drug inhibits DNA polymerase and is used to treat AML?

Back 1037

cytarabine

Front 1038

This drug used to treat Leukemias and Lymphomas is metaboilized by xanthine oxidase

Back 1038

6-mercaptopurine (6-MP)

Front 1039

Used to treat leukemias, lymphomas, choricarcinoma, sacromas, rheumatoid arthritis, psoriasis, and can be an abortifacient; it may lead to myelosuppression

Back 1039

Methotrexate

Front 1040

Used to treat colon cancer and other solid tumors, basal cell carcinoma (topically)

Back 1040

5-Fluorouracil (5-FU)

Front 1041

Myelosuppression by 5-FU is ______

Back 1041

Not reversible

Front 1042

This drug used to treat AML may lead to leukopenia, thrombocytopenia, megaloblastic anemia?

Back 1042

cytarabine

Front 1043

This drugs used to treat CML may lead to pulmonary fibrosis and hyperpigmentation?

Back 1043

Busulfan

Front 1044

____is an alkylating agent acivated by liver that covalently x-links DNA at guanine N-7, and is used to treat non-hodgkin's lymphoma, breast/ovarian carcinomas

Back 1044

cyclophosphamides

Front 1045

____ alkylates DNA after bioactivation and can cross the BBB and treats brain tumors (glioblastoma multiforme)

Back 1045

Nitrosoureas (Carmustine, lomustine, semustine, streptozocin)

Front 1046

____acts like an alkylating agent, x-linking via hyrdolysis of Cl and platinum; used to treat testicular, bladder, lung carcinomas

Back 1046

Cisplatin

Front 1047

This alkylating agent can cause myelosuppression and hemorhagic cystitis

Back 1047

cyclophosphamides

Front 1048

This combination of drugs is used to treat Hodgkin's and myelomas, sarcomas, and solid tumors (breast, ovary, lung)

Back 1048

ABVD: Adriamycin, Bleomycin, Vinblastine, Dacarbazine

Front 1049

____noncovalently intercalates in DNA, creating breaks to decrease replication and transcription

Back 1049

Doxorubicin (adriamycin)

Front 1050

____intercalates DNA strands and induces free radical fromation which causes strand breaks

Back 1050

Bleomycin, Dactinomycin

Front 1051

Which drugs causes cardiotoxicity, alopecia, and myelosuppression?

Back 1051

Doxorubicin (adriamycin)

Front 1052

Which drug is used to trat oat cell carcinoma of the lung and prostate/testicular carcinoma?

Back 1052

Etoposide

Front 1053

This combination of drugs is used to treat lymphoma, CLL, Hodgkin's, Wilm's tumor, choriocarcinoma

Back 1053

MOPP (Mustargen, Oncovin (Vincristine), Procarbazine (Matulane), Prednisone)

Front 1054

Which glucocorticoid may trigger apoptosis and may even work on nondividing cells

Back 1054

Prednisone

Front 1055

This drug is a G2-phase specific inhibitor of Topisiomerase II, leaving double strand breaks in DNA following DNA replication

Back 1055

Etoposide

Front 1056

This drug used to treat testicular cancer and lymphomas may cayse pulmonary fibrosis, skin chnages, and myelosuppression

Back 1056

Bleomycin, Dactinomycin

Front 1057

This drugs used as an immunosuppressant and in lymphomas may cause acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis?

Back 1057

Prednisone

Front 1058

____is an estrogen receptor mixed agonist/antagonist that blocks the binding of estrogen to ER+ cells.

Back 1058

Tomoxifen/Raloxifene

Front 1059

____is n M-phase-specific alkaloid that binds to tubulin and blocks polymerization of microtubules, preventing spindle formation

Back 1059

Vincristine and Vinblastine

Front 1060

____is an M-phase-specific agen that binds to tubulin and hyperstabilizes the polymerized microtubules, so that the mitotic spindle cannot break down

Back 1060

Paclitaxel

Front 1061

What drugs is used to treat breast cancer, but may increas the risk of endometrial carcinomas and hot flashes

Back 1061

Tomoxifen

Front 1062

Side-effects of Vinblastine include….

Back 1062

VinBASTine BLASTs Bone Morraow, causing myelosuppression, as well as neurotoxicity and paralutic ileus.

Front 1063

Side effects of Paclitaxel include….

Back 1063

Myelosuppression and hypersensitivity

Front 1066

Immunosuppressants and Cytokine Therapy

Back 1066

pg 336-337

Front 1067

This drug binds to cyclophilins, blocking differentiation and activation of T cells mainly by inhibiting IL2 production

Back 1067

cyclosporine

Front 1068

This antimetabolite derivative of 6-mercaptopurine interferes with the metabolism and synthesis of nucleic acid, therefore toxic to proliferating lymphocytes

Back 1068

azathioprine

Front 1069

This potent immunosuppressive drug binds to the FK-binding protein and inhibits secretion of IL2 and other cytokines

Back 1069

tacrolimus (FK506)

Front 1070

This drug is used to suppress organ rejection after transplantation, but may predispose patient to viral infections and lymphoma

Back 1070

cyclosporine

Front 1071

Azaothioprine is used to in what setting?

Back 1071

Kidney transplants, autoimmune disorders (glomerulonephritis, hemolytic anemia)

Front 1072

Recombinant Cytokine- Aldesleukin (interleukin-2) is used for?

Back 1072

Renal cell carcinoma, metastatic melanoma

Front 1073

Recombinant Cytokine- Erythropoietin (epoetin) is used for?

Back 1073

anemia

Front 1074

Recombinant Cytokine- Filgrastim is used for?

Back 1074

Recovery of Bone Marrow; it is a granulocyte colony stimulating factor

Front 1075

Recombinant Cytokine- alpha interferon is used for?

Back 1075

Hep B/C, Kaposi's sarcoma, leukemia, malgnant melanoma

Front 1076

Recombinant Cytokine- beta interferon is used for?

Back 1076

Multiple Sclerosis

Front 1077

Recombinant Cytokine- gamma interferon is used for?

Back 1077

Chronic Granulomatous disease

Front 1078

Recombinant Cytokine- oprelvekin (interleukin2) is used for?

Back 1078

Thrombocytopenia

Front 1079

Recombinant Cytokine- sargamostim is used for?

Back 1079

Recovery of Bone Marrow (it is a granulocyte-macrophage colony stimulating factor)

Front 1080

Recombinant Cytokine- thrombopoietin is used for?

Back 1080

Thrombocytopenia

Front 1082

Toxicology

Back 1082

pg 338

Front 1083

What is the antidote for acetaminophen toxicity/overdose

Back 1083

N-acetylcysteine

Front 1084

What is the antidote for salicylates toxicity/overdose

Back 1084

Alkanize urine/dialysis

Front 1085

What is the antidote for antichoinesterase toxicity/overdose

Back 1085

Atropine, pralidoxime

Front 1086

What is the antidote for antimuscarinic/anticholinergic agents toxicity/overdose

Back 1086

physostigimine salicylate

Front 1087

What is the antidote for Beta-blockers toxicity/overdose

Back 1087

glucagon

Front 1088

What is the antidote fordigitalis toxicity/overdose

Back 1088

Stop digitalis, Normalize K+, lodpcaine, anti-digitialis Fab Fragments, Magnesium

Front 1089

What is the antidote for lead toxicity/overdose

Back 1089

CaEDTA, dimercaprol, succimer, penicillamine

Front 1090

What is the antidote for iron toxicity/overdose

Back 1090

Deferoxamine

Front 1091

What is the antidote for aresnic/mercury/gold toxicity/overdose

Back 1091

Dimercaprol (BAL), succimer

Front 1092

What is the antidote for copper, arsenic, gold toxicity/overdose

Back 1092

Penicillamine

Front 1093

What is the antidote N-acetylcysteine used to treat?

Back 1093

Acetaminophen toxicity/overdose

Front 1094

What is the antidote for cyanide toxicity/overdose

Back 1094

nitrite, hydroxocobalamin, thiosoulfate

Front 1095

What is the antidote for methemoglobin toxicity/overdose

Back 1095

methylene blue

Front 1096

What is the antidote glucagon used to treat?

Back 1096

Beta-blocker toxicity/overdose

Front 1097

What is the antidote for carbon monoxide toxicity/overdose

Back 1097

100% oxygen, hyperbaric oxygen

Front 1098

What is the antidote atropine used to treat?

Back 1098

anticholinesterase toxicity/overdose

Front 1099

What is the antidote for methanol toxicity/overdose

Back 1099

Ethanol, dialusis, fomepizole

Front 1100

What is the antidote for opiods toxicity/overdose

Back 1100

Nalozone/naltrexone

Front 1101

What is the antidote for ethylene glycol toxicity/overdose

Back 1101

Ethanol, dialusis, fomepizole

Front 1102

What is the antidote for benzodiazepines toxicity/overdose

Back 1102

Flumazenil

Front 1103

What is the antidote for (TCA) Tricyclic Antidepressants toxicity/overdose

Back 1103

NaHCO3

Front 1104

What is the antidote for Heparin toxicity/overdose

Back 1104

Protamine

Front 1105

What is the antidote Deferoxamine used to treat?

Back 1105

Iron toxicity/overdose

Front 1106

What is the antidote for warfarin toxicity/overdose

Back 1106

vitamin K, fresh frozen plasma

Front 1107

What is the antidote Naloxone/naltrexone used to treat?

Back 1107

opioid toxicity/overdose

Front 1108

What is the antidote for tPA/streptokinase toxicity/overdose

Back 1108

aminocaproic acid

Front 1109

What is the antidote Physostigmine salicylate used to treat?

Back 1109

Antimuscarinic/anticholinergic agents toxicity/overdose

Front 1110

What is the antidote Flumazenil used to treat?

Back 1110

Benzodiazepine toxicity/overdose

Front 1111

What is the antidote Protamine used to treat

Back 1111

Heparin toxicity/overdose

Front 1112

Children living in old houses might eat the paint chips which could cause ____

Back 1112

Lead Poisoning

Front 1113

Signs of Lead poisoning include:

Back 1113

Lead Lines on gingivae and epiphyses of Long bones, Encephalopathy and Erythrocyte Basophilic stippling, Abdominal colic and sideroblastic Anemia, Wrist and Foot Drop

Front 1114

1st line of Treatment for Lead Poisoning include

Back 1114

Dimercaprol and EDTA

Front 1115

Weak acids, such as phenobarbitol, methotreaxate, aspirin, alkanize urine with ____ to increase clearance

Back 1115

bicarbonate

Front 1116

Weak bases, such as amphetamines, acidify urine with NH4Cl to ____ clearance

Back 1116

increase

Front 1117

AUTHOR

Back 1117

Lakshmi Swamy

Front 1118

Drug reactions

Back 1118

p. 339

Front 1119

For each drug reaction, give the pharmacological agents responsible. The number of drugs you should list are given in parentheses. You could also quiz yourself in reverse by going down the list of drugs on the right.

Front 1120

Pulmonary fibrosis (3)

Back 1120

bleomycin, amiodarone, busulfan

Front 1121

Hepatitis (2)

Back 1121

isoniazid, halothane

Front 1122

Focal to massive hepatic necrosis (4)

Back 1122

halothane, valproic acid, acetaminophen, amanita phalloides

Front 1123

Anaphylaxis (1)

Back 1123

penicillin

Front 1124

SLE-like syndrome (4). [mnemonic: it's not HIPP to have lupus]

Back 1124

hydralazine, INH, procainamide, phenytoin

Front 1125

Hemolysis in G6PD-deficient patients (8)

Back 1125

sulfonamides, INH, aspirin, ibuprofen, primaquine, nitrofurantoin, pyrimethamine, chloramphenicol

Front 1126

Thrombotic complications (1 class)

Back 1126

OCPs (e.g. estrogens and progestins)

Front 1127

Adrenocortical insufficiency (withdrawal of what class of drugs causes adrenocortical insufficiency?)

Back 1127

withdrawal of glucocorticoids causes hypothalamic-pituitary-axis suppression

Front 1128

Photosensitivity reactions (3) [mnemonic: SAT for a photo]

Back 1128

Sulfonamides, amiodarone, tetracycline

Front 1129

Induce P-450 system (6)

Back 1129

barbiturates, phenytoin, carbamazepine, rifampin, griseofulvin, quinidine

Front 1130

Inhibit P-450 system (6, including one fruit)

Back 1130

cimetidine, ketoconazole, grapefruit, erythromycin, INH, sulfonamides

Front 1131

Tubulointerstitial nephritis (5)

Back 1131

sulfonamides, furosemide, methicillin, rifampin, NSAIDs (except aspirin)

Front 1132

Hot flashes (1)

Back 1132

Tamoxifen

Front 1133

Cutaneous flushing (4)

Back 1133

niacin, Ca++ channel blockers, adenosine, vancomycin

Front 1134

Cardiac toxicity (2)

Back 1134

doxorubicin (adriamycin), daunorubicin

Front 1135

Agranulocytosis (3, all start with letter C)

Back 1135

clozapine, carbamazepine, colchicine

Front 1136

Stevens-Johnson syndrome (3)

Back 1136

ethosuximide, sulfonamides, lamotrigine

Front 1137

Cinchonism (2)

Back 1137

quinidine, quinine

Front 1138

Tendonitis, tendon rupture and cartilage damage (kids) (1)

Back 1138

fluoroquinolones

Front 1139

Disulfiram-like reaction (4)

Back 1139

metronidazole, certain cephalosporins, procarbazine, sulfonylureas

Front 1140

Otoxicity and nephrotoxicity (3)

Back 1140

aminoglycosides, loop diuretics, cisplatin

Front 1141

Drug-induced Parkinson's (4)

Back 1141

haloperidol, chlorpromazine, resperine, MPTP

Front 1142

Torsades de pointes (two subclasses of antiarrhythmics)

Back 1142

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

Front 1143

Aplastic anemia (3)

Back 1143

chloramphenicol, benzene, NSAIDs

Front 1144

Neuro/nephrotoxicity (1)

Back 1144

polymyxins

Front 1145

Pseudomembranous colitis (2)

Back 1145

clindamycin, ampicillin

Front 1146

Gynecomastia (5) [mnemonic: Some Drugs Create Awesome Knockers]

Back 1146

spironolactone, digitalis, cimetidine, chronic Alcohol use, estrogens, ketoconazole

Front 1147

Atropine-like side effects (1)

Back 1147

tricyclics

Front 1148

Cough (1)

Back 1148

ACE inhibitors (losartan --> no cough)

Front 1149

Gingival hyperplasia (1)

Back 1149

phenytoin

Front 1150

Diabetes insipidus (1)

Back 1150

lithium

Front 1151

Tardive dyskinesia (1)

Back 1151

antipsychotics

Front 1152

Fanconi's syndrome (1)

Back 1152

tetracycline

Front 1153

Gray baby syndrome (1)

Back 1153

chloramphenicol

Front 1154

Extrapyramidal side effects (3)

Back 1154

chlorpromazine, thioridazine, haloperidol

Front 1155

Osteoporosis (2)

Back 1155

corticosteroids, heparin

Front 1157

Alcohol toxicity

Back 1157

p. 340

Front 1158

Ethylene glycol is converted to ------- ------ by alcohol dehydrogenase. This product can lead to acidosis and nephrotoxicity.

Back 1158

oxalic acid.

Front 1159

Alcohol dehyrogenase also converts methanol to formaldehyde and formic acid, which can cause severe ----- and damage to the -------.

Back 1159

acidosis. retina

Front 1160

Ethanol competes with ethylene glycol and methanol (if present) for alcohol dehydrogenase. ADH action on EtOH produces -------.

Back 1160

acetaldehyde

Front 1161

What symptoms does acetaldehyde cause?

Back 1161

nausea, vomiting, headache, hypotension

Front 1162

Acetaldehyde itself can be metabolized by acetaldehyde dehydrogenase to ----- -----.

Back 1162

acetic acid.

Front 1163

Acetaldehyde dehydrogenase is inhibited by what drug?

Back 1163

disulfiram.

Front 1165

Herbal agents

Back 1165

p. 341

Front 1166

Give the clinical uses for the following herbal agents.

Front 1167

echinacea

Back 1167

common cold

Front 1168

ephedra

Back 1168

as for ephedrine

Front 1169

feverfew

Back 1169

migraine

Front 1170

ginko

Back 1170

intermittent claudication

Front 1171

kava

Back 1171

chronic anxiety

Front 1172

milk thistle

Back 1172

viral hepatitis

Front 1173

saw palmetto

Back 1173

benign prostatic hyperplasia

Front 1174

St. John's wort

Back 1174

mild to moderate depression

Front 1175

dehyroepiandrosterone

Back 1175

symptomatic improvement in females with SLE or AIDS

Front 1176

Melatonin

Back 1176

jet lag, insomnia

Front 1178

Give the toxicities for the following herbal agents.

Front 1179

echinacea

Back 1179

GI distress, dizziness, and headache

Front 1180

ephedra

Back 1180

CNS and cardiovascular stimulation; arrhythmias, stroke and seizures at high doses.

Front 1181

feverfew

Back 1181

GI distress, mouth ulcers, antiplatelet actions

Front 1182

ginko

Back 1182

GI distress, anxiety, insomnia, headache, and antiplatelet actions

Front 1183

kava

Back 1183

GI distress, sedation, ataxia, hepatotoxicity, phototoxicity, dermatotoxicity

Front 1184

milk thistle

Back 1184

loose stools

Front 1185

saw palmetto

Back 1185

GI distress, decreased libido, hypertension

Front 1186

St. John's wort

Back 1186

GI distress and phototoxicity; serotonin syndrome with SSRIs

Front 1187

dehyroepiandrosterone

Back 1187

Androgenization (premenopausal women), estrogenic effects (postmenopausal), feminization (young men)

Front 1188

Melatonin

Back 1188

Sedation, suppresses midcycle LH, hypoprolactinemia

Front 1190

Drug name

Back 1190

p. 341

Front 1191

For each drug name ending, give the general category of drug it indicates and an example of a drug in that category.

Front 1192

-ane

Back 1192

inhalational general anesthetic. Halothane

Front 1193

-azepam

Back 1193

benzodiazepine. Diazepam

Front 1194

-azine

Back 1194

phenothiazine (neuroleptic, antiemetic). Chlorpromazine

Front 1195

-azole

Back 1195

antifungal. Ketoconazole

Front 1196

-barbital

Back 1196

barbiturate. Phenobarbital

Front 1197

-caine

Back 1197

local anesthetic. Lidocaine

Front 1198

-cillin

Back 1198

penicillin. Methicillin

Front 1199

-cycline

Back 1199

antibiotic, protein synthesis inhibitor. Tetracycline

Front 1200

-ipramine

Back 1200

tricyclic antidepressant. Imipramine

Front 1201

-navir

Back 1201

protease inhibitor. Saquinavir

Front 1202

-olol

Back 1202

beta antagonist. Propranolol

Front 1203

-operidol

Back 1203

butyrophenone (neuroleptic). Haloperidol

Front 1204

-oxin

Back 1204

cardiac glycoside (inotropic agent). Digoxin

Front 1205

-phylline

Back 1205

methylxanthine. Theophylline

Front 1206

-pril

Back 1206

ACE inhibitor. Captopril

Front 1207

-terol

Back 1207

beta-2 agonist. Albuterol

Front 1208

-tidine

Back 1208

H2 antagonist. Cimetidine

Front 1209

-triptyline

Back 1209

tricyclic antidepressant. Amitriptyline

Front 1210

-tropin

Back 1210

pituitary hormone. Somatotropin

Front 1211

-zosin

Back 1211

alpha-1 antagonist. Prazosin