Usmle Pharm

Front 1

What's Epi/NE's location/effect on: vascular smooth mm.

Back 1

alpha1/beta2

Front 2

What's Epi/NE's location/effect on: Renal vasculature

Back 2

D1 (vasodilation)

Front 3

What's Epi/NE's location/effect on: heart

Back 3

beta-1

Front 4

What's Epi/NE's location/effect on: pulmonary bronchioles

Back 4

beta2

Front 5

What's Epi/NE's location/effect on: pre-synaptic neurons

Back 5

alpha2

Front 6

What's Epi/NE's location/effect on: pupillary sphincter

Back 6

alpha1 - mydriasis

Front 7

What's Epi/NE's location/effect on: kidney JGA

Back 7

Beta1 - renin release and decreased BP

Front 8

What's Epi/NE's location/effect on: Beta cells of pancreas

Back 8

alpha2 - inhibits insulin release

Front 9

What's Epi/NE's location/effect on: alpha cells of pancreas

Back 9

increased glucagon release

Front 10

What's Epi/NE's location/effect on: liver

Back 10

beta2 - glycogenolysis + gluconeogenesis

Front 11

Treatment for: alcohol withdrawal

Back 11

benzos

Front 12

Treatment for: anorexia/bulimia

Back 12

SSRIs

Front 13

Treatment for: anxiety

Back 13

Benzos, buspirone, SSRIs

Front 14

Treatment for:ADHD

Back 14

methylphenidate (ritalin)Amphetamines (dexedrine)dextroamphetamine (adderall)

Front 15

Methylphenidate uses

Back 15

ADHD, major depressive disorder, especially in elderly (as it has quick effect), narcolepsy, daytime sleepiness

Front 16

Treatment for: Atypical depression (mood reactivity, leaden fatigue, rejection sensitivity, reversed vegetative states of increased sleep+appetite)

Back 16

MAOI SSRIs Both better than TCAs

Front 17

Treatment for: Bipolar disorder

Back 17

Mood stabilizers: Lithium Valproic acid, Carbamazepine, Lamotrigine (these three anticonvulsants) Atypical antipsychotics: olanzapine, aripiprazole

Front 18

Treatment for: Depression

Back 18

SSRIs, NSRIs, TCAs

Front 19

Treatment for: Depression with insomnia

Back 19

Mirtazapine (tetracycline), Trazodone, Nefazodone (SNRI)

Front 20

Treatment for: OCD

Back 20

SSRIs, Clomipramine

Front 21

Treatment for: Panic Disorder

Back 21

SSRIs, TCAs, Benzos, beta-blockers, desensitization, CBT

Front 22

Treatment for: PTSD

Back 22

SSRIs, psychotherapy

Front 23

Treatment for: Schizophrenia

Back 23

Antipsychotics

Front 24

Treatment for: Tourette's Syndrome

Back 24

Antipsychotics (haloperidol)

Front 25

Withdrawal symptoms: Post-use crash, including depression, lethargy, headache, stomach cramps, hunger, hypersomnolence [suicidality, fatigue, malaise, severe psychological craving]

Back 25

Amphetamines, [cocaine]

Front 26

Intoxication symptoms: Psychomotor agitation, impaired judgment, pupillary dilation, tachycardia, hypertension, hallucinations

Back 26

amphetamines - inc. prolonged wakefulness and attention, cardiac arrhythmias, delusions, fever Cocaine - hallucinations includng tactile, paranoid ideations, angina, sudden cardiac death

Front 27

Intoxication symptoms: restlessnes, insomnia, arrhythmias

Back 27

caffeine - also: diuresis, muscle twitching Nicotine - anxiety

Front 28

Withdrawal symptoms: Headache, weight gain

Back 28

Caffeine - also lethargy, depression Nicotine - Irritability, anxiety, craving

Front 29

Intoxication Symptoms: respiratory depression, low safety margin

Back 29

Barbs - greater respiratory depression, lower safety margin Benzos - lesser respiratory depression, greater safety margin. Also: amnesia, ataxia, somnolence, additive effects with alcohol

Front 30

Intoxification Treatment: Barbs and Benzos

Back 30

Barbs - symptom management (assist respiration, increase BP) Benzos - Flumazenil (too much can induce withdrawal symptoms)

Front 31

Withdrawal symptoms: Anxiety, seizures, life-threatening

Back 31

Barbs - also delirium, cardiovascular collapse Benzos - rebound anxiety, tremor, insomnia

Front 32

Intoxication Symptoms: Pinpoint pupils, constipation, seizures, CNS depression, nausea, vomiting

Back 32

Opioids - OD is life-threatening b/c of seizures, no tolerance to constipation/pupillary constriction Tx: naloxone, naltrexone

Front 33

Withdrawal Sx: piloerection, rhinorrhea, yawning. Also: insomnia, anorexia, sweating, dilated pupils, fever, nausea, stomach cramps, diarrhea (flu-like symptoms)

Back 33

Opioids
Tx: symptomatic, not life-threatening

Front 34

Intoxication Sx: serum gamma-glutamyltransferase is sensitive indicator of use

Back 34

Alcohol - also emotional lability, slurred speech, disinhibition, ataxia, coma, blackouts. AST>ALT elevation

Front 35

Withdrawal Sx: Life-threatening, tachycardia, hypertension, malaise, nausea, seizures, delirium tremens (DTs), tremulousness, agitation, hallucination (inc. tactile, like crawling bugs)

Back 35

Alcohol
Tx: Benzos

Front 36

Intoxication Sx: belligerence, impulsiveness, homicidality, psychomotor agitation, vertical and horizontal nystagmus, tachycardia, ataxia, psychosis, delirium

Back 36

PCP

Front 37

Withdrawal Sx: depression, anxiety, irritability, restlessness, anergia, disturbances of thought and sleep, homicidality, vertical/horizontal nystagmus, tachycardia, ataxia

Back 37

PCP
actually reintoxication from GI reabsorption

Front 38

Intoxication Sx: flashbacks, visual hallucinations, marked anxiety or depression, delusions, pupillary dilation

Back 38

LSD - no other withdrawal Sx

Front 39

Intoxication Sx - increased appetite, hallucinations, conjunctivitis, euphoria, anxiety, paranoid delusions

Back 39

Marijuana - withdrawal - depression, irritability, insomnia, nausea, anorexia, most symptoms peak in 48 hours, last for 5-7 days, can be detected up to 1 month in urine.

Front 40

Tx: Systemic Mycoses (histo, blasto, coccidio, paracoccidiodo, etc.), local and systemic

Back 40

Local: fluconazole or ketoconazole
Systemic: Amphotericin B

Front 41

Tx: Tinea versicolor

Back 41

topical miconazole, selenium sulfide

Front 42

Tx: Tinea pedis, cruris, corporis, capitis, unguium

Back 42

Topical azoles, except:
ungium/capitis: terbenafine or griseosulvin

Front 43

Tx: Candidiasis

Back 43

nystatin (superficial), amphotericin B (serious systemic)

Front 44

Tx: PCP
Start prophylaxis when?

Back 44

TMP-SMX, pentamidine, dapsone (if sulfa allergy).
Prophylaxis with TMP-SMX when CD4 <200

Front 45

Tx: Sporothrix Schenckii

Back 45

itraconazole or potassium iodide

Front 46

Mechanism of terbinafine

Back 46

antifungal
blocks ergosterol synthesis by blocking squalene epoxidase-catalyzed squalene --> Lanosterol step
(Squalene --> Lanosterol --> Ergosterol)

Front 47

Mechanism of azoles

Back 47

Antifungal
Block ergosterol synthesis from lanosterol
(Squalene --> Lanosterol --> Ergosterol)

Front 48

Mechanism of Griseofulvin

Back 48

Antifungal
Disrupts microtubules

Front 49

Mechanism of Flucytosine

Back 49

Antifungal
Blocks precursors --> Pyrimidines
(which are then converted to nucleic acids)

Front 50

Mechanism of Amphotericin B and Nystatin

Back 50

Antifungals
Form pores in cell wall, disrupting membrane

Front 51

Amphotericin B clinical use

Back 51

wide spectrum of systemic mycoses - crypto, histo, coccidio, aspergillus, blasto, candida, mucor
Given intrathecally (into CSF) for fungal meningitis (does not cross BBB)

Front 52

Clinical use: Nystatin

Back 52

oral candidiasis (swish/swallow)
diaper rash/vaginal (topical)

Front 53

Clinical Use: -azoles

Back 53

Crypto meningitis - fluconazole (also amphotericin B) because it can cross BBB
Candidiasis - Fluconazole
Blasto, Coccidio, Histo, Candida - Ketoconazole
Topical fungal infections - Clotrimazole, miconazole
Hypercortisolism - especially ketoconazole

Front 54

Mechanism: Flucytosine

Back 54

Antifungal
FLUcytosine --> 5-FLUorouracil
Inhibits DNA synthesis

Front 55

Clinical use: Flucytosine (what is it used in combo with?)

Back 55

systemic fungal infections (e.g. candida, crypto) IN COMBINATION with ampho B

Front 56

Mechanism: Caspofungin

Back 56

Antifungal
inhibits cell wall synthesis by inhibiting synthesis of beta-glycan

Front 57

Clinical Use: Caspofungin

Back 57

Antifungal
cASPofungin = invasive ASPergillosis

Front 58

Clinical Use: Terbinafine

Back 58

Antifungal
Used to treat dermatophytoses - oral (because nail [onychomycosis] or follicle [capitis])

Front 59

Griseofulvin

Back 59

Antifungal
Like terbinafine, taken orally to treat superficial infections of nail/follicle

Front 60

Clinical use: Nifurtimox

Back 60

Trypanosoma cruzi (Chagas' disease)

Front 61

Clinical use: Suramine, Pentamidine, Melarsoprol

Back 61

Sleeping sickness
Blood-borne - SURamin + pentamidine
CNS penetration - MELArsoprol
"It SURe is nice to get sleep. MELAtonin helps with sleep)

Front 62

Clinical use: sodium stibogluconate

Back 62

Leishmaniasis

Front 63

Name four malaria Rx combinations

Back 63

1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 64

Monotherapy for Malaria

Back 64

mefloquine

Front 65

Primaquine

Back 65

Malaria drugs
1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 66

Chloroquine

Back 66

Malaria drugs
1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 67

Sulfadoxine

Back 67

Malaria drugs
1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 68

Pyrimethamine

Back 68

Toxoplasmosis
(and...)
Malaria drugs
1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 69

Mefloquine

Back 69

Malaria drugs
1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 70

Quinine

Back 70

Malaria drugs
1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 71

Doxycycline

Back 71

(also antimicrobial)
Malaria drugs
1: Chloroquine + primaquine - prevents relapse of vivax/ovale. Also used as prophylaxis
2: sulfadoxine + pyrimethamine
3: mefloquine (alone)
4: quinine (not approved for restless leg syndrome) + doxycycline

Front 72

Tx for Entamoeba histolytica

Back 72

Metronidazole (GET GAP on the Metro) and iodoquinol

Front 73

Iodoquinol

Back 73

used with Metronidazole for amoebiasis

Front 74

Tx: Enterobius vermicularis

Back 74

Mebendazole (worms BEND)
Pyrantel pamoate

Front 75

Pyrantel pamoate

Back 75

Helminths:
Enterobius vermicularis (pinworm), Ascaris lumbricoides (giant roundworm), Ancylostoma duodenale, Necator americanus (hookworms)

Front 76

Tx: Ascaris lumbricoides

Back 76

Mebendazole (worms BEND)
Pyrantel pamoate

Front 77

Thiabendazole

Back 77

Trichinella spiralis
Strongyloides stercoralis

Front 78

Tx: Ancylostoma duodenale

Back 78

Mebendazole (worms BEND)
Pyrantel pamoate

Front 79

Tx: Necator americanus (hookworms)

Back 79

Mebendazole (worms BEND)
Pyrantel pamoate

Front 80

Tx: Diphyllobothrium latum

Back 80

Praziquantel

Front 81

Tx: Echinococcus granulosus

Back 81

Albendazole

Front 82

Tx: Schistosomes

Back 82

Praziquantel (as with all trematodes - flukes)

Front 83

Tx: Clonorchis sinensis

Back 83

Praziquantel (as with all trematodes - flukes)

Front 84

Praziquantel

Back 84

Helminths:
All Trematodes (Schistosomes, Clonorchis sinensis, Paragonimus westermani)
And two Cestodes (Diphylllobothrium latum and intestinal worms/cysticercosis of Taenia solium)

Front 85

Tx: Pediculosis capitis/pediculosis pubis

Back 85

lice - malathion, pyrethrin, permethrine
crabs - pyrimethamine, pyrethrin, malathion

Lindane not first line because of neurotoxicity

Front 86

Tx: Roundworm

Back 86

BEND drug

Front 87

MAI prophylaxis

Back 87

CD4 < 100 : azithromycin
CD4 < 75 : clarithromycin

Front 88

Tx (alternative): Leprosy

Back 88

Rifampin
Clofazimine/Dapsone combination

Front 89

Tx (primary): Leprosy

Back 89

Long-term dapsone
6 mos - 2 years
Toxicity - hemolysis, methemoglobinemia

Front 90

Tx: Haemophilus influenzae meningitis

Back 90

ceftriaxone
(same for GC meningitis)

Front 91

Tx: atypical pneumonias

Back 91

Macrolides - azithro/erythromycin

Front 92

Tx: Legionella pneumophila

Back 92

erythromycin

Front 93

Block cell wall synthesis by inhibition of peptidoglycan cross-linking

Back 93

penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam, cephalosporins

Front 94

Block peptidoglycan synthesis

Back 94

Bacitracin, vancomycin

Front 95

Disrupt bacterial cell membranes

Back 95

Polymyxins

Front 96

Block nucleotide synthesis

Back 96

Sulfonamides, TMP

Front 97

Block DNA topoisomerases

Back 97

Quinolones

Front 98

Block mRNA synthesis

Back 98

Rifampin

Front 99

Block protein synthesis at 50S subunit

Back 99

Chloramphenicol, macrolides, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid

Front 100

Blocks protein synthesis at 30S subunit

Back 100

Aminoglycosides, tetracyclines

Front 101

Bacteriostatic: ECSTaTiC

Back 101

We're ECSTaTiC about bacteriostatics:
Erythromycin
Clindamycin
Sulfamethoxazole
Trimethoprim
Tetracyclines
Chloramphenicol
All involve nucleotide formation or protein synthesis

Front 102

Bacteriocidal:
Very Finely Proficient At Cell Murder

Back 102

Vancomycin, Fluoroquinolones, Penicillin, Aminoglycosides, Cephalosporins, Metronidazole
Aminoglycosides exceptional for being involved in protein synthesis

Front 103

Penicillin mechanism

Back 103

Bind penicillin-binding proteins
Block transpeptidase cross-linking
Activate autolytic enzymes

Front 104

Clinical use: Penicillin

Back 104

Bactericidal for gram+ve cocci, rods, gram-ve rods (Neisseria), spirochetes. Not penicillinase resistant

Front 105

Mechanism: Methicillin, nafcillin, dicloxacillin

Back 105

penicillinase-resistant penicillins
Same mechanism as PCN
Narrow spectrum
Penicilinase resistant because of bulkier R group

Front 106

Clinical use: Penicillinase-resistant PCNs

Back 106

Nafcillin, methicillin, dicloxacillin
S. aureus (except MRSA - resistant because of altered PCN-binding protein)
Use naf for staph

Front 107

Mechanism - aminopenicillins

Back 107

same as penicillin, wider spectrum, PCNase sensitive. Can combine with clavulinic acid to enhance spectrum

amOxicillin has greater Oral bioavailability than ampicillin (which is given IV)

Front 108

Clavulinic acid, sulbactam

Back 108

block beta-lactamase in gram-ve periplasm (inside the outer cell membrane)

Front 109

Clinical use: aminopenicillins

Back 109

extended-spectrum PCN - certain gram+ve bacteria and gram-ve rods (Haemophilus, E. coli, Listeria, Proteus, Salmonella, enterococci)
"Amp/amox - HELPS kill enterococci and gram+ves"

Front 110

Mechanism: antipseudomonals

Back 110

Same as PCN, extended spectrum

Front 111

Clinical use: antipseudomonals

Back 111

Pseudomonas spp. and gram-ve rods. Susceptible to penicillinase, use with clavulanic acid

Front 112

Beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases - bactericidal

Back 112

Cephalosporins

Front 113

Clinical use:
1st Generation Cephalosporins

Back 113

cefazolin, cephalexin
PEcK + gram+ve
Proteus
E. coli
Klebsiella
+gram+ves

Front 114

Clinical use:
2nd Generation Cephalosporins

Back 114

Cefoxitin, cefaclor, cefuroxime
HEN PEcKS + gram+ve
Haemophilus
Enterobacter aerogenes
Neisseria spp.
Proteus
E. coli
Klebsiella
Serratia
+gram+ves

Front 115

Clinical use:
3rd Generation Cephalosporins

Back 115

ceftriaxone, cefotaxime, ceftazidime
serious gram-ve infections resistant to other beta-lactams
Meningitis (most penetrate BBB)
e.g.s ceftazidime for Psuedomonas, ceftriaxone for gonorrhea

Front 116

Clinical use:
4th Generation Cephalosporins

Back 116

Cefepime
Increased activity against Pseudomonas and gram+ve organisms

Front 117

Cephalosporins through the generations

Back 117

Increasing Gram-ve/decreasing gram+ve spectrum from 1-->3
4 reverses somewhat - increased activity against pseudomonas and gram+ve organisms

Front 118

Mechanism: Aztreonam

Back 118

monobactam resistant to beta-lactamases, inhibits cell wall synthesis, binds PBP
Synergistic with aminoglycosides
(starts with A like them, treats gram-ve rods like them)

Front 119

Clinical use: Aztreonam

Back 119

Synergistic with Aminoglycosides. Like them, acts on severe gram-ve rods, not anaerobes or gram+ves. Ksp: Klebsiella, Serratia, Pseudomonas

For PCN-allergic pts and those with renal insufficiency who cannot tolerate aminoglycosides

Front 120

Mechanism: Imipenem/cilastatin, meropenem

Back 120

imipenem - broad-spectrum, beta-lactamase-resistent carbapenem
Cilastatin - inhibitor of renal dihydropeptidase 1 to decrease inactivation in renal tubules. Meropenem similar but dihydropeptidase 1 resistant

Front 121

Clinical use: Imipenem/cilastatin, meropenem

Back 121

gram+ve cocci, gram-ve rods, anaerobes. Drug of choice for enterobacter. General surgeon's best friend. Only used with life-threatening, refractive infections (b/c of side effects)

Front 122

Mechanism: Vancomycin

Back 122

Bactericidal by binding D-Ala D-Ala portion of cell wall precursors

Front 123

Clinical use: Vancomycin

Back 123

serious, gram+ve multi-drug resistant organisms, including S. aureus, C. dif, coag-ve endocarditis

Front 124

Protein synthesis inhibitors

Back 124

buy AT 30, CCELL at 50
30S
Aminoglycosides (strepto, genta, tobramycin, amikacin [bactericidal])
50S
Chloramphenicol, Clindamycin (bacteriostatic)
Erythromycin (bacteriostatic)
Lincomycin (bacteriostatic)
Linezolid (variable)

Front 125

Mechanism: Aminoglycosides

Back 125

Gentamycin, Neomycin, Amikacin, Tobramycin, Streptomycin
Bactericidal (only protein synthesis inhibitor MEAN enough to kill)
Inhibit formation of initiation complex (bind 30S) and cause misreading of mRNA. Require O2 for uptake

Front 126

Clinical use: Aminoglycosides

Back 126

severe gram-ve rod (e.g. pseudomonas) infections, synergistic with beta-lactams, neomycin for bowel surgery.
Inactive against anaerobes - aminO2glycoside

Front 127

Mechanism: Tetracyclines

Back 127

Bacteriostatic, bind 30S, prevent attachment of aminoacyl tRNA. Limited CNS penetration. GI absorption inhibited by divalent cations

Front 128

Doxycycline

Back 128

Tetracycline that is fecally eliminated (good for pts with renal failure).

Front 129

Clinical use: Tetracyclines

Back 129

VACUUM THe BedRoom
Vibrio, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Tularemia, H. pylory, Borrelia burgdorferi, Rickettsia

Front 130

Mechanism: Macrolides

Back 130

Protein synthesis inhibitors - bind 23S rRNA of 50S subunit, blocking translocation
Bacteriostatic

Front 131

Clinical Use: Macrolides

Back 131

PUS
Pneumonia (atypical)
URIs
STDs (GC/Chlam)

Gram+ve cocci (strep infections for pts with PCN allergies)
Mycoplasma, Legionella, Chlamydia, Neisseria

Front 132

Clinical use: Erythromycin (alternate)

Back 132

Increases GI motility - used in ileus

Front 133

Mechanism: Chloramphenicol

Back 133

Inhibits 50S peptidyltransferase activity.
Bacteriostatic.

Front 134

Mechanism: Linezolid

Back 134

Binds 23S rRNA, interacts with bacterial protein synthesis initiation complex
Oral

Front 135

Mechanism: Binds 23S rRNA, blocks initiation complex

Back 135

Linezolid

Front 136

Mechanism: Inhibits 50S peptidyltransferase activity.

Back 136

Chloramphenicol

Front 137

Mechanism: bind 30S, prevent attachment of aminoacyl tRNA

Back 137

Tetracyclines

Front 138

Binds 23S rRNA on 50S subunit, blocks translocation

Back 138

Macrolides, Clindamycin, Lincomycin

Front 139

Binds 30S, blocking initiation, preventing mRNA reading

Back 139

Aminoglycosides

Front 140

Clinical use: Chloramphenicol

Back 140

Meningitis - H. influenzae, N. meningitidis, S. pneumoniae. Conservative use b/c of toxicities

Front 141

Clinical use: meningitis

Back 141

Chloramphenicol

Front 142

Mechanism: Clindamycin

Back 142

Blocks peptide bond formation at 50S ribosomal subunit. Bacteriostatic

Front 143

Clinical use: Clindamycin

Back 143

anaerobes ABOVE diaphragm (vs. Metronidazole)
Narrow spectrum (imipenem would be broad-spectrum against anaerobes)
Aspiration pneumonia is usually anaerobes, so clinda- good there too, and MRSA is very sensitive to it as well

Front 144

Clinical use: Anaerobes ABOVE diaphragm

Back 144

Clindamycin

Front 145

Clinical use: Anaerobes BELOW diaphragm

Back 145

Metronidazole

Front 146

Mechanism: Sulfonamides

Back 146

PABA antimetabolites inhibit dihydropteroate synthetase (PABA + pteridine make dihydropteroate --> dihydrofolic acid --> THF --> --> DNA, RNA and Proteins)

Front 147

Clinical use: Sulfonamides

Back 147

gram+/-ves - nocardia, chlamydia
Triple sulfas or SMX for simple UTI

Front 148

Clinical use: TMP-SMX

Back 148

Recurrent UTIs, Shigella, Salmonella, PCP, MRSA

Front 149

Mechanism: Nitrofurantoin

Back 149

bacteriocidal, reduced in urine by bacterial proteins, making it active

Front 150

Clinical use: Nitrofurantoin

Back 150

Cystitis, NOT pyelonephritis. Works on E. coli, Staph saprophyticus, NOT proteus

Front 151

Mechanism: [Fluoro]quinolones

Back 151

Inhibit DNA gyrase (topoisomerase II). Bactericidal. Must not be taken with antacids

Front 152

Clinical use: [Fluoro]quinolones

Back 152

Pneumonias, URIs
Gram-ve rods of UTI and GI infections (including Pseudomonas), Neisseria, some gram+ves

Front 153

Mechanism: Metronidazole

Back 153

forms toxic metabolites in bacterial cell that damage DNA. Bactericidal, antiprotozoal

Front 154

Clinical use: Metronidazole

Back 154

GET GAP on the Metro!
Giardia
Entamoeba
Trichomonas
Gardnerella
Anaerobes (bacteroides, clostridium) below diaphragm
h. Pylori (used in triple therapy)

Front 155

Triple therapy

Back 155

1. bismuth, metronidazole and either tetracyclin or amoxicillin
2. (more costly) metronidazole, omeprazole, clarithromycin

Front 156

Mechanism: Polymyxin B and E

Back 156

Myxins MIX up membranes
Bind to cell membranes of bacteria and disrupt osmotic properties. Cationic, basic proteins that act like detergents.

Front 157

Clinical use: Polymyxins

Back 157

Resistant gram-ve infections, Pseudomonas on the skin

Front 158

Antimycobacterial drugs

Back 158

Rifampin, INH, Pyrazinamide, Ethambutol, Azithromycin, Streptomycin, Dapsone, Clofazimine

Front 159

M. tuberculosis prophylaxis/Tx

Back 159

Proph: INH
Tx: Rifampin, Isoniazid, Pyrazinamide, Ethambutol
RIPE for Tx

Front 160

M. avium intracellulare prophylaxis/Tx

Back 160

Proph:
CD4 under 100: Azithromycin
Under 75 - Clarithromycin
Tx:
Azithromycin, Rifampin, Ethambutol, Streptomycin
Go to war on MAI with ARES

Front 161

Tx: M. leprae

Back 161

Dapsone, Rifampin, Clofazimine

Front 162

Tx: Tb

Back 162

1st: Streptomycin, Pyrazinamide, Isoniazid, Rifampin, Ethambutol (INH-SPIRE)
2nd - Cycloserine

Front 163

Tx: Pseudomonas

Back 163

3rd Gen Ceph, Extended Spectrum PCNs (TCP), Aztreonam, Cefepime (4th gen Ceph), Aminoglycosides, quinolones, polymyxins

Front 164

Mechanism: Isoniazid

Back 164

decreased synthesis of mycolic acids

Front 165

Clinical use: Isoniazid

Back 165

M. tuberculosis - only agent used solo in prophylaxis against Tb and dormant Tb

Front 166

Mechanism: Rifampin

Back 166

Inhibits DNA-dependent RNA Polymerase, blocking formation of all three types of RNA

Front 167

Rifampin characteristics - 4 Rs

Back 167

RNA Polymerase inhibitor
Revs up microsomal P-450
Red/orange body fluids
Rapid resistance if used alone

Front 168

Clinical use: Rifampin

Back 168

Tb, delays dapsone resistance in leprosy Tx
Proph: meningococcal/H. influenzae type B
Used with TMP-SMX or Clarithromycin for MRSA (never use alone)

Front 169

Resistance mechanism against:
PCN

Back 169

beta-lactamase cleavage of beta-lactam ring
Altered PBP in case of MRSA or PCN-resistant S. pneumoniae

Front 170

Resistance mechanism against:
Aminoglycosides

Back 170

Modification via acetylation, adenylation, phosphorylation

Front 171

Resistance mechanism against:
Vancomycin

Back 171

Terminal D-ala of cell wall component replaced with D-lac, reducing affinity

Front 172

Resistance mechanism against:
Chloramphenicol

Back 172

Modification via acetylation

Front 173

Resistance mechanism against:
Macrolides

Back 173

Methylation of rRNA near erythromycin's ribosome-binding site

Front 174

Resistance mechanism against:
Tetracycline

Back 174

decreased uptake, increased transport out of cell

Front 175

Resistance mechanism against:
Sulfonamides

Back 175

Altered enzyme (bacterial dihydropteroate synthetase), decreased uptake or increased PABA synthesis

Front 176

Resistance mechanism against:
Quinolones

Back 176

Altered gyrase, reduced uptake

Front 177

Nonsurgical Antimicrobial prophylaxis:
Meningococcal
Gonorrhea
Syphilis
Recurrent UTIs
PCP
Endocarditis with surgical/dental procedures

Back 177

Nonsurgical Antimicrobial prophylaxis:
Meningococcal - Rifampin (drug of choice), minocycline
Gonorrhea - Ceftriaxone
Syphilis - Benzathine PCN G
Recurrent UTIs - TMP-SMX
PCP - CD4 < 200 - TMP-SMX (Drug of choice - Dapsone if sulfa allergy), aerosolized pentamidine
Endocarditis with surgical/dental procedures - PCNs; Ampicillin; 1st generation Cephs

Front 178

Tx: VRE

Back 178

linezolid and streptogramins (quinupristin/dalfopristin)

Front 179

Tx: HSV-1/2, EBV, VZV

Back 179

acyclovir, valacyclovir, famcyclovir

Front 180

Clinical use: Acyclovir

Back 180

HSV-1/2, VZV, EBV
Old, cheap, 5x/day dosing

Front 181

Clinical use: Famcyclovir

Back 181

HSV-1/2, VZV, EBV
Newer than Acyclovir, expensive, less frequent dosing, better compliance.

Front 182

Clinical use: Valacyclovir

Back 182

HSV-1/2, VZV, EBV
Newer than Acyclovir, expensive, less frequent dosing, better compliance.

Front 183

Clinical use: Ganciclovir

Back 183

CMV, especially in IC patients. Greater activity than acyclovir for CMV DNA polymerase

Front 184

Mechanism: Acyclovir, Valacyclovir, Famcyclovir

Back 184

DNA nucleotide analog

monophosphorylated (activated) by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination

Front 185

Mechanism of resistance: Acyclovir, Valacyclovir, Famcyclovir

Back 185

Lack of thymidine kinase

Front 186

Mechanism: Ganciclovir

Back 186

Nucleotide analog
5'-monophosphate formed by CMV viral kinase or HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase

Front 187

Mechanism of resistance: Ganciclovir

Back 187

Mutated CMV DNA polymerase or lack of viral kinase

Front 188

Clinical use: Foscarnet

Back 188

CMV retinitis in IC patients WHEN ganciclovir fails. Acyclovir-resistant HSV. reverse transcriptase inhibitor in HIV

Front 189

Mechanism: Foscarnet

Back 189

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

Front 190

Mechanism of resistance: Foscarnet

Back 190

Mutated DNA polymerase

Front 191

Tx: HCV

Back 191

Interferon-alpha + ribavirin

Front 192

Clinical uses: Amantadine, Rimantidine

Back 192

Flu (no longer used because 90% of influenza A strains resistant)
Parkinson's

Front 193

Mechanism: Amantadine, Rimantidine

Back 193

blocks viral penetration/uncoating (M2 protein), buffers pH of endosome
Causes release of Dopamine from intact nerve terminals.
Rimantidine is a derivative with fewer CNS side effects, does not cross BBB

Front 194

Mechanism of resistance: Amantadine, Rimantidine

Back 194

Mutated M2 protein

Front 195

Mechanism: Zanamivir, oseltamivir

Back 195

Inhibit influenza neuraminidase, deceasing release of progeny virus

Front 196

Clinical use: Zanamivir, oseltamivir

Back 196

Influenza A/B, Avian flu

Front 197

Mechanism: Ribavirin

Back 197

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase

Front 198

Clinical Use: Ribavirin

Back 198

HepC when used with IFN-alpha

Front 199

HIV Prophylaxis

Back 199

ZDV + 3TC

Front 200

HAART

Back 200

highly active antiretroviral therapy - protease inhibitor and RTIs. Initiated when CD4 < 500 or high viral load.

Front 201

Mechanism: Protease inhibitors

Back 201

inhibit maturation of new virus by blocking protease in progeny virions - inhibit assembly

Front 202

Mechanism: RTIs

Back 202

preferentially inhibit RT of HIV, prevent incorporation of DNA copy of viral genome into host DNA

Front 203

Mechanism: Fusion inhibitor

Back 203

bind viral gp41 subunit, inhibit conformational change required for fusion with CD4 cells, blocking entry and subsequent replications

Front 204

Clinical use: Fusion inhibitor

Back 204

in pts. with persistent viral replication in spite of RTI Tx, used in combination

Front 205

Mechanism: Interferons

Back 205

glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis. Induce ribonuclease that degrades viral mRNA

Front 206

Clinical use: Interferons

Back 206

IFN-alpha - chronic HBV/HCV, Kaposi's
IFN-Beta - MS
IFN-gamma - NADPH oxidase deficiency

Front 207

ABs safe in pregnancy for UTIs

Back 207

nitrofurantoin, aminopenicillins, 1st generation Cephs
vs.
Children - TMP-SMX
Adults - fluoroquinolones

Front 208

Mechanism: Hydroxyurea

Back 208

Inhibits Ribonucleotide Reductase (UDP → dUDP, which then goes on to form dUMP and then dTMP)
Works in S-phase

Front 209

Mechanism: 6-MP

Back 209

Blocks de novo purine synthesis

Front 210

Mechanism: Methotrexate (MTX)

Back 210

Inhibits dihydrofolate reductase (DHFR)
Decreases dTMP levels.

Front 211

Drugs that act on MTs

Back 211

Mebendazole/thiabendazole
Griseofulvin
Vincristine/vinblastine (block polymerization)
Paclitaxel (hyperstabilizes MTs, preventing disassembly
Colchicine (anti-gout. Inhibits Macrophage movements/chemotaxis)

Front 212

Effect of glucocorticoids on collagen synthesis

Back 212

Inhibitory. E.g. inject steroids into keloids to decrease abnormally increased production there

Front 213

Clinical use: N-acetylcysteine

Back 213

Inhaled in CF and ventilator pts to loosen mucous plugs (mucolytic - cleaves disulfide bonds within mucous glycoproteins). Prophylaxis to prevent contrast induced nephropathy (give 24 hrs prior and after dye). Antidote to acetaminophen hepatotoxicity induced by intermediate metabolite NAPQI

Front 214

Mechanism: Fomepizole

Back 214

inhibits alcohol dehydrogenase (converts ethanol to acetaldehyde and produces NADH)
vs. Disulfiram, which blocks next step, conversion of acetaldehyde → acetate (also producing NADH)

Front 215

Clinical Use: Benzoate

Back 215

Tx of Ornithine transcarbamoylase (OTC) deficiency

Front 216

Tx: OTC deficiency

Back 216

Benzoate

Front 217

Tx: PKU

Back 217

Replace THB (since PKU pts lack THB cofactor for phenylalanine hydroxylase)

Front 218

Tx: Cystinuria

Back 218

Acetazolamide to alkalinize urine, increasing cystine solubility

Front 219

Tx: Orotic aciduria

Back 219

Oral uridine administration

Front 220

Tx: Abetalipoproteinemia

Back 220

Vitamin E – helps restore lipoproteins

Front 221

Tx: Paroxysmal Nocturnal Hemoglobinuria (PNH)

Back 221

Fe supplementation, warfarin, BM transplant

Front 222

Tx: Chronic granulomatous disease

Back 222

Susceptibility to S. aureus, E. coli, Aspergillus, Candida, Klebsiella. Treat with propylactic TMP-SMX, IFN-gamma

Front 223

Mechanism: Cyclosporine

Back 223

Immunosuppressant
Binds cyclophilins, complex blocking differentiation/activation of T cells by inhibiting calcineurin, preventing production of IL-2 and its receptor.

Front 224

Mechanism: Tacrolimus (FK506)

Back 224

Immunosuppressant
Similar mechanism to cyclosporine. Binds FK-binding protein, then binding calcineurin, inhibiting secretion of IL-2 and other cytokines

Front 225

Clinical use: Cyclosporine

Back 225

Transplantation, some autoimmune disorders

Front 226

Clinical use: Tacrolimus (FK506)

Back 226

Immunosuppressant
Organ transplants.
Topical (called protopic) for eczema

Front 227

Clinical use: Pimecrolimus

Back 227

Immunosuppressant
Used topically for eczema, as with Tacrolimus

Front 228

Clinical use: Muromonab-CD3 (OKT3)

Back 228

Immunosuppressant after kidney transplantation

Front 229

Mechanism: Muromonab-CD3 (OKT3)

Back 229

Immunosuppressant
mAb that binds CD3 on T cell surface, blocking IL-2 production and T-cell signaling.

Front 230

Mechanism: Sirolimus (rapamycin)

Back 230

Immunosuppressant
Binds FK binding protein which inhibits mTOR, inhibiting T cell proliferation in response to IL-2

Front 231

Mechanism: Mycophenolate mofetil

Back 231

Inhibits de novo guanine synthesis and blocks lymphocyte production. Blocks IMP dehydrogenase

Front 232

Clinical use: Mycophenolate mofetil

Back 232

Used for lupus nephritis, kidney/heart/liver transplants

Front 233

Mechanism: Daclizumab

Back 233

mAb with high affinity for IL-2 receptor on activated T cells

Front 234

Mechanism: Thalidomide

Back 234

Anti-angiogenic, affects TNF-alpha primarily
Contraindicated in pregnancy

Front 235

Clinical use: Aldesleukin

Back 235

IL-2
Renal cell carcinoma, metastatic melanoma

Front 236

Clinical use: EPO

Back 236

Anemias, especially in renal failure and chemo

Front 237

Clinical use: Filgrastim

Back 237

filGRAstim – GRAnulocyte colony stimulating factor. Used to recover BM

Front 238

Clinical use: Sargramostim

Back 238

sarGRAmostim – GRAnulocyte-macrophage colony stimulating factor, like IL-3
Used to recover BM

Front 239

Clinical use: alpha-IFN

Back 239

HBV, HCV, Kaposi’s sarcoma, leukemias, malignant melanoma

Front 240

Clinical use: beta-IFN

Back 240

Multiple sclerosis

Front 241

Clinical use: gamma-IFN

Back 241

Chronic granulomatous disease

Front 242

Clinical use: Oprelvekin

Back 242

IL-11
Thrombocytopenia

Front 243

Clinical use: thrombopoietin

Back 243

Thrombocytopenia

Front 244

Tx: Actinic keratosis

Back 244

Can freeze off with 5-FU

Front 245

Volume of distribution Vd

Back 245

Amount given IV / plasma [drug]

Front 246

Clearance of drug

Back 246

C = 0.7 x Vd / t1/2

Front 247

Loading dose

Back 247

LD = CSS x Vd

Front 248

Maintenance dose

Back 248

MD = CSS x Cl

Front 249

Half time

Back 249

t1/2 0.7 x Vd / Cl

Front 250

Elimination of weak acid drugs

Back 250

e.g. Phenobarbital, MTX, TCAs, aspirin. Trapped in basic environments. Treat OD with bicarbonate

Front 251

Elimination of weak base drugs

Back 251

e.g. amphetamines
Trapped in acidic environments. Treat OD with ammonium chloride

Front 252

Phase I metabolism of drugs

Back 252

Reduction, oxidation, hydrolysis, yielding slightly polar, water-soluble metabolites, often still active. CYP450 catalyzed. Lost first in geriatric pts

Front 253

Phase II metabolism of drugs

Back 253

Acetylation, glucuronidation, sulfation, yielding very polar, inactive metabolites, renally excreted

Front 254

Therapeutic index

Back 254

= LD50/ED50

Front 255

G-Protein linked 2nd messengers – G protein classes

Back 255

Qiss qiq siq sqs

Front 256

G-Protein linked 2nd messengers – Sympathetic - qiss

Back 256

Alpha1 – Gq – increased vascular sm mm. contraction, increased pupillary dilator muscle contraction (mydriasis)
Alpha2 – Gi – decreased sympathetic outflow, decreased insulin release, decreased BP
Beta1 – Gs – increased heart rate, increased contractility, increased renin release, increased lipolysis
Beta2 – Gs – vasodilation, bronchodilation, increased heart rate, contractility, lipolysis, glucagon release. Decreased uterine tone.

Front 257

G-protein linked 2nd messengers – Parasympathetic – qiq

Back 257

M1 – Gq – CNS, enteric nervous system
M2 – Gi – decreased heart rate and contractility of atria
M3 – Gq – increased exocrine gland secretions, gut peristalsis, bladder contraction, bronchoconstriction, pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accommodation)

Front 258

G-protein linked 2nd messengers – Dopamine, Histamine, Vasopressin – si-q, s-qs

Back 258

D1 – Gs – relaxes renal vascular sm mm.
D2 – Gi – modulates transmitter release, especially in brain
H1 – Gq – increased nasal/bronchial mucus production, contraction of bronchioles, pruritis, pain
H2 – Gs – increased gastric acid secretion
V1 – Gq – increased vascular sm mm. contraction
V2 – Gs – increased H2O permeability and reabsorption in collecting tubules

Front 259

Gq-coupled G-protein receptors – examples and mechanism

Back 259

QtC (“cutesy”) for gQ and phospholipase/protein kinase C
HAVe 1 M&M
H1, alpha1, V1, M1, M3
Gq → Phospholipase C → Lipids catalyzed to PIP2, which becomes IP3 (increasing [Ca]i) and DAG (increasing protein kinase C)

Front 260

Gi-coupled G-protein receptors – examples and mechanism

Back 260

MAD 2s
M2, alpha2, D2
Gi → adenylyl cyclase → cAMP decreased → decreased PKA

Front 261

Gs-coupled G-protein receptors – examples and mechanism

Back 261

Beta1/2, D1, H2, V2
Gs → adenylyl cyclase → increased cAMP → increased PKA

Rate-limiting step of cholinergic transmission and drug that inhibits
RLS – getting choline into neuron
Hemicholinium inhibits this

Front 262

Mechanism: Vesamicol

Back 262

Experimental anticholinergic drug that blocks Ach transport into secretory vesicles
Col = Chol

Front 263

What toxin blocks Ach release into synapse? What stimulates it?

Back 263

Botulinum inhibits, black widow toxin stimulates

Front 264

What blocks Tyrosine → DOPA conversion?

Back 264

Metyrosine blocks this reaction, catalyzed by Tyr hydroxylase

Front 265

What blocks Dopamine packaging in secretory vesicles?

Back 265

Reserpine (depletory action)

Front 266

What blocks NE release into synapse?

Back 266

Guanethidine, Bretylium

Front 267

What stimulates NE release into synapses?

Back 267

Amphetamine, ephedrine, tyramine

Front 268

What blocks reuptake of NE?

Back 268

Cocaine, TCAs

Front 269

Clinical use: Bethanechol

Back 269

Direct cholinomimetic agonist
Post-op and neurogenic ileus and urinary retention
Activates bowel and bladder

Front 270

Clinical use: Carbachol

Back 270

Direct cholinomimetic agonist
Glaucoma, pupillary contraction, release of intraocular pressure
Contracts ciliary muscle of eye (open angle), pupillary sphincter (narrow angle). Resistant to AChE

Front 271

Clinical use: pilocarpine

Back 271

Direct cholinomimetic agonist
Potent stimulator of sweat, tears, saliva
Used in acute glaucoma emergency
Contracts ciliary muscle of eye (open angle), pupillary sphincter (narrow angle). Resistant to AChE

Front 272

Clinical use: Methacholine

Back 272

Direct cholinomimetic agonist
Challenge test for Dx of asthma
Stimulates muscarinic receptors in airway when inhaled

Front 273

Anti-AchE drugs – net effect

Back 273

Increase of endogenous Ach

Front 274

Clinical use: Neostigmine

Back 274

Post-op and neurogenic ileus and urinary retention, MG, reversal of neuromuscular junction blockade (post-op). “NEO CNS” = No CNS penetration

Front 275

Clinical use: Pyridostigmine

Back 275

Cholinomimetic agent: Indirect agonist (anti-AchE). pyRIDostiGMine gets RID of MG (vs. Edrophonium, used for Dx)
Long acting MG Tx. Does not penetrate CNS, increases strength

Front 276

Clinical use: Edrophonium

Back 276

Cholinomimetic agent: Indirect agonist (anti-AchE)
Dx of MG (vs. Tx as in pyridostigmine) – extremely short acting

Front 277

Clinical use: Physostigmine

Back 277

Cholinomimetic agent: Indirect agonist (anti-AchE)
PHYS is for EYES
Tx for glaucoma (crosses BBB) and atropine OD (“Fix”ostigmine – fixes atropine OD)

Front 278

Clinical use: Echothiphate

Back 278

Cholinomimetic agent: Indirect agonist (anti-AchE)
Glaucoma

Front 279

Tx: Myasthenia Gravis

Back 279

Direct/indirect cholinomimetic agonists, corticosteroids, thymectomy, plasmaphoresis (last ditch).

Front 280

Clinical use: Tropicamide

Back 280

Muscarinic antagonist
Atropine, Homatropine, Tropicamide
Works on eye, producing mydriasis and cycloplegia (paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation)

Front 281

Clinical use: Homatropine

Back 281

Muscarinic antagonist
Atropine, Homatropine, Tropicamide
Works on eye, producing mydriasis and cycloplegia (paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation)

Front 282

Clinical use: Atropine

Back 282

Muscarinic antagonist
Atropine, Homatropine, Tropicamide all work on eye, producing mydriasis and cycloplegia (paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation)

Front 283

Clinical use: Benztropine

Back 283

Muscarinic antagonist
Works on CNS – Parkinson’s disease – PARK my BENZ

Front 284

Clinical use: Scopolamine

Back 284

Muscarinic antagonist
Motion sickness, end of life (decreases nausea, vomiting), sedation. Topical behind ear

Front 285

Mechanism/Clinical use: Ipratropium

Back 285

Competitive Muscarinic antagonist, preventing bronchoconstriction. Also used for COPD. Add albuterol if used for acute asthma exacerbation. Given intranasally to pregnant women
Respiratory – Asthma, COPD – I PRAy I can breathe soon!

Front 286

Clinical use: Oxybutynin

Back 286

Muscarinic antagonist
Genitourinary – reduces urgency in mild cystitis and reduces bladder spasms

Front 287

Clinical use: Glycopyrrolate

Back 287

Muscarinic antagonist
Respiratory – used by anesthesiologists to decrease airway secretions

Front 288

Clinical use: Methscopolamine

Back 288

Muscarinic antagonist
GI – Methscopolamine and Propantheline decrease salivation, GI motility and stomach acid

Front 289

Clinical use: Propantheline

Back 289

Muscarinic antagonist
GI – Methscopolamine and Propantheline decrease salivation, GI motility and stomach acid.
Propantheline – blocks M1 receptors on ECL (enterochromaffin-like cells), decreasing histamine secretion, and M3 receptors on parietal cells (decreasing H+ secretion)

Front 290

Clinical use: Hexamethonium

Back 290

Ganglionic blocker – knocks out entire ANS. Used in experimental models to prevent vagal reflex responses to changes in BP, e.g. prevents reflex bradycardia caused by NE. Effect depends on dominant tone in each organ.
Arteries and veings – SNS – blocking effect → decreased BP, pooling of blood in veins → decreased return → decreased CO.
Most everywhere else – PNS dominant, so hexamethonium causes SNS responses

Front 291

Tx: Alzheimer’s anticholinesterases

Back 291

Donepezil (Aricept)
Galantamine
Rivastigmine

Front 292

Mechanism/selectivity/Application: Epinephrine

Back 292

Sympathomimetic – Direct
Alpha1/2, Beta 1/2, low doses selective for Beta1 (“B-low”)
Anaphylaxis, open angle glaucoma, asthma, hypotension

Front 293

Mechanism/selectivity/Application: Norepinephrine

Back 293

Sympathomimetic – Direct
Alpha1/2 > Beta
Hypotension

Front 294

Mechanism/selectivity/Application: Isoproteronol

Back 294

Sympathomimetic – Direct
Equal activity in beta1/2
Relaxes bronchial smooth muscle (beta2), causes tachycardia (beta1) – same with epinephrine. Used for asthma. Toxicity: AV block (rare)

Front 295

Mechanism/selectivity/Application: Dopamine

Back 295

Sympathomimetic – Direct
D1=D2 > Beta > alpha, inotropic and chronotropic
Shock, heart failure

Front 296

Mechanism/selectivity/Application: Phenylephrine

Back 296

Sympathomimetic – Direct
Alpha1>alpha2
Pupillary dilation, vasoconstriction, nasal decongestion

Front 297

Mechanism/selectivity/Application: Albuterol

Back 297

Sympathomimetic – Direct
Beta2 (relaxes bronchial smooth muscle) > Beta1 (heart)
Acute asthma

Front 298

Mechanism/selectivity/Application: Terbutaline

Back 298

Sympathomimetic – Direct
Beta2 > Beta1
Reduces premature uterine contractions

Front 299

Mechanism/selectivity/Application: Ritodrine

Back 299

Sympathomimetic – Direct
Beta2
Reducsed premature uterine contractions

Front 300

Mechanism: Amphetamine

Back 300

Sympathomimetic – Indirect
Indirect general agonist
Releases stored catecholamines

Front 301

Mechanism: Ephedrine

Back 301

Sympathomimetic – Indirect
Indirect general agonist
Releases stored catecholamines

Front 302

Mechanism: Cocaine

Back 302

Sympathomimetic – Indirect
Indirect general agonist
Uptake inhibitor

Front 303

Clinical use: Amphetamine

Back 303

Narcolepsy, obesity, ADD

Front 304

Clinical use: Ephedrine

Back 304

Nasal decongestion, urinary incontinence, hypotension

Front 305

Clinical use: Cocaine

Back 305

Vasoconstriction and local anesthesia

Front 306

Clinical use: Clonidine

Back 306

Sympathoplegic (decreases sympathetic discharge or its effect on the CNS)
HTN, especially with renal disease (no decrease in renal blood flow). 1/2 life = 8 hours, so dose qx3 to avoid rebound HTN

Front 307

Clinical use: alpha-methyldopa

Back 307

Sympathoplegic (decreases sympathetic discharge or its effect on the CNS)
HTN, especially with renal disease (no decrease in renal blood flow). Safe in pregnancy

Front 308

Effect on BP, HR: Norepinephrine

Back 308

Alpha > Beta
Widening of pulse pressure. Beta1 increase of systolic pressure > alpha1 increase of diastolic
Reflex bradycardia decreases HR

Front 309

Effect on BP, HR: Epinephrine

Back 309

Nonselective
Widening of pulse pressure. Beta1 increase of systolic pressure, Beta2 decrease of diastolic
Beta1 increase of HR

Front 310

Effect on BP, HR: Isoproteronol

Back 310

Beta > alpha
Slight decrease of systolic – Beta1. Greater increase of diastolic – Beta2
Beta1 increases HR, but so does reflex tachycardia due to drop in BP, so greater increase in HR than with Epi

Front 311

Epi/NE effect – which receptors dominate: vascular smooth mm.

Back 311

Alpha1, Beta2

Front 312

Epi/NE effect – which receptors dominate: Renal vasculature

Back 312

D1 – vasodilation

Front 313

Epi/NE effect – which receptors dominate: heart

Back 313

Beta1

Front 314

Epi/NE effect – which receptors dominate: Pulmonary bronchioles

Back 314

Beta2

Front 315

Epi/NE effect – which receptors dominate: Presynaptic neurons

Back 315

Alpha2

Front 316

Epi/NE effect – which receptors dominate: Pupillary Sphincter

Back 316

Alpha1 – mydriasis

Front 317

Epi/NE effect – which receptors dominate: Kidney JGA

Back 317

Beta1 – renin release → increased BP

Front 318

Epi/NE effect – which receptors dominate: beta cells of pancreas

Back 318

Alpha2 – inhibits insulin release

Front 319

Epi/NE effect – which receptors dominate: alpha cells pancreas

Back 319

Beta2 – increased glucagons release

Front 320

Epi/NE effect – which receptors dominate: Liver

Back 320

Beta2 – glycogenolysis and gluconeogenesis

Front 321

Clinical use: selective beta2 agonists

Back 321

Asthma
Terbutaline given sub-Q. Also used to decrease premature uterine contraction or decrease uterine hyperstimulation. Salmeterol – long acting, not a rescue agent.

Front 322

Clinical use: Phenoxybenzamine

Back 322

Pheochromocytome (use phenoxybenzamine before removing tumor, since high levels of released catecholamines will not be able to overcome blockage)

Front 323

Clinical use: Prazosin

Back 323

Hypertension (smooth muscle relaxer)
urinary retension in BPH (relaxes urethral sphincter)

Front 324

Clinical use: Terazosin

Back 324

Hypertension (smooth muscle relaxer)
urinary retension in BPH (relaxes urethral sphincter)

Front 325

Clinical use: Doxazosin

Back 325

Hypertension (smooth muscle relaxer)
urinary retension in BPH (relaxes urethral sphincter)

Front 326

Clinical use: Mirtazapine

Back 326

Depression

Front 327

What’s a good antidepressant for patients with insomnia or anorexia?

Back 327

Mirtazapine – increases appetite (as well as serum cholesterol). Causes sedation

Front 328

Effect of Epi on BP before/after alpha blockage

Back 328

Epi – alpha1/2, Beta 1/2 agonist - nonselective
Before – Net pressor effect, with widening of pulse pressure
After – Net depressor effect because no alpha-1 effect, beta2 mediated. Alpha1 and Beta2 are dominant receptors in vascular smooth muscle, so blocking alpha leaves unopposed beta2 vasodilation

Front 329

Effect of Phenylephrine on BP before/after alpha blockage

Back 329

Phenylephrine pure alpha agonist – alpha1>2
Before – net pressor effect because primarily alpha1 agonist
After – Suppression of pressor effect (no change) because alpha stimulation blocked and no beta stimulation.

Front 330

Beta blocker applications

Back 330

HTN – decreased CO and renin secretion
Angina pectoris – decreased HR and contractility, resulting in decreased O2 consumption
MI – beta blockers cardioprotective, decrease mortality
SVT (propranolol, esmolol) – decrease AV conduction velocity (class II antiarrhythmic)
CHF – slows pregression of chronic failure but can exacerbate very bad HF
Glaucoma (timolol) – decreases secretion of aqueous humor

Front 331

Clinical use: Propranolol

Back 331

SVT, Thyroid storm

Front 332

Tx: SVT, thyroid storm, HTN, CHF

Back 332

Propranolol

Front 333

Tx: Glaucoma, HTN

Back 333

Timolol

Front 334

Beta blocker that’s not cardioprotective?

Back 334

Atenolol

Front 335

Short acting beta blocker given by IV?

Back 335

Esmolol

Front 336

Clinical use: Esmolol

Back 336

See effect of beta blocker on patient with arrhythmia, since it’s short-acting

Front 337

Why is a beta blocker not a good Tx for Cocaine OD?

Back 337

Cocaine blocks uptake of catecholamines, which stimulate Beta1 (increased HR) and Beta2 (vasodilation), both of which would be blocked, but this would leave unopposed alpha1 vasoconstriction → increase in arterial BP

Front 338

Tx: Aortic dissection

Back 338

Beta blockers decrease BP and the slope of the rise in BP during contraction

Front 339

Workup: Pt with tachycardia and 1st degree heart block

Back 339

Test first with Esmolol to see if a Beta-blocker makes heart block worse

Front 340

Things to give pt having (or had) MI – MONA

Back 340

Morphine
O2
Nitrates
Aspirin
Beta blockers important too unless CHF. Also give ACE-I or ARBs. Statin, anti-coagulant

Front 341

Vaso/Venodilators and ACE-I/ARB effects on pre/afterload

Back 341

Preload = ventricular EDV. Afterload = mean arterial pressure
Vasodilators (e.g. hydralazine) decrease afterload
Venodilators (e.g. nitroglycerine) decrease preload
ACE-I and ARB decrease Afterload AND Preload

Front 342

Tx: Wolff-Parkinson-White syndrome

Back 342

Unlike most SVT, adenosine is contraindicated. Can use procainamide and amiodarone

Front 343

Tx: A-fib

Back 343

Warfarin
Rhythm control – get A + V back into normal rhythm – Amiodarone, sotalol
Rate control – beta blockers, non-dihydropyridine Ca channel blockers, digoxin (it only affects resting rate and not if they increase their rate)

Front 344

How do you close a PDA? Keep it open?

Back 344

Indomethacin; PGE2

Front 345

Tx: Epstein’s anomaly

Back 345

Findings: tricuspid leaflets displaced ito RV, hypoplastic RV, Tricuspid regurge and stenosis. 80% of pts with ASD with R→ shunt. Dilated RA, risk of ventricular tachycardia and WPW. Widely split S2, Tricuspid regurge on PE.
Tx: PGE2, digoxin, diuresis, propranolol (for SVT)

Front 346

Tx: Hypertrophic cardiomyopathy

Back 346

Beta blocker or heart-specific calcium channel blocker (e.g. verapamil – not dihydropyridines)

Front 347

Tx: Acute CHF

Back 347

LMNOP
Lasix (furosemide)
Morphine (decreases respiratory distress, vasodilation takes fluid elsewhere)
Nitrates (same vasodilatory effect)
Oxygen
Pressors (e.g. dobutamine)

Front 348

Tx: Thrombosis

Back 348

Can give tPA if massive. Have larger window if applied directly to site of clot
Otherwise, give heparin + warfarin. Warfarin inhibits proteins C+S so makes pt. hypercoagulable for first few days

Front 349

Tx: Pericarditis

Back 349

High dose NSAIDs or Aspirin (if Hx of heart dz) and treatment of underlying dz

Front 350

Tx: Raynaud’s disease

Back 350

Dihydropyridine Ca channel blockers, aspirin, sildenafil

Front 351

Tx: Wegener’s granulomatosis

Back 351

Cyclophosphamide and corticosteroids (steroids the more important treatment in PAN)

Front 352

Tx: Kawasaki dz

Back 352

High dose aspirin, even to kids, to avoid infarctions

Front 353

Tx: Polyarteritis Nodosa

Back 353

Corticosteroids w/ or w/o cyclophosphamide (both in Wegener’s)

Front 354

Tx: Temporal (Giant cell) arteritis

Back 354

High dose steroids for one year

Front 355

Mechanism: Hydralazine

Back 355

Increases cGMP → smooth muscle relaxation. Vasodilates arterioles > veins → afterload reduction

Front 356

Clinical use: Hydralazine

Back 356

Severe HTN, CHF. First line for HTN in pregnancy, with methyldopa

Front 357

Clinical use: Minoxidil

Back 357

Severe HTN

Front 358

Mechanism: Minoxidil

Back 358

Anti-HTN
K+ channel opener – hyperpolarizes and relaxes vascular smooth muscle (arteriolar)

Front 359

Mechanism: Ca Channel blockers

Back 359

Block voltage-dependent L-type Calcium channels of cardiac (non-dihydropyridine, e.g. Verapamil) and smooth muscle (Nifedipine, amlodipine), reducing muscle contractility
Vascular smooth muscle – nifedipine > diltiazem > verapamil (Verapamil = Ventricle)
Heart – Verapamil > diltiazem > nifedipine

Front 360

Clinical use: Ca Channel blockers

Back 360

HTN, angina, arrhythmias (not nifedipine), Prinzmetal’s angina (dihydropyridines), Raynaud’s (Dihydropyridines)

Front 361

Mechanism: Nitroglycerin, Isosorbide dinitrate

Back 361

Vasodilation by releasing NO in smooth mm., causing increase in cGMP and smooth mm relaxation. Dilate veins >> arteries, decreasing PREload

Front 362

Clinical use: Nitroglycerin, Isosorbide dinitrate

Back 362

Angina, pulmonary edema, aphrodisiac and erection enhancer

Front 363

Tx: Malignant HTN

Back 363

Nitroprusside – short acting, increases cGMP via direct release of NO
Fenoldopam – Dopamine D1 receptor agonist, relaxes renal vascular smooth muscle
Diazoxide – K+ channel opener – hyperpolarizes and relaxes vascular smooth muscle

Front 364

Antianginal therapy

Back 364

Goal – reduction of myocardial O2 consumption by decreasing one or more of: EDV, BP, HR, contractility, ejection time. Use Nitrates (affect preload), Beta blockers (affect afterload)

Front 365

Antianginal therapy: Nitrates effect on EDV, BP, Contractility, HR, Ejection time, MVO2

Back 365

Decrease preload
Decreased: EDV, BP, Ejection time, MVO2
Increased: Contractility + HR (both reflex response).
Reflex contractility blocked by beta-blockers. MVO2 decreased more in combination with Beta blockers and more still with ACE-I as well.

Front 366

Antianginal therapy: Beta Blockers effect on EDV, BP, Contractility, HR, Ejection time, MVO2

Back 366

Decrease afterload
Decreased: BP, Contractility, HR, MVO2 (decreased more in combination with Nitrates, and more so with ACE-I as well)
Increased: EDV, Ejection time

Front 367

Antianginal therapy: Nitrates + Beta Blockers

Back 367

Little/no effect: EDV, Contractility, Ejection time
Decreased: BP, HR
Significantly decreased: MVO2

Front 368

Antianginal therapy: Ca Channel Blockers

Back 368

Nifedipine similar to Nitrates in effect. Verapamil similar to Beta blockers in effect

Front 369

Antianginal therapy: Pindolol, Acebutolol

Back 369

Partial Beta agonists – contraindicated in angina

Front 370

Mechanism/Effects: Statins

Back 370

Greatly decrease LDL, increase HDL, Decrease TGs
Blocks second step in: Acetyl-CoA → HMG-CoA → Mevalonate → → → cholesterol

Front 371

Mechanism/Effects: Niacin

Back 371

Lipid lowering agent with significant decrease in LDL and significant increase in HDL. Decreases LDL
Inhibits lipolysis in adipose tissue, reduces hepatic VLDL secretion into circulation

Front 372

Mechanism/Effects: Cholestyramine, Colestipol, Colesevelam

Back 372

Bile Acid Resin Lipid Lowering Agents
Significant decrease of LDL, slight increases in HDL, TGs
Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more. Binds C-dif toxin

Front 373

Mechanism/Effects: Cholesterol absorption blocker

Back 373

Ezetimibe
Significant decrease in LDL, no effect on HDL/TGs
Prevents cholesterol reabsorption at SI brush border

Front 374

Mechanism/Effects: Fibrates

Back 374

Lipid-lowering agents
Greatly decreased TGs, decreased LDL, increased HDL
Upregulate LPL, leading to increased TG clearance
Useful because high TGs lead to pancreatitis → ARDS

Front 375

Mechanism/Effects: Omega-3 Fatty Acids

Back 375

Significantly decrease TGs

Front 376

Cardiac drugs – site of action

Back 376

Na/K pump increases extracellular Na, so that Na/Ca antiport can push Ca out. Ca comes in through Ca channels, triggering Ca release through SR Ca channel. Digoxin blocks Na/K pump. Ca channel/Beta blockers block the PM Ca Channel. Ryanodine, a poison, blocks Ca release from SR. Ca sensitizers increase Ca action on troponin/tropomyosin system. Beta1 receptors are Gs, activate PKA, which phosphorylates L-type Ca Channels and phospholamban, both of which increase intracellular Ca during contraction

Front 377

Common Effect/Toxicity: Class I Antiarrhythmics

Back 377

Decrease slope of Phase 0 and Phase 4 depolarization
Toxicity increased by hyperkalemia
Slow or block conduction (especially in depolarized cells). Increased threshold for firing in abnormal pacemaker cells. State dependent (selectively depolarize tissue that is frequently depolarized)

Front 378

Effect: Class IA Antiarrhythmics

Back 378

Procainamide, Disopyramide, Quinidine
Increased AP duration/ERP/QT
Affect both A and V arrhythmias, especially reentrant and ectopic SVT and Vtach, e.g. WPW (use procainamide almost exclusively for this)
Also block K channels, so have Class III effect – pushing out repolarization and increasing ERP

Front 379

Effects: Class IB Antiarrhyhmics

Back 379

Tocainide, Lidocaine, Mexiletine
Affect ischemic or depolarized purkinje and ventricular tissue. Useful in acute Vtach arrhythmias (esp. post MI) and in digitalis-induced arrhythmias (can also use Phenytoin). Lidocaine is MC used Class I. Shorten phase 3 repolarization, decreasing ERP

Front 380

Effects: Class IC Antiarrhytmics

Back 380

Flecainide Propafenone, Encainide
No effect on AP duration. Useful in Vtachs that progress to Vfib and in intractable SVT. Usually used only as last resort in refractory tach. For patients without structural abnormalities. Drastic slowing of phase 0

Front 381

Mechanism: Class II Antiarrhythmics

Back 381

Propranolol, esmolol, metoprolol, atenolol, timolol
Decrease cAMP and Ca currents. Suppress abnormal pacemakers by prolonging phase 4 depolarization. AV node particularly sensitive – increased PR interval. Esmolol very short acting (used to test potential adverse reaction to anti-arrhythmics)

Front 382

Clinical use: Class II Antiarrhythmics

Back 382

Propranolol, esmolol, metoprolol, atenolol, timolol
Vtach, SVT, slowing ventricular rate during afib and atrial flutter

Front 383

Mechanism/Clinical use: Class III Antiarrhythmics

Back 383

Sotalol, ibutilide, amiodarone
Increase AP duration and ERP, inhibit (pulling to right) Phase III. Increases QT, used when other antiarrhythmics fail. Used in A-fib

Front 384

Mechanism: Class IV Antiarrhythmics

Back 384

Verapamil, Diltiazem
Primarily affect AV nodal cells, decreasing conduction velocity, increasing ERP and PR. Used in prevention of nodal arrhythmias (e.g. SVT). Decrease slope of Phases 1 and 2 and increase slope of Phase 3

Front 385

Effects: Adenosine as a drug

Back 385

Antiarrhythmic
Pushes potassium out of cells → hyperpolarizing cells and decreasing intracellular Ca. Drug of choice in diagnosing/abolishing AV nodal arrhythmias (like SVT. Don’t use in reentrant rhythms like WPW – can convert to a-fib). Very short acting (~15s). Stops heart for few seconds, can see what’s under the large QRS

Front 386

Mechanism: K+ as drug

Back 386

Antiarrhythmic
Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)

Front 387

Mechanism: Mg+2 as drug

Back 387

Effective in torsades de pointes and digoxin toxicity

Front 388

Effect of low Ca, low Mg on PTH. What causes low Mg? What does low Mg cause?

Back 388

Decreased free serum Ca increases PTH secretion. Opposite for Mg
Decreased Mg causes arrhythmias and is caused by diarrhea, aminoglycosides, diuretics, alcohol abuse (last two MCC). Diuretic-induced hypomagnesemia problem in CHF patients, who’ll then get antiarrhythmics. They should be on supplemental Mg

Front 389

Mechanism: Nesiritide

Back 389

ANP analog
Acts on cGMP pathway on ANP receptor → increased cGMP → activation of Protein Kinase G → relaxation of smooth muscle (vasodilation) → relaxes afferent glomerular arterioles → increased GFR → diuresis.

Front 390

Clinical use: Nesiritide

Back 390

ANP analog. Used to treat HF

Front 391

Tx: Heart failure/Hyperaldosteronism

Back 391

Spironolactone, Epleranone
K+ sparing diuretics that act as aldosterone antagonists

Front 392

Clinical use: Epleranone

Back 392

K+ sparing diuretic that acts as aldosterone antagonist, used in Tx of HF and hyperaldosteronism

Front 393

Tx: Acromegaly

Back 393

Pituitary adenoma resection, followed by octreotide administration

Front 394

Mechanism/Clinical Use: Octreotide

Back 394

Somatostatin analog. Inhibits most GI hormones/activity (and hormones in general), can use for pituitary excess (GH, TSH, ACTH), GI endocrine excess (e.g. Z-E syndrome), VIPoma, Carcinoid, Glucagonoma, Insulinoma, bleeding varices (decreases blood flow to splanchnic vessels).

Front 395

Tx: Neuropathic pain in DM

Back 395

Gabapentin or Pregabalin

Front 396

Tx: Diabetic Ketoacidosis

Back 396

Fluids, insulin, K+ (to replete intracellular stores, since H+ pumped into cells and K+ out to decrease acidosis). Glucose if necessary to prevent hypoclycemia. Mg+ also decreased with diuresis. Treat following anion gap, since glucose will normalize before it.

Front 397

Tx: Diabetes Insipidus

Back 397

Adequate fluid intake. For Central DI – intranasal desmopressin (ADH analog). For nephrogenic DI – hydrochlorothiazide (loss of electrolytes, not free water, as in loops. Combats hypovolemia due to increased Na/H2O absorption proximally, leading to less H2O in tubules distally, where ADH acts), indomethacin (decreases PG synthesis. PGs inhibit ADH) or amiloride (used in lithium toxicity in addition to HZT. Closes the Na channels opened by Li. 2nd line)

Front 398

Clinical use: Desmopressin

Back 398

ADH analog
Used in Central DI, von Willebrand’s Disease – promotes release of vWF from endothelial storage sites

Front 399

Insulin for DM – Long/short acting

Back 399

Short acting: Lispro, Aspart, Regular
Intermediate: NPH
Long-acting: Glargine, Detemir

Front 400

Clinical use: Insulin

Back 400

Type I DM, Type 2 DM
Life threatening hyperkalemia (increases muscle uptake of K+) and stress-induced hyperglycemia

Front 401

Mechanism: Sulfonylureas

Back 401

1st gen: tolbutamide, chlorpropamide. 2nd gen: glyburide, glimepiride, glipizide
Close K+ channel in beta cell membrane, so cell depolarizes, triggering increased insulin release via increased Ca influx

Front 402

Clinical use: Sulfonylureas

Back 402

1st gen: tolbutamide, chlorpropamide. 2nd gen: Glyburide, glimepiride, glipizide
Stimulates release of endogenous insulin in Type 2 DM. Requires some islet cell functioning, so useless in Type I DM

Front 403

Tx: DM

Back 403

Type 1 – low sugar diet, insulin
Type 2 – dietary modification, exercise for weight loss, oral hypoglycemics, insulin replacement
Sulfonylureas, Biguanides, Glitazones and alpha-glucosidase inhibitors can be used together or alone

Front 404

Mechanism: Metformin/Biguanides

Back 404

Unknown. Possibly decreases gluconeogenesis, increases glycolysis, decreases serum glucose levels. Overall acts as insulin sensitizer

Front 405

Clinical use: Meformin/Biguanides

Back 405

Oral hypoglycemic. Can be used in patients without islet cell function (vs. sulfonylureas). Used in PCOS, can be used in pregnancy, can be used to decrease weight.

Front 406

Mechanism: Pioglitazone, Rosiglitazone

Back 406

Glitazones (aka thiazolidinediones, aka TZDs)
DM Drugs
Increase target cell response to insulin by acting as PPAR-gamma agonists

Front 407

Clinical use: Glitazone (aka thiazolidinedione, aka TZD)

Back 407

DM Drug
Monotherapy for Type 2 DM or combined with other agents (e.g. Sulfonylureas, Biguanides, Alpha-glucosidase inhibitors)

Front 408

Mechanism: Pramlintide

Back 408

Mimetic – DM drug
Amylin analog. Amylin is secreted by Beta cells, works like insulin, decreased in DM. Decreases glucagons, delays gastric emptying

Front 409

Clinical use: Pramlintide

Back 409

Mimetic – DM 2 drug

Front 410

Mechanism: Exenatide

Back 410

GLP-1 (an incretin) mimetic – DM Drug
Increases insulin, decreases glucagon release

Front 411

Clinical use: Exenatide

Back 411

GLP-1 (an incretin) mimetic – DM 2 Drug

Front 412

Mechanism: Sitagliptin

Back 412

Dipeptidyl-Peptidase-4 (DPP-4) inhibitor, Prolongs incretin secretion, increasing insulin and decreasing glucagon secretions. Delays gastric emptying

Front 413

Clinical use: Sitagliptin

Back 413

Dipeptidyl-Peptidase-4 (DPP-4) inhibitor
DM 2

Front 414

Mechanism: Orlistat

Back 414

Obesity drug – pancreatic lipase inhibitor – so can’t absorb fat and end up excreting

Front 415

Clinical use: Orlistat

Back 415

Obesity drug – pancreatic lipase inhibitor
Long-term obesity management (in conjunction with modified diet)

Front 416

Mechanism: Sibutramine

Back 416

SNRI used for obesity. Peripherally acting, not in CNS.

Front 417

Clinical use: Sibutramine

Back 417

SNRI used for obesity – short- and long-term management

Front 418

Mechanism: Propylthiouracil, Methimazole

Back 418

Inhibit organification and coupling (iodination of tyrosil groups) of thyroid hormone synthesis. PTU also decreases peripheral T4→T3 conversion.

Front 419

What decreases T4→T3 conversion peripherally?

Back 419

PTU, Propranolol, Glucocorticoids, I-

Front 420

Clinical use: Propylthiouracil, Methimazole

Back 420

Hyperthyroidism

Front 421

Clinical use: Somatotropin

Back 421

GH. Used in GH deficiency, Turner’s syndrome (to help with height), Prader-Willi Syndrome

Front 422

Clinical use: Somatostatin

Back 422

Octreotide. Acromegaly, carcinoid, gastrinoma, glucagonoma, insulinoma, etc.

Front 423

Clinical use: Oxytocin

Back 423

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

Front 424

Mechanism: Glucocorticoids

Back 424

Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone, prednisolone (used for liver dz pts)
Decrease production of LTs and PGs by inhibiting Phospholipase A2 and expression of COX-2

Front 425

Clinical use: Demeclocycline

Back 425

SIADH

Front 426

Tx: Malabsorption syndromes

Back 426

Limit fat intake, replace fat-soluble vitamins, give pancreatic enzymes with meals

Front 427

Tx: Crohn’s Dz

Back 427

Corticosteroids, infliximab (anti-TNF). Don’t do surgery because dz will pop up in previously unaffected area

Front 428

Tx: Ulcerative Colitis

Back 428

Sulfasalazine, infliximab, colectomy (curative)

Front 429

Tx: End Stage Liver Dz

Back 429

Propranolol or natalol (decrease bleeding varices risk)
Vit K (help clotting factors)
Lactulose (helps pull toxins out of GI wall and blood – dose to 3-4 bowel movements/day)
Diuretics – for ascites (paracentesis if too much. + albumin IV)
Ascites + fever? – rule out SBP
HepA/B/Flu/Pneumonia vaccines

Front 430

Causes of hepatic steatosis

Back 430

Didanosine (ddI), Stavudine (d4T), alcohol, non-alcoholic steatohepatitis

Front 431

Mechanism: H2 blockers

Back 431

Cimetidine, Ranitidine, Famotidine, Nizatidine
Reversible block of H2 receptors → decreased H+ secretion by parietal cells

Front 432

Clinical use: H2 blockers

Back 432

Peptic ulcer, gastritis, mild esophageal reflux

Front 433

Mechanism: Proton pump inhibitors

Back 433

Omeprazole, Lansoprazole
Big guns, stronger than H2 blockers
Irreversibly bind H+/K+-ATPase in stomach parietal cells

Front 434

Clinical use: Proton pump inhibitors

Back 434

Omeprazole, Lansoprazole
Peptic ulcers, gastritis, esophageal reflux, Z-E syndrome, erosive esophagitis

Front 435

Mechanism: Bismuth, sucralfate

Back 435

Bind to ulcer base, providing physical protection, allow HCO3- secretion to reestablish pH gradient in mucous layer

Front 436

Clinical use: Bismuth, sucralfate

Back 436

Increased ulcer healing, traveler’s diarrhea.
Sucralfate – also used to prevent gastritis and gastric ulcers. Requires acidic environment, so can’t give with antacid

Front 437

Prostaglandin analog used in peptic ulcer treatment

Back 437

Misoprostol

Front 438

Mechanism: Misoprostol

Back 438

PGE1 analog. Increased production and secretion of gastric mucous barrier, decreased acid production

Front 439

Clinical use: Misoprostol

Back 439

PGE1 analog that directly antagonizes NSAID (which decrease PGs) induction of peptic ulcers. Used for maintenance of patent ductus arteriosus
Used to induce labor

Front 440

Mechanism: Pirenzepine

Back 440

Blocks M1 receptors on ECL (enterochromaffin-like cells), decreasing histamine secretion, and M3 receptors on parietal cells (decreasing H+ secretion)

Front 441

Clinical use: Pirenzepine

Back 441

Muscarinic antagonist
Peptic ulcers (rarely used)

Front 442

Mechanism: Infliximab, Etanercept, Adalimumab

Back 442

Monoclonal TNF Ab (etanercept = recombinant form of human TNF receptor, infliximab = mouse variable region, adalimumab = human anti-TNF variable region), blocking inflammation

Front 443

Clinical use: TNF Ab

Back 443

Infliximab, Etanercept, Adalimumab
HLA B27 diseases: Crohn’s, Rheumatoid Arthritis, Ankylosing spondylitis, psoriatic arthritis

Front 444

Mechanism: Sulfasalazine

Back 444

Combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory). Activated by colonic bacteria. Only works in distal ileum and colon because doesn’t become unbound until encounters bacteria

Front 445

Clinical use: Sulfasalazine

Back 445

=sulfapyridine AB and mesalamine (anti-inflammatory). Used in ulcerative colitis, Crohn’s (just give mesalamine if early small intestine affected)

Front 446

Mechanism: 5-HT3 antagonists

Back 446

Ondansetron, Granisetron
Powerful central-acting antiemetics, work on chemotactic trigger zone

Front 447

Clinical use: 5-HT3 antagonists

Back 447

Ondansetron, Granisetron
Control vomiting post-op and in pts undergoing cancer chemo, good for morning sickness

Front 448

Mechanism: Metoclopramide

Back 448

D2 receptor antagonist – increases resting tone, contractility, LES tone, motility. Does not influence colon transport time. Also stimulates 5HT receptors

Front 449

Clinical use: Metoclopramide

Back 449

5HT receptor agonist, D2 receptor antagonist
Diabetic and post-op gastroparesis

Front 450

Drugs and receptors involved in increased gut motility

Back 450

Increased gut motility = Increase in Ach and 5HT (e.g. carcinoid syndrome), decrease in D2
Cholinergic agonists: bethanechol (can use for post-op neurogenic ileus), AchE-I like neostigmine
Metoclopramide: stimulates 5HT, antagonizes D2
Domperidone: anti-D2
Cisapride – 5HT agonist
Macrolides – Stimulate smooth mm. and motilin receptors

Front 451

Clinical Use: Hydroxyurea

Back 451

Increases HbF. Used in SCD pts

Front 452

Tx: SCD

Back 452

Hydroxyurea to increase HbF
BM transplantation (ultimate Tx)

Front 453

Mechanism: Heparin

Back 453

Catalyzes activation of antithrombin III, decreases thrombin and Xa. Short half-life

Front 454

Clinical use: Heparin

Back 454

Immediate anticoagulation for PE, stroke, acute coronary syndrome, MI, DVT. Used during pregnancy (doesn’t cross placenta). Follow PTT. Continuous infusion (short half-life)

Front 455

Mechanism: Enoxaparin

Back 455

Low MW heparin, acts more on Xa, has better bioavailability and 2-4 times longer half life. Can be administered SubQ and without laboratory monitoring. Not easily reversible.

Front 456

Tx: HIT

Back 456

Lepirudin, bivalirudin – hirudin derivatives. Directly inhibit thrombin. Have to give warfarin once HIT is over because pt is still hypersensitized.

Front 457

Mechanism: Hirudin derivatives

Back 457

Lepirudin, Bivalirudin
Anticoagulants – directly inhibit thrombin

Front 458

Mechanism: Argatrovan

Back 458

Direct thrombin inhibitor

Front 459

Mechanism: Warfarin

Back 459

Interferes with normal synthesis and gamma-carboxylation of vit-K dependent clotting factors II, VII, IX, X, Proteins C+S. Metabolized by CYP450. Effects Extrinsic pathway more, followed by PT or INR (window = 2-3). Long half-life

Front 460

Clinical use: Warfarin

Back 460

Chronic anticoagulation. Not used in pregnant women (crosses placenta – vs. heparin). DVT, Afib, PE Hx, genetic hypercoagulability, prosthetic heart valve. Have to give heparin with Warfarin until blood level established because slow acting and action on Proteins C+S causes hypercoagulability for first 2-3 days.

Front 461

Mechanism: Urokinase

Back 461

Like tPA, it stimulates the plasminogen → plasmin conversion, leading to breakdown of Fibrin clots and fibrinogen

Front 462

Mechanism: Anistreplase

Back 462

Activates Plasmin formation and function on fibrinogen. Activates formation of plasmin from plasminogen

Front 463

Mechanism: Streptokinase

Back 463

Activates Plasminogen → plasmin conversion

Front 464

Mechanism: Aminocaproic acid

Back 464

Blocks Plasminogen → plasmin conversion
Thrombolytic antidote

Front 465

Mechanism: Thrombolytics

Back 465

Streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)
Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves fibrin clots, increasing PT and PTT, though not changing platelet count or bleeding time

Front 466

Clinical use: Thrombolytics

Back 466

Early STEMI, early ischemic stroke (have 3 hrs if given generally, 6 if given directly)

Front 467

Mechanism: Aspirin

Back 467

Acetylates and irreversibly inhibits COX-1 and COX2 to prevent Arachidonic Acid → PGs + TxA2 conversion (Tx2 produced by activated platelets - mediates vasoconstriction, platelet aggregation/activation – by mediating expression of GPIIbIIIa for fibrinogen binding). (PGI2 → decreased platelet aggregation/uterine tone, causes vasodilation) (PGE2 → decreased vascular tone, increased pain/uterine tone, temperature, gastric mucus) Increases bleeding time. No effect on PT, PTT.

Front 468

Clinical use: Aspirin

Back 468

Low dose (<300mg/day) – decreased platelet aggregation (lasts 3-5 days)
Intermediate (300-2400) – antipyretic and analgesic
High – anti-inflammatory

Front 469

Mechanism: Clopidogrel, Ticlopidine

Back 469

Inhibit platelet aggregation by irreversibly blocking ADP receptors (released by activated platelets – binds to receptors to further activate platelets). Inhibits fibrinogen binding by preventing GPIIbIIIa expression

Front 470

Clinical use: Clopidogrel, Ticlopidine

Back 470

Acute Coronary Syndrome (MI), coronary stenting, decreases incidence or recurrence of thrombotic stroke

Front 471

Mechanism: Abciximab, Tirofiban, Eptifibatide

Back 471

Monoclonal Ab that binds to GP receptor IIbIIIa on activated platelets, preventing aggregation

Front 472

Clinical use: Abciximab, Tirafiban, Eptifibatide

Back 472

Acute coronary syndromes (NSTEMI – vs. tPA or streptokinase if STEMI), percutaneous transluminal coronary angioplasty

Front 473

Mechanism: MTX

Back 473

S-phase specific antimetabolite. Folic acid that inhibits dihydrofolate reductase, decreasing dTMP and therefore DNA/protein synthesis

Front 474

Clinical use: MTX

Back 474

Leukemias, lymphomas, choriocarcinoma (also use Vincristine/Vinblastine for this), sarcomas, abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis, Wegener’s. Think: WBC tumors and uterine pathology

Front 475

Mechanism: 5-FU

Back 475

S-phase-specific antimetabolite. Pyrmidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase, resulting in decreased dTMP and same decreased DNA/Protein synthesis

Front 476

Clinical use: 5-FU

Back 476

Colon cancer and other solid tumors (vs. Cytaraban for liquid), basal cell carcinoma (topical). Synergy with MTX. Topical for actinic keratosis – highlights all the actinic AKs – redness.

Front 477

Toxicity: 5-FU

Back 477

Myelosuppression, which is NOT reversible with leucovorin. Photosensitivity. Can rescue with thymidine

Front 478

Relationship between 5-FU and MTX

Back 478

dUMP is converted to dTMP by thymidylate synthase. This requires addition of methyl group from methyl-THF, which becomes DHF and is converted back to THF by DHF reductase. 5-FU blocks thymidylate synthase and MTX blocks DHFR. Thus, they are synergistic

Front 479

Mechanism: 6-MP

Back 479

Blocks de novo purine synthesis by blocking PRPP synthetase, which converts ribose → PRPP. Activated by HGPRTase

Front 480

Clinical use: 6-MP

Back 480

Leukemias, lymphomas (not CLL or Hodgkin’s)

Front 481

Mechanism: Cytarabine (ara-C)

Back 481

Inhibits DNA polymerase

Front 482

Clinical use: Cytarabine (ara-C)

Back 482

AML, ALL, high-grade non-Hodgkin’s lympoma. Think: liquid tumors (vs. 5-FU, Doxorubicin, Daunorubicin)

Front 483

Mechanism: Cyclophosphamide, Ifosfamide

Back 483

Alkylating agents; covalently x-link (interstrand) DNA at guanine N-7. Require bioactivation by liver

Front 484

Clinical use: Cyclophosphamide, ifosfamide

Back 484

Non-Hodgkin’s lymphoma, PAN, Wegener’s, breast and ovarian carcinomas, also immunosuppressants (e.g. SLE)

Front 485

Mechanism: Nitrosureas

Back 485

Carmustine, lomustine, semustine, streptozocin
Alkylate DNA, cross BBB → CNS

Front 486

Clinical use: Nitrosureas

Back 486

Carmustine, lomustine, semustine, streptozocin
Think: brain. Brain tumors (including glioblastoma multiforme)

Front 487

Mechanism: Cisplatin, Carboplatin

Back 487

Cross-link DNA

Front 488

Clinical use: Cisplatin, Carboplatin

Back 488

Testicular, bladder, ovary, and lung carcinomas

Front 489

Mechanism: Busulfan

Back 489

Alkylates DNA

Front 490

Clinical use: Busulfan

Back 490

CML. Also for ablating bone marrow in hematopoeitic stem cell transplants

Front 491

Clinical use: Doxorubicin (adriamycin), Daunorubicin

Back 491

Part of the ABVD combination regimen for Hodgkin’s lymphoma; also for myelomas, sarcomas and solid tumors (breast, ovary, lung; 5-FU also used for solid tumors, vs. cytaraban for liquid tumors)

Front 492

Mechanism: Doxorubicin (adriamycin), daunorubicin

Back 492

Generate free radicals and noncovalently intercalate in DNA (creating breaks in DNA strand to decrease replication)

Front 493

Mechanism: Dactinomycin (Actinomycin D)

Back 493

Intercalates in DNA

Front 494

Clinical use: Dactinomycin (Actinomycin D)

Back 494

Wilm’s tumor, Ewing’s Sarcoma, Rhabdomyosarcoma
Children ACT out. ACTinomycin for their tumors

Front 495

Mechanism: Bleomycin

Back 495

Induces formation of free radicals, which cause breaks in DNA

Front 496

Clinical use: Bleomycin

Back 496

Testicular cancer, Hodgkin’s lymphoma (part of ABVD regimen)

Front 497

Clinical use: Hydroxyurea

Back 497

Melanoma, CML, SCD (increases HbF)

Front 498

Mechanism: Etoposide (VP-16)

Back 498

G2-phase specific agent that inhibits Topo II and increases DNA degradation

Front 499

Clinical use: Etoposide (VP-16)

Back 499

Small cell carcinoma of the lung and prostate, testicular carcinoma

Front 500

Mechanism: Prednisone

Back 500

Prototype Corticosteroid
May trigger apoptosis. May even work on nondividing cells. Inhibits synthesis of virtually all cytokines. Inactivates NF-kappaB, the TF that induces production of TNF-alpha, among other inflammatory agents.

Front 501

Clinical use: Prednisone

Back 501

Most commonly used glucocorticoid in chemo-. Used in CLL, Hodgkin’s (Part of MOPP regimen). Immunosuppressant used in autoimmune diseases. First line for chronic asthma. Takes 4 hours to get started regardless of delivery

Front 502

Mechanism/toxicity: Beclomethasone

Back 502

Corticosteroid. Inhibits synthesis of virtually all cytokines. Inactivates NF-kappaB, the TF that induces production of TNF-alpha, among other inflammatory agents. Oral thrush when used for asthma (use spacer to avoid)

Front 503

Clinical use: Beclomethasone

Back 503

Antiinflammatory. First line for Asthma

Front 504

Mechanism: Tamoxifen, Raloxifene

Back 504

SERMs – receptor antagonists in breast, agonists in bone. Block binding of estrogen to estrogen receptor-positive cells

Front 505

Mechanism: Clomiphene

Back 505

SERM. Partial agonist at estrogen receptors in pituitary. Prevents normal feedback inhibition and increases release of LH and FSH, stimulating ovulation.

Front 506

Clinical use: Clomiphene

Back 506

Infertility and PCOS

Front 507

Mechanism: Tamoxifen

Back 507

Antagonist on breast tissue

Front 508

Clinical use: Tamoxifen

Back 508

SERM - Used to treat and prevent occurrence of ER+ BrCa

Front 509

Mechanism: Raloxifene

Back 509

SERM. Agonist on bone

Front 510

Clinical use: Raloxifene

Back 510

Useful in preventing/treating osteoporosis, reduce resorption of bone

Front 511

Mechanism: Trastuzumab (Herceptin)

Back 511

Monoclonal Ab against HER-2 (erb-B2). Helps kill breast cancer cells that overexpress HER-2, possibly through Ab-dependent cytotoxicity

Front 512

Clinical use: Trastuzumab (Herceptin)

Back 512

Metastatic breast cancer

Front 513

Mechanism: Imatinib (Gleevac)

Back 513

Philadelphia chromosome bcr-abl tyrosine kinase inhibitor

Front 514

Clinical use: Imatinib (Gleevac)

Back 514

CML, GI stromal tumors, Philadelphia Cr+ ALL

Front 515

Mechanism: Vincristine, Vinblastine

Back 515

M phase specific alkaloids that bind to tubulin and block polymerization of MTs so that mitotic spindles cannot form. MTs are the “vines” of your cells. Blocks chemotaxis. (Griseofulvin, colchicines, taxols [e.g. Paclitaxel] Bend-y drugs all also interfere with MTs)

Front 516

Clinical use: Vincristine, Vinblastine

Back 516

Part of the MOPP (O = Oncovin [vincristine]) regimen for Hodgkin’s lymphoma. Wilm’s tumor, choriocarcinoma (also use MTX for this), Kaposi’s sarcoma

Front 517

Mechanism: Taxols

Back 517

E.g. paclitaxel. M-phase-specific agents that bind to tubulin and hyperstabilize polymerized MTs so that mitotic spindle cannot break down (anaphase can’t occur). (Griseofulvin, colchicines, taxols [e.g. Paclitaxel] Bend-y drugs all also interfere with MTs)

Front 518

Clinical use: Taxols

Back 518

E.g. paclitaxel. Ovarian and breast carcinomas

Front 519

Tx: Paget’s disease

Back 519

Bisphosphonates to inhibit osteoclasts

Front 520

Tx: Ewing’s Sarcoma

Back 520

Dactinomycin (Actinomycin D)
Kids act up, Use Actinomycin for their tumors

Front 521

Tx: Osteoarthritis

Back 521

1st line = acetaminophen (least complications). Good to schedule it vs. taking as needed
After: NSAIDS, steroid injection into joints every 3 mos, Hyaluronic acid (every 1-3 yrs), Joint replacement surgery (mainstay), Opioids – last resort, chronic.

Front 522

Tx: Rheumatoid Arthritis

Back 522

1st line: NSAIDS
Anti-TNF – can’t give if pt has Tb
Disease modifying drugs stop progression

Front 523

Tx: Gout

Back 523

NSAIDs (e.g. indomethacin) used first, Colchicine (rarely given b/c of toxicities), probenecid (if chronic), allopurinol (if chronic, tophi). Don’t give salicylates – all but highest doses depress uric acid clearance, and even then (5-6g/day) uricosuric activity only minor. Low dose salicylates and diuretics decrease uric acid tubular secretion.

Front 524

Mechanism: Colchicine

Back 524

Depolymerizes MTs, impairing leukocyte chemotaxis and degranulation so Macrophages can’t get to uric acid crystals to phagocytise them.

Front 525

Clinical use: Colchicine

Back 525

Gout, pseudogout

Front 526

Mechanism: Probenecid

Back 526

Inhibits reabsorption of uric acid in proximal convoluted tubule.
Inhibits secretion of PCN

Front 527

Clinical use: Probenecid

Back 527

Chronic gout - Should be used if uric acid is high.
Can lengthen PCN effect (blocks secretion in kidney)

Front 528

Mechanism: Allopurinol

Back 528

Blocks xanthine oxidase (conversion of hypoxanthine to xanthine to uric acid)
Xanthine oxidase also metabolizes azathioprine and 6-MP

Front 529

Clinical use: Allopurinol

Back 529

Chronic gout. Also used in lymphoma, leukemia to prevent tumor lysis-associated urate nephropathy

Front 530

Tx: Pseudogout

Back 530

NSAIDs, colchicines

Front 531

Tx: Seronegative spondyloarthropathies

Back 531

PAIR = Psoriatic arthritis, Ankylosing spondylitis, IBD arthritis, Reiter’s syndrome (can’t see, can’t pee, can’t climb a tree). Tx is Anti-TNF (Infliximab, Etanercept, Adalimumab)

Front 532

Tx: SLE

Back 532

Glucocorticoids, NSAIDS (these MC used)
Cyclophosphamide (if very severe), hydroxychloroquine. Primaquine (have to check 2x/year for renal damage

Front 533

Tx: Sarcoidosis

Back 533

Steroids

Front 534

Tx: Polymyalgia rheumatica

Back 534

Prednisone (just as with temporal arteritis)

Front 535

Tx: Polymyositis/dermatomyositis

Back 535

Steroids

Front 536

Tx: Mixed connective tissue disease

Back 536

Responds to steroids

Front 537

Tx: Fibromyalgia

Back 537

Pregabalin, milnacipran (SNRI), amitryptiline (helps with sleep), low dose fluoxetine

Front 538

Mechanism: NSAIDs

Back 538

Ibuprofen, Naproxen, Indomethacin, Ketorolac
Reversibly inhibit COX-1/2. Block PG synthesis

Front 539

Clinical use: NSAIDs

Back 539

Antipyretic, analgesic, anti-inflammatory. Indomethacin used to close PDA.
Indomethacin strongest, use for gouty arthritis but no longer than 5 days
Ketorolac – very strong, can be given IM, oral

Front 540

Mechanism: Cox-2 inhibitor

Back 540

e.g. Celecoxib
Reversibly inhibit Cox-2 in inflammatory cells and vascular endothelium, mediates inflammation and pain, spares Cox-1, sparing gastric mucosa

Front 541

Clinical use: Cox-2 inhibitor

Back 541

e.g. celecoxib
Rheumatoid Arthritis and Osteoarthritis

Front 542

Mechanism: Acetaminophen

Back 542

Reversibly inhibits COX, mostly in CNS. Inactivated peripherally (so no anti-inflammatory properties)

Front 543

Clinical use: Acetaminophen

Back 543

Antipyretic, analgesic, lacking anti-inflammation. Used instead of aspirin in children to prevent Reye’s syndrome with viral infection.

Front 544

Compare Aspirin, Acetaminophen, NSAIDs

Back 544

Acetaminophen = NSAID – anti-inflammatory activity
Aspirin = NSAID + antiplatelet activity

Or
Acetaminophen + anti-inflammation = NSAID
NSAID + antiplatelet = Aspirin

Front 545

Mechanism: Bisphosphanates

Back 545

Inhibit Osteoclast activity; reduce formation and resorption of hydroxyapatite

Front 546

Clinical use: Bisphosphonates

Back 546

Malignancy associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoporosis, prophylaxis with long-term steroid users. Take on empty stomach and stay upright for 1/2 hour afterward

Front 547

Tx: Osteoporosis

Back 547

Bisphosphanates
Also, stop smoking, alcohol, steroids, PPI (b/c acid needed to absorb Ca)
Give Vitamin D, exercise, hip protectors, PTH (has anabolic effect, decreases hip fractures), testosterone, estrogen, calcitonin

Front 548

Tx: Huntington’s Dz

Back 548

Dopamine antagonist, e.g. haloperidol

Front 549

Prophylaxis: strokes, TIA

Back 549

Aspirin. If pt also has cardiac need, use clopidogrel

Front 550

Tx: Pseudotumor cerebri

Back 550

Acetazolamide, Prednisone. Repeat spinal taps to maintain/control pressure. If untreated, can lead to blindness

Front 551

Tx: Migraine

Back 551

Triptans, ergotamines (e.g. bromocriptine)

Front 552

Tx: Tension headaches

Back 552

NSAIDs

Front 553

Tx: Cluster headache

Back 553

Ergotamines, O2

Front 554

Tx: Absence seizures

Back 554

Ethosuxamide

Front 555

Tx: Brain tumors

Back 555

Nitrosureas (nitros on your mustang – most end in –stine)

Front 556

Mechanism: Epinephrine (in glaucoma)

Back 556

Alpha agonist – decreases aqueous humor synthesis via vasoconstriction

Front 557

Mechanism: Brimonidine

Back 557

Alpha agonist - Decreases aqueous humor synthesis

Front 558

Clinical use: Brimonidine

Back 558

Glaucoma

Front 559

Mechanism: Beta blockers (in glaucoma)

Back 559

Timolol, betaxolol, carteolol
Decrease aqueous humor secretion

Front 560

Mechanism: Acetazolamide (in glaucoma)

Back 560

Decreases aqueous humor secretion due to HCO3 decrease (via inhibition of carbonic anhydrase)

Front 561

Clinical use: Mannitol

Back 561

Glaucoma – emergency Rx
Shock, drug overdose, to decrease intracranial/ocular pressure

Front 562

Mechanism: Mannitol

Back 562

Osmotic diuretic. Increases TF osmolarity producing more urine. Decreasing effects, so best used in emergencies acutely.

Front 563

Mechanism: Cholinomimetics (in glaucoma)

Back 563

pilocarpine, carbachol, physostigmine, echothiophate
Increases outflow of aqueous humor, contracts ciliary muscle and opens trabecular meshwork. Very effective at opening Canal of Schlemm. Use pilocarpine for emergencies.

Front 564

Mechanism: Latanoprost

Back 564

PGF-2alpha
Increases outflow of aqueous humor

Front 565

Clinical use: Latanoprost

Back 565

PGF-2alpha
MC prescribed Rx in glaucoma

Front 566

Tx: Glaucoma (emergency)

Back 566

Pilocarpine (cholinomimetic), Mannitol

Front 567

Mechanism: Opioid analgesics

Back 567

Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan
Opioid receptor agonists (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission. Open K+ channels, close Ca channels → decreased synaptic transmission

Front 568

Clinical use: Opioid analgesics

Back 568

Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan
Pain, cough suppression (DXM), diarrhea (loperamide and diphenoxylate, which slow down peristalsis and can cause constipation), acute pulmonary edema, maintenance programs for addicts (methadone). O in LMNOP for acute CHF. Increase pain threshold, decreasing need for sleep inducer in operations – less chance of waking due to pain.

Front 569

Mechanism: Butorphanol

Back 569

Partial agonist at opioid mu receptors, agonist at kappa receptors

Front 570

Clinical use: Butorphanol

Back 570

Pain; causes less respiratory depression than full agonists. Indications: intranasally for migraines, pregnancy

Front 571

Mechanism: Tramadol

Back 571

Very weak opioid agonist, also blocks serotonin and NE reuptake

Front 572

Clinical use: Tramadol

Back 572

Chronic pain

Front 573

Drugs that work on Simple/Complex Partial Seizures

Back 573

Phenytoin, Carbamazepine, Lamotrigine, Gabapentin (only as adjuvant), Topiramate
Phenobarbital, Valproic acid

Front 574

First line drugs for Generalized Tonic-Clonic seizures

Back 574

Phenytoin, Carbamazepine, Valproic acid

Front 575

Non-First line drugs for Generalized Tonic-Clonic Seizures

Back 575

Lamotrigine, Gabapentin, Topiramate, Phenobarbital

Front 576

First line drug for Absence seizures

Back 576

Ethosuxamide

Front 577

Non-First line drug for Absence seizures

Back 577

Valproic Acid

Front 578

First line drug for prophylaxis: Status epilepticus

Back 578

Phenytoin

Front 579

First line drug for acute Status epilepticus

Back 579

Benzodiazepines

Front 580

Mechanism: Phenytoin

Back 580

Use-dependent blockade of Na+ channels; inhibition of glutamate release from excitatory presynaptic neurons

Front 581

Clinical use: Phenytoin

Back 581

Tonic-clonic seizures (first line), Class IB antiarrhythmic. Treats simple/complex partial seizures and is first line prophylaxis for Status epilepticus

Front 582

Mechanism: Barbiturates

Back 582

Phenobarbital, pentobarbital, thiopental, secobarbital
Used as antiepileptic, anesthetic
Facilitate GABAa action by binding at the receptor and INCREASING DURATION of Cl channel opening (vs. increased frequency in Benzos), thus decreasing neuron firing. “BarbiDURATes increase DURATion.”

Front 583

Clinical use: Barbiturates

Back 583

Phenobarbital, pentobarbital, thiopental, secobarbital
Sedative for anxiety, seizures (phenobarbital used for simple/complex partial seizures and tonic-clonic generalized), insomnia (though long half-life = residual effects, so not commonly prescribed for insomnia), induction of anesthesia (thiopental) – high lipid solubility, rapid entry into brain, effect terminated by slower redistribution into sk. mm. and adipose, decreased cerebral blood flow.
Phenobarbital first line antiepileptic in pregnancy, children

Front 584

Mechanism: Benzodiazepines

Back 584

Facilitate GABAa action by acting at the binding site and INCREASING FREQUENCY (vs. Barbs – increased duration) of Cl channel opening. Decrease REM sleep (treats insomnia but less restful sleep results). Most have long half lives and active metabolites.

Front 585

Clinical use: Benzodiazepines

Back 585

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide (all have “az” in them)
Anxiety, spasticity, status epilepticus (persistent seizure - lorazepam, diazepam), detox (especially for alcohol withdrawal DTs), night terrors, sleepwalking, insomnia (temazepam), short-procedure sedation (midazolam – used with gaseous anesthetics and narcotics), trigeminal neuralgia. Also used for seizures of eclampsia (though first line is MgSO4)

Front 586

Benzo used in insomnia

Back 586

Temazepam
Reduces REM, less restful sleep

Front 587

Benzo used in short-procedure sedation

Back 587

Midazolam

Front 588

Benzo used in alcohol withdrawal, long-acting

Back 588

Chlordiazepoxide

Front 589

Benzos used in status epilepticus (persistent seizure)

Back 589

Diazepam, Lorazepam

Front 590

GABA potentiators used for epilepsy Tx

Back 590

Benzos, Phenobarbital, Valproic acid, Gabapentin, Topiramate

Front 591

Na Channel blockers used in Epilepsy Tx

Back 591

Carbamazepine, Phenytoin, Valproic acid, Lamotrigine, Topiramate
Prevent depolarization

Front 592

Mechanism: Lamotrigine

Back 592

Blocks voltage gated Na channels

Front 593

Clinical use: Lamotrigine

Back 593

Used for Simple/Complex Partial seizures and tonic-clonic

Front 594

Mechanism: Gabapentin

Back 594

GABA potentiator (increases release)

Front 595

Clinical use: Gabapentin

Back 595

Adjuvant seizure med used for simple/complex partial seizures and tonic-clonic seizures. Also used for peripheral neuropathy.

Front 596

Mechanism: Topiramate

Back 596

Blocks Na channels, preventing neuronal depolarization. GABA potentiator (increases release)

Front 597

Clinical use: Topiramate

Back 597

Simple/Complex Partial seizures, Tonic-Clonic seizures

Front 598

Mechanism: Valproic acid

Back 598

GABA potentiator, blocks Na channels, preventing neuronal depolarization

Front 599

Clinical use: Valproic acid

Back 599

First line for tonic-clonic seizures. Used in absence seizures, simple/complex partial seizures, and myoclonic seizures

Front 600

Mechanism: Ethosuximide

Back 600

Blocks thalamic T-type Ca channels

Front 601

Clinical use: Ethosuximide

Back 601

First line for absence seizures

Front 602

Mechanism: Carbamazepine

Back 602

Blocks Na channels, preventing neuronal depolarization

Front 603

Clinical use: Carbamazepine

Back 603

First line for trigeminal neuralgia, First line for tonic-clonic seizures, also used for simple/complex partial seizures

Front 604

Anesthetics: relationship between Lipid/blood solubility, MAC, potency, km

Back 604

High lipid solubility = low MAC (minimum alveolar concentration) = high potency = low km
High blood solubility = slow induction and recovery times
Give both together so as fast one wears off, slower one kicks in

Front 605

How do these anesthetics compare in potency and induction: Isoflurane, N2O, Halothane, Methoxyflurane, Enflurane

Back 605

Decreasing potency/Increasing speed of induction: Methoxyflurane > Halothane + Enflurane > Isoflurane, N2O

Front 606

Mechanism: Inhaled anesthetics

Back 606

Unknown

Front 607

Mechanism: Ketamine

Back 607

Arylcyclohexylamine – PCP analog that acts as dissociative anesthetic. Blocks NMDA receptors. Cardiovascular stimulant

Front 608

Clinical use: Opiates as anesthetics

Back 608

Morphine, Fentanyl

Front 609

Mechanism: Propofol

Back 609

Potentiates GABAa (like benzos and barbs)

Front 610

Clinical use: Propofol

Back 610

rapid anesthesia induction and short procedures. Leaves system rapidly, so good for waking up rapidly.

Front 611

Mechanism: Local anesthetics

Back 611

Block Na channels by binding specific recpeptors on inner portion of channel. Preferentially bind activated Na channels, so most effective in rapidly firing neurons. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form

Front 612

How are Local anesthetics affected by infection, pH?

Back 612

In infected (acidic) tissue, e.g. an abscess, alkaline anesthetics are charged and cannot penetrate the membrane effectively. More anesthetic is needed.

Front 613

Order of nerve blockade for local anesthetics

Back 613

Small diameter fibers > large. Myelinated fibers > unmyelinated. Size effect > myelination, so small myelinated fibers > small unmyelinated > large myelinated > large unmyelinated
Order of loss – pain (lose first) > temperature > touch > pressure (lose last)

Front 614

Clinical Use: Local anesthetics – Use with vasoconstrictors

Back 614

Vasoconstrictors decrease bleeding and increase anesthesia because restricts drug to local area. All but cocaine given with vasoconstrictor (usually epinephrine).

Front 615

Clinical use: Neuromuscular drugs

Back 615

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor

Front 616

Reversal of Depolarizing neuromuscular blockade

Back 616

Phase I – prolonged depolarization – no antidote. Block potentiated by AchE-I. Excess NT release
Phase II – repolarized by blocked – antidote consists of AchE-Is, e.g. neostigmine

Front 617

Reversal of Nondepolarizing neuromuscular blockade

Back 617

Neostigmine, edrophonium, and all other AchE-Is

Front 618

Mechanism: Neuromuscular blockade

Back 618

Depolarizing – Succinylcholine – complications include hypercalcemia and hyperkalemia
Nondepolarizing – competitive inhibition of Ach receptors

Front 619

Mechanism: Dantrolene

Back 619

Prevents release of Ca from SR of sk mm.

Front 620

Clinical use: Dantrolene

Back 620

Malignant hyperthermia (caused by use of inhalation anesthetics – except N2O) and succinylcholine. Also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotics)

Front 621

Mechanism: Bromocriptine, pramipexole, ropinirole

Back 621

Partial dopamine agonists

Front 622

Mechanism: Amantadine

Back 622

May increase dopamine release

Front 623

Clinical use: Amantadine

Back 623

Mild, young Parkinson’s patients, used as antiviral against influenza A (not much anymore because of resistance – use oseltamavir) and rubella

Front 624

Mechanism: L-dopa + Carbidopa/Tolcapone (or entacapone)

Back 624

Increase Dopamine levels in brain. Unlike dopamine, Dopa can cross BBB into brain, where it is converted to dopamine by dopa decarboxylase. Carbidopa inhibits dopa decarboxylase peripherally. Tolcapone and entacapone block COMT conversion of L-dopa to 3-O-methyldopa, which can’t cross into CNS. These add-ons decrease necessary dose of L-dopa

Front 625

Clinical use: L-dopa + Carbidopa/Tolcapone

Back 625

Parkinsonism. L-dopa is the big gun for parkinsons Tx. Almost every Parkinsons patient is on it.

Front 626

Mechanism: Selegiline

Back 626

Selectively inhibits MAO-B, increasing availability of dopamine

Front 627

Clinical use: Selegiline

Back 627

Adjunctive agent to L-dopa in Parkinson’s Tx. Only MAOI used in Parkinson’s. Be careful not to give MAOIs and anti-depressants with L-dopa because too much increase in dopamine leads to conversion to NE → HTN crisis
Dopa → [Melanin +] Dopamine → NE → Epi

Front 628

Mechanism: Sumatriptan

Back 628

5HT 1B/1D agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-life &lt;2 hours

Front 629

Clinical use: Sumatriptan

Back 629

Acute migraines, cluster headache attacks

Front 630

Mechanism: Memantine

Back 630

NMDA receptor antagonist. Helps prevent excitotoxicity (mediated by Ca)

Front 631

Tx: Heroin addiction

Back 631

Naloxone and naltrexone – competitively inhibit opioids, used in OD
Methadone – long-acting oral opiate – long-acting opiate – used for heroin detox or long-term maintenance
Suboxone – naltrexone + buprenorphine (partial agonist) – long acting with fewer withdrawal Sx than methadone; withdrawal symptoms if injected (lower abuse potential)

Front 632

Mechanism: Typical Antipsychotics (neuroleptics)

Back 632

All typical antipsychotics block dopamine D2 receptors

Front 633

Clinical use: Typical Antipsychotics

Back 633

Schiphrenia (primarily positive symptoms), psychosis, acute mania, Tourette’s, agitated demented pt (high potency to avoid worsening dementia)

Front 634

Tx: NMS

Back 634

Antipsychotic complication
Dantrolene, agonists (e.g. bromocriptine)

Front 635

High Potency Typical antipsychotics + toxicities

Back 635

Haloperidol, Fluphenazine, thiothixene
Extrapyramidal effects, not so much anticholinergic

Front 636

Moderate Potency Typical antipsychotics

Back 636

Molindine, Laxopine, Trifluoperazine

Front 637

Low Potency Typical antipsychotics

Back 637

Thioridazine, Chlorpromazine
Anticholinergic side effects, not really extrapyramidal

Front 638

Mechanism: Atypical antipsychotics

Back 638

Clozapine, Olanzapine, Risperidone, Aripiprazole, Quetiapine, Ziprasidone
Block 5-HT2, alpha, H1 and dopamine receptors

Front 639

Clinical use: Atypical antipsychotics

Back 639

Clozapine, Olanzapine, Risperidone, Aripiprazole, Quetiapine, Ziprasidone
First line agents for Szhizophrenia (useful for both + and – symptoms)
Olanzapine – also used for OCD, anxiety, depression, mania, Tourette’s

Front 640

Mechanism: Lithium

Back 640

Not established. Possibly related to inhibition of phosphoinositol cascade

Front 641

Clinical use: Lithium

Back 641

Mood stabilizer for Bipolar disorder. Blocks relapse and acute manic events. Also SIADH

Front 642

Mechanism: Buspirone

Back 642

Stimulates 5HT1A receptors

Front 643

Clinical use: Buspirone

Back 643

Generalized anxiety disorder (not PTSD or panic disorder). Does not cause sedation or addiction. Does not interact with alcohol (vs. barbs and benzos)

Front 644

Mechanism: TCAs

Back 644

SNRIs
Inhibit fast sodium channels. OD can lead to blockage of phase 0 depolarization in myocytes and His-Purkinje system. Tx: hypertonic sodium bicarbonate

Front 645

Clinical use: TCAs

Back 645

Imipramine, Amitriptyline, Desipramine, Nortriptyline, Chlomipramine, Doxepin, Amoxapine
(End in –pin(e), -pramine, -triptyline)
Major depression, bedwetting (imipramine), OCD (clomipramine)

Front 646

Clinical use: SSRIs

Back 646

Fluoxetine, paroxetine, sertraline, citalopram, fluvoxemine
Depression, OCD, anxiety, panic, PTSD, anorexia

Front 647

Mechanism: Bupropion

Back 647

Increases NE and Dopamine by unknown mechanism

Front 648

Clinical use: Bupropion

Back 648

Antidepressant. Can be added to SSRI. Smoking cessation

Front 649

Mechanism: Venlafaxine

Back 649

SNRI

Front 650

Clinical use: Venlafaxine

Back 650

Depression, GAD

Front 651

Clinical use: Milnacipran

Back 651

SNRI used for Fibromyalgia

Front 652

Clinical use: Sibutramine

Back 652

SNRI used in weight loss

Front 653

Mechanism: Duloxetine

Back 653

SNRI, similar to venlafaxine, but more effect on NE

Front 654

Clinical use: Duloxetine

Back 654

Depression, diabetic peripheral neuropathy

Front 655

Mechanism: Mirtazapine

Back 655

Tetracyclic. Alpha2 antagonist (increased release of NE and 5HT) and potent 5HT2/3 receptor antagonist

Front 656

Mechanism: Maprotiline

Back 656

Tetracyclic
NE reuptake inhibitor

Front 657

Mechanism: Trazodone

Back 657

Antidepressant that primarily inhibits 5HT reuptake

Front 658

Clinical use: Trazodone

Back 658

Insomnia (low dose – increases REM sleep), depression (high dose). Given as adjuvant to SSRI

Front 659

Mechanism: MAOI

Back 659

Nonselective MAO inhibition – increases levels of amine NTs

Front 660

Clinical use: MAOI

Back 660

Atypical depression, anxiety, hypochondriasis

Front 661

Things that move K+ out of cells

Back 661

Decreased insulin, beta blockers, acidosis (H/K transporter), digoxin, cell lysis (as in leukemia/treatment)

Front 662

Things that move K+ into cells

Back 662

Insulin, beta agonists (e.g. albuterol), alkalosis (give bicarb for Tx), cell creation/proliferation (e.g. cancer)

Front 663

Mechanism: Acetazolamide

Back 663

Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total body HCO3 stores

Front 664

Clinical use: Acetazolamide

Back 664

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness (respiratory alkalosis. This helps compensation)

Front 665

Mechanism: Loop diuretics

Back 665

Inhibit NaK2Cl cotransport system of thick ascending limb of Loop of Henle. Abolishes hypertonicity of medulla, preventing concentrating of urine. Secretion of isotonic fluid (vs. hypertonic for thiazides). Increased Ca excretion. Loops Lose Calcium (vs. thiazides). Most potent diuretics with excellent efficacy.

Front 666

Clinical use: Furosemide, Bumetanide, Torasemide

Back 666

Most potent diuretics. Edematous states (CHF, Cirrhosis, Nephrotic syndrome, Pulmonary edema), HTN (if CHF also present), hypercalcemia

Front 667

Mechanism: Ethacrynic acid

Back 667

Essentially same as furosemide, but not a sulfonamide (so can give to pts with sulfa allergies)

Front 668

Clinical use: Ethacrynic acid

Back 668

Diuresis in patients allergic to sulfa drugs

Front 669

Mechanism: Hydrochlorothiazide

Back 669

Secretion of hypertonic fluid (vs. isotonic for loops). Inhibits NaCL reabsorption in early distal tubule, reducing diluting capacity of nephron. Decreased Ca excretion

Front 670

Clinical use: Thiazides

Back 670

HTN, CHF, Idiopathic hypercalciuria

Front 671

Mechanism: K-sparing diuretics

Back 671

Spironolactone, Triamterine, Amiloride, Eplerenone
Spironolactone – competitive aldosterone receptor antagonist in cortical collecting tubule
Triamterine, Amiloride –block Na channels in CCT

Front 672

Clinical use: K-sparing diuretics

Back 672

Hyperaldosteronism, K+ depletion, CHF (decrease mortality)

Front 673

Diuretic effects – Urine NaCl

Back 673

Increased by all diuretics

Front 674

Diuretic effects – Urine K

Back 674

Increased by all except K-sparing diuretics

Front 675

Diuretic effects – Blood pH decrease (acidemia)

Back 675

Carbonic anhydrase inhibitors (decreased HCO3 reabsorption), K-sparing diuretics (hyperkalemia → H/K exchange

Front 676

Diuretic effects – Blood pH increase (alkalemia)

Back 676

Loops and thiazides
1. volume contraction → increases ATII → Na/H exchange in proximal tubule → increased HCO3 (contraction alkalosis) 2. K loss → H/K exchange puts H into cells. 3. In low K state, H (instead of K) is exchanged for Na in principal cells, leading to alkalosis and “paradoxical aciduria”

Front 677

Diuretic effects – Urine Ca

Back 677

Increased by loops – abolish lumen-positive potential in thick ascending limb → decreased paracellular Ca reabsorption → hypocalcemia, increased urinary Ca
Decreased by thiazides – block luminal Na/Cl cotransport in DCT → increased Na gradient → interstitial Na/Ca exchange → hypercalcemia

Front 678

Mechanism: ACE-I

Back 678

Captopril, Enalapril, Lisinopril
Inhibit ACE, reducing levels of ATII, preventing inactivation of bradykinin, a potent vasodilator. Renin release is increased due to loss of feedback inhibition

Front 679

Clinical use: ACE-I

Back 679

HTN, CHF, Diabetic renal disease

Front 680

Tx: Menopausal symptoms

Back 680

Estrogen replacement therapy (weigh risks of endometrial, etc. cancers), SSRI (Venlafaxine), Clonidine (Anti-HTN), Gabapentin (especially with anxiety/seizure disorder or neuropathy in addition)

Front 681

Tx: Preeclampsia/eclampsia

Back 681

Delivery of fetus as soon as viable. Otherwise, bed rest, salt restriction, monitoring and treatment of HTN. IV MgSO4 and diazepam to prevent and treat seizures of eclampsia. Benzos controversial; MgSO4 drug of choice, but it can cause hyporeflexia, pulmonary edema, decreased respiratory drive, all signs of overdosing, so check every 4 hrs

Front 682

Clinical use: MgSO4

Back 682

Eclampsia seizures; in conjunction with tocolysis to delay labor (stop contractions).

Front 683

Tx: Ectopic pregnancy

Back 683

If small, MTX to abort. If large, surgery to remove.

Front 684

Tx: Leimyoma (fibroid)

Back 684

Fibroidectomy, OCP (excess bleeding)

Front 685

Tx: PCOS

Back 685

Weight loss OCPs (makes ovaries less sensitive to LH), gonadotropin analogs (leuprolide – use pulsatile when they want to get pregnant), clomiphene (SERM - pts have decreased FSH, amenorrhea, so this can help ovulation), anti-androgens (e.g. spironolactone, ketoconazole – both prevent hirsutism and cause gynecomastia and amenorrhea) or surgery

Front 686

Mechanism: Leuprolide

Back 686

GnRH analog with agonist properties when used in pulsatile fashion, antagonistic when used in continuous fashion

Front 687

Clinical use: Leuprolide

Back 687

Infertility (pulsatile administration), prostate cancer (continuous – use with flutamide), uterine fibroids (continuous), inducing menopause. Prescribe with add back therapy – patient can take estrogen when Sx of menopause too much

Front 688

Tx: BPH

Back 688

Finasteride, alpha blockers, tamsulosin (alpha1A selective, fewer side fx, no decrease in BP). Saw Palmetto (works as finasteride does, but no negative side effects and no change to PSA)

Front 689

Tx: Prostatitis

Back 689

4 weeks fluoroquinolones or TMP-SMX

Front 690

Tx: Epididymitis

Back 690

<35 – GC/Chlamydial infection. Ceftriaxone + Doxycycline
>35 (or Hx of anal sex) – enterobacteria – Fluoroquinolones for 2 weeks (vs. 4 weeks for prostatitis because better blood flow)

Front 691

Mechanism: Finasteride

Back 691

Blocks 5-alpha-reductase conversion of testosterone → DHT

Front 692

Clinical use: Finasteride

Back 692

BPH (shrinks prostate, since DHT promotes prostatic growth. Decreases PSA levels, lowering threshold for prostatic cancer screening). Promotes hair growth, treats male pattern baldness

Front 693

Mechanism: Flutamide

Back 693

Nonsteroidal competitive of androgens at the testosterone receptor

Front 694

Clinical use: Flutamide

Back 694

Prostatic carcinoma

Front 695

Mechanism: Ketoconazole (anti-androgen)

Back 695

Inhibits steroid synthesis

Front 696

Mechanism: Spironolactone (anti-androgen)

Back 696

Inhibits steroid synthesis

Front 697

Mechanism: Sildenafil, Vardenafil, Tadalafil

Back 697

Inhibit cGMP phosphodiesterase, increasing cGMP, smooth mm. relaxation in corpus cavernosum, increased blood flow, penile erection

Front 698

Clinical use: Sildenafil, Vardenafil, Tadalafil

Back 698

Treatment of ED, Pulmonary HTN, Raynaud’s syndrome

Front 699

Mechanism: Mifepristone (RU-486)

Back 699

Competitive inhibitor of progestins at progesterone receptors

Front 700

Clinical use: Mifepristone (RU-486)

Back 700

Termination of pregnancy. Administered with misoprostol (PGE1 – causes contractions).

Front 701

Clinical use: Hormone replacement therapy (HRT)

Back 701

Relief/prevention of menopausal symptoms (e.g. hot flashes, vaginal atrophy) and osteoporosis. Unopposed estrogen replacement therapy (ERT) increases the risk of endometrial cancer, so progesterone is added. Possible increased cardiovascular risk. Some will have testosterone to help with decreased libido, atrophic vaginitis

Front 702

Mechanism: Dinoprostone

Back 702

PGE2 analog that causes cervical dilation and uterine contraction

Front 703

Clinical use: Dinoprostone

Back 703

Labor induction

Front 704

Mechanism: Ritodrine, terbutaline

Back 704

B2 agonists that relax the uterus

Front 705

Clinical use: Ritodrine, terbutaline

Back 705

Delaying premature uterine contractions

Front 706

Clinical use: Anastrozole, Exemestane

Back 706

Aromatase inhibitors used for BrCa in postmenopausal women

Front 707

Clinical use: Testosterone (methyltestosterone)

Back 707

Treat hypogonadism, promote development of secondary sex characteristics; stimulation of anabolism to promote recovery after burn or injury. Treat ER+ BrCa (exemestane). Male with sexual dysfunction or osteoporosis due to decreased testosterone

Front 708

Clinical use: Estrogens (ethinyl estradiol, DES, mestranol)

Back 708

Hypogonadism orovarian failure, menstrual abnormalities, HRT in postmenopausal women; use in men with androgen dependent prostate cancer.

Front 709

Mechanism: Progestins

Back 709

Bind progesterone receptor, reduce growth and increase vascularization of endometrium

Front 710

Clinical use: Progestins

Back 710

Used in oral contraceptives and in the treatment of endometrial cancer and abnormal uterine bleeding

Front 711

Tx: Neonatal respiratory distress syndrome

Back 711

Lecithin: Sphingomyelin < 2.0 in amniotic fluid
Steroids 24 hrs before delivery – matures pneumocytes. Also artificial surfactant for infant

Front 712

Tx: Primary Pulmonary HTN

Back 712

Sildenafil

Front 713

Mechanism: H1-blockers

Back 713

1st generation – Diphenhydramine, Dimenhydrinate, Chlorpheniramine, Hydroxazine
2nd Generation – Loratadine, foxofenadine, Destoratadine, Ceterizine
Reversible inhibitors of H1 histamine receptors (non-stomach locations). Anti-serotonergic, anti-muscarinic, anti-alpha-adrenergic. Increase proportion of inactive H1 receptors ("reverse blockade")

Front 714

Clinical use: H1 Blockers

Back 714

Can help prevent asthma exacerbations in pts with allergies

Front 715

Clinical use: H1 Blockers – 1st generation

Back 715

1st generation – Diphenhydramine, Dimenhydrinate, Chlorpheniramine, Hydroxazine
Allergy, motion sickness, sleep aid

Front 716

Clinical use: H1 Blockers – 2nd generation

Back 716

2nd Generation – Loratadine, foxofenadine, Destoratadine, Ceterizine
Allergies, not sleep

Front 717

Mechanism: Asthma drugs

Back 717

Bronchoconstriction is mediated by 1) inflammatory processes and 2) sympathetic tone. Tx directed at these two

Front 718

Mechanism/Use/Toxicity: Salmeterol

Back 718

Long-acting agent for asthma prophylaxis only. B2 agonist (Bronchial smooth muscle relaxer). Tremor, arrhythmia

Front 719

Clinical use: Cromolyn

Back 719

Clinical use: Cromolyn

Front 720

Mechanism: Cromolyn

Back 720

Prevents release of mediators from mast cells

Front 721

Clinical use/toxicity: Methylxanthines

Back 721

Last resort for COPD pts. Cardiotoxicity, neurotoxicity lead to narrow therapeutic window. CYP450 metabolism

Front 722

Mechanism: Methylxanthines

Back 722

Theophylline, Aminophylline
Likely cause bronchodilation by inhibiting phosphodiesterase, thereby decreasing cAMP hydrolysis

Front 723

Mechanism: Zileuton

Back 723

Anti-leukotriene. 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes

Front 724

Clinical use: Zileuton

Back 724

Good for asthma prophylaxis. Can be given with steroids, albuterol

Front 725

Clinical use: Leukotriene receptor blockers

Back 725

allergies/asthma. Especially good for aspirin-induced asthma
Montelukast – can be given to pts under 5. Zafirlukast – only 5+

Front 726

Mechanism: Guaifenesin

Back 726

Stimulates vagus to decrease viscosity of secretions in bronchial tree

Front 727

Clinical use: Guaifenesin

Back 727

Expectorant. Removes excess sputum, but large doses necessary. Does not suppress cough reflex (need DXM, codeine [opioids] for that)

Front 728

DHFR inhibitors

Back 728

MTX, TMP, Pyrimethamine (used in eukaryotes, prokaryotes and protozoa respectively). Notice each has "meth" in it, and that THF is used to donate methyl groups

Front 729

Mechanism: Azathioprine

Back 729

is converted to 6-MP, which blocks PRPP Amidotransferase, blocking PRPP conversion into 5-P-ribosylamine (replacement of PPi with NH2) in purine synthesis

Front 730

Tx: Mucormycosis

Back 730

surgical debridement and amphotericin B

Front 731

Tx: anovulation

Back 731

Menotropins (human menopausal gonadotropin) - act like FSH - lead to production of one dominant follicle. Followed by one large dose of HCG - simulates LH surge

Front 732

Clinical use/mechanism: Menotropins

Back 732

Used in anovulatory infertility
Human menopausal gonadotropins - act like FSH - lead to production of one dominant follicle

Front 733

Clinical use/mechanism: HCG

Back 733

Used in anovulatory infertility. After menotropins create a dominant follicle, HCG is used to simulate an LH surge

Front 734

Which benzo has the shortest half-life (fastest acting)?

Back 734

Alprazolam - less than 12 hrs
Lorazepam - 10-15 hrs
Chlordiazepoxide, Clonazepam, Diazepam - 25-100 hours

Front 735

Mechanism: Pentazocine

Back 735

Opioid analgesic - partially agonistic and weakly antagonistic at mu receptors. Designed to be effective analgesic with little/no abuse potential. If given to pt with opioid addiction, can induce withdrawal Sx.

Front 736

Mechanism: Lamivudine

Back 736

cytosine analog NRTI. Must be phosphorylated to active lamivudine triphosphate form by intracellular kinases. Blocks HIV Reverse Transcriptase via DNA chain termination.

Front 737

Mechanism: Alpha glucosidase inhibitors

Back 737

miglitol, acarbose
Block disaccharidases, delaying carbohydrate absorption

Front 738

Mechanism: Digoxin

Back 738

75% bioavailability, 20-40% protein bound, half time = 40 hours, urinary excretion

Front 739

Clinical use: Digoxin

Back 739

CHF (increased contractility), a-fib (decreased conduction at AV node and depression of SA node)

Front 740

Clinical use: Bactericidal for gram+ve cocci, rods, gram-ve rods (Neisseria), spirochetes.

Back 740

Penicillins

Front 741

Mechanism of resistance against antitumor drugs

Back 741

Human multidrug resistance (MDR1) gene codes for P-glycoprotein, a transmembrane ATP-dependent pump protein with broad specificity for hydrophobic compounds. Normally expressed in gut epithelium, also in BBB, helping keep or flush out foreign substances.

Front 742

Mechanism: Zolpidem

Back 742

GABAa receptor agonist (similar mechanism to benzos). Rapid onset (15 min), metabolized by CYP450

Front 743

Clinical use: Zolpidem

Back 743

Short-acting hypnotic agent used for short term insomnia treatment. Less risk of tolerance/addiction/withdrawal symptoms than benzos. No anticonvulsant properties in regular doses. No muscle relaxing effects, not used for anesthesia