Fa - Pharm Part 9

Front 1

Metronidazole mech:

Back 1

DIRECT breaking of DNA

Front 2

SMX mech =

Back 2

PABA analog

Front 3

mech of Pyrimethamine:

Back 3

same as TMP and MTX - DHFR inhibitor

Front 4

Choloroquine kills Plasmodium inside RBC’s, then primaquine:

Back 4

kills them in other tissues

Front 5

3 cardio drugs that improve mortality rates:

Back 5

1. ACEI's

2. B-blockers

3. aspirin (right after MI)

Front 6

Thiazides are recommended for recovering MI pts:

Back 6

WITHOUT DM or CHF

- if with, use ACEI's

Front 7

ACEI's not only lower BP, but also:

Back 7

inhibit myocardial remodeling that would occur with aldo

Front 8

"inc. lipids" of Thiazides ~~

Back 8

chol *and* LDL

Front 9

remember that unless they are K+-sparing, diuretics cause:

Back 9

hypoK+

Front 10

nitrates can lead to a reflexive tachycardia b/c:

Back 10

they cause a relative hypotension that the body responds to with SNS/cat's

- B-blockers don't have this problem

Front 11

Lidocaine (class IB) is specific for:

Back 11

rapidly-depolarizing or already-depolarized cells, which ischemic myocardium is

Front 12

Isosorbid mononitrate has:

Back 12

~100% bioavailability

(a nitrate)

Front 13

Digoxin treats:

(2)

Back 13

a-fib,

a-flutter

- a cardiac glycoside

Front 14

ACEI's, nitrates, Ca2+-blockers, and a1-antagonists ALL:

Back 14

cause reflex tachy after they vasodilate

Front 15

combining B-blockers with non-dihydropyridine Ca2+ blockers (Verapamil, Diltiazem) =>

(2)

Back 15

SEVERE bradycardia and hypotension

Front 16

Amiodarone and Sotalol also:

Back 16

lower HR

Front 17

3 low-potency SE’s can be explained by:

Back 17

1. anticholinergic

2. anti-H

3. a1-blocking effects

Front 18

Succinylcholine =

Back 18

depolarizing NMJ blocker

- catabolized by PLASMA cholinesterases

- [Neostigmine] will augment it during Phase 1,
but will reverse it during Phase 2/train of 4

- by leaving ACHE's to allow for more ACH

Front 19

Tubocurarine =

Back 19

nondepol NMJ blocker

- like Pancuronium
- ACH antagonists

- overcome by [Neostigmine], which causes there to be more ACH to compete with them

Front 20

***mechanism of Digoxin:***

Back 20

inhibits Na+/K+ channels in pacemaker cells

=> increase in intracellular Na+

=> decrease Na+/Ca2+ channel activity

=> dec. Ca2+ efflux

=> more Ca2+ inside

=> inc. contractility

Front 21

why is hyperK+ a SE of Digoxin toxicity?

Back 21

b/c Digoxin competes with K+ for the Na/K pump

=> if Digoxin wins, K+ cannot be brought into cardiac cells

=> hyperK+

Front 22

**how does Digoxin/digitalis block the AV node?

Back 22

it binds in the CNS ==> increases vagal tone, dec. SNS

Front 23

tx of HSV =

Back 23

-cyclovirs

Front 24

tx for excess copper =

Back 24

Penicillamine

Front 25

mechanism of TZD's:

Back 25

activate PPAR-y

=> dec. insulin R

Front 26

**MAOI's are best for:

(2)

Back 26

1. atypical depression

2. tx-refractory depression
(e.g. already tried SSRI's)

Front 27

glucocorticoids are primarily:

Back 27

catabolic

- but in the liver, they inc. proteins for GNG, glycogenesis

(proteolytic at skeletal muscle; => inc. BUN)

Front 28

thiopental =

Back 28

general IV anesthetic (actually a Barb)

- highly lipid-soluble => acts incredibly fast on the brain

- but then redistributed to skeletal muscle and adipose => pt wakes up

Front 29

clinically, Selegiline is used to:

Back 29

delay the progression of Parkinson's

Front 30

lipophilic drug ~~

(3)

Back 30

high Vd,

good penetration into the CNS,

preferentially processed in the liver

(not excreted well by the kidney)

Front 31

acyclovir can cause:

Back 31

crystalline nephropathy without aggressive IV hydration

Front 32

clavulanic acid, sulbactam, and tazobactam are all:

Back 32

B-lactamase inhibitors

Front 33

SE's of L-dopa:

Back 33

anxiety and agitation

- due to DA action
- can actually increase with Carbidopa, b/c DA conc. increases

- W/O Carbidopa, n/v

Front 34

Foscarnet inhibits:

(3)

Back 34

1. DNAP

2. RNAP

3. Reverse Transcriptase

- does NOT need to be activated - just gets to it

- administered IV

Front 35

Oseltamivir =

Back 35

neuraminidase inhibitor

- against BOTH influenza A and B (unlike Amantadine/uncoating)

= "-mivir's"

Front 36

remember that Foscarnet SE's ~~

Back 36

nephrotoxicity,

electrolyte abnormalities

Front 37

Zolpidem =

Back 37

non-Benzo hypnotic with lower chance of tolerance

Front 38

SE's of Succinylcholine:

(2)

Back 38

1. Malignant Hyperthermia

2. severe hyperK+
(in pts with burns, myopathies, denervation)

Front 39

mechanism of Succinylcholine:

Back 39

first, depolarizes Na+ channels at the post-synaptic terminal

- then, inactivates them (phase II)

Front 40

Baclofen =

Back 40

muscle relaxant that affects GABA-B channels at the SC

Front 41

Vecuronium =

Back 41

non-depolarizing NMJ blocker

- like Atracurium

Front 42

atypical T-lymphocytes are:

Back 42

reactive CD8+ lymphocytes

- much larger than normal

- release in response to virally-infected B-cells (e.g. EBV)

- plentiful cytoplasm, edges conform to shapes of cells around them

Front 43

why is Primaquine added to Chloroquine?

Back 43

Chloroquine kills P. vivax or ovale in the infected RBC's of the blood,

while Primaquine kills off the vivax or ovale that initially infected the liver hepatocytes

=> Primaquine prevents relapses

Front 44

first-line agents for status epilepticus =

Back 44

Benzo's + Phenytoin [to prevent recurrence]

- so Benzo's are first-line tx, Phenytoin = prophylaxis (prolongs inactivation)

- Phenobarbital if those don't work

Front 45

Colchicine blocks MT polymerization; what does this do?

Back 45

**blocks leukocyte chemotaxis and phagocytosis**

- keeps WBC's from causing pain by reacting to MSU

Front 46

d.o.c. for oropharyngeal Candida =

Back 46

Nystatin

- directly binds ergosterol, ruins cell wall
(like Daptomycin, Polymyxin in bact.)

Front 47

Pentamidine treats:

Back 47

PCP pneumonia

Front 48

IFN-a treats:

(5)

Back 48

1. HBV

2. HCV

3. HCL

4. condyloma acuminatum

5. Kaposi's

Front 49

acyclovir is best for:

Back 49

HSV infs

Front 50

Flucytosine/ 5-FU best for:

Back 50

fungal inf's, like Cryptococcus

Front 51

addition of Spironolactone to HF therapy shows:

Back 51

improvement in morbidity and mortality

- **aldo is what causes ventricular remodeling and cardiac fibrosis**

Front 52

Phenoxybenzamine =

Back 52

long-acting alpha blocker

- used for Pheo

Front 53

Infliximab =

Back 53

TNF-a inhibitor

Front 54

Thiazides are more likely to cause:

Back 54

hyponatremia, hypercalcemia

- loops lose Ca2+

Front 55

COX 1 and 2 are normally:

Back 55

NOT detectable in tissue

- only come out during inflammation

Front 56

3 most notorious causes of necrotizing fasciitis:f

Back 56

1. S. aureus

2. GAS

3. Clostridium perfringens



~~ sudden and severe pain at site of wound
=> hypotension

- must debride

Front 57

GAS not only causes necrotizing fasciitis, but is also:

Back 57

PYR-positive

(replaces Bacitracin)

Front 58

hypertensive crises are associated with:

Back 58

MAOI's

- wine and cheese, sausage

- tyramine is a sympathomimetic

- accumulates, floats out into bloodstream

Front 59

one possible tx for psoriasis =

Back 59

topical Vit. D (Calcipotriene, Tacalcitol)

- inhibits keratinocyte prolif, stimulates differentiation

Front 60

**halos in TB tx =

Back 60

Ethambutol

- includes vision loss, color changes

= all optic neuritis

Front 61

mech. of Ethambutol:

Back 61

inhibits carbohydrate polymerization [by inhibiting arabinosyl transferase]

=> prevents peptidoglycan wall synthesis

Front 62

mech of INH =

Back 62

inhibition of mycolic acid SYNTHESIS

Front 63

mech of Echinocandins:

Back 63

inhibit glucan (polysaccharide) synthesis

=> prevent cell wall formation

Front 64

Nystatin and Amphotericin B are equivalent to:

Back 64

Daptomycin and Polymyxin

- bind ergosterol, cause pore formation => cell death

Front 65

mech of Azoles:

Back 65

inhibit SYNTHESIS of ergosterol

Front 66

role of carbonic anhydrase at the kidney:

Back 66

ultimately allows NaHCO3 reabsorption, with **concurrent H+ excretion**

Front 67

mech and consequences of Acetazolamide:

Back 67

blocks carbonic anhydrase at the PCT

=> HCO3 not reabsorbed

=> remains in tubule

=> water follows

- meanwhile, body does not have HCO3 to buffer H+

=> blood pH becomes acidic

Front 68

Acetazolamide treats:

Back 68

ICP, glaucoma (both types)

(decrease volume in the former, decrease production of aqueous humor via anhydrase in the latter)

Front 69

1st-line for GAD =

Back 69

SSRI's

Front 70

short-acting Benzo's are useful for:

Back 70

minimizing daytime fatigue and impaired judgment

Front 71

2 short-acting Benzo's:

Back 71

1. Triazolam

2. Alprazolam

Front 72

intermediate-acting Benzo:

Back 72

Lorazepam

Front 73

long-acting Benzo's:

(3)

Back 73

1. Diazepam

2. Flurazepam

3. Chlordiazepoxide

Front 74

Phenelzine inhibits MAO's by:

Back 74

IRREVERSIBLE binding

- need to wait a couple of week for new MAO's to be made before starting SSRI's,

to avoid SER syndrome (no reuptake, no degradation = too much SER)

Front 75

problem with 1st-gen antiH's =

Back 75

sedation

e.g. Chlorpheniramine

Front 76

statin SE's =

Back 76

1. myopathy

2. hepatotoxicity
(as do all other lipid-lowering drugs except Fibrates)

rhabdo is rare

Front 77

mech. of loop diuretics:

Back 77

block Na/K/2Cl symporters at the thick ascending limb (impermeable to water)

=> loss of Na+, Cl, and water

Front 78

3 SE's of loops:

Back 78

1. hypoK+

2. hypoMg2+

3. hypoCa2+

Front 79

Vit A is a great tx for:

Back 79

measles

Front 80

unlike neuroleptics, atypical/2nd-gen antipsychotics improve:

Back 80

BOTH positive AND negative symps of schizophrenia

- 1st-gen only improve positive symps

Front 81

2 SE's of nitrates:

Back 81

1. facial flushing

2. HA's

Front 82

remember that B-blockers can treat:

Back 82

hyperthyroid symps,

by opposing thyroid's sympathetic activation

Front 83

remember that Protease inhibitors are used in:

Back 83

HIV

Front 84

steroids in osteoarthritis are:

Back 84

intraarticular,

and don't cause systemic effects like fat redistribution

Front 85

TCA's (Doxepin, "-tylines," "-pramines") have really strong:

Back 85

anticholinergic properties

(remember the 4 class blocking effects)

Front 86

TCA's are commonly used for:

Back 86

painful diabetic retinopathy

Front 87

Naloxone =

Back 87

opioid antagonist

(binds mu > k or d)

- respiratory and cardiac depression occurs at mu channels

Front 88

Glutamate (excitatory) binds to:

Back 88

NMDA r'

- Ketamine et al. block NMDA

Front 89

2 SE's of Vit. A:

Back 89

1. hyperTG

2. teratogen

Front 90

1st-line for myoclonic sez's =

Back 90

Valproic acid

(2nd-line for absence sez's, 1st for all generalized)

Front 91

1st-line for all partial sez's =

Back 91

CBZ

Front 92

Clonidine =

Back 92

anti-sympathetic

- treats HTN, ADHD

Front 93

Baclofen =

Back 93

muscle relaxant that imitate GABA

Front 94

mainstay for acute mania =

Back 94

Li2+ / Valproic acid / CBZ

+

atypical antipsychotic

Front 95

major, rare complication of antithyroid drugs =

Back 95

agranulocytosis

(M, PTU)

- get a WBC count with differential

Front 96

PTU is used more often than Methimazole b/c it:

Back 96

inhibits peripheral conversion of T4 to T3,

and isn't teratogenic like Methimazole

Front 97

Calcineurin =

Back 97

essential protein in the activation of IL-2 ==> CD8+'s

- Cyclosporine and Tacrolimus inhibit Calcineurin

Front 98

Class IC anti-arrhythmics are USE-dependent:

Back 98

prolong the QRS more at higher HR's,

e.g. exercise

- also prolong QT interval more the slower the HR is

Front 99

B1-blockers, Digoxin, and Class IV's do NOT:

Back 99

affect the length/width of QRS

Front 100

Hep A infection ==>

Back 100

hepatocyte ballooning (swelling) and eosinophilic apoptosis (Councilman bodies)