Boards Pharm

Front 1

Km

Back 1

reflects the affinity of the enzyme for its substrate; lower Km corresponds with incr affinity

Front 2

Vmax is proportional to what

Back 2

the enzyme concentration

Front 3

the velocity of a reaction is dependent on which 3 things

Back 3

concentration of enzyme, substrate and product

Front 4

effects of competitive vs. noncompetitive inhibitors

Back 4

competitive: have no effect on Vmax and incr Km, the lines also cross on a graph; non-compet: decr Vmac, no change on Km, don't cross on a graph

Front 5

vol of distribution

Back 5

Vd= amount of drug in body/plasma drug concentration

Front 6

where do drugs with low, med and high Vd distribute

Back 6

low: blood; med: extracellular space, body water; high: tissues

Front 7

drug clearence

Back 7

relates the rate of elimination to the plasma concentration; CL = rate of elimination/plasma drug concentration = Vd X Ke (elimination constant)

Front 8

how many half lifes must a drug be infused at a constant rate to achieve 94% of steady state

Back 8

4

Front 9

half life equation

Back 9

t1/2 = (0.7xVd)/CL

Front 10

bioavailability

Back 10

fraction of an administered drug that reaches the systemic circulation in a chemically unchanged form

Front 11

loading dose

Back 11

LD=(Cp x Vd)/F Cp is target plasma concentration, F is bioavailability

Front 12

maintenence dose

Back 12

MD = (Cp x CL)/F Cp is target plasma concentration, F is bioavailability

Front 13

changes in maintenece or loading doses in pts with renal or hepatic function

Back 13

decr maintenece, same loading

Front 14

zero order elimination and 3 examples

Back 14

rate of elimination is constant, regardless of C (constant amount of drug eliminated per unit time); Ex: phenytoin, ethanol, aspirin

Front 15

phase I vs. phase II metablism

Back 15

phase I: P450, reduction, oxidation, hydrolysis, usually yields slightly polar water soluble metablites which are often active still, this is lost first in geriatric pts; phase II: (conjugation) acetylation, glucuronidation, sulfation, usually yields very polar inactive metabolites which are renally excreted

Front 16

efficacy vs. potency

Back 16

efficacy: max effect a drug can produce (decr by noncompet antagonist); potency: amount of drug needed for a given effect (decr by competitive antagonist)

Front 17

partial agonist

Back 17

has a lower maximal efficacy as a full agonist, can have incr, decr or equal potency (its independent)

Front 18

therapeutic index

Back 18

TI=LD50 (median toxic dose)/ED50 (median effective dose); safer drugs have higher TI values

Front 19

what type of receptors are preganglionic SNS

Back 19

ACh N, PNS and D1 also

Front 20

what type of receptors are NACh and MACh

Back 20

NACh: ligand gated Na/K channels; MACh: G-protein coupled

Front 21

which adrenergic receptor is responsible for incr renin release

Back 21

B1

Front 22

which histamine receptor is responsible for pruritis and vessel permeability

Back 22

H1

Front 23

phospholipase C

Back 23

is activated by Gq 2nd messangers, converts lipids into PIP2 which breaks down into IP3 (which incr Ca) and DAG (activtes PKC)

Front 24

protein kinase A

Back 24

is activated by incr levels of cAMP and vice versa

Front 25

nonselective B blockers (5)

Back 25

propanalol, timolol, naldolol, pindolol, labetelol

Front 26

B1 selective blockers (5)

Back 26

"A BEAM" acebutolol (partial agonist), betaxolol, esmolol, atenolol, metoprolol

Front 27

non selective a and b blockers (2)

Back 27

carvedilol, labetelol

Front 28

partial B agonsts (of b blockers), (2)

Back 28

pindolol, acebutalol

Front 29

findings in lead poisoning

Back 29

lead lines on gingivae and on epiphysis of long bones (only heavy metal that can deposit here), encephalopathy and cerebral edema (related to incr vessel permeability and ALA build up which is toxic to neurons), RBC basophilic stippling, abdominal coloc, sideroblastic anemia, wrist and foot drops (causes demyelination), N/V

Front 30

P450 inducers (8)

Back 30

"Bosten Red Soxs Gotta Play Quality Competitions" to go up: barbituates, rifampin, St Johns wart, griseosulvin, phenytoin/phenobarbital, quinidine, carbamezepine

Front 31

P450 inhibitors (8)

Back 31

"I C(see) KEGS" going down: INH, cimentidine/cipro, Ketoconzale, erythromycin, grapefruit, sulfonamides

Front 32

drugs that cause SLE like syndrome (4)

Back 32

Its not HIPP to have lupus: hydralazine, INH, phenytoin, procainamide

Front 33

drug that causes tendonitis/tendon rupture/cartilage damage

Back 33

fluroquinilones

Front 34

drugs that cause coronary vasospasm (2)

Back 34

cocaine, sumatriptan (migraines)

Front 35

which drugs cause cutaneous flushing (4)

Back 35

niacin, Ca channel blockers, adenosine, vanco

Front 36

which drugs cause agranulocytosis (5)

Back 36

C3: clozapine, carbamexepine, colchicine; plus propythiouriil and methimazole

Front 37

drugs that cause pulm fibrosis

Back 37

bleomycin, busulfan, amiodarone

Front 38

what drug causes acute cholestatic hepatitis

Back 38

macrolides

Front 39

which drugs cause gynecomastia (5)

Back 39

"some drugs cause awesome knockers": spironolactone, digitalis, cimentidine, alcohol (chronic use), ketoconazole

Front 40

what drugs cause interstitial nephritis (3)

Back 40

methicillin, NSAIDs, furosimide

Front 41

fomepizole

Back 41

inhibits alcohol dehydrogenase