Pharm Part Ii

Front 1

Effects of Phenlephrine

Back 1

a-1 agonist - mydriasis w/o cycloplegia

Front 2

clonidine

Back 2

pre & post synaptic a-2 adrenoreceptor agonist

Front 3

ritodrine

Back 3

b-2 agonist , dec uterine contraction in premature labor

Front 4

Epi + b-blocker (propanolol)

Back 4

only a affects (increased BP)

Front 5

Epi effects

Back 5

inc skeletal muscle BF, dec skin, renal & GI BF, inc HR, inc dp/dt, inc CO, SBP, PP; dec DBP

Front 6

what happens if pre-tx w/ reserpine?

Back 6

no indirect adrenergic agonist effects

Front 7

Tyramine containing foods contraindicated w/ which rx's?

Back 7

Phenelzine, tranycypromine (MAOi's)

Front 8

methylphenidate

Back 8

tx ADHD/ADD
s/e- depression, insomnia, decreased appetite, linear growth rate

Front 9

Amphetamine toxicity

Back 9

nervous, excited, agitated, inc HR/BP, toxic psychosis - paranoid schizo, formication w/ excoriations, convulsion w/ OD; difficult to distinguish from effects of cocaine

Front 10

Psychosis tx due to amphetamine OD

Back 10

chlorpromazine

Front 11

ephedrine

Back 11

direct b1, b2, indirect a, no a after reserpine

Front 12

Alpha blockers

Back 12

3 P's - phentolamine, prazosin, phenoxybenzamine

Front 13

partial a agonists

Back 13

ergotamin, dihydroergotamine

Front 14

tx of migraine

Back 14

ergotamine, dihydroergotamine

Front 15

a1a receptor blocker in GU tract

Back 15

tamsulosin (BPH)

Front 16

b1 blockers

Back 16

atenolol, metroprolol

Front 17

b1, b2 blockers

Back 17

propranolol, timolol

Front 18

see charts on page 4 - 5

Back 18

see charts on pg 4-5

Front 19

what is angina

Back 19

dec O2 requirement via dec dp/dt & HR, but LV_EDV inc

Front 20

b blocker heart effects

Back 20

dec HR, AV conduction, dp/dt

Front 21

how do b-blockers dec O2 demand?

Back 21

dec HR, dp/dt and afterload (DBP)

Front 22

Nitroglcyrine efects

Back 22

dec O2 demand by dec VR and LV-EDV

Front 23

S/E of b-blockers

Back 23

CHF, bronchospasm, AV block, delayed recovery of glucose conc in T1DM after sc injection of too much insulin

Front 24

Timolol

Back 24

dec IOP w/o cycloplegia (propanolol causes local anesthesia of cornea)

Front 25

b-blocker w/drawal sx

Back 25

tachycardia, palpitations, tremor, chest pain (DON'T D/C b-blocker w/o consulting MD first)

Front 26

propanolol effects on hyperthyroidism

Back 26

dec tachycardia, termor and prevent peripheral conv of T4 to T3

Front 27

T1DM tx w/ gluacoma drug which causes hypoglycemia. Which drug was given?

Back 27

timolol

Front 28

Reserpine

Back 28

decreased nerve-stimulated NE release. No effect of TAP drugs (tyramine, amphetamine, phenylpropanolamine) after pre-tx w/ reserpine, no a effects of ephedrine after pre-tx

Front 29

guanethidine

Back 29

1) decrease nerve-stimulated NE release 2) comp inhibitor of NE uptake 3) anit-HT effect blocked by TCA's b/c TCA's block entery of guanethidine into neuron

Front 30

Cocaine

Back 30

1) blocks uptake1 of NE, Epi, DA, 5-HT in CNS
2) blocks uptake1 in peripheral sympathetic neurons - potentiates effects of NE and Epi, but not isoproterenol (ISO)
3) Euphoria via release of DA in nucleus accumbens
4) local anesthetic effect via blockade of Na+ channels in sensory neurons
5) toxic doses/OD = dilated pupils, euphoria, hallucinations, excitation, halo vision, itchy skin, ↑ BP/HR, convulsions - difficult to distinguish from amphetamine toxicity/OD
6) withdrawal syndrome = sleepiness, depression, anhedonia

Front 31

MAOi's

Back 31

phenelzine(A&B), tranylcypromine (A&B), selegeline (MAO-B)

Front 32

cheese rxn w/ maoi's

Back 32

HT & Tachycardia, inhibition of MAO-A in gut wall allows dietary tyramine to enter circulation; tyramine releases NE

Front 33

see page 7-8 for charts

Back 33

see page 7-8 for charts

Front 34

clonidine and alpha-methyldopa (α-MD)

Back 34

antihypertensive:
↓ SNS activity via stimulation of α2-receptors in CNS: ↓ plasma NE & renin activity (PRA) , HR
- S/E = sedation, dry mouth, edema, hepatitis, “flu” syndrome, (+) Coomb’s test
- clonidine withdrawal syndrome = sweating, ↑ HR, abrupt return of BP to HT value, abdominal pain, tremor, headache, apprehension (differs from β-blocker withdrawal syndrome =↑ HR with palpitations but no sweating, abdominal pain or↑ BP)

Front 35

Drugs that decrease plasma NE

Back 35

clonidine, α-MD, guanethidine, reserpine, ganglionic blockers

Front 36

Drugs that increase plasma NE

Back 36

alpha blockers, hydralazine, minoxidil, diazoxide, nifedipine, HCTZ, sodium nitroprusside

Front 37

Arterial vasodilators

Back 37

hydralazine, minoxidil, diazoxide
- dilate resistance vessels = ↓ TPR & BP; ↑ HR, dP/dT, CO , PRA and plasma NE

Front 38

S/E - hydralazine

Back 38

edema ;SLE = arthralgia, arthritis, fever, malar (butterfly) rash, glomerulonephritis- d/c hydralazine and tx with steroid

Front 39

minoxidil s/e

Back 39

hirsutism, effect additive w finasteride; edema

Front 40

s/e diazoxide

Back 40

inhibition of insulin release = hyperglycemia; edema

Front 41

Drugs for HT emergency

Back 41

diazoxide, sodium nitroprusside (SNP), labetalol (fenoldopam on USMLE World)

Front 42

sodium nitroprusside (SNP)

Back 42

1) dilates arteries and veins via release of nitric oxide (NO) from SNP molecule
2) balanced vasodilation, NT patient = decreases TPR and venous retrun → CO = n.c. CHF = decreases preload and afterload → leads to increase in CO
3) review thiocyanate (tx w thiosulfate) and CN (tx w nitrite/thiosulfate) toxicity thiocyanate toxicity after SNP infusion in patients w poor renal function = muscle weakness, & spasm, disorientation

Front 43

Ca++ blockers

Back 43

nifedipine, diltiazem, verapamil

Front 44

Ca++ blockers MOA/use

Back 44

) block Ca++ channels at SA/AV nodes, cardiac myocytes, arterial VSM
2) decrease in BP: the -pine drugs cause a greater fall in BP than diltiazem & verapamil
3) verapamil and diltiazem decrease AV conduction via (increase in ERP) & HR
4) the -pine drugs have no effect on AV conduction or HR (HR may increase slightly)
5) angina - decrease oxygen demand (decrease dp/dt, HR and afterload) w increased
oxygen delivery via dilation of coronary arteries and arterioles
6) tx uses: HT, exertional and vasospastic angina, AV nodal re-entry tachycardia (V+D)

Front 45

Drugs which dec dP/dT

Back 45

β-blockers, Ca++ blockers, diisopyramide

Front 46

Effects of Ang II

Back 46

↑ BP, increases SNS activity via CNS, presynaptic enhancement of
NE release, blocks NE uptake1, release of ADH, release of aldosterone, decreases mesenteric BF.

Front 47

Drugs which decrease mesenteric BF to tx GI bleeding

Back 47

NE & Ang II (get escape), ADH (a.k.a. AVP) & octreotide (no escape)

Front 48

ACE inhibitors =

Back 48

captopril, enalapril, prevent conversion of Ang I to Ang II

Front 49

ARBs

Back 49

the -sartans block Ang II rceptors

Front 50

ACEi effects

Back 50

) decrease TPR and BP with no change in HR and CO
2) block formation of Ang II, block enzymatic destruction of bradykinin (BK)
3) S/E = fetal toxicity (category X) , K+ retention, cough; cough caused by BK & PG and
is blocked by aspirin (ACEI’s block metabolism of bradykinin)
4) ACEI’s potentiate the decrease in BP caused by i.v. bradykinin
5) ACEI's increase the plasma concentration of BK

Front 51

losartan

Back 51

ARB...NO COUGH

Front 52

MOA in tx of CHF =

Back 52

increase CO by decreasing preload and afterload; reverses cardiac remodeling caused by angiotensin II (ang II)

Front 53

HT patient with DM

Back 53

- tx w ACEI to↓ BP and ↓ proteinuria (protects kidneys)

Front 54

Pt w DM & microalbuminuria

Back 54

Tx wACEI or -ARB or BOTH to ↓ proteinuria