Trachte Rx Flashcards

1
Q

Paragyline

A

MAOI
a1
b1

increase BP

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2
Q

Cocaine

A
  • axoplasmic pump = block reuptake NE
    a1
    b1

increase BP

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3
Q

Imipramine

A

TCA
- axoplasmic pump = block reuptake NE
a1
b1

increase BP

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4
Q

Tyramine

A

reverse axoplasmic transporter = increase release NE
a1
b1

increase BP

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5
Q

Amphetamine

A

reverse axoplasmic transporter = increase release NE
a1
b1

increase BP

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6
Q

Ephedrine

A

reverse axoplasmic transporter = increase release NE
a1
b1

increase BP

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7
Q

Reserpine

A
  • granular pump = decrease accumulation NE = deplete NE

decrease BP

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8
Q

Guanethidine

A

induce NE release = deplete NE stores

decrease BP

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9
Q

Guanadrel

A

induce NE = release = deplete NE stores

decrease BP

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10
Q

Epinephrine

A

a1 VASOCNX
a2
b1
b2

increase BP

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11
Q

Norepinephrine

A

a1 VASOCNX
a2
b1

increase BP

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12
Q

Isoproterenol

A

b1
b2 RELAX SM

decrease BP

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13
Q

Phenylephrine

A

a1 VASOCNX

increase BP

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14
Q

Clonidine

A

a2 inhibit neural NE release

decrease BP

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15
Q

Alpha methyl Dopa

A

a2 inhibit neural NE release

decrease BP

antihypertensive safe for pregnancy

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16
Q

Guanabenz

A

a2 inhibit neural NE release

decrease BP

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17
Q

Dobutamine

A

b1 INCREASE HR AND FORCE

increase BP

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18
Q

Albuterol

A

b2 RELAX SM
some b1

decrease BP

bronchodilation

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19
Q

Metaproterenol

A

b2 RELAX SM
some b1

decrease BP

bronchodilation

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20
Q

Salmeterol

A

b2 RELAX SM
some b1

decrease BP

bronchodilation

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21
Q

Ritodrine

A

b2 RELAX SM

decrease BP

delay labor

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22
Q

Tertbutaline

A

b2 RELAX SM

decrease BP

delay labor

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23
Q

TPR =

A

8Lv/nr^4

r^4 is only variable

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24
Q

Terazosin

A

a1 ANTAGONIST

decrease vasocnx

decrease BP

25
Q

Propanolol

A

nonspecific b blocker

block b1: decrease HR and contractility
block b2: decrease bronchodilation (not as important)

decrease BP

26
Q

Metoprolol

A

b1 antagonist
b1 blocker

block b1: decrease HR and contractility

decrease BP

*specific to b1 = specific to heart

27
Q

Atenolol

A

b1 antagonist
b1 blocker

block b1: decrease HR and contractility

decrease BP

*specific to b1 = specific to heart

28
Q

a1

A

vascular SM contractility

VASOCONSTRICTION

29
Q

b1

A

1 heart = b1

increase HR and contractility

30
Q

a2

A

don’t need to care about it

inhibit neural NE release

31
Q

b2

A

2 lungs = b2
vascular SM relaxation

VASODILATION

BRONCHODILATION
decreased uterine tone

32
Q

Ceftriaxone

A

3rd gen cephalosporin
CELL WALL INHIBITOR
blocks transpeptidation fo peptidoglycan in bacterial cell walls

Tx: MSSA, strep, some gram (-)

33
Q

Vancomycin

A

CELL WALL INHIBITOR
binds D-ala-D-alanine to prevent transglycosylation

Tx: MRSA, broad gram (+)

34
Q

Empiric treatment of infectious endocarditis (according to PBL)

A

ceftriaxone and vancomycin

35
Q

Penicillin G

A

CELL WALL INHIBITOR
beta-lactam
binds pbp and blocks transpeptidation of peptidoglycan in bacterial cell walls

Tx: some gram (+), basically strep

36
Q

Treatment of most common cause of subacute IE

A

penicillin G

strep viridans = gram (+)

37
Q

Amoxicillin

A

CELL WALL INHIBITOR
AMINO-beta-lactam
binds pbp and blocks transpeptidation of peptidoglycan in bacterial cell walls

Tx: some gram (+) = mainly strep, some gram (-)

can still be inactivated by beta-lactamases, so give with clavulanate

38
Q

Clavulanate

A

beta-lactamase resistant

39
Q

Alteplase

A

t-PA
tissue plasminogen activator: converts plasminogen to plasmin –> break down fibrin clots

Tx: non-hemorrhagic stroke or clot (emboli or thrombi)

CONTRAINDICATED IN ENDOCARDIDITS

40
Q

Morphine

A

OPIOD PAIN RELEIVER/ANALGESIC
acts on mu receptors in three locations:
- presynatpic nociception pathway (blocks calcium pump –> blocks vesicle release)
- postsynatpic nociception pathway (increases K permeability –> blocks depolarization)
- presynatpic descending inhibitory pathway (blocks GABA release –> allos inhibior neuron firing and blocking nociception pathway)

41
Q

Nitroglycerin

A

VENOdilator
forms free radical NO -> activates guanylyl cyclase –> incrase cGMP –> increase MLC phosphatase –> increase MLC dephosphorylation –> SM relaxation –> VEINS vasodilate –> decreased blood returning to heart –> decrease preload

Tx: decrease myocardial activity and oxygen demand –> decrease ischemic damage

42
Q

Clopidogrel

A

ANTI-COAGULANT
INHIBITS PLATELET ACTIVATION
blocks ADP receptors on platelets –> inhibits platelet activation

Tx: post MI anticoagulation therapy

43
Q

Heparin

A

ANTI-COAGULANT
INHIBITS FIBRIN FORMATION
increases activity of antithrombin III –> Inhibits thrombin –> blocks conversion of fibrinogen to fibrin = NO CLOT

Tx: post MI anticoagulation therapy

44
Q

Eptifibatide

A

ANTI-COAGULANT
INHIBITS PLATELET AGGREGATION
binds GPIIb/IIIa receptor on activated platelets –> inhibits binding of fibrinogen –> block initiatino of coagulation cascade post-platelet plug

Tx: post MI anticoagulation therapy

45
Q

Aspirin

A

ANTI-COAGULANT
INHIBITS PLATELET AGGREGATION
irreversibly inhibits COX1/2 –> blocks production of TXA2 –> inhibits platelet aggregation

Tx: used IMMEDIATELY upon suspected MI UNLESS patient recently took aspirin

46
Q

Statins

A

INHIBIT CHOLESTEROL SYNTHESIS
inhibit HMG-CoA reductase
reduces plaque formation in vessels

Tx: dyslipidemia –> decrase atherosclerosis and risk of CAD

47
Q

ACE inhibitors

A

angiotensin converting enzyme inhibitor
SUPPRESSES RAAS system
suppresses RAAS system by inhibitng conversion of angiotensin I to angiotensin II –> decreased aldosterone release –> decreased Na reabsorption in kidney –> DECREASED BLOOD VOLUME AND PRELOAD

DECREASED VASOCNX –> DECREASED AFTERLOAD

Tx: post MI management, chronic CHF management

48
Q

Lisinopril

A

ACE inhibitor
suppresses RAAS system –> dec aldosterone –> DECREASE BLOOD VOLUME AND PRELOAD

DECREASED VASOCNX –> DECREASED AFTERLOAD

Tx: post MI, chronic CHF

49
Q

Enalapril

A

ACE inhibitor
suppresses RAAS system –> dec aldosterone –> decreased Na reabsorption in kidney –> DECREASED BLOOD VOLUME –> DECREASED PRELOAD

DECREASED VASOCNX –> DECREASED AFTERLOAD

Tx: post MI, chronic CHF

50
Q

Beta-blockers

A

block b1 receptors: MAIN ACTIVITY ON HEART:
DECREASE HR AND CONTRACTILITY
decrease myocaridal oxygen demand
decrease BP

Tx: MI to reduce ischemia, post MI, chronic CHF

*contraindicated in acute CHF (need to preserve heart function and complete diuresis first)

51
Q

Metoprolol

A

specific b1 blocker: block b1 receptors: MAIN ACTIVITY ON HEART:
DECREASE HR AND CONTRACTILITY
decrease myocaridal oxygen demand
decrease BP

Tx: MI to reduce ischemia, post MI, chronic CHF

52
Q

Propranolol

A

nonspecific beta blocker (blocks b1 and b2)
block b1 receptors: MAIN ACTIVITY ON HEART:
DECREASE HR AND CONTRACTILITY
decrease myocaridal oxygen demand
decrease BP

Tx: MI to reduce ischemia, post MI, chronic CHF

53
Q

Isosorbide dinitrate

A

same mech as NO

NO –> binds SM –> G-protein coupled receptor –> activates guanyly cyclase –> increase cGMP –> decrease intracellular Ca –> relaxes SM –> VENOdilator –> decrases preload

*longer half-life than NO (60-90 min)

54
Q

Hydralazine

A

increases NO synthesis in endothelium –> NO –> binds SM –> g-protein coupled receptor –> incrase cGMP –> dec intracell Ca –> relaxes SM –> VENOdilator –> decreases preload

*HIGHER SELECTIVITY FOR ARTERIOLES = decrease afterload

55
Q

Aldosterone Receptor Blockers

A

ARBs
Block aldosterone action –> decrease Na reabsorption in kidney –> DECREASES BLOOD VOLUME –> DECREASES PRELOAD

*causes an increase in aldosterone and renin plasma concentration = INHIBITION OF NEGATIVE FEEDBACK

56
Q

Eplerenone

A

ARB

block aldosterone –> decrease BV –> decreases preload

57
Q

Spirinolactone

A

ARB

blocks aldosterone –> decrease BV –> decreases preload

58
Q

Digoxin

A

Inhibits Na/K/ATPase

POSITIVE INOTROPE: increases CONTRACTILITY
NEGATIVE CHRONOTROPE: decreases HR