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Pharm Oral > Catecholamines > Flashcards

Catecholamines Flashcards

1
Q

Epi class

A

endogenous catecholamine that is nonselective adrenergic agonist

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2
Q

Epi MOA

A

binds to alpha1/2 and b1/2 receptors equally- activating g coupled protein receptors to increase cAMP causing an influx of intracellular Ca2+ causing agonist effects

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3
Q

Epi se

A

tachycardia, angina, arrhythmias, HTN, decrease RBF, vasoconstriction of- skin, Gi tract, muscle, liver and kidneys. gangrene in digits, hypoglycemia

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4
Q

Epi ci

A

caution in DM, hyperthyroid, pheochromocytoma, glaucoma, caution in pregnancy. Decrease LA absorption. avoid in peripheral LA blocks in fingers and toes

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5
Q

Epi PK

A 
Onset 1-2 min
DOA 5-10 min
E1/2t 30 sec
Small vd= poor lipid solubility
reuptake or diffusion primary way drug gets out of system then metabolized by Catechol-o-methyltransferase (COMT) and monoamine oxidase enzymes biotransformations in blood, liver, kidneys

Metabolites Excreted in urine

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6
Q

epi dose

A

anaphylaxis- 0.1-1mg. 1mg q3-5min for CV arrest ACLS, 1-2mcg/min beta2 (asthma); 4-5mcg/min beta1 (poor co), 10-20mcg/min alpha and beta

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7
Q

NE/Levophed class

A

direct acting endogenous catecholamine and adrenergic agonist- sympathomimetic

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8
Q

NE MOA

A

binds to alpha 1 and 2 receptors and b1- lacks B2 and activates g coupled protein receptors to increase cAMP causing an influx of Ca2+ causing an agonist effect and increase contractility; potent vasoconstrictor; when it increase BP= causes baroreceptor activation and drops HR and increase SVR preserves coronary and cerebral BF in decrease BP; decrease venous return- CO and HR; low dose causes increase HR/CO; alpha at high doses

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9
Q

NE Pk

A

onset rapid; DOA 5-10min; E1/2 2.5min; reuptake or diffusion primary way metabolized then by MAO and COMT. excreted in urine

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10
Q

NE SE

A

increase SBP, DDBP, MAP; decreases HR bc baroreceptor activation, decrease RBF, HBF and splanchnic BF; organ ischemia and necrosis of extremities and digits

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11
Q

NE CI

A

pheochromocytoma, caution in liver and renal disease; MAOi’s and TCAs, hypovolemai, thrombosis

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12
Q

NE dose

A

4-16mcg/min IV

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13
Q

Dopamine class

A 
dopamine/adrenergic  agonist; sympathomimetic endogenous precursor of NE 
Preg class C
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14
Q

DA MOA

A

stimulates all adrenrgic receptors including DA receptors. extracted from L-dopa on catecholamine synthesis of tyrosine; small doses- DA effects- vasodilation by stimulation of adenyl cyclase-> increasing level of cAMP in vascular SM (renal, coronary and mesenteric beds); medium doses= beta causing increased myocardial contraction and increase HR; large doses= alpha and beta effects causing vasoconstriction of all vascular beds including renal increasing BP, CO, SVR; also increase endogenous NE release (doesn’t work well with decreased catecholamine stores)

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15
Q

DA PK

A

Does not cross BBB, onset rapid, DOA 5-10min; E1/2 2 min; metabolized and elimated by MAO and COMP to 75% inactive and 25%NE. Must protect from light

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16
Q

DA SE

A

tachycardia, arrhythmias, angina, extravasation, N/V, increased IOP and UOP, widen qrs

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17
Q

DA CI

A

right HF, pheochromocytoma, thyroid storm, IOP, caution in CAD/post MI, sulfa allergy. Should not be used with methyldopa, non selective bb, tcas, and MAOIs

synergistic with Dobutamine to decrease SVR and increase CO (Da dilates cutaneous vascular beds while Dobutamine dilates other vascular beds)

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18
Q

DA dose

A

DA1- low dose 1-3mcg/kg/min ( increase GFR, RBF, UOP); beta 1 medium dose 3-10 mcg/kg/min; alpha large dose 10mcg/kg/min

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19
Q

Dobutamine class

A

sympathomimetic; synthetic catecholamine-synthetic analog of isoproterenol

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20
Q

Dobutamine MOA

A

beta 1 selective agonist and weak beta 2 and alpha 1; binds to receptor and activates G protein receptors in increase cAMP causing an influx of Ca2+= increase contractility and CO without increase HR or Bp too much (good for CHF)

21
Q

Dobutamine PK

A

onset 1-2 min; DOA 5-10min, e1/2 2 min, metabolized and eliminated by MAO and COMT reuptake or diffusion away from active site

22
Q

Dobutamine SE

A

minimal increase HR (weak activity at SA node), arrhythmias, angina, HTN, platelet inhibition, thrombocytompenia, coronary artery and pulmonary vasodilator, N, phlebitis

23
Q

Dobutamine CI

A

avoid in hypertrophic cardiomyopathy, MAOis, TCAs, caution in CAD and MI (ok for CHF); not good if need an increased SVR

24
Q

Dobutamine dose

A

Typical dose 2-10mcg/kg/min; (max is 40)

Beta15mcg/kg/min

25
Q

Vasopressin class

A

exogenous antidiuretic peptide and vasopressor

26
Q

Vasopressin MOA

A

vasoconstricts by stimulating the V1a receptors on vascular SM, glomerular efferent arteriole, mesangial cells and vasa recta. Works on V2 receptors in the collecting tubules by stimulating g coupled protein receptor adenylyl cyclase= ATP= cAMP= activates protein kinase that stimulates the vesicles containing aquaporin water channels to be come active and retain water.

27
Q

Vasopressin PK

A

onset fast; e1/2 10-20 min; metabolized by tissue peptidase and urinary excretion

28
Q

Vasopressin SE

A

angina, CA spasm, arrhythmias, increased peristalsis, N/V, abd pain, EKG changes, increase BP, bronchial constriction

29
Q

Vasopressin Ci

A

HTN, CAD (caution), renal disease, NSAIDS increased effect

30
Q

Vasopressin dose

A

40 units IVP for CV arrest ACLS; 20 units for varices; 0.04U/min gtt for sepsis

31
Q

isoproterenol class

A

synthetic catecholamine

32
Q

isoproterenol MOA

A

B1>B2; minimal alpha (cardiac pacemaker), acts on Gproteins to increase cAMP causing an influx of Ca2+ causing increase in contractility with NO change in SVR (can increase HR) , increases SBP, profound decrease DBP with no change in MAP; also is a pulmonary and systemic arterial vasodilator from B2 actions used to treat bronchospasm; used for HB especially 3rd degree, bradyarrhythmias, BB OD

33
Q

isoproterenol PK

A

onset rapid; DOA 5-10min; e1/2 3-5mi; metabolized and eliminated rapidly by COMT in liver and pulmonary with 50% elimated unchanged in the urine

34
Q

isoproterenol SE

A

bradycardia, angina, arrhythmias, decrease CA BF secondary to decrease DBP; B2 effects- peripheral vasodilation and hypotension; B1= increased contractility of the heart and increases o2 demand

35
Q

isoproterenol CI

A

HTn, CAD (increases demand), pheochromocytoma, thyroid stomr, MI, hyper tropic cardiomyopathy, tachycardia, dig toxicity

36
Q

isoproterenol dose

A

0.5-10mcg/min

37
Q

ephedrine class

A

synthetic NON-catecholamine; direct and indirect (primarily) adrenergic agonist

38
Q

ephedrine MOA

A

indirectly affects alpha and beta receptors by stimulating NE release; directly acting on b1 (increase myocardial contractility); increase SBp, DBP, CO and HR; increase CA and skeletal muscle BF; venous>arterial constriction; decrease HBF and splanchnic BF

39
Q

ephedrinePK

A

onset rapid; DOA 1hr; E1/2 3hrs; slower/resistant to MAO metabolism since lacking catecholamines so slower metabolism and excreted 40% unchanged in the urine

40
Q

ephedrine SE

A

arrhythmias, HTN, MI, CNS stimulation, decrease uterine activity; can cause tachyphylaxis

41
Q

ephedrine CI

A

HTN, CAD, MAOis, TCAs, cocaine, caution in trauma, ephedra

42
Q

ephedrine dose

43
Q

phenylephrine class

A

direct acting synthetic NON-catecholamine selective alpha 1 agonist

44
Q

phenylephrine MOA

A

direct stimulation of alpha 1 receptors with venous>arterial constriction, increase MAP, SBP, DBP, SVR and decrease in HR and CO (baroreceptors),

45
Q

phenylephrine PK

A

90%PB, onset <1min, DOA 5-20min, e1/2 2.5hours; metabolized by MAO to phenolic and conjugates excreted in the urine 90%

46
Q

phenylephrine SE

A

rebound nasal congestion, bradycardia, HTN, arrhythmias, decrease RBF and splanchnic BF= decrease UOP; metabolic acidosis

47
Q

phenylephrine CI

A

HTN, arrhythmias, CHF, glaucoma, cocaine, ephedra

can prolong LA

48
Q

phenylephrine dose

A

50-200mcg IVP; 20-50mcg/min gtt- double dilute

Pharm Oral (10 decks)

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