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Year 2 Pharmacology > Autonomic pharmacology V > Flashcards

Autonomic pharmacology V Flashcards

1
Q

EPI is a potent stimulant of which receptors?

A

alpha and beta

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2
Q

why are the effects of EPI so complex?

A

dose dependent, route dependent

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3
Q

what are the cardiac effects of small IV doses of EPI?

A

B1 - increase PP, HR, SV, CO

B2 - decreased TPR

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4
Q

what are the cardiac effects of moderate IV doses of EPI?

A

B1 - increase PP, HR, SV, CO
B2 - decrease TPR, DBP
a1 - increase TPR, BP

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5
Q

what are the cardiac effects of high IV doses of EPI?

A

a1 - increase TPR, BP (potential reflex bradycardia)
B1 - increase PP, HR, SV, CO
B2 - decrease TPR, DBP

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6
Q

what is EPI reversal phenomenon?

A

because EPI activates both alpha and beta receptors, if you block either prior to EPI administration then the effect on remaining unblocked receptors will be much more pronounced

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7
Q

how does EPI reversal phenomenon affect the heart when alpha receptors are blocked?

A
  1. increased EPI induced vasodilation
  2. decrease TPR
  3. decrease MAP
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8
Q

how does EPI reversal phenomenon affect the heart when beta receptors are blocked?

A
  1. EPI induced vasoconstriction unmasked

2. LARGE increase in MAP

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9
Q

what is the main vascular site of action for EPI?

A

arterioles and precapillary sphincters

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10
Q

how does EPI affect cutaneous blood flow?

A

decrease (large)

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11
Q

how does EPI affect skeletal muscle blood flow?

A

increase

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12
Q

how does EPI affect renal blood flow? fractional flow?

A
  1. decrease

2. increase (large)

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13
Q

how does EPI affect the GFR?

A

no effect

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14
Q

how does EPI affect renin secretion? via what receptor?

A

increase (via B1)

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15
Q

how does EPI affect pulmonary blood flow?

A
  1. increase PAP

2. increase PVP

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16
Q

how does EPI affect coronary blood flow?

A

increase (relative diastole and aortic pressure and metabolic stimulation)

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17
Q

how does EPI affect inotropy, lusitropy, and chronotropy?

A

inotropy - increase

lusitropy - increase

chronotropy - increase

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18
Q

how does EPI affect overall cardiac oxygen consumption?

A

increase

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19
Q

the increase in BP by EPI is due to what mechanism?

A

a1 activation on vascular smooth muscle

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20
Q

which receptors are more important to pay attention to during shock - alpha or beta?

A

alpha - vascular effects

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21
Q

what are the adverse effects of EPI toxicity?

A
  1. throbbing headache, tremor, palpitations
  2. cerebral hemorrhage
  3. arryhthmias
  4. angina (CAD)
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22
Q

what are the contraindications to EPI use?

A

beta blockers

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23
Q

what are the therapeutic uses for EPI?

A
  1. hypersensitivity
  2. cardiac arrest
  3. local anesthetic
  4. post-extubation croup, viral croup
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24
Q

why doesn’t NE produce vasodilation?

A

no B2 activation

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25
Q

what receptors does NE stimulate?

A

B1 (same as EPI)

alpha (less than EPI)

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26
Q

how does NE affect BP?

A
  1. increase SBP
  2. increase DBP
  3. increase PP
27
Q

how does NE affect coronary flow?

A

increase

28
Q

how does NE affect TPR?

A

increase

29
Q

how does NE affect renal blood flow?

A

decrease

30
Q

what are the adverse effects of NE?

A

same as EPI, but greater BP spike

31
Q

what is the therapeutic use for NE?

A

low BP (titration necessary)

32
Q

where is DA synthesized in the periphery and what is its function?

A
  1. epithelial cells of proximal tubule

2. local diuretic and natriuretic effects

33
Q

why is DA ineffective when administered orally?

A

it is a substrate for MAO and COMT

34
Q

which vascular DA pathway is dependent on cAMP?

A

renal tubular cells

35
Q

low doses of DA are used for what purpose?

A

increase urine output

36
Q

what are the effects of moderate doses of DA on the heart?

A
  1. positive inotropy, tachycardia (B1)
  2. increase SBP and PP
  3. TPR - same
37
Q

what are the effects of high doses of DA on the vasculature? via what receptors?

A

vasocontriction (a1)

38
Q

what condition should be corrected before DA use?

A

hypovolemia

39
Q

what are the adverse effects of DA?

A
  1. tachycardia, angina, arryhthmias, headache, hypertension

2. extravasation

40
Q

what are the therapeutic uses for DA?

A
  1. severe congestion heart failure (especially in patients with oliguria and low/normal peripheral vascular resistance)
  2. cardiogenic and septic shock
  3. may improve cardiac and renal function in severely ill patients with chronic heart disease or renal failure
41
Q

how is the response of ephedrine affected by prior treatment with reserpine or guanethidine?

A

reduced

42
Q

how does ephedrine affect adrenergic receptors?

A

mixed acting - acts both on the receptor directly and increases release of NE from vesicles

43
Q

how are the effects of indirect-acting adrenergic agonists affected by prior treatment with reserpine or guanethidine?

A

responses are abolished

44
Q

what happens when amphetamine displaces NE in the nerve terminal vesicle?

A

NE release occurs independent of exocytosis

45
Q

activity of amphetamine is affected by drugs that affect what step of catecholamine synthesis?

A

storage

46
Q

what is the effect of amphetamines on the CNS?

A
  1. releases biogenic amines from storage sites in nerve terminals
  2. stimulates medullary respiratory center
  3. stimulates cortex and reticular activating system to prevent fatigue, delays need for sleep
47
Q

what are the cardiovascular effects of amphetamine?

A
  1. activates peripheral a and B
  2. increase SBP and DBP
  3. increase HR
  4. cardiac arrythmias may occur
48
Q

what is the effect of amphetamines on other smooth muscles?

A

large increase in bladder smooth muscle contraction - treatment for enuresis and incontinence

49
Q

what is the role of tyramine?

A

used to synthesize NE and EPI via alternative pathway

50
Q

how is tyramine metabolized?

A

destroyed by MAO in gut wall and liver

51
Q

how is tyramine related to MAO inhibitors?

A

tyramine action is increased with MAO inhibitor treatment - leads to sudden rise in BP due to extra NE

52
Q

which adrenoceptor antagonists have much higher affinity for a1 over a2?

A
  1. prazosin
  2. terazosin
  3. doxazosin
53
Q

which adrenoceptor antagonists have slightly higher affinity for a1 over a2?

A

phenoxybenzamine

54
Q

which adrenoceptor antagonists have equal affinity between a1 and a2?

A

phentolamine

55
Q

which adrenoceptor antagonists have higher affinity for a2 over a1?

A
  1. yohimbine
  2. rauwoscine
  3. torazoline
56
Q

what are the properties of alpha receptor antagonists?

A
  1. reversibly or irreversibly block a-adrenergic receptors
  2. half life determines effects of reversible inhibitors
  3. rate of production of new receptors determines effects of irreversible inhibitors
57
Q

what are the effects of alpha receptor antagonists?

A
  1. lowered BP, orthostatic hypotension
  2. tachycardia
  3. reverse pressor effects of a and B agonists
  4. miosis
  5. nasal stuffiness
  6. lowered resistance to urine flow
58
Q

what are the therapeutic uses for alpha receptor antagonists?

A
  1. pheochromocytoma
  2. hypertensive emergencies
  3. chronic hypertension
  4. peripheral vascular disease
  5. urinary obstruction
  6. erectile dysfunction
59
Q

how does phenoxybenzamine affect a1 receptors?

A

irreversible blockade

also blocks H1, Ach, and 5-HT receptors

60
Q

what is the clinical use for phenoxybenzamine?

A

pheochromocytoma

61
Q

how does prazosin affect a1 receptors?

A

a1 selective

62
Q

what is the effect of prazosin on a1 receptors?

A

relaxes arterial, venous, and prostate smooth muscle

63
Q

how does tamsulosin affect a1 receptors? what is its clinical use?

A
  1. a1A selective

2. BPH

Year 2 Pharmacology (70 decks)

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