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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
what receptors does NE stimulate?
B1 (same as EPI) | alpha (less than EPI)
26
how does NE affect BP?
1. increase SBP 2. increase DBP 3. increase PP
27
how does NE affect coronary flow?
increase
28
how does NE affect TPR?
increase
29
how does NE affect renal blood flow?
decrease
30
what are the adverse effects of NE?
same as EPI, but greater BP spike
31
what is the therapeutic use for NE?
low BP (titration necessary)
32
where is DA synthesized in the periphery and what is its function?
1. epithelial cells of proximal tubule | 2. local diuretic and natriuretic effects
33
why is DA ineffective when administered orally?
it is a substrate for MAO and COMT
34
which vascular DA pathway is dependent on cAMP?
renal tubular cells
35
low doses of DA are used for what purpose?
increase urine output
36
what are the effects of moderate doses of DA on the heart?
1. positive inotropy, tachycardia (B1) 2. increase SBP and PP 3. TPR - same
37
what are the effects of high doses of DA on the vasculature? via what receptors?
vasocontriction (a1)
38
what condition should be corrected before DA use?
hypovolemia
39
what are the adverse effects of DA?
1. tachycardia, angina, arryhthmias, headache, hypertension | 2. extravasation
40
what are the therapeutic uses for DA?
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
how is the response of ephedrine affected by prior treatment with reserpine or guanethidine?
reduced
42
how does ephedrine affect adrenergic receptors?
mixed acting - acts both on the receptor directly and increases release of NE from vesicles
43
how are the effects of indirect-acting adrenergic agonists affected by prior treatment with reserpine or guanethidine?
responses are abolished
44
what happens when amphetamine displaces NE in the nerve terminal vesicle?
NE release occurs independent of exocytosis
45
activity of amphetamine is affected by drugs that affect what step of catecholamine synthesis?
storage
46
what is the effect of amphetamines on the CNS?
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
what are the cardiovascular effects of amphetamine?
1. activates peripheral a and B 2. increase SBP and DBP 3. increase HR 4. cardiac arrythmias may occur
48
what is the effect of amphetamines on other smooth muscles?
large increase in bladder smooth muscle contraction - treatment for enuresis and incontinence
49
what is the role of tyramine?
used to synthesize NE and EPI via alternative pathway
50
how is tyramine metabolized?
destroyed by MAO in gut wall and liver
51
how is tyramine related to MAO inhibitors?
tyramine action is increased with MAO inhibitor treatment - leads to sudden rise in BP due to extra NE
52
which adrenoceptor antagonists have much higher affinity for a1 over a2?
1. prazosin 2. terazosin 3. doxazosin
53
which adrenoceptor antagonists have slightly higher affinity for a1 over a2?
phenoxybenzamine
54
which adrenoceptor antagonists have equal affinity between a1 and a2?
phentolamine
55
which adrenoceptor antagonists have higher affinity for a2 over a1?
1. yohimbine 2. rauwoscine 3. torazoline
56
what are the properties of alpha receptor antagonists?
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
what are the effects of alpha receptor antagonists?
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
what are the therapeutic uses for alpha receptor antagonists?
1. pheochromocytoma 2. hypertensive emergencies 3. chronic hypertension 4. peripheral vascular disease 5. urinary obstruction 6. erectile dysfunction
59
how does phenoxybenzamine affect a1 receptors?
irreversible blockade also blocks H1, Ach, and 5-HT receptors
60
what is the clinical use for phenoxybenzamine?
pheochromocytoma
61
how does prazosin affect a1 receptors?
a1 selective
62
what is the effect of prazosin on a1 receptors?
relaxes arterial, venous, and prostate smooth muscle
63
how does tamsulosin affect a1 receptors? what is its clinical use?
1. a1A selective | 2. BPH

Year 2 Pharmacology (70 decks)

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