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My Pharm II > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

Norepi originates from

A

CNS

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2
Q

Epi originates from

A

adrenal medulla

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3
Q

___________ secrete norepinephrine

A

Postganglia

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4
Q

Big target for these meds – _________ nervous system at the ________ receptors.

A

sympathetic

adrenergic

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5
Q

______________________ converts dopamine to NE

A

Dopamine beta hydroxylase

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6
Q

Metabolism of NE

A
  • Monamine oxidase (MAO)

- Catechol-o-methyltranserase (COMT)

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7
Q

Adrenergic Receptors

A

alpha-1: periphery
alpha-2: central
beta-1: heart
beta-2: other smooth muscle

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8
Q

Alpha-1 Postsynaptic Receptor

A 
Activation increases intracellular calcium
Smooth muscle contraction
Peripheral vasoconstriction
Bronchoconstriction
Inhibits Insulin secretion
Stimulates glycogenolysis and gluconeogenesis
Mydriasis
GI relaxation
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9
Q

Alpha-2 Receptors: Pre/Post synaptic

A

Presynaptic in the PNS

  • Decreases entry of calcium into the cell
  • Limits the release of norepinephrine

Postsynaptic in the CNS

  • Sedation
  • Decreased sympathetic outflow
  • Decreased BP
  • Platelet aggregation
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10
Q

Beta-1 Postsynaptic Receptor:

A
  • Increases HR
  • Increases conduction velocity
  • Increases myocardial contractility
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11
Q

Beta-2 Postsynaptic Receptor:

A
  • Stimulation leads to smooth muscle relaxation
  • Peripheral vasodilitation
  • Decreases BP
  • Bronchodilation
  • Increases insulin secretion
  • Increases glycogenolysis and gluconeogenesis-
  • Decreases GI mobility
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12
Q

Look at slide 17-19

A

.

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13
Q

extended exposure to agonists reduces the number, but not their response. Results in tachyphylaxis.

A

Down regulation

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14
Q

chronic depletion of catecholamines or use of antagonists increases the number of receptors, but not their sensitivity. May account for withdrawal syndrome with beta blockers.

A

Up regulation

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15
Q

Occurs rapidly, Inability of the receptor to bind G protein (alter the function of the receptor)

A

Receptor Uncoupling

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16
Q

Occurs more slowly, Movement of receptors from the cell surface to intracellular compartments

A

Sequestration

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17
Q

Prolonged process, Movement of receptors from the cell surface to intracellular compartments, but then destroyed.

A

Downregulation

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18
Q

Disease of uncontrolled release of catecholamines due to an adrenal gland tumor. Constant SNS stimulation

A

Pheochromocytoma

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19
Q

Catecholamines are both _______________ and __________

A

neurotransmitters

hormones

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20
Q

All are sympathomomymetics, but all are not _____________

A

catecholomines

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21
Q

Compounds that resemble catecholamines except that hydroxyl groups are not present in both the __ and __ positions of the benzene ring.

A

Sympathomimetics

3

4

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22
Q

All sympathomimetics are derived from:

A

β phenylethylamine

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23
Q

Structures: Catechole, amine

A

OH

CN

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24
Q

Other uses of sympathomimetics:

A
  • Treatment of bronchospasm
  • Management of anaphylaxis.
  • Addition to local anesthetic to slow systemic absorption
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25
Q

Catecholamines metab’d by both, non-catecholamines by:

A

MAO

Both are COMT and MAO

26
Q

Look at slide 34

A

.

27
Q

Inhibition of the reuptake of catecholamines uptake mechanism produces a ______ potentiation of effects of epinephrine than does inhibition of either enzyme.

A

greater

28
Q

Parkinsons utilize MAOIs, can be med interactions. Will exibit what response to synthetic non-catecholamines?

A

exaggerated

29
Q

vasoconstrictors direct hemodynamic effects

A

-Increase arterial resistance and afterload
(Increase SVR and usually MAP)

-Increase venous return
(Increase preload and C.O.)

30
Q

Hemodynamic Effects: reflex changes

A
  • Decreased heart rate
  • Decreased conduction
  • Occasionally, decreased contractility
31
Q

Non-cardiac effects of vasoconstrictors

A
  • Bronchodilate
  • Glycogenolysis
  • Insulin, renin, pituitary hormone
  • CNS stimulation (low lipid solubility)
32
Q

Risk of end organ damage and mortality increases with time:

A

MAP < 65 mmHg for 13-28 minutes

MAP < 50 mmHg for 1 minute

33
Q

Contraindications/Complications of vasoconstrictors:

A
  • Can worsen LV Failure
  • Can exacerbate RV Failure
  • Can decrease renal blood flow
  • Can mask hypovolemia
34
Q

Most potent activator of Alpha-1 receptors

A

Epinephrine

35
Q

Epinephrine Stimulates

A

Alpha-1, Beta-1, and Beta-2 receptors

36
Q

Which pressor has highest risk of S/E’s

A

Epinephrine

37
Q

Epi low dose stimulates? Net effect?

A

Alpha-1 receptors in the skin, mucosa, and hepatorenal system while Beta-2 receptors are stimulated in skeletal muscle

Net Effect:

  • decreased SVR and distribution of blood to skeletal muscle
  • MAP remains essentially the same
38
Q

Epinephrine Intermediate doses

A
  • Beta-1
  • Increased H.R. and contractility and increased C.O.
  • Increased automaticity (May lead to dysrrhythmias)
39
Q

Epi increases ____ better than NE

A

rate

40
Q

Epinephrine high doses

A
  • Potent vasoconstrictor including cutaneous, splanchnic and renal vascular beds
  • Used to maintain myocardial and cerebral perfusion
  • Reflex bradycardia can occur
41
Q

Epinephrine

A
  • Hyperglycemia
  • mydriasis
  • platelet aggregation*
  • sweating
  • headache
  • tremor
  • nausea
  • arrhythmias
42
Q

Norepi increases

A

systolic, diastolic, and mean arterial pressure

43
Q

Norepinephrine C.O.

A
  • Cardiac output may increase at low doses, Higher doses - C.O. may decrease because of increased afterload and baroreceptor-mediated reflex bradycardia
  • Refractory hypotension
44
Q

Look at 60-65

A

.

45
Q

Ephedrine works at what receptors

A

Works at Alpha-1 and Beta receptors

46
Q

Ephedrine Principle mechanism is increased __________________.

A

myocardial contractility

47
Q

Ephedrine: ___________ greater than _________ constriction increases ________ and with increased heart rate and myocardial contractility, increases cardiac output (Beta-1 receptor action). Increases what as a result?

A

Venoconstriction

arteriolar

preload

Increases Systolic and Diastolic BP as a result

48
Q

Ephedrine: _____________ can occur – negative feedback loop at adrenergic receptors, no more N.E. (can be in first 24 hours).

A

Tachyphylaxis

49
Q

Ephedrine preserves or increases ________ blood flow.

A

uterine

50
Q

Which non-catecholamine is a bronchial smooth muscle relaxant?

A

Ephedrine

51
Q

Phenylephrine Increases

A

preload > afterload

52
Q

Phenylephrine causes

A
  • reflex bradycardia
  • Decreased renal and splanchnic blood flow
  • Increased pulmonary artery resistance and pressure
  • No dysrrhythmias as a direct effect - but heart can respond to whats happening in periphery
53
Q

look at slide 79

A

.

54
Q

Vasopressin effects

A
  • Stimulates vascular V1a receptors causing intense arterial vasoconstriction.
  • In the renal-collecting ducts increases the permeability of cell membranes resulting in the passive reabsorption of water (V2 effect).
55
Q

Vasopressin tidbits

A
  • AQP2 (auquporin) is a channel allowing fluid back to blood stream from collecting duct
  • V1 receptors increase aldosterone which also increases BP
56
Q

Unlike _____________, effects of _________________ are preserved during hypoxia and severe acidosis.

A

catecholamines

arginine vasopressin

57
Q

Pts on MAOIs do what to the response of vasoconstrictors?

A

exxagerated response

58
Q

treatment for pt on cocaine?

A

Beta blocker and combine wit alpha blocker (labetalol/Coreg)

59
Q

Phentolamine is what?

A

alpha 1 and 2 antagonist

60
Q

what to do if norepi extravasates?

A

phentolamine

elevate extremity

warm compress

My Pharm II (8 decks)

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