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Pharm 2 > Physiology of Sympathomimetics - Week 1 > Flashcards

Physiology of Sympathomimetics - Week 1 Flashcards

1
Q

Sympathetic NS branches from what region the spinal cord?

A

Thoracolumbar (T1-L2)

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2
Q

Where are the sympNS preganglia located?

A

Near the spinal cord

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3
Q

SympNS postglaglia secrete ________

A

Norepinephrine (adrenergic fibers)

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4
Q

What converts dopamine into NE after it enters the synaptic vessel?

A

Dopamine beta hydroxylase

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5
Q

What releases NE from the synaptic vessel?

A

an action potential

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6
Q

3 modes of signal termination from NE

A
  1. Reuptake
  2. Dilution by diffusion
  3. Metabolism by
    • Monamine oxidase (MAO)
    • Catechol-o-methyltransferase (COMT)
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7
Q

Primary sites of action for the adrenergic receptors:

  • Alpha 1
  • Alpha 2
  • Beta 1
  • Beta 2
A
  • Alpha 1: periphery (and some organs)
  • Alpha 2: central (negative feedback loops)
  • Beta 1: heart
  • Beta 2: other smooth muscle (throughout the body; counterbalances A1)
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8
Q

Functions of the alpha 1 postsynaptic receptor

A
  • activation increases intracellular Ca (important for both release of NT’s and for must contraction)
  • smooth muscle contraction
  • peripheral vasoconstriction
  • bronchoconstriction
  • inhibits insulin secretion
  • stimulates glycogenolysis and gluconeogenesis
  • mydriasis (pupils dilate)
  • GI relaxation
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9
Q

Functions of the alpha 2 PREsynaptic receptors in the PNS:

A
  • decreases entry of Ca into the cell

- limits the release of NE

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10
Q

Functions of the alpha 2 POSTsynaptic receptors in the CNS:

A
  • sedation
  • decreased symp outflow
  • decreased BP
  • plt aggregation
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11
Q

Functions of the beta 1 postsynaptic receptor:

A
  • Increases HR
  • Increases conduction velocity (SA and AV nodes)
  • Increases myocardial contractility
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12
Q

Functions of beta 2 postsynaptic receptor:

A
  • smooth muscle relaxation
  • peripheral vasodilation (esp sk musc)
  • decreases BP
  • Bronchodilation (overrides a1)
  • increases insulin secretion
  • increases glycogenolysis and gluconeogenesis
  • Decreases GI motility
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13
Q

ParasympNS (PSNS) originates from what region of the spinal cord?

A

Craniosacral

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14
Q

What cranial nerves and what sacral nerves specifically are associated w the PSNS?

A

Cranial nerves III, VII, IX, and X

Sacral nerves 2,3,4

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15
Q

Where are the PSNS pre ganglia located?

A

near their organs of innervation

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16
Q

What do the post ganglia of the PSNS secrete?

A

Each (cholinergic fibers)

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17
Q

Anticholinergic = ________

A

Antiparasympathetic

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18
Q

What enzyme catalyzes the conversion of choline and Acetyl CoA into acetylcholine

A

Choline acetyltransferase

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19
Q

What mediates an ACh action potential?

A

Calcium

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20
Q

Each is deactivated by __________ into _________ and __________

A

Acetylcholinesterase

Choline and acetate

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21
Q

Up regulation and down regulation are controlled by?

A

Effector cell receptors

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22
Q

What is down regulation?

What does down regulation result in?

A

decrease in number but not response of effector cell receptors

results in tachyphylaxis

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23
Q

What is up regulation?

What is a possible result of up regulation?

A

increase in number but not sensitivity of receptors (d/t chronic depletion of catecholamines or use of antagonists

May account for withdrawal syndrome w B-blockers

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24
Q

The reduction in a physiologic response to a stimulus that is constant over time

A

desensitization

25
Q

Type of desensitization/down regulation which

  • occurs over seconds to minutes
  • the receptor is unable to bind to the G protein (therefore the fx of the receptor is altered)
  • caused by phosphorylation of the receptor and possibly the G protein
A

Uncoupling

26
Q

Type of desensitization/down regulation which:

  • occurs over minutes to hours but is still reversible
  • moves receptors from the cell surface to intracellular compartments
  • the receptors are therefore not accessible to ________?
A

Sequestration

receptors inaccessible to hydrophilic ligands

27
Q

Type of receptor desensitization/down regulation which

  • is the slowest process
  • occurs over hours to days
  • receptors are moved from cell surface to intracellular compartments, and then destroyed
A

Down regulation

28
Q

during down regulation, are receptors available for recycling to the cell surface

A

No. A new receptor protein must be made from RNA to replace the lost receptors

29
Q

What is autonomic tone?

A

Residual basal activity of the autonomic nervous system

30
Q

What is pheochromocytoma?

A

uncontrolled release of catecholamines due to an adrenal gland tumor; constant SympNS stimulation

31
Q

True or False: Catecholamines are both neurotransmitters and hormones

A

True

32
Q

What are sympathomimetics?

A

Compounds that resemble catecholamines except that hydroxyl groups are not present in both the 3 and 4 positions of the benzene ring

33
Q

How are sympathomimetics classified?

A

according to their selectivity for simulating alpha and/or beta receptors

34
Q

Do synthetic non-catecholamines act directly or indirectly? Why?

A

Both

indirectly - cause the release of NE (an endogenous NT) from postganglionic sympathetic nerve endings

directly - activate the adrenergic receptors directly

35
Q

Indirect-acting sympathomimetics are characterized mostly by ______ and _______ adrenergic effects because NE is a weak _______ agonist

A

Alpha and Beta 1

Beta 2

36
Q

Does denervation or depletion of NT, as w repeated doses of sympathomimetic, blunt the pharmacologic responses normally evoked by an indirect-acting sympathomimetic drug?

A

yes

37
Q

Name 2 direct-acting synthetic noncatecholamines

A

phenylephrine and methoxamine

38
Q

T/F: Synthetic noncatecholamines are less potent than catecholamines

A

True

39
Q

Does denervation or depletion of NT prevent the activity of direct-acting sympathomimetics?

A

no

40
Q

T/F: Most direct sympathomimetics activate alpha and beta receptors, but the magnitude of alpha and beta activity varies greatly from pure alpha agonist phenylephrine to pure beta agonist isoproterenol.

A

True

41
Q

3 types of sympathomimetics

A
  • Naturally occurring catecholamines
  • Synthetic catecholamines
  • synthetic non-catecholamines (indirect and direct acting)
42
Q

All Sympathomimetics are derived from:

A

beta phenylethylamine

43
Q

Presence of hydroxyl groups on the 3 and 4 position of the benzene ring of the B phenylethylamine creates a _________. Drugs with this composition are ________.

A

catechol

catecholamines

44
Q

CV/resp pharmacologic effects of sympathomimetics

A
  • vasoconstriction - cutaneous and renal circulations
  • vasodilation - skeletal muscle
  • bronchodilation
  • cardiac stimulation
    • increased HR
    • increased contractility
    • vulnerability to dysrhythmias
45
Q

Other pharmacologic effects of sympathomimetics (hepatic, metab, endocrine, CNS)

A
  • Hepatic - Glycogenolysis
  • Liberation of free fatty acids from adipose tissue
  • Endocrine - modulation of insulin, renin, and pituitary secretion
  • CNS - stimulation
46
Q

What is the only time a vasopressor should be used?

A

When a pt’s BP must be increased immediately to avoid pressure-dependent reductions in organ perfusion w subsequent ischemia

47
Q

The pharmacologic response caused by a sympathomimetic is related to:

A

The density of the alpha and beta receptors in the tissues

48
Q

T/F: An inverse relationship exists b/t the conc’n of available sympathomimetic and the number of receptors.

A

True

For example, increased plasma conc’n’s of NE results in a decrease in the density of B-adrenergic receptors in cell membranes

49
Q

The response evoked by a sympathomimetic is influenced by:

A

The anatomical distribution of a and B receptors

50
Q

Why does NE have minimal effects on airway resistance

A

Because adrenergic receptors in bronchial smooth muscle are mostly B2 and thus not stimulated by this catecholamine

51
Q

Why are epidural and isoproterenol potent bronchodilators?

A

because they are able to activate B2 receptors

52
Q

What structure must a drug have to be rabidly inactivated by both MAO and COMT?

A

3,4 dihydroxybenzene (catecholamine)

53
Q

Name the enzyme present in liver, kidneys, and GI tract that catalyzes oxidative deamination

A

Monoamine oxidase (MAO)

54
Q

Name the enzyme that methylates the hydroxyl group of catecholamines

A

Catechol-o-transferase (COMT)

55
Q

Name 2 ways to potentiate the effects of epinephrine

A
  • inhibition of reuptake

- inhibition of COMT or MAO

56
Q

completeness of this reuptake mechanism and metab is evidenced by:

A

minimal presence of unchanged catecholamines in the urine

57
Q

Name some ways the metabolism of synthetic non-catecholamines differs from the metab of catecholamines

A

synthetic non-catecholamines:

  • lack a 3-hydroxyl group
  • aren’t metab by COMT
  • depend of MAO for metab
  • are metabolized more slowly than catechols
  • duration of action is prolonged by inhibition of MAO
58
Q

How may pts on MAOI’s respond when treated w synthetic non-catecholamines?

A

they may manifest exaggerated responses

Pharm 2 (7 decks)

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