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Pharm Unit 2 MJC > Adrenergic Lectures > Flashcards

Adrenergic Lectures Flashcards

1
Q

What enzyme converts dopamine into NE in the synaptic vesicle?

A

Dopamine beta hydroxylase

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2
Q

What type of G protein is the D1 receptor coupled to?

A

Gs

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3
Q

What are the 3 routes of termination of an adrenergic transmitter?

A

1 neuron specific re-uptake (Highly specific)
2 extra-neuronal uptake, non-specifc, high capacity (a lot in liver cells)
3 Diffusion

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4
Q

What two intracellular enzymes metabolize adrenergic transmitters? Does this play a role in the termination of NE as a neurotransmitter?

A 
Monoamine Oxidase (MAO, on mitochonrial surface)
Catechol-O-methyletransferase (COMT in cytoplasm of many cell, notably liver)
No these doe not play a role in the termination of NE as a neurotransmitter
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5
Q

Plasma levels of what are measured to detect excess adrenergic transmitters in a pheochromocytoma?

A

metanephrine

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6
Q 
Name the receptor that causes the following effects in tissues:
increase HR and force of contraction
Bronchial muscle relaxation
renin secretion from JGA
lipolysis in adipose tissue
dilation of arterioles
increase metabolic effects
A 
B1 - increase HR and force of contraction
B2 - Bronchial muscle relaxation
B1 - renin secretion from JGA
B3 - lipolysis in adipose tissue
B2 - dilation of arterioles
B2 - increase metabolic effects
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7
Q

Name the receptor that causes the following effects in tissues
inhibit NE release and ACh release at presynaptic nerve endings
dilation of renal, mesenteric and cerebral arteries
decrease peripheral sympathetic tone at postsynaptic CNS sites
Constriction of arterioles and veins and uterus and spleen

A

a2 - inhibit NE release and ACh release at presynaptic nerve endings
D1 - dilation of renal, mesenteric and cerebral arteries
a2 - decrease peripheral sympathetic tone at postsynaptic CNS sites
a1 - Constriction of arterioles and veins and uterus and spleen

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8
Q

What types of adrenergic receptors are present in skeletal muscle? Describe the dominant effect at low and high concentrations of Epi?

A

Skeletal muscle has both a1 and B2 receptors. The B2 receptors have a lower threshold and are responsible for the expected response (dilation) at physiological levels (low) of epi. Effects of a1 are dominant (constriction) but are usually only seen with very high levels of Epi as are present in extreme shock.

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9
Q

Correctly order the agonist potency of ISO, EPI, NE, and DA on B1 receptors

A

ISO > Epi >= NE > DA

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10
Q

Correctly order the agonist potency of ISO, EPI, NE, and DA on B2 receptors

A

ISO > Epi&raquo_space; NE&raquo_space; DA

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11
Q

Correctly order the agonist potency of ISO, EPI, NE, and DA on a1 receptors

A

Epi >= NE > DA&raquo_space; ISO

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12
Q

Correctly order the agonist potency of ISO, EPI, NE, and CLON on a2 receptors

A

CLON > Epi >= NE&raquo_space; ISO

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13
Q

How do indirect NE agonists work?

A

Drugs cause release of NE from small cytoplasmic pool (NOT from synaptic vesicles)

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14
Q

What is tachyphylaxis?

A

Acute Tolerance: e.g. when small cytoplasmic pool of NE is rapidly used up with repeated tyramine injections

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15
Q

What are the effects of a low dose of DA?

A

direct action of DA on D1 receptros causes vasodilation; thus increase in blood flow notably at renal, mesenteric, and cerebral vessels; resulting in lowering of BP and increased urine output

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16
Q

What are the effects of a medium dose of DA?

A

Similar to low dose plus some action on B1 receptors in heart, and some indirect action/NE release; thus, positive inotropic effect

17
Q

What are the effects of a high does of DA?

A

Similar to medium dose plus some direct action on vascular a1 receptors, and indirect action/NE release; thus, vasoconstriction (including renal, as a1 activation dominates DA receptor activation) can be used as a pressor

18
Q

What are the effects on HR and BP and Peripheral Resistance with IV infusion (physiological amounts) of NE?

A

HR drops slightly
Diastolic, systolic and MAP rise
PP increases
peripheral resistance increases significantly

The reason HR decreases is dues to baroreceptor response to increase MAP triggering vagus to decrease HR which trumps effects of NE on B1

19
Q

What are the effects on HR and BP and Peripheral Resistance with IV infusion (physiological amounts) of Epi?

A 
HR increases
MAP and systolic increase
diastolic decreases
PP increases
peripheral resistance decreases

At low infusion rate B2 response in skeletal muscle overwhelms a1 response in resistance vessels, skin and mucosa, thus peripheral resistance drops

20
Q

What are the effects on HR and BP and Peripheral Resistance with IV infusion (physiological amounts) of isoproterenol

A 
HR increases
Systolic pressure increases
diastolic and MAP decrease
PP increases
Peripheral resistance decreases significantly.
21
Q

What is the apocrine secretory function mediated by?

A

alpha adrenergic receptors

22
Q

What effects does epinephrine have when given during anaphylactic shock?

A

a1 vasoconstriction
B2 brochodilation
B2 decrease histamine release from mast cells

23
Q

What is an important consideration when stopping the use of a short acting adrenergic antagonist or agonist?

A

You must tapper off to avoid denervation hypersensitivity (antagonist) and desensitization (agonist)

24
Q

What are 3 cautions with using alpha agonists?

A

1 localized ischemia may occur at infusion site
2 avoid extravasation (tissue necrosis)
3 gradually decrease infusion

25
Q

What is more important during shock, increasing BP or tissue perfusion?

A

Tissue perfusion

26
Q

What do the main clinically relevant ergot alkaloids function as?

A

Alpha agonists and serotonin agonists

27
Q

What compound are all ergot derivatives that are commonly used related to?

A

Lysergic acid

28
Q

Where are ergot alkaloids obtained form?

A

extraction of fungus (Claviceps pupurea) parasitic to rye and other grains.

29
Q

What are 4 major side effects of alpha adrenergic agonists?

A

1 hypertension/headache
2 localized ischemia - a1 especially with extravasation
3 Dramatic fall in BP on rapid withdrawal
4 Nervousness, anxiety, insomnia if they cross BBB

30
Q

What is a major controlling area for autonomic output from the brain stem?

A

Nucleus Tractus Solitarus (NTS)

31
Q

How do alpha 2 agonists decrease blood pressure?

A

They act on postsynaptic inhibitory alpha 2 receptors in the NTS which decreases central sympathetic output.

32
Q

What are some side effects of beta adrenergic agonists?

A

Mainly cardiac arrhythmia
-Direct effect from B1 receptor activation
- Indirect response to lowered BP resulting from B2 mediated vasodilation
Occasional skeletal muscle tremor with B2 agonists

33
Q 
What is the selectivity of the following generations of beta blockers?
First Gen
Second Gen
Third Gen A
Third Gen B
A

First Gen - “classical” non-selective B blockers
Second Gen - B1 selective
Third Gen A - Non-selective with additional actions
Third Gen B - B1 selective with addition actions

34
Q

What is the main “additional action” of third gen beta blockers?

A

vasodilation that results from alpha 1 antagonism (A) or Ca2+ channel blocking (B)

35
Q

What generation beta blockers should be used in CHF?

A

Second and Third.

36
Q

What are the major side effects of alpha antagonists?

A

tachycardia and postural hypotension

37
Q

Why does prazosin have less tachycardia and postural hypotension.

A

Since it is selective for only alpha 1, it doesnt interfere with negative feedback of NE release via alpha 2 receptors.

38
Q

Why are alpha blockers less effective in treating peripheral vascular disease?

A

Because stealing occurs in which non affected areas dilate and steal blood away from areas that need it most and are unable to dilate.

Pharm Unit 2 MJC (25 decks)

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