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P&T Block 1 > L6 > Flashcards

L6 Flashcards

1
Q

What is the rate limiting step in NE synthesis?

A

Tyrosine –> DOPA

Tyrosine hydroxylase

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2
Q

What enzyme converts DOPA –> dopamine?

A

DOPA decarboxylase

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3
Q

What enzyme converts dopamine –> NE?

A

Dopamine beta hydroxylase

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4
Q

What transporter brings dopamine into vesicles in the adrenergic nerve terminal?

A

VMAT2

H+ counter transport

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5
Q

Which drug can be used to deplete NE by inhibiting VMAT2?

A

Reserpine

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6
Q

When enzyme converts NE –> E? In what organ?

A

PNMT inside vesicles

Adrenal medulla

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7
Q

What is the mechanism of NE feedback inhibition?

A

Alpha 2 auto-receptors on the pre-synaptic side

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8
Q

What is the primary mechanism for NE inactivation?

A

NET reuptake into pre-synapse

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9
Q

What is the secondary mechanism for NE inactivation?

A

Facilitated diffusion out of cleft by OCT3 into the post-synaptic side

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10
Q

How does cocaine work at adrenergic nerve terminals?

A

Inhibits NET

Increases NE time in synapse

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11
Q

What are the 3 ways NE adrenergic receptors can be regulated on the post-synaptic membrane?

A
  1. Desensitization (sec)
    - Phos the receptor, uncouple action from ligand binding
  2. Sequestration (mins) = aggregation, internalization
  3. Down regulation (hrs) via less mRNA
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12
Q

If the receptor is G protein independent, what is the mechanism by which it will be regulated?

A

B arrestin = signaling molecule to inactivate

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13
Q

If the receptor is G protein dep, what is the mechanism by which it will be regulated?

A

B arrestin = chaperone for INTERNALIZATION

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14
Q

Does MAO or COMT metabolize NE in the pre-synaptic neuron?

A

MAO

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15
Q

Does MAO or COMT metabolize NE in the post-synaptic neuron?

A

COMT

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16
Q

Describe the sympathetic nerve metabolism of NE/E

A
  1. NE/E + MAO –> DHPG
    • COMT –> MHPG
  3. MHPG reduced = glycol
    MHPG oxidized (liver) = VMA
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17
Q

Describe the adrenergic nerve metabolism of NE/E

A
  1. N/E + COMT –> normet/met
    • MAO –> MHPG
  3. MHPG reduced = glycol
    MHPG oxidized (liver) = VMA
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18
Q

What is elevated plasma free (unconj) metanephrines diagnostic of?

A

Pheochromocytoma
Catecholamine secreting paraganliomas
Or pt is on drugs that release or inhibit reuptake of NE

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19
Q

A1 agonist

A

Phenylephrine

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20
Q

A2 agonist

21
Q

B1 agonist

A

Dobutamine

22
Q

B2 agonist

23
Q

B3 agonist

A

Mirabegron

24
Q

3 effects of A1 agonist

A
  1. Smooth muscle contraction - vascular, iris, GU
  2. Secretion - salivary & sweat glands
  3. K+ release from liver
25
Q

4 effects of A2 agonist

A
  1. ↓NE @ nerve term
  2. Contract vasc smooth muscle
  3. ↓ insulin secretion
  4. Platelet aggregation
26
Q

4 effects of B1 agonist

A
  1. ↑HR
  2. ↑contractility
  3. ↑conduction velocity
  4. ↑renin from kidney
27
Q

4 effects of B2 agonists

A
  1. Dilate BVs in skeletal muscle & liver
  2. ↑glucose & K in skeletal muscle
  3. ↑glucose @ liver
  4. Mast cell stablization
28
Q

2 effect of B3 agonists

A
  1. Relax bladder

2. Lypolysis

29
Q

What is the difference between B1 & 2 receptors with NE/E?

A

B1: E=NE agonism
B2: E > NE

30
Q

Are catecholamines hydrophobic or philic - explain effects.

A

Hydrophobic - poor penetration

- Injector topical

31
Q

Do catecholamines have long or short half lives?

32
Q

What is NE’s receptor selectivity?

A

A1, 2

B1; 3

33
Q

What is E’s receptor selectivity?

A

A1, 2

B1, 2

34
Q

What is isoproterenol’s receptor selectivity?

A

= 100% beta agonist

B1, 2, 3 only

35
Q

What is dopamine’s receptor selectivity?

A

B1 - need ↑[ ]

D1 - dilate renal & GI vascular beds, ↑NA excretion at kidneys

36
Q

What is dobutamine’s receptor selectivity?

37
Q

What is the main adrenergic receptor in the heart?

A

B1
Some B2
NO ALPHA

38
Q

What happens if E + SA node?

A 
Epi + beta receptor
- AC --> cAMP --> PKA
↑HR and contractility 
- Faster depol & repol due to ↑PKA
- Faster pacemaker potential due to ↑cAMP
↑freq of impulses
39
Q

What is a downside of using B agonists in the heart?

A

↑risk arrhythmia

↑risk cardiac arrest due to VFib

40
Q

What do A1 & 2 receptors do to vascular smooth muscle: cuteanous, mesenteric, renal, muscle, liver?

A

Vasoconstrict

41
Q

What is the baroreceptor reflex in context of slow NE infusion?

A

+ NE
A1 vasocontrict –> ↑TPR –> ↑BP
B1 at heart means you’d expect ↑HR… but vagal reflex dominates so ↑BP overrides to ↓HR
ACh acts on muscarinic receptors

42
Q

What happens with slow E infusion?

A 
B2 - vasodilation in skeletal muscle
↓TPR --> ↓DBP
↑CO --> ↑SBP
Not dramatic enough rise BP to warrant vagal response - ↑HR & BP at same time
(EXERCISE)
43
Q

What happens with slow isoproterenol infusion?

A

B effects only
Dilation –> ↓DBP
↑HR & CO but overall BP ↓s even if systolic increases slightly due to CO

44
Q

Why use E for cardiac arrest?

A

Peripheral vasoconstriction - ↑coronary perfusion

45
Q

Why use E for anaphylatic shock?

A

↑CO
↑BP (alpha)
Bronchodilate (alpha & B2)
Stabilize mast cells (B2)

46
Q

Why use NE or E for mucosal decongestion?

A

Alpha - vasocontrict to ↓swelling and secretions

47
Q

Why use NE or E for hypotension?

A

Vasopressor short term

48
Q

Why use DO during acute heart failure?

A

Selectively B1 -↑CO

49
Q

Adverse effects E/NE

A

MI
Arrythmia
Hypoxia
Necrosis at IV sites

P&T Block 1 (43 decks)

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