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Pharm 2 > Vasoconstrictors > Flashcards

Vasoconstrictors Flashcards

1
Q

Adrenergic/Cholinergic receptor associated with SNS?

A

Adrenergic is associated with the SNS and cholinergic is associcated with the PNS

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2
Q

What happens when an SNS neuron is stimulated?

A

Stimulation travels the length of the neuron. Once it reaches the presynaptic region, NE is released and is it attaches itself to the postsynaptic receptor (Beta or Alpha).

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3
Q

Where do the SNS nerves originate from?

A

Thoracolumbar origin (T1-L2).

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4
Q

What substance enters the synaptic vessel?

A

Dopamine

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5
Q

What converts Dopamine to Norepinephrine?

A

Dopamine Beta Hydroxylase

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6
Q

T/F: 99% of norepinephrine is metabolized in the body?

A

False; 2/3rds is reuptaken into the presynaptic cleft again.

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7
Q

What are the two enzymes that rapidly inactivate catecholamines?

A
  1. Monoamine oxidase (MAO).

2. Catechol-o-transferase (COMT).

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8
Q

What three ways is norepinephrine’s signal terminated?

A
  1. Reuptake
  2. Dilution by diffusion
  3. Metabolism (MAO/COMT).
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9
Q

What are four main adrenergic receptors?

A

Alpha 1
Alpha 2
Beta 1
Beta 2

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10
Q

Which adrenergic receptor is located primarily in the heart?

A

Beta 1

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11
Q

Which adrenergic receptor is located primarily centrally: alpha 1 or alpha 2?

A

Alpha 2

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12
Q

Which adrenergic receptors are G Proteins?

A

Beta 1 and 2

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13
Q

Which enzyme is responsible for converting ATP into cAMP?

A

(AC) Adenylyl cyclase

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14
Q

What is phosphodiesterase’s role in contractility?

A

Phosphodiesterase breaks down cAMP and stops the action of contraction

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15
Q

Which enzyme (instead if cAMP) does do Alpha receptors use to stimulate contraction in smooth muscle?

A

Inositol triphosphate

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16
Q

What 8 things occur with Alpha 1 Postsynaptic receptor activation?

A
  1. Increased intracellular calcium
  2. Smooth muscle contraction
  3. Peripheral vasocontriction
  4. Bronchoconstriction
  5. Inhibits insulin secretion
  6. Stimulates glycogenolysis and gluconeogensis
  7. Mydriasis
  8. GI relaxation
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17
Q

Which adrenergic receptor system uses a negative feedback system?

A

Alpha 2

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18
Q

What are the effects of Alpha 2 receptors presynaptically?

A
  1. Decreases entry of calcium into the cell

2. Limits the release of norepinephrine

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19
Q

What are the effects of Alpha 2 receptors post-synaptically?

A
  1. Sedation
  2. Decreased sympathetic outflow
  3. Decreased BP
  4. Platelet aggregation
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20
Q

3 Effects of Beta-1 postsynaptic receptor agonism?

A
  1. Increased HR
  2. Increased conduction velocity
  3. Increased myocardial contractility
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21
Q

7 effects of Beta-2 postsynaptic agonism?

A
  1. Smooth muscle relaxation
  2. Peripheral vasodilation
  3. Decreased BP
  4. Bronchodilation
  5. Increased insulin secretion
  6. increased glycogenolysis and gluconeogenesis
  7. Decreased GI mobility
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22
Q

What are the main differences between Alpha 1 and Beta 2 stimulation?

A

Alpha 1 is more fight/flight and will decrease insulin and cause bronchoconstriction and vasocontriction.
Beta 2 increases insulin and causes bronchodilation and vasodilation

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23
Q

Where does the parasympathetic nervous system originate?

A

Craniosacral origin (III,V,VII,X).

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24
Q

Is the preganglia of the PNS near the organ or near the origin ?

A

Near the organ that it innnervates.

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25
Q

What is secreted by the postganglia with PNS stimulation?

A

Acetylcholine

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26
Q

Which electrolytes mediates the action potential of acetylcholine in the ANS?

A

Calcium

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27
Q

What deactivates acetylcholine?

A

Acetylcholinesterase

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28
Q

What are the two different types of cholinergic receptors?

A
  1. Nicotinic

2. Muscarinic

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29
Q

SNS or PNS cause gallbladder relaxation and urinary bladder muscle relaxation/sphincter contraction

A

SNS

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30
Q

What does extended exposure to agonists do to the body?

A

Reduces the number, but not their response. The result is tachyphylaxis/down regulation

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31
Q

What is up regulation?

A

Chronic depletion of catecholamines or use of antagonists increases the number of receptors, but noth their sensitivity. May accoutn for withdrawal syndrome with beta blockers.

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32
Q

What is sequestration of cell receptors?

A

Movement of receptors from the cell surface to intracellular compartments

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33
Q

T/F: Vasoconstrictors we use are all catecholamines, but not all of them are sympathomimetics?

A

False; all are sympathomimetics, but not all have catecholamine structure

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34
Q

What is different about the chemical structure of a NON-catecholamine sympathomimetic?

A

The hydroxyl groups are not present in both the 3 and 4 positions of the benzene ring.

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35
Q

Can a sympathomimetic be an indirect-acting catecholamine?

A

No; indirect acting sympathomimetics are synthetic non-catecholamines

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36
Q

What are the three different types of sympathomimetics?

A
  1. Naturally occurring catecholamines
  2. Synthetic catecholamines
  3. Synthetic non-catecholamines
    a. Indirect
    b. Direct
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37
Q

What substance are all sympathomimetics derived from?

A

B-Phenylethylamine

38
Q

All drugs containing the 3,4 dihydroxybenzene structure are rapidly inactivated by which two enzymes?

A
  1. Monoamine oxidase (MAO).

2. Catechol-o-transferase (COMT)

39
Q

Which has a greater potentiation of effect- inhibition of MAO/COMT or inhibition of reuptake mechanism?

A

Reuptake mechanism

40
Q

How can completeness of reuptake mechanism and metabolism be tested?

A

Checking for presence of unchanged catecholamines in urine

41
Q

Is metabolism of synthetic non catecholamines faster or slower and why?

A

Slower because on MAO can metabolize.

42
Q

Which patients can have dramatic responses to synthetic non-catecholamines?

A

Patients on MAO inhibitors

43
Q

What are MAO inhibitors used for?

A

Used to be used for PTSD/depression, now used for Parkinson’s

44
Q

What are the two hemodynamic effects of vasoconstrictors?

A
  1. Increase arterial resistance and afterload (Increase SVR and MAP).
  2. Increase venous return (increased preload and CO)
45
Q

What are the reflex changes of vasoconstrictors?

A
  1. Decreased HR
  2. Decreased conduction
  3. Occasionally, decreased contractility
46
Q

What are the non-cardiac effects of vasoconstrictors?

A
  1. Bronchodilate
  2. Glycogenolysis
  3. Insulin, renin, and pituitary hormone
  4. CNS stimulation
47
Q

How long does end organ damage take at a MAP <50mmHg? <65mmHg?

A

At <50mmHg takes 1 min

At <65mmHg takes 13-28min

48
Q

What are 4 contraindications/complications of vasoconstrictors?

A
  1. Can worsen LV failure
  2. Can exacerbate RV failure
  3. Can decrease RBF
  4. Can mask hypovolemia
49
Q

What are the three naturally occurring catecholamines?

A
  1. Epinephrine
  2. Norepinephrine
  3. Dopamine
50
Q

What natural catecholamine is the most potent activator of Alpha 1 receptors?

A

Epinephrine (2-10x more potent than NE).

51
Q

What changes in RBF can be seen in epinephrine administration?

A

Decreased RBF even in absence of changes in systemic BP (potent renal vasoconstrictor alpha 1 effect) and stimulates Renin release (indirect effect).

52
Q

What receptor does low dose epinephrine typically stimulate primarily?

A

Beta 2

53
Q

What is the overall net effect of Beta 2 stimulation from low dose epinephrine infusion?

A

Net decrease in SVR and distribution of blood to skeletal muscles.
MAP remains the same

54
Q

What is low dose epi gtt dose?

A

1-2mcg/min

55
Q

What receptors does intermediate dose epinephrine typically stimulate primarily?

A

Beta 1

56
Q

What are the net effects of intermediate dose epinephrine infusion?

A

Increase HR, contractility, CO and automaticity (may lead to dysrrhythmias)

57
Q

What is intermediate dose epi gtt dose?

A

4mcg/min

58
Q

What receptor does high dose epinephrine typically stimulate primarily?

A

Alpha 1

59
Q

What are the net effects of high dose epinephrine infusion?

A

Potent vasoconstriction. Reflex bradycardia can occur, used to maintained myocardial and cerebral perfusion

60
Q

What can be used as treatment for severe croup and post-extubation/airway trauma?

A

Racemic epinephrine

61
Q

Which drug is a potent vasoconstrictor of renal, mesenteric, and cutaneous vascular beds?

A

Norepinephrine

62
Q

Will you see Beta 2 agonist effects with low dose NE infusion?

A

No; beta 2 effects are minimal to none

63
Q

What happens to CO with changes in NE infusion rates?

A

Low dose- may increase CO

High dose may decrease because of increased afterlaod and baroreceptor mediated reflex bradycardia.

64
Q

Which drug do we use often that has both direct and indirect actions?

A

Ephedrine

65
Q

Is ephedrine a catecholamine?

A

no; synthetic non-catecholamine

66
Q

How is ephedrine metabolized?

A

MAO

67
Q

Is the principle effect of ephedrine direct or indirect?

A

Indirect

68
Q

Which has greater likelyhood of dysrrhythmias- ephedrine or phenylephrine?

A

Ephedrine

69
Q

What does long term/high dosages of ephedrine lead to?

A

Tachyphylaxis via Alpha 2 negative feedback loop

70
Q

Which medication is considered a pure Alpha 1 agonist?

A

Phenylephrine

71
Q

What is dose, onset, and duration of ephedrine?

A

2.5-25mg IV, Onset 1 min, duration 5-10min

72
Q

Why is duration longer for ephedrine compared to other medications?

A

Lack of uptake and only 1 enzyme breaks it down (MAO).

73
Q

What should be monitored while administering ephedrine or epinephrine?

A

E=everything

HTN, insomnia, urinary retention, H/A, weakness, tremor, palpitations, psychosis,

74
Q

T/F: Phenylephrine cannot be used to improve coronary perfusion pressure without also having positive chronotropic side effects?

A

False

75
Q

What HR changes can be seen with phenylephrine administration?

A

Reflex bradycardia (no direct effect on the heart)

76
Q

What is dose, onset, duration of phenylephrine?

A

50-100mcgIV, onset 1-2 min, duration 5-10min

77
Q

When comparing posterior pituitary hormones, how do their antidiuretic to vasopressor effect ratios differ?

A

Arginine vasopressin 100:100
Oxytocin 1:1
DDAVP 1200:0.39

78
Q

Which receptor is responsible for vasopressor effects from vasopressin admin?

A

V1a receptor

79
Q

Which receptor is responsible for renal collecting duct permeability increase from vasopressin admin?

A

V2 receptor

80
Q

Which ducts open and allow water to be retained?

A

Aquaporin (AQP2).

81
Q

What are 3 pros to using vasopressin as opposed to epi/NE in shock patients?

A
  1. No major glucose level siwngs
  2. Less renal damage
  3. Vasopressor effects are maintained even during hypoxia and severe acidosis
82
Q

What are the 5 advantages of vasopressin over epinephrine in cardiac arrest?

A
  1. Epi increases myocardial oxygen consumption
  2. Epi may not work well in acidic environments
  3. Vasopressin has better blood flow to vital organs
  4. Better delivery of cerebral oxygen
  5. Better chance of resuscitation with good neurological outcomes
83
Q

What are the two major drug interactions with vasoconstrictors?

A
  1. MAO inhibitors/tricyclic anti-depressants

2. Cocaine

84
Q

How does cocaine interfere with other catecholamines?

A

Interferes with re-uptake of catecholamines both exogenous and endogenous and produces an enhanced effect.

85
Q

What drug can be used in the management of acute cocaine toxicity?

A

Labetolol

86
Q

Why would pure beta blockade be contraindicated with cocaine OD?

A

You will see unopposed HTN

87
Q

What can be given in the event a vasoconstrictor extravasates ?

A

Phentolamine

88
Q

What is Giapreza?

A

Angiotensin II.

89
Q

What is the bad side effect of Giapreza administration?

A

DVT and arterial thrombosis.

90
Q

What should also be administered with Giapreza?

A

Prophylactic treatment for blood clots should be used.

91
Q

Which monomers of Racemic Epinphrine produce vasoconstriction of vessels?

A

L (levo)-monomer and D (dextro)-monomer

Pharm 2 (19 decks)

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