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Apex ANS > ANS > Flashcards

ANS Flashcards

1
Q

ALPHA 1 -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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2
Q

ALPHA 2 -
Signal Transduction
Effector
Second Messenger

A

Gi
Decrease Adenylate cyclase
Decrease cAMP

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3
Q

BETA 1 -
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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4
Q

BETA 2 -
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Incrase cAMP

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5
Q

MUSCARINIC 1/3/5 -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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6
Q

MUSCARINIC 2/4-
Signal Transduction
Effector
Second Messenger

A

Gi
Decrease Adenylate cyclase
Decrease cAMP

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7
Q

NICOTINIC (ANS ganglia, NMJ, & CNS)
Signal Transduction
Effector
Second Messenger

A

Ion channels
N/A
N/A

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8
Q

DOPAMINE 1 (post-synaptic)
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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9
Q

DOPAMINE 2 (pre-synaptic)
Signal Transduction
Effector
Second Messenger

A

Gi
Decrease Adenylate cyclase
Decrease cAMP

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10
Q

VASOPRESSIN 1 (vasculature) -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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11
Q

VASOPRESSIN 2 (renal tubules) -
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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12
Q

HISTAMINE 1 -
Signal Transduction
Effector
Second Messenger

A

Gq
Increase Phospholipase C
Increase IP3, DAG, Ca+2

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13
Q

HISTAMINE 2-
Signal Transduction
Effector
Second Messenger

A

Gs
Increase Adenylate cyclase
Increase cAMP

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14
Q

MYOCARDIUM
SNS Receptor
Action

A

B1

Increased contractility

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15
Q

MYOCARDIUM
PNS Receptor
Action

A

M2

Decreased contractility

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16
Q

CONDUCTION SYSTEN
SNS Receptor
Action

A

B1

Increased HR, Increased conduction speed

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17
Q

CONDUCTION SYSTEN
PNS Receptor
Action

A

M2

Decreased HR, Decreased conduction speed

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18
Q

ARTERIES
SNS Receptor
Action

A

A1 > A2
Vasoconstriction

*No PNS receptors

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19
Q

VEINS
SNS Receptor
Action

A

A2 > A1
Vasoconstriction

*No PNS receptors

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20
Q

MYOCARDIUM VASCULATURE
SNS Receptor
Action

A

B2
Vasodilation

*No PNS receptors

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21
Q

SKELETAL MUSCLE VASCULATURE
SNS Receptor
Action

A

B2
Vasodilation

*No PNS receptors

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22
Q

RENAL VASCULATURE
SNS Receptor
Action

A

DA
Vasodilation

*No PNS receptors

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23
Q

MESENTERIC VASCULATURE
SNS Receptor
Action

A

DA
Vasodilation

*No PNS receptors

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24
Q

BRONCHIAL TREE
SNS Receptor
Action

A

B2

Bronchodilation

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25
Q

BRONCHIAL TREE
PNS Receptor
Action

A

M3

Bronchoconstriction

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26
Q

RENAL TUBULES
SNS Receptor
Action

A

A2
Diuresis

*No PNS receptors

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27
Q

RENIN RELEASE
SNS Receptor
Action

A

B1
Increased renin release

*No PNS receptors

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28
Q

SPHINCTER MUSCLE (IRIS)
SNS Receptor
Action

A

No SNS receptor

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29
Q

SPHINCTER MUSCLE (IRIS)
PNS Receptor
Action

A

M3, M2

Contraction (miosis)

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30
Q

RADIAL MUSCLE (IRIS)
SNS Receptor
Action

A

A1
Contraction (mydriasis)

*No PNS receptor

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31
Q

CILIARY MUSCLE
SNS Receptor
Action

A

B2

Relaxation (far vision)

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32
Q

CILIARY MUSCLE
PNS Receptor
Action

A

M3, M2

Contraction (near vision)

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33
Q

SPHINCTERS
SNS Receptor
Action

A

A1

Contraction

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34
Q

SPHINCTERS
PNS Receptor
Action

A

M

Relaxation

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35
Q

GI MOTILITY & TONE
SNS Receptor
Action

A

A1/A2/B1/B2

Decrease

36
Q

GI MOTILITY & TONE
PNS Receptor
Action

A

M

Increase

37
Q

SALIVARY GLANDS
SNS Receptor
Action

A

A2

Decrease

38
Q

SALIVARY GLANDS
PNS Receptor
Action

A

M

Increase

39
Q

GALLBLADDER & DUCTS
SNS Receptor
Action

A

B2

Relaxation

40
Q

GALLBLADDER & DUCTS
PNS Receptor
Action

A

M

Contraction

41
Q

BETA CELLS - Alpha and Beta
SNS Receptor
Action

A

A2 - Decrease insulin release
B2 - Increase insulin release

*No PNS receptor

42
Q

LIVER
SNS Receptor
Action

A

A1/B2

Increase serum glucose

43
Q

UTERUS - Alpha and Beta
SNS Receptor
Action

A

A1 - Contraction
B2 - Relaxation

*No PNS receptor

44
Q

BLADDER TRIGONE & SPHINCTER
SNS Receptor
Action

A

A1

Contraction

45
Q

BLADDER DETRUSOR
SNS Receptor
Action

A

B2

Relaxation

46
Q

BLADDER TRIGONE & SPHINCTER
PNS Receptor
Action

A

M

Relaxation

47
Q

BLADDER DETRUSOR
PNS Receptor
Action

A

M

Contraction

48
Q

SWEAT GLANDS
SNS Receptor
Action

A

A1

Increase secretion

49
Q

SWEAT GLANDS
PNS Receptor
Action

A

M

Increase secretion

50
Q

ANS innervation of eye

A1 stimulation

A

radial muscle contraction

mydriasis = pupil DILATION

51
Q

ANS innervation of eye

Muscarinic stimulation

A

sphincter muscle contraction

miosis = pupil CONSTRICTION

52
Q

BRR

If the heart rate increases in setting of hypotension OR decrease in setting of hypertension, BRR is said to be

53
Q

Volatile gas

Decrease or Increase effectiveness of BRR

A

Decrease in dose-dependent

54
Q

Volatile gas

which gas impairs BRR lease

A

Iso

mild B1 agonist properties

55
Q

IV Induction agents and BRR

Thiopental

56
Q

IV Induction agents and BRR

Propofol

A

Depresses - decrease in HR with decrease in SVR

57
Q

IV Induction agents and BRR

Ketamine

A

activates SNS - increase HR but no change in SVR

In critically ill pts, with exhausted catecholamine reserve, myocardial depressant effects may be noticed

58
Q

IV Induction agents and BRR

Etomidate

A

No change in HR, small decrease in SVR. Hypovolemic pts my experience hypotension

59
Q

Vasodilators and BRR

Hydralazine

A

Preserves BRR

Decrease in SVR with Increase in HR

60
Q

Vasodilators and BRR

Nitroprusside

A

Preserves BRR

61
Q

Vasodilators and BRR

Nitroglycerine

A

Preserves BRR

62
Q

Beta blockers and BRR

A

May prevent a compensatory rise in HR in setting of hypotension

63
Q

BB and BRR

Labetalol

A

BB
Also antagonizes A-1 receptor
May increase the risk of orthostatic hypotension

64
Q

Catecholamines and BRR

NE

A

Effect on HR is dose-dependent
Lower doses - B1 chronotropic effects prevail
Higher doses - A1 vasoconstrictive effects overshadow B1 = BRR fall in HR

65
Q

Catecholamines and BRR

epi, dobutamine, isoproterenol, dopamine

A

BRR NOT preserved

HR increases

66
Q

Phenylephrine and BRR

A

BRR is preserved
Bradycardia is side effect
Not a catecholamine

67
Q

Adrenergic Agonists

NE

A 
Low dose - B1 selective (increase HR, increase inotropy)
High dose ( - stimulates A1, A2, B1 - increase SVR to increase BP and decrease HR via BRR

0.02-0.4 mcg/kg

68
Q

Adrenergic Agonists
NE
When is ideal to use?

A

Ideal drug for low SVR states like sepsis or post-CPB hypotension due to low afterload

69
Q

Adrenergic Agonists
NE
When to avoid use?

A

In the setting of cardiogenic shock bc it increase afterload and MVO2

70
Q

Treatment of NE extravasation

A

Injection with phentolamine (2.5-10 mg in 10 mL of dilute)

Stellate ganglion block

71
Q

Adrenergic Agonists

Epi

A 
Low dose (0.01-0.03 mcg/kg) - b1 and B2 (increase HR, increase CO, increase inotropy, decrease SVR)
Intermediate dose(0.03-0.15 mcg/kg) - Mixed alpha and beta
High dose (>0.15)- Alpha effects predominate and SVT common
72
Q

Adrenergic Agonists
Epi
Key points

A

Bronchodilation - think bronchospasm!
Mast cell stabilization - think anaphylaxis!
Prolongs duration of LA
Increases serum glucose
Causes hypokalemia due to transcellular K+ shift

73
Q

Adrenergic Agonists

Dopamine

A 
Low dose (1-2 mcg/kg) - Renal vasodilation and incrase RBF 
Intermediate (2-10 mcg/kg) - Increase HR, increase inotropy, increase CO
High dose (10-20 mcg/kg) - Vasopressor effect - Alpha effects overshadow
74
Q

Adrenergic Agonists

Isoproterenol

A

Synthetic catecholamine derived from dopamine
Stimulates B1, B2
0.02-0.5 mcg/kg
increase HR, incrase inotropy, incrase CO
Vasodilation decrease SVR
Can cause dysrthymias and tachycardia

75
Q

Adrenergic Agonists
Isoproterenol
What to be aware/cautious of?

A

reduction in SVR can be so severe as to drop DBP, and this can impair CPP

Also makes it a poor choice for septic shock

76
Q

Adrenergic Agonists
Isoproterenol
Key points

A

chemical PM for bradycardia unresponsive to atropine or for the pt w a denervated heart
Treatment of bronchoconstriction
Treatment of cor pulmonale

77
Q

Adrenergic Agonists

Dobutamine

A

Sympathomimetic amine
Potent B1 and mild B2 agonist
Increase HR, Increase inotropy, increase CO

0.5-15 mcg/kg

78
Q

Adrenergic agent

Phenylephrine

A

Alpha1 receptor
Direct acting

Increases SVR
Increases CPP
Reflex bradycardia
Good for conditions where increase afterload is required, such as hypertrophic cardiomyopathy or tetralogy of Fallot

Infusion 10-200 mcg/min

79
Q

Adrenergic agent

Ephedrine

A

Non-catecholamine
Direct and Indirect
A1, A2, B1, B2
Increase HR, Increase inotropy, increase CO, increase SVR
Multiple doses can cause tachyphylaxis - progressively smaller response to a given dose after multiple administrations

80
Q

Adrenergic agent
Ephedrine
When doesn’t ephedrine work?

A

When neuronal catecholamine stores are:

  1. depleted - SEPSIS
  2. absent - denervated heart (HEART TRANSPLANT)
81
Q

Adrenergic agent
Ephedrine
Pts on MAOI are at risk for what?

A

Hypertensive crisis

82
Q

Adrenergic agent
Vasopressin
Where does it come from?

A

Produced by the hypothalamus and released by the Posterior Pituitary Gland

83
Q

Adrenergic agent
Vasopressin
How does it restore BP?

A
  1. V1 receptor simulation causes intense vasoconstriction
  2. V2 receptor simulation stimulates the synthesis and insertion of aquaporins into the walls of the collecting ducts. This increase water (but not solute) reabsorption and lowers serum osmolarity
84
Q

Adrenergic agent
Vasopressin
Key points

A

IV bolus - 0.5-1 unit
IV infusion - 0.01-0.04 units/min

First line therapy for ACEI or ARB induced vasoplegia that’s refractory to catecholamines
*NOTE: methylene blue is next best drug

85
Q

Adrenergic agent
Vasopressin
Overdose can cause what?

A

Hyponatremia and seizures

86
Q

What causes K+ to shift into cells?

A

Alkalosis - Activating Na+/K+ pump
B2 agonists (albuterol, ritodrine, epi)
Theophylline
Insulin

87
Q

What causes K+ to shift out of cells?

A

Acidosis - Activating H+/K+ pump
Cell lysis
Hyperosmolarity
Succ

Apex ANS (1 decks)

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