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ANS Flashcards

1
Q

What are 4 classifications of receptors?

A
  • Ion channel
  • G-protein coupled receptor
  • Enzyme linked receptor
  • Intracellular receptor
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2
Q

What is signal transduction?

A

The process which a cell converts an extracellular signal into an intracellular response.

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3
Q

Describe the general architecture of the G-Protein second messenger system.

A

1st messenger (extracellular signal)
Receptor (responds to an extracellular signal)
G-protein (turns off or turns on an effector)
Effector (activates or inhibits the second messenger)
Second messenger (the primary intracellular signal)
Enzymatic cascade (a bunch of steps you don’t have to worry about)
Cellular response (causes a physiologic change)

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4
Q

What second messenger system is associated with the alpha-1 receptor?

A

increased Phopholipase C

which increases IP3, DAG, Ca++

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5
Q

What receptors share a similar 2nd messenger pathway as alpha-1?

A
  • Histamine-1
  • Muscarinic-1,3,5
  • Vasopressin-1 (vascular)
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6
Q

What second messenger system is associated with the alpha-2 receptor?

A

Decreased Adenylate cyclase (inhibition)

which decreases cAMP

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7
Q

What receptors share a similar 2nd messenger pathway as alpha-2?

A
  • Muscarinic-2,4

- Dopamine-2 (presynaptic)

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8
Q

What second messenger system is associated with the beta-1 and -2 receptor?

A

Increased Adenylate cyclase

which increases cAMP

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9
Q

What receptors share a similar 2nd messenger pathway as Beta-1 and -2?

A
  • Histamine-2
  • Vasopressin-2 (renal)
  • Dopamine-1 (post-synaptic)
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10
Q

What fibers innervate the heart for the SNS?

A

cardiac accelerator fibers arising from T1-4

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11
Q

What fibers innervate the heart for the PNS?

A

Vagus nerve (CN X)

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12
Q

What affect does stimulation of beta-1 receptors have on the heart?

A

increased contractility, heart rate, and conduction speed

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13
Q

What affect does stimulation of M2 receptors have on the heart?

A

decreased contractility, heart rate, and CV

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14
Q

What receptors are responsible for vasoconstriction?

A

arteries: alpha1 > alpha2
veins: alpha2 > alpha1

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15
Q

What receptors are responsible for vasodilation in the myocardium and skeletal muscle?
Renal and mesenteric?

A

beta-2: myocardium & skeletal muscle

DA- renal, mesenteric

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16
Q

Stimulation of what receptors cause bronchodilation?

A

beta-2

*Beta-2 receptors are not innervated. Instead, they respond to catecholamines in the systemic circulation or in the airway (inhaled).

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17
Q

Stimulation of what receptors cause bronchoconstriction?

A

M3

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18
Q

Stimulation of what receptor causes diuresis (ADH inhibition)?

A

Alpha-2 at the renal tubules

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19
Q

Stimulation of what receptor causes increased renin release?

A

Beta-1

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20
Q

Stimulation of what receptor causes contraction of the sphincter muscles of the iris (miosis)?

A

Muscarinic

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21
Q

Stimulation of what receptor causes contraction of radial muscle of the iris (mydriasis)?

A

Alpha-1

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22
Q

Stimulation of what receptor causes relaxation of the ciliary muscles (far vision)?

A

Beta-2

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23
Q

Stimulation of what receptor causes contraction of the ciliary muscles (near vision)?

A

Muscarinic

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24
Q

Receptor that causes contraction of GI sphincters:

A

Alpha-1

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25
Q

Receptor that causes Relaxation of GI sphincters:

A

Muscarinic

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26
Q

Receptor that decreases GI motility and tone:

A

A1 A2 B1 B2

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27
Q

Receptor that increases GI motility and tone:

A

Muscarinic

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28
Q

Receptor that decreases salivary glands:

A

alpha2

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29
Q

Receptor that increases salivary glands:

A

muscarinic

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30
Q

Receptor that relaxes gallbladder and ducts:

A

Beta2

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31
Q

Receptor that contracts gallbladder and ducts:

A

muscarinic

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32
Q

Receptor that decreases insulin release from islet (beta) cells:

A

Alpha 2

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33
Q

Receptor that increases insulin release from islet (beta) cells:

A

beta 2

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34
Q

Receptor in the liver that increases serum glucose:

A

alpha 1

beta 2

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35
Q

Receptor that increases uterine contraction:

A

alpha 1

36
Q

Receptor that relaxes uterus:

A

beta 2

37
Q

Receptor that contracts bladder trigone and sphincter:

A

alpha 1

38
Q

Receptor that relaxes bladder trigone and sphincter:

A

muscarinic

39
Q

Receptor that relaxes bladder detrusor:

A

beta 2

40
Q

Receptor that contracts bladder detrusor:

A

muscarinic

41
Q

Receptor that increases perspiration:

A

alpha1

muscarinic

42
Q

what is the primary neurotransmitter in the SNS?

A

Norepi

43
Q

list the steps of norepinephrine synthesis:
(what’s the rate limiting step)
(* see ANS section for photo)

A

Tyrosine –(tyrosine hydroxylase)–>DOPA –(DOPA decarboxylase)–> dopamine – (dopamine b-hydroxylase)–> norepinephrine – (phenylethanolamine n-methyltransferase) –> epinephrine

  • norepi –>tyrosine hydroxylase is a negative feedback loop and rate limiting step
  • *phenyl methyl–> epi is in the adrenal medulla
44
Q

3 ways NE can be removed from the synaptic cleft

A
  • Reuptake into presynaptic neuron (80%)
  • diffusion away from the synaptic cleft
  • reuptake by extra neural tissue
45
Q

2 metabolic pathways for NE and EPI?

What is the final metabolic byproduct?

A
  • Monoamine oxidase (MAO)
  • Catechol-O-Methyltransferase (COMT)

Final byproduct: Vanillylmandelic acid (VMA) aka 3-methoxy-4-hydroxymandelic acid.

46
Q

what does an elevated level of VMA in the urine aid in diagnosing?

A

phenochromocytoma

47
Q

3 types of cholinergic receptors and their location in the body:

A
  1. Nicotinic type-M (muscle)
    - Neuromuscular junction
  2. Nicotinic type N (nerve)
    - preganglionic fibers at autonomic ganglia (SNS and PNS)
    - central nervous system
  3. Muscarinic
    - postganglionic PNS fibers at effector organs
    - central nervous system
48
Q

Synthesis, release, and metabolism of acetylcholine:

see photo in ANS module

A

Choline goes from blood to cholinergic neuron.
Acetyl CoA goes from Mitochondria to cholinergic neuron.
Choline + Acetyl CoA use ChAT to form Ach.
Ach enters vesicle then released into NMJ.

It binds with post synaptic M or N receptor.
AchE breaks it down to Acetate and Choline.
Choline is reuptake into cholinergic neuron.

49
Q

5 components of autonomic reflex arc:

A

Sensor –> afferent pathway –> control center –> efferent pathway –> effector

50
Q

Architecture of PNS efferent pathway:

A

Pre-ganglionic: Long, myelinated, B-fiber, release Ach

Post-ganglionic: short, unmyelinated, C-fiber, release Ach

51
Q

Architecture of SNS efferent pathway:

A

Pre-ganglionic: short, myelinated, B-fiber, releases Ach

Post-ganglionic: Long, unmyelinated, C-fiber, release NE
*Ach released at sweat glands, piloerector muscles, and some vessels

52
Q

Origin of the efferent SNS pathways:

A

Thoracolumbar (T1-L3)

Cell bodies arise from the intermediolateral region of the spinal cord and axons exit via ventral nerve roots.

Preganglionic fibers usually synapse with postganglionic fibers in the 22 paired sympathetic ganglia (mass effect).

53
Q

Origin of the efferent PNS pathways:

A

Craniosacral (CN 3, 7, 9, 10, S2-S4)

Preganglionic fibers synapse with postganglionic fibers near or in each effector organ (precise control of each organ)

54
Q

Innervation of adrenal medulla:

A

NO postganglionic fibers.
Preganglionic fibers release Ach onto the chromatin cells, which then release EPI/NE into systemic circulation at a ratio of EPI 80% : NE 20%

*can think of adrenal medulla as autonomic ganglion that is in direct communication with the bloodstream.

55
Q

Hemodynamic management of a pt with pheochromocytoma:

A

Alpha block BEFORE beta block!!

Non-selective alpha blockers: phenoxybenzamine and phentolamine
Alpha1 selective: Doxazosin and prazosin

56
Q

Problems that arise from blocking beta before alpha in phenochromocytoma patients:

A

Beta2 blockade inhibits skeletal muscle vasodilation and increases SVR.
Beta1 blockade reduces inotropy and can precipitate CHF in the setting of increased SVR

57
Q

Things that shift potassium into cells:

A

Alkalosis
Beta-2 agonists
Theophylline
Insulin

58
Q

Things that shift potassium out of cells:

A

Acidosis
cell lysis
hyperosmolarity
succinylcholine

59
Q

Baroreceptor reflex:

see photo in ANS module

A

Regulates short term blood pressure control.

Increased BP –> baroreceptor decreases HR, contractility, and SVR

Decreased BP –> baroreceptor increases HR, contractility, and SVR

60
Q

What mediates long term blood pressure control?

A

RAAS and ADH

61
Q

Describe the Bainbridge reflex:

A

increases HR when venous return is too high (this minimizes venous congestion and promotes forward flow)

Sensor: SA node, RV, Pulmonary veins
Afferent: Vagus nerve
Control: vasomotor center in medulla
Efferent: vagus (inhibitory) 
Effector: SA node increases HR

example: autotransfusion during child birth

62
Q

Describe the Bezold-Jarisch reflex:

A

Decreases HR when venous return is too low. (gives an empty heart adequate time to fill)

Sensor: cardiac mechanoreceptors (venous return) and chemoreceptors (ischemia)
Afferent: Vagus
Control: Vasomotor center in medulla
Efferent: vagus
Effector: SA node decreases HR, AV node decreases conduction velocity

tx: restore pre-load (IVF and leg elevation) increase HR (EPI is best)
ex: cardiac arrest during spinal, massive hemorrhage, myocardial ischemia, shoulder arthroscopy + inter scalene block with epi + sitting position

63
Q

Describe the oculocardiac reflex:

A

Sensor: pressure to eye
Afferent: long/short ciliary n. –>ciliary ganglion –> trigeminal V1 ophthalmic –> gasserian ganglion
Control: vasomotor center in medulla
Efferent: Vagus
Effector: SA node decreases HR, AV decreases CV

tx: remove stimulus, 100% FiO2, ensure proper ventilation, deepen anesthetic, anticholinergic (atropine/robinul)
ex: strabismus repair, ocular trauma, retrobulbar block (can cause or prevent)

64
Q

Primary determinant of CO in heart transplant patients:

consequences?

A

Heart is severed from autonomic influence; HR is determined by intrinsic rate of SA node. (this is why they have resting tachycardia; HR 100-120)

CO is dependent on preload because HR is fixed. They are very sensitive to hypovolemia.

65
Q

Drugs that can be used to augment HR in a heart transplant patient:

A

Direct stimulation of SA node to increase HR (EPI, isoproterenol, glucagon)

Indirect stimulation of the SA node can NOT be used (atropine, glycopyrrolate, ephedrine)

*there is no autonomic input from cardiac accelerator fibers (T1-4) or vagus.

66
Q

Glomus tumor (glomangioma):

A
  • Originate from neural crest cells.
  • Grow in Neuroendocrine tissues close to carotid artery, aorta, glossopharyngeal n., and middle ear.
  • Usually not Malignant.
  • Can release vasoactive substances leading to exaggerated hyper- or hypotension (NE, 5HT3, Histamine, bradykinin)
  • Octreotide to treat carcinoid-like s/s.
  • CN dysfunction (glossopharyngeal, vagus, hypoglossal) can cause swallowing impairment, aspiration and airway obstruction.
  • surgical dissection of gloms tumor that has invaded IJ vein increases risk of air embolism
67
Q

What is multiple system atrophy (aka shy-drawer syndrome):

A

-Causes degeneration of the locus coeruleus, intermediolateral column of the spinal cord (where cell bodies for the SNS efferent nerves live), and peripheral autonomic nerves.

68
Q

Anesthetic considerations for multiple system atrophy (aka shy-drawer syndrome):

A
  • Autonomic dysfunction (orthostatic hypotension)
  • Treat hypotension with volume and direct acting sympathomimetics.
  • Exaggerated HTN response to ephedrine and possibly ketamine.
69
Q

Low dose EPI:

A

0.01-0.03mcg/kg/min

Non-selective beta effects:
B1 increases HR/contractility
B2 vasodilator skeletal muscle
Net effect is increase in CO, decrease SVR, slight decrease in BP, Pulse pressure increased (wider)

70
Q

Intermediate dose EPI:

A

0.03-0.15 mcg/kg/min

Mixed Beta and Alpha effects

71
Q

High dose EPI:

A

> 0.15 mcg/kg/min

alpha > beta
BP rises
SVTs are common and limit usefulness of high does EPI

72
Q

Cardiovascular effects of Isoproterenol:

A

Synthetic catecholamine that stimulates B1/B2

  • increase HR, contractility, and myocardial O2 consumption.
  • decreased SVR, which reduces DBP. this may reduce coronary perfusion pressure.
  • can cause severe dysrhythmias and tachycardia
  • Vasodilates nonessential vascular beds (muscle and skin) which precludes its use in septic shock.
73
Q

Coronary perfusion pressure calculation:

A

CPP = AoDB - LVEDP

74
Q

4 indications for isoproterenol:

A

Chemical pacemaker for bradycardia unresponsive to atropine.
Heart transplant
Bronchoconstriction
Cor Pulmonale

75
Q

When to NOT use ephedrine:

A

Ephedrine uses endogenous catecholamine stores from presynaptic sympathetic nerves.

  • Doesn’t work when catecholamine stores depleted (sepsis) or absent (heart transplant).
  • risk of HTN crisis in pt on MAO-I
  • Conditions where increased HR or contractility is detrimental to hemodynamics.
76
Q

How does Vasopressin increase BP?

A

V1 receptor stimulation causes intense vasoconstriction.
V2 receptor stimulation increases intravascular volume by stimulating the synthesis and insertion of aquaporins into the walls of collecting ducts. This increases water (but not solute) reabsorption and lowers serum osmolarity.

77
Q

Difference between Vasopressin and Aldosterone:

A

Alosterone increases H2O AND sodium reabsorption (serum osmolarity is unchanged).

78
Q

What is Vasoplegic syndrome:

A

Refractory hypotension. The key here is that hypotension doesn’t respond to conventional therapies such as adrenergic agonists, hydration, and reducing depth of anesthesia.

79
Q

Best tx for vasoplegic syndrome:

A

Vasopressin 0.5-1 U IV bolus and 0.03u/min infusion

  • Incidence of vasoplegic syndrome is increased by ACE-I or ARBs
  • Methylene blue is the next best choice.
80
Q

6 drugs selective for Beta1 receptor:

A 
Atenolol
Acebutolol 
Betaxolol
Bisoprolol
Esmolol
Metoprolol
81
Q

6 non-selective Beta blockers:

A 
Carvedilol
Labetalol
Nadolol
Pindolol
Propranolol
Timolol
82
Q

Primary site of metabolism of commonly used beta blockers?

and 2 exceptions?

A

Primary site: liver

Exceptions:

  • Esmolol (RBC esterases; NOT pseudocholinesterase)
  • Atenolol (Kidneys)
83
Q

Beta blockers with LA properties:

How do they work?

A

(aka Membrane stabilizing properties)

Propranolol
Acebutolol

Reduces the rate of rise of the cardiac action potential, however it probably only occurs when these drugs reach toxic levels.

84
Q

What is intrinsic sympathomimetic activity?

Which drugs exert this effect?

A

Beta blockers that exert partial agonist effect, while simultaneously blocking other agonists that have a higher affinity for the beta receptor.

Labetalol and pindolol

85
Q

3 Alpha Antagonists and their MOA:

A

Reduce BP by vasodilation (decreased SVR)

  • Phenoxybenzamine: long acting, non-selective antagonist
  • Phentolamine: Short acting, non-selective, competitive antagonist
  • Prazosin: selective A1 antagonist

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