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APEX ANESTHESIA FLASHCARDS > UNIT 2 ANS > Flashcards

UNIT 2 ANS Flashcards

1
Q

What are the 4 classifications of receptors?

A
  1. ion channel
  2. GPCR
  3. enzyme linked receptor
  4. intracellular receptor
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2
Q

Describe the general architecture of the GPCR second messenger system.

A

1st messenger: extracellular signaling

Receptor: responds

G protein: turns off/on an effector

Effector: activates/inhibits a 2nd messenger

2nd messenger: primary intracellular signal

Enzymatic cascade

Cellular response

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3
Q

What second messenger system is associated w/ alpha-1 receptor? What other receptors share the same pathway?

A

Gq –> phospholipase C –> IP3/DAG/Ca++

others:
- histamine 1
- muscarinic 1, 3, 5
- vasopressin 1

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4
Q

What second messenger is associated w/ alpha-2 receptor? What other receptors share a similar pathway?

A

G1 –> adenylate cyclase –> ATP to cAMP

others:
- muscarinic 2
- dopamine 2

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5
Q

What second messenger system is associated w/ beta1 & beta2 receptors? What other receptors share a similar pathway?

A

Gs –> adenylate cyclase –> ATP to cAMP

others:
- histamine 2
- vasopressin 2
- dopamine 1

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6
Q

describe the autonomic innervation of the heart

A 
myocardium 
- B1 = increased contractility
- M2 = decreased contractility
conduction system 
- B1 = increased HR & conduction speed
- M2 = decreased HR & depressed CV

SNS: cardiac accelerator fibers from T1-T4
PNS: vagus

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7
Q

describe the autonomic innervation of the vasculature

A

vasculature:
arteries a1>a2 –> vasoconstriction
veins a2>a1 –> vasoconstriction

specific vascular beds:

  • myocardium B2 = vasodilation
  • skeletal m B2 = vasodilation
  • renal DA = vasodilation
  • mesenteric DA = vasodilation
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8
Q

Describe the autonomic innervation of the bronchial tree

A 
B2 = bronchodilation
M3 = bronchoconstriction

B2 aren’t innervated, just respond to catecholamines in the systemic circulation or the airway (inhaled)

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9
Q

Describe the autonomic innervation of the kidney

A

renal tubules: a2 = diuresis via ADH inhibition

renin release: B1 = increased renin release

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10
Q

Describe the autonomic innervation of the eye

A

sphincter m (iris) = M = contraction (miosis)

radial muscle (iris) = a1 = contraction (mydiasis)

ciliary m =
B2 = relaxation (far vision)
M = contraction (near vision)

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11
Q

Describe the autonomic innervation of the GI tract

A

sphincters
a1 = contraction
M = relaxation

motility & tone
a1/a2/B1/B2 = decrease
M = increase

salivary glands
a2 = decrease
M = increase

gallbladder & ducts
B2 = relaxation
M = contraction

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12
Q

describe the autonomic innervation of the pancreas

A

islet (beta cells)
a2 = decrease insulin release
B2 = increase insulin release

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13
Q

describe the autonomic innervation of the liver

A

a1/B2 = increase serum glucose

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14
Q

describe the autonomic innervation of the uterus

A 
a1 = contraction
B2 = relaxation
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15
Q

describe the autonomic innervation of the bladder

A

trigone & sphincter
a1 = contraction
M = relaxation

destrusor m
B2 = relaxation
M = contraction

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16
Q

describe the autonomic innervation of the sweat glands

A 
a1 = increase secretion
M = increase secretion
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17
Q

list the steps of NE synthesis. What is the rate limiting step?

A

tyrosine

  • -> DOPA (via tyrosine hydroxylase)
  • -> dopamine (via DOPA decarboxylase)
  • -> NE (via dopamine B-hydroxylase)
  • -> Epi (via phenylethanolamine N-methyltransferase)

Tyrosine hydroxylase is the rate limiting step

All occurs in the adrenal medulla

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18
Q

What are the 3 ways in which NE can be removed from the synaptic cleft? Which is the most important?

A
  1. reuptake (80%)
  2. diffusion away
  3. reuptake by extraneural tissue
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19
Q

What enzymes metabolize NE & Epi? What is the final metabolic byproduct?

A

MAO
COMT

final byproduct = vanillylmandelic acid (VMA) aka 3-methoxy-4-hydroxymandelic acid

elevated VMA in urine aids in diagnosis of pheochromocytoma

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20
Q

list the three types of cholinergic receptors. Where are each of these found inside the body?

A

Nicotinic M type (muscle)
- NMJ

Nicotinic N type

  • preganglionic fibers at autonomic ganglia (SNS & PNS)
  • CNS

Muscarinic

  • postganglionic PNS fibers at effector organs
  • CNS
21
Q

Describe the synthesis, release, and metabolism of acetylcholine

A

choline diffuses into cholinergic neuron; mitochondria produces AcetylCoA

Acetyl CoA + Choline
–> Ach (via ChAT)

released into synaptic cleft onto mAChR or nAChR

converted to choline + acetate

  • choline reuptake
  • acetate into vasculature
22
Q

list the 5 components of the autonomic reflex arc

A
  1. sensor
  2. afferent pathway
  3. control center
  4. efferent pathway
  5. effector
23
Q

compare and contrast the architecture of the SNS & PNS efferent pathways

A

both have pre & post ganglionic nerve fibers

PNS

  • preganglionic: long, myelinated, B fiber, releases ACh
  • postganglionic: short, unmyelinated, C-fiber, releases ACh

SNS

  • preganglionic: short, myelinated, B-fiber, releases ACh
  • postganglionic: long, unmyelinated, C-fiber, releases NE normally
  • releases ACh at sweat glands, piloerector m, and some vessels
24
Q

What is the origin of the efferent SNS pathways?

A

thoracolumber T1-L3
- cell bodies from the intermediolateral region of the SC & axons exit via the ventral nerve roots
preganglionic fibers usually synapse w/ postganglionic fibers in the 22 paired sympathetic ganglia

25
Q

What is the origin of the efferent PNS pathways?

A

craniosacral CN 3, 7, 9, 10 & S2-S4

- preganglionic synapse w/ postganglionic near or in each effector organ

26
Q

describe the innervation of the adrenal medulla. How is it different that then typical SNS efferent architecture?

A

there are no postganglionic fibers

pregang release ACh onto the chromaffin cells & the chromaffin cells release Epi & NE into the systemic circulation at a 80/20 ratio

27
Q

describe the hemodynamic management of the patient with pheochromocytoma

A

MUST a BLOCK BEFORE B BLOCK!!!!
if you dont:
- B2 block inhibits skeletal m vasodilation & increases SVR
- B1 block decreases inotropy & can precipitate CHF in the setting of incresed SVR

a-antagonists:

  • nonselective: phenoxybenzamine & phentolamine
  • a1 selective: doxazosin & prazosin
28
Q

What is the transcellular K+ shift & what causes it to occur?

A

describes a number of processes that alter serum K+ by shifting it in or out of cells

shift into cells = hypokalemia

  • alkalosis
  • B2 agonists
  • theophylline
  • insulin

shift out of cells = hyperkalemia

  • acidsois
  • cell ysis
  • hyperosmolarity
  • succinylcholine
29
Q

describe the anatomy & physiology of the baroreceptor reflex

A

regulates short term blood pressure control

  • high BP, reflex = decreased HR, contractility, & SVR
  • low BP, reflex = increased HR, contractility, and SVR

sensors in the carotid bodies & the aortic arch –> medulla (efferent)

afferent is via SNS/PNS

30
Q

describe the anatomy & physiology of the bainbridge reflex.

A

increases HR when venous return is too high. This is beneficial in minimizing venous congestion & promoting forward flow

sensor = SA node, RV, pulmonary veins
afferent = vagus
control = vasomotor center of medulla
efferent = vagus 
effects = SA node
31
Q

describe the anatomy & physiology of the Bezold-Jarisch reflex

A

decreases HR when venous return is too low. this gives an empty heart adequate time to fill

sensor = cardiac mechanoreceptors & chemoreceptors
afferent = vagus
control = medulla
efferent = vagus
effector = SA node & AV node

tx = restore preload & increase HR

32
Q

describe the anatomy & physiology of the oculocardiac reflex

A

five (V) & dime (X) reflex

sensor = pressure to the eye or globe
afferent = long & short ciliary n. --> ciliary ganglion --> V1 of CN V --> Gasserian ganglion
control = medulla
efferent = vagus
effector = SA node & AV node (decreased HR & conduction velocity)

tx = remove stimulus, 100% FiO2, atropine/glyco

33
Q

What is the primary determinant of CO in the pt w/ a heart transplant? What is the consequence of this?

A

severed from autonomic influence, so HR is determined by intrinsic SA rate. Often have resting tachycardia 100-120

CO is dependent on preload in these patients, they are very sensitive to hypovolemia

34
Q

What drugs can be used to augment HR in the patient w/ a heart transplant?

A

no autonomic input from the cardiac accelerator fibers (T1-T4) or the vagus nerve. Thus, good to use: those that directly stimulate the SA node:

  • epi
  • isoproterenol
  • glucagon

those that indirectly stimulate SA cannot be used (atropine, glyco, ephedrine)

35
Q

A pt presents for removal of a glomus tumor. What are your primary concerns when planning your anesthetic?

A

(glomangiomas) originate from neural crest cells. Tent to grow in the neuroendocrine tissues that lay in close proximity to the carotid artery, aorta, CN IX, and middle ear. Usually not malignant

  • can release vasoactive substances that lead to HTN/hypotension (NE, 5-HT, histamine, bradykinin)
  • octreotide can be used to treat carcinoid-like s/sx
  • CN dysfunction (IX, X, XII) can cause swallowing impairment, aspiration of gastric contents, and a/w obstruction
  • surgical dissection of glomulus tumor that has invaded the IJ vein increass risk of VAE
36
Q

what are the anesthetic considerations for multiple system atrophy?

A

(previously known as Shy-Drager syndrome)

causes degneration of the locus coeruleus, intermediolateral column of the SC (where cell bodies for SNS efferent fibers live), & peripheral autonomic nerves

  • autonomic dysfunction (orthostatic hypotension)
  • tx hypotension w/ volume & direct acting sympathomimetics
  • exaggerated hypertensive response to ephedrine & possibly ketamine
37
Q

Compare & contrast low, intermediate, and high dose epi

A

low (0.01-0.03mcg/kg/min)
- nonselective B effects predominate –> increased CO w/ reduction in SVR & possibly a slight reduction in BP w/ widened pulse pressure)

intermediate (0.03-0.15mcg/kg/min)
- mixed B & a effects

high (>0.15mcg/kg/min)
- a effects prevail –> HTN, risk for SVT

38
Q

describe the cardiovascular effects of isoproterenol

A

synthetic catecholamine that stimulates B1 & B2 receptors

  • increases HR, contractility, & myocardial O2 consumption
  • decreases SVR, which reduces DBP, which may reduce CPP
  • causes severe dysrhythmias & tachycardia
  • vasodilates nonessential vascular beds (i.e. muscle & skin). This precludes its use in septic shock.
39
Q

list 4 clinical indications for isoproterenol

A
  1. chemical pacemaker for bradycardia unresponsive to atropine
  2. heart transplant
  3. bronchoconstriction
  4. cor pulmonale
40
Q

in what situations should ephedrine not be used to treat hypotension?

A
  • when neuronal catecholamine stores are depleted (sepsis) or absent (heart transplant)
  • risk of hypertensive crisis in pts on MAO inhibitors
  • conditions where increased HR or contractility is detrimental to hemodynamics
41
Q

How does vasopressin increase BP

A 
V1 = intense vasoconstriction 
V2 = increases intravascular volume by stimulating the synthesis & insertion of aquaporins into the walls of the collecting ducts (increases water reabsorption & lowers serum osmolarity)
42
Q

What is the best treatment for vasoplegic syndrome

A

aka refractory hypotension. Key = hypotension doesn’t respond to conventional therapies such as adrenergic agonists, hydration, and reducing depth of anesthesia

  • vasopressin is the best tx (0.5-1U IV bolus, 0.03U/min)
  • incidence is increased by ACEI or ARBs
  • methylene blue is the next best choice
43
Q

list 6 drugs that are selective for the B1 receptor

A 
atenolol
acebutolol
betaxolol
bisoprolol
esmolol
metoprolol
44
Q

list 6 nonselective B blockers

A 
coreg
labetalol
nadolol
pindolol
propranolol
timolol
45
Q

what is the primary site of metabolism of the commonly used beta blockers? what are two exceptions?

A

most depend on the liver as their primary site of metabolism

2 exceptions: esmolol (by RBC esterases) & atenolol (by kidneys)

46
Q

which beta blockers have LA properties? What is another name for this?

A

propanolol
acebutolol

another name = membrane stabilizers

effect = reduction in the rate of the rise of the cardiac AP

47
Q

what is intrinsic sympathomimetic activity? Which drugs exert this effect?

A

BB that exert a partial agonist effect, while simultaneous blocking other agonsts that have a higher affinity for the B receptor

labetalol
pindolol

48
Q

list 3 alpha antagonists. What is the MOA for each?

A

reduce BP by causing vasodilation (decreased SVR)

phenoxybenzamine: nonselective, noncompetitive binding, long acting
phentolamine: nonselective, competitive binding, short acting
prazosin: selective alpha1 antagonist

APEX ANESTHESIA FLASHCARDS (14 decks)

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