ANS Flashcards

1
Q

Gq receptor

A

↑ Phospholipase C → ↑ IP3, DAG, Ca2+

  • A1
  • M1, M3, M5
  • V1
  • H1
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2
Q

Gi receptor

A

↓ adenylate cyclase → ↓ cAMP

  • A2
  • M2, M4
  • D2
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3
Q

Gs receptor

A

↑ adenylate cyclase → ↑ cAMP

  • B1, B2
  • D1
  • V2
  • H2
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4
Q

B1 receptor

A
  • myocardium, conduction system → ↑ HR, contractility, conduction speed
  • kidneys → renin release
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5
Q

B2 receptor

A

Bronchial tree → bronchodilation

Myocardial and skeletal muscle vascular beds → vasodilation

Ciliary muscle relaxes (far vision)

Gallbladder and ducts relax

Pancreas islet beta cells release MORE insulin

Liver ↑ serum glucose

Uterus relaxes

Bladder: destrusor relaxes

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6
Q

A1 receptor

A

Vasoconstriction (arteries > veins, but both)

EYES: radial muscle (iris) → contracts → MYDRIASIS

GI: sphincters contract

LIVER: serum glucose ↑

UTERUS: contracts

BLADDER: trigone + sphincter contract

Sweat glands ↑ secretion

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7
Q

A2 receptor

A
  • vasoconstriction (veins > arteries, but both)
  • Kidney: renal tubules → ADH inhibition → DIURESIS
  • pancreas: Islet beta cells ↓ insulin release → hyperglycemia
  • Salivary glands: dries out
  • antishivering
  • promotes platelet aggregation
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8
Q

SNS receptors in kidneys

A

A2 (renal tubules, diuresis via ADH inhibition)

B1 (↑ renin release)

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9
Q

DA receptors

A

-renal and mesenteric vasodilation

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10
Q

M2 receptors

A

-HEART: myocardium, conduction system: → ↓ HR, contractility

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11
Q

M3 receptor

A

BRONCHIAL TREE → bronchoconstriction

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12
Q

Phosphodiesterase III

A
  • metabolizes cAMP to AMP which basically “turns off” a specific protein kinase, the cell is no longer instructed to perform that specific function.
  • If you inhibit PDEIII, the “turn off” mechanism is inhibited and it indirectly ↑ cAMP, maintaining the protein kinases in the “turned on” state.
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13
Q

Lusitropy

A

Increasing the rate of relaxation by speeding up the return of calcium to the SR

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14
Q

Adrenal medulla

A

80% epi, 20% norepi

At rest secretes:

  1. 2mcg/kg/min epi
  2. 05mcg/kg/min norepi

Remember catecholamines in the bloodstream last 5-10X longer than they do in the synaptic cleft

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15
Q

Baroreceptor reflex monitoring locations and innervation: AFFERENT

A
  1. ) carotid sinus —> carotid sinus nerves (nerves of Hering) + CN IX (glossopharyngeal) converge to send afferent impulses to nucleus tractus solitarus in the medulla
  2. ) Transverse aortic arch sends afferent signal via vagus nerve.
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16
Q

Baroreceptor reflex location and innervation: EFFERENT

A

Vasomotor center in medulla and pons

Afferent traffic to nucleus tractus solitarus stimulates rostral ventrolateral medulla and intermediolateral nucleus.

SNS output is ↓ via inhibition of T1-T4 cardio accelerator nerves, neural network to vasculature, and at the same time a reciprocal rise in vagal tone. The net effect is ↓ HR, inotropy, and SVR.

17
Q

Clinical examples of baroreceptor reflex

A

CEA: carotid sinus may cause bradycardia

Mediastinoscopy: pressure from scope on transverse aortic arch may cause bradycardia

Phenylephrine!

18
Q

Drugs that preserve baroreceptor reflex

A

TPL, etomidate, hydralazine, SNP, NTG, norepi

19
Q

ANS receptors: eye

A

A1: contraction radial muscle → mydriasis
B2: relaxation ciliary muscle → far vision

20
Q

ANS receptors: pancreas

A

A2: ↓ insulin release
B2: ↑ insulin release

21
Q

ANS receptors: liver

A

A1: ↑ serum glucose
B2: ↑ serum glucose

22
Q

ANS receptors: uterus

A

A1: contraction
B2: relaxation

23
Q

ANS receptors: bladder

A

A1: trigone + sphincter contraction (facilitates urination)
B2: detrustor relaxation (facilitates retention/storage)

24
Q

Vasopressin receptors

A

V1: Gq
V2: Gs

25
Histamine receptors
H1: Gq H2: Gs
26
How do preganglionic fibers get from spinal cord to SNS chain?
SNS preganglionic fibers exit SC via ventral nerve roots | Enter SNS chain via white rami
27
Steps of norepi synthesis
Tyrosine —(tyrosine hydroxylase) → DOPA → Dopamine → Norepi → Epi Tyrosine hydroxylase is the rate limiting step
28
Where is the origin of efferent PNS pathways?
Craniosacral - CN 3,7,9,10 - S2-S4
29
What drugs can be given to augment HR in a patient who got a heart transplant?
Epi, isoprel, glucagon
30
Glomus tumors
Originate from neural crest cells, tend to grow in neuroendocrine tissues that are near carotid, aorta, CN IX, and middle ear. Usually benign → release vasoactive substances HTN or hypo (NE, 5HT, histamine, bradykinin) → octreotide can be helpful for carcinoid-like sx → CN dysfunction (IX, X, XII) can ↑ aspiration risk, a/w obstruction → resection of a glomus that invaded IJ vein ↑ air embolism risk
31
Low, medium, and high dose epi compare/contrast
Low dose (0.01-0.03mcg/kg/min) → non selective beta. B1 ↑ HR/contractility, B2 → skeletal muscle vasodilation ↑ CO ↓ SVR Intermediate dose (0.03-0.15mcg/kg/min) → mixed alpha beta High dose (>0.15) → alpha prevails, BP ↑, tachyarrythmias
32
4 indications for isopreterenol
Chemical pacemaker if atropine not working Heart transplant Bronchoconstrition Cor pulmonale
33
B1 selective drugs
Atenolol, Esmolol, Metoprolol, Bisoprolol Betaxolol
34
Non selective beta agonists
Propranolol, Labetolol, Carvedilol, Nadolol, Pindolol, Timolol
35
Alpha antagonists
Phenoxybenzamine: long acting nonselective noncompetitive antagonist A1+A1 Phentolamine: short acting nonselective competitive antagonist A1+A2 Prazosin selective A1 antagonist