ANS Pharm: ACEIs, ARBs, Anesthetic Agents Flashcards

1
Q

dry cough from ACEI

A
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2
Q

Which effects of the volatiles are:
ANS mediated?
spinal cord mediated?

A
  • ANS: amnesia, sedation, unconsiousness
  • spinal cord: immobility (MAC)
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3
Q

Which locals are antiarrhythmics?

A

1A: procainamide
1B: Lidocaine

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4
Q

RAAS starts with renin secretion by renal cortical juxtaglom. cells. What causes this?

A

decreased renal perfusion d/t hemorrhage or SNS activation

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5
Q

synthesizes angiotensinogen

A

liver

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6
Q

renin acts on ___ to produce ___

A

cleaves angiotensinogen to produce angiotensin 1

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7
Q

Angiotensin 2 is a potent vasoconstrictor of kidney and mesenteric arterioles via its action on….

A

the angiotensin receptor, type 1 (AT 1).

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8
Q

angiotensin receptor, type 2 (AT2)

A

regulates vascular response, cardiac growth response, and fibrotic response in other tissues

type 1: angiotensin 2 acts there to vasoconstrict

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9
Q

RAAS
role in HTN

A
  • HTN involves RAAS dysfxn
  • RAAS modules NT release (influences SNS outflow)
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10
Q

Actions of angiotensin II

A
  • triggers release of norepi & epinephrine from the adrenal medulla
  • acts on renal tubules to decrease both Na & water elimination while increasing K excretion.
  • stimulates Aldosterone production (amplifies Na retention & K excretion)
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11
Q

T/F:
The result of RAAS is an elevation of venous blood pressure and an increased intravascular volume.

A

false
arterial BP

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12
Q

RAAS

Which hormones come from the adrenal cortex vs the medulla

A

cortex: aldosterone

medulla: epi, norepi

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13
Q

T/F:
Angiotensin 1 and 2 cause vasoconstriction.

A

False
only 2

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14
Q

Although ACEi drugs are potent, they are devoid of the many side effects of other antihypertensives such as…

A

bradycardia, bronchospasm, and rebound hypertension when acutely discontinued

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15
Q

ACEi drugs are best for HTN from increased renin & are first-line therapy for…

A

HTN, CHF, mitral regurgitation, LV dysfunction

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16
Q

ACEI effects

A
  • Decrease angiotensin (↓ aldosterone)
  • Reduce LV afterload
  • reduce arterial tone
  • ↓ water and Na retention
  • decrease bradykinin breakdown (endogenous vasodilator)
  • lowers LDL
  • Do not impair baroreceptors, thus orthostatic hypotension is not an issue.
  • renal protection in diabetics
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17
Q

ACEI prevent bradykinin breakdown. This contributes to 2 important side effects

A

cough
angioedema

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18
Q

ACEIs + vasodilating GA can cause hypoTN that is not responsive to …., so use ___

A

neo, ephedrine, norepi

use vaso (V1)

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19
Q

ACEIs can cause renal dysfxn and this electrolyte imbalance

A

hyperK

my also see fatigue

20
Q

Which ACEI is a prodrug?

21
Q

Which ACEI is excreted unchanged in the urine?

A

lisinopril

22
Q

T/F:
Angioedema from ACEIs is thought t be genetically linked.

A

True
Black people 4.5x more likely

23
Q

the only ACEI available IV

24
Q

Why do ARBs have less SEs than ACEIs?

A

ACEI impair activity at both AT 1 & AT 2 receptors

ARBs only AT1 receptor (more selective)

ARBS have similar SE to ACEi but milder and no dry cough
primary outcome is also similar

25
ARBs receptor activity
* great affinity for AT1r * inhibit angiotensin 2 @ AT1r * better at inhibiting angiotensin 2 than ACEi
26
T/F: ACEi provides renal protection for DM, unlike ARBs.
False both can
27
T/F: Volatiles have anti-seizure activity.
True
28
primary inhibitory & excitatory NT in CNS
GABA glutamate
29
common anesthetics that enhance GABA
* volatiles * prop * etomidate * BZDs * Barbs
30
What explains the CV, respiratory and neuroendocrine effects of anesthetics?
they alter neurotransmission
31
GABAr structure
ligand gated ion channel Cl- influx hyperpolarizes = inhibits neuronal cells
32
ANS modification by volatile inhaled agents:
* ↓ BP, CO, Cl, SVR * ♡ depressant & vasodilates (Alters Ca fxn) * Depress baroreceptor reflex (HD instability) * Antagonizes SA node automaticity (nodal rhythm) & prolong QT interval (inhibition K efflux which repolarizes) * Impairs ventilatory response to CO2 and O2. Low Minute ventilation for a given blood gas tension. * Uncoupling of cerebral blood flow autoregulation (> 0.5 MAC).
33
Volatiles primary receptor target
GABA**A**
34
Volatiles uncouple CBF autoregulation, usually above 0.5 MAC. What does this mean?
* blood flow will be higher than metabolic need * the ability to maintain a consistent blood flow despite changes in blood pressure is disrupted
35
Which anesthetics target GABA A?
* volatiles * Propofol * Etomidate * BZDs
36
T/F: Etomidate blocks the SNS response to laryngoscopy.
True
37
How does etomidate affect CBF?
cerebral vasoconstrictor reduces CBF & ICP
38
Ketamine is a/w CV stability and works to treat depression and pain. What are the limiting SEs?
* emergence delirium * secretions * nystagmus * hallucinations
39
Precedex can decrease MAC by how much?
over 90%
40
Lidocaine is a class 1B antiarrhythmic. How do they work?
1. suppress automaticity by increasing stimulation threshold of the ventricle & His-Purkinje 1. inhibiting spontaneous depolarization during diastole
41
longest doA LAs
bupi & ropi
42
most potent LA
tetracaine followed by chloroprocaine, bupi, ropi
43
What rhythms can lidocaine treat?
* AFIB * PVCs * VTach
44
fast onset LAs
* lidocaine * chloroprocaine * cocaine
45
Why is cocaine unique as a LA?
increases endothelin (vasconstrictor) & impairs nitric oxide production
46
renin