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Therapeutics II > ANS Control of BP + Sympatholytics in Control of BP > Flashcards

ANS Control of BP + Sympatholytics in Control of BP Flashcards

1
Q

Systolic BP

A

pressure inside arteries when the heart pumps

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2
Q

diastolic BP

A

pressure when the heart relaxes between beats

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3
Q

Isolated systolic HTN

A
  • can increase risk of stroke and heart attack

- results from pathophysiologic changes in the arterial vasculature consistent with aging

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4
Q

Chronic HTN damages end organs

A
  • heart (heart failure, coronary artery disease, angina/ischemia, MI)
  • kidney (kidney disease/failure)
  • brain (stroke)
  • eyes (vision loss)
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5
Q

Primary or essential HTN accounts for

A

85 - 90% of all cases

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6
Q

Interrelated Diseases: Diabetes and HTN

A
  • lifestyles that lead to HTN can also lead to diabetes
  • diabetic nephropathy can cause HTN
  • complex mechanism, incompletely understood
  • includes excess Na retention, sympathetic nervous system (SNS) and renin-angiotension-aldosterone system (RAAS) activation, endothelial cell dysfunction (ECD), and increased oxidative stress
  • autonomic neuropathy can lead to orthostatic hypotension
  • glucose and fat can lead to vascular damage
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7
Q

Blood pressure equation

A

= cardiac output x peripheral vascular resistance

  • reduce cardiac output (pace or force)
  • reduce vascular resistance (vasodilation, decrease blood volume)
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8
Q

Targets for antihypertensive drugs

A
  • heart –> reduce cardiac output
  • resistance arterioles
  • veins (SANS)
  • kidney (reduce fluids, reduce blood volume)
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9
Q

Nervous System comprised of _____ and ______

A

Central nervous system AND peripheral nervous system

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10
Q

Peripheral nervous system comprised of _____ and _____

A

Autonomic nervous system AND somatic nervous system

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11
Q

Autonomic nervous system comprised of _____ and _____

A

Sympathetic system AND parasympathetic system

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12
Q

Sympathetic

A

Fight or flight (adrenaline/epinephrine)

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13
Q

Parasympathetic

A

rest and digest

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14
Q

Sympathetic NTs

A
  • norepi

- epi

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15
Q

Parasympathetic NTs

A
  • ACh
  • Muscarinic (exogenous)
  • Nictine (exogenous)
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16
Q

Parasympathetic Pre ganglionic

A

Long

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17
Q

Parasympathetic Post ganglionic

A

Short

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18
Q

Sympathetic Pre ganglionic

A

Short

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19
Q

Sympathetic Post ganglionic

A

Long

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20
Q

Baroreceptor

A

Body’s system to measure and maintain BP

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21
Q

Pressure Equation

A

Cardiac output (CO) x Vascular Resistance (VR)

-vascular resistance primarily controlled by SANS

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22
Q

Cardiac output (CO) equation

A

Stroke volume (SV) x Heart rate (HR)

-SV and HR controlled by PANS and SANS

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23
Q

Electrical Conduction Systems: Chronotropic

A
  • SA node cells = pacemaker cells

- rate of contraction

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24
Q

Electrical Conduction Systems: Inotropic

A
  • AV node
  • Force of contraction
  • Cardiomyocytes
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25
Q

Activation of beta 1 (in the heart)

A

increases HR + Force/SV

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26
Q

Activation of M2 (in the heart)

A

decreases HR + Force/SV

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27
Q

Beta 1 receptors in the kidney

A

control renin release

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28
Q

For the kidney: Sympathetic activation –>

A

NE –> renal beta 1 –> secretion of renin

  • Renin plays a role in increasing BP
  • Part of reason why beta blockers reduce BP
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29
Q

Activation of renal sympathetic nerves release

A

dopamine from proximal tubules

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30
Q

Dopamine is produced in the

A

proximal tubules

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31
Q

Dopamine receptors expressed along the

A

kidney tubules (particularly the Gs-coupled D1 receptors)

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32
Q

Dopaminergic CV effects

A

< 3 mcg/kg/min: D-selective = vasodilation

3 - 7.5 mcg/kg/min: beta 1-AR = increase CO

> 7.5 mcg/kg/min: alpha 1-AR = vasoconstriction (used in hypovolemic cardiogenic shock)

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33
Q

Dopamine causes

A

natriuresis (sodium) –> diuresis

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34
Q

Dopamine –>

A

generates cAMP –> decreases the activity of the Na/H exchanger (luminal membrane) –> diminishes Na reabsorption –> increases Na excretion (primarily in the proximal tubule)

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35
Q

Natriuresis lowers concentration of Na in the blood –>

A

osmotic force –> drag water out of blood circulation and into the urine –> lowers blood volume

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36
Q

M3R promotes

A

vasoconstriction in pathologies in which the vascular endothelium is disrupted (e.g. atherosclerosis)

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37
Q

Beta receptor blockers

A

impact the heart and decrease in force and rate of cardiac contraction

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38
Q

peripherally acting sympatholytics

A

impact the heart and decrease in force and rate of cardiac contraction

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39
Q

diuretics

A

decrease in blood volume

40
Q

angiotension inhibitors

A

decrease in blood volume

41
Q

beta receptor blockers

A

decrease in blood volume

42
Q

peripherally acting sympatholytics

A

relax vascular smooth muscle

43
Q

Ca++ channel blockers

A

relax vascular smooth muscle

44
Q

Direct vasodilators

A

relax vascular smooth muscle

45
Q

Angiotension inhibitors

A

relax vascular smooth muscle

46
Q

Centrally acting sympatholytics

A

decreased sympathetic outflow

47
Q

Beta receptor blockers

A

decreased sympathetic outflow

48
Q

3 - 4th line medications

A
  • CCB
  • ACE-I
  • ARBs more effective
49
Q

weak efficacy as monotherapy

A

due to the homeostatic nature of the ANS on BP via the baroreceptor reflex

50
Q

avoid sympatholytic drugs in

A

-patients that are pregnant, breastfeeding

51
Q

one (maybe 2) sympatholytic outlier that can be used in pregnant and breastfeeding women

A

methyldopa (alpha 2 blocker + labetalol can be okay

52
Q

primary use ‘in patient as rescue antihypertensives’

A
  • IV labetalol (alpha + beta blocker)
  • reduce sudden spikes in BP
  • short acting
  • stroke, heart attack, heart failure, rupture of aorta, renal failure, eclampsia
53
Q

Prazosin

A

alpha 1 selective

decrease BP

no tachycardia

alpha 2 presynaptic negative feedback intact

54
Q

Phentolamine

A

alpha 1 and alpha 2 non selective

baroreceptor reflex

reflex tachycardia

alpha 2 presynaptic negative feedback BLOCKED

55
Q

blockade of alpha1 receptor on blood vessel smooth muscle cells leads to

A

vasodilation and a drop in BP

drop in BP causes a baroreceptor reflex leading to decreased firing to the nucleus tractus

BUT NE wont activate post-synaptic alpha 1 receptors because theyre blocked by prazosin

56
Q

a1 antagonist drug ending

A

-osins

57
Q

alpha antagonists

A

dilate arteries and veins (cause vascular resistance)

58
Q

Primary use of alpha 1 antagonists

A

benign prostatic hyperplasia (relax urinary sphincter muscles)

59
Q

secondary use of alpha 1 antagonists

A

may reduce LDL cholesterol levels

60
Q

SE of alpha 1 antagonists

A
  • First dose: orthostatic hypotension

- slight tachycardia (Na+ and water retention)

61
Q

methyldopa (aldomet)

A

central acting alpha 2 agonists)

prodrug

62
Q

clonidine (catapres)

A

centrally acting alpha 2 agonists

reduces BP

63
Q

Phentolamine (regitine)

A

non-selective alpha blocker

reversible

64
Q

Phenoxybenzamine (dibenzyline)

A

non-selective alpha blocker

irreversible

65
Q

Clinical uses of non-selective alpha blockers

A
  • hypertensive emergency

- cocaine-induced cardiovascular complications

66
Q

A non-selective alpha-blocker also blocks alpha 2 receptors and

A

prevents alpha 2 receptor negative feedback of NE release (blockage cause more NE release, reflex tachycardia, arrhythmias - via cardiac beta 1 receptors)

67
Q

1st generation beta blocker ending

A

-olol names

68
Q

Propranolol

A
  • first beta blocker
  • unselective
  • reduces heart rate and stroke volume (reduce BP, can reduce renin release)
  • SE = bradycardia, AV block, hypotension, bronchospasms, sedation, rebound tachycardia
69
Q

pindolol. acebutalol

A
  • partial agonists

- less bradycardia

70
Q

non-selective beta blocker problems

A
  • can increase risk for diabetes
  • block insulin release from pancreas and glucose release from liver
  • mask signs of low blood sugar (tachycardia
71
Q

non-selective beta blockers contraindicated in

A

asthma, COPD, CHF

72
Q

2nd generation beta blockers

A
  • beta selective –> less bronchoconstriction

- ex: metoprolol tartrate (Lopressor), metoprolol succinate (Toprol XL), atenolol (tenormin)

73
Q

metoprolol tartrate (Lopressor)

A

short acting (2 - 4x)

74
Q

metoprolol succinate (Toprol)

A

long acting (1 - 2x day)

proven effective for CHF

75
Q

3rd generation beta blockers

A
  • beta 1 antagonist

- induce vasodilation

76
Q

3rd generation beta blockers

A
  • nebivolol (bystolic)

- betaxolol (betoptic)

77
Q

nebivolol (bystolic)

A

beta 3 stimulation potentiates NO action

78
Q

betaxolol (betoptic)

A

calcium channel blocking

79
Q

alpha 1/beta blockers (non-selective beta blocker)

A
  • used in HF

- decreases SVR, blocks increase in HR, SV + CO

80
Q

alpha 1/beta blockers (non-selective beta blocker) examples

A
  • carvedilol (coreg)

- labetalol (normodyne)

81
Q

labetalol (normodyne)

A
  • one of the few hypertensives that can be used in pregnancy (or women wanting to get pregnant)
  • useful in aortic dissection
82
Q

baroreceptor reflect counteracts

A

blockage of alpha 1

83
Q

baroreceptor sensitivity

A

the baroreflex elicits reciprocal responses of
the autonomic nervous system: when afferent baroreflex nerve traffic
intensifies (this happens when BP increases), the efferent sympathetic
traffic decreases, while the efferent parasympathetic traffic increases.
The inverse response occurs when BP lowers.

84
Q

drugs that increase BP

A

tend to produce reflex bradycardia

85
Q

drugs that reduce BP

A

attenuate this response and cause reflex tachycardia

86
Q

baroreceptor response is blunted in hypertensive pts

A
  • more able to buffer increases in BP than falls in BP

- for example, hard to avoid orthostatic hypotension

87
Q

autonomic neuropathy

A

can blunt baroreceptor response

88
Q

catecholamine depleters are

A

adrenergic neuron blockers

89
Q

inhibition of VMAT

A

depletes monoamine stores (metabolism) –> decreases synaptic transmission

decrease of NE –> vasodilation

90
Q

catecholamine depleter example

A

reserpine (serpasil)

91
Q

reserpine (serpasil)

A
  • 2nd line antihypertensive
  • MOA: irreversibly block VMAT (depletes DA and NE –> reduced adrenergic function)
  • little postural hypotension
  • SE: GI (diarrhea, cramps, acid secretion), CNS (sedation, nightmares, depression)
92
Q

ALPHA 1

A
  • vasoconstriction
  • increased peripheral resistance
  • increased BP
  • mydriasis
  • increased closure of internal sphincter of the bladder
93
Q

ALPHA 2

A
  • inhibition of norepi release
  • inhibition of ACh release
  • inhibition of insulin release
94
Q

BETA 1

A
  • tachycardia
  • increased lipolysis
  • increased myocardial contractility
  • increased release of renin
95
Q

BETA 2

A
  • vasodilation
  • slightly decreased peripheral resistance
  • bronchodilation
  • increased muscle and liver glycogenolysis
  • increased release of glucagon
  • relaxed uterine smooth muscle

Therapeutics II (12 decks)

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