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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

(95 cards)

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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
Activation of beta 1 (in the heart)
increases HR + Force/SV
26
Activation of M2 (in the heart)
decreases HR + Force/SV
27
Beta 1 receptors in the kidney
control renin release
28
For the kidney: Sympathetic activation -->
NE --> renal beta 1 --> secretion of renin - Renin plays a role in increasing BP - Part of reason why beta blockers reduce BP
29
Activation of renal sympathetic nerves release
dopamine from proximal tubules
30
Dopamine is produced in the
proximal tubules
31
Dopamine receptors expressed along the
kidney tubules (particularly the Gs-coupled D1 receptors)
32
Dopaminergic CV effects
< 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)
33
Dopamine causes
natriuresis (sodium) --> diuresis
34
Dopamine -->
generates cAMP --> decreases the activity of the Na/H exchanger (luminal membrane) --> diminishes Na reabsorption --> increases Na excretion (primarily in the proximal tubule)
35
Natriuresis lowers concentration of Na in the blood -->
osmotic force --> drag water out of blood circulation and into the urine --> lowers blood volume
36
M3R promotes
vasoconstriction in pathologies in which the vascular endothelium is disrupted (e.g. atherosclerosis)
37
Beta receptor blockers
impact the heart and decrease in force and rate of cardiac contraction
38
peripherally acting sympatholytics
impact the heart and decrease in force and rate of cardiac contraction
39
diuretics
decrease in blood volume
40
angiotension inhibitors
decrease in blood volume
41
beta receptor blockers
decrease in blood volume
42
peripherally acting sympatholytics
relax vascular smooth muscle
43
Ca++ channel blockers
relax vascular smooth muscle
44
Direct vasodilators
relax vascular smooth muscle
45
Angiotension inhibitors
relax vascular smooth muscle
46
Centrally acting sympatholytics
decreased sympathetic outflow
47
Beta receptor blockers
decreased sympathetic outflow
48
3 - 4th line medications
- CCB - ACE-I - ARBs more effective
49
weak efficacy as monotherapy
due to the homeostatic nature of the ANS on BP via the baroreceptor reflex
50
avoid sympatholytic drugs in
-patients that are pregnant, breastfeeding
51
one (maybe 2) sympatholytic outlier that can be used in pregnant and breastfeeding women
methyldopa (alpha 2 blocker + labetalol can be okay
52
primary use 'in patient as rescue antihypertensives'
- IV labetalol (alpha + beta blocker) - reduce sudden spikes in BP - short acting - stroke, heart attack, heart failure, rupture of aorta, renal failure, eclampsia
53
Prazosin
alpha 1 selective decrease BP no tachycardia alpha 2 presynaptic negative feedback intact
54
Phentolamine
alpha 1 and alpha 2 non selective baroreceptor reflex reflex tachycardia alpha 2 presynaptic negative feedback BLOCKED
55
blockade of alpha1 receptor on blood vessel smooth muscle cells leads to
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
a1 antagonist drug ending
-osins
57
alpha antagonists
dilate arteries and veins (cause vascular resistance)
58
Primary use of alpha 1 antagonists
benign prostatic hyperplasia (relax urinary sphincter muscles)
59
secondary use of alpha 1 antagonists
may reduce LDL cholesterol levels
60
SE of alpha 1 antagonists
- First dose: orthostatic hypotension | - slight tachycardia (Na+ and water retention)
61
methyldopa (aldomet)
central acting alpha 2 agonists) prodrug
62
clonidine (catapres)
centrally acting alpha 2 agonists reduces BP
63
Phentolamine (regitine)
non-selective alpha blocker reversible
64
Phenoxybenzamine (dibenzyline)
non-selective alpha blocker irreversible
65
Clinical uses of non-selective alpha blockers
- hypertensive emergency | - cocaine-induced cardiovascular complications
66
A non-selective alpha-blocker also blocks alpha 2 receptors and
prevents alpha 2 receptor negative feedback of NE release (blockage cause more NE release, reflex tachycardia, arrhythmias - via cardiac beta 1 receptors)
67
1st generation beta blocker ending
-olol names
68
Propranolol
- 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
pindolol. acebutalol
- partial agonists | - less bradycardia
70
non-selective beta blocker problems
- can increase risk for diabetes - block insulin release from pancreas and glucose release from liver - mask signs of low blood sugar (tachycardia
71
non-selective beta blockers contraindicated in
asthma, COPD, CHF
72
2nd generation beta blockers
- beta selective --> less bronchoconstriction | - ex: metoprolol tartrate (Lopressor), metoprolol succinate (Toprol XL), atenolol (tenormin)
73
metoprolol tartrate (Lopressor)
short acting (2 - 4x)
74
metoprolol succinate (Toprol)
long acting (1 - 2x day) proven effective for CHF
75
3rd generation beta blockers
- beta 1 antagonist | - induce vasodilation
76
3rd generation beta blockers
- nebivolol (bystolic) | - betaxolol (betoptic)
77
nebivolol (bystolic)
beta 3 stimulation potentiates NO action
78
betaxolol (betoptic)
calcium channel blocking
79
alpha 1/beta blockers (non-selective beta blocker)
- used in HF | - decreases SVR, blocks increase in HR, SV + CO
80
alpha 1/beta blockers (non-selective beta blocker) examples
- carvedilol (coreg) | - labetalol (normodyne)
81
labetalol (normodyne)
- one of the few hypertensives that can be used in pregnancy (or women wanting to get pregnant) - useful in aortic dissection
82
baroreceptor reflect counteracts
blockage of alpha 1
83
baroreceptor sensitivity
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
drugs that increase BP
tend to produce reflex bradycardia
85
drugs that reduce BP
attenuate this response and cause reflex tachycardia
86
baroreceptor response is blunted in hypertensive pts
- more able to buffer increases in BP than falls in BP | - for example, hard to avoid orthostatic hypotension
87
autonomic neuropathy
can blunt baroreceptor response
88
catecholamine depleters are
adrenergic neuron blockers
89
inhibition of VMAT
depletes monoamine stores (metabolism) --> decreases synaptic transmission decrease of NE --> vasodilation
90
catecholamine depleter example
reserpine (serpasil)
91
reserpine (serpasil)
- 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
ALPHA 1
- vasoconstriction - increased peripheral resistance - increased BP - mydriasis - increased closure of internal sphincter of the bladder
93
ALPHA 2
- inhibition of norepi release - inhibition of ACh release - inhibition of insulin release
94
BETA 1
- tachycardia - increased lipolysis - increased myocardial contractility - increased release of renin
95
BETA 2
- 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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