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Pharm > ANS and CV System > Flashcards

ANS and CV System Flashcards

1
Q

SNS: fight or flight

A
  • Increased cardiac output
  • Shunting of blood
    GI tract & skin →muscle,
    heart & lungs
  • Increased metabolism
  • Increased mental alertness
  • Dilate pupils
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2
Q

PSNS: rest and digest

A
  • Decreased cardiac output
  • Shunting of blood to
    abdominal organs
  • Increased digestion &
    absorption
  • Decreased metabolism
  • Decreased alertness
  • Focus lens/constrict pupil
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3
Q

Sympathetic Neurotransmitter

A

Sympathetic ganglion –> Nicotinic- Cholinergic Ach Receptor –> Adrenergic Norepi receptor

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4
Q

Parasympathetic Neurotransmitter

A

PNS ganglion –> Nicotinic- Cholinergic Ach Receptor –> Muscarinic Ach receptor

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5
Q

Ach –>

A

Cholinergic –> muscarinic or nicotinic

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6
Q

Norepinephrine –>

A

adrenergic receptor –> alpha or beta

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7
Q

cholinergic receptor –> muscarinic

A

primarily in the peripheral ANS at PSNS post-
ganglionic post-synaptic membrane

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8
Q

cholinergic receptor –> nicotinic

A

– CNS
– Peripheral ANS in preganglionic -postsynaptic membrane
– neuromuscular junctions

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9
Q

alpha one adrenergic receptor

A

vascular smooth muscle

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10
Q

alpha two adrenergic receptor

A

post-synaptic adrenergic membrane

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11
Q

beta one adrenergic receptor

A

heart, kidney and fat cells

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12
Q

beta two adrenergic receptor

A

certain vascular beds, bronchioles

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13
Q

direct agonist

A

drug binds to and stimulates receptor

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14
Q

cholinergic agonist

A
  • bind all acetylcholine (Ach) receptors (R)
  • Non-specific and wide-spread side effects
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15
Q

muscarinic agonist

A
  • bind only the muscarinic subtype Ach R
  • More specific to GI organs and fewer side effects
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16
Q

indirect cholinergic stimulant

A
  • alter degradation of Ach
  • Block acetylcholinesterase so Ach isn’t
    degraded, prolonging neurotransmission
  • Tend to be non-specific (affecting all Ach
    receptors) with a lot of side effects
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17
Q

Uses of muscarinic agonist

A
  • Illius
  • Atony of bladder
  • glaucoma
  • myasthenia gravis
  • reversal of neuromuscular block or anticholinergic toxicity
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18
Q

Uses of muscarinic agonist - Illius

A

a loss of tone (atony) in GI Tract after surgery
or trauma. decreases peristalsis, distension

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19
Q

Uses of muscarinic agonist - Atony of bladder

A

decrease tone in smooth muscle and
distension of bladder. Urinary retention

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20
Q

uses of muscarinic agonist - glaucoma

A

increases in ocular pressure due to accumulation
of aqueous humor in the eye

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21
Q

uses of muscarinic agonist - myasthenia gravis

A

skeletal muscle paralysis due
(autoimmune) loss of Ach receptors

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22
Q

non specificity of cholinergic agonists causes:

A

– bronchoconstriction (acting at muscarinic R in
PSNS nerves to lung)
– excessive salivation
– bradycardia
– difficulty in visual accommodation
– flushing/sweating, especially of face due to
stimulation of special SNS neurons w/ Ach Rs

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23
Q

What are anti-muscarinic drugs used in treatment of?

A

GI disturbances, Parkinson’s Disease, bradycardia (2MI/surgery), motion
sickness, urinary frequency, asthma/breathing
difficulty, poisoning & to produce mydriasis

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24
Q

GI disturbances:

A
  • hyperactivity in ANS- GI
    motility/secretion
  • Anti-muscarinic block both secretion & motility
    since both mediated by Ach at GI muscarinic Rs
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25
Q

what do anti- muscarinics block?

A

both secretion & motility
since both mediated by Ach at GI muscarinic Rs

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26
Q

Uses of anti-muscarinics

A
  • irritable bowel
  • peptic ulcer
  • motion sickness
  • bradycardia
  • parkinson disease
  • urinary frequency/incontinence
  • reparatory distress/asthma
  • produce mydrisis
  • rx poisoning
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27
Q

uses of anti-muscarinics - irritable bowel

A

motility in GI tract
* Anti-muscarinic effectiveness questionable

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28
Q

uses of anti-muscarinics - peptic ulcer

A
  • caused by gastric acid
  • Anti-muscarinics not very effective: H2-blockers & antibiotics more efficacious
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29
Q

uses of anti-muscarinics - motion sickness

A

Scopolamine: inhibit Vestibular Sys.

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30
Q

uses of anti-muscarinics - bradycardia

A

Atropine: blocks vagal tone after MI or with
anesthesia during surgery

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31
Q

uses of anti-muscarinics - parkinson disease

A

blocks Ach inhibition in BG

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32
Q

uses of anti-muscarinics - urinary frequency/incontinence

A

decreases bladder tone/spasm

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33
Q

uses of anti-muscarinics - respiratory distress/asthma

A

block vagal bronchial constriction

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34
Q

uses of anti-muscarinics - produce mydriasis

A

dilate the papillary muscle to allow
for ophthalmologic examination

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35
Q

uses of anti-muscarinics - treat poisoning

A

insecticides, mushrooms, chemical
weapons and other common poisons

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36
Q

side effects of anticholinergics

A
  • similar for all drugs in this class
    – dry mouth
    – blurred vision
    – urinary retention
    – constipation
    – tachycardia
    – CNS symptoms: confusion, nervousness,
    drowsiness (especially anticholinergics)
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37
Q

urinary retention

A

– Muscarinic agonists may be given to patients w/ SCI in first few weeks to prevent urinary retention
– decrease the risk of UTI

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38
Q

Neurogenic bladder (incontinence or frequency)

A

– Anti-cholinergic agents may be given to patients w/ SCI after reflexes return to decrease activity in the bladder and prevent incontinence

39
Q

Rx of autonomic dysreflexia

A

-remove noxious stimulus
- block SNS: Non-specific adrenergic antagonists (Acebutolol), Beta adrenergic blockers (Propranolol), Alpha adrenergic blockers (Phentolamine)
- Alpha 2 receptor agonist –> Clonadine (Catapress)

40
Q

definition of HTN

A

bp > 140/90

41
Q

primary or essential HTN:

A

– cannot be attributed to another disease process
– no straight forward underlying pathology or cause is u/k
– 95% of all patients with HTN

42
Q

secondary HTN

A

– HTN that is due to another disease process
– example: HTN due to chronic renal disease
– only 5% of cases of HTN

43
Q

pathophysiology of HTN on slide 25

A
44
Q

causes of HTN

A

– Complex interaction of genetic & environment
– Genetic factors are variable depending on individual
– Environmental factors: smoking, sedentary life style, obesity, alcohol, personality trait

45
Q

major categories of drugs for HTN

A

– diuretics
– sympatholytic drugs
– vasodilators
– angiotensin converting enzyme (ACE)
inhibitors
– calcium channel blockers

46
Q

Diuretics

A
  • work in kidney
  • decrease plasma volume
47
Q

Sympatholytics

A
  • works on SNS and in hypothalamus
  • decreases SNS influence on heart and vasculature
48
Q

Vasodilators

A
  • peripheral vasculature
  • lower vascular resistance by direct vasodilation
49
Q

ace inhibitors

A
  • work in peripheral vasculature, heart, kidney
  • inhibit ACE enzyme, blocking Ang II formation
50
Q

Ca-channel blockers

A
  • works in Ca channels in smooth and cardiac muscle
  • decrease smooth muscle tone, vasodilation, decrease force and rate of cardiac contraction
51
Q

Thiazide Diuretics

A

Chlorothiazide (Diuril)
Hydrochlorothiazide (Esidrix)

52
Q

pathophysiology of angina pectoris

A
  • Occurs when myocardial O2 demand is
    insufficient to meet the demands of body.
    – Often brought on by exercise/exertion
53
Q

symptoms of angina pectoris

A
  • resulting from myocardial ischemia
    – chest pain (may also be in jaw, shoulder or back)
    – diaphoresis (sweating)
    – chest pressure (intense tightness or constriction)
    – anxiety/ denial
    – SOB or dyspnea
54
Q

see slide 34

A
55
Q

drugs used to treat angina

A

All drugs used to Rx angina either decrease the hearts work load or increase O2 delivery to the heart:
– 1) Drugs that decrease the afterload (force against
which heart pumps)
– 2) Drugs that decrease the preload (thereby
decrease work of the heart)
– 3) Drugs that decrease cardiac contractility
– 4) Drugs that vasodilate coronary arteries

56
Q

how do nitrates work?

A

primarily by decreasing the
workload on the heart, not by coronary
vasodilatation as previously thought

57
Q

Best delivery of nitrates

A
  • Not absorbed well in GI tract so sublingual, buccal or patch works best
  • Sublingual is fastest (2 min) for acute angina attack
58
Q

can tolerance to nitrates develop?

A

yes - remove for at least a few hours

59
Q

side effects of nitrates

A
  • associated with vasodilation
    – headache (secondary to hypotension)
    – orthostatic hypotension
    – nausea
60
Q

how do beta blockers work?

A
  • Directly decrease the work of the heart by
    decreasing contractility
  • Prophylactically to prevent angina attack
61
Q

how do calcium channel blockers work?

A

primarily by blocking Ca2+ entry into
smooth muscle, causing vasodilatation and
decreasing the afterload and preload

62
Q

what is the primary effect of calcium channel blockers

A
  • vasodilation of the coronary arteries: increases myocardial blood flow
  • Also limit Ca2+ entry to myocardium, but this
    affect is important for Rx arrhythmias
63
Q

stable angina

A
  • myocardial oxygen demand exceeds supply during cardiovascular stress in predictable manner
  • treat with beta blockers and/or nitrate
64
Q

variant angina

A
  • myocardial oxygen demand exceeds supply, secondary vasospasm, may occur at rest
  • treat with calcium channel blockers
65
Q

unstable angina

A
  • myocardial oxygen demand exceeds supply at any time
  • treat with combination of calcium channel blocker ply beta blockers and/or nitrate
66
Q

use of nitrates during PT

A

– If a patient is taking nitrates (by patch or
sublingual) then the med should be taken with the patient to PT!
– Monitor patients response to exercise
– Use caution with heat or whirlpool

67
Q

arrhythmia

A

any significant or abnormal deviation in the hearts conduction pattern

68
Q

consequences of arrhythmia

A

syncope, TIA/CVA, MI, heart failure, death

69
Q

R heart failure

A

accumulation in periphery: limbs,
abdomen, liver or other systemic organ

70
Q

L heart failure

A

accumulation in lungs

71
Q

what does “congestive” refer to

A

“backward” failure with fluid accumulation

72
Q

cycle of CHF slide 46

A
73
Q

effects of Digitalis

A
  • Increases the pumping ability of the heart
  • Very narrow “therapeutic window”: the
    dose must be carefully titrated to patient
74
Q

side effects of Digitalis

A

– drug toxicity: 20-25 % of the patients taking it
– GI distress, N&V
– CNS disturbances: drowsiness, fatigue,
confusion, visual disturbances
– Rhythm disturbances: premature atrial and
ventricular contractions, paroxysmal atrial
tachycardia, AV-blocks

75
Q

Target of ACE inhibitors in CHF

A

– cardiac lesion (HTN)
– neurohumoral compensation
– limit the increased cardiac workload
– cell adaptations (cardiac hypertrophy)

76
Q

Treatment of coagulation disorders

A

Body requires a delicate balance between
coagulation an anti-coagulation for vascular
function

77
Q

inadequate clotting

A

hemophilia, hemorrhage

78
Q

excessive clotting

A

embolism & thrombosis

79
Q

Classes of anticoagulants:

A

Heparins
Low molecular weight heparins
oral anticoagulants
- All Inhibit synthesis and function of clotting factors; used primarily to prevent and treat
venous thromboembolism

80
Q

Heparin sodium and LMWH

A

Used for preventing and treating MI AND:
– DVT prophylaxis (prior to THA, TKA surgery,
during periods of immobilization, etc…)
– Treatment of thromboembolism
– Treatment of pulmonary embolism

81
Q

Antiplatelet Drugs (GP-2b3a Inhibitors):
Clopidogrel (Plavix) & Ticlopidine (Ticlid)

A

– New anti-platelet drugs
– Member of the ticlopidin family
– Reduces the risk of re-infarction by 30-35% after MI
– Clopidogrel has fewer adverse effects than other ticlopidins
– Reduces expression of glycoprotein IIb/IIIa (GP-2b-3a), the fibrinogen receptor on platelet surface
– Inhibits ADP-dependent platelet aggregation

82
Q

Heparin

A

primary anticoagulant used clinically, given
parentally for prevention of clots in venous system

83
Q

Warfarin (Coumadin)

A

long term anticoagulation. inhibits production of Vit-K from Vit-K epoxide, preventing completion of clotting cascade
* given orally, but lag time (2-days) before works

84
Q

Aspirin

A

– Anti-platelet action: impairs hepatic synthesis of Factors VII, IX & X
– Rx w/ aspirin shown torisk for MI, or recurrence

85
Q

What do thrombolytic drugs do

A

– Convert plasminogen (profibrinolysin) to plasmin (fibrinolysin)
– Plasmin is the active form of this endogenous enzyme
and dissolves the clot
– Actually break-up clots that already exist

86
Q

uses of thrombolytic drugs

A

MI, stroke, PE, peripheral arterial occlusion
- must be administered within 3-6 hrs

87
Q

hemophilia

A

– Hereditary disease in which a clotting factor is
not produced or produced inadequately
– Hemophilia A: F-VIII (most common)
– Hemophilia A: F-IX (second most common)
– Rx: replacing appropriate F, but it is still obtained from human blood and very expensive (25,000/y)
– risk of HIV, hepatitis-B or C, other viruses

88
Q

Vitamin K deficiencies

A

treat with vitamin supplement

89
Q

excessive bleeding after surgery

A

secondary to over-activation of fibrinolytic system

90
Q

causes of hyperlipidemia

A

familial, diet and life style

91
Q

how are lipids transferred

A
  • as lipo-proteins in blood (HDL, VLDL, LDL and IDL)
    – HDL- removes lipids from vessel wall
    – VLDL, IDL and LDL- deposit lipids on vessel wall
92
Q

Pharmacological strategies to decrease lipids

A

– prevent endogenous formation
* HMG-CoA reductase inhibitors or STATINS
– rid body of cholesterol

93
Q

Special Concern for PT

A
  • Many pt’s seen in PT are on thrombolytic Rx
    secondary to bed rest increases risk of
    embolism/ thrombosis (DVT)
    – hip, knee or other joint surgery
    – post-MI, post-CABG, any re-vascularization
    – valve surgery
    – especially patients Rx w/ streptokinase or t-PA
  • Rehab procedures dealing with open wounds
    (WP, unwrapping dressings) should be done
    with caution secondary to risk of hemorrhage

Pharm (12 decks)

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