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
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
3
Q
Sympathetic Neurotransmitter
A
Sympathetic ganglion –> Nicotinic- Cholinergic Ach Receptor –> Adrenergic Norepi receptor
4
Q
Parasympathetic Neurotransmitter
A
PNS ganglion –> Nicotinic- Cholinergic Ach Receptor –> Muscarinic Ach receptor
5
Q
Ach –>
A
Cholinergic –> muscarinic or nicotinic
6
Q
Norepinephrine –>
A
adrenergic receptor –> alpha or beta
7
Q
cholinergic receptor –> muscarinic
A
primarily in the peripheral ANS at PSNS post-
ganglionic post-synaptic membrane
8
Q
cholinergic receptor –> nicotinic
A
– CNS
– Peripheral ANS in preganglionic -postsynaptic membrane
– neuromuscular junctions
9
Q
alpha one adrenergic receptor
A
vascular smooth muscle
10
Q
alpha two adrenergic receptor
A
post-synaptic adrenergic membrane
11
Q
beta one adrenergic receptor
A
heart, kidney and fat cells
12
Q
beta two adrenergic receptor
A
certain vascular beds, bronchioles
13
Q
direct agonist
A
drug binds to and stimulates receptor
14
Q
cholinergic agonist
A
- bind all acetylcholine (Ach) receptors (R)
- Non-specific and wide-spread side effects
15
Q
muscarinic agonist
A
- bind only the muscarinic subtype Ach R
- More specific to GI organs and fewer side effects
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
17
Q
Uses of muscarinic agonist
A
- Illius
- Atony of bladder
- glaucoma
- myasthenia gravis
- reversal of neuromuscular block or anticholinergic toxicity
18
Q
Uses of muscarinic agonist - Illius
A
a loss of tone (atony) in GI Tract after surgery
or trauma. decreases peristalsis, distension
19
Q
Uses of muscarinic agonist - Atony of bladder
A
decrease tone in smooth muscle and
distension of bladder. Urinary retention
20
Q
uses of muscarinic agonist - glaucoma
A
increases in ocular pressure due to accumulation
of aqueous humor in the eye
21
Q
uses of muscarinic agonist - myasthenia gravis
A
skeletal muscle paralysis due
(autoimmune) loss of Ach receptors
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
23
Q
What are anti-muscarinic drugs used in treatment of?
A
GI disturbances, Parkinson’s Disease, bradycardia (2MI/surgery), motion
sickness, urinary frequency, asthma/breathing
difficulty, poisoning & to produce mydriasis
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
25
what do anti- muscarinics block?
both secretion & motility
since both mediated by Ach at GI muscarinic Rs
26
Uses of anti-muscarinics
- irritable bowel
- peptic ulcer
- motion sickness
- bradycardia
- parkinson disease
- urinary frequency/incontinence
- reparatory distress/asthma
- produce mydrisis
- rx poisoning
27
uses of anti-muscarinics - irritable bowel
motility in GI tract
* Anti-muscarinic effectiveness questionable
28
uses of anti-muscarinics - peptic ulcer
- caused by gastric acid
* Anti-muscarinics not very effective: H2-blockers & antibiotics more efficacious
29
uses of anti-muscarinics - motion sickness
Scopolamine: inhibit Vestibular Sys.
30
uses of anti-muscarinics - bradycardia
Atropine: blocks vagal tone after MI or with
anesthesia during surgery
31
uses of anti-muscarinics - parkinson disease
blocks Ach inhibition in BG
32
uses of anti-muscarinics - urinary frequency/incontinence
decreases bladder tone/spasm
33
uses of anti-muscarinics - respiratory distress/asthma
block vagal bronchial constriction
34
uses of anti-muscarinics - produce mydriasis
dilate the papillary muscle to allow
for ophthalmologic examination
35
uses of anti-muscarinics - treat poisoning
insecticides, mushrooms, chemical
weapons and other common poisons
36
side effects of anticholinergics
* similar for all drugs in this class
– dry mouth
– blurred vision
– urinary retention
– constipation
– tachycardia
– CNS symptoms: confusion, nervousness,
drowsiness (especially anticholinergics)
37
urinary retention
– Muscarinic agonists may be given to patients w/ SCI in first few weeks to prevent urinary retention
– decrease the risk of UTI
38
Neurogenic bladder (incontinence or frequency)
– Anti-cholinergic agents may be given to patients w/ SCI after reflexes return to decrease activity in the bladder and prevent incontinence
39
Rx of autonomic dysreflexia
-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
definition of HTN
bp > 140/90
41
primary or essential HTN:
– cannot be attributed to another disease process
– no straight forward underlying pathology or cause is u/k
– 95% of all patients with HTN
42
secondary HTN
– HTN that is due to another disease process
– example: HTN due to chronic renal disease
– only 5% of cases of HTN
43
pathophysiology of HTN on slide 25
44
causes of HTN
– Complex interaction of genetic & environment
– Genetic factors are variable depending on individual
– Environmental factors: smoking, sedentary life style, obesity, alcohol, personality trait
45
major categories of drugs for HTN
– diuretics
– sympatholytic drugs
– vasodilators
– angiotensin converting enzyme (ACE)
inhibitors
– calcium channel blockers
46
Diuretics
- work in kidney
- decrease plasma volume
47
Sympatholytics
- works on SNS and in hypothalamus
- decreases SNS influence on heart and vasculature
48
Vasodilators
- peripheral vasculature
- lower vascular resistance by direct vasodilation
49
ace inhibitors
- work in peripheral vasculature, heart, kidney
- inhibit ACE enzyme, blocking Ang II formation
50
Ca-channel blockers
- works in Ca channels in smooth and cardiac muscle
- decrease smooth muscle tone, vasodilation, decrease force and rate of cardiac contraction
51
Thiazide Diuretics
Chlorothiazide (Diuril)
Hydrochlorothiazide (Esidrix)
52
pathophysiology of angina pectoris
- Occurs when myocardial O2 demand is
insufficient to meet the demands of body.
– Often brought on by exercise/exertion
53
symptoms of angina pectoris
- 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
see slide 34
55
drugs used to treat angina
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
how do nitrates work?
primarily by decreasing the
workload on the heart, not by coronary
vasodilatation as previously thought
57
Best delivery of nitrates
* Not absorbed well in GI tract so sublingual, buccal or patch works best
* Sublingual is fastest (2 min) for acute angina attack
58
can tolerance to nitrates develop?
yes - remove for at least a few hours
59
side effects of nitrates
- associated with vasodilation
– headache (secondary to hypotension)
– orthostatic hypotension
– nausea
60
how do beta blockers work?
- Directly decrease the work of the heart by
decreasing contractility
- Prophylactically to prevent angina attack
61
how do calcium channel blockers work?
primarily by blocking Ca2+ entry into
smooth muscle, causing vasodilatation and
decreasing the afterload and preload
62
what is the primary effect of calcium channel blockers
- vasodilation of the coronary arteries: increases myocardial blood flow
- Also limit Ca2+ entry to myocardium, but this
affect is important for Rx arrhythmias
63
stable angina
- myocardial oxygen demand exceeds supply during cardiovascular stress in predictable manner
- treat with beta blockers and/or nitrate
64
variant angina
- myocardial oxygen demand exceeds supply, secondary vasospasm, may occur at rest
- treat with calcium channel blockers
65
unstable angina
- myocardial oxygen demand exceeds supply at any time
- treat with combination of calcium channel blocker ply beta blockers and/or nitrate
66
use of nitrates during PT
– 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
arrhythmia
any significant or abnormal deviation in the hearts conduction pattern
68
consequences of arrhythmia
syncope, TIA/CVA, MI, heart failure, death
69
R heart failure
accumulation in periphery: limbs,
abdomen, liver or other systemic organ
70
L heart failure
accumulation in lungs
71
what does "congestive" refer to
“backward” failure with fluid accumulation
72
cycle of CHF slide 46
73
effects of Digitalis
* Increases the pumping ability of the heart
* Very narrow “therapeutic window”: the
dose must be carefully titrated to patient
74
side effects of Digitalis
– 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
Target of ACE inhibitors in CHF
– cardiac lesion (HTN)
– neurohumoral compensation
– limit the increased cardiac workload
– cell adaptations (cardiac hypertrophy)
76
Treatment of coagulation disorders
Body requires a delicate balance between
coagulation an anti-coagulation for vascular
function
77
inadequate clotting
hemophilia, hemorrhage
78
excessive clotting
embolism & thrombosis
79
Classes of anticoagulants:
Heparins
Low molecular weight heparins
oral anticoagulants
- All Inhibit synthesis and function of clotting factors; used primarily to prevent and treat
venous thromboembolism
80
Heparin sodium and LMWH
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
Antiplatelet Drugs (GP-2b3a Inhibitors):
Clopidogrel (Plavix) & Ticlopidine (Ticlid)
– 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
Heparin
primary anticoagulant used clinically, given
parentally for prevention of clots in venous system
83
Warfarin (Coumadin)
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
Aspirin
– Anti-platelet action: impairs hepatic synthesis of Factors VII, IX & X
– Rx w/ aspirin shown torisk for MI, or recurrence
85
What do thrombolytic drugs do
-- 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
uses of thrombolytic drugs
MI, stroke, PE, peripheral arterial occlusion
- must be administered within 3-6 hrs
87
hemophilia
-- 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
Vitamin K deficiencies
treat with vitamin supplement
89
excessive bleeding after surgery
secondary to over-activation of fibrinolytic system
90
causes of hyperlipidemia
familial, diet and life style
91
how are lipids transferred
- 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
Pharmacological strategies to decrease lipids
– prevent endogenous formation
* HMG-CoA reductase inhibitors or STATINS
– rid body of cholesterol
93
Special Concern for PT
* 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
