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cvs Flashcards

1
Q

where does sympathetic nerves arise?

A

emerge from thoracic area of spine

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2
Q

where does parasympathetic nerves arise?

A

from cranial nerves and lumbar sacral areas of spine

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3
Q

length of pre and postsynaptic nerve for sympathetic nerves

A

pre: short
post: long
ganglion: inside sympathetic chain

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4
Q

length of pre and postsynaptic nerve for parasympathetic nerves

A

pre: long
post: short
ganglion: in wall of organ/tissue

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5
Q

explain somatic nerve

A
  • supply skeletal muscle
  • no ganglions
  • voluntary control
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6
Q

main neurotransmitters in ANS?

A

Ach and NE

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7
Q

what organ/tissue in sympathetic pathway with no postsynaptic fibre?

A

adrenal gland

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8
Q

what sympathetic pathway that include both Ach and NE

A

pathway to smooth mucle, cardiac cells and gland cells to contract

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9
Q

functions of parasympathetic

A
  • SLUDD (salivation, lacrimation, urination, digestion, defeacation)
  • anabolic, conserves and stores energy
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10
Q

functions of sympathetic

A
  • fight or flight

- catabolic, mobilises energy, raise BP and body temperature, dilates airways etc

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11
Q

non-adrenergic and non-cholinergic neurotransmitter

A
  • nitric oxide
  • serotonin
  • ATP
  • GABA
  • dopamine
  • purines
  • neuropeptide
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12
Q

Ach synthesis by

A

choline acetyltranferase

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13
Q

hydrolysis of Ach by

A

acetylcholine esterase

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14
Q

choline reuptake by

A

Na+ driven symport

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15
Q

types of Ach receptors

A
  • nicotinic (Nm and Nn)

- muscarinic ( M1, M2, M3)

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16
Q

explain nicotinic receptors

A
  1. muscle-type and nerve-type
  2. cause membrane depolarization
  3. role in neuromuscular junction (skeletal) and ganglionic transmission (nerve)
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17
Q

explain muscarinic M1

A
  1. in CNS, ganglia, gastric, parietal cells
  2. increase IP3, DAG (excitation)
  3. role in memory CNS, gastric acid secretion, GI motility
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18
Q

explain muscarinic M2

A
  1. in cardiac conducting tissue and presynaptic terminals
  2. decrease CAMP (inhibition)
  3. role in cardiac, presynaptic and neural inhibition
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19
Q

explain muscarinic M3

A
  1. exocrine gland, smooth muscle and blood vessels
  2. increase IP3, DAG (excitation)
  3. role in secretion, SM contraction, vasodilatation
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20
Q

cholinoceptor agonists

A
  • acetylcholine
  • carbachol
  • methacholine
  • bethanechol
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21
Q

cholinoceptor agonist that do not hydrolyse by AchE

A

bethanecol

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22
Q

Nicotinic muscular type agonist

A
  • Ach
  • suxamethonium
  • decamethonium
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23
Q

nicotinic muscular type antagonist

A
  • vecuronium

- pancuronium

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24
Q

nicotinic nerve type agonist

A
  • Ach
  • nicotine
  • epibatidine
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25
Q

nicotinic nerve type antagonist

A
  • trimetaphan

- hexamethonium

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26
Q

AchE can be block by

A

serine occlusion

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27
Q

products of hydrolysis of AchE are

A
  • choline
  • acetic acid
  • regenerated enzyme
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28
Q

reuptake of NA is blocked by

A
  • cocaine

- tricyclic antidepressants

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29
Q

adrenoceptor B1

A
  1. in heart, intestine, smooth muscle
  2. increase cAMP
  3. increase BP
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30
Q

adrenoceptor B2

A
  1. In bronchial, vascular and uterine smooth muscle
  2. bronchodilation, vasodilation, uterine SM
  3. increase cAMP
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31
Q

adrenoceptor A1

A
  1. postsynaptic
  2. increase IP3, DAG
  3. increase BP
  4. cause vasoconstriction
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32
Q

adrenoceptor A2

A
  1. presynaptic

2. decrease cAMP

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33
Q

a adrenoreceptors agonist specificity

A

noradrenaline > adrenaline > isoprenaline

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34
Q

a adrenoreceptors antagonist specificity

A

phentolamine

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35
Q

actions of NA terminated by when

A
  1. reuptake into nerve terminal
  2. dilution and diffusion from cleft and uptake at non-neuronal sites
  3. metabolic transformation
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36
Q

enzymes important in biotransformation of cathecholamines

A
  1. COMT (cathecol-0-methyl transferase)

2. MAO (monoamine oxidase)

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37
Q

b adrenoreceptors antagonist specificity

A

propanalol

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38
Q

Example of muscarinic receptors antagonist

A

Atropine (treat bradycardia)

hyoscine

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39
Q

Indirect acting of cholinergic agonist

A

Action of cholinesterase inhibitors (inhibit Ach catabolism)

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40
Q

Example of muscarinic receptors agonist

A
  1. pilocarpine (use as eye drop to treat glaucoma)

2. bethanechol

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41
Q

Two type of cholinergic agonist

A
  1. Choline esters (Ach, bethanechol)

2. Alkaloids (pilocarpine)

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42
Q

What are the effects produced by muscarinic agonists?

A

Parasympathetic-like effects.

  1. Smooth muscle (M1) - Increase GI peristaltic activity
  2. Cardiovascular (M2) - Cardiac slowing, decrease c. output
  3. Eye (M3) - Contraction of ciliary muscle
  4. Secretions (M3) - Stimulation of exocrine glands, sweating, lacrimation, salivation and bronchial secretion.
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43
Q

what is glaucoma?

A

increase intraocular pressure due to increase aqueous fluid production and decreased its trabecular outflow.

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44
Q

Effects produced by muscarinic antagonists

A

Sympathetic-like effects

  1. Smooth muscle (M1) - Bronchial, biliary & urinary tract SM relax. GI transit is inhibited
  2. Cardiovascular (M2) - Tachycardia
  3. Eye (M3) - Dilation of the pupil and relaxation of ciliary muscle
  4. Secrettions (M3) - Inhibition of secretions; dry mouth, bronchial mucociliary clearance is inhibited.
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45
Q

Therapeutic uses of muscarinic antagonists

A
  1. GI actions:
    • treat hyermotility and spasm associated with GI disease (IBS)
    • Dicycloverine
  2. Resp. actions:
    • Treatment of COPD and acute asthma; as bronchodilator
    • Ipratropium
  3. Urinary tract:
    • relieve muscle spasm accompanying infection
  4. CVS actions:
    • Treating bradycardia associated with MI
    • Atropine
  5. Overactive bladder:
    • Reduce spontaneous myocyte activity
    • decrease frequency and intensity of detrusor activity
    • M3 receptor antagonists
    • Adverse reaction - dry mouth, constipation, blurred vision, cardiac arrhythmia
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46
Q

Botulinum toxin..

A
  • Botulinum toxin A (BTX-A) most potent and have a longer duration of action
  • Administered and act in a site specific manner
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47
Q

Type of neuromuscular blocking drugs

A
  1. Non depolarising: Block Ach receptors

2. Depolarising: Agonists at Ach receptors

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48
Q

Examples of competitive antagonists of Ach at mNicotinic receptor:

A

Tubocurarine analogues

  1. Mivacurium
  2. Atracurium
  3. Vecuronium
  4. Pancuronium
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49
Q

How depolarising agent act as neuromuscular blocking drugs?

A
  • Sustained mNicotinic agonism at NMJ -> depolarisation block
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50
Q

Depolarising agent (suxamethonium) is contraindicated in..

A
  1. Neuropathies
  2. Myopathies (esp malignant hyperthermia)
  3. Burns/severe trauma (hyperkalaemia -> risk of arrhythmia)
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51
Q

Example of AchE inhibitors (indirect cholinergic agonist)

A
  1. Short-acting quaternary alcohols:
    - e.g. edrophonium
    - Bind to anionic site -> prevent Ach access
    - Readily reversible -> brief action
    - Used in diagnosis of myasthenia gravis
  2. Medium acting Carbamyl esters
    - e.g. neostigmine, physostigmine (longer acting)
    - Carbamyl transfer to anionic site, then slow hydrolysis
    - As reversal of NMJ block, myasthenia treatment
    - Also Alzheimer’s (doneprezil, tacrine)
  3. Irreversible block
    - e.g. echothiopate (eye drop for glaucoma), dyflos, melathion
    - Phosphorylate ser203 at active site; stable bond so long lasting
    - Reversible within first 1-2 hours using pralidoxome
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52
Q

Types of cholinesterase inhibitors

A
  1. Carbamates (physostigmine, neostigmine)

2. Phosphates (isofluorophate)

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53
Q

Example of beta blockers

A
  1. Atenolol

2. Propanolol

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54
Q

Example of direct acting adrenoreceptor agonists

A
  1. dobutamine
  2. epinephrine
  3. phenylephrine
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55
Q

Example a & b blockers

A

Cervedilol

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56
Q

dobutamine

A
  1. direct adrenoceptor agonist
  2. Effects:
    - Cardiac stimulation (B1)
    - Vasodilation (B2)
  3. clinical use:
    - cardiogenic shock
    - acute heart failure
    - cardiac stimulation during heart surgery
  4. side effect - arrhythmias
57
Q

epinephrine

A
  1. Effects:
    - Vasoconstriction and increase BP (a1)
    - Cardiac stimulation (B1)
    - Bronchodilation (B2)
  2. Side effects:
    - Hypertension
    - Vasoconstriction
    - Arrhythmias
58
Q

cocaine

A
  1. Effects:
    - Inhibition of norepinephrine reuptake
  2. Side effects:
    - hypertension
    - cardiac damage
    - necrosis of nasal mucosa (abuse)
59
Q

Example of indirect acting adrenoreceptor agonists

A
  1. amphetamine
  2. cocaine
  3. ephedrine
60
Q

phenylephrine

A
  1. Effects:
    - Vasoconstriction, increase BP, mydriasis (a1)
  2. Side effects:
    - Bradycardia
    - Hypertension
61
Q

prazosin

A
  1. MOA: competitive a1-blocker
  2. Effects:
    - vasodilation
    - decrease vascular resistance and BP
    - relax bladder neck and prostate
  3. Clinical use: hypertension
  4. Side effects:
    - hypotension
    - tachycardia
    - nasal congestion
62
Q

ephedrine

A
  1. Effects:
    - vasoconstriction (a1)
  2. Clinical use - nasal decongestion
  3. Side effects:
    - hypertension
    - tachycardia
    - insomnia
63
Q

amphetamine

A
  1. Effects:
    - increase norepinephrine release
  2. Side effects:
    - hypertension
    - tachycardia
    - dependence
64
Q

atenolol

A
  1. MOA: B1-blocker
  2. Effects:
    - decrease cardiac rate, output, AV node conduction & O2 demand
    - decrease blood pressure
  3. Clinical use: hypertension, angina, acute MI, arrhythmia
  4. Side effects:
    - Cardiac failure
    - Bronchoconstriction
65
Q

phentolamine

A
  1. MOA: competitive a1 and a2 blocker
  2. Effects:
    - Vasodilation
    - Decrease vascular resistance and BP
  3. Side effects:
    - Hypotension
    - tachycardia
    - nasal congestion
66
Q

Examples of a-blockers

A
  1. Prazosin

2. Phentolamine

67
Q

carvedilol

A
  1. MOA:
    - B1 and B2 blocker
    - a1 blocker
  2. Effects:
    - Vasodilation
    - decrease heart rate and BP in patient with hypertension
    - increase cardiac output in patient with heart failure
68
Q

how to count BP?

A

cardiac output x total peripheral resistance

69
Q

how to count cardiac output(CO)?

A

heart rate (HR) x stroke vol (SV)

70
Q

define preload

A

the ability of the ventricles to stretch and fill with blood

71
Q

define afterload

A

the ability of the ventricle to empty by pushing against systemic vascular resistance

72
Q

parasympathetic effects on the heart

A
  • input via vagus nerve causes decrease HR (dominates)
73
Q

sympathetic effects on the heart

A
  • input to SA node causes increase HR

- increase heart contractility

74
Q

propanolol

A
  1. MOA: B1 and B2 blocker
  2. Effects:
    - decrease cardiac ratem otput, AV node conduction & O2 demand
    - decrease blood pressure
  3. Clinical use: hypertension, angina, arrhythmia, acute MI
  4. Side effects:
    - cardiac failure
    - bronchoconstriction
75
Q

function of renin

A
  • secreted by the kidney to increase BP or blood volume

- converts angiotensinogen -> angiotensin 1

76
Q

function of angiotensin-converting enzyme (ACE)

A

converts angiotensin 1 -> angiotensin 2 in lung

77
Q

actions of angiotensin 2

A
  1. cause vasoconstriction = increase TPR
  2. cause release of aldosterone -> promote Na & water reabsorption in kidney -> increased blood volume
  3. negative feedback to release renin
  4. stimulate thirst in hypothalamus
  5. stimulate sympathetic outflow`
78
Q

Principles of treatment of hypertension

A
  1. Reduce left ventricular systolic performance
    - negative inotropes (beta blockers)
    - Calcium channel blockers (verapamil)
  2. Reduce blood volume
    - Diuretics (thiazide, loop diuretics & potassium sparing diuretic)
  3. Reduce venous tone and thus venous return
    - Central sympatholytics (clonidine) act to reduce synpathetic tone
  4. Reduce arterial tone (resistance)
79
Q

drugs to reduce arterial tone in hypertension eg: resistance

A
  • ACE inhibitors
  • angiotensin receptor blockers
  • K+ channel openers
  • NO donors
  • A1- blockers
  • mixed A and B blockers
80
Q

treatment of cardiac failure

A
  1. diuretics and nitrates (A-blocker) to reduce preload
  2. digoxin to increase capacity of muscle contract
  3. ACE inhibitors and A-blocker to reduce afterload
81
Q

management of chronic heart failure

A
  1. ACE inhibitors
  2. diuretics and nitrates
  3. B-blockers
  4. ACE inhibitor and ARB
82
Q

What are the adaptive response when in cardiac failure?

A
  1. Cardiac dilatation
    - CO increases as length of muscle fibre is increased
  2. Sympathetic drive
    - Increased preload, contractility, afterload
  3. Renin angiotensin system
    - Aldosterone causes sodium retention
    - Angiotensin II causes peripheral vasoconstriction

(increase preload, contractility, afterload = increase O2 demand and eventual decompensation)

83
Q

Principles of treatment of cardiac failure

A
  1. Reduction of preload
    - Diuretics (decrease blood volume)
    - Nitrates
    - a-blocker (venodilation)
  2. Increased capacity of the myocardium to contract
    - Digoxin
  3. Reduction of afterload
    - ACE inhibitors (vasodilation)
    - a-blocker (vasodilation)
  4. Counteract activation of sympathetic nervous system
    - B-blocker
  5. Counteract activation of RAAS
    - ACE inhibitors
84
Q

which type of adrenoreceptors (sympathetic nerves) dilate the arteries/veins?

A

B2 adrenoreceptors

85
Q

what is variant angina?

A

vasospasm and temporary reduction of coronary blood flow

86
Q

define stable angina

A
  • chronic narrowing of coronary arteries due to inadequate blood flow
87
Q

define unstable angina

A
  • formation and dissolution blood clot (thrombosis) in coronary artery
  • coronary blood flow reduced causing decreased O2 supply
  • MI if clot completely occludes coronary arteries
88
Q

Principles of treatment of angina

A
  1. Dilation of arteries and veins
    - Calcium channel blocker
    - Nitrates
  2. Reduction of heart rate and contractility
    - Beta blocker
    - Clacium channel blocker
  3. Prevention of thrombus formation
    - Anticoagulant
    - Anti platelet drugs
89
Q

Class 2: beta blockers are used to treat..

A
  1. Arrhythmia caused by catecholamines
  2. Arrhythmia originating from SA/AV nodes induced by stress
  3. Effective for Sup. Ventricular and Ventricular arrhythmia
  4. Contraindicated in asthma
  5. Side effect: cardia depression and bradycardia
90
Q

Principles of treatment myocardial infarction

A
  1. Vasodilation
    - Nitrates
    - ACE inhibitors
    - ARBs
  2. Cardiac depression
    - beta blockers
  3. Antiarrhythmics
  4. Thrombolysis (primary)
    - Plasminogen activators
  5. Analgesics
    - morphine
  6. Anti thrombotics (secondary)
    - Anticoagulant
    - Anti platelet drugs
91
Q

phase 0 action potential (AP)

A
  1. rapid depolarization

2. Na and Ca2 channels open

92
Q

voltage for resting membrane

A

-70mV

93
Q

phase 3 of AP

A
  1. K+ channels open

2. Hyperpolarization

94
Q

phase 1 and 2 action potential

A
  1. Na and Ca2 channels close
  2. K channels open
  3. Repolarization
95
Q

phase 4 of AP

A
  1. K channels close

2. Recovery

96
Q

How parasympathetic (vagal) nerve endings slows the heart rate?

A

Vagal nerve release Ach, acting on mAChr -> open K+ channels -> decrease slope of pacemaker potential -> decrease HR

(opposite effect of noradrenaline)

97
Q

what phase of AP in RS ECG?

A

phase 1 and 2

98
Q

what phase of AP in Q ECG?

A

phase 0 and 1

99
Q

causes of arrhythmias

A
  1. cardiac ischemic
  2. excessive discharge or sensitivity to autonomic transmitters
  3. exposure to toxic substances
100
Q

what phase of AP in T ECG?

A

phase 3

101
Q

types of vaughan williams classification

A

Class 1: Na channel blockers
Class 2: B-blockers
Class 3: K+ channel blockers
Class 4: Ca2 channel blockers

102
Q

treatment of cardiac arrhytmias

A

use Vaughan Williams Classification

103
Q

Class 1A:

A
  • cause moderate phase 0 depression
  • prolong repolarization
  • increase duration of AP (slowing conduction)
  • decrease HR
  • use only for ventricular arrhythmias
  • drugs: disopyramide
104
Q

non-vaughan williams classification drugs

A
  1. adenosine

2. digoxin

105
Q

Class 1C

A
  • strong phase 0 depression
  • no effect on depolarization and duration of AP
  • inhibit abnormal automaticity
  • drugs: flecainide (slow conductions in all part of heart)
106
Q

Class 1B

A
  • weak phase 0 depression
  • shorten depolarization and repolarization
  • decrease duration of AP
  • drugs: lidocaine (in ventricular cell, and digitalis associated arrhythmia)
107
Q

Class 3

A
  • delay repolarization
  • prolong refractory period and AP
  • use in SVT and VT
  • drugs: amiodarone (could cause Na channel blockade), bretylium, sotalol
  • All 3 agents - torsades de pointes
108
Q

Class 2

A
  • Block sympathetic stimulation of heart
  • increase K+ conductance (slow HR)
  • increase refractory period and prolong AP
  • e.g. propanolol, atenolol, sotalol
109
Q

Drugs used in heart failure

A
  1. Diuretics
  2. Nitrates
  3. ACE inhibitor and ARBs
  4. B-adrenoreceptor blocker
  5. Digoxin
110
Q

Drugs used in hypertension and angina

A
  1. ACE inhibitor and ARBs (v TPR = vasodilation)(^ Blood Vol.)
  2. Calcium channels blockers (v contractility, TPR, HR)
  3. Diuretics (v blood vol.)
  4. Adrenoreceptor acting drugs
  5. Vasodilator (GTN)
111
Q

Class 4

A
  • slow stimulus conduction through the AV node
  • strongly affect conduction from atria to ventricles
  • Very useful for supraventricular arrhythmia (not ventricular)
112
Q

Drugs used in MI

A
  1. Analgesia

2. Thrombolysis & other antiplatelet therapies

113
Q

digoxin (cardiac glycoside)

A
  1. increase vagal tone
  2. decrease HR in atrial fib
  3. prolongs the effective refractory period
  4. positive inotropic effect in heart failure
  5. May induce cardiac arrhythmias:
    - block AV conduction
    - increase ectopic pacemaker activity
114
Q

adenosine

A
  1. depresses Ca current influx
  2. increase K+ conductance
  3. slows AV node conduction
  4. termination of SVT
  5. replaced verapamil for SVT
  6. given IV only
115
Q

Example of ACE inhibitors

A

Captopril

116
Q

MOA of ACE inhibitors

A
  1. Vasodilation: reduce vascular tone

2. Reduction in aldosterone secretion: decrease blood vol.

117
Q

Therapeutic use of ACE inhibitor in hypertension

A
  1. in diabetes mellitus with hypertension
  2. most effective in high renin hypertension
  3. more effective in white vs black patients
  4. excellent for patient with concomitant congestive heart failure
  5. considered in asthma instead of beta blocker
118
Q

drugs for hypertension for <55 years patients

A

ARB

119
Q

Example of ARBs or AT1 receptor antagonists

A

losartan

120
Q

drugs for hypertension for >55 years patients

A
  • Ca channel blocker or

- diuretics

121
Q

Two groups of Calcium channel blockers

A
  1. Non dihydropyridines (verapamil)

2. Dihydropyridines (nifedapine): primary action on arterioles

122
Q

Effects of nifedapine.

A
  1. Dilation of arteries and arterioles
  2. Fall in BP (decreased TPR)
  3. Reflex tachycardia
123
Q

Which drug is the best in low renin hypertension (black and elderly patient) ?

A

Nifedapine

124
Q

the use of non selective alpha blocker (phentolamine)

A
  1. Postural hypotension > induce tachycardia

2. pheochromacytoma

125
Q

clonidine MOA in treating hypertension

A
  1. Central action:
    - reduce sympathetic tone -> vasodilation & reduced HR
  2. Prejunctional action:
    - Reduces noradrenaline release
  3. Vascular smooth muscle:
    - Open Ca2+ channels and cause vasoconstriction
126
Q

losartan (ARB)

A
  1. block angiotensin 2 from stimulate pressor effect at AT1 recep.
  2. antihypertensive effects
  3. lack of bradykinin effects
  4. promote renal excretion of Na and water
127
Q

effects of ACE inhibitors eg: captopril

A
  1. hypotension
  2. reduced glomerular filling pressure
  3. accumulation of bradykinin cause cough
  4. hyperkalemia
  5. hyponatraemia
128
Q

loop diuretics

A
  • act in loop of Henle
  • most effective and commonly used
  • 25% Na retention
  • cause hypokalemia
129
Q

major categories of diuretics

A
  1. loop diuretics (furosemide & bumetanide)
  2. thiazides (hydrochlorothiazide)
  3. potassium-sparing
    - aldosterone antagonist (spironolactane)
    - non aldosterone antagonist (amiloride)
  4. osmotic (mannitol)
130
Q

potassium-sparing

A
  • helps reducing the hypokalemia due to loop diuretic & thiazide.
  • drugs: spironoloctoone
131
Q

thiazides

A
  • act in DCT
  • effective in mild cases only
  • 5% Na retention
  • cause hypokalemia
  • drugs: hydrochlorothiazide
132
Q

nitrates (GTN)

A
  • vasodilator
  • release NO that relaxes vascular SM
  • Antianginal actions:
    • reduce cardiac O2 consumption
    • reduce preload and afterload
    • redistribution of blood flow towards ischaemic area
    • relief of coronary spasm
133
Q

side effects of B-blocker

A
  • bradycardia
  • heart failure
  • bronchospasm
  • coldness of extremities
  • hypoglycaemia
134
Q

amrinone

A
  • PDE inhibitors
  • increase cAMP
  • cAMP phosphprylate Ca channels -> increase Ca entry into the cell
  • increase cardiac muscle contract
  • vasodilating effect
135
Q

inotropes

A
  • increase force of contraction of heart
  • increase intracellular cardiac [ca2+]
  • drugs: digitalis (digoxin), dobutamine, amrinone (PDE inhibitor),
    noradrenaline
136
Q

levosimendan

A
  • calcium sensitizer

- increase contraction at normal Ca levels

137
Q

Example of thrombolytic therapy

A
  1. Streptokinase

2. Recombinant tissue plasminogen activator

138
Q

recombinant tissue plasminogen activators

A
  • directly activates plasminogen
  • not antigenic
  • initiate conversion plasminogen to plasmin to induce fibrin degradation
139
Q

streptokinase

A
  • protein extracted from streptococci
  • activates plasminogen
  • initiate conversion plasminogen to plasmin to induce fibrin degradation

pharmacology (2 decks)

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