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PMY2106 > Cardiovasualar Durgs Lecture 1 > Flashcards

Cardiovasualar Durgs Lecture 1 Flashcards

1
Q

how angina occurs

A

when one or more of the coronary arteries becomes narrowed or blocked, usually by atherosclerosis

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2
Q

adrenoreceptors

A

receptors that mediate central and peripheral actions of the neurotransmitter noradrenaline and the hormone and neurotransmitter adrenaline

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3
Q

where adrenoreceptors are found

A

in nearly all peripheral tissues and on many neuronal populations within the central nervous system

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4
Q

what roles do noradrenaline and adrenaline play

A
  • blood pressure
  • heart rate and force
  • airway reactivity
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5
Q

activating alpha-adrenoreceptors

A

generally contracts smooth muscle, except in the gut

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6
Q

activating beta-1 receptors

A

contracts cardiac muscle
- predominate in the heart

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7
Q

activating beta-2 receptors

A

relaxes smooth muscle
- predominate in the airways

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8
Q

beta-blockers

A

used predominately in treatment of hypertension, angina and cardiac arrhythmias

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9
Q

how beta-blockers work

A

they prevent catecholamines from accessing the beta-adrenergic receptor sites in the heart and other organs

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10
Q

they prevent catecholamines from accessing the beta-adrenergic receptor sites in the heart and other organs

A
  • decreased heart rate and force of contraction
  • decreased renin secretion
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11
Q

Structure-Activity Relationship of beta-blockers

A

see lecture notes for structure

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12
Q

alcohol group

A
  • R-enantiomer of NA is more active than S
  • indicates that secondary alcohol is involved in H-bonding
  • compounds lacking hydroxyl group have greatly reduced interaction, but still posses some activity
  • alcohol group is important, but not essential
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13
Q

amine group

A
  • normally protonated and ionised at physiological pH
  • ^important since replacing it with carbon results in large drop in activity
  • activity affected by number of substituents
  • primary and secondary amines have good adrenergic activity
  • tertiary and quaternary ammonium salts don’t
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14
Q

both phenol substituents

A
  • can be replaced by other groups capable of interacting with binding site of hydrogen bonding
  • particularly true for the meta phenol group
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15
Q

alkyl substitution

A
  • alkyl substitution on the side chain linking the aromatic ring to the amine decreases activity
  • may be a steric effect which blocks h-bonding to the alcohol or prevents molecule adopting active conformation
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16
Q

isoprenaline

A
  • non-selective beta-agonist
17
Q

dichloroisoprenaline

A
  • partial agonist
  • overall acts as an antagonist
18
Q

pronethalol

A
  • replaces di-chloro substitution with aromatic ring
  • partial agonist, but overall beta blocker
  • first beta-blocker to be used clinically
19
Q

propanolol

A
  • produced by experimenting with length of chain between aromatic ring and the amine
  • was a pure antagonist with 10-20x greater activity than pronethalol
20
Q

synthesis of aryloxypropanolamines

A
  • nucleophilic substitution by the phenol, chemoselective for alkyl halide
  • nucleophilic substitution by the amine, regioselective for less substituted part of epoxide
  • synthesis allows variation of aromatic rings and N-substituents
  • racemic products formed
21
Q

first generation beta-blockers

A
  • branched, bulky N-alkyl substituents are good for beta-antagonist activity
  • variation of aromatic ring system possible
  • substitution on side chain methylene group increases stability but lowers activity
  • alcohol group on side chain essential for activity
  • replacing ether oxygen is detrimental
  • n-alkyl substituents longer than isopropyl or t-butyl are less effective but extension with n-arylethyl is beneficial (-CHMe-CH2-Ph)
  • AMINE MUST BE SECONDARY
22
Q

what receptors do first generation beta-blockers act on

A
  • both beta-1 and beta-2 receptors
  • can’t be used with asthmatic patients
23
Q

second generation beta-blockers

A
  • beta-1 selective
  • addition of another side chain on para-position
  • substitution has to be in para for beta-1 selectivity, as another hydrogen bond is formed which isn’t possible with beta-2
24
Q

third generation beta-blockers

A
  • inlude n-arylakyl group
  • extra vasodilating properties through blockade of alpha-adrenergic receptors
  • they have massive extensions after the amide group
25
Q

3rd generation beta blockers: labetalol, carvedilol and bucindolol

A

cause vasodilation through blockage of alpha-1 receptors

26
Q

3rd generation beta blockers: nebivolol

A

causes vasodilation by endothelium-derived NO

27
Q

why is carvedilol an exception to 3rd generation beta-blockers

A

why is carvedilol an exception to 3rd generation beta-blockers

28
Q

beta-blockers on hypertension

A
  • they decrease blood pressure by reducing cardiac output
  • acute treatment with beta-blockers not effective in reducing arterial pressure due to compensatory increase in systemic vascular resistance
29
Q

beta-blockers on angina

A
  • antiangial effects attributed to cardiodepressant and hypotensive actions
  • by reducing heart rate, force and arterial pressure, they reduce work of heart and oxygen demand
  • improves oxygen supply/demand ratio, which can relieve anginal pain
30
Q

beta-blockers on arrhythmias

A
  • antiarrhythmic properties related to beta-blockers ability to inhibit sympathetic influences on cardiac electrical activity
  • sympathetic nerves increase SA node firing
31
Q

kind of heart failure that most patients have

A

systolic dysfunction

32
Q

systolic dysfunction

A

contractile function of the heart is depressed

33
Q

beta-blockers on systolic dysfunction

A
  • some specific beta-blockers improve cardiac function and reduce mortality
  • may be related to blockade of excessive chronic sympathetic influences on the heart, which are known to be harmful to the failing heart
  • however, precise mechanism is poorly understood
34
Q

beta-blocker side effects

A
  • dizziness
  • tiredness
  • slow heartbeat
35
Q

thing to note with beta-blockers

A

lipophilic beta-blockers can cross the BBB, so they have been associated with a low incidence of CNS side effects

PMY2106 (15 decks)

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