Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

notes to flashcards year 2 - LCRS1 > SNS antagonists > Flashcards

SNS antagonists Flashcards

1
Q

what do alpha 2 receptors do to NE release?

A
  • there are pre-synaptic alpha 2 receptors

- alpha 2 receptors have a -ve feedback on NE release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do alpha 1 receptors do?

A

vasoconstriction

relaxation of GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do alpha 2 receptors do

A

inhibition of NT release,
contraction of VSMC,
CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what do beta 1 receptors do?

A

cardiac stimulation,
relaxation of GIT,
renin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what do beta 2 receptors do?

A

bronchodilation,
vasodilation,
relaxation of VSMC,
hepatic glycenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what do beta 3 receptors do?

A

lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

name a non selective (alpha 1 and beta 1) adrenoreceptor ANTAGONIST

A

labetol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

name an alpha 1 and beta 2 ANTAGONIST

A

phentolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

name an alpha 1 antagonist

A

prazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

name a beta 1 and 2 selective antagonist

A

propanolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

name a beta 1 selective anatagonist

A

atenolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is hypertension?

A
  • underlying cause rarely diagnosed
  • defined as DAMP > 90mmHg
  • BP as 140/90mmHg or higher
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the main elements that control hypertension?

A
  • blood volume
  • CO
  • TPR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the 4 different targets for anti-hypertensives?

A
  • SNS nerves that release vasoconstrictor molecules
  • kidney and heart
  • arterioles - control/determine TPR
  • CNS - determine BP set point, regulate some systems involved in BP control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the targets of beta-adrenoceptor antagonists?

A
  • CNS: to reduce sympathetic tone
  • Heart (beta 1): reduce ionotropic and chronotropic effect
  • kidneys (beta 1): reduce renin prodiction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the unwanted effects of beta-adrenoreceptor antagonists?

A
  • bronchoconstriction
  • cardiac failure
  • hypoglycaemia (beta blockers may mask symptoms, non selective also block hepatic glycogenolysis)
  • fatigue (reduced CO)
  • cold extremities (loss of beta receptor mediated vasodilation)
  • bad dreams
17
Q

what is propanolol? what does it cause?

A
  • beta 1 and beta 2 selective
  • in subject at rest = very little effect
  • during exercise can reduce HR, CO and ABP
  • as non-selective, produces all typical adverse effects
18
Q

what is atenolol? what does it do?

A
  • beta 1 selective
  • antagonises effects of NE on heart but affects any organ with beta 1
  • less effect on airways than non-selective but not safe with asthmatic
  • selectivity is concentration dependent (too much and becomes non-selective)
19
Q

what is labetalol? what does it do?

A
  • alpha 1 and beta 1 dual-action antagonist
  • lowers BP via reduction in TPR
  • induces reduction in HR or CO –> wanes with chronic use
20
Q

what is the problem with alpha-adrenoreceptor?

A
  • fall in arterial pressure (as alpha receptors are main mediators of TPR)
  • problem with postural hypotension
  • as there is a fall in TPR, you get reflex tachycardia
21
Q

what is phetolamine and what does it cause?

A
  • non selective alpha-antagonist
  • causes vasodilation and fall in BP
  • but simultaneous blockade of alpha 2 receptors tends to inc. NE release
  • this enhances reflex tachycardia
  • inc. GIT motility and diarrhoea common
  • no longer clinically used
22
Q

what is prazosin and what does it cause?

A
  • alpha 1 antagonist
  • causes vasodilation, fall in BP
  • less reflex tachycardia as don’t block alpha 2 receptors to inc. NE release
  • dramatic hypotenive effect
  • causes a modest dec. in LDL and inc. in HDL = GOOD
23
Q

how is methyldopa an antihypertensive medication?

A
  • methyldopa taken up by noradrenergic neurones
  • methyldopa is decarboxylated and hydroxylated to form alpha-methyl-NA (false NT)
  • methyldopa not broken down within neuron
  • accumulates in larger quantities than NA
  • displaces NA from vesicles
24
Q

what’s the MoA?

A
  • less active than NA on alpha-1 receptors (less effective in causing vasoconstriction)
  • more active on presynaptic alpha 2 receptors (more -ve feedback on NE release)
  • minor effects on CNS
25
Q

what are the benefits of methyldopa?

A
  • renal and CNS blood flow maintained –> used in pt with renal insufficiency or CNS disease
  • recommended in hypertensive pregnant women –> no adverse effects on foetus
26
Q

what are the adverse effects of methyldopa?

A
  • dry mouth
  • sedation
  • orthostatic hypotension
  • male sexual dysfunction
27
Q

what is the main cause of arrythmias?

A
  • myocardial ischaemia
28
Q

what is propanolol?

A
  • non selective beta antagonist class II drug
  • reduces mortality of pt with MI
  • partially successful in arrhythmias that occur during exercise/mental stress
29
Q

what is angina?

A

pain that occurs when the O2 supply to myocardium is insufficient for its needs

30
Q

where does the pain spread in angina?

A
  • spreads down dermatome T1 in chest, arm, and neck

- bought on by exertion of excitement

31
Q

what are the types of angina?

A
  • stable: pain on exertion - due to fixed narrowing of coronary vessels
  • unstable: pain with less exertion and with pain at rest - thrombus but without complete occlusion of artery
  • variable: occurs at rest, caused by coronary artery spams, ass/ w. atheromatous disease
32
Q

how do beta adrenoreceptor antagonists reduce myocardial demand?

A
  • by decreasing ionotropic and chronotropic effect
  • at low doses does not affect bronchial SM, systolic BP
  • reduces oxygen demand whilst maintaining effort
33
Q

what are the adverse effects of beta-adrenoceptor antagonist’s?

A
  • fatigue
  • insomia
  • dizziness
  • sexual dysfunction
  • bronchospasm
  • bradycardia
  • heart block
  • hypotension
34
Q

what is glaucoma caused by?

A
  • poor drainage of aqueous humour

- can permanently damage optic nerve

35
Q

describe the production of aqueous humour

A
  • produced by blood vessels in ciliary body via actions of carbonic anhydrase
  • production is indirectly related to BP
36
Q

describe the flow of aqueous humour

A

posterior chamber –> through pupil to anterior chamber –> trabecular meshword and into veins and canal of Schlemm

37
Q

what beta adrenoceptor antagonists are used in glaucoma treatment? what do they do?

A
  • non selective block of beta 1 and 2
  • timolol maleate, corteolol hydrocholride
  • reduce rate of aqueous humour formation by blocking receptors on ciliary body

notes to flashcards year 2 - LCRS1 (58 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions