Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology year 2 > UMP2005 pharmacology of the sympathetic nervous system > Flashcards

UMP2005 pharmacology of the sympathetic nervous system Flashcards

1
Q

what type of receptor are adrenoreceptors?

A
  • GPCRs
  • g protein coupled receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the subtypes of adrenoreceptors?

A
  • alpha 1 and 2
  • Beta 1,2,3x
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the pathway of alpha 1 adrenoreceptors?

A
  • coupled with Gq protein
  • causes stimulation of phospholipase C which stimulates IP3/DAG which Ca release causing muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the pathway of alpha 2 adrenoreceptors?

A
  • coupled to Gi protein
  • inhibits adenyl cyclase which decreases levels of cAMP causing decreased contraction/excitability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the pathway of beta-adrenoreceptors?

A
  • B 1 = coupled to Gs protein = stimulates adenyl cyclase, increasing cAMP, causing contraction/excitability
  • B2/3 = coupled to either Gs or Gi so either stimulate or inhibit adenyl cyclase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

give an example of a non-selective competitive irreversible alpha adrenoreceptor antagonist

A
  • phenoxybenzamine
    (used in treatment of paroxysmal hypertension and sweating resulting from pheochromocytoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

give an example of a non-selective competitive reversible alpha adrenoreceptor antagonist

A
  • phentolamine
    (used to reverse the effects of an anesthetic medicine in soft tissues, such as the lips and tongue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

give some examples of selective alpha 1 adrenoreceptor competitive reversible antagonists

A
  • prazosin
    (manage and treat hypertension, benign prostatic hyperplasia, PTSD-associated nightmares, and the Raynaud phenomenon)
  • doxazosin
    ( treat symptoms of benign prostatic hyperplasia and hypertension)
  • tamsulosin
    (treat symptomatic benign prostatic hyperplasia and chronic prostatitis and to help with the passage of kidney stones)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

give some examples of selective alpha 2 adrenoreceptor competitive reversible antagonists

A
  • yohimbine
    (used in veterinary medicine to reverse the effects of xylazine in dogs and deer and used to treat erectile dysfunction)
  • idazoxan
    (trials for mental illnesses and neurodegeneration)
  • atipamezole
    (reversal of the sedative and analgesic effects of dexmedetomidine and medetomidine in dogs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

give some therapeutic uses of a1 adrenoreceptor antagonists

A
  • hypertension
  • phaeochromocytoma
  • benign prostatic hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do alpha 1 antagonists work against hypertension?

A
  • prevent noradrenaline from stimulating a1 receptors to constrict, so with the antagonist the blood vessels dilate to decrease blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what happens when alpha 1 adrenoreceptors are blocked?

A
  • decrease blood pressure (vasodilation)
  • postural hypotension = dizziness
  • failure of ejaculation
  • miosis ( pupils constrict )
  • baroreceptor reflex can cause tachycardia and renin cause sodium and water retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do alpha 1 antagonists work against benign prostatic hyperplasia?

A
  • they block receptors from noradrenaline to constrict
  • so the antagonists relax the prostatic smooth muscle
  • helps reduce constriction on urethra, help urine flow more easily
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

give 2 examples of non-selective Beta adrenoreceptor antagonists

A
  • propranolol
    ( treat high blood pressure and other heart problems, but it can also help with the physical signs of anxiety, like sweating and shaking)
  • timolol
    (treat and manage open-angle glaucoma and ocular hypertension)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

give some examples of selective Beta 1 adrenoreceptor antagonists

A
  • atenolol
    (treat hypertension and arrhythmia)
  • bisoprolol
    (treat hypertension and heart failure)
  • metoprolol
    (treat hypertension and arrhythmia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are Beta-adrenoreceptor antagonists with intrinsic sympathomimetic activity and give some examples?

A

beta-blockers that are able to stimulate beta-adrenergic receptors (agonist effect) and to oppose the stimulating effects of catecholamines (antagonist effect) in a competitive way
- pindolol
(treat hypertension)
- oxprenolol
(treat hypertension and arrhythmia)

17
Q

how do beta blockers work?

A
  • block the effect of adrenaline on organs and tissues like the heart
  • this will slow the heart down and thus also decrease blood pressure
18
Q

give 2 examples of combined alpha 1 and beta 1 antagonists

A
  • carvedilol
    (treat hypertension and prevent heart disease)
  • labetatol
    (treat hypertension especially in pregnancy and emergency)
19
Q

give an example of a combined Beta 1 antagonist and Beta 3 agonist

A
  • nebivolol
  • treat hypertension and heart failure
    -induces nitric oxide production from endothelium and myocardium via activation of beta(3)-adrenergic receptors, which improves blood flow
20
Q

give some uses of beta adrenoreceptor antagonists

A
  • treat hypertension, heart failure, angina, arrhythmias, myocardial infarction, thyrotoxicosis, anxiety, migraine, glaucoma
21
Q

what is the differences between lipid and water soluble beta blockers?

A
  • lipid soluble = liver metabolised, shorter half life
  • water soluble = excreted by kidnyes, longer half life
  • lipid soluble antagonists may have more CNS side effects but may be better for anxiety and migraine
22
Q

what are some unwanted side effects of Beta blockers?

A
  • fatigue, bradycardia, cold extremities, hypoglycaemia, sleep disturbance and nightmares
23
Q

what are some contradictions of beta blockers

A
  • can cause bronchospasm = avoid in asthma patients
  • can cause hypoglycaemia = avoid in diabetic patients
  • also avoid in AV block and severe peripheral vascular disease
24
Q

why should beta blockers be avoided in some type 1 diabetic patients?

A
  • they may exacerbate hypoglycaemia in insulin dependent diabetes (mostly type 1)
  • as it blocks Beta-2 mediated glucose release from the liver and also sympathetic responses to hypoglycaemia
25
Q

why should beta blockers be avoided in some type 2 diabetic patients?

A
  • mechanism not clear but non-selective, non-vasodilating, Beta blockers may reduce skeletal muscle blood flow and so insulin dependent glucose uptake
  • Carvedilol and nebicolol have better glycaemic control as they are selective beta and alpha-1 blockers
26
Q

what is the link between adrenoreceptors and hyperlipidaemia?

A
  • beta blockers may increase blood triglycerides and decrease HDL (except carvedilol which may reduce triglycerides and LDL)
  • alpha blockers like doxazosin may reduce blood triglycerides, increase HDL and decrease LDL
27
Q

what does it mean that some beta blockers are inverse agonists?

A
  • some beta blockers display some spontaneous activity
  • metoprolol shown to be a very good inverse agonist on beta blockers
  • they can reduce cAMP and cardiac contractility below basal levels
  • as they can act through both Gs and Gi which oppose each other
28
Q

describe the beta adrenoreceptor arrestin/GRK pathway

A
  • Beta 1 and 2 adrenorecpeotrs linked to Gs coupled protein, stimulates adenyl cyclase which increases cAMP
  • this causes arrestin to activate and GRK to phosphorylate
  • however, as arrestin binds to the GPCR it desensitized, blocking the signalling pathway
    (Beta 3 have no GRK phosphorylation sites so much less desensitization)
29
Q

describe how some beta blockers are biased agonists for the GRK/Arrestin pathway

A
  • carvedilol and nebivolol can stimulate GRK phosphorylation of Beta 1 and 2 adrenoreceptors and stimulate arrestin binding and ERK1/2 kinase activity (basically blocking signalling pathway)
  • this is thought to be cardio protective which may be useful in some patients
30
Q

what are the 3 ways you can interfere with adrenoreceptor stimulation with pre-synaptic processes?

A
  • synthesis
  • storage
    -release
31
Q

give some examples of drugs used to inhibit the synthesis of catecholamines (to reduce adrenoreceptor stimulation)

A
  • a-methytyrosine = block tyrosine hydroxylase which converts L-tyrosine into L-DOPA
  • disulfiram = blocks dopamine B-hydroxylase which converts dopamine into noradrenaline
  • a-methyldopa = competitive inhibitor of dopa decarboxylase which converts L-DOPA into dopamine
32
Q

describe the process of recycling noradrenaline in the presynaptic terminal

A
  • NA is taken back into the presynaptic nerve terminal by NA transporter
  • then MAO breaks down excess NA
  • NA is then uptaken into vesicles by VMAT2
33
Q

what is VMAT2 used for in presynaptic nerve terminals?

A
  • uptake of NA into vesicles
34
Q

how does reserpine work?

A
  • inhibits VMAT2 which allows NA to be uptaken into vesicles in the presynaptic nerve terminal
  • so less NA is released

Pharmacology year 2 (8 decks)

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