Brainscape's Knowledge GenomeTM

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


See full index

Pharm > SNS agonist > Flashcards

SNS agonist Flashcards

1
Q

Outline the signalling mechanisms at each adrenergic recetor

A

a1- PLC, IP3, DAG
a2- decrease cAMP (inhibitory)
B1- increase cAMP
B2- increase cAMP

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

Outline the difference adrenergic receptors present on blood vessels

A

In skeletal muscle blood vessels, lots of B2++ receptors to cause dilation, but in blood vessels to skin, mucous membranes etc. have a1 effects to constrict (learn receptors for all major sites)

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

Outline the selectivity of adrenoceptors for adrenalin and NA

A

noradrnaline more alpha, adrenaline more beta 2

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

Effect of a2 receptors on presynaptic membrane

A

NE can bind and then reduce synpatic transmission

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

Why is adrenaline used in anaphylaxis

A
  • act on a1 receptors of blood vessels to cause vasoconstriction to increase BP
  • acts on b1 reeptors on the heart to cause tachycardia
  • b2 receptor binding cause bronchodilation
  • beta receptors on mast cells which suppresses mediator release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the effect of anaphylactic shock

A

-histamine causes increased permeability of capillary so more fluid loss and vasodilation
Contraction of smooth mscle in resp tract
Contraction of smooth muscle in the GI tract eading to vomiting

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

Other use of adrenaline other than anaphylaxis

A

asthma,

acute bronchospasm due to chronic bronchitis,

cardiogenic shock- b1 inotropic (inability of heart to pump sufficient oxygen rich blood),

spinal anaesthesia a1 (to maintain BP), as lidocaine causes fall due to Na+ blockade

local anaesthesia- vasoconstrict to ensure the LA stays local for longer. A1. (infiltration anaesthesia and nerve block anaesthesia)

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

Side effects of adrenaline

A

Secretions (reduced and thickened mucous)

Minimal CNS

Minimal GIT

Skeletal muscle temor (adrenergic receptors on skeletal muscle)

CVS: PATCH! palipitations,arrhythmias, tachycardia,
COLD EXTREMITIES, hypertension

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

Outline selectivity of phenylephrine

A

a1»a2»>b1/b2

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

Difference between phenylephrine and adrenaline

Use of phenylephrine

A

phenylephrine chemically related to adrenaline but more resistant to COMT breakdown (post-synaptic membrane) but not MAO (mitochondria of the presynaptic)

used as nasal degongestant

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

Why is phenylephrine used as decongestant

A

Congestion due to capillary leakage in vessels travelling around nasal sinus…. stimulate a1 receptors increase vasocnstriction and reduces leakage

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

Other phenylephrine uses

A

Mydriatic (causes pupul dilation)

Anti-glaucoma (as it stimutes constriction of capillaries in the ciliary body, thus preventing movement of substrates from capillaries to ciliary body to make aqeous humour)

(pheNEYElephrine)

N for nose (decongestant)
sounds like EYE for mydriatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Selectivity of clonidine

A

a2»a1»>b1/b2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clonidine mimics sympthetic effects t/f

A

F! Because you get increased stimulation of a2 prejunctional receptor which causes inhibition of synaptic transmission at sympathetic synapse!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which receptors would you need to stimulate to reduce glaucoma

A

a2 receptor agonist- stimulate a2 receptors on epithelium to decrease production of aqueous humour
a1 receptor agonist on the blood vessel so vasoconstrction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical uses of clonidine

A

treatment of hypertension and migraine (reverse vasoconstriction)

17
Q

Mechanism of action of clonidine

A

a2 receptors prejunctionally and also in the CNS,

clonidine has a central action in the brainstem within baroreceptor pathway to reduce sympathetic outflow

AND

a2 adrenoceptor mediated
presynaptic inhibition of NA release

will reduce CO, cause vasodilation etc

18
Q

…

A

……

19
Q

Selectivity of isoprenaline

A

b1=b2»»a1/2

20
Q

Compare isoprenaline to adrenaline

A

chemically related but more resistant to MAO and uptake 1

21
Q

Clincal uses of isoprenaline

A

cardiogenic shock, acute heart failure, myocardial infarction

Normally with heart failure you want to reduce myocardial oxygen demand

but HF is associated with low CO, so this is aimed at increasing CO if the HF gets really bad and the CO is dangerously low

22
Q

Why is the b2 stimulation of isoprenaline a problem

A

b2 stimulation in VSMC in skeletal muscle blood vessels results in fall in venous BP causing reflex tachycardia via stimulation of baroreceptors. So you want less of the beta 2 effects

23
Q

State the selectivity of dobutamine

A

b1»b2»>a1/2

24
Q

Clincal use of dobutamine

A

cardiogenic shock, no relfex tachycadia and also short plasma half life (2 mins due to rapid breakdown by COMT, which is a good thing in this case)

25
Q

T/F dobutamine and salbutamol are both rapidly broken down by COMT

A

F… dobutamine is, but salbutamol is a wynthetic catecholamine derivate with relative resistance to MAO and COMT

26
Q

Action of salbutamol

A

You get increased stimulation of b2 receptors in the lungs, as you get increased cAMP and increased PKA causing bronchodilation due to:

  • opening of K+ channels
  • Increased Na/Ca2+ exchange to reduce Ca2+ in cell

inhibition of release of brochoconstrictor substances from mast cells.

27
Q

Clinical use of ventolin

A

asthma ( b2 relaxation of bronchial smooth muscle, inhibtion of release of bronchoconstrictors from mast cells )

Treatment of threatened premature labour (b2 relaxation of uterine smooth muscle

28
Q

Side effects of ventoiln

A

reflex tachycardia (less than isprenaline but still a bit), tremor and blood sugar dysregulation

29
Q

Outline what happens in anaphylactic shock

A

Upon secondary exposure to antigen, mast cells degranulate, releasing inflammagtory mediarors:

Heart and CVS:
-Capillaries leak in response to histamine, tissues swell (incl. tongue), blood volume decreses, irregular heartbeat, loss of oxygen to tissue

Respiratory tract:
Constriction of smooth muscle and muscles in throat
Difficulty swallowing and breathing

GI tract:
Contraction of smooth muscle, stomach cramps, vomiting

30
Q

Consequences of adrenaline overdose

A

Cerebral haemorrhage

Pulmonary oedema

31
Q

Why do isoprenaline and phenylephrine AND SALBUTAMOLlast longer in the body than endogenous catcholamines

Name a drug that does not share this property

A

Because isoprenaline is more resistant to COMT breakdown

Phenylephrine more resistant to MAO and uptake 1

Salbuatmol has relative resistancew to MAO and COMT

so broken down less quickly than adrenaline

Dobutamine has half life of 2 minutes (RAPIDLY metabolised by COMT!)

32
Q

Why is dobutamine a good drug in emergecny situations

A

In cardiogenic shock emergency

Lacks reflex tachy

Plasma half life just 2 mins (rapidly metabolised by COMT)

33
Q

Mast cells contain which adrenergic receptors

A

b2

Pharm (33 decks)

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