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LCRS Pharma > SNS agonists > Flashcards

SNS agonists Flashcards

1
Q

what are directly acting SNS agonists/ sympathomimetics (DASA) ?

A

mimics the actions of NA/A by binding to and stimulating adrenoreceptors

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2
Q

alpha 1

A

PLC, IP3, DAG

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3
Q

alpha 2

A

decreased cAMP
NA release inhibition

selectively targeted by clonidine to reduce sympathetic tone

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4
Q

beta 1

A

increased cAMP

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5
Q

beta 2

A

increased cAMP

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6
Q

what are the principle target sites for DASAs?

A

CVS
eyes
lungs

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7
Q

alpha 1 locations

A 
eye
liver
trigone and sphincter 
ureter
genitalia male
lacrimal glands 
salivary glands 
skin 
GI
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8
Q

beta 2 locations

A 
trachea and bronchioles
liver
detrusor
salivary glands 
genitalia female 
skeletal muscle
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9
Q

name some beta 1 locations

A

heart

adipose
kidney
salivary glands

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10
Q

how does noradrenaline selectivity change for the adrenoreceptors?

A

a1/a2> b1/b2

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11
Q

how does adrenaline selectivity change for the adrenoreceptors

A

b1/b2> a1/a2

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12
Q

effect of NA binding to alpha 2 receptors?

A

negative feedback effect in NA exocytosis

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13
Q

adrenaline (DASA)

A 
non-selective 
b2- bronchodilator 
b1- tachycardia 
a1- peripheral vasodilation
suppression of mediator release
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14
Q

clinical scenarios to use adrenaline

A
  • asthma, bronchospasm (COPD) for b2
  • glaucoma a1
  • cardiogenic shock b1
  • spinal (maintain BP) and local anaesthesia ( prolong action on a1 to reduce blood flow and remove anaesthetic drug)
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15
Q

how does adrenaline treat glaucoma?

A

the increased IOP is caused by the production of aqueous humour by the ciliary body. Vasoconstriction will reduce blood flow and there aq humour production to release IOP

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16
Q

what are the unwanted effects of adrenaline (DASA)

A
  • secretions are reduced and thickened
  • CNS effect is minimal (BBB not crossed)
  • tachycardia, palpitations, arrhythmia, hypertension
  • cold extremities
  • overdose leads to cerebral haemorrhage and pulmonary oedema
  • GI effect is minimal
  • tremor (beta receptors)
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17
Q

phenylephrine (DASA)

A
  • a1 selective (more than alpha 2, beta 1 and 2)
  • structure similar to A
  • however more resistant to COMT (not MAO) … longer lasting
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18
Q

clinical uses of phenylephrine

A
  • vasoconstriction (e.g. local anaesthetics’ hypotensive effects)
  • mydriasis (dilation)
  • nasal decongestant (vasoconstriction reduces fluid leakage in nasal sinus)
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19
Q

clonidine (DASA)

A
  • a2 selective more than a1, then beta

- acts on presynaptic a2 to inhibit NA release

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20
Q

clinical uses of clonidine

A
  • hypertension
  • migraine
  • reduce sympathetic tone
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21
Q

isoprenaline (DASA)

A
  • beta selective (over alpha)
  • similar to A
  • more resistant to MAO and uptake 1
  • plasma half life of 2 hours ( fast)
22
Q

clinical uses of isoprenaline

A
  • cardiogenic shock
  • acute heart failure
  • MI

however beta2 stimulation causes a drop in venous BP and therefore a reflex tachycardia due to BR stimulation

23
Q

dobutamine (DASA)

A
  • beta 1 selective more than beta 2 (then alpha)
  • rapidly metabolised by COMT
  • administered by IV
  • half life of 2 minutes
24
Q

clinical use of dobutamine

A
  • cardiogenic shock (without the reflex tachycardia)
25
Q

salbutamol [ventolin] (DASA)

A
  • beta 2 selective more than beta 1 (then alpha)
  • synthetic catecholamine derivative
  • resistant to COMT and MAO
26
Q

clinical uses of salbutamol

A
  • asthma (relax smooth muscles b2, inhibit constriction substances)
  • threatened premature labour (relax smooth muscles)
27
Q

side effects of salbutamol

A
  • reflex tachycardia
  • tremor
  • blood sugar dysregulation
28
Q

indirecting acting SNS agonist examples

A

cocaine

tyramine

29
Q

Cocaine (IASA)

A

uptake 1 blocker

30
Q

effects of cocaine on CNS

A

low dose- euphoria, excitement, increased motor activity

high dose- activation of CTZ (then vomiting), CNS depression, respiratory failure, convulsions and death

31
Q

effects of cocaine on CVS

A

low dose- tachycardia, vasoconstriction, raised BP

32
Q

tyramine (IASA)

A
  • acts as false NT
  • normally not a problem when MAO degradation mechanism is in place
  • used to prescribe MAO inhibitors as anti-depressants
33
Q

action of tyramine

A
  1. Weak action at the receptors for NA.
  2. Weak inhibitory effect on the uptake 1.
  3. Displaces NA from the vesicles.
  4. Competes for MAO breakdown so less breakdown of NA.
  5. Leakage of NA out of the vesicles.
34
Q

how can inhibition of MAO with tyramine administration lead to a hypertensive crisis?

A

tyramine competes with left over MAO with NA

NA builds up

35
Q

why is adrenaline used in anaphylactic shock?

A

mast cell degranulation and histamine release leads to bronchoconstriction and vasodilation

adrenaline will counteract these reactions

36
Q

what is cardiogenic shock?

A

mediated by beta 1 (positive inotropic)
the sudden inability to pump sufficient oxygen-rich blood

when you have an MI
or cardiac arrest

37
Q

why is adrenaline used in local anaethesia?

A

to keep the agent restricted to one area by having near by vessels constricted (prevent clearance)

via alpha 1 mediated vasoconstriction

38
Q

why is adrenaline given in spinal anaesthesia?

A

the anaesthesia gets rid of sympathetic outflow so the peripheral vessels relax so BP is not maintained

adrenaline will constrict vessels to maintain the blood pressure

39
Q

what mediated mydriasis?

A

radial muscles of the iris

they have alpha 1 adrenoceptors (use with phenylephrine)

contraction of these muscles–> dilation

40
Q

how is phenylephrine used a nasal decongestant?

A

acts on alpha 1 (vasoconstriction)

this will reduce mucus production and swelling

41
Q

where are alpha 2 uniquely located? what function does this enable?

A

pre-synaptically

auto-inhibitory receptors to reduce the amount of NA released into the synaptic cleft

42
Q

how does clonidine reduce sympathetic drive from the brain?

A

works on baroreceptors in the brainstem

43
Q

how does clonidine treat hypertension and migraine?

A
  • clonidine targets Alpha 2
  • reduce NA levels in synaptic cleft
  • reduce sympathetic tone
  • reduced vascular tone
  • decreased TPR
  • decreased BP

clonidine also works on baroreceptors in the brainstem

44
Q

how does isoprenaline differ to phenylephrine? what do they have in common

A

isoprenaline is more resistant to MAO degradation
- alpha 1 selective

phenylephrine is more resistant to COMT degradation
- beta selective

both are based on the structure of adrenaline

45
Q

why is isoprenaline no longer used?

A

resulted in fatal reflex tachycardia or dysrhythmias due to action on beta 2 adrenoceptors

non selective Beta agonist

46
Q

why is dobutamine better to use than isoprenaline?

A

dobutamine is selective for beta 1 (very little for beta 2)
isoprenaline is non-selective for beta

therefore dobutamine lacks the isoprenaline reflex tachycardia effect

47
Q

how does dobutamine differ to isoprenaline is terms of metabolism?

A

very short half life (2min)
rapidly metabolised by COMT

isoprenaline is MAO degradation resistant

48
Q

why does salbutamol have a longer doa than adrenaline and noradrenaline?

A

synthetic catecholamine derivative resistant to MAO and COMT degradation

49
Q

how does salbutamol treat asthma?

A
  • binds to beta 2–> bronchodilation
  • bronchial smooth muscle relaxed
  • inhibition of bronchoconstriction mediators from mast cells
50
Q

how does salbutamol treat premature labour?

A

beta 2 mediated relaxation of uterine smooth muscle

51
Q

what are some side effects of salbutamol? why must care be taken for some patients?

A
  • reflex tachycardia
  • tremor
  • blood sugar dysregulation

take care in cardiac patients, hyperthyroidism, diabetics as beta 2 stimulated glycogenolysis

52
Q

why must diabetics be careful with salbutamol?

A
  • acts on beta 2

- beta 2 mediated glycogenolysis

LCRS Pharma (32 decks)

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