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LSM3211 > Autonomic Nervous System(adrenergic) > Flashcards

Autonomic Nervous System(adrenergic) Flashcards

1
Q

adrenergic system

A

fight or flight nervous system

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2
Q

physiological changes due to adrenegicsyetem

A

increased heart rate, increased sweating and pupil dilation

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3
Q

two key hormones in sympathetic nervour system

A

noradrenaline(noreponephrine) and adrelanine(epiinephrine)

noradrenaline released first
adrenaline erleasde when circumstances presist

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4
Q

locations where the hormones for sympathetic nervous system are produced

A

noradrenaline : adrenegic neurons adn adrenal medulla
adrenaline: adrenal medulla

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5
Q

location of the adrenagenic receptors

A

effectors organs only

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6
Q

what class do noradrelaine and adrenaline belong to

A

catecholamines
largely derived from the amino acid tyrosine

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7
Q

synthetic deravitive of noradrenaline

A

issoprenaline

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8
Q

catecholamine synthesis steps

A

l tyrosin to l dopa to dopamine to noradrelaine to adrenaline

tyrosine hyroxylase
l aromatic amino acid decarboxylase
dapamine B hydroxylase
phenylmethanomaine -n- methyltransferase

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9
Q

catecholamine sythesis negaative feedback

A

noradreanline to regualre noradrelaine sythesis
inhibit the tyrosine hydroxylase

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10
Q

what breaks down noradrenaline

A

monoamine oxidase (MAO)
MAO present in the cytoplasm

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11
Q

post synaptic receptors for adrenergenic

A

a and b

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12
Q

at synaptic cleft of adrenergic

A

75 % of nor adrenlaine recaptured and transported via noradrenaline transporter
bind ot a and b post snymaptic clift and mediast reaction

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13
Q

what are contorls of non adrelaine release

A

autoinhibitory feedback medicated by a2 receptor on pre snmaptic
when a lot bind to it, prevent further release

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14
Q

where are NA made

A

inside vesicles with dopamine beta hydroxylase

vascular monoamine trasnported allow for NA to enter the vescicel again

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15
Q

a receptors of adrenergic receptors

A

a1: contraction of smooth muscles
a2: feedback inhibition

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16
Q

b receptors of adrenergic receptor

A

b1: heart : increase the rate and force of contraction
b2: lungs : relaxation of smooth muscles

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17
Q

a1 receptor function

A

contraction of smooth muscles
vasoconstriction of smooth muscles of blood vessels
increase in peripheral vascular resistance
increase in blood pressure
– reactivates the baroreceptor and result in reflex(bradycardia)

at smooth muscle causes
- blood vessel constriction
-bronhco construction
gastrointestinal relax
sphincter contract
uterus contract
iris contract

at liver causes : glycogenolysis
at prostate : induced contraction
at heart: increased interaction

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18
Q

a2 receptor function

A

inhibit release of NA (autoinhibitory feedback,, so less A , less adrenergic activity

blood vessel constrict
relax gastrointestinal tract

decrease insulin sectrion from pancreatic islets

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19
Q

agonist potency order for a1

A

NA
A
ISO

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20
Q

agonist potency order for a2

A

A
NA
ISO

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21
Q

agonist potency order for b1

A

ISO
NA
A

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22
Q

agonist potency order for B2

A

ISO
A
NA

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23
Q

B1 receptor function

A

increase rate and force of heart contraction
increase release of renin from juxtaglomerular cells of kidney which raises blood pressurestep

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24
Q

stpes involved when b1 is activated

A

activation of b1 in juxtaglomerular cells
increase renin release
renin catalysed the conversion of angiotensinogen to angiotensin I
ACE converted AGTI into AGTII

AGTII increase aldosterone release at adrenal glands
sodium and water retentions
increased blood pressure

increase heart rate and heart contraction

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25
Q

b2 receptor

A

relax smooth muscles
- vasodilation
-bronchodilation
-relax uterine muscles
relax gastrointestinal tract

promotes relaxation

increase heart rate and heart contraction

@ liver, gylcogenolysis

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26
Q

agonist for which receptor causes bronchoconstriction

A

M3

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27
Q

asthma drug

A

Adregenic B2 agonist

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28
Q

seconadry messengers and effectors(a1)

A

increase inositol triphosphate
inscrease DAG
increase CA2+

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29
Q

seconadry messengers and effectors(a2)

A

decrease CAMP

30
Q

seconadry messengers and effectors(b1)

A

increase CAMP

31
Q

seconadry messengers and effectors(b2)

A

increase CAMP

32
Q

norepinrpherine drug

A

a/b agonist
not clinically used
trasnmitter at postganglionic sympathetic neurons

33
Q

epinephrine

A

a/b agonist
asthma and anaphylactic shock, cardiac attack

34
Q

salbutamol

A

B2 agonist
asthma
premature labor

35
Q

phenylphrine

A

a1 agnoist
nasal decongestion thr vaso constriction; reduce amt of fluid

36
Q

clonidine

A

a2 partial agonist
hypertension
migraine
derease amt of sympathetic activity

37
Q

propranolol

A

b antagnoist (non selctive)
angina
hypertenison
cardia dysrthmias
anxiety
tremor

38
Q

A methyl-p-tyrosine

A

drug that affect NA biosynthesis
tyrosine hyroxylase inhibitor

reduce amt of noradrenaline and adrenaline

39
Q

clinical use of A methyl-p- tyrosine

A

alternative treatmenr option phaenchromocytoma
(NA/ADR secreting tumour of adrenal medulla)
- high heart rate
symptoms representative of over active adrenaline system

40
Q

Reserpine

A

drug that affect NA storage
- inhibitor of VMAT
inhibit uptake of vesicular uptake of NA
- NA remain in cytoplasm and get metabolised by MAO
-depletion of NA : interrupt sympathetic transmission

41
Q

clinical use of resperpine

A

hypertension and mood disorders(schizophrenia)

adverse effect; dizziness, droziness, irregular heart beat , depression

42
Q

name the drugs that affect the relase and uptake of noradrenaline

A

Amphetamine
cocaine
clonidine
yohimbine

43
Q

drugs that are indirect sympathomimetics

A

Amphetamine that increases the relase of NA
cocaine that inhibits the reuptake of NA

44
Q

drusg that are A2 agonist for release and reuptake of noradreanlaine

A

a2 receptor agonist, clonidine that decreases NA release
a2 antagonist yohimbine that increases NA release

45
Q

how does amphetamine work on noradrenaline release

A

since they represent the NA structureally, they are taken up by NET and VMAT in exchange for reduced NA uptake
NA left in the cytosol is metabolized by MAO or escpated via NET back into synaptic cleft
– this causes increase in NA in cleft
- amphetamine have some inhibitory effect on MAO and can also increase dopamine release in a similar manner
– thus nre amt of NA increase
tyramine from chocolate and ephereine have similar action as amphetamine

46
Q

amphetamine effect on NA

A

promote release of NA without depolarising nerve membranes
– bc everything in the pre snymaptinc leaks out

47
Q

cocaine effect on Noradrenaline

A

inhibit reuptake of Noradrenaline into presynaptic by inhbiting respective trasnporters
— thus build up of noradrenaline in synaptic cleft leading to increased sympathetic activity

48
Q

effect of sympathimimimetics

A

increased rate and force of contractility of heart(dose responsive tachycardia)
– construction of blood vessels leading to hypertension
– inhibition of gut motility(die to relaxation of GI tract)
–CNS stimulant
– euphoria(dopamine effect), increased energy and libido, reduced fatigue and appetite, and behavioral responses, such as increased self confidence and alertness

49
Q

dangers of tyramine

A

can be dangerous if given with MAo blocker, which is required for catabolsim of tyramine

50
Q

clinical use of tyramine

A

NA release

no clinica use but present in various foodi

51
Q

clincial use of amphetamine

A

NA release, MAO inhibitor, NET inhibitor, CNS stimulant

CNA stimuant in narcolepsy, also in hyperactive children, appetite suppressant , drug of abuse

52
Q

clinical use of ephedrine

A

NA release, B agonist, weak CNA stimulant action
nasal decongestion

53
Q

a2 receptor agonist and antagonist regarding Noradrenaline

A

clonidine agonist
yohimbine(antagonist)

54
Q

effect of a2 receptor agonist at noradrenaline

A

clonidine
inhibit NA release
clinical use: antihypertension
adverse effect : headache, dizziness, drowsiness, constipation, brandycardia

55
Q

effect of “a” receptor antagonist regarding yohimbine

A

inhibit post snymaptinc a receptor as well,
so no used clinically

56
Q

indirect sympathomimetic drugs- MAO and COMT inhibitors

A

moclabemide, anti depresant

57
Q

how does moclobemide work

A

endogenous and exogenous catecholamine are metabolised mainly by two enzymes :

  • monoamine oxidase and catechol-o-methyl -transferase
    (CoMT metabolism substranets such as L dopa and are absent in the NA neurons)

inhibiting them will increase availability of neurotransmitters such as NA nd dopamine

58
Q

what is the difference between the catecholamine and NA released from the sympathetic nerves

A

duration of activity of the catechoaimines released from the adrenal medulla is longer – so longer activity
NA immeidaytl removed from the neuroeffectory synapse by way of reuptake into the postganglinos neurons however circualtin is inactivate by COMT in liver, as such would have longer period of effect
capable of stimulating tiessies that are not directly innervated by the nerve
NA has limited affinity for B2 receptors, thus circulating A is capable of stimulating these receptors in airway smooth muscles
vascular smooth muscles in skeletal muscles contain a1 and b receptor,
NA which stimular only excitatory a1 receptor causes strong vasoconstriction
however, a which stimulates both type of receptor would cause weaker vasoconstrictions

59
Q

receptors that are linked to blood pressure

A

a1 - vasoconstrictinos
b1- increased cardia output
b1 at juxtaglomerular cells - increase renin - renin causes angiotensinogen into at1-AEC– CONVERT AT1 TO AT2 - at2 increase aldostrong release at adrenal glands, - sodicum and water retention - increase in blood pressure
b2 - vasodilation

60
Q

ISO

A

isoprenaline

61
Q

noradrenaline effect

A

predominantly a agonist
expect vaso constrictions
peripheral resistance will increase
blood pressure increase
heart rate go down bc when blood pressure increase, baroreceptors can sense it and the refex is to lower heart rate

62
Q

isoprenaline effect

A

potent b agnoist
vaso constrictions
peripeherial reisitance decrease
blood pressure decrease

also act on b1 receptor
heaty rate become higher

63
Q

adrenaline effect

A

combines both action od noradrenaline and isoprenaline

activate all receptors – balance

64
Q

what is anaphylactic shock

A

severem life threatening allergic reaction, can occure within seconds of exposure to the allergen ,, bc immune system will release floods fo checmincal that make the person going into a shock , blood pressure plummet airway narros, breathing becoming difficult

65
Q

adrenaline mechanism of action during anaphylaxis

A

decreae the release of medators from mast cell, alleviate obstruction to airflow in the respirator tracts and improves cardiovascular response

  • a1 adrenegic agonist effect : increased vasoconstriction, increased peripheral vascular resistance and decreased mucosal edema
  • b1 adrenergic agonist effect : increased rate and force of contraction
    -b2 adrenergic agonist effect: increased bronchodilator and decreased release of mediatiors of inflammation from mast cell and basophils
66
Q

machanism of a1 receptor

A

plc activated, increased ip3, and dag, increased intracellular ca2+

67
Q

mechanism of a2

A

ac inhibited, decreased cAMP

68
Q

mechanism of b1

A

ac activated - increased camp

69
Q

mechanism of b2

A

ac activated - increased camp

70
Q
A

LSM3211 (14 decks)

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