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LSM3211 > Autonomic Nervous System(adrenergic) > Flashcards

Autonomic Nervous System(adrenergic) Flashcards

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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
b2 receptor
relax smooth muscles - vasodilation -bronchodilation -relax uterine muscles relax gastrointestinal tract promotes relaxation increase heart rate and heart contraction @ liver, gylcogenolysis
26
agonist for which receptor causes bronchoconstriction
M3
27
asthma drug
Adregenic B2 agonist
28
seconadry messengers and effectors(a1)
increase inositol triphosphate inscrease DAG increase CA2+
29
seconadry messengers and effectors(a2)
decrease CAMP
30
seconadry messengers and effectors(b1)
increase CAMP
31
seconadry messengers and effectors(b2)
increase CAMP
32
norepinrpherine drug
a/b agonist not clinically used trasnmitter at postganglionic sympathetic neurons
33
epinephrine
a/b agonist asthma and anaphylactic shock, cardiac attack
34
salbutamol
B2 agonist asthma premature labor
35
phenylphrine
a1 agnoist nasal decongestion thr vaso constriction; reduce amt of fluid
36
clonidine
a2 partial agonist hypertension migraine derease amt of sympathetic activity
37
propranolol
b antagnoist (non selctive) angina hypertenison cardia dysrthmias anxiety tremor
38
A methyl-p-tyrosine
drug that affect NA biosynthesis tyrosine hyroxylase inhibitor reduce amt of noradrenaline and adrenaline
39
clinical use of A methyl-p- tyrosine
alternative treatmenr option phaenchromocytoma (NA/ADR secreting tumour of adrenal medulla) - high heart rate symptoms representative of over active adrenaline system
40
Reserpine
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
clinical use of resperpine
hypertension and mood disorders(schizophrenia) adverse effect; dizziness, droziness, irregular heart beat , depression
42
name the drugs that affect the relase and uptake of noradrenaline
Amphetamine cocaine clonidine yohimbine
43
drugs that are indirect sympathomimetics
Amphetamine that increases the relase of NA cocaine that inhibits the reuptake of NA
44
drusg that are A2 agonist for release and reuptake of noradreanlaine
a2 receptor agonist, clonidine that decreases NA release a2 antagonist yohimbine that increases NA release
45
how does amphetamine work on noradrenaline release
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
amphetamine effect on NA
promote release of NA without depolarising nerve membranes -- bc everything in the pre snymaptinc leaks out
47
cocaine effect on Noradrenaline
inhibit reuptake of Noradrenaline into presynaptic by inhbiting respective trasnporters --- thus build up of noradrenaline in synaptic cleft leading to increased sympathetic activity
48
effect of sympathimimimetics
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
dangers of tyramine
can be dangerous if given with MAo blocker, which is required for catabolsim of tyramine
50
clinical use of tyramine
NA release no clinica use but present in various foodi
51
clincial use of amphetamine
NA release, MAO inhibitor, NET inhibitor, CNS stimulant CNA stimuant in narcolepsy, also in hyperactive children, appetite suppressant , drug of abuse
52
clinical use of ephedrine
NA release, B agonist, weak CNA stimulant action nasal decongestion
53
a2 receptor agonist and antagonist regarding Noradrenaline
clonidine agonist yohimbine(antagonist)
54
effect of a2 receptor agonist at noradrenaline
clonidine inhibit NA release clinical use: antihypertension adverse effect : headache, dizziness, drowsiness, constipation, brandycardia
55
effect of "a" receptor antagonist regarding yohimbine
inhibit post snymaptinc a receptor as well, so no used clinically
56
indirect sympathomimetic drugs- MAO and COMT inhibitors
moclabemide, anti depresant
57
how does moclobemide work
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
what is the difference between the catecholamine and NA released from the sympathetic nerves
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
receptors that are linked to blood pressure
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
ISO
isoprenaline
61
noradrenaline effect
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
isoprenaline effect
potent b agnoist vaso constrictions peripeherial reisitance decrease blood pressure decrease also act on b1 receptor heaty rate become higher
63
adrenaline effect
combines both action od noradrenaline and isoprenaline activate all receptors -- balance
64
what is anaphylactic shock
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
adrenaline mechanism of action during anaphylaxis
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
machanism of a1 receptor
plc activated, increased ip3, and dag, increased intracellular ca2+
67
mechanism of a2
ac inhibited, decreased cAMP
68
mechanism of b1
ac activated - increased camp
69
mechanism of b2
ac activated - increased camp
70

LSM3211 (14 decks)

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