The Adrenergic System Flashcards

1
Q

neurotransmitters of the adrenergic system are

A

catecholamines -

adrenaline and noradrenaline.

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

catecholamines -
adrenaline and noradrenaline.
( physiology - mechanism )
+ look the steps from pic of atlas

A

1) - They are synthesized in the cytoplasm of cells adrenergic neurons from tyrosine which converts in dopa (by tyrosine hydroxilase ) , an amino acid which then transforms into dopamine. ( tyrosine -> DOPA -> DOPAMINE )
2) Dopamine -> NE (noradrenaline) which
is converted into -> epinephrine (adrenaline).
3) Catecholamines are released from the deposit granules by exocytosis.
4) From the synaptic cleft it diffuses and stimulate specific receptors - adrenergic receptors.
5) Termination of the effect of catecholamines is done by passive diffusion,
reuptake and metabolism by 2 enzymes - monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)

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

Sympathomimetics

A

Agents that activate adrenergic receptors

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

Sympatholytics

A

Agents that blocks the activation of adrenergic receptors

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

Adrenergic receptors

A

G protein coupled receptors and are of two

types - α and β.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

α-adrenergic receptors:

A
  • postsynaptic α1 receptors

- presynaptic, postsynaptic and extrasinaptic α2 receptors.

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

adrenergic receptors G coupled + production of 2nd messenger

A

α1 receptors are coupled with Gq proteins. -> ACTIVATES : phospholipase C , producing IP3 & DAG
α2 receptors are coupled with Gi proteins -> INHIBIT : adenyl cyclase , decreasing cAMP formation
β-adrenergic receptors are coupled with Gs proteins -> STIMULATE : Adenyl cyclase with an increase in intracellular cAMP

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

β-adrenergic receptors -

A

β1, β2, β3

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

Effects of adrenergic receptor stimulation

α1 receptors: (6)

A
VASCULAR LEVEL : 
o vasoconstriction, (thus ↑BP);
o decreased bronchial secretion , 
o mydriasis,
GI LEVEL : 
o spleen capsule contraction,
o piloerection,
o decreased insulin secretion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

presynaptic α2 receptors:

A

decreases the release of norepinephrine into the synaptic cleft -
feedback mechanism. ( negative feedback)
- inhibition of neurotransmitter release ( noradrenaline + acetylcholine )

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

α2 postsynaptic receptors:

A

Vasoconstriction

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

extrasynaptic α2 receptors:

A

o stimulates platelet aggregation
+ contraction of vascular smooth muscles
+ inhibition of insulin release

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

β1 receptors:

A

increases the activity of the heart (increases contractility, A-V conduction, excitability)
o stimulates renin secretion
- CNS = anxiety

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

β2 receptors:

A
o vasodilation, ( in skeletal muscle ) 
o bronchodilation,
o relaxes uterine muscles,
o tremor,
o agitation,
o nervousness,
o increases gluconeogenesis and glycogenolysis,
o increases insulin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

β3 receptors:

A

o lipolysis and glycogenolysis.

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

Direct sympathomimetics

A

are substances that have affinity for

adrenergic receptors and intrinsic activity

17
Q

Adrenaline

A
  • stimulates all adrenergic receptors.
    Effects:
  • anxiety, insomnia, nervosity, vasoconstriction in the
    subcutaneous, splanchnic and renal territories and
  • vasodilation in the muscular,
    cardiac and cerebral territories, stimulation of the heart. - Systolic blood pressure
    rises,
  • diastolic blood pressure does not change. - Bronchodilation.

Indications.

  • anaphylactic shock. - type I hypersensitivity reactions
  • acute asthma attack.
  • cardiac arrest
  • antihemorrhagic in association with local anesthetics.

Side effects: increased blood pressure with strokes, severe heart arrhythmias, ventricular fibrillation, worsening of ischemic heart disease,
myocardial infarction, tremor of the extremities, anxiety, psychomotor agitation

18
Q

Noradrenaline ( Norepeinephrine )

A
  • stimulates α adrenergic receptors;
  • no β adrenergic effects.
  • Effects:

1) vasoconstriction in all territories,
2) contraction of the spleen capsule.
3) Increases blood pressure, both systolic and diastolic.

Indications :
hypovolemic shock with collapse
- administration by intravenous infusion

19
Q

Dopamine

A
  • stimulates adrenergic and dopaminergic receptors
  • Effects:
    1) vasodilation in the splanchnic and renal territory.
    2) In high doses the drug can stimulate :
  • β1 adrenergic receptors by increasing heart activity
  • α adrenergic receptors by increasing blood pressure.
    Indications: selected cases of shock in intravenous infusion.
20
Q

Isoprenaline

Dilation

A
  • selective β1 and β2 receptors agonist.
  • Effects:
    o bronchodilation,
    o heart stimulation,
    o vasodilation,
    o decreases diastolic blood pressure and increases systolic blood pressure.

Side effects

  • worsening of ischemic heart disease,
  • acute myocardial infarction,
  • ventricular fibrillation, tachycardia, palpitations,
  • extremity tremor,
  • psychomotor agitation, anxiety
21
Q

Selective α1 sympathomimetics

A

phenylephrine, ethylephrine -
produce vasoconstriction; used in the treatment of particular types of shock or
as a decongestant of the nasal or conjunctival mucosa (local applications)

22
Q

Selective α2 sympathomimetics

A

clonidine - lowers blood pressure -

is used to treat high blood pressure.

23
Q

Selective β1 sympathomimetics

A

dobutamine - increases the

contraction force of the myocardium, increases the cardiac output; used in cardiogenic shock

24
Q

Selective β2 sympathomimetics

A

1) salbutamol,
2) phenoterol,
3) orciprenaline,
4) terbutaline,
5) salmeterol
produce bronchodilation, vasodilation
and relaxation of the uterine smooth muscles. Indications: treatment of asthma,
treatment of painful uterine contractions in pregnant women.
* Inhalatory , oral , injectable ( terbutaline )

EFFECTS :

  • Low-intensity cardiac side effects, * ( angina , tachycardia ,arrythmia - β1 rec activation )
  • tremor of the extremities,
  • increased excitability of the central nervous system,
  • anxiety.
25
Q

Indirect sympathomimetics

  1. amphetamine
  2. Ephedrine
  3. Cocaine
  4. Nafazolin
  5. Tricyclic antidepressants
  6. IMAO antidepressants
A

1) increase the availability of catecholamines
in the synaptic cleft, by increasing the release (ephedrine, amphetamine),
2) preventing the reuptake of catecholamines from the synaptic cleft (cocaine, tricyclic antidepressants) or
3 ) inhibiting their metabolism (antidepressants
IMAO)

26
Q

Ephedrine

A
  • indirect sympathomimetic
  • increases the release of catecholamines into the synaptic cleft.
  • It is effective in oral administration and crosses the blood-brain barrier.
27
Q

Nafazolin

A

mechanism of action identical to that of ephedrine, used as a decongestant of the nasal mucosa.

28
Q

Amphetamine

A

is another indirect sympathomimetic that has

virtually all the effects of ephedrine but the effects on the central nervous system are much more intense

29
Q

Cocaine

A
  • indirect sympathomimetic
  • is a local anesthetic that prevents the reuptake of
    catecholamines from the synaptic cleft.
  • It produces adrenergic side effects, and
    on the central nervous system it produces phenomena similar to those produced by amphetamine.
30
Q

Tricyclic antidepressants

A
  • indirect sympathomimetics
  • increase the availability of catecholamines
    in the synaptic cleft by preventing their reuptake from the synaptic cleft
31
Q

IMAO antidepressants

A

block catecholamine metabolization by blocking MAO enzymes.

32
Q

Sympatholytics

A

are substances that prevent the effects of sympathoadrenergic stimulation

33
Q

Direct sympatholytics

A

have affinity for adrenergic receptors without

intrinsic activity.

34
Q

Tolazoline, phentolamine

A

1 ) non-selectively block both α1 and α2 receptors,
2) producing vasodilation with decreased blood pressure and
3 ) reflex tachycardia.
4 ) Are used in the diagnosis and treatment of pheochromocytoma

35
Q

Selective blockers of α1 adrenergic receptors

A
  • prazosin,
  • doxazosin,
  • tamsulosin
    1) produce vasodilation without reflex tachycardia. Are used in the treatment of hypertension and benign prostatic hypertrophy
36
Q

β Adrenergic receptor blockers

A

1) Decrease the heart activity by :
- blocking the β1 adrenergic receptors and
- aggravate asthma by blocking the β2 adrenergic receptors.

Indications:
1 ) treatment of hypertension,
2) angina pectoris and
3) cardiac arrhythmias,
4) prevention of migraine attacks (propranolol),
5) tremor of the extremities in conditions of anxiety
( propranolol), treatment of glaucoma (timolol) in local administration.

Side effects:

  • excessive hypotension,
  • bradycardia ,
  • atrioventricular block,
  • worsening of asthma or peripheral vascular-spastic diseases.
37
Q

β non-selective blockers

A

propranolol

* ( + Alprenolol + Oxprenolol )

38
Q

β1 selective blockers

A
  • atenolol, metoprolol, acebutolol.
    ( Nevibolol , cervedilol )
  • They have the same indications and the same efficacy as non-selective blockers but can also
    be used in patients with asthma or peripheral ischemia syndromes.
  • they are antiarrythmic , anti- aginal + anti- hypertensive drugs
  • side effects : bronchoconstriction , bradycardia , cardiac failure , cold extremities , insomnia , depression
39
Q

Indirect sympatholytics

A
  • neurosympatholytics, or blockers of sympathetic endings, prevent the accumulation of catecholamines in the synaptic cleft.
  • It works by decreasing the release of the neurotransmitter in the synaptic cleft
  • guanethidine or by depleting catecholamine deposits
  • reserpine