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Pharmacology > 2nd lecture - sympathomimetics > Flashcards

2nd lecture - sympathomimetics Flashcards

1
Q

thoracolumbar outflow also known as

A

Sypathetic nervous system

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2
Q

Sympathetic preganglionic fibers originate from

A

cell bodies localized within the intermediolateral columns of the thoracic and lumbar regions of the spinal cord.

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3
Q

The adrenal medulla is an extremely important component of the

A

sympathetic nervous system.

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4
Q

norepinephrine and epinephrine difference

A

norepinephrine is typically referred to as a mediator and epinephrine, a hormone.

norepi is always vasoconstrictive; epi can be constrictor, dilator, OR pure inotrope depending on dose and location.

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5
Q

The adrenal medulla is embryologically and functionally homologous to a sympathetic ganglion but does not contain postsynaptic neuronal cells. Instead It contains

A

chromaffin cells that release epinephrine and norepinephrine (mediators!) from the adrenal gland.

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6
Q

name 3 mediators of the sympathetic nervous system

A

noradrenaline
adrenaline
dopamine

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7
Q

chemical nature of noradrenaline

A

catecholamine

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8
Q

noradrenaline is broken down by what enzymes? (2)

A

the enzymes MAO (monoamine oxidase) and
COMT (catechol O-methyl transferase)

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9
Q

nature of Adrenaline (epinephrine) and source

A

catecholamine, hormone secreted by the medulla of the adrenal glands

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10
Q

broad categorization for adrenergic receptors

A

otherwise known as adreno-receptors, alfa and beta

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11
Q

alfa receptor subgroups

A

alfa1 and alfa 2

(Subtypes: α1A; α1B; α1D,
α2A; α2B; α2C)

The pharmacological action of different subtypes is in most cases similar.

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12
Q

where are alfa1 receptors (2)

A

postsynapse,
most of all in the arteries

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13
Q

where are alfa2 receptors (3)

A

presynapse,
regulates the release of mediator,
located on smooth muscle cells

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14
Q

where are beta1 receptors (2)

A

postsynapse,
primarily in the heart

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15
Q

where are beta2 receptors (2)

A

postsynapse,
primarily in the bronchi

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16
Q

describe beta3 receptors

A

β3 are found in fat cells

(also other locations, but function needs more investigations)

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17
Q

describe dopamine receptors

A

D1 & D2 receptors can be found

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18
Q

where are beta1 receptors found percentagewise?

A

postsynapse

70-80% in the heart, 20-30% in the lungs

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19
Q

where are beta2 receptors found percentagewise?

A

70-80% in the lungs, 20-30% in the heart

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20
Q

When released in the organism, noradrenaline mainly affects what receptors?

A

beta1 mainly

but when NA is administered IV, its mainly an alfa-mimetic!

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21
Q

When released in the organism, adrenaline mainly affects what receptors?

A

mostly beta 2, also beta1

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22
Q

beta1 stimulation causes?

A

Increase in the heart beat and heart contractility, lipolysis

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23
Q

beta2 stimulation causes?

A

Decrease in the tone of bronchial muscle, thus causes bronchodilation

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24
Q

general beta-mimetic affects (4)

A

Glycogenolysis
Dilation of the blood vessels in the skeletal muscle

Decrease in gastrointestinal motility
Relaxation of the uterine smooth muscle

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25
Q

cardiac beta 1 activation results in (3)

A

Positive inotropic effect
Positive chronotropic effect
Positive dromotropic effect

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26
Q

define Positive inotropic effect

A

increased cardiac contractility

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27
Q

define Positive chronotropic effect

A

increased heart rate

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28
Q

define Positive dromotropic effect

A

accelerated conduction of the cardiac impulse

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29
Q

Pulmonary beta2-mimetic effects (2)

A

relaxation of bronchiolar smooth muscle,
bronchodilation

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30
Q

vascular smooth muscle beta2-mimetic effects (2)

A

mediate vasodilation,
reduce vascular resistance.

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31
Q

General alfa1-mimetic effects (4)

A

vasoconstriction -> blood pressure increase
mydriasis (dilation)
decrease in GI motility
uterine myometrial contractions

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32
Q

alfa2 receptors are mainly found in (3)

A

presynaptic nerve terminals but are not restricted anatomically to neuronal elements.

found in vascular tissue too – in extrasynaptic regions of vascular smooth muscle cells, also in endothelial cells.

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33
Q

Classification of adrenomimetics (3)

A

1) Direct-acting; act directly with regard to receptors.

2) Indirect-acting; increase the amount of noradrenaline in synapse either by encouraging its release or by inhibiting the deactivation.

3) Mixed action (ie. ephedrine); mechnism uses direct and indirect simultaneously

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34
Q

Ephedrine is

A

a central nervous system stimulant that is often used to prevent low blood pressure during anesthesia.

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35
Q

Direct-acting adrenomimetics act how?

A

bind directly with receptors to enhance effects

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36
Q

Indirect-acting adrenomimetics act how?

A

act by increasing the amounts of noradrenaline in the synapse either by encouraging its extra release or by inhibiting its deactivation

37
Q

Mixed action adrenomimetics act how?

A

act both directly on receptors and in-directly enhancing effects of stimulation

38
Q

give an example of a group of Direct acting sympathomimetics

A

Catecholamines

39
Q

what is isoproterenol

A

(also known as isoprenaline) as synthetic direct acting sympathomimetic catecholamine

an analogue of epinephrine that acts exclusively on beta adrenergic receptors

thus is a selective beta agonist

40
Q

name the main catecholamine

A

noradrenaline/norepinephrine

41
Q

what effects does noradrenline have first and foremost? (3)

A

Constricts arteries, veins, arterioles, capillaries (alfa1-agonist properties).

Increases both the arterial and venous blood pressure.

The blood flow is increased to the heart, which causes reflectory decrease of the heart rate (bradycardia).

42
Q

Catecholamine effect of the heart (2)

A

increase the strength of myocardial contractile force and accelerate heart rate.

inotopic and chronotropic

43
Q

what often occurs during the peak pressor response seen after administration of epinephrine and norepinephrine?

A

Catecholamines increase the strentgh of myocardial contractile force and accelerate heart rate.

Despite that, bradycardia often occurs during the peak pressor response. This is dependent upon the hypertensive response causing an increase in vagal discharge via the baroreceptor reflex mechanisms.

It is more pronounced with norepinephrine.

44
Q

Why is noradrenaline harmful if administered non-iv?

A

causes Extremely strong spasm of the blood vessels if it gets under the skin and thus can lead to tissue necrosis.

45
Q

Any kind of mechanical function of the smooth muscle cells of blood vessels depends on the existence of

A

the intracellular calcium ion, Ca2+

The basis for the effect of contracting blood vessels of noradrenaline and adrenaline is the increase in the quantity of intracellular calcium.

46
Q

noradrenaline effect on the eyes

A

contraction of the radial muscle of the iris, dilation of the pupil (mydriasis), contractions of the third eyelid.

47
Q

noradrenaline effect on the GI tract

A

decrease in tone

48
Q

noradrenaline effect on glands?

A

decrease in secretion.

49
Q

noradrenaline pilomotor effect?

A

Both NA and A cause contraction of pilomotor muscle, causing involuntary erection of hairs.

This effect is mediated by the alfa-receptors and can easily be observed in carnivorous animals.

50
Q

Adrenaline (epinephrine) Induces primarily which receptor effects?

A

beta1 and beta2 effects, but in greater concentrations A will also have alfa-receptor effects (different data!)

almost like “spill-over”

51
Q

Adrenaline (epinephrine) effect on metabolism?

A

Glycogenolysis, substantial increase in the level of blood sugar, free fatty acids, lactic acid.

52
Q

Adrenaline (epinephrine) effect on bronchi?

A

beta2-mimetic effect ensures a decrease in the tone of bronchial muscle and a decrease in the secretion of glands.

Relaxation of bronchial smooth muscle is particulary pronounced if the muscle is contracted by other mediators (acethylcoline, histamine) or by anaphylactic or asthmatic conditions.

53
Q

Adrenaline (epinephrine) effect on the GI tract?

A

decrease in tone,
decrease in the secretion of glands,
slow-down of peristalsis

54
Q

adrenaline affect on cardiovascular area?

A

substantial tachycardia (beta1),
increase in contractility and minute volume (there is a risk of heterotopic stimulus formation, extrasystoles),
the oxygen requirement of the heart increases.

55
Q

adrenaline’s effect on the blood vessels depends on

A

the ratio of alfa and beta receptors.

56
Q

how does adrenaline effect alfa 1 receptors?

A

in blood vessels contraction occurs

57
Q

how does adrenaline effect beta 1 & 2 receptors?

A

Beta-1-adrenergic receptors regulate heart rate and myocardial contractility, but in situations of stress with the provocation of epinephrine release stimulation of cardiac beta-2 receptors contribute to additional increases in heart rate and contractility.

58
Q

what does isoproterenol cause

A

Isoproterenol is a beta-1 and beta-2 adrenergic receptor agonist resulting in the following: Increased heart rate. Increased heart contractility. vasodilation, Relaxation of bronchial, gastrointestinal, and uterine smooth muscle.

59
Q

name 2 catecholamines that the GI tract cannot absorb, and 1 that it can

A

Epinephrine and norepinephrine are not absorbed to any appreciable extent following oral administration because of destruction within the GI tract.

Isoproterenol is absorbed following oral or sublingual administration, but in an erratic manner – therapeutically nonuseful.

59
Q

Clinical use of catecholamines broadly (4)

A

cardiac pathologies (arrest, partial and full AV block)

anaphylactic and allergic reactions (restores pressue and relaxes bronchial muscle)

bronchial asthma (muscles relax but bronchial vessels dilate)

hypotension

60
Q

an overdose of NA or A can cause

A

a dangerous increase in the arterial pressure and disturbance of cardiac rythm even ventricular fibrillation.

61
Q

catecholamine effects associated with thyroid conditions?

A

Hyperthyroid conditions, thyroid therapy, digitalis therapy, halogenated hydrocarbon anesthetics and thiobarbiturates predispose a patient to the myocardial toxicity of catecholamines.

62
Q

Dopamine is an Immediate biochemical precursor to

A

norepinephrine

63
Q

Dopamine infusions will increase both

A

blood pressure and cardiac output.

These effects are caused by stimulating cardiac contractility and heart rate via the action on α1 receptors.

64
Q

Dopamine increases the release of norepinephrine from nerve terminals because

A

it is a precursor for norepinephrine.

65
Q

what receptors does dopamine mainly act via

A

D1 & D2 receptors

66
Q

Dopamine’s primary metabolic pathway?

A

L-Phenylalanine →
L-Tyrosine →
L-DOPA (precursor = levodopa) →
Dopamine

67
Q

clinical uses for dopamine (2)

A

Acute management of heart failure, cardiogenic shock.

Acute renal failure (increases renal blood flow, glomerural infiltration rate). (note: Some investigations do not confirm that effect)

68
Q

Dopamine, adverse effects (3)

A

Excessive doses can cause tachycardia and vasoconstriction.

Outside the vein can cause tissue necrosis.

69
Q

dobutamine is

A

a Synthetic catecholamine

mainly used in dogs

70
Q

what type of effect does dobutamine have on the heart?

A

Positive inotropic effect in the heart.

Dose-related increase in myocardial contractility, without changes in ventricular preload or heart rate.

71
Q

what veterinary species is dobutamine usually used in?

A

dogs

72
Q

example of a Non-catecholamine adrenomimetic

A

ephedrine, a CNS stimulant

ephedrine is naturalyl found in a plant but can also be syntehsized

rarely used in vet med

73
Q

Ephedrine exerts its sympathomimetic effects by

A

direct action of adrenergic receptors and release of endogenous norepinephrine. (mixed-acting)

includes mydriasis and relaxtion of bronchial smooth muscle

74
Q

effects of ephedrine on the cardiovascular area

A

the effect is similar to that of adrenaline:
an increase in systolic and diastolic blood pressure,
increase in myocardial contractility,
spasm of the blood vessels of the skin and kidneys.

75
Q

ephedrine vasopressor effect is many times weaker than that of

A

adrenaline but the duration of action is 7-10 times longer.

76
Q

Ephedrine acts how on what receptors

A

Direct-acting symopathomimetic, α1 receptors.
Very little effect on ß receptors?

“Ephedrine is a direct and indirect sympathomimetic amine. As a direct effect, ephedrine activates alpha-adrenergic and beta-adrenergic receptors. As an indirect effect, it inhibits norepinephrine reuptake and increases the release of norepinephrine from vesicles in nerve cells.”

77
Q

main effects of ephedrine?

A

Increases systolic and diastolic blood pressure, reflex bradycardia usually occurs.

78
Q

Phenylpropanolamine is used for

A

Its a Non-catecholamine adrenomimetic (propalin) used for treatment of urinary incontinence in dogs – increases the tone of the urinary sphincter (α1), relaxes the detrussor muscle of the bladder wall and allows for more urinary filling.

79
Q

Selective beta2-mimetics prevent the cardiostimulatory effects resulting from

A

the dilatation of the bronchi upon the use of mixed-type substances (for instance in the case of adrenaline).

80
Q

Most Selective beta2-mimetics are absorbed after oral administration and have prolonged duration of

A

bronchodilator action.

81
Q

name 3 beta2-mimetics

A

Terbutaline,
salbutamol,
albuterol

82
Q

what is Clenbuterol

A

a beta-2 mimetic

83
Q

what is Clenbuterol used for commonly

A

For treatment of recurrent airway obstructions in horses. It improves airway conductance.

Brief tachycardia may occur reflexly due to transient beta2 vasodilation and hypotension.

84
Q

Indirect-acting adrenomimetics cause reaction through what mechanism

A

higher noradrenaline release from presynapse.

85
Q

mechanism of action of alfa2-adrenomimetics such as xylazine, medetomidine and others

A

NA release blockade: paralysis of NA depot mechanism occurs, NA is washed out, causes presynaptic NA accumulation.

86
Q

What is MAO?

A

the enzyme monoamine oxidase is an important enzyme that breaks down noradrenaline

87
Q

What is digitalis/ digitalis therapy?

A

is a cardiac glycoside

Digoxin, sold under the brand name Lanoxin among others, is a medication used to treat various heart conditions. Most frequently it is used for atrial fibrillation, atrial flutter, and heart failure. Digoxin is one of the oldest medications used in the field of cardiology.

It is used to improve the strength and efficiency of the heart, or to control the rate and rhythm of the heartbeat.

88
Q

how do alpha 2 mimetics cause sedation

A

The primary mechanism of action of alpha-2 agonists is stimulation of presynaptic alpha-2receptors in the central nervous system, activating inhibitory neurons which lead to a reduction in sympathetic output via a negative feedback mechanism.

Pharmacology (19 decks)

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