SYMPATHOMIMETIC AGENTS Flashcards

1
Q

Catecholamines any compound

- hydroxyl is on_____carbon positions.

A

any compound that has CATHECOL nucleus (benzene ring with 2 adjacent hydroxyl groups with and amine containing side chain; 3,4

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2
Q

Endogenous catecholamines, 3

A

Epinephrine, norepinephrine, dopamine,

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3
Q

Sympathomimetic drugs does what?

A

mimic action of the SNS via activation of sympathetic receptors

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4
Q

Pharmacologic effects of catecholamines.
SV, HR, Force of contraction via receptor ______

Patients are more vulnerable to develop?

A

Cardiac stimulation (B1 receptors of heart)

  • SV
  • cardiac arrhythmias
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5
Q

Pharmacologic effects of catecholamines.
SVR, BP via receptor ______ mediated vaso________ of blood vessels
Shunts blood to ________(_______non essential organs)
Vasodilation results from _______activation in certain blood vessels such as _____ ______

Lung effect( Brandi/constri)
Inc/dec pulmonary blood flow.
GI effect on : secretions and motility

A

Cardiac stimulation (B1 receptors of heart)
-all increase
-constriction ; to muscle (vasoconstrict)
Alpha 1; skeletal muscle blood vessels.

bronchodilation
Improve pulmonary blood flow
Decreases GI motility and secretions

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6
Q

SYMPATHOMIMETIC

A

Increase nutritional supply

Modulation of the secretion of insulin, renin and pituitary hormones.

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7
Q

The predominant effect seen by the SNS for the ENDOCRINE SYSTEM

A

INHIBITION of INSULIN

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8
Q

Alteration that occur in the ANS in case of injury?

Effect in the eye? Enhancement of ______

A

Fluid retention
renin secretion –> angiontensin II –> Aldosterone
Posterior pituitary hormone secretion (ADH)

MYDRIASIS : far vision

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9
Q

They can alter potassium through?

Remember sodium potassium pump has ____receptors.

A

Beta 2 agonism by plasma epinephrine (Exogenously administered drug) produces HYPOKALEMIA, because Na -K pump has beta 2 receptors, which shift potassium from outside to the inside of the cell (RBCS and muscle cells)

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10
Q

CNS stimulation of Sympathomimetics?

is EPINEPHRINE a powerful CNS stimulant ?

A

Lipophillic enough drugs can cross brain

No; because it is a polar molecule

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11
Q

Analgesia : sympathomimetic with analgesia

A

enhanced specially in the presence of OPIOIDS

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12
Q

Physiological Basis of Adrenergic Receptor Function:

An important factor in the response of any cell, organ tissue to sympathomimetic agents is the _______ _________

A

density and proportion of ALPHA and BETA Adrenergic in various tissues.

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13
Q

For example: Norepinephrine as a drug does not activate

A

B2 receptor.

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14
Q

_________ and _________ can activate beta 2 receptors and are potent ________since they have affinity for _____receptors

A

Isoproterenol and epinephrine ; and Beta2 receptor.; BRONCHODILATORS; B2

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15
Q

NE and EPINEPHRINE cause vasoconstriction of _________ where as ISOPROTERENOL _______ effect on blood vessel. why? ______lacks

A

cause vasoconstriction of these blood vessels, where as ISOPROTERENOL HAS little effect on blood vessels since its lack alpha agonism activity

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16
Q

Explain the reflex homeostatic adjustments

A

The reflex homeostatic adjustments

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17
Q

Phenylephrine can cause ________ (side effect or adverse effect) (1)

A

Reflex BRADYCARDIA

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18
Q

Norepineprhine can cause activation of ______ reflex and ______ ____ tone leading to a ______ in HR.

A

Baroreceptor reflex

and increase VAGAL tone decreasing HR>

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19
Q

The most effective agents for enhancement of analgesia is ________ and __________

A

amphetamine and amphetamine derivatives

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20
Q

All sympathomimetic amines are derived by

A

beta phenylethylamine–> Benzene ring & Ethylamine side chain.

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21
Q

Basic catecholamines structure:

A

are monoamine substances with the presence of hydroxyl groups (-OH) specifically on the 3 and 4 carbon positions on the benzene ring

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22
Q

All sympathomimetic amines are derived by

A

beta phenylethylamine–> Benzene ring & EthylAMINE side chain.

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23
Q

_____makes polar and not lipid soluble. Catecholamines Catecholamines have a brief duration of action and are ineffective when administered orally because they are ?
Which 2 enzymes: _______ & ________

A

Hydroxyl group; rapidly inactivated in the intestinal mucosa and in the liver via both MAO & COMT before reaching the systemic circulation.

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24
Q

Sympathomimetic agents can exert their mechanism of action and pharmacologic effects by either _________ OR __________

A

DIRECTLY binding to and activating alpha-adrenergic, beta-adrenergic, or dopaminergic receptors

INDIRECTLY releasing substances which will bind to alpha-adrenergic, beta-adrenergic, or dopaminergic
receptors which activates the receptors

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25
Q

Epinephrine – binds to α1,

α2, β1, β2 receptors

A

binds to α1, α2, β1, β2 receptors

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26
Q

NE – binds only to ________

A

α1, α2, β1

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27
Q

Isoproterenol – binds only to_______

A

β1 and β2 receptors

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28
Q

Phenylephrine binds

A

SELECTIVELY to only α1 receptors

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29
Q

Synthetic non-catecholamines Generally, do/ don’t have hydroxyl groups on benzene ring. They are metabolized primarily by _______. ________ is an exception

A

Don’t have 3- hydroxyl groups on benzene ring and

Phenylephrine is an exception

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30
Q

____ , ____ and _____ are able to penetrate BBB more readily and have more central nervous system activity? and considerable CNS activity, they are synthetic non catecholamines.

A

ephedrine, amphetamine, methamphetamine exhibit

considerable CNS activity

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31
Q

The potency or affinity of agents to the adrenergic _________between sympathomimetic agents ; depends on

A

varies; depends; on structure binding.

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32
Q

β1 Receptor: _______
β2 Receptor: ________
Alpha 1 receptor:

A

ISO>Epi>NE
ISO>Epi»»NE
Epi >NE»»»»>ISO

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33
Q

Epi slightly more potent at B1 recepotrs

A

yes

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34
Q

The concentration required to give NOREPINEPRHINE to activate alpha 2

A

Would kill a patient.

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35
Q

Isoproterenol

A

Non-selective beta agonist (beta 1 or 2)

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36
Q

Clinical uses of sympathomimetics

A

Shock, vasopressors, positive inotrope

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37
Q

Albuterol is a

A

Sympathomimetic.

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38
Q

Why is the Addition of EPINEPHRINE to local anesthetics? 2 reasons

A

decrease systemic absorption

increase the duration of action of local anesthetics

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39
Q

Caution when using pure α1 agents
The disadvantages of using sympathomimetics that lack significant β1 adrenergic effects to maintain systemic blood pressure include
As a result of this reflex activation, sympathetic tone is ________ and vagal tone is ________

Selective α1 agents produce so much _________that they trigger a r_____________ Since,

CO = HR x SV

A

intense vasoconstriction and associated blood pressure increases that evoke reflex-mediated bradycardia (via the carotid-aortic baroreceptor system), which leads to a decreases in cardiac output
decreased; increased

vasoconstriction
reflex bradycardia response.

decreasing HR will ultimately decrease your CO.

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40
Q

How to classify Sympathomimetic agents:

A

a)Sympathomimetic agents can be classified based on their chemical structure
b)Sympathomimetic agents can ALSO be classified based upon how they activate adrenergic receptors
c)

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41
Q

Endogenous catecholamines :

A

a) Dopamine
b) Norepinephrine
c) Epinephrine

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42
Q

Synthetic catecholamines:

A

a) Isoproterenol

b) Dobutamine

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43
Q

Synthetic non-catecholamines

A

Direct-acting : Phenylephrine
Indirect-acting: Amphetamines
Direct- and indirect-acting: Ephedrine

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44
Q

What are Direct-Acting Sympathomimetic Agents

Give examples
synthetic catecholamines : ____ and ________
What are the only 2 synthetic non-catecholamines that are direct acting ?

A

Agents that bind directly to one or more of the adrenergic receptors and activate the receptor

Natural catecholamines; 
Synthetic catecholamines (Dobutamine, Isoproterenol)

Synthetic non-catecholamines – only Phenylephrine and Methoxamine are the only synthetic non-catecholamines that are direct-acting

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45
Q

Their actions are independent of endogenous stores of NE –> DASA

A

Direct-Acting Sympathomimetic Agents (doesnt need endogenous NE)

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46
Q

**Denervation or depletion of neurotransmitters does not alter activity of these drugs (i.e.: heart transplant, training)

A

Direct-Acting Sympathomimetic Agents

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47
Q

Direct acting sympathomimetic agents Response may be potentiated (increased) by drugs such as_____,______,______more indirect release

A

Response may be potentiated (increased) by drugs such as cocaine, reserpine and guanethidine

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48
Q

Selective agents –

Non-selective agents

A

bind primarily to only 1 adrenergic receptor
binds to more than 1 adrenergic
receptor

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49
Q

Indirect-Acting Sympathomimetic Agents
“Releasing agents” are a type of indirect-acting agent
Most, not all, synthetic non-catecholamine agents are indirectacting agents i.e., __________

A

Agents that increase the release of endogenous NE to stimulate adrenergic receptors
} i.e., Amphetamines

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50
Q

Below lists the 3 mechanisms of how indirect-acting

sympathomimetic agents increase the release of endogenous NE:

A
  1. ***** By releasing or displacing NE from sympathetic nerve varicosities from the presynaptic nerve which increases NE concentrations in the synaptic cleft
  2. By blocking the re-uptake of NE back into sympathetic neurons (i.e.: Cocaine, TCA’s) which increases NE concentrations in the synaptic cleft
  3. By blocking the metabolizing enzymes MAO (called MAOInhibitors) or COMT (called COMT inhibitors)
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51
Q

Their actions are dependent on adequate neuronal stores of endogenous NE

A

Pharmacology of Indirect-Acting Sympathomimetics Agents (IASA)

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52
Q

Pharmacology of Indirect-Acting Sympathomimetics Responses are abolished by prior treatment with _________ __________

A

reserpine or guanethidine ;

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53
Q

Indirect-acting SYMPATHOMIMETICS are characterized mostly by ______ because ______

The actions of indirect-acting sympathomimetic amines are subject to ________ which means_________

A

alpha and beta 1 adrenergic agonists; NE has very little to no B2-adrenergic agonists activity.

Tachyphylaxis ; Repeated administration results in rapidly decreasing effects due to the depletion of neuronal stores of endogenous NE

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54
Q

Denervation (cases such as ________ ________) Clinical question: Would a indirect-acting sympathomimetic agent work in a heart transplant patient?

A

(i.e.: spinal cord injury, heart transplant)

Cant use in those situations because there is damage to nerve ending.

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55
Q

Mixed-Acting Sympathomimetic Agents are :

Denervation or depletion of neurotransmitter reduces or blunts the drug response of these agents

A

Agents that both indirectly release NE AND also directly bind to and activate adrenergic receptors

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56
Q

Examples of Mixed-Acting Sympathomimetic Agents

A

Ephedrine and Dopamine.

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57
Q

For Mixed-Acting Sympathomimetic Agents, drug response is

A

reduced or blunted by prior treatment with reserpine or guanethidine

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58
Q

What effects does Denervation or depletion of neurotransmitter have on Mixed-Acting Sympathomimetic Agents _______

A

reduces or blunts the drug response of these agents

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59
Q

Be careful ENDOGENOUS enzymes metabolizing

A

COMT and MAO enzymes

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60
Q

___________enzyme The circulating catecholamines are primarily metabolized by COMT

A

Catechol-O-methyltransferase (COMT) enzyme

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61
Q

____,____, _____, _____primarily metabolized by COMT (WHEN GIVEN AS A DRUG) –DINE

A

DINE: Epinephrine, norepinephrine, dobutamine and isoproterenol

62
Q

The lungs also act as a filter for central venous blood
_______of circulating NE is extracted during a single passage through the lungs
________of clinical doses of dopamine are cleared by the lungs after a single pass
________- is not broken down or extracted by lungs

A

~25%
~20%
Epinephrine

63
Q

Synthetic non-catecholamines that lack a 3-hydroxyl group are primarily metabolized by ______
These agents are not metabolized by COMT due to the _____________
Metabolism of these agents is ______ than catecholamines, thus these agents have ___________

A

MAO; loss of the hydroxyl group

slower; a longer duration of action

64
Q

Oral administration of catecholamines is NOT effective due to_____________

A

due to the presence of the 3- and 4-hydroxyl groups

65
Q

Catecholamines are ineffective when administered orally

Why?

A

because they are rapidly metabolized by MAO & COMT in the intestinal mucosa and liver before reaching the systemic circulation

66
Q

Mostly given IV but can also be given IM or SQ depending on the specific agent

A

Synthetic non-catecholamines.

67
Q

_______Is an endogenous catecholamine agent that is a potent activator of ____________

A

Epinephrine: both α- and β-adrenergic receptors (non-selective α- and β-adrenergic agent)

68
Q

Is a circulating hormone secreted by the adrenal medulla and constitutes ~80% of the catecholamine content of the adrenal medulla_________

A

Epinephrine

69
Q

________ the prototype drug among the sympathomimetics

A

Epinephrine

70
Q
EPINEPHRINE EFFECT on  myocardial contractility 
heart rate  Vascular smooth muscle
BRONCHIOLES
Sugar and glycogen
Glandular secretions.
A

Increase myocardial contractility (Positive Inotrope)
} Increase heart rate (Positive Chronotrope)
} Vasodilation and vasoconstriction of vascular smooth muscle
} Bronchodilation
} Glandular secretions
} Metabolic processes such as glycogenolysis & lipolysis

71
Q

Use in the treatment of severe asthma and bronchospasm

A

Epinephrine

72
Q

______(drug) Is poorly lipid soluble and does not readily penetrate the CNS which accounts for the lack of __________ ____

A

cerebral effects

73
Q

**The cardiovascular effects of epinephrine are from stimulation of both ___ ____ ____receptors

A

α- and β-adrenergic receptors

74
Q

**For Epinephrine, the higher you go on the dose, the more ______responses predominate and too high can cause _____________

A

***alpha ; severe metabolic acidosis

75
Q

Epinephrine high doses can cause
Which predominates in vascular bed?
And what happens to heart

A

Peripheral vasoconstriction leading to necrosis.

Alpha 1

76
Q

Effects of epinephrine on vascular smooth muscle are

A

DOSE - DEPENDENT

77
Q

Associated with vascular smooth muscle are a large number of ________ relative to ______receptors. However, epinephrine has a ______ affinity for the β2 receptor relative to the _________

A

α1 receptors; β2 receptors.; higher ; α1 receptor.

78
Q

Epi favors _____ as opposed to _____

A

beta 2; alpha 1

79
Q

Epinephrine favors _____ as opposed to _____

A

beta 2; alpha 1

80
Q

Therefore, the effect of epinephrine on

vascular smooth muscle is dependent on 3 things_______ _______ and ____

A

relative affinity for

α1 and β2 receptors AND epinephrine’s concentration.

81
Q

Low dose of epinephrine

A

0.01-0.3 mcg/kg/min

82
Q

At low doses of epinephrine

A
  • selective stimulate beta 2 (smooth muscle relaxation) and decrease in peripheral resistance.
  • the non-selective beta-adrenergic effects predominate with little alpha-adrenergic effects
83
Q

β2 receptor stimulation in vascular smooth muscle (peripheral vasculature) results in __________, predominately in skeletal muscle, which will decrease diastolic blood pressure (caution in
patient with _____

A

vasodilation; diastolic; aortic stenosis)

84
Q

B2 the net effect is typically ______________CO with a ________ in SVR and possibly a ________ in blood pressure. Pulse pressure is _______and MAP is not __________

A

increased cardiac output ; decrease; decrease; increased ; generally elevated

85
Q

Intermediate Dose of epi
Some effects: more pronounced _____ which continues to HR, contractility and SBP
Net effect–> _____in pulse pressure and increase in __BP are greater than increase in ___BP. and MAP ___

A

0.03 - 0.13 mcg/kg/min;
Beta 1 effect; increase HR , contractility and SBP
Increase; SBP, DBP; increases.

86
Q

Epinephrine: High doses: stimulation of ____ _____ ______ still occurs but _______ stimulation effects predominate on most vascular beds, including ____ ______ and _____ vasculature.

A

Stimulation of α1 & β1 & β2 receptors still occurs but α1
stimulation effects predominate on most vascular beds, including cutaneous, splanchnic and renal vasculature.

87
Q

____________ ___________are more common at high

doses which limits the usefulness of high dose epinephrine

A

Supraventricular tachyarrhythmia’s

88
Q

Epinephrine increases heart rate by ___________________which also increases the risk of cardiac dysrhythmias

A

accelerating the rate of spontaneous phase 4 depolarization of nodal tissue,

89
Q

Halothane anesthesia increases _______ ____________by

A

cardiac toxicity with epinephrine by sensitizing the myocardium to the action of epinephrine

90
Q

Epinephrine _________ (inc/dec) conduction velocity and _________(inc/dec) the refractory period in the AV node, bundle of His, Purkinje fibers and ventricular muscles

A

conduction velocity and decreases the refractory period in the AV node, bundle of His, Purkinje fibersn and ventricular muscles

91
Q

For epinephrine

CO, HR, Myocardial contractility and venous return

A

Increased cardiac output reflects epinephrine-induced

increases in HR, myocardial contractility and venous return

92
Q

a) Activation of the β2 receptor by epinephrine would produce _________ while activation of the α1 receptor would result in __________. Stimulation of α2 receptors on vascular smooth muscle also leads to __________
b) Remember, the magnitude of effect is dependent on the _____________ ______

A

a)vasodilation ; vasoconstriction; vasoconstriction

degree of receptor occupancy.

93
Q

Epinephrine does what to the RAAS?

A

Activates the RAAS SYSTEM to raise BP

94
Q

Supratherapeutic doses of epinephrine may lead to heart
failure, myocardial ischemia/infarction, pulmonary edema,
arrhythmias, profound hypertension which may cause
cerebrovascular hemorrhage, metabolic acidosis or kidney failure

A
heart failure
myocardial ischemia/infarction
pulmonary edema,
arrhythmias
profound hypertension which may cause
cerebrovascular hemorrhage
metabolic acidosis or kidney failure
95
Q

Supra-therapeutic doses of epinephrine may lead to :

A
heart failure
myocardial ischemia/infarction
pulmonary edema,
arrhythmias
profound hypertension which may cause cerebrovascular hemorrhage
metabolic acidosis or kidney failure
96
Q

Pancreas has both

A

alpha 2 and Beta 2

97
Q

Insulin secretion is inhibited by________ activation and is enhanced by activation of _______
} Stimulation of β2 & β3 receptors by epinephrine increases
} Liver glycogenolysis/gluconeogenesis (β2)
} Adipose tissue lipolysis (β2 & β3)

A

α2 receptor ; β2 receptors;

98
Q

The predominant effect seen with epinephrine is _________

A

inhibition of insulin secretion

99
Q

Glucagon secretion is enhanced through action on ____receptors of the ______________________

A

beta receptors of the alpha cells of pancreatic islets

100
Q

Stimulation of β2 & β3 receptors by epinephrine increases _______ _________and _________

A

Liver glycogenolysis/gluconeogenesis (β2)

Adipose tissue lipolysis (β2 & β3)

101
Q

*****Norepinephrine does not

A

AGONIZE BETA 2 RECEPTORS

102
Q

Infusions of epinephrine usually increase plasma

concentrations of

A

Glucose (hyperglycemia)
Lactate levels
Free fatty acids
Cholesterol, phospholipids, and low density lipoproteins

103
Q

_________ and ________are minimal with systemic
administration of epinephrine but occur after intradermal
injection

A

Sweating and pilomotor activity

104
Q

Activation of α1 and β2 receptors in the eye

_________(α1) does what to the radial muscles ? therefore _____Pupil.

A

Mydriasis (α1)

contracts the radial muscles of the iris, dilating the pupil

105
Q

SNS regulates the ___________

A

filling phase

106
Q

Epinephrine inhibits uterine tone and contraction during
pregnancy and at parturition via ____________receptors
(meaning causes relaxation) and________________ __________via activation of _______receptors.

A

activation of β2 ; contraction of

pregnant uterus via activation of α1 receptors

107
Q

Use with caution during labor and delivery. Although epinephrine improves maternal hypotension associated with anaphylaxis, it may result in ________,_______,________

A

uterine vasoconstriction, decreased uterine blood flow, and fetal anoxia

108
Q

Blood coagulation is accelerated by epinephrine, presumably by ________________ and _______

A

Increasing factor V activity and inducing platelet aggregation

109
Q

Epinephrine EXTRAVASATION Can cause ________ and _______

A

ischemic tissue necrosis and sloughing of

surrounding tissue

110
Q

***Treatment of EPINEPHRINE

Mix with and inject how ?

A

(Regitine®) Phentolamine mesylate 5-10 mg diluted to local tissue area
Mix 5-10 mg with 10 mL of NS and inject small amount
subcutaneously into the extravasated area

111
Q

****Which class is PHENTOLAMINE?

A

Phentolamine is a competitive, non-selective α1 and α2 antagonist

112
Q

Insulin secretion is both Inhibited by _____ and enhanced by ______

A

alpha 2; beta 2

113
Q

Sympathomimetic effect on nutritional supply

A

Free fatty acids from adipose tissue

Increase rate of metabolic and muscle GLYCOGENOLYsis

114
Q

Pharmacology effect on stress hormone levels

A

INCREASE

115
Q

The receptors in bronchial smooth muscle are largely of the _______ subtype.

A

β2 subtype.

116
Q

Phenylephrine has______ direct effects on the heart since it is a selective for ____ receptors and lacks ____ _agonism activity

A

minimal ; α1 ; Beta 1 agonism activity

117
Q

The ultimate response of a target organ to _________ agents is dictated not only by the _____ effects of the agents by also by the _________ ______adjustments of the organisms that occurs from the effects of the agents

A

sympathomimetic; direct; reflex homeostatic.

118
Q

Sympathomimetic will increase SBP This stimulation elicits compensatory reflexes that are are mediated by the _____ -_____ ________ . As a result, _______ tone is diminished, and _____tone is enhanced. each of these responses leads to a ______ of the heart rate

A

carotid-aortic baroreceptor ; sympathetic tone ; vagal tone; slowing.

119
Q

What happens when a drug lower mean SBP by activating beta ___ receptors? common on vagal tone and sympathetic tone.

A

2; the baroreceptor reflex work to restore blood pressure by REDUCING Vagal tone (parasympathetic) outflow from the CNS to the heart and INCREASING sympathetic tone outflow to the heart and blood vessels.

120
Q

Alpha, beta and dopaminergic receptors are all

A

G protein coupled receptors

121
Q

Adrenergic receptors can be found in

A

both the CNS and PNS

122
Q

What is the characteristics of SYNTHETIC NON-CATECHOLAMINES? Provide the exception

A

Don’t have HYDROXYL GROUP on BENZENE RING 3-OH and 4-OH groups; Phenylepinephrine

123
Q

CNS stimulation is prominent with which kind of agents and why?

A

synthetic NON-CATECHOLAMINES because they don’t have hydroxyl group with makes them able to penetrate BBB more readily

124
Q

What are some of the SYNTHETIC NON-CATECHOLAMINES that can exhibit CONSIDERABLE CNS ACTIVITY ?

A

Methamphetamine
Ephedrine
Amphetamine

125
Q

The absence of polar hydroxyl groups in synthetic non-catecholamines results in

A

LOSS of direct SYMPATHOMIMETIC activity.

126
Q

Clinical use of Sympathomimetics –>

A

a) Addition to local anesthetics to decrease systemic absorption and increase the duration of action of local anesthetics
b) Management of life-threatening allergic reactions, including anaphylaxis
c) Vasopressors to increase systemic blood pressure after sympathetic blockade produced by regional anesthesia.
d )Vasopressors to maintain systemic blood pressure during the time needed to eliminate excess inhaled anesthetics or to restore intravascular fluid volume .

127
Q

Selective α1 agents produce so much vasoconstriction that they trigger a ____ ______response.
Since, CO = _______ decreasing HR will ultimately _______ CO

A

reflex bradycardia

HR x SV; decrease your CO

128
Q

Which is more potent ? Catecholamines or SYNTHETIC CATECHOLAMINES?

A

Catecholamines.

129
Q

________Breaks down catecholamines in food _________

A

MAO; Tyramine

130
Q

The presence of methyl group on the alpha carbon , as with ______ and ______ slows the metabolism by _______ and further increases theses duration of action.

A

EPHEDRINE
AMPHETAMINE
MAO

131
Q

Metabolic of non-synthetic catecholamines is ______ than catecholamines.

A

slower

132
Q

Ephedrine is not ______or _____By _____(organs)

A

Broken down, extracted

133
Q

Certain Medications can cause transmitter depletion

A

Methyldope
Reserpine
Guanethidine

134
Q

How does Reserpine work

A

Inhibits transport of Monoamine into synaptic storage vesicles ultimately leaks to DEPLETION of Catecholamines from nerve endings. in CNS

135
Q

Guanethidine

A

systemic BP response to indirect age is decreased when given in conjunction with these depleting agents

136
Q

RESPONSE OF INDIRECT ACTING SYMPATHOMIMETIC (IASA) AGENTS MAY BE ACCENTUATED BY

A

MAO Inhibitors.

137
Q

The mechanism of the rise in blood pressure, mainly ______due to epinephrine is due to

A
  • direct myocardial stimulation (increase strength ventricular contraction
  • increase in HR
  • Vasoconstriction in vascular bed(skin, mucosa, splanchnic area and kidneys, veins)
138
Q

As the concentration of EPINEPHRINE increases , the predominant effect will be

A

Vasoconstriction; ALPHA 1

139
Q

___________ state present during the intraoperative and post-operative period may reflect stress-associated release of ________

A

HYPERCOAGULABLE

EPINEPHRINE

140
Q

GI EPI effects: ________Through which receptors?
GI muscle tone is
SPHINCTERS and secretion

A

Relaxation of GI smooth muscle in the GI wall ; Beta 2
decreased.
contraction of sphincters and decrease secretion.

141
Q

SNS control of radial muscles

A

Alpha -1 activation causes –> radial muscles to shorten –>

Increase pupil size =mydriasis

142
Q

Epinephrine predominantly stimulates _______ in the _____, mucosa , _________ vasculature producing intense vaso_______

A

Alpha 1 receptors; skin; hepatorenal ; vasoconstriction.

143
Q

In the skeletal vasculature epinephrine principally stimulate _______ receptors producing vaso _______

A

Beta 2; dilation

144
Q

The net effect o f changes in the peripheral vascular tone is _______

A

Distribution of cardiac output to skeletal muscles and increased SVR

145
Q

What happens to myocardial oxygen consumption?

A

Increased with enhanced LV preload
Increased contractility
Increased afterload and
Tachycardia

146
Q

Repeased doses of epinephrine does not lead to _______ like _______do

A

Tachyphylaxis; catecholamines.

147
Q

What is substantially decreased by Epi?

A

Renal blood flow

148
Q

In usual therapeutic doses, epinephrine has relatively ______ ______ action on cerebral arterioles because epinephrine is

A

little vasoconstriction

Poorly lipid soluble.

149
Q

What causes hyperglycemia in perioperative?

A

Release of endogenous epinephrine and the resulting GLYCOGENOLYSIS/ GLUCONEOGENESIS and inhibit of insulin secretion

150
Q

Why is the measurement of serum potassium levels immediately before induction of anesthesia are usually lower than 1- 3 days prep

A

due to STRESS INDUCED RELEASE OF EPINEPHRINE

151
Q

B2 stimulation ________ intracellular concentration of ________ and ______ release of ______Mediatrors associated with bronchial asthma

A

increasing
decreasing
vasoactive

152
Q

The bronchodilator effect of Epinephrine ( is or is not) ________ seen with B2 adrenergic blockade instead, epinephrine induces _______ from stimulation of _______

A

is not
broncho-constriction
alpha receptors.