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CNUR 202 Questions with 100% Correct Answers

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CNUR 202 Questions with 100% Correct Answers

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CNUR 202 Questions with 100% Correct
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Endogenous vs Exogenous

en = within the body - naturally produced

ex = made outside the body - synthetic

Adrenergic Receptors

sites for catecholamines norepinephrine and epinephrine, further divided into beta and alpha

Alpha-Adrenergic-Receptors

two types differentiated by their location relative to nerves, control the release of

neurotransmitters

1- located on the postsynaptic nerve terminal (the tissue that nerve stimulates) NE or E

2- located on presynaptic terminals

beta-adrenergic-receptors

located on postsynaptic effector cells

1- located primarily on the heart

2- located on smooth muscle fibers of the the bronchioles, arterioles, and visceral organs

Adrenergic Drugs

drugs that mimic effects of the SNS neurotransmitters norepinephrine, epinephrine, and

dopamine; known as catecholamines.

can be classified as either selective or non-selective on alpha and/or beta receptors

mechanism of action - adrenergic drugs

,transmission takes place at the junction between nerve and receptor site of the innervated

organ or tissue (effector

mechanism of action - alpha 1 adrenergic stimulators

located on smooth muscles, vasoconstriction occurs and relaxation of GI smooth muscle.

Decreased renin secretion

CNS stimulation

Pupil dilatation

Glycogenolysis & gluconeogenesis

Contraction of pregnant uterus

mechanism of action - alpha 2 adrenergic stimulators

tends to reverse sympathetic activity, inhabitation and relaxation

Inhibit release of NE

Vasoconstriction

Inhibit insulin secretion

Increase platelet aggregation

mechanism of action - beta 1 adrenergic stimulators

effector cells of the heart; increase HR, contractility, BP, and AV conduction, also increases

renin release.

Postive Inotrope

Postive Chronotrope

Postive Dromotrope

+ inotropic effect

increased force of contraction

,+ chronotropic effect

increased HR

+ dromotropic effect

increase in the conduction of cardiac electrical nerve impulses through the AV node

mechanism of action - beta 2 adrenergic stimulators

relaxation and dilation of lungs, vasodilation

Bronchodialtion

Relaxation of pregnant uterus

Decreased motility/tone GI tract

Increased glycogenolysis and gluconeogenesis

vasoactive adrenergics

used to support the cardiovascular system or treat orthostatic hypotension, have a rapid onset

and their effects cease quickly.

Epinephrine Routes and Pharmacokinetics

Subcut: onset 5-10 minutes, peak 20 minutes, variable half life

IV: onset less than 2 minutes, rapid peak, half-life of 5 minutes, duration of action 5-30

minutes

Epinephrine Indications: alpha and beta

B dose used to treat bradycardias, left ventricular dysfunction, or anaphylaxis

A dose used to treat profound hypotension or pulseless cardiac arrest

Salbutamol/Ventolin

, anti-asthmatic, bronchodilator, adrenergic agonist

selective beta 2, stimulating the ability to breathe; bronchodilation and vasodialtion through

metered dose inhaler or nebulizer

Types of Alpha Blockers

nonselective blocking alpha 1 and alpha 2

selective black alpha 1 (alpha 1B, 1A, and 2)

Nonselevtive Alpha Blockers

Can black alpha 1 and alpha 2

alpha 1: vasodilation

aplhpa 2: increase norepinephrine release

Selective Alpha Blockers

Alpha 1A - block receptors in smooth muscle of bladder, neck, and prostate gland; most

affinity for specific sites

Alpha 1B- reduces resistance in peripheral vasculature, decreases BP; works in 2 different

sites

Alpha Blockers

interrupt stimulation of the SNS at alpha adrenergic receptors to work either by direct

competition with NE or noncompete process

Beta Blockers

block SNS stimulation of beta-adrenergic receptors by competing with NE and E, can either

be selective or nonselective

known as the "olols"

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