Mod 7 PNS Flashcards

1
Q

Alpha 1 & Beta 1

A

Vaso CONSTRICTS

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2
Q

Alpha 2 & Beta 2

A

Vaso DILATES & Bronchial DILATES

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3
Q

Describe the effects of BETA 2 STIMULATORS

A

-Bronchial dilation
-Vasodilation
-⇩ GI activity
-Relaxes uterine muscle
Drugs: Albuterol & Salmeterol

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4
Q

Explain the effects of CHOLINERGIC medications
Drugs: -stigmine

A
  1. Act upon acetylcholine (Ach) neurotransmitter
  2. Upon activation:
    -NicotinicN (neuronal): promotes ganglionic transmission and release of epinephrine

-NicotinicM (muscle): promotes contraction of skeletal muscles

-Muscarinic: targets parasympathetic organs, pupils narrow, ⇩ HR, bronchial constriction, relaxes bladder sphincters, ⇧ GI tract activity, generalized sweating, vasodilation

Muscarinic AGONIST (parasympathomimetic): increases rest & digest (PNS) and mimics effects of Ach

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5
Q

Identify the effects of DOPAMINE RECEPTOR activation medication

A

Effects:
-Dopamine receptors causes dilation of renal vasculature
Used in shock to improve renal perfusion
-Dopamine also enhances Beta 1 receptors in the heart
⇧ BP, urine output, and renal perfusion
Dosage Strength:
- Low dose (dopamine receptors only): vasoDILATES to renal blood vessels to ⇧ renal perfusion
- Medium dose (Beta 1 & dopamine receptors): vasoCONSTRICTS
- High dose (Alpha 1, Beta 1, & Dopamine receptors: vasoCONSTRICTION, pupil dilation, bladder sphincter contraction, ejaculation

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6
Q

Identify signs of and drugs used for ANAPHYLACTIC SHOCK

Drug: Epinephrine

A

Signs:
Wheezing, confusion/anxiety, ⇧ HR, lightheadedness, glottis edema, hypotension, difficulty breathing, skin rash,

Drugs: Epinephrine (1st line)
-Activates Alpha 1, Beta 1 and Beta 2 receptors to reverse anaphylactic manifestations
Alpha 1: vasoCONSTRICTION to suppress glottis edema
Beta 1: ⇧ CO to raise BP
Beta 2: bronchial dilation to reduce bronchoconstriction

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7
Q

Explain the consequences of using too much intranasal albuterol and associated patient teaching needed.

A

Consequences:
-If albuterol is administered in large doses, it can lose its Beta 2 selectivity, causing: tachycardia, angina, & tremors

Patient Teaching:
-Do not exceed prescribed dose for albuterol
-Avoid caffeine
-Observe for palpitations or chest pain

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8
Q

Identify the most serious side effect of alpha1-adrenergic receptor blockers.

A

**alpha 1-adrenergic receptor blockers inhibit smooth muscle contraction

ORTHOSTATIC HYPOTENSION: causing dizziness, light-headedness, and syncope

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9
Q

List the contraindications for administering beta blockers.

A

-Bradycardia
-AV block or Heart block
-Diabetes
-Asthma or COPD
-History of anaphylaxis

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10
Q

Describe the nursing interventions for the side effects of clonidine.

Clonidine (Alpha 2 Agonists)
Antihypertensive
Vasodilates
2nd line drug: always used in combination with another antihypertensive med

A

Side Effects:
Drowsiness
Xerostomia (dry mouth)
Rebound hypertension

Interventions:
Avoid driving or hazardous activities
Chewing gum, sucking on candy, sipping on fluids
Tapering clonidine slowly over 2-4 days
Monitor BP

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11
Q

Identify the drug classes that decrease systemic vascular resistance (vasoconstriction).

A

ACE Inhibitors
ARBs
Alpha 1 -Adrenergic Blockers (Prazosin)
CNS Alpha 2 Agonist
Direct vasodilators

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12
Q

Describe the effects of beta-2 adrenergic stimulators.

A

Opens up lung passages and blood vessels
Mimics the natural effects of epinephrine and norepinephrine (sympathomimetics)

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13
Q

Identify the drug of choice for bradycardia treatment.

A

ATROPINE (anticholinergic):
1st line drug for cardiac arrest
Blocks PNS (slow and digest) to ⇧ HR

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14
Q

What are the toxic effects of cholinesterase inhibitors (helps acetylcholine)?

A

SLUDGE:
Salivation
Lacrimation
Urination
Diaphoresis / Diarrhea
GI cramping
Emesis (vomiting)

Killer Bs:
Bradycardia
Bronchospasm
Bronchorrhea (watery mucus)

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15
Q

What is the therapeutic use of norepinephrine?

A

Therapeutic use:
Emergency IV drug for SEVERE HYPOTENSION
VasoCONSTRICTOR
⇧ HR to prevent cardiovascular death/collapse

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16
Q

How is glycogenesis affected by beta blockers?

A

Glycogenesis: glucagon ⇨ glucose (sugar)

Beta blockers can cause exacerbation of hypoglycemia – the mechanism responsible for beta blocker-induced hypoglycemia involves inhibition of hepatic glucose production. ⇩Adrenergic counter regulation = ⇩ glycogenesis.

Glycogenesis can’t occur in a HYPOglycemic patient

Hypoglycemia recovery is dependent on adrenergic response (constricting response)