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40 Cards in this Set

  • Front
  • Back
Schedule 1
highest abuse potential
high physiological and psychological dependence
very limited or no clinical use

Examples: heroin, LSD, MDMA (ecstasy), GHB, marijuana
Schedule 2
high abuse potential
high physiological and psychological dependence
therapeutic use with prescription

Examples: morphine, opium extracts, carfentanil (and most other opioids), cocaine, methamphetamine
Schedule 3
moderate abuse potential
moderate physiological dependence
high psychological dependence
therapeutic use with prescription

Examples: anabolic steroids, buprenorphine, codeine, marinol (synthetic marijuana), ketamine,
Schedule 4
lower abuse potential
lower physiological and psychological dependence
therapeutic use with prescription

Examples: Xanax (alprazolam), diazepam, Brevital (methohexital), Provigil (modafinil), Restoril (temazepam)
Schedule 5
lowest abuse potential
lowest physiological and psychological dependence
therapeutic use without prescription

Examples: OTC drugs, cough medicines with codeine
Nursing Process (5 steps of nursing)
Assessment
Diagnosis
Planning care with goals and outcomes
Implementation of intervention
Evaluating care
Nursing Implications and Interventions for Pharmacotherapy
Administration
Therapeutic effects
Adverse effects
Teaching
Five Rights of Drug Administration
Right client
Right medication
Right dose
Right route of administration (see chapter 4)
Right time of delivery
Enteral
via the digestive tract
Parenteral
not by digestive tract
first-pass metabolism
phenomenon of drug metabolism whereby the concentration of a drug is greatly reduced before it reaches the systemic circulation. It is the fraction of lost drug during the process of absorption which is generally related to the liver and gut wall.

To by-pass first-pass metabolism:
Sublingual
Rectal
Parental
Therapeutic response
= concentration of drug at target tissue

*This is very hard or impossible to measure

Therapeutic response = concentration of drug at target tissue
*This is very hard or impossible to measure

Therapeutic response = plasma concentration of drug
Efficacy
magnitude of maximal response that can be produce by a drug
aka – maximal efficacy
determined by height of dose-response curve

Potency
refers to amount of drug we need to give to elicit an effect
aka - relative potency
determine by position of dose-response curve along x-axis
Norepinephrine (NE)
Neurotransmitter; Autonomic Nervous System; fight or flight

norepinephrine activates a1, a2, b1 only (Adrenergic receptors)
Epinephrine
Hormone; (released from adrenal medulla only, not from neurons); Autonomic Nervous System
epinephrine activates all Adrenergic receptors (a1, a2, b1, b2)
Acetylcholine
Neurotransmitter; Autonomic Nervous System; rest-and-digest
Parasympathetic nervous system (PNS)
"rest-and-digest"

Increase gastric secretion (increase digestion) **
Empty bladder **
Empty bowel **
Focus eyes for near vision **
Constrict pupils **
Slows heart rate
Contract bronchial smooth muscle
Sympathetic nervous system (SNS)
1. “fight-or-flight”
2. Regulation of cardiovascular system
3. Regulation of body temperature


Increase heart rate and blood pressure
Shunting blood flow from skin/vicera to skeletal muscles
Dilation of bronchi to improve oxygenation
Dilation of pupils (improve visual accuity, more light)
Mobilize energy stores – for brain and muscles
Nicotinic receptors (nAChR)
named for nicotine
lots of subtypes!!! (acetylcholine binds to all subtypes, but selective drugs)
at neuromuscular junction (muscle-type) (somatic NS)
on ALL postganglionic neurons (neuronal-type) in PNS and SNS
(across from preganglionic neurons that release ACh)
on adrenal medulla cells

****
promotes ganglionic transmission (in postganglionic neuron)
release Epi from adrenal medulla
contraction of skeletal muscles
Muscarinic receptors (mAChR)
named for muscarine (found in certain mushrooms)
multiple subtypes (acetylcholine binds to all subtypes, but selective drugs)
on organs innervated by postganglionic parasympathetic nerves
(cardiac muscle, smooth muscle, some glands)

* on sweat glands innervated by postganglionic sympathetic nerves

****
causes:
*increased glandular secretions (pulmonary, gastric, intestinal, sweat)
*contraction of smooth muscle (bronchi, bladder, GI tract)
slows heart (decreases HR, decreases force of contraction)
*contract sphincter of iris (miosis = decrease pupil diameter)
contract ciliary muscles of eye (to focus lens for near vision)
**on blood vessels, not innervated, don’t know how or why they are here, BUT cause vasodilation!
Alpha1 (alpha1 = a1)
Iris – pupil dilation
Blood vessels (veins, arterioles) – vasoconstriction
Male sex organs – ejaculation
Smooth muscle of bladder neck and prostatic capsule - contraction
Alpha2 (alpha2 = a2)
On nerve terminals – not clinically relevant in periphery
* relaxes blood vessels
Beta1 (beta1 = b1)
Heart – increase HR, force of contraction, AV conduction
Kidney – renin release→angiotensin release - vasoconstriction
Beta2 (beta2 = b2)
Lungs – bronchial dilation
Arterioles – vasodilation
Liver, skeletal muscle - glycogen → glucose
Uterus – relaxation of smooth muscle
bethanechol (Urecholine)
Muscarinic agonists (parasympathomimetics)

Pharmacological effects:
smooth muscle contraction (bladder, GI tract, bronchi)
exocrine gland secretions (sweat, salivation, bronchi, gastric)
eye – miosis, contract ciliary muscle (near)
heart – bradycardia (slow heart rate)
vascular smooth muscle – dilation - hypotension

Main sites of action: urinary tract and GI tract, contraction

Therapeutic use: urinary retention (constrict bladder, relax sphincter)
- following surgery under general anesthesia
- to treat nonobstructive urinary retention (postpartum)
Administration: p.o., s.c.

Adverse effects:
bradycardia, excessive salivation, abdominal cramps, diarrhea, fainting (syncope), hypotension

Contraindicated in patients with:
gastric ulcers, intestinal obstruction, bladder weakness, asthma, epilespy, Parkinson’s diease
atropine
2. Muscarinic antagonists (anticholinergics, cholinergic blockers)

Pharmacological effects:
smooth muscle relaxation (bladder, GI tract, bronchi)
↓ exocrine gland secretions (sweat, salivation, bronchi, gastric)
eye – mydriasis, relax ciliary muscle (far)
heart – tachycardia (increase heart rate)
vascular smooth muscle – no effect (only in presence of bethanechol)
Main sites of action: all muscarinic receptors
Therapeutic use: reverse bradycardia from anesthetics, for opthalamic procedures, ↓ gastric acid secretions, muscarinic poisoning
Administration: p.o., s.c.

Adverse effects:dry mouth, constipation, urinary retention, tachycardia, CNS excitement, delirium – agitation, convulsions

Contraindicated in patients with: glaucoma, obstructive GI, bladder obstruction, myasthenia gravis, hemorrhage

atropine decreases effects of levodopa (PD)
tricyclic antidepressant
antihistamines
quinidine
procainamide
To reverse poisoning – increase acetylcholine (cholinestera
Tubocurare (curare)
Neuromuscular blocking agents (muscle-type, nicotinic antagonist)

arrow poison causing muscle paralysis
death from paralyzing respiratory muscles
- can use to relax muscles for surgery (VERY UNLIKELY)
Succinylcholine
Neuromuscular blocking agents (muscle-type, nicotinic antagonist)

-in clinical use
-blocks muscle-type nicotinic receptors
-ultra-short acting
-charged molecule, stays in periphery
used for muscle relaxation during endotracheal intubation, and electroconvulsive therapy (ECT) and endoscopy.
neostigmine (Prostigmin)
Cholinesterase inhibitor (anticholinesterase agent)

Mechanism of action: prevent breakdown in ACh
at therapeutic doses – mimics muscarinic agonists and activate nAChR (nicotinic) at NMJ (neuromuscular junction)
Pharmacological effects:
smooth muscle contraction (bladder, GI tract, bronchi)
exocrine gland secretions (sweat, salivation, bronchi, gastric)
eye – miosis, contract ciliary muscle (near)
heart – bradycardia (slow heart rate)
vascular smooth muscle – dilation – hypotension
*NMJ – increase muscle contraction
Main sites of action: cholinesterase enzyme
Therapeutic use: myasthenia gravis
Administration: s.c., IM, IV

Adverse effects:hypotension, bradycardia, excessive salivation, abdominal cramps, diarrhea, fainting (syncope)
phenylephrine
Adrenergic agonists (sympathomimetics)

Mechanism of action: alpha1 agonist
Pharmacological effects:
vasoconstriction of veins, arterioles
pupil dilation

Main sites of action: blood vessels
Therapeutic use: nasal- ↓ congestion by constricting blood vessels in nasal mucosa; constricts blood vessels to reduce hypotension; dilate pupil during examination
Administration: intranasal, opthalmic, IM, s.c., IV

Adverse effects: burning of nasal mucosa, reflex bradycardia
anxiety, restlessness, tremor

Contraindicated in patients with:
glaucoma, heart disease

Drug-drug interactions: MAO inhibitors (hypertensive crisis), tricyclic antidepressants, alpha-blockers, beta-blockers, oxytocin, digoxin (cause arrhythmia)
clonidine
Mechanism of action: alpha2 agonist
Pharmacological effects:
no significant peripheral effects
in CNS
↓ sympathetic flow to heart and blood vessels
treat hypertension
Pharmacological effects:
contraction of heart

Main sites of action: heart
Therapeutic use: heart failure (improve cardiac performance), shock (condition causes hypotension – increase HR and contract force to increase blood supply)
Administration: intracardiac, IV

Adverse effects:
tachycardia, arrhythmia
albuterol (Proventil, Ventolin)
Adrenergic agonists (sympathomimetics)

Pharmacological effects:
bronchodilation
relaxes uterine smooth muscle

Main sites of action: lungs, uterus
Therapeutic use: asthma, premature labor (ritodrine, Yutopar)
Administration: inhalation

Main sites of action: lungs, uterus
Therapeutic use: asthma, premature labor (ritodrine, Yutopar)
Administration: inhalation

Adverse effects:
if using non-selective beta2 agonist (epinephrine), then be aware of beta1 actions on heart (contraindicated in heart conditions) – use selective beta2, inhalation
prazosin
Adrenergic antagonists

Pharmacological effects:
vasodilation (arterioles and veins)
decrease peripheral resistance
decrease blood pressure

Main sites of action: blood vessels
Therapeutic use: hypertension
Administration: p.o.

Adverse effects:
orthostatic hypotension (start with low doses, give at bedtime)
dizziness, drowsiness
reflex tachycardia
nasal congestion
inhibition of ejaculation

Drug-drug interactions: alcohol, antihypertensives, diuretics
atenolol (Tenormin)
Adrenergic antagonists
Mechanism of action: beta1 antagonist
Pharmacological effects:
reduce heart rate
reduce force of contraction
reduce velocity of conduction through AV node

Main sites of action: heart
Therapeutic use: hypertension, angina, “stage fright”
Administration: p.o.

Adverse effects and contraindications:
bradycardia
insufficient tissue perfusion
conduction in heart (AV block)
if withdrawn abruptly, rebound cardiac excitation (arrhythmia, angina)
propranolol (Inderal)
Adrenergic antagonists;
Mechanism of action: beta1 and beta2 antagonist (b-blocker)****
Pharmacological effects:
reduce heart rate (beta1)
reduce force of contraction (beta1)
reduce velocity of conduction through AV node (beta1)
broncoconstriction (beta2)

Main sites of action: heart
Therapeutic use: hypertension, angina, cardiac dysrhythmias, “stage fright”
Administration: p.o.

Adverse effects:
bradycardia
bronchoconstriction
CNS effects (depression, insomnia, nightmares, hallucinations)

Contraindicated for: heart failure, patients with pre-existing AV block

* don’t abruptly stop taking – rebound tachycardia
Epinephrine
non-selective drugs

binds to and activates all adrenergic receptors. Although mainly used for its ability to activate b1 receptors and get the heart pumping, what else will it do?
b1 agonist activity – ↑ HR, ↑ force of contraction, ↑ AV conduction
b2 agonist activity – dilate bronchi
a1 agonist activity - vasoconstriction

adverse effects:
too much stimulation of heart (tachycardia, arrhythmias, angina)
- can give some atenolol/propranolol to slow heart
severe hypertension
- can give a1 blocker/antagonist to decrease BP
Isoproterenol (Isuprel)
b1 and b2 agonist
Human chorionic gonadotropin (hCG)
similar effect to LH  increases testosterone and sperm production
Menotropin (Pergonal)
mixture of follicle stimulating hormone (FSH) and luteinizing hormone (LH)