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The 5 Classes of Scheduled Drugs

I - LSD, Heroin
II - Narcotic analgesics
III - Sedatives, Anabolic steroids
IV - Sedative-Hypnotics
V - Partially controlled: Lomotil

Pharmacokinetics: 4 thing that effect absorption

1. Route of administration
2. Drug solubility and concentration
3. Acid-base composition
4. Site conditions

Cytochrome P450

set of liver enzymes that metabolize drugs

First pass effect

the initial metabolism in the liver of a drug absorbed from the gastrointestinal tract before the drug reaches systemic circulation through the bloodstream

bypass the liver when absorbed

buccal, sublingual, vaginal, rectal, topical & parenteral route meds

parenteral

IV: intravenous
IM: intramuscular
Subq: subcutaneous
Intradermal

Topical

Patches
Inhalants

Pharmacokinetics: Distribution (from the blood stream to the site of action)

Depends on:
good blood supply
good blood pressure
Blood brain barrier
Protein Binding

Protein Binding

Pharmacokinetics: Biotransformation ( Metabolism or inactivating the drug)

Enzyme induction
Enzyme inhibition
First-pass effect
Note: Liver disease or failure --> an increase potential for a toxic or adverse drug effect

Enzyme induction

Increased enzyme activity by certain compounds. Drugs or chemicals have the ability to stimulate the activity of microsomal enzymes. Occurs when certain drugs are administered that have the ability to rev up the cytochrome P450 system. This causes the enzymes to work much more efficiently so the body requires more drug to receive the desired effect.

Enzyme inhibition

The decrease in hepatic enzyme activity that results in reduced metabolism of drugs

Pharmacokinetics: Excretion ( Getting the drugs out of the body)

Lungs
Intestines
Breast milk
Kidney
Note: Kidney disease or failure  an increase potential for a toxic or adverse drug effect

Serum Half-Life

The time it takes for the serum concentration of a drug to decrease by 50%

Therapeutic Medication effects

Palliative
Curative
Supportive
Substitute
Chemotherapeutic
Restorative

cross tolerance

tolerance for a substance one has not taken before as a result of using another substance similar to it eg opioids such as heroin to methadone

Drug effects on the fetus

A - studies done on pregnant women
B - Animal studies
C - Animal studies
D - Evidence of human fetal risk
X - Risk outweighs any potential benefit

Assessment factors

1. ALLERGIES
2. RECREATIONAL DRUGS
3. OTC DRUGS
4. AGE
5. BODY SIZE
6. SEX (teratogenicity)
7. ETHNICITY
8. GENETICS
Pharmacogenetics
Pharmacogenomics
9. DOSE
Dosage
Depends on:
Characteristics of the drug
Characteristics of the patient

Cellular reaction to damage

Injury to cell --> arachidonic acid--> cyclooxygenase--> prostaglandins--> Activating & Sensitizing Pain Receptors

Injury to cell --> bradykinin--> Activating & Sensitizing Pain Receptors

Both cascades happen simultaneously

Vasodilitation (erythema and warmth), edema, pain receptors innervated.

bradykinins

a protein produced that acts to stimulate vasodilation and pain receptor activation. Released during tissue injury and promote pain INFLAMMATORY MEDIATOR

cyclooxygenase

Key enzyme in the prostaglandin metabolic pathway that is blocked by aspirin and other NSAIDs.

3 Categories for Pain Management

1. Opiates/Opioids or narcotics (7-10 on pain scale)
2. Nonopiates: Acetaminiphen, Salicylates (ASA), & NSAIDs (4-6 or combined with opiate, 1-3 alone)
3. Adjuvant analgesics (not known pain relief but for things that go with pain like anxiety, insomnia, nausea): Benzodiazopines, TCA, Corticosteriods

Types of Pain by Origin

Somatic "sharp, burning, throbbing, cramping" can stimulate sympathetic NS
Visceral - thoracic or abdominal, hard to localize, can stimulate parasympathetic vasovagal
Neuropathic - injury to nerves, "shooting"

opioid antagonist examples

Prototype: pentazocine (Talwin)
Stadol, Nubain

opioid agonist

bind to opiate receptors and prevent neurons from sending pain signals

opioid agonist antagonist

Medications in which an opioid antagonist (e.g., naloxone/Narcan) is added to an opioid agonist, in hopes of decreasing opioid abuse.

ADEs of opioids

Depresses CNS
Serious: Respiratory depression
Common: Sedation, dizziness
Depress GI Tract
Common: N&V, constipation
Alters psychological responses to pain
Produces euphoria

clinical uses of opiates

Relief of moderate to severe pain
Pre-op sedation
Labor and delivery
Invasive diagnostic tests
Acute Pulmonary Edema
Severe nonproductive cough
MI

Times for pain relief by route

PO 45-60 min
intramuscular 30 min
IV 5-15 min

Opiate prototype?

morphine

endogenous

from body (eg endorphines)

exogenous

from outside body (eg morphine)

Does morphine have a ceiling?

No, can increase dose indefinitely with tolerance

Opiate agonist-antagonist definition

Developed to decrease addictive qualities of drugs. For new patient will relieve pain, for addict will put into withdrawal because will block some receptors.

Opiate agonist-antagonist prototype?

pentazocine (Talwin)

Opiate antagonist prototype?

Narcan (naloxone)

Opiate antagonist description

NOT a stimulant
Given IV
knocks opiate off receptor sites
Shorter duration of action (2hrs) than opiate so may need to be given again

Drugs to treat opiate withdrawal?

Methadone
Buprenorphine (Suboxone)

Arachidonic acid produces?

Cyclooxygenase I (physiologi/protective prostaglandins) -
Cyclooxygenase II (pathological prostaglandins)

What does cyclooxygenase I do?

Physiological/Protective
GI
Renal
Regulates smooth muscle - bronchodilitation
Regulates blood clotting

What does cyclooxygenase II do?

Inflammation
Edema
Leukocytosis
Release of cytokines - increase inflammatory and pain response

What drugs interfere with arachidonic acid to cyclooxygenase I and II?

Non-selective cycclooxygenase blockers
aspirin, acetaminophen, NSAIDs

Selective cyclooxygenase II inhibitor

celecoxib (Celebrex)

Acetylsalicylic Acid

Aspirin - ASA

ASA function

Analgesic
Anti-inflammatory
Antipyretic
Anti-thrombotic

ASA effect on platelets?

ASA binds irreversibly to platelet for life of platelet (7-10 days) and platelet will not aggregate

ASA ADEs

Tinnitus
Reye's Syndrome
N/V
GI System
Bleeding - heamatoria, heamatemisis, GI bleeds, bruising, epistaxis
During Pregnancy
ASA sensitive asthma
Salisilate Poisoning

Reye's syndrome

Acute encephalitis characterized by an onset of symptoms 1 to 3 weeks following a viral infection. A complication of a viral infection. Associated with salicylate use during viral infections.

Salisilate poison

ASA overdose
if <1hr gastric lavage
if >1 hr (hyperventilation, diaphoresis, thirst, drowsiness, coma) no med to reverse, support

NSAID protoype

ibuprofen (Advil)

NSAID effects

Analgesic
Anti-inflammatory
Antipyretic
Anti-thrombotic (not like ASA, binds to platelet only as long as drug is in circulation)

NSAIDs - Adverse Effects

CNS - depresses a little, dizziness drowsiness,
Eyes - blurred vision
GI System - pain, ulceration, bleeding, N/V
Renal System
Pregnancy

Prototype: acetaminophen (Tylenol) therapeutic use

Analgesic
Antipyretic

Acetominophen ADEs

Serious: liver necrosis,hepatic or renal toxicity (large doses)
Common: rash, urticaria, nausea

Celecoxib functions

Analgesic
Anti-inflammatory

Aceitaminophen overdose

first 24 hours flu symptoms (can use mucomyst)
next 24 hours pain in upper right quadrant
in next 2 days hepatotoxiity - jaundice, elevated liver enzymes, bleeding problems, death

Celecoxib ADEs

increases platelet activity, increases clotting
MI
stroke

Anti-anxiety & Sedatives = Relaxation
Hypnotics = Sleep
The difference between the effects is dosage dependent meaning...

Large doses of anti-anxiety and sedatives = Sleep
Small doses of hypnotics = sedation

antianxiety and sedcatives are like opiates because...

both are CNS depressants

Barbiturates prototype

Phenobarbital

Anxiety action

Amygdala - store memory, associate with memory like anxiety
Hippocampus - same
Neurotransmitter Gamma-aminobutyric acid or GABA inhibition will rid anxiety

Barbiturates are not just sedative-hypnotics

also anticonvulsants

Barbiturates ADEs

no REM sleep
enzyme induction = high tolerance
addiction and abose

Anxiolytic

anti-anxiety

BENZODIAZEPINES protoype

diazapam (Valium)

adavantages to benzodiazepines over barbiturates

doesn't supress REM sleep
less enzyme induction
wider margin safety between therapeutic and toxic dosage

Benzodiazapenes ADEs

CNS depressants
mental and physical activity impairment

Barbiturates, Benzodiazepines, & Miscellaneous ADEs

Serious: Paradoxical reaction
Common: drowsiness, ataxia (lack muscle control), confusion

Barbiturates & Benzodiazepines
Abuse: Drug Synergism Effect
Overdose

Respiratory support
Nasogastric lavage
IV fluids & diuretics
Flumazenil (Romazicon)

sympathomimetic

mimcs SNS stimulation
adrenergic (alpha and beta)

parasympathomimetic

mimics PSNA stim
cholinergic

sympatholytic

blocks/prevents/inhibits SNS
antiadrenergic, alpha and beta adrenergic-blocker

parasympatholytic

blocks/prevents/inhibits PSNS
anticholinergic, cholinergic blocker

Adrenergics neurotransmitter?

9nor)epinephrine

Cholinergics neurotransmitter?

acetylcholine

ADRENERGIC EFFECTS

Heart rate UP - chronotrpoic and ianotropic
Blood vessels - peripheral constriction, UP to heart brain and large muscles
Bronchi OPEN
Pupils OPEN
Feelings TENSION
GI System SLOWS, less blood
Blood sugar UP
Fatty acids UP
Sweating UP
Blood coagulation UP

heart rate up?

positive chronotropic effect

heart rate stronger?

ianotropic

adrenergic ADEs

dysrythmias, tachy,
bronchodilitation

Adrenergic Specific receptors

Alpha
Peripherally vasoconstrict in the arms and legs
Beta 1
Cardiac
HR (chronotropic)
force of contraction (inotropic)
Beta 2
Lungs
Bronchodilation

Catecholamines prototype

epinephrine (Adrenalin)
effects all 3 receptors

Catecholamines effects

Both endogenous and exogenous
Can't be PO
are adrenergic and parasympatholytic
Emergency
Cardiac arrest
Hypotension
Shock
Bronchial asthma
Obstructive pulmonary disease

Non-catecholamines

Similar to catecholamines
Effects last longer
Effective orally
OTC medications

Adrenergic ADEs

Cardiac arrhythmias
Angina
Hypertension
Cerebral hemorrhage
Anxiety, nervousness, insomnia,

Nursing Assessment for Adrenergics

? Diabetes
IV site - can be vasoconstrictor to point of necrosis
Respiratory & cardiovascular assessment

Antiadrenergic Effects

Use for patholigical stimulation, hypertension, tachycardia etc
Blood vessels dilate peripherally
Blood pressure DOWN
Heart Rate DOWN
Bronchoconstriction
Cardiac Output DOWN - negative chronotropic and ianotropic
Weakness, lethargy
Less effective metabolism of glucose --> hypoglycemic

Antiadrenergic ADEs

Circulation to periphery
Orthostatic hypotension
Bradycardia
Resp difficulties
Fatigue
Weakness, insomnia
Hypogylcemia

Antiadrenergic Receptor effects

Alpha
Extremities, arms and legs
Dilation of peripheral arterioles and veins
Beta 1
Cardiac
Negative Chronotropic
Negative Inotropic
Beta 2
Lungs: Bronchoconstriction

alpha adrenergic blockers prototype

prozosin or mini-pres

alpha adrenergic blockers effects

BP down
heart rate can go up from contraction going down
peripheral blood flow up
urinary output out

Clinical Use
Tx of hypertension
Raynaud's, Frostbite
Prevent necrosis 2nd from IV extravasation
Tx Benign Prostatic hypertrophy

Serious ADE: first dose syncope

Beta Adrenergic Blockers prototype

propanolol (Inderal)

Beta Adrenergic Blockers

Review:
 Heart Rate ( neg chronotropic)
 Force of contraction ( neg inotropic)
 CO at rest and w/ exercise
Slowed conduction ( neg dromotropic)
 BP
Bronchoconstriction
Less effective metabolism of glucose
Weakness, insomnia

beta adrenergic blockers

Clinical Use
Tx Hypertension, Angina, MI, Tacky arrhythmias
Glaucoma
Pheochromocytoma
Migraines
Palpitations
Contraindications/ADE
Common: hypotension, bradycardia, heart block, CHF,
asthma, bronchoconstriction, and heart block

Cholinergic effects "WET"

Eye - pupil constriction
Salivary glands
Bronchi - constriction and secretion
Heart - slows, vasodilitation, BP down
GI Tract - increase secretion, pooping
Urinary Bladder - increase flow
Increased sweating
Nicotinic Receptors
in motor nerves and skeletal muscles --> muscle contraction
Muscarinic Receptors
in most internal organs --> secretions

Cholinergic Medications

Prototype: neostigmine (Prostigmine)

neostigmine uses and contraindications

Clinical Uses:
Bladder atony
Dx & Tx MG
Antidote
Glaucoma
Alzheimer's
GI Tract atony
Contraindications:
Urinary or GI tract obstruction
Asthma
Peptic Ulcer
CAD
Pregnancy

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