Pharmacokinetics: Distribution (from the blood stream to the site of action)
Depends on: good blood supply good blood pressure Blood brain barrier 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
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.
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
The time it takes for the serum concentration of a drug to decrease by 50%
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
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
Injury to cell --> bradykinin--> Activating & Sensitizing Pain Receptors
Both cascades happen simultaneously
Vasodilitation (erythema and warmth), edema, pain receptors innervated.
a protein produced that acts to stimulate vasodilation and pain receptor activation. Released during tissue injury and promote pain INFLAMMATORY MEDIATOR
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
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.
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?
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
epinephrine (Adrenalin) effects all 3 receptors
Both endogenous and exogenous Can't be PO are adrenergic and parasympatholytic Emergency Cardiac arrest Hypotension Shock Bronchial asthma Obstructive pulmonary disease
Similar to catecholamines Effects last longer Effective orally OTC medications
? Diabetes IV site - can be vasoconstrictor to point of necrosis Respiratory & cardiovascular assessment
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
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
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