Pharm basics part 3 Flashcards
4 processes: Absorption, distribution, metabolism, excretion
Diff routes - sig; routes most sig for absorption
Liver responsible for metabolism
Drug excreted from kidneys - responsible for excretion
What body does with med
Pharmacokinetics
How the med affects the body - what drug do to body; how actually work to exert effect; part of distribution phase of pharmacokinetics - drug has to get distributed to diff parts of body (tissues, organs) to exert an effect
Drugs act at specific areas on cell membranes called receptor sites
Drugs work by change/altering existing physiological and biochemical processes - utilize receptor sites in lot diff ways
Medications gen work in one of four ways:
Pharmacodynamics
Have Receptor sites all over body
Receptor sites Normally bind things like hormones, neurotransmitters, growth factors, etc.: hormones: insulin, cortisol, ADH - attach to specific receptor sites; neurotransmitters: AcH, epinephrine, norepinephrine
Drugs act at specific areas on cell membranes called receptor sites
1.To replace or act as substitutes for missing chemicals - T1DM: no insulin secretion: give exogenous/synthetic insulin to replace what missing since missing insulin
2.To increase or stimulate certain cellular activities - do with agonist drugs; beta2 agonist - beta2 receptors part sympathetic NS: act sim to sympathetic NS
3.To depress or slow cellular activities - beta antagonists/blocker (opp beta agonist); antihistamines
4.To interfere with the functioning of foreign cells, such as invading microorganisms or neoplasms leading to cell death: antibiotics - working to kill that microorganism; chemo - targeted to kill cancer cells
Medications gen work in one of four ways:
types receptors and How meds interact with them
Agonists
Antagonists
Drug–Enzyme Interactions
Selective Toxicity
Receptor theory: types
Drugs interact directly with receptor sites and causes same activity that natural chemicals would
Cause same activity of natural chemicals would cause at that site
Ex: insulin - interacting with same receptor site as indogenous insulin and causing same activity; beta-agonist
Mimicking what body norm do
Occupy same exact receptor site and work exactly like normal areas of body would
Agonists
blocks/prevents some kind of stimulation/rxn from occurring
Ex: beta-blockers - blocking beta receptor sites of symp NS; anti-histamines
Means blocked/prevented - antagonist, blocker, anti
Occupy receptor sites for natural chemical so no longer get in receptor sites
Antagonists
Drugs that Interferes with enzyme systems that act as catalysts for chemical reactions
Most time drugs are blocking some point of this enzyme interaction so norm effect cannot occur
One interruption (drug) in cascade can block the normal cell function
Ex: Angiotensin converting enzyme inhibitor (ACE-inhibitor) - RAAS - conversion Angiotensin I to II and need ACE because acts as catalyst of conversion from I to II and if inhibit enzyme prevent conversion: lowering BP
Drug–Enzyme Interactions
Ability of a drug to attack only those systems found in foreign cells
Drugs trying to attack certain types of foreign cells
Ex: Penicillin (antibiotic); certain types of chemotherapy drugs - trying to do is directly target cells
Selective Toxicity
Parasympathetic -
Sympathetic -
Receptor theory: ANS
major neurotransmitter: AcH; “rest and digest”
major actions: decreases the HR, constrict bronchioles - resting not need breathing heavy or oxygenating well because not utilizing lot major organs, increases digestion/GI tract, increases/helps to stimulate urination
Parasympathetic -
“fight/flight”
Major actions: increase HR, bronchodilation, increase rate and depth of breathing, slowing of GI/digestive tract, decreased urination - need O2 to tissues
Sympathetic -
Mimics acetylcholine - major neurotransmitter
Agonist (cholinergic agonist) - cholinergic referring to parasym NS: mimicking normal actions of parasym NS
Antagonist (cholinergic-blocking/er) - blocking; aka anti-cholinergic drugs; blocking parasymp NS - because helpful in conditions
ANS: parasym branch
Increases saliva production
Slows heart rate
Constricts bronchioles
Stimulates digestive process
Increases urination
Common use: Alzheimer’s disease - loses neurons (die); goal is increase amount AcH available for use in brain; give this increases amount AcH and mimics norm actions; also have adverse effects because not just affect brain because goes to entire body
Agonist (cholinergic agonist) - cholinergic referring to parasym NS: mimicking normal actions of parasym NS
Decreases saliva/secretions
Increased heart rate
Relaxes bronchioles
Decreased GI motility and peristalsis
Urinary retention
Drowsiness, disorientation
Uses: bowel and bladder disorders - overactive bladder - urinating too much - block parasymp activation which increases urination and block it so not urinate as frequently but also goes systemic so have those adverse effects, Parkinson’s disease, asthma
Also called: anti-cholinergic
Antagonist (cholinergic-blocking/er) - blocking; aka anti-cholinergic drugs; blocking parasymp NS - because helpful in conditions
Adrenergic agonist - mimics action of SNS
Adrenergic antagonist (adrenergic-blocking) - some kind of blocker of some specific cells in SNS
ANS: SNS branch
Tachycardia and vasoconstriction
Increases BP
Increases rate and depth of breathing
Bronchodilation
Decreased GI motility
Glycogenolysis (increased blood glucose)
Constricts bladder sphincter
Uses: cardiac and respiratory
Other name: sympathomimetic - mimicking SNS
Adrenergic agonist - mimics action of SNS
Slows heart rate
Lowers blood pressure
Bronchoconstriction
Masks s/s hypoglycemia
Urinary incontinence
Uses: HTN, BPH
Other name: alpha-, beta-blockers: blocking receptors in sympathetic branch
Block receptor sites: Blocking norm action of SNS - PSNS symp
Adrenergic antagonist (adrenergic-blocking) - some kind of blocker of some specific cells in SNS
