HNC33 1/3
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| Cholinomimetics | Autonomic nervous system
Muscarinic receptors
Acetyl coenzyme A
Parasympathetic
Sjorgren,Myasthenia Gravis, Anticholinergic toxicity, Vagal, Parkinson's,
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| Parasympathetic nerve | Vagus
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| Parasympathetic nervous system | Autonomic nervous system
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| parasympathetic neuron and Autonomic nervous system target organs | Organ, heart, lung, pupils
Muscarinic receptors acetylcholine
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| Shortens syndrome antibodies | Block the acetylcholine choline at the muscarinic receptors on the salivary and lacrimal glands
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| Barriers to absorption |
#Quaternary ammonium compounds -ex.) curare
#Ions- molecules with a net electrical charge that are unable to cross membrane unless very small into the blood stream. Ions do not move well across the blood and will not absorb well
#Ph- dependent
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| Absorption from the GI tract | * entero-hepatic recycling.
*sustained release
*enteric coated
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| )Distribution- olically active) | free floating drugs are metab
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| Effectiveness | inactivation of a drug drug excreted from the kidney more rapidly(the drug needs to be water soluble to excrete from the kidney)
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| inducers | increases cyp450 activity/metabolism therefor levels of the drug drops or not as effective(deactivates) effectiveness of the drug decrease.(ex. phenytoin, carbamazepine(anti-seizure drugs)( chronic alcohol use, st. johns warts, baributates, rifampin, phen
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| inhibitors | drugs that stimulate the liver to synthesis drug metabolism )-decreases activity of cyp450 therefore levels increase(risk for toxicity)(ex. grape fruit juice, alcohol, anti-biotics, anti-fungal, anti-virus, )
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| Excretion- removal of the drug from the body | A. Glomerular Filtration
B. Passive tubular reabsorption
C Active tubular secretion- p-glycoproteins will help pull/transport
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| Factors that influence excretion | A. Ph Dependent ionization
B. Non Renal Excretion
C. Age
D. Competition for active transport
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| therapeutic response- is achieved through control of the |
1. onset of action- when do you start seeing the effect of a drug
2. peak of action- when of the drug concentration is the highest
3. duration of action- when does the drug wear off
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| Selective drug | one that elicits
only the response for which it is given. There is no such thing
as a wholly selective drug because all drugs cause side effects.
Common examples include the drowsiness that can be caused
by many antihistamines; the peripheral edema tha
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| Peak concentration | highest concentration of a drug checked about 1 hour after drug given. peak should be below the toxic level (the level below liver/kidney damage and organ damage).
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| Peak concentration highest concentration of a drug. ex.) | (ex. 2.0 digoxin)
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| Trough concentration | lowest concentration usually measured 30 minutes before you give the next does. should be above the Minimum Effective Concentration.
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| Minimum Effective Concentration. (ex.) | Minimum Effective Concentration. (ex. 0.5 digoxin)
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| Half life | determine dosing intervals, the amount of time required to reduce the amount of drug in the body by 50%. that determines dosing intervals,measures how quickly drug levels will decline through, metabolization, elimination, when levels start to dip on down,
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| Steady state | when the same dose of a medication is given it typically takes 4 half lives to reach
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| Decline of drug level | when dosing is discontinued, 94% of the drug will be eliminated after 4 half lives.
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| Pharmacodynamics | what happens when the drug gets to the receptor and its effects therefore the study of what drugs do to the body and how they do it.
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| Receptors |
Receptors (mimics or blocks what the body is designed to do)
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| Agonist | any drugs that mimic the action of endogenous moleculestherefore activating receptors. but the activation of receptors does not necessarily mean that the rate will be increased because the stimulation of the receptor might decrease the reaction rate.
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| Agonist Drug (ex.) | (ex. Beta agonist)
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| Partial Agonist | mimics the action of endogenous(something that actually exists in the body all ready) molecules at a lower intensity/not as effective as full agonist, therefore the maximal efficacy is lower that the full agonist
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| Partial Agonists wont (ex.) | (ex. wont reduce pain as well or wont lower blood pressure as well)
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| Antagonists-(seat stealers) | have no inherit ability of their own except they are right shape and the right fit. The antagonist block/prevents the effect of endogenous molecules. they prevent endogenous molecules from binding to receptors by occupying the seat/action site. and have n
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| Seat stealer drug (ex.) | opioid antagonist= Narcan( antidote) that has no effect unless there is opioid in the body, therefore blocks morphine/opioids)
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| Antagonists are | Dependent on the presence of an agonists
Non competitive antagonist- irreversibly
Competitive antagonists
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| Factors that influence response | A. Diet
B. Age- infants sensitive / elderly organ degeneration.
C. Body weight/composition- smaller person distributes drugs better. fat people may store fat soluble . women/men
D. Pathophysiology- genetics, race, kidneys, liver, acid balance , tolera
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| Drug interactions | interaction due to physical or chemical properties - precipitation
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| Drug physical or chemical interactions | 1.change in pharmacokinetics- absorption, distribution- metabolism-
2. altered renal excretion-
3. Drug food- change in absorption rate
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| Metabolism drug interaction | cyp450 or grapefruit juice=cyp450 inhibitor that inhibits the concentration of drugs therefore increasing the concentration of the drug in the body.
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| Adverse reactions to drugs | A. Toxicity- Organ damage
B. Allergic reaction- ige
C. Idiosyncratic Effect
D. Latrogenic- chmo, thyroid medications
E. Physical dependence
F. Carcinogenic Effect- malignant
G. Teratogenic Effect - birth defects
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| Minimizing adverse reactions- | *8 rights to Drug Administration
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