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217 Cards in this Set
- Front
- Back
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what are the two parts of the CNS?
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afferent- sensory
efferent - motor |
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what is the efferent system divided up into?
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somatic- skeletal muscle innervation (voluntary)
autonomic- smooth muscle, cardiac muscle, and exocrine glands (reflex, homeostasis) |
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what are the two divisions of the autonomic nervous system?
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sympathetic- fight or flight
parasympathetic- non stress time. |
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what neurotransmitter is primariy stored in vescicles?
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Acetylcholine
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what do you call neurons that release acetylcholine?
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cholinergic
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what do you call drugs that mimic acetylcholine?
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cholinomimetics
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what do you call drugs that oppose the action of acetylcholine?
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cholinoceptor antagonists
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what are the two types of cholinrgeic receptors?
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muscarinic- nerves, heart, smooth muscle, glands, endothelium
nicotinic- skeletal muscle, neuromusclular junctions |
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what neurotransmitter is released at most sympathetic postganglionic neuroeffector junctions?
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norepinephrine
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how is norepinephrine formed?
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tyrosine -> dopamine -> norepinephrine (last step is in vesicles)
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How is Norepinephrine removed after released?
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1. reuptake
2. diffuse into circulation. 3. transported into effector cells (MAO and COMT) |
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where is norepinephrine carried a step further and converted to epinephrine?
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adrenal medualla
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what do you call drugs that mimic norepinephrine?
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adrenergic, or sympathomimetics
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what do you call drugs that oppose NE?
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adrenergic antagonists, or blockers
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what are 2 types of cholinomimetic agents?
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direct acting - bind directly
indirect - inhibits the AChE, increasing ACh. |
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whate are two types of direct cholinomimetic agents?
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choline esters- longer duration than ACh. resist destruction from AChE.
alkaloids- well absorbed, kidney excreted, faster with acidification. |
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what are the 4 cholinomimetic esters?
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acetylcholine- used for miosis during cataract surgery
metacholine- longer DOA, no nicotinic activity Carbachol- more nicotinic activity, used to treat glaucoma bethanechol- muscarinic activity, used for urine retention, has many adverse effects |
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what are the cholinomimetc alkaloids?
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muscarine- no nicotinic agent, (mushroom poisoning)
pilocarpine- miosis, increases gatric secretion, can be to much if diarrhea and vomiting happen. |
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what are the two types of AChE inhobitors?
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mono and bis quaternary amine alcohols
carbamates |
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what are the three AChE amine inhibitors?
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Ambenonium- oral, used for myastenia gravis. long DOA, more ADR's
Demecarium- topical, used for glaucoma Edrophonium- NMB reversal, a diagnostic for myastenia gravis |
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what are the 3 AChE carbamate inhibitors that are reversable?
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Neostigmine- treats myastenia gravis, NMB reversal, post-op non obstructive urinary retention
physostigmine- antidote to muscarinic blockers, easily absorbed Pyridostigmine- myasthenia gravis, NMB reversal, longer DOA than neo. |
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what are the AChE carbamate inhibitors that are irreversable?
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organophosphates- cause miosis, salivation, sweating, bronchisl constriction, NVD. Treat by maintaining ventilation and atropine. (Echothiophte)
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what is glaucoma? How is it treated?
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increased intraocular pressurethat can dmage the optic nerve.
miotics can imporve the aqueous flow(pilocarpine, methacholine, carbacho), cholinesterase inhibitors enhace the ACh to the iris sphincters(physostigmine, demecarium, echothiophate, isoflurophate) |
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what is strabismus?
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turning of one or both eyes from the normal position, treated with echothiophate, demecarium, isoflurophate.
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what is myasthenia gravis?
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impaired neuromuscular transmission at skeletal muscles.
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what do cholinomimetics do to the GI and urinary tracts?
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increase lower esophogus tone, urinary retention, don't use if there is a GI blockage
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how are cholinomimetics used for poisonings?
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good for atropine and tricyclic antidepressant poisoning. If poisoned with them can cause serious behavior disturbances.
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what are cholinergic blocking agents?
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compounds that selectively antagonize the muscarinic responses to ACh. reversible. Bella Donna alkaloids, atropine, and scopoline
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what is Menieres disease?
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recurrent vertigo, ringing in the ears, deafness, nausea and vomiting. Use Scopolamine.
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What drug is used for seasickness?
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scopolamine
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what are cholinergic blocking agent effects on the eye?
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mydriasis (pupil enlargment), cycloplegia (can't contract ciliary muscles), tear reduction.
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what are the cholinergic blocking agents that are normally used in the eyes?
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atropine, scopolamine, cyclopentolate, tropicainamide. Can cause acute glaucoma. Apply presure to lacrimal sac after administration
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what are the effects of cholinergic bocking agents on the cardiovascular system?
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little effect on blood pressure, slight tachycardia. prevents effects of direct acting muscarinic stimulants. low dose = initial bradycardia. larger dose = tachycardia. Only use atropine when hypotension or ventricular arrthymia
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what are the effects of cholinergic blocking agents on the respiratory system?
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bronchodilation, reduction of secretion. Scopolamine also causes amnesia. Glycopyrrolate is useful to reduce secretion in intubated patients.
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What is the best cholinergic blocking agent to use for asthma?
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ipratopium- decreased systemic effects when compared with atropine.
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what effects do cholingeric blocking agents have on the GI tract?
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slows motility, decreases salivation. used for diarrhea, irratable bowel, spasms
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which cholinergic blocking agent is typically used for stomach spasm and pain?
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propantheline, oxybutnin.
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what cholinergic blocking agent is typically used for smooth muscle relaxation?
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oxybutnin
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what effect do cholinergic blocking agents have on the genitourinacry tract?
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slows it down. good to treat urinary frequency, urgency, incontinence
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which cholinergic blocking agents are best to treat overactive bladder
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oxybutnin, and tolterodine (the latter has less adverse affects, and a longer DOA), and solifnacin, and Darifenacin (the last two have the greatest affinity for muscarinic receptors.
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What effect does cholinergic blocking agents have on the sweat glands?
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suppression.
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what is used for cholinesterase inhibitor poisoning?
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cholinergic blocking agents (atropine, need multiple doses becuase DOA is shorter than the poison's) 2-PAM and DAM regenerate active enzyme from the organophosphate cholinesterase complex.
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What are the adverse effects of too much cholinergic blocking agent?
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tachycardia, fever, delirium.
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Under what conditions should you not use Cholinergic blocking agents?
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glaucoma, ulcers, prostatic hyperplasia, urinary retention.
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what is the difference between direct and indirecr acting adrenergic drugs?
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indirect depend on the release of endogenous catecholamines.
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which drugs displace the stored catacholamines from the adrenergic nerve endings?
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amphetamines
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which adrenergic drugs inhibit catacholamine reuptake?
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cocaine and tricyclic antidepressents
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which adrenergic drug is most selective for Alpha receptors? For Beta receptors?
Which does both? |
Alpha- Epinephrine
Beta- Ioproterenol Both- Norepinephrine |
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which drugs are adrenergic alpha blockers?
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phentolamine and phenoxybenzamine
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what are the 2 types of adrenergic beta receptors?
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beta 1- in heart. (equal affinity)
beta 2- in lungs. (higer affinity for EPI) |
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What is receptor sequestration?
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receptors made temporarily unavailable for activation by agonists
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what is down-regulation?
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disappearance of the receptors from the cell.
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what is the major mechanism of desensitization?
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phosphorylationof the receptor
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what is homologous desensitization?
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loss of receptors sensitivity exposed to a drug
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what is heteroologous desensiitization?
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loss of some cell surface receptor sensitivity that have not been activated by the drug.
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What does epinephrine do?
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acts on both alpha and beta receptors. Relaxes bronchospasms, reduces congestion and edema.
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which drug is the best to use with anaphylaxis?
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epinephrine
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what are the side effects of using epinephrine?
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tachycardia, hypertension, increased myocardial 02 demand, anxiety, decreased renal and splanchnic flow
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what does norepinephrine do?
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stimulant for alpha and beta in the heart, but not in the bronchi or peripheral system. Used in shock.
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what are the adverse effects of norepinephrine?
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arrythmias, palpitation, bradycardia, hypertension, chest pain, head ache
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What doe isoproterenol do?
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synthetic, acts on beta receptors. used to treat bronchospasm, shock, cardiac arrest
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what are the adverse effects for isoproterenol?
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premature ventricular contractions, hypotension, chest pain,
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what does dopamine do?
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precursor to NE. both beta and alpha receptors. indirect effect of releasing norepinephirine from storage sites.
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how does the dose of dopamine effect the outcome?
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low dose- D1 receptor, increases urine output.
med dose- B receptors cardiac stimulation high dose- alpha receptors vasoconstriction |
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what are the adverse effects of dopamine?
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tachycardia, vasoconstriction, hypertension, ventricular arrythmias, nausea and vomiting
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What does Dobutamine do?
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B1 receptor. caridac stimulation increases introphy and cardiac output. Has less arrythmia issues than all the others
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what does phenylephrine do?
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pure alpha agonist. decongestant for the eyes.
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What does Ephedrine do?
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releases the stores of catecholamines. nonselective. Nasal decongestant. Ma Huang and herbal teas have it.
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what does pseudoephedrine do?
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ephedrine enantiomer. OTC decongestant
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What are the topical decongestants?
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Xylometazoline and Oxymetazoline, may cause hypotension
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What are the three characteristics of ADD and ADHD?
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impulsiveness, heightened distractability, short attention span
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what are the goals of ADHD medications?
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improve core symtoms, associated symptoms, functional outcomes, allow the child to exert control instead of have the drug control the child
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what do stimulant medications do in regards to ADHD?
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dopamine and norepinephrine reuptake inhibitor. (MOA)
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what is Methylphenidate
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patch worn up to 9 hours a day. Has many adverse effects
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What is Amphetamines?
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Adderall- mix of dextroammphetamie and lisdexamphetamine. Lasts up to 12 hours. CNS stimulation can lead to abuse. Was a study aid.
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Which stimulant medication is used to treat narcolepsy?
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modafinil
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what are SSRI's?
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selective serotonin reuptake inhibitors
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what are the two functions of writing prescriptions?
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1- tells pharmasist specific drug, dosage, concentration, and amount issued
2- directions to patient |
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why prescribe generics?
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flexibility for the pharmasist and savings for the patient
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are generics and brand names always of equal satisfaction?
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no
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how many grams in an ounce? how many ml in an ounce?
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30 gms, 30 mls
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how many ml in a pint?
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500 ml
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how many ml in a teaspoon and a table sppon
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5/15ml
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what are legend drugs?
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require a prescription
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1906?
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interstate regulation
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1914?
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Narcotic drug federal regulation
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1938?
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interstate regulation of drugs that haven't been proven safe
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1952
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prescriptions introduced
Federal warning introduced |
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1962
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drug must demonstrate effectiveness and ingredients
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1965
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accounting of abuseful drugs. Refill limitations
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1970
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controlled substances divided into 5 classes
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1983
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orphan drugs
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what is the law for a controlled drug?
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DEA # required.
I -not prescribed. II -IV -require prescription III-IV can be telephoned and can have up to 5 refills II must be written and signed in ink. |
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What are Schedule I drugs?
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drugs w/ high potential for abuse with no accepted medical use.
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Schedule II?
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high potential for abuse with accepted medical use
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Schedule III?
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lower abuse potential
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Schedule IV?
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lower abuse rate than III
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Schedule V?
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exempt narcotics, very low
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BID?
GM? QD? QID? Q4h? STAT? TID? |
twice a day
gram as required 4 times a day every 4 hours immediately 3 times a day |
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What does the IRB do?
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requires federal funds, reviews studies, protects the rights of those involved in trials
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What is informed consent?
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study subjects have the right to know what will happen to them if they participate
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what are the phases of clinical investigation?
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I - establish safety
II - establish efficacy and dose III - verify efficacy and detect adverse effects IV- obtain additional data following approval |
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Phase I?
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dose level where toxicity first appears.
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Phase II?
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find optimal dose range, patients in test should have no medical problems other than the condition for which the new drug is being administered
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phase III?
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detect adverse effects, over 2 million serious adverse effect reactions a year. 100,000 deaths a year many adverse effects are not discovered until after phase 3
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What does parenteral mean?
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injection - given to uncooperative , good for poorly absorbed
painful |
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what is the difference between solutions, suspensions, emulsions, and dry powders?
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suspensions - decreased water solubility
emulsions- water insoluble dry powders- drugs unstable for long periods |
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Bioavailability?
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fraction of unchanged drug reaching the systemic circulation following administration by any route
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pharmicodynamics?
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what the drug does to the body.
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what do drugs do?
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enhance, discontinue or regulate something the body already does
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what is the pH of most drugs?
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weak acids and bases.
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What is the difference between hormones and xenobiotics?
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xenobiotics are synthesized outside of the body
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what is the difference between a toxin and a poison?
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toxins are organics or biological only. Poisons can be synthetic. Both are of no benefit to the body.
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do all drugs produce their effect by an interaction with a receptor?>
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no
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what determines the concentration of drug required for drug action?
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number of receptors available and affinity for binding
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what is more important? specific nature of a particular drug receptor bond, or drugs with low affinity to their receptors are more selective than drugs that have a high affinity?
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the latter
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what are enantiomers?
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asymetric centers with same chemical makeup
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What is structure activity relationships? (SAR)
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activity is related to chemical structure and affinity for receptors
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what is an agonist?
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drugs that have a direct stimulatory effect on a receptor.
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what is the difference between a full agonist and a partial agonist?
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full- envokes the max response
partial- doesn't elicit full response, even when occupying all the receptors. |
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what is an antagonist
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agents that interfere with the activities of an agonist
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what effect does an antagoinst binding to a receptor site have?
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none, remains inactive
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What is the difference between competitive and noncompetitive antagoinsts?
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competitive- is reversible, can be overcome by increasing the concentration of the agonist
noncompetitive- irreversible, increase in agonist concentration will have no effect on the receptors. |
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what are chemical antagonists?
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drugs that antagonize by binding to and inactivating the agonist
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what are the 2 main functions of a receptor-substrate interaction?
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direct cemical effect on the receptor
involvement of a second messenger |
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what is the dose-response relationship curve?
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relationship where the maximum effect is reached at a dose, or percentage of receptors occupied, lower than what would be expected on a linear graph.
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what is a quantal dose/effect?
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the effect will be either/or. It will either have the desired effect, or it won't.
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what is the ED50 and the LD50 mean?
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ED50- median effective dose, 50% of subjects demonstrate quantal effect
LD50- median lethal dose, 50% die |
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what is the therapeutic index?
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range between the ED50 and LD50 (before the LD50)
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what is a graded response?
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small response to a low dose of drug, and the response increases as the dose increases. It is directly related to the number of receptors with which the drugs effectively interact
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how can the efficacy of the drug be determined?
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it is seen where the drug plateaus on the dose/response curve.
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how can you determine the potency of a drug?
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the concentration at which the drug produces 50% of the maximal effect.
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Can a drug be more potent and less efficient than another?
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yes, it can reach 1/2 maximum effect at a lower dose, but not reach the same efficacy level as the other drug
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does greater potency or greater efficacy determine superiority?
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no, each patient and circumstance is different.
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what are spare receptors?
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receptors still unfilled once the maximal effect has been reached by the drug.
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what do spare recpetors do?
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increase the sensitivityto drugs since lower concentrations of antagonist can be blocking receptors and drug responses can still occur.
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what is pharmicokinetics?
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absorption, distribuition, metabolism, and excretion of the drug. Compares these to the therapeutic effects of the drug.
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how does drug concentration effect absorption?
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rate of diffusion is directly proportional to the concentration.
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how does the physical state of the drug effect absorption?
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the hardness and the interactions among various ingredients plays a role.
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how does the surface area effect absorption?
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smaller surface area = slower absorption
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how does vascularity and blood flow effect absorption?
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more rapid from tissues that are more vascular and inflamed.
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where are most drugs absorbed?
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small intestine
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what is drug distribution?
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the partitioning of a drug among the numerous locations where a drug may be found in the body.
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what kind of drug would be found in the total body water?
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small hydrophilic compounds
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what kind of drug would be found only in the extracellular water?
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large hydrophilic compounds
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what kind of drug would be found in blood plasma?
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strongly plasma bound and charged compounds
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why is the blood brain barrier important to consider before administering a drug?
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it allow diffusion certain chemical to pass along into the CNS. Lipid soluble
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what is the only route of administration that does not require the drug to transport from the sight of administration to the the area desired?
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intravenously
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how can drug binding to protein effect the drug distribution?
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only the free drug that is not bound th protein is available to exert it's biological effect. If a competitor dislodges the drug from the protein, icreased effect or even toxicity results.
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how are drugs effected by metabolism?
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most drugs are acted on by metabolisms and turned into metabolites, which can be excreted ot turn into toxic products.
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what are active metabolites?
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metabolites that still have therapeutic effects
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what are prodrugs?
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drugs that have no therapeutic benefit until it has indergone metabolism first.
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what is first pass metabolism?
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after absorption, portal vein delivers drug to liver before body. Significant metabolism can take place there first.
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when discussing drug metabolism, what are phase 1 reactions?
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drug is made into a more polar metabolite by either masking or unmasking a functional group.
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when discussing drug metabolism, what is enzyme induction?
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acceleration of the metabolism leads to a decrease in drug therapeutic action.
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in discussing drug metabolism, what is enzyme inhibition?
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inhibition of the drug metabolism leads to an increase in drug therapeutic effect, increasing the half life.
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when discussing drug metabolism, what are phase 2 reactions?
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conjugating the drug or metabolite with an endogenous compound more water soluble to be eliminated by the kidney.
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what are the three processes that lead to kidney excretion of drugs?
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glomerular filtration rate, tubular secretion, and reabsorption.
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What is Therapeutic Drug Monitoring? (TDM)
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safe and effective therapeutic management of drugs in an individual patient
It is used to improve efficacy and decrease toxicity. |
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what can be extrapolated about drug concetrations in blood plasma?
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whatever trends are seen in the blood plasma, should be similar in the target tissues as well.
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what is the therapeutic range?
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aid to individualize medications, it is derived from population kinetics, and it provides a guideline for safe and effective medeication use.
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are the boundry concentrations of therapeutic ranges the sane for everyone?
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no
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what factors can cause variability in serum concentration?
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difference in absorption, metabolize, and eliminate ability
disease age drug interactions |
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what is compartmental monitoring?
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estimates an actual physiologic circumstance.
=dose/Vd (amount/volume it is found) |
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what is the difference between one and two compartment modeling?
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one- organs and tissues are grouped into one. Instant distribution is assumed, and elimination does not affect concentration.
second- closer to reality becuase it accounts for quick distribution to the plasma, and slow distribution to the tissues. |
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what is volume of dsitribution?
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the extent into which the drug is distributed. THE Vd DOES NOT CHANGE WITH DOSE.
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what is clearance?
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removal of drug from plasma, and removal from the body. Doesn't say how much, just how fast.
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what is the difference between first order and Zero order elimination?
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1st- fraction remains constant. Amount changes.most drugs exhibit 1st order.
0- amount does not change. Fraction does. |
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What is the elimination rate constant?
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calculated form the first order elimination. amount of drug removed from the body over a given period of time.
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what is half-life?
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time it takes for drug concentrationin the measured compartment to be reduced by half.
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What is steady state?
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when the amount eliminated is equal to the amount taken in. concentration of peak times are consistent. Concentrations of trough times are consistent.
= 5 half lives |
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What is a loading dose?
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amount of drug required for a patient to achieve therapeutic concentration of the drug. It does not reach the steady state faster, but reaches the range fater.
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what is pharmacotherapeutics?
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use of drugs in the diagnosis, prevention, and treatment of a disease.
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what are empircal results?
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results that may occur because the prescribed drug covers a vat range of symptoms beyond the just the one that you are trying to alleve.
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How is the optimal dose determined?
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diagnosis, severity, stage of disease, concurrent disease and drug therapy.
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what are the steps of rational prescribing?
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1- make diagnosis
2- consider pathophysiology of diagnosis 3- select therapeutic objective 4- select drug 5- determin dose 6- plan for observation 7-plan for patient instruction |
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what is pharmacogenetics?
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different drug responses due to heredity
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what is genetic polymorphism?
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variation in structure of a gene or an allele
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what are the important genetic factors to consider?
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1- metabolism rates among different ethnic groups
2- cellular resistence 3- alteration of protein synthesis (in microorganisms and cell lines) 4- transfer of genes that encode a resistence to the drug (in microorganisms and cell lines) 5- excess gene amplification that leads to excess enzyme production that inactivates drugs |
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how is the weight of the patient used to calculate dose?
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get actual weight for obese to use for their loading dose, then use the ideal body weight for their maintenence dose.
Use actual for normal and underweight patients. |
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what type of drugs do most pregnant women on medication take?
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nonprescription
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what is teratogenesis?
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malfunction of fetal organs either structurally or functionally
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do most drugs cross the placenta into the baby?
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yes
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when is the greatest teratogenic susceptability for the fetus?
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1st trimester
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what kind of drugs pass into the fetus most easily and how do they do it?
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lipid soluble drugs- passive diffusion, facilitated transport, and active transport.
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what are the FDA pregnancy safety categories?
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A- sufficent studies with no adverse effects
B- adverse in animals, but not in humans, or no animal risks and not many human studies C- adverse effects, not many human studies, benefits outweigh the risk D- eveidence of fetal risk, but effect still outweighs the risk X- Risk outweighs the benefit |
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where do most drugs taken during pregnancy fall into?
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B and C
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How are drugs passed on to the infant in breatfeeding from the mother?
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bidirectional diffusion. Milk proteins can bind to drug, but bind less well than the proteins in plasma. Emulsified fat in milk can cause drug concentrating
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what is the milk/plasma ratio?
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drug in milk/drug in plasma. are directly porportional. The lower (0.1) the better.
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what is the relative infant dose and absolute infant dose
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absolute- drug concentration in milk X volume of milk per day
relative- infant exposure due to maternal dose. absolute dose/maternal dose X 100 |
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what are the methods to minimize drug exposure to infants because of maternal dose?
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1- withhold or delay feeding
2- change drug route for mother 3- monitor infant adverse effects |
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are adults or children at a greater risk for medication errors?
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children
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how is the body composition different in babies compared to adults
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more water(Vd) and less fat(Vd) than adults
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what are the primary organs for metabolism?
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LIVER, kidneys, intestine, lugs, skin
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what are the two categories of metabolic processes seen in children?
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phase I- decreased P450 enzyme activity in neonates, reaches normal levels around 6 months
phase II- conjugation of drug with endogenous protein to be excreted. |
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what are the types of conjugation reactions seen in infants?
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sulfation- around week
acetylation- around a month glucaron- around 2 months AA conjugation- around 3 months |
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how is elimination rate effects in children?
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lower glomerular filtration rate b/c of fewer nephrons, or fewer functional nephrons.
Tubular function is decreased b/c of secretion and reabsorption low levels |
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what are some good ways to mask medicines?
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chill, popsicle, cold liquid, hold nose, mix with something else
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how does absorption change in elderly patients?
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decreased saliva, teeth, active transport, stomach acid production, GI blood flow, esophogus action.
increased gastric pH, ulcers, diverticulum in colon |
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how is body composition different in elderly patients?
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increased fat, decreased water and plasma. Decreased albumin, increasing free fraction of drugs.
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how is metabolism different for elderly patients?
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decreased liver size, decreased first pass metabolism. Phase I has most change
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How is excretion different for elderly patients?
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less glomeruli, less GFR, less renal blood flow
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what is physiologic reserve in elderly pateints?
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functional reserve capacity and the ability to maintain homeostasis
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what is the functional reserve capacity in elderly?
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ability to perform activities under abnormal sistuations
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what is homeostasis in the elderly?
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ability to maintain a constant enviroment while adjusting to change.
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what patients get the majority of prescriptions in the US?
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elderly (50%)
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what is polypharmacy?
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use of several medications by one patient
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what are 8 risky drugs to use with the elderly and why?
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1- amitriptyline and doxepin- used for neuropathic pain- it dires them out
2- Diazepam and chlordiazepoxide- long half lives, cause sedation hangover anf can injure them selves 3- propoxyphene- causes CNS disfunction due to a toxic metabolite 4- Dipyridamole- used to decrease platelet aggregation, causes standing hypotension 5- Meperidine- creates a toxic metabolite 6- cyclobenzaprine and carisoprodol- has poor efficacy, is a skeletal muscle relaxant 7- COX2 inhibitors- GI ulcers 8- Fluoxetine- long half life |
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what should be done to patients with lver disease that have a prescription for a drug that is either highly or intermediately extracted?
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reduced because the liver diseae will porlong the half life otherwise.
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what is azotemia?
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elevated blood urine nitrogen (BUN) and creatine in urine (can cause vomiting)
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what is uremia?
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metabolic abnormalities and symptoms resulting from the accumulation of uremic toxins
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what is creatinine clearance?
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men= (140-age)(weight)/(72 x serum creatinine)
women= men x .85 |
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how does the loading dose change in patients with organ dysfunction?
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stays the same. The subsequent doses change to account for the degree of organ dysfunction. You can change either the dose or the interval
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what is hyporeactivity and hypereactivity?
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hypo- needs bigger dose
hyper- needs smaller dose |
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what is idiosyncracy?
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unpredicted reaction indepeendent of dose, not an allergic reaction
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What is tachyphylaxis?
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tolerance that quickly develops over only a few doses
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what are 4 types of noncompliance?
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failure to obtain or access medicine
2- failure to take as prescribed 3- failure to start and stop as directed 4- medication sharing |
