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205 Cards in this Set
- Front
- Back
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non-scheduled drug prescription limitations
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unlimited refils
valid for 12 months fax or phone can pre-print no DEA # needed |
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Schedule I drugs
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no accepted medical use
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Schedule II
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DEA # needed
30 days no refills no pre-printing valid for 90 days |
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schedule III, IV, V
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DEA #
5 refill max good for 6 months no pre-printing |
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example given for chemical interaction drug
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antacids
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what type of drug-receptor interaction is irreversible?
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covalent binding
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where do lipid soluble compounds exert their effects?
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intracellular receptors
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what are some hormones that stimulate intracellular receptors?
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corticosteroids
mineralocorticoids Sex hormones Vit D Thyroid hormone p450 inducers |
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what are the 2 pharmacological consequences of drugs that bind intracellular receptors?
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there is a lag period
effects persist even after drug conc has gone to 0 |
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what is the main type of allosterically regulated transmembrane protein?
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Protein tyrosine Kinases
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what type of molecules activate protein tyrosine kinase's
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insulin
EGF PDGF |
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examples given that are signal transduction inhibitors (STI's. protein tyrosine kinase inhibitors)?
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Imatinib
sorafinib sunitinib |
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examples of cytokine receptor ligands
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erythropoietin
GH interferons |
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cytokine receptors activate what signaling pathway?
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JAK/STAT
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what are the 2 ligand gated ion channels emphasized in lecture?
(receptor, ligand, and channel type) |
Ach/nicotinic recep - Na+ channel
GABA/GABAa recep - Cl- channel |
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effect of opening Na+ channels on the membrane?
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depolarization
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effect of opening Cl- channels on the membrane
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hyperpolarization
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what is the difference btw G-protein desensitization and down-regulation?
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desensitization: rapidly reversible, GRK's allow B-arrestin to bind recep and preventmore G-prot activation
down-regulation: lasting decrease in responsiveness, excessive stimulus and B-arrestin binding leads to endocytosis of recep |
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which G proteins increase cAMP levels?
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Gs
(s=stimulate) |
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Which G proteins decrease cAMP levels?
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Gi
(i=inhibit) |
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Epinepherine binds to this receptor and stimulates cAMP formation (Gs)
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B1 & B2
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Norepinepherine binds to this receptor and stimulates cAMP formation (Gs)
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B1 & B2
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Isoproterenol binds to this receptor and stimulates cAMP formation (Gs)
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B1 & B2
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Dopamine binds to this receptor and stimulates cAMP formation (Gs)
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DA1
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Dobutamine binds to this receptor and stimulates cAMP formation (Gs)
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B1
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Histamine binds to this receptor and stimulates cAMP formation (Gs)
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H2
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hormones that increase cAMP production
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FSH
ACTH Glucagon |
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Norepinepherine binds to this receptor and inhibits cAMP formation (Gi)
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a2
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Dopamine binds to this receptor and inhibits cAMP formation (Gi)
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D2
(DA activates) |
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Clonidine binds to this receptor and inhibits cAMP formation (Gi)
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a2
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Ach binds to this receptor and inhibits cAMP formation (Gi)
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M2
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Serotonin binds to this receptor and inhibits cAMP formation (Gi)
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5-HT1
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Morphine binds to this receptor and inhibits cAMP formation (Gi)
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u,K,S(delta)
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what breaks down cAMP within the cell?
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Phosphodiesterase (PDE)
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what inactivates Phosphodiesterase (PDE)?
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caffeine
theophylline |
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what is the main intracellular receptor for cAMP?
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Protein Kinase A
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what can cAMP bind to change gene expression?
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CREBs
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which G protein activates phospholipase C?
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Gq
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which intracellular components are upregulated in response to Gq receptor binding?
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IP3
DAG |
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what is the job of IP3 in the cell?
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increase Ca++ release from stores
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what is the job of DAG in the cell?
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activates protein kinase C
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Ach binds to this receptor to increase IP3 and DAG expression (Gq)?
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M1 & M3
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Norepinepherine binds to this receptor to increase IP3 and DAG expression (Gq)?
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a1
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Serotonin binds to this receptor to increase IP3 and DAG expression (Gq)?
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5-HT1c
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what is the vascular effect of an increase in cGMP?
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vasodilation
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how do you get from M and H receptor stimulation to cGMP?
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M/H- inc Ca++- calmodulin - NO synthase- NO- guanylyl cyclase- cGMP
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agonist
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stimulator
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antagonist
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inhibitor
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EC 50
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Effective concentration @ 50% of Max
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KD
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Drug concentration at which 50% of the receptors are occupied
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potency
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the dose required to elicit a particular effect
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how do you overcome the effects of a competitive inhibitor?
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increase the dose of the agonist to "out compete" the inhibitor
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how do you overcome the effects of a non-competitive inhibitor?
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you dont. they irreversibly bind to the receptor and block its function.
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what is functional antagonism?
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drugs/molecules that have opposite effects on a system
"one says right, the other says left" |
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what is chemical antagonism?
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antagonist directly effects the agonist.
I.E. inactivates its function |
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how can a partial agonist act as an inhibitor?
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via competitive inhibition when combined with a full agonist
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what is a constitutive receptor?
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a receptor that has a basal level of functioning without a ligand present
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what is an inverse agonist?
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a ligand that binds a constitutive receptor and decreases its activity
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what is efficacy?
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max effect of drug
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what is a graded dose-response curve
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a first order plot of dose vs response to that dose
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what is a threshold dose?
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the dose, below which, there is no response
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what is a quantal dose-response curve
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used to determine the dose that produces a therapeutic effect or a lethal effect
ED50 LD50 makes a therapeutic index (TI) |
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how do you determine the therapeutic ratio for mice?
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TR= LD50/ED50
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how do you determine the therapeutic ratio for humans?
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TR=TD50/ED50
TD= toxic dose |
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pharmokinetic tolerance
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the drug induces the enzymes responsible for its own metabolism
metabolic tolerance barbituates inc the metabolism of phenobarbitol and warferin |
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pharmicodynamic tolerance
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cellular tolerance
downregulation of receptors changes in receptor function |
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tachyphylaxis
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rapid development of tolerance
depleating of monoamine pool |
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physiologic tolerance
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functional antagonism
opposite effects |
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chemically induced hyperactivity/sensitivity
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increased catecholamine sensitivity when some patients are under anesthesia. (halothane)
also, some drugs upregulate receptor #s |
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surgically induced hyperactivity
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surgical damage to a pre-synaptic nerve that increases the activity of the post synaptic nerve when chemically stimulated
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examples of a deficiency in degradating enzymes that induces hyperactivity?
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inc in succinylcholine sensitivity with pts that have decreased cholinesterase activity
hemolytic anemia in patients who take primaquine and are G-6-P dehydrogenase deficient |
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how would competition for a binding site induce hyperactivity?
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if one drug displaces another from albumin, effectively increasing available drug in the sys
Warfarin and phenytoin |
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synergism
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the combined effect of both drugs is greater than the sum of the two individual effects
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potentiation
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a drug that does not have a specific effect, increases the effectiveness of another drug
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urticaria
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hives
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angioedema
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swelling beneath the skin
larger than hives |
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Type I hypersensitivity
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anaphylactic
IgE treat with IV epinepherine, .5mL of 1:1000 sln |
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Type II hypersensitivity
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cytotoxic (autoimmune)
IgM IgG usually subsides w/in months after withdrawl of drug |
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Type III hypersensitivity
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Arthus
Ag-Ab complex more common than anaphylaxis urticaria, arthritis, vasculitis, glomerular nephritis, lymphadenopathy subside after withdrawl sulfa, penicillins, thiouracil,anticonvulsants, iodides |
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Type IV hypersensitivity
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cell mediated, delayed hypersensitivity
contact dermatitis T-cell |
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what happens to patients that are administered succynlcholine that have a cholinesterase insufficiency/abnormality
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apnea
paralyzation fo 4-8 hrs |
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how do you determine if a pt has a cholinesterase abnormality?
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dibucaine number
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when should you show extreame caution in prescribing isoniazid?
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in individuals over 35
Slow aceytelators = b6 deficiency fast acytelators = hepatotoxic |
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what happens to slow aceytlators?
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they have low N-aceytltransferase activity and are prone to isoniazid induced, vit B6 deficiencys and anemia
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hemolytic anemia in african american males can be caused by
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primaquine
they are G-6-P dehydrogenase deficient |
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what drug can induce porphyria?
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barbituates
they increase the activity of ALA-synthase, the rate limiting step in porphyrin production |
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aqueous diffusion
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absorption of drugs through:
pores in membranes fenestrations |
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BBB and drug absorption
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brain does not have fenestrated capillaries
choroid plexus, pineal and pituitary, medium eminence, and area pastrema are exceptions to this |
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through what process is L-dopa delivered to the CNS
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facilitated diffusion
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rule of thumb for ionization
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acids like acids
bases like bases strong acids or bases are always ionized in the body |
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factors that influence drug absorption
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pH
circulation contact time solubility concentration route surface dissolution |
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how do you determine the volume of distribution?
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Vd= Dose/Co
Co=initial concentration in plasma |
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is a first order elimination a straight line in a linear plot or a semi-logrythmic plot?
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semi-log plot
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is a zero order elimination a straight line in a linear plot or a semi-log plot?
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linear
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how do you calculate clearance?
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CL= Vd x Kel
CL= Vd x (.7/t1/2) |
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how many half lives does it take to generate a steady state condition and concentration?
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about 5
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what will shortening the dosing interval do to the ss concentration?
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increase it
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what type of drugs can not achieve a ss level?
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drugs with zero order kinetics
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what happens if you give a dose higher than the elimination rate for zero order kinetic drugs?
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it creates toxicity
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how do you determine dosing rate or elimination rate?
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DR=ER= (CL x TC)/ F
F=bioavailability |
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how do you determine the maintenance dose?
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MD= (CL X TC)/F x t
t=dosing interval |
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how do you determine the loading dose?
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LD= Vd x TC
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what are phase I rxns?
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usually convert lipid soluble drugs into polar metabolites by introducing or unmasking functional groups
I.E. OH, SH, NH2 |
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what happens in phase II rxns
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OH- groups are conjugated with glucuronic acid or sulfate
makes the molecule have a larger molecular weight and becomes more polar |
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where are molecules with a molecular weight of less than 350 excreted?
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kidney
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where are molecules with a MW of larger than 350 excreted?
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into bile and subsequently, the GI tract
can be metabolized by microbes, reactivated, and reabsorbed |
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inhibitors of p450
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quinidine- competitive
ketoconazole- non-competitive |
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list some inducers of microsomal oxidase and conjugating systems in the liver
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acetominophen
rifamycins ethanol carbamazepine |
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what is the only phase II enzyme that is microsomal?
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glucoronyl transferase
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asside from p450 what is ethanol metabolized by?
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alcohol dehydrogenase
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what inactivates 6-mercaptopurine
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xanthine oxidase
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what inactivates norepinepherine, tryamine, and 5-hydroxytryptamine
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monoamine oxidase
(MAO) |
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what is warfarin inactivated by?
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a reduction reaction done by CYP2A6
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what groups are most commonly involved in conjugation rxns during Phase II rxns?
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glucuronyl, sulfate, methyl, acetyl, glycyl, and glutathione
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what is the enterohepatic circulation?
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recycling of conjugated drugs that are excreted into the GI from bile.
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enzyme inducers
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Rifamycins
barbituates phenytoin carbamazepine glucocoritcoids smoking grilled foods cruciferate veg dioxin st johns wart |
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CYP3A4 inhibitors
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ketoconazol
itraconazol ritonavir erythromycin clarythromycin diltiazem nicardipine verapamil grapefruit juice fluoxetine cimetidine amiodarone paroxitine |
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CYP2D6 inhibitors
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quinidine
SSRI's |
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acute toxicity
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1 to 2 days
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subacute toxicity
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up to 3 months
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chronic toxicity
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greater than 3 months
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when is a gastric lavage reccomended?
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within 4 hours of ingestion
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contraindications of gastric lavage
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> than 30min after ingestion of a corrosive material
if hydrocarbon solvents have been ingested coma, stupor, delierium, convulsions |
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when should you not use ipecac or induce vomiting?
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same contraindications ad lavage
Also, if under 6 months old |
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drugs that reduce absorption or enhance elimination
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activated charcoal
ipecac ammonium chloride: acidify urine sodium bicarbonate: alkalinize the urine Magnesium sulfate: cathartic mannitol: diuretic |
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drugs that chelate
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deferoxamine mesylate: iron
dimercaperol: arsenic, gold, mercury, lead Edetate: lead penicillamine: wilsons disease, cystinuria, copper succimer: lead |
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drugs that inactivate toxins
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atropine:counteract cholinesterase inhibitor poisons
prolidoxamine chloride: cholinesterase reactivator (only for organophosphates) flumazinil:benzodiazipine overdoses |
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naloxone
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opioid antagonist
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cyanide antidote package
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sodium nitrate
sodium thiosulfate amyl nitrate |
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glucagon is used when
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poisoned with B- blockers
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when do you give ethanol
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to counteract methanol or ethylene glycol ingestion
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fomepizole
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for ethylene glycol poisoning
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when do you give sodium bicarb?
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to treat overdose with cardiac depressants
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diazipam
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for chemical induced convulsions
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pyridoxine
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used for isoniazid
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Mech of botulinum toxin
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prevents the release of Ach from cholinergic vessels
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sympt of botulinum toxin
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vomiting
double vision muscular paralysis |
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treatment of botulinum toxin
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emisis or catharcis (dep on timeframe)
support vitals administer ABE botulinus antitoxin |
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symp of bacterial food poisoning
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vomiting
mild fever dehydration occasionally shock GI inflammation |
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treatment of bacterial food poisoning
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anti-emetic in severe cases
fluid intake supportive treatment |
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symptom of bleach ingestion
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severe irritation
hypotension delirium coma |
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treatment of bleach ingestion
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remove from skin by flooding
give milk, ice cream, beaten eggs, antacids support vital signs |
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agricultural poisons
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organophosphates
carbamates strychnine |
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symp of organophosphate poisoning
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SLUD (salivation, lacrimation, urination, deification)
mild; head ache, dizzy, weak, anxious, moderate: nausea/vomiting, abdominal cramps, sweating, slow pulse, muscle twitching (fasciculations) Severe: pin-point nonreactive pupils, resp diff, pulmonary edema, cyanosis, coma, heart block |
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treatment of organophosphate poisoning
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small dose of atropine, inc as needed
2-PAM to reactivate enzyme emisis if recent support vitals |
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what is the only difference when treating carbamate poisoning vs organophosphates?
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do not use 2-PAM
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mech of strychnine
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competitive antagonist of glycine (inhibitory neurotransmitter)
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sympt of strychnine poisoning
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convulsions with sensitivity to stimuli
death from resp paralysis |
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treatment of strychnine poisoning
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support vitals
IV diazipam or succinylcholine (both for prevention of convulsions) activated charcoal to prevent further absorbtion |
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herbicides mentioned in lecture
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chlorophenoxy compounds
dinitrophenols paraquat |
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complications with herbicide poisoning
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not terribly harmful unless in mass quantities
ROS production inc metobolic rate and temp |
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halogenated hydrocarbons
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CCL4
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Mech, sympt, and treatment for methanol poisoning
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metabolized to formaldehyde and formic acid
acidosis, visual disturbances, resp fail emisis, IV ethanol 50%, fomepizole, sodium bicarb for acidosis |
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treatment of acute alcohol poisoning (500mg)
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hemodialysis
support vitals |
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what is disulfiram?
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inhibits acetylaldehyde dehydrogenase
tha accumulation of acetylaldehyde when mixed with EtOH causes nausea and vomiting |
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sympt and treatment of petrolieum distillates
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pulmonary irritation
CNS depression severe pneumonitis support vitals |
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sympt of aromatic hydrocarbons
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CNS stimulation, followed by depression as dose increases
kidney and liver damage cardiac arrhythmias aplastic anemia and leukemia with prolonged exposure |
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treatment of aromatic hydrocarbon poisoning
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gastric lavage
IV diazipam for convulsions |
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symptoms of oxalic acid and oxalate poisoning
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local irritation and GI corrosion
calcium chelation, leading to muscle convulsions, weakness, or colapse renal tubular damage |
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treatment for oxalate or oxalic acid poisoning
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precepitate it out of the GI by giving calcium in any form
force fluids to prevent Ca++ chelations from damaging the kidney (IV Calcium gluconate) |
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sympt of hydrochloric/ sulfuric acid poisoning
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irritation to necrosis of any part of the GI exposed
death is due to hypovolumic shock |
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treatment of hydrochloric/sulfuric acid poisoning
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No emisis or lavage
dilute with water give analgesics for pain milk of magnesia support vitals |
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sympt of hydroxides/drain cleaners
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irritation to necrosis
more penitrating than acids death due to hypovolumic shock |
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treatment of hydroxides/drain cleaners
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No lavage or emisis
water for dilution support vitals |
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sympt of arsenic poisoning
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Acute: GI disturbences, CNS effects leading to coma, ventricular arrhythmias, renal tubular damage
Chronic: polyneuritis, nephritis, dermititis, cardiac failure, cirrhosis, altered sensorium |
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treatment of arsenic poisoning
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lavage
dimercaprol or penicillamine to chelate |
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sympt of lead poisoning
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lead line on the gums
basophilic erythrocytes accumulation of aminolevulenic acid (inhibition of heme synth) colic CNS effects hyperirritability coma and convulsions wrist and ankle drop |
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treatment of lead poisoning
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remove unabsorbed lead
treat symptoms in severe CNS toxicity, treat with chelation |
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sympt of Iron overdose
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severe GI irritation to necrosis
resulting in acidosis, hypotension, and shock vomiting blood coma shock blue lips and fingernails palor |
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treatment of iron overdose
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lavage within the first hour
IV and Oral deferoxamine support vitals |
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sympt of mercury poisoning
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abdominal pain and vomiting
swollen, bleeding gums mad hatters disease parasthesia ataxia constriction of visual field diarrhea renal necrosis shock |
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treatment of mercury poisoning
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lavage or emesis
milk, raw eggs activated charcoal IV dimercaprol |
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Dimercaperol (BAL) is used for?
|
arsenic, lead, gold, inorganic mercury
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Calsium disodium etetate is used for?
|
lead and zinc
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penicillamine is used for?
|
copper (wilsons disease)
arsenic cystinuria |
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dimercaprol route of administration
|
IM
7-14 days |
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succimer is used for?
|
lead
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What is the benefit for administering succimer?
|
it can be administered orally for lead poisoning
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what is deferoxamine used for?
|
iron chelation
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deferoxamine route of administration
|
orally
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symptoms of nitrite poisoning
|
chocolate blood
hypotension cyanosis coma resp fail |
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what do nitrites do to heme?
|
convert hemoglobin to methemoglobin
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treatment of methemoglobinemia, nitrite poisoning
|
methylene blue
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sympt of CO poisoning
|
cherry red blood
headache, dizzyness, stupor |
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treatment of CO poisoning
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100% O2
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cherry red blood
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CO poisoning
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chocolate blood
|
nitrate or dapsone poisoning
methemoglobinemia |
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what does cyanide smell like?
|
almonds
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mech of cyanide toxicity
|
binds cytochrome oxidase and prevents respiration
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sympt of cyanide poisoning
|
dizzyness
headache hypotension unconciousness convulsions resp failure |
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immediate treatment for a patient in a coma and having seizures
|
airway and seizure control
IV diazipam |
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|
ingested acetominophen and alcohol intake =
|
liver damage
|
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what do ingested saylicates or barbituates do to urine
|
alkalinize the urine
|
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young patient presents with heart attack. first thing you think
|
cocaine
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young patient with psychosis. first thing you think?
|
metamphetamine
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pinpoint pupils
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opiates
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farmer, orchard, SLUD
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organophosphates
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child in renovated house, mental retardation, CNS issues
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Lead poisoning
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use 2-PAM for
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organophosphates
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do not use 2-PAM for
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carbamates (insecticides, polyurethanes)
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where would you find halogenated hydrocarbons
|
fire extinguisher
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treatment for a pt with acidosis and methanol poisoning
|
50% EtOH
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treatment for ethylene glycol poisoning
|
50% EtOH
fomepizole |
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wrist drop and/or ankle drop sign
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lead poisoning
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tremor, stomatitis, emotional instability
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mercury poisoning
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