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43 Cards in this Set

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What is the most common ingestant?
What is the number 1 cause of death due to pharm ingestion?
Salicylates (pKa, protein, dialyzable, tox half life)
pKa = 3.5 (weak acid)
90% protein bound
Easily Dialyzable
Tox Half life = 20hrs.
Salicylates Elimination
Mainly via conjugation but becomes overwhelmed and becomes Michaelis-Menten elim in OD.
Sialicylates TOX mech
Uncouple ox phos leading to increased metabollic rate, hyperventillation, heat production and acidosis. Increased glycolysis leads to hyperglycemia. Kids get hypoglycemia.
Also Interfere with coagulation factors leading to hypoprothrombin, capillary fragility, decreased platelet adhession, and throbocytopenia.
Salicylates antidote
Vit K for coagulation
Sodium bicarbonate for the acidosis and to decrease absorbtion and increase secretion.
Salicylates and Fetus
Crosses placenta. May cause metabolic acidosis in newborn, possible teratogen, contraindicated in 3rd trimester.
Sodium Bicarbonate
Used to correct metabollic adicosis from ethylene glycol poisoning or when there are high loads of acid. Can also fix wide complex ventricular rythems from tricyc antidepressant poisons and other drugs that block Na channel. Used to alkalinize urine, increaseing excretion of weak acids. Also used to decrease crystalization of -globins in renal tubules.
Acetominophen Elimination
Mostly by glucuronidation, but some by CYP 2E1 > NAPQI. NAPQI is detoxed by glutathione.
Peak plasma levels may be delayed if co-ingested with narcs and GI slowing drugs.
Acetominophin TOC mech
If there is insufficient glutathione, NAPQI binds to macromolecules causing hepatic damage.
Used for acetaminophen TOX. Promotes glutathione synth and offers a harmless substitute for active metabolites of acetaminophen to bind to.
NSAIDs types
-Propionic acids (ibuprofen, naproxen, ketoprofen, oxaprozin)
-Acetic acids
Symptoms of an NSAID overdose
-CNS depression
-Resp depression
-Metabolic acidosis
-Renal Insuficiency
NSAID treatment
If 200-400 mg/kg are ingested, should treat with activated charcoal and gastric emptying. >400 is a serious tox risk.
CAD toxicity
-Excessive NE reuptake blockade
-Direct quinidine-like effect (blocks fast inward Na influx in hert)
-Central plus peripheral anticholinergic effects.
NE excess can lead to NE depletion. May see arrhythmias, bradycardia, hypotension, cap collapse.
Tricyclic antidepressants
Direct inward fast sodium and potassium rectifier channel blockers
Cyclic Antidepressant treatment
Alkalinization with NaHCO3 and +/- hyperventillation
NA bolus to overcome sodium channel blockade.
Iron Tox
Free iron is catalyzes redux reactions > lipid peroxidation + free rad formation. Get hypotension, hypovulemia, cellular damae from free radicals. Get acidosis via:
-tissue hypoperfusion and lactate formation
-hydration of ferric ions
-disruption of ox phos.
Chealates iron. Turns urine, sweat, skin red. Adverse effects include hypotension, acute lung injury, anaphylaxis.
Chronic use correlated with hearing and visual loss. Also associated with yersinia sepsis and mucormycosis.
Anticonvulsants names
carbamazepine, valproic acid, phenobarbital, and phenytoin.
Anticonvulsant OD symptoms
Nystagmusm ataxia, depressed sensorium, convulsions, coma.
Carbamazepine (CBZ) TOX
Respiratory depression, apnea, decreased GI motility (causing delay in Cmax)
Crosses placenta and is a terat.
Major metabolite, CBZ-E is toxic and takes a while to peak.
Anticonvulsant mechs and treatment
CBZ is an NA channel blocker. Treat with supportive care and multi dose activated charcoal.
Valproic acid enhances GABA. May consume carnitine and affect mito FA oxidation.
Phenytoin blocks Na channels.
Phenobarbital is GABAergic. Supportive care plus charcoal.
Opiates types
Opiate TOX
-CNS depression/coma
-Seizures (esp. meperidine)
-Resp depression and pulmonary edema.
Opiate antagonist. works on mu-1,2, kappa, and sigma.
Coaine mech
CNS stimulant, blocks repuptake of nori and promotes release. Blocks presynaptic monoamine transporter.
Slow on/off sodium channel blocker, fast on off potassium rectifier.
Early stim, late depression
Cocaine TOX
-CNS hemorrhage
-Pul edema
Cocaine / metabolite ratios
A ration of BE:cocaine > 100:1 means use was more than 10 hours prior (cocaine detected 24-36 hours)
Psychostimulant types
Cocaine, amphetamines and derrivatives, and methylphenidate.
Psychostimulant mechs
Induce catecholamine release and block transporters (DAT)
Amphetamine elimintaion
Resistant to COMT and MAO. Metabolized via p450. Polymorphisms of CYP2D6 are important.
Amphetamine tox
-CNS hemorrhage
PCP mech and tox
Antagonizes effect of glutamate on NMDA receptor by blocking calcium influx. Can cause tachycardia, hypertension, and rhabdomyolysis
7 qualifiers for substance abuse (need 3 or more within a 12 month period)
1) Tolerance leading to more drug needed for effect
2) Diminished effect from continued use of same amount
3) Withdrawal involving tachycardia, tremors, NV, anxiety, hallucinations.
4) Substance taken in larger amounts of for a linger period than intended or an unsuccessful attempt to cut down.
5) SIgnificant time spent obtaining and doing drug.
6) Social/occupational/recreational activities are reduced because of drug
7) Use is continued despite knowledge of it causing a physical or psychological problem.
SSRIs examples and tox
Fluoxtine, paroxetine, sertraline, and fluoxamine. Less toxic than CADs but can cause seritonin toxicity when combined with other drugs.
Sedative/hypnotic mechs
Barbituates cause excess GABA leading to CNS depression and resp. depression.
Benzo increases GABA tone.
Competitive antagonist of benzo at the GABA-a receptor. Dont use if there is possibility of mixed OD leading to seizures (CAD, cocaine, unknown)
Atypical antipsychotics
Safer than conventional. Can cause, hypotension, tachycardia, prolonged QT and widened QRS. Possible hepatotox and electrolyte imbalance.
Atypical antipsychotic with a novel mech. Stabalizes dopamine by causing a D2 blockade in excess but maintains a basal D2 level if at shortage.
OD effects include somnolence, anxiety, ataxia, and dystonia. NMS possible.
Digitoxin mech and tox
In overdose poisons the Na/K ATPase pump. Get increased intracellular calcium, brady cardia, arrhythmias, hyperkalemia.
Cardiac glycosides examples
Digoxin, oleander
Digoxin antidote
Digoxin specificc antibody fragment. Abs reach cardiac sites where digoxin is inhibiting ATPase, binding it and removing it from the tissue.