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43 Cards in this Set

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A pt presents w/ hypotension & bradycardia from a Ca2+ channel blocker overdose, what do you need to do to tx & prevent reflex tachycardia?

Ca2+ Chloride infusion

if CV contractility depressed--> glucagon (used for BOTH Ca2+ or Beta blocker ODs)

Erosives & caustic agents can cause rapid skin toxicity. The higher the _________, the faster the absorption.

higher lipid solubility

In addition to antidotes, what else can be used to help remove toxic substances?

(toxicology txs)

*after tx, hold pt for 48 hrs to monitor for rebound toxicity! (goes into adipose & may redistribute rapidly)

activated charcoal- slows absorption & spread of toxin, can cause N/V & constipation

body surface irrigation- prevents further absorption

Ionized diuresis- enhances excretion of weak acids & bases using sodium bicarb, ammonium Cl, Vit C, cranberry juice, etc

urinary alkalinization- enhance elimination & excretion

What drugs undergo biotransformation & become more toxic (usually become active metabolites)?

organophosphates (irreversible Ach inhibitor--> dumbells)




(aspirin, iron, & acetaminophen are the mc household substances that cause toxicity)

What drugs cause photosensitivity?

(antimicrobials- QSTs)




Q: Pt is recieving a drug w/ a clearance of 100 mL/min. If a target blood level is 1 mcg/mL & pt is going to be injected every 4 hrs, what dose should be injected (maintenance dose)?

A: 24,000 mcg

Maintenance dose = Clearance x concentration at steady state x time (minutes)**

= 100 mL/min x 1 mcg/mL x 240 min (4 hrs)

= 24,000 mcg

(steady state conc = target blood level!)

________cause toxic neoplasm (cancer)

nitrogen mustard

TCA's, cocaine, & amphetamine ODs can all cause __________


Furosamide diuretics & barium salt can cause toxic_________


Spironolactone & ACE inhibitors can cause toxic________


_______ OD causes toxic hepatic injury

d/t accumulation of NAPQI (N-acetyl-para-benzoquinoneimine) in the liver

What causes NAPQI to accumulate?


glutathione depletion

*acetaminophen undergoes glutathione conjugation & gets excreted, w/o glutathione, it undergoes CYT P450 metabolism & toxic NAPQI is produced

*most likely to occur in acetaminophen OD d/t suicide attempt OR in alcoholic pts (alcohol induces glutathione pathway & causes incr NAPQI production)

Large stores of glutathione lead to delayed presentation of acetaminophen OD.

How do pts present?

No sx until initially

12-24 hrs--> N/V, bloody diarrhea, & GI shock

3-5 days--> RUQ tenderness, jaundice, hypoglycemia (liver damage)

*CONFIRM w/ LFT & APAP testing!!

Acetaminophen OD must be tx ASAP!!

__________ is given to replace glutathione, BUT there is no tx to reverse the hepatic damage that has already occurred, ONLY prevent worsening.

*If recent OD, may give activated charcoal to prevent further drug absorption

What else can be given for symptomatic relief?

N-acetylcysteine (NAC)- glutathione precursor, helps replenish glutathione to prevent further NAPQI accumulation & damage

Ondanestron (anti-emetic) can be given to relieve GI sxs

_________ OD causes rapid & toxic CNS depression-->

diminished breathing,

low body temp &

skin reddening

Tx: bicarbonate, why?


bicarbonate reduces proximal tubular reabsorption-->

increases renal excretion

NSAID's & ethylene glycol OD's can cause ______

renal dysfunction

How do you reverse anuria from renal dysfunction?


(osmotic diuresis)

Pt presents w/ CNS & respiratory depression, peripheral neuropathy, nephrotoxicity*, opthalmalogic & GI sx after consuming unknown liquid. Blood tests reveal anion gap & profound metabolic acidosis. Urine reveals oxalate crystals.

What is the liquid?

What antidote should be given to prevent fatal renal failure?

Ethylene glycole


antidote: fomepizole (competitive ADH inhibitor)

if unavailable, infuse ethanol up to 100 mg/dL

Ethylene glycole forms a toxic metabolite ____________ that accumulates in the kidney & leads to serious nephrotoxicity--> renal failure

How should pts be tx if severe nephrotoxicity occurs or if pts become unresponsive?

calcium oxalate

hemodialysis for severe poisoning & unresponsive pts

_______ presents similarly to Ethylene Glycol OD, w/ peripheral neuropathy, ocular damage (--> permanent blindness*), & GI sxs.

Metabolic acidosis & tissue injury occurs occurs d/t formation of toxic formic acid.

How is metabolic acidosis tx?

(for any cause*)


(found in paint thinner & moonshine)

Tx: infusion of sodium bicarbonate-->

keep pH at 7.2 or above

How do you tx peripheral neuropathy caused by ethylene glycol or methanol OD?

ethylene glycol: pyridoxine + thiamine

methanol: leucovorin

Delayed toxicity usually arises d.t redistribution (esp in fat).

Delayed toxicity of __________ is very severe & presents w/ pulmonary fibrosis & smurf skin


Q: Pt on digoxin therapy suddenly develops toxicity w/ a plasma level of 4 ng/mL. Renal function is normal & half-life of digoxin is 1.5 days. How long should you withhold digoxin in order to reach a safer therapeutic dose (1 ng/mL is preferred, toxic about 2)?

A: 4.5 days

(3 half lives--> 4--> 2--> 1)

Pt who works on a farm presents w/ Diarrhea, Urination, Myosis, Bradycardia, Bronchoconstriction, Excitation, Lacrimation, Salivation, & Sweating (DUMBBELSS). Pt begins to experience muscular paralysis.

What toxic compound has he been exposed to?

What is the MOA?


(insecticides, etc)


irreversible acetylcholinesterase inhibitor-->

High lipophilicity, forms covalent irreversible phosphate bond w/ AchE-->

Ach overstimulation-->

desensitized nicotinic receptors at NMJ-->

neuromuscular paralysis

Organophosphate poisoning must be tx ASAP to prevent respiratory failure!

_________ is given as an antidote, but MUST be given quickly to work. Why?

Pralidoxime (2-PAM)

*breaks covalent bonds btwn organophosphate & AchE, but bonds get stronger w/ time "aging process" & 2-PAM no longer works

__________ can be given to reverse the systemic effects of Ach.

*There is no tx to reverse the neuromuscular paralysis (will reverse on own w/i 24 hrs).



-competitive inhibition of Ach muscarinic receptors

*Can't reverse desensitization of nicotinic receptors, need to wait for new receptors to form

_________ toxicity caused hypertension, tachycardia, fever, dry mouth, urinary retention, hallucinations, confusion

"dry as bone, red as a beet, hot as a pistol, blind as a bat, & mad as a hatter!"

how do you tx?


Antihistamines (1st gen- diphenhydramine)

TCA's (meperidine)

Jimson weed, mushrooms

tx: Physostigmine

(AchE inhibitor, that crosses BBB*)

Pt presents w/ tachycardia, hypertension, increased muscle tone, horizontal & frontal nystagmus & is action very agitated & aggressive.

What drug toxicity?



tx: Benzos (sedation), antipsychotics (haloperidol), beta blockers, activated charcoal (if recent)

______ toxicity;

abdominal cramping, seizures, anemia, neuropathy, fatigue-->

encephalopathy, GI shock & bleeding

*inhibits heme biosynthesis


Lead toxicity

(metal contaminants, house dust, occupational exposure)

Tx: antidote= dimecaprol w/ EDTA (chelation therapy)

Benzo for seizures

mannitol & corticosteroids if Incr ICP


Garlic breath & rice water stools*

severe abdominal pain, NV-->

GI hemorrhage-->

Hypotension, shock-->

convulsions, delirium, polyneuropathy

*disrupts oxidative phosphorylation


Arsenic toxicity


Tx: antidote = Dimecaprol (ASAP!)

Gastric lavage

O2 & electrolyte support

_________ toxicity:

severe N/V*, diarrhea, hematemesis-->

GI strictures, bowel perforation-->

CNS depression-->


*disrupts oxidative phosphorylation-->

mitochondrial damage (free radicals)-->

shift to anerobic metabolism

Iron toxicity

How is iron toxicity tx?

*Tx ASAP to prevent renal failure

antidote = deferoxamine mesylate (chelates iron, makes it wate soluble)

Bowel irrigation

__________ toxicity:

tissue ischemia & hypoxia-->

Decreased Cardiac Output-->

tachycardia, hypertension-->

MI, seizures, metabolic acidosis-->


*displaces O2 & forms carboxyhemoglobin (COHgb)


Carbon monoxide (CO)

(car generators, left on)

Tx: Hyperbaric O2 chamber

Benzo for seizures

Rapid infusion of ________ may cause cyanide poisoning.

*cyanide inhibits formation of ATP-->

CV, CNS, & respiratory depression

How is cyanide poisoning tx?


tx: amyl nitrite pearls (if unconscious) or sodium nitrite (cyanide binds methemoglobulin & forms cyanomethemoglobulin)--> then give sodium thiosulfate (breaks bond creating less toxic thiocyanate which is excreted & methemoglobulin)--> followed by methylene blue (if d/t nitroprussimide*)(generates oxyhemoglobin)


Sustained rapid eye movement, shivering, diarrhea, fever, seizures = ___________


Antidepressant toxcicity

* occurs w combos w/ St. John Wort & Meperidine, buproprion

= Serotonin syndrome

Tx: Benzos for seizures

bowel irrigation if sustained release buproprion

______ toxicity---->

anticholinergic effects

reflex tachycardia (alpha antagonist)

postural hypotension


TCA toxicity

tx: IV saline w/ vasopressors for hypotension

________ toxicity--->

tachycardia, hypertension-->

HA, N/V, abdominal cramps, delirium-->

rhabdomyolsis, MI

UA: benzoylecgonine


Cocaine toxicity

*benzoylecgonine is metabolite, remains in urine up to 5 days after use

Tx: nitroglycerin or phentolomine (for severe HTN, NEVER give beta-blocker)

Benzos (for agitation, anxiety, seizures)

Endoscopic removal (if d/t body packing)

O2, dextrose, thiamine

Combining alcohol w/ cocaine, leads to ___________ production-->

CV shock-->



*VERY toxic metabolite

Corrosive acids & alkalies (bleach, sulfuric acid, ammonia, etc) are EXTREMELY toxic-->

tissue burns-->

rapid perforation-->


(skin, GI, any body part in contact)


Tx: Endotracheal intubation (for respiratory distress)

Gastric lavage (stomach irrigation, NOT w/ emesis)

Dilution ASAP (milk or water)

Corticosteroids + Abx*

Toxic__________, can lead to stinging, burning-->

blistering, swelling (histamine release)-->

N/V, weakness, muscle fasciculations-->

hypotensive shock & CV collapse


Toxic Crotaline snake bite (venom)

(rattlesnakes, copperheads, cottonmouths)

tx: Crotaline polyvalent Fab (antivenom) +

Prednisone (Corticosteroids)

IV fluids (hypotension)

Anti-histamines, Antiinflammatories

*instruct pt to remain as still as possible to prevent further venom spread, further degranulation of mast cells & histamine spread

What type of antagonist interacts DIRECTLY w/ an agonist & NOT at all w the receptor?

Physiological antagonist

(Ex: vasodilators & vasoconstrictors, don't share receptors)

A pt taking warfarin following a recent heart valve surgery develops a UTI & is given Trimethoprim-sulfamethoxazole (bactrum). In addition to checking prothrombin time, what else needs to be done?

Reduce warfarin dose*

warfarin is highly bound-->

sulfonamides (bactrum) displaces warfarin-->

toxicity (need to reduce)

A multiple myeloma pt is taking vincristine, cisplatin, bleomycin & methotrexate. They develop declining renal fxn. What drug is responsible?


^alkylating agent, prevents DNA cross-linking, causes nephrotoxicity

________ would be responsible if the multiple myeloma pt presented w/ peripheral nephrotoxicity


^mitotic spindle inhibitor, strips axon sheaths--> peripheral neuropathy