- I: High potential for abuse/dependency no therapeutic value: heroine, PCP et al - II: High potential for abuse/dependency; Written prescription only, No refills - III: Moderate potential for abuse; Written or oral prescription, 5/6mo refills - IV: Limited potential for abuse; Written or oral prescription, 5/6mo refills - V: Limited potential for abuse; Prescription or OTC

- I: serious health effects or death: contaminated Abx - II: temporary or medically reversible adverse health consequences: - III: Not likely to cause any health effects: quantity packaging error

- Activated charcoal: superior to emesis and gastric lavage - Emesis and gastric lavage: especially if < 1 hour postexposure - Cathartics: laxatives or whole bowel irrigation

Two treatment options: - nitrates -> methemoglobin + methylene blue -> hemoglobin - hydroxycolobamin -> cyanocolobamin (soluble excretory product)

Nicotinic receptors are preganglionic autonomics; Sympathetic and parasympathetic activation. Stimulation followed by inactivation - insecticide is highly toxic -> coma, resp arrest, HTN, arrythmias, - Trt: symptomatic; usually if pt survives 4 hours recovery is good

Arsenic and inorganic/elemental mercury - in cases of severe lead poisoning, add it to calcium EDTA - not H2O soluble (admin with 10% peanut oil) - succimer and unithiol superior agents

Use in children with blood [lead] > 45 ng/dl and adults - arsenic and mercury poisoning - water soluble - prodrug: binds cystines to form mixed disulfides - comparable to parenteral EDTA, and is used more commonly now - does not affect other Ca, Zn, Mn

- primarily lead - zinc, manganese, certain heavy radionuclides - 1 hour 1/2 life - nephrotoxicity if not careful (hydration, low adequate dose)

Toxicology Flashcards by Jordan Jacobsen

Drug testing process

Earliest analysis is toxic effects followed by IND application
Clinical trials
- Phase 1: Healthy volunteers; safety concerns and dosages
- Phase II: diseased PTs., toxic effects
- Phase III: large number of PTs., effectiveness, rare side effects
- Phase IV: post marketing research, verification
- ANDA: generic release
- Phase IV: research

How well did you know this?

Not at all

Perfectly

Orphan drugs

Drugs for diseases that have that effect Less than 200,000 people

How well did you know this?

Not at all

Perfectly

Dosage adjustment equation

Body Surface Area(M^3)/1.73 x adult dose

How well did you know this?

Not at all

Perfectly

Category A,D and X

A - no known risks to fetus
D - risk to fetus, therapeutic effect may justify use
X - significant risk to fetus: Do not use in pregnant pt

How well did you know this?

Not at all

Perfectly

Schedules

I: High potential for abuse/dependency no therapeutic value: heroine, PCP et al
II: High potential for abuse/dependency; Written prescription only, No refills
III: Moderate potential for abuse; Written or oral prescription, 5/6mo refills
IV: Limited potential for abuse; Written or oral prescription, 5/6mo refills
V: Limited potential for abuse; Prescription or OTC

How well did you know this?

Not at all

Perfectly

Recall classes

I: serious health effects or death: contaminated Abx
II: temporary or medically reversible adverse health consequences:
III: Not likely to cause any health effects: quantity packaging error

How well did you know this?

Not at all

Perfectly

Dialysis of toxins

Primarily a function of volume of distribution

- High Vd indicates low chance of success and visa versa

How well did you know this?

Not at all

Perfectly

ABC’s of poison treatment

Airway, breathing, circulation, dextrose
- Alcohol: thiamine (avoids Warneke’s encephalopathy)
- Opioid: Naxalone (narcan)
- Benzodiazepine antagonist (flumazenil)
Assess exposure especially if anyone else may have been affected

How well did you know this?

Not at all

Perfectly

Poison treatment physical exam

Vitals, eyes, mouth, CNS, abdomen, skin

How well did you know this?

Not at all

Perfectly

Decontamination

Activated charcoal: superior to emesis and gastric lavage
Emesis and gastric lavage: especially if < 1 hour postexposure
Cathartics: laxatives or whole bowel irrigation

How well did you know this?

Not at all

Perfectly

Acetaminophen toxicity

P450 converts acetaminophen to NAPQI which is then typically converted to an excreta bowl conjugate via glutathione

In an acetaminophen glutathione gets overloaded, and the toxic NAPQI builds up and causes hepatotoxicity
N-acetylcystine, a glutathione precursor is administered to handle the toxic metabolite overload

How well did you know this?

Not at all

Perfectly

Cyanide poisoning

Two treatment options:

nitrates -> methemoglobin + methylene blue -> hemoglobin
hydroxycolobamin -> cyanocolobamin (soluble excretory product)

How well did you know this?

Not at all

Perfectly

Nicotine poisoning

Nicotinic receptors are preganglionic autonomics; Sympathetic and parasympathetic activation. Stimulation followed by inactivation

insecticide is highly toxic -> coma, resp arrest, HTN, arrythmias,
Trt: symptomatic; usually if pt survives 4 hours recovery is good

How well did you know this?

Not at all

Perfectly

Halogenated aliphatic hydrocarbons

Carbon tetrachloride, chloroform

chloriform is a CNS depressant
carbon tet is hepatotoxic
trt: support/symptomatic

How well did you know this?

Not at all

Perfectly

Heavy metal toxicity: Arsenic

Toxin and toxicant (natural and man made)
- MOA: Interferes with oxidative phosphorylation, cell signaling and gene expression
- clinical effects: often seen in manufacturing processes and water supplies/aquatic sources
~ pancytopenia
~ Gastroenteritis
~ Cardiovascular: shock/arrhythmias
~ CNS: encephalopathy, peripheral neuropathy

How well did you know this?

Not at all

Perfectly

Heavy metal toxicity: lead

Organic and inorganic forms
Inorganic: deposits in bone (X-ray diagnosis)
- MOA: interferes with essential cations
- Clinical affects: CNS and peripheral neuropathy, HTN, repro toxicity
- can be excreted in breast milk
Organic:
- MOA: hepatic dealkylation (fast) trialkylmetabolites (slow)
- clinical findings: encephalopathy

How well did you know this?

Not at all

Perfectly

Heavy metal toxicity: elemental mercury

MOA: enzyme inhibition, membrane alteration
clinical findings: tremor, behavioral changes, gingivostomatitis, acrodynia; high dose pneumonitis
Higher tissue distribution then the other mercury types

How well did you know this?

Not at all

Perfectly

Heavy-metal toxicity: inorganic Mercury

MOA: inhibits enzymes; alters membranes

- clinical findings: Acute tubular necrosis, GI

How well did you know this?

Not at all

Perfectly

Heavy metal toxicity: organic mercury

MOA: alters enzymes, microtubules and neuronal structure

- clinical findings: CNS and birth defects

How well did you know this?

Not at all

Perfectly

Heavy metal chelators

Dimercaperol
Succimer
Penicillamine
Calcium EDTA
Ferroxamine
Unithiol
Dferoxamine

How well did you know this?

Not at all

Perfectly

Dimercaperol

Arsenic and inorganic/elemental mercury

in cases of severe lead poisoning, add it to calcium EDTA
not H2O soluble (admin with 10% peanut oil)
succimer and unithiol superior agents

How well did you know this?

Not at all

Perfectly

Succimer

Use in children with blood [lead] > 45 ng/dl and adults

arsenic and mercury poisoning
water soluble
prodrug: binds cystines to form mixed disulfides
comparable to parenteral EDTA, and is used more commonly now
does not affect other Ca, Zn, Mn

How well did you know this?

Not at all

Perfectly

Calcium EDTA

primarily lead
zinc, manganese, certain heavy radionuclides
1 hour 1/2 life
nephrotoxicity if not careful (hydration, low adequate dose)

Ferroxamine

Iron and aluminum

Unithiol

- increases excretion of mercury, arsenic and lead | - associated with sever allergic rxns, Stevens-Johnson syndrome

Penicillamine

- D is less toxic than L isomer - readily absorbed in the gut - copper chelators: Wilson's disease

Deferoxamine

- Iron chelator - in combo with dialysis useful for treatment of aluminum toxicity in renal failure - IM/IV - can cause hypotension and increased susceptibility to yersinia enterocolitica

Chlorinated hydrocarbons (4) ABCD

- insecticides: DDT, Benzine Hexachlorides, cyclodienes, toxaphens

DDT

- Poor dermal absorption - prevents inactivation of Na channels -> depol of neurons - inhibits Ca transport -> increases neuronal excitability - symptomatic treatment

bipyridyl herbicide: paraquat

Oral toxicity - free radical production - initially GI irritation hematemesis, bloody stools - accumulation in lungs-> edema, alviolitis, progressive fibrosis - treat with activated charcoal, gastric lavage and symptomatic care; PROMPT IS KEY

Chlorophenoxy herbicides

- increased risk of Hodgkin's lymphoma - 2,4 D: large doses req for coma/hypotonia. Symptoms last weeks -2,4,5D: coma more muscular effects - TCDD: by product of combustion of organic + chlorine ~ MOA: Aryl Hydrocarbon receptor ~ forest fires, bleaching, waste incineration ~ agent orange ~ Chloracne ~ human tumor promoter

Organophosphates

- MOA: AChE inhibition-> hypercholinergic effect: DUMBELS | - trt: atropine and pralidoxamine (AChE agonist)

Carbamate insecticides

- less toxic, effects more transient | - pralidoxamine is not indicated

Venomous vs. non venomous snakes

- triangular head - pits AND nostrils - elliptical pupil - undecided scales on underside of tail

Jimsom weed

- all parts toxic - contains atropine, scopolamine, hyocyanamine - anticholinergic effect: mydriasis, flushed dry skin, agitation, tachycardia, hyperthermia, hallucinations

Death cap mushroom

- amanitin: inhibits RNA Pol II -> hepatocellular necrosis | - death may occur 4-9 days after infection

Alcohol toxicity treatment

Administration of thiamin helps avoid Wernecke's encephalopathy

Opioid overdose treatment

Naxalone (Narcan)

SO2

- combustion of fossil fuels: colorless irritant - clinical: bronchospasm, pulmonary edema - trt: support

NO2

- waste fires and silage on farms: brown irritant - clinical: bronchial irritation, pulmonary edema - trt: support

- causes tissue hypoxia; HA followed by confusion, deteriorating visual acuity, coma, seizures, death - Trt: pure O2; hyperbaric oxygen therapy may help

Aromatic hydrocarbons

Benzene, toluene, xylene - CNS depression, ataxia, coma - industrial, chemistry settings - trt: support

Rotenone

Plant insecticide - irritant: dermatitis, GI irritation - trt: symptomatic

Pyrethrum

- plant alkaloid insecticide - most commonly irritation: contact dermatitis, CNS excitation -> seizures - trt: generally support, anticonvulsant

Glyphosate

Irritant | Trt: Support

PCB (polychlorinated biphenyls)

- bioaccumulate in food chain, electrical equipment manufacturing - dermatotoxic, screws with liver enzymes

TDCC

by-product of combustion of organic + chlorine ~ MOA: Aryl Hydrocarbon receptor ~ forest fires, bleaching, waste incineration ~ agent orange ~ Chloracne

Membrane depressant cardiotoxic drugs OD

- tricyclic antidepressants, quinidine | - trt: bicarbonate, sodium

Fluoride OD

- calcium channel blockers | - give calcium

Short acting beta-blockers OD

- theophylline, caffeine, metaproterenol | - esmolol

Methanol, ethaleneglycol OD

Ethanol, fomepizol easier to use

Benzo OD

Flumazenil | - Cind: seizures, benzo dependance

Delirium caused by anticholinergic agents

Phyostigmine

B-blocker OD

Glucagon

Fomepezil

Methanol/ethylene glycol antidote

Previously healthy patient presents to the emergency room after burning refuse. He is suffering from headaches, nausea, dizziness and is cyanotic and upon admission begins to seize. His breath has a distinct odor of bitter almonds.

Diagnosis: cyanide poisoning - cytochrome C oxidase inhibition Trt: hydroxycolobamin or nitrates/sodium thiosulfate followed by methylene blue.

45-year-old man previously healthy reports to the ED with Bright cherry red skin on his extremities, nausea/vomiting dizziness, confusion. The wife reports that he was working out in his shop and had a small kerosene heater burning when she found him.

Diagnosis: CO poisoning (looks just like cyanide poisoning: clues in history) Trt: 100% O2 and hyperbaric therapy