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Rosen's > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Mechanism of acetaminophen toxicity

A

APAP metabolized to NAPQI. NAPQI is detoxified by glutathione.
When glutathione stores are depleted, NAPQI can bind to cell proteins in the liver→ hepatic cell death

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2
Q

4 clinical stages of APAP toxicity

  • Name
  • Time course
  • Symptoms
  • Signs
A

1: 0-12h, preinjury
- n/v, anorexia, malaise
- ↑ serum APAP concentration

2: 8-36h, liver injury
- n/v, RUQ pain
- ↑ AST

3: 2-4d, maximum liver injury
- Liver failure - encephalopathy, coagulopathy, acidosis
- Hemorrhage, ARDS, sepsis/SIRS, MOF, cerebral edema

4: >4d, recovery
- No symptoms
- Complete hepatic histologic recovery

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3
Q

Amount of APAP needed for acute ingestion to lead to toxicity?

A

> 10g total
Or >150mg/kg
(forty 325mg tabs, or twenty five 500mg tabs in 80kg adult)

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4
Q

Indication for treatment with NAC in APAP overdose @ 4h

A

APAP level > 150µg/mL at 4 hours

Based off of adaptation of rumack-matthew line

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5
Q

Patients at higher risk for hepatotoxicity with chronic APAP use? (4)

A

Chronic INH ingestion
Chronic etoh ingestion
(↑ CYP2E1 activity)

Malnourished
Severe dehydration

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6
Q

Indications for testing APAP and AST in chronic APAP ingestions for suspect APAP poisoning? (>6yo) (3)

A

Ingestion of >10g/d (or >200mg/kg/d, whichever is smaller) in 24h period

Ingestion of >6g/d (or >150mg/kg/d) over 48h period or longer

Symptomatic (RUQ pain/tenderness/jaundice/vomiting)

** consider if >4g/d for several days, AST >2x normal, evidence of APAP excess (serum >30µg/mL)

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7
Q

Indications for emergent HD following acute APAP ingestion (5)

A

Serum APAP >1000mg/L at 4h post-ingestion

Hepatorenal syndrome (Cr >3.5)

Metabolic acidosis with pH <7.30

Encephalopathy

↑ lactate (>3.5mmol/L)

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8
Q

Pathophysiology of ASA toxicity

A

Uncoupled ox phos → ↑ lactic/pyruvic acid and ↑ lipid metabolism → elevated anion gap acidosis

Stimulation of resp drive → respiratory alkalosis

↓ pH → more of salicylic acid becomes neutral charge → crosses BBB → neurotoxicity

Neuro effects: hypoglycemia, AMS, coma, seizure

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9
Q

Principles of treatment for ASA toxicity

A

Alkalinize blood (convert to charged form and prevent BBB crossing)
Alkalinize urine (enhance excretion)
Treat dehydration
Correct hypokalemia
Correct hypokalemia
HD if severe or refractory to conservative management
Intubate only if absolutely necessary

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10
Q

Manifestations of anticholinergic (antimuscarinic) toxicity

  • Peripheral
  • CNS
A

Peripheral - smooth muscle (intestinal, bronchial, cardiac), secretory glands (salivary and sweat), ciliary body of the eye
– tachycardia, HTN, hyperthermia, mydriasis, dry mouth, dry skin (lack of sweating), skin flushing, ↓ bowel motility, urinary retention

CNS: delirium characterized by confusion, mumbling speech, agitation, hallucinations, picking gestures, myoclonus, tremor, coma

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11
Q

Antimuscarinic (Anticholinergic) toxidrome (8)

A 
Mydriasis - "blind as a bat"
AMS - "mad as a hatter"
Dry mucous membranes - "dry as a bone" 
Dry, flushed skin - "red as a beet" 
Hyperthermia - "hot as hades" 
Urinary retention - "full as a flask" 
↓ bowel sounds/ileus
Tachycardia
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12
Q

Treatment for antimuscarinic/anticholinergic poisoning

A

Usually symptomatic treatment
IV bicarb if evidence of Na-channel blockade (QRS > 120ms)
Benzos for agitation/seizure

Physostigmine

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13
Q

MOA of physostigmine

A

Antidote for anticholinergic/antimuscarinic poisoning

Reversibly inhibits cholinesterases in PNS and CNS → ↑ ACh accumulation and subsequent competition with antimuscarinic blocking agent, occupying the receptor

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14
Q

Mechanism of action of MAOI’s

A

Monoamine oxidase A (MAO-A): deaminates serotonin and NE

Monoamine oxidase B (MAO-B): deaminates phenylethylamine

Both equally metabolize Tyramine and dopamine.

MAOI’s can be selective or non-selective.

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15
Q

Examples of MAOI’s

Early MAOI’s
-Selective MAOI’s

A

Early: phenelzine, isocarboxazid, tranylcypromine - non-selective, irreversible

Selegiline - irreversible MAO-B used for Parkinson’s, metabolized to L-methamphetamine

Linezolid, reversible MAO-A inhibitor

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16
Q

Mechanism of MAOI toxicity with Tyramine

A

Tyramine - indirect acting sympathomimetic present in aged cheese ,red wine, smoked/pickled/aged meats

When MAO-A is inhibited, tyramine is not metabolized in gut/liver → systemic absorption → enters presynaptic vesicles → release of NE and serotonin into synapse → hypertensive crisis, as well as HA, flushing, diaphoresis

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17
Q

Clinical features of MAO-I toxicity

A

Asymptomatic period (up to 24h) → delayed toxicity

Hyperadrenergic symptoms - tachycardia, HTN, hyperthermia

Seizure, rhabdomyolysis, coma, and ultimately cardiovascular collapse once presynaptic catecholamines are depleted

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18
Q

Clinical features of TCA toxicity

A

Anticholinergic symptoms
- BUT with small pupils 2/2 α effects

Altered mental status
- confusion, agitation, hallucinations, coma

EKG changes

  • Wide QRS
  • Prolonged QTc
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19
Q

EKG changes in TCA toxicity

A

WIDE QRS due to Na-channel blockade
>100ms associated with seizures
>160ms associated with ventricular dysrhythmias

Prolonged QTc due to inhibition of K efflux

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20
Q

Triad of serotonin syndrome

Clinical features of serotonin syndrome

A

Autonomic instability
Altered mental status
↑ neuromuscular activity

Clinical features: tremor, akathisia, GI illness, clonus (inducible or spontaneous), rigidity, fevers, autonomic instability

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21
Q

Caustic ingestions:

Mechanism of injury from acidic compounds

A

Acidic compounds desiccate epithelial cells → coagulation necrosis.
An eschar is formed that limits further penetration.

*** strong odor, immediate pain on contact → limits quantity ingested

Squamous epithelium is relatively resistant to coagulation necrosis → esophageal/pharyngeal damage &laquo_space;gastric damage

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22
Q

Caustic ingestions:

Mechanism of injury from alkaline compounds

A

Alkaline compounds cause liquefaction necrosis, fat saponification, protein disruption → further penetration into tissue.

*** colorless, odorless, do not cause immediate pain on contact

Damage typically to squamous epithelial cells of oropharynx, hypopharynx, and esophagus.

Can also cause gastric necrosis, intestinal necrosis, and perforation.

*** Burns below pylorus = 50% mortality, above = 9% mortality.

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23
Q

Caustic ingestions:

Difference between acidic and alkaline ingestions

A

Acidic - coagulation necrosis, strong odor and immediate pain on contact, epithelium of esophagus/pharynx somewhat resistant. Absorption → metabolic acidosis

Alkaline - liquefaction necrosis, colorless/odorless, full-thickness/perforation of esophagus, pharynx, more significant local injury.

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24
Q

Clinical features of hydrofluoric acid exposure

A

Hydrofluoric acid exposure - inhalation, ingestion, or dermal contact (hand size or larger)

Fluoride is absorbed → hypocalcemia
** Requires cardiac monitoring to assess for QTc prolongation, torsades de pointes, or other ventricular dysrhythmias.

Rapid cardiac deterioration can occur.

Determine serum calcium, potassium, magnesium in these cases.

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25
Q

Mechanism of action and clinical effect of Digoxin

A

MOA: inhibits cardiac membrane Na-K-ATPase → ↑ INTRAcellular Na, ↑ EXTRAcellular K
↑ intracellular Na → dysfunction of Na-Ca exchange → ↑ intracellular Ca → ↑ Ca-induced Ca release in sarcoplasmic reticulum → more powerful muscle contraction and ↑ CO.

Clinical effects:

  • ↑ force of myocardial contraction → ↑ CO in pts with heart failure
  • ↓ AV conduction to slow ventricular rate in Afib
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26
Q

Toxic effects of Digoxin

A
  1. Hyperkalemia
  2. Directly blocks generation of impulses in SA node
  3. Depresses conduction through AV node
  4. ↑ sensitivity of SA/AV nodes to catecholamines
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27
Q

EKG findings with digoxin toxicity
1 most common
4 other specific dysrhythmias

A

Most common: ↑↑ PVCs

Specific dysrhythmias (not pathognomonic)

  • Afib with slow/regular ventricular rate (AV dissociation)
  • Non-paroxysmal junctional tachycardia (70-130bpm)
  • Atrial tachycardia with block (atrial rate usually 150-200bpm)
  • Bidirectional ventricular tachycardia

*** Digoxin can produce virtually any dysrhythmia or conduction block, and bradycardias are as common as tachycardias

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28
Q

Plants that may cause cardioactive steroid poisoning (mimicking digoxin poisoning) (3)

A
  1. Oleander - Nerium oleander
  2. Lily-of-the-valley - Convallaria majalis
  3. Aconitine, a Na-channel opening xenobiotic found in common Monkshood (aconitum napellus)
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29
Q

Dosing of DigiFab in Digoxin toxicity:

  1. Based on ingested dose
  2. Based on steady-state digoxin concentration
A
  1. Based on ingested dose:
    Amount ingested x 0.8 (bioavailability of dig tablets)
    e.g. 40yoF ingested fifty 0.25mg tablets
    Amount ingested = 0.25mg x 50 x 0.8 = 10mg
    1 vial = 0.5mg digoxin, therefore administer 20 vials
  2. Based on steady-state digoxin concentration (measured 6-8h after ingestion)
    ( Serum dig concentration x weight in kg ) / 100 + # vials
    e.g. 20kg child with dig level 16ng/mL 8h after ingestion unknown # of digoxin tablets
    ( 16 x 20 ) / 100 = 3 vials
    *** divide by 100 in children, 1000 in adults
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30
Q

Electrolyte abnormalities seen with Digoxin toxicity

A
  1. Hyperkalemia (acute poisoning, chronic may present with hypokalemia)
    - Caution with K repletion; K may increase with administration of DigiFab
  2. Hypocalcemia - Ca held intracellularly
    - Caution with Ca repletion or CaGluconate administration for HypoK; theoretical “stone heart syndrome”
  3. Hypomagnesemia - required for K repletion, suppression of tachydysrhythmias
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31
Q

Treatment for unstable dysrhythmia in Digoxin toxicity (3)

A
  1. DigiFab
  2. Phenytoin - if DigiFab unavailable or while being prepared - may enhance AV conduction - 100mg bolus q5min until dysrhythmia improves OR max 18mg/kg reached
  3. Lidocaine - only if contraindication to Phenytoin or max dose of phenytoin has been reached - 1.5mg/kg IVP → 1-4mg/min infusion (30-50 µg/kg/min).

** most other cardiac drugs (isoproterenol, procainamide, amiodarone, βblockers, CCBs) may worsen dysrhythmias or depress AV conduction in dig poisoned patients and should not be used.

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32
Q

Manifestations and complications of β-blocker OD in order of decreasing frequency (10)

A
  1. Bradycardia
  2. Hypotension
  3. Unconsciousness
  4. Respiratory arrest/insufficiency
  5. Hypoglycemia (uncommon in adults)
  6. Seizures (esp with propanolol)
  7. Symptomatic bronchospasm (uncommon)
  8. VT or VF
  9. Mild hyperK (uncommon)
  10. Hepatotoxicity, mesenteric ischemia, renal failure (very rare)
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33
Q

Treatment for β-blocker toxicity (7)

A
  1. Fluids
  2. Atropine
  3. Calcium - final common pathway for stimulation of β-adrenergic receptors, therefore ↑ in intracellular Ca and deleterious effects on Ca transport may contribute to β-blocker toxicity - give CaCl 1-2g or CaGluconate 3-6g over 10min
  4. Glucagon - has inotropic and chronotropic effects, stimulates production of intracellular CAMP, indepent of β-adrenergic receptor. Also counteracts hypoglycemia. - Give 5-10mg IV bolus
  5. High-dose insulin - profound inotrope with vasodilating properties - MOA involves optimization of use of carbohydrates for fuel and modulation of intracellular Ca - 1U/kg bolus, followed by 1U/kg/h titrate up to 10U.
    + DEXTROSE and K repletion
  6. Sodium Bicarbonate - Na-channel blockade from β-blockers with membrane-stabilizing activity (propanolol) that cause QRS widening - 1-2 mEq/kg IV q3-5min until QRS <120ms
  7. Vasopressors - when MAP <60mmHg after fluid resuscitation, Ca, atropine, Glucagon, and insulin
  8. Salvage therapies - IV fat emulsion (IFE), IABP, LVAD
34
Q

Manifestations of calcium channel OD -

  1. Cardiovascular
  2. Pulmonary
  3. GI
  4. Neuro
  5. Metabolic
  6. Dermatologic
A
  1. Cardiovascular: hypotension, sinus bradycardia/arrest, AV block/dissociation, junctional rhythm, asystole.
  2. Pulm: respiratory depression, apnea, pulmonary edema, ARDS
  3. GI: N/V, bowel infarction (rare)
  4. Neuro: lethargy, confusion, slurred speech, coma, seizure (uncommon), CVA (rare)
  5. Metabolic: lactic acidosis, hyperglycemia, hyperkalemia
  6. Dermatologic: flushing, diaphoresis, pallor, peripheral cyanosis
35
Q

Treatment of CCB intoxication

3 phases

A

Phase 1: Resuscitation
- IV fluid bolus, Calcium, Atropine

Phase 2: Stabilization
- Ca infusion, High-dose insulin+glucose infusion, catecholamine infusion, transcutaneous/transvenous cardiac pacing, invasive monitoring

Phase 3: Salvage therapies
- Methylene blue (increases systemic vascular resistance), IV fat emulsion (IFE), IBP, consider LVAD

36
Q

MOA of clonidine

A

Binds to pre-synaptic α2-adrenergic receptors in brain → inhibiting NE release in neurons in nucleus tractus solitaries

37
Q

Toxic effects of clonidine (5)

A 
Bradycardia
Hypotension
↓ mental status
Miosis
Hypothermia
38
Q

Treatment of clonidine toxicity

A
  1. Fluid resuscitation for hypotension
  2. Catecholamines if not responsive to fluids - NE to maintain MAP of 60
  3. Consider naloxone, up to 10mg if pt obtunded or with unprotected airway
39
Q

MOA of nitrate toxicity

A

Low doses - venous dilation
Higher doses - arterial dilation

Nitrates are converted to nitrites in GI tract (esp in infants <4mo)

Nitrites&raquo_space; nitrates - oxidize Fe2+ to Fe3+ in hemoglobin → methemoglobinemia → ↓ O2 carrying capacity

40
Q

Toxic effects of Nitrates

A
  1. Hypotension, typically accompanied by reflex tachycardia
  2. Headache 2/2 rapid dilation of meningeal arterioles
  3. S&S of methemoglobinemia - fatigue, dyspnea, weakness, dizziness, drowsiness, coma, seizure, death
41
Q

Common products containing methanol?

A

Common products: windshield wiping fluid, antifreeze, embalming fluid, cleaning solution, enamels/paint/stains, paint remover

42
Q

Methanol metabolism?

A

Methanol is primarily metabolized in liver by alcohol dehydrogenase into formaldehyde.

Formaldehyde is metabolized by aldehyde dehydrogenase into formic acid.

43
Q

Toxic metabolite of methanol?

A

Formic acid

44
Q

Clinical features of methanol toxicity?

A

*** VISUAL DISTURBANCES - targets optic disk of retina and retrolaminar optic nerve - presents with seeing spots, blurred vision (snowstorm), altered visual fields, blindness.

↓ pupillary response to light, hyperemia of optic disc → peripapillary retinal edema, loss of optic disk cupping → ↓ visual fields and central scotomata

GI symptoms - n/v from mucosal irritation → hemorrhagic gastritis. Acute pancreatitis.

CNS effects similar to etoh - slurred speech, ataxia, confusion, CNS depression

45
Q

Lab findings with methanol toxicity?

A
  • Anion gap metabolic acidosis + elevated osmolar gap

- Methanol concentration: <20mg/dL not associated with toxicity, > 50mg/dL indicates serious exposure.

46
Q

Treatment for methanol toxicity?

A
  • IV sodium bicarb for pH <7.3
  • Fomepizole - inhibits alcohol dehydrogenase, prevents metabolism of methanol to formaldehyde - loading dose 15mg/kg → 10-mg/kg doses BID up to 48h → 15mg/kg
  • Hemodialysis indications: pH < 7.3, renal failure, vision abnormalities with known methanol exposure, electrolyte imbalances unresponsive to tx (e.g. hyperK), hemodynamic instability, serum methanol concentration >50mg/dL
47
Q

Common products containing ethylene glycol?

A

Antifreeze

Brake fluids, industrial solvents, paints, cosmetics

48
Q

Metabolism of ethylene glycol?

A

Ethylene glycol → glycoaldehyde by alcohol dehydrogenase

Glycoaldehyde → glycolate by aldehyde dehydrogenase

Glycolate → Glyoxylic and oxalic acid

49
Q

Toxic metabolites of ethylene glycol?

A

Glyoxylic acid → profound metabolic acidosis

Oxalic acid + Ca → calcium oxalate crystals
→ precipitate in proximal renal tubules → ATN and renal failure
→ deposit in brain/intestinal mucosa/lungs/heart/spleen
→ systemic hypocalcemia

50
Q

Clinical findings with ethylene glycol poisoning? (3 stages)

A
  1. Acute neurologic stage (<12h) - inebriation and euphoria similar to etoh. Severe poisoning - CNS depression → coma, hypotonia, seizures. Additional findings: nystagmus, ataxia, myoclonic jerks. Cerebral edema from CaOxalate deposition
  2. Cardiopulmonary stage (12-24h) - tachycardia, severe metabolic acidosis, compensatory tachypnea. Hypoxia, pulmonary edema, ARDS. Multiorgan failure with circulatory collapse. *** Most deaths during this stage.
  3. Renal stage (24-72h) - Acute renal failure from CaOxalate crystal deposition. + CVA tenderness, hematuria, proteinuria.
  4. Delayed neuro sequelae - bulbar palsy 5-20d post-ingestion, with CN VII most commonly implicated, also opthalmoplegia, diplopia, nystagmus, facial drop, facial sensory loss, hearing loss, dysphagia, vertigo.
    * ** Facial auditory nerve oxalosis; predelicition for CN VII and VIII
51
Q

Specific features with specific toxic alcohol poisonings?

  1. Methanol
  2. Ethylene Glycol
    3.
A
  1. Methanol - formic acid - visual disturbances
  2. Ethylene glycol - Glycolic acid, oxalic acid - calcium oxalate crystalluria and renal failure, urinary/oral fluorescence under woods lamp 2/2 fluoresence of antifreeze
  3. Profound CNS depression, respiratory depression. ↑ osmolar gap WITHOUT ↑ anion gap, euglycemia
52
Q

Treatment for ethylene glycol poisoning?

A
  1. Sodium bicarb for metabolic acidosis (pH <7.3)
  2. ADH blockade (fomepizole) - prevent further formation of toxic metabolites
  3. HD if indicated
  4. Pyridoxine + Thiamine for pts with vitamin deficiencies (cofactors for glycolic acid metabolism)
53
Q

Common products containing isopropyl alcohol?

A

Rubbing alcohol, antifreeze, disinfectants, cleaning solutions, hair/skin products, hand sanitizers.

54
Q

Metabolism of isopropyl alcohol?

A

Isopropyl alcohol → acetol (hydroxyacetone) by acetone monooxygenase
→ → propylene glycol, methylglyoxal, lactate, formate, acetate → glucose

55
Q

Clinical features of isopropyl alcohol intoxication?

A

2x as inebriating as etoh

Respiratory depression + profound CNS depression

Large doses → peripheral vasodilation, ↓ cardiac inotropy → hypotension

Topical exposure → corneal de-epithelialization, dermal irritation

56
Q

Physical properties of hydrocarbons that increase toxicity (5) + examples.

A
  1. Viscosity - low viscosity allows spread into airway/lungs. e.g. furniture polish, gasoline, lamp oil.
  2. Volatility - high volatility can displace alveolar O2 and cause hypoxia. e.g. Butane and propane.
  3. Surface tension - enables a substance to disperse easily. e.g. Turpentine
  4. Chemical side chains/substitutions - metals (arsenic), halogens (chloride ions in carbon tetrachloride), and those from aromatic structures (toulene)
  5. Lipophilicity - enhances BBB penetration
57
Q

Clinical features of hydrocarbon toxicity

A
  1. Pulmonary toxicity - low viscosity, high volatility, low surface tension has worse effect. Penetrates lower airways → bronchospasm and direct injury → inflammatory response and pneumonitis. Also impairs surfactant lipid function → alveolar instability and collapse.
  2. CNS toxicity - recreational inhalation → systemic absorption without first-pass metabolism → targets NMDA, GABA, dopamine, opioid receptors → mood alteration
  3. Cardiac - intentional inhalation → sudden death. Hydrocarbons induce myocardial sensitization to endo/exogenous catecholamines by inhibition of Ca-signaling → precipitates ventricular dysrhythmias and myocardial dysfunction.
58
Q

Types of hydrocarbons and typical effects (CHAMP)

A

Camphor - neurotoxicity and seizures
Halogenated - dysrhythmias and hepatotoxicity
Aromatics - bone marrow suppression and leukemia
Metals (arsenic, mercury, lead) - neurotoxicity
Pesticides - cholinergic crises, seizures, respiratory depression

59
Q

MOA and toxidrome seen with organophosphate poisoning

A

MOA: cholinesterase inhibitor → ↑ ACh accumulation at multiple receptors (ANS, symp/parasymp, skeletal muscle, CNS)

DUMBBELS 
Diarrhea/diaphoresis
Urination
Miosis
(killer) B's: bronchorrhea/bronchospasm/bradycardia
Emesis
Lacrimation
Salivation
60
Q

Treatment of organophosphate poisoning (4)

A
  1. Decontamination
  2. Supportive care with emphasis on respiratory stabilization
  3. Reversal of ACh excess
  4. Reversal of toxin binding at receptor sites on cholinesterase molecule
61
Q

What type of pesticide are parathion, malathion?

A

Organophosphates

62
Q

You need to intubate a patient with suspect organophosphate poisoning. What type of paralytic do you use?

A

Rocuronium - non-depolarizing paralytic that is not metabolized by cholinesterase

Succinylcholine requires cholinesterase metabolism; because organophosphates are cholinesterase inhibitors, anticipate prolonged paralysis if succinylcholine is used.

63
Q

Treatment for organophosphate poisoning (2) + dosing + MOA of each

A
  1. Atropine - competitive inhibitor of ACh at muscarinic receptors. 1-3mg IV, double dose q5min until control of muscarinic effects (particularly drying of secretions) → infusion to provide 10-20% of total cumulative dose needed to obtain symptom control per hour.
  2. Pralidoxime (2-PAM) - binds to organophosphate-cholinesterase complex → conformational change → cholinesterase resumes normal function. 1-2g bolus followed by infusion (multiple options)
64
Q

MOA of carbamate toxicity.

Difference between carbamates and organophosphates?

A

Carbamates are acetylcholinesterase inhibitors vs organophosphates are cholinesterase inhibitors.

Carbamate toxicity has shorter duration of effect, no process of aging.

65
Q

Treatment of carbamate toxicity

A

Atropine, same tx as for organophosphate poisoning, monitor respiratory status.

Oxime (pralidoxime/2PAM) treatment only for severe poisoning, cannot differentiate between carbamate/organophosphate poisoning.

66
Q

Examples of chlorinated hydrocarbons (2)

A

Dichlorodiphenyltrichloroethane (DDT) - insecticide

Hexachlorocyclohexane (Lindane) - available as rx for 2nd line treatment of head-lice and scabies

67
Q

MOA and clinical manifestations of chlorinated hydrocarbon toxicity

A

Highly lipid soluble

Affect neuronal voltage-gated Na channels
GABA antagonists

Manifestations: Hyperexcitability and irritability of both CNS and PNS
+ ↑ susceptibility to ventricular tachydysrhythmias because of ↑ myocardial sensitivity to circulating catecholamines

68
Q

Clinical features of chlorinated hydrocarbon insecticide toxicity?

A

Neurologic excitation: muscle fasiculations, ataxia, tremors, delirium, weakness, paralysis, paresthesias, seizures, death

Hyperthermia 2/2 muscle fasiculations and seizures.

+/- metabolic acidosis, respiratory failure, acute renal failure

+ Ventricular tachydysrhythmias 2/2 ↑ myocardial sensitivity to circulating catecholamines (often seen at the time of seizures due to catecholamine surge)

69
Q

Treatment of chlorinated hydrocarbon insecticide toxicity?

A

Cessation of seizures with benzodiazepines and barbiturates.

β-blockers for any life-threatening tachydysrhythmias.

External cooling if hyperthermic.
IV hydration for metabolic acidosis, rhabdo, AKI

Alkalinization for rhabdomyolysis if needed.

70
Q

Examples of substituted phenols

A

Dinitrophenol (DNP), pentachlorophenol, dinitrocresol

Used as dyes, wood preservatives, photograph developers, insecticidse.

SNP currently used as weight loss supplement.

71
Q

MOA and clinical manifestation of substituted phenol toxicity

A

Substituted phenols uncouple oxidative phosphorylation → ↓ ATP formation and ↑ heat generation

Acute toxicity - hyperthermia, tachycardia, diaphoresis, tachypnea.

Neuro symptoms: confusion, agitation, seizure, coma.

+/- rhabdo, myocardial injury, AKI, hepatic damage

Death due to cardiovascular collapse.

72
Q

Treatment for substituted phenol toxicity?

A

Supportive care.

Benzos, treatment for hyperthermia, fluid resuscitation, correction of electrolyte derangements.

** consider activated charcoal if pt presents w/in 1h of acute oral ingestion and who is alert/cooperative.

73
Q

MOA and clinical manifestations of chlorophenoxy herbicide toxicity

A

*** Used as herbicides for broad-leaved weeds.

MOA unknown, proposed MOA due to cell membrane damage, forms analogues of acetyl-CoA and acts as false cholinergic messengers. At high doses uncouples ox-phos.

Ingestion → GI symptoms including vomiting, abd pain, diarrhea, oropharyngeal burning, GI hemorrhage.

Primary organ of toxicity: Skeletal muscle.
- Muscle fasiculations, weakness, myotonia, ↓ DTRs.
May → rhabdo and metabolic acidosis

74
Q

Examples of bipyridyl herbicides (2)

A

Paraquat

Diquat

75
Q

MOA and clinical manifestations of bipyridyl herbicide poisoning

A

Paraquat&raquo_space; diquat
Causes production of superoxides created during cyclic oxidation-reduction reactions in tissues → oxygen radical damage → cell death

** Paraquat selectively concentrates in the lungs/alveolar cells (high O2 concentrations) → ARDS, progressive pulmonary fibrosis, respiratory failure.

Corrosive - n/v, caustic injury to oropharynx, esophagus, GI tract. Dermal exposure can cause corrosive injury to the skin

Systemic toxicity → multiorgan failure and death

76
Q

Treatment for bipyridyl herbicide poisoning

A

Corrosive injury to upper airway → intubation

Because of O2 radical damage, supplemental O2 with target oxyhemoglobin of 95%

Supportive care for multiorgan failure

Dialysis indicated to increase elimination if renal failure, metabolic acidosis, or electrolyte imbalance develops as result of poisoning

77
Q

Pyrethrin - what is it?
MOA of toxicity?
Clinical manifestations?
Treatment?

A

Pyrethrin - naturally occurring from chrysanthemum plant. Pyrethroids are synthetic derivatives, more stable in environment. Used to treat human infestations of scabies and lice.

Block voltage-gated Na channels, voltage-gated Ca channels, and Cl channels on GABA receptors.

Sensitivity reactions with skin exposure (erythema)

Inhalation → rhinitis, sneezing, oral mucosa irritation, cough, dyspnea, wheezing, chest pain.

Ingestion → n/v, abd pain, diarrhea

Massive ingestion → neuro symptoms including numbness, tremors, ataxia, paralysis.

Tx: supportive care

78
Q

Glyphosate - examples?
MOA of toxicity?
Clinical manifestations?
Treatment?

A

Glyphosate (Roundup) - one of the most commonly used pesticides in the US.

Human toxicity thought to be 2/2 surfactant included in glyphosate preparation.

Poor dermal absorption.
Concentrated (41%) solutions → mucosal injury.
** Residential concentration is 1%.

Unintentional ingestion → mild GI symptoms.

Massive ingestions/concentrated ingestion may → sore throat, n/v, abd pain, hyperthermia, respiratory distress, acute lung injury, renal failure, coma.

Metabolic acidosis may develop as result of cardiovascular compromise.

Poor prognostic features: AMS, hyperK, renal failure

Treatment: supportive

79
Q

What type of toxin?

Jimson weed

A

Anticholinergic toxin

aka Datura stramonium

80
Q

What type of toxin?

Deadly Nightshade

A

Anticholinergic toxin

aka Atropa belladonna

Rosen's (25 decks)

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