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Toxicology Flashcards

1
Q

LPT for OD

A

Bring all pills

Call poison control

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2
Q

OD; ask

A

Poison; What, when, how much, why,

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3
Q

Reduction of absorption

A

Ipecec - rarely used
Gastric lavage (stomach pump)
Activated charcoal
Cathartics enhance elimination, whole bowel irrigation

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4
Q

The 4 anticholinergics

A

Antihistamine, psychotic, depressant, parkinsonian
Red, dry, blind, mad, hot
Flushing, dry skin and membranes, mydriasis (dilation), fever, altered LOC, tachycardia

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5
Q

TCA names -ine

A

Amitriptyline (elavil), amoxapine (asendin), clomipramine (anafranil), doexpin (sinequan)

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6
Q

Pharmacologic properties of TCA

A 
Inhibits reuptake of norepi and reotonin
Antichol actions
Alpha-adrenergic blockade
Inhibit potassium in heart
Inhibits sodium in brain and heart
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7
Q

TCA on the heart

A

Block fast sodium - QRS prolongation, tall R wave in aVR)
Inhibits K+ channels (QTc prolongation, direct myocardial depression)
M1, H1 and A1 blockade as well
QRS > 100ms predictive of seizures
QRS > 160ms predictive of ventricular arrhythmias

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8
Q

ECG features of sodium channel blockade

A 
IVCD 
Terminal R wave > 3mm in aVR
R/S ratio >0.7 in aVR
Sinus tach due to M1 blockade
Heart blocks
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9
Q

TX of TCA OD

A 
40mL/kg fluid
Cardiotoxicity - bicarb 1mEq/kg (refractory hypotension or QRS >0.10 or ventricular dysrhythmia) 
Benzos for seizures
2g mag in 50mL over 5 if needed
Norepi for pressors
Avoid a
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10
Q

Activated charcoal

A

Charcoaid
Class absorbent
Contras - need an OG/NG if altered, don’t give if corrosive agent (vomit) 1g/kg for everyone

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11
Q

Antiarrhythmics in TCA

A

Avoid Ia and IC, beta blockers and ami as these may all worsen hypotension or conduction abnormalities
LITFL says lido after bicarb and hyperventilation, tins says no evidence of this
Overdrive pacing or isoprotenolol in tins…maybe

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12
Q

Things that cause cholinergic tox

A

Nictotine, muscarine mushrooms, neostigmine, cevimeline, organophosphates

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13
Q

S&S of chol tox

A 
BM SLUDGE
Bradycardia/bronchospasm/bronchorrhea
Miosis
Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
Miosis
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14
Q

Cholinergic toxicity MOA

A

Cholinesterase inhibitors have high affinity for ACHe which metabolizes ACh.

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15
Q

TX for chol tox (SLUDGEM)

A 
Decontamination
Assisted resps
Monitor for torsades
Atropine 2mg IV/IO q 5 until reversal 
Avoid succs (prolonged paralysis) 
Pulmonary edema 
2-PAM
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16
Q

Pralidoxime hydrochloride

A

2-PAM. Regenerates ACHe activity, must be given early

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17
Q

Metabolic considerations

A

Rhado/renal failure

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18
Q

Stim OD protocol

A 
Cool
12lead
5IV midaz 2.5 q 5 max 20
10IM midaz 5mg q 10 max 20
Bicarb for QRS widening 1mEq/kg q 5 ma 2 mEq
Refractory chest pain treat ACS
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19
Q

Beta blocker theory for stim OD

A

Unopposed alpha because if B2 is blocked (peripheral vasodilation) and A1 still stimulated you get sky high BP
(propanolol is non selective B)
Metoprolol (selective B1) or Isoprotenolol (blocks alpha and beta) can be given according to LITFL.
Tins says you can give

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20
Q

Tins antipyschotics

A

Haloperidol may decrease seizure threshold, contribute to hyperthermia, and increase QT prolongation. Still give, but after beta blockers

21
Q

Anxiolytics OD presentation

A

Benzos/barbs
Decreased LOC, delirium, slurred speech, combative, resp depression, hypotension, bradycardia, diaphoresis, hypothermia, nystagmus

22
Q

Barbs and bicarb

A

Alkalization of urine enhances elimination of phenobarb by ion trapping. Just used for long acting barbs

23
Q

Zero order kinetics

A

A set amount of drug is eliminated per unit of time

Happens to salicylates after liver is saturated, the kidneys become primary route of excretion at this point

24
Q

Salicylate tox and alkalinization

A

Serum alkalinization used to keep drug in plasma and out of tissue
Urinary pH above 7.5 keeps ASA from being reabsorbed

25
Q

pH salicylate tox

A

Direct stimulation of resp center causes tachypnea, hypernea and resp alkalosis
Inhibition of metabolism produces acidosis that overwhelms alkalosis and may create late resp acidosis (coingestion of other drugs may cancel resp center stimulation)

26
Q

Salicylate tox sugars

A

Initial mobilization of glycogen stores causing hyperglycemia but inhibits gluconeogensis so pts are often normoglycemic (tins says hypoglycemia is rare)
Profound decrease in brain glucose despite normal serum glucose meaning.

27
Q

Salicylate lungs

A

Can cause noncardiogenic pulmonary edema - may also cause cerebral edema

28
Q

Salilcylate GI

A

Corrosive injury of GI with abdo pain N/V and occasionaly hematemsis with volume loss, metabolic alkalosis and hypokalemia

29
Q

Salicylate OD tx

A

ABCs, fluid, control hyperthermia, sugar for sugars benzos for seizures and maybe bicarb
Activated charcoal within 60 minutes

30
Q

Beta blocker TXs

A

Fluid, pacing, epi or dope, glucagon and CaCl as beta blockers inhibit calcium entr

31
Q

Common CCB

A

Verpamil (isoptin) Nifedipine (adalat) Diltiazem (cardizem)

32
Q

4 cardio effects of CCB

A

Negative ino chrono and dromotropy plus vasodilation

33
Q

S&S CCB OD

A

Hypotension, bradycardia, heart block
Altered LOC/seizures
Hyperglycemia

34
Q

MOA CCBs

A

Bind to L-type calcium channel causing it to favour closed state and decreasing Ca2+ entry during phase 2.
Verapamil at high concentration occupies and completely blocks channel

35
Q

3 classes of CCB

A

phenylalkylamines (verapamil and gallopamil)
benzothiazepines (diltiazem)
Dihydropyridines (nifedipine, amlodipine)

36
Q

TX of CCB

A

CaCl, insulin, TCP, glucagon (N/V) pressors of epi or dope

37
Q

Dig presentation

A

Headache, irritability, psychosis, yellow-greenish vision, anorexia, N/V, palpitations, syncope, dyspnea, atrial tachycardia with block, junctional tachy ectopy
Tachyarrhythmias and heart blocks

38
Q

Dig Tox TX

A

12-lead, fluid, TCP/atropine, hyperK+ tx with digibind THEN calcium

39
Q

Digibind dose

A

400mg IV over 15 minutes

800mg IVP if in arrest

40
Q

Ethylene glycol

A

Antifreeze, can produce intox, severe toxicity

41
Q

Methanol

A

Primary in windshield fluid

42
Q

Methanol/ethylene glycol MOA

A

Metabolized by same enzyme as ETOH - dehydrogenase, but into toxic by-products that lead to severe multi-system toxicity

43
Q

Ethylene glycol metabolites

A

glycolic acid, glyoxylic acid, oxalic acid, lactic acid

44
Q

Methanol metabolites

A

formic acid and lactic acid

45
Q

Methanol/ethylene S*S

A

May just show as intox for first 6 hours

Both produce severe metabolic acidosis with elevated anion gap and osmolar gaps

46
Q

Ethanol as tx

A

Competitive substrate for enzyme alcohol dehydrogenase
Pyridoxine (vit B6) - cofactor in enzymatic breakdown of glyoxylic acid into non-toxic by products
Folic acid - enzyme cofactor
B1(thiamine) 100mg IV/IM - cofactor in enzymatic breakdown glyoxylic acid

47
Q

MDMA

A

Jaw clenching, teeth grinding, scratching, nystagmus, dilated pupils, tachycardia, HTN, hyperthermia, sensation of chills, elevated temp, severe dehydration with hyponatremia, decreased LOC, coma, seizure, death, DIC, malignant hyperthermia
TX with fluids and cooling

48
Q

Hydrocarbons

A

Kerosene, gasoline, lighter fluid, turpentine, mineral oil, petroleum jelly, paraffin wax

49
Q

Hydrocarbons S*S

A

Euphoria, anxiety, choking/gagging/coughing, N/V/D upsetstomach pepto bismal hypoglycemia

Advanced medical (24 decks)

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