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Rosh Review > Toxicologic Disorders > Flashcards

Toxicologic Disorders Flashcards

1
Q

Mechanism of action and clinical effects of clonidine (overdose)

A

Alpha-2 adrenergic agonist
Stimulation of centrally acting alpha-2 receptors inhibits release of peripheral catecholamines -> decrease HR, contractility, peripheral vascular resistance
Paradoxical hypertension can occur immediately after ingestion due to peripheral alpha-2 adrenergic stimulation, but ultimately manifests in hypotension and bradycardia

Also stimulates mu-receptors causing miotic pupils and lethargy

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2
Q

What type of toxidrome does “paint stripper” cause?

A

Solvent = methylene chloride or dichloromethane is metabolized by liver to carbon monoxide

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3
Q

What is the problem with tar and asphalt?

A

Dermal hydrocarbon injuries commonly in construction workers

Apply mineral oil, antibacterial ointments, petroleum jelly to dissolve and remove the substance to ensure proper burn management

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4
Q

INR Reversal Guidelines

A

*Table from Question 232838

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5
Q

What medication is obtained in oil of wintergreen?

A

Salicylates

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6
Q

Salicylate toxicity effects on organ systems

A

***Q174111 pic

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7
Q

Treatment for salicylate toxicity

A
  • Activated charcoal if <2 hours from ingestion
  • Urine alkalinization with bicarb gtt (ion-trapping) with pH goal 7.5-8
  • K+ prior to alkalinization
  • Dialysis
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8
Q

Dialysis indications in salicylate toxicity

A
  • Level >100 mg/dL
  • Severe acidosis
  • Coma, seizure, AMS
  • Rising levels despite alkalinization
  • Renal failure
  • Pulmonary edema
  • Clinical deterioration
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9
Q

Clinical presentation of GHB overdose

A

Low dose - euphoria; increasing dose - sedation with amnesia; high dose - coma, respiratory depression

  • Hypothermia, bradycardia, hypotension
  • Agitation, nystagmus, dizziness
  • U waves on ECG
  • Pupils small and minimally responsive
  • Respiratory depression
  • Classic presentation is comatose patient requiring intubation then has an abrupt awakening
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10
Q

What is the main complication of GHB other than respiratory depression?

A

Rhabdomyolysis

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11
Q

Beta-blocker toxicity clinical presentation

A
  • Bradycardia
  • Hypotension
  • AMS/seizures (propranolol - will also widen QRS)
  • Hypothermia
  • Hypoglycemia (due to interference with gluconeogenesis and glycogenolysis)
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12
Q

Tx for beta-blocker toxicity

A
  • Glucagon (bypasses antagonized beta-receptors by independently activating myocardial adenylate cyclase, increasing intracellular cAMP, improving myocardial contractility
  • Adrenergic receptor agonists (norepi, epi, phenylephrine)
  • Calcium
  • High-dose insulin
  • Sodium bicarb if QRS prolonged
  • Lipid emulsion therapy
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13
Q

Which beta-blocker prolongs QTC?

A

Sotalol due to blockade of potassium channels

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14
Q

What is sarin gas?

A

Organophosphate nerve agent

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15
Q

Examples of potent cholinesterase inhibitors

A

Organophosphates: parathion, fenthion, malathion, diazinon
Carbamates: methomyl, aldicarb
Nerve agents: sarin, tabun, soman

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16
Q

Cholinergic toxicity mnemonics

SLUDGE and DUMBBELLS

A

Salivation; Lacrimation; Urination; Diarrhea; GI cramps; Emesis

Diarrhea; Urination; Miosis; Bradycardia; Bronchospasm; Emesis; Lacrimation; Lethargy; Salivation; Seizures

Also nicotinic effects such as fasciculations, muscle weakness, paralysis

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17
Q

Tx for cholinergic toxicity

A
  • Decontamination
  • Atropine (anticholinergic… does not bind nicotinic receptors)
  • Pralidoxime - regeneration of cholinesterase -> HAS TO BE GIVEN WITHIN 4-6 HOURS AFTER EXPOSURE
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18
Q

Adverse effects of carbamazepine

A
  • Ataxia
  • Diplopia
  • Hepatotoxicity
  • Blood dyscrasias (aplastic anemia, agranulocytosis)
  • SIADH
  • SJS
  • Teratogenicity
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19
Q

Acute toxicity of carbamazepine

A
  • CNS depression
  • Nystagmus
  • Ataxia
  • Hypertonicity
  • Anticholinergic toxidrome
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20
Q

Compounds that can be removed by dialysis

A
  • Amanita mushrooms
  • Barbiturates
  • Ethylene glycol, methanol, isopropanol
  • Isoniazid
  • Lithium
  • Metformin
  • Salicylates
  • Theophylline
  • Carbamazepine
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21
Q

Indications for dialysis in salicylate toxicity

A
  • AMS
  • Seizures
  • Pulmonary edema
  • New hypoxemia
  • pH = 7.2
  • Initial salicylate levels >100 mg/dL
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22
Q

Over ingestion of sulfonylureas (chlorpropamide, glyburide, glipizide) causing hypoglycemia can be treated with what agent?

A

Octreotide

Sulfonylureas have a high affinity to inhibit potassium channels on pancreatic beta cells -> opens voltage-gated calcium channels and influx of Ca = release of endogenous insulin

Octreotide inhibits Ca entry through the voltage-gated Ca channels, prevents further insulin release

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23
Q

What medications ingested by children can result in hypoglycemia?

A
  • Oral hypoglycemics
  • Ethanol
  • Salicylates
  • Beta-blockers
  • Pentamidine
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24
Q

Clinical manifestations of hydrogen peroxide ingestion

A

Small ingestions can liberate large amount of oxygen!

Cardiac and cerebral gas emboli with symptoms similar to those seen in diving related decompression injuries

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25
Q

Treatment for hydrogen peroxide ingestion

A

Hyperbaric oxygen

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26
Q

Which patients with carbon monoxide toxicity should be treated with hyperbaric oxygen?

A
  • Neurologic abnormalities
  • Cardiovascular instability
  • COHb level >25% (or 15% in pregnant women)
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27
Q

Classic EKG findings in patients who present with TCA overdose?

A

Sinus tachycardia
Prolonged PR, QRS and QT
Terminal R wave in aVR
Negative S wave in lead I

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28
Q

What medication should be administered for hypoglycemia if IV access is unavailable?

A

Glucagon

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29
Q

Vital sign changes with specific calcium channel blocker overdose

A

Dihydropyridines (“-pines”): hypotension

Non-dihydropyridines (dilt, verapamil): bradycardia

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30
Q

Signs and symptoms of local anesthetic systemic toxicity

A

CNS:

  • Tinnitus
  • Circumoral numbness
  • Metallic taste
  • Agitation
  • Dysarthria
  • Seizures
  • LOC
  • Respiratory arrest

CV:

  • Hypotension
  • Bradycardia
  • Ventricular dysrhythmias
  • Cardiovascular collapse
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31
Q

Dose for lipid emulsion therapy pin systemic anesthetic toxicity

A

20% lipid emulsion in adults >70kg -> bolus 100mL IV over 2-3 minutes followed by infusion of 200-250 mL over 15-20mins

In children or adults <70kg -> bolus 1.5mL/kg IBW over 2-3 mins followed by infusion at 0.25mL/kg/min
(Max dose of lipid emulsion approx 12mL/kg IV)

Repeat bolus once or twice and double infusion rate for cardiovascular instability

Continue infusion for at least 10 minutes after hemodynamic stability is achieved

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32
Q

S/S of lead poisoning

A
  • Headache
  • Joint pain
  • Peripheral neuropathy
  • Constipation
  • Encephalopathy
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33
Q

Lab/Img findings of lead toxicity

A

Lab: normocytic, hypochromic anemia and basophilic stippling on peripheral smear
Imaging: hyperdense lines at meatphyses, radioopaque foreign bodies

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34
Q

Tx based on lead levels

A

5-20 mcg/dL - exposure history, education, continued monitoring of levels
>20 mcg/dL - neurodevelopmental exam, investigation and hazard reduction, lab work, abdominal x-ray
45 mcg/dL - chelation therapy
>70 - hospitalization and immediate chelation

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35
Q

Tx of lead toxicity

A

Oral succimer or IV EDTA (calcium disodium edetate, given after dimercaprol)

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36
Q

Other clinical effects of opioids

A

Top 3: CNS depression, respiratory depression, miosis

  • Hypothermia
  • Bradycardia
  • Hypotension
  • Noncardiogenic pulmonary edema
  • Decreased GI motility
37
Q

How long do the effects of naloxone last?

A

Reverses opiate effects for 1-2 hours

38
Q

Early clinical features of acute salicylate overdose

A
  • N/V
  • Tinnitus
  • Tachypnea -> resp alkalosis
39
Q

Clinical effects of TCA overdose and the mechanisms that lead to them

A
  1. Dry skin, tachycardia, mydriasis, hot, AMS, urinary retention (anticholinergic)
  2. Peripheral vasodilation and hypotension (inhibition of central sympathetic reflexes and inhibition of alpha-1 adrenergic receptors)
  3. Prolonged QRS (Sodium channel blockade)
  4. Prolonged QT
  5. Terminal R wave in aVR (Right bundle branch more affected due to longer refractory period)
  6. Sedation (antihistamine effects)
  7. GABA receptor antagonism may contribute to seizures
40
Q

Tx for TCA overdose

A

Sodium bicarb 1-2mEq/kg IV bolus followed by infusion of 150mEq in 1,000 cc of D5W administered IV at twice maintenance

41
Q

Treatments contraindicated in TCA overdose

A

Phenytoin - due to sodium blockade

Physostigmine - lowers seizure threshold

42
Q

Clinical effects of clonidine overdose

A

Alpha-2-adrenergic agonist

Initial transient HTN (due to peripheral effects causing release of norepi) -> hypotension and bradycardia

Also with hypoventilation, hypoxia, Cheyne-Stokes respiration, periodic apnea, miosis

43
Q

Tx for clonidine overdose

A

Supportive care; naloxone at high doses (4-10mg) sometimes effective

44
Q

How long does GHB generally last?

A

<6-8 hours

45
Q

Why do some athletes and bodybuilders use GHB?

A

Thought to elevate levels of human growth hormone

46
Q

Heparin reversal in patients with bleeding is with what?

A

Protamine sulfate

47
Q

What kind of risk does protamine sulfate pose?

A

Hypotension and anaphylaxis

48
Q

Heparin function?

A

Reduce thrombin and fibrin formation by binding and activating antithrombin III

  1. Unfractionated heparin - inhibits factors Xa and IIa in equal proportions
  2. LMWH - higher ratio of inhibition of Xa as apposed to IIa
49
Q

What can be administered within 1 hour of ingestion of TCA?

A

Activated charcoal - if patient awake and cooperative

50
Q

Indications for sodium bicarb in TCA overdose

A
  • QRS > 100ms
  • Terminal right axis deviation greater than 120 degrees
  • Brugada pattern
  • Ventricular dysrhythmias
51
Q

What is target when sodium bicarb given for TCA overdose?

A

Target pH 7.50-7.55

52
Q

What is initial dose of sodium bicarb for TCA toxicity?

A

1-2mEq/kg

53
Q

What is the end point of tx with atropine in patients with organophosphate poisoning?

A

Dry respiratory secretions and cessation of bronchoconstriction

54
Q

What type of toxicity can occur in patients who receive large or continuous infusions of benzodiazepines?

A

Propylene glycol - the diluent used in parenteral formulations of diazepam, lorazepam, phenobarbital, phenytoin, nitroglycerin

55
Q

Propylene glycol toxicity presentation

A
  • Anion gap metabolic acidosis
  • Skin and soft tissue necrosis from extravasation
  • Hemolysis
  • Cardiac dysrhythmias
  • Hypotension
  • Lactic acidosis
  • Seizure
  • Coma
  • Multisystem organ failure
56
Q

Why should you exercise caution when using flumazenil?

A

It can cause withdrawal seizures

57
Q

T/F: The use of pralidoxime decreases requirement for atropine?

A

True

58
Q

Mnemonic to remember symptoms of NMS

A 
FEVER
Fever
Encephalopathy
Vitals unstable
Elevated CK
Rigidity

Usually mental status changes and rigidity precede hyperthermia and autonomic instability

59
Q

Tx for NMS

A

Aggressive control of hyperthermia
Benzos
Bromocriptine

60
Q

Jimsonweed overdose presents with what toxidrome

A

Anticholinergic because of belladonna alkaloids

61
Q

What are the indications for physostigmine in anticholinergic poisoning?

A

Tachycardia uncontrolled with standard therapy and agitation uncontrolled with sedatives

62
Q

Rigid chest syndrome is a noted adverse effect of which medication?

A

Fentanyl

63
Q

Which opioid, due to anticholinergic metabolites, can result in seizures, agitation, and psychosis at therapeutic doses?

A

Meperidine

64
Q

What can cyanide toxicity smell like?

A

Bitter almonds

65
Q

Mild-moderate-severe signs of cyanide toxicity

A

Mild
- tachycardia, headache, drowsiness, dyspnea, tachypnea

Mod-Severe
- bradycardia, hypotension, CV collapse, asystole, seizures, coma, apnea

66
Q

Maximum dose of bupivacaine

A

2 mg/kg or 0.4 mL/kg

67
Q

What is the first-line antidysrhythmic in a patient with dysrhythmia from systemic lidocaine toxicity?

A

Amiodarone

68
Q

What nonopioids can cause a false-positive opioid drug screen?

A

Poppy seeds and fluoroquinolones

69
Q

What kind of effect does lithium toxicity have on renal system?

A

Nephrogenic diabetes insipidus - renal collecting system becomes resistant to antidiuretic hormone

70
Q

Indications for hemodialysis in lithium toxicity

A
  • Impaired renal function and lithium concentration > 4 mEq/L
  • Lithium concentration > 5 mEq/L
  • Presence of seizure, dangerous dysrhythmia, altered mental status
  • Elevated lithium level in symptomatic patient with contraindication to aggressive hydration (e.g. heart failure)
71
Q

What medication has been shown to help minimize further accumulation of lithium in patients with mild-moderate nephrogenic diabetes insipidus due to chronic lithium use?

A

Amiloride

72
Q

Acute lithium toxicity symptoms

A

More GI sx early
Delayed neuro symptoms
Cardiovascular symptoms: prolonged QT interval, ST/T wave changes
Leukocytosis

73
Q

Chronic lithium toxicity symptoms

A

Early neuro symptoms
CV: myocarditis
Aplastic anemia
Dermatitis, ulcers, edema

74
Q

What is the mechanism of action of glucagon in the treatment of beta blocker toxicity?

A

Stimulates production of intracellular cyclic adenosine monophosphate

75
Q

What type of toxicity produces an osmolal gap with normal anion gap?

A

Isopropyl alcohol poisoning
Metabolized to acetone by alcohol dehydrogenase
“Ketosis without acidosis”

76
Q

Calculation for serum osmolarity

A

2 x Na + (glucose/18) + (BUN/2.8) + (Ethanol/4.6)

Normal = 275-295

77
Q

Indications for hemodialysis in isopropyl alcohol toxicity

A
  • Refractory hypotension despite conventional therapy
  • Comatose
  • Isopropyl alcohol levels > 400 mg/dL
78
Q

For which volatiles can fomepizole be used?

A

Methanol and ethylene glycol (not isopropyl alcohol)

79
Q

Medications that can precipitate lithium toxicity

A

Nephrotoxic - NSAIDs, ACEI, diuretics due to decreased kidney excretion of lithium

80
Q

What is ergotism?

A

When Ergot derivatives such as dihydroergotamine increase serotonin activity in CNS and have alpha-adrenergic agonist effects peripherally

Can occur when medications used in excess or drug interactions with macrolide antibiotics and triptans

  • Miosis
  • Burning sensation in extremities
  • Cerebrovascular or cardiac ischemia
  • GI disturbances
  • Seizures
  • Bradycardia
81
Q

What ancillary lab test can aid in diagnosis of valproic acid poisoning?

A

Serum ammonia level

82
Q

Which three anticonvulsant drugs are typically associated with seizure in overdose?

A

Tigabine
Iamotrigine
Carbamazepine

83
Q

Lab results in Wilson disease

A

LOW ceruloplasmin
LOW serum copper
INCREASED urine copper

84
Q

Tx for Wilson Disease

A

Chelation with penicillamine

85
Q

Substances known to cause acquired methemoglobinemia

A
  • Dapsone
  • Topical anesthetics, especially mucous membrane use of benzocaine (although also reported with lidocaine, tetracaine, or prilocaine)
  • Nitrates
  • Antimalarials
86
Q

What has the odor of fresh hay?

A

Phosgene

- plastics, textiles, pharmaceuticals

87
Q

What chemical is liberated when phosgene mixes with the fluid of the epithelial lining of skin?

A

Hydrochloric acid

88
Q

What drug commonly causes hyponatremia and associated seizures?

A

MDMA - increase release of antidiuretic hormone

89
Q

Effects of MDMA

A
  • Hyperthermia
  • Dysrhythmia
  • Rhabdomyolysis
  • DIC

Rosh Review (22 decks)

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