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Wrap-Up Block > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What are your options regarding the specific management of intoxicants

A

1) Decrease the absorption of the intoxicant
2) Increase the elimination of the intoxicant
3) Use a specific antagonist/ antidote

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2
Q

Provided that some of the toxicant stays in the GI tract to be absorbed, what could the physician administer?

A

Activated Charcoal…absorbs the toxin and is then excreted in the feces

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3
Q

What is essential when administering charcoal for toxicity?

A

Airway protection

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4
Q

The greatest benefit of charcoal is within how long of ingestion

A

1 hr…..and don’t give it unless the pt has protected airways

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5
Q

Syrup of Ipecac most likely useless after how long?

A

30 minutes

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6
Q

Hemodialysis can be effective if the toxin has what:

A
  • Water solubility
  • Low volume of distribution
  • Low Molecular Wt Molecular Wt under 500 Da
  • Low Plasma Protein Binding

Useful for methanol, ethylene glycol, salicyclates, lithium, sotalol

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7
Q

Hemoperfusion can be used in place of hemodialysis when?

A

When there is a high degree of plasma protein binding.

Phenobarbital, carbamezapine, theophyline

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8
Q

What are some of the sympathomimetics

A
  • Cocaine, amphetamine, Methamphetamine, caffeine, theophyline …..so mostly stimulants
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9
Q

Treatment of sympathomimetic overdose

A
  • Phentolamine, nitrates, or calcium channel blockers for HTN
  • Benzos for agitation
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10
Q

Top three causes of toxicity causing arrhythmias

A

1) Amphetamines
2) TCAs
4) Digitalis

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11
Q

Most potent Beta Blocker

A

Propanolol

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12
Q

Beta Blocker toxicity treatment

A

Glucagon

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13
Q

Alternative to glucagon as treatment for Beta Blocker Toxicity?

A

High-dose insulin along with glucose suplementation

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14
Q

Calcium Channel Blocker Toxicity

A
  • Charcoal if it hasn’t been very long
  • Treat the hypotension and bradycardia with Calcium chloride or calcium gluconate.
  • Give epinephrine and gluconate
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15
Q

Realize that Beta Blockers and Calcium Channel Blockers also lead to hyperglycemia, hypoinsulinemia, and acidosis by blocking specific channels in the pancreas.

A

The administration of Insulin may reverse this.

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16
Q

Isoniazid produces acute brain toxicity how?

A

Reduces the amount of brain P5P….Results in low levels of CNS GABA which leads to seizures

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17
Q

Treatment of Isoniazid induced seizures

A

Pyridoxine and a beno if necessary

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18
Q

Acetaminophen and Aspirin (salicilate) poisoning

A

Phase 1- 30 min -4 hrs: anorexia, pallor, N/V, diaphoresis

Phase II (24-48 hrs)- Symptoms less severe, potential right upper quad pain. liver enzymes become abnormal

Phase III (3-5 days)- hepatic necrosis, jaundince, coag defects, death due to renal failure

Phase IV- 4 days to 2 weeks- death or resolution

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19
Q

Antidote for acetaminophen od

A

N-Acetylecysteine (replenishes the glutathione)

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20
Q

Antidote for Salicylates

A

NaHCO3 (alkalinize urine)

Also give glucose containing fluids to reduce the risk of cerebral hypoglycemia.

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21
Q

What do Salicylates do that cause harm?

A
  • Uncouple cellular oxidative phosphorylation which leads to acidosis and excess heat
  • Stimulate respiratory center in brainstem which leads to tachypnea
  • You see metablic acidosis and respiratory alkalosis
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22
Q

High Anion Gap Acidosis produced by what drugs

A

MUDPILES CAT

Methanol or Metformin
Uremia
DKA
P
Iron, INH, Ibuprofen
Lactic Acidosis
Ethylene Glycol
Salicylates
Cyanide
Alcohol or acids
Toluene or Theophyline
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23
Q

Serotonin syndrome antidote

A

Cyproheptadine

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24
Q

Charcoal doesn’t work for hydrocarbons

A

ok

25
Q

Describe the vital sign findings of a pt experiencing toxicity from adrenergic drug

A

RR- up
HR- up…beta 1
BP- up
Temp- up

26
Q

Physical exam findings for a pt experiencing overdose on adrenergic drug

A
  • Alert/agitated
    Pupils: dilated
    mucus: wet
    Increased bowel sounds increased urine, increased everything basically.
27
Q

Vital sign findings for an anti-cholinergic overdose

A

RR- No change
HR- up
BP- no change
T-Up

28
Q

Mental status findings for anti-cholinergic overdose

A

depressed, confused, hallucinating

29
Q

Vital sign findings for opiod overdose

A

Low rr, hr, bp, and fever

30
Q

pupils in opioid overdose?

A

constricted…the only time you’ll see constricted pupils is in opioid overdose and cholinergic agonist overdose

31
Q

Vital sign findings in serotonergic overdose

A

Inc in everything…think serotonin syndrome

32
Q

How do you treat the bradycardia and hypotension associated with beta blocker toxicity

A

IVglucagon

33
Q

Propanolol overdose

A

IV lipid emulsion can help

34
Q

Calcium channel blocker toxicity treatment

A

treat hypotension and bradycardia with IV clcium chloride or calcium gluconate

Epinephrine can also raise HR

35
Q

Insulin and detrose used during Beta Blocker toxicity and Calcium channel blocker toxicity why>

A

Because they somehow improve heart function…not real clear how. We know that insulin promotes the uptake of glucose into skeletal and cardiac muscles and adipose tissue, it also shifts potassium intracellularly.

36
Q

Isoniazid is used to treat what

A

TB

37
Q

How is isoniazid toxic?

A

produces acute toxic effects by reducing brain pyridoxal 5-phosphate, the active form of vitamin B6. All of this results in low GABA and thus seizures,

ALSO, inhibits the conversion of lactate to pyruvate in the liver thus exacerbating the lactic acidosis resulting from seizures.

38
Q

What is the antidote for Isoniazid toxicity

A

Pyridoxine

39
Q

Salicylate poisoning?

A

Causes tinnitus, vertigo, change in mental status, confusion

  • Directly stimulates the respiratory center which may lead to respiratory alkalosis early, respiratory acidosis late.
  • Adult overdose shows respiratory alkalosis and metabolic acidosis

HYPERTHERMIA- damages the innermitochondrial membrane and oxidative energy is released as heat

40
Q

How do you diagnose salicyclate poisoning

A

High anion gap + positive salicylate test

41
Q

Treatment of salicylate poisoning

A

IV sodium bicarbonate which alkalinizes the urine and enhances renal salicylate excretion by trapping the salicylate anion in the urine

42
Q

Cyproheptadine is what

A

An Antihistamine that also has alti-serotonin activity

43
Q

Where does cyproheptadine work?

A

GI smooth muscle and other locations

44
Q

WHat is in a cyanide kit and how does it work

A

Amyl Nitrate + Sodium Nitrite + Sodium thiosulfate

You take the amyl nitrite as an inhalant and then IV sodium nitrite which converts a portion of your hemoglobin to methemoglobin, Cyanide is strongly drawn to the methemoglobin than to cytochrome oxidase in cells. Once the cyanide binds the methemoglobin, it becomes cyanomethemoglobin. The sodium thiosulfate and cyanomethemoglobin become thiocyanate, releasing the hemoglobin for renal elimination

45
Q

What are the two types of insecticides we need to know

A
  • Organophosphates- malathion

- Carbamates- carbofuran

46
Q

How do the organophosphates and carbamates cause toxicity?

A 
Inhibit acetylcholinesterase and thus acetylcholine levels go way up and you get cholinergic effects....sludgebbb
Salivation
Lacrimation
Urination
Defecation
GI probs
Emesis
Bronchorrea
Bronchospasm
Bradycardia
47
Q

Treatment of insecticide poisoning

A

Protopam (cholinesterase restarter) + Atropine (anti-cholinergic)

48
Q

How do botanical insecticides work?

A

Work on voltage gated ion channels

49
Q

How does acid cause harm

A
  • On the skin it causes coagulative necrosis
  • Stomach is the most commonly involved organ ans the esophagus and pharynx are relatively resistant.

Causes Gastric/intestinal perforation, upper GI hemorrhage, metabolic acidosis, hemolysis, acute renal failure and death

50
Q

Caustic alkalis

A

Tissue injury by liquefactive necrosis
DOES affect the epithelium of the oropharyx, hypopharynx, and esophagus. Tissue edema occurs immediately and may progress to airway obstruction

51
Q

High protoporphyrin =

A

lead toxicity

52
Q

The presence of lead, even at low levels, impacts what in children?

A

Neural development

53
Q

Lead toxicity is reversed by?

A

Chelators such as:
Succimer- mild cases
Dimercaprol- for severe symptoms
Calcium EDTA-

54
Q

Remember that lead levels will fall and then rise again as lead is mobilized from tissue, thus the use of chelators is not a one and done thing, must be used as a series

A

ok

55
Q

Lead Toxicity

A

GI: Colic and constipation
Nerves: Peripheral neuropathy due to demyelination
Blood: Anemia, microcytic
Kidneys: Impairment of prox tubule function
CNS: Interferes with PKC and neurotransmitters

56
Q

Arsenic poisoning treated with

A

Dimercaprol in adults

Succimer in kids

57
Q

Mercury posoning treatment

A

Dimercaprol and Succimer…..do not reduce neurotoxicity

58
Q

The pattern of symptoms in iron supplement toxicity in kids

A

Nausea and hemorrhagic diarrhea with abdominal pain

At 6-12 hrs the GI symptms resolve and there is apparent recovery

24 hours: metabolic acidosis

Long term is GI tract scarring with obstruction

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