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WRAP UP > PHARM_TOXICOLOGY > Flashcards

PHARM_TOXICOLOGY Flashcards

1
Q

antidote for acetaminophen

A

n-acetylcysteine

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2
Q

antidote for anticholinergics

A

physostigmine

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3
Q

antidote for arsenic, lead, and mercury

A

dimercaprol (first line for arsenic; for severe lead cases) Succimer (for mild lead cases) d-penicillamine

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4
Q

antidote for benzodiazepines

A

flumazenil

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5
Q

antidote for beta-blockers

A

glucagon, insulin & glucose

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6
Q

antidote for CCBs?

A

calcium, glucagon, insulin, and glucose

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7
Q

antidote for cyanide

A

hydroxycobalamin

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8
Q

antidote for cyanide, hydrogen sulfide

A

Na thiosulfate + nitrate hydroxycobalamin

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9
Q

antidote for hydrofluoric acid

A

calcium gluconate

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10
Q

antidote for iron overdose

A

deferoxamine

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11
Q

antidote for lead

A

DMSA (Succimer), EDTA

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12
Q

antidote for opioids

A

naloxone, nalmefene

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13
Q

antidote for organophosphates and carbamates

A

atropine, protopam

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14
Q

antidote for sulfonylureas

A

octreotide

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15
Q

antidote for TCAs

A

bicarbonate

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16
Q

name some drugs/drug classes that are pot’lly fatal in small children in small amounts?

A

antimalarials antidysrhythmics benzocaine beta-blockers CCBs opioids TCAs theophylline

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17
Q

what is the mnemonic to remember for general pt management of intoxication?

A

A-Airway B-Breathing C-Circulation D-disability DEFG-don’t ever forget glucose G-get basic observations

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18
Q

what are the ways you can manage toxicity of a pt?

A
  1. decreased absorption 2. increase elimination 3. using a specific antagonist
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19
Q

what is the most important thing to remember about administering activated charcoal to a pt?

A

airway protection is essential

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20
Q

when is the greatest benefit seen with single dose activated charcoal (SDAC)?

A

within 1 hr of ingestion -note there is no evidence that AC improves outcome

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21
Q

what kind of pts should get gastric decontamination?

A

pts with potentially life-threatening exposure

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22
Q

what is gastric lavage?

A

instill/remove several liters of water pt has to maintain airways (may have increased risk of aspiration)

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23
Q

what are some of the complications of gastric lavage?

A

GI perforation, hypoxia, aspiration

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24
Q

what is whole bowel irrigation?

A

1-2L/hr PEG electrolyte soln -speeds elimination of sustained-release or enteric coated drug preps -not for use in pts with unprotected airway

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25
Q

what are some of the contraindications for whole bowel irrigation?

A

bowel obstruction or perf. hemorrhage ileus hemodynamic instability or intractable vomiting

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26
Q

when is hemodialysis used for intoxication?

A

for toxins with: -water soluble -low Vd -molecular weight <500 Da -low plasma protein binding

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27
Q

what kind of drug intoxications could be alleviated by hemodialysis?

A

methanol, ethylene glycol, salicylates, lithium, sotalol

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28
Q

what is hemoperfusion?

A

passage of blood through absorptive-containing cartridge (usually charcoal)

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29
Q

when would you using hemoperfusion ?

A

removes substances with high degree of plasma protein binding option for: carbamazepine, phenobarbital, phenytoin, & theophylline

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30
Q

name the toxins requiring quantitative levels at a set point

A

acetaminophen

carbon monoxide

ethanol,

ethylene glycol

heavy metals (24 hr urine)

iron

methanol

methemoglobin

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31
Q

name the toxins requiring quantitative serial levels

A

aspirin/salicylates tegretol digoxin phenobarbital phenytoin valproic acid theophylline

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32
Q

name the toxidrome: alert/agitated, dilated pupils, wet mucus membranes, diaphoretic, increased reflexes, increased bowel sounds, increased urine output, increased RR, HR, BP, Temp

A

adrenergic

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33
Q

name the toxidrome: depressed/confused/hallucinating, dilated pupils, dry mucus membranes, dry skin, decreased bowel sounds, decreased urine output, increased temp

A

anticholinergic

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34
Q

name the toxidrome: depressed/confused, constricted pupils, wet mucus membrnaes, diaphoretic, increased bowel sounds, increased urine output, muscle fasciculations, vomiting, decreased HR

A

cholinergic

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35
Q

name the toxidrome: depressed mental status, constricted pupils, decreased bowel sounds, decreased urine output, decreased RR

A

opioid

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36
Q

name the toxidrome: normal vitals, depressed mental status

A

sedative-hypnotics

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37
Q

name the toxidrome: agitated/euphoric/hypomanic, dilated pupils, dry mucus membranes, diaphoretic, increased reflexes, increased bowel sounds, increased: RR, HR, BP, Temp, muscle rigidity, tremor, ataxia/loss of coordination, nystagmus

A

serotonergic

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38
Q

what is the treatment for sympathomimetic toxidrome?

A

Mostly supportive: for HTN: phentolamine, nitrates or CCBs for agitation: BNZs

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39
Q

explain how using bicarbonate work for treating TCA toxicity?

A

bicarb displaces drug from Na+ channels ; increase

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40
Q

how would you treat theophylline toxicity?

A

beta-blockers/muscarinic antagonists for hypotension, tachycardia

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41
Q

what are 4 drug classes that are classic culprits for causing arrhythmias?

A

1, ephedrine, amphetamines, cocaine 2. TCAs 3. Digitalis 4. Theophylline

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42
Q

which drugs are the culprits for seeing blunt force trauma during intoxication?

A

hallucinogens (PCP), ethanol Treatment= protect airways, supportive care

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43
Q

what are the 2 MC signs/symptoms of beta-blocker toxicity?

A

bradycardia & hypotension

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44
Q

how do you treat beta-blocker toxicity?

A
  1. give IV glucagon, followed by infusion
  2. high-dose insulin w/ glucose
  3. membrane-depressant effects (wide QRS interval) may respond to bolus of sodium bicarb
  4. intravenous lipid emulsion has treated propanolol overdose
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45
Q

how does glucagon work to treat beta-blocker toxicity?

A

can increased HR & BP in high doses by raising intracellular cAMP

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46
Q

how is insulin an effective treatment for beta-blocker overdose ?

A
  1. makes heart use carbs which increases lactate uptake and decreases anaerobic metabolism, also increases contractility w/o increasing demand
  2. improves BP & switches metab. from FA’s to Carbs (which results in improved cardiac function) Note: now considered more favorable option
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47
Q

why would you be able to decontaminate the pt with CCB overdose before the drug is absorbed in the GI tract?

A

many CCBs are slow-release formula (use activated charcoal + supportive care)

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48
Q

how do you treat CCB toxicity?

A
  1. For Hypotension & Bradycardia: IV calcium chloride or calcium gluconate (Ca2+ most useful for negative inotropic effects, less effective for AV nodal blockade & bradycardia)
  2. epinephrine infusion & glucagon
  3. high doses of insulin + dextrose (to maintain euglycemia)
  4. intralipid emulsion (can help adsorb drug and improve hemodynamics)
49
Q

what effect does insulin have on blood glucose and potassium?

A

uptake of glucose into skeletal and cardiac muscles and adipose tissue shifts potassium intracellularly

50
Q

what effect does insulin-dextrose have on cardiac contractility and PVR?

A

increases inotropy, and increases PVR

51
Q

what effect do CCBs have on insulin secretion?

A

decrease insulin secretion by blocking pancreatic L-type calcium channels

52
Q

what effect do beta-blockers have on insulin?

A

block insulin secretion; by blocking pancreatic beta-2 receptors

53
Q

describe the 4 phases of APAP poisoning?

A

Phase I: 30 mins - 4 hrs (anorexia, pallor, N/V; may be normal) Phase II: 24-48 hrs (symptoms less severe; RUQ pain, hepatic damage, increased PT, decreased renal function) Phase III: 3-5 days (hepatic necrosis, coagulopathy, jaundice, renal failure, hepatic encephalopathy w/ centrilobular necrosis) Phase IV: 4 days-2wks (resolution or death)

54
Q

how do you know when you should give n-acetylcysteine in acetaminophen toxicity?

A

if the APA conc. > risk line on the Rumack-Matthew nomogram for APAP toxicity

55
Q

what is the most important rule when using n-acetylcysteine with APAP poisoning?

A

don’t stop n-acetylcysteine once started -can use metoclopramide for N/V

56
Q

explain how salicylates cause acid base disorders?

A

uncouple cellular oxidative phosphorylation (anaerobic metab. & excessive prod. of lactic acid and heat; interfere w/ several krebs cycle enzymes) stimulate brainstem causing tachypnea ABGs show respiratory alkalosis & metabolic acidosis

57
Q

what is the clinical presentation of acute ingestion of salicylate excess?

A

N/V; sometimes gastritis

58
Q

describe moderate salicylate intoxication?

A

hypernea, tachycardia, tinnitus

59
Q

describe serious salicylate intoxication?

A

agitation confusion seizures CV collapse pulm. edema hyperthermia-death

60
Q

what is the mnemonic for high anion gap metabolic acidosis? MUDPILES CAT

A

M-methanol or metformin

U-uremia

D-DKA

P-propylene glycol

I-Iron, INH, ibuprofen

L-lactic acidosis

E-ethylene glycol

S-salicylates

(late C-cyanide A-alcohol or acids (valproate) T-toluene or theophylline

61
Q

how do you diagnose salicylate poisoning?

A

anion gap + positive stat salicylate test

62
Q

how do you treat salicylate poisoning?

A
  1. activated charcoal by gastric tube
  2. glucose-containing fluids to reduce risk of cerebral hypoglycemia
  3. Treat metabolic acidosis w/ IV Na+bicarb Note: hemodialysis for pts w/ severe metabolic acidosis or markedly altered mental status
63
Q

what are the clinical features of CO toxicity?

A

headache dizziness N/V seizures coma

64
Q

how do you treat CO poisoning?

A

100% O2

65
Q

what are the clinical features of gas irritants like chlorine, ammonia, sulfur dioxide?

A

cough stridor wheezing pneumonia

66
Q

how do you treat gas irritants (chlorine, ammonia, sulfur dioxide) toxicity?

A

humidified O2 and bronchodilators

67
Q

what is the mechanisms of gas irritant (chlorine, ammonia, sulfur dioxide) toxicity?

A

corrosive effects on upper and lower airways

68
Q

explain the mechanism of cyanide toxicity?

A

blocks O2 binding to cytochrome C

69
Q

what are the clinical features and treatment of cyanide toxicity?

A

headache, N/V, syncope, seizures, coma Treat w/ CN antidote kit

70
Q

what are the clinical features of hydrogen sulfide toxicity?

A

smell of rotten eggs, no specific antidote

71
Q

what is the mechanism of oxidizing agents (nitrogen oxides) toxicity?

A

can cause methemoglobinemia treat w/ methylene blue

72
Q

what comes in a cyanide kit?

A

sodium nitrite + sodium thioulfate + amyl nitrite

73
Q

how does the cyanide kit work to treat cyanide toxicity?

A

small inhaled dose of amylnitrite followed by IV sodium nitrite converts a portion of hgb into methemoglobin

  • cyanide is more strongly drawn to methemoglobin than to cytochrome oxidase
  • once bound w/ cyanide the methemoglobin becomes cyanmethemoglobin
  • the sodium thiosulfate and cyancyanmethemoglobin become thiocyanate, releasing hgb and thiocyanate for renal elim.
74
Q

what is the clinical presentation of solvents (hydrocarbons) toxicity?

A

coughing, gagging, choking w/i 30 mins but can be delayed by hours

  • headache, lethargy & decreased mental status
  • Dyspnea or syncope
  • myocardial sensitization to catecholamines
  • local rxn: perioral rash are not uncommon
75
Q

how do you treat solvents (hydrocarbons) toxicity?

A

decontaminate + ABCs, keep calm -supportive care -intubation if resp. failure -mg2+ & K+ for arrhythmias -lidocaine or beta-blockers for V-fib

76
Q

what treatment for solvents (hydrocarbons) toxicity clearly doesn’t work?

A

charcoal

77
Q

what do you have to remember when treating industrial exposure toxicities?

A

decontaminate, before transportation

78
Q

the organophosphates like malathion and carbamate like carbofuran inhibit what enzyme?

A

inhibit acetylcholinesterase via phosphorylation or carbamoylation Note: phosphates-some target neuronal esterase increasing neurotoxicity + paralysis

79
Q

what is the mnemonic to remember with cholinergic toxicity?

A

S-salivation

L-lacrimation

U-urination

D-defecation

G-GI symptoms

E-emesis

B-bronchorrea

B-bronchospasm

B-bradycardia

80
Q

what is the treatment for cholinergic toxicity?

A

supportive treatment + atropine

81
Q

explain the clinical effects of nicotine-botanical insecticide toxicity via skin or oral ingestion?

A

stimulation of postsynaptic nicotinic receptor followed by depolarizing blockade

82
Q

explain the mechanism of pyrethrum-botanical toxicity via inhalation or ingestion?

A

cns toxicity via voltage-sensitive Na+, Ca2+, Cl- channels presentation: excitation, convulsions, and tetanic paralysis, contact dermatitis Note: provide symptomatic support and control of seizures

83
Q

explain the clinical presentation of rotenone toxicity via skin or oral ingestion?

A

GI irritation, rhinitis, pharyngitis, dermatitis note: provide symptomatic support

84
Q

what are some of the characteristic signs/symptoms of herbicide (2,-4-D) toxicity?

A

metabolic acidosis increased CPK sometimes myoglobinuria breath odor, confusion, and bizarre behavior

85
Q

how do you treat herbicide (2,4-D) toxicity?

A

IV fluids + forced alkaline diuresis (Nabicarb acelerates urinary excretion); control for electrolyte (K+, Ca2+ losses)

86
Q

explain how paraquat (herbicide) causes toxicity?

A

slowly evolving free-radical tissue damage

87
Q

what are some of the acute clinical sequelae of paraquat toxicity?

A

pain & swelling of mouth and throat N/V, abd. pain & bloody diarrhea

88
Q

what is the clinical presentation of the slower onset (speed depends on dose) paraquat (herbicide) toxicity?

A

liver, kidney, heart or lung failure

  • lung scarring
  • CNS toxicity
89
Q

what are some common acid sources?

A

toilet bowl cleaner car battery liquid rust remover metal cleaner cement cleaners drain cleaners

90
Q

what are some common alkali sources?

A

drain cleaner ammonia containing brands oven cleaner swimming pool cleaner dishwashing detergent bleaches cement

91
Q

what kind of tissue injury is caused by caustic acids?

A

coagulative necrosis -eschar or coagulum sloughs in 3-4 days, replaced with granulation tissue

92
Q

which organ is most commonly involved with caustic acids?

A

stomach -pharynx and esophagus are relatively resistant -small bowel in 20% of cases

93
Q

what are some of the clinical signs/symptoms of caustic acids?

A

GI perf, upper GI hemorrhage, metabolic acidosis, hemolysis, acute renal failure & death

94
Q

what kind of tissue injury is caused by caustic alkalis?

A

liquefactive necrosis -emulsification & disruption of cellular membranes

95
Q

which organs are most commonly involved with caustic alkalis?

A

epithelium of oropharynx, hypopharynx, and esophagus (most commonly involved)

96
Q

what are some of the clinical features of caustic alkalis?

A

tissue edema immediately-may persist to 48 hrs (progresses to airway obstruction)

  • over time, granulation tissue replaces necrotic tissue
  • scar tissue thickens and forms strictures 2-4 wks
97
Q

what is the treatment for caustic acids and bases?

A

NO EMETICS

  • gastric lavage
  • NGT suction of liquid products
  • DON’T dilute acids with water (EXCESSIVE HEAT)
98
Q

what are some common sources of lead?

A

pain chips industrial pollution water lead glazed ceramics fishing weights

99
Q

lead poisoning inhibits which 2 enzymes in heme synthesis?

A

delta-aminolevulinic acid dehydratase & ferrochelatase

100
Q

what are some of the clinical effects of lead toxicity?

A
  1. colic and constipation (decreased ACh release, Na+/K+ ATPase inhib.)
  2. slowed nerve conduction (peripheral neuropathy)
  3. Sideroblastic anemia (typically microcytic)
  4. acute impairment of proximal tubule function (aminoaciduria, glycosuria, hyperphosphaturia)
  5. CNS encephalopathy (interferes w/ PKC & NTs’)
101
Q

what are the dermatologic effects seen with chronic exposure to arsenic?

A

hyperpigmentation and both palmar and solar keratoses

102
Q

what is the most serious consequence of arsenic poisoning?

A

malignant change in almost all organs of the body also has increased risk of CVD, peripheral vascular dz, resp, dz, DM, & neutropenia

103
Q

how do you treat lead toxicity?

A

Succimer: mild cases

Dimercaprol: severe cases & encephalopathy

Ca2+ EDTA: can increase CNS Pb levels (used only in conjunction w/ dimercaprol) “used as a series of treatments”

104
Q

describes the general results of chelation therapy with lead poisoning?

A

lowers blood level (can’t reverse existing damage) Rapid fall in Pb levels, then rebound as Pb mobilized from tissues

105
Q

what is first line agent for arsenic toxicity?

A

dimercaprol

106
Q

what are some of the problems with using dimercaprol in arsenic toxicity?

A

formulated in peanut oil for IM injection -issues with hypersensitivity; G6PD deficiency; concurrent iron suppplement therapy -may be nephrotoxic, sterile abscesses (etc.)

107
Q

which antidote is approved for childhood lead poisoning but is efficacious for arsenic intoxications?

A

succimer (hydration is important as its renally excreted)

108
Q

what is the clinical presentation of mercury poisoning?

A

interstitial pneumonitis w/ vapor exopsure

—intention tremor

—inflamm. of gums w/ excessive salivation

—psych symptoms: (irritability, insomnia)

Acrodynia (dequamative rash) in small kids

Paresthesias around mouth

Dose related nephrotic syndrome (ATN w/ severe exposure)

109
Q

what is the treatment for mercury toxicity?

A

supportive care chelation therapy: dimercaprol + succimer Exchange transfusion as last resort

110
Q

Penicillamine is used for what 2 dzs?

A

rheumatoid arthritis wilson’s

111
Q

why is penicillamine experiencing declining use?

A

fatal thrombocytopenia, aplastic anemia, renal failure, neural effects, lots of adverse rxns

112
Q

describe the mechanisms of toxicty of iron supplements?

A
  1. corrosive toxicity to mucosa (hematemesis & diarrhea)
  2. mitochondrial toxin (decrease ox. phos.)
  3. primarily affects liver
113
Q

describe the clinical presentation of iron toxicity?

A

Nausea & bloody diarrhea w/ abd. pain

6-12 hrs: resolution of GI symptoms, apparent recovery

>24 hrs: metabolic acidosis, venous pooling & 3rd-spacing of fluids; increased liver enzymes & bilirubin plus coagulopathy; hypoglycemia

Long: term: GI tract scarring with obstruction

114
Q

what are some of the adverse effects of using deferoxamine?

A

red urine (not blood) Tachycardia, hypotension, & shock

115
Q

brown recluse spider has what kind of toxin and presentation?

A

venom produce endothelial damage, platelet aggregation, rbc lysis (small vessel occlusion & necrosis) Presentation w/ pain, redness, enlarging blister

116
Q

what is loxoscelism?

A

rare complication of brown recluse spider bite including: fever, chills, N/V, arthralgia, convulsions, rash

117
Q

what type of venom does black widow spider have?

A

neurotransmitter dysregulator

118
Q

describe presentation of black widow spider bite?

A

initially redness & induration at bite site cramping develops headache, restlessness, anxiety, fatigue and insomnia (not usually fatal)

119
Q

how do you treat black widow spider bite?

A

antivenin (latrodectus mactans antivenin) -equine protein allergy -reserved for pts at high risk for severe complications

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