PHARM_TOXICOLOGY Flashcards
1
Q
antidote for acetaminophen
A
n-acetylcysteine
2
Q
antidote for anticholinergics
A
physostigmine
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
4
Q
antidote for benzodiazepines
A
flumazenil
5
Q
antidote for beta-blockers
A
glucagon, insulin & glucose
6
Q
antidote for CCBs?
A
calcium, glucagon, insulin, and glucose
7
Q
antidote for cyanide
A
hydroxycobalamin
8
Q
antidote for cyanide, hydrogen sulfide
A
Na thiosulfate + nitrate hydroxycobalamin
9
Q
antidote for hydrofluoric acid
A
calcium gluconate
10
Q
antidote for iron overdose
A
deferoxamine
11
Q
antidote for lead
A
DMSA (Succimer), EDTA
12
Q
antidote for opioids
A
naloxone, nalmefene
13
Q
antidote for organophosphates and carbamates
A
atropine, protopam
14
Q
antidote for sulfonylureas
A
octreotide
15
Q
antidote for TCAs
A
bicarbonate
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
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
18
Q
what are the ways you can manage toxicity of a pt?
A
- decreased absorption 2. increase elimination 3. using a specific antagonist
19
Q
what is the most important thing to remember about administering activated charcoal to a pt?
A
airway protection is essential
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
21
Q
what kind of pts should get gastric decontamination?
A
pts with potentially life-threatening exposure
22
Q
what is gastric lavage?
A
instill/remove several liters of water pt has to maintain airways (may have increased risk of aspiration)
23
Q
what are some of the complications of gastric lavage?
A
GI perforation, hypoxia, aspiration
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
25
what are some of the contraindications for whole bowel irrigation?
bowel obstruction or perf. hemorrhage ileus hemodynamic instability or intractable vomiting
26
when is hemodialysis used for intoxication?
for toxins with: -water soluble -low Vd -molecular weight \<500 Da -low plasma protein binding
27
what kind of drug intoxications could be alleviated by hemodialysis?
methanol, ethylene glycol, salicylates, lithium, sotalol
28
what is hemoperfusion?
passage of blood through absorptive-containing cartridge (usually charcoal)
29
when would you using hemoperfusion ?
removes substances with high degree of plasma protein binding option for: carbamazepine, phenobarbital, phenytoin, & theophylline
30
name the toxins requiring quantitative levels at a set point
acetaminophen
carbon monoxide
ethanol,
ethylene glycol
heavy metals (24 hr urine)
iron
methanol
methemoglobin
31
name the toxins requiring quantitative serial levels
aspirin/salicylates tegretol digoxin phenobarbital phenytoin valproic acid theophylline
32
name the toxidrome: alert/agitated, dilated pupils, wet mucus membranes, diaphoretic, increased reflexes, increased bowel sounds, increased urine output, increased RR, HR, BP, Temp
adrenergic
33
name the toxidrome: depressed/confused/hallucinating, dilated pupils, dry mucus membranes, dry skin, decreased bowel sounds, decreased urine output, increased temp
anticholinergic
34
name the toxidrome: depressed/confused, constricted pupils, wet mucus membrnaes, diaphoretic, increased bowel sounds, increased urine output, muscle fasciculations, vomiting, decreased HR
cholinergic
35
name the toxidrome: depressed mental status, constricted pupils, decreased bowel sounds, decreased urine output, decreased RR
opioid
36
name the toxidrome: normal vitals, depressed mental status
sedative-hypnotics
37
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
serotonergic
38
what is the treatment for sympathomimetic toxidrome?
Mostly supportive: for HTN: phentolamine, nitrates or CCBs for agitation: BNZs
39
explain how using bicarbonate work for treating TCA toxicity?
bicarb displaces drug from Na+ channels ; increase
40
how would you treat theophylline toxicity?
beta-blockers/muscarinic antagonists for hypotension, tachycardia
41
what are 4 drug classes that are classic culprits for causing arrhythmias?
1, ephedrine, amphetamines, cocaine 2. TCAs 3. Digitalis 4. Theophylline
42
which drugs are the culprits for seeing blunt force trauma during intoxication?
hallucinogens (PCP), ethanol Treatment= protect airways, supportive care
43
what are the 2 MC signs/symptoms of beta-blocker toxicity?
bradycardia & hypotension
44
how do you treat beta-blocker toxicity?
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
45
how does glucagon work to treat beta-blocker toxicity?
can increased HR & BP in high doses by raising intracellular cAMP
46
how is insulin an effective treatment for beta-blocker overdose ?
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
47
why would you be able to decontaminate the pt with CCB overdose before the drug is absorbed in the GI tract?
many CCBs are slow-release formula (use activated charcoal + supportive care)
48
how do you treat CCB toxicity?
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
what effect does insulin have on blood glucose and potassium?
uptake of glucose into skeletal and cardiac muscles and adipose tissue shifts potassium intracellularly
50
what effect does insulin-dextrose have on cardiac contractility and PVR?
increases inotropy, and increases PVR
51
what effect do CCBs have on insulin secretion?
decrease insulin secretion by blocking pancreatic L-type calcium channels
52
what effect do beta-blockers have on insulin?
block insulin secretion; by blocking pancreatic beta-2 receptors
53
describe the 4 phases of APAP poisoning?
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
how do you know when you should give n-acetylcysteine in acetaminophen toxicity?
if the APA conc. \> risk line on the Rumack-Matthew nomogram for APAP toxicity
55
what is the most important rule when using n-acetylcysteine with APAP poisoning?
don't stop n-acetylcysteine once started -can use metoclopramide for N/V
56
explain how salicylates cause acid base disorders?
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
what is the clinical presentation of acute ingestion of salicylate excess?
N/V; sometimes gastritis
58
describe moderate salicylate intoxication?
hypernea, tachycardia, tinnitus
59
describe serious salicylate intoxication?
agitation confusion seizures CV collapse pulm. edema hyperthermia-death
60
what is the mnemonic for high anion gap metabolic acidosis? MUDPILES CAT
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
how do you diagnose salicylate poisoning?
anion gap + positive stat salicylate test
62
how do you treat salicylate poisoning?
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
what are the clinical features of CO toxicity?
headache dizziness N/V seizures coma
64
how do you treat CO poisoning?
100% O2
65
what are the clinical features of gas irritants like chlorine, ammonia, sulfur dioxide?
cough stridor wheezing pneumonia
66
how do you treat gas irritants (chlorine, ammonia, sulfur dioxide) toxicity?
humidified O2 and bronchodilators
67
what is the mechanisms of gas irritant (chlorine, ammonia, sulfur dioxide) toxicity?
corrosive effects on upper and lower airways
68
explain the mechanism of cyanide toxicity?
blocks O2 binding to cytochrome C
69
what are the clinical features and treatment of cyanide toxicity?
headache, N/V, syncope, seizures, coma Treat w/ CN antidote kit
70
what are the clinical features of hydrogen sulfide toxicity?
smell of rotten eggs, no specific antidote
71
what is the mechanism of oxidizing agents (nitrogen oxides) toxicity?
can cause methemoglobinemia treat w/ methylene blue
72
what comes in a cyanide kit?
sodium nitrite + sodium thioulfate + amyl nitrite
73
how does the cyanide kit work to treat cyanide toxicity?
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
what is the clinical presentation of solvents (hydrocarbons) toxicity?
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
how do you treat solvents (hydrocarbons) toxicity?
decontaminate + ABCs, keep calm -supportive care -intubation if resp. failure -mg2+ & K+ for arrhythmias -lidocaine or beta-blockers for V-fib
76
what treatment for solvents (hydrocarbons) toxicity clearly doesn't work?
charcoal
77
what do you have to remember when treating industrial exposure toxicities?
decontaminate, before transportation
78
the organophosphates like malathion and carbamate like carbofuran inhibit what enzyme?
inhibit acetylcholinesterase via phosphorylation or carbamoylation Note: phosphates-some target neuronal esterase increasing neurotoxicity + paralysis
79
what is the mnemonic to remember with cholinergic toxicity?
S-salivation
L-lacrimation
U-urination
D-defecation
G-GI symptoms
E-emesis
B-bronchorrea
B-bronchospasm
B-bradycardia
80
what is the treatment for cholinergic toxicity?
supportive treatment + atropine
81
explain the clinical effects of nicotine-botanical insecticide toxicity via skin or oral ingestion?
stimulation of postsynaptic nicotinic receptor followed by depolarizing blockade
82
explain the mechanism of pyrethrum-botanical toxicity via inhalation or ingestion?
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
explain the clinical presentation of rotenone toxicity via skin or oral ingestion?
GI irritation, rhinitis, pharyngitis, dermatitis note: provide symptomatic support
84
what are some of the characteristic signs/symptoms of herbicide (2,-4-D) toxicity?
metabolic acidosis increased CPK sometimes myoglobinuria breath odor, confusion, and bizarre behavior
85
how do you treat herbicide (2,4-D) toxicity?
IV fluids + forced alkaline diuresis (Nabicarb acelerates urinary excretion); control for electrolyte (K+, Ca2+ losses)
86
explain how paraquat (herbicide) causes toxicity?
slowly evolving free-radical tissue damage
87
what are some of the acute clinical sequelae of paraquat toxicity?
pain & swelling of mouth and throat N/V, abd. pain & bloody diarrhea
88
what is the clinical presentation of the slower onset (speed depends on dose) paraquat (herbicide) toxicity?
liver, kidney, heart or lung failure
- lung scarring
- CNS toxicity
89
what are some common acid sources?
toilet bowl cleaner car battery liquid rust remover metal cleaner cement cleaners drain cleaners
90
what are some common alkali sources?
drain cleaner ammonia containing brands oven cleaner swimming pool cleaner dishwashing detergent bleaches cement
91
what kind of tissue injury is caused by caustic acids?
coagulative necrosis -eschar or coagulum sloughs in 3-4 days, replaced with granulation tissue
92
which organ is most commonly involved with caustic acids?
stomach -pharynx and esophagus are relatively resistant -small bowel in 20% of cases
93
what are some of the clinical signs/symptoms of caustic acids?
GI perf, upper GI hemorrhage, metabolic acidosis, hemolysis, acute renal failure & death
94
what kind of tissue injury is caused by caustic alkalis?
liquefactive necrosis -emulsification & disruption of cellular membranes
95
which organs are most commonly involved with caustic alkalis?
epithelium of oropharynx, hypopharynx, and esophagus (most commonly involved)
96
what are some of the clinical features of caustic alkalis?
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
what is the treatment for caustic acids and bases?
NO EMETICS
- gastric lavage
- NGT suction of liquid products
- DON'T dilute acids with water (EXCESSIVE HEAT)
98
what are some common sources of lead?
pain chips industrial pollution water lead glazed ceramics fishing weights
99
lead poisoning inhibits which 2 enzymes in heme synthesis?
delta-aminolevulinic acid dehydratase & ferrochelatase
100
what are some of the clinical effects of lead toxicity?
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
what are the dermatologic effects seen with chronic exposure to arsenic?
hyperpigmentation and both palmar and solar keratoses
102
what is the most serious consequence of arsenic poisoning?
malignant change in almost all organs of the body also has increased risk of CVD, peripheral vascular dz, resp, dz, DM, & neutropenia
103
how do you treat lead toxicity?
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
describes the general results of chelation therapy with lead poisoning?
lowers blood level (can't reverse existing damage) Rapid fall in Pb levels, then rebound as Pb mobilized from tissues
105
what is first line agent for arsenic toxicity?
dimercaprol
106
what are some of the problems with using dimercaprol in arsenic toxicity?
formulated in peanut oil for IM injection -issues with hypersensitivity; G6PD deficiency; concurrent iron suppplement therapy -may be nephrotoxic, sterile abscesses (etc.)
107
which antidote is approved for childhood lead poisoning but is efficacious for arsenic intoxications?
succimer (hydration is important as its renally excreted)
108
what is the clinical presentation of mercury poisoning?
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
what is the treatment for mercury toxicity?
supportive care chelation therapy: dimercaprol + succimer Exchange transfusion as last resort
110
Penicillamine is used for what 2 dzs?
rheumatoid arthritis wilson's
111
why is penicillamine experiencing declining use?
fatal thrombocytopenia, aplastic anemia, renal failure, neural effects, lots of adverse rxns
112
describe the mechanisms of toxicty of iron supplements?
1. corrosive toxicity to mucosa (hematemesis & diarrhea)
2. mitochondrial toxin (decrease ox. phos.)
3. primarily affects liver
113
describe the clinical presentation of iron toxicity?
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
what are some of the adverse effects of using deferoxamine?
red urine (not blood) Tachycardia, hypotension, & shock
115
brown recluse spider has what kind of toxin and presentation?
venom produce endothelial damage, platelet aggregation, rbc lysis (small vessel occlusion & necrosis) Presentation w/ pain, redness, enlarging blister
116
what is loxoscelism?
rare complication of brown recluse spider bite including: fever, chills, N/V, arthralgia, convulsions, rash
117
what type of venom does black widow spider have?
neurotransmitter dysregulator
118
describe presentation of black widow spider bite?
initially redness & induration at bite site cramping develops headache, restlessness, anxiety, fatigue and insomnia (not usually fatal)
119
how do you treat black widow spider bite?
antivenin (latrodectus mactans antivenin) -equine protein allergy -reserved for pts at high risk for severe complications
