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MLSCI 466 > Clinical Side of Tox > Flashcards

Clinical Side of Tox Flashcards

1
Q

most common route of exposure for POISON

A

ingestion (83%)
inhalation next with 7%

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2
Q

fundamental approach to the poisoned patient

A

airway
breathing
circulation
decontamination or avoid abs
elimination or enhance excretion
find an antidote

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3
Q

airway can be in danger due to:

A
  • sedation = low airway smooth muscle tone
  • inhalation of toxin or vomit (ASPIRATION)
  • increased secretions

protect airway early and continually assess!!

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4
Q

if breathing effort poor but patient’s airway is open =

A

sedation
aspiration

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5
Q

if breathing is poor, you or machine must breathe for the poisoned pt

A

mouth to mouth
bag-valve mask ventilation (BVM)
advanced airway

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6
Q

how to position for ventilation

A

head tilt, chin lift
jaw thrust

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7
Q

circulation assesses for signs of..

A

poor perfusion
- heart rate, BO, skin temp, pulses, urine output
- establish vascular access early in poisoned pt

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8
Q

where to check for pulse

A

carotid or radial pulse

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9
Q

CPR is as easy as …

A

Compression = push hard and fast on victim’s chest
Airway = tilt victim’s head and lift chin to open airway
Breathing = give mouth-to-mouth rescue breaths

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10
Q

signs of POOR perfusion

A
  • tachycardia
  • tachypnea
  • hypotension
  • mottled skin
  • altered mental status
  • weak pulses
  • delayed capillary refill
  • cool skin
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11
Q

treatment for poor perfusion

A

IV fluids
meds to increase BP = inotropes = epi, norepi, dopamine, dobutamine

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12
Q

what is the goal of decontamination

A

to prevent or minimize absorption

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13
Q

options for decontamination

A

activated charcoal
emesis
whole bowel irrigation
gastric levage

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14
Q

when is gastric lavage ideally performed

A

in first 4 hrs

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15
Q

complications of gastric lavage

A

aspiration pneumonitis
GI tract perforation

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16
Q

when do we ideally give activated charcoal for decontam?

A

within first hour
- complications: aspiration, small bowel obstruction

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17
Q

when will activated charcoal fail?

A

PHAILS
pesticides
hydrocarbons
acids and alkali
iron
lithium
solvents

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18
Q

how does whole bowel irrigation help with decontamination?

A

decrease absorption by decreasing transit time

uses PEG through nasogastric tube

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19
Q

greatest utility of whole bowel irrigation

A

iron
lead
lithium OD
sustained release tablets

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20
Q

only the sickest or those w potential for severe deterioration do we use THIS technique

A

ELIMINATION

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21
Q

elimination techniques

A

urine alkalization
hemodialysis

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22
Q

urine alkalization

A
  • NAHCO3 intravenously to produce urine pH >/=7.5
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23
Q

urine alkalization increases urine elimination of:

A

chlorpropamide (type II DM)
2,4-dichlorophenoxyacetic acid and Mecoprop (herbicides)
fluoride
methotrexate (chemotherapy)
phenobarbital (antiseizure)
salicylate

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24
Q

medication properties of hemodialysis

A

low Vd (<1L/kg)
single compartment kinetics
low endogenous clearance (<4 ml/min/kg)
MW <500 daltons
water sol
not bound to plasma proteins

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25
Q

examples of hemodialysis

A

salicylates
theophylline
uremia
methanol
barbiturates
lithium
ethylene glycol

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26
Q

antidote: acetaminophen

A

N-acetylcysteine (NAC)

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27
Q

antidote: anticholinergic

A

physostigmine

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28
Q

antidote: benzodiasepines

A

flumazenil

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29
Q

antidote: CO

A

oxygen

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30
Q

antidote: cyanide

A

hydroxocobalamin, sodium nitrite, sodium thiosulfate

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31
Q

antidote: digoxin

A

digoxin-specific Fab

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32
Q

antidote: ethylene glycol

A

ethanol, fomepizole

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33
Q

antidote: iron

A

deferoxamine

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34
Q

antidote: methanol

A

ethanol, fomepizole

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35
Q

antidote: methemoglobinemia

A

methylene blue

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36
Q

antidote: opioids

A

naloxone

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37
Q

antidote: organophosphates

A

atropine, pralidoxime

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38
Q

4 key questions in history taking

A

what
when
how much
what is patient’s weight?

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39
Q

tox physical exam (5)

A

vital signs = HR, BP, R, T, O2 sat
skin
pupils
bowel sounds
neuro exam

other clues?

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40
Q

miotic

A

little pupil

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41
Q

mydriatic

A

big pupil

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42
Q

bitter almonds toxin

A

cyanide

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43
Q

carrots smell toxin

A

water hemlock

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44
Q

fishy smell toxin

A

zinc or aluminum phoshide

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45
Q

fruity smell toxin

A

ethanol, acetate, isopropyl alcohol, chloroform

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46
Q

garlic smell toxin

A

arsenic
DMSO
organophosphates
yellow phosphorus

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47
Q

glue smell toxin

A

toluene, solvents

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48
Q

pear smell toxin

A

paraldehyde
chloral hydrate

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49
Q

rotten egg smell toxin

A

hydrogen sulphide
DMSA
N-acetylcysteine

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50
Q

shoe polish smell toxin

A

nitrobenzene

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51
Q

wintergreen smell toxin

A

methyl salicylate

52
Q

T or F. Everys ingle tox patient gets an ECG

A

T

53
Q

common toxidromes

A

sedative/hypnotic
opioids
cholinergic
antichloniergic
sympathomimetic

54
Q

Quaaludes

A

sedative/hypnotic
methaqualone

55
Q

sed/hypnotic drugs

A

quaaludes
benzos
barbiturates
ethanol

56
Q

effects of sed/hypnotic drugs

A
  • general anesthesia
  • complete loss of awareness and reflex
  • mixing common here = dangerous!!
57
Q

sed/hypnotic signs

A

pupil = normal
RR = decreased
BP,HR = slightly decreased
Skin = normal
mental status = sedated
bowel sounds = normal

58
Q

antidote for sed/hypnotic

A

flumazenil for benzo but need t be cautious

59
Q

opioids drugs

A

heroin
morphine
codeine
oxycodone
fentanyl
opium
hydromorphone
Percocet (Tylenol and oxy)
tramadol

60
Q

triad of symptoms in opioid overdose

A

pinpoint pupils
uconsciousness
respiratory depression

61
Q

T or F. pronounced resp depression in opioid intake

A

T! RR often diminished before decreases in BP/HR occur

62
Q

opioid symptoms

A

pupil = small, fixed or pinpoint
RR = decreased
BP,HR = slightly decreased
Skin = normal
mental status = euphoria to coma
bowel sounds = decreased

63
Q

antidote for opioids

A

naloxone

64
Q

these are common in terrorist attacks

A

cholinergic

65
Q

what arecholinergic drugs

A

organc phosphorus compounds = pesticides, nerve gases such as sarin gas
carbamates
mushrooms = boletus, Clitocybe sp, Inocybe sp

RARE

66
Q

foundation of nerve agents

A

cholinergic

67
Q

Cholinergic drugs can harm these healthcare workers

A

first responders!!! giving mouth-to-mouth

68
Q

symptoms of cholinergic toxidrome

A

pupil = small, fixed, lacrimation
RR = normal/increased
BP,HR = increased/decreased
Skin = wet
mental status = conusion/drowsiness to coma, seizures
bowel sounds = increased
other = SLUDGE and killer B’s, pulmonary edema, fasciculations,
weakness -> paralysis

69
Q

antidote for cholinergic

A

atropine, pralidoxi,e (2-PAM) = cholinesterase regenrator

70
Q

this toxidrome is due to massive discharge of parasymp nervous system

A

cholinergic

71
Q

killer B’s

A

bronchorrhea
bronchospasm
bradycardia

cholinergic

72
Q

SLUDGE

A

cholinergic

salivation
lacrimation
urination
diarrhea
GI distress
emesis

73
Q

anticholinergic drugs

A

anticholinergic
antihistamines
antipsychotics
antidepressants
Jimson weed

74
Q

symtoms of anticholinergic toxidrom

A

pupil = big, fixed, blurred vision (CARTOON-like)
RR = normal
BP,HR = HR increased
Skin = dry, hot, flushed
mental status = delirium, coma, seizures
bowel sounds = decreased
other = urinary retention (sometimes can’t communicate so insert catheter to decrease pt agitation)

75
Q

anticholinergic memory aid

A

mad as a hatter, hot as hades, red as a beet, dry as a bone, blind as a bat. the bowel and bladder lose their tone and the heart goes on alone

76
Q

sympathomimetic drugs

A

stimulants

amphetamines
cocaine
ephedrine (Ma Huang)
meth
phenylpropanolamine (PPA’s)
pseudoephedrine

77
Q

sympathomimetic symptoms

A

pupil = large, reactive
RR = increased
BP,HR = increased
Skin = wet
mental status = agitation, delirium, psychosis
bowel sounds = increased
other = tremor, myoclonus, increased temp

78
Q

antidote for sympathomimetic

A

none but benzos for agitation

79
Q

antidote for anticholinergic drugs

A

consider phygostigmine

80
Q

massive sympathomimetic overdoses symptoms

A

cardiovascular collapse = hypotension
shock
dysrhythmias

81
Q

piloerection may be seen in this toxidrome

A

sympathomimetic

82
Q

blood gases

A

pH
hemoglobin
lytes
glucose
lactate
CO level
methemoglobin level

look at each result then calculate AG and OG

83
Q

a normal pH and anion gap rules out many ingestions

A

ASA
cyanide
toxic alcohols

84
Q

metabolic acidosis with resp alkalosis

A

salicylates

85
Q

metabolic acidosis with increased lactate

A

metformin

86
Q

anion gap

A

cations - anions
sodium - (bicarb + chloride)

87
Q

if AG is >____, this implies unmeasured ______ from a toxic or metabolic source

A

12; anions

88
Q

elevated AG is strongly suggestive of this

A

metabolic acidosis

89
Q

high anion gap metabolic acidosis drugs

A

MUDPILES
methanol
uremia
diabetic ketoacidosis, etc.
paraldehyde
iron, isoniazid
lactic acidosis
ethylene glycol
salicylates

90
Q

osmolal gap

A

measured - calc osmoles

  • should be 0-10 (-12 to 1)
  • unaccounted osmoles (elevated OG) may signify a toxic alc ingestion
    = but not sensitive enough to rule out
91
Q

calculated osmoles

A

2(Na+) + urea + glucose

290-300

92
Q

these caused increased OG

A

SAGMMAP
sorbitol
alcohols
glycerol
maltose
mannitol
acetone
polyethylene glycol, propylene glycol

93
Q

what is the tox screen?

A

urine screen for various drugs of abuse
= rarely results in ID of ingestion agent
= results not usually available until hrs/days after most of acute treatment decisions are made
= very expensive!

94
Q

one pill can kill

A

cardiac medications
antidepressants
antimalarials
isoniazid
iron
sulfonylureas
rec sympathomimetic drugs
opiates
oil of wintergreen

95
Q

ASA toxic dose

A

150-200 mg/kg

96
Q

severe intoxication of ASA

A

300-500 mg/kg

97
Q

what do we initially see after ASA ingestion?

A

resp alkalosis
- direct stimulation of medulla/breathing center

then develop elevated AG metabolic acidosis
- impaired renal function due to acid production
- interference w Krebs
- uncoupling oxidative phosphorylation

98
Q

clinical presentation of ASA ingestion

A

vomiting
hyperpnea (increase depth and breathing rate)
lethargy
tinnitus

mixed resp alk and metabolic acidosis

99
Q

severe ASA intoxication presentation

A

coma
seizure
hypoglycemia
hyperthermia
pulmonary edema

100
Q

ASA decontam

A

gastric decontam : activated charcoal and consider whole bowel irrigation if enteric coated

101
Q

elimination for ASA

A

urinary alkalization
- indicated when symptomatic, acute salicylate level >2.5 mmol/L or rising, significant acid-base disturbance

hemodialysis
- indicated when >7mmol/L, chronic >3.5, altered mental status (coma, seizure), intubation, pulmonary edema, renal or hepatic failure, failure of urinary alkalinization

102
Q

acetaminophen toxic dose

A

> 150 mg/kg

103
Q

overdose PK of acetaminophen

A

sulfation and glucuronidation pathways become saturated, shunting acetaminophen towards P450 pathway resulting in increased NAPQI production

detox of NPQI depletes glutathione

glutathione below 30% = NAPQI binds non-specifically to intracellular proteins resulting in cell dysfunction

104
Q

phases of acetaminophen poisoning

A

phase I (<24h)
- anorexia, nausea/vomiting, malaise

phase II
- most symptoms resolve
- right upper quadrant abdominal pain
- start seeing abnormal labs such as high AST/ALT, high bili, high INR

phase III
- sequelae of hepatic necrosis = jaundice, coagulopathies, encephalopathy, hypoglycemia
- renal failure
myocardial dysfunction

phase IV
- 4d-2wk
- after hepatic failure
- complete resolution of injury; no residual liver dysfunction
- need for urgent liver transplantation
- death

105
Q

this is available to help decide if treatment is needed for acetaminophen level

A

nomogram
- indicated only in acute ingestions
- need time of ingestion

106
Q

NAC

A

N-acetylcysteine
- glutathione precursor/substitute
- enhances sulfation
- free radical scavenger
- enhances hepatic oxygen delivery
- decreases cerebral edema and hypotension
- initiate within 8hrs
- 21hr protocol
- oral or IV dosing

107
Q

Decontam and antidote for Acetaminophen

A

charcoal
NAC

107
Q

what does CO bind with?

A

hemoglobin (250x greater affinity than O2)
myoglobin
cytochrome oxidase
induces lipid peroxidation also

108
Q

what causes CO poisoning?

A

incomplete combustion of fossil fuels
> fires
> engine exhaust
> propane-powered vehicles
> home heating, gas stoves, dryers, water heaters

methylene chloride (paint strippers)

108
Q

T or F. CO shifts oxygen dissociation curve to right

A

F! shits to left

109
Q

Rate of elimination for CO depends on …

A

rate of dissociation

110
Q

clinical symptoms of CO

A

CNS:
headache, nausea, blurred vision, altered LOC, ataxia, seizures, coma

CVS:
dyspnea, weakness, angina, palpitations, hypotension, MI, dysrhythmias

111
Q

this percentage of CO is rapidly fatal

A

> 80&

60-70% = seizures/death

112
Q

this percentage of CO is normal

A

1-5%
5-10% in smokers

113
Q

management for CO poisoning

A

remove from source
ABCs
F: 100% supplemental O2 = hyperbaric O2 if indicated

labs
- COHb level by co-oximetry (NOT PULSE)
- assess end-organ damage
- preg test

114
Q

T or F. Ethanol is not a toxic alcohol

A

T! b/c metabolite not toxic
- CNS depression, resp depression and hypoglycemia due to inhibition of gluconeogenesis

115
Q

clinical presentations of ethylene gkycikl

A

stage I: acute neurologic, slurred speech, ataxia, vomitting
stage II: cardiopulmonary: hypertension, tachycardia, tachypnea, ARDS, CV collapse
III: renal; flank pain, hematuria, proteinuria, oliguria => anuria

116
Q

labs for eth glycol

A

elevated OG
high AG metabolic acidosis without signifcant lactates/ketones
hypocalcemia from formation of oxylate

117
Q

this is used in gas line antifreeze and windshield washer fluid

A

methanol

118
Q

clinical findings for methanol

A

inebriation
visual changes
abdominal complaints

119
Q

labs for methanol

A

high AG metabolic acidosis without significant lactate or ketones
pH <7.2 predictive of impaired visual acuity
elevated OG

120
Q

treatment for toxic alcohol ingestion

A

block alc dehydrogenase (ADH)
> ethanol or Fomepizole
> risk of hypotension, tachycardia, CNS/resp depression, hypoglycemia, electrolyte derangement, gastritis

sodium bicarb to correct acidosis

adjuncts (folate, pyridoxine, thiamine)

dialysis to remove parent alc and metabolites

121
Q

what is fomepizole?

A

competitive inhibitor of ADH
benefits over alcohol:
- no increased sedation or resp depression
- avoid hypoglycemia

BUT EXPENSIVE!

122
Q

indications for hemodialysis

A

met acidosis
renal failure
deterioration despite other treatments
electrolyte disturbances
visual disturbance (methanol)
methanol level >15 mmol/L
ethylene glycol >8 mmol/L

123
Q

elim for toxic alcs

A

hemodialysis

124
Q

adjuncts for toxic alcohols

A

folate, pyridoxine, thiamine
sodium bicarb

MLSCI 466 (19 decks)

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