Clinical Side of Tox Flashcards
(126 cards)
1
Q
most common route of exposure for POISON
A
ingestion (83%)
inhalation next with 7%
2
Q
fundamental approach to the poisoned patient
A
airway
breathing
circulation
decontamination or avoid abs
elimination or enhance excretion
find an antidote
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!!
4
Q
if breathing effort poor but patient’s airway is open =
A
sedation
aspiration
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
6
Q
how to position for ventilation
A
head tilt, chin lift
jaw thrust
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
8
Q
where to check for pulse
A
carotid or radial pulse
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
10
Q
signs of POOR perfusion
A
- tachycardia
- tachypnea
- hypotension
- mottled skin
- altered mental status
- weak pulses
- delayed capillary refill
- cool skin
11
Q
treatment for poor perfusion
A
IV fluids
meds to increase BP = inotropes = epi, norepi, dopamine, dobutamine
12
Q
what is the goal of decontamination
A
to prevent or minimize absorption
13
Q
options for decontamination
A
activated charcoal
emesis
whole bowel irrigation
gastric levage
14
Q
when is gastric lavage ideally performed
A
in first 4 hrs
15
Q
complications of gastric lavage
A
aspiration pneumonitis
GI tract perforation
16
Q
when do we ideally give activated charcoal for decontam?
A
within first hour
- complications: aspiration, small bowel obstruction
17
Q
when will activated charcoal fail?
A
PHAILS
pesticides
hydrocarbons
acids and alkali
iron
lithium
solvents
18
Q
how does whole bowel irrigation help with decontamination?
A
decrease absorption by decreasing transit time
uses PEG through nasogastric tube
19
Q
greatest utility of whole bowel irrigation
A
iron
lead
lithium OD
sustained release tablets
20
Q
only the sickest or those w potential for severe deterioration do we use THIS technique
A
ELIMINATION
21
Q
elimination techniques
A
urine alkalization
hemodialysis
22
Q
urine alkalization
A
- NAHCO3 intravenously to produce urine pH >/=7.5
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
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
25
examples of hemodialysis
salicylates
theophylline
uremia
methanol
barbiturates
lithium
ethylene glycol
26
antidote: acetaminophen
N-acetylcysteine (NAC)
27
antidote: anticholinergic
physostigmine
28
antidote: benzodiasepines
flumazenil
29
antidote: CO
oxygen
30
antidote: cyanide
hydroxocobalamin, sodium nitrite, sodium thiosulfate
31
antidote: digoxin
digoxin-specific Fab
32
antidote: ethylene glycol
ethanol, fomepizole
33
antidote: iron
deferoxamine
34
antidote: methanol
ethanol, fomepizole
35
antidote: methemoglobinemia
methylene blue
36
antidote: opioids
naloxone
37
antidote: organophosphates
atropine, pralidoxime
38
4 key questions in history taking
what
when
how much
what is patient's weight?
39
tox physical exam (5)
vital signs = HR, BP, R, T, O2 sat
skin
pupils
bowel sounds
neuro exam
other clues?
40
miotic
little pupil
41
mydriatic
big pupil
42
bitter almonds toxin
cyanide
43
carrots smell toxin
water hemlock
44
fishy smell toxin
zinc or aluminum phoshide
45
fruity smell toxin
ethanol, acetate, isopropyl alcohol, chloroform
46
garlic smell toxin
arsenic
DMSO
organophosphates
yellow phosphorus
47
glue smell toxin
toluene, solvents
48
pear smell toxin
paraldehyde
chloral hydrate
49
rotten egg smell toxin
hydrogen sulphide
DMSA
N-acetylcysteine
50
shoe polish smell toxin
nitrobenzene
51
wintergreen smell toxin
methyl salicylate
52
T or F. Everys ingle tox patient gets an ECG
T
53
common toxidromes
sedative/hypnotic
opioids
cholinergic
antichloniergic
sympathomimetic
54
Quaaludes
sedative/hypnotic
methaqualone
55
sed/hypnotic drugs
quaaludes
benzos
barbiturates
ethanol
56
effects of sed/hypnotic drugs
- general anesthesia
- complete loss of awareness and reflex
- mixing common here = dangerous!!
57
sed/hypnotic signs
pupil = normal
RR = decreased
BP,HR = slightly decreased
Skin = normal
mental status = sedated
bowel sounds = normal
58
antidote for sed/hypnotic
flumazenil for benzo but need t be cautious
59
opioids drugs
heroin
morphine
codeine
oxycodone
fentanyl
opium
hydromorphone
Percocet (Tylenol and oxy)
tramadol
60
triad of symptoms in opioid overdose
pinpoint pupils
uconsciousness
respiratory depression
61
T or F. pronounced resp depression in opioid intake
T! RR often diminished before decreases in BP/HR occur
62
opioid symptoms
pupil = small, fixed or pinpoint
RR = decreased
BP,HR = slightly decreased
Skin = normal
mental status = euphoria to coma
bowel sounds = decreased
63
antidote for opioids
naloxone
64
these are common in terrorist attacks
cholinergic
65
what arecholinergic drugs
organc phosphorus compounds = pesticides, nerve gases such as sarin gas
carbamates
mushrooms = boletus, Clitocybe sp, Inocybe sp
**RARE**
66
foundation of nerve agents
cholinergic
67
Cholinergic drugs can harm these healthcare workers
first responders!!! giving mouth-to-mouth
68
symptoms of cholinergic toxidrome
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
antidote for cholinergic
atropine, pralidoxi,e (2-PAM) = cholinesterase regenrator
70
this toxidrome is due to massive discharge of parasymp nervous system
cholinergic
71
killer B's
bronchorrhea
bronchospasm
bradycardia
cholinergic
72
SLUDGE
cholinergic
salivation
lacrimation
urination
diarrhea
GI distress
emesis
73
anticholinergic drugs
anticholinergic
antihistamines
antipsychotics
antidepressants
Jimson weed
74
symtoms of anticholinergic toxidrom
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
anticholinergic memory aid
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
sympathomimetic drugs
stimulants
amphetamines
cocaine
ephedrine (Ma Huang)
meth
phenylpropanolamine (PPA's)
pseudoephedrine
77
sympathomimetic symptoms
pupil = large, reactive
RR = increased
BP,HR = increased
Skin = wet
mental status = agitation, delirium, psychosis
bowel sounds = increased
other = tremor, myoclonus, increased temp
78
antidote for sympathomimetic
none but benzos for agitation
79
antidote for anticholinergic drugs
consider phygostigmine
80
massive sympathomimetic overdoses symptoms
cardiovascular collapse = hypotension
shock
dysrhythmias
81
piloerection may be seen in this toxidrome
sympathomimetic
82
blood gases
pH
hemoglobin
lytes
glucose
lactate
CO level
methemoglobin level
**look at each result then calculate AG and OG**
83
a normal pH and anion gap rules out many ingestions
ASA
cyanide
toxic alcohols
84
metabolic acidosis with resp alkalosis
salicylates
85
metabolic acidosis with increased lactate
metformin
86
anion gap
cations - anions
sodium - (bicarb + chloride)
87
if AG is >____, this implies unmeasured ______ from a toxic or metabolic source
12; anions
88
elevated AG is strongly suggestive of this
metabolic acidosis
89
high anion gap metabolic acidosis drugs
MUDPILES
methanol
uremia
diabetic ketoacidosis, etc.
paraldehyde
iron, isoniazid
lactic acidosis
ethylene glycol
salicylates
90
osmolal gap
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
calculated osmoles
2(Na+) + urea + glucose
290-300
92
these caused increased OG
SAGMMAP
sorbitol
alcohols
glycerol
maltose
mannitol
acetone
polyethylene glycol, propylene glycol
93
what is the tox screen?
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
one pill can kill
cardiac medications
antidepressants
antimalarials
isoniazid
iron
sulfonylureas
rec sympathomimetic drugs
opiates
oil of wintergreen
95
ASA toxic dose
150-200 mg/kg
96
severe intoxication of ASA
300-500 mg/kg
97
what do we initially see after ASA ingestion?
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
clinical presentation of ASA ingestion
vomiting
hyperpnea (increase depth and breathing rate)
lethargy
tinnitus
mixed resp alk and metabolic acidosis
99
severe ASA intoxication presentation
coma
seizure
hypoglycemia
hyperthermia
pulmonary edema
100
ASA decontam
gastric decontam : activated charcoal and consider whole bowel irrigation if enteric coated
101
elimination for ASA
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
acetaminophen toxic dose
>150 mg/kg
103
overdose PK of acetaminophen
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
phases of acetaminophen poisoning
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
this is available to help decide if treatment is needed for acetaminophen level
nomogram
- indicated only in acute ingestions
- need time of ingestion
106
NAC
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
Decontam and antidote for Acetaminophen
charcoal
NAC
107
what does CO bind with?
hemoglobin (250x greater affinity than O2)
myoglobin
cytochrome oxidase
induces lipid peroxidation also
108
what causes CO poisoning?
incomplete combustion of fossil fuels
> fires
> engine exhaust
> propane-powered vehicles
> home heating, gas stoves, dryers, water heaters
methylene chloride (paint strippers)
108
T or F. CO shifts oxygen dissociation curve to right
F! shits to left
109
Rate of elimination for CO depends on ...
rate of dissociation
110
clinical symptoms of CO
CNS:
headache, nausea, blurred vision, altered LOC, ataxia, seizures, coma
CVS:
dyspnea, weakness, angina, palpitations, hypotension, MI, dysrhythmias
111
this percentage of CO is rapidly fatal
>80&
60-70% = seizures/death
112
this percentage of CO is normal
1-5%
5-10% in smokers
113
management for CO poisoning
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
T or F. Ethanol is not a toxic alcohol
T! b/c metabolite not toxic
- CNS depression, resp depression and hypoglycemia due to inhibition of gluconeogenesis
115
clinical presentations of ethylene gkycikl
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
labs for eth glycol
elevated OG
high AG metabolic acidosis without signifcant lactates/ketones
hypocalcemia from formation of oxylate
117
this is used in gas line antifreeze and windshield washer fluid
methanol
118
clinical findings for methanol
inebriation
visual changes
abdominal complaints
119
labs for methanol
high AG metabolic acidosis without significant lactate or ketones
pH <7.2 predictive of impaired visual acuity
elevated OG
120
treatment for toxic alcohol ingestion
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
what is fomepizole?
competitive inhibitor of ADH
benefits over alcohol:
- no increased sedation or resp depression
- avoid hypoglycemia
BUT EXPENSIVE!
122
indications for hemodialysis
met acidosis
renal failure
deterioration despite other treatments
electrolyte disturbances
visual disturbance (methanol)
methanol level >15 mmol/L
ethylene glycol >8 mmol/L
123
elim for toxic alcs
hemodialysis
124
adjuncts for toxic alcohols
folate, pyridoxine, thiamine
sodium bicarb
