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Unit 1 Emerg/Surg > L3: AMS + Toxicology > Flashcards

L3: AMS + Toxicology Flashcards

1
Q

If you don’t ask person, place, and time, what should document about someone’s mental status?

A

Alert and appropriate

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2
Q

Alert is defined as

A

Awake, fully aware of surroundings, appropriate response to normal stimuli
Does not imply capacity to focus attention

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3
Q

Spectrum of level of conciousness

A 
alert
lethargic/somnolent
obtunded
stuporous/semicomatose
comatose
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4
Q

Lethargic or somnolent is defined as

A

not fully alert, drifts off to sleep when not stimulated, spontaneous movements decreased, awareness limited

Unable to pay close attention, loses train of thought

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5
Q

Obtunded is defined as

A

Difficult to arouse and when aroused, confused

Constant stimulation required to elicit minimal cooperation

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6
Q

Stuporous or semicomatose means

A

Does not arouse spontaneously

Vigorous stimulation→ little response, moaning/mumbling when aroused

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7
Q

Coma

A

unarousable unresponsiveness

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8
Q

When to intubate someone according to the glasgow coma scale

A

Score <8 for >72 hours

very poor prognosis

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9
Q

Major neurocognitive disorder aka

A

Dementia

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10
Q

Major neurocognitive disorder diagnosis per DSM 5

A

Evidence of significant cognitive decline in at least one domain:
learning + memory, language, executive function, complex attention, perceptual motor function, social cognition

Impairment is acquired + a significant decline from previous functioning

Interferes with independence in everyday activities

Not exclusively in context of delirium

Not better explained by another mental disorder

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11
Q

Delirium diagnosis per DSM 5

A

Disturbance in attention + awareness

Develops over a short period of time, represents a change from baseline, fluctuates throughout day

Additional disturbance in cognition→ memory deficit, disorientation, language, visuospatial ability, perception

Spectrum: drowsy/lethargic vs agitated and confused, visual hallucinations, tremulousness, myoclonus/asterixis

Not better explained by a different neurocognitive disorder and isn’t due to severely reduced level of arousal such as coma

Evidence that disturbance is caused by a medical condition, substance intoxication/withdrawal, or medication side effect

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12
Q

How prevalent is delirium?

What are its complications?

A

30% of older patients experience delirium, usually while hospitalized

Doubles morbidity + mortality of a medical condition

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13
Q

Factors that increase risk of delirium

A

Underlying brain disease → dementia, stroke, Parkinson’s

Age >80

M>F

Infection, fracture, medical problems

Polypharmacy

ETOH use

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14
Q

Possible cardiac etiologies of AMS

A

Acute coronary syndrome
cardiac arrhythmia
hypertensive encephalopathy

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15
Q

Possible pulmonary etiologies of AMS

A

Pneumonia
pulmonary embolism
hypoxia
hypercarbia

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16
Q

Possible metabolic etiologies of AMS

A 
Hyponatremia
hypercalcemia
renal failure
thyroid disorder
hypoglycemia
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17
Q

Possible infectious etiologies of AMS

A

Pneumonia
UTI
meningitis
bacteremia

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18
Q

Possible neurologic etiologies of AMS

A 
CVA
encephalopathy
meningitis/encephalitis
seizure
malignancy
intracranial hemorrhage
spinal cord injury
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19
Q

Possible psychiatric etiologies of AMS

A

Dementia
delirium
Wernicke’s encephalopathy
conversion disorders

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20
Q

“Other” possible etiologies of AMS

A

Alcohol or benzodiazepine withdrawal
medication/drug effect
shock
post-op state

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21
Q

AEIOU-TIPS acronym for common etiologies of AMS

A 
Alcohol
Epilepsy/Endocrine/Exocrine/Electrolyte
Infection
Overdose, opioids, oxygen deprivation
Uremia
Trauma, Temperature, Toxins
Insulin
Psychosis
Stroke, Shock
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22
Q

MOVE STUPID acronym for common etiologies of AMS

A 
Metabolic→ hyponatremia, hypernatremia, hypercalcemia
Oxygen→ hypoxia
Vascular→ CVA, bleed, MI, CHF
Endocrine→ hypoglycemia, thyroid
Seizure→ postictal state
Trauma, Temperature, Toxins
Uremia
Psychogenic
Infection
Drugs→ intoxication or withdrawal
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23
Q

The first interventions you should do for all patients with AMS

A

O2
finger stick glucose
EKG
place IV/draw labs

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24
Q

The initial workup for AMS should include

A 
Serum electrolytes
creatinine
glucose
calcium
CBC
UA
pregnancy test
TSH, Folate, B12
\+/- blood alcohol, urine drug screen, specific drug levels
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25
Q

If a patient with AMS has CAD or is older than 50 years

A

ECG

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26
Q

If a patient with AMS has respiratory symptoms or a fever

A

CXR

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27
Q

If a patient with AMS has focal neurological exam findings or history of trauma

A

Head CT

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28
Q

If an AMS patient has a negative head CT, but you’re still super suspicious

A

MRI brain or EEG

29
Q

If a patient with AMS is hypoxic, or you suspect metabolic acidodis

A

ABGs

30
Q

If you suspect meningitis or encephalitis in a patient with AMS

A

Lumbar puncture

31
Q

Medical interventions you can give to any AMS patient that won’t cause them harm if it isn’t the cause of their AMS

A

folate
dextrose
naloxone

32
Q

If a patient with AMS is really aggressive….

A

Physical restraints are a LAST RESORT

Use frequent touch, reassurance and verbal orientation from familiar persons

33
Q

If a patient with AMS has potential to harm themselves or others

A

psychotropic medication trial:

low dose haloperidol

34
Q

Benzos + AMS

A

avoid
UNLESS:
sedative drug/alcohol withdrawal
sympathomimetic or anticholinergic poisonings

35
Q

Cholinesterase inhibitors + AMS

A

rivastigmine, donepezil
Avoid
not effective, bad side effects

36
Q

Your patient was working in the garage: what kind of poisoning?

A

Carbon monoxide

37
Q

Your patient was fumigating a ship: what kind of poisoning?

A

Cyanide

38
Q

Your patient was applying chemical to crops: what kind of poisoning?

A

Organophosphates

39
Q

Physiological excitation

A

CNS stimulation

Elevated HR, BP, RR, temp

40
Q

Physiological depression

A

Depressed mental status and reductions in HR, BP, RR, temp

41
Q

Mixed physiologic effects

A

Polydrug ODs
exposure to metabolic poisons
heavy metals
Agents with multiples MOAs

42
Q

Exposures that cause physiological excitation

A

Anticholinergics
Sympathomimetics
Central hallucinogen drugs
ETOH withdrawal

43
Q

Exposures that cause physiological depression

A 
ETOH, methanol, ethylene glycol
Sedative hypnotics
Opiates
Cholinergics
Sympatholytics
44
Q

Exposures that cause mixed physiologic effects

A 
Metformin
Sulfonylurea
ASA
Iron
Cyanide
Mixing of street drugs
45
Q

Example anticholinergics

A

diphenhydramine
dextromethorphan
atropine
some antidepressants

46
Q

Example sympathomimetics

A

cocaine
meth
bath salts
epi/NE

47
Q

Example sedative hypnotics

A

benzodiazepines

barbiturates

48
Q

Example cholinergics

A

organophosphates

49
Q

Example sympatholytics

A

Clonidine

alpha and beta blockers

50
Q

Topical decontamination

A

Copious water or saline irrigation

51
Q

Ingestion decontamination

A 
activated charcoal
gastric lavage
whole bowel irrigation
endoscopy
surgery
dilution
cathartics
52
Q

Enhanced elimination methods

A

forced diuresis
urine ion trapping
hemodialysis
exchange transfusion

53
Q

Flumezenil

A

benzos antidote

caution: can cause seizures in chronic benzodiazepine patients

54
Q

Possible MOAs of antidotes

A

Prevent absorption
Bind and neutralize poisons directly
Antagonize end-organ effects
Inhibit conversion to more toxic metabolites

55
Q

If the antidote has a shorter half life than the toxin (ex: naloxone)

A

Toxicity may reoccur

Prevent using repeated administration or IV dosing

56
Q

Get these labs for ALL poisonings, toxidromes, and AMS

A

Serum pregnancy test
Fingerstick glucose
Acetaminophen and Salicylate testing

57
Q

Anticholinergic toxidrome presentation

A

“Blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel and bladder lose their tone and the heart runs alone”

Hyperthermia
dry flushed skin
dilated pupils
agitation
hallucinations
delirium
tachycardia (earliest/most reliable sign but nonspecific), HTN
Urinary retention
decreased bowel sounds
seizures (rare)
58
Q

Anticholinergic toxidrome diagnosis

A

clinical

serum drug levels are not helpful

59
Q

Anticholinergic toxidrome treatment

A

Agitation→ benzos

Relatively recent ingestion→ activated charcoal
Patient must have normal mental status and ability to protect their airway

Moderate to severe poisoning→ +- Physostigmine

60
Q

Sympathomimetic toxidrome presentation

A 
Hyperthermia
tachycardia/dysrhythmia
HTN
diaphoresis
agitation
hallucinations
paranoia
dilated pupils
seizures
*Appears similar to alcohol withdrawal*
61
Q

Sympathomimetic toxidrome treatment

A

Supportive care

Benzos

62
Q

Anticholinergic vs Sympathomimetic: bowel sounds

A

Anticholinergic: hypoactive
Sympathomimetic: hyperactive

63
Q

Anticholinergic vs Sympathomimetic: skin

A

Anticholinergic: dry, dry mucous membranes
Sympathomimetic: diaphoresis

64
Q

Opioid toxidrome presentation

A 
Hypothermia
bradycardia
hypotension
bradypnea/apnea
flash pulmonary edema
CNS depression
coma
miosis
65
Q

Opioid toxidrome treatment

A

Supportive care

+/- Naloxone (Narcan)

66
Q

Naloxone (Narcan)

A

opioid antagonist, duration of action 45 mins→ repeat dosing/continuous IV

Chronic narcotic users that are breathing→ small dose .4 mg→ avoid precipitating withdrawal

67
Q

Sedative-hypnotic toxidrome presentation

A 
Hypothermia
normal vitals or bradycardia/ hypotension
bradypnea/apnea
CNS depression
coma
hyporeflexia
*variable pupils*
68
Q

Sedative-hypnotic toxidrome treatment

A

Supportive care

Tincture of time

+/- flumazenil (rare, induces seizures in chronic benzo users)

Unit 1 Emerg/Surg (10 decks)

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