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MCC Part 1 > Emergency Medicine > Flashcards

Emergency Medicine Flashcards

1
Q

Dx

  • IgE-mediated, immediate onset reaction to protein antigen
  • prior sensitizing exposure to antigen required
A

Anaphylaxis

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2
Q

Dx

  • occurs on initial exposure to antigen
  • not IgE mediated but clinically identical to anaphylaxis
A

Anaphylactoid reaction

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3
Q

When does biphasic anaphylactic reaction occur?

A

4-32h after initial episode

  • due to release of secondary mediators, causing late-phase response
  • > IL4, IL5, TNF-alpha
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4
Q

What is protracted anaphylaxis?

A
  • refractory resp distress or hypotension despite appropriate medical rx
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5
Q

Type of hypersensitivity reaction

- immediate hypersensitivity - IgE mediated (e.g. urticaria)

A

Type I

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6
Q

Type of hypersensitivity reaction

- cytotoxic reaction - IgM and IgG mediated (e.g. Goodpasture syndrome)

A

Type II

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7
Q

Type of hypersensitivity reaction

- immune complex reaction - soluble immune complexes and complement mediated (e.g. serum sickness)

A

Type III

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8
Q

Type of hypersensitivity reaction

- delayed-type reaction - lymphocyte mediated (e.g. contact sensitivity)

A

Type IV

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9
Q

What cells degranulate in anaphylaxis?

A

Mast cells and basophils

  • release of preformed primary mediators (histamines, proteases, eosinophil and neutrophil chemotactic factors, and heparin)
  • due to membrane bound IgE on cells
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10
Q

Common causes of urticaria?

A
  • IgE mediated
  • direct mast cell release
  • complement mediated
  • arachidonic acid metabolism
  • physical (cold, sun, etc)
  • mastocytosis
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11
Q

Management of anaphylaxis?

A

ABCs

  • d/c antigen exposure
  • 2 large bore IV
  • cardiac and O2 monitoring

EPI

  • 0.3-0.5 mg IM adults
  • 0.01 mg/kg IM kids (max dose 0.3mg)
  • repeat 5-15min x1 if no response
  • epi drip if no response and pt in extremis
    0. 1mL of 1:1,000 epi diluted in 10cc NS at 1-2cc/min IV

methylprednisolone 1-2mg/kg IV (leukotriene production in delayed phase response)
diphenhydramine 1mg/kg IV (block H1 receptors)
ranitidine 1mg/kg IV (block H2 receptors)

  • observe 6-8h
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12
Q

Standard management in bites?

A
  • irrigate!!!
  • tetanus, rabies vaccine, prophylactic abx prn
  • check FB in wound
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13
Q

What do you administer to hypotensive pt not responding to bolus treated for anaphylaxis, if pt on b-blocker?

A

refractory hypotension = glucagon IV

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14
Q

What us Skeeter syndrome?

A
  • local immune reaction to mosquito bites
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15
Q

What are mosquito vectors?

A
  • malaria
  • West Nile virus
  • yellow fever
  • dengue
  • filariasis
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16
Q

What are tick vectors?

A
  • Rocky Mountain spotted fever

- Lyme disease

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17
Q

What is potential pathogen in human bites that is resistant to Piperacillin and Ticarcillin?

A
  • Eikenella corrodens
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18
Q

Treatment for human/dog/cat bite with established infection or prophylaxis for high risk bite?

A 
Amoxicillin/Clavulante 
or Doxycycline (kid>9 yr), Ceftriaxone
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19
Q

Treatment mod-severe infection from human/dog/cat bite?

A

Ceftriaxone IM/IV +/- metronidazole
or Ticaricillin/clavulante or Pip-Tazo

if Pen allergy in adult
Ciprofloxacin +/- clindamycin
Pen allergy in kid
TMP/SMX +/- clindamycin

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20
Q

3 distinct zones of tissue in full thickness burns?

A
  • zone of coagulation - white, charred central portion, necrotic tissue
  • zone of stasis - red, may blanch with pressure initially but fragile blood supply may give way to AVN
  • zone of hyperaemia - red, blanches with pressure, intact blood supply
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21
Q

Classification of burns

A
  • thermal
  • electric
  • chemical
  • radiation
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22
Q

Sequelae of electric burns?

A
  • cardiac arrhythmia
  • MSK injury to muscle/ligament/bone (high resistance of tissues) - compartment syndrome +/- rhabdo
  • renal ATN due to CK
  • CNS LOC, paralysis, resp depression, amnesia
  • eye cataracts and keraunoparalysis from lightening (fixed dilated pupils)
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23
Q

Do you neutralize acid/alkali burns?

A

NO - exothermic reaction can worsen burn

-> irrigate with WATER

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24
Q

Do alkali burns cause coagulation or liquefaction more commonly?

A
  • Liquefaction

alkali dissolves protein and collagen (liquefaction) penetrating deeper than acid burns

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25
Q

What systems more commonly affected by radiation burns? Best prognostic factor?

A

GI and hematologic (rapidly dividing cells)

- best prognostic indicator is absolute lymphocyte count within 48h of whole body exposure

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26
Q

How do you estimate TBSA?

A

Rule of 9s

  • hand 1%
  • head 9% (4.5% each front/back)
  • trunk 18% front, 18% back
  • arms 9% (4.5% front/back)
  • legs 18% (9% front, 9% back)
  • groin 1%
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27
Q

Indications of transfer to burn centre?

A
  • partial thickness >10% BSA
  • burns involving face, hands, feet, genetalia, perineum, major joints
  • any third degree burn
  • electrical (incl lightening) or chemical burns
  • preexisting medical condition with potential impact on recovery
  • concomitant trauma where burn = worst thing
  • kids in hospital without peds
  • special emotional/social/rehab required
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28
Q

Dx degree of burn

  • red
  • epidermis involved
  • ++painful, tender to touch, intact 2 point discrim
  • complete healing ins several days
A

Superficial (first degree)

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29
Q

Dx degree of burn
- red/blanched white, fluid-filled blisters
- epidermis, superficial (papillary) +/- deep (reticular) dermis involved
- ++ painful, tender to touch, 2 point discrimination intact or diminished
+/- scarring, may be hypertrophic with contractors across joints, healing 2wk

A

Superficial-Partial thickness (superficial second degree)

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30
Q

Dx degree of burn

  • white and leathery or black and charred
  • epidermis and both layers of dermis involved
  • numb with loss of 2 point discrimination
  • extensive time to heal (3-4wk) but may require wound excision and skin grafting
A

Deep partial thickness (deep second degree)

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31
Q

Dx degree of burn

  • white and leathery or black and charred
  • epidermis, dermis and subcutaneous tissues (fascia/ muscle/ bone) involved
  • numb with loss of 2 point discrim
  • extensive debridement, reconstruction of specialized tissues, skin grafting
A

Full thickness (third degree)

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32
Q

Management burns

A
  • Td immunization prn
  • neomycin/ polymyxin B or Bacitracin creams -> ensure good antimicrobial coverage without risk of allergic reaction and able to be removed easily to view wound bed
    +/- blister debridement
    Foley to monitor ins and outs
    Analgesia
    Fluids - Parkland formula
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33
Q

How do you decrease half life of CO-Hbg in blood?

A

100% O2

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34
Q

When do you use gastric tube for burn pt?

A

> 20% BSA can develop ileus lasting 4-5d

- increased metabolic rate requires nutritional support too

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35
Q

Parkland formula

A

fluid requirement = 4x body wt x % TBSA (partial and full thickness only)

  • half in first 8h and the other half over next 16h
  • electrical and full thickness require more fluids
  • adjust based on urine output (adult = 0.5 mL/kg/h; child = 1mL/kg/h; infant = 2 mL/kg/h) and vitals
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36
Q

Investigations for burn pt?

A
  • CBCD, lytes, BUN, Cr, glucose, INR, PTT, ABG with CO-Hgb, b-hCG
  • ECG, CK-MB, trop, UA for urine Mgb
  • type and screen if anticipate OR debridement
  • CXR, CT head if altered LOC, bronchoscopy if serious inh injury
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37
Q

Key Q on facial injury pt?

A
  • is your bite normal (malocclusion)
  • any numbness (trigeminal nerve injury)
  • seeing double (orbital #/ impaired EOMs)
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38
Q

Hyperthermia - is it pathologic or adaptive?

A
  • hyperthermia is pathologic thermoregulatory failure

- fever is adaptive, cytokine-mediate response

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39
Q

Define hyperthermia

A
  • core body temp >38 not due to fever
  • rise in body temp above hypothalamic set point when heat-dissipating mechanisms are impaired (drugs/ disease) or overwhelmed by extern or internal heat
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40
Q

Where are peripheral thermoreceptors?

A

Skin

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41
Q

Where are central thermoreceptors?

A

Anterior hypothalamus

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42
Q

Where is the central integrative area?

A

Posterior hypothalamus

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43
Q

Dx temp >37.5

  • cramping of most worked muscle groups
  • caused by replacement with isotonic fluid after ++ perspiration
A

Heat cramps

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44
Q

Dx temp >37.5

  • ventilation -> orthostatic pooling -> increased ADH/ aldosterone
  • commonly seen in non acclimatized or elderly pt
A

Heat edema

r/o other causes of edema

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45
Q

Dx temp >37.5

  • similar mechanism as heat edema
  • commonly in elderly
  • transient LOC
A

Heat syncope

r/o other causes syncope

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46
Q

Dx temp >37.5

  • superficial pruritic vesicles on erythematous base
  • generally confined to clothed areas
A

Prickly heat rash/ malaria rubra/ lichen tropicus/ sweat rash

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47
Q

Dx

  • temp 37.5 - 40.5
  • mental function intact
  • malaise, fatigue, headache
  • increased HR, orthostatic hypotension, clinically dehydrated
A

Heat exhaustion

48
Q

Dx

  • temp >40.5
  • CNS dysfunction (ataxia, coma, sz)
  • liver dysfunction (delayed 24-48h - leaking of transaminases from centrilobular necrosis)
  • up to 80% mortality if untreated
A

Heat stroke

  • ataxia often first CNS sign because cerebellum most sensitive to heat
  • 20% will have persistent neurologic dysfunction
49
Q

Management rhabdomyolysis (in setting hyperthermia)?

A
  • +++ fluids
  • mannitol
  • HCO3
50
Q

Management MH, possibly NMS (setting hyperthermia)?

A
  • dantrolene (lowers myoplasmic Ca++ by blocking Ca channels in sarcoplasmic reticulum of muscle fibres)
51
Q

Cooling techniques

A

first line

  • evaporation
  • ice water submersion

adjuncts

  • ice packs to axilla/ groin
  • cooling blankets
  • cardiopulmonary bypass (ECHMO)

not recommended

  • cool fluid lavage
  • cold IV fluid (worsen preexisting edema)
52
Q

Rule of resuscitation re: minimum pt body temp?

A

At least 35 degrees

53
Q

Define hypothermia

A

Core temp <35
- disruption in balance between heat production and heat dissipation

mild 32.2 - 35
moderate 28 - 32.2
severe <28

54
Q

ECG moderate hypothermia?

A
  • junctional bradycardia and afib; Osborn waves
55
Q

Management hypothermia?

A
  • external rewarming
  • warm crystalloids
  • invasive active rewarming
56
Q

Toxidrome category of

  • antihistamine
  • TCAs
  • phenothiazine
  • atropine
A

Anticholinergic

57
Q

Toxidrome category of

  • insecticides
  • nerve agents
  • nicotine
  • pilocarpine
  • urecholine
A

Serotonergic

58
Q

Toxidrome category of

  • heroin
  • morphine
  • benzos
  • barbiturates
  • meprobamate
  • EtOH
A

Cholinergic

59
Q

Toxidrome category of

  • MAOIs
  • SSRIs
  • meperidine
  • TCA
  • benzos
  • L-tryptophan
A

Opioid/ sedative/ hypnotic

60
Q

Toxidrome category of

  • cocaine
  • amphetamines
  • MDMA
  • ephedrine
  • theophylline
A

Sympathomimetics

61
Q

Causes elevated osmolar gap?

A
  • EtOH
  • isopropyl alcohol
  • ethylene glycol
  • methanol
  • ethanol
62
Q

Causes of elevated anion gap acidosis?

A

MUDPILES

  • methanol
  • uremia
  • diabetic/ alcoholic ketoacidosis
  • paraldehyde
  • isoniazid/ iron
  • lactate
  • ethylene glycol
  • salicylate
63
Q

Causes of narrow AG?

A

HARDUPS

  • hyperventilation
  • acetazolamide, acids, Addision disease
  • renal tubular acidosis
  • diarrhea
  • ureterosigmoidostomy
  • pancreatic fistula
  • saline
64
Q

Increase in OG or AG first noticed in toxic alcohol ingestion?

A

OG

65
Q

AG calculation

A 
AG = [Na] - [Cl] - [HCO3]
normal = 8-14
66
Q

Osmolar gap calculation

A

OG = difference between measured serum osmolality and calculated serum osmolarity
normal <10 mOsm/L

Osm(calc) = 2 (Na) + BUN + Glucose

67
Q

Dx

  • increased BP, HR, temp +/- RR
  • delirium
  • increased pupils
  • reduced bowel sounds
  • dry, red skin
A

Anticholinergic

  • hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter
68
Q

Dx

  • increased RR +/- BP/HR, normal temp
  • n/depressed LOC
  • +/- pupils (nicotinic dilates; muscarinic constricts)
  • increased bowel sounds
  • wet skin
A

Cholinergic

  • sludge (muscarinic sx - salivation, lacrimation, urination, diarrhea, GI distress, emesis)
  • the Killer Bs (bronchospasm, bronchorrhea)
  • fasciculations/ muscle cramps (nicotinic sx)
69
Q

Dx

  • decreased vitals
  • depressed LOC
  • reduced bowel sounds
  • normal skin
  • reduced reflexes, ataxia
A

Opioids and sedative/hypnotics

70
Q

Dx

  • labile BP; increased HR, RR, temp
  • tremor, agitation, hallucination
  • increased bowel sounds
  • wet skin
  • increased reflexes, vomiting
A

Serotonergic

71
Q

Dx

  • increased vitals
  • agitated, increased psychomotor activity
  • increased pupils
  • increased bowel sounds
  • wet skin
  • tremors, seizures
A

Sympathomimetics

72
Q

Dx

  • increased vitas
  • agitated, hallucinations
  • increased pupils
  • increased bowel sounds
  • wet skin
  • tremors, seizures
A

Withdrawal of sedatives/ EtOH

73
Q

Dx

  • vitals usually increased, temp can be normal
  • anxious
  • increased pupils
  • increased bowel sounds
  • wet skin
  • GI upset, yawning, rhinorrhea, piloerection
A

Withdrawal of opioids

74
Q

Methods of decontamination

A
  • orogastric lavage
  • whole bowel irrigation
  • activated charcoal/ multi-dose activated charcoal
75
Q

Antidote of acetaminophen

A

N-Acetylcysteine (NAC)

76
Q

Antidote of opioid OD

A

Naloxone

77
Q

Antidote of Warfarin

A

Vit K and/or prothrombin complex

78
Q

Antidote of ethylene glycol/ methadone

A

Fomepizole or ethanol

79
Q

Antidote of flumazenil

A

Benzo

80
Q

Antidote of carbon monoxide

A

O2

81
Q

Antidote of TCAs

A

sodium bicarbonate

82
Q

Antidote of CCB

A

IV calcium

83
Q

Antidote of b-blocker

A

glucagon

84
Q

Antidote of organophosphates/ insecticides

A

atropine

85
Q

Dx

  • reduced LOC, ataxia, lethargy, coma
  • blurry vision, reduced VA, snowstorm vision
  • Parkinsonism in late stage
  • delated presentation common

Tx?

A

Methanol
- hepatic metabolism by alcohol dehydrogenase to formic acid and depletion of folate stores

Rx - fomepizole or EtOH drip

  • hemodialysis if severe
  • folate
86
Q

Salicylate toxic ingestion - pathophys, toxic dose and rx?

A
  • resp alkalosis due to CNS chemoreceptors
  • metabolic acidosis late
  • toxic dose = 150mg/kg

rx - fluids +++
+/- K, dextrose
- urinary alkalization
- hemodialysis if severe

87
Q

Acetaminophen toxicity - pathophys, 4 phases and rx?

A
  • toxic metabolites conjugated in liver using glutathione
  • glutathione depleted in OD -> metabolites = hepatotoxicity
    toxic dose >150mg/kg or >7.5g

4 phases

  • 24-48h - GI upset and diaphoresis
  • d2-3 - GI improves, mild abdo pain, transaminases climb
  • d3-4 - GI upset, jaundice, metabolic acidosis
  • d>5 - multi organ failure with improvement or death

rx

  • 4h post ingestion levels -> Rumack-Matthew nomogram
  • NAC protective within 8h
88
Q

TCAs - pathophys, dx, rx?

A
  • block Na channels and serotonin reuptake
  • anticholinergic and antihistaminic effects
  • sx within 6h
  • clinical dx (no labs) - nonspecific presentation with dizziness, agitation, confusion +/- anticholinergic effects
  • ECG - long QRS, QT or PR +/- RAD of terminal 40ms of QRS

rx

  • supportive
  • charcoal if <2h
  • NaHCO3 if ECG changes
  • benzo for seizure
89
Q

Wounds through what skin layer scar?

A

Through dermis

90
Q

Timing to close wounds?

A

Within 12h, 24h if on face

91
Q

Can you put chlorhexidine in wound to clean?

A

No - causes tissue damage

92
Q

Maximum dose of lidocaine? + epi?

A

5 mg/kg

+ epi = 7 mg/kg

93
Q

Maximum dose of bupivacaine? + epi?

A

2 mg/kg

+ epi = 3 mg/kg

94
Q 
Size of suture:
back/trunk
scalp
arms/legs
hands/feet
face
A 
back/trunk: 3.0- 4.0
scalp: 4.0
arms/legs: 4.0 - 5.0
hands/feet: 5.0
face: 6.0
  • smaller suture = bigger number
95
Q

Type of closure

  • immediate skin closure in wounds with low infection risk
  • within 12h (24h if face)

CI?

A

Primary closure

CI

  • punctures
  • bites
  • extensive crush or debridement
96
Q

Type of closure

  • would left open to heal by granulation and contraction
  • for contaminated infected wounds
  • wounds presenting outside acceptable time for primary closure

CI?

A

Secondary closure

CI

  • cosmetics significant concern
  • unable to control bleeding
97
Q

Type of closure

  • wound initially left open, kept covered with antimicrobial mesh dressing, then closed 3-5d later if no signs of infection
  • for high risk of infection but significant cosmetic concern
  • wounds with significant tension

CI?

A

Delayed primary closure

CI n/a

98
Q

When do administer Td or Tdap? Tig?

A

Td or Tdap:

  • uncertain or <3doses
  • last booster >10yr (>3doses initially received)
  • last booster >5yr for wounds not clean/minor

Tig
- uncertain or <3 doses in wounds not clean/minor

99
Q

What is result when person’s airway goes below surface of liquid?

A

Submersion -> resp impairment

100
Q

What electrolytes can increase in dead sea submersions?

A
  • increased Mg++ and Ca++ from absorption of sea water
101
Q

What is the diving reflex?

A

cold water to face -> apnea + bradycardia -> shunting blood to brain and heart
- can be protective in infants and children

102
Q

Systemic effects of submersion injuries?

A

CNS
- hypoxia and acidosis -> cerebral edema

CVS
- hypoxia, acidosis and hypothermia -> arrhythmia (CPR until core body temp >32)

Resp
- aspiration washes out surfactant -> pulmonary edema -> ARDS
+/- laryngospasm

Metabolic

  • mixed resp/metabolic acidosis
  • dead sea: lyte abnormalities

Renal
- hypoxia + acidosis -> myoglobinuria + ATN

103
Q

Define shock

A

tissue hypoxia and end-organ dysfunction secondary to tissue hypo perfusion

104
Q

Dx shock

  • increased CO (HR/contractility)
  • increased SVR (vasoconstriction)
  • BP = narrow pulse pressure
  • skin cold
A

Hypovolemic

105
Q

Dx shock

  • reduced CP (reduced preload)
  • reduced SVR (vasodilation)
  • BP = wide pulse pressure
  • skin warm
A

Distributive

106
Q

Dx shock

  • reduced CO (reduced contractility)
  • increased/normal SVR
  • BP reduced
  • skin cold
A

Cardiogenic

107
Q

Dx shock

  • reduced CO
  • increased SVR (veno congestion)
  • reduced BP
  • cold skin
A

Obstructive

108
Q

Is lactate increased or decreased in shock?

A

mitochondrial dysfunction -> anaerobic metabolism -> increased lactate

109
Q

Is glucose increased or decreased in shock?

A

stress hormone release (catecholamines, glucocorticoids, glucagon) -> glyconeogenesis, lipolysis, insulin resistance -> increased glucose

110
Q

Result of inflammatory events in shock?

A

inflammatory events -> activated neutrophils bind vascular endothelium -> release free radicals and proteolytic enzymes -> damage to cell membrane and DNA

111
Q

Causes of multi-system organ failure in shock?

A

increased lactate, increased glucose, damage to cell membrane and DNA ->
ion pump malfunction -> cellular edema -> cellular dysfunction with dysregulation of intracellular pH -> cellular necrosis and death ->
multi system organ failure ->
death

112
Q

Dx

  • appears unwell
  • tachycardia, tachypnea, hypotensive, hypoxemic
  • increased serum lactate
  • reduced u/o
A

hypovolemic shock

113
Q

Can positive pressure ventilation affect pneumothorax?

A

Yes - can turn into tension pneumothorax

114
Q

Areas where significant bleeding can occur?

A
  • chest
  • abdo
  • pelvis (3L)
  • thigh (1L each)
  • retroperitoneal space
115
Q

Investigations for trauma pt?

A
  • CBC, type and screen, INR/PTT, lytes, BUN, Cr, b-hCG, lactate
    +/- ABG/VBG, lipase, LFTs, toxicology workup

CXR, pelvic XR, spine films (re: C-spine rules)
XR suspected injuries
CT chest, abdo, pelvis, spines prn

116
Q

Management of unstable pt with peritonitis?

A

Direct to OR for laparotomy

-> NO imaging

MCC Part 1 (22 decks)

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