Other

Question 1

Salicylate poisoning symptoms, treatment?

Answer 1

Confusion/agitation, tachypnea, hyperglycemia, anion gap acidosis, seizure

Ingestion of >300 mg/kg can be fatal

Treatment: Increase urinary excretion through alkalinization (drug won’t give up H+ if urine is acidic, nonpolar form gets reabsorbed), activated charcoal, hemodialysis

Sodium bicarb infusion: 0.5 mEq/kg/hr, watch for hypokalemia

Question 2

Treatment for cyanide poisoning

Answer 2

Hydroxycobalamin

Sodium nitrite or sodium thyosulfate

Sodium nitrite creates methemoglobin, ferric ion binds cyanide liberating it from cytochrome oxidase

Question 3

Treatment of clonidine overdose?

Answer 3

Naloxone 0.1 mg/kg – reverses neurologic but not cardiovascular effects in some patients

Question 4

What is most common genetic mutation associated with neonatal familial HLH?

Answer 4

Perforin gene (PRF1)

Perforin is released by cytotoxic T cell and NK cells to perforate target cell membranes; when absent, these cells activity is disrupted and cytokines/activated macrophages are unchecked

Question 5

Glasgow coma scale

Answer 5

Eyes (4): spontaneous, to speech, to pain, none

Verbal (5): coo and babble, irritable cry, cry to pain, moan to pain, none

Motor (6): spontaneous and purposeful, withdraw to touch, withdraw to pain, abnormal flexion to pain, abnormal extension to pain, none

Question 6

What is three column model of spine injury?

Answer 6

Spine is made up of anterior column (anterior ligament and anterior 2/3 of vertebral body), middle column (posterior ligament and posterior 2/3 of vertebral body), posterior column (pedicles, facets, lamina, spinous processes)

Need two intact to maintain stability, otherwise likely surgery with hardware

Question 7

Pediatric burn stabilization

Answer 7

ABCDE
Consider early intubation (airway edema)
Early imaging for other injuries

Depth and surface area:
1. superficial-damage to epidermis but will heal (sunburn)
2. partial thickness-variable damage to dermis, areas of injured cells that will evolve, blisters and moist; deep partial thickness less painful, >50% of dermis is damaged, potential severe scaring, pink to pale white, less edema, all of epidermis and significant portion of dermis
3. full thickness-complete dermal destruction with almost no capacity for skin regeneration, need to excise (bright white, leathery)

Surface area = only count partial and full thickness
Rule of 7s for smaller kids, rule of 9s for older and adults

Burn physiology: loss of skin barrier (fluid loss) with vasoactive mediator release
TBSA>15% develop a systemic inflammatory response, hypermetabolic response with protein needs 3 g/kg/d

Excise early to blunt the global inflammatory response (first postinjury week), get improved healing, decreased infection, and improved survival; best coverage is autograft, in large burns can supplement with cadaver allograft

Question 8

Parkland formula for burn resuscitation

Answer 8

4mL x TBSA x weight in kg
First half over 8 hours from start of burn, second half over 16 hours

Question 9

Inhalational injury

Answer 9

Look for: hoarse voice, stridor, wheezing, soot in pharynx or nares, singed nose hairs

Bronchospasm then PARDS
Early bronch to remove carbonaceous material
No role for steroids

Question 10

How does carbon monoxide impact body?

Answer 10

Cytochrome oxidase system, electron transport chain and production of ATP

Hgb oxygen dissociation curve is shifted left, mild acidosis may actually be helpful

Question 11

How does cyanide impact the body?

Answer 11

Often co-exists with carbon monoxide poisoning, burning of household materials

Binds with cytochrome a3, a component of the cytochrome c oxidase complex in mitochondria, prevents cells from using oxygen

Antidote is hydroxocobalamin

Question 12

Snake bite

Answer 12

In the United States, most venomous snakebites are from members of the Crotalinae subfamily, including rattlesnakes, copperheads, and water moccasins.
Crotalid venom contains multiple enzymes and proteins, which can cause hypofibrinogenemia and thrombocytopenia, resulting in persistent coagulopathy.
Coral snake antivenom is no longer commercially available.

Question 13

What are symptoms of cholinergic toxicity (e.g. organophosphate)?

Answer 13

Cholinergic toxicity
SLUDGE - salivation, lacrimation, urination, defacation, GI cramps, emesis/edema
Bradycardia, miosis, faciculations

Question 14

What is pralidoxime (2-PAM) used for?

Answer 14

Treat organophosphate toxicity - breaks the bond between oganophosphate and acetylcholinesterase (enzyme that should break down acetylcholine)

Question 15

What causes damage in acetaminophen toxicity?

Answer 15

Acetaminophen metabolized by glucuronidation, sulfonation, and …

CYP-450 oxidation > N-acetyl-p-benzoquinoneimine (NAPQI) > reduced by glutathione to a clearable metabolite

When glutathione stores are depleted, NAPQI accumulates causing hepatotoxicity

N-acetylcysteine replaces glutathione stores, helpful within 8hrs of ingestion

Question 16

Toxic dose of acetaminophen?

Answer 16

10x usual dosing

Child: 150 mg/kg
Adult: 10 g

Question 17

Salicylate poisoning

Answer 17

salicylate toxidrome includes vomiting, tinnitus, tachypnea, and confusion/agitation. Patients may develop hyperreflexia, hypotension, noncardiogenic pulmonary edema, and acute respiratory distress syndrome with severe salicylate intoxication. There is typically a mixed respiratory alkalosis and anion gap metabolic acidosis

30-60-90 rule for salicylate ingestions may be helpful: levels greater than 30 mg/dL require urinary alkalinization; levels greater than 60 mg/dL for chronic use and 90 mg/dL for acute ingestions may be life threatening and require hemodialysis

Question 18

Thiamine role

Answer 18

Thiamine is important for mitochondrial activity and energy production. Thiamine deficiency affects the entrance of pyruvate into the mitochondria resulting in lactate formation. Decreased levels of thiamine can result in impaired oxidative phosphorylation and carbohydrate metabolism resulting in lactic acidosis and cell death.

Question 19

Treatment for cyanide toxicity?

Answer 19

Hydroxycobalamin

Combines with cyanide, turns urine red, interferes with lab tests

If unavailable, cyanide antidote kit: sodium nitrite and sodium thiosulfate

sodium nitrite - downside is methemoglobinemia
sodium thiosulfate - give with sodium nitroprusside, serves as a sulfur donor in reaction converting cyanide to thiocyanate (excreted)

Question 20

Symptoms of hemlock ingestion

Answer 20

Combo of cholinergic and sympathomimetic (selective agonist for nicotinic-type acetylcholine receptors)

Cholinergic: bronchorrhea, bronchospasm, vomiting, salivation, urination

Sympathomimetic: hypertension, tachycardia, tremor, mydriasis, seizure, rhabdo

Other: bronchoconstriction, difficulty walking, hypothermia, coma

Question 21

What kind of damage is caused by bleach or alkaline ingestion?

Answer 21

Saponification of fats > liquifaction necrosis, high risk of perforation and stricture (more than acidic ingestion)

High dose methylpred can prevent stricture formation

Acid ingestion causes coagulation necrosis

Caustic ingestion and syptomatic should generally get an EGD

Don’t induce emesis - increases mucosal contact

Question 22

Iron ingestion

Answer 22

Ferrous sulfate tablets are 20% elemental iron (60mg in a tablet)

Ferrous fumarate tabs are 33% elemental (107mg in a tablet)

> 40 mg/kg ingestion requires hospital evaluation; severe toxic effects >60 mg/kg

iron level <300 ok, moderate 500-100 ug/dL, >1000 ug/dL severe

Negative inotrope, inhibits thrombin, interferes with oxidative phosphorylation

Phase 1: N/V/D, intestinal bleeding
Phase 2: metabolic acidosis
Phase 3 (12-24hrs): worsening metabolic acidosis, shock, coagulopathy, hemodynamic instability
Phase 4: hepatotoxicity
Phase 5 (3-6 weeks): GI strictures, fistula formation

Rx: deferoxamine (red urine
Charcoal not effective
Not dialyzable

Question 23

Marfan Syndrome

Answer 23

FBN1 gene mutation, autosomal dominant

CV: Aortic dilation, risk of dissection, mitral valve prolapse, TV prolapse; most common cause of mortality is Ao root disease leading to aneurysmal dilation, AI, and dissection

Treat with Bblocker and ARB

Question 24

Signs of cyanide toxicity

Answer 24

shock, neurologic impairment, lactic acidosis and a low arterial-venous oxygen difference

Question 25

Demonstration of malpractice four requirements

Answer 25

1. Presence of professional duty owed to the patient
2. Breach of that duty
3. Breath caused injury
4. Damage resulted

Negligence = failed to adhere to the standard practices of a reasonably careful and knowledgeable physician under similar circumstances

Litigation far more common when family feels they haven’t received clear and open communication

Question 26

Characteristic finding of Menkes disease

Answer 26

coarse, twisted, hypopigmented hair

• Low copper, low ceruloplasmin
• Cooper transport disorder
• Identified at 2-3 months of age, progressive developmental regression, low tone, feeding difficulty, FTT, seizure
• Death by age 3

Question 27

Tay-Sachs disease

Answer 27

HEXA gene mutation, deficiency of hexosaminidase A, accumulation of GM2 ganglioside in brain and spinal cord

Loss of developmental milestones at 6mo, cognitive and motor deterioration after that

Seizure, intellectual disability, paralysis, death by 5 years

Cherry red macular spot

Question 28

First order vs. zero order kinetics

Answer 28

First order: constant proportion of drug eliminated per time

Zero order: constant amount of drug eliminated per time

Question 29

Time to steady state and time to 97% elimination of a drug if it exhibits first order kinetics

Answer 29

5 half lives

Question 30

Equation for half life in first order kinetics

Answer 30

(0.693 x volume of distribution) / clearance

Question 31

Radiation syndrome

Answer 31

GI: vomiting, diarrhea, cramping
Neuro: confusion, nervousness, lethargy, headache, cerebral edema, seizure
Cutaneous: erythema, hair loss Hematologic: reduced absolute lymphocyte count

chromosome aberration cytogenetic bioassay to confirm estimated dose

lymphocyte count can be used to determine level of injury, <300 don’t survive

Question 32

List the 5 key nontechnical skills of crisis resource management

Answer 32

1. Leadership and followership
2. Communication
3. Teamwork
4. Resource use
5. Situational awareness

Question 33

Management of electrical burns

Answer 33

3 types: low voltage, high voltage, lightning

LOW VOLTAGE:
- Alternating house current (electrical cords, outlets)
- Superficial/contact burns, often heal on their own
- ECG to assess for changes, most of which resolve, CK to assess for deeper injuty
- Often discharge after 6-8hrs obs

HIGH VOLTAGE
- Power lines
- Creatinine kinase to assess for deeper muscular injury
- Deep tissue more likely to occur in high-voltage, rarely occur with lightning strike
- Compartment syndrome
- Trauma from getting thrown

LIGHTNING:
- Special kind of high voltage
- ECG: changes are common after lightning strike, most resolve spontaneously, troponin elevation common but non-prognostic
- Rare to have deep tissue injury
- Lichtenberg figure (tattoo)
- Keraunoparalysis - blue, mottled, pulseless extremities mimicking compartment syndrome but usually gets better on its own
- High urine output and cerebral salt wasting?
- Eye/ear injuries

Question 34

Antibiotic dosing adjustment

Answer 34

1. Duration of time that free drug remains above MIC
   - want this as close as possible to 100% (B-lactam effect is time-dependent, want 40-70%)
2. Ratio of max drug concentration to MIC
   - effect of aminoglycosides is concentration-dependent not time dependent, 8-10x MIC
3. Ratio of area under concentration-time curve over 24hrs to MIC

Trough > 2 mg/L for aminoglycoside is associated with higher toxicity (want <0.5-1 mg/L)

Question 35

Flumazenil vs. fomepizole

Answer 35

Flumazenil - benzo antagonist
Fomepizole - alcohol dehydrogenase