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Step 2 CK > Emergency Medicine > Flashcards

Emergency Medicine Flashcards

1
Q

When is gastric lavage the right answer after toxic ingestion?

A

When ingestion is extremely recent (can be attempted up to 2 hours after ingestion)

One hour after ingestion = 50% effective

2 hours after ingestion = 15% effective

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2
Q

When is gastric lavage dangerous (i.e., contraindicated)?

A

Patients with altered mental status (may cause aspiration)

Caustic ingestion (causes burning of the esophagus and oropharynx)

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3
Q

What is ipecac?

A

Used to induce vomiting

Always the WRONG ANSWER in the ED (needs 15-20 minutes to work and delays the administration of antidotes)

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4
Q

When is whole bowel irrigation indicated?

A

Placing a gastric tube and flushing out the GI tract with polyethylene glycol-electrolyte solution (GoLYTELY) is almost always the wrong answer

Indications = massive iron ingestion, lithium, and swallowing drug-filled packets

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5
Q

Gastric emptying of any kind is always wrong with:

A

Caustics (acids and alkali)

AMS

Acetaminophen overdose

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6
Q

When the answer is not clear and the cause of overdose is asked, say:

A

Acetaminophen or

Aspirin

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7
Q

What is the most appropriate next step when a patient presents after overdose confused, disoriented, and lethargic?

A

The best initial management of AMS of unclear etiology is an opiate antagonist (Naloxone) and glucose (dextrose)

Opiate ingestion and diabetes are extremely common; naloxone and glucose work instantaneously and have no adverse effects (if they do not work, perform intubation)

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8
Q

Difference between the management of opiate and benzodiazepine overdose

A

Opiate overdose is fatal = give naloxone immediately

BZ overdose by itself is not fatal and acute withdrawal after chronic use causes seizures = do NOT give flumazenil

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9
Q

True/False

Charcoal is benign and should be given to anyone with a pill overdose

A

True

It may not be effective for every overdose, but it is not dangerous in anyone (removes toxic substances even after they have been absorbed)

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10
Q

Toxicity of acetaminophen may occur with ingestions greater than…

A

8-10 grams (approximately 0.5 grams per pill, 16 pills = toxic)

12-15 grams may be fatal (24 pills)

Note: alcoholism decreases the amount of acetaminophen needed to cause toxicity

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11
Q

If a clearly toxic amount of acetaminophen has been ingested (more than 8-10 grams/16 pills), what is the next step?

A

Give N-acetylcysteine

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12
Q

If acetaminophen overdose was more than 24 hours ago when the patient presents, what is the next step?

A

There is no therapy

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13
Q

If the amount of acetaminophen ingestion is unclear, what is the next step?

A

Drug level

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14
Q

Does charcoal make N-acetylcysteine ineffective?

A

No

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15
Q

Overdose of unknown substance

Tinnitus

Hyperventilation

A

Aspirin overdose

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16
Q

How does aspirin cause metabolic acidosis?

A

Aspirin interferes with oxidative phosphorylation and results in anaerobic glucose metabolism, which produces lactate

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17
Q

Treatment for aspirin overdose

A

Sodium bicarb

Alkalinizing the urine = increased rate of excretion

ASA is a weak acid; charged particles, which ASA would be in an alkaline enviroment, are not reabsorbed in the tubules (i.e., excreted)

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18
Q

Blood gas in aspirin overdose

A

Look for respiratory alkalosis progressing to metabolic acidosis*

pH 7.46, pCO2 22, HCO2 16

*ASA directly stimulates the respiratory center (hyperventilation = respiratory alkalosis), its interference with oxidative phosphorylation leads to metabolic acidosis

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19
Q

A patient ingested multiple toxic substances. You know for certain that this is the first time they took BZs. You give flumazenil and the patient immediately seizes. What happened?

A

BZs can prevent seizures from TCA toxicity. When you reverse BZs, you remove the suppression and can induce a seizure

Flumazenil will only cause seizures with chronic BZ dependence

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20
Q

What is the best initial test for suspected TCA toxicity

A

EKG

TCA toxicity is rapidly detectable on EKG (will show widening of the QRS complex that progresses to Torsades)

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21
Q

What is the treatment for TCA overdose

A

Sodium bicarbonate

Unlike for aspirin, bicarbonate will not increase urinary excretion of TCAs but it does protect the heart (competes for binding on Na fast channels)

If EKG shows torsades, give Magnesium

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22
Q

Dyspnea

Lightheadedness

Confusion

Seizures

MI

Pt was in a burning house

A

CO poisoning

The LV cannot distinguish between anemia, carboxyhemoglobin, and a stenosis of the coronary arteries (why death from CO is often from MI)

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23
Q

Blood gases for CO poisoning

A

pH 7.35, pCO2 26, HCO3 18

Prevents O2 release to tissues, so lactic acidosis develops

Note: pO2 is normal

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24
Q

When is hyperbaric oxygen indicated (over 100% oxygen via nonrebreather) for CO poisoning

A

For severe disease:

CNS symptoms

Cardiac symptoms

Metabolic acidosis (low bicarb and low pH)

It shortens the half-life of carboxyhemoglobin even more than 100% O2

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25
Q

Difference between methemoglobinemia and CO poisoning?

A

In methemoglobinemia, hemoglobin will never pick up the oxygen; with carboxyhemoglobin, the oxygen is picked up, but will not release is to tissues

CO = abnormally red blood

Methemoglobinemia = abnormally brown blood

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26
Q

What causes methemoglobinemia

A

Idiosyncratic reaction of hemoglobin to certain drugs (oxidized hemoglobin gets locked into the ferric state) such as:

Benzocaine and other anesthetics

Nitrites and nitroglycerin

Dapsone

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27
Q

Test and Treatment for Methemoglobinemia

A

Most accurate test = methemoglobin level

Best initial therapy = 100% oxygen

Most effective therapy = methylene blue

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28
Q

Cyanosis

normal pO2

A

Methemoglobinemia

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29
Q

Salivation

Lacrimation

Polyuria

Diarrhea

Bronchospasm and respiratory arrest

A

Organophosphate (insecticide) poisoning and nerve gas

It causes a massive increase in the level of ACh by inhibiting its metabolism

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30
Q

Treatment for organophosphate poisoning?

A

Give atropine first (blocks the effects of ACh that is already increased)

Then give pralidoxime (reactivates acetylcholinesterase, but does not work as instantaneously as atropine)

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31
Q

How are potassium and digoxin related

A

They compete for binding at the same site on the Na/K ATPase

Hypokalemia predisposes to digoxin toxicity

Digoxin toxicity causes hyperkalemia

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32
Q

Diagnostic testing for digoxin toxicity

A

Best initial test = potassium level and EKG (downsloping of the ST segment in all leads)

Most accurate = digoxin level

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33
Q

What are the strongest indications for giving digoxin-binding antibodies?

A

CNS and cardiac involvement

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34
Q

Abdominal pain

ATN

Anemia

Wrist drop

Memory loss

A

Lead poisoning

35
Q

Diagnostic test for lead poisoning

A

Best initial = increased level of free erythrocyte protoporphyrin*

Most accurate = lead level

*The free erythrocyte protoporphyrin (FEP) test measures the concentration of nonheme protoporphyrin in red blood cells. Protoporphyrin comprises the predominant porphyrin in red blood cells, which combines with iron to form the heme portion of hemoglobin.

36
Q

Treatment for lead poisoning

A

Chelating agents

Succimer is the only oral form of lead chelator

EDTA (ethylenediaminetetraacetic acid) and BAL (dimercaprol) are parenteral agents

37
Q

Difference between mercury poisoning from oral ingestion vs inhaled?

A

Oral = neurological problems (nervous, jittery, twitchy, and hallucinations)

Inhaled = lung toxicity that presents as interstitial fibrosis

38
Q

Treatment for mercury poisoning

A

There is no therapy to reverse pulmonary toxicity (inhaled)

Chelating agents such as dimercaprol and succimer are effective for neurological toxicity (can prevent progression of pulmonary disease)

39
Q

Difference between Methanol and Ethylene Glycol intoxication

A

Methanol

From wood alcohol, cleaning solutions, and paint thinner

Toxic metabolite = formic acid/formaldehyde

Presentation = ocular toxicity (retinal inflammation on exam)

Ethylene Glycol

From antifreeze

Toxic metabolite = oxalic acid/oxalate

Presentation = renal toxicity (look for hypocalcemia 2/2 precipitation of calcium in oxalate crystals*)

*Calcium oxalate crystals are enveloped shaped

40
Q

Treatment for methanol and ethylene glycol intoxication

A

Both give an osmolar gap and are treated with fomepizole and dialysis

Fomepizole inhibits alcohol dehydrogenase and prevents production of the toxic metabolites

Dialysis effectively removes methanol and ethylene glycol from the body

41
Q

Death from bites is from:

A

Hemolytic toxin: hemolysis and DIC

Neurotoxin: respiratory paralysis

42
Q

Treatment for snake bites

A

Pressure, Immobilization (decreases movement of venom), and Antivenin

Ineffective/dangerous treatment = tourniquet, ice, and incision/suction

43
Q

Difference between black widow and brown recluse bite?

A

Black widow

Abdominal pain, Hypocalcemia

Treat with calcium and antivenin

Brown recluse

Local skin necrosis

Treat with debridement, steroids, and dapsone

44
Q

Management of dog, cat, and human bites

A

Amoxicillin/clavulanate

Tetanus vaccination booster if more than 5 years since last injection

  • Dog and Cats = Pasteurella multocida*
  • Humans = Eikenella corrodens (most damaging)*
45
Q

True/False

Both epidural and subdural hematomas are associated with a lucid interval

A

True

46
Q

Treatment for large subdural/epidural hematomas

A
  1. Intubation and hyperventilation (cerebral circulation constricts when the pCO2 is low; a small decrease in volume results in a large decrease in pressure)
  2. Mannitol
  3. Drainage (evacuation)
47
Q

What are clear indications for stress ulcer prophylaxis with a PPI?

A

Head trauma

Burns

Intubation

Coagulopathy (platelets < 50,000 or INR > 1.5) with respiratory failure

48
Q

When to intubate a burn patient?

A

Any signs of airway injury:

stridor

hoarseness

wheezing

burns insides the nasopharynx or mouth

49
Q

How to calculate fluid replacement for burn patients

A

(4 mL) x (% BSA burned) x (weight in kg)

Give one-half in the first 8 hours, then give the second half over the next 16 hours

50
Q

How to estimate BSA in burns

A

Head = 9%

Arms = 9% each

Legs = 18% each

Chest or back = 18% each

  • Each hand width is one percent of BSA*
  • For children, Head = 18% and each Leg = 14%*
51
Q

The most common cause of death from hypothermia is…

A

cardiac arrhythmia

look for an intoxicated person with a low body temp

best initial step = EKG

52
Q

What does the EKG show for hypothermia

A

Marked elevation of the J point

J waves are where the QRS hits the ST segment

53
Q

What is always the wrong answer for management of patients recovering from drowning?

A

Seroids and Abx

Correct answer = positive pressure ventilation

54
Q

Besides CPR, therapy for asystole is with…

A

epinephrine (vasopressin is an alternative)

by constricting blood vessels in tissues (like the skin), they shunt blood into critical central areas

55
Q

The best initial therapy for v fib

A

immediate, unsynchronized cardioversion (aka defibrillation) followed by the resumption of CPR if not effective

Only VF and VT without a pulse get unsynchronized cardioversion

56
Q

When is amiodarone given for v fib

A

After shock, epi, shock, epi, shock

(order is shock, drug, shock, drug, shock…and amiodarone is given after 2 doses of epi are unsuccessful)

57
Q

Hemodynamically stable vs unstable VT

A

Stable = amiodarone, then lidocaine, then procainamide (cardiovert if medical therapy fails)

Unstable = electrical cardioversion several times, followed by medications

58
Q

What constitutes hemodynamic instability

A

Chest pain

Dyspnea

Hypotension

Confusion

59
Q

Why do we synchronize the delivery of electricity in the cardioversion of VT

A

To prevent worsening of the arrhythmia into ventricular fibrillation or asystole

60
Q

normal EKG and no pulse

A

PEA

Give CPR and correct the underlying cause (tamponade, tension pneumo, massive PE, potassium disorders)

61
Q

Irregularly irregular rhythm

A

Think a fib

62
Q

Atrial fibrillation vs Atrial flutter

A

Fibrillation = irregular rhythm

Flutter = regular rhythm

Flutter will either go back into sinus rhythm or deteriorate into fibrillation

63
Q

What defines chronic atrial fibrillation

A

Lasting for more than 2 days

The distinction is important because acute a fib does not need anticoagulation prior to cardioversion, whereas chronic a fib does

64
Q

Why is cardioversion of chronic atrial fibrillation (even after anticoagulation) not routinely indicated?

A

Most will revert to fibrillation

Shocking the patient into sinus rhythm does not correct a dilated LA (chronic a fib is caused by anatomic abnormalities of the atria or from HTN or valvular heart disease)

65
Q

Treatment for a fib

A

Rate control and anticoagulation (same for atrial flutter)

Best initial therapy = beta blocker, CCB, or digoxin

Once the rate is under 100 per minute, the most appropriate next step is to give warfarin, dabigatran, or rivaroxaban

66
Q

Is heparin necessary prior to starting warfarin on a patient with a fib?

A

No (unless there is evidence of an existing clot)

67
Q

CHADS Score

A

C: CHF or cardiomyopathy

H: hypertension

A: age > 75

D: diabetes

S: stroke or TIA (2 points)

When CHADS score is 1 or less use aspirin

2 or more use warfarin, dabigatran, rivaroxaban, or apixaban

68
Q

Best initial step for SVT

A

Look for a patient with palpitations who is hemodynamically stable

  1. Vagal maneuvers (carotid massage, valsalva, ice immersion)
  2. Adenosine
  3. Beta blockers (metoprolol), CCB (diltiazem), or digoxin
69
Q

Narrow complex tachycardia without P waves, fibrillatory waves, or flutter waves

A

SVT

70
Q

SVT alternating with ventricular tachycardia

SVT that gets worse after diltiazem or digoxin

Observing the delta wave on the EKG

A

WPW Syndrome

71
Q

Most accurate test for WPW

A

Cardiac electrophysiology (EP) studies

They will tell you where the anatomic defect is

72
Q

Acute and chronic therapy for WPW

A

Acute = procainamide or amiodarone

Chronic = radiofrequency catheter ablation

73
Q

Why are digoxin and CCBs dangerous in WPW

A

They block the normal AV node and force conduction into the abnormal pathway

74
Q

3 different P-wave morphologies and associated with COPD

A

MAT

Treat as you would atrial fibrillation, but AVOID beta blockers for rate control because of their lung disease

75
Q

Treatment for sinus brady

A

Asymptomatic = no treatment

Symptomatic:

best initial = atropine

most effective = pacemaker

76
Q

Wenckebach block

A

aka Mobitz I

Progressively lengthening PR interval that results in a “dropped” beat

Often a sign of normal aging of the conduction system

77
Q

Mobitz II

A

Drops a beat without the progressive lengthening of the PR interval

Mobitz II progresses, or deteriorates into third-degree AV block

EVERYONE gets a pacemaker, even if they are asymptomatic

78
Q

P waves and T waves have no fixed relationship to each other

A

Third-degree or complete heart block

Pacemaker

79
Q

What determines the risk of recurrence of a ventricular arrhythmia?

A

Ejection fraction (get an echo)

A normal ejection fraction = low risk of recurrence

80
Q

The most common cause of death in the 72 hours surrounding an acute MI

A

Ventricular arrhythmia

If the arrhythmia is from ischemia, correct the ischemia (angiography and angioplasty or bypass)

81
Q

Most appropriate next step in a patient with multiple episodes of syncope and an EKG showing ventricular tachycardia

A

Implantable defibrillator (will prevent the next episode of sudden death or syncope)

Metoprolol is NOT sufficient when syncope or sudden death has occurred

82
Q

HEART Score

A

Used to predict the risk of a MACE (major adverse cadiac event) within the next month

  • History*
  • EKG*
  • Age*
  • Risk Factors*
  • Initial Troponins*

0-3 = low risk, >7 = 50-65% risk

83
Q

Wells Criteria

A

Objectifies risk of PE

Clinical signs and symptoms

PE is #1 diagnosis

HR > 100

Immobilization

Previous PE/DVT

Hemoptysis

Malignancy w/ treatment within the last 6 months

The original intent of this tool was to determine who was low risk (<2 points) enough to rule out testing with a d-dimer

84
Q

PERC

A

The PERC rule can be applied to patients where the diagnosis of PE is being considered, but the patient is deemed low-risk

  • Age > 50*
  • HR > 110*
  • SaO2 < 95*
  • Unilateral leg swelling*
  • Hemoptysis*
  • Recent surgery/trauma*
  • Prior DVT/PE*
  • Hormone use*

If no criteria are positive and clinician’s pre-test probability is <15%, PERC Rule criteria are satisfied. PERC negative patients do not require utilization of the d-dimer, which has a high sensitivity but low specificity.

Step 2 CK (18 decks)

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