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USMLEStep2Lesson1:Cardiology:MyocardialInfarction

Internal Medicine Highlights

Conrad Fischer, MD

Maimonides Medical Center

Residency Director

Cardiology

Myocardial Infarction

Differential of Chest Pain

A 52-year-old man comes to the ER with 1 hour of severe chest pain on exertion. He is nauseated and diaphoretic with

slight shortness of breath. The pain does not change with respiration or bodily position. Exam shows normal vitals,

clear lungs, no murmurs, and no tenderness.

Changes With Respiration

Pneumonia

Pneumothorax

Pulmonary embolus

Pleuritis

Pericarditis

All can give fever - so can MI.

Changes With Position

Pericarditis only

when lying back causes more pain

Changes With Palpitation

Costochondritis only

EKG shows 2 mm of ST segment elevation in V2-V4

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Anything 1 mm in 2 electrically connected leads is sufficient for diagnosing acute MI

II, III F: Inferior wall

: Anterior Wall

I,L, : Lateral wall

What would you do next?

Cardiac Enzymes

Do not answer enzyme testing next:

Takes too long to obtain results

Treatment should be initiated first

Won't be positive yet

Wont change what to do, regardless of results (positive or negative) at this time

Cardiac Enzymes

Begins to
Elevate
Lasts

CPKMB
46hr
2days

Troponin
46hr
12wk

Myoglobin
14hr
s

LDH
1224hr
s

LDH currently is not useful. Never answer it.

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Best Answers:

Which has the best sensitivity, but poor specificity?

Myoglobin

Which has the best specificity?

Troponin

CPK-MB is sensitive and specific, but not as sensitive as myoglobin or as specific as troponin.

Treatment of Acute MI in ALL Patients

Decrease
Mortality
Time
Dependant

Aspirin
YES(25%)
YES

Nitrates
??
?

Morphine(Analgesics)
??
?

Thrombolytic
YES(25%)
YES

-Blockers
YES(1020%)
NO

Special Circumstances
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Angioplasty
o Patients with major bleeding or risk of bleeding
o Patients who cant receive thrombolytics for any reason
o Patients failing thrombolytics and progressing to hemodynamic instability
o Equal in efficacy to thrombolytics

Special Circumstances

ACE Inhibitor
o Patients with decreased left ventricle function or CHF

Lidocaine
o Never as prophylaxis
o All patients who develop major vertricular arrhythmias (ventricular tachycardia or fibrillation)

Pacemakers

Anything slow or that could become slow

Third-degree AV block

Mobitz II second degree block

Left bundle branch block

USMLEStep2Lesson2:Cardiology:CongestiveHeartFailure

Cardiology

Congestive Heart Failure

Congestive Heart Failure/Pulmonary Edema

A 67-year-old woman comes to the ER with 1-2 hours of severe shortness of breath. She has a history of

two MIs in the past. She comes with a pizza in one hand and a bag of Doritos in the other, and she is

chewing a sausage. Her respiration rate is 34; BP, 130/82; and PUD, 18. Jugulovenous distention is

present. Chest: rales to apices. Heart:3/6 systolic murmur at Apex 1. S3 gallop. Abd: Enlarged liver.3+
 Page |5

Edema of lower extremities to mid-thigh.

What would you do next?

Do Not Answer Lab Tests

CXR:Congestion of vasculature, enlarged heart, effusion

Arterial blood gas: Hypoxia, respiratory alkalosis

EKG: Sinus tachycardia

Echocardiogram (never used in acute cases): decreased ejection fraction, mitral regurgitation, abnormal

motion of anterior and, inferior walls

Radionuclide ventriculogram:(MUGA) never use acute scan, most accurate method of assessing

ejection fraction

Treatment of Pulmonary Edema

Sit the patient upright

Give Oxygen

Treatment of Pulmonary Edema

First Step: Preload reduction

Diuretics any loop diuretic intravenously

Morphine

Nitrates
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Second Step: Only if preload reduction is ineffective

Positive inotropes

Dobutamine

Amrinone

Treatment of Pulmonary Edema

Third Step: Afterload reduction

Ace inhibitors - IV

Nitroprusside

Congestive Heart Failure

Treatment when the patient has been stabilized

Ace inhibitors

Diuretics

Digoxin

Blockers (carvedilol or metoprolol)

Blockers

Reduce mortality

Increase ejection fraction

Improve symptoms

USMLEStep2Lesson3:InfectiousDiseases:Intro.to
Antibiotics

Infectious Deseases

Introduction to Antibiotics
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Introduction to Antibiotics

The organisms that cause diseases have largely not changed

The antibiotics that go with the organisms change

The most important aspect of infectious diseases: ascribe the antibiotics that go with each

group of organisms

Think in terms of groups of antibiotics

Gram-positive Cocci: Staphylococcus and Streptococcus

Penicillins:
o Oxacillin
o Cloxacillin
o Dicloxacillin
o Nafcillin

Gram-positive Cocci: Staphylococcus and Streptococcus

With mild penicillin allergy

First-generation cephalosporins:
o Cefazolin
o Cephalexin
o Cephradine
o Cefadroxil

Gram-positive Cocci: Staphylococcus and Streptococcus

With severe penicillin allergy

Clindamycin

Macrolides (erythromycin, clarithromycin, azithromycin): Used for minor, non-life-threatening

infections

Vancomycin, Synercid, Linezolid: Used for gram-positive infections with life-threatening

allergy to penicillin and methicillin-resistant Staphylococcus

 Page |8

Gram-negative Bacilli

For E. coli, Proteus, Enterobacter, Klebsiella, Morganella, and Pseudomonas, ALL of following

provide >90% coverage:

Aminoglycosides (gentamicin, tobramycin, amikacin)

Aztreonam

Quinolones (ciprofloxacin, levofloxacin)

Gram-negative Bacilli

For E. coli, Proteus, Enterobacter, Klebsiella, Morganella, and Pseudomonas, ALL of following

provide >90% coverage:

Carbapenems (imipenem, meropenem)

Extended-spectrum penicillins (piperacillin, ticarcillin, azlocillin, mezlocillin)

Third-generation cephalosporins (especially ceftazidime)

Fourth-generation cephalosporins (especially cefepime)

Second-generation cephalosporins (eg, cefoxitin, cefotetan,

cefuroxime)

Good for gram-positive coverage like first-generation cephalosporins

Good for gram-negative coverage but NOT for Pseudomonas

Cefoxitin and cefotetan are good for anaerobes

Anaerobes

Oral anaerobes (anything above the diaphragm)

Clindamycin

Penicillin (any penicillin EXCEPT the Ox/Clox/Diclox/Naf group)

Abdominal anaerobes (below the diaphragm)

Metronidazole

Imipenem
 Page |9

Second-generation cephalosporins

Beta-lactam/ Beta-lactamase inhibitor combinations

Antivirals

Herpes simplex and varicella

Acyclovir, valacyclovir, famciclovir

Herpes simplex, and varicella AND Cytomegalovirus

Ganciclovir, foscarnet, cidofovir

Antivirals

Influenza

Oseltamivir, zanamivir

Amantadine, rimantadine: Becoming archaeologic

Hepatitis B

Lamivudine or interferon

Hepatitis C

Interferon and ribavirin in combination

Antifungals

Life-threatening infections (eg, endocarditis, meningitis, fungemia)

Amphotericin

Candida infections

Azoles
 P a g e | 10

Fluconazole, ketoconazole, itraconazole

Onychomycosis

Terbinafine, itraconazole

Griseofulvin is as useful as a rotary telephone

USMLEStep2Lesson4:CentralNervousSystemInfections

Infectious Deseases

Central Nervous System Infections

Central Nervous System Infections

A 48-year-old man comes to the ER with 1 day of fever, headache, nausea.

What could this be?

ANY of the CNS infections can present with fever, headache, and
nausea. To determine which one, the question will provide the following
clues:

Meningitis

The patient also has photophobia and nuchal rigidity (stiff neck) on exam.

Encephalitis

The patient is disoriented confused and lethargic with difficulty thinking.

ANY of the CNS infections can present with fever, headache, and
nausea. To determine which one, the question will provide the following
clues:
P a g e | 11

Abscess

The patient has focal neurological deficits found on examination.

Note: There is considerable overlap between these diseases. If the question state that he has

a stiff neck AND confusion/lethargy AND focal findings, then neither you nor anyone else could

determine the precise diagnosis.

Which patients require a CT scan of the head BEFORE lumbar

puncture?

Focal findings

Papilledema

Altered mental status

If CT is required before lumbar puncture, ALWAYS answer give

treatment (ceftriaxone) before the lumbar puncture:

Treatment is more important than the specific diagnosis

Cell count, chemistry (protein level), gram-stain, and bacterial antigen testing can still give the

diagnosis if the antibiotics sterilize the culture

Meningitis

Diagnostic testing on lumbar puncture: Everything depends on the specific question asked!

MOST SPECIFIC test is CULTURE

MOST SENSITIVE test is PROTEIN

NEXT BEST or BEST INITIAL test on CSF is CELL COUNT. (Cell count is not as specific as

culture or as sensitive as protein level but it is the best combination of both.)

Cultures

In general, culture is the answer to the

What is the BEST - Most Accurate - Most Likely to lead to specific diagnosis type of
P a g e | 12

question.

HOWEVER:Dont answer, Wait for the cultures before initiating treatment.

Meningitis

A 48-year-old man comes to the ER with 1 day of fever, headache, and nausea. He has

photophobia and a stiff neck. He has no focal neurological deficits or papilledema and is fully

oriented and alert. Lumbar puncture shows an elevated protein, cell count of 3,502, and a

negative gram stain. Culture is sent.

Which type of meningitis is this?

Cell Count on CSF

Any type of meningitis can cause an elevated cell count; the differential on the cell count gives more

specific information.

Neutrophils Bacterial:

Streptococcus pneumonia: most common

Neisseria: look for a rash, particularly a petechial rash in the presentation

Haemophilus: particularly in children, although greatly diminished because of vaccination

Treatment of Bacterial Menigitis

Cell Count on CSF

Lymphocytes (look for these specific features):

Rocky Mountain spotted fever: rash on wrists/ankles, moving centrally towards the body

Lyme: Facial palsy, target lesion rash (erythema migrans)

Cryptococcus: HIV+ patients with <100 CD4 cells

TB: Very high protein in CSF,and very low glucose, TB in lungs

Viral: Everything negative; no particular association. Exclude the other causes

Treatment of Bacterial Meningitis

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A 48-year-old man comes to the ER with 1 day of fever, headache, nausea. He has

photophobia and a stiff neck. He has no focal neurological deficits or papilledema and is fully

oriented and alert. Lumbar puncture shows an elevated protein, cell count of 3,502, and a

negative gram stain. Culture is sent. The differential shows 92% neutrophils.

What is the best initial therapy?

Treatment of Bacterial Meningitis

What is the best intial therapy?

Ceftriaxone unless T-cell immune deficit present.

Ceftriaxone AND Ampicillin if there is steroid use, neutropenia, pregnancy lymphoma,

leukemia, HIV or if the patient is elderly or a neonate. Ampicillin covers Listeria.

Treatment of Bacterial Meningitis

A 48-year-old man comes to the ER with 1 day of fever, headache, nausea. He has

photophobia and a stiff neck. He has no focal neurological deficits or papilledema and is fully

oriented and alert. Lumbar puncture shows an elevated protein, cell count of 3,502, and a

negative gram stain. Culture is sent. The differential shows 92% neutrophils.

What is the best initial therapy?

Treatment of Bacterial Meningitis

What is the best intial therapy?

Ceftriaxone unless T-cell immune deficit present.

Ceftriaxone AND Ampicillin if there is steroid use, neutropenia, pregnancy lymphoma,

leukemia, HIV or if the patient is elderly or a neonate. Ampicillin covers Listeria.

USMLEStep2Lesson5:PPDTesting
P a g e | 14

Infectious Diseases

PPD Testing

PPD Testing

When to use the PPD? What's it for?

To screen the asymptomatic: do not use as primary method for diagnosing TB in acutely symptomatic

patients

What is considered a positive PPD?

>10 mm induration, not erythema in most patients; >5 mm in HIV+ patients and close contacts

Always get CXR after a positive PPD

Treatment for a positive PPD means INH alone

Treat all PPD+ patients if the risk of developing TB is greater than risk of hepatitis from the isoniazid:

ANY recent (past 2 years) converter

ANYONE with severe immune deficiency (eg, HIV, steroid use, leukemia, diabetes, lymphoma)

ANYONE <35 years old

What is the effect of BCG on these recommendations?

BCG has NO effect on these recommendations.

Which of the following patients should receive isoniazid prophylactic

therapy?

A 19-year-old, HIV- woman entering college with 8 mm of induration and a negative test last

year.

Which of the following patients should receive isoniazid prophylactic

therapy?

A 32-year-old, HIV- physician from India who received BCG as a child and has never been
P a g e | 15

tested before. She has 12 mm of induration at health screening before starting an internship in

the US.

Which of the following patients should receive isoniazid prophylactic

therapy?

A 47-year-old HIV+ man who had never been tested before and has 7 mm of induration.

A 95-year-old, HIV-, female nursing home resident who was PPD- last year and has 11 mm of

induration this year.

Which of the following patients should receive isoniazid prophylactic

therapy?

A 3,725-year-old Egyptian mummy who was PPD- last year and is PPD+ this year.

Which of the following patients should receive isoniazid prophylactic

therapy?

The 19-year-old woman: NO

The 32-year-old physician: YES

The 47-year-old-HIV+ man: YES

The 95-year-old nursing home resident: YES

The 3725-year-old Eqyptian mummy:

YES, YES, YES!

USMLEStep2Lesson6:HIV

Infectious Diseases

HIV

HIV
P a g e | 16

A 37-year-old man comes to your office after having been recently diagnosed with HIV. He

has no symptoms. His physical examination is normal. His CD4 count is 575, and his viral

load is 1,000.

Which medications are appropriate for this patient?

None for this patient: CD4>500, viral load <20,000

Antiretroviral Medications and their most common adverse effects

Nucleoside reverse transcriptase inhibitors

Zidovudine (anemia)

Didanosine (pancreas, neuropathy)

Stavudine (pancreas, neuropathy)

Zalcitabine (pancreas, neuropathy)

Lamivudine

Protease inhibitors: hyperlipidemia, hyperglycemia

Nelfinavir

Ritonavir

Indinavir

Saquinavir

Amprenavir

When to start therapy?

CD4 < 500 or viral load > 20,000

What to start?

Any two reverse transcriptase inhibitors AND any protease inhibitor

A 37-year-old man comes to your office after having been recently diagnosed with HIV. He

has no symptoms. His physical examination is normal. His CD4 count is 575, and his viral

load is 1,000.

NONE for this patient: CD4 >500, viral load <20,000

P a g e | 17

A 37-year-old man comes to your office after having been recently diagnosed with HIV. He

has no symptoms. His physical examination is normal. His CD4 count is 275, and his viral

load is 1,000.

What medications are appropriate?

Any two nucleosides AND a protease inhibitor

A 37-year-old man comes to your office after having been recently diagnosed with HIV. He

has no symptoms. His physical examination is normal. His CD4 count is 575, and his viral

load is 71,000.

What medications are appropriate for this patient?

Any two nucleosides AND a protease inhibitor

A 37-year-old man comes to your office after having been recently diagnosed with HIV. He

has no symptoms. His physical examination is normal. His CD4 count is 175, and his viral

load is 31,000

Any two nucleosides AND a protease inhibitor AND . . .

Pneumocystis Prophylaxis: when the CD4 <200 Trimethoprim/Sulfamethoxazole(first

choice) Dapsone Atovaquone

A 37-year-old man comes to your office after having been recently diagnosed with HIV. He

has no symptoms. His physical examination is normal. His CD4 count is 45, and his viral load

is 31,000.

Any two nucleosides AND a protease inhibitor + trimethoprim/sulfamethoxazole AND .

. . Mycobacterium avium complex prophylaxis: when the CD4 <50

Azithromycin (once a week)

A 37-year-old man comes to your office after having been recently diagnosed with HIV. He

has no symptoms. His physical examination is normal. His CD4 count is 5, and his viral load

is 371,000

Any two nucleosides AND a protease inhibitor AND trimethoprim/sulfamethoxazole

P a g e | 18

AND azithromycin AND

NOTHING!!

USMLEStep2Lesson7:Hematology:MicrocyticAnemia

Hematology

Microcytic Anemia

Microcytic Anemia

A 32-year- old woman presents with several weeks of fatigue. She complains of nothing else.

Initial CBC reveals an hematocrit of 28%.

Symptoms of anemia are largely based on severity not etiology. Iron deficiency with

hematocrit of 28% will give the same symptoms and the anemia of chronic disease,

folate deficiency, thalassemia, etc, with hematocrits of 28%.

A 32-year-old woman presents with several weeks of fatigue. She complains of nothing else.

Initial CBC reveals hematocrit of 28%. The other portions of the CBC are normal, and the MCV

is 70 (normal 80-100).

What is the most likely diagnosis?

After determining that the patient has anemia, the next most useful step is to determine

the cell size. This is the next easiest clue as to the etiology of the anemia.

Low MCV

Iron deficiency

Anemia of chronic disease (can also be normocytic)

Sideroblastic

Thalassemia
P a g e | 19

High MCV

Vitamin B12 deficiency

Folate deficiency

Alcohol

Drug toxicity

Normal MCV

Hemolysis

A 32-year-old woman presents with several weeks of fatigue. She complains of nothing else.

Initial CBC reveals an hematocrit of 28%; other portions of the CBC are normal, and MCV is 70

(normal 80-100).

What is the next best step in the management of this microcytic patient? (ie: What is the

best initial diagnostic test?)

What is the next best step in the management of this microcytic patient?

Iron Studies

Iron deficiency: low ferritin, high iron binding capacity

Chronic disease: high ferritin, low iron binding capacity

Sideroblastic: high serum iron

Thalassemia: normal iron studies

After the iron studies, how would you address other questions about the
specifics of the various low MCV anemias? (What is the most accurate
diagnostic test?)

Iron Deficiency

High red cell distribution of width (RDW)

What is the most specific test? Bone marrow for stainable iron.

Sideroblastic anemia
P a g e | 20

What is the most specific test? Prussian blue stain for ringed sideroblasts

Thalassemia
What is the most specific test? Hemoglobin electrophoresis

What is the best therapy for this patient?

Iron Deficiency

Iron replacement

Ferrous sulfate tablets

Chronic Disease

Correct the underlying disease

What is the best therapy for this patient?

Sideroblastic anemia

Pyridoxine

Thalassemia trait

No therapy

USMLEStep2Lesson8:Hematology:MacrocyticAnemia

Hematology

Macrocytic Anemia

A 32-year-old woman presents with several weeks of fatigue. Initial CBC reveals an hematocrit

of 28%.
P a g e | 21

Symptoms of anemia are largely based on the severity not the etiology. Iron deficiency

with hematocrit of 28% will give the same symptoms and the anemia of chronic disease,

folate deficiency, thalassemia, etc, with an hematocrit of 28%.

A 32-year-old woman comes to the office with several weeks of fatigue. In addition, she

complains of a sensation of pins and needles in her hands and feet. She drinks almost a quart

of vodka per day. Initial CBC reveals an hematocrit of 28%. The MCV is 120 (normal 80-100).

What is the next best step in the management of this macrocytic patient?

Macrocytic anemia is largely due to either vitamin or folate deficiency, although several

drug toxicities (eg, severe alcoholism, zidovudine or methotrexate use) can do it as well. You

do NOT need neurological symptoms to have anemia from deficiency. However the

presence of neurological symptoms means it cannot be folate deficiency alone. Alcohol can

give neurological symptoms as well.

Which neurological problems can occur with B12 deficiency?

Motor, sensory, psychiatric, ataxia, position, vibratory, cognitive, autonomic, sexual

ANY neurological symptom can occur with deficiency

Which is the most common neurological symptom with B12 deficiency?

Peripheral neuropathy

B12 Deficiency

What is the best intial test?

Presence of hypersegmented neutrophils and a low B12 level (NOT a Schilling test).

Folate Deficiency
P a g e | 22

What is the best initial test?

Presence of hypersegmented neutrophils and a low folate level.

Alcohol or other drug toxicity

What is the best initial test?

Absence of hypersegmented neutrophils and to exclude the B12 and folate deficiency and look

for the drug in the history.

What are the specific tests you would do to determine the specific
etiology of the B12?

Elevated methylmalonic acid and elevated LDH are characteristic of deficiency.

Antibodies to intrinsic factor and an elevated gastrin level are characteristic of pernicious

anemia

Schillings test is the least often used but most specific way to determine precisely how a

patient is malabsorbing . Do NOT answer Schillings test if the case gives you the elevated

LDH, antibodies to intrinsic factor and elevated gastrin level.

What is the best therapy?

B12 deficiency: Replace the B12

Folate deficiency: Replace the folate

Drug/Alcohol toxicity: Stop the drug/alcohol

USMLEStep2Lesson9:Hematology:Hemolysis

Hematology

Hemolysis

Hemolysis

A 42-year-old man is admitted to the hospital because of weakness, fatigue, and dark urine.
P a g e | 23

On examination he appears jaundiced with scleral icterus. Initial CBC shows an hematocrit of

28% with a normal MCV. His indirect bilirubin, LDH level and reticulocyte count are all

elevated.

What is the cause of his anemia?

All forms of hemolysis present with elevated LDH levels, reticulocyte count, and indirect

bilirubin. The dark urine can be either from hemoglobin filtered into the urine in intravascular

hemolysis or from the bilirubin alone. Sometimes the MCV can be slightly elevated because

reticulocytes are slightly larger.

Which clues in the history will tell you which type of hemolytic anemia it
is?

Autoimmune:Lupus, lymphoma, leukemia, rheumatoid arthritis, viral infections, penicillin or

quinidine use

Glucose 6 phosphate dehydrogenase deficiency (G6PD): Very sudden onset, current

infection, oxidant stress from drugs (eg, dapsone, primaquine, or sulfa) or fava bean ingestion

Which clues in the history will tell you which type of hemolytic anemia it
is?

Paroxysmal nocturnal hemoglobinuria (PNH): Dark morning urine, major venous

thrombosis such as the portal vein

Hemolytic uremic syndrome (HUS): Renal failure and thrombocytopenia

Which clues in the history will tell you which type of hemolytic anemia it
is?

Thrombotic thrombocytopenic purpura (TTP): Renal failure and thrombocytopenia and

neurological symptoms and fever

Hereditary spherocytosis: Splenomegaly

Which diagnostic testing is useful to distinguish between these?

All EXCEPT the hereditary spherocytosis can also give:

P a g e | 24

low haptoglobin level

hemoglobinuria

Hemosiderinuria

Hereditary spherocytosis will not give these because it is extravascular hemolysis. Extravascular means

it occurs in the spleen.

Which of the following tests is the most specific, most accurate, and
most likely to lead to a definite diagnosis in each of these forms of
anemia?

Autoimmune: Coombs test

G6PD: G6PD level

PNH: Sugar-water and Hams test

HUS: Finding renal failure and thrombocytopenia with hemolysis; no specific test

TTP:Finding renal failure, thrombocytopenia, and neurological symptoms and fever with

hemolysis; no specific test

Hereditary spherocytosis:Spherocytes on the smear AND an osmotic fragility test

Which of the following is the best intitial therapy and most definitive
therapy?

Autoimmune:: Initially, steroids; with life-threatening hemolysis, IV immunoglobulin; recurrent,

splenectomy

G6PD:Avoid the oxidant stress

PNH:Steroids

HUS:Initially, spontaneous resolution; with life-threatening disease, plasmapheresis

TTP:Plasmapheresis

Hereditary spherocytosis:Splenectomy
P a g e | 25

USMLEStep2Lesson10:Nephrology:AcuteRenalFailure

Nephrology

Acute Renal Failure

An 87-year-old woman with a history of gout and osteoarthritis is found on the floor of her apt.

by her family. It is not clear how long she has been on the floor. She uses NSAIDs for joint

pain. In the ER she is found to be confused. Her temperature is 102 F, pulse is 117, and

systolic BP blood is 92; rales are heard on lung examination. She has a head CT with contrast

to evaluate her confusion and receives penicillin and gentamicin for her pneumonia. She has

no urine output since admission. On hospital day 2 her BUN and creatinine begin to rise.

How many causes of renal failure can you identify in this patient?

The first step in evaluating a patient with acute renal failure is to determine whether there is a

problem inside the kidney (tubules, glomeruli, vascular) or with the perfusion of the kidney

(prerenal) or drainage out of the kidney (postrenal).

The fever, tachycardia, relatively low BP, and the fact that she was found on the floor are

all sufficient suggestions of pre-renal azotemia.

The best initial tests to determine whether it is pre-renal azotemia is as

follows:
P a g e | 26

Pre-renal
Acute
Tubular
Necrosis
BUN/Creatini
ne
Ratio
> 20:1
10.1

Urine Sodium
Low < 20
High > 40

Urine
Osmolality
High > 500
Low < 350

To exclude post-renal azotemia (obstruction to drainage OUT of the

kidney) the following are useful:

Physical examination to detect enlarged bladder

Ultrasound to look for bladder size and hydronephrosis

Urinary catheter placement

Do NOT assume that the decreased urine output described is from the renal failure. The renal failure

could simply be from decreased urine output and obstruction.

Intra-renal Damage (ATN)

Damage to the kidney could affect tubules, glomeruli, or vasculature. It is NOT very useful to

think of the diseases as cortical or medullary. Glomerular diseases, eg, lupus, Goodpasture,

Alport syndrome, Berger disease, or even post-streptococcal disease, are unlikely to occur this

acutely and without other history of systemic disease. The same is true of vascular diseases,

eg, polyarteritis nodosa, Wegener granulomatosis, TTP, HUS, or Henoch Schonlein purpura.

Intra-renal Damage (ATN)

Acute renal failure such as this is most often from tubular diseases, which are most often from

various toxins combined with possible ischemia from hypoperfusion.

P a g e | 27

How many different toxins can you identify in this case?

An 87-year old woman with a history of gout and osteoarthritis is found on the floor of her

apartment by her family. It is not clear how long she has been on the floor. She uses NSAIDs

for joint pain. In the ER she is found to be confused. Her temperature is 102 F, pulse is 117,

and systolic BP blood is 92; rales are seen on lung examination. She has a heat CT with

contrast to evaluate her confusion and receives penicillin and gentamicin for her

pheumonia. She has no urine output since admission. On hospital day 2 her BUN and

creatinine began to rise.

You could simply say that the tubular diseases are from toxins. However, since the

answers to questions concerning initial and best tests and treatments are different, they

must be subdivided so they can be addressed individually.

Direct Toxins

Gentamicin acts directly as a toxin to the kidney's tubule. Other drugs include amphotericin,

cisplatin, NSAIDs, and cyclosporine. Contrast agents also act in the same way.

Best test: Exclude other causes of renal failure. There is no test to determine the specific

etiology of any toxin-mediated organ toxicity. Biopsy will NOT determine the specific agent.

Direct Toxins:

Best therapy: Stop the offending agent. There is no specific therapy to reverse ANY toxin-

mediated organ damage beyond this. Dialysis does NOT reverse the damage; it supports the

patient while waiting for the kidneys to come back to life on their own.

Allergic Interstitial Nephritis:

Penicillin causes damage to the kidney, as it causes an allergic reaction against the kidney

tubule. Other drugs include sulfa drugs, allopurinol, phenytoin, rifampin and NSAIDs.

Keys to recognizing this as the cause of the renal failure are fever and rash, although

these do not have to be present.

Allergic Interstitial Nephritis:

P a g e | 28

Best initial test: Measure blood and urinary eosinophils. IgE levels are not sufficiently

sensitive. Renal biopsy is the most accurate test but should seldom, if ever, be used.

Best initial therapy: Stop the medications. Very severe cases can be treated with steroids.

Crystals:

Uric acid crystals from the gout as well as from oxalate crystals from ethylene glycol ingestion

can also damage the tubules. Look for gout or ethylene glycol ingestion in the history.

Best initial test: Urinalysis to look for crystals.

Therapy: Either allopurinol for gout or ethanol infusion for the ethylene glycol ingestion.

Pigments:

Myoglobin from rhabdomyolysis and hemoglobin from hemolysis are directly toxic to the tubule.

The fact that this patient was found lying on the floor of her apartment is suggestive of

rhabdomyolysis. Clues to pigments as the cause of the renal failure are hemolysis or muscle

breakdown, as dark urine, on history.

Pigments:

Best initial tests: EKG to exclude signs of life-threatening hyperkalemia and urinalysis to

show dipstick positive for blood with no RBCs on the microscopic examination.

Most accurate and specific tests: Myoglobin in urine and elevated CPK level in blood for

rhabdomyolysis.

Best initial therapy: Hydration and alkalinization of the urine with bicarbonate.

USMLEStep2Lesson11:Nephrology:Hyponatremia

Nephrology

Hyponatremia
P a g e | 29

A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the hospital

because of mild confusion, which has developed over the past several days. His sodium level

is 119 (normal 135-145)

What is the etiology of his hyponatremia?

The first step in evaluating hyponatremia is to determine the volume

status of the patient.

Hypervolemic (presence of rales, edema, jugulovenous distention):

o Congestive heart failure
o Nephrotic syndrome
o Cirrhosis

The first step in evaluating hyponatremia is to determine the volume

status of the patient.

Hypovolemic (orthostasis, dry mucous membranes, decreased skin turgor):

o GI fluid loss
o Urinary loss, diuretics
o Skin losses, sweating, fever, burns

The above also require replacement with free water to drive sodium down

The first step in evaluating hyponatremia is to determine the volume

status of the patient.

Normal volume:

Addisons disease does not require free water to drive the sodium down.

Psychogenic polydipsia

Pseudohyponatremia

Syndrome of inappropriate antidiuretic hormone (SIADH)

Hypothyroidism

A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the hospital
P a g e | 30

because of mild confusion, which has developed over the past several days. His sodium level

is 119 (normal 135-145). Physical examination reveals normal skin turgor and no

orthostasis, edema, or rales.

What is the best initial test?

If a normal persons sodium were suddenly driven below normal, the bodys response would be

to immediately shut off all ADH secretion, allowing the maximal amount of free water to be

released. The normal response would be to maximally dilute the urine. The normal response to

hyponatremia would be to have a urine osmolality at the lowest possible amount. The range of

urine osmolarity is 50-1200 mOsm/kg. The normal response would be urine osmolarity around

50 mOsm/kg and urine osmolality less than serum osmolarity. Urine sodium should also be

low.

The best initial test is the

urine osmolality

A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the hospital

because of mild confusion, which has developed over the past several days. His sodium level

is 119 (normal 135-145). Physical examination reveals normal skin turgor and no orthostasis,

edema, or rales. His serum osmolality is 250 mOsm/kg (normal 280-300), urine osmolality

is 425 mOsm/kg and urine sodium is 42 mEq/L.

What is the best therapy for this patient?

The urine osmolality in this patient is higher than the serum osmolality. Combined with a high

urine sodium level this is confirmatory of SIADH. We do not use ADH levels.

Therapy for SIADH is divided as follows:

Mild, asymptomatic hyponatremia: Fluid restriction to 1/L/day

Moderate hyponatremia with mild or moderate neurological symptoms: Saline infusion and

loop diuretic

Severe hyponatremia with severe symptoms: 3% hypertonic saline sometimes combined with

diuretic
 P a g e | 31

What are the complications of changing sodium levels too rapidly?

(>1-2 mEq/L/hr)

Too rapid a RISE => central pontine myelonolysis

Too rapid a DROP => cerebral edema

The patient described above has his sodium corrected by normal saline infusion and a diuretic.

His neurological symptoms resolve.

What is the next best step in his management?

This patients underlying problem probably cant be corrected; lung cancer at the carina

typically cant be resected. Hence, as soon as the saline and diuretic therapy is stopped the

hyponatremia will recur. He will probably not be thrilled with maintaining lifelong fluid restriction.

What is the management of chronic SIADH?

Demeclocycline to block the effect of the ADH at the level of the kidney tubule on a

chronic basis.

USMLEStep2Lesson12:Nephrology:Hyperkalemia

Nephrology

Hyperkalemia

A 27-year-old man presents to the ER at your hospital after having just taken the physical exam to join the

NY City Fire Department. As part of this exam he must do 50 push-ups followed by suddenly lifting a 175-

lb bag of sand. He then has to run up and down 3 flights of stairs and across a balance beam followed by

50 more push-ups. He comes to see you because of severe muscle pain, muscle tenderness, and dark

urine developing over the next several hours.

What is the most important first step in his management?

 P a g e | 32

The patient seems to have rhabdomyolysis on the basis of severe, sudden exertion. Several tests are

needed: CPK level, urinalysis looking for blood on dipstick, urine microscopic exam, potassium level, and

possibly urine myoglobin level. However, you must choose the MOST URGENT test. No matter how high

the CPK level is, hyperkalemia is more immediately life-threatening. Even if the potassium level is

elevated, it is more important to know whether there are EKG abnormalities from the hyperkalemia, which

mean he will suddenly die of an arrhythmia.

The EKG shows peaked T-waves

What is the NEXT best step in management?

Calcium chloride or calcium gluconate is given intravenously

What is the NEXT best step in management?

Half normal saline infusion and bicarbonate as well as an ampule of 50%

dextrose is given with insulin.

The original potassium level (on entry, before therapy) comes back at 7.9 mEq/L. His CPK level is

markedly elevated at 48,000 and the urinalysis is dipstick positive for blood, but no RBCs are seen on

microscopic exam.

What is the NEXT best step in management?

The fluid and bicarbonate infusion is continued.

Kayexalate is given orally to remove potassium from body.

Repeat potassium level 2 hours later is 6.8 mEq/L. A further level 2 hours after that is 5.8 mEq/L.

USMLEStep2Lesson13:EmergencyMedicine:Overdose

Emergency Medicine

Overdose

A 25-year-old medical student gets very depressed while preparing for USMLE Step 2. After
P a g e | 33

finishing studying at midnight she takes a bottle of pills at 12:15 am in an attempt to commit

suicide. She removes the label from the bottle so no one can determine what she took. After

12:15 she finds that her last practice test score was 87% and she will easily pass. She walks

across the street to the ER at 12:30 am to seek treatment.

What is the best initial step in the management of this patient?

Ipecac is given immediately

Gastric emptying with ipecac has limited utility because it must be given within the first hour of

management. Do NOT give ipecac with ingestions of caustic substances since they will burn

the GI tract and mouth on their way out.

Do NOT answer toxicology screen. This takes too long to come back to be useful and it will

not change management. No matter what pills she took, the initial answer in the first hour of

management is to empty the stomach.

Why NOT the gastric lavage?

Gastric lavage with an oropharyngeal hose is not very useful, and most awake patients do not

need this and will not tolerate it. Use gastric lavage in patients with an acute overdose who

have an altered mental status in the first hour after a pill ingestion. You cannot give ipecac to

these patients because they will aspirate.

Perform endotracheal intubation with gastric lavage to protect the airway when the

patient has altered mental status.

Do NOT lavage patients with caustic, acid or alkali ingestion.

After the ipecac, what is the NEXT best step in management?

Activated charcoal

Charcoal is useful in almost all overdoses and is not dangerous in anybody. In addition,

charcoal will even remove drug from the body that has already been absorbed into the blood

stream.

A 25-year-old medical student gets very depressed while preparing for USMLE Step 2. After

finishing studying at midnight she takes a bottle of pills at 12:15 am in an attempt to commit
P a g e | 34

suicide. She removes the label from the bottle so no one can determine what she took. At

12:30 am she finds that her last practice test score was 87% and she will easily pass. She

walks across the street to the ER at 1:00 am to seek treatment.

The patient is confused, disoriented, lethargic, sleepy, and

obtunded and is not thinking so well.

What is the best initial step in the management of this patient?

Naloxone

Thiamine

Dextrose

Although you will want to intubate the patient to perform gastric lavage, you
must FIRST give the naloxone, thiamine, and dextrose. If the patient took an
opiate or is hypoglycemic she will awaken immediately. You will NOT have to
do lavage then because the problem will have been solved.

She awakens after being given the naloxone, dextrose and thiamine.

What is the NEXT best step in management?

Activated charcoal for the same reasons as described above.

After this management, then toxicology and specific drug levels are used to determine the

specific etiology of the overdose.