microsoft word viewer - internal medicine 1,conrad fisch

8/8/2019 Microsoft Word Viewer - Internal Medicine 1,Conrad Fisch

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USMLE Step 2 Lesson 1: Cardiology: Myocardial Infarction

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

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

CPK-MB 4-6 hr 2 days

Troponin 4-6 hr 1-2 wk

Myoglobin 1-4 hr s

LDH 12-24 hr s

LDH currently is not useful. Never answer it.

Best Answers:

Which has the best sensitivity, but poor specificity?

Myoglobin

Which has the best specificity?


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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 (10-20%) NO

Special Circumstances

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 Neveras prophylaxis

o All patients who develop major vertricular arrhythmias (ventricular

tachycardia or fibrillation)


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Pacemakers

Anything slow or that could become slow

Third-degree AV block

Mobitz II second degree block

Left bundle branch block

USMLE Step 2 Lesson 2: Cardiology: Congestive Heart

Failure

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+ 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


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Treatment of Pulmonary Edema

Sit the patient upright

Give Oxygen


First Step: Preload reduction

Diuretics any loop diuretic intravenously Morphine

Nitrates

Second Step: Only if preload reduction is ineffective

Positive inotropes

Dobutamine

Amrinone


Third Step: Afterload reduction

Ace inhibitors - IV


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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

USMLE Step 2 Lesson 3: Infectious Diseases: Intro. to

Antibiotics

Infectious Deseases

Introduction to Antibiotics

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


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o Cloxacillin

o Dicloxacillin

o Nafcillin


With mild penicillin allergy

First-generation cephalosporins:

o Cefazolin

o Cephalexin

o Cephradine

o Cefadroxil


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

Gram-negative Bacilli

ForE. coli, Proteus, Enterobacter, Klebsiella, Morganella, and Pseudomonas, ALL of

following provide >90% coverage:

Aminoglycosides (gentamicin, tobramycin, amikacin)

Aztreonam

Quinolones (ciprofloxacin, levofloxacin)

Gram-negative Bacilli


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ForE. 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 forPseudomonas

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

Second-generation cephalosporins

Beta-lactam/ Beta-lactamase inhibitor combinations

Antivirals

Herpes simplex and varicella

Acyclovir, valacyclovir, famciclovir

Herpes simplex, and varicella AND Cytomegalovirus


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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

Fluconazole, ketoconazole, itraconazole

Onychomycosis

Terbinafine, itraconazole

Griseofulvin is as useful as a rotary telephone

USMLE Step 2 Lesson 4: Central Nervous System Infections


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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 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

of3,502, and a negative gram stain. Culture is sent.


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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


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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.


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?


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.

USMLE Step 2 Lesson 5: PPD Testing

Infectious Diseases

PPD Testing


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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


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A 32-year-old, HIV- physician from India who received BCG as a child and has never

been 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.



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



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!

USMLE Step 2 Lesson 6: HIV

Infectious Diseases

HIV


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HIV

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 is575, and his viral load is 1,000.

Which medications are appropriate for this patient?

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

Whatto start?

Any two reverse transcriptase inhibitors AND any protease inhibitor



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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


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Azithromycin (once a week)


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 AND azithromycin AND

NOTHING!!

USMLE Step 2 Lesson 7: Hematology: Microcytic Anemia

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 of28%.

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.


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Low MCV

Iron deficiency

Anemia of chronic disease (can also be normocytic)

Sideroblastic

Thalassemia

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 of28%; 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


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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

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


Sideroblastic anemia

Pyridoxine

Thalassemia trait

No therapy


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USMLE Step 2 Lesson 8: Hematology: Macrocytic Anemia

Hematology

Macrocytic Anemia

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

hematocrit of28%.

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


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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

What is the best initial test?

Presence of hypersegmented neutrophils and a low folate level.

Alcohol or other drug toxicity


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


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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:

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


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

Which of the following is the best intitial therapy and mostdefinitive 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

USMLE Step 2 Lesson 10: Nephrology: Acute Renal Failure

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).


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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-renalazotemia is as follows:

Pre-renalAcute Tubular

Necrosis

BUN/Creatinine

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


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often from various toxins combined with possible ischemia from hypoperfusion.

How many different toxins can you identify in this case?

An 87-year old woman with a history ofgoutand 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


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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:

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 glycolingestion.

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.


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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.

USMLE Step 2 Lesson 11: Nephrology: Hyponatremia

Nephrology

Hyponatremia

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 severaldays. 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



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



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Normal volume:

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

Psychogenic polydipsia

Pseudohyponatremia

Syndrome of inappropriate antidiuretic hormone (SIADH)

Hypothyroidism


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.


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


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


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is 42 mEq/L.


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

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


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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.

USMLE Step 2 Lesson 12: 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?

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



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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 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?


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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.


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.

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