Special thanks to Chris Rombaoa and RayRay for taking the time and energy to organize the jacket orders. If you haven’t heard by now, our new Valley jackets have arrived!!! If you ordered one, please do come by the chiefs office to pick it up so you can look as fly as Dr. Minh Le.

Teaching Pearls:

• Hypercoagulable etiologies: Acquired vs inherited causes.
• Inherited Hypercoagulable work-up: Protein C, Protein S, Factor V Leiden, Antithrombin 3, Prothrombin G2021A
• Acquired causes: prolonged rest, high risk surgery, hospitalization, medications, age
• In acute infection/acute clot, the Protein C, protein S and Antithrombin 3 levels may be decreased, giving a false positive result. The Factor 5 Leiden and Prothrombin Gene mutation are gene studies so they are not affected by acute illness.
• You can see both arterial and venous clots in Anti-phospholipid syndrome and Paroxysmal Nocturnal Hematuria (think myelosuppression and thrombosis, intravascular hemolysis)
• Thrombosis plus thrombocytopenia –> Think HIT, APS, PNH
• Clinical Diagnosis of APS: Unexplained thrombocytopenia, spontaneous miscarriages, arterial/venous thrombosis
• Laboratory Diagnosis of APS: aCL, B2GP, LA, timing requires positivity of markers even after three months due to false positive serologic studies

Inherited Thrombophilia

A special thank you to Dr. Polesky, Dr. Young, and Dr. Roosevelt for joining us at Morning Report today.

Teaching Pearls: 

• For needlestick injuries, post-exposure HIV prophylaxis entails a 28 day course of Truvada and an integrase inhibitor (Raltegravir or Dolutegravir). See PEP Guidelines.
• AIDS is defined as a CD4<200 or presence of an AIDS-defining illness.
• PCP in an AIDS patient is a medical emergency with high mortality if left untreated! Make sure to get an ABG and CT Chest. Hypoxemia is an important distinguishing feature of PCP Pneumonia. Significant lymphadenopathy on CT is not commonly seen with PCP pneumonia and may push you towards TB or other etiologies.
• When PCP pneumonia is clinically suspected, start treatment right away. Make sure to get input from Pulmonology and Infectious Diseases.
• CXR findings can be normal in a patient with PCP.
• LDH is a sensitive but not specific test for PCP. Beta-D-Glucan can be helpful but again is not specific to PCP and can take a long time to result.
• Treatment of PCP with Bactrim can cause rapid destruction of the PCP organism and lead to widespread inflammation cause respiratory failure. Steroids are indicated when the A-a Gradient is > 35 mmHg or the PaO2 < 70 mmHg.
• Once you start treatment for PCP, make sure to closely monitor their respiratory status closely as patients can clinically worsen before improving.

Teaching Pearls:

• Often present with jaundice, abdominal pain and distension, leukocytosis.
• Many patients may actually stop alcohol use a few weeks prior to admission due to worsening symptoms.
• Severe alcoholic hepatitis defined by DF>32
• First-line treatment for alcoholic hepatitis is ALWAYS alcohol cessation.
• Studies have shown that 6-month mortality could be as high as 40%.
• Medical management includes prednisolone or pentoxifylline. Prednisolone is preferred assuming there are no contraindications.
• Recent STOPAH trial in NJEM 4/2015 showed no additional benefit with combo of prednisolone + pentoxifylline compared to prednisolone alone. No benefit with pentoxifylline alone compared to placebo.
• Many patients with alcoholic hepatitis are also very malnourished. Hence these patients should be taking 1-1.5 grams protein/kg body weight daily.

Thanks to Madison Pham for presenting today!

Teaching Pearls:

• Cameron Lesions are associated with large hiatal hernias and are linear erosions in the gastric mucosa secondary to the mechanical sliding through the hernia
• The most common causes of Upper GI Bleeds are:
  • Peptic Ulcer Disease (38%)
  • Esophageal Varices (16%)
  • Esophagitis (13%)
  • Malignancy (7%)
  • Angioectasias (6%)
• Uncommon causes of UGIB: Mallory-Weiss Tear, Dieulafoy lesions, Cameron lesions, Gastric Antral Vascular Ectasia, Portal Hypertensive Gastropathy, Hemobilia, Osler-Weber-Rendu
• MKSAP Pearl: Polyps >1cm or villous features require repeat colonoscopy in 3 years.

Teaching Pearls: 

• Calculate the osmolar gap in patients with an anion gap acidosis of unknown etiology. Causes of Elevated Osmolar Gap includes methanol, ethanol, ethylene glycol, propylene glycol, isopropyl alcohol, mannitol. Remember that Isopropyl alcohol causes an osmolar gap without an anion gap.
• The cough syrup/drug “Lean” can sometimes contain propylene glycol.
• Causes of Rhabdomyolysis includes:
  • Direct Injury/Trauma: Lightning strike, malignant hyperthermia, NMS, ischemic limb injury, exertional causes such as marathon running
  • Infectious: Viral, bacterial
  • Inflammatory: Polymyositis, dermatomyositis
  • Metabolic/Endocrinological: Electrolyte imbalance, hypothyroidism, thyrotoxicosis, DKA
  • Genetic Causes
• The treatment of Rhabdomyolysis includes fluid resuscitation and intravenous bicarbonate to alkalanize the urine to prevent myoglobin toxicity

• First rule out fulminant liver failure. Fulminant Liver Failure: no history of liver disease, transaminitis, coagulopathy, and encephalopathy.
• For patients with AST/ALT in the thousands, think: Viral, ischemic, toxins, or autoimmune etiologies
• Hemoarthroses: think of hemophilia (Factor 8/9 deficiency), platelet dysfunction more likely to cause petechiae.
• Alcoholic liver disease normally presents with AST and ALT in the 300-400s. AST/ALT ratio >1
• Hep A and B more likely to cause transaminitis in the 1000s. Unlikely to be seen in acute HCV infection, hemochromatosis, alcoholic liver disease.
• Check HAV IgM for acute hep A infection. Transmitted via fecal oral route. More likely to cause significant transaminitis in adults vs children.

• Important to determine whether serum is hypo-osmolar, iso-osmolar, or hyperosmolar.
• If hypo-osmolar, determine overall fluid status.
• Using urine osmolality and urine sodium can assist with history and physical to determine etiology
• Patients with significant vomiting can present with very low chloride levels (<60) due to high concentration of chloride within gastric lumen. Parietal cells secrete HCl into stomach lumen so excessive vomiting can significantly decrease serum chloride levels.
• Metabolic alkalosis and hypokalemia can result from excessive vomiting. Hypokalemia could also be worsened with intracellular shift due to alkaline conditions.
• Main trigger for renin aldosterone system is low volume status.
• Main trigger for ADH secretion is elevated osmolality. Second trigger is low volume status.
• Low volume status results in a higher urine osmolality and low urine sodium level, in the setting of proper renal function.
• Low volume status with low solute intake (as in alcoholics) may display lower values of urine osmolality in addition to low urine sodium level.
• May check urine chloride in a patient with hyponatremia, hypokalemia, and alkalosis:
  • If urine chloride low, suggestive of excessive vomiting.
  • If urine chloride high, suggestive of diuretic use.
  • If urine chloride normal, suggestive of possible Gitelman/Barttner syndrome

• Urea splitting organisms include Proteus, Klebsiella, Pseudomonas, and Enterobacter
• Xanthogranulomatous pyelonephritis can occur in patients with chronic pyelonephritis with recurrent urinary tract infections causing accumulation of granulomatous tissue containing lipid-laden macrophages which can destroy a kidney. Usually this is unilateral and the treatment is nephrectomy. Look for a bear paw on CT!

• The differential for wide complex tachycardia includes ventricular tachycardia, SVT with aberrancy, and SVT with a bypass track (WPW).
• Characteristics of V tach include capture/fusion beats, AV dissociation, Northwest axis, precordial concordance.
• Akhtar Criteria: In patients with a history of MI, new onset wide complex tachycardia is >95% ventricular tachycardia
• Remember Idiopathic V-Tach (often from the right ventricular outflow tract) and Arrhythmogenic right ventricular dysplasia as causes of V-tach in a young person