Category Archives: Morning Report

Morning Report 9/24/15 Bleedin’ and Clottin’

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

Conditions Epidemiology MOA Severity of Hypercoagulability
Factor V Leiden Most common cause, 5% of Caucasians Point mutation in one active site of protein C, decreased ability to inactivate factor V Moderate
Prothrombin Gene Mutation Second most common cause More stabilized prothrombin (harder to inactivate) Moderate
Protein C Less Common  Protein C inactivates factors Va and VIIIa. Severe
Protein S  Less Common  Protein S is a cofactor for protein C Severe
AT Deficiency  Less Common  Antithrombotic protein that inhibits factor II and X  Severe

Morning Report 9/23/15 PCP Pneumonia

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.

Intern Report 9/22/15 – Alcoholic hepatitis

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.

9/21/15 Morning Report – Cameron Lesions

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.

Morning Report 9/15/15: Rhabdomyolysis

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

Morning Report! Approach to Transaminitis in the 1000s

  • 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.

9/10/15 – Morning Report – Hyponatremia

  • 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

8/31/15 Morning Report – Staghorn Calculi and Proteus Pyelonephritis!

  • 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!
Kidney Stones Composition PH Visibility on Xray
Calcium Stones (80%)

   

Calcium Oxalate 90%

Calcium Phosphate 10%

Insoluble in Acidic pH (except Ca phosphate) Radiopaque
Struvite (<10%) Magnesium Ammonium Phosphate

Calcium Carbonate Apatite

Insoluble in Alkaline PH Radiopaque (but can be variable)
Uric Acid Stones (~10%) Uric Acid Crystals Insoluble in Acidic pH Radiolucent
Cystine (rare) Cystine (Congenital Cystinuria) Insoluble in Acidic PH Radiolucent

8/26/15 Morning Report

  • 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

8/20/15 The All-of-Endocrinology-in-ONE-hour AM Report!

Clinical Pearls:

  • Over 90% of hypercalcemia is caused by primary hyperparathyroidism or malignancy.
  • Malignancy etiologies could be due to bone metastasis and/or PTHrP
  • Granulomatous diseases can cause hypercalcemia by expressing 1a-hydroxylase, which induces production of active Vitamin D.
  • Severe hypercalcemia (over 13mg/dL) is usually associated with malignancy and is most commonly seen in the inpatient setting
  • Mild to moderate hypercalcemia (11-13mg/dL) is usually seen in patients with primary hyperparathyroidism. It is most commonly seen in the outpatient setting.
  • Metastatic tumors to the hypothalamus/pituitary space are usually caused by lung or breast cancer
  • Management of hypercalcemia
    • IV Fluids to improve GFR immediately for calcium excretion.
    • Calcitonin intermediate onset of 4-6 hours. Be aware of tachyphylaxis
    • IV bisphosphonates, onset 24-48 hours (pamidronate, zolendronate)
  • A normal to high level of PTH in a patient with hyperparathyroidism almost always suggests primary hyperparathyroidism as the etiology.
  • V1 receptors are present in the blood vessels whereas V2 receptors are present in the collecting tubule. Activation of V2 receptors causes aquaporin channels within the membrane to allow reabsorption of water.
  • The hypernatremia from Diabetes insipidus may be masked until the patient is unable to satisfy their thirst or if they are unable to access water (for example, outpatients with DI usually don’t have hypernatremia because they can obtain free water from the most powerful sensing mechanism – thirst)
  • The etiologies for hypernatremia include poor water intake (inability to access water) versus diabetes insipidus.
  • Central DI will respond appropriately to ddAVP whereas nephrogenic DI will have a suboptimal response
  • Nephrogenic DI can be caused by electrolyte abnormalities (hypercalcemia, hypokalemia), medications (lithium, demeclocycline, etc), and genetic factors
  • Prolactin levels will INCREASE with pituitary stalk compression due to the lack of inhibition from hypothalamic dopamine, while all other anterior pituitary hormones (FSH, LH, ACTH, TSH, GNRH) would decrease.

A Very Special Thank you to Dr. Crapo for joining us!!! Also a special thank you to Dr. Kevin Ku for bringing in yummy bagels!