Morning Report 9/28/15 – Hypertensive Urgency/Emergency

Teaching Pearls:

  • Distinguish whether elevated blood pressure is secondary to other etiologies, including brain bleed, aortic dissection, drug use, etc
  • Hypertensive emergency/urgency is a diagnosis of exclusion. Defined as very high blood pressure with active end organ damage. End-organ damage includes:
    • Acute encephalopathy
    • Pulmonary edema
    • Aortic dissection
  • Cushing’s Reflex: Hypertension, Bradycardia, and Respiratory variation.
  • In LVH, you can commonly see T wave inversions along lateral leads due to repolarization abnormalities.
  • Hypokalemia, Metabolic Alkalosis, Hypertension –> consider hyperaldosteronism, bilateral renal artery stenosis, or Cushing’s syndrome. Check Renin and Aldosterone levels:
    • Elevated Renin/Elevated Aldosterone –> bilateral renal artery stenosis
    • Low Renin, Elevated Aldosterone –> Conn’s syndrome
    • Low Renin, Low Aldosterone –> Consider Cushing’s syndrome as corticosteroids can still bind to mineralocorticoid receptors.
  • Treatment for Hypertensive emergency: Decrease of blood pressure 10-20% within the first hour. Then 5-15% for the next 23 hours. No more than 25% within the first 24 hours to prevent hypoperfusion.
  • Two exceptions are acute CVA and aortic dissection.
    • Acute CVA – no need to treat unless BP>185/110 with consideration of tPA, or BP>220/120
    • Aortic Dissection – Important to treat aggressively to goal SBP 100-120. Use beta blockers.
  •  Medications For Treatment
    • Nitroglycerin gtt, Nitroprusside (fast onset, short half life, risk factors for cyanide toxicity include AKI, increased infusion rate)
    • Beta Blockers – Labetalol or esmolol
    • Calcium Channel Blockers – Nicardipine

9/25/15 Friday!

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.
MINH Jacket

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.