All posts by vmcimchiefs

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!

8/19/15 Morning Report

Clinical Pearls!

  • Dengue fever can present as a separate clinical entity called Dengue Hemorrhagic Fever which presents with shock from plasma leakage syndrome, marked thrombocytopenia, and spontaneous bleeding
  • Fever Pattern with Dengue infection: Continuous or occasionally the fever abates for a day and then returns, a pattern referred to as “saddleback fever”
  • Lab abnormalities in Dengue Fever Include: Thrombocytopenia, Leukopenia, Anemia is less common, AST elevation

Morning Report 8/13/15: Serotonin Syndrome

Great Discussion!

  NMS Serotonin Syndrome
Etiology Too Little Dopamine Too much serotonin
Onset Days to Weeks Usually < 24 hours (more acute than NMS)
Neuromuscular Findings Bradyreflexia, severe muscular rigidity Hyperreactivity (tremor, myoclonus, reflexes, ocular clonus)
Pupils Normal Dilated
Treatment Supportive care, consider bromocriptine Benzodiazepines, cyproheptadine in certain cases
Resolution Days to weeks < 24 hours

Intern Morning Report 8/11/15 – Endocarditis Review

We went over a fascinating case of MSSA endocarditis in the setting of immunosuppression. Below are some of the clinical pearls:

  1. Modified Duke Criteria for infective endocarditis
  • Major criteria
    • Positive blood cultures
      • Typical microorganism from two separate blood culture
      • Single positive blood culture for Coxiella burnetii
      • Persistently positive blood cultures
    • Echocardiogram findings of vegetation
    • New valvular regurgitation
  • Minor criteria
    • Predisposing heart condition or IVDU
    • Fever >38C
    • Vascular phenomena
      • Major arterial emboli
      • Septic pulmonary infarcts,
      • Mycotic aneurysm
      • intracranial hemorrhage
      • conjunctival hemorrhages
      • Janeway Lesions
    • Immunologic phenomena
      • glomerulonephritis
      • Osler nodes
      • Roth spots
      • Rheumatoid factor
  • Clinical Diagnosis
    • 2 Major criteria OR
    • 1 major and 3 minor criteria OR
    • 5 minor criteria

2. Surgical Indications for treatment of endocarditis:

  • Valve dysfunction causing heart failure
  • Para-valvular involvement causing abscess, fistula or heart block
  • Difficult to treat organisms (fungal)
  • Persistent bacteremia
  • Recurrent septic emboli with vegetations despite appropriate antibiotic therapy

3. Most common bacteria associated with endocarditis

  • Viridans streptococci
  • Staphylococcus (MRSA or MSSA)
  • Enterococci

Ophtho-Medicine Morning Report

Thanks to Zach, one of the Stanford ophthalmology residents, for teaching us about the eye today at morning report! Here are some of the highlights:

  • Eye Pain: Usually related to pathology with the ANTERIOR segment of the eye. If pain resolves with topical anesthetic, think about dry eyes/external irritant.
  • Photophobia: Usually caused by ciliary body spasm
  • Inflammation from outside to inside:
    • Blepharitis: Eyelid inflammation
    • Conjunctivitis: Bacterial/viral/allergic
    • Scleritis/Episcleritis: Can be associated with collagen vascular disease (RA common)
    • Keratitis: Corneal inflammation, HSV classic cause
    • Iritis: Inflammation of the Iris
    • Uvea = Ciliary body + Choroid + Iris
      • Anterior Uveitis
      • Posterior Uveitis
    • Retinitis: Pt’s may report flashing lights
  • Retinal Detachment is classically described as a curtain over the eyes
  • Cherry red spot is seen in central retinal artery occlusion 

Morning Report: Staph Endocarditis Causing Glomerulonephritis?

Clinical Pearls:

  • Purpura = red-purple lesions that indicate extravasation of blood into the skin, they do not blanch
    • Purpura can be palpable or non-palpable
    • Purpura can result from abnormalities in 1) Platelets 2) Plasma Coagulation Factors 3) Blood Vessels
    • Non-palpable purpura:  described as petechiae (<3mm) or ecchymoses (>5mm), this is usually non-inflammatory. Causes include abnormal platelet function, DIC, infection, thrombocyptopenia, skin weakness, high intravscular pressure (blood pressure cuffs)
    • Palpable purpura: hallmark sign of leukocytoclastic vasculitis (small vessel vasculitis), occurs due to immune complex deposits in vessel walls, can also be caused by septic emboli
  • Cerebral edema is the most common cause of death in fulminant hepatic failure and is related to hyperammonemia
  • Dr. Young pointed out that Staphylococcus associated GN is not a classic type of post-infectious GN. As opposed to Strep associated GN which manifests classically manifests weeks after your infection, Staph associated GN often occurs at the same time as your infection. Also it is very important to distinguish HSP from the IgA dominant GN of MRSA infection as the treatments are very different but presentation can be similar. Absolutely don’t treat infection related GN with steroids (See references Below)!
  • HCV associated glomerulonephritis can be caused by Type 2 mixed cryoglobulinemia, which is a small vessel vasculitis mediated by antigen-antibody complexes depositing in small blood vessels

References:

  • Glassock RJ1 et al. Staphylococcus-related glomerulonephritis and poststreptococcal glomerulonephritis: why defining “post” is important in understanding and treating infection-related glomerulonephritis. Am J Kidney Dis. 2015 Jun;65(6):826-32. doi: 10.1053/j.ajkd.2015.01.023. Epub 2015 Apr 15.
  • Satoskar AA et al. Henoch-Schönlein purpura-like presentation in IgA-dominant Staphylococcus infection – associated glomerulonephritis – a diagnostic pitfall. Clin Nephrol. 2013 Apr;79(4):302-12. doi: 10.5414/CN107756.

AM Report SIM Session

Great session with our pulmonary critical care attendings Dr. Friedenberg and Dr. Gohil. This is our safe environment to practice rapid response/code scenarios and receive feedback which we do monthly. Thanks to everyone who participated!

Clinical Pearls: 

  • ABCDEFG: ABCs…don’t ever forget glucose! Make sure to check the fingerstick glucose during codes. It’s quick, easy, and can save lives!
  • During a code, no “air orders” and make sure to close the loop
  • As the code leader, be concrete with your instructions and delegation of tasks
  • Carry your code cards and take a look at the H’s and T’s when you are stuck
  • Remember that patients who are altered and unable to protect their airways are not good candidates for BIPAP, these patients often just need intubation
  • Post-intubation codes: Remember that sedation, hypotension from decreased preload/positive pressure ventilation, air-trapping from hyperventilation, and ventilator dysynchrony can lead to post-intubation code situations.

Morning Report: An Uncommon Presentation of an Uncommon Disease

Clinical Pearls:

  • Guillan-Barre Miller Fisher Variant: Classical triad is ophthalmoplegia, ataxia, areflexia but all three are not necessary. About 25% of these patients will have limb weakness. Additionally, you can see a descending paralysis rather than ascending paralysis.
  • Romberg Test: Maintaining balance while standing requires 2 out of 3 of the following – Proprioception, vision, vestibular apparatus. Patient’s with cerebellar ataxia will generally be unable to balance with their eyes open so the Rhomberg’s test is not a test of cerebellar function.
  • Albumino-cytologic dissociation on LP, preceding viral URI or Gastroenteritis, 30% Campylobacter
  • TCA Toxicity can cause numbness, tingling, transaminitis, extrapyramidal symptoms, ataxia.