Category Archives: Morning Report

10/27/15 Morning Report SLE

Teaching Pearls: 

  • ANA negative lupus, check SSA/SSB which are associated with neonatal lupus and congenital heart block
  • ANA positive in 99% of patients with lupus, but low specificity
  • double stranded DNA antibodies are used to monitor disease severity in lupus
  • check C3, C4, and double stranded DNA to work up possible lupus flare
  • Drug induced lupus: Look for positive ANA and anti-histone antibodies. Also look for exposure to procainamide, hydralazine, chlorpromazine, PTU, phenytoin, minocycline, and TNF inhibitors.
Steroid Duration Equivalent Dosing
Dexamethasone Long-acting 1 mg
Methylprednisolone Intermediate-acting 4 mg
Prednisone Intermediate-acting 5 mg
Hydrocortisone Short-acting 20 mg

10/22/15 Morning Report Hyperthyroidism

  • Pathophysiology of T4 secretion: TSH secreted in the anterior pituitary and stimulates the TSH receptor in the thyroid to secrete thyroid hormone
  • Clinical presentation of Hyperthyroidism: Hyperdefecation (not diarrhea), osteoporosis, oligomenorrhea in pre-menopausal females, hair changes, palpitations, arrhythmias
  • Etiologies of hyperthyroidism
    • Grave’s Disease (most common cause of hyperthyroidism)
    • Destructive thyroiditis (subacute, silent, postpartum)
    • Multinodular Goiter/Toxic Adenoma
    • Medication-induced (amiodarone, lithium, IFN-a, etc)
    • Factitious
  • Antibodies
    • Anti-TPO and anti-thyroglobulin Ab seen with Hashimoto’s Disease (hypothyroidism)
    • TSI (thyroid stimulating immunoglobulin) and TBII associated with Graves Disease.
      • TSI binds to TSH receptors on thyroid gland, stimulating production of thyroid hormone.
      • TSI also binds to TSH receptors located on fibroblasts, stimulating proliferation and glycosaminoglycan production in retro-orbital space.
  • Clinical Presentation specific to Graves include pretibial myxedema (5% patients with Graves), exophthalmos (25% of patients with Graves)
  • Work-up of Hyperthyroidism
    • If evidence for Graves Disease, then GD likely diagnosis.
    • Evidence of nodules on physical Exam:
      • If None: Perform RAI uptake scan and antibody studies.
        • If increased uptake, elevated thyroid hormone due to over-synthesis
          • If diffuse uptake, think Graves Disease
          • If patchy uptake, think toxic multinodular goiter
        • If decreased uptake, think of factitious or destructive causes (subacute, silent, postpartum.
      • If Present: Get RAIU scan and thyroid ultrasound to distinguish TNG vs TA and/or evidence of cold nodules. Check for any concerning factors for thyroid cancer.
    • Thyroglobulin: Precursor to thyroid hormone production. Combined with iodine to produce T4.
      • May be used to differentiate factitious vs destructive thyroiditis, surveillance for thyroid cancer.
  • Treatment Options:
    • Thionamides – Methimazole versus PTU
      • Watch for drug rash and/or agranulocytosis
    • Radioactive iodine ablation
      • Do not use in patients with Graves Disease with severe ophthalmopathy as this can worsen symptoms.
    • Surgery
  Grave’s Disease Multinodular Goiter Subacute Thyroiditis
Clinical Course/Exam

 

 

Exophthalmos

Pre-tibial Myxedema

Hyperthyroid symptoms

Palpable nodules

Preceded by URI sx, Pain around the neck, pain with palpation, initially hyperthyroid (6 weeks) but progresses to hypothyroid (6 weeks), then normalizes
Diagnosis Tests

 

 

 

Low TSH

High Free T4

TSI

RAIU

TSH/T4

RAI

Thyroid US

TSH, Free T4

RAI – low uptake

Thyroid US – diffuse enlargement

Treatment

 

 

 

PTU

Methimazole (don’t use in 1st trimester of pregnancy). Watch for agranulocytosis.

RAIA, then will require

Surgical. Don’t use RAIA for patients with exophthalmos.

If compressive sx (dysphagia, etc) then surgery

If no compressive symptoms, can treat with RAIU. Toxic patients can also be treated with thionamides

NSAIDS, supportive

Then Prednisone if poor response

Symptomatic treatment, such as propranolol or beta blockers

Thionamides not indicated

Intern Report 10/20 – Bloody Diarrhea

Teaching Pearls

  • Duration of Diarrhea
    • Acute < 14 days
    • Chronic >4 weeks
  • Types of Diarrhea
    • Secretory
      • Stool osmole gap <50
    • Osmotic
      • Stool osmole gap >100
    • Inflammatory
      • Evidence of blood and/or mucoid stools
    • Malabsorption
      • Protein-losing enteropathy
      • CHO malabsorption
      • Fat malabsorption
  • Bacterial Causes of Blood Diarrhea
    Source Presentation Complications Treatment
    STEC (EHEC) Uncooked hamburger meat.

    Fecal-oral route

    Abd pain with bloody diarrhea +/- fever HUS No antibiotics indicated; supportive care
    Shigella Shellfish, fecal oral route Dysentery (bloody mucoid stools), tenesmus, fever, abdominal pain Reiters Disease Flouroquinolone; 3rd generation cephalosporin
    Salmonella Undercooked raw eggs, chicken, fruits Fever, abdominal pain, occult/overt bleeding Bacteremia, aortitis, osteomyelitis in those with sickle cell disease Only treat when symptoms are severe
    Campylobacter Poultry Occult bleeding Reiters disease, Guillain-Barre Syndrome Treat only if severe with macrolides

10/17/15 – Valley Residents Present at ACP in San Francisco!

A shout out to our poster presenters and brave Jeopardy Team! It wouldn’t have been possible without all our housestaff who graciously covered our presenters – thank you very much!  Saloni, Courtney, and Joe Li advanced to the finals in the poster competition. Three fascinating ID cases (cutaneous blastomycosis, rat bite fever, and pseudallescheria boydii) which is testament to all the cool ID we see here at Valley! 

Alex

SaloniCrazypic 3

Morning Report 10/14/15 Obscure Occult and Overt??

Teaching Pearls:

MKSAP Boards Question Review – Bipap has been shown to decrease mortality, decrease need for intubations, and decrease hospital stay in select patients with COPD exacerbations.

  • Definitions
    • Overt Bleeding – GI bleed that is clinically evident. Hematemesis, hematochezia, melena, etc
    • Occult Bleeding – Slow bleed manifested by iron deficiency anemia and/or positive guiac tests
    • Obscure Bleeding – Evident GI bleed without clear source of bleed despite standard work-up
  • Common etiologies for obscure occult GI bleed
    • Angioectasia
    • Cameron lesions
    • NSAID ulcer
    • Malignancy
  • Common etiologies for obscure overt GI bleed
    • Dieulafoy lesion
    • Meckel’s diverticulum
    • Angioectasia
    • Colonic diverticulum
  • Tachycardia suggests blood loss of 15-30%. Patients develop hypotension once blood loss >30%.
  • If unable to find source with EGD/colo, next step is to perform EGD and/or colonoscopy again as 30-50% can be identified
  • Capsule – can detect lesions without active bleeding. Diagnostic in 50-75% of cases. Only offers diagnostic benefits
  • Tagged RBC scan – good sensitivity but poor specificity. Does not offer therapeutic intervention. Ideal for bleeds 0.1-0.5cc/min.
  • Angiography – best for overt bleeding (>1cc/min), allows for immediate therapy.
  • Chronic Hepatitis B Treatment Goals:
    • Treat HBeAg Positive patients if:
      • ALT>2xULN
      • HBV DNA >20,000IU/ml
    • Treat HBeAg Negative patients if:
      • ALT>2xULN
      • HBV DNA >2,000IU/ml

Morning Report 10/13/15: COPD and Acid/Base

Teaching Pearls:

  • Only two interventions shown to reduce the progression of COPD: Smoking cessation and supplemental O2
  • Stepwise Approach to Acid Base: 
    • Acidic or Alkalotic?
    • Primary Disturbance? Respiratory or Metabolic
    • Calculate the Anion Gap
    • If Anion Gap present, calculate the Delta Gap
    • If metabolic acidosis present, use Winter’s formula to calculate whether there is appropriate respiratory compensation
  • For every 10 increase in pCO2, the bicarb should increase by 1 in acute respiratory acidosis and 3.5 in chronic respiratory acidosis
  • BIPAP can be used to improve respiratory acidosis, increase pH, decrease risk of intubation, and to reduce the pCO2
  • Contraindications of BIPAP include respiratory arrest, CV instability, altered mental status, aspiration risk/significant secretions, nasopharyngeal abnormalities, cranofacial trauma
  • Right Bundle Branch Block: Causes include RVH, cor pulmonale, PE, ischemic HD, myocarditis. Look for Broad QRS > 120ms, RSR prime in V1-V3, wide slurred S in the lateral leads V5-V6

Morning Report 10/8/15 West Nile Virus

A special thanks to the ID service for joining us today!

Clinical Pearls: 

  • Kernig and Brudinski’s sign (thanks to Dan for demonstrating!)
  • PRES: Posterior Reversible Encephalopathy Syndrome presents as headaches, confusion, seizures, and visual loss often in the setting of elevated blood pressure. Thought to be secondary to problems in cerebral autoregulation. Associated with immunosuppression, renal failure, eclampsia, hypertension, lupus.
  • Obtain a CT scan prior to an LP to evaluate for mass lesions that can cause brain herniation in the following patients:
    • Age >60
    • Immunocompromised
    • History of CNS disease
    • Seizure within one week of presentation
  • Empiric treatment for suspected bacterial meningitis includes Ceftriaxone (2gm IV q12 for CNS penetration), Vancomycin (resistant Strep pneumonia), and Ampicillin (immunocompromised and elderly patients for Listeria coverage, use Bactrim for penicillin allergies)
  • Start IV Acyclovir to cover possible HSV meningitis/encephalitis. HSV-1 is associated with encephalitis while HSV-2 can cause recurrent aseptic meningitis (Mollaret’s meningitis).
  • West Nile Virus
    • Flavivirus which was first detected in the US in 1999, over 500 cases in California last year
    • Asymptomatic in 80% of patients, symptomatic patients present with West Nile Fever (20%) or West Nile Neuroinvasive Disease (<1%)
    • Can manifest with acute flaccid paralysis, extrapyramidal signs
    • Detection of West Nile Virus IgM antibody in the CSF of symptomatic patients is diagnostic of West Nile Neuroinvasive Disease
    • Serologic cross-reactivity with other flaviviruses can cause false-positives (for example recent Yellow Fever vaccination or dengue infection)
    • Treatment of WNV is supportive 

10/7/15 Simulation Session

Nice work everyone! Thank you to Dr. Friedenberg and Dr. Gohil for running the case.

Some pearls:

  • Avoid Air Orders! Designate a “Code Leader” early on and stand at the head of the bed.
  • For PEA, start CPR ASAP and go ahead and ask for 1mg of epinephrine
  • During codes, make sure to ask for the Past Medical History, Medications, and Allergies.
  • Start antibiotics early for neutropenic fever.
  • Remember the sepsis core measures! If SBP < 90mmHg and/or MAP <65mmHg, recommend 30ml/kg of IVF bolus.

SIM picture

Intern Report 10/6 – New Onset Heart Failure

Teaching Pearls:

  • MKSAP Board Review Question – Thrombotic Thrombocytopenic Purpura (TTP) pentad: thrombocytopenia, microangiopathic hemolytic anemia (presence of schistocytes), renal failure, fever, neurological deficits.
    • Need only thrombocytopenia and MAHA (presence of schistocytes) for diagnosis.
    • Hematologic emergency. Treatment with plasmapheresis.
  • Left ventricular thrombus occurs in up to 10% of patients with post-MI and EF<30%.
    • Due to combination effects of blood stasis and replacement of endothelium with fibrotic tissue.
    • Diagnosis: Echocardiogram with Definity study
    • Treatment involves anticoagulation for 3-6 months
  • Etiologies of Heart Failure
    • Ischemic
    • Hypertensive heart disease
    • Valvular disease
    • Toxin/drug-induced
    • Medication-induced
    • Infiltrative disease
    • Infectious etiologies
    • Stress cardiomyopathy
    • Idiopathic
  • Presence of low voltage on EKG suggestive of tissue, air, or fluid surrounding the heart. Ex: obesity, pericardial effusion, etc.
  • Isolated Q wave can be present in lead III in a normal heart.
  • NT pro-BNP is primarily used as a helpful adjunct in distinguishing between heart failure and other etiologies of dyspnea. However if your patient clearly is coming in with symptoms of heart failure, it is not necessary to order it.
  • FREEDOM Trial
    • In patients with 3V disease, left main disease, and 2V disease with DM, CABG has demonstrated better clinical outcomes in CV mortality and MI compared to PCI.
    • Increased risk of stroke seen with CABG vs PCI.

10/5/15 Morning Report DIC versus TTP

– Clinical presentation of platelet disorders vs factor disorder. Epistaxis and petechiae are more suggestive of platelet disorders. Factor deficiency is usually associated with larger bleeds such as hemoarthrosis.
– Palpable purpura….think Leukocytoclastic Vasculitis.
– Thrombocytopenia Framework: Decreased production, increased breakdown, sequestration, dilutional
– Treatment for APL is ATRA. Remember to consider ATRA differentiation syndrome which can present with pleural effusions, edema, shortness of breath, and fever. Treat ATRA differentiation syndrome with Prednisone.
– Causes of MAHA: DIC, TTP/HUS, malignant hypertension, mechanical valves, HELLP/Pre-eclampsia, Scleroderma renal crisis
– It is important to distinguish between TTP and DIC because the treatment is different. DIC – treat the underlying cause and supportive care. TTP – treat with Plasmapharesis.
TTP DIC
Thrombocytopenia x x
Fibrin Degradation Products x
Elevated D-Dimer x
Low Fibrinogen x
Elevated LDH x x
Elevated PT and PTT x
MAHA/Schistocytes x x
ADAMTS13 x
Leukopenia x