AM Report 9/27/2016 – Graves Disease

Causes of High Output Heart Failure:
– Obesity (most common ~ 31%)
– Systemic AV shunts (22.5%)
– Hepatic disease (22.5%)
– Lung disease (i.e. COPD ~ 16%)
– Myeloproliferative disorders (multiple myeloma, myelofibrosis)
– Sepsis/Fever
– Hyperthyroidism
– Anemia

Increased thyroid hormone → increased metabolism → decreased SVR → increased cardiac output → increased contractility of heart muscle → increased myocardial oxygen demand/consumption

Physical Exam:
– tachycardia / atrial fibrillation
– hyperdynamic precordium
– systolic hypertension with widened pulse pressure
– brisk carotid/peripheral arterial pulsations
– loud first heart sound
– fine tremor
– warm moist skin
– exophatalmos (occurs in 20-25% of Graves patients)
– pretibial myxedema

– return patient to euthyroid state with antithyroid medication or RAI
– caution BB use – can reduce myocardial contractility in patients with impaired LVSF

Radioiondine Uptake Scan Interpretation:

Normal/Elevated Uptake:
[Autoimmune] – Graves disease, Hashimotos thyroiditis
[Autonomous Thyroid Tissue] – Toxic adenoma, toxic multinodular goiter
[TSH-mediated] – pituitary tumor

Low/Absent Uptake:
[Thyroiditis] – de Quervain’s thyroiditis, radiation thyroiditis, amiodarone thyroiditis
[Exogenous Thyroid Hormone] – excessive replacement, factitious hyperthyroidism
[Ectopic Hyperthyroidism] – Struma ovarii, metastatic follicular thyroid cancer

AM Report 9/26/2016 – Malaria


Transmission: Anopheles mosquito (nighttime bites)
Cause: Protozoan parasite (5 types) – P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi
Clinical Presentation: fever, headache, chills, vomiting – can progress to severe illness/death
Incubation Period: variable 12-14 days (early) to months
Diagnosis: Thick/Thin smear (gold standard), RDTs, PCR, serology/IFA (NOT FOR ACUTE DIAGNOSIS)
Treatment: Depends on uncomplicated vs. severe, suspected species, and drug-resistance

* Remember that P. vivax and P. ovale can remain dormant for months/years in your liver (hyponozoites)
* Remember to test for G6PD before administering primaquine given the risk for hemolytic anemia
* Negative Duffy blood group is protective against P. vivax – since it requires the Duffy antigen for cell entry.

Dengue Fever
Transmission: Aedes mosquito (day and night bites)
Cause: viral infection (Dengue single-stranded RNA virus 4 serotypes)
Clinical Presentation: Maculopapular rash on face, thorax, and flexor surfaces, abdominal pain, nausea/vomiting, diarrhea, saddleback fever – fever abates for a day and returns
Incubation Period: 3-14 days; >2 weeks UNLIKELY to be dengue
Diagnosis: IgM capture ELISA – serologic assay, viral RNA, NS protein-1 antigen
Treatment: Supportive care; self-limited illness

Transmission: Aedes mosquito (day and night bites)
Cause: Viral infection (Chikungunya virus – arbovirus)
Clinical Presentation: Fever, joint pain (common); headache, muscle ache, joint swelling, rash
Incubation Period: 3-7 days after infection
Diagnosis: IgM anti-chikungunya ELISA
Treatment: Supportive care; self-limited illness

Typhoid Fever
Transmission: Fecal/oral from infected humans
Cause: Bacteria: Salmonella Typhi
Clinical Presentation: High fever, weakness, abdominal pain, constipation (early) followed by diarrhea (later), salmon/rose-colored rash, HSM
Incubation Period: 8-14 days usually; can range from 3 days to 1 month
Diagnosis: Culture blood/stool/bone marrow for S. Typhi; serologic testing for S. Typhi antibodies
Treatment: Flouroquinolones (resistance growing), ceftriaxone, azithromycin


AM Report 9/22/2016 – Cauda Equina Syndrome

Cauda Equina  Syndrome:

Cauda Equina: set of intradural nerves that provide sensory/motor innervation from L2-S5

Nerve Roots of Cauda Equina:

  • Hip muscles
  • Lower extremity muscles
  • Urinary and anal sphincters
  • Sexual organ muscles

Causes of Cauda Equina:

  • Disc herniation (MOST COMMON)
  • Lumbar stenosis (OA)
  • Trauma
  • Infection/abscess
  • Metastatsis/neoplasma (Metastasis most common, ependymoma or schwannoma possible)
  • Inflammatory disease (CIPD, Paget’s, ankylosing spondylitis)

Symptomsbased on level 
Low back/radiating LE pain with at least one below

  • Urinary incontinence/retention
  • Fecal incontinence/retention
  • Loss of anal sphincter tone
  • Sexual dysfunction
  • Saddle anesthesia/hypoesthesia


– urgent neurosurgical evaluation to reduce side/eliminate mass
– eradicate causative organisms

Most common organisms:
– staph (63%)
– strep (9%)
– gram negative anaerobes (16%)

Empiric antibiotic regimen: vancomycin and cephalosporin +/- nafcillin

Steroids indications:
– within 8 hours of traumatic spinal cord injury
– metastatic disease (followed by surgery/radiation)

9/20/2016 AM Report – Cannabinoid Hyperemesis Syndrome

Cyclic Vomiting Syndrome

  • Stereotypical episodes of vomiting <1 week
  • 3 episodes in past year, 2 in past 6 months, at least one week apart
  • Absence of vomiting between episodes

3 Phases – Interepisodic, Prodromal, and Vomiting



  • More common in children
  • More frequent bouts in children (12/year) vs. adults (4/year)
  • Broad age of onset for adults
  • Symptoms longer for adults prior to diagnosis
  • Nausea between episodes is more common in adults

Differential diagnosis:


  • Acute gastroenteritis (rotovirus, enteric aderovirus, norovirus)
  • Post-operative nausea/vomiting
  • Vestibular neuritis
  • Chemotherpy/Drugs


  • Pregnancy
  • Chronic nausea/vomiting syndrome
  • Gastroparesis
  • Gastric outlet obstruction
  • CVS
  • Rumination syndrome

Cannabinoid Hyperemesis Syndrome

  • Stereotypical episodic vomiting similar to CVS (onset, duration, frequency)
  • Presentation after prolonged/excessive cannabis use
  • Relief of symptoms with sustained (1 week) cessation of cannabis*

* often associated with pathologic bathing behavior (prolonged hot baths/showers) – considered pathognomonic for CHS

9/7/2016 AM Report – IgA Nephropathy

Nephrotic Syndrome:
– Proteinuria (>3.5 g/24h or urine/creatinine > 3.5 mg/mg)
– Hypoalbuminemia
– Clinical evidence of edema
* Other clinical manifestations (hyperlipidemia, coagulation abnormalities) are related to losses of proteins other than albumin or caused by increased protein synthesis.

Nephrotic Range Proteinuria: > 3 g/24h without other findings

Nephritic Syndrome:
Characterized by: proteinuria, hematuria, pyuria, and often decreased kidney function and hypertension
– due to injury or inflammation within the glomerulus that allows the passage of protein, erythrocytes, and leukocytes into the renal tubule.
– resulting damage can lead to decreased GFR, kidney function, and abnormal blood pressure

IgA Nephropathy:
– most common primary glomerulonephritis
– an immune complex disease in which IgA antigen-antibody complexes are depositied primarily in the mesangium
– may be primarily involve the kidney or may be secondarily associated with other conditions

occurs at any age, but usually found in men (20-30 yo) who are white or Asian
– develops to ESRD in approximately 20-30% of patients within 10-20 years of onset

Risk factors for progression:
younger age at onset, hypertension, proteinuria > 1 g/24h, elevated creatinine, and low GFR

Clinical manifestations:

– typically asymptomatic at presentation with only microscopic hematuria and proteinuria on urine evaluation
– common presentation: recurrent gross hematuria occuring synchronously with an episode of respiratory or GI infection

confirmed by kidney biopsy

Management: ACE inhibitors or ARBs, with goal urine protein excretion < 1 g/24h

Simplified Approach to GN:
Step 1: determine the broad cause of the acute or progressive renal failure
– Pre-renal, intrinsic renal, or post-renal
– FENa (if oliguric to differentiate pre-renal from ATN), UA (evaluated for sediment), and renal US (rule out obstruction)
– If INTRINSIC renal than the differential is either: Glomeruli, Tubules, Interstitum, Vessels

Step 2: If a glomerular cause – differentiate between GLOMERULONEPHRITIS pattern from a NEPHROTIC SYNDROME pattern
– UA, renal US, 24 hour urine protein (urine protein:creatinine ratio)
– Look for active sediment (UA with protein and RBCs, dysmorphic RBCs, and/or RBC casts)

Step 3:
Use the serum complement levels to differentiate cause of GN
Low Complement GN:
Systemic: SLE, endocarditis, cyroglobulinemia
Isolated Renal: post-infectious GN, MPGN

Normal Complement GN:
Systemic: HSP, ANCA-associated, Goodpasture’s syndrome, hypersensitivity vasculitis
Isolated Renal: IgA nephropathy, anti-GBM disease, RPGN