Thanks to Dr. Wentzein for joining us!

• Paroxysmal Atrial Fibrillation is defined as intermittent episodes lasting less than 7 days. Persistent Atrial fibrillation lasts > 7 days
• Indications for cardioversion in Atrial Fibrillation: Hemodynamically unstable, refractory to medical interventions, severe CHF symtpoms, unstable angina
• The ARISTOTLE trial: In patients with nonvalvular atrial fibrillation and at ≥1 risk factor, apixaban is associated with a greater reduction in rates of stroke or systemic embolism while having a lower rate of lower bleeding than warfarin.
• CHADS VASC: 
  • CHF, HTN, Age 65-75, DM2, Prior stroke
  • Vascular disease, Age >75, Female
• In general, don’t combine beta-blockers with calcium channel blockers due to the risk of complete heart block.
• The AFFIRM trial: In patients with nonvalvular AF, there is no survival benefit between rate and rhythm control.
• Causes of High Output Heart Failure: Systemic AV Fistulas, hyperthyroidism, anemia, beriberi, psoriasis, sepsis, kidney/liver disease
• Side-effects of Amiodarone include thyroid disorders, lung toxicity, hepatotoxicity, and corneal deposits
• For Atrial Fibrillation > 48 hours, start antiocoagulation three weeks before and continue four weeks after DCCV
• For atrial fibrillation < 48 hours, continue anticoagulation for four weeks
• The ACUTE trial showed that with TEE guided cardioversion (to evaluate for a thrombus), anticoagulation is still needed

Teaching Pearls:

• Etiologies of hypernatremia include:
  • Dehydration
  • Diabetes Insipidus
• Dehydration
  • More likely to occur in those with CNS lesions, impaired thirst mechanism, inability to obtain free water, etc
  • High urine osmolality
• Diabetes Insipidus
  • Low urine osmolality
  •  Central
    • Secondary to poor ADH release from the posterior pituitary gland
  • Nephrogenic
    • Secondary to poor response to ADH
• Test of Choice to Differentiate Polyuria – between dehydration and Diabetes Insipidus
  • Water Deprivation Test
• Treatment for Correcting Hypernatremia
  • D5W – Find out the Free Water Deficit and correct sodium levels by 0.5mEq/L per hour correction. Avoid overcorrection to prevent cerebral edema.
  • If patient is very hypovolemic, fluid resuscitate with normal saline first

Teaching Pearls:

• Primary hyperparathyroidism and malignancy comprise of >90% of cases of hypercalcemia.
• Primary hyperparathyroidism is the most common cause of hypercalcemia in outpatient settings.
  • Patients are often asymptomatic and/or have a history of kidney stones
• Malignancy is the most common cause of hypercalcemia in inpatient admissions.
  • Labs often display severe hypercalcemia
• Initial Workup – First measure the PTH level
  • High PTH: diagnosis is likely primary hyperparathyroidism
  • High normal to mild elevation: think of primary hyperparathyroidism or Familial hypocalciuric hypercalcemia (FHH)
  • Low PTH: proceed onto further tests
• Other work-up labs include PTHrP and vitamin D metabolites. Other considerations include SPEP/UPEP, TSH, Vitamin A, etc.
• FHH differs from primary hyperparathyroidism in that the fractional excretion of Ca in FHH is low, whereas primary hyperparathyroidism is high.
  • Decreased fractional excretion of Calcium leads to lack of nephrolithiasis development.
• Primary hyperparathyroidism has three different pathologic conditions:
  • Adenoma – 89-90%
  • Hyperplasia – 6.8%
  • Carcinoma – 1.2%
• Should consider parathyroid carcinoma in patients with primary hyperparathyroidism and the following:
  • Severe elevations in calcium
  • Severe elevations in PTH

Special thanks to Dr. Patricia Salmon for coming to morning report to participate with our discussion today!

• Autoimmune hepatitis: Type 1 (associated with Anti-smooth muscle antibody which is very specific) and Type 2 (Anti-LKM), more common in women 4:1, can also be associated with elevated IgG
• Diagnose autoimmune hepatitis with liver biopsy showing interface hepatitis
• Treatment for autoimmune hepatitis includes prednisone plus azathioprine  or prednisone alone, liver transplantation when no contraindications
• Generally lupus is not usually a cause of liver disease but can be associated with autoimmune hepatitis
• SLE: Anti-DS DNA is used to follow disease progression

https://soundcloud.com/liluoke/the-hemophagocytic-lymphocystiocytosis-hlh-song

Compliments of our budding Hematologist/singer song-writer Eric Lau!!

Teaching Pearls

• Etiologies for Dilated Cardiomyopathy
  • Ischemic
    • Most common cause
  • Stress-induced
    • “Broken Heart syndrome”
    • Takotsubo cardiomyopathy
    • Middle to older age females with recent stressor event
  • Infectious
    • Chagas Disease
      • Most common cause of DCM in those from south and central America
    • Lyme’s Disease
      • More classically associated with heart block
    • Viral
      • Parvovirus B19
      • HIV
      • Coxackie
      • CMV
      • HHV-6
      • adenovirus
  • Toxins
    • Cocaine, meth, alcohol
    • Web Beriberi – thiamine deficiency
  • Medications
    • Chemotherapy (anthracyclines)
  • Idiopathic
• Ground Glass Opacities on CT
  • Due to filling of alveolus (airspace disease) or interstitial lung disease
  • Acute findings
    • Edema
      • Heart failure
      • ARDS
    • Pulmonary hemorrhage
    • Pneumonia (viral, mycoplasma, PCP)
    • Acute eosinophilic PNA
  • Chronic findings
    • Hypersensitivity pneumonitis
    • Organizing pneumonia
    • Alveolar proteinosis
    • Chronic eosinophilic pneumonia
    • Bronchoalveolar carcinoma
    • Lung fibrosis

Teaching Pearls:

• Pathophysiology
  • Involves excessive splanchnic vasodilation due to production of nitric oxide, causing increased decreased flow to the renal circulation.
  • MAP = CO x SVR
    • In patients with HRS, SVR is decreased due to the splanchnic vasodilation. Hence treatment is geared towards improving SVP and MAP.
• Diagnosis of Exclusion
  • Normal urinary sediment
  • No nephrotoxic meds
  • No hypotension
  • Urine studies similar to pre-renal AKI
    • UNa low, elevated FENa or FEUrea
  • Cannot distinguish between HRS and and pre-renal AKI
• Requires fluid challenge with albumin to distinguish between HRS and pre-renal AKI
  • 1g/kg albumin (max 100g) daily x 2 days
  • If renal function improves, suggestive of pre-renal AKI
  • If renal function continues to worsen, suggestive of HRS
• Types
  • Type I
    • Two-fold increase in Cr to Cr>2.5 within two weeks
    • Very poor prognosis
  • Type II
    • Less severe disease, associated with diuretic resistance
• Treatment of Choice
  • Liver Transplantation
  • Medical Management
    • If in ICU
      • Treat with norepinephrine and albumin
    • If non-ICU
      • Treat with midodrine, octreotide, and albumin

• Autosomal Dominant Polycystic Kidney Disease
  • Type 1: ~85%, average age of developing ESRD is around 50yo
  • Type 2: ~15%, average age of developing ESRD is around 70yo
• Cardiovascular disease is the most common cause of death in ADPKD and ADPKD is the most common inherited kidney disease
• For an infected renal cyst, use a lipophilic antibiotic (for good cyst penetration) such as quinolones or bactrim
• ADPKD is present in 5-10% of dialysis patients in the US
• Renal manifestations include recurrent UTIs, cyst infection, hematuria from cyst hemorrhage, and nephrolithiasis (usually uric acid stones)
• Extra-renal manifestations of ADPKD include diverticulosis, abdominal hernias, cysts in liver/thyroid/pancreas/seminal vesicles/etc, mitral valve prolapse, and cerebral aneurysms.
• The biggest risk factor for cerebral aneurysms in patients with ADPKD is a family member with cerebral aneurysms
• DDAVP for uremic platelets works by increasing vwF from endothelial cells

• Diagnostic Criteria for APLS: Need ONE lab criteria (confirmed 12 weeks apart) and ONE clinical criteria.
  • LAB Criteria: B2 Glycoprotein, Anti-Cardiolipin antibody, or lupus anticoagulant (as measured by prolonged DRVVT which does not correct with a mixing study)
  • CLINICAL Criteria: Any Thrombosis (venous/arterial) OR fetal loss/miscarriage
• APLS can be a primary disorder or secondary to other disease (usually Lupus)
• Clinical Features of APLS: 50% have prolonged PTT, 20% with livedo reticularis, cardiac valvular disease (MR), 32% DVT, 13% stroke, 7% hemolytic anemia
• Massive PE refers to PE causing hemodynamic instability (SBP < 90) while submassive PE refers to PE causing right heart strain without hypotension
• Right heart strain from PE: Look for signs of right ventricular hypertrophy and dilatation on EKG, Echo. McConnell’s sign on ECHO is RV hypokinesis with apical sparing

Teaching Pearls:

• Average Age 30-55 years old; F:M ratio 3:1
• Symmetric polyarthritis
• Morning stiffness >1 hour that improves with activity
  • OA worsens with activity
• Joint Involvement:
  • Almost always involves MCP, PIP, wrist, MTP
  • Spares the DIP and lumbar spine
    • Think of OA with DIP involvement
  • Can occasionally affect large joints
  • Swan Neck Deformity
  • Boutonniere deformity
  • Ulnar Deviation
  • C1-C2 subluxation (Atlanto-axial instability)
    • This specifically can also be seen in Downs syndrome
  • Peri-articular osteopenia
• RA is an independent risk factor for pre-mature coronary artery disease
• RA + pancytopenia + splenomegaly = Felty Syndrome
• RA is a systemic disease that can affect multiple organs. Can be a cause for secondary amyloidosis.
• Amyloidosis – deposition disease that clinically affects the kidneys, liver, and heart.
  • Kidney – can lead to nephrotic syndrome
  • Hepatomegaly
  • Restrictive cardiomyopathy
  • Thickening of tongue – lateral scalloping seen on exam
  • Waxy skin
  • Coagulopathy – amyloid protein causes binding to factor X
  • Neuropathy
  • GI – causing a malabsorptive syndrome
• Diagnosis requires abdominal fat pad biopsy with Congo red stain to check for apple-green birefringence.