MKSAP Question: Understand the difference between between dehydration and hypovolemia – dehydration is defined as loss of free water.

Thanks to Fernando for presenting an interesting case!

Teaching Pearls:

• Asthma affects approximately 5% of the population.
• Commonly present in adolescent/young adults, but can also present in the elderly.
• Risk Factors for Asthma Exacerbations: 1) Prior Intubations 2) # of Hospitalizations in Last Year 3) Not on inhaled corticosteroids or PO steroids 4) Tobacco/Polysubstance Abuse 5) Psychosocial Issues 6) Non-compliance 7) Multiple Medical Co-morbidities
• PFTs will demonstrate obstructive airway disease with FEV1/FVC <70%. With bronchodilators, reversibility will be seen.
  • FEV1 improvement of 12% with total change >200cc demonstrates reversibility.
  • TLC will be elevated.
  • DLCO should be normal (Watch out for any false positive and false negative results)
• Antibiotics are not routinely recommended in patients with asthma exacerbation in the absence of a consolidation.
• Beware of a “normal” pCO2 in a patient who is hyperventilating and admitted with asthma exacerbation.
• Treatment of Asthma Exacerbation: Steroids, Short Acting Beta Agonists +/- anticholinergic medications. Needs continual reassessment.

Teaching Points:

• Clinical Manifestations:
  • Nocturia (usually first sign), polydipsia, polyuria
• At baseline, [Na] resides in the high normal range as long as patient is able to replete free water.
  • Patients become hypernatremic when they are in an altered stated and unable to replete their free water needs.
  • Ex: Pts are strapped down, kept NPO during acute stresses
• Sodium level becomes impaired during the following conditions:
  • When thirst is impaired or cannot be expressed
  • CNS lesions who have hypodipsia or adipsia.
  • Impaired adults who cannot independently access free water.
• Nephrogenic DI is the most common side effect of lithium.
• Water Deprivation test should be used to distinguish etiologies of polyuria and polydipsia.
• Lithium enters the principal cells via ENaC. Accumulation leads to interference of aquaporin production.
• Chronic Lithium use can lead to irreversible nephrogenic DI.
• Treatment of Li-induced Nephrogenic DI
  • Discontinuation of Lithium
  • If Lithium is to be used, treat with amiloride
    • Only shown to work with mild to moderate nephrogenic DI.
    • Need to check Lithium level as a result of fluid depletion.
  • Other treatment modalities:
    • NSAIDs
    • HCTz and low sodium diet
  • Can also potentially cause RTA and nephrotic syndrome.

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