GOUT

GOUT
By:
Wayne Blount, MD, MPH
Professor, Emory Univ. S.O.M.

OBJECTIVES

* Identify diagnostic criteria for gout
* Identify 3 treatment goals for gout
* Name the agents used to treat the acute flares of gout and the chronic disease of gout


Why Worry About Gout ?
* Prevalence increasing
* May be signal for unrecognized comorbidities : ( Not to point of searching)
Obesity (Duh!)
Metabolic syndrome
DM
HTN
CV disease
Renal disease

URATE, HYPERURICEMIA & GOUT
* Urate: end product of purine metabolism
* Hyperuricemia: serum urate > urate solubility (> 6.8 mg/dl)
* Gout: deposition of monosodium urate crystals in tissues

HYPERURICEMIA & GOUT
* Hyperuricemia caused by
Overproduction
Underexcretion
* No Gout w/o crystal deposition
THE GOUT CASCADE
* Urate
* Oevrproduction Underexcretion
* Silent Gout Renal Associated
* Tissue manifestations CV events &
* Deposition mortality

GOUT: A Chronic Disease of 4 stages
* Asymptomatic hyperuricemia
* Acute Flares of crystallization
* Intervals between flares
* Advanced Gout & Complications

ACUTE GOUTY FLARES
SITES OF ACUTE FLARES
INTERVALS SANS FLARES
FLARE INTERVALS
ADVANCED GOUT
* Chronic Arthritis
* X-ray Changes
* Tophi Develop
* Acute Flares continue
* Chronic Arthritis
* Polyarticular acute flares with upper extremities more involved

TOPHI
TOPHI RISK FACTORS
RADIOLOGIC SIGNS
X-RAYS
DIAGNOSING GOUT
SERUM URATE LEVELS
GOUT RISK FACTORS
DIFFERENTIAL DIAGNOSIS
* Pseudogout: Chondrocalcinosis, CPPD
* Psoriatic Arthritis
* Osteoarthritis
* Rheumatoid arthritis
* Septic arthritis
* Cellulitis
Gout vs. CPPD
RA vs Gout
REDNECK MEDICAL TERMS
TREATMENT GOALS
ENDING ACUTE FLARES
Acute Flare Med Choices
MED Considerations
PROTECTION VS. FUTURE FLARES
PREVENT DISEASE PROGRESSION
URICOSURIC AGENTS
XANTHINE OXIDASE INHIBITOR
WHICH AGENT ?
NEW AGENTS
URICASE ENZYMES
CASE STUDIES
WHAT ARE J.F.’s RISK FACTORS FOR GOUT ?
HOW WOULD YOU DX GOUT ?
NEXT STEP FOR J.F. ?
IN WHAT STAGE OF GOUT IS M.B. ?
WOULD YOU CHANGE MD’S RX ?
WHAT OTHER ISSUES WOULD YOU CONSIDER ?
CONCLUSIONS

GOUT.ppt

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Celiac Disease

Celiac Disease
By:Lianne Beck, MD
Assistant Professor
Emory Family Medicine

Celiac disease
* Autoimmune disorder with a prevalence of approximately 0.5 to 1 percent in the United States. (1 in every 100-200 persons)
* Inappropriate immune response to the dietary protein gluten, which is found in rye, wheat, and barley.
* After absorption in the small intestine these proteins interact with the antigen-presenting cells in the lamina propria causing an inflammatory reaction that targets the mucosa of the small intestine.
* Manifestations range from no symptoms to overt malabsorption with involvement of multiple organ systems and an increased risk of some malignancies.
* Most all patients with celiac disease express human leukocyte antigen (HLA)-DQ2 or HLA-DQ8, which facilitate the immune response against gluten proteins
* Concordance rates of 70 to 75 % among monozygotic twins and 5 to 22 % among first-degree relatives.

Risk Factors for Celiac Disease
Dermatitis Herpetiformis
Signs and Symptoms
* Common
o Diarrhea
o Fatigue
o Borborygmus
o Abdominal pain
o Weight loss
o Abdominal distention
o Flatulence
* Uncommon
o Osteopenia/ osteoporosis
o Abnormal liver function
o Vomiting
o Iron-deficiency anemia
o Neurologic dysfunction
o Constipation
o Nausea

Differential Diagnosis of Celiac Disease
* Anorexia nervosa
* Autoimmune enteropathy
* Bacterial overgrowth
* Collagenous sprue
* Crohn's disease
* Giardiasis
* Human immunodeficiency
virus enteropathy
* Hypogammaglobulinemia
* Infective gastroenteritis
* Intestinal lymphoma
* Irritable bowel syndrome
* Ischemic enteritis
* Lactose intolerance
* Pancreatic insufficiency
* Soy protein intolerance
* Tropical sprue
* Tuberculosis
* Whipple's disease
* Zollinger-Ellison syndrome

* Consider testing in symptomatic patients at high risk for celiac disease with any of the following conditions:
o Autoimmune hepatitis
o Down syndrome
o Premature onset of osteoporosis
o Primary biliary cirrhosis
o Unexplained elevations in liver transaminase levels
o Unexplained iron deficiency anemia

Test selectively as part of the medical evaluation when symptoms could be secondary to celiac disease:
o Autoimmune thyroid disease
o Cerebellar ataxia
o First- or second-degree relative with celiac disease
o Irritable bowel syndrome
o Peripheral neuropathy
o Recurrent migraine
o Selective immunoglobulin A deficiency
o Short stature (in children)
o Sjögren's syndrome
o Turner's syndrome
o Type 1 diabetes mellitus
o Unexplained delayed puberty
o Unexplained recurrent fetal loss

SEROLOGY
* Serum immunoglobulin A (IgA) endomysial antibodies and IgA tissue transglutaminase (tTG) antibodies. Sensitivity and specificity > 95%.
* Testing for gliadin antibodies is no longer recommended because of the low sensitivity and specificity for celiac disease.
* The tTG antibody test is less costly because it uses an enzyme-linked immunosorbent assay; it is the recommended single serologic test for celiac disease screening in the primary care setting.
* When the prevalence is low, as in the general U.S. population, the risk of a false-positive result is high even with an accurate test . PPV 49.7%, NPV 99.9%
* Confirmatory testing, including small bowel biopsy, is advised.

SMALL BOWEL BIOPSY
Normal small intestine
Villous atrophy
Normal villi
Patient presents with symptoms of celiac disease
Perform serologic IgA tTG antibody testing
High clinical suspicion?
Low probability of celiac
Evaluation for Celiac Disease
Treatment
COMORBIDITIES
Follow-up
Screening
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Key clinical recommendation Evidence rating
Quiz
Reference

Celiac Disease.ppt

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Hyponatremia

Hyponatremia
By:James Yost, MD, MS, MBA
Emory Family Medicine

Hyponatremia
* Definition
* Epidemiology
* Physiology
* Pathophysiology
* Types
* Clinical Manifestations
* Diagnosis
* Treatment

* Definition:
o Commonly defined as a serum sodium concentration 135 meq/L
o Hyponatremia represents a relative excess of water in relation to sodium.
* Epidemiology:
* Physiology
o Serum sodium concentration regulation:
+ stimulation of thirst
+ secretion of ADH
+ feedback mechanisms of the renin-angiotensin-aldosterone system
+ renal handling of filtered sodium
+ Aldosterone

* Pathophysiology
Hypovolemic hyponatremia
* Nonrenal loss
* Renal Loss
Euvolemic hyponatremia
Redistributive hyponatremia
* Pseudohyponatremia
* Clinical Manifestations
* Diagnosis
* Laboratory tests
* Treatment
* Symptomatic or Acute
* IV Fluids
* Example:
* Asymptomatic or Chronic

Hyponatremia.ppt

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