Sandbox : anmol: Difference between revisions

Jump to navigation Jump to search
No edit summary
No edit summary
Line 1: Line 1:
__NOTOC____NOTOC__
__NOTOC__
{{Hyperparathyroidism}}
{{Hyperparathyroidism}}



Revision as of 18:27, 30 October 2017

Hyperparathyroidism Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Hyperparathyroidism from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Sandbox : anmol On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Sandbox : anmol

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Sandbox : anmol

CDC on Sandbox : anmol

Sandbox : anmol in the news

Blogs on Sandbox : anmol

Directions to Hospitals Treating Hyperparathyroidism

Risk calculators and risk factors for Sandbox : anmol

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]


Pathogenesis

  • GSD type 1 results due to defects in the function of microsomal enzyme glucose-6-phosphatase (G6Pase).
  • G6Pase catalyzes the conversion of glucose-6-phosphate to glucose during glycogenolysis and gluconeogenesis.
  • G6Pase is primarily expressed in expressed primarily in the gluconeogenic the liver and kidney. It is also expressed to a lesser extent in the intestine and pancreas.
  • 80% Cases of GSD 1 are of GSD type 1a.

References