A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.

A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.

 

PMH-noncontributory. No surgeries or major medical problems. Usual colds and ear infections as a child

Allergies-none know

Family history- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process

Social-denies alcohol, tobacco or illicit drug use. Not sexually active. Junior at local high school and works in a fast food store after school and on weekends.

Labs in office: random glucose 220 mg/dl.

Based on his symptoms and the glucose level, the pediatrician makes a tentative diagnosis of Diabetes Mellitus type 1 and refers the boy and his parents to an endocrinologist for further work up and management plan.

Question 6 of 6:

How do genetics and environmental factors contribute to the development of Type 1 diabetes?

      
Correct Answer:  

 

Islet cell autoantibodies (ICAs) were detected in serum from patients with autoimmune polyendocrine deficiency. They have subsequently been identified in 85 percent of patients with newly diagnosed type 1 diabetes and in prediabetic people.

Autoantigens form on insulin producing beta cells and circulate in the blood and lymphatics. This leads to processing and presentation of autoantigen by antigen presenting cells

There is activation of T helper 1 lymphocytes and T helper 2 lymphocytes There is activation of macrophages that release IL-1 and TNFα and activation of autoantigen specific T cytotoxic CD8 cells.

There is activation of B lymphocytes to produce islet cell autoantibodies and antiGAD65 antibodies. This cascade results in destruction of beta cells with decreased insulin production.

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