Flashcards in Type 1 Diabetes Deck (25):
Cell Types of Pancreas (4)
ß: 60-80% cells; secrete insulin
alpha: 20-30%; secrete glucagon
∆: secrete somatostatin, which suppresses both insulin and glucagon
PP: unknown function
Preproinsulin processed to proinuslin in ER
Proinsulin processed to C-peptide and insulin in golgi
What is significance of C-peptide?
Can be measured to estimate insulin production
Requirements for Insulin Function (4)
Islet ßcell mass
Glucose-dependent insulin secretion
Insulin signaling at target cells
How many granules does a ß-cell contain? How many does it secrete each day?
Contains 10,000 and secretes 10^12 in a given day
Insulin Metabolism: What are immediate effects of rise in blood glucose? More delayed effects?
Immediate effect of blood glucose is exocytosis of granules
If persistently high glucose, will see increased insulin synthesis in beta cells
Insulin functions (4)
Trasmembrane transport of glucose/amino acids
Glycogen formation in liver/muscles
Glucose conversion to triglycerides
Nucleic acid and protein synthesis
Special signs in T1DM
DKA (25-30%), coma (5%)
How does glycosuria occur?
Hyperglycemia-->filtration in kidneys results in too much glucose in filtrate; it cannot all be reabsorbed so it is excreted
Who is most likely to get Type I Diabetes?
Northern european ancestry
Peak ages: 5-7, onset of puberty, 1/3 above 18
Incidence higher during winter
Risk Factors for T2DM
Viral infections (coxsaccie, congenital rubella, enterovirus)
Immunizations, diet, high SES, obesity, vit D deficiency
What autoantibodies are seen in T1DM? (4)
Islet cell antibodies (ICA)
Insulin autoantibodies (IAA)
Antibodies to Glutamic acid decarboxylase (GAD)
ZnT8 autoantibodies (80% newly diagnosed T1DM)
How does chronic insulitis develop?
Genetic susceptibility and environmental trigger lead to development of autoantibodies
High risk MHC
Cellular infiltrate (lymphocytes ,mø)-->Destruction of ß-cells
What is Latent Auto-immune Diabetes of Adulthood?
Basically an non-obese adult that shows up with T2DM symptoms but is antibody positive
How is LADA managed?
Can initially be controlled with glucose lowering pills....but eventually will become insulin dependent
First symptoms in LADA?
Loss of 1st insulin response
Treatment of Type 1 Diabetes (3)
Insulin replacement therapy
Screening: blood glucose and complications
Diabetics should adjust insulin doses according to _____ (3)
Blood glucose profile
Impact of Intensive Therapy
Reduced retinopathy, nephropathy, neuropathy, CVD mortality and atherosclerosis
Body perceives state of starvation when no insulin is detected and utilizes alternate energy sources
DKA: loss of insulin effects in liver, muscle, adipose
Liver: glucose output-->glucosuria-->polyuria-->dehydration
Muscle: Muscle wasting-->weight loss
Adipose: increased lipolysis-->increased ketogenesis (ß-hydroxybutyrate/acetoacetate)-->Ketoacidsois
DKA Symptoms (big list)
nausea/vomiting, thirst/polyuria, weakness/anorexia, abdominal pain, visual disturbances, somnolence, tachycardia, hypotension, dehydration, kussmaul respiration (hyperventilation), fruity odor on breath, altered mental status
Insulin IV (until anion gap is resolved)
Correction of fluid/electrolyte imbalance
What increases with increasing glycemic control?
Risk for hypoglycemia