Type 1 Diabetes Flashcards Preview

Endocrinology > Type 1 Diabetes > Flashcards

Flashcards in Type 1 Diabetes Deck (25):
1

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

2

Insulin Processing

Preproinsulin processed to proinuslin in ER
Proinsulin processed to C-peptide and insulin in golgi

3

What is significance of C-peptide?

Can be measured to estimate insulin production

4

Requirements for Insulin Function (4)

Islet ßcell mass
Insulin synthesis
Glucose-dependent insulin secretion
Insulin signaling at target cells

5

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

6

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

7

Insulin functions (4)

Trasmembrane transport of glucose/amino acids
Glycogen formation in liver/muscles
Glucose conversion to triglycerides
Nucleic acid and protein synthesis

8

Special signs in T1DM

DKA (25-30%), coma (5%)

9

How does glycosuria occur?

Hyperglycemia-->filtration in kidneys results in too much glucose in filtrate; it cannot all be reabsorbed so it is excreted

10

Epidemiology:
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

11

Risk Factors for T2DM

Viral infections (coxsaccie, congenital rubella, enterovirus)
Immunizations, diet, high SES, obesity, vit D deficiency

12

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)

13

Pathogenesis:
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

14

What is Latent Auto-immune Diabetes of Adulthood?

Basically an non-obese adult that shows up with T2DM symptoms but is antibody positive

15

How is LADA managed?

Can initially be controlled with glucose lowering pills....but eventually will become insulin dependent

16

First symptoms in LADA?

Loss of 1st insulin response

17

Treatment of Type 1 Diabetes (3)

Insulin replacement therapy
Education
Screening: blood glucose and complications

18

Diabetics should adjust insulin doses according to _____ (3)

Carbohydrate intake
Exercise regimen
Blood glucose profile

19

Impact of Intensive Therapy

Reduced retinopathy, nephropathy, neuropathy, CVD mortality and atherosclerosis

20

DKA Concept

Body perceives state of starvation when no insulin is detected and utilizes alternate energy sources

21

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

22

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

23

DKA Treatment

Insulin IV (until anion gap is resolved)
Correction of fluid/electrolyte imbalance

24

What increases with increasing glycemic control?

Risk for hypoglycemia

25

What is relative hypoglycemia?

Symptoms of hypoglycemia despite normal/elevated blood glucose due to patient being in a chronic hyperglycemic state