Diabetes Mellitus

Type 1-
Begins commonly in early childhood or adolescence.
-the body produces little to no insulin
-insulin dependent
-people with type 1 diabetes need injections of insulin
-Beta cells are destroyed.
Beta cells makes insulin

Beta cells: make insulin
Rehualtes Carbohydrates
C

Hyperglycemia- too much sugar in the blood
Hypoglycemia- abnormal low values of sugar or glucose in the blood

Type 2-
-most common
-adult-on set or age-onset
-usually on overwight patients or those who do not exercise
-usually a slow developing. Usually develops within years
-can usually be controlled with diet and oral medication
-nonisulin-dependent but might need injections if diet and medications are not working
-gestational diabetes develop during pregnancy and generally resolves after birth

Causes:
Type 1- usually the immune system is triggered by a virus that attack insulin producing cells in the pancreas
Type 2: heredity, age, obesity, family history
Pancreas produces insulin but is not effective

Some medications can impair the body’s use of insulin causing secondary diabetes.
Medications for High BP, oral contraceptives ( hormonal), anti-inflammation
Drugs that treat mood disorders can impair glucose absorption (ie antidepressants, adrenergic agonists)
Heparin, cimetidine, nicotinic acid, isoniazid

Ketoacidosis- condition due to starvation or uncontrolled diabetes
Common in type 1 diabetes.
Symptons: abdmonial pain, vomiting, rapid breathing, extremem lethargy and drowsiness
Type 2 symptoms may no be evident for years

Endocrine Pancreatic Hormones and Glucose Homeostasis
-cells that produce these hormones are clustered in groups of cells called the islets of Langerhans

Glucagon-ALPHA
-forms carbohydrates in the liver
-glucagon stimulates the breakdown of glycogen in the liver
-breakdown of lipis in both the liver and adipose tissue
-primary function decrease glucose oxidation and increase blood glucose levels
-glucagon is initaitied in most people when blood glucose falls below 70mg/dl

Insulin- BETA CELLS
-facilitaes the movement of glucose across cell membranes into cells thus decrasing blood glucose levels.
-prevents excessive breakdown of glycogen
-facilitaes lipid formation
-protein synthesis
-travels directly to the liver
-it increases when blood glucose is high and it decreases when blood glucose levels decrease

Amylin-affects post meal glucose levels
Secreted with insulin
Impairs glucagon secretion and slows the rate and slows the rate at which glucose travels to the small intestine

Delta- somatostatin. Inhibits the production of insulin

GLP-1 and GIP – SMALL INTESTINE
-lower blood glucose levels follwin intake of a meal
-stimulate insulin secretion after a meal has been digested
-INCRETIN EFFECT
-MEDICATION- BYETTA incretin mimetic used for TYPE 2

Not all body organs need insulin for glucose uptake,
Do not need:
-BRAIN
-LIVER
-INTESTINES
-RENAL TUBULES

Do require:
-cardiac muscle
-skeletal muscle
-adipose tissue

increase blood glucose levels, amino acids, and fatty stimulate insulin production as cardiac cells, adipose tissue and skeletal muscle take up glucose plasma of nutrients decrease suprresing the stimulus to produce insulin.

Type 1; Immune-mediated or Idiopathic (has no known eiologic causes. Most patients are of African or Asian descent,
-usually inheridited
-viral infection or a chemical toxin are believed to trigger 1 DM

-glucose molecules accumulate in the blood stream = hyperglycemia
-draws blood into the general circulation.
-increased blood volume increases renal blood flow which increases urine output- POLYURIA
-GLUCOSORIA- Increae of glucose in urine renal threshold for glucose is 180 mg/dL

Manifestations of Type 1 Dm
-polyuria( increase urine_
-polydispsia (increase thirst)
-polyphagia ( increase hunger)

Type 2-
-insulin resistance
-function of insulin is impaired
-liver produces more glucose than normal,
-CH0 are not metabolized
-pancreas secretes less than adequate