Diabetes Type II

CV: CAD, MI, CHF, HTN, CV accidents. L vent hypertrophy
Cancer: Colon, Prostrate, breast, ovary, endometrail, cervical, gall bladder, bile ducts.
Metabolic: Insulin resistance, hyperlipidimai
Endocrine: PCOD, decreased tertosrone
Rhuematic, Joints
Liver: Cholestrol gallstones,
Pulmonary, Sleep apnea, snoring, incresed work to breathe, obesity hyperventilation syndrome.

Hyperlipidmia
Hypertriglycerdimia
Hypertension
Insulin resistance
artherosclerosis

Coronary Artery Disease
HTN
Adult
Onset diabetes
Stroke

increased adipodicity-decreased adiponectin, increased resistan, increases insuline resistance

periphral resistance, post receptor problem,

excess fatty acid, affect insulin senstivity in other tissues, deposition of fat affects insulin sensititvty.

Viceral fat: central fat, surrounding abdominal viscera, induces insulin resistance, MS
responsive to epinephrine, free fatty acid mobility, Apple shaped

Subcutanious fat-metabolically neutral, pear shaped

Primary defect in signaling: receptor muations, IAA, genetics

2 to endocrine: Cushings, Acromegaly, Pheo, Clucagonoma, Hyperthyroidism, Insulinoma

2 to other disorders: Viceral fat, stress, uremia, hyperglycermia, liver disease, AIDS, neuromuscular disorders

2 to normal states: Pregnancy, Puberty, Starvation

2 to medications: Glucocorticoids, Niacin, Thiazide Diuretics, Esotrogens, b-blockers

Type II diabetes
Acanthosis nigricans--skin condition, dark, velvety skin thickening on back of neck and skin folds. TO MUCH IGF-1!!
Pseudoacromegaly
PCOD
HTN
HyperTG

Obesity: adiponectin and resistin, decrease senstivty

Increased insuline resistance: need more insulin for same effects.

B-cell faliure: limits ability to produce or secrete insulin. genetic mutations. increased fatty acids have deletarious effects on b-cells.

Type I: Leptin, LeptinR, POMC, MC4R mutations

Type II: 50-90% concordance twin studies.

Materially Inherited diabetes and deafness syndrome: mitochondra have DNA, exclusively from the mother. egg contains normal and abnormal DNA-heteroplamy, quite diffent syndromes depending on degree of heteroplasmy.

MIDD, not obese, diabetes in middle age, relative insulin deficency, tRNA gene, defects in oxidative PO, impaired glucose sensing and insuline secreation.

Inheritance: autosomal, heterozygous mutations cause disease

MODY2: Glucokinases genes decreases g-6PO, decreased insulin

MODY1-6: Beta-cell transciption factors, interfere with normal function or production and replacement of b-cells

DKA-uncommon, insulin levels are still enough to suppress glucagon, inhibit b-oxidation
only in stress/infeection, underlying insulin definency

Hyperosmolarity-more later

macrovascular complications, HTN, MI, stroke, amputation, caused by syndrome X. same as type one long term complications but less frequency.

protection: Diet management, Blood pressure and cholestrol managment, low saturated fat diet, aspirin therapy, stop smoking.

increase glucose, glucosuria, osmotic diresis. Free water loss causes hyperosmolarity. cognitive function, mental status declines, hyperosmolic coma!

fluid losses, fever burns, diarrehea, vomiting, lack of water intake, stress, surgey, elderly precipites risk

Tx: correct osmolarity slowly!

1st/3rd trimester problems.

1. optimal control before conception
2. monitor and control of glucose during pregnancy.
3. fetus is nutrient sink!
4. mom, increase insulin resistance, gluc mom-baby
5. Gestational diabetes