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15 Cards in this Set

  • Front
  • Back
medical consequences of Obesity
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.
Metabolic syndrome

Insulin resistance

Coronary Artery Disease
Onset diabetes
Etiology of metabolic syndrome
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 vs subcutaineous fat
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
Causes of Insulin Resistance
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
Consequences of Insuline Resistance
Type II diabetes
Acanthosis nigricans--skin condition, dark, velvety skin thickening on back of neck and skin folds. TO MUCH IGF-1!!
Type II Diabetes etiology: Obesity, Insuline resistance, B-cell failure
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.
Genetics of Diabetes: Type I and Type II
Type I: Leptin, LeptinR, POMC, MC4R mutations

Type II: 50-90% concordance twin studies.
How is Mitochondrial genes inherited?
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.
How does mito DNA cause diabetes?
MIDD, not obese, diabetes in middle age, relative insulin deficency, tRNA gene, defects in oxidative PO, impaired glucose sensing and insuline secreation.
Maturity Onset Diabetes of the Young
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
Short Term complications of TII diabetes
DKA-uncommon, insulin levels are still enough to suppress glucagon, inhibit b-oxidation
only in stress/infeection, underlying insulin definency

Hyperosmolarity-more later
Long term compliations of TII diabetes
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.
Hyperosmolarity in TII diabetes
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!
Steps to prevent adverse complications in pregnancy
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