Diabetes Pathophys.csv

Beta: insulin. Alpha: glucagon. Delta: somatostatin.

Storage: striated mm ( gluc and aa uptake + glycogen synthesis). adipose (gluc uptake and lipogenesis). liver (glycogen synth lipogenesis and decrease in gluconeogenesis.)

Commonly from acute hyperglycemia: polydipsia; polyuria; weight loss. Less frequently; polyphagia; blurred vision; and pruitis. DKA in 25% of cases.

Insiduous; co-morbid CV disease lethargy; fatigue.

Diabetes I: autoantibody test. Diabetes II: >126 fasting or >200 2hr-post prandial/random or A1C>6.5. IFG: 110-125. IGT 140-200.

Presence of glucose intolerance during pregnancy; usually returns to normal after pregnancy. Screening at 2nd trimester; 50gm 1hr post prandial challenge (>140). Mild predisposition to DM2.

Environmental insult: trigger virus/compound. Genetic susceptibility (HLA-DR3/DR4). Autoimmunity: CD8/4 and macrophages destroy Beta-cells; distruciton-recovery cycle; eventual clinical manifestation; honeymoon phase.

Insulin resistance (defective intracellular signlaing following insulin binding); B-cell dysfunction (early: hypersecretion of insulin; late: can't keep up; insulin secretion drops); dysregulated hepatic glucose production (HGP); abnormal intestinal glucose absorption; obesity.

MODY-maturity onset diabetes of the young. AD inheritence; early onset <25; absence of obesity; absence of beta-cell Ab.

KCNJ11 or ABCC8 mutation; permenant activation of K channel; hyperpolarization; hypoinsulinemic diabetes.

Maternally inherited diabetes and deafness

Type A insulin resistance; insulin receptor mutations

lipoatrophic diabetes

Polyuria; hyperglycemia pulls in water. Polydipsia; osmotic diuresis leads to dehydration. Polyphagia; starvation mode can't take up glucose.

glucose intolerance in skeletal mm and fat. liver increase heptatic glucose output; beta cells dysfunctional from glucotoxisity.

elevated PPG can predit fasting hyperglycemia; perdic diabete before symptoms arise. PPG control in diabetes patients assoicated with lowered cardiovascular risk and mortality

SMBG performed fasting; preprandial; 2hrs postprandial; and bedtime glucose for tight contorl of glucose. HBA1c average blood glucose in 2-3 months; not diagnositc. preprandial fasting glucose (<100); post prandial glucose (<140); bedtime glucose 110. HbA1c<6.5

LDL<100 (<70 in established CV risk). HDL >45 in men; 55 in women. TG<150.

Standard therapy (1-2 injections). Intensive insulin therapy: multiple daily injections or insulin pumps. For intensive therapy-give 40-50% total daily dose; rest is given during the day as prandial insulin.

Hypoglycemia at night causes rebount hyperglycemia in the morning. Usually from poor insulin injection technique. Increase evening dose or alter timing of insulin dosing.

Hyper glycemia; keosis (ketonemia and moderate ketonuria) acidosis

infection (respiratory/UTI); new onset diabetes; insulin administration; stress

nausea; vomiting; thirst; polydipsia; polyuria; abdominal pain; weakness; fatigue and anorexia. Tachycardia; orthostatic hypotension; poor skin turgor; warm/dry skin and mucus membranes; hyperventiliation or Kussmaul respiration; hypothermia; ketons on breath; weight loss; altered mental status; coma.

Restore circulating volume; maintenance of CO and renal function. (Hyper glycemia pulls water away). Fluid replacement therapy as in DKA

Occures exclusively in T2DM who are elderly and physically impaired. Marked hyperglycemia and dehydration in absence of acidosis; ketonemia. Fluid replacement theraphy as in DKA