Type 1 DM Etiology & Pathology

4. Type 1 DMEtiology & Pathology • Formerly known as insulin-dependent DM or juvenile diabetes • An autoimmune ds in which autoantibodies are directed against the islet cells • Once the islet cells are destroyed, the pancreas can no longer produce insulin • On order to control glucose levels, daily exogenous insulin is required.

5. Type 11 DMEtiology & Pathology • Formerly known as non-insulin dependent DM • Although the amount of endogenous insulin produced may be WNL, the problem is that insulin cannot bind with cell receptor sites to promote transport of glucose into the cell. • Do not usually require exogenous insulin, but if they do, it is called insulin-requiring DM

6. Diabetes MellitusSomogyi and Dawn phenomenon • Hypoglycemia usually at night followed by compensatory rebound hyperglycemia ( lasts 12 to 72 hours). Usually caused by too much insulin or an increase in insulin sensitivity. Can be stabilized by gradual lowering of insulin dose and increase in diet at the time of the hypoglycemic reaction. • Dawn phenomenon-BS normal until 3 am-begins to rise in early morning hours. Glucose released from liver in early A.M.- needs to be controlled.Altering time and dose of insulin (NPH or ultralente) by two or two units-stabilizes the pt.

7. Diabetes MellitusSigns & Symptoms • The “ 3 P’s” (less severe in type 11 DM) > Polyuria > Polydipsia > Polyphagia • Fatigue • Pruitus • Ketosis (more common in Type 1 DM) • Blurred vision (retinopathy) • Tingling, numbness, or pain in the extremities (neuropathy).

8. Diabetes MellitusDiagnosis • Symptoms of DM plus casual plasma Glu concentration of 200 mg/dl or higher OR • Fasting plasma Glu level of 126 mg/dl or higher or • 2-hr plasma Glu level of 200 mg/dl or greater during an oral glucose tolerance test.

9. Diabetes MellitusTreatments • Diet – 60% CHO, 20% fats, 20% protein • Exercise • Insulin therapy: goal is to mimic the pattern of normal insulin secretion. Rapid-acting (e.g. Humulin R (or regular) Intermediate-acting (e.g. NPH) Long-acting (e.g. Humulin U) Mixtures (e.g. Humulin 70/30)

11. Acute Complications of DMDiabetic Ketoacidosis (DKA) • Usually occurs in type 1 DM • Develops when both insulin deficiency & excess stress hormones occur • Hyperglycemia, acidosis, & ketosis must all be present for dx • Blood Glu levels between 300-800 mg/dl • Ketones produced from lipolysis • Blood pH < 7.35 • Serum osmolality < 350 mOsm/kg • This is considered a medical emergency; if untreated coma & death can occur.

13. Acute Complications of DMDiabetic Ketoacidosis (DKA) treament • Major goals include correcting the following: Insulin therapy Reestablish fluid balance Replace electrolyte loss Patient family teaching

15. Acute Complications of DMHyperosmolar Nonacidotic Diabetic (HNAD) • Usually occurs in type 11 DM • Blood Glu levels between 600-1200 mg/dl • No ketones produced • Serum osmolality > 350 mOsm/kg • Blood pH WNL • Because the onset is gradual, condition can be missed or mis-dx for several weeks.

16. Acute Complications of DMHyperosmolar Nonacidotic Diabetic (HNAD • Signs & Symptoms: > Neurologic abnormalities (confusion, seizures, hemiparesis, aphasis, central hyperthermia). > Hyperglycemia, hyperosmolality & osmotic diuresis. > Hypotension • Primary Goals are to: > Reestablish fluid balance > Replace electrolytes loss > Insulin therapy > Patient/family teaching

18. Acute Complications of DMHypoglycemia • Also called insulin shock or insulin reaction • Occurs when blood Glu levels fall below 50 mh/dl • Signs & symptoms: > Range from mild to severe tremors, diaphoresis, confusion, blurred vision, drowsiness, convulsions. • Treatment: > Rapid administration of glucose.

21. Chronic Complications of DMMicrovascular • Retinopathy- progressive impairment of retinal circulation that eventually causes vitreous hemorrhage with vision loss. Assessment: > Impaired vision. • Implementation: Assist in ways to maintain independence & self-esteem. Instruct in actions that prevent or reduce complications:stable Blood glucose levels.

22. Chronic Complications of DMMicrovascular • Neuropathy- general deterioration that affects the peripheral and autonomic nervous systems. Assessment: • Peripheral neuropathy: > Pain in the legs > Aching and burning sensations in lower ext. • Alterations in bowel & bladder function-constipation, diarrhea, nocturnal fecal incontinence,infrequent voiding, weak stream, dribbling, signs of UTI. • Autonomic nervous system- sexual dysfunction, orthostatic hypotension, pupillary changes

23. Chronic Complications of DMMicrovascular • Circulatory abnormalities- skin breakdown and signs of infection, thick toenails: suggestive of circulatory impairment, athlete’s feet, thin, shiny, atropic skin, weak peripheral pulses. • Implementation: • Assist to deal with pain- encourage walking for exercise, provide foot cradle when in bed. • Assist to deal with bladder-bowel problems-provide privacy,encourage fluids, administer drugs for diarrhea. • Allow to ventilate abt. sexual impotence • Prevent moisture from accumulation bet. toes • Instruct in well-fitting shoes. Don’t go barefoot

24. Chronic Complications of DMMicrovascular • Nepropathy-intercapillary glomerulosclerosis- Kimmelstiel-Wilson syndrome-pathologic changes in the kdney that reduce kidney function-due to chronic DM. • Assessment: > proteinuria, azotemia,frequent UTI, neurogenic bladder. > BUN, creatinine elevated > Thirst and fatigue

25. Chronic Complications of DMMicrovascular • Implementation:Administer meds. To prevent UTI. Instruct to keep BS levels WNL. Maintain adequate fluid intake Instruct in 20 to 40 grams protein diet Restrict sodium and potassium in diet Prepare for dialysis therapy if appropriate. • Male erectile dysfunction (ED)- inability to maintain an erection. Caused by neuropathy,vascular disease, psychological disorders. Autonomic neuropathy are responsible for persistent ED.

26. Chronic Complications of DMMacrovascular • Cardiovascular- Hypertension-the goal to reduce BP less than 130/80 mm hg. • Lifestyle modification- weight loss, Na restriction, exercise. Ace inhibitors- Calcium channel blockers.Beta blockers- mask hypoglycemia-worsening of insulin resistance. • Atherosclerosis- elevated low-density lipoprotein,elevated triglycerides. • PVD- Diabetic Foot- neuropathy- ischemia-sepsis.