Diabetes Mellitus- 18 pts

Diabetes is absolute (type I) or relative (type II) insulin deficiency

• - Characterized by chronic hyperglycemia
• - Disturbances of carbs, protein and fat metabolism
• - A whole body disease that affects the brain, eyes, heart, pancreas, kidneys, & blood vessels

• *"Absolute insulin deficiency" or "Insulin dependent"
• Auto-immune disorder: Body mistakenly destroys insulin producing beta cells!

• 1. Stomach changes food into glucose.
• 2. Glucose enters blood stream.
• 3. The pancreas makes little to no insulin. (because body destroys the insulin producing beta cells)
• 4. Little or no insulin enters the blood stream.
• 5. Glucose builds up in the blood stream.

Unknown- thought to be result of gene-environment interaction: Primary B cell (lymphocyte) defect or failure

• -Other possible causes include:
• Auto-antibodies
• Airal infections
• Cows milk before 3-4 months (immune response to protein in milk)
• prescription drug use
• o2 free radicals formed as byproduct of chems in body

• Usually affects Children and young adults under 30
• Caucasions

• Rapid onset of symptoms!-- "the 3 P's!"
• - Polydipsia: secondary to cell dehydration
• - Polyuria: secondary to hyperglycemia acting as osmotic diuretic
• - Polyphagia: secondary to cell starvation
• -Weight Loss: secondary to loss of fats and proteins used for energy
• -Fatigue : secondary to metabolic changes

• - Symptoms + random blood glucose > 200
• - Fasting blood glucose of > 126 (on 2 occasions)
• - Glycohemoglobin Test (HgAIC) = glucose trends rather than day-to-day fluctuation - goal is less than 7%
• - C-peptide Test = determines type of diabetes by--Body releases C-peptide equal to insulin, if no insulin is produced (like in type I), no C-peptide is produced therefore Type I
• - Ketone Test- DKA= diabetic ketoacidosis-- ketones are waste product that build up with any diabetes but most common in one!

A combination of insulin, meal planning, and exercise are used to manage the disease

Increased thirst

(Take a "dip" in the pool)

Increased hunger

Increased urination

• Most common form (90-95%)
• "relative insulin dependent" (used to be "non-insulin dependent")
• -When the cells resist insulin.
• Relative insulin deficiency
• Beta cells function
• Cause unknown, genetics are complex and
• not clearly defined
• Insulin resistance increases with obesity
• NOT autoimmune
• Cellular resistance is a factor in 60-80%
• of individuals with DM II.

(Cellular resistance is facton in 60-80% of DM type II)

• 1. The stomach changes food into glucose.
• 2. Glucose enters the blood stream.
• 3. The pancreas makes insulin.
• 4. Insulin enters the blood stream.
• 5. Glucose can't get into the cells of the body (cells resist insulin). Glucose builds up in blood vessels.

Unknown but thought to be interaction of metabolic, genetic and environmental factors.

• B-cells work BUT as available insulin is not used, because cells resist insulin, body reacts by producing less insulin.
• ncreases with obesity

• Obese: increased BMI, insulin resistance increases
• Age: primarily effects ppl over 40
• Family history of type II
• Ethnic minority: Native Americans, Blacks, Hispanics
• Puberty:
• Gender: Males more likely
• Metabolic syndrome: (atleast 3 of these- high blood pressure, abdominal obesity, high triglyceride levels, low HDL levels, and high fasting levels of blood sugar)

• Develop Gradually
• - usually vague and long standing
• - Usually non-specific
• - Patient typically overweight and hyperlipidemic
• -"Classics": pruritus (itching), recurrent infections, visual changes, paresthesias (pricking, tingling, creeping on skin)

Same diagnostc testing as type 1

• Goal is to restore blood glucose levels to normal (euglycemia) and correction of related metabolic disorder.
• 1. Meal Planning: balance ration of fats, carbs, protein
• 2. Weight Loss: Lower body's resistance to insulin
• 3. Exercise: take glucose from blood and use for energy
• 4. Oral hyperglycemic drugs: used if others do not work
• 5. Insulin therapy: used if oral meds not enough

• Hypoglycemia: insulin shock, blood glucose <70 or <90 w. symptoms
• DKA: Diabetic Ketoacidosis- Severe hyperglycemia
• HHNKS: Hyperosmolar hyperglycemia nonketoic syndrome- uncommon, mirrors DKA but no ketones in blood or urine
• Somogyi effect: PM regular glucose and then undetected hypoglycemia in middle of night followed by rebound hyperglycemia in mo
• Dawn phenomenon: AM high blood glucose with no__hypoglycemia

• >Diabetic neuropathies (peripheral or autonomic): most common, gradual nerve disorders
• >Microvascular disease: affects small blood vessels
• >Macrovascular disease: effects large blood vessels, causes morbidity and death.
• >Infection: high risk factor
• Chronic Complications of Diabetes
• Mellitus

1. Diabetic neuropathies: most common complication of diabetes

• Painful
• peripheral neuropathies

Mononeuropathy (wrist/foot drop)

• Autonomic
• neuropathy: such as delayed gastric emptying, diabetic diarrhea, altered
• bladder function, and orthostatic
• hypotension

• Chronic
• hyperglycemia can also cause cognitive changes

• 2. Microvascular disease: thickening of the capillary basement
• membrane

resulting in decreased tissue prefusion

• -Diabetic retinopathy: visual changes occur in response to
• retinal ischemia from blood vessel changes

• -Diabetic nephropathy: <diabetes is the most common cause
• of ESRD>glomerular changes lead to decreased perfusion/blood flow to the
• kidney, decreased glomerular filtration leads to acidosis/anemia/uncontrolled
• hypertension and renal failure.

3. Macrovascular disease: causes morbidity and mortality

in poorly controlled diabetics

• -Coronary Artery Disease (CAD): most common cause of death for those
• with DMII, because of insulin resistance, hyperlipedemia, platelet abnormalities and endothelial
• cell dysfunction.

• -Cerebral Vascular Accident (CVA)/Stroke:
• twice as common in the diabetic vs. nondiabetic
• population

• -Peripheral Vascular Disease (PVD): high risk for lesions, ulcers and
• gangrene secondary to occlusions of the small arteries and arterioles

• 4. Infection: is a high risk factor in diabetics
• because of:

• Senses:
• impaired vision, impaired touch

• Hypoxia: from
• compromised skin integrity, plus glycosated hemoglobin in RBC’s slows the release of
• oxygen to tissues

• Pathogens: glucose
• provides energy for pathogens to proliferate/grow rapidly

• Blood supply: decreased blood supply results from
• vascular changes and decreases the supply of white blood cells to the affected
• area.

White cells: these cells suffer impaired function

• Diabetic Ketoacidosis is a acute complication of diabetes
• What: blood glucose >400
• Etiology: -Not enough insulin, -too much food, -less exercise w.o. changing diet or insulin; -Stress; -Infection
• Patho: A serious acute complication r/t a deficiency of insulin and increase in counter regulatory hormones
• Symptoms: fatigue, sleepy, warm, flush, feel full, polydipsia, slow breath, glucosuria, increase BG lvl. Advanced: decrease UO, Kussmaul respirations, elevated K+, ketonuria, fruity breath, CAn lead to coma & death
• Diagnosis and Treatment: hydration, hourly BG and UO measurements, serum electrolyte assess, Insulin, IV k+ when U/O increases

Hyperosmolar Hyperglycemia NonKetoic Syndrome--uncommon acute complication of diabetes type II

• Mirrors DKA but no ketones in blood or urine
• What: Blood Glucose>500 mg/dl
• High mortality rate
• Patho: High BG and serum osmotic pressures lead to severe dehydration, low blood volume, low perfusion pressure

• Cause- (chronic hyperglycemia)
• Peripheral- more common, problem w. movement or feeling, pain and paresthesia--temporary or permanent
• Mononeuropathy- only one side of body- foot/wrist
• Autonomic: delayed gastric emptying, diabetic diarrhea, alt bladder function, orthostatic hypotension, cognitive changes

• -cause small vessels to thicken which decreases tissue perfusion
• Diabetic retinopathy- visual changes
• Diabetic nephropathy- ESRD

• -causes large vessels to thicken which decreases perfusion
• Coronary Artery Disease (CAD): most common cause of death in type II bcus insulin resistance
• Cerebral Vascular Accident (CVA): Stroke- twice as likely in diabetic patient
• Peripheral Vascular Disease (PVD): narrowing and hardening of the arteries that supply the legs and feet- high risk for lesions, ulcers, gangrene

Impaired senses, Hypoxia from skin integrity and slow release of O2, glucose provides energy for pathogens to proliferate, Decrease blood supply which decreases WBC supply

• We eat>>>>serum glucose rises
• Pancreas responds with >>>insulin
• Beta cells release insulin into>>>plasma
• Cells have insulin receptors on membranes
• Insulin binds with >>>receptor sites
• Intracellular activation mechanism responds. Glucose enters the cells>>>serum glucose levels drop.
• Pancreas senses drop in serum glucose>>>stops secreting insulin
• When serum glucose drops, alpha cells secrete>>>glucagon into plasma
• Glucagon travels to the liver and>>>stimulates release of stored glucose into serum
• Liver releases>>>glucose
• Serum glucose>>>increases

**(Summary)**

• Dietary
• glucose>>Increase serum glucose>>insulin>>decreased serum glucose>>glucagon>>increase serum glucose

• **Normal (fasting) glucose range is
• 70-100 mg/dl**