DIABETES

metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia)

a hormone produced by the pancrease (beta cells), controls levels of glucose in the blood by regulating the production & storage of glucose

hormone produced by the alpha islet cells of the pancreas, serves to complete gluconeogensis in the hypoglycemic state

stored glucose in liver and muscles

antidiabetic; stimulates secretion of insulin.

Chlorpropamide (Diabinese)

Long lasting: 24-72 hrs

antidiabetic: stimulates the release of insulin and increases sensitivity to insulin.

Glipizide (Glucatrol)

Short half life, good in elderly

Both for Type II, both taken with first meal of the day.

SE: hypoglycemia

• raise blood sugar
• treatment of severe hypoglycemia in diabetes and adjunct for GI radiography.

• Improves insulin sensitivity in Type II in liver, muscle and fat cells.
• Pioglitazone (Actos)
• Rosiglitazone (Avandia)

hepatotoxicity: liver function, and fluid overload, edema

inhibitors of intestinal flucose production and absorption. Target is liver, small intestine and peripheral tissues. Has no effect on pancreatic beta cells

Lactic Acidosis. Must avoid it in renal failure or uncontrolled HF. Not to be used w/sulfonylureas or the pt will go hypoglycemic.

Type II- delays absorptoin of glucose from GI tract - target is small intestine. lowers BS by inhibiting alphaglucosidase in GI tract.

• flatulence diarrhea, abdominal pain
• must be taken immidiatly before meal
• delays absorption of glucose in intestinal system

dizziness, tremors, tachycardia, anxiety, sweating, hunger, weakness

• These are for Type II, and stimulates the secretion of insulin.
• Target - pancreatic beta cells.
• Fast Acting
• Repaglinide (Prandin)
• neteglide (Starlix)

polydipsia, polyuria, headache, N&V, ABD pain, air hunger, acetone/fruity breath, dim vision, drowsiness, unconsciousness, dehydration

• delayed or omission of a meal, excessive exercise, insulin overdose
• injection-unused tissue, ASA

infection, trauma, stress, omitted insulin, loss of pancreatic insulin secretion

• hypoglycemia:
• BS <50, ketones 0-norm, HCO2 24-32-norm.
• DKA:
• BS >300, ketones 4+, HCO2 low (Met Res) 4-16

glucose, glucagon, oral forms of sugar, D50W IVP

insulin, HCO2, fluid replacement, Potassium replacement is usually required after acid/base balance, Foley catheter

• T1DM: is no insulin production, HLA (destruction of beta cells)
• T2DM: is decreased insulin or insulin resistant

• DKA: hyperglycemia in a Type 1
• Hyperglycemic hyperosmolar nonketotic syndrome: Type 2: hyperglycemia, no ketones are produced.

• Macrovascular: coronary artery disease, cerebrovascular disease, peripheral vascular disease
• Microvascular: Kidney and eye disease, Neuropathic complications

Glucogon hormone

liver as glycogen

• enhance storage of dietary fat in adipose tissue
• accelerates transport of amino acids into cells
• inhibits breakdown of stored glucose, protein and fat

during fasting, the pancreas releases a small amount of insulin on a continuous basis for our basal levels

glucose is released by the liver to provide energy to keep us breathing such as using the diaphragm

production of glucose from glycogen

glucose from the breakdown of non carb substances such as proteins

HLA human leukocyte antigen

virus and toxins

• glucose spilled in the urine 180-200 mg/dl
• Also loss of electrolytes

• KETONES
• Increasing the Acid balance = DKA

• usually under 30. They have no insulin, are very dehydrated and they feel like they have the flu - vomiting, no energy
• Caused by: absence or inadequate amount of insulin, Hyperglycemia, acidosis, electrolyte loss. amount of glucose entering cells is reduced & liver produces more glucose.

• fluid replacement Normal Saline
• tx of hyperglycemia
• electrolyte stabilizaiton
• tx of underlying risks such as lack of education.

usually K+ will correct when fluid replacement and regular insulin is given. Don't replace K+ until pt has stabalized

over 30 and obese

• slow and insiduous process of glucose intolerance or insulin resistance
• 75% of cases dx incidentally

• weight loss (as most pts obese)
• oral antidiabetic medications
• then insulin if other measures are ineffective

insulin

• HHNS is slower in onset
• some insulin is present
• profound dehydration

• Fluid replacement if indicated
• trmt of hyperglycemia, electrolyte stabilization

Fatigue, weak, sudden vision changes, tingling or numbness in hands or feet. dry skin and sores that are slow to heal due to poor circulation.recurrent infections, ABD pain , Nausea, Vomiting

• polydipsia
• polyuria
• polyphalgia

• >126mg/dl FPG
• >200 mg/dL Random PG

7%+

• glycosylated hemoglobin measured every 3 months. It gives a tale of the last 90 days.
• Normal is 4.4% - 6.4%
• 12 is very bad

History (3 P's), Physical examination (eyes, cardiovscular, renal impairment), Labs: HgbA1C, Microalbuminuria or 24 hr urine q year (notes renal failing), Fasting lipids annually

• 1. nutrition therapy
• 2. exercise
• 3. monitoring
• 4. Phrmacologic therapy
• 5. education

normalize insulin activity and blood glucose level to reduce the incident of vascular and neuropathic complications

• Take insulin/oral med as usual
• test BS & urine ketones q 3-4 hrs
• call MD if BS >300 or ketones present in urine
• make sure to eat, take liquids

• adv - allows pt control
• dis - requires fine motor skills, visual acuity

poor nutrition, decrease in lean body mass, alterred insulin secretions, decrease in circulation

nutritionist, podiatrist, ophthalmologist

exercise lowers blood glucose levels by increasing uptake of glucose

250... ketones

• Humalog, Novolog, Regular Insulin.
• Onset 10-15 minutes
• Peak 1-2 hrs
• Duration 3 hrs

• NPH & Lente (cloudy) must eat food near the onset and peak of action
• Onset 3-4 hrs
• peak 4-12 hrs
• Duration 16-20 hrs

• Long lasting: Ultralente
• Onset is 6-8 hrs
• peak 12-16 hrs
• duration is 20-30 hrs
• Needs to be supplemented w/short acting insulin

• local & systemic allergic reactions
• lipodystrophy, insulin resistance, morning hyperglycemia

stimulate pancreas to secrete insulin

• delay absorption of glucose
• decreases glucose prodcution in liver (metformin) Glucophage

• heart- coronary arteries
• brain- cerebral vascular accident
• main veins- peripheral vessels of lower limbs

retinopathy, nephropathy, neuropathies

DKA

ABD pain, nausea, vomiting, hyperventilation, fruity odor of breath

126 mg/dL

biguanides

Thiazolidinediones such as Actos and Avan

• delay of absorption of glucose in the GI such as Acarbose (Precose)
• lowers BS by inhibiting alphaglucosidase in GI tract

15 g of fast acting simple carbs such as 3-4 commercially prepared glucose tabs. 6 oz fruit juice, regular soda, 6-10 hard candies

• Stroke, MI
• CAD
• cerebrovascular disease
• peripheral vascular disease

60-120 in diabetic

Kussmaul's respirations, dry skin, hypotension, and bradycardia are signs of diabetic ketoacidosis

Polyuria, polydipsia, polyphagia, and weight loss are classic signs

anxiety, restlessness, headache, irritability, confusion, slurred speech, incoordiantion, diaphoresis, cool skin, tremors, coma, and seizures

• insulin resistance (decreased sensitivity)or impaired insulin secretion
• body tries to compensate by increasing the production of insulin
• no ketones, rare
• pts typically obese
• pt has no islet antibodies
• > 30
• HHNS

• glucose derived from food cannot be stored in the liver and remains circulating in the blood, leading to postprandial hyperglycemia
• desctruction of beta cells results in unchecked glucose production by the liver and fasting hyperglycemia
• pt usually thin at Dx
• pt needs insulin to preserve life
• pt often has islet cell antibodies
• onset can occur at any age

Lipotrophy is loss of subcutaneous fat and appears as a slight dimpling or more serious pitting of subcutaneous fat.

• hypotension
• profound dehydration
• tachycardia
• neuro- seizures

diabetic retinopathy

loss of sensation to pain and pressure

• increased skin dryness
• formation of skin fissures

muscular atrophy

inadequate and compromised lower extremity circulation interfers with ability to get nutrients to wound to promote healing and prevent gangrene.

hyperglycemia impairs leukocytes ability to destroy bacteria, thus lowering resistance to infection

insulin regulates the procution and storage of glucose: in diabetes the pancreas stops making insulin or the cells stop responding to it. hyperglycemia results and can lead to acute metabolic complications (DKA, HHNS)

• type 1: characterized by an absence of insulin production and secretion due to autoimmune destruction of the beta cells
• type 2: characterized by deficiency of insulin production and decreased insulin action as well as insulin resistance

describes how much a given food increases the BG level compared with an equivalent amount of glucose