Unit 5

Hypoglycemia

Promote glucose uptake in skeletal muscle and adipose tissue

storage of glycogen and fatty acids

fluid shifts resulting from osmotic effects of hyperglycemia

HHNS lacks ketonuria

both may be caused by an infection or some other stress

• excessive dose of insulin
• too much exercise
• eating too little

defined as a 2-hour oral glucose tolerance test with a glucose concentration of between 140-200 (prediabetes)

glucose concentration between 110-125 (prediabetes)

• limited beta-cell response to hyperglycemia. Beta cells chronically exposed to high levels of glucose and become less efficient. Called desensitization
• resistance to the biologic activity of insulin in both liver and peripheral tissues. known as insulin resistance. Clients have decreased senstivity to glucose levels which results in continued hepatic glucose production

• decreased glucose utilization
• increased fat metabolism
• increased proetein utilization

Glucose is not getting to cells due to lack of insulin, blood sugar levels rise, and the elevation continues b/c the liver can't store glucose as glycogen w/o sufficient insulin levels. To try to get blood sugars back to normal the kidneys excrete the extra glucose and it appears in the urine (glucosuria)

When glucose is not available body turns to fat stores. Fat breakdown procudes ketones. These accumulate and are excreted through kidneys and lungs. (fruity breath) ketones produce H+ causing metabolic acidosis. Ketones are excreted as well as sodium (hyponeutric). Leads to increased fluid loss and increased atherosclerosis

lack of insulin leads to protein wasting. Amino acids are converted to glucose in the liver, further elevating glucose levels. these people look emaciated

• polyuria
• polydipsia
• polyphagia

• abdominal pain
• anorexia
• dehydration
• fruity odor or breath
• hyperpnea or Kussmaul's
• hypotension
• impaired LOC or coma
• N/V
• polyuria
• somnolence
• tachycardia
• thirst
• visual disturbances
• warm, dry skin
• weakness
• weight loss

• symptoms of diabetes plus a casual plasma glucose value greater than 200 mg/dl
• fasting plasma glucose level greater than 126 mg/dl
• plasma glucose value in the 2-hr oral glucose tolerance test (OGTT) greater than 200 mg/dl. Using a load of 75gm of anhydrous glucose

drawn when client has not ate anything besides water for at least 8 hours. Reflects glucose level from hepatic production. Blood glucose level is greater than 126 to confirm diabetes. Preferred method of dx DM

postload (after a meal) glucose level. drawn 2 hours after meal and reflects the efficiency of insulin-mediated glucose uptake by peripheral tissues. Normally BG returns to fasting levels w/in 2 hrs. Greater than 200 indicates DM

Random blood glucose level over 200 mg/dl. Drawn anytime of the day w/o fasting.

glucose normally attached itself to the hemoglobin moecule on a RBC. Therefore the higher the BG the higher the levels of HbA1c. Is an avg blood glucose measured over the previous 3 months. Keep this level below 7%.

standard dose of glucose is ingested by mouth and blood levels are checked 2 hours later. pt is instructed to fast 8-12 hrs prior to test. Taken to determine how quickly glucose is cleared from the body.

early manifestation of kidney disease. testing the urine for microalbuminuria shows early nephropathy.

• Sulfonylureas (glipizide)
• Biguanides (metformin)
• Megalintinides
• Thiasolidinediones (Avandia)
• Alpha glucosidase

Increase tissue response to insulin and decreases glucose production by the liver

increases tissue response to insulin (increases periperhal insulin sensitivity esp in muslce tissue), decreases the hepatic prodcution of the liver, decreases absorption of glucose from the small intestine and decreases the triglyceride and low-density lipoprotein levels

Increase insulin action at the receptors and post receptors and post receptors in hepatic and periperhal tissue to decrease insulin resistance and often decrease triglyceride levels.

delay the digestion of complex carbs and certain sugars to blunt the peak of BG levels after meals

works to lower BG level by promoting the transport of glucose into cells and by inhibiting the conversion of glycogen and amino acids to glucose

• Humalog (insulin lispro)
• Novolog (insulin aspart)

• onset - 5-10 minutes
• peak - 1 hour
• duration - 2-4 hours

• Humulin R (regular)
• Novolin R (regular)

• onset - 0.5-2 hours
• peak - 2-4 hours
• duration - 4-6 hours

• Humulin N (NPH)
• Humulin L (lente)
• Humulin 70/30

• Onset - 2-4 hours
• Peak - 4-10 hours
• Duration -10-16 hours

• Onset - .5-1 hour
• peak - dual
• duration - 10-16 hours

• humulin U (ultralente)
• Lantus (insulin glargine)

• onset - 1 hour
• peak - none
• duration - 24 hours

Inhaled insulin, removed from market due to increase in lung cancer

when BG levels are less than 50-60 mg/dl

• overdose of insulin
• exercise w/o additional carb compensation
• omitting a meal or eating less food than usual
• nutritional and fluid imbalances caused by N/V
• sleeping later than usual
• excessive ETOH intake

Normally the body triggers counterregulatory hormones, glucagon and epi to promptly increase BG by stimulating glucose release from the liver and inhibiting insulin secretion

Increase epi. Occurs during rapid decrease in BG levels. Most common in poorly controlled DM. See shakiness, irritability, nervousness, tachy, tremor, hunger, sweating, pallor, paresthesias

decreased glucose to the brain. Decreased cognitive functioning. See headache, mental illness, inability to concentrate, slurred speech, blurred vision, LOC, coma, seizure, death

• 8-24 hours after strenuous exercise
• middle of the night
• during exercise

CAD, CVD, HTN, PVD, Infections

insulin therapy may actually increase incidence of atherosclerotic disease b/c insulin therapy often leads to weight gain and increased BP

ACE inhibitors and Calcium-channel blockers are choice for treatment. Beta blockers may increase glucose tolerance

• inhibition of polymorphonuclear leukocytes activity while glucosuria is present
• diabetic neuropathies
• vascular insufficiency (can't fight off infection)

retinal, renal and peripheral capillaries

• major cause of blindness in DM. Has 3 stages
• nonproliferative-early phase - microaneurysms and intraretinal hemorrhages
• preproliferative - further progression of the hemorrhages and decreasing visual acuity
• proliferative - final and most vision-threatening type. in response to ischemia may rupture causing retinal hemorrhage and exudates

• single most cause of stage 5 chronic kidney disease
• involves damage to and from eventual obliteration of the capillaries that supply gloeruli of the kidney
• kidneys can't filtrate

• most common chronic complication of DM
• Lack of O2 going to nerve endings and nerve fibers
• These clients experience nerve pain like numbness, stabbing, tingling
• HTN and smoking increases this incidence due to vasoconstriction

involves single nerve group. Produces sharp, stabbing pains. caused by an infarction of blood supply. Muscles innervated by nerves affected by focal neuropathies are painful and at risk for atrophy of the foot

• diffuse neuropathy, involves the sensory and autonomic nverves, sensory is most common, affects lower extremities, clients feel numness, tingling, burning, treatment includes foot care.
• Don't even know when blisters are on their foot, then the foot can't heal

manifests in its effects on pupillary, cardiovascular, GI and GU

• interferes with pupils ability to adapt to dark
• pupil dilation is inadaqueate
• problem with night driving

• evidenced by abnormal response to exercise
• orthostatic hypotension

dysphagia, ab pain, nausea, vomiting, constipation, may contribute to anorexia

• bladder hypertonicity, straining with urination, infrequent urge to urinate, erectile dysfunction
• neurogenic bladder = can't fee when bladder is full
• urinary statis leads to UTI