Unit 5

Card Set Information

Author:
shannonm2003
ID:
150485
Filename:
Unit 5
Updated:
2012-04-27 13:47:47
Tags:
Diabetes
Folders:

Description:
Unit 5
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user shannonm2003 on FreezingBlue Flashcards. What would you like to do?


  1. What can happen if you give too much insulin?
    Hypoglycemia
  2. One major action of insulin is to
    Promote glucose uptake in skeletal muscle and adipose tissue
  3. What does insulin increase
    storage of glycogen and fatty acids
  4. The polydipsia and polyuria related to diabetes are caused primarily by what
    fluid shifts resulting from osmotic effects of hyperglycemia
  5. What is the difference between hyperglycemic hyperosmolar nonketotic syndrome and DKA
    HHNS lacks ketonuria
  6. DKA and HHNK coma are alike in which way
    both may be caused by an infection or some other stress
  7. What are some factors that could cause hypoglycemia in a diebetic client
    • excessive dose of insulin
    • too much exercise
    • eating too little
  8. What is impaired glucose tolerance
    defined as a 2-hour oral glucose tolerance test with a glucose concentration of between 140-200 (prediabetes)
  9. what is impaired fasting glucose level
    glucose concentration between 110-125 (prediabetes)
  10. What are the two pathophysiologic processes of type 2 diabetes
    • 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
  11. What are the 3 major metabolic problems that occur w/o insulin
    • decreased glucose utilization
    • increased fat metabolism
    • increased proetein utilization
  12. what is decreased glucose 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)
  13. What is increased fat metabolism
    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
  14. what is increased protein utilization
    lack of insulin leads to protein wasting. Amino acids are converted to glucose in the liver, further elevating glucose levels. these people look emaciated
  15. what are the 3 cardinal signs of DM
    • polyuria
    • polydipsia
    • polyphagia
  16. What are common manifestations of DKA
    • 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
  17. What are 3 ways to diagnose Diabetes
    • 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
  18. What is a fasting blood glucose test
    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
  19. What is a postload blood glucose test
    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
  20. What is a casual blood glucose test
    Random blood glucose level over 200 mg/dl. Drawn anytime of the day w/o fasting.
  21. What is a glycosylated hemoglobin (HbA1c) test
    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%.
  22. what is an oral glucose tolerance test (OGTT)
    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.
  23. What is proteinuria
    early manifestation of kidney disease. testing the urine for microalbuminuria shows early nephropathy.
  24. What are the 5 oral anti-diabetes agents avialable?
    • Sulfonylureas (glipizide)
    • Biguanides (metformin)
    • Megalintinides
    • Thiasolidinediones (Avandia)
    • Alpha glucosidase
  25. What does glipizide (sulfonylureas) do
    Increase tissue response to insulin and decreases glucose production by the liver
  26. What does metformin (biguanides) do?
    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
  27. What does avandia (thiazolidinediones) do?
    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.
  28. What do alpha glucosidase inhibitors do?
    delay the digestion of complex carbs and certain sugars to blunt the peak of BG levels after meals
  29. What does insulin do
    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
  30. What are the rapid-acting insulins
    • Humalog (insulin lispro)
    • Novolog (insulin aspart)
  31. When are the rapid acting insulin onsets, peaks, and duration
    • onset - 5-10 minutes
    • peak - 1 hour
    • duration - 2-4 hours
  32. What are the short-acting insulins
    • Humulin R (regular)
    • Novolin R (regular)
  33. What are the short acting insulin onset, peak and durations?
    • onset - 0.5-2 hours
    • peak - 2-4 hours
    • duration - 4-6 hours
  34. What are the intermediate-acting insulins
    • Humulin N (NPH)
    • Humulin L (lente)
    • Humulin 70/30
  35. What are Humulin N and L (intermediate-acting insulins) onset, peak, and durations?
    • Onset - 2-4 hours
    • Peak - 4-10 hours
    • Duration -10-16 hours
  36. What is Humulin 70/30 (intermediate acting) insulins onset, peak and duration
    • Onset - .5-1 hour
    • peak - dual
    • duration - 10-16 hours
  37. What are the long-acting insulins
    • humulin U (ultralente)
    • Lantus (insulin glargine)
  38. What are the onset, peak and duration of lantus?
    • onset - 1 hour
    • peak - none
    • duration - 24 hours
  39. What is exubera?
    Inhaled insulin, removed from market due to increase in lung cancer
  40. When does hypoglycemia usually occur
    when BG levels are less than 50-60 mg/dl
  41. What is hypoglycemia caused by
    • 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
  42. What does body normall do when in a hypoglycemic state
    Normally the body triggers counterregulatory hormones, glucagon and epi to promptly increase BG by stimulating glucose release from the liver and inhibiting insulin secretion
  43. What is an adrenergic response
    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
  44. What is a neuroglycopenic response
    decreased glucose to the brain. Decreased cognitive functioning. See headache, mental illness, inability to concentrate, slurred speech, blurred vision, LOC, coma, seizure, death
  45. When are the most common times hypoglycemia occurs
    • 8-24 hours after strenuous exercise
    • middle of the night
    • during exercise
  46. What are the macrovascular complications of DM
    CAD, CVD, HTN, PVD, Infections
  47. How does CAD effect clients with diabetes
    insulin therapy may actually increase incidence of atherosclerotic disease b/c insulin therapy often leads to weight gain and increased BP
  48. What are drug choices for HTN pts with diabetes
    ACE inhibitors and Calcium-channel blockers are choice for treatment. Beta blockers may increase glucose tolerance
  49. What are the 3 factors that contribute to infections in DM pts
    • inhibition of polymorphonuclear leukocytes activity while glucosuria is present
    • diabetic neuropathies
    • vascular insufficiency (can't fight off infection)
  50. What are the microvascular complications of DM
    retinal, renal and peripheral capillaries
  51. What is diabetic retinopathy
    • 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
  52. What is nephropathy
    • 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
  53. what is neuropathy
    • 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
  54. What is mononeuropathy
    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
  55. What is polyneuropathy
    • 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
  56. what is autonomic neuropathy
    manifests in its effects on pupillary, cardiovascular, GI and GU
  57. What happens with pupillary response in autonomic neuropathy
    • interferes with pupils ability to adapt to dark
    • pupil dilation is inadaqueate
    • problem with night driving
  58. what happens with cardiovascular response in autonomic neuropathy
    • evidenced by abnormal response to exercise
    • orthostatic hypotension
  59. What happens in GI system with autonomic neuropathy
    dysphagia, ab pain, nausea, vomiting, constipation, may contribute to anorexia
  60. what happens in GU system in autonomic neuropahty
    • 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

What would you like to do?

Home > Flashcards > Print Preview