Diabetes Flashcards Preview

Nursing > Diabetes > Flashcards

Flashcards in Diabetes Deck (95):
1

Diabetes

A disease in which the body is unable to manufacture or utilize insulin thus resulting in a chronic state of hyperglycemia


2

Characterized by :

 Disturbances of carbohydrate, lipid and protein metabolism
 Beta-cell destruction leading to absolute insulin deficiency (Type 1)
OR
 Insulin resistance with relative insulin deficiency (Type 2)
 Secretory deficit with insulin resistance (Type 2)
 Systemic organic changes as a result of vascular pathology

3

Facts about DM:

• Affects 7% of pop
• 7th leading cause of death in the US
• Leading cause of blindness, end-stage renal disease and amputations in the US
• 2-4x more likely to have heart disease
• **MI and CVA are leading cause of death for clients with DM

4

Pancreas: exocrine function

 98% of pancreas is digestive enzymes

5

Pancreas: endocrine fumction

 Islets of Langerhans…scattered through the organ most prominently found in the tail
 Alpha, Beta, Delta
 Secretion of hormones: Glucagon, Insulin and Somatostatin

6

Insulin

• A protein made up of amino acids
• Allows the glucose to move into the cells for energy
• Insulin reaches the liver first where it helps the liver produce and store glycogen and inhibits glycogen breakdown into glucose
• Increases protein and lipid synthesis
• Limits ketogeneisis (conversion of fats to acids) and gluconeogenesis (conversion of proteins to glucose)
• Keeps lipid levels in normal range and prevents glucose levels from being too high

7

Ketogenesis

conversion of fats to acids

8

Gluconeogenesis

conversion of protein to glucose

9

Lack of insulin

• Unable to store glucose
• Cells starve …fats break down for energy... ketones form
• Stored glucose dumps into bloodstream
• Glucose breaks down into CO2 +H2O
• Fluid and electrolyte imbalances
• Polyuria, polydipsia, polyphagia

10

Polyphagia

excessive hunger

11

Polydipsia

excessive thirst

12

Risk factors:

• Genetics
• Obesity > 20% IBW or BMI >25 kg/m2
• Body shape: apple v. pear
• Habitually inactive
• Ethnic group (AA, American Indian, Hispanic American, Asian American, Pacific Islander)
• HTN > 140/90
• HDL 250
• PMH Gestational diabetes or babies >9 pounds
• Polycystic ovary syndrome
• IFG or IGT on previous testing

13

Type 1 Diabetes

• Insulin dependent
◦ Absolute insulin deficiency
◦ Ketoacidosis (DKA)
◦ Usually younger than 30 y/o
◦ <10% of all DM

14

Type 2 Diabetes

• Non-insulin dependent
◦ Insulin resistance
◦ Abnormal secretion of insulin
◦ Impaired gluconeogenesis
◦ Obesity in 80% of clients
◦ 90% of DM

15

Treatment: Type 1

◦ Exogenous insulin
◦ Dietary control

16

Treatment: Type 2

◦ Lifestyle changes
 Dietary control
 Weight reduction
 Exercise
◦ May require oral hypoglycemic therapy or exogenous insulin
– Insulin when oral hypoglycemic medications can no longer provide glycemic control

17

Diagnosis: health history

◦ Age
◦ Weight and weight changes
◦ Excessive hunger
◦ Excessive urination
◦ Excessive thirst
◦ Excessive fatigue
◦ Slow wound healing
◦ Infections
◦ Family hx DM

18

Diagnosis: blood glucose

◦ FBS > 126 (fasting = NPO x 8h)
◦ 2-hour plasma glucose > or = 200 mg/dL during an OGTT
◦ Symptoms of DM and random BG >200mg/dl
◦ The above 3 should be repeated to confirm Dx of DM

19

Diagnosis: HbA1C

◦ HbA1C > or = 6.5% (newly recognized as diagnostic criterion)
◦ Used to monitor glycemic control and predict risk for chronic complications

20

Target labs for diabetic patients:

- Blood Glucose
- Fasting: 90-130 (70-100 in non-diabetics)
- Bedtime: 100-140
- HbA1C: < or =7%
- Lipids
LDL: < 100 mg/ dL
HDL: >40 (men)
> 50 (women) ( with exercise and good fats)
Triglycerides: < 150
- Blood pressure: 130/80

21

Prevention of progression:

• Lifestyle changes
 Increase in physical activity
 Decrease in dietary fat
 Modification of food intake
• Smoking cessation
• Tx of HTN
• Tx of hyperlipidemia
• Tight control of blood glucose levels
• Regular F/U with HCP or endocrinologist
• Yearly vision testing
 Yearly urine microalbumin levels

22

Secondary diabetes

 Pregnancy (Gestational diabetes)
◦ Weight gain, increased estrogen levels and placental hormones
 Pharmacological:
◦ Insulin antagonists
◦ Adrenal corticosteroids
◦ Contraceptives (po)
◦ Estrogen replacements
◦ Atypical antipsychotics
 Surgical removal of pancreas or pancreatitis
 Adrenal or pituitary gland disorders
 Viral infections
◦ CMV, rubella, mumps, adenovirus

23

Hyperglycemia: S/s

 Hot, dry skin
 Dehydration
 Rapid, deep respirations; Kussmaul
 From alert to stuporous; coma
 N/V, cramps
 Tachycardia, orthostatic hypotension
 Positive ketonuria
 Notify HCP:
 BS >250
 Cannot take food or fluids
 Ill more than 1-2 days
 Ketonuria lasts more than 24 hours

24

Sick Days:

 Notify HCP of illness
 Monitor BG q4h
 Test urine for ketones
 Continue taking insulin or po antidiabetics
 Increase fluids, eat regular meals
 Get plenty of rest
 Treat symptoms as directed by HCP
 Know when to call HCP!

25

Acute Complications of DM:

1.Diabetic ketoacidosis (DKA)
 Lack of insulin
 Presence of ketones
2.Hyperglycemic-hyperosmolar state (HHS)
 Insulin deficiency
 Profound dehydration
3. hypoglycemia

26

DKA

 Total or partial lack of insulin
 Occurs with Type 1 diabetes
 Most often starts with infection
 Death – up to 10% of cases…even with appropriate treatment!
o Mortality highest in older adults with accompanying stroke, MI, vascular thrombosis, intestinal obstruction, or pneumonia
 Increased renal and liver glucose production
 Decreased use of glucose in tissues
 Production of ketoacids – ketonemia and ketonuria – metabolic acidosis
 Osmotic diuresis - dehydration and electrolyte loss

27

DKA: S/s

 Sudden onset
 Polyuria, polydipsia, polyphagia
 Weight loss
 Vomiting, abdominal pain
 Dehydration, dry skin, weakness
 Altered mental status – total alertness to coma
 Shock
 Kussmaul respirations, fruity breath (from acetone exhaled)

28

DKA: lab findings

 Glucose: >300 mg/dL
 Serum ketones: positive
 Serum pH: < 7.35
 Serum HCO3: 20 mg/dL
 CrS: >1.5 mg/dL
 Urine ketones: positive

29

DKA: Monitor

o VS q 15mins til stable
o Labs: hourly BGM, lytes
o I/O: hourly outputs
o IVF replacement
 Insulin drips
o Neuro status
 Keep safe
o Airway

30

DKA: managing fluids and electrolytes

1. Restore volume - isotonic normal saline 1 - 2 L over hour ;
2. replace total body fluid loss - 0.45 NS, when sugar < 250 : D 5 + 0.45 NS - to prevent hypoglycemia and cerebral edema

31

DKA: drug therapy

1. Insulin: decrease sugar 75-150 mg/dL/hr - continuous IV insulin drip ( half life 4 min);
2. Watch for hypokalemia ( fatigue, muscle weakness, shallow respiration, paraletic ileus, hypotension, wek pulse); Give K+
3. Severe acidosis: bicarb (pH < 7)

32

HHS

 Formerly known as hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
 Acute hyperglycemic crisis that can result in coma or death from severe dehydration
 End result of sustained osmotic diuresis
 Renal insufficiency – extremely high BG levels
 Kidneys capacity to reabsorb glucose is exceeded
 Decreased kidney perfusion associated with hypovolemia
 More common in older adults with Type 2

33

Difference between DKA and HHS

Both have hyperglycemia and dehydration. With HHS there are little or no ketones present; and glucose is much higher.

34

HHS: S/s

◦ Gradual onset
◦ May have seizures, myoclonic jerking, and reversible paralysis
◦ Serum glucose: >600 mg/dL
◦ Serum ketones: negative
◦ Serum pH: >7.4
◦ Serum HCO3: >20
◦ Urine ketones: negative

35

HHS: TX

 Rehydrate: BS levels may drop 80-200 mg/dl with fluids alone
 Caution with the elderly with hx cardiac a/o renal problems
 Correct electrolytes
 Hold insulin if K+ is less than 3.3
 Na, Phosphorous and Mg++ replaced according to labs
 Provide insulin to restore and maintain normal glucose
 Hydration is key! Insulin is not always required once the client is re-hydrated

36

HHS: monitor

 VS q 15 til stable
 Labs: hourly BGM, electrolytes
 I/O -hourly outputs
 IVF replacement
 Insulin drips
 Airway
 Neuro status
 Keep safe

37

Hypoglycemia

 BG < 70 mg/dL
 Clinical criteria is used to categorize severity rather than BG levels
 Precipitating factors include:
◦ Too much oral med or insulin
◦ Increased activities
◦ Recent illness
◦ Wt loss
◦ Skipped or delayed meals
◦ Liver dysfunction
◦ ETOH without food

38

Hypoglycemia: S/s

 Cool, clammy skin
 Profuse perspiration
 Anxiety, nervousness
 Irritability, mental confusion, seizures, coma
 Weakness
 Double vision, blurred vision
 Hunger
 Tachycardia, palpitations

39

Hypoglycemia: nursing considerations

 All diabetics should be on hypoglycemia protocol while in hospital
 Document all episodes
 Notify MD for insulin/medication adjustment as needed
 More likely to have another episode in next 24 hrs because glycogen stores in the liver have been depleted
 Pts with chronic hyperglycemia may have s/s of hypo without going below a BG of 70mg/dl

40

Systemic effects of DM

 25% of Medicare’s TOTAL budget is spent on treatment of diabetes and the chronic complications that go along with it
 2 categories of chronic complications
◦ Macrovascular complications
◦ Microvascular complications

41

Macro-vascular changes

 Refers to arteriosclerotic and atherosclerotic changes in moderate- to large-sized arteries and veins
 Coronary artery disease, cerebral artery disease and peripheral artery disease fall into this category

42

Micro-vascular changes

 Refer to disease of the small vessels
 Nephropathy: damage to glomeruli
 Retinopathy: damage to vessels of the retina
 Neuropathy: damage to nervous system

43

CAD

◦ Most common complication of DM
◦ 2-3x greater risk than non-diabetics
◦ MI leading cause of death in diabetics

44

CVA

cerebra-vascular accident (stroke);
◦ Risk for stroke from vascular damage.
◦ Risk increased with HTN, hyperlipidemia, nephropathy, PVD and etoh/tobacco

45

PVD

◦ Poor blood flow to extremities
◦ 86,000 amputations/year and 85% of the time preceded by a foot ulcer

46

Targets for healthier heart

 A1c < 6.5%
 Blood pressure < 200mg/dl
 HDL >40mg/dl for men; > 50 mg/dl for women
 LDL < 100 mg/dl
 Triglycerides < 150 mg/dl
 Smoking cessation
 Increase activity
 Weight loss

47

Diabetic Retinopathy

 Leading cause of blindness in America
 Biggest fear of diabetics
 Related to duration of DM
◦ Type I - after 20 years close to 100%
◦ Type II - after 20 years > 60%
 Linked to FBG > 129 mg/dL
 Hyperglycemia and HTN increase the rate of retinopathy development in Type 1
 Maintenance of near-normal BG levels reduces risk

48

Neuropathy

 Common complication, often involves all parts of the body
 Progressive deterioration of nerves, loss of nerve function
 Results in pain and/or loss of sensation, muscle weakness
 Peripheral neuropathy – numbness, tingling, burning sensation in hands and feet

49

Peripheral Neuropathy treatment:

◦ Normalization of blood sugars
◦ Medications like gabapentin (Neurontin

50

Autonomic Neuropathy treatment

◦ BG normalization
◦ Symptom relief with meds
◦ Smaller frequent meals, low fat and low fiber (gastroparesis)
◦ Hydration and elastic stockings for orthostatic BP

51

Goals for foot care:

1. Relieve pressure
◦ Proper foot wear
◦ Examination by HCP-deformities/nail care
2. Prevent ulcers
◦ Daily feet inspection
◦ Moisturizers (not between toes)
3. Prevent amputations
◦ Risk factor modification is essential!!!!!!!!!!

52

Foot care DO's

◦ Wash feet daily in warm water
◦ Dry feet thoroughly
◦ Inspect daily for cuts, blisters, redness, calluses
◦ Exercise daily
◦ Custom made shoes
◦ See a podiatrist

53

Foot care DON'T

◦ Hot water
◦ Hot water bottles
◦ Heating pads
◦ Apply ice
◦ Soak feet
◦ Use OTC wart remedies
◦ Trim toenails
◦ Walk barefoot
◦ High impact aerobics
◦ Smoke

54

Nephropathy

 Pathologic change in the kidney that reduces renal function and leads to kidney failure.
 Leading cause of end-stage kidney disease (ESKD) and kidney failure
 Diagnosed by laboratory tests
 Risk factors:
◦ 10-15 year history of DM
◦ Diabetic retinopathy
◦ Poor BG control
◦ Uncontrolled HTN
◦ Genetics

55

Nephropathy: treatment and prvention

 Annual screening (including albumin level in urine)
 BG control
 BP control
 Antihypertensive medications to protect the kidneys
 Protein restriction
 Avoid nephrotoxic drugs ( NSAIDS, pcn, dyes)
 Avoid ETOH

56

Dental Disease

 Higher risk for dental caries and gum disease due to increased glucose in saliva and damage to vessels of the gums
 Dental exam every 6 months

57

DM: treatment

 EDUCATE EDUCATE EDUCATE
 Prevention
 Diet
 Exercise
 Monitor BS, HbA1C, Lipids, BP
 Lifestyle modification
 Insulin and/or oral hypoglycemics

58

Principles of nutrition:

1. Individualized diet plan:Meet with dietician
- Protein:15-20% of total daily calories (depending on renal function)
-Carbohydrates: 45-65% of total daily calories;Minimum intake of 130 g/day
- Fat and cholesterol: Saturated fatty intake < 7% of total daily calories;
- Dietary cholesterol < 200 mg/day
- Fiber (improves carbohydrate metabolism)
- ETOH (only with or after meal; in moderation)
- Diets: Exchange system based on 3 food groups; CHO counting; more flexible

59

Exercise

 First see HCP
 Start slow and build
 Can cause hypoglycemia due to increased muscle glucose uptake and inhibited glucose release from the liver
◦ Up to 24 hours after exercise
 Benefits
◦ Better regulation of BG levels and lower insulin requirements
◦ Increased insulin sensitivity
◦ Decreased risk for CVD
 Don’t exercise if BG 250!!

60

Oral Hypoglycemics

1. Sulfonylureas (oldest)
2. Meglitinides
3. Biguanides
4. Alpha-glucosidase inhibitors
5. Thiazolidinediones (TZDs)

61

Indications for oral hypoglycemics

 They are used to lower blood sugar levels in patients when diet and exercise have failed.
 The patient must have some pancreatic function left.
 They can be used as a monotherapy or in conjunction with other oral hypoglycemics.

62

Sulfonylureas

 Stimulate the pancreas to secrete more insulin
 Usually well-tolerated and safe
 Hypoglycemia possible
 Weight gain
 Peaks and valleys (snack?during peak time)
 Many are only effective for a few years, then may stop working

63

Meglitinides

 Action similar to sulfonylureas
 Increase insulin secretion from the pancreas
 repaglinide (Prandin)
 nateglinide (Starlix)
 Designed to increase meal-related insulin secretion
 Rapidly absorbed
 Short duration of action

64

Biguanides

 Decrease liver production of glucose and improve insulin receptor sensitivity in tissues
 Metformin does not produce hypoglycemia or weight gain;
 Relatively low cost;
 Few adverse effects: abdominal discomfort and diarrhea;
 Recommended by ADA as initial tx for Type 2

65

Alpha-glucosidase Inhibitors

 acarbose (Precose)
 miglitol (Glyset)
- Reversibly inhibit the enzyme alpha-glucosidase in the small intestine
 Result: delayed absorption of glucose and digestion of starches
◦ Must be taken with meals to prevent excessive postprandial blood glucose elevations (with the “first bite” of a meal)

66

Thiazolidinediones (TZDs)

 Decrease insulin resistance
 Improves glucose control
◦ Increase glucose uptake and use in skeletal muscle
◦ Inhibit glucose and triglyceride production in the liver
 pioglitazone (Actos)
 rosiglitazone (Avandia)

67

Insulins:

 Substitute for & same effects as endogenous insulin
 Restores the diabetic patient’s ability to:
◦ Metabolize carbohydrates, fats, and proteins
◦ Store glucose in the liver
◦ Convert glycogen to fat stores
- Most now human-derived, using recombinant DNA technologies
 Goal: tight glucose control by mimicking the pancreas’ normal insulin release pattern
- To reduce the incidence of long-term complications

68

Rapid -Acting Insulin

1. Insulin aspart (Novolog) (0.25; 1-3; 3-5 hr)
2. Insulin glulisine (Apidra)
3. Human lispro inj. (Humalog)

69

Short -Acting Insulin

1. Regular human insulin inj. (0.5; 2-4; 5-7 hr)

70

Intermediate - Acting Insulin

1. NPH inj (1.5; 4-12; 16-24+ hr)
2. Lente

71

Long-Acting Insulin

1.Ultralente
2. Insulin Glargine (2-4;none; 24)

72

Insulin : pharmacological therapy

 Type I diabetics need insulin to survive
 Type II diabetics may need insulin as time goes on
 Insulin that is in use may be at room temperature for up to 28 days
 Insulin that is not being used should be stored in the fridge
 Discard insulin as per manufacturer recommendations
 Use insulin syringe once and dispose of properly

73

Factors affecting absorption rate of insulin

 The longer the duration of action, the more unpredictable is absorption
 Larger dose – prolonged absorption
 Increased blood flow from the injection site increases absorption
◦ Application of heat
◦ Massage of area
◦ Exercise of area
 Scarring from repeated injections slow absorption rate

74

Injection depth of insulin

 Injections should be made into SC tissue
◦ Most people grasp skinfold and inject at 90o
◦ Thin pt may need to inject at 45o to avoid IM
 IM injection has faster absorption rate

 Assess older patient’s ability to inject properly
 Arrange for assistance when self-care not possible

75

Timing of injection

- Interval between pre-meal injection and eating is called “lag time”
- Lag time can be utilized to increase or decrease the absorption of insulin, therefore affecting the post-prandial BG level

76

Lipoatrophy

◦ The loss of fat tissue at site of repeated injections
◦ Caused by immune response to impurities in insulin
◦ Tx: injection of insulin at the edge of the atrophied area.

77

Lipohypertrophy

◦ Increased swelling of fat that occurs at site of repeated injections
◦ Decreased sensitivity, can become large and unsightly
◦ Tx: rotating the injection site among different body areas

78

Dawn phenomenon

◦ Morning hyperglycemia due to nighttime release of growth hormone causing BG elevation
◦ Occurs early: 5-6 a.m.
◦ Tx: provide more insulin for the overnight period

79

Somogyi phenomenon

◦ Morning hyperglycemia caused by the counterregulatory response to nighttime hypoglycemia
◦ Tx: ensure adequate dietary intake at bedtime and evaluate insulin dose and exercise program to prevent conditions that lead to hypoglycemia
 Both are diagnosed by BGM during the night

80

Nursing care: Insulin

1. BG monitoring
2. Administration utilizing 5 rights and 2 identifiers
3. Know onset, peak and duration of action
4. Look at pt’s trends for 24 hr
5. What is po status? (Lantus and Levamier have no peak and can be given)
6. Plan ahead for procedures and surgery
7. Know s/s of hyper/hypoglycemia
8. Patient teaching in self-administration
9. Site rotation

81

Lispro

Humalog - 0.5 -1.5 hr ( rapid - acting insulin)

82

Regular

Humulin R and Novolin R - 2-5 hr ( short-acting insulin)

83

NPH

Humulin N and Novolin N - 6-12 hr ( intermediate-acting insulin)

84

Glargine

Lantus - none ( long-acting insulin) never mixed .

85

FBG

fasting blood glucose < 100 ( > 126 )

86

OGTT

oral glucose tolerance testing ( 2 hr post) < 140 ( > 200 )

87

HbA1C

shows the average blood glucose levels during the previous 120 days - 4-6 % ( > 6.5 %)

88

Tolbutamide

Sulfonylurea agent; increase insulin secretion; take after meals; hypoglycemia.

89

Glipizide

Second generation sulfonylurea agent; increase insulin secretion; 30 min before meal; hypoglycemia; monitor for impaired renal function.

90

Metformin

Biguanide; (Glucophage); reduce hepatic glucose production; take with food; monitor renal and liver, cardiopulmonary function ; lactic acidosis; withhold for 48 hours before use of iodinated contrast materials.

91

Lactic acidosis

Lactic acid is produced when oxygen levels in the body drop.

92

Conditions that increase risk for lactic acidosis

Reduced renal function; liver impairment; respiratory insufficiency; severe infection; alcohol abuse.

93

S/s of lactic acidosis

Malaise, unusual muscle pain; respiratory and abdominal distress

94

Avandia

Thiazolidinedione (TZD); improves tissue sensitivity to insulin; Not for patients with moderate to severe liver impairment, jaundice ; may interfere with oral contraceptives ; monitor weight, assess for edema; continue therapy - response can take 2-3 month.

95

Pancreas secrets

40-50 units of insulin