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488 > Class 8: Endocrine > Flashcards

Class 8: Endocrine Flashcards

1
Q

Diabetes diagnostic studies (positive results)

A

-FBG ≥ 7 mmol/L
-Two-hour glucose level ≥11.1 mmol/L during 75 g oral glucose tolerance test (OGTT)
-Random glucose level ≥11.1 mmol/L
-A1C ≥ 6.5% (in adults)

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2
Q

Hemoglobin A1C test

A

-Useful in determining glycemic levels over time; amount of glucose attached to hemoglobin molecules over RBC life span (90-120 days)
-Regular assessments required

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3
Q

Ideal A1C test results

A

Ideal goal; Canadian Diabetes Association (CDA) ≤7.0%, normal range is <6.0%

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4
Q

Normal A1C does what

A

Reduces risks pathy’s: Retinopathy, nephropathy, and neuropathy

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5
Q

DM collaborative care

A

-Oral antihyperglycemic agents and noninsulin injectables
-ACEI or ARBs
-BP control; target is <130/80 mm Hg
-Drug therapy

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6
Q

DM collaborative care cont’d

A

-Exercise & nutritional therapy
-Teaching and follow-up programs
-Self monitoring of blood glucose (SMBG)
-Vascular protection

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7
Q

Drug therapy for DM

A

-Enteric-coated acetylsalicylic acid (ASA)
-Insulin
-Lipid-lowering drugs

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8
Q

Exogenous insulin

A

-MUST be used for Type 1 Diabetes; may be additional treatment for Type 2 Diabetes
-Always includes separate rapid/short acting + intermediate or long acting

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9
Q

Just bc a pt is on insulin…

A

Does not mean they have been diagnosed with type 1 diabetes

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10
Q

Preparations of rapid-acting (bolus) clear insulin

A

-Injected 0-15 minutes before meal
-Onset: 10-15 minutes, peak; 60- 90 min, duration; 3-5h

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11
Q

Preparations of short-acting (bolus) clear insulin

A

-Injected 30-45 minutes before meal
-Onset; 30-60 min, peak; 2-4h, duration; 5-8h

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12
Q

Preparations of intermediate-acting (basal) cloudy insulin

A

-BID; am & pm (not specific to meals)
-Onset; 1-3h, peak; 6-8h, duration; 12-16h

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13
Q

Preparations of long-acting (basal) insulin

A

-Injected OD at bedtime OR in the morning
-Onset; 1-2h, peak; none, duration; 24+h
-Released steadily and continuously, CANNOT be mixed with any other insulin or solution

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14
Q

Slide 9

A

Conflicts with slide 8…. Figure out which one is right

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15
Q

Rapid-acting (clear) insulins

A

-Novorapid, apidra & humalog
-NAH

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16
Q

Short acting (clear) insulins

A

-Humulin R, novolin GE, Toronto

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17
Q

Intermediate (cloudy) insulins

A

Humulin N, novolin GE NPH

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18
Q

Long acting (clear) insulin

A

Lantus

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19
Q

Long acting insulin

A

Levemir

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20
Q

Intermediate insulins are…

A

The only cloudy insulins

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21
Q

Insulin therapy regimens

A

-Basal-bolus; long-acting (basal) OD & rapid/short-acting (bolus) before meals
-Fixed combination insulins
-Sliding scale insulin dosing

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22
Q

Basal-bolus insulin…

A

Closely mimics endogenous insulin production

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23
Q

Premixed insulin (cloudy)

A

-Ratio of rapid/fast-acting to intermediate acting insulin: Humulin (rapid) 30/70 & novolin GE (fast acting) 30/70
-Not for Type 1 diabetes

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24
Q

Insulin therapy considerations

A

-Regimens should be adapted to tx goals, lifestyle, capacity and general health

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25
Q

Administration of insulin (routes)

A

-Cannot be taken PO
-SC injection for self-administration
-IV administration of Regular insulin ONLY

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26
Q

Administration of insulin (sites)

A

-Fastest absorption from abdomen, followed by arm, thigh, and buttock
-Abdomen is the preferred site
-Rotate injections within one particular site (think – checkerboard)
-Do not inject in site to be exercised

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27
Q

Administration of insulin (preparation)

A

No alcohol swab on site needed before injection (home therapy)

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28
Q

Slide 15 (checkerboard rotation)

A
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29
Q

Insulin syringe sizes

A

-1.0, 0.5 & 0.3 mL
-The 0.5mL size may be used for doses of 50 units or less, and the 0.3mL syringe can be used for doses of 30 units or less
-The 0.5mL & 0.3mL syringes are marked in 1-unit increments

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30
Q

Giving an insulin injection

A

-Wash hands with soap & water
-Do not recap needle
-45-90 degree angle (depending on fat)

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31
Q

Slide 18&19

A
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32
Q

Insulin pump

A

-Continuous SC infusion (basal rate)
-Potential for tight glucose control

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33
Q

PO hypoglycemic agents (OHA)

A

-Used for patients with type 2 diabetes, NOT type 1
-Patients may be on both OHA’s and insulin, but they will still be classified as a patient with Type 2 Diabetes

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34
Q

Insulin drug classes

A

-Sulfonylurea
-Alpha glucosidase inhibitor
-Biguanide
-Megltinide
-SABM

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35
Q

Biguanide

A

-Reduces production & output of sugar by the liver, acts on the liver
-Metformin

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36
Q

Sulfonylurea

A

-Promotes insulin secretion, acts on the pancreas
-Gliclazide, Glyburide & Chlopromaide

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37
Q

Megltinide

A

-Promotes insulin secretion, acts on the pancreas
-Regaglinide & nateglinide

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38
Q

Alpha glucosidase inhibitor

A

-Prevents breakdown of carbs and delays carb digestion, acts on the small intestine
-Acarbose & sitagliptin

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39
Q

Biguanide (metformin) MOA

A

-Decreases glucose production
-Lowers glucose absorption & enhances insulin receptor uptake

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40
Q

Biguanide (metformin) AE

A

GI upset & lactic acid

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41
Q

Biguanide (metformin) contraindications

A

-Hepatic & renal failure
-Respiratory insufficiency & hypoxemic conditions
-Alcohol abuse

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42
Q

Biguanide (metformin) does…

A

-NOT cause hypoglycemia
-Take with food

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43
Q

Biguanide (metformin) dosing

A

-250-2500 mg/day
-May be divided doses dependent on the patient’s needs

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44
Q

Sulphonylurea (liclazide, glyburide & glimepiride) MOA

A

-Stimulates beta cell insulin release
-Increases peripheral glucose utilization & insulin receptor sensitivity
-Decreases hepatic glucose production

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45
Q

Sulphonylurea (liclazide, glyburide & glimepiride) AE

A

-Hypoglycemia, weight gain, hyperinsulemia
-Caution with renal/liver dysfunction (reduce dose)

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46
Q

Sulphonylurea (liclazide, glyburide & glimepiride) dosing

A

-Take 30min before meals

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47
Q

Meglitinides (repaglinide) MOA

A

-Short acting secretagogue
-Binds to beta cell to stimulate insulin release at a different site than sulfonylureas

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48
Q

Meglitinides (repaglinide) rule of thumb

A

No meal, no dose; extra meal, extra dose (take 15 minutes before meal)

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49
Q

Meglitinides (repaglinide) AE

A

Weight gain & hypoglycemia

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50
Q

Meglitinides (repaglinide) interactions

A

Interacts with CYP 3A4

51
Q

Alpha-Glucosidase Inhibitor (acarbose) MOA

A

Inhibits intestinal amylase and alpha-glucosidase, therefore delaying breakdown of complex carbohydrates and slows glucose absorption

52
Q

Alpha-Glucosidase Inhibitor (acarbose) AE & cautions

A

-Flatulence, diarrhea & cramps
-Caution in patient with GI disorders

53
Q

Alpha-Glucosidase Inhibitor (acarbose) administration considerations

A

-Not absorbed, decreased hypoglycemia (except with sulfonylureas)
-Take with first bite of food, no food no dose

54
Q

Thiazolidinediones (glitazones): (pioglitazone & rosiglitazone) MOA

A

Enhances insulin sensitivity at the cell level

55
Q

Thiazolidinediones (glitazones): (pioglitazone & rosiglitazone) AE

A

Hypertensive effect, headache, upper respiratory infection, anemia, edema & weight gain

56
Q

Dipeptidyl Peptidase 4 (DPP-4) inhibitors (sitagliptin) MOA & AKA

A

-Also known as ‘gliptins’
-Delays breakdown of incretin hormones by inhibiting the enzyme DPP-4
-Reduces postprandial and fasting glucose concentrations

57
Q

Dipeptidyl Peptidase 4 (DPP-4) inhibitors (sitagliptin) AE

A

Respiratory tract infection, headache & diarrhea

58
Q

Combination therapy options

A

-Glyburide & metformin
-Avandamet (avandia and metformin)

59
Q

Combination therapy MOA

A

-Increases effectiveness of drugs by targeting different sites at the same time
-Minimizes side effects because lower doses are used

60
Q

Combination therapy considerations

A

May add up to 3-4 OHA’s before placing patient on insulin with/without OHA (primarily metformin)

61
Q

Diabetic medication drug interactions

A

-Alcohol & sulfonylureas
-Arcabose & sulfonylureas
-Antihypertensives
-Beta-blockers
-Digoxin & propranolol

62
Q

Diabetic medications + alcohol & sulfonylureas

A

-Disulfiram-like reaction (flushing, nausea, dizzines & tachycardia)

63
Q

Diabetic medications + antihypertensives

A

-(Thiazides, furosemide & CCBS)
-Cause hyperglycemia

64
Q

Diabetic medications + beta-blockers

A

-Mask hypoglycemia

65
Q

Diabetic medications + beta-blockers

A

-Mask hypoglycemia

66
Q

Diabetic medications + fibrates & cholestyramine

A

Cause hypoglycemia

67
Q

Diabetic medications + digoxin or propanolol

A

-Decrease absorption of digoxin or propranolol

68
Q

Diabetic medications + sulfonylureas & acarbose

A

-Causes hypoglycemia (treat with honey, dextrose tabs or milk)

69
Q

General diabetes management

A

Diet, exercise & glucose monitoring

70
Q

Type 1 DM nutritional therapy (total calories)

A

Increase in caloric intake possibly necessary to achieve desirable body weight and restore body tissues

71
Q

Type 1 DM nutritional therapy (effect of diet)

A

Diet & insulin necessary for glucose control

72
Q

Type 1 DM nutritional therapy (distribution of calories)

A

Equal distribution of carbohydrates through meals or adjustment of carbohydrates for insulin activity

73
Q

Type 1 DM nutritional therapy (consistency of daily intake)

A

Necessary for glucose control

74
Q

Type 1 DM nutritional therapy (uniform timing of meals)

A

Crucial for NPH insulin programs; flexibility with multidose rapid-acting insulin

75
Q

Type 1 DM nutritional therapy (intermeal & bedtime snacks)

A

Frequently necessary

76
Q

Type 1 DM nutritional therapy (nutritional supplement for exercise programs)

A

Carbohydrates 20 g/hr for moderate physical activities

77
Q

Type 2 DM nutritional therapy (total calories)

A

Reduction in caloric intake desirable for overweight or obese patient

78
Q

Type 2 DM nutritional therapy (effect of diet)

A

Diet alone possibly sufficient for glucose control

79
Q

Type 2 DM nutritional therapy (distribution of calories)

A

Equal distribution recommended; low-fat diet desirable; consistency of carbohydrate at meals desirable

80
Q

Type 2 DM nutritional therapy (consistency in daily intake)

A

Desirable for weight reduction and moderation of blood glucose levels

81
Q

Type 2 DM nutritional therapy (uniform timing of meals)

A

Desirable but not essential, unless using insulin or sulphonylureas

82
Q

Type 2 DM nutritional therapy (intermeal & bedtime snacks)

A

Based on patient’s eating habits and preferences; may be necessary if using insulin or sulphonylureas

83
Q

Type 2 DM nutritional therapy (nutritional supplement for exercise programs)

A

May be necessary if patient’s blood glucose levels are controlled on sulphonylureas or insulin

84
Q

Slide 36

A
85
Q

Food composition

A

-Protein; 15-20% of energy
-Fat: <35% of energy
-Fibre
-Carbohydrates: 45-60% of energy

86
Q

Diabetic neuropathy + protein

A

Limit intake to 15% of energy & closely monitor

87
Q

Saturated & trans-fatty acids

A

Should be reduced to less than 7% of energy intake

88
Q

Polyunsaturated fat

A

Should be limited to 10% of energy intake

89
Q

Fibre intake

A

25-50g/day

90
Q

Carbohydrates

A

-Pts should try to consume high fibre carbohydrates
-<10% of energy intake should come from sucrose
-Low carbohydrate diets are not recommended for DM management

91
Q

Glycemic index (slide 38)

A

-Low GI (55 or less); great
-Medium GI (56-69); okay
-High GI (70 or more); not great

92
Q

Basic carb counting

A

-Make healthy choices, focus on the carbohydrate, set carbohydrate goals
-Determine carbohydrate content
-Monitor effect on BG

93
Q

Slide 40 & 41

A
94
Q

Continuous glucose monitoring

A

Updates every 1-5 minutes, helps identify patterns

95
Q

Slide 45

A
96
Q

Nursing care of DM

A

-Foot care, BP & cholesterol monitoring

97
Q

Hypoglycemia

A

<4mmol/L

98
Q

Manifestations of hypoglycemia

A

-Confusion, irritability, diaphoresis, tremors
-Hunger, weakness & visual disturbances

99
Q

Untreated hypoglycemia can…

A

Progress to loss of consciousness, seizures, coma, and death

100
Q

Hypoglycemia unawareness

A

-Person does not experience usual warning signs
-R/t autonomic neuropathy
-Unsafe for patients with risk factors for hypoglycemic unawareness to aim for tight blood glucose control because a major drawback of intensive treatment is hypoglycemia

101
Q

Those at risk for hypoglycemia unawareness

A

Elderly patients and patients who use β-adrenergic blockers

102
Q

Causes of acute hypoglycemia

A

Mismatch in timing of meals and peak action of medications

103
Q

At the first sign of acute hypoglycemia

A

-Check BG
-If <4 mmol/L, begin treatment
-If >4 mmol/L, investigate further for cause of S&S
-If monitoring equipment not available, treatment should be initiated

104
Q

Acute hypoglycemia tx

A

-15-20g of a simple carbohydrate, 175 mL of fruit juice, or a soft drink
-Check BG 15 min after & again in 45 min
-Repeat until BG >4mmol/L

105
Q

Acute hypoglycemia tx considerations

A

-Avoid foods with fat as they decrease absorption of sugar
-Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia

106
Q

Acute hypoglycemia tx if pt cannot swallow

A

-1 mg of glucagon IM or SC; side effect: rebound hypoglycemia
-Have patient ingest a complex carbohydrate after recovery
-20-50 mL of 50% dextrose IV push in acute care settings

107
Q

Pediatric considerations of hypoglycemia

A

-Children are often able to detect the onset of hypoglycemia; some are too young to implement treatment
-Parents should be able to recognize the onset of symptoms
-Give children 10-15mg simple carbs
-Illness can alter diabetes management; insulin requirements may increase or decrease

108
Q

DKA

A

-Caused by profound deficiency of insulin
-Most likely to occur in Type 1 DM

109
Q

Precipitating factors of DKA

A

-Illness, infection, inadequate insulin dosage, undiagnosed type 1, poor self-management or neglect

110
Q

DKA pathophysiology

A

-Insufficient insulin prevents glucose from being used for energy
-Body breaks down fat & ketones are a by-product of fat metabolism

111
Q

Ketones

A

-Alter pH balance, causing metabolic acidosis
-Ketone bodies are excreted in urine
-Electrolytes become depleted

112
Q

DKA manifestations

A

-Lethargy/weakness (early symptoms)
-Dehydration (tachycardia)
-Abdominal pain (anorexia & vomiting)
-Kussmaul respirations (rapid deep breathing to reverse metabolic acidosis, sweet fruity odor)

113
Q

Management of DKA

A

-Airway; O2
-Correct fluid & electrolytes; NaCl restores urine output & raises BP
-When BG levels approach 14 mmol/L (downward); 5% dextrose
-K+ replacement & Na+ bicarbonate

114
Q

Acute management of DKA + insulin therapy

A

-Witheld until fluid resuscitation has begun
-Bolus followed by regular insulin drip

115
Q

Pediatric considerations of DKA

A

-Children should be admitted to PICU
-Priorities = IV access
-Aim to decrease BG by 2.8-5 mmol/L per hour, keep BG 6.7-13.3mmol/l
-Cardiac and neuro monitoring: Risk of cerebral edema; caution with rehydration & risk of hypokalemia; watch for ecg changes

116
Q

Pediatric considerations of DKA cont’d

A

-After acute period of DKA is over, goal is regulating insulin dosage in relation to diet and activity
-In children, often presentation with DKA is the first diagnosis of diabetes

117
Q

Hyperosmolar hyperglycemic syndrome (HHS)

A

-Life-threatening syndrome, less common than DKA
-Often occurs in patients older than 60 years with type 2 DM
-Pt has enough circulating insulin that ketoacidosis does not occur, fewer symptoms in earlier stages
-Neurological manifestations occur because of ↑ serum osmolality

118
Q

HHS common etiology’s/hx

A

-Inadequate fluid intake
-Increasing mental depression
-Polyuria

119
Q

HHS lab values

A

-BG >34 mmol/L
-Increase in serum osmolality
-Absent/minimal ketone bodies

120
Q

HHS is a…

A

-Medical emergency with a high mortality rate

121
Q

HHS therapy

A

-Similar to DKA except HHS requires greater fluid replacement

122
Q

Nursing management of DKA/HHS (administration)

A

-IV fluids, insulin & electrolytes

123
Q

Nursing management of DKA/HHS (assessment)

A

-Renal & cardiopulmonary status
-Cardiac & VS monitoring
-LOC, signs of potassium imbalance

124
Q

Incretin

A

-A group of metabolic hormones that augment the secretion of insulin

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