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N324 > Ch. 59 Concepts of Care for Patients w/ DM > Flashcards

Ch. 59 Concepts of Care for Patients w/ DM Flashcards

1
Q

Diabetes Mellitus (DM)

A

Common, chronic, complex disorder of impaired nutrient metabolism

Describes diseases of abnormal carbohydrate metabolism with a characteristic of hyperglycemia

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2
Q

Classification of Diabetes

A

Underlying problem causing a lack of insulin

Action and the severity of insulin deficiency

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3
Q

Type 1 DM

A

Insulin production is absent d/t autoimmune pancreatic beta-cell destruction

Abrupt onset, thirst, hunger, increased urine output, wt loss

Usually <30 yr old

All dependent on insulin

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4
Q

Type 1 DM Causes

A

Susceptible genes

Autoantigens

Environmental factors

Viruses - coxsackievirus, rubella, cytomegalovirus, EPV

Diet - early exposure to cow’s milk, high nitrates in water, low vitamin D

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5
Q

Type 1 DM Clinical Manifestations

A

Polyuria
Polyphagia
Polydipsia
Wt loss
Fatigue
Increased frequency of infections

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6
Q

Type 2 DM

A

Insulin resistance and decreased insulin secretion

Inability to suppress hepatic glucose production

Impaired glucose uptake

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7
Q

Type 2 DM Causes

A

Some beta cell dysfunction
Genetics
Ethnic groups - American Indians, Hispanics, Asians

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8
Q

What causes insulin resistance?

A

Develops from obesity and physical inactivity in a genetically susceptible adult

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9
Q

Type 2 DM is characterized by what?

A

Hyperglycemia d/t progressive loss of insulin secretion in beta cells > causes insulin resistance and insulin deficiency

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10
Q

Type 2 DM Clinical Manifestations

A

Polyuria
Nocturia
Polydipsia
Polyphagia
Recurrent infections
Prolonged wound healing
Visual changes
Fatigue
Decreased energy

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11
Q

Metabolic Syndrome

A

Simultaneous presence of metabolic factors that increase risk for developing type 2 DM and CVD

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12
Q

Metabolic Syndrome Characteristics

A

Abdominal obesity - waist circumference greater then or equal to 40in (men); greater then or equal to 35in (female)
Hyperglycemia
Hypertension
Hyperlipidemia
HDL < 40 (male); <50 (female)

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13
Q

Absence of Insulin

A

Lack of production or a problem with insulin use at cell receptors

Causes glucose to build up on the blood, causing hyperglycemia

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14
Q

What is required for glucose regulation?

A

Insulin to move glucose into many tissues

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15
Q

Basal Insulin Secretion

A

Low-level secretion during fasting

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16
Q

Prandial

A

Two-phase release after eating

An early burst of insulin secretion occurs within 10 minutes of eating, followed by an increasing release that lasts until BG levels return to normal

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17
Q

Classic Symptoms of DM

A

Polyuria
Polydipsia
Polyphagia (cells are starving)
Blurred vision
Weight loss

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18
Q

Acute Complications of Diabetes

A

Diabetic ketoacidosis (DKA)
Hyperglycemic-hyperosmolar state
Hypoglycemia

All 3 require emergent treatment and can be fatal if treatment is delayed or incorrect

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19
Q

Chronic Complications of Diabetes

A

Macrovascular - large blood vessels

Microvascular - small blood vessels

Develop from chronic hyperglycemia

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20
Q

Macrovascular Complication - Cardiovascular Disease (CVD)

A

CVD risk factors

Treatment is aggressive management of: HTN, hyperglycemia, hyperlipidemia

Priority - reduce modifiable risk factors by lifestyle modifications

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21
Q

CVD Risk Factors

A
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22
Q

Macrovascular Complication - Cerebrovascular Disease

A

Risk for stroke 2-4x higher in adults w/ DM

Increases likelihood of severe carotid atherosclerosis

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23
Q

Macrovascular Complication - Cerebrovascular Disease Additional Risk Factors

A

HTN
Hyperlipidemia
Nephropathy
Peripheral vascular disease
Alcohol
Tobacco

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24
Q

Macrovascular Complication - Reduced Immunity

A

Combination of vascular changes and hyperglycemia by reducing WBC activity, inhibiting gas exchange in tissues, and promoting growth of microbes

WBCs do not like to swim around in a sugary environment

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25
Q

Microvascular Complication - Eye & Vision

A

Blindness is 25x more common

Diabetic retinopathy r/t duration of diabetes

R/t blocked retinal blood vessels and cause them to leak, leading to retinal hypoxia

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26
Q

Proliferative Diabetic Retinopathy

A

Growth of new retinal blood vessels which are thin, fragile, and bleed easily leading to vision loss

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27
Q

Microvascular Complication - Diabetic Peripheral Neuropathy

A

Progressive deterioration of nerve function = muscle weakness, damage to nerve fibers

Damage causes pain at first, which is followed by loss of sensation

Onset slow

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28
Q

Microvascular Complication - Diabetic Autonomic Neuropathy

A

Due to failure of heart and arteries to respond to position changes by increasing HR and vascular tone

CAN, orthostatic hypotension, syncope

Can affect entire GI system (gastroparesis, neurogenic bladder, defective balancing hormones)

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29
Q

Microvascular Complication - Diabetic Nephropathy

A

Causes progressive albumin excretion and declining GFR

Changes in kidney = reduced function = kidney failure

Leading cause of ESRD = diabetic-kidney disease

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30
Q

Diabetic Nephropathy Risk Factors

A

10-15 yr history of DM

Poor blood glucose control

Uncontrolled HTN

Genetic predisposition

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31
Q

Microvascular Complication - Sexual Dysfunction

A

Due to damage to both nerve tissue and vascular tissue

Affects M & F

Made worse by poorly controlled BG levels

Other risk factors: obesity, HTM, tobacco use, some prescribed drugs

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32
Q

Microvascular Complication - Cognitive Dysfunction

A

Due to neuron damage, brain atrophy, cognitive impairment

DM increases risk for developing all types of dementia

Increases complications of neuropathy and retinopathy

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33
Q

Indications for Testing People for Type 2 Diabetes

A

BMI > 25

First-degree relative w/ DM

Physically inactive

High-risk ethnic population

Gave birth to baby weighing > 9 or had gestational diabetes

Hypertensive

A1C > 5.7%

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34
Q

Criteria for Diagnosis of Diabetes

A

A1C >6.5%

Fasting BG > or = to 126

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35
Q

Normal Blood Glucose Values

A

Fasting BG < 100 mg/dL

Glycosylated hemoglobin (A1C) 4%-6%

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36
Q

A1C Levels

A

Q6Months or quarterly

5.7%-6.4% prediabetes

> 6.5% diabetes

> 8% poorly controlled diabetes

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37
Q

Preventing Injury From Hyperglycemia

A

Maintaining BG levels in optimal target range

A1C maintained < or = to 7.0%

Majority of premeal BG levels 70-130

Peak after meal BG <180

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38
Q

Drug Therapy for Diabetes

A

Indicated for type 2

Type 1 requires insulin therapy

Insulin therapy indicated for type 2 when BG levels cannot be met

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39
Q

What is the most important thing to teach the patient on drug therapy with DM?

A

Antidiabetic drugs are not a substitute for dietary modification and exercise

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40
Q

Sulfonylureas (SU)

A

Insulin Stimulator

Glyburide; Glipizide

Used for patients who are still able to produce insulin

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41
Q

Sulfonylureas (SU) MOA

A

Stimulate insulin release from pancreatic beta cells

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42
Q

Sulfonylureas (SU) Pt Teaching

A

S/S of hypoglycemia

Take w/ or just before meals to prevent hypoglycemia

Report to provider any OTC or supplement use

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43
Q

Metformin

A

1 drug for type 2 DM

Biguanides

44
Q

Metformin MOA

A

Lower BG by inhibiting liver glucose production, decreasing intestinal absorption of glucose, and increasing insulin sensitivity

45
Q

Metformin Pt Teaching

A

Do not drink alcohol

Must be stopped before using contrast agents and not started again for 48 hr after testing d/t increased risk for kidney damage and lactic acidosis

Administer with meals to minimize GI effects

May cause hypoglycemia if combined w/ a sulfonylurea

46
Q

Thiazolidinediones (TZDs or “glitazones”)

A

Insulin Sensitizers

Pioglitazone

Black-box warning (risk of HF)

47
Q

Thiazolidinediones MOA

A

Increase cellular use of glucose, which lowers BG levels

48
Q

Thiazolidinediones Pt Teaching

A

Weigh daily (report >2 lbs in one day or 4 lbs in one wk)

Report vision changes immediately

Weight gain and peripheral edema are common side effects

49
Q

Dulaglutide

A

Incretin Mimetics (GLP-1 Agonists)

Can cause hypoglycemia when used with insulin, sulfonylureas, or meglitinides

50
Q

Dulaglutide MOA

A

Reduces liver glucose production, and delaying gastric emptying

51
Q

Dulaglutide Pt Teaching

A

S/S of hypoglycemia

How to inject themselves, only available as SQ injection

Read pens carefully as some extended-release form is only injected WEEKLY

Report persistent abdominal pain and nausea

52
Q

Alogliptin

A

Dipeptidyl peptidase-4 (DPP-4) inhibitors

53
Q

Alogliptin MOA

A

Breaks down natural gut hormones (GLP-1 and GIP)

Reduce BG levels by delaying gastric emptying

Works w/ body’s insulin

54
Q

Alogliptin Pt Teaching

A

S/S of hypoglycemia

Report a rash or other signs of allergic reaction

Report persistent abdominal pain

Notify HCP if SOB, dyspnea on exertion, cough especially when lying down

55
Q

Canagliflozin

A

Sodium-glucose cotransparent inhibitors (SGLT2)

56
Q

Canagliflozin MOA

A

Glucose is excreted in urine rather than moved back into the blood

High risk of UTI & yeast infection

57
Q

Canagliflozin Pt Teaching

A

S/S of hypoglycemia

S/S of dehydration

S/S of hyponatremia

S/S of UTI

S/S of genital yeast infection

Report any swelling, tenderness or redness of genitals or perineal skin

58
Q

Insulin Therapy

A

Used for type 1 & 2

Prandial - where pancreas produces additional mealtime insulin to prevent BG elevations after meals

Post-prandial - first 4 hr after eating or drinking, BG begins to rise within a few min after eating

59
Q

Insulin Therapy Pt Teaching

A

Insulin types

Injection technique

Site of injection can affect absorption, onset, degree, and duration of insulin activity

60
Q

Rapid Acting Insulin

A

Lispro (Humalog)

61
Q

Short Acting Insulin

A

Regular (Humulin R)

62
Q

Intermediate Acting Insulin

A

NPH (Humulin N)

63
Q

Long-Acting Insulin

A

Glargine (Lantus)

64
Q

Lispro (Humalog)

A

Onset: 5-30 min
Peak: 30-90 min
Duration: 3-5 hr

65
Q

Regular (Humulin R)

A

Onset: 30-60 min
Peak: 2-4 hr
Duration: 5-7 hr

66
Q

NPH (Humulin N)

A

Onset: 1-2 hr
Peak: 4-12 hr
Duration: 18-24 hr

67
Q

Glargine (Lantus)

A

Onset: 3-4 hr
Peak: none
Duration: 24 hr +

68
Q

Insulin Absorption

A

Injection site

Rotation within one anatomic site is preferred

Heat, massaging the area, exercising injected area increases insulin absorption

Scarred areas slow insulin absorption

69
Q

Injection Timing

A

Affects BG levels

Rapid onset - give within 10 min before mealtime

Regular insulin - give 20-30 min prior to mealtime

70
Q

Insulin Storage

A

Refrigerate (no longer than 28 days)

Prevent exposure to sunlight

May be kept at room temp up to 28 days

Avoid excessive shaking

Do not freeze

Discard after 28 days

71
Q

Pt Teaching: BG Monitoring

A

Teach to assess BG frequently for:
S/S of hypo or hyperglycemia
Hypoglycemic unawareness
Periods of illness
Before and after exercise
Gastroparesis
Adjustment of anti diabetic drugs
Pregnancy

72
Q

Pt Education: Nutrition Therapy

A

Registered dietitian nutritionist (RDN)

Diabetic educator

Consider cultural background, financial status, lifestyle

Carbohydrate intake

Dietary fat and cholesterol

Alcohol consumption

73
Q

Pt Education: Exercise Therapy

A

Improves glycemic control

Decreases mortality and improves A1C

Exercise a minimum of 50 min, 3 times/wk

Can cause hypoglycemia in Type 1 (monitor BG before and after)

74
Q

What is the best exercise type for people with diabetes?

A

Swimming

75
Q

Swimming With Diabetes

A

Gentle on feet and joints

Excellent cardiovascular exercise

Improves BG control

76
Q

Swimming Precautions w/ Diabetes

A

Avoid if any wounds are present

Never walk barefoot around the deck, locker room, or shower

Hydrate well

77
Q

Stress Hyperglycemia

A

May occur during severe illness in adults without DM

Caused by a combination of factors:
Increased serum cortisol, catecholamines, glucagon, GH
Leads to increased gluconeogenesis and glycogenolysis, and insulin resistance

Associated with poor outcomes

78
Q

BG Control in Hospitalized Patients

A

Hyperglycemia develops when withholding oral anti diabetics and when giving corticosteroids and changes in nutrition

Maintain BG between 140-180 for critically ill

Pre-meal <140

Random BG <180

79
Q

NPO Status

A

Give reduced dose of basal insulin

80
Q

Pancreas Transplant Indications

A

Severe metabolic complications

Consistent failure of insulin-based therapy

ESKD who have had or plan to have a kidney transplant

81
Q

Preventing Injury From Peripheral Neuropathy

A

Practice proper foot care

Identify factors that increase risk of injury

Maintain intact skin on feet

82
Q

Peripheral Neuropathy

A

Motor - damages nerves of foot muscles

Autonomic - loss of normal sweating and skin temp regulation; dry, thinking skin; skin cracks and fissures

Sensory - tingling or burning; numbness and reduced sensory perception

83
Q

Diabetic Foot Assessment

A

Dry, cracked, fissured skin
Ulcers
Toenails: thickened, long nails; ingrown
Symptoms of claudication
Pedal and tibial pulse reduced
Cap refill
Presence or absence of hair growth on top of foot
Calluses, corns
Clawed toes, hammertoes, bunions
Limited ROM

84
Q

Foot Care Instructions/Education

A

Inspect feet daily

Wash daily in lukewarm water, mild soap, dry thoroughly especially btw toes

Apply fragrance free moisturizer top and bottom; avoid btw toes

Clean cotton socks daily

Breathable shoes

Trim nails straight across, smooth w/ emery board

Teach family how to inspect and provide foot care

85
Q

Foot Care “DO NOT” List

A

Do not treat blisters, sores, or infections at home

Do not smoke or use nicotine

Do not step into bathtub w/out checking temp of water w/ wrist or thermometer

Do not use very hot or cold water or warm devices on feet

Do not treat corns, blisters, bunions, calluses, or ingrown toenails yourself

Do not go barefooted

Do not wear sandals w/ open toes or straps btw toes

Do not cross legs or tight stockings that constrict blood flow

Do not soak feet

86
Q

Reducing the Risk for Kidney Disease

A

BG control

ACE or ARB (BP in range)

Annual kidney function evaluation

Cholesterol management

Avoid nephrotoxic agents

Smoking cessation

87
Q

Preventing Complications From Hypoglycemia

A

Causes specific symptoms and resolves when BG concentration increases

Avoid levels <70 and never higher than 200

Apply 15-15 rule

88
Q

Hypoglycemia Clinical Manifestations

A

Cool, clammy, sweaty

Anxious, nervous

Irritable, confusion

Seizure, coma

Weakness, double or blurred vision

Hunger

Tachycardia

Palpitations

89
Q

Hyperglycemia Clinical Manifestations

A

Warm, dry, vasodilated skin

S/S of dehydration

Rapid, deep respirations

Rotten fruity breath

Abdominal cramps

N/V

BG >250

90
Q

TIRED

A

For hypoglycemia

T = tachycardia
I = irritable
R= restless
E = excessive hunger
D = diaphoresis, depression

91
Q

15-15 Rule

A

BG <70 or s/s of hypoglycemia

Give 15 g of carbs

Recheck BG in 15 min
(still low = give 15 g of carb)

Avoid giving high potassium options such as orange juice

Dysphagia = IV dose of concentrated dextrose or SQ glucagon

92
Q

High Potassium Foods

A

Prunes and prune juice
Oranges and orange juice
Milk
Low-sodium cheese
Nuts
Beef
Chicken
Bananas
Raisins
Potatoes

93
Q

15g Carbohydrate Options

A

Glucose tablets or glucose gel

Half cup (120 mL; 4 oz) fruit juice or regular soft drink

8 ounces (240 mL) skim milk

6-10 hard candies

4 cubes of sugar or 4 tsp of sugar

6 saltines

3 graham crackers

1 tbsp (15 mL) honey or syrup

94
Q

Survival Skills For Diabetics

A

Pathophysiology

Prepare and inject insulin

How to take anti diabetics

Recognition, treatment, and prevention of hypo or hyper glycemia

Basic diet information

How to monitor BG and urine ketones

Teach sick day management rules

Where to buy diabetic supplies

When and how to follow-up with HCP

95
Q

Dawn Phenomenon

A

Abnormal early-morning hyperglycemia

Do not skip breakfast

96
Q

Dawn Phenomenon Management

A

Additional insulin at 10 pm instead of evening meal

Avoid carbs before bedtime

Increase evening exercise

Increase protein intake

97
Q

Somogyi Phenomenon

A

Begins as hypoglycemic episode overnight

Body has a hormonal response that causes hyperglycemia

98
Q

Somogyi Phenomenon Causes

A

Excess insulin

Inadequate calorie intake w/ insulin therapy

99
Q

Diagnosing Dawn/Somogyi Phenomenon

A

Check BG around 2-3 am for several nights in a row

100
Q

DKA

A

Most common precipitating factor is infection

101
Q

DKA S/S

A

Dehydration w/ electrolyte loss

The 3 P’s

Rotting citrus fruit odor to breath

Vomiting, abdominal pain, dehydration, weakness, confusion, shock, coma

Kussmaul respirations

102
Q

Interventions for Preventing DKA

A

BG management

Fluid and electrolyte management

Drug therapy - regular insulin IV continuous and then switch to SQ

103
Q

Sick Day Rules

A

Monitor BG at least Q4H

Test urine for ketones when BG level >240

Continue to take insulin unless instructed not to

Drink 8-12 oz of sugar-free liquids every hour

Continue to eat meals

Unable to tolerate solid food d/t nausea, consume more easily tolerated foods or liquids equal to carb content of usual meal

104
Q

Sick Day Rules: When to call HCP

A

Persistent N/V

Moderate or high ketones

BG elevation after 2 supplemental doses of insulin

High temp or increasing fever; fever more than 24 hr (101.5)

105
Q

Hyperglycemic-Hyperosmolar State (HHS)

A

Develops only in pt who still receive insulin

Caused by sustained osmotic diuresis leading to extremely high BG levels

Differs from DKA - absent or low ketone levels and BG levels higher (600)

106
Q

HHS Interventions

A

Fluid replacement - restore blood volume; NS used if shock or sever hypotension, if not then half NS

Assess hourly for signs of cerebral edema (AMS, N/V, HA, lethargy)

N324 (18 decks)

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