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NU 340 > Ch. 56 > Flashcards

Ch. 56 Flashcards

1
Q

diabetes mellitus

A
  • chronic endocrine disorder of impaired glucose regulation
  • can affect every body system
  • very common
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2
Q

pathophysiology of diabetes

A
  • pancreas: organ (beta cells) in charge of insulin production; insulin helps keep blood glucose levels within normal range
  • liver: organ in charge of glucose production
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3
Q

what is the function of the pancreas (r/t DM)?

A
  • organ (beta cells) in charge of insulin production
  • insulin helps keep blood glucose levels within normal range
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4
Q

what is the function of the liver (r/t DM)?

A
  • organ in charge of glucose production
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5
Q

Type 1 DM

A

autoimmune disorder with beta cell destruction leading to absolute insulin deficiency

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6
Q

Type 2 DM

A

insulin resistance

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7
Q

types of diabetes

A
  • type 1
  • type 2
  • gestational
  • other specific conditions resulting in hyperglycemia
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8
Q

pathophysiology of type 1 DM

A
  • genetically susceptible individuals develop islet cell autoantibodies months to years before diagnosis of type 1
  • pancreas: progressive autoimmune destruction of beta cells (80-90% reduction) leads to hyperglycemia and diagnosis of type 1
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9
Q

pathophysiology of type 2 DM

A
  • muscle: insulin resistance, caused by inherited defect in insulin receptors, is a universal finding in patients with type 2. precedes development of impaired glucose tolerance and type 2 by as much as 3-4 decades. insulin resistance stimulates a compensatory increased insulin production by beta cells in pancreas
  • pancreas: beta-cell defect results in decreased insulin secretory capacity below the amount needed for the degree of insulin resistance leading to hyperglycemia and the diagnosis of diabetes
  • liver: excessive hepatic glucose production causes increased hyperglycemia in the fasting and postprandial state
  • adipose tissue: adipokines from adipose tissue have a role in altered glucose and fat metabolism
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10
Q

type 1 DM: symptom start

A
  • symptoms usually start in childhood or young adulthood
  • people often seek medical help because they are seriously ill from sudden symptoms of high blood sugar
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11
Q

type 1 DM: episodes of low blood sugar

A

episodes of hypoglycemia are common

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12
Q

type 1 DM: prevention

A

cannot be prevented

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13
Q

type 2 DM: symptom start

A
  • the person may not have symptoms before diagnosis
  • usually the disease is discovered in adulthood but an increasing number of children are being diagnosed with the disease
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14
Q

type 2 DM: episodes of low blood sugar

A

fewer episodes of low blood sugar level, unless person is taking insulin or certain diabetes meds

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15
Q

type 2 DM: prevention

A

*can be prevented or delayed with
- healthy lifestyle
- maintaining a healthy weight
- eating sensibly
- exercising regularly

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16
Q

proinsulin is secreted by and stored in ___

A

the beta cells of the islets of Langerhans in the pancreas

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17
Q

how is proinsulin transformed to active insulin?

A

the liver

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18
Q

insulin attaches to ____

A

receptors on target cells
- promotes glucose transport into the cells through the cell membranes

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19
Q

effects of absence of insulin

A
  • hyperglycemia
  • polyuria (pee a lot)
  • polydipsia (thirsty)
  • polyphagia (hungry)
  • ketone bodies present in a urine test
  • hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion, hypoxia
  • metabolic acidosis, kussmaul respiration
  • hypokalemia, hyperkalemia, or normal serum potassium levels
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20
Q

simultaneous presence of metabolic factors that increase risk for type 2 DM:

A
  • abdominal obesity-waist circumference
  • hyperglycemia
  • hypertension
  • hyperlipidemia
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21
Q

long term complications of DM (hyperglycemia)

A
  • microvascular: smaller blood vessels
    - diabetic retinopathy: leading cause of blindness in working-age adults
    - eye, feet,
  • macrovascular: large blood vessels
    - diabetic nephropathy: leading cause of end-stage renal disease
  • stroke
  • cardiovascular disease
  • diabetic neuropathy: leading cause of non-traumatic lower extremity amputations
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22
Q

microvascular

A
  • smaller blood vessels
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23
Q

macrovascular

A
  • large blood vessels
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24
Q

what is the major focus for health promotion activities of DM

A
  • control of diabetes
  • its complications
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25
Q

diabetic diet

A
  • low-calorie, low carbohydrate
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26
Q

diabetic “healthy lifestyle”

A

adopt a healthy lifestyle changes aimed at weight loss:
- low calorie, low carbohydrate diet
- increased physical activity

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27
Q

risk factors for type 2 DM

A

Family history
Sedentary lifestyle
*Obesity
*Ethnic background: african american, hispanic
Delivery of baby > 9 lbs
*Gestational DM (mom is at risk of developing type 2)
Hypertension
High cholesterol
Polycystic ovarian syndrome
History of Vascular Disease

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28
Q

type 2 DM assessment: history

A

Risk factors
OB history
Weight changes: weight gain
Infections: frequent- skin, UTI, yeast
Changes in vision or sense of touch

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29
Q

type 2 DM assessment: blood tests

A

Fasting plasma glucose (FPG)
Oral glucose tolerance test (OGTT)
HgA1C
Other blood tests for diabetes
Screening for diabetes
Ongoing assessment—urine tests, tests for renal function

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30
Q

type 2 DM health promotion and maintenance

A

Control of diabetes and its complications is a major focus for health promotion activities

Maintain serum glucose between 80 and 130 mg/dL

Managing lipids to prevent hyperlipidemia, usually through drug therapy (statins)

Ensuring BP is maintained below 140/90 or, in younger patients, below 130/80, usually through drug therapy to manage hypertension

Promoting a healthy lifestyle of smoking cessation, balanced diet, and regular activity or exercise

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31
Q

normal blood glucose levels

A

fasting: 70-100
after eating: 170-200
2-3 hours after eating: 120-140

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32
Q

impaired glucose blood glucose levels

A

fasting: 101-125
after eating: 190-230
2-3 hours after eating: 140-160

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33
Q

diabetic blood glucose levels

A

fasting: 126 +
after eating: 220-300
2-3 hours after eating: 200 plus

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34
Q

general management of A1C level

A

the higher the A1C the higher the blood glucose is
A1C of 6 is = BG 126 (diabetic)

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35
Q

The priority collaborative problems for patients with diabetes DM include

A

Potential for injury due to peripheral neuropathy
Potential for injury due to hypoglycemia
Potential for kidney disease due to reduced kidney perfusion
Potential for surgical complications due to health complexities with DM
Potential for acute complications associated with glucose related emergencies

36
Q

treatment options for type 2 DM

A

Medication therapies (ie metformin)
Insulin
Nutritional considerations
Exercise
Surgical intervention (such as transplantation)

37
Q

diabetic agents specific to Type 2 DM

A
  • biguanides: Metformin (hold 24 hours for contrast dye) (PO)
  • sulfonylureas: Glipizide (watch for hypoglycemia; need to eat with this med) (PO)
  • GLP-1 Agonists: Liraglutide, Semaglutide (SQ)
  • Insulin (SQ)
38
Q

GLP-1 Agonists

A

Mimic the GLP-1 hormone that is naturally released in the gastrointestinal tract in response to eating
Regulate appetite by sending signals to the brain to tell the body it is full

39
Q

which GLP-1 agonists are FDA approved for patients without DM?

A

Liraglutide and semaglutide are approved by the FDA for weight loss in patients without DM

40
Q

GLP-a RAs are effective in: (effects)

A

Improved weight loss
Low risk for hypoglycemia
Reduction in glycated hemoglobin (HgA1c)

41
Q

types of insulin

A

Rapid-acting: Lispro, Aspart
Short-acting: Regular
Intermediate-acting: NPH
Long-acting: Glargine, Detemir
Ultra long-acting: Degludec
Combined – NPH 70/30

42
Q

insulin onset, peak, duration: insulin aspart

A

onset: 10-20 min
peak: 1-3 hr
duration: 3-5 hr

43
Q

Injection sites for insulin

A

adipose tissue in
- abdomen
- back of the arms
- top of the buttocks
- top of the quads

*rotate sites!!

44
Q

complications of insulin therapy

A
  • lipoatrophy
  • lipohypertrophy
  • dawn phenomenon
  • somogyi’s phenomenon
45
Q

lipoatrophy

A

Loss of fat tissue at area of repeated injections
Immune reaction to impurities of insulin
Treatment - inject at edge of atrophied area
** complication of insulin

46
Q

lipohypertrophy

A

ncreased swelling of fat at area of repeated injections
Treatment – rotate sites
** complication of insulin

47
Q

dawn phenomenon

A

hyperglycemia in early morning (at dawn) due to night-time release of the growth hormone (adrenal hormone), no hypoglycemia during the night

RX: increase dose of nighttime insulin to prevent hyperglycemia in the morning

48
Q

somogyi’s phenomenon

A

hyperglycemia in the morning; hypoglycemia in the night in response to bedtime insulin, the body has a rebound effect by mobilizing glucose

RX: decrease dose of nighttime insulin and make sure that they have a bedtime snack to prevent hypoglycemia overnight (which leads to hyperglycemia in the morning)

49
Q

alternative methods of insulin administration

A
  • continuous SQ infusion
  • injection devices (pens- dial it to a certain number)
  • new technology
  • continuous blood glucose monitoring systems: dexcom- continuous glucose monitoring- readings on cellphone, sensor applied to SQ tissue
  • pancreatic transplants
50
Q

patient education for insulin

A

Insulin storage: kept in the refrigerator to maintain potency
Dose preparation: make sure patient is capable of drawing up or get the pens
Syringes: orange marked in units
Blood glucose monitoring: morning and night (with meals)
Infection control measures: washing hands before checking sugars/injecting insulin
Diet therapy: use dietician, educate number of carbs

51
Q

nutrient balance with diabetics:

A

carbohydrates (breads, pasta, potatoes)
protein
fat

Alcohol consumption affects blood glucose levels
- Levels are not affected by moderate use of alcohol when DM is well controlled
- Teach patients that two alcoholic beverages for men and one for women can be ingested with, and in addition to, the usual meal plan
- When alcohol is consumed by adults taking insulin or an insulin stimulation drug, the risk for delayed hypoglycemia is increased

When a diabetic is sick, nutrition is altered as is metabolic rate – check glucose more frequently

Share diet information with person who prepares meals

Screening for food insecurity should be done frequently

52
Q

carbohydrates include

A

Starch and sugar: Complex and simple carbohydrates
Glycemic index
Fiber
Sugar substitutes: Nutritive and nonnutritive

53
Q

diet management

A

General planning according to type of diabetes
Develop plan to meet individual needs
- Food exchange system
- Carbohydrate counting

54
Q

exercise therapy

A

Regular exercise is an essential part of a diabetic treatment plan
Benefits of exercise: lowers glucose level in the blood, weight loss
Exercise in the presence of long-term complications of diabetes
Assessment before initiating an exercise program
Guidelines for exercise: check sugar and eat something with carbohydrates before exercising to prevent hypoglycemic episode

55
Q

proper foot care

A

Foot injury is the most common complication of diabetes leading to hospitalization
Prevention of high-risk conditions
Neuropathy – keep blood sugar in normal range to delay ulcers and amputations
Peripheral sensation management – examine at least yearly
Footwear - shoes with soles
Foot care: washing feet, dry between toes, no lotion between toes (don’t want bacteria); see pediatrist a few times a year

56
Q

testing sensation of the feet: locations

A

ball of the foot (few locations), and on bottom of big toe
- testing for neuropathy
- want patient keep their eyes closed during the test so that they can’t see when you’re touching

57
Q

ineffective tissue perfusion: renal- interventions

A

Control of blood glucose levels
Yearly evaluation of kidney function (usually done more than once a year- any time they get blood work)
Control of blood pressure and cholesterol (high BP and high cholesterol = heart attack risk)
Prompt treatment of UTIs
Avoidance of nephrotoxic drugs (NSAIDs- motrin every day)
Diet therapy (carb-controlled diet; if have HTN: low sodium too)
Smoking cessation (decreases blood perfusion to kidneys)

58
Q

acute complications of diabetes

A

Hypoglycemia from too much insulin or too little glucose (not eating enough carbs)
Diabetic ketoacidosis: acute complication of extremely elevated blood glucose
Hyperglycemic-hyperosmolar state (HHS): acute complication of extremely elevated blood glucose

59
Q

high blood glucose (hyperglycemia) symptoms

A

thirst*
hunger*
frequent urination*
dry skin
fatigue
nausea
blurred vision
headache
nervousness
confusion

3 Ps: polydipsia (thirsty), polyphagia (hungry), polyuria (pee a lot)
*pts typically don’t show systems if elevated 150-200s, sx around 500

60
Q

causes of high blood glucose

A

too much food
too little exercise
too little medicine
stress
illness
injury
short time between meals and snacks

61
Q

low blood glucose (hypoglycemia) symptoms

A

*shakiness
*sweaty
*hungry
anxiety
nervousness
confusion
acting angry or irritable
slurred speech
headache
double vision

*more common to show sx than hyperglycemic patients

62
Q

causes of low blood glucose

A

too little food
too much medicine
more activity than usual
too long between meals or snacks
alcohol

63
Q

hypoglycemia onset

A

rapid, 1-3 hours

64
Q

hypoglycemia: blood sugar level

A

< 70mg/dL

65
Q

diet therapy for hypoglycemia

A

carbohydrate replacement

66
Q

drug therapy for hypoglycemia

A

glucagon injection
50% dextrose through IV

67
Q

prevention strategies for hypoglycemia

A

control insulin excess
avoid deficient food intake
monitor insulin/eat before exercise
avoid alcohol

68
Q

hypoglycemia: home management

A
  1. eat/drink 15g carbs = 4 oz juice/milk + graham crackers
  2. wait 15 minutes
  3. check blood glucose levels
  4. less than 70mg/dL? repeat steps 1-4
69
Q

diabetic ketoacidosis (DKA)

A

Defined by uncontrolled hyperglycemia, metabolic acidosis, and increased ketones
Results from insulin deficiency and metabolizing triglycerides and amino acids for energy
Severe dehydration and electrolyte loss

70
Q

diabetic ketoacidosis (DKA) s/sx

A

Fruity breath,
vomiting,
three P’s,
Kussmaul respirations

71
Q

hyperglycemic-hyperosmolar state (HHS)

A

Extremely high glucose levels and osmotic diuresis
CNS impairment – confusion to coma
Pt still has some insulin so DKA does not develop

72
Q

key treatment of hyperglycemic-hyperosmolar state (HHS)

A

IVF rehydration and reduction of glucose is key

73
Q

people with diabetes need essential skills and knowledge of:

A

Understand nature of diabetes
Nutrition: Develop sound food plan
Insulin: Know type, duration of action, combinations
Monitor glucose levels
Control emergencies, illness (make sure that they are checking their sugar levels and taking meds even if they are sick, ie with the flu)
Identification bracelet (that says diabetic)

74
Q

evaluation of a diabetic patient

A

Achieve blood glucose control
Avoid acute and chronic complications of diabetes
Avoid injury
Experience relief of pain
Maintain optimal vision (eye doc on yearly basis)
Maintain a urine output in the expected range (BUN/creatinine on yearly basis- to assess kidney fx)
Have an optimal level of mental status functioning
Have decreased episodes of hypoglycemia
Have decreased episodes of hyperglycemia

75
Q

diagnosis of diabetes (reading value)

A

2 fasting glucose readings > 126

76
Q

HgA1C purpose

A

average blood glucose over the past 3 months

76
Q

normal HgA1C

A

goal < 7

77
Q

difference between type 1 and type 2 DM

A

type 1: body does not make insulin
type 2: body makes insulin, but does not respond to it (immune)

78
Q

insulin onset, peak, duration: insulin glulsine

A

onset: 10-15 min
peak: 1-1.5 hr
duration: 3-5 hr

79
Q

insulin onset, peak, duration: insulin lispro (humalog)

A

onset: 15-30 min
peak: 0.5-2.5 hr
duration: 3-6 hr

80
Q

insulin onset, peak, duration: regular insulin

A

onset: 30-60 min
peak: 1-5 hr
duration: 6-10 hr

81
Q

insulin onset, peak, duration: NPH insulin

A

onset: 60-120 min
peak: 6-14 hr
duration: 16-24 hr

82
Q

insulin onset, peak, duration: insulin glargine U-100

A

onset: 70 min
peak: none
duration: 18-24 hr

83
Q

insulin onset, peak, duration: insulin detemir

A

onset: 60-120 min
peak: none
duration: 12-24 hr

84
Q

insulin onset, peak, duration: insulin degludec

A

onset: 30-90 min
peak: none
duration: 24+ hr

85
Q

what is important about fast-acting insulin?

A

patients need to eat within onset period so that their blood sugar does not bottom out (about 15 minutes)

86
Q

neuropathy

A

impaired sensation in the feet as a complication of diabetes
- safety issues, falling, can’t feel their feet, burns (temperature of shower)

NU 340 (26 decks)

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