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Nursing 20G > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is diabetes?

A
  • Abnormal insulin production
  • impaired insulin utilization
  • or both
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2
Q

What cells signal the release insulin?

A

Pancreas
*glucuse breakdown and absorption

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3
Q

What does diabetes lead too?

A

High blood sugar levels which can damage organs, b.v, nerves

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4
Q

What is type I DM?

A

The pancreas is unable to produce insulin (insulin is absent)

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5
Q

What is type II DM?

A

Pancreas does not produce insulin or the body does not effectively use the insulin that is produced.
- insulin insufficient
- insulin poorly utilized

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6
Q

Where is the pancreas located?

A

Behind the lower part of stomach

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7
Q

What hormones in the Islet of Langerhans?

A

Insulin secreted by beta cells
Glucagon secreted by alpha cells

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8
Q

What is fct of pancreas?

A
  • Endocrine: manage blood sugar leveles
  • Exocrine: enzymes that break down food
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9
Q

What effect does insulin have?

A

A hypoglycemic effect

After eat a meal:
1. Blood glucose increase
2. pancreas secrete insulin from beta cells
3. Insulin key: allow glucose to leave blood and enter cells.

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10
Q

What stops the pancreas from secreting insulin?

A

When blood glucose stabilizes.

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11
Q

What is the effect of glucagon?

A

Hyperglycemic effect

  • Antagonist to insulin
  • Lvls of glucose low: glucagon secrete from islets of Langerhans
  • stimulate LIVER to break down glycogen to be released
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12
Q

When would glucose lvls be low?

A

If individual not eaten or overnight

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13
Q

What is done with excess glucose?

A

Stored as glycogen in liver (skeletal muscle) => remain until body needs it

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14
Q

What is normal condition of glucose?

A

Continuously released into blood stream in small increments (basal rate) => meet need for quick energy.

W/increased bolus when food ingested

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15
Q

What is average amount of insulin secreted die?

A

40-50 units

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16
Q

What are the ranges for insulin secretion?

A
  • 1hr after meal: insulin concentration rises rapidly
  • After, insulin decline bc carb absorption from GI tract decline
  • After carb absorption and night: [insulin] low and constant
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17
Q

What is the normal level of glucose level?

A

Balance b/w insulin and glucagon
4-6 mmol/L
- No caloric intake for at least 8 hours

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18
Q

What is HbA1C (glycosylated hemoglobin)?

A

<6.5% in adults
Average of blood glucose in past 2-3 months
Determine glycemic control over
Hgb last 120 days
- What % of Hgb coated in glucose
- Higher A1c = poorer blood sugar control

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19
Q

What is fasting plasma glucose lvl (FPG)?

A

4-6 mmol/L (no caloric intake for 8 hrs)

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20
Q

What is oral glucose tolerance test (OGTT)?

A

<11.1 mmol/L
- Glucose given orally and test done 1 hr after

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21
Q

What is random blood glucose lvl?

A

< or equal to 11.1 mmol/L taken at any time of the day

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22
Q

What are urine ketones

A

Poor use of glucose for energy and using fat as source of energy. Not be present within urine

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23
Q

Urine glucose?

A

elevated urine levels (glycosuria) is an indicator of diabetes

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24
Q

Urine proteins

A

kidney damage

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25
Q

Type 1 diabetes

A
  • progressive destruction of beta cells in Islets of Langerhans (months to years before onset)
  • immune sys attacks and kills the beta cells of pancreas
  • Absence of insulin: insulin deficiency
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26
Q

When type 1 DM dev?

A
  • generally before 30 years of age
  • not preventable
  • approx 10% of ppl have DM I
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27
Q

How manage type 1?

A

Insulin SC (exogenous insulin => outside source)
- Insulin-dependent: need it to survive

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28
Q

Clinical manifestation type 1?

A

Elevate plasma glucose lvls
- Polyuria
- Polydipsia (excessive thirst)
- Polyphagia (excessive hunger)

fatigue, weight loss, lack energy

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29
Q

What type 2 DM?

A

some endogenous => inside body insulin (insufficient), inefficient use of insulin
- Insulin resistance: insulin receptors unresponsive
- in ppl over 35 years old
- 90% of people w/diabetes

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30
Q

Clinical manifestation type 2?

A

Early stages: no symptoms => when have symptoms (gradual or very subtle)

  • feeling tired
  • frequent infections (bacteria feed off glucose)
  • blurred vision
  • slow healing of cuts or sores
  • tingling or numbness in hands and feet
  • Slow dev of 3 polys (unnoticed)
  • Dx from MD => elevated fastin plasma glucose lvls
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31
Q

What is prediabetes?

A

high risk for dev DM => prevent diabetes w/appropriate lifestyle changes

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32
Q

What are blood values for prediabetes?

A

HbA1c: 6.0 - 6.4%
Fasting plasma glucose: 6.1-6.9 mmol/L
oral glucose tolerance test: 7.8 to 11.0 mmol/L

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33
Q

What are risks for DM II?

A

Increase risk of heart disease
- prediabetes + HTN +DLP + elevated triglycerides + abd obesity + sedentary lifestly

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34
Q

What are goals of diabetes?

A
  • Nutritional therapy
  • Exercise
  • Self-monitor blood-glucose
  • Drug therapy
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35
Q

How to do SMBG?

A

Self-monitor blood glucose
- Allow pt to do so
- Portable blood glucose meters: disposable lancets and glucose test strips
- better control of blood glucose lvls

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36
Q

What is other terms for SMBG?

A
  • Acuchaeck
  • CBGM: capillary blood glucose monitoring
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37
Q

What to teach pt to when monitoring BG?

A
  1. How and when to perform SMBG
  2. How to record results
  3. Meaning of various BG lvls
  4. How behavior and actions affect SMBG results/
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38
Q

What is the frequency of SMBG?

A

depend individually
- avg: 2-4 times a day for pt w/insulin (before meals, 2 hrs after meals and/or at bedtime)

  • At least die if not receiving insulin
  • When suspect hyper/hypoglycemia
  • Any change in med, activity or health.
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39
Q

What are possible causes of hypoglycemia?

A
  • not enough food
  • excessive exercise
  • too much insulin
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40
Q

What are S&S of hypoglycemia?

A
  • ANS: Trembling, palpations, sweating, anxiety, hunger, nausea
  • CNS: Diffuculty concentrating, confusion, weakness, drowsiness, blurred/doble vision, dizziness, loss of consciousness
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41
Q

What is mild hypoglycemia?

A

ANS present: Trembling, palpations, sweating, anxiety, hunger, nausea
- individual able to self treat

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42
Q

What is moderate hypoglycemia?

A

ANS and CNS symptoms
- able to self treat

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43
Q

What is severe hypoglycemia?

A
  • assistance of another prs
  • may be unconscious
  • plasma glucose <2.8 mmol/L
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44
Q

What are steps to address hypoglycemia?

A
  1. Recognize symptoms
  2. Conform blood glucose <4 mmol/L
  3. Treat with fast sugars (15 g)
  4. RETEST in 15 min for BG >4 mmol/:
  5. Eat snack or meal
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45
Q

What is the 15:15 rule

A
  • Eat 15 g of fast sugar
  • Wait 15 min and check again

Do three times in hospital before further intervention required

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46
Q

What are examples of 15 g simple carb?

A
  • Glucose tablets
  • 3 teaspoons or 3 packets of sugar in water
  • 175 mL of juice
  • 6 Lifesavers
  • 15 mL of honey ( Tbs)
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47
Q

What do w/severe hypoglycemia (unconscious)?

A
  • No IV => IM or SC glucagon => tell liver to release glucose into bloodstream
  • w/IV: 10-25 g of glucose (220-50 mL of D50W) 1-3 minutes
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48
Q

How to prevent hypoglycemia?

A

Pt education (causes and early signs of hypoglycemia)
- Eat and exercise at reg times
- Always eat smt with alcohol => cause hypoglycemia till up to 24 hrs after + insulin secretion, liver work to remove alcohol from the blood instead of regulating blood sugar

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49
Q

What are the possible causes of hyperglycemia?

A

BG > 7 mmol/L
- Too lil or no diabetes meds
- excessive food intake
- inactivity
- emotional or physical stress
- illness/infection
- some medications (corticosteroids)

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50
Q

What are the clinical manifestations of hyperglycemia?

A

initial: Increased glucose levels > 6 mmol/L
later: classic signs (polyuria, polydipsia, polyphagia) fatigue, drowsiness, weakness

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51
Q

What is blood glucose lvls like in the hospital?

A

Hyperglycemia normal
- 1/3 of pt have hyperglycemia
- pre-existing DM

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52
Q

What are adverse effects of hyperglycemia?

A
  • Increased risk of post-op infections
  • vaginal yeast infections
  • UTIs (glucose in urine)
    => prolong hospital stay => increase resource utilization
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53
Q

What are macrovascular DM complications?

A
  • stroke
  • heart disease & HTN
  • PVD
  • ulcers and amputation
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54
Q

What are microvascular DM complications?

A
  • Diabetic eye disease: retinopathy
  • renal disease (kidney)
  • neuropathy
  • foot problems
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55
Q

How is CV health affected by DM?

A
  • long-term => poor tissue perfusion from b.v. damage
  • DM => elevate cholesterol => vessel damage => atherosclerotic plaque => decrease in arterial supply to tissues => tissue damange or death
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56
Q

What is the vascular protection checklist?

A

A: A1C usually ≤7%
B: BP <130/80
C: Cholesterol - LDL ≤2mmol/L
D: Drug protect heart
A - ACEi or ARB, S - Stain, A - ASA
E: Exercise/Eating healthy
S: Smoking cessation

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57
Q

How does DM affect peripheral arteries disease/peripheral neuropathy?

A

Nerve damage + poor blood flow to legs and feet
- Less likely to feel foot injury (blister or cut)
- make harder to heal
- untreated => amputation

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58
Q

What are complications of foot and lower extremities?

A
  • Sensroy neuropathy: reduced pt awareness
  • PVD: delayed wound helaing
  • Poor vision inability see small lesion
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59
Q

What could nutrition therapy do?

A
  • Reduce HbA1C by 1% to 2%
  • reduce calory intake
  • space out carbs intake regularity in meal consumption control BG and wt
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60
Q

What is an integral part of DM treatment?

A

Nutrition therapy and counselling
- Maintain or improve quality of life
- maintain or improve nutritional and physiological health
- prevent and treat acte and long-term complications of DM

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61
Q

What BMI # should wt loss be done?

A

For Patients with BMI ≥25 kg/m2…
- Nutritionally balanced, calorie-reduce diet be followed for lower, healthier body wt
- wt loss 5-10% of initial body wt
- improve insulin sensitivity, glycemic control, BP, lipid lvls

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62
Q

What is nutritional therapy for DM 1?

A

Meal: plan same as pt usual diet and BALANCED with insulin and exercise
- insulin managed day to day
- assess for hypoglycemia

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63
Q

What is nutritional therapy DM 2?

A

Achieving glucose, lipid and BP goals
- calorie reduction

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64
Q

Why choose healthy fats?

A

Good fat: avocado, nuts, olive oil, fish
- Unsaturated liquid at room temp
- Bad saturated fats: solid at room temp

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65
Q

What health carbohydrates to choose?

A

Dietary fibre: 30-50 g a day
- oats, barley, konjac noodles, beans, peas, chickpeas, lentils, vegetables, fruit, broccoli

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66
Q

How to read labels for carbs and fibers?

A
  1. Look at serving size and the whole amount of the food
  2. Fiber should be substracted from total carbohydrates (not raise BG)
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67
Q

Why to consume less Na?

A

Increase BP bc retains fluid and increases volume
- diuretic to void

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68
Q

What is GI?

A

a ranking of carbs in food and how affect blood glucose lvls.

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69
Q

What does it mean carbs low GI value?

A
  • 55 or less
  • slower release of glucose in blood: no peak and then drop.
  • regulated and gradual BG
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70
Q

What does high GI value mean?

A
  • spike in blood glucose lvl: rapidly digested.
  • Fluctuations in blood glucose lvls
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71
Q

What are examples of low, medium and high GI?

A
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72
Q

What to evaluate effectiveness of diet?

A
  • Blood glucse 2 hrs before and after meal
  • HbA1C lvls: under 6%
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73
Q

What exercise should pt do?

A

decrease med need in DM 2 w/diet and exercise

IF not working then oral meds and then insulin

  • walking
  • in the water: min barriers such as arthritis (walking briskly, swimming)
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74
Q

Cautions for diabetes in exercise?

A
  • Risk of hypoglycemia: highest risk at peek time of med action or if food intake insufficient to maintain blood glucose lvls
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75
Q

Best time for pt to exercise?

A

Blood glucose at peak (~1 hr after meal or snack)
- have fast acting glucose available WHEN exercise

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76
Q

What recommended exercises and time?

A
  • min of 150 mins moderate aerobic exercise per week
  • resistance exercise ≥ 2 times a week
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77
Q

Pre-exercise assessment why?

A

Predisposed to injury before px exercise regimen

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78
Q

What to include in pre-exercise assessment?

A
  • neuropathy: have sensation
  • retinopathy: can see
  • CAD-resting ECG: exercise stress rest
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79
Q

How to do resistance exercise?

A

6-8 exercises for major grp muscles
- 3 sets of 8-12 reps, 1-2 min rest

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80
Q

How to perform aerobic exercises?

A
  • walk: 5-15 min
  • progress over 12 wks to 50 min per session
  • 10 min x3 die
81
Q

What should ppl with diabetes do?

A
  • specific physical activity goals
  • anticipate barriers to physical activity (weather) => dev strategies to overcome barriers
  • record physical activity
  • dev strategies overcome barriers
82
Q

Example of nursing dx?

A

Unmet for nutrition d/t altered metabolism r/t poorly controlled blood glucose

83
Q

What to assess for when dx w/diabetes?

A
  • Medications
  • CV
  • family hx
  • Recent surgery: infection, wound healing
  • symptoms: 3 polys
    - malaise
    - wt loss
    - hunger
    - poor healing
    - Kussmaul’s respirations: ketoacidosis (remove excess CO2), pH lvl, blood lvls acidic
84
Q

What is the nursing dx?

A
  • Ineffective health management
  • Risk for injury
  • Risk for unstable blood glucose levels
  • Risk for peripheral neuro-vascular dysfunction
85
Q

What do you plan for?

A
  • active ct participation
  • few to no ep of hype/hyperglycemia
  • normal BG lvls
  • prevent or delay chronic complications
  • lifestlye adjustments with min stress
86
Q

Who is at risk?

A
  • CV problems
  • fam hx
  • overweight adults at 45 yeards old
  • usually dx of DM 2 @ 35
    screen w/fasting blood glucose lvls preferred
87
Q

What do you implement?

A

Health promotion: identify those at risk, routine screening

88
Q

What are cute implementations?

A
  • Hypoglycemia
  • Diabetic ketoacidosis
  • Hyperosmolar hyperglycemic nonketotic syndrome
89
Q

What are interventions for stress of illness and surgery?

A
  • increases blood glucose level
  • continue reg meal plan
  • inc. intake of noncaloric fluids
  • take oral agents and insulin
  • monitor blood glucose: ketone testing if glucose > 14 mmol/L (need MD order)
90
Q

What are ambulatory and home care?

A
  • care for self at home: monitor blood glucose lvls
  • personal hygiene
  • ## med identification and travel card
91
Q

What to evaluate for?

A
  • Knowledge
  • Balance of nutrition
  • Immune status
  • Health benefits
  • No injuries
92
Q

What is diabetic ketoacidosis (DKA)?

A

Profounds deficiency of insulin
characterized by:
- hyperglycemia
- ketosis
- acidosis
- dehydration

Most likely in type 1

93
Q

What are precipitating factors to DKA?

A
  • lllness
  • infection
  • inadequate insulin
  • poor self-management
94
Q

How is DKA dev?

A

Insulin supply insufficient => glucose unable to be used for energy
- Break down of fats => ketone => urine
- Blood becomes acidic

Prs doing:
- alter pH balance, metabolic acidosis
- removing as much acid as possible (Kussmaul’s breathing and urinating)

95
Q

What is angiopathy?

A

Disease of b/v
macrovascular
- large and med b.v.
- greater frequency and earlier onset in DM
- altered lipid metabolism common to diabetes

96
Q

What are risk factors to aniopathy?

A

risk factors:
- smoking
- obesity
- hypertension
- high fat
- sedentary lifestyle

97
Q

What is microvascular angiopathy?

A

Dislipidemia
- thickening of b.v. membranes and capillaries and arterioles bc of HYPERGLYCIMIA => speciic to DM

98
Q

What is most noticeably affected by microvascular angiopathy

A

Retinopathy: eyes
Neuropathy: nerves
nephropathy: kidneys

99
Q

When do clinical manifestations appear for microvascular angiopathy?

A

10-20 years after DM

100
Q

What is diabetic retinopathy?

A

microvascular damage to retina from hyperglycemia
- Most common cause of new blindneess in ppl of working age

treatment
- laser photocoagulation (prevent further vision loss), vitrectomy (aspirate blood, membrane and fibers inside eye

101
Q

What is nephropathy?

A

Damage to small b.v. that supply kidney
- LEAD to end-stage renal disease

102
Q

How to prevent nephropathy?

A
  • Tight glucose control
  • Blood pressure management
  • Angiotensin-converting enzyme (ACE) inhibitors => Used even when not hypertensive
  • Angiotensin II receptor antagonists
103
Q

What are interventions for diabetic nephropathy?

A

yearly screening: microalbumin in urine, serum creatinine

104
Q

What is diabetic neuropahty?

A
  • 40-50% have degree of neuropathy
  • due METABOLIC derangements of DM
  • distal symmetric => affect bilateral hands and feet
    Characteristic: loss of sensation, abn sensation, pain, paresthesias
  • foot injury and ulcers without pt having pain
  • atrophy of small muscles
105
Q

Treatment of neurpathy drugs?

A

TIGHT BG control

drug therapy:
- Topical creams
- Tricyclic antidepressants
- Selective serotonin and norepinephrine reuptake inhibitors
- Antiseizure drugs

106
Q

What are autonomic diabetic neuropathy complications?

A

Affect nearly all body sys

complications: gastroparesis (delayed gastric emptying, CV abnormalities

  • Alter sexual fct & neurogenic bladder
  • Foot complications: most common cause of hospitalization (micro&macro vascular disease)
107
Q

What do you implement?

A

Health promotion: identify those at risk, routine screening

108
Q

What values to dx pt in FPG?

A

Fasting Plasma Glucose: ≥7 mmol/L (no caloric intake for 8hrs)

109
Q

What values to dx in HgA1c?

A

≥6.5% in adults

110
Q

What values in random blood glucose for dx?

A

≥ 11.1 mmol/L

111
Q

What is antidiabetic drug for DM I?

A

Insulin => always required for DM I
- pt endogenous insulin absent

112
Q

What is antidiabetic drug for DM II?

A

Inadequate insulin for their needs

Antihyperglycemic agents +/- insulin PRN

113
Q

What do the antidiabetic drugs aim to produce?

A
  • normoglycemic state
  • euglycemic state

=> NORMAl BG

114
Q

What is the purpose of glucose?

A

No a cure for DM
- control hyperglycemia

Goal: TIGHT glucose control
- reduce long-term complications

115
Q

Where does originate from?

A
  1. From domesticated animals: pigs (porcine insulin)
116
Q

How is insulin made in lab?

A

Synthesized using RECOMBINANT DNA tech
- from common bacteria or yeast cells
- human biosynthetic insulin

117
Q

How to alter pharmacokinetic properties of Human Insulin?

A

Onset, peak, duration

  • Adding zinc, acetate buffers and protamine to insulin => diff insulin preparations
118
Q

What are the four major classes of insulin?

A
  1. Rapid Acting
  2. Short ACting
  3. Intermediate
  4. Long acting
119
Q

What are rapid-acting insulin?

A

lispro (Humalog)
aspart (NovoRapid)
glulisine (Apidra)

appearance: clear, colourless

120
Q

What is onset of rapid acting?

A

10-15 min

121
Q

What is peak action of rapid acting insulin?

A

1 to 2 hours

122
Q

What is duration of action?

A

3 to 5 hours

123
Q

When to admin rapid-acting insulin?

A

Admin 0-15 ac meals (before)

124
Q

What are short acting insulin?

A

Reg insulin
(Humulin R, Novolin ge, Toronto)

appearance: clear, colourless

125
Q

What is onset of short acting?

A

30 min

126
Q

What is peak action?

A

2 to 3 hours

127
Q

What is duration of action?

A

6.5 hours

128
Q

When to admin short-acting insulin?

A

30 mins before a meal
ONLY insulin admin IV route

129
Q

What are characterisitcs of rapid and short acting insulin?

A
  • admin in association w/meals => control BG rise after meals
  • Glycemin control b/w meals and at NIGHT, rapid/short acting insulin used w/intermediate OR long-acting insulin => TYPE I
130
Q

What are intermediate-acting insulin?

A

Isophane insulin suspension (Humulin N, Novolin, NPH)
- cloudy, white

131
Q

What is onset of intermediate acting insulin?

A

1-3 hours

132
Q

What is peak action of intermediate insulin?

A

5-8 hours

133
Q

What is duration of intermediate insulin?

A

up to 18 hours

134
Q

How intermediate insulin combined?

A

Combined with regular insulin to reduce amount of injection die

135
Q

How is intermediate insulin release longer?

A

Conjugating regular insulin with protamine (large protein) => delay absorption
- Onset delayed and duration of action extended

136
Q

What are long acting insulin?

A

glargine (Lantus)
detemir (Levenir)

clear/colorless

137
Q

What is onset of long acting insulin?

A

90 min

clear/colorless

138
Q

What is peak of long acting insulin?

A

NO peak (hypoglycemia risk reduced)
- constant lvl of insulin in body

139
Q

When to admin long acting insulin?

A

glargine admin at bedtime
detemir admin 1-2 x die

140
Q

What to know about detemir?

A

long-acting insulin
- duration of action: dose dependent
- lower doses => bid
- higher doses => die

141
Q

What more to know about long acting insulin?

A

Slow onset and prolonged duration => provide BASAL GLYCEMIC CTRL
- NOT meant control hyperglycemia immediately after meal

142
Q

What does an insulin regimen look like?

A

combo of…
- rapid/short acting insulin => manage surges of BG after meals
- intermediate or long-acting insulin => period b/w meals when blood glucose lvls are lower

require: mixing and admin of diff types of insulin

143
Q

What insulin are you able to mix?

A

Insulin NPH in longer-acting insulin (intermediate) MIX with rapid or short acting-insulin

144
Q

Can you mix detemir or glargine?

A

NO bc pH incompatible

145
Q

What are premixed insulins?

A

Fixed ratio of insulin: % of rapid or short-acting insulin to intermediate-acting insulin

146
Q

What is bolus insulin?

A

Insulin taken at meal times to keep blood glucose lvls under control following a meal
- Act quickly and short-acting insulin or rapid insulin

147
Q

What is basal insulin?

A
  • keep BG consistent lvls during fasting periods
  • act over long period of time: long or intermediate acting insulin
148
Q

What is sliding-scale insulin dosing?

A

Doses of short-acting (reg) or rapid-acting (lispro or apart) insulins adjusted based off of BG results

149
Q

Where is sliding-scale insulin dosing used?

A

Hospitalized pt: insulin requirement vary
- stress: infection, surgery, acute illness
- inactivity

150
Q

What is the sliding scale like?

A

For Humulin R SC
Blood glucose ≤ 10 0 units
Blood glucose 10.1 – 12.0 2 units
Blood glucose 12.1 – 14.0 4 units
Blood glucose 14.1 – 16.0 6 units
Blood glucose 16.1 – 18.0 8 units
Blood glucose ≥ 18.1 10 units and call MD

151
Q

What to do when insulin sliding scale used at bedtime?

A

Admin HALF of indicated dose => check cap refill glucose after 2hrs of injection

152
Q

What to know abt PO insulin admin?

A

Insulin inactivated by gastric juices => not taken PO

USUALLY SC (syringe, insulin pen, or continuous SC infusion)

153
Q

What can be given by IV?

A

Only regular insulin

154
Q

How to admin insulin SC using a syringe?

A
  • only use insulin syringes => calibrated in units + 28-29G and 1/2” length
  • Admin at 90 degree angle unless emaciated (abn thin) => 45 degree
155
Q

What is the concentration of insulin?

A

Number of units per mL of insulin

156
Q

How to admin NPH or pre-mixed insulin?

A
  • Cloud appearance

before prep dose
- NOT shake => roll b/w hands (avoid air trapped in syringe and inaccurate dose admin

157
Q

What are insulin pumps?

A
  • computerized devices
  • Insulin doses delivered through catheter => through skin => S/C tissue of abd
  • Alternative to multiple insulin injections
158
Q

When to change catheter sie infusion?

A

Change q3 days around 1” away from old one

159
Q

How to program pumps?

A

Programmed to release small doses of insulin continuously (basa) and/or a bolus dose close to mealtime
-> closely mimic body’s natural release of insulin

160
Q

How to set a basal lvl in insulin pump?

A

Infuse insulin continuously at a slow but steady rate

161
Q

How does pump provide bolus dose?

A

Match in size to the carbohydrate content of each meal => could be triggered manually

162
Q

What is used in insulin pumps?

A

regular, lispro, aspart, glulisine

163
Q

How to store unopened insulin?

A

Vials and pen catridges => up to three months in the fridge

164
Q

How to store insulin when opened?

A

Room temperature for up to one month

165
Q

How to never admin insulin?

A

Cold => trigger tissue atrophy

166
Q

What is lipodystrophy?

A

Tissue become hardened (lumps) w/orange peel appearance

167
Q

What does lipodystrophy do?

A

Alter insulin absorption, delay onset
- result if same site injection are used repeatedly

168
Q

How is lipodystrophy resolved?

A

Area unused for min of 6 months

169
Q

What is current practice for injection sites?

A
  • Rotation to diff anatomical site not recommended => variability in insulin absorption
  • enter blood at diff speed in diff site injections
170
Q

What is best practice site for insulin injection?

A

Abd => insulin work fastest
- insulin arrive a little more slowly from upper arms and more slowly from thighs and buttocks

171
Q

Site rotation

A
172
Q

What is recommended for each mealtime injection?

A

Ex:
breakfast insulin injecxtion => abd
supper ac insulin injection => leg die

=> give more BG results

173
Q

What to know about allergies?

A

Allergies to insulin rare bc of human insulin creation
- Zinc and protein are used as preservatives in insulin and latex rubber stoppers

174
Q

What are insulin adv effects

A
  • hyperglycemia, lipodystrophyl, allergic rxn, insulin insensitivity
175
Q

What are potential drug interactions that anatogonize hypoglycemic effect?

A
  • Antagonize hypoglycemic effects of insulin: cortico steroids, thyroid gland, furosemide => elevated BG lvls
176
Q

What are drug interactions that increase BG lvls?

A
  • Increase hypoglycemic effect => lower blood glucose lvls, alcohol, saulfa antibiotics, salicytes
177
Q

What are families for oral antihyperglycemic agents?

A
  • decrease amount of glucose release by the liver
  • increase amount of endogenous insulin produced by the pancreas
  • improve way endogenous insulin is used (decrease insulin resistance)
  • delay intestinal absorption of glucose
178
Q

Can DM I use oral hyperglycemic agents?

A

No, pt must have some circulating endogenous insulin

179
Q

What are biguanide?

A

metformin (Glucophage)
- commonly used for DM II
- first-line drug

180
Q

What is primary action of metformin?

A

Decreases glucose production by the liver
- Lower amount of glucose released into the blood by the liver

181
Q

What is metformin commonly used w/?

A

sulfonylurea agents when each drug not results in adequate glycemic control

182
Q

What are adverse effects of metformin?

A

GI tract
- abd bloating, nausea, cramping, feeling fullness and diarrhea

not cause hypoglycemia => not stimulate pancreas to release insulin

183
Q

Who is well suited for metformin?

A

Ppl who skip meals: not lower blood glucose any further

184
Q

What is a rare but serious risk in for biguanide?

A

Lactic acidosis => use consciously w/pt w/renal insufficiency

185
Q

When to withhold metformin?

A

if pt requires any test that uses contrast medium (increased risk for nephrotoxicity)
- resume when serum creatinine lvls have been assessed.

186
Q

What are sulphonylureas?

A

glyburide (Diabeta)
gliclazide (Diamicron)

187
Q

What is the prim actino of sulphonylureas?

A

Stimulate insulin production and secretion by the beta cells of the pancreas
- Helps the pancreas to make more insulin

  • Lower BG lvls in pt when diet and lifestyle have failed and A1C lvls remain elevated
188
Q

What is the most frequent adverse effects?

A

Hypoglycemia

Effect GI sys: N, epigastric fullness, heartburn, increased appetite

189
Q

What are meglitinides?

A

repaglinide (GlucoNorm)
nateglinide (Starlix)

190
Q

What is the actions of meglitinides?

A

Structurally diff than sulfonylurea
- increase insulin production and secretion by beta cells of pancreas

191
Q

What to know about duration of action in meglitinides?

A

Quicker and shorter duration of action: less chance of hypoglycemia bc of BG

192
Q

What are thiazolidinediones (glitazones) ?

A

rosiglitazone (Avandia)
pioglitazone (Actos)

193
Q

what is the prim action of thiazolidinediones (glitazones)?

A

Not increase insulin ffrom pancreasa

  • enhance sensitivity of insulin receptors
  • allows cells to respond to available endogenous insulin more efficiently
  • increased glucose uptake by muscle and adipose tissue
194
Q

What are α-Glucosidase Inhibitor examples?

A

acarbose (Glucobay)

195
Q

What are α-Glucosidase Inhibitor?

A
  • “starch blockers” slows/delays absorption of carbs from small intestine => smaller increase in BG glucose lvls
  • glucose absorbed into blood more slowly
  • enzymes break down carbs = inhibited
196
Q

When is What are α-Glucosidase Inhibitor admin?

A

Beginning of each meal (first bite)
- med cannot directly lower fasting blood glucose

197
Q

What are Incretin enhancers examples?

A

sitagliptin (Januvia)

198
Q

What are Incretin enhancers?

A

enhacne incretin hormones (endogenous compounds )
1) stimulate release of insulin
2) suppress release of glucagon

Nursing 20G (5 decks)

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