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Nursing Semester 2 > Monica - Week 7 - Exam 2 > Flashcards

Monica - Week 7 - Exam 2 Flashcards

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1
Q

what is diabetes mellitius?

A
  • CHO metabolism disorder

- ↑ blood glucose d/t inability to produce or utilize insulin

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2
Q

what are 2 major risk factors for diabetes?

A

obesity and sedentary lifestyle

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3
Q

T/F diabetes is preventable and reversible in pre-diabetes stage

A

TRUE, BUT once you have actual diabetes → it can’t be cured; it can be managed

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4
Q

why is diabetes called a multi-factorial, multi-organ condition?

A

chronic ↑ in BG overtime can cause damage to other systems → CVD, renal damage, PVD, eyes (diabetic retinopathy), and nervous system disorders (peri. neuropathy)

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5
Q

diabetes is the leading cause of ____? (3)

A

blindness, renal failure, and non-traumatic lower extremity amputations

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6
Q

what are the immediate complication of hyperglycemia?

A
  • ↓ immune function and wound healing (↓ WBC function efficiently → less able to fight infection)
  • ↑ coagulability (thromboembolic events)
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7
Q

what are the long-term MICROvascular angiopathy and arteriosclerosis of hyperglycemia?

A
  • retinopathy (small hemorrhage, cotton wool spots → blindness)
  • neuropathy ( sensory motor nerves; ↓ blood flow → demylenation and degeneration)
  • nephropathy = microalbuminuria/proteinuria (leading cause of KF in adults; damage to capill. (filter) → hyperpermeable → protein released in urine)
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8
Q

what is arteriosclerosis?

A

narrowing d/t the inflammation of arterial line

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9
Q

what are the long-term MACROvascualar angiopathy?

A
  • coronary = angina, MI (leads to chest pain, ↓ O2 = MI)
  • cerebral = TIA, CVA (↓ O2 to brain→TIA “mini stroke”; ↑ risk for CVA cerebrovascular accident)
  • peripheral = peripheral vascular disease (PVD), limb loss
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10
Q

T/F diabetic’s TPA (natural clot buster) is effected, so they are not able to break down clots.

A

TRUE

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11
Q

what cells produce insulin?

A

beta cells

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12
Q

what stimulates an insulin release?

A

blood glucose rise

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13
Q

what happens to excess glucose?

A

converted to glycogen or converted to fatty acids

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14
Q

an inability to make insulin, failure to control BG, or insulin resistance is characteristics of ?

A

diabetes

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15
Q

what do alpha cells produce?

A

glucagon (counteracts insulin secretion and ↑ BG)

  • glycogenolysis (break down of gly in liver)
  • gluconeogenesis (make new glucose from fat/amino acids → ketones → DKA)
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16
Q

Type 1: where is is most common?

A

most common in children and adolescents < 20y/o

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17
Q

Type 1: possible causes?

A

genetic predisposition or autoimmune response (destruction of beta cells)

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18
Q

Type 1: characterized by?

A

a complete lack of endogenous insulin

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19
Q

Type 1: treatment?

A

need long term insulin therapy

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20
Q

Type 1: presenting condition?

A
  • hyperglycemia (700-800)

- DKA

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21
Q

Type 2: can still make endogenous insulin but ______?

A
  • not making enough = glucose can’t move into cell
  • tissues poorly using insulin (cellular resistance)
  • or both
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22
Q

Type 2: when there is a cellular resistance to insulin the liver attempts to _____–?

A

compensate by making more → hyperinsulinemia → beta cell exhaustion → blood sugars slowly rise

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23
Q

Type 2: contributing factors?

A

obesity and physical inactivity

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24
Q

Type 2: treatment?

A

may need oral and/or insulin treatment

***↑ exercise → can make cells more sensitive to insulin, weight loss, ↑ glucose use, good for ♥; ↑ HDL and ↓ LDL`

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25
Q

look at process map

A

understood

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26
Q

what are the uncontrollable risk factors of diabetes?

A
  • age
  • family hx of type 2 DM
  • hx of GDM
  • ethnicity (african-american, asian-american, hispanic, and native american) → ↑ rate of obesity
  • genetic mutation → insulin resistance
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27
Q

what are the controllable risk factors of diabetes?

A
  • obesity
  • lack of physical inactivity
  • metabolic syndrome (3 of each factor)
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28
Q

what are the characteristics of metabolic syndrome?

A
  • ↓ HDL
  • ↑ glucose levels, ↑ BP, ↑ triglycerides
  • abdominal obesity
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29
Q

what are the complications of metabolic syndrome?

A

CAD, PVD, thrombotic events.

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30
Q

what are the 5 different tests to diagnose diabetes?

A
  • fasting glucose (8hr fasting)
  • random glucose (anytime, non-fasting)
  • fingerstick blood glucose (FSBG - used in conjunction w insulin - not as reliable)
  • oral glucose tolerance test (OGTT)
  • glycosylated hemoglobin (hbg A1C/A1C)
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31
Q

what occurs in a OGTT?

A
  • ingest a 75g glucose load drink and assess BG 2 hrs later (challenge test)
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32
Q

what occurs in a Hbg A1C?

A

looks at BG control over the preceding 3 months → glucose attaches to Hbg molecule and stays on for the life of the cell)
shows effectiveness of diabetic therapy

33
Q

what is the normal, prediabetes, and diabetes levels for fasting blood glucose?

A

N: = 99
PD: 100 - 125
D: >/= 126

34
Q

what is the normal, prediabetes, and diabetes levels for HgA1C?

A

N: = 5.6
PD: 5.7 - 6.4
D >/= 6.5

35
Q

what is the normal, prediabetes, and diabetes levels for 2 hr post OGTT?

A

N: = 139
PD: 140 - 199
D: >/= 200

36
Q

what is the normal, prediabetes, and diabetes levels for random blood glucose?

A

N: NA
PD: NA
D: >/= 200 + symptoms (polydipsia, polyuria, polyphagia)

37
Q

what are the three way to lifestyle mainstays?

A
  1. following a meal plan
  2. increasing activity level + weight loss (if needed)
  3. self-monitoring of BG
38
Q

what 3 characteristics of following a meal plan?

A

• Balance CHO intake with pancreas function or insulin
injections
• Reduce demand on pancreas
• Reduce post-prandial BG spikes and A1c

39
Q

what 2 characteristics of ↑ activity and ↓ weight?

A
  • Reduce blood glucose directly

* Reduce insulin resistance

40
Q

what 2 characteristics of self monitoring BG?

A
  • Identify individual patterns and help target therapy

* Routine monitoring of glucose levels and A1c

41
Q

Protein: glucose effects

A
  • Very little converted to glucose
  • Stimulates some insulin secretion
  • Slows digestion
  • Intake: 15-20% calories/day
42
Q

fat: glucose effects

A
  • Slows digestion, slow ↑ of BG
  • Blunts post meal spike; ↑ risk of CVA
  • Promotes satiety
  • Less saturated fat (<7%)0
  • Poly- and monounsaturated
  • Low cholesterol, low Na+
  • Intake: 25-30% calories/day
43
Q

alcohol: glucose effects

A
  • Inhibits gluconeogenesis - good in some way; can cause hypoglycemia in conjunction w/ insulin or oral drug
  • Best to drink with meals
  • Sugar-free mixes
  • Dry, light wines
44
Q

CHO: glucose effects

A 
• Greatest effect on post-prandial
spikes
• Whole grains, fruits, veggies
healthier 
• Daily allowance 130 gm/day
• Intake: 50% of calories/day
45
Q

3 different methods of CHO counting?

A
  • consistent CHOs
  • “exchange” list system
  • myPlate
46
Q

what are the 3 characteristics of consistent CHOs?

A
  • CHO load divided equally into 3-4 meals
  • 1 serving of CHO = 15 grams
  • 45-60 grams/meal and 15-30 grams/snack
47
Q

what are 2 characteristics of exchange list system?

A

• 1 serving of food choice = 15 grams of CHO
• food choice can be exchanged for another within list
ex: 1 ear of corn for 1/3 cooked pasta

48
Q

what is myPlate system?

A

• ½ plate with veggies and fruit, ¼ starch, ¼ protein, dairy

49
Q

what are food items with 15 grams of CHO?

A

1 slice bread, ½ c. cooked oatmeal, ½ banana,
1 small baked potato, ⅓ c. cooked beans or rice,
½ c. croutons, 1 small apple, 1 c. milk, ½ c. fruit juice

50
Q

what is the indication for metformin?

A
  • management of type 2 DM and pre diabetes
  • introduced when lifestyle mod are inefficient in control
  • first line drug of choice
51
Q

what type of med is metformin?

A

biguanide

52
Q

what are the actions of metformin?

A

o makes tissues less resistant to endogenous insulin
o ↓ amount of glucose produced by the liver
o ↓ intestinal glucose absorption

53
Q

what are AEs of metformin?

A

nausea, diarrhea, abdominal bloating, metallic taste

54
Q

what are NIs with metformin?

A

o take with meals
o assess BG and Kidney function → contraindicated w/renal insufficiency o DC before procedures requiring radiographic contrast
media
- hold for 1 - 2 days prior to procedure and 48 hrs. post-procedure
- HCP to assess renal function and restart

55
Q

what are the 3 common sulfonylureas?

A

glipizide, glyburide, glimepiride

56
Q

how do the sulfonylureas work?

A

o stimulate the release of insulin from the pancreas (pt needs functional beta cells)
o ↑ sensitivity to insulin at receptor sites
o may ↓ hepatic glucose production

57
Q

what are the AEs of sulfonylureas?

A

hypoglycemia (shaky, sweating, confusion, aggitation) and increased appetite (weight gain)

58
Q

what are the NIs for sulfonylureas?

A

o administer 30 mins. before meals
o cross-sensitivity with sulfonamide allergy (sulfa)
o may be combined with metformin
o hold post-op until able to intake regular meal

59
Q

what are incretins?

A

hormones found in GI tract

60
Q

what do incretins do?

A

stimulate pancreatic insulin secretion

61
Q

what does incretin dysfunction result in?

A

post-prandial hyperglycemia

62
Q

what does dipeptidyl peptidase (DDP-4) do?

A

destroys incretin hormones

63
Q

what 3 actions do DDP-4 inhibitors do?

A
  • inhibit enzyme from destroying incretin
    hormones
  • stimulates pancreas to secrete insulin
  • reduces fasting and post-prandial glucose
64
Q

what are the DDP-4 drug names?

A

Drugs: sitagliptin and saxagliptin

65
Q

what is the name of the DDP-4 combo drug and what is the combo?

A

Combo: Janumet (sitagliptin and metformin)

66
Q

what is the drug-drug interaction for DDP-4?

A

may ↑ risk of hypoglycemia with

sulfonylureas or insulin

67
Q

what are the NIs for DDP-4?

A

o assess for hypoglycemic sxs

○ no regard to food

68
Q

what is the purpose of insulin?

A
  • mimic the pancreatic secretory patterns of insulin

* achieved through basal and post-prandial insulin

69
Q

what are the different types of insulin?

A

rapid-, short-, intermediate-, and long-acting

forms

70
Q

what is the goal of insulin combination therapy?

A

combined w/therapy to stimulate fasting and postprandial pancreatic insulin

71
Q

when should rapid acting insulin be given?

A

15 min before a meal; 3 - 4 times a day

72
Q

when should short acting insulin be given?

A

30 min w/in time frame

73
Q

when should intermediate acting insulin be given?

A

1 - 2 a day

74
Q

when should long acting insulin be given?

A

once a day; can be given in conjunction with spikes; steady release

75
Q

refer to sliding scale insulin picture

A

understood

76
Q

what are the effects of corticosteroids and stress hyperglycemia (physical/emotional/recovery stress)?

A
  • ↑ blood glucose levels

* insulin therapy may be needed • patient teaching

77
Q

what should be considered with IV therapy?

A
  • may ↑ blood glucose depending on solution
  • assess type of IVFs and oral intake
  • assess need for IVFs if taking PO
78
Q

what should we do as far as patient education?

A
  • assess knowledge
  • teach monitoring and management therapy
  • meal plans
79
Q

T/F: people are normally prediabetic for 10 years prior to their diabetes diagnosis

A

T

Nursing Semester 2 (21 decks)

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