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NU 360 > Ch. 56 > Flashcards

Ch. 56 Flashcards

1
Q

metabolic syndrome is

A

the simultaneous presence of metabolic factors that increase the risk for Type 2 DM

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2
Q

metabolic syndrome includes

A
  • abdominal obesity
  • hyperglycemia
  • hypertension
  • hyperlipidemia
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3
Q

incidence and prevalence of DM

A
  • more than 34 million people in the US are living with DM
  • 7.3 million in US are undiagnosed
  • 86 million in the US with prediabetes
  • 2.2 million adults in Canada
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4
Q

health promotion and maintenance of DM

A
  • control of DM and its complications is the major focus of health promotion activities
  • low-calorie diet
  • increase acitivity
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5
Q

Type 1 DM

A
  • beta cell destruction = absolute insulin deficiency
  • autoimmune
  • idiopathic
  • not controlled by diet
  • ONLY treated by insulin
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6
Q

Type 2 DM

A
  • insulin resistance to insulin deficiency
  • later onset
  • risk factors can be mitigated
  • can be treated w/ insulin, diet, exercise, mult. treatment options
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7
Q

ethnic disparities in DM in the US

A

African Americans: 12.6%
Hispanics: 11.8%
Asian Americans: 8.4%
Non-Hispanic Whites: 7.1%
American Indians in Southern AZ: 24.1%

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8
Q

DM assessment: risk factors

A
  • decreased PA
  • obesity/high BMI
  • poor diet
  • genetics/ fam history
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9
Q

DM assessment: s/sx

A
  • always tired
  • frequent urination
  • sudden weight loss
  • wounds that won’t heal
  • sexual problems
  • vaginal infections (yeast)
  • always thirsty
  • numb or tingling hands or feet
  • blurry vision
  • always hungry
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10
Q

DM assessment: labs/screenings

A
  • glycosylated hemoglobin (A1c)
  • FBG
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11
Q

Hgb A1c levels

A

healthy: < 5.3
trending 5.3-5.5
prediabetic: 5.6-6.4
diabetic: > 6.4

lifespan of Hgb: 3 months

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12
Q

patient problems related to DM

A
  • potential for injury
  • potential for poor wound healing
  • potential for kidney disease (damage to blood vessels causes kidneys to not function properly)
  • potential for complications
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13
Q

nursing actions with DM

A
  • preventing injury from hyperglycemia
  • enhancing surgical recovery
  • preventing injury from peripheral neuropathy
  • reducing risk for kidney disease
  • preventing complications
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14
Q

PO medication for DM

A
  • sulfonylurea agents: glipizide, glyburide, glimepiride
  • meglitinide analogues: repaglinide
  • biguanides: metformin
  • thiazolidinediones: pioglitazone, rosiglitazone
  • DPP-4 inhibitors: sitagliptin (januvia)
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15
Q

insulin therapy: types of insulin

A
  • rapid: aspart, lispro, humalog
  • short: regular, humalin
  • intermediate: NPH
  • long: glargine/lantus
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16
Q

mixing insulin

A
  • make sure that they can be mixed/compatible
  • regular and NPH: clear before cloudy (R before N)
  • inject air into NPH, then inject air in R, draw up R, then draw up NPH
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17
Q

factors that influence insulin absorption

A
  • fat scarring
  • injection site (abdomen is fastest site)
  • high temperature (hot shower, bath, water bottle, spa, sauna)
  • massaging/vigorously rubbing injection site
    **(heat increases, cold decreases absorption)
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18
Q

rapid-acting insulin

A

aspart, lispro, humaLOG
- onset: 10-20 min
- peak: 1-3 hours
- duration: 3-5 hours
- take with meals?: want food tray in the room

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19
Q

short-acting insulin

A

regular (given IV route only), humaLIN
- onset: 30-60 min
- peak: 1-5 hours
- duration: 6-10 hours
- take with meals?: 30 mins before each meal

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20
Q

intermediate-acting insulin

A

NPH
- onset: 60-120 min
- peak: 6-14 hours
- duration: 16-24 hours
- take with meals?: 30-45 mins before meals

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21
Q

long-acting insulin

A

glargine (lantus)
- onset: 70 min
- peak: none
- duration: 18-24 hours
- take with meals?: same time every day, usually within 1 hour of breakfast

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22
Q

health teaching of DM

A
  • normal values
  • Hgb A1c
  • how to take a glucose finger stick?
  • exercise: promotes uptake of glucose without insulin, also to decrease weight
  • prevent complications: peripheral neuropathy
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23
Q

what do meglitinide analogues do?

A

stimulate insulin release
- actually stimulate the beta cells to make insulin
- CAN cause hypoglycemia

24
Q

what do biguanides do?

A

improves insulin sensitivity, decrease liver glucose production
- makes the liver not make as much sugar/glycogen, makes tissue more sensitive to take in glucose/less resistant to insulin
- will NOT cause hypoglycemia!!
- hard on kidneys!- CT scan, will need to hold metformin

25
Q

what do thiazolidinediones do?

A

increase cellular use of glucose
- more insulin receptive

26
Q

what do DPP-4 inhibitors do?

A

reduced liver glucose production, delay gastric emptying
- make less sugar/glycogen

27
Q

dawn phenomenon

A

nighttime release of adrenal hormones, glucose elevated 5-6AM; give insulin later at night

morning hyperglycemia because insulin did not cover the whole night

28
Q

somogyi effect

A

morning hyperglycemia, rebound from nighttime hypoglycemia; eat more at night, monitor insulin dose

morning hyperglycemia because too much insulin/not enough glucose at night caused hypoglycemia

29
Q

inhaled insulins*

A
  • comes w/ inhaler
  • “afrezza” is an ultra-rapid/short- acting mealtime insulin
30
Q

insulin pumps*

A

small computerized device that delivers insulin to help people with diabetes manage their blood glucose level
- can deliver in bolus before meals or continuously
- Usually for type 1 diabetics

31
Q

principles of nutrition

A
  • protein (high)
  • dietary fat and cholesterol (low)
  • fiber (high)
  • sweeteners (low)
  • alcohol (low)
32
Q

chronic complications of DM can be

A
  • macrovascular
  • microvascular
33
Q

macrovascular complications

A
  • stroke
  • heart disease or HTN
  • peripheral arterial disease
  • foot problems*
34
Q

microvascular complications

A
  • diabetic eye disease (retinopathy and cataracts)
  • renal disease
  • neuropathy
  • foot problems*
35
Q

acute complications of DM: hypoglycemia

A

Low blood sugar
(cold and clammy needs some candy)
- act quickly, more emergency than hyper because sugar is falling while youre talking, time sensative

36
Q

acute complications of DM: DKA

A

Very very high blood sugar
(hot and dry, sugar high)
- fat is broken down for energy
- have to be acidic to have DKA
- this is an INFECTION
- medical emergency

37
Q

acute complications of DM: HHS

A

Very high blood sugar
(hot and dry, sugar high)

38
Q

causes of hypoglycemia

A

rapid onset (1-3 hours)
- insufficient food intake
- excess insulin
- excess exercise
- history

39
Q

s/sx of hypoglycemia

A
  • anxious
  • sweaty
  • hungry
  • confused
  • blurred or double vision
  • shaky
  • irritable
  • cool, clammy skin
40
Q

treatment of hypoglycemia

A
  • rule of “15”
  • under 70, 15 grams of carbs, recheck in 15 mins
  • need BS increased!

eating is ideal treatment if they can eat (awake and alert) NO FOOD to drooling, unconscious- give glucagon

41
Q

DKA patho

A
  • onset over 4-10 hours
  • causes: lack of insulin, GI upset, febrile illness, history
  • biggest reason: infection
  • BG >300
42
Q

s/sx of DKA

A
  • Polyuria (peeing a lot)**
  • Polydipsia (thirsty)**
  • Polyphagia**
  • Fruity Breath (smell ketones on breath)***
  • Nausea/Vomiting
  • Abdominal Pain
  • Dehydration signs
  • Weakness
  • AMS
  • Kussmaul’s respirations***
  • Electrolyte Imbalance***
  • could come in comatose or walk in flushed
43
Q

management of DKA

A
  • airway
  • LOC
  • hydration status: start NS, then 1/2NS until BS at 250, then D5 1/2NS (add sugar to balance) *aggressive fluid resuscitation (get IV in asap)
  • electrolytes: K+ high (ketones are acidic, acid pushes the K+ out of the cells and into the blood- hyperkalemia = cardiac issue), sodium bicarbonate
  • blood glucose level (>300)
  • vital signs Q15min until stable

needs: hydration, insulin, electrolyte replacement

44
Q

hyperglycemic-hyperosmolar state (HHS) aka HHNK (broken down)

A
  • old patient (> 65)*
  • type 2 DM*
  • uncontrolled DM for weeks
  • usually absent N/V/abd pain
  • dehydration, polyuria, hypotension, CV collapse
  • altered mental state*, lethargy, coma, seizures
  • underlying precipitants: sepsis, MI, stroke, medication (diuretics, phenytoin, corticosteroids)
  • NO ketosis or acidotic breathing
45
Q

s/sx of HHS

A
  • AMS
    -Neurological signs
  • Dehydration signs
  • Polyuria
  • Polydispsia
  • Polyphagia
46
Q

HHS management

A
  • fluid therapy: NS - 1/2NS
  • LOC/AMS
  • electrolytes
  • blood glucose level

think slow up, slow down

47
Q

diabetic keto-acidosis DKA (broken down)

A
  • young patient (< 65)
  • type 1 DM (type 2 under conditions of extreme stress)
  • often 1st time dx
  • N/V/abd pain
  • dehydration, thirst, polyuria, volume depletion
  • altered mental state, lethargy, coma
  • underlying precipitants: infection, infarction, drugs (cocaine)
  • SOB, ketotic/acidotic breathing (Kussmauls)
48
Q

normal BS levels

A

74-106 mg/dL

49
Q

peripheral neuropathy: teaching points

A
  • shoes always
  • inspect feet daily
  • bathe daily- test water before with thermometer
  • nail clippers- straight across
  • dry between toes
50
Q

low glycemic food choices (good choices)

A
  • banana
  • F1
  • white corn
  • peanut
  • sweet potato
  • apple
  • tomato
  • green tea
  • milk
  • brown rice
51
Q

high glycemic food choices (bad choices)

A
  • baguette
  • doughnuts
  • rice cakes
  • white rice
  • potato
  • noodles
  • corn
  • cola
  • instant noodles
  • popcorn
52
Q

relationship between insulin and potassium

A

insulin will push the K+ back into the cells, causing hypokalemia

*MUST CHECK K+ LEVEL BEFORE GIVING INSULIN

52
Q

really bad complication/ side effect of DKA

A

cerebral edema

53
Q

HHS patho

A
  • slow onset
  • not as aggressive to treat as DKA
  • very high concentration in blood, bring down slowly
  • **NEURO (to detect improvement)
  • BG >600
54
Q

hyperglycemia blood sugar level

A

> 106

NU 360 (12 decks)

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