Diabetes Flashcards

1
Q

Risk factors for DM

A

x

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2
Q

Signs and Symptoms of

1) Hyperglycemia
2) Hypoglycemia

A
Hyperglycemia:
BG > 7.0 mmol/L
Polyuria – excessive urination
Polyphagia – increased hunger
Polydipsia – increased thirst
Glucosuria – high levels of glucose in the urine
Weight loss
Fatigue 

Hypoglycemia:

BG

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3
Q

Labs key to DM

A
B.G. (blood glucose)
FBG (fasting blood glucose) 
GGT (glucose tolerance test)
A1C
Cholesterol
Urine - Ketones

BP

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4
Q

Glucose TOlerance test =

A

Glucose Tolerance Test – done after FBG – the patient drinks a standard solution of glucose to challenge his/her system – followed by a second BG test at specific intervals to track ‘glucose challenge’

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5
Q

Blood glucose monitoring

  • How do errors typically occur?
  • Important considerations for self monitoring?
A

Errors d/t:

  • Blood amount too small
  • Improper maintenance of machine
  • Damaged monitor strips

Dependent on skill level, cognitive ability, visual acuity, technology, comfort, cost…teaching and eval critical!

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6
Q

Microalbuminuria (Proteinuria)

A

Albumin found in urine

r/t damage to kidneys in which filtering is impaired and proteins escape into urine

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7
Q

Hgb A1C

A

x

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8
Q

Pharmacological interventions for DM?

A

**Typically see polypharmacy!!

In order to reach A1C, BP and lipid targets, people with diabetes typically require many medications:

  • To lower blood glucose: 1-3 pills and/or insulin
  • To lower cholesterol: 1 or 2 pills
  • To lower blood pressure: 2 or 3 pills
  • For general vascular protection: aspirin

** Adherence to complex drug regimens can be a challenge for patients.

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9
Q

Glycemic Index

A

x

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10
Q

What occurs in severe metabolic acidosis?

Long term effects?

A

When blood glucose reaches 150mg/100ml (normal = 80-120), glycosuria begins…large fluid quantity excreted as well (polyuria) → dehydration occurs → blood vol dec → blood flow dec → less O2 → anaerobic resp → lactic acid poors out of muscles into bloodstream

  • Lipids utilized → acidic ketone bodies enter bloodstream
  • Protein also metabolized
  • As cells die, release Na+ and K+, lost in excessive polyuria

-Long term effects = vascular narrowing leading to kidney, heart + retinal dysfx

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11
Q

Which people with DM need extra close monitoring because may not experience the initial symptoms of hypo/hyperglycemia?

A

Those with autonomic neuropathy or those on Beta blockers may not experience initial symptoms (adrenergic)

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12
Q

All with diabetes should wear?

A

BRacelet or tag

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13
Q

Important consideration for family when teaching about DM?

A

•Family members need to know symptoms of hypoglycemia, esp any change in behavior

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14
Q

Key nutritional aspects of managing diabetes?

A

Nutrition, diet, weight control + exercise = foundation for DM management

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15
Q

What is the most important objective with regard to DM and diet?

A

• Most important objective is caloric intake to attain or maintain reasonable body weight + control of blood glucose levels

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16
Q

Nutritional management goals for DM?

A

o Providing all essential food constituents (vitamins, minerals, etc.) for optimal nutrition
o Meeting energy needs
o Achieving & maintaining reasonable weight
o Preventing wide daily fluctuations in blood glucose levels
o Dec serum lipid levels (if elevated) to reduce risk for macrovascular disease

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17
Q

What aspect of DM is obestity r/t?

A

Inc insulin resistance

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18
Q

How important is weight loss with DM?

A

• Weight loss alone can eliminate need for medication in Type 2 with diabetics with obesity (loss as small as 5-10% may sig improve glucose levels, insulin sensitivity, pretension, and dyslipidemia)

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19
Q

How is weight distribution important for DM?

A

•Location of adipose tissue critical – check waist circ

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20
Q

Is skipping meals a good way to reduce caloric intake in DM?

A

• Reduce calories but DON’T skip meals! Easier on pancreas if pacing food throughout day

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21
Q

• 3 major acute complications r/t short-term imbalances in blood glucose levels:

A

hypoglycemia, DKA and HHNS

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22
Q

DKA =

A

Diabetic Ketoacidosis

*Deficit of insulin results in disorders in metabolism of CHO, proteins, and fat

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23
Q

HHNS =

A

hyperglycemic hyperosmolar nonketotic coma or hyperglycemic hyperosmolar syndrome

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24
Q

Normal range for blood glucose?

A

3.9-11 mmol/L

VIHA

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25
Q

Hypoglycemia = ?

A

•Glucose level

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26
Q

What is hypoglycermia d/t?

A

•D/t too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity

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27
Q

When can hypoglycemia occur (day or night?) and when does it often occur?

A

• May occur day or night; often before meals (esp if meals delayed or snacks missed)

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28
Q

How does an NPH insulin cause hypoglycemia in the middle of the night?

A

•Delay in NPH insulin’s associated with peak causing hypoglycemia a while after taking (middle of the night hypoglycemia may occur d/t pre-dinner NPH

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29
Q

2 groups of clinical manifestations of hypoglycemia?

A

1) Adrenergic symptoms = sympathetic system stimulated in early stage of hypoglycemia → surge of NorE and E → sweating, tremor, tachycardia, palpitation, nervousness and hunger
2) CNS symptoms: in moderate hypo, brain cells deprived of energy → inability to concentrate, headache, light-headedness, confusion, memory lapses, numbness of lips and tongue, slurred speech, impaired coordination, emotional changes, drowsiness (adrenergic symptoms continue)

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30
Q

SYmptoms of severe hypoglycemia?

A

Severe hypoglycemia: CNS fx so impaired that will require aid from another person – disoriented behavior, seizures, difficulty arousing from sleep, loss of consciousness

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31
Q

Difference between type1 and type 2 diabetes?

A

Type 1 diabetes (5-10%)

Body’s own immune system attacks the cells in the pancreas that produce insulin

Type 2 diabetes (90 - 95%)

The pancreas does not produce enough insulin and/or the bodies’ tissues do not respond properly to the actions of insulin – insulin resistant

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32
Q

What is gestational diabetes?

A

Diabetes with first onset or recognition during pregnancy

Puts women and the child at higher risk for type 2 DM later in life

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33
Q

WHat is pre- diabetes?

A

When a persons blood sugar levels are higher than normal but not enough to be diagnosed with Type 2

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34
Q

Non-modifable risk factors for diabetes?

A

Age, Gender, Race & Ethnicity, Family History

35
Q

Modifiable risk factors for DM?

A

1) Overweight/Obesity
2) Smoking
3) Physical Inactivity
4) HTN – leads to risks for myocardial infarction, stroke, eye problems and kidney disease.
5) Hyperlypidemia
6) High Blood Glucose
7) Inflammation/Hypercoagulation – these two factors are known to underlie cardio-metabolic risk.

36
Q

Macrovascular complications of DM?

A
  • Stroke
  • heart disease and htn
  • Peripheral vacular disease
  • Ulcers and amputations
37
Q

Microvascular complications of DM?

A
  • Diabetic eye disease (retinopathy and cataracts)
  • Renal disease
  • Neuropathy
  • Foot problems
38
Q

What is DM a MAJOR risk factor for?

A
factor for heart disease and stroke
Acute MI (heart attack) occurs 15 to 20 years earlier in people with diabetes
39
Q

Eye problems and DM

  • DM is leading cause of?
  • In risk of what other problems?
A

Diabetes is the leading cause of adult-onset blindness

Increased risk of macular edema, cataracts, glaucoma

40
Q

What is the leading cause of kidney failure?

A

DM

41
Q

Other complications of DM?

A
- Digestive problems
Thyroid problems (hypothyroidism)
- Sexual dysfunction in men (50-70% of all male diabetes patients suffer from erectile dysfunction)
- Urinary tract and vaginal infections
- Carpal tunnel syndrome
42
Q

Key aspects of care for patient with DM?

A

Exercise
Nutrition

Diagnostics:
(B.G., FBG, GGT, A1C, BP, Cholesterol, Urine, Ketones)

Pharmacological Therapy

Education

Develop a diabetic teaching plan with your patient and family

43
Q

How does Glucose Tolerance Test work?

A

done after FBG – the patient drinks a standard solution of glucose to challenge his/her system – followed by a second BG test at specific intervals to track ‘glucose challenge’

44
Q

What does HbA1C show?

A

glycosylated hemoglobin – reflects average B.G. levels over 2-3 months. The longer the glucose levels are elevated in the blood the more glucose attach to hemoglobin. This is permanent and lasts the life of the RBC (120 days).

45
Q

What are the ABC’s of DM important for nurse to remember?

Target values of each?

A

A1C: ≤7.0% (or ≤6.0%)
BP: ≤130/80 mm Hg
Cholesterol: LDL-C

46
Q

Urine testing

pros and cons?

A
Non invasive strip, inexpensive
Not accurate result
Does not detect hypoglycemia
Some drugs interfere with results
ASA, Vit. C, some Abx
47
Q

Significance of ketones in urine? Why are we looking for this?

A
No effective insulin available
Body breaks down stored fat for energy
Ketones are by products of fat metabolism
Accumulate in blood and urine
Puts patient at risk for DKA
Diabetic Ketoacidosis
48
Q

Oral hyperglycemics taken in what kind of DM?

Action?
Insulin also required?
example?

A
  • Type 2
  • Common action of lowering BG levels
  • Single, dual, or triple therapy may be used
  • May require Insulin
  • ex: metformin
49
Q

Important considerations for administering anti-hyperglycemics w/ regard to adverse effects?

A
  • Watch for hypoglycemia!
  • Consider pharmacokinetics of your patient
    (Absorption, distribution, metabolism, excretion)
  • Drug to drug interactions
    Other medications may increase glucose levels
    (Diuretics, steroids, anti-seizure, anti-coagulants, contraceptives)
50
Q

1 adverse effect of insulin and oral anit-hyperglycemics?

A

Hypoglycemia

51
Q

Does a urine test detect hyperglycemia?

Hypoglycemia?

A

Yes to hyper - will show elevated glucose levels

No to hypo

52
Q

Are hypo/hyper glycemic symptoms the same in everyone?

A

o Range of where symptoms are experienced is individual

  • Those with diabetes for many years may have decreased hormonal response, may be related to autonomic neuropathy (a chronic diabetic complication) → no surge in adrenaline, may not detect hypo until has become moderate or severe
53
Q

Why might DM be less well monitored in the elderly?

A

hypo of particular concern because may live alone & may not recognize symptoms

dec renal fx = longer for oral hypo meds to be excreted

dec appetite = possible skipped meals

dec visual acuity = errors with insulin

54
Q

What to do when someone is hypoglycemic?

A
- Give 15g CHO
• 3-4 glucose tablets
• 120-180mL fruit juice or soft drink
• 6-10 life-savers or other hard candy
• 10-15mL sugar or honey

Reteset glucose in 15 mins, and again if

55
Q

teaching regarding hypoglycemia?

A

o Must know to carry sugar with them at all times
o Eat anything if no glucose avail
o Refrain from eating high calorie, high fat desserts to treat hypo
oNot to see hypoglycemic episodes as time for treats → should teach to incorporate occasional deserts into meal plan instead

56
Q

Why are high fat deserts not a good option for treating hypoglycemia?

A

fat delays glucose absorption so results not seen as fast; may eat more → sever hyper later & weight gain

57
Q

Emergency measures for hypoglycemia?

A

o Sucut or IM 1mg glucagon
o Give concentrated source of CHO and snack on awakening (glucagon only lasts 12-27mins)
o May experience nausea with glucagon – turn on side to prevent aspiration

o In hospital: unsconscious or cannot swallow receive 25-50mL D50W IV

58
Q

How long may it take someone to regain consciousness after passing out from hypoglycemia?

A

May take 20 mins

59
Q

3 main clinical features of DKA?

A

1) Hyperglycemia
2) Dehydration + electrolyte loss
3) Acidosis

60
Q

3 main causes of DKA?

A

1) Decreased or missed dose of insulin
2) Illness or infection
3) Undiagnosed and untreated diabetes

61
Q

Misconceptions about insulin use when sick? How should someone approach insulin admin when sick?

A

Errors in insulin possibly d/t ill thinking that if eating less or vomiting require less insulin…do not need to dec when ill, rather may need to increase dose

Illness + infections associated with insulin resistance → inc stress hormones interfere with glucose use by muscle & fat + cause liver to produce glucose (counteracting insulin)

o Must be taught “sick day” rules for managing diabetes when ill
o Most important = do not eliminate insulin when naursea + vomiting; instead keep up reg doses + try to have small amounts of CHOs
o Keep sick day foods available, urine test strips

62
Q

Clinical manifestations of DKA?

A

o Hyperglycemia leads to Polyuria–> dehydration, weakness, headache, polydypsia
o Inc ketone bodies → leads to acetone breath (fruity odour), poor appetite, nausea; resulting acidosis causes nausea, vomiting, abdominal pain, inc in RR
o LOC varies greatly, may be alert to comatose → depend on plasma osmolarity

63
Q

What sort of diagnostic findings would you see with someone with DKA?

A

o Glucose levels: 16.6 to 44.4mmol/L or greater
o Low serum bicarbonate and low pH vlaues
o Low PCO2 level because compensating through Kussmal breathing
o Accum of ketone bodies in blood and urine
o Elev levels of creatinine, BUN, Hb and HCt with dehydration

64
Q

Is the severity of acidosis predictable based on glucose levels?

A

No, is highly individual

65
Q

Important signs of dehydration in lab values?

A

Elev levels of creatinine, BUN, Hb and HCt with dehydration

66
Q

3 goals of medical management in DKA?

A

1) Rehydration
2) Restoring electrolytes
3) Reversing acidosis

67
Q

What IV infusion given to restore hydration with acidosis?

A

NS initially - may require 6-10L!

•When glucose controlled, may switch to D5W to keep levels

68
Q

What will be important to monitor when rehydrating pt?

A

Monitor for fluid overload (BP, resp assess, intake/output)

69
Q

What electrolyte is of main concern when restoring electrolytes in pt dehydrated by acidosis?
Effect of insulin on this electrolyte?
Potential problem?

A

K is main concern
• Insulin enhances movement of K from ECF into cells
• Careful replacement of K essential for avoiding dysrhythmias – monitor ECG

70
Q

Nursing management with acidosis?

A
  • Focus on monitoring fluid + electrolyte status & glucose levels
  • Admin of fluids, insulin, other meds
  • Preventing fluid overload
  • ECG monitored for dysrhythmias
  • Vital signs, ARB’s on flow sheet
  • As resolves must check: no signs of hyperkalemia, lab vales of K normal or low, pt is urinating
71
Q

What must be established before admin of K electrolytes?

A

Urine output established before admin K to prevent hyperkalemia

72
Q

What occurs with HHNS?

A
  • Basic biochemical defect = lack of effective insulin (insulin resistance)
  • Hyperosmolarity + hyperglycemia predominate
  • Simultaneously, ketosis is minimal or absent (normal serume and urine ketone levels)
  • Glucosuria + dehydration → hypernatremia and inc osmolarity occur
73
Q

HHNS
Who is this most likely to occur in?
Precipitating events?

A
  • Occurs most often in older people with no known hx of diabetes or mild Type 2
  • Precipitating events: acute illness (pneumonia, stroke), meds that exacerabate hyperglycemia (thiazides), or tx such as dialysis
74
Q

Key difference between DKA and HHNS?

A

Unlike DKA, in HHNS, enough insulin to keep glucose levels high enough to prevent breakdown of fats

75
Q

What symptom of HHNS migh patients experience for a long time and not report?

A

• Days to weeks of polyuria → may adequate manage this with inc intake, not seek medical attn until neurological changes occur

76
Q

Clinical manifestations of HHNS?

A

hypotention, profound dehydration (dry mucous membranes, poor skin turgor), tachycardia, and variable neurologic signs → morality rate high d/t underlying illness

77
Q

Assessment & Diagnostic Findings of HHNS

A

o Glucose, electrolytes, BUN, CBC, serum osmolarity, ABG’s
o Glucose + osmolarity will be seen to be exceptionally high
o Lytes + BUN show severe dehydration
o Mental status changes, focus neuologic deficits, hallucinations,
o Postural hypotension d/t dehydration

78
Q

Nursing management for HHNS:

A

o Close monitoring of VS, fluid status, lab values
o Measure to ensure safety of pt with changes in sensorium secondary to HHNS
o High risk for renal failure d/t dehydration → output + fluid status regulated
o Nursing care for underlying illness

79
Q

Medical management of HHNS?

How important is insulin here?

A

o Similar to DKA: fluid replacement, correction of lyte imbalance, insulin admin
o Because in elderly, fluid overload, HF, and dysrhythmias very important
**Insulin admin less important than DKA because no needed for reversal of acidosis
o Other tx d/t underlying illness

80
Q

3 general categories of long term complications of DM?

A

1) Macrovascular disease
2) Neuropathy
3) Retinopathy

81
Q

Etiology of long term compications of DM?

A

Etiology not entirely understood – linked to high glucose + HTN

82
Q

Do both types of DM experience long term complications? WHen do they typically occur?

A

• Present in both types, usually appear 5-10yrs after disease develops

83
Q

Which complications are more prevalent in each type?

A

Renal (microvascular) disease more prev in Type 1

CV (macrovascular) more prev in Type 2

84
Q

Important teaching in foot care for pt’s with DM?

A

o Wash feet + inspect daily
o Apply lotion - but not in between toes! (creates moisture, risk for breakdown)
o Nail care: after bath
o Trim nail straight across (file edges so not sharp)
o Do not cut cuticles
o Teach to not go barefoot