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NURS 232 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Is type 1 or type 2 more common in Canada?

A

Type 2 (90%), Type 1 (10%)

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2
Q

3 factors for why the prevalence of diabetes is increasing

A
  1. Obesity from poor diets
  2. Population is aging
  3. More sedentary lifestyles
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3
Q

When was an insulin injection first used and who discovered it?

A

1922 - Banting

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4
Q

Describe DM

A

A metabolic disorder characterized by the presence of hyperglycemia due to defective insulin secretion, action, or both.

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5
Q

How long do you fast before taking a FPG (fasting plasma glucose)?

A

8 hours

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6
Q

Describe gestational diabetes

A

Effects the growth of babies, larger because they are getting too much sugar. 1st recognized during pregnancy.

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7
Q

Describe secondary diabetes

A

Health conditions or medications bring on secondary diabetes. ex, pancreatic or endocrine diseases

*not the same as Type 2 diabetes which is caused by lifestyle factors

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8
Q

Primary prevention for type 2 diabetes

A

Diet (leads to insulin resistance), exercise, HTN, dyslipidemia

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9
Q

What cells secrete insulin in the pancreas?

A

Beta cells

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10
Q

What cells secrete glucagon in the pancreas? Function of glucagon?

A

Alpha cells. Glucagon increases stored glucose release by the liver when there is low glucose.

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11
Q

3 other hormones that increase blood glucose

A

Stress hormones increase blood glucose:
1. EP
2. Cortisol
3. Growth hormones

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12
Q

When are manifestations of type 1 diabetes seen?

A

When 80-90% of normal beta-cell function is destroyed

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13
Q

Describe Type 1 Diabetes and 2 possible causes

A
  • lack of insulin secretion
  • autoimmune process as the body destroys its own beta cells
  • possible causes: genetic predisposition of the immune disorder, virus
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14
Q

Describe Type 2 Diabetes

A
  • insulin resistance
  • desensitization
  • often inherited defect in insulin receptors
  • adipokines from adipose tissue cause altered glucose and fat metabolism
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15
Q

What does desensitization mean in regards to type 2 diabetes?

A

Decreased responsiveness of beta cells to hyperglycemia

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16
Q

Describe how cachexic can appear in diabetes?

A

Glucose is not getting to any cells, so the body breaks down carbs and fats instead

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17
Q

Compare the onset of diagnosis between DM1 and DM2

A

DM1 - younger age < 30, abrupt diagnosis
DM2 - older age, slow gradual onset

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18
Q

Compare the insulin requirements and blood sugar maintenance between DM1 and DM2

A

DM1 - insulin required for survival, often difficult to control BS
DM2 - oral hypoglycemic agents or insulin may be necessary, relatively stable BS

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19
Q

Compare the precipitated causes of DM1 and DM2

A

DM1 - often stress or illness
DM2 - often a combination of genetic and environmental factors

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20
Q

4 ways diabetes can be diagnosed. MUST MEMORIZE!

A
  1. Symptoms of DM + random (any time of the day) plasma glucose value ≥ 11.1 mmol/L

OR

  1. Fasting plasma glucose (FPG) ≥ 7.0 mmol/L

OR

  1. Plasma glucose value in the 2-h sample (2hPG) of a 75g oral glucose tolerance test (OGTT) ≥ 11.1 mmol/L

OR

  1. A1C ≥ 6.5% (in adults)
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21
Q

What is an A1C test?

A

A measurement of blood sugar serum over 3 months to show how much glucose is binding to hemoglobin.

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22
Q

3 ways prediabetes can be diagnosed

A
  1. FPG of 6.1-6.9

OR

  1. 2hPG in a 75g OGTT of 7.8-11.0

OR

  1. A1C of 6.0-6.4%
23
Q

Clinical Manifestations of Type 1 DM

A

3 Ps: polyuria (getting rid of glucose), polydipsia (excessive thirst), polyphagia (excessive hunger)

2 Ws: Weight LOSS, weakness/fatigue

2 Ks: Ketonuria (pee), ketoacidosis (blood)
- causes fruity breath

2GU: N&V, ab pain

24
Q

Clinical Manifestations of Type 2 DM

A

Often fatigue is the only symptom

Some S&S associated w/ prolonged hyperglycemia:
- chronic blurred vision
- recurrent infections
- slow wound healing
- neuropathic pain
- Weight GAIN

25
Q

4 goals for management of DM

A
  1. Reduce symptoms
  2. Prevent & manage acute complications
  3. Prevent & manage long term complications
  4. Attain a desirable body weight
26
Q

Describe sick day management of DM

A
  • stress hormones increase blood glucose, so may need more insulin
  • assess blood glucose Q3-4H
  • check urine for ketones if CBG > 14 mmol/L
  • assess for dehydration and hold SADMANS meds if dehydrated
27
Q

Effects of exercise on glucose uptake and insulin resistance

A

↑ glucose uptake into cells
↓ insulin resistance

28
Q

Effects of stress on glucose levels and insulin resistance

A

↑ glucose levels in blood
↑ insulin resistance

29
Q

What percent of people with DM will die of heart disease or stroke?

A

65-80%

30
Q

What races are most at risk for diabetes?

A

Hispanic, Asian, South Asian, African, Indigenous

31
Q

3 Acute Complications of DM

A
  1. Hypoglycemia
  2. Diabetic ketoacidosis
  3. Hyperosmolar hyperglycemic nonketotic syndrome (HHS)
32
Q

Explain how electrolyte abnormalities occur in patients with DKA

A

Body pulls H+ into the cells but K+ are already in the cells so the K+ ions are pulled out. Hyperglycemia causes intracellular potassium depletion and K+ goes into the bloodstream (intracellular hypokalemia)

33
Q

How are ketones tested?

A

Through beta hydroxybutyrate which releases H+ that circulates and contributes to metabolic acidosis

34
Q

Describe DKA

A

Diabetic Ketoacidosis:
FATS METABOLIZED in absence of insulin
-> ketosis, acidosis
- most likely seen in type 1
- profound deficiency of insulin -> hyperglycemia and dehydration

35
Q

Describe HHNS

A

Hyperosmolar hyperglycemic nonketotic syndrome:
Has enough insulin to prevent DKA
Not enough insulin to prevent:
1. Severe hyperglycemia
2. Osmotic diuresis (increased urine)
3. Extracellular fluid depletion

  • primarily a type 2 problem
  • less common than DKA
  • higher mortality rate than DKA
  • mostly to older adults who lose thirst protective mechanism
36
Q

4 Causes of hypoglycemia

A
  1. Mismatch timing of intake and peak of insulin
  2. Excessive insulin
  3. Insufficient carb intake
  4. Excessive exercise
37
Q

S&S of hypoglycemia

A

SNS is triggered releasing EP which causes:
- diaphoresis
- tremors
- hunger
- anxiety
- pallor
- palpitations

When the CNS is not getting enough glucose
- irritability
- visual disturbances
- dysarthria (difficulty speaking)

38
Q

How does asymptomatic hypoglycemia occur?

A

When there is autonomic neuropathy -> impaired secretion of the counter regulatory hormones (EP)

Needs BG managed more

39
Q

Tx of hypoglycemia

A

If BG < 4:
Administer 15-20g of simple carbs
Check BG in 15 mins

If BG > 4:
Administer longer-acting starch & protein
Check BG in an hour

40
Q

What is the response of the liver and kidneys to hyperglycemia?

A

Liver tries to make more glucose for the CELL and converts glucagon to glucose. Fat is broken down into ketones.

Kidneys recognize glucose pulling fluid into vascular space as too much volume causing polyuria. The glomerulus filters more glucose than the proximal tubule can reabsorb causing glycosuria.

41
Q

6 Causes of DKA

A
  1. Illness
  2. Infection
  3. Insulin Omission
  4. Inappropriate management or undiagnosed T1DM
42
Q

S&S of DKA

A

[ BG > 14 and pH < 7.35 ]
- Tachycardia
- Hypotension
- Kussmaul RR (rapid to get rid of acid)

3 Ps: polyuria (getting rid of glucose), polydipsia (excessive thirst), polyphagia (excessive hunger)

2 Ws: Weight LOSS, weakness/fatigue

2 Ks: Ketonuria (pee), ketoacidosis (blood)
- causes fruity breath

2GU: N&V, ab pain

43
Q

Tx of DKA

A
  • ABCDs, blood work
  • Need NS bolus dose of 1-2L before insulin because it could cause fluid and electrolyte shifts like a severe serum potassium drop
  • NS lowers BG through dilution
  • Once BG is at 14, give dextrose to prevent hypoglycemia
  • Fluid resuscitation until urine output > 30 ml/hr
44
Q

Explain Osmotic Diuresis

A

Glucose in the blood creates osmosis of water from the interstitial spaces in cells to dilute the intravascular hypertonic hyperglycemia. This leads to dehydration and increased urine output.

45
Q

S&S of HHNS

A

Fewer symptoms cause late recognition
- Increased serum osmolality (glucose > serum)
- BG > 34 !!!
- ketone bodies absent in blood and urine
- coma, seizures, aphasia

46
Q

How does DM affect the vascular system?

A

Prolonged high blood sugar can damage blood vessels and the nerves that control your heart. Diabetics often have comorbidities that increase the risk of CVD. that raise the risk for heart disease: High BP increases the force of blood through arteries and can damage artery walls.

47
Q

Why are diabetics more prone to infection?

A

Increased glucose is a breeding ground for more bacteria.

48
Q

Chronic complications of DM

A

Infections, macrovascular (CAD, MI, HTNL, PVD) and microvascular (retinopathy, nephropathy, neuropathy) complications

49
Q

What is the most common form of diabetic sensory neuropathy?

A

Distal symmetrical neuropathy. Risk for foot ulcers, reduced BF due to atherosclerosis, slow wound healing.

50
Q

What are the only two ways to treat diabetic neuropathy?

A
  1. Control of BG
  2. Foot care
51
Q

ABCDESSS of Diabetes Care

A

A - A1C (<7% optimal glycemic control)
B - BP (<130/80)
C - Cholesterol (<2.9 mmol/L)
D - Drugs (statin, ACE inhibitors)
E - Exercise and eating healthy
S - Screening for complications
S - smoking cessation
S - self management

52
Q

How to give pt education for foot care

A

Keep feet dry
Wear proper shoes
Inspect foot daily
Recognize and treat wounds promptly
If ulceration occurs: debride wound, give antibiotics, bed rest, prevent edema

53
Q

Relationship between obesity and diabetes

A
  1. Obesity-linked inflammation contributes to insulin resistance: cells resist letting insulin move glucose into them.
  2. The area of your liver where excess glucose is usually stored is filled with fat. Therefore, glucose staying in the blood.

NURS 232 (11 decks)

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