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KIN 187 Clinical Exercise Physiology > Metabolic Disease: Diabetes Mellitus > Flashcards

Metabolic Disease: Diabetes Mellitus Flashcards

1
Q

Statistics of Diabetes

A

7% of the US population

1.5 Million new cases diagnosed each year

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2
Q

Diabetes Mellitus

A

A group of metabolic disease with hyperglycemia over a prolonged period

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3
Q

Hyperglycemia

A

elevated blood glucose levels

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4
Q

`Acute complications caused by DM

A

diabetic ketoacidosis, nonketotoic hyperomolar coma, death

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5
Q

Chronic Complications caused by DM

A

Heart Disease, stroke, chronic kidney failure, neuropathies, retinopathy, nephropathy

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6
Q

Polyuria

A

Excessive urination

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7
Q

Polydipsia

A

Excessive drinking/thirst

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8
Q

Polyphagia

A

Excessive eating/hunger

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9
Q

Symptoms of DM

A

polyuria, polydipsia, polyphagia, blurred vision, weight loss

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10
Q

Type 1

A

Insulin dependent diabetes mellitus/juvenile
Auto immune destructiON of beta cells in the pancreas
10% of DM

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11
Q

Type 2

A

non insulin, adult onset
insulin resistance in skeletal muscle, liver, and adipose tissue +insulin secretory defect
90% of DM

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12
Q

Other types of DM

A

gestational, specific genetic syndrome, drugs, surgery and other illnesses

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13
Q

Fasting Plasma Glucose Prediabetic

A

100-125 mg/dl

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14
Q

Fasting Plasma Glucose diabetic

A

> or equal to 126

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15
Q

A1C values-diabetic

A

> or equal to 6.5%

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16
Q

Oral Glucose Tolerance Test-diabetic

A

> or equal to 200

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17
Q

Oral Glucose Tolerance Test-normal

A

<140 mg/dl

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18
Q

Fasting Plasma Glucose-Normal

A

<100 mg/dl

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19
Q

Normal A1C

A

<5.7%

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20
Q

Oral Glucose Tolerance Test-prediabetic

A

140-199 mg/dl

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21
Q

HbA1C

A

Glycosylated Hemoglobin

60-80% attach of glucose to N terminal amino acid valine of the beta chain of hemoglobin

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22
Q

Advantages of HbA1C

A

predictive of vascular conditions, helps management decisions, easy to measure, relatively cheap

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23
Q

Limitations of HbA1C

A

Only provides an approximate measure of glycemia
Unable to address GV or hypoglycemia
Unreliable in certain conditions (RF, Hb abnormalities, other)

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24
Q

Beta Cells

A

Insulin-promotes the storage of glucose, amino acids, and fats

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25
Q

Alpha Cells

A

Glucagon-promotes the mobilization of fatty acid and glucose

26
Q

Causes of Type 1

A

loss of beta cells of the islets of langerhans in the pancreas
Idiopathic
T-cell mediated autoimmune attack leads to loss of beta cells
Ketoacidosis is common

27
Q

Causes of Type 2

A

insulin resistance
insensitivity of receptors
lifestyle factors and genetics

28
Q

Type 1 is autoimmune… why

A

at the diagnosis… -presence of anti insulin and anti-islet cell antibodies

  • presence of inflammatory cells around the islets
  • Activation of T-lymphocytes
  • Association of diabetic genes with the incidence of development of diabetes
29
Q

When you lose 80-90% of beta cells mass

A

Lack of insulin, abnormalities occur in the muscle and liver
Excessive hepatic glucose production (gluconeogenesis)
Decreased muscle glucose uptake
Glucose intolerance

30
Q

Metabolism shift from CHO to Fat ketoacidosis

A
  • NO glucose into the cell so the body switches to other forms for fuel
  • Increased fat metabolism results in increased keto acid levels (ketone bodies)
  • Sodium is excreted in the urine with the excess keto acids (Helps to neutralize the acid)
  • Sodium is replaced by hydrogen ions in the extracellular fluid, increasing the acidosis
31
Q

Diabetic Ketoacidosis

A

Seen in severe cases of uncontrolled diabetes
Kussmaul respiration
Can develop into acidotic coma and death when the pH of the blood falls below 7.0

32
Q

Normal blood pH

33
Q

Kussmaul respiration

A

rapid and deep breathing, can result in loss of the bicarbonate content in the extracellular fluid

34
Q

Insulin

A

transfers the glucose from the blood to the cells

35
Q

Type 2 pathophysiology

A

Enough insulin is produced but the insulin is resistant, the liver is resistant to the effects of insulin, glucose cant get into the body’s cells leaving too much in the bloodstream,

36
Q

Type 2 pathophysiology (pancreas)

A
  • decrease in insulin secretion
  • increase in beta-cell apoptosis
  • decrease in beta cell mass
  • Hyperglucagonemia
37
Q

Type 2 pathophysiology (Gut)

A

impaired incretin effect

38
Q

Type 2 pathophysiology(Liver)

A
  • Insulin resistance

- Increase hepatic glucose output

39
Q

Type 2 pathophysiology (Muscle)

A

Insulin Resistance

40
Q

Type 2 pathophysiology (Adipocytes)

A
  • Increase in circulating fatty acids

- Hyperlipidemia

41
Q

Insulin inhibits

A

glycogenolysis (liver)

gluconeogensis (liver)

42
Q

Insulin stimulates

A

transport of glucose into muscle and adipose tissue

storage of glucose as glycogen

43
Q

Sources of blood glucose

A
  • intestinal absorption of food

- Glycogenolysis and gluconeogenesis

44
Q

Glycosuria (or Gluco)

A

When blood glucose level is high over time…

Glucose is excreted in the urine

45
Q

When glucose is excreted in the urine

A

Osmotic pressure of urine increases
It inhibits water reabsorption
It increases urine production =polyuria

46
Q

Exercise Testing

A

Occurs when the patient wants to start a vigorous program and has a > or equal to 10% risk of a cardiac event over a 10 year period

47
Q

FITT (aerobic)

A

3-7 days/week
Moderate intensity (40-50 rpe)
150 min /wk for moderate or 75 for vigorous

48
Q

FITT (resistance)

A

min of 2 nonconsecutive days
moderate (50-69%)
to vigorous
8-10 exercises, 1-3 sets of 10-15 reps

49
Q

FITT (flex)

A

2-3 days/wk
stretch to the point of tightness or slight discomfort
Hold for 10-30 seconds, 2-4 reps
Static or dynamic

50
Q

Hypoglycemia

A

blood glucose is less than 70 mg/dl

-could occur during exercise and or delayed up to 12 hr post exercise -Most serious for DM patients who exercise

51
Q

Symptoms of Hypoglycemia

A

shakiness, sweating, weakness, nervousness/anxiety

52
Q

Neuroglycopenic symptoms of hypoglycemia

A

headache, visual disturbances, mental dullness, seizures, coma

53
Q

CGM

A

Continuous glucose monitoring

54
Q

Preventing Hypoglycemia

A
  • timing of exercise and timing/dose of insulin, -increasing CHO consumption
  • Exercise with a partner
  • CGM before and several hours after
55
Q

DM + retinopathy

A

avoid activities that dramatically elevate BP

56
Q

DM + Autonomic Neuropathy

A

Chronotropic incompetence, blunted BP response, attenuated VO2 kinetics
Monitor potential silent ischemia (Unusual shortness of breath or back pain)
Monitor BP to look for hyper/hypo tension
Monitor HR and BP
Use RPE to assess exercise intensity

57
Q

DM Acute response to exercise dependent on…

A

use and type of medication, timing, blood glucose level prior to exercise
timing, amount, and type of food intake
presence and severity of diabetic complications
Intensity, duration and type of exercise

58
Q

Exercise like Insulin

A

Lowers blood glucose levels
stimulates glucose transport and metabolism
Increases blood flow to exercising muscle
More glucose to enter the muscle to be utilized for energy production

59
Q

Rx of exercise

A
  1. Whole body
  2. Combined aerobic and resistance
  3. Modulate exercise mode and intensity to increase skeletal muscle fiber recruitment
60
Q

Indirect effects of exercise on DM

A

lower HbA1C
lower insulin secretion
lower micro complications

61
Q

Direct effects of exercise on DM

A

increase vasodilator signaling
increase capillary density
increase insulin/p13K signaling (increase glycogen synthesis, increase glute 4 trans)

62
Q

Overall effects of exercise on DM

A

-Improvement in blood glucose control (improve glucose tolerance)
-increased insulin sensitivity on skeletal muscle cells (therefore reducing insulin requirements with Type 1 DM)
Vascular Adaptation

KIN 187 Clinical Exercise Physiology (16 decks)

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