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
Alpha Cells
Glucagon-promotes the mobilization of fatty acid and glucose
26
Causes of Type 1
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
Causes of Type 2
insulin resistance insensitivity of receptors lifestyle factors and genetics
28
Type 1 is autoimmune... why
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
When you lose 80-90% of beta cells mass
Lack of insulin, abnormalities occur in the muscle and liver Excessive hepatic glucose production (gluconeogenesis) Decreased muscle glucose uptake Glucose intolerance
30
Metabolism shift from CHO to Fat ketoacidosis
- 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
Diabetic Ketoacidosis
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
Normal blood pH
7.35-7.45
33
Kussmaul respiration
rapid and deep breathing, can result in loss of the bicarbonate content in the extracellular fluid
34
Insulin
transfers the glucose from the blood to the cells
35
Type 2 pathophysiology
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
Type 2 pathophysiology (pancreas)
- decrease in insulin secretion - increase in beta-cell apoptosis - decrease in beta cell mass - Hyperglucagonemia
37
Type 2 pathophysiology (Gut)
impaired incretin effect
38
Type 2 pathophysiology(Liver)
- Insulin resistance | - Increase hepatic glucose output
39
Type 2 pathophysiology (Muscle)
Insulin Resistance
40
Type 2 pathophysiology (Adipocytes)
- Increase in circulating fatty acids | - Hyperlipidemia
41
Insulin inhibits
glycogenolysis (liver) | gluconeogensis (liver)
42
Insulin stimulates
transport of glucose into muscle and adipose tissue | storage of glucose as glycogen
43
Sources of blood glucose
- intestinal absorption of food | - Glycogenolysis and gluconeogenesis
44
Glycosuria (or Gluco)
When blood glucose level is high over time... | Glucose is excreted in the urine
45
When glucose is excreted in the urine
Osmotic pressure of urine increases It inhibits water reabsorption It increases urine production =polyuria
46
Exercise Testing
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
FITT (aerobic)
3-7 days/week Moderate intensity (40-50 rpe) 150 min /wk for moderate or 75 for vigorous
48
FITT (resistance)
min of 2 nonconsecutive days moderate (50-69%) to vigorous 8-10 exercises, 1-3 sets of 10-15 reps
49
FITT (flex)
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
Hypoglycemia
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
Symptoms of Hypoglycemia
shakiness, sweating, weakness, nervousness/anxiety
52
Neuroglycopenic symptoms of hypoglycemia
headache, visual disturbances, mental dullness, seizures, coma
53
CGM
Continuous glucose monitoring
54
Preventing Hypoglycemia
- timing of exercise and timing/dose of insulin, -increasing CHO consumption - Exercise with a partner - CGM before and several hours after
55
DM + retinopathy
avoid activities that dramatically elevate BP
56
DM + Autonomic Neuropathy
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
DM Acute response to exercise dependent on...
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
Exercise like Insulin
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
Rx of exercise
1. Whole body 2. Combined aerobic and resistance 3. Modulate exercise mode and intensity to increase skeletal muscle fiber recruitment
60
Indirect effects of exercise on DM
lower HbA1C lower insulin secretion lower micro complications
61
Direct effects of exercise on DM
increase vasodilator signaling increase capillary density increase insulin/p13K signaling (increase glycogen synthesis, increase glute 4 trans)
62
Overall effects of exercise on DM
-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