Metabolic Disease: Diabetes Mellitus Flashcards
Statistics of Diabetes
7% of the US population
1.5 Million new cases diagnosed each year
Diabetes Mellitus
A group of metabolic disease with hyperglycemia over a prolonged period
Hyperglycemia
elevated blood glucose levels
`Acute complications caused by DM
diabetic ketoacidosis, nonketotoic hyperomolar coma, death
Chronic Complications caused by DM
Heart Disease, stroke, chronic kidney failure, neuropathies, retinopathy, nephropathy
Polyuria
Excessive urination
Polydipsia
Excessive drinking/thirst
Polyphagia
Excessive eating/hunger
Symptoms of DM
polyuria, polydipsia, polyphagia, blurred vision, weight loss
Type 1
Insulin dependent diabetes mellitus/juvenile
Auto immune destructiON of beta cells in the pancreas
10% of DM
Type 2
non insulin, adult onset
insulin resistance in skeletal muscle, liver, and adipose tissue +insulin secretory defect
90% of DM
Other types of DM
gestational, specific genetic syndrome, drugs, surgery and other illnesses
Fasting Plasma Glucose Prediabetic
100-125 mg/dl
Fasting Plasma Glucose diabetic
> or equal to 126
A1C values-diabetic
> or equal to 6.5%
Oral Glucose Tolerance Test-diabetic
> or equal to 200
Oral Glucose Tolerance Test-normal
<140 mg/dl
Fasting Plasma Glucose-Normal
<100 mg/dl
Normal A1C
<5.7%
Oral Glucose Tolerance Test-prediabetic
140-199 mg/dl
HbA1C
Glycosylated Hemoglobin
60-80% attach of glucose to N terminal amino acid valine of the beta chain of hemoglobin
Advantages of HbA1C
predictive of vascular conditions, helps management decisions, easy to measure, relatively cheap
Limitations of HbA1C
Only provides an approximate measure of glycemia
Unable to address GV or hypoglycemia
Unreliable in certain conditions (RF, Hb abnormalities, other)
Beta Cells
Insulin-promotes the storage of glucose, amino acids, and fats
Alpha Cells
Glucagon-promotes the mobilization of fatty acid and glucose
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
Causes of Type 2
insulin resistance
insensitivity of receptors
lifestyle factors and genetics
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
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
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
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
Normal blood pH
7.35-7.45
Kussmaul respiration
rapid and deep breathing, can result in loss of the bicarbonate content in the extracellular fluid
Insulin
transfers the glucose from the blood to the cells
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,
Type 2 pathophysiology (pancreas)
- decrease in insulin secretion
- increase in beta-cell apoptosis
- decrease in beta cell mass
- Hyperglucagonemia
Type 2 pathophysiology (Gut)
impaired incretin effect
Type 2 pathophysiology(Liver)
- Insulin resistance
- Increase hepatic glucose output
Type 2 pathophysiology (Muscle)
Insulin Resistance
Type 2 pathophysiology (Adipocytes)
- Increase in circulating fatty acids
- Hyperlipidemia
Insulin inhibits
glycogenolysis (liver)
gluconeogensis (liver)
Insulin stimulates
transport of glucose into muscle and adipose tissue
storage of glucose as glycogen
Sources of blood glucose
- intestinal absorption of food
- Glycogenolysis and gluconeogenesis
Glycosuria (or Gluco)
When blood glucose level is high over time…
Glucose is excreted in the urine
When glucose is excreted in the urine
Osmotic pressure of urine increases
It inhibits water reabsorption
It increases urine production =polyuria
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
FITT (aerobic)
3-7 days/week
Moderate intensity (40-50 rpe)
150 min /wk for moderate or 75 for vigorous
FITT (resistance)
min of 2 nonconsecutive days
moderate (50-69%)
to vigorous
8-10 exercises, 1-3 sets of 10-15 reps
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
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
Symptoms of Hypoglycemia
shakiness, sweating, weakness, nervousness/anxiety
Neuroglycopenic symptoms of hypoglycemia
headache, visual disturbances, mental dullness, seizures, coma
CGM
Continuous glucose monitoring
Preventing Hypoglycemia
- timing of exercise and timing/dose of insulin, -increasing CHO consumption
- Exercise with a partner
- CGM before and several hours after
DM + retinopathy
avoid activities that dramatically elevate BP
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
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
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
Rx of exercise
- Whole body
- Combined aerobic and resistance
- Modulate exercise mode and intensity to increase skeletal muscle fiber recruitment
Indirect effects of exercise on DM
lower HbA1C
lower insulin secretion
lower micro complications
Direct effects of exercise on DM
increase vasodilator signaling
increase capillary density
increase insulin/p13K signaling (increase glycogen synthesis, increase glute 4 trans)
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