Diabetes Flashcards

1
Q

Diabetes

A

patients w/ diabetes are classified in 2 groups
- Type 1 (insulin-dependent) 10% of cases
- 20,000 new patients
- Type 2 (non-insulin dependent) 90% of cases
- 180,000 new patients
- number of people developing type 2 diabetes increasing due to aging population, rise in obesity, lack of excercise

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2
Q

Diabetes Mellitus

A

Not a single disease, but a group of diseases caused by increased fasting blood glucose levels due to relative or absolute deficiency of insulin
- glucose remains in blood despite not having eaten

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3
Q

Chronic elevated blood glucose leads to

A
  • Nerve damage, blindness, impotence, amputation
  • Major cause of premature kidney failure, heart attack and stroke
  • leads to blindness possibly due to improper glycosylation of proteins (not fully known)
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4
Q

Type 1 diabetes

A
  • Caused by absolute deficiency of insulin as a result of autoimmune attack on the B-cells of the pancreas
  • Requires both environmental stimulus and genetic determinant allowing B-cells to be targeted by immune system
  • not instantaneous loss of insulin
  • over time will decrease B-cells
  • once reach pink line no longer enough insulin and diabetes will begin to present symptoms (abrupt)
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5
Q

Diagnosis of Type 1 Diabetes

A
  • Onset occurs during childhood or puberty
  • patients present with polyuria (freq. urination), polydipsia (excessive thirst) and polyphagia (escessive hunger)
  • symptoms include fatigue, weight loss and weakness
  • Diagnosed w/ fasting blood glucose > 126 mg/dl (normal is around 70)
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6
Q

Metabolic changes

A
  • Profoundly affects metabolism in liver, muscle and adipose
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7
Q
  1. Hyperglycemia and ketoacidosis
A
  • Liver increases glucose production, while muscle and adipose take up less glucose
  • Increased mobilization of FAs from adipose combined w/ increased ox. of FAs in liver and increased ketone body synthesis
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8
Q
  1. Hypertriacylglyceridemia
A
  • Liver cannot dispose of all FAs so packages them into VLDL
  • Chylomicrons and VLDL in plasma increase because lipoprotein lipase activity is decreased; accumulate in blood
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9
Q

Treatment of Type 1 diabetes

A
  • Patients not producing insulin so cannot respond to changing blood glucose levels
  • rely on exogenous insulin
  • Standard insulin treatment; 1 or 2 daily insulin injections
  • Intensive insulin treatment; 3 or more daily injections, more freq. monitoring of blood glucose, decreases complications by 60% compared to standard
  • Elevated blood glucose leads to formation of glycosylated hemoglobin (A1C) which is a marker of blood gucose
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10
Q

Hypoglycemia in Type 1 diabetes

A
  • Therapeutic goal; reduce blood glucose to minimize complications of disease
  • difficult to achieve approprate doses of insulin
  • too much insulin. is most common complication and leads to hypoglycemia
  • hypoglycemic episodes are elevated in intensive insulin therapy compared to standard insulin therapy
  • Hypoglycemia is NOT a symptom of diabetes; it is strictly a complication of the therapeutic drugs
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11
Q

Type 2 Diabetes

A
  • Most common form
  • has a strong genetic component
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12
Q

Type 2 diabetes results from combination of

A
  1. Insulin resistance- inability to target tissues (liver, adipose, muscle) to respond to normal levels of insulin - most common (obesity)
  2. Non-functional B-cells- If B-cells are normal they can compensate by increasing amount of insulin
    - can overcome barrier of resistance
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13
Q

Metabolic abnormalities of Type 2 diabetes

A

Milder than type 1
- limited insulin secretion can still slow down ketogenesis and lessen ketoacidosis

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14
Q

Diagnosis of type 2 Diabetes

A
  • Develops gradually; some develop polyuria, polydipsia, polyphagia
  • Diagnosis based on hyperglycemia; blood glucose conc > 126
  • Patients do not require insulin injections to sustain life
  • eventually B-cells fail completely leading to req. of insulin therapy
  • benefit from standard therapies
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15
Q

Insulin rise in obese patients

A
  • Obese patients have 3x the amount of insulin but still can compensate and have same blood glucose level as normal patient
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16
Q

Insulin Resistance

A
  • Decreased ability of liver, adipose, muscle to respond to normal levels of insulin
  • characterized by uncontrolled liver production of glucose and decreased glucose uptake by muscle and adipose
  • Obesity is most common cause of insulin resistance but most obese insulin resistant patients do not develop diabetes
  • insulin secretion is 2-3 fold higher in obese patients
  • to compensate for lowered effect of insulin
  • Keeps blood glucose levels the similar to lean subjects
17
Q

Causes of insulin resistance

A
  • Insulin resistance increases w/ weight gain
  • decreases w/ weight loss
  • excess adipose is key in its dev.
  • adipose does not simply store energy, but also is a secretory organ
  • changes in adipose secretions in obesity leads to insulin resistance
18
Q

Metabolic changes in type 2 diabetees

A
  • Result from insulin resistance of liver, muscle, and adipose tissue
    1. Hyperglycemia- increased production of liver glucose combined w/ decreased tissue usage of glucose
  • ketosis is minimal because presence of insulin lowers ketogenesis
    2. Hypertriacylglyceridemia- low lipoprotein breakdown in adipose due to low levels of lipoprotein lipase
19
Q

Chronic effects and prevention of disease

A
  • Hyperglycemia is moderated by therapies but do not fully normalize metabolism
  • chronic hyperglycemia causes blindness, renal faliure, heart attack/stroke
  • As control of glucose improves incidence of retinopathy decreases
  • no preventative treatment for type 1
  • Type 2 risk is decreased by modification of diet, wight loss, excercise
  • hypoglycemic drugs
20
Q

Incidence of Type 2 Diabetes

A
  • Weight gain and lack of excercise promote development of type 2 diabetes
  • Hypertension (high blood pressure) and elevated low density lipoproteins (LDL) promote type 2 diabetes
  • Elevated high density lipoproteins (HDL) may retard development of type 2 diabetes