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Diabetes, Acute complication, Pathogenesis, Metabolic abnormalities =>…
Diabetes
Hormones
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Insulin
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Glucose transporters:
- Bc mb are permeable = glucose transporter
Glucagon
Actions of glucagon
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Increase the transport of AA into the liver and stimulates their conversion into glucose = Gluconeogenesis
Secretion of glucagon
Rich protein meal = stimulate glucagon secretion and the conversion of AA to glucose = maintain body's glucose levels
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Glucagon is believed to be secreted by other tissue:
- Gut cells
- Catecholamines
- Growth hormones
- Glucocorticoids
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Diabetes mellitus
- Disorder of carbohydrate, protein, and fat metabolism = imbalance between insulin availability and insulin need
Can be due to:
- Insulin deficiency
- Impaired released of insulin by pancreatic 𝛽 cells
- Defective insulin R
- Inactive insulin
- Insulin destroyed
Etiology
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Type 2
- More prevalent type
- Insulin resistance (impaired ability to the tissue to use insulin)
- Lack of insulin or impaired release of insulin
Type 1 diabetes
- Disorder in which circulating insulin is absent
- Glucagon level elevated
- Pancreatic 𝛽 cells fail to respond to all insulin-producing stimuli
- Insulin inhibits lipolysis
- Ketosis develops = when FA are released and converted to ketoacids in the liver
- Type 1A require exogenous insulin replacement to control blood glucose level and prevent ketosis
Type 2 diabetes
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Describes a condition of fasting hyperglycemia, despite the availability of insulin
Diabetes management
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Nutrition therapy, exercise, and antidiabetic agents
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Diabetes Mellitus
- High prevalence
- Chronic complications
- High mortality
Risk factors:
- Age
- Obesity
- Family history
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Chronic complications:
- Neuropathy 25%
- Retinopathy 32%
- Nephropathy 23%
Pathogenesis
1.Insulin resistance initially stimulates insulin secretion
- Later the insulin response by the beta cells declines= elevated blood glucose
- These patients are less prone to ketoacidosis than are people with type 1 diabetes (still produce some insulin)
Insulin resistance produce:
- High levels of plasma triglycerides
- Low levels of high-density lipoproteins
- Hypertension
- Abnormal fibrinolysis
- And coronary heart disease
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Clinical manifestations of diabetes:
- Type 1 = suddenly
- Type 2 = Insidiously
Polydipsia:
- Intracellular dehydration
Polyphagia:
- Not present in type 2 diabetes
- In type 1 diabetes, it probably results from cellular starvation and the depletion of cellular stores of carbohydrates, fats, and proteins.
Polyuria:
- Glycosuria accompanied by large losses of water in the urine
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Diabetes:
- Disorder of energy metabolism
- Imbalance between insulin availability and insulin need
Insulin + Glucagon (with the liver) = Control availability and utilization of:
- Glucose
- Fat
- Protein
<=> As a fuel for metabolic processes
Acute complication
Ketoacidosis
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Hyperglycemia, ketosis, and metabolic acidosis = 3 major metabolic derangement in DKA
1-2 days of:
- Polyuria
- Polydipsia
- Nausea
- Vomiting, and marked fatigue with eventual stupor that can progress to coma
- Abdominal pain
- Fruity smell
- Hypotension and tachycardia = because of a decrease in blood volume (dehydration)
- Kussmaul breathing = try to eliminate acetone from their lungs
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Other types of diabetes
Gestational diabetes
- Affect pregnant women typically during 3rd semester
- Gestational hormones may interfered with insulin
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Pathogenesis
Type 1 diabetes is thought to result from:
- A genetic predisposition
- A environmental agent could trigger the disorder
- The genetic abnormality affects self-tolerance control of immune
system
- T-cells can recruit other immune cells that coordinate an attack on
beta-cells.
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Chronic complications
Diabetic foot ulcers
Diabetes cause ulceration and infection, eventually resulting in amputation
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Nephropathies
Most common kidneys lesions:
✦ Capillary basement membrane thickening
✦ Diffuse glomerular sclerosis
✦ Nodular glomerulosclerosis
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Activation of kinase result in phosphorylation of the 𝛽 subunit -> activates some enzymes and inactivates other
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