Unit 4 - Endocrine Diseases pt 1 Flashcards
Diabetes Mellitus (DM)
Condition characterized by impaired glucose metabolism. There are two major types.
3rd leading cause of death and leading cause of blindness and lower extremity amputations
diabetes and kidney disease
leading single cause of kidney disease in the US
diabetic nephropathy: elevated protein albumins in the urine
diabetes process/terminology
inc blood glucose levels –> hyperglycemia
regulated by insulin (produced and secreted by beta/islet cells)
insulin activity
Insulin attaches to receptors
Activates Glucose Transporters (G4) to transport Glucose across the Cell Membrane
Alpha Cells secrete Glucagon - Raises blood glucose
Converts Liver Glycogen to Glucose
Type 1
Juvenile onset – (~ 5% Type 1)
are insulin dependent
Type 2
Maturity onset – (~ 95% Type 2)
not an insulin deficit, but poor response to insulin secretion
Commonalities-Types I & II
3Ps
Polyphagia-excessive appetite
Polyuria-osmotic diuresis
Polydipsia-excessive thirst
commonality: hyperglycemia s/s
dry mouth inc thirst blurred vision weakness headache frequent urination
commonality: glucosuria
glucose from the blood spills over into the urine
glucose renal t-max above 180 mg%
other commonalities:
- elevated blood lipids
- poor wound healing and circulation
- peripheral neuropathy (mx weakness, decreased DTRs)
- assessed by glucose tolerance test
- hyperesthesia
- anesthesia
- atherosclerosis
- infections, gangrene, amputations
etiology/risk factors of type 1
loss of Pancreatic Islet Beta Cells Loss of Insulin Production/Secretion Causes ?? Autoimmune mechanism Viruses Rubella Coxsackie Mumps (Rubulavirus) CMV
etiology/risk factors of type2
Decreased sensitivity to insulin by insulin receptors
Decreased number of insulin receptors
Contributing Causes Genetic predisposition Lifestyle!!! Excess bodyweight/obesity Sedentary behavior
differences in type 1 and 2
Type 1:
- Normal Body Type
- No Central Obesity
- insulin shock
- ketoacidosis
- exogenous insulin required
- autoimmune disease
- diabetic coma
Type 2:
- obesity
- respond to oral hypoglycemics
criteria for the diagnosis of diabetes
A1C > 6.5% or
FPG > 126mg/dL (fasting is defined as no caloric intake for at least 8 hours) or
2 hour plasma glucose > 200 mg/dL (following glucose load containing equivalent of 75 g of anhydrous glucose dissolved in water) or
Random plasma glucose > 200 mg/dL with classic symptoms of hyperglycemia
urine glucose test
metabolic syndrome
condition characterized by the presences of several risk factors in a single individual that greatly increase the risk of cardiovascular disease and diabetes
indicators of metabolic syndrome
Central obesity (excessive fat tissue in and around the abdomen)
Hyperlipidemia (blood fat disorders — mainly high cholesterol & triglycerides and low HDL’s
Elevated blood pressure (130/85 mmHg or higher)
Insulin resistance or glucose intolerance (the body can’t properly use insulin or blood sugar)
Prothrombotic state (e.g. high fibrinogen or plasminogen activator inhibitor in the blood)
Proinflammatory state (e.g. inflamation present- C-reactive protein in the blood)
diagnosis of metabolic syndrome
Three or more of the following risk factors in a single individual would constitute the presence of metabolic syndrome.*
Abdominal obesity Men >102 cm (>40 in) Women >88 cm (>35 in) Triglycerides >150 mg/dl HDL cholesterol Men <40 mg/dl Women <50 mg/dl Blood pressure >130/>85 mm Hg Fasting glucose >110 mg/dl
ketoacidosis
“Diabetic Coma”- (“much more likely with Type 1”)
Unable move glucose into the cell due to insufficient insulin levels. Blood sugar levels continue to rise.
Acidic state caused by elevated ketones in the blood due to incomplete breakdown of fatty acids .
Hyperglycemia
Ketone bodies (Acetone) are formed
Metabolic acidosis results (pH < 7.35)
Symptoms/consequences – “potentially life-threatening”
nausea, vomiting, abdominal discomfort, altered breathing pattern, coma, and death.
“acetone breath”
tx of ketoacidosis
IV fluids
insulin
correction of electrolyte disturbance
may also require sodium bicarbonate if pH remains low despite the measures listed above
Diabetic Gastroparesis
Autonomic Neuropathy
Delayed Gastric emptying
Ileus-decreased Peristalsis
Poor appetite
diabetes insipidus
Affects the posterior pituitary and hypothalamus
The posterior pituitary releases the Anti-diuretic Hormone (ADH) or Vasopressin
ADH acts on the kidneys to conserve H20 and reduce urine output
ADH secretion is reduced or absent
Urine volume increases
Patient becomes dehydrated
Electrolyte imbalance (concentrated)
causes of DI
Head injury
CNS Infection
Neurosurgery
Tumors
nephrogenic DI
Occurs when the kidneys do not respond to ADH
Usually occurs due to:
Heredity
Acquired- adverse medication response
Inappropriate ADH-hypersecreton of ADH
Retention of fluid Dilutional Hyponatremia Nausea Vomiting Confusion Seizures
