NR507 Week 7 Quiz Diabetes Type I Pathophysiology (ANS-
Autoimmune-mediated: environmental-genetic factors tiggers cell-mediated
destruction of pancreatic beta cells.
Idiopathic or non-immune: Secondary to other disease like pancreatitis.
Autoantigens bind to beta cells and circulate blood and lymph-->Activation of T helper 1 + 2 lymphocytes-->Macrophages with releases of IL and TNFa, T cytotoxic cells, B lymphocytes to produce islet cells autoantibodies-->Destruction of beta cells with decreased insulin secretion.
Diabetes Mellitus type 1 Classic Signs (ANS- Polydipsia, polyuria, polyphagia, weight loss, fatigue.
DM Causes
(ANS- Type I:
Autoimmune: Environmental-Genetic predisposition
Idiopathic: secondary to other disease (ex. pancreatitis)
Type II:
Genetic Predisposition Obesity
BOTH: Lack of endogenous insulin
Diabetes Insipidus Kidney Function (ANS- Nephrgenic DI: inadequate response of the renal tubules to Anti Diuretic Hormone (ADH). Acquired or genetic. Gradual onset.
Urine output for DI: 8-12 L/Day.
DM chronic complications (ANS- Neuropathy Nephropathy 1 / 2
Retinopathy Macrovascular Disease Infection
Commons signs for DM Type I and Type II (ANS- Polyuria, polydipsia, fatigue.
DI caused by dysfunction of:
(ANS- Pituitary System
DI Defined (ANS- The inability to concentrate urine and the production of copious amounts of dilute urine.
Pancreatic, insulin secreting cells (ANS- Beta cells; endocrine gland.
DM End Result on cellular level (ANS- Cellular starvation d/t lack of glucose in cells-->liver stores of glycogen depleted-- >use of fat and protein-->Ketones are byproduct of fat catabolism-->Diabetic Ketone Acidosis (DKA) due to ketone build up
OR if less severe: Prevention of lysis of fats-->No ketone formation--
>Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK).
polydipsia (ANS- Excessive thirst.Elevated blood glucose-->water osmotically attracted from cells into blood-- >Intracellular dehydration-->hypothalmic stim. of thirst.
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