Endocrine System - created from Mind Map

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Type 1 DM

Type 2 DM

Diabetic Ketoacidosis (DKA)

an absolute deficiency of insulin

clinical manifestations: 3 P's - polydipsia, polyuria, polyphagia. tachycardia, weight loss and fatigue

results from beta cell destruction

PATHOPHYSIOLOGY - Genetic factors OR viral infections causing an immune response against beta cells -> beta cell destruction -> lack of insulin released -> GLUT-4s are not activated -> glucose unable to be taken up by the cells -> release of glucagon -> liver continues to release glucose = HYPERGLYCAEMIA

TREATMENT: insulin

reliant on insulin replacement

POLYDIPSIA -excessive thirst LINK - high blood sugars cause kidneys to produce more urine in order to get rid of extra glucose = causing you to become more thirsty

POLYURIA - frequent urination. LINK - excess levels of sugar that should be redirected into the blood, ends up in urine where it then pulls more water and results in more urine

POLYPHAGIA - excessive hunger. LINK - the lack of insulin does not transport glucose from the blood stream to cells like its supposed to and instead glucose leaves in the urine. Leaving the cells without glucose and telling you to eat more food in order to gain more glucose

GLUT- 4s : insulin-regulated glucose transporter that is responsible for insulin-regulated glucose uptake into fat an muscle cells

GLUCAGON - a glucoregulatory peptide hormone that counteracts the actions of insulin by stimulating hepatic glucose production and thereby increase BGL

BETA CELL normal function: stored in the PANCREAS, produces, stores and releases the hormone insulin.

when blood glucose levels start to rise beta cells respond by secreting insulin

insulin resistance due to:

PATHOPHYSIOLOGY: high glucose stimulates insulin release from pancreas. insulin receptors do not work properly or as efficiently, pancreas believes it needs to secrete more insulin as it is not being properly received in the cells. excess glucose = glucosuria -> polyuria

TREATMENT: diet and exercise, close monitoring of BGL's, oral hypoglycaemic agents (OHA), insulin

decreased beta cell responsiveness to increased glucose levels

decreased insulin production

increased insulin resistance at the cell

reduction in the number of insulin binding sites

decrease in the amount of insulin binding to receptors

condition related to hyperglycemia which gradually develops over hours/days. the body starts breaking down fat as a rate that is too fast, ketones then build up in your blood

PATHOPHYSIOLOGY: hyperglycemia -> glucosuria/polyuria -> dehydration and hypovolemia ->

LAB markers: BGL >11mmol/L, ketones present in blood and urine, pH <7.3, K+ and Na+ changes, fruity breath, polyuria, polydipsia

Management: correction of dehydration - fluid resus IVF 24-72 hours, reverse ketosis - insulin infusion, dextrose infusion with/without KCI, acid-base and electrolyte corrections - regular 1/24 BGL's, ABG's, urine ketone and monitoring of U&E

Later signs and symptoms: sunken eyes, tachycardia, dry skin, headache, fatigue, seizures and coma

without enough insulin, the body cant use sugar for energy. this prompts the release of hormones that break down fat as fuel to produce acids known as ketones. excess ketones in blood eventually spill over and end up in urine