• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/34

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

34 Cards in this Set

  • Front
  • Back
Types of Diabetes- 4
IDDM
NIDDM
Gestational Diabetes
Diabetes Insepidus
IDDM Diabetes
Insulin dependent- Pancreas no longer produces insulin. 10% and juvenile onset
NIDDM
Non insulin dependent- Pancreas does not produce enough insulin or body doesnt use insulin, 90% and adult onset.
Risk factors for type 1 diabetes
Race,family history. Aboriginal/latin american/African
Risk factors for type 2 diabetes
Age >45, obesity, large baby, impaired glucose tolerance(IGT)
Symptoms type 1 diabetes
urination,thirst,hunger,weightloss,fatigue,nausea,vomiting,sweet breath.
Symptoms type 2 diabetes
Same as type 1 but also,infections, slow wound healing,tingling/numbness in extremities, skin/gum/bladder infections.
Pancreatic hormones made where?
Islet of Langerhans
Islet Cells
Beta cells, A1 (D) cells, A2 (A) cells.
What do beta cells do? What percentage of islet cells are beta?
Secrete insulin, 50%
What do Alpha 1(D) cells do?
Release somatostatin.
What do Alpha 2(A) cells do?
Release glucagon
What does somatostatin do?
decreases insulin and glucagon release
What does glucagon do?
increase blood sugar and insulin release
What is glucose dependent insulin release?
A graded response, more glucose more insulin
What does biphasic insulin release mean?
Normal insulin released immediatly, NIDDM delayed and lower, IDDM no insulin released.
Stimulants of insulin release
Glucose,Amino acids(Arg,Leu), FA's(acute), Sulphonylureas
What is a insulin secretagogue
Stimulant of insulin release
Inhibitors of insulin release
Somatostatin, Sympathetic activation(A2 on beta cells), Decreased blood glucose.
Action of insulin
Increased uptake,utlizating and storage of glucose, aas and fats.
Mechanism of insulin
Insulin receptor, RTK dimerizes, autophosphorylates receptor, phosphorylate target proteins, gene expression altered.
Actions of glucagon
Glycogen bdown, gluconeogenesis, lypolysis-increased
gylcogen synthesis and glucose oxidation decreased.
Raises blood glucose
Glucagon raised by, lowered by
Raised by Arginine,low blood glucose, sympathetic/parasympathetic activation
Lowered by High glucose,somatostatin
Characteristics of Diabetes Mellitus
Hyperglycemia,Glycosuria, Dysfunctional protein metabolism, ketosis
Pathologies of diabetes
Macrovascular, Hypertension, Retinopathy, Neuropathy, Nephropathy
People with diabetes in 2010
239 million
Cost of diabetes in Canada
12 billion annually
What is congenital dysfuction of insulin release called?
Persistant Hyperinsulinemic Hypoglycemia of Infance. PHHI
What is PHHI? What causes it? What gene is it linked to? Treatment
Excessive insulin secretion. Autosomal recessive 11p15.1 mutations on beta-cell Katp
Diazoxide,somatostatin,partial removal of pancreas
Link between Katp mutations and diabetes?
Decreased Katp= More insulin secretion
Increased Katp= Less insulin secretion=Diabetes
What does post prandial mean?
After eating a meal
What is an Incretin
Incretins are a group of gastrointestinal hormones that cause an increase in the amount of insulin released from the beta cells of the islets of Langerhans
Difference between IR and Diabetes?
Need IR and beta cell dysfunction to develope T2DM.
Therepeutic targets of T2DM? Three
Increase insulin secretion
Increase insulin sensitivity
Lower blood glucose independent of insulin