Diabetes Mellitus 2
Terms
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- What is Diabetes?
- A disturbance in the carbohydrate homeostasis regulated by the opposing actions of INSULIN and GLUCAGON
- Diabetes definition again?
- a state of CHRONIC HYPERGLYCEMIA due to deficiency of INSULIN or a combination of inuslin receptor abnormalities and inadequate insulin secretion to compensate.
- What else with Diabetes?
-
-Accompanying disturbances in carbohydrate, fat and protein metabolism.
-80-90% of pancreatic Beta cells dysfxn is present even with early diagnosis of DM-1 - Pancreas?
- -Both an endocrine and exocrine gland
- Islets of Langerhans?
-
-Insulin
-Glucagon - What are the 3 types of HORMONE secreting cells?
-
-Alpha cells = Glucagon
-Beta cells= Insulin
-Delta cells= Gastrin/Somatostatin - What cells secrete Glucagon?
- Alpha cells
- What cells secrete Insulin?
- Beta cells
- What cells secrete Gastrin/Somatostatin?
- Delta cells
- Acinar cells?
-
-Amylase
-Lipase - What kind of lipase and amalyse levels does a diabetic usually have?
- Normal levels
- Beta cells?
-
-Pro-insulin into inuslin via proteolytic enzymes.
-C-peptide is the catalyst that breaks the disufic bonds
see notes ask* - Regulation on Insulin?
-
Chemcal:
-Insulin (neg feedback)
-Glucose (hyper and hypoglycemia)
-Amino and fatty acids
-Glucagon
Para/sympathetic stim
Hormones:
Proarglandins - Insulin enhances?
- Glucose uptake
- Without Insulin=
- -no glucose=no ATP!
- GLUT 4?
-
Transporter
Glut 4 is transported outside the cell membrane where it connects and transports glucose into the cells of
-Skeletal muscle
-Cardiac muscle
-Liver
-Adipose tissue
*Facilitates intracellualr transport of K+ - 4 muscles that util. Glucose?
-
-Sk Muscle
-Cardiac muscle
-Liver
-Adipose tissue - Insulin is a Anabolic Hormone, what the hell does that mean?
-
Anabolic=Builder
-Stimulates cellular metabolism using glucose as fuel
-SYNTHESIS in liver, muscle, and adipose of:
-Protein
-Carbs
-Lipids
-Nucleic Acids - Where does Insulin metabolism occur?
- -Liver and Kindey (enzymatic catabolism of disulfide bonds)
- Glucogenisis?
- Glucose---Glycogen
- Glycolysis?
- Glycogen---simple sugars
- Sites of Insulin Activity?
-
-Liver
-Muscle
-Adipose tissue - Insulin metabolism?
-
-increases cell metabolism
-Decreases overall blood glucose
-facilitates intracellular transport of K+ - Glucagon?
-
-Inverse relationship with Insulin
-Prod in pancreatic alpha cells
-Secretion inhib by high glucose/stim by low glucose.
-Secretion stim by high protein diet - Glucagon in the liver?
-
-Stim glucoeogenesis and glycogenolysis
-Antagonizes Insulin
-Stim Lipolysis with ketogenic effect - Which is best to treat hypoglycemic state?
- Glucagon
- Pancreatic Somatostatin and Carbohydrate Metabolism?
-
-Metabolizes fat, protein, carbs
(homeostasis of ingested nutrients)
-Regulates Pancreatic A and B fxn
-Inhibits insulin and glucagon secretion
-Prevents excess secretion of inuslin - How many in US have diabetes?
-
-18.2 in US
-5-10%= Type 2
-90-95%=Type I - What group is most suscept to Type I?
-
AA
Hispanics
Pima Indians - What is DM I?
-
-Pancreatic Islet Beta cell autoimmune destruction
-pts are Insulin dependant
-Pts are prone to Ketoacidosis
-Usu under 30yo at time of dx
-Peak indicence at school age and adolescence
-Highest incidence in Northern Europe and in the US - Bascially DM I?
- -Beta cell failure
- What is the most common DM?
- DM Type II!
- DM II?
-
-Most common type
-Due to insulin resistance and lack of insulin secreation compensation
-pts may require Insulin
-HTN, Hyperlipidemia, atherosclerosis are usu. present or at hight risk to develop.
Pts usu. greater than 40 yo - Insulin Resistance Syndrome?
-
AKA Syndrome X/Metabolic syndrome
-Hyperglycemia
-Hyperinsulinemia
-Dyslipidemia
-HTN
-Increased CAD, MI, PVD, Stroke
*25% of the general non obese pop. have insulin resist. - MODY?
-
Maturity Onset Diabetes of the Young
-Rare form of NIDDM
-six types
-Genetic mutation of Beta cells
-Non-obese