DIABETES MELLITUS Flashcards
explain what is diabetes mellitus
-chronic disease
-insulin deficiency or resistance
-hyperglycemia bc of lipid, cho, protein metabolism disturbances
Mechanism of diabetes insipidus?
-hyperglycaemia bc of excessive water loss
= hypertonic blood volume
-antidiuretic hormone dysregulation
-not insulin related
what is amylin?
Where and how much secreted?
peptide hormone thats released with insulin by beta cells (100:1 insulin)
what cells secrete insulin? glucagon? somatostatin?
insulin = beta
glucagon = alpha
somatostatin = delta
all in the pancreas
Purpose of amylin?
blood glucose regulation via
1. decreased food intake
2. delayed gastric emptying
3. decreased glucose production
how would amylin delaying gastric emptying help regulate blood glucose?
delayed absorption of glucose
= slower time from GIT to bloodstream
=stable post-meal glucose levels
Explain the role of insulin
- Mediates transport of glucose from blood to muscle or adipose cells
- inhibit glycogenolysis and gluconeogenesis
- promotes energy storage via glycogen/fat production and body tissues building via proteins
is insulin catabolic?
No anabolic bc it creates molecules in body and uses energy in process
role of glucagon?
- promote glycogenolysis + gluconeogenesis
- inhibit energy storage (glycogen and fat production) and building of tissue via proteins
is glucagon anabolic?
no its catabolic bc breaks down molecules and releases energy.
what GLUT transporter is mediated by insulun, and where can we find it?
GLUT-4
-commonly in muscle and adipose tissues
List GLUT transporters
GLUT 1 - RBC, brain
GLUT 2 - liver * fruc and galac too
GLUT 3 - brain
GLUT 4 - skm and adipose
GLUT 5 - fructose in intestinal level
classifications of DM
- pre diabetes (IFG or IGT)
- t1d
- t2d
- pre existing DM in pregnancy (T1 or T2)
- GDM
- hypoglycemia
Improvements in Canada for diabetes needed?
treatment, screening, access and education
whats the differences between IFG vs IGT?
higher levels of glucose fasted state vs hyperglycemia post prandial
new vs more established
risks of diabetes and CVD vs higher risk of CVD
both show no symptoms
blood levels for IGT? IFG?
IGT : 7.8-11
IFG: 6.1 -6.9
what is the overload hypothesis?
related to the development of T1D
stress exposure to fetus = autoimmune response triggered
explain the etiology of T1D
autoimmune disease/susceptible
typically have antibodies for beta cells, insulin or beta cell antigens that destroy them
- development of autoantibodies triggered via environment-gene interaction
- around 2 years of life then manifested later in life
huge genetic component
in t1d, what is the thresholfd for when minimal insulin is secreted
loss of 80-90% beta cells
Acute effects of T1DM
- hyperglycemia
- glucosuria (glucose spills into urine)
- polyuria - osmotic diuresis bc glucose spills into urine
- polydipsia - thirst
- polyphagia -increased food intake
- dehydration
- fatigue
- weight loss even with increased apetite
why do T1D patients lose weight even tho they are more hungry?
combination of all the acute effects
- inability to uptake glucose in cells so body perceives this as a state of energy deficit even tho you have high blood glucose levels
-protein and fat broken down instead of cho
-excretion of water
-loss of calories through urine
severe effects of T1D?
Ketones broken down for fuel
-ketosis- acumulation of ketones in blood
-ketoacidosis - lower blood PH bc of uncontrolled ketosis
-diabetic ketoacidosis DKA - lowered blood pH
What happens during DKA?
complete deficiency in insulin
blood pH decrease = hyperapnea
brain uses ketones for energy
= stupor
=coma
Can we prevent or treat T1D?
yes, we can delay the onset
-manage life stressors
-avoid autoimmune responses that triggers inflammation (gluten ex.)
