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.)
What is T2D?
-chronic disease
-mainly insulin resistance
-overtime pancreas may stop making insulin
-disease of aging and obesity rather than genetics and environmental factors
T2D etiology
- Genetic
- Obesity
- Diet high in ADDED saturated fats and low GI/GL foods
what percentage of diabetics are obese (BMI>30)
60-80%
Explain the progression to T2D over the years
- insulin resistance
- hyperinsulinemia
- Prediabetes - IGT/IFG
- T2D
what is hyperinsulinemia
high levels of insulin in the blood due to IR
–pancreas secreting more insulin to manage glucose levels but body not responding
short term effects of t2d
- classic symptoms of DM
- mild fatigue
- mild or no weight loss
- mild ketosis NOT DKA
2 types of hypoglycemia
- fasting/spontaneous
- Reactive/ functional
Explain fasting/spontaneous hypoglycemia
-Due to tumours, liver disease, alcoholism, endocrinopathies
-relative of absolute lack of insulin relative to counter-reg hormones
explain reactive functional hypoglycemia
-post prandial/absorptive
-occurs in DM when too much insulin OR too little food (intake vs insulin mismatch)
-can be DM prior diagnosis (insulin release vs sensitivity mismatch)
what type of hypoglycemia would you see in dm patients?
reactive functional
hypoglycemia bc of too much insulin or too little food is…
mismatch between insulin and food intake
hypoglycemia in prediabetes is an example of
insulin release and sensitivity mismatch
symptoms of hypoglycemia
specific to DM patients treated with insulin
insulin shock
=fatigue
coma
sometimes death
what is brittle DM
diabetes thats hard to control due to fluctuations of blood sugar
-mostly in type 1
-anxiety around controlling levels
-brain damage if not controlled
