Case 6 Flashcards
1
Q
What are the genetic causes of TIDM?
A
- loss of self tolerance among T cells that attack the beta cells antigens therefore t cells call other t cells to have a coordinated attack on beta cells
- HLA system on chromosome 6 that code for MHC complex which is important for self tolerance
- many diabetic patients have the genes
- HLA -DR3
- HLA-DR4
- Susceptibility genes:
- DQB1*0201
- DQBI*0302
2
Q
What are the Environmental causes of TIDM?
A
- Viruses: directly infect and destory betal cells or may cause betal cells destruction indirectly by exposing autoantigens activating autoreactive lymphocytes
- Diet: exposure of infants to cow’s milk
- low vit D
- early or late exposure to gluten
3
Q
What are the effects of a lack of unsulin on the liver?
A
- Decreased glucose uptake
- decreased glycogen breakdown and gluconeogenesis
- conversion of of fatty acids to ketone bodies
4
Q
What are the effects of a lack of insulin on the muscle?
A
- decreased glucose uptake
5
Q
Whar are the effects of a lack of insulin on adipose tissue?
A
- decreased glucose uptake and storage
- increased breakdown of fat and release of Fatty acids
6
Q
Describe and explain the pathogeneisis of TIDM?
A
- Genetic predisposition linked to HLA
- Environmental challenge possibly viral causes onset leading to inflammation of islets (insulitis) and changes the nature of beta cells so that they become a target for the immune system
- Beta cell destruction
- As a result from the lack of insulin blood glucose levels are raised both before and after a meal in the fasting state
- The cells cannot uptake the glucose available int he blodo therefore the body is in astate of hypoglycaemia
- all regulatory mechanisms against hypoglycaemia are activated:
- increase in lipolysis - resulting in plasma FFA
- increase in ketone bodies - ketoacidosis
- compensated by Kussmaul’s respiration
7
Q
What are the symptoms of TIDM?
A
- Hyperglycaemia
- loss of glucose in urine
- osmotic drag of glucose on water
- water and glucose lost in urine - glycosuria
- electrolytes lost along with water
- increased urine - polyuria and nocturia
- dehydration - increased thirst - polyuria
- eating a lot - polyphagia
8
Q
What is T2DM?
A
- A syndrome due to insulin receptor insensitivity, igher levels of insulin are required to achieve the same effect, a disorder of insulin deficiency
- progressive decline in beta cell function
9
Q
What is sarcopenia and what are its effects?
A
- Loss of muscle mass
- results in increased insulin resistance
10
Q
What are the non-modifable risks associated with T2DM?
A
- Age
- Ethnicity
- Afro-Caribean
- Middle Eastern
- Asian
- Family history of T2DM
- history of gestational diabetes
- polycystic ovary syndrome
11
Q
Whare are the modifiable risk factors of T2DM?
A
- Obesity/Overweight
- Sedentary lifestyle
- Glucose intolerance
- dietary factors
- intrauterine environment
- inflammation
- metabolic syndrome
- Hypertension
- Decreased HDL cholesterol
- Increased triglycerides
12
Q
What is the minimum blood sugar level for diabetic patients
A
- 4mmol/L
13
Q
What are the effects of a low blood sugar level?
A
- Neuroglycopenia
- mild cognitive impairement below that level
- activation of autonomic systems
- sweting
- tremor
- elevated HR
- Coma
- death
14
Q
What are the symptoms of hyperglycaemia?
A
- Ketoacidosis in T2DM
- polydipsia
- polyphagia
- diabetic retinopathy leads to blindness
- fatigue
- headache
- blurred vision
15
Q
Explain the mechanism of insulin release from beta cells?
A
- Brain is dependent on glucose
- Insulin is produced from pancreatic beta cells which have calcium and k-ATPase channels
- glucose enters the cell and is broken down to produce ATP
- The ATP deactivates the K-ATPase channel shutting it down therefore the cell retains potassium and depolarises the membrane
- calcium channel opens
- calcium influx results in insulin granules being re;eased
- in the absence of glucose beta cells don’t produce insulin