WEEK 7 - WHEN INFLAMMATION PERSISTS

Question 1

Diabetes type 1

Answer 1

• beta cells in the pancreas are destroyed by the immune system
• induced by genetic factors
• less insulin is produced, therefore less glucose is let into the cells, leaving most in the blood
• sudden onsets, before the age of 20
• treated with insulin supplements

Causes

• Environmental event (infection)
• T-lymphocyte mediated hypersensitivity against β cell antigen. A cell mediated immune
  response.
• Genetic predisposition (multiple potentially identified genes, not one singled out)
• May also be idiopathic
• insulin dependant

Symptoms
- naseau, vomitting
- increased urination + sweating
- polydypsia (thirst) + polyphagia (hunger)
- weight loss
- blurred vision

Question 2

Diabetes type 2

Answer 2

• issues with receptor binding or insulin signalling inside the cells occurs.
• Insulin receptors on the surface of liver, adipose tissue and skeletal muscle tissue. These receptors are stimulated when bound to by insulin, and promote the uptake of glucose.
• target cells are non-responsive to insulin, leaving excess glucose in the blood stream
• Persistent blood glucose - glucose travels to kidneys where it is secreted in urination (glucosuria) leading to osmotic diuresis, which is the loss of water in urine as water dilates the glucose. This leads to polyuria (excess urination, loss of water and electrolytes).
• Insulin resistance also leads to polyphagia, (hunger), as the body is depleted and requires energy due to the poor uptake of glucose.

causes
- genetic factors predispose susceptibility to the disease
- lifestyle factors (obesity, sedentary lifestyle, poor diet)
- adult onset, symptoms occur gradually

Question 3

atherosclerosis description

Answer 3

• a disease of artieries characterised by fatty deposits (plaque) in their inner walls
• chronic condition
  
  • occurs in big elastic arteries, like aorta, iliac arteries, carotid arteries, renal arteries, coronary arteries and arteries going to the brain.

Question 4

risk factors leading to atherosclerosis (non- modifiable (4), modifable (7))

Answer 4

non-modifiable

• age - 40—60
• sex - males at higher risk
• post menopausal - in females
• genetic predisposition

modifiable

• hypertension
• Dyslipidemia - high density of bad fats(LDLs)
• Diabetes malitis
• Smoking
• increased alcohol consumption
• high tryglyceride levels
• sedentary lifestyle

Question 5

atherosclerosis pathogenesis

Answer 5

1. normal vessels
2. endothelial injury - leads to cells binding to the endothelial layer (platletes, WBC), releasing growth factors into the vascular wall.
3. endothelial —> permeable - Low density Lipid proteins (LDLs) fill the intima and accumulate. Monoctyes also pass through into the fatty core, specialising into macrophages and destroying LDL’s.
4. fatty streak - these macrophages filled with LDL’s build up and are known as foam cells. This inflammatory response also leads to the uptake of collagen, further building the fatty core.
5. advanced plaque