Pathology Diabetes Flashcards Preview

Jason's Metabolism Block > Pathology Diabetes > Flashcards

Flashcards in Pathology Diabetes Deck (30):
1

DM is a group of conditions resulting in?

chronic hyperglycaemia

2

conservative or aggressive glycaemic control better?

aggressive

3

what is the major insulin-responsive site?

muscle

4

Insulin receptor activation does 3 things:

1. send GLUT4 to allow glucose in
2. PI-3K: lipid, protein, glycogen synthesis/cell survival
3. MAP kinase: growth

5

Type 2 severe hyperglycaemic you get?

hyperosmolar coma

6

3 areas of pathology for DM/hyperglycaemia?

Macrovascular
Microvascular
Cellular/extravascular

7

What kind of macrovascular effects do you get with hyperglycaemia?

atheroma in larger vessels
10x risk of CVD/stroke

8

What can happen at kidney macrovascularly with hyperglycaemia?

atheroemboli

9

3 big regions with microvascular effects of hyperglycaemia?

kidney
retina
delayed wound healing

10

Glycosalation of proteins in 2 steps:

1. initially labile (Schiff bases)
2. Stable (Advance glycation end products - AGEs)

11

initial presenation of diabetic nephropathy?

proteinuria

12

hyperglycaemia and immune system?

impaired neutrophils

13

How does DM cause renal failure? 4 things:

1. diabetic glomerulosclerosis
2. infection
3. papillary necrosis
4. renal infarcts

14

balls of collagen in the mesangium in diabetic nephropathy are called?

Kimmelstiel-Wilson nodules

15

AGEs stand for?

Advanced glycation end products

16

arteriolar wall thickening in kidney called?

hyaline arteriolosclerosis

17

basement membrane in diabetic nephropathy?

thickened: though still allow protein leakage

18

primary cause of diabetic retinopathy?

ischaemia to retinal artery due to glycosalation

19

what are Kimmelstiel-Wilson nodules?

balls of collagen in the mesangium in diabetic nephropathy

20

Why delayed wound healing in DM2?

1. impaired perfusion
2. impaired neutrophils=infection=gangrene
3. impaired sensation=trauma

21

3 pathways for hyperglycaemia tissue damage?

1. AGEs
2. Protein Kinase C
3. Intracellular Polyols

22

AGEs bind to what 3 things?

RAGE (receptor) on
1. Macrophages, T-cells
2. endothelial cells
3. vascular smooth muscle

23

what is primary source of AGEs?

diet, normally well controlled, AGEs only problem with higher levels in DM

24

AGEs bound to a vessel does what 4 things?

1. release cytokines
2. reactive O2
3. increase pro-coagulant
4. thicken vessel walls

25

Medication for AGEs?

perhaps RAGE antagonist?

26

What else can AGEs do besides receptor mediated effects?

Cross linking Type 1 and 4 collagen, trapping LDL > atheroma

27

Protein Kinase C mainly affects?

capillary beds, thickening, constriction

28

Peripheral nerve damage in DM just vascular problem?

Combo of:
1. AGEs
2. Polyols
3. microvascular injury

29

How can liver be involved in DM?

Non-alcoholic steatohepatitis (NASH) Fibrosis increases risk of insulin resistance, hyperglycaemia

30

Common cause of DM death?

Macrovascular (MI, stroke, renal failure)