Vascular and interstitial disease Flashcards Preview

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Flashcards in Vascular and interstitial disease Deck (25):
1

What is the phenotype of normal blood vessels?

Anticoagulant form

Lining of the vessel wall is kept smooth by anticoagulant molecules on cell surfaces

2

What happens when there is damage to the endothelial layer lining the blood vessels?

Anticoagulant surface is disrupted with platelets, thrombin and complement

Procoagulant phenotype is expressed

Expression of prothrombotic molecules

3

How do endothelial cells change following vessel damage?

No longer flat and anticoagulant -> pulled apart, plumper and active

Basement membrane is exposed

Procoagulant surface is formed

Stimulates platelets and procoagulant molecules to stick to the basement membrane

4

Condition where clot occludes blood vessels leading to the organ distal to the occlusion becoming ischaemic

Thrombotic microangiopathy

5

Why do RBC become damaged in occluded vessels?

RBC try to work their way through a clot and become damaged

6

What are some causes of thrombotic microangiopathy?

Drugs - chemotherapy

Antibodies binding to endothelium following infectious events or autoimmunity

Complement activation

Vessel wall damage

7

What causes vessel wall damage?

Stress force or hypertension

8

What is the coagulation pathway?

Stimulates blood clot formation

9

What is the complement pathway?

Deposition of complement molecules on endothelial surfaces

10

What happens to the balance of coagulation and complement pathways in pathology?

If the regulators of the balance are insufficient in number or have a genetic abnormality

There is over activation of the pathway

Disease follows

Can also lead to formation of antibodies against the complement pathway

11

Which diseases lead to thrombotic microangiopathy?

Scleroderma - deposition of antibdodies on blood vessel wall

Accelerated hypertension

Haemolytic anaemia

12

What are antiphospholipid antibodies?

Abnormal antibodies against phospholipids on blood vessel walls that increase blood clotting

13

How does haemolytic anaemia lead to TMA?

Complement regulatory proteins are abnormal

Complement pathways is therefore always switched on

This means that complement will get stuck to the endothelium

Leads to endothelial damage

14

What is an example of haemolytic anaemia?

Haemolytic uraemic syndrome

15

What is vasculitis?

Blood vessel inflammation due to activation of leukocytes

Leads to damage of endothelial cells

16

What is the pathophysiology of systemic vasculitis?

Inappropriate activation of WBC due to antigen

WBC release cell contents

Causing damage to the capillary wall

This activates more blood cells to be recruited

Capillary loop stops functioning

Less filtration happens at the glomerulus

Leads to glomerulonephritis

17

Which antibodies are normally associated in systemic vasculitis?

Anti-neutrophil cytoplasm antibodies

18

What is a simple test that can be done to detect proteins present in inflammation?

Dipstick urine test

19

What is tubulointerstitial nephritis characterised by?

Infestation of WBC in tubules

20

Why are the tubules more predisposed to injury than other parts of the nephron?

Filter the urinary filtrate so exposed to antigens present in the kidney

21

What cell types cause damage to the tubules?

Leukocytes, antibodies and complement

22

How do WBC respond to antigens in the tubules?

Stimulate an inflammatory response

23

What are causes of tubulointerstitial nephritis?

Infections

Drugs

Autoimmunity

Unkown - inflammation resolves as quickly as it started

24

Which drugs commonly cause tubulointerstitial nephritis?

NSAIDS

Proton pump inhibitors

25

Which cell is the main WBC in drug-induced TN?

Eosinophils