PHARM; Lecture 16, 17 and 18 - Haemostasis and thrombosis, Atherosclerosis & lipo metabolism, NSAIDS Flashcards Preview

Y2 LCRS 1 - Pharm, Endo, Reproduction > PHARM; Lecture 16, 17 and 18 - Haemostasis and thrombosis, Atherosclerosis & lipo metabolism, NSAIDS > Flashcards

Flashcards in PHARM; Lecture 16, 17 and 18 - Haemostasis and thrombosis, Atherosclerosis & lipo metabolism, NSAIDS Deck (77)
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1

What are the constituents of blood?

2

What is the balance between clotting and bleeding?

3

What is haemostasis?

Essential physiological process -> blood coagulation prevents excessive blood flow

4

What is thrombosis?

Pathophysiological process -> blood coagulates within blood vessel and obstructs blood flow. Can be dangerous if it dislodges from the vessel

5

What is the difference between red vs white thrombi?

Red = venous thrombi with high fibrin components. Whiite = arterial with high platelet components

6

What is atherosclerosis?

Pathophysiological process -> thrombus forms within atherosclerotic plaque; plaque rupture (thrombus released into lumen)

7

Why does a thrombus form?

Virchow's triad -> 1) rate of blood flow 2) consistency of blood 3) blood vessel wall integrity (!!!!)

8

What is the cell based theory of coagulation and which drugs act on which stage?

NB: all 3 drugs work on all 3 components (but easy to remember)

9

What is the initiation phase of the cell based theory of coagulation?

x

10

Which drugs can act on the initiation stage of the cell based theory of coagulation?

11

What is the amplification phase of the cell based theory of coagulation?

12

How are platelets activated?

13

Which drugs can act on the platelet aggregation phase of the cell based theory of coagulation?

14

What is the propagation phase of the cell based theory of coagulation?

15

Which drugs can act on the propagation phase of the cell based theory of coagulation?

16

What is DVT/PE and how is it managed?

17

What are acute coronary syndromes?

If clot present then treat with fibrinolytics

18

How do you treat different thrombosis diseases?

19

What are lipoprotein particles?

Cholesterol, TG and PL. HDL (A1) v LDL (B) the apoproteins are the main differences; which allow them to circulate in the blood

20

How do we get exogenous lipids for metabolism?

Dietary TG and cholesterol are broken down an packaged into chylomicrons which are then broken down further into chylomicron remnants, which can end up in the adipose tissue and the blood vessels

21

How do we get endogenous lipids for metabolism?

Liver is the main organ that deals with cholesterol -> most are metabolised and most do very little but a small proportion ends up in walls of blood vessels

22

What is reverse cholesterol transport?

Mediated largely by HDL -> cholesterol can't be broken down in body, so eliminated intact via HDL from peripheral tissues to liver

23

How does atherosclerosis occur?

Foam cells (macrophages/smooth muscle cells - filled with cholesterol/HDL/LDL) - remnant cholesterol is pro-inflammatory.

24

How does the endothelial layer become dysfunctional?

  • Characterised by series of early changes that precede lesion formation.
    • Greater permeability of endothelium,
    • upregulation of leucocytes and endothelial adhesion molecules 
    • migration of leucocytes into artery wall

25

What is fatty streak formation in atherosclerosis?

  • Earliest recognisable lesion of atherosclerosis;
  • caused by aggregation of lipid rich foam cells within tunica intima and inner most part of artery wall.
  • Later lesions will include smooth muscle cells -> formed usuallly in direction of blood flow

26

How does the complicated atherosclerotic plaque form?

Results from death and rupture of foam cells in fatty streak, migration of smooth muscle cells into intima and lay down collagen fibres forming protective fibrous cap around lipid core

27

What are the types of atherosclerotic lesions?

  • Complicated lesions often contain Ca;
  • CAD can be detected doing CT scan of heart to detect Ca -> more Ca = more symptomatic

28

What is the vulnerable atherosclerotic plaque?

  • Vulnerable plaques are characterised by a thin fibrous caps, a core rich in lipid and macrophages, and less evidence of smooth muscle proliferation.
  • In contrast, the stable plaque has a relatively thick fibrous cap protecting the lipid core from the contact with blood.
  • Vulnerable plaques are prone to rupture and ulceration, followed by rapid development of thrombi.
  • The size of the plaque does not appear to predict whether a plaque is prone to rupture, stable plaques more often show luminal narrowing detectable by angiography than do vulnerable plaques.
  • Rupture usually occurs at sites of thinning (particularly at the shoulder area of the plaque) and is associated with regions where there are relatively few smooth muscle cells but abundant macrophages and T cells.
  • Rupture is associated with greater influx and activation of macrophages, accompanied by release of matrix metalloproteinases that are involved with the breakdown of collagen.

29

What is LDL?

  • LDL cholesterol has been shown to be strongly associated with the development of atherosclerosis and the risk of CHD events in patients with established CHD (history of angina pectoris, MI etc.) and in those without CHD.
  • This applies to women as well as men, but in women the general level of CHD risk is lower.
  • A 10% increase in LDL cholesterol is associated with an approximate 20% increase in risk for CHD.
  • The association between LDL cholesterol and the risk of CHD events is considerably modified by other risk factors, such as low HDL cholesterol, smoking, hypertension and diabetes.
  • This modification is apparent especially when total cholesterol and LDL cholesterol are only moderately elevated.

30

What is the vulnerable atherosclerotic plaque?

  • Characterised by thin fibrous caps, a core rich in lipid and macrophages, and less evidence of smooth muscle proliferation -> stable has thick fibrous cap.
  • Vulnerable plaques are prone to rupture and ulceration, followed by rapid development of thrombi.
  • Rupture usually occurs at sites of thinning and is associated with regions where there are relatively few smooth muscle cells but abundant macrophages and T cells.
  • Rupture is associated with greater influx and activation of macrophages, accompanied by release of matrix metalloproteinases that are involved with the breakdown of collagen.

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