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MEDICAL BIO > WEEK 5-7 - thrombosis > Flashcards

WEEK 5-7 - thrombosis Flashcards

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USMLE® Step 1 flashcards Biology 101 flashcards
1
Q

haemostasis versus thrombosis

A

normal response
- the activation of platelets and clotting to prevent excessive blood loss at sites of injury
- negatively regulated by intact endothelium

disease scenario
- unwanted formation of a blood clot thrombus (which can block vessels

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2
Q

arterial thrombosis

A

typically caused by vessel disease leading to atherosclerotic plaque rupture (platelets)

Chronic inflammatory reaction
Big problem when it ruptures

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3
Q

venous thrombosis

A

due to slow blood flow, endothelial dysfunction or altered blood properties (coagulation)

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4
Q

atherosclerosis
occurs?

A

occurs at sites in arteries where laminar flow is disrupted
(e.g. at branch points)

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5
Q

atherosclerosis
progression

A

1) healthy arterial wall
2) fatty streak
3) lesion progression
4) plaque rupture

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6
Q

atherosclerosis
causes
environmental/lifestyle

A

western high fat diet
high blood cholesterol
physical inactivity
smoking
high blood pressure
obesity

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7
Q

atherosclerosis
causes
inherited

A

strong familial tendency
multiple genes responsible

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8
Q

atherosclerosis
rupture of plaque

A

Macrophages unable to deal with
End up with inflammatory response
- T cells
- Extracellular deposits

Rupture of plaque
Exposure to blood
Platelets think this is a normal wound and form a thrombus
Becomes a problem when have narrow arteries (blocking blood flow)

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9
Q

atherosclerosis
rupture of plaque
can cause

A

heart attack
- If in major artery to the heart
- When part of the heart dies the whole heart tends to stop beating

stroke
- clot stops flow of blood to area in brain

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10
Q

heart attack and stroke in the UK

A

most common cause of death

someone has a heart attack every 2 mins
a third never make it to the hospital and half die within a month
someone has a stroke every 5 mins
stroke is a major cause of disability

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11
Q

atherosclerosis
treatment
to deal with high blood cholesterol

A

statins
- cholesterol lowering drugs

widely used to treat atherosclerosis

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12
Q

atherosclerosis
treatment

A

standard treatment:
- aspirin
- clopidogrel
–> Bleeding risk
(because they inhibit platelets)

integrin inhibitors have high bleeding risk in long term use
- used during stenting

Voropaxar recently approved but now discontinued due to bleeding

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13
Q

atherosclerosis
treatment
percutaneous coronary intervention

A

e.g. stenting and angioplasty

restoring vessel to normal diameter

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14
Q

anti-platelet therapy

A

effectiveness balanced against acceptable bleeding risk

aim is not to completely inhibit the platelet response
most common treatment is aspirin
finding new drug targets is a major research area

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15
Q

venous thrombosis

A

Major component of venous thrombus:
Red blood cells

Causes spontaneous clots to form
Caused by coagulation cascade

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16
Q

venous thrombosis
main risk factors
inherited

A

factor V Leiden
- activated protein C resistance

Protein C, protein S or antithrombin deficiency
(factors that limit coagulation)

prothrombin, polymorphism
- increased levels

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17
Q

venous thrombosis
main risk factors
acquired

A

prolonged immobility
postoperative
cancer
contraceptive pill and hormone replacement therapy
heart failure
varicose veins

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18
Q

venous thrombosis
pulmonary embolism

A

a life-threatening condition that occurs when a blood clot blocks an artery in the lungs

symptoms include pain and swelling in the affected area

death can occur if pices of the clot break off (embolisation) and lodge in the lungs

20,000 UK death per year

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19
Q

venous thrombosis
traditional treatments

A

Warfarin
- vitamin K antagonist
- acts against: VIIa, Xa, IXa and thrombin

Heparin
- activates anti-thrombin
- acts against: Xa and thrombins

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20
Q

venous thrombosis
traditional treatments
limitations

A

limitations of warfarin and heparin

variable anti-coagulant response due to
- drug-drug interactions
- drug-food interactions
- genetic polymorphisms

effective dose varies between patients

routine coagulation monitoring is required to maintain a therapeutic effect

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21
Q

venous thrombosis
treatment: direct oral anticoagulants

A

factor X inhibitors
- apixaban
- edoxaban
- rivaroxaban

thrombin inhibitor
- dabigatram

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22
Q

venous thrombosis
treatment: direct oral anticoagulants
advantages

A

safer than warfarin and heparin
- less intracranial bleeding

convenient dosing
- predictable anticoagulant effect

quick onset and offset of action

fewer drug-food interactions

23
Q

venous thrombosis
treatment: direct oral anticoagulants
licensed for:

A

licensed for:
deep vein thrombosis and pulmonary embolism

post-operative for hip and knee replacements

stroke prevention in atrial fibrillation

24
Q

atrial fibrillation

A

a major risk factor for ischaemic stroke

one of the most common forms of abnormal heart rhythm (over one million people in UK)

causes abnormal blood flow

five-fold increased chance of stroke

25
Q

acute treatment of ischaemic stroke by…

A

thrombolysis or ‘clot busters’

e.g. streptokinase
only effective within 3 hours of the event
- any longer than brain damage is permanent

26
Q

thrombosis summary:
arterial thrombosis

A

typically caused by platelets following the rupture of atherosclerotic plaques

27
Q

thrombosis summary
venous thrombosis

A

typically caused by coagulation a result of slow blood flow and/or blood hypercoagulability

the endothelium remains intact

28
Q

SEARCH FOR NOVEL ANTI-PLATELET THERAPIES
aim of platelet research

A

to prevent heart attack and stroke by inhibiting platelet activation

to ensure that platelets are not 100% inhibited otherwise the patient might suffer bleeding complications

29
Q

SEARCH FOR NOVEL ANTI-PLATELET THERAPIES
hypothesis

A

identification of new platelet receptors may lead to new drug targets to prevent heart attack and stroke

30
Q

SEARCH FOR NOVEL ANTI-PLATELET THERAPIES
strategy to identify new platelet surface proteins

A

1) purify platelets
2) separate membrane proteins by gel electrophoresis
3) identify proteins by mass spectrometry

31
Q

SEARCH FOR NOVEL ANTI-PLATELET THERAPIES
identification of a new platelet surface protein

A

136 surface proteins identified

one of the most interesting was CD-148

CD148 is important in activating proteins in other cell types

32
Q

SEARCH FOR NOVEL ANTI-PLATELET THERAPIES
how can we study the roll of platelet CD148

A

knock out CD148 expression in platelets

but this is impossible in human platelets

however, we can use CD148-knock out mice
- Can then study these platelets

33
Q

SEARCH FOR NOVEL ANTI-PLATELET THERAPIES
CD148 importance

A

impaired platelet spreading without CD148

impaired in vitro thrombus formation without CD148
- much slower to form thrombus and thrombus much smaller (than wild type)

platelets not completely impaired
- no signs of bleeding problems in mice

34
Q

HEART ATTACK CASE STUDY
major risk factors for atherosclerosis

A

raised low-density lipoprotein cholesterol

reduced high-density lipoprotein cholesterol

high blood pressure

diabetes

smoking

obestity

physical inactivity

genetic e.g. familial hypercholesterolaemia

35
Q

HEART ATTACK CASE STUDY
cholesterol

A

a membrane lipid

also a precursor for bile, vitamin D and steroid hormones

36
Q

HEART ATTACK CASE STUDY
lipoprotein transport

A

cholesterol and lipids are transported in the bloodstream as lipoproteins

four classes of lipoprotein
- HDL –> contain apoA (7-20nm diameter)
- LDL –> contain apoB-100 (20-30nm)
- VLDL –> contain apoB-100 (30-80nm)
- chylomicrons –> contain apoB-48 (100-1000nm)

37
Q

HEART ATTACK CASE STUDY
lipoprotein structure

A

hydrophobic core containing triacylglycerols and cholesterol esters

surrounded by apolipoproteins

38
Q

HEART ATTACK CASE STUDY
structure of cholesteryl esters

A

has long carbon tail

major form of cholesterol transported

39
Q

HEART ATTACK CASE STUDY
triglycerides

A

glycerol with 3 fatty acids chains

function as energy source and storage for unused caloried

40
Q

HEART ATTACK CASE STUDY
cholesterol transport

A

Cholesterol is transported in the body through a series of processes that involve lipoproteins, enzymes, and receptors:

41
Q

HEART ATTACK CASE STUDY
Dyslipdaemia

A

abnormal amount of lipids in the blood

primary dyslipidaemia due to combination of
- diet
- genetics (e.g. familial hypercholesterolaemia)

secondary dyslipidaemia due to other conditions
- e.g. diabetes, alcoholism

42
Q

HEART ATTACK CASE STUDY
cholesterol production

A

Cholesterol production
The body absorbs dietary cholesterol from the intestine and carries it to the liver in chylomicrons.

43
Q

HEART ATTACK CASE STUDY
Cholesterol packaging

A

The liver packages cholesterol into lipoproteins, which are particles that transport cholesterol, cholesteryl esters, and triglycerides.

44
Q

HEART ATTACK CASE STUDY
Cholesterol transport from liver to tissues

A

Low-density lipoprotein (LDL) particles carry cholesterol and other lipids from the liver to peripheral tissues.

45
Q

HEART ATTACK CASE STUDY
Cholesterol transport from tissues to liver

A

High-density lipoprotein (HDL) particles transport cholesterol and other lipids from peripheral tissues back to the liver.

46
Q

HEART ATTACK CASE STUDY
Cholesterol esterification

A

Lecithin-cholesterol acyltransferase (LCAT) converts cholesterol to cholesteryl esters.

47
Q

HEART ATTACK CASE STUDY
Cholesterol transfer

A

Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters between HDL2, serum triglycerides, VLDL, and LDL.

48
Q

HEART ATTACK CASE STUDY
Cholesterol uptake

A

The liver LDL receptor takes up LDL.

49
Q

HEART ATTACK CASE STUDY
Cholesterol hydrolysis

A

Hepatic lipase regulates the hydrolysis of HDL2 to HDL3.

50
Q

HEART ATTACK CASE STUDY
Cholesterol catabolism

A

Lipoprotein lipase catabolizes serum triglycerides and transports free cholesterol into HDL.

51
Q

HEART ATTACK CASE STUDY
what type of mechanism is likely to be involved in the uptake of LDL by cells
what is the fate inside the cell

A

Uptake of LDL: Endocytosis (receptor mediated). LDL is taken up into cells by receptor mediated endocytosis Surface receptors recognise the apolipoprotein in LDL cluster together.
In cells, broken down by fusing with lysosome

52
Q

HEART ATTACK CASE STUDY
what is the significance of HMG0CoA reductase in cholesterol biosynthesis

A

It is the rate limiting step
The decrease in HMG-Coa reductase activity is to reduce the amount of cholesterol being produced

53
Q

HEART ATTACK CASE STUDY
pharmacological agents prescribed (to treat atherosclerosis)

A
  1. Oral cholestyramine
    ○ Used to lower high cholesterol levels in the blood
    ○ This helps to prevent cholesterol clogging blood vessels
    ○ Works by removing bile acid from the body (by forming insoluble complexes with the bile so it is excreted)
    Lovastatin
    ○ class of medications called HMG CoA reductase inhibitors (statins)
    ○ It competitively inhibits HMG CoA
    ○ Slows the production of cholesterol in the body to decrease the build up of cholesterol on blood vessels
    Other pharmacological agents prescribed
    ○ Fibrates
    ○ Nicotinic acid
    ○ Fish oil derivatives
    PCSK9 inhibitors
54
Q
A

MEDICAL BIO (16 decks)

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