Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MEDICAL BIO > WEEK 5-7 - thrombosis > Flashcards

WEEK 5-7 - thrombosis 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

arterial thrombosis

A

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

Chronic inflammatory reaction
Big problem when it ruptures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

venous thrombosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

atherosclerosis
occurs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

atherosclerosis
progression

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

atherosclerosis
causes
environmental/lifestyle

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

atherosclerosis
causes
inherited

A

strong familial tendency
multiple genes responsible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

atherosclerosis
treatment
to deal with high blood cholesterol

A

statins
- cholesterol lowering drugs

widely used to treat atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

atherosclerosis
treatment
percutaneous coronary intervention

A

e.g. stenting and angioplasty

restoring vessel to normal diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

venous thrombosis

A

Major component of venous thrombus:
Red blood cells

Causes spontaneous clots to form
Caused by coagulation cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

venous thrombosis
main risk factors
acquired

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

venous thrombosis
treatment: direct oral anticoagulants

A

factor X inhibitors
- apixaban
- edoxaban
- rivaroxaban

thrombin inhibitor
- dabigatram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
acute treatment of ischaemic stroke by...
thrombolysis or 'clot busters' e.g. streptokinase only effective within 3 hours of the event - any longer than brain damage is permanent
26
thrombosis summary: arterial thrombosis
typically caused by platelets following the rupture of atherosclerotic plaques
27
thrombosis summary venous thrombosis
typically caused by coagulation a result of slow blood flow and/or blood hypercoagulability the endothelium remains intact
28
SEARCH FOR NOVEL ANTI-PLATELET THERAPIES aim of platelet research
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
SEARCH FOR NOVEL ANTI-PLATELET THERAPIES hypothesis
identification of new platelet receptors may lead to new drug targets to prevent heart attack and stroke
30
SEARCH FOR NOVEL ANTI-PLATELET THERAPIES strategy to identify new platelet surface proteins
1) purify platelets 2) separate membrane proteins by gel electrophoresis 3) identify proteins by mass spectrometry
31
SEARCH FOR NOVEL ANTI-PLATELET THERAPIES identification of a new platelet surface protein
136 surface proteins identified one of the most interesting was CD-148 CD148 is important in activating proteins in other cell types
32
SEARCH FOR NOVEL ANTI-PLATELET THERAPIES how can we study the roll of platelet CD148
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
SEARCH FOR NOVEL ANTI-PLATELET THERAPIES CD148 importance
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
HEART ATTACK CASE STUDY major risk factors for atherosclerosis
raised low-density lipoprotein cholesterol reduced high-density lipoprotein cholesterol high blood pressure diabetes smoking obestity physical inactivity genetic e.g. familial hypercholesterolaemia
35
HEART ATTACK CASE STUDY cholesterol
a membrane lipid also a precursor for bile, vitamin D and steroid hormones
36
HEART ATTACK CASE STUDY lipoprotein transport
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
HEART ATTACK CASE STUDY lipoprotein structure
hydrophobic core containing triacylglycerols and cholesterol esters surrounded by apolipoproteins
38
HEART ATTACK CASE STUDY structure of cholesteryl esters
has long carbon tail major form of cholesterol transported
39
HEART ATTACK CASE STUDY triglycerides
glycerol with 3 fatty acids chains function as energy source and storage for unused caloried
40
HEART ATTACK CASE STUDY cholesterol transport
Cholesterol is transported in the body through a series of processes that involve lipoproteins, enzymes, and receptors:
41
HEART ATTACK CASE STUDY Dyslipdaemia
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
HEART ATTACK CASE STUDY cholesterol production
Cholesterol production The body absorbs dietary cholesterol from the intestine and carries it to the liver in chylomicrons.
43
HEART ATTACK CASE STUDY Cholesterol packaging
The liver packages cholesterol into lipoproteins, which are particles that transport cholesterol, cholesteryl esters, and triglycerides.
44
HEART ATTACK CASE STUDY Cholesterol transport from liver to tissues
Low-density lipoprotein (LDL) particles carry cholesterol and other lipids from the liver to peripheral tissues.
45
HEART ATTACK CASE STUDY Cholesterol transport from tissues to liver
High-density lipoprotein (HDL) particles transport cholesterol and other lipids from peripheral tissues back to the liver.
46
HEART ATTACK CASE STUDY Cholesterol esterification
Lecithin-cholesterol acyltransferase (LCAT) converts cholesterol to cholesteryl esters.
47
HEART ATTACK CASE STUDY Cholesterol transfer
Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters between HDL2, serum triglycerides, VLDL, and LDL.
48
HEART ATTACK CASE STUDY Cholesterol uptake
The liver LDL receptor takes up LDL.
49
HEART ATTACK CASE STUDY Cholesterol hydrolysis
Hepatic lipase regulates the hydrolysis of HDL2 to HDL3.
50
HEART ATTACK CASE STUDY Cholesterol catabolism
Lipoprotein lipase catabolizes serum triglycerides and transports free cholesterol into HDL.
51
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
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
HEART ATTACK CASE STUDY what is the significance of HMG0CoA reductase in cholesterol biosynthesis
It is the rate limiting step The decrease in HMG-Coa reductase activity is to reduce the amount of cholesterol being produced
53
HEART ATTACK CASE STUDY pharmacological agents prescribed (to treat atherosclerosis)
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

MEDICAL BIO (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions