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Cardiovascular disease Flashcards

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1
Q

Haemostasis

A

Appropriate response to blood vessel injury

Cooperation between platelets, coagulation system and endothelium

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2
Q

Thrombosis

A

Formation of a thrombus following inappropriate activation of haemostat mechanisms

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3
Q

Platelet response to vascular injury stages

A

Adhesion
Activation and secretion
Aggregation

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4
Q

Adhesion

A

Injury to endothelium exposes ECM so can bind to Gp1b on the platelet via vWf

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5
Q

Activation and secretion

A

Shape change of the platelets from discs to plates to cover more surface area via modification of GpIIb/IIIa
Secretion of alpha and dose granules to release TXA2, ADP, Ca2+ etc for clotting

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6
Q

Aggregation

A

Bridging between platelets via GpIIb/IIIa cross links by fibrinogen to give primary haemostat plug
Converted to secondary haemostat plus by action of thrombin on fibrinogen to give fibrin

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7
Q

Where do coagulation system reactions happen

A

On phospholipid rich surfaces e.g platelets, Microparticles

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8
Q

Convergence of the coagulation system

A

On the activation of factor X; by Factor VIIa (extrinsic), VIIIa and IXa

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9
Q

Activation of prothrombin

A

Xa, Va and Ca2+ as cofactor

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10
Q

Haemophilia A

A

Factor VIII deficiency

X linked

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11
Q

Fibrinolytic system

A

Plasminogen activated to plasmin by tPA, streptokinase, XIIa

Plasmin can break fibrin down into soluble D dimers

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12
Q

Anti-thrombotic

A

NO
PGI2
Thrombomodulin (binds thrombin)
Protein C

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13
Q

Pro-thrombotic

A

wVF
Tissue factor
Microparticles
Thromboplastin

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14
Q

Virchow’s triad

A

Changes in vessel wall
Changes in blood flow
Changes in blood constituents

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15
Q

Changes in blood flow

A

In veins: stasis due to slow flow

In arteries: turbulent flow; can directly damage the vessels

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16
Q

Arterial thrombus appearance

A

Compact, granular, firm

Laminations called lines of Zahn

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17
Q

Venous thrombus appearance

A

Pale head with long red tail pointing towards hear

Harder to see laminations

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18
Q

Blood clot compared to thrombus

A

Can arise outside of circulation
Only involves coagulation system
Softer

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19
Q

Fate of thrombi

A 
Lysis
Propagation in stagnant blood
Stenosis/vessel occlusion
Organisation 
Infection 
Embolisation
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20
Q

Organisation of thrombi

A

Retraction of the thrombus by WBCs releasing enzymes, ingrowth of smooth muscle cells and fibroblasts, growth of endothelium, ECM synthesis

Then can be pulled into vessel wall
Or form new vessels through it

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21
Q

Embolus

A

Intravascular mass carried by blood flow to impact at distant site

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22
Q

Emboli from systemic veins or R side of heart

A

Lodge in pulmonary artery cause hypoxia, heart failure,,

can cause myocardial hypertrophy

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23
Q

Emboli from L side of heart or aorta

A

Go to brain, gut, kidney

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24
Q

Atherosclerosis

A

Disease affecting the intimacy of medium and large arteries

Focal thickening called plaques made of fibrous tissues and lipids associated with necrosis and inflammatory cells

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25
LDL
Delivers cholesterol to the tissues
26
Native LDL receptor pathways
Hepatocytes mainly | Transcription regulated by negative feedback by cholesterol levels
27
Scavenger receptor pathway for LDL
By macrophages to take up modified lipoprotein | No -ve regulation so get uncontrolled cholesterol accumulation to form foam cells
28
Dyslipoproteinaemia
Abnormality in constitution/concentration of lipoproteins in the blood May be inherited e.g FH Secondary e.g from diabetes mellitus
29
Atherogenesis
Process by which atherosclerosis occurs | Chronic inflammatory process with prolonged endothelial injury response
30
Activated macrophage effects
``` Endothelial cell activation via IL-1 and TNFalpha Recruiting monocytes Activating SMCs Modify ECM with collagenase Oxidise/ingest lipoproteins Antigen presentation ```
31
Vascular smooth muscle
Activated by macrophages via growth factors Proliferate and migrate from media to intima Change from contractile to synthetic cells and secrete ECM and remodelling enzymes
32
Lipoprotein contribution having been oxidised in plaques
To local T cell response | + act as chemoattractant for monocytes
33
Structure of plaque
Fibrous cap with collagen, SMCs, macrophages, T cells Lipid core with foam cells, necrotic core, extracellular lipid Shoulder has lots of angiogenesis so prone to haemorrhage
34
Ischaemia
Inadequate local blood supply to an organ due to insufficient quantity of blood (rather than quality)
35
Infarctions
Necrosis due to ischaemia
36
Causes of ischaemia
``` External stenosis Internal stenosis Spasm Capillary blockage Shock ```
37
Causes of capillary blockage
Cerebral malaria | Sickle cell disease
38
Types of shock
Cardiogenic Hypovolaemic Septic Anaphylactic
39
Reversible morphological changes
Swelling, membrane blebs, chromatin clumping
40
Irreversible changes
ER disintegration, pyknosis (nuclear shrinkage), lysosome rupture
41
Predominan cytoplasmic change if ischaemia is cause
Eosinophilia (rather than nuclear fragmentation)
42
Cell susceptibility to hypoxia
Neurons > renal tubule epithelium > myocardium > skeletal muscle > macrophages, fibroblasts
43
Ischaemic reperfusion injury
Restoring blood flow can - Allow generation of fresh mediators of injury - Initiate acute inflammation via delivery of immune cells
44
Macroscopic shape of infarcts
conical in 3D | wedge in 2D
45
Red infarct
Due to blood in infarcted tissue Ischaemia due to venous occlusion, so blood still enters from artery Or in spongy tissue like lungs that don't resist blood infiltration Or those with collateral supply
46
Pale infarct
Tissue is solid so blood doesn't enter Pale with red margins due to vasodilation Fibrinous exudate on surface and granulation tissue
47
Septic infarcts
Happen in lung | Check if anywhere else
48
Cystic infarct
Liquefication necrosis and cyst formation e.g in brain
49
Myocardial infarction
Mainly LV Due to coronary artery atherosclerosis Pale infarct Pericardial surface gets fibrin deposition (fibrinous pericarditis can happen)
50
Mural thrombosis
Where a thin layer of scar tissue forms at apex of heart due to an infarct This isn't functional so causes turbulent flow and can get thrombosis (this LV thrombus may become infected)
51
Anaemia
Reduced total mass of circulating red cells
52
Adult haemoglobin major form
HbA alpha2beta2
53
Fetal haemoglobin form
HbF alpha2gamma2
54
Main causes of anaemia
Impaired RBC generation Increased haemolytic Blood loss
55
Megaloblastic anaemia
B12 or folate deficiency Impaired thymidine production causing defective cell division; but still get RNA/protein production Megaloblasts; abnormally large erythroblast Macrocytosis; larger RBCs Neutrophils have hyperhsegmented nuclei Right shift on price jones
56
B12 absorption
``` Binds haptocorrin (from salivary glands) in the stomach which protects it from stomach acid Pancreatic enzymes digest haptocorrin in duodenum Binds intrinsic factor; IF receptors in ileum absorb complex Transported in the blood by transcobalamin ```
57
Folate absorption
Taken up in diet linked to fpolyglutamic acid | Absorbed in duodenum, jejunum, prox small bowel as methyltetrahydrofolate
58
B12 storage
In liver for 5 years
59
Folate storage
For 3 months
60
Iron deficiency anaemia
Females need 15mg per day | Males need 7mg per day
61
Iron absorption
In duodenum and small bowel Taken up by mucosal cells and transported out using ferroportin Negative feedback based on inhibitory hepcidin
62
Haemoglobinopathies
Structural abnormalities: Sickle cell disease | Diminished production: thalassaemia
63
Beta thalassaemia
Major: B0/B0, B+/B+, B0/B+ Minor: B0/B, B+/B Can be loss of chain or inadequate synthesis Genes are on chromosome 11
64
Alpha thalassaemia
Due to deletion of 1 to 4 copies of the gene | Genes are on chromosome 16

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