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BOD > Cardiovascular disease > Flashcards

Cardiovascular disease Flashcards

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
Q

LDL

A

Delivers cholesterol to the tissues

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26
Q

Native LDL receptor pathways

A

Hepatocytes mainly

Transcription regulated by negative feedback by cholesterol levels

27
Q

Scavenger receptor pathway for LDL

A

By macrophages to take up modified lipoprotein

No -ve regulation so get uncontrolled cholesterol accumulation to form foam cells

28
Q

Dyslipoproteinaemia

A

Abnormality in constitution/concentration of lipoproteins in the blood
May be inherited e.g FH
Secondary e.g from diabetes mellitus

29
Q

Atherogenesis

A

Process by which atherosclerosis occurs

Chronic inflammatory process with prolonged endothelial injury response

30
Q

Activated macrophage effects

A 
Endothelial cell activation via IL-1 and TNFalpha
Recruiting monocytes 
Activating SMCs
Modify ECM with collagenase
Oxidise/ingest lipoproteins
Antigen presentation
31
Q

Vascular smooth muscle

A

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
Q

Lipoprotein contribution having been oxidised in plaques

A

To local T cell response

+ act as chemoattractant for monocytes

33
Q

Structure of plaque

A

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
Q

Ischaemia

A

Inadequate local blood supply to an organ due to insufficient quantity of blood (rather than quality)

35
Q

Infarctions

A

Necrosis due to ischaemia

36
Q

Causes of ischaemia

A 
External stenosis
Internal stenosis
Spasm
Capillary blockage 
Shock
37
Q

Causes of capillary blockage

A

Cerebral malaria

Sickle cell disease

38
Q

Types of shock

A

Cardiogenic
Hypovolaemic
Septic
Anaphylactic

39
Q

Reversible morphological changes

A

Swelling, membrane blebs, chromatin clumping

40
Q

Irreversible changes

A

ER disintegration, pyknosis (nuclear shrinkage), lysosome rupture

41
Q

Predominan cytoplasmic change if ischaemia is cause

A

Eosinophilia (rather than nuclear fragmentation)

42
Q

Cell susceptibility to hypoxia

A

Neurons > renal tubule epithelium > myocardium > skeletal muscle > macrophages, fibroblasts

43
Q

Ischaemic reperfusion injury

A

Restoring blood flow can

  • Allow generation of fresh mediators of injury
  • Initiate acute inflammation via delivery of immune cells
44
Q

Macroscopic shape of infarcts

A

conical in 3D

wedge in 2D

45
Q

Red infarct

A

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
Q

Pale infarct

A

Tissue is solid so blood doesn’t enter
Pale with red margins due to vasodilation
Fibrinous exudate on surface and granulation tissue

47
Q

Septic infarcts

A

Happen in lung

Check if anywhere else

48
Q

Cystic infarct

A

Liquefication necrosis and cyst formation e.g in brain

49
Q

Myocardial infarction

A

Mainly LV
Due to coronary artery atherosclerosis
Pale infarct
Pericardial surface gets fibrin deposition (fibrinous pericarditis can happen)

50
Q

Mural thrombosis

A

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
Q

Anaemia

A

Reduced total mass of circulating red cells

52
Q

Adult haemoglobin major form

A

HbA alpha2beta2

53
Q

Fetal haemoglobin form

A

HbF alpha2gamma2

54
Q

Main causes of anaemia

A

Impaired RBC generation
Increased haemolytic
Blood loss

55
Q

Megaloblastic anaemia

A

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
Q

B12 absorption

A 
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
Q

Folate absorption

A

Taken up in diet linked to fpolyglutamic acid

Absorbed in duodenum, jejunum, prox small bowel as methyltetrahydrofolate

58
Q

B12 storage

A

In liver for 5 years

59
Q

Folate storage

A

For 3 months

60
Q

Iron deficiency anaemia

A

Females need 15mg per day

Males need 7mg per day

61
Q

Iron absorption

A

In duodenum and small bowel
Taken up by mucosal cells and transported out using ferroportin
Negative feedback based on inhibitory hepcidin

62
Q

Haemoglobinopathies

A

Structural abnormalities: Sickle cell disease

Diminished production: thalassaemia

63
Q

Beta thalassaemia

A

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
Q

Alpha thalassaemia

A

Due to deletion of 1 to 4 copies of the gene

Genes are on chromosome 16

BOD (7 decks)

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