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Tamsin - Pathology > Blood vessels > Flashcards

Blood vessels Flashcards

1
Q

Describe the layers of a normal vessel wall

A

INTIMA: Endothelial cells overlying a thin ECM sheet

MEDIA: Smooth muscles and ECM

ADVENTITIA: Loose connective tissue, nerve fibres and smaller cells

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2
Q

What is arteriosclerosis?

A

Abnormal thickening and loss of elasticity of arterial walls.

There are 3 types

  1. Arteriolosclerosis - affects small arteries and arterioles, primarily associated with hypertension and diabetes
  2. Monckeberg medial calcific sclerosis - calcific deposits in muscular arteries, not of clinical significance
  3. Atherosclerosis - The most frequent and clinically important pattern
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3
Q

What is the definition of atherosclerosis?

A

A slowly progressive disease of large to medium sized arteries, marked by elevated intimal based plaques (atheroma) composed of lipids, proliferating smooth muscle cells (SMC), inflammatory cells and increased ECM

They cause pathology by:

  1. Mechanically obstructing flow - atherosclerotic stenosis
  2. Acute plaque change
  3. Plaque rupture leading to vessel thrombosis
  4. Weakening the underlying vessel wall and leading to aneurysm formation
  5. Causing vasoconstriction due to endothelial dysfunction
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4
Q

Which vessels are most heavily affected by atherosclerosis?

A
  1. Abdominal aorta
  2. Coronary arteries
  3. Descending thoracic
  4. Internal carotid
  5. Branches of circle of Willis
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5
Q

What are the 3 key components of atherosclerotic plaques?

A
  1. Cells including smooth muscle cells
  2. Connective tissue extracellular matrix including collagen, elastic fibres and proteoglycans
  3. Intracellular and extracellular deposits
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6
Q

What are the major modifiable and non-modifiable risk factors for atherosclerosis?

A

Modifiable:

  • Hypertension (increases risk by 60%)
  • Smoking
  • Hypercholestrolaemia (increased LDL and decreased HDL confers increased risk) HDL clears cholestrol from vessel wall lesions
  • Diabetes

Non-modifiable:

  • Increasing age
  • Male gender (although in postmenopausal females risk rapidly increases
  • Family history (most significant independant risk factor)

Other:

  • Inflammation
  • Hyperhomocysteinaemia
  • Metabolic syndrome
  • LipoproteinA
  • Haemostatic factors
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7
Q

Describe the pathogenesis of atherosclerosis

A

A chronic inflammatory and healing response of the arterial wall to EC injury. In turn EC injury causes increased endothelial permeability, white blood cell and platelet adhesion and coagulation activation.

These events induce chemical mediator release and activation followed by recruitment and subsequent proliferation of SMC in the intima to produce the characteristic intimal lesion

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8
Q

Describe the stages in the pathogenesis of atherosclerosis

A
  1. Endothelial injury caused by hypercholestrolaemia, haemodynamic disturbances, smoking, hypertension, toxins and infectious agents
  2. Monocyte and platelet adhesion and growth factor eg PDGF release
  3. Smooth muscle cell recruitment and proliferation in the intima and increased matrix synthesis
  4. Foam cells result when macrophages and smooth muscle cells accumulate cholestrol throughthe uptake of LDL
  5. Circulating HDL can help remove cholestrol from these accumulations
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9
Q

Describe the morphology of atherosclerotic plaque

A
  • Superficial fibrous cap compromised of smooth muscle cells, few leukocytes and dense connective tissue
  • Cellular area beneath and to the side of the cap consisting of macrophages, smooth muscle cells and T-lymphocytes
  • Deep necrotic core with disorganised mass of lipid material, cholestrol clefts, cellular debris and lipid laden foam cells
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10
Q

What are the features of vulnerable vs stable plaques

A

Vulnerable plaques have large deformable atheromatous cores, thin fibrous caps and/or increased inflammatory cell content

Stable plaques have minimal atheromatous cores and thicker, well collagenised fibrous caps with relatively less inflammation

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11
Q

What is the AHA classification of atheromas?

A

Type 1: Initial - isolated macrophage foam cells

Type 2: Fatty streak- Intraceullular lipid accumulation

Type 3: Intermediate - small extracellular pools

Type 4: Atheroma - core of extracellular lipid

Type 5: Fibroatheroma - lipid core with fibrotic layer

Type 6: Complicated -surface defect

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12
Q

What is clinically significant hypertension?

A

Sustained diastolic BP more than 89 mmHg or systolic pressures more than 139 mmHg

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13
Q

What is malignant hypertension?

A
  • Systolic BP more than 200mmHg, diastolic BP more than 120 mmHg, renal failure and retinal haemorrhages
  • Affects 5% of hypertensive patients
  • If untreated, leads to death in 1-2 years
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14
Q

What are the determinants of blood pressure?

A

Blood pressure = cardiac output x peripheral vascular resistance

  • Cardiac output is determined by myocardial contractility, heart rate and blood volume
  • Blood volume is affected by:
    • Sodium load
    • Mineralocorticoids (aldosterone)
    • natriuretic factors than influence sodium excretion
  • Vascular resistance is primarily determined at the arteriole level
    • Vasoconstrictors: angiotensin 2, catecholamines, thromboxane, leukotrienes, endothelin
    • Vasodilators: kinins, prostaglandin, nitric oxide, adenosine
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15
Q

Describe the mechanism of essential hypertension

A

Cumulative effects of non-genetic environmental factors and multiple genetic polymorphisms in vasomotor tone or blood volume regulation conspire to cause high blood pressure

  1. Genetic factors
    • Mutations in enzymes that influence aldosterone syhtensis lead to increased aldosterone production
    • Mutations in the renal epithelial Na+ channel protein lead to increased sodium resorption (Liddle syndrome)
  2. Reduced renal sodium excretion > expansion of plasma and ECF volume
  3. Vasoconstriction > increased peripheral resistance
  4. Environmental factors eg obesity, salt intake, stress modify impact of genetic determinants
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16
Q

Describe the role of the RAAS in regulation of BP

A
  • Juxtaglomerular cells of the kidney release renin
  • Renin converts angiotensinogen to angiotensin 1
  • ACE converts angiotensin 1 to angiotensin 2
  • Angiotensin 2 causes
    • Increased peripheral resistance (direct action on SMCs)
    • Increased blood volume (stimulates aldosterone secretion > reabsorption of sodium)
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17
Q

What is the role of natriuretic factors in regulation of BP

A
  • Secreted by atrial and ventricular myocardium in response to volume expansion
  • Inhibit sodium resorption in the distal tubules > sodium excretion + diuresis
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18
Q

What is the vascular pathology seen in hypertension?

A
  1. Hyaline arteriolosclerosis
    • ​Typically in elderly patients with mild HTN/DM​
    • EC injury > plasma leakage into arteriolar walls > increased SMC matrix synthesis
    • Diffuse pink hyaline arteriolar wall thickening with lumen stenosis
  2. Hyperplastic arteriolosclerosis
    • Occurs in malignant hypertension
    • Concentric laminated arteriolar thickening with reduplicated basement membrane and SMC proliferation
    • Frequently associated with fibrin deposition and wall necrosis called necrotising arteriolitis
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19
Q

List some of the causes of secondary hypertension

A

Renal

  • Acute glomerulonephritis
  • CRD
  • PKD
  • Renal artery stenosis
  • Renal artery fibromuscular dysplasia
  • Renal vasculitis
  • Renin producing tumours

Endocrine

  • Cushings
  • Primary aldosteronism
  • CAH
  • Licorice ingestion

Cardiovascular

  • Coarctation of the aorta
  • Polyarteritis nodosa
  • Increased intravascular volume
  • Increased cardiac output
  • Rigidity of the aorta

Neurologic

  • Psychogenic
  • Increased intracranial pressure
  • Sleep apnoea
  • Acute stress, including surgery
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20
Q

What is the difference between a true aneurysm, false aneurysm and dissection?

A

True aneurysm is bounded by all 3 vessel wall layers (intima, media, adventitia)

False aneurysm is an extravascular haematoma that communicates with the intravscular space through a breach in the vascular wall

Dissection occurs when blood enters the arterial wall itself as a haematoma dissecting between layers

21
Q

Describe the pathogenesis of aneurysms

A
  • Poor intrinsic quality of the vessel matrix eg
    • Marfan syndrome - aberrant transforming growth factor B (TGF-b) activation and progressive loss of elastic tissue matrix
    • Loeys-Dietz syndrome - TGF-b receptor mutations cause elastic tissue loss
  • Degradation of collagen in the vessel wall
    • Increased MMP activity by inflammatory cells causes net medial ECM degradation eg in atherosclerosis or vasculitis
  • Loss of medial smooth muscle cells or change in SMC synthesis
    • Ischaemia of the innermost aspect of the aoritc media in atherosclerosis
    • Narrowing or arterioles of vasa vasorum
22
Q

What are the most common causes of aortic aneurysms ?

A

Atherosclerosis (particularly in abdominal aorta)

Hypertension (particularly in ascending thoracic aorta)

Syphilis

Trauma vasculitis

Congenital defects eg Berry anuerysms

Mycotic aneurysms from septic emoblisation

23
Q

What are the complications of aneurysms?

A
  1. Rupture
  2. Impingement
  3. Occlusion
  4. Emoblism
24
Q

What is the most common site of AAA?

A

Below the renal arteries and above the iliac bifurcation

25
Q

What is the risk of rupture from a AAA?

A

<5cm low

5-6 cm 11%

>6cm 25%

26
Q

What is the morphology of a AAA?

A
  • Localised dilatation of the AA
  • Usually infrarenal and above the bifurcation of the iliacs
  • Atheromatous ulcers
  • Mural thrombi
  • Thinning and destruction of the media
27
Q

What are the sequnce of changes seen in the vessel wall in aortic dissection?

A
  1. Intimal tear into media of the aorta
  2. Strips along the laminar planes
  3. Formation of intramural blood filled channel which may then rupture outwards
28
Q

Which groups are most commonly affected by aoritc dissection?

A
  1. Hypertensive men aged between 40-60
  2. Younger individuals with connetive tissue defects

Other causes: trauma, complications of arterial cannulation, pregnancy

29
Q

Describe the morphology of aortic dissection

A

Cystic medial degeneration

Often a tear within first 10cm above the aortic valve annulus

The dissection plane can extend retrograde to the heart and/or anterograde which extends into the great arteries or other major branches

Rupture through the wall of the aorta causes massive haemorrhage

30
Q

What is the DeBakey and Stanford classifications of aortic dissection?

A

De Bakey

1. Both ascending and descending aorta

2. Ascending aorta

3. Descending aorta (after left subclavian origin)

Remember BAD

Stanford

Type A Affects Ascending Aorta

Type B Begins Beyond Brachiocephalic vessels

31
Q

What are the 2 most common pathogenic mechanisms of vasculitis?

A
  1. Immune mediated inflammation
  2. Direct invasion of vascular walls by infectious pathogens
32
Q

What causes immune-complex associated vasculitis?

A
  • Vascular deposition of circulating antigen-antibody complexes eg DNA/anti DNA complexes in SLE
  • Vascular injury arises from complement activation or the recruitment of Fc receptor-bearing cells
33
Q

What are ANCAs?

A

Heterogenous group of autoantibodies directed against the constituents of neutrophil primary granules

34
Q

What is p-ANCA?

A
  • Anti-myeloperoxidase - directed against the lysosomal constituent involved in generating oxygen free radicals .
  • Characteristically seen in microscopic polyangitis and Churg-Strauss syndrome
35
Q

What is c-ANCA?

A
  • Anti-proteinase 3 - directed against a neutrophil azurophiic granule constituent.
  • Characteristically associated with Wegener Granulomatosis
36
Q

Characterised by focal granulomatous inflammation of medium sized and small arteries, cheifly cranial vessels. It can also involve the aorta. The primary etiology is likely a T cell mediated immune response

A

Giant cell arteritis

37
Q

What is the morphology of giant cell arteritis?

A
  • Granulomatous vasculitis
  • Elastic tissue fragmentation
  • Multinucleated giant cells
  • Intimal fibrosis with medial scarring and luminal narrowing
38
Q

Granulomatous vasculitis of medium to large arteries characterised by transmural fibrous thickening of the aortic arch and virtual obliteration of the great vessel branches

A

Takayasu arteritis

39
Q

What is the morphology of Takayasu arteritis?

A
  • Irregular aortic thickening with intimal hyperplasia
  • Early stages: Adventitial perivascular mononuclear cell infiltrates
  • Later stages: Medial fibrosis with granulomas and acellular intimal thickening- indistinguishable from giant cell arteritis
40
Q

What are the clinical features of Takayasu arteritis?

A
  • Fatigue, fever, weight loss
  • Ocular and neurologic disturbances
  • Marked weakening of upper extremity perfusion pressures
  • Pulmonary artery involvement in 50%
  • Coronary and renal artery involvement - can cause hypertension
41
Q

What is polyarteritis nodosa

A
  • Systemic disease characterised by necrotising vasculitis involving small to medium arteries, kidney, heart, liver, GI tract. Pulmonary circulation is spared
  • Morphology: Lesions are sharply demarcated, induce thrombosis causing distal ischaemic injury
    • Acute lesions are characterised by sharply circumscribed arterial fibrinoid necrosis
    • Healed lesions show marked fibrotic thickening of the artery
  • Clinical features: Largely a disease of young adults with non-specific symptoms
42
Q

What is Kawasaki disease?

A
  • Acute, febrile, usually self-limited illness of infants and children
  • Associated with medium-large vessel arteritis
  • Aetiology is T cell hypersensitivity to yet-unidentified antigens
  • Lesions resemble those of PAN
  • Symptoms: CRASH + burn
    • ​Conjunctivitis
    • Rash
    • Adenopathy
    • Strawberry tongue
    • Mucosal involvement
    • Fever
  • Aspirin and IV gamma globulin reduce the coronary arteritis incidence (risk of aneurysms that rupture or thrombose)
43
Q

Necrotising vasculitis of vessels smaller than those invovled in PAN with lesions typically at the same histological stage.

A

Microscopic polyangiitis

44
Q

Allergic granulomatosis and angiitis - Small vessel necrotising vasculitis associated with asthma, allergic rhinitis, peripheral eosinophilia and extravascular necrotising granulomas

A

Churg Strauss syndrome

45
Q

What is the triad of Wegener Granulomatosis?

A
  1. Necrotising or granulomatous vasculitis of small to medium vessels mostly in the lung and upper airway
  2. Necrotising granulomas of the upper and lower respiratory tract
  3. Glomerulonephritis

c-ANCA is a good marker of disease activity

Without treatment 80% die within 1 year. 90% respond to immunosupression

46
Q

What is thromboangiitis obliterans?

A
  • Buerger disease
  • Segmental thrombosing, acute and chronic inflammation of intermediate and small arteries and veins in the extremities
  • Typically encountered in heavy smokers
47
Q

What is the difference between primary and secondary Raynaud phenomenon?

A

Primary - young women, exaggerated vasomotor response to cold or emotion

Secondary - vascular insufficiency due to arterial narrowing induced by other conditions ag SLE, athersosclerosis, systemic sclerosis

48
Q

Which diseases affect whice size vessels?

A

Tamsin - Pathology (2 decks)

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