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2a- Cardiology > Cardiovascular pathology - BLOOD VESSELS > Flashcards

Cardiovascular pathology - BLOOD VESSELS Flashcards

1
Q

What is atherosclerosis?

A

A degenerative condition of arteries characterised by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis

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2
Q

What is seen in the initiation stage of atherosclerosis?

A
  1. Endothelial dysfunction and injury around sites of damage, with subsequent lipid accumulation at sites of impaired endothelial barrier
  2. Local cellular proliferation and incorporation of oxidised lipoproteins occurs
  3. Mural thrombi (thrombi adhered to vessel wall) heal the vessel and repeat of cycle
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3
Q

What is seen in the adaption stage of atherosclerosis?

A
  1. As plaque progresses to 50% of lumen size, vessel can no longer compensate by re- modelling
  2. Becomes narrowed – drives cell turnover within the plaque
  3. New matrix surfaces and degradation of matrix
  4. May progress to unstable plaque
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4
Q

What is seen in the clinical stage of atherosclerosis?

A
  1. Plaque continues to encroach upon the lumen and runs the risk of haemorrhage
  2. T cell accumulation is stimulated
  3. Inflammatory reaction against the plaque contents – complications develop incl. ulceration, fissuring, calcification and aneurysm change
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5
Q

What is seen in the pathological stages of atherosclerosis?

A
  • Fatty streak – these show as macrophages filled with abundant lipid (foam cells) but also smooth muscle cells with fat
  • Intimal cell mass – these are collections of muscle cells and connective tissue without lipid cushions
  • The atheromatous plaque
  • Complicated plaque = calcification, mural thrombus, vulnerable plaque
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6
Q

What are the complications of plaque rupture?

A
  • Acute occlusion due to thrombus
  • Chronic narrowing of vessel lumen with healing of the local thrombus
  • Aneurysm change
  • Embolism of thrombus +/- plaque lipid content
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7
Q

What are risk factors for atherosclerosis?

A
  • Hypertension
  • Serum cholesterol level
  • Tobacco smoking
  • Diabetes
  • Increasing age
  • Male > female
  • Inactive and stressful life patterns
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8
Q

What is the hypertension background of atherosclerosis?

A
  • Altered renin-angiotensin system elevates BP by impairing sympathetic output, increasing mineralocorticoid secretion and direct vaso-constriction
  • This is balanced by atrial natriuretic factor
  • Changes to auto-regulation produce an increase in peripheral resistance, which would normally allow increased BP, diuresis and restoration of normal pressure and volume
  • Hypertension alters blood vessel walls whereby the lumen size is decreased as the wall thickness increases
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9
Q

What are the acquired causes of atherosclerosis?

A
  • Chronic vascular disease
    • Diabetes
    • Primary elevation of
      aldosterone
    • Cushing syndrome
    • Hyperthyroidism
  • Exogenous (drugs) agents
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10
Q

What is arteriosclerosis?

A
  • Hyaline arteriosclerosis shows a deposition of basement membrane-like material and accumulation of plasma proteins within the vessel wall
  • Accelerated in diabetic and hypertensive individuals
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11
Q

What is malignant hypertension defined as?

A

> 160/110mmHg

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12
Q

What is vasculitis?

A

An inflammatory and variably necrotic process centred on the blood vessels that may involve arteries, veins or capillaries

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13
Q

What is the immune background of vasculitis?

A
  • Deposition of immune complexes
  • Direct attack on vessels by antibodies
  • Cell mediated immunity
  • Viral infection
  • Serum sickness = model
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14
Q

Which viral antigens can be found in human vasculitis cases?

A

HSV, CMV, Parvovirus

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15
Q

What is Polyarteritis nodosa (PAN)?

A
  • Affects medium and small muscular arteries
  • Patchy necrotising arteritis with neutrophils, lymphocytes, plasma cells and macrophages
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16
Q

What is Hypersensitivty angiitis?

A
  • Affects the smallest arteries and arterioles
  • Microscopically fibrinoid necrosis and inflammation around small vessels
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17
Q

What is Churg-Strauss syndrome?

A
  • Necrotising legions of small medium arteries, arterioles and veins affecting lungs/ spleen/ kidney/ heart/ liver/ CAN
  • Strong association with asthma
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18
Q

What is the most common type of vasculitis?

A

Giant cell arteritis

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19
Q

Describe the features of giant cell arteritis?

A
  • Can involve large arteries (aortic aneurysm/dissection)
  • Genetic background with family
  • Thickened blood vessel, often palpable
  • Granulomatous inflammation involving full thickness of the wall with macrophages, lymphocytes, plasma cells, neutrophils and occasionally eosinophils
  • Giant cells tend to congregate around Internal elastic lamina
  • Variable necrosis
  • Old areas of inflammation show up as focal scars with fragmentation of elastic laminae, thrombosis may occur
  • Often benign, but if affects ocular artery it results in blindness
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20
Q

What is Wegener’s granulomatosis?

A

Vasculitis of the respiratory tract and kidney, may involve small arteries and veins

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21
Q

What are the symptoms of Wegener’s granulomatosis?

A

skin rash, joint pains, neurological changes

22
Q

What is Takayasu’s arteritis?

A
  • Involves artery of aorta
  • Asian bias
23
Q

What is Kawasaki disease?

A
  • Arteritis principally affecting the coronary arteries
  • May progress death due to thrombosis with acute myocardial infarction
24
Q

What is Buerger disease?

A
  • An inflammatory disease of medium and small arteries affecting the distal limbs
  • Distal ischaemic symptoms and necrosis
  • Strong association with smoking – cessation may lead to remission
25
Q

What is an aneurysm?

A
  • Dilated areas of vasculature suggesting either congenital or acquired weakness of the wall of the vessels
  • Incidence rises with age
26
Q

What are the types of aneurysm?

A
  • Fusiform
  • Saccular
  • Dissecting
  • Arterio-venous
27
Q

What is an AAA?

A

Abdominal aortic aneurysm

28
Q

Describe features of an AAA

A
  • Greater than 50% dilatation of aortic diameter
  • Strong association with atheromatous disease
  • Majority below renal arteries
  • Local inflammatory changes can be profound and involve ureters and local nerves
  • Fragmentation of the luminal thrombus leads to distal embolisation and ischaemic damage
29
Q

What is the major problem with AAA?

A

RISK OF ANEURYSM RUPTURE

30
Q

What lowers the mortality risk in AAA?

A
  • Prophylactic replacement with Dacron graft/endoluminal prosthesis
  • Rather than waiting for rupture
31
Q

What is a berry aneurysm?

A
  • Rounded berry-like vascular dilatation particularly common in the cerebral circulation
  • It is the consequence of longstanding hypertension/ focal area of weakness within the arterial substructure
32
Q

When is a berry aneurysm dangerous?

A
  • Dangerous if near the circle of Willis – if a subarachnoid haemorrhage occurs it will lead to sudden death
33
Q

What is a dissecting aneurysm?

A
  • A haematoma within the arterial wall with blood entering under pressure from the luminal surface and dissecting along the length of the media
  • Majority occur just above the aortic ring
  • Prunes off the large arteries supplying the head
  • May rupture into local soft tissues, may rupture into pericardium
  • Double-barrelled aorta if blood re-enters circulation
34
Q

What is syphilis?

A
  • Inflammatory disease affecting the vasa vasorum
  • May produce degeneration of the media and subsequent aneurismal change
35
Q

What are varicose veins?

A

Enlarged and torturous veins, principally affecting the superficial leg veins

36
Q

What are the risk factors for varicose veins?

A
  • Age
  • Female (pregnancy related)
  • Hereditary
  • Posture
  • Obesity
37
Q

What does progressive incompetence of vein valves lead to?

A

Venous hypertension

38
Q

What are reasons lymphatic vessels can become obstructed?

A
  • Infestation of the lymph nodes and lymphatic vasculature by tropical parasites
  • Tumour obstruction
  • Surgical clearance (particularly breast surgery)
  • Inherited lymphoedema – Milroy disease
39
Q

What are some vascular tumours?

A
  • Haemangioma
  • Glomus tumour
  • Haemangioendothelioma
  • Angiosarcoma
  • Kaposi’s sarcoma
40
Q

What is a haemangioma?

A

a benign proliferation of blood vessel tissue, which varies in name and structure depending on site and age of patient

41
Q

What is a Glomus tumour?

A
  • a benign neoplasm involving the glomus body
  • Mainly affects the hands (painful)
42
Q

What is a Haemangioendothelioma?

A
  • a vascular tumour of endothelial cells of low grade malignancy
  • May metastasise to other sites around the body
43
Q

What is an Angiosarcoma?

A
  • high aggressive malignant neoplasm of endothelial cells
  • Rapidly enlarging haemorrhagic tumour with rapid dissemination to other organs – skin, soft tissue, breast, bone, liver and spleen
44
Q

What is Karposi’s sarcoma?

A
  • linked to HIV, associated with human herpes virus 8
  • Painful purple/brown nodule on skin between 1-10mm diameter
45
Q

What are risk factors of deep vein thrombosis?

A
  • Venous flow stasis from any cause (e.g. cardiac failure, chronic venous insufficiency)
  • Injury (trauma, surgery, child birth)
  • Hypercoagulability (pregnancy, cancer, inherited thrombophilic disorders)
  • Advanced age
  • Sickle cell disease
46
Q

What features can form after DVT?

A
  • Lysis
  • Organisation
  • Provocation
  • Embolisation
47
Q

What can an embolism cause?

A
  • May be asymptomatic and small
  • May produce transient dyspnoea for relatively small emboli
  • May produce focal pulmonary infarction with chest pain, haemoptysis and secondary effusion
  • Can produce CV collapse and sudden death (saddle embolus)
48
Q

What is a Paradoxical embolism?

A

Embolus that travels through the venous circuit then across from the right to the left side of the heart through a patent foramen ovale

49
Q

What do systemic arterial embolisms usually cause?

A

Usually causes infarction of the tissue as the material impacts in the nutrients/oxygen supplying vasculature

50
Q

What can cause systemic arterial embolisms?

A
  • Atherosclerotic plaques, mural thrombus in heart or vasculature
  • Infective endocarditis
  • Sites particularly vulnerable – brain, intestine, distal limbs, kidneys and coronary circulation
51
Q

What are other types of embolism?

A
  • Air embolism
  • Acute decompression sickness
  • Amniotic fluid embolism
  • Fat embolism
  • Bone marrow embolism
  • Talc/cotton/other material from intravascular injection

2a- Cardiology (7 decks)

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