1- Diseases of the blood vessels Flashcards
(26 cards)
what are diseases of the blood vessels
Arteriolosclerosis
Aneurysm
Aortic dissection
Vasculitis
arteriosclerosis classifications
Arteriosclerosis literally means “hardening of the arteries”; it is a generic term for arterial wall thickening and loss of elasticity. there are three general patterns of arteriosclerosis:
- arteriolosclerosis- affects small vessels arteries and arterioles. ==can be hyaline or hyperplastic==
- mönckeberg medial stenosis- characterised by calcification of the walls of muscular arteries
- atherosclerosis- affects large and medium sized blood vessels
artherosclerosis consists of?
Chronic inflammatory disorder of intima of large arteries characterized by formation of fibrofatty plaques called atheroma.
> [!NOTE]
> ### Composition of an Atheroma:
> 1. Lipid Core:Contains cholesterol, cholesterol esters, and cellular debris.
> 2. Fibrous Cap:Composed of smooth muscle cells, collagen, and extracellular matrix, which covers the lipid core.
> 3. Inflammatory Cells:Macrophages, foam cells (lipid-laden macrophages), and T-cells are present, indicating an inflammatory process.
> 4. Calcium Deposits:In advanced stages, calcification may occur, making the plaque hard and brittle.
risk factors for artherosclerosis
non-modifiable
Genetic abnormalities
Family history
Increasing age
Male gender
modifiable
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes
Inflammation
unquantifiable/ possibly lesser risk factors
Lack of exercise
Type “A” personality
Obesity
“Trans”-unsaturated fat intake
Postmenopausal
Estrogen deficiency
High carbohydrate diet
Chlamydia pneumoniae
Hyperhomocystinemia
Lipoprotein (a)
Inhibitors of fibrinolysis
Low PA-1 Inhibitor
C-reactive protein
Pathogenesis of artherosclerosis
Endothelial Dysfunction: Damage to the inner lining of arteries due to risk factors like high cholesterol, smoking, or high blood pressure.
Lipid Accumulation: LDL cholesterol enters the damaged wall, gets oxidized, and is taken up by macrophages, forming foam cells and fatty streaks.
Inflammation: Immune cells are recruited, releasing cytokines that worsen inflammation and promote plaque growth.
Plaque Formation: Smooth muscle cells migrate, producing a fibrous cap over a lipid-rich necrotic core.
Complications: Plaques can rupture, causing blood clots that block arteries, leading to heart attacks or strokes.
common blood vessels involved in artherosclerosis
In descending order, the most extensively involved vessels are:
A- abdominal aorta
C- carotid artery
P- popiteal artery
D- descending thoracic aorta
I- internal carotid artery
C- circle of willis
Complications of artherosclerosis
H- haemorrhage into a plaque
A- Aneurysm
C- calcification
U- ulceration or rupture
T- thrombosis
E- embolism
Aneurysm definition and types
Aneurysm is a localized abnormal dilation of a blood vessel or the wall of the heart. It is of two types:
True aneurysm: Involves intact attenuated arterial wall or thinned ventricular wall of the heart.
The common causes include Atherosclerosis, syphilis and post-MI ventricular aneurysms.
False/Pseudo- aneurysm: It is characterised by a breach in the vascular wall leading to extravascular hematoma communicating with intravascular space.
The two commonest causes of pseudo-aneurysm are post-MI rupture and leakage at the site of vascular anastomosis
aneurysm classification based is size and shape
Saccular aneurysms: They are spherical outpouchings involving only a portion of the vessel wall; they vary from 5 to 20 cm in diameter and often contain thrombus e.g Berry aneurysm.
Fusiform aneurysms: They are diffuse, circumferential dilations of a long vascular segment; they vary in diameter (up to 20 cm) and in length; and can involve extensive portions of the aortic arch, abdominal aorta, or even the iliacs
Other causes of Hypertension
common causes of hypertension include:
- Hypertension: commonest cause of ascending aortic aneurysms
Inherited or congenital causes of aneurysm include:
- Marfan’s syndrome: defective synthesis of the protein fibrillin
- Ehlers-Danlos syndrome: defect in collagen type III
- Loeys Dietz syndrome: defect in elastin and collagen types I and III due to mutation in TGF-b receptor.
- Fibromuscular dysplasia
- Berry aneurysms
Aortic dissection
Aortic dissection occurs when blood separates the laminar planes of the media to form a blood-filled channel within the aortic wall
Aortic dissection occurs principally in two groups of patients:
Men aged 40 to 60 years with antecedent hypertension (more than 90% of cases)
Younger adults with systemic or localized abnormalities of connective tissue affecting the aorta (e.g., Marfan’s syndrome).
Causes of aortic dissection
Hypertension: major risk factor for aortic dissection.
Inherited or acquired connective tissue disorders with defective vascular extracellular matrix: e.g Marfan’s syndrome, Ehlers-Danlos syndrome, defects in copper metabolism
Iatrogenic: e.g following arterial cannulations during coronary catheterization procedures or cardiopulmonary bypass.
Classification of Aortic dissection
Debekey 1, 2 and 3
Pathogenesis of Aortic Dissection
An aortic dissection usually initiates with an intimal tear
Aortas of hypertensive patients have medial hypertrophy of vasa vasorum resulting in ischaemic injury due to diminished blood flow, and associated degenerative changes in the media such as loss of medial smooth muscle cells and disorganized extracellular matrix.
Morphology of Aortic Dissection
The most frequent pre-existing histologically detectable lesion is cystic medial degeneration.
- Inflammation is characteristically absent
- In the vast majority of spontaneous dissections, the tear occurs in the ascending aorta, usually within 10 cm of the aortic valve
- Such tears are typically transverse with sharp, jagged edges up to 1 to 5 cm in length.
- The dissection can extend retrogradely toward the heart as well as distally, sometimes into the iliac and femoral arteries.
- The dissecting hematoma spreads characteristically along the laminar planes of the aorta, usually between the middle and outer thirds
- It can rupture through the adventitia causing massive haemorrhage (e.g. into the thoracic or abdominal cavities) or cardiac tamponade (haemorrhage into the pericardial sac).
- In some instances, the dissecting haematoma re-enters the lumen of the aorta through a second distal intimal tear, creating a new false vascular channel (“double-barreled aorta”).
Vasculitis
vasculitis is inflammation of the blood vessels
The two common pathogenic mechanisms of vasculitis are: immune-mediated inflammation and direct invasion of vascular walls by infectious pathogens.
Physical and chemical injury, such as from irradiation, mechanical trauma, and toxins, can also cause vasculitis
classification of vasculitis based on vessel size
- large vessel vasculitis
- medium vessel vasculitis
- small vessel vasculitis
Large vessel vasculitis
- Giant cell (Temporal) arteritis/Cranial arteritis
- takayasu arteritis
Giant cell (temporal) arteritis/cranial arteritis
It is the most common type of vasculitis in adults (usually >50 years)
Characterized by granulomatous arteritis of the aorta and its major branches particularly the extracranial branches of the carotid artery.
Also known as temporal arteritis because Superficial temporal artery is the commonest involved vessel.
Clinical features include constitutional symptoms like fever, fatigue, weight loss, jaw Pain (most specific symptom), facial pain, localized headache (commonest symptom; most intense along the anatomical course of the superficial temporal artery) and sudden onset of blindness (due to involvement of ophthalmic artery)
Biopsy of temporal artery is the investigation of choice.
Microscopically, there is presence of granulomatous inflammation with multinucleated giant cells and fragmentation of internal elastic lamina.
Takayasu Arteritis
It is seen in adult females < 50 years of age.
This condition is characterized by granulomatous vasculitis followed by irregular thickening of the vessel wall with intimal hyperplasia of the aortic arch and decreased or obliterated lumen of the vessels arising from the aortic arch.
The pulmonary, renal and coronary arteries may also be involved.
Clinical features include weak pulses in the upper limbs (so, the disease is also known as pulseless disease), ocular disturbances, hypertension and neurological defects.
Medium vessel vasculitis
- Classic Polyarteritis Nodosa (PAN)
- Kawasaki’s disease (Mucocutaneous Lymph Node Syndrome)
Classic Polyarteritis Nodosa (PAN)
It is a systemic vasculitis of medium sized muscular arteries (no involvement of arterioles/capillaries/venules).
The most frequently involved vessels are those of the kidney and other viscera vessels.
The vessels of the pulmonary circulation are typically not involved.
Characteristic feature of this disease is sharp segmental lesions showing transmural inflammation of vessel wall accompanied by fibrinoid necrosis and existence of all stages of inflammation in the same vessel.
30% patients have association with Hepatitis B antigen in their serum.
No glomerulonephritis is seen.
It is the commonest cause of mononeuritis multiplex
Kawasaki’s disease (Mucutaneous lymph node syndrome)
It is the vasculitis affecting children < 5 years of age.
It is characterized by fever, conjunctivitis and oral erythema, skin rash often with desquamation, erythema of palms and soles and cervical lymphadenopathy.
For diagnosis of Kawasaki disease, there must be presence of fever ( i.e most important constitutional symptom) > 5 days plus any 4 of the following:
C - Conjunctivitis (non-exudative; non purulent conjunctivitis)
R - Rash (polymorphous non-vesicular)
E - Edema (or erythema of hands or feet)
A - Adenopathy (cervical, often unilateral and non- suppurative)
M - Mucosal involvement (erythema or fissures or crusting at times referred as strawberry tongue)
It is the most important cause of acquired heart disease in children in USA.
It may present with myocardial infarction in children.
It is associated with presence of anti-endothelial cell antibodies.
Morphologically, there is typically intimal proliferation and mononuclear infiltration of vessel wall.
It may also be associated with thrombophilia (i.e increased platelet count)
Small Vessel vasculitis
- Granulomatosis with Polyangiitis (Wegener’s granulomatosis )
- Churg-strauss syndrome
