Just like our lecture on atherosclerosis and hypertension, the learning outcomes are a bit broad so I'll be using a different style of headings for this post (rather than simply using learning outcomes as headings).
Aneurysms
Aetiology and predisposing factors
The main causes of aneurysms are congenital, mycotic (the name suggests fungal infections, but in this case the term actually refers to any kind of infection, including bacterial), inflammatory, and traumatic.
Pathogenesis and pathophysiology
Aneuryms are abnormal dilations of the blood vessel or heart wall that may be due to some kind of weakness in the tunica media (or myocardium, if the aneurysm is in the heart). Aneurysms are most common in arteries and the left ventricle.
Classification scheme
Aneurysms can be classified as true or false aneurysms. True aneurysms are bounded by components of the arterial wall. False aneurysms are formed due to leakage of blood through a breach in the vascular wall, forming a haematoma.
Aneurysms can also be classified by morphology. Bubble-like aneurysms that only affect part of the artery wall are known as saccular aneurysms. Swelling that involves the whole wall is called a fusiform aneurysm.
Aneurysms can also be classified by cause and/or location.
Morphological changes and clinical features
One common type of aneurysm is the berry aneurysm, or cerebral saccular aneurysm. Berry aneurysms are usually found at branch points in the Circle of Willis (a circle of arteries in the brain). They usually form where there are some congenital defects in the tunica media. Note that the aneurysm itself is not congenital; however, it is the conditions that allow the aneurysm to form that are congenital. (In fact, the aneurysm itself normally doesn't form until around 30-60 years of age) Berry aneurysms may compress cranial nerves and may affect vision if they press on the optic nerve. If berry aneurysms rupture, patients may experience a sudden headache that feels like a "thunderclap." The resulting subarachnoid haemorrhage can be highly fatal if untreated and of the survivors, around 50% have permanent neurological damage. Berry aneurysms may be diagnosed by imaging and subarachnoid haemorrhage may be detected by looking at cerebrospinal fluid.
Aortic aneurysms similarly occur due to some kind of abnormality in the tunica media. However, in aortic aneurysm, the most common cause of such abnormalities are atherosclerosis. Abdominal aortic aneurysms are fairly common (2-4% of Caucasians) but is usually not the cause of death in these patients. Rupture is rapidly fatal due to the size of the aorta. Another consequence of abdominal aortic aneurysm is the formation of blood clots due to disturbance of blood. Clots may break off and occlude downstream arteries.
Thoracic aortic aneurysms are mainly associated with hypertension. They may press on airways or the oesophagus. If the aortic root is dilated, aortic regurgitation may result.
Complications and clinical sequelae
Aneurysms may rupture, leading to haemorrhage that can be rapidly fatal. They may also cause disturbance of blood within the arteries, resulting in thrombus formation. Aneurysms may also push against surrounding structures and compress them.
Aortic Dissection
Aortic dissection is not an aneurysm, but since it was covered in this slide, I'll talk about it anyway. In aortic dissection, there is a tear in the intima of the aorta, allowing blood to enter and separate the intima and media. Many patients with aortic dissection experience a sudden excruciating pain in the chest or back between the shoulder blades. Aortic dissection usually occurs due to weakening of the tunica media (just like most aneurysms, even though aortic dissection isn't an aneurysm). In hypertension or some genetic conditions, like Marfan syndrome, there are fewer elastic fibres and excess polysaccharides in the tunica media: a change known as cystic medial necrosis. Cystic medial necrosis can, in turn, lead to aortic dissection (as well as aortic aneurysms).
Vasculitides
Aetiology and predisposing factors
Vasculitis just refers to inflammation of the blood vessels, which can be due to a range of factors. Some types of vasculitis, such as temporal giant cell arteritis, have no known cause. Others may be due to infection, malignancy, medications, etc.
Pathogenesis and pathophysiology
Often, vasculitis starts off by the deposition of immune complexes in the blood vessels. These immune complexes can activate the complement cascade and cause propagation of the inflammatory response. Antibodies may also directly attack the blood vessel wall.
Classification scheme
Vasculitis is mainly classified by the size of the vessels affected. Large-vessel vasculitis includes takayasu arteritis and temporal giant cell arteritis. Medium-vessel vasculitis includes polyarteritis nodosa and Kawasaki's disease. Small-vessel vasculitis includes granulomatosis with polyangiitis (a.k.a. Wegener's granulomatosis), Churg-Strauss Syndrome, and Henoch-Schonlein purpura. (Note that this is not an exhaustive list of all of the types of vasculitis.) In this post, we will be focusing on temporal giant cell arteritis, polyarteritis nodosa, and granulomatosis with polyangiitis.
Morphological changes and clinical features
Temporal giant cell arteritis involves inflammation of large- and medium-sized arteries, especially the carotid and temporal arteries. It is usually diagnosed by a biopsy of the temporal artery, though an issue with this is that you could just as easily remove a part of the temporal artery that is unaffected.
Polyarteritis nodosa primarily affects medium-sized vessels, usually the renal and mesenteric arteries. However, it does not involve pulmonary arteries. In polyarteritis nodosa, there is infiltration of the arterial wall by neutrophils, lymphocytes, and plasma cells, and fibrinoid necrosis of the arterial wall.
Granulomatosis with polyangiitis, also known as Wegener's granulomatosis, is a small-vessel vasculitis that primarily affects the respiratory and renal systems. It can affect people of any age and it affects males and females equally.
Complications and clinical sequelae
The inflammation in vasculitis may lead to narrowing of the lumen or disrupted blood flow leading to thrombosis. In both cases, there may be ischaemia to tissues supplied by the blood vessel.
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