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Classification of vasculitis

  1. Gastroepato
  2. Cardiology
  3. Classification of vasculitis
  4. Abdominal aortic aneurysms
  5. Dissection of aorta, classification
  6. Aortic aneurysm
  7. Aneurysms and aorta dissection

notes by dr Claudio Italiano

Suddenly some reddish spots appeared on your body and the fever rose to 38 ° C.
You feel bad, you have pain in the joints, headache, visual disturbances and other strange signs. Before the appearance of these signs you felt good, then you have something and you see a black spot in the groin, after you're back from a trip to the mountains and you're sitting in the grass.
Go to your doctor or emergency room right away.

You could have a vasculitis after an insect sting, maybe a tick.

Several microorganisms can cause inflammation of blood vessels, whether they are small caliber or large caliber, such as coronary vessels.
Vasculitis includes a huge spectrum of diseases that are shared by the presence of a primary inflammation of the vessel wall of the blood vessel (eg endothelium or subendothelial connective tissue of a large vase).

They recognize the most different genesis, but can be determined as a result of infection by viral or bacterial agents. For example, severe vasculitis is determined during Rickettsia infection, or in Mycobacterium tuberculosis infection. In the course of the vasculitic inflammation, however, the immunological responses are different: we can have a granulomatous and histiocytic reaction (leprosy and tuberculosis), a proliferative response (rickettiosis) to a hemorrhagic response (anthrax bacillus). In arteritis luetica, adventitious fibrosis with lymphoplasmocytic infiltrates is appreciated. It is true, however, that the angioites have a different genesis, not on an infectious basis but on an allergic or autoimmune basis.

A recent classification of the angioites includes the subdivision into:

Churg-Strauss syndrome, very high eosinophilia,
red cells with a blue nucleus

1. Infectious angioitis

Lue
mycobacteria
Pyogenic bacteria or fungi
rickettsia
Virus
Whipple's bacillus

2. Non-infectious angioitis

A. with large, medium and small caliber vessels
Takayasu's arteritis
Granulomatous giant cell arteritis
Giant cell arteritis of cranial vessels (temporal arteritis) and extracranial vessels
Disseminated visceral granulornatose angiitis
Granulomatous angiote of the central nervous system
Arteritis of rheumatoid disease and spondylohytropathies

B. mainly by medium and small caliber vessels
Thromboangioitis obliterans (Buerger's disease, see smoke)
Polyarteritis nodosa
Kawasaki disease
Granulornotosi and allergic peferic aparioitis
Granulomatosis of Wegener
Vasculitis of collagenopathies
Rheumatic fever
Rheumatoid arthritis
Systemic sclerosis
Seronegative arthropathies
Sjogren's syndrome
Systemic lupus erythematosus
Behçet syndrome
Dermatorniosite / polymyositis
C. Mostly dependent on small vessels

Angioitis in the course of temporal arteritis,
the vessel is obliterated, in the center

Hypersensitivity angiitis or allegory vasculitis

Serum sickness
Mixed cryoglobulinemia
Schoein-Henoch purple
Drug-induced angioitis
hypocomplementemia
Inflammatory intestinal diseases
Vasculitis associated with malignant neoplasms
Primary biliary cirrhosis
Retroperitoneal fibrosis
Goodpasture syndrome

Etiopathogenesis

Vasculitis can be classified according to the size of the vessel where the predominant effects are shown:
- vasculitis of small vessels, which includes the manifestation in arterioles, capillaries and venules;
- vasculitis of the medial vessels, which mainly affects the medium-sized arteries;
- vasculitis of the large vessels, which involves the aorta and its main branches.


They can also be classified according to pathogenesis:
- granulomatose: Wegener's granulomatosis, Takayasu's arteritis, Churg-Strauss syndrome, temporal arteritis (with giant or Horton cells), isolated CNS vasculitis
- from immune complexes: Polyarteritis nodosa classico (PAN), Microscopic polyangiitis (PAM), Kawasaki disease, Schonlein-Henoch purple, Systemic lupus erythematosus, cryoglobulinemic vasculitis, Goodpasture's syndrome

Topics of Gastroepato

Cardiology

Dermatology

Diabetology

Hematology

Gastroenterology

Neurology

Nephrology
and Urology


Pneumology

Psychiatry

Oncology
Clinical Sexology

Purpura of Schonlein-Henoch
Initial form with deposit of amorphous
eosinophilic material and increase of
semiluna-shaped cells.

Purpura of Schonlein-Henoch
Late form. Involute glomerulus with
deposit of eosinophilic material and
proliferation of semiluna cells

Symptoms

These are strange and vague symptoms, such as fever, sometimes itching, purple, necrosis and ulcers. Livedo reticularis, arthralgias, myositis, myalgias, mononevrites, headache, tinnitus, stroke, myocardial infarction, thrombosis, glomerulonephritis, loss of invasive visual acuity, bleeding of the respiratory and gastrointestinal tract. A patient who performs bio-temporal examinations that document the signs of vasculitis may be increased erythrocyte sedimentation rate (ESR), increased C-reactive protein (PCR), anemia, increased white blood cell count, and eosinophilia. Other indicators may be elevated levels of neutrophil anti-cytoplasm antibodies and haematuria. Specific abnormalities depend on the degree of involvement of the various organs, for example signs of renal failure.

Differences between the various vasculitides

- Takayasu's arteritis, affects young women, localizes on large vessels, NO ANCA +, possible eosinophilia, No leukocytoclastic vasculitis, fibrinoid necrosis, granuloma presence
- Temporary arteritis, affects between 50-60 years, affects large vessels, NO ANCA +, possible eosinophilia, No leukocytoclastic vasculitis, fibrinoid necrosis, no presence of granulomas
- Polyarteritis nodosa, affects subjects Around 40 years, Middle vessels, NO ANCA +, No leukocytoclastic vasculitis, fibrinoid necrosis, no presence of granulomas
- Microscopic polyangioitis, affects subjects of 50-60 years, Small and medium vessels, SI ANCA +, possible eosinophilia, no vasculitis, high fibrinoid necrosis
- Wegener's granulomatosis, affects subjects of 50-60 years, Small and medium vessels, Yes, cANCA +, minimal eosinophilia, no leucocytoclastic vasculitis, fibrinoid necrosis, granulomas
- Churg-Strauss syndrome, affects the subjects of 50-60 years, Small and medium vessels, Yes, pANCA, very high eosinophilia, no leukocytoclastic vasculitis, fibrinoid necrosis, no granulomas
- Essential mixed cryoglobulinemia, affects subjects aged 50-60 years. affects small vessels, NO ANCA +, possible eosinophilia, elevated leukocytoclastic vasculitis, minimal fibrinoid necrosis, no granulomas
- leukocytoclastic vasculitis, affects 40-year-old subjects, small vessels, NO ANCA +, minimal eosinophilia, elevated leukocytoclastic vasculitis, fibrinoid necrosis, no granulomas
- Schönlein-Henoch purple, affects children 7-10 years, Small vessels, NO ANCA +, possible eosinophilia, elevated leukocytoclastic vasculitis, minimal fibrinoid necrosis, no granulomas

Coronary arteries can also be affected by angioitis and any type of Gram-positive or Gram-negative organism may be involved. Myocarditis with abscesses and pericarditis are often associated with infectious coronary angiitis. Mucormycosis, aspergillosis and Candida are examples of fungal infections and systemic yeasts that are associated with coronary angiitis. Malaria parasites and red blood cells parasitized by them can also occlude major coronaries. Schistosoma haematobium was found in a major coronary artery, even associated with myocardial infarction. Rickets infections can cause angioitises in small vessels of the heart; these infections cause a lymphomononuclear infiltrate associated or not with thrombosis. A direct toxic effect of the rickettsies can cause anxiety. Viruses can also be involved in vasculitides by direct invasion by immunologic mechanisms. In humans, virus vasculitis is represented by polyarteritis associated with antigenemia for hepatitis B and herpes zoster.

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