Joints, Vasculitis, Diseases of Immunity QandA explanations Flashcards
Rubin’s 21, Joints: Juvinile arthritis
can have polyarticular juvenile arthritis with prominent systemic symptoms including fever, rash, HSM, lymphadenopathy, pleuritis, and anemia; could develop RA, ankylosing spondylitis, psoriatic arthritis, and other CT diseases; also the PERICARDIAL FRICTION RUB
Robbins 30 Joints: Woman with a form of chronic arthritis
that is the late, or stage 3, manifestation of Lyme, which can be remitting and migratory, involving primarily the LARGE JOINTS. Presence of lymphoplasmacytic infiltrate with endothelial prolif is characteristic of Lyme arthritis; infectious agent is Borrelia burgdorferi (spirochete spread by deer tick)
Robbins 37 Joints: what does the picture show, and what could have beget this condition?
Calcium pyrophosphate dihydrate deposition, which can be primary or secondary, like hemochromatosis or preexisting joint damage. Patient here shows evidence of hemochromatosis-caused skin pigmentation, heart failure, diabetes, and cirrhosis.
Robbins 44 Joints: A _____ cyst has a thin wall and clear, ____ content
ganglion; mucoid;
it arises in the CT of a joint capsule or tendon sheath, and extensor surfaces of the hands are the most common sites, particularly the region of the wrist. Ganglion cysts probably arise after trauma from focal myxoid degen of CT to produce a cystic space
Robbins 11 BV’s: a man with a thoracic aorta with a dilated root and arch, giving intimal surface a tree-bark appearance. There is an olberative endarteritis of the vasa vasorum. What could this be?
Description is suggestive of syphilitic aortitis, a complication of tertiary syphilis; with characteristic involvement of the thoracic aorta: the obliterative endarteritis is NOT a feature of other forms of vasculitis
Robbins 27 DOI: CD4 lymphocytes are
thought to respond to some unknown antigenic stimulation, releasing cytokines that activate further macrophages and mast cells. The result is EXTENSIVE DERMAL FIBROSIS that produces the clinical appearance of sclerodactyly in scleroderma!!
Rubin’s 9 BV: Obliteration of the vasa vasorum
causes focal necrosis and scarring of the media, with disruption and disorganization of the elastic lamellae; see tree bark appearance, and the outer and middle third of the aora encircled by lymphocytes, plasma cells and macrophages
Rubin’s 12 BV: Malignant hypertension refers to
an elevated BP that could lead to rapidly progressive vascular disease affecting brain, heart, and kidney; disease injures endothelial cells, causing increased vascular perm, leading to insudation of plasma proteins into vessel wall and fibrinoid necrosis!!
Rubin’s 16 BV: Most common morphologic of PAN is
fibrinoid necrosis in the affected arteries, when medial muscle and adjacent tissue are fused into an eosinophilic mass that stains for fibrin
Rubin’s 18 BV: Hypersens angiitis refers to
broad spectrum of inflamm lesions that represent a rxn to foreign materials (e.g. bacterial products or drugs like sulfa); also called LEUKOCYTOCLASTIC VASCULITIS, cutaneous vasulitis, or cutaneous necrotizing venulitis when vascular lesions are confined to the skin
Rubin’s 23 DOI: Immune complex (type III) hypersens reactions cause
vasculitis. Ag-Ab complexes are either formed in circulation and deposited in the tissues or formed in situ. IMmune complexes induce a localized inflamm response by fixing complement, which leads to recruitment of neutrophils and monocytes. This hypersens is seen with HS purpura and PAN.
Rubin’s 8 DOI: Type II hypersens reactions are mediated by
Ab’s directed against fixed antigens. Here, preformed Ab’s in patient’s blood attached to foreign antigens on membranes of transfused erythrocytes. Complement cascade leads to destruction of the target cell through formation of a membrane attack complex (MAC).
