Immune system Flashcards
Most common clinical manifestations of SLE
Hematologic
Fatigue
Arthritis, arthralgia or myalgia
Skin
Renal
“SOAP BRAIN, MD” mnemonic for SLE criteria
Serositis
Oral ulcers
Arthritis
Photosensitivity
Blood disorders
Renal involvement
ANAs
Immuno. (andi-dsDNA, anti-Sm, antiphospholipid antibodies)
Neurological disorders
Malar or Discoid rash
Genes that create genetic predisposition to SLE
HLA-DRA2 & HLA-DRA3
Most widely used method for detection of ANAs
Indirect immunofluorescence
Complement proteins deficient in SLE
C1q, C2 and C4
Common triggers of SLE, have not been proved as a cause for the disease.
UV light and EBV
Air particles or substances that increase the risk of developing SLE.
Cigarette smoking and silica
Type of hypersensitivity causing systemic lesions in SLE.
Type III hypersensitivity
Mechanism through which blood vessels are damaged in lupus.
Increased vascular permeability, complement activation and accuulation of PMNs that secrete enzymes.
Most dangerous clinical manifestation in SLE because of its high morbidity and mortality.
Renal involvement
Parts of the kidney where immune complexes deposit in SLE.
Glomerular basement membrane, mesangium and sometimes in the glomerulus.
Most common glomerular disease pattern in SLE.
Class IV
Class 1 is the least common
Types of class IV SLE kidney disease (diffuse lupus nephritis)
50% or more glomeruli with lesions:
IV-S: Lesions involving <half of glomerular tuft.
IV-G: Lesions involving >half of glomerular tuft.
Classes with which membranous lupus nephritis (V) can occur
III and IV
SLE nephritis in which 90% or more of the flomeruli are globally sclerosed.
VI. Advanced sclerotic lupus nephritis.
These deposits may cause the thickening of the capillary wall of the glomerulous, forming the wire loops structures on class IV SLE nephtropaty.
Subendothelial immune complex
Diffuse thickening of the glomerulous capillary walls.
Membranous lupus nephritis class V
Sclerosis of more than 90% of the glomeruli in SLE.
Advanced sclerosing lupus nephritis class VI
Findings in HE stained skin in SLE
Vacuolar degeneration of the basal layer of the epidermis.
Variable edema and perivascular inflammation in the dermis.
SLE skin finding with IF
Deposition of Ig and complement in the dermoepidermal junction.
Type of joint involvement in SLE
Non-erosive synovitis with little deformity
Histopathologic finding of the spleen in SLE
Perioarteriolar fibrosis (onion skinning)
Concentric intimal and smooth muscle cell hyperplasia
Histopathologic finding of the bone marrow in SLE
LE or hematoxylin bodies
Histopathologic skin findings in chronic discoid lupus erythematosus
Follicular plug (carpet tack)
Liquefaction degeneration
Thick basement membrane
Type of lupus with predominant skin involvement, initial widespread superficial and non-scarring rash and no genetic association, with extreme photosensitivity.
Subacute cutaneous lupus erythematosus
Drugs that may cause drug-induced LSE
Hydralazine, procainamide, isoniazid and D-penicillamine
Type of synovitis of RA
Non-suppurative, proliferative and inflammatory
Genes associated to RA
HLA-DR4 & HLA-DR1
Articular lesions in RA
Symmetrical polyarthritis
Z deformity
Tenosynovitis
Carpal tunnel syndrome
Skin finding in RA
Bursitis and rheumatoid nodules
Finger discoloration finding in RA
Raynaud phenomenon
Citrullinated protein that mimics the epitope on microbes and is presented by class II HLA-DR4 molecule on RA.
Vinculin
CC produced by Th1 cells in RA that activates macrophages and resident synovial cells.
IFN-y
CC produced by Th17 cells in RA that recruits neutrophils and monocytes.
IL-17
Factor expressed by activated T cells in RA, simulates bone resorption.
RANKL
An activated macrophage producing TNF and IL 1 in RA, will stimulate synovial cells to produce________ to ______
MMP and ADAMTS to destroy cartilage
Diagnostic markers found in serum in RA
Anti-citrullinated peptide antibodies (ACPA)
Ig that form rheumatoid factor in RA
IgM and IgA, not specific.
Radiologic finding that differentiates RA from osteoarthritis
RA involves the non-weight bearing portion of the knee.
First joints affected in RA
Small joints, first in hands (metacarpo-phalangeal and proximal interphalangeal)
Necrotizing skin granulomas with central fibrinoid necrosis surrounded by activated macrophages.
Rheumatoid nodules
These organisms infect in mantained anti-TNF therapy
Opportunistic microorganisms (M. tuberculosis)
Swelling of popliteal fold in RA
Baker cyst
Cells infected and attacked by HIV
CD4+ T cells
Receptor and correceptors used by HIV
R: CD4
Correceptor: gp120, CCR5 and CXCR4
Pathway activated by HIV to increase the number of cells infected
Inflammasome pathway (more cell recruitment)
Organs where HIV infection of macrophages and DCs takes place.
lungs and brain
Predominant cell type infected with HIV.
Microglia
Most common neoplasm in patients with AIDS
Kaposi Sarcoma
Tinción que resalta hongos (hifas y esporas)
PAS y grocott (argénica de plata)
Afección de los virus en las células
Inclusiones virales
Virus que causa inclusión en saco de canicas (vesículas con núcleos contaminados), sólo se ve en epitelio escamoso
Herpes simple
Centro necrótico, rodeado de linfocitos con células gigantes multinucleadas.
Granuloma
Protozoarios sugestivos de VIH
Cryptosporidium, P. jirovecii y toxoplasma
Hongos sugesitos de VIH
Candida, Cryptococous en SNC, Coccidioides, Histoplasma
Patient with HIV presents interstitial pneumonia and cavitations.
Alveolar biopsy shows alveolar exudate.
Grocott stain is requested and black spots are shown.
P. jirovecii infection
Viral inclusion shown as only 1 owl eye everywhere in the body, often in HIV.
CMV
Person with HIV presents chronic diarrhea refractary to treatment. Most common coinfection?
Cryptosporidium
HIV patient with meningitis and encephalitis, grocott stain of CSF is asked.
Cryptococcous pneoformans
HIV infected patient presents encephalitis
T. gondii
For a patient to develop a Kaposi Sarcoma it must be infected with
Herpes virus 8
Escala utilizada para graduar el rechazo renal
Clasificación de Banff
Complement and coagulation activation after blood restorage in a transplant for HLA recognition and preformed antibodies.
Hyperacute rejection
Rejection within days or weeks or transplant, or after immunosuppressive treatment is suspended with possible damage to blood vessels.
Acute rejection
Renal tubulitis after transplantation, with infiltrates in the tubules.
Acute kidney transplant rejection
Explain the diagram and structures.
Acute rejection
B: acute cellular rejection (tubulitis)
C: vascular rejection