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48 Cards in this Set
- Front
- Back
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C3a
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-vasoactive
-increases release of HISTAMINE -anaphylotoxin |
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Bradykinin
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-vasodilation
-increases PAIN -increase endothelial stimulation -increase capillary permeability |
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CHemokines
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chemotactic for N0/ B0/ E0/ lymphocytes
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M0 secretes in healing process
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-platelet-derived GF
-IL-1 -fibroblast-GF -TNF |
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Fever Chemokines
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IL-1
IL-6 TNF-a |
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Epitheliod cells
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aggregations of M0 seen in granulomatous infections
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C3b FXN
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increase phagocytosis
OPSONIN |
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Activates Hageman Factor
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Factor XII
-activates Kalirien cascade -activates intrinsic coagulation pathway -activates plasminogen |
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C5a
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chemotactic for N0
vasoactive anaphylotixin |
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Phospholipase C
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releases ARACHIDIONIC ACID
generated from platelet activation |
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PAF
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released by N0/ M0/ endothelial cells/ platelets
INCREASES: -vascular permeability -N0 aggregation -platelet activation |
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Premature degranulation
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release of enzymes and free radicals
causes PUS and ABSCESS formation |
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Frustrated Phagocytosis
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release of injurious free radicals and enzymes by leukocytes attempting to PHAGOCYTOSE LARGE OBJECTS
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Cachexia
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severe, long-lasting inflammation
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Acute Phase Proteins
How are they made? |
synthesized w/in HOURS of onset
made in LIVER after stimulation of IL-1, IL-6, and TNF-a |
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Examples of ACUTE PHASE PROTEINS
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CRP
fibronigen, plasminogen, prothrombin serum amyloid protein |
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ESR
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erythrocyte sedimentation rate
indicative of increased ACUTE PHASE PROTEINS CRP more specific |
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CRP
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made in liver
acute phase protein bings to PHOSPHOCHOLINE moieties in LPS activates CLASSICAL COMPLEMENT PATHWAY |
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exudate v. transudate
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EXUDATE = high protein
sp. gravity > 1.020 TRANSUDATE= low protein sp. gravity < 1.020 |
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Granulation Tissue
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fibrous CT
newly formed blood vessels (ANGIOGENESIS) |
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STEROIDAL ANTI-INFLAMMATORY DRUGS
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prevent PLA-2 formation--->
prevents PAF release inhibit synthesis of NF-KB via IKB inhibit chemokine, lymphokine HLA synthesis apoptosis of TC and BC |
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Phospholipase A-2
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creates PAF
inhibited by steroidal anti-inflammatory drugs |
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TxA2
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vasoconstriction
platelet activation |
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Fibrosis v. GLiosis
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FIBROIS= proliferation of fibroblasts (collagen) w. filling of mesenchymal tissue
GLIOSIS= if no mesenchymal tissue available, proliferation of glial cells |
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Healing by primary intention
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clean surgical incision
perfectly aligned very little tissue destruction w/ little ingrowth of GRANULATION TISSUE--> scar tissue |
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Liver regeneration
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regeneration if 80% is lost
lobules larger than previous |
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Loss of renal parenchyma
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enlargement of remaining nephrons
75%- hypertrophy 25%- hyperplasia |
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Loss of Endocrine tissue
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hyperplasia of glandular tissue
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fibrous tissue
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reults when organa scaffolding degenerates
preceeded by granulation tissue (ANGIOGENESIS) |
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DEHISCENCE
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WOUND RUPTURE
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Ab-(SS-B/ SS-A)
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Sjogren's Syndrome
auto-anti-RIBONUCLEOPROTEINS |
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Pemphigus
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autoimmune
Type II HS |
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Direct Targer HA
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Type II
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HS: complement-dependant and ADCC
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Type II
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Hashimoto's thyroiditis
HS |
Type II
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Arthus Reaction
HS |
Type III
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RA HS
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Type III
Type IV |
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antibuclear antibodies
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SLE
Type III and IV |
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Bruton's Agammaglobulinemia
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x-linked
no serum Ig |
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x-linked
no serum Igs |
Bruton's Agammaglobulinemia
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HIV-Rapid Progressors
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HLA-A29
HLA-B22 |
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HIV-Non Progressors
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HLA-B14
HLA-C8 |
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Myeloperoxidase
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in AZUROPHILIC granules of N0
H202---> HOCl-' destroys phagocytosed organisms via HALOGENATION |
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Leukotriene B4
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chemoattractant
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MOA (Inheritance) Chronic Granulomatous Disease
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1/3 autonomic rec.
2/3 X-linked |
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MOA Chronic Granulomatous Disease
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def. NADPH Oxidase sustem
-Staph -Pseudomonas -Aspergillus -Serratia -Nocardia |
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IFN-y
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secreted by TC
mediates GRANULOMATOUS FORMATION activates M0---> epitheliod cells |
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TNF-a
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fever
-activates TC -proliferation of FIBROBLASTS |
