High yield (inflam) Flashcards
Histamine is responsible for the rubor, calor (both: vasodilatation on arterial end) and tumor (inc permeability on venular end) of acute inflammation.
Bradykanin (degraded by ACE) and PGE2 are responsible for the dolor.
- C5A, LTB4 => chemotaxis, make adhesion molecules.
- IgG, C3B => opsonization
- C3A, C5A => anaphylatoxins (stimulate mast cells to release histamine)
- I-cell disease (lysosomal storage disease): can’t add mannose 6 phosphate residues to lysosomal enzymes => no proper trafficking => empty lysosomes.
- Oxygen dependant myeloperoxidase system: O2 is converted by NADPH oxidase in cell membrane of neutrophils + monocyes (not MP) into superoxide (free radical), that gives off energy => oxygen burst – can be measured by radiation detector or NBT dye test: if working ok => bluish color, if not ! chronic granulomatous disease of childhood (X-linked, no NADPH oxidase).
Superoxide is converted to peroxide which together with chloride (catalyzed by myeloperoxidase) to form bleach (kills bacteria).
- Microglial cells are the MP of the CNS.
- Dendritic cells (MP outside CNS) are located in lymph nodes.
Catalase (Staph. Aureus) breaks down peroxide and prevent its utilization in CGD. Strep doesn’t have catalase, so it can be killed even in CGD patient.
In Myeloperoxide deficiency (AR), there is a respiratory burst, but no bleach
Adhesion/B integrin defect => impaired adhesion, phagocytosis => umbilical cord doesn’t fall off (removed surgically), no neutrophils lining the small vessels.
- NO is used in treatment of pulmonaty hypertension, big role in septic shock.
- IL-1 => stimulate hypothalamus to produce PG => fever (reduced by aspirin).
- Corticosteroids inhibit PLA2 => no release of retinoic acid from PL => no PG, IL. => Decrease adhesion molecules (along with epi and NE) => neutrophil count increase (more circulating instead of being stuck to endothelium).
- Addison’s disease => dec neutrophils, inc eosinphils.
- MI => inc epi => inc neutrophil
- Omega 3 (like aspirin) inhibits platelet aggregation.
- Zileuton inhibits 5 lipoxygenase, works in asthma
- TXA2 made in platelets => vasoconstrictor, bronchoconstrictor, platelet aggregation.
- PGI2 made in endothelial cells => vasodilator, inhibits platelet aggregation.
- PGE2 => vasodilator in kidney, patent ductus arteriosus, mucus barrier in stomach, dismenorrhea, increases uterine contractility.
- Dipyridamole inhibits TX synthase, used in stress test in coronary artery disease.
- Alveolar MP have a lot of lysosomes which are seen as black dots on EM.
- Lamellar bodies (where lechitin is located) are seen in pneumocyte type 2.
- Vitamin E neutralizes oxidized LDL
- 60% of lymphocytes are T. Th:Tc ratio is 2:1.
- Plasma cell has a lot of ribosomes, because of Ig production. It is located in germina follicle.
- Eosinophils have crystals in their cytoplasm. In asthma, degenerating eosinophils form Charcot-Leyden crystals seen in sputum.
- Major basic proteins are released by eosinphils in type 2 H-S to kill helminths.
- Mast cells release histamine and eosinophil chemotactic factor in type 1 H-S. Eosinophils here release histaminase and leukotriene neutralizing agents.
- CD3 = marker in antigen recognition site for all T cells
- CD1 = antigen marker for histiocyte
- CD10 = CALLA antigen (common ALL antigen)
- CD15, 30 = Reed Sternberg
- CD21 = B cell, EBV hooks on it
- CD45 = all leukocytes
- Antipyretics reduce the oxygen in neutrophils (disturbs O2 dep. myelo system)
- Fever is not good for viral and bacterial reproduction.
Pus coming out of lactiferous duct in post partum => Staph. Aureus
Osteomyelitis (yellowish abscess) => Staph. Aureus. In Sickle cell anemia, it is usually cause by Salmonella Typhimurium. Hematogenous spread.
- Cellulitis => Strep. Pyogens
- C. dyphteria toxin damages the sub/mucosa => psedomembrane (like C. difficile)
- Bread and butter pericarditis = fibrinous inflammation => SLE, MI, coxsackie
- Dressler’s syndrome: pericarditis which develops about 6 weeks after an MI or heart surgery.
- Most common organism causing infection in 3rd degree burns is Pseudomonas Aeruginosa. Pus color is green due to pyocyanin.
- Fibronectin is an adhesion molecule and fibroblast chemotactic in healing process. Granulation tissue starts at day 3, peak on day 5.
- Type 4 collagen in basement membrane.
- Type 1 collagen is in bone, skin, tendons and ligaments
- Type 3 collagen is in the initial stages of wound repair. Broken by type 3 collagenase.
- Metalloenzyme (need zinc) helps turn type 3 into type 1.
- Maximal tensile strength in a wound by 3 months is 80%.
- Most common cause of poor wound healing is infection.
- Ehlers danlos syndrome: defect in collagen.
- Marfan syndrome: defect in fibrillin.
- Scurvy: defect in hydroxylation of proline and lysine => no cross bridges => weak
abnormal collagen => hemorrhage, no wound healing, hemoarthrosis. - Keloid (hypertrophied scar) = excess of type 3 collagen deposition.
- SCC is common in the setting of scars related to 3rd degree burns or chronically draining sinus tracts (in osteomyelitis).
- IgM is the most potent activator of the complement system, because it had 10 antigen recognition sites. Main Ig of Acute inflammation. IgG complement activation doesn’t go beyond C3 (no C5A and so on). Main Ig of chronic inflammation.
- Pus is not a characteristic of chronic (only of acute) inflammation.
- Tc killing neoplastic cells or virally infected cells is also Type 4 H-S.
- MP and Th are the key cells of TB.
- Th type 1 are involved in type 4 H-S. MP release IL-12 => memory T cells.
- Langerhans cells are the MP of the skin, phagocytose PPD, process it and present it to Th type 1 that has memory of previous exposure => release cytokines that produces the inflammatory reaction which is part of the positive PPD.
- HIV: less/no type 4 H-S (Th dec), no granuloma formation in HIV. PPD of 5 cm is enough to say positive in HIV.
- Scar tissue: heart muscle, kidney (especially straight portion of PT, TAL).
- Na-K-Cl pump generates free water (80ml for those 4 ions). Blocked by lasix.
- Type 2 pneumocytes: 1. produce surfactant, 2. repair cells, even replace type 1.
- Astrocytes: can proliferate, cause gliosis (reaction to injury in the brain)
- Schwann cells myelinate PNS axons, Oligodendrocytes myelinate CNS axons.
- Schwannoma = acoustic neuroma (if involves VIII nerve), seen in neurofibromatosis.
- IgG and/or fibrinogen inc => ESR inc
- IgM, cryoglobulin cause RBC to stick (cold agglutination => Raynaud’s phenomenon). High association of Hep.C with cryoglobulin.
- IgG => MM, IgM => macroglobulinemia (both increase ESR)
- Greater than 10% band neutrophils is left shift.
- Acute inflammation: absolute increase in neutrophils, toxic granulation, left shift.