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1: is synthesised by mast cells
2: mediates vascular spasm
3: is an antagonist of platelet aggregation
4: production is inhibited by aspirin
Robbins 6th ed. Page: 70-71
1: is located in lysosomes
2: is visible by light microscopy in routine paraffin sections
3: is stored in mononuclear phagocytic cells
4: levels in serum reflect iron stores except in inflammation
Robbins 5th ed. PAGE: 28-29; 610
1: act locally on immediately adjacent cells
2: have individual actions in modulating cell function which are specific for each cytokine
3: bind to non-specific receptors on target cells
4: are involved in stimulating cell growth but not cell differentiation
Refer to Robbins, 6th Ed, Ch 7, page 191-192
1: when released systemically, protecting against shock
2: enhancing leukocyte-endothelial adhesion in acute inflammation
3: activating fibroblast migration and collagen synthesis
4: influence on the hypothalamus resulting in fever
IL-1/TNF is all pro-inflammation, pro-healing (including healing by fibroplasia). Hence, responses 2, 3 and 4 are all True (fibroplasia and collagen synthesis are stimulated). However, the vasoactive and prothrombocoagulant effects can be devastating when there is avid systemic release/activation of IL-1/TNF systemically (as, for example in severe bacteraemia [septicaemia in non-Robbins terms]), when widespread vasodilatation and increased vascular permeability contribute to the syndrome of irreversible shock (and to DIC also).
1: inhibiting proliferation of T helper cells
2: endothelial cell activation
3: hypothalamus-mediated fever induction
4: enhancement of monocyte/macrophage bactericidal capacity
Robbins 5th ed. Chapter: 3 Pages: 71, 174
1: may be activated in the absence of immune complexes
2: is important in the formation of granulomas
3: binds to the mast cell membrane and inhibits degranulation
4: kills target cells by triggering apoptosis
Refer to Roitt, 9th Ed, page 11-14
A. increasing vascular permeability
B. phagocytosis of bacteria
C. release of histamine from mast cells
D. activation of fibrinolysis
E. destruction (killing) of bacteria
Robbins, 6th ed, Ch 3 and 5
Complement activation is critical to a successful acute inflammatory reaction and to opsonisation of bacteria in the early phases of acute inflammation in immunologically ‘unprimed’ individuals. This must protect the person until infection is controlled by innate mechanisms or until an immune response is generated. Subgroup 4 of IgG does not (after reacting with specific Ag) activate C?; IgG2 is a poor C? activator. However, the phenomenon under discussion has nothing to do with subgroup IgG activation of C? - this important ‘bypass activation’ of C? takes place far earlier than the immunologic production of Ig capable of dealing with this ‘new’ bacterium and is the ‘stopgap’ protection, pending Ig release.
2: lysis of bacteria
3: chemotaxis of neutrophils
Roitt 9th Edition PAGE: 12-16 Robbins 5th ed. PAGE: 182-183
1: thromboxane A2 (TxA2)
2: nitric oxide
4: adenosine triphosphate ATP
Robbins 6th Edition Page: 120-122
15923 – The following mediators are synthesised ‘on the spot’ and immediately released by injured/ stimulated cells
1: tissue thromboplastin
2: leukotriene B4 (LTB4)
3: Interleukin-2 (IL-2)
4: C3b opsinic factor
Platelets (activated) and endothelial cells (injured), in particular, manufacture tissue thromboplastin. LTB4 is a product of the lipoxygenase pathway metabolism of arachidonic acid (from cell membrane phospholipid). IL-2 production is particularly the province of CD4+, TH2 cells in B cell ‘help’. Complement is, of course, a plasma protein system.
1: platelet activating factor
2: major basic protein
3: C3b opsinic factor
Platelet activating factor is stored in granules within some cells and manufactured ‘on the spot, on demand’ by others. Major basic protein is a product of eosinophil leukocytes - very effective in destroying multicellular parasites (and also bystander host cells). Complement components are, of course, plasma components (though some components are present in some cells also). Plasmin is another ‘cascade’ enzyme systems - contact activated.
2: expression of adhesion molecules on endothelial cells
4: platelet activating factor (PAF)
Fibroblast proliferation and differentiation appears to be largely under the control of growth-promoting and growth-controlling cytokines. The influence of other factors such as extracellular matrix products (particularly fibronectin, laminin, etc and fibrino-peptides), although persuasive, is still equivocal. The endothelial adhesion molecules include members of the immunoglobulin family of proteins - they have no known influence on fibroblast ( or other ECM cell ) activity and the same goes for the two cell membrane phospholipid derivatives LT and PAF.
1: platelet activating factor (PAF)
2: gamma interferon
Platelet activating factor is derived from cell membrane phospholipid by phospholipase (PLA2) action, but not via pathways of prostaglandin or HETE/leukotriene metabolism. In low concentrations, it is an extremely potent inducer of vasodilator and permeability, as well as other aspects of the inflammatory process. Bradykinin and histamine are also both 'classic' permeability factors. Gamma-interferon has no effect on endothelial cells (other cytokines may act indirectly through endothelium-activation in pavementing, thus aiding ‘leukocyte-mediated’ permeability - but not directly).
1: acute anaphylaxis
2: adult respiratory distress syndrome
3: serum sickness
Robbins 5th Edition Page: 55&68 vs 180, 184&(677)
1: prostacyclin (PGI2)
2: nitric oxide (NO)
3: leukotriene B4 (LTB4)
4: neutrophil lysosomal enzymes
Prostacyclin and nitric oxide are both powerful vasodilating agents, both produced by intact endothelium. Leukotriene B4 is produced from arachidonic acid through the lipoxygenase pathway; it has powerful chemotactic effects, but does not directly influence either vascular flow or permeability. Neutrophil lysosomal enzymes appear to have no effect on vasodilatation and, in any case, are not active in the zone until acute inflammation is well established.
Muramic acid-N acetyl glucosamine bond is found in the cell wall of all bacteria. Lysozyme specifically hydrolyses the bond, thus damaging the bacterial cell wall.
1: processing and presentation of antigens
2: control of fibroblast proliferation
3: induction of neutrophil adhesion molecules on endothelial cells
4: secretion of endogenous pyrogen, IL-1
Robbins 5th ed. CHAPTER: 2 PAGES: 701; 76
1: morphologically resemble lymphocytes
2: are derived from stem cells in the germinal centres of lymph nodes
3: undergo chemotaxis in response to IgE antibody
4: are mainly transformed blood monocytes
Robbins 5th ed. Chapter: 5 Pages: 59; 74; 76
3: activated complement products4: activated T helper lymphocyte (TH1) secretions
The amines which are important in acute inflammation are vasoactive, but not chemotactic. Cytokines (IL-8 family) and complement products (C5a) are chemotactic for PMN and monocytes. TH1 secretions include the ‘lymphokines’ of which MCF is a prominent member!
2: adenosine diphosphate (ADP)
3: an inhibitor of plasminogen activation (tPA inhibitor)
4: prostacyclin (PGI2)
It is useful to assume that all of the actions of the intact endothelium are anticoagulant and antiplatelet (the endothelium also secretes a plasminogen activator (tPA), inducing fibrinolysis, nitric oxide, a powerful vasodilator, as well as heparin-like glycosaminoglycans etc) Materials secreted by the injured endothelium are procoagulant (eg vWF secretion) and proplatelet (eg ‘switch-off’ of PGI2 and tPA secretion), as well as ‘thromboplastic’ material. Review July 2004 re: entire question.
A. complement activation product (C5a)
B. thromboxane A2 (Tx-A2)
C. high molecular weight kininogen (HMWK)
D. leukotriene (LTB4)
The two chemoattractants for granulocytes shown are C5a and LTB4. Of the two, LTB4 is generally stated to be the most powerful naturally occurring in inflammation. HMWK is an intermediate metabolite for the various ‘cascade’ enzyme systems active in inflammation and coagulation systems. Fibronectin is certainly chemotactic for fibroblasts (and perhaps also endothelial cells) in healing and possibly also has a role in chemotaxis for some cancers during the invasive process. Question being reviewed at March 04 meeting for further referencing (20/02/04).
1: prostacyclin (PGI2)
3: activated complement products
4: oxygen-derived free radicals
Prostacyclin and other cyclo-oxygenase pathway arachidonic acid derivatives are vasoactive, but not chemotactic. The same goes for bradykinin and the free radicals (NO as a vasodilator - probably the oxygen-derived free radicals only influence vascular actions through direct endothelial cell damage). C5a, on the other hand, is strongly chemotactic.
1: leukotriene (LTB4)
3: prostacyclin (PGI2)
4: nitric oxide (NO)
Leukotriene is the most potent chemotactic agent known. Others include C5a, bacterial products and cytokines ( IL-8 ‘family’). Products of the cyclo-oxygenase arm of arachidonic acid metabolism have no chemotactic action. Bradykinin causes increased vascular permeability, while NO mediates vasodilatation and tissue damage.
1: increased binding activity of integrins
2: P-selectin/ICAM-1 (intercellular adhesion molecule-1)interaction in low-flow conditions
3: induction of endothelial adhesion molecules
4: redistribution of P-selectin by histamine stimulation
Robbins 6th ed. Chapter: 3 Page: 57-59
2: ligand action of thromboxane-A2 (Tx-A2)
3: adhesion molecules expressed on endothelial cells
4: adhesion molecules expressed on leukocytes
Direct causes of the phenomena of leukocyte adhesion to endothelium in zones of acute inflammation are the interactive adhesion molecules expressed on the surfaces of leukocytes and endothelial cells. These include redistribution of P-selectin and increased activity of integrins in leukocytes, together with cytokine-induced induction of endothelial adhesion molecules (these are of the immunoglobulin family). Expression of these interactive adhesion molecules is stimulated variously by histamine, thrombin, IL-1 and chemotactic agents. Bradykinin and Tx-A>Sub>2 have no influence, either direct or indirect.
This question is currently under review by the Pathology Sub Committee. 28 June 2002.
Pathology Sub Committee comments: This question relates to molecules having a direct influence on leukocyte pavementing. 1. It is resonable to assess mediators directly causing pavementing (ie. leukocyte - endothelial adhesion) as the interactive adhesion molecules (selectins, integrins, ICAM-1, VCAM-1) on endothelial cells and leukocytes; 2. Mediators indirectly influencing pavementing are those which induce expression of those adhesion molecules on the surfaces of endothelial cells (IL-1, TNF) and of leukocytes (C5a at least); 3. Anything even more remote from direct indluence (including bradykinin) is surely highly speculative as having any effect. Bradykinin certainly has no direct effect (ie. as an adhesion molecule per se) or even at the next level (ie influencing the expression of those adhesion molecules).
This question has been reviewed.
1: ligand action of LTB4
2: complement activation by-product (C5a)
3: adhesion molecules on endothelial cells
4: adhesion molecules of neutrophil leukocytes
A number of chemical mediators of the acute inflammatory reaction influence the expression of adhesion molecules on both endothelial cells (these adhesion molecules are generally members of the immunoglobulin superfamily) and granulocytes (these are generally integrins). However they may be influenced to be expressed, it is the adhesion molecules themselves which are responsible for the adhesion (and therefore, for the pavementing).
Pending Review Jan 2004
4: bacterial permeability increasing protein
Robbins, 6th ed, Ch 3
A. n-acetyl muramindase (lysozyme)
B. peroxide-myeloperoxidase-halide system
D. superoxide hydroxyl radical system
E. major basic protein
The production of hypochlorite (OHCl) by this enzyme system results in the most powerful bactericidal effect against pygenic bacteria. MPO-deficient leukocytes are capable of killing bacteria (albeit more slowly), by virtue of the other oxygen-dependent enzyme systems. Individuals who cannot generate the superoxide radical suffer a major disorder of bacterial killing, chronic granulomatous disease (usually an X-linked disorder).
A. requires prior opsonisation of the organism
B. results in a phagocytic vacuole which will fuse with lysosome(s)
C. results in degranulation of the granulocyte
D. frequently requires production of hydrogen peroxide to cause bacterial destruction
E. does not necessarily ensure death of the bacteria
Robbins 5th ed. CHAPTER: 6 PAGES: 62-64
1: n-acetyl muramidase (lysozyme)
2: hypochlorite ion
3: hydrogen peroxide
4: major basic protein
Oxygen-derived free radicals and their metabolic derivatives may be released extracellularly from leukocytes by a number of stimuli. Their action is dependent on the activation of the NADPH oxidative system and the generation of superoxide (?). This, in turn, is converted to H2O2, OH-, NO derivatives and, through the myeloperoxidase-halide system, to OHCl-. Lysozyme and major basic protein are lysosomal enzymes and not free radicals.
1: catalase reaction
2: interaction with iron
3: interaction with glutathione peroxidase
4: oxidase (e.g. xanthine oxidase) reactions
Robbins 6th ed. Chapter: 1 Page: 12-14
1: cysteine and methionine-containing ‘remedies’
2: paracetamol (acetaminophen) poisoning
3: prolonged positive pressure ventilation at FIO2 of 1.0
4: immune complex-induced PMN chemotaxis in acute glomerulonephritis
Cysteine and methionine are antioxidant amino acids and are therefore protective. Paracetamol is metabolised to form a toxic ‘free radical’ product by the liver. This is usually detoxified by reduced glutathione (GSH), but the system may be overwhelmed with paracetamol overdose. Normal oxygen partial pressure intracellularly result in formation of reactive oxygen species - rapidly detoxified; this formation is intensified (mass action) by raising the FIO2 which can cause tissue damage (to lung pneumocytes and endothelial cells in particular - ARDS). PMN are direct pathogenetic suppliers of the damage (via exocytosis - toxic oxygen radicals and enzymes) in acute glomerulonephritis.
1: cytochrome enzyme system
2: superoxide dismutase enzyme system
3: catalase enzyme system
4: glycolytic (Embden-Meyerhof) pathway enzymes
Glycolytic and cytochrome enzyme systems are concerned with glycolysis (E-M with anaerobic glycolysis and cytochrome system with electron transfer) - they have no protective effect from or detoxification action of reactive oxygen (or other ‘free radical’) species. Superoxide dismutase ‘dismutes’ superoxide (?)!; catalase metabolises H2O2 to water and oxygen - both are detoxicants and are therefore protective.
4: C3b and fibronectin
The two major opsonins are the Fc fragment of immunoglobulin G and C3b, the so-called ‘opsonic fragment of C3’. The corresponding phagocyte receptors are FcgR which recognises the Fc fragment of IgG, and complement receptors CR 1, 2 and 3, which interact with C3b and C3bi. CR 3 also binds laminin and fibronectin; it is responsible for non-opsonic binding of some bacteria. The cytokines have no opsonic activity, although some may 'activate' phagocytes. IL-8 (‘family’) is chemotactic
1: formation of nitric oxide
2: production of superoxide radicals
3: production of the complement C1q
4: production of hydroxyl radicals
Essential Immunology 9th ed. Pages: 8-10
1: simultaneous binding of C3b and fibronectin to leukocyte receptor
2: interleukin (IL-6) receptor binding
4: receptor binding to IgFc
C3b requires simultaneous binding with fibronectin for effective opsonin action. Fc receptors are present on granulocytes and macrophages - this ligand action of the Fc fragment of Ig is, of course, activated by the binding of the Fab fragment with antigen. Phagocytosis is most avid when both C3b and Fc ligands bind simultaneously to their respective receptors on the phagocyte; clearing of bacteria is enormously enhanced by the presence of both.
1: immunoglobulin G subtypes
3: a derivative of complement component C3
4: intercellular adhesion molecule (ICAM)
Robbins 6th ed. Chapter: 3 Page: 59; 62
1: removed via lymphatics
2: replaced by reticulin
3: phagocytosed by macrophages
4: replaced by granulation tissue
Refer to Robbins, 6th Ed, Ch 3, page 78
1: pneumococcal pneumonia
2: uncomplicated healing of a sutured surgical incision
3: pulmonary infarct
4: paracetamol-induced hepatic necrosis
In both pneumococcal pneumonia and paracetamol poisoning, although there may be cell injury and necrosis (of pneumocytes and hepatocytes respectively), the basement membrane is not damaged and remains as a framework along which regenerating cells can migrate. Despite careful suturing of a skin incision, there is always some scarring and dermal appendages do not regenerate. Basement membrane does not survive pulmonary infarction - scarring results (although, interestingly, elastic tissue survives).
1: renal papillary necrosis
2: acute viral hepatitis
3: hypovolaemic acute renal tubular necrosis
4: liver abscess
Renal papillary necrosis and liver abscess both result in total destruction of the ‘framework’ of the tissue involved - healing by scarring is the best possible outcome here. In acute viral hepatitis (apoptotic cell death, not necrosis), cells regenerate along the intact basement membrane framework as they also do following acute renal tubular necrosis. Although oliguric renal failure caused by hypovolaemic shock is a hazardous disorder, when recovery occurs without complications (eg infection etc), eventual complete restoration of ‘pre-injury’ renal structure and function occurs.
1: a compact mass of immature granulation tissue
2: a compact mass of lymphocytes and plasma cells
3: a mass of macrophages and giant cells
4: a mass of epithelioid cells and giant cells
The clear distinction between epithelioid cells and macrophages and the clear implications of their different morphologies and functions is poorly dealt with in Robbins. Nevertheless, at least the book makes it clear that there are both innate (non-immune - characterised by macrophages, ie. phagocytic) and immune (characterised by epithelioid cells - which are not phagocytic, but are synthetic and secretory and probably also fulfil a ‘barrier’ function before fibrosis). Granulomas are not composed of granulation tissue, not primarily made up of immunocytes (lymphocytes and plasma cells), though both may be present.
1: primary syphilis
3: Echinococcus granulosus infestation
4: the reaction to yersiniae
Robbins, 6th ed, Ch 3; Ch 9 and Ch 16
1: Crohn's disease
2: primary biliary cirrhosis
4: cat scratch lymphadenitis
Refer to Robbins, 6th Ed, page 83, 878, 817
1: lepromatous leprosy
2: mycobacterial infections in AIDS patients
3: Cryptococcus neoformans infections
Robbins 6th ed. Chapter: 3; 7; 9 Page: 83-84; 248; 351; 386. Question to be reviewed at March 04 meeting re: option C (23/02/04)
1: cause wound contraction
2: contain contractile cytoplasmic filaments
3: secrete collagen
4: develop from fibroblast progenitor cells
Myofibroblasts are important cells in wound healing and variants of this (chronic inflammation, tumour fibroplasia etc). In all of these , ‘wound contraction’ leads to a scar which, in uncomplicated healing, is smaller than the original tissue it replaces; in other circumstances, this leads to such problems as bowel obstruction in cancer, Crohn disease etc. All of the suggested functions and the cell origin are true. ‘Wound contraction’ is common and important - that message does not come through clearly in Robbins, but the gist of the phenomenon and its importance is clear - where there is granulation tissue, there is wound contraction, occurring early in connective tissue healing.
1: contains abundant amounts of dense collagen
2: is commoner in males than in females
3: is commoner in Negroes than in white races
4: usually shows premalignant changes
Robbins 5th ed. Page: 90
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