1748171
Description
Flashcards by Marielle83, updated more than 1 year ago
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Created by Marielle83
over 9 years ago
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| Question | Answer |
| Shediak-Higashi syndrome? | Defective phago-lysosomal fusion (cats, cows, minks, killer whales) |
| Interaction b/w lymphocytes and macrophages in chonic inflammation? | Activated T lymphocytes recruit inflammatory cells (through TNF and other) and activate macrophages (through INF gamma). In return, activated macrophages stimulate T cells by presenting antigens and via secretion of inflammatory mediators (like IL12). |
| Name the cell-derived mediators of inflammation | Platelets, neutrophils, monocytes/macrophages, mast cells + Pre-existing (intracellular granules) E.g. histamine in mast cells Synthesized de novo (PGs, cytokines) |
| Name some plasma derived mediators of inflammation | E.g. complement proteins, kinins - Made in liver - Circulate as inactive precursors |
| What stimulates mediators? | Necrotic material (PAMPs and DAMPs) + Proteins of complement, kinin, and coagulation systems |
| Which vaso-active amine is mainly released by mast cells but also basophils and platelets? | Histamine |
| What is the effect of histamine release? | Dilation of arterioles & increased permeability of venules (via binding to H1 receptors on endothelium) |
| Which vaso-active amine is mainly released by platelets and neuroendocrine cells in an inflammatory response and what stimulates its release? |
Serotonine stimulated by platelet aggregation
Image:
2014-12-03_1649 (image/png)
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| What are the 2 major classes of eicosanoids? | Cyclooxygenase pathway (PGs) Lipoxygenase pathway (LTs and lipoxins) |
| Leukotrienes- produced by lipoxygenases, secreted by leukocytes have effects on? | Vasculature (permeability, constriction) Chemotaxis (call in other cells) Smooth muscle (bronchospasm) |
| Lipoxins - produced by lipoxygenase have what effect in inflammation? | INHIBITORS of inflammation (particularly inhibit leukocyte recruitment) |
| Prostaglandins - produced by actions of cyclooxygenases: COX-1 (constitutively expressed) and COX-2 (inducible) prostacyclin, thromboxane have effects on? | Vasculature (dilation, constriction) Platelets (aggregation or inhibition) Smooth muscle Chemotaxis Pain / fever |
| Out of COX-1 and COX-2, which one is always activated and which one only activated in inflammation? | COX-1 Always COX- 2 Inflammation |
| Which pathway does NSAIDs act on and which eicosanoid pathway does it not have an effect on? | Cyclooxygenase pathway! (COX-inhibitors) No effect on Lipoxygenase pathway |
| Cytokines TNF and IL-1 are relased from activated macrophages in response to what? | Physical injury Endotoxins and other microbial products Immune complexes etc. |
| Complement system functions? (3) | Inflammation(C3a, C5a) Phagocytosis (C3b is opsonin) Cell lysis (deposition of MAC on cell) |
| What are kinins? | Vasoactive peptides e.g. bradykinin with similar effects to histamine |
| Can you live a normal life without factor XII (Hageman factor) ? | Yes |
| True or false: Inflammatory mediators are long-acting and require a specific STOP signal | False Short half-lives with rapid decay or proteolysis |
| List two effects of histamine | Vasodilation Increased vascular permeability |
| What stimulates the release of inflammatory mediators? | Microbial products (PAMPs), necrotic material (DAMPs), other mediators |
| What are the 2 pathways of the arachidonic acid metabolism, and what is produced by each? | Cyclooxygenase: PGs Lipoxygenase: leukotrienes and lipoxins |
| Where does arachidonic acid come from? | Cell membranes |
| How are lipoxins different from the other classes of eicosanoids? | Inhibition of inflammation |
| Which part of the arachidonic acid pathway do cortocosteroids inhibit? | Entire thing (NSAIDS inhibit Cox-1 and Cox-2; not lipoxygenase) |
| Where do "plasma-derived" proteins actually come from? | Originally made in liver; circulate in inactive form |
| List 2 effects of cytokines tnf and IL-1 | Leukocyte recruitment Fever |
| What is the key step in complement fixation that is common to all pathways? | C3 proteolysis |
| What are the 3 functions of the complement system? And what proteins are most involved with each function? | Inflammation (C3a and C5a) Phagocytosis (C3b) Cell lysis (MAC attack complex) |
| What mediator is involved in eliciting pain? | Bradykinin |
| Activation of what substance is involved in activating the four systems involved in inflammation? | Hageman factor (Factor XII) |
| List the 3 major pathogen routes of entry into lung | Inhaled (aerogenous) Hematogenous Direct entry |
| List 4 types of pneumonia and their route of entry | Bronchopneumonia (inhaled) Interstitial (inhaled or hematogenous) Granulomatous (inhaled or hematogenous) Embolic (hematogenous) |
| Name the etiologies involved in enzootic pneumonias and shipping fever | Enzootic pneumonia = mycoplasmas (ovipneumoniae and hyopneumoniae) Shipping fever = Mannheimia hemolytica |
| List two causes of granulomatous pneumonia | Fungal: blastomycosis, histoplasmosis, coccidiomycosis, cryptococcosis Mycobacterium bovis |
| Recall a predisposing condition for aspiration pneumonia | Megaesophagus, handfeeding, cleft palate, downer animal |
| Identify two predisposing conditions in a cow for embolic pneumonia | Hepatic abscesses Vegetative valvular endocarditis |
| Identify two predisposing conditions in a cow for embolic pneumonia | Hepatic abscesses Vegetative valvular endocarditis |
| What is the origin of the neoplastic cells in Jaagsiekte (OPA) | Alveolar epithelial cells (type II pneumocytes and Clara cells) |
| What bug is the cause of shipping fever? | Mannheimia haemolytica |
| What type of pneumonia is shipping fever? | Acute fibrinous bronchopneumonia (can also be suppurative or fibrinosuppurative) |
| BALT? | Bronchus Associated Lymphoid Tissue |
| Metaplasia? | The reversible replacement of one differentiated cell type with another mature differentiated cell type |
| Gross findings at interstitial pneumonia? | Diffuse distribution and large lungs that do not deflate, rubbery texture "meaty" |
| Gross findings in granulomatous pneumonia | Multifocal firm nodules (any lobe) with white/grey/tan crumbly material |
| Which pathogens may cause suppurative bronchopneumonia? | P. multocida B. bronchiceptica A. pyogenes Strep spp. Distemper virus Parainfluenza virus |
| Which type of pneumonia may be ventilator induced? | Interstitial |
| Which bacteria is the major cause of granulomatous pneumonia? | Mycobacterium bovis |
| Which parasites may cause granulomatous pneumonia? | Dictycaulus Muelleria capillaris |
| Via what route does embolic pneumonia enter the lungs? | Haematogenous |
| What are the 3 possible causes of embolic pneumonia? | Vegetative valvular endocarditis Hepatic abscesses Any septicaemia |
| How could you grossly differentiate b/w embolic pneumonia and for example tumours or an M. capillaris infection? | Lesions in embolic pneumonia are soft like normal tissue and not nodular |
| Jaagsiekte is what type of cancer, and what is the cause? | Pulmonary adenocarcinoma Jaagseikte Sheep Retrovirus (JSRV) |
| List the events in the resolution of acute inflammation | Neutralisation/decay/degradation of chemical mediators Normalisation of vascular permeability Cessation of leukocyte migration |
| Name 4 types of inflammatory stimuli | Infectious agents Tissue damage Foreign bodies Immune reactions |
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