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Inflammation - Marcador
Inflammation - Detalles
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154 preguntas
| 🇬🇧 | 🇬🇧 |
| Edema, presence of neutrophils in tissue | Hallmarks of acute inflammation |
| Infection, Tissue necrosis | Causes of acute inflammation |
| Activators of Toll-like receptors (TLRs) | Pathogen-associated molecular pattern (PAMP) |
| Releases arachidonic acid from plasma membrane | Phospholipase A2 |
| Produces prostaglandins from AA | Cyclooxygenase |
| Mediates arterial vasodilation and increased vascular permeability at the postcapillary venule | PGI2, PGD2, PGE2 |
| Location of increased vascular permeability | Postcapillary venule |
| Produces leukotrienes from AA | 5-lipoxygenase |
| Slow reacting substances of anaphylaxis; mediates vasoconstriction, vasospasm and increased vascular permeability | LTC4, LTD4, LTE4 |
| Tissue trauma, C3a and C5a, crosslinking of surface IgE by an antigen | Activators of mast cells |
| LTB4, C5A, IL-8, Bacterial products | Activators of neutrophils |
| Degranulation-> histamine release -> arteriolar vasodilation, increased vascular permeability of postcapillary venule | Immediate response of mast cells |
| Leukotriene release and activation | Delayed response of mast cells |
| C1 binds to IgG or IgM bound to an antigen ("GM makes CLASSIC cars") | Classical complement pathway |
| Microbial products directly activate complement | Alternative complement pathway |
| MBL binds to mannose on microorganisms and activates complement | Mannose-binding lectin (MBL) pathway |
| Cleaves C3 -> C3a and C3b | C3 convertase |
| Cleaves c5 -> c5a and c5b | C5 convertase |
| C5bC6C7C8C9; lyses microbes by creating a hole on cell membrane | Membrane attack complex |
| Rubor, calor, tumor, dolor | Cardinal signs of inflammation |
| Histamine | Key mediator of rubor and calor |
| Induced by TNF and IL-1 | E-selectin |
| Binding site of selectins on leukocytes | Sialyl Lewis X |
| Intercellular/Vascular Cell Adhesion Molecule found on endothelium; upregulated by TNF and IL-1 | ICAM, VCAM |
| Leukocytes cross the endothelium of postcapillary venules and are attracted to chemotactic agents | Transmigration and Chemotaxis |
| Autosomal recessive microtubule defect leading to a protein trafficking defect and impaired phagolysosome formation | Chediak Higashi Syndrome |
| Increased risk of pyogenic infections, neutropenia, giant granules in leukocytes, defective primary hemostasis, albinism, peripheral neuropathy | Clinical features of Chediak Higashi Syndrome |
| Most effective mechanism of destroying phagocytosed material | O2 dependent killing |
| Produces HOCl from H2O2 | Myeloperoxidase |
| Conversion of superoxide from O2 by NADPH oxidase | Oxidative burst |
| Autosomal recessive or X-linked NADPH oxidase defect -> Poor O2 dependent killing | Chronic Granulomatous Disease (CGD) |
| Catalase positive bacteria associated with recurrent infection in CGD | Staph aureus, Pseudomonas cepacia, Serratia marcescens, Nocardia, Aspergillus |
| Screening test fo CGD | Nitroblue tetrazolium test |
| Enzyme in eosinophil utilized in O2-independent killing | Major basic protein |
| Macrophages replace neutrophils and predominate | 48-76 hours post-inflammation |
| Primary mechanism of destruction of phagocytosed materials by macrophages | O2-independent killing |
| Stimulated by macrophages through antigen presentation to CD4+ helper T cells | Chronic Inflammation |
| CD4+ T cells (4 x 2 = 8) | MHC Class II |
| CD8+ T cells (8 x 1 = 8) | MHC Class I |
| Perforin and Granzyme release-> apoptosis; FasL expression -> apoptosis | CD8+ Cytotoxic T cell killing |
| Surface immunoglobulins for naïve B cells | IgM and IgD |
| Located on B-cell, binds with CD40L from helper T-cell to provide 2nd activation signal | CD40 receptor |
| Epithelioid histiocytes | Hallmark of granulomatous inflammation |
| Activated macrophages with abundant pink cytoplasm | Epithelioid histiocytes |
| No central necrosis; Arises from foreign materials, sarcoidosis, beryllium exposure, Crohn's disease, cat scratch disease | Noncaseating granuloma |
| With central necrosis; Associated with Tuberculosis and fungal infection | Caseating granuloma |
| Stellate shape granuloma | Characteristic finding for cat scratch disease |
| Secreted by activated macrophages to induce CD4+ helper T-cells to differentiate into TH1 subtype | IL-12 |
| Developmental failure of third and fourth pharyngeal pouches leading to absent thymus and parathyroid | DiGeorge Syndrome |
| Causes DiGeorge syndrome | 22q11 microdeletion |
| Defective cell mediated and humoral immunity | Severe Combined Immunodeficiency (SCID) |
| A possible etiology of SCID wherein there is decreased ADA activity leading to buildup of adenosine and deoxyadenosine which are toxic to lymphocytes | Adenosine Deaminase (ADA) Deficiency |
| Disordered B-cell maturation -> complete lack of immunoglobulins; recurrent bacterial infection, entreovirus, Giardia infection | X-linked Agammaglobulinemia |
| X-linked Agammaglobulinemia | Mutated Bruton Tyrosine Kinase (BTK) |
| Low immunoglobulin due to B-cell or helper T-cell defect; Rik for bacterial, enterovirus and Giardia infection in late childhood | Common Variable Immunodeficiency |
| GI pathology associated with IgA deficiency | Celiac disease |
| Elevated IgM levels with low IgA, IgG and IgE; Risk for recurrent pyogenic infections especially at mucosal sites | Hyper-IgM syndrome |
| Second signal is not delivered, cytokines for class switching are not released | Mutated CD40L (helper T-cell) or CD40 Rc (B-cell) |
| Triad of thrombocytopenia, eczema and recurrent infections | Wiskott-Aldrich Syndrome |
| X-linked condition; Wiskott-Aldrich Syndrome | Mutated WASP gene |
| Complement deficiency associated with increased risk for Neisseria gonorrhoeae and Neisseria meningitides infection | C5-C9 deficiency |
| Hereditary angioedema | C1 inhibitor deficiency |