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USMLE - Inflammation
USMLE - Goljan, Chapter 2 Inflammation and Repair
| Question | Answer |
|---|---|
| Leukocyte adhesion deficiency - type 1 | autosomal recessive disorder in which there is a DEFICIENCY of beta2 INTEGRINS on the surface of neutrophils (CD11a:CD18) |
| Leukocyte adhesion deficiency - type 2 | autosomal recessive disorder in which there is a DEFICIENCY of SELECTINS, the molecults on the surface of endothelial cells that bind neutrophils and cause neutrophil ROLLING along vascular endothelium |
| What should you suspect when it takes longer than 1 month for umbilical cord to separate? | leukocyte adhesion deficiency (LAD) -- neutrophils important in cord separation |
| Patient comes in complaining of these sx's: severe gingivitis and poor wound healing. You do labs and find neutrophilic leukocytosis (lots of neutrophils in the blood). What should you suspect? | leukocyte adhesion deficiency (LAD) |
| Bruton's agammaglobulinemia | X-linked mutation in Bruton's tyrosine kinase (BTK). Without BKT, B cells don't differentiate and mature and you don't get B-cell differentiation into IgG --> no IgG to act as opsonins --> impaired neutrophil recognition and ingestion of bacteria. |
| Chediak Higashi Syndrome (CHS) | autosomal recessive; defect in MEMBRANE FUSION; leukocytes can't form phagolysosomes --> increased susceptibility to infection. |
| What organism are children with CHS more susceptible to? | Staph aureus |
| Selectins | expressed on EC's; neutrophils attach to them to "ROLL" on the endothelium before extravasation |
| B2-integrins | adhesion molecules expressed on neutrophils; bind to ICAM and VCAM expressed on EC's |
| what is a granuloma? | collection of macrophages -- can develop as a result of chronic inflammation |
| What is chronic granulomatous disease? | CDG is when NADPH oxidase in cell membranes of neutrophils and monocytes is absent --> no respiratory burst --> decreased production of superoxide radical, which is essential in O2-dependent killing of bacteria |
| What can catalase-positive organisms do? | Break down peroxide (H2O2) |
| What happens to catalase+ organisms in CDG? | Calalase+ bacteria are ingested but not killed; H2O2 degraded --> can't synthesize bleach to kill the bacteria |
| What happens to baceria in someone with MPO deficiency? | no MPO --> can't make bleach --> can't kill bacteria |
| One consequence of G6PD deficiency? | Can't regenerate NADPH --> defect in O2-dependent bactericidal mechanism |
| Lactoferrin | O2-independent system; binds Fe necessary for bacterial reproduction |
| What is major basic protein? | Made by eosinophils; is toxic to helminths |
| What is bradykinin activated by? | Factor 7 (XII) in the kinin-kallikrein system |
| What is the relationship between ACE and bradykinin? | ACE breaks down bradykinin --> dry cough |
| What does bradykinin do to blood vessels and bronchioles?? | Vasodilation and increases permeability of vessels; bronchoconstriction |
| Where is complement synthesized? | Liver |
| C3a and C5a | stimulate mast cell release of histamine |
| C3b | opsinization |
| C5a | like LTB4; activation of neutrophil adhesion molecules (integrins); chemotaxis |
| C5-C9 | membrane attack complex -- cell lysis |
| IL-6 | release of neutrophils from bone marrow |
| IL-8 | chemotaxis |
| What does histamine do to blood vessels? | vasodilation and increases permeability |
| What cells make histamine? | Mast cells (primary), platelets |
| Name two functions for nitic oxide (NO) | vasodilation and is bactericidal |
| What two cells make NO? | macrophages and ED's |
| What does serotonin do to blood vessels? | vasodilation and increases permeability |
| What cells make serotonin? | mast cells and platelets |
| What is the most important mediator of ACUTE inflammation? | Histamine |
| what is the most common cause of skin abscess? | S. aureus |
| Types of acute inflammation - what is the difference: purulent, fibrinous, pseudomembranous | puru - pus is produced (coagulase fr S.aureus cleaves fibrinogen into fibrin & traps bacteria & neutroph); fib - fibrin-rich exudate deposited due to incr vessel permeability; pseudo - damage of mucosal membrane producing shaggy membrane of necrotic tissu |
| role of fever in inflammation (2) | 1. R-shift O2 binding curve so O2 is let go easier and more O2 available for O2-dependent MPO bactericidal system; hostile environment for bacterial and viral reproduction |
| What is the most common cause of chronic inflammation? | infection |
| What is the difference between macrophages and monocytes? | Monocyte is the precursor of the macrophage. Monocyte becomes macrophage when monocyte when it enters damaged tissue to phagocytose. |
| What are the primary leukocytes in chronic inflammation? | monocytes and macrophages |
| What is granulation tissue? | Highly vascular tissue compoased of newly formed blood vessels and activated fibroblasts; essential in nl wound healing; converted into scar tissue |
| What is fibronectin? | key adhesion glycoprotein in the extracellular matrix required for the formation of granulation tissue in wound healing |
| What is does fibronectin bind to? | collagen, fibrin, cell surface receptors such as integrins |
| VEGF | vascular endothelial growth factor --> attracts endothelial cells to form new blood vessels (angiogenesis) |
| BFGF | basic fibroblast growth factor --> attracts fibroblasts --> fibroblasts synthesize collagen --> collagen needed to build blood vessels |
| What is granulomatous inflammation | Type of chronic inflammation; associated with caseous necrosis if due to infection; noncaseating (hard granulomas) if noninfectious cause |
| What are the cell types you can find in a granuloma? | Macrophages and CD4 helper T cells |
| What are epithelioid cells? | macrophages that have been activated for some purpose by gamma-interferon (released by CD4 helper T cells) |
| What are multinucleated giant cells composed of? | Fusion of activated macrophages (epithelioid cells) |
| G0 phase of cell cycle | Resting |
| G1 phase of cell cycle | Synthesis of RNA, protein, organelles, and cyclin D (regulatory protein) |
| What is the most variable phase in the cell cycle? | G1 |
| S phase of cell cycle | Synthesis of DNA, RNA, protein |
| G2 phase of cell cycle | Synthesis of tubulin, necessary for formation of mitotic spindle |
| M phase of cell cycle | mitosis - 2 daughter cells produced |
| Regulation of cell cycle between G1 and S | Growth factors produce cyclin D and Cdk4 --> cyclin D binds Cdk4 --> this complex phosphorylates RB (retinoblastoma) gene --> enters S phase |
| RB gene | phosphorylated by Cdk4 --> makes cell move from G1 phase to S phase of cell cycle |
| TP53 gene | inhibits Cdk4 from phosphorylating RB gene --> arrests cell in G1 phase to repair DNA; if too much DNA damage --> activate BAX gene --> apoptosis |
| BAX gene | inhibits BCL-2 (which suppresses apoptosis by preventing release of cytochrome c from mitochondria) --> apoptosis |
| What is laminin? | key adhesion protein in basement membrane that is required for normal tissue repair |
| Ehlers-Danlos Syndrome | defect in collagen types I and III --> hypermobile joints, aortic dissection (most common cause of death), poor wound healing, bleeding into skin (ecchymoses), hyperplastic skin -- like Jim Carrey's face |
| most common cause of impaired wound healing | infection |
| what do glucocorticoids do for wound healing? | prevents scar formation; inhibits activation of neutrophil adhesion molecules --> increased neutrophils in blood; sequesters eosinophils, B and T cells in lymph nodes and signals for apoptosis of lymphocytes --> decreased B, T, and eosinophils in blood; |
| keloid scar | excessive synthesis of Type III collagen; common in AA's |
| what is the key repair cell of the lungs? | Type II pneumocytes |
| What are microglial cells? | macrophages in the brain; remove debris in brain |
| What is the key cell in peripheral nerve regeneration? | Schwann cell |
| What is predominant Ig in acute inflammation? Chronic inflammation? | IgM in acute; IgG in chronic |
| ESR | nonspecific screening test (testing how fast RBC's form rouleaux -- stack up together) that indirectly measures how much inflammation is in the body; elevated in acute and chronic inflammation |
| Name two factors that increase RBC rouleaux formation | increased fibrinogen --> decrease RBC negative charge --> faster rouleaux; anemia (must have normal shape) --> faster rouleaux |
| C-Reactive Protein | Sensitive indicator of necrosis associated with acute inflammation (esp atherosclerotic plaques and bacterial infxns); excellent monitor of dz activity (i.e. rheumatoid arthritis) |
| What happens to serum albumin in acute inflammation? | Decreases slightly because 1. catabolic effect of inflammation, 2. aa are used by liver to synthesize acute phase reactants |
| What happens to serum albumin in chronic inflammation? | Greater decrease in serum albumin than acute; inc in gamma-globulin peak due to inc IgG |
| What is the key cell type in acute inflammation? | Neutrophil |
| Charcot-Leyden crystals in sputum of asthmatics | signify presence of eosinophils |
Created by:
christinapham
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