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USMLE - Inflammation

USMLE - Goljan, Chapter 2 Inflammation and Repair

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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