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105 Cards in this Set

  • Front
  • Back
When does repair begins in inflammation?
At the early phases.
Who are inflammatory connective tissue cells?
MAST CELLS, fibroblasts, resident macrophages and lymphocytes.
Where are Mast cells located?
Connective tissue.
Redness, swelling, pain, heat- symptoms of which inflammation?
Acute.
What causes Exudate (SG>1.020)?
What causes Transudate (SG<1.015)?
Exudate: changes in permeability of small blood vessels.
Transudate: changes in hydrostatic/oncotic pressure.
What is pus?
EXUDATE, rich in leukocytes (mostly neutrphiles), debris of dead cells and often microbes.
What are some stimuli for acute inflammation I never think about?
Blunt trauma
Burns
Tissue necrosis
Which vessels are affected by vasodilation?
First arterioles, and then you see opening of new capillary beds.
What causes vasodilation in inflammation?
Histamine and NO, that affect smooth muscle cells.
What does the permeability cause?
Loss of fluid -> concentration of RBC -> increased viscosity -> STASIS.
What is the "immediate transient response"? Which vessel is affected?
(permeability)
Permeability due to gaps between endothelial cells.
Venules.
How long does the immediate transient response last?
(permeability)
15-30 minutes.
Immediate transient response: which mediators cause it? What is the mechanism in each reponse?
(permeability)
Histamine: contraction of endothelial cells (contractile proteins).
Cytokines: structural reorganization of cytoskeleton.
What is the difference between the effect of Histamine vs. Cytokines in the Immediate Transient Response?
(permeability)
Cytokines requires reorganization of cytoskeleton, and thus take longer to and are more long-lived.
What is the Immediate Sustained Reponse?
(permeability)
Direct endothelial damage, causing necrosis and detachment.
(burns)
Affects all microvasculature.
What is Delayed Prolonged Leakage?
(permeability)
begins 2-12 hours, lasts for several hours/days.
(sunburn)
Where does Leukocyte-mediated endothelial injury usually occur?
(permeability)
Vascular sites, like the glomerulus, where they can adhere for prolonged periods.
What is Transcytosis?
What mediator cause it?
(permeability)
Channels consisting of interconnected, uncoated vesicles- mostly in venules.
VEGF.
What are the 3 phases of increased permeability in acute inflammation?
1. Immediate transient response- venules- 30 min or less.
2. Delayed response, 2-8 hours.
3. After direct endothelial injuru: Prolonged response.
Can any endothelial cell bind leukocytes?
No, it has to be activated (by histamine, PlateletActivatingFactor, thrombin).
What causes margination of leukocytes?
Blood stasis
Where can you find P-Selecting?
Endothelial cells, Platelets.
Which cells express ICAM1/VCAM1? What do they bind?
Endothelial cells, bind integrins on leukocytes.
What is CD31? What does it bind?
Also called PECAM on endothelial cells.
Binds ... CD31 on leukocytes.
What causes rolling of leukocytes?
P,E Selectins that bind Sialyl-Lewis X on leukocytes.
Which cytokines induce expression of VCAM1/ICAM1 on endothelial cells?
TNF, IL-1.
How are rolling leukocytes activated?
Chemokines cause change of integrins to high affinity state, so they can stick and stop rolling.
Common chemokines?
Exogenous factors like bacterial products.
C5a, Leukotrienes, IL-8.
What type of receptor do chemokines have?
GPCR.
What does leukocyte activation cause?
1. Increase in Ca.
2. Activatoin of Protein C.
3. Activation of Phospholipase A2 (causes production of Arachinodic Acid metabolites).
Which receptors are involved in leukocyte activation?
(4)
1. TLR (cause production of microbicidal substances).
2. GPCR.
3. Cytokine receptors in phagocytes.
4. Opsonin receptors in phagocytes.
What receptors activate phagocytosis?
(meaning, they exist on neutrophiles and macrophages)
Mannose receptor.
Scavenger Receptor (also activate uptake of LDL by macrophages).
Popular opsonins?
IgG, C3b, MBL, CRP, fibronectin, fibrinogen.
What happened (cytoskeleton-wise) during phagocytosis?
Polymerization of actin.
What does NADPH Oxidase do?
Reduce oxygen to O2-. Can spontaneously go -> H2O2, that can be reduced to OH.
Who breaks down most of the H2O2?
Catalase enzyme.
What does the enzyme MPO do?
Which cells contain it?
Converts H2O2 to HOCL (bleach).
Neautrophiles (Azuraphilic granules).
When do the acid hydrolases begin to work?
After killing in the phagolysosome.
What products do neutrophiles and macrophages release to the extracellular fluid during phagocytosis?
(3)
1. Lysosomal enzymes.
2. ROS intermediates.
3. Products of AA metabolism.
What causes release of products to the extracellular fluid during phagocytosis?
1. Regurgiation during feeding.
2. Frustrated phagocytosis- ingestible materials.
3. Cytotoxic release- after damage to the membrane of the phagolysosome (like asfter engluding urate crystals).
4. Sometimes, exocytosis..
What do neutrophiles do after phagocytosis?
Apoptosis.
What are LAD1/2?
Defects in leukocyte adhesion.
LAD1: recurrent baterial infections, impaired wound healing.
LAD2: milder.
What happens in Chediak-Higashi syndrome?
AR.
Defect in forming phagolysosomes.
(thought to result from aberrant organelle fusion).
What happens in Chronic Granulomatose Disease?
Inherited defects in NADPH oxidase.
Recurrent bacterial infections.
How is acute inflammation terminated?
1. Mediators have short half-lives.
2. Mediators are degraded after release.
3. Active anti-inflammatory mechniasms ("stop signals").
Are plasma-derived mediators active, or precursors?
Precursors.
Which cells secrete Histamine?
MAST CELLS, basophils, platelets.
Which cells secrete Serotonin?
Platelets (after aggregation), Enterochromaffin.
What are the actions of Serotonin?
Similar to histamine.
What are the 3 complement pathways?
1: Classical- C1 is fixated to antibody+antigen.
2. Alternative: Triggered without antibody.
3. Lectin: MBL binds the microbe, and activates C1.
What do C3a, C5a and C4a do?
Cause release of Histamine from Mast cells.
What does C5a do?
1. Cause release of Histamine from Mast cells.
2. Activate the Lipooxygenase pathway in neutrophiles and macrophages.
3. Chemotactic factor for many leukocytes.
Who are the most important inflammatory mediators among the complement components?
What can activate them?
C3 and C5.
Can be activated by proteolytic enzymes within the inflammatory exudate, like plasmic.
What are Kallikreins?
Proteases, cleave Kininogen to create Bradykinin.
What activates Kallikreins?
Activated Hageman factor (12a).
What are the effects of Bradykinin?
Similar to Histamine.
What does Kallikrein do, besides cleavage of Kininogen to create Bradykinin?
1. Activate Hageman factor.
2. Convert C5 to C5a.
What does Thrombin do?
(just some)
1. Activate fibrin, from fibrinogen.
2. Activate PAR1 (induces inflammation).
What does Hageman factor do?
1. Initiate the Kinin system.
2. Initiate the instrinsic clotting system.
3. Initiate the fibrinolytic system (via plasmin).
4. Activate the complement system.
Which are the most important plasma proteases?
(clotting)
Bradykinin, C3a, C5a, Thrombin.
What is an Autocoid?
Short-range hormone.
How do we obtain Arachidonic Acid?
1. Dietary sources.
2. Conversion from linoleid acid.
What are Eicasinoids?
AA metabolites.
Synthesized by COX & Lipooxygenase.
What does the COX pathway create?
Prostaglandins (also Thromboxane).
COX1 - constitutive and during inflammation.
COX2 - only during inflammation (the bad guy).
What do prostaglandins cause during inflammation?
Pain and fever.
What is created by the lipooxygenase pathway? What do the products do?
Leukotrienes.
Cause vasoconstriction and increase permeability much more than Histamine.
What are Lipoxins?
Eicasinoids- precursor created in neutrophiles, final factor in platelets.
What do you use Lipooxygenase inhibitors for?
Asthma, as leukotrienes cause bronchospasm.
What is effected by C-X-C chemokines?
C-C chemokines?
C-X-C : Neutrohpiles
C-C: Everybody else.

They use GPCR receptors.
What other effects does NO have?
Microbicidal!
What is the difference between specific and azuophil granules in neutrophiles?
Specific granules are secreted extra-cellulary, and more readily (=by lower concentrations of agonist).
Azuraphil granules are more destructive, and release their content into phagolysosomes less readily.
What do extra-cellular ROS do?
Amplify inflammatory cascade.
What is substance P?
What does it do?
Who secretes it?
Neuropeptide, plaus a role in the initiation and propagation of the inflammatory response.
Secreted from nerve fibers.
What causes Gout?
The pro-inflammatory action of uric acid.
What do we need in order to achieve complete resolution after acute inflammation?
Limited/short lived injury.
Little tissue destruction.
The parenchymal cells can regenerate.
When do we resort to healing by fibrosis?
Substantial tissue destruction, or the parenchymal cells cannot regenrate, or there is abundant fibrin exudation.
What is Serous Inflammation?
Outpouring of fluid (effusion)- can be in pleura etc. or under/within epidermis.
What is Gibrinous inflammation?
Comes with more severe injuries- such great permeability that larger molecules, like fibrinogen, pass and deposit fibrin.
Can also happen is there is a procoagulant stimulus in the interstitium (like cancer cells).
What is "organization"?
conversion of fibrin exudate to scar tissue.
What is purulent inflammation?
Large amounts of pus.
(also abscesses)
What are abscesses?
localized collection of purulent inflammatory tissue, in a confined space.
What is an Ulcer?
Defect of the surface of an organ, produced by the shedding of inflammatory necrotic tissue.
Obviously, can only occur when it exists on/near a surface..
(in mouth, legs in people with circulatory disturbances)
What happens in chronic inflammation?
Active inflammation, tissue destruction and repair, simultaneously.
What kind of immune reaction is chronic inflammation caused by organisms?
Delayed-type hypersensitivity.
What type of cells infiltrate in chronic inflammation?
Mainly mononuclear- macrophages and lymphocytes.
Which cell type is dominant in chronic inflammation?
Macrophages.
What is the half-life of blood monocytes?
Tissue macrophages?
Monocytes: 1 day.
Macrophages: months.
When do macrophages emigrate during acute inflammation?
Pretty early- after 48 hours they are often the dominant cell.
What causes macrophage accumulation during chronic inflammation?
1. Recruitment of monocytes from the circulation.
2. Local proliferation of macrophages (happens in atheromatous plaques).
3. Immobilization of macrophages.
What do the products of activated macrophages do in chronic inflammation?
Tissue injury.
What is one of the major hallmarks of chronic inflammation?
Tissue destruction.
What can happen in strong chronic inflammation, lymphocytes-wise?
The reaction, because of the accumulation of lymphocytes, APC and plasma cells, may look like a lymph node- germinal follicles and all.
What is a granuloma?
Focus of chronic inflammation, consisting of aggregation of epitheloid cells, surrounded by a collar of mononuclear leukocytes (mainly lymphocytes).
What do older granulomas develop?
an enclosing rim of fibroblasts and connective tissue.
What are giant cells?
Fusion of several epitheloid cells.
20+ small nuclei.
What is a difference between granulomatous inflammation and other granulomatous diseases?
Granolumatous inflammation often has central caseous necrosis (think tuberculosis).
What happens to lymph flow during inflammation?
Increases, to help drain the edema.
What is Lymphangitis?
Inflammation in Lymph.
What is Lymphadenitis?
Inflammation in lymph nodes.
What usually causes nodal enlargement?
HyperPLASIA of lymphoid follicles and phagocytic cells (lining the sinuses).
Termed Reactive Lymphadenitis.
What happens in Acute Phase Response?
1. Fever (in response to pyrogens).
2. Leukocytosis (left shift)- called Leukemoid Reaction.
3. Acute Phase Proteins, made by the liver, appear.
Name two acute phase proteins
CRP, Fibrinogen.
What do acute phase proteins do?
(3)
1. Act as opsonins.
2. Aid in the clearing of necrotic cell nuclei (bind chromatin).
3. Target HDL to macrophages, so they have more sources for energy.
What affects the Erythrocyte Sedementation Rate?
Fibrinogen makes RBCs form stacks, which decreases ESR.
Since Fibrinogen is a marker of systemic inflammation, so is ESR..
What can prolonged production of acute phase proteins cause?
Secondary Amyloidosis.