Term
|
Definition
| Defect in phagolysosome formation. Susceptible to recurrent bacterial infection (especially catalase positive bacteria). |
|
|
Term
| How to diagnose Chediak-Higashi Syndrome |
|
Definition
| Identify giant granules in neutrophils. |
|
|
Term
| Chronic Granulomatous Disease (CGD) |
|
Definition
| Defective NADPH (phagocyte) oxidase means neutrophils can't produce ROS, so macrophages try to control infection. Macrophages group around the infectious agent, creating a granuloma. |
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Term
|
Definition
| tissue necrosis, infiltration of monocytes |
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Term
| CGD diagnosis and treatment |
|
Definition
genetic testing
and IFN-gamma (a cytokine that induces NAPH production) |
|
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Term
|
Definition
|
|
Term
| How does S. aureus protein A prevent phagocytosis? |
|
Definition
| Binds to the Fc region of IgG, preventing opsonization. |
|
|
Term
| Where are most neutrophils located in the body? |
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Definition
|
|
Term
| T/F, the most abundant cell type produced by the bone marrow is RBCs. |
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Definition
|
|
Term
| The neutrophil goes through several stages during its development. Which is the biggest? |
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Definition
|
|
Term
| At what stage in neutrophil development does the cell stop dividing? |
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Definition
|
|
Term
| List the stages of neutrophil development in order. |
|
Definition
| stem cell, myeloblast, promyelocyte, myelocyte, metamyelocyte, band, PMN |
|
|
Term
| How long does PMN development take? |
|
Definition
|
|
Term
| What is a "shift to the left"? |
|
Definition
| The shift to the use of less mature neutrophils. Shown by the presence of band neutrophils in the blood. |
|
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Term
|
Definition
| low neutrophil count (<1500/mm3) |
|
|
Term
| What is a typical first oral manifestation of neutropenia? |
|
Definition
| ulceration of the gingiva |
|
|
Term
|
Definition
| Neutrophil count <200mm3 3-6 days/21 days |
|
|
Term
|
Definition
| Stimulates the neutrophil development pathway. |
|
|
Term
| How to diagnose cyclic neutropenia. |
|
Definition
| WBC blood count every 2-3 days for 8 wks. |
|
|
Term
| Pt has oral ulceration every 3 wks, and a 1% PMN count. What do you suspect? |
|
Definition
|
|
Term
|
Definition
| Discontinue any meds that may have precipitated. Antibiotics, G-CSF, oral hygiene. |
|
|
Term
| During inflammation, when do neutrophil levels peak, macrophage? |
|
Definition
neutrophil: 2 days
macrophage: 3 days |
|
|
Term
| What is the most important degenerative change that occurs when the heart can no longer compensate for hypertrophy? |
|
Definition
| Loss of myofibrillar contractile elements. |
|
|
Term
| Does breast tissue undergo hyperplasia? Does heart muscle? |
|
Definition
|
|
Term
| When part of the liver is removed, through which process does is grow back to its normal size? |
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Definition
|
|
Term
| Most forms of pathologic hyperplasia are caused by excessive _____ stimulation. |
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Definition
|
|
Term
| Do papillomaviruses cause hypertrophic or hyperplastic epithelial lesions? |
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Definition
|
|
Term
| The mechanisms of atrophy are decreased ____ synthesis and increased ____ degradation. |
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Definition
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|
Term
| Degradation of cellular proteins occurs mainly through the _____ pathway. |
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Definition
|
|
Term
| Epithelial metaplasia in smokers: ciliated columnar cells are replaced with ______. |
|
Definition
| stratified squamous cells |
|
|
Term
| Deficiency of what vitamin may induce epithelial metaplasia in the respiratory tract? |
|
Definition
|
|
Term
| In GERD metaplasia in the esophagus, what becomes what? |
|
Definition
| stratified squamous becomes columnar |
|
|
Term
| Do necrosis and apoptosis elicit an inflammatory response? |
|
Definition
necrosis: yes
apoptosis: no |
|
|
Term
| With ischemia, how long does it take myocytes to beccome non-contractile? To die? |
|
Definition
| 1-2 minutes; 20-30 minutes |
|
|
Term
| Which two phenomena consistently characterize irreversible cell injury? |
|
Definition
| Inability to correct mitochondrial dysfunction and profound disturbances in membrane function. |
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|
Term
| The enlargement of which organelle in which cells is responsible for barbiturate tolerance? |
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Definition
|
|
Term
| Injured cells may show increased _____ staining. |
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Definition
|
|
Term
| Clumping of ____ and detachment of ____ from ____ is associated with reversible cell injury. |
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Definition
|
|
Term
| Which cell response is characterized by large amorphous densities and intracytoplasmic myelin figures? |
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Definition
|
|
Term
| Which pattern of necrosis can only be detected by histologic examination? |
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Definition
|
|
Term
| ____ necrosis is characteristic of infarcts in all solid organs except the ____, in which liquefactive necrosis may be seen due to an infarct. |
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Definition
|
|
Term
| Bacterial infection causes which necrosis pattern? |
|
Definition
|
|
Term
| What is gangrenous necrosis? |
|
Definition
| Coagulative necrosis with an infection that adds some liquefactive properties. |
|
|
Term
| Fat necrosis typically results from the release of what kind of enzymes? |
|
Definition
|
|
Term
| Which necrosis pattern is a result of saponification? |
|
Definition
|
|
Term
| Where is the "fibrinoid" of fibrinoid necrosis found? |
|
Definition
| In the walls of arteries. |
|
|
Term
| The principal targets of cell injury include these three cellular components and homeostasis of this element. |
|
Definition
| mitochondria, membranes, DNA, calcium |
|
|
Term
| During ischemia, there is less ATP available and the sodium pump cannot function properly. This results in influx of what? Efflux of what? |
|
Definition
Influx: Na, Ca, H2O
Efflux: K+ |
|
|
Term
| During anaerobic glycolysis, lactic acid production causes pH to fall, resulting in what change in the nucleus? |
|
Definition
|
|
Term
| Are Ca2+ levels higher in the cytoplasm or in extracellular fluid? |
|
Definition
| In extracellular fluid (up to 10,000x more) |
|
|
Term
| How does increased cytosolic Ca cause membrane breakdown? |
|
Definition
| It activates phospholipases that directly damage the membrane and proteases that damage the cytoskeleton, which leads to membrane damage. |
|
|
Term
| Is death from hypoxia in the form of necrosis, apoptosis, or both? |
|
Definition
| Both, but mostly necrosis. Apoptosis occurs with release of pro-apoptotic enzymes from damaged mitochondria. |
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|
Term
| In the presence of ___, H202 is converted to the highly reactive hydroxyl radical *OH through the ____ reaction. |
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Definition
|
|
Term
| In order for ____ to cross biologic membranes, it must first be converted to H2O2. |
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Definition
|
|
Term
| Reactive oxygen species are produced mainly by what WBCs? |
|
Definition
| neutrophils and macrophages |
|
|
Term
| What is the "respiratory burst"? |
|
Definition
| The process by which phagosomes produce hypochlorite from superoxide. |
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|
Term
| Leukocytes use the free radical NO to react with superoxide to form ____. |
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Definition
|
|
Term
|
Definition
|
|
Term
| Both glutathione peroxidase 1 and catalase catalyze the breakdown of _____ |
|
Definition
|
|
Term
| What is ischemia-reperfusion injury? |
|
Definition
| Return of blood flow to reversibly injured cells results, paradoxically, in their death. |
|
|
Term
| Which enzyme is usually responsible for converting non-active chemicals to toxic metabolites? |
|
Definition
|
|
Term
| Apoptosis is activated by which enzymes? |
|
Definition
|
|
Term
| What is the "intrinsic" pathway of apoptosis? |
|
Definition
| The mitochondrial pathway. |
|
|
Term
| What is the "extrinsic" pathway of apoptosis? |
|
Definition
| The death receptor pathway. |
|
|
Term
|
Definition
| Pro-apoptotic mitochondrial proteins. |
|
|
Term
| phosphatidylserine (in re apoptosis) |
|
Definition
| An "eat me" protein. If flips to the outer leaflet to initiate apoptosis. |
|
|
Term
| What is the most common exogenous pigment? |
|
Definition
|
|
Term
| What is the "wear and tear pigment"? |
|
Definition
|
|
Term
|
Definition
| The accumulation of lipofuscin (typically in heart, brain, or liver). |
|
|
Term
| What is the difference between dystrophic and metastatic calcification? |
|
Definition
Dystrophic: dead or dying tissue
Metastatic: otherwise healthy tissue |
|
|
Term
| Which calcification process requires hypercalcemia, dystrophic or metastatic? |
|
Definition
|
|
Term
| Metastatic calcification is usually caused by hypercalcemia due to excessive _____ hormone. |
|
Definition
|
|
Term
|
Definition
| Advanced aging bc cells can't divide as many times. |
|
|
Term
| Which WBC is associated with acute inflammation? With chronic? |
|
Definition
Acute: neutrophils
Chronic: lymphocytes and macrophages |
|
|
Term
| What are the two most important families of pattern recognition receptors in activating inflammation? |
|
Definition
| Toll-like receptors (for infections) and the inflammasome (for dead cells) |
|
|
Term
| The inflammasome activates caspase-1, which in turn activates _____. |
|
Definition
|
|
Term
| What are the two main vascular changes associated with acute inflammation? |
|
Definition
| vasodilation and increased vascular permeability |
|
|
Term
| In regards to inflammation, what is stasis? |
|
Definition
| When fluid leaks out of vessels, the blood becomes more viscous. RBCs are packed together and blood flow slows. |
|
|
Term
|
Definition
| The process by which leukocytes (primarily neutrophils) accumulate on vascular endothelial surfaces. |
|
|
Term
| What do exudates contain that transudates do not? |
|
Definition
|
|
Term
| The weak and transient interactions involved in rolling are mediated by the ____ family of adhesion molecules. |
|
Definition
|
|
Term
|
Definition
| The selectin present on the surface of most leukocytes. If binds to L-selectin ligands on endothelial cells during rolling. |
|
|
Term
| E-selectin is mostly absent from unactivated endothelial cells. Which to compounds cause it to be expressed? |
|
Definition
|
|
Term
| Adhesion is mediated by ____ on leukocyte cell surfaces. |
|
Definition
|
|
Term
| What caused integrins to be convert to their high-affinity state? |
|
Definition
|
|
Term
| Extravasation of leukocytes through endothelial cell junctions is called _____. |
|
Definition
|
|
Term
| On what cells is PECAM-1 (aka CD31) expressed? |
|
Definition
| On both the leukocytes and the endothelial cells. |
|
|
Term
| With acute inflammation, how long does is take for the predominant cell type to switch from neutrophils to monocytes? |
|
Definition
|
|
Term
| The most important opsonins are antibodies of the ___ class, portions of the complement protein ___, and collectins. |
|
Definition
|
|
Term
| In the neutrophil lysosome, the enzyme ____ converts H2O2 to the radical _____, a powerful microbicidal molecule. |
|
Definition
| MPO; HOCl (hypochlorous radical) |
|
|
Term
|
Definition
| Neutrophil extracellular traps. Fibrillar networks with granule proteins and stuff that trap microbes. |
|
|
Term
| NETs kill neutrophils. T/F |
|
Definition
| True. Essentially, the neutrophil is destroyed in the process of creating the NET. |
|
|
Term
| A skin blister from a burn represents which type of inflammation morphology? |
|
Definition
|
|
Term
| Which cell types produce leukotrienes and prostaglandins? |
|
Definition
| leukocytes and mast cells |
|
|
Term
| What inflammatory mediators do platelets produce? |
|
Definition
|
|
Term
| Which cells produce inflammatory chemokines? |
|
Definition
| leukocytes and macrophages |
|
|
Term
| What are the three main classes of plasma derived inflammatory mediators? |
|
Definition
| complement, kinins, and proteases |
|
|
Term
| What are the inflammatory mediators that are vasoactive amines? |
|
Definition
|
|
Term
| What is histamine's action as an inflammatory mediator? |
|
Definition
| vasodilation and vascular permeability |
|
|
Term
| What is serotonin's action as an inflammatory mediator? |
|
Definition
| vasoconstriction during clotting |
|
|
Term
| What are the AA-metabolites? |
|
Definition
| leukotrienes, prostaglandins, and lipoxins |
|
|
Term
| What is another name for AA-metabolites? |
|
Definition
|
|
Term
| Do prostaglandins cause vasodilation or vasoconstriction? |
|
Definition
|
|
Term
| What are the two major enzymatic pathways of AA metabolism? |
|
Definition
COX: prostaglandins and thromboxanes
lipoxygenase: leukotrienes and lipoxins |
|
|
Term
| Two main actions of leukotrienes. |
|
Definition
| bronchoconstriction (think back to pharm) and vascular permeability |
|
|
Term
| Because they inhibit neutrophil chemotaxis, ____ act as antagonists of leukotrienes, another AA metabolite. |
|
Definition
|
|
Term
| Which AA-metabolite is mainly anti-inflammatory? |
|
Definition
|
|
Term
| Prostacyclin and thromboxane A2 have opposing effect. What are they? |
|
Definition
PGI2: vasodilation, platelet inhibition
TXA2: vasoconstriction, platelet aggregation |
|
|
Term
| Main actions of platelet-activating factor. |
|
Definition
| Activates platelets, bronchoconstriction, vasodilation, permeability |
|
|
Term
| What is the principal role of TNF and IL-1 in inflammation? |
|
Definition
|
|
Term
| Where do macrophages come from? |
|
Definition
| circulating monocytes become macrophages after they migrate into the tissue |
|
|
Term
| What is the opsonin of the complement pathway? |
|
Definition
|
|
Term
| The kinin system, the clotting system, the fibrinolytic system, and the complement system are all initiated by the activation of what factor? |
|
Definition
| the Hageman factor (factor XIIa) |
|
|
Term
| What is an M1 macrophage? |
|
Definition
| Classically activated (by microbes, IFN-y, and foreign substances). Function: phagocytosis and inflammation. |
|
|
Term
| What is an M2 macrophage? |
|
Definition
| Alternatively actived (by non-IFN-y cytokines). Function: tissue repair, anti-inflammatory |
|
|
Term
| What do mast cells release when they encounter allergens? |
|
Definition
|
|
Term
| Which dz is prototypical of granulomatous inflammation? |
|
Definition
|
|
Term
| What is the acute phase reaction? What are its most important mediators? |
|
Definition
| Systemic effects of inflammation. TNF, IL-1, IL-6. |
|
|
Term
| What does the eythrocyte sedimentation rate test for? |
|
Definition
| Systemic inflammation. (Fibrinogen released in acute inflammation causes RBCs to form stacks.) |
|
|
Term
| What is a "shift to the left"? |
|
Definition
| Increased numbers of circulating immature leukocytes. |
|
|
Term
| What is organization (in re repair)? |
|
Definition
| A fibrosis that develops in a space occupied by an inflammatory exudate. |
|
|
Term
| Nondividing cells are in cell cycle arrest in the ___ phase. |
|
Definition
|
|
Term
| Is the pancreas labile, stable, or permanent? |
|
Definition
|
|
Term
| What is asymmetric replication of stem cells? |
|
Definition
| The stem cell divides and only one daughter cell becomes differentiated. |
|
|
Term
| What do mesenchymal stem cells differentiate to? |
|
Definition
| chondroblasts, osteoblasts, myoblasts |
|
|
Term
| What is granulation tissue (in re repair)? |
|
Definition
| The collection of connective tissue, vessels, and leukocytes that form in the initial phases of scar formation |
|
|
Term
| Angiogenesiss is the process of new blood vessel development primarily from which type of existing vessels? |
|
Definition
|
|
Term
| What are the two most important growth factors in angiogenesis? |
|
Definition
| VEGF and FGF-2 (basic fibroblast growth factor) |
|
|
Term
| VEGF promotes vasodilation by stimulating the production of ____. |
|
Definition
|
|
Term
| Why is granulation tissue often edematous? |
|
Definition
| Because newly forming vasculature is leaky due to incomplete junctions and NO production stimulated by VEGF. |
|
|
Term
| Collagen synthesis by _____ in scars begins about 3-5 days after injury. |
|
Definition
|
|
Term
| As a scar matures, does vascularization increase or decrease? |
|
Definition
|
|
Term
| What does TGF-b do during repair? |
|
Definition
| Stimulates production of scar components and helps terminate the inflammatory response. |
|
|
Term
| What does PDGF do during scar formation? |
|
Definition
| Causes migration and proliferation of fibroblasts. |
|
|
Term
| Enzymes in the ECM, most notably _______, degrade the ECM to permit remodeling and extension of the vascular tube. |
|
Definition
| matrix metalloproteinases (MMPs) |
|
|
Term
| Which ion are MMPs dependent on? |
|
Definition
|
|
Term
|
Definition
| tissue inhibitors of metalloproteinases. They shut down MMP activity after scar formation is complete. |
|
|
Term
| Glucocorticoids may inhibit the activity of this growth factor, leading to weak scar formation. |
|
Definition
|
|
Term
| Which is likely to have a larger wound contraction, healing by first intention, or healing by second intention? |
|
Definition
| healing by second intention |
|
|
Term
| How strong can a wound be compared to normal skin? |
|
Definition
| After 3 mos, 70-80% strength. |
|
|
Term
| What is the difference between a scar and fibrosis? |
|
Definition
| They are the same, but fibrosis usually refers to collagen deposition in chronic diseases. |
|
|
Term
What is this?: http://trialx.com/curetalk/wp-content/blogs.dir/7/files/2011/05/diseases/Chediak-1.jpg
How do you know? |
|
Definition
| Chediak-Higashi syndrome. Giant granules in neutrophils. |
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