Pathology Exam 1

#separator:tab #html:true "the study of disease and provides the scientific foundation for medicine"pathology  "refers to the steps in the development of a disease or how a disease develops "pathogenesis "refers to the gross and microscopic appearance of cells and tissue"morphology What are possible etiologies of disease"immunologic abnormalities genetic abnormalities nutritional imbalances infections toxins trauma <img src=""paste-fe38b6015b96ffbc7c01ae441760c601fb47f2b0.jpg"">" What are adaptations "reversible changes in size, number, phenotype, metabolic activity, or function of cells in response to changes in their environment" different types of adaptations hypertrophy hyperplasia atrophy metaplasia dysplasia What is hypertrophy"<div>An increase in size of cells that results in an increase in the size of the affected organ</div>" what does hypertrophy result fromcellular protein production  What are examples of tissue that can undergo hypertrophyskeletal and cardiac muscle can be pathologic or physiologic meaning that it can be due to weight lifting or disease  What is hyperplasia"<div>Increase in the number of cells in an organ or tissue in response to a stimulus</div>" what can hyperplasia occur withhypertrophy what is pathologic hyperplasia often due to "excessive actions of hormones or growth factors acting on target cells" what is physiologic hyperplasia often due to "<div>the action of hormones or growth factors  when there is a need for compensatory increase after damage or resection.</div>" what is metaplasia"<div>Reversible change in which one differentiated cell type is replaced by another cell type</div>" "<div>Often represents an adaptive response in which one cell type that is sensitive to a particular stress is replaced with another cell type that is better able to withstand the adverse environment</div>"Metaplasia what is an example of metaplasiacolumnar cells to squamous cells in the respiratory tract secondary to chronic inflammation like tobacco smoking  "<div>Stimuli that cause metaplasia may persist and cause [...] in metaplastic cells </div>""<div>Stimuli that cause metaplasia may persist and cause malignant transformation in metaplastic cells </div> " what is dysplasia"disordered growth  constellation of changes which include a loss in the uniformity of cells as well as a loss of architectural  orientation" when does dyspalsia often occurin metaplastic epithelium what is an example of dysplasiapleomorphism large hyperchromatic nuclei and increased nuclear/cytoplasmic ratio (nucleus too big)  does dysplasia mean a progress to cancer no  may be reversible  "When dysplastic changes are marked and involve the entire thickness of the epithelium without penetrating beyond the basement membrane it is called: ""carcinoma in situ" what is anaplasialack of differentiation  where is anaplasia seen in malignant neoplasms  implies a reversal of differentiation to a more primitive level of cell "<div>Implies a reversal of differentiation to a more primitive level of a cell</div>"anaplasia what are changes in cells and tissue caused byprolonged stimulation lack of stimulation  lack of oxygen lack of nutrients chronic injury  what is cell injury caused by"<div>change in the cell’s homeostasis (the ability to handle physiologic demands while maintaining a healthy steady state)</div>" 2 types of cell deathapoptosis and necrosis  most important cause of cell injuryhypoxia What are the mechansisms of cell injurydepletion of ATP mitochondrial damage influx of calcium inside cell accumulation of O2 derived free radicals  defects in membrane permability ischemiadecrease in blood supply hypoxemialow partial pressure of oxygen in the blood forms of hypoxiaischemia hypoxemia decreased oxygen what happens to a cell when the activity of the sodium pump is reduced cell swells  what does depletion of ATP do to protein synthesis decreases protein synthesis  what does mitochondria damage do to the membrane increased permability lets things get through and out  what is the biggest issue with the increased permeability of mitochondria in damage"<div>Leakage of cytochrome c with alteration of electron transport chain leading to cell death</div>" cell injury is accompanied by this ion coming in the cellcalcium where can the influx of intracellular calcium come form during injuryextracellular fluid mitochondrial compartment  rough ER why is the influx of intracellular calcium so badamplifies the effects of hypoxia  by activating several enzymes  are the changes to a cell due to influx of calcium reversible or irreversibleinitially reversible but then can become irreversible what does influx of calcium result in lower ATP  lower phospholipids disruption of membrane and cytoskeletal proteins  chromatin damage  how do we consume oxygen derived free radicals radiant energy  chemicals or drugs reduction oxidation reactions  transition metals like Fe or Cu Nitric oxide  what are free radicals single unpaired electron  why are free radicals an issuebecause they have an unpaired electrons, they are unstable af and react with organic and inorganic chemicals  ya know like the stuff were made out of  what WBC produces free radicals neutrophils  to destroy bacteria  how do free radicals damage cells lipid peroxidation  DNA lesions  Cross linking proteins  what is cross linking of proteins caused by free radicals and causes inactivation of enzymes  why are free radicals bad for DNAThey may block DNA transcription and cause mutations What are examples of free radicals "O2- H2O2 -OH  <img src=""paste-ffb72173e3aa490f95d224e968a53ca1ef7869e0.jpg"">" how are free radicals removed antioxidants  binding of metals like Fe or Cu enzymes can break down free radicals what are antioxidants examples vitamin E  vitamin A absorbic acid glutathione What can result from membrane permeabilitymitochondrial dysfunction  loss of membrane phospholipids  cytoskeletal abnormalities ROS lipid breakdown products what happens if damage to proteins is too severe"<div>it may not be able to be corrected and the cells may initiate a “suicide” program and dies by apoptosis</div>" what happens if improperly folded proteins accumulate apoptosis  irreversible cell injury leads to death what is reversible injury characterized by acute cellular swelling  depleted glycogen reduced intracellular pH reduction in protein synthesis  What is irreversible injury characterized byincreased calcium in mitochondria damage to plasma membrane swelling of lysosomes  leakage in intra cellular proteins into the blood what are the mechanisms of irreversible injuryloss of membrane phospholipids cytoskeletal abnormalities  toxic oxygen radicals lipid breakdown products  What is the difference between reversible and irreversible injury"<img src=""paste-f8e514b8382d2137f8eba99492dc032d1c9e5b99.jpg"">" what is the issue with drug therapy chemical injury is a common problem in drug therapy what organ is a target of chemical injuryliver because many chemicals and medications and metabolized in the liver  what can promote recovery of cells that have been reversible injured in ischemic tissuerestoration of blood flow does ischemia reperfusion always workno  sometiems the blood flow is restored to ischemic cells it can accelerate tissue damage  what is ischemia reperfusion caused by"inflammation reactive oxygen and nitrogen species the activation of the complement system" heterophagya cell eats another cell autophagy"cell eats its own contents  can be implicated in some physiologic states such as exercise and aging pathologic processes" does autophagy and heterophagy both have residual bodies"yes  can be implicated in some physiologic states such as exercise and aging pathologic processes" what organelle metabolises chemicalsSER organelle for p450 modificationSER what are intracellular accumulations fatty change cholesterol proteins glycogen pigments "produced at normal or increased rate with inadequate metabolism in intracellular accumulations"endogenous substance the homogenous glassy pink change in cells or extracellular space in vesselshyaline cartilage when can glycogen accumulate diabetes  glycogen storage disease what are exogenous pigmentscarbon with arthracosis  what are endogenous pigments lipofuscin melanin hemosiderin what is steatosisfat build up in an organ usually liver or heart when does cholesterol or cholesterol esters build upathersclerosis  xanthomas inflammation and necrosis  when do proteins accumulatereabsorbsion droplets in proximal renal tubules excessive amounts of secretory protein defects in protein folding russel bodiesexcessive amount of secretory protein Dystrophic calcification intracellular and extracellular calcification necrosis that can cause necrosis  dystrophic calcification can be accentuated byhypercalcemia where does metastatic calcification occurnormal tissues  gastric mucosa kidneys and lungs does metastatic calcification cause clinical dysfunctionusually no  replicative senescencelimited dividing of cells  "Cellular swelling ,protein denaturation, and organellar breakdown  "necrosis programmed cell deathapoptosis difference between necrosis and apoptosis"<img src=""paste-a7cfbfcdae9c58653f9d03e23d84c78cecaf8e6d.jpg"">" what is the morphology of apoptosiscell shrinkage chromatin condensation  cytoplasmic blebs and apoptotic bodies phagocytic of apoptotic cells biochemical features of apoptosisprotein cleavage: capsases DNA breakage phagocytic recognitiion what are the parts of the mechanisms to apoptosisexecution phase  removal of dead cells (phagocytosis) examples of necrosiscoagulative liquerfactive caseous fat  fibrinoid  gangrenous  what is necrosiscells lose membrane integrity  elicit inflammation denatures intracellular proteins  enzymatic digestion of the cell what are the myelin figures in necrosis curled up phospholipids masses derived from damaged cell membranes with replace cells what are the nuclear changes in necrosis karyolysis pyknosis karyorrhexis degenerative cellular process involving fragmentation of the nucleus and the breakup of the chromatin into unstructured granuleskaryorrhexis the shrinkage or condensation of a cell with increased nuclear compactness or densitypyknosis the melting of nucleus chromatin with enzymes (nucleases) released from the lysosomes of the dead cellkaryolysis what is karyolysisfading of the basophilia of the nuclear chromatin nuclear shrinkagepyknosis a pyknotic nucleus undergoes fragmentation example of coagulative necrosismyocardial infarct what occurs during coagulative necrosispreservation of the structural outline of the cell denaturing of structural and enzymatic proteins characterized by cheesy appearance of a central necrotic areacaseous necrosis example of caseous necrosisTB  what happens during caseous necrosisfragmented or lysed cells cell outlines and architecture is lost  example of fat necrosispancreatitis release of lipases  what happens during fat necrosis"Focal areas of fat destruction, lipases split triglyceride esters to release fatty acids, which combine with calcium to produce chalky white deposits" liquefactive necrosis complete digestion of dead cells  often seen in bacterial or fungal infections  illicit an acute inflammatory response resulting in the release of enzymes that LIQUEFY tissue where may liquefactive necrosis be seenCNS "involves a lower limb that has lost its blood supply which results in coagulative necrosis of multiple cell layers"gangrenous necrosis what is wet gangreneliquefactive + gangrenous necrosis is fibrinoid necrosis visible by light microscopyyes  when is fibrinoid necrosis usually seen"immune reactions where antigens and antibodies are deposited in the walls of arteries" how does fibrinoid necrosis occur"<div>The deposits and fibrin produce a pink amorphous material that  forms in the walls hence the term fibrinoid</div>" What is the purpose of inflammation"<div>The goal is to eliminate the cause of injury and repair any damage</div>" What kind of response does inflammation requirevascular  cellular humoral three main events in inflammationhemodynamic changes increased permeability of vessels emigration of leukocytes from vessels to tissue along with eliminating or neutralizing the cause of injury, what is the other important role of inflammationmust repair damage caused by the injuirious agents  what is a general issue that can arise with inflammation"<div>Sometimes, the inflammatory response can produce major tissue damage </div>" Five R's of inflammationrecognize the injurious agent recruitment of leukocytes removal of the agent regulation of the response resolution or repair microbes and necrotic tissue trigger what cells "macrophages  dendritic cells mast cells  recognition by macrophages other sentinel cells in tissues  <img src=""paste-a40fd22892e6b2eefe81f9b116f668f2923d9c79.jpg"">" what are the mediators that the innate immune system releases to trigger recruitment of leukocytes"amines and cytokines <img src=""paste-a40fd22892e6b2eefe81f9b116f668f2923d9c79.jpg"">" vasodilation or increased vascular permeability can lead to edema macrophages send what to fibroblasts to trigger repair"cytokines and growth factors <img src=""paste-a40fd22892e6b2eefe81f9b116f668f2923d9c79.jpg"">" acute vs chronic inflammation"acute: immediate reaction to injury, lasts a few hours to days  chronic: lasts longer maybe months or longer" main cells of acute inflammationneutrophils  main cells of chronic inflammationlymphocytes  plasma cells  macrophages acute inflammation is regulated by mediators found where the plasma or secreted by cells what are the mediators of acute inflammationvasoactive amines coagulation factors  complement proteins  arachadonic acid derivatives cytokines in acute inflammation where do intravascular leukocytes move toward the site of pathogens  the vessels are source of what mediators NO cytokines  mast cells are source of what mediators histamine  purpose of polymorphonuclear leukocytes elimination of microbes and dead tissue purpose of plasma proteins complement: mediators of inflammation, elimination of microbes clotting factors: clotting factors and kiinogens (mediators of inflammation)  five signs of acute inflammationheat (calor) redness (rubor) swelling (tumor) pain (dolor) loss of function (factio leasa)  "an excess of fluid in tissues or serous body cavities"edema exudatehigher protein content transudatelower protein content three main causes of edema"<div>1.Increased hydrostatic pressure in microcirculation: vessel dilatation with influx of blood can cause a transudate</div> <div>2.Increased permeability of blood vessels: vessels become leaky from the mediators of inflammation</div> <div>3.Reduced osmotic pressure of the plasma: loss of proteins can increase the movement of fluid into the interstitial space</div>" what happesn to vasculature during reactions of acute inflammation"both the arteriole and venule dilate increasing blood flow and allowing for leakage of plasma and neutrophils  <img src=""paste-c5052df6de05fb119ee7f8c51e516da5d24ef831.jpg"">" normally in the endothelium what is the relationship between colloid osmotic pressure and hydrostatic pressure "they are equal <img src=""paste-788f645c777c9071ce9af604a549b0948b869823.jpg"">" what causes retraction of endothelial cells histamine or other mediators  is retraction of endothelial cells quick or slowrapid and short lived are endoethlial injuries rapid or slowrapid and maybe long lived  what are endothelial injuries cased byburns and some microbial toxins what happens if inflammation sticks arounddamages normal tissue as well not too long what are examples of sentinel cells macrophages dendritic cells mast cells  some of the first to recognize inflammatory cascase What are monocytes called when they move out of the blood vesselmacrophages  throw pseudopods around to eliminate acute inflammation cause change in blood flow change in blood flow allows for intravascular leukocytes to move where they are needed component of acute inflammation associated with liquid portion of bloodplasma proteins think complement cascase cells that line blood vesselendothelial why are acute injuries red and hotvasodilation tumor portion of acute inflammationedema as proteins are lost in plasma what happens to osmotic pressuredecreases contributes to fluid leaking out  2 forms of edematransudate and exudate can a transudate and exudate occur togetheryes what is the hydrostatic pressure in vessel trying to dopush fluid out of blood vessel colloid is trying to keep in so net balance  what happens to the hydrostatic and colloid osmotic pressure in inflammationit is disrupted what occurs during a transudatehydrostatic pressure is particuarly large forcing out mostly fluid and not much protein because gaps arent that wide  what occurs during an exudate increase in fluid leaving but also gaps open up so protein molecules can leave as well  what decresaes osmotic colloid pressure (transudate)anything that decreases plasma proteins liver disease: cant make proteins kidneys malfunction: breaking down proteins  transcytosis fluid transmitted across cytoplasm through endothelial  why are new blood vessels often leakynot mature yet  what mediates the gaps in endotheliumvenules or vasoactive mediators  what causes cytoskeleton to reorganizecytokines and hypoxia what kind of reponse comes with leukocyte dependent injurylate  when does leukocyte activation occurwhen microbes or dead cells induce several responses cytokines also play a key role  how do leukocytes attach to the walls of the endotheliumnormally the leukocytes flow with blood fast but during vasodilation the blood slows down and gives the leukocytes the ability to attach to the walls of endothelium allowing for attachment what mediators can macrophages releaseTNF IL-1 margination when the WBC start to accumulate around margins of vessels rollingWBC bouncing through endothelium what are the selectinsE P L selectin selectins allow for what rolling and transient stickiness of wall what gives the firmer attachment of WBC to the wallICAM-1 VCAM-1 LFA-1 mac-1 and PCAM-1 things like PCAM allow for what passing through endothelium what is stasisslow down of blood flow chemotaxisallows for movement of WBC along chemical gradients where they are needed and activated what are involved in chemotaxis and activationN Formyl Methionine C5a LTB4 IL8 what contributes to leukocyte activationprod of arachadonic acid  degranulation and secretion of lysosomal enzymes secretion of cytokines modulation of leukocyte adhesion molecules 2 major phagocytes neutrophils and macrophages degranulation vs phagocytosisphagocytosis is grabbing and eating and degran is breaking down steps of phagocytosis and degranulationrecognition and attachment engulfment degredation what engulfts the microbe during phagocytossipseudopods fake arms  what happens after pathogen has been engulfed during phagocytosis it fuses with a lysosome to become a phagolysosome and is degraded  what could be a cause of leukocyte defectsdefects in adhesion defects in chemotaxis or phagocytossi  defects in microbial activity  what are the cell derived mediators of inflammation vasoactive amines histamine and seratonin why are cell derived mediators often the first mediators to be released during inflammationbecause they are already made and stored in cells  arachadonic acid metabolitesprostoglandins leukotrienes platlet activating factor cytokines  NO oxygen derived free radicals lysosomal constituents  what enzyme converts phospholipids to AAphospholipase releases phospholipids from bilayer  what inhibits phospholipasesteroids  2 pathways AA can takecyclooxengenase and lipooxygenase  thromboxane A2 functioncauses vasoconstriction promotes platelet aggregation prostacyclin PGI2 functioncauses vasodilation  inhibits platelet aggregation which AA pathway makes the prostoglandinscyclooxenenase  what inhibits cyclooxenenaseCOX-1 and COX-2 inhibitors asprin  indomethacin what AA Pathway makes the leukotrieneslipooxenease  what pathway are PDG2 and PGE2 madecyclooxegenase  why are corticosteroids so potent in blocking inflammationbecause they block the initial pathway of phospholipase so nothing is made mediator that causes bronchospasm leukotrienes lipoxin functioninhibit neutrophil adhesion and chemotaxis causes vasoconstriction and platelet aggregationTXA2 vasodilation and edemaPDG2 PGE3 and PGF2 overall what do prostaglandins cause pain and fever  where are plasma proteins like the complement system made (organ)liver  Factor XII Haegman functionkin system activation and coagulation  made in liver  leukotrienes and lipoxins are derived from what pathwaylipoxgenase pathway what is a feature of asthma that is being targeted to fixbronchospasms caused by leukotrienes roles of paltelet activating factorplatelet stimulation vasoconstriction bronchoconstriction  what does low levels of PAF causeincreased vascular permeability and vasodilation  what produces nitric oxideendothelial cells  macrophages  some neurons what is nitric oxidepotent and short acting vasodilator also decreaeses platelet aggregation and adhesion  what does nitric oxide do to microbeslimits replication of bacteria, viruses and protazoa where are lysosomal granules found neutrophils and monocytes types of lysosomal granules acid proteases neutral protease antiprotease function of acid protease degrade bacteria within phagolysosomes  lysosomal granule function of neutral protease degrade ec componenets  lysosomal granule  lysosomal granule if unchecked can produce tissue damageneutral protease  what checks the effects of some of the acid and neutral proteases antiproteases alpha 1 antitrypsin what does oxygen derived free radicals do to antiproteasesinactivates antiproteases  what does ROS do to cells injures  increased IL-1 and TNF does what do endotheliumincrease leukocyte ahderence increase PGI synthesis  increase procoagulant activity decrease anticoagulant increase IL-1 8 6 and PDGF what are the acute phase reactions of IL-1 and TNFincrease sleep  increase acute phase proteins decrease appetite  IL-1 TNF effects on fibroblasts increase  proliferation collagen synthesis collagenase  protease PGE synthesis what is the effect of IL-1 and TNF on leukocyte effects cytokine secretion  plasma proteins play a role in which systemscomplement kinin clotting  what does the complement system consist of proteins that aid in inflammation phagocytosis and cell lysis  these systems are intimatley connected resulting in clot formation and contributing to the complement cascadecoagulation and kinin systems what are cytokinesgeneral forms of messenger molecules  chemokines are specific type of cytokines that direct migration of white blood cells to areas of infected or damaged tissues specific type of cytokinechemokines leukocytosisincrease in WBC  where are the precursors of WBC bone marrow  blood is being made. progenitors are produced here so mediators can sitmulate more  TNF does what to cardiac outputlowers  TNF effect on insulinresistance  what happens if damaged tissue does not go back to complete resolution after acute inflammationit gets replaced with scar tissue what is an abcesswalling off a group of bacteria so best thing to do is  wall it off so it just kills the WBC around it but those dying cells are creating an abcess can disease skip acute and go right to chronicyes  another name for abcesspus serous inflammationprotein poor  fibrinous inflammationincreased vascular permeability suppurative inflammationabcesses and pus ulceration inflammationeroded epithelium example of serous inflammationfirst degree burn get that little bubble that is serous fluid  What are the dark cells of micrscopic lung neutrophils  purulent inflammation example of fibrinous inflammationfibrinous pericarditis  causes of chronic inflammationpersistant infection (TB) prolonged exposure to toxins  autoimmune diseases plasma cells are derived fromB lymphocytes Why do macrophages and monocytes release ROSto kill cells and bacteria function of eicosanoids chronic inflammatory cell involved in signaling molecules that induce swelling and inflammation monocytes and macrophages have a reciprocal relationship with which cells T cells  activation what are eosinophils for parasitic infection what do plasma cells produce `antibodies what do eosinophils look like"bright granules  <img src=""paste-cc0fde5e58fc64fd130c2d04f2db5c2c09af1be8.jpg"">" what do plasma cells look lik"eccentric nucleus with a perinuclear hoff <img src=""paste-cc0fde5e58fc64fd130c2d04f2db5c2c09af1be8.jpg"">" granulomatous inflammation is seen in what type of inflammation mostlychronic what is granulomatous inflammationaccumulations of activated macrophages are granulomatous inflammation the same and ganulation tissueno they are different what are the examples of infections of granulomatousTB fungi and parasites what are the examples of inorganic metals and dust with granulomatous inflammationsilicosis or berlliiiosis  what is the example of foreign body granulomatoussutures  sarcoidosis multi organ disease resulting in deposition of granulomas that occurs mostly in the lungs  caseouating necrosis is associted mostly with what disease TB why are granuloma in TB giant cells result from fusion of macrophages  true or false: not all granulomas have necrosis true  what is chronic inflammation characterized bypersistent inflammation  tissue injury  attempted repair by scarring what happens to tissue when it encounters mild superficial injurybasement membrane still in tact  inflammation but cells can regenerate and bounce back what happens when there is severe injury in tissuedestorys epithelium and breaks throgh basement membrane and gives a more robust response  tissue is so dmaaged it cannot regenerate and is replaced by scar tissue what is regenerationthe ability to regenerate depends on the proliferative potential of cells main cell types in regeneraterationlabile stable  permanent  cells that constantly enter the cell cycle labial cells  examples of permanent cells cardiac monocytes and neurons nondividing for the most part quiescent stable cells examples hepatocytes G0  cell proliferation is driven bysignals provided by growth factors and extracellular matrix  where are most growth factors producedactivated macrophages  besides macrophages where is growth factor produced epithelial and stromal cells  these activate signaling pathways that produce proteins that aid in driving cells through cell cycle growth factors  cells use these to bind to extracellular matrix proteinsintegrins what are the extracellular components laid down during repaircollagens  adhesive proteins  proteoglycans  What are the adhesive proteins of the ECMfibronectin laminin function of fibronectinbinds to ECM function of laminincomponenet of basement membranes smooth and skeletal muscles  what is the function of proteoglycansregulate ECM structure and permeability PDGF, EGF and FGF are examples of growth factors  platelet derived growth factor that plays a role in chemotaxisPDGF growth factor that stimulates granulation tissue and stimulates grwoth of skin cells and fibroblasts EGF growth factor that is for angiogenesis, fibroblast growth, mitogenic for keratinocytesFGF growth factor for fibrogenesis chemotaxis for neutrophils macrophages lymphcytes and angiogenesisTGF-B growth factor for angiogenesis and vascular permeabilityVEGF cytokines that are growth factors IL-1 TNF  fibroblasts  collagen these can be growth factors but also growth inhibitors TGF-B and TNF what is repair by connective tissuescar tissue formation steps in scar formationangiogenesis granulation tissue maturation and organization of scar what is angiogenesisnew blood vessel growth how does angiogenesis occurthe parent vessel basement membrane is degraded then the cells migrate to the endothelium where they can proliferate and mature  blood vessels look like branches off a tree why is angiogenesis important for growing new tissueyou cannot grow new tissue without a good blood supply  what are the starting cells of angiogenesisangioblasts  what is granulation tissuesoft pink granular gross appearance made of fibroblasts blood vessels and loose ECM what is granulation tissue made of fibroblasts  blood vessels  loose ECM where does fibrosis occuroccurs on granulation tissue framework on new vessels and ECM parenchymal cells functional cells of a tissue or organ liver: hepatocytes  what is the main goal of wound healingto restore tissue function  if damage is too severe or due to a permanent cell will just get scar tissue when does healing by first intention occursurgical incision and nice clean cut with no stuff and suture it close will get inflammation and stuff but granulation tissue will go in and itll heal with minimal scar what is healing by second intentionoccurs in big woulds that cannot be sutured together. is often necrotic and just have to keep clean and let heal by itself what healing intention has a much more robust healing response second intention what are keloidsexacerbated scar tissue begins normal wound healing but then there is excess collagen production   keloids are due toexcess collagen production  difference between edema and effusions edema are accumulations of fluids in tissues and effusions are accumulations of fluid in body cavities like the pleural space  can edema be inflammatory and noninflammatoryyes  elevated hydrostatic pressure and or decreased colloid osmotic pressure leads to increased movement of fluid out of the vessels  lymphatic obstruction can lead t oedema where does the fluid that comes out of the capillary bed go to lymphatics to be eventually drained what can exaccerbate the causes of edema sodium and water retention  what is a localized increase in hydrostatic pressureimpaired venous outflow of venous blood like a deep vein thrombosis blood cannot be drained so hydrostatic pressure in that one localized area what is generalized increased hydrostatic pressure systemic venous pressure is increasing  CHF makes build up of venous blood pressure everywhere reduced osmotic pressure is an effect due to plasma proteins  anything that results in loss of proteins or making too much proteins can result in edema result of plasma porteins retaining fluid in vessel nephrotic syndromeloss of protein through urine  proteins are usually too large for nephrons but if kidney is damaged then they can get through why can cirrhosis and malnutrition reduce osmotic pressure not as much protein synthesis  what can block lymphatics parasites and cancer  what happens during lymphatic obstructionimpaired lymphatic drainage  when does sodium and water retention occurwhen there is acute reduction of renal function  what does sodium and water retention result in increased hydrostatic pressure due to intravascular fluid volume expansion  why does decreased colloid pressure cause sodium water retention too much fluid dilutes the blood and diluting proteins what are the two systems that are usually the cause during sodium water retentionrenal fuction cardivascular disorder (compromise renal perfusion)  how does heart failure cause edemaincrease central venous pressure increase capillary pressure  edema due to hydrodynamic derangments and are protein poor and low specific gravitytransudate  are a transudate or exudate associated with noninflamamtory transudate are an exudate or transudate associated with inflammatoryexudate what is the significance of the increased vascular permeability in an exudate larger protein molecules to leave blood vessels making protein rich exudate  type of edema with lower specific gravitytransudate  type of edema with higher specific gravityexudate presentations of edemasubcutaneous edema pulmonary edema cerebral edema  what is the most immediate life threatening of all the edemascerebral edema brain swells  hyperemiaactive process due to arteriolar dilation congestionpassive process due to impaired outlow of blood what causes that impariment depends  hemorrhagic disorders are disorders associated withabnormal bleeding  what do hemorrhagic disorders result fromdefects in one or more of the following: vessels walls platelets coagulation factors  coagulation factors are produced in the liver hematomapalpable mass of blood  can be in brain skin or just about anywhere in the body petechiaepinpoint hemmorrhages  purpuraslightly larger than petechiae  3 mm ecchymosis hemorrhage of 1 to 2 cm in size extraversion of blood from ruptured BV hemorrhage  what maintains hemostasis and thrombosisvascular walls platelets  coagulation cascade (clotting( main goal of hemostasis devleop blood clot or thrombin at site of injury why is there vasoconstriction in hemostasis limit blood loss short lived steps of hemostasis1. arteriolar vasoconstriction  2. primary hemostasis 3. secondary hemostasis 4. clot stabalization and resoption  hemostasis vasoconstriction secretes what endothelin  potent endothelium derived vasoconstrictor  what happens during primary hemostasis formation of a platelet plug  what is the process of forming a platelet plug during primary hemostasis 1. disruption of endothelium via VWF and collagen which promotoes platelet activation 2. activation of platelets chaning their shape and allowing them to release secretory granules to recruit more platelets  potent platelet activator TXA  secondary hemostasis goalconsolidate the initial platelet plug with deposition of fibrin  purpose of tissue factor the procoagulant in secondary hemostasis once it is exposed at the site of injury it binds and activates factor VII to aggregate thrombin what does thrombin cleave circulating fibrinogen into insoluble fibrin  creating a meshwork and also activate more platelets leading to more platelet aggregation at the site of injury  cleaves circulating fibrinogenthrombin  where is fibrin in relation to platlelets fills in the gaps like plug  what is tPAcounter regulatory mechanism to limit clotting at site of injury  so clots are limited to point of injury  endothelin is produced by endothelium constrictor  what does endothelin react withsmooth muscle von willebrand factor and collagen effects promotes platelet activation secondary hemostasis involves deposition of fibrin  TF is released whensecondary hemostasis  what does thrombin work on in secondary hemostasis fibrinogen  why does fibrin and platelet aggregate to form a plug to prevent further bleeding  when is tpa releasedonce stable clot has been formed heparin like molecules are what anticoagulants  what makes endothelium prothromboticendothelial injury  cytokines where do platelets adhere to ECM  these help induce platelet aggregation TXA2 and Thrombin  what inhibits TXA2asprin where does TXA2 come from from secretory granules what do platelets exposephospholipid complexes  stimulates the formation of hemostatic plugADP what ion holds clots together calcium  examples of anticoagulants antithrombins proteins C and S plasminogen plasmin system proteins C and S are anticoagulants that are dependent on what vitaminK what does the plasminogen plasmin system dobreaks down fibrin and interferes with fibrin polymerization  thrombosis is initated usually byendothelial injury  MI, trauma and smoking how do alterations to normal blood flow cause thrombosisif blood in vessel is not moving like it should that promotes a blood clot  turbulence or stasis  what causes hyperviscositydehydration and some other diseases that cause increase RBC hypercoagulability can be primary or secondary how is clot removed once it is no longer neededTPa breaks off fibrin giving degredation products which induces anti clotting cascade what is the big purpose of virchows triad"it shows how endothelial injury, abnormal blood flow and hypercoagulability relates to thrombosis  <img src=""paste-5d01568afb2614aabf1d21e2e5428b8162211c5b.jpg"">" due to virchows triad what is most likely to cause thrombosis"endothelial injury <img src=""paste-5d01568afb2614aabf1d21e2e5428b8162211c5b.jpg"">" in virchows triad what can abnormal blood flow result in"hypercoagulability and endothelial injury <img src=""paste-5d01568afb2614aabf1d21e2e5428b8162211c5b.jpg"">" in virchows triad what can hypercoagulability result from "endothelian injury and abnormal blood flow  <img src=""paste-5d01568afb2614aabf1d21e2e5428b8162211c5b.jpg"">" in virchows triad what can endothelial injury cause "abnormal blood flow and hypercoagulability <img src=""paste-5d01568afb2614aabf1d21e2e5428b8162211c5b.jpg"">" the morphology of thrombi depends on the location of the thrombi  arterial thrombi is usually caused byendothelial injury  turbulence  coronary  cerebral  femoral occlusive  venous thrombi is caused bystasis  lower extremities perioprostatic pelxis difference between arterial and venous thrombiarterial is usually due to a blockage where venous is usually due to blood now flowing enough (like sitting too much)  where does venous thrombi usually occurlower extremities mural thrombis is where wall of heart  due to arrhythmias or MI  a MI causes what kind of thrombi morphologymural wall where are lines of zahn seenantimortum thrombus what are lines of zahnlayers of platelets, fibrin and RBC's can you get thrombi formation in a dead person yes but it is a passive process  lines of zahn  how do lines of zahn appear very organized fates of a thrombuspropogate embolize dissolute  recanalization what does it mean when a thrombus propogates accumulates platelets and fibrin what does it mean when a thrombus embolizes dislodges and transports to other sites  what does it mean when a thromus dissolutes removed by fibrinolytic activity  what does it mean for when a thrombus is recanalized it is incorporated into the wall leading to form a new lumen  how does a pulmonary embolism occurwhen a clot breaks off and travels to the venous system where it will end up stuck in a vein in the lung  can be very dangerous what is disseminated intravascular coagulation or DICwhen clots form throughout the entire body how does DIC progressstarts off by having too many clots but then turns into an issue of not having enough platelets to make a clot so can cause life threatening bleeding  is DIC a primary disease no it is usually due to something else  what can cause DIC birthing complications  sepsis GSW what is an embolustravels through the blood stream like a clot that usually shouldnt be  pulmonary embolis is usually created by a thrombi in the lower extremeties  where does pulmonary embolus originate fromdeep leg veins  what is a saddle emboluspulmonary embolus goes up right ventricle and pumps in pulm artery and it just sits there and that is fatal what does a saddle embolus result inright sided heart failure secondary to pulmonary problem what does it mean for PE to be clinically silentmost of us probably have had one in our lifetime but our fibrinolytic systems break them down so it is not an issue where do systemic thromboembolism travel withinarterial circulation  where do systemic thromboembolism originate fromcardiac mural thrombi what happens in systemic thromboembolismclot in walls of the heart breaks off and eventually travels systemically because thats how blood works and those embolus can end up in a variety of sites what does fat embolus result fromfractures of long bones  tibia and femur how does fat embolus occurwhen bone fractures it exposes the bone marrow and there is a lot of fat in the bone marrow which now gets into circulation and that does a lot of damage  why does a fat embolus result in anemiaRBC break apart when get to fat  a fat embolus can result in small areas of hemmorage in what part of the brainwhite matte r what are the ways to get an air embolusscuba diving (bends) and oral sex (nice) how does scuba diving cause air embolusperson goes in deeper depths that puts pressure on body which results in tissues resorbed by tissues and if person ascends too quickly the nitrogen precipitates into tissue which is not good why can oral sex cause air embolusamniotic membrane is semipermeable to air so the air might be put into vaginal wall that makes it way into placental membranes to cause embolus how is an amniotic fluid emblus createdduring a rough delivery of a fetus tearing of placental membrane and tearing uterine veins to seperate from tissues  what is the danger of the amniotic fluid embolusif pulmonary vessels break off they can release squamous cells, fat and mucin which is dangerous for the maternal blood supply  dyspenia cyanosis shock and coma amniotic fluid embolus is complicated by DIC what is the difference between an infarct and infarctioninfarction is the process and infarct is indicating some kind of cell death  infarcts result in area of necrosis  what are infarcts caused byocclusion of arteries or veins  what are common locations of infarctbrain heart  lungs  bowel what shape are many of the infarcts in the lungs wedge shaped  apex of wedge is where clot originated from red infarcts are associated with what occlusionvenous ovaries and testes  two types of infarcts red and white infarcts why are the ovaries and testes subject to red infarctsthose organs are pedunculated and can twist and can cut venous blood supply. blood can get there but cannot be removed and it builds up  where could red infarcts be seenloose tissues  dual circulation tissues congested tissues  places where there is new reestablisment of blood from from prebious sites  white infarcts are due to what occlusionarterial  where are white infarcts seenin solid organs where the tissue limits the amount of hemorrhage that seeps into the area of ischemic necrosis form adjoining capillary beds like the heart spleen and kidney why are they called white infarctsaretery is occluded margins of an infarct become better defined with time if the person survives  if the infarct is so severe and they die immediatley they will not be able to mount an inflammatory response in time coagulative necrosis most common type of infarct seen in the heart and kidney  liquefactive necrosis is often seen here brain what type of vascular supply is more susceptible to infarct single supply  dual can shunt  what does a quick developing infarct result in prominent infarct if it is gradual they might develop collateral circulation in order to bypass the infarct what are the cells that are vulnerable to hypoxianeurons and myocardial cells what types of cells can survive longer without oxygenskeletal how does oxygen in blood cause infarctif someone is anemic and doesnt have enough RBC there wont be enough O2 delivery CHF what causes shock hypoperfusion of organs  what can cause shockdecreased cardiac output  decrease in blood volume from bleeding out vasodilation (hypotension)  cellular hypoxia types of shockcardiogenic hypovolemic neurogenic anaphylactic  what is cardiogenic shockmyocardial pump failure  infarction what is hypovolemic shockloss of blood plasma  hemorrhage or trauma what is neurogenic shockspinal cord trauma what is anaphylactic shockhypersensitivity response  most common type of shockcardiogenic  arrhytmia or infarction so organs cannot get blood shock that results from hemorrhage or trauma hypovolemic shock that results from myocardial pump failure cardiogenic what type of shock results from spinal cord trauma neurogenic  what type of shock results from hypersensativity response anaphylactic allergic reactionanaphylactic  chain reaction vasodilation and hypoperfusion  septic shock is due to what kind of bacteriagram negative  produces endotoxin in bacterial wall like LPS why is the LPS and other endotoxins released by gram negative bacteria so dangerous the LPS can trigger TNF and cytokine cascade  result in vasodilation and lack of perfusion and damage endothelial cells (coagulation cascade)  what complicates septic shock DIC how does LSP trigger cascade LPS  TNF  IL-1 IL-6 and 9 NO and PAF  inflammation, systemic effects and septic shock NO and PAF in low quantites gives monocyte and macrophage activation endothelial cell activation  complement acitvation local inflammation NO and PAF in moderate quantities can givefever  acute phase reactants from the liver systemic effects NO and PAF in high quantites is defined byseptic shock  low cardiac output low peripheral resistance  ARDS in lungs  local inflammation is associated with what level of quantities of NO and PAF`low  what level of quantities of NO and PAF is assocaited with systemic effects moderate quantities what level of quantites of NO and PAF are associated with septic shock high  stages of shocknonprogressive progressive irreversible stage of shock associated with BP drops but body compensates nonprogressive stage of shock associated with tissue hypoperfusion with worsening of circulatory and metabolic imbalanesprogressive  stage of shock associated with severe cellular and tissue injuryirreversible stage morphology of shock in brainbrain is energy hungry so it is very susceptible to shock so get ischemic encephalopathy morphology of shock in heartcoagulation necrosis subendocardial hemorrhae  morphology of shock in the kidneystubular ischemic injury  oliguria  anuria electrolyte disturbances morphology of shock in the lungdiffuse alveolar damage morphology of shock in the GIT mucosal hemorrhages morphology of shock in the liver fatty change  necrosis  anuriano urine output  if GI doesnt have a good blood supply what will happen will bleed  damages  what do t lymphocytes mediatecellular immunity these t lymphocytes secrete cytokinesCD4 helper cells these T lymphocytes kill virus infected cells and tumor cells to cytotoxicityCD8 suppressor cells T lymphocytes make up how many of the peripheral lymphocytes 60 to 70%  B cells make up how many of the peripheral lympocytes 10 to 20%  what do b cells formlymphoid follicles  what do b cells mediate humoral immunity location of b cells lymph nodes white pulp of spleen  these form plasma cells which produce immunoglobulinsb cells function of macrophages present antigens to T cells to induce cell mediated immunity what do macrophages produce cytokines what do macrophages do to tumor cells lyse them  macrophages are important in what delayed hypersentitivtiy reactions where are dendritic cells lymphoid tissue where are langerhan cells epidermis  what do dendritic and langerhan cells doantigen presentation to the T cells What do NK cells do recognize and destroy severly distressed or abnormal cells  NK cells make up how much of peripheral lymphocytes 10 to 15% What kind of cells do NK cells target severly distressed or abnormal ones do not want those one propogating which can lead to malignancy what CD are associated with NK cells CD 16 and CD 56  what do NK cells secrete cytokines  activates macrophages what happens to cell when it successfully binds to inhibitory and activating receptor of NK cell"no lysis  <img src=""paste-7d8fb7879cb0985edaf4d02afd05d49b2f38636f.jpg"">" what happens to a cell when it binds to the activating receptor of an NK cell but not the inhibitory receptor "Lysis  <img src=""paste-7d8fb7879cb0985edaf4d02afd05d49b2f38636f.jpg"">" what would a tumor cell be lacking that allows an NK cell to cause it to lysean inhibitory receptor what does a B cell recognize microbe what does a helper T cell recognizemicrobial antigen presented by APC  what does a cytotoxic T cell recognizeinfected cell presenting microbial antigen what are the functions of B cells neutralization of microbe  phagocytosis  complement activation what is the function of helper T cells activation of macrophages  inflammation killing of infected cells this is all triggered by cytokiens released by the Helper T cell what is the function of the cytotoxic T cells killing of infected cell what cytokines mediate natural immunityIL-1  TNF IL-6  interferons  what cytokines regulate lymphocyte growth activation and differentiation IL-2  IL-4 IL-12  TGF B what cytokines are chemotactic factors IL-8 what cytokines activate inflammatory cells TNF  what cytokines stimulate hematopoiesis IL-3 IL-7 where are complements produced in the liver  when are complement proteins released during inflammation  complements are part of white immune response innate function of MHA or HLAto display peptide fragments of protein antigens for recognition by antigen specific T cells  genes encoding HLA are present on which chromosome6 what does it mean that HLA system is very polymorphicgives differences. this is the reason we have match issues to organ transplants we have different HLA alleles that makes us differ form others  HLA class I lociHLA-A HLA-B HLA-C HLA class 1 are present where almost all nucleated cells and platelets  what do HLA class I do restricts action of cytotoxic CD8 T cells  HLA Class II lociDP DQ DR  HLA-D subregions  where are HLA class II mostly found monocytes  macrophages B cells T cells (some)  T cells proliferate in response to foreign class II HLA what does HLA class II do to CD4 helper cells restricts the action What do HLA class III do components of the complement system what cell response does organ transplantation evokehumoral and cell mediated MS, Lupus and Hashimotos are examples of what class of HLA diseaseclass II what is the benefit of HLA and autoimmune diseaes since HLA are genomic sequences, we can screen for these diseases since we know where they are and what to look for  however this might be not great since all the diseases do not have cures so its kinda depressing what are autoimmne diseasesbody lacks self tolerance  immune system acts against slef tissue autoimmune diseases immune reactions against what self antigen how many organs does lupus involvemany what are the genetic factors of lupus HLA-DR HLA-DR3 HLA-C2 HLA-C4 HLA-DEF what can cause symptoms of lupus drugs and UV light  lupus patients have deficiencies in what compliment C2 and C4 what kind of anti antibodies are involved with lupus anti DNA so that is why there are many organs affected  what is vasculities which is seen in patients with lupus inflammation of blood vessels  what does lupus often involve rahses and diffuse erythematous macules  exacerbated by UV what does lupus do to the heartpercarditis and libman sacks endocardidtis where can you really see lupus labratoryin histological pictures of the epidermis can see that DNA antibody RA usually affects whowomen in their 30s or 40s  where does RA start small joints of the hands and feet  what is seen with RA it is a chronic disease that shows proliferation of the synovium but has acute inflammation due to neutrophils  sinoviumlining of joints  seen in proliferation of RA what is the pannus formation in RAhistocytes plasma cells and lymphocytes in the spaces of the joints  what is the rhematoid factor autoantibodies against Fc portion of IgG Rheumatoid factor are autoantibodies against Fc portion of what antibodyIgG what is sjogrens syndrom characterized bydry eyes and mouth  from destruction of salivary and lacrimal glands  how does sjogrens syndrom happenexocrine glands are infiltrated by T cells and that damages the glands and the function of glands  dry eyes and mouth sjogrens syndrome increases the abiltiy to develop what lymphoma what should you think when you see sclerosisa hardening of somethign  systemic sclerosis causes fibrosis of what the skin GIT heart and lungs  what causes systemic fibrosis fibroblasts produce a large amount of collagen  what is raynauds phenomenonwhen the vasulature of hands doesnt perfuse as well so hands become pale and numb what is systemic sclerosis associated with CREST syndrome calcinosis Raynaud phenomenon esophageal dysmotility sclerodactyly telangiesctasia what is agammaglobulinemia of brutonx linked disorder that is a virtual absence of b cells due to abnormal maturation  agammglobulinemia is absence of what kind of cells B cells  what happens during agammaglobulinemia of bruton recurrent infections: bronchitis, pneumonia and skin infections  why can someone with agammaglobulinemia of bruton handle pathogens like fungi or viruses because AGB only affects B cells so the remaining T cells can still properly deal with fungi and viruses just not bacteria as well what cell is variable in DiGeorge syndrome T cells  what is characterized in DiGeorge syndrome developmental delay facial dymorphism hypoparathroidism congenital heart defects  what are the 2 forms of retrovirus of AIDS HIV-1 and HIV-2  what can AIDS give rise to opportunistic infections secondary neoplasms and neurologic problems  how is AIDS spreadsexual contact what does AIDS targetimmune system and CNS can AIDS be spread from mother to newbornyes  what is the morphology of HIV spherical retrovirus with 2 strands of RNA  core proteins  reverse transcriptase  glycoproteins  how is HIV internalized and integrated into cells glycoprotein 120 of HIV binds with CD4 cells and macrophages  what part of HIV allows it to attach to cells glycoprotein 120 why is the core of HIV important includes a variety of enzymes like reverse transcriptase integrase and protease to propogate virus  what cell receptor does glycoprotein 120 interact with CCR5  what serves as the resivoir of HIV monocytes and macrophages  what are likely the mode of transmission of HIV to the central nervous systemmonocytes  normally what is the ratio of CD4 and CD8 cells normally there are more CD4 than CD8 cells  in HIV what is the ratio of CD4 and CD8 cells more CD8 than CD4 inversion  why is the inversion of the ratio of CD4 to CD8 cells bad CD4 is the source of things like IL-2 and IFN and other chemotactic factors and when you lose them you lose the ability to put up an immune response  HIV antibodies are detected how long after exposure 3 to 17 weeks  what is the incubation period of HIV 2 to 8 years  HIV is represented by a CD4 count of less than 200  why is the 2 to 8 year incubation period of HIV significant becasue most of the time HIV patients are intially asymptomatic but still have the ability to transmit HIV even though they do not know it  screening is recommended even for people who do not think they have it  why is it that people do not realize they have HIV for so long the latency period for HIV is a slow burn so the CD4 cells will decrease slowly and go unnoticed but what is the issue is when the CD4 is so low now opportunistic diseases before that go unnoticed due to healthy immune system are now ravishing the body how does HIV affect the brainaseptic meningitis encephalitis leukoencephalopathy dementia complex what is encephalitis inflammation of brain tissue leukoencephalopathywhite matter degredation can HIV affect any organ in the bodyyes  sometimes may be more specific to one system why is the transmission rate of HIV during oral sex lowbecause it requires a break in the musoca how is HIV transmitted sharing of needles anal and vaginal sex transfusion of blood products  vertical transmission from mother to child in utero or during breastfeeding  can someone get HIV from a needle stickyes  but transmission is very low  what are the neoplasms (tumors) associated with AIDSkaposi sarcoma CNS lymphomas immunoblastic lymphoma systemic lymphomas (burkitt)  primary effusion lymphoma squamous cell carcinoma why are there so many neoplasms associated with AIDS people with AIDS have no immune system and our bodies continue to fight off neoplasm causing pathogens everyday so once the defense is down it is open season on the body disorder of the mouth with AIDS herpes and thrush disorders of the lungs with AIDS pneumonia disorders of the large intestine with AIDScolitis and proctisis  disorders of the kidneys with AIDS focal flomerulosclerosis  disorders of the skin with AIDS dermatitis and folliculitis  what is thrushyeast infection of candida accumulates  califlower ear is due to a degredatino of what cartilage  who is most likely to get califlower ear wrestlers, MMA fighters, boxers  can also be seen in child abuse cases  what part of the ear is affected in califlower ear external what is malignant external otitisnecrotizing inflammation of the external ear canal  what is malignant external oitits caused by pseudomonas bacteria  what types of people are malignant external otitis seen in people with diabetes melitus or are immunocompromised what can malignant external otitis lead to meningitis what bone can malignant external otitis spread to temporal bone  why can malignant external otitis lead to meningitisas it leaks through the bone it may find its way to the brain and the meningies are the covering of the brain  what does malignant external otitis require to treat potential debris removal and aggressive antibiotic treatment what is otitis media often caused bybacteria  strep penumoniae or haemophilus (acute) what occurs in chronic otitis media recurring infections result in drainage from the ear drum and tympanic membrane perforates  common in young children what is chronic otitis media often seen in young children "their eustacian tube connected ear to mouth is horizontally oriented and if feeded, they might have problems draining because of the horizontal position of the tube  <img src=""paste-e9853dee88a8dccedf99d792454b77a65c227559.jpg"">" what is seen in a swolen tympanic membranethe membrane is bright red when it should be more pink  tense (fluid building up and pushing membrane outward)   what is cholesatomamass of material comprised of keratin and cholesterol crystals that expands in middle ear  what causes cholesteatomagrowth of squamous epithelium into the middle ear through a perforated tympanic membrane. those squamous cells produce keratin  cholesteatoma is often infected by bacteria  where can cholesteatoma erode intobone  what is cholesteatoma seen in people who experience explosions explosion changes air pressure in short amount of time and that strikes ears and perforates tympanic membrane  what does a cholesteatoma look like pearly white mass what kind of disorder is otosclerosis autosomal dominant  most common cause of hearing loss in young adults otosclerosis  what causes hearing loss due to otosclerosisin your ear there are little bones that transmit sound waves to brain to be interpreted and otosclerosis causes bone deposition around the stapes which fuses those three bones together and your ear can no longer transmit info to the brain otosclerosis causes bone deposition around which bone stapes  most common neoplasms of the middle ear after squamous cell cancer paragangliomas can skin cancer affect ear yes  skin around ear is exposed to UV which gets cancer  what are mengiomas benign tumors of the lining of the brain what bone could the meningiomas arise from petrous bone  where in the ear can meningiomas invade middle ear  acoustic neuroma is a benign tumor of which cranial nerve 8 vestibulocochlear  if someone has a paraganglioma what would an otoscopy reveal vascular mass behind the eardrum  is a paraganglioma fast or slow growing slow  are paragangliomas benign or malignantmost are benign but some are malignant and can metastasize why are removals of paragangliomas dangerousthey tend to bleed a bit what does a paraganglioma look like nest of round to oval cells with clear or granular eosinophilic cytoplasm seperated by delicate vascular septae little pleomorphism and scant mitoses are indicitive of what kind of paragnagliomabenign acoustic neuroma arises from what cells schwann cells does acoustic neuroma occur in one or two ears usually one  unilateral  when does acoustic neuroma peak5th and 6th decades how can acoustic neuroma cause vertigogait and balance is also centered in middle ear  what is the issue with benign acoustic neuromas even though those tumors a benign they may cause increased intracranial pressure with nausea and vomiting  why might someone with acoustic neuroma have a palsy or weakness in face "because there is not much room to grow in the space where an acoustic neuroma grow so it can put pressure on the adjacent nerves like the facial nerve  <img src=""paste-b3581acae9c4435e27203195863f6e607d252c38.jpg"">" rhinitis is inflammation of what the nose  rhinitis is commonly from what originviral  chronic forms are often allergic in origin if pt presents with rhinitis few years on and off might not be viral and instead is an allergic reaction  is rhinitis treatablenot if it is viral but there is allergy medication if chronic inflammatory polyps are unusually before what age 20  in children inflammatory polyps may indicate what cystic fibrosis  the edematous stroma of the inflammatory polyps are filled with what plasma cells and eosinophils large inflammatory polyps can result in difficulty breathing what types of cells usually line inflammatory polyps"columnar cells  <img src=""paste-980cc36a63869b3788f538bac1366179567ba9b3.jpg"">" plasma cells have what kind of positioning in terms of their nucleus eccentrically located what is the new name for granulomatosis granulomatosis with polyangiitis  granulomas forming and inflammation in various blood vessels what can granulomatosis with polyangiitis result innecrotizing infections in the sinus  can affect hard and soft palate of the mouth why can wegeners granulomatosis cause gangreneaffect blood vessels in extremeties  what is positive c-ANCAanti neutrophil cytoplasm test to test for wegeners  what can wegeners do to the lungsproduce big areas of necrosis in the lungs  see cavity what does it mean that sinonasal papilloma is benign but locally aggresive although benign it can grow into the adjactent structures like nasal space what type of cells compose the sinonasal papillomasquamous or columnar epithelium what virus has been identified in lesions of sinonasal papillomaHPV 6 and 11 suggest infectious eitiology to this three types of sinonasal papillomaexophytic inverted cylindrical what is the most clinically significant type of sinonasal papillomainverted  which can recur and extend into the orbit or cranial vault what does sinonasal papillomas present withepistaxis or a mass nose bleed  sinonasal papilloma is seen with whoolder men sinonsasal papilloma may recur if notcompletely excised how do the squamous cells grow in inverted sinonasal papillomainward fasion  why is inverted sinonasal papilloma the most dangerous or problematicthat is the one that tends to grow into bone and orbit and facial bones which can be more problematic than the other ones  what does olfactory neuroblastoma arise fromneuroectodermal olfactory cells in the mucosa when does olfactory neuroblastoma peak15 and 50 bimodal age distribution what does olfactory neuroblastoma look likesmall blue round cells forming nests surrounded by vascular connective tissue  what does the prognosis of olfactory neuroblastoma depend on stage and grade like most cancers  what are the treatment options for olfactory neuroblastomachemotherapy surgery radiation why do olfacotry neuroblastoma have large blue nuclei"they have very little cytoplasm scant <img src=""paste-b08167fd17bfccb529011c113a5c3c1b19f4e92d.jpg"">" what are the peak ages of nasopharyngeal carcinoma20 and 65 what virus is nasopharyngeal carcinoma associated with Epstein Barr Virus  what does nasopharyngeal carcinoma present with nasal obstruction epistaxis unilateral lymph node metastasis  what does it mean when nasopharyngeal carcinoma can be clinically occult for long periodsmay remain clinically insignificant and not obvious  what is a marker for nasopharyngeal carcinomapositive epithelial membrane antigens  standard treatment of nasopharyngeal carcinomaradiotherapy close to brain so challenge to treat what does nasopharyngeal carcinoma look like histologically"syncytium like clusters of epithelial cells with abundant lymphocytes  <img src=""paste-5bdf7e22c4a469a903ae8af3047963319ab63bd6.jpg"">" what is angiofibromamass consisting of fibers tissues and blood vessels why does angiofibroma usually happen in adolescent males because it is androgen dependent so typically occurs in adolesecent males when they start to hit puberty and testosterone levels rise  what is angiofibroma comprised of mixture of blood vessels and fibrous stroma  why is angiofibroma tough to remove very vascular tumor and if you remove can result in blood loss  death can occur form hemorrhage and intracranial extension acute epiglottitis is an infection with what h influenze  what is acute epiglottitis characterstic lookred swollen epiglottis why does acute epiglottitis cause obstruction of airwaythe epiglottis is the punching bag at the back of you throat that prevents food from going into airway when eating. It is usually thin and not a problem but grows in size when inflammed what would you see in someone wit hacute epiglotitis excessive salivartion  appears apprehensive what is important in treating someone with acute epiglottitis do not move their neck too much cuz that can result in occlusion what does the epiglottis look like "positive thumb sign  <img src=""paste-112b80d761c68b8da2a6a2d929450689af5bed0a.jpg"">" people with contact ulcers present wit hwaht symptoms of hoarsness, dysphagia and pain what is dysphagia (seen in contact ulcers of the larynx)painful swallowing or painful eating  what can cause contact ulcers of the larnyxvocal cord abuse shouting  intubation (more commonly) coughing bilateral laryngeal nodulesingers nodule  unilateral laryngeal nodule vocal cord polyps  how can laryngeal nodules happenvocal cord abuse  think from pitch perfect what can laryngeal nodule result in stromal edema with fibroblast proliferation who is laryngeal carcinomas most common in men over 40 what is laryngeal carcinoma linked to smoking  HPV is becoming an increasingly important risk factor  what kind of cell cancer is laryngeal carcinomasquamous cell cancer what is becoming an increasingly important risk factor for laryngeal carcinomaHPV what is laryngeal carcinoma usually preceded by varying degrees of dysplasia how does laryngeal carcinoma appeargrossly as gray ulcerating plaques, red or white focal thickening of the tissue  what does laryngeal carcinoma present as hoarsness how many of the cases of laryngeal carinoma are fatal1/3

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