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151 Cards in this Set
- Front
- Back
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pinpoint hemorrhages up to 1 mm
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petechia
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hemorrhages up to few cm, paint brush apearance
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ecchymosis
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petechia and ecchymosis on mucus membranes
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purpura
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causes of hemorrhage
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*local factors affecting blood vessels
*systemic factors affecting either vessels or the blood |
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Primary effects of hemorrhage
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*rapid blood loss can lead to shock
*hemorrhage may form space occupying lesion with disastrous consequences |
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secondary effects of hemorrhage
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1. resorption of fluid
2. erythrocytes lysed 3. fibrinolysis 4. potential scarring |
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hyperemia and congestion
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*defined as an increase in the amount of blood in the vasculature in a given part of the body due to local vascular dilation
**hyperemia is an active process; primarily due to arteriolar dilation **congestion is a passive process; primarily due to venous engorgement |
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causes of hyperemia
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*active dilation of arterial channels
*physiologic *inflammation |
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causes of congestion
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*decrease in venous return with pooling of blood in tissue
--mechanical --cardiac failure --gravity |
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effects of congestion
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*relative hypoxia or complete anoxia
*hemorrhage *thrombosis *edema *fibrosis |
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Types of congestion
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*acute passive: sudden occlusion of vessels leading to congestion +/- severe anoxia
*chronic: long standing interference which does not cause complete ischemia --local --generalized |
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causes of congested liver
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interference with blood flow into or through the right heart
1.right heart failure 2.valvular insufficiency or stenosis 3.obstruction of blood flow through lung 4.obstruction of posterior vena cava |
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congested liver appearance
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*enlarged with rounded edges
*dark red to purple with prominent architecture or "nutmeg" appearance *pathogenesis:centrilobular hypoxic cell injury with loss of hepatocytes and fibrosis |
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congested lung
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*causes:interference with blood flow through the left heart due to valvular insufficiency or stenosis
*left ventricular failure *leads to pulmonary edema; if longstanding there may be pulmonary fibrosis with hemosiderosis (heart failure cells) |
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congested spleen
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common incidental finding after barbiturate euthanasia
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hypostatic congestion
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*ante or post-mortem gravitational settling of blood in tissues
**post-mortem **can occur in recumbent animals, e.g. during surgery or in debilitated animals |
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edema
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*edema- accumulation of watery fluid in extravascular spaces
*tissue are swollen and pit *excess fluid separates tissue planes |
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types of edema
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Effusion:clear low protein
Transudate:more protein Exudate:even more protein/cells often inflammatory |
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generalized edema
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*cardiac edema- venous congestion with Na and water retention resulting in increased blood volume and increased hydrostatic pressure
*renal failure- urinary protein loss leading to decreased oncotic pressure *hepatic failure or malnutrition/malabsortion- leading to decreased plasma oncotic pressure |
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localized edema
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*venous obstruction- elevated intravascular hydrostatic pressure
*lymphatic obstruction- decreased fluid drainage from tissues *inflammatory edema- increased vascular permeability |
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cerebral edema
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*hypoxia/hyperthermia- swelling results in compression of medulla and death
*herniation of the vermis is present |
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hemostasis
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defined as the termination of blood loss from the vasculature
**delicate balance of pro and anti coagulant mechanisms maintains normal hemostasis |
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trombosis
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formation of a solid adherent blood clot (thrombus) within the lumen of a vessel or the heart
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events in hemostasis
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*vasoconstriction- transient neurogenic reflex
*platelet plug- platelets adhere to damaged endothelial cells or collagen and adhere to one another (aggregation) *coagulation- enzymatic cascade involving pre-formed clotting factors in blood |
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coagulation system mechinism
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*intrinsic and extrinsic systems converge at factor x
*enymatic cascade |
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stuff in platelets
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*integrin membrane receptors, p selectin
*arachidonic acid: esp. thromboxane A2 *alpha granules: fibrinogen, fibronectin, factors V & VIII, thrombospondin, PDGF & TGF-B *electron dense bodies: ADP, Ca, histamine, serotonin & epinephrine |
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platelet activation
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1. adhesion and shape change
2. aggregation 3. secretion (release reaction) |
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platelet adhesion
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von Willebrand's factor binds subendothelial collagen, platelets bind von Willebrand's factor via gplb surface integrins
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platelet aggregation
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*ADP and thromboxane A2 promote platelet aggregation; producing the temporary or primary hemostatic plug
*thrombin production promotes further aggregation and polymerizes fibrin; producing the definitive or secondary hemostatic plug |
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platelet aggregators
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*ADP and thromboxane A2
*thrombin *collagen *epinephrine *immune complexes *platelet activating factor |
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platelet secretion
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*both alph and dense granule contents are secreted
*ADP promotes platelet aggregation *Ca is an important coagulation cofactor *phospholipid complex on platelet surface forms that binds and activates clotting factors |
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fibrinogen binding by platelets
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*ADP activated platelets bind fibrinogen via gpIIb, IIIa; which links platelets with adjacent platelets promoting further aggregation
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procoagulant properties of endothelium
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1. stimulation of platelet aggregation
*a. von Willebrand's factor *b. synthesized by enodthelial cells *c. links platelets to collagen via gpIb 2. production of procoagulant factors 3. inhibition of fibrinolysis |
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Procoagulant factors
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*endothelial cells express tissue factor in response to cytokines to cytokines and endotoxin
*endothelial cells have binding sites for activated clotting factors *endothelial cells produce platelet activating factor |
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Inhibition of fibrinolysis
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tissue type plasminogen activator inhibitor
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control of clotting overview
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*blood stasis favors clotting: activated factors are not swept away
* local control of clotting **antithrombins **proteins C & S **plasminogen-plasmin system |
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Anticoggulant properties of endothelium
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1. covers thrombogenic subendothelial collagen (surface glycocalyx)
2. inhibits platelet aggregation 3. inhibits thrombin 4. fibrinolysis 5. a2 macrogloblin- cleans up clotting factors |
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Inhibition of platelet aggregation
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*PG12 & NO
-formed by endothelial cells -potent vasodilators -inhibit platelet aggregation |
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inhibition of thrombin
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*heparin-like surface molecules activate antithrombin III, which inactivates thrombin (and others)
*thrombomodulin binds activated thrombin and this complex activates proteins C and S, which cleave activated clotting factors |
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Antithrombins
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*Antithrobin III is the prototype, others: C1 esterase inhibitor, alpha 1 antitrypsin alpha 2 antiplasmin
*AT III activated by binding heparin-like surface molecules on endothelial cells *activated antithrombin III inhibits actions of activated clotting factors 2 & 10 |
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Proteins C & S
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*vitamin K dependent
*activated by binding the thrombomodulin/thrombin complex on endothelial cells *inhibit activated clotting factors V & VIII |
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fibrinolysis
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endothelial cells synthesize tissue type plasminogen activator which promotes fibrinolysis
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plasminogen-plasmin system
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*plasminogen present in plasma and platelet membranes
*plasminogen binds fibrin, then is cleaved by plasminogen activators to form plasmin *plasmin digests polymerized fibrin |
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plasminogen activation
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1. tissue type plasminogen activator, produced by activated endothelial cells
2. urokinase like plasminogen activator, present in plasma |
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plasminogen activation inhibitors
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*endothelial cells also make factors that inhibit binding of fibrin by tissue type plasminogen activator
*effect depends on balance of endothelial secretion of activators and inhibitors *alph 2 antitrypsin: circulating factor that inhibits fibrin binding of plasmin |
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Disseminated intravascular coagulation
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thrombohemorrhagic disorder characterized by widespread activation of clotting mechanisms with consumption of platelets and clotting factors, activation of fibrinolysis, and widespread hemorrhage
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causes of disseminated intravascular coagulation
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1. infection
2. trauma 3. Neoplastic disease |
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pathogenesis of disseminated intravascular coagulation
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*massive release of tissue factor or thromboplastic substances into the circulation
*widespread endothelial injury |
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disseminated intravascular corgulation mechanism w/ gram negative sepsis
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1.endotoxin induces expression of tissue factor in monocytes and macrophages
2.these cells also secrete IL-1 and TNF which induces tissue factor expression in endothelial cells 3.IL-1 and TNF also upregulate binding of WBC to endothelium by production of oxygen radicals 4. widespread activation of clotting in microvasculature 5. widespread activation of fibrinolysis 6.platelets and clotting factors are consumed 7. fibrin degradation products inhibit further platelet aggregation and fibrin polymerization 8.terminal microvascular hemorrhage |
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von willebrand's disease
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*lack of this factor and associated loss of factor VIII documented in over 50 breeds of dogs, cats and horses
*the most common inherited bleeding disorder in animals *von willebrand's factor binds VIII and prolongs factor VIII lifespan in circulation |
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A bleeding disorder common in basset hounds, simmental cattle, otterhounds, foxhounds, and scottish terriers. Caused by miscellaneous defects in a certian cell type.
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platelet defects
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some common causes of acquired thrombocytopenia are?
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1.infectious diseases: Rickettsial Diseases
2.Immune mediated 3.Disseminated intravascular coagulation 4.neoplasia |
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What is hemophilia A?
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bleeding disorder of the intrinsic coagulation system. It is sex linked and results in a factor VIII deficiency in cats and dogs, males bleed
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What is hemophilia B?
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Bleeding disorder of the intrinsic coagulation system. It is sex linked and causes a deficiency in factor IX in cats and dogs, males bleed
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A factor VII deficiency in beagles is an example of what kind of bleeding disorder?
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bleeding disorder of the extrinsic coagulation system
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Which clotting factor has the shortest half life?
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factor VII
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What is coumarin poisoning?
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inhibition of vitamin K dependent factor generation (2,7,9,&10). Sources are rodent baits and moldy clover forages. Also called D-con poisoning
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Is thrombosis a normal component of hemostasis?
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No, thrombi are caused by normal clotting mechansims, but control is lost and excessive or inappropriate clot forms
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Define thrombosis
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formation of a solid adherent blood clot (thrombus) within the lumen of a blood or lymph vessel or the heart
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What is a chicken fat clot?
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post mortem clot; incidental, not a lesion. It is not attached to endothelium
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What are the 3 types of clots?
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1.normal clots
2.thrombi 3.post mortem |
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What are the 3 parts of virchow's triad for the pathogenesis of thrombosis?
how many of the 3 parts do you need for a likey occurance of a thrombus |
1.damage to vessel wall and endothelium
2.changes in the blood itself (hypercoagulability) 3.hemodynamic and rheological(flow) changes *need two parts |
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What are some causes of damage to vessel wall or endothelium?
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1.vasculitis: viral and rickettsial diseases, septicemia, toxemia and uremia
2.Endocarditis: bacterial colonization of valves 3.Disseminated intravascular coagulation 4.Trauma, burns, surgery 5.Depositional injury: diabetes, amyloidosis, atherosclerosis |
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What are some causes of increased coagulability?
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1.severe trauma, burns ,surgery
2.Malignant neoplasia 3.acute infections with septicemia 4.Disseminated intravascular coagulation 5.pregnancy and periparturient period 6.hyperadrenocorticism |
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What are some causes of alteration in blood flow which predispose an animal to thrombosis?
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1.congestive heart failure or valvular lesions
2.stenosis or aneurysmal dilation 3.compression |
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T/F arterial thrombi are more common than venous thrombi.
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F, venous flow is more sluggish and more likely to have stasis, turbulence or sluggish flow
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What do arterial thrombi look like?
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usually pale and dry, firm but frialbe; composed of fibrin and platelets in alternating bands
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What do venous thrombi look like?
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often large, dark red, soft, gelatinous and shiny;contain many entrapped RBC
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What are the 4 fates of thrombi?
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1.propagation:occurs on surface of existing thrombus in direction of blood flow
2.Fibrinolysis:digestion of fibrin polymer by plasmin 3.organization and recanalization:by macrophages, fibrolasts and endothelial cells 4.embolism:portion breaks off, "sails down" vessel and lodges |
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what are some different types of common emboli
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1.thrombi
2.hair 3.fat 4.cartilage 5.neoplastic cells 6.bacteria 6.air 7.pharmaceutical suspensions |
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Emboli often produce ______
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infarcts
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define infarct
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name given to a localized area of tissue necrosis caused by ischemia
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define infarction
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the name given to the process of in farct formation
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T/F infarction from arterial blockage is more common than venous blockage
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T
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What are some common causes of vessal blockage
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1.thrombi
2.emboli 3.vasospasm 4.external compression |
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put theses sets of oragns in order of most susceptibility to least suceptibility to be damaged from infarction:
A)skeletal muscle, viscera B)lung, liver C)brain, renal cortex, heart |
1.C)brain, renal cortex, heart:these oragans have single vessel perfusion
2.A)skeletal muscle, viscera: these organs have a parallel system 3.B)lung, liver: these organs have a dual blood suppply |
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What is the appearance of an infarct
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1.irregularly shaped
2.sharply demarcated 3.peripheral zone of hyperemia 4.raised or depressed 5.anemic or hemorrhagic |
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what causes anemic or pale infarcts?
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arterial occlusion results in little blood in tissues
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what are some causes of hemorrhagic infarcts?
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1.early infarcts
2.venous occlusion 3.tissue with dual circulation(liver, lung) 4.previously congested tissues 5.venous infarcts |
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old infarcts are composed of _____tissue which appears paler than adjacent tissue
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scar
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What are the 3 ways in which neutrophils cause damage to host tissue?
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1.lysosomal suicide
2.frustrated phagocytosis 3.regurgitation while feeding |
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T/F chemical mediators of inflammation are deactivated or opposed by other products present in the inflammatory response
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T, natural inhibitors exist in plasma
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what are the 3 plasma derived chemical mediators of inflammation?
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1.Hageman factor
2.complement components 3.kininogens |
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What plasma derived mediator of inflammation is activated in the first step of intrinsic coagulation cascade by negatively charged surfaces
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Hageman factor
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Hageman factor initiates generation of what 4 processes?
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1.clotting
2.fibrinolysis 3.kinin generation 4.complement cascade |
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What are the actions and types of kinins involed in inflammation
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Bradykinin is prototype, luekokinins alos important
actions: vasodilation, increased vascular permability, and pain |
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complement pathways converge at ____, leading to formation of the "membrane attack complex"
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C3
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Classic complement pathway is initiated by __________.
Alternative complement pathway is iniatiated by _________________. |
Classic complement pathway is initiated by _immune complexes__.
Alternative complement pathway is iniatiated by _contact with fungal and bacterial cell walls or prarsite cuticle_. |
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complement fragment actions>
C3b and C3bi are good ______. C3a and C5a are ___________. C1 and C4 help _________ virus when titers are low |
complement fragment actions>
C3b and C3bi are good _opsonins__. C3a and C5a are _anaphylotoxins_. C1 and C4 help __neutralize_ virus when titers are low |
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What do C3a and C5a anaphylotoxins do?
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1.nonvascular smooth muscle constriction
2.increase vascular permeability 3.cause mast cell degranulation (histamine release) 4.activate WBC: lipoxygenase, degranulation, phagocytosis, adhesion, chemotaxis |
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What are the 2 cell derived pre formed mediators of inflammation and what do they do?
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Histamine and serotonin
they are stored in mast cells, basophils and platelet granules. They are released by allergens that bind IgE, C5a and C3a, snake and insect venoms. They cause vasodilation, increased vascular permeability , and nonvascular smooth muscle contraction |
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What are the cell derived newly synthesized mediators of inflammation and where do they come from?
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arachidonic acid derivitatves (autocoids). There formation is stimulated by cytokines, chemotatctic peptides, and many others. They are formed by phospholipids acting on cell membranes
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What are the 2 pathways of arachidonic acid derivitaves (autocoids)
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1.cyclooxygenase
2.lipoxygenase |
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Which cox is induced in inflammation
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cox-2
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How do glucocorticoids inhibit inflammation?
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glucocorticoids induce lipocortin expression which inhibits phospholipase and cox-2
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cyclooxygenase products:
What does prostacyclin (PG12) do |
vasodilation, inhibits platelet aggregation
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cyclooxygenase products:
What does thromboxane A2 do? |
vasoconstriction, promotes platelet aggregation
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cyclooxygenase products:
What do prostaglandins D2, E2, F2 alpha do? |
vasodilation and promote edema
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What are cyclocooxygenase products?
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prostaglandins and thromboxanes
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What produces leukotrienes?
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lipoxygenase
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Lipoxygenase:
What do 5-HETE and LTB4 do? |
chemotaxis, enhances adhesion, degranulation, ROS generation
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Lipoxygenase:
What do leukotrienes C4, D4, and E4 do? |
also known as slow release substance of anaphylaxis and cause: vasoconstriction, bronchospasm, and increased vascular permeability
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pmn
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Polymorphonuclear leukocytes (neutriphils)
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How are lipoxins made?
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transcellular biosynthesis; requires physical contact between pmn and platelet. pmn LTA4 acted on by platelet enzymes to produce lipoxins; LX-A4 and B4
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What do lipoxins do?
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decrease pmn adhesion and chemotaxis and promote monocyte adhesion
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What does platelet activating factor do in inflammation?
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It is a lipid derived from most inflammatory cells and is a very potent mediator, can produce all the cardinal signs of inflammation
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Reactive oxygen species are produced by activated _________ and increase _______ and activate ________. ROS cause damage to microbes as well as the _________
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Reactive oxygen species are produced by activated __phagocytes__ and increase _vascular permeability_ and activate _neutrophils_. ROS cause damage to microbes as well as the _host_
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What are the 2 isoforms of Nitric Oxide?
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Constitutive (homeostasis function) and Inducible (infammation)
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what is the difference between constitutive and inducible nitric oxide isoforms?
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Constitutive: are regulated by Ca, have intermittent activity, and produce picomoles of NO.
Inducible: is regulated by expression, has sustained activity, and produces micromoles of NO |
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location of constitutive and inducible forms of Nitric oxide
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Constitutive: endothelium, neurons, adrenal gland, cardiac myocytes, pancreatic islets and more.
Inducible: macrophages, hepatocytes, chondrocytes, vascular smooth muscle, and many more. |
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Expression of inducible nitric oxide synthase is up regulated by______________________ and down regulated by ________________
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up regulation of: bacterial products, IL-1, TNF alph, IFN gamma.
Down regulation: TGF beta, IL-4, IL-10 and glucocorticoids |
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What organsims are susceptible to Nitric oxide?
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mycobacteria, staphylococcus, many fungi, leishmania, trypanosoma, plasmodium and schistosoma
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What are the 5 cytokine classes?
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1.regulate lymphocytes: IL-2, 4, 10
2. natural immunity: TNF, IL-1, IL-6 3. activate inflammatory cells: IFN, TNF 4. stimulate hematopoiesis: IL-3,5,7 CSFs 5. chemokines |
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What are the 4 types of chemokines
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1. C-X-C(alph) act on pmn and IL-8
2.C-C (beta) cells other than pmn; MCP-I eotaxin 3.C (gamma) act on lymphocytes 4. C-X3-C bound on endothelial surface; chemotactic and adhesive for monocytes and lymphocytes |
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cytokines:
_______ and _______ increase leukocyte adherence and procoagulant potential of endothelium. _ produced by macrophages and other cells, strongly chemotactic for neutrophils |
IL-1_ and _TNF_ increase leukocyte adherence and procoagulant potential of endothelium.
_IL-8_ produced by macrophages and other cells, strongly chemotactic for neutrophils |
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What is the acute phase response?
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survival oriented response that may occur in bouts of either acute or chronic inflammatory disease. Term used to describe either: patholphysiologic and behavioral changes hat occur in illness, or plasma proteins whose concentrations change by greater than 25% in adaptive response to illness
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acute phase response is largely mediated by what?
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cytokines: IL-1, TNF, and IL-6
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What are the outcomes of acute inflammation?
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1.complete resolution
2.scarring 3.abscessation 4.chronic inflammation |
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chronic inflammation is associated with persistent or recurrent injury often persistent_________stimulus
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antigenic
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What is the hallmark of chronic inflammtion?
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neovasculariztion and fibrosis
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What is the key cell type in chronic inflammation?
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macrophage: produces pro-inflammatory, immunomodulatory and fibrogenic mediators
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Cells type in chronic inflammation is primarily mononuclear but when it includes neutrophils it is called?
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chronic active
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What is the most important facotr that must occur from chronic inflammation?
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macrophage accumulation through continued recruitement (C5a, chemokines, growht factors, fibrin degradation products)
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In chronic inflammation feedback/ cytokine cross talk between macrophages and lymphoid cells promotes _________ _________
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lesion formation
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The form of chronic inflammation in which epitheliod macrophages predominate is called?
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granulomatous inflammation ( may be in sheets admixed with other cells types, ie pyogranulomatous, eosinophilic granulomatous, lymphogranulomatous)
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discrete aggregate of epithelioid macrophages with mantle of lymphoid cells and peripheral fibrosis is called?
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granuloma/ may also have central necrotic debris, mineralized debris, multinucleate giant cells
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what are 2 types of granulomas?
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1.Foreign body: formed in response to indigestible material; keratin , hair, plant material
2. immune granuloma: persistent antigen with T-cell response |
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What are the 2 types of healing and repair?
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1.parenchymal regeneration
2.replacement by fibrous tissue |
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When does replacement fibrosis occur?
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1.stromal framework is destroyed
2.permanen cell population is damaged 3.exudate cannot be reabsorbed |
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What are labile cells?
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cells which ordinarily have high turnover in life
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What are stable cells?
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cells which have low mitotic activity , but are capable of rapid replication
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What are permanent cells?
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terminally differentiated and incapable of mitotic acticity
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What are the function of platelet derived growth factor?
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1. chemotactic
2.mitogenic 3.stimulates glycosaminoglycan and fibronectin synthesis |
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What are the functions of transforming growth factor and fibroblast growht factor?
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Matrix:
fibrolast mitogens, collagen, glycosaminoglycan and fibronectin synthesis, FGF induces collagenase activity |
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What is the function of macrophage derived growth factors?
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fibroblost proliferation, angiogenesis, wound contraction
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What is the function of vascular endothelial growth factor?
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potent angiogenic factor
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Granulation tissue provides proliferation of fibrovascular tissue that:_____________________________________________
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fills tissue defect and provides framework for elaboration of fibrous tissue
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What are the 3 phases of granulation tissue formation?
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1.inflammatory phase: inflammatory response initiates healing process
2.proliferative phase: rapid growth of delicate fibrovascular tissue 3.remodeling phase: collagen fivers are replaced and reorganized, vasculature regresses |
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What are the 3 main cells of granulation tissue?
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1.macrophages: remove exudate, secrete fibrogenic and angiogenic factors
2.Fibroblasts: lay down collagen matrix, myofibroblasts have contractile activity reducing wound volume 3.endothelial cells: provide vascular supply |
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What are the 6 phases of wound healing?
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1.inflammation
2.cell migration 3.matrix deposition 4.vascular proliferation 5.collagen synthesis 6.remodeling |
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What are the 2 types of wound healing?
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first intention:wound edges opposed, rapid healing with minimal scar tissue
second intention: defect filled with granulation tissue, prolonged course, potential for signigicant scarring |
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define keloid
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too much scar tissue during healing
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What is proud flesh?
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excess granulation tissue
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What are some adverse outcomes of healing?
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1.adhsion
2.ankylosis:bones fixed together 3.stricture:scar around lumen 4.contracture:limb 5.critical tissue replaced by fibrous tissue |
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What autosomal recessive disease has sign these signs abnormal gray hair coat, cyclic neutropenia, 11 day periodicity, defect in neutrophil maturation, severe recurrent bacterial infections, and death by one year of age
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canine cyclic neutropenia
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what gentic defect is a result of substitution of one base which results in defective CD 18 beta chain of Mac 1. Severe neutrophilia in face of tissue demand. Oral ulcers, pneumonia, diarrhea and is a lethal trait
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bovine leukocyte adhesion deficiency
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What disorder is common in arabian and quarterhorses. Has recurrent pyogenic bronchopenumonia, and septicemia and the cause is unknown
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selective IgM deficiency
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Usually highly virulent organisms with adhesion/invasion strategy invade ______________ while opportunsists of low virulende usually enter the body to cause infection through _________
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Usually highly virulent organisms with adhesion/invasion strategy invade __GI, Respirtory, genitourinary__ while opportunsists of low virulende usually enter the body to cause infection through _disonctinuites in the skin_
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the sensing of endotoxin requires what 3 things?
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1.LBP
2.CD 14 recptor 3.toll-like receptors |
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what is the difference between bacteremia and septicemia
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bacteremia is bacteria in the blood. Septicemia is systemic disease associated with the presence oand persistence of pathogenic microoraganisms and their toxins in the blood
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What is the arthus reaction?
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Large quantities of antigen and antibody preciptating in cutaneous vessel walls resulting in necrotizing cutaneous vasculitis and hemorrhage; occurs following injection of antigen when there is high level of circulating antibody
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