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53 Cards in this Set
- Front
- Back
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What is meant by the terms active hyperaemia?
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increased blood volume within a tissue due to arteriolar dilation and expansion of the perfused capillary bed
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What is meant by the terms passive congestion?
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a passive process in which increased blood volume within a tissue results from impairment of venous outflow
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What is meant by the terms pulmonary hypertention?
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increased blood pressure within the pulmonary artery
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What is meant by the terms systemic hypertension?
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abnormally high systemic arterial blood pressure
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In what circumstances does active hyperaemia develop?
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an increase in tissue metabolism and oxygen consumption
●food ingestion → ↑d blood flow to gastrointestinal tract ●excercise → ↑d blood flow to skeletal muscle |
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In what circumstances does localised passive congestion develop?
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blood pooling withing venous channels and capillaries
●luminal obstruction of vein or external compression of eins ●intestinal strangulation due to torsion or volvulus ● hypostatic or dependent congestion (gravitational pooling of venous blood in dependent areas in recumbent or inactive animals) |
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In what circumstances does generalised passive congestion develop?
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●heart failure
●heperthermia ●shock left-sided congestive heart failure → venous blood pools in the pulmonary veins and alveolar capillaries of the lung right-sided congestive heart failure → venous blood pools in the venae cavae and especially the liver, spleen |
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How would you grassly distinguish between active hyperaemia and passive congestion of an organ or tissue in a live animal?
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Active
-red due to oxygenated blood -warm Passive -blue-red to blue-black due to engorgement of vessels with poorly oxygenated venous blood -cooler than normal Both -swollen -turgid -wet cut surface -concurrent oedema |
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What are the potential consequences of passive congestion of tissues of organs?
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●oedema formation
●diapedesis of erythrocytes from blood vessels into tissues ●capillary rupture with haemorrhage ●parenchymal cell degeneration or necrosis oand reparative fibrosis |
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What is the renin-angiotensin-aldosteron system?
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decrease in blood pressure leads to renin release from renal juxtaglomerular cells. Renin cleaves angiotensinogen to angiotensin Ⅰ. AⅠis then cleaved to AⅡ and AⅢ.AⅡ and AⅢ cause an increase in both the cirbulating blood volume and the total peripheral vasular resistance. AⅡ also stimulates release of anti-diuretic hormone to paromote water resorption by the kidneys
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What is meant by the terms active hyperaemia?
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increased blood volume within a tissue due to arteriolar dilation and expansion of the perfused capillary bed
|
|
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What is meant by the terms passive congestion?
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a passive process in which increased blood volume within a tissue results from impairment of venous outflow
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What is meant by the terms pulmonary hypertention?
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increased blood pressure within the pulmonary artery
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What is meant by the terms systemic hypertension?
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abnormally high systemic arterial blood pressure
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In what circumstances does active hyperaemia develop?
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an increase in tissue metabolism and oxygen consumption
●food ingestion → ↑d blood flow to gastrointestinal tract ●excercise → ↑d blood flow to skeletal muscle |
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In what circumstances does localised passive congestion develop?
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blood pooling withing venous channels and capillaries
●luminal obstruction of vein or external compression of eins ●intestinal strangulation due to torsion or volvulus ● hypostatic or dependent congestion (gravitational pooling of venous blood in dependent areas in recumbent or inactive animals) |
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In what circumstances does generalised passive congestion develop?
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●heart failure
●heperthermia ●shock left-sided congestive heart failure → venous blood pools in the pulmonary veins and alveolar capillaries of the lung right-sided congestive heart failure → venous blood pools in the venae cavae and especially the liver, spleen |
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How would you grassly distinguish between active hyperaemia and passive congestion of an organ or tissue in a live animal?
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Active
-red due to oxygenated blood -warm Passive -blue-red to blue-black due to engorgement of vessels with poorly oxygenated venous blood -cooler than normal Both -swollen -turgid -wet cut surface -concurrent oedema |
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What are the potential consequences of passive congestion of tissues of organs?
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●oedema formation
●diapedesis of erythrocytes from blood vessels into tissues ●capillary rupture with haemorrhage ●parenchymal cell degeneration or necrosis oand reparative fibrosis |
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What is the renin-angiotensin-aldosteron system? What triggers its activation and what are the consequences of its activation?
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System performed by the kidney to regulate blood pressure. Decrease in blood pressure leads to renin release from renal juxtaglomerular cells. Renin cleaves angiotensinogen to angiotensin Ⅰ. AⅠis then cleaved to AⅡ and AⅢ.AⅡ and AⅢ cause an increase in both the cirbulating blood volume and the total peripheral vasular resistance. AⅡ also stimulates release of anti-diuretic hormone to paromote water resorption by the kidneys
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What is a potential consequence of sustained pulmonary hypertension?
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development of cor pulmonale (
= pulmonary hypertensive herat disease) characterised by right ventricular dilation or hypertrophy and potentially right-sided hart failure |
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What are common causes of systemic hyper tension in cats and dogs?
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Secondary to another disease
-renal disease -hyperadrenocorticism -hyperthyroidism -obisity -liver disease etc... |
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What are the potential consequences of sustained systemic hypertension?
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high perfusion pressure can damage delicate capillaryies!
-capillary hypoxia, tissue damage, haemorrhage and tissue infarction with organ dysfunction -left ventricular concentric hypertrophy -blindness due to acute retinal haemorrhage -polyuria/dipsia -cardiac murmur -epistaxis(鼻血） |
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What is meant by the term oedema?
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accumulation of excess extracellular fluid in the interstitium and/or body cavities
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What are the major factors that control the movement of water (and electrolytes and other small solutes) between the interstitium and the microvasculature and normally prevent the development of oedema?
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Balance between two opposing forces
1.Forces promoting fluid movement from the plasma into the interstitium (plasma hydrostatic pressure & interstitial colloid psmotic pressure) 2.Forces promoting fluid movement from the interstitium into the plasma (plasma colloid osmotic pressure & interstitial hydrostatic pressure) The slight excess of fluid moving into the interstitium is removed via interstitial lymphatics and returned to the bloodstream via the thoracic duct |
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What is meant by the term ascites?
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=hydroperitoneum
accumulation of oedema fluid within the peritoneal cavity |
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What is meant by the term hydrothorax?
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accumulation of oedema fluid within the pleural cavity
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What is meant by the term hydropericardium?
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accumulation of oedema fluid within the pericardial sac
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What is meant by the term hydrocoele?
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acumulation of oedema fluid within the cavity of the tunica vaginalis of the scrotum
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What is meant by the term anasarca?
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severe, generalised oedema (oftern most prominently in the subscutis but with accompanying body cavity effusions)
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What are the five main mechanisms that can lead to oedema development?
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1. decreased plasma colloid osmotic pressure
2. increased plasma hydrostatic pressure 3. lymphatic obstruciton 4. increased vascular permeability 5. sodium retention |
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Which of five mechanisms provokes localised oedema?
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●increased plasma hydrostatic pressure
●lymphatic obstruction ●increased vascular permeability (as inflammatory oedema) |
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Which of five mechanisms can lead to generalised oedema and why?
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●decreased plasma colloid osmotic pressure
●increased plasma hydrostatic pressure ●sodium retention (●lymphatic obstruction:rare!) (●increased vascular permeability) |
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What gross features would allow you to recognize oedematous tissues or organs in the live or dead animal?
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●oedematous tissues are wet, shiny or glistening, swollen, heavy or rubbery, firm but doughy and they ooze fluid when incised
●oedematous organs have overall increase in size and weight and a bulging (腫れる) cut surface ●distended lymphatics may be visible over serosal surfaces of oedematous viscera and within adjacent mesenteries |
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What are the potential consequences of oedema?
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●impair wound healing
●promote wound dehiscence post-surgery ●susceptible to 2ndary bacterial infection ●fibroplasia & fibrosis ●cerebral & pulmonary oedema may be potentially fetal |
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What is meant by the term haemostasis?
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the sequence of events that follows vascular injury to rapidly produce a localised plug to prevent blood loss
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What are the key events in formation of the primary haemostatic plug following injury to a blood vessel?
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endothelial injury → exposure of highly thrombogenic subendothelial extracellular matrix → adhesion of platelets → activation of adherent platelets by collagen → release of products that cause recruitment of additional platelets to form a primary haemostatic plug
*collagen is the only matrix protein that promotes both platelet adhesion and activation |
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What is meant by the terms platelet adhesion?
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adhesion of platelets to a non-platelet surface
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What is meant by the terms platelet secretion?
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release of the contents of the alpha and dense granules and of lysosomes
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What is meant by the terms platelet aggregation?
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sticking of platelets to each other
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Why is von Willebrand's factor imprtant in primary haemostasis?
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without vWf, platelets will be dislodged from collagen by the high shearing forces of flowing blood in arteries and arterioles
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What are the key events in formation of the secondary haemostatic plug following injury to a blood vessel?
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injury to a blood vessel → formation of primary haemostatic plug → activation of coagulation cascade → generation of thrombin → further platelet aggregation & the conversion of fibrinogen to fibrin → formation of viscous metamorphosis under the influence of thrombospondin → viscous metamophosis and fibrin form secondary haemostatic plug
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What is meant by the terms intrinsic, extrinsic and common coagulation cascades?
What activates the intrinsic and extrinsic cascades? |
Intrinsic system & extrinsic system are the compartments of the coagulation cascade
●Intrinsic coagulation pathway involves components normally present in the circulation ●Extrinsic pathway is initiated by tissue factor; a membrane glycoprotein that is exposed following cell injury ●Common system is a final common pathway leading to fibrin formation |
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Which is considered to be more important in activation coagulation in vivo: the intrinsic or the extrinsic pathway?
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the extrinsic pathway which is the major route of activation of coagulation in vivo
the intrinsic pathway is not involved in the initiation of coagulation in vivo |
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Why can an animal be deficient in some intrinsic system coagulation factors and yet not be predisposed to haemorrhage?
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there are redundancies in the coagulation cascade because of connections between the intrinsic and extrinsic systems.
Factor Ⅸ is activated by both intrinsic and extrinsic pathway. Platelets also can activate factor ⅩⅡ and ⅩⅠ which are activated by the intrinsic system. |
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What are the major regulatory mechanisms that oppose haemostasis? are all of these mechanisms essential?
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●the antithrombin Ⅲ system
●the protein C and protein S system ●the tissue factor pathway inhibitor ●the fibrinolytic system each of these systems is essential for normal control of haemostasis and each controls different aspects of normal coagulation any imbalance → hypercoagulable state promoting thrombosis |
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What is meant by the terms fibrinolysis, fibrin degradation products, plasmin and plasminogen activators?
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●fibrionlysis=breakdown of fibrin
●fibrin degradation products= ●plasmin=enzyme that cleaves factor 5 & 8 and splits fibrin into fibrin degradation products ●plasminogen activators= activate plasminogen into plasmin, may be intrinsic or extrinsic |
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What is meant by the term thrombosis?
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formation of a pathological blood clot (thrombus) withing the cardiovascular system (ante mortem process, always intravascular and attached to the vessel wall)
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What are the three major mechanisms that predispose to thrombosis? Which of these is the most important predisposing mechanims?
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●endothelial injury
●absormal harmodynamics ●blood hypercoagulability Endothelial injury is the most important factor predisposing to thrombosisq |
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How does endothelial damage promote thrombosis?
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endo damage allows adhesion of platelets to the underlying extracellular matrix by means of von Willebrand factor. Injured endo cells lead to exposure of membrane-bound tissue factor which activates the extrinsic coagulation cascade.
Injury endothelial cells results in a procoagulant phenotype that augments local blood coagulation |
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How do blood turbulence and blood stasis predispose to thrombosis?
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●Both may disrupt laminar flow and sllow platelets and coagulation factors to contact endothelium, prevent dilution oand removal of activated coagulation factors by fresh flowing blood, retard arrival of coagulation factor inhibitors and permit build-up of thrombi, and promote activation of endothelium to a procoagulant state
●turbulence may directly damage endothelium ●blood stasis may produce local hypoxaemia promoting endothelial release of tissue factor to initiate extrinsic coagulation |
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In what circumstances does blood hypercoagulability develop?
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increased procoagulant factors or decreased inhibitory factors
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What is meant by the terms thrombus propagation, mural thrombus and occlusive thrombus?
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Thrombus propagation = gradual enlargement of the thrombus by additional coagulation occurring on its surface
Mural thrombus = intra-cardiac thrombi involving the wall of a heart chamber Occlusive thrombus = |
