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87 Cards in this Set
- Front
- Back
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What is active hyperaemia? Give an example of when this happens. |
Engorgement of vessels due to increased inflow of blood (vesselse dilate). May happen in exercise or inflammation. |
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What causes active hyperaemia? |
Pre-capillary sphincter relaxation |
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What is passive hyperaemia (congestion)? When might this happen? |
Engorgement of vessels due to decreased outflow, resulting in build up of deoxygenated blood. May happen with a blockage or obstruction to flow. |
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What can localised passive hyperaemia eventually result in? |
Hypoxic necrosis of tissue |
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What is the main cause of generalised venous congestion? What happens here? |
Congestive heart failure - Heart fails to work properly and blood pools behind congestion. |
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What circulation is most effected by left-sided heart failure? |
Pulmonary circulation |
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What circulation is most effected by right-sided heart failure?
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Hepatic (or jugular) circulation |
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What are the main causes of congestion? |
Generalised: Faulty valves, damage to muscle, compression, neoplasia. Localised: Compression is a large cause. |
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Name 2 heart valve disorders. |
Endocardiosis Endocarditis |
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Give an example of a disease which effects heart muscle. |
Hypertrophic cardiomyopathy (in cats) |
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How can the heart become suppressed? |
Pericardium fills with fluid e.g. blood, pus. |
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What is "hardware" disease, and what species does it primarily effect? |
Traumatic reticulitis carditis - Cows may eat sharp objects which lodge in reticulum and may penetrate reticulum and diaphragm upon contraction, this releases microbes into the pericardium. Neutrophils, fibrin etc. build up and collagen forms, making contraction difficult. |
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How does congestion of the lungs appear grossly? |
Acute - Dark red and heavy Chronic - Brown(ish) |
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How does congestion of the lungs appear microscopically? |
Capillaries appear congested (many RBC) Haemosiderin present in macrophages in alveoli. |
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How does congestion of the liver appear grossly? |
Acute - Enlarged, dark red Chronic - "Nutmeg" appearance pattern |
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What is the gross appearance of a congested spleen? |
Enlarged, dark red (euthanasia and anthrax) |
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What is the appearance of post-mortem congestion? |
Gravity-dependent redenning (white at pressure points) livor mortis |
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Define oedema. |
Accumulation of fluid in interstitium or body cavities. |
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What are the two main types of oedema and what do they involve? |
Inflammatory oedema: High protein, high cells. Produces exudates (cells) Non-inflammatory: Low protein, low cells. Produces transudate (blood) |
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What intermediates are present that fit neither of the two main categories of oedema? |
High protein modified transudate High cell modified transudate |
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How can a protein exit the lumen of blood vessels? |
Vesicular transport by endothelial cells. |
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What factors are included in retaining fluid in the circulation? |
Plasma osmotic pressure (Na+, proteins) Selectively permeable endothelium |
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What factors retain fluid in the interstitium and body cavities? |
Hydrostatic pressure of interstitium Osmotic pressure in the interstitium |
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What are the two main factors that cause oedema? |
An imbalance in the fluid-retaining factors Blockage of the lymphatic flow |
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What 5 things can result in an imbalance of fluid, resulting in oedema? |
Reduced plasma osmotic pressure Increased capillary permeability Increased capillary hydrostatic pressure Increased osmotic pressure in interstitium Reduced lymphatic drainage |
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What can cause a decrease in plasma osmotic pressure and how does this happen? |
Loss/decreased synthesis of plasma proteins Loss - malnutrition, parasitism, diarrhoea, renal disease Synthesis - liver disease |
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What can cause increased capillary permeability and how? |
Endothelial damage (e.g. by toxins, chemicals) Inflammation (vasoactive substances) |
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What can cause increased capillary hydrostatic pressure? |
Increased venous pressure Decreased venous outflow Vasodilation in inflammation |
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What is the name given to fluid build up in the abdominal cavity? |
Ascites |
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What is the name given to fluid build up in the thorax? |
Hydrothorax |
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What is the name for oedema that gathers where gravity is drawing it? |
Dependent oedema |
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What is a haemorrhage and how is it caused? |
Escape of blood from vessels - caused by some sort of damage to blood vessels (e.g. trauma, rupture) |
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What is another name for haemopericardium (haemorrhage in pericardium)? |
Cardiac tamponade |
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What is the name given to a haemorrhage in tissue? |
Haematoma (bruise) |
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What is the name given to a haemorrhage coming from the nose? |
Epistaxis (but can be from anywhere e.g. pulmonary) |
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What happens to blood that enters the stomach (normally via inflammation or ulcer)? What is this called? |
Blood is partially digested and blackens - Malena (in faeces)
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What is haematemesis? |
Vomiting fresh blood Passing melena in faeces(?) |
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What are the terms given to the haemorrhage that causes fresh blood to be passed in faeces? What is the difference between these? |
Dysentry - Diarrhoea containing blood. Haematochezia - Formed stools with blood on surface |
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What is haematuria? |
Blood in urine |
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State the 3 names given to different sized haemorrhages, indicating their size. |
petechiae - "pin-point" ecchymoses - 1-3cm Suffusive/"paint brush" - anything larger |
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What type of haemorrhage is primary haemostasis often associated with? |
petechiae |
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What type of haemorrhage is secondary haemostasis often associated with? |
ecchymosis Suffusive/"paint-brush" |
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Give some examples of how an endothelium may be directly or indirectly damaged to cause haemorrhage? |
Direct: Septicaemia, toxaemia Indirect: Immune complexes, vasculitis |
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What may cause failure of clotting, thus haemorrhage? |
Haemophilia Anti-coagulants Consumption coagulopathies |
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Briefly describe primary haemostasis. |
Local vasoconstrction Platelets adhere to sub-endothelial matrix Endothelial cells release vWF vWF forms bridges between sub-endothelial collagen Platelet release reaction (dense bodies, alpha-granules) GP-IIb and IIIa binds fibrinogen, linking platelets in loose aggregate Dense platelet plug |
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Which factors are involved in the extrinsic, intrinsic and common pathways for secondary haemostasis? |
Intrinsic: XII, XI, IX, VIII Extrinsic: III, VII Common: X, V, II, I |
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Which factor activates prothrombin to thrombin? |
X |
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What does thrombin (serine protease) do in secondary haemostasis, and what happens finally to form a stable fibrin clot? |
Activates fibrin from fibrinogen as well as factor VIII to form factor VIIIa. Factor VIIIa then acts on the fibrin to form a stable clot. |
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Which factors are vitamin K dependent? Which pathways does this affect? |
XI, VII, X and II - All pathways |
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What pathway does an activated partial thromboplastin time (APTT) test examine? |
Intrinsic secondary haemostasis pathway (time to clot). |
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What does a Prothrombin time (PT) test examine? |
Extrinsic secondary haemostasis pathway (time to clot).
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What does a CBC test look at? |
Platelet concentration |
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What tests only the common pathway in secondary haemostasis? |
Activated clotting time |
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What does buccal mucosal bleeding time (BMBT) examine? |
Primary haemostasis |
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What does EDTA, fluoride-oxolate and citrate do? |
Binds divalent calcium, stopping the coagulation cascade. |
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What does heparin do? |
Potentiates antithrombin III |
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What is factor II? |
Thrombin |
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How is coagulation in areas other than that affected prevented? |
Anti-thrombins and thrombin-modifiers (e.g. antithrombin III, heparin). |
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What do endothelial cells release to cleave fibrin? What inhibits this? |
Active plasmin Inhibited by plasminogen activator inhibitors (restrict plasminogen activation) |
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Name 3 disorders of secondary haemostasis? |
Haemophilia Liver damage Vitamin K deficiency |
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Name 4 disorders of primary haemostasis? |
Thrombocytopenia (reduced platelets) Thrombocytopathy (impaired platelets) Septicaemia/Toxaemia Von Willebrand disease |
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What does disseminated intravascular coagulation ultimately result in? |
Ischaemia and haemorrhage |
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What is thrombosis? |
Inappropriate coagulation in uninjured vessel/heart. |
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What is Virchow's triad? |
1. Change of inner surface of vessel (endothelial injury) 2. Change in normal pattern of blood flow 3. Change in blood constituents (hypercoagubility) |
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Give some possible causes of endothelial injury. |
Turbulence Infections Toxins Inflammation Free radicals Injection Neoplasia |
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What can change blood flow? |
Vessel compression Cardiac disease |
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What can cause hypercoagulability? |
Increased number/adhesiveness of platelets Increased fibrin/clotting factor Reduced fibrinolytic activity Reduced antithrombin concentration |
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What does arterial/cardiac thrombi constitute? |
Non-occlusive Begin at endothelial injury/turbulence Grey, red lines - lines of zahn Left ventricle and valves most affected |
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What does venous thrombi constitute?
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Occlusive Start at stasis Red-blue Veins of distal limbs most affected |
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What will eventually happen to a thrombus? |
Dissolution Vessel obstruction Organisation and recanalisation Embolisation (fragments break away) Propogation (growth) |
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What is an embolus? |
And intravascular bolus carried away from site of origin and lodging elsewhere. |
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Name some types of embolism. |
Thromboembolism Fat embolism (e.g. bone marrow) Tumour Fibrocartilage (intervertebral disc) Parasites Bacterial/infectious Gas |
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Where are venous and arterial emboli normally lodged? |
Venous - pulmonary circulation Arterial - Aortic bifurcation (e.g. iliac arteries) |
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Which areas are most affected by a short period of anoxia by embolism? |
Heart, brain, kidneys |
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What can occlusion of an end artery result in? |
Ischaemic necrosis |
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What is ischaemia? |
Decreased blood flow |
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What can cause ischaemia? |
Thrombosis Embolism Compression Vasoconstriction Vasculitis |
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What is infarction? |
Death of tissues as a result of ischaemia. |
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What is a focal infarct? |
A blockage of a small terminal or artery, causing local infarction. |
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What is a global infarction? |
Blockage of larger, more proximal arteries causing more extensive infarction. |
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What can reperfusion injury result in? |
Free radicals |
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What is shock? |
State of tissue hypoperfusion? |
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What can cause shock? |
Reduced effective circulating volume Reduced peripheral vascular resistance |
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What are the three main categories of shock? |
Hypovolaemic Cardiogenic Blood maldistribution |
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What percentage of blood may be lost to cause hypovolaemic shock? |
More than 35% (less than 10% is fine) |
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What can cause cardiogenic shock? |
Heart attack |
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What may result from blood maldistribution? |
Anaphylaxis - mast cell degranulation Neurogenic - autonomic stimulation Septic - infectious organisms cause release of cytokines and such chemical mediators |
