Term
| Potential vascular changes and circulatory disturbances |
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Definition
-oedema
-hyperaemia
-congestion
-haemorrhage
-thrombosis
-embolisation
-infarction
-shock |
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Term
| What are the 5 mechanisms of oedema formation? |
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Definition
1. changes in vasc. permeability
(associated w. inflam!)
2. increased hydrostatic P
(associated w. inflam!)
3. Decr. plasma oncotic P (hypoproteinaemia)
4.Lymphatic obstruction
5. Sodium retention |
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Term
| What can cause an incr. in vasc. permeability that results in oedema? |
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Definition
-usually seen in inflam and involves an exudate (or transudate if mild)
e.g.vasculitis, allergic reaction (serous inflam)
-toxins, chemicals or infectios agents that may damage the endothelium |
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Term
| What can cause an incr. in hydrostatic P that results in oedema? |
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Definition
-occur w. inflam (hyperaemia - incr. blood flow)
-occur w. congestion i.e. passive accumulation of blood |
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Term
| What can cause an congestion as a cause of incr. hydrostatic P that results in oedema? |
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Definition
-local congestion - due to impaired venous drainage e.g. blocked (thrombus) or due to external P (e.g. tumour, bandage)
-generalised w. congestive H failure (backward P as blood that is not pumped forward backs up) |
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Term
| How does reduced plasma oncotic P / hypoproteinaemia result in oedema? |
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Definition
-lowers the osmotic P of blood
-fluid moves into interstitial tissues |
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Term
| What can cause reduced plasma oncotic P / hypoproteinaemia that results in oedema? |
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Definition
-loss of protein -via kidneys (protein losing nephropathy PLN) / gut (protein losing enteropathy) - may have parasitic cause PLE)
-dietary protein deficiency or cachexia e.d. severe wastage, where proteins used for E
-dec. albumin synthesis due to liver dz.
-water intoxication |
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Term
| Why does lymphatic obstruction result in oedema? |
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Definition
| -excess fluid in the vasc. compartment is unable to enter the lymphatic system |
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Term
| In lymphatic obstruction is oedema generally localised or generalised? |
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Definition
| localised - due to a focal/local obstruction of lymphatic(s) or LN(s) |
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Term
| What can cause lymphatic obstruction that results in oedema? |
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Definition
-trauma, incl. surgery
-malformations
-inflam of lymphatics or LNs
-neoplasia |
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Term
| How does sodium retention result in oedema |
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Definition
| -incr salt (and obligated incr. water) causes an incr. hydrostatic P (incr. volume) and decr. colloid osmotic P (due to dilution) |
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Term
| What causes sodium retention which results in oedema? |
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Definition
-any acute reduction in renal function e.g. acute renal failure, glomerulonephritits
-over-consumption of salt esp. w. ltd water - brain adapts to dehydration in the short term but on rehydration the brain cannot pump ions out fast enough and so fluid enters brain due to osmosis
- |
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Term
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Definition
INCREASED BLOOD FLOW
-active process
-incr. inflow of blood due to arteriolar dilation |
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Term
| What is hyperaemia usually associated w.? |
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Definition
-inflam or exposure to heat
-also physiologically e.g. exercise |
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Term
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Definition
IMPAIRED OUTFLOW OF BLOOD
-passive
-vessels become dilated and engorged w. blood
-can be local or systemic |
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Term
| What is chronic passive congestion? |
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Definition
| stasis of poorly oxygenated blood |
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Term
| What is the consequence of chronic passive congestion? |
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Definition
chronic hypoxia and so cell degeneration or death
e.g. nutmeg liver in chronic heart failure |
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Term
| What is hypostatic congestion? |
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Definition
Congestion caused by gravity
e.g. recumbency. Incl. anaes. esp LA |
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Term
| Purpose of normal haemostasis? |
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Definition
-ensure blood is maintained in fluid, clot-free state
-induces rapid formation of localised haemostatic plug at site of vasc. injury to arrest bleeding |
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Term
| What does normal haemostasis involve? |
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Definition
-vasc. wall and endothelial contraction
-platelets to form haemostatic plug
-coagulation cascade
-fibrinolysis to limit clot size |
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Term
| How is the vascular wall involved in haemostasis? |
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Definition
Prothrombotic if injured (hence inflam results in haemostasis!)
-endothelium constricts
-platelets adhere to ECM (via release of vWF)
-coagulation stimulated (TF synthesised by endot)
NB: normally endothelium is antithrombotic:
-blocks platelet adhesion
-interferes w. coag. cascade |
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Term
| How are platelets involved in haemostasis? |
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Definition
-form haemostatic plug
-plug small defects in b.v. and promote coag.
-adhere to ECM via vWF bridge (become activated)
-secrete granules containing Ca++ (required in coag. cascade) and ADP (mediates platelet aggregation)
-expose surface phospholipid complexes (used in coag. cascade)
NB: WBCs and RBCs also adhere to platelets and endothelium |
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Term
| How is the coagulation cascade involved in haemostasis? |
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Definition
-results in thrombin formation
-thrombin converts fibrinogen --> fibrin
-thrombin converts XII --> XIIa
-XIIa converts fibrin --> cross-linked fibrin i.e. fibrin clot |
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Term
| How is fibrinolysis involved in haemostasis? |
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Definition
-development of fibrin clot must be restricted to site of injury - fibrinolysis limits clot size and dissolves the clot post-healing
-generates plasmin from plasminogen
-plasmin breaks down fibrin --> FDPs |
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Term
| Describe normal haemostasis |
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Definition
-initial injury to b.v. wall
-transient vasoconstriction
-primary haemostasis - haemostatic plug formation
-secondary haemostasis - coag. cascade
-thrombus and anti-thrombotic events i.e. regulatory mechanisms to limit haemostasis to site of injury |
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Term
| Describe primary haemostasis |
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Definition
i.e. haemostatic plug formation
-exposure of ECM allows platelets to adhere to it and become activated. Therefore further adhesions etc. |
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Term
| Regulation of haemostasis |
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Definition
-coagulation inhibitors e.g. antithrombin III
-fibrinolytic inhibitors e.g. plasminogen activation inhibitor |
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Term
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Definition
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Term
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Definition
-occurs w. abnormalties in factors affecting haemostasis
-usually due to b.v. rupture or damage e.g. inflam, degen, necrosis, tumour invasion, trauma
-also rupture of weakened b.v. e.g. aneurysm
-passive congestion (rupture due to incr. P)
-failure to clot
-some toxins may interfere w. coagulation e.g. warfarin
-some inf. dz. damage endothelium e.g. black leg, blue tongue, canine inf. hepatitis, leptospirosis
-some deficiencies cause haemorr e.g. vit C causes collagen defect (guinea pigs) or vit K (needed in many factors) |
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Term
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Definition
-Petechiae: pinpoint haemorr.
-Ecchymoses: haemorr. spots <3cm
-Haemorr. into body cavity e.g. haemothorax
-Haematoma: blood +/-clotted blood in tissues (forms tumour-like enlargement) |
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Term
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Definition
| Inappropriate/pathological activation of haemostasis leading to formation of thrombi |
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Term
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Definition
-Aggregation of platelets, fibrin, WBSc, RBCs within the CVS, following inappropriate activation of haemostasis.
-Always have point of attachment
-can be anywhere in CVS incl. heart valves, aa, vv, capillaries |
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Term
| Difference between thrombus and clood clot |
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Definition
Clots do not form in flowing blood and so are not pathological
Thrombi are pathological |
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Term
| Thrombi predisposing factors |
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Definition
-ENDOTHELIAL INJURY - loss of endothelium / dysfunction endotheliun
-altered BF - turbulence / stasis
-hypercoagulability |
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Term
| How does endothelial injury predispose to thrombus formation? |
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Definition
Loss of endothelium
e.g. from endocardial surface w. cardiomyopathy / due to injury (e.g. Strongylus vulgaris, catheter placement)/ inflam
Dysfunctional endothelium
i.e. altered balance of pro-thrombotic factors |
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Term
| How does altered blood flow predispose to thrombus formation? |
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Definition
Turbulence - causes endothelial injury and pockets of static blood
Stasis - causes incr. viscosity e.g. dilated atria, aneurysms, cardiac insufficiency, polycythaemia (incr. RBC) |
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Term
| How does hypercoagulability predispose to thrombus formation? |
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Definition
-primary i.e. genetic
-secondary / acquired e.g. ATII deficiency w. glomerular or liver dz |
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Term
| Arterial / cardiac chamber thrombi |
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Definition
-usually at site of endothelial injury / turbulence
-red(mostly RBCs)/grey (platelets and fibrin), can be laminated i.e. lines of Zahn (indicates at site of blood flow, not stasis)
-usually, but not always, occlusive |
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Term
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Definition
-usually red (more RBCs c.f. arterial) and no laminations
-can be v. long
-almost always occlusive |
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Term
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Definition
-usually occur w. valve damage e.g. bact/fungal inf.
-can be sterile in hypercoag. states |
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Term
| Poss sequelae to thrombosis (if patient survives!) |
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Definition
-dissolution: recent thrombi are removed by fibrinolysis and macrop. (must be before extensive polymerisation of fibrin)
-propagaton: thrombus accumulates fibrin and platelets and obstructs b.v.
-embolisation: thrombus / fragments dislodge and travel elsewhere
-organisation and recanalisation: BF may re-establish via new capill. and/or organised thrombus may contract |
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Term
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Definition
-obstructs b.v. (esp. imp. if no collateral supply)
-source of emboli
e.g. saddle embolus in cats (lodge in terminal aorta / iliac trifurcation resulting in paralysis of hind limbs. Usually due to HCM but also DCM and RCM) |
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Term
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Definition
| -a detached, intravasc. solid / liquid / gas mass that is carried by blood to a site distant from its origin |
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Term
|
Definition
| -area of ischaemic necrosis, caused by occlusion of art. supply or venous drainage |
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Term
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Definition
-usually thrombotic or embolic
-can be due to compression of b.v. e.g. tumours, torsion of b.v. (e.g. LI volvulus in horse) |
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Term
| Gross description of infarct |
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Definition
-usually wedge-shaped in parenchymal organs w. occluded b.v. at apex
-may be red i.e. haemorrhagic (due to b.v. damage and back flow into tissue) or if spongy tissue (i.e. lung, spleen)
-may be white i.e. anaemic (due to art. occlusion of end aa. / haemolysis) or if in solid tissue where P can force blood out |
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Term
| What do consequences of an infarct depend on? |
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Definition
-if collateral supply
-speed of development of occlusion (if slow, less likely to cause infarction as alternative perfusion may develop)
-vunerability of tissue to hypoxia (neurons, myocardium v. sensitive and damaged in mins, c.f. fibroblasts rel. insensitive and can tolerate hrs of ischaemia)
-oxygen content of blood (if low partial pressure of oxygen then even only partially occluded b.v. can cause infarction) |
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Term
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Definition
Circulatory collapse w. marked hypotension, which causes hypoperfusion and so hypoxia
- cells therefore shift to anaerobic metabolism, and so get cell. degen. and death if unresolved |
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Term
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Definition
-decr. CO (cardiogenic shock) or circulating BV (hypovolaemic shock)
-inappropriately low peripheral vasc. resistance (vasculogenic shock) |
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Term
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Definition
| Blood or fluid loss leads to decr. BV (>10% loss results in shock) |
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Term
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Definition
| in heart failure, inadequate blood is pumped around the vasculature |
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Term
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Definition
Decr. peripheral R and so peripheral blood pooling
Incl. septic (usually endotoxic), neurogenic (e.g. SC injury) and anaphylatic (generalised HS rection w. vasodil and incr. vasc. perm). |
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