Term
| Disturbances in Circulation (types) |
|
Definition
INCREASED BLOOD IN THE VASCULAR BED
1.hyperaemia
2.Congestion
DECREASED BLOOD IN THE VASCULAR BED
1.ischaemia
2.infarction
3.hemorrhage
4.shock
5.edema
6.thrombosis |
|
|
Term
|
Definition
The acute, active process by which increased numbers of RBC's in an area give the tissue a general redness and small arterioles and venuoles may stand out visually.
This may be physiological (blushing) or pathological (inflammation). |
|
|
Term
|
Definition
pooling of blood in a tissue due to obstructed flow of blood out of the tissues. It is caused by
1. physical obstruction - within or surrounding veins
2. failure of forward flow- failing heart. Blood accumulates in the tissues giving a dark red/blueish color. |
|
|
Term
|
Definition
1. localized congestion: local retriction of blood flow. Can be due to a thrombus or external pressure on the vein.
2. systemic venous congestion (generalized congestion): commonly seen in heart failure, blood dams back in the great veins.
3. Hypostatic congestion: lividity |
|
|
Term
|
Definition
If there congestion is gradual in onset, then there may be time for a collateral blood supply to be established = no effects. When passsive congestion (local or systemic) is chronic then effects may include:
1.edema
2.ischaemia
3.diapediesis (loss of whole RBC's through intact capillary walls) |
|
|
Term
| Morphology of congestive Heart Failure |
|
Definition
Left: there is an increase in pulmonary vascular pressure resulting in alveolar capillary walls becoming distended with blood. Edema and diapedesis occur and macrophages follows to clean up. They engulf the RBC's and hemosiderin is left in their cytoplasm = "heart failure cells"
Right: there is congestion in systemic vasculature, in particular the liver. a congested liver appears larger and darker in color and may have a mottled appearance = nutmeg liver. The build-up in pressure around the central veins eventually causes necrosis of the adjacent liver cells and fibrosis of the central veins (cardiac cirrhosis). Hemosiderin deposits in local macrophages may also be seen histologically. |
|
|
Term
|
Definition
| a condition of inadequate blood supply to an area of tissue relative to its needs. |
|
|
Term
|
Definition
in adequate blood supply results in:
1. hypoxia or anoxia
2. local nutrient deprivation
3. failure to remove waste products- the accumulation of metabolites is probably the cause of pain in ischaemic tissue. |
|
|
Term
|
Definition
1.cardiac arrest -ex. during anaesthesia (if longer than 4 mins = brain damage)
2.arterial obstruction:
a.thrombosis
b.embolism
c.arterial wall spasm -ergot poisoning
d.arteritis
e.occlusive external pressure -bandage
f.arterial occlusion- gastric volvulus
3.venous obstruction
4.capillary damage -bed sores
5.hypovolemia
6.severe vasodilation |
|
|
Term
| factors modifying the effects of ischaemia |
|
Definition
effects are those that are mediated by hypoxia or anoxia.
1.sensitivity to hypoxia -ie the brain
2.duration and speed of onset- faster and longer produce more effects
3.blood oxygenation state
4.temperature of the tissue- lower temps. lower metabolic rate and therefore O2 demand, thus lowering damage |
|
|
Term
|
Definition
| ischaemic tissue damage becomes worse when the blood supply is restored because restoration of oxygen to anoxic tissues results in free radical production which cause irreversible damage to the cells. In some cases neutrophils may be present which release cell mediators which further damage the tissue. |
|
|
Term
|
Definition
| a localized area of necrotic tissue that occurs as a result of ischaemia. Most are caused by obstruction of the arterial blood supply although venous infarcts can occur. Organs most affected:kidney, spleen, limbs, brain and intestines. Organs with dual blood supply (liver, lungs)seldom develop infarcts. |
|
|
Term
|
Definition
| following obstruction, hydostatic pressure is reduced and backward flow of venous blood results = acute infarcts are red. Hypoxia or venous and capillary walls results in fluid loss and sometimes hemorrhage. Evnetually the tissue becomes degenerate and necrotic with a good line or demarcation. Loss of tissue fluid and RBC's results in paler tissue with time. If the individual lives then macropages and neutrophils invade and a fibrotic scar is left. |
|
|
Term
|
Definition
bleeding from a transected or ruptured blood vessel or from the heart. It is caused by:
1.trauma
2.vascular disease
3.collagen defects- weak BV's
4.local high blood pressure- severe exertion
5.abnormal clotting mechanisms
Hemorrhage can be local (trauma) or diffuse (mucosal surfaces in clotting disorders) |
|
|
Term
|
Definition
| localized collection of blood, usually clotted that forms like a swelling in tissues |
|
|
Term
|
Definition
| very small hemorrhages up to 1-2mm (pin-prick hemorrhages) |
|
|
Term
|
Definition
| slightly larger foci of hemorrhage (paint-brush hemorrhages) |
|
|
Term
|
Definition
| a disease characterized by hemorrhages of the skin, mucous membranes and viscera. |
|
|
Term
|
Definition
1. local effects- small hemorrhages are little affect (per se). exception would be in the brain and brain stem. Larger hemorrhages can form "space occupying lesions" which can cause:
a.mechanical effects- hemopericardium
b.asphyixa
c.joint pain
2. systemic effects- depends on the total amount of blood loss and the speed at which it is lost. If blood loss is chornic and in small amounts (ex. gastric ulcers) then anemia and Fe+ deficiency may occur.
a. accute/sudden loss =shock and death if more than 20% blood is lost. |
|
|
Term
| Hemorrhage (compensatory mechanisms) |
|
Definition
3 phases:
1. redistribution of blood to vital centers: Occurs by splenic contraction and arterial consriction of non-vital tissues. Vital centers = brain, heart and diaphragm.
2.Restoration of plasma volume: arteriolar constriction results in a decrese in intravascular pressure, therefore ECF flows in = hemodilution. PCV will give a good indication of blood loss 2 days after hamorrhage but not just after it.
3.Replacement of RBC's: erythropoiesis by the bone marrow. Within 5-6 days the reticulocyte (immature RBC's) count may reach 10% which indicates active RBC formation. This usually decreases about 12 days later, if not then there's recurrent hemorrhage. |
|
|
Term
|
Definition
the predisposition to hemorrhage. Abnormal bleeding is a feature or many diseases and is often associated with:
1.blood clotting disorders
2.disorders if the vascular system: vasculitis (BV inflammation) which can be due to:
a.endotheliotropic viruses
b.bacterial toxins
c.rickettsial agents (intacellular bacteria-like organisms)
3.weakness of the supporting connective tissues:
a.congenital- collagen defects
b.aquired- scurvy (Vit. C deficiency) |
|
|
Term
|
Definition
| a condition of peripheral circulatory failure resulting from a disparity between the volume of blood available and the volume- capacity of the vascular system. |
|
|
Term
|
Definition
| caused by a sudden decrease in circulating blood volume (hypovolemia) and/or increased vascular space (systemic vasodilation) |
|
|
Term
|
Definition
1.hypovolemic shock
2.vascolgenic (septic) shock
3.cardiogenic shock |
|
|
Term
|
Definition
this form of shock is due to a decrease in circulating blood volume, which can be due to:
1.severe acute hemorrhage (>20ml blood/kg BWT)
2.prolonged diuresis: loss of dilute fluid in the urine
3.persistent emesis: vomiting or diarrhoea
4.torsion: twisting or GIT obstruction
5.extensive burns |
|
|
Term
| Vasculogenic (septic) shock |
|
Definition
occurs due to changes in venous capacitance or peripheral resistance. Causes:
1.vasodilation due to endotoxins produced by bacteria
2.widespread endothelial damage
3.decreased CO with pooling of blood in the splanchnic areas
4.neurogenic shock |
|
|
Term
|
Definition
causes:
1.acute changes in myocardial function
2.improper filling with blood -cardiac temponade
3.heart failing to empty adequately - ex. increased TRP or ruptured chordae tendinae
4.decrease in myocardial contractility -disrhythmias |
|
|
Term
|
Definition
Shock may be reversible or irreversible.
Reversible: if an animal is bled to an extent that there is considerable hypotension and then the blood volume is immediately replaced, the BP returns to normal.
Irreversible: if the animal is allowed to remain in a hypotnesive state (shock), then the blood volume is restored by transfusion, BP will not return to normal= death. Associated with irreversible shock is an inadequate oxygen supply to the tissues and therefore a tendancy towards anaerobic glycolysis for energy requirements which further decreases vascular tone. Fluid may be lost and RBC's may aggregate = "blood sludging." Shock causes cooling to the skin and a decreased overall body heat production. |
|
|
Term
|
Definition
an excessive accumulation of ECF. If it is generalized it is called anasarca. If fluid accumulates in serou cavities it can be called:
1.ascites -peritoneal cavity
2.hydothorax- pleural cavity
3.hydropericardium- preicardial sac |
|
|
Term
| Edema: formation and drainage of tissue fluid |
|
Definition
| Development of edema is related to the control of normal fluid balances between the blood and the tissues as explained by the Starling Equilibrium. Combined differences in hydorstatic pressure and colloid osmotic pressure casue fluid and low molecular weight solutes (not protein)to flow into the tissue spaces. This explains the movement of nutrients, waste and O2 to and from the tissues. Much of the tissue fluid that is left behind is drawn off in the lymphatics but when this extra capacity is exceeded or there is lymphatic obstruction, edema results. |
|
|
Term
| Edema: mechanisms of development |
|
Definition
there are 4 mchanisms:
1.increased hydorstatic pressure
2.decreased colloid osmotic pressure
3.lymphatic blockage
4.increased vascular permeability |
|
|
Term
| Edema: Increased Hydorstatic Pressure |
|
Definition
Increased hydorstatic pressure results from increased fluid within vessels. Since pressure in the capillary bed is mostly affected by venous and not arterial pressure, disturbances in venous flow are most imporatant. This can occur locally (ex.venous obstruction, venous occulsion, torsion of a luminal organ) or systemically (Ex.cardiac failure). Cardiac edema is facilitated via the RAAS system:
1. reduced CO
2.arterial constriction
3.kidney arterial constriction -> renin
4.angiotensinogen activation ->AT1
5.AT1 ->AT2 via the lungs
6. AT2-> aldosterone release via adrenal cortex
7. aldosterone = Na+/water retention
8.retention = increased plasma volume
9. increased edema |
|
|
Term
| Edema: decreased colloid osmotic pressure |
|
Definition
circulating proteins (mostly albumin) are responsible for most of the osmotic pressure of plasma. Hypoalbuminaemia is the leading cause of decreased osmotic pressure. Therefore this edema is always generalized. Clinically it appears as ascites, hydorthorax and peripheral subcutaneous edema. Hypoalbuminemia occurs via:
1.decreased albumin formation (liver disease or protein malnutrition)
2.increased albumin loss (whole blood, GIT loss (protein losing enteropathy), renal loss (nephrotic syndrome)). |
|
|
Term
| edema:lymphatic blockage (lymphoedema) |
|
Definition
| Edema occurs if there is extensive tumor invasion of a regional lymph node or if the lymph node was surgically removed. Obstruction can be internal or external (external mass pressing on the lymph vessels). |
|
|
Term
| Edema: increased vascular permeability |
|
Definition
| This tends to occur locally and most commonly from local inflammation. Inflammation products are released and cause an increase in permeability by enlaring the gaps between vascular endothelial cells. AS a result fluid, proteins and inflammatory cells are lossed to the interstital space. This fluid (high in protein and cell contents) = exudate. Other forms of edema result in a clear transudate. |
|
|
Term
| Specific syndromes associated with edema |
|
Definition
1.Hepatic disease:often seen as ascites and edema fluid can be produced as a result of:
a.lack of protein synthesis
b.fibrosis (cirrhosis) and portal vein hypertension
c. liver may not inactivate hormones = hormone build-up and thus further Na+ retention by aldosterone
2.congestive heart failure
3.pulmonary edema: left sided heart failure, inhalation of irritant gases, respiratory infections or anaphylaxsis
4.cerebal edema: head trauma and tumors
5.nephrotic syndrome |
|
|
Term
|
Definition
| Coagulation = blood clotting. Ante-mortem clotting = thrombosis. Thrombosis can be divided into large vessel thrombosis and microvascular thrombosis or (DIC). A thrombus = a solid structure formed within the flowing blood stream from the normal blood constituents. |
|
|
Term
|
Definition
Thrombi can form due to:
1.damage to vascular walls -results in activation of tissue factor which triggers the clotting cascade.
2.abnormal blood flow - blood stasis(dilated BV's, aneurysms, poor peripheral circulation) or disturbances in laminar flow (vessel branches,vessel wall irregularities).
3.changes in blood composition- severe dehydration (hemoconcentration) |
|
|
Term
|
Definition
phase 1. platelet plug formation
phase 2. activation of intrinsic clotting mechanism results in the formation of layered fibrin strands
phase 3. more layering of platelets and fibrin strands. A thrombus may have an layered "onion skin" appearance |
|
|
Term
| Classification of Thrombi |
|
Definition
1. Size
a.large vessel thrombi
b. microvascular thrombi (DIC)
2.physical characteristics
a.color- red = with RBC's white= slow growing without RBC's
b.main components- platelet thrombi or hyaline thrombi (mainly fibrin)
c.occluding thrombi |
|
|
Term
|
Definition
A thrombus that is attached to a BV may:
1. lyse if small
2. shrink (retraction) if rich in fibrin. Later endothelium forms over it = recanalization
3. if it remains after lysis and recanalization it can become organized (formation of granular tissue.
4. may detach to form emboli
5. death or severe organ dysfunction if it occludes the BV causing ischaemia. |
|
|
Term
|
Definition
emboli- an abnormal mass circulating the blood stream
embolism- when an emboli becomes stuck in a BV and occludes it. |
|
|
Term
|
Definition
1.thromboemboli - formed from a thrombus and can be bland or septic.
2.gas (ex. bends)
3.fat (usually follows orthopedic injury)
4.neoplasms
5.foreign bodies, parasites, clumps of bacteria, pus or injected material
6. cartilage derived from intervertebral discs (lodged in the vessels of the spinal chord) |
|
|
Term
|
Definition
1. infected or neoplastic emboli will spread infection or cancer
2. infarction
3. if the emboli are small and bland and the ogan has good collateral circulation then there may be little effect. |
|
|
