1
Q
What are the two components of the circulatory system?
A
1) Collection system 2) Distribution system
2
Q
What does the collection system do?
A
Transports deoxygenated blood from the periphery to the heart.
3
Q
What does the distribution system do?
A
Pumps oxygenated blood from the heart into the periphery.
4
Q
What is microcirculation?
A
The circulation that occurs in the blood vessels and capillaries, where the exchange of blood, nutrients, and waste materials takes place.
5
Q
What is the role of venules in microcirculation?
A
Transport blood from a cell towards the heart.
Venules in the microcirculation contain more muscle and the capillaries and have a low-resistance pathway. They are also able to store large amounts of blood compared to the capillaries that only contain 5% of blood.
6
Q
What is the role of capillaries in microcirculation?
A
Transport blood to the cell from the heart.
7
Q
Why do capillaries have slow blood flow?
A
To allow better exchange with tissues.
8
Q
What is the significance of capillaries?
A
They are important for fluid balance.
9
Q
How do venules differ from capillaries?
A
Venules contain more muscle and have a low-resistance pathway, storing larger amounts of blood.
10
Q
What are the two types of transport across the capillary wall?
A
1) Direct diffusion 2) Transcytosis
11
Q
What is the nature of the capillary wall?
A
The capillary is a semi-permeable membrane.
12
Q
What occurs during direct diffusion?
A
Materials can pass passively through the semi-membrane or via interendothelial pores.
13
Q
What materials can pass through interendothelial pores?
A
Water, ions, glucose.
14
Q
What occurs during transcytosis?
A
Vesicles are used to transport material across the capillary wall.
15
Q
What determines water distribution between plasma and interstitium?
A
Differences in hydrostatic pressure and osmotic pressure.
16
Q
What happens at the arterial end of the capillary?
A
Fluid exits due to increased hydrostatic pressure greater than blood colloidal osmotic pressure.
17
Q
What occurs near the mid capillary?
A
The pressure inside reduces until net filtration pressure is zero.
There is no movement between the interstitium and the capillary since the hydrostatic pressure of the capillary is equal to the plasma osmotic pressure of the interstitium
18
Q
What happens towards the venous end of the microcirculation?
A
Fluid re-enters the capillary as hydrostatic pressure is less than outside blood colloidal osmotic pressure.
19
Q
What is oedema?
A
A disorder characterized by excess fluid in the interstitial space.
20
Q
What does oedema look like under a histo slide?
A
Increased thickness of layers, lightly stained eosinophilic or clear fluid, and dilated lymphatics.
21
Q
What are the four main mechanisms leading to oedema?
A
1) Increased hydrostatic pressure 2) Reduced plasma osmotic pressure 3) Reduced lymphatic drainage 4) Increased vascular permeability.
22
Q
How does increased hydrostatic pressure cause oedema?
A
It prevents fluid accumulation towards the venous end, causing fluid to move into the interstitium.
23
Q
What can generalised oedema be caused by?
A
Heart failure.
Generalised oedema can be caused by heart failure since the heart is responsible for blood pressure and thus the increased hydrostatic pressure in the capillaries.
24
Q
What causes localised oedema?
A
-local impaired venous drainage/obstruction of veins
-local lymphatic obstruction
-local inflammation
.
25
How does right-sided heart failure affect oedema?
It results in generalised oedema due to blood being stuck in circulation.
26
How does left-sided heart failure affect oedema?
passive congestion and oedema in lungs
If the left heart fails this causes the dilation of pulmonary vessels (L pulmonary vein) and thus an edema which causes pulmonary congestion
27
What causes reduced plasma colloid osmotic pressure?
Not enough plasma proteins, leading to hypoalbuminaemia.
Plasma has high conc of proteins than the capillaries - this is what drives the colloid osmotic p gradient
28
What can cause hypoalbuminaemia?
1) Renal failure 2) Intestinal damage 3) Malabsorption/starvation 4) Liver failure.
29
What are the causes of lymphatic obstructions?
Mechanical pressure, inflammation, obstruction by neoplasia or infectious processes.
30
What causes increased vascular permeability?
Inflammation - inflammatory mediators (vasodilation), direct endothelial damage.
31
What are localised oedemas caused by?
Local impaired venous drainage, local lymphatic obstruction, local inflammation.
32
What are generalised oedemas caused by?
1. Increased hydrostatic pressure (heart failure)
2. decreased colloidal osmotic pressure (hypoproteinaemia).
33
What is hyperaemia?
Hyperaemia is an increased blood flow within vessels.
34
What are the two types of hyperaemia?
1. Active 2. Passive/congestion
35
What characterizes active hyperaemia?
Active hyperaemia involves the engorgement of vascular beds due to increased arteriolar flow. It is an active process with increased inflow of oxygenated blood.
36
What are examples of pathological active hyperaemia?
Inflammation causes the release of inflammatory mediators that dilate arterioles, often associated with oedema.
37
What are examples of physiological active hyperaemia?
1. Exercise - active hyperaemia of the muscles 2. Digestion - increased blood flow to stomach and intestine 3. Heat dissipation - increased blood flow to skin
38
What is passive or congestive hyperaemia?
Passive or congestive hyperaemia is when there is a decreased outflow of venous blood, is only pathological, and contains deoxygenated blood.
39
What causes local congestion?
Local congestion can be caused by a displacement of an organ obstructing venous blood flow, leading to a buildup of low-pressure venous blood.
40
What is generalised congestion?
Generalised congestion occurs in the heart or lungs, causing pulmonary congestion if the left heart fails or generalised congestion if the right heart fails (from the systemic circulation)
41
How do you differentiate between active and congestive hyperaemia in gross features?
Active hyperaemia is usually more red and highly oxygenated, while congestive hyperaemia is darker red and low oxygenated.
42
How do you differentiate between active and congestive hyperaemia in histological specimens?
Active hyperaemia shows capillaries engorged with blood, +/- inflammatory cells, and oedema. Congestion shows capillaries engorged with poorly oxygenated blood, local hypoxia, and degeneration.
43
What is the resolution of haemorrhage?
1. Activation of primary and secondary haemostasis 2. Formation of the fibrin plug 3. Reabsorption of serum via lymphatic vessels 4. Phagocytosis of cell debris by macrophages 5. Cytokines secreted by macrophages 6. Secretion of fibrolytic enzymes for clot removal 7. Formation of a collagenous mass (scar)
44
What is oedema?
Oedema is excess fluid in the interstitium.
45
What is haemorrhage?
Haemorrhage is blood outside of blood vessels.
46
What is the difference between haemorrhage and hyperaemia/congestion?
A haemorrhage is characterized by blood outside of blood vessels, while hyperaemia is when there is an increased flow of blood inside the blood vessels. congestion- there is a decreased outflow of venous blood but increased amount of blood overall in venous side.
47
What is a haematoma?
Haematoma is a localized haemorrhage or collection of blood.
48
What is haemopericardium?
Haemopericardium is a collection of blood in the pericardial sac.
49
What is haemothorax?
Haemothorax is a collection of blood in the thorax.
50
What is haemoperitoneum?
Haemoperitoneum is a collection of blood in the abdomen.
51
What are petechiae?
Petechiae are very small pinpoint haemorrhages due to capillary damages.
52
What are ecchymoses?
Ecchymoses are large blotchy haemorrhages.
53
What are the two important players in preventing haemorrhage?
1. Blood vessel integrity 2. Haemostasis
54
What are the three main issues that can cause haemorrhages?
1. Loss of endothelial integrity or damage to blood vessels 2. Platelet pathology 3. Defects in coagulation factors
55
What are the clinical implications of haemorrhages based on?
The clinical implications are based on how much blood is being lost, where the haemorrhage is, and how quickly blood is being lost.
56
Why is a hematoma in the brain concerning?
A hematoma in the brain is concerning because the brain lacks a lymphatic system to drain excess fluids.
57
Describe Hyperaemia (LA)
Hyperaemia is an increased blood flow within vessels.
Hyperaemia has 2 types : 1. Active and 2. Passive/congestion
Active hyperaemia involves the engorgement of vascular beds due to increased arteriolar (arterial blood) flow. This is an active process, has an increased inflow of blood, contains more oxygenated blood and can be pathological or physiological.
Examples of pathological Active hyperaemia:
Inflammation- cause release of inflammatory mediators - cause dilation of arterioles
-Often associated with oedema
Examples of physiological Active hyperaemia:
Exercise - active hyperaemia of the muscles
Digestion - increased blood flow to stomach and intestine
Heat dissipation - increased blood flow to skin
Inflammation- inflammatory markers dilate blood vessels which cause an increase in arterial blood flow.
Passive or congestive hyperaemia is when there is a decreased outflow of venous blood. This is only pathological. This is a passive process, contains deoxygenated blood, and is caused by a blockage of venous drainage.
Local congestion can be caused by e.g a displacement of an organ which will obstruct blood flow causing a buildup of low-pressure venous blood and no supply of arterial blood. This will cause stagnant blood to be rapidly deoxygenated.
58
Describe generalised congestion (LA)
This occurs in the heart or lungs.
If the left heart fails this causes the dilation of pulmonary vessels (L pulmonary vein) and thus an edema which causes pulmonary congestion
If the right heart fails,(blue) this causes the blood to get stuck in the main circulation causing a generalised congestion and oedema
59
How do you differentiate between active and congestive hyperaemia in a histological specimen?
Active - capillaries engorged with blood, +/- inflammatory cells, oedema
Congestion - capillaries engorged with blood, chronic stagnation of poorly oxygenated blood, local hypoxia, degeneration
60
Describe the Resolution of Haemorrhage (LA)
Activation of primary and secondary haemostasis - to arrest the haemorrhage
Haemorrhage blocked by the formation of the fibrin plug
Reabsorption of serum via lymphatic vessels
Phagocytosis of cell debris and RBCs by macrophages - RBC breakdown - produced haemosiderin - which is then phagocytosed by macrophages
Macrophages remove necrotic debris and simultaneously start the repair process
Cytokines secreted by macrophages into capillaries and fibrocytes growing into fibrin clot
Secretion of fibrolytic enzymes by macrophages for clot removal
Formation of a collagenous mass (scar)
61
What is important in preventing haemorrhage and why (LA)
There are two important ‘players’ in preventing haemorrhage.
Blood vessel integrity
Haemostasis
Haemorrhages can be caused by 3 main issues
Loss of endothelial integrity or damage to blood vessels - trauma, vascular erosion/damage by inflammatory cells, toxins etc
Platelet pathology - decreased number of platelets (reduced production, increased destruction of platelets or increased use) -abdnormal platelet function (genetic, drug-induced)
Defects in coagulation factors - Inherited, acquired (decreased production- liver failure (liver produces coagulation factors, increased use)
62
For the clinical implications of hemorrhages it's based on three different factors:
How much blood is being lost
Where the hemorrhage is
How quickly blood is being lost
63
64
What is thrombosis?
Thrombosis is inappropriate coagulation that occurs when clotting is initiated unnecessarily within veins or arteries.
65
Where does thrombosis occur?
Thrombosis occurs in uninjured or mildly injured vessels.
66
What happens if clots in blood vessels are not resolved?
If clots are not resolved, they will progress into a thrombus.
67
What does a thrombus look like in veins and arteries?
A thrombus looks red in veins and white in arteries.
68
What are the three conditions needed for thrombosis?
1. Altered blood flow
2. Endothelial injury
3. Hypercoagulability
69
What is altered blood flow?
Altered blood flow refers to turbulence or disruption of blood that can lead to endothelial injury and faster coagulation.
70
What is endothelial injury?
Endothelial injury can be major or minor and initiates the thrombotic process.
71
What is hypercoagulability?
Hypercoagulability is an increased concentration of clotting factors, often due to genetic conditions.
72
What are the three major consequences of a thrombus?
1. Local Ischaemia
2. Occlusion of blood vessels and infarction
3. Embolism
73
What is DIC?
DIC, or Disseminated Intravascular Coagulation, is caused by widespread thrombi in small vessels and is associated with sepsis and hypovolaemic shock.
74
What are the physical symptoms of DIC?
Physical symptoms include disseminated petechiae due to multiple thrombi caused by hyperactivation of coagulation factors.
75
What is ischaemia?
Ischaemia is the interruption of blood flow, which can cause infarction.
76
What are the causes of ischaemia?
1. Local obstruction of a vessel
2. Decreased cardiac output
3. Local congestion
77
What is infarction?
Infarction is necrosis due to interrupted blood flow from occlusion of arterial supply or venous drainage.
78
What are common causes of infarction?
Common causes include thrombosis, embolism, and vascular occlusion.
79
What histological features indicate necrosis?
In histology, necrosis shows pale tissue around blood vessels.
80
What factors influence the development of an infarction?
1. Vulnerability of affected tissue to hypoxia
2. Anatomy of blood supply
3. Rate of vessel obstruction
81
What does hyperaemic mean?
Hyperaemic means increased blood supply.
82
What is shock?
Shock is cardiovascular collapse that occurs when blood pressure is inadequate for tissue perfusion.
83
What can cause shock?
Causes include microbial sepsis, severe haemorrhage, extensive trauma or burns, myocardial infarction, and severe pulmonary embolism.
84
What are the symptoms of shock?
Symptoms include weakness, extremely pale mucous membranes, and slow capillary refill time.
85
What are the three main types of shock?
1. Hypovolaemic shock
2. Cardiogenic shock
3. Blood maldistribution
86
What causes hypovolaemic shock?
Causes include blood loss (>20% of circulating blood) and fluid loss (e.g., vomiting, diarrhea, burns).
87
What causes cardiogenic shock?
Cardiogenic shock is caused by cardiac pathology such as cardiomyopathy, conducting problems, or vascular disease.
88
What causes blood maldistribution?
Blood maldistribution is caused by systemic inflammation, anaphylaxis, and sepsis.
89
Define Thrombosis (LA)
Thrombosis -is inappropriate coagulation- This occurs when clotting is initiated unnecessarily within veins or arteries
Thrombosis occurs in uninjured or mildly injured vessels
Usually clots in blood vessels are eventually resolved during the normal coagulation process however if this does not happen then it will progress into a thrombus.
Thrombus looks red in veins and white in arteries.This is because in the veins the circulation is slow and leads to a buildup of blood, while in the artery there is a buildup of more cells than RBCs
90
What 3 conditions are needed for a thrombosis? (LA)
Altered blood flow
Endothelial injury
Hypercoagulability
Altered blood flow:
Turbulence/disruption of blood can lead to further endothelial injury and mixing of reagents will cause a faster coagulation cascade
Stasis of blood can lead to dilution of clotting factors and the buildup of thrombi.
Endothelial injury:
-Major or minor injury can initiate thrombotic process
-platelets and fibrin do not adhere to normal endothelium of blood vessels
Hypercoagulability:
-Increased concentration of clotting factors - this is usually a genetic condition
91
There are 3 major consequences of a thrombus: (LA)
Local Ischaemia (reduced blood supply)
Occlusion of blood vessels and infarction (necrosis of nearby tissue)
Embolism - pieces of thrombi travel in blood and get stuck in distant organs e.g brain
92
DIC - Disseminated Intravascular Coagulation
DIC - Disseminated Intravascular Coagulation is a condition caused by the widespread thrombi in small vessels. It is associated with sepsis and hypovolaemic shock.
Physical symptoms of DIC include disseminated petechiae - multifocal pinpoint cutaneous haemorrhages; this is due to multiple thrombi caused by hyperactivation of coagulation factors. There is widespread clotting in this animal and therefore the clotting factors are consumed by the clotting even though the coagulation is hyper-activated, therefore it is not enough to avoid haemorrhages. This is a quick process and causes multiple haemorrhages.
93
Define Ischaemia (LA)
Ischaemia - interruption of blood flow. This causes infarction. This can be stagnant (still?) or cessation of blood flow.
Causes are:
Local obstruction of a vessel
Decreased cardiac output
Local congestion
These cause a reduced blood supply and accumulation of metabolic by-products which result in cell death. The outcomes depend on the nature of cells e.g CNS, Kidney, and heart cells are very sensitive to ischaemia and infarction.
94
Define Infarction (LA)
Infarction is necrosis due to interrupted blood flow (ischaemia) from occlusion of arterial supply or venous drainage. Occlusions of the arteries are more common.
Causes for infarction include: thrombosis, embolism, vascular occlusion from twisting of a vessel. In animals, they are mostly found in pulmonary, intestinal, and renal.
In a histological sample what will you see if there is necrosis vs a gross sample? Pale tissue around blood vessels in histology. In a gross sample, wedge-shaped, early infarct = ill define and hyperamic margin, late infarct= pale colour.
95
There are 3 factors that will influence the development/characteristics of an infarction. What are they? (LA)
:
Vulnerability of affected tissue to hypoxia - Renal, pulmonary and CNS are sensitive
Anatomy of blood supply - dual supply = less prone to infarction (liver>kidney)
Rate of vessel obstruction
Rate of vessel obstruction:
-Acute occlusion = infarction
-Slow occlusion = formation of a collateral circulation - this is a circulation that forms upstream of the occlusion to provide the same tissue with blood.
96
Define shock (LA)
Shock - Is cardiovascular collapse that occurs when blood pressure is inadequate for tissue perfusion.
The following can cause shock: Microbial sepsis, severe haemorrhage (lose blood), extensive trauma or burns, myocardial infarction, severe pulmonary embolism. In general, congestion, necrosis, and lesions can cause shock e.g pulmonary and liver congestion, kidney - acute tubular necrosis, neuronal cell death in brain, pallor skeletal muscle.
Symptoms: weakness, extremely pale mucous membranes, slow capillary refill time.
97
Describe in detail the main types of shock (LA)
There are 3 main types of shock:
Hypovolaemic shock
Cardiogenic shock
Blood maldistribution
The main causes of Hypovolaemic shock are
Blood loss (>20% of circulating blood)
Fluid loss (V++, D++, burns)
When blood/fluid is reduced this reduces blood volume which will reduce blood pressure and thus reduced perfusion in tissues.
Cardiogenic shock is caused by cardiac pathology such as cardiomyopathy, conducting problems, vascular disease. Issues with the heart will lead to no blood pumping or blood stagnation and thus tissue hypoperfusion (tissues aren’t perfused enough). Pale patches in heart due to myocardial damage.
Blood maldistribution caused by systemic inflammation, anaphylaxis, sepsis.
-Systemic vasodilation causes pooling of blood in the periphery which leads to a drop in blood pressure.
-Anaphylaxis can cause blood maldistribution since the inflammation can cause the release of vasoactive amines.
-Sepsis causes endotoxin release from bacteria which activates endothelial cells and WBCs to release cytokines and thus vasodilation.
Vets2007
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