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principles of disease > pathology of circulation week 7 > Flashcards

pathology of circulation week 7 Flashcards

1
Q

what is the structure of an artery from inside out

A
  • lumen in middle (where blood flows)
  • endothelial cells line lumen
  • endothelial cells make basal lamina to sit on
  • smooth muscle cells around the basal lamina
  • around the smooth muscle cells are interstitial collagen fibres
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2
Q

what does the lumen of an artery contain

A
  • red blood cells, white blood cells and platelets
  • platelets aren’t normally exposed to interstitial collagen fibres!!
  • lumen also contains plasma
  • plasma contains clotting factors
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3
Q

what is serum

A
  • serum is plasma without the clotting factors
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4
Q

where are clotting factors produced

A
  • mainly in the liver but also by enodthelial cells
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5
Q

what is the clotting cascade

A
  • an amplification system
  • damage results in the release of a tissue factor
  • prothrombin converts into thrombin
  • thrombin converts fibrinogen into fibrin
  • fibrin forms a mesh of strands
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6
Q

what is meant by initial damage in the clotting cascade

A
  • one way is trauma

- trauma leads to 1. exposure of interstitial collagens and 2. exposure of a molecule called tissue factor (TF)

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7
Q

what happens when there is trauma to a blood vessel

A
  • trauma results in defects in vessels
  • blood leaks out and plasma comes into contact with interstitial collagen fibres
  • plasma clotting factors can now be activated as they contact interstitial collagens
  • tissue factor is also released from smooth muscle
  • tissue factor can now bind a particular clotting factor and initiate the clotting cascade
  • TF can then result in fibrin deposition as a result of the cascade
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8
Q

how does a clotting factor become activated

A
  • many clotting factors are serine proteases (they have a serine amino acid in them)
  • they cleave other clotting factors to form the active molecule
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9
Q

what is the endpoint of the clotting cascade

A
  • production of insoluble fibrin strands that form a meshwork
  • (fibrinogen are small molecules and combine to form fibrin which is a large network of stands)
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10
Q

where are platelets produced and from what cell

A
  • produced in bone marrow

- bud off as fragments from cell called megakaryote

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11
Q

how do platelets work

A
  • trauma to vessel leads to exposure of platelets to interstitial collagen
  • platelets adhere together and try to form bridge to close the gap on the surface of the vessel
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12
Q

when do platelets become activated

A

when they interact with the interstitial collagen

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13
Q

what does thrombin do

A

converts soluble fibrinogen into insoluble fibrin

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14
Q

what are the two types of coagulation

A
  1. thrombus formation (in flowing blood)

2. clot formation (in stagnant blood)

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15
Q

what is a thrombus

A
  • occurs in flowing blood!
  • a pure thrombus is pale cream coloured
  • a thrombus consists of platelets and a mesh like network of fibrin strands
  • thrombosis is the process of thrombus formation and it occurs in flowing blood
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16
Q

why does a thrombus of platelets and fibrin occur in flowing blood

A
  • platelets have molecules on their surfaces which allow adherence to interstitial collagen even when blood flow is flowing past them
  • the clotting cascade deposits factor VIII which enhances this further
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17
Q

what is the process of clot formation

A
  • blood leaks out of a vessel and becomes stagnant
  • within the stagnant blood, sitting next to interstitial collagen, the clotting cascade is activated
  • a clot consists of a network of fibrin strands and red blood cells
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18
Q

what does a clot consist of

A
  • network of fibrin strands and red blood vessels
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19
Q

how is bleeding stopped in a wound

A
  • vasoconstriction helps reduce bleeding
  • clot formation occurs in space around vessel and may fill void of wounded tissue
  • thrombus forms in flowing blood and stops bleeding from gaps in vessel
  • (then process of inflammation, granulation tissue, etc.)
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20
Q

how does the body remove a clot or thrombus

A
  • a blood protein called plasminogen converts to plasmin
  • plasmin cuts up fibrin into smaller fragments as a way of removing fibrin
  • in a thrombus this is called thrombolysis
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21
Q

how is excess clot or thrombus removed

A
  • in blood there is a fibrinolytic system which removes fibrin and stops thrombi gathering
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22
Q

when is the formation of thrombus and clotting normal

A
  • wound healing

- stopping bleeding in menstruation

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23
Q

what are the three main causes of thrombosis

A
  1. changes in the intimal surface of a vessel
  2. changes in the pattern of blood flow
  3. changes in the blood constituents
24
Q

what is haemostasis

A

the stopping of bleeding

25
Q

what is Virchow’s triad

A
  • the three main causes of thrombosis
    1. changes in the intimal surface of a vessel
    2. changes in the pattern of blood flow
    3. changes in the blood constituents
26
Q

what is atheroma

A

disease of the coronary arteries which results in a build up of lipid under the intimal surface
- the lipid can result in abnormal blood flow, can get both slow and turbulent blood flow

27
Q

how can coronary artery thrombosis as a result of smoking result in all three Virchow’s triad

A
  • smoking increases ‘stickiness’ of platelets, so easier for them to group together and makes it more likely for thrombus to occur
  • this is a change in blood constituents (one of Virchow’s triad)
  • smoking can also predispose to atheroma in the coronary arteries (build up of lipid under intimal surface), the atheroma narrows the lumen of the vessel
  • this can result in abnormal blood flow, can be slow and turbulent, slowed blood flow predisposes to fibrin and platelet clumping
  • this is a change in the pattern of blood flow (one of Virchow’s triad)
  • lipid and collagen can also rupture through the intimal surface of the vessel (one of Virchow’s triad)
  • platelets and fibrin now exposed to collagen and are deposited as thrombus
  • thrombus blocks lumen of coronary artery and clot can now form in stagnant blood behind it
28
Q

what are lines of Zahn

A

multiple layers of thrombus and clot

29
Q

what is an example of change in the intimal surface of a vessel

A
  • atheroma lipid coming onto surface

- trauma

30
Q

what is an example of changes in pattern of blood flow

A
  • a bulge of atheroma changing the flow of blood
31
Q

what is an example of changes in the blood constituents

A

smoking makes it more likely that platelets aggregate (group together)

32
Q

what are the consequences of a thrombus blocking an artery

A
  • complete obstruction leads to no blood flow beyond blockage
  • partial obstruction leads to decreased blood flow
33
Q

what is ischaemia

A

poor blood flow or lack of blood flow

34
Q

what happens when there is a partial obstruction due to thrombus

A
  • tissue supplied by artery receives less blood flow (ischaemia)
  • if it severe enough ischaemia leads to decreased oxygenation of tissues (hypoxia)
  • ischeamic heart tissue is often painful
35
Q

what happens when there is severe or total blockage of vessel due to thrombus

A
  • lack of blood flow (ischaemia) leads to severe lack of oxygen (hypoxia) and a localised area of tissue dies
  • process of tissue dying is called necrosis
36
Q

what is an infarct

A
  • infarct or infarction

- a name reserved for necrosis as a result of ischaemia

37
Q

what is an embolism

A
  • a mass of material moving in the vascular system and able to become lodged in a vessel and block its lumen
  • most emboli are derived from thrombi or clots
  • they break off and go elsewhere in the circulation
38
Q

what is a thromboembolism

A

when thrombi/clots embolise

39
Q

what are other forms of embolism besides thromboembolism

A
  • fracture a leg, marrow enters ruptured vein, marrow embolisms to lung vessels = marrow embolism
  • knife wound to the neck, air enters vein, air embolisms to heart = air embolism
40
Q

what is pulmonary embolism

A
  • sluggish flow in veins leads to thrombosis and clot formation (maybe someone who had operation and didn’t move calf for several days)
  • a part of thrombosis (and clot) breaks off and travels up the vein, so it embolisms
  • emboli passes into the inferior vena cava, then right heart, then pulmonary trunk and lodges in the pulmonary artery branch
  • emboli blocks pulmonary artery and get pulmonary infarction
41
Q

what is circulatory shock

A
  • profound circulatory failure causing poor perfusion of vital organs
  • in practice it is low blood pressure and its physiological consequences
42
Q

what is normal arterial pressure

A

120/80

  • 120 is the pressure when the pulse comes past
  • 80 is the resting pressure when the pulse isn’t there
43
Q

what does normal blood pressure rely on

A
  • enough blood in the system
  • smooth muscle in vessels having a certain tone
  • heart pumping blood
44
Q

why do you need enough blood in the system for normal blood pressure

A
  • no blood in the vessel causes it to collapse and blood pressure becomes low and then unrecordable
45
Q

why does the smooth muscle in blood vessels need to have a certain tone to maintain normal blood pressure

A
  • if smooth muscle tone is decreased the vessel will dilate

- if enough vessels are affected then blood pressure may fall

46
Q

how does the body detect blood pressure and oxygen

A

using the carotid body and sinus on either side of the bifurcation of the artery
- there are two carotid bodies and two carotid sinuses on either side of the neck

47
Q

what do the carotid bodies do

A
  • sense the partial pressure of oxygen
48
Q

what do the carotid sinuses do

A
  • respond to blood pressure
  • if blood pressure drops carotid arteries sense this, they are connected to nerves and they send off signals to the brain stem, brain stem tells heart to pump faster via the sympathetic nervous system
49
Q

what is the physiological response to low blood pressure

A
  • faster pulse
50
Q

what does stimulation of the sympathetic nervous system in response to low blood pressure result in

A
  • sympathetic nervous system stimulation causes increased vascular tone in vessels in limbs and abdomen which pushes blood back up to chest and head
  • also causes adrenal glands to secrete adrenaline which makes the heart pump even faster
51
Q

in practice circulatory shock is present if…

A
  • low blood pressure combined with a fast pulse
52
Q

what are the 3 main causes of circulatory shock

A
  1. hypovolaemic (not enough blood)
  2. septic (vessels dilate, issues with vascular tone)
  3. cariogenic (heart doesn’t pump properly)
  4. other
53
Q

what happens when you have hypovolaemic shock

A
  • low blood pressure reflects severe reduction in volume of blood in circulation
  • blood vessels collapse due to the little blood
  • carotid sinuses sense lower blood pressure
  • carotid sinuses unregulate the sympathetic nervous system and this results in the patient feeling ‘ill’, rapid breathing, fast heartbeat!!, pale and sweaty skin
  • in summary, low blood pressure and very high pulse e.g. BP = 60/40 and bpm = 120
54
Q

what happens when you have cariogenic shock

A
  • heart doesn’t pump properly
  • (not due to blood loss so venous pressure is normal or even increased)
  • e.g. heart disease, heart starts failing, give drugs to increase heart function
55
Q

what happens when you have septic shock

A
  • infection in blood causing generalised vasodilatation (issue with vascular tone)
  • results in pooling of blood in veins e.g. in legs and not enough blood gets back to the heart
  • in severe cases of septic shock muscle of the heart, just like muscle of the vessels loses it tone (may then get slow heart rate - bradycardia)
56
Q

what are the complications of shock

A
  1. decreased perfusion (ischaemia) of brain, initially reversible but then permanent and you get infarctions, so dead tissue in the brain which will give you a stroke
  2. decreased perfusion of kidneys, initially reversible but then can become more serious and can end up with ischaemic necrosis of renal tubules
  3. many other complications

principles of disease (19 decks)

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