PoD - Circulation Flashcards

1
Q

what is the structure of a normal blood vessel?

A
  • endothelial cells lines lumen
  • endothelial cells make basal lamina (basement membrane)
  • basal lamina is surrounded by smooth muscle
  • smooth muscle cells surrounded by interstitial collagen fibres
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2
Q

what does an artery contain?

A
  • RBCs
  • WBCs
  • platelets (not normally exposed to collagen)
  • plasma (water, proteins, clotting factors etc)
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3
Q

what is the clotting cascade?

A
  • amplification system - so many more molecules at end compared to starting factors
  • one step’s product = next step’s substrate
  • aim to produce thrombin
  • thrombin converts fibrinogen to fibrin (forms meshwork)
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4
Q

what are the key factors to remember?

A
  • tissue factor (TF)
  • prothrombin
  • thrombin
  • fibrinogen
  • fibrin
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5
Q

how does the clotting cascade develop?

A
  • trauma causes defects in the vessel
  • this causes blood to leak out and plasma comes into contact w/ interstitial collagen fibres
  • plasma clotting factors exposed
  • tissue factor is released from smooth muscle as a result of trauma
  • TF can now bind a particular clotting factor and initiate the clotting cascade
  • clotting factor (protease) cleaves next clotting factor = activation
  • clotting cascade leads to production of thrombin from prothrombin
  • thrombin converts solute fibrinogen to insoluble fibrin
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6
Q

what are platelets?

A
  • produced in bone marrow
  • megakaryocytes undergo nuclear division but cell doesn’t divide = huge cell with many nuclei
  • platelets bud off as v.small fragments
  • platelets aim to form bridges to close gap - clot
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7
Q

what are the 2 types of coagulation?

A
  • thrombus formation

- clot formation

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8
Q

what happens to form a thrombus?

A
  • occurs in flowing blood
  • pure thrombus is cream coloured
  • contains platelets and a mesh like network of fibrin strands
  • platelets have molecules on their surfaces which allow them to adhere to interstitial collagen, means thrombus is formed in flowing blood (factor 8 enhances stickiness)
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9
Q

what happens to form a clot?

A
  • clots occur in stagnant blood (blood leaks out of a vessel)
  • clot consists of a network of fibrin strands and RBCs (clot = red from RBCs)
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10
Q

what is haemostasis?

A
  • the mechanism by which we stop bleeding
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11
Q

describe the process of haemostasis

A
  • trauma disrupts one side of vessel
  • blood leaks out
  • clotting system is activated by collagen and the stagnant blood (clot)
  • this may not work properly and wound may continue to bleed
  • the vessel vasoconstrictor to decrease blood loss
  • platelet and fibrin thrombus bridges gap between the ends of the vessel adjacent to flowing blood
  • the skin now stops bleeding - haemostasis
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12
Q

how can the body repair injury?

A
  • new vessels can grow into area of the wound
  • new vessels = granulation tissue
  • granulation tissues with blood vessels can oxygenate the area of the wound and keep it alive?
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13
Q

how is a thrombus removed?

A
  • plasminogen is converted to plasmin
  • plasmin cuts up fibrin into smaller fragments as a way of removing fibrin
  • in a thrombus, this is sometime called thrombolysis
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14
Q

describe the fibrinolytic system

A
  • fibrinolytic system removes fibrin and stops thrombi from spreading, allows blood to flow
  • fibrinolytic system is normally in balance with clotting system
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15
Q

what are the three main causes of thrombus formation?

- Virchow’s Triad

A
  • changes in intimal surface of a vessel
  • changes in the pattern of blood flow
  • changes in the blood constituents
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16
Q

give an example of a pathological thrombus

A

Coronary Artery Thrombosis

  • coronary arteries supply blood to heart muscle (myocardium)
  • smoking cigarettes increases the ‘stickiness’ of platelets (easier to aggregate)
  • stickier platelets make it more likely a thrombus will form (= change in blood constituents)
  • cigarette smoking (high blood lipid) can also deposit lipids in the blood = atheroma
  • atheroma is a build-up of lipid under the intimal surface
  • lipid deposition can cause abnormal (slow/turbulent) blood flow because the artery is narrowed
  • slowed blood flow predisposes thrombus formation (= change in pattern of blood flow)
  • lipids can also rupture the intimal surface (= change in intimal surface)
  • platelets and fibrin are now exposed to an abnormal substance (lipid & collagen) and turbulent flow - deposited as a thrombus
  • thrombus blocks the lumen of the coronary artery
  • clot can now form in the stagnant blood behind the thrombus
17
Q

what are the consequences of a thrombus blocking an artery?

A
  • complete/partial obstruction means there is a lack of blood flow to tissues beyond the blockage
  • when a tissue receives less blood flow = ischaemia
  • ischaemia can lead to decreased oxygenation of tissues = hypoxia
  • in severe or total blockage of blood flow, the ischaemia and hypoxia causes the tissue to die = infarct (ischaemic necrosis)
18
Q

what is an embolism?

A
  • a mass of material moving in the vascular system that is able to break off and become lodged in a vessel elsewhere, blocking its lumen
  • most emboli are derived from thrombi or clots
  • when thrombi/clots embolise = thromboembolism
19
Q

what happens in a pulmonary embolism?

A
  • occurs due to sluggish flow in leg veins - leads to thrombosis and clot formation
  • part of the thrombus/clot breaks up and travels through the circulatory system
  • the embolus can travel through the blood stream from legs to lungs (femoral vein –> ileac vein –> inferior vena cava –> right atrium –> pulmonary arteries)
  • embolism can block pulmonary artery and cause pulmonary infarction
20
Q

what is circulatory shock?

A
  • profound circulatory failure causing poor perfusion of vital organs
21
Q

what is a normal BP?

A

120/80

22
Q

what does normal BP rely on?

A
  • enough blood in system (no blood in vessel causes it to collapse, BP decreases)
  • smooth muscle in vessels having a certain tone (if muscle tone is decreased, vessel will dilate, if enough vessels are affect then BP may fall)
  • heart pumping blood (if heart doesn’t pump enough blood, BP will fall)
23
Q

how is the BP detected?

A
  • the carotid bodies (either side of neck)
  • detects blood flow, BP, oxygen
  • 2 carotid bodies have groups of cells which sense blood going past them
  • respond to partial pressure of oxygen
24
Q

what happens if BP drops?

A
  • if BP drops, so does partial pressure of oxygen
  • carotid bodies respond by sending nerve signals to brain stem
  • brain stem tells heart to pump harder and faster
  • if heart pumps faster, pulse is faster
  • physiological response to low BP –> faster heart/pulse rate
25
Q

what characteristics need to be present to diagnose circulatory shock?

A
  • low BP - arterial pressure (60/40)

- fast pulse (>100)

26
Q

what are the 3 main causes of circulatory shock?

A
  • hypovolaemia (severe blood/fluid loss)
  • septicaemia (bacterial infection)
  • heart failure (cardiogenic)
27
Q

what occurs in hypovoaemic shock?

A
  • severe blood or fluid loss occurs
  • as blood flows out, there is blood present in other vessels = vessels collapse
  • less blood in the inferior vena cava
  • of inferior vena cava has no blood in it, then venous pressure falls
  • no blood travels to R side of the heart
  • no blood travels to the lungs
  • very little blood/oxygen goes to brain and tissues
  • systemic BP drops
  • carotid bodies sense lower pressure of oxygen
  • this regulates the sympathetic nervous system (low BP, feeling ill, rapid breathing, fast heartbeat, pale/sweaty skin)
  • can be partially combatted with blood transfusion and stopping the leak
28
Q

what happens in septic shock?

A
  • occurs when infectious bacteria spreads into the blood
  • molecules released cause generalised vasodilation
  • vasodilation is general and blood pools in veins
  • not enough blood gets back to the heart
  • not enough blood can go to brain and rest of the body
  • infection in blood causing generalised vasodilation and shock = septic shock
29
Q

what is cardiogenic shock?

A
  • occurs when heart starts to fail
  • heart can no lunger pump enough to maintain BP
  • as BP fails, pulse rate goes up
    NO BLOOD LOSS
30
Q

what are the complications of shock?

A
  • decreased perfusion of brain - initially reversible but then permanent
  • decreased perfusion of kidneys -initially reversible, then more severe
  • brain injury = ischaemic infarction of brain tissue
  • renal injury - ischaemic necrosis of renal tubules