PoD - Circulation Flashcards
what is the structure of a normal blood vessel?
- 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
what does an artery contain?
- RBCs
- WBCs
- platelets (not normally exposed to collagen)
- plasma (water, proteins, clotting factors etc)
what is the clotting cascade?
- 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)
what are the key factors to remember?
- tissue factor (TF)
- prothrombin
- thrombin
- fibrinogen
- fibrin
how does the clotting cascade develop?
- 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
what are platelets?
- 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
what are the 2 types of coagulation?
- thrombus formation
- clot formation
what happens to form a thrombus?
- 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)
what happens to form a clot?
- 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)
what is haemostasis?
- the mechanism by which we stop bleeding
describe the process of haemostasis
- 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
how can the body repair injury?
- 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?
how is a thrombus removed?
- 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
describe the fibrinolytic system
- fibrinolytic system removes fibrin and stops thrombi from spreading, allows blood to flow
- fibrinolytic system is normally in balance with clotting system
what are the three main causes of thrombus formation?
- Virchow’s Triad
- changes in intimal surface of a vessel
- changes in the pattern of blood flow
- changes in the blood constituents
give an example of a pathological thrombus
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
what are the consequences of a thrombus blocking an artery?
- 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)
what is an embolism?
- 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
what happens in a pulmonary embolism?
- 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
what is circulatory shock?
- profound circulatory failure causing poor perfusion of vital organs
what is a normal BP?
120/80
what does normal BP rely on?
- 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)
how is the BP detected?
- 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
what happens if BP drops?
- 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
what characteristics need to be present to diagnose circulatory shock?
- low BP - arterial pressure (60/40)
- fast pulse (>100)
what are the 3 main causes of circulatory shock?
- hypovolaemia (severe blood/fluid loss)
- septicaemia (bacterial infection)
- heart failure (cardiogenic)
what occurs in hypovoaemic shock?
- 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
what happens in septic shock?
- 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
what is cardiogenic shock?
- 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
what are the complications of shock?
- 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