Blood flow Flashcards
Basal state vs activated state of endothelial cells
Endothelial cells property/function and mediators/products
When stimulated, smooth muscle cells can…
Proliferate, Upregulate ECM collagen, elastin, and proteoglycan production, Secrete growth factors and cytokines and mediate the vasoconstriction or vasodilation that occurs in response to physiologic or pharmacologic stimuli
Blood pressure =
How is blood pressure regulate?
What is hypertension?
How does the vascular wall respond to injury?
What 3 things lead to a thrombosis? (Virchows triad)
Endothelial injury leads to…
- Promotes Platelet adhesion and aggregation
- Causes the production of pro-coagulant factors
- In heart and arterial circulation:
- Over ulcerated plaques in Atherosclerosis
- Endocardial injury in MI- mural thrombus
- Traumatic or inflammatory vascular injury - vasculitis
What are 2 causes of abnormal blood flow?
• Stasis (venous thrombosis)
– allows platelets to encounter endothelium (due to loss of laminar blood flow) and slows the washout of activated clotting factors
• Turbulence (arterial, near valves/cardiac thrombosis) – Physical trauma to endothelial cells or dysfunction
– Countercurrents and local pockets of stasis
Primary vs secondary hypercoagulable state
- Primary
• Leiden factor V mutation, Congenital deficiency of
antithrombin III, protein C & S, - Secondary: increased concentration of fibrinogen and prothrombin
• Immobilization, MI, neoplasia, tissue damage (surgery, fracture, burns), cancer, prosthetic cardiac valves
• Heparin induced thrombocytopaenia syndrome
• Antiphospholid antibody syndrome
Arterial vs venous thrombus
What are the fates of a thrombus?
- Lysis: due to the potent thrombolytic activity of the blood.
- Propagation (increase in size): because the thrombus acts as a focus for further thrombosis.
- Organisation: the eventual invasion of connective tissue elements, which causes a thrombus to become firm and greyish white.
- Canalisation: by which new lumens lined by endothelial cells form in an organised thrombus.
- Embolization: in which part or all of the thrombus becomes dislodged, travels through the circulation, and lodges in a blood vessel some distance from the site of thrombus formation
What is infarction?
Ischaemic necrosis of tissue secondary to:
- Arterial occlusion (arterial infarct) by • Thrombosis
• Emboli
• Vasospasm or compression of a vessel - Venous occlusion (venous infarct) by • strangulated bowel in hernia
• Torsion- testicular/ovarian torsion, bowel volvulus
In most tissues the histological characteristic of infarction is ischemic coagulative necrosis (except in the brain it is liquefactive necrosis)
Red vs white infarcts
-
Red (haemorrhagic) Infarcts
1. Venous blockage
2. Loosetissues(lungs)
3. Dualcirculation(small intestine)
4. Congestedorgans
5. Re-establishedbloodflowin an infarcted tissue -
White (anaemic) infarcts
1. Arterial occlusions
2. Solid organs
3. End arterial circulation organs:
• heart, spleen and kidney
4. Dense tissues
What are the factors that influence infarct development?
- Anatomy of the vascular supply:
• The presence or absence of an alternative blood supply is the most important factor in determining whether occlusion of an individual vessel causes damage. - Rate of occlusion:
• Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral blood supplies. - Tissue vulnerability to hypoxia:
• Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes.
• Myocardial cells die after only 20 to 30 minutes of ischemia
Athero vs arteriolosclerosis
What is atherosclerosis and what are the risk factors?
Genetic, family history, age, sex, hyperlipidaemia, HTN, smoking, DM and inflammation
What is the pathogenesis of atherosclerosis?
- Normal wall under chronic endothelial injury (smoking, HTN)
- Chronic injury leads to dysfunction. Shown as increased permeability which leads to leukocytes adhesion.
- Accumulation of lipoproteins (mainly oxidized LDL and cholesterol crystals) in the vessel wall
- Monocyte and smooth muscle cell migration into the intima, with macrophage activation.
- Macrophage and smooth muscle cell uptake of modified lipids, with further activation.
- Intimal smooth muscle cell proliferation with extracellular matrix production, forming a well-developed plaque
What is the atherosclerotic plaque fate?
What are the clinicopathologic consequences of atherosclerosis?
What are the types of aneurysms?
What are the classifications of dissections?
Mean arterial pressure=
the average pressure over a complete cardiac cycle and is calculated as follows:
- Pa = DP + 1/3 Pulse pressure
- normal value range is 70-100mmHg
Velocity=
Flow=
ΔP/R
Q is flow (ml/min)
ΔP is pressure difference (mm Hg)
R is resistance (mm Hg/ml/min)
Series vs parallel resistance
- Series resistance is illustrated by the arrangement of blood vessels within a given organ.
- Parallel resistance is illustrated by the distribution of blood flow among the various major arteries branching off the aorta.
What poiseuilles law?
What is laminar flow and turbulent flow?
- The flow in CVS is laminar.
- It is smooth parabolic.
- The velocity of blood flow highest in the centre of the vessel and lowest toward the vessel walls
- When an irregularity occurs in a blood vessel, the laminar stream is
disrupted and blood flow may become turbulent. - Laminar flow is silent, while turbulent flow is audible.
- For example: Korotkoff sounds & murmurs.
What is Reynolds number?
What is local vascular control?
What are the physiological consequences of local control?
What is central vascular control?
Noradrenaline acts on α1 -> vasoconstriction
Adrenaline acts on β2 -> vasodilation
What is hormonal vascular control?
What is endothelial vascular control?
