Blood flow

Question 1

Basal state vs activated state of endothelial cells

Answer 1

Question 2

Endothelial cells property/function and mediators/products

Answer 2

Question 3

When stimulated, smooth muscle cells can…

Answer 3

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

Question 4

Blood pressure =

Answer 4

Question 5

How is blood pressure regulate?

Answer 5

Question 6

What is hypertension?

Answer 6

Question 7

How does the vascular wall respond to injury?

Answer 7

Question 8

What 3 things lead to a thrombosis? (Virchows triad)

Answer 8

Question 9

Endothelial injury leads to…

Answer 9

• 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

Question 10

What are 2 causes of abnormal blood flow?

Answer 10

• 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

Question 11

Primary vs secondary hypercoagulable state

Answer 11

• 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

Question 12

Arterial vs venous thrombus

Answer 12

Question 13

What are the fates of a thrombus?

Answer 13

• 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

Question 14

What is infarction?

Answer 14

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)

Question 15

Red vs white infarcts

Answer 15

• 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

Question 16

What are the factors that influence infarct development?

Answer 16

1. 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.
2. Rate of occlusion:
   • Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral blood supplies.
3. 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

Question 17

Athero vs arteriolosclerosis

Answer 17

Question 18

What is atherosclerosis and what are the risk factors?

Answer 18

Genetic, family history, age, sex, hyperlipidaemia, HTN, smoking, DM and inflammation

Question 19

What is the pathogenesis of atherosclerosis?

Answer 19

1. Normal wall under chronic endothelial injury (smoking, HTN)
2. Chronic injury leads to dysfunction. Shown as increased permeability which leads to leukocytes adhesion.
3. Accumulation of lipoproteins (mainly oxidized LDL and cholesterol crystals) in the vessel wall
4. Monocyte and smooth muscle cell migration into the intima, with macrophage activation.
5. Macrophage and smooth muscle cell uptake of modified lipids, with further activation.
6. Intimal smooth muscle cell proliferation with extracellular matrix production, forming a well-developed plaque

Question 20

What is the atherosclerotic plaque fate?

Answer 20

Question 21

What are the clinicopathologic consequences of atherosclerosis?

Answer 21

Question 22

What are the types of aneurysms?

Answer 22

Question 23

What are the classifications of dissections?

Answer 23

Question 24

Mean arterial pressure=

Answer 24

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

Question 25

Velocity=

Answer 25

Question 26

Flow=

Answer 26

ΔP/R Q is flow (ml/min) ΔP is pressure difference (mm Hg) R is resistance (mm Hg/ml/min)

Question 27

Series vs parallel resistance

Answer 27

- 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.

Question 28

What poiseuilles law?

Answer 28

Question 29

What is laminar flow and turbulent flow?

Answer 29

- 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.

Question 30

What is Reynolds number?

Answer 30

Question 31

What is local vascular control?

Answer 31

Question 32

What are the physiological consequences of local control?

Answer 32

Question 33

What is central vascular control?

Answer 33

Noradrenaline acts on α1 -> vasoconstriction Adrenaline acts on β2 -> vasodilation

Question 34

What is hormonal vascular control?

Answer 34

Question 35

What is endothelial vascular control?

Answer 35