Cardiovascular pathology

Question 1

Why are arteries more elastic?

Answer 1

To accommodate the higher pressures

Question 2

What structurally allows veins to prevent backflow?

Answer 2

Valves

Question 3

What is the value range of someone who is deemed to have hypertension?

Answer 3

> 140/90mmHg

Question 4

What values are used to calculate blood pressure?

Answer 4

cardiac output and total peripheral resistance

Question 5

What regulates vascular tone and how do they do it?

Answer 5

Endothelial cells via the secretion of hormones affecting calcium concentrations, sympathetic nerves via neurotransmitters affecting calcium concentrations, circulating hormones by activating endothelial cells or smooth muscle

Question 6

How does nitric oxide affect calcium levels?

Answer 6

Nitric oxide is made through the conversion of L-arginine via eNOS. It causes calcium levels to decrease by dilating the smooth muscle

Question 7

How does prostacyclin affect calcium levels?

Answer 7

It is made through the conversion of arachidonic acid via COX. it moves out of the endothelium and interacts with prostacyclin receptor IPR causing the smooth muscle to dilate and calcium levels to decrease

Question 8

How does endothelin-1 affect calcium levels?

Answer 8

Made through the conversion of big-ET-1 via ECE (shortens the polypeptide). it then interacts with endothelin receptors causing the smooth muscle to contract, increasing calcium levels

Question 9

How does angiotensin II affect calcium levels?

Answer 9

Made through the conversion of angiotensin I via ACE. It then interacts with AT1 receptor causing the smooth muscle to contract, increasing calcium levels

Question 10

How does noradrenaline affect calcium levels?

Answer 10

It interacts with alpha-adreno receptors following release causing contraction of the smooth musce, increasing calcium levels

Question 11

What is atherosclerosis?

Answer 11

Thickening and inelasticity of arterial wall

Question 12

Where does atherosclerosis usually occur?

Answer 12

Medium and large arteries

Question 13

What does LDL stand for?

Answer 13

Low-density lipoprotein

Question 14

How does an abundance of LDL lead to a thrombus? (Long answer)

Answer 14

LDL is oxidised following damage to endo cells. Macrophages phagocytose oxidised-LDL and become foam cells, these degenerate and release contents forming atheroma in the wall. Calcium salts and fibrous tissue accumulate on this and create plaque narrowing the lumen. the endothelium will eventually rupture due to the narrowing of the lumen causing increased pressure, exposing collagen. Platelets will bind to the exposed collagen to form a blood clot and thrombus

Question 15

How do statins increase cholesterol synthesis?

Answer 15

They inhibit HMG-CoA reductase

Question 16

Describe the normal process following an injury to a blood vessel

Answer 16

vasoconstriction, platelets binding to exposed subendothelial connective tissue (collagen), primary haemostatic plug formation, secondary plug formation, clearance, inhibition and inactivation

Question 17

What factors make up Virchow’s triad?

Answer 17

Hypercoagulability, damage to vessel wall and change in blood flow

Question 18

Endothelial tissue has antithrombotic properties, what are they?

Answer 18

Nitric oxide and prostacyclin inhibit platelet function by stopping contact with subendothelial connective tissue

Question 19

When do venous thrombi usually occur?

Answer 19

Inapporpriate activation of coagulation cascade

Question 20

What is Factor V Leiden?

Answer 20

The most common inherited venous thrombi, but can also be caused by a mutation causing the individual to be less susceptible to the breakdown of protein C