CVS - CHD and Thromoembolic CV Pathologies

Question 1

Atherosclerosis

Answer 1

narrowing of the arteries

Question 2

Ischemia

Answer 2

less oxygen

Question 3

Coronary system

Answer 3

get blood when heart relaxes

Question 4

Coronary circulation:

Answer 4

pressure excreted to aortic arch, when aorta relaxed there is a backflow to the blood

Question 5

hyperlipidaemia/ atherosclerotic lesions

Answer 5

narrow coronary arteries and reduce ability to dilate

Question 6

lesions rupture and stimulate platelet aggregation/thrombus formation LEADS to

Answer 6

occludes the artery and PREVENTS blood flow/suppy

Question 7

How does NO dilate the blood vessel? (vascular smooth muscle)

Answer 7

1. NO stimulates cytoplasmic guanylyl cyclase
2. Elevation of intracellular [cGMP]
3. Activation of protein kinase G
4. Smooth muscle relaxation (vasodilation)
5. PDE isoform breaks down cGMP

Question 8

Antianginal drugs - what are the 1st line options?

Answer 8

• BB = beta blockers (‘lol’) drugs
  for pateints w angina or HF
• CCB = Calcium channel blocker

Question 9

what are the 2nd line options?

Answer 9

• sodium-channel blocker
• potassium channel activator

Question 10

Progressive coronary heart disease;

Answer 10

myocardial infarction

Question 11

What does myocardial infarction require?

Answer 11

thrombolytics or surgical

Question 12

PC heart disease effect on vessels?

Answer 12

severe coronary artery narrowing, transient occlusion or microembolization of thrombis or atheromatous material

Question 13

NSTEMI

Answer 13

Non-ST segment elevation MI

Question 14

NSTEMI explained

Answer 14

myocardial ischaemia and necrosis - still functional (some blood flow)
changes in TROPONIN & no change in ECG

Question 15

why is STEMI worse than NSTEMI?

Answer 15

complete and prolonged occlusion of an epicardial coronary blood vessel

Question 16

ST segment elevation of Mi (STEMI)

Answer 16

Dysfunction and death (necrosis) of cardiac myocytes in the ventricular wall

Question 17

explain the troponin and ECG levels in an occurance of STEMI?

Answer 17

troponin level RISE

elevation of ST segment in ECG

Question 18

thrombosis

Answer 18

blood clotting in artwery

Question 19

embolism

Answer 19

b,ood clot/ endogenous materials (embolus) moving in blood the vessel and obstruct blood flow

Question 20

What are the charicteristics of thrombocytes/ fragments/ platelets?

Answer 20

• no nucleus
• mitochondria in them
• play a role in blood clotting

Question 21

what is the process of maemostasis of blood clotting

Answer 21

physiological process to stop bleeding - staying still

Question 22

Blood clotting - haemostasis. explain in 3 steps:

Answer 22

1) vasular spasm

2) Platelet activation

3) Coagulation- patch (fibrin mesh)

Question 23

1) vasular spasm

Answer 23

pain reflux, constriction of vasuclar smooth muscle , trigger clotting chemicals/ factors needed & directed to site of injury

Question 24

2) Platelet activation

Answer 24

+ive feedback mechanism

Endothelial Damage
Exposed Collagen

Platelets stick to exposed collagen (swell like star shaped cells)

Platelets stimulate ADP, Thromboxane A2 and Serotonin

Von Willebrand Factor- Stabilise collagen-platelet adhesion

Question 25

3. Coagulation- Patch

Answer 25

Clotting factors/procoagulants in Liver
Vitamin K, the biosynthesis clotting factors
Plasma proteins I to XIII

Question 26

What is the last process of blood clotting ? forming a mesh?

Answer 26

Intrinsic (blood) and exrinsic (tissue) > PROthombin activation > PROthombin > thrombin > fibrinogen (soluble) > fibrin (INsoluble) > fribrin (MESH)

Question 27

What happens in the clotting process in ATHEROSCLEROSIS?

Answer 27

the thrombin-mediated platelet activations becomes abrupt and accelerated due to the endothelial dysfunction/damage

Question 28

What is the HEALTHY thrombin mediated process?

Answer 28

Protease-activated receptor causes THROMBIN to activate the platelets via PAR

AT-III binds to HEPARIN (released from endothelial cells)
Anti-thrombin III- heparin complex inhibit throbin activity

Question 29

ATHERSCLEROSIS, hwo does, how does ADP- mediated platelet plug formation work?

Answer 29

becomes abrupt and accelerated due to endothelial dysfunction or damage

PLATELETS stimulate ADP, thromboxane A2 and serotonin

Question 30

Explain the process of pltelet-endothelial interaction (ADP-mediated process- healthy)

Answer 30

ACTIVATED platelets stimulate the release of ADP whioch acts on P2Y receptors in platelets to actiavte +ive feedback

in healthy ADP binds to P2Y receptor and stimulate the release of prostacycin and NO from endothelial cells to prevent plug formation

Question 31

Platelet-Fibrin Plug Formation (GPIIb/IIIa-mediated process- Healthy)

Answer 31

Von Willebrand factor acts as a bridge between collagen, exposed in damaged blood vessels, and the glycoprotein receptors, GPIIb/IIIa expressed in activated platelets

Glycoprotein receptors, GPIIb/IIIa binds to fibrinogen and form platelet-fibrin plug

Question 32

Clot retraction concurrent with vessel repair

Answer 32

The actin and myosin in platelets contract and pulls on fibrin strands
Platelet-derived growth factor (PDGF)
Stimulate smooth muscle and fibroblast division
Vascular endothelial growth factor (VEGF)
Rebuild endothelial lining by multiplying endothelial cells

Question 33

What is Fibrinolysis?

Answer 33

Plasminogen, plasma protein trapped in clot- converted Plasmin-digest Fibrin