IHD

Question 1

2 Main causes of IHD - what does this centre around?

Answer 1

Disease of the coronary arteries (fatty plaque build up / atherosclerosis)
Non-acute coronary syndrome: stable angina
Angina
Atherosclerosis

Question 2

What is meant by ischaemia?

Answer 2

Resitriction of blood flow to tissues

Question 3

Atherosclerosis features

Answer 3

Atherosclerosis –> restricts blood flow to tissues (ISCHAEMIA), blocks arteries, progressive with age, has modifiable risk factors

Question 4

Angina features

Answer 4

Blood, o2, nutrients, cannot reach the myocardium
Results in chest pain and cell death of the myocardium
Pain in chest seems to occur with less and less exertion

Question 5

Stable angina - why is it different?

Answer 5

NOT an acute coronary syndrome

Occurs due to emotional or physical stress

Question 6

Acute coronary syndromes- what are they ?

Answer 6

Unstable angina
NSTEMI (non st elevation myocardial infarction)
STEMI (st elevated myocardial infarction)

Question 7

What can normally be found in a completely blocked artery

Answer 7

Both a thrombus and a fatty plaque

Question 8

What is seen to distinguish a STEMI from other ACS

Answer 8

No relief from GTN (nitrate treatment)
Troponin present (released as a result of damaged cardiac muscle)
Abnormal ECG (elevated ST)

Question 9

What is seen to distinguish a N-STEMI from other ACS

Answer 9

No relief from GTN
Troponin present
Abnormal ECG (but no elevation of ST)

Question 10

What is seen to distinguish stable angina from other ACS

Answer 10

Relief from GTN
No troponin present
Normal ECG

Question 11

What is seen to distinguish unstable angina from other ACS

Answer 11

Relief from GTN
No troponin
Normal ECG

Question 12

Angina treatment - stable and unstable?

Answer 12

Characterised by crushing pain in the chest
Relieved by rest (no exercise)
- Stable = asparin, ca2+ channel blocker
- Unstable = TREAT AS MI - anti platelet meds, asparin

Question 13

Treatment of ischaemia - what do we aim to do?

Answer 13

Restore blood flow (prevents HF and death of myocardium)
Stenting (opens blocked arteries)
Reduce coagulation (prevents blockage of arteries - warfarin and asparin)
Reduce myocardial o2 demand (reducing work/contractility of the heart)
Control risk factors (stop smoking/good diet!)

Question 14

Features of stent - how soon does it need to be applied? Drugs coating device? Overall process?

Answer 14

PCI (percutaneous coronary intervention)
Ideally needs to happen <120 minutes (door -> balloon time)
Catheter used to dilate vessel and push plaques away
Stent coated with RAPAMYCIN which inhibits proliferation of cells

Question 15

Stenting - overall process, what does it aim to do, how can it be personalised

Answer 15

• Restores blood flow in coronary arteries
• Balloon placed inside the stent, balloon inflated, balloon removed
• Can get balloons of different sizes for personalised aspect

Question 16

What must be done after PCI? Additional benefits?

Answer 16

• After treatment DAPT (dual anti platelet therapy)
  Plavix/asparin
• Up to a year after stenting
• Adverse effects = excessive bleeding
• Additional benefits = anti inflammatory as has positive pleiotropic effects on neutrophils

Question 17

Pharmacological treatments for IHD - prognostic (in anticipation of future event)

Answer 17

• Statins
• Ace –|s
• Asparin/DAPT

Question 18

Pharmacological treatments for IHD - symptomatic (reduces associated symtoms)

Answer 18

• Nitrates
• Asparin/antiplatelet
• Ca2+/K+ channel blockers

Question 19

Nitrates – what is their mechanism of action?

Answer 19

Metabolises release of NO (causes production of GNP from GTP –> activates PKG)
Relaxes vascular smooth muscle and veins

Question 20

Where do nitrates mainly target/

Answer 20

Large muscular arteries

They decrease cardiac work and redirect ischaemic flow

Question 21

Adverse effects of nitrates

Answer 21

• Tolerance
• Headaches
• Hypotension
• Dilation in the collateral vessels of the heart

Question 22

How is IHD treatment personalised?

Answer 22

• Length of stents
• Mapping of coronary arteries
• Can measure activity of platelets in patients to work out the best drugs for their dynamics

Question 23

Ca2+ channel blockers - name an example? Features and mechanism?

Answer 23

VERAPAMIL
Target L type channels
Cardioselective
Few side effects
Disrupt movement of Ca2+ through channels to prevent release from sarcoplasmic reticulum

Question 24

ASPARIN - adverse effects?

Answer 24

Gastric bleeding
Resistance
Self poisoning risk
Deafness/tinnitus

Question 25

Asparin - mechanism of action?

Answer 25

Bind to active site of COX1 enzyme - acetylates serine residue
Prevents Arachodonic acid from doing so
This prevents the production of Prostoglandin H2 which means it cannot be converted into Thromboxane A2 which activates platelets via TP receptors

Platelets don’t have nucleus so until more COX1 is produced platelets cannot coagulate (IRREVERSIBLE)

Question 26

HEPARINS - mechanism of action, adverse effects

Answer 26

Activation of anti clotting factors including ANTITHROMBIN |||a - this inactivates Thrombin and Factor Xa which prevents clot formation
Can result in EXCESSIVE BLEEDING

Question 27

Analgesia - main example - why is it used and where does it exert its’ action?

Answer 27

Very powerful painkiller which is well tolerated when correctly administered
Binds to Opoid receptors Go and Gi in the brain
Coupled to ion channels

Question 28

Analgesia - adverse effects

Answer 28

Induces release of histamines 
Dependance 
Vomiting and nausea
Decreased gut tone and mobility 
Respiratory depression

Question 29

Treatment summary - unstable angina -

Answer 29

1) DAPT
2) Heparin
3) Analgesics
Then move onto secondary prevention drugs such as ACE–|s, B blockers and Statins

Question 30

Treatment summary - NSTEMI

Answer 30

1) DAPT
2) Heparin
3) Platelet inhibitor
Then if ECG changes, stent within 72 hours and analgesics must be applied

Question 31

Treatment summary - STEMI

Answer 31

1) PCI
2) IV clot buster (catheterisation)
3) Antiplatelet drugs (DAPT - asparin + clopidogrel)
If this doesn’t work you’re fucked (lifelong meds ACE-|s, asparin, statins, b blockers)