Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Personalised Medicine - Cardiovascular > L11 - Ischaemic Heart Disease > Flashcards

L11 - Ischaemic Heart Disease Flashcards

1
Q

What is the path-biology of IHD?

A

Disease of coronary arteries that progresses gradually culminating in heart attack, heart failure and dysrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When does IHD occur?

A

Occurs when a fatty/fibrotic plaque (atherosclerosis) blocks the coronary artery
Blood flow to tissues is restricted –> less nutrients to tissue –> ischaemia
Oxygen demand of the myocardium exceeds supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does IHD present itself as?

A

Chest pain (angina)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What potentially causes angina?

A

Release of K+, H+ and adenosine can sensitise or stimulate nociceptors
Typically central in the chest and can radiate to arms neck and jaw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How many cases of IHD are they a year in the UK?

A

21,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the prevalence of IHD in the UK?

A

> 55yrs
12% men
5% for women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Death rates from IHD have halved in the last 10 years mainly due to efforts to reduce which two types of risk factors?

A

Non-modifiable

Modifiable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are non-modifiable risk factors?

A

Advanced age
Male
Personal history of ischaemic heart disease
Positive family history of heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are modifiable risk factors?

A 
High BP 
Diabetes/obesity 
Smoking 
High cholesterol 
Poor diet
Chronic kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 acute coronary syndromes IHD patients are susceptible to?

A

Unstable angina
NSTEMI - non ST elevation
STEMI - ST elevation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is unstable angina?

A

Pre MI condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is NSTEMI?

A

Type of MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is STEMI?

A

Caused by a complete blockage of one of the main coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When do the acute coronary syndromes present themselves in IHD patients?

A

Syndrome presents when the plaque ruptures –> platelet clots and blockage of coronary artery –> ACS –> ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the prevalence of ACS?

A
  1. 6% in 35-74

2. 3% in age >74

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How many new causes of ACS are there a year in the UK?

A

233,600

75% of these are NSTEMI or unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How many people does STEMI affect in the UK a year?

A

5 in 1000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Is the prevalence of STEMI or NSTEMi rising?

A

NSTEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is angina characterised by?

A

Characterised by heavy or central crushing pain on exertion

Relieved by rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the two types of angina?

A

Stable - if pain occurs under exertion

Unstable - if pain with little exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you treat stable angina?

A 
Reduce cardiac work
- Nitrates
- Ca antagonists
Treat the underlying condition
- Statin 
Prophylaxis	
- An anti-platelet drug like aspirin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do you treat unstable angina?

A

Treat as for a heart attack using DAPT and nitrates

- Dual anti-platelet therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What 3 things do you look at to help distinguish between different acute coronary syndromes?

A

If glycerol trinitrates give relief
If ECG trace is normal
If troponin concentration increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is troponin?

A

A cardiac muscle specific protein

Released when myocytes in ventricles die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which form of angina is an acute coronary syndrome?

A

Unstable angina - can progress to STEMI and NSTEMI

Stable is different in terms of pathology, risk and treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which forms of ACS give GTN relief?

A

Stable angina

Unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which forms of ACS have a normal ECG?

A

Stable angina

Unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

In which forms of ACS are troponin concentrations raised?

A

NSTEMI

STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the main treatment for ischaemia?

A

Restore blood flow – and quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why do you need to restore blood flow so quickly in ischaemia?

A

Need treatments within 2 hours of chest pain

If blood flow is not restored –> necrosis of the heart muscle –> myocardial infarction –> can lead to heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the 4 aims of ischaemia treatment?

A 
Reopen blocked arteries 
- Done by cardiologist – use a stent 
Reduce the coagulability of blood
- Anti-platelts, heparins, aspirin 
Control risk factors
- Statins 
Reduce myocardial oxygen demand
32
Q

What are the two ways you can restore blood flow in ischaemia?

A

Nitrates

PCI - for patients with uncontrolled angina

33
Q

What is PCI?

A

Percutaneous Coronary Intervention

34
Q

How does PCI work?

A

Non-surgical technique - aim to widen the artery using dilation from within
Insertion of metallic stent via brachial or radial artery into heart
- Track a catheter under fluoroscopic guidance into the coronaries

35
Q

What drugs are stents coated in?

A

Popular drugs inhibit cell re-growth e.g. rapamycin or taxol

Rapamycin – inhibits cells in G1/S

36
Q

What is the door balloon time for STEMI?

A

2 hours

37
Q

How does stenting work?

A

Underneath the stent is a balloon which is inflated – 8 atmospheres
- Helps keep the stent up against the vessel wall
Then remove balloon leaving behind stent

38
Q

What treatments do patients have after stenting?

A

DAPT

39
Q

What is DAPT therapy?

A

Aspirin plus an anti-platelet or anti-clotting drug

E.g. PLAVIX (clopidogrel) or Brilinta (ticagrelor)

40
Q

What are the adverse effects of DAPT?

A

Must be continued for up to a year after stenting

Excess bleeding

41
Q

What are the benefits of DAPT?

A

Stent doesn’t block

Positive effects upon neutrophils and therefore reduction in pulmonary infections

42
Q

What is the main aim of pharmacological treatments of IHD?

A

To keep the coronary plaques as stable as possible to avoid an acute clot blockage (occlusion) which can be partial or full and to reduce pain

43
Q

What are the symptomatic pharmacological treatments for IHD?

A 
Reduce strain on the heart
Increase vasodilation of arteries and veins
Nitrates
- Glyceryl trinitrate (short acting)
- Isosorbide mononitrate (long acting)
Aspirin and antiplatelet drugs
Ca channel blockers e.g. amlodipine
K channel activators e.g. Nicorandil 
Analgesia e.g. morphine
44
Q

What are the prognostic pharmacological treatments for IHD?

A

Aspirin
Statins/PCSK9 inhibitors
Beta blockers
oACE inhibitor
Anti-inflammation approaches are being developed
- Inhibit IL-1 – can use microtubule inhibitor

45
Q

How are nitrates administered?

A

First line agent - GTN as a short acting spray given sublingually

46
Q

What are the primary effects of nitrates?

A

Relax smooth muscle and veins –> reduces central venous pressure –> reduces preload –> reduces cardiac work
Mainly impacts larger muscular arteries –> coronary vasodilation –> increases coronary flow

47
Q

What are the secondary effects of nitrates?

A

Reduces cardiac work
Redirection of flow towards ischemic areas of heart muscle
- Evidence from animals that GTN diverts blood from normal to ischemic areas through dilatation of collaterals in the heart
Improves coronary artery spasm

48
Q

What is the mechanism of action of nitrates?

A

GTN metabolism releases NO
NO –> guanylyl cyclase –> GTP converted to cGMP –> PKG –> relaxation of smooth muscle via dephosphorylation of myosin chains and sequestration of intracellular Ca

49
Q

What are the adverse effects of nitrates?

A

Possible hypotension - administer sitting down
Headaches
Tolerance - possibly because of depletion of –SH groups
- More common with longer acting agents

50
Q

What is GTN inactivated by?

A

Hepatic/liver metabolism

51
Q

How long do nitrates take to act?

A

Sublingual delivery effective in 1-2 minutes

  • Conversion from TN to di and mononitrates in minutes
  • Length of effect 30 min
  • Transdermal patches or lung acting forms also available
52
Q

What do nitrates reduce?

A

Ishaemia - not mortality

53
Q

What is the mechanism of action of Ca channel blockers?

A

Block receptor response –> prevent channel opening –> prevent influx of calcium
This non-selectively blocks the contraction of smooth muscle
Dilate coronary vessels

54
Q

What 3 types of drugs act on L-type Ca channels?

A

Phenylalkylamines (e.g.verapamil)
Dihydropyridines (e.g. amlodipine)
Benzothiazepines (e.g. diltiazem)

55
Q

Where does verapamil act?

A

More active on the heart

56
Q

Where does nifedipine act?

A

On smooth muscle

57
Q

What are the side effects of Ca channel blockers?

A

Flushing and headache due to vasodilator action

Verapamil - constipation due to effects on gastrointestinal nerves or smooth muscle

58
Q

What does aspirin reduce?

A

Reduces mortality and risk of a future heart attack

59
Q

When/how is Aspirin administered?

A

Given immediately on presentation and daily thereafter
75mg/day suppresses platelet function
Given orally

60
Q

What is the mechanism of action of aspirin?

A

Inhibits COX-1 receptor on platelets –> irreversibly acetylates COX enzymes –> prevents conversion of arachadonic acid to thromboxane A2  reduces platelet aggregation
Effects last for the lifetime of the platelet - 10 days
- Platelets do not have a nucleus so cannot replace enzymes
- Have to be made in bone marrow

61
Q

Where is aspirin hydrolysed/protonated?

A

A weak acid so protonated in the stomach and able to pass across the mucosa
Rapidly hydrolysed to salicylate by esterases in the liver (75%) and plasma

62
Q

How does aspirin cause its anti-inflammatory actions?

A

Through inhibition of nFkB

63
Q

What are the side effects of aspirin?

A

Gastric bleeding
Deafness/tinnitus (with larger doses/overdoses)
Risk of self poisoning
Resistance to aspirin is known - no genetic tests available
Interacts with warfarin increasing warfarin concentration

64
Q

What do anticoagulants do?

A

Anticoagulants prevents blood clotting and inhibit clotting factors in clotting cascade

65
Q

What are heparins?

A

Glycosaminoglycans found in mast cells and basophils

66
Q

What do heparins do?

A

Activate antithrombin IIIa –> inactivates thrombin and factor Xa –> prevents formation of a stable clot/thrombus

67
Q

What are the side effects of anti-coagulants/heparins?

A

Bleeding

68
Q

What is a second anti-platelet approach?

A

Second antiplatelet approach alongside aspirin use thienopyridines – Clopidogrel and Tiagrelor

69
Q

What can be used to treat analgesia?

A

Opiates and antiemetics

70
Q

Where does morphine bind?

A

Binds to opioid receptors (Gi/G0 coupled to ion channels) in the brain as a partial agonist
- Binds the mu receptor

71
Q

What are the side effects of morphine?

A

Respiratory depression – modulated by mu receptors as well
Nausea and vomiting (40%)
- Because opioids have their effects in the postrema in the medulla where chemical stimuli act and cause vomiting
Reduced tone and motility in the gut
Histamine release
Tolerance

72
Q

Overall what are the 5 steps to treat unstable angina?

A
  1. DAPT - aspirin plus clopidogrel or ticagrelor
  2. Heparin
  3. Analgesics
  4. Secondary prevention - statin, ACE inhibitor or beta blocker
  5. Once stabilised - elective (planned) PCI
73
Q

Overall what are the 5 steps to treat NSTEMI?

A
  1. Antiplatelet and anti-thrombotic therapy
    a. Antiplatelets only active in the arterial circulation not the venous circulation
    i. Anticoagulants active in both
  2. Additional platelet inhibitor if ECG changes are rapid
  3. Analgesics
  4. PCI within 72 hours to determine lesion severity and suitability for stenting or bypass surgery.
  5. Persistent pain plus markers
74
Q

What are the key markers of STEMI?

A

Most severe presentation - must have clear ST elevation on ECG and chest pain of less than 12h duration

75
Q

Overall what are the 4 steps to treat STEMI?

A
  1. First - primary PCI at heart attack centre
  2. If heart attack centre is too far - clot buster drug used intravenously
    a. Clot buster drugs stimulate the breakdown of stable fibrin clots
    b. Not to be used with anti-platelets
  3. Antiplatelet medications – aspirin and ticagrelor
  4. Lifelong medications after STEMI
    - Aspirin 75mg/day
    - Antiplatelet agent for 1 year
    - Statins
    - ACE inhibitors
    - Beta blockers to aid myocardial recovery
76
Q

What is the mortality for STEMI patients who reach hospital?

A

4.4%

30% die before reaching hospital

77
Q

What are 3 ways to personalise treatments for STEMI?

A

1 - Bedside device at the time of PCI after STEMI to measure individual platelet reactivity
2 - Individualised maps of a patient’s coronary arteries help decide which lesions
3 - Inflammation

Personalised Medicine - Cardiovascular (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions