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Year 3 Medicine > Angina > Flashcards

Angina Flashcards

1
Q

Vicious cycle of myocardial ischaemia

A

Myocardial demand exceeds myocardial oxygen supply

This leads to myocardial ischaemia

The ischaemia causes further vasoconstriction, continuing the cycle

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2
Q

Drug targets for angina

A
  • increase supply: nitrates
  • reduce demand: beta blockers
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3
Q

Difference between angina pectoris and myocardial infarction

A
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4
Q

Pathophysiology of atherosclerosis

A

Endothelial damage occurs (by whatever means e.g. metabolic stress), this allows lipoprotein to collect in the intima. As the lipoproteins are free from plasma antioxidants they will then become oxidatively modified. Next leukocytes are recruited and finally mononuclear phagocytes differentiate into macrophages and transform into lipid laden foam cells

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5
Q

Definition of angina pectoris

Non ischaemic causes of angina pectoris

A

Chest discomfort due to myocardial ischaemia associated with coronary artery disease

Other causes: aortic stenosis, hypertrophic obstructive cardiomyopathy

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6
Q

Types of angina

A

Stable

Unstable

Prinzmetal/variant

Syndrome X

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7
Q

Stable angina

A

Angina occurring over several weeks without major deterioration, although symptoms may vary considerably over time (eg with extertion, stress)

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8
Q

Unstable angina

A

Abrutptly worsening angina or new angina at low work load

When plaque goes from being stable to unstable

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9
Q

Prinzmetal angina

A

Spontaneous (i.e. no precipitating cause) angina with ST elevation on ECG.

Coronary artery spasm, often near the site of plaque formation.

Classic symptom: chest pain at night

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10
Q

Syndrome X

A

Happens in perimenopausal or menopausal women.

Angina with objective evidence of myocardial ischaemia (eg ST depression) in the absence of evident coronary atherosclerosis or epicardial (large vessel) disease

Triad:

  1. Anginal chest pain
  2. Positive exercise test on treadmill
  3. Angiographically smooth coronary arteries

Doesn’t often respond to classic anti-anginal therapy

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11
Q

ECG findings in prinzmetal’s angina

A

Profound ST elevation

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12
Q

Key to diagnosis of prinzmetal’s angina

A

Chest pain when going to bed

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13
Q

Decubitus angina

A

Comes on when patient is lying in bed.

Due to severe coronary artery stenosis.

Physiology:

  • increased venous return when lying down
  • increased myocardial work

-

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14
Q

Characteristics of the pain

A

Site- typical angina is central

Character- dull ache is typical. Sometimes it’s not “pain”, it’s “squeezing”

Mode of onset- sudden (likely to be MSK) vs gradual (likely to be cardiac)

Progression

Radiation- often goes to the neck and arm

Positional body function- if its worse upon neck movement for eg we know its MSK

Precipitating or relieving factors- whether activity makes it worse?

Treatment eg GTN BUT BEWARE, because GI reflux also causes chest pain and GTN relaxes lower end of oesophagus (confounding!)

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15
Q

Other chest pains

A

MI: sudden, severe, SWEATING

Aortic dissection: tearing pain- abdo or back. Suspect in relatively eldelry patients.

Pericarditis- usually viral aetiology. Sharp, sudden chest pain. Worse upon breathing, postural differences. Can usually hear a pericardial RUB

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16
Q

Investigations for angina

A

Blood pressure

Lipids

ECG- resting is usually normal in CHD. May pick up old infarct (Q waves).

Stress test- look for ST segment depression.

Angiography- if you already suspect it and want to assess the severity. Usually in patients who’ve had an MI and want to assess

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17
Q

What measurement is used to classify the relationship between exercise capacity and post-MI mortality?

A

Bruce score.

Bruce score <10 mis=9% mortality

Bruce score >10 mins= 2 % mortality

18
Q

What finding on the ECG in a stress test would indicate CHD?

A

ST depression > 1mm

19
Q

What finding on ECG would indicate previous MI?

A

Q waves (Q waves that are longer than normal)

20
Q

When to stop an exercise test?

A
  • severe chest pain
  • rapidly dropping ST segment
  • drop in blood pressure (shows reduction in cardiac output)
  • arrhythmias (Detected on ECG)
21
Q

What is the cause of death of cardiac myocytes in myocardial infarction?

A
  • lack of oxygen
  • cessation of sodium-potassium ATPase
  • cells fill up with sodium
  • water comes in so cells swell and die
22
Q

What is the blood pressure like in aortic stenosis?

A

LOW blood pressure

23
Q

Male vs female incidence of hypertrophic obstructive cardiomyopathy

A

Equal sex ratio

24
Q

Overview of angina management

A
  1. education/lifestyle- exercise
  2. anti-anginal drugs
  3. anti-platelet drugs- avoids complications
  4. revascularisation therapy- CABG or PCI
25
Q

Reasons for supply and demand problems in angina

A

Low supply

  • coronary insufficiency- vasospasm or stenosis
  • Outflow obstruction- aortic stenosis or hypertrophic cardiomyopathy
  • anaemia

High demand

  • arrythmias (AF), sinus tachycardia
  • thyrotoxicosis
  • high afterload (systemic hypertension)

-

26
Q

Anti-anginal drugs

A
27
Q

FIrst line therapy for angina

A

Beta blockers- because of prognostic benefit eg post-MI and hypertensives

28
Q

Beta blocker contraindications

A

Erectile dysfunction

29
Q

2 main categories of CCBs

A
30
Q

Which 3 drugs are often used synergistically for angina?

A

Beta blockers

CCBs

Nitrates- relax vascular smooth muscle, improving blood supply to the heart

31
Q

Calcium antagonists

A
  • used with or instead of beta-blockers
  • heart: negatively inotropic. Blood vessels: peripheral vasodilation
  • amlodipine is more vasoselective than nifedipine, so has less of a -ve inotropic effect- preferred
  • diltiazam and verapamil are also NEGATIVE CHRONOTROPES
  • the non-DHPs are particualrly useful for vasospastic angina
  • short-acting DHPs may increase adverse cardiac events
32
Q

Contraindications and side-effects of CCBs

A
33
Q

Nitrates

A
34
Q

Side effects and ocntraindications of nitrates

A
35
Q

Nicorandril

A

MOst useful when there are contraindications to CCBs o BB

36
Q

What shold all patients with variable angina be on?

A

ANTI-PLATELET THERAPY

37
Q

How is coronary angiogram carried out?

A

Tube inserted from artery in groin- goes towards coronary arteries, which are X-rayed with a dye inserted.

38
Q

Benefits of PTCA (percutaneous transluminal angioplasty)?

A
  1. Chronic stable angina: no benefits on longevity.
  2. MI: beneficial.

With chornic stable angina main treatment is drugs and exercise.

39
Q

Schematic of angioplasty

A
  • first they carry out coronary angiogram to find out where the blockage is
  • insert a balloon, which is inflated and pushes the narrowing out towards the wall
  • SOMETIMES they put a stent in along with it to HOLD the widened part open
40
Q

What is revascularization?

A

Two methods: CABG OR PCI

PCI: percutaneous intervention.. Includes coronary angioplasty ALONG WITH STENT insertion.

41
Q
A

Year 3 Medicine (9 decks)

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