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JG Year 1 > 126 Angina > Flashcards

126 Angina Flashcards

1
Q

Define hypoxia

A

Lack of O2 in tissues leading to decreased aerobic oxidative respiration followed by cell injury

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2
Q

Define ichaemia

A

INadequate blood flow to a part of the body caused by constriction or occlusion of artery or decreased venous drainage leading to lack of O2 and essential metabolites

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3
Q

What are the 4 things which cause cell damage?

A
  1. Decreased ATP
  2. Membrane damage
  3. Increased intracellular calcium
  4. Increase in O2 derived free radicals
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4
Q

What is the outcome when there’s decreased ATP in the cell?

A
  • decreased Na+/K+ pump therefor influx of Ca2+,H2O and Na+ and efflux of K+ causing ER swelling and loss of microvilli
  • Increased anaerobic glycolysis —> decreased glycogen and decreased pH –> clumping of chromatin
    • detachment of ribosomes meaning decreased protein synthesis
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5
Q

What is the outcome of membrane damage of a cell?

A
  • decreased ATP synthesis including decreased phosphlipid synthesis
  • increased intracellular Ca2+ which activates phospholipases and proteases which causes breakdown of the cytoskeleton
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6
Q

Which 4 enzymes are activated by increased intracellular calcium during cell injury?

A
  1. ATPase
  2. Phospholipase
  3. Protease - breakdown of the cytoskeleton and membrane
  4. Endonuclease - breakdown of chromatin
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7
Q

What is reperfusion injury?

A

Reperfusion of ischaemic tissues - the WBC returning to the tissues release ILs and free radicals which further damages the cells. Re-introduction of O2 to the tissue causes damage to proteins, DNA and cell membrane

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8
Q

What is the contents of the core of an artherosclerotic plaque?

A
  • LDL cholesterol
  • cellular debris
  • cholesterol crystals
  • foam cells
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9
Q

Which cells form foam cells within the core of an artherosclerotic plaque?

A

Macrophages

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10
Q

What is the initial step in the formation of an atherosclerotic plaque?

A

Irritation of the endothelium causing endothelial dysfunction

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11
Q

What do foam cells release within an atherosclerotic plaque?

A

Proteinases which break down collagen

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12
Q

Which layer of the artery wall does LDL cholesterol accumulate in to cause formation of an atherosclerotic plaque?

A

Tunica intima

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13
Q

Which cells form the fibrous cap on an atherosclerotic plaque?

A

Smooth muscle cells - lay down collagen, elastin and proteoglycan

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14
Q

Which cells are seen in histology of myocardium 4-12 hours post MI?

A

Eosinophils

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15
Q

How long after an MI does coagulation necrosis start?

A

4-12 hours

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16
Q

How long after an MI does neutrophil infiltration start?

A

12-24 hours

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17
Q

How long after an MI does phagocytosis of myocardium by macrophages happen?

A

3-7 days

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18
Q

Define angina pectoris

A

Reversible ischaemia to the myocardium brought on by increased workload and releived by rest which is normally caused by CAD

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19
Q

Name the 4 life threatening causes of chest pain

A
  1. MI
  2. PE
  3. TnPTx
  4. Dissecting aortic aneurism
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20
Q

Name some pulmonary causes of chest pain (4 listed)

A
  1. PE
  2. TnPTx
  3. Pneumonia
  4. Pleuritis
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21
Q

Name some GIT causes of chest pain (8 listed)

A
  • oesophagitis
  • oesophageal spasm
  • reflux
  • cholecystitis
  • cholecholithiasis
  • ascening cholangitis
  • peptic ulcer
  • pancreatitis
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22
Q

Name 3 causes of non-atherosclerotic CAD (6 listed)

A
  1. congenital anomalies of the coronary arteries
  2. arteritis
  3. coronary ectasia (abnormal dilation of the coronary arteries)
  4. Radiotherapy induced CAD
  5. Syndrome X (normal coronary arteries but with micrvascular disease)
  6. Prinzmentals angina
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23
Q

What is syndrome X?

A

Angina but with normal coronary arteries - microvascular disease

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24
Q

What is Prinzmentals angina?

A

Spasm of the coronary arteries which happens cyclically - even at rest.

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25
Q

What is defined as Class I angina?

A

Pain with strenuous excercise

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26
Q

What is defined as Class IV angina?

A

Inability to perform activities of daily living and angina at rest

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27
Q

Which functional tests can be performed to diagnose angina? (5 listed)

A
  • ETT
  • Stress echo
  • Myocardium perfusion testing
  • PET scan
  • Stress MRI
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28
Q

Which drug is used in a stress echo for diagnosis of angina? What is its MOA?

A

Dobutamine - cardiac stimulant action by directly stimulating β1 receptors to increase contractility and stroke volume

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29
Q

Which drug is used in myocardial perfusion testing (scintigraphy)? MOA?

A

Adenosine - inhibits slow inward Ca2+ current and activation of adenylate cyclase in SM cells –> relaxation and increased blood flow to coronary arteries.

Relatively low perfusion seen in stenotic coronary arteries

30
Q

Which anatomical tests enables visualisation of the histology of the coronary arteries?

A

Invasive coronary angiography with intravascular ultrasound

31
Q

What can CT coronary angiography allow visualisation of?

A

Atherosclerotic plaques

32
Q

What is the 1st line treatment for rapid symptomatic relief of angina?

A

Glyceryl trinitrate sublingually

33
Q

Whatis the MOA of GTN spray?

A
  • glyceryl trinitrate is converted into NO which activates guanyate cyclase
  • stimulates production of cGMP
  • kinase dependent phosphorylatio of SM cells and dephosphorylation of myosin light chain
  • causing relaxation of the SM
34
Q

What in addition to GTN should be prescribed as 1st line treatment of angina pectoris?

A

β-blockers eg bisoprolol

35
Q

What is the MOA of β-blockers?

A
  • Blocks the catecholamine action on the β1-adrenergic receptors in heart and vascular smooth muscle
  • Reduciton of sympathetic drive –> lowered HR, and decreased myocardial contractilty
  • Improves excercise tolerance and relives symptoms
36
Q

What are the contraindications for β-blockers? (3 listed)

A
  • asthma
  • bradycardia
  • HF
37
Q

Which drug can be used if β blockers are contraindicated?

A

Verapamil - Ca2+ blocker

38
Q

What type of drug is amlodopine?

A

Ca2+ channel blocker

39
Q

What is the 2nd line added in treatment for angina pectoris?

A

Ca2+ channel blockers

40
Q

What is the MOA of Ca2+ channel blockers in angina pectoris?

A
  • inhibits the influx of Ca2+ ions by inhibiting the voltage gated calcium channels
  • causes relaxation of SM –> relaxation of the coronary arteries and peripheral vascular smooth muscle
41
Q

What is isorbide mononotrate and what is it used to treat?

A

Long acting glyceryl trinitrate for the 2nd line treatment of angina

42
Q

What kind of drug is ivabridine?

A

K+ channel activator

43
Q

What is the 3rd line added in treatment for angina? give an e.g.

A

K+ channel activators

e.g. Nicorandil

44
Q

What is the MOA of K+ channel activators?

A

They’re NO donors which activate cGMP to cause SM relaxation.

Open K+ channels which causes efflux of K+ and decreased Ca2+ entry therefore SM relaxation

45
Q

When is ranolasine added in for pharmacological treatment of angina?

MOA?

A
  • If the pt is still symptomatic after all other treatment.
  • Inhibits late Na+ channels
    • decreased Ca2+ overload to cause SM relaxation
46
Q

What is the treatment for acute coronary syndrome?

A
  • Morphine
  • Oxygen
  • Nitrates
  • Anti-platelet therapy - eg aspirin 300mg/clopidogrel
47
Q

What is the pharmacological prevention following acute coronary syndrome? MI-5

A
  1. Aspirin
  2. Clopidogrel
  3. ACEI
  4. β-blocker
  5. Statin
48
Q

Where in the blood vessel is the highest velocity of blood flow?

A

In the centre of the lumen

49
Q

Which vessels are resistance vessels?

A

Arterioles

50
Q

What units is blood resistance measured in?

A

R units

51
Q

If mean aortic pressure is 90mmHg and output is 90ml/s, what is the resistance?

A

= 1 R unit

52
Q

What happens to the flow of blood after reaching its ‘critical velocity’?

A

Changes from laminar to turbulent

53
Q

What does Darcy’s law state?

A

That flow is proportional to the pressure difference - this is in laminar flow, not turbulent

54
Q

Why are systolic murmurs more frequent in anaemic people?

A

There is a lower viscosity to the blood which causes more turbulence

55
Q

Above what value of reynolds number is turbulence seen in bloodflow?

A

>3000

56
Q

Below what value of Reynolds number is laminar flow present in blood?

A

<2000

57
Q

In which vessels is the highest and lowest velocity of blood?

A

Highest = aorta

Lowest = capillaries

58
Q

What is the total cross sectional area of the capillaries in comparison to the aorta?

A

x1000 more cross sectional area

59
Q

What does the Poiseuille-Hagen formula describe? How is this useful in the body?

A

The relationship between flow, viscosity and radius of a tube.

Organ perfusion is maintained by this - a small increase in the diameter of blood vessels = pronounced effect on systemic arterial pressure

60
Q

What is the relationship of flow to radius of a tube?

A

flow ∝ 1/r4

61
Q

What is the Fahraeus-Lindqvist effect?

A

The viscosity of blood changes with the diameter of the tube it travels through. Decrease in viscosity when decrease in diameter

62
Q

What does the ‘cell free zone’ in the lumen of larger vessels allow?

A

Lubrication of blood to decrease the viscosity

63
Q

Where is bolus flow seen?

A

Capillaries - much less friction ∴ lower viscosity

64
Q

What is haematocrit?

A

Volume percentage of RBCs in the blood

65
Q

What happens to the viscosity of blood if haematocrit is raised?

A

Increases

66
Q

What does Kery’s tissue clearance measure?

A

Blood flow by measuring the rate of distribution of blood through the body with radioactive isotope

67
Q

How can Fick’s prinicple be used to measure blood flow?

A

Measuring bloodflow through the lungs - rate of O2 uptake is measured

68
Q

Explain venous occlusion plethysmography

A
  • Studying blood flow through the periphery
  • Arm sealed in a water tank
  • venous drainage occluded
  • rate of increase in volume of water in tank = function of arterial blood flow
69
Q

What is active hyperaemia?

A
  • Active hyperemia is the increase in organ blood flow (hyperemia) that is associated with increased metabolic activity of an organ or tissue.
  • increased oxygen consumption of during muscle contraction stimulates the production of vasoactive substances that dilate the resistance vessels in the skeletal muscle
70
Q

Which hormones act to constrict blood vessels? (2 listed)

A
  • Adrenaline
  • Angiotensin II

JG Year 1 (27 decks)

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