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JG Year 1 > 126 Angina > Flashcards

126 Angina Flashcards

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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
What is defined as Class I angina?
Pain with strenuous excercise
26
What is defined as Class IV angina?
Inability to perform activities of daily living and angina at rest
27
Which functional tests can be performed to diagnose angina? (5 listed)
* ETT * Stress echo * Myocardium perfusion testing * PET scan * Stress MRI
28
Which drug is used in a stress echo for diagnosis of angina? What is its MOA?
Dobutamine - cardiac stimulant action by directly stimulating β1 receptors to increase contractility and stroke volume
29
Which drug is used in myocardial perfusion testing (scintigraphy)? MOA?
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
Which anatomical tests enables visualisation of the histology of the coronary arteries?
Invasive coronary angiography with intravascular ultrasound
31
What can CT coronary angiography allow visualisation of?
Atherosclerotic plaques
32
What is the 1st line treatment for rapid symptomatic relief of angina?
Glyceryl trinitrate sublingually
33
Whatis the MOA of GTN spray?
* 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
What in addition to GTN should be prescribed as 1st line treatment of angina pectoris?
β-blockers eg bisoprolol
35
What is the MOA of β-blockers?
* 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
What are the contraindications for β-blockers? (3 listed)
* asthma * bradycardia * HF
37
Which drug can be used if β blockers are contraindicated?
Verapamil - Ca2+ blocker
38
What type of drug is amlodopine?
Ca2+ channel blocker
39
What is the 2nd line added in treatment for angina pectoris?
Ca2+ channel blockers
40
What is the MOA of Ca2+ channel blockers in angina pectoris?
* 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
What is isorbide mononotrate and what is it used to treat?
Long acting glyceryl trinitrate for the 2nd line treatment of angina
42
What kind of drug is ivabridine?
K+ channel activator
43
What is the 3rd line added in treatment for angina? give an e.g.
K+ channel activators e.g. Nicorandil
44
What is the MOA of K+ channel activators?
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
When is ranolasine added in for pharmacological treatment of angina? MOA?
* If the pt is still symptomatic after all other treatment. * Inhibits late Na+ channels * decreased Ca2+ overload to cause SM relaxation
46
What is the treatment for acute coronary syndrome?
* **M**orphine * **O**xygen * **N**itrates * **A**nti-platelet therapy - eg aspirin 300mg/clopidogrel
47
What is the pharmacological prevention following acute coronary syndrome? MI-5
1. Aspirin 2. Clopidogrel 3. ACEI 4. β-blocker 5. Statin
48
Where in the blood vessel is the highest velocity of blood flow?
In the centre of the lumen
49
Which vessels are resistance vessels?
Arterioles
50
What units is blood resistance measured in?
R units
51
If mean aortic pressure is 90mmHg and output is 90ml/s, what is the resistance?
= 1 R unit
52
What happens to the flow of blood after reaching its 'critical velocity'?
Changes from laminar to turbulent
53
What does Darcy's law state?
That flow is proportional to the pressure difference - this is in laminar flow, not turbulent
54
Why are systolic murmurs more frequent in anaemic people?
There is a lower viscosity to the blood which causes more turbulence
55
Above what value of reynolds number is turbulence seen in bloodflow?
\>3000
56
Below what value of Reynolds number is laminar flow present in blood?
\<2000
57
In which vessels is the highest and lowest velocity of blood?
Highest = aorta Lowest = capillaries
58
What is the total cross sectional area of the capillaries in comparison to the aorta?
x1000 more cross sectional area
59
What does the Poiseuille-Hagen formula describe? How is this useful in the body?
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
What is the relationship of flow to radius of a tube?
flow ∝ 1/r4
61
What is the Fahraeus-Lindqvist effect?
The viscosity of blood changes with the diameter of the tube it travels through. Decrease in viscosity when decrease in diameter
62
What does the 'cell free zone' in the lumen of larger vessels allow?
Lubrication of blood to decrease the viscosity
63
Where is bolus flow seen?
Capillaries - much less friction ∴ lower viscosity
64
What is haematocrit?
Volume percentage of RBCs in the blood
65
What happens to the viscosity of blood if haematocrit is raised?
Increases
66
What does Kery's tissue clearance measure?
Blood flow by measuring the rate of distribution of blood through the body with radioactive isotope
67
How can Fick's prinicple be used to measure blood flow?
Measuring bloodflow through the lungs - rate of O2 uptake is measured
68
Explain venous occlusion plethysmography
* 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
What is active hyperaemia?
* 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
Which hormones act to constrict blood vessels? (2 listed)
* Adrenaline * Angiotensin II

JG Year 1 (27 decks)

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