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Cardiovascular System > Atherosclerosis (atheroma, Thrombosis & Embolism, Myocardial Infarction, Ischaemic Heart Disease & Angina, ACS & SCAD) > Flashcards

Atherosclerosis (atheroma, Thrombosis & Embolism, Myocardial Infarction, Ischaemic Heart Disease & Angina, ACS & SCAD) Flashcards

1
Q

What is an atheroma? Where does it form?

A

Atheroma = formation of focal elevated lesions (plaques)

Forms in the intima (innermost membrane) of large and medium-sized arteries

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2
Q

What are the consequences of arteromatous plaques in coronary arteries?

A

Plaques narrow the lumen —> ischaemia
Serious consequences:
- angina (chest pain due to reduced blood flow to heart muscles) due to myocardial ischaemia
- complications due to thromboembolism

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3
Q

What is the 2-step process of development of atheromatous plaque?

A
  1. Injury to endothelial lining of artery

2. Chronic inflammatory and healing response of vascular wall to agent causing injury

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4
Q

How does the endothelium get injured(2)? What are the consequences of this(3)?

A

Many causes including:
• Haemodynamic disturbances (turbulent flow)
• Hypercholesterolaemia (impairs endothelial function, lipoproteins can aggregate in intima and are modified by free radicals)

Consequences:

  • accumulation of lipoproteins in vessel wall
  • monocytes migrate into intima and transform into foamy macrophages
  • platelets adhere
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5
Q

What are the 4 stages of atherogenesis?

A

Fatty streak:
- earliest significant lesion
- found in young children
- no clinical significance (may disappear)
Early atheromatous plaque:
- found in young adults and onwards
- smooth yellow patches in intima
Fully developed atheromatous plaque:
- central lipid core with fibrous tissue cap, covered by arterial endothelium
- inflammatory cells reside in fibrous cap
- highly thrombogenic (forms thrombus or clot when in contact with blood)
Complicated atheroma:
- haemorrhage into plaque (calcification)
- plaque rupture/fissuring
- thrombosis

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6
Q

Causes/risk factors of atheroma (6)

A 
Hypercholesterolaemia is most important risk factor (causes plaque formation in absence of other known risk factors)
Smoking 
Hypertension
Diabetes mellitus
Male 
Elderly
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7
Q

What are the signs of Hyperlipidaemia(3)?

A

Corneal Argus - deposit of cholesterol, phospholipds, triglycerides in arc on the iris
Tendon xanthomata - cholesterol deposits in tendons (often on knuckles and Achilles)
Xanthelasmata - yellow deposits of cholesterol underneath skin (usually on/around eyelids)

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8
Q

What are high grade plaque stenosis? What is stenoses atheromatous coronary artery? (What if its severe?)

A

Stenosis of 50-75% of vessel lumen —> critical reduction of blood flow in distal arterial bed —> reversible tissue ischaemia

E.g. stenoses atheromatous coronary artery = stable angina
Severe stenosis = unstable angina (ischaemic pain at rest)

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9
Q

What is acute atherothrombotic occlusion?

A

Ruptured plaque exposes thrombogenic plaque contents to blood stream —> coagulation cascade and thrombotic occlusion short time

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10
Q

What is a total atherothrombotic occlusion? With examples

A

Total occlusion —> irreversible ischaemia —> necrosis (infarction) of tissues

Examples:

- myocardial infarct (coronary artery)
- stroke (carotid, cerebral artery)
- lower limb gangrene (ileal, femoral, popliteal artery)
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11
Q

What is embolisation of the distal arterial bed?

A

Detachment of small thrombus fragments from thromboses atheromatous arteries —> embolise distal to ruptured plaque

Embolism occlusion of small vessels —> small infarcts in organs
(Common cause of stroke - cerebral infarct/TIA)

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12
Q

What is a ruptured atheromatous abdominal aneurysm?

A

Aneurysm - bulge in blood vessel
Media beneath atheromatous plaques gradually weakened —> gradual dilation of vessel
Vessel suddenly ruptures —> massive retroperitoneal haemorrhage (high mortality)

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13
Q

What are primary prevention measures for atheromatous plaques (5)?

A 
Stop smoking 
Control blood pressure 
Weight loss
Regular exercise 
Dietary modification
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14
Q

What are secondary prevention measures for atheromatous plaques?

A

Cholesterol lowering drugs (inhibits platelet aggregation to decrease risk of thrombosis on established atheromatous plaques)

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15
Q

What defects can occur in blood flow (2)?

A

Stasis - stagnation of flow

Turbulence - forceful, unpredictable flow

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16
Q

What is Virchow’s triad?

A
  1. Changes in blood vessel wall - e.g. atheromatous of coronary artery
  2. Changes in blood constituents - e.g. hyperviscosity
  3. Changes in pattern of blood flow - e.g. stasis (post-operatively), turbulence (atheromatous plaque)
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17
Q

What is a thrombosis

A

formation of a solid mass from the constituents of blood within the vascular system during life

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18
Q

What are common clinical scenarios of thrombosis (3)?

A

Deep vein thrombosis - blood clot developing in deep vein in body (usually leg)
Ischaemic limb - sudden decrease in limb perfusion that threatens viability of limb
Myocardial infarction

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19
Q

What are the 2 types of embolus?

A

Systemic thromboembolus

- travel to wide variety of sites: often lower limbs, brain
- consequences dependent on: vulnerability of affected vessel to ischaemia, calibre of occluded vessel

Venous thromboembolus

- originate from deep venous thromboses 
- travel to pulmonary arterial circulation 
- consequences dependent on size of embolus 
- multiple over time —> pulmonary hypertension & right ventricular failure
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20
Q

Risk factors for DVT and pulmonary thromboembolism (7)

A 
Cardiac failure 
Severe trauma/burns
Post-op/post-partum (time after baby birth)
Nephrotic syndrome
Old age 
Oral contraceptive 
Bed rest/immobile
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21
Q

What are the types of embolus (9)

A

Fat (after major fractures)
Gas (decompression sickness - N bubbles lodge in capillaries)
Air (head and neck wounds, surgery, central venous catheter)
Tumour (spread of tumour)
Septic material (infective endocarditis)
Amniotic fluid (cause of collapse in childbirth)
Bone marrow (fractures - CPR)
Foreign bodies (sutures)

22
Q

What is ischaemia?

A

Relative lack of blood supply to tissue/organ leading to inadequate O2 supply to meet needs of tissue/organ

23
Q

4 types of hypoxia

A
  1. Hypoxic - low inspired O2 level/normal inspired O2 but low PaO2
  2. Anaemic - normal inspired O2 but abnormal blood
  3. Stagnant - normal inspired O2 but abnormal delivery (occlusion of vessel)
  4. Cytotoxic - normal inspired O2 but abnormal at tissue level
24
Q

What are the supply (5) and demand (2) causes of ischaemic heart disease?

A 
Supply:
Coronary artery atheroma 
Cardiac failure (flow)
Pulmonary function (e.g. pulmonary oedema)
Anaemia 
Previous MI
Demand:
Heart has high intrinsic demand 
Exertion/stress
25
Q

Clinically correlate atheromatous stages to conditions

A

Established atheroma in coronary artery = stable angina
Complicated atheroma in coronary artery = unstable angina
Complicated ruptured plaque —> thrombosis —> ischaemia/infarction
Atheroma in aorta —> aneurysm

26
Q

Functional effects of ischaemia

A

Blood/O2 supply fails to meet demand due to insufficient supply or too high a demand (or both)

27
Q

Effects of acute and chronic ischaemia

A

Acute - sudden decrease in limb perfusion that threatens viability of limb
Chronic - peripheral arterial disease resulting in reduced blood flow to limbs (commonly lower)

28
Q

Biochemical and cellular effects of ischaemia

A

Insufficient O2 to meet demand therefore aerobic metabolism —> anaerobic metabolism —> cell death
Different tissues have variable O2 requirements and are variably susceptible to ischaemia - dependent on metabolic rate

29
Q

What is a myocardial infarction?

A

Coronary arterial obstruction —> decreased blood flow to region of myocardium —> ischaemia + rapid myocardial dysfunction —> myocyte death

30
Q

What is the time scale of myocardial ischaemia

A

Seconds = anaerobic metabolism & onset of ATP depletion
<2minutes = loss of myocardial contractility (—> heart failure)
Few minutes = ultrastructural changes (myofibrillar relaxation, cell and mitochondrial swelling) potentially reversible
20-30minutes = severe ischaemia —> irreversible damage
20-40minutes = myocyte necrosis
1hour = injury to microvasculature

31
Q

How is a myocardial infarction diagnosed?

A

Detection of cardiac cell death = positive cardiac biomarkers (troponin levels increase significantly- STEMI, not so much NSTEMI)

AND one of:

  • Symptoms of ischaemia
  • New ECG changes
  • Evidence of coronary problem on coronary angiogram or autopsy
  • Evidence of new cardiac damage on another test
32
Q

What are non-coronary causes of troponin rise?

A 
Arrhythmia 
Pulmonary embolism 
Cardiac contusion
Sepsis
Anaemia

(Elevated troponin levels on own just indicate some degree of myocardial cell injury)

33
Q

What does the ECG tell you about myocardial infarction? What does this indicate?

A

If there is ST elevation (STEMI) in ECG there will be complete coronary occlusion
If there is ST depression, T wave inversion or normal there may be a partial coronary occlusion

34
Q

Modifiable and non-modifiable risk factors of stable angina

A

Modifiable:
Smoking
Lifestyle - exercise and diet
Diabetes mellitus (glycemic control reduces CV risk)
Hypertension (BP control reduces CV risk)
Hyperlipidaemia (lowering reduces CV risk)

Non-modifiable:
Age
Gender
Family history 
Genetic factors
35
Q

What is angina

A

a discomfort in the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis

36
Q

What is the pathophysiology of stable angina

A

Mismatch between supply of O2 and metabolites to myocardium and myocardial demand for them
Commonly due to reduction in coronary artery blood flow to the myocardium (most common cause is coronary atheroma)

37
Q

What presenting features make angina likely?

A

Site of pain (retrosternal)
Character of pain (tight band/pressure/heaviness)
Radiation sites (neck/jaw/down arms)
Aggravating (exertion/emotional stress)
Relieving factors (rapid improvement with glycerol trinitrate)

38
Q

What presenting features make angina unlikely?

A

Sharp/stabbing pain (more likely pleuritic or pericardial)
Associated with body movements or respiration
Very localised
Superficial with/or without tenderness
No pattern to pain (particularly if often occurring at rest)
Begins some time after exercise
Lasts hours

39
Q

What are the 4 degrees of stable angina activity?

A
  1. ordinary physical activity doesn’t cause angina – symptoms only on significant exertion
  2. slight limitation of ordinary activity – symptoms on walking > 1 flight of stairs or 2 blocks
  3. marked limitation – symptoms on walking only 1-2 blocks or 1 flight of stairs
  4. symptoms on any activity – getting washed/dressed causes symptoms
40
Q

What are the types of myocardial infarcts (3)?

A

Transmural infarction
Subendocardial infarction
Acute infarcts

41
Q

What is a transmural infarction

A

Ischaemic necrosis affecting full thickness of myocardium

42
Q

What is a subendocardial infarction

A

Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

43
Q

What is an acute infarct?

A

Acute infarcts classified according to whether there is elevation of the ST segment on the ECG

44
Q

What are some complications of myocardial infarction (8)?

A 
Sudden death
Angina
Arrhythmias
Cardiac failure
Cardiac rupture (ventricular wall, septum, papillary muscle)
Reinfarction
Pericarditis 
Pulmonary embolism
45
Q

Name 2 acute coronary syndromes

A

Myocardial infarction

Unstable angina pectoris

46
Q

Name 2 stable coronary artery diseases

A

Angina pectoris

Silent ischaemia

47
Q

What is stable coronary artery disease?

A

Arises due to mismatch in myocardial blood/oxygen supply and demand
Attacks of angina may be precipitated by anything which increases heart rate, stroke volume or blood pressure

48
Q

What is demand ischaemia? What are determinants of demand ischaemia (4)?

A

Ischaemia during stress (physical/emotional)

Determinants of demand ischaemia:
Heart rate 
Systolic blood pressure
Myocardial wall stress
Myocardial contractility
49
Q

What is supply ischaemia? What are determinants of supply ischaemia (4)?

A

Ischaemia at rest

Determinants of supply:
Coronary artery diameter and tone
Collateral blood flow
Perfusion pressure
Heart rate (duration of diastole)
50
Q

What are acute coronary syndromes?

A

Collection of symptoms related to a problem with coronary arteries

Cardiovascular System (37 decks)

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