Clinico-pathological Conference Flashcards

1
Q

Potential causes of an anterolateral MI

A
  • rupture of atherosclerotic plaque
    • rupture of erosion
    • platelet adhesion and aggregation
    • intracoronary coagulation
  • thrombus formation
  • embolism
  • sponatenous coronary dissection
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2
Q

Treatment of an STEMI

A
  • immediate percutaenous revascularisation
  • primary percutaneous coronary intervention
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3
Q

What is the main measure of inflammation?

A

C-reactive protein

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4
Q

Timeline of CRP

A
  • Injury, infectious agent
  • innate immune system respond to injury
  • inflammatory cytokines released into the blood and go to the liver where they engage with receptor cells
  • CRP + fibrinogen = Activated acute system causes down regulation of some genes producing protein
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5
Q

Draw a diagram showing the pathogenisis and natural history of ACS

A
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6
Q

Describe the vascular phenotypes driven by the inhibition of IL-1

A
  • reduces atheroclerosis in animal models
  • reduces neintima formation of POBA and stenting
  • reduces vascular oxidative stress
  • restores endothelial function in fat fed models
  • UP REGULATED in coronary atherosclerosis
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7
Q

Drug treatment after an acute MI

A
  • Aspirin
  • Ticagrelor
  • ACE I
  • Beta-Blocker
  • Statin
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8
Q

Causes of a loud systolic murmur?

A
  • blood in pericardium - lV rupture
  • ventricular spetal rupture - papillary muscle necrosis
  • mitral regurgitation
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9
Q

Complications of Acute MI

A
  • arrhythmia
    • bradycardia = heart block
    • Tachycardia = AF, VT and VF
  • Myocardial death
    • pericarditis, VSD, free wall rupture, papillary muscle necrosis
  • LV thrombus and embolisation
  • Heart failure
    • pump failure
    • LV dilation
    • LV aneurysm
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10
Q

How to pronounce someone dead

A
  • Cessation of the circulation
    • no pulses
    • no cardiac acitivity
      • no heart sounds or electrical activity
  • Cessation of respiration
  • Cessation of cerebral function
    • fixed dilated pupils (do not constrict to light)
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11
Q

Pathology of an MI

A
  • myocyte death
  • coagulation
  • inflammation
    • neutrophil recruitment
    • monocyte recruitment and macrophage formation
    • digestion and removal of debris
  • Granulation and scar formation
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12
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

0-1hrs

A
  • normal
  • normal
  • ST Elevation
  • None
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13
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

1-4hrs

A
  • N/A
  • Coagulation necrosis
  • ST elevation and troponin elevated
  • hypokinesia on echo
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14
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

4-12hrs

A
  • Motting
  • coagulation necrosis, oedema, haemoorhage
  • ST elevation and Q waves, Troponin elevated
  • hypokinesia
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15
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

12-24 hrs

A
  • Dark motting
  • Coagulation necrosis, cintraction band necrosis
  • ST elevation and Q waves, peak troponin
  • hypokinesia
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16
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

1-3 days

A
  • Yellowish
  • Necrosis continues, loss of nuclei, inflammation
  • ST elevation and Q waves, tropnin elevated
  • Hypokinesia
17
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

3-7 days

A
  • yellow centre, hyperaemia at borders
  • disintegration of structures and macrophage infiltration
  • Q waves, troponin elevated
18
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

7-10 days

A
  • yellow
  • start of ganulation, hypokinsia tissue
  • Q waves, troponin negative
19
Q

Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:

10days - 3 months

A
  • white grey
  • collagen and dense scar formation
  • Q waves
  • LV dilation
20
Q

Type 1 respiratory failure =

A

hypoxemia and normocapnia

V/Q mismatch and loss of functional alveoli

  • “Pure” emphysema – the Pink Puffer
  • Acute pulmonary oedema
  • Pulmonary embolism
  • Pneumonia
  • ARDS
21
Q

Type 2 respiratopry failure =

And acute causes

A

hypoxemia and hypecapnia

hypoventilation

  • Lung disease (COPD infective exacerbations, severe asthma) • Mechanical (overdose, neuromuscular, flail chest)
  • Obstruction (anaphylaxis, epiglottitis, croup)
  • Pickwickian syndrome (primary hypoventilation)
22
Q

What is respiratory failure?

A
  • Inability to maintain a normal arterial oxygen level
  • Defined as a PaO2 < 8 kPa
  • NORMAL VALUES
    • PaO2 12.5±0.7 kPa
    • PaCO2 5.3±0.3 kPa
23
Q

Treatment of type 1 respiratory failure

A

Oxygen

Mechanical ventilation (if FiO2 of 0.6 cannot be maintained)

24
Q

Causes of chronic respiratory failure

A

Arterial pH is normal but bicarbonate is raised due to renal retention

  • COPD
  • Other chronic lung disease
  • Neuromuscular disease
  • Massive obesity
  • Chest wall deformity
25
Q

Symptoms of chronic resp. failure

A
  • morning headache
  • daytime somnolence
  • mood swins
  • intellectual decline
26
Q

Signs of COPD

A
  • The “Blue Bloater”
  • Loss of hypercapnic respiratory drive
  • Hypoventilation plus alveolar loss

SIGNS
Vasodilatation, tremor, confusion, cyanosis DIAGNOSIS ONLY ON BLOOD GASES

27
Q

Treatment for chronic respiratory failure

A
  1. Domiciliary oxygen therapy
  2. Continuous positive airways pressure
  3. Non-invasive ventilation