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
Symptoms of chronic resp. failure
* morning headache * daytime somnolence * mood swins * intellectual decline
26
Signs of COPD
* The “Blue Bloater” * Loss of hypercapnic respiratory drive * Hypoventilation plus alveolar loss SIGNS Vasodilatation, tremor, confusion, cyanosis DIAGNOSIS ONLY ON BLOOD GASES
27
Treatment for chronic respiratory failure
1. Domiciliary oxygen therapy 2. Continuous positive airways pressure 3. Non-invasive ventilation