Clinico-pathological Conference Flashcards
Potential causes of an anterolateral MI
- rupture of atherosclerotic plaque
- rupture of erosion
- platelet adhesion and aggregation
- intracoronary coagulation
- thrombus formation
- embolism
- sponatenous coronary dissection
Treatment of an STEMI
- immediate percutaenous revascularisation
- primary percutaneous coronary intervention
What is the main measure of inflammation?
C-reactive protein
Timeline of CRP
- 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
Draw a diagram showing the pathogenisis and natural history of ACS
Describe the vascular phenotypes driven by the inhibition of IL-1
- 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
Drug treatment after an acute MI
- Aspirin
- Ticagrelor
- ACE I
- Beta-Blocker
- Statin
Causes of a loud systolic murmur?
- blood in pericardium - lV rupture
- ventricular spetal rupture - papillary muscle necrosis
- mitral regurgitation
Complications of Acute MI
- 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
How to pronounce someone dead
- 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)
Pathology of an MI
- myocyte death
- coagulation
- inflammation
- neutrophil recruitment
- monocyte recruitment and macrophage formation
- digestion and removal of debris
- Granulation and scar formation
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
0-1hrs
- normal
- normal
- ST Elevation
- None
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
1-4hrs
- N/A
- Coagulation necrosis
- ST elevation and troponin elevated
- hypokinesia on echo
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
4-12hrs
- Motting
- coagulation necrosis, oedema, haemoorhage
- ST elevation and Q waves, Troponin elevated
- hypokinesia
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
12-24 hrs
- Dark motting
- Coagulation necrosis, cintraction band necrosis
- ST elevation and Q waves, peak troponin
- hypokinesia
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
1-3 days
- Yellowish
- Necrosis continues, loss of nuclei, inflammation
- ST elevation and Q waves, tropnin elevated
- Hypokinesia
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
3-7 days
- yellow centre, hyperaemia at borders
- disintegration of structures and macrophage infiltration
- Q waves, troponin elevated
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
7-10 days
- yellow
- start of ganulation, hypokinsia tissue
- Q waves, troponin negative
Describe the appearance, histology, ECG and troponin and imaging of a STEMI at:
10days - 3 months
- white grey
- collagen and dense scar formation
- Q waves
- LV dilation
Type 1 respiratory failure =
hypoxemia and normocapnia
V/Q mismatch and loss of functional alveoli
- “Pure” emphysema – the Pink Puffer
- Acute pulmonary oedema
- Pulmonary embolism
- Pneumonia
- ARDS
Type 2 respiratopry failure =
And acute causes
hypoxemia and hypecapnia
hypoventilation
- Lung disease (COPD infective exacerbations, severe asthma) • Mechanical (overdose, neuromuscular, flail chest)
- Obstruction (anaphylaxis, epiglottitis, croup)
- Pickwickian syndrome (primary hypoventilation)
What is respiratory failure?
- 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
Treatment of type 1 respiratory failure
Oxygen
Mechanical ventilation (if FiO2 of 0.6 cannot be maintained)
Causes of chronic respiratory failure
Arterial pH is normal but bicarbonate is raised due to renal retention
- COPD
- Other chronic lung disease
- Neuromuscular disease
- Massive obesity
- Chest wall deformity
Symptoms of chronic resp. failure
- morning headache
- daytime somnolence
- mood swins
- intellectual decline
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
Treatment for chronic respiratory failure
- Domiciliary oxygen therapy
- Continuous positive airways pressure
- Non-invasive ventilation
