T9-L3: Cardiovascular Pathology 3

Question 1

What are the clinical features for acute peripheral vascular disease?

Answer 1

Acute 6Ps - Pale, Pulseless, Perishingley Cold, Paraesthesia, Paralysis, Pain

Chronically there is time for collateral vessels to open. Initially may just be reduced pulses. As severity increases you may get intermittent claudication. Critical limb ischemia can shoe rest pain and tissue loss (and necrosis).

Question 2

What are the clinical features of giant cell arteritis?

Answer 2

• General flu-like symptoms - fatigue, weight loss, pain
  
  • Pain - tender superficial temporal artery/sca ; jaw claudication (pain when eating)
  • Vision problems
    Stroke (rare)

Question 3

What clinical features do we see in infective endocarditis?

Answer 3

• Splenic infarct
• Osler’s nodes
• Splinter haemorrhages
• Janeway Lesions
• Roth spots

Question 4

What is the pathogenesis of infective endocarditis?

Answer 4

1. Damage to the endothelium over the valve
2. Fibrin deposition
3. Circulating bacteria colonise this fibrin
4. Vegetations form. This leads to:
   - Vegetations damage the valve causing murmer and heart failure
   - Bacteria in vegetations form local abscess and can lead to AV block
   - Bits of vegetations break off and emboli infect or infract distant organs lea dinging to Janeway Lesions, Splinter Haemorrhages, Splenic infarct , Kidney infarct etc.
   - Immune response causing fever, weight loss, immune complex formation etc.

Question 5

What is the aetiology of infective endocarditis?

Answer 5

• Bacteria: Streptococcus viridans (dental procedures) and strep. Bovis (Colorectal cancer), Staphylococcus aureus - can effect anyone - and staph epidermis (prosthetic valves
  Fungi - candida or aspergillus (rare)

Question 6

What is the aetiology of Pericarditis?

Answer 6

• Infectious - viruses (Coxsachie B), bacteria, TB, fungi, parasite
  
  • Autoimmune - RD, SLE, Scleroderma, Drug hypersensitivity, Post-MI (Dressler’s syndrome)
    Miscellaneous - Uraemia, radiation, Neoplasia,
  • Trauma (Inc. surgery)

Acute can be classified further based on the fluid is composed of such as serofibrinous (due to fibrin), caseous (TB), haemorrhagic (think malignancy) and purulent (neutrophils and so possible bacterial cause). Chronic tends to be constrictive.

Question 7

Give the aetiology of myocarditis.

Answer 7

Infections
• Viruses (COVID-19, Adenovirus “common cold”, Coxsackie A&B, ECHO, influenza, HIV, CMV)
• Bacteria (C. diphtheriae, N. meningococcus, Borrelia)
• Fungi (Candia, histoplasma)
• Protozoa (Trypanosoma cruzi “Chagas disease”)
• Helminths (Trichonosis)

	Immune Mediated
	• Post Group A streptococcus
	• SLE/ other autoimmune conditions
	• Drugs (methyldopa, sulphonamides)
	• Rejection of heart transplant

Other - Sarcoidosis

Question 8

What are the 4 types of cardiomyopathies?

Answer 8

1. Dilated cardiomyopathy - impaired ventricular filling. Left ventricular outflow obstruction (1/3rd of cases) and relative ischaemia
2. Hypertrophic cardiomyopathy - Dilated and thin walled ventricles
3. Restrictive cardiomyopathy- Impaired ventricular filling
4. Arrthmogenic right ventricular cardiomyopathy - RV myocyte adhesion is impaired due to mutation in desmosome proteins. The cells detach and so a fibrofatty tissue forms in attempt to repair damage. This interferes with muscle contraction