CVS Pathology Flashcards
1
Q
Describe the pathogenesis of an aortic dissection
A
- Medial weakness (commonly from HTN), medial hypertrophy vasa vasorum, intimal tear, blood flow dissects the media -> medial haematoma.
- Cystic medial degeneration (HTN)
- Risk factors – HTN, CT disease (e.g. Marfan’s, Ehlers-Danlos), iatrogenic (e.g. arterial cannulation), pregnancy, trauma
2
Q
How are aortic dissections classified?
A
By site of involvement:
Stanford
Proximal (A) and distal (B)
DeBakey
I – ascending and descending
II – ascending only
III – descending only (better prognosis)
3
Q
What are the potential consequences of aortic dissection?
A
- Rupture back into intima or out through adventitia
- Most common cause of death is rupture into pericardial, pleural or peritoneal cavities
- Other outcomes include cardiac tamponade, aortic insufficiency, MI, extension into any of the branches of the aorta causing obstruction +/- ischaemia, transverse myelitis
4
Q
What are the causes of Aortic valve stenosis?
A
- Post-inflammatory scarring (Rheumatic fever)
- Senile calcific Ao Stenosis
- Calcification of congenitally deformed valve
5
Q
What is calcific aortic stenosis?
A
- Ao Stenosis most common valvular abnormality (2%)
- Wear and tear => calcification on normal or cong bicuspid valves (1%). Newer evidence implicates chronic injury from HTN, hyperlipdaemia & inflammation.
- Clinically significant in 6-7th decade in bicuspid valves, 8-9th decade in prev. normal valves
- Heaped up calcified masses within cusps=> protrude through to outflow tracts. Functional valve area decreased.
6
Q
What are the consequences of calcific aortic stenosis?
A
- LV outflow obstruction=> increased pressure gradient over valve. (Severe when valve area 0.5-1 cm2)
- CO maintained by concentric LVH. Hypertrophied myocardium ischaemic.
- Impaired systolic and diastolic function.
- Decompensation => angina, CCF, syncope
7
Q
What are the causes of acute pericarditis?
A
- Infectious; viral, pyogenic bacteria
- Immune mediated (presumed); Rheumatic fever, SLE, Scleroderma, post cardiotomy. Post MI (Dressler’s), Drug hypersensitivity reaction.
- Other; AMI, uraemia, post cardiac surgery, neoplastic, trauma, radiation
8
Q
What types of pericardial fluid exudate occur?
A
- Serous; usually non-infectious inflammation, RF, SLE, uraemia, tumours
- Fibrinous/serofibrinous; (most common) post MI, Dressler’s, trauma, post surgery but also as in 1.
- Purulent/suppurative; almost always bacterial invasion from local infection, lymphatic or blood seeding, or at operation
- Haemorrhagic
- Caseous
9
Q
Describe the clinical features of pericarditis
A
- Pericardial rub (may be absent if large effusion).
- Pain, fever (chills and rigors if suppurative)
- Signs of cardiac failure
10
Q
Outline the steps involved in the pathogenesis of atherosclerosis
A
Response to injury hypothesis:
- Endothelial injury and dysfunction
- Lipoprotein (mainly LDL) accumulation and oxidation in vessel wall
- Monocyte adhesion and migration into intima and transformation into foam cells and macrophages
- Platelet adhesion
- Smooth muscle cell migration from media into intima
- Subsequent smooth muscle cell proliferation in intima
- Enhanced lipid accumulation within intimal cells (macrophages and smooth muscle cells)
11
Q
List the potential causes of endothelial injury?
A
- Hyperlipidaemia,
- Hypertension,
- Smoking
- Haemodynamic factors (disturbed flow patterns)
- Homocysteine
- Toxins
- Viruses
- Immune reactions
12
Q
List the major risk factors for aortic dissection?
A
- Hypertension
- Connective tissue diseases eg. Marfan Syndrome,
- Iatrogenic: coronary artery catheterisation, coronary artery by pass.
- Pregnancy
- Trauma
13
Q
Describe the morphological features of aortic dissection
A
- Most frequent pre-existing = medial degeneration of elastic tissue
- Intimal tear aorta extends into the media.
- Haematoma spread between the middle and outer thirds along the laminar planes of the media and formed a blood filled channel.
- Disrupts outward causing massive haemorrhage or re-rupture into the lumen of the aorta producing a false lumen.
14
Q
What are the consequences of aortic dissection?
A
- Dissects proximally towards the aortic valve and vessels of the neck and causes disruption of the aortic valve, cardiac tamponade, myocardial infarction, cerebral vascular accident.
- Dissects distally into the renal, mesenteric, iliac & femoral arteries causing ischaemia.
- Compression of the spinal vessels causing transverse myelitis.
15
Q
Describe the pathological changes in myocardium following occlusion of a coronary artery
A
- Loss of contractility (<2mins); loss of ATP (50% at 10min, 10% at 40min); irreversible cell injury (20-40min); microvascular injury (>1hour); coagulative necrosis.
- Minutes: myofibrillar relaxation, glycogen depletion, mitochondrial and cell swelling.
- 40minutes: sarcolemmal disruption, mitochondrial amorphous densities.
- Necrosis first in subendocardium, endocardium is spared. 4-12hour coag necrosis, edema, haemorrhage
