Pathology

Question 1

what is a dysrhythmia

Answer 1

any variation from normal rhythm of the heart beat = palpitation, flutter

Question 2

symptoms of dysrhythmia

Answer 2

sob
fainting
fatigue
chest pain

Question 3

what are the 3 mechanisms underlying dysrhythmia?

Answer 3

altered impusle formation
altered impulse conduction
triggered activity

Question 4

what can alter impulse formation to trigger an arrhythmia

Answer 4

changing the automaticity of pacemakers - too fast, too slow (and if too slow, other cells may take over)

may have abnormal generation AP at sites other than SA node

changes can occur in the ionic environment
may have damage of tissue/conducting pathway

Question 5

what can cause altered impuse conduction to trigger dysrthythmia

Answer 5

conduction block - ventricles adopt their own slower rate

re-entry - additional pathways of conduction, that allow circulation of signal back to atrium from ventricle -> get extra beats

Question 6

what can cause triggered activity to trigger dysrthythmia

Answer 6

early/late after-depolarsiation

after the refractory period you have a ‘slow period’ - stray currents can set off AP here

cause: excess sympathetic activation

Question 7

strategies for managing dysrhythmias

Answer 7

Always consider the no treatment option

• many anti-arrhythmics have pro-arrhythmic activity **
• may worse arrhythmia and cause sudden death

Where possible, manage underlying causes
drugs
- ionic balance
- ischaemia, infarct, fibrosis

Question 8

What is atherosclerosis?

Answer 8

Type of arteriosclerosis (general term for thickening and hardening of walls of arteries)

Question 9

Pathogenesis of an atheroma

Answer 9

Endothelial dysfunction initiated via a variety of risk factors
= Hyperlipidemia, hypertension, smoking, toxins, hemodynamic factors, immune reactions, viruses

LDL entry and oxidation e.g. via ROS

Cytokine production

Recruitment of monocytes

Expression of leukocyte adhesion molecules on endothelium
= Selectins
= VCAM-1, ICAM-1

Chemoattractant signals e.g. IL8, MCP

Phagocytosis of lipids and formation of foam cells
= foam cells - trigger formation of fibrous tissue (want to trap them)
= foam cells also produce “tissue factor” - can lead to thrombosis

Recruitment of lymphocytes

Recruitment of smooth muscle cells from the media and formation of extracellular matrix e.g. stimulated by PDGF and TGF beta

Degeneration of components of plaque by e.g. apoptosis and matrix metalloproteinases, forming lipid rich necrotic core

Initial remodelling of vessel wall preserves lumen diameter

Continued endothelial dysfunction: altered release of vasoactive substances, alteration of normal antithrombotic properties

Eventually variable combination of vessel stenosis, impaired vasodilation, plaques vulnerable to rupture, local prothrombotic environment

Question 10

What do you see macroscopically with fatty streaks, and atherosclerosis

Answer 10

fatty streaks - ill-defined yellow streaks
(early manifestation, doesn’t necessarily progress)

atherosclerosis

• irregular, slightly elevated plaques
• dark blobs - thrombus / ulcers