Flashcards in MOD Deck (186)
What is the difference between arterial and venous thrombi?
Arterial more platelet based - pale, granular, striated with lines of Zahn
Venous more thrombin based - red and gelatinous
What are the outcomes of thrombosis?
Propagation (proximally in veins, distally in arteries - direction of flow)
Reorganisation (ingrowth of fibroblasts and capillaries - granulation like tissue)
What is an embolism?
What is the commonest cause?
A blockage of a blood vessel by a solid, liquid or gas distant from its site of origin.
90% are thromboembolisms
What are common origins and sites of embolisms?
Systemic veins - lungs
Carotid arteries - cerebral arteries
Abdominal aorta - arteries of the leg
Heart - cerebral arteries
What are risk factors for DVTs?
Post op hypercoagubility
What are mitigations for DVT risk?
Heparin / anticoagulation
Filters in IVC
Intermittent leg compression during surgery
Differentiate athroma, athroscleosis and arteriosclerosis
Athroma - accumulation of extra and intra cellular lipids in the intima and media of medium and large arteries
Athrosclerosis - hardening of arteries as a consequence of athroma
Arteriosclerosis - thickening hardening of arteries, e.g. Hypertension, DM
What are the stages of atroma formation?
What is the macroscopic appearance of each?
Fatty streak - slightly raised white or yellow streak
Simple plaque - raised yellow or white plaque
Complex plaque - raised plaque with haemorrhage, infarction, aneurysm and calcification
How does a complicated athroma appear histologically?
Fibrosis, necrosis, cholesterol clefts, disruption of internal elastic lamina, ingrowth of blood vessels, fissues.
What is the histological appearance of simple athroma?
Proliferated smooth muscle cells and foam cells
What are common locations of athromas with related consequences
Coronary arteries - angina / mi
Cerebral arteries - cva / cve
Superior mesenteric artery - ischemic colitis
Legs - pvd
What are risk factors for athroma formation?
What is the process of athroma formation?
Adhesion of platelets and release of PDGF
Proliferation of smooth muscle, macrophage arrival
Phagocytosis of lipids and ldl by smc and macrophage (foam cells)
Macrophages move into intima
Lipoproteins undergo glycosylation
Smc produce unstable matrix weakening plaque
Cytokines from macrophages recruit more inflammatory cells
Neutraphils secrete proteases causing local damage weakening plaque
Lymphocytes stimulate smooth muscle cells
What cells are involved in athroma formation?
Smooth muscle cells
What are possible outcomes of a cell to growth signals?
What are the categories of cell growth signals?
What are growth factors?
What are the odd things they effect?
Local mediators that bind to receptors to stimulate transcription of genes causing increased return from, G0 and shortening interphase.
Locomotion, contractility, differentiation, viability, angiogenesis.
Give some examples of growth factors
Epidermal growth factor
Vascular endothelial growth factor
Platelet derived growth factor
Granulocyte colony stimulating factor
What are the checkpoints in the cell cycle?
G1 end checkpoint - restriction point
G2 end checkpoint
What does the restriction point do in the cell cycle?
Checks cell size, environment and for dna damage
What does the g2 checkpoint do in the cell cycle?
Ensures all dna has replicated and the cell is of sufficient size.
Which cell checkpoint is the most important in the cell cycle?
How is cell movement through the cell cycle controlled?
What cyclins move the cell through the different stages?
S to G2 is A
G2 to M is B
M to G1 is D (low)
G1 to S is E
How do cyclins work to control cell cycle?
Bind to a cyclin dependant kinase which phosphorylates a regulatory protein.
How do growth factors effect cyclins?
Increase cyclin dependent kinase
Decreased cyclin dependent kinase inhibitors
How are cell losses in tissues replaced?
Division of a stem cell - one daughter cell remaining undiferentiated, one daughter cell replacing the lost cell.
In what ways can cells adapt to stress?
What feature of regeneration aids immunity?
Replacement cells aren't immediately mature / fully functional and therefor infection may not be able to colonise or replicate within them.