Pathology Flashcards
What are the three types of necrosis?
Caseous- occuring in tb
Liquefactive- liquid formed where cell death has occured
Coagulative- where there is an outline of the cells that have died
Why does angina occur?
When there is less oxygen reaching the heart than needed
Describe the effects of hypoxic injury to the heart
What is the window for recovery of a heart attack
No ATP from aerobic respiration means the na/k pump fails, causing swelling of the cell from accumulation of potassium.
The calcium pump fails so there is increased Ca+ in cell stimulating pathways that cause harm
20 minute window
Within 24 hours/ 3-7days/ 20 minutes after a heart attack what are the cellular observatiobs
- 24 Acute inflammation occurs, heart is redder/ yellow parts
- 3-7 huge necrosis so risk of cardiac rupture, yellower colour of heart
- 20 minutes cell death occurs displaying marginal contraction bands in cardiac tissue.
How can apoptosis be signalled?
Extriniscally by a death receptor (FAS) activated located on the cell membrane. Neutrophils bind to this and cause it to undergo cell death
Intrinsically (mitcochondrial pathway) where pro-apoptopic bodies make holes in the mitochondria which releases cytochrome C inducing apoptosis. Also by P53 stopping the cell cycle.
What are the four stages of the cell cycle, what do they do?
G1- inital growth stage and synthesis of organelles. CDK4 synthesises Rb to release e2f which drives dna replication
S phase- duplication of the chromatids. Involving cyclin A and CDK2
G2 - second growth phase with synthesis of proteins. P53 will check the cell at this point
m phase- PMAT occurs
Define hyperplasia, hypertrophy, atrophy
Hyperplasia- increased no of cells
Hypertrophy- increase in cell size
Atrophy- decrease in cell size
What growth factor pathways can initiate hyperplasia/ hypertrophy?
- producing more growth factors through:
1. Intrinsic receptor tyrosine kinase pathway
2. G protein coupled receptor (spanning membrane 7 times with nh2/cooh terminals)
3. Receptor with no intrinsic TK activity (can phosphorylate on own)
How does atrophy occur?
From protein degradation by lysosomes, can be from hormone stimulus from glucorticoids and thyroid hormones.
- decreased workload, loss of innervation/ blood supply/ hormonal stimulation/ , inadequate nutrition, ageing (neurones), pressure from endo/exogenous structures
What is the definition of malignant cell
A cell that has passed the basal membrane of a tissue
What are some of the precursors for malignancy?
Dysplasia- disordered growth, where there are abnormal cell types in a tissue e.g stratified cuboidial ciliated squamous cell in the gut.
Metaplasia- differentiated group of cells to a different function e.g stratified squamous cells in oesophagus to glandular epithelium to cope with acid reflux
Hyperplasia- increase in cell number
What are some of the categories that lead to malignancy (7)
- Inherited disposition (gene hot spots),
- obesity (causes hyperplasia as cholesterol similar molecule to oestrogen so causes proliferation of endometrium),
- red meat types (contain polycylic aromatic hydrocarbons= carcinogen),
- radiation (UVB from sun beds),
- infections (HPV’s protein E7 binds to RB so e2f can dna replicate),
- Chemicals (smoking, beta-naphyylamine)
- Chronic inflammation (calor (heat), dolor (pain), rubor (redness), tumour (swelling))
When can resolution occur?
When there is good blood supply, oxygen supply, basal lamina in tact, good nutrition
What are granulomas
Collection of WBCs like neutrophils to wall off a pathogen
What does supparation involve? Pathological or physiological?
Pathological
Necroris, phagocytosis, neutrophils and abscess formation
What are the hallmarks of cancer
- Inducing angiogenesis by VEGF
- Sustained growth signalling
- Loss of growth factor inhibition
- Ability to invade other areas and metastasis
- Unlimited replicative potential
- Resisting apoptosis
- Disordered repair mechanisms
- Evasion of the immune system
How does a tumour get sustained growth signalling?
Overexpression of genes in the mapk/erk pathway giving a contant green light to replication like MYC , EGFR and RAS mutations
How does a tumour get loss of growth inhibition?
Describe the functions of the P inhibitor molecules
By mutations in any of the p53, pten, p27, p21 will cause unlimited cell replication
PTEN= inactivation of PI3 kinase dependent signalling P27 = arrest of cell cycle at g1 and able to inhibit cdk2. P21= inhibits CDK2 and CDK4 complexes so regulates cell cycle at g1 and sphase
What are the four types of tumours?
Epithelial (including bladder, glandular and squamous epithelium)
Mesenchymal (connective tissue)
Haemopoetic (blood)
Other (CNS)
What two inflammatory mediators increase selectin expression on endothelial walls?
Histsamine and thrombin
