Histopath Flashcards
which cells are associated with acute inflammation v chronic inflammation (histpaht)
neutrophils - acute
Lymphocytes and plasma cells - chronic
Bilobed nucleus with red granulocytes
Eosinophils
Eosinophils are associated with (3)
Allergic reactions
Parasitic infections
Tumours e.g. Hodgkin’s - they are reactive processes to tumourgenesis
Cell with very large granules containing inflammatory mediators
mast cells
associated with allergic reactions
Lots of cytoplasm, associated with late acute and chronic inflammation
Macrophages
primary role is to phagocytose debris
secondary role to secrete the inflammatory mediators
A true sputum sample will contain macrophages - T/F
T
Even in non-smokers, because marcophages are need to clear up any inhaled pollutants including industrial fumes and especially cigarette smoke
2 features of squamous cell carcinomas
Keratin production + intracellular bridges
2 features of adenocarcinomas
Glands and mucin production
You can stain for mucin using special stains which cause goblet cells to appear bright blue
Name the stain for melanin
Fontana stain - chemical reaction with melanin that makes it more pigmented (appears black)
histochemical stians v immunohistochemical stains?
name examples (*2-3 each)
histochemical is based on CHEMICAL reaction between stain and tissue e.g. H&E, Prussian blue for iron, congo red for amyloid
immuno stain is based on antigen and antibody interaction e.g. immunofluorescence or immunoperoxidases e.g .CD45 (pan-lymphocyte stain), cytokeratin (stain for ketarin used in SCC)
Staining for amyloid (2)
Congo red + apple green birefringence under polarised light
Sheets of plasma cells
Lymphoma
Langerhan type giant cell
Granulomas formed by activated macrophages
Resembles both stratified squamous and stratified cuboidal depending on degree of organ stretch
Transitional epithelium
Seen in bladder, ureters and part of urethra, allows the bladder to expand and contract when needed
Smokers cancer type
Squamous cell carcinoma (also the most common lung cancer overall)
Non-smoker lung ca
Adenocarcinoma (more peirpheral)
Smoking is most associated with these 2 types of lung ca
SCC and small cell carcinoma
*Adenocarcinoma is more in non-smokers
Types of histology samples for a ?lung Ca
- Biopsy at bronchoscopy
- Per-cutaneous CT guided biopsy for peripheral tumours
- Mediastinoscopy and lymph node biopsy for staging
- Open biopsy at time of surgery
- Resection specimen - confirm full excision and staging
Pathogenesis of lung SCC
Normal epithelium -> hyperplasia -> squamous metaplasia -> dysplasia -> carcinoma in situ -> invasive carcinoma
- Tends to arise from proximal airways
- Smoking irritates epithelium which undergoes hyperplasia in response
- No cilia on the airways and deposits of carcinogens from cigarettes stays there
- Metaplasia is characterised by instability which increases risk of accumulating mutations → dysplastic changes
- Stopping smoking can reverse these genetic changes
- But when threshold of mutations reached, cells form carcinoma in situ
- Breakthrough of basement membrane → invasive carcinoma
- Hirsch et al 2001, at each stage, there is accumulation of specific genetic mutations
Clinical features of lung SCC
- who gets it
- Risk factors
- site
- behaviour
Smokers
Usually centrally located, arising from bronchial epithelium
Local spread, mets late
This specific type of lung Ca shows prominent capillary loops underneath dysplastic epithelium
- there is keratinisation and intercellular bridges
angiosqaumous SCC
specific type of SCC, sen in high risk smokers, clinical significance is uncertain
Histology of SCC
Keratinisation
intercellular ‘prickles’ representing desmosome
Adenocarcinoma clinical features
- who gets it
- Risk factors
- site
- behaviour
*BONUS QN: what is a new targetted therapy for adenoCa
Non-smoker, usually females, far east
site: peripheral and often multi-centric, specifically arises from terminal alveoli wall
behaviour: mets early and common, especially extra-thoracic, 80% present with mets
Tarceva (anti-EGFR) which is the most common mutation in adneoCa for non-smoker.
*smoker version of kras, p53 = useless
precursor cells of lung adenoCa
what is the pathogenesis
Atypical adenomatous hyperplasia
Normal terminal alveoli wall lined by type 1 pneumocytes -> develop atypically into type 2-like pneumocytes with large nuclei -> these abnormal cells then grow like a caterpillar along the alveoli wall (adenoCa in situe) -> acquires invasive phenotype to break through basement membrane by destroying elastin