Pathology Flashcards
Inflammation
Local physiological response to tissue injury
2 types of inflammation
Acute
Chronic
2 Cells involved in acute inflammation
Neutrophils (Day 1)
Monocytes (Day 2)
4 Neutrophil functions
Phagocytose pathogens
Pathogens ingested to form phagosome
Lysosomes released to kill pathogens
Respiratory burst
1 Macrophage function
Secrete chemical mediators for chemotaxis
5 Causes of Acute Inflammation
Microbial infections Hypersensitivity reactions Physical agents Chemicals Tissue Necrosis
4 Stages of acute inflammation
1) Changes in vessel calibre
2) Fluid exudate
3) Cellular exudate (accumulation of neutrophil polymorphs in extracellular space)
4) Chemotaxis
5 Cardinal signs of acute inflammation - SHLRP
Swelling (Oedema) Redness (Dilated blood vessels) Heat (Increased blood flow - hyperaemia) Pain (Stretching of tissues to inflammatory oedema) Loss of function
4 Outcomes of acute inflammation - ROSP
Resolution (Tissues restored to normal)
Suppuration (Pus formation)
Organisation (Tissue replaced by granulation tissue as part of healing process)
Progression to Chronic inflammation
Chronic inflammation
Unresolved acute inflammation
3 examples of chronic inflammation - AUF
Ulcer
Abscess
Fibrosis
Causes of chronic inflammation
Resistance of infective agent to phagocytosis
Endo/Exogenous materials
Autoimmune conditions
Primary granulomatous diseases
3 Cells involved in chronic inflammation - PML
Macrophages
Lymphocytes
Plasma cells
3 ways chronic is different to acute inflammation
Less exudative
Longer onset
Long-lasting effects
3 Histological features of chronic inflammation
Cellular infiltrate consists of PML
Tissue destruction
Tissue repair
Granuloma
Aggregate of epithelioid histiocytes
5 Systemic granulomatosis diseases - TCLSS
TB (Tuberculosis) Crohn's disease Leprosy Sarcoidosis Schistosomiasis
Special type of Granuloma cell in TB
Langhans giant cell
Thrombus
Solid mass of blood constituents
Part of healing and repair
Physiological - Haemostasis (to prevent bleeding outside vessels)
Pathological - Imbalance in coagulation
Virchow’s triad - SHE
Stasis of blood flow
Endothelial injury
Hypercoagulability
5 Features of venous thrombosis
Due to stasis
Low pressure
Red thrombus (Composed of coagulation factors, RBCs)
Lead to DVT/PE
Treated with anti-coagulants (Warfarin, heparin, NOAC (New Oral Anti-Coag))
5 Features of arterial thrombosis
Superimposed on atheroma High pressure White thrombus (Platelets) Lead to MI/Stroke Treated with anti-platelets (Aspirin, clopidogerel
Atherosclerosis - MLS
Accumulation of lipid, macrophages and smooth muscle cells in intimal plaques in the coronary arteries.
5 Arteries affected by atherosclerosis - 2 Heart, 2 Brain, 1 Pelvic
Aorta Coronary Carotid Cerebral Common iliac and femoral
3 Contents of a plaque - MLS
Macrophages
Lipids
Smooth muscle cells
Pathogenesis
1) Endothelial cell dysfunction (lots of cholesterol damages wall)
2) High levels of LDL in blood accumulate in arterial wall.
3) Macrophages attracted to site of damage and take up lipid to form foam cells (inflammatory response)
4) Formation of a fatty streak (early stage plaque)
5) Activated macrophages release their own products (Cytokines and growth factors)
6) Smooth muscle proliferation to intima around the lipid core and formation of a fibrous cap (collagen)
Hypertrophy
Increased organ/tissue size due to increased cell size
Can be via increased protein synthesis or increased size of intracellular organelles
Exercise increases skeletal muscle mass
Hyperplasia
Increased organ/tissue size due to increased cell number
Uterine enlargement
Atrophy
Decreased organ/tissue size due to decreased cell size
Decreased exercise
Endometrium
Metaplasia
Replacement of one differentiated tissue by another
Barret’s oesophagus
Dysplasia
Presence of abnormal cell types within a tissue
Increased cell growth and Decreased differentiation
Variation in size and shape of cells
High nuclear : cytoplasmic ratio
Increased nuclear DNA
Pre-cancer state
Apoptosis
Programmed cell death
Non-inflammatory
Cell and its organelles are intact/undamaged/retained
Embryological development
Necrosis
Morphological changes following apoptosis
Inflammatory
Cell and its organelles are destroyed/damaged/released
Gangrene
MI
Carcinogenesis
Transformation of normal cells to neoplastic cells through permanent mutations (genetic alterations)
Benign tumours
Does not invade basement membrane Exophytic (grows outwards) Low mitotic activity Circumscribed (limited spread) Necrosis/ulceration rare
Malignant tumours
Invades basement membrane Endophytic (grows inwards) High mitotic activity Poorly circumscribed (spread out) Necrosis/ulceration common
4 Effects of Benign tumours
Pressure on adjacent vital organs
Paraneoplastic effects
Anxiety
Transformation to malignant tumour
4 Effects of Malignant tumours
Metastases
Paraneoplastic effects
Anxiety
Pain
4 Histological features of malignant tumours
Poorly defined border
Hyperchromatic nuclei
High mitotic activity
Pleomorphism (altered cell size/shapes)
Metastasis
Tumours spread from site of origin to form tumours at distant sites
2 Signs of metastasis
Bone pain
Palpable lymph nodes
Mechanism of metastasis
1) Detachment of tumour cells from neighbours
2) Invasion into surrounding connective tissue
3) Intravasation into vessel lumen
4) Evasion of host defence mechanisms (natural killer cells in blood)
5) Adherence to endothelium at remote location
6) Extravasation of cells from vessel lumen into surrounding tissue
See peer teaching pathology pres slide 39 for useful pic
3 Routes of Metasasis - HTL
Haematogenous (blood)
Transcoelomic (peritoneum)
Lymphatic
