Flashcards
Week 3 General Pathology
Cards in this deck (67)
- 1InflammationLocal reaction of tissue to irritation or injury
- 2CausesAnything that leads to injury or necrosis
Microbes
Allergies
Trauma
Toxins
Heat/cold - 3Naming suffix-itis
- 4Purpose of inflammationRemove the cause of the injury and injured cells to promote healing
- 5Acute inflammation processInflammatory agent recognised
Reaction of blood vessels
Leukocyte activation
Destruction and elimination of agent - 6Chronic InflammationReaction to inflammatory agent not eliminated. Cycle of acute inflammation, tissue damage and tissue healing. Failure or repeat of acute phase
- 7What is the acute phase responseSystemic response mediated by IL-1 due to recognition of agent by TLR
Increased WBC and acute phase proteins - 85 classic signs of inflammationHeat
Redness
Swelling
Pain
Loss of function - 9Phases of acute phase response (3)Fluid phase
Cellular phase
demolition phase - 10Fluid/Vascular phaseHeat and redness caused by vasodilation
Contraction of endothelial cells forces fluid into extracellular space causing swelling. Delivers nutrients, Fibrinogen and antibodies to cells while diluting toxins - 11Consequence of swelling during fluid phase on blood compositionBlood more viscous with a slower blood flow, increases amount of blood cells in affected area and increases WBC contact with endothelium
- 12Cellular phaseDelivery of white blood cells to injured area
Prevents spread of bacteria, produces mediators, removes necrotic debris and liquefies clotted fibrin to increase repair - 13What is margination?Increased contact of white blood cells with the endothelial cells during inflammation
- 14What are the stages of emigration? (4)1. Tethering: weak binding between WBC ad endothelium leads to slow rolling
2. Activation: firm adhesion occurs when both cells produce new receptors 3.Movement of white blood cells between gaps of endothelial cells
4.Chemotaxis - 15Cells involved in inflammation (5)1. Neutrophils
2. Monocytes and Macrophages
3. Mast cells
4. Eosinophils
5. Lymphocytes - 16Function of neutrophilsFirst to arrive, live 24-48 hours
Release enzymes to tissue and phagocytic - 17Function of macrophagesArrive after 24-48 hours
Kill microbes and remove necrotic debris via phagocytosis
Produce cytokines and control inflammatory response - 18Types of inflammatory exudates (4)Serous - watery. Low protein, no cells.
Fibrinous: High fibrinogen with neutrophils present
Catarrhal: mucus, due to MM inflammation
Purulent: Neutrophils, necrotic debris and fluid - 19Function of chemical mediatorsStimulate, amplify or inhibit inflammation
Short half life to prevent reaction from going out of control - 20How to NSAIDs work?COX enzyme inhibitors preventing prostaglandin synthesis
- 21Demolition phase of inflammationBreakdown and removal of necrotic tissue via phagocytosis and liquefaction to prepare for repair and regeneration
- 22How does liquefaction occur?Lysosomal enzymes released from neutrophils into tissue
- 23Outcomes of acute inflammationComplete resolution
Healing by CT replacement
Chronic inflammation - 24Cells involved in chronic inflammation (4)Macrophage
Lymphocytes
Fibroblasts
Plasma cells - 25Phases of wound healing (4)Haemostasis
Inflammation
Proliferation
Remodelling - 26Process of haemostasisPrevention of bleeding:
Vasoconstriction
Platelet plug
Fibrin plug
24 hours post injury - 27Process of proliferationFormation of granulation tissue and replacement of epithelial cells
Macrophages release growth factors for proliferation of fibroblasts and epithelial cells.
4 days post injury - 28What is granulation tissue?Fibrous connective tissue and capillaries
- 29Remodelling phase3-4 weeks post injury after inflammatory phase. Granulation tissue replaced by mature connective tissue.
- 30Healing by primary intentionWounds with minimal tissue damage and closely apposed edges
Surgical incisions - 31Healing by secondary intentionLarge amounts of tissue involved that is traumatic, unsutured or infected
- 32Wound contractionIn second intention healing.
Myofibroblasts at wound edge contract to make the wound smaller
Continues after wound has healed leading to pitted appearance and skin immobility - 33Factors that affect wound healing process (6)Age
Diet
INFECTION
concurrent disease
Foreign bodies in wound
Blood supply to area - 34Classifications of wounds (4)Clean
Clean contaminated
Contaminated
Dirty - 35What is a pathological fractureAbnormal fracture due to minimal trauma or weight bearing Can be secondary to systemic disease or localised lesion
- 36Types of fractures (6)Simple
Comminuted
Impacted
Compound
Greenstick
Avulsion - 37Stages of fracture repair (6)Haematoma formation
Necrosis of adjacent bone
Mesenchymal cell proliferation
Callus formation
Maturation of callus
Remodelling of callus - 38Fracture callusInitially fibrous tissue and hyaline cartilage
Cartilage replaced by trabecular bone then to lamellar bone - 39Factors affecting fracture repairsInadequate blood supply
Infection
Instability of fracture - 40AntigenSubstance that promotes production of antibodies or induces an immune response
- 41AntibodyProtein that targets antigen for destruction
- 42Abnormalities of the immune system (3)Inadequate response eg. FIV
Abnormal response eg. Allergies
Uncontrolled response eg. Neoplasia - 43Serological testsMeasure Ag:Ab reactions, quantified by colour change
ELISA - 44What are hypersensitivity reactions?Inappropriate, misguided immune reactions.
Type 1-4 - 45Type 1 hypersensitivityAllergies due to IgE reaction to environmental antigen. Mast cells, basophils and eosinophils release inflammatory mediators
Eg. allergic rhinitis - 46Type 2 hypersensitivityDevelopment of antibodies to self antigens leading to cell destruction
Eg. Immune mediated haemolytic anaemia - 47Type 3 hypersensitivityFormation of antigen/antibody complexes that circulate in blood and arrest in capillaries. Neutrophil enzymes destroy the surrounding tissue
eg. Lupus, rheumatoid arthritis - 48Type 4 hypersensitivityT lymphocyte sensitisation to antigen leading to chronic inflammation
Eg. mycobacterium infection, Johnes disease - 49Immunological testsTo diagnose immune abnormalities
eg. Coombs test for haemolytic anaemia
Immunoglobin measurement - 50What is a neoplasmA new growth of cells that have undergone changes that are unresponsive to normal growth controls
- 51NeoplasiaProcess of developing a neoplasm
- 52Naming benign neoplasms-oma suffix
- 53Naming malignant neoplasms of epithelial origin-carcinoma
- 54Naming malignant neoplasms of mesenchymal origin-sarcoma
- 55LeukaemiaNeoplasms of haematopoietic cells. There is an increase in malignant cells in the bloodstream
- 56Gross visual features to decide of growth benign or malignant (5)Signalment of animal and breed
Speed of growth
Necrosis
# masses
Infiltration - 57Clinical effects of neoplasms on the bodyInterference with tissue or organ function
Rupture of blood vessels and haemorrhage
Ulceration & peritonitis
Anaemia and infections
Hormone imbalances
Depression, malaise and weight loss - 583 methods of neoplasm spread in the bodyDirect expansion and infiltration
Metastasis
Transcoelomic spread - 59Direct expansion and infiltrationMultiplication of abnormal cells infiltrates the tissue spaces between normal cells. First phase of growth and normally leads to lymph and blood vessel infiltration
- 60MetastasisNeoplasm infiltrates lymph or blood vessel. Cells break off from original neoplasm forming embolus and arrest downstream to form a secondary neoplasm
- 61Transcoelomic spreadFollows infiltration, where neoplasm enters and spreads through a body cavity
- 62Malignant epithelial gland neoplasmadenocarcinoma
- 633 groups of carcinogensRadiant energy
Chemicals
Viral infection - 64TeratogenEnvironmental agent that causes malformation of a foetus
- 65Teratogenic agentsViruses
Toxins
Ionising radiation
Nutritional imbalance - 66AnaplasiaLack of differentiation in cells
High mitosis with cellular and nuclear pleomorphism - 67Things to consider when diagnosing a neoplasmSignalment
History
Clinical exam: Location, spread, necrosis and nearby LN
Cytology
Histology
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- Pathology Flashcards on Week 3 General Pathology, created by Kelly Scott on 09/02/2020.
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- Kelly Scott
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