Lecture 19: How the Body Responds to Injury Flashcards
what are the cells involved in acute inflammation
neutrophil granulocytes and polymorphs
what are the 5 Rs of the inflammatory process
Recognition Recruitment Removal Regulation Resolution
what happens during vasodilation
- increased amount of blood but slower blood flow
- causes stasis of blood and an increase in hydrostatic pressure beyond normal levels
what happens during acute inflammation
1) vasodilation
2) increased vascular permeability and extravasation of fluid
3) emigration of leukocytes, primarily neutrophil polymorphs
what are the types of oedema
- exudate: high in proteins and may contain some white and red blood cells
- transudate: mainly the leaking of fluids, low in proteins
how are tissues drained of fluid
tissues drained through lymph nodes back into venous system via thoracic duct
what causes increased vascular permeability
histamine and NO cause endothelial cells to contract
how do phagocytic leukocytes leave the vasculature and what are the processes mediated by
- margination and rolling along the vessel wall. mediated by selectins upregulated by TNF and IL-I
- adhesion to the activated endothelium. mediated by VCAM-I and ICAM-I integrins upregulated by TNF and IL-I
- emigration through the vessel wall into the surrounding tissues. mediated by CD31 / PECAM-I
what allows amoeboid movement of the leukocytes
leukocyte forms processes from contractile cytoplasmic microtubules
what are the mediators in vasodilation
- histamine
- NO
- prostaglandins
what are the mediators in increased vascular permeability
- histamine
- bradykinin
- leukotrienes
- complement C3a and C5a
what are the mediators in chemotaxis and leukocyte recruitment
- TNF
- IL-I
- complement C3a and C5a
what are the mediators in fever
- TNF
- IL-I
- prostaglandins
what are the mediators in pain
- prostaglandins
- bradykinin
what are the mediators in tissue and cell damage
- ROS
- NO
- lysosomal enzymes from leukocytes
what are the types of harmful inflammation and what do they look like
- serous inflammation because of effusion (collection of fluid)
- fibrinous inflammation with effusion and lots of fibrin
- purulent inflammation because of effusion and lots of pus and neutrophils
- ulceration (destruction of an epithelial structure due to abscess)
causes of chronic inflammation
- immune mediated inflammatory diseases, eg Crohn’s disease
- persistent infections, eg some viral and fungal infections
- inability to heal, eg chronic peptic ulcer of the stomach
- prolonged exposure to toxic agents, eg silicosis of the lung
what is a granuloma
- an area of activated epithelioid macrophages
- pallisated if surrounded by leukocytes, naked if not
- caseating if shows central necrosis, non-caseating if not
- may fuse to form giant multinucleated cells
what are granulomas characteristic of
- mycobacterial infection
- sarcoidosis
- may be idiopathic or caused by drugs
what are the dominant cells in acute and chronic inflammation
acute: neutrophil
chronic: lymphocyte
what is eosinophil accumulation mediated by
IgE produced by plasma cells
what is healing by primary and secondary intention
- primary: when the skin edges come together properly
- secondary: wound is too large / other factors interfere with skin edges coming together properly
what are important examples of metaplasia
- oesophagus: squamous epithelium –> columnar epithelium due to gastric content reflux (Barrett’s)
- bronchus: pseudostratified ciliated columnar epithelium –> squamous epithelium due to smoking
- cervix: columnar endocervical mucosa –> squamous epithelium sue to HPV infection
