2. Acute Inflammation Flashcards
what are the signs of inflammation? (5)
redness, swelling, heat, pain, loss of function
pathogenesis of a inflammatory response
- change in blood flow (vasoconstriction, vasodilation)
- increased permeability of capillaries/venules
- white cell events (emigration/migration –chemotaxis)
neutrophils
involved in acute inflammatory response, usually following bacterial infection
band cells
immature neutrophils
eosinophils
involved in allergic reactions and parasitic infections
basophils
involved in immune, parasitic and allergic reactions, they recruit helper T cells
mast cells
involved in allergic reactions, releasing histamines and prostaglandins and cause immediate inflammation
lymphocytes (what type of inflammation is it involved in?)
chronic inflammation
types of macrophages: monocytes
immature macrophages
types of macrophages: kuppfer cells
liver macrophages
types of macrophages: histiocytes
connective tissue under skin
types of macrophages: microglial cells
brain macrophages
types of macrophages: osteoclasts
bone macrophages
giant cells
fusion of macrophages, chronic inflammation only
dendritic cells
antigen presenting cells, generally found at entry points
transudate
exudate, but less protein, cell and/or dead cell material content
exudate
a mass of fluid and cells that have seeped out of blood vessels (due to increased capillary permeability)
serous exudate
very little protein, watery
fibrinous eudate
fibrin leaks from capillaries as well, only occurs with greater injury when greater capillary permeability occurs
suppurative/purulent exudate
pus, contains masses of neutrophils, bacteria, dead tissue and fluid. if encased it is an abscess
exudate removal process
transudate - moves back into vessel
exudate - removed by the lymphatic system
swelling of lymph nodes
hyperplasia of lymphocytes in presence of a pathogen
bradykinin
vasodilation of blood vessels, constriction of non-vascular smooth muscle, pain
complement factors
lead to inflammation in response to antigen-antibody binding
C3a
increased permeability, also acts as opsonin for phagocytosis
C5a
chemotaxis
C5b-C9
MAC (membrane attack complex)
histamine
immediate vasodilation and increased permeability
prostaglandin E2 & its inhibition
vasodilation and inhibition of platelet activity (inhibited by aspirin and corticosteroids)
thromboxane A2
induces platelet aggregation and arterial constriction
prostacyclin
vasodilation and inhibition of platelet activity
leukotrienes & its inhibition
powerful inflammatory mediator (inhibited by corticosteroids)
benefits and harms of vasoconstriction
benefit: bacteria can’t spread to other areas
harm: prolonged can lead to ischaemia/gangrene
benefits and harms of vasodilation
benefit: increased blood flow, WBC and nutrient delivery
harm: if widespread, can reduce BP
benefits and harms of increased permeability
benefit: movement from blood vessel to injured tissue
harm: can severely reduce O2 exchange with fluid accumulation in lungs
benefits and harms of WBC activity
benefit: decreased risk of infection and increased rate of healing
harm: rheumatoid arthritis, multiple sclerosis, emphysema
benefits and harms of exudates
benefit: wound healing
harm: fibrinous especially - can cause adhesions, difficulty breathing, GIT movement affected etc
benefits and harms of lymphatic drainage
benefit: removes excess fluids, cells, proteins
harm: lymphangitis
