pathology Flashcards
what do mast cells release
histamine, prostaglandins and NO causing vasodilation
what releases histamine
mast cells, eosinophils, basophils and platelets involving c3a and c5a
where does acute inflammation begin
arterioles and moves to capillary bed close to the site of injury
what does vasodilation do
decrease BP
what does serotonin do
increase permuability of capillaries, blow flow slows
what adheres to blood vessel walls in acute inflammation
leukocytes
what makes the walls sticky
proteins expressed on endothelium
what do endothelial cells do
contract to allow fluid into surrounding tissues
what do endothelial cells express
ICAM and VCAM
what increases expression of VCAM and ICAM
tumour necrosis factor and IL-1
what binds to glycoproteins on neutrophils
selectins
what binds to itegrins on leukocytes
ICAM abd VCAM
white cells slowly rollig along the vessels is known as
pavementing
what are chemokines
signalling proteins inducing chemotaxis and attracting other leucocytes
what do chemokines do
activate chemokine receptors making integrin bind tighter to ICAM
diapedesis / margination
leukocytes migrate accross the vessel wall by extending pseudopods through the gaps and pulling themselves in
chemotaxis
leukocyte following a chemical gradient guided by signalling molecules
what do nuetrophils do at the site of injury
carry out phagocytosis
phagocytosis
recognition and attachment, engulfment by pseudopods, phagolysosome, killing and degradtation by reactive oxidative species
phenylketonuria
guthrie test, phenylalaine accumulates, metabolic disorder, loss of enzyme, inherit
chronic inflammation
involves lymphocytes, macrophages (monocyte if within tissue) and plasma cells occurs if there is a persistant injury (foreign material), infectious agnet (virus / mycobacteriu), autoummine injury (transplant rejection, empyema or abscess
granulomas
aggregation of epithelioid histocytes (macrophages), associated with parasites, worms, malignancy, syphilis, mycobacterium
mechanism of apoptosis
p53 activates caspases in DNA damage at G1, S + G2/M, extrinsic (death receptor, mediated by TNF/Fas) and intrinsic pathway (mitochondria Bak, cytochrome C )
labile cell
multiply constantly - eg GI tract, bone marrow
stable cell
hepatocytes, endothelium
epithelial cancer
carcinoma
glandualar cancer
adenoma or adenocarcinoma
squamous cancer
papilloma or squamous cell carcinoma
bladder cancer
urothelial cell carcinoma, transitional
transport into cells
diffusion, via transport proteins, incorporation into vesicles