Path processes Flashcards
what are the four causes if hypoxia?
- hyperaemic hypoxia: arterial content of oxygen low
- anaemic hypoxia: decreased ability of haemoglobin to carry oxygen (CO poisoning)
- ischaemic hypoxia: interruption to blood supply
- histiocytic hypoxia: inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes (eg cyanide poisoning)
what are the cell components most susceptible to injury?
cell membranes - plasma and organellar membrane
nucleus- DNA
protein- structural
mitochondria- oxidative phosphorylation
describe the process of reversible ischaemic injury
- mitochondria decrease oxidative phosphorylation
- decreased amount of ATP production
- NA pump decreases- causes increase in calcium, water and sodium and decrease in potation => cell swells
- by anaerobic respiration glycolysis increases which decreases pH => clumping of nuclear chromatin
- detachment of ribosomes decreases protein synthesis => lipid deposition
describe the process of irreversible prolonged hypoxia
increased cytosolic calcium- from mitochondria andER
- activates ATPase which decreases ATP
- activates phospholipase- decreases phospholipids
- activates protease- disruption of membrane and cytoskeletal proteins
- activates endonuclease- nuclear chromatin damage
how are free radicals produced?
- normal metabolic reactions eg oxidative phosphorylation
- inflammation eg oxidative burst of neutrophils
- radiation
- contact with unbound metals within the body eg iron and copper
- drugs and chemicals
how does the body control free radicals?
- antioxidant scavengers ( vit ACE)
- metal carrier and storage proteins ( transferrin, ceruloplasmin)- sequester iron and copper
- enzymes that neutralise free radicals ( superoxide dismutase, catalase, glutathione peroxidase)
how do free radicals injure cells?
- cause lipid peroxidation- leads to generation of free radicals
- oxidise proteins, carbohydrates and DNA
what are the clinical features of acute inflammation?
rubor (redness) tumor (swelling) calor (redness) dolor (pain) loss of function
what are the key changes in blood flow during acute inflammation?
vasoconstriction
vasodilation - arterioles then capillaries
increased permeability of blood vessels
increased conc of RBCs in small vessels
what is the primary WBC in inflammation?
neutrophil