Path processes Flashcards

1
Q

what are the four causes if hypoxia?

A
  • 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)
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2
Q

what are the cell components most susceptible to injury?

A

cell membranes - plasma and organellar membrane
nucleus- DNA
protein- structural
mitochondria- oxidative phosphorylation

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3
Q

describe the process of reversible ischaemic injury

A
  • 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
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4
Q

describe the process of irreversible prolonged hypoxia

A

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
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5
Q

how are free radicals produced?

A
  • 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
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6
Q

how does the body control free radicals?

A
  • 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)
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7
Q

how do free radicals injure cells?

A
  • cause lipid peroxidation- leads to generation of free radicals
  • oxidise proteins, carbohydrates and DNA
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8
Q

what are the clinical features of acute inflammation?

A
rubor (redness)
tumor (swelling)
calor (redness)
dolor (pain)
loss of function
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9
Q

what are the key changes in blood flow during acute inflammation?

A

vasoconstriction
vasodilation - arterioles then capillaries
increased permeability of blood vessels
increased conc of RBCs in small vessels

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10
Q

what is the primary WBC in inflammation?

A

neutrophil

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