Pathology Flashcards
aetiology
causative element in disease
pathogenesis
sequence of events leading from healthy state to clinical disease
sequelae
range of possible outcomes of a disease process
outcome
patients health or illness at defined time
apoptosis
Programmed cell death
Defence against inherited and injury
p53
Protein that if lost can cause cancer which will be resistant to treatment
Tumour supressor gene (transcription factor)
Activated by cell stress
Loss of membrane integrity
Failure of ion pumps
Disruption of membrane
Alterations of lipids
Cross-linking of membranes
free radicals
Particularly O2
Creates chain reaction leading to lipid peroxidation
non-lethal cell injury
Hydropic change
Fatty change
Membrane shedding
Necrosis
Death of tissues
Pathological
Elicits adjacent tissues response
Coagulative necrosis
Proteins coagulate
Colliquative necrosis
Necrotic material becomes softened and liquefied
Caseous Necrosis (Cheese like)
TB
Gangrenous necrosis
cell death by necrosis, then infection on top
fibrinoid necrosis
fibre desposition
fat necrosis
acute pancreatitis
metabolic disorder
Biochemical abnormality which may itself be deleterious, can also cause target organ damage due to accumulation of injurious agent
Can be inherited or acquired
inherited metabolic disorder
Autosomal recessive
Loss of function
Gene encodes enzymes in metabolic pathway
Phenylketonuria
Inborn error of metabolism that results in decreased metabolism of the amino acid phenylalanine
Phenylketonuria tests
Guthrie test (blood test) due to accumulation of phenylanine caused by deficiency in enzyme which converts phenylaline to tryosine
acute inflammation phases
Vascular changes
Cellular changes
Chemical mediators
Morphologic patterns
Vascular changes
dilatation and increased permeability of blood vessels
Cellular phase
fluids and cells escape venules
Neutrophils in extracellular space = diagnostic feature
Beneficial effects of acute inflammation
Toxin dilution Entry of antibodies Fibrin formation Drug transport Oxygen and nutrient delivery Immune response stimulation
Harmful effects of acute inflammation
Wrong inflammatory response - type 1 hypersensitivity
Swelling
Digestion of normal tissues
chronic inflammation
Subsequent and often prolonged tissue reactions follow initial response
Recurrence of acute inflammation may lead to chronic
characteristics of chronic inflammation
Redness = dilatation of small blood vessels
Heat = increased blood flow
Swelling = accumulation of fluid in extracellular space
Pain = distortion of tissues
Loss of function = inhibited by pain or swelling
fluid exudate
proteins including immunoglobulins
Fibrinogen ->
Fibrin on contact with ECM, acutely inflamed organ surfaces commonly covered in fibrin
neutrophils are an
inflammatory stimulus
Margination
loss of intracellular fluid and increased plasma viscosity allows neutrophils into plasma
surface adhesion molecule expression increased by
C5a
Leukotrine B2
TNF
endothelial expression of adhesion molecules increased by
IL 1
Endotoxins
TNF
chemotaxis
locomotion along a chemical gradient
Chemical mediators
Histamine Serotonin Chemokines Leukotrines Prostaglandinds
Histamine causes
Vascular dilatation
histamine is released by
mast cells, eosinophils, basophils, platelets
histamine release stimulated by
C3a, C5a and lysosomal proteins
seratonin
increases vascular permeability
chemokines
attract various leukocytes to site of inflammation