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PATH20001: Lecture 2 Stress & Injury, : - Coggle Diagram
PATH20001: Lecture 2 Stress & Injury
Nomenclature
Aetiology
cause of disease e.g. smoking
Pathogenesis
mechanism causing disease e.g. genetic alteration
Pathology
molecular and morphological changes to cells or tissues e.g. lung tumour
Clinical manifestations
Signs & symptoms e.g. breathlessness
Complications
secondary, systemic or remote consequences of disease e.g. metastasis
Prognosis
anticipated course of disease e.g. death/remission
Epidemiology
incidence, prevalence and distribution e.g. risk 1/100
Cellular injury
the cell cannot return to normal even if stimulus is removed
types of cell injury
hypoxia
causes include pneumonia, carbon monoxide poisoning and ischemia
chemical agents
e.g. poisons, tobacco, alcohol
infectious agents
prion infection
immunologic reactions
autoimmunity, hypersensitivities, graft rejection
genetic defects
congenital malformations, single bae mutations
nutritional imbalance
deficiency e.g. Rickets, or excess e.g. obesity
physical agents
mechanical trauma e.g. abrasions, thermal injury, ionising radiation
aging
Cellular adaptation
if stimulus is removed, cell returns to normal
occurs due to increased demand or stress
types of adaptation
hypertrophy
increase in cell size and organ size
physiological e.g. body builder forming larger muscles
pathological e.g. hypertension leads to an enlarged heart
hyperplasia
increase in cell number and organ size
physiological e.g. tissue growth during puberty
pathological e.g. endometriosis
atrophy
decrease in cell size/number and organ size
physiological e.g. uterus shrinks following pregnancy
pathological e.g. muscular dystrophy
metaplasia
change in cell type
e.g. cigarette smoking causes ciliated columnar cells to become stronger stratified squamous cells
Physiological adaptation: cellular response to normal stimulation
Pathological adaptation: cellular response to stimulation secondary to underlying disease, or to avid injury
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