Cells and Inflammation

Hypertrophy and Atrophy : change in cell size

Hyperplasia: change in cell numbers

Hyperplasia: change in cell type

Dysplasia : change in cell size, shape and organization

Apoptosis : controlled cell death 

Necrosis: cells killed before its time

Coagulative Necrosis: from hypoxia (typically) primarily in kidneys, heart and adrenal glands

Liquefactive Necrosis : from bacterial infection. Results from ischemia to neutrons and glial cells in the brain

Caseous Necrosis : Common in lungs, combinations of coagulative and liquifactive necrosis 

Fat Necrosis : common in breasts, pancreas and other abdominal organs

Gangrenous necrosis : when a large mass of tissue undergoes necrosis 

Inflammation: non-specific response of body to local injury 

Acute inflammation – Vascular response

  • Arterioles vasodilator -> Increased blood flow -> Increase redness and heat -> Permeability of capillaries increases-> Leads to swelling ->Pain results from tissue swelling 

Acute inflammation – Cellular response

  • Mast cells/ basophils in blood ->Releases histamine ->Neutrophils cleans up debris and dead cells  -> Monocytes turn in to macrophages -> Helps destroy injurious agent by phagocytosis-> Natural killer cells patrols the blood and lymph for “bad”guys and attacks  -> releases perforins 

Response of WBC’s to inflammation

  • Margination ( adheres to the endothelial cells) -> Emigration ( leukocytes travel through the “walls” and into the injured tissue) -> Chemotaxis ( leukocytes move towards injured site due to chemical signals) -> Phagocytosis

Chronic inflammation :  lasts weeks, months or years 

  • macrophages and lymphocytes instead of neutrophils are the major WBC moving to site

Non-specific chronic inflammation: fibroblasts proliferate and leads to scar tissue 

Granulomatous lesion: a small lesion that is infiltrated with macrophages that are surrounded by lymphocytes from splinters, sutures, silica

  • Fibroblasts make scar tissue 
  • Scar tissue is non-contractile

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