L8 Acute Inflammation 3 Flashcards
Fibrosis
excessive scar formation that may interfere with normal function
Describe Proliferative capacity in labile tissue
multiply constantly throughout life
− Continuously lost and replaced
− Doesnot enter G0
ever
− Maturation of stem cells or
proliferation of mature cells
− Tissue can regenerate if stem cells reserve and tissue structure intact
Eg.
Hematopoietic cells Epithelial cells (skin, GIT etc)
Describe Proliferative capacity in stable tissue
− Quiescent
− Enter G0
− Reenter cell cycle if stimulated by loss of cells
− Limited capacity to regenerate (exception liver)
Eg.
Parenchyma( functional tissue of an organ as distinguished from the connective and supporting tissue) of most solid organs (liver and kidney)
Endothelial (angiogenesis) and smooth muscle cells, fibroblasts
liver, vascular smooth muscle
Describe Proliferative capacity in permanent tissue
− Terminally differentiated
− Enter G0
− Cannot reenter the cell cycle
− Limited stem cell replication (not sufficient for regeneration)
Eg.
Neurons, cardiac muscle cells and (skeletal muscle cells)
Morphology-Serous Inflammation
• Watery cell poor fluid- effusion
− Plasma
− Mesothelial cells that form the serous membrane of serous cavities
o Peritoneal (abdomen)
o Pleural (lung)
o Pericardial (heart)
Effusion can prevent the lung for expanding properly
• Irritation of serous membranes
• Skin blister
− viral infection eg chicken pox
− burn
Morphology-Fibrinous Inflammation
− Associated with increased vascular permeability
− Exudate contains large molecules (fibrinogen)
− Form fibrin which is deposited in the extravascular space
− Characteristic of inflammation of meninges, pericardium, pleura
− Fibrinous exudate may be removed by fibrinolysis and macrophages
− If fibrin is not removed the exudate may be converted to scar tissue-organization
Collagen being laid down within exudate
− Scar may compromise the function of the tissue/ organ
eg scar tissue over the heart
Morphology-Supparative (purulent)- PUS
− Purulent exudate composed of neutrophils, liquifactive necrosis and oedema
− Indicative of prominent cellular components
− Associated with pyogenic (pus causing) bacterial infection (staphylococci)
− Heme of neutrophil MPO gives this exudate its characteristic color
− Abscesses: confined spaced filled with cellular inflammatory exudate- neutrophils
− Focal collections of purulent inflammatory tissue buried in a confined space
Morphology Ulceration
− Necrosis and inflammation on or near the surface
− Shedding of inflamed necrotic tissue
− Mucosa of mouth, GIT, genitourinary tract
− Lower extremities with poor circulation
Lost epithelial layer and mucosa, injury has formed in the submucosa
Acute phase response-clinical manifestations
Fever
• Elevation of body temperature (+1-4oC)
• Release of pyrogens (molecules that cause fever)
− Exogenous (bacterial and viral molecules)
− Endogenous pyrogens (cytokines), cytokines released by macrophages
• Prostaglandin synthesis
− Reset the temperature set point in the hypothalamus
− Thought to ward of infection and induce heat shock proteins.
Increase body temperature to slow down pathogens and to give immune system time to retaliate
- Increased heart rate,
- Increased blood pressure,
- Decreased sweating
- Rigors and chills (temperature set point)
- Anorexia, somnolence, malaise (action of cytokines on brain)
- Cachexia (wasting due to TNF mediated appetite suppression and mobilization of fat stores)
Acute phase response-pathologic manifestations
• Acute-phase proteins (chemical markers of acute phase response)
− C-reactive protein (CRP)
− Serum amyloid A (SAA)
Both bind to microbial cell wall • Opsonin and C’
− Fibrinogen (binds RBC, RBCs stack together basis of erythrocyte sedimentation rate)
Leukocytosis
• Increased leukocyte count
− Neutrophilia (bacteria)
− Lymphocytosis (viral infection)
− Eosinophilia (hypersensitivities and parasitic infections)
Acute Phase Response
Sepsis
Sepsis: systemic inflammatory response
− Severe microbial infection (microorganism or their
products-secreted toxins in the blood)
− Stimulates enormous production of cytokines
− TNF and IL-1
− Disseminated intravascular coagulation-blood clots forming
− Metabolic disturbances - hyperglycemia
− Hypotensive shock –drop in blood pressure
Systemic vasodilation throughout entire body-more volume –bigger blood vessels but same amount of blood -> drop in blood pressure
Regeneration or repair by scar formation
Repair/healing
2 main categories
• Regeneration: proliferation of cells to replace lost structures.
− Tissues composed of cells with proliferative capacity AND
− The underlying structure of the tissue has not been too severely damaged
• Repair by scar formation (connective tissue)
− Tissues composed of cells with limited or no proliferative
capacity
eg myocytes of the heart
− The underlying structure of the tissue is lost
Proliferative capacity-labile tissue,
− Continuously lost and replaced
− Does not enter G0
ever
− Maturation of stem cells or
proliferation of mature cells
− Tissue can regenerate if stem cells reserve and tissue structure intact
Eg.
Hematopoietic cells Epithelial cells (skin, GIT etc)
Proliferative capacity-stable tissue
− Quiescent
− Enter G0
− Reenter cell cycle if stimulated by loss of cells
− Limited capacity to regenerate (exception liver)
Eg.
Parenchyma( functional tissue of an organ as distinguished from the connective and supporting tissue) of most solid organs (liver and kidney)
Endothelial (angiogenesis) and smooth muscle cells, fibroblasts
Proliferative capacity-permanent tissue
− Terminally differentiated
− Enter G0
− Cannot reenter the cell cycle
− Limited stem cell replication (not sufficient for regeneration)
Eg.
Neurons, cardiac muscle cells and (skeletal muscle cells)
