Path (Inflammation) - Exam 2 Flashcards
What are the 3 stages of cellular injury?
- Aetiology (cause)
- Pathogenesis
- Morphology
What are the three types of aetiology?
a) environmental (bacteria, viruses, chemical)
b) genetic (inherited, acquires, auto-immune)
c) physical (mechanical, heat, UV)
What are reversible cellular responses?
- swelling
- cytoplasmic inclusions
- accumulations of pigments
- steatosis (fatty change)
What are irreversible cellular responses?
- abnormal mitochondria
- irregular contours
- eosinophilia
- nuclear deformities
What are two examples of Hydropic Swelling and what do they look like?
- Toxic injury (mostly reversible) - swelling with lipid accumulation
- Adaptive swelling - i.e. blebbing. Cell to cell communication lost
What does hydropic swelling look like?
Cell Sub-structure is dilated, therefore pale and ER is disorganised.
What are three examples of inclusions?
- mallory body in an alcoholic liver. Very pink with weird clumping due to damaged intermediate filaments.
- toxoplasma infection of AIDS
- virus in skin cells - amphiphilic
How are accumulations and pigments categorized?
- Intracellular or extracellular
- Endogenous or exogenous
NOTE: endogenous is normally present, but there is an abnormal accumulation, whereas exogenous is not normally there.
Give an example of both intracellular and extracellular accumulations.
Intracellular:
Lysosomal Storage Disease (glycogen accumulates in lysosomes)
Extracellular:
Amyloid-myocardium = deposits of amyloid (protein stuff)
Give an example of both endogenous and exogenous pigments.
Endogenous:
Haemachromatosis (too much stored iron=haemosiderin in liver)
Exogenous:
- anthracosis (carbon deposits on lung)
- ferrunginous bodies (asbestos fibbers coated in iron)
What is steatosis?
Steatosis is the infiltration of liver cells with fat, associated with disturbance of the metabolism by, for example, alcoholism, malnutrition, pregnancy, or drug therapy.
What does abnormal mitochondria look like and what could cause it?
Mitochondria is swollen and cristae no longer well organised.
Ischaemic injury
What could cause nuclear deformities?
- Cells arrested at metaphase and therefore separated chromosomes.
Colchine treatment for gout - Multinucleation
Chemo, HSV infection
What are the potential effects of cell injury?
a) none
b) adaptive response
c) reversible damage
d) irreversible (lethal) damage
What changes occur during necrosis?
- Initial biochemical damage
- Delay 4-12 hours
- Morphological changes
What are the two types (and subtypes) of microscopic changes that occur during necrosis?
- Non Specific (mainly cytoplasmic) i.e. blabbing, swelling, eosinophilia etc
- Specific
a) Nuclear Changes
b) Changes resulting from membrane rupture and enzyme release
What nuclear changes can occur during necrosis?
a) Pyknosis - nuclear shrinkage and condensation
b) karyorrhexis - nuclear rupture and fragmentation
c) karyolysis - disappearance
What are the changes resulting from membrane rupture and enzyme release during necrosis?
a) Intracellular:
- Digestion of organelle membranes and contents
- Denaturation of proteins
b) Extracellular:
- digestion of neighbouring cells
- inflammation response
What are macroscopic effects of necrosis?
- Coagulative
- Colliquative (liquefactive) necrosis
- Caseous Necrosis
OTHERS:
- gangrene
- fat necrosis
- fibrinoid change
- autolysis
What is the most common cause of coagulative necrosis?
Ischemia. Resultant lesion is an INFARCT and the process is INFARCTION.
What is the timeline of coagulative necrosis?
- Architecture remains for days/weeks
- increased anaerobic respiration
- denaturation of proteins
- breakdown of cells (some days later)
- inflammatory reaction
- haemorrhagic border
- regeneration or fibrosis
What does coagulative necrosis look like?
- Tissue is softer but still firm.
- Either pale (ischaemic) or red (haemorrhagic).
- Haemorrhagic border.
What are the two types of coagulative necrosis and where do they occur?
- Ischaemic Necrosis = pale. Blood seeps away from area.
- kidney
- heart
- brain - Haemorrhagic infarct = red
- lung
- venous occlusion
What happens during colliquative necrosis?
- Powerful hydrolytic enzymes are released instead of denatures, so the entire cell dissolves
- Inflammatory reaction - liquid material removed by ,macrophages, leaving CYSTIC SPACE, often with FIBROUS periphery.
What are the main reasons for colliquative necrosis?
- Pyogenic organisms (pus forming)
2. Brain Ischaemia
What does caseous necrosis look like and where is it usually seen?
Cheese-like
Tuberculosis
What are the types of gangrene?
- Wet
- Dry = ‘mummification’
- Gas (usually due to gram + bacteria)
What causes fat necrosis?
- enzymatic digestion of fat due to abnormal release of activated pancreatic enzymes. Chalky deposits
- Traumatic fat necrosis - rupture of fat cells (i.e. boobs, not a problem)
What does fibrinoid necrosis look like?
Pink around blood vessels and protein leaks to damages area.
What is the difference between apoptosis, necrosis, autolysis and autophagy?
Apoptosis - normal cell death activated by caspases
Necrosis - premature death of cells in LIVING tissue
Autolysis - self digestion AFTER DEATH
Autophagy - process for mopping up damaged cell parts. NOT always associated with cell death, i.e. lysosomal vesicles.
What does the outcome of necrosis depend on?
- Tissue involved (ability to regenerate)
- Extent of necrosis (intensity and duration)
- Time elapsed
What are the innate physical barriers?
skin and mucosal surfaces, pH, mucous, flushing
What are the innate cells and their primary functions?
macrophages, DC,
neutrophils, eosinophils, basophils, NK cells.
What are the main professional antigen presenting cells?
- monocytes
- B cells
- macrophages
- DCs
What are professional antigen presenting cells?
Professional APCs specialize in presenting antigen (peptide epitopes) to Th cells with MHC class II.
They have high concentrations of MHC class II on their surface