Cellular Injury and Adaptation Flashcards
Protective factors against free radicals
- antioxidants (vitamin A, E, C)
- superoxide dismutase
- glutathione peroxidase
- catalase
Necrotic connective tissue histologically resemble fibrin, eosinophilic homogenous appearance, due to acute immunologic injury and vascular hypertensive damage
Fibrinoid necrosis
Combination of coagulative and liquefaction necrosis. Typical example of it.
- caseous necrosis
- granulomatous disease (ex, TB, histoplasma capsulatum, nocardia)
Barret’s esophagus and polycythemia are classical examples of what type of cell adaptation
- Metaplasia
- Hyperplasia
Intracytoplasmic accumulation of immunoglobulins in plasma cells. What scenario lead this?
- Russel bodies (intracellular hyaline change)
- proteinuria
*occur in proximal renal tubules
Damage produced at CNS by vitamin B12 deficiency
Degeneration of the posterior and lateral white columns of the spinal cord
*spastic paraparesis, sensory ataxia, paresthesia, principally in lower limbs. Megaloblastic anemia
As some irreversibly cellular damage, phospholipases are activated, what factor mediate its activation?
Calcium
*loss of cellular permeability to ions and loss of integrity. During the initial stages of cell death, calcium is released from the mitochondria.
Type of necrosis where there is a loss of nuclei, although the shape of the cell is maintaine
Coagulative necrosis
*most solid organs following ischemic damage.
Exception in ischemic damage where type of necrosis is liquefaction no coagulative
Central nervous system (brain)
In chronic pancreatitis what mechanism is associated with the produce of calcium deposits?
Lipase ▶️ release triglycerides ▶️ binds to calcium (saponification)
*dark-blue on H&E stain
Which scenarios do you expect find fibrinoid necrosis?
- Vasculitis
- Malignant hypertension
What is the consequence of over expression of Bcl-2? What is the mechanism? Example of this situation.
⬇️ Caspase activation and ⬆️ tumorigenesis
Bcl-2 ▶️ (-) APAF-1 ▶️ (+) caspase 9 ▶️ initiate caspase cascade ⏩ APAF-1 overinhibited
Follicular lymphoma t(14;18)
Consequence of Fas mutation
⬆️ number of self-reactive lymphocytes (failure of clonal deletion)
*Fas-FasL needed for thymic medullary (-) selection
Sequence of events of coagulative vs liquefactive necrosis, why does that difference occur?
- ischemia/infarction ▶️ protein denature ▶️ enzymatic degradation
- abscess/brain infarction ▶️ neutrophils release enzymes ▶️ enzymatic degradation ▶️ protein denature
Most vulnerable regions and cells at brain to hypoxia/ischemia
- Purkinje cells of cerebellum, pyramidal cells of hippocampus and neocortex
- ACA, MCA, PCA boundary areas
- watershed areas
