| What happens when cells encounter physiological stress or pathological stimuli? | Cells undergo adaptation to achieve a new state and preserve viability and function
These adaptations are Hypertrophy, hyperplasia, atrophy, metaplasia
This may be reversible when stress is done, and may lead to cell injury if stress level exceeds adaptive capacity.
Some injuries are reversible, others are not and lead to cell death by necrosis or apoptosis |
| What is hypertrophy? | Cell size increase thus organ size increase, occurs when cells have limited capacity to divide, in response to increased workload.
Induced by growth factor, could occur with accompanying hyperplasia leading to enlarged organ |
| What is hyperplasia? | It occurs for tissues capable of replication, induced by growth factors, can be pathologic or physiologic.
Two types: hormonal (like female breast hypertrophy) or compensatory (by removal or loss of an organ part)
Most pathological ones are caused by hormonal excess |
| Give examples on pathological hyperplasia? | Endometrial hyperplasia by disturbed estrogen and progesterone levels, causing abnormal menstrual bleeding.
Growth factors repair vessels and tissues by proliferating fibroblasts
Viral infections also increase growth factor (like papilloma causing skin warts and mucosal lesions) |
| What is the relationship between hyperplasia and cancer? | Usually hyperplasia is responsive to normal regulatory control mechanisms, if they get out of control , we reach cancer.
Also hyperplasia is a fertile soil to get cancer (pt with endometrial hyperplasia have an increased risk to get endometrial cancer) |
| What is atrophy? | It is the shrikage in size of cells, may lead to shrikage in organs if nb of cells is big.
Due to decreased cell activity by decreased workload (immoblization of limb), loss of innervation, diminished blood supply, nutrition, endocrine stimulation , and aging |
| What is metaplasia? | It is replacement of a cell type to another in response to chronic stress and irritation in order to further adapt to this irritation
Like squamous metaplasia, although protective to cells, but leads to loss of function (like mucus secretion) and may be malignant (lung cancer)
Sometimes can get from squamous to columnar (like in case of gastric reflux
Can occur to mesenchyma pathology (bone erosion to soft tissue) |
| What is reversible cell injury? | During early injury it is still reversible where no severe membrane damage or nuclear dissolution occurs |
| What are the causes of cell injury? | Hypoxia, chemical agents, infection, autoimmunity, genetic defects, nutritional imbalances, physical agents, and aging |
| How does hypoxia cause cell injury and death? | It interferes with oxidative respiration, it is different then ischemia which is loss of blood supply, as it may also be caused by pneumonia, anemia, or CO poisoning (which complexes with Hb and form a stable form) |
| How to distinguish a reversible cell injury? | Two manifestations (swelling and fatty change)
swelling due to no ion pumps, fatty change is appearance of small or large lipid vacuoles in cytoplasm |
| What is cellular swelling? | First manifestation of cell injury, reversible, seen better when whole organ is affected by increasing its mass, turgor and pallor (capillary compression)
AKA hydropic change or vacuolar degeneration |
| What is fatty change? | Appearance of lipid vacuoles in cytoplasm, cells participating in fat metabolism (liver cells) also shows eosinophilic staining with progression to necrosis becomes more pronounced |
| What are cellular changes in reversible injury? | Plasma membrane alteration (blebbing, distortion of microvilli)
Mitochondrial changes (swelling, phopholipid rich density)
ER dilation (detachment of ribosomes)
Nuclear alterations (clumping of chromatin) |
| What is cell death? | As damage continues, cells get to a point of irreversible damage and thus death, two types (necrosis and apoptosis)
that differ in mechanism, morphology and disease physiology |
| What is necrosis? | It is a pathway of cell death, where cytoplasmic membranes are damaged releasing toxins to the cell.
Cytoplasm gets more eosinophilic, more glassy appearance due to glycogen loss, increased myelin figures, vacuolated month-eaten cytoplasm due to organelle digestion by enzymes
Nuclear changes are karyolysis (no more basophilia due to DNA damage), pyknosis (nuclear shrink due to DNA decondesation), karyorrhexis (fragmented nucleus)
1-2 days nucleus disappears |
| What happens to necrotic cells after death? | May either be digested by enzymes, or replaced by myelin figures and either phagocytosed or degraded into fatty acids which may bind calcium and get tissue calcification. |
| What are the patterns of necrosis? | Coagulative, liquifactive, gangrenous, caseous, fat necrosis, fibrinoid necrosis |
| What is coagulative necrosis? | Characteristic of infarcts in all solid organs except brain.
It is death of cells with preservation of underlying architecture, and dead tissue forms a firm texture.
Dead cells are not directly removed, it need leucocytosis in order to start degradation (takes days or weeks) |
| What is liquefactive necrosis? | In bacterial/ fungal infections where inflammation and enzymes liquify the tissue, usually in CNS, completely digested dead cells.
If by bacteria it forms pus |
| What is gangrenous necrosis? | Limb lost blood supply and had caogulative necrosis involving many tissue layers, could be accompanied by liquification if bacteria is present and attracts leukocytes (wet-gangrene) |
| What is caseous necrosis? | In TB, cheese like, Fragmented or lysed cells, amorphous pink appearance in H&E stain, completely obliterated cellular outline and tissue architecture.
If enclosed in an inflammatory border then it is called a granuloma. |
| What is fat necrosis? | Focal areas of fat destruction, due to release of pancreatic lipases in acute pancreatitis, liquify membranes of fat cells in peritoneum that may combine with calcium (fat saponification) |
| What is fibrinoid necrosis? | Special form where Ab-Ag complexes accumulate in arterial walls, leaks out of the vessels producing an amorpous bright pink appearance called fibrinoid |
| What is apoptosis? | When no GF or DNA is damaged cell kills itself.
Nuclear dissolution without loss of membrane integrity.
Not necessarily pathological, no inflammatory response. |
