cell injury, cell death, adaptations

what organs in the adult body do not proliferate its cells?

what organs in the adult body do not proliferate its cells?

heart and brain

what is hypertrophy?

the increase in the size of each cell without proliferation

examples of physiologic hypertrophy

muscle hypertrophy due to exercise uterus hypertrophy from pregnancy

What induces uterus hypertrophy during pregnancy?

hormones

what can be observed in the uterus after menopause?

atrophy

example of pathological hypertrophy

increased workload on the heart due to hypertension. (hypertrophy of the cardiac muscle, especially the left ventricle)

what is brown atrophy of the heart?

the heart cells become thinner due to aging. lipofuscin accumulates and a dense number of nuclei will be visible (may look like hyperplasia)

what is hyperplasia?

the increase in proliferation or the number of cells in a tissue

physiological hyperplasia examples

hormone/growth factor-induced hyperplasia (proliferation of mammary glands during puberty) bone marrow proliferation in response to massive bleeding endometrium hyperplasia during menstrual cycle

examples of pathological hyperplasia

excessive release of hormones, leading to benign hyperplasia (prostate and endometrium) HPV-induced

2 symptoms caused by HPV

skin warts, mucosal lesion

what is atrophy?

reduction in the size OR number of cells

factors that contribute to atrophy

decreased workload, denervation (nerve damage), diminished blood supply, inadequate nutrition, loss of endocrine stimulation, pressure

what is metaplasia?

reversible changes in the type of cell proliferating

examples of metaplasia

epithelial metaplasia (squamous, intestinal, pseudopyloric, etc.) mesenchymal metaplasia (formation of catilage, bone and adipose)

What is barrett esophagus?

when a patient has chronic GERD, the lower parts of the esophagus undergo metaplasia and become a simple columnar epithelium to tolerate the gastric acid rising to the esophagus.

causes of cell injury

hypoxia/ischemia toxins (such as pollutants and CO) infectious agents immunologic reactions, such as inflammatory response genetic abnormalities nutritional imbalance physical agents

how can down syndrome cause cell injuries?

down syndrome causes congenial malformations which lead to cell injury

examples of reversible injury of the membrane

blebbing, distortion of microvilli, loose intercellular exattachments.

reversible injury of the mitochondria

swelling, phospholipid-rich amorphous densities

reversible injury of ER

dilation/swelling, detachment of polysome/ribosome

reversible injury of the nucleus

clumping of chromatin

reversible injury of the cytoplasm

myelin figures

what is fatty change?

loss of lipid-metabolizing enzymes in the liver resulting in accumulation of fat.

examples of fatty change

artherosclerosis and xanthomas

what is atherosclerosis?

cholesterol accumulation in tunica intima

what is xanthoma?

cholesterol/TAG accumulation under the skin

what are russel bodies?

protein accumulation in plasma cells

what are mallory bodies?

cytoskeletal protein accumulation in cells

what is amyloidosis?

accumulation of amyloid

2 types of pathological calcification in the heart

dystrophic (when serum calcium levels are normal) and metastatic (when serum calcium levels are elevated)

changes observed in the nucleus of necrotic cells

pyknosis (nucleus is small), karyorrhexis (the nucleus is bursted), and karyolysis (no nucleus)

changes observed in the cytoplasm of necrotic cells

cytoplasm is eosinophilic, myelin figues, calcium soaps, changes in the mesenchyma.

changes observed in the membrane/extracellular space of necrotic cells

membrane breakage, leakage of intracellular enzymes into the blood (LDH, CK, etc)

What is observed in coagulative necrosis

cells look swollen, firm, and pale. infarcts of solid organs (heart, spleen, kidney) can be seen.

what is observed in caseous necrosis?

cells are white/yellow, cheese-like. can be seen in granulomas

what types of changes are observed in what order when there is cell injury?

biochemical, ultrastructural, light-microscopic, and morphological

characteristics of apoptosis

there is no inflammation. caused by antagonism of BCK2, which leads to the activation of BAX/BAK, release of cytochrome c, and the caspase cascade.

what is autophagy?

cells digest their own organelles and recycle them to provide energy and substrates. If the stress is too severe for the process to cope with it, it results in cell death by apoptosis.

how can ATP levels initiate necrosis?

low levels of ATP cause cell injury and necrosis

how can levels of ROS (reactive oxygen species) initiate necrosis?

high levels of ROS leads to cell injury

3 causes of hypoxia

reduced blood flow due to ischemia and artherosclerosis decreased oxygen affinity of the RBCs due to CO, anemia, and etc. inadequate oxygenation of blood due to low functions of the heart

excessive influx of calcium into the cells result in...

activation of phospholipase, protease, endonuclease, and ATPase

what substance released from a damaged mitochondrium contributes to cell injury and necrosis?

H+

what substance released from a damaged mitochondrium contributes to apoptosis?

cytochrome c

3 immediate results of accumulation of free radicals

lipid peroxidation protein modification or misfolding DNA damage

3 causes of membrane permeability defects

phospholipid loss, accumulation of lipid breakdown products, and cytoskeletal damage

what are the 5 classifications of degeneration?

cellular swelling, fatty change, hyaline change, amyloid change, mucoid change

what are the 5 types of cellular accumulation?

water, fat, amyloid (protein), glycogen, pathologic calcification