Pathoma: Growth adaptations, cell injury and death Flashcards
Hypertrophy
increase in size of the organ
involves gene activation, protein synthesis, and production of organelles
Hyperplasia
increase in number of cells in the organ
involves the production of new cells from stem cells
Permanent Tissues
Cardiac muscle
skeletal muscle
nerve
cannot make new cells
undergo hypertrophy only
Pathologic hyperplasia progresses to
dysplasia and eventually cancer
exception - benign prostatic hyperplasia, does not increase the risk for prostate cancer
Atrophy
decrease in stress leads to decrease in organ size by a decrease in size and number cells
what process decreases the number of cells in atrophy
apoptosis
what processes decreases the cell size in atrophy
ubiquitin-proteasome degradation of cytoskeleton - intermediate filaments of cytoskeleton are tagged with ubiquitin and destroyed by proteasomes
autophagy of cellular components - generation of autophagic vacuoles - fuse with lysosomes whose hydrolytic enzymes breakdown cellular components
metaplasia
change in stress on an organ leads to a change in cell type - most commonly one epithelium to another better able to handle the new stress
occurs via reprogramming stem cells
may be reversible by treating stressor
persistent stress - can progress to dysplasia and eventually cancer
Barrett’s Esophagus
Barrett’s Esophagus
esophagus normally lined by nonkeratinizing squamous epithelium - can handle friction of food bolus
acid reflux from the stomach causes metaplasia to nonciliated, mucin-producing columnar cells- better able to handle stress of acid
Vitamin deficiency that can lead to metaplasia
vitamin A
necessary for differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye
vit A deficiency can cause goblet cell/columnar epithelium of conjunctiva to undergo metaplasia into keratinizing squamous epithelium
dry eyes (xerophtalmia) can lead to destruction of the cornea and blindness
What condition occurs in response to healing in trauma that causes mesenschymal tissues to undergo metaplasia
myositis ossificans
connective tissue within muscle changes to bone during healing after trauma
Dysplasia
disordered cellular growth
most often refers to proliferation of precancerous cells
often arises from longstanding pathologic hyperplasia or metaplasia
Aplasia
failure of cell production during embryogenesis
ex. unilateral renal agenesis
hypoplasia
decrease in cell production during embryogenesis, resulting in a relatively small organ
ex. streak ovary in Turner syndrome
Common causes of cell injury
inflammation nutritional deficiency or excess hypoxia trauma genetic mutations
hypoxia
low oxygen delivery to tissue
oxygen is the final electron acceptor in the electron transport chain of oxidative phos
decreased oxygen impairs ox phos, resulting in decreased ATP production
lack of ATP leads to cell injury
causes of hypoxia
ischemia
hypoxemia
decreased oxygen carrying capacity of blood
ischemia
decreased blood flow through an organ
decreased arterial perfusion - atherosclerosis
decreased venous drainage - Budd-Chiari syndrome
Shock - generalized hypotension -> poor tissue perfusion
hypoxemia
low partial pressure of oxygen in the blood - PaO2 decreased PaO2
hypoventilation - increased PaCO2 -> decreased PaO2
diffusion defect - PaO2 not able to push as much O2 into the blood due to a thicker diffusion barrier (interstitial pulmonary fibrosis)
V/Q mismatch - blood bypasses oxygenated lung or oxygenated air cannot reach blood
decreased O2 carrying capacity
hemoglobin loss or dysfunction
anemia - normal PaO2
carbon monoxide poisoning - PaO2 normal - cherry red appearance of skin, early sign is HA
Methemoglobinemia - iron in heme is oxidized to Fe3+ which cannot bind oxygen - PaO2 normal - seen in oxidant stress - cyanosis with chocolate colored blood - Tx is intravenous methylene blue which helps reduce Fe3+ back to Fe2+
hallmark of reversible cellular injury
cellular swelling - cytosol swelling results in loss of microvilli and membrane blebbing
swelling of the rough ER results in dissociation of ribosomes and decreased protein synth
Hallmark of irreversible cellular injury
membrane damage - results in cytosolic enzymes leaking into the serum (cardiac troponin), additional calcium entering cell
End result is cell death