Pathoma: Growth Adaptations, Cell Injury and Cell Death Flashcards
By what mechanism does cellular hypertrophy occur?
Gene activation, protein synthesis and increased production of organelles
By what mechanism does hyperplasia occur?
Stem cell activation
Tissues that cannot undergo hyperplasia
Cardiac, nervous and skeletal muscle
Pathologic hyperplasia that does not increase risk of cancer?
BPH
3 mechanisms by which organ atrophy occurs?
Apoptosis, ubiquitin-proteosome degradation of cytoskeletal intermediate filaments and autophagy via vaculole-lysosomal degredation.
Mechanism by which the columnar cells in Barrett’s esophagus underwent metaplasia?
Stem cell reprogramming
Type of metaplasia that carries no increased risk for cancer?
Apocrine metaplasia of the breast
How does vitamin A deficiency cause keratomalacia?
Vitamin A is necessary for production of the thin squamous lining of conjunctiva. When it is absent, those cells undergo metaplasia to stratified keratinized squamous epithelium.
What is dysplasia?
Disordered cellular growth
When is dysplasia irreversible?
When cellular stress persists and it transitions to a carcinoma.
What is hypoxia?
Low oxygen delivery to tissue
Common causes of hypoxia
Ischemia (decreased arterial perfusion, decreased venous drainage or shock), hypoxemia (PaO2
Common causes of hypoxemia
High altitude, hypoventilation, diffusion defect and V/Q mismatch
First sign of CO poisoning?
Headache
PaO2 and SaO2 in CO poisoning and methemoglobinemia?
PaO2 is normal. SaO2 is decreased.
Why treat patients with methemoglobinemia with methylene blue?
It helps reduce Fe3+ to Fe2+
How does hypoxia cause cellular injury?
Low O2 = low ATP production. Low ATP results in multiple problems:
- Na/K ATP pump dysfunction causes Na and H2O to build up in the cell and it swells
- Ca2+ ATP pump dysfunction causes Ca2+ build-up in cytosol
- Lactic acid build-up denatures proteins and precipitates DNA
Cellular features that indicate reversible injury
Loss of microvilli and membrane blebbing secondary to cellular swelling.
Decreased protein synthesis from ribosomal dissociation from rER secondary to swelling.
Signs of irreversible cellular injury
Plasma membrane damage results in enzyme leakage (troponins) and increased Ca entry.
Mitochondrial membrane damage results in loss of function of the ETC and cytochrome C leakage into cytosol.
Lysosomal membrane damage results in release of hydrolytic enzymes that are activated by already high intracellular Ca levels.
How does the nucleus change as the cell dies?
Pyknosis -> Karyorrhexis -> Karyolysis -> No nucleus
Characteristic histologic pattern of cell death in every organ except the brain?
Coagulative necrosis. Nucleus is absent, but cellular architecture is preserved by protein coagulation. Note that the area of infarcted tissue is typically wedge-shaped and pale. The area of infarction is red if blood re-enters after infarction.
Characteristic histologic pattern of necrosis in the brain?
Liquefactive necrosis. This is a result of enzymatic lysis of cells and proteins. This also occurs in abscess (neutrophilic enzymes) and the pancreas (pancreatic enzymes)
Characteristic histologic pattern of ischemia in a patient with lower limb or GI tract ischemia?
Gangrenous necrosis is coagulative necrosis that looks mummified, there may be superimposed liquefactive necrosis if the dead tissue becomes infected
Characteristic histologic pattern of necrosis in a Tb or fungal infection?
Caseous necrosis. This occurs due to accumulation of fungal wall or mycobacterium in the infected necrotic tissue.
