Pathology (Gen Principles) Flashcards
Hypertrophy
increase in size
involves gene activation and *protein synthesis, and production of organelles (for cellular fxn - mitochondria)
Hyperplasia
increase in cell number
production of new cells from stem cells - classic response to hormone stimulation
Ex: breast growth at puberty, liver regeneration (donation) and bone marrow (anemia)
physiologic changes of the uterus during pregnancy
smooth muscle undergoes hypertrophy and hyperplasia
Important note about permanent tissues
canNOT make new cells - so cannot undergo hyperplasia - hypertrophy ONLY
3 permanent tissues:
cardiac myocytes
skeletal muscle
nerves
3 permanent tissues
“terminally differentiated”
cardiac myocytes
skeletal muscle
nerves
pathologic hyperplasia
hyperplasia that progresses to dysplasia and cancer
ex: endometrial hyperplasia - due to estrogen
exception: benign prostatic hyperplasia (BPH) - due to androgens - not related to cancer and no increase in cancer risk
Atrophy
decrease in stress on the organ (less stress) - decrease in size and number
Mechanism:
apoptosis (decrease # of cells)
ubiquitin-proteasome degradation (decrease in cell size)
mechanism of atrophy
- decrease in # - apoptosis
- decrease in size
a. ubiquitin-proteasome degradation pathway - destroying the cytoskeleton
b. autophagy of cellular components and then destroyed by lysosomes
Metaplasia
change cell type in response to stress
most common involves surface epithelium
metaplastic cells are better to handle the new stress
Mechanism of metaplasia
REVERSIBLE reprogramming of stem cells - can progress to cancer
ex: Barrett esophagus and respiratory epithelium w/ cigarette smoke (to stratified squamous cell epithelium)
exception: apocrine metaplasia (fibrocystic change of the breast - does not increase the risk of breast cancer)
the exception to metaplasia as an increased risk to cancer
apocrine metaplasia (fibrocystic change of the breast - does not increase the risk of breast cancer)
Which vitamin deficiency can lead to metaplasia?
Vitamin A deficiency
- night blindness
- also necessary for immune cell maturation (PML - trapped in blast state (derivative of Vitamin A is a tx)
- can result in metaplasia (necessary for maintenance of specialized epithelial - conjunctival and upper respiratory tract - pulmonary infections)
ex: keratomalacia
keratomalacia - clouding and drying (xerophthalmia) of the eye caused by a Vitamin A deficiency
Mesenchyme tissues
Connective tissues
- blood vessels, bone, fat, cartilage
presence of bone within skeletal muscle
myositis ossificans (ex of an mesenchyme metaplasia) - muscle going to bone
bone is normal - look careful and see that there is a distinct separation between the bone and muscle (is not growing off the bone - so not a bone issue like osteosarcoma)
Dysplasia
REVERSIBLE disordered cellular growth
proliferation of precancerous cells (ex: CIN) - arises from long standing hyperplasia (endometrial hyperplasia) or metaplasia (Barrett esophagus)
if stress persists - leads to cancer IRREVERSIBLE
Aplasia
failure of growth/cellular production during embryogenesis
ex: unilateral renal agenesis (fails to develop one kidney)
Hypoplasia
decrease in cell production during embryogenesis - results in small organ
Ex: streak ovary in Turner syndrome
Characteristic changes that indicate dysplasia
pleomorphism, abnormal nuclei (hyperchromatic or large), and mitotic figures (clumped chromatin)
Hypoxia
low oxygen delivery to tissues - O2 final electron acceptor - needed for ATP/energy - impairs oxidative phosphorylation -cellular injury (Na+/K+ failure)
CO poisoning
carbon monoxide is an odorless gas that binds Hb more tightly than 02; PaO2 will be normal but SaO2 will be decreased - (O2 is in the blood, just not bound to Hb)
Ex: smoke from fires, exhaust from cars (suicide) and gas heaters
Clinical manifestation: cherry red appearance of the skin, early sign of *headache and then confusion until it gets to coma and death
Methemoglobinemia
iron in heme is oxidized to Fe3+ (normally in Fe2+ state) - so now Hb can no longer bind O2
PaO2 is normal, SaO2 decreased - (O2 is in the blood, just not bound to Hb)
Seen in oxidant stresses (sulfa and nitrate drugs) and in newborns
Clinical manifestation: chocolate-colored blood w/ cyanosis Tx: IV methylene blue (reduce Fe3+ to Fe2+)
Low ATP in cells
ATP needed for Na+/K+ pump (pushes Na+ out to maintain gradient) w/ failure Na+ will build up inside the cell - H20 follows - swelling (first signs of cellular injury)
Also:
Ca2+ pump - high cyclic Ca2+ (enzyme activator) and aerobic glycolysis
Initial phase in reversible injury
hallmark = cellular swelling
leads to loss of microvilli, membrane blabbing and swelling of the RER (ribosomes pop pff the ER - decreased protein synthesis)