(2) Cell Injury and Adaption Flashcards
4 Cellular Responses to Injury
- alter physiology/non-lethal stimulus
ie. Increased demand, GF, less nutrients, chronic irritation
→ Hyperplasia/hypertrophy/atrophy/metaplasia - Reduced O2, chemical injury, microbial infection
ie. Acute/transient and progressive/severe
→Acute reversible injury like swelling or fatty change
→Irreversible like necorsis/apoptosis - Metabolic change/genetic/aquired change/chonic
-→intracellular accumulations, calcifications - Cumulative sub-lethal injury overtime
→ cellular aging
Labile cells and examples
continously dividing
→hematopoetic cells or surface epi (chemo would affect these)
Stable tissues
quiescent; divide, but not often
→ in response to injury
→ the parenchyma of solid organs
→ endothelial cells, fibroblasts, sm msl cells
Permanent Tissues
non-proliferative
→ neurons and cardiac muscle cells
↑SIZE of cells; increase size organ
HYPERtrophy
- more proteins/organelles
- d/t tropic(GFs) or mechanical triggers
- occurs in cells w/ limited capacity to divide
Hypertrophy
Physiologic Hypertrophy:
d/t increased fnx demand or hormonal stimulation. Like wt lifting or preg uterus
CC: Patho hypertrophy =
heart mscl in HTN
*thick lf ventricle and increased mass; in response to increased work load in HTN
See also w/ aortic vavle stenosis
*myofibers enlarge; increase filaments. Initially no change but leads to heart fail
In microscope: see enlarged nuclie and myofiber width
↑# of cells
*cells capable of division(labile and stable)
HYPERplasia:
Physiologic hyperplasia:
female boobs puberty/preg
- Compensatory hyperplasia of liver after partial resection
- CT response to wound healing
- preg uterus both hypertrophy/hyperplasia
CC: Patho hyperplasia
Excessive stimulation by GF or hormones
-Endometrial hyperplasia; reversible and cells respond normally to regulatory mech. Puts you at increased risk for cancer
Microscope: increased # and crowding of glands with cells closely packed liking glands. Glands should be round
Benign Prostatic Hyperplasia
men >50
*nodules in prostate/perurethral = obstruction
cause=?
d/t androgen induced relesase of GF→ increased proliferation of stromal cells, decreased death of epithelial cells
*no increased risk of cancer
BPH pathogenesis:
androgen induced released of GF–> increased proli of stromal cells, decreated death of epithelial cells
↓size of a cell d/t loss of substance
- severe leads to decreased organ size
- decreased protein synth + increased degredation
- decreased function but not death
Atrophy:
Causes of Atrophy
- Physiologic:
- Pathologic:
- loss of hormonal simulation (endometrium, menopaus)
2. decreased functional demand/loss of innervation/inadequte nutrition
cell type replaced by other adult cell type more able to handle stress
-Adaptive process to chronic stress+/or persisten cell injury
Metaplasia:
- cells become reprogrammed but is reversible
- can increase risk cancer
metaplasia
Epithelial metaplasia in smoker: pathophysiology
Ciliated columnar epi→ squam epi (trachea of smokers)
*stimulus causing change may predispose to devo of malignant neoplasm
Barrett Esophagus pathogenesis
sq epithelium at distal eso→ glandular epithelum like in stomach (protect reflux acid)
***predisposes devo of glandular carcinoma = adenocarcinoma
Barretts Esophagus predisposes you to what type of cancer?
adenocarcinoma
Causes of Squamos metaplasia at endocervix
- columnar→ squamos at endocervix
- increase risk of HPV infection
bone formation in soft tissue (msl/CT)at sites of injury
Mesenchymal metaplasia:
inadequate oxygenation of blood (lung disease or lack of O2 in ambient air)
-reduced O2 carry capacity of blood (anemia, cyanide)
Hypoxia
lack of blood to site (coronary art diseae/stroke/ heart attack)
Ischemia:
Causes of Cell death
- O2 deprevation: hypoxia and ischemia
- Physical agents: trauma/temp extremes/ radiation
- Chemical agents
- Infections agents: virus/fungi/bacteria/parasites
- Immunologic rxns: autoimmune/hypersentivity
- Genetic derangements
- NUTRITION imbalance or aging
- can’t reverse mitochondiral dysfnx (lack of oxidative phosphorlyation and ATP generations)
- mess up membrane fnx
- have apoptosis and necrosis
Irreversible Cell Death
Hallmark of irreverisble cell death
mitochondiral dyxfnx; lack of oxidative phosphorylation and ATP generations
swelling/ pyknosis, karyorjexis, karyolysis/ enZ may leak out of cell/ disrupted pl membrane/often adjacent inflammation/always pathologic
Necrosis:
shrinkage/framementation to nucleosomes/ intact plasma membrane/ contents are intact and released as apoptotic bodies/ no inflammaiton/ often physiologic, sometimes pathologic
Apoptosis:
Two examples of Reversible Cell Change
Fatty change and vacuole change (hydopic change)
lipid vacuoles in cytoplasm dt toxi or hypoxic injury. In cells dependent on fat metabolism
CC: fatty liver secondary to alcohol
Fatty Change: Reversible
- d/t failure of mmb pump to maintain homeostasis = mmb blebs~ failure of Na/K pump
- see vacuoles in cells corresponding to distended ER
*Cell swelling: hydorpic change or vacuolar degen
Cause steatosis:
alcohol, obesity, malnutrition, anoxia, diabetes
What happens in steatosis
-hepatocytes are injured → intracell accumulation of triGs, liver gets big, elevated liver enZ from leaky hepatos
Clincal manifestations depend on cause/severity; can be reverible if cause removed. If mild, no effect on cell fnx but sever we see fucked cell fnx, cell death, cirrhosis
What does a liver cell with steatosis look like under microscope
Microscopy: intracell accumulation of fat = liposome, will push aside nucleus
