Unit 1: Cell Adaptation Flashcards
What do cells respond to?
microenvironment (adjacent cells, ECM, vascular elements), signaling (hormones), physical signals (stretch, temp)
quiescent cells vs labile vs stable cells
- Labile: divide continuously= skin, hair, mucosa, bone marrow
- Quiescent: only divide in situations of stress or repair
- Stable: cannot divide
aplasia- 1. define, 2. pathologic or adaptive response
total lack of stem cell division nearly always pathologic (ie NOT adaptive)
atrophy
- Define
- Why does this happen? Pathological or Physiological?
- pathophysiology
- decrease in the SIZE or NUMBER of cells
- to decrease function and metabolic demand of tissue/cell.
- Physiologically with AGE/decreased endocrine stimulation
- pathologically: ischemia, malnutrition, disuse, loss of innervation, pressure
- Decrease in SIZE: catabolism of cell components (ubiquitin pathway or autophagic vacuoles),
- Decrease in NUMBER: cell death (necrosis or apoptosis), or loss of proliferative factors (hormones/GF).
dysplasia
- define
- cause
- occurs in what cells?
- pre-cancerous changes in CELL STRUCTURE and TISSUE ARCHITECTURE and function that can progress to neoplasia
- damage to DNA
- only cells that can divide!
hyperplasia-
- define
- which tissues, why?
- how?
Pathological OR physiological
- increase in the number of cells
- requires proliferative tissues (stem cells). Does not occur in neurons, heart or skeletal muscle
- increase in proliferative signals (hormonal or growth factors)
hypertrophy
- define
- which tissues, why?
- how?
physiological or pathological
- increase in SIZE of cells
- Almost all tissues. The ONLY adaptive response in non proliferating cells to increase function
- due to increase in synthesis of cell components (usually proteins) or genetic changes
Examples of hyperplasia –physiological and pathological
Physiological-
- Hormonal control: uterus in pregnancy, lactation, puberty
- Local growth factors: wound healing
Pathological
- hormone secretion is out of control (ex: HPV- warts)
- endometrial hyperplasia post-menopause
- hyperkeratosis of skin
- gynecomastia in men (secondary to alcoholism)
- benign nodular prostatic hyperplasia
metaplasia
- Define
- etiology
- adaptive/pathological; reversible/irreversible
- downside?
- replacement of one NORMALLY DIFFERENTIATED cell type with another type due to CHRONIC stress/irritation/infection/injury
- STEM CELLS differentiate into a different cell type that can better withstand stress/irritation
- ADAPTIVE REVERSIBLE response
- loss of functions (ciliary function, mucous secretion)
neoplasia
- Define (pathologic or adaptive?)
- Etiology
- what cell types?
- PATHOLOGIC change that results in unregulated cell growth, mass formation, and tissue destruction==cells are altered in form and function and arise from SINGLE MOTHER CELL (ie monoclonal)
- abnormal expression of damaged DNA
- Only in dividing cells
Big differences between neoplasia and hyperplasia…..?
- Neoplasia= irreversible;
- hyperplasia= reversible
- Neoplasia= not under control of external signals,
- hyperplasia= hormonal control, can be withdrawn to reverse changes
Hypertrophy- examples of physiological and pathological
Physiological: skeletal muscle growth from increased exercise Pathological: heart muscle hypertrophy due to chronic hemodynamic overload (ie: htn)
Tissue adaptation
- etiology
- examples
- reversible/irreversible?
- cell’s attempt to RE-ESTABLISH HOMEOSTASIS due to physiologic or pathologic change in cell’s environment
- hyperplasia, hypertrophy, atrophy, metaplasia
- reversible
Hypoplasia
- Define
- Etiology
- examples?
- lack of development of a tissue or organ
- genetic or mechanical (ex: uterine constraint)
- hypoplastic left heart syndrome, hypoplastic (nondescended) testes
These two are ALWAYS pathologic changes
dysplasia, neoplasia
hypoplasia of Bone marrow – causes
genetic or nutritional deficiency cannot support adequate red cell production, causing anemia
Aplastic anemia
toxin or virus results in loss of viable stem cells –> red cells cannot be made OFTEN IRREVERSIBLE
LV Hypertrophy
- Caused by?
- defining characteristic
- pathophysiology
- eventually….
- secondary to chronic increased resistance to cardiac outflow–usually due to systemic hypertension
- LV>1cm thick
- increased stretch activates transcription factors to increase actin and myosin filaments (fetal myosin heavy chain) and increased production of ANP
- compensation is not enough, cells degenerate==> cardiac dilation and heart failure
Regeneration
A) hyperplasia in tissues that can divide
B) scar tissue in non dividing tissue (fibroblasts and collagen)
Regeneration following liver biopsy- timeline
- increase in DNA synthesis within 12 hrs,
- peaks in 1-2 days 10% of cells divide (vs .5%)
- regeneration complete in 1-2 weeks
What are residual bodies?
[Following atrophy] Residual bodies–often lipofuscin granules— are cellular debris that resists degradation during autophagy
What is brown atrophy?
discolored tissue following atrophy due to leftover lipofuscin granules
Examples of metaplasia with regards to…..
- Lungs
- Vitamin A
- Esophagus
- Bladder
- bronchial: columnar to squamous epithelial (from smoke)
- Vit A def: columnar to squamous (in lung?)–Vit A needed for normal epithelial differentiation
- Barretts Esophagus: squamous to columnar (from acid)
- Schistosoma haematobium= transitional to squamous
atypia
changes in cell morphology–seen in dysplasia
Major differences between DYSPLASIA and METAPLASIA
Metaplasia- cell differentiates regularly, despite the fact that it’s a different cell type ==>reversible ==>NOT precancerous
Dysplasia- irregular differentiation= altered architecture and organization due to GENETIC changes ==>reversible or irreversible ==>precancerous
Structural changes in cell adaptation are initiated by…..
response to signal transduction from cell surface receptors (TBL ?)
