Exam 1 Study Guide
Cellular Responses 1o Injury
1. Discuss the types of adaptations. Provide examples.
– Atrophy--decrease in cell size: muscle shrinking from disuse (cast), lack of
nutrients, denervation, ischemia, endocrine dysfunction, persistent cell injury
Endocrine: pituitary gland injury causing lack of growth (trophic) hormones
Persistent cell injury: chronic inflammation/infection
– Hypertrophy--increase in cell mass due to augmented functional capacity
Increase in cellular protein content
Functional demand (exercise, heart working too hard in HBP + CHF)
Increase in trophic hormones (breasts and uterus during pregnancy)
Only occurs in cells that are unable to undergo mitotic division
– Hyperplasia--increase in number of cells in MITOTIC cell types
Increased physiologic demand (RBC increase in higher altitudes)
Hormonal stimulation (uterus during uterine cycle; pathologic hyperplasia in
thyroid and prostate enlargement)
Chronic irritation of epithelial cells (calluses and corns, bladder cystitis)
– Metaplasia--replacement of one cell type with another REGULAR cell type
Persistent injury--replacement of of ciliated columnar epithelium of bronchial
mucosa to non-ciliated stratified squamous epithelium with cigarette smoke
SEE Q. 3
New cell type better adapted to injurious stimulation (Ciliated columnar: one
layer, cilia trap toxins
Stratified squamous: multiple layers, more resistant to physical injury)
– Dysplasia--disorganized appearance of cells, abnormal variation in
size/shape/arrangement atypical hyperplasia
Adaptive effort gone astray--hip dysplasia
Heightened risk of cancer
2. Are adaptations reversible? Are dysplastic cells cancerous?
Adaptations are reversible upon removal of the stimuli
No, they are precancerous (preneoplastic- neoplastic = abnormal new growth)
3. Explain the adaptation that occurs with smoking and GERD.
GERD (Gastroesophageal Reflux Disease) -- The normal esophageal cells
(squamous epithelium) are sensitive to the refluxed acid and die. They are
replaced with the columnar cells of the stomach that are resistant to the stomach's
acidity. This pathological condition is known as "Barrett's Esophagus."
Smoking
Squamous Metaplasia (SQM) is a pre-neoplastic change of the bronchial
epithelium observed in lungs in response to toxic injury induced by cigarette
smoke. The change in the cells of the trachea and bronchi of chronic
, cigarette smokers from ciliated columnar epithelium to non-ciliated stratified
squamous epithelium. The replacement cells lack the defense mechanism
performed by the cilia in moving particles up and out of the trachea
(mucociliary escalator)
4. Díscuss hypoxíc cell ínjury mechanísms. Crea1e a concep1 map descríbíng hypoxíc cell ínjury mechanísms
Hypoxia come common cell injury
• Aerobic vs. anaerobic metabolism
– Aerobic: Ischemia causes cells to generate reactive oxygen molecules. Free
radicals can form from oxidative reactions during normal aerobic
metabolism. These free radicals cause destruction of cell membranes and
structures. This includes nuclear DNA, mitochondrial DNA.
– Anaerobic: Hypoxia cuts off O2 supply from mitochondria decreasing ATP
production (cellular respiration). The cell uses its glycogen stores to generate
ATP. Pyruvate end products converted to lactate→ dec in cell pH
o High cell pH causes dysfunction of cell proteins and enzymes
• ATP
– ATP production stops due to lack of O2. Has many effects:
, o Na/K and Calcium pumps dysfunction causing hydropic swelling
• Na/Ca exchange
• Na/K pump
Cellular Responses 1o Injury
1. Discuss the types of adaptations. Provide examples.
– Atrophy--decrease in cell size: muscle shrinking from disuse (cast), lack of
nutrients, denervation, ischemia, endocrine dysfunction, persistent cell injury
Endocrine: pituitary gland injury causing lack of growth (trophic) hormones
Persistent cell injury: chronic inflammation/infection
– Hypertrophy--increase in cell mass due to augmented functional capacity
Increase in cellular protein content
Functional demand (exercise, heart working too hard in HBP + CHF)
Increase in trophic hormones (breasts and uterus during pregnancy)
Only occurs in cells that are unable to undergo mitotic division
– Hyperplasia--increase in number of cells in MITOTIC cell types
Increased physiologic demand (RBC increase in higher altitudes)
Hormonal stimulation (uterus during uterine cycle; pathologic hyperplasia in
thyroid and prostate enlargement)
Chronic irritation of epithelial cells (calluses and corns, bladder cystitis)
– Metaplasia--replacement of one cell type with another REGULAR cell type
Persistent injury--replacement of of ciliated columnar epithelium of bronchial
mucosa to non-ciliated stratified squamous epithelium with cigarette smoke
SEE Q. 3
New cell type better adapted to injurious stimulation (Ciliated columnar: one
layer, cilia trap toxins
Stratified squamous: multiple layers, more resistant to physical injury)
– Dysplasia--disorganized appearance of cells, abnormal variation in
size/shape/arrangement atypical hyperplasia
Adaptive effort gone astray--hip dysplasia
Heightened risk of cancer
2. Are adaptations reversible? Are dysplastic cells cancerous?
Adaptations are reversible upon removal of the stimuli
No, they are precancerous (preneoplastic- neoplastic = abnormal new growth)
3. Explain the adaptation that occurs with smoking and GERD.
GERD (Gastroesophageal Reflux Disease) -- The normal esophageal cells
(squamous epithelium) are sensitive to the refluxed acid and die. They are
replaced with the columnar cells of the stomach that are resistant to the stomach's
acidity. This pathological condition is known as "Barrett's Esophagus."
Smoking
Squamous Metaplasia (SQM) is a pre-neoplastic change of the bronchial
epithelium observed in lungs in response to toxic injury induced by cigarette
smoke. The change in the cells of the trachea and bronchi of chronic
, cigarette smokers from ciliated columnar epithelium to non-ciliated stratified
squamous epithelium. The replacement cells lack the defense mechanism
performed by the cilia in moving particles up and out of the trachea
(mucociliary escalator)
4. Díscuss hypoxíc cell ínjury mechanísms. Crea1e a concep1 map descríbíng hypoxíc cell ínjury mechanísms
Hypoxia come common cell injury
• Aerobic vs. anaerobic metabolism
– Aerobic: Ischemia causes cells to generate reactive oxygen molecules. Free
radicals can form from oxidative reactions during normal aerobic
metabolism. These free radicals cause destruction of cell membranes and
structures. This includes nuclear DNA, mitochondrial DNA.
– Anaerobic: Hypoxia cuts off O2 supply from mitochondria decreasing ATP
production (cellular respiration). The cell uses its glycogen stores to generate
ATP. Pyruvate end products converted to lactate→ dec in cell pH
o High cell pH causes dysfunction of cell proteins and enzymes
• ATP
– ATP production stops due to lack of O2. Has many effects:
, o Na/K and Calcium pumps dysfunction causing hydropic swelling
• Na/Ca exchange
• Na/K pump
