Advanced Patho Altered Cellular Function and Cancer Questions with
Answer Graded A+ 2025/2026
Dysplasia - E: cells abnormal changes in shape, size, organization P:
caused by cell injury/irritation, characterized by disordered cell growth. aka
atypical hyperplasia or pre-cancer Ex:pap smears often show dysplastic
cells of the cervix that must undergo laser/surgical tx
Metaplasia - E: reversible change, one type of cell changes to another type
for survival P: results from exposure of the cells to chronic stressors, injury,
or irritation Ex: Columnar cells change to squamous cells in lungs of
smoker
Atrophy - Physiologic: shrinking of thymus during childhoodPathologic: -
paralyzed person, skeletal muscle atrophy-occurs as result of decrease in
workload, pressure, use, blood supply, nutrition, hormonal stimulation, or
nervous stimulation
Hypertrophy - Physiologic:skeletal muscle hypertrophy for persons doing
heavy work/weight lifting. one kidney removed, the other kidney increases
in size to accommodate for workloadPathologic:Cardiomegaly results from
HTN or heart valve problems
Hyperplasia - Physiologic: removal of part of the liver lead to hyperplasia of
hepatocytes. uterine or mammary gland enlargement during pregnancy
Pathologic:abnormal proliferation of normal cells usually caused by
increased hormonal stimulation. increase of production of local growth
factors
Dysplasia - Physiologic:Is not a true adaptive process
Pathologic:Dysplastic cells of cervix found on Pap smear.
Metaplasia - Physiologic: Barrett Esophagus- normal squamous cells
change to columnar epithelial cells in response to reflux, aka intestinal
metaplasia Pathologic: Smokers- normal ciliated epithelial cells of the
bronchial linings are replaced by stratified squamous epithelial cells.
Cancer can arise from this area, stimulus induces a reprogramming of stem
cells under the influence of cytokines and growth factors
Hypoxic Injury - Etiology:decreased O2,loss of Hgb or Hgb function,
decreased RBC production, disease of heart/lungs, ischemia Clinical
, Manifestations: ischemia which progresses to hypoxia. Intracellular
enzymes as follows: CK-most muscle cells, including heart,LDH- muscle
cells, liver cells, heart cells, RBCs, brain,AST- liver cells,ALT- liver cells
Troponin- cardiac cells Patho: lack of O2 causes decrease in mitochondrial
function, causing decrease ATP production and increases anaerobic
metabolism (generating ATP from glycogen), eventually anaerobic
metabolism will stop and the cell will die. Reduction of ATP impairs Na/K
pump, leads to increased Na/Ca in cell, K is diffused out of cell, water
diffuses into cell causing swelling, ribosomal dilation and malfunction occur.
Ribosomes produces protein and when it malfunctions causes decrease in
protein synthesis. Death will occur if injury is not stopped.
Free Radical and Reactive Oxygen Species (ROS) - Etiology:Free Radical-
have unpaired electron in its outer shell, making molecule unstable and
highly reactive. aka being oxidized ROS-byproduct of ATP production in the
mitochondria Clinical Manif: FR- to stabilize self, it will steal an electron
from another molecule or give up an electron. The free radical will often
steal an electron from another molecule, making that molecule a free
radical ROS- can overwhelm mitochondria and exhaust intracellular
antioxidants, causing cell injury/disease Patho: ROS are produced by
absorption of high energy sources such as radiation or UV light, have role
in development of Alzheimer's, Parkinson's, Amyotrophic Lateral Sclerosis
(ALS). ROS cause lipid peroxidation, damage proteins which maintain ion
pumps and cellular transport, fragment DNA and causes less protein
synthesis, cause chromatin destruction, and damage mitochondria.
Antioxidants are our body's defense against ROS- reducing agents that
provide missing electron, stabilizing the free radical
Ethanol - Etiology: ETOH is metabolized to acetaldehyde in the cytoplasm
of the cell, enzyme alcohol dehydrogenase (ADH) helps with conversion
Clinical Manifestation: adverse effects on liver and causes nutritional
disorders. acute effects in the liver include inflammation, fatty infiltration,
hepatomegaly, acute liver necrosis and suppressed fatty acid oxidation.
liver failure is irreversible effect of chronic abuse Patho: Conversion
oxidized niacin (NAD+) is reduced to NADH. In the mitochondrial
acetaldehyde is further converted by ADH to acetate and further oxidized
niacin (NAD+) is reduced to NADH. the increased NADH/NAD+ ratio in the
liver causes the following Pyruvate change to lactic acid causing lactic
acidosis Oxaloacetate converted to malate, preventing gluconeogenesis
leading to fasting hypoglycemia Glyceraldehyde to glycerol which combines
Answer Graded A+ 2025/2026
Dysplasia - E: cells abnormal changes in shape, size, organization P:
caused by cell injury/irritation, characterized by disordered cell growth. aka
atypical hyperplasia or pre-cancer Ex:pap smears often show dysplastic
cells of the cervix that must undergo laser/surgical tx
Metaplasia - E: reversible change, one type of cell changes to another type
for survival P: results from exposure of the cells to chronic stressors, injury,
or irritation Ex: Columnar cells change to squamous cells in lungs of
smoker
Atrophy - Physiologic: shrinking of thymus during childhoodPathologic: -
paralyzed person, skeletal muscle atrophy-occurs as result of decrease in
workload, pressure, use, blood supply, nutrition, hormonal stimulation, or
nervous stimulation
Hypertrophy - Physiologic:skeletal muscle hypertrophy for persons doing
heavy work/weight lifting. one kidney removed, the other kidney increases
in size to accommodate for workloadPathologic:Cardiomegaly results from
HTN or heart valve problems
Hyperplasia - Physiologic: removal of part of the liver lead to hyperplasia of
hepatocytes. uterine or mammary gland enlargement during pregnancy
Pathologic:abnormal proliferation of normal cells usually caused by
increased hormonal stimulation. increase of production of local growth
factors
Dysplasia - Physiologic:Is not a true adaptive process
Pathologic:Dysplastic cells of cervix found on Pap smear.
Metaplasia - Physiologic: Barrett Esophagus- normal squamous cells
change to columnar epithelial cells in response to reflux, aka intestinal
metaplasia Pathologic: Smokers- normal ciliated epithelial cells of the
bronchial linings are replaced by stratified squamous epithelial cells.
Cancer can arise from this area, stimulus induces a reprogramming of stem
cells under the influence of cytokines and growth factors
Hypoxic Injury - Etiology:decreased O2,loss of Hgb or Hgb function,
decreased RBC production, disease of heart/lungs, ischemia Clinical
, Manifestations: ischemia which progresses to hypoxia. Intracellular
enzymes as follows: CK-most muscle cells, including heart,LDH- muscle
cells, liver cells, heart cells, RBCs, brain,AST- liver cells,ALT- liver cells
Troponin- cardiac cells Patho: lack of O2 causes decrease in mitochondrial
function, causing decrease ATP production and increases anaerobic
metabolism (generating ATP from glycogen), eventually anaerobic
metabolism will stop and the cell will die. Reduction of ATP impairs Na/K
pump, leads to increased Na/Ca in cell, K is diffused out of cell, water
diffuses into cell causing swelling, ribosomal dilation and malfunction occur.
Ribosomes produces protein and when it malfunctions causes decrease in
protein synthesis. Death will occur if injury is not stopped.
Free Radical and Reactive Oxygen Species (ROS) - Etiology:Free Radical-
have unpaired electron in its outer shell, making molecule unstable and
highly reactive. aka being oxidized ROS-byproduct of ATP production in the
mitochondria Clinical Manif: FR- to stabilize self, it will steal an electron
from another molecule or give up an electron. The free radical will often
steal an electron from another molecule, making that molecule a free
radical ROS- can overwhelm mitochondria and exhaust intracellular
antioxidants, causing cell injury/disease Patho: ROS are produced by
absorption of high energy sources such as radiation or UV light, have role
in development of Alzheimer's, Parkinson's, Amyotrophic Lateral Sclerosis
(ALS). ROS cause lipid peroxidation, damage proteins which maintain ion
pumps and cellular transport, fragment DNA and causes less protein
synthesis, cause chromatin destruction, and damage mitochondria.
Antioxidants are our body's defense against ROS- reducing agents that
provide missing electron, stabilizing the free radical
Ethanol - Etiology: ETOH is metabolized to acetaldehyde in the cytoplasm
of the cell, enzyme alcohol dehydrogenase (ADH) helps with conversion
Clinical Manifestation: adverse effects on liver and causes nutritional
disorders. acute effects in the liver include inflammation, fatty infiltration,
hepatomegaly, acute liver necrosis and suppressed fatty acid oxidation.
liver failure is irreversible effect of chronic abuse Patho: Conversion
oxidized niacin (NAD+) is reduced to NADH. In the mitochondrial
acetaldehyde is further converted by ADH to acetate and further oxidized
niacin (NAD+) is reduced to NADH. the increased NADH/NAD+ ratio in the
liver causes the following Pyruvate change to lactic acid causing lactic
acidosis Oxaloacetate converted to malate, preventing gluconeogenesis
leading to fasting hypoglycemia Glyceraldehyde to glycerol which combines
