PATHOPHYSIOLOGY CHAMPION TEST WITH QUESTIONS
AND ANSWERS UPDATED 2025/2026 LATEST VERSION
Etiology
Causative factors in a particular disease
Iatrogenic
produced by treatment
Epidemiology
risk factors and distribution in populations
Incidence
number of new cases
Hyperplasia
increase in number of cells in an organ/tissue as a response to injury that results from an increased rate
of cellular division
compensatory Physiologic hyperplasia
is an adaptive mechanism that enables certain organs to regenerate. Occurs in skin, intestines,
hepatocytes, bone marrow, and fibroblasts. Ex. Is when skin gets callus in response to mechanical
stimulus.
Hormonal physiologic hyperplasia
Hormonal occurs mainly from estrogen dependent organs such as uterus and breasts.Ex- after ovulation
estrogen stimulates endometrium to grow/thicken for fertilized ovum.
Pathologic hyperplasia
he abnormal proliferation of normal cells and can occur as a response to excessive hormonal stimulation
or the effects of growth factors on target cells. These cells have enlargement of the nucleus, clumping of
chromatin (package and protect DNA), and the presence of one or more large nucleoli. Ex. Benign
prostatic hyperplasia (BPH) and endometriosis-both the result of hormonal imbalance.
Metaplasia
reversible replacement of one mature cell type (epithelial or mesenchymal) by another, sometimes less
differentiated, cell type.
Cause of metaplasia
develops from reprogramming of stem cells. Found in association with tissue damage, repair, and
regeneration.
pathophysiology of metaplasia
Adaptive replacement cell may be more suitable to the changed conditions in the surrounding
environment. Ex. GERD damages squamous epithelium of the esophagus, cells are replaced by glandular
,epithelium which may tolerate the acid better. Not always beneficial. Ex. Smoking causes changes in
bronchi cells, which don't have cilia or secrete mucus, causing loss of protective mechanism.
What is the significance of metaplasia
Can be reversed if stimulus is removed. If continues, can cause malignant transformation.
Dysplasia
abnormal changes in the size, shape, and organization of mature cells. mostly found in epithelia
Significance of dysplasia
can be reversed if it does not involve the entire epithelium. When dysplastic changes penetrate the
basement membrane it is considered a preinvasive neoplasm (carcinoma in situ)
mechanisms of cell injury
ATP depletion, mitochondrial damage, accumulation of oxygen and oxygen-derived free radicals
membrane damage
protein folding defects
DNA damage defects
calcium level alterations
reperfusion injury
injury to tissue that occurs after blood flow is restored
restoration of needed oxygen is accompanied by oxidative stress with the generation of toxic oxygen
radicals which damage cellular membranes and mitochndria
What helps reperfusion injury?
antioxidants and anti-inflammatory drugs
examples of cell injury
ischemic and hypoxic injury
ischemia-reperfusion injury
oxidative stress or accumulation of oxygen-derived free Prevalence
number of existing cases both new and old
clinical manifestations
signs, symptoms, and diagnostic criteria
how are symptoms and signs different
symptoms are what the patient reports
signs are objective or measurable
outcomes
cure, remission, chronicity, or death
,primary prevention
Efforts to prevent an injury or illness from ever occurring.
secondary prevention
-focuses on early identification of individuals or communities experiencing illness, providing treatment,
and conducting activities that are geared to prevent worsening health status
-examples: communicable disease screening and case finding; early detection and treatment of
diabetes; exercise programs for older adult clients who are frail
Tertiary prevention
-aims to prevent the long-term consequences of a chronic illness or disability and to support optimal
functioning
-examples: prevention of pressure ulcers as complication of a spinal cord injury; promoting
independence for the client who has traumatic brain injury
Atrophy
Decrease or shrinkage in cellular size.Most common in skeletal muscle, heart, secondary sex organs, and
brain.
Physiologic atrophy
occurs with early development. Ex. Thymus gland gets physiologic atrophy during childhood.
pathologic atrophy
occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation,
and nervous stimulation
hypertrophy
Increase in the size of the cells that increase the size of the affected organ. Heart and kidneys
(responsive to enlargement) and skeletal muscle.
physiologic hypertrophy
occurs with increased demand, stimulation of hormones, and growth factors. Ex. Pregnancy causes
hormone induced hypertrophy of the uterus, in skeletal muscle occurs as a response to heavy workload.
pathologic hypertrophy
results from chronic hemodynamic overload. Ex. Hypertension or heart valve dysfunction. Hypertrophic
cells have increased accumulation of ER, plasma membrane, myofilaments, mitochondria (not cellular
fluid). Nucleus is also hypertrophic with increased DNA synthesis. Triggers for cardiac hypertrophy
include mechanical signals (stretch) and trophic signals (growth factors and vasoactive agents).
radicals induced injury
chemical injury
Cell injury: ATP depletion
, loss of mitochondrial ATP and decreased ATP synthesis
results include:
cellular swelling
decreased protein synthesis
decreased membrane transport
lipogenesis
all changes that contribute to loss of integrity of the plasma membrane
Cell injury: Oxygen and oxygen-derived free radicals
lack of oxygen is key in progression of cell injury in ischemia (reduced blood supply)
activated oxygen species (free radicals) cause destruction of cell membranes and cell structure
Cell Injury: Intracellular calcium and loss of calcium steady state
Normally intracellular cytosolic calcium concentrations are very low; ischemia and certain chemicals can
cause an increase in cytosolic Ca concentrations
sustained levels of Ca continue to increase with damage to plasma membrane
Ca causes intracellular damage by activating enzymes
Cellular events that occur with ischemia-hypoxic injury
-Decrease in oxygen reaching the cell
-decrease in ATP production within mitochondria
-failed NA+/K pump
-Na, Ca enter cell, K leaves
-organelle swelling
-protein synthesis stops
-ATP via oxidative phosphorylation declines, glycolysis increases
-glycogen stores depleated
-lactic acid produced
-decrease in intracellular Ph declines
-rupture of lysosomes
-autodigestion of the cell contents and membrane
Deleterious effects of free radicals on cells
-unstable compounds with an unpaired electron in outer ring
-anxious to "mate" with other substances
affinity for lipid substances
(there is a phospholipid bilayer membrane around cell)
-combine avidly with cell and organelle membranes
-lipid peroxidation - dissolution of the membrane
-"drills a hole"
examples o diseases linked to oxygen-derived free radicals
aging
atherosclerosis
AND ANSWERS UPDATED 2025/2026 LATEST VERSION
Etiology
Causative factors in a particular disease
Iatrogenic
produced by treatment
Epidemiology
risk factors and distribution in populations
Incidence
number of new cases
Hyperplasia
increase in number of cells in an organ/tissue as a response to injury that results from an increased rate
of cellular division
compensatory Physiologic hyperplasia
is an adaptive mechanism that enables certain organs to regenerate. Occurs in skin, intestines,
hepatocytes, bone marrow, and fibroblasts. Ex. Is when skin gets callus in response to mechanical
stimulus.
Hormonal physiologic hyperplasia
Hormonal occurs mainly from estrogen dependent organs such as uterus and breasts.Ex- after ovulation
estrogen stimulates endometrium to grow/thicken for fertilized ovum.
Pathologic hyperplasia
he abnormal proliferation of normal cells and can occur as a response to excessive hormonal stimulation
or the effects of growth factors on target cells. These cells have enlargement of the nucleus, clumping of
chromatin (package and protect DNA), and the presence of one or more large nucleoli. Ex. Benign
prostatic hyperplasia (BPH) and endometriosis-both the result of hormonal imbalance.
Metaplasia
reversible replacement of one mature cell type (epithelial or mesenchymal) by another, sometimes less
differentiated, cell type.
Cause of metaplasia
develops from reprogramming of stem cells. Found in association with tissue damage, repair, and
regeneration.
pathophysiology of metaplasia
Adaptive replacement cell may be more suitable to the changed conditions in the surrounding
environment. Ex. GERD damages squamous epithelium of the esophagus, cells are replaced by glandular
,epithelium which may tolerate the acid better. Not always beneficial. Ex. Smoking causes changes in
bronchi cells, which don't have cilia or secrete mucus, causing loss of protective mechanism.
What is the significance of metaplasia
Can be reversed if stimulus is removed. If continues, can cause malignant transformation.
Dysplasia
abnormal changes in the size, shape, and organization of mature cells. mostly found in epithelia
Significance of dysplasia
can be reversed if it does not involve the entire epithelium. When dysplastic changes penetrate the
basement membrane it is considered a preinvasive neoplasm (carcinoma in situ)
mechanisms of cell injury
ATP depletion, mitochondrial damage, accumulation of oxygen and oxygen-derived free radicals
membrane damage
protein folding defects
DNA damage defects
calcium level alterations
reperfusion injury
injury to tissue that occurs after blood flow is restored
restoration of needed oxygen is accompanied by oxidative stress with the generation of toxic oxygen
radicals which damage cellular membranes and mitochndria
What helps reperfusion injury?
antioxidants and anti-inflammatory drugs
examples of cell injury
ischemic and hypoxic injury
ischemia-reperfusion injury
oxidative stress or accumulation of oxygen-derived free Prevalence
number of existing cases both new and old
clinical manifestations
signs, symptoms, and diagnostic criteria
how are symptoms and signs different
symptoms are what the patient reports
signs are objective or measurable
outcomes
cure, remission, chronicity, or death
,primary prevention
Efforts to prevent an injury or illness from ever occurring.
secondary prevention
-focuses on early identification of individuals or communities experiencing illness, providing treatment,
and conducting activities that are geared to prevent worsening health status
-examples: communicable disease screening and case finding; early detection and treatment of
diabetes; exercise programs for older adult clients who are frail
Tertiary prevention
-aims to prevent the long-term consequences of a chronic illness or disability and to support optimal
functioning
-examples: prevention of pressure ulcers as complication of a spinal cord injury; promoting
independence for the client who has traumatic brain injury
Atrophy
Decrease or shrinkage in cellular size.Most common in skeletal muscle, heart, secondary sex organs, and
brain.
Physiologic atrophy
occurs with early development. Ex. Thymus gland gets physiologic atrophy during childhood.
pathologic atrophy
occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation,
and nervous stimulation
hypertrophy
Increase in the size of the cells that increase the size of the affected organ. Heart and kidneys
(responsive to enlargement) and skeletal muscle.
physiologic hypertrophy
occurs with increased demand, stimulation of hormones, and growth factors. Ex. Pregnancy causes
hormone induced hypertrophy of the uterus, in skeletal muscle occurs as a response to heavy workload.
pathologic hypertrophy
results from chronic hemodynamic overload. Ex. Hypertension or heart valve dysfunction. Hypertrophic
cells have increased accumulation of ER, plasma membrane, myofilaments, mitochondria (not cellular
fluid). Nucleus is also hypertrophic with increased DNA synthesis. Triggers for cardiac hypertrophy
include mechanical signals (stretch) and trophic signals (growth factors and vasoactive agents).
radicals induced injury
chemical injury
Cell injury: ATP depletion
, loss of mitochondrial ATP and decreased ATP synthesis
results include:
cellular swelling
decreased protein synthesis
decreased membrane transport
lipogenesis
all changes that contribute to loss of integrity of the plasma membrane
Cell injury: Oxygen and oxygen-derived free radicals
lack of oxygen is key in progression of cell injury in ischemia (reduced blood supply)
activated oxygen species (free radicals) cause destruction of cell membranes and cell structure
Cell Injury: Intracellular calcium and loss of calcium steady state
Normally intracellular cytosolic calcium concentrations are very low; ischemia and certain chemicals can
cause an increase in cytosolic Ca concentrations
sustained levels of Ca continue to increase with damage to plasma membrane
Ca causes intracellular damage by activating enzymes
Cellular events that occur with ischemia-hypoxic injury
-Decrease in oxygen reaching the cell
-decrease in ATP production within mitochondria
-failed NA+/K pump
-Na, Ca enter cell, K leaves
-organelle swelling
-protein synthesis stops
-ATP via oxidative phosphorylation declines, glycolysis increases
-glycogen stores depleated
-lactic acid produced
-decrease in intracellular Ph declines
-rupture of lysosomes
-autodigestion of the cell contents and membrane
Deleterious effects of free radicals on cells
-unstable compounds with an unpaired electron in outer ring
-anxious to "mate" with other substances
affinity for lipid substances
(there is a phospholipid bilayer membrane around cell)
-combine avidly with cell and organelle membranes
-lipid peroxidation - dissolution of the membrane
-"drills a hole"
examples o diseases linked to oxygen-derived free radicals
aging
atherosclerosis
