PATH 3610 FINAL EXAM QUESTIONS
AND ANSWERS ALL CORRECT
What's neoplasia? - Answer- An abnormality in cellular differentiation, maturation and
control of growth
Resulting mass of abnormal tissue termed neoplasm or tumor
For normal structure of a tissue to be maintained the rate of cell proliferation must
balance w/ the rate of what? - Answer- The rate of differentiation (leading to cell death)
What's hyperplasia? - Answer- Increased size of tissue consisting of labile and stable
cells, results when the cells of a tissue are stimulated to undergo mitosis, increased risk
of becoming cancerous
What's hypertrophy? - Answer- -The only method of adaptation in permanent cells for
an increased functional demand unable to be met by cell multiplication
-Increase in amount of cytoplasm and the numbers of cytoplasmic organelles
T/F
Hyperplasia and hypertrophy are irreversible - Answer- False
Both are reversible if the demand is removed
What's atrophy? - Answer- Reduction in the structural components of the cell, due to
decreased synthesis, increased catabolism, or both (appears "wasted" away)
Atrophy is considered the opposite of what? - Answer- Hyperplasia and hypertrophy
What is an example of disuse atrophy? - Answer- Osteoporosis
What causes disuse atrophy? - Answer- A prolonged lack of activity or use of muscles
-When a muscle isn't used, there is a rapid decrease in the size of the muscle cells
(fibers)
-Can be reversed by activity
What's denervation atrophy? What causes it? - Answer- Result of lack of stimulation of
muscle fibres by lower motor neurons
-This type of atrophy is seen in the limbs of people who have spinal cord injuries
-Physical therapy and electrical stimulation of muscles are used to help prevent loss of
muscle fibres
Atrophy can also occur due to: - Answer- -Lack of tropic hormones
,-Severe malnutrition
-Ischemia (due to pressure on blood vessels)
What's metaplasia? - Answer- A reversible change, in which the normal phenotype of
mature cells is replaced by another type of mature cell, which is not normal for that site
Why does metaplasia occur? - Answer- -New type of cell might survive under certain
stresses the previous type couldn't
-In response to chronic irritation
-Is reversible if the cause of metaplastic change is removed
-Can be cancerous if metaplastic transformation persists
What's dysplasia? - Answer- -Abnormal development of tissue
-Abnormality seen in differentiation and maturation
-Characterized by nuclear abnormalities, loss of uniformity, & disruption of normal
architectural orientation
-Premalignant lesion & associated w/ increased risk of cancer
How does dysplasia differ from neoplasia? - Answer- Dysplastic lesions are not invasive
(cancer is invasive), and may (spontaneously) revert to normal (unlike cancer).
However, there is a very fine line between dysplasia and cancer
For this reason, the term carcinoma in situ is sometimes used for dysplastic lesions;
they look like cancer but are not yet showing unequivocal evidence of invasive
behaviour
This is central to carcinogenesis - Answer- Non-lethal DNA damage
What are some possible causes of degeneration and necrosis? - Answer- Depletion of
ATP, Impaired cell membrane function, Intracellular accumulation, Genetic
Abnormalities
What is hypoxia/ischemia? - Answer- Insufficient oxygen in the cells & reduced blood
supply
What would cause a depletion of ATP? - Answer- Hypoxia/ischemia, hypoglycemia,
enzyme inhibition, uncoupling of oxidative phosphorylation
What is hypoglycemia? - Answer- Low blood glucose
What are the effects of defective energy production? - Answer- Intracellular
Accumulation of Water: water/sodium channels not working properly, w/o that balance
water starts to fill the cell
Swelling of Cytoplasmic Organelles: the above causes organelles, like the mitochondria,
to swell, causing the uncoupling of oxidative phosphorylation
Switch to Anaerobic Glycolysis: leads to increase of lactic acid, pH decreases, further
disruption of organelle membranes
,What causes impaired membrane function? - Answer- Free radicals (damaging the
membrane), Activation of complement system, & Direct Lysis of the membrane (direct
insertion, lysis by immune response)
What are the effects of impaired membrane function? - Answer- Loss of Structural
Integrity: if bad enough, cell will rupture and die
Loss of Function: swelling -> loss of function
Deposition of Lipofuscin: damaged bits of cell membrane is deposited in the cytoplasm
result from free radical peroxidation, considered normal in aging
What could cause triglyceride accumulation in the liver? - Answer- Increased
mobilization of adipose tissue, so increased amounts of fatty acids reach the liver.
Overactivity of certain enzyme systems increase the conversion of fatty acids into
triglycerides. The oxidation of triglycerides to other forms is decreased. Apoprotein
synthesis is decreased.
How does iron accumulate in the body? - Answer- Hemoglobin (Hb) is broken down at
sites of hemorrhage (local hemosiderosis). Usually deposited in macrophages or
connective tissue as hemosiderin. Not generally harmful, unless too extreme
How is bilirubin formed and excreted? - Answer- -Old/damaged RBCs broken down &
recycled by macrophages
-Porphyrin ring (from Hb) is catabolized to bilirubin
-Bilirubin binds to albumin (unconjugated/lipid soluble) and travels to the liver
-In the liver, it's conjugated to glucuronide (now water soluble) and excreted by liver
cells into the bile duct
-Removed via the feces w/ the bile
How does jaundice come about? - Answer- Jaundice is the accumulation of bilirubin
-Hemolysis (destruction of RBCs): if RBC break down increases too much, the
production of bilirubin also increases, liver cannot conjugate it fast enough,
Unconjugated serum bilirubin increases
-Hepatocellular dysfunction: if liver is injured, uptake, conjugation and excretion of
bilirubin will be affected, conjugated and unconjugated levels will both increase
-Obstruction to bile flow (cholestasis): an obstruction to the bile duct will affect excretion,
Conjugated bilirubin will reflux into the plasma, causing jaundice
What are the three types of morphological evidence of necrosis? - Answer- -Gross
Evidence: microscopic changes that can be seen by the unaided eye
-Cytoplasmic Evidence: cytoplasm becomes deeply stained and more homogenous,
may have a bubbly or vacuolated appearance, abnormal deposits of calcium
-Nuclear Evidence: nuclear chromatin clumps, and the nucleus becomes smaller and
more densely staining
What is coagulation necrosis? - Answer- Cell death due to ischemia
, What is liquefaction necrosis? - Answer- Dead cells liquefy (pus) because of release of
cell enzymes from inflammatory cells
What is gangrenous necrosis/ gangrene? - Answer- Condition of a limb (usually a leg)
that has lost its blood supply & has undergone coagulation necrosis involving multiple
tissue layers
What is caseous necrosis? - Answer- A form of coagulative necrosis in which a thick,
yellowish, cheesy substance forms
What is fat necrosis? - Answer- A specialized form of liquefaction necrosis caused by
the action of lipolytic enzymes
What are some clinical problems associated with tissue necrosis? - Answer- -Altered
function: can result if sufficient numbers of cells become necrotic
-Loss of Tissue: severe cell and tissue death can result in loss of the affected tissue or
organ
-Secondary Infection: necrotic tissue often contains little-to-no inflammation; necrotic
tissue can become an ideal growth medium for infection (usually if moist), as they are
beyond the reach of inflammatory cells and the immune system
-Systemic Effects: fever and increased white blood cell counts
-Local Effects: depends on what tissue is affected and extent of necrosis
-Release of Enzymes from a Necrotic Cell
What are some differences between apoptosis and necrosis? - Answer- -Necrosis is
passive and disorderly, Apoptosis is active, organized and orderly, requires energy and
follow a "plan"
-Necrosis is fragmented and intracellular proteins leak out, while Apoptosis keeps its
cellular outlines intact
-Necrosis produces cell debris and releases inflammatory mediators, while Apoptosis
produces neatly packaged cell fragments
Describe the mitochondrial pathway of apoptosis. - Answer- -BH3-only proteins (part of
the Bcl-2 family which controls mitochondria permeability), sense a lack of survival
signals or DNA or protein damage
-These BH3-only proteins activate effector molecules that increase mitochondrial
permeability
-The mitochondria become leaky and various substances, such as cytochrome c, enter
the cytosol and activate caspases
-Activated caspases induce the changes that culminate in cell death and fragmentation
Describe the death receptor pathway of apoptosis - Answer- -Signals from plasma
membrane receptors (Fas & TNF receptor) lead to the assembly of adaptor proteins into
a "death-inducing signaling complex"
-Which activates caspases
AND ANSWERS ALL CORRECT
What's neoplasia? - Answer- An abnormality in cellular differentiation, maturation and
control of growth
Resulting mass of abnormal tissue termed neoplasm or tumor
For normal structure of a tissue to be maintained the rate of cell proliferation must
balance w/ the rate of what? - Answer- The rate of differentiation (leading to cell death)
What's hyperplasia? - Answer- Increased size of tissue consisting of labile and stable
cells, results when the cells of a tissue are stimulated to undergo mitosis, increased risk
of becoming cancerous
What's hypertrophy? - Answer- -The only method of adaptation in permanent cells for
an increased functional demand unable to be met by cell multiplication
-Increase in amount of cytoplasm and the numbers of cytoplasmic organelles
T/F
Hyperplasia and hypertrophy are irreversible - Answer- False
Both are reversible if the demand is removed
What's atrophy? - Answer- Reduction in the structural components of the cell, due to
decreased synthesis, increased catabolism, or both (appears "wasted" away)
Atrophy is considered the opposite of what? - Answer- Hyperplasia and hypertrophy
What is an example of disuse atrophy? - Answer- Osteoporosis
What causes disuse atrophy? - Answer- A prolonged lack of activity or use of muscles
-When a muscle isn't used, there is a rapid decrease in the size of the muscle cells
(fibers)
-Can be reversed by activity
What's denervation atrophy? What causes it? - Answer- Result of lack of stimulation of
muscle fibres by lower motor neurons
-This type of atrophy is seen in the limbs of people who have spinal cord injuries
-Physical therapy and electrical stimulation of muscles are used to help prevent loss of
muscle fibres
Atrophy can also occur due to: - Answer- -Lack of tropic hormones
,-Severe malnutrition
-Ischemia (due to pressure on blood vessels)
What's metaplasia? - Answer- A reversible change, in which the normal phenotype of
mature cells is replaced by another type of mature cell, which is not normal for that site
Why does metaplasia occur? - Answer- -New type of cell might survive under certain
stresses the previous type couldn't
-In response to chronic irritation
-Is reversible if the cause of metaplastic change is removed
-Can be cancerous if metaplastic transformation persists
What's dysplasia? - Answer- -Abnormal development of tissue
-Abnormality seen in differentiation and maturation
-Characterized by nuclear abnormalities, loss of uniformity, & disruption of normal
architectural orientation
-Premalignant lesion & associated w/ increased risk of cancer
How does dysplasia differ from neoplasia? - Answer- Dysplastic lesions are not invasive
(cancer is invasive), and may (spontaneously) revert to normal (unlike cancer).
However, there is a very fine line between dysplasia and cancer
For this reason, the term carcinoma in situ is sometimes used for dysplastic lesions;
they look like cancer but are not yet showing unequivocal evidence of invasive
behaviour
This is central to carcinogenesis - Answer- Non-lethal DNA damage
What are some possible causes of degeneration and necrosis? - Answer- Depletion of
ATP, Impaired cell membrane function, Intracellular accumulation, Genetic
Abnormalities
What is hypoxia/ischemia? - Answer- Insufficient oxygen in the cells & reduced blood
supply
What would cause a depletion of ATP? - Answer- Hypoxia/ischemia, hypoglycemia,
enzyme inhibition, uncoupling of oxidative phosphorylation
What is hypoglycemia? - Answer- Low blood glucose
What are the effects of defective energy production? - Answer- Intracellular
Accumulation of Water: water/sodium channels not working properly, w/o that balance
water starts to fill the cell
Swelling of Cytoplasmic Organelles: the above causes organelles, like the mitochondria,
to swell, causing the uncoupling of oxidative phosphorylation
Switch to Anaerobic Glycolysis: leads to increase of lactic acid, pH decreases, further
disruption of organelle membranes
,What causes impaired membrane function? - Answer- Free radicals (damaging the
membrane), Activation of complement system, & Direct Lysis of the membrane (direct
insertion, lysis by immune response)
What are the effects of impaired membrane function? - Answer- Loss of Structural
Integrity: if bad enough, cell will rupture and die
Loss of Function: swelling -> loss of function
Deposition of Lipofuscin: damaged bits of cell membrane is deposited in the cytoplasm
result from free radical peroxidation, considered normal in aging
What could cause triglyceride accumulation in the liver? - Answer- Increased
mobilization of adipose tissue, so increased amounts of fatty acids reach the liver.
Overactivity of certain enzyme systems increase the conversion of fatty acids into
triglycerides. The oxidation of triglycerides to other forms is decreased. Apoprotein
synthesis is decreased.
How does iron accumulate in the body? - Answer- Hemoglobin (Hb) is broken down at
sites of hemorrhage (local hemosiderosis). Usually deposited in macrophages or
connective tissue as hemosiderin. Not generally harmful, unless too extreme
How is bilirubin formed and excreted? - Answer- -Old/damaged RBCs broken down &
recycled by macrophages
-Porphyrin ring (from Hb) is catabolized to bilirubin
-Bilirubin binds to albumin (unconjugated/lipid soluble) and travels to the liver
-In the liver, it's conjugated to glucuronide (now water soluble) and excreted by liver
cells into the bile duct
-Removed via the feces w/ the bile
How does jaundice come about? - Answer- Jaundice is the accumulation of bilirubin
-Hemolysis (destruction of RBCs): if RBC break down increases too much, the
production of bilirubin also increases, liver cannot conjugate it fast enough,
Unconjugated serum bilirubin increases
-Hepatocellular dysfunction: if liver is injured, uptake, conjugation and excretion of
bilirubin will be affected, conjugated and unconjugated levels will both increase
-Obstruction to bile flow (cholestasis): an obstruction to the bile duct will affect excretion,
Conjugated bilirubin will reflux into the plasma, causing jaundice
What are the three types of morphological evidence of necrosis? - Answer- -Gross
Evidence: microscopic changes that can be seen by the unaided eye
-Cytoplasmic Evidence: cytoplasm becomes deeply stained and more homogenous,
may have a bubbly or vacuolated appearance, abnormal deposits of calcium
-Nuclear Evidence: nuclear chromatin clumps, and the nucleus becomes smaller and
more densely staining
What is coagulation necrosis? - Answer- Cell death due to ischemia
, What is liquefaction necrosis? - Answer- Dead cells liquefy (pus) because of release of
cell enzymes from inflammatory cells
What is gangrenous necrosis/ gangrene? - Answer- Condition of a limb (usually a leg)
that has lost its blood supply & has undergone coagulation necrosis involving multiple
tissue layers
What is caseous necrosis? - Answer- A form of coagulative necrosis in which a thick,
yellowish, cheesy substance forms
What is fat necrosis? - Answer- A specialized form of liquefaction necrosis caused by
the action of lipolytic enzymes
What are some clinical problems associated with tissue necrosis? - Answer- -Altered
function: can result if sufficient numbers of cells become necrotic
-Loss of Tissue: severe cell and tissue death can result in loss of the affected tissue or
organ
-Secondary Infection: necrotic tissue often contains little-to-no inflammation; necrotic
tissue can become an ideal growth medium for infection (usually if moist), as they are
beyond the reach of inflammatory cells and the immune system
-Systemic Effects: fever and increased white blood cell counts
-Local Effects: depends on what tissue is affected and extent of necrosis
-Release of Enzymes from a Necrotic Cell
What are some differences between apoptosis and necrosis? - Answer- -Necrosis is
passive and disorderly, Apoptosis is active, organized and orderly, requires energy and
follow a "plan"
-Necrosis is fragmented and intracellular proteins leak out, while Apoptosis keeps its
cellular outlines intact
-Necrosis produces cell debris and releases inflammatory mediators, while Apoptosis
produces neatly packaged cell fragments
Describe the mitochondrial pathway of apoptosis. - Answer- -BH3-only proteins (part of
the Bcl-2 family which controls mitochondria permeability), sense a lack of survival
signals or DNA or protein damage
-These BH3-only proteins activate effector molecules that increase mitochondrial
permeability
-The mitochondria become leaky and various substances, such as cytochrome c, enter
the cytosol and activate caspases
-Activated caspases induce the changes that culminate in cell death and fragmentation
Describe the death receptor pathway of apoptosis - Answer- -Signals from plasma
membrane receptors (Fas & TNF receptor) lead to the assembly of adaptor proteins into
a "death-inducing signaling complex"
-Which activates caspases
