PATHOPHYSIOLOGY 370 NEW VERSION EXAM QUESTIONS AND
VERIFIED ANSWERS PRESENTED IN A CLEAR FORMAT TO HELP
YOU PASS WITHOUT STRESS
PATHO 370
1. What is hypertrophy? Increase in cell size leading to increased organ size,
often due to increased workload or hormonal stimulation.
2. What is hyperplasia? Increase in the number of cells in an organ or tissue,
usually in response to hormonal stimulation or compensatory mechanisms.
3. What is atrophy? Decrease in cell size and number, leading to reduced
tissue mass, often from disuse, denervation, or decreased blood supply.
4. What is metaplasia? Reversible change where one differentiated cell type is
replaced by another cell type, often as an adaptation to stress.
5. What is dysplasia? Abnormal cell growth and organization; considered a
precancerous condition that may progress to malignancy.
6. What is the difference between necrosis and apoptosis? Necrosis is
uncontrolled cell death with inflammation; apoptosis is programmed cell death
without inflammation.
7. What is coagulative necrosis? Cell death preserving tissue architecture,
commonly seen in ischemic injury to most organs except the brain.
8. What is liquefactive necrosis? Cell death resulting in liquid viscous mass,
typically seen in brain infarcts and bacterial infections.
9. What is caseous necrosis? Cheese-like tissue death characteristic of
tuberculosis infections.
10. What is fat necrosis? Death of adipose tissue, often seen in acute
pancreatitis or breast trauma.
11. What causes cellular swelling? Failure of ATP-dependent sodium-
potassium pump, leading to sodium and water accumulation inside cells.
12. What are free radicals? Unstable molecules with unpaired electrons that
can damage cellular components including DNA, proteins, and lipids.
,13. What is reperfusion injury? Paradoxical tissue damage that occurs when
blood flow returns to ischemic tissue, generating free radicals.
14. What is ischemia? Reduced blood supply to tissue, causing oxygen and
nutrient deprivation.
15. What is hypoxia? Decreased oxygen availability to tissues, which can
result from various causes including ischemia.
16. What are heat shock proteins? Protective proteins produced by cells in
response to stress that help refold damaged proteins.
17. What is the role of calcium in cell injury? Excessive intracellular calcium
activates enzymes that damage cell membranes, proteins, and DNA.
18. What is oxidative stress? Imbalance between free radical production and
antioxidant defenses, leading to cellular damage.
19. What is the difference between reversible and irreversible cell injury?
Reversible injury allows cell recovery if stress is removed; irreversible injury
leads to cell death.
20. What is chromatolysis? Dissolution of Nissl substance in neurons
following injury to their axons.
21. What is lipofuscin? Yellow-brown "wear and tear" pigment accumulating
in aging cells, representing residual bodies from lysosomal digestion.
22. What is hemosiderin? Iron-containing pigment derived from hemoglobin
breakdown, appearing in tissues with excessive iron or hemorrhage.
23. What is anthracosis? Black pigmentation of lungs from carbon particle
accumulation, common in urban dwellers and smokers.
24. What is pathologic calcification? Abnormal calcium salt deposition in
tissues, either dystrophic (damaged tissue) or metastatic (elevated calcium
levels).
25. What is hydropic change? Cellular swelling with water accumulation in
the cytoplasm, an early sign of reversible cell injury.
26. What causes cellular aging? Progressive accumulation of cellular and
molecular damage over time, involving telomere shortening, DNA damage, and
protein dysfunction.
27. What is autophagy? Cellular self-digestion process where cells break down
their own components for energy or removal of damaged organelles.
, 28. What is gangrene? Tissue necrosis with decomposition, classified as dry
(coagulative) or wet (liquefactive with bacterial infection).
29. What is pyknosis? Nuclear condensation and shrinkage seen in necrotic or
apoptotic cells.
30. What is karyolysis? Dissolution and fading of the nucleus due to DNase
activity during cell death.
Inflammation and Healing (Questions 31-60)
31. What is acute inflammation? Rapid-onset, short-duration response to
injury characterized by vascular changes and neutrophil infiltration.
32. What are the cardinal signs of inflammation? Redness (rubor), heat
(calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
33. What is chronic inflammation? Prolonged inflammation lasting weeks to
years, characterized by lymphocytes, macrophages, and tissue destruction.
34. What are the main cells in acute inflammation? Neutrophils are the
predominant cells, followed by monocytes/macrophages.
35. What are the main cells in chronic inflammation? Macrophages,
lymphocytes, and plasma cells.
36. What is exudate? Protein-rich fluid that leaks from blood vessels during
inflammation due to increased vascular permeability.
37. What is transudate? Low-protein fluid accumulation due to increased
hydrostatic pressure or decreased osmotic pressure without inflammation.
38. What is chemotaxis? Directed migration of cells toward chemical signals
(chemokines) at sites of injury or infection.
39. What is margination? Process where leukocytes move to the periphery of
blood vessels along the endothelium during inflammation.
40. What is diapedesis? Migration of leukocytes through intact blood vessel
walls into tissues.
41. What is opsonization? Coating of pathogens with antibodies or
complement proteins to enhance phagocytosis.
42. What is phagocytosis? Cellular process of engulfing and digesting
particles, pathogens, or debris.
VERIFIED ANSWERS PRESENTED IN A CLEAR FORMAT TO HELP
YOU PASS WITHOUT STRESS
PATHO 370
1. What is hypertrophy? Increase in cell size leading to increased organ size,
often due to increased workload or hormonal stimulation.
2. What is hyperplasia? Increase in the number of cells in an organ or tissue,
usually in response to hormonal stimulation or compensatory mechanisms.
3. What is atrophy? Decrease in cell size and number, leading to reduced
tissue mass, often from disuse, denervation, or decreased blood supply.
4. What is metaplasia? Reversible change where one differentiated cell type is
replaced by another cell type, often as an adaptation to stress.
5. What is dysplasia? Abnormal cell growth and organization; considered a
precancerous condition that may progress to malignancy.
6. What is the difference between necrosis and apoptosis? Necrosis is
uncontrolled cell death with inflammation; apoptosis is programmed cell death
without inflammation.
7. What is coagulative necrosis? Cell death preserving tissue architecture,
commonly seen in ischemic injury to most organs except the brain.
8. What is liquefactive necrosis? Cell death resulting in liquid viscous mass,
typically seen in brain infarcts and bacterial infections.
9. What is caseous necrosis? Cheese-like tissue death characteristic of
tuberculosis infections.
10. What is fat necrosis? Death of adipose tissue, often seen in acute
pancreatitis or breast trauma.
11. What causes cellular swelling? Failure of ATP-dependent sodium-
potassium pump, leading to sodium and water accumulation inside cells.
12. What are free radicals? Unstable molecules with unpaired electrons that
can damage cellular components including DNA, proteins, and lipids.
,13. What is reperfusion injury? Paradoxical tissue damage that occurs when
blood flow returns to ischemic tissue, generating free radicals.
14. What is ischemia? Reduced blood supply to tissue, causing oxygen and
nutrient deprivation.
15. What is hypoxia? Decreased oxygen availability to tissues, which can
result from various causes including ischemia.
16. What are heat shock proteins? Protective proteins produced by cells in
response to stress that help refold damaged proteins.
17. What is the role of calcium in cell injury? Excessive intracellular calcium
activates enzymes that damage cell membranes, proteins, and DNA.
18. What is oxidative stress? Imbalance between free radical production and
antioxidant defenses, leading to cellular damage.
19. What is the difference between reversible and irreversible cell injury?
Reversible injury allows cell recovery if stress is removed; irreversible injury
leads to cell death.
20. What is chromatolysis? Dissolution of Nissl substance in neurons
following injury to their axons.
21. What is lipofuscin? Yellow-brown "wear and tear" pigment accumulating
in aging cells, representing residual bodies from lysosomal digestion.
22. What is hemosiderin? Iron-containing pigment derived from hemoglobin
breakdown, appearing in tissues with excessive iron or hemorrhage.
23. What is anthracosis? Black pigmentation of lungs from carbon particle
accumulation, common in urban dwellers and smokers.
24. What is pathologic calcification? Abnormal calcium salt deposition in
tissues, either dystrophic (damaged tissue) or metastatic (elevated calcium
levels).
25. What is hydropic change? Cellular swelling with water accumulation in
the cytoplasm, an early sign of reversible cell injury.
26. What causes cellular aging? Progressive accumulation of cellular and
molecular damage over time, involving telomere shortening, DNA damage, and
protein dysfunction.
27. What is autophagy? Cellular self-digestion process where cells break down
their own components for energy or removal of damaged organelles.
, 28. What is gangrene? Tissue necrosis with decomposition, classified as dry
(coagulative) or wet (liquefactive with bacterial infection).
29. What is pyknosis? Nuclear condensation and shrinkage seen in necrotic or
apoptotic cells.
30. What is karyolysis? Dissolution and fading of the nucleus due to DNase
activity during cell death.
Inflammation and Healing (Questions 31-60)
31. What is acute inflammation? Rapid-onset, short-duration response to
injury characterized by vascular changes and neutrophil infiltration.
32. What are the cardinal signs of inflammation? Redness (rubor), heat
(calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
33. What is chronic inflammation? Prolonged inflammation lasting weeks to
years, characterized by lymphocytes, macrophages, and tissue destruction.
34. What are the main cells in acute inflammation? Neutrophils are the
predominant cells, followed by monocytes/macrophages.
35. What are the main cells in chronic inflammation? Macrophages,
lymphocytes, and plasma cells.
36. What is exudate? Protein-rich fluid that leaks from blood vessels during
inflammation due to increased vascular permeability.
37. What is transudate? Low-protein fluid accumulation due to increased
hydrostatic pressure or decreased osmotic pressure without inflammation.
38. What is chemotaxis? Directed migration of cells toward chemical signals
(chemokines) at sites of injury or infection.
39. What is margination? Process where leukocytes move to the periphery of
blood vessels along the endothelium during inflammation.
40. What is diapedesis? Migration of leukocytes through intact blood vessel
walls into tissues.
41. What is opsonization? Coating of pathogens with antibodies or
complement proteins to enhance phagocytosis.
42. What is phagocytosis? Cellular process of engulfing and digesting
particles, pathogens, or debris.
