UTMB 5355 PATHOPHYSIOLOGY EXAM COMPLETE
QUESTIONS AND 100% VERIFIED ANSWERS
1. What is hypertrophy? Hypertrophy is an increase in cell size that results in
an increase in organ size without an increase in cell number. It occurs in
response to increased workload or hormonal stimulation.
2. What is hyperplasia? Hyperplasia is an increase in the number of cells in an
organ or tissue, resulting in increased mass. It can be physiologic
(compensatory or hormonal) or pathologic.
3. What is atrophy? Atrophy is a decrease in cell size and number, resulting in
reduced tissue or organ size. Causes include disuse, denervation, ischemia,
malnutrition, and aging.
4. What is metaplasia? Metaplasia is a reversible change where one
differentiated cell type is replaced by another cell type. Example: bronchial
epithelium changing from columnar to squamous in smokers.
5. What is dysplasia? Dysplasia is disordered cell growth characterized by loss
of uniformity and architectural orientation. It is considered a pre-cancerous
change.
6. What are the major causes of cellular injury? Hypoxia, physical agents
(trauma, temperature), chemical agents, infectious agents, immunologic
reactions, genetic defects, and nutritional imbalances.
7. What is apoptosis? Apoptosis is programmed cell death characterized by
cell shrinkage, chromatin condensation, and formation of apoptotic bodies
without inflammation.
8. What is necrosis? Necrosis is unprogrammed cell death resulting from
severe cellular injury, characterized by cell swelling, membrane rupture, and
inflammatory response.
9. What is coagulative necrosis? A type of necrosis where tissue architecture
is preserved for several days. The tissue appears firm and pale. Common in
ischemic injury except in the brain.
,10. What is liquefactive necrosis? Necrosis characterized by digestion of dead
cells, resulting in liquid viscous mass. Typical of brain infarcts and bacterial
infections.
11. What is caseous necrosis? A type of necrosis with a cheese-like
appearance, characteristic of tuberculosis infection. Contains fragmented cells
and debris.
12. What is fat necrosis? Necrosis of adipose tissue typically seen in breast
trauma or acute pancreatitis, where lipases break down triglycerides releasing
fatty acids.
13. What is gangrenous necrosis? Not a specific pattern but refers to ischemic
coagulative necrosis of limbs. Dry gangrene has no bacterial infection; wet
gangrene includes bacterial infection.
14. What are free radicals? Unstable molecules with unpaired electrons that
cause cellular damage by oxidizing lipids, proteins, and DNA. Examples
include superoxide, hydroxyl radical, and hydrogen peroxide.
15. What is reperfusion injury? Cellular damage that occurs when blood flow
returns to tissue after ischemia. Paradoxically causes more damage through free
radical generation and calcium overload.
16. What is ischemia? Reduced blood flow to tissue resulting in decreased
oxygen delivery, leading to cellular injury and potentially necrosis if prolonged.
17. What is the role of calcium in cell injury? Excessive intracellular calcium
activates enzymes (proteases, phospholipases, endonucleases) that damage
cellular components, leading to cell death.
18. What are heat shock proteins? Protective proteins produced by cells in
response to stress that help refold damaged proteins and prevent aggregation.
19. What is oxidative stress? An imbalance between free radical production
and antioxidant defenses, leading to cellular damage.
20. What are the morphologic changes in reversible cell injury? Cellular
swelling, plasma membrane blebbing, loss of microvilli, mitochondrial
swelling, and dilation of the endoplasmic reticulum.
21. What are the morphologic changes in irreversible cell injury? Severe
mitochondrial damage with amorphous densities, membrane disruption,
lysosomal rupture, and nuclear changes (pyknosis, karyorrhexis, karyolysis).
, 22. What is pyknosis? Nuclear shrinkage and increased basophilia seen in
necrotic cells.
23. What is karyorrhexis? Nuclear fragmentation seen in necrotic cells.
24. What is karyolysis? Nuclear fading due to DNase activity seen in necrotic
cells.
25. What is autophagy? A cellular process where cells digest their own
components through lysosomal degradation, serving as a survival mechanism
during stress.
SECTION 2: INFLAMMATION AND HEALING (Questions 26-50)
26. What is acute inflammation? A rapid-onset, short-duration response to
injury characterized by vascular changes, edema, and neutrophil infiltration.
27. What are the five cardinal signs of inflammation? Rubor (redness), calor
(heat), tumor (swelling), dolor (pain), and functio laesa (loss of function).
28. What is chronic inflammation? Prolonged inflammation characterized by
lymphocytes, macrophages, and plasma cell infiltration, along with tissue
destruction and fibrosis.
29. What are the major chemical mediators of inflammation? Histamine,
prostaglandins, leukotrienes, cytokines (IL-1, TNF), complement proteins, and
bradykinin.
30. What is the role of histamine in inflammation? Histamine causes
vasodilation and increased vascular permeability, leading to edema. It's released
from mast cells and basophils.
31. What is the function of prostaglandins in inflammation? Prostaglandins
cause vasodilation, increased vascular permeability, and pain. They also induce
fever. NSAIDs work by inhibiting prostaglandin synthesis.
32. What are leukotrienes? Lipid mediators that cause vasoconstriction,
bronchoconstriction, and increased vascular permeability. Important in asthma
and allergic reactions.
33. What is the complement system? A cascade of plasma proteins that
enhances inflammation, promotes phagocytosis (opsonization), and causes cell
lysis through membrane attack complex.
34. What is chemotaxis? The directed migration of cells (especially
leukocytes) toward a chemical stimulus or gradient.
QUESTIONS AND 100% VERIFIED ANSWERS
1. What is hypertrophy? Hypertrophy is an increase in cell size that results in
an increase in organ size without an increase in cell number. It occurs in
response to increased workload or hormonal stimulation.
2. What is hyperplasia? Hyperplasia is an increase in the number of cells in an
organ or tissue, resulting in increased mass. It can be physiologic
(compensatory or hormonal) or pathologic.
3. What is atrophy? Atrophy is a decrease in cell size and number, resulting in
reduced tissue or organ size. Causes include disuse, denervation, ischemia,
malnutrition, and aging.
4. What is metaplasia? Metaplasia is a reversible change where one
differentiated cell type is replaced by another cell type. Example: bronchial
epithelium changing from columnar to squamous in smokers.
5. What is dysplasia? Dysplasia is disordered cell growth characterized by loss
of uniformity and architectural orientation. It is considered a pre-cancerous
change.
6. What are the major causes of cellular injury? Hypoxia, physical agents
(trauma, temperature), chemical agents, infectious agents, immunologic
reactions, genetic defects, and nutritional imbalances.
7. What is apoptosis? Apoptosis is programmed cell death characterized by
cell shrinkage, chromatin condensation, and formation of apoptotic bodies
without inflammation.
8. What is necrosis? Necrosis is unprogrammed cell death resulting from
severe cellular injury, characterized by cell swelling, membrane rupture, and
inflammatory response.
9. What is coagulative necrosis? A type of necrosis where tissue architecture
is preserved for several days. The tissue appears firm and pale. Common in
ischemic injury except in the brain.
,10. What is liquefactive necrosis? Necrosis characterized by digestion of dead
cells, resulting in liquid viscous mass. Typical of brain infarcts and bacterial
infections.
11. What is caseous necrosis? A type of necrosis with a cheese-like
appearance, characteristic of tuberculosis infection. Contains fragmented cells
and debris.
12. What is fat necrosis? Necrosis of adipose tissue typically seen in breast
trauma or acute pancreatitis, where lipases break down triglycerides releasing
fatty acids.
13. What is gangrenous necrosis? Not a specific pattern but refers to ischemic
coagulative necrosis of limbs. Dry gangrene has no bacterial infection; wet
gangrene includes bacterial infection.
14. What are free radicals? Unstable molecules with unpaired electrons that
cause cellular damage by oxidizing lipids, proteins, and DNA. Examples
include superoxide, hydroxyl radical, and hydrogen peroxide.
15. What is reperfusion injury? Cellular damage that occurs when blood flow
returns to tissue after ischemia. Paradoxically causes more damage through free
radical generation and calcium overload.
16. What is ischemia? Reduced blood flow to tissue resulting in decreased
oxygen delivery, leading to cellular injury and potentially necrosis if prolonged.
17. What is the role of calcium in cell injury? Excessive intracellular calcium
activates enzymes (proteases, phospholipases, endonucleases) that damage
cellular components, leading to cell death.
18. What are heat shock proteins? Protective proteins produced by cells in
response to stress that help refold damaged proteins and prevent aggregation.
19. What is oxidative stress? An imbalance between free radical production
and antioxidant defenses, leading to cellular damage.
20. What are the morphologic changes in reversible cell injury? Cellular
swelling, plasma membrane blebbing, loss of microvilli, mitochondrial
swelling, and dilation of the endoplasmic reticulum.
21. What are the morphologic changes in irreversible cell injury? Severe
mitochondrial damage with amorphous densities, membrane disruption,
lysosomal rupture, and nuclear changes (pyknosis, karyorrhexis, karyolysis).
, 22. What is pyknosis? Nuclear shrinkage and increased basophilia seen in
necrotic cells.
23. What is karyorrhexis? Nuclear fragmentation seen in necrotic cells.
24. What is karyolysis? Nuclear fading due to DNase activity seen in necrotic
cells.
25. What is autophagy? A cellular process where cells digest their own
components through lysosomal degradation, serving as a survival mechanism
during stress.
SECTION 2: INFLAMMATION AND HEALING (Questions 26-50)
26. What is acute inflammation? A rapid-onset, short-duration response to
injury characterized by vascular changes, edema, and neutrophil infiltration.
27. What are the five cardinal signs of inflammation? Rubor (redness), calor
(heat), tumor (swelling), dolor (pain), and functio laesa (loss of function).
28. What is chronic inflammation? Prolonged inflammation characterized by
lymphocytes, macrophages, and plasma cell infiltration, along with tissue
destruction and fibrosis.
29. What are the major chemical mediators of inflammation? Histamine,
prostaglandins, leukotrienes, cytokines (IL-1, TNF), complement proteins, and
bradykinin.
30. What is the role of histamine in inflammation? Histamine causes
vasodilation and increased vascular permeability, leading to edema. It's released
from mast cells and basophils.
31. What is the function of prostaglandins in inflammation? Prostaglandins
cause vasodilation, increased vascular permeability, and pain. They also induce
fever. NSAIDs work by inhibiting prostaglandin synthesis.
32. What are leukotrienes? Lipid mediators that cause vasoconstriction,
bronchoconstriction, and increased vascular permeability. Important in asthma
and allergic reactions.
33. What is the complement system? A cascade of plasma proteins that
enhances inflammation, promotes phagocytosis (opsonization), and causes cell
lysis through membrane attack complex.
34. What is chemotaxis? The directed migration of cells (especially
leukocytes) toward a chemical stimulus or gradient.
