NR283 / NR-283: PATHOPHYSIOLOGY | CHAMBERLAIN COLLEGE OF NURSING |
COMPLETE REAL EXAM QUESTIONS AND CORRECT ANSWERS | NEWEST
2026/2027 VERSION (PASS GUARANTEE)
Q1. What is atrophy? ANSWER Decrease in cell size
Q2. What causes atrophy? ANSWER Decreased workload, ischemia,
malnutrition, loss of hormonal/neural stimulation
Q3. What is hypertrophy? ANSWER Increase in cell size
Q4. What causes hypertrophy? ANSWER Increased workload/demand (e.g.,
skeletal muscle from weightlifting, cardiac muscle from hypertension)
Q5. What is hyperplasia? ANSWER Increase in the number of cells
Q6. What is dysplasia? ANSWER Disordered, defective cell growth with loss of
uniformity and architectural orientation; considered pre-cancerous
Q7. What is metaplasia? ANSWER Replacement of one differentiated cell
type with another; often a response to chronic irritation
Q8. What is neoplasia? ANSWER Abnormal, uncontrolled cell growth (tumor
formation)
Q9. What is apoptosis? ANSWER Programmed cell death; a normal,
controlled process
Q10. What is necrosis? ANSWER Cell death caused by external factors such as
trauma, infection, or toxins; uncontrolled and pathological
Q11. What are the four types of necrosis? ANSWER Coagulative, liquefactive,
caseous, and fat necrosis
Q12. What is coagulative necrosis? ANSWER Tissue maintains shape;
commonly seen in ischemia of solid organs (heart, kidney, spleen)
Q13. What is liquefactive necrosis? ANSWER Tissue turns to liquid; seen in
brain infarcts and bacterial infections/abscesses
,Q14. What is caseous necrosis? ANSWER "Cheese-like" appearance;
characteristic of tuberculosis
Q15. What is fat necrosis? ANSWER Breakdown of fat tissue; seen in
pancreatitis and breast trauma
Q16. What is the difference between reversible and irreversible cell injury?
ANSWER Reversible: cellular swelling, fatty changes. Irreversible: membrane
damage, mitochondrial swelling, nuclear changes (pyknosis, karyorrhexis,
karyolysis)
Q17. What is hypoxia? ANSWER Insufficient oxygen supply to tissues
Q18. What is ischemia? ANSWER Insufficient blood flow to an organ or tissue
Q19. What is reperfusion injury? ANSWER Damage caused when blood
supply returns to tissue after a period of ischemia; free radicals are generated
Q20. What are free radicals? ANSWER Unstable molecules with unpaired
electrons that damage cells, lipids, proteins, and DNA
Q21. What is the role of antioxidants? ANSWER Neutralize free radicals (e.g.,
vitamin E, vitamin C, superoxide dismutase, catalase, glutathione peroxidase)
Q22. What is cellular swelling? ANSWER Earliest sign of cell injury; caused by
failure of the Na+/K+ pump due to lack of ATP
Q23. What is fatty change (steatosis)? ANSWER Accumulation of triglycerides
in cells; commonly seen in liver (alcohol, diabetes, obesity)
Q24. What is calcification? ANSWER Deposition of calcium salts in tissues;
dystrophic (damaged tissue) or metastatic (elevated serum calcium)
Q25. What is gangrene? ANSWER Massive tissue necrosis; dry gangrene
(ischemia), wet gangrene (infection), gas gangrene (Clostridium perfringens)
Inflammation & Healing (Questions 26–50)
Q26. What are the cardinal signs of acute inflammation? ANSWER Heat,
redness, swelling, pain, loss of function
Q27. What causes vasodilation in inflammation? ANSWER Histamine,
prostaglandins, and nitric oxide
, Q28. What causes increased vascular permeability in inflammation? ANSWER
Histamine and bradykinin cause endothelial cell contraction, creating gaps
Q29. What is chemotaxis? ANSWER Movement of leukocytes toward a
chemical gradient (chemoattractants)
Q30. What is opsonization? ANSWER Coating of pathogens with antibodies or
complement to enhance phagocytosis
Q31. What are the phases of wound healing? ANSWER Inflammatory phase,
proliferative phase, maturation (remodeling) phase
Q32. How long does the inflammatory phase of wound healing last? ANSWER
1–4 days
Q33. How long does the proliferative phase of wound healing last? ANSWER
4–24 days
Q34. How long does the maturation phase of wound healing last? ANSWER
21 days to 2 years
Q35. What is primary intention healing? ANSWER Wound edges are
approximated (sutured); minimal scarring
Q36. What is secondary intention healing? ANSWER Wound edges are not
approximated; granulation tissue fills the gap; more scarring
Q37. What is granulation tissue? ANSWER New connective tissue and tiny
blood vessels that form on wound surfaces
Q38. What is a keloid? ANSWER Excessive scar tissue that extends beyond
the original wound boundaries
Q39. What is a hypertrophic scar? ANSWER Excessive scar tissue that stays
within the original wound boundaries
Q40. What is dehiscence? ANSWER Separation of wound edges
Q41. What is evisceration? ANSWER Protrusion of organs through a wound
opening
Q42. What cells are involved in chronic inflammation? ANSWER
Macrophages, lymphocytes, plasma cells, fibroblasts
COMPLETE REAL EXAM QUESTIONS AND CORRECT ANSWERS | NEWEST
2026/2027 VERSION (PASS GUARANTEE)
Q1. What is atrophy? ANSWER Decrease in cell size
Q2. What causes atrophy? ANSWER Decreased workload, ischemia,
malnutrition, loss of hormonal/neural stimulation
Q3. What is hypertrophy? ANSWER Increase in cell size
Q4. What causes hypertrophy? ANSWER Increased workload/demand (e.g.,
skeletal muscle from weightlifting, cardiac muscle from hypertension)
Q5. What is hyperplasia? ANSWER Increase in the number of cells
Q6. What is dysplasia? ANSWER Disordered, defective cell growth with loss of
uniformity and architectural orientation; considered pre-cancerous
Q7. What is metaplasia? ANSWER Replacement of one differentiated cell
type with another; often a response to chronic irritation
Q8. What is neoplasia? ANSWER Abnormal, uncontrolled cell growth (tumor
formation)
Q9. What is apoptosis? ANSWER Programmed cell death; a normal,
controlled process
Q10. What is necrosis? ANSWER Cell death caused by external factors such as
trauma, infection, or toxins; uncontrolled and pathological
Q11. What are the four types of necrosis? ANSWER Coagulative, liquefactive,
caseous, and fat necrosis
Q12. What is coagulative necrosis? ANSWER Tissue maintains shape;
commonly seen in ischemia of solid organs (heart, kidney, spleen)
Q13. What is liquefactive necrosis? ANSWER Tissue turns to liquid; seen in
brain infarcts and bacterial infections/abscesses
,Q14. What is caseous necrosis? ANSWER "Cheese-like" appearance;
characteristic of tuberculosis
Q15. What is fat necrosis? ANSWER Breakdown of fat tissue; seen in
pancreatitis and breast trauma
Q16. What is the difference between reversible and irreversible cell injury?
ANSWER Reversible: cellular swelling, fatty changes. Irreversible: membrane
damage, mitochondrial swelling, nuclear changes (pyknosis, karyorrhexis,
karyolysis)
Q17. What is hypoxia? ANSWER Insufficient oxygen supply to tissues
Q18. What is ischemia? ANSWER Insufficient blood flow to an organ or tissue
Q19. What is reperfusion injury? ANSWER Damage caused when blood
supply returns to tissue after a period of ischemia; free radicals are generated
Q20. What are free radicals? ANSWER Unstable molecules with unpaired
electrons that damage cells, lipids, proteins, and DNA
Q21. What is the role of antioxidants? ANSWER Neutralize free radicals (e.g.,
vitamin E, vitamin C, superoxide dismutase, catalase, glutathione peroxidase)
Q22. What is cellular swelling? ANSWER Earliest sign of cell injury; caused by
failure of the Na+/K+ pump due to lack of ATP
Q23. What is fatty change (steatosis)? ANSWER Accumulation of triglycerides
in cells; commonly seen in liver (alcohol, diabetes, obesity)
Q24. What is calcification? ANSWER Deposition of calcium salts in tissues;
dystrophic (damaged tissue) or metastatic (elevated serum calcium)
Q25. What is gangrene? ANSWER Massive tissue necrosis; dry gangrene
(ischemia), wet gangrene (infection), gas gangrene (Clostridium perfringens)
Inflammation & Healing (Questions 26–50)
Q26. What are the cardinal signs of acute inflammation? ANSWER Heat,
redness, swelling, pain, loss of function
Q27. What causes vasodilation in inflammation? ANSWER Histamine,
prostaglandins, and nitric oxide
, Q28. What causes increased vascular permeability in inflammation? ANSWER
Histamine and bradykinin cause endothelial cell contraction, creating gaps
Q29. What is chemotaxis? ANSWER Movement of leukocytes toward a
chemical gradient (chemoattractants)
Q30. What is opsonization? ANSWER Coating of pathogens with antibodies or
complement to enhance phagocytosis
Q31. What are the phases of wound healing? ANSWER Inflammatory phase,
proliferative phase, maturation (remodeling) phase
Q32. How long does the inflammatory phase of wound healing last? ANSWER
1–4 days
Q33. How long does the proliferative phase of wound healing last? ANSWER
4–24 days
Q34. How long does the maturation phase of wound healing last? ANSWER
21 days to 2 years
Q35. What is primary intention healing? ANSWER Wound edges are
approximated (sutured); minimal scarring
Q36. What is secondary intention healing? ANSWER Wound edges are not
approximated; granulation tissue fills the gap; more scarring
Q37. What is granulation tissue? ANSWER New connective tissue and tiny
blood vessels that form on wound surfaces
Q38. What is a keloid? ANSWER Excessive scar tissue that extends beyond
the original wound boundaries
Q39. What is a hypertrophic scar? ANSWER Excessive scar tissue that stays
within the original wound boundaries
Q40. What is dehiscence? ANSWER Separation of wound edges
Q41. What is evisceration? ANSWER Protrusion of organs through a wound
opening
Q42. What cells are involved in chronic inflammation? ANSWER
Macrophages, lymphocytes, plasma cells, fibroblasts
