Practice questions for Pathology

Cellular adaptations:
1. What is Pathology?
a) Study of plants
b) Study of diseases and their causes
8
c) Study of geological structures
d) Study of celestial bodies

2. What do pathologists do?

a) Design buildings
b) Investigate the causes of diseases
G
c) Write prescriptions
d) Perform surgeries

3. What is the primary focus of Pathology?

O
a) Functional changes in cells
b) Economic changes in society
c) Political changes in government
d) Atmospheric changes in weather

4. What is hypertrophy?
a) Decrease in cell size
O
b) Increase in cell size
c) Increase in cell number
d) Decrease in cell number

5. Which of the following is an example of physiologic hypertrophy?

a) Left ventricular hypertrophy in hypertension
⑧
b) Muscle hypertrophy in bodybuilders
c) Benign prostatic hyperplasia
d) Atrophy of the uterus in pregnancy

6. What are the mechanisms involved in hypertrophy of the heart?

a) Endocrine stimulation
b) Increased protein degradation
c) Vasoactive agents and growth factors
O
d) Apoptosis

7. How is hypertension classified?

a) Based on age
b) Primary and Secondary
O
c) Based on gender
d) Systolic and Diastolic

8. What is the consequence of hypertension on the heart?

a) Hypertrophy of the left ventricle
O
b) Atrophy of the atria
c) Hyperplasia of the coronary arteries
d) Metaplasia of the myocardium

9. What is hyperplasia?
a) Increase in cell size
b) Increase in cell number
G
c) Decrease in cell size
d) Decrease in cell number

10. What is the main risk factor for endometrial hyperplasia?

a) Aging
O
b) Prolonged estrogenic stimulation
c) Pregnancy
d) Hormonal imbalance

11. What is Barrett’s esophagus?

a) Physiologic hyperplasia of the esophagus
b) Pathologic hypertrophy of the esophagus
c) Squamous metaplasia of the esophagus
d) Columnar metaplasia of the esophagus
⑧

12. What is the relationship between GERD and Barrett’s esophagus?

a) GERD causes atrophy of the esophagus
b) GERD is unrelated to Barrett’s esophagus
c) GERD can lead to columnar metaplasia in the esophagus
O
d) GERD is a cure for Barrett’s esophagus

13. What is the main type of metaplasia seen in response to H. pylori infection?
a) Squamous metaplasia
b) Columnar metaplasia
c) Intestinal metaplasia
O
d) Connective tissue metaplasia

14. Which infection is associated with progressive mucosal squamous metaplasia and
dysplasia in the bladder?
a) Schistosoma haematobium
O
b) Helicobacter pylori
c) Myositis ossificans
d) Tuberculosis

15. What is the mechanism of metaplasia?

a) Reprogramming of stem cells
O
b) Increased protein synthesis
c) Apoptosis
d) Vasoconstriction

16. What is atrophy?

a) Increase in size of an organ
b) Decrease in size of an organ
c) Increase in cell number
O
d) Decrease in cell size

17. Which of the following is an example of physiologic atrophy?

a) Immobilization-induced muscle atrophy
b) Hypopituitarism-induced atrophy
c) Pressure-induced atrophy in cystic fibrosis
d) Notochord atrophy during embryogenesis
O
18. What are the mechanisms of atrophy?
a) Increased protein synthesis
b) Decreased protein degradation
c) Apoptosis
d) Decreased protein synthesis and increased protein degradation
O

19. What is the main mechanism of protein degradation in atrophy?

O
a) Ubiquitin-proteasome pathway
b) PI3K/AKT pathway
c) G-protein-coupled receptor pathway
d) TGF-B pathway

20. What is the significance of GATA4 in hypertrophy?

O
a) Increases synthesis of contractile proteins
b) Decreases synthesis of contractile proteins
c) Activates the ubiquitin-proteasome pathway
d) Induces apoptosis

21. What is the role of growth factors in hypertrophy?

a) Decrease protein synthesis
b) Increase protein degradation
c) Increase cell size
O
d) Inhibit cell growth
22. Which type of hyperplasia is associated with the risk of endometrial carcinoma?
a) Physiologic hyperplasia
b) Hormonal hyperplasia
c) Compensatory hyperplasia
O
d) Pathologic hyperplasia

23. What is the main cause of primary hypertension?

a) Reduced sodium excretion
O
b) Increased sodium intake
c) Hypersecretion of aldosterone
d) Overactivity of the sympathetic nervous system

24. What is the consequence of hypertension on arterioles?

a) Thinning of vessel walls
b) Decreased peripheral resistance
c) Thickening of vessel walls
O
d) Atrophy of arterioles

25. What is the consequence of increased afterload in hypertension?

⑧
a) Hypertrophy of the left ventricle
b) Atrophy of the left ventricle
c) Hyperplasia of the left ventricle
d) Metaplasia of the left ventricle

26. What is the primary type of metaplasia associated with chronic smoking?
a) Intestinal metaplasia
b) Columnar to squamous metaplasia
8
c) Squamous to columnar metaplasia
d) Connective tissue metaplasia

27. What is the precursor lesion for invasive squamous cell carcinoma in the lungs?
a) Barrett’s esophagus
O
b) Squamous metaplasia
c) Tuberculosis
d) Pneumonia

28. How is Barrett’s esophagus diagnosed endoscopically?

a) Pale, glossy appearance of the mucosa
b) Salmon-colored and coarse appearance of the columnar mucosa
O
c) Presence of goblet cells
d) Increased acid production
29. What is the increased risk associated with both GERD and Barrett’s esophagus?
a) Liver cirrhosis
b) Adenocarcinoma of the distal esophagus
O
c) Lung cancer
d) Breast cancer

30. What is the definition of GERD?

a) A condition causing troublesome symptoms due to stomach reflux
O
b) A condition with no symptoms related to stomach reflux
c) A condition causing heartburn episodes
d) A condition cured by Barrett’s esophagus

31. What is the main type of metaplasia seen in response to H. pylori infection in the
stomach?
a) Columnar to squamous metaplasia
b) Squamous to columnar metaplasia
O
c) Intestinal metaplasia
d) Connective tissue metaplasia

32. What is the consequence of H. pylori infection progressing to the gastric body and
fundus?
a) Increased acid production
g
b) Reduced parietal cell mass
c) Increased risk of gastric adenocarcinoma
d) Decreased risk of gastric ulcer

33. What is the association between Schistosoma haematobium and metaplasia?

a) Adenocarcinoma of the lung
b) Squamous metaplasia in the bladder
O
c) Intestinal metaplasia in the stomach
d) Connective tissue metaplasia in the muscles

34. What is myositis ossificans?

a) Formation of bone in muscles
O
b) Formation of adipose tissue in muscles
c) Formation of cartilage in muscles
d) Formation of connective tissue in muscles

35. What is the timeframe for myositis ossificans following intramuscular hemorrhage?
a) 1-2 days
b) 2-4 weeks
c) 4-7 weeks
O
d) 8-12 weeks
36. What is the mechanism of metaplasia?
a) Reprogramming of stem cells
O
b) Decreased protein degradation
c) Increased protein synthesis
d) Inhibition of cytokines

37. What is the primary mechanism of atrophy?

a) Increased protein synthesis
b) Increased apoptosis
c) Increased protein degradation
O
d) Decreased protein degradation

38. Which of the following is not a type of metaplasia mentioned in the provided
information?
a) Columnar to squamous
b) Squamous to columnar
c) Cuboidal to squamous
O
d) Intestinal to squamous

Answers:
1. b
2. b
3. a
4. b
5. b
6. c
7. b
8. a
9. b
10. b
11. d
12. c
13. c
14. a
15. a
16. b
17. d
18. d
19. a
20. a
21. c
22. d
23. a
24. c
25. a
26. b
27. b
28. b
29. b
30. a
31. c
32. c
33. b
34. a
35. c
36. a
37. c
38. c

CELL INJURY NECROSIS

1. What is the result of irreversible cell injury in most cases?

a) Apoptosis
b) Necrosis
c) Inflammation
d) Liquefactive necrosis

2. What are the two important points that determine irreversible injury?
a) Increased eosinophilia and nuclear changes
b) Mitochondrial dysfunction and altered membrane function
c) Denaturation of proteins and enzymes
d) Phagocytosis and inflammation

3. Which type of necrosis is caused by ischemia to tissues and is the most commonly seen
type?
a) Coagulative necrosis
b) Liquefactive necrosis
c) Caseous necrosis
d) Gangrenous necrosis

4. What is the primary mechanism of coagulative necrosis?

a) Release of proteases
b) Denaturation of proteins and enzymes
c) Accumulation of iron sulphide
d) Rapid myocyte dysfunction

5. Which clinical condition is characterized by paroxysmal chest discomfort caused by

transient myocardial ischemia?
a) Myocardial infarction
b) Stable angina
c) Unstable angina
d) Prinzmetal angina

6. What is the main objective in the treatment of myocardial infarction?

a) Antibiotic therapy
b) Revascularization
c) Analgesic administration
d) Immunosuppressive drugs

7. Which enzyme is used for monitoring myocardial infarction and rises within 6 to 8 hours?
a) Amylase
b) Lipase
c) Troponin
d) CK-MB

8. What is the first sign of myocardial myocyte death (necrosis)?

a) Increased eosinophilia
b) Karyolysis
c) Disruption of sarcolemmal membrane
d) Amorphous densities in mitochondria

9. Which type of necrosis is caused by focal bacterial or fungal infection and is seen in
abscess formation?
a) Coagulative necrosis
b) Liquefactive necrosis
c) Gangrenous necrosis
d) Caseous necrosis

10. What is the unique form of coagulative necrosis seen in tuberculosis?

a) Fat necrosis
b) Caseous necrosis
c) Liquefactive necrosis
d) Fibrinoid necrosis

11. What is the most common cause of fat necrosis?

a) Myocardial infarction
b) Trauma
c) Alcohol
d) Inflammation

12. What is the mechanism of fat destruction in fat necrosis?

a) Denaturation of proteins
b) Release of proteases
c) Activation of lipases
d) Accumulation of iron sulphide

13. Which type of necrosis is associated with immune vasculitis and malignant hypertension?
a) Coagulative necrosis
b) Fibrinoid necrosis
c) Gangrenous necrosis
d) Liquefactive necrosis

14. What is the phenomenon called when necrotic cells become calcified due to the
deposition of calcium salts?
a) Dystrophic calcification
b) Metastatic calcification
c) Caseation
d) Saponification

15. Which type of angina is triggered by smoking, cocaine, and amphetamines and is
unrelated to physical activity?
a) Stable angina
b) Prinzmetal angina
c) Unstable angina
d) Exertional angina

16. Which enzyme is specifically used for diagnosing myocardial infarction and is highly
sensitive?
a) Lipase
b) Amylase
c) Troponin
d) CK-MB

17. What is the primary mechanism of gangrenous necrosis in diabetic foot?

a) Coagulative necrosis
b) Liquefactive necrosis
c) Caseous necrosis
d) Fibrinoid necrosis

18. What is the clinical presentation of myocardial infarction classically characterized by?
a) Short-lived chest discomfort
b) Prolonged chest pain
c) Weak pulse
d) Rapid breathing

19. Which conduits are most commonly used in Coronary Artery Bypass Graft (CABG)?
a) Left internal thoracic artery and greater saphenous vein
b) Radial artery and femoral artery
c) Pulmonary artery and aorta
d) Brachial artery and popliteal artery

20. What is the primary cause of liquefactive necrosis in the brain?

a) Ischemia
b) Trauma
c) Bacterial infection
d) Fungal infection

21. Which of the following is a morphologic change associated with necrosis?

a) Increased cell division
b) Denaturation of proteins
c) Enhanced mitochondrial function
d) Decreased inflammatory response

22. In coagulative necrosis, what is the mechanism behind the preservation of cell outlines,
producing a "tombstone" appearance?
a) Activation of lipases
b) Denaturation of proteins and enzymes
c) Blockage of complete proteolysis
d) Leakage of lysosomal enzymes

23. What is the primary clinical correlation of stable angina?

a) Prolonged chest pain
b) Myocardial infarction
c) Transient myocardial ischemia
d) Vasospastic angina

24. In myocardial infarction, which enzyme is released due to disruption of the sarcolemmal
membrane, allowing leakage of proteins into circulation?
a) Amylase
b) Lipase
c) Troponin
d) CK-MB

25. What is the significance of a left internal thoracic artery graft in Coronary Artery Bypass
Graft (CABG)?
a) Associated with higher long-term patency rates
b) Reduces inflammatory response
c) Prevents vasospasm
d) Minimizes denaturation of proteins

26. Which type of necrosis is associated with slowly developing occlusion of blood vessels
and is commonly seen in diabetic foot?
a) Coagulative necrosis
b) Liquefactive necrosis
c) Gangrenous necrosis
d) Caseous necrosis

27. What is the primary mechanism of traumatic fat necrosis in the breast?
a) Denaturation of proteins
b) Activation of lipases
c) Accumulation of iron sulphide
d) Release of proteases

28. What is the clinical presentation of gangrenous necrosis in the gastrointestinal tract,
specifically in diabetic patients?
a) Prolonged chest pain
b) Acute abdomen
c) Substernal discomfort
d) Rapid pulse

29. Which form of gangrenous necrosis involves a combination of coagulative and

liquefactive necrosis?
a) Dry gangrene
b) Wet gangrene
c) Liquefactive gangrene
d) Caseous gangrene

30. In brain ischemia leading to liquefactive necrosis, what is observed in the affected area on
electron microscopy?
a) Amorphous densities in mitochondria
b) Increased eosinophilia
c) Dissolution of neural tissue
d) Formation of granulomas

ANSWERS
1. b) Necrosis
2. b) Mitochondrial dysfunction and altered membrane function
3. a) Coagulative necrosis
4. b) Denaturation of proteins and enzymes
5. b) Stable angina
6. b) Revascularization
7. c) Troponin
8. c) Disruption of sarcolemmal membrane
9. b) Liquefactive necrosis
10. b) Caseous necrosis
11. c) Alcohol
12. c) Activation of lipases
13. b) Fibrinoid necrosis
14. a) Dystrophic calcification
15. b) Prinzmetal angina
16. c) Troponin
17. a) Coagulative necrosis
18. b) Prolonged chest pain
19. a) Left internal thoracic artery and greater saphenous vein
20. c) Bacterial infection
21. b) Denaturation of proteins
22. c) Blockage of complete proteolysis
23. c) Transient myocardial ischemia
24. c) Troponin
25. a) Associated with higher long-term patency rates
26. c) Gangrenous necrosis
27. b) Activation of lipases
28. b) Acute abdomen
29. b) Wet gangrene
30. c) Dissolution of neural tissue