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Pathology Exam Answers

The document contains answers to a pathology exam, including multiple-choice questions and detailed explanations of key concepts such as hypertrophy, types of necrosis, inflammation signs, and mechanisms of disease onset. It also discusses morphological changes in necrosis and apoptosis, as well as the role of caspases and microbial killing. The information is structured into sections for easy reference.

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166 views3 pages

Pathology Exam Answers

The document contains answers to a pathology exam, including multiple-choice questions and detailed explanations of key concepts such as hypertrophy, types of necrosis, inflammation signs, and mechanisms of disease onset. It also discusses morphological changes in necrosis and apoptosis, as well as the role of caspases and microbial killing. The information is structured into sections for easy reference.

Uploaded by

alamsheraz23
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd

Pathology Exam Answers

Section I: MCQ Answers

1. d
2. a
3. b
4. d
5. d
6. a
7. a
8. b
9. d
10. a
11. a
12. d
13. d
14. d
15. d
16. b
17. d
18. a
19. a
20. d

Section II: Short Question Answers

1. Hypertrophy:
Hypertrophy is the increase in the size of individual cells, which leads to an increase in the size of
the organ. It occurs in response to increased workload, such as in skeletal muscles or the heart.

2. Types of Necrosis:
- Coagulative - heart, kidney infarcts.
- Liquefactive - brain, abscesses.
- Caseous - TB.
- Fat - pancreas.
- Fibrinoid - vessels.

3. Signs of Inflammation:
Redness, heat, swelling, pain, and loss of function are the five classic signs.

4. Mechanism of Increased Permeability:


Due to endothelial contraction, direct injury, or leukocyte-mediated damage, allowing fluid and cells
to escape into tissue.

5. Chronic Inflammation:
Lasts long, involves lymphocytes, macrophages, causes tissue destruction and fibrosis. Seen in TB
and autoimmune diseases.

6. Serous Inflammation:
Outpouring of watery fluid, like in viral infections or burns. Example: skin blister.

7. Metaplasia:
A reversible change where one adult cell type is replaced by another. Seen in smokers' lungs
(columnar to squamous).

Section III: Long Question Answers

1. Mechanism of Disease Onset:


Disease starts with an etiology (cause), which can be genetic or acquired. It leads to cellular injury,
triggering inflammation. The body tries to adapt or cells may die (necrosis/apoptosis). Healing
follows through regeneration or scarring.

2. Morphological Changes in Necrosis:


Includes cell swelling, membrane damage, increased eosinophilia. Nuclear changes: pyknosis
(shrinkage), karyorrhexis (fragmentation), karyolysis (dissolution). Inflammation usually occurs.

3. Difference Between Dry and Moist Gangrene:


Dry: ischemia, black/dry tissue, no infection. Moist: infected, wet, soft, foul smell. Moist is more
dangerous due to sepsis.

4. Types of Caspases:
Initiator: Caspase-8, 9. Effector: Caspase-3, 6, 7. Caspases are enzymes that initiate and execute
apoptosis by breaking cellular proteins.

5. Morphological Changes in Apoptosis:


Cell shrinkage, chromatin condensation, membrane blebbing, apoptotic bodies form. No
inflammation. Organelles remain intact till late.
6. Oxygen-dependent Microbial Killing:
Neutrophils/macrophages use ROS like superoxide and H2O2. NADPH oxidase and MPO are key
enzymes. ROS kill microbes in phagosomes.

7. Physiological Stress and Types:


Stress disturbs homeostasis. Body responds via hormones and immunity. Types: physical (injury),
chemical (toxins), emotional (fear), biological (infection).

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