PATHOLOGY

ANNUAL
Section-A: General Pathology

1. Define inflammation. Describe vascular and cellular response of inflammation. Write differences
between acute and chronic inflammation. [2+5+3]

Answer:

- Definition of Inflammation:

Inflammation is a protective response of body tissues to harmful stimuli like pathogens, damaged
cells, or irritants. It aims to eliminate the initial cause of cell injury, clear out necrotic cells and
tissues, and establish tissue repair.

- Vascular Response:

- Vasodilation: Blood vessels widen to increase blood flow to the affected area, causing redness and
warmth.

- Increased Vascular Permeability: Blood vessels become more permeable, allowing plasma proteins
and leukocytes to leave the bloodstream and enter the tissues, leading to edema (swelling).

- Stasis and Margination: Slowing of blood flow allows leukocytes to adhere to the vessel walls.

- Cellular Response:

- Leukocyte Migration: White blood cells, especially neutrophils, migrate towards the site of injury.

- Phagocytosis: Neutrophils and macrophages engulf and destroy pathogens and dead cells.

- Release of Inflammatory Mediators: Chemicals like histamine, cytokines, and prostaglandins are
released to sustain the inflammatory response.

- Differences between Acute and Chronic Inflammation:

Feature Acute Inflammation Chronic Inflammation

Onset Rapid (minutes to hours) Slow (weeks to years)
Duration Short-term Long-term
 Cell Type Neutrophils Macrophages, lymphocytes
Outcomes Resolution, abscess formation Tissue destruction, fibrosis
Signs Redness, heat, swelling, pain Persistent inflammation,
fibrosis

2. Define shock. Enumerate different types of shock. Write pathophysiology of different stages of
shock. [2+4+4]

Answer:

- Definition of Shock:

Shock is a life-threatening condition characterized by inadequate tissue perfusion and oxygen

delivery, resulting in cellular and organ dysfunction.

- Types of Shock:

1. Hypovolemic Shock: Due to significant loss of blood or fluids.

2. Cardiogenic Shock: Due to heart failure.

3. Distributive Shock: Includes septic, anaphylactic, and neurogenic shock, characterized by

excessive vasodilation.

4. Obstructive Shock: Due to physical obstruction of blood flow (e.g., pulmonary embolism).

- Pathophysiology of Shock Stages:

- Initial Stage: Decreased oxygen delivery leads to anaerobic metabolism, resulting in lactic acidosis.

- Compensatory Stage: The body activates compensatory mechanisms like increased heart rate,
vasoconstriction, and hormonal responses (release of catecholamines, ADH).

- Progressive Stage: Prolonged hypoperfusion leads to worsening metabolic acidosis, cell damage,
and potential multi-organ failure.

- Irreversible Stage: Severe tissue hypoxia and acidosis lead to irreversible damage and often result
in death.

3. Write short notes on any four: [2.5×4]

a) Differentiate between Humoral and Cellular Immunity

-Humoral Immunity: Mediated by B cells that produce antibodies to neutralize extracellular

pathogens.

-Cellular Immunity: Mediated by T cells that destroy infected cells directly or help other immune
cells.
 Aspect Humoral Immunity Cellular Immunity

Mediating Cells B lymphocytes T lymphocytes

Primary Function Antibody production Cell-mediated destruction

Pathogens Targeted Extracellular Intracellular (e.g., viruses)

b) Atherosclerosis - Risk Factors and Complications

- Risk Factors: Hypertension, hyperlipidemia, smoking, diabetes, obesity.

- Complications: Myocardial infarction, stroke, peripheral artery disease, aneurysms.

c) Pathways of Spread of Malignant Lesion

- Direct Invasion: Tumor invades surrounding tissues.

- Lymphatic Spread: Tumor cells travel via lymphatic system to lymph nodes.

- Hematogenous Spread: Tumor cells enter blood vessels and spread to distant organs (e.g., liver,
lungs).

- Transcoelomic Spread: Tumor spreads across body cavities (e.g., peritoneal cavity).

d) Differentiate between Apoptosis and Necrosis

Feature Apoptosis Necrosis

Nature Programmed cell death Accidental cell death
Inflammation No inflammation Causes inflammation
Cell Membrane Intact Disrupted
Energy ATP-dependent Not energy-dependent

e) Stages of Repair after Injury

1. Hemostasis: Immediate response to stop bleeding.

2. Inflammation: Removal of pathogens and dead cells.

3. Proliferation: Formation of granulation tissue, angiogenesis, and re-epithelialization.

4. Remodeling: Collagen remodeling and tissue maturation to restore function.

1. Type of necrosis associated with tuberculosis:

- Answer: b. Caseous necrosis

2. Which of the following is responsible for the production of antibodies?

- Answer: b. B lymphocytes

3. The term "Metaplasia" means:

- Answer: d. Replacement of one cell type with another cell type

4. Which cytokine is primarily responsible for acute-phase response during inflammation?

- Answer: a. IL-6 (interleukin-6)

5. Metastatic calcification is due to:

- Answer: b. Hypercalcemia

1ST INTERNAL
# Definition of Apoptosis (2 marks):

Apoptosis is a form of programmed cell death that occurs in a regulated, controlled manner, without
causing inflammation. It plays a key role in maintaining homeostasis by eliminating damaged or
unnecessary cells.

# Pathways of Apoptosis (4 marks):

1. Intrinsic Pathway (mitochondrial pathway):

- Triggered by cellular stress such as DNA damage, oxidative stress, or nutrient deprivation.

- Involves the release of cytochrome c from mitochondria into the cytoplasm, activating caspases
(proteases) that cleave cellular components.

- The key proteins involved include Bcl-2 family members (e.g., Bax and Bcl-2) that regulate
mitochondrial membrane permeability.

2. Extrinsic Pathway (death receptor pathway):

- Initiated by the binding of death ligands (e.g., Fas ligand, TNF-α) to their respective cell surface
receptors (e.g., Fas receptor, TNF receptor).

- This activates caspases through adaptor proteins, leading to apoptosis.

# Difference Between Necrosis and Apoptosis (4 marks):

- Necrosis:

- Cause: Typically caused by external factors such as infection, toxins, or trauma.

- Process: The cell swells, and its contents leak into the extracellular space, causing inflammation.

- Outcome: Leads to tissue damage and inflammation.

- Morphology: Cells show nuclear swelling, membrane rupture, and inflammation.

- Apoptosis:

- Cause: Results from intrinsic or extrinsic signals, such as DNA damage, hormonal signals, or
developmental cues.

- Process: The cell undergoes controlled shrinking and fragmentation into apoptotic bodies that are
cleared by phagocytes, with minimal inflammation.

- Outcome: No tissue damage or inflammation.

- Morphology: Cells show shrinkage, chromatin condensation, and membrane blebbing.

4. Answer Any Four of the Following

I. Primary vs Secondary Wound Healing (2.5 marks):

- Primary Healing: Occurs when the wound edges are brought together (e.g., surgical incisions). It
involves minimal tissue loss and a faster healing process, with minimal scarring.

- Secondary Healing: Occurs in larger or more complex wounds (e.g., ulcers, traumatic injuries). It
involves significant tissue loss, prolonged inflammation, and more extensive scarring, with
granulation tissue formation and eventual reepithelialization.

II. Benign vs Malignant Tumors (2.5 marks):

- Benign Tumors:

- Well-differentiated and slow-growing.

- Encapsulated, non-invasive, and do not metastasize.

- Example: Fibroma, lipoma.

- Malignant Tumors:

- Poorly differentiated, fast-growing, and invasive.

 - They invade surrounding tissues and have the potential to metastasize.

- Example: Carcinoma, sarcoma.

III. Innate vs Adaptive Immunity (2.5 marks):

- Innate Immunity:

- Present at birth, nonspecific, and includes physical barriers (skin), phagocytes, and natural killer
cells.

- Provides immediate defense but lacks memory.

- Adaptive Immunity:

- Develops after exposure to specific pathogens, involves T and B lymphocytes.

- Highly specific, slower to respond but has immunological memory, leading to a more efficient
response upon re-exposure.

IV. Metaplasia (2.5 marks):

- Metaplasia is the reversible transformation of one differentiated cell type into another, usually as
an adaptive response to environmental stress (e.g., smoking leading to squamous metaplasia in the
respiratory epithelium). However, prolonged metaplasia can lead to dysplasia and cancer.

V. Peripheral Blood and Bone Marrow in Megaloblastic Anemia (2.5 marks):

- Peripheral Blood: Features include macrocytic anemia with large, oval-shaped red blood cells
(macrocytes), hypersegmented neutrophils, and anisocytosis.

- Bone Marrow: Hypercellular with abnormal large, immature erythroblasts (megaloblasts). The
erythroid precursors show delayed nuclear maturation relative to cytoplasm.

5. Single Most Appropriate Answer (1x5)

I. Higher in Exudate Compared to Transudate Except:

d) Glucose concentration

II. Benign Tumor:

a) Fibroma

III. Not an Important Opsonin:

 c) C3a

IV. All are Cellular Responses of Adaptation Except:

c) Dysplasia

V. Not a Common Antigen-Presenting Cell:

c) T Cell

2ND INTERNAL

I. Difference Between Innate and Adaptive Immunity (2.5 marks):

- Innate Immunity: The first line of defense, present at birth, non-specific, and includes physical
barriers (e.g., skin), cellular components (e.g., neutrophils, macrophages), and proteins (e.g.,
complement system). It responds rapidly but lacks memory.

- Adaptive Immunity: Highly specific and includes the activation of T and B lymphocytes. It provides
long-lasting immunity due to memory cells (e.g., memory T and B cells), and takes longer to develop
after first exposure.

II. Difference Between Red Infarct and White Infarct (2.5 marks):

- Red Infarct: Occurs in organs with a dual blood supply (e.g., lungs, liver), where the infarction is
hemorrhagic due to reperfusion or venous congestion.

- White Infarct: Typically seen in solid organs with a single blood supply (e.g., heart, kidney, spleen),
where the infarct is pale due to lack of blood flow and ischemia.

III. Classification of Bone Tumors (2.5 marks):

Bone tumors can be classified as:

1. Benign Bone Tumors:

- Osteochondroma

- Osteoid osteoma

- Giant cell tumor of bone

2. Malignant Bone Tumors:

- Osteosarcoma

- Chondrosarcoma
 - Ewing's sarcoma

IV. Definition of Embolism and Types of Embolism (2.5 marks):

- Embolism: The obstruction of a blood vessel by an embolus, which can be a clot, air, fat, or foreign
substance, traveling through the bloodstream.

Types of Embolism:

1. Thromboembolism: Clot (thrombus) traveling through the bloodstream.

2. Fat Embolism: Fat droplets, often from fractures of long bones.

3. Air Embolism: Air bubbles entering the bloodstream.

4. Septic Embolism: Infected emboli, often associated with infective endocarditis.

5. Amniotic Fluid Embolism: Amniotic fluid entering the maternal circulation during childbirth.

V. Difference Between Cell-Mediated Immunity and Humoral Immunity (2.5 marks):

- Cell-Mediated Immunity: Involves T lymphocytes and is responsible for defending against

intracellular pathogens (e.g., viruses, fungi) and tumors. Key players include cytotoxic T cells (CD8+)
and helper T cells (CD4+).

- Humoral Immunity: Involves B lymphocytes and the production of antibodies (immunoglobulins) to

target extracellular pathogens (e.g., bacteria). Antibodies neutralize the pathogens or mark them for
destruction by phagocytes.

4. Most Appropriate Answers (1x5)

I. Not an Important Cytokine Released from TH2 Cell:

c) IL-6

II. Prefers Hematogenous Route of Metastasis:

c) Renal Cell Carcinoma

III. Usual X-ray Picture of Osteosarcoma:

a) Sun Ray

IV. Inhibitory Cytokine:

d) IL-10

V. Not a Common Feature of Memory Lymphocytes:

b) Are Important for 1st Episode of Ag Exposure

3RD INTERNAL

3. Answer Any Four of the Following

I. Short Note on Delayed-Type Hypersensitivity Reaction (2.5 marks):

- Delayed-type hypersensitivity (DTH) is a cell-mediated immune response mediated primarily by

CD4+ T-helper cells and macrophages.

- Mechanism: Upon exposure to an antigen, the immune system mounts a response that peaks
around 48-72 hours. The activated T-cells release cytokines that recruit and activate macrophages,
leading to inflammation and tissue damage.

- Example: Tuberculin skin test (positive test indicates prior exposure to Mycobacterium
tuberculosis), contact dermatitis (e.g., poison ivy).

II. Diagnostic Criteria of SLE (2.5 marks):

- The diagnosis of Systemic Lupus Erythematosus (SLE) is based on the ACR/EULAR criteria:

1. Clinical Criteria: Butterfly-shaped malar rash, discoid lupus, photosensitivity, oral ulcers, arthritis,
pleuritis, etc.

2. Immunological Criteria: Positive antinuclear antibodies (ANA), anti-dsDNA, anti-Smith antibodies,

antiphospholipid antibodies, low complement levels.

3. Serologic Tests: A positive ANA test is often the first step in diagnosis, though it is not specific to
lupus.

- A diagnosis requires the presence of at least 4 criteria, with at least 1 clinical and 1 immunologic
criterion.

III. Risk Factors and Complications of Atherosclerosis (2.5 marks):

- Risk Factors:

1. Modifiable: Hypertension, hyperlipidemia, smoking, diabetes, physical inactivity, obesity.

2. Non-modifiable: Age, male gender, family history, genetic predisposition.

- Complications:
 1. Myocardial Infarction: Due to rupture of an atherosclerotic plaque and thrombus formation.

2. Stroke: Atherosclerosis of cerebral arteries can lead to ischemic strokes.

3. Peripheral Arterial Disease: Decreased blood flow to the extremities.

4. Aneurysms: Due to weakening of the vessel wall (e.g., abdominal aortic aneurysm).

IV. Diagnosis of Diabetes Mellitus (2.5 marks):

- Criteria for Diagnosis:

1. Fasting Plasma Glucose (FPG): ≥ 126 mg/dL after at least 8 hours of fasting.

2. Oral Glucose Tolerance Test (OGTT): 2-hour plasma glucose ≥ 200 mg/dL after a 75g glucose load.

3. Random Plasma Glucose: ≥ 200 mg/dL with symptoms of hyperglycemia.

4. HbA1c: ≥ 6.5% is diagnostic for diabetes.

- Confirmatory Tests: A diagnosis should be confirmed by a second test, except when the patient has
classic symptoms of hyperglycemia.

V. AML vs ALL (2.5 marks):

- Acute Myeloid Leukemia (AML):

- Affects myeloid lineage (granulocytes, monocytes).

- Characterized by myeloblasts with auer rods in peripheral blood or bone marrow.

- More common in adults.

- Acute Lymphoblastic Leukemia (ALL):

- Affects lymphoid lineage (B-cells or T-cells).

- Characterized by lymphoblasts (larger than myeloblasts) in blood or bone marrow.

- More common in children.

4. Most Appropriate Answers (1x5)

I. Defect in Platelet Adhesion is Seen in:

a) vWF deficiency
II. Not an Usual Feature of Multiple Myeloma:

c) ↑Blood Hemoglobin

III. Useful Investigation for the Diagnosis of HIV Infection in the Window Period is Detection of:

c) P24

IV. Which of the Following is a Diaphyseal Tumor:

a) Osteosarcoma

V. Basophilia is Seen in:

c) CML (Chronic Myelogenous Leukemia)