INFLAMMATION

Question 1

Duration and primary cell type of Acute Inflammation

Answer 1

Onset is Immediate; cell type is mainly Neutrophils {PMCs}.

Question 2

Duration and primary cell types of Chronic Inflammation

Answer 2

Onset is Delayed; cell types are Lymphocytes, Macrophages, and Plasma Cells.

Question 3

Acute inflammation exception showing Relative Lymphocytosis

Answer 3

Typhoid is the notable exception where acute inflammation shows an increase in Lymphocytes.

Question 4

Chronic inflammation exception showing Neutrophils

Answer 4

Chronic Pseudomonas infection is the exception where chronic inflammation still shows an increase in Neutrophils.

Question 5

Classification: Inflammation with watery fluid (low protein)

Answer 5

Serous inflammation.

Question 6

Classification: Inflammation with thread-like, fibrin-rich exudate

Answer 6

Fibrinous inflammation.

Question 7

Appearance of Sero-Fibrinous Pericarditis {RHD}

Answer 7

The Bread & Butter appearance, containing both watery and thread-like fluid.

Question 8

Classification: Inflammation characterized by pus (Neutrophils + Necrotic cells)

Answer 8

Purulent inflammation (e.g., Abscess).

Question 9

Classification: Most common inflammation type characterized by mucus and water

Answer 9

Catarrhal inflammation (e.g., Common Cold).

Question 10

First vascular event in Acute Inflammation

Answer 10

Vasoconstriction (a transient event lasting for a few seconds).

Question 11

Vascular events consists

Answer 11

Vasoconstriction
Vasodilation
Increased vascular permeability
Stasis

Question 12

Hallmark event of acute inflammation

Answer 12

Increased vascular permeability (most commonly seen in post capillary Venules)

Question 13

Effect of increased vascular permeability in acute inflammation

Answer 13

Formation of exudate (protein-rich fluid) in the extravascular space.

Question 14

Key mediators that causes vasodilation and increased vascular permeability

Answer 14

Histamine and serotonin

Question 15

What is stasis

Answer 15

When plasma comes out from blood vessels, the RBCs become concentrated. In other words, viscosity is increased
This results in sluggish blood flow

Question 16

What is the most common mechanism of increased vascular permeability?

Answer 16

Endothelial cell contraction/retraction → formation of gaps between endothelial cells.

Question 17

What are all endothelial cells positive for?

Answer 17

CD34 (marker for endothelial cells).

Question 18

What mediators cause endothelial contraction/retraction?

Answer 18

Histamine and Serotonin.

Question 19

What type of response is endothelial contraction?

Answer 19

Immediate and transient.

Question 20

What happens in direct endothelial injury?

Answer 20

Direct damage → necrosis and detachment of endothelial cells → delayed prolonged (eg: delayed sun burn) or immediate sustained response (eg: sepsis).

Question 21

What is transcytosis?

Answer 21

Passage of fluid/proteins through endothelial cells via Vesiculo-Vacuolar Organelle (VVO) tunnels.

Question 22

What are the mediators of transcytosis?

Answer 22

Histamine and VEGF.

Question 23

Why are new vessels “leaky” in angiogenesis?

Answer 23

Because immature endothelial junctions are incomplete → leaky channels.

Question 24

What mediators are involved in angiogenesis?

Answer 24

Histamine and VEGF.

Question 25

In cellular injury what does “MRATCOP” stand for in inflammation?

Answer 25

M – Margination R – Rolling A – Adhesion T – Transmigration (Diapedesis) C – Chemotaxis O – Opsonization P – Phagocytosis

Question 26

What is normal laminar flow of blood in blood vessel ?

Answer 26

Blood vessel cells are in center of blood vessel

Question 27

Which is center most cell in laminar flow ?

Answer 27

RBC

Question 28

What happens during margination?

Answer 28

WBCs move from the central flow to the vessel margin.

Question 29

What molecules mediate rolling?

Answer 29

Selectins.

Question 30

Name the three types of selectins and their locations.

Answer 30

P-selectin: Platelets & Endothelial cells. E-selectin: Endothelial cells. L-selectin: Leukocytes.

Question 31

What is the ligand for P-selectin and E-selectin?

Answer 31

Sialyl-Lewis X on leukocytes.

Question 32

What is the ligand for L-selectin?

Answer 32

GlyCAM-1, MadCAM, or CD34 on endothelium.

Question 33

What molecules mediate firm adhesion?

Answer 33

Integrins on leukocytes binding to ICAM and VCAM on endothelium.

Question 34

Which integrins bind VCAM and ICAM?

Answer 34

α4β1 (VLA-4) → binds VCAM. β2 (LFA/MAC or CD11/18) → binds ICAM.

Question 35

What molecule mediates transmigration?

Answer 35

A: PECAM-1 (CD31) — between endothelial cells.

Question 36

Flashcard 21 Q: What enzyme helps WBCs cross the basement membrane? A: Matrix Metalloproteinase (MMP) – Zn-dependent enzyme. Flashcard 22 Q: What other molecules are involved in adhesion/transmigration? A: ICAM and VCAM. Flashcard 23 Q: What pathogens attach to ICAM? A: Rhinovirus and Plasmodium falciparum. 🔹 5. Chemotaxis Flashcard 24 Q: What is chemotaxis? A: Unidirectional movement of leukocytes toward a chemical attractant. Flashcard 25 Q: What are exogenous chemotactic agents? A: Bacterial products. Flashcard 26 Q: What are endogenous chemotactic agents? A: LTB4, IL-8, C5a (complement fragment). 🔹 6. Opsonization Flashcard 27 Q: What is opsonization? A: Coating of microbes with molecules that enhance phagocytosis — makes them “tastier.” Flashcard 28 Q: What are the main opsonins? A: IgG (main antibody opsonin). C3b (main complement opsonin). 🔹 7. Phagocytosis Flashcard 29 Q: What are the two killing mechanisms in phagocytosis? A: Oxygen-dependent (H₂O₂–MPO–Halide system). Oxygen-independent (enzymes/proteins from granules). Flashcard 30 Q: What enzyme is key to oxygen-dependent killing? A: NADPH oxidase, encoded by PHOX gene. Flashcard 31 Q: Which cell mainly performs oxygen-independent killing? A: Eosinophils — via Major Basic Protein (MBP) against parasites. Flashcard 32 Q: Which system is more potent—oxygen dependent or independent? A: Oxygen-dependent is more potent. ⚡ Quick Integrations Flashcard 33 Q: Which mediators appear repeatedly in permeability, angiogenesis, and transcytosis? A: Histamine and VEGF. Flashcard 34 Q: CD markers to remember: A: CD34 – endothelial cells. CD31 (PECAM) – transmigration. CD11/18 – leukocyte integrins.

Question 37

What enzyme helps WBCs cross the basement membrane?

Answer 37

Matrix Metalloproteinase (MMP) – Zn-dependent enzyme.

Question 38

What other molecules are involved in adhesion/transmigration?

Answer 38

ICAM and VCAM.

Question 39

What pathogens attach to ICAM?

Answer 39

Rhinovirus and Plasmodium falciparum.

Question 40

What is chemotaxis?

Answer 40

Unidirectional movement of leukocytes toward a chemical attractant.

Question 41

What are exogenous chemotactic agents?

Answer 41

Bacterial products.

Question 42

What are endogenous chemotactic agents?

Answer 42

LTB4, IL-8, C5a (complement fragment).

Question 43

What is opsonization?

Answer 43

Coating of microbes with molecules that enhance phagocytosis — makes them “tastier.”

Question 44

What are the main opsonins? A: IgG (main antibody opsonin). C3b (main complement opsonin). 🔹 7. Phagocytosis Flashcard 29 Q: What are the two killing mechanisms in phagocytosis? A: Oxygen-dependent (H₂O₂–MPO–Halide system). Oxygen-independent (enzymes/proteins from granules). Flashcard 30 Q: What enzyme is key to oxygen-dependent killing? A: NADPH oxidase, encoded by PHOX gene. Flashcard 31 Q: Which cell mainly performs oxygen-independent killing? A: Eosinophils — via Major Basic Protein (MBP) against parasites. Flashcard 32 Q: Which system is more potent—oxygen dependent or independent? A: Oxygen-dependent is more potent. ⚡ Quick Integrations Flashcard 33 Q: Which mediators appear repeatedly in permeability, angiogenesis, and transcytosis? A: Histamine and VEGF. Flashcard 34 Q: CD markers to remember: A: CD34 – endothelial cells. CD31 (PECAM) – transmigration.

Question 45

What are the main opsonins?

Answer 45

IgG (main antibody opsonin). C3b (main complement opsonin).

Question 46

What are the two killing mechanisms in phagocytosis?

Answer 46

Oxygen-dependent (H₂O₂–MPO–Halide system). Oxygen-independent (enzymes/proteins from granules).

Question 47

What enzyme is key to oxygen-dependent killing?

Answer 47

NADPH oxidase, encoded by PHOX gene.

Question 48

Which cell mainly performs oxygen-independent killing?

Answer 48

Eosinophils — via Major Basic Protein (MBP) against parasites.

Question 49

Which system is more potent—oxygen dependent or independent?

Answer 49

Oxygen-dependent is more potent.

Question 50

Which mediators appear repeatedly in permeability, angiogenesis, and transcytosis?

Answer 50

Histamine and VEGF.

Question 51

CD markers to remember:

Answer 51

CD34 – endothelial cells. CD31 (PECAM) – transmigration. CD11/18 – leukocyte integrins.

Question 52

What are NETs (Neutrophil Extracellular Traps)?

Answer 52

Networks of extracellular chromatin released by neutrophils to trap and kill pathogens when phagocytosis is insufficient.

Question 53

When are NETs formed?

Answer 53

In severe infections, especially sepsis, when phagocytosis alone is ineffective.

Question 54

What happens to the neutrophil during NET formation?

Answer 54

The nucleus ruptures and chromatin is released, killing microbes but also killing the neutrophil itself → “beneficial suicide.”

Question 55

Which amino acid is essential for NET formation?

Answer 55

Arginine.

Question 56

What autoimmune disease can NETs contribute to?

Answer 56

Systemic Lupus Erythematosus (SLE) — NETs release nuclear material → formation of antinuclear antibodies (ANA).

Question 57

NETs vs Phagocytosis — location of killing?

Answer 57

NETs: Extracellular killing Phagocytosis: Intracellular killing

Question 58

What types of pathogens can NETs trap?

Answer 58

Bacteria, yeast, protozoa, and fungal hyphae.

Question 59

What is Emperipolesis?

Answer 59

A phenomenon where one cell enters another living cell without being destroyed — a “cell-within-a-cell” appearance.

Question 60

What is the main difference between emperipolesis and phagocytosis?

Answer 60

In emperipolesis, there is no killing of the engulfed cell.

Question 61

Which cell is usually the host in emperipolesis?

Answer 61

Macrophage (the larger cell).

Question 62

Mnemonic for conditions showing emperipolesis – MARC

Answer 62

M: Myelodysplastic/Myeloproliferative syndromes (MDS/MPN) A: Autoimmune Hepatitis (AIH) R: Rosai–Dorfman Disease C: Chronic Lymphocytic Leukemia (CLL)

Question 63

What is the common feature of all LAD (leukocyte adhesion defect) types?

Answer 63

Autosomal recessive, recurrent bacterial infections, and impaired neutrophil migration.

Question 64

What is defective in LAD Type 1?

Answer 64

β₂-integrin (CD11/18) defect → failure of firm adhesion.

Question 65

Classic feature of LAD Type 1?

Answer 65

Delayed separation of the umbilical cord stump.

Question 66

What is defective in LAD Type 2?

Answer 66

Sialyl Lewis X deficiency → failure of rolling.

Question 67

What is the blood group of LAD Type 2 patients?

Answer 67

Bombay Blood Group.

Question 68

What antigens and antibodies are found in Bombay blood group?

Answer 68

Antigens absent: H, A, B Antibodies present: Anti-H, Anti-A, Anti-B

Question 69

What gene is defective in LAD Type 3?

Answer 69

FERMT3 gene (encodes Kindlin-3).

Question 70

What additional symptom is seen in LAD Type 3 besides infection?

Answer 70

Severe bleeding (due to platelet integrin defect).

Question 71

“Delayed separation of umbilical cord is seen in which condition?”

Answer 71

LAD Type 1 (β₂ integrin defect).