8.1

Question 1

What is the main purpose of acute inflammation (AI)?

Answer 1

To eliminate offending agents and initiate tissue repair.

Question 2

How long does acute inflammation typically last?

Answer 2

2–3 days, up to 2–3 weeks.

Question 3

How is chronic inflammation different from acute inflammation?

Answer 3

Chronic inflammation is prolonged, involves a shift in cell types, and features simultaneous tissue destruction and healing.

Question 4

What are the 5 Rs of inflammation?

Answer 4

Recognition, Recruitment, Removal, Regulation, Repair.

Question 5

What are the clinical signs of AI and their causes?

Answer 5

Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Loss of function – due to vasodilation, vascular permeability, and soluble mediators.

Question 6

What is the vascular response to injury?

Answer 6

Vasoconstriction, vasodilation, stasis, increased permeability, and endothelial activation.

Question 7

What causes vasodilation in early inflammation?

Answer 7

Histamine acting on arteriolar smooth muscle.

Question 8

What is leukocyte extravasation?

Answer 8

The process by which leukocytes exit the bloodstream and migrate to the site of inflammation.

Question 9

What are the steps of leukocyte extravasation?

Answer 9

Margination, rolling, adhesion, transmigration, chemotaxis.

Question 10

Name key chemoattractants.

Answer 10

IL-8, C5a, leukotriene B4.

Question 11

What are PAMPs and DAMPs?

Answer 11

PAMPs: Pathogen-associated molecular patterns; DAMPs: Damage-associated molecular patterns.

Question 12

What receptors detect these signals?

PAMP/DAMPs

Answer 12

Pattern recognition receptors (PRRs) like TLRs and NLRs.

Question 13

What is opsonisation?

Answer 13

Tagging of microbes with antibodies/complement for easier phagocytosis.

Question 14

What is a transudate?

Answer 14

Low protein (<30 g/L), low cell fluid; non-inflammatory.

Question 15

What is an exudate?

Answer 15

High protein (>30 g/L), high cell count; inflammatory.

Question 16

What is oedema?

Answer 16

Excess interstitial fluid; can be inflammatory or non-inflammatory.

Question 17

What are major cell-derived mediators?

Answer 17

Histamine, serotonin, cytokines, chemokines, prostaglandins, leukotrienes.

Question 18

What are sources of these mediators?

Answer 18

Mast cells, leukocytes, macrophages, lymphocytes.

Question 19

What is the effect of histamine?

Answer 19

Vasodilation, increased permeability, eosinophil chemotaxis.

Question 20

What is the effect of serotonin?

Answer 20

Vasoconstriction, pain, vascular changes.

Question 21

What enzyme releases arachidonic acid?

Answer 21

Phospholipase A2.

Question 22

What enzymes metabolise arachidonic acid?

Answer 22

Cyclooxygenase (COX) and lipoxygenase.

Question 23

What are the key metabolites of arachidonic acid?

Answer 23

Prostaglandins, thromboxanes, leukotrienes, lipoxins.

Question 24

What are the possible outcomes of AI?

Answer 24

Complete resolution, healing by fibrosis, chronic inflammation, abscess/ulcer formation.

Question 25

What are the major classes of anti-inflammatory drugs?

Answer 25

Steroids, NSAIDs, DMARDs, anticytokines, antihistamines, gout drugs.

Question 26

What is the difference between steroidal and non-steroidal drugs?

Answer 26

Steroids modulate gene transcription; NSAIDs inhibit COX enzymes.

Question 27

What is the genomic effect of glucocorticoids?

Answer 27

Bind nuclear receptors to modulate gene transcription: ↑ anti-inflammatory, ↓ pro-inflammatory genes.

Question 28

What are the non-genomic effects of glucocorticoids?

Answer 28

Membrane stabilisation, reduced leukocyte trafficking.

Question 29

How do glucocorticoids modulate immune cells?

Answer 29

Suppress T cell activity, reduce neutrophil migration, decrease antigen presentation.

Question 30

What pro-inflammatory enzymes do glucocorticoids inhibit?

Answer 30

COX-2 and phospholipase A2.

Question 31

What are some endocrine/metabolic side effects?

Answer 31

Adrenal suppression, hyperglycemia.

Question 32

What are immune-related side effects?

Answer 32

Immunosuppression, delayed wound healing.

Question 33

Name 3 other categories of glucocorticoid side effects.

Answer 33

GI (e.g., hypertension), neuropsychiatric (e.g., mood changes), dermatologic (e.g., acne).

Question 34

How do NSAIDs exert their primary effect?

Answer 34

Inhibit COX enzymes to reduce prostaglandin and thromboxane synthesis.

Question 35

What are the roles of COX-1 and COX-2?

Answer 35

COX-1: physiological functions; COX-2: inducible, inflammation-related.

Question 36

What are the three major effects of NSAIDs?

Answer 36

Anti-inflammatory, analgesic, antipyretic.

Question 37

What renal side effects are associated with NSAIDs?

Answer 37

Decreased renal perfusion, fluid retention.

Question 38

What GI risks do NSAIDs pose?

Answer 38

Ulcers, bleeding, dyspepsia.

Question 39

What are some cardiovascular risks?

Answer 39

Thrombosis, hypertension.

Question 40

What platelet effect is seen with NSAIDs like aspirin?

Answer 40

Irreversible inhibition of COX-1 in platelets → ↓ thromboxane A2 → ↓ platelet aggregation.

Question 41

What are examples of non-selective COX inhibitors?

Answer 41

Aspirin, ibuprofen, diclofenac, indomethacin.

Question 42

Name selective COX-2 inhibitors.

Answer 42

Celecoxib, etoricoxib, parecoxib.

Question 43

What drugs are poor anti-inflammatories but used as analgesics/antipyretics?

Answer 43

Paracetamol, metamizole, nefopam.

Question 44

GCC SE

Answer 44

* endocrine and metabolic: adrenal suppression * Immune system; Immunosuppression * Dermatological: Skin thinning and acne. * GI: hypotension