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A set of 20 medical pathology flashcards on cell injury, necrosis, inflammation, and tissue repair, postgraduate medical level, clean white cards with bold question on front and detailed answer on back, organized in a grid layout

Here are your 20 postgraduate-level pathology flashcards on Cell Injury, Necrosis, Inflammation & Repair, sourced from Robbins, Cotran & Kumar - Pathologic Basis of Disease.

🃏 Flashcard 1

Q: What are the hallmark morphologic features of necrosis on H&E staining?

A: Eosinophilia of cytoplasm (loss of RNA + denatured proteins binding eosin); nuclear changes - pyknosis (shrinkage), karyorrhexis (fragmentation), karyolysis (dissolution); breakdown of plasma and organellar membranes; myelin figures; enzymatic digestion of cell contents. Elicits local inflammation (unlike apoptosis).

🃏 Flashcard 2

Q: Distinguish coagulative from liquefactive necrosis - mechanism, location, and morphology.

A: Coagulative: protein denaturation dominates over enzymatic digestion; architecture preserved ("ghost cells"); seen in ischemic infarcts of solid organs (heart, kidney, spleen) EXCEPT brain. Liquefactive: enzymatic digestion dominates; tissue becomes liquid/creamy; seen in brain infarcts and bacterial abscesses (due to neutrophil-derived proteases).

🃏 Flashcard 3

Q: What is caseous necrosis? What condition is it pathognomonic of, and what do you see microscopically?

A: A variant combining features of coagulative and liquefactive necrosis - gross appearance is white-yellow "cheesy" material. Microscopically: structureless, granular, eosinophilic debris with complete loss of cellular architecture, surrounded by a granulomatous rim of macrophages and lymphocytes. Pathognomonic of tuberculosis (and other mycobacterial/fungal infections).

🃏 Flashcard 4

Q: What is fibrinoid necrosis? Where is it characteristically seen, and what is its pathogenesis?

A: Seen in blood vessel walls; caused by deposition of immune complexes + plasma proteins (including fibrin) that appear bright pink and amorphous on H&E. Pathogenesis: antigen-antibody complexes activate complement and inflammatory mediators → vascular wall damage. Classically seen in malignant hypertension, polyarteritis nodosa, and autoimmune vasculitides.

🃏 Flashcard 5

Q: How does apoptosis differ from necrosis in terms of mechanism, morphology, and inflammatory response?

A: Apoptosis is a regulated, energy-dependent cell suicide program. Key differences: (1) Membrane integrity - preserved in apoptosis, destroyed in necrosis; (2) Inflammation - absent in apoptosis (apoptotic bodies are rapidly phagocytosed before contents leak), present in necrosis; (3) Morphology - apoptosis shows cell shrinkage, chromatin condensation, membrane blebbing, apoptotic body formation; necrosis shows cell swelling, membrane rupture; (4) Scope - apoptosis affects single cells; necrosis affects groups of cells.

🃏 Flashcard 6

Q: What are the two pathways of apoptosis and their key molecular mediators?

A: (1) Intrinsic (mitochondrial) pathway: triggered by DNA damage, oxidative stress, growth factor withdrawal → pro-apoptotic BCL-2 family proteins (BAX, BAK) overwhelm anti-apoptotic members (BCL-2, BCL-XL) → cytochrome c released → apoptosome → caspase 9 → executioner caspases 3/6/7. (2) Extrinsic (death receptor) pathway: FasL binds Fas (CD95) or TNF binds TNFR → FADD recruitment → caspase 8 activation → executioner caspases. Both converge on caspase 3.

🃏 Flashcard 7

Q: What are DAMPs and what role do they play in sterile inflammation?

A: Damage-Associated Molecular Patterns (DAMPs) are endogenous molecules released from necrotic/injured cells - includes ATP (from damaged mitochondria), uric acid (DNA breakdown product), HMGB1, and DNA. They are recognized by pattern-recognition receptors (e.g., TLRs, NLRs) on macrophages and other cells, triggering cytokine production and phagocytosis without a microbial trigger. This is the basis of sterile inflammation (e.g., gout, myocardial infarction, crystal-induced arthritis).

🃏 Flashcard 8

Q: Describe the sequence of leukocyte recruitment to an inflammatory site - from rolling to transmigration.

A: (1) Margination and rolling: leukocytes marginate due to stasis; roll along endothelium via selectin-carbohydrate interactions (P-selectin/E-selectin on endothelium bind sialyl-Lewis X on leukocytes); (2) Firm adhesion: cytokines (TNF, IL-1) upregulate ICAM-1/VCAM-1 on endothelium; integrins (LFA-1/MAC-1 binding ICAM-1; VLA-4 binding VCAM-1) mediate firm arrest; (3) Transmigration (diapedesis): leukocytes squeeze between endothelial cells at junctions, aided by CD31 (PECAM-1) homotypic interactions; (4) Chemotaxis: directed migration toward C5a, LTB4, IL-8, bacterial products (fMLP).

🃏 Flashcard 9

Q: What is the predominant leukocyte at 0-24 hrs, 24-48 hrs, and >48 hrs in acute inflammation? Explain why.

A: 0-24 hrs: Neutrophils - most abundant in blood, fastest responders to chemokines (C5a, IL-8, LTB4, fMLP); short-lived (survive hours-days). 24-48 hrs: Monocytes/Macrophages - slower recruitment but longer lived; take over as neutrophils undergo apoptosis. >48 hrs: Macrophages + Lymphocytes - in viral infections, lymphocytes may predominate from the start. Notable exceptions: viral infections (lymphocytes early), Pseudomonas (neutrophils persist), helminthic infections (eosinophils dominate).

🃏 Flashcard 10

Q: What distinguishes an exudate from a transudate? What are the mechanisms behind each?

A: Exudate: high protein concentration, specific gravity >1.020, contains cells/debris; results from increased vascular permeability due to inflammatory mediators (histamine, VEGF) - gaps form between endothelial cells. Transudate: low protein, specific gravity <1.012, few cells; results from hydrostatic/osmotic imbalance without increased permeability - seen in heart failure, cirrhosis, nephrotic syndrome. Clinically: Light's criteria (protein ratio, LDH ratio) differentiate pleural exudates from transudates.

🃏 Flashcard 11

Q: Name the major chemical mediators of acute inflammation and their primary actions.

Histamine (mast cells, basophils, platelets): vasodilation, increased permeability - earliest mediator
Serotonin (platelets): similar to histamine
Prostaglandins (PGE2, PGD2): vasodilation, increased permeability, fever, pain
LTB4: potent neutrophil chemoattractant
LTC4/D4/E4: bronchoconstriction, increased permeability (important in asthma)
C3a/C5a: mast cell degranulation, chemotaxis (C5a strongest)
IL-1/TNF: fever, acute phase response, endothelial activation
Bradykinin: vasodilation, increased permeability, pain
PAF: platelet aggregation, bronchoconstriction, vasodilation at low doses

🃏 Flashcard 12

Q: How do NSAIDs and corticosteroids differ in their mechanism of action on the inflammatory cascade?

A: NSAIDs (aspirin, ibuprofen): inhibit cyclooxygenase (COX-1 and COX-2) → block conversion of arachidonic acid to prostaglandins and thromboxane. Aspirin irreversibly acetylates COX; selective COX-2 inhibitors (celecoxib) spare gastric mucosa but increase thrombotic risk. Corticosteroids: induce lipocortin (annexin A1) → inhibits phospholipase A2 → blocks release of arachidonic acid from membrane phospholipids → suppresses synthesis of ALL eicosanoids (prostaglandins + leukotrienes) plus reduces transcription of cytokines (TNF, IL-1, IL-6, IL-12).

🃏 Flashcard 13

Q: What are Neutrophil Extracellular Traps (NETs)? How are they formed and what is their pathologic relevance?

A: NETs are extracellular chromatin meshworks laden with antimicrobial granule proteins (MPO, elastase, defensins) that trap and kill bacteria/fungi. Formation: ROS activate arginine deaminase → citrullination of histones → chromatin decondensation; MPO and elastase enter nucleus → nuclear envelope rupture → chromatin release → neutrophil death (NETosis). Pathologic roles: excessive NET formation contributes to thrombosis (NETs provide scaffold for platelet/fibrin deposition), vasculitis, ANCA-associated nephritis, and COVID-19 coagulopathy.

🃏 Flashcard 14

Q: Define granulomatous inflammation. What cells form it and what are the two main categories of granulomas?

A: Granulomatous inflammation is a form of chronic inflammation characterized by nodular aggregates of activated macrophages (epithelioid cells), often with multinucleated giant cells (Langhans or foreign-body type), T lymphocytes, and plasma cells ± central necrosis. Two categories: (1) Immune granulomas (T cell-mediated, often with necrosis - e.g., TB, leprosy, sarcoidosis, Crohn's disease, fungal infections, berylliosis); (2) Foreign-body granulomas (no T-cell response needed; reaction to indigestible material - e.g., suture, silica, talc).

🃏 Flashcard 15

Q: What are the three CD4+ T-helper cell subsets involved in chronic inflammation, and what cytokines do they produce?

Th1: produces IFN-γ → classical macrophage activation (kills intracellular pathogens, forms granulomas); involved in autoimmune diseases, defense against bacteria/viruses
Th2: produces IL-4, IL-5, IL-13 → alternative macrophage activation; IgE production; eosinophil recruitment; important in helminthic defense and allergic inflammation
Th17: produces IL-17 → induces chemokine secretion → recruits neutrophils and monocytes; important in defense against extracellular bacteria/fungi and in autoimmune diseases (psoriasis, ankylosing spondylitis)

🃏 Flashcard 16

Q: What are tertiary lymphoid structures (TLS)? Where are they seen and what is their significance?

A: TLS are organized lymphoid follicles (resembling lymph node germinal centers) that form at sites of chronic inflammation when accumulated lymphocytes, APCs, and plasma cells cluster together. Seen in: rheumatoid arthritis synovium, Hashimoto thyroiditis, Sjögren syndrome, and in tumor microenvironments. Significance: thought to perpetuate chronic immune reactions by providing local sites for antigen presentation and B/T cell activation; presence in tumors may correlate with better response to immunotherapy.

🃏 Flashcard 17

Q: What is dystrophic calcification versus metastatic calcification? Distinguish their pathogenesis and serum calcium levels.

A: Dystrophic calcification: occurs in dead or dying tissue (areas of necrosis, atheroma, aging heart valves, calcified parasites); serum calcium is normal; mechanism involves release of membrane phospholipids that bind calcium + alkaline phosphatase generating phosphate ions. Metastatic calcification: occurs in normal tissue due to hypercalcemia (hyperparathyroidism, vitamin D toxicity, sarcoidosis, bone metastases, multiple myeloma); affects kidneys, lungs, blood vessels, gastric mucosa preferentially because they excrete acid and create locally alkaline pH.

🃏 Flashcard 18

Q: What is α1-antitrypsin deficiency and how does it mechanistically link neutrophil function to tissue destruction?

A: α1-Antitrypsin (AAT) is the major serum inhibitor of neutrophil elastase. In AAT deficiency (most commonly Z allele homozygotes): neutrophil elastase goes unchecked in the lung → destroys elastic support fibers of alveolar walls → panacinar emphysema (predominantly lower lobe). Concurrently, misfolded AAT polymer accumulates in hepatocyte ER → ER stress → hepatocyte injury → cirrhosis. This case illustrates how failure to regulate leukocyte-derived proteases directly causes chronic tissue damage.

🃏 Flashcard 19

Q: What are the outcomes of acute inflammation? Under what circumstances does each occur?

Complete resolution: restoration of normal tissue; occurs when injury is limited/short-lived and tissue has regenerative capacity (e.g., mild lobar pneumonia)
Healing by fibrosis/scarring: occurs when there is substantial tissue destruction or non-regenerative tissue involvement (e.g., myocardial infarction)
Progression to chronic inflammation: when agent persists (e.g., TB, persistent foreign body), or the inflammatory response is abnormal
Abscess formation: walled-off collection of pus in suppurative inflammation; usually requires surgical drainage
Systemic effects: fever (IL-1, IL-6, TNF → hypothalamic PGE2), acute phase response (CRP, fibrinogen, serum amyloid A via IL-6 → liver), leukocytosis (demargination + increased marrow output)

🃏 Flashcard 20

Q: Describe the cellular and molecular basis of tissue repair - what determines regeneration versus scarring?

A: After injury, repair proceeds by: (1) Regeneration (if stem cells/progenitors survive and scaffolding is intact) or (2) Scarring (if parenchymal loss is too great or stroma is destroyed). Key determinants:

Labile cells (epithelium, bone marrow): continuously cycling - regenerate readily
Stable cells (liver, kidney, endocrine): quiescent but retain regenerative capacity - can regenerate if architecture preserved
Permanent cells (neurons, cardiac myocytes, skeletal muscle): cannot regenerate - always scar
Key mediators: PDGF (fibroblast recruitment), TGF-β (collagen synthesis, the master fibrosis cytokine), VEGF (angiogenesis), EGF/HGF (epithelial proliferation), MMPs (ECM remodeling), TIMPs (inhibit MMPs)
Scar maturation: type III collagen replaced by type I; cross-linking by lysyl oxidase increases tensile strength (reaches ~70-80% of original by 3 months)

Source: Robbins, Cotran & Kumar - Pathologic Basis of Disease (10th ed.), Chapters 2 & 3

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