A patient with congestive heart failure develops ankle edema. The fluid is low protein due to hydrostatic/oncotic imbalance. What is it called?
A. Exudate
B. Seroma
C. Transudate
D. Hematoma

C. Transudate

A swollen joint aspirate is cloudy and protein-rich from increased vascular permeability. What is this fluid?
A. Exudate
B. Transudate
C. Seroma
D. Lymph

A. Exudate

A macrophage senses cytosolic ATP and low intracellular K+ during tissue damage. Which receptor family detects these danger signals?
A. Toll-like receptors
B. Selectins
C. Integrins
D. NOD-like receptors

D. NOD-like receptors

Inflammasome activation most directly increases production of:
A. IL-4
B. IL-1
C. IL-10
D. IFN-γ

B. IL-1

The initiating step of inflammation begins with recognition of microbial components by:
A. Toll-like receptors
B. MHC I molecules
C. B-cell receptors
D. T-cell receptors

A. Toll-like receptors

In postcapillary venules, the initial rolling of neutrophils along endothelium is mediated by:
A. Integrins
B. PECAM-1
C. Selectins
D. Cadherins

C. Selectins

The main ligands for selectins on leukocytes are:
A. Collagen fibers
B. Sialylated oligosaccharides
C. Complement fragments
D. Fibrin polymers

B. Sialylated oligosaccharides

Endothelial cells increase coordinated adhesion molecule expression primarily in response to:
A. IL-4 and IL-5
B. IL-6 and IL-8
C. IFN-α and IFN-β
D. TNF and IL-1

D. TNF and IL-1

A patient twists an ankle and develops rubor, calor, tumor, dolor, and impaired use. Which sign completes this classic set?
A. Loss of function
B. Blistering
C. Cyanosis
D. Pruritus

A. Loss of function

Which pairing correctly matches inflammation type with its dominant tissue change?
A. Acute: fibrosis
B. Chronic: exudation
C. Acute: granulomas
D. Acute: fluid exudation

D. Acute: fluid exudation

In acute inflammation, vasodilation occurs first at the:
A. Capillaries
B. Arterioles
C. Venules
D. Lymphatics

B. Arterioles

Vasodilation in acute inflammation is quickly followed by:
A. Basement membrane synthesis
B. Platelet aggregation
C. Increased microvascular permeability
D. Smooth muscle hypertrophy

C. Increased microvascular permeability

Endothelial cell retraction causing leakage is induced by:
A. Histamine serotonin thromboxane
B. IL-12 IL-23 IL-17
C. TNF IFN-γ IL-2
D. Histamine bradykinin leukotrienes

D. Histamine bradykinin leukotrienes

The system that generates multiple inflammatory mediators (e.g., anaphylatoxins) is the:
A. Renin-angiotensin system
B. Complement system
C. Coagulation cascade only
D. Kinetochore complex

B. Complement system

In autoimmune disease, inflammation is commonly driven by:
A. Cytokines from B cells
B. Histamine from mast cells
C. Cytokines from T lymphocytes
D. IgE cross-linking only

C. Cytokines from T lymphocytes

In tuberculosis, infectious granulomas can become poorly perfused; the combination of hypoxia and free-radical–mediated injury most classically produces which type of necrosis within the granuloma?
A. Coagulative necrosis
B. Caseous necrosis
C. Liquefactive necrosis
D. Fat necrosis

B. Caseous necrosis

Which is a major component of acute inflammation involving movement from blood to tissue?
A. Fibroblast proliferation
B. Collagen deposition
C. Granuloma formation
D. Leukocyte emigration to injury

D. Leukocyte emigration to injury

In the general steps of inflammation, controlling and shutting down the reaction corresponds to:
A. Recognition
B. Regulation
C. Recruitment
D. Repair

B. Regulation

The initiating step of inflammation is best described as:
A. Recognition of harmful stimulus
B. Fibrosis of injured tissue
C. Epithelial regeneration
D. Antibody class switching

A. Recognition of harmful stimulus

Red streaks tracking proximally from a skin wound most strongly suggest:
A. Allergic urticaria
B. Sterile inflammation
C. Bacterial infection
D. Autoimmune vasculitis

C. Bacterial infection

In resting endothelium, P-selectin is stored in a specific granule type and later redistributed to the cell surface during inflammation. Where is it stored?
A. Specific neutrophil granules
B. Weibel-Palade bodies
C. Rough ER cisternae
D. Lysosomal granules

B. Weibel-Palade bodies

Early, weak rolling interactions that slow leukocytes and create time for endothelial binding are mediated by:
A. Selectins
B. Cadherins
C. Integrins
D. PECAM-1

C. Integrins

During endothelial activation, ligands for integrins are upregulated primarily by which cytokines?
A. TNF and IL-1
B. IL-4 and IL-5
C. IL-10 and TGF-β
D. IFN-α and IFN-β

A. TNF and IL-1

A neutrophil squeezes between endothelial cells (diapedesis). This transmigration occurs mainly in:
A. Arterioles
B. Capillaries
C. Small arteries
D. Postcapillary venules

D. Postcapillary venules

A key immunoglobulin-superfamily molecule for leukocyte diapedesis is CD31, also called:
A. ICAM-1
B. PECAM-1
C. VCAM-1
D. E-selectin

B. PECAM-1

A patient with bacterial cellulitis has strong neutrophil recruitment. The most common exogenous chemoattractant signal is:
A. N-formylmethionine peptides
B. Leukotriene B4
C. IL-8 chemokines
D. Complement fragments

A. N-formylmethionine peptides

Which set contains only endogenous chemoattractant sources listed in these notes?
A. Histamine, bradykinin, serotonin
B. Albumin, fibrinogen, IgM
C. Cytokines, complement, leukotriene B4
D. Myeloperoxidase, elastase, defensins

C. Cytokines, complement, leukotriene B4

Chemotactic agents guide leukocytes by binding to:
A. Nuclear steroid receptors
B. Ligand-gated ion channels
C. Cytosolic tyrosine kinases
D. Transmembrane G-protein receptors

D. Transmembrane G-protein receptors

In the first 6–24 hours of acute inflammation, the dominant inflammatory infiltrate is:
A. Eosinophils
B. Neutrophils
C. Macrophages
D. Plasma cells

B. Neutrophils

Once recruited to a site of infection/cell death, leukocytes recognize offending agents primarily via:
A. Toll-like receptors
B. T-cell receptors
C. MHC class II
D. Fcε receptors

A. Toll-like receptors

Leukocyte activation triggers signaling with increased cytosolic ion levels plus enzyme activation. Which option matches these notes?
A. ↓Ca2+, inhibits PKC
B. ↑cAMP, inhibits PLA2
C. ↓Ca2+, activates NOS
D. ↑Ca2+, activates PKC and PLA2

D. ↑Ca2+, activates PKC and PLA2

A bacterium is coated to enhance phagocytosis. Which trio lists the major opsonins from these notes?
A. IgG, C3b, plasma lectins
B. IgE, C5a, albumin
C. IL-1, TNF, IL-6
D. LTB4, histamine, bradykinin

A. IgG, C3b, plasma lectins

A receptor that binds and mediates endocytosis of LDL particles and microbial particles is best described as a:
A. Toll-like receptor
B. Selectin receptor
C. Scavenger receptor
D. Complement receptor only

C. Scavenger receptor

The primary mechanism listed for killing ingested microbes by phagocytes is:
A. Complement MAC formation
B. Reactive oxygen species
C. Antibody secretion
D. Collagen synthesis

B. Reactive oxygen species

ROS are produced mainly within the:
A. Cytosol
B. Nucleus
C. Extracellular space
D. Phagolysosome

D. Phagolysosome

The most potent bactericidal system in neutrophils (per these notes) is the:
A. Complement MAC pathway
B. Nitric oxide pathway
C. H2O2–MPO–halide system
D. Lactoferrin chelation system

C. H2O2–MPO–halide system

An inherited deficiency of components of the phagocyte oxidase system causes:
A. Leukocyte adhesion deficiency
B. Chronic granulomatous disease
C. Chediak-Higashi syndrome
D. Hyper-IgE syndrome

B. Chronic granulomatous disease

A macrophage generates the gas NO for antimicrobial activity. NO is produced from which amino acid via which enzyme?
A. Ornithine via nitric oxide synthase
B. Arginine via arginase
C. Tyrosine via nitric oxide synthase
D. Arginine via nitric oxide synthase

D. Arginine via nitric oxide synthase

Neutrophil specific (secondary) granules contain lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and ALP. Which is a secondary granule component?
A. Lactoferrin
B. Myeloperoxidase
C. Defensins
D. Elastase

A. Lactoferrin

The two major phagocytes emphasized in acute inflammation are:
A. Basophils, eosinophils
B. NK cells, dendritic cells
C. Neutrophils, macrophages
D. Mast cells, plasma cells

C. Neutrophils, macrophages

A neutrophil’s azurophilic (primary) granules carry enzymes for antimicrobial killing. Which primary-granule protein is classically present?
A. Lactoferrin
B. Collagenase
C. Myeloperoxidase
D. Gelatinase

C. Myeloperoxidase

A lab isolates neutrophil primary granules (azurophilic). Which set best matches their contents?
A. Defensins, elastase, cathepsin G
B. Lysozyme, ALP, histaminase
C. Lactoferrin, gelatinase, collagenase
D. Plasminogen activator, ALP, lysozyme

A. Defensins, elastase, cathepsin G

Neutrophil extracellular traps (NETs) require an enzyme that converts arginine → citrulline to drive downstream nuclear changes. Which enzyme is cited here?
A. Nitric oxide synthase
B. Lipoxygenase-5
C. Phospholipase A2
D. Arginine deaminase

D. Arginine deaminase

In NET formation, arginine-to-citrulline conversion most directly leads to:
A. Microtubule stabilization
B. Chromatin decondensation
C. Ribosomal shutdown
D. Membrane lipid peroxidation

B. Chromatin decondensation

A patient develops recurrent cold abscesses and is unusually susceptible to fungal and bacterial infections due to impaired neutrophil recruitment. Loss of which cytokine best fits?
A. IL-17
B. IL-10
C. TNF
D. IL-1

A. IL-17

Resolution of inflammation can occur when anti-inflammatory cytokines are liberated. Which pair best dampens the response?
A. IL-1 and TNF
B. IL-17 and TNF
C. TGF-β and IL-10
D. IL-1 and IL-17

C. TGF-β and IL-10

Histamine and serotonin are among the earliest mediators released in inflammation. Histamine IS NOT ACTIVATED BY:
A. Physical injury
B. Antigen cross-links IgE
C. C3a/C5a fragments
D. Leukotriene B4

D. Leukotriene B4

In leukocytes, arachidonic acid is freed from membrane phospholipids by:
A. Cyclooxygenase-2
B. Phospholipase A2
C. Lipoxygenase-5
D. Myeloperoxidase

B. Phospholipase A2

Leukotrienes are generated in leukocytes and mast cells mainly through:
A. Lipoxygenase
B. Nitric oxide synthase
C. Myeloperoxidase
D. Inflammasome protease

A. Lipoxygenase

In neutrophils, 5-lipoxygenase converts arachidonic acid into which intermediate that precedes leukotrienes?
A. Prostaglandin H2
B. Thromboxane A2
C. 5-hydroxyeicosatetraenoic acid
D. Lipoxin A4

C. 5-hydroxyeicosatetraenoic acid

A patient with acute bronchospasm has mediator-driven airway narrowing. Which leukotriene set is the cysteinyl group that causes intense vasoconstriction and bronchospasm?
A. LTB4, LTA4, LTB5
B. LTC4, LTD4, LTE4
C. LXA4, LXB4, LTB4
D. PGE2, PGI2, TXA2

B. LTC4, LTD4, LTE4

Lipoxins primarily:
A. Suppress inflammation, inhibit chemotaxis
B. Amplify inflammation, activate chemotaxis
C. Increase vasodilation, increase edema
D. Activate complement, activate IL-1

A. Suppress inflammation, inhibit chemotaxis

A patient on high-dose corticosteroids has reduced inflammatory gene expression. Which target is explicitly downregulated in these notes?
A. Arginine deaminase
B. Lipoxygenase-5
C. Cathepsin G
D. TNF

D. TNF

IL-1 generation depends on the:
A. Membrane attack complex
B. Phagolysosome
C. Inflammasome
D. NET scaffold

C. Inflammasome

Prolonged TNF production can cause:
A. Urticaria
B. Cachexia
C. Polycythemia
D. Thrombocytosis

B. Cachexia

A cytokine program driven by IL-1 and TNF induces chemokines that act primarily on neutrophils. Which chemokine class fits?
A. C chemokines
B. CX3C chemokines
C. C-C chemokines
D. C-X-C chemokines

D. C-X-C chemokines

C-C chemokines act on monocytes, eosinophils, basophils, and lymphocytes. Which mediator selectively recruits eosinophils?
A. Eotaxin
B. IL-1
C. Lipoxin
D. IL-17

A. Eotaxin

Which chemokine class is relatively specific for lymphocytes?
A. C-C chemokines
B. C-X-C chemokines
C. C chemokines
D. CX3C chemokines

C. C chemokines

Which chemokine family promotes strong adhesion of monocytes and T cells?
A. C-X-C chemokines
B. CX3C chemokines
C. C-C chemokines
D. C chemokines

B. CX3C chemokines

In complement activation, the critical step is proteolysis of C3. Which trio lists the pathways that can cleave C3?
A. Terminal, MAC, lytic
B. IgE, histamine, serotonin
C. Neutrophil, monocyte, mast
D. Classical, alternative, lectin

D. Classical, alternative, lectin

A patient mounts an antibody response; immune complexes form on a pathogen surface. Which event initiates the classical complement pathway?
A. C1 binds IgM/IgG on antigen
B. MBL binds microbial mannose
C. C3a binds neutrophil receptors
D. Factor H cleaves C3b

A. C1 binds IgM/IgG on antigen

In the classical pathway, C1 binds to which immunoglobulins after they have bound antigen?
A. IgA or IgE
B. IgG or IgM
C. IgD or IgA
D. IgE or IgM

B. IgG or IgM

A septic patient has complement activation triggered directly by microbial surface molecules without antibody involvement. Which pathway matches, per these notes?
A. Classical pathway
B. Lectin pathway
C. Alternative pathway
D. Terminal pathway

C. Alternative pathway

In these notes, the alternative pathway is described as being triggered when microbial surface molecules activate:
A. C3a
B. C1 inhibitor
C. C4a
D. CD59

A. C3a

A child with recurrent infections has impaired lectin-pathway recognition. The initiating binding molecule is:
A. C1 inhibitor
B. Mannose-binding lectin
C. Decay accelerating factor
D. Complement factor H

B. Mannose-binding lectin

In the lectin pathway, mannose-binding lectin binds carbohydrates on microbes and then:
A. Directly activates C1
B. Directly activates CD59
C. Cleaves C3b to iC3b
D. Blocks C3 convertase

A. Directly activates C1

All three complement activation pathways converge on formation of which enzyme complex?
A. C1 inhibitor
B. Membrane attack complex
C. C3 convertase
D. Lipoxygenase

C. C3 convertase

The key action of C3 convertase is to:
A. Split C5 into C5a/C5b
B. Split C3 into C3a/C3b
C. Split C4 into C4a/C4b
D. Split IgG into fragments

B. Split C3 into C3a/C3b

Which trio of complement fragments is listed as mediators of inflammation?
A. C3b, iC3b, C5b
B. C5a, C3a, C4a
C. C1q, C2, C9
D. Factor H, DAF, CD59

B. C5a, C3a, C4a

A lab studies leukocyte chemotaxis and finds a complement fragment strongly attracting multiple leukocyte types. Which fragment is chemotactic here?
A. C4a
B. C3b
C. C5a
D. C5b

C. C5a

In these notes, C5a is chemotactic for:
A. Neutrophils, monocytes, eosinophils, basophils
B. Lymphocytes, plasma cells, platelets, RBCs
C. Fibroblasts, myocytes, osteocytes, neurons
D. Hepatocytes, adipocytes, chondrocytes, keratinocytes

A. Neutrophils, monocytes, eosinophils, basophils

Beyond chemotaxis, C5a also activates which pathway (explicitly noted as not complement) ?
A. Cyclooxygenase pathway
B. Lipoxygenase pathway
C. Nitric oxide pathway
D. Kallikrein pathway

B. Lipoxygenase pathway

Opsonization is impaired in a patient with complement dysfunction. Which complement proteins act as opsonins here?
A. C3a and C4a
B. C5a and C5b
C. C3b and iC3b
D. C1 and C2

C. C3b and iC3b

A patient has recurrent swelling episodes due to uncontrolled complement activation. Which regulator normally blocks activation of C1?
A. CD59
B. DAF
C. C1 inhibitor (C1INH)
D. Factor H

C. C1 inhibitor (C1INH)

Deficiency of C1 inhibitor most directly causes:
A. Hemolytic uremic syndrome
B. Hereditary angioedema
C. Paroxysmal nocturnal hemoglobinuria
D. Macular degeneration

B. Hereditary angioedema

Two complement regulators are membrane-linked by a specific anchor; loss of that anchor predisposes RBCs to lysis. What anchor links DAF and CD59?
A. GPI anchor
B. Actin anchor
C. Integrin anchor
D. Collagen anchor

A. GPI anchor

Decay accelerating factor (DAF) protects cells by preventing formation of:
A. C3 convertases
B. C1 complexes
C. C5a fragments
D. Bradykinin

A. C3 convertases

CD59 protects cells by inhibiting formation of the:
A. C3 convertase
B. Membrane attack complex
C. Mannose lectin complex
D. C1 inhibitor complex

B. Membrane attack complex

Defective enzymes that create GPI anchors cause excess RBC lysis in:
A. Hereditary angioedema
B. Hemolytic uremic syndrome
C. Paroxysmal nocturnal hemoglobinuria
D. Macular degeneration

C. Paroxysmal nocturnal hemoglobinuria

Complement factor H inhibits the alternative pathway by promoting:
A. Proteolysis of C3
B. Cleavage and destruction of C3b
C. Assembly of MAC
D. Activation of C1

B. Cleavage and destruction of C3b

A patient has thick yellow “pus” draining from a wound; the reaction is purulent. The most common cause of purulent inflammation is:
A. Viral cytolysis
B. Autoimmune reaction
C. Fungal infection
D. Bacterial infection

D. Bacterial infection

A tender, fluctuant skin lesion is incised and a localized collection of pus is released. This lesion is a(n):
A. Abscess
B. Ulcer
C. Granuloma
D. Serous blister

A. Abscess

Endoscopy shows a crater-like defect/excavation on mucosa caused by sloughing of inflamed necrotic tissue. This is a(n):
A. Abscess
B. Seroma
C. Ulcer
D. Granuloma

C. Ulcer

Compared with acute inflammation, chronic inflammation is best characterized by:
A. Neutrophils only, no repair
B. Mononuclear cells, destruction, repair
C. Vasodilation only, no cells
D. Edema only, no injury

B. Mononuclear cells, destruction, repair

Which cell types are commonly present at sites of chronic inflammation (beyond macrophages)?
A. Basophils and platelets
B. Neutrophils and mast cells
C. Erythrocytes and fibroblasts
D. B cells and plasma cells

C. Erythrocytes and fibroblasts

Classical macrophage activation (M1) is induced by microbial products plus:
A. Interferon-gamma
B. IL-4
C. IL-13
D. IL-10

A. Interferon-gamma

Alternative macrophage activation (M2) is most strongly induced by:
A. IL-1 and TNF
B. IFN-gamma and IL-17
C. IL-4 and IL-13
D. C3a and C5a

C. IL-4 and IL-13

A cytokine that predominates in classical macrophage activation (not alternative) is:
A. IL-5
B. Interferon-gamma
C. IL-4
D. IL-13

B. Interferon-gamma

Which pairing correctly matches macrophage activation pathway to primary role?
A. Classical repair; Alternative defense
B. Classical eosinophils; Alternative neutrophils
C. Classical antibodies; Alternative complement
D. Classical defense; Alternative repair

D. Classical defense; Alternative repair

CD4+ T lymphocytes at inflamed sites primarily:
A. Neutralize toxins directly
B. Phagocytose microbes
C. Promote and shape inflammation
D. Secrete IgG antibodies

C. Promote and shape inflammation

A CD4+ subset drives classical macrophage activation by producing IFN-gamma. Which subset is this?
A. Th1
B. Th2
C. Th17
D. Treg

A. Th1

A CD4+ subset secretes IL-4, IL-5, IL-13, recruits eosinophils, and promotes alternative macrophage activation. Which subset is this?
A. Th1
B. Th2
C. Th17
D. Treg

B. Th2

A CD4+ subset secretes IL-17, inducing chemokines that recruit neutrophils and monocytes. Which subset is this?
A. Th2
B. Treg
C. Th1
D. Th17

D. Th17

Th1 and Th17 responses are most involved in defense against:
A. Helminths and allergy
B. Protozoa only
C. Bacteria, viruses, autoimmunity
D. Tumors only

C. Bacteria, viruses, autoimmunity

Th2 responses are most involved in defense against:
A. Helminths and allergy
B. Bacteria and viruses
C. Autoimmune diseases
D. Intracellular bacteria only

A. Helminths and allergy

A long-standing T-cell–macrophage interaction in chronic inflammation can result in:
A. Serous blistering
B. Granuloma formation
C. Immediate pus formation
D. Pure edema only

B. Granuloma formation

In granulomatous inflammation, which cell types are typically elevated at the lesion?
A. Eosinophils and basophils
B. Neutrophils and platelets
C. T lymphocytes and macrophages
D. RBCs and fibroblasts

C. T lymphocytes and macrophages

Foreign body granulomas characteristically occur in the absence of:
A. Neutrophil recruitment
B. Complement activation
C. Antibody production
D. T cell responses

D. T cell responses

In immune granulomas, elevated IFN-gamma is most associated with production by:
A. Th1 cells
B. Th2 cells
C. B cells
D. Mast cells

A. Th1 cells

In IgE-mediated allergy and parasitic reactions, which pairing is correct?
A. Eosinophil: IgE Fc receptor; Mast: MBP
B. Mast: IgE Fc receptor; Eosinophil: MBP
C. Mast: MBP; Eosinophil: prostaglandins
D. Eosinophil: histamine; Mast: MBP

B. Mast: IgE Fc receptor; Eosinophil: MBP

In tuberculosis, infectious granulomas can become poorly perfused; the combination of hypoxia and free-radical–mediated injury most classically produces which type of necrosis within the granuloma?
A. Coagulative necrosis
B. Caseous necrosis
C. Liquefactive necrosis
D. Fat necrosis

A. Coagulative necrosis

Which three cytokines are the most important mediators of the acute-phase reaction?
A. IL-4, IL-5, IL-13
B. IFN-γ, IL-2, IL-12
C. TGF-β, IL-10, IL-35
D. TNF, IL-1, IL-6

D. TNF, IL-1, IL-6

A patient with pneumonia has fever, leukocytosis, elevated acute-phase proteins, and increased heart rate/blood pressure with reduced sweating. This systemic pattern is best termed the:
A. Acute-phase response
B. Type I hypersensitivity
C. Complement deficiency syndrome
D. Granulomatous inflammation

A. Acute-phase response

Which pair are the key endogenous pyrogens?
A. IL-6 and TGF-β
B. IFN-γ and IL-17
C. IL-1 and TNF
D. Histamine and serotonin

C. IL-1 and TNF

During the acute-phase reaction, the prostaglandin that drives neurotransmitter production involved in hypothalamic temperature regulation is:
A. PGI2
B. PGE2
C. TXA2
D. PGD2

B. PGE2

Which acute-phase protein is most IL-1/TNF–dependent?
A. C-reactive protein
B. Fibrinogen
C. Albumin
D. Serum amyloid A

D. Serum amyloid A

Which mediator reduces iron availability to erythroid progenitors in bone marrow?
A. Transferrin
B. Ferritin
C. Hepcidin
D. Haptoglobin

C. Hepcidin

A CBC shows leukocytosis with a marked neutrophil predominance after a new lobar pneumonia. This leukocyte pattern most strongly suggests:
A. Bacterial infection
B. Viral infection
C. Helminth infestation
D. Typhoid fever

A. Bacterial infection

Which pairing correctly matches the condition with its expected leukocyte pattern?
A. Viral infection: neutrophilia
B. Bacterial infection: lymphocytosis
C. Typhoid: eosinophilia
D. Helminths: eosinophilia; typhoid: leukopenia

D. Helminths: eosinophilia; typhoid: leukopenia

A patient with severe infection develops disseminated intravascular coagulation (DIC), hypotensive shock, and insulin resistance with hyperglycemia. This “clinical triad” is most consistent with:
A. Acute-phase response alone
B. Septic shock triad
C. Viral syndrome
D. Granulomatous inflammation

B. Septic shock triad

Following tissue injury, repair proceeds through two core processes. Which pair correctly names them?
A. Chemotaxis and exudation
B. Necrosis and apoptosis
C. Regeneration and scarring
D. Vasodilation and edema

C. Regeneration and scarring

After a fibrin-rich exudate fills a tissue space, fibrovascular ingrowth produces fibrosis within that exudate-occupied space. This outcome is called:
A. Organization
B. Regeneration
C. Caseation
D. Metaplasia

A. Organization

In wound healing, the highly vascular granulation tissue that initially fills the defect is gradually replaced by:
A. Fibrin
B. Elastin
C. Keratin
D. Collagen

D. Collagen

The macrophage population most associated with repair and wound healing is predominantly derived from which activation pathway?
A. Classically activated macrophages
B. Alternatively activated macrophages
C. Neutrophil-derived macrophages
D. Plasma-cell derived macrophages

B. Alternatively activated macrophages

In liver regeneration, Kupffer cells release a cytokine that “primes” hepatocytes (makes them competent) before growth factors push cell-cycle entry. Which cytokine is this?
A. IL-6
B. IL-4
C. IL-10
D. IFN-γ

A. IL-6

In the second phase of hepatocyte proliferation, which growth factors act on primed hepatocytes to stimulate metabolism and move them from G0 toward G1?
A. VEGF and FGF-2
B. TNF and IL-1
C. HGF and TGF-alpha
D. Angiopoietin-1 and -2

C. HGF and TGF-alpha

After hepatocytes complete the replication phase, return to quiescence is driven by which antiproliferative cytokine?
A. IL-6
B. HGF
C. TGF-alpha
D. TGF-beta

D. TGF-beta

If liver injury is too severe for mature hepatocytes to restore mass effectively, which cells become primarily responsible for repair?
A. Stellate cells
B. Progenitor cells
C. Kupffer cells
D. Endothelial cells

B. Progenitor cells

During angiogenesis, the earliest step includes vasodilation and increased permeability. Which pair matches this step?
A. NO and VEGF
B. VEGF and endothelin
C. Histamine and serotonin
D. FGF-2 and IL-6

A. NO and VEGF

Which factors are most associated with maturation of the new vessel wall?
A. VEGF and NO
B. FGF-2 and Angiopoietin-1
C. Angiopoietin-1 and -2
D. Nitric oxide and Angiopoietin-1

C. Angiopoietin-1 and -2

Stabilization of newly formed vessels and pericytes is primarily mediated by:
A. VEGF and FGF-2
B. PDGF and TGF-beta
C. IL-1 and TNF
D. IL-4 and IL-13

B. PDGF and TGF-beta

PDGF stabilizes newly formed vessels mainly by:
A. Inhibiting endothelial proliferation
B. Increasing metalloproteinases
C. Driving vessel branching
D. Recruiting smooth muscle cells

D. Recruiting smooth muscle cells

TGF-beta stabilizes new vessels mainly by:
A. Suppressing endothelium, increasing ECM
B. Recruiting smooth muscle cells
C. Stimulating neutrophil chemotaxis
D. Triggering mast cell degranulation

A. Suppressing endothelium, increasing ECM

Sprouting and branching of new vessels is regulated by the:
A. MAPK signaling pathway
B. JAK-STAT signaling pathway
C. NOTCH signaling pathway
D. Hedgehog signaling pathway

C. NOTCH signaling pathway

VEGF promotes vessel branching by stimulating expression of:
A. Notch ligands
B. Smooth muscle actin
C. C3 convertase
D. Myofibroblast networks

A. Notch ligands

During angiogenic sprouting, ECM proteins aid vessel extension by binding:
A. Selectins
B. Toll-like receptors
C. Cadherins
D. Integrins

D. Integrins

ECM remodeling and vascular tube extension are enabled by:
A. Tight junction proteins
B. Matrix metalloproteinases
C. Sialylated oligosaccharides
D. Complement anaphylatoxins

B. Matrix metalloproteinases

Connective tissue deposition is driven by macrophage-released:
A. IL-1, TNF, IL-6
B. VEGF, NO, Angiopoietins
C. PDGF, FGF-2, TGF-beta
D. Histamine, serotonin, bradykinin

C. PDGF, FGF-2, TGF-beta

The growth factors for connective tissue deposition are mainly released by:
A. Th1 lymphocytes
B. Neutrophils
C. Mast cells
D. M2 macrophages

C. Mast cells

The single most important cytokine for connective tissue synthesis/deposition is:
A. TGF-beta
B. IL-6
C. IFN-gamma
D. IL-17

A. TGF-beta

TGF-beta decreases ECM degradation primarily by:
A. Activating lipoxygenase
B. Increasing elastase release
C. Inhibiting metalloproteinases
D. Upregulating complement pathways

C. Inhibiting metalloproteinases

A factor that prolongs inflammation and increases local tissue injury is:
A. Rapid re-epithelialization
B. Early wound contraction
C. Angiogenesis maturation
D. Infection

D. Infection

Glucocorticoids inhibit inflammation partly by decreasing:
A. TGF-beta production
B. Notch ligand expression
C. PDGF receptor density
D. Integrin binding affinity

A. TGF-beta production

Healing by first intention most typically involves:
A. Large tissue defects
B. Skin wounds
C. Deep abscess cavities
D. Extensive necrotic slough

B. Skin wounds

In second intention healing, type III collagen is replaced over weeks by:
A. Type II collagen
B. Type IV collagen
C. Type I collagen
D. Type V collagen

C. Type I collagen

Wound contraction is driven primarily by networks of:
A. Keratinocytes
B. Endothelial cells
C. Neutrophils
D. Myofibroblasts

D. Myofibroblasts

Venous leg ulcers result from chronic venous hypertension and often show:
A. Hemosiderin deposits
B. Amyloid plaques
C. Bilirubin crystals
D. Melanin accumulation

A. Hemosiderin deposits

Arterial ulcers most often develop in patients with:
A. Chronic venous hypertension
B. Peripheral artery atherosclerosis
C. Prolonged tissue compression
D. IgE-mediated reactions

B. Peripheral artery atherosclerosis

Pressure sores are skin ulcerations/necrosis caused by:
A. Immune complex deposition
B. Ischemia from vasculitis
C. Prolonged compression against bone
D. Excessive collagen breakdown

C. Prolonged compression against bone

Excessive formation of repair components most directly causes:
A. Caseous necrosis
B. Serous effusion
C. Purulent exudate
D. Hypertrophic scars and keloids

D. Hypertrophic scars and keloids

Scar tissue that grows beyond the original wound boundary is a:
A. Keloid
B. Contracture
C. Ulcer
D. Granuloma

A. Keloid

Hypertrophic scars commonly follow thermal/traumatic injury involving:
A. Epidermis
B. Deep dermis layers
C. Mucosa
D. Subcutaneous fat

B. Deep dermis layers

Contractures are most prone to develop in the:
A. Neck, scalp, face
B. Abdomen, flank, back
C. Palms, soles, anterior thorax
D. Hips, thighs, calves

C. Palms, soles, anterior thorax

Liver progenitor cells are found within the:
A. Space of Disse
B. Central vein
C. Portal triad artery
D. Canals of Hering

D. Canals of Hering