front 1 A patient with congestive heart failure develops ankle edema. The
fluid is low protein due to hydrostatic/oncotic imbalance. What is it
called? | back 1 C. Transudate |
front 2 A swollen joint aspirate is cloudy and protein-rich from increased
vascular permeability. What is this fluid? | back 2 A. Exudate |
front 3 A macrophage senses cytosolic ATP and low intracellular K+ during
tissue damage. Which receptor family detects these danger
signals? | back 3 D. NOD-like receptors |
front 4 Inflammasome activation most directly increases production
of: | back 4 B. IL-1 |
front 5 The initiating step of inflammation begins with recognition of
microbial components by: | back 5 A. Toll-like receptors |
front 6 In postcapillary venules, the initial rolling of neutrophils along
endothelium is mediated by: | back 6 C. Selectins |
front 7 The main ligands for selectins on leukocytes are: | back 7 B. Sialylated oligosaccharides |
front 8 Endothelial cells increase coordinated adhesion molecule expression
primarily in response to: | back 8 D. TNF and IL-1 |
front 9 Which pairing correctly matches inflammation type with its dominant
tissue change? | back 9 D. Acute: fluid exudation |
front 10 In acute inflammation, vasodilation occurs first at the: | back 10 B. Arterioles |
front 11 Vasodilation in acute inflammation is quickly followed by: | back 11 C. Increased microvascular permeability |
front 12 Endothelial cell retraction causing leakage is induced by: | back 12 D. Histamine bradykinin leukotrienes |
front 13 The system that generates multiple inflammatory mediators (e.g.,
anaphylatoxins) is the: | back 13 B. Complement system |
front 14 In autoimmune disease, inflammation is commonly driven by: | back 14 C. Cytokines from T lymphocytes |
front 15 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? | back 15 B. Caseous necrosis |
front 16 Which is a major component of acute inflammation involving movement
from blood to tissue? | back 16 D. Leukocyte emigration to injury |
front 17 The initiating step of inflammation is best described as: | back 17 A. Recognition of harmful stimulus |
front 18 Red streaks tracking proximally from a skin wound most strongly
suggest: | back 18 C. Bacterial infection |
front 19 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? | back 19 B. Weibel-Palade bodies |
front 20 Early, weak rolling interactions that slow leukocytes and create time
for endothelial binding are mediated by: | back 20 C. Integrins |
front 21 During endothelial activation, ligands for integrins are upregulated
primarily by which cytokines? | back 21 A. TNF and IL-1 |
front 22 A neutrophil squeezes between endothelial cells (diapedesis). This
transmigration occurs mainly in: | back 22 D. Postcapillary venules |
front 23 A patient with bacterial cellulitis has strong neutrophil
recruitment. The most common exogenous chemoattractant signal
is: | back 23 A. N-formylmethionine peptides |
front 24 Which set contains only endogenous chemoattractant sources listed in
these notes? | back 24 C. Cytokines, complement, leukotriene B4 |
front 25 Chemotactic agents guide leukocytes by binding to: | back 25 D. Transmembrane G-protein receptors |
front 26 In the first 6–24 hours of acute inflammation, the dominant
inflammatory infiltrate is: | back 26 B. Neutrophils |
front 27 Once recruited to a site of infection/cell death, leukocytes
recognize offending agents primarily via: | back 27 A. Toll-like receptors |
front 28 Leukocyte activation triggers signaling with increased cytosolic ion
levels plus enzyme activation. Which option matches these
notes? | back 28 D. ↑Ca2+, activates PKC and PLA2 |
front 29 A bacterium is coated to enhance phagocytosis. Which trio lists the
major opsonins from these notes? | back 29 A. IgG, C3b, plasma lectins |
front 30 A receptor that binds and mediates endocytosis of LDL particles and
microbial particles is best described as a: | back 30 C. Scavenger receptor |
front 31 The primary mechanism listed for killing ingested microbes by
phagocytes is: | back 31 B. Reactive oxygen species |
front 32 ROS are produced mainly within the: | back 32 D. Phagolysosome |
front 33 The most potent bactericidal system in neutrophils (per these notes)
is the: | back 33 C. H2O2–MPO–halide system |
front 34 An inherited deficiency of components of the phagocyte oxidase system
causes: | back 34 B. Chronic granulomatous disease |
front 35 A macrophage generates the gas NO for antimicrobial activity. NO is
produced from which amino acid via which enzyme? | back 35 D. Arginine via nitric oxide synthase |
front 36 The two major phagocytes emphasized in acute inflammation
are: | back 36 C. Neutrophils, macrophages |
front 37 A neutrophil’s azurophilic (primary) granules carry enzymes for
antimicrobial killing. Which primary-granule protein is classically
present? | back 37 C. Myeloperoxidase |
front 38 A lab isolates neutrophil primary granules (azurophilic). Which set
best matches their contents? | back 38 A. Defensins, elastase, cathepsin G |
front 39 Neutrophil extracellular traps (NETs) require an enzyme that converts
arginine → citrulline to drive downstream nuclear changes. Which
enzyme is cited here? | back 39 D. Arginine deaminase |
front 40 In NET formation, arginine-to-citrulline conversion most directly
leads to: | back 40 B. Chromatin decondensation |
front 41 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? | back 41 A. IL-17 |
front 42 Resolution of inflammation can occur when anti-inflammatory cytokines
are liberated. Which pair best dampens the response? | back 42 C. TGF-β and IL-10 |
front 43 Histamine and serotonin are among the earliest mediators released in
inflammation. Histamine IS NOT ACTIVATED BY: | back 43 D. Leukotriene B4 |
front 44 In leukocytes, arachidonic acid is freed from membrane phospholipids
by: | back 44 B. Phospholipase A2 |
front 45 Leukotrienes are generated in leukocytes and mast cells mainly
through: | back 45 A. Lipoxygenase |
front 46 In neutrophils, 5-lipoxygenase converts arachidonic acid into which
intermediate that precedes leukotrienes? | back 46 C. 5-hydroxyeicosatetraenoic acid |
front 47 A patient with acute bronchospasm has mediator-driven airway
narrowing. Which leukotriene set is the cysteinyl group that causes
intense vasoconstriction and bronchospasm? | back 47 B. LTC4, LTD4, LTE4 |
front 48 Lipoxins primarily: | back 48 A. Suppress inflammation, inhibit chemotaxis |
front 49 A patient on high-dose corticosteroids has reduced inflammatory gene
expression. Which target is explicitly downregulated in these
notes? | back 49 D. TNF |
front 50 IL-1 generation depends on the: | back 50 C. Inflammasome |
front 51 Prolonged TNF production can cause: | back 51 B. Cachexia |
front 52 A cytokine program driven by IL-1 and TNF induces chemokines that act
primarily on neutrophils. Which chemokine class fits? | back 52 D. C-X-C chemokines |
front 53 C-C chemokines act on monocytes, eosinophils, basophils, and
lymphocytes. Which mediator selectively recruits eosinophils? | back 53 A. Eotaxin |
front 54 Which chemokine class is relatively specific for lymphocytes? | back 54 C. C chemokines |
front 55 Which chemokine family promotes strong adhesion of monocytes and T
cells? | back 55 B. CX3C chemokines |
front 56 In complement activation, the critical step is proteolysis of C3.
Which trio lists the pathways that can cleave C3? | back 56 D. Classical, alternative, lectin |
front 57 A patient mounts an antibody response; immune complexes form on a
pathogen surface. Which event initiates the classical complement
pathway? | back 57 A. C1 binds IgM/IgG on antigen |
front 58 In the classical pathway, C1 binds to which immunoglobulins after
they have bound antigen? | back 58 B. IgG or IgM |
front 59 A septic patient has complement activation triggered directly by
microbial surface molecules without antibody involvement. Which
pathway matches, per these notes? | back 59 C. Alternative pathway |
front 60 In these notes, the alternative pathway is described as being
triggered when microbial surface molecules activate: | back 60 A. C3a |
front 61 A child with recurrent infections has impaired lectin-pathway
recognition. The initiating binding molecule is: | back 61 B. Mannose-binding lectin |
front 62 In the lectin pathway, mannose-binding lectin binds carbohydrates on
microbes and then: | back 62 A. Directly activates C1 |
front 63 All three complement activation pathways converge on formation of
which enzyme complex? | back 63 C. C3 convertase |
front 64 The key action of C3 convertase is to: | back 64 B. Split C3 into C3a/C3b |
front 65 Which trio of complement fragments is listed as mediators of
inflammation? | back 65 B. C5a, C3a, C4a |
front 66 A lab studies leukocyte chemotaxis and finds a complement fragment
strongly attracting multiple leukocyte types. Which fragment is
chemotactic here? | back 66 C. C5a |
front 67 In these notes, C5a is chemotactic for: | back 67 A. Neutrophils, monocytes, eosinophils, basophils |
front 68 Beyond chemotaxis, C5a also activates which pathway (explicitly noted
as not complement) ? | back 68 B. Lipoxygenase pathway |
front 69 A patient has recurrent swelling episodes due to uncontrolled
complement activation. Which regulator normally blocks activation of
C1? | back 69 C. C1 inhibitor (C1INH) |
front 70 Deficiency of C1 inhibitor most directly causes: | back 70 B. Hereditary angioedema |
front 71 Two complement regulators are membrane-linked by a specific anchor;
loss of that anchor predisposes RBCs to lysis. What anchor links DAF
and CD59? | back 71 A. GPI anchor |
front 72 Decay accelerating factor (DAF) protects cells by preventing
formation of: | back 72 A. C3 convertases |
front 73 CD59 protects cells by inhibiting formation of the: | back 73 B. Membrane attack complex |
front 74 Defective enzymes that create GPI anchors cause excess RBC lysis
in: | back 74 C. Paroxysmal nocturnal hemoglobinuria |
front 75 Complement factor H inhibits the alternative pathway by
promoting: | back 75 B. Cleavage and destruction of C3b |
front 76 A patient has thick yellow “pus” draining from a wound; the reaction
is purulent. The most common cause of purulent inflammation
is: | back 76 D. Bacterial infection |
front 77 A tender, fluctuant skin lesion is incised and a localized collection
of pus is released. This lesion is a(n): | back 77 A. Abscess |
front 78 Endoscopy shows a crater-like defect/excavation on mucosa caused by
sloughing of inflamed necrotic tissue. This is a(n): | back 78 C. Ulcer |
front 79 Compared with acute inflammation, chronic inflammation is best
characterized by: | back 79 B. Mononuclear cells, destruction, repair |
front 80 Which cell types are commonly present at sites of chronic
inflammation (beyond macrophages)? | back 80 D. B cells and plasma cells |
front 81 Classical macrophage activation (M1) is induced by microbial products
plus: | back 81 A. Interferon-gamma |
front 82 Alternative macrophage activation (M2) is most strongly induced
by: | back 82 C. IL-4 and IL-13 |
front 83 A cytokine that predominates in classical macrophage activation (not
alternative) is: | back 83 B. Interferon-gamma |
front 84 Which pairing correctly matches macrophage activation pathway to
primary role? | back 84 D. Classical defense; Alternative repair |
front 85 CD4+ T lymphocytes at inflamed sites primarily: | back 85 C. Promote and shape inflammation |
front 86 A CD4+ subset drives classical macrophage activation by producing
IFN-gamma. Which subset is this? | back 86 A. Th1 |
front 87 A CD4+ subset secretes IL-4, IL-5, IL-13, recruits eosinophils, and
promotes alternative macrophage activation. Which subset is
this? | back 87 B. Th2 |
front 88 A CD4+ subset secretes IL-17, inducing chemokines that recruit
neutrophils and monocytes. Which subset is this? | back 88 D. Th17 |
front 89 Th1 and Th17 responses are most involved in defense against: | back 89 C. Bacteria, viruses, autoimmunity |
front 90 Th2 responses are most involved in defense against: | back 90 A. Helminths and allergy |
front 91 A long-standing T-cell–macrophage interaction in chronic inflammation
can result in: | back 91 B. Granuloma formation |
front 92 In granulomatous inflammation, which cell types are typically
elevated at the lesion? | back 92 C. T lymphocytes and macrophages |
front 93 Foreign body granulomas characteristically occur in the absence
of: | back 93 D. T cell responses |
front 94 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? | back 94 A. Coagulative necrosis |
front 95 Which three cytokines are the most important mediators of the
acute-phase reaction? | back 95 D. TNF, IL-1, IL-6 |
front 96 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: | back 96 A. Acute-phase response |
front 97 Which pair are the key endogenous pyrogens? | back 97 C. IL-1 and TNF |
front 98 During the acute-phase reaction, the prostaglandin that drives
neurotransmitter production involved in hypothalamic temperature
regulation is: | back 98 B. PGE2 |
front 99 Which acute-phase protein is most IL-1/TNF–dependent? | back 99 D. Serum amyloid A |
front 100 Which mediator reduces iron availability to erythroid progenitors in
bone marrow? | back 100 C. Hepcidin |
front 101 A CBC shows leukocytosis with a marked neutrophil predominance after
a new lobar pneumonia. This leukocyte pattern most strongly
suggests: | back 101 A. Bacterial infection |
front 102 A patient with severe infection develops disseminated intravascular
coagulation (DIC), hypotensive shock, and insulin resistance with
hyperglycemia. This “clinical triad” is most consistent with: | back 102 B. Septic shock triad |
front 103 Following tissue injury, repair proceeds through two core processes.
Which pair correctly names them? | back 103 C. Regeneration and scarring |
front 104 After a fibrin-rich exudate fills a tissue space, fibrovascular
ingrowth produces fibrosis within that exudate-occupied space. This
outcome is called: | back 104 A. Organization |
front 105 In wound healing, the highly vascular granulation tissue that
initially fills the defect is gradually replaced by: | back 105 D. Collagen |
front 106 The macrophage population most associated with repair and wound
healing is predominantly derived from which activation
pathway? | back 106 B. Alternatively activated macrophages |
front 107 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? | back 107 A. IL-6 |
front 108 In the second phase of hepatocyte proliferation, which growth factors
act on primed hepatocytes to stimulate metabolism and move them from
G0 toward G1? | back 108 C. HGF and TGF-alpha |
front 109 After hepatocytes complete the replication phase, return to
quiescence is driven by which antiproliferative cytokine? | back 109 D. TGF-beta |
front 110 If liver injury is too severe for mature hepatocytes to restore mass
effectively, which cells become primarily responsible for
repair? | back 110 B. Progenitor cells |
front 111 During angiogenesis, the earliest step includes vasodilation and
increased permeability. Which pair matches this step? | back 111 A. NO and VEGF |
front 112 Which factors are most associated with maturation of the new vessel
wall? | back 112 C. Angiopoietin-1 and -2 |
front 113 Stabilization of newly formed vessels and pericytes is primarily
mediated by: | back 113 B. PDGF and TGF-beta |
front 114 PDGF stabilizes newly formed vessels mainly by: | back 114 D. Recruiting smooth muscle cells |
front 115 TGF-beta stabilizes new vessels mainly by: | back 115 A. Suppressing endothelium, increasing ECM |
front 116 Sprouting and branching of new vessels is regulated by the: | back 116 C. NOTCH signaling pathway |
front 117 VEGF promotes vessel branching by stimulating expression of: | back 117 A. Notch ligands |
front 118 During angiogenic sprouting, ECM proteins aid vessel extension by
binding: | back 118 D. Integrins |
front 119 ECM remodeling and vascular tube extension are enabled by: | back 119 B. Matrix metalloproteinases |
front 120 The growth factors for connective tissue deposition are mainly
released by: | back 120 C. Mast cells |
front 121 The single most important cytokine for connective tissue
synthesis/deposition is: | back 121 A. TGF-beta |
front 122 TGF-beta decreases ECM degradation primarily by: | back 122 C. Inhibiting metalloproteinases |
front 123 A factor that prolongs inflammation and increases local tissue injury
is: | back 123 D. Infection |
front 124 Glucocorticoids inhibit inflammation partly by decreasing: | back 124 A. TGF-beta production |
front 125 Healing by first intention most typically involves: | back 125 B. Skin wounds |
front 126 In second intention healing, type III collagen is replaced over weeks
by: | back 126 C. Type I collagen |
front 127 Wound contraction is driven primarily by networks of: | back 127 D. Myofibroblasts |
front 128 Venous leg ulcers result from chronic venous hypertension and often
show: | back 128 A. Hemosiderin deposits |
front 129 Arterial ulcers most often develop in patients with: | back 129 B. Peripheral artery atherosclerosis |
front 130 Pressure sores are skin ulcerations/necrosis caused by: | back 130 C. Prolonged compression against bone |
front 131 Excessive formation of repair components most directly
causes: | back 131 D. Hypertrophic scars and keloids |
front 132 Scar tissue that grows beyond the original wound boundary is
a: | back 132 A. Keloid |
front 133 Hypertrophic scars commonly follow thermal/traumatic injury
involving: | back 133 B. Deep dermis layers |
front 134 Contractures are most prone to develop in the: | back 134 C. Palms, soles, anterior thorax |
front 135 Liver progenitor cells are found within the: | back 135 D. Canals of Hering |