I85PREP
⌘ K
RCPA BPS Exam study materials
RCPA BPS Exam study resources

RCPA BPS Exam practice questions

One question at a time. Build your RCPA BPS Exam understanding.

First 50 of 200 questions. Each one lists the choices, the correct answer, and an explanation. The checker at the top of this page saves progress in this browser when it is available.

Continue in the practice tool above to load more questions, 50 at a time.

Question 1Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which morphological change is the earliest light-microscopic feature of reversible cell injury?

  1. Calcification of the mitochondrial matrix
  2. Nuclear pyknosis with chromatin clumping
  3. Coagulative necrosis with ghost cells
  4. Cellular swelling with membrane blebbing Correct answer.

Explanation

Reversible injury first disturbs ion pumps, so sodium and water enter the cell and the cell swells with plasma membrane blebs. Nuclear pyknosis and coagulative necrosis are features of irreversible injury and cell death, which occur later. Dystrophic calcification also follows cell death rather than preceding it.

Question 2Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A 60-year-old man has a myocardial infarct. Which histological pattern is expected in the infarcted myocardium after several days?

  1. Coagulative necrosis with loss of nuclei and preserved cell outlines Correct answer.
  2. Liquefactive necrosis with a cystic cavity
  3. Fibrinoid necrosis of arteriolar walls
  4. Caseous necrosis with granulomatous rimming

Explanation

Ischaemic injury in solid organs such as heart produces coagulative necrosis, in which proteins denature and cells keep their outlines while nuclei are lost. Liquefactive necrosis characterises brain infarcts and abscesses. Caseous necrosis occurs in tuberculosis, and fibrinoid necrosis affects vessel walls in vasculitis or malignant hypertension.

Question 3Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which process describes a change from one mature differentiated cell type to another mature type?

  1. Anaplasia
  2. Dysplasia
  3. Metaplasia Correct answer.
  4. Hyperplasia

Explanation

Metaplasia is the reversible replacement of one mature differentiated cell type by another, often in response to chronic irritation. Dysplasia denotes disordered growth with cytological atypia, hyperplasia is an increase in cell number, and anaplasia is loss of differentiation in malignancy.

Question 4Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which cell is the principal effector of type I collagen synthesis in healing wounds?

  1. Endothelial cell
  2. Neutrophil
  3. Mast cell
  4. Fibroblast Correct answer.

Explanation

Fibroblasts are the main source of type I collagen and other extracellular matrix proteins during granulation tissue formation and scar maturation. Neutrophils provide early phagocytic defence, endothelial cells form new vessels, and mast cells release mediators.

Question 5Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which epithelium lines the normal trachea and bronchi?

  1. Stratified squamous keratinised epithelium
  2. Simple squamous epithelium
  3. Pseudostratified ciliated columnar epithelium Correct answer.
  4. Transitional epithelium

Explanation

The conducting airways are lined by pseudostratified ciliated columnar epithelium with goblet cells, forming the mucociliary escalator. Simple squamous epithelium lines alveoli and serosae, stratified squamous epithelium lines skin and oesophagus, and transitional epithelium lines the urinary tract.

Question 6Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which connective tissue fibre is the principal component of the dermis and tendon?

  1. Type I collagen Correct answer.
  2. Reticulin fibre
  3. Elastic fibre
  4. Type II collagen

Explanation

Type I collagen is the most abundant collagen and forms the thick eosinophilic bundles of dermis, tendon and bone. Type II collagen predominates in hyaline cartilage, elastic fibres provide recoil in vessels and lung, and reticulin forms delicate supporting networks.

Question 7Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Apoptosis differs from necrosis in which key respect?

  1. Apoptosis provokes a strong neutrophilic inflammatory response
  2. Apoptosis causes cell swelling and membrane rupture
  3. Apoptosis results from severe ATP depletion and ion pump failure
  4. Apoptosis is an energy-dependent, caspase-mediated process with intact membranes Correct answer.

Explanation

Apoptosis is an active, ATP-dependent programme driven by caspases, with cell shrinkage, chromatin condensation and membrane-bound bodies that are phagocytosed without inflammation. Necrosis typically involves swelling, membrane rupture and an inflammatory response.

Question 8Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which organelle is the primary site of ATP generation by oxidative phosphorylation?

  1. Lysosome
  2. Golgi apparatus
  3. Mitochondrion Correct answer.
  4. Rough endoplasmic reticulum

Explanation

Mitochondria house the electron transport chain and ATP synthase on the inner membrane, generating most cellular ATP. The endoplasmic reticulum and Golgi handle protein synthesis and processing, and lysosomes carry out intracellular digestion.

Question 9Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A patient with chronic hypertension develops left ventricular hypertrophy. Which cellular adaptation underlies this change?

  1. Metaplasia of myocardium to squamous epithelium
  2. Apoptotic loss of cardiomyocytes
  3. Pathological hypertrophy of cardiomyocytes Correct answer.
  4. Hyperplasia of cardiomyocytes

Explanation

Cardiomyocytes are terminally differentiated and cannot divide, so a chronic pressure load causes them to enlarge, producing pathological hypertrophy. Hyperplasia requires a proliferative compartment, metaplasia involves a change of cell type, and apoptosis would reduce rather than increase myocardial mass.

Question 10Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

In a chronic smoker, the bronchial epithelium changes from ciliated columnar to stratified squamous. What is this adaptation called?

  1. Adenocarcinoma in situ
  2. Goblet cell hyperplasia
  3. Squamous metaplasia Correct answer.
  4. Dysplasia

Explanation

Chronic irritation by smoke can reversibly replace the ciliated respiratory epithelium with stratified squamous epithelium, termed squamous metaplasia. Dysplasia would require cytological atypia and disordered maturation, and adenocarcinoma in situ is a malignant lesion.

Question 11Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A woman with a long-standing cervical lesion has a biopsy showing disordered maturation with nuclear atypia but an intact basement membrane. Which term best describes this finding?

  1. Carcinoma in situ invading stroma
  2. Metaplasia
  3. Hyperplasia without atypia
  4. Dysplasia Correct answer.

Explanation

Disordered maturation with nuclear atypia confined by an intact basement membrane defines dysplasia, which may be pre-malignant. Metaplasia is a change of mature cell type without atypia, and invasion through the basement membrane would indicate invasive carcinoma.

Question 12Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which mechanism best explains cell swelling in acute ischaemic injury?

  1. Loss of plasma membrane cholesterol with osmotic shrinkage
  2. Failure of the Na+/K+ ATPase with net sodium and water influx Correct answer.
  3. Increased activity of the Na+/K+ ATPase with potassium influx
  4. Enhanced lysosomal exocytosis with extracellular water loss

Explanation

Ischaemia reduces ATP, so the Na+/K+ ATPase fails and intracellular sodium rises, drawing water into the cell and causing swelling. Increased pump activity would extrude sodium, and cholesterol loss does not explain the osmotic shift.

Question 13Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which feature first marks the transition from reversible to irreversible cell injury?

  1. Severe mitochondrial dysfunction with membrane integrity loss Correct answer.
  2. Cellular swelling
  3. Ribosomal detachment from rough endoplasmic reticulum
  4. Fatty change in hepatocytes

Explanation

Irreversible injury is marked by profound mitochondrial damage, ATP depletion and loss of membrane integrity, which commits the cell to death. Ribosomal detachment and swelling are reversible changes, and fatty change is a sublethal accumulation.

Question 14Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which pattern of necrosis is characteristic of an acute pancreatic enzyme leak into surrounding fat?

  1. Fibrinoid necrosis of capillaries
  2. Coagulative necrosis of adipocytes
  3. Caseous necrosis with granulomas
  4. Enzymatic fat necrosis with saponification Correct answer.

Explanation

Released pancreatic lipases digest adipose tissue, and liberated fatty acids bind calcium to form chalky saponified deposits, the hallmark of enzymatic fat necrosis. Coagulative, caseous and fibrinoid patterns reflect different mechanisms and tissues.

Question 15Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A cerebral infarct undergoes softening and cavity formation. Which necrotic pattern is this?

  1. Caseous necrosis
  2. Fat necrosis
  3. Liquefactive necrosis Correct answer.
  4. Coagulative necrosis

Explanation

Brain infarction causes liquefactive necrosis because enzymatic digestion predominates over protein denaturation, leaving a cystic cavity. Coagulative necrosis occurs in most solid organs, caseous necrosis in tuberculosis, and fat necrosis in pancreatitis or breast trauma.

Question 16Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which change represents physiological apoptosis during normal tissue turnover?

  1. Fibrinoid necrosis in a small artery
  2. Caseous necrosis in a tuberculous lymph node
  3. Coagulative necrosis of hepatocytes in viral hepatitis
  4. Loss of intestinal crypt cells balancing proliferation Correct answer.

Explanation

Apoptosis maintains constant cell numbers by removing senescent cells, as in the intestinal crypt where loss balances proliferation. The other options describe necrotic patterns caused by infection, ischaemia or immune injury.

Question 17Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which pathway of apoptosis is triggered by cytochrome c release from mitochondria?

  1. Necroptotic RIPK pathway
  2. Extrinsic death receptor pathway
  3. Complement membrane attack pathway
  4. Intrinsic mitochondrial pathway Correct answer.

Explanation

The intrinsic pathway is initiated by mitochondrial outer membrane permeabilisation with cytochrome c release, which assembles the apoptosome and activates caspase-9. The extrinsic pathway uses death receptors such as Fas, and complement and necroptosis use different mechanisms.

Question 18Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which pigment accumulates in the cytoplasm of hepatocytes and macrophages in chronic haemolysis?

  1. Haemosiderin Correct answer.
  2. Lipofuscin
  3. Biliverdin crystals
  4. Melanin

Explanation

Excess iron from haemoglobin breakdown is stored as haemosiderin, a golden-brown pigment visible in macrophages and hepatocytes. Lipofuscin is a wear-and-tear pigment, melanin derives from melanocytes, and biliverdin is rapidly reduced to bilirubin rather than stored as a stable pigment.

Question 19Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which intracellular accumulation is characteristic of alcoholic liver disease?

  1. Glycogen within lysosomes
  2. Calcium phosphate in the cytosol
  3. Haemosiderin in hepatocyte nuclei
  4. Mallory-Denk bodies composed of cytokeratin Correct answer.

Explanation

Alcoholic liver injury causes accumulation of damaged intermediate filaments, forming eosinophilic Mallory-Denk bodies rich in cytokeratin. Iron accumulates in haemochromatosis, calcium deposits occur in necrosis, and glycogen is stored in the cytosol rather than lysosomes in normal hepatocytes.

Question 20Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which cell junction anchors intermediate filaments to the extracellular matrix at the basal surface of epithelial cells?

  1. Gap junction
  2. Desmosome
  3. Hemidesmosome Correct answer.
  4. Tight junction

Explanation

Hemidesmosomes use integrins to attach the basal keratin intermediate filament network to the basal lamina. Desmosomes link adjacent cells, gap junctions allow small molecule exchange, and tight junctions seal the paracellular space.

Question 21Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A tissue shows increased numbers of cells in an organ, all of normal appearance, in response to a hormonal stimulus. Which adaptation is present?

  1. Hypertrophy
  2. Atrophy
  3. Dysplasia
  4. Hyperplasia Correct answer.

Explanation

Hyperplasia is an increase in cell number within a tissue, often driven by hormonal or growth factor stimulation, as in the endometrium or prostate. Hypertrophy increases cell size, atrophy reduces cell size and number, and dysplasia introduces atypical disordered growth.

Question 22Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which process describes autophagic removal of damaged organelles during nutrient deprivation?

  1. Necroptosis with membrane rupture
  2. Macroautophagy with lysosomal degradation Correct answer.
  3. Apoptotic caspase-3 activation
  4. Coagulative necrosis of the cell

Explanation

Macroautophagy sequesters cytoplasm and organelles in double-membrane autophagosomes that fuse with lysosomes for degradation, recycling nutrients during starvation. Apoptosis and necroptosis are death programmes, and coagulative necrosis is a post-ischaemic pattern.

Question 23Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A tumour shows marked nuclear pleomorphism, high mitotic activity and loss of glandular architecture. Which term best captures the loss of differentiation?

  1. Anaplasia Correct answer.
  2. Hyperplasia
  3. Metaplasia
  4. Dysplasia

Explanation

Anaplasia denotes loss of differentiation and architectural organisation in malignant cells, with pleomorphism and atypical mitoses. Metaplasia and hyperplasia are non-neoplastic adaptations, and dysplasia is disordered growth that may precede but does not by itself define complete loss of differentiation.

Question 24Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which mechanism explains dystrophic calcification in necrotic tissue despite normal serum calcium?

  1. Calcium binding to exposed acidic phospholipids and denatured proteins in dead cells Correct answer.
  2. Systemic hypercalcaemia driving calcium phosphate deposition
  3. Active osteoblast-mediated bone formation in the lesion
  4. Increased renal tubular reabsorption of phosphate

Explanation

Dystrophic calcification occurs in dead or dying tissue when membrane breakdown exposes acidic phospholipids and denatured proteins that bind calcium, even with normal serum levels. Hypercalcaemia causes metastatic calcification, and osteoblastic bone formation is unrelated.

Question 25Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which ultrastructural feature distinguishes myofibroblasts in granulation tissue from ordinary fibroblasts?

  1. Prominent rough endoplasmic reticulum with peripheral contractile actin bundles Correct answer.
  2. Apical cilia with basal bodies
  3. Numerous free ribosomes with no cytoskeletal filaments
  4. Abundant lysosomes with phagocytosed debris

Explanation

Myofibroblasts combine the synthetic machinery of fibroblasts, a well-developed rough endoplasmic reticulum, with peripheral bundles of actin and myosin that enable wound contraction. Lysosome-rich phagocytes are macrophages, and cilia are epithelial specialisations.

Question 26Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

Which type of epithelium lines the inner surface of the urinary bladder and ureter, and what property does it possess?

  1. Simple squamous epithelium, which permits rapid diffusion of water and solutes
  2. Pseudostratified ciliated columnar epithelium, which propels mucus along the surface
  3. Stratified squamous keratinised epithelium, which resists abrasive wear
  4. Transitional epithelium, whose superficial umbrella cells can flatten and stretch in response to distension Correct answer.

Explanation

The urinary tract is lined by transitional (urothelial) epithelium, a stratified epithelium whose superficial umbrella cells change shape and allow the mucosa to accommodate large changes in luminal volume without rupture. It also forms a barrier against the hypertonic, potentially toxic urine.

Question 27Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A tissue section shows cells arranged in a single layer resting on a basement membrane, with nuclei at varying heights so that not every cell reaches the surface. Which description fits this epithelium?

  1. Stratified cuboidal epithelium
  2. Pseudostratified columnar epithelium Correct answer.
  3. Simple columnar epithelium
  4. Simple squamous epithelium

Explanation

In pseudostratified epithelium all cells contact the basement membrane, but because nuclei lie at different levels the layer appears stratified. True stratification requires cells stacked in several tiers, with only the basal layer touching the basement membrane.

Question 28Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

After a myocardial infarct, the necrotic muscle is replaced over weeks by a collagen-rich scar. Which cell is the principal source of this new collagen?

  1. Circulating neutrophils
  2. Myofibroblasts derived largely from fibroblasts Correct answer.
  3. Endothelial cells of newly formed capillaries
  4. Resident cardiac myocytes

Explanation

Healing by fibrosis depends on myofibroblasts, which are induced by TGF-beta and other mediators and secrete large amounts of type I collagen while generating contractile force. Cardiac myocytes are permanently post-mitotic and cannot regenerate the lost muscle.

Question 29Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A young man has recurrent bacterial infections, and electron microscopy of his respiratory epithelium shows cilia with absent dynein arms. Which functional consequence follows directly from this defect?

  1. Failure of microtubule sliding, so cilia cannot beat effectively and mucus clearance is impaired Correct answer.
  2. Loss of tight junction sealing, so the epithelium becomes leaky to ions
  3. Loss of actin microvilli, so the apical surface area for absorption is reduced
  4. Failure of intermediate filament assembly, so basal cells detach from the basement membrane

Explanation

Ciliary movement depends on dynein motor proteins sliding adjacent microtubule doublets within the axoneme. When dynein arms are absent the sliding cannot occur, the cilia are immotile, and mucociliary clearance fails, predisposing to recurrent respiratory infection.

Question 30Cell and Tissue Biology (cell injury, adaptation, death, and basic histology)

A biopsy of chronically inflamed tissue shows numerous plasma cells. Which ultrastructural feature would best identify these cells at electron microscopy?

  1. Numerous secondary lysosomes packed with pigment
  2. Abundant rough endoplasmic reticulum arranged in concentric whorls Correct answer.
  3. Large numbers of mitochondria between myofilaments
  4. A prominent brush border of long microvilli

Explanation

Plasma cells are dedicated antibody-secreting cells, so their cytoplasm is dominated by rough endoplasmic reticulum and a prominent Golgi region for protein synthesis and export. The nucleus typically shows a clock-face chromatin pattern with a perinuclear clearing.

Question 31General Pathology (inflammation, repair, regeneration, and wound healing)

Which cell type is the first to arrive at the site of acute inflammation, typically within minutes to a few hours?

  1. Plasma cell
  2. Neutrophil Correct answer.
  3. Fibroblast
  4. Macrophage

Explanation

Acute inflammation is dominated by neutrophils, which are recruited earliest by chemotactic signals such as IL-8 and complement C5a and marginate and emigrate within minutes to hours. Macrophages follow and predominate later, while plasma cells and fibroblasts belong to chronic repair phases. This temporal sequence defines the classic acute inflammatory infiltrate.

Question 32General Pathology (inflammation, repair, regeneration, and wound healing)

Increased vascular permeability in acute inflammation is most directly caused by which mechanism?

  1. Reduced hydrostatic pressure in capillaries
  2. Decreased plasma oncotic pressure
  3. Increased lymphatic drainage
  4. Endothelial cell contraction creating intercellular gaps Correct answer.

Explanation

Endothelial contraction, mediated by histamine, bradykinin and leukotrienes, causes reversible gap formation between endothelial cells and allows protein-rich exudate to escape. This produces the swelling and protein-rich edema of acute inflammation. Changes in lymphatic drainage, hydrostatic pressure or oncotic pressure produce transudates rather than inflammatory exudates.

Question 33General Pathology (inflammation, repair, regeneration, and wound healing)

Which adhesion molecule pair mediates the firm adhesion (not rolling) of leukocytes to activated endothelium?

  1. Integrin on leukocyte binding ICAM-1 on endothelium Correct answer.
  2. P-selectin binding PSGL-1
  3. CD31 binding CD31
  4. Selectin on leukocyte binding sialyl-Lewis X on endothelium

Explanation

Firm adhesion requires activation of leukocyte integrins (such as LFA-1 and Mac-1) which bind endothelial ICAM-1 and VCAM-1. Selectin-ligand interactions mediate the earlier rolling step, and CD31 participates in transmigration rather than firm adhesion. This stepwise model explains the sequential rolling, adhesion and transmigration of leukocytes.

Question 34General Pathology (inflammation, repair, regeneration, and wound healing)

A 40-year-old develops a localized abscess. Which process most directly explains the pus formation?

  1. Neutrophil accumulation with necrosis and liquefactive breakdown of tissue Correct answer.
  2. Fibrinoid necrosis of vessel walls
  3. Caseous necrosis with granuloma formation
  4. Coagulative necrosis with preserved tissue architecture

Explanation

Abscess formation reflects a dense neutrophilic infiltrate that releases enzymes and reactive oxygen species, causing liquefactive necrosis of tissue and accumulation of pus. Caseous necrosis with granulomas is typical of tuberculosis, coagulative necrosis follows ischemia, and fibrinoid necrosis occurs in immune vasculitis. The dominant neutrophil response distinguishes an abscess.

Question 35General Pathology (inflammation, repair, regeneration, and wound healing)

Which chemical mediator is a preformed vasoactive amine stored in mast cell granules and released early in inflammation?

  1. Interleukin-1
  2. Histamine Correct answer.
  3. Prostaglandin E2
  4. Leukotriene B4

Explanation

Histamine is preformed and stored in mast cell and basophil granules, causing rapid vasodilation and increased venular permeability. Prostaglandins and leukotrienes are synthesized de novo from arachidonic acid, and IL-1 is a newly synthesized cytokine. Preformed versus newly synthesized mediators explains the timing of the vascular response.

Question 36General Pathology (inflammation, repair, regeneration, and wound healing)

Which enzyme is the principal target of aspirin's anti-inflammatory action?

  1. Cyclooxygenase Correct answer.
  2. Phospholipase A2
  3. 5-lipoxygenase
  4. Myeloperoxidase

Explanation

Aspirin irreversibly acetylates cyclooxygenase, reducing prostaglandin and thromboxane synthesis. Phospholipase A2 liberates arachidonic acid and is targeted by steroids, 5-lipoxygenase drives leukotriene production, and myeloperoxidase is a neutrophil enzyme. This explains why aspirin reduces prostaglandin-mediated pain and fever.

Question 37General Pathology (inflammation, repair, regeneration, and wound healing)

A defect in NADPH oxidase causes which disorder?

  1. Chediak-Higashi syndrome
  2. Complement C3 deficiency
  3. Chronic granulomatous disease Correct answer.
  4. Leukocyte adhesion deficiency type 1

Explanation

NADPH oxidase generates superoxide for the respiratory burst, and its deficiency causes chronic granulomatous disease with recurrent catalase-positive bacterial and fungal infections. Leukocyte adhesion deficiency involves integrin defects, Chediak-Higashi involves lysosomal trafficking, and C3 deficiency impairs opsonization. The respiratory burst defect is specific to NADPH oxidase.

Question 38General Pathology (inflammation, repair, regeneration, and wound healing)

Which cytokine is the most important for fever production in inflammation?

  1. Interleukin-1 Correct answer.
  2. Interleukin-4
  3. Transforming growth factor beta
  4. Interleukin-10

Explanation

Interleukin-1, together with TNF and IL-6, acts on the hypothalamus to increase prostaglandin E2 and raise the thermoregulatory set point, producing fever. IL-4 drives Th2 responses, IL-10 is anti-inflammatory, and TGF-beta promotes fibrosis. These latter cytokines do not mediate the febrile response.

Question 39General Pathology (inflammation, repair, regeneration, and wound healing)

Which pattern of inflammation is most characteristic of a viral infection such as hepatitis?

  1. Mononuclear infiltrate with lymphocytes and macrophages Correct answer.
  2. Neutrophilic infiltrate with abscess formation
  3. Eosinophil-rich infiltrate with Charcot-Leyden crystals
  4. Granulomatous infiltrate with caseation

Explanation

Viral infections typically evoke a mononuclear infiltrate rich in lymphocytes and macrophages, reflecting cell-mediated immune responses. Neutrophils dominate pyogenic bacterial infections, eosinophils dominate parasitic and allergic responses, and caseating granulomas indicate tuberculosis. The predominant cell type helps classify the inflammatory stimulus.

Question 40General Pathology (inflammation, repair, regeneration, and wound healing)

Which statement best describes a granuloma?

  1. A collection of neutrophils surrounding necrotic tissue
  2. A proliferation of plasma cells in lymphoid tissue
  3. A collection of activated macrophages often with multinucleated giant cells Correct answer.
  4. A localized accumulation of eosinophils and mast cells

Explanation

Granulomas are organized collections of activated macrophages (epithelioid cells), often with multinucleated giant cells and a rim of lymphocytes, formed in response to persistent antigens. They occur in tuberculosis, sarcoidosis and foreign body reactions. Neutrophilic, eosinophilic or plasmacytic aggregates do not define a granuloma.

Question 41General Pathology (inflammation, repair, regeneration, and wound healing)

In wound healing by primary intention, which event occurs first?

  1. Formation of a fibrin clot and hemostasis Correct answer.
  2. Remodeling of collagen to type I
  3. Wound contraction by myofibroblasts
  4. Deposition of type III collagen

Explanation

Healing begins with hemostasis, forming a fibrin clot that provides a scaffold and releases platelet-derived growth factors. Granulation tissue with type III collagen forms over the following days, contraction occurs later, and remodeling to type I collagen takes weeks to months. This sequence explains why clot formation is the earliest event.

Question 42General Pathology (inflammation, repair, regeneration, and wound healing)

Which collagen type predominates in mature, remodeled scar tissue?

  1. Type IV
  2. Type III
  3. Type I Correct answer.
  4. Type II

Explanation

Early granulation tissue contains type III collagen, which is progressively replaced by stronger type I collagen during remodeling. Type II is found in cartilage, and type IV is a component of basement membranes. The shift from type III to type I increases tensile strength of the scar.

Question 43General Pathology (inflammation, repair, regeneration, and wound healing)

A surgical wound in a healthy patient achieves approximately what proportion of its original tensile strength after several months?

  1. About 100 percent
  2. About 20 percent
  3. About 70 to 80 percent Correct answer.
  4. About 5 to 10 percent

Explanation

Wound strength rises rapidly over weeks and reaches roughly 70 to 80 percent of uninjured tissue by several months, but rarely returns fully to normal. Early strength is low because of the weak clot and granulation tissue. The residual deficit reflects the inferior organization of scar collagen.

Question 44General Pathology (inflammation, repair, regeneration, and wound healing)

Which factor most impairs wound healing by reducing collagen synthesis?

  1. Early mobilization
  2. Topical antibiotic use
  3. Mild postoperative anemia
  4. Chronic glucocorticoid therapy Correct answer.

Explanation

Glucocorticoids suppress inflammation and inhibit fibroblast proliferation and collagen synthesis, delaying healing and reducing wound strength. Topical antibiotics, mild anemia and early mobilization do not impair collagen deposition. This is why steroid-treated patients are at risk of wound dehiscence.

Question 45General Pathology (inflammation, repair, regeneration, and wound healing)

Which vitamin deficiency classically impairs hydroxylation of proline and lysine, causing defective collagen cross-linking and poor wound healing?

  1. Vitamin C Correct answer.
  2. Vitamin D
  3. Vitamin K
  4. Vitamin B12

Explanation

Vitamin C is a cofactor for prolyl and lysyl hydroxylase, and deficiency (scurvy) produces weak collagen and impaired wound healing. Vitamin K is required for clotting factors, B12 for DNA synthesis and myelin, and vitamin D for calcium homeostasis. Only vitamin C directly affects collagen hydroxylation.

Question 46General Pathology (inflammation, repair, regeneration, and wound healing)

A wound that reopens after abdominal surgery on the fifth postoperative day most likely reflects which underlying problem?

  1. Defective collagen synthesis or increased wound tension Correct answer.
  2. Overproduction of granulation tissue
  3. Excessive neutrophil recruitment
  4. Excess vitamin C intake

Explanation

Dehiscence in the first week occurs before collagen deposition has provided significant tensile strength, so poor collagen synthesis, malnutrition, steroids or excessive mechanical tension predispose to it. Neutrophil recruitment is part of normal healing, and excess granulation tissue produces proud flesh rather than dehiscence. Vitamin C excess does not weaken wounds.

Question 47General Pathology (inflammation, repair, regeneration, and wound healing)

Which process best describes regeneration rather than repair?

  1. Replacement of lost tissue by cells of the same type with restored function Correct answer.
  2. Replacement of lost tissue by fibrous scar
  3. Contraction of a wound by myofibroblasts
  4. Organization of an exudate into fibrous tissue

Explanation

Regeneration restores the original tissue architecture and function by proliferation of surviving parenchymal cells, as occurs in the liver and in healing skin epithelium. Repair replaces tissue with fibrous scar and does not restore specialized function. Scar organization and wound contraction are features of repair.

Question 48General Pathology (inflammation, repair, regeneration, and wound healing)

Which tissue has the greatest capacity for regeneration after injury?

  1. Hepatic parenchyma Correct answer.
  2. Central nervous system neurons
  3. Cardiac muscle
  4. Skeletal muscle

Explanation

The liver has high regenerative capacity, illustrated by restoration of hepatic mass after partial hepatectomy. Cardiac muscle and central neurons are essentially permanent tissues with minimal regenerative capacity, and skeletal muscle regenerates only limited and imperfectly through satellite cells. This hierarchy underlies why hepatic injury can resolve without scarring.

Question 49General Pathology (inflammation, repair, regeneration, and wound healing)

Which cell type is considered a stable (quiescent) cell that can re-enter the cell cycle after injury?

  1. Neuron
  2. Cardiomyocyte
  3. Hepatocyte Correct answer.
  4. Erythrocyte

Explanation

Stable cells such as hepatocytes and renal tubular cells normally rest in G0 but can proliferate after injury. Neurons and cardiomyocytes are permanent cells that cannot regenerate, and erythrocytes are terminally differentiated without a nucleus. This classification predicts regenerative potential.

Question 50General Pathology (inflammation, repair, regeneration, and wound healing)

Which growth factor is most strongly associated with angiogenesis during wound healing?

  1. Insulin-like growth factor 1
  2. Vascular endothelial growth factor Correct answer.
  3. Erythropoietin
  4. Interleukin-10

Explanation

Vascular endothelial growth factor, produced by macrophages, platelets and hypoxic cells, drives endothelial proliferation, migration and new vessel formation during granulation tissue development. Erythropoietin stimulates erythroid precursors, and IL-10 is anti-inflammatory. IGF-1 supports growth but is not the principal angiogenic signal.