A 32-year-old woman presents with amenorrhea and galactorrhea. MRI shows a pituitary adenoma. Histological examination of the surgical specimen shows cells arranged in cords and nests with sinusoidal capillaries. Special staining reveals three distinct cell types: chromophobes (50%), acidophils (40%), and basophils (10%). Immunohistochemistry shows the tumor cells staining strongly for prolactin. Evaluate the relationship between normal pituitary architecture and tumor development to determine which cell type most likely gave rise to this neoplasm.
Q2
A 65-year-old man with progressive shortness of breath undergoes transbronchial biopsy. Microscopy shows thickened alveolar septa with increased collagen deposition. Type I pneumocytes are decreased, and there is proliferation of type II pneumocytes. Alveolar macrophages are present. The patient has a history of environmental asbestos exposure 30 years ago. Evaluate the histological progression and synthesize the most likely diagnosis considering the temporal relationship and cellular changes.
Q3
A 40-year-old woman presents with difficulty swallowing. Esophageal biopsy shows non-keratinized stratified squamous epithelium in the upper two-thirds and columnar epithelium with goblet cells in the lower third. Submucosal glands are present throughout. Evaluate these findings and synthesize a diagnosis considering the clinical significance of the epithelial transition zone.
Q4
A 50-year-old man with chronic pancreatitis undergoes pancreatic biopsy. Microscopy shows distinct acinar cells with basophilic basal cytoplasm and eosinophilic apical zymogen granules. Scattered among the acini are pale-staining clusters of cells with few granules and rich capillary networks. Immunostaining reveals insulin, glucagon, somatostatin, and pancreatic polypeptide in different cells within these clusters. Analyze the microarchitecture and predict which histological feature best explains the systemic effects of a tumor arising from these clusters?
Q5
A 35-year-old woman with hyperthyroidism undergoes thyroid biopsy. Microscopy shows follicles of varying sizes lined by cuboidal epithelium. The follicular lumens contain eosinophilic colloid material. In her condition, the follicular cells have become columnar with scalloped colloid borders and decreased colloid content. Analyze these changes and determine which cellular process is most enhanced?
Q6
A 70-year-old man with progressive dyspnea undergoes lung biopsy. Microscopy reveals cuboidal cells lining the alveolar septae, interspersed with very thin squamous cells. The cuboidal cells contain lamellar bodies on electron microscopy and stain positive for surfactant proteins. Analyze the relationship between these cell types and predict what would occur if the cuboidal cells were selectively damaged?
Q7
A 55-year-old man with chronic kidney disease undergoes renal biopsy. Microscopy shows the glomerulus with a specialized capillary network. Between the capillary endothelium and the visceral epithelial cells (podocytes), a thick basement membrane is visible. The podocytes have interdigitating foot processes creating filtration slits. Apply this structural knowledge to determine which component would be most affected in minimal change disease?
Q8
A 28-year-old woman presents with amenorrhea. Ovarian biopsy reveals primordial follicles consisting of primary oocytes arrested in prophase of meiosis I, surrounded by a single layer of flattened follicular cells. Under hormonal stimulation, these cells will transform. Apply your knowledge to identify what these follicular cells become during follicular development.
Q9
A 62-year-old man with a history of chronic hepatitis C infection undergoes liver biopsy. Microscopy shows plates of hepatocytes separated by sinusoids lined with fenestrated endothelium. Between the hepatocytes and sinusoidal endothelium, a space contains stellate-shaped cells with lipid droplets. Which cell type in this space is primarily responsible for hepatic fibrosis in chronic liver disease?
Q10
A 45-year-old woman undergoes endoscopic biopsy for evaluation of chronic dyspepsia. Microscopy reveals glands lined by tall columnar cells with basally located nuclei and apical mucin granules, along with deep invaginations forming gastric pits. Scattered parietal cells with eosinophilic cytoplasm are noted. Which region of the gastrointestinal tract was most likely biopsied?
Organ-specific histology US Medical PG Practice Questions and MCQs
Question 1: A 32-year-old woman presents with amenorrhea and galactorrhea. MRI shows a pituitary adenoma. Histological examination of the surgical specimen shows cells arranged in cords and nests with sinusoidal capillaries. Special staining reveals three distinct cell types: chromophobes (50%), acidophils (40%), and basophils (10%). Immunohistochemistry shows the tumor cells staining strongly for prolactin. Evaluate the relationship between normal pituitary architecture and tumor development to determine which cell type most likely gave rise to this neoplasm.
A. Somatotrophs (acidophils producing growth hormone)
B. Lactotrophs (acidophils producing prolactin) (Correct Answer)
C. Corticotrophs (basophils producing ACTH)
D. Gonadotrophs (basophils producing FSH/LH)
E. Chromophobes (null cells with no secretory granules)
Explanation: ***Lactotrophs (acidophils producing prolactin)***
- These cells are classified as **acidophils** based on their staining characteristics and are responsible for the secretion of **prolactin**, consistent with the patient's **amenorrhea** and **galactorrhea**.
- Although the tumor specimen contains various cell types, the **immunohistostaining** specifically identifying **prolactin** confirms these cells as the source of the neoplasm.
*Somatotrophs (acidophils producing growth hormone)*
- While these are also **acidophilic** cells, they secrete **Growth Hormone (GH)**, and a tumor of this type would present with **acromegaly** or gigantism rather than galactorrhea.
- They do not typically stain for **prolactin**, unless the tumor is a rare plurihormonal adenoma, which is not indicated here.
*Corticotrophs (basophils producing ACTH)*
- These cells are **basophils** and produce **ACTH**; an adenoma arising from them would lead to **Cushing's disease** due to hypercortisolism.
- Histologically, they would not correspond to the strong **prolactin** staining observed in this immunohistochemical evaluation.
*Gonadotrophs (basophils producing FSH/LH)*
- These are **basophilic** cells that produce **FSH** and **LH**, and tumors originating from them are usually non-functional or present with mass effects rather than hormonal excess.
- They are clinically and histologically distinct from **prolactin-producing** lactotrophs.
*Chromophobes (null cells with no secretory granules)*
- **Chromophobes** lack significant cytoplasmic staining due to a lack of hormone granules; they often represent cells that have depleted their secretory stores.
- While they occupy 50% of the specimen, the **strong prolactin staining** identifies the active neoplastic process as originating from the hormone-producing lineage.
Question 2: A 65-year-old man with progressive shortness of breath undergoes transbronchial biopsy. Microscopy shows thickened alveolar septa with increased collagen deposition. Type I pneumocytes are decreased, and there is proliferation of type II pneumocytes. Alveolar macrophages are present. The patient has a history of environmental asbestos exposure 30 years ago. Evaluate the histological progression and synthesize the most likely diagnosis considering the temporal relationship and cellular changes.
A. Chronic hypersensitivity pneumonitis with granulomas
B. Idiopathic pulmonary fibrosis with usual interstitial pneumonia pattern
C. Asbestosis with interstitial fibrosis and ferruginous bodies (Correct Answer)
D. Sarcoidosis with non-caseating granulomas
E. Acute respiratory distress syndrome with diffuse alveolar damage
Explanation: ***Asbestosis with interstitial fibrosis and ferruginous bodies***
- The histological findings of **thickened alveolar septa**, **type I pneumocyte loss**, and **type II pneumocyte hyperplasia** characterize chronic **interstitial fibrosis** consistent with **asbestosis** in the context of exposure.
- Asbestos fibers are ingested by **alveolar macrophages**, triggering a fibrogenic response that typically manifests after a **latency period** of 20 to 30 years.
*Chronic hypersensitivity pneumonitis with granulomas*
- This condition is an immunologic reaction to inhaled organic antigens, characterized by **poorly formed non-caseating granulomas**.
- While it causes **interstitial fibrosis**, it lacks the specific association with **asbestos exposure** and the long-term temporal progression described.
*Idiopathic pulmonary fibrosis with usual interstitial pneumonia pattern*
- **IPF** presents with a **Usual Interstitial Pneumonia (UIP)** pattern, featuring **fibroblastic foci** and **honeycombing** with temporal heterogeneity.
- While similar in appearance, this diagnosis is reserved for cases of **unknown etiology** where occupational exposures like asbestos are absent.
*Sarcoidosis with non-caseating granulomas*
- **Sarcoidosis** typically presents with **well-formed non-caseating granulomas** distributed along **lymphatic pathways** and bronchovascular bundles.
- It is a systemic disease that primarily affects **hilar lymph nodes**, which is not the pathology described in this biopsy.
*Acute respiratory distress syndrome with diffuse alveolar damage*
- **ARDS** is characterized by an acute onset with **hyaline membranes** lining the alveolar spaces during the **diffuse alveolar damage (DAD)** phase.
- The scenario describes a **chronic, progressive** clinical course rather than the acute, critical illness seen in respiratory failure.
Question 3: A 40-year-old woman presents with difficulty swallowing. Esophageal biopsy shows non-keratinized stratified squamous epithelium in the upper two-thirds and columnar epithelium with goblet cells in the lower third. Submucosal glands are present throughout. Evaluate these findings and synthesize a diagnosis considering the clinical significance of the epithelial transition zone.
A. Normal histological finding representing the gastroesophageal junction
B. Barrett esophagus with intestinal metaplasia requiring surveillance (Correct Answer)
C. Esophageal stricture with squamous hyperplasia
D. Normal columnar epithelium of the lower esophageal sphincter
E. Eosinophilic esophagitis with epithelial transformation
Explanation: ***Barrett esophagus with intestinal metaplasia requiring surveillance***
- The presence of **columnar epithelium** with **goblet cells** (specialized intestinal metaplasia) replaces the normal squamous lining in the lower esophagus, which is the hallmark of **Barrett esophagus**.
- This condition is a **premalignant change** resulting from chronic **GERD** and carries an increased risk for **esophageal adenocarcinoma**, necessitating regular endoscopic surveillance.
*Normal histological finding representing the gastroesophageal junction*
- Normal esophageal histology consists entirely of **non-keratinized stratified squamous epithelium**; any columnar lining with goblet cells above the junction is abnormal.
- While the **Z-line** is the transition point, the biopsy describes this change within the **esophagus** itself (distinguished by esophageal submucosal glands), indicating pathology.
*Esophageal stricture with squamous hyperplasia*
- **Squamous hyperplasia** involves an increase in the thickness of the squamous layer, not a complete transformation into **columnar epithelium**.
- While **strictures** can cause difficulty swallowing, they are a physical narrowing and do not explain the histological finding of **goblet cells**.
*Normal columnar epithelium of the lower esophageal sphincter*
- The **lower esophageal sphincter** region is anatomically part of the esophagus and should be lined by **squamous epithelium**, not columnar cells with intestinal features.
- **Goblet cells** are never a normal component of the esophageal lining and always signify **intestinal metaplasia**.
*Eosinophilic esophagitis with epithelial transformation*
- **Eosinophilic esophagitis** is characterized by dense **eosinophilic infiltration** (>15 per HPF) and clinical features like **food impaction**.
- It typically presents with **stacked rings** or linear furrows on endoscopy and does not involve **metaplastic columnar transformation**.
Question 4: A 50-year-old man with chronic pancreatitis undergoes pancreatic biopsy. Microscopy shows distinct acinar cells with basophilic basal cytoplasm and eosinophilic apical zymogen granules. Scattered among the acini are pale-staining clusters of cells with few granules and rich capillary networks. Immunostaining reveals insulin, glucagon, somatostatin, and pancreatic polypeptide in different cells within these clusters. Analyze the microarchitecture and predict which histological feature best explains the systemic effects of a tumor arising from these clusters?
A. Lymphatic drainage to regional nodes for hormone distribution
B. Autonomic nerve fiber density for neurocrine release
C. Direct connection to pancreatic ducts for hormone delivery
D. Rich fenestrated capillary network allowing direct hormone entry to bloodstream (Correct Answer)
E. Gap junctions with acinar cells for paracrine signaling
Explanation: ***Rich fenestrated capillary network allowing direct hormone entry to bloodstream***
- The pale-staining clusters described are **Islets of Langerhans**, which are **endocrine** structures characterized by a dense network of **fenestrated capillaries** for rapid hormone delivery.
- Unlike exocrine glands, endocrine tumors (pancreatic neuroendocrine tumors) utilize this **vascular proximity** to release hormones directly into the systemic circulation, leading to immediate **systemic effects**.
*Lymphatic drainage to regional nodes for hormone distribution*
- While lymphatics are crucial for tumor **metastasis**, they are not the primary route for physiological or pathological **hormone secretion** into the general circulation.
- Hormone distribution relies primarily on the **fenestrated venous system** to reach target organs like the liver and muscle quickly.
*Autonomic nerve fiber density for neurocrine release*
- Autonomic fibers regulate the **rate of secretion** from islet cells but do not serve as the medium for **systemic transport** of the hormones.
- The term **neurocrine** refers to localized signaling, whereas systemic effects of tumors like **insulinomas** or **gastrinomas** depend on blood-borne transport.
*Direct connection to pancreatic ducts for hormone delivery*
- Islet cells are **ductless** (endocrine); only the **exocrine acinar cells** discharge their secretions (enzymes) into the pancreatic ductal system.
- If hormones were released into the ducts, they would be **digested by proteases** or neutralized by bicarbonate before reaching the systemic circulation.
*Gap junctions with acinar cells for paracrine signaling*
- **Gap junctions** facilitate localized communication between adjacent cells (paracrine) but cannot account for **distal systemic symptoms** associated with endocrine tumors.
- This feature aids in coordinating **islet-acinar** interactions rather than the widespread metabolic changes seen in **neuroendocrine syndromes**.
Question 5: A 35-year-old woman with hyperthyroidism undergoes thyroid biopsy. Microscopy shows follicles of varying sizes lined by cuboidal epithelium. The follicular lumens contain eosinophilic colloid material. In her condition, the follicular cells have become columnar with scalloped colloid borders and decreased colloid content. Analyze these changes and determine which cellular process is most enhanced?
A. Follicular cell apoptosis
B. Parafollicular cell calcitonin secretion
C. Interfollicular fibrosis
D. Colloid synthesis and storage
E. Thyroglobulin endocytosis and hormone release (Correct Answer)
Explanation: ***Thyroglobulin endocytosis and hormone release***
- In hyperthyroidism (such as **Graves' disease**), high activity leads to **scalloped margins** of the colloid, which represent active **endocytic vacuoles** consuming thyroglobulin.
- Transition from cuboidal to **columnar epithelium** and decreased colloid volume indicate an enhanced rate of thyroid hormone secretion into the bloodstream.
*Follicular cell apoptosis*
- **Apoptosis** would lead to a decrease in cell number and glandular atrophy, whereas hyperthyroidism typically displays **hyperplasia** and hypertrophy.
- The histological signs of **scalloping** and increased cell height are markers of high metabolic activity, not programmed cell death.
*Parafollicular cell calcitonin secretion*
- **Parafollicular cells** (C-cells) are responsible for **calcitonin** production, which regulates calcium levels and is not directly involved in thyroxine (T4) hyperthyroidism.
- The description specifically mentions **follicular cell** morphology and changes in the **colloid**, which are unrelated to C-cell function.
*Interfollicular fibrosis*
- **Fibrosis** is a characteristic of chronic inflammatory conditions like **Riedel thyroiditis**, not the active secretory state of hyperthyroidism.
- Active hyperthyroidism typically shows **increased vascularity** and cellularity rather than the deposition of dense connective tissue.
*Colloid synthesis and storage*
- While synthesis occurs, the hallmark of this histological picture is the **rapid depletion** and utilization of colloid, rather than its accumulation.
- Inactive follicles or **hypothyroidism** typically show flattened cells and **distended lumens** due to excessive colloid storage.
Question 6: A 70-year-old man with progressive dyspnea undergoes lung biopsy. Microscopy reveals cuboidal cells lining the alveolar septae, interspersed with very thin squamous cells. The cuboidal cells contain lamellar bodies on electron microscopy and stain positive for surfactant proteins. Analyze the relationship between these cell types and predict what would occur if the cuboidal cells were selectively damaged?
A. Increased gas exchange efficiency due to thinner barrier
B. Alveolar collapse due to increased surface tension (Correct Answer)
C. Enhanced immune defense against pathogens
D. Accelerated regeneration of alveolar epithelium
E. Decreased capillary permeability
Explanation: ***Alveolar collapse due to increased surface tension***
- The cuboidal cells described are **Type II pneumocytes**, which are responsible for secreting **pulmonary surfactant** from their **lamellar bodies**.
- A deficiency in surfactant leads to high **surface tension** at the air-liquid interface of the alveoli, resulting in **atelectasis** (alveolar collapse) and decreased lung compliance.
*Increased gas exchange efficiency due to thinner barrier*
- Damage to **Type II pneumocytes** would actually impair gas exchange because these cells are the **progenitors** for **Type I pneumocytes**.
- Loss of these cells prevents the repair of the **blood-air barrier**, eventually leading to fibrosis or persistent alveolar damage rather than a more efficient barrier.
*Enhanced immune defense against pathogens*
- **Type II pneumocytes** play a positive role in innate immunity by secreting **collectins** (surfactant proteins A and D) that aggregate pathogens.
- Selective damage to these cells would **compromise immune defense** in the lung, making the patient more susceptible to infections.
*Accelerated regeneration of alveolar epithelium*
- **Type II pneumocytes** act as the **stem cells** of the alveolar epithelium; they proliferate and differentiate into **Type I pneumocytes** after lung injury.
- If these cells are damaged, the **regenerative capacity** of the alveoli is lost, often leading to **interstitial fibrosis** instead of healthy epithelial repair.
*Decreased capillary permeability*
- Damage to the alveolar epithelium typically causes **increased permeability** due to the loss of the epithelial barrier and the subsequent inflammatory response.
- This increase in permeability allows fluid to leak into the alveolar space, further worsening the **pulmonary edema** associated with surfactant loss.
Question 7: A 55-year-old man with chronic kidney disease undergoes renal biopsy. Microscopy shows the glomerulus with a specialized capillary network. Between the capillary endothelium and the visceral epithelial cells (podocytes), a thick basement membrane is visible. The podocytes have interdigitating foot processes creating filtration slits. Apply this structural knowledge to determine which component would be most affected in minimal change disease?
A. Glomerular basement membrane thickness
B. Mesangial cell proliferation
C. Podocyte foot process effacement (Correct Answer)
D. Endothelial fenestration loss
E. Bowman's capsule rupture
Explanation: ***Podocyte foot process effacement***
- **Minimal change disease (MCD)** is specifically defined by the **effacement (fusion)** of the podocyte foot processes, which is only visible under **electron microscopy**.
- This structural damage disrupts the **slit diaphragm**, leading to a loss of the negative charge barrier and resulting in **massive selective proteinuria** (mainly albumin).
*Glomerular basement membrane thickness*
- The **glomerular basement membrane (GBM)** typically appearing normal under light microscopy is a hallmark of MCD, unlike **membranous nephropathy** where the GBM is thickened.
- MCD does not involve structural thickening or "splitting" of the basement membrane as seen in **Alport syndrome** or **MPGN**.
*Mesangial cell proliferation*
- **Mesangial hypercellularity** is absent in MCD, as the glomeruli appear completely **normal under light microscopy**.
- This feature is more characteristic of conditions like **IgA nephropathy** or **membranoproliferative glomerulonephritis**.
*Endothelial fenestration loss*
- While the **fenestrated endothelium** is the first layer of the filtration barrier, it remains intact in MCD.
- Endothelial damage or loss is more commonly associated with **thrombotic microangiopathies** or acute inflammatory states rather than primary nephrotic syndromes like MCD.
*Bowman's capsule rupture*
- **Bowman's capsule rupture** is a severe pathological finding typically associated with **crescentic (rapidly progressive) glomerulonephritis**.
- MCD is a non-inflammatory condition and does not cause the architectural destruction required to rupture the capsule or form **extracapillary crescents**.
Question 8: A 28-year-old woman presents with amenorrhea. Ovarian biopsy reveals primordial follicles consisting of primary oocytes arrested in prophase of meiosis I, surrounded by a single layer of flattened follicular cells. Under hormonal stimulation, these cells will transform. Apply your knowledge to identify what these follicular cells become during follicular development.
A. Theca interna cells
B. Theca externa cells
C. Granulosa cells (Correct Answer)
D. Corpus luteum cells
E. Stromal cells
Explanation: ***Granulosa cells***
- In the transition from a primordial to a primary follicle, the **flattened follicular cells** proliferate and become cuboidal **granulosa cells**.
- These cells develop **FSH receptors** and are essential for producing **estrogen** and supporting the maturation of the oocyte.
*Theca interna cells*
- These cells differentiate from the **ovarian stroma** outside the basal lamina during the secondary follicle stage, not from the original flattened follicular cells.
- They are highly vascularized and primarily responsible for secreting **androgens** (androstenedione) under the influence of **LH**.
*Theca externa cells*
- This layer is the outermost connective tissue capsule of the follicle and does not arise from the **primordial follicular cells**.
- It is composed mainly of **smooth muscle cells** and collagen, playing a role in follicular rupture during **ovulation**.
*Corpus luteum cells*
- These cells form from the remains of the **granulosa** and **theca interna** only after **ovulation** has occurred.
- While they represent a later stage, the question specifically asks what the flattened cells become during **follicular development** (the primary follicle stage).
*Stromal cells*
- **Stromal cells** are the connective tissue cells of the ovary that surround the follicles rather than being part of the initial follicular casing.
- They serve as the precursors to the **theca layers** but are distinct from the cells that directly surround the **primary oocyte** in a primordial follicle.
Question 9: A 62-year-old man with a history of chronic hepatitis C infection undergoes liver biopsy. Microscopy shows plates of hepatocytes separated by sinusoids lined with fenestrated endothelium. Between the hepatocytes and sinusoidal endothelium, a space contains stellate-shaped cells with lipid droplets. Which cell type in this space is primarily responsible for hepatic fibrosis in chronic liver disease?
A. Kupffer cells
B. Hepatic stellate cells (Correct Answer)
C. Sinusoidal endothelial cells
D. Pit cells
E. Cholangiocytes
Explanation: ***Hepatic stellate cells***
- Also known as **Ito cells**, these reside in the **space of Disse** and are the primary storage site for **vitamin A** (lipid droplets) in a healthy liver.
- Upon chronic injury (e.g., Hepatitis C), they activate into **myofibroblasts**, producing excessive **Type I collagen** and extracellular matrix, leading to **fibrosis**.
*Kupffer cells*
- These are specialized **macrophages** located within the hepatic sinusoids rather than the space of Disse.
- Their primary role is **phagocytosis** of debris and pathogens; while they secrete cytokines that activate stellate cells, they do not produce the collagen matrix.
*Sinusoidal endothelial cells*
- These cells form a **fenestrated lining** of the liver sinusoids, allowing for the exchange of materials between blood and hepatocytes.
- While they regulate blood flow and vascular tone, they are not the primary source of **fibrotic tissue** synthesis.
*Pit cells*
- These are liver-resident **Natural Killer (NK) cells** found inside the sinusoidal lumen.
- They provide **antitumor immunity** and defense against viral infections but have no structural role in **collagen deposition**.
*Cholangiocytes*
- These are epithelial cells that line the **bile ducts** and regulate the composition of bile.
- They are involved in **biliary pathologies** (like primary biliary cholangitis) but do not reside in the space of Disse or drive global hepatic **parenchymal fibrosis**.
Question 10: A 45-year-old woman undergoes endoscopic biopsy for evaluation of chronic dyspepsia. Microscopy reveals glands lined by tall columnar cells with basally located nuclei and apical mucin granules, along with deep invaginations forming gastric pits. Scattered parietal cells with eosinophilic cytoplasm are noted. Which region of the gastrointestinal tract was most likely biopsied?
A. Esophageal mucosa
B. Gastric fundus (Correct Answer)
C. Gastric antrum
D. Duodenal mucosa
E. Ileal mucosa
Explanation: ***Gastric fundus***
- The presence of **parietal cells** (large, eosinophilic cells) and **chief cells** within deep gastric pits is the hallmark of the **oxyntic mucosa** found in the fundus and body of the stomach.
- Tall columnar cells with apical **mucin granules** (foveolar cells) line the surface and pits, providing protection against the acidic environment produced by these glands.
*Esophageal mucosa*
- Normal esophageal lining consists of **non-keratinized stratified squamous epithelium**, which is structurally different from the glandular epithelium described.
- It lacks **gastric pits** and specialized acid-secreting **parietal cells** under physiological conditions.
*Gastric antrum*
- The **antrum** contains much shallower gastric pits and the glands are primarily composed of **mucus-secreting cells** and **G cells**.
- While a few **parietal cells** may be present, they are scattered and significantly less abundant compared to the fundic region.
*Duodenal mucosa*
- The duodenum is characterized by **villi**, **crypts of Lieberkühn**, and the presence of **Brunner's glands** in the submucosa.
- It contains **goblet cells** and **enterocytes** with a brush border, rather than the pure foveolar-parietal cell population seen in the stomach.
*Ileal mucosa*
- The ileum features **villi**, numerous **goblet cells**, and specialized lymphoid aggregates known as **Peyer's patches** in the lamina propria.
- It does not contain **parietal cells** or the specific glandular structure of the gastric **oxyntic mucosa**.
