Cytopathology — MCQs

A 7-year-old boy sustained an open compound fracture of the right tibia and fibula. On physical examination, the fractured bones are visible protruding from the skin wound. The fracture is managed with external manipulation and skin closure. One year later, he experiences persistent pain in the right leg and has developed a draining sinus tract in the lateral lower right leg. A radiograph of the lower right leg is most likely to show which of the following?

Q46Medium

Rapidly progressive glomerulonephritis can be associated with all of the following, except?

Q47Easy

Karyopyknotic index is a method for?

Q48Medium

How can a surgeon confirm intraoperatively that a resected margin of tissue does not contain suspicious tissue?

Q49Medium

Which cytological feature of necrotizing sialometaplasia most closely resembles?

Q50Easy

Birbeck granules in the cytoplasm are seen in which of the following cells?

Cytopathology Indian Medical PG Practice Questions and MCQs

Question 41: Which of the following is NOT a morphological feature of celiac disease?

A. Increase in intraepithelial lymphocytes
B. Increase in crypt:villous ratio
C. Distended macrophages with PAS positive granules in lamina propria (Correct Answer)
D. Elongated hyperplastic and tortuous crypts

Explanation: **Explanation:** The correct answer is **C**. Distended macrophages with PAS-positive, diastase-resistant granules in the lamina propria are the hallmark histological feature of **Whipple’s Disease** (caused by *Tropheryma whipplei*), not Celiac disease [1]. In Celiac disease, the lamina propria typically shows an increase in plasma cells and lymphocytes, but not PAS-positive macrophages. **Analysis of other options (Features of Celiac Disease):** * **Option A:** An increase in **intraepithelial lymphocytes (IELs)**, specifically >25 per 100 epithelial cells, is the earliest and most sensitive histological marker of Celiac disease (Marsh Grade 1) [2]. * **Option B & D:** Celiac disease is characterized by **villous atrophy** and compensatory **crypt hyperplasia** [2]. In a healthy small intestine, the villous-to-crypt ratio is 3:1 or 4:1. In Celiac disease, this ratio increases (e.g., 1:1) as crypts become elongated, tortuous, and hyperplastic to replace damaged surface enterocytes [2]. **NEET-PG High-Yield Pearls:** * **Marsh Classification:** Used to grade Celiac disease severity (Stage 0: Normal; Stage 3: Villous atrophy). * **Gold Standard Diagnosis:** Duodenal biopsy (usually multiple samples from the second part of the duodenum/bulb). * **Serology:** Anti-tissue Transglutaminase (anti-tTG) IgA is the screening test of choice; Anti-endomysial antibody (EMA) is the most specific [3]. * **Genetics:** Strongly associated with **HLA-DQ2** (95%) and **HLA-DQ8** [3]. * **Complications:** Increased risk of Enteropathy-associated T-cell lymphoma (EATL) and Small bowel adenocarcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 798-799. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 789-790. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 360-361.

Question 42: What is the normal cytoplasm-to-nucleus ratio?

A. 1:1
B. 1:4
C. 6:1 (Correct Answer)
D. 3:1

Explanation: ### Explanation In cytopathology, the **Nucleus-to-Cytoplasm (N:C) ratio** is a critical diagnostic parameter used to differentiate between normal, reactive, and malignant cells. **Why 6:1 is Correct:** In a healthy, mature cell (such as a superficial squamous cell), the cytoplasm is abundant compared to the size of the nucleus. The standard **Cytoplasm-to-Nucleus ratio** is approximately **6:1**. This indicates that the cytoplasmic volume is significantly larger than the nuclear volume, reflecting a state of cellular maturity and metabolic stability. **Analysis of Incorrect Options:** * **A (1:1) and B (1:4):** These ratios represent a "High N:C ratio." A 1:1 ratio (where the nucleus occupies half the cell) or a 1:4 ratio (where the nucleus dominates) is a hallmark of **malignancy** or extreme immaturity (e.g., blast cells). In cancer, the nucleus enlarges due to increased DNA content and rapid division, while the cytoplasm diminishes. * **D (3:1):** While this shows more cytoplasm than the nucleus, it is still considered a "decreased" ratio compared to normal mature cells. This may be seen in dysplastic cells or lower-level maturation stages (like parabasal cells). **High-Yield Clinical Pearls for NEET-PG:** * **N:C Ratio vs. C:N Ratio:** Always read the question carefully. Most textbooks refer to the **N:C ratio**, which is normally **1:4 to 1:6**. If the question asks for the **Cytoplasm-to-Nucleus ratio**, the numbers are reversed (**4:1 to 6:1**). * **Malignancy Criteria:** An increased N:C ratio is one of the most reliable morphological indicators of malignancy, alongside nuclear pleomorphism, hyperchromasia, and irregular nuclear membranes. * **Exception:** Small cell carcinomas and lymphomas typically exhibit the highest N:C ratios, often appearing as "naked nuclei" with barely visible rims of cytoplasm.

Question 43: A 35-year-old female presents with a lump in the anterior triangle of the neck. What is true about Fine Needle Aspiration Cytology (FNAC)?

A. FNAC can diagnose follicular carcinoma.
B. FNAC can diagnose papillary carcinoma. (Correct Answer)
C. Presence of follicular cells indicates follicular carcinoma.
D. FNAC can differentiate follicular carcinoma and adenoma.

Explanation: **Explanation:** The core principle of Fine Needle Aspiration Cytology (FNAC) is the evaluation of **cytological (cellular) features** rather than architectural patterns. [1] **Why Option B is Correct:** Papillary Thyroid Carcinoma (PTC) is diagnosed based on characteristic nuclear features that are easily visible on a smear [1], [2]. These include **Orphan Annie eye nuclei** (clearing), **nuclear grooves**, and **intranuclear pseudoinclusions** [1]. Since these are cellular details, FNAC is highly sensitive and specific for diagnosing PTC [1]. **Why Other Options are Incorrect:** * **Options A & D:** The differentiation between a **Follicular Adenoma** and **Follicular Carcinoma** depends entirely on **architectural evidence**—specifically the presence of capsular or vascular invasion [3]. FNAC only samples cells and cannot visualize the intact capsule or vessel walls. Therefore, FNAC can only suggest a "Follicular Neoplasm," but histopathology (biopsy) is required for a definitive diagnosis of carcinoma. * **Option C:** The presence of follicular cells is a common finding in many conditions, including a normal thyroid, multinodular goiter, or adenomas. It is not pathognomonic for malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **Bethesda System:** Used for reporting thyroid cytopathology (Category IV is "Suspicious for Follicular Neoplasm"). * **Psammoma Bodies:** Often seen in FNAC smears of Papillary Carcinoma (concentric calcifications). * **Limitation of FNAC:** It cannot reliably distinguish between Hürthle cell adenoma and carcinoma for the same reasons as follicular lesions. * **Medullary Carcinoma:** Can be diagnosed via FNAC by identifying spindle-shaped cells and confirming with **Congo Red stain** for amyloid [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1099. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 429-430. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1099-1100. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103.

Question 44: Which of the following is NOT a feature of Minimal Change Disease?

A. Good response to steroids
B. Effacement of podocytes on electron microscope, normal on light microscope
C. Nil deposit disease
D. NSAIDs are a primary cause (Correct Answer)

Explanation: **Explanation:** Minimal Change Disease (MCD) is the most common cause of nephrotic syndrome in children [1]. Understanding its pathogenesis and clinical features is crucial for NEET-PG. **Why Option D is the correct answer:** While NSAIDs are indeed associated with MCD, they are considered a **secondary cause**, not a primary (idiopathic) cause. Primary MCD is typically idiopathic, often linked to T-cell dysfunction and the release of glomerular permeability factors. Secondary causes include drugs (NSAIDs, Lithium), malignancies (Hodgkin Lymphoma), and allergies. **Analysis of other options:** * **Option A (Good response to steroids):** This is a hallmark of MCD. Over 90% of children show a dramatic response to corticosteroid therapy [1], which is a key diagnostic and therapeutic feature. * **Option B (Morphology):** MCD is characterized by a "minimal" change. Under **Light Microscopy**, the glomeruli appear completely **normal**. However, **Electron Microscopy** reveals the diagnostic feature: **diffuse effacement (fusion) of podocyte foot processes** [1]. * **Option C (Nil deposit disease):** This is an alternative name for MCD because **Immunofluorescence (IF)** shows no significant deposits of immunoglobulins or complement (Negative/Nil deposits) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common presentation:** Sudden onset of heavy proteinuria (selective proteinuria, mainly albumin) [1]. * **Pathogenesis:** Loss of the glomerular polyanionic charge (heparan sulfate), leading to albumin leakage. * **Lipiduria:** "Maltese cross" appearance under polarized light due to cholesterol esters in urine. * **Prognosis:** Excellent in children; however, adults may take longer to respond to steroids and have a higher rate of relapse [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 922-928.

Question 45: A 7-year-old boy sustained an open compound fracture of the right tibia and fibula. On physical examination, the fractured bones are visible protruding from the skin wound. The fracture is managed with external manipulation and skin closure. One year later, he experiences persistent pain in the right leg and has developed a draining sinus tract in the lateral lower right leg. A radiograph of the lower right leg is most likely to show which of the following?

A. Cortical nidus with surrounding sclerosis
B. Involucrum and sequestrum (Correct Answer)
C. Osteolysis with osteosclerosis
D. Soft-tissue hemorrhage and swelling

Explanation: ### Explanation **Correct Answer: B. Involucrum and sequestrum** The clinical presentation describes a classic case of **Chronic Osteomyelitis** following an open fracture. Open fractures are highly susceptible to bacterial contamination (most commonly *Staphylococcus aureus*). When the infection becomes chronic, the following pathological hallmarks occur: 1. **Sequestrum:** Increased intraosseous pressure and inflammation lead to ischemia, causing a segment of bone to die. This necrotic bone is called a sequestrum [1]. 2. **Involucrum:** The periosteum is lifted by pus, but remains viable. It begins depositing new bone around the dead bone, forming a reactive sheath called the involucrum [1]. 3. **Sinus Tract:** The persistent infection often finds a path to the skin surface (cloaca), resulting in a draining sinus tract, as seen in this patient. **Analysis of Incorrect Options:** * **A. Cortical nidus with surrounding sclerosis:** This is the radiographic hallmark of **Osteoid Osteoma**, a benign bone tumor characterized by nocturnal pain relieved by aspirin. It is not associated with trauma or sinus tracts. * **C. Osteolysis with osteosclerosis:** While these features can be seen in various bone pathologies (like Paget’s disease or certain metastases), they lack the specific structural hallmarks (sequestrum/involucrum) diagnostic of chronic osteomyelitis. * **D. Soft-tissue hemorrhage and swelling:** These are acute findings seen immediately after a fracture. They would not persist for one year nor explain a draining sinus tract. **NEET-PG High-Yield Pearls:** * **Most common organism:** *Staphylococcus aureus* (overall); *Salmonella* (in Sickle Cell patients); *Pseudomonas* (in IV drug users or puncture wounds through sneakers). * **Brodie’s Abscess:** A localized form of subacute/chronic osteomyelitis, typically appearing as a radiolucent lesion in the metaphysis surrounded by reactive sclerosis [1]. * **Complication:** Long-standing chronic osteomyelitis with a draining sinus tract carries a risk of developing **Squamous Cell Carcinoma** (Marjolin’s ulcer) at the sinus site. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1197-1198.

Question 46: Rapidly progressive glomerulonephritis can be associated with all of the following, except?

A. Goodpasture syndrome
B. Lupus nephritis
C. Diabetic nephropathy (Correct Answer)
D. Post-infectious glomerulonephritis

Explanation: **Explanation:** Rapidly Progressive Glomerulonephritis (RPGN) is a clinical syndrome characterized by a rapid decline in renal function (usually a 50% decline in GFR within 3 months) and the histological hallmark of **crescent formation** in the majority of glomeruli [1]. **Why Diabetic Nephropathy is the correct answer:** Diabetic nephropathy is a **non-inflammatory, chronic, and slowly progressive** microvascular complication of diabetes. Histologically, it is characterized by glomerular basement membrane thickening, mesangial expansion, and **Kimmelstiel-Wilson (nodular glomerulosclerosis) lesions**, rather than the acute inflammatory crescentic changes seen in RPGN. **Analysis of Incorrect Options:** * **Goodpasture Syndrome (Type I RPGN):** Caused by anti-GBM antibodies. It presents with linear IgG deposits and is a classic cause of RPGN [2]. * **Lupus Nephritis (Type II RPGN):** Specifically Class IV (Diffuse Proliferative GN), which is immune-complex mediated and can frequently present with a crescentic, rapidly progressive course [1]. * **Post-infectious GN (Type II RPGN):** While most cases resolve, a small percentage of patients (especially adults) develop severe inflammation leading to crescent formation and RPGN [2], [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Classification of RPGN:** * **Type I:** Anti-GBM (e.g., Goodpasture). * **Type II:** Immune Complex (e.g., SLE, PSGN, Henoch-Schönlein Purpura). * **Type III:** Pauci-immune (e.g., Wegener’s/GPA, Microscopic Polyangiitis) – associated with ANCA [3]. * **Crescent Composition:** Formed by the proliferation of **parietal epithelial cells** and the migration of **monocytes/macrophages** into Bowman’s space, triggered by fibrin leakage [1]. * **Most common cause of RPGN overall:** Type III (Pauci-immune) [1], [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 528-529. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 916-917.

Question 47: Karyopyknotic index is a method for?

A. Ovarian carcinoma
B. Hormonal evaluation (Correct Answer)
C. Dysplasia measurement
D. Measurement of cells in active replication

Explanation: **Explanation:** The **Karyopyknotic Index (KPI)** is a cyto-hormonal evaluation tool used primarily in vaginal cytology. It measures the percentage of **superficial squamous cells** (cells with small, shrunken, dense "pyknotic" nuclei) compared to intermediate cells in a lateral vaginal wall smear [2]. **1. Why Hormonal Evaluation is Correct:** The maturation of the vaginal epithelium is directly influenced by steroid hormones. **Estrogen** promotes full maturation, leading to an increase in superficial cells with pyknotic nuclei [2]. Therefore, a high KPI indicates high estrogenic activity. Conversely, **Progesterone** causes maturation to stop at the intermediate cell stage [3]. By calculating the ratio of these cells, clinicians can assess the hormonal status of a patient (e.g., evaluating menopause, primary amenorrhea, or threatened abortion). **2. Why Other Options are Incorrect:** * **Ovarian Carcinoma:** While some functional ovarian tumors secrete hormones that alter the KPI, the index itself is a measure of hormonal effect, not a diagnostic tool for malignancy. * **Dysplasia Measurement:** Dysplasia is assessed using the Bethesda System (LSIL/HSIL) based on nuclear-to-cytoplasmic ratios and chromatin patterns, not the KPI [1], [2]. * **Cells in Active Replication:** This is typically measured using flow cytometry (S-phase fraction) or immunohistochemical markers like **Ki-67** [1]. **Clinical Pearls for NEET-PG:** * **Maturation Index (MI):** Expressed as a ratio of Parabasal: Intermediate: Superficial cells (e.g., 0/40/60). * **Estrogen Effect:** Shifts the MI to the **right** (increased superficial cells). * **Progesterone/Pregnancy Effect:** Shifts the MI to the **middle** (increased intermediate cells/Navicular cells). * **Atrophy (Post-menopause):** Shifts the MI to the **left** (increased parabasal cells). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1007-1008. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, p. 1010. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1011-1012.

Question 48: How can a surgeon confirm intraoperatively that a resected margin of tissue does not contain suspicious tissue?

A. Punch biopsy
B. Brush biopsy
C. Frozen section (Correct Answer)
D. Exfoliative cytology

Explanation: **Explanation:** The primary goal of intraoperative consultation is to provide a rapid diagnosis that influences immediate surgical management. **Why Frozen Section is correct:** The **Frozen Section** is the gold standard for intraoperative diagnosis [1]. It involves rapidly freezing the tissue specimen (usually using a cryostat at -20°C to -30°C), which hardens the tissue enough to be sliced into thin sections without the lengthy process of formalin fixation and paraffin embedding [1]. This allows a pathologist to provide a diagnosis within 15–20 minutes, enabling the surgeon to confirm **negative margins** (ensuring no residual tumor remains) or identify unknown lesions before closing the patient [1]. **Why other options are incorrect:** * **Punch Biopsy:** This is a diagnostic procedure used primarily in dermatology to obtain a full-thickness core of skin. It requires routine histopathology (FFPE), which takes 24–48 hours. * **Brush Biopsy:** A form of abrasive cytology used to collect cells from mucous membranes (e.g., bronchus or esophagus). It provides cytological detail but cannot assess tissue architecture or margin status [1]. * **Exfoliative Cytology:** This involves examining cells shed naturally (e.g., Pap smear) or scraped from surfaces [1]. Like brush biopsy, it lacks the architectural context required to confirm a "clear margin." **NEET-PG High-Yield Pearls:** * **Indications for Frozen Section:** Margin assessment, identifying unknown lesions, and confirming if sampled tissue (e.g., a lymph node) is representative. * **Contraindications:** Never used for calcified tissues (bone), heavily fatty tissues (breast margins can be difficult), or when a definitive diagnosis requires immunohistochemistry (IHC). * **Common Stain:** Rapid H&E or Toluidine Blue is typically used for frozen sections. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 25-26, 231-232.

Question 49: Which cytological feature of necrotizing sialometaplasia most closely resembles?

A. Pleomorphic adenoma
B. Mucoepidermoid carcinoma (Correct Answer)
C. Warthin's tumor
D. Adenoid cystic carcinoma

Explanation: **Explanation:** **Necrotizing Sialometaplasia (NS)** is a benign, self-limiting inflammatory condition of the salivary glands (most commonly the hard palate) that clinically and microscopically mimics malignancy. **Why Mucoepidermoid Carcinoma (MEC) is the correct answer:** The hallmark of NS is **squamous metaplasia** of the salivary acini and ducts. On cytology, this presents as clusters of atypical squamous cells and reactive ductal cells. Because NS involves tissue infarction and inflammation, the background often contains **mucin** (from ruptured ducts) and inflammatory debris. This combination of **squamous cells, mucinous material, and mild nuclear atypia** closely mimics the cytological triad of **Mucoepidermoid Carcinoma**, leading to frequent false-positive diagnoses of malignancy [1]. **Why other options are incorrect:** * **Pleomorphic Adenoma:** Characterized by a biphasic pattern of epithelial cells and a characteristic **fibrillar, chondromyxoid stroma** [1]. NS lacks this specific mesenchymal-like stroma. * **Warthin’s Tumor:** Shows a distinct pattern of **oncocytes** (granular cytoplasm) and a dense background of small lymphocytes [1]. * **Adenoid Cystic Carcinoma:** Defined by highly cohesive "basaloid" cells forming **hyaline globules** (cylindromatous pattern), which are not a feature of the squamous metaplasia seen in NS [1]. **NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Typically presents as a "deep, painless crater-like ulcer" on the hard palate. * **Pathogenesis:** Ischemic necrosis of salivary gland lobules (often post-trauma or local anesthesia). * **Key Histology:** Preservation of the **lobular architecture** despite necrosis (a vital clue to distinguish it from SCC or MEC). * **Management:** Spontaneous healing in 6–8 weeks; biopsy is essential to rule out malignancy, but overdiagnosis must be avoided. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 751-755.

Question 50: Birbeck granules in the cytoplasm are seen in which of the following cells?

A. Mast cells
B. Langerhans cells (Correct Answer)
C. Thrombocytes
D. Myelocytes

Explanation: **Explanation:** **Birbeck granules** are the pathognomonic ultrastructural hallmark of **Langerhans cells** [1]. These are specialized dendritic cells (antigen-presenting cells) primarily found in the stratum spinosum of the epidermis. On electron microscopy, Birbeck granules appear as rod-shaped, pentalaminar cytoplasmic organelles with a central striated line and a bulbous end, giving them a classic **"tennis racket" appearance** [1]. They are composed of **Langerin (CD207)**, a protein involved in the endocytosis of pathogens [1]. **Analysis of Options:** * **Mast cells (A):** Characterized by dense, membrane-bound granules containing histamine, heparin, and ECF-A. On electron microscopy, these granules often show a "scroll-like" or "whorled" pattern. * **Thrombocytes (C):** Contain alpha-granules (containing fibrinogen, vWF) and dense granules (containing ADP, ATP, Calcium, Serotonin), but do not possess Birbeck granules. * **Myelocytes (D):** These are precursors in the granulocytic series (neutrophils, eosinophils, basophils) and contain primary (azurophilic) and secondary (specific) granules. **High-Yield Clinical Pearls for NEET-PG:** * **Langerhans Cell Histiocytosis (LCH):** A group of disorders (e.g., Letterer-Siwe disease, Hand-Schüller-Christian disease) characterized by the proliferation of these cells [1]. * **Immunohistochemistry (IHC) Markers:** Langerhans cells are positive for **S-100**, **CD1a**, and **Langerin (CD207)** [1]. * **Function:** They capture antigens and migrate to regional lymph nodes to present them to T-lymphocytes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 630.

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Basic Principles of Cytopathology

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Specimen Collection and Processing

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Urinary Tract Cytology

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Effusion Cytology

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Fine Needle Aspiration Cytology

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Gastrointestinal Tract Cytology

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