100+ Free Facharzt FMH Pathologie Practice Questions

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2026 Statistics

Key Facts: Facharzt FMH Pathologie Exam

SGPath / SSPath

Exam Body

Swiss Society of Pathology

Practical + written + oral; pass 75%

Exam Format

SIWF Weiterbildungsprogramm 4.4/4.6

CHF 700 / 1'200

Exam Fee

SGPath Fee Schedule

EN written; DE/FR/IT oral

Official Languages

SIWF Weiterbildungsprogramm 4.5.5

5 Years

Residency Training

SIWF Pathologie Curriculum

100

Practice Bank Items

OpenExamPrep

The Facharzt FMH Pathologie confers independent diagnostic signing authority in histopathology and autopsy across Switzerland under SIWF and SGPath governance. The official examination is a practical slide and oral assessment (CHF 700 members / CHF 1'200 non-members). This bank provides 100 high-yield English-language MCQ practice items covering surgical pathology, cytopathology, IHC, and molecular diagnostics. Note: This is an English MCQ study adaptation, not an official exam simulation or clinical substitute.

Sample Facharzt FMH Pathologie Practice Questions

Try these sample questions to test your Facharzt FMH Pathologie exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 58-year-old man with a 15-year history of gastroesophageal reflux disease undergoes surveillance endoscopy for Barrett esophagus. Biopsies of salmon-colored columnar-lined mucosa show crowded glandular architecture, loss of nuclear polarity, marked nuclear pleomorphism with hyperchromasia extending to the mucosal surface, atypical mitotic figures near the luminal surface, and complete absence of surface maturation. Immunohistochemistry for p53 demonstrates strong, diffuse, unequivocal nuclear overexpression in 100% of the atypical epithelial cells. What is the most accurate pathological diagnosis according to current WHO classification criteria?

A.Barrett esophagus with high-grade dysplasia (HGD).

B.Barrett esophagus with low-grade dysplasia (LGD).

C.Barrett esophagus negative for dysplasia with florid reactive/regenerative atypia.

D.Intramucosal esophageal adenocarcinoma with submucosal invasion.

Explanation: High-grade dysplasia (HGD) in Barrett esophagus is characterized by marked architectural complexity, loss of cellular and nuclear polarity, full-thickness cytologic atypia extending to the epithelial surface, and prominent mitoses in upper crypts. Aberrant p53 expression (either complete absence / null-phenotype or diffuse strong 'block-like' overexpression in >80% of crypt cells) strongly supports the diagnosis of HGD. Interobserver reproducibility is highest when high-grade architectural distortion accompanies severe cytological atypia.

2An endoscopic mucosal resection (EMR) specimen from the distal esophagus reveals a 1.2 cm ulcerated lesion. Histology demonstrates sheets of malignant polygonal cells with abundant dense eosinophilic cytoplasm, prominent intercellular bridges, and focal keratin pearl formation infiltrating the lamina propria. Immunohistochemistry confirms diffuse strong positivity for p40 and cytokeratin 5/6, while CK7 and CDX2 are completely negative. How should this entity be diagnosed and distinguished from conventional distal esophageal adenocarcinoma?

A.Adenocarcinoma with squamous metaplasia; staged as pT1b.

B.Esophageal squamous cell carcinoma (SCC); distinguished by p40/CK5/6 positivity and keratinization.

C.Adenosquamous carcinoma of the gastroesophageal junction; driven by HER2 gene amplification.

D.Poorly differentiated neuroendocrine carcinoma (small cell type); confirmed by p40 expression.

Explanation: Squamous cell carcinoma (SCC) of the esophagus is characterized histologically by intercellular bridges, keratin pearl formation, and squamous differentiation. Immunohistochemically, SCC shows robust and diffuse expression of basal squamous markers including p40 (DeltaNp63) and CK5/6, with absence of glandular markers such as CK7 and CDX2. In contrast, esophageal adenocarcinoma is typically CK7 positive, CDX2 positive, and p40/CK5/6 negative.

3A total gastrectomy specimen from a 42-year-old woman with a family history of gastric cancer shows diffuse thickening and linitis plastica of the gastric corpus. Microscopic examination reveals non-cohesive, round-to-oval neoplastic cells diffusely infiltrating the muscularis propria as single cells and small loose clusters, with prominent intracytoplasmic mucin vacuoles displacing the nuclei peripherally (signet-ring cell morphology). Glandular/tubular formations are entirely absent. According to the Lauren classification and molecular pathology, which diagnosis and genetic alteration are most characteristic?

A.Intestinal-type gastric adenocarcinoma; associated with APC and TP53 mutations.

B.Gastric hepatoid adenocarcinoma; characterized by alpha-fetoprotein (AFP) secretion.

C.Diffuse-type gastric adenocarcinoma; associated with germline or somatic CDH1 (E-cadherin) alterations.

D.Gastric glomus tumor; driven by NOTCH2 translocations.

Explanation: Under the Lauren classification, diffuse-type gastric adenocarcinoma (poorly cohesive carcinoma / signet-ring cell carcinoma) is characterized by dyscohesive neoplastic cells infiltrating singly or in small chords throughout the gastric wall, frequently leading to linitis plastica. Loss of cell-cell adhesion in diffuse gastric cancer is predominantly driven by inactivating mutations, deletions, or promoter hypermethylation of the CDH1 gene (encoding E-cadherin). Hereditary Diffuse Gastric Cancer (HDGC) is an autosomal dominant syndrome caused by germline CDH1 mutations.

4A diagnostic biopsy of an advanced gastric adenocarcinoma is submitted for predictive biomarker assessment to determine eligibility for targeted trastuzumab therapy. Immunohistochemistry for HER2 (clone 4B5) is performed. Which of the following staining patterns on a biopsy specimen meets the standard diagnostic criteria for HER2-positive (IHC 3+) status in gastric cancer?

A.Weak-to-moderate complete membranous staining in >=10% of tumor cells.

B.Strong circumferential membranous staining in >50% of tumor cells only, with incomplete staining interpreted as negative.

C.Nuclear immunoreactivity for HER2 in >20% of viable malignant cells.

D.Strong complete, basolateral, or lateral membranous staining in a cluster of at least 5 contiguous tumor cells, regardless of the overall percentage.

Explanation: Due to the frequent histologic heterogeneity and glandular polarity in gastric cancer, the ASCO/CAP and European guidelines define HER2 IHC 3+ in gastric endoscopic biopsy specimens as a cluster of at least 5 contiguous viable tumor cells displaying strong (intense) complete, basolateral, or lateral ('U-shaped') membranous reactivity. Unlike breast cancer, circumferential (complete circular) staining is not mandatory because gastric glandular cells often stain only along the basolateral membranes. Biopsy specimens with IHC 3+ qualify directly for trastuzumab therapy without mandatory FISH reflex.

5Gastric biopsies from a 55-year-old woman with severe vitamin B12 deficiency show complete loss of specialized parietal and chief cells with extensive pseudopyloric and intestinal metaplasia strictly limited to the oxyntic mucosa of the body and fundus. The antral mucosa demonstrates preserved architectural structure with no active inflammation and an increased gastrin-positive G-cell population. Chromogranin A immunohistochemistry reveals linear and micronodular hyperplasia of enterochromaffin-like (ECL) cells in the corpus. What is the diagnosis and the underlying mechanism responsible for the ECL hyperplasia?

A.Autoimmune atrophic gastritis (AAG); hypergastrinemia driven by achlorhydria causes trophic ECL cell stimulation.

B.Helicobacter pylori pangastritis; direct bacterial CagA toxin stimulation of mucosal endocrine cells.

C.MEN1 syndrome; primary germline loss of menin in ECL neuroendocrine progenitors.

D.Zollinger-Ellison syndrome; autonomous gastrin secretion by a duodenal/pancreatic gastrinoma causing parietal cell hypertrophy.

Explanation: Autoimmune atrophic gastritis (AAG / Type A gastritis) involves autoantibodies directed against parietal cell H+/K+-ATPase and intrinsic factor, leading to selective destruction of oxyntic glands in the corpus and fundus with sparing of the antrum. Destruction of parietal cells results in profound achlorhydria, which eliminates normal somatostatin negative feedback and induces marked antral G-cell hyperfunction and secondary hypergastrinemia. Circulating hypergastrinemia exerts a continuous trophic and proliferative effect on ECL cells, producing linear/micronodular ECL hyperplasia and predisposing to Type 1 gastric neuroendocrine tumors.

6A 34-year-old man presents with chronic malabsorptive diarrhea and iron deficiency anemia. Duodenal biopsies show marked intraepithelial lymphocytosis (>35 intraepithelial lymphocytes per 100 enterocytes), pronounced crypt hyperplasia with increased mitotic figures, and subtotal (marked) blunting and flattening of the intestinal villi. How is this lesion categorized according to the Marsh-Oberhuber classification of celiac disease?

A.Marsh 1 (Infiltrative lesion).

B.Marsh 3b (Destructive lesion with subtotal villous atrophy).

C.Marsh 0 (Pre-infiltrative normal mucosa).

D.Marsh 2 (Hyperplastic lesion without villous flattening).

Explanation: Under the Marsh-Oberhuber classification for gluten-sensitive enteropathy (celiac disease), Marsh 3 represents the destructive stage combining intraepithelial lymphocytosis (>25 IELs/100 enterocytes), crypt hyperplasia, and villous atrophy. Marsh 3 is further subclassified into Marsh 3a (partial villous atrophy), Marsh 3b (subtotal villous atrophy with markedly blunted, stubby villi), and Marsh 3c (total villous atrophy with flat mucosa).

7A 28-year-old patient undergoes colonoscopy for chronic bloody diarrhea and tenesmus. Biopsies from the rectum, sigmoid, and descending colon show a continuous, diffuse inflammatory process restricted to the mucosa, marked crypt architectural distortion with crypt branching, extensive crypt abscesses, and dense basal plasmacytosis. The terminal ileum is completely normal, and non-caseating granulomas are absent. Which histological feature is the most reliable criterion of chronicity distinguishing this condition from acute self-limiting infectious colitis?

A.Neutrophilic infiltration of crypt epithelium (cryptitis).

B.Focal mucosal erosions and intraluminal fibrinopurulent exudate.

C.Basal plasmacytosis with crypt branching and shortening.

D.Transmural lymphoid aggregates and knife-like fissuring ulcers.

Explanation: Basal plasmacytosis (the presence of plasma cells between the crypt bases and the muscularis mucosae) and crypt architectural distortion (branching, shortening, and loss of parallelism) are the most reliable histological hallmarks of mucosal chronicity. These features definitively distinguish chronic inflammatory bowel disease (such as ulcerative colitis) from acute self-limiting infectious colitis, in which crypt architecture remains straight and basal plasmacytosis is absent. Ulcerative colitis characteristically presents with diffuse, continuous mucosal involvement starting in the rectum.

8A 48-year-old patient with long-standing pancolitis undergoes surveillance chromoendoscopy. A biopsy from a flat, non-polypoid area in the transverse colon demonstrates crowded glands with nuclear stratification, marked hyperchromasia, enlarged round nuclei with loss of nuclear polarity extending to the surface, multiple atypical mitotic figures, and complete absence of cytoplasmic mucin. Immunohistochemistry demonstrates diffuse, intense p53 nuclear positivity in >90% of crypt cells. What is the appropriate diagnostic categorization according to ECCO/SCENIC consensus guidelines?

A.Mucosa indefinite for dysplasia with severe regenerative changes.

B.Low-grade dysplasia (LGD) in inflammatory bowel disease.

C.Sporadic tubular adenoma without colitis association.

D.High-grade dysplasia (HGD) in inflammatory bowel disease.

Explanation: According to the ECCO and SCENIC guidelines, the diagnosis of high-grade dysplasia (HGD) in IBD is established when severe cytological atypia (loss of nuclear polarity, marked nuclear pleomorphism, enlarged vesicular or hyperchromatic round nuclei, prominent nucleoli, and abnormal surface mitoses) is present in the absence of overwhelming inflammation. Diffuse, strong p53 nuclear overexpression (aberrant pattern) provides valuable objective confirmation of true neoplastic transformation driven by TP53 alteration, distinguishing HGD from regenerative inflammatory atypia.

9A screening colonoscopy in a 61-year-old woman reveals an 8 mm flat, pale mucosal lesion in the cecum. Microscopic examination demonstrates serrated crypt architecture with dilated, horizontally branching crypt bases (boot-shaped or inverted 'L/T'-shaped crypts) abutting the muscularis mucosae, alongside mature goblet cells extending into the deep crypt bases. Conventional cytological dysplasia is absent. Which of the following is the most accurate pathological diagnosis and associated molecular feature?

A.Sessile serrated lesion (SSL); characterized by frequent BRAF V600E mutation and predisposition to the CIMP/MSI-H pathway.

B.Microvesicular hyperplastic polyp (MVHP); driven by APC gene inactivation and lacking malignant potential.

C.Traditional serrated adenoma (TSA); characterized by ectopic crypt formations and primary KRAS mutations.

D.Tubular adenoma with low-grade dysplasia; characterized by beta-catenin nuclear translocation.

Explanation: According to the WHO 5th edition classification of digestive system tumours, the presence of at least one unequivocally architecturally distorted crypt (dilated, horizontally branching L-shaped, boot-shaped, or inverted T-shaped crypt base touching the muscularis mucosae) is sufficient to diagnose a sessile serrated lesion (SSL). SSLs typically arise in the right colon, are driven by activating BRAF V600E mutations, and represent the precursor lesion for the serrated neoplasia pathway that progresses via CpG island methylator phenotype (CIMP) and MLH1 promoter hypermethylation to microsatellite instability-high (MSI-H) colorectal adenocarcinoma.

10A 44-year-old man undergoes resection of a right-sided ascending colon adenocarcinoma. Immunohistochemistry for DNA mismatch repair (MMR) proteins reveals complete loss of nuclear expression for MLH1 and PMS2 within the tumor cells, with preserved nuclear staining in internal non-neoplastic stromal and lymphoid cells. Nuclear expression of MSH2 and MSH6 is completely retained. To differentiate between a sporadic MSI-H carcinoma and Lynch syndrome, which molecular test should be performed next?

A.Sequencing of APC and TP53 genes to evaluate chromosomal instability.

B.BRAF V600E mutation testing and/or MLH1 promoter hypermethylation analysis.

C.Testing for KRAS and NRAS exon 2-4 mutations to guide anti-EGFR antibody selection.

D.FISH analysis for ERBB2 (HER2) gene amplification.

Explanation: Concurrent loss of MLH1 and PMS2 expression is the most common MMR deficiency pattern in colorectal carcinoma. Approximately 80-85% of MLH1/PMS2-deficient cases are sporadic and caused by somatic epigenetic hypermethylation of the MLH1 promoter, which strongly correlates with somatic BRAF V600E mutations. The presence of a BRAF V600E mutation or MLH1 promoter hypermethylation effectively rules out Lynch syndrome, whereas the absence of both warrants germline genetic testing for Lynch syndrome.

About the Facharzt FMH Pathologie Exam

The Facharzt FMH für Pathologie (Spécialiste FMH en pathologie) is the official Swiss federal medical specialist qualification certifying physicians for independent diagnostic practice in surgical pathology, cytopathology, molecular pathology, and autopsy pathology. Governed by the SIWF and the Schweizerische Gesellschaft für Pathologie (SGPath / SSPath), obtaining the title requires 5 years of accredited postgraduate training, completed e-Logbook documentation, and passing the practical Facharztprüfung. Note on study adaptation: This question bank is an independent English-language MCQ practice resource created by OpenExamPrep—not an official release of SGPath or SIWF—designed to reinforce core theoretical, visual-morphological, immunohistochemical, and molecular diagnostic knowledge.

Assessment

Three-part examination (Weiterbildungsprogramm 4.4). (1) Practical part: histopathology — written diagnosis or differential diagnosis plus the further work-up required, on slides from 20–30 patients spanning biopsy and autopsy diagnostics, 180–240 minutes; cytopathology — gynaecological and non-gynaecological preparations from 10–15 patients assessed in multiple-choice form, 30–60 minutes; molecular pathology, 30–60 minutes. (2) Theoretical-written part: 20–30 multiple-choice questions across the whole Anforderungskatalog including autopsy, biopsy, cytopathology and molecular pathology, 90–120 minutes. (3) Oral part: an individual oral-practical examination on one drawn sub-area — autopsy, tumour board, molecular pathology or macropathology — 30–45 minutes. Everyday diagnostic textbooks may be used during the practical part but not in the written or oral parts. The written part is held in English; the oral and practical parts are held in German, French or Italian, and in English with the candidate's agreement.

Time Limit

Histopathology 180–240 min; cytopathology 30–60 min; molecular pathology 30–60 min; theoretical-written 90–120 min; oral 30–45 min — sat on the single published examination day

Passing Score

At least 75% of the maximum attainable points (Weiterbildungsprogramm 4.6). Every section is scored on a scale fixed in advance by the examination commission and communicated to candidates; results are given at the end of the examination and discussed on request.

Exam Fee

SGPath member fee CHF 700 / non-member fee CHF 1'200 for the Facharztprüfung, plus SIWF title issuance fee (Schweizerisches Institut für ärztliche Weiter- und Fortbildung (SIWF / FMH) & Schweizerische Gesellschaft für Pathologie (SGPath / SSPath))

Facharzt FMH Pathologie Exam Content Outline

20%

Gastrointestinal, Hepatic & Pancreatobiliary Pathology

Barrett esophagus dysplasia grading, gastric adenocarcinoma (Lauren classification, HER2, MMR, PD-L1 CPS), celiac disease Marsh staging, inflammatory bowel disease (Crohn vs UC histological features), colorectal adenocarcinoma staging and molecular pathways (CIN vs MSI-H vs CIMP), appendiceal neoplasms (LAMN), liver cirrhosis etiology, hepatocellular carcinoma vs intrahepatic cholangiocarcinoma, hepatic adenomas (HNF1a, beta-catenin, inflammatory), and pancreatic neoplasms (PDAC, IPMN, PanNET grading).

20%

Gynecologic, Breast & Urologic Pathology

Breast carcinoma (invasive NST vs lobular with E-cadherin loss, Nottingham histological grading, hormone receptors ER/PR, HER2 IHC/FISH ASCO/CAP guidelines, triple-negative subtypes, DCIS vs LCIS, phyllodes tumor), endometrial carcinoma (TCGA/ProMisE molecular classification), ovarian epithelial tumors (HGSC vs LGSC, clear cell, endometrioid, mucinous), cervical SIL (p16/Ki-67), prostate adenocarcinoma (ISUP Grade Groups 1-5, perineural invasion, IDC-P), urothelial carcinoma (non-invasive vs muscularis propria invasion), and renal cell carcinoma subtypes (clear cell, papillary, chromophobe, oncocytoma vs chromophobe, FH-deficient RCC).

20%

Pulmonary, Mediastinal, Cardiovascular & Soft Tissue/Bone Pathology

Lung carcinoma (adenocarcinoma histological patterns: lepidic, acinar, papillary, micropapillary, solid; squamous cell carcinoma p40/CK5/6; neuroendocrine spectrum; predictive biomarkers EGFR, ALK, ROS1, BRAF, RET, MET, PD-L1 TPS), interstitial lung disease patterns (UIP vs NSIP), mediastinal thymoma (WHO types A, AB, B1, B2, B3, thymic carcinoma), pleural mesothelioma (BAP1/MTAP), soft tissue tumors (liposarcoma MDM2, GIST KIT/PDGFRA, leiomyosarcoma, synovial sarcoma SS18, DFSP COL1A1-PDGFB), bone tumors (osteosarcoma, chondrosarcoma, giant cell tumor H3F3A), and myocardial infarction dating.

15%

Dermatopathology, Head & Neck, and Neuropathology

Cutaneous melanoma (Breslow depth, Clark level, ulceration, mitotic rate, subtypes, BRAF V600E, SOX10/Melan-A), non-melanoma skin cancer (BCC subtypes, SCC, Merkel cell carcinoma MCPyV/CK20 dot), inflammatory dermatoses (psoriasiform, lichenoid, spongiotic), head & neck SCC (HPV/p16 status in OPSCC), salivary gland tumors (pleomorphic adenoma, Warthin, adenoid cystic MYB-NFIB, mucoepidermoid MAML2), and CNS tumors (WHO 5th ed: Glioblastoma IDH-wildtype vs Astrocytoma IDH-mutant, Oligodendroglioma 1p/19q co-deleted, meningioma grading, schwannoma vs neurofibroma).

15%

Hematopathology & Lymph Node Pathology

Reactive lymphadenopathy patterns (follicular hyperplasia, Castleman disease, Kikuchi-Fujimoto), classical Hodgkin lymphoma (nodular sclerosis, mixed cellularity; CD30+, CD15+, PAX5 weak+, CD20-, CD45-) vs NLPHL, diffuse large B-cell lymphoma (cell of origin: GCB vs non-GCB Hans algorithm, double-hit MYC/BCL2/BCL6), follicular lymphoma (grading 1-3B, t(14;18)), mantle cell lymphoma (cyclin D1, SOX11, t(11;14)), marginal zone / MALT lymphoma, Burkitt lymphoma (MYC, Ki-67 ~100%), peripheral T-cell lymphomas, and plasma cell myeloma.

10%

Cytopathology, Molecular Pathology & Quality / Autopsy Standards

Thyroid cytopathology (The Bethesda System 3rd ed, PTC features, NIFTP), serous effusion cytopathology (mesothelioma BAP1/MTAP vs adenocarcinoma claudin-4 vs reactive mesothelium), cervical Pap smear (Bethesda system), molecular diagnostic techniques (NGS panels, liquid biopsy ctDNA, FISH, PCR, MSI testing), pre-analytical variables (cold ischemia time, 10% neutral buffered formalin 6-72h, decalcification effects on nucleic acids), diagnostic immunohistochemistry quality control (Qualab / EQA), and Swiss legal autopsy standards (StPO/CPP Art. 253 extraordinary death, HFG / Human Research Act biobanking).

How to Pass the Facharzt FMH Pathologie Exam

What You Need to Know

Passing score: At least 75% of the maximum attainable points (Weiterbildungsprogramm 4.6). Every section is scored on a scale fixed in advance by the examination commission and communicated to candidates; results are given at the end of the examination and discussed on request.
Assessment: Three-part examination (Weiterbildungsprogramm 4.4). (1) Practical part: histopathology — written diagnosis or differential diagnosis plus the further work-up required, on slides from 20–30 patients spanning biopsy and autopsy diagnostics, 180–240 minutes; cytopathology — gynaecological and non-gynaecological preparations from 10–15 patients assessed in multiple-choice form, 30–60 minutes; molecular pathology, 30–60 minutes. (2) Theoretical-written part: 20–30 multiple-choice questions across the whole Anforderungskatalog including autopsy, biopsy, cytopathology and molecular pathology, 90–120 minutes. (3) Oral part: an individual oral-practical examination on one drawn sub-area — autopsy, tumour board, molecular pathology or macropathology — 30–45 minutes. Everyday diagnostic textbooks may be used during the practical part but not in the written or oral parts. The written part is held in English; the oral and practical parts are held in German, French or Italian, and in English with the candidate's agreement.
Time limit: Histopathology 180–240 min; cytopathology 30–60 min; molecular pathology 30–60 min; theoretical-written 90–120 min; oral 30–45 min — sat on the single published examination day
Exam fee: SGPath member fee CHF 700 / non-member fee CHF 1'200 for the Facharztprüfung, plus SIWF title issuance fee

Keys to Passing

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Facharzt FMH Pathologie Study Tips from Top Performers

1Master Diagnostic Immunohistochemical Algorithms: Practice key diagnostic panels to resolve common diagnostic dilemmas (e.g. adenocarcinoma vs mesothelioma with calretinin/WT1/D2-40 vs claudin-4/Ber-EP4; lung adeno vs squamous with TTF-1/napsin A vs p40/CK5/6; breast lobular vs ductal with E-cadherin).

2Internalize WHO 5th Edition Tumor Classifications: Review updated diagnostic criteria, especially molecularly defined entities in CNS tumors (IDH-mutant vs IDH-wildtype glioblastoma, 1p/19q co-deletion), endometrial carcinomas (POLE, MMRd, p53abn, NSMP), and soft tissue sarcomas (MDM2, SS18, EWSR1).

3Consolidate Predictive Biomarker Scoring Guidelines: Memorize ASCO/CAP scoring criteria for HER2 IHC/FISH in breast and gastric cancer, PD-L1 scoring systems (TPS, CPS, IC), and mismatch repair (MMR) IHC interpretation (MLH1/PMS2, MSH2/MSH6 loss patterns).

4Review Pre-analytical Requirements & Swiss Quality Standards: Understand cold ischemia time limits, 10% neutral buffered formalin fixation duration (6–72 hours), decalcification artifacts on DNA/RNA, and Swiss statutory regulations for clinical autopsies (StPO Art. 253) and research biobanking (HFG).

Frequently Asked Questions

What is the Facharzt FMH für Pathologie title?

The Facharzt FMH für Pathologie is the federally accredited specialist title in anatomical and clinical pathology in Switzerland awarded by SIWF/FMH in partnership with SGPath. It confers full diagnostic authority for histological and cytological examination of surgical and autopsy specimens. Note: This question bank is an English-language MCQ study adaptation—not an official translation, not a simulation of microscope slide examination or autopsy practicals, and not a substitute for residency slide diagnostic training.

In what format and languages is the official SGPath Facharztprüfung conducted?

Language depends on the format: under Weiterbildungsprogramm 4.5.5 the written part is conducted in English, while the oral and practical parts may be taken in German, French or Italian — or in English if the candidate agrees. The examination has three parts: a practical part (histology slides from 20–30 patients over 180–240 minutes, cytology preparations from 10–15 patients answered in multiple-choice form over 30–60 minutes, and molecular pathology over 30–60 minutes), a theoretical-written part of 20–30 multiple-choice questions over 90–120 minutes, and a 30–45 minute oral examination on one drawn sub-area (autopsy, tumour board, molecular pathology or macropathology). Standard diagnostic textbooks are available during the practical part only. At least 75% of the maximum points is required to pass.

What are the fees for the Swiss Pathology Specialist Examination?

The examination fee set by the Swiss Society of Pathology (SGPath / SSPath) is CHF 700 for SGPath members and CHF 1'200 for non-members, plus the statutory SIWF/FMH administrative title issuance fee.

What classification and diagnostic systems are emphasized on the exam?

The examination is strictly aligned with the current WHO Classification of Tumours (5th Edition Blue Books), UICC/AJCC TNM 8th and 9th edition cancer staging, ASCO/CAP predictive biomarker guidelines (HER2, ER/PR, PD-L1, MMR), and The Bethesda Systems for thyroid and cervical cytopathology.

What core pathology subspecialties are tested in this practice bank?

The practice bank covers 6 core syllabus areas: Gastrointestinal & Hepatopancreatobiliary (20%), Gynecologic, Breast & Urologic (20%), Pulmonary, Mediastinal & Soft Tissue/Bone (20%), Dermatopathology, Head & Neck & Neuropathology (15%), Hematopathology (15%), and Cytopathology, Molecular Pathology & Autopsy Standards (10%).

100+ Free Facharzt FMH Pathologie Practice Questions

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