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AP RCPA VIVA > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

Pink Inclusions in Hepatocytes

A

Non-neoplastic:
Apoptotic bodies
Mallory hyaline
Fibrinogen
Megamitochondria

Congenital:
Alpha 1 antitrypsin
Glycogen storage disorder

Neoplastic: HCC, embryonal sarcoma

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2
Q

Neutrophils in Liver

A

Non - Neoplastic:
“surgical hepatitis”
CMV
Ascending cholangitis
NASH / ASH

Neoplastic: in association with malignant tumours, both primary and secondary

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3
Q

Liver Special Stains

A

Reticulin: Architecture, plate thickness

Trichrome: Staging of fibrosis

PAS: BM, AIAT globules, storage disorders

PERLS: presence, site, grading of iron

Rhodanine: Copper deposition (Wilson, cholestasis)

Orcein: elastic fibres, Cu associated binding protein, Hep B surface antigen

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4
Q

Subtypes of HCA

A

1) HNF1A inactivated (loss of LFABP)
2) Inflammatory adenoma (express CRP / SAA in 50%)
3) Beta catenin activated. (nuclear BCat of diffuse GS)
4) SHH activated (ASS1 +, increased risk of bleeding)
5) Unclassified

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5
Q

IPX for Primary Liver Carcinoma

A

HCC: HepPar1, arginase +, CK 7 / CK 20 -

CC: CK7 / CK 19 +, albumin RNA ISH +

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6
Q

HCA versus Well Diff HCC

A

HCA:
Younger, female, hormones, non cirrhotic
Bland cytology, no reticulin loss, low Ki67
Glypican and HSP70 negative

HCC:
Older, cirrhotic or chronic liver disease
Glandular / acinar formation, loss of reticulin network
Increased atypia and mitoses
Ki67 increased c.f. background
Glypican 3 and HSP70 positive

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7
Q

DDx Granulomas in the Liver

A

PBC
Sarcoidosis
Infection (Hep C, Tb, atypical Mb)
Drugs
Paraneoplastic syndrome
Idiopathic

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8
Q

MMR / BRAF in GI Cancers

A

Loss of MLH1 / PMS2
= promoter hypermethylation
or germline mutation (Lynch)

BRAF V600E positive = most likely promoter hypermethylation (sporadic)

Isolated loss of PMS2
Loss of MSH2 / MSH6
= most likely to be germline mutation

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9
Q

Synoptic Report Malignant Polyps

A

Site and size of polyps, pedunculated or sessile

Precursor polyp type
Histologic type of cancer
Histologic grade
Size of invasive carcinoma
LVI
PNI
Tumour budding score
Margin status

MMR / BRAF
Other: NE markers, Ki67 as needed

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10
Q

Haggitt versus Kikuchi

A

Haggitt =

Adenocarcinoma in a pedunculated polyp

Four levels: depth of invasion from head of stalk to submucosa (level 4)

Kikuchi =

Adenocarcinoma in a sessile polyp

Three levels: depth of invasion within submucosa (sm1 - 3)

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11
Q

Explain how to Cut Up This Specimen

A
  1. PPE, 3 points of ID, orient and photograph
  2. Review MDM and imaging (where is tumour located, size)
  3. Measure stomach, duodenum, pancreas, ducts, gallbladder, fat. Open stomach / duodenum and fix.
  4. Ink pancreatic margin, SMV / vascular groove, uncinate (SMA)
  5. Take margins: stomach, duodenum, bile duct and pancreatic margin
  6. Section superior to inferior, lay out slices and photograph
  7. Describe tumour - border, size, cut surface distance to margins
  8. Block tumour to closest margins and anatomy documenting this on photo blocking diagram
  9. Look for lymph nodes
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12
Q

Explain how to cut up this Specimen

A
  1. PPE, 3 points of ID, orient and photograph
  2. Review MDM notes / imaging ? site, size of tumour, relationship to structures, prior NAT
  3. Measure length and diameter of specimen, width of mesocolon to apical tie, measure distance of PPR and APR to distal margin. Comment on completeness of mesorectum and ink mesorectum. Open and fix.
  4. Margins from proximal, distal and apical tie including apical lymph node.
  5. Look for polyps, diverticulae / other pathology.
  6. Measure tumour, distance to proximal and distal margins and relationship to anterior peritoneal reflection.
  7. Slice from superior to inferior, lay out slices of tumour and photograph. Describe depth of invasion and closest CRM.
  8. Block 6 - 8 blocks of tumour - background polyp, depth of invasion and closest CRM. Document on photo blocking diagram.
  9. Look for lymph nodes.
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13
Q

Explain how to cut up this Specimen

A
  1. PPE, 3 points of ID, orient specimen.
  2. Review MDM notes and imaging - ?size / site of tumour, relationship to adjacent structures, NAT
  3. Measure lesser curve, greater curve, width, proximal and distal resection margins, omentum in 3 dimensions. Inspect serosal surface.
  4. Ink circumferential resection margin. Open along greater curve and pin out on board to fix.
  5. Photograph specimen. Describe gastric mucosa including site, size, appearance of tumour. Measure tumour to proximal and distal margins. Take shave margins to prox and distal.
  6. Section stomach through tumour. Lay out slices and photograph. Describe deepest point of invasion and distance to circumferential resection margin.
  7. Block tumour to closest margins and anatomy. Block background mucosa. Record on photo diagram.
  8. Look for lymph nodes.
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14
Q

Syndromes Associated with GI Polyps and Tumours

A

1. Lynch: AD, MMR proteins

  • colorectum, stomach, small bowel, pancreaticobiliary, endometrial, ovary, upper urothelial tract

2. Muir-Torre: AD, MSH2, MLH1

  • phenotypic variant of Lynch, sebaceous adenomas and carcinomas and keratoacanthomas

3. FAP: AD, APC

  • Small and large intestine, periampullary adenocarcinoma, fundic gland polyps with dysplasia in stomach. Cribiform morular thyroid neoplasms. Nasopharyngeal angiofibromas in males.

Gardner - variant of FAP, adenomas plus: soft tissue and ovarian fibromas, fibromatosis, osteomas, supernumerary teeth

4. Turcot: variant of FAP or Lynch. Either:

Medulloblastoma plus FAP or

GBM and Lynch.

Other:

Serrated polyposis syndrome

Peutz Jegher syndrome

Juvenile polyposis syndrome

Cowden (PTEN hamartoma) syndrome

Cronkhite-Canade syndrome

Herediatry diffuse gastric cancer syndrome

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15
Q

Syndromes Associated with GIST

A

1. Carney - Stratakis syndrome (AD, SDH genes)

  • SDH deficient GIST
  • Paragangliomas
  • SDH deficient RCC

2. Carney Triad (SDHC hypermethylation)

  • SDH deficient GIST
  • Paragangliomas
  • Pumonary chondromas

3. NF1

4. KIT and PDGRFA mutated syndromic GIST’s

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16
Q

Genes involved in development of GIST

A

C-KIT (imatinib)

PDGFRA

SDH

NF1

17
Q

Synoptic Reporting of GIST

A
  1. Focality (uni / multi), site, size
  2. Histologic subtype (spindled, epithelioid, mixed)
  3. Mitotic count per 5 mm2 to determine grade
    - < 5 per 5 = low grade, > 5 per 5 = high grade
  4. Necrosis
  5. Pre- resection therapy / treatment effect
  6. Risk assessment: based on size, site and mitotic count
  7. Margins status, nodes, distant metastases

Ancillary tests: CKIT, DOG1, SDH, PDGFA, NF1

pT Stage based on size: cutoffs 2, 5, 10 cm

18
Q

Explain Principles of EMR

A

EMR (endomucosal resection) is a technique for the treatment and staging of superficial neoplasms of the GIT

Most commonly used for Barrett’s oesophagus, early gastric cancers and colon polyps.

Techinque performed under endoscopy and involves injecting a lifting agent under the lesion followed by ligation. Specimen should be retireved, oriented and pinned flat to board before fixation.

19
Q

Synoptic Report EMR / ESD Oesophagus

A
  1. Procedure type, specimen size and location (upper, mid, lower, GOJ), tissue layers included
  2. Tumour focality (uni, multi), histologic type, histologic grade, size of invasive tumour, depth of invasion, LVI
  3. BE and dysplasia (LGD, HGD) present
  4. Margins to invasive carcinoma and dysplasia
20
Q

Criteria for Sessile Serrated Polyposis Syndrome

A
  1. Presence of 20 or more serrated polyps anywhere in colon
  2. Presence of 5 or more serrated polyps proximal to sigmoid colon at least two of which are >1cm in size
  3. Any serrated polyp in a person who has a family history of SPS
21
Q

Explain Criteria for Tumour Budding

A

Tumour budding = presence of single cells or small clusters of less than five cells at the advancing edge of the tumour.

High tumour budding associated with:

  • increased risk of LN metastases in polypectomy specimen - need resection
  • increased risk of LN metastases in stage II resection patients - need CTX

Tumour budding counts:

  • should be done on H&E in a hot spot area
  • count total number of buds in an area 0.785mm2 (20x on some microscopes but need to check normalisation table in CAP protocol)
  • report both total number of tumour buds and three tier score (low 0-4, intermediate 5 -9 and high 10 +)

Issues:

  • don’t count in post NAT specimens (no data)
  • difficult subtypes e.g micropapillary, mucinous (don’t count groups suspened in mucin) and medullary (obscured by TIL’s, can us CK to identify but count on H&E)
22
Q

Risk Factors for Cholangiocarcinoma

A

Congenital:

Choledochal cysts, multiple VMC, congenital hepatic fibrosis

Infectious:

Liver flukes, HCV and HBV

Inflammatory / Other:

Hepatolithiasis, PSC

23
Q

Risk Factors for HCC

A

Majority of the risk factors for HCC result in cirrhosis.

Hepatotropic viruses

Alcohol Use

NAFLD

Metabolic / Hereditary disorders: A1AT, tyrosinemia, glycogen storage disease, hereditary haemochromotosis

Drugs and toxins: thorotrast, anabolic steroids, Aspergillus flavus

24
Q

Definition of Barretts Oesophagus

A

Definition of BE depends on geography. In USA, Australia and NZ:

  1. Replacement of oesophageal squamous mucosa with metaplastic columnar epithelium which includes goblet cells and…
  2. ..in an area of endoscopically abnormal mucosa (salmon pink)..
  3. …>1cm above GOJ

Should receive four quadrant biopsies at 2 cm intervals along the entire length of altered mucosa for assessment.

Assess for presence of BE and the negative for dysplasia, indeterminate for dysplasia, LGD, HGD.

After diagnosis patients receive anti-reflux medication and regular surveillance (interval depends on RF e.g. length, dysplasia)

HGD can be treated with endoscopic ablative therapy or EMR

25
Q

Interpretation of HER2 in GOJ / Gastric Adenocarcinoma

A

HER2 is a receptor tyrosine kinase present on the surface of cells.

Member of the epidermal growth factor receptor EGFR, family and is encoded by the HER2/neu oncogene.

Amplification or overexpression of this oncogene is associated with the development and progression of certain breast and gastric carcinoma types.

HER2 receptor can be targeted by monoclonal antibodies (e.g. trastuzumab) for therapy.

In GOJ / gastric adenocarcinomas: HER2 amplification can be assessed by IPX or ISH studies.

With IPX assessment is based on basolateral staining, intensity of the staining and the number of cells staining (biopsy 5 cells or more, resection >10% of tumour cells)

26
Q

Grading of NET’s

A

NET’s and NEC’s are graded on the basis of mitotic count per 2mm2 / 10 HPF and Ki67 proliferation index.

Ki67 counted in a hot spot area.

Count at least 500 cells.

“eyeball” / manual count / or digital image analysis

Mitoses count in ~50 HPF and report average per 10 HPF

Cut offs:

Ki67 < > 3%

Mitoses < > 2 / 10 HPF

27
Q

IPX for Metastatic NET

A

SATB2: rectum / appendix

CDX2: small intestine

PAX8 / IL1: pancreas

TTF1: lung

28
Q

Coeliac Serology

A

Tissue transglutaminase antibody

Deamidated gliadin eptide

IgA levels

HLA-DQ2/DQ8 typing for people at risk of CD (first degree relatives, T1DM, IgA deficiency, other autoimmune disease, Trisomy 21)

29
Q

Refractory Coeliac Disease

A

Persistent villous blunting, LP inflammation and IEL despite 6 - 12 months of strict gluten free diet

_Consider and exclud_e: collagenous sprue, tropical sprue, autoimmune enteropathy and immune deficiency eg CVID.

Type 1 RCD:

IEL phenotype identical to usual Coeliac disease i.e. CD8=CD3+ IEL’s. TCR gene rearrangement polyclonal.

Can use immunosuppression. No increased risk of EATL.

Type 2 RCD:

CD8 lost in >50% of CD3+ IEL’s. Loss of surface CD3, CD7, CD8. TCR gene studies oligo/monoclonal.

Increased risk of EATL.

30
Q

Pigment in Liver

A

Bile

Iron (PERLS +)

Copper (Rhodanine +)

Lipofuscin (Fontana-Masson +)

31
Q

Reporting Elements Metastatic CRC to Liver

A

Number of tumours, size of each, distance to margins

Histologic type and grade of tumour

Treatment response to NAT - tumour regression score (Rubrei and Grant, only fibrosis counts, presence and %)

MMR / BRAF

Background liver: including sinusoidal obstruction syndrome due to oxiplatin and any concurrent disorder

32
Q

Defining Steatosis in Liver (& Causes)

A

Steatosis = Abnormal accumulation of fat within hepatocytes

Steatohepatitis = Fat + Injury (balloon cells and lobular inflammation)

These are part of the same disease process, and both lead to fibrosis, but steatohepatitis leads to fibrosis faster

Changes usually seen in Zone 3 first. Portal infiltrates may be present, but are usually mild. If they are severe, consider additional Dx’s

Macrovesicular steatosis: Change in lipid metabolism. Nucleus pushed to the side by usually a single medium to large sized droplet. Causes: metabolic disease, obesity, TPN, PEM, steroid therapy.

Microvesicular steatosis: Usually represents mitochondrial injury. Nucleus remains central with innumerable, fine fat droplets. Only use this term if it is a diffuse change. Causes: Acute fatty liver of pregnancy, Reye syndrome, in born errors of fatty acid metabolism, alcohol.

Quantifying Fat

< 5% Normal

5 - 33% Mild

33-66% Moderate

>66% Severe

33
Q

Grading and Staging of Steatohepatitis

A

Grading:

% of fat (mild, moderate, severe)

Lobular inflammation

Hepatocyte Ballooning

Staging:

Fibrosis

Systems: SAF, NASH-CRN score

34
Q

Causes of Excess Iron in Liver

A

Haemochromatosis

Thalassemia

Excess RBC transfusions

Small amounts of iron also seen in many chronic liver diseases e.g. NAFLD, ALD, Hep B / C, cirrhosis

35
Q

Grading of Iron in Liver Biopsy

A

Modified Scheurer

Grade 0 - discrete granules not visible or barely discernible at 400x

Grade 1 - discrete granules barely discernible at 250x, easily seen at 100x

Grade 2 - discrete granules resolved at 100x

Grade 3 - discrete granules resolved at 25x

Grade 4 - masses visible with naked eye or at 10x

36
Q

Classification of Gastric Cancer

A

Lauren Classification: Diffuse, Intestinal or Mixed

WHO Classification: Tubular, Poorly cohesive (includes signet ring cell carcinoma), Mixed, Mucinous, Papillary, Micropapillary, Hepatoid, Adenosquamous, SCC, Undifferentiatiated / Anaplastic, Gastroblastoma, SCNEC, LCNEC, MANEC

37
Q

Appendiceal Mucinous Neoplasms

A

In appendix: LAMN and HAMN

In peritoneum:

WHO 5th edition:

G1: Low grade peritoneal mucinous neoplasia

G2: High grade peritoneal mucinous neoplasia

G3: High grade peritoneal mucinous neoplasia with signet ring cells

PSOG:

Low grade mucinous carcinoma peritonei

High grade mucinous carcinoma peritonei

High grade mucinous carcinoma peritonei with signet ring cells

* submit 1 / cm of mucinous deposits

* search for and sample solid areas

38
Q

Tumour Regression Score in GIT

A

Modified Ryan Scheme

Score 0: No viable cancer cells (complete response)

Score 1: Single cells or rare groups of cells (near-complete response)

Score 2: Residual cancer with evident regrssion but more than single cells or rare groups of cells (partial response)

Score 3: Extensive residual cancer without evidence of tumour regression (poor or no response)

39
Q

Causes of Copper Deposition in Liver

A

Wilson’s diseae

Chronic cholestatic liver disease PBC, PSC (periportal hepatocytes)

Indian childhood cirrhosis

PFIC

AP RCPA VIVA (14 decks)

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