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U17 + 18 > GI patho > Flashcards

GI patho Flashcards

1
Q

Define chronic and granulomatous

A
  • Chronic inflammation - temporal sequence, non neutrophilic inflammatory response, eosinophils in GIT-subacute.
  • Granulomatous inflammation - often vaguely referred to by many clinicians eg, post of granuloma, stitch granuloma, pyogenic granuloma - all misnomers
  • Granulomatous inflammation - chronic, defined as collection of epitheliod histiocytes with typical slipper foot nuclei. Giant cells common of various/ variable types and may calcify over time-diagnostically useful.
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2
Q

Define an ulcer, sinus, fistula

A
  • Ulcer - discontinuity in surface epithelium due to acute inflammatory reactioon- temporal sequence- constituted by neutrophils (polymorphs/polymorphouclear neutrphils).
  • Sinus = ulcerated tracj +/- epithelial lining opneing to a surface or hollow viscus.
  • Fistula - Ulcerated track +/- eputhelial lining connectin two hollow viscera or one hollow viscus to a different surface- diversion/bypss.
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3
Q

Ischaemia and infarction

A
  • ischaemia - reduced to absent vascular supply to cells, tissue and organ
  • Infarction - ischaemia resulting in tissue necrosis, when collateral vascular channels fail to develop or are inufficiently developed
  • Important - infarction in bowel mzy be venous in nature due to reduced to absent venous drainage.
  • Infarction - leads to gangrene - dry and then wet and supeadded putrefaction (bacterial)
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4
Q

Metaplasia

A
  • metaplasia - conversion of a temrinallydifferentiated tissue to yet another terminally differentiated phenotype (trans-differentiation) reflective of an innate adaption to an abnormal and hotile environment
  • Barretts oesophagus - GORD leading to cephalad prolongation of columnar mucosa replacing the native oesophageal squamous mucosa- reflecting a favourable (short term) phenotype
  • Neo-metaplasia- retro-differentiation in tumour- reversal of ontogeny- e.g., yolk sac areas in adult granulosa cell tumour of ovary or YST like areas in colorectal carcinoma (enteroblastic)- foetal reprogramming- so not mature or terminally differentiated but immature
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5
Q

Dysplasia (abnormal development deifnition)

A

■Abnormal proliferation-maturation uncoupling in epithelium leading to a non- invasive cancer or a pre-cancerous state with intact basement membrane or incapacity to avail lymphovascular access

■Many exceptions- dysplastic naevus, dysplastic kidney, dysplastic hip, fibrous dysplasia, myelodysplasia, osseous dysplasia etc

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6
Q

Intraepithelial neoplasia development in to occult invasive carcinoma

A
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7
Q

What is acute appendicitis

A

■Luminal inflammation- pain around umbilicus- Dermatomal rule (referred pain).Mural and serosal inflammation (peritonitis) - shifts to RIF

■Peri appendicitis- only serosal inflammation without mural or luminal inflammation

■Usually related to the other D/D RIF pain- PID (pelvic inflammatory disease), typhlitis/caecitis and mesenteric lymphadenitis due to Yersenis often with appendicitis- serology and typical suppurative granulomas/follicles/germinal centres

The appendix = phylogenetically relatedto bursa fabricus (clacal end of avian species). Physiological diverticulum (cul de sac). Vesitgial organ, diverted from faecal stream - prominent lymphoid follicles

ACE appendix- appendicostomy for antegrafr continence enema - diversion to faecal stream- loss of fllicles.

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8
Q

Peritonitis

A
  • Acute - inflammation of the outermost layer of serosa of any peritonealised intra-abdominal organ (hollow viscus) - visceral peritonitis. Or the outer layer of peritoneum related to the abdominal wall (parietl peritonitis)
  • Rebound tenderness , guarding + rigidity
  • Greater omentum acts as abdominal policeman to localise the inflammation - abdominal apron
  • Common end result of disparate pathologic processes.
  • Regional - visceral, localised to the organ involved,
  • Diffuse - parietal
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9
Q

Diverticulum

A
  • Herniation of the mucosal layer through a weak point of the muscle coat due to increased intra luminal pressure- colon (sigmoid)
  • Rarely as anatomical variation or congenital anomaly- Meckels diverticulum
  • urinayr bladder, small intestine, oeosphagus (abnormally tight upper sphincter - Zenkers diverticulum)
  • Proximal colonic diverticulosis- strong genetic predispoition in individuals of asia pacific heritage
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10
Q

Pathology of sigmoid diverticular

A
  • Western low fibre diet
  • Relatively less genetic influence cf proximal diverticulosis of Asia- pacific
  • Chronic constipation
  • Diverticulitis, peridiverticulitis, diverticular abscess- pain abdomen
  • Peritonitis - acute abdomen
  • Serious complications - stricture leading to intestinal obstruction, colovesical and colovaginal fistula
  • Misdiagnosis - crohns segmental colitis, due to granuloma and deep skin inflammation
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11
Q

Diverticular disease

A

■Sac like protrusion

■Diagnosed on endoscopy and CT scan

■Concertina like appearance on resection

■Port of perforating artery is a weak point of the wall

■Presentation- abdominal pain, per rectal bleeding, constipation, fever if complicated

■Acute presentation- intestinal obstruction, sepsis, pyrexia of unknown origin

■DO NOT BIOPSY AN INVERTED POLYP/DIVERTICULAR POLYP- WILL PERFORATE

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12
Q

Intestinal obstruction

A

■Intrinsic- lumen- tumour- polyp, intussusception, cancer and worms (tropical)

■Intrinsic- wall/mural- stricture

■Extrinsic- usually extra tubal compression by mass

■Proximal dilation- vomiting

■Distal collapse- inability to pass flatus and faeces

■Double barrel obstruction- volvulus- collapse of both afferent and efferent limbs

■Perforation and peritonitis- caecum, site of election, as most dependent and fixed

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13
Q

Vascular supply of the intestine

A
  • Foregut- coeliac axis
  • Midgut- SMA- Superior mesenteric artery
  • Hindgut- IMA- Inferior
  • Junctions are watershed zones and prone to ischaemia
  • Atherosclerosis, thrombosis
  • Venous occlusion, strangulated hernia
  • Vasculitides- e,g IgA vasculitis (Henoch-Sconlein purpura)
  • Drugs rare- 5’ Azacytidine
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14
Q

Ischaemic Bowel

A
  • Acute emergency - acute abdomen, blood in stool
  • Strangulated hernia
  • Dusky cyanosis, irreversible, no change of colour on hot mop compress
  • Must keep margins viable
  • Needs histiologial confirmation
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15
Q

Factors in ischaemia

A
  • Previous damage
  • Susceptibility - metabolic demand for 02
  • Presence of anastomosis
  • Time of onset- suficient or not for collaterals to develop - will decide if acute bowel ischaemia or chronic ischaemic colitis (latter usually in atherosclerotic arteripathy)
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16
Q

Ischaemic colitis

A
  • Vascular proliferation
  • Crypt withering
  • Mucin loss
  • Focal active cryptitis
  • Pseudomembrane
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17
Q

IBD

A

■Chronic idiopathic condition

■May have extra intestinal manifestations/involvement

■First presentation may be acute- pain, diarrhoea, blood in stool, fever, anaemia, extreme fatigue

■Relapsing remitting disorder requiring long term medical intervention

■Predisposition to malignancy

■2 main prototypes

■Overlaps and may be indeterminate/unclassified

■Initial diagnosis needs exclusion of infection, drugs

18
Q

Aetiology

A

■Genetic susceptibility

■Immune dysregulation

■HLA B27 link

■May be part of other immune dysregulation diseases- uveitis, primary sclerosing cholangitis, ankylosing spondylitis/enteropathic arthropathy

■More for Crohn’s>Ulcerative colitis

■Minority transform from other microscopic colitis (collagenous colitis)

19
Q

Ulcerative colitis vs crohns disease

A

UC:

  • Colonic disease mostly with some backwash ileitis
  • Distal involvement with ascending progression but typically spares the anal canal (common in CD)
  • Exception - caecal patch variant
  • COnfluent mucosal involvement but superficial

Crohns disease:

  • Regional enteritis, predominately ileal but may involve stomodeum (mouth) to proctodeum (anus)
  • Occaisonally non-gut site
  • Skipped mucosal involvement with deep mural involvement

3 genotypic groups - UC, ileal CD, Colonic CD. 3rd phenotype is PSC-IBD

20
Q

Crohns disease- macro and micro features

A

Macro:

  • Sharp linear fissuring ulcers
  • Intervening polypoid mucosa
  • Cobble stone appearance
  • Pseudopolyps
  • Creeping fat substitution/fat wrapping- mesenteric fat doe snot stop but creeps to wrap around

Micro:

  • Sharp deeo falciform, knife edge ulcer or saucer shaped
  • Ulcer associated cell lines - pyloric or pseudo pyloric metaplasia
  • perivasclar subserosal lymphoid rosaries/beads
  • Non necrotic granuloma (not related to crypt rupture)
  • Mesenchymal manifestations - neuromatous hyperplasia
  • Hypercrinia (retained mucin)
  • Lymphangectasia (dilated lymphatics)
21
Q

Ulcerative colitis - macro and micro

A

Macro:

  • Confluent distally predominant superficial involvement
  • Exception - rectal involvement may reduce with sulfasalazine enema and caecal patch variant

Micro:

  • Acute inflammation limited to mucosa
  • Basal plasmacytosis
  • Crypt distortion
  • Cryptolytic granuloma- associated with imploding crypts
  • Mucin loss
  • Lack of other CD features
  • Loss of gradient of distribtuion of mononuclear inflammatory cells,

In surgical emegrency - toxic mega colon- UC, may show allf eatures of CD and may be indistinguishable-often called indeterminate but mostly re true UC

22
Q

Complications of IBD - CD/UC

A
  • Untreated
  • Treated
  • Medical vs surgical management
  • Intestinal complications
  • Extra-intestinal complications- mainly associations, predominately CD.

CD: Stricture, Perforation, sinus, fistula. Dysplasia and malignancy- partocularly in PSC-IBD rightt sided phenotype. Toxic megacolon less common.

UC: stricture less common, exceptional, dysplasia and malignancy (UC>CD), toxic megacolon - acure dilation.

Colitis associated neoplasia/CAN

23
Q

Extra intestinal comlictions (associations)

A

■CD- typically- uveitis, PSC, enteropathic axial arthropathy/ankylosing spondylitis

■CD- involvement of oral cavity, oesophagus, stomach and anal canal

■Upper GI- paediatric age group typically

■Anal canal- skin tags, sinus, fistula. If multiple- water can perineum (sieve like)- historical in developed countries

■Orogenital involvement- typically adults

■Episcleritis, scleritis, iritis, sacrolilitis, peripeheral enteropathic arthropathy

■Pyoderma gangrenosum (commonest skin manifestation)

■Sweet syndrome (neutrophilic dermatosis), erythema nodosum, psoriasis, thromboembolism

24
Q

Treatment associated complications: medical for UC/CD

A

■Mainstay immunomodulation/suppression

■Steroids- CMV colitis (cytomegalo virus)- CD=UC

■Detected on histology and serology

■Important clue- refractory and increasingly symptomatic on full dose steroids

■Usually not a problem with biologics and biosimilar

■Biologics- Monoclonal antibodies- , clue- -mab, commonest Infliximab

■Biosimilars- cheaper, follow on biologics or second entry, not original but equipotent

■Methotrexate, thiopurines and anti TNF- increased risk of lymphoma/lymphoproliferative disease/myelodysplastic syndrome/myeloid leukaemia

25
Q

Surgicla treatment associated complications for UC/CD

A

■Surgical management- stricture, fistula, sinus, perforation

■Toxic megacolon- may be total colectomy or ileorectal anastomosis (TC-IRA)

■Or more commonly total proctocolectomy (stoma) and later ileoanal pouch (IAP- restorative proctocolectomy)

■Pouch failure- CD much higher late biological failure than UC

■Early failures- vascular, mechanical, septic in both UC and CD

26
Q
A

Crohns anasotmotic stricture

27
Q

Define tumour, neoplasia, cancer, carcinoma, adenocarcinoma

A

■Tumour- swelling ( remember- 5 signs of inflammation)

■Neoplasia- Uncontrolled clonal proliferation of cells (new growth)

■Cancer- malignant- Neoplasia invading across tissue planes with capacity to spread to locoregional lymph nodes and distant sites/organs (metastasis)

■Carcinoma- malignancy of epithelial cells

■Adenocarcinoma- carcinoma of glandular origin/differentiation (recapitulation)

28
Q

Colorectal cancer staging principles

A
  • Leading cause morbidity and mortlaity in western countries.
  • NHSBCSP = bowel cancer screenign program as early detectin for precancerous biologu, detectable and points of intervention, outcome and management are well known in disease with high pop burden
  • Staging - spread at given point
  • At detection - clinical staging - not accurate but good enough to dictate management
  • At defintiive surgery - pathological staging- accurate to dictate subsequent management
  • Pathological staging - dukes, modified dukes, turnball modification, aster coller modification, TNM staging (AJCC-UICC/TNM). All common principles of local spread across tissue planes and landmarks, extend of nodal involvement and distant metastasis.
  • Nodal burden of disease internationally accepted as worsening stage rather than level of spread in CRC. Still recorded in pathology reports as aspical node involvement. Lymph node staiton not recognised in TNM.
29
Q

TNM staging of CRC

A
30
Q

Stages of CRC

A
31
Q

Bowel cancer screening - when, and what

A
  • After 60th until 74th brthday
  • 2 yearly invitation
  • FIT (faecal immunocemical test) >FOBT (foecal occult blood test)
32
Q

Principles of screening

A

■High disease burden/prevalence

■Known natural history of disease

■Consensus on treatment and points of intervention

■Early intervention reduces mortality and/or morbidity

■Acceptable procedure

■Reasonable specificity and sensitivity of screening test

■Balance against psychological stress/anxiety/harm

33
Q
A

What we dont want - marrow involvement, myelopthisis

34
Q
A

What we want to see, polyp cancer, preferably fully excised

35
Q

Surgicla principles in CRC management and further management

A

■Complete resection

■Adequate nodal clearance

■Lymphatic drainage, vascular supply, anatomical restoration

■TME- Total mesorectal excision

■ELAPE- Extra levator abdominoperineal excision

■TEMS/EMR/SMD- trans anal endoscopic mucosal excision/endoscopic mucosal resection/submucosal dissection

Chemo/radiation further management depends on: T4, venous invasion, CRM involvement, nodal metastasis, micro satellite instability plus work up. MMR status influences immuno-oncology decisions. Optional parameters - perneural invasion, tumour budding, host response. Grade

TME and nodal harvest are credentialing factors for surgeons and surgeons and/or pathologists, ELAPE is no longer a quality mesaure

36
Q

Nodal basin clearance in CRC surgery

A

■Midgut- origin of SMA (superior mesenteric artery)

■Hindgut- origin of IMA (inferior mesenteric artery)

■Median harvest of 12 nodes in any series of 50 consecutive cases

■Dutch pathologists routinely record tumour to high tie distance as a quality indicator

37
Q

TME - total mesorectal excision

A

■Excision of the entire mesorectal fat below the anterior peritoneal reflection covered by fascia

■Initially proposed by Quirk (Leeds) and Nagtegaal (Netherlands) as prognostic factor

■With increased and universal adoption in developed countries- quality indicator/credentialing factor

38
Q

grading quality of mesorectal excision in TME specimens

A
39
Q

TME grading -recap

A

■TME3- Smooth fascia, no defects, no coning

■TME1- muscle fibres visible at any point

■TME2- between 1 and 3

40
Q

ELAPE - extra levator abdominoperineal excision

A

ELAPE: No longer wuality indicator, but a tumour dpeendent surgical varibale

41
Q

Subsequent surgical managements decided by pathological parameter sincluding tumour budding and grade:

Minimally invasive techniques for polyps etc

A

■EMR- endoscopic mucosal resection

■TEMS- trans anal endoscopic mucosal surgery

■ESD- endoscopic submucosal dissection

■Very early or undiagnosed cancers

■Often polyps with limited invasion at the base

■No endoscopic or imaging concerns

U17 + 18 (22 decks)

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