L16 GI Malig Flashcards

1
Q

LO2: desc how GI der infec or CA may spread.

A

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2
Q

LO3: desc incid of var comm CA of GIT.

A
  • oesoph carcinoma- wide geog var. 2% malig in UK. Male more than fem. low US. High arnd Caspian Sea. High China. Squad less, adeno increasing.
  • gastric CA- 15% CA deaths world. Poor prog- present adv, vague symps, stom large so while for eff, esp in yng when seen as unlikely, less early endosc. 5 yr surv under 20%. Men more than wom. Japan, Columbia, Finland high. Assoc with gastritis, H pylori. More comm in blood grp A so genet compon.
  • colorectal CA most comm E and W 25000 new case per yr. carcinoma of stom 2nd with 11000 new cases per yr. decreasing in UK. Panc 5500 per yr. then oesoph.
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3
Q

LO4: desc histol app of comm GI CA.

A

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4
Q

LO1: gastric

A

GASTRIC CA:
-clinic- symps often vague, epigastric pain, vom, weight loss.
-investig- endosc, biop, barium less often. Stranding is feat of mailing stricture.
-macro feats- fungating or diffuse infilt- leather bott stom. Ulcerative. Infiltrative (linitus plastica). Early- not adv but still CA.
-microsc feats- int var deg gl format. Diffuse sing cells and small grps, signet ring cells full mucin.
-early- confined to mucosa/submuc. Uk us Id after spread further. Japan screen Id early, lesions not prod symps. Good prog.
Adv- furth spread, X stom wall, somet perit to liv etc. Comm UK. 10% 5yr surv.
-spread- direc through gastric wall. LN- local and L supraclavic fossa. Liver. Trans coelomic- perit, ovaries.
-tx- surg, chemo, herceptin.
-H pylori- gen assoc of chronic inflamm with CA, schistosomiasis, IBD etc. Gastric CA comm where high Hp eg Colombia. Serologic and epidem ev.
-gastric lymphoma- most comm GI lymphoma. Starts as low grade lesion. Str assoc Hp. Erad Hp can= tum regress. Hp stim B lymphoc, clinal prolif, one becomes domin and changes to lymphomotous stage, so look for lymphoma in gastric biop too. Prog better than gastric CA.
-GI stromal tums- uncomm. Der from int cells of cajal (pacemaker). C-kit (CD117) marker. Specif targeted tx- imantinib. Unpredictable behav- pleomorphism, mitosis, necrosis. Mostly get all out, some receurr or metast. Size of lesions and mitot count Indic recurr/metast risk. Histol bundles of spindle cells interweaving.
-bezoar made of hair is trichobezoar NOT tum.

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5
Q

LO1: LI

A

TUMS OF LI: SI gen few tums.
-adenomas, adenocarcinomas, polyps, anal carcinoma.
LI ADENOMAS:
-Macro- sessile (flat) or pedunculated. Micro- var deg of dysplasia, all show dysplasia in LI not other sites, low and high grade. Behav- definite malig often, assoc with dev colorectal adenocarcinomas.
-Incid- incr with age in W pop, genet synds incr incid.
-Genet conds-
famil adenomatous polyposis- autos domin, chrom 5, 1000s adenomas by 20, high risk CA, only real tx rem colon and rectum. Gardners synd- simil to FAP, bone and soft tiss.
-Adenoma to carcinoma seq- sim geog distrib. Anat distrib simil too. Synchronous lesions. Metachronous lesions. Adenomas with invas.
-Sessile adenoma arises straight from mucosa. Pedunculated stalk, dark metaplastic epith. FAP many adenomas.

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6
Q

LO1: LI

A

COLORECTAL ADENOCARCINOMA:
-macro- 60-70% rectosigm. Fungating esp R side, on R unlikely obstruc as big and distensib, often present with iron defic anaemia. U+L endosc if over 60. Stenotic esp L side.
-link= basis screen prog. Blood Indic large adenoma twist/ulcer or adenocarcinoma. Are other reasons. Polyps for biop, rem. Tx for carcinomas. Rid adenomas, rid preCA risk.
-barium enema or CT now- apple core stricture- colonic adenocarcinoma. Mushroom. Low down CA can prolapse.
-microsc- Maj are mod diff. Occas mucinous. Occas signet ring cell type. Expanded glob mucus, signet pushed one side.
-spread- direc through bowel wall to adj organs eg bladder. Via lymphat to mesenteric LN. Via port ven sys to liv.
-dukes staging for colon: A confined to bowel wall. B through wall, but LN clear. C LN inv. C1/2 highest node clear/inv. TNM- T deps on how far through wall, N is nodal metast, M metast.
-genetics- FAP. RAS mut- cetuximab works only if intact k-RAS path. 18q(DCC) delet. 17q (p53) loss or inactiv. N-RAS. Braf infl prog.
-incid- peak 60-70, uncomm in yng unless precip dis. High UK/USE, low Japan. Polyposis synds. UC and crohns.
-aetiol- low resid diet, fibre reduc constit, divert, piles. Slow transit time, allow contact noxious molec and mucous longer. High fat intake. Genet. Predisp. High fibre dilutes harmf thing in diet, more stool, toxin decr conc.
-outc- surv decr with incr dukes stage or TNM. Liver metast comm in adv dis. Chemo palliative. Resection of liv deposits good outc. Local radio therap- not colon as surr tiss dam, can loc to rectum, often tx bef surg shrink tum and sterilise area of malig cells for recurr.
-other LI tums-
Carcinoid tum- rare neuroendoc tum, unpredictable. Can get anywhere in GIT, are malig many don’t kill or metast, comm appendix. Some grow and metast to liv.
Lymphoma- rare, may be prim or spread from elsewhere.
Smooth musc/stromal tum- more comm, anywhere in GIT, most in stom. Rare and unpredictable.

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7
Q

LO1: panc

A

CARCINOMA OF PANC:

  • early symps vague. often not diag til metast. Unless block bile duct early=jaund. Slow symp- weight loss, jaund, troussaeu’s sign rash. Imaging for diag- better biop now, most diag rely radiology, diffic to acc. Diffic prove CA bef whipple.
  • morphol- 2/3 in head. Firm pale mass. Cut surf- necrotic, haemorr, cystic. May infilt adj strucs eg spleen if tail.
  • histol- 80% duct all adenocarcinoma. Well formed gl +/- mucin. Soma acinar tum cont zymogen grans. All types poor prog.
  • carcinoma of ampulla of vater- obstruc bile duct early. Big op but high chance cure as small lesion. Jaund and silver black stool. Malabs and lack bile.
  • islet cells tum rare- insulinoma=hypog. Glucagonoma= skin rash. VIPoma-Werner Morrison synd. Gastrinoma- zollinger Ellison.
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8
Q

LO1: liver

A

TUMS OF LIV:
- benign- hepat adenoma. Bile duct adenoma/hamartoma somet ID dur surg, if metast CA stop surg. Haemangioma BV tum, app in scans for metast dis, char.
-malig/prim- HCC. Cholangiocarcinoma. Hepatoblastoma. Malig can be prim or sec. Most malig tum in liv are metast.
Secondary tum in liv- multip metast. Can excise, ablate, freeze etc.

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9
Q

LO1: desc comm GI CA and clinic present.

A

OESOPH CARCINOMA:
-clinic feats- Dysphagia prog worse. Weight loss.
-Investig- endoscopy, biop, barium to see stricture.
-Pathol feats-
squamous cell carcinoma- most comm, can occ at any lev. Adenocarcioma- less comm but getting more, lower 1/3, Barrett’s.
-Aetiol/ pathogenesis- squamous carcinoma- HPV, tannin, vitA defic, riboflavin defic, presumed prog through dysplasia. Adenocarcinoma- arises in metaplastic epith of Barrett’s oesoph after contin inflamm- squamous to gl mucosa (eg histol see mucin in goblet) to protec from ac. Prog through dysplasia to adeno. Controversy over foll up. US more endosc, finan invent.
-prog- adv dis at present us. Direc spread through oesoph wall. Only 40% respectable- due to spread or other conds, radio or chemo poss bef surg but decr fitn. Lot pt have tube through tum to swall. 5% 5 yr surv.

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