MOD (tumors, GI path) Flashcards

1
Q

Adenocarcinoma vs SCC risk factors?

A

Adeno–obesity, alc

SCC–HPV!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 types/ ease of removal of esoph cancer?

A

Polyploid/ exophytic (most, golf ball, easy to excise)
Ulcerated/excavated (harder to remove)
Flat/diffuse (least)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What histo changes happen in Barretts?

A

intestinal metaplasia of esoph!
Non-ker stratified squamous epith of esoph is replaced with intestinal, non-cil columnar epith (with goblet cells!)
(BE comes from GERD, most ppl with BE will not get a carcinoma!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do goblet cells in esoph mean? what risk is it assoc with?

A

Indicate chronic mucosal injury/ metaplasia

Assoc with incr risk of adenocarc in esoph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

4 types of esoph cancer invasion/spread? (eg where does it spread to)?

A

1 Intra esophageal (resect and bring up stomach)
2 Direct extensions (to lungs, aorta and nearby structures etc)
3 Lymphatic spread (to lymph nodes, drain to celiac trunk and can metast)
4 Distant disease (spread to retroperitoneal and celiac LNs, metast to liver and lung) (cant remove w surgery if spread to nodes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 most common locations for esoph cancer metastases?

A

Lungs
Liver
Retroperitoneal/Celiac lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

SCC vs adeno risk factors?

A

SCC: n-nitrous cpds (smoked meat), red meat
Adeno: GERD/ZE/H pylori, antichols, etc
both smoking and alc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TNM tumor staging?

A

T size
N nodal spread
M metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Major benign esoph tumors? sx?

A

Leiomyoma (soft tissue tumor), trouble swallowing can be resected (also papilloma, polyp, fibroma hemangioma etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Most “common” stomach cancers? (location?)

Pop for lymphomas?

A

Lymphomas (immunosuppr/HIV etc)
Carcinoids
Malig stromal tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diffs between intestinal and diffuse gastric cancer classifications?
(Histo, differentiation, M:F, etc)

A

Intestinal gastric cancer– polypoid, elev, well diff, males

Diffuse gastric cancer– ulcerated/fung, poorly diff, SIGNET RING, = M:F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Grade vs stage?

A

Grade–differentiation

Stage–invasion/metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Early vs Advanced gastric cancer?

A

Early: confined to mucosa/submuc, good survival, removed with margin
Advanced: inflitrates into muscularis propria, lymph, nodes, poor px and low survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Carcinoid tumor def?

Appearance gross/histo?

A

Epithelial neoplasm with neuroendocrine differentiation (grade 1 NET, grade 2, and NEC neuroendo carcinoma)

Gross: pedunculated, vascular/red
Histo: cells who organoid arrangements, uniform nuclei with salt and pepper chromatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common tumors in stomach (3)
Esoph?
Duod? (which chemicals are produced?)

Sx? Most common?

A
  • Stomach: Type I NET (most common) with pernicious anemia and gastrinemia, autoimm), typie II net assoc with MEN-1 and ZE from gastrin-secreting tumor (elev gastrin), and type III NET (poor px, large)
  • Esoph: mostly carcinoid or NEC
  • Duod: Non-MEN-1 NET prod gastrin, or somatostatin, and MEN-1 which prod gastrin (NET)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Zollinger-Ellison syndrome?

A

Gastrin secreting tumor causes peptic ulcers! (sporadic or MEN-1) (can give Ca2+ stim to identify if gastrin doesnt show up as elev during dx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Benign liver tumors? (3)

Which is most common?

A

Cavernous hemangioma (most common benign liver tumor!)
Focal nodula hyperplasia
Hepatocellular adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cavernous hemangioma

Pop? Histo/Gross? Px? *Complications?

A

Most common!
Appearance: see on a CT scan commonly, large squishy cherry spot, histo is reddish hemorrhage of vasc
-Complications: DIC coag in extreme sports/ KAsabach Merrit (tumor sucks up platelets), and Rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Focal Nodular Hyperplasia etiology?

Appearance?

A
  • From localized hyperperfusion due to presence of anomalous artery, fibrosis of liver tissue can cause central scar, intact arc but abnormal vasc
  • females (like prev), most asmp, X on scan
20
Q
HEPATOCELLULAR ADENOMA 
Pop?
Risks?
Sx?
Px/size?
Results/ compl?
Histopath/layers?
Subtypes?
A
  • women (sex hormones, contraceptives, glycogen storage dis)
  • solitary lesion
  • sx: abd pain, referred pain bc liver doesn’t have nerve endings
  • can rupture (ESP if pregnant and HTN) center can get necrotic (high risk at >5cm), can lead to HELLP (hemolysis/elev liver enz/low platelets), can turn into hepatocell carc
  • histopath: absence of portal triads/bile ducts, hepatocytes everywhere instead (but normal nucl), 2 or fewer layers, aberrant arteries
  • subtypes: Beta-catenin activated HCA has HIGHEST risk for malig!
21
Q

Types of malig liver tumors? (4 + metast)

A

Hepatocellular carcinoma (incl fibrolamellar)
Choliangiocarcinoma
Hepatoblastoma (bbys)
Angiosarcoma

22
Q

Hepatocellular carcinoma
risks?
Histopath/layers?

A
  • risks: HEP B!!!, virus can cause scarring, (other causes like aflatoxin, NASH steatohep, type II DM, alc/smoking, A1-AT herid dis etc)
  • histo: scarring with large atypical cells with mitosis, 3+ layers!
23
Q
Hepatocell carc (cont)
Gross
Dx
Tx
Invazn
Mutation
A
  • gross: nodular brown firm liver, with golden tumor in center
  • dx: hypervasc masses on imaging (big and white), glypican-3, elev AFP
  • tx: resect (can resect a lot if small, transplant or ablation if big)
  • invazn: portal vein
  • mut: TERT telomere stability, p53, beta-catenin
24
Q

Fibrolamellar HCC?

Pop? gross/histo? px?

A
younger pts (30 etc)
-large tumor, better px than HCC, but metast, fibrosis
25
Q

Cholangiocarcinoma

  • Types (3) and most common
  • sx
  • risks
  • histo
  • px
  • tx
A

Cancer of bile ducts!

  • types: intrahepatic, hilar, extra hep (last 2 cause jaundice bc obstruct bile duct)
  • sx: jaundice
  • risk factors: sclerosing of ducts, ulcerative colitis/flukes/cysts/nitrosamines in diet
  • histo: cells prolif/fibrosis, klastskin tumor (hilar CCA), skip lesions
  • px is better with intrahep (can also be mixed CCA and HCC which is worse px), resect, transplant (but can be bad)
26
Q
Hepatoblastoma
Pop?
Assoc/sx?
Causes?
Lvls?
Histo?
Tx?
Px?
A
  • babies within first 5 yr
  • assoc with anemia, and thrombo
  • elev AFP!
  • histo: tumor cells look like fetal hepatocytes, epith, sometimes pink mesenchymal bone, or small cell pattern
  • Tx: neoadjuvent hemo then operate, decent survival
27
Q

Angiosarcoma
Px?
Appearance?
Cause?

A

-bad px
-v vascular, red and black; hemorrhage w diffuse enlargement of liver w nodular appearance, malig prolif of endoth cells
-cause: from polyvinyl chloride eg tires, males
(liver and bile duct cancers have increased mortality)

28
Q

Which hepatic malig is most common?
Metast from?
Tx?
Mutations?

A

Metastatic disease!
Can come from colorectal cancer
Tx with surg ablation neoadj chemo
KRAS mutation (need more chemo, but too much can cause fatty liver cirrhosis)

29
Q

Diaphragmatic hiatal hernia compl?

A

can be from incompl during dev, compli is pulm hypoplasia

30
Q

Pyloric stenosis and congen assocs/sx?

A

Hyperplasia of pyloris that obstructs gastric outlfow
Sx: nonbiliary vomiting newborn with distended stomach
Assoc with Trisomy 18 and Turners

31
Q

Gastric heterotopia and assocs?

A

displaced tissue in GI, large/red, normal mucosa with oxyntic glands, inlet patch
-assoc with barrets, adenocarc (acid release), even ectopic pancr tissue

32
Q

If gastric mucos makes way into colon this cause?

A

occult blood loss

33
Q

What are the cells/secretions in the body vs antrum of stomach?

A

Body–parietal cells secr HCl (and intrinsic factor)

Antrum–G cells secrete gastrin (which stim par cells to secr more HCl)

34
Q

Protective mechs of stomach from acid?

A
Tight junctions
Mucin
Bicarb
Turnover
PGs! (help w. all of above! NSAIDS inhibit this!)
35
Q

Acute gastritis causes/mechs?

Mild acute?

A

Transient inflam mucosa
Can be from NSAIDS which inhibit PGs
sx pain nausea vomit bleed
-Mild acute: Lamina prop congested but BM ok, transient mucosal but no hemorr, surface epith intact

36
Q

Which cells infiltrate in acute vs chronic gastritis?

A

Acute– NEUTROS!

Chronic–LYMPHOS! (and plasma cells)

37
Q

Erosive hemorrhagic gastritis?

appearance?

A

erosion (superficial epith lost, prululent exudate with fibrin) and hemorr (ulcer where entire mucosa is gone, can extend into submucosa),
-darker black spots in bright red mucosa on gross

38
Q

Chronic gastritis and most common cause

A
  • Most common cause is H pylori
  • gland atrophy w/ lymphos
  • nausea/vomiting/pain
39
Q
H pylori 
appearance
results
cells and features
complications
MALT
A
  • Most common cause of CHRONIC GASTRITIS
  • spiral shaped gram neg, lil dark rods on GIEMSA
  • assoc with poverty, foreign etc
  • lymphocytic and neutrophilic bc bact, interstit metaplasia (looks columnar and has goblet cells!), poorly diff glands, MALT lymphoma (neoplastic B cell lymphoma in mucosa)
  • compl include gland atrophy
40
Q

Antral vs pangastritis? leads to?

A

antral gast- high acid, (can lead to ulcers)

pan gast-decr acid bc mucosal atrophy (can lead to adeno)

41
Q

Tests for H pylori?

Tx?

A

GOLD STD: histo! GIEMSA stain
-do if pt has dyspepsia w/o alarm sx, can also use serologic test for IgG against pylori for current/past, stool antigen test for active infxn, urea breath test, can have false negatives (esp if antibios PPIs etc)

42
Q
Autoimmune gastritis
Def
Sx
Causes/ assoc
Cx
Etiology
Compl
Histo
Tx
A
  • sx smooth beefy RED TONGUE, atrophic glossitis of tongue
  • assoc with folate/B12 deficiency (pernicious/ megaloblastic anemia) always
  • not in antrum, cx is loss of parietal cells (so no HCl and IF decr B12 abs in ileum causing megalob anemia)
  • women, autoimmune conds
  • compl: periph neurop, spinal cord, cerebral etc
  • tx: IM so b12 can get in
  • histo: lympho/macro infilt, glandular atrophy
43
Q

Other uncommon gastritis?

A

IgE allergic eosinophilic gastritis
Lympho gastritis assoc with celiacs
Granulomatous

44
Q

Acute ulcer types?
Tx?
diff between acute and chronic ulcer appearance?

A

ulcer breaches mucosa

  • acute: from acute erosive gastritis, ICU, stress, curling/cushing etc; small round, many, with marked borders, no scarring (chronic has scarring)
  • tx acute with PPI and H2 blocker
  • chronic PUD: H pylori or NSAIDS (smoking, steroids etc), gastric hyperacid from H pylori, gastrin, ZE assoc, benign near lower, elev borders, bleeding/perfor, various tx
45
Q

Ulcerated gastric carcinoma and diff with benign ulcers?

Sx/alarm features and location?

A

Ba px, assoc with iron def anemia and wt loss (alarm features that indicate cancer)
-larger ulcers with heaped up margins (Benign are smaller with raised margins), antrum

46
Q

Types of polyps and diffs?

Pop? assocs? appearance?

A
  • Hyperplastic/inflam polyps: assoc with chronic gastritis, rxn causes polyp growth (can elim by elim pylori)
  • Fundic gland polyps, women, assoc with PPI tx, decr acid secr increases gastrin secr by G cells, G/gland prolif (collectionof polyps), not malig, increased risk for gastric adenoma