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GI Exam 1 > Small and Large Intestines > Flashcards

Small and Large Intestines Flashcards

1
Q

Inflammatory bowel disease (IBD) definition:

example diseases?

A
  • chronic relapsing inflammatory disorders of intestinal tract of obscure origin affecting GI tract
  • Crohns and ulcerative colitis
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2
Q

pathogenesis of IBD

A

not well understood - could result from unregulated and exaggerated immune responses to normal gut flora

-M-cells have some abnormal regulation or presentation

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3
Q

WHcih immune cells are primary culprits in Crohns and UC?

A

T-cells and their products

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4
Q

which hypersensitivity reslts in Crohns?

A

chronic delayed type

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5
Q

Excessive stimulation of TH2 cells in which condition?

A

IBD –> ulcerative colitis!

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6
Q

TH2 cells stimulated in which condition?

A

UC

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7
Q

Which condition is a transmural inflammation - through bowel wall?

A

CD

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8
Q

CD - defintion:

A

-idiopathic, chronic ulceroconstrictive inflammatory bowel disease characterized by:
~sharply delimited and typically transmural involvement of bowel by an inflammatory process with mucosal damage
~presence of non-caseating granulomas
~fissuring with formation of fistulae
~sytemic manifestations in some patients

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9
Q

Whcih condition has inflammation that is limited to mucosa?

A

UC

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10
Q

Affected area CD vs UC?

A

Crohns can be anywhere in GI tract vs UC only in intestines

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11
Q

People affected - CD:

A
  • peak in 20s and 30s but any age
  • Whites
  • Females
  • jewish population
  • SMOKING IS A STRONG RISK FACTOR
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12
Q

CD patient presentation:

A
  • All have diarrhea - can be bloody
  • fever
  • pain,
  • WL
  • weakness
  • anemia

ALL DUE TO TRANSMURAL INFLAMMATION

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13
Q

Which condition has higher CA risk, CD or UC?

A

UC has higher risk

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14
Q

CD - long term issues:

A
  • malabsorption
  • inc risk of carcinoma (but not as high risk as with UC)
  • amyloidosis
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15
Q

Morphology of CD

A
  • segmental - skip lesions
  • Early APHTHOID ulcers - linear
  • COBBLESTONE MUCOSA
  • thickened, inflexible way (RUBBER HOSE) - Luminal narrowing
  • CREEPING FAT - dull gray, granular serosa
  • Fissures and fistulous tracts, abscess formation
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16
Q

Whcih condition has skip lesions and which is continuous?

A

CD=skip lesions but transmural

UC=continuous but only in mucosa

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17
Q

**Main histological difference bw UC and CD?

A

**CD has non-caseating granulomas

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18
Q

String sign on radiology?

A

thickening of bowel in CD

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19
Q

wHich condition has more primary sclerosing cholangitis?

A

UC more than CD!

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20
Q

Crohns disease extraintestinal manifestations:

A
  • migratory polyarthritis
  • sacroiliitis
  • ankylosing spondylitis
  • erythemia nodosum
  • clubbing of fingertips
  • primary sclerosing cholangitis (less than seen with UC)
  • mild hepatic pericholangitis
  • uveitis
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21
Q

UC- definition:

A

ulceroinflammatory disease limited to colon and affecting only mucosa, submocusa

  • extends CONTIGUOUSLY (NO SKIP LESIONS) proximally from rectum
  • NO GRANULOMAS
  • systemic disorder
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22
Q

NO granulomas with which condition?

A

UC!

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23
Q

Thinning of the bowel vs thickening of the bowel conditions?

A 
Thinning = UC
THickening = CD
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24
Q

First place affected in 50% of UC patients? How it presents?

A

rectum = BLOODY MUCOID DIARRHEA!*

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25
Q

Ulcerative colitis morphology:

A
  • rectum involved
  • continuous proximal involvement
  • BACKWASH ILEITIS - debris washed back into ileum if through whole colon
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26
Q

Chronic UC has:

A

-coalescence of ulcers and pseudopolyps

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27
Q

Complication of UC?

A

toxic megacolon

perforation

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28
Q

Only affect part or all of colon?

A

UC

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29
Q

Histology of

1) Active UC:
2) chronic UC:

A

1) -mononuclear infiltrate in lamina propria
- crypt abscesses (PMNs in crypts)
- dystortions of crypts
- ulcerations
- granulation tissue
- NO GRANULOMAS!!!!

2) ulcerations
- submucosal fibrosis
- POSSIBLE CARCINOMA
- flat dysplasia
- atrophy
- mucosal glad disarray

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30
Q

Inflammatory pseudopolyps seen in:

A

UC!

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31
Q

Muscularis propria and serosa are unaffected in which condition?

A

UC

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32
Q

Presentation UC?

A
  • remitting and relapsing with stress as precipitant
  • lower abdominal pain, cramps
  • relieved by pooping
  • BLOODY MUCOID POOP
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33
Q

MAIN COMPLICATION OF UC?

What drives this complication?

A

CARCINOMAS!! - usually no obvious mass!!! - early diagnosis is critical

DNA damage and microsatelite instability in mucosal cells

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34
Q

***Results of transmural infiltration in CD?

A 
Serosa inflamed
adhesions
fistulas
perianal abscess and fistula
granulomas
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35
Q

Does UC or CD have potential for megacolon?

A

UC!

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36
Q

Ischemic colitis is what kind of disease?

Where most often occurs?

A
  • vascular disorder

- most often occurs in “watershed” areas of splenic flexure (SMA and IMA) or rectosigmoid (IMA and hypogastic)

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37
Q

causes of Ischemic colitis?

A
  • multifactorial!
  • arterial embolism
  • arterial thrombosis
  • low flow states (non-occulusive)
  • venous thrombosis
  • miscellaneous - radiation, volvulus, stricture, herniation
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38
Q

transmural infarction is due to:

A

Its gangrene due to acute vascular obstruction

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39
Q

Mural and mucosal infarction due to?

A

acute or chronic hypoperfusion

NO SEROSAL INVOLVEMENT

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40
Q

What kind of diarrhea with mural and mucosal infarct?

A

bloody diarrhea

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41
Q

Transmural infarction (gangrene):

  • what layers involved?
  • most common cause?
  • mortality?
A
  • all layers! comprise of MAJOR blood vessels
  • thrombosis or embolism of SMA in 50% of cases
  • rapid progression to shock and death - for sure dead if not immediately removed
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42
Q

Cronic ischemia:

  • think of what kind of patient
  • what happens?
A

-older patient with inflammatorry bouts
inflammation ulceration and fibrosis - may lead to stricture
-may have some bloody diarrhea

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43
Q

Angiodysplasia

  • what is it?
  • what layers involved?
  • problem with most cases?
A
  • non-neoplastic vascular dilation and malformation of submucosal blood vessels in cecum and ascending colon
  • mucosa and submucosa
  • significant bleeding of lower intestines = trouble
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44
Q

Lots of frank red blood flowing think which disease?

A

angiodysplasia
or
diverticular disease

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45
Q

diverticular disease

-due to?

A

increased abdominal pressure
meat eating
others tuff

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46
Q

where is most diverticular disease?

A

sigmoid colon - weak areas of submucosa and muscularis propria where small mesenteric vessels penetrate muscularis propria

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47
Q

pathogenesis of diverticular disease?

A
  • focal weakness in colonic wall coupled with increased luminal pressure
  • low fiber diet
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48
Q

Clinical presentation of diverticular disease

A

most are asymptomatic

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49
Q

What do diverticula look like with barium CT?

A

saw-tooth pattern

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50
Q

complications of diverticular disease:

A
  • when inflammed - deverticulitis = most common

- when rupture

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51
Q

Intestinal obstruction

  • what part of intestine most often affected?
  • conditions most patients with this have?
A
  • usually involves small bowel

- Hernias, adhesions, intussusception, volvulus

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52
Q

Why does obstruction cause pain?

A

bc distention can cause pain!!

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53
Q

Hernias:

  • definition:
  • typical regions?
  • may cause what issues?
A
  • outpouching of peritoneum through defect or weakness in abdominal wall; serosa lined sac of peritoneum; external herniation
  • typically inguinal and femoral regions
  • umbilical if surgical scars
  • may cause incarceration and strangulation
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54
Q

Inguinal hernias

-types:

A

direct: IN ADULTS- medial to inf epigastric vessels - weakness in hasselbacks triangle
indirect: lateral to inf epigastric vessels - congenital or acquired in adulthood - can go down into testes

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55
Q

adhesions

  • what are they?
  • when can they happen?
  • what can happen because of adhesions?
A
  • fibrous bridges between bowel segments or abdominal wall
  • following inflammation (peritonitis), surgery, infection, endometriosis - RARELY CONGENITAL
  • viscera can slide between the fibrous bridges and become trapped
  • obstruction and infarction
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56
Q

intussusception
what is it?
issue with this?

A
  • proximal egment of bowel telescopes into a distal segment of bowel by wave of peristalsis
  • leads to infarction
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57
Q

volvulus think:

A

TWISTING OF BOWEL

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58
Q

Volvulus:

  • issues when this happens?
  • most frequent in who and which bowel?
A
  • ischemia and necrosis
  • most frequent in children - small bowel
  • adults get in small and large bowel
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59
Q

steatorrhea definition:

A

malabsorption of fat - abnormal bulky, frothy, greasy, yellow or gray stools

60
Q

symptoms of malabsortion

A
  • steatorrhea
  • WL
  • anorexia
  • abdominal distention
  • borborygami
  • muscle wasting
61
Q

Most common Malabsorptive disorders in US?

A

-celiac sprue
chronic pancreatitis
-crohns

62
Q

Malabsorptive disorder cause in OUS?

A

problems of infectious causes

63
Q

celiac sprue;

1) what is it?
2) characteristic mucosal biopsy?
3) diagnosis?
4) TX?
5) issues?

A

1) genetic susceptibility - exposure to gliadin = T-cell mediated chronic inflammatory reaction
2) vilous atrophy
3) Hx, biopsy, response to diet
4) gluten free diet
5) malabsorption

64
Q

Tropical sprue

1) what is it?
2) where is it?
3) what happens?

A

1) Entire small intestine affected –> folate and/or B12 deficiency (megaloblastic changes) in intestinal epithelial cells
2) tropical disease - india, caribbean, africa, SE Asia, Central and S America
3) Bacterial overgrowth = use borad spectrum antibiotics

65
Q

Whipple Disease

1) what is it?
2) what does it effect?
3) who is affected?

A

1) tropheryma whippelii - organism lives in macrophages
2) systemic disorder - intestine CNS and joints = severe malabsorption, diarrhea, steatorrhea, emaciation, fever, polyarthritis
3) middle ages whites - 10 Males to 1 Female

66
Q

Whipple disease - hallmark

A
  • macrophages are stuffed with PAS + granules from Tropheryma whippelii a gram pos actinomycete
  • pretty mcuh goes everywhere
67
Q

Vili with foamy macrophages and stains PAS + what issue?

A

Whipple Disease

68
Q

WHat is the most common tumor of GI tract?

A

adenocarcinomas

69
Q

most common tumors of small bowel?

A

adenocarcinomas and carcinoid

small bowel tumors not as common as large bowel

70
Q

Most frequent benign tumors of small intestines?

A

adenomas, mesenchymal tumors (GISTs)

71
Q

most common site for adenoma of small bowel?

A

ampulla of vater - where common bile duct comes in == pateints present with jaundice

72
Q

What genetic condition increases risk for small bowel adenoma?

A

familial polyposis coli (FPC)

73
Q

What inflammatory condition increases risk of small bowel adenoCARCINOMA?

A

crohn disease

74
Q

small bowel adenocarcinoma - distinctive feature:

A

“napkin ring” - encircling pattern or as polypoid masses similar to colonic carcinomas

75
Q

Adenocarcinoma more common where and hwat part?

A

more common in large bowel - rectum to sigmoid is hotspot

76
Q

polyps start wth what appearance and grow to have?

A

all are sessile and form stalk (pedunculated)

77
Q

most non-neoplastic polyps how formed?

A

formed as result of abnormal mucosal maturation, inflammation, or architecture (HYPERPLASTIC POLYP)

78
Q

most common neoplastic polyps:

A

adenomatous polyps (adenomas) - precursors to CA = epithelial polyps arise as result of proliferation and dysplasia

79
Q

Hyperplastic polyps: are these common? ***where are they? what kind?

A

common

***benign in recto-sigmoid area

80
Q

harmartomatous polyps:are these common? where are they? what kind?

A

-normal tissue components arranged abnormally

may be part of familial syndrome

81
Q

inflammatory polyps - seen with what disease>

A

seen in IBD

82
Q

cause of hyperplastic polyps:

malignant potential?

A
  • pdecreased epithelial cell turnover and delayed shedding with accumulation of mature cells on surface
  • no neoplastic potential
83
Q

Which polyps are juvenile and retention polyps?

A

juvenille LARGER happen in childern = hamartomatous polyps

rentention SMALLER polyps happen in adults

84
Q

What happens with juvenile polyposis syndrome?

A

young patient has juvenille polyps (hamartomatous) but has increased risk of adenomas and adenoCA

85
Q

Peutz jeghers polyps - how happens? new risks?

A
  • a hamartomatour polyp WITH MUCOCUTANEOUS PIGMENTATION but there is a mutation in STK11 gene
  • risk for intussusception!
86
Q

adenomas polyp is precursor to

A

colorectal CA

87
Q

most important determinant of adenomas?

A

SIZE!!

88
Q

four types of neoplastic adenomatous polyps?

A

tubular
tubulovillous
vilous
serrate

89
Q

Most common adenomatous polyp?

A

tubular

90
Q

TUbular adenomas:

A

most common, least likely to be malignant, larger ones pedunculated (stalk)

91
Q

tubulovillous adenomas:

A

mostly tubular, malignancy risk intermediate

92
Q

vilous adenomas:

A

sessile, broad based tumors

usually large frequently contain carcinoma

93
Q

serrated adenomas:

A

overlap with hyperplastic polyps histologically; most in right colon, full thickness serration

94
Q

intramucosal carcinoma

A

breached basement membrane to invade lamina propria or muscularis mucosa, no metastatic potential

95
Q

Villous adenomas: when is there an increased risk for CA?

A

if it is >4cm

96
Q

Villous adenomas - propensity to be where in GI? Causes?

A

rectum and rectosigmoid

causes bleeding - protein losing enteropathy

97
Q

What is trouble with removing villous adenomas?

A

they have no stalk

98
Q

Tubulovillous adenomas

  • appearance?
  • risk of CA?
A
  • usually have a stalk

- CA risk depends on how villous it is

99
Q

factors determining dev of CA in adenomatous polyps?

A

SIZE
proportion of villous component
degree of dysplastic change

100
Q

Adenomas presentation?

present secondary to?

A

usually asymptomatic

bleeding - esp anemias / iron def anemia

101
Q

Villous adenoma presentation?

A

symptomatic - overt rectal bleed and mucous secretion which can lead to hypoproteinemia, hypokalemia

102
Q

Whcih adenoma type has little or no metastatic potential?

A
  • intramucosal CA with lamina propria
  • hgih grade displasia (CIS)

==> these are benign

103
Q

Which adenoma type can metastasize?

A

invasive adenoCA - Crosses muscularis mucosa

104
Q

3 criteria that must be met to have adequate excision of pedunculated adenoma with invasive CA?

A

1) AdenoCA is superficial, does no approach margin of excision across base of stalk
2) no vascular or lymphatic invasion
3) CA is not poorly differentiated

105
Q

surgery for invasive CA arising in pedunculated or sessile polyp -

A

cannot use polypectomy- must remove part of bowel - complete resection

106
Q

colorectal CA risk factors:

A

1) increasing ages
2) prior colorectral CA or polyps
3) UC or CD
4) genetics
5) diet

107
Q

older male patient with iron deficiency anemia… what must be ruled out?

A

GI carcinoma until proven otherwise

108
Q

GI carcinomas like to send mets to…

A

LN, LIVER, LUNGS and BONE

109
Q

What is cause of left side colorectal CA?

A

solid stool passing by - tumor is a little smaller maybe

110
Q

What is cause of Right sided colorectal CA?

A

anemia 2ndary to blood loss - watery poop still in this area so tumor can grow a lot more

111
Q

Thin pencil like poops?

A

annular CA on left side - napkin ring lesion

112
Q

Classical FAP syndrome due to what mutation?

A

mutations in adenomatosis polyposis coli (APC) gene

113
Q

Classic FAP syndrome - prognosis

A

ALL will develop CA before age 30

114
Q

Attenuated FAP syndrome due to what mutation?

A

APC and MUTYH

115
Q

Presentation of attenuated FAP?

A

delayed appearance of colon cancer - around age 50

116
Q

Location of most tumors in Attenuated FAP?

A

proximal colon

117
Q

Gardner syndrome - how different from FAP?

A
  • same everything as FAP but ALSO distinctive extraintestinal manifestations (skull and mandible, epidermal cysts, cancer near teeth … lots more)
118
Q

Turcot syndrome:

  • what is it?
  • how different from FAP?
A
  • combo of colonic polyposis and tumors of CNS
  • 2/3 have development of medulloblastomas if APC gene mutated
  • 1/3 have glioblastomas due to mutations in DNA repair genes
119
Q

Turcot think:

A

COLON AND BRAIN

120
Q

What is Lynch Syndrome? where affect?

A

–HNPCC- hereditary nonpolyposis colorectal cancer

–usually right colon but increased risk of many organ extraintestinal adenoCA (especially endometrial)

121
Q

Hallmark of HNPCC (Lynch syndrome) - which defects?

A

mutations in genes for detection, excision, and repair of DNA during replication
*MSH2 and MLH1**

122
Q

MSH2 and MLH1 think what disease?

A

Lynch - or HNPCC

123
Q

HNPCC inheritance pattern?

A

autosomal dominant

124
Q

Poorly differentiated colon CA may have what appearance?

A

signet ring

125
Q

staging for colorectal adenomCA?

A 
TNM staging
0 in mucosa
1 in mucosa and muscularis propria
2 deeper in muscularis propria
3 = into LN
4 = seeded to other organs
126
Q

Modified dukes staging (astler coller)

Stage A and B?

A 
A= limited to mucosa
B1 = extending into muscularis propria
B2 = transmural but no LN

A and B best 5 yr survival

127
Q

Carcinoid tumors - main sites?

A

GI tract and lung

128
Q

Most common site for carcinoid tumors?

A

appendix

129
Q

Carcinoid appendix and rectal cancers and metastasis

VS

ileal, gastric, and colonic corcinoids and metastasis?

A

rarely metastasize

FREQUENTLY METASTASIZE

130
Q

If a carcinoid tumor gives met to liver we call it

features:

A

carcinoid syndrome - flushing of skin, cyanosis, diarrhea, cramps, nausea, vomiting

131
Q

What kind of cell and secretion from carcinoid tumor?

A

neuroendocrine tumor

secretes serotonin

132
Q

TEst for carcinoid tumor?

A

check for serotonin metabolism product in urine 5-HIAA

133
Q

Most common extra nodal side for lymphoma? what cell type?

A

GI - B-CELLS

134
Q

Three main types of GI lymphona:

A

MALT
sprue associated
mediterranean

135
Q

Mediterranean GI lymphoma

  • which cell?
  • prognosis?
A

B- cell - plasma cells that secrete IgA heavy chains

B-cell prognosis better

136
Q

Sprue associated GI lymphoma

  • which cell?
  • prognosis?
A

-T-cell
- younger PATIENTS 30-40 yrs
poorer prog than with B-cell

137
Q

Main risk factor for GI lymphoma?

A

H Pylori! aka chronic gastritis

138
Q

Malt lymphoma

  • which cell?
  • prognosis?
A
  • B-cell
  • better than t-cell
  • most common in stomach SInce MALTOMA CAN BE IN ANY GI LYMPH TISSUE - H Pylori related
139
Q

immunoproliferative small intestine disease is also called?

A

mediterranean lymphoma

140
Q

GIST tumors from what cell type

what mutation?

A

kajal cells - MASS OF SPINDLE DELLS

mutation in c-KIT a tyrosine kinase receptor

141
Q

mass of spindle cell tumor -which is it?

A

GIST!

142
Q

most common acute abdominal condition?

A

appendicitis

143
Q

First clinical sign of appendicitis?

THEN?

A

LOSS OF APPETITE

Periumbilical pain inRLQ

144
Q

Histologic criterion for appendicitis?

A

PMNs inmuscularis propria

145
Q

Most common tumor of appendix?

A

carcinoid

146
Q

Nests of uniform looking cells whcih tumor?

A

carcinoid

GI Exam 1 (11 decks)

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