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GI Final > Disorders of the Small Bowel and Colon > Flashcards

Disorders of the Small Bowel and Colon Flashcards

1
Q

If there’s Chronic Diarrhea, is it likely to be infectious?

A

no

-it’s gonna be something like IBD or something like that

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2
Q

What are the most common infectious causes of bloody diarrhea?

A
  • salmonella
  • shigella
  • E. coli (0157 H7)
  • Campylobacter
  • Yersinia enterocolitica (sometimes)… that one is psuedo appendicits
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3
Q

Salmonella Typhi

A
  • Gram - enteric bacillus
  • fever
  • Endotoxin like the rest of gram negative things AND Vi antigen
  • Relative bradycardia
  • Rose spots
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4
Q

What can be a chronic reservoir for Salmonella Typhi?

A

Gallbladder

-healthy asymptomatic carrier

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5
Q

What does MEN1 have?

A
  • pituitary adenoma*
  • parathyroid hyperplasia
  • pancreatic tumors
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6
Q

What does MEN2a have?

A
  • parathyroid hyperplasia
  • Medullary thyroid carcinoma
  • Pheochromocytoma
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7
Q

What doe MEN2b have ?

A
  • mucosal neuromas*
  • MArfanoid body habitus*
  • Medullary thyroid carcinoma
  • Pheochromocytoma
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8
Q

If the diarrhea is osmotic, what will decrease the stool volume?

A

fasting

-there will be a high osmotic gap

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9
Q

If the diarrhea is secretory, what will it be like?

A
  • large volume (>1L a day)
  • normal osmotic gap
  • stool sodium will be high
  • little change with fasting
  • hyponatremia and nonanion gap metabolic acidosis
  • Villous adneoma
  • Bile salt malabsorption
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10
Q

What should we think if we see fecal calprotectin?

A

IBD

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11
Q

What are the most common causes of Chronic diarrhea?

A
  • meds
  • IBS
  • Lactose intolerance
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12
Q

What is the stool osmotic gap?

A

difference between measured osmolality of the stool and the estimated stool osmolality
-Normal is <50 mOsm/kg

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13
Q

if chromogranin A is positive, what is it?

A

VIPoma

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14
Q

If calcitonin is high, what’s up?

A

Medullary thyroid cancer

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15
Q

If gastrin is high, what’s up?

A

ZE syndrome

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16
Q

If we see fecal calprotectin, what’s up?

A

IBD

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17
Q

What do we think of if we see 5-HIAA in the urine?

A

Carcinoid tumor

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18
Q

What is IBS?

A
  • chronic functional disorder
  • Not expleained by the presence of structural or biochemical abnormalities
  • Dx: based on the presence of a compatible profile (ROME III)
  • it’s idiopathic
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19
Q

What is the ROME II criteria for IBS Dx?

A

-abdominal discomfort or pain at least 3 days/month for the past 3 months, with symptom onset>6 months before diagnosis and at least 2/3: relieved with defecation, onset associated with a change in frequency of stool, onset associated with a change in form of stool

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20
Q

What is FODMAPS?

A

Fermentable monosaccharides and short chain carbohydrates

-exacerbate bloating, flatulence, and diarrhea in some patients

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21
Q

Is high fiber a good thing in IBS patients?

A

“appears to be of little value in helping IBS patients”

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22
Q

What do we use to treat C diff?

A

Metronidazole

-harry potter and voldemort

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23
Q

What is colitis from antibiotics caused by?

A

C diff

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24
Q

What are most cases of antibiotic associated diarrhea from?

A

adverse effects of antibiotics

  • NOT c diff
  • mild and self limited
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25
Q

What two toxins does C diff form?

A

TcdA (enterotoxin)

TcdB (cytotoxin)

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26
Q

So, what do we need to check if we suspect C diff?

A

check stool for toxin assay

  • flex sig used if atypical symptoms and positive toxins
  • CT or Abd Xray if severe or fulminant symptoms to look for megacolon or perforation
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27
Q

What antibiotics will we usually see used in a question stem if C diff is cookin?

A

ampicillin
clindamycin
3rd gen cephalosporins and fluoroquinolones
-hospitalizations

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28
Q

What’s a weird thing that can happen with fecal impaction?

A

paradoxical or “overflow” diarrhea

-the only thing that can get past is liquid

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29
Q

How do you treat constipation/fecal impaction?

A

enemas
digital disruption
-long term- good bowel regimen

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30
Q

What is Microscopic colitis?

A
  • idiopathic
  • sometimes medications can cause it
  • R/o celiac
  • chronic or intermittent watery diarrhea
  • *normal mucosa on endoscopy
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31
Q

How do you treat microscopic colitis?

A

stop offending medication

-loperamide, budesonide, bile-slat binding agents, or 5-ASA’s

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32
Q

What are some risk factors for diverticular disease of the colon?

A
  • old

- CT disease: Ehlers-Danlos, Marfan syndrome, Scleroderma

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33
Q

What is diverticulosis?

A
  • Asymptomatic, Dx on colonoscopy or barium enema
  • usually sigmoid and descending colon, can be anywhere in the colon
  • symptomatic complications: GI bleed, Diverticulitis
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34
Q

What is diverticulitis?

A
  • macroscopic inflammation of diverticulum
  • may have microperforation with localized paracolic inflammation
  • may have macroperforation with abscess or peritonitis
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35
Q

How do you treat Diverticulitis?

A
  • maybe Abx

- NPO/clear liquid diet

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36
Q

What should people with diverticulitis do after symptom resolution?

A

undergo diagnositc imaging to exclude colonic neoplasms

-CT with contrast

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37
Q

What is the most common type of polyp?

A

Mucosal adenomatous polyps (70%)

  • tubular
  • tubulovillous
  • villous
38
Q

What do mucosal serrated polyps look like?

A
  • hyperplastic
  • sessile serrated polyps
  • traditional serrated adenoma
39
Q

What are some mucosal nonneoplastic polyps?

A

Juvenile
hamartomas
inflammatory

40
Q

What are some submucosal lesions that can happen in the colon?

A

Lipomas
Lymphoid aggregates
Carcinoids
Pneumatosis cystoides intestinalis

41
Q

What do 95% of cases of Colon adenocarcinoma come from?

A

Adenomas and serrated polyps

-high risk of prgressing to malignancy if they are: >1 cm, contain villous features, have high grade dysplasia

42
Q

What will we see in a patient who has asymptomatic colon cancer?

A

FOBT positive

Iron deficiency anemia

43
Q

What is the Gold standard for detecting polyps?

A

Colonoscopy

44
Q

What are potential complications of colonoscopy?

A

Bleeding and perforation

45
Q

FOBT

A 
Fecal occult blood testing
-Guaiac based
-detect pseudoperoxidase activity of heme or hemogloblin
-need predietary restrictions
-
46
Q

FIT

A 
Fecal immunochemical test
-Tests for hgb
-no predietary restrictions
preferred over FOBT
-more sensitive than Guaiac based tests
-Screening for CRC and advanced adenomas
47
Q

Fecal DNA

A

Tests for stool Hgb

-measures a variety of mutated genes and methylated gene markers from exfoliated tumor cells

48
Q

Does intussusception happen more in adults or kids?

A

kids!

-more common in kids, rare in adults

49
Q

FAP

A

Familial adenomatous polyposis

  • eraly development of a shit ton of polyps and adenocarnicoma
  • Extracolonic: dudoenal adenomas, desmoid tumors, osteomas
50
Q

What gene is associates with FAP?

A

-APC gene (90%) or MUTYH gene mutation

51
Q

Tx of FAP

A
  • prophylactic colectomy (CRC inevitable by age 50)

- family needs to be testing and genetic counseling

52
Q

Peutz Jeghers Syndrome

A
  • Hamartomatous polyposis syndrom
  • auto dominant
  • Hamartomatous polyps thorughout GI tract, mostly small intestine
  • Mucocutanious pigmented macules on the lips, buccal mucosa, or skin
53
Q

Are Hamartomas malignant?

A

NO!

54
Q

What kinds of cancer can develop in Peutz Jeghers?

A

GI malignancy in 40-60%

  • Breast CA in 30-50%
  • Gonadal or pancreatic CA
55
Q

What gene is there a defect in in Puetz Jeghers?

A

Threonine kinase II gene

56
Q

Familial Juvenile polyposis

A
  • Hamartomatous polyposis syndrome
  • auto dominant
  • > 10 juvenile hamartomataus polyps (mostly in colon)
57
Q

What genetic defects are in Familial Juvenile polyposis?

A

Loci on 18q and 10q

-MADH4 and BMPR I A

58
Q

Cowden disease

A
  • PTEN multiple hamartoma syndrome
  • hamartomatous polyps and lipomas throughout the GI tract
  • Trichilemmomomas: benign tumor at the root of the hair follicle
  • Cerebellar lesions
  • Increased rate of malignancy (thyroid, breast, and urogenital tract)
59
Q

Lynch syndrome

A
  • aka: Hereditary nonpolyposis colon cancer (HNPCC)
  • autosomal dominant
  • Gene mutation: MLH1, MSH2
  • increased risk of CRC, endometrial CA, and others at a young age
  • Rapid poly transformation benign to malignant in 1-2 years
60
Q

When should we suspect Lynch syndrome?

A

person early onset CRC

-FH of CRC, edonmetrial CA, or lynch syndrome

61
Q

Dx of Lynch syndrome?

A
  • Besthesda criteria
  • tumor tissue immunohistochemcial staining for mismatch repair proteins
  • testing for microsatellite instability
  • confirmed by genetic testing
62
Q

Screening for lynch syndrome

A
  • colonoscopy every 1-2 yrs begin age 25, or 5 yrs younger than age of youngest affected family member at diagnosis
  • pelvic exam, transvaginal US, and endometrial sampling for Women starting at age 30-35
  • upper endoscopy every 2-3 years beginning at age 30-35 to look for gastric cancer
  • prophylactic hysterectomy with oophorectomy age 40 or once done childbearing
63
Q

Besthesda Criteria?

A
  • CRC under age 50
  • Synchronous CRC or lynch syndrome-associated tumor regardless of age (enometrial, stomach, ovary, pancreas, ureter, renal, biliary, brain)
  • CRC with one or more first degree relations with CRC or lynch syndrom erelated cancer with one of the cancers occurring before age 50
  • CRC with two or more second degree relative with CRC or LS
  • Tumors with infiltrating lymphocytes, mucinous/signet ring differentiation or medullary growth pattern in patients younger than 60 yo
64
Q

Gardner’s syndrome

A
  • adenomatous colon polyps
  • 95% develop cr polpyps
  • Osteomas of mandible, skull and long bones
  • supernumerary teeth, epidermoid and sebaceous teeth, thyroid and adrenal tumors. desmoid (fibrous) tumors
  • Autosomal dominant
65
Q

Turcot’s syndrome

A
  • Adenomatous colon polyps
  • brain tumors
  • colorectal cancer–100% over 40 years of age
  • Auto dominant
66
Q

Pernicious anemia/ Autoimmune Gastritis

A
  • Autoimmune destruction of fundic glands
  • loss of them
  • achlorhydria… pronounced hypergastrinemia (kinda like ZE)
  • induce hyperplasia of gastric enterochromaffin-like cells
  • development of small, multicentric carcinoid tumors (5% of patients)
67
Q

in Autoimmune gastritis, what is the result of the loss of fundic glands?

A

achlorhydria
decreased IF secretion
Vitamin B12 malabsorption

68
Q

Celiac disease

A

IgA tissue tansglutaminase

  • if IgA deficiency, check IgG to deamidated gliadin peptide (anti-DGP)
  • Wgt loss, chronic diarrhea, abdominal distention, growth retardation
  • Dermatitis herpetiformis, iron deficiency anemia, osteoporosis
69
Q

What part of the GI tract does Celiac disease damage most?

A

proximal small intestinal mucosa

70
Q

What is the weird gene that is with celiac disease?

A

HLA-DQ2 or DQ8

71
Q

Whipple disease

A
  • rare multi system disease
  • fever, LAD, Arthralgias, Wgt loss, malabsorption, chronic diarrhea
  • Encephalitis, ocular abnormalities
72
Q

Dx Whipple disease

A

Duodenal bx with PAS + periodic acid schiff macrophages with characteristic bacillus

73
Q

What is the characteristic bacillus in Whipple disease?

A

Tropheryma whippelli

-gram positive bacilli (not acid fast

74
Q

Tx of whipple disease

A

Abx

75
Q

Bacterial overgrowth

A
  • distention, flatulence, diarrhea, weight loss
  • increased qualitative and quantitative fecal fat
  • reduced absorption of B12 and carbs
  • need to check serum iron
  • osmotic and secretory diarrhea
76
Q

When should we think of bacterial overgrowth?

A

in the elderly with malabsorption

77
Q

Dx of bacterial overgrowth

A

Breath tests (hydrogen, methane, glucose, lactulose, or C-xylose)

78
Q

Tx of bacterial overgrowth

A

Abx duh!

79
Q

Short bowel syndrome

A
  • removal of significant segments of small intestine

- crohn, volvulus, tumor resection, trauma…

80
Q

Terminal ileum resection

A
  • bile salts and vit B12 malabsorption
  • Increased chance of oxylate kidney stones
  • Increased chance of cholesterol gallstones
81
Q

how do you treat that B12 malabsorption?

A

B12 injections, bile salt binding resins, low fat diet, fat soluble vitamin replacements

82
Q

what to do about the oxylate kidney stones in short bowel syndrome?

A

Give calcium supplementation

83
Q

How much of the proximal jejunum is required to maintain oral nutrition?

A

at least 200cm

-if there’s no colon and less than 100-200 cm of proximal jejunum, they require parenteral nutrition (TPN)

84
Q

Lacatase deficiency

A

diarrhea, bloating, flatulence, abdominal pain AFTER ingestion of milk-containing product

  • Dx: symptomatic improvement with lactose free diet (confirm by hydrogen breath test)
  • Lactase-brush border enzyme hydroyzes disaccharide lactose into glucose and galactose
85
Q

Urea breath test

A

H. pylori

86
Q

Hydrogen breath test

A

Lactose intolerance

-can also do for bacterial overgrowth

87
Q

Glucose, lactulose, or 14C-xylose breath test

A

-bacterial overgrowth

88
Q

Pernicious anemia

A
  • rare
  • AI destruction of gastric fundic glands
  • loss of inhibition to gastrin G cells
  • may cause hyperplasia of gastric enterochromaffin-like cells (can lead to small carcioid tumors)
  • decreased intrinsic factor secretion
  • B12 malabsorption
89
Q

What does the histology look like on pernicious anemia?

A

severe gland atrophy and intestinal metaplasia

90
Q

What is the big risk that was bolded on the pernicious anemia slide?

A

3 FOLD INCREASED RISK OF GASTRIC ADENOCARCINOMA

GI Final (13 decks)

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