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(J2) GI II Test 1 > Small Intestine and Colon > Flashcards

Small Intestine and Colon Flashcards

1
Q

What are the main causes of mechanical bowel obstruction?

(epi)

A

major causes:

  • hernia (most common globally)
  • adhesions (most common US)
  • intussuseption (most common in children)
  • volvulus
  • tumors (most common LBO)

less common:

-infarction

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2
Q

What is paralytic ileus?

What are the main causes?

A

Functional bowel obstruction:

-interupted passage of bowel contents due to imparied peristalsis

Causes:

  • post-operative ileus (most common)
  • hypokalemia
  • hypothyroidism
  • drugs (opioids, anticholinergics)
  • infections
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3
Q

What are common symptoms of GI obstruction?

A
  • abdominal pain
  • distension
  • constipation (w/ inability to pass gas)
  • vomting
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4
Q

How does vomiting in GI obstruciton change with location of obstruction?

A
  • non-bilious at pylorus
  • bilious in SBO
  • feculent in LBO (late)
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5
Q

What exam and imaging findings are associated with mechanical GI obstruction?

A

Exam:

  • colicky pain
  • distention
  • high-pitched BS (early) -> absent BS (late)

Imaging:

  • dilated loops of bowel proximally
  • air-fluid levels
  • collapsed bowel distally
  • no air in rectum
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6
Q

What are hernias?

A

protrusions of portion of GI tract through a weakness/deformity in muscular wall of abdomen

most common casue of obstruction worldwide

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7
Q

What complications can occur with hernias?

A
  • obstruction
  • imapired venous drainage -> edema -> incarceration (can’t be manually reduced) -> strangulation (vascular compromise)
  • > infarction (necrosis)
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8
Q

What is an adhesion?

A

fibrous bridge connecting connecting parts of GI tract with itself or to the abdominal wall

most common cause of obstruction in US

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9
Q

What are cause of adhesions?

A

Acquired:

  • surgery/trauma (hence prominence in US)
  • peritonitis
  • endometirosis

Congenital:

-rare, but can still occur

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10
Q

What are complications of adhesions?

A
  • obstruction
  • formation of closed loops of bowel -> internal herniation (complications similar to external herniation)
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11
Q

What is a volvulus?

Where does it most commonly occur?

A

twisted loop of bowel on mesentary -> obstruction and strangulation/ischemia

  • occurs in redundant loops of bowel
  • sigmoid colon >>> cecum > midgut/SI
  • can be caused by congenital intestinal malrotation
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12
Q

What is intussusecption?

(mechanism)

A

“telescoping” of bowel in on itself

-occurs at a lead point (anomoly in GI wall that restricts motion) during peristalsis; lead point does not dilate during peristalsis and collsapses into proximally dilated portion

  • highly associated with immune reactions in Peyer’s patches of children (viral infections and rotovirus vaccine)
  • can be associated with tumor/polyps in older groups
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13
Q

What are complications of intussusception?

A
  • obstruction
  • ischemia (mesentary trapped as well) -> infarction
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14
Q

What are the sources of blood supply of the GI tract?

A
  • celiac artery
  • superior mesenteric artery
  • inferior mesenteric artery
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15
Q

What are the main causes of chronic and acute bowel ischemia?

A

Chronic (hypoperfusion related):

  • cardiac failure
  • shock
  • dehydration
  • vasoconstrictors

Acute (obstruction related):

  • atherosclerosis
  • AAA
  • embolized cardiac vegetations
  • venous thrombosis
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16
Q

How does the bowel respond to chronic and actue vascular compromise?

A

Chronic/progressive:

-numerous collaterals allow for adaptation

Acute:

-can cause large portions of bowel to become ischemic

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17
Q

How does acute bowel ischemia present?

What symptoms indicate surgery?

A
  • periumbilical pain disproportionate to exam findings
  • bloody diarrhea
  • thumbprinting (ABD XR)

peritoneal signs/infarction indicate surgery:

  • absent BS
  • cessation of stools
  • guarding/rebound
  • shock
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18
Q

How does chronic bowel ischemia present?

A

“Abdominal angina”

  • dull periumbilical pain
  • worse with with increased GI activity -> worse following meals
  • “food fear”
  • weight loss
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19
Q

What factors affect severity of injury in ischemic bowel disease?

What causes the most damage in acute bowel ischemia?

A
  • severity of compromise
  • time of compromise
  • vessel affected (more proximal or larger area supplied = worse)
  • reperfusion injury: toxic substances from hypoxic injury and potentially the intenstial lumen enter blood stream causing systemic effects
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20
Q

What is angiodysplasia?

Where does it most commonly occur and what is is associated with?

A

abnormal tortuous, dilated blood vessels (typically veins) in the mucosa and submucosa

most common in cecum and ascending colon

associated with episodic GI bleeding later in life

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21
Q

What is diarrhea?

A

increase in one of the following:

-frequency (>3/day)

-water content (>75%)

-mass (>200mg/day) of stool

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22
Q

What are the types of diarrhea?

A

Exudative diarrhea:

  • due to inflammation
  • bloody, purulent stool
  • persists with fasting

Secretory diarrhea:

  • increased cAMP -> active secretion of water
  • persists with fasting

Osmotic diarrhea:

  • water drawn into stool by unabsorbed solutes in the lumen
  • abates with fasting

Malabsorptive diarrhea:

  • general malabsorption -> increased fat in stool; steatorrhea
  • abates with fasting
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23
Q

What is malabsorption?

A

Mechanisms:

  • impaired intraluminal digestion of macromolecules
  • impaired terminal digestion of oligosaccharides/pepetides at intestinal surface
  • impaired epithelial transport
  • imparied lymph transport of lipids

failure of absorption of (one or multiple):

  • fat
  • fat/water soluble vitamins
  • proteins
  • carbohydrates,
  • electrolytes/minerals
  • water
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24
Q

What conditions cause malabsorption and associated diarrhea?

A

Maldigestion:

  • pancreatitis/exocirne pancreatic insufficiency
  • bile acid deficiency
  • cystic fibrosis
  • hypo/achlorhydria

Malabsorbtion:

  • IDB (CD/UC)
  • lactase deficiency/lactose intolerance
  • abetalipoproteinemia
  • environmental/autoimmune enteropathy
  • infectious gastroenteritis
  • Whipple
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25
Q

How do conditions of malabsorption typically present?

A

General malabsorptions:

  • diarrhea, particularly steatorrhea
  • weight loss (if chronic)
  • distension
  • flatulence
  • associated deficiencies

Specific malabsorptions:

-varies, dependent on what is not absorbed or associated deficiency

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26
Q

What is cystic fibrosis?

A

genetic defect in Cl ion transporter, CFTR, found in exocrine glands as well as respiratory, GI, and reproductive epithelium -> imparied water transport and thickened secretions

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27
Q

What mechanism of malabsorbtion occurs in cystic fibrosis and how does it present?

A

Failed intraluminal digestion:

  • pancreatic duct obstruction due to thickend secretions -> pancreatitis/exocrine pancreatic insufficiency -> carbs, lipids, and proteins not digested
  • general malabsorption due to lack of digestive enzymes -> steatorrhea and malnutrition
  • impaired water secretion into GI lumen -> viscid mucous -> obstruction
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28
Q

What is the mechanism of celiac disease?

A

gluten-sensitive, immune-mediated enteropathy:

  • autoimmune reaction triggered by gluten leading to damage of intestinal epithelium
  • gliadin trigger epithelial cells to release IL-15 -> activates CD8+ T cells expressing NKG2D
  • NKG2D binds MIC-A expressed on stressed enterocytes -> cell-mediated damage of epithelium -> malabsorption
  • gliadin also binds HLA-DQ2 and HLA-DQ8 on APCs -> activate CD4+ T cells -> activate B cells -> production of anti-gliadin, anit-tTG, and anti-endomysial abs
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29
Q

What characteristics of celiac disease are used in its diagnosis?

(lab and histology)

A

Lab:

  • anti-tTG IgA (gold standard)
  • anti-endomysial IgA
  • both high sens. and spec.

Histo:

  • villous atrophy (loss of villi)
  • crypt hyperplasia (elogation of crypts
  • increased intraepithelial CD8+ T cells
  • none are unique to celiac disease
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30
Q

What is the epidemiology of celiac disease?

A

Bimodal

Children:

  • onset with introduciton of wheat products to diet ~6-24 months
  • M=F

Adults:

  • 30-40
  • F>M
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31
Q

What are the clinical features of celiac disease in adults?

A

Classical:

  • chronic diarrhea
  • bloating/cramping
  • malabsorption -> iron/vitamin deficiency -> anemia -> -chronic fatigue
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32
Q

What non-GI condition is associated with celiac disease?

A

dermatitis herpatiformis:

-autoimmune blistering disease associated with anti-tTG produced in celiac disease

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33
Q

What are the clinical features of celiac disease in children?

A

Often onsets at young age and pt may not be able to describe symptoms.

GI:

  • chronic diarrhea/steatorrhea
  • abdominal distension/pain -> irritability
  • malabsorption -> failure to thrive/weight loss

Extraintestinal (impact of malabsorption on growth):

  • arthritis
  • growth restriction -> short
  • delayed puberty
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34
Q

What causes many cases of celiac disease to go undetected/delay detection?

A

Most cases are atypical in their presentation, delaying testing for celiac disease

many cases are asymptomatic and go undetected

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35
Q

How is celiac disease treated?

A

No treatment available -> gluten-free diet to prevent symptoms

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36
Q

What is environmental enteropathy?

A

Environmental sprue/non-tropical sprue

similar to celiac disease (which is alternatively called non-tropical sprue) in presentation/appearance but:

-cause is unknown

  • associated with poor sanitation/hygiene -> responds to antibiotics
  • endemic to the tropics (***visiting or from there***)

Presentation:

  • chronic diarrhea/steatorrhea
  • bloating/cramping
  • malabsorption -> iron/vitamin deficiency -> anemia -> chronic fatigue

Biopsy:

-villous atrophy

-cryptic hyperplasia

37
Q

How is environmental enteropathy treated?

A

antibiotics

38
Q

What are helpful factors in distinguishing between celiac sprue and environmental sprue?

A
  • celiac predominates in the duodenum; environmental predominates in the ileum and jejunum (B12/folate deficiency)
  • environmetal responds to Abx
  • environmental is typically preceeded by infectious diarrhea
39
Q

What is autoimmune enteropathy?

(etiology and presentation)

A

IPEX - Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked

  • X-linked autoimmune disorder associated with mutation in FOXP3 -> loss of Treg cells
  • presents early in life

Presentation:

  • eczema
  • T1DM
  • malabsorption -> chronic diarrhea -> failure to thrive
40
Q

What antibodies are found in autoimmue entropathy?

A
  • anti-enterocyte
  • anti-goblet cell
  • anti-parietal cell
  • anti-islet cell (-> T1DM)
41
Q

How is autoimmune enteropathy treated?

A

immune supression:

-cyclosporine

42
Q

What is lactase deficiency?

A

Lactase: brush-border enzyme, breaks down lactose -> galactose and glucose

-when deficient, lactose remains in lumen and exerts osmotic force, pulling water into stool -> osmotic diarrhea

43
Q

What is the etiology/epidemiology of lactase deficiency?

A

Congenital:

  • mutation in lactase gene
  • very rare

Acquired:

  • downregulation of lactase gene
  • common in Native American, Africian American, and Chinese
  • can be acquired following gastroeneteritis and gradually improve over time
44
Q

What is the presentation of lactase deficiency?

A

Following consumption of milk:

  • watery, frothy diarrhea (osmotic)
  • cramping
  • flatulence

Symptoms are more variable in aquired due to variance in active lactase

45
Q

What is abetalipoproteinemia?

(presentation and findings)

A

autosomal recessive disorder associated with microsomal triglyceride transfer protein, MTP

  • blood has no lipoprotein B
  • body is unable to transport fats and fat soluble vitamins from the intestine
  • diarrhea/steatorrhea
  • failure to thrive
  • lipid accumulation in enterocytes
  • membrane defects -> acanthocytes/spur RBCs
46
Q

What is IBS?

(presentation and cause)

A

Irritable bowel syndrome:

chronic, relapsing:

  • abdominal pain
  • bloating
  • change in bowel habits

It has no known cause:

  • diagnosed using Rome criteria
  • diagnosed by elimination of DDx’s
47
Q

What changes are associated with IBS?

A

NONE; GI tract has a normal macroscopic and microscopic appearance

48
Q

What is the epidemiology of IBS?

A
  • women
  • 20-40 years
49
Q

What is diversion colitis?

A

blind ending segment of colon resulting from surgery that produced an ostomy

50
Q

What is microscopic colitis?

What are the types?

A

Normal gross appearing colon but with microscopic abnormalities

Symptoms:
-chronic diarrhea (non-bloody)

  • weight loss
  • abdominal pain

Collagenous colitis: increased subepithelial collagen

Lymphcytic colitis: intraepithelial lymphocyte infiltrate; commonly in setting of celiac dz or autoimmune dz

51
Q

How does GVHD most commoly present in the GI tract?

A

SI and colon involved in most cases of GVHD

  • watery diarrhea
  • apoptosis of crypt cells
52
Q

What are colonic diverticula?

A

false divertiucla/outpouchings of the mucosa and submucosa of the colon through discontinuities in the muscular layer

53
Q

What is the epidemiology of colon diverticular disease?

How does this relate to likley location of the diverticula?

A

Epi:

  • rare <30
  • prevalence increases with age -> 50% by age 60
  • more common in Western countries (left-sided diverticula)
  • less common in Asia and Africa (right sided diverticula)
54
Q

How do diverticula present?

A

most are asymptomatic

Those that are symptomatic (20%):

  • painless lower GI bleed/hematochezia
  • lower abdominal pain/cramping
  • constipation
  • sensation of not being able to empty the rectum
55
Q

What is diverticulitis?

What complications can be associated with it?

A

inflammation of diverticula

Complicaitons:

  • abscess
  • fistula formation
  • perforation
56
Q

Where are polyp most commonly found?

A

colo-rectal, but can be found throughout GI tract

57
Q

What are the morphological appearances of polyps?

A

Sessile polyps:

-small elevations of mucosa w/o stalks

Pedunculated polyps:

  • protrusions of mucosa w/ stalks
  • typcially preceded by a sessile precursor
58
Q

What are the non-neoplastic polyp variants?

A
  • hyperplastic
  • inflammatory
  • hamartomatous
59
Q

What are hyperplastic polyps?

(description and location)

A

Benign epithelial proliferation:

  • decreased epithelial turnover and decreased sheding leading to “piling up” of NORMAL cells (no dysplasia)
  • small (<5 cm) sessile polyp

-serrated crypts

-tufting of surface due to crowding

-left/descending colon

60
Q

What is significant about hyperplastic polyps?

A

very similar in presentation to serrated, sessile adenoma which is malignant, and must be ruled out

61
Q

What are inflammatory polyps?

(description and location)

A

Benign polyp:

  • caused by repeated injury and healing of the mucosa
  • typcially assocaiated with solitary rectal ulcer sundrome (SRUS) where anorectal sphincter fails to relax -> recurrent abrasion/ulceration

Appearance:

  • mixed inflammatory infiltrates
  • erosion
  • epithelial hyperplasia w/ fibromuscular hyperplasia
62
Q

What are hamartomatous polyps?

(etiology)

A

disorganized growth of mature cells native to local tissue

  • autosomal dominant inheritance (if genetic etiology)
  • involved genes tend to be tumor supressors or protooncogenes -> increased risk of malignancy
  • the polyps themselves tend to be benign
63
Q

What are the main hamartomatous syndromes?

A
  • juvenile polyposis syndrome
  • Peutz-Jeghers syndrome
  • Cowden syndrome
  • Cronkhite-Canada syndrome
64
Q

What is juvenile polyposis?

(symptoms/complications and cancer risk)

A

Autosomal dominant syndrome (SMAD4)

  • presents <5 years
  • >10 polyps (mostly colon, can involve stomach and SI)
  • high risk of bleeding -> rectal bleeding -> anemia
  • risk of intussusception and obstruction

Increased risk of gastric, SI, and colon adenocarcinoma

65
Q

What is Peutz-Jeghers syndrome?

(symptoms and cancer risk)

A

Autosomal dominant syndrome (STK11):

  • mucocutaneous hyperpigmentation, especially oral (mucosal “freckles”)
  • arborizing polyps (most commonly SI, can occur in colon, stomach, bladder and lungs)
  • can cause intussusception

Increased risk of colorectal, breast, lung, and pancreatic cancer

66
Q

What are adenomatous polyps?

A

pre-malignant lessions that have a high risk becoming adneocarcinomas

-typcially distinguished from other, more benign polyps by the pressence of a stalk and dysplasia

67
Q

What adenoma does not fit the typical description/classification of adenoma?

(why is this significant)

A

Sessile serrated adenomas:

  • still a pre-malingnant lesion
  • lack a stalk -> sessile
  • lack dysplasia -> hyperplastic

Very similar in appearance to benign hyperplastic polyps, but can become malignant:

  • crypts are serrated to their base; more common in right colon (adenoma)
  • crypts are only serrated partway down; more common in left colon (hyperplastic)
68
Q

What is the most significant prognostic factor of colorectal adenomas progressing to colorectal adenocarcinoma?

A

size:

  • <1cm -> minimal risk
  • >4cm -> 40%
69
Q

What are the two genetic pathways associated with development of colonic adenocarcinoma?

(compare)

A

Classic, adenoma-carncinoma sequence:

  • associated with FAP or sporadic mutations in APC/WNT pathway (growth supression) (APC-> K-RAS -> P53)
  • 70-80% of sporadic CRC
  • polypoid precursor -> non-mucinous adneocarcinoma
  • typcially left-sided (sporadic only; FAP has no preference)

MMR sequence:

  • associated with NHPCC or sporadic mutations in mismatch repair pathway (MLH1/MSH2)
  • 10-15% of sporadic CRC
  • most common inherited CRC (HNPCC)
  • non-polypoid, serrated sessile precursor -> mucinous adneocarcinoma
  • typcially right-sided
70
Q

What drug impedes classic, adneoma-carcinoma sequence progression?

A

Aspirin/NSAIDs

-increased COX expression is part of transformation so COX inhibitors impede progression

71
Q

What is familial adenomatous polyposis (FAP)?

(extra-GI manifestations and cancer risk)

A

autosomal dominant syndrome:

  • development of >100, potentially 1000’s of adenomatous polyps
  • mutation in Adenomatous Polyposis Coli (APC) gene
  • associated with congenital retinal pigmented epithelium hypertrophy (can be deceted at birth)

100% risk of developing adenocarcinoma by age 45

72
Q

What is MYH-associated polyposis?

A

Very similar to FAP but is more mild (<100 polyps) and slower progression (CRC around 50 y/o)

-MYH gene is affected instead of APC

73
Q

How is FAP treated?

A

-prophylactic proctocolectomy w/ ileoanal anastamosis (prior to age of 20) otherwise colorectal cancer is inevitable

74
Q

What is Gardner syndrome?

A

variant of FAP (APC mutation):

-additional risk of osteoma and soft tissue tumors

75
Q

What is Turcot syndrome?

A

variant of FAP (APC mutation):

-additional risk of brain tumors

76
Q

What is Lynch syndrome?

A

Hereitary nonpolyposis colorectal cancer (HNPCC):

  • autosomal dominant mutations in mismatch repair genes (MSH2/MLH1)
  • atypical adenomas (sessile instead of pedunculated) with high rate of prgression to CRC
  • most common inherited cause of CRC
77
Q

What cancers have an increased risk in Lynch syndrome?

A
  • colon (HNPCC)
  • endometrium
  • stomach
  • ovary
78
Q

What is the difference in appearance and presentation colon cancer based on location?

A

Right-sided/proximal:

  • flat, exophytic masses; “inverted mushroom”
  • LIGB -> anemia
  • rarely casue obstruction

Left-sided/distal:

  • annular, “napkin-ring” constrictions
  • blood streaked stools
  • change in bowel habits
  • may lead to obstruction
79
Q

Where are colon adneocarcinomas most likely to metastasize to?

A
  • LNs
  • liver
80
Q

What are the most important prognostic factors for colorectal adenocarcinoma?

A
  • depth of invasion
  • metastasis to LNs

less important but still prognostic:

  • mucinous (MMR/sessile serrated)
  • poorly differentiated
81
Q

What findings should always trigger investigation for possible GI cancer?

A
  • fatigue/weakness from IDA in older men or postmenopausal women (anemia of unknown origin)
  • GI bleed
  • most common presenting complaint in colon cancer and frequent with others
82
Q

Where are carconoid tumors most likley to be found in the lower GI tract?

What do they secrete? (symptoms?)

A

most found in jejunum/ileum (most common site of carcinoid tumors in whole GI tract)

Secrete serotonin

  • serotonin is mostly release into portal circulation -> metabolisim in liver (first-pass effect)
  • if high tumor burden or directly secreted into systemic circulation -> carcinoid syndrome

Cacinoid syndrome:

  • flushing, sweating
  • bronchospasm
  • colicky abdominal pain, diarrhea
  • right-sided cardiac valve fibrosis (pulmonary system metabolizes 5HT preventing it from reaching L heart)
83
Q

What infection is associated with colorectal carcinoma?

A

Streptococcus gallolyticus/bovis endocarditis

84
Q

What tumor marker is associated with CRC?

A

CEA

  • not reliable in screening as it is not always present
  • can be used to monitor CRC known to produce CEA or similarly look for relapse
85
Q

What genes are associated with juvenile polyposis?

A

SMAD4

86
Q

What genes are associated with Puetz-Jeghers syndrome?

A

STK11

87
Q

What genes are associated with adenomatous polyps?

A

APC (chromosome 5)

Adenomatous Polyposis Coli gene

88
Q

What genes are associated with the classical sequence of CRC (stalked polyps)?

A

APC -> β-catenin -> K-RAS -> TP53, DCC, COX-2

89
Q

What genes are associated with the MMR sequence of CRC (sessile polyp)?

A

MLH1, MSH2

(J2) GI II Test 1 (14 decks)

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