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Pathology dt2 > Chapter 15: Small and Large Intestines > Flashcards

Chapter 15: Small and Large Intestines Flashcards

1
Q

Describe what herniation is.

A

Herniation occurs when the intestine pushes through the abdominal wall at the site of previous abdominal surgery (for example). In general this happens when there’s a weakness or defect in the wall of the peritonel cavity.

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2
Q

Describe what adhesions are.

A

Loops of the intestine are attached to eachother.

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3
Q

Describe what volvulus is.

A

It means that the intestine has rotated so that blood supply is limited.

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4
Q

Describe what intussusception is.

A

It occurs when a segment of the intestine, constricted by a wave of peristalsis, telescopes into the immediately distal segment. In children younger than 2 years this is the most common cause of intestinal obstruction.

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5
Q

What is Hirschsprung Disease?

A

It is a congenital defect in colonic innervation.

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6
Q

How do patients (infants) present the Hirschsprung Disease?

A

As neonates, they fail to pass meconium followed by obstructive constipation.

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7
Q

What gene is mutated in familial Hirschsprung Disease?

A

Mutations in the receptor tyrosine kinase RET

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8
Q

Fill in: Hirschsprung disease always affects the …, but the length of the additional involved segments varies

A

rectum (and sigmoid colon)

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9
Q

Just read

A

Ischemic Bowel Disease: Ischemic damage to the bowel can range from mucosal infarction, extending no deeper than the muscularis mucosa; to mural infarction of mucosa and submucosa; to transmural infarction involving all three layers of the wall.

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10
Q

What factors determine the severity of ischemic bowel disease?

A

Severity of vascular compromise, time frame during which it develops and vessels affected.

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11
Q

Intestinal responses to ischemia occur in two phases. What is the first phase?

A

The initial hypoxic injury occurs at the onset of vascular compromise and although some damage occurs, intestinal epithelial cells are relatively resistant to transient hypoxia.

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12
Q

Intestinal responses to ischemia occur in two phases. What is the second phase?

A

The second phase is reperfusion injury which is initiated by restoration of the blood supply and associated with the greatest damage. Reperfusion injury involves free radical production, neutrophil infiltration and inflammatory mediators.

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13
Q

What are watershed zones?

A

Intestinal segments at the end of their respective arterial supplies that are particularly susceptible to ischemia.

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14
Q

What is the influence of the patterns of intestinal microvessels on ischemic injury?

A

Intestinal capillaries run alongside the glands, from crypt to surface, before making a hairpin turn at the surface to empty into the postcapillary venules. This configuration leaves the surface epithelium particularly vulnerable to ischemic injury.

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15
Q

What can be seen in this picture?

A

Ischemia, you can see partially detached villous epithelium in acute jejunal ischemia. Note the hyperchromatic nuclei of proliferating crypt cells.

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16
Q

What are hemorrhoids?

A

Dilated (peri)anal collateral vessels that connect the portal and caval venous systems to relieve elevated venous pressure within the hemorrhoid plexus

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17
Q

What are external and internal hemorrhoids?

A

External hemorrhoids are collateral vessels within the inferior hemorrhoidal plexus which are located below the anorectal line. Internal hemorrhoids are a result of dilation of the superior hemorrhoidal plexus within the distal rectum.

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18
Q

On histologic examination, what are characteristics of hemorrhoids?

A

Hemorrhoids are thin-walled, dilated submucosal vessels beneath anal or rectal mucosa.

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19
Q

What is diarrhea?

A

An increase in stool mass, frequency, or fluidity, typically to amounts greater than 200 grams per day.

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20
Q

What four categories of diarrhea are there?

A

Secretory, osmotic, malabsorptive and exudative diarrhea.

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21
Q

What are characterisations secretory diarrhea?

A

Isotonic stool and persists during fasting.

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22
Q

What is osmotic diarrhea?

A

Luminal solutes are unabsorbed and create osmotic forces that cause (osmotic) diarrhea. (Condition abates with fasting)

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23
Q

Wht is malabsorptive diarrhea?

A

Diarrhea caused by inadequate nutrient absorption. (This diarrhea is relieved by fasting.)

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24
Q

What is exudative diarrhea?

A

Diarrhea due to inflammatory disease and is characterized by purulent, bloody stools that continue during fasting.

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25
Q

What is a hallmark of malabsorptive diarrhea?

A

Steattorrhea

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26
Q

Malabsorption results from disturbance in at least one of the four phases of nutrient absorption. Which phases are these?

A
  • Intraluminal digestion (of proteins, carbohydrates and fat).
  • Terminal digestion (in brush border of small-intestinal mucosa).
  • Transepithelial transport (transport and process within small-intestinal epithelium).
  • Lymphatic transport of absorbed lipids.
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27
Q

What is celiac disease?

A

An intestinal immune reaction to gluten.

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28
Q

Explain shortly how celiac disease can occur.

A

When gluten is present in the intestines, it can usually be digested by luminal and brush border enzymes. When a certain enzyme (gliadin) is deamidated (by transglutaminase) it is able to interact with HLA molecules. This produces an immune reaction where lymphocytes and antibodies are produced against certain enzymes (like gliadin and transglutaminase).

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29
Q

Which parts of the intestines are exposed to the highest concentration of gluten?

A

Second portion duodenum or proximal jejunum.

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30
Q

What are characteristics of the histopathology of celiac disease?

A

Increased numbers of T lymphocytes with intraeptihelial lymphocytosis, crypt hyperplasia and villous atrophy.

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31
Q

What are classic and non-classic symtoms of celiac disease (don’t learn this by heart)?

A

Classic symptoms present at a young age and are irritability, abdominal distention, anorexia, diarrhea, failure to thrive, weight loss or muscle wasting. Nonclassic symptoms present at older age and present with abdominal pain, nausea, vomiting, bloating or constipation.

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32
Q

What two cancers are common in celiac disease?

A

Enteropathy-associated T cell lymphoma and small-intestinal adenocarcinoma.

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33
Q

What does the term environmental enteric dysfunction mean?

A

It refers to a syndrome of stunted growth and impaired intestinal function that is common in developing countries.

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34
Q

What disorder can cause osmotic diarrhea?

A

Lactase deficiency

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35
Q

What is the cause of congenital lactase deficiency? What is the cause of acquired lactase deficiency?

A

The cause of congenital lactase deficiency is a mutation in the lactase gene. The cause of acquired lactase deficiency is downregulated lactase gene expression.

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36
Q

What is abetalipoproteinemia?

A

A(n autosomal recessive disease) characterized by an inability to secrete triglyceride-rich lipoproteins.

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37
Q

What is microscopic colitis?

A

Microscopic colitis encompasses two entities, collagenous colitis and lymphocytic colitis. Both of these idiopathic diseases manifest with chronic, nonbloody, watery diarrhea without weight loss.

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38
Q

Colonic diverticula tend to develop under conditions of ….

A

elevated intraluminal pressure in the sigmoid colon.

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39
Q

Just read about why colonic diverticula can develop under elevated intraluminal pressure.

A

This is facilitated by the unique structure of the colonic muscularis propria, where nerves, arterial vasa recta, and their connective tissue sheaths penetrate the inner circular muscle coat to create discontinuities in the muscle wall. In other parts of the intestine, these gaps are reinforced by the external longitudinal layer of the muscularis propria, but in the colon, this muscle layer is discontinuous, being gathered into three bands termed taeniae coli.

40
Q

What are morphological characteristics of colonic diverticula?

A

They have thin walls composed of a flattened or atrophic mucosa, compressed submucosa and attenuated musclaris propia (or completely absent).

41
Q

What is diverticulitis?

A

Inflammatory changes due to obstruction of diverticula with stasis of contents.

42
Q

What is a complication of diverticulitis?

A

Perforation

43
Q

What is inflammatory bowel disease (IBD)?

A

A chronic condition resulting from complex interactions between intestinal microbiota and host immunity in genetically predisposed individuals resulting an inappropriate mucosal immune activation

44
Q

What two diseases are encompassed by inflammatory bowel disease (IBD)?

A

Crohn disease and ulcerative colitis.

45
Q

What is the difference between Crohn disease and ulcerative colitis?

A

Ulcerative colitis is limited to the colon and rectum and extends only into the mucosa and submucosa. By contrast, Crohn disease, also referred to as regional enteritis (because of frequent ileal involvement), may involve any area of the gastrointestinal tract and is frequently transmural.

46
Q

What is a feared long-term complication of ulcerative colitis and colonic Crohn disease?

A

Development of neoplasia (colitis-associated neoplasia)

47
Q

What is meant by sessile polyps? And by pedunculated polyps?

A

Sessile polyps are polyps without stalks. Pedunculated polyps are polyps with stalks

48
Q

In general, intestinal polyps can be classified as nonneoplastic or neoplastic. What is the most common neoplastic polyp?

A

Adenoma, which has the potential to progress to cancer.

49
Q

Nonneoplastic colonic polyps can be classified into…

A

Inflammatory, hamartomatous or hyperplastic.

50
Q

The solitary rectal ulcer syndrome is associated with a purely inflammatory polyp. What are three clinical manifestations of a inflammatory polyp?

A

Triad of rectal bleeding, mucus discharge and an inflammatory lesion of the anterior rectal wall.

51
Q

What is the cause of solitary rectal ulcer (or inflammatory polyp)? (to illustrate)

A

Impaired relaxation of the anorectal sphincter, creating a sharp angle. This leads to recurrent abrasion and ulceration of the overlying rectal mucosa. Chronic cycles of injury and healing produce a polypoid mass composed of inflamed and reactive mucosal tissue.

52
Q

What are hamartomatous polyps?

A

Polyps that occur sporadically or are part of a genetically or acquired syndrome. Hamartomas are disorganized, tumorlike growths composed of mature cell types normally present at the site at which the polyp develops.

53
Q

What two hamartomous polyps are there?

A

Juvenile polyps and Peutz-Jeghers Syndrome

54
Q

Can all three types of polyps result in adenocarcinoma?

A

No, only the ones who display dysplasia (so only adenomas).

55
Q

What’s the goal of screening for colorectal cancer?

A

To find individuals who are predisposed to developing colorectal cancer, because they have an adenoma which displays dysplasia. In short: identification of high risk subjects and early detection.

56
Q

Just read and see.

A

In this picture you can see a juvenile polyp (hamartomous). You can see the surface erosion and cystically dilated crypts filled with mucus, neutrophils and debris.

57
Q

Just read and see.

A

In this picture you can see a Peutz-Jeghers (hamartomous) polyp. You can see complex glandular architecture and bundles of smooth muscle.

58
Q

Where do colonic hyperplastic polyps usually result from?

A

Epithelial proliferations or decreased epithelial cell turnover/shedding leading to a pileup of goblet cells.

59
Q

What is a characterisation/hallmark/precursor of colorectal adenocarcinoma?

A

The presence of epithelial dysplasia.

60
Q

Are adenomas pedunculated or sessile?

A

They can be either of the two or both.

61
Q

Adenomas can be classified on the basis of their architecture. What are these three types?

A

Tubular, tubulovillous or villous.

62
Q

Just know that 2/3 of all polyps are tubular adenomas, but 95% does not progress to colorectal cancer. Thus tubular cancer is rare.

A

Okay

63
Q

What is Familial Adenomatous Polyps (FAP)?

A

An autsomal dominant disorder marked by the appearance of numerous (>100) colorectal adenomas by the teenage years.

64
Q

By what is Hereditary Nonpolyposis Colorectal Cancer (HNCC) caused?

A

By inherited germ line mutations in genes that encode proteins responsible for the detection, excision, and repair of errors that occur during DNA replication.

65
Q

The goal of screening is to identify high risk subjects. This is done by finding/selecting individuals who have advanced adenomas. When is referred to an advanced adenoma?

A

When there’s high grade dysplasia, or if they have a size > 10 mm, or when there’s a villous component.

66
Q

What is difficult in diagnosing of advanced adenomas during screening of individuals who may have advanced adenomas?

A

A size > 10 mm is easily seen, but high grade dysplasia can only be seen when the polyp is first removed. So it’s not always easy to define an advanced adenoma. But for succesful screening colorectal tumors should be discoverd and removed at a premalignant stage (adenoma). But adenomas occur frequently and only 5% of adenomas progress to carcinoma.

67
Q

Which two pathways have been described in the pathogenesis of adenomacarcinoma?

A

The APC/β-catenin pathway and the microsatellite instability pathway.

68
Q

What is meant by the classic adenomacarcinoma sequence?

A

A sequence which accounts for as much as 80% of sporadic colon tumors and typically involves mutation of the APC tumor suppressor in early neoplastic process.

69
Q

What is the only way adenomas can develop?

A

When both of the copies of the APC gene are functionally inactivated, either by mutation or epigenetic events.

70
Q

Describe the normal APC pathway.

A

The APC protein normally binds to and promotes degradation of β-catenin. This prevents it from translocating to the nucleus, where it acts as a transcription factor for proliferation genes.

71
Q

What happens when APC function is lost?

A

β-catenin accumulates and translocates to the nucleus, here it activates the transcription of genes, such as those encoding MYC and cyclin D1, that promote proliferation.

72
Q

Other mutations follow after loss of function of APC. What other gene will mutate and how?

A

A activating mutation of KRAS, which also promotes growth and prevents apoptosis

73
Q

How can we conclude that KRAS mutation is a late event?

A

By observation that mutations are present in fewer than 10% of adenomas that are less than 1 cm in diameter, 50% of ademos that are greater than 1 cm in diameter and 50% of invasive adenocarcinomas.

74
Q

What other genes can be mutated during neoplastic progression of adenomacarcinoma?

A

Tumor suppressor genes like SMAD2 and 4, which encode effectors of TGF-β signaling (TGF-β normally inhibits the cell cycle).

75
Q

What gene is mutated in 70-80% of colon cancers but is uncommanly mutated in adenomas (and with that occurs at a late stage of tumor progression)?

A

TP53

76
Q

What is a hallmark of the APC/β-catenin pathway (in oncogenesis)?

A

Chromosomal instability -> Loss of function of TP53 and other tumor suppressor genes is often caused by chromosomal deletions, highlighting chromosomal instability as a hallmark of the APC/β-catenin pathway

77
Q

Explain the microsatellite instability pathway in short.

A

The microsatellite instability pathway is where mutations accumulate in microsatellite repeats. ((Generally these repeats are located in noncoding regions, but other repeats can be located in coding/promotor regions of genes involved in regulation of cell growth, such as those encoding the type II TGF-β receptor and the pro-apoptotic protein BAX.))

78
Q

In a subset of colon cancers with microsatellite instability, there are no mutations in DNA mismatch repair enzymes. What phenotype do these tumors demonstrate?

A

CpG island hypermethylation (phenotype (CIMP)).

79
Q

What is typical of tumors with CpG hypermethylation (CIMP)?

A

The MLH1 promotor region is hypermethylated, this reduced the MLH1 expression and repair function.

80
Q

KRAS and TP53 are not typically mutated in CpG hypermethylation. But what other gene besides MLH1 is commonly mutated?

A

BRAF oncogene, the mutation makes the gene active.

81
Q

Cecal and other right-sided colon cancers most often are called to clinical attention by the appearance of fatigue and weakness due to iron-deficiency anemia. What can be concluded from this?

A

That the underlying cause of iron-deficiency anemia (in an older male or mostmenopausal female) is gastrointestinal cancer (until proven otherwise).

82
Q

What influences the survival of a patient with colon cancer? (don’t learn this by heart)

A

-Depth of invasion (submucosa > submucosa/muscularis propria) -Presence of lymph node metastases -Distant metastases

83
Q

Describe what you can see here (histologic appearance of colorectal carcinoma).

A

Well-differentiated adenocarcinoma. Note the elongated, hyperchromatic nuclei. Necrotic debris, present in the gland lumen, is typical.

84
Q

Describe what you can see here (histologic appearance of colorectal carcinoma)

A

Poorly differentiated adenocarcinoma forms a few glands but is largely composed of infiltrating nests of tumor cells.

85
Q

Just read

A

Acute appendicitis can be initiated by progressive increase in intraluminal pressure that compromises venous outflow. It can also be caused by luminal obstruction. Ischemic injury and stasis of luminal contents, which favor bacterial proliferation, trigger inflammatory responses.

86
Q

Four facts about GI tumors (for illustration).

A

-GI tumors comprise 27% of all cancer related mortality -High incidence -Present in late stage of disease -> poor prognosis

87
Q

What is meant by primary prevention of cancer?

A

Interfering with the etiology of cancer development (changing lifestyle)

88
Q

What is meant by secundairy prevention of cancer?

A

Interfering with the pathogenesis of cancer development

89
Q

What can be seen when comparing individuals that were diagnosed due to a screening with individuals that weren’t diagnosed through screening?

A

That the amount of individuals that were diagnosed in a later stage of cancer, was much lower in the group that got screened.

90
Q

Describe what can be seen in this histologic picture of a colonic adenomacarcinoma

A

Irregular shaped cells and cytonuclear atypia

91
Q

How long can it take for an adenoma to progress to colorectal carcinoma?

A

10-15 years

92
Q

Why do we need to improve the screening quality/What is a problem during screening?

A

During a screening the feces of individuals is examined and when blood is found, the indivual is invited for a colorectal scopie. If adenomas are found, they are always treated. This results in overtreatment, because only 5% of adenomas progress to carcinoma.

93
Q

What can be concluded when looking at the size of adenomas and their % with malignancy?

A

Only a very low percentage (1.3%) of the adenomas removed that were <1 cm were malignant while the percentage with malignancy in adenomas that were >2 cm was much higher (46.0%).

94
Q

What is the reason that still 7.0% of cancer originate from adenomas <1 cm if the % with malignancy in adenomas <1 cm is so low?

A

Because the prevalence of small adenomas is still very high (1469 (<1 cm) against 430 (>2 cm))

95
Q

What type of adenoma has a high % with malignancy and what type has a low % with malignancy?

A

Tubular adenomas have a low % with malignancy (but a high prevalence), villous adenomas have a high % with malignancy (but a low prevalence).

96
Q

Just know (and hopefully logical) that a higher grade of dysplasia displays a higher % with malignancy (but a lower prevalence and vice versa).

A

Okay

97
Q

What genes are usually mutated in an adenoma, what in malignant polyps and what in carcinoma?

A

Adenoma: APC (methylated APC results in abnormal epithelium). Malignant polyp (adenoma class I, II and III): Kras/Nras and DCC Carcinoma: p53

Pathology dt2 (39 decks)

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