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2H SystemicPatho GIT > Chapter17: INTESTINES:Malabsorption and Diarrhea > Flashcards

Chapter17: INTESTINES:Malabsorption and Diarrhea Flashcards

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1
Q

What is malabsorption?

A

Malabsorption, which presents most commonly as chronic diarrhea, is characterized by
_defective absorption of fats, fat- and water-soluble vitamins, proteins, carbohydrates,
electrolytes and minerals, and water._

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2
Q

What is the characteristic of chronic malabsorption?

A

Chronic malabsorption can be accompanied by :

  • weight loss,
  • anorexia,
  • abdominal distention
  • , borborygmi,
  • and muscle wasting.
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3
Q

What is the hallmark of
malabsorption?

A

Steatorrhea, characterized by excessive fecal fat and bulky, frothy, greasy, yellow or clay-colored stools..

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4
Q

What is Steatorrhea?

A

characterized by excessive fecal fat and bulky, frothy, greasy, yellow or clay-colored stools.

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5
Q

What are the chronic malabsorptive disorders most commonly encountered in the United States

A
  • pancreatic insufficiency,
  • celiac disease, and
  • Crohn disease ( Table 17- 6 ).
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6
Q

What is an important cause of malabsorption and diarrhea
after allogeneic bone marrow transplantation?

A

Intestinal graft-versus-host disease

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7
Q

TABLE 17-6 – Defects in Malabosorptive and Diarrheal Disease

A
  1. Celiac disease
  2. Tropical sprue
  3. Chronic pancreatitis
  4. Cystic fibrosis
  5. Primary bile acid
    malabsorption
  6. Carcinoid syndrome
  7. Autoimmune enteropathy
  8. Disaccharidase deficiency
  9. Whipple disease
  10. Abetalipoproteinemia
  11. Viral gastroenteritis
  12. Bacterial gastroenteritis
  13. Parasitic gastroenteritis
  14. Inflammatory bowel
    disease
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8
Q

Celiac disease

A

Pathogenesis:

  1. Terminal Digestion
  2. Transepithelial Transport
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9
Q

What process is abnormal inTropical sprue ?

A

Pathogenesis:

  • Terminal Digestion
  • Transepithelial Transport
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10
Q

What process is abnormal in Chronic pancreatitis ?

A

Intraluminal
Digestion

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11
Q

What process is abnormal in Cystic fibrosis ?

A

Intraluminal
Digestion

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12
Q

What process is abnormal in Primary bile acid
malabsorption ?

A
  • Intraluminal Digestion
  • Transepithelial Transport
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13
Q

What process is abnormal in Carcinoid syndrome?

A

Transepithelial
Transport

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14
Q

What process is abnormal in Autoimmune
enteropathy?

A
  • Terminal Digestion
  • Transepithelial Transport
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15
Q

What process is abnormal in Disaccharidase
deficiency?

A

Terminal
Digestion

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16
Q

**** What process is abnormal in Whipple disease?

A

Lymphatic Transport

****Among the defects in Malabosorptive and Diarrheal Disease, this is the only disease with a pathology exhibiting in lympahtic transport.

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17
Q

What process is abnormal in Abetalipoproteinemia?

A

Transepithelial
Transport

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18
Q

What process is abnormal in Viral gastroenteritis?

A
  • Terminal Digestion
  • Transepithelial Transport
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19
Q

What process is abnormal inBacterial
gastroenteritis?

A
  • Terminal Digestion
  • Transepithelial Transport

*** same with Viral and parasitic gastroenteritis.

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20
Q

What process is abnormal in Parasitic gastroenteritis?

A
  • Terminal Digestion
  • Transepithelial Transport
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21
Q

What process is abnormal in Inflammatory bowel
disease?

A
  • Intraluminal Digestion
  • Terminal Digestion
  • Transepithelial Transport
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22
Q

Malabsorption results from disturbance in at least one of the four phases of nutrient absorption:

A
  • (1) intraluminal digestion
  • (2) terminal digestion
  • (3) transepithelial transport
  • (4) lymphatic transport
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23
Q

What is being broken down in intraluminal digestion?

A

in which proteins, carbohydrates, and fats are broken down into
forms suitable for absorption

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24
Q

What is involved in terminal digestion?

A

which involves the hydrolysis of
carbohydratesandpeptides by disaccharidasesandpeptidases, respectively, in thebrush
border of the small intestinal mucosa;

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25
Q

What is involved in transepithelial transport?

A

in which nutrients, fluid, and electrolytes are transported across and processed within the small intestinal epithelium

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26
Q

What is involved inlymphatic transport?

A

of absorbed lipids

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27
Q

What is the reason why malabsorption syndromes resemble each other more than they differ?

A

In many malabsorptive disorders a defect in one of these processes predominates, but more
than one usually contributes.

As a result, malabsorption syndromes resemble each other more
than they differ.

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28
Q

What is the general symptom for malabsorption?

A

General symptoms include:

  • diarrhea (from nutrient malabsorption and excessive intestinal secretion),
  • flatus,
  • abdominal pain, and
  • weight loss.
  • Inadequate absorption of vitamins and minerals can result in anemia and mucositis due to pyridoxine, folate, or vitamin B12

deficiency; bleeding, due to vitamin K deficiency; osteopenia and tetany due to calcium,
magnesium, or vitamin D deficiencies; or peripheral neuropathy due to vitamin A or B12
deficiencies. A variety of endocrine and skin disturbances may also occur

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29
Q

What is diarrhea?

A

Diarrhea is defined as an increase in stool mass, frequency, or fluidity, typically greater than 200 g per day.

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30
Q

In severe cases stool volume can exceed how many L per day?

A

14 L per day and, without fluid resuscitation, result in death.

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31
Q

What is dysentery?

A

Painful, bloody, small-volume diarrhea is known as dysentery.

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32
Q

Diarrhea can be classified according to four major categories:

A
  • Secretory diarrhea
  • • Osmotic diarrhea
  • • Malabsorptive diarrhea
  • • Exudative diarrhea
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33
Q

What is Secretory diarrhea?

A

is characterized by isotonic stool and persists during fasting

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34
Q

What is osmotic diarrhea?

A

Osmotic diarrhea, such as that which occurs with lactase deficiency, is due to the excessive osmotic forces exerted by unabsorbed luminal solutes.

The diarrhea fluid is over 50 mOsm more concentrated than plasma and abates with fasting.

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35
Q

What is Malabsorptive diarrhea?

A

follows generalized failures of nutrient absorption and is
associated with steatorrhea and is relieved by fasting

36
Q

What is exudative diarrhea?

A

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

37
Q

What is the pathogenesis of cystic fibrosis regarding malabsorption?

A

Due to the absence of the epithelial cystic

  • *fibrosis transmembrane conductance regulator (CFTR),** individuals with cystic fibrosis have
  • *defects in intestinal chloride ion secretion.**

This interferes with bicarbonate, sodium, and water
secretion,ultimately resulting in defective luminal hydration.

Formation of intraductal concretions can begin in utero, leading to duct obstruction, low-grade chronic autodigestion of the pancreas, and eventual exocrine pancreatic insufficiency in more than 80% of patients .

The result is failure of the intraluminal phase of nutrient absorption, which can be effectively treated
in most patients with oral enzyme supplementation.

38
Q

What is celiac disease?

A

Celiac disease is also known as celiac sprue or gluten-sensitive enteropathy.

It is an immunemediated
enteropathy triggered by the ingestion of gluten-containing cereals, such as wheat,
rye, or barley, in genetically predisposed individuals.

In countries where most people are
Caucasians of European ancestry, celiac disease is a common disorder, with an estimated
prevalence of 0.5% to 1%.

39
Q

Why is Celiac disease a unique intestinal immune disorder?

A

because the environmental precipitant,
gluten, is known.

40
Q

What is gluten?

A

Gluten is the major storage protein of wheat and similar grains, and the alcohol-soluble fraction of gluten, gliadin, contains most of the disease-producing components.

41
Q

How is gluten digested?

A

Gluten is digested by luminal and brush-border enzymes into amino acids and peptides,
including a 33–amino acid α-gliadin peptide that is resistant to degradation by gastric,
pancreatic, and small intestinal proteases ( Fig. 17-25 ).

42
Q

What is the pathogenesis of Celiac disease?

A

The network of immune reactions to
gliadin that are thought to result in celiac disease is illustrated below.

Some gliadin peptides induce epithelial cells to express IL-15, which in turn triggers activation and proliferation of CD8+ intraepithelial lymphocytes that are induced to express NKG2D, a natural killer cell
marker.

These **lymphocytes become cytotoxic and kill enterocytes with surface MIC-A, an HLA
class I–like protein** expressed in response to stress.

NKG2D is the receptor for MIC-A.

Thus,
unlike the CD4+ T cells, these NKG2D+ CD8+ T cells do not recognize gliadin.

The resulting epithelial damage may contribute to the process by which other gliadin peptides cross the
epithelium to be deamidated by tissue transglutaminase.

Deamidated gliadin peptides are then able to interact with HLA-DQ2 or HLA-DQ8 on antigen-presenting cells and be presented to
CD4+ T cells. These T cells produce cytokines that contribute to tissue damage and the
characteristic mucosal pathology.

43
Q
A

FIGURE 17-25 The left panel illustrates the morphologic alterations that may be present
celiac disease, including villous atrophy, increased numbers of intraepithelial lymphocytes
(IELs), and epithelial proliferation with crypt elongation (compare to Fig. 17-26 ). The right
panel depicts a model for the pathogenesis of celiac disease. Note that both innate and
adaptive immune mechanisms are involved in the tissue responses to gliadin.

44
Q

Why does host factors determine whether disease develops or not in celiac disease?

A

While nearly all people eat grain and are exposed to gluten and gliadin, most do not develop
celiac disease.

Thus, host factors determine whether disease develops

45
Q

Wha is seem to be critical host factors in Celiac Disease?

A

. Among these, HLA proteins seem to be critical, since almost all people with celiac disease carry the class II HLADQ2 or HLA-DQ8 allele.

However, the HLA locus accounts for less than half of the genetic component of celiac disease.

Remaining genetic factors may include polymorphisms of immuneregulatory
genes, such as those encoding IL-2, IL-21, CCR3, and SH2B3, [46] and genes that determine epithelial polarity. [47,] [48]

46
Q

There is also an association of celiac disease with other immune diseases including what?

A
  • type 1 diabetes,
  • thyroiditis, and
  • Sjögren syndrome, as well as
  • ataxia,
  • autism,
  • depression,
  • some forms of epilepsy,
  • IgA nephropathy,
  • Down syndrome, and
  • Turner syndrome.
47
Q

What is generally
diagnostic in celiac disease?

A

Biopsy specimens from the second portion of the duodenum or proximal jejunum, which are exposed to the highest concentrations of dietary gluten, are generally diagnostic in celiac disease.

48
Q

What is the histopathologic characteristic of Celiac disease?

A

The histopathology is characterized by increased numbers of intraepithelial CD8+ T lymphocytes (intraepithelial lymphocytosis), crypt hyperplasia,
and villous atrophy ( Fig. 17-26 ).

This loss of mucosal and brush-border surface area
probably accounts for the malabsorption.

In addition, increased rates of epithelial turnover reflected in increased crypt mitotic activity, may limit the ability of absorptive enterocytes to
fully differentiate and contribute to defects in terminal digestion and transepithelial transport.

49
Q

Other features of fully developed celiac disease include

A
  • increased numbers of plasma cells,
  • mast cells,
  • and eosinophils, especially within the upper part of the lamina propria.
50
Q

What is a marker for a marker of less advanced celiac disease?

A

. With increased frequency of serologic screening and early detection of disease-associated antibodies, it is now appreciated that an increase in the number of intraepithelial lymphocytes, particularly within the villus, is a marker of less advanced celiac disease. [49

However, intraepithelial lymphocytosis and villous atrophy are not specific for celiac disease and can be

present in other diseases, including viral enteritis.

​The combination of histology and serology

is most specific for diagnosis of celiac disease

51
Q

What is most specific for diagnosis of celiac disease?

A

​The combination of histology and serology

is most specific for diagnosis of celiac disease

52
Q
A

FIGURE 17-26 Celiac disease.

  • A, Advanced cases of celiac disease show complete loss of villi, or total villous atrophy. Note the dense plasma cell infiltrates in the lamina propria.
  • B, Infiltration of the surface epithelium by T lymphocytes, which can be recognized by their densely stained nuclei (labelled T). Compare to elongated, pale-staining epithelial nuclei (labelled E).
53
Q

In adults, celiac disease presents most commonly between the ages

A

of 30 and 60.

However, many cases escape clinical attention for extended periods because of atypical presentations.

54
Q

What is silent celiac disease?

A

Some patients may have silent celiac disease, defined as positive serology and villous atrophy
without symptoms.

55
Q

What is latent celiac disease?

A

in which positive serology is _not accompanied by
villous atrophy._

56
Q

Symptomatic adult celiac disease is often associated with what?

A
  • anemia,
  • chronic diarrhea,
  • bloating, or
  • chronic fatigue.
57
Q

Although there is no gender preference, celiac disease is

detected two- to threefold more commonly in what women and what is the reason for this?

A

women, perhaps because monthly menstrual
bleeding increases the demand for iron and vitaminsand accentuates the effects of impaired
absorption.

58
Q

Pediatric celiac disease, which affects males and females equally, may present with what?

A

malabsorption or atypical symptoms affecting almost any organ. [50]

59
Q

What are the classic symptoms of celiac disease in pediatric patients?

A

In those with classic
symptoms, disease typically begins between ages of 6 and 24 months, after introduction of
gluten to the diet, and includes:

  • irritability,
  • abdominal distention,
  • anorexia,
  • chronic diarrhea,
  • failure to thrive,
  • weight loss, or
  • muscle wasting. [50]
60
Q

What are the nonclassic symptoms of children with celiac disease?

A

Children with nonclassic symptoms tend to

present at older ages with complaints of abdominal pain, nausea, vomiting, bloating, or
constipation.

Common extra-intestinal complaints include arthritis or joint pain, seizure disorders, aphthous stomatitis, iron deficiency anemia, pubertal delay, and short stature.

61
Q

What characteristic presentation is seen in 10% of pediatric patients?

A

A characteristic itchy, blistering skin lesion, dermatitis herpetiformis, can be present in as many
as 10% of patients, and the incidence of lymphocytic gastritis and lymphocytic colitis is also
increased.

62
Q

Unfortunately,what is the only treatment currently available for celiac disease ?

A

a glutenfree diet, but, despite the challenges of adhering to this diet, it does result in symptomatic
improvement for most patients.

A gluten-free diet may also reduce the risk of long-term
complications including anemia, female infertility, osteoporosis, and cancer

63
Q

What diagnostic procedure in celiac disease is done prior to biopsy ?

A

Noninvasive serologic tests are generally performed prior to biopsy. [51]

64
Q

What are the most The most sensitive
tests for celiac disease?

A
  • presence of IgA antibodies to tissue transglutaminase
  • or IgA or IgG antibodies to deamidated gliadin.
65
Q

What tests are highly specific for celiac disease?

A

Anti-endomysial antibodies are highly specific but less sensitive than other antibodies.

66
Q

What is done in cases with negative IgA tests in testing for celiac disease?

A

In cases with negative IgA tests, IgA deficiency, which is more common in celiac patients, should be ruled out.

If IgA deficiency is present, titers of IgG antibodies to tissue
transglutaminase and deamidated gliadin should be measured. The absence of HLA-DQ2 or
HLA-DQ8 is useful for its high negative predictive value, but the presence of these alleles is not
helpful in confirming the diagnosis.

67
Q

Individuals with celiac disease have a higher than normal rate of malignancy.

What is the most common
celiac disease–associated cancer?

A

enteropathy-associated T-cell lymphoma ,

-is an aggressive lymphoma of intraepithelial T lymphocytes.

Small intestinal adenocarcinoma is also more
frequent in individuals with celiac disease.

Thus, when symptoms such as abdominal pain,
diarrhea, and weight loss develop despite a strict gluten-free diet, cancer or refractory sprue, in
which the response to a gluten-free diet is lost, must be considered.

It is, however, important to
remember that failure to adhere to a gluten-free diet is the most common cause of recurrent
symptoms,and that most people with celiac disease do well with dietary restrictions and die of
unrelated causes.

68
Q

Why is cancer or refractory sprue is considered to patients when symptoms such as abdominal pain,
diarrhea, and weight loss develop despite a strict gluten-free diet?

A

response to a gluten-free diet is lost, must be considered.

69
Q

What is Tropical sprue?

A

is a malabsorption syndrome that occurs almost exclusively in people living in or
visiting the tropics,including _Puerto Rico, the Caribbean, northern South America, West Africa,
India, and Southeast Asia._

Inexplicably, it is uncommon in Jamaica.

The disease is generally
endemic, although epidemics have occurred.

70
Q

What are the histological changes in tropical sprue?

A

are similar to celiac disease, but total villous atrophy is
uncommon,andtropical sprue tends to involve the distal small bowel.

The latter probably
explains the frequency of folate or vitamin B12 deficiencies with enlarged (megaloblastic) nuclei
within epithelial cells that are reminiscent of those seen in pernicious anemia

71
Q

What explains the frequency of folate or vitamin B12 deficiencies with enlarged (megaloblastic) nuclei
within epithelial cells that are reminiscent of those seen in pernicious anemia in tropical sprue?

A

tropical sprue tends to involve the distal small bowel.

72
Q

What is the clinical course of Tropical sprue?

A

Malabsorption usually becomes apparent within days or a few weeks of an acute diarrheal
enteric infection in visitors.

Although no definite causal organism has been identified, overgrowth of aerobic enteric bacteria has been documented, and broad-spectrum antibiotics
usually effect rapid recovery.

Various infections, including Cyclospora or enterotoxigenic bacteria, have been suggested as etiologic factors.

73
Q

What is Autoimmune enteropathy?

A

is an X-linked disorder characterized by severe persistent diarrhea and autoimmune disease that occurs most often in young children.

74
Q

What is IPEX?

A

A particularly _severe familial
form, termed IPEX_, an acronym denotingimmunedysregulation, polyendocrinopathyenteropathy, and X-linkage, is due to a germline mutation in theFOXP3gene, which is located on the X chromosome.

75
Q

What is FOXP3?

A

is a transcription factor expressed in CD4+ regulatory T cells, [53] and individuals with IPEX and FOXP3 mutations have defective T-regulatory function.

Other defects in regulatory T cell function have also been linked to less severe forms of autoimmune enteropathy.

Autoantibodies to enterocytes and goblet cells are common, andsome patients may have antibodies to parietal or islet cells.

Within the small intestine
intraepithelial lymphocytes may be increased, but not to the extent seen in celiac disease, and
neutrophils are often present.

Therapy includes immunosuppressive drugs such as
cyclosporine and, in rare cases, bone marrow transplantation.

76
Q

The disaccharidases, including lactase, are located in the where?

A
  • *apical brush-border membrane** of the
  • *villus absorptive epithelial cells.**
77
Q

Because the defect is biochemical, biopsy histology is generally unremarkable

. Lactase deficiency is of two types:

A
  1. Congenital lactase deficiency
  2. Acquired lactase deficiency
78
Q

What is Congenital lactase deficiency?

A

caused by a mutation in the gene encoding lactase, [55] is an autosomal recessive disorder.

The disease is rare and presents as _explosive
diarrhea with watery_, frothy stools and abdominal distention upon milk ingestion.
Symptoms abate when exposure to milk and milk products is terminated, thus removing
the osmotically active but unabsorbable lactose from the lumen.

79
Q

What is Acquired lactase deficiency ?

A

is caused by down-regulation of lactase gene expression and is particularly common among Native Americans, African-Americans, and Chinese
populations.

80
Q

What is the presentation of acquired lactase deficiency?

A

Disease presents after childhood, perhaps reflecting the fact that, before farming of dairy animals, lactase was unnecessary after children stopped drinking
mothers’ milk.

81
Q

When is the Onset of acquired lactose deficiency?

A

is sometimes associated with enteric
viral or bacterial infections.

82
Q

What are the symptoms of acquired lactase deficiency?

A

Symptoms, including _abdominal fullness, diarrhea, and
flatulence_, due to fermentation of the unabsorbed sugars by colonic bacteria, are triggered by ingestion of lactose-containing dairy products.

83
Q

What is Abetalipoproteinemia?

A

rare autosomal recessive disease characterized by an inability to secrete triglyceride-rich lipoproteins.

84
Q

What is the pathogenesis of Abetalipoproteinemia?

A

It is caused by a mutation in the microsomal triglyceride transfer protein (MTP) that catalyzes transport of triglycerides, cholesterol esters, and
phospholipids.

MTP-deficient enterocytes are unable to export lipoproteins and free fatty acids.
_As a result, monoglycerides cannot be assembled into chylomicrons and triglycerides
accumulate within the epithelial cells_.

The malabsorption of abetalipoproteinemia is therefore a failure of transepithelial transport.

Lipid vacuolization of small intestinal epithelial cells is evident under the light microscope and can be highlighted by special stains, such as oil red-O,
particularly after a fatty meal.

85
Q

Wha is the presentation of Abetalipoproteinemia?

A

Abetalipoproteinemia presents in infancy and the clinical picture is dominated by failure to thrive, diarrhea, and steatorrhea.

Patients also have a _complete absence of all plasma
lipoproteins containing apolipoprotein B,_although the gene that encodes apolipoprotein B itself
is not affected.

Failure to absorb essential fatty acids leads to deficiencies of fat-soluble vitamins as well as lipid membrane defects that can be recognized by the presence of acanthocytic red cells (burr cells) in peripheral blood smears.

86
Q

What is the reason for the appearance of acanthocytic red cells (burr cells) in peripheral blood smears in Abetalipoproteinemia?

A

Failure to absorb essential fatty acids leads to deficiencies of fat-soluble vitamins as well as lipid membrane defects

87
Q
A

2H SystemicPatho GIT (34 decks)

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