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bowel diseases: small intestine Flashcards

1
Q

diseases of the sm. intestine: Malabsorption

A 
Celiac disease
Whipple disease
Bacterial overgrowth
Short bowel syndrome
Lactase Deficiency
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2
Q

Celiac disease is also called ??

is what??

A

sprue, celiac sprue, and gluten enteropathy
is a permanent dietary disorder caused by an immunologic response to gluten, a storage protein found in certain grains, that results in diffuse damage to the proximal small intestinal mucosa with malabsorption of nutrients

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3
Q

celiac disease prevalence??

A

Disease is present in 1:100 whites of Northern European ancestry, in whom a clinical diagnosis of celiac disease is made in only 10% (most go undiagnosed)

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4
Q

Symptoms and signs of celiac disease depend on ??

“Classic” symptoms ??

A

the length of small intestine involved and the patient’s age

Malabsorption!
Diarrhea, steatorrhea, weight loss, abdominal distention, weakness, muscle wasting, or growth retardation

*slide 8,9: dermatitis herpatiformis (complication of celiac disease)

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5
Q

Celiac disease labs

A 
Microcytic anemia due to iron deficiency
Megaloblastic anemia due to folate or vitamin B12 deficiency
Low serum calcium 
Elevated alkaline phosphatase 
Elevations of prothrombin time
Decreased vitamin A, vitamin D
Low serum albumin
Nonanion gap acidosis
Hypokalemia
Mild elevations of aminotransferases

chart on pg. 11
*steaorrhea: dec. serum cholesterol, dec. serum carotene, vit A, D
malabsorbed TGs, FAs, PLs, cholesterol, vit ADEK
*paresthesia: tetany, + Trousseaus’s/Chvostek signs: dec. serum Ca2+, Mg+

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6
Q

case: ddx

A 
appendicitis
ectopic pregnancy
uterine fibroids
pancreatitis
Crohn's
diverticulitis
malrotatio/vovulus
medial edematous polypsis
*just bc it is in lower quadrant doesn't mean it can't be an UQ problem
ascending cholangitis  (RUQ, fever, jaundice (Charcot's triad)
cholelithiasis
(other choles)
viral gastroenteritis
FBI
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7
Q

case: labs

A 
CBC (anemia)
CNP (LFT's)
lipase (pancreatitis)
UA (pyelonephritis)
hemoccult
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8
Q

case: imaging

A

US

possible CT

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9
Q

Celiac disease Abs dx

A

IgA tissue transglutaminase (IgA tTG) antibody
Antigliadin antibodies are NOT recommended
IgA antiendomysial antibodies are NOT recommended

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10
Q

??? is the gold standard method for confirmation of the diagnosis in patients with a positive serologic test for celiac disease or patients with negative serologies when symptoms and laboratory studies are strongly suggestive of celiac disease

Histology reveals ??

A

Endoscopic mucosal biopsy of the proximal duodenum (bulb) and distal duodenum

*Atrophy or scalloping of the duodenal folds may be observed (slide 13)

Histology reveals abnormalities ranging from intraepithelial lymphocytosis alone to extensive infiltration of the lamina propria with lymphocytes and plasma cells with hypertrophy of the intestinal crypts and blunting or complete loss of intestinal villi
slide 14: “lawn mower effect?”

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11
Q

celiac disease tx

A

Removal of all gluten from the diet is essential to therapy: all wheat, rye, and barley

  • may also have lactose intolerance either temporarily or permanently and should avoid dairy products
  • Dietary supplements (folate, iron, calcium, and vitamins A, B12, D, and E) initially
  • Confirmed osteoporosis may require long-term calcium, vitamin D, and bisphosphonate therapy
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12
Q

celiac disease px
Associated with ??

Celiac disease that is truly refractory to gluten withdrawal occurs in ??

A

Excellent prognosis**
-other autoimmune disorders, including Addison disease, Graves disease, type 1 diabetes mellitus, myasthenia gravis, scleroderma, Sjögren syndrome, atrophic gastritis, and pancreatic insufficiency

-less than 5% and generally carries a poor prognosis

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13
Q

Whipple disease

A

Rare multisystem illness caused by infection with the bacillus Tropheryma whippelii
Most commonly affects white men in the fourth to sixth decades (30s-50s)
“foamy whipped cream in a can”

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14
Q

Whipple disease clinical manifestations

A

*Arthralgias (80%, migratory, nondeforming)
Diarrhea, abdominal pain (75%)
*Weight loss (almost 100%) with protein-losing enteropathy with hypoalbuminemia and edema
Intermittent low-grade fever (50%) of cases
Generalized lymphadenopathy
*Cardiac involvement: Heart failure, Valvular regurgitation
*CNS: Dementia, lethargy, coma, seizures, myoclonus, or hypothalamic signs, Ophthalmoplegia, nystagmus

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15
Q

Whipple disease clinical manifestations 2

A 
Low-grade fever
Malabsorption 
Lymphadenopathy 
Heart murmurs 
Peripheral joints edema, erythema
Neurological findings
Hyperpigmentation on sun-exposed areas
Hypotension ** (happens later)
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16
Q

Whipple dx

A

Endoscopic biopsy of the duodenum with histologic evaluation:

  • Infiltration of the lamina propria with PAS+ macrophages that contain G+ bacilli (which are not acid-fast) and -dilation of the lacteals
  • Whipple bacillus has a characteristic trimellar wall appearance on electron microscopy
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17
Q

Because asymptomatic central nervous system infection occurs in 40% of patients, examination of the ??

A

cerebrospinal fluid by PCR for T whippelii should be performed routinely

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18
Q

Whipple disease tx

A

Antibiotic therapy results in a dramatic clinical improvement within several weeks

  • Complete clinical response usually is evident within 1–3 months
  • Relapse may occur in up to one-third of patients after discontinuation of treatment
  • Prolonged treatment for at least 1 year is required
  • Drugs that cross the BBB are preferred
  • If untreated, the disease is fatal
  • Prevent neurological progression
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19
Q

Bacterial overgrowth in the small intestine of whatever cause may result in malabsorption via a number of mechanisms

A
  • Bacterial deconjugation of bile salts may lead to inadequate micelle formation, resulting in decreased fat absorption with steatorrhea and malabsorption of fat-soluble vitamins (A, D)
  • Microbial uptake of specific nutrients reduces absorption of vitamin B12 and carbohydrates
  • Bacterial proliferation also causes direct damage to intestinal epithelial cells and the brush border, further impairing absorption of proteins, carbohydrates, and minerals
  • Passage of the malabsorbed bile acids and carbohydrates into the colon leads to an osmotic and secretory diarrhea and increased flatulence
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20
Q

Bac OG

A 
Gastric achlorhydria (PPIs)
Anatomic abnormalities of the small intestine with stagnation 
Small intestine motility disorders 
Gastrocolic or coloenteric fistula 
Miscellaneous disorders
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21
Q

Bac OG presentation

A 
Many asymptomatic*
Flatulence
Weight loss
Abdominal pain
Diarrhea
Steatorrhea
Vitamin and mineral deficiencies
Fat-soluble vitamins A or D, vitamin B12, and iron
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22
Q

Bac OG labs

A

Qualitative or quantitative fecal fat assessment typically is abnormal
Stool collection should be obtained for confirmation of steatorrhea
Measure vitamins A, D, B12
Measure serum iron should be measured
Small bowel barium radiography or CT enterography study

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23
Q

Bac OG Gold standard for diagnosis: ??

next one??

another one??

A

aspirate and culture of proximal jejunal secretion that demonstrates over 105 organisms/mL

Noninvasive breath tests are easier to perform: Breath hydrogen and methane tests with glucose or lactulose

Empiric antibiotic trial **Brown doesn’t advocate

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24
Q

bac OG tx

A

Fix anatomic defect if one exists
1–2 weeks with oral broad-spectrum antibiotics effective against enteric aerobes and anaerobes usually leads to dramatic improvement

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25
Q

bac OG tx: In patients in whom symptoms recur off antibiotics, ??
For severe intestinal dysmotility use ??

A

cyclic therapy; continuous antibiotics should be avoided, if possible, to avoid development of bacterial antibiotic resistance.

octreotide

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26
Q

Short Bowel Syndrome

A 
Malabsorptive condition that arises secondary to removal of significant segments of the small intestine:
Crohn disease
Mesenteric infarction
Radiation enteritis
Volvulus
Tumor resection
Trauma
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27
Q

Short Bowel Syndrome: Type and degree of malabsorption depend on ??

A

the length and site of the resection and the degree of adaptation of the remaining bowel

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28
Q

Short Bowel Syndrome: Resection of the terminal ileum

A

Malabsorption of bile salts and vitamin B12

  • Low serum vitamin B12 levels or resection of over 50 cm of ileum require monthly subcutaneous or intramuscular vitamin B12 injections
  • In patients with less than 100 cm of ileal resection, bile salt malabsorption stimulates fluid secretion from the colon, resulting in watery diarrhea treated with bile salt-binding resins
  • Resection of over 100 cm of ileum leads to a reduction in the bile salt pool that results in steatorrhea and malabsorption of fat-soluble vitamins treatment is with a low-fat diet and vitamins supplemented with medium-chain triglycerides
  • Unabsorbed fatty acids bind with calcium, reducing its absorption and enhancing the absorption of oxalate and oxalate kidney stones may develop
  • Calcium supplements should be administered to bind oxalate and increase serum calcium
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29
Q

Short Bowel Syndrome: Resection of up to ?? of the total length of small intestine usually is well tolerated

A more massive resection may result in ??

A

40–50%

“short-bowel syndrome”:
-Weight loss and diarrhea due to nutrient, water, and electrolyte malabsorption
Patients with less than 100–200 cm of proximal jejunum remaining almost always require parenteral nutrition (TPN, only want to use temporarily)
-Death is most commonly due to TPN-induced liver disease, sepsis, or loss of venous access
-Teduglutide is a glucagon-like peptide-2 analogue that stimulates small bowel growth and absorption and is FDA approved for the treatment of short-bowel syndrome **

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30
Q

Lactase is a brush border enzyme that hydrolyzes the ??

A

disaccharide lactose into glucose and galactose

31
Q

Lactase Deficiency epi

A

Approximately 50 million people in the United States have partial to complete lactose intolerance
90% of Asian Americans, 70% of African Americans, 95% of Native Americans, 50% of Mexican Americans, and 60% of Jewish Americans are lactose intolerant compared with less than 25% of white adults
-hard to diagnose

32
Q

Lactase deficiency may also arise secondary to other ??

A

gastrointestinal disorders that affect the proximal small intestinal mucosa:
Crohn disease, sprue, viral gastroenteritis, giardiasis, short bowel syndrome, and malnutrition

33
Q

Lactase Deficiency presentation

A

A large number of false self diagnosis
Most patients with lactose intolerance can drink one or two 8 oz glasses of milk daily without symptoms if taken with food at wide intervals
Mild to moderate amounts of lactose malabsorption:
Bloating, abdominal cramps, and flatulence
Higher lactose ingestions patients will experience osmotic diarrhea

34
Q

Lactase Deficiency tx

A

Find patient “threshold” of intake at which symptoms will occur
By spreading dairy product intake throughout the day in quantities of less than 12 g of lactose (one cup of milk), most patients can take dairy products without symptoms and do not require lactase supplements
-Lactase enzyme replacement is commercially available as nonprescription formulations
-May need calcium supplementation

35
Q

Intestinal motility disorders

A

Acute paralytic ileus
Acute colonic pseudo-obstruction (Ogilvie Syndrome)
Chronic Intestinal Pseudo-obstruction and Gastroparesis

36
Q

Acute Paralytic Ileus: Ileus is a condition in which there is ??

A

neurogenic failure or loss of peristalsis in the intestine in the absence of any mechanical obstruction

37
Q

Causes of ileum

A

Intra-abdominal processes such as recent GI/abd surgery or peritoneal irritation

  • Severe medical illness such as pneumonia, respiratory failure requiring intubation, sepsis or severe infections, uremia, diabetic ketoacidosis, and electrolyte abnormalities
  • Meds that affect intestinal motility (*opioids, anticholinergics, phenothiazines)
  • Following surgery, small intestinal motility usually normalizes first (often within hours), followed by the stomach (24–48 hours), and the colon (48–72 hours)
38
Q

Acute Paralytic Ileus presentation

A

Mild diffuse, continuous abdominal discomfort with nausea and vomiting
Generalized abdominal distention is present with minimal abdominal tenderness but no signs of peritoneal irritation
Bowel sounds are diminished to absent
Laboratory abnormalities are attributable to the underlying condition

39
Q

Acute Paralytic Ileus: imaging

A

Plain film radiography of the abdomen demonstrates distended gas-filled loops of the small and large intestine; air-fluid levels may be seen
A CT scan may be useful in such instances to exclude mechanical obstruction, especially in postoperative patients (if pts looks bad)

40
Q

Acute Paralytic Ileus tx

A

Primary medical or surgical illness that has precipitated adynamic ileus should be treated

  • Most cases respond to restriction of oral intake with gradual liberalization of diet as bowel function returns
  • Severe or prolonged ileus requires NG suction and parenteral administration of fluids and electrolytes
41
Q

FYI: ?? is a peripherally acting mu-opioid receptor antagonist with limited absorption or systemic activity that reverses opioid-induced inhibition of intestinal motility (waking gut back up)

A

Alvimopan

42
Q

Ogilvie Syndrome

A

Spontaneous massive dilation of the cecum and proximal colon may occur in a number of different settings in hospitalized patients

  • Progressive cecal dilation may lead to spontaneous perforation with dire consequences
  • Early detection and management are important to reduce morbidity and mortality
43
Q

Ogilvie Syndrome 2

A

Colonic pseudo-obstruction is most commonly detected in postsurgical patients (mean 3–5 days), after trauma, and in medical patients with respiratory failure, metabolic imbalance, malignancy, myocardial infarction, heart failure, pancreatitis, or a recent neurologic event

44
Q

Liberal use of ?? may precipitate colonic pseudo-obstruction in susceptible patients. It may also occur as a manifestation of ??

A

opioids or anticholinergic agents
colonic ischemia

Etiology of colonic pseudo-obstruction is unknown

45
Q

slide 39

A

Ogilvie Syndrome, looks like toxic megacolon

46
Q

Ogilvie Syndrome: presentation

A

Abdominal distention is frequently noted by the clinician as the first sign
Some patients are asymptomatic
Most report constant but mild abdominal pain
Nausea and vomiting may be present
Bowel movements may be absent, but up to 40% of patients continue to pass flatus or stool

47
Q

Ogilvie Syndrome: labs

A

Laboratory findings reflect the underlying medical or surgical problems
Significant fever or leukocytosis raises concern for colonic ischemia or perforation

48
Q

Ogilvie Syndrome: imaging

A

Radiographs demonstrate colonic dilation, usually confined to the cecum and proximal colon
-Because the dilated appearance of the colon may raise concern that there is a distal colonic mechanical obstruction due to malignancy, volvulus, or fecal impaction, a CT scan or water-soluble enema may sometimes be performed.

49
Q

Ogilvie Syndrome tx

A

Conservative treatment is the appropriate first step for patients with no or minimal abdominal tenderness, no fever, no leukocytosis, and a cecal diameter smaller than 12 cm

  • Treat underlying illness
  • A nasogastric tube and a rectal tube should be placed
  • pts should be ambulated or periodically rolled from side to side and to the knee-chest position in an effort to promote expulsion of colonic gas (decompress)
  • All drugs that reduce intestinal motility should be discontinued if possible
  • *Enemas may be administered judiciously if large amounts of stool are evident on radiography
50
Q

Ogilvie Syndrome tx 2

what is NOT helpful

A

Oral laxatives are NOT helpful and may cause perforation, pain, or electrolyte abnormalities.
-Conservative treatment is successful in over 80% of cases within 1–2 days
Pts must be watched for signs of worsening distention or abdominal tenderness; cecal size should be assessed by abdominal radiographs every 12 hours

51
Q

Ogilvie Syndrome: Intervention should be considered in patients with any of the following:

A
  • no improvement or clinical deterioration after 24–48 hours of conservative therapy
  • cecal dilation greater than 10 cm for a prolonged period (more than 3–4 days)
  • pts with cecal dilation greater than 12 cm
  • Neostigmine injection should be given unless contraindicated
  • Colonoscopic decompression is indicated in patients who fail to respond to neostigmine
52
Q

Gastroparesis and chronic intestinal pseudo-obstruction are chronic conditions characterized by??

A

intermittent, waxing and waning symptoms and signs of gastric or intestinal obstruction in the absence of any mechanical lesions to account for the findings

53
Q

Gastroparesis and chronic intestinal pseudo-obstruction: Caused by a heterogeneous group of ??

A

endocrine disorders (DM), postsurgical conditions, neurologic conditions, rheumatologic syndromes, infections, amyloidosis, paraneoplastic syndromes, medications, eating disorders, and idiopathic

54
Q

Gastroparesis and chronic intestinal pseudo-obstruction: Small bowel involvement:
Gastric involvement:

A

abdominal distention, vomiting, diarrhea, and varying degrees of malnutrition can result in constipation or alternating diarrhea and constipation

Chronic or intermittent symptoms of postprandial fullness (early satiety), nausea, and vomiting (1–3 hours after meals)

55
Q

Gastroparesis and chronic intestinal pseudo-obstruction: imaging

A
  • Plain film radiography may demonstrate dilation of the esophagus, stomach, small intestine, or colon resembling ileus or mechanical obstruction
  • Mechanical obstruction of the stomach, small intestine, or colon is much more common than gastroparesis or intestinal pseudo-obstruction and must be excluded
  • Gastric scintigraphy with a low-fat solid meal is the optimal means for assessing gastric emptying (see it moving thru)
  • Small bowel manometry is useful for distinguishing visceral from myopathic disorders and for excluding cases of mechanical obstruction
56
Q

Chronic Intestinal Pseudo-obstruction and Gastroparesis: tx

A

No specific therapy for gastroparesis or pseudo-obstruction
Acute exacerbations are treated with nasogastric suction and intravenous fluids
Long-term treatment is directed at maintaining nutrition
Agents that reduce gastrointestinal motility should be avoided

57
Q

?? and ?? before meals are each of benefit in treatment of gastroparesis but not small bowel dysmotility

?? is another antidopaminergic agent that enhances gastric emptying and has efficacy as an antiemetic agent

A

Metoclopramide (Reglan) and erythromycin

Domperidone (not in US, not FDA approved)

58
Q

other Diseases of the Small Intestine

A

Appendicitis
Intestinal tuberculosis
Protein-losing enteropathy

59
Q

Appendicitis

A

Most common abdominal surgical emergency, affecting approximately 10% of the population

  • Most commonly between the ages of 10 and 30 years
  • Initiated by obstruction of the appendix by a fecalith, inflammation, foreign body, or neoplasm
60
Q

appendicitis: Obstruction leads to ??

A

increased intraluminal pressure, venous congestion, infection, and thrombosis of intramural vessels
If untreated, gangrene and perforation develop within 36 hours**

61
Q

appendicitis symptoms

A

Begins with vague, often colicky periumbilical or epigastric pain
Within 12 hours the pain shifts to the right lower quadrant, manifested as a steady ache that is worsened by walking or coughing
Almost all patients have nausea with one or two episodes of vomiting
Low-grade fever

62
Q

appendicitis signs

A

Localized tenderness with guarding in the right lower quadrant at McBurney’s point:

  • Psoas sign (pain on passive extension of the right hip)
  • Obturator sign (pain with passive flexion and internal rotation of the right hip)
63
Q

appendicitis Atypical presentations

A

Retrocecal appendix
In the elderly
In pregnancy

64
Q

Both abdominal ?? are useful in diagnosing appendicitis

A

ultrasound and CT scanning

65
Q

appendicitis tx

A

The tx of early, uncomplicated appendicitis is surgical appendectomy in most pts

  • When possible, a laparoscopic approach is preferred to open laparotomy
  • Prior to surgery, pts should be given broad-spec abx with G- and anaerobic coverage to reduce the incidence of postop infections
  • Emergency appendectomy is required in patients with perforated appendicitis with generalized peritonitis
66
Q

Intestinal Tuberculosis

A

Intestinal tuberculosis is common in underdeveloped countries

  • US incidence has been rising in immigrant groups and patients with AIDS
  • Caused by both Mtb and M bovis
  • Active pulmonary disease is present in less than 50% of patients
  • The most frequent site of involvement is the ileocecal region
67
Q

Intestinal Tuberculosis: May cause ??

A

mucosal ulcerations or scarring and fibrosis with narrowing of the lumen

68
Q

Intestinal Tuberculosis: presentation

A

May be without symptoms or complain of chronic abdominal pain, obstructive symptoms, weight loss, and diarrhea

  • An abdominal mass may be palpable
  • Complications include intestinal obstruction, hemorrhage, and fistula formation
69
Q

Intestinal Tuberculosis dx

A

The purified protein derivative (PPD) skin test may be negative, especially in patients with weight loss or AIDS
Barium radiography may demonstrate mucosal ulcerations, thickening, or stricture formation
Abdominal CT may show thickening of the cecum and ileocecal valve and massive lymphadenopathy

70
Q

Intestinal Tuberculosis dx/tx

A

Colonoscopy may demonstrate an ulcerated mass, multiple ulcers with steep edges and adjacent small sessile polyps, small ulcers or erosions, or small diverticula, most commonly in the ileocecal region
gold standard:
endoscopic or surgical biopsy revealing acid-fast bacilli, caseating granuloma, or positive cultures from the organism
-Detection of tubercle bacilli in biopsy specimens by PCR is now the most sensitive means of diagnosis
Treatment with standard antituberculous regimens is effective

71
Q

Protein-Losing Enterpathy

A

A number of conditions that result in excessive loss of serum proteins into the gastrointestinal tract
Hypoalbuminemia and an elevated fecal alpha-1-antitrypsin level

72
Q

Protein-Losing Enterpathy: Proteins may be lost through one of three mechanisms:

A

Mucosal disease with ulceration
Lymphatic obstruction
Idiopathic change in permeability of mucosal capillaries and conductance of interstitium, resulting in “weeping” of protein-rich fluid from the mucosal surface

73
Q

Protein-Losing Enterpathy: dx

A

In most cases, protein-losing enteropathy is recognized as a sequela of a known gastrointestinal disorder
Protein-losing enteropathy must be distinguished from other causes of hypoalbuminemia
Confirmed by determining the gut alpha-1-antitrypsin clearance
Laboratory evaluation of protein-losing enteropathy includes serum protein electrophoresis, lymphocyte count, and serum cholesterol
Serum ANA and C3 levels are useful to screen for autoimmune disorders
Stool samples should be examined for ova and parasites
Evidence of malabsorption is evaluated by means of a stool qualitative fecal fat determination

74
Q

Protein-Losing Enterpathy: dx/tx

A

Intestinal imaging is performed with small bowel enteroscopy biopsy, CT enterography, or wireless capsule endoscopy of the small intestine
Colonic diseases are excluded with colonoscopy
A CT scan of the abdomen is performed to look for evidence of neoplasms or lymphatic obstruction
In some situations, laparotomy with full-thickness intestinal biopsy is required to establish a diagnosis
Treatment is directed at the underlying cause

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