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Block 10 week 5 > GI path-Usera > Flashcards

GI path-Usera Flashcards

1
Q

When does pyloric stenosis present?

How does it present?

A

2nd or 3rd week of life

-new onset regurgitation and persistent, projectile nonbilous vomiting.

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2
Q

Pyloric stenosis results from hypertrophy of the (blank) that results in obstruction.

A

muscularis propria

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3
Q

Pyloric stenosis is associated with (blank) and (blank)

A

Turner syndrome

Trisomy 18

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4
Q

Acquired pyloric stenosis occurs due to (blank) and (blank)

A

antral gastritis

ulcers close to the pylorus

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5
Q

Meckel diverticulum occurs in the ileum due to failed involution of the (blank)

A

vitelline duct (connects the developing gut lumen to the yolk sac)

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6
Q

A true diverticuum that occurs on the (blank) side of the bowel.

A

antimesenteric

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7
Q

What are the rules of 2 associated with meckels diverticulum?

A
  • 2% of pop
  • w/in 2 ft of the ileocecal valve
  • 2 inches long
  • 2x as common in males than females
  • pnts symptomatic by age 2
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8
Q

What is this:
congenital aganglionic megacolon
Why does this occur?

A

Hirschsprung disease

-an arrest in normal migration of neural crest cells from cecum to rectum AND ganglion premature death

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9
Q

In Hirschsprung disease, the distal intestinal segment lacks both (blank) and (blank). Coordinated perstaltic contractions are (blank) and (blank) with proximal dilation occurs

A

Meissner submucosal
Auerbach myenteric plexus
absent
functional obstruction

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10
Q

What is this:
presents neonatally with failure to pass meconium with obstruction later

How do you treat it?

A

Hirschsprung disease

resection of aganglionic segment and anastomosis of the normal colon to the rectum

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11
Q

What can cause acquired megacolon?

A
  • Chagas disease (T. cruzi)
  • Stricture
  • Ulcerative colitis
  • Visceral myopathy
  • Psychosomatic disorders
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12
Q

The GI tract is a (blank) tube lined by (blank) membrane that exhibits regional variation reflecting the changing functions of the system from mouth to anus

A

muscular

mucous

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13
Q

The mucous membranes can be classified as (blank x 3)

A

protective-esophagus
secretory- stomach
absorptive- small and large intestine

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14
Q

What are the four distinct functional layers of the lower GI tract?

A
  • Mucosa
  • Submucosa
  • Muscularis propria
  • Adventitia
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15
Q

The small intestine begins after the (blank) and consists of three segments, which are (blank x 3)

A

pyloric sphincter

Duodenum, Jejunum, Ileum

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16
Q

What is the prinicipal site for absorption of digestion products from the GI tract?

A

small intestine

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17
Q

What are the cell types found in the small intestine?

A
  • enterocytes
  • goblet cells
  • paneth cells
  • neuroendocrine cells
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18
Q

What is the most numerous cell type in the small intestine and what do they look like?

A

Enterocytes

tall and collumnar with microvilli that creates a brush border

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19
Q

What are scattered among the enterocytes and produce mucin for lubrication of intestinal contents?

A

goblet cells

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20
Q

What are found in the small
intestine at the base of crypts?
What do they contain and what are they a part of?

A

Paneth cells

  • apical eosinophilic granules
  • innate immune system of GI tract
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21
Q

(blank) produce locally acting hormones that regulate GI motility and secretion

A

Neuroendocrine cells

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22
Q

The duodenum is identified by the presence of (blank).

A

brunners glands

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23
Q

The jejunum and ileum are histologically indistinguishable.

T or F

A

T

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24
Q

What are the principle functions of the large intestine?

A

-recovery of water and salt from feces and propulsion of solid waste to the rectum

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25
Q

Large intestine begins after the (blank) and is organized into segments. What are the segments and how can you distinguish them from on another?

A

-ileocecal valve

  • Cecum
  • Appendix
  • Ascending colon
  • Transverse colon
  • Descending colon
  • Sigmoid colon
  • Rectum

you cant

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26
Q

How is the colon organized and what are the 2 cell types found in it?

A

as glands and crypts

-absorptive enterocytes and goblet cells

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27
Q

Obstruction can occur at any level but is most common at the (blank) due to its relatively narrow lumen.
What are the causes of this?

A

small intestine

Hernias, intestinal adhesions, intussuception, volvulus, tumors and infarction

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28
Q

What are the clinical features of obstruction?

A

ab pain
distention
vomiting
constipation

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29
Q

What is this:

protrusion of a serosa lined pouch of peritoneum due to a weakness or defect in the wall of the peritoneal cavity

A

Hernias

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30
Q

(blank) herniation is of concern due to possible incarceration and strangulation.
Where do hernias most commonly occur?

A

External herniation (visceral protrusion)

in small bowel but can contain omentum and colon

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31
Q

What is this:
fibrous tissue connects bowel segments
What is it due to?

A

Adhesions

surgical procedures, infection, endometriosis or other causes of peritoneal inflammation

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32
Q

What is of concern with adhesions?

A

internal herniation of viscera w/ obstruction and strangulation

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33
Q

What is this:
complete twisting of a loop of bowel around its mesenteric base of attachment

This produces (blank) and (blank) compromise

Where does it occur most often?

A

Volvulus

luminal and vascular

sigmoid colon, cecum, small bowel, stomach, and transverse colon

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34
Q

What are the clinical features of volvulus?

A

obstruction and infarction (rare)

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35
Q

What is this:

segment of the intestine that is constricted by a wave of peristalsis telescopes into the immediately distal segment

A

Intussuscpetion

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36
Q

In intussusception, the invaginated segment is propelled by (Blank) and pulls the (blank) along

A

peristalsis

mesentary

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37
Q

In intussuscpetion, children have no anatomic defects but some cases are associated with (blank)

A

rotavirus

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38
Q

In older children and adults, what is normally the cause of intussuscpetion?
What is the tx for intussuscpetion?

A

intraluminal mass

barium enema and surgical intervention

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39
Q

The majority of the GI tract is supplied by the (blank x 3) arteries

A

celiac, superior mesenteric, inferior mesenteric arteries

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40
Q

How does the bowel tolerate slow progressive blood loss? Acute compromise can lead to (blank)

A

collateral circulation

infarction

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41
Q

What is this:
necrosis extends no further than the muscularis mucosa.
What is it due to?

A

mucosal infarction

due to acute or chronic hypoperfusion

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42
Q

What is this:
necroses extends from mucosa to submucosa

What is it due to?

A

Mural infarction

acute and chronic hypoperfusion

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43
Q

What is this:
necrosis extends throughout the wall from mucosa to serosa

What is it due to?

A

Transmural infarction

Acute vascular compromise

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44
Q

The severity of bowel necrosis is determined by (blank x 3)

A

severity of vascular compromise
time frame
vessels affected

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45
Q

In ischemic bowel disease, if the vessels are affected, what are the 2 presentations seen?

A
  • watershed areas (splenic flexure)

- crypt sparing with epithelial sloughing

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46
Q

Injury causing ischemic bowel disease occurs in 2 phases, what are they?

A
  • hypoxia

- reperfusion injury (greatest damage)

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47
Q

What are the causes of ischemic bowel disease?

A 
Severe atherosclerosis
Aortic aneurysm
Hypercoagulable states
Oral contraceptive use
Embolization of cardiac vegetations
Aortic atheromas
Cardiac failure
Shock
Dehydration
Vasoconstrictive drugs
Systemic vasculitis
Venous thrombosis
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48
Q

What are the clinical features of ischemic bowel disease?

A 
Older people with coexistent cardiac or vascular disease
Abdominal pain
Nausea
Vomiting
Diarrhea
Melanotic stools
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49
Q

Malabsorption is characterized by defective absorption of (blank x 5)

A
  • fats
  • fat-soluble and water-soluble vitamins
  • proteins
  • carbs
  • electrolytes and minerals
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50
Q

How does malabsorption present?

A
  • chronic diarrhea (increase in stool mass, frequency, fluididy > 200 g/day)
  • Steatorrhea (excess fecal fat and greasy, yellow clay-colored stools)
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51
Q

malabsorptions results from disturbance in at least 1 phase of absorption. What are the phases?

A
  • Intraluminal digestion (breakdown of nutrients)
  • Terminal digestion (hydrolysis of nutrients by brush border in SI)
  • Transepithelial transport
  • Lymphatic transport (absorbed lipids)
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52
Q

What are the clinical features of malabsorption?

A
  • Diarrhea
  • Flatus
  • Abdominal pain
  • Weight loss
  • Signs of vitamin deficiency (anemia, bleeding, peripheral neuropathy, osteopenia)
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53
Q

What are the four ways that diarrhea can be classified?

A
  • secretory
  • osmotic
  • malabsorptive
  • exudative
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54
Q

What kind of diarrhea is this:

isotonic stool and persists during fasting

A

Secretory

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55
Q

What kind of diarrhea is this:

due to excessive osmotic forces exerted by unabsorbed luminal solutes

A

Osmotic

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56
Q

What kind of diarrhea is this:

associated with steatorrhea and is relieved by fasting

A

malabsorptive

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57
Q

What kind of diarrhea is this:

due to infammatory disease and is characterized by purulent, bloody stools that continue during fasting

A

Exudative

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58
Q

Cystic fibrosis can cause malabsorption and is due to mutations of (blank). patients have defective intestinal chloride ion secretion.

A

CFTR

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59
Q

CF interferes with (blank x 3) secretion leading to defective luminal hydration

A

bicarb
sodium
water

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60
Q

In CF you have failure of the (bank) phase of nutrient absorption

A

intraluminal phase

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61
Q

(blank) also known as celiac sprue or gluten sensitive enteropathy

A

Celiac disease

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62
Q

Celiac’s disease is an immune mediated (blank) triggered by the ingestion of gluten

A

enteropathy

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63
Q

Celiacs is associated with other autoimmune diseases and (blank or blank)

A

HLA-DQ2

HLA-DQ8

64
Q

What are the clinical features of celiac disease?

A 
Anemia
Diarrhea
Bloating
Fatigue
Failure to thrive
Weight loss 
Dermatitis herpetiformis
65
Q

How do you diagnose celiac’s disease?

A

serologic tests

  • IgA antibodies to tissue transglutaminase (sensitive)
  • IgA or IgG to deaminated gliadin (sensitive)
  • Antiendomysial antibodies (specific)
66
Q

What is this:
occurs in people living in or visiting the tropics (except Jamaica).
Various infectious organisms are the suspected cause.

What part of the GI tract does it affect?

A

Tropical sprue

small bowel

67
Q

What is this:
X-linked disorder characterized by severe persistent diarrhea and autoimmune disease

Autoantibodies to (blank) and (blank) may be present.

What is the therapy?

A

Autoimmune enteropathy

Enterocytes and goblet cells

immunosuppressive drugs

68
Q

What is this:
Rare autosomal recessive disorder caused by a mutation in the (blank) that catalyzes the transport of triglycerides, cholesterol esters and phospholipids

A

Abetlipoproteinemia

MTP (microsomal triglyceride transfer protein)

69
Q

What is abetalipoproteinemia characterized by?

A

inability to secrete TAG rich proteins since enterocytes can not export lipoproteins and FFAs

70
Q

In abetlipoproteinemia, (blank) cannot be assembled into chylomicrons and TAGs accumulate in the epithelial cells and you get (blank) due to transepithelia transport.

A

monoglycerides

malabsorption

71
Q

What are the cinical features of abetalipoproteinemia?

A

presents in infancy w failure to thrive, diarrhea, steatorrhea

  • complete absence of apolipoprotein B
  • fat-soluble vitamin deficiency
  • acanthocytes on peripheral blood smears
72
Q

(blank) is located on the apical brush border. Defect is biochemical so not histologic changes.

A

Disaccharidase (lactase)

73
Q

What are the 2 types of lactase deficiency and what causes each?

A
  • Congenital: AR disorder with mutation in lactase

- Acquired: down-regulation of lactase gene expression after childhood

74
Q

What is this:
an idiopathic disorder that reuslts from a combination of defects in host interactions with intestinal microorganisms, intestinal epithelial dysfunction and aberrant mucosal immune responses

What are the 2 disorders that maket his up?

A

inflammatory bowel disease

Chron’s disease
Ulcerative colitis

75
Q

The increasing incidence of IBD is due to (blank) and (Blank).
Why?

A

improved food storage
decreased food contamination

-reduced frequency of enteric infections-> reduced immunity-> allowing pathogens that should cause self-limited diseases to trigger overhwleming immune responses and chronic inflammatory disease

76
Q

Epidemiology, genetics and clinical studies support the theory that IBD is due to (blank)

A

aberrant mucosal immune responses

77
Q

What gender is IBD more common in and what ages?
Increased risk with family members?
Genetics?

A

females in teen and early 20s

yes
50% concordance with monozygotic twins

NOD2, ATG16L1, IRGM seen in patients with Chrons

78
Q

In IBD, Transepithelial flux of luminal (blank) components activates innate and adaptive immune responses

A

bacterial

79
Q

In genetically susceptible hosts, TNF and other immune mediators cause (blank) which establishes a self-amplifying cycle in which any stimulus can intiate IBD

A

increased tight junction permeability

80
Q

(blank) is also called regional enteritis. May involve any area of the GI tract and shows transmural inflammation

A

Chron’s disease

81
Q

Ulcerative colitis is a severe ulcerating inflammatory disease that is limited to the (blank) and (blank) and extends from the mucosa to the (blank)

A

colon and rectum

mucosa to the submucosa

82
Q

Where does chrons disease occur?

A

-any area of the GI tract but most common in terminal ileum, ileocecal valve, and cecum

83
Q

What are the earliest lesions of Chrons disease?

A

apthous ulcers

84
Q

(blank) are characteristic of Chrons disease and gives the mucosa a cobblestone appearance

A

Skip lesions (sharply delineated areas of disease)

85
Q

In chrons disease you can get fissures between mucosal folds that may develop and lead to the formation of (blank) or (blank)

A

fistula tracts or perforation

86
Q

In chrons disease what will the intestinal wall look like? What is it due to?

A

thickened and rubbery
-transmural edema, inflammation, submucosal fibrosis, muscularis propria hypertrophy and contribute to strictures formation

87
Q

Chrons disease has creeping fat, what does this mean?

A

mesentaric fat extends around the serosal surface

88
Q

What are the clinical features of chrons disease?

A 
Intermittent attacks of mild diarrhea
Fever
Abdominal pain
Right lower quadrant pain
Bloody diarrhea 
Asymptomatic periods that last weeks to months
Disease reactivation with cigarette smoking (risk factor)
Malabsorption and serum protein loss
Uveits
Extra-intestinal manifestations
89
Q

What do you see via microscopy in Chrons disease?

A
  • abundance of neutrophils
  • crypt abscesses
  • ulceration
  • distortion of mucosal architecture
  • non-caseating granuloma formation
90
Q

In ulcerative colitis, the disease is limited to the (blank) and (blank) but in a continous fashion

A

colon and rectum

91
Q

What are the extraintestinal manifestations of ulcerative colitis?

A
  • migrating polyarthritis
  • sacroilitis
  • ankylosing spondylitis
  • uveitis
  • skin lesions
  • pericholangitis
  • primary sclerosing cholangitis
92
Q

What does the colon look like in ulcerative colitis?

A

red and granular with extensive broad based ulcers

93
Q

What makes the pseudopolyps seen in ulcerative colitis?

A

-isolated islands of regenerating mucosa bulge into the lumen

94
Q

Chronic ulcerative colitis leads to mucosal (blank) and a flat and smooth (blank) surface that lacks normal folds

A

atrophy

mucosal surface

95
Q

In ulcerative colitis, mural thickening is (blank) the serosal surface is normal and (blank) do not occur

A

NOT present

strictures

96
Q

In ulcerative colitis, toxic megacolin is a possible consequence of (blank) damage

A

muscularis propria

97
Q

What are the clinical features of ulcerative colitis?

A

Bloody diarrhea with stringy mucoid material
Lower abdominal pain
Cramps temporarily relieved by defecation
Symptoms may persist for days, weeks or months before they subside
Colectomy is curative
Attacks may initially be precipitated by infectious colitis, psychological stress

98
Q

What is the microscopic appearance of ulcerative colitis?

A
  • Abundance of neutrophils
  • Crypt abscesses
  • Distortion of the mucosal architecture
  • Inflammatory process limited to the mucosa and superficial submucosa
  • Granulomas are not present
99
Q

What is this:
Definitive diagnosis of Crohn disease or ulcerative colitis is not possible in 10% of patients with IBD
These patients do not have small bowel involvement, but grossly do have continuous colonic disease with a histologic picture of fissure or discontinuous disease

A

indeterminate colitis

100
Q

WHat is a long term complication of colitis?

What are the risk factors for this?

A

neoplasia

Disease for 8-10 years
Pancolitis
Greater frequency and severity of active inflammation
Primary sclerosing cholangitis

101
Q 
What is this:
found only in colon
diffuse
doesnt have strictures
thin wall
A

Ulcerative colitis

102
Q 
What is this:
found in the ileum and colon
skip lesions
strictures
thick wall
A

Chrons disease

103
Q 
What is this:
transmural inflammation
some pseudopolyps
deep ulcers
granulomas are present
fistulas are present
LOTS of lymphoid reaction
Lots of fibrosis
Lots of serositis
A

Chrons disease

104
Q

What is this:
perianal fistulas
malabsorption

A

Chrons disease

105
Q

What is this:

can result in toxic megacolon and has malignant potential

A

Ulcerative colitis

106
Q 
What is this:
lots of pseudopolyps
superficial ulcers
inflammation limited to mucosa
limited fibrosis and serositis
A

Ulcerative colitis

107
Q 
What is this:
muscle hypertrophy
cobblestone appearance
fissures
fat wrapping
A

Crohn’s Disease

108
Q

What is this:

idiopathic disease that presents with chronic, nonbloody, watery diarrhea without weight loss

A

Microscopic colitis

109
Q

In microscopic colitis what will the radiographic and endoscopic studies show?

A

They will be normal

110
Q

What are the 2 forms of microscopic colitis?

A
  • Collagenous colitis

- Lymphocytic colitis

111
Q

What is this:

dense subepithelial collagenous layer, increased intraepithelial lymphocytes and mixed LP inflammation

A

Collagenous colitis

112
Q

What is this:
increased intraepithelial lymphocytes and mixed LP inflammation
No subepithelial collagen

A

Lymphocytic colitis

113
Q

What kind of colitis is this:
Chronic colitis can occur at the site of an (blank).
microscopically numerous mucosal lymphoid follicles develop

A

Diversion colitis

Ostomy

114
Q

What is this:

nodules or masses that project above the level of the surrounding mucosa

A

Polyps

115
Q

Where do polyps most commonly occur?

A

in the colon

but may occur in the esophagus, stomach or small intestine

116
Q

What are the 2 types of polyps?

A
  • sessile (small elevations of mucosa)

- pedunculated (have stalks)

117
Q

Are polyps neoplastic?

A

can be neoplastic or non-neoplastic

118
Q

(blank) polyps are part of the solitary rectal ulcer syndrome and forms due to repeated cycles of (blank) and (blank)

A

inflammatory

injury and healing

119
Q

(blank) are tumor like growths composed of mature tissues that are normally present at the site in which they develop

Why do these occur?

A

hamartomas

sporadically or due to genetic or acquired syndromes

120
Q

What are all the hamartomas?

A

Juvenile polyps
Peutz-Jeghers syndrome
Cowden syndrome
Cronkhite-Canada syndrome

121
Q

What are these;
focal malformation of mucosal epithelium and lamina propria that occur most often in the rectum (stomach or small intestine may occur)

What causes this?

A

Juvenile polyp

sporadic or syndromic but are histologically indistinguishable

122
Q

Juvenile polyps occur typically in whom?

A

children under 5 but can occur in adults who present with rectal bleeding.

123
Q

Syndromic juvenile polyposis may present with (blank to blank) polyps

A

3 to 100

124
Q

Peutz-Jeghers syndrome is a rare (bank) syndrome characterized by multiple GI (blank) and mucocutaneous (Blank)

A

AD
hamartomatous polyps
hyperpigmentation

125
Q

T or F

Peutz-Jeghers syndome has an increased risk of carcinoma, but the harmatoms are not preneoplastic.

A

T

126
Q

Where can you get carcinomas from peutz jeghers syndrome?

A 
Colon
Pancreas
Breast
Lung
Ovary
Uterus
Testicle
127
Q

Cowden syndrome is a (AR/AD) hamartomatous polyp syndrome associated with the loss of function of (blank)

A

AD

PTEN

128
Q

(blank) is a well characterized tumor suppressor gene that is associated with a loss of function mutation

A

PTEN

129
Q

Cowden syndrome is characterized by (blank), (blank) and (blank)

A

macrocephaly
intestinal hamartomatous polyps
benign skin tumors

130
Q

People with Cowden syndrome have increased risk of (blank), (blank) and Blank) cancer. Is there increased incidence of Gi carcinoma?

A

Breast carcinoma
thyroid follicular carcinoma
endometrial carcinoma
No

131
Q

What is this:

nonhereditary and develops in individuals over 50 years old.

A

Cronkhite-Canada syndrome

132
Q

What are the features of cronkhite canada syndrome?

Polyps are histologically indistinguishable from juvenile polyps

A

-hamartomatous polyps of the stomach, small intestine and colorectum

133
Q

What are hyperplastic polyps due to?

Is there malignant potential?

A

decreased epithelial cell turnover and delayed shedding of surface epithelial cells

-NO!

134
Q

any neoplastic mass may produce a polyp including (Blank X 4)

A
  • neuroendocrine tumors
  • stromal tumors
  • lymphomas
  • metastasis
135
Q

(blank) are benign polyps that are precursors to colorectal adenocarcinoma. How would you describe adenomas? What should you do if you have a family history of this? The rest of the population should have surveillance by (blank)

A

adenomas

  • intraepithelial neoplasms w/ epithelial dysplasia
  • surveillance is required
  • 50
136
Q

Familial adenomatous polyposis is a (AR/AD) disorder caused by mutations of the (blank) gene

A

AD

APC

137
Q

Patients with familial adenomatous polyposis develop numerous (blank) as teenagers. At least (blank) polyps are required for diagnosis. How do you treat this?

A

colorectal adenomas
100
prophylactic colectomy and carcinoma will develop in 100% of untreated patients

138
Q

What are the extra-intestinal manifestations of familial adenomatous polyposis?

A

congenital hypertrophy of retinal pigment epithelium

139
Q

(bank) is an autosomal dominant form of polyposis characterized by the presence of multiple polyps in the colon together with tumors outside the colon. Where are the tumors located outside the colon?

A

Gardners syndrome

Intestinal adenomas
Osteomas of the mandible, skull and long bones
Epidermal cysts
Desmoid tumors
Thyroid tumors
Dental abnormalities
140
Q

What is Turcot syndrome, what are the manifestations and what is the mutation?

A

A familial polyp syndrome with APC mutation and intestinal adenomas and CNS tumors

141
Q

What is this:
hereditary non-polyposis colorectal cancer

What is it caused by?

A

Lynch syndrome

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

142
Q

What are the 2 main mismatch repair genes affected in hereditary non-polyposis colorectal cancer?
How do pnts get it?

A

MSH2 and MLH1

patients inherit one mutated gene, the other is lost through mutation

143
Q

Hereditary nonpolyposis colorectal cancer is associated with which carcinomas?

A 
Associated with  carcinomas:
Endometrium 
Colorectum
Endometrium
Stomach
Ovary
Ureters
Brain
Small intestine
Hepatobiliary tract
Skin
144
Q

(blank) is the most common malignancy of the colon while the small intestine is an uncommon site for benign or malignant neoplasms

What are the risk factors?

What are the clinical features?

A

Adenocarcinoma

low intake of fiber
high intake of carbs and fat

fatigue, weakness, iron deficiency anemia

145
Q

What are the 2 pathways associated with adenocarcinomas?

A

APC/WNT -classic adenoma-carcinoma sequence (80%)
Microsatellite instability pathway-defects in DNA mismatch repair
(pathways involve stepwise accumulation of multiple mutations)

146
Q

What is the APC/WNT pathway?

A

APC mutation-> inactivation of normal alleles-> proto-oncogene mutations (KRAS)-> loss of additional suppressor gene -> additional changes

147
Q

What is the microsatellite instability?

A

MLH1 and MSH2 mutations of mismatch repair gene-> microsatellite instability-> accumulated mutations in apoptosis, growth and differentiation

148
Q

What is this:
acquired pseudodiverticular outpouchings of colonic mucosa and submucosa.

When multiple, the clinical syndrome is referred as (blank)

What does it result from?

A

Diverticular disease

Diverticulosis

taenia coli of muscularis propria and elevated intraluminal pressure in the sigmoid colon

149
Q

What is this:
characterized by malformed submucosal and mucosal blood vessels

Where does it most often occur?

Accounts for more than (blank)% of major episodes of lower intestinal bleeding

A

angiodysplasia

cecum and right colon

20%

150
Q

What is this:
Characterized by chronic, relapsing abdominal pain, bloating and change in bowel habits
Gross and microscopic pathology is normal

A

Irritable bowel syndrome

151
Q

IBS occurs more in (females/males). It is a (chronic/acute) pain disorder.

A

Females

chronic

152
Q

What is the diagnostic criteria for IBS?

A
  • ab pain/discomfort for at least 3 days over 3 months
  • improvement with defecation
  • change in stool frequency or form
153
Q

What are the serious long term sequelae of IBS?

What is prognosis determined by?

A

there isnt one.

duration of symptoms

154
Q

What is the:
a normal true diverticulum of the cecum

What is it prone to?

What are the clinical features of appendicitis?

A 
appendix
acute and chronic infection
Periumbilical pain/ RLQ pain
Nausea
Vomiting
Fever
Elevated white count
McBurney’s sign
155
Q

What are the most common appendiceal tumors?

A

neuroendocrine tumors

156
Q

What are the mucus producing lesion of the appendix?

A

Mucocele
Mucinous cystadenoma
Pseudomyxoma peritonei

Block 10 week 5 (3 decks)

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