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Large intestines I Flashcards

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1
Q

What is the difference between diverticulosis and diverticulitis?

A

Diverticulosis is an outpouching. Diverticulitis is inflammation of that outpouching

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2
Q

What is the pathogenesis of diverticula?

A

Focal weakness in colonic wall, coupled with increased luminal pressure

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3
Q

What is the usual presentation of someone with diverticula?

A

Asymptomatic

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4
Q

What are the acquired form of diverticula?

A

Composed of mucosa, submucosa, with absent muscularis propria

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5
Q

What is the most common site of diverticula?

A

Sigmoid colon

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6
Q

Near what structures do diverticula usually form?

A

Mesenteric vessels d/t weakness in the wall of the intestines

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7
Q

What happens to the peristaltic contractions in with diverticula?

A

Overexaggerated

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8
Q

What are the three common causes of BRBPR?

A

Angiodysplasia
Diverticulitis
Hemorrhoids

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9
Q

What is the radiological findings of diverticula?

A

Sawtooth like appearance

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10
Q

What can happen if feces is stuck in one of the diverticula?

A

Fecalith can cause inflammation

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11
Q

What are the complications of diverticular disease?

A

Gross perforation
Abscesses
Fistulas
Peritonitis (if rupture)

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12
Q

Where do intestinal obstructions usually occur?

A

Small bowel

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13
Q

What are the causes of intestinal obstruction? (4)

A

Hernia
Adhesions
Intussusception
Volvulus

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14
Q

What are the three pseudo-obstruction causes?

A

Paralytic ileus
Vascular (bowel infarction)
Myopathies and neuropathies

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15
Q

What is the problem with hernias?

A

can becomes strangulated or incarcerated

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16
Q

True or false: volvulus is a medical emergency

A

True

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17
Q

Direct inguinal hernias occur where?

A

Hesselbach’s triangle

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18
Q

What are the border’s of hesselbach’s triangle?

A

Inguinal ligament
Inferior epigastric a
Lateral margin of the rectus sheath

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19
Q

What are indirect inguinal hernias?

A

Those that pass through the inguinal canal

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20
Q

What is the treatment for hernias?

A

Surgery with mesh

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21
Q

What is the cause of umbilical hernias?

A

Weakness of the rectus abdominus

Prego

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22
Q

What is diastasis recti?

A

Weakness of the rectus abdominus–usually presents in infants, and resolves on its own

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23
Q

What are adhesions?

A

Fibrous bridges between bowel segments or abdominal wall

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24
Q

What can cause adhesions?

A

Surgery

Infection/inflammation

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25
What is the problems with adhesions?
Viscera may slide between the fibrous areas, it can become incarcerated an infarct
26
Where in infants does intussusception occur?
Small bowel
27
What causes the death of the intestines with intussusception?
Infarction secondary to vessel blockage
28
What does intussusception signify in adults?
Intraluminal mass or tumors as potin of traction
29
What is the cause of intestinal death with a volvulus?
Cut off blood supply
30
Where do volvuli usually occur?
SB in infants | SB and LB in adults
31
Why is it that the left side is more susceptible to obstruction?
Stool is harder and has lower water content
32
How does malabsorption usually present?
Diarrhea and steatorrhea
33
What is the cause of steatorrhea?
malabsorption of fat
34
What is abetalipoproteinemia? Ssx?
Inability to make apoB100 (liver) and B48 (small intestinal), thus leading to steatorrhea
35
What are the part of terminal digestion?
Hydrolysis of carbs and peptides by enzymes in the brush border of SB mucosa
36
Where does intraluminal digestion begin?
Mouth with saliva
37
What are the hematopoietic symptoms of malabsorption?
Macrocytic anemia (B12 and folate) Bleeding (Vit K) Microcytic anemia (Fe)
38
What are musculoskeletal effects of malabsorption?
Osteopenia, tetany
39
Which vitamin deficiency presents with neurological symptoms: b12 or folate?
B12
40
What are the three most common malabsorptive disorder in the US?
Celiac Chronic pancreatitis IBS
41
What is the pathogenesis of celiac sprue?
T cell reaction to gliadin
42
What are the genes implicated in celiac sprue?
DQ2, HLA B8
43
What are the histology of celiac sprue?
Proximal villous atrophy
44
What is the risk of celiac sprue?
T cell lymphomas | Carcinomas
45
Giant cells = ?
Chronic inflammation
46
What is tropical sprue? How do you treat it?
Tropical disease caused by bacteria overgrowth Broad spectrum abx
47
What is whipple disease?
Infection with tropheryma whippelii (gram + actinobacteria) causes CNS and joint symptoms, malnutrition
48
Where is tropheryma whippelii found?
within macrophages throughout the body
49
The majority of tumors in the small and large intestines are of what origin?
Epithelial
50
What is the most common type of cancer of the GI tract?
Adenocarcinoma and carcinoids
51
What is the most common site for GI tumors?
Colon
52
What are the most frequent benign tumors of the GI tract?
Adenoma | Mesenchymal tumors
53
What is the most common cause of SB tumors?
FAP or Gardener's syndrome
54
What is the most common site of adenomas in the GI tract?
Ampulla of vater
55
What is the characteristic growth pattern of small bowel carcinomas?
Napkin ring encircling pattern
56
What are polyps? What causes them?
Small elevations of he mucosa; mass protruding into gut lumen abnormal mucosal transformation
57
Are most polyps benign or malignant?
Benign
58
What is the most common neoplastic polyp?
Adenomatous polyp
59
What are the three non-neoplastic polyps?
Hyperplastic polyps Hamartomatous polyps Inflammatory polyps
60
What are hyperplastic polyps?
Normal tissue swollen up
61
Where do hyperplastic polyps usually occur?
Rectosigmoid areas
62
What is the cause of hyperplastic polyps?
Decreased epithelial cell turnover and delayed shedding
63
What is the morphology of hyperplastic polyps?
Well formed glands and crypts, lined by non-neoplastic mature goblet and absorptive cells
64
True or false: most hyperplastic polys have no neoplastic potential
True
65
What are hamartomatous polyps?
focal hamartomatous malformations of mucosal epithelium and lamina propria
66
Juvenile polyps are usually of what type?
Hamartomatous polyps
67
in whom does retention polyps usually form?
Adults
68
In what polyps in juvenile polyposis syndrome is the chance of developing into CA increased?
NOT in the hamartomatous polyps
69
What is Peutz-Jeghers syndrome?
an autosomal dominant genetic disease characterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa
70
What is the genetic cause of Peutz-Jeghers syndrome?
STK11 mutation
71
What are the polyps of Peutz-Jeghers syndrome made of?
Smooth muscle, lined by intestinal epithelium
72
What are patient with Peutz-Jeghers syndrome more susceptible to? (2)
Intussusception and carcinoma in many places in the body
73
What are the oral findings of Peutz-Jeghers syndrome?
Hyperpigmented macules
74
True or false: adenomas are precursor to colrectal CA?
True
75
When do adenomas of the GI tract become adenocarcinomas?
When they penetrate the Basement membrane
76
What are the four types of neoplastic polyps?
Tubular adenoma Tubulovillous adenoma Villous adenoma Serrate adenoma
77
What is the biggest prognostic factor for the malignancy risk with adenomas? What are the other, lesser two?
Size Histological architecture Severity of dysplasia
78
What are tubular adenomas?
stalk with piled up cells on top (strawberry on a stick)
79
What are villous adenomas?
Flat carcinoma with finger like projections coming up
80
What are serrated adenomas?
Saw tooth pattern that lacks dysplastic features

Gastrointestinal (42 decks)

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