Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MS2 GI > 10/8- Small Intestine Pathology > Flashcards

10/8- Small Intestine Pathology Flashcards

1
Q

What is the widest part of the small intestine?

A

Duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What part of the small intestine does the jejunum comprise?

  • Location
  • Describe relative dimensions
  • Histology
A

Upper 2/5, around umbilicus and L iliac fossa

  • Wider, thicker, more vascular
  • Villi are larger; no Peryer’s patches in upper part
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What part of the small intestine does the ileum comprise?

  • Location
  • Describe relative dimensions
  • Histology
A

Lower 3/5, umbilical, hypogastric, R iliac and pelvic region

  • Narrow, smaller, thinner layers; less vascular
  • Numerous and larger Peyer’s patches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the normal villous to crypt length ratio?

A

3-5: 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is seen here?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Compare jejunum and ileum (picture)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Jejunum or ileum?

A

Jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Jejunum or ileum?

A

Ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T/F: Obstruction may occur at any level of the GIT?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where is the most common site of obstruction in the small intestine?

  • Other sites/causes?
A

Mostly small intestine (narrow lumen)

  • 80% of mechanical obstructions = hernias, intestinal adhesions, intussusception and volvulus
  • 10-15% of small bowel obstructions = tumors and infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some clinical manifestations of intestinal obstruction?

A
  • Abdominal pain and distention
  • Vomiting
  • Constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment of intestinal obstruction?

A

Surgery in cases of mechanical obstruction or severe infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a hernia?

A

Weakness/defect in the wall of the peritoneal cavity

  • Hernia sac = protrusion of serosa-lined pouch of peritoneum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Are acquired hernias more commonly anterior or posterior? Where?

A

Acquired are more anterior

  • Inguinal and femoral canals or umbilicus or surgical scars
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens with pressure at the neck of a hernia?

A

Impair venous drainage

  • > stasis and edema
  • > increase in size
  • > permanent entrapment (incarceration)
  • > arterial and venous compromise (strangulation)
  • > infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is adhesion/what causes it?

  • Characteristics
  • Complications?
A

Surgical procedures, infection, or peritoneal inflammation may cause adhesions between bowel segments, abdominal wall and operative sites

  • Rarely congenital

Fibrous bridges, closed loops; other viscera may slide -> become entrapped: internal herniation

Complications:

  • Obstruction
  • Strangulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is seen here?

A

Small bowel infraction secondary to intraperitoneal fibrous band

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is volvulus?

  • What does it cause
  • Clinical presentation
  • Common locations
A

Complete twisting of a loop of bowel about its mesenteric base of attachment

  • Luminal and vascular compromise

Clinical presentation: features of obstruction and infarction

Most often in:

  • Sigmoid colon, then
  • Cecum
  • Small bowel
  • Stomach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is intussusception?

  • Prognosis
A

A segment of the intestine, constricted by a wave of peristalsis, telescopes into the immediately distal segment

  • Once trapped, the invaginated segment is propelled by peristalsis and pulls the mesentery along
  • Untreated intussusception… intestinal obstruction, compression of mesenteric vessels and infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is seen here?

A

Jejunum with big mass in distal portion; pulled rest of jejunum along

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes intussusception in kids? Adults?

A

Infants and children:

  • Usually no underlying anatomic defect
  • Association with rotavirus infection

Older children and adults:

  • Intraluminal mass or tumor; leading point of traction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How to treat intussusception in kids? Adults?

A

Infants and young children: barium enema

Older patient: surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe blood supply to the small/large intestine?

A

Arterial supply:

  • Celiac a
  • Superior and inferior mesenteric arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the most common cause of intestinal ischemia?

A

Arterial insufficiency if large and small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute compromise of any major vessel causes what?

A

Infarction of several meters of intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does ischemic bowel disease present?

A

Older individuals with coexisting cardiac or vascular disease

Acute mesenteric ischemia (95%):

  • Abdominal pain, N/V and hematochezia
  • Little or no pain in elderly until advanced stages
  • Shock and vascular collapse within hours as a result of blood loss

Chronic mesenteric ischemia (< 5%):

  • Postprandial abdominal pain; 30 min after a meal, peaks in one hour and resolves in 3 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is found on the physical exam of someone with ischemic bowel disease?

  • Prognosis
A

Bowel sounds diminish or disappear, and muscular spasm creates rigid abdomen (acute abdomen)

  • Delayed or missed diagnosis: disastrous consequences
  • Mucosal barrier breaks down, bacteria enter the circulation and sepsis; mortality >50%
28
Q

What is seen here?

A

Ischemic bowel disease (or just infarction?)

29
Q

What is the etiology of acute arterial obstruction: non-occlusive?

A

Non-occlusive: failure to deliver sufficient oxygen due to inadequate blood flow without an obstruction

  • Severe atherosclerosis
  • Hypotension, shock and dehydration
  • Vasoconstrictor drugs: digitalis, vasopression and propranolol
30
Q

What is the etiology of acute arterial obstruction: occlusive?

A
  • Intraluminal
  • Thromboemboli: the most common cause
  • Atherosclerosis, dissecting aneurysms..
  • Intramural: drugs causing vasospasm: cocaine, snake venom
  • Extramural: compresion by tumors, volvulus, torsion..
31
Q

What is the most common cause of acute arterial obstruction?

A

Thromboemboli

32
Q

Describe the pathogenesis of acute arterial obstruction- 2 big stages?

A
  1. Initial hypoxic injury
  2. Reperfusion injury
33
Q

What happens in the initial hypoxic injury?

A
  • At the onset of vascular compromise
  • Some damage (epithelial cells relatively resistant to transient hypoxia)
34
Q

What happens in the reperfusion injury?

A
  • Restoration of the blood supply
  • Greatest damage …trigger multiorgan failure
  • Free radical production, neutrophil infiltration, and release of inflammatory mediators (complement proteins and TNF )
35
Q

Extent of damage in obstruction/ischemia depends on what?

A
  • Severity of vascular compromise
  • Time frame
  • Size of obstructed vessel and its degree of collateral circulation
36
Q

What is seen on microscopic examination of ischemia?

How does occlusive differ from non-occlusive?

A

Similar changes, except that in occlusive disease ischemia is segmentally distributed and affected regions uniformly affected whereas in non-occlusive patchy, variable in severity and often widespread

37
Q

What layer is most susceptible to hypoxia?

What layer most easily regenerates?

A

Mucosa on both counts!

  • Mucosa is the most susceptible layer to hypoxia, also has the greatest regenerative capacity
38
Q

What is seen here?

A

Ischemia

  • Attenuated villi
  • Ulcerated
39
Q

What is Celiac disease?

  • Mechanism
  • Epidemiology
A
  • Gluten sensitive enteropathy
  • Autoimmune-mediated disorder that results in damage to small intestinal mucosa and malabsorption of nutrients

Most common in countries with European descent population (1% prevalence):

  • Europe
  • America
  • Australia
40
Q

What does celiac disease look like in adults?

A

Mild disease : fatigue due to anemia

  • Silent disease: positive serology and villous atrophy without symptoms
  • Latent disease: positive serology but no villous atrophy
41
Q

More on celiac disease:

  • Symptoms
  • Other associations
  • Gender prevalence
A

Symptoms:

  • Abdominal discomfort
  • Diarrhea and steatorrhea

Also: FTT, infertility, neurologic disorders, dermatitis herpetiform

Female = Male

42
Q

What is the pathogenesis of celiac disease?

  • What is gluten biochemically?
  • What normally digests it
A
  • Gluten: the major storage protein of wheat and similar grains
  • Gliadin: alcohol-soluble fraction of gluten; which has most of the disease-producing components
  • Gluten is digested into AAs and peptides, including a 33-AA α-gliadin peptide, resistant to degradation by gastric, pancreatic, and small intestinal proteases
43
Q

Describe what’s going on here?

A

(Missed the beginning- Ab mediation?)

  • Gliadin enters, passes epithelial cells to reach lamina propria
  • Gliadin is deaminated by tissue transglutaminase (tTG)
  • It effects antigen presenting cellswtih DQ2/8 to activate cytotoxic T cells
  • Stimulated to kill more lymphocytes
  • T cells also stimulate B cells to produce Abs against gliadin
44
Q

What are the genetics behind celiac disease?

A
  • Class II HLA-DQ2 or HLA-DQ8 allele: less than half of the genetic component
  • Polymorphisms of immune-regulatory genes, such as those encoding IL-2, IL-21, CCR3, and SH2B3, and genes that determine epithelial polarity
45
Q

What other diseases/conditions celiac disease associated with?

A
  • Type 1 diabetes
  • Thyroiditis
  • Sjögren syndrome
46
Q

What serology should be done to identify Celiac disease?

A

Most sensitive tests:

  • IgA Abs to tissue transglutaminase
  • IgA or IgG Abs to deamidated gliadin

Anti-endomysial Abs are highly specific but less sensitive

If IgA test is negative, rule out IgA deficiency:

  • IgA deficiency: IgG antibodies to tissue transglutaminase and deamidated gliadin

Absence of HLA-DQ2 or HLA-DQ8

  • High negative predictive value
47
Q

What is seen grossly in celiac disease?

A
  • Reduced or absent duodenal folds
  • Totally flat mucosa with dramatic clinical and morphologic response to removal of gluten
48
Q

What is seen on the microscopic exam in celiac disease?

A

Atrophic or absent villi

  • Villous/crypt ratio: 1 or less (normal: 2.5+)
  • Increased in T lymphocytes
49
Q

What is the most common celiac disease associated cancer? Others?

A

Enteropathy-associated T-cell lymphoma

  • Also small intestinal adenocarcinoma
50
Q

What are symptoms of small intestinal adenocarcinoma?

A
  • Abdominal pain
  • Diarrhea
  • Weight loss

Despite a strict gluten free diet (failure to adhere to gluten-free diet is the most common cause of recurrent symptoms)

51
Q

What is seen here?

A

Giardia in lumen

52
Q

What is seen here?

A

Giardia

  • Pear shaped, 2 symmetric nuclei
53
Q

What are Giardia?

  • Characteristics
  • Disease
  • Location
  • Resistance
A

Giardia characteristics:

  • Pear shaped trophozoites
  • 2 symmetric nuclei each with 1 necleoli

Cause Giardiasis

  • Most common diarrheal disease transmitted by contaminated water

Located in duodenum

  • Only human protozoa that resides here

Cysts are resistant to chlorine

54
Q

How is Giardiasis transmitted?

A
  • Transmitted through streams and domestic water supplies
  • Contaminated with cysts from human or wildlife feces, fecal-oral in day-care and oral-anal sex
55
Q

Symptoms of Giardiasis?

A
  • Severe diarrhea
  • Cramping and malabsorption
56
Q

Diagnosis of Giardiasis?

A
  • Trophozoites or cysts in stool
  • Surgical biopsies
  • Serology (ELISA) may be helpful
57
Q

What is seen here?

A

Giardia???

58
Q

What is strongyloides stercoralis?

  • Epidemiology/demographics
  • Associated with what
A

Threadworm Worldwide distribution:

  • Southern US
  • Mental institutions
  • Adults, hospitalized, chronic illness and immunocompromised

Associated with

- Steroids

- HTLV1

59
Q

What are symptoms of Strongyoides stercoralis?

A
  • Diarrhea
  • Abdominal pain and tenderness
  • N/V
  • Weight loss
  • GI bleed
60
Q

How does the Strongyloides stercoralis worm cause disease?

  • How is infection diagnosed?
A

Worm penetrates skin.. veins.. lung.. small intestine

  • Aauto-infection; can be fatal especially in immunossuppressed

Diagnosis

  • Larvae or egg in stool
  • Adult worm in intestinal biopsy
  • Serology
61
Q

What is seen here?

A

Strongyloides stercoralis

62
Q

What is seen here?

A

Strongyloides stercoralis (?)

  • Many lymphocytes?
63
Q

What is Whipple’s disease?

  • Other organ systems
  • Histology
A

Intestinal lipodystrophy

Can involve:

  • LN
  • Heart, lung
  • Liver, spleen
  • Adrenal glands and nervous system

Histology:

  • Large macrophages crowding lamina propria
  • Distorting the villi and alternating with empty spaces
  • Histiocytes have diastase resistant, PAS+ material
64
Q

What is the clinical presentation of Whipple’s disease?

A

Triad:

  1. Diarrhea
  2. Weight loss
  3. Malabsorption
65
Q

What causes Whipple’s disease?

Differential diagnosis?

A

Tropheryma whippelli

  • Malabsorption due to impaired lymphatic transport

Treatment: response to antibiotic

Main differential diagnosis

  • MAI
  • Ingestion of mineral oil can cause similar changes in intra-abdominal lymph nodes
66
Q

What is seen here?

A

Whipple’s disease

MS2 GI (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions