Brainscape's Knowledge GenomeTM

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


See full index

MHD2 > Block 7 (GI) - L4 to L6 > Flashcards

Block 7 (GI) - L4 to L6 Flashcards

1
Q

What are the layers of the intestine?

A
  1. Mucosa (villi, crypts, lamina propria, muscularis mucosa)
  2. Submucosa + Meissner’s plexus
  3. Muscularis propria (inner circular layer, Auberach’s plexus, outer longitudinal layer)
  4. Serosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a defect involving all layers of the abdominal wall that leads to evisceration of bowel loops and other structures and is not covered with a sac?

A

Gastroschisis

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

What is incomplete closure of the abdominal musculature and visceral herniation into a membranous sac?

A

Omphalocele

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

Meckel diverticulum develops due to failed involution of the ___, leading to a blind outpouching.

A

Vitelline duct

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

Is Meckel diverticulum true or false?

A

True

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

What two types of ectopic tissue can be present in Meckel diverticulum?

A

Gastric and pancreatic - gastric tissue can secrete acid, leading to peptic ulceration

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

Discuss the disease of 2’s of Meckel diverticulum.

A 
2% of population
2:1 (M:F)
2" in length
2 feet from ileocecal valve
2 years of age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the difference between a true diverticulum (Meckels’s) and a false diverticulum (diverticulosis)?

A

True: involves all three layers of the intestinal wall (mucosa, submucosa, muscularis propria)
False: only involves the mucosa/submucosa

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

What is Hirschprung Disease?

A

Premature arrest or death of neural crest cells migrating from the cecum to the rectum

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

What mutation is commonly seen in Hirschprung disease?

A

RET proto-oncogene mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the symptoms of Hirschprung Disease?

A

Failure to pass meconium, obstruction/constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which part of the colon is always involved in Hirschprung idsease?

A

Rectum

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

What are potential complications of Hirschprung disease?

A

Fluid/electrolyte disturbances, eneterocolitis, perforation, peritonitis, congenital megacolon (proximal dilation that can rupture)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are associations with Hirschsprung disease?

A

Down Syndrome

Serious neurologic abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the histopathology of Hirschsprung disease.

A

Complete lack of ganglion cells in both Meissner’s and Auberach’s plexuses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is necrotizing enterocolitis?

A

Acute, necrotizing inflammation of small and/or large intestines (cause uncertain)

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

How does necrotizing enterocolitis present?

A

Premature infants

Bloody stools, circulatory collampse, abdominal distension

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

Which parts of the intestine does necrotizing enterocolitis typically involve?

A

Terminal ileum, cecum, right colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is celiac disease?

A

Immune-medaited enteropathy triggered by the ingestion of gluten-containing foods in genetically predisposed individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Gluten is a major storage protein of wheat and similar grains - which component is largely responsible for celiac disease?

A

Gliadin

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

What is the clinical presentation of celiac disease?

A

Most common in 30-60 year olds

Diarrhea, bloating, fatigue, anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the HLA types associated with celiac disease?

A

HLA-DQ2

HLA-DQ8

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

What are other important associations with celiac disease?

A

Dermatitis Herpetiformis (skin blistering disease) and other autoimmune diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the pathogenesis of celiac disease.

A

Gliadin is taken up into cells and processed by ttG, forming deamidated gliadin. APCs pick up gliadin, rpesent to T-cells, and ultimately form anti-gliadin Ab.

Also, IL-15 is expressed by epithelial cells, CD8 cells become cytotoxic and kill enterocytes

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

Describe the histopathology seen in celiac disease.

A

Increased intraepithelial lympohcytes and blunting of villi

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

What Ab can be tested for in celiac disease?

A
  1. IgA Ab to tissue transglutamine (most sensitive)
  2. IgA anti-endomysial (specific but less sensitive) Ab
  3. Anti-gliadin Ab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does the absence of HLA-DQ2 and DQ8 indicate?

A

Good negative predictive value, but not helpful in confirming a diagnosis when they are present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are risks associated with celiac disease?

A

Enteropathy associated T-cell lymphoma and small intestinal adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the gross appearance of the intestine in celiac disease.

A

Atrophic mucosa and flattened folds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is tropical sprue?

A

Disease similar to celiac sprue seen in the tropics, leading to chronic bouts of diarrhea and nutritional deficiencies as a ressult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the symptoms of pseudomembranous colitis?

A

Abdominal pain, fever, watery diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What causes pseudomembranous colitis?

A

Disruption fo normal colonic microbiota by antibiotics leads to C. diff. overgrowth. C. diff. releases Toxins A and B, which ribosylate small GTPases, leading to cytoskeleton disruption, tight junction barrier loss, cytokine release, and apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How is pseudomembranous colitis tested for?

A

Detection of C. diff. toxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the pathology of pseudomembranous colitis.

A

Colonic mucosa covered by a yellow/green false membrane composed of mucus and neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is Whipple disease?

A

Rare multisystem chronic disease caused by a Gram positive rod shaped actinomycete (Tropheryma whipplei)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the triad of symptoms seen in Whipple disease?

A

Diarrhea, weight loss, arthralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some extra-intestinal symptoms of Whipple disease?

A

Arthritis, lymphadenopathy, neurologic, cardiac, pulmonary disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Discuss the pathogenesis of Whipple disease.

A

Macrophages (filled with organisms) accumulate in the lamina propria of the SI and lymph nodes, leading to lymphatic obstruction. The impaired lymphatic transport results in malabsorptive diarrhea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the histopathology of Whipple Disease.

A

Distended foamy macrophages filled with organisms (PAS+, diastase resistant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the two types of inflammatory bowel disease?

A

Crohn’s disease and Ulcerative colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Compare the location of Crohn’s and ulcerative colitis.

A

CD: upper GI tract involvement - segmental with skip lesions; cobblestone appearance

UC: colon only - diffuse, continuous disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Compare the symptoms of Crohn’s and ulcerative colitis.

A

CD: +/- bloody diarrhea
UC: bloody diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Compare the rectal involvement of Crohn’s and ulcerative colitis.

A

CD: variable
UC: rectum involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Compare the microscopic findings of Crohn’s and ulcerative colitis.

A

Both: architectural distortion and crypt abscesses/cryptitis

CD: transmural lymphoid aggregates and granulomas
UC: NO granulomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Compare the complications of Crohn’s and ulcerative colitis.

A

CD: fissures, sinuses, fistulous tracts
UC: NO fissures, toxic megacolon

Both: colon adenocarcinoma (more common in UC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Compare the extra-intestinal manifestions of Crohn’s and ulcerative colitis.

A

CD: pyoderma gangrenosum, erythema nodosum

UC: primary sclerosing cholangitis (p-ANCA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the difference between cryptitis and a crypt abscess?

A

Cryptitis - neutrophils within the epithelium of a colonic gland

Crypt abscess - colonic gland filled with neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is creeping fat, seen in Crohn’s?

A

Normally, fat is located along the mesenteric area of the bowel; creeping fat refers to fat that is moving along the serosal surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Which disease has pseudopolyps?

A

Ulcerative colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the frequency of the basal electric rhythm of the duodenum and ileum respectively?

A

Duodenum: 12 waves/minute

Ileum: 8-9 waves/minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where is iron absorbed in the small bowel?

A

Duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Where is vitamin B12 absorbed in the small bowel?

A

Ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is diverticular disease?

A

Acquired herniation of mucosa and submucosa leading to the formation of a false diverticula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is diverticulitis?

A

When a diverticula becomes inflamed, usually due to obstruction with stool/mucus, leading to bacterial overgrowth/infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Diverticular disease is associated with a ___ diet.

A

Low-fiber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the symptoms of diverticular disease?

A

Left lower quadrant pain, fever (diverticulitis), bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where is diverticular disease most common?

A

Left colon, particularly the sigmoid colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are complications of diverticular disease?

A

Perforation, peritonitis, fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How is diverticular disease treated?

A

Antibiotics and surgical intervention if complciations arise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is a hernia?

A

Weakness or defect of abdominal wall that allows for a serosal-lined out-pouching of peritoneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is incarceration?

A

When a loop of intestines becomes trapped within a hernia sac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is strangulation?

A

When the bowel is compressed and twisted at the mouth of the hernia, compromising blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are adhesions?

A

Fibrous bridges or band-like portions of scar tissue between loops of intestines caused by prior surgery, infection, or other inflammation; may result in obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is intussusception?

A

In-folding or telescoping of one segment of bowel into the adjacent distal segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is a volvulus?

A

Obstruction due to rotation or twisting of a loop of bowel around its mesenteric base of attachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the most common site of volvulus?

A

Sigmoid colon, followed by the cecum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is ischemic bowel disease?

A

Bowel hemorrhage and necrosis secondary to hypoxic injury and/or reperfusion injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What types of patients get ischemic bowel disease?

A

Patients >70 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the symptoms of ischemic bowel disease?

A

Sudden severe abdominal pain and bloody diarrhea (can lead to shock, sepsis, and death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are some causes of acute arterial occlusions that can cause ischemic bowel disease?

A
  1. Atherosclerosis
  2. Aortic aneurysm
  3. Hypercoagulable states
  4. Oral contraceptive use
  5. Embolization of cardiac vegetations or aortic atheromas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are some causes of intestinal hypoperfusion that can cause ischemic bowel disease?

A

Cardiac failure, shock, dehydration, and vasoconstrictors

72
Q

What are some rare causes of ischemic bowel disease?

A

Systemic vasculitis and mesenteric venous thrombosis

73
Q

What part of the colon is prone to infarction?

A

Splenic flexure

74
Q

What are hemorrhoids?

A

Dilated veins of the hemorrhoidal plexus

75
Q

What are risk factors for hemorrhoids and anal varices?

A

Straining at defecation, venous stasis of pregnancy, portal HTN

76
Q

What are the symptoms of hemorrhoids/anal varices?

A

Rectal bleeding and pain

77
Q

What are the two major differences between internal and external hemorrhoids?

A

Internal: above pectinate line, visceral innervation = not painful

External: below pectinate line, somatic innervation = painful

78
Q

Compare the arterial supply of internal and external hemorrhoids.

A

Internal: superior rectal artery (branch of IMA)

External: inferior rectal artery (branch of internal pudendal artery)

79
Q

Compare the venous drainage of internal and external hemorrhoids.

A

Internal: superior rectal vein -> inferior mesenteric vein -> portal system

External: inferior rectal vein -> internal pudendal vein -> internal iliac vein -> common iliac vein -> IVC

80
Q

Compare the lymphatic drainage of internal and external hemorrhoids.

A

Internal: internal iliac lymph nodes

External: superficial inguinal lymph nodes

81
Q

What are the 4 types of benign intestinal polyps?

A
  1. Inflammatory
  2. Juvenile
  3. Hamartomatous
  4. Hyperplastic
82
Q

Where are inflammatory polyps located most commonly?

A

Anterior wall of the rectum

83
Q

Describe the pathogenesis of inflammatory polyps.

A

Impaired relaxation of the anorectal sphincter leads to sharp angle at the anterior rectal shelf. This becomes abraded and ulcerated, and polyps form over time.

84
Q

What are juvenile polyps?

A

Focal malformations of mucosal epithelium and lamina propria; considered hamartomatous

Seen in children younger than age 5 in the rectum

85
Q

What syndrome are juvenile polyps associated with?

A

Juvenile polyposis - autosomal dominent, SMAD4 gene mutation

86
Q

What is Peutz-Jeghers syndrome?

A

Autosomal dominant condition that forms large polyps with arborizing projections

87
Q

What is the mutation associated with Peutz-Jeghers syndrome?

A

LKB1/STK11 gene (tumor suppressor)

88
Q

What is seen clinically in Peutz-Jeghers syndrome?

A
  1. Hamartomatous polyps (SI most common, but can be anywhere in the GI tract)
  2. Melanotic mucosal and cutaneous pigmentation
  3. Increased cancer risk
89
Q

What are hyperplastic polyps?

A

Benign, non-neoplastic polyps that are common, asymptomatic, and similar to adenomas

90
Q

Where are hyperplastic polyps commonly found and what causes them?

A

Left side of colon; proliferation of mature goblet cells

91
Q

Compare the locations of the 4 types of polyps.

A

Inflammatory: rectum (anterior wall)
Juvenile: rectum
Peutz Jeghers Syndrome: small intestine
Hyperplastic: left side of colon

92
Q

Compare the gross appearance of the 4 types of polyps.

A

Inflammatory: polypoid lesion, ulceration
Juvenile: pedunculated smooth surface
Peutz Jeghers syndrome: pedunculated, large
Hyperplastic: small (<0.5 mm)

93
Q

Compare the microscopic appearance of the 4 types of polyps.

A

Inflammatory: epithelial hyperplasia, lamina propria fibrosis
Juvenile: hamartomatous (disorganized normal tissue)
Peutz Jeghers Syndrome: arborizing smooth muscle core
Hyperplastic: glands with serrated surface, goblet cell proliferation

94
Q

What are the 4 neoplastic polyps?

A
  1. Tubular Adenoma
  2. Tubulovillous Adenoma
  3. Villous Adenoma
  4. Sessile Serrated Adenoma
95
Q

What are Tubular/Tubulovillous/Villous adenomas?

A

Neoplastic polyps that are precursors to the majority of colorectal adenocarcinoma; majority do not progress; occur anywhere in the colon

96
Q

Describe the composition of a tubular adenoma.

A

Composed entirely of tubular glands

97
Q

Describe the composition of a villous adenoma.

A

Composed of finger-like villous projections

98
Q

Where is sessile serrated adenoma most common?

A

Right side of colon

99
Q

Describe the appearance of sessile serrated adenoma.

A

Histologically lacks the typical features of dysplasia

Serrated, sessile (flat) appearance, broad base that sits on the muscularis mucosa

100
Q

What is the cause of sessile serrated adenoma?

A

DNA mismach repair (and others)

101
Q

What is the mutation that causes familial adenomatous polyposis?

A

Autosomal dominant

APC gene on chromosome 5q21

102
Q

Describe familial adenomatous polyposis.

A

Defined as patients with a minimum of 100 polyps

100% of patients develop colorectal adenocarcinoma

103
Q

How is familial adenomatous polyposis treated?

A

Prophylactic colectomy

104
Q

Discuss the normal function of APC.

A

Normally, APC negatively regulates B-catenin. It binds B-catenin and promotes its degradation. When this cannot occur, B-catenin accumulates, translocates to the nucleus, and promotes transcription.

105
Q

What is Gardner’s syndrome?

A

Autosomal dominant variant of FAP; involves osteomas of the mandible, skull and long bones, epidermal cysts, desmoid (soft tissue) tumors, thyroid tumors, and dental abnormalities

106
Q

What is Turcot’s syndrome?

A

Variant of FAP causing tumors of the CNS

107
Q

What is Lynch Syndrome?

A

Hereditary nonpolyposis colorectal cancer (HNPCC)

108
Q

Discuss the mutation of Lynch Syndrome.

A

Autosomal dominant

Mutation in DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2) that leads to microsatellite instability

109
Q

What are microsatelllites?

A

Repetitive DNA with certain motifs repeated that are located throughout the genome

110
Q

What are etiologic factors of colon adenocarcinoma?

A

Low content of unabsorbable vegetables

High content of refined carbohydrates

Decreased intake of protective micronutrients

111
Q

What is the pathogenesis of colon adenocarcinoma?

A

Combination of molecular events with genetic and epigenetic abnormalities

112
Q

What are the genetic events leading to colon adenocarcinoma?

A
  1. APC/beta-catenin pathway

2. Microsatellite instability

113
Q

What are the epigenetic events leading to colon adenocarcinoma?

A

Methylation-induced gene silencing which may enhance progression along either pathway

114
Q

What are the 2 most important prognostic factors for colon adenocarcinoma?

A
  1. Depth of invasion

2. Presence/absence of lymph node metastasis

115
Q

Discuss right sided colon adenocarcinoma.

A

Often asymptomatic for a long time as the lumen is wide in the right colon

Symptoms: possible iron deficiency anemia due to surface ulceration and blood loss

116
Q

Discuss left sided colon adenocarcinoma.

A

More commonly symptomatic (smaller lumen)

Symptoms: change in bowel habits or obstruction, blood in stool

117
Q

What are the 4 stages of colon cancer?

A

T1: invasion into submucosa
T2: invasion into muscularis propria
T3: invasion into subserosal tissues
T4: invasion into vasiceral peritoneum, other organs, or perforation

118
Q

What are the symptoms of appendicitis?

A

Acute nausea/vomiting, with periumbilical pain localizing to the RLQ

119
Q

What is the etiology of appendicitis?

A

Obstruction that leads to impaired blood flow and bacterial contamination

120
Q

What is the pathology of appendicitis?

A

Transmural and luminal acute inflammation

121
Q

What is the most common tumor of the appendix?

A

Carcinoid tumor (well-differentiated neuroendocrine neoplasm most often located in the tip of the appendix)

122
Q

How do carcinoid tumors appear in the appendix?

A

Salt and pepper chromatin

123
Q

What are mucinous appendiceal neoplasms?

A

General term for a dilated appendix filled with mucin - may be a mucinous cystadenoma or cystadenocarinoma

124
Q

What is the difference between a mucinous cystadenoma and cystadenocarcinoma?

A

Cystadenoma: proliferation of benign neoplastic cells with dilation by mucinous material

Cystadenocarinoma: neoplastic cells invade through the appendiceal wall

125
Q

What is the peritoneum?

A

Lining composed of mesothelial cells

126
Q

What is the visceral and parietal peritoneum?

A

Visceral: covers organs
Parietal: covers abdominal wall

127
Q

What are etiologies of peritoneal inflammation?

A
  1. Sterile peritonitis (bile or pancreatic juices)
  2. Surgery
  3. Endometriosis
  4. Rupture of GI tract (appendicitis, diverticulitis, salpingitis)
128
Q

What is the presence of abundant mucinous material on peritoneal surfaces?

A

Pseudomyxoma peritonei

129
Q

What are three major organisms that cause infectious diarrhea?

A
  1. Vibrio
  2. Campylobacter
  3. Helicobacter
130
Q

Broadly, what microbial factors contribute to infectious diarrhea?

A
  1. Attachment (surface fimbriae, effacing adherence, invasion)
  2. Toxin production (entero/cytotoxins)
  3. Invasiveness
131
Q

Describe the characteristics of non-inflammatory diarrhea.

A

No fecal WBC’s, watery, tends to occur in the small intestine

132
Q

What types of organisms cause non-inflammatory diarrhea?

A
  1. Toxigenic bacteria (ETEC, V. cholerae)
  2. Viruses (kill enterocytes)
  3. Protozoa
  4. Bacteria (preformed toxin in food)
133
Q

Describe the characteristics of inflammatory diarrhea.

A

Fecal WBC’s, low stool volume, mucus/blood/pus, tends to occur in the large intestine

134
Q

What are examples of organisms that cause inflammatory diarrhea?

A
  1. Bacteria (Shigella, Campylobacter, some E. coli)
  2. Protozoa (Entamoeba histolytica)
  3. Toxin-mediated (C. diff, EHEC)
135
Q

Vibrio cholerae is a ___ (shape), Gram ___ organism found in ___ (environment).

A

Curved rod; salt water

136
Q

Describe the virulence factors of V. cholerae.

A
  1. Single polar flagellum (motility)
  2. Toxin coregulated (TCP) pili
  3. LPS
  4. AB type ADP-ribosylating toxin (potent enterotoxin)
137
Q

How does the entertoxin AB of V. cholerae function?

A

B binds to GM-1 ganglioside; A1 is released from A2 and enters the cell by translocation

138
Q

Describe the cultural characteristics of V. cholerae:

  1. Growth conditions
  2. Oxygen status
  3. Oxidase ___
A
  1. Grows in alkaline conditions (pH 8.0-9.5, inhibits other GN bacteria)
  2. Facultative anaerobe
  3. Oxidase positive
139
Q

Which serogroups of V. cholerae cause cholera?

A

O-1 and O-139

140
Q

How is V. cholerae transmitted?

A

Excreted in stool, contaminates water, ingested by a person

141
Q

Where is cholera endemic?

A

Sub-Saharan Africa and South Asia

142
Q

What does V. cholerae use for adherence?

A

Tcp pili

143
Q

Explain the pathogenesis of V. cholerae.

A
  1. Break down mucus, use flagella to reach to the cell surface.
  2. Attach, multiply, and produce toxin.
  3. B subunit of toxin binds to GM1 and the toxin is taken into the cell.
  4. Here, it breaks apart, and A combines with NAD to ribosylate a G-protein.
  5. This attaches to adenylyl cyclase, which produces cAMP from ATP. This activates PKA, which phosphorylates CFTR OR blocks an NqCl absorptive system, resulting in accumulation of large amounts of water in the lumen.
144
Q

Describe the electrolyte composition of the stool in a patient with cholera.

A

Electrolyte rich

145
Q

Who is more susceptible to cholera?

A

People who have decreased acid (lower inoculum required to produce disease)

146
Q

Describe the clinical manifestations of cholera -

  1. Incubation period
  2. Symptoms
  3. Sequelae
A
  1. Incubation period of 1-3 days
  2. Nonspecific prodrome (abdominal discomfort, vomiting, loose stools

Rapid onset of profuse watery diarrhea (clear, odorless, rice water)

NO fever
3. Dehydration, hypotension, acidosis, death

147
Q

How is cholera diagnosed?

A
  1. Gram stain (early)
  2. Culture: blood agar or TCBS agar (selective)
  3. PCR
148
Q

How is cholera managed?

A
  1. Rehydration

2. Antibiotics (doxycycline, azithromycin for women and children)

149
Q

What electrolytes are supplemented in the IV rehydration solution for cholera?

A

Potassium and bicarbonate

150
Q

If you add ___ to a solution of electrolytes, you can rehydrate patients orally.

A

Glucose (it is linked to Na+ absorption)

151
Q

Which type of Vibrio is found in sea water (instead of coastal waters)?

A

V. vulnificus

152
Q

Which type of Vibrio causes wound infection and septicemia in persons with liver disease?

A

V. vulnificus

153
Q

Which type of Campylobacter is found in poultry primarily?

A

C. jejuni

154
Q

Which type of Campylobacter is found in pigs primarily?

A

C. coli

155
Q

Which type of Campylobacter is found in cattle and sheep primarily?

A

C. fetus

156
Q

Which type of Campylobacter is found in dogs and cats primarily?

A

C. upsiliensis

157
Q

Which type of Campylobacter causes septicemia (not gastroenteritis)?

A

C. fetus

158
Q

Describe the morphology of Campylobacter.

A

Curved, motile GN rod found in pairs (seagull appearance)

159
Q

Describe the cultural characteristics of Campylobacter:

  1. Oxygen status
  2. Oxidase ___
  3. Growth temperature
  4. Biochemical activity
A
  1. Microaerophilic
  2. Oxidase positive
  3. Grows better at 42 C than 37 C
  4. Biochemically inactive
160
Q

What is the common reservoir of C. jejuni?

A

GI and GU tracts of sheep, cattle, and chickens

161
Q

What is the most common source of Campylobacter?

A

Chicken consumption

162
Q

Discuss the pathogenesis of C. jejuni.

A
  1. Attaches via fimbriae/adhesions
  2. Motility via flagella
  3. Toxins
  4. Invasion
163
Q

C. jejuni is linked to ___ syndrome. What happens?

A

Guillain-Barre’ Syndrome, an autoimmune inflammatory neuropathy; bacterial ganglioside-like LOS structures and human peripheral nerve gangliosides cross-react, triggering demyelination and axonal degeneration

164
Q

C. jejuni is also associated with what condition?

A

Reactive arthritis

165
Q

Describe the clinical manifestations of Campylobacter.

A
  1. Incubation period
  2. Fever, abdominal pain, diarrhea (bloody)
  3. Some relapse
166
Q

How is Campylobacter diagnosed?

A
  1. Culture (selective media, microaerophilic conditions, elevated temperature)
  2. PCR is replacing culture
167
Q

How is Campylobacter treated?

A
  1. Erythromycin or azithromycin (shorten course and prevent relapse) for 5 days
  2. Ciprofloxacin (alternative, as resistance is increasing)
  3. No treatment for uncomplicated infection
168
Q

___ colonizes, persists, and causes inflammation in gastric mucosa and is linked to ___ diseases.

A

Helicobacter pylori; upper GI (gastritis, gastric/duodenal ulcer/gastric carcinoma/gastric MALT)

169
Q

Describe the cultural characteristics of Helicobacter:

  1. Shape/Gram
  2. Motility
  3. Oxygen status
  4. Oxidase ___
  5. Urease ___
  6. Non-___, non-___
A
  1. Curved, GN rods
  2. Corkscrew motility
  3. Microaerophilic
  4. Oxidase positive
  5. Urease positive
  6. Non-oxidative, non-fermatative
170
Q

How is Helicobacter transmitted?

A

Ingestion and person-to-person

171
Q

Describe the unique characteristics of H. pylori that allow barrier penetration and persistence in hostile environment.

A
  1. Mucinase (penetrates GASTRIC mucosa)
  2. Flagella
  3. Adherence to GASTRIC mucosa
  4. Urease (creates alkaline environment)
  5. Genetic variation
  6. Vacuolating cytotoxin
172
Q

How does H. pylori adhere to gastric mucosa?

A

Forms membrane attachment pedestals, BabA binds to fucosylated Lewis blood group Ag receptor expressed on intestinal mucosal cells

173
Q

How does the H. pylori cytotoxin work?

A

The exotoxin inserts into the cell membrane, forming a pore that releases nutrients. It targets the mitochondrial membrane, which releases cytochrome c and induces apoptosis.

174
Q

The ___ pathogeneicity island of H. pyloria contains 30 genes, including a ___ that inserts Cag A into the cell. What does this do?

A

cag; Type IV secretory system; promote cytokine production, especially IL-8, that activates and attracts neutrophils

175
Q

What are the clinical manifestations of H. pylori?

A
  1. Gastritis (fullness, epigastric pain, nausea, vomiting, bleeding)
  2. Gastric and duodenal ulcer (pain and bleeding)
  3. Gastric cancer
  4. Gastric MALT (pain or discomfort, loss of appetite, weight loss, bleeding)

Associated with ITP

176
Q

How is H. pylori diagnosed?

A
  1. Serology
  2. Breath test (measures ammonia)
  3. Stool Ag test
  4. Urease test (urease activity in gastric biopsy material)
  5. Histology

Culture is difficult and PCR is not used

177
Q

How is H. pylori treated?

A

PPI + 2 antibiotics (amoxicillin, clarithromycin, metronidazole, tetracycline) for 10-14 days

MHD2 (34 decks)

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