Block 7 (GI) - L4 to L6 Flashcards
1
Q
What are the layers of the intestine?
A
- Mucosa (villi, crypts, lamina propria, muscularis mucosa)
- Submucosa + Meissner’s plexus
- Muscularis propria (inner circular layer, Auberach’s plexus, outer longitudinal layer)
- Serosa
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
3
Q
What is incomplete closure of the abdominal musculature and visceral herniation into a membranous sac?
A
Omphalocele
4
Q
Meckel diverticulum develops due to failed involution of the ___, leading to a blind outpouching.
A
Vitelline duct
5
Q
Is Meckel diverticulum true or false?
A
True
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
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
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
9
Q
What is Hirschprung Disease?
A
Premature arrest or death of neural crest cells migrating from the cecum to the rectum
10
Q
What mutation is commonly seen in Hirschprung disease?
A
RET proto-oncogene mutation
11
Q
What are the symptoms of Hirschprung Disease?
A
Failure to pass meconium, obstruction/constipation
12
Q
Which part of the colon is always involved in Hirschprung idsease?
A
Rectum
13
Q
What are potential complications of Hirschprung disease?
A
Fluid/electrolyte disturbances, eneterocolitis, perforation, peritonitis, congenital megacolon (proximal dilation that can rupture)
14
Q
What are associations with Hirschsprung disease?
A
Down Syndrome
Serious neurologic abnormalities
15
Q
Describe the histopathology of Hirschsprung disease.
A
Complete lack of ganglion cells in both Meissner’s and Auberach’s plexuses
16
Q
What is necrotizing enterocolitis?
A
Acute, necrotizing inflammation of small and/or large intestines (cause uncertain)
17
Q
How does necrotizing enterocolitis present?
A
Premature infants
Bloody stools, circulatory collampse, abdominal distension
18
Q
Which parts of the intestine does necrotizing enterocolitis typically involve?
A
Terminal ileum, cecum, right colon
19
Q
What is celiac disease?
A
Immune-medaited enteropathy triggered by the ingestion of gluten-containing foods in genetically predisposed individuals
20
Q
Gluten is a major storage protein of wheat and similar grains - which component is largely responsible for celiac disease?
A
Gliadin
21
Q
What is the clinical presentation of celiac disease?
A
Most common in 30-60 year olds
Diarrhea, bloating, fatigue, anemia
22
Q
What are the HLA types associated with celiac disease?
A
HLA-DQ2
HLA-DQ8
23
Q
What are other important associations with celiac disease?
A
Dermatitis Herpetiformis (skin blistering disease) and other autoimmune diseases
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
25
Describe the histopathology seen in celiac disease.
Increased intraepithelial lympohcytes and blunting of villi
26
What Ab can be tested for in celiac disease?
1. IgA Ab to tissue transglutamine (most sensitive)
2. IgA anti-endomysial (specific but less sensitive) Ab
3. Anti-gliadin Ab
27
What does the absence of HLA-DQ2 and DQ8 indicate?
Good negative predictive value, but not helpful in confirming a diagnosis when they are present
28
What are risks associated with celiac disease?
Enteropathy associated T-cell lymphoma and small intestinal adenocarcinoma
29
Describe the gross appearance of the intestine in celiac disease.
Atrophic mucosa and flattened folds
30
What is tropical sprue?
Disease similar to celiac sprue seen in the tropics, leading to chronic bouts of diarrhea and nutritional deficiencies as a ressult
31
What are the symptoms of pseudomembranous colitis?
Abdominal pain, fever, watery diarrhea
32
What causes pseudomembranous colitis?
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
33
How is pseudomembranous colitis tested for?
Detection of C. diff. toxin
34
Describe the pathology of pseudomembranous colitis.
Colonic mucosa covered by a yellow/green false membrane composed of mucus and neutrophils
35
What is Whipple disease?
Rare multisystem chronic disease caused by a Gram positive rod shaped actinomycete (Tropheryma whipplei)
36
What is the triad of symptoms seen in Whipple disease?
Diarrhea, weight loss, arthralgia
37
What are some extra-intestinal symptoms of Whipple disease?
Arthritis, lymphadenopathy, neurologic, cardiac, pulmonary disease
38
Discuss the pathogenesis of Whipple disease.
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.
39
Describe the histopathology of Whipple Disease.
Distended foamy macrophages filled with organisms (PAS+, diastase resistant)
40
What are the two types of inflammatory bowel disease?
Crohn's disease and Ulcerative colitis
41
Compare the location of Crohn's and ulcerative colitis.
CD: upper GI tract involvement - segmental with skip lesions; cobblestone appearance
UC: colon only - diffuse, continuous disease
42
Compare the symptoms of Crohn's and ulcerative colitis.
CD: +/- bloody diarrhea
UC: bloody diarrhea
43
Compare the rectal involvement of Crohn's and ulcerative colitis.
CD: variable
UC: rectum involved
44
Compare the microscopic findings of Crohn's and ulcerative colitis.
Both: architectural distortion and crypt abscesses/cryptitis
CD: transmural lymphoid aggregates and granulomas
UC: NO granulomas
45
Compare the complications of Crohn's and ulcerative colitis.
CD: fissures, sinuses, fistulous tracts
UC: NO fissures, toxic megacolon
Both: colon adenocarcinoma (more common in UC)
46
Compare the extra-intestinal manifestions of Crohn's and ulcerative colitis.
CD: pyoderma gangrenosum, erythema nodosum
UC: primary sclerosing cholangitis (p-ANCA)
47
What is the difference between cryptitis and a crypt abscess?
Cryptitis - neutrophils within the epithelium of a colonic gland
Crypt abscess - colonic gland filled with neutrophils
48
What is creeping fat, seen in Crohn's?
Normally, fat is located along the mesenteric area of the bowel; creeping fat refers to fat that is moving along the serosal surface
49
Which disease has pseudopolyps?
Ulcerative colitis
50
What is the frequency of the basal electric rhythm of the duodenum and ileum respectively?
Duodenum: 12 waves/minute
Ileum: 8-9 waves/minute
51
Where is iron absorbed in the small bowel?
Duodenum
52
Where is vitamin B12 absorbed in the small bowel?
Ileum
53
What is diverticular disease?
Acquired herniation of mucosa and submucosa leading to the formation of a false diverticula
54
What is diverticulitis?
When a diverticula becomes inflamed, usually due to obstruction with stool/mucus, leading to bacterial overgrowth/infection
55
Diverticular disease is associated with a ___ diet.
Low-fiber
56
What are the symptoms of diverticular disease?
Left lower quadrant pain, fever (diverticulitis), bleeding
57
Where is diverticular disease most common?
Left colon, particularly the sigmoid colon
58
What are complications of diverticular disease?
Perforation, peritonitis, fistula
59
How is diverticular disease treated?
Antibiotics and surgical intervention if complciations arise
60
What is a hernia?
Weakness or defect of abdominal wall that allows for a serosal-lined out-pouching of peritoneum
61
What is incarceration?
When a loop of intestines becomes trapped within a hernia sac
62
What is strangulation?
When the bowel is compressed and twisted at the mouth of the hernia, compromising blood supply
63
What are adhesions?
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
64
What is intussusception?
In-folding or telescoping of one segment of bowel into the adjacent distal segment
65
What is a volvulus?
Obstruction due to rotation or twisting of a loop of bowel around its mesenteric base of attachment
66
What is the most common site of volvulus?
Sigmoid colon, followed by the cecum
67
What is ischemic bowel disease?
Bowel hemorrhage and necrosis secondary to hypoxic injury and/or reperfusion injury
68
What types of patients get ischemic bowel disease?
Patients >70 years old
69
What are the symptoms of ischemic bowel disease?
Sudden severe abdominal pain and bloody diarrhea (can lead to shock, sepsis, and death)
70
What are some causes of acute arterial occlusions that can cause ischemic bowel disease?
1. Atherosclerosis
2. Aortic aneurysm
3. Hypercoagulable states
4. Oral contraceptive use
5. Embolization of cardiac vegetations or aortic atheromas
71
What are some causes of intestinal hypoperfusion that can cause ischemic bowel disease?
Cardiac failure, shock, dehydration, and vasoconstrictors
72
What are some rare causes of ischemic bowel disease?
Systemic vasculitis and mesenteric venous thrombosis
73
What part of the colon is prone to infarction?
Splenic flexure
74
What are hemorrhoids?
Dilated veins of the hemorrhoidal plexus
75
What are risk factors for hemorrhoids and anal varices?
Straining at defecation, venous stasis of pregnancy, portal HTN
76
What are the symptoms of hemorrhoids/anal varices?
Rectal bleeding and pain
77
What are the two major differences between internal and external hemorrhoids?
Internal: above pectinate line, visceral innervation = not painful
External: below pectinate line, somatic innervation = painful
78
Compare the arterial supply of internal and external hemorrhoids.
Internal: superior rectal artery (branch of IMA)
External: inferior rectal artery (branch of internal pudendal artery)
79
Compare the venous drainage of internal and external hemorrhoids.
Internal: superior rectal vein -> inferior mesenteric vein -> portal system
External: inferior rectal vein -> internal pudendal vein -> internal iliac vein -> common iliac vein -> IVC
80
Compare the lymphatic drainage of internal and external hemorrhoids.
Internal: internal iliac lymph nodes
External: superficial inguinal lymph nodes
81
What are the 4 types of benign intestinal polyps?
1. Inflammatory
2. Juvenile
3. Hamartomatous
4. Hyperplastic
82
Where are inflammatory polyps located most commonly?
Anterior wall of the rectum
83
Describe the pathogenesis of inflammatory polyps.
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
What are juvenile polyps?
Focal malformations of mucosal epithelium and lamina propria; considered hamartomatous
Seen in children younger than age 5 in the rectum
85
What syndrome are juvenile polyps associated with?
Juvenile polyposis - autosomal dominent, SMAD4 gene mutation
86
What is Peutz-Jeghers syndrome?
Autosomal dominant condition that forms large polyps with arborizing projections
87
What is the mutation associated with Peutz-Jeghers syndrome?
LKB1/STK11 gene (tumor suppressor)
88
What is seen clinically in Peutz-Jeghers syndrome?
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
What are hyperplastic polyps?
Benign, non-neoplastic polyps that are common, asymptomatic, and similar to adenomas
90
Where are hyperplastic polyps commonly found and what causes them?
Left side of colon; proliferation of mature goblet cells
91
Compare the locations of the 4 types of polyps.
Inflammatory: rectum (anterior wall)
Juvenile: rectum
Peutz Jeghers Syndrome: small intestine
Hyperplastic: left side of colon
92
Compare the gross appearance of the 4 types of polyps.
Inflammatory: polypoid lesion, ulceration
Juvenile: pedunculated smooth surface
Peutz Jeghers syndrome: pedunculated, large
Hyperplastic: small (<0.5 mm)
93
Compare the microscopic appearance of the 4 types of polyps.
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
What are the 4 neoplastic polyps?
1. Tubular Adenoma
2. Tubulovillous Adenoma
3. Villous Adenoma
4. Sessile Serrated Adenoma
95
What are Tubular/Tubulovillous/Villous adenomas?
Neoplastic polyps that are precursors to the majority of colorectal adenocarcinoma; majority do not progress; occur anywhere in the colon
96
Describe the composition of a tubular adenoma.
Composed entirely of tubular glands
97
Describe the composition of a villous adenoma.
Composed of finger-like villous projections
98
Where is sessile serrated adenoma most common?
Right side of colon
99
Describe the appearance of sessile serrated adenoma.
Histologically lacks the typical features of dysplasia
Serrated, sessile (flat) appearance, broad base that sits on the muscularis mucosa
100
What is the cause of sessile serrated adenoma?
DNA mismach repair (and others)
101
What is the mutation that causes familial adenomatous polyposis?
Autosomal dominant
APC gene on chromosome 5q21
102
Describe familial adenomatous polyposis.
Defined as patients with a minimum of 100 polyps
100% of patients develop colorectal adenocarcinoma
103
How is familial adenomatous polyposis treated?
Prophylactic colectomy
104
Discuss the normal function of APC.
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
What is Gardner's syndrome?
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
What is Turcot's syndrome?
Variant of FAP causing tumors of the CNS
107
What is Lynch Syndrome?
Hereditary nonpolyposis colorectal cancer (HNPCC)
108
Discuss the mutation of Lynch Syndrome.
Autosomal dominant
Mutation in DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2) that leads to microsatellite instability
109
What are microsatelllites?
Repetitive DNA with certain motifs repeated that are located throughout the genome
110
What are etiologic factors of colon adenocarcinoma?
Low content of unabsorbable vegetables
High content of refined carbohydrates
Decreased intake of protective micronutrients
111
What is the pathogenesis of colon adenocarcinoma?
Combination of molecular events with genetic and epigenetic abnormalities
112
What are the genetic events leading to colon adenocarcinoma?
1. APC/beta-catenin pathway
| 2. Microsatellite instability
113
What are the epigenetic events leading to colon adenocarcinoma?
Methylation-induced gene silencing which may enhance progression along either pathway
114
What are the 2 most important prognostic factors for colon adenocarcinoma?
1. Depth of invasion
| 2. Presence/absence of lymph node metastasis
115
Discuss right sided colon adenocarcinoma.
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
Discuss left sided colon adenocarcinoma.
More commonly symptomatic (smaller lumen)
Symptoms: change in bowel habits or obstruction, blood in stool
117
What are the 4 stages of colon cancer?
T1: invasion into submucosa
T2: invasion into muscularis propria
T3: invasion into subserosal tissues
T4: invasion into vasiceral peritoneum, other organs, or perforation
118
What are the symptoms of appendicitis?
Acute nausea/vomiting, with periumbilical pain localizing to the RLQ
119
What is the etiology of appendicitis?
Obstruction that leads to impaired blood flow and bacterial contamination
120
What is the pathology of appendicitis?
Transmural and luminal acute inflammation
121
What is the most common tumor of the appendix?
Carcinoid tumor (well-differentiated neuroendocrine neoplasm most often located in the tip of the appendix)
122
How do carcinoid tumors appear in the appendix?
Salt and pepper chromatin
123
What are mucinous appendiceal neoplasms?
General term for a dilated appendix filled with mucin - may be a mucinous cystadenoma or cystadenocarinoma
124
What is the difference between a mucinous cystadenoma and cystadenocarcinoma?
Cystadenoma: proliferation of benign neoplastic cells with dilation by mucinous material
Cystadenocarinoma: neoplastic cells invade through the appendiceal wall
125
What is the peritoneum?
Lining composed of mesothelial cells
126
What is the visceral and parietal peritoneum?
Visceral: covers organs
Parietal: covers abdominal wall
127
What are etiologies of peritoneal inflammation?
1. Sterile peritonitis (bile or pancreatic juices)
2. Surgery
3. Endometriosis
4. Rupture of GI tract (appendicitis, diverticulitis, salpingitis)
128
What is the presence of abundant mucinous material on peritoneal surfaces?
Pseudomyxoma peritonei
129
What are three major organisms that cause infectious diarrhea?
1. Vibrio
2. Campylobacter
3. Helicobacter
130
Broadly, what microbial factors contribute to infectious diarrhea?
1. Attachment (surface fimbriae, effacing adherence, invasion)
2. Toxin production (entero/cytotoxins)
3. Invasiveness
131
Describe the characteristics of non-inflammatory diarrhea.
No fecal WBC's, watery, tends to occur in the small intestine
132
What types of organisms cause non-inflammatory diarrhea?
1. Toxigenic bacteria (ETEC, V. cholerae)
2. Viruses (kill enterocytes)
3. Protozoa
4. Bacteria (preformed toxin in food)
133
Describe the characteristics of inflammatory diarrhea.
Fecal WBC's, low stool volume, mucus/blood/pus, tends to occur in the large intestine
134
What are examples of organisms that cause inflammatory diarrhea?
1. Bacteria (Shigella, Campylobacter, some E. coli)
2. Protozoa (Entamoeba histolytica)
3. Toxin-mediated (C. diff, EHEC)
135
Vibrio cholerae is a ___ (shape), Gram ___ organism found in ___ (environment).
Curved rod; salt water
136
Describe the virulence factors of V. cholerae.
1. Single polar flagellum (motility)
2. Toxin coregulated (TCP) pili
3. LPS
4. AB type ADP-ribosylating toxin (potent enterotoxin)
137
How does the entertoxin AB of V. cholerae function?
B binds to GM-1 ganglioside; A1 is released from A2 and enters the cell by translocation
138
Describe the cultural characteristics of V. cholerae:
1. Growth conditions
2. Oxygen status
3. Oxidase ___
1. Grows in alkaline conditions (pH 8.0-9.5, inhibits other GN bacteria)
2. Facultative anaerobe
3. Oxidase positive
139
Which serogroups of V. cholerae cause cholera?
O-1 and O-139
140
How is V. cholerae transmitted?
Excreted in stool, contaminates water, ingested by a person
141
Where is cholera endemic?
Sub-Saharan Africa and South Asia
142
What does V. cholerae use for adherence?
Tcp pili
143
Explain the pathogenesis of V. cholerae.
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
Describe the electrolyte composition of the stool in a patient with cholera.
Electrolyte rich
145
Who is more susceptible to cholera?
People who have decreased acid (lower inoculum required to produce disease)
146
Describe the clinical manifestations of cholera -
1. Incubation period
2. Symptoms
3. Sequelae
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
How is cholera diagnosed?
1. Gram stain (early)
2. Culture: blood agar or TCBS agar (selective)
3. PCR
148
How is cholera managed?
1. Rehydration
| 2. Antibiotics (doxycycline, azithromycin for women and children)
149
What electrolytes are supplemented in the IV rehydration solution for cholera?
Potassium and bicarbonate
150
If you add ___ to a solution of electrolytes, you can rehydrate patients orally.
Glucose (it is linked to Na+ absorption)
151
Which type of Vibrio is found in sea water (instead of coastal waters)?
V. vulnificus
152
Which type of Vibrio causes wound infection and septicemia in persons with liver disease?
V. vulnificus
153
Which type of Campylobacter is found in poultry primarily?
C. jejuni
154
Which type of Campylobacter is found in pigs primarily?
C. coli
155
Which type of Campylobacter is found in cattle and sheep primarily?
C. fetus
156
Which type of Campylobacter is found in dogs and cats primarily?
C. upsiliensis
157
Which type of Campylobacter causes septicemia (not gastroenteritis)?
C. fetus
158
Describe the morphology of Campylobacter.
Curved, motile GN rod found in pairs (seagull appearance)
159
Describe the cultural characteristics of Campylobacter:
1. Oxygen status
2. Oxidase ___
3. Growth temperature
4. Biochemical activity
1. Microaerophilic
2. Oxidase positive
3. Grows better at 42 C than 37 C
4. Biochemically inactive
160
What is the common reservoir of C. jejuni?
GI and GU tracts of sheep, cattle, and chickens
161
What is the most common source of Campylobacter?
Chicken consumption
162
Discuss the pathogenesis of C. jejuni.
1. Attaches via fimbriae/adhesions
2. Motility via flagella
3. Toxins
4. Invasion
163
C. jejuni is linked to ___ syndrome. What happens?
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
C. jejuni is also associated with what condition?
Reactive arthritis
165
Describe the clinical manifestations of Campylobacter.
1. Incubation period
2. Fever, abdominal pain, diarrhea (bloody)
3. Some relapse
166
How is Campylobacter diagnosed?
1. Culture (selective media, microaerophilic conditions, elevated temperature)
2. PCR is replacing culture
167
How is Campylobacter treated?
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
___ colonizes, persists, and causes inflammation in gastric mucosa and is linked to ___ diseases.
Helicobacter pylori; upper GI (gastritis, gastric/duodenal ulcer/gastric carcinoma/gastric MALT)
169
Describe the cultural characteristics of Helicobacter:
1. Shape/Gram
2. Motility
3. Oxygen status
4. Oxidase ___
5. Urease ___
6. Non-___, non-___
1. Curved, GN rods
2. Corkscrew motility
3. Microaerophilic
4. Oxidase positive
5. Urease positive
6. Non-oxidative, non-fermatative
170
How is Helicobacter transmitted?
Ingestion and person-to-person
171
Describe the unique characteristics of H. pylori that allow barrier penetration and persistence in hostile environment.
1. Mucinase (penetrates GASTRIC mucosa)
2. Flagella
3. Adherence to GASTRIC mucosa
4. Urease (creates alkaline environment)
5. Genetic variation
6. Vacuolating cytotoxin
172
How does H. pylori adhere to gastric mucosa?
Forms membrane attachment pedestals, BabA binds to fucosylated Lewis blood group Ag receptor expressed on intestinal mucosal cells
173
How does the H. pylori cytotoxin work?
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
The ___ pathogeneicity island of H. pyloria contains 30 genes, including a ___ that inserts Cag A into the cell. What does this do?
cag; Type IV secretory system; promote cytokine production, especially IL-8, that activates and attracts neutrophils
175
What are the clinical manifestations of H. pylori?
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
How is H. pylori diagnosed?
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
How is H. pylori treated?
PPI + 2 antibiotics (amoxicillin, clarithromycin, metronidazole, tetracycline) for 10-14 days
