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H pylori Flashcards

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1
Q

80% of gastric cancers are related to

A

h. pylori infections

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2
Q

5% of cancers WW are related to

A

h. pylori infections

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3
Q

If something is going on w/ the patient’s stomach and they are not taking NSAIDs it is likely

A

h. pylori infections

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4
Q

h. pylori is a group ___ carcinogen

A

1

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5
Q

h. pylori infections may increase the risk for:

A

gastric/duodenal ulcers, PUD, chronic superficial gastritis, hypertrophic gastropathy (Ménétrier’s Disease), atrophic gastritis, recurrent hyperplastic polyps of the stomach

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6
Q

h. pylori infections are associated with increased risk for _____________, an extra- gastrointestinal effect

A

Atrial fibrillation

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7
Q

What genetic polymorphisms increase the likelihood of developing gastric cancer from h. pylori infections

A

IL-1b, IL-1bR, TNF-a, IL-10

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8
Q

h. pylori properties

A

GN curved rod, facultative intracellular, non-invasive, Oxidase (+), urease (+), catalase (+), extremely acid tolerant, Microaerophilic, motile via sheathed flagella

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9
Q

Urease

A

ESSENTIAL for survival! production in h. pylori, converts urea to ammonia + CO2, which neutralizes stomach acid

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10
Q

Why is urease necessary to h. pylori

A

h. pylori is acid resistant NOT acid stable

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11
Q

50% of h. pylori strains are + for

A

cagA and vacA cytotoxins; remaining 50% of h. pylori secretes 1 or the other, few are double -

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12
Q

cytotoxin cagA mechanism

A

effector protein that is injected into stem-like cells in the due to Type IV secretion system, causes rearrangement of cytoskeleton, alters cell signaling, and perturbs cell cycle. Increases expression of DNA editing enzyme, which leads to mutations in p53

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13
Q

cytotoxin vacA mechanism

A

Causes dysfunction autophagy, in chronic infection reduces cathepsin enzyme activities and hinders the fusion of autophagosomes with lysosomes, accelerating the replication of H. pylori

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14
Q

CagA-negative h. pylori strains will cause

A

only chronic gastritis and have only a small chance of developing peptic ulcer disease or gastric cancer.

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15
Q

cagA toxin is associated with the development of

A

cancer and other cellular changes, peptic ulcer disease

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16
Q

vacA toxin is required for the development of

A

REQUIRED for ulcer formation and gastritis

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17
Q

Cag A-negative h. pylori strains will cause

A

only chronic gastritis and have only a small chance of developing peptic ulcer disease or gastric cancer

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18
Q

Oxidase (+) strains causing diarrheal illnesses

A

Vibrio, Campylobacter, Helicobacter, Aeromonas

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19
Q

Weight Loss presenting WITH Fever=

A

Balantidium Coli

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20
Q

Weight Loss presenting WITHOUT Fever=

A

Hymenolepsis Nana

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21
Q

H. pylori LPS affects

A

production of acid and secretion of pepsinogen

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22
Q

Virulence Factors of H. pylori

A

urease, cagA, vacA, and LPS

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23
Q

Which h. pylori virulence factor is necessary for survival?

A

urease; organism is acid-resistant, not acid-stable, after 30-60min will be killed if it does not neutralize toxins

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24
Q

Enterohepatic Helicobacter species (All species other than pylori) may cause

A

extragastric diseases - colonization of the hepatobiliary tract causing chronic biliary disorders (diseases of pancreas, liver, gall bladder primarily)

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25
Chronic biliary disorders caused by Enterohepatic Helicobacter species include:
cholecystitis, cholelithiasis, gallbladder carcinoma and bile tract carcinoma and some liver diseases, such as primary sclerosing cholangitis, primary biliary cirrhosis and hepatocellular carcinoma; chronic pancreatitis and pancreatic cancer, as well as IBD
26
Prevalence of h. pylori
50% of the world's pop is infected, more common in low socioeconomic areas
27
What percentage of h. pylori infected individuals will develop peptic ulcers or gastric malignancies in their lifetime
15-20%
28
Transmission of h. pylori occurs by
interfamilial spread (aerosolized vomit), gastric-oral/oral-oral (burping)
29
Risk Factors for h. pylori
familial spread, crowding, gastroenterologist, MHC-II genotype
30
MHC-II genotype that is at increased risk for h. pylori-associated gastritis
HLA-DR, because HLA-DR is cross-reactive with h. pylori peptides and initiates gastric autoimmune responses due to the molecular mimicry from h. pylori --> gastritis and inflammation
31
Which h. pylori virulent factor reduces capthesin activity?
vacA
32
Carriage rate for h. pylori
increases w/ age
33
Principle reservoir for h. pylori
humans
34
Most frequent symptoms of a h. pylori infection
gnawing, burning pain in the epigastric region below the rib cage, gradual onset of weeks to months, pain typically occurs when stomach is empty (b/w meals or in the morning), pain lasts minutes – hours, relieved by eating or antacids, bad breath despite + oral hygiene
35
Less frequent symptoms of a h. pylori infection
n/v, loss of appetite, black stools, vomiting blood or coughing up blood
36
Extraintestinal Hematological Disease caused by chronic h. pylori infection (Mechanism?)
iron-deficient anemia (sideropenic/refractory); h. pylori infection itself can cause iron-deficient anemia in the absence of bleeding (pregnancy or children)
37
How would you treat iron-deficient anemia due to h/ pylori infection?
Treat h. pylori! H. pylori decreases the response to iron therapy
38
Extraintestinal Hematological Disease caused by chronic h. pylori cagA infection (Mechanism?)
ITP; this may be due to molecular mimicry between anti-platelet antibodies and H. pylori protein cagA
39
How would you treat ITP related to h. pylori infection?
Treat h. pylori! Should show complete or partial response.
40
In iron-deficient anemia, what would you see on a peripheral smear?
microcytic, hypochromic (central pallor is increased), RBCs are small and size/shape varies
41
In ITP, what would you see on a peripheral smear?
increased platelet size (same size as RBCs), morphology of platelets is typically normal
42
Chronic ITP treated w/ abc resolved in _____% of the cases.
50%
43
What other disorders may be caused by molecular mimicry of h. pylori's cagA?
ITP (x w/ platelet proteins), vascular disease, and coronary instability, ischemic heart, unstable angina (x w/ protein in atherosclerotic plaques) resulting in autoimmune response
44
What other disorders may be associated with h. pylori infections?
Lichen planus, rosacea, idiopathic parkinsonism, Diabetes: increased HbA1c, metabolic syndrome
45
How may h. pylori play a role in diabetes?
it plays a role in ghrelin and leptin regulation, can increase HbA1c and gastritis may play a role in metabolic syndrome!
46
A h. pylori infection in early childhood may cause an increased risk for
biochemical aberrations that may lead to schizophrenia in predisposed ind. (dopaminergic dysfunction, decreased polyunsaturated fats, homocysteine alterations)
47
Which test is diagnostic for H. pylori infection?
+ IgG titer for H. pylori
48
What disorder may be improved by a h. pylori infection?
Asthma in children
49
What invasive test may be done to test for H. pylori?
Endoscopic brush biopsy
50
What would you test for w/ an endoscopic brush biopsy
Urease
51
How would you culture suspected h. pylori specimen?
Microaerophilically (low O2 levels)
52
What test for H. pylori is preferred for children under 10?
Breath Test
53
How would you perform a Breath Test?
Patient ingests C-13 urea, measure 13-CO2
54
What are good predictive markers for development of gastric cancer?
serum pepsinogen and H. pylori Ab’s
55
What test is best for an initial diagnosis and following H. pylori treatment/erradication?
Stool Antigen Test (SAT)
56
Stool Antigen Test (SAT)
mAb to test for novel antigens (non-invasive, reliable, results in 10min)
57
Treatment of H. pylori - Triple Therapy
PPI + Clarithromycin + amoxicillin/metronidazole
58
Treatment of H. pylori - Sequential Therapy
Bismuth Subsalicylate... Clarithromycin...Amoxicillin...
59
What test would confirm if the abc are efficiently eradicating the infection?
IgG Titer should decreases by 1-3 mo; monitor patient using SAT
60
Prevention of H. pylori
Hand-washing (w/ SOAP)
61
Presence of schistocytes on a peripheral smear would indicate?
That the anemia is not caused by ITP, most likely agent would NOT be H. pylori

Micro Exam 4 (8 decks)

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