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Micro Exam 4 > H pylori > Flashcards

H pylori Flashcards

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
Q

Chronic biliary disorders caused by Enterohepatic Helicobacter species include:

A

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
Q

Prevalence of h. pylori

A

50% of the world’s pop is infected, more common in low socioeconomic areas

27
Q

What percentage of h. pylori infected individuals will develop peptic ulcers or gastric malignancies in their lifetime

A

15-20%

28
Q

Transmission of h. pylori occurs by

A

interfamilial spread (aerosolized vomit), gastric-oral/oral-oral (burping)

29
Q

Risk Factors for h. pylori

A

familial spread, crowding, gastroenterologist, MHC-II genotype

30
Q

MHC-II genotype that is at increased risk for h. pylori-associated gastritis

A

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
Q

Which h. pylori virulent factor reduces capthesin activity?

A

vacA

32
Q

Carriage rate for h. pylori

A

increases w/ age

33
Q

Principle reservoir for h. pylori

A

humans

34
Q

Most frequent symptoms of a h. pylori infection

A

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
Q

Less frequent symptoms of a h. pylori infection

A

n/v, loss of appetite, black stools, vomiting blood or coughing up blood

36
Q

Extraintestinal Hematological Disease caused by chronic h. pylori infection (Mechanism?)

A

iron-deficient anemia (sideropenic/refractory); h. pylori infection itself can cause iron-deficient anemia in the absence of bleeding (pregnancy or children)

37
Q

How would you treat iron-deficient anemia due to h/ pylori infection?

A

Treat h. pylori! H. pylori decreases the response to iron therapy

38
Q

Extraintestinal Hematological Disease caused by chronic h. pylori cagA infection (Mechanism?)

A

ITP; this may be due to molecular mimicry between anti-platelet antibodies and H. pylori protein cagA

39
Q

How would you treat ITP related to h. pylori infection?

A

Treat h. pylori! Should show complete or partial response.

40
Q

In iron-deficient anemia, what would you see on a peripheral smear?

A

microcytic, hypochromic (central pallor is increased), RBCs are small and size/shape varies

41
Q

In ITP, what would you see on a peripheral smear?

A

increased platelet size (same size as RBCs), morphology of platelets is typically normal

42
Q

Chronic ITP treated w/ abc resolved in _____% of the cases.

A

50%

43
Q

What other disorders may be caused by molecular mimicry of h. pylori’s cagA?

A

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
Q

What other disorders may be associated with h. pylori infections?

A

Lichen planus, rosacea, idiopathic parkinsonism, Diabetes: increased HbA1c, metabolic syndrome

45
Q

How may h. pylori play a role in diabetes?

A

it plays a role in ghrelin and leptin regulation, can increase HbA1c and gastritis may play a role in metabolic syndrome!

46
Q

A h. pylori infection in early childhood may cause an increased risk for

A

biochemical aberrations that may lead to schizophrenia in predisposed ind. (dopaminergic dysfunction, decreased polyunsaturated fats, homocysteine alterations)

47
Q

Which test is diagnostic for H. pylori infection?

A

+ IgG titer for H. pylori

48
Q

What disorder may be improved by a h. pylori infection?

A

Asthma in children

49
Q

What invasive test may be done to test for H. pylori?

A

Endoscopic brush biopsy

50
Q

What would you test for w/ an endoscopic brush biopsy

A

Urease

51
Q

How would you culture suspected h. pylori specimen?

A

Microaerophilically (low O2 levels)

52
Q

What test for H. pylori is preferred for children under 10?

A

Breath Test

53
Q

How would you perform a Breath Test?

A

Patient ingests C-13 urea, measure 13-CO2

54
Q

What are good predictive markers for development of gastric cancer?

A

serum pepsinogen and H. pylori Ab’s

55
Q

What test is best for an initial diagnosis and following H. pylori treatment/erradication?

A

Stool Antigen Test (SAT)

56
Q

Stool Antigen Test (SAT)

A

mAb to test for novel antigens (non-invasive, reliable, results in 10min)

57
Q

Treatment of H. pylori - Triple Therapy

A

PPI + Clarithromycin + amoxicillin/metronidazole

58
Q

Treatment of H. pylori - Sequential Therapy

A

Bismuth Subsalicylate… Clarithromycin…Amoxicillin…

59
Q

What test would confirm if the abc are efficiently eradicating the infection?

A

IgG Titer should decreases by 1-3 mo; monitor patient using SAT

60
Q

Prevention of H. pylori

A

Hand-washing (w/ SOAP)

61
Q

Presence of schistocytes on a peripheral smear would indicate?

A

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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