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Pathophysiology > W.10: Pathophys. of GI tract > Flashcards

W.10: Pathophys. of GI tract Flashcards

1
Q

Enzymes that are secreted by the chief cells?

A
  • Pepsinogen

- Lipase

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2
Q

Hormones that are secreted by the endocrine cells?

A
  • Gastrin
  • Sertotonin
  • Somatostatin
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3
Q

What does parietal cells secrete?

A
  • HCl

- IF

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4
Q

Pathways of Vagus n. stimulation of parietal cells (3)?

A

Vagus n. –> M3 (Acetylcholine receptor)
–> Stimulation of parietal cell secretion of HCl

Vagus n. –> ECL cell (enterochromaffin- like cell) –> H2 (Histamin receptor) –> Stimulation of parietal cell secretion of HCl

Vagus n. –> G cell –> CCK3 (Gastrin receptor) –> Stimulation of parietal cell secretion of HCl

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5
Q

Which other cell type acts on H2 receptor?

A

Mast cells

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6
Q

Where are ECL cells found?

A

In corpus and fundus.

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7
Q

Which other pathway fo G- cells stimulate?

A

ECL- cell pathway.

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8
Q

Pathway of G- cell?

A

G cell –> CCK3 (Gastrin receptor) –> Stimulation of parietal cell secretion of HCl

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9
Q

Pathway of ECL- cells?

A

ECL cell (enterochromaffin- like cell) –> H2 (Histamin receptor) –> Stimulation of parietal cell secretion of HCl

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10
Q

Mode of action of Aspirin (NSAID)

A

Inhibition of COX2, thereby inhibition of AA binding to PGE2 receptor –> lack of inhibition mode of action of H2 receptor.

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11
Q

Mode of action of somatostatin?

A

Inhibition of gastric acid secretion by action upon inhibition of gastrin.

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12
Q

Possible reactions to an H. pylori infection (6)?

A
  • Symtom free carrier 80%
  • Duodenal ulcer 12%
  • Chronic atrophic gastritis 4%
  • Gastric ulcer 2%
  • Gastric adenocaricnoma 1%
  • MALT lymphoma <1%
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13
Q

Mode of action of bicarbonate?

A

pH of bicarbonate is 7, while that of gastric acid is 2. HCO3- protects the mucous layer by making it harder for H+ to penetrate the mucous layer which protect the gastric epithelium.

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14
Q

Main cause of duodenal cancer?

A

H. pylori infection.

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15
Q

Two main causes of formation of gastric ulcer?

A
  1. H. pylori

2. NSAID

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16
Q

One method used for detection of H. pylori?

A

Measurement of urease activity.

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17
Q

How does H. pylori colonosation affect gastric acid secretion?

A

NH4+ will increase the pH –> decrease of Somatostatin –> Increase of Gastrin –> Stimulation of parietal cells –> Increased HCl

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18
Q

Which pathogenetic factors lead to increased accidity?

A
  • Urease

- OMP and outer membrane proteins

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19
Q

Pathogenetic factors leading to gastritis?

A
  • Flagella
  • Adhesion (adhesion fimbriae)
  • Porins
  • Toxins
    • CagA (Cytotoxin Associated Gene) 50- 70%
    • Vac (VACuolising toxin=
    • LPS (Lipopolysaccharide = endotoxin)
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20
Q

Pathway of H. pylori by CagA

A

H. pylori –> CagA –> IL-8 –> Neutrophils –> Neutrophil/ macrophage –> ROIs –> Type IV secretion system

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21
Q

By which pathway does H. pylori lead to alterations in mucous glycoproteins which leads to epithelial damage? (2)

A

H. pylori –> PLA2 –> Alterations in mucous glycoproteins –> Epithelial damage

H. pylori –> Urase, LPS, Porin –> Macrophage –> IL-1beta, TNFalfa
–> Alterations in mucous glycoproteins –> Epithelial damage

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22
Q

H. pylori with its pathogenetic factors will lead to hyperacidity which will lead to? (2)

A
  • Reflux (GERD)

- Duodenal cancer

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23
Q

Genetic predisposition eg. cytokine polymorphism will cause?

A

Mucosal atrophy (atrophic gastritis)

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24
Q

Mucosal atrophy (atrophic gastritis) may cause what? (2)

A
  • Gastric ulcer

- Gastric carcinoma

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25
Q

Pharmacologic inhibition of gastric acid secretion? (4)

A

H2 antagonist (Cimetidin, Ranitidin).

Prostaglandin analoges (Misoprostol) --> PGE/I-2 receptor 
--> Inhibition of H2

Proton- pump- inhibitors (Omeprazol, Losec) –> Inhibition of H+/ K+ pump.

Antacids (Al(OH)3, Mg(OH)2, CaCO3, NaHCO3) –> Bind HCl

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26
Q

Mode of action of Bizmut on H. pylori?

A

Bacteriostatic

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27
Q

Effect of Bizmut combined with Amoxicillin on H. pylori?

A

Bacteriocid

28
Q

Bizmut + Amoxicillin is combinde with?

A

Proton- pump- inhibitor (PPI)

29
Q

Problems in treatment of H. pylori?

A
  • Resistance

- Costs

30
Q

GERD

A

Gastro- Esophageal- Reflux- Disease

31
Q

Percentage of GERD that lead til serious complications?

A

10%

32
Q

Possible cause to reflux?

A

Disfunction of LES (Lower Esophageal Sphincter) due to:

  • Weakness
  • Sponatenous relaxation
33
Q

At which age does maturration of LES occur?

A

6 months

34
Q

Physiologic form of G to E reflux may be caused by:

A
  • Loose LES
  • Too much:
    • Eating
    • Swallowing of too much air (–> burping)
35
Q

GERD may lead to?

A
  • Vomiting
  • Foreful
  • Painful
  • Persistent, not onlu after eating
36
Q

Complications of GERD?

A

Inflammation: Reflux esophagitis
–> Barrets esophagus –> Esophageal cancer

Strictures –> Axhalasie or nutcracker esophagus

37
Q

Definition of Barrets esophagus?

A

Cuboidal epithelial metaplasia of the lower esophagus

normal type of epithelium of esophagus is sqamous non- keratinized ep.

38
Q

Which complications may be seen due to Barrets metaplasia?

A
  • Barrets ulcer

- Esophageal adenocarcinoma

39
Q

Definition of Achalasia?

A

Narrowing of esophagus.

(possible complaints: difficulty of swallowing solid food).

40
Q

Percentage that GERD lead to complications?

A

25%

41
Q

Which TLR is expressed by the flagellum of H. pylori?

A

TLR5

42
Q

Which TLR is expressed by endotoxin (LPS)?

A

TLR4

43
Q

How can TLR signaling be inhibited?

A

By miRNAs.

H. pylori –> Inflammation –>
miRNA activation –> Inhibition of inflammatory signaling (negative feedback)

44
Q

Which interleukins are produced by the H. pylori?

A

IL-1 and IL-6.

45
Q

Which genetic syndromes may have a role in development of colorectal cancer in the 10% of the population?

A
  • Familiar adenomatous polyposis (FAP) = Multiple papillary adenoma
  • Hereditary non- polyposis colorectal cancer (HNPCC)
46
Q

What may lead to HNPCC?

A

DNA micro satellite instability (MSI)

47
Q

What is a micro satellite?

A

2- 5 nucleotide which repeats 5- 50X. Has high mutation rate.

48
Q

Ususally DNA mismatch repair (MMR) enzyme corrects errors caused by DNA polymerase. In case of MMR deficiency, what might develop?

A

Micro satellite deficiency.

4 different mutations of MMR cause HNPCC.

49
Q

What is the patomechanism behind development of Polyposis coli?

A

Patomechanism is unknown. H. pylori eradication may cure it.

50
Q

Untreated FAP may lead to?

A

Increased risk of developing colon carcinoma by 100%, before the age of 40.

51
Q

Cause of FAP?

A

APC mutation.

APC: Adenomatous polyposis coli-= Tumour supressor gene.

52
Q

Diagnosis of colorectal carcinoma is done by?

A
  • Colonoscopy
  • Videocapsule endoscopy
  • Virtual endoscpoy
53
Q

Percentage of mortality in pancreatic cancer?

A

85%

54
Q

What might be the underlying cause of development of pancreatic cancer?

A
  • Chronic pancreatitis

- Cytokine polymorphism

55
Q

Underlying causes in development of IBD?

A
  • Inflammation

- Autoimmunity

56
Q

Difference in Crohn’s disease (CD) and Ulcerative colitis (US)?

A

Crohn’s disease: Illeitis terminalis - anywhere discontinous.

Ulcerative colitis (UC): Only colon - continous, ascending.

57
Q

What may Crohn’s disease lead to in the small intestine?

A

Stenosis of the small intestine and formation of fistulas.

58
Q

What is the endoscopic image in Crohn’s disease?

A

Cobbelstone pattern

59
Q

Which may be the causes leading to Crohn’s disease?

A

Genetic defects:

  • Family history
  • > 70 genes (intestinal immune system)
  • NOD2- CARD mutation, 205 of Crohn’s patients

Damage to the intestinal- barrier function:

  • NSAIDs
  • Intestinal- infections (Salmonella, E.coli)
  • Immune response against normal flora
60
Q

Abbreviation NOD2- CARD stands for?

A

Nucleotide- binding Oligomerization Domain containing 2- CAspase Recruitment Domain family member 15.

61
Q

Therapy of Crohn’s focuses on?

A

Inhibition of inflammatory (Th1) cytokines with antibodies.

  • TNF- alfa
  • IFN- gamma
  • IL- 2, 12
62
Q

Pathology Colitis ulcerosa

A
  • Only superficial mucosal damage

- Chronic disease –> Interstinal wall scarring, shortening of the colon.

63
Q

Pathomechanism of Colitis ulcerosa?

A
  • Autoimmunity
  • Intestinal bacteria: H2S, red meat/ alcohol sulfur content
  • Cigarette smoke: HCN (may be protective)
64
Q

Leading symptoms of Colitis ulcerosa?

A
  • Fever
  • Flatulence
  • Anemia
65
Q

Diagnosis of Colitis ulcerosa is made by?

A
  • Colonoscopy

- Histology

66
Q

Therapy for Colitis ulcerosa?

A
  • Anti- inflammatory drugs
  • Immunosuppression
  • Biologicals (antibodies: TNF- alfa, IFN- gamma, IL-2, 12)

Pathophysiology (14 decks)

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