lec 7

Question 1

types of peptic ulcer.

Answer 1

Gastric and duodenal ulcers

Question 2

Causes of peptic ulcer

Answer 2

(1) Helicobacter Pylori (HP) infection,
(2) Use of non-steroid anti-inflammatory Drugs (NSAIDs)
(3) Stress-relatedmucosal disease (SRMD)

Question 3

Stress-relatedmucosal disease (SRMD) includes

Answer 3

stress-related injury (superficialmucosal damage)

stress ulcers (focal deep mucosal damage).

Question 4

Both types of Stress-relatedmucosal disease (SRMD) are caused by

Answer 4

mucosal ischemia

Question 5

Stress-related mucosal damage onset is

Answer 5

usually acute

Question 6

Both types of Stress-relatedmucosal disease (SRMD) show a propensity ميلfor

Answer 6

the acid-producing body and fundus

Question 7

Stress-related mucosal damage is thought to be caused by factors such as

Answer 7

low mesenteric perfusion rather than HP or NSAIDs

Question 8

Stress-related mucosal damage in a

Answer 8

small proportion of patients may progress to deep ulceration and hemorrhage

Question 9

Less common causes of peptic ulceration include

Answer 9

1. Zollinger- Ellison syndrome (ZES),
2. cancer chemotherapy/ radiation,
3. illicit-drug

Question 10

illicit-drug cause

Answer 10

vascular insufficiency.

Question 11

ZES is caused

Answer 11

by a gastrin-producing tumor called a gastrinoma found in pancreases and
results in gastric acid hyper-secretion.

Question 12

Helicobacter pylorus normally resides in

Answer 12

in the human stomach

Question 13

Helicobacter pylorus is transmitted via

Answer 13

the fecal-oral route or

through ingestion of fecal-contaminated water or food

Question 14

Helicobacter pylorus Infection is more common in developing countries because

Answer 14

of crowded conditions and

 the presence of contaminated food and water

Question 15

Helicobacter pylorus Cellular active infection is usually

Answer 15

asymptomatic and

leads to chronic active gastritis

Question 16

Helicobacter pylorus colonization does not necessarily reflect an

Answer 16

active infection since the organism can attach itself to the gastric epithelium without invading
cells

Question 17

Helicobacter pylorus Cellular invasion is

Answer 17

necessary for an active infection

Question 18

Helicobacter pylorus are

Answer 18

(a) gram-negative
(b) micro-aerophilic
(c) rod shape
(d) S-shaped bacterium
(e) multiple flagella

Question 19

) multiple flagella that initially invade the

Answer 19

gastric antrum but migrates to the more

proximal sections

Question 20

Helicobacter pylori causes

Answer 20

75% of gastric ulcers
90% of duodenal ulcers
mucosa-associated lymphoid tissue (MALT) lymphoma
adenocarcinoma

Question 21

The outcome of the disease depends on

Answer 21

environmental factors,
the host and
the bacterium

Question 22

Bacterial factors in Helicobacter pylori pathogenesis

Answer 22

1. Urease and survival under acidic stomach conditions
2. Flagella and movement toward epithelium cells
3. Adhesins and attachment to cellular surface receptors
4. Toxin and host tissue damage

Question 23

Intra-bacterial urease activity

Answer 23

is regulated by the proton-gated urea channel (UreI)

Question 24

Extra-bacterial urease activity

Answer 24

one note

Question 25

UreI

Answer 25

permits urea entry | only under acidic conditions (5.0-7.0 pH

Question 26

Urease will

Answer 26

liquefy the mucous and Decrease elasticity make Hp to swim easily through it

Question 27

Flagella considered

Answer 27

early stage colonization/virulence factor

Question 28

movement toward epithelium cells

Answer 28

Helicobacter pylori moves through the gastric mucosa gel layer to the basal layer where the pH value is close to 7.0 by the action of 4–7 polar

Question 29

Adhesins

Answer 29

1.attach to the surface of the bacterium 2.can recognize the structures of glycans expressed on the surface of gastric epithelial cell 3.

Question 30

the interaction of bacterial adhesins with cellular receptors

Answer 30

1.protects the bacteria from displacement from the stomach by forces such as those generated by peristalsis and gastric emptying 2.bacteria get metabolic substrates and nutrients to improve growth through releasing toxins to damage the host cells

Question 31

Types of adhesin

Answer 31

1. Blood group antigen binding adhesin (BabA & BabB) 2. sialic acid-binding adhesin (SabA) 3. Neutrophil activating protein A (NAP) 4. Heat shock protein 60 (Hsp60) 5. Adherence-associated lipoproteins (AlpA & AlpB) 6. Lacdinac-binding adhesin (LabA)

Question 32

Blood group antigen binding adhesin (BabA & BabB)

Answer 32

The structure of the BabA receptor is like the O type blood antigen, and the statistics of epidemiology reveal the correlation between type O blood and gastric related diseases

Question 33

Cytotoxin-associated gene A (CagA) associated with

Answer 33

acute gastritis, gastric ulcer, and gastric cancer development

Question 34

The Cytotoxin-associated gene A pathogenicity island (cag A PAI) is located on

Answer 34

``` chromosome in H. pylori, It is 35–40 kilobase pairs of DNA (kb), It contains more than 30 genes It represents the pathogenicity island of H. pylor ```

Question 35

cag A PAI It contains

Answer 35

cagI and cagII region

Question 36

cagI and cagII contain a gene involve | in coding

Answer 36

Type IV secretion system (T4SS

Question 37

The cagA gene is found

Answer 37

within cagI, but not cagII.

Question 38

Type IV secretion system (T4SS)

Answer 38

forms needle-like pili, who’s binding to the integrin in injection of the Cag A oncoprotein.

Question 39

ما هي فوائد | Disruptions of tight junctions للبكتيريا

Answer 39

a) allow the bacterial cells access to the basement membrane | b. beneficial for colonization and persistence at the host epithelial surface

Question 40

ما هي اضرار Disruptions of tight junctions للخلايا ال host

Answer 40

``` abnormal receptor activation + stimulation of signaling pathways involved in inflammation, proliferation, migration, and invasion ```

Question 41

Disruptions of tight junctions causes

Answer 41

1. expose extracellular matrix proteins | 2. abnormal receptor activation

Question 42

ما الذي يحدد الconsequences of disease and result in disease development

Answer 42

``` stimulation of signaling pathways involved in inflammation, proliferation, migration, and invasion ```

Question 43

The pathogenicity of bacteria that colonize the human mucosa is influenced by

Answer 43

H.P capacity to invade and survive within epithelial cellsالبكتيريا كلها جوا الHOST 2.Helicobacter pylori internalization the virulence proteins Cag A and Vac Aالبكتيريا تدخل العامل الامراضي

Question 44

The multiplication of Helicobacter pylori within cells provides

Answer 44

1. resistance to antibiotic | 2. impact on its biological life cycle

Question 45

Helicobacter pylori capacity to invade and survive within epithelial cells

Answer 45

1. ability and rates of Helicobacter pylori positive correlation disease severity gastric cancer and ulcers were higher than the rate of strains found in gastritis 2. بس دخل بتحيط نفسها بحويصله تتكاثر داخلها

Question 46

اهمية وجود الحويصلة

Answer 46

1. the location of replication | 2. the degradation of the replicating bacteria after fusion with lysosomes

Question 47

CagA can alter host cell signaling in

Answer 47

phosphorylation-dependent | 2.phosphorylation-independent manner

Question 48

phosphorylation-dependent affects the:

Answer 48

.1host cell adhesion, spreading, and migration of 2.Host cell induction of Nitric oxide and Cyclooxygenase (COX-2 3.stimulating the gastric epithelium cells to secrete IL-8 (Interleukin-8) 2.NF-κB 4. سلايد 15

Question 49

phosphorylation-independent manner

Answer 49

the proliferation and inflammation of cells (neutrophil | infiltration) via the Akt signaling pathway, which activates NF- κB and β-cateni

Question 50

The effects of Vacuolating cytotoxinA (Vac A)]

Answer 50

1.membrane channel formation 2.vacuolization 3.Previous studies also indicate that VacA may affect 4.It also can induce acute inflammatory responses t

Question 51

The effects of Vacuolating cytotoxinA (Vac A)]

Answer 51

1.membrane channel formation 2.vacuolization 3.Previous studies also indicate that VacA may affect 4.It also can induce acute inflammatory responses t 5.disturb epithelial barrier,