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PHYSIOLOGY GIS > lec 7 > Flashcards

lec 7 Flashcards

1
Q

types of peptic ulcer.

A

Gastric and duodenal ulcers

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2
Q

Causes of peptic ulcer

A

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

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3
Q

Stress-relatedmucosal disease (SRMD) includes

A

stress-related injury (superficialmucosal damage)

stress ulcers (focal deep mucosal damage).

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4
Q

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

A

mucosal ischemia

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5
Q

Stress-related mucosal damage onset is

A

usually acute

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6
Q

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

A

the acid-producing body and fundus

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7
Q

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

A

low mesenteric perfusion rather than HP or NSAIDs

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8
Q

Stress-related mucosal damage in a

A

small proportion of patients may progress to deep ulceration and hemorrhage

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9
Q

Less common causes of peptic ulceration include

A
  1. Zollinger- Ellison syndrome (ZES),
  2. cancer chemotherapy/ radiation,
  3. illicit-drug
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10
Q

illicit-drug cause

A

vascular insufficiency.

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11
Q

ZES is caused

A

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

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12
Q

Helicobacter pylorus normally resides in

A

in the human stomach

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13
Q

Helicobacter pylorus is transmitted via

A

the fecal-oral route or

through ingestion of fecal-contaminated water or food

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14
Q

Helicobacter pylorus Infection is more common in developing countries because

A

of crowded conditions and

 the presence of contaminated food and water

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15
Q

Helicobacter pylorus Cellular active infection is usually

A

asymptomatic and

leads to chronic active gastritis

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16
Q

Helicobacter pylorus colonization does not necessarily reflect an

A

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

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17
Q

Helicobacter pylorus Cellular invasion is

A

necessary for an active infection

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18
Q

Helicobacter pylorus are

A

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

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19
Q

) multiple flagella that initially invade the

A

gastric antrum but migrates to the more

proximal sections

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20
Q

Helicobacter pylori causes

A

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

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21
Q

The outcome of the disease depends on

A

environmental factors,
the host and
the bacterium

22
Q

Bacterial factors in Helicobacter pylori pathogenesis

A
  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
23
Q

Intra-bacterial urease activity

A

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

24
Q

Extra-bacterial urease activity

A

one note

25
Q

UreI

A

permits urea entry

only under acidic conditions (5.0-7.0 pH

26
Q

Urease will

A

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

27
Q

Flagella considered

A

early stage colonization/virulence factor

28
Q

movement toward epithelium cells

A

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

29
Q

Adhesins

A

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

30
Q

the interaction of bacterial adhesins with cellular receptors

A

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

31
Q

Types of adhesin

A
  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)
32
Q

Blood group antigen binding adhesin (BabA & BabB)

A

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

33
Q

Cytotoxin-associated gene A (CagA) associated with

A

acute gastritis, gastric ulcer, and gastric cancer development

34
Q

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

A 
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
35
Q

cag A PAI It contains

A

cagI and cagII region

36
Q

cagI and cagII contain a gene involve

in coding

A

Type IV secretion system (T4SS

37
Q

The cagA gene is found

A

within cagI, but not cagII.

38
Q

Type IV secretion system (T4SS)

A

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

39
Q

ما هي فوائد

Disruptions of tight junctions للبكتيريا

A

a) allow the bacterial cells access to the basement membrane

b. beneficial for colonization and persistence at the host epithelial surface

40
Q

ما هي اضرار Disruptions of tight junctions للخلايا ال host

A 
abnormal receptor activation 
\+
stimulation of signaling pathways involved in
inflammation, 
proliferation, 
migration, and 
invasion
41
Q

Disruptions of tight junctions causes

A
  1. expose extracellular matrix proteins

2. abnormal receptor activation

42
Q

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

A 
stimulation of signaling pathways involved in
inflammation, 
proliferation, 
migration, and 
invasion
43
Q

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

A

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

44
Q

The multiplication of Helicobacter pylori within cells provides

A
  1. resistance to antibiotic

2. impact on its biological life cycle

45
Q

Helicobacter pylori capacity to invade and survive within epithelial
cells

A
  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
46
Q

اهمية وجود الحويصلة

A
  1. the location of replication

2. the degradation of the replicating bacteria after fusion with lysosomes

47
Q

CagA can alter host cell signaling in

A

phosphorylation-dependent

2.phosphorylation-independent manner

48
Q

phosphorylation-dependent affects the:

A

.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

49
Q

phosphorylation-independent manner

A

the proliferation and inflammation of cells (neutrophil

infiltration) via the Akt signaling pathway, which activates NF- κB and β-cateni

50
Q

The effects of Vacuolating cytotoxinA (Vac A)]

A

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

51
Q

The effects of Vacuolating cytotoxinA (Vac A)]

A

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,

PHYSIOLOGY GIS (17 decks)

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