PUD Flashcards

1
Q

What is the gastro intestinal system responsible for?

A

breakdown and digestion of foods, absorption of nutrients from foods and the removal of wastes

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2
Q

what does the GIS consist of?

A

gastro intestinal tract and accessory glands
tract= mouth/ ossiphageous/ stomach/ small and large intestine/ anus
assessory organs- liver/ pancreases and gallbladder

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3
Q

what does a cross section of GIT look like?

A

tube surrounded by mucosa (innermost), submucosa, muscalaris and serosa

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4
Q

what is dyspepsia?

A

upper GIT symptoms which are present for more than 4 weeks

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5
Q

what are the symptoms of dyspepsia?

A

upper abdominal pain or discomfort/ acid reflux/ heart burn/ nausea vomiting

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6
Q

what could symptoms of acid reflux and heartburn also be?

A

GURD

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7
Q

what symptoms require referal for dyspepsia?

A
  • Weightloss
  • Iron-deficiency anaemia
  • GIbleeding
  • Persistent vomiting
  • Dysphagia
  • Epigastricmass
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8
Q

what are ulcers?

A

they are open sores (leisons) on an epithelial tissue caused by superficial loss of tissue

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9
Q

where are ulcers found?

A

on the skin surface ( foot) or on mucus membranes such as the stomach or mouth

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10
Q

what are ulcers usually a result of?

A

arterial and venous disease (irregular blood flow and circulation)

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11
Q

what is a peptic ulcer?

A

it is a sore of the ailmentary canal mucosa- mucosa is exposed to gastric acid
it penetrates through the thick layers of the mucosa

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12
Q

where does a duodenal ulcer occur?

A

first part of the intestines after the pylorus of the stomach

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13
Q

what is the difference between gastric and duodenal ulcer?

A
duodenal :pain relieved by meal
occurs 2/3 hr after meal
dark stool
gastric: pain inc by meal
occurs 30-1 hour after meal
not as common
vomiting occurs
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14
Q

what is in the inner surface of the stomach?

A

lined by mucus membrane ( gastric mucosa )

this mucosa is covered by a thick layer of mucus

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15
Q

what is the role of gastric mucus?

A

lubrication
movement
protective layer over the epithelial lining against own enzymes

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16
Q

what are the types of gastric cells?

A

•Mucus- secreting cells ecretes gel forming mucin.
•Parietal cells secrete HCl, intrinsic factor ,bicarbonate ions.
•Chief cell produces and secretes pepsinogen and gastric lipase.
•Delta-cell(D-cell) produces and secretes somatostatin, which acts directly and inhibits the acid-producing parietal cells
.•Gastrin cells (Gcells) secrete gastrin, which binds to CCK2 receptor on parietal cells and enterochromafin like cells (ECLcells)➔HCL secretion.
•ECL cell synthesizes and secretes histamine in response to stimulation by gastrin.

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17
Q

how does acid secretion work?

A

h+/k+ ATPase or proton pump

18
Q

how is acid secretion controlled?

A

it is controlled through 3 types of receptors:
ACH is controlled by m3
histamine by H2
gastrin by CCK2

19
Q

how is gastrin secretion from parietal cells regulated?

A

regulation of gastrin/ histamine/ ach/ somastatin

20
Q

what inhibits gastric secretion?

A

somastatin and prostaglandins

21
Q

where is somastatin secreted?

A

by the delta cells in the pylorium, duodeum and the pancreatic islets

22
Q

what causes peptic ulcers?

A

1- hylercobacter pylori

2- NSAIDS

23
Q

what are the risk factors of using NSAIDS?

A
history of peptic ulcers/ bleeding
age -60+
co- admin of NSAIDs
high doses NSAIDS
treatment with anticoagulants or glucocortsteroids
24
Q

what risk factors make you more susceptible for developing peptic ulcers?

A

family history
smoking
excessive alcohol use

25
where is h.pylori found ?
in the mucus, on the surface and occasionally inside epithelial cells
26
what effect does the h. pylori have?
affects the lining of the stomach by several mechanisms: 1-uses chemotaxis - avoid low ph areas 2-neutralises acids by producing large amounts of ureases (urea=co2 +nh3)
27
what does the intensity of the h. pylori inflamation depend on?
strain and host factors/ duration of infection/ location
28
what does the area of h. pylori colonisation depend on?
distribution of acidity in the stomach
29
where does h. pylori produce in people with large amounts of acid?
near the pyloric anterum- exit
30
where does the h. pylori colonise with people producing small amounts of acid?
in the stomach
31
what happens when h pylori colonizes other areas of the stomach?
inflam response can result in atrophy
32
what happens in h. pylori inflamation?
* reduces the number of somatostatin-producing cells(D-cells)causing hypergastrinemia. * increases gastric acid secretion➔ * causes the appearance of gastric metaplasia➔ * Further infection by H. Pylori causing duodenit is followed by peptic ulcer formation.
33
what can Hypergastrinemia result from?
H.Pylori reduction of D-cells omatostatin production and increasing G-cell gastrin production
34
what is Gastric metaplasia?
apperaracne of clusters in epithelial cells in gastric pheno type in non-gastric epithelium
35
inhibition of COX 1/2 causes what?
- decreases mucus and bicarbonate production - mucusoal blood flow/ roliferation - inc gastric acid sec
36
what does inhibition of platelt activity by NSAIDS do?
increase the risk of bleeding from those ulcers
37
what are other causes of h. pylori ulcers?
smoking/ alcohol/ co-morbidities
38
how many patiensts are symptomatic with PUD?
1/3
39
what are the symptoms of PUD?
symptoms occur when stomach empty/ worse when wakening | may worsen when they eat
40
what are the 4 peptic ulcer complications?
1. UpperGIbleeding: 2. Perforation: 3. Pyloricstenosis 4. Penetration
41
how do you diagnose peptic ulcers?
1- urea tests 2- blood tests 3- stool 4-endoscopy