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PHA 223 > PUD > Flashcards

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
Q

where is h.pylori found ?

A

in the mucus, on the surface and occasionally inside epithelial cells

26
Q

what effect does the h. pylori have?

A

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
Q

what does the intensity of the h. pylori inflamation depend on?

A

strain and host factors/ duration of infection/ location

28
Q

what does the area of h. pylori colonisation depend on?

A

distribution of acidity in the stomach

29
Q

where does h. pylori produce in people with large amounts of acid?

A

near the pyloric anterum- exit

30
Q

where does the h. pylori colonise with people producing small amounts of acid?

A

in the stomach

31
Q

what happens when h pylori colonizes other areas of the stomach?

A

inflam response can result in atrophy

32
Q

what happens in h. pylori inflamation?

A
  • 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
Q

what can Hypergastrinemia result from?

A

H.Pylori reduction of D-cells omatostatin production and increasing G-cell gastrin production

34
Q

what is Gastric metaplasia?

A

apperaracne of clusters in epithelial cells in gastric pheno type in non-gastric epithelium

35
Q

inhibition of COX 1/2 causes what?

A
  • decreases mucus and bicarbonate production
  • mucusoal blood flow/ roliferation
  • inc gastric acid sec
36
Q

what does inhibition of platelt activity by NSAIDS do?

A

increase the risk of bleeding from those ulcers

37
Q

what are other causes of h. pylori ulcers?

A

smoking/ alcohol/ co-morbidities

38
Q

how many patiensts are symptomatic with PUD?

A

1/3

39
Q

what are the symptoms of PUD?

A

symptoms occur when stomach empty/ worse when wakening

may worsen when they eat

40
Q

what are the 4 peptic ulcer complications?

A
  1. UpperGIbleeding:
  2. Perforation:
  3. Pyloricstenosis
  4. Penetration
41
Q

how do you diagnose peptic ulcers?

A

1- urea tests
2- blood tests
3- stool
4-endoscopy

PHA 223 (42 decks)

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