stomach Flashcards

1
Q

morphological forms of gastritis

A

Catarrhal gastritis
Fibrinous gastritis
Phlegmonous gastritis
Necrotic (corrosive) gastritis
Hemorrhagic gastritis
Pseudomembranous gastritis

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2
Q

causes of gastritis

A

NSAIDS (Asprin)
Bacterial or viral infection e.g.: H. pylori, Salmonella, C. albicans, herpes virus
Alcohol
Smoking
Stress (trauma, burns, surgery)
Uremia
Chemotherapy drugs

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3
Q

features of gastritis

A

Epigastric or central pain
Vomiting
Acute upper GI haemorrhage

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4
Q

diagnosis of gastritis

A

Detailed history: foods taken, medication
Physical examination: pain when pressure applied to the epigastric region
Endoscopy- to rule out ulcer disease
Edematous mucosa, leukocytes infiltrating the mucosa

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5
Q

management of acute gastritis

A

Anti-emetic – Domperidone
Antacid – cimetidine
PPI Omeprazole 20mg
Spasmolytic
Prostaglandin E1 analog: protect stomach mucosa & inhibit gastric acid secretion

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6
Q

special forms of gastritis

A

Lymphocytic gastritis - Extremely rare

esosiniophlic gastroenteritis

giant fold gastritis - mentors disease (most common symptom associated is pain )

Gastritis in the context of Crohn’s disease

sarcoidosis + Tb - others

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7
Q

Lymphocytic gastritis

A

its a chronic gastritis Linked with celiac disease in children and in connection with H. pylori infection

dense infiltration of t lymphocytes
Treatment would be through H.Pylori eradication therapy and appropriate glutenfree diet

diagnosis - increased lymphocyte count
least 25 lymphocytes per 100 gastric epithelial cells is now required for the diagnosis.

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8
Q

types of cells in stomach

A

chief cells- pepsinogen
parietal cells- IF + ccl
mucous cells-

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9
Q

giant cell gastritis

A

Unknown cause although H.Pylori suspected to be triggering factor
Mucosal folds become enlarged: chief & parietal cells degenerate resulting in
hypoplasia (little/no acid output) → excessive mucus production
Most cases asymmtomatic: diarrhoea and intestinal protein loss with anaemia and
edema are rare
Usually discovered accidentally during endoscopic examination - folds remain stable,
even with maximum air insufflation
Treatment: folds may be removed via gastric resection.

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10
Q

eosiiniphilic gastroenteritis

A

parasite infection or an allergic reaction

In a large part of the cases, eosinophilia and elevated serum IgE
Histopathology - eosinophilic infiltration, crypt hyperplasia, villous atrophy, and
ulcerations
Management: Dietary measures and glucocorticoids, possibly supported by lowdose maintenance therapy

google:

  1. eosiniphic infiltrate (not just to stomach but most likely y stomach and duodenum but can be eaosophgus colone etc
  2. GI complaints, abdo pain, diarrhoea, weight los

A history of atopy or food allergies is often present.

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11
Q

tx of pernicious anemia

A

life long therapy of b12, and preparation for the eventual development of iron deficiency anemia

Moreover, these patients should be advised about possible gastrointestinal long-term consequences, such as gastric cancer and carcinoids.

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12
Q

haematological labs for pernicious anemia

A

A low haemoglobin level
High mean corpuscular volume (MCV)
High mean corpuscular haemoglobin (MCH)
Normal mean corpuscular haemoglobin concentration (MCHC)
Abnormally large and oval-shaped RBCs in the blood smear
Low vitamin B12 serum level
Low or normal folic acid serum level
Low reticulocyte count
Antibodies against intrinsic factor and/or parietal cell may be present in pernicious anaemia

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13
Q

symptoms of b12 deficiency

A

paraetsheisa
ataxia when walking
s.o.b
glossitis
psychiatric disttrbances

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14
Q

classification of chronic gastritis and how common

A

ABC

a- 5 %
b- 80%
c- 15%

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15
Q

antibodies found in autoimmune gastritis

A

Anticancaliculat parietal cell antibodies (PCA), H+/K+-ATPase antibodies and
Intrinsic factor antibodies (IFA)

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16
Q

labs for autoimmune gastritis

A

Lead to low/no HCL output, hypergastrinemia and pernicious anaemia

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17
Q

causes for the chemical gastritis

A

bile reflex following a gastrectomy

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18
Q

end result of chronic h.pylori infection

A

damage of the cells causing hypochlorydia - same as autoimmune

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19
Q

urease test

A

H.pylori , looks for the enzyme which converts urea into ammonia + co2,done at the same time as a gastroscopy to collect a sample and then you put the sample in a culture that contains urea and you will see an increase inPH

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20
Q

triple therapy

A

ppi + macrolide+ amoxicillin

21
Q

quadruple

A

PPI + antacid (bismuth salt) 120mg/4x daily +
metronidazole 3x 500mg daily + tetracycline 500mg/4times day (1 week)

22
Q

mucosal protector

A

sucralfate 100mg

23
Q

rf for gastric cancer

A

chronic gastritis
pernicious anemia
smoking
alcohol
Japan (food) Dietary nitrosamines
Blood group A
Adenomatous polyps
Achlorhydria (as seen in Menetrier’s disease)
diet low in fruits and veg (however too much can damage the lininging )

24
Q

Gastric carcinoma can be split up into two types of cancer:

A
  1. intestinal (associated with h.pylori, smoking) chlorhydria and chronic gastritis

The intestinal-type is the end-result of an inflammatory process that progresses from
chronic gastritis to atrophic gastritis and finally to intestinal metaplasia and dysplasia.

more common in elederly men

Commonly on lesser curvature of the stomach

  1. diffuse (not associated with h.pylori- contradictory ? associated with signet cells.

the leather bottle stomach and is seen more in women

25
Q

Krucken berg tumour

A

These cells readily secrete mucin and readily metastasize to the ovaries.
Patients often present with abdominal bloating, ascites or pain during intercourse.

26
Q

linitis plastica

A

iffuse malignant infiltration of the stomach.
The muscles of the stomach wall become thicker and more rigid. The stomach holds less food as it cannot stretch and transition of food is slower due to decreased relaxation of the stomach
It is sometimes known as leather bottle stomach

27
Q

presentation

A

Anaemia (iron deficient)
Loss of weight
Anorexia (early satiety)
Recent onset/progression of symptoms
Melaena/haematemesis
Swallowing difficulty (dysphagia)

signs
ascites
hepatomegaly - metasistis
vrichows node
siste rmary joseph
bloating- ovarian
acanthuses Nigricans

28
Q

tx gastric cancer

A

n gastric cancer, locally invasive disease is managed with partial or total gastrectomy. Moreover, neoadjuvant chemotherapy has been shown to improve outcomes in those undergoing surgery. There is no scope for radiotherapy alone, however when used in combination with chemotherapy (fluorouracil) can be used as a potential curative in a non-surgical candidate.

In advanced cases, palliation can be managed with:

Surgery – To relieve obstruction or haemorrhage
Chemotherapy – Improves quality of life

29
Q

worser prognosis stomach

A

proximally placed tumours have a worse prognosis than distal ones - due
to thinner musularis mucosae (easier invasion) and that they are in a more advanced
staged at the time of presentation (late presentation of symptoms)

30
Q

types of advanced gastric cancer

A

Polypoid fungating: may grow very large but tend to have a better
prognosis

malignant ulcer- looks like benign but has a ncetroci centre

Infiltrating carcinomas:- leather bottle VERY POOR PROFNOIS

31
Q

signed ring cell

A

infiltrating carcinomas where large mucin droplets displace the nuclei
laterally producing the so-called ‘signet ring appearance’.

32
Q

what do most stomach tumours look like under microscope

A

well differentiated apart form the signet ring cell which is the infiltatrtive type

33
Q

diagnos s

A

ANEMIA
FECAL OCCUTLS BLOOD
ENDOSCOPY + BIOPSYS

34
Q

SURGERY FOR GASTRIC

A

gastrojejunostomY - completely block of duodenum

partial or total gastrectomy which involves removing the lN’s and fatty tissue

35
Q

NB most common cancers rof the stomach

A

adenocarcinoma, then lymphoma then SCC

36
Q

NB lymphoma

A

gastric lymphoma they require only chemotherapy and no
surgical resection - since they are very sensitive to it so we don’t need to risk surgery

37
Q

What diseases can present with massive haematochezia

A

ulcerative colitis and diverticulosis

37
Q

What diseases can present with massive haematochezia

A

ulcerative colitis and diverticulosis

38
Q

classification of ulcers endoscopically

A

forest

39
Q

pneumopertioneum is a classic sign of

A

perfrated gastric ulcer

40
Q

where can heterotopic gastric mucosa be found?

A

The proximal esophagus
b. Gastric metaplasia in the duodenum
c. Within a Meckel’s diverticulum
d. In the rectum

41
Q

Which is the most common type of fistula formation in peptic ulcer disease?

A

Which is the most common type of fistula formation in peptic ulcer disease?
Gastrocolic fistula. A gastric ulcer of the greater curve may cause a gastrocolic fistula.

42
Q

forest classifcation how many types

A

3

  1. active bleed, spurting, oozing
  2. recent , visable vessel, adherant clot, flat spot
  3. not bleeding
43
Q

vagotomy

A

medical intervention to interrupt signals carried by your vagus nerve. Your vagus nerve communicates with many organs in your body. In current medical practice, a vagotomy usually means cutting the branch of the vagus nerve that tells your stomach to secrete gastric acid.

44
Q

what are the classifications we use in ulcers

A

forest

johnsons

45
Q

how mnay stages does johnson have

A

5

46
Q

how mnay stages does johnson have

A

5

47
Q

which ulcers are associated with acid hypersecretion

A

types 2 + 3

48
Q

j

A