Peptic Ulcer [Written Summary] PDF (NICE)

Peptic Ulcer [Written Summary] PDF

Peptic Ulcer (1)

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Summary Topics:

  1. Blood supply & venous drainage of stomach
  2. Nerve supply of stomach
  3. Histology of the stomach
  4. Surgical Physiology >>> Gastric motility, Gastric secretion,
  5. Phases of gastric secretion>>> 1/ Cephalic (neural) phase , 2/ Gastric Phase , 3/ Intestinal Phase
  6. Pathology of Peptic Ulcer
  7. Special Forms of Peptic Ulceration: 1/ Stress ulcer2/ Curling’s ulcer , 3/ Cushing’s ulcer
  8. Sites: 1) Duodenum,  2) Stomach , 3) Esophagus , 4) Jejunum5) Meikle’s diverticulum
  9. Etiology >> 1/ Acute peptic ulcer  2/ Chronic peptic ulcer
  10. and more…….
    N.B
    G.U in Post. wall → erode to pancreas
    G.U in Ant. wall → erode to liver

File Size: 637 KB

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Sample of the summary::

( 17 pages )

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Peptic Ulcer

Blood supply & venous drainage of stomach:

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Nerve supply of stomach: 1/ Sympathetic

2/ Parasympathetic:

– ant.vagal trunk → hepatic branch → descend along lesser c urvature &

supply ant. wall of stomach

– post.vagal trunk → coelic branch

→ supply back wall of stomach

Vagus

⅔ ⅓

Read More

Ant & Post vagus hepatic branch celiac b. Stomach liver & gall bladder -pancreas

-S.Intestine -transverse

colon

Histology:

1/ Columnar epith :

Lines the whole stomach

2/ Cardiac gland:

Secrete mucous and electrolytes

Occupy a small ring around the oesophagogastric junction

3/ Oxyntic glands:

Occupy the fundus and body of stomach

a- parietal cells:

produce H+ & intrinsic factor

it is double its # in duodenal ulcer & 4х in Zollinger Ellison syndrome its # is ↓ in gastric ulcer b- peptic (chief) cells: in the fundus &

produce pepsinogen

4/ Pyloric glands: In the antrum

Secrete mucous & electrolytes

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5/ G-cells:

In the antrum

Secrete gastrin

Its # increase only in duodenal ulcer

Surgical Physiology:

1/ Gastric motility:

Body & fundus act as a reservoir for food.

Antrum acts as a mill, mix & grind the food & expel it to the duodenum.

Gastric motility is controlled by intrinsic neural plexus which are regulated by the extrinsic nerve supply (vagus) Truncal vagotomy affects & reduces gastric motility. Also, sympathetic n. inhibit gastric motility.

2/ Gastric secretion:

 Mucus is secreted in all regions of stomach & protects surface

epith. against acid and pepsin.

 Acid & pepsin secretion is regulated by a neurocrine, endocrine

& paracrine factors.

 Neurocrine: Ach from vagus

 Endocrine: Gastrin from antrum

 Paracrine: Histamine from cells near to parietal or peptic cells  Parietal (w secrete H+) & pepsin (w secrete pepsin) cells has

specific receptor for each of the 3 stimulants.

 The action of each stimulant is potentiated by the other two. Eg;

Gastrin & Ach release histamine from mucosal stares.

Ach stimulate secretion by inhibit the release of somatostatin. In truncal vagotomy not only Ach stimulation is affected, but also gastrin & histamine efficacy is reduced.

Phases of gastric secretion: 1/ Cephalic (neural) phase:

 Sight, smell, taste or though stimulate vagal center  Vagus → stimulate pept ic & parietal cells (direct) → stimulate gastrin release from antrum (indirect)

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2/ Gastric Phase:

 Distention of gastric antrum & products of protein digestion

stimulate gastrin release from antral mucosa.

3/ Intestinal Phase:

 Food in small bowel release enteroxyntin (duodenal gastrin)

that increases acid release.

Pathology:

Due to imbalance between gastric acid – pepsin secretion and the ability of the GI mucosa to define against them. This imbalance occurs due to:

a. Hyper secretion of acid and pepsin. (D.U) b. Defect in mucosal defense. (G.U) c. H.pylori infection.

Special Forms of Peptic Ulceration: 1/ Stress ulcer:

 Occur after major surgery, trauma or sever illness.

 Multiple small superficial ulcers in the stomach or duodenum.

2/ Curling ’s ulcer:

 In patient with sever burns.  In the duodenum.

3/ Cushing’s ulcer:

 In patient with neuro-surgical illness or head injury.  In both stomach or duodenum.

Sites:

1) Duodenum:

o The 1 st part of the duodenum is the commonest. o If it is in the Ant. surfac e → perforation.

o If it is in the Post. surface → He by erosion of arteries.

2) Stomach:

o Type 1 (1ry GU): often in the lesser curvature. o Type 2: same as type 1 plus a D.U.

o Type 3: in pyloric channel or prepyloric area.

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3) Esophagus:

o At the lower end.

o Due to reflux of acid and pepsin from the stomach.

4) Jejunum:

o Zollinger-Ellison syndrome. o After gastro-jejunostomy.

5) Meikle’s diverticulum:

o Due to the presence of ectopic gastric mucosa.

N.B

G.U in Post. wall → erode to pancreas G.U in Ant. wall → ero de to liver

Etiology:

1/ Acute peptic ulcer:

 May be without apparent cause.

 Or associated with ingestion of alcohol, NSAID or steroidal

therapy.

 Also it can be associated with stress ulcer, curling’s ulcer or

cushing’s ulcer.

2/ Chronic peptic ulcer:

I. Genetic & blood group

Blood group O 3x likely to get D.U α¹ – antitrypsine deficiency

II. Neurogenic therapy

Vagal stimulation → hyper secretion & hyper motility ← Stress & anxiety +→ vagus

III. Accessory causes (factors)

Alcohol

Excessive smoking Vitamine deficiency

And More………………..

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