Stomach and small intestine Flashcards

1
Q

What are the causes of acute gastritis ?

A

– Alcohol
– Drugs such as NSAIDs, steroids
– Smoking
– Corrosives (acids and alkalis)
– Stress such as Shock, trauma, ischaemia, burns
– Uraemia
– Gastric irradiation

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2
Q

What is the presentation of acute gastritis ?

A

– Epigastric pain
– N&V
– Anaemia (from bleeding)
– Haematemesis
– Melaena

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3
Q

What is the pathophysiology of chronic gastritis ?

A

It is characterised by non-erosive chronic mucosal changes causing mucosal atrophy and epithelial metaplasia which has a risk of causing gastric carcinoma through dysplasia.

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4
Q

What are the three main types of chronic gastritis syndromes?

A

– Helicobacter-associated gastritis
– Autoimmune chronic gastritis
– Chemical / reflux gastritis

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5
Q

What is peptic ulcer ?

A

Peptic ulcers are open sores that develop on the inside lining of the stomach and the upper portion of small intestine.

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6
Q

What is gastric ulcer ?

A

These are ulcers that forms along the lesser curvature of the stomach and gastric antrum.

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7
Q

What is duodenal ulcer ?

A

These are ulcers at the first part of duodenal bulb.

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8
Q

What are erosive gastric ulcers ?

A

These are acute inflammation of the stomach that do not extend beyond the muscularis mucosae.

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9
Q

When to suspect cancer in GI ulcers ?

A

When the ulcers are present in atypical locations.

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10
Q

What are the causes of peptic ulcers ?

A
  • Helicobacter Pylori
  • NSAID use
  • Idiopathic
  • Zollinger-Ellison
  • Viral Infections
  • Cushing’s Ulcer
  • Curling’s Ulcer
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11
Q

What is the clinical presentation of PUD ?

A

Patients commonly presents with epigastric pain worsened by food and hunger. They often have waterbrash and heartburn due to acid reflux or ulcers itself.

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12
Q

What are the ALARM symptoms of PUD ?

A

A- Anaemia
L- Loss of wieght
A- Anorexia and early satiety.
R- recent onset
M- Melina and hematemesis

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13
Q

What are the complications of PUD ?

A

– Gastric outlet obstruction
– Penetration and fistulisation
– Perforation  peritonitis

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14
Q

What are the bedside investigations in PUD ?

A

– Vital Signs
– Blatchford Score

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15
Q

What are the blood works in PUD ?

A
  • FBC and cross matching.
  • urea
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16
Q

What is the radiological study in peptic ulcer ?

A

Erect CXR

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17
Q

What is the purpose of OGD in PUD?

A

It is both diagnostic and therapeutic. It can be used to do rapid urea test ( CLO test) . The OGD can be used to collect tissue for biopsy and H. pylori pathology. It can also be used for hemostasis in active ulcers.

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18
Q

What are the ivestigations in H. pylori ?

A

– Urea Breath Test
– Serum Antigen Test
– Stool Antigen Test

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19
Q

What is the pathophysiology of H.Pyllori gastric carcinoma ?

A

Chronic active superficial gastritis progress to atrophic gastritis. which will gradually cause intestinal metaplasia, dysplasia and finally gastric adenocarcinoma.

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20
Q

What are the preventive measures in PUD ?

A

smoking and alcohol cessation.

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21
Q

What is the key goal of acute an emergent management of PUD ?

A

The bleeding should be managed medically or endoscopically.

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22
Q

What is the management of symptomatic non-bleeding PUD ?

A
  • Proton Pump Inhibitors
  • H2 antagonists Ranitidine.
  • Antacids
23
Q

What are the elements of triple therapy for H. Pylori ?

A

BD PPI + x 2 Antibiotics BD for 14 days:
* Esomeprazole 40mg BD
* Amoxicillin 1g BD / Metronidazole for penicillin allergy.
* Clarithromycin 500mg BD x14 days

24
Q

What are the elements of quadruple therapy for H. Pylori ?

A

– BD PPI + x2 Antibiotics + Bismuth x10 days
* Esomprazole 40mg BD
* Metronidazole + Tetracycline
* Bismuth

25
Q

What are the clinical features of Zollinger- Ellison syndrome ?

A
  • Associated with MEN1
  • Clinical & Laboratory Features are
    1. Duodenal Ulcers (no H Pylori)-
    failure to heal with PPI/H2
    2. Diarrhoea
    3. Hypergastraemia
    4. Hypercalcaemia
    5. Endocrinopathy
26
Q

What is pyloric stenosis ?

A

It is an idiopathic thickened pyloric muscles causing stenosis and obstruction to food. It is typically seen in infants. They present with non-belious vomiting, hunger, weight loss, and dehydration. The management of choice is surgery.

27
Q

What is the triad seen in pyloric stenosis ?

A

Projectile vomiting, visible peristalsis, and epigastric olive sized lesion.

28
Q

What is the acid base disturbance seen in pyloric stenosis ?

A

Hypoclrorimic/ hypokalemic metabolic acidosis.

29
Q

Upper GI bleeding occurs above ___?

A

Ligament of Treitz

30
Q

Lower GI bleeding occurs below ____?

A

Ligament of Treitz

31
Q

Heamatemsis indicates ?

A

Vomiting of blood proximal to the
duodeno-jejunal junction

32
Q

Melaena indicates ?

A

Black ‘tarry’ stools due to
digestion of Hb by intestinal
bacteria

33
Q

What are the key steps of UGI bleed assessment ?

A
  1. Stable or Unstable patient?
  2. Clarify where the blood is
    coming from
  3. Establish Severity
    – Volume
    – Blatchford Scoring (0-1 = Low
    Risk, Outpatient)
    * Hb, Urea
    * BP, HR
    * Presentation with Melaena
    * Presentation with Syncope
    * Liver disease or heart failure
34
Q

What is Osler Weber Rendu syndrome?

A

Hereditary haemorrhagic telangiectasia (HHT) is an inherited genetic disorder that presents with AVMs of the intestine causing bleeding.

35
Q

What are the endoscopic markers of increased risk for esophageal variceal bleeding ?

A
  • Cherry red spots
  • Haemocystic spots
  • Red wale markings
  • All indicate increased risk of variceal bleeding
36
Q

~50% of pts with upper GI bleed has ?

A

PUD

37
Q

gastric or duodenal ulcers are more likely to bleed ?

A

Duodenal.

38
Q

What is the Forest classification for predicting risk of re-bleeding ?

A
  • Clean-based ulcer: 1% risk of recurrent haemorrhage
  • Flat, pigmented spot: 7% risk of recurrent bleeding
39
Q

What is Rockall score for UGI bleeding prognosis indicates ?

A
  • <3 good prognosis
  • > 8 high mortality risk
40
Q

When should blood transfusion done in GI bleeding ?

A

Hb < 8gm/dL

41
Q

what is the management of unstable varicial bleeding ?

A
  • Stabilize the patient by securing airway, NPO, blood transfusion, Terlipression 2mg IV and 3rd generation cephalosporin IV, and Vitamin K.
  • Endoscopy with varicial banding, if unsuccessful consider TIPS, Sendstaken Blackmore tube.
  • Commence secondary prevention + prophylactic antibiotics for gram negative bacteria.
42
Q

What is the management of nonvaricial UGI bleeding ?

A
  • Stabilize the patient by securing airway, NPO, IV access and blood transfusion.
  • IV PPI infusion.
  • OGD to locate the source of bleeding
  • Control bleeding using either Adrenaline, clips, hemospray or GOLD probe.
  • If hemostasis is not achieved CTAngio + interventional radiology or surgical referral.
43
Q

What are the signs of Lymphovascular / transcoelomic spread of gastric cancer ?

A

– Virchow’s node
– Sister Mary Joseph Nodule
– Jaundice

44
Q

What are the signs of peritonial spread of gastric cancer?

A

– Krukenburg tumour
– Blumer’s shelf- metastatic tumor deposit in rectouterine, or rectovesical pouch on digital rectal or vaginal examination
* Ascites
* Jaundice or liver mass

45
Q

What is small bowel obstruction ?

A

It occurs when normal flow of intraluminal contents is disrupted and can be functional or mechanical. The obstruction leads to dilation of the bowel proximal to the obstruction and decompression of the bowel distally. The Bowel wall becomes edematous, absorptive function is lost, fluid is sequestered into the lumen. If prolonged and bowel dilation is excessive, bowel wall blood supply can become compromised and ischemia/necrosis can occur.

46
Q

What is the symptomatology of small bowel obstruction ?

A
  • acute nausea and vomiting
  • Absence of flatus/bowel movements (obstipation)
  • Abdominal pain is typically crampy, diffuse
47
Q

What are the abdominal examination findings in small bowel obstruction ?

A

– Distended
– Hypoactive bowel sounds
– High-pitched tinkling sound at point of obstruction

48
Q

What is the management of small bowel obstruction ?

A
  • NGT to help decompress from
    above.
  • NPO and IVF
  • FBC, U&E and lactate to estimate the severity.
49
Q

What are the imaging in SBO ?

A

Plain film followed by CT-A and P.

50
Q

What is the indication for surgery in SBO ?

A

most cases resolves without surgery. However, surgery is indicated in cases where there is risk of perforation proximal to the obstruction.

51
Q

What is Ileus ?

A

It is the disruption of the normal peristaltic actions of the small intestine. Most cases are due to functional obstruction following surgery and the presentation is similar to SBO. The examination will show distended abdomen with hypoactive bowel sounds and N/V.

52
Q

What is the treatment of ileus ?

A

– Bowel rest
– Pain control
– Ambulation
– Correction of electrolyte abnormalities
– NGT if vomiting present
– Serial abdominal examination

53
Q

what are the elements of rule of 2 of Merckel’s diverticulum?

A

– <2 yrs
– 2:1 M:F
– 2% of population
– 2 feet proximal to ICV
– 2 inches in length
– 2% adults are symptomatic
– 2 ectopic tissue present (gastric
and pancreatic)

54
Q

What is the first-line treatment of intusussuception?

A
  • Treatment with liquid contrast enema or air contrast enema
  • If failed, then surgical reduction