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7: Digestive System > Chapter 91 Stomach > Flashcards

Chapter 91 Stomach Flashcards

1
Q

Label the diagram

A
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2
Q

What anatomical landmark distinguishes body from antrum?

A

Angular incisure

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3
Q

Name the three portions of greater omentum

A
  • Splenic
  • Bursal
  • Veil
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4
Q

Label the diagram

A

N.B.

Hepatic artery gives off branches to liver and GB then

–> gives off right gastric artery

–> then HA becomes gastroduodenal artery

–> gives off right gastroepiploic + becomes cranial pancreaticoduodenal

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5
Q

Label the diagram

A
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6
Q

What are the three branches of the celiac artery?

A

Hepatic, left gastric, splenic

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7
Q

What LNs drain the stomach?

A

Gastric, splenic, hepatic

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8
Q

What are the muscle layers of the stomach, from outside to in

A

Longitudinal

Circular (not present in fundus)

Oblique

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9
Q

What is type of epithelium lines the stomach?

A

Columnar surface epipheium

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10
Q

Name the three types of gland in the stomach.

Name the 5 sub-types of one of these.

A
  • Cardiac –> serous
  • Pyloric –> mucous
  • Gastric
    • Chief cells –> Pepsinogen
    • Parietal –> intrisic factor + acids
    • Mucous
    • Endocrine –> histamine, gastrin, serotonin
    • Neck
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11
Q

What is normal gastric pH?

A

2 - 3

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12
Q

What is the role of intrinsic factor?

A

Binds to B12 (= cobalamin) for absorbtion in ilium

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13
Q

What size of particle is able to pass through pylorus?

A

<2mm.

(food particles ususlly 0.1 - 0.6mm in size)

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14
Q

What is the process of food being churned in stomach called?

A

Contractile retropulsion

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15
Q

When is a defect considered an ulcer

A

when extends into submucosa –> fibrotic repair

(vs epithelial regeneration if mucosa only)

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16
Q

How does collagen production in GI tract differ from elsewhere?

A

Usually only produced by fibroblasts, but in GI tract smooth muscle also produces collagen.

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17
Q

In what % of dogs undergoing prtho procedures was GER present?

and in what % was it clinically noted?

A

Present in 57% but only noted in 14%

i.e. likely goes unnoticed

If anticipated give PPI or H2 blocker pre-operatively and poss anticholinergic like atropine or glycopyrrolate

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18
Q

Name 2 ligaments that anchor stomach

A

Hepatogastric and hepatoduodenal

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19
Q

Name 3 inverting suture patterns

A

E) Cushing

F) Connell

G) Lembert

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20
Q

When is an inverting pattern conraindicated in stomach

A

If –> compromise of luminal diameter

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21
Q

When submerged in gastric fluid, what was halflives of polyglyconate (Maxon), poliglecaperone 25 (Monortyl) and polydioxanone (PDS)?

A
  • polyglyconate (Maxon) 75d
  • poliglecaperone 25 (Monocryl) 15d
  • polydioxanone (PDS) 12d
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22
Q

What layer is endoscopic biopsy able to sample

A

Mucosa

i.e. need full thickness for anything affectign serosa, muscularis or submucosa

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23
Q

How accurate is subjective criteria for assessing gastric viability?

What 4 factors were assessed when juding subjectve viability?

List 3 other potential methods (n.b. actually less accurate than subjective criteria)

A

85%

  • Gastric wall thickness
  • Serosal colour
  • Peristalsis
  • Serosal capillary perfusion

Could also do doppler, scintigraphy, flouoscein dye injection.

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24
Q

How can inadequate functional lumen diameter after gastric resection be managed?

A

Autologous Si submucosal graft

25
Q

Name 2 complications following gastric invagination

A

Gastric ulceration.

Obstruction due to sloughed material.

(Abcessation. + a case at QMHA became anaemic)

26
Q

Name 6 gastropexy methods

Which is reported to be strongest?

A
  • Incisional
  • Belt loop
  • Circumcostal
  • Incorporating
  • Gastrocolopexy
  • Minimally invasive
    • Grid approach
    • Endoscopically assisted
    • Laparoscopic

Cicumcostal and belt loop strongest (109 N, vs 60-85N for incisional)

27
Q

Name 2 complictions of circumcostal gastropexy

A

Pneumothorax

Rib fracture

28
Q

Name 3 types of pyloromyotomy/pyloroplasty

A
  • Pyloromyotomy (Fredet-Ramstedt)
  • Transverse pyloroplasty (Heineke - Mikulicz)
  • Y-U pyloroplasty
29
Q

What is bilroth I and bilroth II

A

Bilroth I = pylorectomy + gastroduodenostomy

Bilroth II = Gastrojejunostomy (side-to-side). Cholecystoenterostomy often required too.

30
Q

What is a whipple procedure?

A

Pancreaticoduedenectomy

–> gastrojejunostomy

–> choledochojejunostomy

–> pancreaticojejunostomy

31
Q

Name the 4 types of hiatal hernia

A

A, Normal anatomy of the junction of the esophagus and stomach.

B, Type I sliding hiatal hernia in which the gastroesophageal junction has moved cranial to the diaphragm.

C, Type II paraesophageal hernia occurs when a portion of the stomach moves into the caudal thorax through the hiatus adjacent to the esophagus.

D, Type III hiatal hernia combines the movement of the gastroesophageal junction into the thorax as well as movement of a portion of the stomach into the thorax adjacent to the esophagus.

Type IV herination of abdo organs other than stomach

E, Gastroesophageal intussusception.

32
Q

What breeds are prone to type I hiatal hernia?

A

Shar pei + English bulldog

33
Q

Comment on the images

A

Type I sliding hiatal hernia.

A, Positive contrast image. Note the gastroesophageal junction cranial to the diaphragm.

B, In this reverse-contrast image the “apple core” effect is demonstrated at the gastroesophageal junction, which is cranial to the diaphragm.

34
Q

List the three aims of medical management for hiatal hernia

A
  1. Reduce gastric acid secretion
  2. Provide oesophageal mucosal protection
  3. Increase rate of gastric emptying while augmenting lower oesophageal sphincter tone
35
Q

What pre-op management should be initiated in animls undergoing sx for hiatal hernia?

A

Antacids + prokinetics

36
Q

List 3 surgical techniques for management of type 1 hiatal hernia

A
  1. Phrenoplasty
  2. Oesophagopexy (to diaphragm)
  3. L gastropexy
37
Q

What surgical step is necessary for access to the oesophageal hiatus?

A

Transection of L triangular ligament and mobilisation of L lobes to r side

38
Q

What are 2 most common c/s of gastrooesophageal intussusception?

A

V + R

Often associated with esophageal disease eg megaoesophagus, enlared hiatus, altered oesophageal motility

39
Q

What canbe seen on radiographs with gastrooesophageal intussuception

A
  • ST mass in caudal oesophagus
  • Lack of gastric gas bubble/pyloru in cranial abdo
  • Dilated oesophagus

A, In this plain film, radiopaque gastric contents may be seen in the caudal thorax superimposed over the left diaphragmatic crus and dorsocaudal lung field (arrows).

B, In this esophagram, barium outlines the cranial aspect of the intussusception (arrows). The large soft tissue mass in the caudal dorsal thorax is the stomach intussuscepted into the caudal esophageal lumen. Note the barium coating of the gastric rugal folds, making them appear as filling defects.

40
Q

What is reported success of endoscopic sewing needle removal

A

High!

8/9 dogs and 18/19 cats

41
Q

What is most common castric neoplasm in dogs?

And in cats

A

Dogs = adenocarcinoma

Cats = lymphoma

42
Q

What are most common sites of gastric adenocarcinoma?

What are the types?

What is rate of metastasis and usual sites?

A
  • Sites: Pylouric antrum + lesser cyrvature
  • Types:
    • Linitis plastica = diffuse
    • groups of ulcerated mucosal plaques
    • discrete polypoid mass
  • Metastasis: 70-80%
    • Lungs
    • Liver
    • LN
43
Q

From what cells are GISTs derived?

What IHC marker is used to distinguish GIST from leiomyosarcoma?

A
  • Interstitial cells of Cajal –> GIST
  • GIST IHC = c-kit = CD117. (SMA or Desmin for leiomyosarcoma)
44
Q

What fungal disease can affect stomach?

What is clinical finding?

Which area most commonly affected?

A
  • What fungal disease can affect stomach?
    • Pythium insidiosum (in US)
  • What is clinical finding?
    • severe transmural thickening
  • Which area most commonly affected?
    • Gastric outflow area

Usually young dogs <2 years

45
Q

List 4 most common caused of gastric ulceration.

List 2 most common caused of gastric perforation

A

List 4 most common caused of gastric ulceration.

  • Hepatic disease (decreased histamine and gastrin degradation)
  • Kidney disease (decreased gastin clearance or increased secretion)
  • NSAIDs/Corticosteroids
  • Neoplasia

List 2 most common caused of gastric perforation

  • NSAIDs
  • Neoplasia (boht primary gastric but consider also gastrinoma and systemic mastocytosis!)
46
Q

What are the two proposed mechanisms of gastric ulceration due to NSAIDs

A
  1. Direct topical effect of weakly acidic NSAID on gastric mucosa
  2. Systemic inhibition of Cox –> reduced protective prostaglandin.
47
Q

List 4 drugs for medical management of gastric ulceration

A
  • PPI
  • H2 blocker
  • Sucralfate
  • Misoprostol (= prostaglandin analogue)
48
Q

List 3 H2 receptor anatgonists in order of increasing potency

A
  • Cimetidine. Tid dosing + inhibits hepatic cytochrome p-450 system
  • Ranitidine. Bid dosing
  • Famotidine. Sid dosing. No cytochrome P-450 inhibition but effectiveness of famotidine decreases within a few days
49
Q

What is sucralfate?

How does it work?

A

Sulphated disaccharide-aluminum hydroxide complex

Acidic environment –> dissociation into component parts –> sucrose octasulfate portion undergoes polymerization to form thick substance that binds to electrostatically chared proteins in base of ulcer.

50
Q

What is misoprostol and how does it work

A

Synthetic prostaglandin analogue

  • Increased bicarb secretion
  • Increases mucous production
  • Increases mucosal blood flow
51
Q

List 2 surgical options for management of gastric ulcer

A

excision or serosal patch

52
Q

Endoscopy was diagnostic for gastric perf in what % of cases?

A

only 17%!

53
Q

List risk factors for GDV

A
  • Increased thoracic depth:width
  • First degree family member with GDV
  • Feeding fewer meals/day
  • Eating rapidly
  • Aggressive/nervous character
  • Smaller food particle size
  • Increased hepatogastric ligament lenght
  • Exercise/stress after meal
54
Q

List 5 pathophysiological changes encountered with GDV

A
  1. Blood Flow
    • ​​Reduced venour return + portal vein compression –> portal hypertension
  2. Cardiac dysfuntion
    • ​​Inadequate coronary vessel flow + myocardial depressant factor
  3. Gastric wall necrosis ​
  4. Bacterial translocation
    • ​​Portal hypertension –> venous stasis, mucosal death, bacterial translocation
  5. Reperfusion injury
55
Q

When is treatment of arrythmias warrated?

A
  • Pulse deficits/poorperipheral perfusion
  • Likely to progress to fibrillation
56
Q

What is recurrence rate of GDV after gastropexy?

A

0-6%

57
Q

List 8 factors that have been associated with mortality due to GDV

A
  • Clinical signs >6 hours
  • Gastric wall necrosis
  • Concurrent gastrectomy or splenectomy
  • Hypotension
  • Pre-op arrythmias
  • Peritonitis
  • Sepsis
  • DIC
58
Q

Bases on serial lactate measurements in dogs with GDV, list 3 factors associated with survival.

A

​Predictors of survival:

  • Absolute change in lactate >4 mmol/L
  • >42.5% decrease in lactate
  • Final lactate <6.4 mmol/L
59
Q

What is lifetime risk of GDV in predisposed breeds?

How is this affected by prophylactic gastropexy?

A

4-37%

prophylactic gastropexy –> x29 decreased risk!

7: Digestive System (12 decks)

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