STOMACH DUODEUNM Flashcards

1
Q

effect secretin on gastrin

A

Secretin inhibits gastrium

careful, separate and stimulation test increase his gastrin with gastrinoma

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2
Q

stimulation of gastrin realease

A
gastric distention
 vagus input
 pH  up
 amino acid
Calcium
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3
Q

pathway of gastrin release

A

antrum G. cells release gastrin to

stimulate parietal cells to release HCL (and intrinsic factor)

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4
Q

what cells secrete intrinsic factor and where

A

parietal cells
careful, same cells that release gastrin

stomach

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5
Q

how is B12 resorbed

A

terminal ileum

with intrinsic factor from stomach and

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6
Q

treatment of perforated duodenal ulcer from chronic nonsteroidal anti-inflammatory use

A

omental patch

PPI and treatment of H. pylori postoperatively

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7
Q

Marjolin’s ulcer

A

Majors have scars and burns

squamous cell carcinoma chronic wound

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8
Q

Cameron’s ulcer

A

associated with hiatal hernia

lesser curve

mechanical trauma or ischemia and peptic injury

may require treatment of hiatal hernia for bleeding

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9
Q

curling ulcer

A

hot curling iron

gastric ulcer

Severe burn injury

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10
Q

Cushing ulcer

A

Cushing’s reflux

elevated intracranial pressure

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11
Q

marginal ulcer

A

margin of tissue not capable handling gastric secretion

gastro-J.
bypass

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12
Q

risk factors for afferent limb obstruction

A

long limb

Antecolic position

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13
Q

physiologic effects of chronic partial afferent limb obstruction

A

DEconjugated bile acid
bacterial overgrowth

decreased vitamin B12 absorption

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14
Q

treatment of efferent limb obstruction

A

surgical reduction

closure of internal defect

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15
Q

most common metabolic consultation after Roux-en-Y gastric bypass

A

dehydration - most common short-term

most common long term:
B12 deficiency
iron deficiency

Dumping syndrome - also relatively common

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16
Q

alkaline reflux cause, diagnosis

A

after Billroth II reconstruction

increased bile reflux

Symptoms of
biliary vomiting
Iron deficiency anemia
weight loss

diagnoses:
HIDA scan easily diagnostic demonstrating bili secretion into the stomach and even into the esophagus

upper endoscopy can also be performed with biopsies

mucosa is beefy-red friable with ulcerations

treatment:
Convert to Roux-en-Y
Roux limb lengthened to at least 40 cm.

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17
Q

where somatostatin released from, what cells

A

antrum of the stomach
D Cells

inhibits:
gastrin
bicarbonate secretion

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18
Q

metabolic syndrome

A

type 2 diabetes
Impaired glucose tolerance
Dyslipidemia
Hypertension

Associated with obesity-central

NOT associated with nonalcoholic steatohepatitis

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19
Q

best treatment for H. pylori

A

PPI

Amoxicillin or Clarithromycin or tetracycline
( careful, do not confuse with ampicillin)

AND

Flagyl

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20
Q

treatment of dumping syndrome after Billroth II

A

Small frequent meals with
high-protein and fat

octreotide

failed conservative management:
Jejunal pouch for reservoir
Long Roux-en-Y limb delayed emptying

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21
Q

mechanism of omeprazole

A

inhibition of H+/K+ ATPase

irreversible

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22
Q

most common locations of gastrointestinal stromal tumors

A
stomach 60-70%
Small bowel 20- 25% ( more common JEJUNUM)
( careful, carcinoid is ileum)
Colorectum 5%
Esophagus 5%
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23
Q

treatment carcinoid of the stomach

A

this is rare-8%

The treatment for localized carcinoids is complete removal.

For small pedunculated lesions, this can be accomplished endoscopically. Larger lesions may require wedge resection or partial gastrectomy. Patients with multiple gastric carcinoids may require total gastrectomy. For patients with recurrent or metastatic disease, somatostatin analogues can be used to decrease the burden of disease and treat carcinoid syndrome.

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24
Q

Carcinoid tumors most common locations

A

appendix #1 45% - most common mass (careful, not most common malignancy-adenocarcinoma)

the small intestine #2 ileum 28% - most likely to cause carcinoid syndrome

rectum 16% - does not produce serotonin

stomach 2-8%

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25
Q

prognosis of carcinoid

A

location, size, depth of invasion, and growth pattern.

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26
Q

prognosis of gastrointestinal stromal tumor

A

tumor size and mitotic index.

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27
Q

workup of gastrointestinal stromal tumor

A

no Percutaneous core or intraoperative biopsy

yes endoscopic biopsy is okay

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28
Q

stimulation of secretin from the duodenum and its effect

A

Secretin “ secretes” bicarbonate

stimulated by: 
fat 
acid and duodenum
 bile
 (careful,  paradoxical since acid stimulates)

( also careful, CCK stimulated secretin and and vice versa)

most important mediator of the secretion of water, bicarbonate, and other electrolytes into the duodenum

inhibited gastrin

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29
Q

stimulation of CCK and its effect

A

ipid, protein, and carbohydrates inside the duodenum

CCK by I cells present in the duodenal mucosa

main mediator of the secretion of pancreatic enzymes.

induces the release of pancreatic enzymes by acinar cells.

cause the release of acetylcholine, vasoactive intestinal peptide, and gastrin-releasing peptide,

CCK induces the relaxation of the sphincter of Oddi

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30
Q

percent acid suppression associated with truncal vagotomy

A

50%

Improved with antrectomy

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31
Q

Indications for truncal vagotomy

A

refractory type II ulcer and body of the stomach and duodenum

Type III ulcer in the pyloric channel within 3 cm of the pylorus - was caused by from hypersecretion of acid

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32
Q

complications of truncal vagotomy

A

loss of vagal tone

Empty LIQUIDS after because loss of repeat receptive relaxation

solids moved more slowly-loss of churning

postoperative diarrhea usually improves in a few months

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33
Q

Which vagus nerve is more difficult to find

A

PR

posterior right

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34
Q

best initial screening test for H. pylori

A

serology testing for IgG

careful, best test for eradication is urea breath test

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35
Q

which testes for H. pylori if patient needs endoscopy for concern of brisk bleeding or perforation on initial evaluation

A

Rapid urease assay-single can be achieved with scope

36
Q

describe helicalbacter pylori organism

A

gram-negative
Spiral
Motile

37
Q

mechanism action of erythromycin

A

binds motilin receptors on smooth muscle cells

38
Q

prokinetic agent decide erythromycin

A

metoclopramide

dopamine antagonist

stimulates acetylcholine release

39
Q

management of recurrent ulcers after parietal cell vagotomy

A

PPI

40
Q

hormone responses to acid in the duodenum

A

somatostatin increased from D cells to put the breaks on
GIP increased to dcr acid secretion and stimulate insulin
secretary and increased to inhibit gastrium and stimulated bicarbonate secretion
motility and is activated and to aid in gastrointestinal motility

41
Q

best test to evaluate for delayed gastric emptying and diabetes - and normal times

A

nuclear medicine gastric emptying study
scintigraphy
Transit time of fried-egg sandwich with sulfur colloid

thought half-life 60-105 minutes

liquid half-life 10-45 minutes

42
Q

how long may a MALT lymphoma need treatment this the results

A

remission gently achieved within 12 months

Relapse 10%

43
Q

alternative H. pylori treatment regimens

A

omeprazole or lansoprazole, clarithromycin, and amoxicillin

omeprazole or lansoprazole, metronidazole, and clarithromycin

omeprazole or lansoprazole, bismuth, metronidazole, and tetracycline.

44
Q

surveillance needed for MALT

A

After treatment:
2 months post treatment endoscopy Surveillance and biopsies

then every 6 months for 2 years

45
Q

management of rebleed after endoscopic clipping and epinephrine injection of duodenal ulcer

A

rescoped!
75% of excess in repeat endoscopy

if fails: This emergency surgery

46
Q

described used to check for bleeding gastroduodenal artery duodenal ulcer

A

superior inferior and MEDIAL

47
Q

treatment of MALT gastric lymphoma who are H. pylori negative

A

chemoradiation
And
Radiation

48
Q

risk factors for gastric cancer

A

diet
Gastric polyps!:
ALL Adenomatous polyp - Including tubular!
Hyperplastic polyps are benign but presents may often be due to chronic gastritis which is a risk factor

Type a blood
Smoking
Previous gastric surgery - including bypass
Nitrates
Previous H. pylori infection
49
Q

risk of bleeding with gastric ulcer

A

highest- visible vessel - even of nonbleeding
active bleeding

intermediate-adherent clot

low-ulceration with black spot
of clean base

50
Q

gastrin stimulates

A

gastric acid
Pepsinogen secretion
Mucosal growth

51
Q

where is gastrin released

A

BOTH
Antrum and duodenum
from G. cells

52
Q

what stimulates gastrin release

A
meal / food
 protein
Antral distention
Vagus
AND Adrenergic-epinephrine! (Careful)
 gastrin releasing peptide
53
Q

waht inhibits gastrin

A

passage and the lumen

Somatostatin

54
Q

risk with prolonged hypergastrinemia

A

mucosal hyperplasia
Increased number of:
Enterochromaffin-like cells

associated development of gastric carcinoid tumor

55
Q

described in mechanism and pump of parietal cell HCl secretion

A

H+/K+ ATPase exchange and chloride channel

Secretion of chloride is accomplished through a chloride channel moving chloride from the parietal cell cytoplasm to the gastric lumen.

56
Q

risk factors for afferent loop syndrome with Billroth II

A

limb greater than 30-40 cm - usually the problem

Antecolic anastomosis to stomach

internal herniation behind the efferent limb,

stenosis of the gastrojejunal anastomosis,

redundant twisting of the afferent limb with a resultant volvulus

adhesions involving the afferent limb.

57
Q

two treatment options of afferent loop syndrome with Billroth II

A

enteroenterostomy below the stoma, which is technically easier.

Creation of a Roux-en-Y can also be done.

58
Q

management of symptomatic duodenal periampullary diverticulum

A

uncomplicated duodenal diverticula:

diverticulectomy with primary closure

If perforation of diverticula:
diversion

gastrojejunostomy
or
duodenojejunostomy

cause pancreatitis or cholangitis do require surgical intervention

59
Q

The accepted treatment for H.pylori includes

A

a triple medication regiment. This includes a PPI and two antibiotics.

The best choices for antibiotics are
Amoxicillin, Flagyl,
Tetracycline, and Clarithromycin.

PPI’s are superior to H2 blockers.

60
Q

Laparoscopic adjustable gastric bands compare to bypass

A

can produce the same weight loss and improvement in comorbidities as roux-en-Y gastric bypass!

The caveat is that LAGB usually requires patients who are more motivated to lose weight.

Patients who undergo gastric bypass usually lose weight faster but weight loss steadily continues after LAGB.

The two procedures can show similar total excess weight loss at the 3- year mark.

5 –year-outcomes for patients receiving LAGB show about 60% of excess weight loss.

Improvement in hypertension in patients status post LAGB has been quoted as high as 55%. Similarly improvements are seen in GERD, diabetes, obstructive sleep apnea and quality of life.

Operative mortality after LAGB is estimated to be 0.1%. It is a safe procedure that is usually done on an outpatient basis.

61
Q

for patients with acute NSAID-related perforation of duodenum what is recommended treatment

A

In general, simple patch closure, typically with omentum, is appropriate

(provided that use of the drugs can be discontinued post-operatively)

and for patients who have never been treated for peptic ulcer disease.

Simple patch repair should also be used for patients with ongoing shock, delayed evaluation, considerable co-morbid disease, or marked peritoneal contamination.

3-0 silk or PDS sutures

62
Q

The most common and effective procedures for Gastroparesis

A

insertion of gastric pacers

pyloroplasty.

NOT endoscopy with botox injections or stent placement,

As a last resort, some patients may need to have a surgical feeding tube placed or started on TPN if their nutritional state is critical, but this should only be used once all other options have failed.

Cisapride use has been discontinued due to its side effect profile which includes prolonged QT syndrome and sudden cardiac arrest.

63
Q

Gastroparesis most common cause

A

3 vagal injuries.

most common cause is idiopathic!!

other causes:
#2 Diabetes is the second most common cause 

The most common surgical procedure that leads to a vagal injury is a Nissen fundoplication.

Other causes:

narcotics
octreotide
scleroderma
electrolyte abnormalities.

64
Q

The gold standard in diagnosis Gastroparesis

A

gastric emptying study which will show a slowed transit of radiolabelled ingested food over the course of several hours.

If gastroparesis is suspected, it is important to perform an upper endoscopy to ensure there is no true mechanical obstruction, such as a mass or ulcer, which is the cause for the symptoms.

A sham feeding test can help determine if there is poor vagal function after eating a meal.

65
Q

accepted treatment for gastroparesis

A

Reglan

if fail med - pyloroplasty / pacemaker

66
Q

Sleeve gastrectomy vascular moves to address greater curve

A

During the operation for sleeve gastrectomy, the greater curvature of the stomach is completely devascularized prior to being resected.

67
Q

Sleeve gastrectomy Blood supply

A

Blood supply to the gastric sleeve is received from the left and right gastric arteries as well as branches from the right gastroepiploic.

68
Q

comparing a parietal cell vagotomy to a truncal vagotomy for an acid suppressing surgery

A

Parietal cell vagotomy has less

post-operative diarrhea than a truncal vagotomy

recurrence rates depend on the experience of the surgeon

Drainage procedures are not required with a parietal cell vagotomy - preservation of the innervation to the gastric antrum.

Truncal vagotomy patients more frequently have post-operative dumping syndrome

Generally speaking, the caveat is an increased recurrence rate of ulcers due to the increased complexity of the surgery.

69
Q

Most recurrent ulcers after a parietal cell vagotomy are treated with

A

MEDICAL therapy alone to achieve cessation of symptoms!

70
Q

Bleeding duodenal ulcers are usually a result of

A

a posterior perforation into the gastroduodenal artery.

71
Q

treatment of a posterior perforation into the gastroduodenal artery.

A

Stable patients:

endoscopy clip or inject the vessel for hemostasis.

If the patient rebleeds but remains stable:
a second attempt at endoscopic therapy can be used.

ANY hemodynamic instability or the need for over 4 units of blood:

operative intervention.

In a patient with a HISTORY / KNOWN ulcer disease:
truncal vagotomy with pyloroplasty after oversewing the vessel through an anterior duodenotomy

72
Q

If dietary modifications fail, what is next step in tx of gastroparesis

A

promotility agents can be used.

Reglan is a dopamine antagonist that has shown to be effective in increasing gastric motility.

Erythromycin is also commonly used and acts upon the motilin receptors to aid in gastric function.

73
Q

A final treatment option for gastroparesis

A

surgery, and this includes gastric pacer implantations,

pyloroplasty,

botox injections (most be injecting sympathetic here?)

partial gastrectomy.

These have varying degrees of effectiveness and should be used as a last resort.

74
Q

Gastric carcinoid

A

rare,
10% of all GI carcinoids
and
2% of all gastric tumors.

The median age at diagnosis is 64,

Gastric carcinoid tumors have been divided into three types, primarily on the basis of their association (or lack thereof) with hypergastrinemia.

75
Q

For patients with multiple or recurrent gastric carcinoid tumors what is the treatment

A

antrectomy to remove the source of the hypergastrinemia.

For patients with type II (MEN ASSO) lesions, treatment is similar to that for patients with type I lesions, with the extent of gastric resection determined by the size and number of lesions.

All patients undergoing a less than total gastrectomy should be followed with serial endoscopy at regular intervals.

Endoscopic polypectomy or open resection via gastrotomy (local excision) is the procedure of choice for patients with small, SOLITARY type I tumors.

Distal or total gastrectomy with extended lymph node dissection is the treatment of choice for patients with type III (SPORATIC AGGRESSIVE) lesions.

76
Q

what is the pump responsible for secretion of HCl into the gastric lumen?

A

H+/K+ exchange and chloride channel

H+/K+ ATPase

final common pathway for gastric acid secretion by the parietal cell.

Cytosolic hydrogen is secreted by the H+/K+ ATPase in exchange for extracytoplasmic potassium.

The secretion or exchange of hydrogen for potassium, however, does require energy in the form of adenosine triphosphate (ATP), because hydrogen is being secreted against a gradient of more than a million-fold.

Secretion of chloride is accomplished through a chloride channel moving chloride from the parietal cell cytoplasm to the gastric lumen.

77
Q

In patients who are stable and do not warrant an endoscopic evaluation, confirmation of H.pylori can best be achieved with what test

A

serologic studies.

This method has high sensitivity and specificity, is cost effective, and is the least invasive.

78
Q

After treatment, the best test for eradication of the bacteria is with

A

urea breath test.

Testing should be delayed for four weeks to ensure reliable results.

Bottom Line: The best diagnostic test for H.pylori is serology and for eradication is the urea breath test.

79
Q

If the patient needs to be evaluated with endoscopy for concern of brisk bleeding or perforation upon initial evaluation, then what is best test

A

Endoscopic bx with rapid urease assay is recommended for diagnosis.

80
Q

Type 1 hiatal hernias

A

called a sliding hernia

most common

gastroesophageal (GE) junction lying above the diaphragm.

only type that can be treated non-operatively with proton pump inhibitors.

81
Q

Type II hiatal hernias

A

paraesophageal hernia,

GE junction is fixed
true hernia sac where the fundus of the stomach herniates into the chest.

Regardless of the severity of symptoms paraesophageal hernias should be electively repaired once found because of the risk of incarceration

82
Q

Type III hiatal hernias

A

second most common

GE junction lies above the diaphragm

stomach (and possibly other organs) herniate into the chest

Enlargement of the hernia allows the stomach and sometimes other organs to protrude through the hernia sac

83
Q

most common nonepithelial cell tumors of the small bowel

A

GISTs

84
Q

GIST most common locations

A

50% gastric
25% small bowel
15% rectal
10% colonic in origin

85
Q

Rates of laparoscopic adjustable gastric band slippage have been reduced by utilization of what technique

A

the pars-flaccida technique.

This method utilizes dissection through the fatty tissue posterior to the gastroesophageal junction to create a tunnel in which the band sits.

The band is held in place by this connective tissue and reduces the chances that the posterior stomach, which is relatively mobile, will slip past the band.

86
Q

Today band slipping should occur with what percent with LAGB

A

less than 3% of patients with LAGB placed using the pars-flaccida technique.

87
Q

After band placement, the first band fill usually occurs

A

6 weeks later.

This allows time for local edema to subside.