Acid Peptic Disease Flashcards

1
Q

First line of defense mucosal defense system

A

mucus-bicarbonate-phospholipid layer

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2
Q

two principal gastric secretory products capable of inducing mucosal injury

A

Hydrochloric acid

pepsinogen

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3
Q

the principal contributors to basal acid secretion

A

Cholinergic input via the vagus nerve

histaminergic input from local gastric sources

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4
Q

released from endocrine cells found in the gastric mucosa (D cells) in response to HCl

A

somatostatin

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5
Q

synthesizes and secretes pepsinogen

A

chief cells in gastric fundus

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6
Q

define ulcer

A

breaks in gastric mucosa greater than 5 mm in size

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7
Q

Active site of H K ATPase pump

A
alpha subunit
function of B subunit is unclear
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8
Q

where is the chief cell primarily found

A

gastric fundus

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9
Q

Peak incidence of Gastric ulcers

A

6th decade of life
less common than DUs,
affects males

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10
Q

MC location of duodenal ulcers

A

first portion of duodenum >95%

90% located within 3 cm of the pylorus

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11
Q

Size giant ulcer

A

3-6 cm

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12
Q

MC location of benign GUs

A

distal to the junction between the antrum and the acid secretory mucosa

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13
Q

NSAID related GUS

A

foveolar hyperplasia
epithelial regeneration in the absence of H pylori
deem of lamina propia

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14
Q

Gastric ulcers
occur within 3 cm of the pylorus and are commonly accompanied by duodenal ulcers and normal or high gastric acid production

A

Type III

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15
Q

Gastric ulcers

found in the cardia and are associated with low gastric acid production

A

Type IV

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16
Q

Gastric ulcers

occur in the gastric body and tend to be associated with low gastric acid production

A

Type I

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17
Q

Gastric ulcers

occur in the antrum and gastric acid can vary from low to normal

A

Type II

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18
Q

H. pylori

A

Gastric mucosa-associated lymphoid tissue (MALT) lymphoma

gastric adenocarcinoma

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19
Q

previous name of H pylori

A

Campylobacter pyloridis

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20
Q

somatostatin is released from endocrine cells found in the gastric mucosa (D cells) in response to

A

HCl

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21
Q

Theories for increased ulcer diathesis in cigarette smokers

A

> altered gastric emptying
decreased proximal duodenal bicarbonate production
increased risk for H. pylori infection
cigarette-induced generation of noxious mucosal free radicals

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22
Q

Chronic disorders with strong association to pUD

A

(1) Systemic mastocytosis,
(2) chronic pulmonary disease,
(3) chronic renal failure,
(4) cirrhosis,
(5) nephrolithiasis
(6) 1-antitrypsin deficiency

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23
Q

Chronic disorders with POSSIBLE association to pUD

A

(1) hyperparathyroidism,
(2) coronary artery disease
(3) polycythemia vera
(4) chronic pancreatitis

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24
Q

Non HP non NSAID ulcer infectious causes

A

Cytomegalovirus
Herpes simplex virus
H. heilmannii

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25
Q

most frequent finding in patients with GU or Du

A

epigastric tenderness

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26
Q

% of pig tenderness in GU/DU patients found at R of the midline

A

20%

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27
Q

MC pUD complicatio

A

GI bleeding- 15%

with5-10% mortality rate

28
Q

2nd MC PUD complication

A

perforation 6-7%

29
Q

form of perforation which the ulcer bed tunnels into an adjacent organ

A

penetration

30
Q

Diff between peneration patterns of DUs and GUs

A
DU= penetrate into pancreas
GU= penetrate into L hepatic lobe, gastrocolic fistulas
31
Q

Least common observed PUD complication

A

Gastric outlet obstruction 1-2%

32
Q

Appearance of benign GU

A

discrete crater with radiating mucosal folds originating form the ulcer margin

33
Q

% of GUS=s radiogragically benign that are malignant

A

8%

34
Q

location of GU with malignant potential

A

body and fundus

35
Q

GU repeat endoscopy to check healing

A

8-12 weeks

36
Q

Refractory ulcers

A

GU=12 weeks

DU= 8 weeks

37
Q

How to exclude ZES (high output state) in refractory ulcers

A

fasting gastrin or

secretin stimulation test

38
Q

Aetiologies of refractory ulcers

A
ischemia
Crohn's disease
amyloidosis
sarcoidosis
lymphoma
eosinophilic gastroenteritis
39
Q

MC ulcer related complication

A

hemorrhage 15-25%

40
Q

%__ perforation

A

2-3% of DU

41
Q

%___

concomitant perforation and Hge

A

10%

42
Q

Complication of truncal and selective (preserve celiac and hepatic branches) vagotomy

A

gastric atony

so we should drain theoygh pyloropasty or gastroduodenostomy

43
Q

Sx to minimize gastric dysmotility

A

Highly selective vagotomy

parietal cell, super selective, proximal vagotomy

44
Q

lowest rates of ulcer recurrence

A

vagotomy + antrectomy

45
Q

vasomotor and GI signs and symptoms occurring in patients who have undergone vagotomy and drainage

A

Dumping syndrome

46
Q

Explain pathophy of dumping syndrome
Early phase: (15-30 mins after meal)
crampy abdominal discomfort, nausea, diarrhea, belching, tachycardia

A

rapid emptying of hyperosmolar contents into the small intestine, resulting in a fluid shift into the gut lumen with plasma volume contraction and acute intestinal distention

47
Q

Explain pathophy of dumping syndrome
Late phase: 90 min-3h
light headedness diaphoresis palpitations tachycardia

A

hypoglycaemia from excessive insulin release

48
Q

RX late phases of dumping

A

acarbose

ocreotide

49
Q

Postvagotomy diarrhoea common in

A

truncal vagotomy

50
Q

post partial gastrectomy patients with and pain, early satiety nausea

A

Bile or alkaline reflux gastropathy/gastritis

51
Q

severe peptic ulcer diathesis secondary to gastric acid hypersecretion due to unregulated gastrin release from a non- cell endocrine tumor (gastrinoma)

A

Zollinger Ellison Syndrome

52
Q

Role of gastrin in acid secretion

A

acts through gastrin receptors on parietal cells and by inducing histamine release from ECL cells

53
Q

The gastronoma triangle where 80% of gastronomes are

A

S: confluence of the cystic and common bile ducts
I: junction of the second and third portions of the duodenum
Medial: junction of the neck and body of the pancreas

54
Q

most common nonpancreatic lesion; between 50 and 75% of gastrinomas are found here

A

Duodenal tumors

55
Q

% of gastronomes malignant

A

> 60%

56
Q

MC s/s of gastrinoma

A

> 90% PUD

50% Diarrhea

57
Q

% of gastronome in MEN I

A

25%
PANcreas
PARAthyroid
PITuitary

58
Q

Gastrin levels of gastronome patients

A

> 150-200

normal

59
Q

When to obtain fasting serum gastric level

A

Multiple ulcers
Ulcers in unusual locations; associated with severe esophagitis; resistant to therapy with frequent recurrences; in the absence of NSAID ingestion or H. pylori infection
Ulcer patients awaiting surgery
Extensive family history for peptic ulcer disease
Postoperative ulcer recurrence
Basal hyperchlorhydria
Unexplained diarrhea or steatorrhea
Hypercalcemia
Family history of pancreatic islet, pituitary, or parathyroid tumor
Prominent gastric or duodenal folds

60
Q

differentiate between the causes of hypergastrinemia in patients with indeterminate acid secretory studies

A

Gastrin provocative tests :

  1. secretin stimulation test- most famous
  2. calcium infusion study
61
Q

Why should you stop PPI 1 week before testing for secretin test

A

PPI induced hypochlorhydria or achlorhydria may lead to a false-positive secretin test

62
Q

Rx ZES

A

PPIs

ocreotide in somatostatin receptor positive

63
Q

Gastritis

related to H pylori infection

A

Type B Gastritis

64
Q

Gastritis

antral predominant

A

Type B= ANtral

Type A= Body

65
Q

Gastritis
antibodies to parietal cells/ pernicious anaemia
autoimmune

A

Type A