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GI > Acid Peptic Disease > Flashcards

Acid Peptic Disease Flashcards

(65 cards)

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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
most frequent finding in patients with GU or Du
epigastric tenderness
26
% of pig tenderness in GU/DU patients found at R of the midline
20%
27
MC pUD complicatio
GI bleeding- 15% | with5-10% mortality rate
28
2nd MC PUD complication
perforation 6-7%
29
form of perforation which the ulcer bed tunnels into an adjacent organ
penetration
30
Diff between peneration patterns of DUs and GUs
``` DU= penetrate into pancreas GU= penetrate into L hepatic lobe, gastrocolic fistulas ```
31
Least common observed PUD complication
Gastric outlet obstruction 1-2%
32
Appearance of benign GU
discrete crater with radiating mucosal folds originating form the ulcer margin
33
% of GUS=s radiogragically benign that are malignant
8%
34
location of GU with malignant potential
body and fundus
35
GU repeat endoscopy to check healing
8-12 weeks
36
Refractory ulcers
GU=12 weeks | DU= 8 weeks
37
How to exclude ZES (high output state) in refractory ulcers
fasting gastrin or | secretin stimulation test
38
Aetiologies of refractory ulcers
``` ischemia Crohn's disease amyloidosis sarcoidosis lymphoma eosinophilic gastroenteritis ```
39
MC ulcer related complication
hemorrhage 15-25%
40
%__ perforation
2-3% of DU
41
%___ | concomitant perforation and Hge
10%
42
Complication of truncal and selective (preserve celiac and hepatic branches) vagotomy
gastric atony | so we should drain theoygh pyloropasty or gastroduodenostomy
43
Sx to minimize gastric dysmotility
Highly selective vagotomy | parietal cell, super selective, proximal vagotomy
44
lowest rates of ulcer recurrence
vagotomy + antrectomy
45
vasomotor and GI signs and symptoms occurring in patients who have undergone vagotomy and drainage
Dumping syndrome
46
Explain pathophy of dumping syndrome Early phase: (15-30 mins after meal) crampy abdominal discomfort, nausea, diarrhea, belching, tachycardia
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
Explain pathophy of dumping syndrome Late phase: 90 min-3h light headedness diaphoresis palpitations tachycardia
hypoglycaemia from excessive insulin release
48
RX late phases of dumping
acarbose | ocreotide
49
Postvagotomy diarrhoea common in
truncal vagotomy
50
post partial gastrectomy patients with and pain, early satiety nausea
Bile or alkaline reflux gastropathy/gastritis
51
severe peptic ulcer diathesis secondary to gastric acid hypersecretion due to unregulated gastrin release from a non- cell endocrine tumor (gastrinoma)
Zollinger Ellison Syndrome
52
Role of gastrin in acid secretion
acts through gastrin receptors on parietal cells and by inducing histamine release from ECL cells
53
The gastronoma triangle where 80% of gastronomes are
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
most common nonpancreatic lesion; between 50 and 75% of gastrinomas are found here
Duodenal tumors
55
% of gastronomes malignant
>60%
56
MC s/s of gastrinoma
>90% PUD | 50% Diarrhea
57
% of gastronome in MEN I
25% PANcreas PARAthyroid PITuitary
58
Gastrin levels of gastronome patients
>150-200 | normal
59
When to obtain fasting serum gastric level
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
differentiate between the causes of hypergastrinemia in patients with indeterminate acid secretory studies
Gastrin provocative tests : 1. secretin stimulation test- most famous 2. calcium infusion study
61
Why should you stop PPI 1 week before testing for secretin test
PPI induced hypochlorhydria or achlorhydria may lead to a false-positive secretin test
62
Rx ZES
PPIs | ocreotide in somatostatin receptor positive
63
Gastritis | related to H pylori infection
Type B Gastritis
64
Gastritis | antral predominant
Type B= ANtral | Type A= Body
65
Gastritis antibodies to parietal cells/ pernicious anaemia autoimmune
Type A

GI (9 decks)

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