Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med III Exam 1 > PUD and Gastric CA > Flashcards

PUD and Gastric CA Flashcards

1
Q

PUD definition

A

defect in gastric or duodenal mucosa that extends through the muscularis mucosa into deeper layers of the wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Layers of stomach wall

A

mucosa, submucosa, muscularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Etiology of PUD

A
  1. H. pylori *
  2. NSAIDs *
  3. Other
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Most common cause of PUD

A

H. pylori; incidence increases w/ age

may predispose to gastric CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Inhibit gastrin release

A

low pH
prostaglandins
SS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Increase gastrin release

A

stomach distention

presence of peptides/AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Gastrin role

A

increase gastric motility

stimulate parietal cells to secrete HCl and pepsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Secretin role

A

inhibit stomach motility
decrease bile secretion
increase bicarb secretion from pancrea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

1 cause of GI bleed

A

PUD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

H. pylori description

A

gram (-) rod
Motile flagella (attaches to gastric mucosa)
oral-oral or fecal-oral route
disrupts protective properties by decreasing gastric mucus and mucosal bicarb secretion
raises pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Increase risk of PUD w/ NSAIDs

A
  • prior hx of PUD/ulcer complications
  • H. pylori infection
  • > 75 YO
  • increased dose, time, duration of use
  • concomitant use of steroid, other NSAID, anticoag, low dose ASA, SSRI, alendronate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

H. pylori virulence factors

A
  1. flagella- attach, move
  2. urease - hydrolyze gastric urea to form ammonia, that helps neutralize gastric acid, enabling it to penetrate gastric mucosa
  3. Adhesins: adhere to epithelial cells
  4. Cause inflammation: causes G cells in antrum to secrete gastrin and therefore HCl increases

(ulcers are immediately friable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Concomitant drugs that worsen PUD from NSAID

A 
steroid
other NSAID
anticoagulants
ASA
SSRI
alendronate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

NSAIDs

A

ibuprofen
ASA
naproxen
toradol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MOA of PUD w/ NSAIDs

A

NSAIDs block COX, therefore preventing prostaglandin synthesis (PGE2) – prostaglandins inhibit gastrin secretion and increase mucous secretion, and promote epithelial cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prostaglandin role in stomach health

A
  • inhibit gastrin secretion
  • increase mucous secretion
  • promote epithelial cell proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Presentation of PUD

A

asymptomatic (70%)
Abdominal pain/discomfort

dyspepsia (belching, bloating, distention)
Nausea, early satiety, comiting

Complications: hematemesis, melena, fatigue, dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Gastric vs. duodenal ulcers

A

gastric: worse after meal (30min-1hr), vomiting, more likely to hemorrhage/hematemesis; weight loss/anorexia
duodenal: relieved by meals! (worse 2-3 hrs post meal), vomiting uncommon), less likely to hemorrhage (melena), weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Melena

A

duodenal ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hematemesis

A

gastric ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Worse w/ meals

A

Gastric ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

vomiting uncommon

A

duodenal ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

weight gain

A

duodenal ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

PUD alarm sx

A 
bleeding
unexplained IDA
early satiety
unintentional weight loss
progressive dysphagia/odynophagia
acute onset of upper ab pain
persistent vomiting
family hx of UGI CA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Complications of PUD

A

bleeding (most common)
perforation
penetration
gastric outlet obstruction (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hemorrhage in PUD

A

hematemesis, melena or hematochezia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Dx/Tx of hemorrhage in PUD

A

stabilize with IV fluids or PRBCs
start IV PPI
perform EGD!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Dark tarry store (melena)

A

UGI

29
Q

Hematemesis

A

UGI (gastric)

30
Q

Hematochezia

A

bad sign! hemorrhaging fast and can’t digest the blood

31
Q

Tx of bleeding

A

thermal coagulation
hemoclip placement
injection tx

32
Q

Perforation presentation

A 
severe, diffuse, abdominal pain
tachycardia
weak pulse
N/V
may progress to "board-like abdominal rigidity"
33
Q

Dx of perforation

A

hx/PE
UPRIGHT CHEST AND ABDOMINAL X-RAY
possible CT to localize

34
Q

Tx of perforation

A 
IV fluid
NG tube
NG suction for gastric decompression
IV PPI
broad spectrum abx
SURGERY!!!
35
Q

Contraindicated with perforation

A

UGI with barium (use gastrografin)

36
Q

Dx of hemorrhage

A

EGD

37
Q

Dx of perforation

A

Upright chest/ab X-ray

38
Q

Penetration definition

A

penetration of ulcer through bowel wall w/o free perforation and leakage of luminal contents into peritoneal cavity;

goes into some other structure – pancreas!

39
Q

Presentation of penetration

A

sx due to affected structure
sx like pancreatitis
pain w/o meal association, more intense pain, pain referral to back

40
Q

Gastric outlet obstruction cause

A

scarring/fibrosis or inflammation/edema in pyloric channel; blockage of contents leaving stomach into duodenum

41
Q

Presentation of gastric outlet obstruction

A 
vomiting
early satiety
bloating
epigastric pain
weight loss 
anorexia
42
Q

Dx of gastric obstruction

A

imaging- dilated stomach

43
Q

Tx of gastric obstruction

A

IV fluid
NG tube- gastric decompression
IV PPI

EGD w/ endoscopic balloon dilation or surger – if fail w/ medical tx

44
Q

PE for PUD

A

ab exam: epigastric tender, RUQ tender, peritoneal signs (perforation), succussion splash

Vitals: hypotension, tachy (complications)

Rectal exam: melena, hemoccult positive, bright red blood

45
Q

Succussion splash

A

place stethoscope over upper abdomen and rock the pt back and forth at hips; retained gastric material >3 hours after meal will generate splash sound and indicate presence of hollow viscus filled w/ both fluid a gas

46
Q

Succussion splash suggests

A

gastric outlet obstruction

47
Q

Dx of PUD

A

EGD - gold standard
UGI

H. pylori:

  • urea breath test
  • fecal antigen test
  • serology
  • bx during EGD (most specific and sensitive!!!)
48
Q

Urea breath test

A

identifies active H. pylori infection

  • discontinue PPI 2 weeks prior and bsimuth/abx 4 weeks prior
  • drink urea, urease converts to CO2 and NH3, test measures radioactive CO2
49
Q

Fecal antigen test

A

antigen in feces

discontinue PPI 2 weeks prior
discontinue bismuth/abx 4 weeks prior

50
Q

Serology

A

identifies IgG antibody to H. pylori
HIGH FALSE POSITIVE; AND FALSE NEGATIVE
* not recommended *

51
Q

Tx of PUD

A
  1. eradicate H. pylori and confirm eradication in 4 weeks after treatment
  2. PPI if h. pylori absent or sx after eradication
  3. if sx persist, treat 8-12 weeks with TCA!
  4. if sx persist, treat 4 weeks w/ PROKINETIC
  5. if sx persist, perform EGD

(discontinue NSAID, ASA, alcohol, tobacco)

52
Q

H. pylori treatment

A

Bismuth quadruple therapy x 14 days:

  • PPI BID
  • Bismuth 524 mg QID
  • Tetracycline 500 mg QID
  • metronidazole 250 mg QID
53
Q

Zollinger-Ellison Syndrome (ZES): what is if?

A

gastrinoma (dudoenum or pancreas) hypersecretes gastrin

  • increased HCl
  • increased gastric motility (absorption issues)

more common in men

54
Q

Etiology of ZES

A

sporadic (80%)

MEN1 (20%) - also in pituitary tumors, pancreas, parathyroid

55
Q

Presentation of ZES

A

recurrent PUD - often distal to duodenal bulb* (multiple on EGD***)
abdominal pain
diarrhea (steatorrhea)

56
Q

Dx of ZES

A

fasting serum gastrin >1000 pg/mL (10x)
gastric pH <2
Secretin stimulation test (gastrin should dec but it doesn’t)
CT abdomen to localize tumor

57
Q

Tx of ZES

A

PPI*

or H2 blocker

58
Q

Gastric CA risk factors

A 
gastric ulcers***
adenomatous polyps
intestinal metaplasia
dietary (nitroso compounds, high-salt diet w/ few veggies)
ETOH/tobacco use
Chronic H.pylori infection
59
Q

Sx of gastric CA

A 
early: asymptomatic
weight loss
persistent ab pain
early satiety
nausea, anorexia, dysphagia
Gastric ulcer hx (25%)
Occult GI bleed
Late: palpable stomach mass, succussion splash, paraneoplastic syndromes
60
Q

Dx of gastric CA

A

EGD* - gastric vs esophageal CA
UGI- 2nd line
Staging (TNM)

determine nodal involvement, distant lesions, invasion of vasculature, depth of tumor

61
Q

Most common type of gastric CA

A

adenocarcinomas (95%)

62
Q

Gastric CA on EGD

A

subtle polypoid protrusion, superficial plaque, mucosal discoloration, depression or ulcer

63
Q

Signs of metastatic disease

A

Virchow’s node (most specific)
sister Mary Joseph’s node/nodule
Left axillary node (irish node)

64
Q

Virchow’s node

A

left supraclavicular lymph node (most common); most specific for gastric cancer

65
Q

Sister Mary Josephs nodule

A

periumbilical nodule

66
Q

irish node

A

left axillary node (nonspecific)

67
Q

Tx of Gastric CA

A

early (rare)- endoscopic mucosal resection

advanced- total or partial gastrectomy if resection possible

unresectable - chemo vs chemoradiotherapy

68
Q

Workup for dyspepsia

A

> 60 YO: EGD!!!

  • PUD- treat
  • no organic cause, either function of H. pylori

<60 YO: EGD if any of the following:

  • weight loss
  • overt GI bleed (visible)
  • > 1 alarm feature
  • Rapidly progressive alarm features

if no EGD- test for H. pylori

69
Q

Alarm features

A 
unintentional weight loss
progressive dysphagia
odynophagia
unexplaind IDA
persistent vomiting
palpable mass or LAD
family hx of UGI CA

Clin Med III Exam 1 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions