Lecture 80 -- Disease of the stomach Flashcards

1
Q

Peptic Ulcer Disease:

Erosion vs Ulcer

A

Erosion – a break in the mucosal lining

Ulcer -a break with depth into the submucosa

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2
Q

Peptic Ulcer Disease: causes

A

Causes: “PH, HP, nough SAID”

pH, H. Pylori, NSAID – 90%

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3
Q

Peptic Ulcer Disease:

pathogenesis

A

Pathogenesis:
1) Injurants to the lining –
Gastric acid or bile acid
NSAIDs

	2) Impaired mucosal Defenses: 
		Impaired mucus and bicarbonate secretion 
		Poor Blood Flow
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4
Q

what are Stress Ulcers ?
who get’s them?

what’s a Cushing’s ulcer?
what’s a Curling ulcer?

A

Stress Ulcers – -occur with severe physiological distress
ICU Patients, Intubated Patients, Post Trauma Patients,

	Cushing's Ulcer  = patients with increased Intra cranial pressure 

Curling Ulcer — in burn patients

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5
Q

4 complications of Ulcers?
which is the most common?
why is incidence decreasing?

A

Perforations – non sterile contents of the GI lumen break open into the peritoneal cavity

Bleeding - the most common complication

Penetration – ulcer breaks into adjacent organ

Obstruction – such as with an ulcer situated at the pyloric outlet

have largely been resolved with the use of PPIs

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6
Q

H. Pylori –
where will the ulcers be?

course of the infection ?

A

Gastric + Duodenal Ulcers
90% of Duodenal Ulcers; 80% of Gastric Ulcers are H pylori associated?

Initial Infection —>
Almost everyone will get chronic gastritis
10% Gastric or Duodenal Ulcers
Atrophic Gastritis – precursor for gastric cancer
Lymphoproliferative MALT Lymphoma (MALToma)

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7
Q

H. Pylori –

diagnostic techniques

A

serum antibody – this can be used for initial detection, but not thereafter as it will always be positive

stool antigen

Breath test – H pylori is urease producing; therefore give patient radiolabelled Urea, and detect if CO2 on exhalation is also radiolabelled; indicates presence of urease

Biopsy – spiral shaped bacteria in the mucosa
Giemsa, Genta or Silver Stains

CloTest – bx of the stomach and put in on an assay
If urease is present it will be positive

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8
Q

H. Pylori –treatment

A

Treatment – 2 antibotics + PPI
Amoxcillin, tetracyclin, metronidazole, clarithromycin

					If you eradicate the organism, risk of recurrent ulcer decreases
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9
Q

NSAIDs and Gastric Ulcers

pathogenesis?

A

NSAIDS = COX inhibition
therefore there is less: prostaglandins, thromboxane and prostacyclin
These are very important for protection of the gastric Mucosa

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10
Q

NSAID Ulcers: Risk factors:

concurrnet use of what drug is bad?

A

> 60 yo, past hx of ulcer, high doses of NSAID

Concomitant Steroid Use

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11
Q

NSAID Ulcers:

treatment and prevention

A

Prevention:
Avoid NSAIDs, Use COX2 selective NSAIDs (Celebrex)
Concomitant use of H2 blockers or PPI –
Misoprostol – PGE1 analog

	Treatment: Stop NSAID, start PPI
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12
Q

Zollinger Ellison Syndrome and Ulcers

what is ZE?
Prevalence in the US?
what % have Multiple endocrine neoplasia?

A

What is it? Gastrin secreting non beta cell tumor of the pancreas (Gastrinoma); which constitutively secretes Gastrin (loss of negative feedback from low pH), leading to gastric acid hypersecretion from parietal cells

		25% of ZE patients  have MEN 

1 in a million Americans have ZE

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13
Q

Manifestations of ZE

A

Gastric and Small intestinal ulcers,

Diarrhea (due to the volume of the extra acid and malabsorption from inhibition of pancreatic enzymes),

Severe GERD

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14
Q

Diagnosis of ZE

A

hypergastrinemia in the setting of Low pH

Secretin Provocation Test (normally secretin inhibits gastrin release)

Localizing the Tumor:

Ocreotide

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15
Q

Treatment of ZE

A

Treatment:
Resection
High Dose PPI
Ocreotide – somatostatin analog

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16
Q

Acute Gastritis –
What is it:
Causes

A

What is it: gastritis is inflammation without breaks, but it can be erosive or hemorrhagic

Causes:  Toxins and drugs: EtOhH, Aspirin, NSAIDs, Chemo Physical Agents: Radiation Vascular: Ischemia, Vasculitis  --- patients who are hypotensive  Gastro-Duodenal Reflux - post gastrectomy (as part of Whipple?)--- bile reflux gastritis  Stress Gastritis
17
Q

Describe the normal metabolism of B12?
what cells secrete intrinsic factor?
what is pernicious anemia?

A

Salivary Complex — Haptocorrin (R factor) + B12
Pancreatic enzymes – cleave B12 from Haptocorrin
B12 binds to intrinsic factor (from the parietal cell)
B12 is then absorbed into the terminal ileum

Pernicious Anemia – lack of B12 leading to macrocytic anemia in the setting of antibody destruction of the GI

	Cause: gastric atrophy and loss of IF production 
	Autoimmune tendencies
18
Q

diagnosis of pernicious anemia –
what features must be present ?

what test is rarely done (but commonly tested on boards) and what isit?

A

Low B12, macrocytic anemia, intrinsic factor/parietal cell antibodies

Achlorhydria – neutral pH

Schilling test (rarely done but commonly tested) – give high dose B12; and some radioactive B12;

		If it appears in the urine -- indicative of dietary insufficiency; 

		If it does NOT appear in the urine -- not just a dietary insufficiency  given them IF with the radioactive B12, to prove it was due to IF deficiency \ could also give them pancreatic enzymes to see if the deficiency is there
19
Q

Gastric Neoplasia:

benign lesions

A

Hyperplastic polyps – (do have pre-malignant potential, but along are totally benign)

	Adenomatous polyps  -- some can become adenocarcinoma 

	Leiomyomas -- smooth muscle 

	Lipomas - fatty
20
Q

Gastric Neoplasia:
Malignant lesions

(GISTs are responsive to what therapy?)

A

Adenocarcinoma – most common (“gastric cancer”
Lymphoma –
GIST – Gastro-intestinal stromal tumors == responsive to Gleevac (imatinib) (anti BCR-ABL)

	Carcinoid Tumors
	Kaposi Sarcomi
21
Q

Gastric Adenomcarcinoma –

  • if in the distal stomach … associated with?
  • if in the proximal stomach.. associated with?

early and late symptoms

A

distal – a/w H pylori

PRoximal – not associated with H pylori

Early: No symptoms; often diagnosed late; not screened for
But is screened for in Asian countries
Late: Anorexia, early satiety, N/V, weight loss, melena, hematemesis

22
Q

Gastric Adenomcarcinoma – physical exam findngs?
(common mets and their epynoyms)
-

A

epigastric mass, enlarged liver (from gastric mets)

Mets:
Hepatomegaly,
Left Supraclavicular Nodes – Virchow’s Node (common for gastric cancers)

Rectal Shelf Metastasis – Blumer’s Shelf
Umbilical Nodes – Sister Mary and Joseph Nodules

23
Q

three vsacular lesions of Stomach…

which has the worst mortality with bleeding?

A

Angiodysplasia (aka Arteriovenous Malformation, AVM)

Watermelon Stomach / Gastric Antral Vascular Ectasia:

Gastric Varicies --  30% mortality with active bleeder
24
Q

Gastroparesis:
• What is it?

Cause

Diagnosis

A
  • What is it?
    * Delayed gastric emptying
    * Disordered peristalsis
    * Complicated process involving interaction of sympathetic, parasympathetic, plexi, smooth muscle cells

Cause: any diseases that affect the NS of the gut
• Diabetes is most common cause:
others include — slceroderma, Post viral, anti-cholinergis, anti-histamines, opiates

25
Q

Gastroparesis

Treatment

side effects

A
  • Metoclopramide – most common cause for litigation; good drug for gastric emptying but lots of bad side effects such as tardive dyskinesia which can be permanent
    * Domperidone – not available in the US; can prolong QT interval; lactation
26
Q
Miscellaneous gastric Diseases: 
Congenital 
Anatomical 
Menetrier's Disease
Bezoar (name three kinds)
A

Congenital – Hypertrophic pyloric stenosis

Anatomical -- Diaphragmatic Hernia; Volvulus 

Menetrier's Disease -- Thickened folds of the stomach; gastric hyperplasia of mucosa. 

Bezoar – conglomeration of indigestible materials
(phyto (vegetables), Tricho (hair), Pharmaco (eg ASA))

27
Q

Upper gastrointestinal bleeding:
what is meant by “upper”

Hemetemesis: BRB vs COffee Ground

Melena

Hematochezia

Causes:

A

Upper = ligament of treitz (duo - jejunal junction)

Hematemesis –
BRB – brisk bleeding
coffee ground – oxidized

Melena -- dark tarry, foul smelling stool 

Hematochezia -- red blood through stool 
Causes: 			
i. Peptic ulcer
ii. Gastritis
iii. Esophagitis
iv. Mallory Weiss Tear --- tearing with forceful 
v. Gastro esophageal Varices
Dieulafoy Lesion
28
Q

Treatment for GI bleeds:

A

Treatment for GI bleeds:
i. Stabilize patient
□ Two large bore IVs
□ Isotonic fluids
□ Blood products – type and crossed
ii. Check Labs – CBC, H&H, Liver tests, platelets, coags
iii. Start PPIs — blood clots better in neutral environment
iv. Nasogastric Lavage – what type of blood
v. Urgent Endoscopy

Endoscopic Therapy

			1. Cautery
			2. Hemoclips
			3. Epinephrine Injection
			4. Banding