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1 > Pathophys & tests for upper GI pathology > Flashcards

Pathophys & tests for upper GI pathology Flashcards

1
Q

H pylori serology

A

Infection elicits a local and systemic IgG-mediated immune response
ELISA and rapid office-based immunoassays
Serology is the test of choice when endoscopy is not indiated
90% sensitivity, specificity
-‘s: antibody titres can remain high for up to a year, cannot test for eradication

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2
Q

Urea breath test

A

Carbon-labeled urea
H. pylori can hydrolyze urea
sensitivity and specificity >95%
ingest urea labelled with either 14C or 13C - 13C requries mass spec, but 14C radiation
Urea metabolized to ammonia and labelled bicarb in the presence of H. pylori
Less expensive than endoscopy, samples the entire stomach
false-negatives can occur if the test is done too soon afte treatment, so test 4 weeks post-tx
best method to test for eradication

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3
Q

Esophagogastroduodenoscopy (EGD)

A

Visualization and biopsy
Surgical procedure
Recommended with suspicious of esophagitis, but not required for every patient undergoing reflux evaluation
Method of choice for PUD
Biopsy from esophagus, stomach, and duodenum for histology and H. pylori
Hemostatic therapy

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4
Q

Barium X-ray (upper GI)

A 
can often demonstrate peptic ulcers
Radiation exposure
lack of technicians
visualize obstructions/strictures
limited utility in modern practice
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5
Q

Esophageal manometry

A

assessment of LES pressure and relaxation, peristaltic activity (contraction amplitude, duration, and velocity
generally not indicated in evaluation of uncomplicated GERD because most have a normal resting LESP.

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6
Q

24h ambulatory pH monitoring

A

GERD
Indications:
- document excessive acid reflux in suspected GERD but withoud endoscopic esophagitis
- evaluate efficacy of surgical/medical therapy

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7
Q

Achalasia

A

Poorly relaxing LES without known cause

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8
Q

Diffuse esophageal spasm

A

normal peristalsis intermittently interrupted by simultaneous contractions with uncertain cause

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9
Q

Hypercontractile esophagus

A

Esophageal contraction pressure above normal (2SD)
“Nutcracker” esophagus when high pressure occurs in esophageal body and hypertensive LES when resting LES pressures are raised

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10
Q

Hypocontracting esophagus

A

non-specific motility disorders
motility tracings characterized by:
- low amplitude (<30 mmHg) peristalsis
- simultaneous contractions in distal esophagus
- failed peristalsis: wave does not transverse entire length of distal esophagus

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11
Q

Secondary esophageal motility abnormalities

A

abnormal motility patterns secondary to systemic disease

e.g. scleroderma, Chagas’ disease, Amyloidosis

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12
Q

GERD

A

transient relaxation of LES, allowing for spontaneous or stress (increased abdominal pressure) reflux

other causing factors:

  • decreased clearance of acid from esophagus due to decreased peristalsis, or salivary secretion
  • reduced resistance of esophageal mucosa to gastric content
  • delayed gastric emptying
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13
Q

Risk factors for GERD

A 
hiatal hernia
pregnancy
diabetes mellitus
CT disorder
obesity
chocolate, caffeine, alcohol, high fat foods)
NSAIDs, opioids, anticholinergics
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14
Q

Stress gastritis

A

stress-related mucosal erosions and subepithelial hemorrhages typically found in critically ill patients
Despite normal/decreased acid secretion

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15
Q

H. pylori gastritis

A

causes gastric mucosal inflammation with PMNs and lymphocytes despite not being invasive

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16
Q

Pernicious anemia gastritis

A

autoimmune, involves fundic glands
resultant achlorhydria and vit B12 malabsorption (gastritis caused by autoimmune disorder, anemia caused by decreased IF released from damaged parietal cells, therefore less B12 absorbed)

17
Q

Peptic ulcer disease

A

disruption of mucosal integrity of the stomach/duoenum caused by local inflammation resulting from imbalance between damaging effects of noxious substances and ability of mucosa to defend against them

Etiology: H. pylori, NSAIDs and acid hypersecretory states such as Zollinger-Ellison syndrome
Risk factors: smoking, alcohol, stress, cocaine, FHx

18
Q

H. pylori ulcer formation

A

survival due to urease activity
Epithelial cell disruption from secretion of CagA, VacA
Induction of local immune responses and cytokine secretion
increased gastrin and gastric acid secretion due to cytokine-induced gastrin secretion, reduced antral somatostatin secretion, local alkaline environment
other factors contributing to local tissue injury

19
Q

Gastric cancer

A

diffuse: poorly differentiated, lacks glandular structure, poorer prognosis

Intestinal form: gland-like tubular structures mimicking intestinal glands, closely linked to environmental and dietary factors, also H. pylori, cigarette smoking

S/S: weight loss, abdominal pain, fatigue, early satiety, hematemesis, melena, nausea, vomiting, supraclavicular lymphadenopathy, periumbilical lymphadenopathy (Sister Mary Joseph Nodes)

20
Q

GIST tumours

A

gastrointestinal stromal tumours
most common mesenchymal tumour in the digestive tract
most are symptomatic and large lesions can ulcerate and bleed

21
Q

Barrett’s esophagus

A

Distal squamous mucosa replaced by metaplastic columnar epithelium with goblet cells due to prolonged injury from GERD
gross: red velvety GI Type mucosa between pale squamous mucosa of lower esophagus and lush pink gastric mucosa

Major risk for gastric adenocarcinoma - higher risk >2cm Barrett’s esophagus

Diagnosis: endoscopic appearance and histological findings

long segment: >3cm from GE junction
need endoscopy every 1-2 y

22
Q

Esophageal cancer

A

Most common: squamous (smoking/alcohol) and adenocarcinoma (likely from GERD)
Both carry a poor prognosis
Risk factors: tobacco, alcohol, GERD, obesity, history of head and neck cancer, history of breast cancer treated with radiotherapy, frequent consumption of extremely hot beverages
S/S: weight loss, dysphagia, odynophagia, GERD
Lymphadenopathy in Virchow’s node, hepatomegaly, pleural effusion

Diagnostic: barium swallow (esophagogram)
Tx: chemo/radiotherapy, surgery

23
Q

Triple therapy for H. pylori

A

patient has not received a macrolide previously

PPI + clarithromycin + amoxicillin

if allergic to penicillin - PPI + clarithromycin + metronidazole

eradication rate 70-85%

24
Q

Quadruple therapy for H. pylori

A

Allergic to penicillin, or failed triple therapy

Bismuth + metronidazole + tetracycline + PPI

eradication rate 75-90%

25
Q

Vomiting mechanism

A

gastric relaxation, inspiration, close glottis, diaphragm and abdominal muscles contract, gastric contents forced outward

Vagal afferent from GI
controlled by vomiting centre in medula oblongata

26
Q

Causes of acute upper GI bleeding

A 
PUD
esophagitis
portal HTN
neoplasm
vascular disorder
traumatic - Mallory-weiss
27
Q

causes of chronic upper GI bleeding

A 
esophagitis
portal hypertensive gastropathy
malignancies
angiodysplasia
radiation
IBD
28
Q

H. pylori strain

A

CagA+ more seen in symptomatic patients

29
Q

DU symptom referral indication

A

> 45 yo, “alarming” symptoms - weight loss, blood, etc

30
Q

DU indications for surgery

A 
bleeding
perforation
obstruction
intractability
suspicions for gastric cancer
31
Q

Operations for DU

A

sectioning the vagus - vagotomy
eliminating hormone stimulation from the antrum (antruectomy)
decreasing the number of parietal cells (gastric resection)

32
Q

NSAID-related ulcer characteristics

A

more common in the elderly
often large
more likely to bleed

33
Q

Causes of esophagitis

A

GERD
eosinophilic esophagitis
infections - candida, herpes simplex
drug: caustic injury, sclerosant injury, “pill esophagitis”

34
Q

Causes of SCC in esophagus

A 
smoking
alcohol
fungal contamination of food
nitrosamines in food and water
vitamin and mineral deficiencies
HPV
35
Q

Acute gastritis

A

hemorrhagic/erosive gastritis

36
Q

Chronic gastritis

A

H. pylori
multifocal atrophic gastritis
autoimmune gastritis
others

37
Q

Atrophic gastritis

A

rare in NA, common in 3rd world countries
develops from H. pylori gastritis
hypochlorhydria
histologically characterized by the presence of intestinal metaplasia
may be a precursor for gastric cancer

38
Q

Autoimmune gastritis

A

immune destruction of secretory glands
may have serum antibodies to parietal cells/IF
could lead to pernicious anemia

39
Q

Precursor lesions of gastric carcinoma

A 
H. pylori gastritis
Chronic atrophic gastritis
intestinal metaplasia
pernicious anemia
adenoma
previous partial gastrectomy
dysplasia

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