PEPTIC ULCER DISEASE IN CHILDHOOD Flashcards
Peptic ulcer is _________ or a _________ of the ________________________ with penetration to the _____________ and exposure of the _________.
discontinuity ; disruption
gastric or duodenal mucosa
muscularis mucosae ; submucosa.
Compared to ulcers, Erosions are (more or less?) superficial and _______________________.
More
do not involve the muscularis mucosae
PUD
Commoner in __________ and __________ than in the __________.
PUD has been reported worldwide in children.
Age :8-17yrs(mean 11yrs)
M:F ratio for all childhood PUD is 1.5:1. For primary PUD equal sex predilection has been described for in infants or young children.
adults ; teenagers
young children.
CLASSIFICATION of PUD
________
____________
________________
Primary
Secondary
Hypersecretory states
Primary PUD
Occur in otherwise healthy individuals.
•______ onset , (acute or chronic?)
• Usually _________.
• associated with ________ (15% of cases)
• Blood group O, Familial (30-40% of cases)
Recovery is the rule with proper medical therapy
Insidious; chronic
duodenal; H.pylori
Secondary PUD
Intracranial lesion( ________)
————,———-,—————————
Uraemia
______________ dx
Drugs: NSAIDS, Corticosteroids, Fe preps, Herbal medications
Hypoglycaemia
Cystic fibrosis
Cushion’s
Sepsis
Shock
Severe burns(Curling’s)
Collagen vascular
Gastric Ulcers
Secondary ulcers.
Commoner in __________
Benign gastric ulcers are normally found on the ___________, although they can occur anywhere in the stomach, rare in the gastric ________
Treatment (more or less?) difficult with (shorter or longer?) treatment duration.
More association with malignancy
younger children
lesser curvature; fundus
More; longer
Duodenal ulcers
(Primary or Secondary?) ulcers
>_______% associated with H.pylori.
Other risks: NSAIDS, family history.
occur most often in D1 ~90% located within 3 cm of the __________ ;
usually <1 cm in diameter, rarely 3 to 6 cm (giant ulcer).
• ulcer base often consists of a zone of ___________ with surrounding _________.
Malignant DUs are extremely (common; rare?)
Primary; 75
pylorus
eosinophilic necrosis; fibrosis
Rare
HYPER SECRETORY STATES
• ____________ syndrome
• Hyper___________
• ________ hyperplasia or hyperfunction
• Systemic mastocytosis(mast cells deposited in skin, lungs, liver, bone etc)
• _____________ syndrome
Zollinger Ellison syndrome
Hyperparathyroidism
G cell
Short bowel syndrome
AETIOLOGY/RISK FACTORS
Genetic: Genetic heterogeneity (Family history in 20-70%),
GU close relatives are at ______ fold risk, (same or not same?) for DU,
______zygoticTwins
Blood group _____
- Diet and Environment: _______,________,________, ________ –yes
3; not same
Mono; O
Hot Spices, Caffeine ?, Smoking, Alcohol
AETIOLOGY/RISK FACTORS
3. Helicobacter Pylori
Gram-__________ _______ ___________
Mainly acquired in ___________
Most infected individuals are asymptomatic;
____% develop peptic ulcer disease, ____% develop gastric cancer.
negative ; microaerophilic
spirochete ; childhood
15%; 1%
H.Pylori
Has unique survival abilities in the acidic environment of the stomach by producing
_________ : which allows it to ________ its microenvironment . Other virulence factors such as catalase, vacuolating cytotoxin, and lipopolysaccharide
Urease; alkalinize
AETIOLOGY/RISK FACTORS
- Emotional Factors
________
Acid secretion:
____ : low acid secretion or normal
_____: hypersecretors for acid. - Secondary factors
- Hypersecretory states
Stress
GU; DU
PATHOGENESIS OF PUD
In general, PUD results from an interaction between :
Protective forces that ___________ in the integrity of the gastric and duodenal mucosa and
Disruptive forces : those that contribute to mucosal ________ and _________
prevent a breach
inflammation and ulceration
Protective /Mucosal defensive Mechanisms
1. Surface mucus _________ secretion
2. _________ secretion into mucus
3. Mucosal _________
4. Apical epithelial cell transport
5.Epithelial _________ capacity
6.Elaboration of ____________
7. Protective _________
- Surface mucus gastric secretion
- Bicarbonate secretion into mucus
- Mucosal blood flow
- Apical epithelial cell transport
5.Epithelial regenerative capacity
6.Elaboration of prostagladins - Protective phospholipids
Disruptive mucosal mechanisms
- Gastric _________
- Acid-dependent _________
- Mucosal _________
- _________ infection
- Sepsis
- Traumatic injuries and _________
- Drugs (, NSAIDs, Steroids)
- Alcohol
- Cigarette smoking
- Stress
Gastric hyperacidity
2. Acid-dependent pepsin
3. Mucosal ischemia
4. Helicobacter pylori infection 5. Sepsis
6. Traumatic injuries and burns 7. Drugs (, NSAIDs, Steroids) 8. Alcohol
9. Cigarette smoking
10. Stress
CLINICAL PRESENTATION : HISTORY
Abdominal Pain : In younger children often a challenge. In toddlers and preschool age : dull and vague, and may or may not be aggravated by food intake. The older child and adolescent may, however, present in the typical adult fashion with sharp and burning pain localized to the __________ or _____________ regions. Pain may exhibit periodicity with frequent exacerbations and remissions over weeks to months.
Dyspepsia
periumbilical or epigastric
Dyspepsia
Major Criteria
___________ abdominal pain
Recurrent __________ (at least ____/mo)
Epigastric
vomiting; 3
Dyspepsia
Minor Criteria
1.Symptoms associated with eating (_______/_______)
2. _______ awakening the child at night
4. Heartburn
5. Oral _________
6. Chronic _______
7. Excessive belching/hiccuping 8. Early satiety
9. Periumbilical abdominal pain
10. Family history of peptic ulcer disease, dyspepsia
anorexia/weight loss
Pain; regurgitation
CLINICAL PRESENTATION : HISTORY
To elicit history of dyspepsia you need to have ______ major and _____ minor criteria.
Dietary history should be obtained in an effort to identify specific foods that ____________.
Family history of disease is important
Drug history the use of potentially causative medications (eg, NSAIDs, steroids, alcohol, smoking, and acid- suppressive medications).
One; two
CLINICAL PRESENTATION
GI __________ : common with secondary ulcers
Recurrent/Intractable ________: Gastric outlet obstruction(___________ common in children)
Weight loss
bleeding ; vomiting
pyloric stenosis
The natural history of peptic ulcers in children has been well correlated with age.
In early life (2–6 years), there is a tendency towards _________ and _________.
In the age group of 7–11 years, the ulcers are usually (acute or chronic?) , may _________, and (rarely or commonly?) bleed or become chronic.
In children older than 11 years of age, the behavior of the ulcers approximates that seen in _________
bleeding ; perforation.
acute ; perforate; rarely
adults
Physical examination
General examination impt: Pallor, clubbing, fluffy hair, other findings etc
Anthropometry
Abdominal examination: ________ tenderness, ________ tenderness, features of __________ occasionally if perforation has occurred(5%)
________ exam is important: _______ disease etc
Other systemic examn to rule out comorbid conditions
Epigastric; Periumbilical
peritonitis; Rectal; Perianal
DIFFERENTIAL DIAGNOSIS
Functional Abdominal Pain
_________________ disease
______________ /Gall stones
Acute/Chronic ____________
UTIs
__________ ____________
Inflammatory bowel
Acute cholescytitis
pancreatitis
Meckel’s Diverticulum
COMPLICATIONS of PUD
List 4
Bleeding
Penetration
Perforation
Gastric outlet obstruction
INVESTIGATIONS
Full blood count , blood film appearance
H.pylori testing:
_____________ , very useful in children
______________ not useful in young children
Stool for _____,_______,_________
Upper GI ________ + __________,
Biopsy : Rapid urease test,
____________________ is the recommended mode of diagnosis in children
Culture of biopsies –(slow or fast?) and yield is (low or high?)
Stool fecal antigen
Urea breath test
ova, parasites, occult blood.
endoscopy + Biopsies
Gastric Biopsy for Histology
Slow; low
INVESTIGATIONS
If GI endoscopy is not available then :
Upper GI series: demonstrate ulcer crater with ____________________ ( high false positive rates up to 30%).
_____________ estimation may be useful in cases of suspected Zollinger-Ellison syndrome:(Elevated or Depressed?) serum gastrin and gastric pH below _______ is strongly suggestive.
deformity of the duodenal cap
Serum gastrin; Elevated
2
Management of PUD
Therapy must achieve the following:
1._________________ /______________ therapy.
2. ____________ of ____________ if present.
For Acid Peptic disease: _______ are recommended
Acid suppression /buffering
Eradication of H. pylori
H. PYLORI TREATMENT
First-line therapy(_______ therapy) is the use of ________ and ______________ for ——— to __________ days.
This can be either:
____________ + ____________ + ____________; or
• ____________ + ____________ + ____________
or • ____________ + ____________ + ____________
Eradication rates:70-85%
Triple
one PPI and two antibiotics
10 to 14
omeprazole + amoxicillin + clarithromycin; or
• omeprazole + amoxicillin + metronidazole
or • omeprazole + clarithromycin + metronidazole
H. PYLORI TREATMENT
Second-line therapy (___________ therapy):
___________ + ___________ + ___________ + ___________ or ___________ for _____ days;
or
___________ + ___________ + ___________ + ___________ for ________ days.
Eradication rates :75-93%
Quadruple
omeprazole + bismuth subsalicylate + metronidazole + amoxicillin or
Tetracycline
14 days
Ranitidine + bismuth citrate + clarithromycin + metronidazole for14 days.
Levofloxacin based triple therapy-
______ + ________ +_______ for _____ days. (86% eradication)
Others
Rifabutin+Amox+PPI BD for 10days (79% eradicattion but Marrow toxicity)
Furazolidone + Amox +PPI for 14 days
lev+Amox+PPI for 10 days.
Sequential therapy :
————- +________ for ____ days, followed by ________ therapy for another ____ days with ________ and 2 alternative antibiotics
PPI +Amoxyl for 5 days, followed by triple therapy for another 5 days with PPI and 2 alternative antibiotics
• Concomitant therapy
_________ + _________ , _________ + _________ or _________ for_______ days
• Concomitant therapy
PPI + amoxicillin , clarithromycin + tinidazole or metronidazole for 7-14 days
Treatment of PUD
Dietary Intervention : Important for ulcer disease recalcitrant to therapy. It may be useful to exclude from the diet _________ causing increased acid secretion eg ———-,———-,_________
__________ diet is not particularly very useful
Exclude only foods that patient complains about(esp _______ fooods)
• •
beverages
tea, coffee and cola.
Bland; spicy
Treatment of PUD
Surgery is indicated when _____________
For secondary ulcers treat underlying disease.
H.pylori: After ____________ of treatment repeat H.pylori testing to ensure eradication of the disease.
Monitor for recurrent of symptoms
there are complications.
one month
PREVENTION
Prevention involves the avoidance of predisposing factors, such as ingestion of NSAIDs, coffee, smoking, and alcohol in older children and adolescents.
Secondary peptic ulceration in severely stressed and traumatized patients can be prevented by ___________ and ______________
Early recognition and evaluation of —————- will prevent the development of complications of PUD.
prophylactic antacids and H2-receptor blockers or PPIs.
abdominal pain
PROGNOSIS AND OUTCOMES
Peptic ulcer is usually a benign disease without a high mortality if diagnosed and treated early.
With modern therapy and eradication of H.pylori, the cure rate is more than _____%.
Mortality rates remain highest in _________ as well as in infants and children with systemic illness or injury who present with acute bleeding or perforation.
90
neonates
REFRACTORY ULCERS
Ulcers are considered refractory if healing is not evident after _____________ of therapy; the latter time frame is most appropriate for larger gastric ulcers (GU)
8 to 12 weeks
refractory symptoms vs refractory ulceration
Persistent symptoms in the absence of an active ulcer on endoscopy suggest that ???
other etiologies for the pain should be sought
TREATMENT OF ULCERS NOT ASSOCIATED WITH HP
(usually associated with _______)
Discontinue drug if possible,
concurrent use of __________,_________, or __________ agents (__________)
Use of selective cyclooxygenase 2 (COX 2) inhibitors
NSAIDS
PPI ; H2RA
cytoprotective ; misoprostol
