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
