GIT Flashcards

1
Q

Meconium ileus mainly due to….

A

pancreatic insufficiency, the distal ileum becomes impacted with thick, viscous meconium. This is associated with cystic fibrosis in most cases, with 20% of newly diagnosed children developing meconium ileus

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2
Q

Most common site of Duplication cysts

A

the ileocecal region

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3
Q

Presentation of Duplication cysts

A

Presentation may be with an abdominal mass, or obstruction

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4
Q

What is most common defect in midgut rotation

A

duodenum lying to the right of the vertebral column instead of the left, with the caecum lying in the upper abdomen to the left of the duodenum

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5
Q

Ix of choice of Midgut malrotation

A

A barium meal is then the investigation of choice as it can show the position of the duodenal–jejunal flexure.

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6
Q

Incidence of Meckel’s diverticulum?

A

(2–4% of newborn infants)

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7
Q

Cause of Meckel’s diverticulum?

A

when the remnant of the omphalomesenteric duct does not fully regress and remains attached to the ileal mucosa (F

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8
Q

Ix of choice in Meckel’s diverticulum

A

technetium-99m scan (the sensitivity of this is 85% in children with a specificity of 95%).

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9
Q

Incidence of Gasrtoschesis

A

4 per 10,000 births

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10
Q

Risk factors of Gastroschesis

A

low maternal age,
drug misuse,
low socioeconomic status,
smoking
ethnic origin.

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11
Q

Site of herniation in Gastroschesis

A

through the anterior abdominal wall on the right-hand side of the umbilicus

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12
Q

What is the cause of Gastroschesis

A

spontaneous herniation of the intraabdominal wall in utero (possibly at the site of the right omphalomesenteric artery) or

from incomplete reduction of the abdominal contents following rotation during the first weeks of fetal life.

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13
Q

معلومة

A

In Gastroschesis

There is a high risk of intrauterine death (15%) due to ischaemia and thus serial antenatal ultrasound scans are recommended

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14
Q

Type of surgery in Gastroschesis

A

primary closure, or secondary

if the defect is too large to replace all the contents in one stage without causing respiratory compromise from splinting of the diaphragm.

In this case, a silo may be used to preserve the intestinal contents while complete closure is awaited.

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15
Q

Incidence of Hirschsprung’s disease

A

1 in 5000 live births

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16
Q

Cause of Hirschsprung’s disease

A

absence of ganglion cells in a variable segment of bowel (aganglionosis).

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17
Q

Most common affected site in Hirschsprung’s disease

A

sigmoid and rectum

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18
Q

Type of Intestinal obstruction in Hirschsprung’s disease and why?

A

functional bowel obstruction.

Due to lack of ganglion cells causes an inability of the bowel to relax.

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19
Q

‘explosive diarrhoea’. ?

A

Occurs in Hirschsprung’s disease as Dramatic decompression occurs on digital examination

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20
Q

Dx of Hirschsprung’s disease

A

rectal suction biopsy to confirm the absence of ganglion cells (in older children, a strip rectal biopsy)

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21
Q

Major post op complication in Hirschsprung’s disease

A

Enterocolitis

22
Q

Post op complication of Hirschsprung’s disease

A

malaise, fever, diarrhoea and generalized sepsis.

23
Q

The most common site in intussusception

A

ileocaecal junction

24
Q

Sx of intussusception

A

acute onset abdominal pain, drawing up of the legs and pallor.

25
Q

What is a late sign in intussusception

A

have ‘redcurrant jelly’ stool

26
Q

Dx of intussusception

A

ultrasound scan, which shows a target-shaped mass

27
Q

Intussusception Mx

A

Treatment aim is to reduce the intussusceptions with an air enema, but surgical reduction may be necessary.

28
Q

swallowing centre in…..

A

cerebral medulla

29
Q

Swallowing is under control of which nerve?

A

cranial nerves V, IX and X.

30
Q

Antral peristalsisemptying

A

3 per minute

31
Q

Which part is responsible for the mixing of food.

A

The antral peristaltic contractions

32
Q

What is the amount of gastric fluid in well hydrated child

A

10 and 20 mL/kg of gastric fluid per day

33
Q

Gastric ph at birth

A

6-8

34
Q

1 day infant Gastric PH

A

1-3

35
Q

معلومة

A

Only by age 3 years does the production of acidity reach adult capacity.

36
Q

Aspirin and gastric ph

A

at low pH aspirin is absorbed from the stomach almost as rapidly as water, but, as the pH of the stomach rises, aspirin is absorbed more slowly.

37
Q

What contents delay gastric empting

A

fats

38
Q

cotransport Na +including:

A

• Amino acids (e.g. glycine)

• Dipeptides

• Tripeptides

.Glucose

39
Q

Why there is watery secretory diarrhea in cholera or Ecoli infections?

A

Cholera toxin and E.coli cause an increase in the levels of cAMP, so driving chloride flow across the brush border into the lumen, and hence the net movement of water with it. This results in watery, secretory diarrhoea.

40
Q

The maximal absorptive capacity of the adult large bowel is……

A

2–3 L/day

41
Q

Input into small intestine……

A

9 L/day (diet: 1.8 L; e enous secretions: 7.2 L)

42
Q

Output of fluid in faeces

A

100–200 mL/day

43
Q

Pancreatic exocrine secretions are controlled by……

A

secretin and cholecystokinin. Secretin is produced in response to the presence of acidic chyme in the duodenum. Cholecystokinin is produced when fat is present in the duodenum.

44
Q

secrete bicarbonate and mucus. The latter provides a protective barrier against damage from mechanical trauma from peristalsis, autodigestion and acid.

A

Mucous neck cells

45
Q

produce pepsinogen. Pepsinogen is a ally a precursor of pepsin, and must be converted to pepsin in order to allow protein digestion to amino acids.

A

Chief cells

46
Q

produce hydrochloric acid and i sic factor. Hydrochloric acid activates pepsinogen to its active form, pepsin, and helps break down connective tissue fibres within food contents whilst destroying microorganisms within the food. Intrinsic factor is important for the absorption of vitamin B 12 in the terminal ileum.

A

Parietal cells

47
Q

found in the pyloric area and secrete the hormone gastrin, which is integral in stimulation of the parietal and chief cells to produce their enzymes.

A

G cells

48
Q

cells produce histamine, which in turn stimulates gastric acid secretion by the parietal cells.

A

Enterochromaffin-like cells

49
Q

produce somatostatin, whose functions include the inhibition of acid secretion.

A

S cells

50
Q

histological findings of coeliac disease include:

A

• Flattened duodenal mucosa with loss of crypt architecture

• Intraepithelial lymphocytosis

• Glandular hyperplasia