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Gastro > oesophagus + stomach > Flashcards

oesophagus + stomach Flashcards

1
Q

Embryology of oesophagus:
- tissue it develops from
- distinguishable at what gestation

A
  • from post-pharyngeal foregut
  • distinguishable from stomach by 4/40
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2
Q

epithelium of oesphagus vs stomach, and where it switches

A

oesophagus = stratified squamous
at GOJ, changes to stomach simple columnar

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3
Q

compare the UES vs LES
- location
- muscle type
- pressures

A

UES
- at cricopharyngeus muscle
- 50 mmHg
- Striated muscle

LES
- at gastroesophageal sphincter – INTRA-ABDOMINAL
- Tonically contracted
- 5-10 mmHg
- Smooth muscle
- Relaxation by NO +/- VIP

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4
Q

types of muscle in oesophagus

A

Upper 1/3 striated
- Innervated by spinal accessory nerves
- Allows for voluntary initiation of swallowing

Middle 1/3 mixed
- Innervated by dorsal motor nerve of vagus

Distal 1/3 smooth muscle
- Innervated by dorsal motor nerve of vagus

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5
Q

4 causes of extrinsic oesopahgeal obstruction

A
  1. oesophageal duplication cysts
  2. neurenteric cysts
  3. mediastinal LN (infection e.g. TB, or neoplasm)
  4. vascular anomalies
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6
Q

oesophageal duplication cysts:
- embryology - how they form
- associated with
- how can they present

A
  • aberrant foregut division 3-4/40
  • a/w vertebral anomalies
  • most commonly resp distress from airway compression. Also lined with gastric epithelium, can have infection/perf.
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7
Q

most common cause of paediatric oesophageal obstruction, and kind of dysphagia is causes?

A

EoE - mechanical, so solid only at first. intermittent.

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8
Q

solid food dysphagia:
- means what
- intermittent vs progressive causes

solid and liquid food dysphagia:
- means what
- intermittent vs progressive causes

A

solid food = mechanical obstruction
- intermittent e.g. lower ring/web, EoE
- progressive e.g. peptic stricture, cancer

solid + liquid = neuromuscular obstruction
- intermittent e.g. DOS
- progressive
…. reflux? -> scleroderma
… respiratory Sx? -> achalasia

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9
Q

cricopharyngeal achalasia vs incoordination

A

achalasia = failure of complete relaxation of UES
incoordination = full relaxation of the UES but incoordination of the relaxation with the pharyngeal contraction

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10
Q

mean age of achalasia onset in chidlren

A

8.8y

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11
Q

define (oesophageal) achalasia

A

Primary esophageal motor disorder characterised by
1) Loss of LES relaxation (resting pressure > 30 mmHg)
2) Loss of esophageal peristalsis

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12
Q

pathogenesis of achalasia

A
  • theory: inflammation and degeneratin of neurons
  • Loss of inhibitory myenteric ganglion cells that innervate the smooth muscle of distal oes/LES. These use nitrous oxide.
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13
Q

triple A syndrome (or Allgrove syndrome) triad

A

12q13 gene mutation, AR:
1) achalasia
2) alacrima
3) ACTH insensitivity (low BSL)

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14
Q

achalasia: ways to Ix, and signs. Which is the gold standard test for achalasia

A
  1. CXR - no air in stomach, dilates oes
  2. Ba fluoro - birds beak
  3. manometry (GS) - aperistalsis, LES not relaxing
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15
Q

complications of achalasia

A
  1. respiratory: asp, bronchiectasis, abscess
  2. GI: malnutrition, inflam-> cancer
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16
Q

DOS:
- what
- main symptoms other than dysphagia
- radiological sign

A
  • normal peristasis, but intermittent high pressure waves
  • Chest pain
    a. Barium esophagogram – corkscrew pattern, pseudo-diverticula caused by spasm
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17
Q

types of hiatus hernia

A

type I = sliding = GOJ into thorax (more reflux)
type II = paraesophageal (more full after eating)
type III = both

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18
Q

GER vs GERD

A

GERD = reflux with one of
1) histopath diagnosis
2) cx of reflux e.g. asp, FTT

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19
Q

peak age of GER

A

at 4mo 2/3 of children will have at least 1 ep per day
at 12 mo, only 5%

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20
Q

pill oesophagitis causes

A

PAINT

P = potassium chloride
A = alendronate
I = iron
N = NSAIDS
T = tetracyclines

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21
Q

primary pathophys problem of GER in kids.
what are other pathophys of GER?
(total 5 causes)

A
  1. transient LES relaxation, reducing LES pressure to 0-2 mm Hg lasting > 10 seconds
  2. hernia
  3. dec LES pressure
  4. dec motility e.g. achalasia, scleroderma, diabetes
  5. gastric emptying
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22
Q

what is sandifer syndrome?

A

symptom of GERD:
sudden onset, intermittent posturing - back arch, neck torsion, chin lift
will also refuse food

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23
Q

normal oesophageal pH vs in GERD

A

normal pH 7.0. GERD pH <4, reaching nadir within 30s

24
Q

agents that decrase LES tone

A

anticholinergics, nicotine, ETOH

25
Q

side effects of PPIs

A

Respiratory infections
C diff infections
Bone fractures
Hypomagnesmia + low B12
Tubulointerstitial nephritis

26
Q

complications of GERD

A
  1. oesophagitis > strictures, Barett’s > cancer
  2. nutritional: FTT
  3. resp: apnoea / BRUE, stridor, asp
27
Q

common presenting Sx of EoE in kids

A

Feeding dysfunction (median age 2.0 years)
Vomiting (median age 8.1 years)
chest/abdominal pain (median age 12.0 years)
Dysphagia (median age 13.4 years)
Food impaction (median age 16.8 years)

28
Q

diagnostic criteria EoE

A

All three of:
1) Symptoms of esophageal dysfunction
- esp if also atopic
- esp if endoscopy finds: rings, furrows, exudates, edema, stricture, narrowing, and crepe paper mucosa

2) ≥15 eos/hpf (∼60 eos/mm2) on biopsy
3) Assessment of non-EoE disorders that cause or potentially contribute to esophageal eosinophilia

29
Q

compare EoE vs GERD

A

EoE:
- atopic history +++
- food impaction +++
- male 3:1 cf 1:1 for GERD
- long furrows and rings more characteristic in EoE (but could happen in reflux oesophagitis)

30
Q

Cx of EoE

A
  1. stricture
  2. perf

*no risk of cancer

31
Q

Mx of EoE

A
  1. diet:
    - 6food: milk, egg, soy, wheat, peanuts/tree nuts, fish/shellfish
    - or just 4 food (without last two)
    - milk and wheat are the worst
  2. Rx: PPI and budesonide/fluticasone 8 weeks
32
Q

mAbs for EoE

A

anti IL-5 Abs: mepolizumab, relizumab

33
Q

infectious oesophagitis, Rx for:
Candida
HSV
CMV

Which bug most common?

A

Candida (most common) = fluconazole
HSV = aciclovir
CMV = ganciclovir, foscarne

34
Q

areas of narrowing at oesophagus for risk of FB

A

a. Cricopharyngeus (upper esophageal sphincter)
b. Aortic arch
c. Left main stem bronchus
d. Diaphragmatic hiatus

35
Q

Rx for oesophageal obstruction (besides endoscopy to fish it out)

A

Glucagon 1 mg IV (maximum 2 mg) - causes the LES to relax!

36
Q

embryology of GI tract - which tissues does it derive from

A

foregut = upper GI tract including esophagus, stomach and duodenum to the level of bile duct insertion
midgut = rest of small bowel and large bowel to the midtransverse colon
hindgut = colon and upper anal canal

37
Q

muscularis externa of oesphagus vs stomach

A

oesophagus: two layers
stomach: three layers - outer longitudinal, middle circular and inner oblique

38
Q

5 special cell types in the stomach, where on the gland and in the stomach they’re located, and their function

A
  1. Mucous cells = mucous (thick and alkaline)
    - cardia and pyloric regions.
    - neck of the gland where it opens into pit
  2. Oxyntic cells/ parietal cells in body + pylorus
    - secrete HCl and intrinsic factor for B12
    - in top half of gland
  3. chief cells
    - activated by acid to release pepsinogen+ lipase
    - deactivated by duodenum high pH
    - lower half of gland. in body only
  4. Enterochromaffin-like cells
    - secrete histamine for digestion regulation
    - lower end of gland
  5. D cells = somatostatin - inhibits acid
  6. G cells = gastrin - stimulates acid
    - in antrum
39
Q

how is HCl released in the stomach?

A
  1. carbonic anhydrase in parietal cell:
    CO2 + H2O = H2CO3 = HCO3 + H
  2. H+ then pumped into the stomach by H-K antiporter
  3. K+ enters cell then exits again down concentration gradient
  4. Gradient maintained by Na-K+ ATPase on basal membrane
  5. bicarbonate is exchanged for chloride in the blood creating chloride shift and chloride is pumped into lumen to join H+
40
Q

which hormones regular gastric HCl production?

A

stimulation:
1) gastrin: from vagus > G cells > G rec. Ca dep
2) ACh: from vagus directly > M rec. Ca dep
3) HA: gastrin and ACh stim ECL cells. Ca INdep

inhibitiion:
1) D cells somatostatin
2) S cells secretin
3) K cells GIP
4) I cells CCK

41
Q

omeprazole:
- MOA
- irreversible or reversible
- metabolism

A
  • blocks H/K ATPase
  • dose dependent irreversible inhibition; max effect day 5
  • completely by CYP450 - inhibits some other drug metabolsim e.g. phenytoin
42
Q

main location of gastric vs duodenal ulcers

A

gastric: lesser curvature
duodenal ulcers: 90% at duodenal bulb

43
Q

two main causes of PUD

A
  1. H Pylori (duodenal 90%, gastric 30%)
  2. NSAIDs (duodenal 7%, gastric 35%)
44
Q

gastric vs duodenal ulcers

A

gastric:
- worse with meal, and 1-2 hours after meal recurs
- nocturnal pain (HCl highest)
- vomiting common, haematemesis / malaena

duodenal:
- relieved by meal, recurs 2-4 hours later
- malaena

45
Q

h.pylori complications

A

GI
- GERD
- gastritis
- PUD
- MALT / adenocarcinoma

extra-GI
- short / FTT

46
Q

how is h.pylori spread

A

faecal-oral > oral-oral

47
Q

PUD complications need to know

A
  1. Upper GI bleed (15%)
    - esp posterior - gastroduodenal artery
  2. Perforation (7%)
    - anterior duodenal ulcers
  3. Gastric outlet obstruction (2%) from oedema/scarring
  4. penetration
    - posterior duodenal ulcers can erode into pancreas
48
Q

NTBM DDx of PUD

A

crohn’s and cancer

49
Q

Rx for H.Pylori

A

triple therapy 10-14 days:
- amox
- clarith
- omep

50
Q

what is zollinger-ellison syndrome?

A

triad pathology of:
1) gastrinoma > excess gastrin
2) excess gastrin > parietal cell hyperplasia > more acid
3) PUD
also diarrhoea/steatorrhoea bc acidic chyme means panc enzymes dont act

51
Q

ZE syndrome associated with what 3 other conditions?

A

MEN1 (25%)
NF1
tuberous sclerosis

52
Q

what is the most important predictor of h.pylori infections

A

SES

53
Q

h.pylori investigations for active infection

A

urea breath test - false neg with PPI
stool antigen - most cost effective, and can Dx, monitor and confirm eradication
endoscopy -> biopsy (GS)
culture for sensis

serology is shit. doesnt tell you about active infection

54
Q

3 meds for gastroparesis after diet mod and MOA

A

Nizatidine – prokinetic
Domperidone – dopamine receptor antagonist
Erythromycin – acts on motilin receptors in stomach

55
Q

symptoms of gastroparesis

A

nausea, vomiting, early satiety, belching, bloating, and/or upper abdominal pain

Gastro (4 decks)

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