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Delta Med - Gastroenterology > Gastroenterology 1 - Upper GI Issues > Flashcards

Gastroenterology 1 - Upper GI Issues Flashcards

1
Q

Where is gastrin produced?

A

In the G cells of the antrum of the stomach. Stimulates H+ production in parietal cells, and production of somatostatin in D-cells, which inhibits gastrin production from G-cells.
Gastrin is stimulated by digested protein and amino acids.

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2
Q

Where is somatostatin secreted in the stomach and it’s function?

A

Released by D-cells in the antrum and body - inhibits G-cell production of gastrin, and inhibits the production of histamine from ECL cels in the body. Inhibits the production of H+ by parietal cells in a paracrine manner.

Is stimulated by ACh release from post ganglionic vagus nerves.

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3
Q

What is the histamine in the stomach?

A

released by ECL cells in the body, and acts on parietal cells to release H+ via H2 receptors. Stimulated by ACh and inhibited by somatostatin

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4
Q

What are features of peptide hormones in the stomach?

A

Gastrin and CCK
Produced in response to triggers, and produced as preprohormones - secretory granules in the golgi apparatus
several sized versions are produced with differing actions

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5
Q

What is the rate limiting step in H+ secretion in the stomach?

A

H/K/ATPase pump

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6
Q

Increases in what conditions have been associated with PPI use in case control studies?

A

Pneumonia - RR 1.89
Gastroenteritis (campylobacter, salmonella) - RR2.9
Osteoporosis OR1.44

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7
Q

What is the odds ratio for C. difficile infection in PPI treated patients?

A

OR 1.47-2.85, p

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8
Q

Is there an interaction between clopodigrel and PPIs?

A

Conflicting data - 2C19 interaction in vitro ? significant clinically?

post hoc analyses have shown no conclusive link

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9
Q

What is the proposed theoretical mechanism for increased CVD in PPI?

A

ADMA destruction inhibited by PPIs - which decreases NO production and decreased vascocontstriction

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10
Q

What are causes of hypergastrinaemia?

A

Prolonged acid suppression (PPI, ranitidine)
Atrophic gastritis - pernicious anaemia, Hpylori
Vagotomy, SB resection
Gastrin secreting tumours
Renal failure
Hypercalcaemia
Hyperlipidaemia (artefact)

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11
Q

What are features of ZES?

A

1/3 of patients have MEN1: hyperparathyroisism, pancreatic and pituitary tumours.

Chromosome 11q13 - 90% have positive genetic test.

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12
Q

Where are tumours found in ZES, and what are lab findings?

A

90% in the head of pancreas/duodenal area, 10% in the tail of pancreas.

fasting gastrin >1000, secretin provocation, gastrin >200, hypersecretion BAO >10mEq/hr

Gatate PET-CT is new standard.

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13
Q

Where do parasympathetic fibres originate?

A

vagal and sacral (Craniosacral)

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14
Q

Where do the sympathetic fibres originate?

A

thoracic and lumbar spine

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15
Q

What segments of the GIT are innervated by the SNS/pSNS?

A

Vagus innervates the oesophagus to upper 1/3 large intestine
Sympathetic - whole gut
Pelvic - large intestine

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16
Q

What is the intrinsic nervous system in the gut?

A

mysenteric plexus - as many neurons as the CNS

peristalsis controlled by ‘pacemaker cells’ - interstitial cells of Cajal

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17
Q

What are properties of slow wave conduction in the GUT?

A

Slow waves propagate without decrement in regions with ICC, but decay in regions without ICC

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18
Q

What are adult disorders of gut motility associated with loss of ICC?

A 
Slow transit constipation, chronic idiopathic constipation
Internal anal sphincter achalasia
Gastroparesis (idiopathic/diabetic)
Afferent loop syndrome
Megacolon/megaduodenum
Paraneoplastic dysmotility
Crohn's disease
Chaga's disease
Achalasia of LES
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19
Q

What are causes of acute pancreatitis?

A 
Alcohol
Gallstones
Infection
Drugs
Metabolic
Post ERCP
Ischaemia
Pancreas divisum
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20
Q

What are causes of chronic pancreatitis?

A 
Alcohol
genetic
Duct obstruction
Tropical
Systemic disease
Autoimmune
Idiopathic
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21
Q

What is the appropriate management of microlithiasis/sludge?

A

Appropriate to proceed to lap chole - decreased future risk of pancreatitis

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22
Q

What are important metabolic causes of pancreatitis?

A

increased chylomicrons and triglycerides increase the risk of pancreatitis

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23
Q

What is the effect of statins and fibrates upon the risk of pancreatitis?

A

Statins reduce the risk of pancreatitis in patients with hypercholesterolaemia.
Fibrates possibly increase the risk of pancreatitis in patients with hypertriglyceridaemia.

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24
Q

What is the effect of smoking and alcohol upon chronic pancreatitis?

A

smoking cessation reduces rates of pancreatic calcification at 6 years.
alcohol cessation has no impact upon calcification at this time

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25
Q

What is the optimal treatment strategy for post ERCP pancreatitis?

A

Can use NSAIDs periprocedurally to reduce risk (RR 0.36) of post ERCP pancreatitis - no AEs detected in study

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26
Q

What are causes of inherited pancreatitis?

A 
Hereditary pancreatitis
SPINK1 mutation
CF gene mutations
Varian common chromotrypsin C
Autoimmune pancreatitis
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27
Q

What are features of autoimmune pancreatitis?

A 
Autosomal dominant
80% penetrance
Recurrent mild attacks from age 5
Chromosome 7q35, with 20 variants
Trypsinogen gene PRSS1
Increased risk of cancer
Genetic testing is available
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28
Q

What are features of SPINK1 mutation in chronic pancreatitis?

A

recently described mutation in patients with chronic pancreatitis and normal trypsinogen levels.
1/4 of adolescent patients with no FHx
most common missense mutation at codon 34

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29
Q

What is the relationship between CFTR gene mutations and idiopathic chronic pancreatitis?

A

RR 3.0 in patients with CFTR gene mutations
5T allele intron 8
also assoc with male infertility
mild mutations may be factor in other causes of pancreatitis

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30
Q

What is the relationship between variant common chymotrypsin C

A 
Cofactor only
Increases risk of pancreatitis along with:
EtOH
smoking
CFTR
SPINK1
31
Q

What are features of autoimmune pancreatitis?

A 
Rare, mild recurrent attacks
May present with mass - DDx - Cancer
Associated with Sjogren's, PBC, RA
Raised serum IgG
Responds to steroids, both histologically and clinically
32
Q

What are features of necrotising pancreatitis?

A

Traditional treatment = early surgery and necrosectomy
Recent RCT showed that there were lower major complications in those treated with percutaneous radiological drainage first, followed by necrosectomy if needed

33
Q

What are features of helicobacter pylori and cag a?

A

Cag A +ve = more virulence
assoc w Vac A - Vaculolating cytotoxin
Clinically = more duodenal ulcers, worse gastritis, higher risk of relapse, ? less cancer (assoc with atrophic gastritis and IM)

34
Q

What are features of antrum-predominant gastritis?

A

associated with Vac A positive H. pylori.

Gastric histo:
Chronic inflammation and polymorph activity,

increased acid output,

Duodenal histo
gastric metaplasia and active chronic inflammation,

with risk of duodenal ulceration

35
Q

What are features of pan-gastritis?

A

Gastric histo:
Chronic inflammation, polymorph activity, atrophy and intestinal metaplasia

Reduced acid output

Normal duodenal pathology

Risk of gastric ulcration

36
Q

What is the rate of reinfection following h. pylori elimination?

A

1% / year

verify eradication with breath test

37
Q

What are symptoms of eosinophilic oesophagitis?

A 
Dysphagia
Food impaction
Chest pain
Heart burn
Abdominal pain
refractory GORD
38
Q

What are typical histological findings in oesophagitis?

A

> =15 eosinophils per HPF on histology
basal zone hyperplasia
dilated intercellular spaces

39
Q

What are features of eosinophilic oesophagitis?

A

Th2 driven - ? asthma like
assoc with carbamazepine hypersensitivity syndrome
young men, dysphagia, food impaction and heartburn

40
Q

What is current treatment of EoE?

A

Empiric Six food elimination diet - histological remission in 81%
Compliance is difficult
most common triggers are milk and wheat
(milk, wheat, egg, soy, peanuts, seafood)

Can do guided diet by skin prick testing - less accurate (histologic remission in 65%)

Four food elimination diet also possible (milk, wheat, eggs and soy)

41
Q

What are other investigation options for EoE other than Bx?

A

Oesophageal string test is a possible method of Dx EoE

42
Q

What are features of PPI responsive oesophageal eosinophilia

A

Typical EoE symptoms and histology
do not have GERD on endoscopy/pH monitoring
Exhibit clinical and histological response to PPIs

43
Q

What are possible mechanisms for PPI responsive EoE?

A

PPIs may have anti-oxidant, inhibitory neutrophil function, decrease CK pdn by endo/epithelial cells, decrease adhesion molecule production by endothelial cells and neutrophils

may have Ix negative GERD (NERD) or respond to anti-inflammatory effects of PPIs

44
Q

What are current Mx guidelines for EoE?

A

trial of PPI for 2 months, even if Sx suggest EoE vs GORD
4 food elimination diet as effective as 6 food - with better compliance
Should assess success at symptomatic improvement at 6 weeks.

45
Q

How is achalasia diagnosed?

A

On barium swallow - bird beak sign with lack of gastric bubble.

On manometry, failure of LES relaxation on swallow.

46
Q

What is the treatment of achalasia?

A

Surgery - modified heller myotomy - mortality 0.3%, response 85% at 5 years
Botulinum toxin - similar efficacy to dilatation, safe, but requires multiple treatments, 12/12 duration
Dilatation, pneumatic - perforation rate 5%, mort 0.2%, response 65% at 5 years, no longer performed

POEM - endoscopic myotomy, also an option

47
Q

What are causes of malabsorption?

A

Luminal phase:
- enzyme deficiency - chronic pancreatitis
- nutrient consumption - bacteria o’growth (Vit b12)
Mucosal phase - coeliac disease
Post-absorptive phase - lymphangectasia

48
Q

What are causes of vitamin B12 Deficiency?

A 
Dietary - vegans
Gastric:
- pernicious aneamia
- atrophic gastritis
- gastrectomy
Small bowel:
- bacterial overgrowth
- pancreatic insufficiency
- crohn's disease
- blocking agents - e.g. neomycin
49
Q

What is HLA types are associated with coeliac disease?

A

HLA DQ2, DQ8

95% of patients with coeliac disease are positive for these - useful rule out test.

50
Q

What are histological features in coeliac disease?

A

villous atrophy
crypt hyperplasia
increased intraepithelial lymphocytes

51
Q

What diseases are associated with coeliac disease?

A

Dermatitis herpetiformis
Autoimmune conditions - IDDM, hypothyroidism, IgA deficiency
Down snydrome

52
Q

What are characteristics of coeliac serology?

A 
Anti-gliadin Abs: IgA, IgG
traditionally used
Endomysial Abs - IgA
Tissue transglutaminase Ab - IgA
- most accurate test
- may be used with endomysial Ab
Deamindated anti gliadin Ab
- IgG antibody, useful in IgA deficiency
- Not quite as Sn as TTG
53
Q

What are the relative Sn and Sp of Ab in Coeliac Disease?

A 
IgA Gliadin Sn 85, Sp 90
IgG Gliadin Sn 75, Sp 80
EMA Sn 95, Sp 100
tTG Sn 95, Sp 100
Deaminated gliadin Sn 90, Sp 100
54
Q

What is the Dx approach for coeliac disease?

A

Histology is still required for diagnosis
Indeterminate cases:
-HLA typing
- Exclude other causes of villous atrophy
(bact overgrowth, giardiasis, lymphoma, gastroenteritis, CVID, norovirus, NSAIDs, MMF and olmesartan)
Recheck after gluten challenge

55
Q

What are features of lymphocytic duodenosis?

A

AKA Marsh 1
>25 IELS/100 enterocytes
Normal architecture
10-20% part of spectrum of gluten sensitivity
Also NSAIDs, H. pylori, Crohn’s, Sjogren’s syndrome

56
Q

What is the most common cause of GORD?

A 
transient lower oesophagel relaxations
cause of reflux if resting LES is normal
mechanism responsible for belching
increased prevalence in obesity
vagally mediated (not by pharynx)
57
Q

What are causes of a low resting LES tone?

A 
Gastric distension
Alcohol
Caffeine
Fat
CCK
Smoking
58
Q

What are features of Grade A reflux oesophagitis?

A

One or more mucosal break, no longer than 5mm, that doesn’t extend between folds

59
Q

What are features of Grade B reflux oesophagitis?

A

One or more mucosal break, more than 5mm long, that does not extend between folds

60
Q

What are features of Grade C reflux oesophagitis?

A

One or more mucosal breaks that extends between two or more mucosal folds, but which involves less than 75% of the circumference

61
Q

What are features of Grade D reflux oesophagitis?

A

One or more mucosal breaks that involves at least 75% of the mucosal circumference

62
Q

What is the relationship between severity of reflux symptoms and grade of oesophagitis?

A

Similar between grades of oesophagitis

63
Q

What is the relationship between GORD and H. pylori?

A

questionable
H pylori causes gastric disease
Hp may be protective in patients with atrophic gastritis and low acid production

64
Q

What are complications of GORD?

A

Oesophagus - metaplasia, malignancy, ulceration, strictures

Extra-oesophageal - refluxate can exacerbate pharyngeal, laryngeal, pulmonary structures

65
Q

What is the relationship between cough and GORD?

A

43-75% of patients with GERD related cough have no reflux symptoms
GORD related cough may respond to PPI
up to 40% of cases of chronic cough are caused by GORD

66
Q

What is the possible MoA of chronic cough in GORD?

A

Possibly vagally mediated cough, stiumlation by refluxate to cough centre

67
Q

What are surgical treatments for GORD?

A

Nissen fundoplication gold standard - 90% symptomatic improvement at 5 years
Dysphagia 6%
10-65% still on PPI
Must exclude achalasia (LES

68
Q

What is the definition of barrett’s oesophagus?

A

Metaplasia of squamous epithelium to columnar epithelium in the lower oesophagus in response to low pH refluxate

69
Q

What is the relationship between reflux and BE?

A

Barrett’s is associated with prolonged reflux episodes and increased frequency of reflux episodes.

Prevalence increases with duration of reflux symptoms.

Significant predominance in white males, who are fat

70
Q

What is the role of HALO in BE?

A

eradicates metaplasia and low and high grade dysplasia in barrett’s oesophagus

71
Q

What are current guidelines for barrett’s surveillance?

A

Nil dysplasia - q3-5yr surveillance endoscopy with Bx
Low-grade dysplasia - Bx - surveillance endoscopy with Bx every six months - 1yr
High grade dysplasia - surveillance endoscopy with Bx every 3 months - or proceed to resection or ablation

72
Q

What is the relationship between BE and adenocarcinoma risk?

A

between 40-125x increased risk of oesophageal adenocarcinoma

73
Q

What is the most common cause of oesophageal SCC?

A

smoking

Delta Med - Gastroenterology (3 decks)

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