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Gastro Flashcards

1
Q

What is achalasia?

A

Disorder of motility of lower oesophageal sphincter - impaired peristalsis and failure to relax

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2
Q

What are the symptoms of achalasia?

A

Dysphagia of both solids and liquids
Regurgitation
Heartburn

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3
Q

How is achalasia diagnosed?

A

Gold standard - oesophageal manometry –> XL LOS tone

Bird’s beak on barium swallow

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4
Q

What is the treatment of achalasia?

A

Pneumatic dilation
Nifedipine
Heller myotomy

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5
Q

What are the risk factors for oesophageal cancer?

A

Barrett’s oesophagus
GORD
Excessive smoking or alcohol

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6
Q

What is a pharyngeal pouch?

A

AKA Zenker’s diverticulum

Posteromedial herniation between hyropharyngeus and cricopharyngeus muscles through Killian’s dehiscience

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7
Q

What are the risk factors for eosinophilic oesophagitis?

A 
Asthma/atopy
Males
FH
Caucasian
Autoimmune disease
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8
Q

How is eosinophilic oesophagitis diagnosed?

A

Endoscopy and biopsy

Doesn’t respond to PPI

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9
Q

What is the treatment of eosinophilic oesophagitis?

A

Elemental diet
Fluticasone/budesonide
Dilation

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10
Q

What is the triad of Plummer-Vinson syndrome?

A

Dysphagia secondary to oesophageal webs
Glossitis
IDA

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11
Q

Where is the most common location for oesophageal varices?

A

Distal oesophagus and proximal stomach

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12
Q

What is the management of UGIB?

A 
Terlipressin
Balloon tamponade
Prophylactic antibiotics
Band ligation
TIPS
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13
Q

What is the mechanism of action of terlipressin?

A

Constriction of splanchnic vessels

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14
Q

What is TIPS procedure?

A

Connection created between hepatic and portal vein, therefore reducing portal pressure

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15
Q

Why does TIPS procedure cause an exacerbation of hepatic encephalopathy?

A

Blood now bypasses the liver so toxins are delivered in greater quantity to the cerebral circulation

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16
Q

When should prothrombin complex concentrate be given?

A

If actively bleeding and on warfarin

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17
Q

When should FFP be given?

A

Fibrinogen<1g/L OR

PT/APTT>1.5x normal

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18
Q

What is prophylaxis for variceal bleeding?

A

Propanolol

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19
Q

What are the risk scores for UGIB?

A

Blatchford

Rockall after endoscopy

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20
Q

What is the histology of gastric cancer?

A

Signet ring cells - large vacuole of mucin which displaces nucleus to one side

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21
Q

What are the risk factors for gastric cancer?

A 
H. pylori
Blood group A
Gastric polyps
Pernicious anaemia
Smoking
Diet high in salt/spice/nitrates
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22
Q

What is the best method of staging gastric cancer?

A

Endoscopic ultrasound - assessment of mural invasion

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23
Q

What is the management of gastric cancer?

A

Proximal >5-10cm from OG junction: subtotal gastrectomy
<5cm from OG junction: total gastrectomy
Type 2 junctional tumours: oesophagogastrectomy

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24
Q

What are 4 associations of h.pylori?

A

Peptic ulcer disease
Gastric cancer
B cell lymphoma of MALT tissue
Atrophic gastritis

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25
Q

What is the eradication regime for h.pylori?

A

7 days PPI + amoxicillin + clari/metro

OR

7 days PPI + clari + metro

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26
Q

What is the most common electrolyte in refeeding syndrome?

A

Low phosphate

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27
Q

What factors are high risk for refeeding syndrome?

A

BMI<16
Unintentional weight loss >15% over 3-6 months
Little intake 10 days
Low K, Phosphate, magnesium prior to feeding

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28
Q

What is the mechanism of PPIs?

A

Irreversible blockade of H/K/ATPase of gastric parietal cell

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29
Q

What are the side effects of PPIs?

A

Low Na/Mg
Osteoporosis
Microscopic colitis
Increased risk of c diff

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30
Q

What is Zollinger-Ellinson syndrome?

A

Gastrin secreting tumour - gastrinoma

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31
Q

Which cells produce gastrin?

A

G cells

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32
Q

What is the function of gastrin?

A

Increases H+ secretion by parietal cells

Increases gastric motility

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33
Q

Whic/h cells secrete CCK

A

I cells in upper small intestine

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34
Q

What is the function of CCK?

A

Contraction of gallbladder
Relaxation of sphincter of Oddi
Decreases gastric emptying
Secretion of pancreatic fluid

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35
Q

D cells produce what?

A

Somatostatin

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36
Q

What is the function of somatostatin?

A

Decreases acid and pepsin secretion
Insulin and glucagon secretion
Pancreatic enzyme secretion

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37
Q

What is the most common cause of diarrhoea after ileocaecal resection, and the diagnosis and treatment?

A

Bile acid malabsorption
SeHCAT test
Cholestyramine

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38
Q

Name 5 complications of coeliac disease

A 
Hyposplenism
Osteoporosis
Subfertility
Oesophageal Ca
Enteropathy-associated T cell lymphoma of small intestine
39
Q

What are the symptoms of small bowel overgrowth syndrome?

A

Chronic diarrhoea
Bloating and flatulence
Abdo pain

40
Q

How is small bowel overgrowth syndrome diagnosed and managed?

A

Hydrogen breath test

Rifaximin

41
Q

What are the symptoms of VIPomas?

A

Large volume diarrhoea
Weight loss
Diarrhoea
Hypokalaemia, hypochlorhydia

42
Q

What is Heyde’s syndrome?

A

Angiodysplasia, IDA, aortic stenosis

43
Q

How is angiodysplasia diagnosed?

A

Colonoscopy/endoscopy

Capsule endoscopy

44
Q

What is Whipple’s disease?

A

Multisystem disorder caused by tropheryma whippelii infection

45
Q

What are the symptoms of Whipple’s disease?

A 
Malabsorption
Large joint arthralgia
Lymphadenopathy
Hyperpigmentation and photosensitivity
Pleurisy/pericarditis
46
Q

How is Whipple’s disease diagnosed?

A

Jejunal biopsy - deposition of macrophages containing Periodic-acid Schiff (PAS) granules

47
Q

What is the treatment of Whipple’s disease?

A

PO co-trimoxazole for one year

48
Q

Where is the most common location for ischaemic colitis?

A

Splenic flexure

Watershed area between IMA and SMA

49
Q

What is seen on AXR in ischaemic colitis?

A

Thumbprinting

50
Q

What is a RF for ischaemic colitis?

51
Q

What are the genetics of sporadic colorectal Ca?

A

50% show allelic loss of APC gene

Other- activation of K-ras oncogene, deletion of DCC tumour suppressor genes

52
Q

What is the inheritance of HNPCC?

A

Autosomal dominant

MSH2 (60%) and MLH1 (30%)

90% develop cancers

53
Q

What other cancer are patients with HNPCC at risk of?

A

Endometrial

54
Q

What is the genetics of FAP?

A

Autosomal dominant

Mutation of Adenomatosis polyposis coli gene (APC) on chromosome 5

55
Q

What is Gardner’s syndrome?

A

Variant of FAP

Features skull and mandible osteomas, retinal pigmentation, thyroid carcinoma

56
Q

What is the most common cause of HCC?

A

Chronic hep C

57
Q

What is the management of HCC?

A

Resection (Child-Pugh A, no portal HTN, single lesion<2cm)

Radiofrequency ablation and Tx (Child-Pugh A and B, 2-3 tumours<3cm or 1 tumour 2-5cm, no spread)

Sorafenib (Child-Pugh A and B, vascular invasion/spread)

Best supportive care (Child-Pugh C)

58
Q

What is the syndrome of hepatic vein thrombosis?

A

Budd-Chiari syndrome

59
Q

What is the triad of Budd-Chiari syndrome?

A

Sudden onset severe abdo pain
Ascites
Tender hepatomegaly

60
Q

What is the gold standard diagnosis of Budd-Chiari syndrome?

A

USS doppler

61
Q

What LFT derangement is seen in a cholestatic/hepatitic picture?

62
Q

Which drugs cause cholestasis or hepatitis?

A

COCP
Penicillins/erythromycin
Anabolic steroids
Sulphonylureas

63
Q

What LFT derangement is seen in hepatocellular picture?

64
Q

Which drugs cause hepatocellular injury?

A

V-PAN-AM

Valproate and phenytoin
Paracetamol overdose
Atorvastatin, amidarone
Nitrofurantoin
Alcohol, anti-tuberculous drugs
MAOs, methyldopa
65
Q

Which drugs cause cirrhosis?

A

Methotrexate
Methyldopa
Amiodarone

66
Q

What is the pathophysiology of decompensated ALD?

A

Excess collagen and extracellular matrix deposition in peripheral and pericentral zone leading to formation of regenerative nodules

67
Q

What criteria do Child-Pugh and MELD use?

A

Child-Pugh: bilirubin, albumin, PT, encephalopathy, ascites

MELD: bilirubin, creatinine, INR

68
Q

What causes ascites in ALD?

A

Hypoalbuminaemia (impairment of hepatic synthetic function)

Fluid overload due to hyperaldosteronism

69
Q

How is ascites managed?

A

Spiro reverses hyperaldosteronism
Furosemide used as an adjunct but less effective as monotherapy
If hyponatraemic <125 - fluid restriction
Abdominal paracentesis

70
Q

What are the indications for HAS?

A

Volume replacement after LVP
Hepatorenal syndrome
SBP

71
Q

What is the pathophysiology of hepatorenal syndrome?

A

Vasoactive mediators cause splanchnic vasodilation
This reduces systemic vascular resistance –> underfilled kidneys
Sensed by JG apparatus which activates RAAS causing renal vasoconstriction, which is not enough to counter balance the effects of splanchnic vasodilation

72
Q

What are the types of HRS?

A

1: rapidly progressive, often occurs following an acute event
2: slower progression, associated with refractory ascites

73
Q

What is the management of ascites?

A

Terlipressin
HAS
TIPS

74
Q

What is diagnostic for SBP?

A

Paracentesis: neutrophils >250cells/ul

75
Q

Which patients have SBP prophylaxis and what is it?

A

Prev episode of SBP
Fluid protein <15g/l
Child PUgh>8
HRS

Oral cipro

76
Q

What is the pathophysiology of NAFLD?

A

Insulin resistance

77
Q

What are the features of NAFLD?

A

Asymptomatic
ALT>AST, ratio >3
Increased echogenicity on US

78
Q

What is the cause of hereditary haemochromatosis?

A

Autosomal recessive

Defect of HFE gene on chromosome 6

79
Q

What are the features of haemochromatosis?

A 
Symptomatic 40-60s
Fatigue, weakness
Arthropathy
ED
Diabetes
Bronzing of the skin
Cirrhosis
Arrhythmias
Dilated cardiomopathy
80
Q

How is haemochromatosis diagnosed?

A

High fasting transferrin sats >55% M >50% women

High ferritin, low TIBC

Liver biopsy with Perl’s stain

81
Q

Which features of haemochromatosis are reversible with treatment?

A

Cardiomyopathy

Skin pigmentation

82
Q

What is the screening test for haemochromatosis?

A

General popu: transferrin sats

Family members: HFE genetic testing

83
Q

What are the associations of PBC?

A

Sjogrens in 80%
RA
Systemic sclerosis

84
Q

What are the ?symptoms of PBC

A 
Fatigue
Pruritus
Incidental raised ALP
Hyperpigmentation over pressure points
10% RUQ pain
85
Q

What is the immunology of PBC?

A

Anti-mitochondrial antibodies M2 subtype
SM antibodies
Raised serum IgM

86
Q

What is the treatment of PBC?

A

Ursodeoxycholic acid
Cholestyramine
Liver tx

87
Q

What is the increased risk of HCC in PBC?

88
Q

What is the gene mutation in Wilson’s disease?

A

ATP7B on chromosome 13

89
Q

What are the symptoms of Wilson’s disease?

A 
Liver failure
Psychiatric disorders
Dysarthria and tremor
Chorea
Kayser-Fleischer ring/sunflower cataracts
90
Q

How is wilson’s disease diagnosed?

A

Low serum caeruloplasmin
Low serum copper
Elevated 24h urianry copper
Liver biopsy

91
Q

What is the treatment of Wilson’s disease?

A

Penicillamine

92
Q

What are the most common organisms causing liver abscesses?

A

Children: s.aureus
Adults: e.coli

93
Q

What is the most important risk factor for the progression of hepatitis B to cirrhosis?

A

HBV DNA titres

94
Q

What is the frequency of endoscopy in Barrett’s oesophagus monitoring?

A

No dysplasia: every 2-5 years
Low grade dysplasia: every 6 months, and repeat endoscopy with biopsies every cm
High grade dysplasia: every 3 months

If a visible lesion is present - endoscopic ablation with mucosal resection

MRCP (17 decks)

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