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MRCP Part 1 > Gastro > Flashcards

Gastro Flashcards

1
Q

Causes of Acute liver failure(4)

A
  1. paracetamol overdose
  2. alcohol
  3. viral hepatitis (usually A or B)
  4. acute fatty liver of pregnancy
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2
Q

the ratio ofAST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of

A

Acute alcoholic hepatitis

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3
Q

liver function tests’ do not always accurately reflect the synthetic function of the liver. This is best assessed by looking at

A
  1. the prothrombin time
  2. albumin level.
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4
Q

Treatment of Pseudocysts

A

Treatment is either with

  1. endoscopic or
  2. surgical cystogastrostomy or
  3. aspiration
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5
Q

Treatment of Pancreatic abscess

A
  1. Transgastric drainage is one method of treatment,
  2. endoscopic drainage is an alternative
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6
Q

Drugs causing Acute pancreatitis (8)

A
  1. azathioprine
  2. mesalazine
  3. steroids
  4. furosemide
  5. bendroflumethiazide
  6. pentamidine
  7. didanosine
  8. sodium valproate

*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine

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7
Q

7 factors indicating severe pancreatitis include:

A
  1. age > 55 years
  2. hypocalcaemia
  3. hyperglycaemia
  4. hypoxia
  5. neutrophilia
  6. elevated LDH and AST
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8
Q

Which test may be used to assess exocrine function of pancreas if imaging inconclusive

A

faecal elastase

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9
Q

Treatment of chronic pancreatitis

A
  1. pancreatic enzyme supplements
  2. analgesia
  3. antioxidants: limited evidence base - one study suggests benefit in early disease
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10
Q

Treatment of Alcoholic ketoacidosis

A

The most appropriate treatment is aninfusion of saline & thiamine.

Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.

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11
Q

management notes for alcoholic hepatitis:

A
  1. glucocorticoids( prednisolone) are often used during acute episodes of alcoholic hepatitis
  2. pentoxyphylline is also sometimes used

Maddrey’s discriminant function (DF)is often used during acute episodes to determine who would benefit from glucocorticoid therapy

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12
Q

Maddrey’s discriminant function (DF)is often used during acute episodes to determine who would benefit from

A

glucocorticoid therapy in alcoholic hepatitis

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13
Q

SAAG <11g/L

A
  • Hypoalbuminaemia
  1. nephrotic syndrome
  2. severe malnutrition (e.g. Kwashiorkor)
  • Malignancy
  1. peritoneal carcinomatosis
  • Infections
  1. tuberculous peritonitis
  • Other causes
  1. pancreatitis
  2. bowel obstruction
  3. biliary ascites
  4. postoperative lymphatic leak
  5. serositis in connective tissue diseases
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14
Q

SAAG > 11g/L
(indicates portal hypertension)

A
  • Liver disorders are the most common cause
  1. cirrhosis/alcoholic liver disease
  2. acute liver failure
  3. liver metastases
  • Cardiac
    1. right heart failure
    2. constrictive pericarditis
  • Other causes
    1. Budd-Chiari syndrome
    2. portal vein thrombosis
    3. veno-occlusive disease
    4. myxoedema
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15
Q

Management of ascites

A
  1. reducing dietary sodium
  2. fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
  3. Aldactone & lasix
  4. drainage if tense ascites
  5. TIPS
  6. prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. ‘ oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved
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16
Q

hepatic encephalopathy on EEG

A

triphasic slow waves on EEG

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17
Q

8 Precipitating factors Of Hepatic encephalopathy

A

infection e.g. spontaneous bacterial peritonitis

GI bleed

post transjugular intrahepatic portosystemic shunt

constipation

drugs: sedatives, diuretics

hypokalaemia

renal failure

increased dietary protein (uncommon)

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18
Q

Diagnosis of SBP

A

paracentesis:neutrophil count > 250 cells/ul

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19
Q

the most common organism found on ascitic fluid culture is

A

E. coli

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20
Q

Management of SBP

A

Iv cefotaxime

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21
Q

a marker of poor prognosis in SBP

A

Alcoholic liver disease

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22
Q

Antibiotic prophylaxis should be given to patients with ascites if:

A
  1. patients who have had an episode of SBP
  2. patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
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23
Q

TIPSS connects …….to ……

A

connects the hepatic vein to the portal vein

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24
Q

Screening for hepatocellular cancer

A

liver ultrasound every 6 months (+/- alpha-feto protein)

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25
Q

screening for cirrhosis NICE made a specific recommendation, suggesting to offer transient elastography

A
  1. people with HCV infection
  2. people diagnosed with alcohol liver disease
  3. men who drink alcohol over 50 units per week
  4. women who drink alcohol over 35 units per week
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26
Q

pathophysiology of HRS

A

vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance.

This results in ‘underfilling’ of the kidneys.

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27
Q

Type 1 HRS

A
  • Rapidly progressive Doubling of serum creatinine to > 221 µmol/L or a having of the creatinine clearance to < 20 ml/min over a period of less than 2 weeks
  • Very poor prognosis
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28
Q

Autoimmune hepatitis associated with

A

hypergammaglobulinaemia and

HLA B8, DR3

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29
Q

Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present

A

Tpye 1 : “Affects both adults and children”
- ANA
- ASMA

Type 2: “ Affects children only”
- LKM1

Type 3: “ Affects adults in middle-age”
- Soluble liver-kidney antigen

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30
Q

Management of autoimmune hepatitis

A

steroids, other immunosuppressants e.g. azathioprine

liver transplantation

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31
Q

Haemochromatosis is an autosomal ……disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies ofchromosome ……

A
  1. autosomal recessive
  2. chromosome 6
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32
Q

Reversible complications of haemochromatosis

A
  1. Cardiomyopathy
  2. Skin pigmentation
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33
Q

Typical iron study profilein patient with haemochromatosis

A
  1. transferrin saturation > 55% in men or > 50% in women
  2. raised ferritin (e.g. > 500 ug/l) and iron
  3. low TIBC
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34
Q

Screening for iron overload

A
  1. transferrin saturation
  2. genetic testing for HFE mutation
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35
Q

Liver biopsy in haemochromatosis indicated if

A

only used if suspected hepatic cirrhosis

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36
Q

Management of haemochromatosis

A
  1. venesectionis the first-line treatment
  • monitoring adequacy of venesection:transferrin saturation should be kept < 50% and the serum ferritin concentration < 50 ug/l
  1. desferrioxamine may be used second-line
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37
Q

Wilson’s disease is ………….disorder

A

an autosomal recessive

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38
Q

Wilson’s disease is caused by a defect in the………..gene located on chromosome ……..

A

in the ATP7B gene located on chromosome 13.

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39
Q

Investigations of Wilson disease

A
  1. slit lamp examination for Kayser-Fleischer rings
  2. reduced serum caeruloplasmin
  3. reduced total serum copper(counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
  • free (non-ceruloplasmin-bound) serum copper is increased
  1. increased 24hr urinary copper excretion
  2. the diagnosis is confirmed by genetic analysis of the ATP7B gene
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40
Q

Management of Wilson’s disease

A
  1. penicillamine(chelates copper) has been the traditional first-line treatment
  2. trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
  3. tetrathiomolybdate is a newer agent that is currently under investigation
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41
Q

4 Risks of ERCP

A
  1. Bleeding 0.9% (rises to 1.5% if sphincterotomy performed)
  2. Duodenal perforation 0.4%
  3. Cholangitis 1.1%
  4. Pancreatitis 1.5%
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42
Q

Management of Acute cholecystitis

A

Imaging (USS) and cholecystectomy (ideally within 48 hours of presentation)

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43
Q

Management of Gallbladder abscess

A

Imaging with USS +/- CT Scanning
Ideally, surgery although subtotal cholecystectomy may be needed if Calot’s triangle is hostile
In unfit patients, percutaneous drainage may be considered

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44
Q

Management of Cholangitis (4)

A
  1. Fluid resuscitation
  2. Broad-spectrum intravenous antibiotics
  3. Correct any coagulopathy
  4. Early ERCP
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45
Q

Management of Gallstone ileus

A

Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction and not at the site of obstruction. The fistula between the gallbladder and duodenum should not be interfered with.

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46
Q

Management of Acalculous cholecystitis

A

If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy

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47
Q

Causes of hepatosplenomegaly

A
  1. chronic liver disease* with portal hypertension
  2. infections: glandular fever, malaria, hepatitis
  3. lymphoproliferative disorders
  4. myeloproliferative disorders e.g. CML
  5. amyloidosis
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48
Q

Contraindications to percutaneous liver biopsy

A
  1. INR > 1.4
  2. low platelets (e.g. < 60 * 109/l)
  3. anaemia
  4. extrahepatic biliary obstruction
  5. hydatid cyst
  6. haemoangioma
  7. uncooperative patient
  8. ascites
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49
Q

The most common organisms found in pyogenic liver abscesses are………….in children and…….in adults.

A

Staphylococcus aureus in children

Escherichia coli in adults.

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50
Q

Management of pyogenic liver abscesses

A

drainage (typically percutaneous) and antibiotics

amoxicillin + ciprofloxacin + metronidazole

if penicillin allergic: ciprofloxacin + clindamycin

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51
Q

Budd Chiari syndrome
classically a triad of:

A

abdominal pain: sudden onset, severe

ascites → abdominal distension

tender hepatomegaly

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52
Q

studiesis very sensitive and should be the initial radiological investigation in Budd-Chiari syndrome

A

ultrasound with Doppler flow

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53
Q

In liver failure all clotting factors are …. 1….., except …..2. Because….3..

A
  1. Low
  2. factor VIII which is paradoxically supra-normal.
  3. because factor VIII is synthesised in endothelial cells throughout the body, unlike the other clotting factors which are synthesised purely in hepatic endothelial cells.
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54
Q

Pathogenesis of Primary biliary cholangitis

A

Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis

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55
Q

Primary biliary cholangitis
Association with

A

Sjogren’s syndrome (seen in up to 80% of patients)

rheumatoid arthritis

systemic sclerosis

thyroid disease

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56
Q

Diagnosis of Primary biliary cholangitis

A

anti-mitochondrial antibodies

smooth muscle antibodies in 30% of patients

raised serum IgM

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57
Q

In Primary biliary cholangitis
required before diagnosis to exclude an extrahepatic biliary obstruction by

A

Ultrasound or MRCP

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58
Q

Management of PBC

A
  1. first-line:ursodeoxycholic acid

slows disease progression and improves symptoms

  1. pruritus:cholestyramine
  2. fat-soluble vitamin supplementation
  3. liver transplantation

e.g. if bilirubin > 100 (PBC is a major indication)

recurrence in graft can occur but is not usually a problem

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59
Q

Complications of PBC

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage

osteomalacia and osteoporosis

significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

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60
Q

Primary sclerosing cholangitis is characterised by …?

A

inflammation and fibrosis of intra and extra-hepatic bile ducts.

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61
Q

Primary sclerosing cholangitis
Association with

A
  1. ulcerative colitis: 4% of patients with UC have PSC,80% of patients with PSC have UC
  2. Crohn’s (much less common association than UC)
  3. HIV
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62
Q

Primary sclerosing cholangitis
Investigations

A
  • raised bilirubin + ALP
  • ERCP or MRCP are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance.
  • P-ANCA
  • there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

-

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63
Q

Complications of Primary sclerosing cholangitis

A
  • cholangiocarcinoma (in 10%)
  • increased risk of colorectal cancer
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64
Q

Ascending cholangitis

  1. Which is the most common organism?
  2. What is the most common predisposing factor ?
A
  1. E.coli
  2. Gallstones
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65
Q

Charcot’s triad

A
  1. right upper quadrant (RUQ) pain,
  2. fever
  3. jaundice
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66
Q

Investigations of Ascending cholangitis

A

ultrasoundis generally used first-line in suspected cases to look for bile duct dilation and bile duct stones

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67
Q

Management of Ascending cholangitis

A
  1. Iv antibiotics
  2. ERCP after 24-48 hours to relieve any obstruction
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68
Q

Hydatid cysts are caused by

A

caused by the tapeworm parasite Echinococcus granulosus.

These cysts are allergens which precipitate atype 1 hypersensitivity reaction

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69
Q

Investigations of Hydatid cysts

A

imaging

  1. ultrasound if often used first-line
  2. CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts

serology

  1. useful for primary diagnosis and for follow-up after treatment
  2. wide variety of different antibody/antigen tests available
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70
Q

Treatment of Hydatid cysts

A

Surgery is the mainstay of treatment(the cyst walls must not be ruptured during removal and the contents sterilised first).

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71
Q

8 Associations of Pancreatic cancer

A

increasing age

smoking

diabetes

chronic pancreatitis (alcohol does not appear an independent risk factor though)

hereditary non-polyposis colorectal carcinoma

multiple endocrine neoplasia

BRCA2 gene

KRAS gene mutation

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72
Q

Investigations of Pancreatic cancer

A
  • ultrasound has a sensitivity of around 60-90%
  • high-resolution CT scanning is the investigation of choiceif the diagnosis is suspected
  • imaging may demonstrate the’double duct’ sign- the presence of simultaneous dilatation of the common bile and pancreatic ducts
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73
Q

Management of Pancreatic cancer

A
  • less than 20% are suitable for surgery at diagnosis
  • a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
  • adjuvant chemotherapy is usually given following surgery
  • ERCP with stenting is often used for palliation
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74
Q

drugs tend to cause a hepatocellular picture (10)

A
  1. paracetamol
  2. sodium valproate, phenytoin
  3. MAOIs
  4. halothane
  5. anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
  6. statins
  7. alcohol
  8. amiodarone
  9. methyldopa
  10. nitrofurantoin
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75
Q

drugs tend to cause cholestasis (+/- hepatitis):(7)

A
  1. combined oral contraceptive pill
  2. antibiotics:flucloxacillin,co-amoxiclav, erythromycin*
  3. anabolic steroids, testosterones
  4. phenothiazines: chlorpromazine, prochlorperazine
  5. sulphonylureas
  6. fibrates
  7. rare reported causes: nifedipine
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76
Q

Drugs causing Liver cirrhosis (3)

A
  1. methotrexate
  2. methyldopa
  3. amiodarone
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77
Q

Inherited causes of jaundice

Unconjugated hyperbilirubinaemia

A
  1. Gilbert’s syndrome
  2. Crigler-Najjar syndrome
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78
Q

Inherited causes of jaundice

conjugated hyperbilirubinaemia

A
  1. Dubin-Johnson syndrome
  2. Rotor syndrome
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79
Q

Gilbert’s syndrome ?

A
  1. autosomal recessive
  2. mild deficiency of UDP-glucuronyl transferase
  3. benign
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80
Q

Crigler-Najjar syndrome?

  • type 1
  • type 2
A

Crigler-Najjar syndrome, type 1

  • autosomal recessive
  • absolute deficiency of UDP-glucuronosyl transferase
  • do not survive to adulthood

Crigler-Najjar syndrome, type 2

  • slightly more common than type 1 and less severe
  • may improve with phenobarbital
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81
Q

Dubin-Johnson syndrome

A
  1. autosomal recessive disorder resulting inhyperbilirubinaemia (conjugated, therefore present in urine). Relatively common in Iranian Jews
  2. mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin
  3. results in a grossly black liver
  4. benign
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82
Q

Rotor syndrome

A
  1. autosomal recessive
  2. defect in the hepatic uptake and storage of bilirubin
  3. benign
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83
Q

Gilbert’s syndrome

  • Features
  • Investigation
  • management
A

Features

  • unconjugated hyperbilirubinaemia (i.e. not in urine)
  • jaundice may only be seen during anintercurrent illness, exercise or fasting
  • rise in bilirubin following prolonged fasting or IV nicotinic acid
  • no treatment required
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84
Q

The most common cause of biliary disease in patients with HIV is ….?

A

sclerosing cholangitis due to infections such as CMV, Cryptosporidium and Microsporidia

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85
Q

Cause of Pancreatitis in patients with HIV ….?

A

may be secondary to anti-retroviral treatment (especially didanosine) or

by opportunistic infections e.g. CMV

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86
Q

the main risk factor for cholangiocarcinoma

A

Primary sclerosing cholangitis

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87
Q

Features of Cholangiocarcinoma

A
  1. persistent biliary colic symptoms
  2. associated with anorexia, jaundice and weight loss
  3. a palpable mass in the right upper quadrant (Courvoisier sign)
  4. periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
  5. raised CA 19-9 levels
    - often used for detecting cholangiocarcinoma in patients with primary sclerosing cholangitis
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88
Q

HELLP syndrome

A

Haemolysis, Elevated Liver enzymes, Low Platelets

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89
Q

Acute fatty liver of pregnancy is rare complication which may occur in the ……. trimester or ……

A
  1. Third
  2. the period immediately following delivery.
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90
Q

Features of Acute fatty liver of pregnancy

A

abdominal pain

nausea & vomiting

headache

jaundice

hypoglycaemia

severe disease may result in pre-eclampsia

ALT is typically elevated e.g. 500 u/l

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91
Q

Management of Acute fatty liver of pregnancy

A

support care

once stabilised delivery is the definitive management

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92
Q

What is the most common liver disease of pregnancy.

A

Intrahepatic cholestasis of pregnancy (also known as obstetric cholestasis)

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93
Q

Features of Intrahepatic cholestasis of pregnancy

A

pruritus, often in the palms and soles

no rash (although skin changes may be seen due to scratching)

raised bilirubin

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94
Q

Management of Intrahepatic cholestasis of pregnancy

A
  1. ursodeoxycholic acid is used for symptomatic relief
  2. weekly liver function tests
  3. women are typically induced at 37 weeks
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95
Q

What is the most common cause of HCC worldwide?

A

Chronic hepatitis B is the most common cause of HCC worldwide with chronic hepatitis C being the most common cause in Europe.

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96
Q

The main risk factor for developing HCC

A
  1. liver cirrhosis, for example secondary* tohepatitis B & C, alcohol,haemochromatosisand primary biliary cirrhosis.
  2. alpha-1 antitrypsin deficiency
  3. hereditary tyrosinosis
  4. glycogen storage disease
  5. aflatoxin
  6. drugs: oral contraceptive pill, anabolic steroids
  7. porphyria cutanea tarda
  8. male sex
  9. DM , metabolic syndrome
97
Q

Screening of HCC with ….

A

ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:

patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis

men with liver cirrhosis secondary to alcohol

98
Q

Management of HCC

A

early disease: surgical resection

liver transplantation

radiofrequency ablation

transarterial chemoembolisation

sorafenib: a multikinase inhibitor

99
Q

HBV vs breastfeeding

A

hepatitis B cannot be transmitted via breastfeeding (in contrast to HIV)

100
Q

Achalasia due to degenerative loss of

A

ganglia from Auerbach’s plexus

101
Q

Treatment of achalasia

A
  • pneumatic (balloon) dilationis increasingly the preferred first-line option

less invasive and quicker recovery time than surgery

patients should be a low surgical risk as surgery may be required if complications occur

  • surgical intervention with aHeller cardiomyotomyshould be considered ifrecurrent or persistentsymptoms
  • intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
  • drug therapy (e.g. nitrates, CCB ) has a role but is limited by side-effects
102
Q

Glasgow-Blatchford score helps clinicians decide ……

A

whether patient patients can be managed as outpatients or not

103
Q

theRockall score is usedafterendoscopy provides a percentage …..?

A

Risk of rebleeding and mortality

104
Q

Barrett’s can be subdivided into ……?

A

Short if < 3 cm

Long if > 3 cm

105
Q

Risk factors of Barrett’s oesophagus

A
  1. GERD
  2. MALE
  3. SMOKING
  4. CENTRAL OBESITY
106
Q

Management of Barrett’s oesophagus

A
  • high-dose proton pump inhibitor
  • ifdysplasia of any grade is identified endoscopic interventionis offered. Options include:
  • radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia
  • endoscopic mucosal resection
107
Q

Barrett’s oesophagus
endoscopic surveillance with biopsies

A

for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years

108
Q

Risk factors of gastric cancer

A
  1. Helicobacer pylori
  • triggers inflammation of the mucosa → atrophy and intestinal metaplasia
  1. atrophic gastritis
  2. diet
  • salt and salt-preserved foods
  • nitrates
  1. smoking
  2. blood group A
109
Q

Management of Gastric cancer

A
  1. surgical options depend on the extent and side but include:
    - endoscopic mucosal resection
    - partial gastrectomy
    - total gastrectomy
  2. chemotherapy
110
Q

Gastric MALT lymphoma associated with

A

H. pyloriinfection in 95% of cases

good prognosis

111
Q

Indications for upper GI endoscopy in GERD

A
  1. age > 55 years
  2. symptoms > 4 weeks or persistent symptoms despite treatment
  3. dysphagia
  4. relapsing symptoms
  5. weight loss
112
Q

In patients with GERD If endoscopy is negative consider …….

A

24-hr oesophageal pH monitoring (the gold standard test for diagnosis)

113
Q

Drugs causing dyspepsia

A

NSAIDs

bisphosphonates

steroids

The following drugs may cause reflux

calcium channel blockers*

nitrates*

theophyllines

114
Q

In Eosinophilic oesophagitis , oesophageal biopsy will show

A

show dense infiltrate of eosinophils in the epithelium

115
Q

Risk factors for developing eosinophilic oesophagitis

A
  1. Allergies/ asthma: suffering from food/ environmental allergies or atopic dermatitis and asthma increases the risk of diagnosis
  2. Male sex
  3. Family history of eosinophilic oesophagitis or allergies
  4. Caucasian race
  5. Age between 30-50
  6. Coexisting autoimmune disease e.g. coeliac disease
116
Q

eosinophilic oesophagitis

Investigations

A

Endoscopy: diagnosis can only be made on the histological analysis of an oesophageal biopsy.
Histologically, the diagnosis is made more likely in the presence of epithelial desquamation, eosinophilic microabscesses, and abnormally long papillae

PPI trial: persistence of eosinophilia and no improvement of symptoms after trialling a proton pump inhibitor. This can help the clinician differentiate between eosinophilic oesophagitis and GORD, which can be a tricky task

117
Q

Management of

A

Dietary modification:

Topical steroids e.g. fluticasone and budesonide are options when dietary modification fails. This requires the patient to swallow
solutions of the steroid to line the oesophagus. This should be done for eight weeks before being reassessed

Oesophageal dilatation: 56% of patients require this at some point in their treatment to reduce the symptoms associated with oesophageal strictures

118
Q

Zollinger-Ellison syndrome are found in which parts of GIT

A

are found in thefirst part of the duodenum, with the second most common location being the pancreas.

119
Q

Diagnosis of Zollinger-Ellison syndrome

A
  1. fasting gastrin levels: the single best screen test
  2. secretin stimulation test
120
Q

Treatment of Pernicious anaemia

A

vitamin B12 replacement

no neurological features:3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections

more frequent doses are given for patients with neurological features

121
Q

Helicobacter pylorihas 2 main mechanisms to survice in the acidic gastric environment:

A
  1. chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
  2. secretesurease→ urea converted to NH3→ alkalinization of acidic environment → increased bacterial survival
122
Q

pathogenesis mechanism, Helicobacter pylorireleases bacterial cytotoxins (e.g. CagA toxin) lead to

A

disruption of gastric mucosa

123
Q

Urea breath test should not be performed

within……. of treatment with an antibacterial or

within ……….. of PPI

A

within4 weeks of treatment with an antibacterial or within 2 weeks of PPI

124
Q

Pyloric stenosis is caused by

A

It is caused by hypertrophy of the circular muscles of the pylorus.

125
Q
  1. projectile’ vomiting, typically 30 minutes after a feed
  2. constipation and dehydration may also be present
  3. a palpable mass may be present in the upper abdomen
  4. hypochloraemic, hypokalaemic alkalosisdue to persistent vomiting

Features of what?

A

Pyloric stenosis

126
Q

Pyloric stenosis
Diagnosis is most commonly made by………….

A

Diagnosis is most commonly made byultrasound.

127
Q

Management of Pyloric stenosis

A

Management is withRamstedt pyloromyotomy.

128
Q

Boerhaave syndrome?

A

Severe vomiting → oesophageal rupture

129
Q

Adverse effects of Metoclopramide

A

extrapyramidal effects

acute dystonia e.g.oculogyric crisis

this is particularly a problem in children and young adults

diarrhoea

hyperprolactinaemia

tardive dyskinesia

parkinsonism

130
Q

In Oesophageal cancer

Location of Adenocarcinoma in ….1….
Location of Squamous cell cancer ….2….

A
  1. Lower third - near the gastroesophageal junction
  2. Upper two-thirds of the oesophagus
131
Q

Risk factors of Oesophageal Adenocarcinoma

A

GORD

Barrett’s oesophagus

smoking

obesity

132
Q

Risk factors of Oesophageal Squamous cell cancer

A

smoking

alcohol

achalasia

Plummer-Vinson syndrome

diets rich in nitrosamines

133
Q

Diagnosis of oesophageal cancer

A

Upper GI endoscopy with biopsy is used for diagnosis

Endoscopic ultrasoundis the preferred method for locoregional staging

CT scanning of the chest, abdomen and pelvis is used for initial staging

FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans.

Laparoscopy is sometimes performed to detect occult peritoneal disease

134
Q

Treatment of oesophageal cancer

A

Operable disease (T1N0M0) is best managed bysurgical resection- the most common procedure is an Ivor-Lewis type oesophagectomy

The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis

In addition to surgical resection many patients will be treated with adjuvant chemotherapy

135
Q

The amount of energy that may be derived from 1 gram of food is as follows:

carbohydrates:

protein:

fat:

A

carbohydrates: 4 kcal

protein: 4 kcal

fat: 9 kcal

136
Q

Patients identified as being malnourished if

A
  1. BMI < 18.5
  2. unintentional weight loss of > 10% over 3-6/12
  3. BMI < 20 and unintentional weight loss of > 5% over 3-6/12
137
Q

AT RISK of malnutrition

A
  1. Eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
  2. Poor absorptive capacity
  3. High nutrient losses
  4. High metabolism
138
Q

complications of enteral feeding

A
  1. Diarrhoea
  2. Aspiration
  3. Hyperglycaemia
  4. Refeeding syndrome
139
Q

The following brush border enzymes are involved in the breakdown of carbohydrates:

maltase: cleaves disaccharide maltose to ……..

sucrase: cleaves sucrose to …….

lactase: cleaves disaccharide lactose to ………

A

maltase: cleaves disaccharide maltose to glucose + glucose

sucrase: cleaves sucrose to fructose and glucose

lactase: cleaves disaccharide lactose to glucose + galactose

140
Q

In Refeeding syndrome
The metabolic consequences include:

A
  1. hypophosphataemia

this is the hallmark symptom of refeeding syndrome

may result in significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)

  1. hypokalaemia
  2. hypomagnesaemia: may predispose totorsades de pointes
  3. abnormal fluid balance
141
Q

Patients are considered high-risk of Refeeding syndrome if one or more of the following:

A
  1. BMI < 16 kg/m2
  2. unintentional weight loss >15% over 3-6 months
  3. little nutritional intake > 10 days
  4. hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
142
Q

Patients are considered high-risk of Refeeding syndrome if two or more of the following:

A
  1. BMI < 18.5 kg/m2
  2. unintentional weight loss > 10% over 3-6 months
  3. little nutritional intake > 5 days
  4. history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids
143
Q

if a patient hasn’t eaten for > 5 days, aim to re-feed at …….

A

no more than 50% of requirements for the first 2 days.

144
Q

Source of Gastrin

A

G cells in antrum of the stomach

145
Q

Actions of Gastrin

A
  1. Increases acid secretion by gastric parietal cells,pepsinogenand IF secretion,
  2. increases gastric motility,
  3. stimulates parietal cell maturation
146
Q

Source of CCK

A

I cells in upper small intestine

147
Q

Actions of CCK

A
  1. Increases secretion of enzyme-rich fluid from pancreas,
  2. contraction of gallbladderand relaxation of sphincter of Oddi,
  3. decreases gastric emptying, trophic effect on pancreatic acinar cells, induces satiety
148
Q

Source of Secretin

A

S cells in upper small intestine

149
Q

Actions of secreting

A
  1. Increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells,
  2. decreases gastric acid secretion, trophic effect on pancreatic acinar cells
150
Q

Source of VIP

A
  1. Small intestine,
  2. pancreas
151
Q

Actions of VIP

A
  1. Stimulates secretion by pancreas and intestines,
  2. inhibits acid secretion
152
Q

Source of Somatostatin

A

D cells in the pancreas & stomach

153
Q

Actions of Somatostatin

A
  1. Decreases acidandpepsinsecretion,
  2. decreases gastrin secretion,
  3. decreases pancreatic enzyme secretion,
  4. decreases insulin and glucagon secretion
  5. inhibits trophic effects of gastrin,
  6. stimulates gastric mucous production
154
Q

Diagnosis of Angiodysplasia by

A
  1. colonoscopy
  2. mesenteric angiography if acutely bleeding
155
Q

Management of Angiodysplasia

A

endoscopic cautery or argon plasma coagulation

antifibrinolytics e.g. Tranexamic acid

oestrogens may also be used

156
Q

Conditions associated with coeliac disease include

A
  1. dermatitis herpetiformis (a vesicular, pruritic skin eruption)
  2. autoimmune disorders (T1DM and autoimmune hepatitis)
157
Q

Which condition is strongly associated withHLA-DQ2 (95% of patients)and HLA-DQ8 (80%).

A

Coeliac disease

158
Q

Complications of Coeliac disease

A

anaemia:iron, folate and vitamin B12 deficiency(folate deficiency is more common than vitamin B12 deficiency in coeliac disease)

hyposplenism

osteoporosis,osteomalacia

lactose intolerance

enteropathy-associated T-cell lymphoma of small intestine

subfertility, unfavourable pregnancy outcomes

rare: oesophageal cancer, other malignancies

159
Q

If suspected Codliac disease in patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at………. prior to testing.

A

At least 6 weeks

160
Q

Serology of coeliac disease

A
  1. TTG antibodies (IgA) are first-choiceaccording to NICE
  2. endomyseal antibody (IgA)
  • needed to look for selective IgA deficiency, which would give a false negative coeliac result
  1. anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
  2. anti-casein antibodies are also found in some patients
161
Q

What is the ‘gold standard’ for diagnosis - this should be performed in all patients with suspected coeliac disease to confirm or exclude the diagnosis ?

A

Endoscopic intestinal biopsy

162
Q

findings supportive of coeliac disease in biopsy

A

villous atrophy

crypt hyperplasia

increase in intraepithelial lymphocytes

lamina propria infiltration with lymphocytes

163
Q

Complications of diverticulitis include:

A

abscess formation

peritonitis

obstruction

perforation

164
Q

Management of diverticulitis

A

mild attacks can be treated with oral antibiotics

more significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given

165
Q

In Bile-acid malabsorption the ,test of choice is

A

SeHCAT

166
Q

Severity of C.diff

A

Mild: NORMAL WBC

MODERATE: WBC < 15

Severe: WBC > 15 or rise in Creatinine > 50 % above baseline or T > 38.5 or evidence of severe colitis ( abdominal or radiological signs)

Life-threatening : Hypotension, partial or complete ileus toxic megacolon
Or CT evidence of severe disease

167
Q

Treatment of First episode ofC. difficileinfection

A

first-line therapy isoral vancomycinfor 10 days

second-line therapy:oral fidaxomicin

third-line therapy:oral vancomycin +/- IV metronidazole

168
Q

Treatment of Recurrent episode c.diff

A

within 12 weeks of symptom resolution: oral fidaxomicin

after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin

169
Q

Treatment of Life-threateningC. difficileinfection

A

oral vancomycin AND IV metronidazole

specialist advice - surgery may be considered

170
Q

Preventing the spread ofC. difficileinfection

A

isolation in side room: the patient should remain isolated until there has been no diarrhoea

171
Q

cause of jejunal villous atrophy

A

coeliac disease

tropical sprue

hypogammaglobulinaemia

gastrointestinal lymphoma

Whipple’s disease

cow’s milk intolerance

172
Q

In Melanosis coli, Histology demonstrates……..

A

pigment-laden macrophages.

173
Q

Melanosis coliis associated with

A

laxative abuse, especially anthraquinone compounds such as senna

174
Q

In IBS, First-line pharmacological treatment - according to predominant symptom

A

pain: antispasmodic agents

constipation: laxatives but avoid lactulose

diarrhoea: loperamide is first-line

175
Q

Diagnosis of Small bowel bacterial overgrowth syndrome by

A

Hydrogen breath test

176
Q

Treatment of Small bowel bacterial overgrowth syndrome

A
  1. correction of the underlying disorder
  2. antibiotic therapy:
    rifaximinis now the treatment of choice due to relatively low resistance. Co-amoxiclav or metronidazole are also effective in the majority of patients.
177
Q

Peutz-Jeghers syndrome is anautosomal …….condition

A

dominant

178
Q

Peutz-Jeghers syndrome is also associated

A

associated with numerous hamartomatous polyps in the gastrointestinal tract, pigmented freckles on the lips, face, palms and soles.

179
Q

In Peutz-Jeghers syndrome, responsible gene encodes …….

A

serine threonine kinase LKB1 or STK11

180
Q

Management of Peutz-Jeghers syndrome

A

conservative unless complications develop

181
Q

Whipple’s disease is a rare multi-system disorder caused by……..

A

Tropheryma whippeliiinfection.

182
Q

Whipple’s disease is more common in those who are ………

A

HLA-B27 positive and inmiddle-aged men.

183
Q

Whipple’s disease, jejunal biopsy shows …..

A

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

184
Q

Management of Whipple’s disease

A

oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin

185
Q

Intestinal causes of malabsorption

A

coeliac disease

Crohn’s disease

tropical sprue

Whipple’s disease

Giardiasis

brush border enzyme deficiencies (e.g. lactase insufficiency)

186
Q

Pancreatic causes of malabsorption

A

chronic pancreatitis

cystic fibrosis

pancreatic cancer

187
Q

Biliary causes of malabsorption

A

biliary obstruction

primary biliary cirrhosis

188
Q

Deep ulcers,skip lesions-‘cobble-stone’ appearance

Seen in ?

A

Crohn’s disease

189
Q

appearance of pseudopolyps seen in

A

Ulcerative colitis

190
Q

Hirschsprung’s disease is associated with

A

Down’s syndrome

191
Q

Investigations of carcinoid syndrome

A

urinary 5-HIAA

plasma chromogranin A y

192
Q

Management of carcinoid syndrome

A

somatostatin analogues e.g.octreotide

diarrhoea: cyproheptadine may help

193
Q

Risk factors of anal cancer

A
  1. human papillomavirus (HPV)
  2. Anal intercourse
  3. Smoking
  4. Those with HIV and those taking immunosuppressive medication
  5. Immunosuppressive drugs used in transplant recipients
  6. Women with a history of cervical cancer or cervical intraepithelial neoplasia
194
Q

familial adenomatous polyposis, It is due to a mutation in a tumour suppressor gene called……………..

A

adenomatous polyposis coli gene (APC), located on chromosome 5.

195
Q

hereditary non-polyposis colorectal carcinoma(Lynch syndrome),
The mostcommon genes involvedare:

A

MSH2 (60% of cases)

MLH1 (30%)

196
Q

Colorectal cancer: screening

With

A

Faecal Immunochemical Test (FIT)screening to older adults

patients with abnormal results are offered a colonoscopy

197
Q

Crohn’s disease commonly affects ……..

A

the terminal ileum and colon

198
Q

Crohn’s disease: management
Inducing remission

A
  1. glucocorticoids (oral, topical or intravenous) are generally used to induce remission
  2. 5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
  3. azathioprine or mercaptopurine* may be used as an add-on medication to induce remission but is not used as monotherapy. Methotrexate is an alternative to azathioprine
  4. infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
  5. metronidazole is often used for isolated peri-anal disease
199
Q

Maintaining remission, Crohn’s disease

A

1.lmazathioprine or mercaptopurineis used first-line to maintain remission

  1. methotrexate is used second-line
200
Q

TPMT activity should be assessed before offering methotrexate, azathioprine or mercaptopurine therapy in

  • thiopurine methyltransferase (TPMT) activity
A

Crohn’s disease

201
Q

patients with symptomatic perianal fistulae are usually given oral

A

metronidazole

202
Q

the investigation of choice for suspected perianal fistulae

A

MRI

203
Q

Factors may trigger an ulcerative colitis flare

A
  1. stress
  2. medications (NSAIDs & antibiotics)
  3. cessation of smoking
204
Q

Mild ulcerative colitis

A

4 < stools daily with or without blood

205
Q

Moderate ulcerative colitis

A

4- 6 stools daily with minimal systemic disturbance

206
Q

Severe ulcerative colitis

A
  1. > 6 stools a day, containing blood
  2. Evidence of systemic disturbance, e.g.

fever

tachycardia

abdominal tenderness, distension or reduced bowel sounds

anaemia

hypoalbuminaemia

207
Q

In ulcerative colitis, Factors increasing risk of cancer

A

disease duration > 10 years

patients with pancolitis

onset before 15 years old

unremitting disease

poor compliance to treatment

208
Q

Colonoscopy surveillance in inflammatory bowel disease patients should be decided following risk stratification.

A

By follow up colonoscopy

  1. Low risk: 5 years
  2. Intermediate risk: 3 years
  3. High risk: 1 year
209
Q

Adverse effects of Cholestyramine

A

constipation

decreases absorption of fat-soluble vitamins

cholesterol gallstones

may raise level of triglycerides

210
Q

Treatment of diarrhea following bowel resection in crohn’s disease

A

Cholestyramine

211
Q

Treating mild-to-moderate ulcerative colitis

proctitis

A
  1. topical (rectal) aminosalicylate
    If no improvement after 4 weeks then
  2. Oral aminosalicylate

If no improvement then

  1. Oral or topical steroids
212
Q

Treating mild-to-moderate ulcerative colitis
proctosigmoiditis and left-sided ulcerative colitis

A
  1. topical (rectal) aminosalicylate

If no improvement after 4 weeks then

  1. high-dose oral aminosalicylateOR switch to a high-dose oral aminosalicylate and a topical corticosteroid

If no improvement after 4 weeks then

  1. oral aminosalicylate andan oral corticosteroid
213
Q

Treating mild-to-moderate ulcerative colitis

extensive disease

A
  1. topical and a high-dose oral aminosalicylate

if remission is not achieved within 4 weeks

  1. stop topical treatments and offer a high-dose oral aminosalicylate and anoral corticosteroid
214
Q

Treatment of Severe ulcerative colitis

A
  1. Iv steroids are usually given first-line
    * iv ciclosporin may be used if steroid are contraindicated
  2. if after 72 hours there has been no improvement, consider adding iv ciclosporin to iv corticosteroids or consider surgery
215
Q

Maintaining remission

Following a mild-to-moderate ulcerative colitis flare

proctitis and proctosigmoiditis

A
  1. Topical aminosalicylate
    Or
  2. Topical and oral aminosalicylate
    Or
  3. Oral aminosalicylate
216
Q

Maintaining remission

Following a mild-to-moderate ulcerative colitis flare

Following a severe relapse or >=2 exacerbations in the past year

A

oral azathioprine or oral mercaptopurine

217
Q

Associated factors of NAFLD

A
  1. Obesity
  2. T2DM
  3. hyperlipidaemia
  4. jejunoileal bypass
  5. sudden weight loss/starvation
218
Q

In patients with non-alcoholic fatty liver disease, …….. testing is recommended to aid diagnosis of liver fibrosis

A

enhanced liver fibrosis (ELF) testing

219
Q

Side effects of Sulphasalazine

A

1.rashes,
2.oligospermia
3. headache
4. Heinz body anaemia,megaloblastic anaemia
5. lung fibrosis

220
Q

Side effects of Mesalazine

A
  1. GI upset
  2. headache
  3. agranulocytosis,
  4. pancreatitis,
  5. interstitial nephritis
221
Q

What can stimulate the release of gastrin from G-cells?

A

Distension of stomach,

vagus nerves (mediated by gastrin-releasing peptide),

luminal peptides/amino acids

222
Q

The combination of deranged LFTs combined with secondary amenorrhoea in a young female strongly suggest ……

A

autoimmune hepatitis

223
Q

What is the strongest risk factor for anal cancer

A

HPV infection

224
Q

non-specific lower gastrointestinal symptoms

secretory diarrhoea may occur

microcytic anaemia

hypokalaemia

Features of

A

Villous adenomas

225
Q

Perianal itching in children, possibly affecting other family members →

A

Enterobius vermicularis(threadworms)

226
Q

what percentageof patients with a positive faecal occult blood test have colorectal cancer

A

5 - 15 %

227
Q

What percentage of patients with Peutz-Jeghers syndrome will have died from a related cancer by the age of 60 years?

A

50 %

228
Q

Hepatorenal syndrome is primarily caused by …….. vasodilation

A

splanchnic vasodilat

229
Q

What is the function of MSH2 gene.

A

DNA mismatch repair

230
Q

biospy shows pigment laden macrophages =

A

laxative abuse

231
Q

Which one of laxatives is shown to have to carcinogenic potential?

A

Co-danthramer

232
Q

Non-caseating granulomas is features of ….

A

Crohn’s disease

233
Q

SeHCAT is the investigation of choice for …..

A

bile acid malabsorption

234
Q
  1. increased goblet cells in …..
  2. depletion of goblet cellsand mucin from gland epithelium in ……
A
  1. CD
  2. UC
235
Q

Screening for haemochromatosis

general population: ………

family members: ………

A

Screening for haemochromatosis

general population: transferrin saturation > ferritin

family members: HFE genetic testing

236
Q

familial adenomatous polyposis (FAP) is Autosomal …….

A

Autosomal dominant.

237
Q
  • anti-mitochondrial antibodies
  • smooth muscle antibodies
  • Raise serum IgM
A

PBC

238
Q

Treatment of Small bowel bacterial overgrowth syndrome

A

rifaximin

  • Tetracyclines are no longer commonly used due to widespread bacterial resistance.

MRCP Part 1 (15 decks)

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