Gastroenterology Flashcards

1
Q

How many units of alcohol is the recommendation?

A

Men and women should drink no more than 14 units of alcohol per week!

If you do drink as much as 14 units per week, it is best to spread this evenly over 3 days or more

If you are pregnant or planning a pregnancy, the safest approach is not to drink alcohol at all, to keep risks to your baby to a minimum.

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2
Q

What is the commonest cause of hepatocellular carcinoma?

A

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

The main risk factor for developing HCC is liver cirrhosis, for example secondary to hepatitis B & C, Alcohol, Haemochromatosis and Primary Biliary Cirrhosis. Other risk factors include:

  • alpha-1 antitrypsin deficiency
  • hereditary tyrosinosis
  • glycogen storage disease
  • aflatoxin
  • drugs: oral contraceptive pill, anabolic steroids
  • porphyria cutanea tarda
  • male sex
  • diabetes mellitus, metabolic syndrome
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3
Q

Signs and symptoms of HCC?

A

Features of liver cirrhosis or failure may be seen:

  • Jaundice
  • Ascites,
  • RUQ pain
  • Hepatomegaly
  • Pruritus
  • Splenomegaly

Possible presentation is decompensation in a patient with chronic liver disease.
- Raised AFP
- Tends to present late

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4
Q

What is the acute treatment for variceal haemorrhage?

A

Acute treatment of variceal haemorrhage:

  1. ABC: patients should ideally be resuscitated prior to endoscopy
  2. Correct clotting: FFP, vitamin K
  3. Vasoactive agents:
    - Terlipressin is currently the only licensed vasoactive agent. Benefit in initial haemostasis and preventing rebleeding.
    - Octreotide may also be used although there is some evidence that Terlipressin has a greater effect on reducing mortality.
  4. Prophylactic antibiotics. Quinolones are typically used. Offer prophylactic intravenous antibiotics for people with cirrhosis who have upper GI bleeding.
  5. Endoscopy: endoscopic variceal band ligation is superior to endoscopic sclerotherapy. NICE recommend band ligation
  6. Sengstaken-Blakemore tube if uncontrolled haemorrhage
  7. Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail
    - connects the hepatic vein to the portal vein
    - exacerbation of hepatic encephalopathy is a common complication
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5
Q

What drug is given for prophylaxis of variceal haemorrhage?

A

Propranolol: reduced rebleeding and mortality compared to placebo

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6
Q

What is Wilson disease? Mode of inheritance?

A

Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.

The onset of symptoms is usually between 10 - 25 years. Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease

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7
Q

Signs and symptoms of wilson disease?

A

Features result from excessive copper deposition in the tissues, especially the BRAIN, LIVER and CORNEA:

  • Liver: hepatitis, cirrhosis
  • Neurological:
  • basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia
  • Speech, behavioural and psychiatric problems are often the first manifestations
  • also: asterixis, chorea, dementia, parkinsonism
  • Kayser-Fleischer rings
    green-brown rings in the periphery of the iris
    due to copper accumulation in Descemet membrane
  • renal tubular acidosis (esp. Fanconi syndrome)
  • haemolysis
  • blue nails
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8
Q

How is Wilsons disease investigated?

A
  • Slit lamp examination for Kayser-Fleischer rings
  • Reduced serum caeruloplasmin
  • Reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin). Free (non-ceruloplasmin-bound) serum copper is increased
  • Increased 24hr urinary copper excretion
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9
Q

Which drug is given in management of Wilsons disease?

A

Penicillamine (chelates copper) has been the traditional first-line treatment.

Trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future

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10
Q

What are the associated factors for NAFLD?

A

Non-alcoholic fatty liver disease (NAFLD) is now the most common cause of liver disease in the developed world. It is largely caused by obesity and describes a spectrum of disease ranging from:
- steatosis - fat in the liver
- steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH)
- progressive disease may cause fibrosis and liver cirrhosis

Associated factors:
- obesity
- type 2 diabetes mellitus
- hyperlipidaemia
- jejunoileal bypass
- sudden weight loss/starvation

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11
Q

Investigations for NAFLD?

A

(Incidental finding of NAFLD - typically asymptomatic fatty changes on liver ultrasound)
in these patients, NICE recommends the use of the Enhanced Liver Fibrosis (ELF) blood test to check for advanced fibrosis.

if the ELF blood test was not available:
Non-invasive tests may be used to assess the severity of fibrosis.
These include the FIB4 score or NALFD fibrosis score
these scores may be used in combination with a FibroScan (liver stiffness measurement assessed with transient elastography).

This combination has been shown to have excellent accuracy in predicting fibrosis

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12
Q

Management for NAFLD?

A

Management:

The mainstay of treatment is lifestyle changes (particularly weight loss) and monitoring.

there is ongoing research into the role of gastric banding and insulin-sensitising drugs (e.g. metformin, pioglitazone)

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13
Q

Anti-smooth muscle antibodies (SMA) is associated with which condition?

A

Autoimmune hepatitis

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14
Q

What is the main stay of coeliac disease management?

A

The management of coeliac disease involves a GLUTEN-FREE DIET. Gluten-containing cereals include:
- wheat: bread, pasta, pastry
- barley: beer
- rye
- oats

Some notable foods which are gluten-free include:
- rice
- potatoes
- corn (maize)

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15
Q

What antibody is checked to check for compliance to a gluten-free diet?

A

Tissue transglutaminase antibodies

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16
Q

Diarrhea, the stool floats in the toilet water, but there is no blood. What is the most likely causative organism?

A

Giardia lamblia causes fat malabsorption, therefore greasy stool can occur

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17
Q

What is the first line pharmacological treatment for IBS?

A

First-line pharmacological treatment - according to predominant symptom:

Pain: antispasmodic agents
Constipation: laxatives but avoid lactulose
Diarrhoea: Loperamide is first-line

General dietary advice:
- have regular meals and take time to eat
- avoid missing meals or leaving long gaps between eating
- drink at least 8 cups of fluid per day, especially water or other non-caffeinated drinks such as herbal teas
- restrict tea and coffee to 3 cups per day
- reduce intake of alcohol and fizzy drinks
- consider limiting intake of high-fibre food (for example, wholemeal or high-fibre flour and breads, cereals high in bran, and whole grains such as brown rice)
- reduce intake of ‘resistant starch’ often found in processed foods
- limit fresh fruit to 3 portions per day
- for diarrhoea, avoid sorbitol
- for wind and bloating consider increasing intake of oats (for example, oat-based breakfast cereal or porridge) and linseeds (up to one tablespoon per day).

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18
Q

What are the features of hepatic encephalopathy?

A

Hepatic encephalopathy is largely believed to occur from accumulation of ammonia in the blood stream due to the livers decreased ability to detoxify ammonia that is produced and transported from the gastrointestinal tract.

Features:
- Confusion, altered GCS
- Asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
- Constructional apraxia: inability to draw a 5-pointed star
- Triphasic slow waves on EEG
- Raised ammonia level (not commonly measured anymore)

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19
Q

What is the first line treatment for hepatic encephalopathy?

A

Management:

  1. Treat any underlying precipitating cause
  2. NICE recommend LACTULOSE first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
    - lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
  3. Antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production
  • other options include embolisation of portosystemic shunts and liver transplantation in selected patients
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20
Q

What is the investigation of choice for crohn’s disease? What is usually seen?

A

Crohn’s disease is a form of inflammatory bowel disease. It commonly affects the terminal ileum and colon but may be seen anywhere from the mouth to anus.

Bloods:
C-reactive protein correlates well with disease activity

Colonoscopy is the investigation of choice!
- features suggestive of Crohn’s include deep ulcers, skip lesions

Histology
- inflammation in all layers from mucosa to serosa
- goblet cells, granulomas

Small bowel enema
- high sensitivity and specificity for examination of the terminal ileum
- strictures: ‘Kantor’s string sign’
- proximal bowel dilation
- ‘rose thorn’ ulcers
- fistulae

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21
Q

Commonest organism found in ascitic culture of spontaneous bacterial peritonitis?

A

Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.

Features:
Ascites
Abdominal pain
Fever

Diagnosis:
- Paracentesis: neutrophil count > 250 cells/ul
- The most common organism found on ascitic fluid culture is E. coli

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22
Q

What is the antibiotic given for SBP? What is the prophylaxis?

A

Management of SBP:
Intravenous Cefotaxime

Antibiotic prophylaxis should be given to patients with ascites if:

  • Patients who have had an episode of SBP
  • Patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
  • Offer prophylactic 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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23
Q

What is Courvoisir’s law?

A

Courvoisier’s law states that in the presence of a palpably enlarged gallbladder and accompanied with mild jaundice, the cause is unlikely to be gallstones.

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24
Q

Signs and symptoms of pancreatic cancer?

A
  • Classically painless jaundice
  • Pale stools, dark urine, and pruritus
  • Cholestatic liver function tests
  • Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
  • However, patients typically present in a non-specific way with anorexia, weight loss, epigastric pain
  • Loss of exocrine function (e.g. steatorrhoea)
  • Loss of endocrine function (e.g. diabetes mellitus)
  • Atypical back pain is often seen

migratory thrombophlebitis (Trousseau sign) is more common than with other cancers

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25
Q

Investigation of choice for suspecte pancreatic cancer?

A
  • Ultrasound has a sensitivity of around 60-90%
  • High-resolution CT scanning is the investigation of choice if 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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26
Q

What procedure is done for pancreatic ca?

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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27
Q

What is the management for haemochromatosis?

A
  • Venesection is the first-line treatment
    monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
  • Desferrioxamine may be used second-line
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28
Q

Which drugs are given in Crohn’s to induce and maintain remission?

A

Patients should be strongly advised to stop smoking!

Inducing remission:

  • Glucocorticoids (oral, topical or intravenous) are generally used to induce remission. Budesonide is an alternative in a subgroup of patients.
  • 5-ASA drugs (e.g. Mesalazine) are used second-line to glucocorticoids but are not as effective
  • 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
  • Infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
  • metronidazole is often used for isolated peri-anal disease

Maintaining remission:

  • As above, stopping smoking is a priority (remember: smoking makes Crohn’s worse, but may help ulcerative colitis)
  • Azathioprine or mercaptopurine is used first-line to maintain remission
  • Methotrexate is used second-line
  • 5-ASA drugs (e.g. mesalazine) should be considered if a patient has had previous surgery

Surgery:
- around 80% of patients with Crohn’s disease will eventually have surgery

Crohn’s disease is notorious for the developmental of intestinal fistulae; these may form between the rectum and skin (perianal) or the small bowel and skin. Fistulation between loops of bowel may also occur and result in bacterial overgrowth and malabsorption. Management of enterocutaneous fistulae involves controlling sepsis, optimising nutrition, imaging the disease and planning definitive surgical management.

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29
Q

What are the symptoms and signs of haemochromatosis?

A

Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation.

Presenting features:

  1. Early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
  2. ‘bronze’ skin pigmentation
  3. diabetes mellitus
  4. liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
  5. Cardiac failure (2nd to dilated cardiomyopathy)
  6. Hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
  7. Arthritis (especially of the hands)
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30
Q

Signs and symptoms of acute appendicitis?

A

Abdominal pain is seen in the vast majority of patients:

  • Peri-umbilical abdominal pain (visceral stretching of appendix lumen and appendix is midgut structure) radiating to the right iliac fossa (RIF) due to localised parietal peritoneal inflammation.
  • The migration of the pain from the centre to the RIF has been shown to be one of the strongest indicators of appendicitis. patients often report the pain being worse on coughing or going over speed bumps. Children typically can’t hop on the right leg due to the pain.

Other features:

  • Vomit once or twice but marked and persistent vomiting is unusual
  • Diarrhoea is rare. However, pelvic appendicitis may cause localised rectal irritation of some loose stools. A pelvic abscess may also cause diarrhoea
  • Mild pyrexia is common - temperature is usually 37.5-38oC. Higher temperatures are more typical of conditions like mesenteric adenitis
  • Anorexia is very common. It is very unusual for patients with appendicitis to be hungry
  • Around 50% of patients have the typical symptoms of anorexia, peri-umbilical pain and nausea followed by more localised right lower quadrant pain
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31
Q

What are the examinations performed in suspected appendicits?

A

Examination:

  • Generalised peritonitis if perforation has occurred or localised peritonism
  • Retrocaecal appendicitis may have relatively few signs
  • Digital rectal examination may reveal boggy sensation if pelvic abscess is present, or even right-sided tenderness with a pelvic appendix
  • Rovsing’s sign (palpation in the LIF causes pain in the RIF) is now thought to be of limited value
32
Q

What is the management of appendicitis?

A
  1. Appendicectomy which can be performed via either an open or laparoscopic approach. Laparoscopic appendicectomy is now the treatment of choice!
  2. Administration of prophylactic intravenous antibiotics reduces wound infection rates.
  3. Patients with perforated appendicitis (typical around 15-20%) require copious abdominal lavage.
  4. Patients without peritonitis who have an appendix mass should receive broad-spectrum antibiotics and consideration given to performing an interval appendicectomy.
  5. be wary in the older patients who may have either an underlying caecal malignancy or perforated sigmoid diverticular disease.

trials have looked at the use of intravenous antibiotics alone in the treatment of appendicitis. The evidence currently suggests that whilst this is successful in the majority of patients, it is associated with a longer hospital stay and up to 20% of patients go on to have an appendicectomy within 12 months.

33
Q

Colicky abdominal pain RUQ, worse postprandially, worse after fatty foods

A

Biliary colic

34
Q

Triad of symptoms seen in Budd-Chiari syndrome?

A

Budd-Chiari syndrome presents with the triad of sudden onset abdominal pain, ascites, and tender hepatomegaly.

Budd-Chiari syndrome is a condition characterized by obstruction to hepatic venous outflow. It usually occurs in a patient with a hypercoagulative state (e.g. antiphospholipid syndrome) but can also occur as a result of physical obstruction (e.g. tumour). The venous congestion can cause hepatomegaly and portal hypertension which can can also result in splenomegaly and ascites.

35
Q

What is the test to detect for H.pylori?

A

Testing for H. pylori infection:

Initial diagnosis: NICE recommend using a carbon-13 urea breath test or a stool antigen test, or laboratory-based serology ‘where its performance has been locally validated’

Test of cure:
- there is no need to check for H. pylori eradication if symptoms have resolved following test and treat

  • however, if repeat testing is required then a carbon-13 urea breath test should be used
36
Q

How long must symptoms be present for to diagnose IBS?

A

The diagnosis of IBS should be considered if the patient has had the following for AT LEAST 6 MONTHS:
1. abdominal pain, and/or
2. bloating, and/or
3. change in bowel habit

A positive diagnosis of IBS should be made if the patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form, in addition to 2 of the following 4 symptoms:
- altered stool passage (straining, urgency, incomplete evacuation)
- abdominal bloating (more common in women than men), distension, tension or hardness
- symptoms made worse by eating
- passage of mucus

Features such as lethargy, nausea, backache and bladder symptoms may also support the diagnosis

37
Q

Investigations for IBS in primary care setting?

A

Suggested primary care investigations are:
- Full blood count
- ESR/CRP
- Coeliac disease screen (tissue transglutaminase antibodies)

38
Q

Risk factors for diverticulosis?

A

Diverticulosis is an extremely common disorder characterised by multiple outpouchings of the bowel wall, most commonly in the sigmoid colon.

Risk factors:
- Increasing age
- Low-fibre diet

Diverticulosis can present in a number of ways:
- Painful diverticular disease: altered bowel habit, colicky left sided abdominal pain. A high fibre diet is usually recommended to minimise symptoms

39
Q

What is the presentation for dicerticulitis?

A

One of the diverticular become infected. The classical presentation is:

  1. Left iliac fossa pain and tenderness
  2. anorexia, nausea and vomiting
  3. diarrhoea
  4. features of infection (pyrexia, raised WBC and CRP)

Management:
- 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

Complications of diverticulitis include:
- abscess formation
- peritonitis
- obstruction
- perforation

40
Q

Causes of liver cirrhosis?

A
  • Alcohol
  • Non-alcoholic fatty liver disease (NAFLD)
  • Viral hepatitis (B and C)
41
Q

Investigation to detect liver cirrhosis?

A

Transient elastography is now the investigation of choice to detect liver cirrhosis

Brand name ‘Fibroscan’
uses a 50-MHz wave is passed into the liver from a small transducer on the end of an ultrasound probe
measures the ‘stiffness’ of the liver which is a proxy for fibrosis

42
Q

What causes c.diff infection?

A

Clostridium difficile is a Gram positive rod often encountered in hospital practice. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis. Clostridium difficile develops when the normal gut flora are suppressed by broad-spectrum antibiotics.

Clindamycin is historically associated with causing Clostridium difficile but the aetiology has evolved significantly over the past 10 years. Second and third generation cephalosporins are now the leading cause of Clostridium difficile.

Other than antibiotics, risk factors include:
- proton pump inhibitors

Features:
- diarrhoea
- abdominal pain
- a raised WBC count is characteristic
- if severe toxic megacolon may develop

Diagnosis:
- is made by detecting Clostridium difficile toxin (CDT) in the stool
- Clostridium difficile antigen positivity only shows exposure to the bacteria, rather than current infection

43
Q

What is the first line drug for c.diff infection?

A

First episode of C. difficile infection:

  1. First-line therapy is oral Vancomycin for 10 days
  2. second-line therapy: oral Fidaxomicin
  3. Third-line therapy: oral vancomycin +/- IV metronidazole
44
Q

Toxic megacolon is associated more commonly in which conditions?

A

Toxic megacolon is an acute form of colonic distension. It is characterized by a very dilated colon (megacolon), accompanied by abdominal distension (bloating), and sometimes fever, abdominal pain, or shock.

Toxic megacolon is usually a complication of inflammatory bowel disease, such as ulcerative colitis and, more rarely, Crohn’s disease, and of some infections of the colon, including Clostridium difficile infections, which have led to pseudomembranous colitis.

45
Q

What are the risk factors for Barrett’s esophagus?

A
  • Gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
  • male gender (7:1 ratio)
  • smoking
  • central obesity
46
Q

What is the investigation performed for suspected coeliac disease?

A

Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption. Conditions associated with coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis).

If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks prior to testing.

Immunology:
- Tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
- Endomyseal antibody (IgA)

Duodenal biopsy:
- villous atrophy
- crypt hyperplasia
- increase in intraepithelial lymphocytes
- lamina propria infiltration with lymphocytes

47
Q

What are the causes of Ascites with a serum-ascites albumin gradient (SAAG) <11 g/L?

A

A low SAAG (<11g/L) suggests the ascitic fluid is an EXUDATE.

  • Malignancy
  • Infection
  • Pancreatitis
  • Nephrotic syndrome
48
Q

What are the causes of Ascites with a serum-ascites albumin gradient (SAAG) >11 g/L?

A

A high SAAG (>11g/L) indicates PORTAL HYPERTENSION. The ascitic fluid is a TRANSUDATE.

  • Liver cirrhosis
  • Hepatic failure
  • Cardiac ascites
  • Venous occlusion (e.g. Budd Chiari syndrome)
  • Alcoholic hepatitis
  • kwashiorkor malnutrition.
49
Q

Triad of Plummer-Vinson syndrome?

A

Triad of:

  • Dysphagia (secondary to oesophageal webs)
  • Glossitis
  • Iron-deficiency anaemia
50
Q

Treatment with which drug is associated with a high risk of Clostridium difficile?

A

Clindamycin

51
Q

What is the management to eradicate H.pylori?

A

Eradication may be achieved with a 7 day course of:

a proton pump inhibitor + amoxicillin + clarithromycin

OR

a proton pump inhibitor + metronidazole + clarithromycin

52
Q

Rovsing’s sign

A

positive if palpation of the left lower quadrant of the abdomen increases the pain felt in the right lower quadrant. This may be an indicator of appendicitis, although it is not positive in all cases.

53
Q

Psoas sign/ Cope’s test

A

Patient lies on their left side and the clinician extends the right hip with the knee fully extended. Abdominal pain on this movement indicates irritation of iliopsoas and possible appendicitis. This test usually indicates an appendix that lies in the retrocaecal position.

54
Q

McBurney’s point location?

A

The site where the pain from appendicitis is usually most severe on palpation. The point is on the right side of the abdomen, approximately one-third of the distance from the anterior superior iliac spine to the umbilicus

55
Q

Which antibody is characteristically associated with primary biliary cholangitis?

A

Anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific for primary biliary cholangitis.

56
Q

What is achalasia?

A

Esophageal achalasia is an esophageal motility disorder involving the smooth muscle layer of the esophagus and the lower esophageal sphincter (LES). It is characterized by incomplete LES relaxation, increased LES tone, and lack of peristalsis of the esophagus (inability of smooth muscle to move food down the esophagus) in the absence of other explanations like cancer or fibrosis.

Achalasia is characterized by difficulty in swallowing, regurgitation, and sometimes chest pain. Unknown underlying cause.

57
Q

What is achalasia?

A

Esophageal achalasia is an esophageal motility disorder involving the smooth muscle layer of the esophagus and the lower esophageal sphincter (LES). It is characterized by incomplete LES relaxation, increased LES tone, and lack of peristalsis of the esophagus (inability of smooth muscle to move food down the esophagus) in the absence of other explanations like cancer or fibrosis.

Achalasia is characterized by difficulty in swallowing, regurgitation, and sometimes chest pain. Unknown underlying cause.

Dysphagia equally to BOTH SOLIDS AND LIQUIDS from the outset is suggestive of achalasia. A barium swallow which shows a grossly expanded oesophagus that tapers at the lower oesophageal sphincter (‘bird’s beak’ appearance) confirms the diagnosis.

58
Q

What is seen in barium enema in Ulcerative colitis?

A
  • Loss of haustrations
  • superficial ulceration, ‘pseudopolyps’
  • Long standing disease: colon is narrow and short -‘Lead pipe colon’
59
Q

What is the most common extra-intestinal feature in both crohn’s and UC?

A

Arthritis is the most common extra-intestinal feature in both CD and UC.

60
Q

Which features are common to both CD and UC? which features are found more in one than the other?

A

Common:
- Diarrhea
- erythema Nodosum
- Arthritis
- Pyoderma gangrenosum

UC (more common features):
- Ileocaecal valve to rectum. CONTINUOUS disease
- No inflammation beyond SUBMUCOSA, crypt abscess
- Bloody diarrhea
- Primary sclerosing cholangitis
- Uveitis
- Colorectal Cancer

CD (more common features):
- Non bloody diarrhea
- Weight loss
- Abdominal pain
- Mouth to anus, SKIP LESIONS
- Inflammation all layers. Goblet cells, granulomas
- Bowel obstruction, FISTULA

61
Q

Examples of proton pump inhibitors?

A

Proton pump inhibitors (PPI) cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell.

Examples include Omeprazole and Lansoprazole.

62
Q

Comparison of CD and UC:

A

CD:
- Diarrhoea usually non-bloody
- Weight loss more prominent
- Upper gastrointestinal symptoms, mouth ulcers, perianal disease
- Abdominal mass palpable in the right iliac fossa
- Obstruction, fistula
- Lesions may be seen anywhere from the mouth to anus. Skip lesions may be present
- Inflammation in all layers from mucosa to serosa
- Deep ulcers, skip lesions - ‘COBBLE-STONE’ appearance

Small bowel enema:
- strictures: ‘Kantor’s string sign’
- ‘rose thorn’ ulcers
- fistulae

UC:
- Bloody diarrhoea more common
- Abdominal pain in the left lower quadrant
- Tenesmus
- PSC more common
- Risk of colorectal cancer high in UC than CD
- Inflammation always starts at rectum and never spreads beyond ileocaecal valve. Continuous disease
- No inflammation beyond submucosa (unless fulminant disease) -

Barium enema:
- loss of haustrations
- superficial ulceration, ‘pseudopolyps’
- long standing disease: colon is narrow and short -‘Lead Pipe colon’

63
Q

Wernicke’s encephalopathy is due to a deficiency of?

A

Wernicke’s encephalopathy is a neuropsychiatric disorder caused by thiamine (vitamin B1) deficiency which is most commonly seen in alcoholics.

64
Q

What is the classical triad of wernicke’s encephalopathy?

A

Classically, Wernicke encephalopathy is characterised by the triad
1. Ophthalmoplegia/nystagmus
2. Ataxia
3. Confusion.

65
Q

Which drug is contraindicated in parkinsonism for GORD?

A

Metoclopramide.

As metoclopramide is a dopamine antagonist it may worsen symptoms in patients with Parkinson’s disease.

Metoclopramide is a D2 receptor antagonist* mainly used in the management of nausea. Other uses include:
gastro-oesophageal reflux disease
prokinetic action is useful in gastroparesis secondary to diabetic neuropathy

Adverse effects:
1. extrapyramidal effects: oculogyric crisis. This is particularly a problem in children and young adults
2. hyperprolactinaemia
3. tardive dyskinesia
4. parkinsonism

66
Q

Which other cancer is commonly associated with HNPCC besides colorectal ca?

A

Endometrial cancer.

HNPCC, an autosomal dominant condition, is the most common form of inherited colon cancer. Patients with HNPCC are also at a higher risk of other cancers, with endometrial cancer being the next most common association, after colon cancer.

67
Q

H.Pylori is mostly strongly associated with which condition?

A

Associations:

  1. Peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
  • gastric cancer
  • B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
  • atrophic gastritis
68
Q

Example of Aminosalicylate drug? (used for IBD)

A

Mesalazine
- mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis

Sulphasalazine
- a combination of sulphapyridine (a sulphonamide) and 5-ASA

69
Q

Antibody found in PBC?

A

Anti-mitochondrial antibodies

70
Q

What is triple therapy for H.Pylori eradication? ‘Test and treat’

A

Triple therapy after positive H.pylori test:
PPI and 2 antibiotic combination for 1 week.

  • Lansoprazole
  • Amoxicillin
  • Clarithromycin

If H.Pylori test negative then give acid suppression alone (omeprazole or ranitidine).

71
Q

First line treatment for primary biliary cholangitis?

A

Ursodeoxycholic acid.

Pruritus: cholestyramine

72
Q

Investigation for carcinoid syndrome?

A

Carcinoid syndrome: usually occurs when metastases are present in the liver and release serotonin into the systemic circulation.

Flushing (often the earliest symptom)
Diarrhoea
Bronchospasm
Hypotension

Ix: Urinary 5-HIAA

Mx: Somatostatin analogues e.g. Octreotide

73
Q

Clotting factor results seen in liver failure?

A

Liver failure: all clotting factors are low except for factor VIII which is high.

This is because factor VIII is synthesised in endothelial cells throughout the body, unlike the other clotting factors which are synthesised purely in hepatic endothelial cells.

74
Q

Which TB medication causes peripheral neuropathy?

A

Isoniazid.

Usually, prophylactic pyridoxine is prescribed at the same time as Isoniazid to prevent the peripheral neuropathy.

75
Q

Transformation in Barrett’s oesophagus?

A

Barrett’s oesophagus is a condition in which the normal squamous epithelium of the oesophagus is replaced by columnar epithelium.

typically as a result of chronic gastro-oesophageal reflux disease (GORD).

76
Q

Antibody tested for pernicious anaemia?

A

Anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%)

77
Q
A