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Exam - M - GI Diseases > PassMedicine > Flashcards

PassMedicine Flashcards

1
Q

What is the test used to diagnose liver cirrhosis

A

Transient elastography

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2
Q

Who should be offered a screening for liver cirrhosis

A
  • People with hepatitis C
  • Men who drink >50 units of alcohol per week
  • Women who drink >35 units of alcohol per week
  • People diagnosed with alcohol-related liver disease
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3
Q

How are patients with liver cirrhosis followed up

A
  • Upper endoscopy to check for varies after initial diagnosis
  • Liver ultrasound every 6 months (+/- alfa fetoprotein) for hepatocellular carcinoma
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4
Q

What are the common presenting symptoms of coeliac disease

A

Bloating
Flatulence
Abdominal pain
Fatigue
Weight loss
Dermatitis herpetiformis
Anaemic
Low Ferritin
Low folate

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5
Q

What is the gold standard test for diagnosing coeliac disease

A

Endoscopic intestinal biopsy
- villous atrophy
- crypt hyperplasma
- increased intraepithelial lymphocytes
- lamina propria infiltration with lymphocytes

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6
Q

What is barrels oesophagus

A

Were squamous epithelium is replaced with columnar epithelium

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7
Q

What is the management of Barretts oesophagus

A

Metaplasia - endoscopic surveillance every 3-5 years

Dysplasia - Endoscopic intervention - Radiofrequency ablation is 1st line, endoscopic mucosal resection can also be done

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8
Q

What are the main signs of acute mesenteric ischaemia

A

Sudden onset, severe abdominal pain

Vomiting and a rapid episode of bloody diarrhoea

Pain out of proportion with the clinical findings

TriadL Cardiovascular disease (usually AF), raised lactate and soft but tender abdomen.

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9
Q

What VBG findings will there be in acute mesenteric ischaemia

A

Metabolic acidosis
Elevated lactate

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10
Q

What imaging is used to diagnose ischaemic bowel

A

CT angiography abdomen and pelvis with contrast

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11
Q

What type of inheritance is haemochromatosis

A

Autosomal recessive

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12
Q

Who requires an urgent referral for upper GI

A
  • All patients with dysphagia
  • All patients with an upper abdominal mass

Patients >55 with weight loss AND:
- Upper abdominal pain
- Reflux
- Dyspepsia

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13
Q

Who requires a non-urgent GI referral

A
  • Patients with haematemesis

-Patients > 55 with:
- Treatment resistant dyspepsia
- Upper abdo pain with low haemoglobin levels
- Raised platelet count and symptoms
- Nausea or vomiting with weight loss, reflux, dyspepsia and upper ando pain

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14
Q

What are the signs of acute cholecystitis

A
  • Pain in RUQ - more severe and persistent than biliary colic
  • Pain may radiate to back or right shoulder
  • Pyrexia
  • Murphys sign positive - arrest of inspiration on palpation of RUQ
  • NOT jaundiced
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15
Q

What are the signs of ascending cholangitis

A

Triad of: Charcots triad
- Fever
- RUQ pain
- Jaundice

If very severe - Reynolds pentad:
- Fever
- RUQ pain
- Jaundice
- Shock (low bp, tachycardia)
- Altered mental status

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16
Q

What are the causes of vitamin B12 deficiency

A
  • Pernicious anaemia (most common)
  • Atrophic gastritis (secondary to H pylori)
  • Gastrectomy
  • Malnutrition (alcoholism)
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17
Q

What is the pathophysiology of pernicious anaemia

A

Antibodies are created against intrinsic factor (+/- gastric parietal cells)

  1. Intrinsic factor antibodies bind to intrinsic factor - this blocks vitamin B12 binding sight
  2. Gastric parietal cell antibodies - caused reduced acid production and atrophic gastritis. This causes reduced intrinsic factor which again causes reduced vitamin B12 absorption.
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18
Q

What is the role of vitamin B12

A
  • Production of blood cells
  • Myelination of nerves

A deficiency causes megaloblastic anaemia and neuropathy

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19
Q

What are the features of vitamin B12 deficiency?

A

Anaemia:
- Lethargy, pallor, dyspnoea

Neurological:
- Peripheral neuropathy (pins and needle), numbness (symmetrical) and affects the legs more than the arms.
- Subacute combined degeneration of the spinal cord (progressive weakness, ataxia, parasthesias, spasticity, paraplegia).

Psychiatric:
- memory loss, poor concentration, confusion, depression, irritability

Other:
- Mild jaundice, glossitis, angular cheilitis

** Increased risk of gastric cancer - vitamin B therapy resolves the anaemia but the atrophic gastritis remains **

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20
Q

what are the signs and symptoms of vitamin C deficiency (scurvy) Vitamin C = Ascorbic acid

A
  • ecchymosis (easy bruising)
  • Poor wound healing
  • Follicular hyperkeratosis and perifollicular hyperkeratosis (cork screw hairs)
  • Gingivitis + bleeding and receding gums
  • Sjogren’s syndrome
  • Arthralgia
  • Oedema
  • Weakness, malaise, anorexia, depression
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21
Q

What are the classic features of pancreatic cancer

A
  • Painless jaundice
  • Pale stools, dark urine, pruritus
  • Abdominal masses (hepatomegaly, gallbladder, epigastric mass)
  • Cholestatic liver function tests
  • Anorexia, weight loss, epigastric pain
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22
Q

What is Boerhaave syndrome

A

Rupture of the oesophagus

Causes crepitus on examination

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23
Q

What is the pattern of inheritance of Gilberts syndrome

A

Autosomal Recessive

Isolated increase of UNCONJUGATED bilirubin

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24
Q

What is the treatment for alcoholic hepatitis

A

Glucocorticoids (for example, prednisolone)

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25
Q

What histology is seen in Crohns

A

Inflammation in all layers from mucosa to serosa

Increased goblet cells

Granulomas

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26
Q

What histology is seen in Ulcerative Colitis

A

No inflammation beyond the submucosa

Crypt abscesses

Depletion of goblet cells and mucin

Granulomas are infrequent

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27
Q

How is primary biliary cholangitis diagnosed

A

The M rule:
Anti-mitochondrial antibodies
Raised IgM
Middle aged females
Abnormal liver function tests (raised ALP and yGT)1

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28
Q

What is the difference between primary biliary cholangitis and primary sclerosis cholangitis

A

Both are cholestatic liver diseases that can cause liver cirrhosis and liver failure.

Both cause poor flow of bile through the liver and bile ducts.

Primary sclerosis cholangitis:
- A chronic, progressive condition characterised by inflammation, scarring and structuring of the intrahepatic and extra hepatic bile ducts’.
- Some segments are unaffected so it gives a bead appearance.
- 2x as common in males, a strong link with ulcerative colitis
- Survival is 15 years
- Cholangiocarcinoma

Primary Biliary Cholangitis:
- A chronic, progressive, autoimmune condition leading to destruction of the small intrahepatic bile ducts
- More common than PSC
- more common in females, middle aged
- Associated with other autoimmune diseases

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29
Q

What is the treatment for primary biliary cholangitis

A

First line:
Ursodeoxycholic acid

Itch - cholecystramine

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30
Q

What is non-alcoholic fatty liver disease

A

Excessive fat in the liver cells, specifically triglycerides. The fat deposits interfere with functioning of the liver cells.

It can progress to cause hepatitis or lover cirrhosis.

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31
Q

What are the risk factors for non-alcoholic fatty liver disease

A

Same risk factors as CVD and diabetes

25% of the population is thought to have NAFLD
- Middle aged
- Obesity
- Type 2 diabetes
- High cholesterol
- Hypertension
- Smoking

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32
Q

What are the investigations for non-alcoholic fatty liver disease

A
  • Raised ALT (often 1st indication of NAFLD)
  • Liver ultrasound (for hepatic steatosis - fatty liver)
  • Enhanced liver fibrosis blood test (for fibrosis)
    • Transient elastography (used for fibrosis)
  • Liver biopsy is gold standard

Transient elastography is most commonly done

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33
Q

Which blood test is characteristic of alcoholic hepatitis

A

The AST/ALT ratio being >2:1

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34
Q

What is the management for C difficile infection

A

stop all opioids - Reduce gut motility and clearance of C. difficult which increases risk of toxic megacolon.

First line: Oral vancomycin for 10 days

Second line: Oral fidaxomicin

Third line-: Oral vancomycin +/- IV metronidazole

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35
Q

How is Ulcerative colitis classified

A

Mild:
<4 stools/day, only a small amount of blood

Moderate:
4-6 stools/day, varying amount of blood, no systemic upset

Severe:
>6 bloody stools/day, features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

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36
Q

How is mild - moderate ulcerative colitis managed to induce remission

A

Proctitis:
- Topical (rectal) aminosalicylate (mesalazine)
- If remission isn’t achieved within 4 weeks - add oral aminosalicylate
- If remission isn’t achieved - add topical or oral corticosteroid (prednisolone)

Proctosigmoiditis + left-sided UC:
- Topical (rectal) aminosaclytate
- If remission isn’t achieved within 4 weeks - add a high dose oral aminosalicylate OR high dose oral aminosalycilate and topical corticosteroid
- If remission still isn’t achieved - stop topical treatment and offer oral aminosalycilate and oral corticosteroid

Extensive disease:
- Topical (rectal) aminosalicylate and a high dose oral aminosalycilate
- If remission isn’t achieved within 4 weeks - stop topical treatment and add a high dose oral aminosalicylate and an oral corticosteroid

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37
Q

How is severe ulcerative colitis managed to induce remission

A

Should be treated in hospital

First line:
- IV steroids

Other:
- IV cyclosporin if steroids contraindicated

If no improvement after 72 hours:
- add IV cyclosporin to the IV steroids OR consider surgery

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38
Q

How is remission maintained in ulcerative colitis after a mild-moderate flare

A

Proctitis and proctosigmviditis:
- Topical aminosalycylate alone
OR
- An oral aminosalicylate + topical aminosalicylate

Left-sided and extensive ulcerative colitis:
- Low maintenance dose of an oral aminosalicylate

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39
Q

How is remission of a severe episode of ulcerative colitis maintained

A

Severe relapse or >2 exacerbations in the past year:
- Oral azathioprine or oral mercaptopurine

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40
Q

Which scoring systems are used to classify the severity of liver cirrhosis

A

Child-Pugh OR Model for End stage liver disease (MELD)

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41
Q

What are the associations of H. Pylori Infection

A

Peptic ulcer disease - 95% duodenal, 75% gastric (most common)

gastric Cancer

B cell lymphoma

Atrophic gastritis

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42
Q

How is H. Pylori infection treated

A

A 7 day course of:
- PPI + Amoxicillin + (clarithromycin OR metronidazole)

  • If penicillin allergy - PPI + metronidazole + clarithromycin
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43
Q

What is achalasia

A

Failure of oesophageal peristalsis and relaxation of the lower oesophageal sphincter due to the degenerative loss of ganglia from Auerbachs plexus

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44
Q

What is the treatment for achalasia

A

First-line:
- Pneumatic balloon dilatation

If recurrent or persistent symptoms:
- Heller cardopmyotomy

Other:
- Intra-sphincter injection of botulinum toxin
- Drug therapy (nitrates, calcium channel blockers)

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45
Q

What is Wilson’s disease

A

An autosomal recessive condition characterised by the toxic accumulation of copper in the liver and brain.

Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.

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46
Q

What are the features of Wilsons disease

A
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47
Q

What are the features of Wilsons disease

A

Symptom onset is usually between 10-25 years.

Children - present with liver disease
Young adults - Present with neurological disease

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48
Q

What are the signs of Wilsons disease

A

Liver - hepatitis, cirrhosis
Neurological - speech, behaviour and psychiatric problems, asterisks, chorea, dementia, Parkinsonism
Kayser-Fleischer rings
Blue nails
Haemolysis
Renal tubular acidosis

49
Q

Where is most copper deposited in Wilsons disease

A

In the brain most coper is deposited in the basal ganglia, particularly in the putamen and globes pallid us

50
Q

What are the investigations for wilsons disease

A

Liver biopsy - definitive diagnosis
24 hour copper urine assay
Slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
Reduced total serum copper
Diagnosis confirmed by genetic analysis of ATP7B gene

51
Q

What is the treatment for Wilsons disease

A

First line - Penicillamine

Alternative - Tridentine hydrochloride

52
Q

What type of bacteria is clostridioides difficile

A

A gram positive rod

53
Q

Which antibiotic is most likely to cause C difficile infection

A

Clindamycin
Cephalosporins - Ceftriazone, ceftazidime

54
Q

What is the management of a first episode of C difficile infection

A

First-line - oral vancomycin for 10 days
Second-line - Oral fidaxomicin
Third line - Oral vancomycin +/- IV metronidazole

55
Q

What is the management of a recurrent episode of C difficile

A

Within 12 weeks of symptoms resolution - Oral fidaxomicin
After 12 weeks of symptom resolution - Oral vancomycin OR fidaxomicin

56
Q

What s the treatment for life threatening C difficile infection

A

Oral vancomycin AND IV metronidazole

57
Q

What acid base disturbance is seen with prolonged vomiting

A

Metabolic alkalosis + Hypokalaemia

58
Q

What is the treatment for IBS

A

Pain - Antispasmodic agents

Constipation - Laxiatives (ispaghulta husk). AVOID lactulose.

Diarrhoea - Loperamide is first line

59
Q

Which antibiotic is most likely to cause spontaneous bacterial peritonitis

A

E. coli

60
Q

What is the treatment for spontaneous bacterial peritonitis

A

IV cefotaxime

If patients have ascites - can give antibiotic proplhyaxis (ciprofloxacin or norfloxacin

61
Q

What are the anatomical borders of ulcerative colitis

A

Inflammation starts at the rectum and does not spread beyond the ileocaecal valve

62
Q

What investigation is done to diagnose a Mallory-Weiss syndrome

A

Endoscopy - Treated with ablation

63
Q

What is small bowel bacterial overgrowth syndrome

A

A disorder caused by an excessive amount of bacteria in the small bowel resulting in gastrointestinal symptoms.

64
Q

What are the conditions that give an increased risk of small bowel bacterial overgrowth syndrome

A

Scleroderma
Diabetes mellitus
Neonates with GI abnormalities

65
Q

How is small bowel bacterial overgrowth syndrome diagnosed

A

Hydrogen breath test

Often gets better after a trial of antibiotics

66
Q

What is the treatment of small bowel bacterial overgrowth syndrome

A

Rifampicin

OR

Co-amoxiclav or metronidazole

67
Q

Malnutrition Diagnosis

A
  1. BMI <18.5
  2. BMI <20 and unintentional weight loss >5% within the last 3-6 months
  3. Unintentional weight loss >10% within the last 3-6 months
68
Q

What is the triad used to diagnose Plummer-Vinson syndrome

A
  1. Dysphagia (secondary to oesophageal webs)
  2. Glossitis
  3. Iron-deficiency anaemia
69
Q

Which levels are used to monitor haemochromatosis

A

Ferritin
Transferrin saturation

70
Q

What is the screening for haemochromatosis

A

General population - Transferrin saturation > ferritin

Family members - HFE genetic testing

71
Q

What is the screening for Wilsons disease

A

Caeruloplasmin

72
Q

What are some of the common side effects of proton pump inhibitors

A

Hyponatraemia
Hypomagnasaemia (muscle weakness)
Osteoporosis
Microscopic colitis
Increased risk of C difficile infection

73
Q

What is transferrin

A

The bodys carrier of iron around the blood

ID - In states of iron deficiency, transferrin increases to try and make the most of what iron it has left

ACD - Decreases

74
Q

What is total iron binding capacity

A

Measures the number of binding sites on transferrin available for iron.

ID - increases

ACD - decreases

75
Q

What are the signs of spontaneous bacterial peritonitis

A

Ascites
Abdominal pain
Fever

76
Q

How is spontaneous bacterial peritonitis diagnosed

A

Paracentesis - neutrophil count >250 cells

77
Q

What are the signs of ischaemic colitis

A
  • most common in the splenic flexure area
  • thumb printing seen on abdominal x-ray
  • bloody diarrhoea
  • conservative management
  • large bowel
  • transient, less severe symptoms
78
Q

What is Budd-Chiari syndrome

A

AKA hepatic vein thrombosis.

Usually seen in the context of other haematological disease or another procoagulant condition.

79
Q

What are the causes of Budd-Chiari syndrome

A

Polycythaemia rubra vera
thrombophilia
pregnancy

80
Q

What are the signs of Budd-Chiari syndrome

A

Abdominal pain - sudden onset, severe pain
Ascites
Tender hepatomegaly

Investigated using ultrasound with doppler flow studies

81
Q

What is the m most common cause of inherited colon cancer

A

HNPCC (Lynch syndrome)

82
Q

What is Lynch syndrome

A

An autosomal dominant condition.

90% of patients with the condition develop cancer:
- Often in the proximal colon
- Endometrial cancer is the second most common

83
Q

What is Familial adenomatous polyposis

A

An autosomal dominant condition which leads to the formation of hundreds of polyps by the age of 30-40.

84
Q

What is Familial adenomatous polyposis

A

An autosomal dominant condition which leads to the formation of hundreds of polyps by the age of 30-40.

It causes a mutation in a tumour suppressor gene.

85
Q

How is vitamin B12 replaced

A

Intramuscularly

No neurological features:
- 3 injections per week for 2 weeks (1mg)
- followed by 3 monthly treatment injections (1mg)

86
Q

What is primary sclerosis cholangitis

A

A chronic condition of unknown cause affecting the gallbladder and liver.

Inflammation and scarring of the bile duct occur and result in obstruction of the duct system and eventually cirrhosis and failure.

87
Q

what is done to diagnose primary sclerosis cholangitis

A

Either MRCP OR ERCP can be used first line.

Will show alternating biliary strictures and dilatation inside and/or outside the liver - hallmark beaded appearance.

p-ANCA might be positive.

88
Q

What is primary sclerosis cholangitis associated with

A

Ulcerative colitis

4% of patients with UC have PSC
80% of patients with PSC have UC

Can cause cholangiocarcinoma or colorectal cancer

89
Q

what are the features of primary sclerosis cholangitis

A

Cholestasis:
- pruritus
- jaundice
- raised bilirubin + ALP
- RUQ pain
- Fatigue

90
Q

What is the mechanism of action for loperamide

A

Reduces gastric motility through stimulation of opioid receptors

91
Q

What is metaplasia

A

The replacement of one mature cell type with another mature cell type - as an adaptive response

92
Q

What is dysplasia

A

Replacement of one mature cell type with a less mature cell type

the development of abnormal types of cells within a tissue

can be pre cancerous

93
Q

what is neoplasia

A

The uncontrolled, abnormal growth of cells or tissues in the body. Causing a tumour = neoplasm.

The neoplasm can be benign or malignant.

94
Q

what is the treatment for Barretts oesophagus

A

High dose PPI

Metaplasia (but no dysplasia):
- Endoscopic surveillance every 3-5 years

dysplasia:
- endoscopic mucosal resection and removal of cancerous cells
- radiofrequency ablation

95
Q

What is usually deficient in coeliac disease

A

Mixed picture anaemia

Iron
Folate
B12

96
Q

What is the treatment for gallstones

A

Asymptomatic gallstones located in the gallbladder are common and do not require treatment.

If stones are present in the common bile duct - theres an increased risk of cholangitis or pancreatitis and surgical management should be considered.

Symptomatic gallstones = laparoscopic cholecystectomy

97
Q

What is the treatment for hepatic encephalopathy

A

First line - Lactulose

Secondary prophylaxis - rifaximin

98
Q

What are the signs of acute liver failure

A

jaundice
raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure
fetor hepaticus (hepatic encephalopathy)

Check coagulation and albumin - liver enzymes usually remain normal for a long time

99
Q

What is the treatment used to induce remission in crohns

A

First line: Glucocorticoids

Second line: Mesalazine

Add on: Aathioprine or mercaptopurine (or methotrexate)

Refractory disease: Infliximab

Isolated peri-anal disease: Metronidazole

100
Q

What is the treatment used to maintain remission in crohns disease

A

Azathioprine or mercaptopurine

Stopping smoking

Second line: Methotrexate

101
Q

which gene mutations are associated with HNPCC

A

MSH2/MLH1

102
Q

Which test is most specific at diagnosing an acute liver failure

A

A raised prothrombin time

103
Q

How long before an upper GI endoscopy should PPI be stopped

A

2 weeks before

104
Q

When should someone with G ORD be investigated with an upper GI endoscopy

A
  • Age >55
  • symptoms > 4 weeks or persistent despite treatment
  • Dysphagia
  • Relapsing symptoms
  • Weight loss

If endoscopy is negative - use 24hr oesophageal pH monitoring (gold standard test for diagnosis)

105
Q

What must patients have before being considered for fundoplication surgery

A

Oesophageal pH
Manometry studies

106
Q

Which metabolic disturbances can occur due to refeeding symdrome

A
  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia (torsades des pointes)
  • Abnormal fluid balance
107
Q

Who is at risk of refeeding syndrome

A

One of the following:
- BMI <16
- Unintentional weight loss >15% over 3-6 months
- Little nutritional intake >10 days
- Hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding

Two or more of the following:
- BMI <18.5
- Unintentional weight loss >10% over 3-6 months
- Little nutritional intake >5 days
- History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics, antacids

108
Q

What is the recommendation for re-feeding

A

If a patient hasn’t eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days

109
Q

What are the causes of raised bilirubin

A

Unconjugated bilirubin - Prehepatic or hepatic jaundice.

Conjugated bilirubin - Hepatocellular injury or cholestasis

110
Q

Which site is most affected by crohns disease

A

The ileum (causes weight loss because theres malabsorption)

111
Q

What are the risk factors for developing gallstones

A

Increasing age
family history
sudden weight loss
loss of bile salts (crohns)
diabetes
oral contraception

112
Q

What are the features of appendicitis

A
  • Right sided tenderness on PR exam
  • Peri-umbilical abdominal pain radiating to the right iliac fossa
  • mild pyrexia
  • anorexia
  • pain worse going over speed bumps or coughing
  • children can’t hop of the right leg due to pain
113
Q

what test is gold standard for the diagnosis of coeliac disease

A

Jejunal biopsy

114
Q

what is used to treat symptoms of carcinoid syndrome

A

Octreotide

115
Q

which part of the bowel is most affected in ulcerative colitis

A

Rectum

116
Q

what are the most common signs of ulcerative colitis

A

Bloody diarrhoea
urgency
tenesmus
abdominal pain - particularly left lower quadrant

Extra clinic features:
primary sclerosing cholangitis
uveitis
colorectal cancer

117
Q

which drugs cause a hepatocellular picture of liver disease

A

paracetamol
sodium valproate
phenytoin
MAOI
anti-tuberculosis
statins
alcohol
amiodarone
methyldopa
nitrofurantoin

118
Q

Which drugs can cholestasis

A

COCP
antibiotics - flucloxacillin, co-amoxiclav, erythromycin

Exam - M - GI Diseases (35 decks)

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