Gastroenterology Flashcards

1
Q

What test is used to monitor treatment in haemochromatosis?

A

Transferrin saturation and ferritin

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2
Q

What is achalasia?

A

Failure of oesophageal peristalsis and relaxation of the LOS due to degenerative loss of ganglia from Auerbach’s plexus.

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3
Q

What are the clinical features of achalasia?

A
  • Dysphagia to solids and liquids.
  • Heartburn
  • Regurgitation of food
  • Variation in severity of sx
  • Malignant change in small number of patients.
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4
Q

What can often be seen on CXR when someone has achalasia?

A

Retrocardic air-fluid level.

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5
Q

How would you investigate achalasia?

A
  • Oesophageal manometry (diagnostic).
  • Barium Swallow (bird beak appearance)
  • CXR (retrocardic air-fluid level)
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6
Q

What is the first line treatment for Achalasia?

A

Pneumatic dilation (balloon).

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7
Q

What are second line options for the treatment Achalasia?

A
  • Surgical intervention (Heller cardiomyotomy)
  • Botulinum toxin injection into sphincter
  • Drug therapy with CCBs and nitrates.
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8
Q

Which marker is used to monitor the recurrence of colorectal cancer?

A

CEA (carcinoembryonic antigen).

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9
Q

What are some causes of liver decompensation?

A
  • Constipation
  • Infection
  • Electrolyte imbalances
  • Alcohol intake
  • Dehydration
  • UGIB
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10
Q

What are the causes of liver cirrhosis?

A
  • Alcohol
  • Hepatitis B and C
  • NALFD
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11
Q

What is transient elastography?

A

-Known as Fibroscan
- 50 Mhz wave passed into liver from end of US probe
- Measures stiffness of liver

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12
Q

What are risk factors for gastric cancer?

A
  • Smoking
  • Nitrates in diet
  • Pernicious anaemia
  • H.pylori infection
  • Blood group A
  • Atrophic gastritis
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13
Q

What are typical features of gastric cancer?

A
  • Abdominal pain (typically vague epigastric)
  • Weight loss
  • Nausea and vomiting
  • Dysphagia
  • UGIB
  • Lymphadenopathy (Virchow’s and Sister Mary Joseph’s node)
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14
Q

How is gastric cancer diagnosed?

A

Oesopho-gastro-duodenoscopy with biopsy (signet ring cells, more cells = worse prognosis).

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15
Q

Where is secretin secreted from?

A

S cells within the upper small intestine.

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16
Q

What is the action of secretin?

A
  • Increases secretion of bicarbonate rich fluid from pancreas and hepatic duct cells.
  • Decreases gastric acid secretion
  • Trophic affect on pancreatic acinar cells
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17
Q

Where is Gastrin secreted from?

A
  • G cells in antrum of stomach.
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18
Q

What is the action of Gastrin?

A
  • Increases acid secretion by gastric parietal cells
  • Pepsinogen and If secretion
  • Increases gastric motility
  • Stimulates parietal cell maturation
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19
Q

Where is CCK secreted?

A

I cells in upper small intestine

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20
Q

What is the action of CCK?

A
  • Increases secretion of enzyme rich fluid in pancreas,
  • Increases contraction of gallbladder and relaxation of sphincter of Oddi.
  • Decreases gastric emptying
  • Trophic affect on pancreatic acinar cells
  • Induces satiety
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21
Q

Where is Vasoactive Intestinal peptide (VIP) secreted from?

A

Small intestine and Pancreas

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22
Q

What is the action of Vasoactive Intestinal Peptide (VIP)?

A
  • Stimulates secretion from small intestine and pancreas
  • Inhibits gastric acid secretion.
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23
Q

Where is somatostatin secreted from?

A

D cells in the pancreas and stomach

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24
Q

What is the action of somatostatin?

A
  • Decreases acid and pepsin secretion
  • Decreases Gastrin secretion
  • Decreases pancreatic enzyme secretion
  • Decreases insulin and glucagon secretion
  • Inhibits trophic effects of gastrin
  • Stimulates gastric mucous production
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25
Q

What is the investigation of choice in Primary sclerosing cholangitis?

A

MRCP/ERCP

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26
Q

What is primary sclerosing cholangitis?

A

Inflammation and fibrosis of intra and extra hepatic bile ducts.

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27
Q

What conditions is PSC associated wtih?

A
  • Ulcerative colitis
  • HIV
  • Crohn’s (much less common than UC)
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28
Q

What are the features of PSC?

A
  • Jaundice
  • Pruritus
  • Raised bilirubin + ALP
  • RUQ pain
  • Fatigue
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29
Q

What are the complications of PSC?

A
  • Cholangiocarcinoma in 10% of patients
  • Increased risk of colorectal cancer
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30
Q

What is the mode of inheritance of Peutz-Jeghers syndrome?

A

Autosomal dominant

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31
Q

What is Peutz-Jeghers syndrome?

A

Autosomal dominant condition characterised by numerous hamartomatous polyps forming in GI tract. Pigmented freckles on face, lips, palms and soles.

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32
Q

What is Whipple’s disease?

A

Rare, multi-system disorder caused by Tropheryma whippelii infection. More common in Men and HLA B27 positive individuals.

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33
Q

What are the features of Whipple’s disease?

A
  • Malabsorption: diarrhoea, weight loss.
  • Large joint arthralgia
  • Skin hyperpigmentation and photosensitivity.
  • Pleurisy
  • Pericarditis
  • Neurological (rare): dementia, myoclonus, ataxia, seizures, ophthalmoplegia.
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34
Q

How would Whipple’s disease be identified on jejunal biopsy?

A

Deposition of macrophages containing Periodic acid-Schiff (PAS) granules.

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35
Q

What is the management of Whipple’s disease?

A

Oral co-trimoxazole for 1 year.
Occasionally preceded by course of IV penicillin.

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36
Q

Which mode of investigation is best suited for staging oesophageal/gastric cancer?

A

Endoscopic ultrasound

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37
Q

What are the main risk factors to developing hepatocellular carcinoma?

A
  • Chronic hepatitis B or C
  • Alcohol
  • Haemochromatosis
  • 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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38
Q

What are the features of hepatocellular carcinoma?

A
  • Tends to present late
  • Liver cirrhosis or failure (pruritus, jaundice, ascites, RUQ, hepatosplenomegaly)
  • raised AFP
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39
Q

Who are at high risk of developing hepatocellular carcinoma and should be considered for screening?

A
  • patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
  • men with cirrhosis secondary to alcohol
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40
Q

What are the management options for hepatocellular carcinoma?

A
  • Surgical resection in early disease
  • Liver transplant
  • Radiofrequency ablation
  • Transarterial chemoablation
  • sorafenib: a multikinase inhibitor
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41
Q

Which condition affecting the liver does is the exception that does not cause hepatocellular carcinoma?

A

Wilson’s Disease

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42
Q

What is Primary biliary cholangitis?

A

Chronic liver disorder typically seen in middle aged females.
- Autoimmune condition
- Interlobular bile ducts are damaged by inflammation causing chronic cholestasis (slow bile) and leads to cirrhosis.

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43
Q

What conditions are associated with Primary biliary cholangitis?

A
  • Sjogren’s syndrome (80% patients)
  • Rheumatiod arthritis
  • Thyroid disease
  • Systemic sclerosis
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44
Q

What are the clinical features of Primary Biliary Cholangitis?

A
  • fatigue
  • pruritus
  • cholestatic jaundice
  • raised ALP
  • RUQ pain
  • hyperpigmentation (pressure points)
  • xanthelasmas, xanthomata
  • clubbing
  • hepatosplenomegaly
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45
Q

How is primary biliary cholangitis diagnosed?

A
  • anti-mitochondrial antibodies M2 subtype (present in 98%)
  • smooth muscle antibodies
  • raised serum IgM
  • RUQ US or MRCP to rule out obstruction
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46
Q

What is the management of Primary biliary cholangitis?

A
  • first-line: ursodeoxycholic acid (slows progression)
  • pruritus: cholestyramine
  • fat-soluble vitamin supplementation
  • liver transplantation
47
Q

What is Coeliac disease?

A

Autoimmune disease caused by a sensitivity to gluten. Leads to villous atrophy causing malabsorption.

48
Q

What conditions are associated with coeliac disease?

A
  • Autoimmune thyroid disease
  • Dermatitis herpetiformis
  • Irritable bowel syndrome
  • Type 1 diabetes
  • First-degree relatives (parents, siblings or children) with coeliac disease
49
Q

What are the signs and symptoms of coeliac disease?

A
  • Chronic or intermittent diarrhoea
  • Failure to thrive or faltering growth
  • Persistent or unexplained GI symptoms including N&V.
  • Prolonged fatigue
  • Recurrent abdominal pain, cramping or distension
  • Sudden or unexpected weight loss
  • Unexplained iron-deficiency anaemia, or other unspecified anaemia
50
Q

What complications are associated with 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
51
Q

What are the features of Crohn’s disease?

A
  • Diarrhoea (usually non bloody)
  • Weight loss
  • Prominent upper GI sx
  • Mouth ulcers
  • Perianal disease
  • Palpable mass in R iliac fossa.
52
Q

What are the extra intestinal features of Crohn’s?

A

Gallstones (due to reduced bile absorption)
Oxalate renal stones

53
Q

What are the complications of Crohn’s?

A

-Intestinal obstruction
- Fistula
- Colorectal cancer

54
Q

What are the pathological findings of Crohn’s?

A

Mouth to anus
Skip lesions

55
Q

What are the histological findings of Crohn’s?

A
  • Inflammation in all layers (mucosa to serosa)
  • Increased goblet cells
  • Granulomas
56
Q

What are the endoscopic findings of Crohn’s?

A

Skip lesions - Cobblestone appearance
Deep ulcers

57
Q

What are the radiological findings of Crohn’s?

A

Kantor’s string sign - strictures
Proximal bowel dilation
Rose thorn ulcers
Fistulae

58
Q

What are the features of UC?

A

Bloody diarrhoea
LLQ abdominal pain
Tenesmus (inclination to evacuate bowels)

59
Q

What are the extra intestinal features of UC?

A

Primary sclerosing cholangitis

60
Q

What complications are associated with UC?

A

Colorectal cancer (higher risk than Crohn’s)

61
Q

What are the pathological findings of UC?

A

Inflammation begins in rectum and never goes beyond ileocaecal valve.
Continuous disease

62
Q

What are the histological findings of UC?

A

No inflammation beyond submucosa
Inflammatory cell infiltrate in lamina propria:
- crypt abscesses
- depleted goblet cells
- depleted mucin

63
Q

What are the endoscopic findings in UC?

A

Widespread ulceration (pseudopolyps)

64
Q

What are the radiological findings of UC?

A

Loss of haustrations
Superficial ulceration (pseudopolyps)
Drainpipe colon in longstanding disease

65
Q

What are some secondary causes of bile-acid malabsorption?

A

Crohn’s
Cholecystectomy
Coeliac disease
Small intestinal bacterial overgrowth

66
Q

What is the investigation of choice for bile-acid malabsorption?

A

SeHCAT
Scans are done 7 days apart to assess retnetion/loss of radiolabelled SeHCAT

67
Q

How is bile-acid malabsorption managed/

A

Bile acid sequestrants e.g. Cholestyramine

68
Q

What are the main side effects of sulfasalazine?

A

Rashes
Oligospermia
Headache
Heinz body anaemia
Megaloblastic anaemia
Lung fibrosis
GI upset
Agranulocytosis

69
Q

What are the common side effects of mesalazine?

A

GI upset
Headache
Agranulocytosis
Pancreatitis
Interstitial nephritis

70
Q

What are some recognised associations with Autoimmune hepatitis?

A

-Other autoimmune disorders e.g. coeliac, T1DM, pernicious anaemia
- Hypergammaglobulinaemia
- HLA B8 and DR3 antibodies.

71
Q

What are the features of autoimmune hepatitis?

A
  • Signs of chronic liver disease
  • Acute hepatitis : fever, jaundice etc.
  • Amenorrhoea
  • ANA/SMA/LKM1 antibodies
  • Raised IgG levels
  • ‘Piecemeal necrosis’ on liver biopsy (inflammation extending beyond limiting plate)
72
Q

What antibodies are involved in Type 1 autoimmune hepatitis

A

Anti-nuclear antibodies (ANA) +/- anti-smooth muscle antibodies (SMA)

Affects both children and adults

73
Q

What antibodies are involved in type 2 autoimmune hepatitis?

A

Anti-liver/kidney microsomal type 1 antibodies (LKM1)

Affects children only.

74
Q

What antibodies are involved in type 3 autoimmune hepatitis?

A

Soluble liver/kidney antigen

Affects middle aged adults.

75
Q

What is the management of autoimmune hepatitis?

A

-Steroids
- Immunosuppressants e.g. azathioprine
- Liver transplant

76
Q

Where are the majority of gastrinomas located?

A

First part of the duodenum

77
Q

What is Zollinger-Ellison syndrome?

A

Condition characterised by excessive levels of gastrin secondary to a gastrin secreting tumour.
Commonly found in first part of duodenum or pancreas.
30% occur as part of MEN type 1 syndrome.

78
Q

What are the features of Zollinger-Ellison syndrome?

A
  • Multiple gastroduodenal ulcers
  • Diarrhoea
  • Malabsorption
79
Q

How is Zollinger-Ellison syndrome diagnosed?

A
  • Fasting gastrin levels
  • Secretin stimulation test
80
Q

What is eosinophilic oesophagitis?

A

Allergic inflammation of the oesophagus. Dense infiltrate of eosinophils within epithelium.
3:1 male to female ratio.
30-50yrs

81
Q

What are risk factors for developing eosinophilic oesophagitis?

A
  • Allergies/asthma
  • Male sex
  • Family history
  • Caucasian
  • Aged 30-50years
  • Coexisting autoimmune disease
82
Q

What are the typical features of eosinophilic oesophagitis?

A
  • Dysphagia
  • Strictures/fibrosis
  • Food impaction
  • Regurgitation
  • Vomiting
  • Anorexia
  • Weight loss
83
Q

What investigations should be performed for eosinophilic oesophagitis?

A

-Endoscopy : diagnosis requires histological analysis, >15 eosinophils per microscopy field.
- Trial of PPI: no improvement in sx.

84
Q

What is the management of eosinophilic oesphagitis?

A
  • Dietary modification: targeted elimination diet, elemental diet or exclusion of 6 food groups.
  • Topical steroid e.g. fluticasone, budesonide 8/52 course
  • Oesophageal dilatation
85
Q

What complications are associated with eosinophilic oesophagitis?

A
  • Strictures
  • Impaction
  • Mallory-Weiss tears
86
Q

What are common adverse effects of PPis?

A
  • Hyponatraemia
  • Hypomagnasaemia
  • Osteoporosis
  • Microscopic colitis
  • Increased risk of C.difficile
87
Q

What is helicobacter pylori?

A

Gram negative bacteria associated with variety of GI problems, principally peptic ulcer disease?

88
Q

What is the pathophysiology of H.pylori?

A
  • Chemotaxis away from low pH areas, using flagella to burrow into mucous lining to reach epithelial cells
  • Secretes urease resulting in alkalinisation of acid environment
  • Releases bacterial cytotoxins that disrupt gastric mucosa.
89
Q

What conditions are associated with H.pylori infection?

A
  • Peptic ulcer disease
  • Gastric cancer
  • B cell lymphoma of MALT tissue
  • Atrophic gastritis
90
Q

What is the management of H.pylori infection?

A

7 day course of PPI + Amoxicillin + (clarithromycin or metronidazole)

If pen allergic PPI + Metronidazole + Clarithromycin

91
Q

What are the features of carcinoid tumours?

A
  • Flushing
  • Diarrhoea
  • Bronchospasm
  • Hypotension
  • R heart valvular stenosis
  • Increased serotonin secreted by mets.
  • Pellagra
92
Q

What investigations diagnose Carcinoid tumours?

A

Urinary 5-HIAA
Plasma chromogranin A y

93
Q

What is the management of carcinoid tumours?

A

Somatostatin analogues e.g. octreotide
Cyproheptadine may help diarrhoea.

94
Q

What are the NICE guidelines for referral for bariatric surgery?

A

Early referral for very obese patients (BMI >40kg/m2)especially with conditions associated with obesity e.g. T2DM, hypertension.

95
Q

What are the different types of bariatric surgery?

A
  • Primary restrictive operations: Laparoscopic-adjustable gastric banding (LAGB), Sleeve gastrectomy, Intragastric balloon.
  • Primarily malabsorptive operations: Biliopancreatic diversion with duodenal switch (BMI >60).
  • Mixed operations: Roux-en-Y gastric bypass.
96
Q

What is ischaemic colitis?

A

Acute but transient compromise to blood flow to large bowel. May lead to inflammation, ulceration and haemorrhage.

97
Q

Where is ischaemic colitis most likely to occur?

A

Splenic flexure

98
Q

What condition does thumbprinting on AXR suggest?

A

Ischaemic colitis

99
Q

What is the mainstay treatment for hydatid cysts?

A

Surgery

100
Q

What are the clinical features of hydatid cyst infection?

A
  • Cysts usually occur in liver and lungs
  • Usually asymptomatic until cysts >5cm in diameter.
  • Biliary colic, jaundice and urticaria in biliary rupture
  • Infection
  • Organ dysfunction
101
Q

What investigations should be performed in hydatid cysts?

A

AUSS 1st line
CT to differentiate hydatid cysts from other types.
Serology
Antibody/antigen testing

102
Q

What findings within LFTs suggest ALD?

A

Gamma-GT elevated
AST:ALT >2.
AST:ALT >3 strongly suggests acute alcoholic hepatitis

103
Q

What medication is used to treat alcoholic hepatitis?

A

Glucocorticoids e.g. prednisolone
Pentoxyphylline occasionally used

104
Q

What are causes of ascites that have a serum ascites albumin gradient >11?

A
  • Liver disorders (most common)
    -Cardiac: R heart failure, constrictive pericarditis
  • Budd-Chiari syndrome
  • Portal vein thrombosis
  • Veno-occlusive disease
  • Myxoedema
105
Q

What are causes of ascites that have a serum ascites albumin gradient <11

A

-Hypoalbuminaemia: nephrotic syndrome, severe malnutrition
- Malignancy: peritoneal carcinomatosis
- Infection: tuberculosis, peritonitis
- Pancreatitis
- Bowel obstruction
- Biliary ascites
- Post-op lymphatic leak
- Serositis in CTD

106
Q

What are the management options for ascites?

A
  • Reduce dietary sodium
  • Fluid restriction if Na <125mmol
  • Aldosterone antagonists e.g. spironolactone
  • Drainage if tense (large vol requires albumin cover)
  • Prophylactic antibiotics to reduce risk of SBP, ciprofloxacin or norfloxacin
  • TIPS in some patients
107
Q

What is angiodysplasia?

A

Vascular deformity of GI tract which predisposes individuals to bleeding and iron deficiency anaemia.

108
Q

What condition is associated with angiodysplasia?

A

Aortic stenosis

109
Q

What is the management of angiodysplasia?

A

Endoscopic cauterisation or argon plasma coagulation.
Antifibrinolytics e.g. tranexamic acid
Oestrogens may also be used

110
Q

What is the first line treatment for a mild-moderate flare of UC?

A

Topical aminosalicylates

111
Q

How is UC classified?

A

Mild = <4 stools/day, minimal blood
Moderate= 4-6 stools/day, varying amounts of blood, no systemic upset.
Severe = >6 bloody stools/day + systemic upset

112
Q

What is the treatment for severe UC?

A
  • IV steroids (ciclosporin if steroid contraindicated)
  • Add ciclosporin to Iv steroids if no improvement after 72hrs.
  • Surgery
113
Q

What is the first line diagnostic test for small bowel overgrowth syndrome?

A

Hydrogen breath test (significant rise suggest disease).

114
Q

What vasoactive agents are used in the acute management of oesophageal varices?

A

Terlipressin (1st line and only licensed)
Octreotide may also be used.