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ΩΩ 4 Bateman - Specialities + Endo + GI + Liver > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is the blood supply to these regions?

Foregut

Midgut

Hindgut

A
  1. Foregut - Coeliac Trunk
  2. Midgut - Superior mesenteric artery
  3. Hindgut - Inferior mesenteric artery
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2
Q

WHAT IS HELIOCBACTER PYLORI?

A

Gram negative, curved motile rod, microaerophilic.

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3
Q

What is heliocbacter pylori’s key biochemical feature?

A

Urease positivity-used in testing.

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4
Q

How is heliocbacter pylori spread?

A

Oro-fecal or oral-oral.

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5
Q

What is the pathogenesis of heliocbacter pylori?

A

Adapted to living in gastric mucus Colonises over gastric but not intestinal epithelium.

Induces inflammation

Stimulates increased gastrin

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6
Q

What are some disease associations with heliocbacter pylori?

A

Ulcers.

In the absence of NSAIDS or Zollinger-Ellison syndrome.

Gastric cancer.

Gastric lymphoma.

Oesophageal disease.

Barrett’s oesophagus.

Others.

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7
Q

What are the usual symptoms of heliocbacter pylori?

A
  1. Acquisition usually asymptomatic but may cause nausea and epigastric pain.
  2. Chronic diffuse superficial gastritis
  3. Followed by a period of achlorrydria.
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8
Q

What investigations can you do for HP?

A
  1. Serology
  2. Stool antigen
  3. Urea breath test
  4. Endoscopy with urease test
  5. Histology ± culture
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9
Q

What is the treatment for H.pylori?

A
  1. Eradication may be achieved with a 7-day course of
    • a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
    • if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
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10
Q

WHAT IS PERITONITIS?

A

Inflammation of peritoneum.

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11
Q

What are the causes of peritonitis?

What is the most common bacteria?

A
  1. Perforation of GI tract i.e. trauma
  2. E. coli
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12
Q

What are the symptoms of peritonitis?

A
  1. Pain
  2. Rebound tenderness
  3. Guarding reflex
  4. Fever
  5. Increase in WBC
  6. Shoulder tip pain in sepsis
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13
Q

What are the investigations of peritonitis?

What are the investigations for SBP?

A

Erect CXR - air under diaphragm.

USS/CT

Neutrophil count >250 cells/microlitre

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14
Q

How can you treat peritonitis?

What is the prophylaxis for SBP?

A
  1. IV fluids
  2. Antibitoics
    • Metronidazole for anaerobes and cephalexin for aerobes
  3. Electrolytes
  4. Surgery laparotomy

Prophylaxis - ciprofloxacin

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15
Q

Who should prophylaxis be given to after peritonitis?

What is the prophylaxis?

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
  3. NICE recommend: ‘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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16
Q

WHAT IS THE DEFINITION OF INTESTINAL OBSTRUCTION?

A

Blockage to the lumen of gut Intestinal

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17
Q

What are some causes of bowel obstruction?

A
  1. Adhesions
  2. Hernias
  3. Tumour
  4. Crohn’s
  5. Volvulus
  6. Gallstone Ileus
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18
Q

How is bowel obstruction classified?

A

According to site - e.g. small vs large intestine

Extent of luminal obstruction

Mechanical / True ( intraluminal / extraluminal)

Paralytic (Pseudo obstruction)

Simple Closed loop Strangulation Intussusception

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19
Q

WHAT ARE THE CAUSES OF SMALL BOWEL OBSTRUCTION?

A
  1. Tumours
  2. Intussusception
  3. Gallstone ileus
  4. Impacted faeces
  5. Meconium
  6. Bezoars
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20
Q

What are the symptoms of small bowel obstruction?

A
  1. Abdominal pain, colicky, i.e. returns to normal periodically. Felt in mid-abdomen. Need to know site, radiation, duration and relieving factors.
  2. No flatus; constipation is present
  3. Distention, early in the course of the illness if the obstruction is high
  4. Vomiting, again earlier in the course if the obstruction is relatively proximal in the bowel
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21
Q

What are the investigations for small bowel obstruction?

A
  1. Blood urea and electrolytes
  2. White cell count
  3. Radiology:
    • Supine: obstructive picture of dilated small bowel
    • Sitting: multiple air/fluid levels in obstruction
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22
Q

What is the treatment for small bowel obstruction?

A

Drip and suck
A nasogastric tube is placed in small bowel obstruction or if the patient is vomiting

Nil by mouth and given intravenous fluids

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23
Q

WHAT ARE THE CAUSES OF LARGE BOWEL OBSTRUCTION?

A
  1. The principal cause of large bowel obstruction is carcinoma, which together with diverticulitis accounts for 90% of cases.
  2. Colonic volvulus is a rare cause of obstruction
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24
Q

What are the symptoms of large bowel obstruction?

A

Present quite late with:

  1. Faecel vomiting
  2. Weight loss
  3. Appetite loss.
  4. Colicky abdominal pain.

Signs include:

  1. Succussion splash
  2. Dehydration
  3. Mass due to the tumour, either in the epigastrium or in the lymph nodes
  4. Hepatomegaly
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25
Q

What is the treatment for large bowel obstruction?

A
  1. Drip and suck
    • A nasogastric tube is placed in small bowel obstruction or if the patient is vomiting
  2. Nil by mouth and given intravenous fluids
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26
Q

What are the indications for immediate surgery of a bowel obstruction?

A
  1. Crescendo pain
  2. Localised peritonism, implying perforation or ischaemia
  3. Complete colonic obstruction with competent ileocaecal valve and caecum dilated to greater than 8cm
  4. “Closed loop” seen radiologically
  5. Obstruction occurring as a result of hernial incarceration
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27
Q

WHAT IS A VOLVULUS?

A

A twist / rotation of segment of bowel

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28
Q

What are the types of volvulus?

A
  1. Sigmoid (most common)
  2. Cecal
  3. Midgut
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29
Q

What is the cause of a sigmoid volvulus?

A
  1. Pregnancy
  2. Middle aged and eldery constipation
  3. Adhesions
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30
Q

What can cause a cecal volvulus and what can cause a midgut volvulus?

A

Same as sigmoid, mesenteric join loose

Abnormal fetal development for midgut

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31
Q

What can happen to a volvulus?

A

Can twist and stop blood flow to that part

Can release bacteria into body

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32
Q

What are the symptoms of a volvulus?

A
  1. Colicky abdominal pain
  2. Vomiting (earlier with small bowel)
  3. Constipation (earlier with large bowel).
  4. Distension and tinkling bowel sounds.
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33
Q

What are the tests for a volvulus?

A
  1. Abdo X-ray
    • Coffee bean
  2. Barium enema
    • Bird’s beak
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34
Q

What is the treatment for a volvulus?

A

Sigmoidoscopy

Endoscopy

Surgery

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35
Q

What is a Hartmann’s procedure?

A
  1. Hartmann’s procedure is performed when a carcinoma of the rectum is found to be unresectable either due to local invasion or because the patient is unfit for a major resection
  2. When resection of the sigmoid colon is performed and an end colostomy is fashioned the operation is referred to as a Hartmann’s procedure
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36
Q

What is Paul-Mikulicz procedure?

A

A Paul-Mikulicz procedure is used to treat obstructed colonic carcinoma, volvulus or localized diverticular disease

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37
Q

WHAT IS A HERNIA?

A

Protrusion of organ or tissue out of the body cavity in which it normally lies

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38
Q

What are some causes of hernias?

A
  1. Age
  2. Chronic cough
  3. Trauma damage
  4. Failure of abdo wall to close properly in womb
  5. Constipation
  6. Heavy weight lifting
  7. Pregnancy
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39
Q

What are the different meanings for these?

Irreducible

Reduction

Incarceration

Obstructed

Strangulated

A

Irreducible= hernia cannot be pushed back into the right place

Reduction = pushing tissue/organ back into place

Incarceration = contents of hernialsac are stuck inside by adhesions

Obstructed = bowel contents cannot pass through them

Strangulated = if ischaemic occurs

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40
Q

What are the different types of hernia?

A
  1. Hiatal
  2. Inguinal
  3. Femoral
  4. Incisional (after surgery)
  5. Umbilical (<6m, normally corrects itself)
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41
Q

What is the most common hernia and why?

A

Inguinal hernia

70%

More common in MEN because after testicles descend through canal after birth the canal doesn’t always close properly so is weakened

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42
Q

What is a direct inguinal hernia?

A

Protrudes DIRECTLY into inguinal canal

Medial to inferior epigastric vessels

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43
Q

What is an indirect inguinal hernia?

A

Protrudes through internal inguinal ring

Lateral to inferior epigastric vessels

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44
Q

What is a hiatus hernia?

A

Part of stomach herniates through oesophageal hiatus of diaphragm

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45
Q

How does a hiatal hernia occur?

A

Sliding
GO junction slides through hiatus and lies above diaphragm

Para-oesophageal hernia
Gastric fundus rolls up through hiatus alongside oesophagus, GO junction remains below diaphragm

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46
Q

What are the symptoms of a sliding hernia?

A

None unless gastric oesophageal reflux occurs

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47
Q

What are the symptoms of a para-oesophageal hernia?

A

Serious risk of complications (gastric volvulus, bleeding)

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48
Q

What are the investigations for a hernia?

A

Made clinically with history and examination

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49
Q

What are the treatments for hernias?

A

May require surgical repair

Reducing the hernia can prevent strangulation from occurring

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50
Q

WHAT IS DIVERTICULOSIS?

https://www.youtube.com/watch?v=TL9_WKuNfu0

A

Little pouches at the side of the gut

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51
Q

What is diverticular caused by?

A

High pressure within the lumen pushes part of the intestine out

Classically, diverticular disease is believed to occur as a result of deficiency of dietary fibre.

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52
Q

Where do most diverticulums occur?

A

Sigmoid colon

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53
Q

What causes incresed risk of diverticulosis?

A

Low fiber foods leads to constipation

Fatty foods and red meat

Marfan’s syndrome

Ehlers-danlos syndrome

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54
Q

WHAT IS DIVERTICULAR DISEAESE?

A

Diverticula + complications e.g. infection, hemorrhage, infection

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55
Q

What is the symptoms of diverticular disease

A

Usually no symptoms

Sometimes stomach pain and bleeding

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56
Q

What can happen if a diverticular outpouching ruptures?

A
  1. Can form a fistula
  2. Connection between it and another organ
  3. Most commonly the bladder
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57
Q

What is the tests for diverticular disease?

A

Diagnosis of exclusion

Contrast CT Abdo Pelvis

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58
Q

What are the treatment options for diverticular disease?

A
  1. Diet
    • ​More fibre
  2. Attacks
    • Antibiotics
  3. Recurrent attacks
    • Colonic resection
  4. Smooth muscle relaxants
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59
Q

WHAT IS DIVERTICULITIS?

A

Inflammation of diverticula

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60
Q

How can a diverticulosis become a diverticulitis?

A

Inflammation

Through high pressures erroding the wall
OR
Lodged fecalith

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61
Q

What are the symptoms of acute diverticulitis?

A

LIF pain

Fever

Abdoguarding

Tachycardia (similar to appendicitis but on the left)

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62
Q

What are the symptoms of chronic diverticulitis?

A

Chronic diverticulitis exactly mimics the local clinical features of carcinoma of the colon:

  1. Mucus/bloody diarrhoea alternating with constipation
  2. Which progresses to large bowel obstruction with
  3. Vomiting
  4. Distension
  5. Colicky abdominal pain
  6. Constipation
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63
Q

What are the tests for diverticulitis?

A
  1. Diagnostic - Contast CT Abdo Pelvis
  2. Bloods (ESR, CRP)
  3. USS
  4. Sigmoidoscopy
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64
Q

What is the treatment of diverticulitis?

A
  1. Generally treated with bed rest
  2. If mild
    • Oral antibiotics, liquid diet and analgesia
  3. If symptoms don’t settle within 72 hours
    • IV fluids, analgesics
    • IV antibiotics - for example cefuroxime and metronidazole - and antispasmodics
  4. Surgical removal - not usually done
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65
Q

WHAT ARE THE RISK FACTORS FOR OESOPHAGUS CANCER?

A

Two main risk factors

  1. Gastro-oesophageal reflux
  2. Obesity
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66
Q

What is the most common cancer found in oesophageal cancer?

A

Squamous cell carcinoma (SCC) upper 2/3rds

Adenocarcinoma lower 1/3rd

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67
Q

What is the staging for oesophageal cancer?

A

TNM

T = primary tumour

N = lymph nodes

M = metastisis

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68
Q

What are the symptoms of oesophageal cancer?

A
  1. Dysphagia: the most common presenting symptom
  2. Anorexia and weight loss
  3. Vomiting
  4. Other possible features include:
    • Odynophagia - solid foods then soft foods progression
    • Hoarseness
    • Melaena
    • Cough
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69
Q

What are the investigations for oesophageal cancer?

A
  1. Endoscopy
    • in patients with ALARM symptoms
    • Aged 55 or older with unexplained dyspepsia
  2. Barium oesphagography
  3. CT
    • Staging

Apple core sign

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70
Q

What is the treatment for oesophageal cancer?

A
  1. Operable disease is best managed by surgical resection - the most common procedure is an
    • Ivor-Lewis type oesophagectomy
  2. The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
  3. In addition to surgical resection many patients will be treated with adjuvant chemotherapy
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71
Q

WHAT ARE THE RISK FACTORS FOR STOMACH CANCER?

A
  1. H.pylori
  2. Age
  3. Sex
  4. Ethnic origin - Black African or Caribbean
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72
Q

What is the most common cancer type for stomach cancer?

A

Adenocarcinomas

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73
Q

What are the clinical features of stomach cancer?

A

Dyspepsia

Later features include:
Anorexia and weight loss
Palpable mass

Troisier’s sign - palpable left supraclavicular lymph node; this is called Virchow’s node.

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74
Q

What are the investigations for stomach cancer?

A
  1. Endoscopy and biopsy
  2. Chest X-ray, liver enzymes and liver ultrasound
  3. Anaemia
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75
Q

What is the staging of stomach cancer?

A

TNM

T = primary tumour

N = lymph nodes

M = metastisis

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76
Q

What is the treatment for stomach cancer?

A

Surgery ONLY

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77
Q

WHAT IS THE MOST COMMON CANCER OF THE SMALL INTESTINE?

A

Adenocarcinoma

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78
Q

What are the clinical features of small intestine cancer?

A
  1. Occult bleeding
  2. Obstruction
  3. Epigastric pain
  4. Vomiting
  5. Jaundice
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79
Q

What are the investigations for small intestine caner?

A

Endoscopy + biopsy

Barium studies

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80
Q

What is the treatment for small intestine cancer?

A

Surgical resection

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81
Q

WHAT ARE THE RISK FACTORS FOR COLORECTAL CANCER?

A

Age

Male

Environmental factors - red meat and processed meat

Obesity

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82
Q

What is the most common type of cancer for colorectal cancer?

A

Adenocarcinoma

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83
Q

When would you offer screening for colorectal cancer?

A
  1. age > 40
  2. family history of colorectal cancer
  3. personal history of colorectal cancer
  4. familial adenomatous polyposis coli
  5. ulcerative colitis
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84
Q

What are the symptoms of colorectal cancer?

A

Pain common to both types

  1. Right colonic carcinoma
    • Weakness and anaemia
  2. Left colonic carcinoma
    • Change in bowel habit
  3. Rectal carcinoma
    • Rectal bleeding
    • Change in bowel habit
    • Tenesmus
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85
Q

What are the investigations for colorectal cancer?

A

Colonoscopy

Barium enema, flexible sigmoidoscopy

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86
Q

What is the treatment for colorectal cancer?

A

Surgical resection

+ chemotherapy

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87
Q

What is Duke classificaiton?

A

Staging colorectal carcinoma

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88
Q

What are the Dukes classifications?

A

COLORECTAL CANCER

  1. Duke A in gut.
  2. Duke B just outside gut.
  3. Duke C lymph node.
  4. Duke D high tie lymph node.
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89
Q

WHAT IS A PEPTIC ULCER?

https://www.youtube.com/watch?v=26Rdx2EiBaA

A

Having one or more sores in the stomach, gastric ulcers or duodenum, duodenal ulcers

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90
Q

What increases the risk of a peptic ulcer?

A

Stress

Use of NSAIDs

Smoking

Helicobacter pylori

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91
Q

What are the symptoms of peptic ulcers?

A

Epigastric pain - aching in abdomen

Bloating

Belching

Vomiting

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92
Q

When do symptoms improve for gastric and duodenal ulcers?

A

Gastric when not eating

Duodenal when eating

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93
Q

What is the diagnosis of peptic ulcers?

A

Endoscopy + biopsy

C13 Urea breath test
H pylori

Biopsy
Check for malignancy
H.pylori

Gastrin Levels
If Zollinger-Ellinson syndrome - gastric tumour

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94
Q

How could you treat peptic ulcers?

A

H.pylori
Antibiotics (Omeprazole, Metronidazole, Clarithromycin)

Acid lower medications

  1. Proton pump inhibitors - Lansoprazole
  2. H2 blocker - Rantidine

Surgery

95
Q

What makes gastric ulcers worse?

A
  1. NSAIDs
  2. Smoking
  3. Caffiene
  4. Alcohol
96
Q

WHAT IS GASTRITIS?

A

Irritation of stomach lining without an ulcer

97
Q

What are the causes of gastritis?

A

Excessive alcohol

NSAIDs

Spicy foods

Stress

98
Q

What are the symptoms of gastritis?

A

Epigastric pain

Loose stools

Vomiting

Haematemesis.

99
Q

How can you diagnose gastritis?

A

Endoscopy + biopsy

100
Q

What is the treatment for gastritis?

A
  1. Ranitidine or PPI; eradicate H. pylori as needed.
  2. Troxipide PO improves gastric mucus.
  3. Endoscopic cautery may be needed.
101
Q

WHAT IS THE STRUCTURE OF THE SMALL INTESTINE?

A
  1. Villi and crypts.
  2. Crypts provide new cells for the villi
102
Q

What are the different types of malabsorption?

A
  1. Insufficient intake.
  2. Defective intraluminal digestion.
  3. Insufficient absorptive area.
  4. Lack of digestive enzyme.
  5. Defective epithelial transport.
  6. Lymphatic obstruction.
103
Q

What is Giardia lamblia?

A

Giardia lamblia, also known as Giardia intestinalis, is a flagellated parasite that colonizes and reproduces in the small intestine, causing giardiasis.

The parasite attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission.

104
Q

WHAT IS CROHN’S DISEASE?

A

Massive inflammation and associated ulcers.

Transmural granulomatous inflammation

105
Q

What is the cause of crohn’s?

A

Immune response occurs in reponse to pathogen but is wide and damages cell in GI tract

Defect in epithelial wall which lets bacteria in

106
Q

What are the bacteria thought to be responsible for Crohn’s?

A

Mycobacterium paratuberculosis

Pseudomonas

Listeria

107
Q

Where in the GI tract is Crohn’s disease most common?

A

Terminal Ilieum.

108
Q

Where can ulceration/granulomatous inflammation be found in Crohn’s?

A

Whole length of the GI tract

PATCHY

Throughout the mucosa, submucosa, muscular propriety and fat of the gut.

109
Q

Where do crohn’s ulcers extend?

A

All the way through muscle layer

Ulcerative colitis does not

110
Q

What are the symptoms of crohn’s?

A
  1. Pain in assocaited areas
    • RLQ
  2. Diarrhoea and blood in stool
  3. If affecting large bowel
  4. Malabsorption
    • If affect small bowel
111
Q

What are the test for crohn’s disease?

A
  1. Colonoscopy (and biopsy)
    • DIAGNOSITIC
  2. Histology
    • inflammation in all layers from mucosa to serosa
    • goblet cells
    • granulomas
  3. Small bowel enema
    • Kantor’s string sign
    • Rose thorn ulcers
  4. CT
    • Shows areas of wall thickening
112
Q

What does the histology look like for crohn’s?

A

Skip Lesions

Transmural inflammation

Increase in Goblet cells

Non-Caseating Granulomas

113
Q

What are the treatment option for crohn’s?

A

Maintenance:

  1. Azathioprine
  2. Mercaptopurine / Methotrexate
  3. TNF-alpa inhibitors (all the –imabs)
  4. Surgery eg. Strictures, resection

Flares:

  1. 7 days prednisolone then taper dose for 7 weeks
  2. If systemically unwell – admit for IV hydrocortisone and monitoring (incl Xrays). Supportive – fluids, transfusion if <80Hb).
  3. Switch to oral pred once improving or biologics if not improving
114
Q

What are some Crohn’s disease complications?

A
  1. Malabsorption
    • Disease extent -surgical resections
  2. Obstruction
    • Acute swelling -chronic fibrosis
  3. Perforation
    • Acute abdomen
  4. Fistula formation
  5. Osteoporosis
  6. Neoplasia
    • Colorectal cancer
115
Q

What different surgical resections are there in crohns?

A
  1. Ileocolonic anastomosis
  2. Jejunocolonic anastomosis
  3. End-jejunostomy
116
Q

WHAT IS ULCERATIVE COLITIS?

A

Inflammation in the large intestine forming ulcers including colon and rectum

117
Q

What are the categories of mild, moderate, or severe for ulcerative collitis?

A
118
Q

What is the cause of ulcerative collitis?

A

Autoimmune

Stress and diet make it worse

119
Q

What trait do a large amount of people with ulcerative collitis have?

Blood test result

A
  1. p-ANCAs
    • Thought to be due to bacteria mimicary
  2. Increase in Sulfide gut bacteria
120
Q

What is the epidemology of ulcerative collits?

A
  1. Family history positive
  2. Women
  3. 30s
  4. Caucasions and eastern europeans
121
Q

Where does ulcerative collitis start and what does it look like inside the lumen?

A

Rectum

Makes way round with no breaks

Circumfrential and continuous

122
Q

What can ulcerative colitis involve?

A
  1. Inflammatory disorder of the colonic mucosa.
  2. Does not involve the muscle
  3. Forming ulcers
123
Q

How do you distinguish ulcerative colitis from Crohn’s disease?

A
124
Q

What are the symptoms of ulcerative colitis?

A
  1. Pain in LLQ
  2. Episodic or chronic diarrhoea
  3. Cramps abdominal discomfort
  4. Bowel frequency relates to severity
  5. Urgency/tenesmus.
  6. Fever, malaise, anorexia, weight.
125
Q

What are some complications of ulcerative colitis?

A
  1. Skin
    • Erythema nodosum
    • Pyoderma gangrenosum
  2. Colon
    • Blood loss toxic megacolon dilatation
    • Colorectal cancer
  3. Joints
    • Ankylosing Spondylitis
  4. Eye
    • Iritis
    • Uveitis
126
Q

What would show on histology for UC?

A
  1. Continuous superficial inflammation
  2. Crypt Abscesses
  3. Goblet cell depletion
  4. Ulcers
  5. Only rectum affected (not proximal to ileocaecalvalve)
127
Q

What investigations can be done for ulcerative colitis?

A
  1. Sigmoidoscopy and biopsy -
    • ***DIAGNOSTIC
    • Colonoscopy if not severely ill
  2. BARIUM SWALLOW
    • Loss of haustrations and drain pipe colon
  3. XR
    • No faecal shadows; mucosal thickening/islands, colonic dilatation
  4. Stools
    • Exclude bacteria
  5. Colonoscopy
    • Look for inflammatory infiltrate; goblet cell depletion; glandular distortion; mucosal ulcers; crypt abscesses.
128
Q

What is the most important investigation to do in a UC flare?

A

Abdo X-ray

129
Q

What are the principles of management for ulcerative colitis?

A

Maintenance:

  1. TOPICAL OR ORAL Mesalazine (which is an aminosalicylate or 5-ASA)
  2. Azathioprine
  3. Mercaptopurine / Methotrexate
  4. TNF-alpa inhibitors (all the –imabs)
  5. Surgery eg. Strictures, resection, stoma

Flares:

  1. Rectal Mesalazine
  2. Oral Mesalazine
  3. 7 days prednisolone then taper dose for 7 weeks
  4. If unwell – admit for IV steroids and monitoring (incl Xrays). Supportive – fluids, transfusion if <80Hb).
130
Q

What happens in barrett’s oesophagus?

A

Change from squamous epithelium to glandular columnar

131
Q

What is the treatment for barrett’s oesophagus?

A
  1. Endoscopic surveillance with biopsies
  2. high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett’s the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited

Endoscopic surveillance

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

If dysplasia of any grade is identified endoscopic intervention is offered. Options include:

  1. Endoscopic mucosal resection
  2. Radiofrequency ablation
132
Q

WHAT IS IBS?

A

Recurrent abdominal pain and abnormal bowel motility

133
Q

What are the symptoms of IBS?

A

Constripation and/or diarrhoea

Symptoms improve after voiding

Does not involve inflammation

134
Q

What is the cause of IBS?

A

Unknown

135
Q

What happens with visceral hypersensitivity in IBS?

A
  1. Sensory nerve endings
  2. Abnormaly stong response to stimuli
  3. When eating
  4. Recurrent abdo pain
136
Q

How does increased bowel motitlity work with IBS?

A
  1. Short-chain carbohydrates
  2. Fructose and lactose act as solutes
  3. Draw water into lumen
  4. Stretch lumen causing pain
  5. Smooth muscle spasm and diarrhoea
  6. Gut flora metabolise short chain and produce gas
137
Q

What is the epidemology of IBS?

A

North america
Middle aged women

Other parts
Both sexes equally

138
Q

What are some risk factors for IBS?

A
  1. Gastroenteritis
    • Norovirus
    • Rotovirus
  2. Stress
139
Q

What is the treatment of IBS?

A
  1. First-line pharmacological treatment - according to predominant symptom
    • pain: antispasmodic agents
    • constipation: laxatives but avoid lactulose
    • diarrhoea: loperamide is first-line
  2. Second-line pharmacological treatment
    • Low-dose tricyclic antidepressants - amitriptyline
  3. CBT
  4. LOW FODMAP

Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols

140
Q

How do you distinguish between IBS and IBD?

A

Faecal calprotectin

141
Q

WHAT IS COELIACS DISEASE?

https://www.youtube.com/watch?v=nXzBApAx5lY

A

Autoimmune response which attacks the small intestine

142
Q

What is the main culprit of coeliacs?

A

Gliadin found in gluten

143
Q

What screening tests can be used to detect coeliacs disease?

A

Anti-tTG and anti-endomyseal useful in severe cases

144
Q

What are the signs seen in the intestinal wall for coeliac’s?

A

Villus atrophy

Crypt hyperplasia

Lymphocyte infiltration

145
Q

How does coeliac’s disease present?

A

Classical

  1. Diarrhoea
  2. Steatorrhoea
  3. Weight loss
  4. Failure to thrive

Non-classical

  1. Irritable bowel type symptoms
  2. Iron Deficiency
  3. Anaemia
  4. Osteoporosis
  5. Chronic Fatigue
  6. Dermatitis Herpitiformis
  7. Ataxia
  8. Peripheral neuropathy
  9. Hyposplenism
  10. Ammenorhoea Infertility
146
Q

What is Dermatitis Herpetiformis?

A
  1. Rash common with coeliac disease patients.
  2. Bumpy skin rash which pops up from IgA antibodies
  3. Transglutaminase in dermal papillae
  4. Neutrophils come by and start reaction
147
Q

How do you test for coeliac’s disease?

A

MUST EAT GLUTEN FOR 6 WEEKS BEFORE TEST

  1. Serology
    • Tissue transglutaminase (tTG)
    • Anti-endomysial antibody (EMA)
    • Anti-gliadin
    • Anti-casein
  2. Endoscopy + Duodenal biopsies - GOLD STANDARD
    • Villous atrophy
    • Crypt hyperplasia
    • Increase in intraepithelial lymphocytes
    • Lamina propria infiltration with lymphocyts
148
Q

How do you manage coeliac’s disease?

A
  1. Gluten free diet – strict and lifelong
  2. Patients with coeliac disease often have a degree of functional hyposplenism
    - - Pneumococcal vaccine
  3. DEXA scan- osteoporotic risk
  4. Prescription entitlement Inform 10% risk in 1st degree relatives.
149
Q

What happens if coeliac’s disease is left untreated?

A
  1. Persistent symptoms
  2. Osteoporosis
  3. Subfertility
  4. Cancer risk - enteropathy-associated T-cell lymphoma
  5. Quality of life.
150
Q

WHAT IS TROPICAL SPRUE?

https://www.youtube.com/watch?v=In1uajyiSxE

A

GI disease that results in malabsorption of nutrients in water

151
Q

What is the cause of tropical sprue?

A

Unknown

Maybe E. coli

152
Q

What happens to the villi in tropical sprue?

A

Villi become flattened

153
Q

What is thought to be the pathology of tropical sprue?

A

Bacteria, virus or protazoa initially damage gut wall

Cause inflammation

Enteroglucagon released by enterocytes

Decreases intentinal motility

154
Q

What are the bacteria in tropical sprue?

A

Klebsiella

E.Coli

Enterobacter

155
Q

What are the symptoms of tropical sprue?

A

Has flare ups

Diarrhoea

Abdominal pain

Fatigue

Weight loss

Dehydration

156
Q

What is the diagnosis of tropical sprue?

A

Lived in tropics and have long standing GI symptoms

  1. Fat malabsorption
    • 72 hour stools test on prescribed diet
  2. Carbohydrate malabsorption
    • D-xylose absorption test
  3. Imaging techniques
    • Endoscopy
      • Villi atropy
    • Barium swallow
      • Intestinal wall thickening
  4. Tissue biopsy of jejenum
157
Q

What is the treatment for tropical sprue?

A
  1. Antibiotics
    • Tetracycline 250mg QDS
  2. Nutrition
    • Folate
    • B12
158
Q

What is a complication of tropcial sprue?

A

Megaloblastic anaemia

Large immature RBCs

159
Q

WHAT IS MALLORY-WEISS TEAR?

https://www.youtube.com/watch?v=YEaP_P5HrLQ

A

A longtitudinal tear in the mucosa lining at the gastroesophageal opening

160
Q

What is the cause of mallory-weiss?

A

Anyhting that causes a suddden rise in intragastric pressure

  1. Normaly prolonged vomiting
  2. Persistant retching
  3. Intentse coughing
  4. Alcholic binge drinking
  5. Beluimic
  6. Gastritis
161
Q

What are the symptoms of Mallory-Weiss?

A
  1. Upper GI pain
  2. Severe vomiting
  3. Vomiting blood (Hematemisis)
  4. Bloody or black stools (Melena)
162
Q

How can you diagnose Mallory-weiss?

A
  1. Pateint history and presenting complaint
    • Binge drinking?
    • Bulimic?
  2. Upper GI endoscopy - FIRST LINE
    • See tear in mucosa
  3. FBC
    • Low RBC
163
Q

What are the treatment options for Mallory-weiss?

A

Most of the time it heals itself

  1. IV fluid
  2. Oesophagus balloon tamponade
  3. Oesophageal clips
  4. Sclerotherapy (medications close off vessel)
  5. Coagulation therapy
164
Q

WHAT IS BOERHAAVE SYNDROME?

A

Mackler triad for Boerhaave syndrome: vomiting, thoracic pain, subcutaneous emphysema.

165
Q

What happens in boerhaave syndrome?

A

Severe vomiting → oesophageal rupture

166
Q

WHAT ARE OESOPHAGO-GASTRIC VARICES?

https://www.youtube.com/watch?v=06nBQxYro8s&t=37s

A

The dilated veins that are in the distal oesophagus

167
Q

What causes varices?

A

Increase in portal venous system

168
Q

What diseases cause varices?

A

Liver cirhosis

Alcoholics

169
Q

How does liver cirrhosis cause varices?

A

progressive liver fibrosis + regenerative nodules produce contractile elements in the liver’s vascular bed

Portal hypertension

Causes veins in oesophagus to become engorged and serpentine

170
Q

What are the symptoms of varices?

A
  1. History
    • Alcoholic
  2. Upper GI bleeding
    • More than Mallory Weiss
171
Q

How do you diagnose varices?

A
  1. Endoscopy
  2. FBC
  3. PT
  4. PTT
  5. LFT
172
Q

What is the treatment for varices?

A
  1. Endoscopic banding
    • Put rubber band around enlarged veins
  2. TIPS
    • Transjugular, intrahepatic portosystemic shunting
    • Bypass between portal and hepatic venous circulations
  3. Octreotide IV
    • Decreases blood flow
    • Inhibits vasodilation
  4. Non-selective beta blockade - PROPHYLAXIS
    • Propanalol
173
Q

What is the treatment for non-variceal bleeding?

A
  1. NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
  2. If further bleeding then options include repeat endoscopy, interventional radiology and surgery
174
Q

WHAT IS ACHALASIA?

https://www.youtube.com/watch?v=Ck5Xhre-UZU&t=1s

A

Lower esopahgeal sphincter does not relax

Esophagus dilates

175
Q

What is the cause of achalasia?

A
  1. Contraction of lower oesophagael by loss of spinchter nerve innervation
  2. BY loss of ganglion cells (Auerbach’s plexus)
176
Q

What is the pathophysiology of achalasia?

A
  1. Impaired of peristalsis
  2. Lack of relaxation of LOS
  3. Increased pressure
177
Q

What are the symptoms of achalasia?

A
  1. dysphagia of BOTH liquids and solids
  2. Typically variation in severity of symptoms
  3. Heartburn
  4. Regurgitation of food
  5. May lead to cough, aspiration pneumonia etc
  6. Malignant change in small number of patients
178
Q

What is the diagnosis of achalasia?

A
  1. Oesophageal monometry - catheter down esophagus
    • Assess peristalsis
    • 100% failed peristalsis
    • Function of LOS
    • Incomplete relaxation
    • Increased pressure
  2. Barium swallow
    • Fluid stuck in esophagus
    • Bird’s beak
  3. Chest x-ray
    • Wide mediastinum
    • Fluid level
179
Q

What is the treatment for achalasia?

A
  1. Pneumatic (balloon) dilation is 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
  2. Surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
  3. Intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
  4. Drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects
180
Q

WHAT IS SCLERODERMA?

A

Collagen deposition in skin and other organs

181
Q

What is the epidemology of scleroderma?

A

30-50 years

Women more than men

182
Q

What is the cause of scleroderma?

A

Unknown agent causes disease in suseptable host

183
Q

What antibody is involved with scleroderma?

A

Limited: Anticentromere

Diffuse: Antitopoisomerase-1

184
Q

What are the symptoms of scleroderma?

A

CREST

Calcinosis
Raynaud’s phenomenom
Esophageal dysfunction - acid reflux and decrease in motility
Sclerodactyly - thickening and tightening of the skin on the fingers and hands
Telangiectasis - dilation of capillaries causing red marks on surface of skin

Skin develops hard texture
Cannot be wrinkled

Face is expressionless

Claw like fingers

185
Q

What is the diagnosis of sclermoderma?

A

Radiography
Diffuse widening of peridontal ligament space

Microscopy
Excess collagen in stroma of organ involved

186
Q

What is the cure of scleroderma?

A

No cure

Immunosuppresants
Cyclophosphamide

187
Q

WHAT IS GASTROINTESTINAL REFLUX?

A

Symptoms or mucosal damage produced by abnormal reflux of gastric content into the oesophagus

188
Q

What are some causes of GI reflux?

A

Obesity

Eating large meals

Tight clothing

Pregnancy

Drugs
Tricylic depressants
Anticholinergics

189
Q

What are the symptoms of GI reflux?

A

Heartburn

Acid regurgitation

190
Q

What is the mechanism in GI reflux?

A
  1. In the normal individual the pressure in the intra-abdominal pressure exceeds the intra-thoracic pressure.
  2. This differential is exacerbated in the obese person.
191
Q

What are the investigations for GI reflux?

A

Endoscopy

Barium radiology

24 hour oesophageal pH monitoring

192
Q

What is the management for GI reflux?

A
  1. Endoscopically proven oesophagitis
    • full dose proton pump inhibitor (PPI) for 1-2 months
    • if response then low dose treatment as required
    • if no response then double-dose PPI for 1 month
  2. Endoscopically negative reflux disease
    • full dose PPI for 1 month
    • if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
    • if no response then H2RA or prokinetic for one month
  3. Fundoplication surgery
    • ​​REQUIRES OESOPHAGEAL PH AND MANOMETRY STUDIES
193
Q

What is a condition that is closely related to GORD?

Produces acid taste, chest discomfort

A

Laryngopharyngeal reflux

194
Q

What are the comoplications of GI reflux?

A
  1. Oesophageal carcinoma
  2. Barrett’s oesophagus
  3. Anaemia
  4. Benign strictures
195
Q

WHAT IS ISCHAEMIC COLITIS?

A

Ischaemic colitis is typically, a chronic segmental process in elderly patients affecting the watershed areas of the splenic flexure or rectosigmoid area. It is caused by transient critical ischaemia.

196
Q

What is the cause of ischaemic colitis?

A

The most common cause is arterial occlusion, usually of the superior mesenteric artery

197
Q

What are the clinical features of ischaemic colitis?

A
  1. Cramp-like, left sided abdominal pain which lasts for a few hours, and is followed by rectal bleeding.
  2. The bleeding is dark red, often without faeces, and may occur 2-3 times over a period of 12 hours.
  3. Most common at splenic flexure
198
Q

What are the investigations for ischaemic colitis?

A

Plain abdominal x-ray - may reveal mucosal oedema at the splenic flexure, so called “thumb printing”; a single segment is affected with symmetrical stricture

199
Q

What is the treatment for ischaemic colitis?

A

May resolve

Strictures may develop which require surgical resection

200
Q

WHAT IS A PILONIDAL SINUS?

A

‘Pilonidal’ means a nest of hairs.

A pilonidal sinus is a sinus that contains a tuft of hairs.

These sinuses are commonly found in the skin covering the sacrum and coccyx but can occur between the fingers, particularly in barbers, and at the umbilicus.

201
Q

What are the clinical features of a pilonidal sinus?

A
  1. Recurrent episodes of pain or sepsis.
  2. There are often periods of several months between episodes.
  3. As the size of the sinus increases the frequency of painful episodes also increases
202
Q

What is the management of a pilinidal abscess?

A
  1. If a pilonidal sinus is small, then it may only require antibiotic treatment. If the sinus develops into an acutely inflamed abscess, then it will require drainage.

There are three alternative procedures that may be undertaken:

  1. the lesion can be incised and laid open
  2. the lesion can be completely excised
  3. the lesion can be curetted and injected with phenol
203
Q

WHAT IS ACUTE MESENTERIC ISCHAEMIA?

A
  1. Acute mesenteric ischaemia is typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery.
  2. Classically patients have a history of atrial fibrillation.
204
Q

What is the management of acute mesenteric ischaemia?

A
  1. urgent surgery is usually required
  2. poor prognosis, especially if surgery delayed
205
Q

What is the difference between mesenteric ischaemia and ischaemic colitis?

A
206
Q

WHAT IS COSTRIDIUM DIFFICILE INFECTION?

A
  1. 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.
207
Q

What are the causes of c.diff?

A
  1. 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
  2. Ompeprazole also a risk factor
208
Q

What are the features of c.diff infection?

A
  1. Diarrhoea
  2. Abdominal pain
  3. A raised white blood cell count (WCC) is characteristic - DETERMINES SEVERITY
  4. If severe toxic megacolon may develop
209
Q

How is c.diff diagnosed?

A
  1. Is made by detecting Clostridium difficile toxin (CDT) in the stool
  2. Clostridium difficile antigen positivity only shows exposure to the bacteria, rather than current infection
210
Q

What is the treatment of c.diff?

A

STOP OPIOIDS DURING TREATMENT

  1. First episode of Clostridium difficile infection
    • first-line therapy is oral vancomycin for 10 days
    • second-line therapy: oral fidaxomicin
    • third-line therapy: oral vancomycin +/- IV metronidazole
  2. Recurrent episode
    • recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode
    • within 12 weeks of symptom resolution: oral fidaxomicin
    • after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
  3. Life-threatening Clostridium difficile infection
    • oral vancomycin AND IV metronidazole
    • specialist advice - surgery may be considered
211
Q

WHAT IS PERNICIOUS ANAEMIA?

A
  1. Pernicious anaemia is an autoimmune disorder affecting the gastric mucosa that results in vitamin B12 deficiency. I
  2. t is helpful to remember that pernicious means ‘causing harm, especially in a gradual or subtle way’ - the symptoms of signs are often subtle and diagnose is often delayed.
212
Q

What is the pathophysiology of pernicious anaemia?

A
  1. antibodies to intrinsic factor +/- gastric parietal cells
  2. intrinsic factor antibodies → bind to intrinsic factor blocking the vitamin B12 binding site
  3. gastric parietal cell antibodies → reduced acid production and atrophic gastritis. Reduced intrinsic factor production → reduced vitamin B12 absorption
  4. vitamin B12 is important in both the production of blood cells and the myelination of nerves → megaloblastic anaemia and neuropathy
213
Q

What are the features of pernicious anaemia?

A
  1. anaemia features
    • lethargy
    • pallor
    • dyspnoea
  2. neurological features
    • peripheral neuropathy: ‘pins and needles’, numbness. Typically symmetrical and affects the legs more than the arms
    • subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia
    • neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritabiltiy
  3. other features
    • mild jaundice: combined with pallor results in a ‘lemon tinge’
    • glossitis → sore tongue
214
Q

What are the investigations for pernicious anaemia?

A
  1. full blood count
    • macrocytic anaemia: macrocytosis may be absent in around of 30% of patients
    • hypersegmented polymorphs on blood film
    • low WCC and platelets may also be seen
  2. vitamin B12 and folate levels
    • a vitamin B12 level of >= 200 nh/L is generally considered to be normal
  3. antibodies
    • anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%)
    • anti gastric parietal cell antibodies in 90% but low specificity so often not useful clinically
  4. Schilling test is no longer routinely done
    • radiolabelled B12 given on two occasions, firstly on its own, secondly with oral IF. Urine B12 levels are then measured
215
Q

What is the management of pernicious anaemia?

A
  1. vitamin B12 replacement
    • usually given intramuscularly
    • 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
    • there is some evidenace that oral vitamin B12 may be effective for providing maintenance levels of vitamin B12 but it is not yet common practice
  2. folic acid supplementation may also be required
216
Q

WHAT IS HNPCC (LYNCH SYNDROME?)?

A
  1. HNPCC (Lynch syndrome), an autosomal dominant condition, is the most common form of inherited colon cancer. Around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive. Currently seven mutations have been identified, which affect genes involved in DNA mismatch repair leading to microsatellite instability. The most common genes involved are:
  2. MSH2 (60% of cases)
  3. MLH1 (30%)
217
Q

What other cancer is lynch syndrome associated with?

A

Endometrial cancer

218
Q

WHAT IS REFEEDING SYNDROME?

A

Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism.

219
Q

What are the metabolic consequences of refeeding syndrome?

A
  1. Hypophosphataemia
  2. Hypokalaemia
  3. Hypomagnesaemia: may predispose to torsades de pointes
  4. Abnormal fluid balance
220
Q

WHAT IS THE MOST COMMON ORGANISM FOR A PYOGENIC LIVER ABSCESS?

A

Staph aureus in children and e.coli in adults

221
Q

What does this scan show?

A

Liver abscess

222
Q

What is the management of a liver abscess?

A
  1. drainage (typically percutaneous) and antibiotics
  2. amoxicillin + ciprofloxacin + metronidazole
  3. if penicillin allergic: ciprofloxacin + clindamycin
223
Q

WHAT TYPE OF DIARRHOEA DOES ENTEROTOXIGENIC E.COLI PRODUCE?

A

Watery stools

224
Q

What type of stools does C.jejuni produce?

A

Bloody stools

225
Q

WHAT IS LUDWIG’S ANGINA?

A

Cellulitis of the floor of the mouth

226
Q

HOW CAN YOU DIFFERENTIATE A LOWER AND UPPER ABDOMINAL BLEED?

A

High urea in upper bleed

227
Q

What landmark indicates upper vs lower GI bleed?

A

Ligament of Trietz

228
Q

WHAT IS ZOLLINGER-ELLISON SYNDROME?

A

Zollinger-Ellison syndrome is condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Around 30% occur as part of MEN type I syndrome

229
Q

What is the diagnosis for zollinger-ellison syndrome?

A
  1. fasting gastrin levels: the single best screen test
  2. secretin stimulation test
230
Q

WHAT DOES ETHE RED PULP AND WHITE PULP OF THE SPEEN DO?

A
  1. Red pulp - filter and destroy defunct red blood cells
  2. White pulp - lymphoid tissue, acts part of defensive system
231
Q

What is need for a patient after a splenectomy?

A
  1. Lifelong antibitoics
  2. Immunisations
232
Q

WHAT IS THE INTITAL INVESTIGATION FOR AN ANAL FISTULA?

A

Pelvic MRI

233
Q

What are the different types of fistula?

A
  1. Enterocutaneous
    • These link the intestine to the skin. They may be high (>500ml) or low output (<250ml) depending upon source. Duodenal /jejunal fistulae will tend to produce high volume, electrolyte-rich secretions which can lead to severe excoriation of the skin. Colo-cutaneous fistulae will tend to leak faeculent material. Both fistulae may result from the spontaneous rupture of an abscess cavity onto the skin (such as following perianal abscess drainage) or may occur as a result of iatrogenic input. In some cases it may even be surgically desirable e.g. mucous fistula following subtotal colectomy for colitis.
    • Suspect if there is excess fluid in the drain.
  2. Enteroenteric or Enterocolic
    • This is a fistula that involves the large or small intestine. They may originate in a similar manner to enterocutaneous fistulae. A particular problem with this fistula type is that bacterial overgrowth may precipitate malabsorption syndromes. This may be particularly serious in inflammatory bowel disease.
  3. Enterovaginal
    • Aetiology as above.
  4. Enterovesicular
    • This type of fistula goes to the bladder. These fistulas may result in frequent urinary tract infections, or the passage of gas from the urethra during urination.

ΩΩ 4 Bateman - Specialities + Endo + GI + Liver (6 decks)

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