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Sirpi's Phase 2A Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

inWhat is the anatomical critera for an upper GI bleed classification?

A

If it occurs above the ligament of treitz.

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2
Q

Aetiology of an upper GI bleed

A

Peptic ulcers
Oesophageal varices
Mallory-Weiss tear

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3
Q

Clinical presentation of an upper GI bleed

A

Melaenia (black stools).
Haematemesis - looks like coffee grounds
Abdominal pain

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4
Q

What score can be used to assess a patients condition in a suspected upper GI bleed?

A

Glasgow-Blatchford score

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5
Q

Acute management of upper GI bleed

A

ABCDE

Fluid resuscitation
Blood transfusion

Keep patient nil by mouth

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6
Q

What are the 2 types of upper GI bleeds?

A

Variceal and non-variceal bleed.

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7
Q

What features of a patient’s history would indicate an non-variceal bleed?

A

Peptic ulcers
NSAID use
Anticoagulants, antiplatelets

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8
Q

What features of a patient’s history would indicate an variceal bleed?

A

Alcoholism
PMH of liver disease

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9
Q

Management of non-variceal bleed

A

Blood transfusion
Stop NSAIDs, anticoagulants
Endoscopy within 24 hours

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10
Q

Management of oesophageal variceal bleed

A

ABCDE
Terlipressin (ADH analogue)
Antibiotics
Endoscopy within 12 hours.
Oesophageal band ligation surgery.

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11
Q

Define small bowel obstruction

A

SBO is a form of Intestinal failure

Inability of the gut to absorb necessary water, nutrients and electrolytes sufficient to sustain life, requiring intravenous supplementation or replacement.

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12
Q

Aetiology of small bowel obstruction

A

Intestinal adhesions
Hernias
Cancerous tumours

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13
Q

What are the 3 types of intestinal obstruction that can occur?

A

Intraluminal
Intramural
Extraluminal

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14
Q

Aetiology of intraluminal small bowel obstruction

A

Gastrointestinal tumour
Diaphragm disease
Meconium ileus
Gallstone ileus

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15
Q

Aetiology of intramural small bowel obstruction

A

Inflammatory- Crohn’s disease, diverticulitis
GI Tumours
Hirschsprung’s disease

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16
Q

Clinical presentation of small bowel obstruction

A

Abdominal colic
Bilious vomiting - green color
Constipation follows vomiting
Abdominal distension

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17
Q

Examination of small bowel obstruction

A

PR exam - bloating = gas is getting through so not likely to be obstructed.

Tinkling bowel sounds upon auscultation

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18
Q

Investigation of small bowel obstruction

A

FBC - to check for anaemia, infection
CRP to assess for inflammation.
U + E
Serum lactate - marker of anaerobic respiration.

CT abdomen and pelvis with contrast - gold standard

Gastrografin challenge: Administration of oral X ray contrast, perform AXR to see how far contrast has got.

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19
Q

General management of small bowel obstruction

A

Supportive Management

Pain: analgesia (usually opiates, IV since vomiting).

Assess fluid balance: Nasogastric tube, urinary catheter.

Resusciate: IV fluids

Alleviate nausea: Antiemetics

Nutrition: If >5 days without intake, may need parenteral feed.

Surgical removal of obstruction for unstable patients.

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20
Q

Management of small bowel obstruction due to adhesions

A

Signs of ischaemia/shock = resuscitate, operate.
If non-ischaemic, non-operative management for up to 3 days.

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21
Q

Complications of small bowel obstruction surgeries

A

Renal failure
Sepsis
Arrythmias

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22
Q

What medication is contraindicated for bowel obstructions?

A

Laxatives

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23
Q

Aetiology/risk factors for Barret’s oesophagus

A

GORD
Hiatus hernia
Obesity

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24
Q

Pathophysiology of Barret’s oesophagus

A

Metaplasia of the oesophageal epithelium from squamous epithelium to columnar epithelium in lower third of oesophagu

Caused by acid reflux which kills the squamous cells.

Regenerated columnar cells have a layer of mucous that protects from further acidic damage.

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25
Q

Complications of Barrett’s oesophagus

A

Oesophageal cancer

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26
Q

How would normal oesophageal squamous epithelium appear on endoscopy?

A

White tissue due to light reflection.

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27
Q

How would columnar epithelium due to Barret’s oesophagus appear on endoscopy?

A

Red tissue

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28
Q

Risk factors for gastic carcinoma

A

Dietary nitrosamines
H.pylori infection
Tobacco smoking
E.cadherin protein mutation

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29
Q

Clinical presentation of gastric cancer

A

ALARM symptoms +/-

Epigastric pain
Nausea/vomiting
Anaemia
Dysphagia if pressing on pyloric sphincter.

Virchow’s node - supraclavicular node enlargement.

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30
Q

Where can gastric cancer commonly metastasize to?

A

Ovaries - Krukenburg tumour
Liver- jaundice

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31
Q

Management of oesophageal, gastric and bowel cancer

A

Surgical resction of tumour + chemotherapy.

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32
Q

Aetiology of familial adenomatous polyposis

A

Genetic mutation in APC gene.

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33
Q

Pathophysiology of familial adenomatous polyposis

A

Causes formation of several adenomatous polyps in the colon

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34
Q

Complication of familial adneomatous polyposis

A

Can become malignant and turn into colon cancer.

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35
Q

Aetiology of lynch syndrome (hereditary non polyposis colorectal cancer)

A

Mutation in DNA protein repair genes

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36
Q

Pathophysiology of lynch syndrome

A

Can result in non-responsiveness to chemotherapy due to inactivation of apoptosis.

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37
Q

What type of cancer is gastric, small, and large bowel cancer?

A

Adenocarcinomas.

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38
Q

Aetiology of extraluminal small bowel obstruction

A

Bowel adhesions
Volvulus - twisting of the bowel.
Peritoneal tumour

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39
Q

How do normal gut flora prevent infection?

A

Inhibiting overgrowth of endogenous pathogens

Preventing colonisation by exogenous pathogens.

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40
Q

Bacterial aetiology of diarrhoea

A

Shigella
Salmonella
E.coli
C.difficile, C.perfringens
Campylobacter jejuni
V.cholerae
Bacillus cereus

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41
Q

Non-infective aetiology of diarrhoea

A

IBD - Crohn’s/ulcerative colitis
Bowel cancer
Hyperthyroidism
Pancreatitis

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42
Q

Which bacteria can cause secretory diarrhoea?

A

Vibrio cholerae
ETEC E.coli
Clostridium perfringens
Bacillus cereus

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43
Q

Which bacteria can cause dysentery?

A

Shigella
Salmonella
E.coli (EIEC, EHEC)
C.difficile
Campylobacter jejuni

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44
Q

Viral aetiology of diarrheoa

A

Norovirus
Rotavirus

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45
Q

Parasitic aetiology of diarrhoea

A

Giardia lamblia
Cryptosporidium
Entamoeba histolytica

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46
Q

What organism can cause diarrhoea from re-heated food/takeaways, etc?

A

C.perfringens
Bacillus cereus

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47
Q

What organisms can cause diarrhoea from petting zoos?

A

E.coli
Cryptosporidum
Salmonella

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48
Q

What is traveller’s diarrhoea?

A

Occurs a few days after arrival in a new country.

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49
Q

Aetiology of traveller’s diarrhoea

A

ETEC
Campylobacter
Cholera

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50
Q

Aetiology of clostridium difficile infection

A

Broad spectrum antibiotic use:
Co-amoxiclav
Cephalosporins
Clindamycin
Ciprofloxacin

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51
Q

Pathophysiology of clostridium difficile infection

A

Contains endospores which can survive stomach acidity.

BSA use kills normal gut flora which allows C.diff flourishing.
Releases toxin A + B causing mucosal damage and dysentery

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52
Q

Clinical presentation of clostridium difficile infection

A

Fever
Dystentery
Abdominal pain

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53
Q

Management of clostridium difficile infection

A

Oral Metronidazole + oral vancomycin

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54
Q

Complication of clostridium difficile infection

A

Pseudomembraneous colitis.

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55
Q

Aetiology of vibrio cholerae infection

A

Shellfish, saline environments (floods, etc)

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56
Q

Pathophysiology of vibrio cholerae infection

A

Release of cholera toxin which causes intestinal Cl- secretion and fluid loss through diarrhoea.

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57
Q

Clinical presentation of vibio cholerae infection

A

Profuse, rice-water diarrhoea
Vomiting
Dehydration

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58
Q

What is the most common cause for diarrhoea in children?

A

Rotavirus

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59
Q

Medical management of diarrhoea in children

A

Fluid Replacement/oral rehydration salts to prevent dehydration

What goes out must come in - e.g 1 l a day excretion means administer same amount gradually over the day (sips).

Zinc treatment

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60
Q

Preventative management of diarrhoea in children

A

Rotavirus and measles vaccinations

Promote breastfeeding + Vitamin A supplementation

Promote hand washing with soap

Water treatment & safe household storage

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61
Q

Why can formula feeding in LEDCs cause an increased risk of diarrhoea?

A

Water used to mix the formula with may not be sanitary.

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62
Q

What are some red-flag signs to point towards gastrointestinal cancer?

A

Anaemia
Loss of weight
Anorexia (loss of appetite)
Recent onset of progressive symptoms
Melena/masses
Swallowing difficulties.

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63
Q

What is gastritis?

A

Inflammation of the stomach mucosa.

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64
Q

Aetiology of acute gastritis

A

Helicobacter pylori infection
Alcohol abuse
Stress (critically ill, major surgery)
NSAIDs (COX inhibitor → inhibits prostaglandin synthesis→ less alkaline mucus secretion)

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65
Q

Aetiology of chronic gastritis

A

H.pylori infection
Autoimmune gastritis

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66
Q

Pathophysiology of autoimmune gastritis

A

Anti-parietal cell antibodies cause destruction resulting in loss of intrinsic factor and HCl production.

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67
Q

Complications of autoimmune gastritis

A

Can lead to decreased vitamin B12 absorption and pernicious anaemia.

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68
Q

Clinical presentation of gastritis

A

Dyspepsia (indigestion)
Epigastric pain
Anorexia
Nausea & vomiting
Bloating

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69
Q

Investigation of gastritis

A

For H.pylori infection:
Urea breath test
Stool antigen test

Endoscopy

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70
Q

Management of gastritis

A

Omit causative agent, e.g NSAID use, alcohol

H.pylori infection:
First line - triple therapy of PPI + amoxicillin 1g + clarithromycin 500mg

If penicillin allergy, replace amoxicillin with metronidazole 400mg.

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71
Q

Management of autoimmune gastritis

A

IM Hydroxycobalamin (vit.B12 replacement for pernicious anaemia)

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72
Q

Complications of chronic gastritis

A

Increased risk of peptic ulcers (H.pylori infection) and pernicious anaemia (autoimmune gastritis)

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73
Q

What are the types of peptic ulcers

A

Gastric and duodenal ulcers.

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74
Q

Aetiology of peptic ulcers

A

NSAIDs
H.pylori infection
Gastritis

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75
Q

Clinical presentation of peptic ulcers

A

Localised burning epigastric pain.
Dyspepsia
Anorexia/weight loss

Can prevent with haematemesis/weight loss of artery perforation.

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76
Q

How is the nature of the pain in a gastric ulcer?

A

Worsens after eating due to increased HCL production to digest food.

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77
Q

How is the nature of the pain in a duodenal ulcer?

A

Better right after eating due to closure of pyloric sphincter to prevent acid from entering duodenum during gastric digestion.

Gets worse a while after eating due to food and acid entering duodenum.

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78
Q

What arteries can be perforated with peptic ulcers?

A

Gastric ulcer: Left gastric artery
Duodenal ulcer:Gastroduodenal artery

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79
Q

Investigation of peptic ulcers

A

Gold standard - endoscopy
H.pylori tests - urea breath test and stool antigen test.

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80
Q

Complication of gastric ulcers

A

Increased risk of gastric carcinoma

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81
Q

Aetiology of malabsorption

A

Defective intraluminal digestion - cystic fibrosis, biliary obstruction.

Insufficient absorptive area - - coeliac disease, giardia lamblia infection

Defective epithelial transport - Abetalipoproteinaemia

Lack of digestive enzymes - disaccharide deficiency

Lymphatic obstruction - lymphoma, TB

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82
Q

Clinical presentation of malabsorption

A

Unexpected weight loss
Steatorrhea - fat is not getting digested/absorbed
Diarrhoea
Anaemia - iron deficiency

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83
Q

Aetiology of coeliac disease

A

Associated with HLADQ 2 and HLADQ 8

Associated with other autoimmune conditions - T1DM, hashimoto’s, dermatitis herpetiformis.

Associated with IgA deficiency

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84
Q

Pathophysiology of coeliac disease (gluten sensitive enteropathy)

A

T4 hypersensitivity reaction.

Prolamins (gliadin protein in wheat) pass through intestinal epithelium and are deaminated by tissue transglutaminase.

APCs present the peptides to T-cells through HLADQ 2 and HLADQ 8.

Result in inflammatory response and synthesis of
anti-tissue transglutaminase (anti-tTG) and anti-endomysial (anti-EMA) antibodies.

Causes villous atrophy and malabsorption.

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85
Q

Clinical presentation of coeliac disease

A

Symptoms of malabsorption -
Anaemia
Steatorrhoea
Diarrhoea
Weight loss

Dermatitis herpetiformis - itchy bumps
Angular stomatitis - ulcers on the corners of mouth.

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86
Q

Investigation of coeliac disease

A

First line - serology - Raised anti-tTG Ab
Second line - serology - Raised anti-EMA Ab

Gold standard - endoscopic duodenal biopsy

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87
Q

Management of coeliac disease

A

Lifelong gluten-free diet

May require vitamin and mineral supplements.

Recommend regular immunisation as coeliac disesae can cause hyposplenism.

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88
Q

What could be seen histologically for coeliac disease?

A

Villous atrophy, crypt hyperplasia.

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89
Q

What conditions comprise inflammatory bowel disease (IBD)?

A

Crohn’s disease
Ulcerative colitis

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90
Q

Aetiology/risk factors of IBD

A

Family history
NSAID use
Smoking - increases risk of CD but not UC

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91
Q

Where can IBD occur?

A

CD: From mouth to anus, can be rectal sparing.

UC: Colon, always with rectal involvement, does not go more proximal than ileocaecal valve.

92
Q

What is the nature of the lesions in IBD?

A

CD: Skip lesions, areas of inflammation with gaps of normal tissue in between.

UC: Continuous lesions.

93
Q

What is the macroscopic morphology of the inflammation in IBD?

A

CD: Transmural inflammation with cobblestone-like appearance

UC: Only superficial (mucosal and submucosal) inflammation.
Friable (easily bleeding) mucosa.

94
Q

What is the microscopic morphology of the inflammation in IBD?

A

CD: Can have non-caseating granulotamous inflammation, presence of goblet cells.

UC: Can have crypt abscesses, no goblet cells or granulomas.

95
Q

What are some gastrointestinal presentations of IBD?

A

CD: Diarrhoea
Lower right quadrant pain usually.

UC: Dysentery
Lower left quadrant pain

Both: Symptoms of malabsorption - anaemia, weight loss, steatorrhoea

96
Q

What are some extra-intestinal presentations of IBD?

A

Ankylosing spondylitis (HLA B27)
Aphthous ulcers / amyloidosis
Clubbing

Pyoderma gangrenosum
Iritis (aka anterior uveitis)
Erythema nodosum
Sclerosing cholangitis

97
Q

Investigation of IBD

A

FBC - Anaemia, neutrophilia, thrombophilia

ESR and CRP - elevated

Serology - pANCA (Perinuclear Anti-Neutrophil Cytoplasmic Antibodies)

Stool samples - faecal calprotectin

Gold standard - colonoscopy (or endoscopy for CD) with biopsy

Abdominal imaging - barium swallow and AXR.

98
Q

What would serology reveal for IBD?

A

CD - negative pANCA
UC - positive pANCA

99
Q

What would abdominal imaging reveal for IBD?

A

CD: String sign upon barium X-ray
UC: Lead-pipe appearance for UC on AXR.

100
Q

What are some complications of IBD?

A

CD: Fistula formation, amyloidosis, malabsorption

UC: Toxic megacolon, colorectal cancer, sclerosing cholangitis.

101
Q

What is the age distribution of clinical presentation like for IBD?

A

CD: Bimodal distribution with peaks from ages 15-30 and ages > 60.

UC: Risk increases with age, mainly presents in15-30 y/o.

102
Q

Medical management of Crohn’s disease

A

First line - steroids e.g prednisolone/hydrocortisone/budesonide.

Second line - add DMARDs such as azathioprine or methotrexate

If still severe - infliximab (anti-TNF monoclonal antibody)

Maintaining remission - azathioprine + methotrexate

103
Q

Medical management of Ulcerative Colitis

A

Mild:
First line - mesalazine (aminosalicylate)
Second line - add prednisolone (steroid)

Severe:
IV fluid resuscitation
IV hydrocortisone
Prophylaxis with LMWH to prevent clot formation.

If still unresponsive, infliximab (anti-TNF monoclonal antibody)

104
Q

Surgical management of IBD

A

Subtotal colectomy with end ileostomy.

105
Q

What are functional gut disorders/disorders of gut-brain interaction?

A

Symptoms occur in the absence of any structural abnormalities and can affect the gut-brain axis to cause issues such as:

Visceral hypersensitivity
GI dysmotility
Alteration of gut microbiome

106
Q

What are examples of compose functional gut disorders/disorders of gut brain interaction?

A

Irritable bowel syndrome (IBS)
Functional dyspepsia

107
Q

Aetiology/risk factors for IBS

A

Mood disorders - depression
Anxiety/stress

108
Q

Clinical presentation of IBS

A

Recurrent abdominal pain that eases with defacaetion
Bloating
Changes in stool habits (diarrhoea/constipation)
Symptoms worse after eating.

Can have urinary and gynaecological symptoms

109
Q

Differential diagnosis for IBS

A

Coeliac disease, lactose intolerance, bile acid malabsorption, IBD, colorectal cancer.

110
Q

Investigation of IBS

A

Rule out differentials

FBC - check for anaemia

ESR & CRP - check for inflammation

Stool sample - IBS has negative faecal calprotectin

Serology - endomysial antibody and tissue transglutaminase antibody negative = not coeliac

Colonoscopy - rule out colorectal cancer.

111
Q

Management of IBS

A

Low FODMAP diet

Diarrhoea - anti-motility agents (Loperamide)

Constipation - laxatives (prucalopride)

112
Q

Aetiology of dyspepsia

A

Functional (idiopathic) dyspepsia
H.pylori infection
Peptic ulcers
Gastritis

113
Q

Clinical presentation of dyspepsia

A

Posprandial fullness
Early satiety
Epigastric pain/burning sensation
Bloating
Acid reflux, can be when lying down

114
Q

What are the ALARMS symptoms?

A

Anaemia
Loss of weight
Anorexia (loss of appetite)
Recent onset of progressive symptoms
Masses / Melena (black stools) → or bleeding from any part of GI tract
Swallowing difficulties

115
Q

What do the ALARMS symptoms indicate?

A

Gastrointestinal cancer.

116
Q

Aetiology of a Mallory-Weiss tear

A

Heavy coughing
Vomiting - alcoholic dry heaving.
Weight lifting
Hiatus hernia

117
Q

Pathophysiology of a Mallory-Weiss tear

A

Sudden increase in intra-abdominal pressure can cause mucosal tear in near gastro-oesophageal junction.

118
Q

Clinical presentation of Mallory-Weiss tear

A

Haematemesis
Abdominal pain
Postural hypotension
Dizziness

119
Q

Investigation of Mallory Weiss tear

A

Endoscopy

120
Q

Management of Mallory-Weiss tear

A

Endoscopic injection therapy

121
Q

Aetiology of Achalasia

A

Mainly idiopathic
Chagas disease

122
Q

Pathophysiology of Achalasia

A

Ganglionic degeneration in auerbach’s plexus causes lack of contraction of lower oesophageal sphincter and lack of peristalsis.

123
Q

Clinical presentation of Achalasia

A

Dysphagia of solids and liquids

Food regurgitation - can cause aspiration pneumonia

Spontaneous chest pain due to oesophageal spasm.

124
Q

Investigation of Achalasia

A

CXR - dilated oesophagus

Endoscopy

Barium swallow fluoroscopy - bird’s beak sign

GS: Manometry (oesophageal motility study) = gold

125
Q

Management of Achalasia

A

Lifestyle - Smaller, more frequent meals.

Medical - Nitrates/CCBs to relax LOS such as isosorbide dinitrate/nifedipine

Interventional - Endoscopic pneumatic dilation, laporoscopic cardiomyotomy

126
Q

Complications of Achalasia

A

Aspiration pneuomonia during sleep
Increased risk of oesophageal squamous cell carcinoma

127
Q

Aetiology of GORD

A

Obesity
Pregnancy
Hiatus hernias
Smoking
NSAIDs, Caffeine, Alcohol
Male gender (2x more likely)
Hypersecretion of acid

128
Q

Pathophysiology of GORD

A

Reduced tone of LOS causes gastric acid reflux into oesophagus.

129
Q

Clinical Presentation of GORD

A

Heartburn - burning chest pain aggravated by bending, stooping or lying down.

Pain becomes worse with spicy food/hot drinks.

Cough
Increased belching
Epigastric pain

Regurgitation of stomach contents - worse when lying down.

Hoarse voice due to laryngopharyngeal reflux

130
Q

Investigation of GORD

A

Endoscopy - presence of Barret’s or oesophagitis is diagnostic.

Intraluminal pH monitoring.

131
Q

Management of GORD

A

Lifestyle:
Smoking cessation
Reduced alcohol intake
Eating smaller meals
Avoiding eating 3-4 hours before sleeping.

Medical:
FL: PPI e.g omeprazole

Can also use:
Alginate containing antacids - magnesium trisilicate
H2 receptor antagonists - cimetidine, ranitidine.

Interventional - Nissen fundoplication

132
Q

Where is the appendix located?

A

McBurney’s point - 1/3 of the way between ASIS and umbilicus.

133
Q

Aetiology of appendicitis

A

Faecoliths (hardened stool)
Lymphoid hyperplasia
Intestinal worms

134
Q

Pathophysiology of appendicitis

A

Luminal obstruction causes stasis of faecal matter and overgrowth of bacteria causing infection and inflammation.

135
Q

Examination of Appendicitis

A

Rovsing’s sign - palpation of LIF causes pain in RIF
Psoas sign - RIF pain upon right hip extension.
Obturator sign - RIF upon right hip flexion and internal rotation.
Guarding - reflect contraction of abdo muscles upon palpation.
Rebound tenderness - pain when pressure is removed during palpation.

136
Q

Investigation of Appendicitis

A

FBC: Leukocytosis

Raised ESR, CRP

Abdominal US (in children and pregnant women)
Abdominal CT with contrast - gold standard

Urinalysis (exclude UTI)

Pregnancy test

137
Q

Management of Appendicitis

A

Antibiotics: Cefuroxime + Metronidazole

Surgical appendectomy

138
Q

What are the 3 types of bowel ischaemias?

A

Acute mesenteric ischaemia

Chronic mesenteric ischaemia (AKA intestinal angina)

Ischaemic colitis (AKA chronic colonic ischaemia)

139
Q

What areas of the bowel are most susceptible to ischaemia?

A

Splenic flexure and caecum due to them being watershed regions.

140
Q

Aetiology of acute mesenteric ischaemia

A

SMA atheroma/embolism causing thrombosis.
Embolus from heart in a patient with AF is most common.

Mesenteric vein thrombosis - more common in younger patients

Hypotension, shock, decreased cardiac output.

141
Q

Clinical presentation of acute mesenteric ischaemia and ischaemic colitis

A

Severe diffuse abdominal pain (left sided for ischaemic colitis)
Pallor, weak rapid pulse due to shock (rapid hypovolemia)
Nausea/vomiting.
Absence of bowel sounds.
Haematochezia

142
Q

Investigation of acute mesenteric ischaemiaand ischaemic colitis

A

1st line: CT abdomen with contrast or angiography
ABG: Metabolic acidosis
Gold standard: colonoscopy

143
Q

Management of acute mesenteric ischaemia and ischaemic colitis

A

IV gentamicin and metronidazole
IV heparin
Surgery - bowel resection.

144
Q

Complications of bowel ischaemia and appendicitis

A

Bowel necrosis and appendix rupture can result in bacterial spreading leading to:
Sepsis
Peritonitis

145
Q

Risk factors/aetiology of pseudomembraneous colitis

A

C.difficile infection
Recent antibiotic usage
CMV infection & immunocompromisation
Stay in a healthcare center/nursing home.

146
Q

Pathophysiology of pseudomembraneous colitis

A

C.diff infection causes colonic mucosa to become inflamed, ulcerated, and covered by an adherent membrane-like material.

147
Q

Investigation of pseudomembranous colitis

A

FBC - leukocytosis

Stool sample - C.diff infection

Colonoscopy - raised yellow plaques

Histology - owl eyes inclusion bodies for CMV

148
Q

Management of pseudomembranous colitis

A

Stop original antibiotic - replace with oral metronidazole + vancomycin.

Maybe need faecal microbiota transplant.

149
Q

Aetiology of large bowel obstruction

A

Malignancy (90%)
Sigmoid volvulus (5%) (coffee bean appearance on abdo X-Ray)
Diverticulitis
Intussusception (more common in children) is when the bowel fold within itself

150
Q

Clinical presentation of large bowel obstruction

A

Continuous abdominal pain
Severe abdominal distension
Constipation first, followed by vomiting (initially bilious, then faecal vomiting)
Absent bowel sounds

151
Q

Investigation of large bowel obstruction

A

1st line: Abdo XRay
Dilation of the large bowel >6cm
Dilation of the caecum >9cm

Gold standard: CT of the abdomen and pelvis with contrast

152
Q

Management of large bowel obstruction

A

ain: analgesia (usually opiates, IV since vomiting).

Assess fluid balance: Nasogastric tube, urinary catheter.

Resusciate: IV fluids

Alleviate nausea: Antiemetics

Nutrition: If >5 days without intake, may need parenteral feed.

153
Q

What can be caused by an H.pylori infection?

A

Gastritis - usually antral.
Peptic ulcers
Gastric cancer

154
Q

Pathophysiology of h.pylori inection

A

Secretion of urease which convertes CO2 to ammonia.

Ammonia combines with stomach H+ to form ammonium which is toxic to the alkaline gastric mucus.

155
Q

Investigation of h.pylori infection

A

Urea breath test - screening.

Stool antigen test - monoclonal antibodies to detect antigen.

Endoscopy - histoligical sampling and culturing.

156
Q

Management of h.pylori infection

A

Triple therapy - 2 antibiotics (clarithromycin and amoxicicillin/metronidazole if allergic) + PPI (omeprazole/lanzoprazole)

157
Q

What is a diverticulum?

A

Outpouchings of the gastrointestinal tract wall.

158
Q

What is diverticulosis?

A

The presence of diverticula

159
Q

What is diverticulitis and where does it mainly occur?

A

The presence of inflamed diverticula

Most comonly occurs in sigmoid colon, espesially in regions with perforating arteries.

160
Q

Aetiology/risk factors of colonic diverticulosis

A

Constipation (low fiber diet)
Obesity
NSAIDs
Smoking

161
Q

Pathophysiology of colonic diverticulosis

A

High colonic pressures causes regions of mucosa to outpouch and extrude through the mucosal wall.

Often has muscle thickening.

162
Q

Pathophysiology of colonic diverticulitis

A

When faecal obstruction due to the diverticulum causes stagnation and bacterial overgrowth.
Can lead to infection and infection of the diverticula.

163
Q

Clinical presentation of colonic diverticulitis

A

Bowel habits changed
Bloating / flatulence
Left illiac fossa pain
Nausea/vomiting
Haematochezia
Fever

164
Q

Examination of colonic diverticulitis

A

Tenderness + guarding
Tympanic to percussion - gas/bloating.
Diminished bowel sounds.

165
Q

Investigation of colonic diverticulitis

A

FBC - Leukocytosis

Raised ESR and CRP

Gold standard - CT colonography

166
Q

Management of colonic diverticulitis

A

If uncomplicated:
High fiber diet
Analgaesia (paracetmol)/antispasmodics (mebeverine)

Complicated:
- Antibioitics - co-amoxiclav.

167
Q

What is a hernia?

A

The profusion of a viscus (organ) or part of a viscus through a defect of the walls of its cavity into an abnormal position.

168
Q

What are some examples of hernias?

A

Inguinal hernia (direct and indirect)
Femoral hernia
Hiatal hernia

169
Q

Pathophysiology of Zencker’s diverticulum

A

Esophageal dysmotility causes herniation of mucosal tissue in Killians triangle - area between cricopharyngeus and thyropharyngeus muscle.

Can cause food to get stuck there.

170
Q

Clinical presentation of Zencker’s diverticulum

A

Bad breath, dysphagia, choking.

171
Q

What is the most common congenital gastrointestinal disorder?

A

Meckel’s diverticulum.

172
Q

Pathophysiology of Meckel’s diverticulum

A

Persistence of vitelline duct, can cause intussusception, volvulus, or obstruction near terminal ileum

173
Q

What is malrotation?

A

Anomaly of midgut rotation during fetal
development can cause improper positioning of bowel.

174
Q

What is intussusception?

A

Telescoping of a proximal bowel segment into
a distal segment, most commonly at ileocecal
junction.

175
Q

Example of intussusception in children

A

Meckel’s diverticulum.

176
Q

What is a volvulus?

A

Twisting of portion of bowel around its
mesentery.

177
Q

What type of volvulus is more common in infants/children?

A

Midgut volvulus

178
Q

What type of volvulus is more common in adults?

A

Sigmoid volvulus.

179
Q

Pathophysiology of Hirschprung disease

A

Congenital megacolon characterized by lack of innervation from enteric plexuses, leading to lack of motility.

180
Q

What are haemorrhoids?

A

Disrupted and dilated anal cushions - masses of spongy vascular tissue due to swollen veins around the anus

181
Q

Aetiology/risk factors of haemorrhoids

A

Constipation
Chronic coughing
Heavy lifting
Pregnancy

182
Q

Clinical presentation of haemorrhoids

A

Bright red bleeding (on wiping. Not mixed in stool
Pruritus ani (anal itching)
Constipation
Lump around or inside the anus

183
Q

Investigation of haemorrhoids

A

Digital rectal exam
Proctoscopy - see internal haemorrhoids

184
Q

What are the classifications of haemorrhoids?

A

1st degree - internal, no bleeding
2nd degree - prolapsed but spontaenously reduces
3rd degree - prolapsed but requires manual reduction
4th degree - prolapsed but does not reduce

185
Q

Management of haemorrhoids

A

Increased fluid and fiber intake
Laxatives

1st and 2nd degree - rubber band ligation, sclerosant injection

3rd & 4th degree - haemorrhoidectomy, haemhorroidal artery ligation operation (HALO)

186
Q

What is an anal fistula?

A

Abnormal open connection between the anal canal and the skin of the gluteus maximus.

187
Q

Aetiology of anal fistula

A

Anorectal abscess (70%)
Crohn’s ulcerations (30%)
TB

188
Q

Clinical presentation of anal fistula

A

Throbbing pain, worse when sitting
Blood/mucus in stool
Pruritus ani

189
Q

Investigation of anal fistula

A

Digital rectal exam
Endoanal ultrasound

190
Q

Management of anal fistula

A

Surgical fistulotomy

191
Q

What is an anal fissure?

A

Painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line.

192
Q

Aetiology of anal fissure

A

Constipation
Anal trauma
Associated with IBD.

193
Q

Clinical presentation of anal fissure

A

Extreme pain on passing stools
Blood in stool / on wiping

194
Q

Management of anal fissure

A

Increase dietary fiber and fluid intake

Lidocaine + GTN

195
Q

Clinical presentation of anal abscess

A

Anal discharge/pus
Pain
Possible fever

196
Q

Investigation of anal abscess

A

Endoanal ultrasound

197
Q

Management of anal abscess

A

Surgical drainage and antibiotics

198
Q

Aetiology of anal abscess

A

IBD
Anal trauma
Anal fistula

199
Q

Aetiology of pilonidal sinus/abscess

A

Ingrown hairs

200
Q

Pathophysiology of pilonidal sinus/abscess

A

Hair follicles get stuck under the skin in the natal cleft (butt crack) resulting in irritation and inflammation leading to small tracts which can become infected

201
Q

Clinical presentation of pilonidal sinus/abscess

A

Painful swelling
Systemic infectin symptoms - fever, etc
Foul smelling discharge/pus.

202
Q

Management of pilonidal abscess

A

Sinus excision and antibiotics.

203
Q

What enteric pathogens can be identified by light microscopy?

A

Protozoans like cryptosporidium, entamoeba histioloitica and giardia lambila.

204
Q

What is the purpose of XLD agar?

A

Can be used to differentiate between shigella and salmonella.

205
Q

How would salmonella appear on an XLD agar?

A

Black spots

206
Q

How would shigella appear on an XLD agar?

A

Red spots

207
Q

Investigation of oesophageal and gastric cancer

A

Endoscopy (gastroscopy) + biopsy
CT chest/abdomen for metastasis

208
Q

What are the 2 types of gastric cancer

A

T1 - intestinal type
T2 - diffuse type

209
Q

Risk factors for t1 (intestinal) gastric cancer

A

Males, older age

210
Q

Risk factors for t2 (diffuse) gastric cancer

A

Females, younger age

211
Q

What regions of the stomach is affected by t1 gastric cancer?

A

Antrum + lesser curvature

212
Q

What regions of the stomach can be affected by t2 gastric cancer?

A

Any region

213
Q

Which type of gastric cancer is more metastatic?

A

T2 (diffuse) so has worse prognosis.

214
Q

What is the histological distinction between t1 and t2 gastric cancer

A

T1: well formed tubules
T2: poorly differentiated signet ring cells

215
Q

Clinical presentation of oesophageal cancer

A

Progressive dysphagia (solids followed by liquid)
Weight loss
Anorexia
Hoarse voice (pressing on recurrent laryngeal nerve)
Odynophagia (painful swallowing)
Red flags (ALARMS)

216
Q

What are the 2 types of oespophageal cancer

A

Adenocarcinoma (lower 1/3)
Squamous cell carcinoma (upper 2/3)

217
Q

Risk factors/aetiology of oesophageal adenocarcinoma

A

GORD
Barret’s oesophagus
Obesity
Male gender
Caucasian

218
Q

Risk factors/aetiology of oesophageal squamous cell carcinoma

A

Smoking
Alcohol
BAME ethnicity
Achalasia

219
Q

Investigation of bowel cancer

A

Gold standard = colonoscopy + biopsy
CT chest abdo pelvis for staging.

220
Q

What screening tests is used to check for bowel cancer?

A

Faecal immunochemical test (FIT) test.

221
Q

What bacteria are associated with causing peritonitis?

A

Gram negative: E.coli, kleibsiella pneumoniae

Gram positive: S.aureus, Mycobacterium tuberculosis,

222
Q

Aetiology/risk factors of peritonitis

A

Appendicitis, ascites, liver failure, cirrhosis, surgery, TB infection

223
Q

Pathophysiology of spontaneous bacterial peritonitis

A

Bacteria infects ascitic fluid

224
Q

Presentation of peritonitis

A

Abdominal pain worse on movement (localised or spread)
Guarding
Pyrexia
Nausea/vomiting
Can have shoulder tip pain

225
Q

Investigation of sponteneous bacterial peritonitis

A

Ascitic tap – raised ascitic fluid neutrophils

Ascitic fluid culture – shows causative organisms

ESR + CRP

226
Q

Management of spontaenous bacterial peritonitis

A

ABCDE

IV antibiotics (cefotaxime)

Supportive therapy (IV fluids, analgesics, electrolytes)

Paracentesis

227
Q

Examination of diverticulitis

A

Rebound tenderness
Guarding

Sirpi's Phase 2A Medicine (13 decks)

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