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Gastroenterology Flashcards

1
Q

What are the causes of upper GI bleed?

A

Peptic ulcers (most common)
Oesophageal varices
Mallory-Weiss tear (split in oesophagus often caused by forceful vomiting)
Gastritis/gastric erosions
Reflux oesophagitis
Malignancy
Drugs (NSAIDs, anticoagulants, alcohol)

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2
Q

What are the signs/symptoms of an upper GI bleed?

A

Melaena (black tar-like stool, contains digested blood)
Haematemesis
Coffee ground vomiting

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3
Q

What is the treatment for an upper GI bleed?

A

ABCDE
Fluids
Blood transfusion (if needed)
Endoscopy

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4
Q

What is the difference in management of variceal and non-variceal bleed?

A

Variceal bleed: suspect if history of liver disease and alcohol excess, give antibiotics and terlipressin (vasodilator), endoscopy within 12 hours
Non-variceal bleed: suspect if history of peptic ulcers, NSAIDs, anticoagulation, antiplatelets, consider proton pump inhibitors, endoscopy within 24 hours

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5
Q

Define bowel obstruction

A

A form of intestinal failure due to mechanical blockage in the intestine, or ileus (temporary lack of gut motility), categorised as small or large bowel obstruction
Can be intraluminal, intramural, or extraluminal

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6
Q

Describe the epidemiology of small bowel obstruction

A

Most common cause of emergency laparotomy, most common age is 70-80

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7
Q

What are the causes of small bowel obstruction?

A

Adhesions = most common (fibrous scar tissue from previous surgery causing loops/kinks)
Hernia (inguinal, femoral)
Cancer (intraluminal or extraluminal, primary or secondary)

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8
Q

What are the causes of large bowel obstruction?

A

Colon cancer
Constipation
Diverticular stricture
Volvulus (sigmoid)

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9
Q

What are the signs/symptoms of bowel obstruction?

A

Abdominal pain
Vomiting
Bloating/distention
Weight loss
Dehydration
Hernias
*small bowel obstruction: vomiting occurs earlier, pain is higher in abdomen, less distention
*large bowel obstruction: pain is more constant, can have constipation

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10
Q

What investigations are needed for small bowel obstruction

A

FBC: check for anaemia, infection, inflammation
U&E: renal function (risk of AKI)
CT scan: diagnostic, shows location, cause, and ischemia

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11
Q

What is the treatment of bowel obstruction?

A

Analgesia (not oral due to vomiting)
Fluid balance: NG tube, urinary catheter
Replace fluids IV
Alleviate nausea: NG tube, antiemetics
Nutrition (may need parenteral feed)
Surgery (key hole/open, divide scar tissue)

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12
Q

Define diarrhoea

A

Increased stool frequency and volume, and decreased consistency

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13
Q

What are the causes of diarrhoea?

A

Infection
IBS
IBD
Colorectal cancer
Drugs (laxatives)
Food allergy/intolerance
Hyperthyroidism
Pancreatic insufficiency

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14
Q

What infections commonly cause gastroenteritis?

A

Vibrio cholerae: e.g. travelling in south Asia, Africa
Escherichia coli: e.g. from animal products
Shigella, salmonella, campylobacter: e.g. food poisoning
Clostridium difficle: e.g. associated with antibiotic use and hospital admission
Norovirus: e.g. outbreaks in care homes, schools, cruise ships
Giardia: e.g. parasite from infected water

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15
Q

What are some associated symptoms of diarrhoea?

A

Fever
Vomiting
Pain
Weight loss
Dehydration
Anaemia
Abdominal/rectal masses
Nocturnal diarrhoea
Stress/anxiety
Blood in stools (likely to be campylobacter, shigella, salmonella, E.coli, IBD, or colorectal cancer)
Mucus in stools (likely to be IBS or colorectal cancer)

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16
Q

What are the investigations needed for diarrhoea?

A

Faecal sample for microbiology, calprotectin, and blood
FBC: anaemia
TFTs
ESR/CRP: raised in inflammation
Antibodies for coeliac disease
Sigmoidoscopy/colonoscopy: detect malignancies/inflammation

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17
Q

What are the treatments of diarrhoea?

A

Treat the cause
Rehydration: oral is best, but IV if vomiting
Electrolyte replacement
Drugs: codeine phosphate or loperamide, avoid antibiotics unless infective diarrhoea causes systemic symptoms
Public health indication: high-risk people (food handlers, healthcare workers, care home residents), food poisoning, outbreaks in community or hospitals

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18
Q

Describe the epidemiology of GI cancers

A

More common in men
Distribution increases with age
Increasing incidence of oesophageal and colorectal cancers, but decreasing incidence of gastric cancer
Low survival rate due to late presentation (colorectal cancer has higher survival rates than others)

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19
Q

Describe the disease progression of oesophageal cancer

A

Gastroesophageal reflux causes normal oesophageal squamous epithelium to change to metaplastic oesophageal glandular epithelium (same as stomach lining)
Continued reflux and other factors change this into dysplastic oesophageal glandular epithelium, then neoplastic oesophageal glandular epithelium

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20
Q

What are the risk factors associated with oesophageal cancer

A

Smoking
Heavy alcohol
Severe reflux
Obesity

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21
Q

Describe the disease progression of gastric cancer?

A

Smoked/pickled food, preserved meat, helicobacter pylori, and pernicious anaemia causes intestinal metaplasia of the normal gastric mucosa
Genetic changes cause dysplasia, then changes to intramucosal carcinoma, then to invasive carcinoma

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22
Q

Describe the disease progression of colorectal cancer

A

Polyps (adenomas) develop on the normal epithelium (e.g. in IBD, prevented with NSAIDs), these can develop into adenocarcinomas (treated with surgical resection), then metastatic colorectal adenocarcinoma (treated with chemotherapy and palliative care)

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23
Q

Define familial adenomatous polyposis

A

An inherited condition causing 1000s of polyps to develop due to a mutation of the adenomatous polyposis coli gene causing high levels of beta catenin which enters the nucleus and damages DNA
If not removed, will lead to colorectal cancer in their early 20s

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24
Q

Define hereditary nonpolyposis colorectal cancer (HNPCC)

A

An inherited condition caused by an absent DNA repair protein gene and mutation in the other gene, which stops the repair of DNA and leads to colorectal cancer

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25
Define coeliac disease
An immune-mediated disorder, characterised by inflammatory small bowel enteropathy triggered by a dietary gluten
26
What causes coeliac disease?
Genetic factors predispose some individuals to coeliac disease, causing an abnormal T-cell response to gluten in the small bowel, resulting in villous atrophy and malabsorption
27
What are the associations of coeliac disease?
T1DM Primary biliary/sclerosing cholangitis Dermatitis herpetiformis Autoimmune hepatitis
28
Describe the epidemiology of coeliac disease
Can affect any age (but peaks in childhood and 50-60y/o) Slightly more common in females Increased risk if a 1st degree relative is affected
29
Describe the sings/symptoms of coeliac disease?
Diarrhoea Steatorrhoea Abdominal pain Bloating Nausea + vomiting Weight loss Fatigue + weakness (anaemia) Angular stomatitis Osteomalacia/osteoporosis
30
What are the investigations needed for coeliac disease?
FBC: low Hb (anaemia) Serum B12 and folate: low Antibodies: positive IgA tissue transglutaminase antibody (tTGA), or IgG endomysial antibody (EMA) if IgA deficient LFTs: raised Biopsy: diagnostic
31
What are the treatments for coeliac disease?
Life-long gluten free diet Referral to dietitian (if concerned about intentional or inadvertent gluten exposure) Nutritional supplements if not responsive/adherent to gluten-free diet DEXA scans to assess bone density
32
What are the complications of coeliac disease?
Reduced quality of life (social implications of gluten-free diet) Depression, anxiety, and eating disorders Faltering growth and delayed puberty in childhood Nutritional deficiencies and anaemia due to malabsorption Reduced bone density causing osteoporosis Hyposplenism (increasing risk of infection) Infertility Malignancy (increased risk of lymphoma)
33
Define irritable bowel syndrome
A mixed group of chronic abdominal symptoms often exacerbated by stress, for which no organic cause can be found, classified as a functional gut disorder/disorder of gut-brain-interaction
34
What are the causes of irritable bowel syndrome?
Abnormal gut-brain interactions Visceral hypersensitivity Motility disturbances Altered immune function or gut microbiome *Unknown pathophysiology but thought to have biological, psychological, and social factors
35
What are the signs/symptoms of irritable bowel syndrome
Diarrhoea (subtype = IBS-D) Constipation (subtype = IBS-C) *sub type IBS-M = mixed, fluctuating between diarrhoea and constipation, or sub type IBS-U = unclassified Abdominal pain: - associated with change in stool type/frequency - relieved by defaecation Abdominal bloating/distension Mucus in stools Extra-intestinal symptoms: lethargy, nausea, back pain, headache, gynaecological, bladder symptoms
36
What are the investigations needed for IBS?
FBC, B12, folate: normal (rules out anaemia) CRP: normal (rules out inflammation/infection) Coeliac serology: normal (rules out coeliac disease) Stool faecal calprotectin: normal (rules out IBD) Stool microbiology: normal (rules out infection) In women, CA-125: normal (rules out ovarian cancer) With alarm features: colonoscopy, CT (if suspecting cancer)
37
What are the alarm features of irritable bowel syndrome?
Age >45 Short history of symptoms Unintentional weight loss Nocturnal symptoms Family history of GI cancer/IBD GI bleeding Abdominal mass/lymphadenopathy Evidence of iron deficient anaemia/inflammation
38
What are the treatments for irritable bowel syndrome?
Patient education and lifestyle advice (diet, fluid intake, exercise, stress) Pharmacological based on symptoms: e.g. laxatives for constipation, loperamide (antimotility) for diarrhoea, then neuromodulator (amitriptyline) Psychological therapies: CBT, gut hypnotherapy
39
Define GORD
Gastro-oesophageal reflux disease is a chronic condition of reflux of the gastric contents back into the the oesophagus, causing dyspepsia (upper GI symptoms e.g. heartburn, acid regurgitation)
40
What are the causes of GORD?
Transient relaxation (reduced tone) of the lower oesophageal sphincter (e.g. drugs, trigger foods) Increased intra-gastric pressure (e.g. straining/coughing/pregnancy) Delayed gastric emptying (e.g. diabetes, drugs) Smoking/alcohol
41
What are the risk factors for GORD?
Stress/anxiety Smoking and alcohol Trigger foods (e.g. coffee reduces lower oesophageal sphincter tone, fatty foods delay gastric emptying) Obesity Drugs that decrease lower oesophageal sphincter tone (e.g. anticholinergics, nitrates, tricyclics, NSAIDs) Pregnancy Hiatus hernia Family history
42
What are the signs/symptoms of GORD?
Heartburn (retrosternal burning after meals, lying, straining, reduced by antacids) Belching Acid +/- bile regurgitation Increased saliva Pain when swallowing Extraoesophageal symptoms: chronic cough, hoarseness, asthma
43
What are the investigations needed for GORD?
Endoscopy: if over 55 or alarm symptoms, may show oesophagitis (inflammation and mucosal erosions) 24h oesophageal pH monitoring Oesophageal manometry
44
What are the treatments for GORD?
Lifestyle changes: smoking cessation, weight loss, reduce trigger foods/drinks, eat smaller meals, avoid eating <3h before bed Pharmacological: antacids (e.g. gaviscon), PPIs (e.g. lansoprazole), H2 blocker (e.g. ranitidine) Surgical: laparoscopic fundoplication
45
What are the complications of GORD?
Oesophageal ulcers, haemorrhage, stricture Anaemia Barrett's oesophagus (columnar metaplasia of the distal oesophagus with malignant potential and progression to adenocarcinoma)
46
Define peptic ulcers
A breach in the epithelium of the gastric or duodenal mucosa which is confirmed with endoscopy, causing dyspepsia (upper GI symptoms e.g. epigastric pain)
47
What are the causes of peptic ulcers?
Increased acid (e.g. certain foods, stress, Zollinger-Ellison syndrome) Bile reflux Decreased defence from mucin (e.g. mucosal ischemia, or genetic cause of change in constancy) H. pylori infection Smoking and alcohol Drugs (NSAIDS, steroids)
48
What are the signs/symptoms of peptic ulcers?
Can be asymptomatic or non-specific Epigastric pain (after eating, relived by food and antacids) Nausea Belching Heartburn (more commonly associated with GORD) Weight loss
49
What investigations are needed for peptic ulcers?
FBC: iron-deficiency anaemia H. pylori testing Endoscopy (if over 55 or alarm symptoms)
50
What are the treatments for peptic ulcers?
Lifestyle changes: avoid drug causes, smoking cessation Treat H. pylori infection PPIs (e.g. lansoprazole) or H2 blocker (ranitidine) to reduce acid and treat ulcers Endoscopic intervention to treat bleeding ulcers
51
What are the complications of peptic ulcers?
Erosion of blood vessels leading to haematemesis or melaena (upper GI bleed) Perforation (causing acute abdomen) Scarring of the duodenum (leading to pyloric stenosis and reduced gastric outflow) Malignancy (increased risk with H. pylori infection
52
Define gastritis
Inflammation of the gastric mucosa, causing dyspepsia (upper GI symptoms e.g. epigastric pain, vomiting)
53
What are the causes of gastritis
H. pylori infection Alcohol NSAIDs Increased acid production (Zollinger-Ellison syndrome) Bile reflux Stress Autoimmune
54
What are the signs/symptoms of gastritis
Can be asymptomatic Epigastric pain Nausea and vomiting Loss of appetite Feeling full soon during/after a meal Bloating
55
What are the investigations needed for gastritis?
FBC: may show anaemia H. pylori testing Endoscopy (if over 55 or alarm symptoms)
56
What are the treatments for gastritis?
Lifestyle changes: smoking cessation, alcohol abstinence, avoid trigger foods, eater smaller meals, reduce stress) Avoid drug causes Treat H. pylori infection Drugs: antacids, PPI (e.g. lansoprazole), H2 blocker (e.g. ranitidine)
57
What are the complications of gastritis?
Gastric ulcers
58
What are the alarm features of dyspepsia (GORD, gastritis, peptic ulcers)?
ALARMS Anaemia (iron deficient) Loss of weight Anorexia Recent onset/progression Melaena/haematemesis Swallowing difficulties
59
How is H. pylori tested for?
Carbon-13 breath test Stool antigen Serology
60
What are the treatments for H. pylori infection?
PPI (e.g. lansoprazole) 2 antibiotics (e.g. amoxicillin/clarithromycin)
61
Define appendicitis
Acute appendicitis is the sudden inflammation of the appendix, usually due to obstruction of the lumen
62
Describe the pathophysiology of appendicitis?
The aetiology and pathogenesis is largely unknown, but 50% of cases are caused by luminal obstruction due to... - faecolith (hard mass of faecal matter) - lymphoid hyperplasia - foreign body - tumour Luminal obstruction leads to... - increased mucus production - bacterial overgrowth - impaired lymphatic and venous drainage - eventual ischemia and necrosis
63
Describe the epidemiology of appendicitis?
It is the most common surgical emergency Highest incidence is between 10 and 20 years old
64
What are the signs/symptoms of appendicitis?
Pain: - periumbilical, moving to right iliac fossa - aggravated by moving, coughing, breathing Nausea, vomiting, anorexia Constipation (sometimes diarrhoea) Fever (low-grade) Tachycardia Guarding and rebound tenderness in RIF
65
What investigations are needed for appendicitis?
Bloods: leucocytosis, raised CRP Imaging: US, CT Rule out: pregnancy, UTI
66
What are the treatments for appendicitis?
GOLD STANDARD: appendicectomy (in 10-20% of cases), often laparoscopic Antibiotics (for uncomplicated cases)
67
What are the complications of appendicitis?
Perforation (high risk in elderly people/young children) Appendix mass: omentum (fat layer) and small bowel adhere to appendix Appendix abscess Generalised peritonitis Sepsis Bowel obstruction
68
Define diverticular disease
Diverticular disease is the presence of symptomatic diverticula (outpouching of the gut wall) Diverticulosis is the presence of non-symptomatic diverticula Diverticulitis refers to the inflammation of diverticula (usually due to infection)
69
Describe the pathogenesis of diverticular disease
High intra-luminal pressures (e.g. due to low-fibre diet) prompts the herniation of the mucosa through the muscle layers of the gut at weak points adjacent to penetrating vessels
70
What are the risk factors for diverticular disease?
Older age Low-fibre diet Smoking Obesity NSAIDs and opioids Immunosuppression Genetic factors
71
What are the signs/symptoms of diverticular disease?
Pain: - lower left quadrant - intermittent - triggered by eating - relieved by passage of stool Nausea Bloating Altered bowel habits Rectal bleeding
72
What are the signs/symptoms of diverticulitis?
Pain: - hypogastrium or lower left quadrant - constant Fever Sudden change in bowel habits Significant rectal bleeding or mucus in stools Abdominal mass or distention
73
What are the investigations needed for diverticular disease/diverticulitis?
FBC: raised WBC in diverticulitis CRP: raised in diverticulitis DIAGNOSTIC = Imaging: colonoscopy, CT
74
What are the treatments of diverticular disease?
High-fibre diet Adequate fluid intake Avoid NSAIDs and opioids Laxatives Simple analgesia (e.g. paracetamol) Antispasmodics (e.g. mebeverine) Blood transfusion (if significant blood loss) Surgical resection (occasional)
75
What are the treatments for diverticulitis?
Mild attacks: bowel rest (fluid only) +/- antibiotics (co-amoxiclav), diet and lifestyle advice Managed in hospital (if pain not managed, hydration is not maintained, significant comorbidity): IV fluid and antibiotics, surgical resection, drainage
76
What are the complications of diverticular disease?
Perforation Haemorrhage Fistulae Abscesses Obstruction (strictures) Sepsis
77
Define inflammatory bowel disease
A chronic, relapsing-remitting inflammatory disease of the GI tract, categorised as ulcerative colitis or Chron's disease (or unclassified)
78
Describe the epidemiology of ulcerative colitis
Typically presents between 20-40 yrs
79
Describe the epidemiology of Chron's disease
Typically presents between 20-40 yrs, with 2nd peak at 60-80 yrs
80
Describe the pathophysiology of inflammatory bowel disease?
An abnormal immune response of inflammation to gut bacteria in genetically susceptible individuals, with environmental triggers
81
What are the risk factors for ulcerative colitis?
Family history Drugs (e.g. NSAIDs) *appendicectomy and smoking are protective
82
What are the risk factors for Chron's disease?
Family history Smoking Infectious gastroenteritis Appendicectomy Drugs (NSAIDs)
83
Describe the pathophysiology of ulcerative colitis
Superficial, continuous inflammation of the mucosa, only affecting the colon Histology: cryptitis, crypt abscesses
84
Describe the pathophysiology of Chron's disease
Transmural, patchy inflammation of the mucosa, affecting any part of the GI tract (most common site = terminal ileum and caecum) Histology: granulomas
85
What are the signs/symptoms of inflammatory bowel disease?
Non-specific: fatigue, malaise, anorexia, fever Diarrhoea (blood +/- mucus = UC more likely) Faecal urgency and/or incontinence Nocturnal defecation Abdominal pain (lower left quadrant, may improve after defecation) Abdominal distention/mass Weight loss Perianal fistulae/abscess Extraintestinal: clubbing, arthritis, osteoporosis, mouth ulcers, uveitis, erythema nodosum, ankylosing spondylitis
86
What are the investigations needed for inflammatory bowel disease?
FBC: check for anaemia CRP/ESR: raised with inflammation U&E: asses electrolytes and dehydration LFTs: abnormal suggests Chron's TFTs: rule out hyperthyroidism causing diarrhoea Coeliac serology: rule out coeliac disease Stool microscopy and culture: rule out C. diff and others Faecal calprotectin: raised with inflammation Colonoscopy/endoscopy and biopsy: diagnosis, differentiate between Chron's and UC, asses severity
87
What are the treatments of ulcerative colitis?
1. 5-aminosalicylates (e.g. mesalazine): 1st line for remission induction/maintenance 2. Corticosteroid (e.g. prednisolone): remission induction if not affective with 5-ASA 3. Immunosuppressants (e.g. methotrexate, thiopurines): maintain remission in more severe cases and if not maintained by 5-ASA 4. Anti-TNFs (e.g. infliximab): induce remission in severe active disease if conventional therapy is not effective/tolerated 5. Surgery: colectomy/terminal ileostomy
88
What are the treatments for Chron's disease?
1. Corticosteroids (e.g. prednisolone): induce remission, gradually taper dose, not used to maintain remission 2. Immunosuppressants (e.g. azathiopurine, or methotrexate): add to steroids, can be used for maintaining remission 3. Anti-TNFs (e.g. infliximab): for severe active disease or if conventional therapy is not effective/tolerated 4. 5-aminosalicylates (e.g. mesalazine): much less of a role than in UC, only used if steroids are contraindicated/not tolerated 5. Surgery: colostomy/ileostomy (permeant/temporary)
89
What are the complications of inflammatory bowel disease
Psychosocial impact Toxic dilation of the colon (risk of perforation) Bowel obstruction Intestinal strictures Fistulae Anaemia Malnutrition Colorectal cancer

Phase 2a (14 decks)

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