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Phase 2a > Gastroenterology > Flashcards

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
Q

Define coeliac disease

A

An immune-mediated disorder, characterised by inflammatory small bowel enteropathy triggered by a dietary gluten

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26
Q

What causes coeliac disease?

A

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

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27
Q

What are the associations of coeliac disease?

A

T1DM
Primary biliary/sclerosing cholangitis
Dermatitis herpetiformis
Autoimmune hepatitis

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28
Q

Describe the epidemiology of coeliac disease

A

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

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29
Q

Describe the sings/symptoms of coeliac disease?

A

Diarrhoea
Steatorrhoea
Abdominal pain
Bloating
Nausea + vomiting
Weight loss
Fatigue + weakness (anaemia)
Angular stomatitis
Osteomalacia/osteoporosis

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30
Q

What are the investigations needed for coeliac disease?

A

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

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31
Q

What are the treatments for coeliac disease?

A

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

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32
Q

What are the complications of coeliac disease?

A

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)

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33
Q

Define irritable bowel syndrome

A

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

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34
Q

What are the causes of irritable bowel syndrome?

A

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

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35
Q

What are the signs/symptoms of irritable bowel syndrome

A

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

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36
Q

What are the investigations needed for IBS?

A

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
Q

What are the alarm features of irritable bowel syndrome?

A

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
Q

What are the treatments for irritable bowel syndrome?

A

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
Q

Define GORD

A

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
Q

What are the causes of GORD?

A

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
Q

What are the risk factors for GORD?

A

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
Q

What are the signs/symptoms of GORD?

A

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
Q

What are the investigations needed for GORD?

A

Endoscopy: if over 55 or alarm symptoms, may show oesophagitis (inflammation and mucosal erosions)
24h oesophageal pH monitoring
Oesophageal manometry

44
Q

What are the treatments for GORD?

A

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
Q

What are the complications of GORD?

A

Oesophageal ulcers, haemorrhage, stricture
Anaemia
Barrett’s oesophagus (columnar metaplasia of the distal oesophagus with malignant potential and progression to adenocarcinoma)

46
Q

Define peptic ulcers

A

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
Q

What are the causes of peptic ulcers?

A

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
Q

What are the signs/symptoms of peptic ulcers?

A

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
Q

What investigations are needed for peptic ulcers?

A

FBC: iron-deficiency anaemia
H. pylori testing
Endoscopy (if over 55 or alarm symptoms)

50
Q

What are the treatments for peptic ulcers?

A

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
Q

What are the complications of peptic ulcers?

A

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
Q

Define gastritis

A

Inflammation of the gastric mucosa, causing dyspepsia (upper GI symptoms e.g. epigastric pain, vomiting)

53
Q

What are the causes of gastritis

A

H. pylori infection
Alcohol
NSAIDs
Increased acid production (Zollinger-Ellison syndrome)
Bile reflux
Stress
Autoimmune

54
Q

What are the signs/symptoms of gastritis

A

Can be asymptomatic
Epigastric pain
Nausea and vomiting
Loss of appetite
Feeling full soon during/after a meal
Bloating

55
Q

What are the investigations needed for gastritis?

A

FBC: may show anaemia
H. pylori testing
Endoscopy (if over 55 or alarm symptoms)

56
Q

What are the treatments for gastritis?

A

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
Q

What are the complications of gastritis?

A

Gastric ulcers

58
Q

What are the alarm features of dyspepsia (GORD, gastritis, peptic ulcers)?

A

ALARMS
Anaemia (iron deficient)
Loss of weight
Anorexia
Recent onset/progression
Melaena/haematemesis
Swallowing difficulties

59
Q

How is H. pylori tested for?

A

Carbon-13 breath test
Stool antigen
Serology

60
Q

What are the treatments for H. pylori infection?

A

PPI (e.g. lansoprazole)
2 antibiotics (e.g. amoxicillin/clarithromycin)

61
Q

Define appendicitis

A

Acute appendicitis is the sudden inflammation of the appendix, usually due to obstruction of the lumen

62
Q

Describe the pathophysiology of appendicitis?

A

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
Q

Describe the epidemiology of appendicitis?

A

It is the most common surgical emergency
Highest incidence is between 10 and 20 years old

64
Q

What are the signs/symptoms of appendicitis?

A

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
Q

What investigations are needed for appendicitis?

A

Bloods: leucocytosis, raised CRP
Imaging: US, CT
Rule out: pregnancy, UTI

66
Q

What are the treatments for appendicitis?

A

GOLD STANDARD: appendicectomy (in 10-20% of cases), often laparoscopic
Antibiotics (for uncomplicated cases)

67
Q

What are the complications of appendicitis?

A

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
Q

Define diverticular disease

A

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
Q

Describe the pathogenesis of diverticular disease

A

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
Q

What are the risk factors for diverticular disease?

A

Older age
Low-fibre diet
Smoking
Obesity
NSAIDs and opioids
Immunosuppression
Genetic factors

71
Q

What are the signs/symptoms of diverticular disease?

A

Pain:
- lower left quadrant
- intermittent
- triggered by eating
- relieved by passage of stool
Nausea
Bloating
Altered bowel habits
Rectal bleeding

72
Q

What are the signs/symptoms of diverticulitis?

A

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
Q

What are the investigations needed for diverticular disease/diverticulitis?

A

FBC: raised WBC in diverticulitis
CRP: raised in diverticulitis
DIAGNOSTIC = Imaging: colonoscopy, CT

74
Q

What are the treatments of diverticular disease?

A

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
Q

What are the treatments for diverticulitis?

A

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
Q

What are the complications of diverticular disease?

A

Perforation
Haemorrhage
Fistulae
Abscesses
Obstruction (strictures)
Sepsis

77
Q

Define inflammatory bowel disease

A

A chronic, relapsing-remitting inflammatory disease of the GI tract, categorised as ulcerative colitis or Chron’s disease (or unclassified)

78
Q

Describe the epidemiology of ulcerative colitis

A

Typically presents between 20-40 yrs

79
Q

Describe the epidemiology of Chron’s disease

A

Typically presents between 20-40 yrs, with 2nd peak at 60-80 yrs

80
Q

Describe the pathophysiology of inflammatory bowel disease?

A

An abnormal immune response of inflammation to gut bacteria in genetically susceptible individuals, with environmental triggers

81
Q

What are the risk factors for ulcerative colitis?

A

Family history
Drugs (e.g. NSAIDs)
*appendicectomy and smoking are protective

82
Q

What are the risk factors for Chron’s disease?

A

Family history
Smoking
Infectious gastroenteritis
Appendicectomy
Drugs (NSAIDs)

83
Q

Describe the pathophysiology of ulcerative colitis

A

Superficial, continuous inflammation of the mucosa, only affecting the colon
Histology: cryptitis, crypt abscesses

84
Q

Describe the pathophysiology of Chron’s disease

A

Transmural, patchy inflammation of the mucosa, affecting any part of the GI tract (most common site = terminal ileum and caecum)
Histology: granulomas

85
Q

What are the signs/symptoms of inflammatory bowel disease?

A

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
Q

What are the investigations needed for inflammatory bowel disease?

A

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
Q

What are the treatments of ulcerative colitis?

A
  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
Q

What are the treatments for Chron’s disease?

A
  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
Q

What are the complications of inflammatory bowel disease

A

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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