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Emily Phase 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What are the different symptoms for ulcerative colitis and Crohn’s?

A

UC
- bloody diarrhoea
- mucus
- weight loss
- abdominal pain

Crohn’s
- NON-bloody diarrhoea
- abdominal pain
- significant weight loss
- aphthous ulcers

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2
Q

What is the epidemiology of Crohn’s and UC?

A

Crohn’s = bimodal age distribution
UC = even spread across the ages

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3
Q

What is the aetiology of IBD?

A

combo of:
- bacteria
- environmental factors
- genetic susceptibility

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4
Q

What different effect does smoking have on UC and crohns?

A

UC = reduced risk
Crohn’s = increases risk

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5
Q

What is the difference in location of UC and Crohn’s?

A

UC
- starts in rectum + spreads proximally towards the ileocaecal valve
(never spreads into small bowel or anus)

Crohn’s
- any part of GI tract from mouth to anus
(MC is terminal ileum)

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6
Q

What is the difference in histology between UC and Crohn’s?

A

UC
- mucosal + submucosal ulceration only
- crypt abscess with neutrophil infiltration
- shallow ulcers with pseudopolyps

Crohn’s
- transmural inflammation (all layers + surrounding fat)
- granulomas
- increase in goblet cells
- skip lesions
- cobblestone mucosa
- deep ulcers

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7
Q

What are the different complications for UC and Crohn’s?

A

UC
- toxic megacolon (dilatation)
- strictures
- liver problems (inflammation, fibrosis)
- problems in joints
- problems in eyes (iritis, uveitis)
- problems in skin

Crohn’s
(mainly in bowel)
- fissures
- fistulas
- strictures

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8
Q

What does a ‘lead pipe’ bowel on a CT signify?

A

UC
- colon loses haustra and looks very straight due to dilation

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9
Q

How does UC or Crohn’s affect risk for colorectal cancer?

A

UC = marked increase
Crohn’s = slight increase

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10
Q

What is the management for UC?

A
  • resuscitate
  • prophylactic LMWH (given to all hospital patients to reduce risk of DVT)
  • IV steroids
  • monitor BM
  • stool cultures
  • stool chart
  • AXR
  • flexible sigmoidoscopy
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11
Q

What are the key things to remember for Crohn’s? (mnemonic)

A

NESTS
N- No blood or mucus
E- entire GI tract
S- Skip lesions
T- Terminal ileum and transmural
S- Smoking is a big risk factor

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12
Q

What it the Truelove and Witts criteria for UC?

A

> 6 bloody stools/day AND
Tachycardia >90bpm OR
pyrexia >37.8 OR
Hb<10.5g/dl OR
ESr >30 mm/h OR

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13
Q

What are the surgery options for UC and Crohn’s?

A

UC = surgery is curative
Crohn’s = only use surgery for complications such as strictures

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14
Q

When and what surgery could be used to treat Crohn’s?

A

When distal ileum is inflamed can surgically resect the area to prevent flare ups

Also used to treat strictures and fistulas

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15
Q

What antibodies are found in patients with UC?

A

p-ANCAs -perinuclear antineutrophilic cytoplasmic antibodies) in their blood - antibodies that target antigens in the body’s own neutrophil

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16
Q

What are the key things to remember for UC? (mnemonic)

A

CLOSEUP
C- Continuous inflammation
L- Limited to colon and rectum
O- only superficial
S- Smoking protects
E- Excrete blood and mucus
U- Use Aminosalicylate
P- Primary sclerosis cholangitis

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17
Q

What are the extra intestinal signs of IBD?

A

A PIE SAC
- Ankylosing spondylitis (HLA B27! - spine + other areas become inflamed)
- Pyoderma gangrenosum (painful nodules become ulcers)
- Iritis (aka anterior uveitis - inflammation of iris)
- Erythema nodosum (swollen fat under the skin causing bumps)
- Sclerosing cholangitis
- Aphthous ulcers / amyloidosis
- Clubbing

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18
Q

How common is cancer in the small intestine? and what are the types?

A

SI relatively resistant to the development of neoplasia.

Types: adenocarcinomas (MC) or lymphomas

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19
Q

What are the RF for small intestine cancer?

A

Coeliac disease
Crohn’s disease

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20
Q

What is the difference between ulcerative and granulomous inflammation?

A

Ulcer = can be caused by bacteria, NSAIDs etc.
Granuloma = chronic inflammation with build up of macrophage surrounded by lymphocytes

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21
Q

What are the investigations for small intestine cancer?

A

Ultrasound
Endoscopic biopsy = histology
CT scan = may show wall thickening + lymph node involvement

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22
Q

What are the types of benign oesophageal cancer?

A

Leiomyomas (MC), papillomas, fibrovascular polyps, haemangiomas, lipomas

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23
Q

What are leiomyomas?

A

A benign smooth muscle tumour

Occur in the oesophageal wall, stomach, bladder, intestine, uterus

  • They are intact, well encapsulated and are within the overlying mucosa
  • Slow growing
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24
Q

What are the symptoms of benign oesophageal cancers?

A

Usually asymptomatic
Dysphagia, retrosternal pain, food regurgitation, recurrent chest infections

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25
Q

What are FAP and HNPCC in colorectal cancer?

A

Both autosomal dominant mutations that increase chance of getting colorectal cancer

FAP = familial adenomatous polyposis

HNPCC = Hereditary non-polyposis colon cancer/ Lynch syndrome

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26
Q

What is the difference in genotype of FAP and HNPCC?

A

FAP
- loss of function mutation in a tumour suppressor on chromosome 5

HNPCC
- mutations in DNA mismatch repair genes lead to microsatelltite instability

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27
Q

What are different colon locations that FAP and HNPCC affect?

A

FAP = left colon + rectum

HNPCC = right colon

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28
Q

What are the different rates of transformation to colorectal cancer for FAP and HNPCC?

A

FAP = 100% colon/rectal cancer
- patients usually have a total colectomy + ileo-anal pouch in 20-30s

HNPCC = 50-80% colon cancer
- right sided poorly differentiated, right sided mutinous or adenocarcinoma

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29
Q

What can reduce absorption?

A
  • coeliac
  • crohns
  • short bowel syndrome
  • parasites (guardia lambia)
  • infarcted small bowel
  • SI resection or bypass
  • lack of enzymes (lactose intolerant)
  • lymphoma obstruction
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30
Q

When would a small intestine resection occur?

A
  • procedure for morbid obesity
  • crohn’s disease
  • infarcted all bowel
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31
Q

What defective epithelial transporters reduces absorption?

A
  • abetalipoproteinemia
  • primary bile acid malabsorption

(inherited disorder that impairs the normal absorption of fats and certain vitamins)

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32
Q

What are gallstones?

A
  • cholesterol supersaturation
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33
Q

Why do people get gallstones?

A
  • diet/weight loss
  • hormonal influence
  • haemolytic anaemias
  • genetics (genes that code for reduced smooth muscle motility)
  • cirrhosis
  • sickle cell
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34
Q

What causes bile to be released?

A

Responds to CCK and then is released from the gallbladder into duodenum

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35
Q

How do you diagnose someone with coeliac disease?

A

1) Gluten challenge = 6 week gluten containing diet to see if they have villous atrophy when they eat gluten

(villious atrophy, crypt hyperplasia, intraepithelial lymphocytes)

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36
Q

What is the management for coeliac disease?

A
  • strict gluten free diet
  • dietitian review
  • bone density assessment
  • coeliac UK info
  • immunisations
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37
Q

What are the genes that can cause coeliac disease?

A

HLA-DQ2
HLA-DQ8

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38
Q

What are the two auto-antibodies associated with coeliac disease?

A

Anti-TTG
Anti-EMA

These antibodies relate to disease activity and will rise with more active disease and may disappear with effective treatment.

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39
Q

What are the risks of not going gluten free?

A
  • enteropathy associated T-cell lymphoma
  • small bowel adenocarcinoma
  • vitamin deficiencies
  • osteoporosis
  • hyposplenism
  • malnutrition
  • infertility
  • depression
  • delayed puberty
  • anaemia
  • iron + folate deficiencies
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40
Q

What other conditions can be improved by going gluten free?

A

Hashimoto’s thyroiditis
T1DM
Sjogren’s syndrome (affects moisture producing glands)
Primary biliary cholangitis
Primary sclerosing cholangitis
Autoimmune hepatitis
Dermatitis herpetiformis

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41
Q

What happens in someone with coeliac disease?

A

Inflammation affects the small intestine particularly the jejunum. This causes atrophy of the intestinal villi and crypt hypertrophy

These villi are used to help absorb nutrients so coeliac will result in malabsorption.

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42
Q

What are the extra intestinal symptoms of coeliac disease?

A

Dermatitis herpetiformis (blistering skin condition)
Angular stomatitis (red sore corners of mouth)
Mouth ulcers
failure to thrive

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43
Q

What are the intestinal symptoms of coeliac disease?

A

Diarrhoea
Weight loss
Bloating
B12 deficiency

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44
Q

What 2 things are needed to indicate coeliac disease?

A
  • IgA-tTG (detect IgA deficiency)
  • villous atrophy
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45
Q

Define functional gut disorders

A

Chronic GI symptoms in the absence of organic disease to explain the symptoms
e.g. IBS, functional dyspepsia (stomach)

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46
Q

What are some of the causes of functional gut disorders?

A
  • visceral hypersensitivity
  • motility disturbances
  • altered mucosal + immune function
  • altered CNS processing
  • Altered gut microbiota
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47
Q

What is functional dyspepsia?

A
  • signs and symptoms of indigestion that have no obvious cause
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48
Q

What are the symptoms of IBS?

A
  • chronic frequent abdominal pain
  • altered bowel habit
  • bloating commonly associated
  • symptoms relieved by opening bowel
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49
Q

What are the differential diagnosis of IBS?

A
  • coeliac disease
  • IBD
  • colorectal cancer
  • ovarian cancer
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50
Q

What are the alarm features that it might be more serious than IBS?

A
  • age >45 yrs
  • short history of symptoms
  • unintentional weight loss
  • nocturnal symptoms
  • family history of GI cancer/IBD
  • GI bleeding
  • palpable abdominal mass or lymphadenopathy
  • evidence of Fe anaemia
  • evidence of inflammation on blood/stool testing
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51
Q

How to make a diagnosis of IBS?

A
  1. history
  2. examination
  3. 1st line: FBC, CRP, stool faecal calprotectin (indicate inflammation), coeliac serology
  4. if alarm features = endoscopy, ultrasound
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52
Q

What is faecal calprotectin?

A

Attracted into bowel from blood by high volume of WBCs in bowel
- indicates inflammation

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53
Q

What is post infectious IBS?

A

After having food poisoning, gastroenteritis or another infection can trigger symptoms of IBS

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54
Q

What is the function of the peritoneum?

A

In health:
Visceral lubrication
Fluid and particulate absorption

In disease:
Pain perception.
Inflammatory and immune responses
Fibrinolytic activity

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55
Q

What is peritonitis?

A

Inflammation of the peritoneum

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56
Q

What are the causes of peritonitis?

A

Bacterial, gastrointestinal and non-gastrointestinal
Chemical, e.g. bile, barium
Traumatic, e.g. operative handling
Ischaemia, e.g. strangulated bowel, vascular occlusion
Miscellaneous, e.g. familial Mediterranean fever

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57
Q

What are the pathways that infection can spread to the peritoneum?

A

Gastrointestinal perforation, e.g. perforated ulcer, appendix, diverticulum
Transmural translocation (no perforation), e.g. pancreatitis, ischaemic bowel, primary bacterial peritonitis
Exogenous contamination, e.g. drains, open surgery, trauma, peritoneal dialysis
Female genital tract infection, e.g. pelvic inflammatory disease
Haematogenous spread (rare), e.g. septicaemia

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58
Q

What are the clinical features of localised peritonitis?

A

S&S of the underlying condition
Pain
Nausea and vomiting
Fever
Tachycardia
Localised guarding (involuntary contraction of the abdominal wall)
Rebound tenderness
Shoulder tip pain ( subphrenic)
Tender rectal and / or vaginal examination (pelvic peritonitis).

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59
Q

What are the clinical features of diffuse/generalised late peritonitis?

A

Generalised rigidity
Destension
Absent bowel sounds
Circulatory failure
Thready irregular pulse
(Hippocratic face - the face as death approaches, sunken eyes and mouth)
Loss of consciousness

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60
Q

What are the clinical features of generalised early peritonitis?

A

Abdominal pain ( worse by moving or breathing)
Tenderness
Generalised guarding
Infrequent bowel sounds cease ( paralytic ileus)
Fever
Tachycardia

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61
Q

What are the investigations for peritonitis?

A

Urine dipstix for urinary tract infection.
ECG if diagnostic doubt (as to cause of abdominal pain) or cardiac history.
Bloods:
U&Es
Full blood count (WCC)
Serum amylase (acute pancreatitis/ others like perf DU)
Group and save - identify blood group + checks for antibodies that will affect a future transfusion

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62
Q

What is the management for peritonitis?

A

CORRECTION OF FLUID LOSS AND CIRCULATING VOLUME

URINARY CATHETERISATION ± GASTROINTESTINAL DECOMPRESSION

ANTIBIOTIC THERAPY

ANALGESIA

Surgical = repair perforation, drainage, peritoneal lavage

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63
Q

What are different special forms of peritonitis?

A

Bile peritonitis (bile leaks)
Spontaneous bacterial peritonitis (infection of ascitic fluid)
Primary pneumococcal peritonitis (genital infection in young girls)
Tuberculous peritonitis (TB of GI spread through hematogenous route or perforation)
Familial Mediterranean fever (periodic peritonitis - hereditary inflammatory disorder)

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64
Q

What is ascites?

A

An accumulation of excess serous fluid within the peritoneal cavity.

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65
Q

What are the 4 classification of ascites?

A

Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
Stage 2 easily detectable but of relatively small volume.
Stage 3 obvious, not tense ascites. (moderate)
Stage 4 tense ascites. (Large)

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66
Q

What are the transudates causes of ascites?

A

Transudates (protein <25g/L)

(-trans = moves across membrane + think causes of fluid shifting)
- Low plasma protein concentrations: Malnutrition
- Nephrotic syndrome Protein-losing enteropathy
- High central venous pressure: Congestive cardiac failure
- Portal hypertension: Portal vein thrombosis /Cirrhosis

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67
Q

What are the exudate causes of ascites?

A

Exudates (protein >25g/L)
Peritoneal malignancy
Tuberculous peritonitis
Budd–Chiari syndrome (hepatic vein occlusion or thrombosis)
Pancreatic ascites
Others: Chylous ascites, Meigs’ syndrome

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68
Q

What is the main cause of ascites?

A

cirrhosis

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69
Q

What is the clinical presentation of ascites?

A
  • abdominal distension (gaining weight)
  • nausea, LOA
  • constipation
  • cachexia - wasting?
  • pain/discomfort = malignant or non-malignant
  • puddle sign
  • shifting dullness (moves as fluid moves around)
  • flank dullness (due to fluid pooling at bottom of stomach)
  • fluid thrill/wave (in large ascites, tap on one side and feel fluid vibration at hand on other side of stomach)
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70
Q

What are the investigations for ascites?

A
  • underlying cause (LFTs, cardiac function)
  • Imaging (X-ray, ultrasound, CT)
  • ascitic aspiration
  • fluid for microscopy, cytology culture
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71
Q

What is the treatment for ascites?

A
  • Treatment of the specific cause
  • Sodium restriction
  • Diurectics
  • Paracentesis (up to 4-6 L / day with colloid replacement - drain)
  • Indwelling drain ( home paracentesis , smaller volumes)
  • Peritoneovenous shunting ( for rapidly accumulating ascites: abandoned)
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72
Q

What are the Duke stagings for Bowel cancer?

A

A = limited to submucosa
B = limited to muscular layer
C = spread to at least 1 lymph node
D = Distant metastatic spread

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73
Q

Which part of the GI tract does coeliac disease affect?

A

Small intestine

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74
Q

What is pseudomembranous colitis?

A

Severe inflammation of the colon lining after taking antibiotics
- normally due to a rise in C.difficile bacteria, that then cause inflammation

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75
Q

What are owl eye inclusions bodies and what do they signify?

A

Nuclei of cells infected by CMV (cytomegalovirus)
- usually in immunosuppressed patients

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76
Q

What is Zenker’s diverticulum?

A

(pharyngeal pouch)
- some food goes down pouch instead of totally down the oesophagus

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77
Q

What are the symptoms of Zenker’s diverticulum?

A

Smelly breath - food is accumulating in oesophagus
Regurgitation and aspiration of food

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78
Q

What is Meckel’s diverticulum?

A

Commonest congenital malformation of the small bowel
- failure of vitelline duct to obliterate so an intestinal pouch forms

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79
Q

What are the complications of meckel’s diverticulum?

A

Majority are asymptomatic
- GI bleeding, obstruction, inflammation or perforation

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80
Q

What is the treatment for meckel’s diverticulum?

A

surgical resection, either with a laparoscopic or open approach

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81
Q

What are the causes of acute gastritis?

A

H.Pylori infection
Alcohol abuse
Stress (critically ill/post surgery)
NSAIDs

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82
Q

What are the causes of chronic gastritis?

A

H.Pylori infection
Autoimmune gastritis (parietal and intrinsic factor antibodies)

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83
Q

How does H.Pylori cause gastritis?

A
  • It produces urease which converts urea to ammonia and CO2 which is toxic since the ammonia will react with HCL to form ammonium.
  • The ammonium will damage the gastric mucosa resulting in less mucus production
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84
Q

What are the clinical manifestations of gastritis?

A

Nausea
Abdominal bloating
Vomiting
Epigastric pain
Indigestion
Haematemesis- “coffee ground” vomiting and melaena
Iron deficiency anaemia due to constant bleeding

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85
Q

What is the general investigation for gastritis?

A

Endoscopy will show gastric inflammation and atrophy

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86
Q

How would you test for autoimmune gastritis?

A

Testing for autoimmune gastritis

  • Look for anti-IF (intrinsic factor) antibody and anti-parietal cell antibodies
  • Raised gastrin levels, reduced pepsinogen
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87
Q

What are the tests for H.Pylori?

A
  • CLO test Urea breath test
  • Stool antigen test

Before testing, stop PPI for at least 2 weeks; antibiotics for 4 weeks

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88
Q

How would you treat gastritis not caused by H.Pylori?

A
  • Remove causative agents such as alcohol/NSAIDs
  • Reduce stress
  • H2 antagonists e.g. ranitidine or cimetidine - to reduce acid release
  • PPIs e.g. lansoprazole or omeprazole - to reduce acid release
  • Antacids - neutralise acid to relieve symptoms
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89
Q

How do you treat a H.Pylori infection?

A

Triple threat (PPI and 2 antibiotics) twice a day for 7 days
- 1st line PPI, 1g amoxicillin and clarithromycin 500mg

If penicillin allergy then give metronidazole 400mg as well as instead

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90
Q

What are the complications of gastritis?

A

Peptic ulcers
Bleeding and anaemia
MALT lymphoma (mucosa-associated lymphoid tissue)
Gastric cancer

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91
Q

What is Peptic ulcers disease?

A

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter.

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92
Q

What are more common gastric or duodenal ulcers?

A

Duodenal ulcers are more common than gastric ulcers.

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93
Q

What drugs can cause Peptic Ulcer Disease?

A
  • NSAIDs inhibit COX enzyme which is needed for prostaglandin synthesis
  • SSRIs, steroids and bisphosphonates can also cause as they break down the protective layer
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94
Q

What lifestyle factors can cause Peptic Ulcer Disease?

A

Smoking and alcohol: may lead to increased acid.
Caffeine: may lead to increased acid.
Stress: may lead to increased acid.

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95
Q

What other health conditions can cause PUD?

A
  • Zollinger-Ellison syndrome:a gastrinoma (tumour) that results in numerous peptic ulcers due to elevated gastrin levels
  • Blood type O
  • Raised intracranial pressure:causes vagal stimulation which increases acid production (Cushing’s ulcer).
  • Severe burn: hypovolaemia secondary to a burn causes reduced perfusion of the stomach leading to necrosis (Curling ulcer)
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96
Q

What are the signs of PUD?

A

Hypotension and tachycardia
Epigastric tenderness

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97
Q

What are the symptoms of PUD?

A

Burning epigastric pain
Nausea
Hematemesis or melaena- caused by the perforation of an artery
Indigestion (Dyspepsia)
Reduced appetite

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98
Q

What is the gold standard test for PUD?

A

Endoscopy and biopsy.
It excludes malignancy. Will not be performed for non-bleeding ulcers

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99
Q

What is used to stratify the risk for a GI bleed?

A

Glasgow Blatchford score

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100
Q

What factors are considered in the Glasgow Blatchford S?

A

HB
Urea
BP
Gender
Tachycardia
Melaena
Syncope
Hepatic disease history
Cardiac failure present

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101
Q

What is the difference in pain onset between a gastric and duodenal ulcer?

A

Gastric ulcer is worse straight after eating and duodenal is better 1-2 hours after eating but then worsens 2 hours after

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102
Q

Which artery is perforated in gastric vs duodenal ulcers?

A

Gastric= Left gastric
Duodenal= Gastroduodenal

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103
Q

What are the signs of perforation in gastric vs duodenal ulcers?

A

Gastric= haematemesis and melena
Duodena= Melaena and haematochezia (fresh blood through anus)

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104
Q

How would you treat an active peptic ulcer bleed?

A

First line:
- IV crystalloid
- Blood transfusion
- Endoscopy
- High dose IV PPI

Second line
Surgery or embolization (blocking abnormal vessels) by interventional radiology: reserved for cases where adequate haemostasis is not achieved at endoscopy

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105
Q

What are the complications of PUD?

A
  1. Perforation: life-threatening as ulcer penetrates the duodenum or stomach into the peritoneal cavity causing peritonitis. May also allow air to collect under the diaphragm and irritate the phrenic nerve causing referred shoulder pain. Requires surgical intervention!
  2. Gastric outlet obstruction/ pyloric stenosis: caused by obstruction of the pylorus due to an ulcer and subsequent scarring. Presents with abdominal pain, distension, vomiting and nausea after eating
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106
Q

What is GORD?

A

Reflux of stomach contents into the oesophagus.

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107
Q

What are the lifestyle risk factors for developing GORD?

A

Obesity
Pregnancy
Smoking
NSAIDs, caffeine and alcohol

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108
Q

What are the biological risk factors for GORD?

A
  • Hiatus hernia- pushes the stomach up into the diaphragm
  • Male sex
  • Scleroderma: muscle of the lower oesophageal sphincter is replaced by connective tissue, so it can’t contract properly.
  • Zollinger-Ellison syndrome: increased gastrin causes increased HCl secretion
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109
Q

Describe the pathophysiology of GORD?

A
  1. When there is very low pressure in the oesophagus reflux will persist for longer becoming pathological.
  2. Persistent acid reflux damages the mucosa causing inflammation.
  3. This will eventually lead to oedema and erosion of the mucosa.
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110
Q

What happens to the oesophageal mucosa as GORD progresses?

A
  1. The epithelium will become damaged and replaced by scar, making the walls thicker and the lumen narrower
  2. As there is damage there will be metaplasia of the cells going from stratified squamous to simple columnar (Barret’s oesophagus).
  3. This can eventually lead to adenocarcinoma (3-5%)
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111
Q

What are the key symptoms of GORD?

A

Heart burn
Regurgitation which is worse when lying down

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112
Q

What are some other symptoms of GORD?

A

Epigastric pain
Dysphagia (difficulty swallowing)
Dyspepsia (indigestion)
Extra-oesophageal: cough, asthma, dental erosion

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113
Q

What are the initial investigations for GORD in people without red flag symptoms?

A

Can be diagnosed based on clinical presentation and based on whether PPI trial would resolve the symptoms
PH monitoring

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114
Q

What are the the red flag symptoms for GORD? (mnemonic)

A

ALARMS
A- Anaemia
L- Loss of weight
A- Anorexia
R- Recent onset
M- Melaena
S- Swallowing difficulties

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115
Q

When would you refer for 2 week endoscopy?

A

Dysphagia or
Age ≥ 55yo with weight loss and 1 of the following:
- Upper Abdo pain
- Reflux
- Dyspepsia

116
Q

What investigations would you perform for a clinical diagnosis of GORD?

A
  • FBC (anaemia)
  • 24-hour pH monitoring (pH <4 for more than 4% of the time is abnormal)
  • Upper GI endoscopy
  • Manometry (rule out motility disorders)
117
Q

What are lifestyle changes for managing GORD?

A

Weight loss
Reduce alcohol intake
Eat smaller meals
Avoid eating before going to bed (no food 2 hours before bed)

118
Q

What are the medical managements for GORD

A

PPI- this will lower acid production within the stomach

H2 receptor antagonist e.g., ranitidine reduces stomach acid

Antacids e.g., Gaviscon

119
Q

What is the surgical management for GORD?

A

Nissen fundoplication = wrapping the fundus of the stomach around the lower oesophagus to tighten the sphincter

120
Q

What is Barret’s oesophagus defined as?

A

Barrett’s oesophagus describes metaplasia (transformation of one differentiated cell type to another differentiated cell type) of the lower oesophageal lining from stratified squamous epithelium to mucous secreting columnar epithelium with goblet cells.

Barrett’s is classified as short segment (< 3 cm) and long segment (> 3 cm).

121
Q

What is appendicitis?

A

Acute appendicitis is an acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix.

122
Q

What are the different positions of the appendix?

A
  • Most commonly the descending intraperitoneal or retrocaecal position
  • Retrocaecal and pelvic appendicitis are often more difficult to distinguish clinically
123
Q

What causes appendicitis?

A
  1. Normally occurs due to luminal obstruction
  2. As the appendix continues to secrete mucus the fluid and mucus build up and increase the pressure this causes it to get bigger and push on the visceral nerve fibres causing pain
  3. This will lead to bacterial overgrowth
124
Q

What can cause the luminal obstruction in appendicitis?

A

Faecolith (hard mass of stool),
Undigested seeds,
Foreign body,
Pinworm infection,
Lymphoid hyperplasia of Peyer’s patches,
Fibrous strictures.

125
Q

What are the mechanisms of pain in appendicitis?

A
  • Peri-umbilical pain: inflammation of the appendix and visceral peritoneum irritates autonomic nerves of the embryological midgut → referred pain to the umbilical region
  • Right iliac fossa pain: due to localised inflammation of the parietal peritoneum
126
Q

What are the key presentations of appendicitis?

A

Central abdominal pain which migrates to the right iliac fossa, low-grade pyrexia and anorexia.

50% of patients present with this characteristic history

127
Q

What are the signs of appendicitis ?

A
  1. RIF pain on palpation worse when hand is released (rebound tenderness)
  2. Rovsing’s sign- pain in right iliac fossa is worsened by pressing on the left iliac fossa
  3. ** Psoas sign** pain is worse on hip extension
  4. Obturator sign pain is worse by flexing and inwardly rotating the hip
128
Q

What are the symptoms of appendicitis?

A
  • Periumbilical pain (referred pain) which migrates to the right iliac fossa (McBurney’s point)
  • Reduced appetite and anorexia
  • Nausea and vomiting
  • Diarrhoea
  • Low grade fever
129
Q

What are the investigations for appendicitis?

A

Blood test (WCC, ESR, CRP)
Abdominal US (in children and pregnant women)
Abdominal CT with contrast
Urinalysis (exclude UTI)
Pregnancy test

130
Q

What is guarding and rebound tenderness?

A

Guarding - when abdominal muscles tense up

Rebound tenderness - slow press on abdomen and then release quickly, pain felt on release of pressure (sign of peritonitis)

131
Q

What is the management for appendicitis?

A

Fluids
Analgesia
Antiemetics (ondansetron)
IV antibiotics pre surgery (ceftriaxone and metronidazole)

Prompt appendectomy

132
Q

What is diverticular disease?

A

Diverticular disease may be defined as any clinical state caused by symptoms pertaining to colonic diverticula and includes a wide-ranging spectrum from asymptomatic to severe and complicated disease

133
Q

What is diverticulosis?

A

The presence of diverticula (out-pouching) in an asymptomatic patient

134
Q

What is diverticulitis?

A

Diverticulitis refers to inflammation and infection of diverticula.

135
Q

Describe how diverticula form?

A
  • Large intestine contains areas of smooth muscle. Where this muscle is penetrated with blood vessels are areas of weakness.
  • Increased pressure in the lumen causes a gap to form in this muscle allowing the mucosa to herniate through. - It happens in areas that are not covered by teniae coli
136
Q

Why do diverticula not form in the rectum?

A

As the rectum has an extra layer of longitudinal muscle that surrounds it this adds extra support.

137
Q

Where is the most common area for the formation of diverticula?

A

Mainly form in sigmoid colon but can also affect right colon

138
Q

What are the risk factors for developing diverticular disease?

A

Increasing age
Low fibre diets
Obesity
NSAIDs
Smoking

139
Q

What can cause diverticulitis?

A
  • When faecal matter becomes lodged in the diverticula or more often due to the erosion of the diverticular wall from high luminal pressure
  • This can cause inflammation and the rupture of vessels leading to bleeding
140
Q

What are the symptoms of diverticular disease?

A

Bowel habits changed
Bloating + flatulence
Left lower quadrant pain
Nausea and vomiting

141
Q

What are the signs and symptoms of diverticulitis?

A
  • Pyrexia
  • Left lower quadrant or iliac fossa tenderness and guarding: in diverticulitis
  • Left iliac fossa tender mass: suggests an abscess (20%)
  • Rigidity, guarding, rebound or percussion tenderness: suggests perforation
  • Digital rectal examination: fresh blood and pelvic tenderness
  • Tachycardia and hypotension: if septic
142
Q

What are the investigations for diverticular disease?

A
  • Examinations: tenderness and guarding, distended and tympanic to percussion, no bowel sounds
  • FBC will show inflammation
  • GOLD STANDARD = Contrast CT scan
143
Q

When should colonoscopy be used for diverticular disease?

A

Colonoscopy = should generally be avoided in acute diverticulitis due to the risk of perforation, and is used if the diagnosis is unclear or alternative pathology is suspected

144
Q

What is the management for mild diverticulitis?

A

Oral co-amoxiclav (at least 5 days)
Analgesia (avoiding NSAIDs and opiates, if possible)
Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
Follow-up within 2 days to review symptoms

145
Q

How would you manage severe diverticulitis?

A
  1. Supportive management:NBM, IV fluids and analgesia
  2. IV antibiotics:co-amoxiclav is typical but depends on local guidelines
  3. Acute PR bleeding: transfuse blood products and arrange angiographic embolization (blocks blood vessels) if available, otherwise, surgery is required
  4. Surgery
146
Q

What surgical procedure would be performed for diverticulitis?

A

Hartmann’s procedure = removing the affected section of the bowel and creating an alternative path for faeces to be passed

147
Q

What are the complications of diverticulitis?

A

Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage requiring blood transfusions
Fistula (e.g., between the colon and the bladder or vagina)
Ileus / obstruction

148
Q

What is a Mallory-Weiss tear (MWT)?

A

Mallory-Weiss tear (MWT) refers to longitudinal lacerations limited to the mucosa and submucosa, at the border of the gastro-oesophageal junction.

149
Q

What are the risk factors for MWT?

A

Persistent vomiting
Alcoholism
Chronic cough
Hiatus hernia
Heavy lifting or straining

150
Q

What causes a MWT?

A

A sudden rise in intra-abdominal and transmural pressure across the gastro-oesophageal junction secondary to wrenching or vomiting in the presence of a pre-existing damaged gastric mucous membrane, which is often related to alcoholism.

151
Q

What are the symptoms of MWT?

A

Fresh blood following period of vomiting particularly after drinking alcohol.
Melaena
Epigastric pain

152
Q

What is the gold standard investigation for a MWT?

A

Upper GI endoscopy:
- gold-standard required for all patients as an inpatient or outpatient depending on the Glasgow Blatchford score
- Usually shows a single longitudinal tear (there can be multiple tears) in the mucosa at the gastro-oesophageal junction

153
Q

What is Boerhaave’s syndrome?

A

Spontaneous perforation of the oesophagus, usually due to vomiting, which ruptures all the layers of the oesophageal wall

154
Q

What is the first line treatment for MWT?

A

Mild bleeding doesn’t require treatment

Upper GI endoscopy- mechanical clipping using adrenaline, then thermal coagulation then Sclerotherapy with adrenaline (delivers medication to the tear to stop bleeding)

155
Q

What are the complications of MWT?

A
  • Rebleeding: usually occurs within the first 24 hours, but is rare after endoscopy
  • Hypovolaemic shock: only occurs with life-threatening, persistent bleeds, which are very rare following MWT
  • Oesophageal perforation: a rare complication
156
Q

What is diarrhoea?

A

The abnormal passage of three or more loose or liquid stools per day.

157
Q

What is the most common cause of diarrhoea?

A

viral = norovirus (cruise ships, hospitals, restaurants)

158
Q

What is the most common viral diarrhoea in children?

159
Q

What is another cause of viral diarrhoea?

A

Traveller’s diarrhoea- symptoms are fever, nausea, vomiting, cramps or bloody stools during trip abroad

160
Q

What is the most common cause of bacterial diarrhoea? investigations + treatment?

A

Campylobacter jejuni

Investigate: Charcoal Cefazolin Sodium Deoxycholate Agar (CCDA) or PCR
Cause: Undercooked chicken (after BBQs!)
Usually self limiting = no treatment

161
Q

What is clostridium difficile infection?

A
  • Some antibiotics interfere with the balance of the bacteria in the bowel which can cause the C. diff bacteria to multiply and produce toxins
  • Antibiotics all start with C
  • Investigate with stool antigen or PCR
162
Q

How do you treat a C. diff infection?

A

Metronidazole, vancomycin, stop antibiotics

163
Q

What are the two types of parasitic diarrhoea?

A
  1. Giardia lamblia – most common
    Treat: metronidazole
  2. Cryptosporidium (helminth parasite)
164
Q

What bacteria cause watery diarrhoea?

A

Vibrio cholerae
E. coli (ETEC)
Clostridium perfringens
Bacillus cereus
S. Aureus

165
Q

What bacteria cause bloody mucoid diarrhoea?

A

Shigella
E. coli (EIEC, EHEC)
Salmonella enteridis
V. parahaemolyticus
C. diff
C. jejuni

166
Q

What is a bowel obstruction and what are the 3 types?

A

The interruption of passage through the bowel. Can be a surgical emergency
1. Small bowel obstruction (most common)
2. Large bowel obstruction
3. Pseudo-obstruction

167
Q

What are the causes of a small bowel obstruction?

A
  • Bowel adhesions post surgery they are the most common cause (75%)
  • Hernia (most likely femoral or inguinal)
  • Stricture formation from crohn’s
  • Gallstone ileus - gallstone within lumen of small bowel
168
Q

Describe the pathophysiology of SBO?

A
  • When peristalsis occurs against a obstruction it results in pain, distension and constipation
  • Dilation of the proximal bowel leads to compression of the mesenteric vessels and mucosal oedema.
  • This results in transudation of large volumes of electrolyte-rich fluid into the bowel (‘third-spacing’).
  • Eventually, as arterial supply is compromised, bowel ischaemia occurs with risk of perforation and subsequent faecal peritonitis and sepsis
169
Q

What are the signs of SBO?

A
  • Abdo tenderness and distension (less severe than LBO)
  • Tinkling bowel sounds in mechanical and absent in functional
  • Rectal exam will be empty
  • Tachycardia and hypotension due to third spacing of fluid
170
Q

What are the symptoms of SBO?

A

colicky, central or generalised Abdo pain
Nausea and vomiting early sign in SBO
Abdominal bloating

171
Q

What is the first line investigation for SBO?

A

Abdominal x-ray will show small bowel dilation of greater than 3 cm (coiled-spring appearance)

172
Q

What is the gold standard investigation for SBO?

A

CT abdomen and pelvis with contrast

173
Q

What is the first-line treatment for SBO?

A

‘drip’ (IV fluids) and ‘suck’ (NG tube)
also IV antibiotics (cefotaxime and metronidazole)
Analgesia and anti-emetics

174
Q

What are the surgical treatments for SBO?

A

Emergency laparotomy would be performed in cases where there is:
- Evidence of bowel ischaemia
- A non-adhesional cause e.g., hernia
- Failure of conservative management

Adhesiolysis- performed for a adhesional obstruction and recurrent adhesional obstructions

175
Q

What are the complications of SBO?

A

Bowel ischaemia
Sepsis
Aspiration pneumonia
Short gut syndrome
–

176
Q

What are the causes of LBO?

A
  • Colorectal cancer is the most common (90% of cases)
  • Volvulus- torsion of the colon around itself and the mesentery
  • Stricture
  • Intussusception (more common in children) is when the bowel fold within itself
  • Hirschprung’s disease: where neonates are born without innervation to the colon or rectum
177
Q

What are the symptoms of LBO?

A

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

178
Q

What would you see on an abdominal x-ray for LBO?

A

Dilation of large bowel greater than 6cm
Dilation of caecum greater than 9cm

179
Q

What is pseudo-obstruction?

A

Clinical picture mimicking colonic obstruction but with no mechanical cause
dilation without obstruction

Also known as Ogilvie syndrome.

180
Q

What can cause a pseudo-bowel obstruction?

A

Puerperium: the period after child birth
Post operative states
Trauma/sepsis
Drugs
cardiorespiratory and neurological disorders

181
Q

What is the pathophysiology of pseudo-obstruction

A

Parasympathetic nerve dysfunction → absent smooth muscle

Complication: bowel ischaemia and perforation

182
Q

What are the symptoms of pseudo-obstruction?

A

Rapid progressive abdominal distension

183
Q

What is the first line investigation for pseudo-bowel obstruction and what would it show?

A

X-ray

A large gas filled bowel greater than 10cm dilated

184
Q

How would you treat a pseudo-bowel obstruction?

A

Drip and suck
IV neostigmine- can encourage motility

Endoscopic colonic decompression can be used in those failing to respond.
Those at increasing risk of or who have developed complications (e.g. necrosis, perforation) will typically need surgical managment

185
Q

What is achalasia?

A

Degeneration of ganglions in Auerbach’s/myenteric plexus (in muscularis externa)

failure to relax lower oesophageal sphincter

186
Q

What is the pathophysiology of achalasia?

A

The nerves in the LOS don’t work properly. This means the LOS can’t relax leading to an obstruction

187
Q

What are the symptoms of achalasia?

A

Dysphagia: unable to swallow both solids and liquids (Oesophageal cancer: Solids first, then unable to swallow liquids over time)
Heartburn
Food regurgitation

188
Q

What are the first line investigations for achalasia?

A

Endoscopy
Barium swallow (Bird beak sign)

189
Q

What is the gold standard test for achalasia?

A

Manometry
- senses the pressure and constriction of muscles in the esophagus as you swallow

190
Q

What is the treatment for achalasia?

A

Lifestyle
Nitrates/CCB to relax LOS
Botox to relax LOS
Surgery: cardiomyotomy (upper part of stomach is sutured onto lower oesophagus)

191
Q

What is ischaemic colitis?

A

Bowel ischaemia that affects the large bowel. Due to pathology in the inferior mesenteric artery.

192
Q

What are the non-occlusive causes of ischaemic colitis?

A

Heart failure
Septic shock
Vasopressors
Recent CABG
Renal impairment
PVD
Cocaine use

193
Q

What are the occlusive causes of IC?

A

Arterial/venous thrombus
Embolism
Hernia/Volvulus/tumours

194
Q

What are the risk factors for IC?

A

Atrial fibrillation major risk factor
IE- can cause in younger patient’s
Vasculitis- can cause in younger patient’s

195
Q

What are the signs of IC?

A

Abdominal tenderness and distension
Haemodynamic instability (Shock)
Abdominal bruit (turbulent blood flow)

196
Q

What are the symptoms of IC?

A

Colicky lower left side abdominal pain- wore after eating
Diarrhoea
Haematochezia- passage of fresh blood
Fever
Abdominal bruit

197
Q

What area is most likely to be affected in IC?

A

The splenic flexure as it is the most distal despite duel supply. The rectum is resistant to ischaemia due to duel supply from IMA and internal iliac

198
Q

What are the investigations for IC?

A

ABG will show metabolic acidosis (raised lactate)
1st line would be CT contrast/angiography
GOLD STANDARD colonoscopy

199
Q

What is the supportive management for IC?

A

Nil by mouth (NG tube potentially)
IV fluids
Broad spectrum antibiotics
Unfractionated heparin

200
Q

What are the surgical treatments of IC?

A

Embolectomy
Thrombolysis
Mesenteric angioplasty and stenting
Laparotomy and resection of ischaemic/ necrotic segments
Stoma formation

201
Q

What are the complications of IC?

A
  • Bowel infarction and perforation: ischaemia can result in necrosis and subsequent perforation. This can lead to peritonitis and profound sepsis
  • Systemic inflammatory response syndrome (SIRS) progressing into a multi-organ dysfunction syndrome, mediated by bacteria translocation across the dying gut wall
  • Strictures: patients with ischaemic bowel managed conservatively have a risk of developing strictures
202
Q

What is mesenteric ischaemia?

A

Bowel ischaemia which affects the small bowel. It refers to pathology affecting the superior mesenteric artery.

203
Q

What are the differences between IC and mesenteric ischaemia?

A

The area that is affected and mesenteric tends to be more serious

204
Q

What is chronic mesenteric ischaemia?

A

The result of narrowing of the mesenteric blood vessels by atherosclerosis. This results in intermittent abdominal pain, when the blood supply cannot keep up with the demand.

205
Q

What are the symptoms CMI?

A

Central colicky abdominal pain after eating
Weight loss
Abdominal bruit

206
Q

What is the management for CMI?

A

Reducing modifiable risk factors
Secondary prevention (statins and antiplatelet)
Revascularisation to improve blood flow

207
Q

What is mesenteric ischaemia?

A

Bowel ischaemia which affects the small bowel. It refers to pathology affecting the superior mesenteric artery.

208
Q

What are the two types of oesophageal cancer?

A

Adenocarcinoma and squamous cell carcinoma

209
Q

Where are adenocarcinomas more common?

A

Developed world

210
Q

Where are squamous cell carcinomas more common?

A

Developing world

211
Q

What are the risk factors for an adenocarcinoma of the oesophagis?

A

Barret’s oesophagus
Obesity
Male sex
Smoking
Coeliac disease

212
Q

What are the risk factors for SSC?

A

Smoking- more associated than with adenocarcinoma
Alcohol
Achalasia
Plummer-Vinson syndrome: rare disease characterised by difficulty swallowing, iron-deficiency anaemia, glossitis,
Hot drinks
Nitrosamines(dietary)

213
Q

What causes SSC and what part of the oesophagus is affected?

A
  • Arises from squamous epithelium. It occurs in the upper 2/3rds of the oesophagus.
  • Occurs when tissue is exposed to risk factors like cigarette smoke, alcohol or hot fluids meaning there are more cell divisions increasing the risk of a malignant tumour
214
Q

What causes adenocarcinomas and what part of the oesophagus is affected?

A

Arises form columnar glandular epithelium in the lower 1/3rd of the oesophagus.
It most frequently occurs as a result of GORD.

215
Q

What are the symptoms of oesophageal cancer?

A

Progressive dysphagia
Regurgitation
Vomiting
Hoarseness
Weight loss

216
Q

What is the first-line investigation for SSC/adenocarcinoma?

A

Upper GI endoscopy (OGD) and biopsy: first-line investigation and allows for visualisation of masses and biopsy

217
Q

What would be used to determine the severity of the cancer (oesophageal)?

A

CT/MRI of the chest and abdomen (staging and metastases)

218
Q

What is the treatment for an localised adenocarcinoma/SSC?

A

Surgical resection and chemoradiotherapy

219
Q

What treatment is used for HER2 positive metastatic cancer/

A

Trastuzumab (Herceptin)

220
Q

What are the 4 types of gastric cancer?

A
  1. Adenocarcinoma
  2. Lymphoma-chronic H.Pylori infection, can cause excessive B-cell proliferation, which makes these cells more prone to have mutations and develop lymphoma.
  3. Carcinoid- - Originates in the neuroendocrine cell e.g. G-cells of the stomach.
  4. Leiomyosarcoma- smooth muscle cells from the gastric wall.
221
Q

What are the two types of adenocarcinoma?

A

Intestinal (type 1), or well-differentiated adenocarcinoma; and diffuse(type 2), or undifferentiated adenocarcinoma. Intestinal is the most common!

222
Q

What are the risk factors for developing a gastric intestinal vs gastric diffuse adenocarcinoma?

A

Intestinal:
Male
Older age
H.Pylori- accounts for 60%
Chronic/atrophic gastritis

Diffuse:
Female
Younger age
Blood type A
H.Pylori

223
Q

Describe the pathophysiology of intestinal gastric adenocarcinoma?

A

H.Pylori releases virulence factors e.g., cagA. This causes damage and leads to an inflammatory response (gastritis)
The normal epithelium of the stomach gets continuously damaged and repaired. Over time, the stomach cells in the epithelium undergo metaplasia and eventually dysplasia

occurs in the antrum and lesser curvature

224
Q

What is the histology of intestinal gastric adenocarcinoma

A

Well-differentiated tubular

225
Q

What gene is mutated in diffuse gastric adenocarcinoma?

226
Q

Describe the pathophysiology of a diffuse gastric adenocarcinoma?

A
  • CDH1 gene codes for tumour suppressor protein E-cadherin. Helps cells stick to each other and controls cell cycle
  • When it isn’t working cells detach and divide uncontrollably. Can spread very easily
227
Q

What can diffuse gastric adenocarcinoma cause?

A

Gastric linitis plastica- where the stomach wall grows thick and hard and looks like a leather bottle

228
Q

What is the histology of diffuse gastric adenocarcinoma?

A

Poorly differentiated signet ring cells

229
Q

What are the symptoms of gastric cancer?

A

Weight loss
Haematemesis and melaena
Dysphagia
Anorexia
Epigastric pain

230
Q

What are the signs of gastric cancer/

A
  • Acanthosis nigricans: darkening of the skin at the axilla and other skin folds
  • Troisier’s sign: an enlarged, hard Virchow’s node (left supraclavicular node)
  • Iron deficiency anaemia
231
Q

What are investigations for gastric cancer?

A

Upper GI endoscopy (gastroscopy) + biopsy
Endoscopic ultrasound
CT/MRI of the chest and abdomen (staging and metastases)

232
Q

What are the risk factors for developing bowel cancer?

A

Familial adenomatous polyposis (FAP)
Hereditary nonpolyposis colorectal cancer (HNPCC)
IBD
Diet high in red and processed meat and low in fibre

233
Q

What is the blood test used for testing bowel cancer?

A

CEA tumour marker used not in screening but testing relapse

234
Q

What are some other tests for bowel cancer?

A

Sigmoidoscopy = involves an endoscopy of the rectum and sigmoid colon only. This may be used in cases where the only feature is rectal bleeding. There is the obvious risk of missing cancers in other parts of the colon.

CT colonography = is a CT scan with bowel prep and contrast to visualise the colon in more detail. This may be considered in patients less fit for a colonoscopy but it is less detailed and does not allow for a biopsy.

235
Q

What is the at home screening test for bowel cancer?

A

Faecal immunochemical test looks for the amount of human haemoglobin in the stool

Test used to be faecal occult blood test which detected blood in stools but used to detect meat blood

236
Q

Who are FIT tests sent to?

A

sent every 2 years for people from 60-74

237
Q

What is assessed in the tumour part of TMN staging?

A

Tx- unable to assess size
T1- submucosa involvement
T2- Involvement of the muscle
T3- involvement of the subserosa and serosa (outer layer), but not through the serosa
T4- Spread through the serosa and reaching other tissues and organs

238
Q

What is assessed in the node part of TMN?

A

NX- unable to asses
N0- No nodal spread
N1- spread 1-3
N2- spread to more than 3 nodes

239
Q

What is assessed in the metastasis part of TMN?

A

M0- no metastasis
M1- Metastasis

240
Q

What is the management for bowel cancer?

A

Surgical resection
Radiotherapy
Chemotherapy

241
Q

What is pseudomembranous colitis? (PMC)

A

Inflammation of the colon due to a overgrowth of C.diff and a recent history of antibiotic use

242
Q

What are the risk factors for developing PMC?

A

Recent antibiotic use
Staying in a hospital/nursing home
older age
IBD
Use of PPI
Immunocompromised

243
Q

What are the investigations for PMC?

A

FBC will show raised WCC
Stool sample (presence of C.diff)
Colonoscopy (raised yellow plaques)

244
Q

How do you treat PMC?

A

Stop causative agent
Start another antibiotic that is effective against C.difficile
Oral fidaxomicin, vancomycin, metronidazole

245
Q

What are haemmorrhoids?

A

A normal spongy vascular structure that acts as a cushion for stools as they pass through
Haemorrhoidal disease is when they get disrupted swollen and inflamed

246
Q

What are internal and external haemorrhoids

A

Internal are above the dentate line
external are below the dentate line

247
Q

What is the dentate line

A

a line which divides the upper two-thirds and lower third of the anal canal.

248
Q

What are the four grades of internal haemorrhoids?

A

Grade I: no protrusion outside the anal canal.

Grade II: protrusion outside the anus during bowel movement, but they retract spontaneously.

Grade III: prolapsed haemorrhoids that don’t retract spontaneously, but they can be pushed back in manually.

Grade IV: prolapsed haemorrhoids that cannot be manually pushed back in.

249
Q

What can cause haemorrhoids?

A

Straining during bowel movements
Chronic diarrhoea
Anal sex
Congestion from a pelvic tumour, pregnancy, congestive heart failure and portal hypertension

250
Q

What are the symptoms haemorrhoids?

A

Usually asymptomatic
Can cause itching, burning and vague discomfort
Painless passage of bright red blood not mixed in with the stools
Straining
Constipation
Lump around or inside the anus

251
Q

What are the investigations for haemorrhoids?

A

External haemorrhoids are visible on inspection

Internal haemorrhoids can sometimes be felt on a digital rectal exam

** GOLD STANDARD** proctoscopy is required for proper visualisation and inspection

252
Q

What do internal haemorrhoids look like with proctoscopy?

A

Internal haemorrhoids look like bulging purplish-blue veins
Prolapsed internal haemorrhoids appear dark pink, glistening, and are sometimes tender masses at the anal margin

253
Q

What are the differentials for haemorrhoids?

A

Anal fissures
Diverticulosis
Inflammatory bowel disease
Colorectal cancer

254
Q

What is the conservative management for haemorrhoids?

A

Topical treatments e.g., Anusol
Give treatment for constipation of present

255
Q

What are the treatments for the first and second degree haemorrhoids?

A

Rubber band ligation
Infrared coagulation
Injection scleropathy
Bipolar diathermy

256
Q

What are the surgical treatments for 3rd and 4th degree haemorrhoids?

A

Haemorrhoidectomy
Stapled haemorrhoidectomy
Haemorrhoidal artery ligation

257
Q

What is an anal fistula?

A

An abnormal connection between the epithelial surface of the anal canal and skin - it is essentially a track that communicates between the skin and anal canal/rectum

258
Q

What are the causes of an anal fistula?

A

Perianal sepsis
Abscesses
Crohn’s
TB
Diverticular disease

259
Q

What are the signs and symptoms of an anal fistula?

A

Throbbing pain worse when sitting, defecation or activity
Malodorous discharge
Pruritis ani
Perianal skin may become inflamed

260
Q

What are the investigations for an anal fistula?

A

MRI
Endoanal ultrasound

261
Q

What is the management for a anal fistula?

A

Surgical - Fistulotomy (cutting along the whole length of the fistula to open it up so it heals as a flat scar) and excision

262
Q

What is an anal fissure

A

A tear in the lower anal canal distal to the dentate line usually due to trauma

263
Q

What are the causes of an anal fissure?

A

Hard faeces
Anal trauma
Rarely Crohn’s/TB

264
Q

What are the symptoms of an anal fissure?

A

Extreme pain on passing motion
Blood in stool on wiping

265
Q

What are the conservative treatments of an anal fissure?

A

Increase dietary fibre and fluids
Use of stool softener

266
Q

What are the medical treatments of an anal fissure?

A

Lidocaine ointment + GTN ointment or topical diltiazem

2nd line: Botulinum toxin injection (botox) and topical diltiazem

Surgery if medication fails: lateral partial internal sphincterotomy
(the internal sphincter is divided to lower its resting pressure, which helps improve blood supply to the fissure and allows faster healing).

267
Q

What is an anal absecess?

A

Superficial infection that appears as a tender red lump under the skin near the anus.

268
Q

Risk factors for anal abscess?

A

Perianal abscesses make up 45% of anorectal abscesses (most common type)
F>M
2-3 times more common in those who have anal sex

269
Q

How does an abscess form?

A

An abscess forms when normal tissue is split apart and that new space is invaded by nearby pathogens like bacteria. This leads to an immune response.

270
Q

What is the treatment for an abscess?

A

Surgical excision and drainage
Treatment with antibiotics

271
Q

What is the surgical treatment for achalasia?

A

Heller cardiomyotomy
- muscles of cardia are cut allowing food and liquids to pass to the stomach.
(as LOS fails to relax properly)

272
Q

Why should people with coeliac disease get the pneumoccal vaccination?

A

Coeliac disease causes hyposplenism
- spleen produces IgM memory B cells, that are important in opsonisation and phagocytosis of encapsulated bacteria
- so more susceptible to illness caused by pneumococcal infection

273
Q

What are the 2 most common causes of pancreatitis?

A
  • gallstones
  • heavy alcohol use
274
Q

What is the Glasgow prognostic score for pancreatitis?

A

Presence of 3 or more of these is indicative of severe pancreatitis:
PANCREAS
pO2 <8 kPa (60 mm Hg)
Age >55 years
Neutrophils: WBC >15 x 109/L
Calcium <2 mmol/L
Renal function: Urea >16 mmol/L
Enzymes: LDH >600 units/L, AST/ALT >200 units
Albumin <32 g/L
Sugar: Glucose >10 mmol/L

275
Q

What is Budd-Chiari syndrome?

A

hepatic vein thrombosis
- triad = painful hepatomegaly, jaundice, and ascites

276
Q

WHat types of granulomatous disease is Crohn’s?

A

Crohns - NON-caseating

like sarcoidosis + leprosy
But TB is caseating

277
Q

What is a blood marker for granulomatous disease?

A

ACE
(raised in Crohn’s)

278
Q

What is Toxoplasma Gondii?

A

A protozoa
- it infects the body via the GI tract, lung or broken skin
- human infection occurs from consumption of undercooked meat or food or water contamination with the oocytes

279
Q

How does Toxoplasma Gondii cause an infection?

A

Oocysst release trophozoites which migrate widely around the body including the eye, brain and muscle
- oocytes are produced in the cat’s intestines and shed it its faeces

280
Q

What are the symptoms of toxoplasma gondii infection?

A

most infections are asymptomatic

  • fever, malaise and lymphadenopathy
  • brain mass lesion
  • headache
  • confusion
  • seizures
  • focal neurologic deficits
  • meningoencephalitis
  • myocarditis
281
Q

What patients are most at risk of a toxoplasma gondii infection?

A

AIDs patients
- cerebral toxoplasmosis should be at top of list if one presents with focal neurological symptoms

282
Q

What will investigations show for toxoplasmosis gondii show?

A

CT/MRI head
- ring enhancing lesion with oedema
- solitary lesions or cortical atrophy
(MRI more sensitive)

283
Q

What is the treatment for toxoplasma gondii?

A

Pyrimethamine plus sulphadiazine

284
Q

What are the causes of oral thrush?

A

Inhaled corticosteroids
Diabetes mellitus
Recent course of antibiotics
Elderly false teeth

285
Q

What is the presentation of oral thrush?

A

White patches on mouth can be easily wiped off
Underlying red base layer that is painless

286
Q

What is the treatment for oral thrush?

A

Oral fluconazole (widespread)
Miconazole gel or nystatin suspension (localised)

287
Q

What is the mechanism of action of Mesalazine?

A

(aminosalicylates)
- reduces inflammation in GI tract
- prevents leucocyte recruitment into bowel wall

  • inhibit chemotactic response to ILB4
  • reduce synthesis of platelet activating factor
  • inhibit leucocyte adhesion molecule upregulation

Emily Phase 2a (15 decks)

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