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Medicine Phase 2a > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

How can The causes of Upper GI bleeds be broken classified?

A

Oesophagus

Stomach

Duodenum

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2
Q

What are the Oesophageal causes of Upper GI Bleeds?

A

Oesophagitis
Varices
Malignancy
Gastro-oesophageal reflux disease (GORD)
Mallory-Weiss tear

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3
Q

What are the stomach causes of Upper GI Bleeds?

A

Peptic ulcer disease
Mallory-Weiss tear
Gastric varices
Gastritis
Malignancy

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4
Q

What are the duodenal causes of Upper GI Bleeds?

A

Peptic ulcer disease
Diverticulum
Aortoduodenal fistula
Duodenitis

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5
Q

What are some key causes for Upper GI bleeding?

A

Peptic ulcer disease (50%)
Oesophageal Varices
Mallory Weiss Tear
Cancers of stomach/duodenum

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6
Q

What is Peptic ulcer disease?

A

Break in the mucosal lining of the stomach, duodenum or lower Oesophagus more than 5mm diameter.

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7
Q

What can cause a peptic ulcer?

A

Imbalance between factors promoting mucosal damage and those promoting duodenal defence

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8
Q

What are some factors that cause mucosal damage and therefore increase risk of peptic ulcers?

A

Gastric acid - high volumes

H.Pylori

NSAIDs

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9
Q

Explain how H. pylori can lead to PUD?

A

Lives in gastric mucus
Secretes urease which splits urea in stomach into CO2 + ammonia
Ammonia + H+ 🡪 ammonium
Ammonium, proteases, phospholipases and vacuolating cytotoxin A damages gastric epithelium
Causes inflammatory response reducing mucosal defense 🡪 mucosal damage
Also causes increased acid secretion
Gastrin release (from G cells) 🡪 more acid secretion
Triggers release of histamine 🡪 more acid secretion
Increases parietal cells mass 🡪 more acid secretion
Decreases somatostatin (released from D cells) 🡪 more acid secretion

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10
Q

Explain how NSAIDs lead to PUD?

A

Mucus secretion stimulated by prostaglandins
COX-1 needed for prostaglandin synthesis
NSAIDs inhibit COX-1
No COX-1 = mucous isn’t secreted
Reduced mucosal defense 🡪 mucosal damage

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11
Q

Explain how Mucosal Ischaemia can lead to PUD?

A

Stomach cells not supplied with sufficient blood
Cells die off and don’t produce mucin
Gastric acid attacks those cells
Cells die 🡪 formation of ulcer
Treatment - H2 blocker

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12
Q

Explain how an increase in stomach acid can lead to PUD?

A

Overwhelms mucosal defence
Acid attacks mucosal cells
Cells die 🡪 formation of ulcer
Stress can increase acid production
Treatment – PPI and H2 blocker

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13
Q

Explain how Bile Reflux leads to PUD?

A

Duodeno-gastric reflux
Regurgitated bile strips away mucus layer
Reduced mucosal defense

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14
Q

What factors can increase acid production?

A

Stress
Alcohol
Caffeine
Smoking
Spicy Foods

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15
Q

What are some protective factors of the upper GI tract that are reduced that can lead to peptic ulcers?

A

Reduced Prostaglandins (NSAIDs) leading to poor muscosal production

Mucus damage (via H.pylori)

Bicarbonate loss leading to no neutralisation of stomach acid

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16
Q

What are the main areas where a Peptic Ulcer develops?

A

Gastric ulcer - stomach
Duodenal Ulcer

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17
Q

What is the most common area for a peptic ulcer?

A

Duodenal ulcers

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18
Q

What arteries are eroded in gastic ulcers and duodenal ulcers?

A

Gastric Ulcer - Left gastric

Duodenal Ulcer - Erodes gastroduodenal artery

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19
Q

Who is typically affected by peptic ulcers?

A

More common in men than women
Prevalence 11-20% for men

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20
Q

What are the risk factors for Peptic Ulcers?

A

Increasing age
H.Pylori infection
NSAIDS
Drugs - SSRIs, Corticosteroids
Smoking
Alcohol

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21
Q

What are the clinical signs of of peptic ulcer disease?

A

Evidence of bleeding
Hypotension
Tachycardia
Melaena
Epigastric Tenderness
Pallor - due to anaemia

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22
Q

What are some signs of Upper GI bleeding via peptic ulcers?

A

Burning Epigastric pain
Nausea & Vomiting
Haematemesis
Melaena
Reduced appetite
Weight loss
Fatigue - Anaemia

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23
Q

What is the pain like in an Upper GI bleed from a peptic ulcer?

How can this be used to distinguish the site of the ulcer?

A

Burning pain

Gastric ulcer - pain worsened by eating

Duodenal Ulcer - Pain relieved by eating and worse a couple e
of hours after eating or when hungry

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24
Q

Why is the pain in a duodenal ulcer relieved by eating?

A

Duodenal ulcers are less painful after eating bc the pyloric sphincter closes during digestion, preventing acid from going into duodenum

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25
Q

What investigations would be done if the patient had no red flags/was not bleeding with a suspected peptic ulcer?

A

Urea breath test
Stool antigen test

Looking for H.pylori infection as a possible cause

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26
Q

If testing for H.pylori infection what must be done?

A

The patient must be off PPI for 2+ weeks to prevent false negative results

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27
Q

What are the investigations that you would do in a suspected peptic ulcer that is currently bleeding?

A

Upper GI endoscopy:
Diagnostic and therapeutic

FBC

H.Pylori Tests

U&E:
urea is raised

LFTs - Assess severity of Liver disease

Venous Blood Gas - raised lactate

Erect CXR - concerned about perforation

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28
Q

What is the Glasgow Blatchford Score (GBS)

A

Scoring system used in a suspected upper GI bleed. Those with a score of >0 require admission.

Drop in Haemoglobin
Rise in Urea
Systolic BP
HR
Melaena
Hx of Syncope
Hepatic disease Hx
HF

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29
Q

What is the Rockall Score?

A

Used for Px who have had an endoscopy. it is a % risk for rebleeding. considers:
Age
Features of Shock - Tachycardia/Hypotension
Co-morbidities
Causes of bleeding
Endoscopic Stigmata

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30
Q

What is the first line treatment for a peptic ulcer that is not bleeding?

A

Conservative Lifestyle Tx - treat RFs

H.pylori Neg:
PPI - omeprazole

H.pylori Pos:
Tripple Therapy - Omeprazole, Clarithromycin, Amoxicillin

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31
Q

What is the general management for an upper GI bleed?

A

ABATED:
ABCDE
Bloods
Access - 2 bore cannula
Transfuse
Endoscopy - urgent within 24 hrs
Drugs - Stop anticoagulants and NSAIDs

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32
Q

What is the first line treatment for a peptic ulcer that is bleeding?

A

First Line:
ABCDE
Blood transfusion - if blood loss
Upper GI endoscopy - within 24 hrs

High dose IV PPI - after Endoscopy

If H.pylori positive - CAP

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33
Q

What is the Second line treatment for a Peptic ulcer which is bleeding?

A

Surgery or embolisation

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34
Q

What are some complications of peptic ulcer disease?

A

Perforation

Gastric outlet obstruction

peritonitis - caused by an ulcer/haemorrhage of an ulcer passing straight through into the stomach

Pancreatitis - can also occur as a result of peritonitis

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35
Q

What are the red flags for Cancer causing an Upper GI Bleed?

A

Unexplained weight loss
Anaemia
Evidence of GI bleeding e.g. melaena or haematemesis
Dysphagia
Upper abdominal mass
Persistent vomiting

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36
Q

What are Oesophageal Varices?

A

Dilated submucosal veins within the lower 1/3rd of the oesophagus that develop as a consequence of portal hypertension

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37
Q

What is the cause of oesophageal varices?

A

Portal Hypertension

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38
Q

What is the pathogenesis of oesophageal varices?

A
  • Increased vascular resistance in portal venous system
  • Causes splanchnic dilations and
  • compensatory Increase in CO
  • Results in fluid overload in portal vein
  • This opens venous collaterals - connecting portal and systemic venous systems.
  • Venous collaterals shunt blood to gastroesophageal veins causing varices
  • Higher pressures can cause the veins to rupture causing an upper GI bleed
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39
Q

Why are Oesophageal Varices prone to rupture?

A

As these vessels are thin and not meant to transport higher pressure blood, they can rupture
Rupture 🡪 haematemesis
Rupture 🡪 blood digested 🡪 melaena

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40
Q

What are the risk factors for oesophageal varices?

A

Liver Cirrhosis (50% of Px have varices)

Portal HTN

Decompensated liver Cirrhosis

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41
Q

What are the clinical signs of oesophageal varices?

A

Hypotension
Tachycardia
Pallor
Signs of chronic liver damage – jaundice, easy bruising (liver not produced coagulation factors) and ascites
Splenomegaly
Ascites

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42
Q

What are the symptoms of oesophageal varices?

A

Haematemesis
Melaena

Sx of blood loss:
Dizziness
dyspnoea
Chest pain
Syncope

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43
Q

What are the primary Investigations for oesophageal varices?

A

Upper GI endoscopy:
Diagnostic

FBC - Anaemia

LFTs - assess liver disease severity

U&Es - Urea is raised in upper GI bleed

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44
Q

What is the management for bleeding oesophageal varices?

A

Resus:
ABCDE
IV Fluids - if in shock
Terlipressin
Blood transfusion
Vit K if bleeding abnormality
Prophylactic Abx

Endoscopic Band Ligation within 24 hrs

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45
Q

What is Terlipressin and what does it do?

What is used if Terlipressin is CI such as in IHD?

A

ADH analogue that can cause splanchnic vasoconstriction to reduce blood flow in the portal vein and reduce portal pressure

CI: use IV somatostatin instead

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46
Q

What Abx are given in oesophageal varices as prophylaxis?

A

Quinolones:
eg. ciprofloxacin

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47
Q

What is the definitive management of oesophageal varices?

A

1st line:
Variceal Band ligation

Sclerotherapy and transjugular intrahepatic portosystemic shunt (TIPS) are also able to be used

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48
Q

What prophylactic Tx should be given to prevent formation or rupture of oesophageal varices?

A

Beta blocker - acts on B2 receptors to cause them to vasoconstrict and propranolol to reduce blood flow to the portal vein to reduce portal pressure

Variceal band ligation

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49
Q

What are some complications of Oesophageal varices?

A

Rupture and GI bleeding
Rebleeding once fixed

Encephalopathy

Infection

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50
Q

What are the different classifications of bowel obstruction?

A

Site of blockage:
Simple
Intra luminal
In the wall
Outside the bowel

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51
Q

What are some causes of bowel obstruction?

A

Crohn’s
Adhesions
Malignancy
Diverticulitis
Volvulus
Hernias
Hirschsprung’s disease

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52
Q

What are some intraluminal causes of bowel obstruction?

A

Tumours:
- Carcinoma
- Lymphoma

Diaphragm disease - NSAIDs cause repeated ulceration then fibrosis

Gallstone ileus – rare form of small bowel obstruction caused by an impaction of a gallstone within the lumen

Meconium ileus – in neonates, content of bowel is sticky 🡪 blockage

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53
Q

What are some within the wall causes of Bowel obstruction?

A

Tumours
Crohn’s – inflammation, fibrosis and contraction
Diverticulitis – outpouchings in the sigmoid

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54
Q

What are some Outside the Bowel causes of Bowel obstruction?

A

Tumours – disseminated malignancy of peritoneum
Ovarian cancer can spread into peritoneum

Adhesions – fibrosis after surgery
Post-surgery
Fibrous connections between loops of small bowel 🡪 bowel becomes kinked
Corrected surgically

Volvulus – sigmoid colon has a “floppy” mesentery
Sigmoid colon can twist
Causes obstruction of the sigmoid
If there is ischaemia and infarction, sigmoid colon is resected

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55
Q

What are the main causes of a large bowel obstruction?

A

Malignancies - colorectal cancer (90% of all causes)

Stricture - complication of diverticulitis and IBD

Volvulus - Sigmoid / Caecal

Hirschsprung’s Disease

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56
Q

What are the main causes of a small bowel obstruction?

A

Adhesions -75% (from previous surgeries)

Hernias - 10%

Crohns - Strictures

Malignancy

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57
Q

What is Hirschsprung’s Disease?

A

Congenital disorder where there is defective relaxation and peristalsis of the distal colon causing a bowel obstruction.

Neonates born with incomplete Innervation of the colon to rectum.
A ganglionic segments of the bowel cannot contract (peristalsis) leading to obstruction

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58
Q

What is a Volvulus and what are the 2 main types?

A

occurs when a loop of intestine twists around itself and the mesentery that supplies it, causing a bowel obstruction.

Sigmoid is most common (80%) - associated with elderly Px

Caecal is less common associated with Pregnancy and can occur at any age.

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59
Q

Define a small bowel obstruction (SBO)?

A

Inability of the gut to absorb the necessary nutrients sufficient to sustain life due to a mechanical blockage of the small intestine

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60
Q

What is the pathophysiology of a SBO (same for a LBO)?

A

Mechanical or functional obstruction of the small intestine preventing the normal passage of abdominal contents.

This leads to dilation of the proximal bowel and compression of mesenteric vessels.

Causes transudation of large volumes of electrolyte rich fluid into the bowel (third spacing).

Arterial supply is compressed and you get ischaemia

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61
Q

What is the most common indication for emergency laparoscopy?

A

Small bowel obstructions

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62
Q

What is the average age of a Px who has a small bowel obstruction?

A

70s

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63
Q

What are the main causes of a SBO?

A

Bowel adhesions (50%) - due to previous abdominal surgery

Incarcerated hernias (15%)

Crohn’s Disease

Volvulus - rarely SBO but commonly LBO

Paralytic ileus

Malignancy

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64
Q

What is a Pseudo-Obstruction of the bowel?

A

Where there is no blockage to the bowel however the intestine is unable to contract and push food, stool and air through the digestive tract

(Failure of Peristalsis)

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65
Q

How do surgeries lead to bowel adhesions?

A

Formation of fibrous scar tissue between organs and tissue can constrict and adhere to the bowel preventing expansion

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66
Q

What is a Paralytic Ileus?

A

Functional Obstruction due to failure of peristalsis:
Often caused post abdominal surgery

May also be due to electrolyte imbalances (hypokalaemia)

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67
Q

What are the clinical signs of a Large and small bowel obstruction?

A

Abdominal tenderness and distension
Tinkling bowel sounds
Rectal exam - empty or blood suggesting strangulation
Tachycardia
Hypotension

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68
Q

What are the symptoms of a small bowel obstruction?

A

Colicky pain - typically in umbilical region
Nausea and Vomiting - Early sign in SBO
Tinkling Bowel Sounds
Bloating/distension
Absolute constipation - Late sign in SBO

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69
Q

What are the Symptoms of a Large bowel obstruction?

A

Continuous abdominal pain
Severe Bloating and distension
Absolute constipation - Early sign in LBO
Nausea and Vomiting - Late sign in LBO (first bilious then faecal)
Absent Bowel Sounds

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70
Q

What is a good way to distinguish whether a Px has a small or large bowel obstruction based off their Symptoms?

A

SBOs present with nausea and vomiting first before constipation

LBOs present with constipation first before nausea and vomiting

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71
Q

What is the cause of the pain felt in SBO?

A

When there is a mechanical obstruction to the SBO and peristalsis occurs this can lead to pain.

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72
Q

Which tests are ordered in the diagnosis of Large/small bowel obstruction?

A

(1st Line) - ABDO XR - Dilation of SB >3 or LB >6cm

(GS) Abdo CT Scan w/contrast - diagnostic for an obstruction

FBC - anaemia/infection
U&Es - Likely have renal dysfunction secondary to hypovolaemia
Venous blood gas/Lactate - may be increased
CRP/ESR - inflammatory

Potentially Gastrograffin contrast scan

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73
Q

What are seen on AXR in bowel obstruction?

A

distended loops of the jejunum/ileum/large colon

Absence of gas in the bowel distal to the obstruction
SBO - central gas shadow
LBO - Peripheral Gas Shadow

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74
Q

What is the 3, 6, 9 rule on abdo XR for bowel obstructions?

A

Dilation of Small bowel > 3cm
Dilation of Large bowel > 6cm
Dilation of Caecum > 9cm
Sigmoid Volvulus - Coffee Bean Sign

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75
Q

What is the gold standard diagnostic test for a Large/small bowel obstruction?

A

Abdo CT Scan w/ contrast:
Diagnostic
Location and cause may also be indicated

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76
Q

What is the treatment for all patients with a Large/small bowel obstruction?

A

Conservative (stable patients)
A-E assessment
‘Drip and suck’
Insert IV cannula → Resuscitate with IV fluids
Nil-by-mouth (NBM)
Insert nasogastric tube to decompress stomach
Catheter (monitor urine output)
Analgesia, antiemetics, antibiotics

Unstable:
Surgical Tx according to cause

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77
Q

What is the treatment for patients with a small bowel obstruction due to adhesions?

A

Signs of Ischaemia or Shock:
Resus and Operate

No-ischaemia:
Gastrografin challenge and determine whether there is a need to operate

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78
Q

What is the treatment for all patients with a small bowel obstruction due to a hernia?

A

Inguinal/Femoral/Umbilical - operate and repair

Incisional Hernia - Treat as adhesive SBO

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79
Q

What are the complications of a Small Bowel Obstruction?

A

Intestinal necrosis

Sepsis

Multi-organ failure particularly renal

Intestinal perforation

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80
Q

What are the 2 types of oesophageal cancer?

A

Adenocarcinoma
Squamous cell carcinoma

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81
Q

What type of oesophageal cancer is most common?

A

Squamous cell carcinoma (90%) in upper 2 thirds

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82
Q

What most commonly predisposes Oesophageal adenocarcinoma?

A

Barret’s metaplasia where glandular columnar epithelium replaces the squamous epithelium in the lower oesophagus

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83
Q

What is the location of an adenocarcinoma of the Oesophagus?

A

Lower third of the oesophagus near gastro-oesophageal junction

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84
Q

What is the location of a Squamous cell carcinoma of the oesophagus?

A

Usually upper or middle third of the oesophagus

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85
Q

What are the risk factors for adenocarcinoma of the Oesophagus?

A

Barrett’s Oesophagus
GORD
Obesity
Smoking

Coeliac Disease
Scleroderma

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86
Q

What are the risk factors for SSC of the oesophagus?

A

Smoking
Alcohol
Achalasia
Plummer Vinson syndrome
Hot beverages
Nitrosamines

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87
Q

Who is more commonly affected by oesophageal cancer?

A

Males
80 years old
Western world

SSC is more common in Japan

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88
Q

What are the clinical signs of oesophageal cancer?

A

Lymphadenopathy
Vocal Cord Paralysis
Pallor - anaemia
Melaena - due to oesophageal bleeding

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89
Q

What are the symptoms of oesophageal cancer?

A

ALARMS:
Anaemia
Loss of Weight
Anorexia
Recent sudden Sx worsen
Melaena/Haematemesis
Swallowing - Progressive Dysphagia (solids then liquids)

Hoarse Voice - due to pressure on recurrent laryngeal nerve

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90
Q

What may be a differential diagnosis when a Px presents with symptoms of dysphagia?

A

Achalasia
This however is non progressive and so Px dont say at first it was difficult to swallow then fluids then food etc.

Barretts Oesophagus

Oesophageal Strictures

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91
Q

What is the primary investigation for oesophageal cancer?

A

Upper GI Endoscopy (OGD) and Biopsy

Staging Ix:
CT Chest abdo pelvis (CAP)

Endoscopic ultrasound (EUS)

HER2 Testing

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92
Q

What is the first line staging investigation for oesophageal cancer?

A

CT chest, abdomen and pelvis (CAP)

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93
Q

When would you do a 2 week endoscopy referral?

A

In Px with:
Dysphagia
OR
Age >55 with Wgt Loss and 1 of the following:

  • Upper Abdo pain
  • Reflux
  • Dyspepsia
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94
Q

What is the management of Oesophageal cancer for both Adenocarcinoma and SCC?

A

If operable:
Adenocarcinoma - Oesophagectomy
SCC - Radical chemoradiotherapy

Advanced/Metastatic:
Chemotherapy
Palliation - Stenting for Dysphagia
Trastuzumab for HER2 Positive

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95
Q

When does Oesophageal cancer tend to present and what is the prognosis?

A

Tends to present late
Has a prognosis of 15% 5yr survival

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96
Q

What are the main types of cancer is a gastric cancer?

A

Adenocarcinoma (90-95%)
SCC (5%)

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97
Q

What are the main types of Adenocarcinoma Gastric cancer?

A

Type 1 (Intestinal 80%) - Usually exophytic or ulcerating

Type 2 (Diffuse 20%) - Flat, causing linitus plastica

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98
Q

What are the features of Intestinal Gastric cancer?

A
  • Better Prognosis
  • Affects Males, H.pylori, chronic/atrophic gastritis
  • Develops from inflammatory process
  • Affects antrum and lesser curvature
  • Well formed and differentiated tubular/glandular structures
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99
Q

What are the features of Diffuse gastric cancer?

A
  • Has a much worse prognosis
  • Female, Young, Blood Type A, Genetic
  • Develops from linitis Plastica
  • Poorly cohesive - signet ring cells
    Infiltrates the gastric wall
  • Can affect any part of the stomach
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100
Q

What are the modifiable risk factors for Gastric cancer?

A

H.pylori infection (significant)
smoking
alcohol
diet
Obesity

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101
Q

What are the non-modifiable risk factors for gastric cancer?

A

Genetics - CDH-1 gene (mutated Cadherin)
Male
Increased age
Pernicious anaemia
Blood type A
Gastric Adenomatous polyps

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102
Q

Where is gastric cancer most common?

A

Japan

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103
Q

What are the clinical signs of gastric cancer?

A

Virchows Nodes - Supraclavicular
Palpable mass
Melaena
Leser-Trelat sign - sudden onset keratosis

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104
Q

What are the symptoms of gastric cancer?

A

Severe epigastric Abdominal pain
Dyspepsia
Anorexia and weight loss
Dysphagia
Nausea and vomiting
Haematemesis and Melaena

Signs of Metastasis - Liver dysfunction etc

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105
Q

What are the main lymph nodes that Gastric cancer may spread to?

A

Virchow’s Node - Supraclavicular

Sister Mary Joseph Node - Umbilical

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106
Q

What is the primary investigation of gastric cancer?

A

Upper GI Endoscopy and Biopsy

1st line staging - CT-CAP

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107
Q

What is the management of Gastric cancer?

A

Surgery only indicated if no evidence of metastatic disease

Surgery - remove tumour/stomach

Advanced disease:
Chemotherapy - 5-Fluorouracil/Cisplatin
Palliative gastrectomy

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108
Q

What are some complications of Gastric cancer?

A

Bleeding
Gastric outlet obstruction
Perforation
Metastasis

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109
Q

What is Bowel Cancer?

A

Usually an adenomatous cancer that typically affects the colon (colorectal) more than it affects the small bowel

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110
Q

What is the prevalence of bowel (colorectal) cancer?

A

4th most prevalent cancer in the UK.
Behind breast, prostate and lung

3rd most Prevalent world wide

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111
Q

How do bowel cancers arise?

A

sporadic cancers arising from:
Adenomatous Polyp to progress to adenocarcinoma
Defects in DNA repair genes

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112
Q

What are the risk factors for Bowel cancer?

A

50+
Increasing age
Smoking
Obesity
IBD
FHx - FAP, HNPCC

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113
Q

What is Familial adenomatous Polyposis (FAP)?

A

Autosomal dominant
Malfunctioning tumour suppressor genes of APC (adenomatous polyposis coli)
Leads to many Polyps developing which can progress to cancer

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114
Q

What is the pathogenesis of FAP?

A

Apc bound to GSK
Beta catenin binds apc complex in high levels of apc
In mutations, apc protein misfolded so can’t bind to beta catenin
Beta catenin able to move into nucleus 🡪 endothelial proliferation 🡪 adenoma

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115
Q

What is Hereditary Nonpolyposis Colorectal Cancer (HNPCC)?

A

Lynch syndrome
Autosomal dominant
Mutations in DNA mismatch repair genes (MMR)
Increases the risk of multiple cancers particularly colorectal

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116
Q

What are the 2 broad areas of colorectal cancers?

A

Left sided (LS) Colorectal cancer
Right Sided (RS) colorectal cancer.

These may have different signs and Sx

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117
Q

What are the symptoms of bowel cancer?

A

Change in bowel habit
Weight loss
Anaemia (iron deficiency)
Tenesmus (feeling to keep having to go empty your bowels)
Abdominal pain
PR bleed
Red flags (ALARMS)

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118
Q

What are the Symptoms of Right sided colorectal cancer?

A

Usually asymptomatic until they present with iron deficiency anaemia due to bleeding
May present with a mass
Weight loss
Abdominal pain

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119
Q

What are the clinical signs of Bowel cancer?

A

LS CC - rectal mass, PR bleeding

RS CC - Iron Deficiency anaemia

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120
Q

What is the Diagnostic investigation used for Bowel cancer diagnosis?

A

FIT Test - screening test for micro blood particles in faeces

Gold standard - Colonoscopy and Biopsy

Digital Rectal exam
38% of colorectal cancers can be detected by DRE

1st Line staging - CT-CAP

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121
Q

What is the FIT test?

A

Faecal immunochemical Test for bowel cancer screening:
Looks for Hb in stool.

Performed in anyone over 50 with unexplained Weight loss and no other symptoms.
Performed in over 60s with a change in bowel habit

done in ages 65-74 years every 2 years

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122
Q

What is the staging classification for bowel cancer?

A

Dukes staging:

TNM Staging:
Tumour: TX - T4
Nodes: NX-N2
Metastasis: M0-M1

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123
Q

What is the Dukes staging of Bowel Cancer?

A

Duke stage:
A – 95% 5 year survival - confined to submucosa

B - 75% 5 year survival, invasion through muscularis (no lymph involvement)

C - 35% 5 year survival, involvement of regional lymph nodes
C1 - 1-4 nodes
C2 - >4 nodes

D - 10% 5 year survival - mets

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124
Q

What is the TNM classification for bowel cancer?

A

T1 - submucosa
T2 - musclaris
T3 - Serosa
T4 - Breached serosa invading other structures

N0 - no tumour in regional lymph nodes
N1 - Tumour seen in 1-3 regional lymph nodes
N2 - Tumour seen in 4+ regional lymph nodes

M0- Not Mets
M1 - Mets

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125
Q

What is the Treatment for Bowel cancer?

A

Surgical resection - curative if no mets
+ chemotherapy

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126
Q

What are some differential Diagnoses of Colorectal Cancer?

A

Anorectal pathology
Haemorrhoids
Anal fissue
Anal prolapse

Colonic pathology
Diverticular disease
IBD
Ischaemic colitis

Small intestine and stomach pathology
Massive upper GI bleed – haematochezia
Meckel’s diverticulum

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127
Q

What is Dyspepsia?

A

Functional Dyspepsia is a form of a Functional Gut disorder like IBS where there are Sx of Indigestion without any other clear cause.

Dyspepsia can also be a symptom of certain conditions such as PUD

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128
Q

What are the Sx of Dyspepsia?

A

Early satiation
Epigastric pain and Reflux (like GORD)
Heartburn
Bloating
Hoarse Cough
Extreme Fullness.

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129
Q

What is the Epidemiology of Dyspepsia?

A

Common – affecting up to 25% of population a year

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130
Q

What is the cause of Dyspepsia?

A

Functional Dyspepsia - Unknown Cause.
Other causes may be PUD.

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131
Q

What are the diagnostic investigations for Dyspepsia?

A

Endoscopy is used to find an underlying cause.
If there is no obvious cause then it may be functional dyspepsia

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132
Q

What is the Treatment for Dyspepsia?

A

If underlying cause then Tx.

If functional - Give reassurance and dietary review.

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133
Q

What is a Mallory-Weiss Tear (MWT)?

A

Longitudinal lacerations limited to the mucosa and submucosa
Found at the border of the gastro-oesophageal junction (GOJ)

Caused by sudden increases in intra-abdominal pressure

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134
Q

What is the pathophysiology of a MWT?

A

Dilations and tears caused by a sudden rise in intra abdominal and transmural pressure across the GOJ secondary to vomiting and retching in the presence of pre existing gastric mucosal damage.

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135
Q

What are the risk factors for MWT?

A

Any condition that predisposes retching/vomiting:
Gastroenteritis, Bulimia etc.

Alcoholism
Chronic cough
Hiatus hernia
GORD

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136
Q

Who is typically affected by a MWT?

A

Male with acute Hx of retching after a night out.
40-60yrs

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137
Q

What are the symptoms of a MWT?

A

Preceding retching and vomiting
Haematemesis
Melaena - rare
Epigastric pain

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138
Q

What are the primary investigations for a MWT?

A

Calculate Glasgow Blatchford score and Rockall Score (post Endoscopy)

1st Line:
FBC - anaemia
U&Es - raised urea

GS:
Upper GI endoscopy

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139
Q

What is the management of a MWT?

A

Usually self limiting - manage contributing factors

If persistent bleeding:
ABCDE assessment
Upper GI endoscopy - clipping/thermal coagulation
High dose IV PPI (pantoprazole) - give after endoscopy

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140
Q

What is the difference between a MWT and an oesophageal varices?

A

A MWT is caused by increased intraabdominal/transmural pressures that cause tears in preexisting mucosal damage.

An oesophageal varices is a consequence of portal HTN due to decompensated liver failure which causes dilation of the oesophageal blood vessels that then become prone to rupture.

Both can cause an upper GI bleed

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141
Q

What are some differential Diagnoses for a Mallory Weiss Tear?

A

Gastroenteritis
Peptic ulcer
Cancer
Oesophageal varices

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142
Q

If you have a patient with acute haematemesis what should you consider?

A

Hx of Liver disease + portal HTN = Oesophageal Varices

No Hx of liver disease but acute Hx of Retching = MWT

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143
Q

Describe h.pylori.

A

A gram negative bacilli with a flagellum that is present in 50% of the populations gastric mucosa

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144
Q

How does helicobacter pylori infection cause gastric damage?

A

Lives in gastric mucus
Secretes urease which splits urea in stomach into CO2 + ammonia
Ammonia + H+ 🡪 ammonium
Ammonium, proteases, phospholipases and vacuolating cytotoxin A damages gastric epithelium
Causes inflammatory response reducing mucosal defense 🡪 mucosal damage

Also causes increased acid secretion
Gastrin release (from G cells) 🡪 more acid secretion
Triggers release of histamine 🡪 more acid secretion
Increases parietal cells mass 🡪 more acid secretion
Decreases somatostatin (released from D cells) 🡪 more acid secretion

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145
Q

What conditions can arise as a result of H.pylori infection?

A

Peptic Ulcer Disease (PUD)
Gastritis
Gastric carcinomas

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146
Q

What is the diagnostic test to investigate H.pylori infection?

A

1st line: Urea breath test
Stool antigen test

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147
Q

What is the treatment of H.pylori infection?

A

Triple-therapy: For 7 days
Proton Pump Inhibitor - Omeprazole
Clarithromycin
Amoxicillin (metronidazole if CI)

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148
Q

What is Inflammatory bowel disease?

A

Umbrella term for 2 main diseases causing inflammation of the GIT Tract.
Ulcerative Colitis and Crohn’s Disease.

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149
Q

What is Crohn’s Disease?

A

Form of IBD
Granulomatous inflammation of any part of the gut
Characterised by Skip lesions arising anywhere between the mouth and anus.
Transmural inflammation with granuloma formation

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150
Q

What can cause Crohn’s Disease?

A

NOD-2 mutation
Bacterial immune mediated response - TNFalpha, IL-1, IL-6

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151
Q

What are the features of Crohn’s Disease?

A

Crohn’s (Crows NESTS):
N - No Blood or mucus in stool
E - Entire GI Tract - from mouth to anus can be affected
S - Skip Lesions on Endoscopy
T - Terminal Ileum is most affected and Transmural inflammation
S - Smoking is a risk factor - dont set the nest on fire

CHRISTMAS:
C - Cobblestones
H - High temperature
R - Reduced lumen
I - Intestinal fistulae
S - Skip lesions
T - Transmural
M - Malabsorption
A - Abdominal pain
S - Submucosal fibrosis

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152
Q

Where is the most commonly affected region of the GI tract in Crohn’s Disease?

A

The Terminal ileum and colon.

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153
Q

What is the inflammation like in Crohn’s Disease?

A

Transmural - full thickness
Occurs in skip lesions (points of inflammation and no inflammation) across GIT
Can lead to fistulas, Strictures and adhesions

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154
Q

What are the Micro and Macro features of Crohn’s Disease?

A

Macroscopically
Skip lesions
Cobblestone appearance due to ulcers and fissures in mucosa
Thickened and narrow

Microscopically
Transmural – affects all layers of bowels
Non-caseating granulomas (aggregations of epithelioid histiocytes)
Increased Goblet cells

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155
Q

Who is typically affected by Crohn’s Disease?

A

Highest incidence and prevalence in Northern Europe, UK and North America
F>M
Presents mostly at 20-40

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156
Q

What are the risk factors for Crohn’s Disease?

A

FHx - NOD2 mutation
Caucasian
Female
NSAIDs
Depression
HLA-B27
Smoking
Chronic Stress

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157
Q

What is the pathophysiology of Crohn’s Disease?

A
  • Faulty GI Epithelium - Pathogens enter wall
  • Exaggerated inflammatory response
  • Formation of Granuloma + destruction of GI tissues
  • Transmural ulcers + skip lesions
  • Cobblestone appearance due to fissures forming.
  • As the wall is healing
    Fistulas
    Adhesions form
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158
Q

What are the signs of Crohn’s Disease?

A

Abdominal tenderness (RLQ)
Fever, Weight loss and fatigue
Malabsorption
Changes in bowel habit
Blood, fistulas, fissures on PR exam
Aphthous - mouth ulcers

Extra-intestinal Manifestations: (less common in Crohns’)
Erythema nodosum
Anal fissures
Episcleritis

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159
Q

What are the symptoms of Crohn’s Disease?

A

Diarrhoea
RLQ abdominal pain (ileum)
Fatigue, fever, Nausea, vomiting
Tenderness

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160
Q

What is Ulcerative Colitis?

A

Form of IBD
Inflammation of the rectum which extends proximally but never beyond the ileocecal valve.
Mucosal and Submucosal inflammation with crypt abscesses and neutrophil infiltration.

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161
Q

What can Cause Ulcerative Colitis?

A

Unknown aetiology
NSAIDs - associated with IBD onset and flares
Potentially autoimmune as it is associated with HLA-B27 gene and pANCA

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162
Q

Where is the most commonly affected region in Ulcerative colitis?

A

Only affects the rectum (proctitis) and continuous colon.
Never past the ileocecal valve to the small bowel

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163
Q

What is the inflammation like in Ulcerative Colitis?

A

continuous inflammation of the Large bowel.
Mucosal and Submucosal layers are affected (not transmural)
Can lead to crypt abscesses and neutrophil infiltration.

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164
Q

What are the Macro and Micro features of Ulcerative Colitis?

A

Macroscopically
Continuous inflammation (no skip lesions)
Ulcers
Pseudo-polyps

Microscopically
Mucosal inflammation
No granulomata
Depleted goblet cells
Increased crypt abscesses

Paneth cells are involved in innate immunity and suggest an inflammatory condition when found in the descending colon

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165
Q

What are the features of Ulcerative Colitis?

A

U-C = CLOSEUP:
Continuous inflammation From distal (rectum) to proximal (ileocaecal valve (never past it))
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary Sclerosing Cholangitis

ULCERATIONS:
Ulcers
Large intestine
Carcinoma – risk of
Extra-intestinal manifestations – uveitis, erythema nodosum, sclerosing cholangitis
Remnants of older ulcers - pseudo polyps
Abscesses in crypts
Toxic megacolon – risk of
Inflamed, red, granular mucosa
Originates at rectum
Neutrophil invasion
Stool is bloody and has mucous

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166
Q

Who is typically affected by ulcerative Colitis?

A

Highest incidence in Northern Europe, UK and North America
Affects males and females equally
Presents mostly at 15-30
Non-Smokers

Bimodal age distribution from 15-25yrs to 55-75yrs

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167
Q

What are the risk factors for Ulcerative Colitis?

A

FHx
HLA-B27
Caucasian
Non-smoker - Smoking relieves UC
NSAIDs – associated with onset of IBD and flares of disease
Chronic stress and depression triggers flares

168
Q

What are the clinical signs of Ulcerative Colitis?

A

Abdominal Tenderness (LLQ)
Fever
Fresh Blood on rectal exam
Blood Diarrhoea
Extra-intestinal manifestations (more common in UC)

169
Q

What are the symptoms of Ulcerative Colitis?

A

Diarrhoea
Blood and Mucus in stool
Urgency and Tenesmus (rectal defaecation pain)
Abdominal pain - particularly in the LLQ
Weight loss and malnutrition - more common in Crohn’s

170
Q

What are the Extra-intestinal manifestations of IBD?

A

A PIE SAC:
Ankylosing Spondylitis (HLA-B27)

Pyoderma Gangrenosum
Iritis
Erythema Nodosum

Sclerosing Cholangitis
Aphthous Ulcers/Amyloidosis
Clubbing

171
Q

What is the most common extra intestinal manifestation in IBD?

A

Arthritis

172
Q

What are the investigations for Crohn’s Disease?

A

Colonoscopy – diagnostic
Biopsy
Barium enema

Stool sample – rules out infectious diseases

FBC
Raised ESR/CRP
Often low Hb due to anaemia
Malabsorption - Low Iron, Vit B, Folate
Faecal calprotectin – indicates IBD but not specific

173
Q

What are the investigations for Ulcerative Colitis?

A

Colonoscopy - diagnostic
Biopsy – crypt abscesses
Barium enema

Bloods:
FBC – raised ESR and CRP, low Hb
Test for pANCA – negative in Crohn’s
Iron deficiency anaemia
Faecal calprotectin - Indicates IBD

Stool sample – rule out infectious causes

CT/MRI
Abdominal X-ray - Toxic Megacolon

174
Q

What are the diagnostic investigations for IBD?

A

Routine Bloods - anaemia, infection, LFTs, TFTs, Kidney function

CRP - inflammation and active diseaes

Faecal Calprotectin - 90% sensitive and specific to IBD

Endoscopy (OGD and colonoscopy) + biopsy is diagnostic

Imaging - CT/Abdo USS for complications - fistulas, fissures, strictures

175
Q

What is the main raised inflammatory marker in IBD?

A

Faecal Calprotectin levels:
released by the intestines when inflamed can help distinguish between IBD and IBS.

176
Q

What is the gold standard diagnostic test for IBD?

A

Endoscopy/Colonoscopy + biopsy

177
Q

What is the First line treatment in inducing remission in Crohn’s Disease?

A

Steroids - oral prednisolone or IV Hydrocortisone

If ineffective alone then add immunosuppressant:
1st - Azathioprine
2nd - Methotrexate
3rd - Infliximab + Mercaptopurine
Adalimumab

178
Q

What is the first line treatment for maintaining remission of Crohn’s disease?

A

First line:
Azathioprine/Mercaptopurine + Methotrexate

179
Q

When is it possible to use surgery to treat Crohn’s Disease?

A

When the disease only affects the distal ileum
Can also be used to treat strictures and fistulas secondary to Crohn’s

Usually a Right Hemi-colectomy

180
Q

What is the First line treatment in inducing remission in Ulcerative Colitis?

A

Mild to moderate disease:
First line - Aminosalicylate (Mesalazine)
Second line - Corticosteroids (prednisolone)

Severe Disease:
First line - IV Corticosteroids (hydrocortisone)
Second Line - IV Ciclosporin

(Gold) Surgery - Colectomy

181
Q

What is the first line treatment for maintaining remission of Ulcerative Colitis?

A

Aminosalicylate - Mesalazine
Azathioprine
Mercaptopurine

182
Q

What aminosalicylate is used to treat Ulcerative Colitis?

A

Mesalazine - oral or rectal

183
Q

When is Surgery used in Ulcerative Colitis?

A

Typically UC only affects the colon and rectum
Surgery to remove these can remove the disease leaving the patient with a ileostomy (stoma)

184
Q

What are some complications of Crohn’s Disease?

A

Peri-anal Abscess
Anal Fissure
Anal Fistula
Strictures and obstruction
Perforation and Sepsis
Anaemia and Malabsorption
Osteoporosis

185
Q

What are some complications of Ulcerative Colitis?

A

Toxic Megacolon
Perforation
Colonic Adenocarcinoma
Strictures and Obstruction
Extra-intestinal Manifestations

186
Q

How is Toxic Megacolon identified?

A

AXR or CT

187
Q

What are the differential diagnoses to exclude for IBD?

A

Alternative causes of diarrhoea should be excluded
Salmonella spp.
Giardia intestinalis
Rotavirus

188
Q

What is Irritable Bowel Syndrome?

A

Irritable bowel syndrome is a chronic, functional bowel disorder characterised by abdominal pain and altered bowel habits with no underlying pathology.

189
Q

What are functional Gut disorders?

A

These are disorders of the gut-brain interaction that do not have a detectable structural or biochemical abnormality.
They are abnormal symptoms within a normal gut.

190
Q

What part of the GI Tract is often affected in irritable bowel Syndrome?

A

The lower GI Tract.

191
Q

What is the Prevalence of IBS and who does it typically affect?

A

Prevalence - Up to 20% of the population.
Affects more women than men
Common in younger adults.

192
Q

What are the different types of IBS?

A

IBS-C = mostly constipation
IBS-D = mostly diarrhoea
IBS-M = mostly mixed (mix of C/D)

193
Q

What are some possible risk factors for IBS?

A

Female sex
FHx
GI infection/inflammation
Dietary factors
Psychosocial Factors - stress/anxiety/depression
Drugs

194
Q

When should you consider a diagnosis of IBS?

A

In a Px who has had any of these symptoms for at least 3+ months:
Abdominal Pain
Bloating
Changing in bowel habits

With NO UNDERLYING CAUSE

195
Q

What are the symptoms of IBS?

A

Abdominal Pain
Bloating
Change in bowel habit
Constipation
Diarrhoea
IMPROVED AFTER OPENING BOWELS
worse after eating.

196
Q

How is IBS Diagnosed?

A

Roman IV Criteria:
IBS is defined as recurrent abdominal pain that has occurred, on average, at least:
one day per week
over the last three months
and symptoms begin at least six months ago.
In addition, pain is associated with ≥2 of the following criteria:

Relieved by defaecation
Change in Bowel Appearance
Change in Bowel Frequency

All with normal results on Ix

197
Q

What Investigations should be done to rule out other causes of Sx in IBS?

A

Diagnosis of exclusion:
Blood Tests - FBC, CRP, ESR all normal
Faecal Calprotectin - negative (excludes IBD)
Anti -TTG Abs - Excludes Coeliacs
Colonoscopy - Cancer is excluded

198
Q

What is the Initial Conservative management of IBS?

A

Positive Diagnosis - Tell them that although they have no pathology present they do have IBS (a condition)

Advice and reassurance - no serious underlying pathology present.

Adequate fluid intake and Regular physical activity.

General healthy diet advice - eg. more fibre if IBS-C (LOW FODMAP Diet)

Probiotic supplements - 4 weeks

Second Line = Medications

199
Q

What are the first and second line medications used in IBS? (second line management)

A

Sx Management:
First Line:
Loperamide - if diarrhoea is key symptom
Linaclotide/Ispaghula Husk - if constipation is key symptom
Antispasmodics - Mebeverine

Second Line:
Tricyclic antidepressants - amitriptyline (5-10mg)

Third Line:
SSRI - Citalopram

CBT - help Px psychologically manage the condition.

200
Q

What dietary foods should IBS Px avoid?

A

FODMAP:
Fermentable - CHOs
Oligosaccharides
Disaccharides
Monosaccharides
And
Polyols

201
Q

What are some complications of IBS?

A

Mood disorders - increased risk of depression and anxiety

Poor Quality of Life

202
Q

What are some differential diagnoses for IBS?

A

IBD
Colorectal cancer
Ovarian cancer

203
Q

What are the alarm features of GI conditions?

A

Age >45
Hx of Symptoms
Unintentional Weightloss
Nocturnal Sx
FHx of GI cancer or IBD
GI bleeding
Palpable mass or lymphadenopathy
Evidence of Fe anaemia
Evidence of Inflammation on blood/stool sample.

204
Q

What is Coeliacs Disease?

A

An autoimmune conditions where exposure to gluten peptides causes an autoimmune reaction that causes inflammation in the small intestine.

This results in malabsorption

205
Q

What foods can contain gluten peptides?

A

Wheat
Barley
Rye

206
Q

What are the Genes and the auto antibodies associated with coeliacs disease?

A

HLA DQ2, HLA DQ8
Anti-tissue transglutaminase (anti-TTG)
Anti-endomysial (Anti-EMA)

207
Q

What is the pathophysiology of Coeliacs Disease?

A

Type IV hypersensitivity
Gluten Peptides (Gliadin) binds to secretory IgA in mucosal membrane

Gliadin-IgA is transcytosed to the lamina propria where the enzyme Tissue Transglutaminase (TTG) deaminates Gliadin which increases its Immunogenicity.

Deaminated gliadin is taken up by macrophages and expressed on MHC II complex via HLA DQ2 and DQ8

APCs present Gliadin antigen to T helper cells so they release inflammatory cytokines and stimulate B cells

This causes villous atrophy, crypt hyperplasia and intraepithelial lymphocyte infiltration

🡪 reduced SA to absorb nutrients 🡪 B12, folate and iron cannot be absorbed 🡪 anaemia

208
Q

What is the prevalence of Coeliacs disease in the UK?

A

1%

209
Q

What are the risk factors for Coeliacs disease?

A

FHx
HLA DQ2/HLA DQ8
PHx of autoimmune disease
IgA deficiency
Downs
Turners

210
Q

How does Coeliacs disease often present?

A

Often ASx

Can present with:
Diarrhoea
Steatorrhea – fatty stools due to reduced fat absorption in intestines
Abdominal pain
Abdominal distension
Weight loss
Rash on Elbows - dermatitis Herpatiformis
Failure to thrive
Nutritional deficiency
Anaemia - secondary to Fe, Vit B12 or folate def.

211
Q

What skin condition is associated with coeliacs disease?

A

Dermatitis Herpetiformis
An itchy vesicular skin eruption caused by deposition of IgA

Treated with Dapsone

212
Q

What should patients with suspected coeliacs disease do prior to investigation?

A

Gluten challenge:
Should be ON a gluten containing diet for 6 weeks prior to investigations

213
Q

What diagnostic investigations are carried out for coeliacs disease?

A

Carried out Post gluten challenge:
Serology:
1st Line: Raised anti-TTG Abs
Total IgA - exclude IgA deficiency - must also be done

2nd Line: Raised anti-EMA Abs
Anti-Gliadin

Gold Standard Endoscopy and Duodenal biopsy:
Crypt hypertrophy
Villous Atrophy
Increased intraepithelial lymphocytes

FBC:
Low Hb
Low B12
Low Folate
Low Ferritin

214
Q

What is the gold standard diagnostic test for Coeliacs disease?

A

Small bowel biopsy and Histology

215
Q

How is the biopsy assessed for Coeliacs?

A

Marsh Classification:
0 normal
1 raised intra epithelial lymphocytes (IEL)
2 raised ILE + crypt hyperplasia
3a partial villous atrophy (PVA)
3b subtotal villous atrophy (SVA)
3c total villous atrophy (TVA)

216
Q

What other investigations may you consider for coeliacs disease?

A

FBC
Nutritional Status
HLA Testing

217
Q

What autoimmune conditions is Coeliacs disease associated with?

A

T1DM
Thyroid disease
Autoimmune Hepatitis
PBC
PSC

218
Q

What are some complications of untreated coeliacs disease?

A

Vitamin Deficiency
Malabsorption
Anaemia
Osteoporosis
Ulcerative jejunitis
Non-hodgkin lymphoma
Enteropathy associated T cell lymphoma of the intestine

219
Q

What is the management of coeliacs disease?

A

A lifelong gluten free diet - can be curative but will relapse upon consuming gluten

Dietary supplements - Ca Vit D, Fe if the Px diet is insufficient

Test all new cases for T1DM

Dexa-scan for osteoporotic risk.

220
Q

How does Lactose intolerance lead to gas.

A

cant break down lactose.
Once in the colon, the bacteria can ferment the unbroken down lactose leading to gas production.

221
Q

Define Malabsorption?

A

The failures to fully absorb nutrients in the small intestine either because of the destruction to the epithelium or due to a problem in the lumen meaning food cannot be digested

222
Q

What disorders of the intestine can lead to malabsorption?

A

Coeliac disease
Tropical Sprue
Crohn’s
Parasitic infection

223
Q

What are some pathological reasons for malabsorption?

A

defective epithelial transport

insufficient absorptive area - gluten sensitive enteropathy (coeliacs)/ Inflammation (Crohn’s)

Defective intraluminal digestion - lack of digestive enzymes (pancreatic, CF, bile secretion)

bowel resection or bypass.

Lymphatic obstruction

224
Q

What are the symptoms of malabsorption?

A

Weight loss
Steatorrhea
Diarrhoea
Anaemia

225
Q

What are the signs of malabsorption?

A

Anaemia – decreased iron, B12, folate
Bleeding disorders – decreased Vitamin K
Oedema – decreased protein
Metabolic bone disease – decreased vitamin D
Neurological features - B12

226
Q

What are the investigations for malabsorption?

A

FBC
Increased/decreased MCV
Decreased calcium/iron/B12 and folate
Increased INR
Stool sample microscopy
Coeliac tests

227
Q

What is Tropical Sprue?

A

Severe malabsorption (of 2 or more substances) accompanied with diarrhoea and malnutrition of unknown cause from the tropics

228
Q

Where does Tropical Sprue occur?

A

To visitors or residents of tropical areas such as Asia, Caribbean Islands, and South America

229
Q

What are the signs and symptoms of Tropical Sprue

A

Diarrhoea/Steatorrhoea
Weight loss
Abdominal Pain
Fatigue
Dehydration
Malabsorption

230
Q

What are the investigations for tropical sprue?

A

GOLD Ix - Jejunal tissue biopsy
Shows incomplete Villous atrophy

231
Q

What is the treatment for Tropical Sprue

A

Drink Treated water + tetracycline for 6 months

232
Q

What is acute gastritis?

A

Inflammation of the stomach that tends to present with nausea and vomiting

233
Q

What is Enteritis?

A

Inflammation of the intestines that tends to present with diarrhoea

234
Q

What is Gastroenteritis?

A

Inflammation of the GI Tract from the stomach all the way through the intestines.
This tends to present with nausea, vomiting and diarrhoea

235
Q

What is the most common cause of gastroenteritis?

A

Viral infection

236
Q

What are the common viral causes of gastroenteritis?

A

Rotavirus
Norovirus
Adenovirus

237
Q

Who is typically affected by gastroenteritis?

A

It can affect anyone and people generally recover well.

It can be serious in Px who are immunocompromised, very young or very old.

238
Q

What must be done if a patient has gastroenteritis in a healthcare environment?

A

Isolate the patient to prevent spread to other patients

239
Q

What are the clinical features of viral gastroenteritis?

A

Diarrhoea
Nausea
Vomiting

240
Q

How long until symptoms are resolved for the main viral causes of gastroenteritis?

A

Rotavirus - 3-8 days
Norovirus - 1-3 days
Adenovirus - 1-2 weeks

241
Q

What are the risk factors for gastroenteritis?

A

Ingestion of undercooked food
Reheating meals
poor sanitary conditions
Travelling to endemic areas - SE Asia, Sub Saharan Africa
Immunosuppression

242
Q

What are the general symptoms of gastroenteritis?

A

Vomiting
Diarrhoea
Abdominal cramps
Fever
Lethargy

243
Q

What are the general clinical signs of a Px with gastroenteritis?

A

Dehydration
Electrolyte imbalance
Hypotension
Tachycardia
Reduced Urine Output

244
Q

What are the potential causes of gastritis?

A

Autoimmune
Increased acid - overcome mucosal buffer
H. pylori - stimulates more acid production
NSAIDs - inhibit COX and prostaglandin synthesis
Mucosal ischaemia - loss of barrier function
Campylobacter infection
Viral infection

245
Q

How do NSAIDs lead to gastritis?

A

NSAIDs inhibit COX which prevents prostaglandin synthesis.

This means that prostaglandins cannot stimulate mucin production and therefore there is reduced mucosal defence.

This allows the stomach acid to then attack the gastric wall leading to ulcer formation and gastritis

246
Q

What is the gold standard diagnostic test for gastritis?

A

Endoscopy + biopsy

247
Q

What are the key bacterial causes of Gastroenteritis?

A

E.coli - particularly E.coli 0157 (HTEC/STEC)
Campylobacter
Shigella
Salmonella
Bacillus Cereus
Yersinia

248
Q

What investigations should be done for a patient with gastroenteritis?

A

If mild/moderate - no Ix required and Px are discouraged from attending hospital to prevent spread

Ix to consider:
FBC
Raised ESR/CRP - infection/inflammation
U&E
Stool culture - for bacteria
Stool Microscopy
PCR- Viruses

249
Q

What is the main parasitic cause of diarrhoea?

A

Giardia Lamblia
Tx with Metronidazole

250
Q

What is the management for gastroenteritis?

A

Viral - usually self limiting - 7 days

Mild-moderate:
Bland diet, oral rehydration

Sx management:
- Antiemetics - metoclopramide
- Antimotility - loperamide
Broad Spec Abx - ciprofloxacin, ceftriaxone

Severe:
IV fluids

251
Q

What should be avoided in gastroenteritis caused by E.coli 0157?

A

Antibiotics as these can lead to HUS.

252
Q

What are some complications of gastroenteritis?

A

Dehydration
Malnutrition
Post infectious IBS

253
Q

What is GORD?

A

Gastro-oesophageal Reflux Disease

Where acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus.

254
Q

What is the lining of the lower oesophagus and the lining of the stomach?

A

Oesophagus - Non- keratinised stratefied Squamous epithelial lining

Stomach - Columnar Epithelial Lining

255
Q

What can GORD be caused by?

A

Increased sphincter relaxation
Raised Intragastric pressure - Pregnancy/Obesity
Reduced Sphincter tone
Hiatus Hernia
Anatomical abnormalities of the GOJ
Oesophageal Dysmotility

256
Q

What are the risk factors of GORD?

A

Increasing Age
FHx
Obesity - raised Intragastric Pressure
Pregnancy - raised intragastric pressure
Hiatus Hernia - disrupts GOJ
Smoking and alcohol
Drugs - nitrates, caffeine, CCBs
Fatty foods

257
Q

What are the Symptoms of GORD?

A

Heartburn
Acidic taste at back of mouth
Dysphagia
nausea
Hoarseness and chronic cough
Dyspepsia

258
Q

What are the diagnostic investigations for GORD?

A

Clinical Diagnosis
Endoscopy if red flags (>55yrs)

FBC - Anaemia
H.pylori test - stool antigen/Urea breath test

Endoscopy - often normal

24 hr pH study - pH <4 for more than 4% of time is abnormal

Oesophageal manometry - functionality test of LOS - rule out motility disorders

259
Q

What is the conservative management of GORD?

A

Lifestyle advice:
weight loss
avoidance of triggering foods
smaller lighter meals
stop smoking
avoid heavy meals before bed
Sleep with head tilted upwards

260
Q

What medical management could be used for GORD?

A

Acid neutralising medication - Gaviscon, Rennie

PPI - omeprazole, Lansoprazole

H2 receptor antagonist - ranitidine, cimetidine

Surgery - Laparoscopic fundoplication

261
Q

What are some complications of GORD?

A

Barrett’s Oesophagus
Oesophageal ulceration/stricture.

262
Q

What bacteria leads to an increased risk of GORD/ barrett’s Oesophagus?

A

Helicobacter Pylori:
Gram negative aerobic bacteria

263
Q

What is Barrett’s Oesophagus?

A

The constant reflux of acid into the lower oesophagus causes a change in the epithelium called metaplasia.

This is a change from the stratified squamous epithelium to the columnar epithelium for the stomach.

Barrett’s Oesophagus is considered premalignant.

264
Q

What does barrett’s Oesophagus predispose a patient to?

A

Considered premalignant.
Predisposes the Px to adenocarcinoma.

265
Q

What is the treatment of Barrett’s Oesophagus?

A

Using Proton Pump Inhibitors + Endoscopic Surveillance
Omeprazole

Ablation therapy in Px with Dysplasia may be used to destroy the epithelium for it to be replaced with normal tissue.

266
Q

What is Achalasia?

A

An oesophageal motility disorder characterised by an inability for the LOS (lower oesophageal sphincter) to relax in response to swallowing.

267
Q

What is the pathophysiology of Achalasia?

A

Unknown but thought to be due to a loss of inhibitory neurones secreting VIP and NO within the Auerbach plexus.

This leads to the constant contraction of the LOS and dilation of the oesophagus above the LOS.

268
Q

What are the risk factors for achalasia?

A

Increasing Age
Genetics
Infection - Chagas disease (Trypanosoma Cruzi)
Autoimmune disease

269
Q

What are the symptoms of Achalasia?

A

NON PROGRESSIVE DYSPHAGIA -
BOTH solids and liquids (dysphagia)

Regurgitation

Heartburn

Coughing when lying down

Weight loss - due to reduced oral intake.

270
Q

What are the primary investigations of Achalasia?

A
  1. Upper GI Endoscopy (OGD) - low sensitivity for achalasia but excludes malignancy.
  2. Barium Swallow - Bird beak - diagnostic except in early disease.
  3. Oesophageal Manometry - GS for establishing the diagnosis
271
Q

\What is the gold standard investigation for establishing a diagnosis of achalasia?

A

Oesophageal manometry:
Incomplete relaxation of the LOS +
Oesophageal aperistalsis

272
Q

What is the management of Achalasia?

A

Lifestyle: Smaller more frequent meals

Medical:
1. CCBs (nifedipine) + nitrates to reduce the pressure and relax LOS.
(often ineffective)
2. Botox to relax LOS
3. Surgical - Heller’s Cardiomyotomy is first line for those fit for surgery.

Balloon Stent

273
Q

What are some complications of Achalasia?

A

GORD - as a complication of cardiomyotomy.

Malignancy

Aspiration pneumonia due to regurgitation

perforation.

274
Q

What are the risk factors for barrett’s Oesophagus?

A

GORD
Middle age
male - 7x more likely
Caucasian
smoking
obesity

275
Q

What are the Ix for Barrett’s Oesophagus?

A

upper GI Endoscopy and Biopsy

Reveals metaplasia

276
Q

What are the 2 types of bowel Ischaemia?

A

Mesenteric Ischaemia - Small bowel

Ischaemic Colitis - Large bowel

277
Q

What is Bowel Ischaemia?

A

Diminished blood flow to the bowel where there is not enough oxygen or nutrients supplied to the bowel that leads to inflammation

278
Q

What causes Ischaemic colitis?

A

Atherosclerosis
Thrombosis
Emboli
Affecting the IMA (sometimes SMA)

Decreased CO and arrhythmias
Vasculitis

279
Q

What are the most common sites affected in ischaemic colitis?

A

Watershed areas:
Splenic Flexure (most common)
Sigmoid Colon + Cecum

280
Q

What are the causes of Mesenteric Ischaemia?

A

Superior mesenteric artery thrombosis – most common

Superior mesenteric artery embolism (e.g. due to AF)

Mesenteric vein thrombosis – common in younger patients with

hypercoagulable states

Non-occlusive diseases

281
Q

What are the two types of Mesenteric Ischaemia?

A

Acute mesenteric Ischaemia (AMI) - acute attack, abdominal MI

Chronic Mesenteric Ischaemia (CMI) - long lasting over months, Abdominal Angina

282
Q

What is Chronic Mesenteric Ischaemia?

A

Similar to Angina:
Narrowing of GI blood vessels causing decreased supply to bowel.
RFs are same as cardio RFs

283
Q

What are the symptoms of Chronic Mesenteric Ischaemia?

A

Central colicky abdo pain (post Prandial)
Weight Loss
Abdominal Bruit (due to turbulent blood flow)

284
Q

What are the Investigations and Treatment for Chronic Mesenteric Ischaemia?

A

Ix - CT contrast/angiograpghy

Tx - Lifestyle, Secondary Prevention, Surgery

285
Q

What are the risk factors for bowel ischaemia?

A

Increasing age
Atrial Fibrillation
CVD RFs
Endocarditis
Malignancy
Cocaine use
Vasculitis

286
Q

What are the symptoms of Ischaemic colitis?

A

LLQ pain
Bright bloody stool
Abdominal Bruit/Cardiac Issues (AF/Aneurysm)
+/- signs of hypovolaemic shock

+ N&V
Melaena/Haematochezia
Abdo Distension

287
Q

What is a major risk factor for Acute Mesenteric Ischaemia?

A

Atrial Fibrillation
+other cardio RFs

288
Q

What are the symptoms of Acute mesenteric Ischaemia?

A

Triad of:
Central/RIF acute severe abdominal pain post prandial (disproportionate pain to clinical findings)

No abdominal signs on exam
(guarding/rebound tenderness)

Rapid Hypovolaemic Shock – pale skin, weak rapid pulse, reduce urine output, confusion

289
Q

What is the diagnostic investigation of Ischaemic Colitis?

A

Bloods: Metabolic Acidosis - raised lactate

1st Line: CT/MRI Angiography

GS: Colonoscopy + biopsy
Only after Px is fully recovered.

Rule out other causes (h.pylori)

290
Q

What is the diagnostic investigation of Acute mesenteric Ischaemia?

A

1st Line: CT angiogram
+ FBC, ABG to look for persistent metabolic acidosis
(Raised Lactate)

GS - Colonoscopy

291
Q

What is the management of Ischaemic Colitis?

A

Conservative:
Symptomatic Tx
IV fluids,
Heparin if bleeding
Prophylactic Abx

Surgery if infected colon - bleeding, peritonitis etc.

292
Q

What is the management of Acute Mesenteric Ischaemia?

A

Emergency:
Fluid Resus
Abx
IV Heparin - lower thrombo-emboli and reduce clotting

Surgery - remove infarcted bowel

293
Q

What is appendicitis?

A

Acute inflammation and bacterial infection of the appendix.

294
Q

What is the pathogenesis of appendicitis?

A

Luminal obstruction of the appendix leads to the trapping of pathogens and bacteria within the appendix causing infection and inflammation.

The inflammation may proceeds to gangrene and rupture via perforation.

This will release faecal contents and infective material into the peritoneum causing peritonitis

295
Q

What can cause appendicitis?

A

Obstruction:
Faecolith – stones made of faeces
Filarial worms
Undigested seeds
Lymphoid hyperplasia – can obstruct tube and lymphoid follicles can grow during viral infection
Bacteria – Campylobacter jejuni, Yersinia, salmonella, bacillus cereus

296
Q

What are complications of a ruptured appendix?

A

Peritonitis
Sepsis
Death

297
Q

What is the appendix and where is it located?

A

a small thin tube arising from the caecum .
Located in the Right Ileac Fossa (RIF) at the point where the 3 teniae coli meet.

298
Q

What are the risk factors for appendicitis?

A

Typically affects young age - 10-20yrs
Male
Frequent Abx use
Smoking

299
Q

What is the key clinical sign of appendicitis?

A

periumbilical pain which migrates to the RIF over the first 24hrs where it becomes localised.

Often tenderness at Mcburney’s Point on palpation.

300
Q

What is McBurney’s Point?

A

2/3 distance from umbilicus to the ASIS

301
Q

What are some other symptoms of appendicitis?

A

classical abdominal pain.
Low grade fever
Reduced appetite and anorexia
Nausea and Vomiting
Diarrhoea - rare

302
Q

What are the clinical signs associated with appendicitis?

A

RIF tenderness - rebound or percussion tenderness.

Rovsing’s Sign - pain in RIF when pressing on the LIF

Guarding on abdominal palpation.

Obturator and Psoas signs

303
Q

What are psoas and Obturator signs?

A

Psoas - RIF pain on right hip extension

Obturator - RIF pain on right hip flexion and internal rotation

304
Q

What are the signs of appendix rupture?

A

Tachycardia, hypotension and generalised peritonism

Rebound tenderness on RIF

Percussion tenderness

305
Q

What is Rebound Tenderness?

A

increased pain when suddenly releasing deep palpations

306
Q

What can cause appendicitis?

A

Fae Colith - hard solidified faeces causing a obstruction to appendix

Lymphoid Hyperplasia - in peyer’s Patches

other blockages

307
Q

What are the primary investigations for appendicitis?

A

Mostly a clinical diagnosis

CT abdo + pelvis = GS for diagnosis (Abdo USS in children/preggo

Raised inflammatory markers on FBC (Increase WCC), CRP/ESR

Exclude ectopic pregnancy by serum hCG

308
Q

What are the key differential diagnoses of appendicitis?

A

Ectopic pregnancy
Crohn’s Disease
UTI
Diverticulitis
Perforated Ulcer
Food poisoning

309
Q

What is the management of appendicitis?

A

Abx and then Appendectomy (laparoscopic)

Must drain abscesses - these are resistant to Abx

310
Q

What must be ruled out in an appendicitis diagnosis? How is this done?

A

Ectopic pregnancy in females of child bearing age.

Perform pregnancy test

Bloods have Serum hCG test.

311
Q

What is Diverticular Disease?

A

A Symptomatic outpouching of the intestinal Mucosa (diverticula) most commonly affecting the sigmoid colon in the absence of inflammation/infection

This is without inflammation and infection

312
Q

What are some different definitions within diverticular disease?

A

Diverticulum
Diverticulosis
Diverticular disease
Diverticulitis

313
Q

What is the Diverticulum?

A

An outpouching/pocket in the intestinal wall often located at perforating artery sites.

314
Q

What is Diverticulosis?

A

The presence of an outpouching in an Asymptomatic patient.
(95% of diverticula are ASx)

When this is Symptomatic this is diverticular disease

315
Q

What is Diverticulitis?

A

Inflammation of an outpouching due to infection typically causing lower abdominal pain.

316
Q

What is the pathophysiology of diverticular disease?

A

Wall of large intestine has a layer of circular muscle.
The points where arteries enter are areas of weakness.
Increased pressure over time can cause the mucosa to herniate through the muscle layer and pouch causing a diverticulum.

If faecal matter of bacteria gather –> this can lead to inflammation and rupture of the vessels causing GI bleeding

317
Q

Where do you not get diverticula forming?

A

The rectum as it is surrounded by an outer layer of longitudinal muscle preventing the herniation of the bowel mucosa

318
Q

What are some risk factors for diverticular disease?

A

High pressures in Colon:
Constipation
Obesity/Sedentary Lifestyle
NSAIDs
Smoking
Increasing age (>50yrs)
Low Dietary fibre
Connective Tissue Disorders - EDH/MF

319
Q

What are the symptoms of diverticular disease?

A

BBL:
Bowel Habits Changed - Constipation
Bloating and Flatulence
LLQ pain
+ N&V/ +/- Urinary Symptoms

320
Q

What are some additional signs/symptoms of acute diverticulitis?

A

BBL:
Bowel Habits Changed - Constipation
Bloating and Flatulence
LLQ pain

PLUS
N&V/ +/- Urinary Symptoms
Pyrexia
Bleeding
Raised inflammatory markers - CRP, ESR WCC
May have haematochezia

321
Q

What are the primary investigations for diverticular disease?

A

Exam:
Tenderness and Guarding - peritoneum irritated
Distended and Tympanic percussion (GAS)
Bowel Sounds diminished

FBC: inflammatory picture
Increased WCC
U&Es - Urea increased
CRP/ESR - Elevated
Venous blood gas
Blood cultures

Colonoscopy (used for acute bleeds)

Gold Standard: CT Abdo + pelvis with contrast

322
Q

What is the gold standard Ix for diverticular disease?

A

CT Abdo and Pelvis with contrast

323
Q

What is the management of Diverticulosis?

A

Conservative
Watch and Wait

324
Q

What is the management of Diverticular disease?

A

Bulk forming laxatives (ispaghula Husk)
Surgery is possible

325
Q

What is the management of Diverticulitis?

A

Abx - Co-Amoxiclav
Paracetamol (analgesia)
IV Fluid
Liquid Food

Surgery if bleeding is not controlled

326
Q

What are some possible complications of Diverticulitis?

A

Perforation
Peritonitis
Peridiverticular abscess
GI Bleed (Large haemorrhage requiring blood transfusions)
Fistula (e.g., between the colon and the bladder or vagina)
Bowel obstruction
Mucosal Inflammation

327
Q

What is Meckel’s Diverticulum?

A

Paediatric disorder
Failure of obliteration of vitelline duct

Rule of 2s:
2 yrs old
2 inches long
2 ft from ileocaecal valve

Dx is Technitium Scan

328
Q

What is Diarrhoea?

A

A presenting Sx with many DDx
Often 3+ watery stools daily

but could be a increase in the normal bowel passage for an individual Px

329
Q

What level of the Bristol Stool chart symbolises Diarrhoea?

A

5-7

330
Q

What are the Different types of Diarrhoea?

A

Secretory
Osmotic
Exudative
Steatorrhea
Inflammatory
Dysentery

331
Q

What is Dysentery?

A

Severe bloody diarrhoea

332
Q

What are the different time frames for diarrhoea?

A

Acute - <14 days
Subacute - 14-28 days
Chronic >28 days

333
Q

What are the 2 overarching causes of diarrhoea?

A

Infective causes

Non-infective causes

334
Q

Give 5 causes of acute diarrhoea?

A

Abx Associated
Viral
Bacterial
Parasitic
Drugs

335
Q

What are some non-infective causes of diarrhoea?

A

Neoplasms - colorectal cancer
Inflammatory - IBD
Irritable bowel - IBS
Coeliacs
Hormonal - Hyperthyroidism
Radiation
Chemical

336
Q

What kind of diarrhoea can infective causes cause?

A

Non-bloody

Bloody (dysentery)

337
Q

What is the chain of infection?

A

Agent
Mode of transmission
Portal of entry
Host
Person to person spread
Reservoir
Portal of exit

338
Q

What are some diarrhoeal diseases?

A

Dysentery
Typhoid
Hepatitis
Cholera

339
Q

What are the different groups of infective causes of diarrhoea?

A

Viral - most common
Bacterial
Worms
Abx - leading to C.diff
Parasites

340
Q

What are the main viral causes of diarrhoea?

A

Rotavirus - kids
Norovirus - adults

341
Q

What are the main bacterial causes of Diarrhoea?

A

Campylobacter - most common
E.coli
Salmonella
Shigella
Cholera
Clostridium Difficile

342
Q

What are some parasitic causes of Diarrhoea?

A

Giardia lamblia
Entamoeba Histolytica

343
Q

What kind of diarrhoea is caused by E.coli (ETEC) What is the incubation period?

A

0-3 days

Watery stools
Abdominal cramps

This is often travellers Diarrhoea

344
Q

What type of diarrhoea is caused by Bacillus Cereus and what is the incubation period?

A

Abrupt onset vomiting and diarrhoea often after reheating/undercooked rice.

<6hrs

345
Q

What type of diarrhoea is caused by S.aureus? What is the incubation period?

A

Severe vomiting and diarrhoea.

2-4 hrs

346
Q

What type of diarrhoea is caused by Shigella? How is it acquired and what is the incubation period?

A

Bloody diarrhoea
abdominal pain and vomiting

From contaminated food/water
0-3 days incubation

347
Q

What type of diarrhoea is caused by Campylobacter? how is it acquired and what is the incubation period?

A

Flu like prodrome
Bloody diarrhoea
Abdominal pain and fever

Typically from undercooked poultry
2-4 days

348
Q

What type of diarrhoea is caused by Cholera, How is it acquired and what is the incubation period?

A

Profuse “Rice water stool” watery diarrhoea
Severe dehydration due to 20+L lost

0-5 days

349
Q

What type of diarrhoea is caused by Salmonella, how is it acquired and what is the incubation period?

A

Bloody diarrhoea
Vomiting, abdominal cramps and fever

Typically from undercooked meats, raw eggs.
0-3 days.

350
Q

What bacterial infections will lead to low volume bloody diarrhoea?

A

Shigella / E.coli 0157 (EHEC)
Salmonella
Campylobacter

351
Q

What is the incubation period of norovirus?

A

12-48 hrs
Symptoms resolve in 1-3 days

352
Q

What is the incubation period of Rotavirus?

A

2-3 days
Symptoms resolve in 3-8 days

353
Q

What are the treatments for diarrhoea?

A

Viral - often self limiting

Bacterial - depends on the type of infection

Non-infective - Tx underlying cause

354
Q

What is the most serious complication of diarrhoea, how is it counteracted?

A

Dehydration and electrolyte loss

Give fluids + diuralite

355
Q

What cause of diarrhoea should you think of if the Px presents with diarrhoeal symptoms if they are under the age of 3?

A

Rotavirus

356
Q

What cause of diarrhoea should you think of if the Px presents with A Hx of broad spectrum Abx?

A

Clostridium Difficile

357
Q

What cause of diarrhoea should you think of if the Px presents with Ricewater stools?

A

Cholera

358
Q

What cause of diarrhoea should you think of if the Px presents with Guillain Barre?

A

Campylobacter

359
Q

What is the general management for diarrhoea?

A

Often self limiting.

Abx may cause HUS in Shigella/E.coli 0157 cause.

360
Q

What Abx may predispose a patient to C.diff infection?

A

5 Cs:
Clindamycin,
Co-amoxiclav
Cephalosporins
Ciprofloxacin
Carbapenems

361
Q

When may you use Abx in shigella infection? what would you prescribe?

A

In severe infection/diarrhoea

Prescribe Azithromycin or Ciprofloxacin

362
Q

What is Clostridium Difficile?

A

Gram +tve spore forming bacillus

363
Q

What causes C.diff?

A

Induced by Abx (Ciprofloxacin, Co-amoxiclav, Cephalosporin, Clindamycin) which kill normal gut flora and allow C.diff to colonise.

364
Q

What is the Treatment for C.diff infection?

A

Ix:
Stool antigen test or PCR

Tx:
Stop C’s Abx
Vancomycin is now first line against C.diff
+ metronidazole

365
Q

What strains of E.coli cause Watery diarrhoea?

A

ETEC (Travellers)
EPEC
EAEC

366
Q

What Strain of E.coli Causes bloody diarrhoea?

A

EHEC (Enterohaemorrhagic E.Coli)
Also known as E.coli 0157

367
Q

What can happen if you treat EHEC with Abx?

A

Cause Haemoloytic Uremic Syndrome (HUS)

However can be treated with Amoxicillin or Trimethoprim/Nitrofurantoin.

368
Q

What condition does C.difficile Cause?

A

Pseudomembranous Colitis

369
Q

What is Pseudomembranous Colitis?

A

Inflammation of the colon caused by C.diff infection leading to watery diarrhoea, nausea fever

370
Q

What are the risk factors for pseudomembranous colitis?

A

Recent Abx Use - (4 C’s)
Staying in hospital/nursing home
Older age
IBD
Use of PPI
Immunocompromised - CMV infection

371
Q

What are the investigations for pseudomembranous Colitis?

A

Bloods:
Raised WCC

Stool Sample - C.diff infection

Abdo XR or CT - colonic dilation

Colonoscopy - raised yellow plaques

Histology - OWL EYE inclusion bodies for CMV colitis

372
Q

What is the treatment for pseudomembranous colitis?

A

Stop causative agent (Abx)

Give vancomycin + metronidazole
Hydration and electrolyte replacement

Infection control - hand hygeine and isolation

Faecal microbiota transplant in recurrent infections

373
Q

What is Meckel’s Diverticulum?

A

Most common congenital abnormality of the GI Tract when there is incomplete obliteration of the vitelline duct.

Affects 2-3% of the population
Usually a diverticulum in the ILEUM

374
Q

What are the Symptoms of Meckel’s Diverticulum?

A

Often ASx

In 50% of cases the distal ileum contains gastric mucosa that secretes HCL which can lead to peptic ulcers causing bleeding and GI pain.

375
Q

What is the treatment of Meckel’s Diverticulum?

A

Surgical Removal of the Diverticula
(often laparoscopically)

376
Q

What are the different Perianal disorders?

A

Haemorrhoids
Fistulae
Fissures
Perianal Abscesses
Pilonidal Sinus/Abscess

377
Q

What are some differential Diagnoses of Perianal Disorders?

A

Causes of Rectal Bleeding:
Colorectal cancer
IBD
Diverticular Disease

Other perianal Disorders

378
Q

What are Haemorrhoids?

A

Swollen veins surrounding the anus disrupting the connective tissue cushions.

379
Q

How do Haemorrhoids develop?

A

Multifactorial:

Conditions that raise intraabdominal pressure (eg. constipation, COPD,)
+
Straining leads to swelling of the haemorrhoid tissue causing a swell/bleed.

380
Q

What is the most common cause of Haemorrhoids?

A

Constipation with increased straining.

Anal Sex

381
Q

What are the risk factors for Haemorrohoids?

A

Constipation +/- straining
Heave lifting
Increasing age
Anal Sex
Raised Intra-abdominal pressure

382
Q

What are the types of haemorrhoids?

A

Internal
External

383
Q

What are internal Haemorrhoids?

A

Originate ABOVE the dentate line internally.
Painless covered in mucus
Less painful due to a reduced sensory supply.
May feel like incomplete emptying
Graded 1-4

384
Q

What are External Haemorrhoids?

A

Originate BELOW the Dentate Line at anal opening
Very painful - Px may not be able to sit down.
Covered in skin sometimes

385
Q

What is the Dentate line?

A

Divides the anal canal into an upper 2/3rds supplied by the inferior mesenteric plexus

Lower 1/3rd supplied by the pudendal nerve

386
Q

What are the symptoms of Haemorrhoids?

A

Bright red rectal bleeding on wiping
Often not painful
Pruritis ani (itchy bum)
Lump in or around anus/Bulging pain
Straining/Constipation

387
Q

What are the diagnostic investigations for Haemorrhoids?

A

PR exam - external piles are palpable (may be visible)

Proctoscopy - for internal Haemorrhoids

388
Q

What is the first line treatment for haemorrhoids?

A

Conservative management:
Increased dietary fibre and fluid intake

Analgesia - paracetamol

Topical Tx - anusol

389
Q

What are the second line treatments for Haemorrhoids?

A

For 1st and Second Degree:

Rubber band Ligation
Infrared coagulation
Injection Scleropathy
Bipolar Diathermy

390
Q

What is a Perianal Abscess?

A

Walled off collection of stool + bacteria around the anus.

391
Q

What is the most common cause of a perianal abscess?

A

Anal sex causing anal gland infection

392
Q

What are the symptoms of a perianal abscess?

A

Puss in stool
Constant pain and tenderness around anus

393
Q

What is the treatment of a perianal abscess?

A

Surgical drainage and removal

Abx resistant due to the walling off.

394
Q

What is an anal fistula?

A

Abnormal connection “Tracks” between the epithelialized surface of the anal canal and the skin.

395
Q

What are the causes of an anal fistula?

A

often progress from perianal abscesses

abscess discharges (toxic substances) which aids the production of a fistula as the abscess grows.

396
Q

What are the symptoms of a anal fistula?

A

Bloody mucusy discharge
Throbbing pain - worse when sitting
often visible
Pruritus ani

397
Q

What is the treatment for an anal fistula?

A

Surgical - Fistulotomy
Drain Abscess + Abx.

398
Q

What is an Anal Fissure?

A

Tear in the mucosa of the lower anal canal

These are very painful due to the strong sensory supply.

399
Q

What is the most common cause of anal fissures?

A

Hard faeces

400
Q

What is the symptoms of an anal fissure?

A

Extreme defaecation pain
Pruritus ani
Anal bleeding

401
Q

What are the treatments for anal fissures?

A

Increased dietary fibre and fluids - soften stool

Topical creams - lidocaine ointment, GTN ointment,

Surgery if medication fails

402
Q

What are Pilonidal Sinuses?

A

Hair follicles that get stuck in the natal cleft (bum crack) resulting in inflammation, irritation and can become infected

403
Q

Who is more commonly affected by Pilonidal Sinus?

A

Males + hairy people
20-30yrs

404
Q

What are the symptoms of Pilonidal Sinus?

A

Swollen pus filled smelly abscess on bum crack
Visible on exam
Painful swelling over days

405
Q

What is the treatment of Pilonidal Abscesses?

A

Surgical removal of the sinus tract
Hygiene Advice

406
Q

What viral infection can cause colitis?

A

CMV colitis

Characterised by Owl Eye Inclusion bodies

407
Q

What is CMV infection a sign of?

A

Immunosuppressed Px
An AIDS defining illness

408
Q

What is Zenker’s DIverticulum?

A

“Pharyngeal Pouch)

When the cricopharyngeal muscle overtightens causing the throat above it to outpouch.

Food can enter this pouch and accumulates leading to smelly breath and regurgitations

409
Q

Give examples of functional gut disorders?

A

IBS (bowel)
Functional Dyspepsia (stomach)

410
Q

What are functional gut disorders?

A

Chronic GI symptoms in the absence of organic disease to explain the symptoms.

411
Q

What is the prevalence of Functional Gut disorders?

A

One of the most common GI conditions that doctors encounter (1 in 3)
More common in women - due to hormones
More common in young people

412
Q

Explain how NSAIDs lead to PUD?

A

Mucus secretion stimulated by prostaglandins
COX-1 needed for prostaglandin synthesis
NSAIDs inhibit COX-1
No COX-1 = mucous isn’t secreted
Reduced mucosal defense 🡪 mucosal damage

413
Q

Why is a raised urea suggestive of an Upper GI bleed?

A

Raised urea is more suggestive of an upper GI bleed; It occurs due to proteins in the blood being digested by enzymes in the upper GI tract, causing an increase in nitrogenous waste.

This is especially true if the creatinine is within normal limits, which confirms the urea rise is not due to impaired renal function.

414
Q

What are the GI Red Flag Signs?

A

ALARMS:
Anaemia
Loss of weight
Anorexia
Recent onset of progressive symptoms
Massess/Melena - or bleeding from any part of GIT
Swallowing Difficulties

+55yrs

415
Q
A

Medicine Phase 2a (20 decks)

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