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gastroenterology - final Flashcards

1
Q

definition of IBS

A

an idipathic GI disorder characterised by chronic abdomial pain and altered bowel habits (diarrhoea and/or constipation)

  • abnormal functioning of otherwise normal bowel

(usually linked to stress)

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2
Q

what are the subtypes of IBS

A

*IBS-C (IBS with predominant constipation) = > 25% motions are usually constipation (types 1 and 2) and <25% are types 6 and 7

*IBS-D (IBS with predominant diarrhoea) ) = > 25% motions are usually diarrhoea (type 6 and 7), <25% are types 1 and 2

*IBS-M (IBS with mixed bowel habits) ) = alternating diarrhoea and constipation, more than 25% types 1 and 2,AND more than 25% type 6 and 7

*IBS-U (IBS unclassified – can’t accurately classify into one of the 3 subtypes) – change in stool consistency is insufficient to categorise

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3
Q

what is the normal age range for a pt presenting with IBS

A

pts often present as teens or in their 20s

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4
Q

RFs for IBS?

A
  • female gender
  • younger age (20-40)
  • PTSD
  • physical and sexual abuse
  • stress/anxiety
  • Hx of mental health disorders (MDD)
  • Hx of GI infections (post-infectious IBS) - gastroenteritis
  • FHx of IBS
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5
Q

Associated conditions (can make IBS worse or IBS can make these conditions worse)

A

other functional disorders

  • Comorbid psychiatric disease e.g. major depression (MDD)
  • Fibromyalgia – associated with stress
  • Chronic fatigue syndrome (CFS) - associated with stress
  • GERD and functional dyspepsia
  • Sexual dysfunction
  • Premenstrual syndrome (PMS) – hormonal changes, can make Sx worse
  • Somatisation (headache, joint pain)
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6
Q

Aetiology of IBS

A

cause = unknown, combination of factors, disorder of gut brain interaction - NO ORGANIC CAUSE

*abnormal gut motility - longer transit time
*alterations in gut microbiome (overgrowth of certain specied
*hypersensitivity to gut stimuli
* psychological factors: stress anxiety can influence expression of Sx
*food hypersensitivity (short chain carbs are metabolised by bacteria → gas and bloating)

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7
Q

signs of IBS

A

abdominal distension (gas)
mild abdominal tenderness

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8
Q

symptoms of IBS

A

mostly occur in the daytime and are relieved with defaecation

ABC: abdominal discomfort, bloating, change in bowel habits

  • chronic abdo pain + discomfort (exacerbated with stress/meals/mensturation)
  • bloating
  • change in bowel habits: diarrhoea (non-bloody), constipation or a combo of both
  • diarrhoea w/ mucous discharge
  • tenesmus may be present (sensation of incomplete bowel emptying)
  • nausea
  • fatigue
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9
Q

Ix for IBS

A

Initial tests - rule out DDx
* FBC, ESR, CRP (inflammation)
* Coeliac testing (anti-TTG or anti-EMA)
* faecal calprotectin (IBD)

Note that the following tests are NOT required: abdominal ultrasound, sigmoidoscopy/colonoscopy, TFTs, FOBT, faecal ova and parasite test, hydrogen breath test.

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10
Q

describe how IBS is diagnosed

A

Rome IV criteria:
A positive Dx of IBS should be made if the pt has abdominal pain relieved by defaecation or associated with altered bowel frequency/stool form (appearance) in addition to 2 of the following 4 Sx:
* Altered stool passage (straining, urgency, incomplete evacuation)
* Abdominal bloating (more common in women than men), distension, tension or hardness
* Sx made worse by eating
* Passage of mucus

Some other features may support the diagnosis:
* Lethargy
* Nausea
* Backache
* Bladder symptoms

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11
Q

List some DDx of IBS

A
  • IBD
  • coeliac disease
  • lactose intolerance
  • food allergies
  • GI infections
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12
Q

What are some complications of IBS

A

IBS doesn’t increase the risk of colon cancers

  • Dehydration
  • Electrolyte imbalance
  • Bowel impaction
  • Haemorrhoids – due to bowel habit changes
  • Anxiety/depression – IBS can increase risk
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13
Q

What red flag Sx should be ruled out before a Dx of IBS

A
  • Rectal bleeding
  • Unexplained/unintentional weight loss: > 10% in 3 months
  • FHx of bowel/ovarian cancer
  • Onset after 60 years of age – change in bowel habits is worrying in this group of pts
  • Palpable abdominal mass
  • Nocturnal diarrhoea (night time Sx - IBS Sx are usually during the day)
  • Fever
  • Anaemia
  • Lab abnormalities
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14
Q

Management of IBS

A

1st line = lifestyle and dietary advice
o Stress management (exercise/meditation)
o Regular meals
o Reducing alcohol/caffeine (max 3 cups)
o Increasing soluble fibre (Ispaghula powder – if constipated) and reducing insoluble fibre (bran)
o Probiotics (trial for 4 weeks)
o if unsuccessful –> dietician review –> e.g. low FODMAP diet (apples, cherries, peaches, lactose, legumes, green veg)
o Regular meals, good hydration (8 cups per day).

2nd line = medications
o Pain: Antispasmodics (Mebeverine, Buscopan)
o Constipation: Laxatives e.g. Isphagula husk (avoid lactulose due to bloating) → Linaclotide (only if max tolerated dose of previous med doesn’t work AND they have had constipation for at least 12 months) → Prucalopride (when all other laxatives fail)
o Diarrhoea: Loperamide (Imodium)

if still no better
* TCAs - warn about drowsiness, takes 4-6 weeks to have an effect
* if TCAs not tolerated, move on to SSRIs

3rd line = psychological therapy
o CBT
o Hypnotherapy

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15
Q

What are the different types of stool according to the bristol stool chart

A

type 1: hard lumps like nuts (constipation)
type 2: sasuage shaped lumpy
type 3: sausaged shaped with cracks at surface
type 4: sausage shaped (normal)
type 5: soft blobs with clear cut edges
type 6: fluffy and mushy with ragged edges
type 7: watery, entirely liquid (diarrhoea)

  • the higher the number the higher the water content of the stool
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16
Q

definition of constipation

A
  • passing stool < 3 times per week
  • hard/lumpy/dry stool
  • difficulty of passage: excessive straining/tenesmus (sense of incomplete evacuation)
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17
Q

pathophysiology of constipation

A
  • reduced colonic motility - motility is needed to propel stool through colon to rectum
  • impaired rectal sensation and function - normally rectum senses presence of faecal matter and urge to defaecate
  • defaecation disorders - pelvic floor dysfunction (inability to relax anal sphincter)
  • psychological factors - stress, anxiety, and depression, can alter the functioning of the GI tract
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18
Q

RFs for constipation

A
  • elderly (age > 65)
  • female sex
  • lower socioeconomic status
  • african ancestry
  • toileting habits - rushing, witholding
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19
Q

common causes of constipation

A
  • inadequate fibre/fluid intake
  • immobility
  • IBS - may alternate with diarrhoea
  • post-op pain
  • hospital environment - lack of privary and using bedpan
  • elderly (age)
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20
Q

causes of constipation: bowel disease

A
  • colorectal carcinoma
  • anal fissures - pain can cause reluctance to defaecate
  • anal stricture
  • rectal prolapse
  • pelvic mass (foetus - pregnancy, fibroids)
  • bowel obstruction
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21
Q

causes of constipation: metabolic/endocrine

A
  • hypothyroidism - reduced metabolism
  • hypercalcemia
  • hypokalaemia
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22
Q

causes of constipation: medications

A
  • opioid analgesics: morphine, codeine
  • anticholnergics: TCAs (Amitryptyline)
  • iron tablets
  • CCBs
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23
Q

causes of constipation: neurological

A
  • diabetic neuropathy
  • Parkinson’s
  • spinal cord lesion
  • depression (especially in pts who somatise more)
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24
Q

Ix for constipation

A
  • DRE: check anal sphincter tone and presence of faecal matter
  • bloods: FBC, TFTs (hypo), Ca (hyper), U&E
  • abdo x-ray: if secondary cause of constipation is suggested
  • barium enema: if suspected impaction or mass
  • colonoscopy: if suspicion of lower GI malignancy
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25
Q

management of constipation

A

treat underlying pathology - treatment depends on cause

  • lifestyle modifications: increase fibre (wholemeal carbs, bran, fruits)
  • more exercise - keep mobile

ONLY give medication if the above doesn’t work

  • enemas if impaction
  • suppository e.g. glycerol
  • bulk-forming laxatives e.g. isphagula, methylcellulose (increase faecal mass to promote peristalsis)
  • osmotic laxatives e.g. lactulose (retain fluid in bowel)
  • stool softeners e.g docusate sodium
  • stimulant laxatives e.g. senna
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26
Q

complications of constipation

A
  • haemorrhoids (swollen and inflammed veins due to straining)
  • anal fissures (tears in the skin of the anus)
  • faecal impaction (hard stools that won’t pass as rectum is stretched out leading to muscle dysfunction)
  • overflow diarrhoea (faeces above blockage may travel around it and out the anus)
  • acute urinary retention (impacted stool may press on bladder)
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27
Q

red flags for constipation

A

the following may indicate GI malignancy:
* sudden weight loss
* dark stools
* abdominal mass
* loss of appetite
* recal bleeding

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28
Q

definition of coeliac disease

A

Autoimmune condition where exposure to gluten causes inflammation in the small bowel.

Gluten is a protein found in wheat, rye and barley

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29
Q

epidemiology of coeliac disease (age, ethnicity)

A

bimodal peak incidence for age but can present at any age
* 1-3yrs when first exposed to gluten in diet (e.g. cereal)
* adults 50-60

more common in irish ancestry

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30
Q

RFs for coeliac disease

A
  • FHx of coeliac disease: First degree relatives (parents/siblings/children) with coeliac disease
  • Autoimmunity
  • Genetic predisposition - 95% of patients have HLA-DQ2 allele, and 80% have HLA-DQ8 allele
  • IgA deficiency: allows increased gluten peptides to circulate in the submucosa
  • Down’s syndrome
  • Turner’s syndrome
  • William’s syndrome
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31
Q

what conditions are associated with coeliac disease

A

other autoimmune conditions

  • T1DM - all new cases of T1DM are tested for coeliac disease even if they don’t have Sx as the conditions are linked
  • autoimmune thyroid disease: Grave’s, Hashimoto’s
  • autoimmune hepatitis
  • PBC (primary biliary cirrhosis)
  • PSC (primary sclerosing cholangitis)
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32
Q

what skin condition is associated with coeliac disease

A

dermatitis herpetiformis = red vesicular, blistering pruritic (itchy) red eruptions

locations: extensor surfaces (shoulders, elbows, knees), trunk, scalp

cause: IgA deposits (anti-epidermal transglutaminase) in epidermis

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33
Q

what is the most common type of pancreatic cancer and where is it typically located

A

pancreatic adenocarcinomas are most common and are found in the head of the pancreas (80%)

cancer of the epithelial cells that have a gland-like appearance under microscopy

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34
Q

prognosis of pancreatic cancer

A

poor as disease is usually advanced at time of diagnosis

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35
Q

symptoms of pancreatic cancer

A
  • painless (obstructive) jaundice: pruritus (generalised itching), yellowing of sclera + skin, pale stools, dark urine
  • this happens as tumours of the head of the pancreas compress the common bile duct
  • epigastric pain radiating to the back
  • anorexia and weight loss (due to malignancy/malabsorption)
  • steatorrhoea (foul smelling, fatty stool, difficult to flush)
  • N + V 🤮
  • faitgue
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36
Q

signs of pancreatic cancer

A
  • Courvosier’s sign: painless palpation of gallbladder with jaundice = unlikely to be a gallstone and is likely to be pancreatic Ca/ cholangiocarcinoma
  • Trousseau’s sign = migratory thrombophlebitis - small blood clots in the superficial veins, that are associated with inflammation (feel like small bumps under skin)
  • worsening of T2DM (or new onset in elderly) - due to loss of endocrine function- presentation of the tumour in the body/tail (presentation: thirst, polyuria, nocturia, weight loss)
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37
Q

where does pancreatic cancer metastasise to

A

first metastasises to the LYMPH NODES (including Virchow’s node):
* peritoneum
* LIVER (via portal vein) - ascites
* LUNGS
* BRAIN
* bowels - constipation

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38
Q

what are the primary Ix for pancreatic cancer

A
  • LFTs: likely to show an obstructive picture with raised ALP, GGT and bilirubin
  • coagulation profile: to assess synthetic function of liver to determine possibility of metastasis
  • abdominal USS: part of initial work-up (pts with jaundice)
  • HRCT of pancreas (gold standard - Ix of choice): for diagnosis + biopsy (for histology)
  • Biopsy can be done: percutaneously (USS/CT) or EUS (endoscopy with US guidance)
  • CA-19-9 (tumour marker) - used to monitor disease but is NOT diagnostic
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39
Q

what are the RFs for pancreatic Ca

A

main RF: smoking
alcohol only indirectly increases risk

non-modifiable RFs:
* FHx (genes) e.g. BRCA2
* age (60+)
* male

modifiable RFs:
* smoking
* obesity
* diet high in fat

associated conditions:
* liver cirrhosis
* chronic pancreatitis
* T2DM
* MEN (multiple endocrine neoplasia)

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40
Q

management of pancreatic Ca

A

surgical resection (to remove tumour - only hope for cure)
* distal pancreatectomy (tumour of tail)
* whipple’s procedure (pancreaticoduodenectomy) = removal of pylorus of stomach, head of pancreas, common bile duct, gallbladder, proximal duodenum and relevant lymph nodes
* modified whipple’s ‘PPPD’ = pylorus sparing

chemo: adjuvant or neoadjuvant

palliative care:
* stenting via ERCP to relieve obstruction of bile duct
* palliative chemo
* palliative radiotherapy
* surgery to bypass biliary obstruction

pancreatic enzyme replacement

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41
Q

describe the referral criteria for pancreatic cancer

A

urgent referral (2WW to be seen in a clinic) if > 40 with jaundice

referral for direct access CT abdo ( to be done within 2 weeks) = over 60 with weight loss and one of:
* nausea
* vomiting
* back pain
* abdo pain
* constipation
* new onset diabetes

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42
Q

describe the typical presentation of pancreatic cancer

A

pt ages 65-75 with painless obstructive jaundice and weight loss

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43
Q

what are some of the Ix to consider in pts with pancreatic cancer

A

done if CT is inconclusive:
* PET-CT: for staging if disease is localised and pt is having treatment
* EUS: allows FNA and can identify small tumours
* ERCP: allows for biliary drainage and biopsy, can be used to insert stent to relieve Sx

imaging may demostrate ‘double duct’ sign due to simultaneous dilation of the pancreatic and common bile ducts

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44
Q

what are the cancer-related complications of pancreatic cancer

A
  • VTE: pancreatic adenocarcinoma is thrombogenic
  • new-onset diabetes mellitus: loss of endocrine function due to cancer growth + surgical resection
  • cholangitis: obstruction of biliary tree increases risk of infection
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45
Q

what are the surgery-related symptoms of pancreatic cancer

A

DUMPING SYNDROME = when sugar moves too quickly into the small intestine

  • early dumping syndrome (30 mins after a meal): fluid moves into intestine due to high osmotic load → DIZZINESS AND PALPITATIONS
  • late dumping syndrome (2 hours after meal): as glucose is rapidly absorbed in the intestine → reactive hyperinsulinamiea and subsequent hypoglycaemia

PEPTIC ULCER DISEASE

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46
Q

what is a Mallory Weiss Tear

A

a longitudinal tear in the muscosa of the oesophagus at the GOJ due to a rapid increase in intra-abdominal pressure (leading to bleeding from submucosal arterial/venous plexus)

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47
Q

aetiology and RFs for Mallory Weiss syndrome

A
  • male
  • age: 40-60
  • conditions that cause vomiting: hyperemesis gravidarum, bulimia, gastroenteritis
  • chronic cough: COPD, asthma, bronchiectasis
  • alcohol: binge drinking, damages mucosa and causes vomiting
  • hiatus hernia
  • GORD
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48
Q

what are the DDx for Mallory Weiss syndrome

A
  • reflux oesophagitis: irregularly shaped ulcerations would be seen
  • Boerhaave syndrome = transmural oesophageal tear
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49
Q

clinical features of Mallory Weiss tear

A
  • haematemesis
  • epigastric pain/back pain
  • malaena
  • shock (hypovolemic): postural hypotension, tachycardia, drop in BP, dizziness
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50
Q

what are the Ix for Mallory Weiss syndrome

A
  • FBC (anaemia)
  • U&E (raised urea as RBCs are digested into urea)
  • LFTs (to check for liver disease, usually NORMAL - if deranged may suggest a variceal bleed)
  • coagulation studies (prothrombin time etc) - to look for coaugulopathies and thrombocytopenia
  • cardiac workup (to look for myocardial ischaemia): ECG, troponins, creatine kinase
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51
Q

what is the diagnostic Ix for Mallory Weiss syndrome and what does it show

A

upper GI endoscopy - should be done in ALL pts once they’re stabilised (after resus)

a single longitudinal tear that appears as a red break in the mucosa

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52
Q

describe the management of Mallory Weiss syndrome

A

most tears self-resolve
main Rx:
* resuscitation to stabilise pt (fluid resus and blood replacement)
* diagnostic and therapeutic endoscopy (for definitive management)
* manage precipitating and exacerbating factors: PPI, antiemetics
* monitor for complictions: ECG for myocardial ischaemia

1) ABC
* fluid resus: IV fluids
* blood transfusion, blood products

anti-emetics is pt is vomiting e.g. ondansetron

2) endoscopy +/- adrenaline injection (vasoconstriction)
* thermocoagulation
* band ligation/haemoclip (mechanical compression)

3) PPI - given post endoscopy (otherwise it can mask bleeding)
* protecting stomach acid from causing further damage to mucosa

4) surgery - if endoscopic therapy isn’t successful = arterial embolisation (angiotherapy) - left gastric artery is blocked (to prevent blood flow to its oesophageal branches so bleeding is prevented)

5) lifestyle changes
* reduce alcohol consumption
* CBT for bulimia

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53
Q

what are the complications of mallory weiss tear

A
  • rebleeding - lacerations can bleed again (usually occurs within 24hrs)
  • hypovolemic shock
  • oesophageal perforation
  • myocardial ischaemia
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54
Q

what are the scoring systems for upper GI bleeds

A

1) Glasgow-Blatchford score (GBS) - done to risk stratify pts before endoscopy
* score of 0: pt can be dishcharged, outpatient endoscopy can be arranged for a later time
* score > 0 = pt is admitted and inpatient endoscopy is done within 24 hours
* score based on: urea, Hb, HF, intial SBP, gender, tachycardia (HR), melaena, Hx of syncope, hepatic disease Hx

2) Rockall score - done after endoscopic treatment to assess risk of adverse outcomes
* based on: age, BP, comorbities, endoscopic findings

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55
Q

what are oesophageal varices

A

dilated veins of the oesophageal submucosa at the junction between portal circ and systemic venous system- these veins are not used to holding high pressure blood and therefore are prone to rupture which can cause heaving bleeding

rupture of oesophageal varices is life-threatening and comes with a high risk of mortality

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56
Q

what causes oesophageal varcies

A

caused by portal hypertension (mainly secondary to liver cirrhosis - commonly from alcoholism) → blood is shunted to other routes

main shunt: portal vein → left gastric vein → oesophageal veins (become distended and tortuous)→ azygous vein → back to heart

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57
Q

what is the diagnostic Ix for oesophageal varices

A

GOLD STANDARD = OGD (oesophagogastroduodenoscopy) ‘

aka: upper GI endoscopy’

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58
Q

what is the management of an acute oesopheageal variceal bleed

A
  • ABC: IV fluids
  • blood transfusion - for massive blood loss
  • correct coagulopathy: vitamin K, FPP, platelet infusions
  • Terlipressin (ADH analogue): causes splanchnic vasoconstriction which reduced portal pressure
  • Broad spectrum Abx: reduce mortality by reducing risk of bacteraemia and spontaneous bacterial peritonitis

Once patients have been haemodynamically resuscitated is important to arrange urgent endoscopy, ideally within 24 hours.
* At endoscopy, variceal band ligation is the treatment of choice.
* Balloon tamponade: If bleeding is uncontrollable, a Sengstaken-Blakemore tube may be inserted as a temporary measure to tamponade the bleeding varices
For patients with a history of alcoholism, thiamine may be required to correct any deficiency.

If there is refractory bleeding: TIPS may be needed (Transhepatic, Intrahepatic, Portosystemic Shunt) - metal stent is inserted to connect the portal vein to the hepatic vein which reduced portal vein pressure - potential complication = hepatic encephalopathy (as well as nutrients, toxins like ammonia can enter the liver faster)

For patients with a history of alcoholism, thiamine may be required to correct any deficiency.

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59
Q

what is the prophylaxis for oesophageal varices

A
  • beta-blockers (non-selective) e.g. Propanolol - to reduce portal pressure (by causing splanchnic vasoconstrition - vasoconstriction of GI organs reducing blood flow to portal vein)
    and/or
  • endoscopic band ligation = putting rubber band around varices
  • screening endoscopy for pts with cirrhosis
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60
Q

what is Barrett’s oesophagus

A

metaplasia of the cells of the lower oesophageal muscosa from squamous epithelial cells to columnar epithelial cells w/ goblet cells

this new columnar epithelium is similar to that of the stomach/intestine, better at handling HCl and goblet cells release mucous to counteract the acid

happens due to long-standing GORD and chronic inflammation

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61
Q

what are the RFs for Barrett’s oesophagus

A
  • GORD (single strongest RF) - oesophageal lining is damaged, over time epithelium erodes which promotes inflammatory cells that cause necrosis. This chronic damage leads to replacement of normal squamous epithelium with columnar epithelium
  • smoking
  • truncal (central) obesity and hiatus hernia: both of these lower the tone of the lower oesophageal sphincter which makes it easier for acid reflux to happen
  • smoking
  • male (7:1 ratio)
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62
Q

what cancer does Barrett’s oesophagus increase the risk of

A

Oesophageal adenocarcinoma

metaplasia to columnar epithelium → dysplasia of glandular cells = adenocarcinoma

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63
Q

describe the management of Barrett’s oesophagus

A
  • high-dose PPI
  • OGD + biopsy - for pts with metaplasia (and no dyplasia), endoscopy is recommended every 3-5yrs
  • if dysplasia is identified - endoscopy is recommended - 2 options
    1) radiofrequency ablastion (1st line)
    2) endoscopic mucosal resection
  • lifestyle: smoking cessation, small regular meals, no hot drinks/alcohol/eating < 3 hrs before bed, avoid tight clothing
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64
Q

what are the symptoms of Barret’s oesophagus

A

Barrett’s oesophagus itself is asymptomatic but will have the symptoms of the coexistent GORD:
* pyrosis (heartburn) - worse with eating, lying flat at night, wearing tight clothing
* dyspepsia
* dysphagia
* dysphonia (hoareseness)
* belching
* cough

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65
Q

describe the pathophysiology of coeliac disease

A
  • gliadin (part of gluten) is deaminated during digestion by tTG (tissue transglutaminase) → a complex is formed composing of tTG and gliadin
  • coeliac disease = an autoimmune response to this complex which causes intestinal damage
  • in pts with coeliac disease the deaminated peptides are presented to APCs via the molecules HLA-DQ2/DQ8 to T helper cells which triggers an immune response
  • immune activation leads to: villous atrophy (therefore malabsorption), lymphocyte accumulation, intestinal crypt hyperplasia (due to mucosal damage)
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66
Q

clinical features of coeliac disease (GI/extra-intestinal)

A

Sx arise due to MALABSORPTION of nutrients

GI
* diarrhoea
* bloating
* N+V
* steatorrhoea
* abdo pain/discomfort
* weight loss (unexpected)
* constipation

other:
* anaemia (secondary to iron/folate/B12) deficient - fatigue ‘tired all the time’ + pallor
* osteoporosis (vit D and Ca malabsorption) → fractures
* bruising (vit K deficiency)
* mouth ulcers + angular stomatitis

neurological (rare)
* non-hereditary cerebellar ataxia
* idiopathic peripheral neuropathy
* epilepsy (seizures due to poor absorption of folate)

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67
Q

clinical features of coeliac disease in children

A

children:
* diarrhoea and/or constipation
* failure to thrive
* vomiting and anorexia
* abdominal distension
* wasted buttocks and short stature (due to malnutrition)

68
Q

what are the 1st and 2nd line Ix for coeliac disease

A

1st line: anti-tTG Abs (IgA) + check total IgA (if pt with coeliac disease has IgA deficiency, you will get a false negative result)

2nd line: anti-EMA - if anti-tTG is weak positive (more specific but less sensitive) = anti-tTG Abs that bind to tTG in the endomysium (part of connective tissue sheath of muscles)

69
Q

what is the gold standard Ix for coeliac disease and what would it shown

A

gold standard = small bowel biopsy (duodenal) - confirms diagnosis

all pts with positive serology should be referred for this

ideally this should be carried out before gluten is withdrawn from the diet and repeated after gluten withdrawal (to demonstrate resolution)

classic findings:
* crypt hyperplasia
* epithelial lymphocytosis
* villous atrophy

70
Q

what are some of the other Ix that can be done for coeliac disease

A
  • FBC: anaemia (macrocytic = folate/B12 def, microcytic = iron def/bleeding, normocytic = chronic inflam)
  • U&E, bone profile: impaired vit D absorption
  • LFT (albumin may be low due to malabsorption)
  • nutritional status: vit D, Ca, iron, B12, folate
  • skin biopsy: if there’s evidence of dermatitis herpetiformis
  • HLA-DQ2/DQ8 testing only done in specialist setting (e.g. in a child who can’t have a biopsy)
71
Q

Mx of coeliac disease

A

life-long gluten free diet = essentially curative (consuming gluten can lead to a relapse of the condition)

avoid:
* wheat: pasta, bread and pastry
* rye
* barley (beer)
* oats

NB: rice, corn and potatoes are gluten free

dietary supplements: vit D, Ca, iron

72
Q

what vaccinations are offered to those with coeliac disease and why

A

pneumococcal (one off with booster every 5 years) - coeliac disease causes functional hyposplenism (due to excess loss of lymphocytes)

hyposplenism increases risk of pneumococcal infection

73
Q

what are some of the steps in monitoring a pt with coeliac disease

A
  • check Abs
  • check adherence to gluten-free diet
  • screen for complications
  • annual review: BMI, diet, Sx, FBC, LFT, Ca, albumin, folate, TFT, glucose
  • DEXA: 1-3 yrs after Dx and at menopause (or age 55 men)
74
Q

what are the complications of coeliac disease

A

dermatitis herpetiformis - may need treatment with Dapsone is persistent, usually seen in active disease and resolves with dietary changes

malabsorption:
* anaemia
* osteoporosis (bone mineral density is checked after 1 yr of gluten free diet in those with other RFs for osteoporosis)
* Ca and vit D deficiency: may lead to secondary hyperparathyroidism and osteomalacia
* peripheral neuropathy (B12/folate def)

ulcerative jejunitis: fever, abdo pain, bleeding

malignancy (coeliac disease increases risk - risk normalises after a few yrs of gluten restriction)
* EATL (enteropathy associated T-cell lymphoma)
* small bowel adenocarcinoma

subfertility and recurrent miscarriages (due to nutrient deficiencies affecting reproductive function)

coeliac crisis: life-threatening
* associated with: signigicant metabolic derangements, severe unexplained diarrhoea and malabsorption
* Rx = rehydration with electrolytes + steroids (to reduce pain and inflammation)

75
Q

what is GORD

A

recurrent reflux of gastric contents (including HCl) into the lower oesophagus due to reduced LOS (lower oesophageal sphincter) tone - this causes burning and inflammation

76
Q

aetiology of GORD

A
  • reduced LOS tone (i.e. increased relaxation) - things that reduce LOS tone: alcohol, smoking, caffeine
  • anatomical abnormality of GOJ which disurpts functioning of the sphincter: hiatal hernias = when part of the oesophagus slides up the oesophageal hiatus in the diaphragm
  • increased acid production: NSAIDs, smoking and alcohol, Zollinger-Ellison syndrome
  • raised intragastric pressure: delayed emptying of gastric contents (gastroparesis), large meals, obesity, pregnancy
77
Q

RFs of GORD

A
  • age: more common in elderly
  • stress and anxiety
  • trigger foods: chocolate, caffeine (reduce LOS tone), fatty foods (delay gastric emptying)
  • drugs (that reduce LOS pressure): NSAIDs, TCAs, anticholinergics, alpha&beta blockers, nitrates, CCBs
  • obesity
  • pregnancy
  • hiatus hernia
  • smoking and alcohol
78
Q

clinical features of GORD (oesophageal)

A
  • heartburn (retrosternal burning pain): worse when lying down (acid pools in oesophagus)/after meals
  • regurgitation
  • belching
    *odynophagia (pain when swallowing)
  • dysphagia (especially if cancer or strictures)
  • unpleasant taste: sour/bitter taste of acid at the back of the mouth
  • nausea
79
Q

clinical features of GORD (extra-oesophageal)

A

gastric contents can reflux into pharynx, larynx and tracheobronchial tree (aspiration):
* worsening of asthma (due to bronchial inflammation - noctural in particular)
* chronic cough
* laryngitis - HOARSENESS if vocal cords are irritated
* sinusitis

  • dental erosions, gum recession
80
Q

what are the Ix for GORD

A
  • clinical Dx: heartburn + regurg, relief with antacids, worse when lying down and after large/fatty meals
  • 8 week trial of PPI to pts with typical Sx

if no response to PPI trial/alarm Sx: OGC (endoscopy) - (STOP PPI 2-4 WEEKS BEFORE THIS) which may be normal or show:
* oesophagitis: erosions, ulcerations, strictures
* Barrett’s oesophagus

alarm Sx: dysphagia, over 55, low Hb (anaemia), raised platelets, treatment resistant dyspepsia, unintentional weight loss

if Dx still uncertain:
* 24 hour ambulatory pH: pH < 4, 4% of the time = Dx GORD
* oesophageal manometry (evaluates oesophageal contractions and LOS function): rules out other disorders like achalasia, diffuse oesophageal spasm or other motility disorders

81
Q

describe the management of GORD

A

lifestyle changes:
* reduce alcohol, smoking cessation
* weight loss (if obese)
* avoid trigger foods: chocolate, tomatoes, fatty/spicy food
* eat smaller meals
* have evening meal 3-4 hrs before bed
* sleep with head of bed raised

review pt’s medication: consider stopping any meds that may exacerbate pt’s Sx e.g. CCBs, nitrates, TCAs

PHARMACOLOGICAL THERAPY

Endoscopically proven oesophagitis
full dose proton pump inhibitor (PPI) for 1-2 months
if response then low dose treatment as required
if no response then double-dose PPI for 1 month

Endoscopically negative reflux disease
full dose PPI for 1 month
if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
if no response then H2RA or prokinetic for one month

PPI:
* give full dose for 4 weeks to aid healing
* If symptoms persist, use a PPI at the lowest dose possible to control symptoms and may be given PRN

If there is evidence of severe oesophagitis on endoscopy and symptoms are not settling with initial treatment, double dose PPI can be used for 1 month followed by full dose maintenance therapy

Histamine-receptor antagonist:
* if symptoms persist, can add in a histamine receptor (H2) antagonist particularly if the patient has nocturnal symptoms and evidence of oesophagitis

SURGERY (in treatment-refractory cases): Laparascopic fundoplication
* mobilisation of the fundus of the stomach which is then wrapped around the lower oesophagus to increase LOS pressure

82
Q

what are the complications of GORD

A
  • oesophagitis - acid can cause inflammation and ulceration of the oesophagus
  • stricture formation - if the oesophagus keeps on getting inflamed it will undergo fibrotic reaction for healing which narrows the lumen
  • GI bleeding - may occur if acid erodes all the way through to the BVs in oesophageal wall (→anaemia and fatigue)
  • Barrett’s oesophagus - metaplasia of cells due to acid damage into better adapted columnar epithelial which can become dysplastic and lead to oesophageal adenocarcinoma
  • Pneumonia - may be caused by aspiration
  • dental problems: erosions, gingivitis, halitosis
83
Q

what is the definition of achalasia

A

oesophageal motility disorder where the LOS is unable to relax in response to swallowing and there is no peristalsis of the lower oesophagus

84
Q

describe the pathophysiology of achalasia

A

loss of inhibitory neurons (which normally release VIP and NO → relaxation) in the myenteric plexus (b/w longitudinal and circular muscle layers) which means the LOS can’t relax (unopposed excitatory neurons release ACh and stimulate smooth muscle contraction → failure of LOS relaxation and peristalsis → as food is unable to pass through to the stomach, it builds up in the oesophagus, causing dilation

most causes are idiopathic (unknown)

85
Q

what are some of the RFs for achalasia

A
  • infection (viral/parasitic): Chagas disease (trypanasoma cruzi), Measles, HSV (Abs against these have been found in pts with Achalasia)
  • autoimmunity: Abs against myenteric plexus neurons, pts with other autoimmune diseases and HLA class 2 antigens
  • genetic factors: Allgrove syndrome is a rare autosomal recessive condition associated with achalasia, alacrima (lack of tears), ACTH insensitivity and autonomic disturbance
86
Q

clinical features of achalasia

A
  • dysphagia of both solids and liquids - “knot” of food stuck in the oeosphagus

the dysphagia is compensated by eating more slowly and lifting neck/throwing shoulders back to improve emptying of oesophagus

  • regurgitation of undigested food → aspiration, cough, pneumonia
  • weight loss - due to limited oral intake
  • heartburn + chest pain - due to food sitting in the oesophagus
87
Q

Ix for achalasia: 1st, gold standard, other? - what would they show

A
  • OGD (endoscopy) = performed first to rule out malignancy
  • oesophageal manometry = GOLD STANDARD
  • would show absence of peristalsis and incomplete relaxation of LOS
  • barium swallow - would show ‘Bird’s Beak sign’ due to dilation of the oesophagus and then stricture near the GOJ

other Ix:
CXR: widened mediastinum, fluid level may be seen

88
Q

describe the management of Achalasia

A

initial = medical therapy to reduce LOS pressure:
nitrates (isosorbide dinitrate), CCBs (Nifedipinde, Verapamil) - INEFFECTIVE but used while awaiting definitive treatment

first line surgery = Heller cardiomyotomy - small incision is made in sphincter to release pressure

pneumatic dilation (balloon) of LOS - perforation is a risk

botox injection (causes ACh release and therefore LOS relaxation) - done in those where surgery isn’t suitable or surgery doesn’t help

89
Q

what are the complications of achalasia

A
  • aspiration
  • malignancy - increased risk of squamous cell carcinoma
  • GORD - may be a complication of cardiomyotomy (if fundoplication is done at the same time, then outcomes may be improved)
  • perforation
90
Q

what is peptic ulcer disease

A

breakdown in the mucosal lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer) leading to the formation of ulcers

91
Q

what are the causes of peptic ulcer disease

A

certain things make the stomach prone to erosion:
* breakdown of protective layer of stomach and duodenum
* increased production of acid

there is a protective layer above the mucosa made of bicarbonate and mucus, this layer can be broken down by:
* medications: NSAIDs, steroids, SSRIs, bisphosphonates
* H.pylori (a type of bacteria - chronic inflam)

increased acid can result from:
* spicy foods
* stress
* alcohol
* smoking
* caffeine

other RFs:
* increasing age
* Zollinger-Ellison syndrome - secretes gastrin

92
Q

what are the clinical features of peptic ulcer disease

A
  • epigastric pain
  • gastric ulcer: eating WORSENS pain
  • duodenal ulcer: eating IMPROVES pain
  • dyspepsia (indigestion)
  • nausea and vomiting
  • bleeding - haematemesis (coffee ground), malaena
  • iron deficiency anaemia due to the bleeding
93
Q

what is used to make the diagnosis of peptic ulcer disease and what are some other Ix

A
  • endoscopy is used to look for ulcers ( in the stomach/ proimal duodenum) - GOLD STANDARD
  • a biopsy can be done to exclude malignancy (cancers look similar to ulcers)
  • a rapid urease test (CLO) [carbon-13 urea test] can be done to rule out H.pylori - pt must be off PPIs for 2 weeks and off Abx for 4 weeks prior to this (otherwise may give a false negative)
  • FBC
  • Fasting gastrin level: if suspected Zollinger-Ellison syndrome e.g.recurrent, treatment-resistant peptic ulcers
  • VBG: if lactate is high this may indicate poor tissue perfusion due to bleeding
  • Erect CXR: if concerned about perforation, an erect CXR may demonstrate pneumomediastinum
94
Q

describe the management of peptic ulcer disease

A
  • treat RFs e.g. stop NSAIDs,
  • if H.pylori negative: high dose PPI - for 1 month until ulcer has healed
  • endoscopy to check if the ulcer has healed
95
Q

what are the complications of peptic ulcer disease

A
  • bleeding
  • strictrures: which can cause pyloric stenosis (reduced emptying of stomach) –> abdominal pain + distension, nausea and vomiting esp upon eating
  • perforation –> “acute abdomen” and peritonitis - needs laparoscopic repair
96
Q

A 60-year-old lady presents with burning epigastric pain that is exacerbated by eating. She has been taking ibuprofen regularly for her osteoarthritic knees.

what condition is this a common presentation of

A

peptic ulcer disease

  • arthritis - people take NSAIDs for this
  • epigastric pain worsened by eating
97
Q

which ulcers are more common, gastric or duodenal and whereabouts do they typically occur

A

duodenal ulcers are the most common, normally occurring in D1, ulcers can potentially erode into the gastroduodenal artery which can cause significant bleeding

98
Q

how do NSAIDs cause peptic ulcers

A

inhibit cyclo-oxygenase (COX) resulting in reduced prostaglandin which normally reduces acid secretion and increases mucus production

99
Q

If there is pain relieved by eating and worse when hungry what type of peptic ulcer would it be

A

duodenal ulcer

100
Q

what is the treatment of peptic ulcer disease if the patient is found H.pylori positive

A

7 day course of triple eradication therapy
* PPI, clarithromycin, Amoxicillin
* Omeprazole, clarithromycin and metronidazole, if penicillin-allergic

101
Q

what are the potential causes of an upper GI bleed

A
  • MWT (Mallory Weiss Tear)
  • ulcers of stomach/duodenum
  • cancers of stomach/duodenum
  • oesophageal varices
102
Q

what counts as an upper GI bleed and what are the most common causes

A

any bleeding above the ligament of Triez at the duodenojejunal junction
i.e. bleeding of the oesophagus, stomach, duodenum

most common causes: peptic ulcers, oesophageal varices

103
Q

describe the management of a non-variceal upper GI bleed

A

A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

Send bloods for:
* Haemoglobin (FBC)
* Urea (U&Es): urea is raised in an upper GI bleed (protein in RBCs is digested into urea in the GI tract), whilst pre-renal acute kidney injury may also be present
* Coagulation (INR, FBC for platelets)
* Liver disease (LFTs): assess severity of liver disease
* Crossmatch 2 units of blood

Transfusion is based on the individual presentation:

  • Transfuse blood, platelets and clotting factors (fresh frozen plasma) to patients with massive haemorrhage
  • Transfusing more blood than necessary can be harmful
  • Platelets should be given in active bleeding and thrombocytopenia (platelets < 50)
  • Prothrombin complex concentrate can be given to patients taking warfarin that are actively bleeding

There are some additional steps if oesophageal varices are suspected, for example in patients with a history of chronic liver disease:
* Terlipressin
* Prophylactic broad spectrum antibiotics

The definitive treatment is oesophagogastroduodenoscopy (OGD) to provide interventions that stop the bleeding, for example banding of varices or cauterisation of the bleeding vessel.

104
Q

what are the different types of gastric tumours

A
  • adenocarcinomas (account for the majority of gastric tumours)
  • lymphomas - occurs in MALT (B lymphocyte proliferation due to chronic H pylori infection)
  • carcinoid tumours - neuroendocrine cells (G-cells)
  • leiomyosarcomas (rare) - smooth muscle in gastric wall
105
Q

what are the 2 subtypes of adenocarcinoma

A

1) intestinal (well-differentiated)
2) diffuse

106
Q

describe the pathophysiology of intestinal adenocarcinoma

A
  • chronic H.pylori infection releases virulent factors which causes damage to the epithelium and overtime causes chronic inflam which leads to gastritis
  • as the epithelium is contantly damaged and repaired, metaplasia occurs as these cells start to change and resemble intestinal cells
  • as these cells become metaplastic, they can accumulate mutations in the genes that control the cell cycle (tumour surpressor genes and proto-oncogenes)
  • this type of adenocarcinoma usually appears as an ulcer with heaped up edges
  • the cells are histologically well-differentiated i.e. they resemble intestinal cells
107
Q

describe the pathophysiology of diffuse gastric adenocarcinoma

A
  • these people tend to have inherited mutations in the CHD1 which codes for the protein E-cadherin
  • E-cadherin normally allows epithelial cells to stick together and controls which positions the cells are at in the cell cycle
  • if there are mutations in E-cahderin, the cells fall apart and start to divide uncontrollably (therefore this type of adenocarcinoma has an increased ability to spread and invade neighbouring structures)
  • this leads to ‘linitis plastica’ where the connective tissue of the submucosa is invaded and is made to become thick + hard (and resembles a leather bottle)
  • histologically these cells have a signet ring appearance (there is a large vacuole in the cell that pushes the cytoplasm and nucleus right to the edge)
108
Q

where does gastric cancer metastasise to

A
  • peritoneum
  • lymph nodes: around the umbilicus, Virchow’s node (left supraclavicular node)
  • liver (is the main organ that is metastasises to)
109
Q

what are some of the paraneoplastic syndromes associated with gastric cancer

A

paraneoplastic syndrome = caused by effect of the primary tumour on other organs but isn’t necessarily a mestastasis

  • Lesser-Trelat sign: brown spots as cancer cells promotes growth factors which in turn promotes keratinocytes
  • Polyarteritis nodosa: inflam/necrosis of medium sized arteries including those supplying kidneys and heart –> could lead to renal failure or MI
  • Trousseau’s sign (migratory thrombososis of veins): cancer cells activate tissue factor which activates the coagulation cascade, causing thrombosis
110
Q

describe the differences in histopathology between the intestinal and diffuse subtypes of gastic cancer

A

intestinal:
* arises from intestinal metaplasia
* most commonly involves the lesser curvature of the stomach

diffuse:
* diffuse infiltration of the gastric wall ‘linitus plastica’
* Signet ring cells: large vacuole of mucin displacing the nucleus; higher numbers are associated with a worse prognosis
* can occur anywhere within the stomach

111
Q

describe the epidemiology of gastric cancer - what countries is it most common in and which part of the stomach is most commonly affected

A

more common in korea/japan and south america (columbia)

the antrum is most commonly affected (but the incidence of tumours affecting the cardia is increasing)

112
Q

what are the modifiable RFs for gastric cancer

A
  • H.pylori infection - strongest RF esp for intestinal subtype
  • smoking
  • alcohol
  • diet: smoked/pickled foods (N-nitroso compounds), nitrosamines, salty and spicy foods
  • obesity: more proximal and advanced cancers (may be why there’s increasing incidence of cancers affecting the cardia
113
Q

what are the non-modifiable RFs for gastric cancer

A
  • male gender
  • increasing age: peak incidence is at age 70-80
  • pernicious anaemia
  • autoimmune gastritis
  • blood type a
  • gastric adenomatous polyps
114
Q

what are the clinical features of gastric cancer

A

usually pts are unsymptomatic or may have non-specific Sx

initial: malaise, reduced appetite, dyspepsia (burning sensation in upper abdo)

after progression: epigastric pain, N+V, weight loss

if ulcers/bleeding: melaena (on DRE), haematemesis, anaemia (iron deficiency: chelitis, pallor, koilonychia)

paraneoplastic syndromes: Lesser-Trelat sign

acanthosis nigricans: darkening of axilla and other folds

sister mary joseph sign: mass around belly button due to lymph node metastasis and enlargement

troissier’s sign: large virchow’s node due to metastasis

if gastric Ca grows near GOJ –> dysphagia

115
Q

describe the referral criteria for a pt with suspected gastric cancer

A

NICE recommends referring patients for an urgent 2-week upper GI endoscopy if they have :
* Dysphagia (difficulty swallowing) or

≥ 55 years with weight loss and one of:
* Epigastric pain
* Reflux
* Dyspepsia (burning sensation)

116
Q

what are the Ix for gastric cancer

A
  • upper GI endoscopy and biopsy

staging Ix:
* CT CAP: if biopsy reveals malignancy, CT imaging is usually the first-line staging investigation to detect metastatic disease
* PET: offered after CT when metastatic disease is suspected and assists with staging; particularly for junctional tumours
* Staging laparoscopy: all patients with potentially curable disease should have a staging laparoscopy to exclude occult peritoneal metastasis
* Endoscopic ultrasound: assists with staging, particularly for patients where curative surgery is being considered
* HER2 testing: patients with HER2-positive metastatic gastric cancer may be responsive to trastuzumab (Herceptin)

117
Q

describe the management of gastric cancer

A

Importantly, surgery (other than palliative) is only indicated if there is no evidence of metastatic disease.

localised disase:
* Oesophagogastrectomy
* Total gastrectomy:
* patrial gastrectomy
* Endoscopic muscosal resection
* Chemotherapy: offer chemotherapy before and after surgery to all patients with gastric cancer

advanced/metastatic disease:
* chemo/chemoradiotherapy
* palliative gastrectomy
* Trastuzumab (Herceptin): for HER2 positive metastatic gastric cancer

118
Q

what are the cancer related complications of gastric cancer

A
  • Bleeding
  • Gastric outlet obstruction: tumour blocks the gastric outlet causing non-bilious post-prandial vomiting
  • Perforation: ulceration of a neoplastic lesion can weaken the stomach wall and if left untreated could lead to perforation
  • Metastasis: Virchow’s node, lung, liver, peritoneum, ovaries (Krukenberg tumour - has lots of signet ring cells and mainly assoc w/ diffuse type)
    *Pseudoachalasia: if tumour is near GOJ
119
Q

what are the gastrectomy related complications of gastric cancer

A

Malabsorption:
* Vitamin B12 deficiency (reduced intrinsic factor)
* Iron deficiency due to reduced conversion of Fe2+ to Fe3+ in the stomach and hence reduced absorption

Small bowel bacterial overgrowth: post gastrectomy, a blind-ending bowel loop is created to allow the gall bladder to drain into. Bacterial overgrowth within this portion of the bowel can lead to malabsorption

Dumping syndrome: occurs when sugar moves too quickly into the small bowel and associated with gastrectomy

120
Q

what are some of the protective measures against gastric cancer

A

having a diet high in fruits and vegetables as well as fibre and folate

121
Q

what is ulcerative colitis

A

a type of inflammatory bowel disease that affects the rectum (proctitis) and colon characterised by diffuse inflammation of the colonic mucosa and a relapsing, remitting course

122
Q

describe the pattern of inflammation and ulceration in UC

A
  • inflammation of the rectum extends proximally and continuously (entire lumen) to affect a variable length of the colon
  • it never affects the anus or the bowel past the iliocecal valve
  • histoppathology will reveal inflammation of the mucosa and submcosa only as well as crypt abscesses with neutrophil infiltration
123
Q

describe the aetiology and pathophysiology of UC

A

mix of genetics and environmental factors

  • increased amount of cytotoxic T cells are seen in pts
  • these pts also may have raised p-ANCA levels, it’s thought that these Abs cross react with our own neutrophils due to the presence of gut bacteria that have a structural similarity to our own cells
  • environmental factors: like increased amounts of sulfide producing gut bacteria
  • genetic predisposition: if you have a FHx of UC you’re more likely to be affected by it, more common in younger females and jewish populations
124
Q

what are some of the RFs for UC

A
  • FHx
  • caucasian
  • non-smoker
  • HLA-B27
125
Q

what are the clinical features of UC

A
  • left lower quadrant pain (as this corresponds to the rectum)
  • frequent bouts of diarrhoea often with blood+mucus (colon dysfunction leads to diarrhoea, as ulcers are eroded, this may cause bleeding) - fresh blood seen on rectal examination
  • urgency and tenesmus
126
Q

what are the Ix for UC

A
  • faecal calprotectin: will be raised (marker of inflam in GIT)
  • FBC: leukocytosis during flare, anaemia if bleeding
  • LFTs: should be checked every 6-12 months to screen for PSC; low albumin may suggest protein-losing enteropathy
  • CRP/ESR: raised during acute inflammation of the bowel (flare)
  • Colonoscopy and biopsy: investigation of choice and allows for biopsy
127
Q

what would colonscopy and biopsy show in a pt with UC

A
  • Red and raw mucosa with widespread shallow ulceration
  • No inflammation beyond the submucosa, unless fulminant disease
  • Lamina propria inflammatory cell infiltrates
  • Pseudopolyps: mucosa adjacent to ulcers is preserved, which has the appearance of polyps
  • Crypt abscesses due to neutrophil migration through gland walls
  • Goblet cell depletion, with infrequent granulomas
128
Q

what are some Ix to consider in a pt with UC

A
  • Sigmoidoscopy: preferred to colonoscopy in acute flares to avoid perforation; similar findings to colonoscopy but limited examination
  • Abdominal X-ray: can assess for toxic megacolon (see complications), ‘lead-pipe’ appearance
  • Stool microscopy and culture: to exclude infective gastroenteritis or pseudomembranous colitis
  • Nutritional status: vitamin B12, folate, ferritin, and vitamin D may be low
  • CT abdomen and pelvis: helps assess the distribution of disease
  • Barium enema: loss of haustrations, widespread superficial ulceration and ‘pseudopolyps’; may demonstrate a ‘lead-pipe’ colon in longstanding disease as the colon is narrowed and shortened
  • Serum antibody markers: to help differentiate UC vs. Crohn’s disease, particularly in the paediatric population
    pANCA is more associated with ulcerative colitis
    (ASCA is more associated with Crohn’s disease)
129
Q

what are the features of MILD UC (Truelove and Witt’s severity index)

A
  • < 4 bowel movements per day
  • No blood or only small amounts of blood in stool
  • HR < 90
  • apyrexial
  • no anaemia
  • ESR < 30mm/hour
130
Q

what are the features of MODERATE UC (Truelove and Witt’s severity index)

A
  • 4-6 bowel movements per day
  • blood in stools is between mild and severe
  • HR < 90
  • apyrexial
  • no anaemia
  • ESR < 30mm/hour
131
Q

what are the features of SEVERE UC (Truelove and Witt’s severity index)

A
  • ≥6 bowel movements per day and at least one feature of systemic upset (marked with*)
  • HR > 90*
  • pyrexical*
  • anaemic*
  • ESR > 30mm/hour*
  • visible blood in stools
132
Q

describe the management of UC in general

A
  • depends on severity and location
  • methotrexate is NOT indicated in UC Rx (unlike in Chrohn’s)
  • There may be a role for probiotics in preventing relapse in patients with mild to moderate disease
133
Q

how is remission INDUCED in MILD-MODERATE UC: PROCTITIS

A
  • First line: topical ASA (superior to rectal steroids or oral ASA)
  • Second line (if remission not achieved within 4 weeks): add oral ASA
  • Third line: add topical/oral corticosteroid if remission still not achieved
134
Q

how is remission MAINTAINED in MILD-MODERATE UC: PROCTITIS

A
  • Topical ASA (daily or intermittent) OR
  • Oral ASA with topical ASA (daily or intermittent) OR
  • Oral ASA alone: less effective than other two options
135
Q

how is remission INDUCED in MILD-MODERATE UC: PROCTOSIGMOIDITIS AND LEFT-SIDED COLITIS (limited to splenic flexure)

A
  • First line: topical ASA
  • Second line (if remission not achieved within 4 weeks): add high-dose oral ASA
    OR
    switch to high-dose oral ASA AND topical corticosteroid
  • Third line: stop topical therapy and commence high-dose oral ASA AND oral corticosteroid
136
Q

how is remission MAINTAINED in MILD-MODERATE UC: PROCTOSIGMOIDITIS AND LEFT-SIDED COLITIS (limited to splenic flexure)

A
  • Proctosigmoiditis: treat as for proctitis
  • Left-sided colitis: low maintenance dose of oral ASA
137
Q

how is remission INDUCED in MILD-MODERATE UC: EXTENSIVE DISEASE (extends proximal to the splenic felxure)

A
  • First line: topical ASA and high-dose oral ASA
  • Second line (if remission not achieved within 4 weeks): stop topical therapy and commence high-dose oral ASA AND oral corticosteroid
138
Q

how is MAINTAINED in MILD-MODERATE UC: EXTENSIVE DISEASE (extends proximal to the splenic felxure)

A

Low maintenance dose of oral ASA

139
Q

how is remission INDUCED in ACUTE SEVERE COLITIS: any site

A
  • First line: admit to hospital and IV corticosteroid (or ciclosporin if steroids are contraindicated)
  • Second line: add IV ciclosporin if no improvement within 72h (or IV infliximab if ciclosporin is contraindicated)
  • Third line: Colectomy
140
Q

how is remission MAINTAINED in ACUTE SEVERE COLITIS: any site

A
  • Oral azathioprine or oral mercaptopurine

Consider oral ASA if the above are contraindicated

141
Q

describe the management of UC if there have been ≥ 2 exacerbations in the past year or remission not maintained by ASAs

A

Offer oral azathioprine or oral mercaptopurine

142
Q

describe the criteria for fulminant disease (UC) and the management

A

Fulminant refers to an abrupt and severe onset of a UC flare

Suggested by one of the following:
* >10 bowel movements per day
* Continuous bleeding
* Abdominal tenderness and distention
* Toxicity
* Colonic dilation
* The need for blood transfusion

Fulminant disease may require early surgical intervention

143
Q

what are the extra-intestinal manifestations of IBD that are RELATED TO DISEASE ACTIVITY

A
  • erythema nodosum
  • pauci-articular arthritis
  • osteoporosis
  • episcleritis (more common in chrohn’s than UC)
144
Q

what are the extra-intestinal manifestations of UC that are NOT RELATED TO DISEASE ACTIVITY

A
  • pyroderma gangrenosum
  • axial arthritis
  • polyarthritix: symmetrical
  • clubbing
  • uveitis (more common in UC than chrohn’s)
  • PSC (UC&raquo_space;> chrohn’s)
  • autoimmune hepatitis (UC > chrohn’s)
145
Q

which is the most common extra-intestinal feature of IBD (Chrohn’s and UC)

A

arthritis

146
Q

what are the complications of UC

A
  • Toxic megacolon: this is an acute form of colonic distension and patients can become septic and perforate. Requires supportive care, bowel rest, NG decompression and antibiotics. Requires a colectomy if no improvement within 24-48 hours
  • Perforation: associated with high mortality
  • Colonic adenocarcinoma: higher risk than Crohn’s disease
  • Strictures and obstruction: bowel loops can develop strictures following chronic inflammation and this can lead to bowel obstruction
  • Extraintestinal manifestations
147
Q

what is Chrohn’s disease

A

A form of IBD where there is transmural inflammation which can occur anywhere along the GIT from the mouth to anus

148
Q

Describe the pattern of inflammation in Chrohn’s disease

A
  • transmural (from mucosa to serosa) - can lead to fistulas, strictures and adhesions
  • scattered inflammation, there will be patches of healthy tissue in between which gives a “cobblestone” appearance
  • most commonly affected areas are: terminal ileum and colon
  • granulomas are formed within the intestinal wall
149
Q

Describe the aetiology and pathophysiology of Chrohn’s

A
  • thought to be due to uncontrolled immune response to pathogens in the GIT (listeria, pseudomonas, mycobacterium paratuberculosis)
  • NOD2 (CARD-15) genetic mutation causes a frameshift which might cause a dysfunctional protein to be encoded
  • there may be a defect in the epithelial barrier which may allow pathogens to enter inside the GIT wall more easily
150
Q

Describe the aetiology and pathophysiology of Chrohn’s

A
  • thought to be due to uncontrolled immune response to pathogens in the GIT (listeria, pseudomonas, mycobacterium paratuberculosis)
  • NOD2 (CARD-15) genetic mutation causes a frameshift which might cause a dysfunctional protein to be encoded
  • there may be a defect in the epithelial barrier which may allow pathogens to enter inside the GIT wall more easily
151
Q

what are the extra-intestinal features specific to UC

A

cholangiocarcinoma

152
Q

what are the extra-intestinal features specific to Chrohn’s

A

these are unrelated to disease activity
* calcium oxalate renal stones
* gallstones

153
Q

what are the Ix for Chrohn’s

A

same as for UC
* FBC: leukocytosis during a flare; anaemia due to vitamin B12, folate or iron deficiency
* U&Es: to assess for electrolyte disturbance and signs of dehydration
* Stool microscopy and culture: to exclude infective gastroenteritis or pseudomembranous colitis (including Clostridium difficile toxin)
* Colonoscopy: investigation of choice and allows for biopsy

other Ix
* CT abdomen pelvis: demonstrates inflammatory bowel changes and their distribution, as well the presence of fistulae or abscesses
* AXR: may show bowel inflammation (thumbprinting)
* Barium fluoroscopy (small bowel enema): Kantor’s ‘string sign’ (suggests strictures), ‘rose thorn’ ulcers, proximal bowel dilatation and fistulae may be present
High specificity and sensitivity for examining the terminal ileum

154
Q

what is seen on colonoscopy for Chrohn’s

A

Mucosal inflammation, deep ulcers, skip lesions and cobblestone mucosa

Histology: transmural inflammation, granulomas and goblet cells

155
Q

Describe the management of Chrohn’s disease in general

A
  • advice regarding smoking cessation is very important
  • There is some evidence to suggest that use of NSAIDs or the COCP may increase the risk of relapse
156
Q

how does MILD Chrohn’s PRESENT

A

First presentation OR 1 exacerbation in 12 months

157
Q

how does MODERATE Crohn’s PRESENT

A

≥2 exacerbations in 12 months OR
Glucocorticoid cannot be tapered for management of mild disease

158
Q

how does SEVERE Chrohn’s PRESENT

A

Unresponsive to conventional therapy AND
≥ 1 symptoms e.g. weight loss, fever, severe abdominal pain AND
Usually >3 loose stools/day

159
Q

how is remission INDUCED in MILD chrohn’s

A
  • 1st line: Glucocorticoid (PO or IV)
  • 2nd line: Aminosalicylate (e.g. mesalazine)
  • Distal ileal or ileocaecal disease: Budesonide (a type of steroid medication)
160
Q

how is remission INDUCED in MODERATE chrohn’s

A

Add in the following:

1st line: Azathioprine or mercaptopurine
2nd line: Methotrexate

161
Q

how is remission INDUCED in SEVERE chrohn’s

A

As monotherapy or combined with other immunosuppressant:

1st line: Infliximab or adalimumab (anti-TNF)
2nd line: Other biological therapies

162
Q

Describe the management of Chrohn’s that is refractory to medical therapy or disease limited to the distal ileum

A

Surgery

163
Q

Describe how remission of Chrohn’s disease is MAINTAINED

A
  • NICE advises that patients can either have no treatment, or pharmacological therapy as below depending on their risk of relapse and this should be discussed with the patient
  • Glucocorticoids or budesonide should not be offered

1st line: Azathioprine or mercaptopurine

2nd line: Methotrexate

Post-surgery: consider azathioprine, with or without methotrexate

164
Q

what are the intestinal complications of chrohn’s disease

A
  • Peri-anal abscess: peri-anal abscesses should be incised and drained under general anaesthetic due to the possibility of a fistula.Antibiotics are generally not required unless evidence of systemic infection
  • Anal fissure: a small tear in the lining of the anus
  • Anal fistula: an abnormal connection between 2 epithelial surfaces, e.g. from the anal canal to skin surface
  • Strictures and obstruction: bowel loops can develop strictures following chronic inflammation and this can lead to bowel obstruction
  • Perforation: chronic inflammation can weaken the bowel wall and predispose to subsequent perforation
  • Malignancy: colorectal cancer (relative risk, 2.59; less than UC) and small bowel cancer (relative risk, 33.2)
  • Osteoporosis
  • Anaemia and malnutrition
165
Q

what are the treatment complications of chrohn’s disease

A
  • Infection: increased risk of opportunistic infections due to immunosuppressive therapy
  • Myelosuppression: azathioprine and mercaptopurine require weekly FBC for the first month and then at least every 3 months after that
  • Non-melanoma skin cancer: increased risk with thiopurines; people should be monitored for skin cancer and given appropriate sun protection advice
166
Q

what are the clinical features of Chrohn’s

A
  • right lower quadrant pain (associated with the ileum)
  • diarrhoea (may be with blood, blood is more common in UC)
  • weight loss and lethargy
  • delayed puberty in children
  • Rectal examination: blood, skin tags, erythema, fissures, fistulas, ulceration
  • apthous mouth ulcers

finals - MT (9 decks)

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