GI&L

Question 1

what is oesophagus lined by?

Answer 1

stratified squamous epithelium, which extends
distally to the squamocolumnar junction where the oesophagus joins the
stomach, recognised endoscopically by a zigzag (‘Z’) line, just above the most
proximal gastric folds

Question 2

what is the lower oesophageal sphincter responsible for?

Answer 2

prevention of gastric reflux

Question 3

GORD epidemiology?

Answer 3

• people who overeat
• smokers
• alcohol users
• pregnancy
• drugs; antimuscarinics, CCB and nitrates

Question 4

aetiology of GORD?

Answer 4

• lower oesophageal sphincter hypotension
• hiatus hernia (80% due to sliding -> where the gastro-oesophageal junction and part of the stomach slide up into chest and 20% rolling -> where the gastro-oesophageal junction remains in abdomen BUT part of fungus prolapses)

Question 5

pathophysiology of GORD?

Answer 5

• in GORD -> MUCH MORE transient lower oesophageal sphincter
  relaxations as the LOS has reduced tone thereby allowing gastric acid to flow
  back into the oesophagus

Question 6

clinical presentations of GORD?

Answer 6

• oesophageal -> heartburn, nelching, acid brash and painful swallowing
• extra-oesophageal -> nocturnal asthma, chronic cough, laryngitis and sinusitis

Question 7

Ddx of GORD?

Answer 7

• CAD
• biliary colic
• peptic ulcer disease

Question 8

investigations of GORD?

Answer 8

• if there are no alarm bell signs (weigh loss and haemtemesis and dysphagia) then treatment without investigation
• if alarm bells then endoscopy and barium swallow

Question 9

treatment for GORD?

Answer 9

• lifestyle changes
• pharma -> antacids (MAGNESIUM TRISLICATE MIXTURE s/e diarrhoea), alginates (GAVISCON), PPI (LANSOPRAZOLE) and h2 receptor antagonist (CIMETIDINE)

Question 10

GORD complications?

Answer 10

• peptic stricture (oesophagiitis which narrows the oesophagus -> worsening dysphagia -> treatment endoscopic dilation and long term PPI therapy)
• Barrets oesophagus (distal oesophageal epithelium metaplasia from squamous to columnar)

Question 11

what is mallory-weiss tear?

Answer 11

• linear mucosal tear occurring at oesphagogastic junction and produced by sudden increase in intra-abdominal pressure
• seen after alcoholic dry heaves -> follows counts of coughing or retching

Question 12

risk factors for mallory-weiss tear?

Answer 12

• alcoholism
• forceful vomiting
• eating disorders
• Male
• NSAID abuse

Question 13

clinical features of mallory-weiss tear?

Answer 13

• vomiting
• haematemesis
• postural hypotension

Question 14

investigations and treatment of mallory-weiss tear?

Answer 14

endoscopy

most bleeds are minor and heal in 24hrs

Question 15

dyspepsia?

Answer 15

upper abdominal
symptoms such as; heart burn, acidity, epigastric pain or discomfort, fullness or
belching
(postprandial fullness, early satiety and epigastric pain >4 weeks)

Question 16

clinical presentation of dyspepsia?

Answer 16

• reflux when lying flat
• heartburn
• acid taste
• blowing
• indigestion

Question 17

dyspepsia -> cancer?

Answer 17

if cancer;

• unexplained weight loss
• anaemia
• evidence of GI bleed
• dysphagia
• upper abdominal mass
• persistant vomiting

Question 18

management fo dyspepsia?

Answer 18

• dietary review
• antidepressants- SSROS (CITALOPRAM)
• endoscopy

Question 19

stomach layers?

Answer 19

• (outer longitudinal,

inner circular and innermost oblique layers)

Question 20

duodenum muscle layers?

Answer 20

(outer longitudinal and inner smooth muscle)

Question 21

pariental cells
chief cells
ECL cells?

Answer 21

Parietal cells - secrete HCl
• Chief cells - produce pepsinogen and thus initiate proteolysis - the
digestion of proteins
• Enterochromaffin-like (ECL) cells - releases histamine (stimulates acid
release)

Question 22

what is in antral mucosa?

Answer 22

• Mucus secreting cells - secrete mucin (protects gastric
  mucosa) and BICARBONATE
  • G cells - secrete gastrin which stimulates acid release
  • D cells - secrete somatostatin that is a suppressant of acid
  secretion

Question 23

prostaglandins in mucosal barrier?

Answer 23

Prostaglandins stimulate the secretion of mucus and their synthesis is
INHIBITED by ASPIRIN and NSAIDs, which inhabit cyclo-oxygenase

Question 24

duodenal mucosa?

Answer 24

Has villi like the rest of the small bowel and also contains Brunner’s glands
which secrete alkaline mucus

Question 25

peptic ulcer disease?

Answer 25

break in the superficial epithelial cells penetrating down to the muscularis mucosa of either the stomach or the duodenum; there is a fibrous base and an increase in inflammatory cells

Question 26

most common peptic ulcer?

Answer 26

duodenal

Question 27

peptic ulcer disease, epidemiology?

Answer 27

- elderly - developing countries due to H pylori - NSAID use - decline in incidence in men and now rising in women

Question 28

aetiology of peptic ulcer disease?

Answer 28

- h pylori - NSAIDs - increased gastric acid secretion - smoking - delayed gastric emptying - O blood group

Question 29

pathophysiology of peptic ulcer disease? NSAIDs

Answer 29

Ulcers result in gastritis (inflammation of the gastric cells) - Usually the gastric mucosa is protected by a layer of MUCIN that is produced by gastric cells - Mucous secretion is stimulated by prostaglandins (in inflamed tissue, prostaglandin triggers inflammatory response thus inhibition = less inflammation) • Cyclo-oxygenase 1 is needed for prostaglandin synthesis • NSAIDS inhibit cylclo-oxygenase 1 • Thus reduced mucosal defence

Question 30

pathophysiology of peptic ulcer disease? H pylori

Answer 30

• Highly adapted to the stomach environment and exclusively colonises gastric epithelium and inhabits the mucous layer or just beneath it • Causes major destruction to the mucin layer that protects the mucosa • Causes the decrease in duodenal HCO3- thereby increasing the acidity of the stomach as there will be less alkali to buffer the acid • Secretes urease, splitting urea into CO2 and ammonia • Ammonia + H+ = ammonium • Ammonium is toxic to gastric mucosa resulting in less mucous produced • Secreted proteases, phospholipase & vacuolating cytotoxin A can then begin attacking the gastric epithelium further reducing mucous production • Results in an inflammatory response and less mucosal defence • Also increases gastrin (released from G cells) release thereby causing more acid secretion from parietal cells and also triggering the release of histamine which further increases acid secretion • Also increases parietal cell mass meaning more acid production • Also decreases somatostatin (released from D cells) release (which reduced acid secretion) resulting in increased acid release • Increased acidity overwhelms the protective mucin resulting in mucosal damage and ulceration

Question 31

clinical presentations of peptic ulcer disease?

Answer 31

- recurrent burning epigastric pain - nausea - anorexia and weight loss

Question 32

complications of ulcers

Answer 32

- duodenal ulcers can go to gasproduodenal artery and cause haemorrhage - can cause peritonitis if enters peritoneum - can cause acute pancreatis

Question 33

investigations of peptic ulcer disease?

Answer 33

- <55 yrs -> non-invasive testing eg serological test (tests for IgG antibodies), breath test (C-urea for H pylori) or stool antigen ( uses monoclonal antibodies to test for H pylori) - >55 endoscopy

Question 34

treatment of peptic ulcer disease?

Answer 34

- lifestyle adjustments - stop NSAIDs - If h pylori positive; triple therapy ( PPI and METRONIDAZOLE/CLARTIHROMYCIN OR QUONOLONES - H2 antagonists -> RANTIDINE

Question 35

oesophageal gastric varices?

Answer 35

A varices is just a dilated vein which is at risk of rupture resulting in haemorrhage and in the GI system can result in GI bleeding

Question 36

types of portal hypertension?

Answer 36

- Pre-hepatic; blockage of the hepatic portal vein before the liver - Intra-hepatic; distortion of the liver architecture, either pre-sinusoidal (e.g. schistosomiasis) or post-sinusoidal (e.g. cirrhosis) - Post-hepatic; venous blockage outside the liver (RARE)

Question 37

epidemiology og oesophageal gastric varicose?

Answer 37

Around 90% of patients with CIRRHOSIS will develop gastro-oesophageal varices over 10 years - but only a third of these will bleed

Question 38

aetiology of oesophageal gastric varices

Answer 38

- alcoholism and viral cirrhosis - preheptaic -> thrombosis in portal or splenic vein - intra hepatic -> cirrhosis and schistomiasis - post hepatic -> budd-chiari syndrome (tumour or thrombosis obstruction hepatic vein)

Question 39

pathophysiology of oesophageal gastric varices?

Answer 39

Following liver injury and fibrogenesis e.g due to cirrhosis, the contraction of activated myofibroblasts (mediated by endothelin, nitric oxide and prostaglandins) contributes to increased resistance to blood flow - This leads to portal hypertension → splanchnic vasodilation → drop in BP → increased cardiac output to compensate for BP → salt and water retention to increase blood volume and compensate → hyperdynamic circulation (high circulatory volume)/increased portal flow → Formation of collaterals between the portal and systemic systems e.g. in the lower oesophagus and gastric cardia → Gastro-oesophageal varices develop one portal pressure is above 10mmHg and start to bleed i.e. rupture when above 12mmHg - this can occur RAPIDLY and could result in MAJOR HAEMORRHAGE

Question 40

clinical presentations of oesophageal gastric varcices?

Answer 40

- signs of chronic liver damage - splenomegaly - ascites - hyponatreamia - If ruptured: • Haematemesis • Abdominal pain • Shock - if major blood loss • Fresh rectal bleeding - associated with shock in acute massive GI bleed • Hypotension and tachycardia • Pallor • Suspect varices as the cause of GI bleeding if there is alcohol abuse or cirrhosis

Question 41

investigations for oesophageal gastric varices?

Answer 41

endoscopy

Question 42

treatment for oesophageal gastric varices?

Answer 42

BLOOD TRANSFUSION aiming to get Hb to 80g/L - Correct clotting abnormalities - administer VITAMIN K and PLATELET TRANSFUSION - Vasopressin - IV TERLIPRESSIN - to cause vasoconstriction, use IV SOMATOSTATIN if terlipressin is contraindicated e.g. in ischaemic heart disease - Variceal banding - where a band is put around varice using an endoscope, after a few days the banded varix degenerates and falls off leaving a scar - Ballon tamponade to reduce bleeding by placing pressure on varice if banding fails - Transjugular intrahepatic portoclaval shunt (TIPS) - only used when bleeding cannot be controlled wither acutely or following a rebleed, essentially a shunt between the systemic and portal systems which reduces sinusoidal and portal vein pressure

Question 43

achalasia?

Answer 43

difficulties passing food and liquid down oesophagus into stomach

Question 44

epidemiology of achalasia?

Answer 44

- F=M | - long history of dysphagia

Question 45

pathophysiology of achalasia?

Answer 45

The lower oesophageal sphincter fails to relax due to degeneration of the mesenteric plexus of the oesophagus with reduction of ganglion cell numbers

Question 46

clinical presentation of achalasia?

Answer 46

- dysphagia - regurgitation of food at night - weight loss - spontaneous chest pain

Question 47

investigations of achalasia?

Answer 47

- CXR - barium swallow - gold standard-> MANOMETRY -> shows failure of relaxation of lower oesophageal sphincter

Question 48

treatment of achalasia?

Answer 48

- relief of symptoms -> NIFEDIPINE, NITRATES | - surgery -> endoscopic balloon dilation or botox injections to relax sphincter

Question 49

SCLERODERMA/SYSTEMIC SCLEROSIS:

Answer 49

Scleroderma/Systemic sclerosis is a multi-system disease that affects the body by hardening connective tissue

Question 50

Scleroderma/Systemic sclerosis, epidemiology?

Answer 50

- F>M | - 30-50 yrs peak

Question 51

Scleroderma/Systemic sclerosis, risk factors?

Answer 51

- vinyl chloride | - silica dust

Question 52

Scleroderma/Systemic sclerosis, pathophysiology?

Answer 52

- Diminished peristalsis and oesophageal clearance due to the replacement of the smooth muscle by fibrous tissue - Lower oesophageal sphincter pressure is decreased thereby allowing GORD with consequent mucosal damage - Strictures may develop

Question 53

clinical presentations, Scleroderma/Systemic sclerosis

Answer 53

- initially no symptoms | - dysphagia

Question 54

Scleroderma/Systemic sclerosis, investiahtions

Answer 54

- barium swallow - gold standard - CXR - manometry

Question 55

gastritis?

Answer 55

Gastritis is inflammation that is associated with mucosal injury

Question 56

aetiology of gastritis?

Answer 56

- H pylori - autoimmune - Virus - reflux - Aspirin and NSAIDs - alcohol

Question 57

pathophysiology of gastritis?

Answer 57

- Autoimmune gastritis - affects the fundus and body of the stomach leading to atrophic gastritis and loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia (low RBCs due to low B12) - Aspirin and NSAIDs e.g. Naproxen will inhibit prostaglandins (which stimulate mucus production) via the inhibition of cyclo-oxygenase resulting in less mucus production and thus gastritis

Question 58

clinical presentations of gastritis?

Answer 58

- nausea - abdominal bloating - epigastric pain - indigestion - vomiting

Question 59

investigations for gastritis?

Answer 59

- endoscopy - gold - biopsy - Pylori urea and stool test

Question 60

treatments for gastritis?

Answer 60

- lifestyle change - triple therapy; PPI, METRONIDAZOLE/CLARTHROMYCIN and CIPROFLOXACIN - h2 antagonist - RANITDINE - antacids

Question 61

diseases that result in malabsorption?

Answer 61

- coeliac - tropical sprue - crohns - parasite infection

Question 62

causes of malabsorption; defective intraluminal digestion?

Answer 62

Pancreatic insufficiency: - Pancreas produce majority of digestive enzymes such as amylase (breaks down starch) - Pancreatitis causes damage to most of the glandular pancreas meaning less or no enzymes are released - Cystic fibrosis results in the blockage of the pancreatic duct due to excess mucus meaning enzymes fail to be released • Defective bile secretion (lack of fat solubilisation): - Biliary obstruction e.g. gall stone - Ileal resection - we reabsorb bile salts in the terminal ileum so if removed then bile salt reuptake will be decreased • Bacterial overgrowth

Question 63

causes of malabsorption; insufficient absorptive area?

Answer 63

Essentially anything that damages microvilli and villi thereby reducing absorptive surface area and thus absorption potential • Coeliac disease (gluten sensitive enteropathy): - Villi are very short if present at all, since there is villous atrophy and crypt hyperplasia - Lots of lymphocytes in the epithelium • Crohn’s: - Causes inflammatory damage to the lining of the bowel resulting in cobblestone mucosa with significant reduction of absorptive surface area • Giardia lamblia: - Extensive surface parasitisation of the villi and microvilli - Parasites coat the surface of the villi thus food cannot be absorbed • Surgery - small intestine resection or bypass - in small bowel infarction Lack of digestive enzymes: • Disaccharidase deficiency (lactose intolerance) - cannot break down the lactose in milk into glucose which can then be absorbed. The undigested lactose passes into the colon where it is then eaten up by bacteria and CO2 is released leading to wind and diarrhoea • Bacterial overgrowth resulting in brush border damage - Defective epithelial transport: • Abetalipoproteinaemia - lack of transporter protein to transport lipoprotein across cell • Primary bile acid malabsorption - mutations in bile acid transporter protein - Lymphatic obstruction: • Lymphoma • Tuberculosis

Question 64

what is coeliac disease?

Answer 64

Condition in where there is inflammation of the mucosa of the upper small bowel that improves when gluten is withdrawn from the diet and relapses when gluten is reintroduced

Question 65

epidemiology of coeliac disease?

Answer 65

Occurs at any age but peaks in infancy and 50-60yrs - Affects males and females equally - 10% risk in 1st degree relatives and 30% risk in siblings

Question 66

risk factors for coeliac disease?

Answer 66

Other autoimmune diseases since having one will increase risk of others: • Type 1 diabetes • Thyroid disease • Sjorgrens - IgA deficiency - Breast feeding - Age of introduction to gluten into diet - Rotavirus infection in infancy increases risk

Question 67

pathophysiology of coeliac disease?

Answer 67

In wheat, in gluten the prolamin a-GLIADIN is toxic and resistant to digestion by pepsin and chymotrypsin because of their high glutamine and proline content and remain in the intestinal lumen thereby triggering immune responses The gliadin peptides pass through the epithelium and are deaminated by tissue transglutaminase, which increases their immunogenicity - The gliadin peptides then bind to antigen-presenting cells which interact with CD4+ T cells in the lamina propria via HLA class II molecules DQ2 or DQ8 These two HLA class II molecules DQ2 (95%) or DQ8 (5%) ACTIVATE the gluten-sensitive T cells - These T cells produce pro-inflammatory cytokines and initiate an inflammatory cascade - The cascade releases metaloproteinkinases and other mediators, which contribute to the VILLOUS ATROPHY, CRYPT HYPERPLASIA and intraepithelial lymphocytes that are typical of the disease and result in malabsorption - The mucosa of the PROXIMAL SMALL BOWEL is predominantly affected - This mucosal damage can mean that B12, folate and iron CANNOT be absorbed resulting in ANAEMIA

Question 68

clinical presentations of coeliac disease?

Answer 68

1/3 are asymptomatic (silent disease) and only detected on routine blood tests (raised MCV) - Stinking stools/fatty stools (steatorrhoea) - Diarrhoea - Abdominal pain - Bloating - Nausea & vomiting - Angular stomatitis - inflammation of one or both corners of mouth - Weight loss - Fatigue - Anaemia - Osteomalacia - softening of bones due to impaired bone metabolism due to lack of phosphate, calcium and vitamin D leading to OSTEOPOROSIS - Dermatitis hepetiformis - red raised patches, often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks

Question 69

investigations for coeliac disease?

Answer 69

``` should maintain gluten for at least 6 weeks before testing to get true results!: - FBC; low Hb, B12 and ferritin - GOLD STANDARD -> duodenal biopsy - serum antibody testing (IgA) ```

Question 70

treatment for coeliac disease?

Answer 70

- lifelong gluten free diet | - correction and vitamins and mineral deficiencies

Question 71

what is tropical sprue?

Answer 71

``` severe malabsorption (of two or more substances) accompanied by diarrhoea and malnutrition ```

Question 72

epidemiology of tropical sprue?

Answer 72

Occurs in residents or visitors to tropical areas where the disease is endemic; most of Asia, some Caribbean islands, Puerto Rico and parts of South America

Question 73

pathophysiology of tropical sprue?

Answer 73

Villous atrophy with malabsorption - Onset is acute and occurs either a few days or many years after being in the tropics - Epidemics can break out in villages, affecting thousands of people at the same time

Question 74

clinical presentations of tropical sprue?

Answer 74

Diarrhoea - Anorexia - Severe malabsorption - Weight loss - Abdominal distension

Question 75

investigation of tropical sprue?

Answer 75

- FBC | - jejunal biopsy - Jejunal mucosa is abnormal showing partial villous atrophy

Question 76

treatment of tropical sprue?

Answer 76

Leave area - FOLIC ACID daily and antibiotic to ensure complete recovery e.g. TETRACYCLINE for up to 6 months - Severe cases require resuscitation with fluids and electrolytes for dehydration and nutritional deficiencies should be corrected and B12 given

Question 77

major forms of IBD?

Answer 77

- Ulcerative colitis (UC) - which affects ONLY the COLON | - Crohn’s disease (CD) - can affect ANY PART of the GI tract (mouth-anus)

Question 78

epidemiology of IBD?

Answer 78

- jewish people more prone?

Question 79

epidemiology of UC?

Answer 79

- Highest incidence and prevalence in Northern Europe, UK and North America - M=F - more common in non/ex smokers

Question 80

risk factors of UC?

Answer 80

- family history - NSAIDs - chronic stress

Question 81

pathophysiology of UC?

Answer 81

- Begins in the rectum and extends to ileocaecal valve - Circumferential and continuous inflammation - NO SKIP LESIONS • Mucosa looks reddened and inflamed and bleeds easily (friability) • Ulcers and pseudo-polyps (regenerating mucosa) in severe disease - no granulotoma - depleted goblet cells

Question 82

clinical presentations of UC?

Answer 82

- LLQ pain - episodic or chronic pain with blood/mucus - cramps - clubbing, oral ulcers and Erythema nodusum

Question 83

investigations for UC?

Answer 83

- blood test; low Hb, raised WCC and platelets, high ESR and CRP and LFT abnormal - pANCA may be positive - stool samples - faecal calprotein (IBD but not specific) - GOLD STANDARD - colonoscopy with mucosal biopsy

Question 84

treatment for UC?

Answer 84

``` -5-ASA aminosalicylates are SULFASALAZINE, MESALAZINE or OLSALAZINE - glucocorticoid - ASA intolertant - AZATHIOPRINE - surgery ```

Question 85

churns disease?

Answer 85

chronic inflammatory GI disease characterised by transmural (goes deep into mucosa) granulomatous inflammation affecting ANY part of the gut from mouth to anus (especially in TERMINAL ILEUM and PROXIMAL COLON)

Question 86

epidemiology of chrons?

Answer 86

- Highest incidence and prevalence in Northern Europe, UK and North America - F>M - smoking increases risk

Question 87

risk factors for chrons?

Answer 87

- stronger genetic association (chr 16) - smoking - NSAIDs

Question 88

pathophysiology of chrons?

Answer 88

NOT CONTINUOUS i.e. there are SKIP LESIONS/patchy areas where there is a gap between affected and unaffected mucosa • Involved bowel is usually thickened and is often narrowed • COBBLESTONE appearance due to ulcers and fissures in mucosa • Affect ANY part of GI tract Inflammation EXTENDS through ALL LAYERS (transmural) of the bowel • Increase in chronic inflammatory cells and there is lymphoid hyperplasia • Granulomas present in 50-60% - these are non-caseating epithelioid cell aggregates with Langhans’s giant cells • Goblet cells are present • Less crypt abscesses’ than UC

Question 89

clinical presentation?

Answer 89

- weigh loss - abdo pain - lethargy - abdominal mass - anal strictures

Question 90

investigations of chrons?

Answer 90

- examination - tenderness RIGHT ILIAC FOSS - bloods; low Hb but no b12 - raised ESR and WWC - NEGATIVE pANCA - colonoscopy

Question 91

treatment of chrons?

Answer 91

- smoking cesstion - corticosteroids (mild - BUDESONIDE, moderate PREDNISOLONE and severe IV HYDROCORTISONE) - if no improvements, INFLIMAB - AZATHIOPRINE or METHOTEXATE given - surgery

Question 92

hirshprungs disease?

Answer 92

In neonates they are born without complete innervation of colon to rectum • Results in gut dilatation and the filling of faeces which remains since no ganglion cells to result in peristalsis and movement of contents - resulting in obstruction

Question 93

adhesions - obstruction?

Answer 93

Sticking together of abdominal structures to one another, bowel loops, omentum, other solid organs or the abdominal wall by fibrous tissue - This is the MOST COMMON CAUSE of OBSTRUCTION in adults (80%) Commonly occurs after surgery - In the intestines, the loops of the small and large intestines can normally move around freely within the abdominal cavity - When adhesions form, the intestines are no longer able to mover around freely because they become tethered to each other, the abdominal wall or to other abdominal organs - At the sites where the adhesions occur, the intestine can twist on itself, resulting in the obstruction of blood supply or the normal movement of the contents of the intestines - the small intestine in particular

Question 94

volvulus?

Answer 94

- A twist/rotation of segment of bowel e.g. sigmoid colon which is on a long mesentery can twist on itself resulting in obstruction - ALWAYS occurs at the part of bowel with mesentery - Type of closed loop bowel obstruction

Question 95

epidemiology of small bowel obstruction?

Answer 95

Accounts for 60-75% of intestinal obstruction - Majority is caused by previous surgery (60%) - Crohn’s disease is also a significant cause (25%)

Question 96

aetiology of small bowel obstructions?

Answer 96

Adhesions (60% of SBOs): - Usually secondary to previous abdominal surgery - Increased incidence in; pelvic, gynaecology and colorectal surgery ``` Hernia Abnormal protrusion of an organ or tissue out of the body cavity in which it normally lies - Particularly in the developing world - Untreated can result in strangulation ``` Malignancy Chrons disease

Question 97

pathophysiology of small bowel obstruction?

Answer 97

Mechanical obstruction is most common e.g. adhesions, hernia and Crohn’s - Obstruction of the bowel leads to bowel distension above the block with increased secretion of fluid into the distended bowel - Also leads to proximal dilatation, above the block, resulting in: • Increased secretions and swallowed air in the small bowel • More dilatation results decreased absorption and mucosal wall oedema • Increased pressure with the intramural vessels becoming compressed resulting in ischaemia and or perforation

Question 98

clinical presentation of small bowel obstruction?

Answer 98

Pain - initially colicky (starts and stops abruptly) then diffuse, pain is higher in the abdomen than in LBO - Profuse vomiting that follows pain - VOMITING occurs EARLIER in SBO compared to LBO - Less distension as compared to LBO (since the more distal the obstruction the greater the distension) - increased bowel sounds

Question 99

investigations for small bowel obstruction?

Answer 99

- GOLD standard - CT - Xray - FBC

Question 100

treatment of short bowel obstruction?

Answer 100

Aggressive fluid resuscitation - Bowel decompression - Analgesia and antiemetic - Antibiotics - Surgery - to remove obstruction done by laparotomy (open surgery)

Question 101

epidemiology of Large bowel obstruction?

Answer 101

- less common 25% | - africa -> volvulus

Question 102

pathophysiology of large bowel obstruction?

Answer 102

The colon proximal to obstruction dilates - There is increased colonic pressure and decreased mesenteric blood flow resulting in mucosal oedema - transudation of fluid and electrolytes from the lumen - This can compromise the arterial blood supply and also cause mucosal ulceration resulting in full thickness necrosis as well as perforation - Bacterial translocation can also occur resulting in sepsis

Question 103

presentation large bowel obstruction?

Answer 103

Abdominal pain that is more constant than in SBO - Abdominal distension - Bowel sounds normal then increased then quiet later - Palpable mass e.g. hernia, distended bowel loop or caecum - Late vomiting which is more faecal like - suggestive of LBO - vomiting may be absent tho - constipation

Question 104

investigations of large bowel obstruction?

Answer 104

- DRE - FBC - Xray - CT

Question 105

treatment of large bowel obstruction?

Answer 105

Aggressive fluid resuscitation - Bowel decompression - Analgesia and antiemetic - Antibiotics - Surgery - to remove obstruction done by laparotomy (open surgery) • Obstruction due to malignancy required colorectal stents followed by elective surgery

Question 106

pseudo-obstruction?

Answer 106

Clinical picture mimicking obstruction but with no mechanical cause

Question 107

pseudo-obsruction, aetiology?

Answer 107

``` Intra-abdominal trauma • Pelvic, spinal and femoral fractures • Postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic and neuro • Intra-abdominal sepsis - pneumonia - opiate use ```

Question 108

clinical presentation fo pseudo -obstruction

Answer 108

Patients present with rapid and progressive abdominal distension and pain

Question 109

investigation and treatment for pseudo obstruction?

Answer 109

X-ray shows a gas-filled large bowel | - treatment -> IV NEOSTIGMINE

Question 110

types of bowel ischemai?

Answer 110

Acute mesenteric ischaemia - Chronic mesenteric ischaemia (AKA intestinal angina) - Ischaemic colitis (AKA chronic colonic ischaemia)

Question 111

acute mesenteric ischemia, epidemiology?

Answer 111

Usually seen in those over 50 | - Almost always involves the small bowel

Question 112

aetiology of acute mesenteric ischemia?

Answer 112

Superior mesenteric artery (SMA) thrombosis - COMMONEST CAUSE • Superior mesenteric artery (SMA) embolism (e.g. due to AF) - rarer now • Mesenteric vein thrombosis - common in younger patients with hypercoagulable states and tends to affect small lengths of bowel • Non-occlusive disease - occurs in low flow states and reflects poor cardiac output

Question 113

clinical presentation fo acute mesenteric ischemia?

Answer 113

TRIAD - acute - severe abdominal pain - rapid hypovolemia -> shock - AF (atrial fibrillation)

Question 114

investigations for acute mesenteric ischemia?

Answer 114

- FBC - AXR - GOLD STANDARD - laparotomy - CT/MRI angiography

Question 115

treatment for acute mesenteric ischemia?

Answer 115

Fluid resuscitation - Antibiotics e.g. IV GENTAMICIN & IV METRONIDAZOLE - IV HEPARIN to reduce clotting - Surgery to remove dead bowel

Question 116

ischemic colitis?

Answer 116

Usually follows low flow in the inferior mesenteric artery (IMA) territory and ranges from mild ischaemia to gangrenous colitis

Question 117

epidemiology and risk factors of ischemic colitis?

Answer 117

- elderly - underlying atherosclerosis and vessel occlusion RF Thrombosis • Emboli • Decreased cardiac output and arrhythmias • Drugs e.g. oestrogen, antihypertensives, vasopressin • Surgery e.g. cardiac bypass, aortic dissection and repair, aortoiliac reconstruction • Vasculitis e.g. SLE, sickle cell disease and polyarthritis nodosa (hep B & C) • Coagulation disorders

Question 118

pathophysiology of ischemic colitis?

Answer 118

Occlusion of branched of the superior mesenteric artery (SMA) or inferior mesenteric artery (IMA), often in the older age group - The anatomy of the vascular supply to the colon results in a watershed area at the splenic flexure - which is thus the MOST COMMON SITE AFFECTED

Question 119

clinical presentation of ischemic colitis

Answer 119

- Sudden onset lower LOWER LEFT SIDE abdominal pain - Passage of bright red blood with/without diarrhoea - May be signs of shock (pale skin, weak rapid pulse, reduce urine output, confusion) and evidence of underlying cardiovascular disease

Question 120

investigation of ischemic colitis?

Answer 120

Urgent CT scan to exclude perforation - Flexible sigmoidoscopy: • Biopsy shows epithelial cell apoptosis - Colonoscopy and biopsy - GOLD STANDARD: • Only done AFTER patient has fully recovered to exclude stricture formation at the site of disease and confirm mucosal healing - Barium enema: • Thumb printing of submucosal swelling at splenic flexure

Question 121

treatment of ischemic colitis?

Answer 121

Fluid replacement - Antibiotics - to reduce infection risks due to translocation of bacteria across possibly dying gut wall

Question 122

what is haemorrhoids?

Answer 122

Disrupted and dilated anal cushions (masses of spongy VASCULAR (veins and arteries) tissue due to swollen veins around the anus

Question 123

epidemiology of haemorrhoids

Answer 123

- 45-65 yrs | - M=F

Question 124

aetiology of haemorrhoids

Answer 124

- constipation - diarrhoea - anal intercoruse - pregnancy

Question 125

pathophysiology of haemorrhoids

Answer 125

The normal/healthy anus is lined by discontinuous masses of spongy vascular tissue - the anal cushions, which contribute to anal closure - They are attached by smooth muscle and elastic tissue but are prone to displacement and disruption, either singly or together - The effects of gravity (erect posture), increased anal tone (possibly due to stress) and the effects of straining when defecating may make them become both bulky and loose, and so protrude to form piles (from latin, pila - ball) They are very vulnerable to trauma (e.g. from hard stools) and bleed readily from the capillaries of the underlying lamina propria - Since blood loss is from capillaries, it is bright red - Since there are no sensory fibres above the dentate line (squamomucosal junction), piles are not painful unless they thrombus when they protrude and are gripped by the anal sphincter, blocking venous return - There is a vicious circle; the vascular cushions protrude through a tight anus → become more congested and hypertrophy → protrude again more readily

Question 126

classification of haemorrhoids?

Answer 126

INTERNAL 1st - Remain in rectum - 2nd - Prolapse through the anus on defecation but spontaneously reduce - 3rd - Prolapse but can be reduced manually - 4th - Remain persistently prolapsed EXTERNAL - originate below dentate line so painful as they protrude

Question 127

treatment for haemorrhoids

Answer 127

- 1st degree - increase fluid, fibre and stool softener - 2/3rd degree - rubber band litigation or infra-red coagulation - 4th degree - excision haemorrhoidectomy

Question 128

what is anal fistula?

Answer 128

An abnormal connection between the epithelised surface of the anal canal and skin - essentially a track communicates between the skin and anal canal/rectum

Question 129

aetiology of anal fistula?

Answer 129

``` Perianal sepsis • Abscesses • Crohn’s • TB • Diverticular disease • Rectal carcinoma ```

Question 130

clinical presentation of anal fistula?

Answer 130

- pain - discharge - Pruritus ani (itchy bottom) - Systemic abscess if it becomes infected

Question 131

investigation of anal fistula?

Answer 131

- MRI | - endoanal US

Question 132

treatment of anal fistula?

Answer 132

Surgical - Fistulotomy and excision | - Drain abscess with antibiotics if infected

Question 133

anal fissure?

Answer 133

Painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line resulting in pain on defecation

Question 134

epidemiology and aetiology of anal fissure?

Answer 134

- F>M | - cause; hard faeces, syphilis, herpes, trauma, chrons

Question 135

investigation of anal fissure?

Answer 135

- perianal inspection

Question 136

treatment for anal fissure?

Answer 136

Increase dietary fibre and fluids to make stools softer - LIDOCAINE OINTMENT + GTN OINTMENT or topical DILTIAZEM - BOTULINUM TOXIN (botox) INJECTION (2nd line)

Question 137

perianal access? epidemiology, presentation, diagnosis and treatment?

Answer 137

Epidemiology: - 2/3 times more common in gay sex and in those who have anal sex • Clinical presentation: - Painful swellings - Tender - Discharge • Diagnosis: - MRI - Endoanal ultrasound • Treatment: - Surgical excision - Drainage with antibiotics

Question 138

pilonidal sinus/abcess?

Answer 138

Hair follicles get stuck under the skin in the natal cleft (butt crack) resulting in irritation and inflammation leading to small tracts which can become infected (abscess)

Question 139

epidemiology of pilonidal sinus?

Answer 139

Much more common in MALES than females | - Commonly presents between 20-30 yrs

Question 140

risk factors of pilonidal sinus?

Answer 140

Obese caucasians and those from Asia, Middle East and Mediterranean are at increased risk - Large amount of body hair - Sedentary job - Occupation involving sitting or driving - Family history

Question 141

treatment of pilonidal sinus?

Answer 141

Surgery: • Excision of the sinus tract and primary closure and pus drainage • Pre-op antibiotics - Hygiene and hair removal advice (near sinus)

Question 142

IBS?

Answer 142

mixed group of abdominal symptoms for which no organic cause can be found

Question 143

IBS epidemiology?

Answer 143

Age of onset is under 40 - More common in FEMALES than males - Common, in western world

Question 144

aetiology of IBS?

Answer 144

``` Depression, anxiety • Psychological stress and trauma • GI infection • Sexual, physical or verbal abuse • Eating disorders ```

Question 145

types of IBS?

Answer 145

* IBS-C - with constipation * IBS-D - with diarrhoea * IBS-M - with constipation and diarrhoea

Question 146

pathophysiology of IBS?

Answer 146

Dysfunction in the brain-gut axis results in disorder of intestinal motility and or enhanced visceral perception (visceral hypersensitivity)

Question 147

clinical presentation of IBS?

Answer 147

``` Painful period • Urinary frequency, urgency, nocturia and incomplete emptying of bladder • Back pain • Joint hypermobility • Fatigue ``` ABC abdominal pain, bloating and change in bowel habit

Question 148

investigations of IBS?

Answer 148

ruling out! - FBC - ESR and CRP - EMA and tTg test - faecal calprotectin - colonoscopy

Question 149

treatment for IBS?

Answer 149

- lifestyle and diet changes - soluble fibre is good, insoluble makes it worse - LOW FODMAP DIET - antispasmodics eg MEBEVERINE - laxatives MAVICOL/SENNA - anti-motility LOPERAMIDE - tricyclic antidepressants AMITRIPTYLINE

Question 150

diverticular disease and diverticulitis definitions?

Answer 150

Diverticulosis = presence of diverticula • Diverticular disease = diverticula are symptomatic • Diverticulitis = inflammation of a diverticulum

Question 151

epidemiology of diverticular disease?

Answer 151

- >50 yrs | - sigmoid colon most frequent

Question 152

aetiology of diverticular disease?

Answer 152

``` Low fibre diet: - Commonly eaten in developed countries - Rare in rural Africa • Obesity • Smoking • NSAIDs ```

Question 153

pathophysiology of diverticula

Answer 153

Diverticular forms at gaps in the wall of the gut where blood vessels penetrate • In a low fibre diet, the colon must push harder to move things along (fibre helps gut motility) so pressure increases • This pressure increase results in pouches of mucosa being extruded through the muscular wall through weakened areas near blood vessels leading to diverticula formation • There is also thickening of the muscle layer

Question 154

pathophysiology of acute diverticulitis

Answer 154

Occurs when faeces obstruct the neck of the diverticulum, causing stagnation and allowing bacteria to multiply and produce inflammation • This can then lead to bowel perforation (peridiverticulitis), abscess formation, fistulae into adjacent organs, haemorrhage and generalised acute peritonitis and possibly death

Question 155

clinical presentation of diverticular disease?

Answer 155

Asymptomatic in 95% of cases and is usually detected incidentally on colonoscopy or barium enema examination • In symptomatic cases: - Intermittent left iliac fossa pain - Erratic bowel habit • In severe cases: - Severe pain and constipation due to luminal narrowing

Question 156

acute diverticulitis clinical presentation?

Answer 156

- severe pain LEFT ILIAC FOSSA - fever - constipation - tachycardia

Question 157

complications of diverticular disease

Answer 157

- perforation - fistula formation - intestinal obstruction - bleeding - mucosal inflammation

Question 158

investigation for diverticular disease and acute diverticulitis

Answer 158

``` diverticular disease - COLONOSCOPY acute diverticulitis - ESR and CRP raised - gold standard CT COLONOGRAPY ```

Question 159

diverticular disease treatment?

Answer 159

In uncomplicated symptomatic disease recommend a well-balanced HIGH FIBRE DIET with smooth muscle relaxants i.e. antispasmodics e.g. MEBEVERINE

Question 160

acute diverticulitis treatment

Answer 160

Mild attacks can be treated with oral antibiotics e.g. CIPROFLOXACIN and METRONIDAZOLE • Those with signs of systemic upset (fevers, tachycardia) and significant abdominal pain require bowel rest, IV fluids and IV antibiotics • Surgical resection is occasionally required

Question 161

merkel diverticulum?

Answer 161

Most common congenital abnormality of the GI tract • Affects 2-3% population Acute inflammation of the diverticulum also occurs and is indistinguishable clinically from acute appendicitis • Treatment is surgical removal of diverticula, often laparoscopically (keyhole)

Question 162

acute appendicitis, where is it?

Answer 162

Located at McBurney’s point which lies 2/3 of the way from the umbilicus to the Anterior Superior Iliac Spine (ASIS)

Question 163

epidemiology of appendicitis?

Answer 163

More common in MALES than females - Can occur at any age although highest incidence is between 10-20 yrs - Rare before age of 2 since appendix is cone shaped with a larger lumen

Question 164

pathophysiology of appendicitis

Answer 164

Occurs when the lumen of the appendix becomes obstructed by lymphoid hyperplasia, filarial worms or a FAECOLITH (most common) resulting in the invasion of gut organisms into the appendix wall - This leads to oedema, ischaemia, necrosis and perforation as well as INFLAMMATION - If the appendix ruptures then infected and faecal matter will enter the peritoneum resulting in life threatening peritonitis

Question 165

clinical presentation of appendicitis

Answer 165

- pain moves from epigastrium to right iliac fossa - anorexia - pyrexia - nausea and vomiting

Question 166

investigations for appendicitis

Answer 166

- blood tests; raised WCC, CRP &ESR - USS - CT - GOLD STANDARD

Question 167

treatment for appendicitis

Answer 167

- surgery | - IV antibiotic pre-op eg IV METRONIDAZOLE

Question 168

acute pancreatitis, aetiology?

Answer 168

I GET SMASHED ``` I - idiopathic G - gallstones (60%) E - ethanol (30%) T - trauma S- steroids M - mumps A - autoimmune S - scorpion venom H - hyperlipidemia E- ERCP D- drugs (diuretics, ACE inhibitors) ```

Question 169

pathophysiology of acute pancreatitis?

Answer 169

Acute pancreatitis is caused by the destructive effect of premature activation of pancreatic enzymes which causes self-perpetuating pancreatic inflammation by enzyme-mediated AUTOdigestion The prematurely activate enzymes also cause leaky vessels by digesting vessel walls in the pancreas leading to the leakage of fluid into the tissues causing OEDEMA, INFLAMMATION and HYPOVOLAEMIA Destruction of blood vessels by enzymes causes haemorrhage - Destruction of the adjacent islets of Langerhans can result in hyperglycaemia as beta cells will be destroyed resulting in less insulin

Question 170

gallstone pancreatitis pathophysiology?

Answer 170

Accumulation of enzyme-rich fluid WITHIN the pancreas due to OBSTRUCTION of the pancreatic duct by gallstones • Intracellular Ca2+ increases and causes the early activation of trypsinogen • In this situation, trypsinogen is cleaved (by cathepsin B) to trypsin, and trypsin degradation (by chymotrypsin C) is impaired and overwhelmed leading to a buildup of trypsin and thus increased enzymatic digestion of the pancreas and inflammation leading to extensive acinar damage

Question 171

alcohol induced pancreatitis pathophysiology?

Answer 171

Alcohol is shown to interfere with Ca2+ homeostasis in increased stimulation of enzyme secretion and obstruction of the duct due to contraction of the ampulla of Vater

Question 172

clinical presentation of acute pancreatitis?

Answer 172

Gradual or sudden severe epigastric or central abdominal pain that radiates to the back - sitting forward may relieve - Anorexia, nausea and vomiting - Tachycardia - Fever - Jaundice - hypotension - Periumbilical ecchymosis (skin discolouration due to blood under skin due to bruising) - Cullen’s sign - Left flank bruising (skin discolouration due to blood under skin due to bruising) - Grey Turner’s sign

Question 173

investigation for acute pancreatitis?

Answer 173

- blood test; serum amylase raised, urinaru amylase raised, CRP raised, serum lipase raised - XCR - AUSS - CT - MRI

Question 174

treatment for pancreatitis?

Answer 174

- analgesia - Prophylactic antibiotics like beta-lactams e.g CEFUROXIME or another type e. g. METRONIDAZOLE to reduce risk of infected pancreatic necrosis

Question 175

chronic pancreatitis?

Answer 175

Debilitating continuing inflammatory process of the pancreas resulting in progressive loss of exocrine pancreatic tissue which is replaced with by fibrosis

Question 176

chronic pancreatitis, epidemiology?

Answer 176

- M>F - alcohol use - CKD - hereditary

Question 177

pathophysiology of chronic pancreatitis?

Answer 177

Obstruction or reduction in bicarbonate secretion, which produces an alkaline pH which in turn stabilises trypsinogen, leads to the activation of trypsinogen as pH rises making it more unstable and causing its activation into trypsin which leads to pancreatic tissue necrosis with eventual fibrosis

Question 178

clinical presentation of chronic pancreatitis?

Answer 178

- epigastric pain that goes to the back - nausea and vomiting - exocrine dysfunction - exocrine dysfunction

Question 179

investigations for chronic pancreatitis?

Answer 179

- serum amylase and lipase may be elevated but not in advanced disease - AUSS and contrast CT - GOLD STANDARD

Question 180

treatment of chronic pancreatitis?

Answer 180

- alcohol sessation - NSAIDs, opiates and trycylci antidepressants - duct drainage - PPI

Question 181

autoimmune chronic pancreatitis?

Answer 181

Chronic pancreatic inflammation which results from an autoimmune process • High prevalence in Japan • Presentation is very similar to normal chronic pancreatitis • There are elevated levels of serum gammaglobulins and immunoglobulin G (IgG) levels - IgG4 • Autoantibodies such as antinuclear cytoplasmic antibody (ANCA) and rheumatoid factor may also be elevated • This condition is steroid responsive with glucocorticoid therapy e.g. ORAL PREDNISOLONE for 4-6 weeks

Question 182

presentation of acute liver injury?

Answer 182

- malaise - nausea - anorexia - maybe jaundice

Question 183

presentation of chronic liver injury?

Answer 183

- ascites - oedema - haematemesis - bruising - hepatomegaly

Question 184

what is serum albumin?

Answer 184

Marker of synthetic function and is useful for gauging the severity of chronic liver disease: a falling serum albumin is a bad prognostic sign • In acute liver disease, initial albumin levels may be normal

Question 185

bilirubin test?

Answer 185

- Is normally all CONJUGATED • In liver disease, increased serum bilirubin is usually accompanied by other abnormalities in liver biochemistry

Question 186

AST?

Answer 186

Also present in heart, muscle, kidney and brain • High levels are seen in hepatic necrosis, myocardial infarction, muscle injury and congestive cardiac failure

Question 187

ALT?

Answer 187

More specific to the liver | • A rise only occurs with liver disease

Question 188

Alkaline phospahte test?

Answer 188

Present in liver but also in bone, intestine and placenta - Raised in both intrahepatic and extrahepatic cholestatic disease of any cause, due to increased synthesis - Raised levels also occur with heaptic infiltrations (e.g. metastases) and in cirrhosis

Question 189

bilirubin and haem catabolism?

Answer 189

When the erythrocytes is ingested it is broken down into haem and globin globin is broken down into amino acids and then used to generate new RBC in bone marrow haem further broken down into biliverdin and fe2+ biliverdin is reduced to UNCONJUGATED bilirubin (BILIVERDIN REDUCTASE). this is toxic and insoluble so transported bound to ALBUMIN to liver In liver it undergoes glucuronidation to make is soliaable using UDP GLUCURONYL TRANSFERASE -> CONJUGATED bilirubin CONJUGATED bilirubin travels to small intestine to ileum where by intestinal bacteria it is reduced to UROBILINOGEN UROBILINOGEN is lipid soluble so 10% reabsorbed into blood and bound to albumin to the liver (can go to the kidney where it is excreted, causing yellow urine) remaining 90% of UROBILINOGEN is oxidised by different intestinal bacteria to form STERCOBILIN -> faeces to make it brown

Question 190

types of jaundice?

Answer 190

PRE HEPATIC unconjugated - gilberts syndrome - UDP GLUCURONYL TRANSFERASE deficiency - haemolysis ``` HEPATIC conjugated - liver disease - hepatitis - ischemia ``` POST HEPATIC - gallstones - stricture - blocked stent

Question 191

what is biliary colic?

Answer 191

The term used for the pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder - The pain of stone-induced ductular obstruction is of sudden onset, severe but constant and has a crescendo characteristic

Question 192

epidemiology of gallstones?

Answer 192

- >30 yrs - F>M - more common with Scandinavians - obese

Question 193

risk factors for gallstones?

Answer 193

Female - Fat - Fertile - more kids = increased risk of gallstones - Smoking

Question 194

pathophysiology of gallstones?

Answer 194

CHOLESTEROL AND BILE PIGMENT CHOLESTEROL STONE - formed due to cholesterol crystallisation in bile BILE PIGMENT STONES - mainly formed of ca2+ - main cause is haemolysis - two types black ( calcium bilirubinate seen in haemolytic anaemia) and brown (calcium salts seen in bile stasis)

Question 195

clinical presentation of gallstones?

Answer 195

- most asymptomatic - celiac pain - start off epigastric pain and then RUQ pain - biliary celiac has no fever and jaundice - acute cholecystisis has no jaundice - cholangitis has jaundice, RUQ pain and fever

Question 196

investigations of gallstones?

Answer 196

- biliary colic - AUSS | - acute cholecystitis - AUSS and blood tests and examination

Question 197

treatment of gallstones?

Answer 197

- laparoscopic cholecystectomy - opiates - IV antibiotics - CEFTRIAXONE - stone dissolution using ORAL URSODEXOYCHOLIC ACID - shock wave lithotripsy

Question 198

stone in common bile duct and acceding cholangitis, aetiology?

Answer 198

- common bile duct obstruction by gallstones - benign biliary strictures following surgery - cancer of head of pancreas

Question 199

ascending chlangitis treatment?

Answer 199

- IV antibiotics | - ERCP - biliary drainage

Question 200

acute v chronic hepatitis?

Answer 200

Acute hepatitis is defined as hepatitis within 6 months of onset • Chronic hepatitis is defined an any hepatitis lasting for 6 months or longer

Question 201

acute hepatitis clinical presentations and investigations?

Answer 201

- general malaise - myalgia - RUQ pain - raised AAST, ALP and bilirubin

Question 202

causes of acute hepatitis?

Answer 202

- Viral - HEP A & E, herpes - non viral; Coxiella - alcohol, drugs, pregnancy

Question 203

chronic hepatitis clinical presentations and investigation?

Answer 203

- clubbing - palmar erythema - dupuytren contracture - spider naevi - LFTs can be normal

Question 204

causes of chronic hepatitis?

Answer 204

- HEP B&C | - alcohol, drugs, autoimmune

Question 205

HEP A, epidemiology?

Answer 205

- most common acute in world - endemic in Africa and South America - children and young adults - contaminated food/water

Question 206

spread of HEP A?

Answer 206

Spread via the faeco-oral route

Question 207

risk factors of HEP A?

Answer 207

Shellfish - Travellers - Food handlers

Question 208

pathophysiology of hEP A?

Answer 208

Hep A is a picornavirus - Replicates in the liver, is excreted in bile and then excreted in the faeces for about 2 weeks before the onset of clinical illness and for up to 7 days after - Disease is maximally infectious JUST BEFORE the onset of jaundice - Short incubation period of 2-6 weeks - Causes ACUTE HEPATITIS ONLY - Usually is self-limiting (3-6 weeks) - very rarely causes fulminant hepatitis (rapid liver injury that can quickly cause liver failure) - 100% immunity after infection

Question 209

clinical presentation of HEP A?

Answer 209

- nausea, fever and malaise | - 1-2 weeks -> jaundice (dark urine and pale stools)

Question 210

investigations of HEP A?

Answer 210

``` before jaundice - serum bilirubin will be normal - raised AST or ALT after jaundice - serum bilirubin will rise ``` - blood test (LOW WCC & RAISED ESR) - viral markers (HAV antibodies and IgM)

Question 211

treatment for HEP A??

Answer 211

- supportive treatment - avoid alcohol - manage close contacts PREVENTION!! - good hygiene and immunisation

Question 212

HEP E, epidemiology?

Answer 212

- older men - common in UK - self limiting

Question 213

HEP E, transmission route?

Answer 213

Faeco-oral route of transmission - water or food-borne

Question 214

HEP B, epidemiology?

Answer 214

- present world wide | - endemic in Far East and Africa

Question 215

HEP B, transmission route?

Answer 215

- blood borne -> needle stick, sex, mother -> child

Question 216

risk factors for HEP B?

Answer 216

Healthcare personnel - Emergency and rescue teams - CKD/dialysis patients - Travellers - Homosexual men - IV drug users

Question 217

pathophysiology of HEP B?

Answer 217

- DNA virus - The complete virus comprises of an inner core or nucleocapsid surrounded by an outer envelope of surface protein (Hepatitis B surface antigen (HBsAg)) HBsAg is produced in excess by the infected hepatocytes and can exist separately from the whole virus in serum and body fluid - After penetration into hepatocyte the virus loses its coat and the virus core is transported to the nucleus without processing - Following infection, which may be subclinical (i.e. little symptoms), around 1-10% of patients will not clear the virus and will develop chronic Hep B Around 1-5% will develop chronic infection which can lead to cirrhosis and then decompensated cirrhosis and then liver failure Both cirrhosis and chronic infection can lead to HEPATOCELLULAR CARCINOMA - VERY BAD

Question 218

clinical presentations of HEP B?

Answer 218

- nausea, fever, malaise - rash - 1-2 weeks - jaundice - heptaospleomegaly

Question 219

investigations of HEP B?

Answer 219

HBsAg is present 1-6 months after exposure - HBsAg presence for more than 6 months implies carrier status - Anti-HBs - antibodies to hepatitis B - IgG

Question 220

treatment for HEP B?

Answer 220

- supportive - avoid alochol CHRONIC - SC PEGYLATED INTERFERON-ALPHA 2A: - oral TENOFOVIR - nucleotide analogues that inhibit viral replication

Question 221

HEP D, epidemiology?

Answer 221

common in eastern Europe

Question 222

HEP D, transmission?

Answer 222

blood borne

Question 223

pathophysiology of HEP D?

Answer 223

Hepatitis D virus is an incomplete RNA particle enclosed in a shell of Hep B surface antigen (HBsAg) - Virus is UNABLE to REPLICATE ON ITS OWN but is activated by the presence of HBV - If acquired simultaneously with HBV (co-infection) causes increased severity of acute infection - Can either occur as co-infection or superinfection co infection - infection of HBV and HBD - has IGM for D and B superinfection - when a person who has chronic HBV gets HBV - raised AST or ALT

Question 224

treatment for HEP D?

Answer 224

SC PEGYLATED INTERFERON-ALPHA 2A:

Question 225

HEP C, epidemiology?

Answer 225

- Egypt - IV drug users - rare vertical transmission

Question 226

HEP C, transmission?

Answer 226

blood and blood products

Question 227

pathophysiology of HEP C?

Answer 227

RNA flavivirus - 7 genotypes; genotype 1a and 1b account for 70% cases in USA and 50% in Europe - Rapid mutations so envelope proteins change rapidly so its hard to develop a vaccine - Can result in chronic hepatitis and thus risk of HEPATOCELLULAR CARCINOMA

Question 228

clinical presentation of HEP C?

Answer 228

- 70% have chronic infection can lead to cirrhosis or liver failure and hepatocellular carcinoma

Question 229

investigations of HEP C?

Answer 229

- HCV antibody (4-6 weeks) | - HCV RNA

Question 230

treatment for HEP C?

Answer 230

SC PEGYLATED INTERFERON-ALPHA 2A/B + ORAL RIBAVIRIN triple therapy of direct acting anti-virals eg, LEDIPASVIR + SOFOSBUVIR + ORAL RIBAVIRIN expensive!

Question 231

cirrhosis?

Answer 231

it is an end stage of all progressive chronic liver diseases; which once fully developed is irreversible and may be associated clinically with symptoms and signs of liver failure and portal hypertension

Question 232

causes of cirrhosis?

Answer 232

- chronic alcohol abuse - NAFLD - hep B + D - hep c - hertitary haemochormatosis - Wilsons disease - alpha anti-tripsin deficiency

Question 233

pathophysiology of cirrhosis?

Answer 233

Chronic liver injury results in inflammation, matrix deposition, necrosis and angiogenesis all of which lead to FIBROSIS Liver injury causes necrosis and apoptosis, releasing cell contents and reactive oxygen species (ROS) - This activates hepatic stellate cells and tissue macrophages (Kupffer cells) cells release cytokines that attract neutrophils and macrophages to the liver which results in further inflammation and thus necrosis and eventual fibrosis

Question 234

types of cirrhosis regression?

Answer 234

Micronodular cirrhosis: - Regenerating nodules are usually < 3mm in size with uniform involvement of the liver - Often caused by alcohol or biliary tract disease • Macronodular cirrhosis: - There nodules are of varying size and normal acini (functioning unit of liver) may be seen within the larger nodules - Often caused by chronic viral hepatitis

Question 235

clinical presentation of cirrhosis?

Answer 235

- clubbing - palmar erythema - Dupuytren’s contracture - spider naiava - abdo pain - oedema - hepatomegaly

Question 236

investigations of cirrhosis?

Answer 236

- GOLD STANDARD - liver biopsy - LFTs (low serum albumin and high PPT) - raised AST and ALT - Alpha-fetoprotein is highly suggestive of HEPATOCELLULAR CARCINOMA - child-pugh SCORE -> looks for ascites, encephalopathy, high bilirubin, low albumin and long PTT

Question 237

complications of cirrhosis?

Answer 237

Coagulopathy; fall in clotting factors II,VII, IX & X • Encephalopathy - liver flap (asterixes - flapping tremor with wrist extended) & confusion/coma • Hypoalbuminaemia resulting in oedema • Portal hypertension: - Ascites - Oesophageal varices

Question 238

treatment of cirrhosis?

Answer 238

- half yearly USS screening - avoid NSAIDs - reduce salt intake - liver transplant

Question 239

portal hypertension, main causes?

Answer 239

PRE HEAPTIC portal vein thrombosis INTRA HEPATIC cirrhosis schistomaiasis sarcocodosis POST HEPATIC RHF IVC obstruction

Question 240

clinical presentations of portal hypertension?

Answer 240

Patients are often asymptomatic - Only clinical sign being splenomegaly which is unspecific Haematemesis and melaena from ruptured gastro-oesophageal varice or portal hypertensive gastropathy -

Question 241

initial management of VARICEAL HAEMORRHAGE:

Answer 241

Resuscitate until haemodynamically stable - If anaemic then BLOOD TRANSFUSION aiming to get Hb to 80g/L - Correct clotting abnormalities - administer VITAMIN K and PLATELET TRANSFUSION - Vasopressin - IV TERLIPRESSIN - to cause vasoconstriction, use IV SOMATOSTATIN if terlipressin is contraindicated e.g. in ischaemic heart disease - Prophylactic antibiotics to treat and prevent infection as well as reduce early rebleeding and mortality e.g. CEPHALOSPORIN - Variceal banding - where a band is put around varice using an endoscope, after a few days the banded varix degenerates and falls off leaving a scar - Ballon tamponade to reduce bleeding by placing pressure on varice if banding fails

Question 242

primary biliary cirrhosis? epidemiology?

Answer 242

- F>M - 40-50 yrs - immunological

Question 243

risk factors for primary biliary cirrhosis?

Answer 243

Positive family history - Many UTIs - Smoking - Past pregnancy - Other autoimmune disease - Use of nail polish/hair dye

Question 244

pathophysiology, primary biliary cirrhosis?

Answer 244

Interlobar bile ducts are damaged by CHRONIC AUTOIMMUNE GRANULOMATOUS INFLAMMATION resulting in cholestasis which may lead to fibrosis, cirrhosis and portal hypertension - Serum anti-mitochondrial antibodies (AMA) found in almost all patients - Likely than an environmental factor acts on genetically predisposed hosts to trigger disease

Question 245

clinical presentation of primary biliary cirrhosis?

Answer 245

- itchy (pruitus) early symptom - lethargy and fatigue - jaundice and hepatomegaly - xanthelasma - yellow fat deposit on eyelid

Question 246

investigation of primary biliary cirrhosis?

Answer 246

- raised alkaline phosphate - raised serum cholesterol - Igm and AMA postive - USS - liver biopsy

Question 247

treatment for primary biliary cirrhosis?

Answer 247

URSODEOXYCHOLIC ACID: COLESTYRAMINE works for itch but unpalatable • NALOXONE and NALTREXONE (opioid antagonists) shown to help

Question 248

alcoholic liver disease, aetiology?

Answer 248

ALCOHOL genetics immunological mechanisms

Question 249

pathophysiology for fatty alcoholic liver disease?

Answer 249

Metabolism of alcohol produces fat in the liver • This is minimal with small amounts of alcohol, but with larger amounts the cells become swollen with fat (steatosis) • There is no liver cell damage • The fat disappears on stopping alcohol • In some cases, collagen is laid down around the central hepatic veins and this can sometimes progress to cirrhosis without a preceding hepatitis • Alcohol directly affects stellate cells, transforming them into collagen- producing myofibroblast cells

Question 250

pathophysiology of alcoholic hepatitis liver disease?

Answer 250

infiltration by polymorphonuclear leucocytes and hepatocyte necrosis • Dense cytoplasmic inclusions called Mallory bodies are sometimes seen in hepatocytes and giant mitochondria are also a feature • If alcohol consumption continues, alcoholic hepatitis can progress to cirrhosis

Question 251

pathophysiology of alcoholic cirrhosis liver disease?

Answer 251

Classically of the MICRONODULAR TYPE but mixed pattern is also seen accompanying fatty change, and evidence of pre-existing alcoholic hepatitis may be present

Question 252

clinical presentation of alcoholic liver disease

Answer 252

FATTY no specific signs or symptoms - mainly nausea, diarrhoea and heptaomegaly ALCOHOLIC HEP can be mild jaundice and signs of chronic liver disease (ascites, bruising and clubbing) or severe with jaundice CIRRHOIS presents as well with few symptoms

Question 253

investigations of alcoholic liver disease?

Answer 253

FATTY - raised ALT and AST - gold standard USS or CT ALCOHOLIC HEP - leucocytosis - raised bilirubin, AST, ALT and PTT CIRRHOSIS - liver biopsy

Question 254

treatment for alcoholic liver disease

Answer 254

- stop alcohol - IV THIAMINE to prevent Wernicke-Korsakoff encephalopathy - reduce salt intake - healthy diet

Question 255

paracetamol poisoning

Answer 255

Large amounts of paracetamol are metabolised by oxidation because of saturation of the sulphate conjugation pathway (Phase II reaction) - Liver GLUTATHIONE stores become depleted so that the liver is unable to conjugate and activate NAPQI (TOXIC) - This results in hepatotoxicity as well as paracetamol-induced kidney injury

Question 256

clinical features of paracetamol poisoning?

Answer 256

- Metabolic acidosis - HYPOglycaemia (since overdose will inhibit glucose production (gluconeogenesis) ) - Prolonged prothrombin time - Raised creatinine

Question 257

treatment of paracetamol poisoning?

Answer 257

Gastric decontamination - ACTIVATED CHARCOAL - Give IV N-ACETYLCYSTEINE which acts by replenishing cellular glutathione stores (s/e rash)

Question 258

hereditary haemochromatosis?

Answer 258

- Inherited disorder of iron metabolism in which there is increased intestinal iron absorption leads to iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin

Question 259

epidemiology of hereditary haemochromatosis?

Answer 259

- Caucasians | - M>F

Question 260

aetiology of hereditary haemochromatosis?

Answer 260

HFE gene mutation on chromosome 6, this is an AUTOSOMAL RECESSIVE gene (i.e. sufferer must be homozygous) - MOST COMMON CAUSE • There are other gene mutations responsible and one is AUTOSOMAL DOMINANT - but not as common, but means sufferer can be heterozygous * High intake of iron and chelating agents (e.g. ascorbic acid) * Alcoholics may have iron overload

Question 261

pathophysiology of hereditary haemochromatosis?

Answer 261

The HFE gene protein interacts with the transferrin receptor 1, which is a mediator in intestinal iron absorption - Iron is taken up by the mucosal cells of the small intestine inappropriately, EXCEEDING the binding capacity of transferrin - Hepcidin, a protein synthesise in the liver, is central to the control of iron absorption; it is increased in iron deficiency states and decreased with iron overload - Hepatic expression of the hepcidin gene is decreased in HFE haemochromatosis thereby facilitating iron overload - Excess iron is then gradually taken up by the liver and other tissue over a long period - The iron content is particularly increased in the liver and pancreas but also in other organs e.g. heart, skin and endocrine glands - In established cases, the liver shows extensive iron deposition and fibrosis - Cirrhosis is a late feature

Question 262

clinical presentation of hereditary haemochromotosis?

Answer 262

- tiredness and joint pain - hypogonadism - slate grey appearance, signs of chronic liver disease and osteoporosis - later -> bronze skin pigment

Question 263

investigations of hereditary heamatochromosis?

Answer 263

- raised serum iron, ferritin - genetic tests - liver biopsy - MRI

Question 264

treatment for hereditary heamtochromosis?

Answer 264

- venesection - testosterone replacement - iron low diet - avoid food high in vit C

Question 265

Wilsons disease?

Answer 265

Rare inherited disorder of biliary copper excretion with too much copper in the liver and CNS (basal ganglia i.e. globus pallidus and putamen)

Question 266

epidemiology of Wilsons disease?

Answer 266

- More common in caucasians than in Indians and Asians | - autosomal recessive chr 13

Question 267

pathophysiology of Wilsons disease?

Answer 267

Dietary copper is normally absorbed from the stomach and upper small intestine - Copper is transported to the liver loosely bound to albumin - Once in the liver it is incorporated into a glycoprotein called CAERULOPLASMIN synthesised in the liver and secreted into the blood - The remaining copper is normally excreted in the bile and excreted in faeces - Wilson’s disease is a very rare inborn error of copper metabolism that results in copper deposition in various organs, including the liver, the basal ganglia of the brain and the cornea

Question 268

clinical presentation of Wilsons disease?

Answer 268

- children - hepatic problems - young adults - CNS problems - terror, dysphagia, dyskinesia - kaiser-fleischer ring - green/brown pigment in eye caused by copper

Question 269

Wilsons disease, investigations?

Answer 269

Serum copper and caeruloplasmin are usually reduced but can be normal - 24 hour urinary copper excretion is high - Liver biopsy shows increased hepatic copper, hepatitis and cirrhosis - but note high copper levels are also found in chronic cholestasis

Question 270

treatment for Wilsons disease?

Answer 270

Avoid foods that are high in copper e.g. liver, chocolate, nuts, mushrooms and shellfish - Lifelong chelating agent e.g. PENICILLAMINE used to chelate copper

Question 271

alpha 1 anti-tripsin deficiency? epidemiology

Answer 271

- Caucasians - family history chr 14 - autosomal recessive

Question 272

alpha anti-trypsin deficiency, pathophysiology?

Answer 272

Alpha-1-antitrypsin is produced in the liver and its main role is to inhibit the proteolytic enzyme - NEUTROPHIL ELASTASE - In the lung, alpha-1-antitrypsin protects against tissue damage from neutrophil elastase - a process that is also induced by smoking - Deficiency results in: • Emphysema • Liver cirrhosis • Hepatocellular carcinoma

Question 273

alpha antitrypsin deficiency, clinical presentation

Answer 273

- children present with liver disease | - adults present with respiratory problems

Question 274

investigations and treatment for alpha anti trypsin deficiency?

Answer 274

investigations Serum alpha-1-antitrypsin levels are LOW treatment there is non by stop smoking and manage liver and lungs

Question 275

hepatic encephalopathy

Answer 275

As the liver fails, nitrogenous waste e.g. ammonia builds up in the circulation and passes to the brain which can result in permanent brain damage as ammonia is neurotoxic to the brain since it halts the Krebs cycle resulting in IRREPARABLE CELL DAMAGE and neural cell DEATH Also as astrocytes try to clear ammonia (using a process involving the conversion of glutamate to glutamine), the excess glutamine causes an osmotic imbalance and a shift of fluid into these cells - hence cerebral oedema - resulting in damage

Question 276

ascites?

Answer 276

accumulation of free fluid within the peritoneal cavity

Question 277

epidemiology of ascites?

Answer 277

- post op | - high sodium diet

Question 278

aetiology of ascites?

Answer 278

- local inflammation - low protein - low flow due to clots

Question 279

clinical presentation of ascites?

Answer 279

- listened abdomen - mild abdo pain - respiratory distress

Question 280

investigations of ascites?

Answer 280

- diagnostic aspiration of 10-20ml using ascitic tap protein measurement of ascitic fluid from ascitic tap

Question 281

treatment for ascites?

Answer 281

- reduce sodium - diuretic - ORAL SPIROLACTONE - drain fluid - TIPS shunts

Question 282

peritonitis?

Answer 282

The inflammation of the peritoneum

Question 283

peritonitis, aetiology?

Answer 283

- bacterial | - chemical; bile, old clotted blood

Question 284

clinical presentation of peritonitis?

Answer 284

perforation = sudden onset which causes severe abdominal pain and shock/collapse poorly localised pain which moves to one pint and becomes localised patients feel better lying still

Question 285

investigations of peritonitis?

Answer 285

- blood tests raised WCC and CRP - HCG to exclude pregnancy - AXRY and CT scan

Question 286

treatment of peritonitis?

Answer 286

- antibiotics | - surgery

Question 287

types of oesophageal tutors?

Answer 287

Squamous cell carcinoma occurs in the middle third (40% of all oesophageal cancer) and in the upper third (15%) of the oesophagus • Adenocarcinomas occur in the lower third of the oesophagus and at the cardia and represent around 45% of tumours

Question 288

oesophagus squamous cell carcinoma, epidemiology and aetiology?

Answer 288

epidemiology - middle and upper 3rd - M>F causes - high levels of alcohol consumption - achalasia - smoking - obesity

Question 289

pesphagus adenocarcinoma epidemiology and aetiology?

Answer 289

``` epidemiology - lower 3rd - causes - barrets oesphagus - gORD - smoking - obesity ```

Question 290

clinical presentation of oesophageal cancer?

Answer 290

- no physical signs - progressive dysphagia (dysphasia to solids and liquids from the start = benign) - weigh loss - lymphadenopathy - anorexia - hoarseness and cough

Question 291

diagnosis of oesophageal cancer?

Answer 291

- gold standard; oesphagoscopy with biopsy - barium swallow - CT scans and PET to se metastases

Question 292

treatment of oesophageal cancer?

Answer 292

- surgical resection with combined chemotherapy and or radiotherapy

Question 293

benign oesophageal tumours, aetiology?

Answer 293

- barrets oesophagus - GORD - obesity

Question 294

pathophysiology of benign oesophageal tumours?

Answer 294

Leiomyomas are smooth muscle tumours arising from the oesophageal wall - They are intact, well encapsulated and are within the overlying mucosa - Slow growing

Question 295

clinical features of benign oesophageal tumours?

Answer 295

Usually asymptomatic, found incidentally on barium swallow - Dysphagia - Retrosternal pain - Food regurgitation - Recurrent chest infections

Question 296

investigations and treatment of benign oesophageal tumour?

Answer 296

Endoscopy - Barium swallow - Biopsy to rule out malignancy treatment - endoscopic removal or surgical removal

Question 297

gastric adenocarcinoma, epidemiology?

Answer 297

- M>F | - peak age 50-70

Question 298

aetiology of gastric adenocarcinoma?

Answer 298

- smoking - H, pylori - diet (high salt and nitrates) - loss of p53 - family history - pernicious anaemia

Question 299

pathophysiology of gastric adenocarcinoma?

Answer 299

Helicobacter pylori infection: • Normal gastric mucosa → H.pylori infection → ACUTE GASTRITIS → Chronic active gastritis → Atrophic gastritis → Intestinal metaplasia → DYSPLASIA → ADVANCED GASTRIC CANCER 2 types; Intestinal (type 1): - Well formed and differentiated glandular structures - distal stomach involved diffuse (type 2) Poorly cohesive undifferentiated cells - Tend to infiltrate the gastric wall - Can involve any part of the stomach, especially the cardia - Has a worse prognosis than intestinal

Question 300

clinical presentation of gastric adenocarcinoma?

Answer 300

- epigastric pain - nausea and anorexia - vomiting - dysphagia - anaemia - palpable lymph node

Question 301

gastric adenocarcinoma investigations?

Answer 301

- gastroscopy and biopsy's GOLD STANDARD - endoscopy - CT/MRI/PET

Question 302

treatment of gastric adenocarcinoma?

Answer 302

- nutritional support | - surgery and combined chemotherapy ECF (EPIRUBICIN + CISPLATIN + 5- FLUOROURACIL)

Question 303

small intestinal tumours, risk factors?

Answer 303

- coeliac disease | - crohns disease

Question 304

small intestinal tumour types?

Answer 304

Adenocarcinoma is the most common tumour of the small intestine, accepting for up to 50% of primary tumours Lymphomas (Non-Hodgkin's type) are most frequently found in the ileum and are less common than adenocarcinomas

Question 305

clinical presentation of small intestine tumours?

Answer 305

Pain, diarrhoea, anorexia, weight loss, anaemia | - May be a palpable mass

Question 306

small intestine tumour investigations and treatment?

Answer 306

- endoscopic biopsy GOLD STANDARD - CT scan treatment - surgery and radiotherapy

Question 307

colon polyps?

Answer 307

abnormal growth of tissue projecting from the colonic | mucosa

Question 308

types of inherited polyps?

Answer 308

Familial adenomatous polyposis (FAP): • Autosomal dominant condition arising from a mutation in the APC gene • Characterised by the presence of hundreds to thousands of colorectal and duodenal adenomas • Develop adenomas at 16 and cancer develops at 39 • Often given prophylactic colectomy and ileorectal anastamosis - Lynch syndrome (Hereditary Non-Polyposis Colon Cancer (HNPCC)): • Polyps are formed in the colon and may rapidly progress to colon cancer • Autosomal dominant condition caused by a mutation in one of the DNA mismatch repair genes, usually hMSH2 or hMSH1 • These genes are responsible for maintaining the stability of DNA during replication - this defect causes naturally occurring, highly repeated, short DNA sequences known as micro satellites that are shorter or longer than normal • This increases the risk of DNA damage in replication and thus colorectal carcinoma development • Thus instead of taking 10-15 years for polyps to develop into colorectal carcinoma it occurs more rapidly

Question 309

colorectal carcinoma, epidemiology?

Answer 309

Usually ADENOCARCINOMA - Majority occur in DISTAL COLON - Majority of presentations are in those over 60 yrs - M>F

Question 310

risk factors of colorectal carcinoma?

Answer 310

- low fibre diet - sugar - polyps - alcohol and smoking - obesity - UC - increasing age - genetic

Question 311

pathophysiology of colorectal cancer?

Answer 311

Normal epithelium → Adenoma → Colorectal adenocarcinoma Polypoid mass with ulceration - Spreads by direct infiltration through the bowel wall then spread to lymphatic and blood vessels and metastasis to LIVER and LUNG

Question 312

clinical presentation of colorectal cancer?

Answer 312

- RIGHT SIDED - asymptomatic - mass - weigh loss - low Hb LEFT SIDED - change in bowel habits - diarrhoea - constipation - blood in stools RECTAL - blood in stools

Question 313

investigations for colorectal cancer?

Answer 313

colonoscopy GOLD STANDARD - feacal occult blood - barium enema - CT colonoscopy - MRI

Question 314

treatment of colorectal cancer?

Answer 314

- surgery | - endoscopic stenting radiotherapy & chemo

Question 315

liver tumours, epidemiology?

Answer 315

Common in China | - More common in MALES than females

Question 316

risk factors of liver tumours?

Answer 316

Carriers of HBV and HCV (higher risk) have an extremely high risk of developing HCC - Associated with cirrhosis such as alcohol cirrhosis, non-alcoholic fatty liver disease and haemochromatosis

Question 317

pathophysiology of liver tumours?

Answer 317

Tumour is either single or occurs as multiple nodules throughout the liver - Consists of cells resembling hepatocytes - It can metastasise via the heaptic or portal veins to the lymph nodes, bones and lungs

Question 318

INVESTIGATION OF LIVER TUMOURS?

Answer 318

- liver biopsy GOLD STANDARD - CT - USS

Question 319

treatment of liver tumours?

Answer 319

- surgery | - liver transplant

Question 320

cholangiocarcinoma, epidemiology and risk factors?

Answer 320

Epidemiology: - Cancer of the biliary tree - Responsible for 10% of liver primaries • Risk Factors: - Associated with infestation with parasitic worms (flukes) e.g. Clonorchis sinensis - Biliary cysts - Inflammatory bowel disease e.g. UC and Crohn’s

Question 321

clinical presentation and treatment of cholangiocarcinoma?

Answer 321

clinical presentation - Fever - Abdominal pain +/- ascites - Malaise - Raised bilirubin - jaundice - Raised alkaline phosphate Treatment: - Surgical resection is rarely possible and patients die within 6 months - Liver transplant is contraindicated

Question 322

secondary liver tumour, clinical presentation

Answer 322

Variable - Weight loss - Malaise - Upper abdominal pain - Hepatomegaly with/without jaundice

Question 323

investigation and treatment of secondary liver your?

Answer 323

Diagnosis: - Ultrasound is primary investigation with CT or MRI to define metastases and look for a primary - Serum alkaline phosphatase is raised Treatment: - Depends on site of the primary and the burden of liver metastases - Removal of primary tumour and hepatic resection - Chemotherapy is used, particularly with breast cancer

Question 324

pancreatic andemocarcinoma, epidemiology?

Answer 324

- 99% is exocrine - M>F - >60 yrs

Question 325

risk factors for pancreatic adenocarcinoma?

Answer 325

- smoking - alcohol and coffee - aspirin - diabetes - family history

Question 326

pathophysiology, pancreatic adenocarcinoma?

Answer 326

- starts at ductal epithelium - metastasise early - 60% in head, 25% in body and 15% in tail

Question 327

clinical presentation of pancreatic adenocarcinoma?

Answer 327

``` Weight loss - Diabetes - Acute pancreatitis - Head of pancreas: • PAINLESS obstructive jaundice - pale stools and dark urine - Body and tail of pancreas: • Epigastric pain that radiates to the back and is relieved by sitting forward ```

Question 328

investigations of pancreatic adenocarcinoma?

Answer 328

- transabdominal US and CT to find pancreatic mass | - BIOPSY

Question 329

treatment for pancreatic adenocarcinoma?

Answer 329

- surgery | - palliative therapy

Question 330

bacterial abscess aetiology?

Answer 330

- unknown - elderly = biliary sepsis - trauma - bacteria -> e.coli most common

Question 331

bacterial abscess clinical presentation?

Answer 331

- fever - vomiting - weigh loss - RUQ pain

Question 332

investigations of bacterial abscess?

Answer 332

- blood culture - Alkaline phosphatase, ESR and CRP raised - CT and USS

Question 333

treatment of bacterial abscess?

Answer 333

- aspirate | - antibiotics - CO-AMOXICALV

Question 334

amoebic abscess investigations and treatment?

Answer 334

Cyst aspiration shows ‘anchovy sauce pus’ - DIAGNOSTIC treatment is METRONIDAZOLE for 10 days

Question 335

infective diarrhoea, aetiology?

Answer 335

VIRAL - children - rotavirus - adults - Nora virus and campylobacter BACTERIA - children - e.coli, salmonella and shingllla - antibiotic associated ( C antibiotics; CLINDAMYCLIN, CO-AMOXICLA, CEPHALOSPORINS) -> c.diff (treatment is METRONIDAZOLE AND ORAL VANCOMYCIN) PARASITE - giardia lamblia

Question 336

investigations of diarrhoea?

Answer 336

BLOODS Low MCV and or Fe deficiency e.g. coeliac disease or colon cancer High MCV if alcohol abuse or decreased B12 absorption e.g. coeliac disease or Crohn’s raised WCC if parasites Raised ESR and CRP indicate infection, Crohn’s, UC or cancer - Stools: • Stool culture if suspect bacteria, parasites or C.diff toxin - Sigmoidoscopy with biopsy

Question 337

treatment of diarrhoea?

Answer 337

Anti-emetics - treat vomiting e.g. METOCLOPRAMIDE - Antibiotics - Anti-motility agents e.g LOPERAMIDE HYDROCHLORIDE