GI&L Flashcards

Question

peptic ulcer disease?

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

• 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

Answer 6

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

Answer 7

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

Answer 8

- <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

Answer 9

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

Answer 10

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

Answer 11

- 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)

Answer 12

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

Answer 13

- 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)

Answer 14

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

Answer 15

- 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

Answer 16

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

Answer 17

difficulties passing food and liquid down oesophagus into stomach

Answer 18

- F=M | - long history of dysphagia

Answer 19

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

Answer 20

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

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

- F>M | - 30-50 yrs peak

Answer 25

- vinyl chloride | - silica dust

Answer 26

- 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

Answer 27

- initially no symptoms | - dysphagia

Answer 28

- barium swallow - gold standard - CXR - manometry

Answer 29

Gastritis is inflammation that is associated with mucosal injury

Answer 30

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

Answer 31

- 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

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

- coeliac - tropical sprue - crohns - parasite infection

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

``` 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) ```

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

- jewish people more prone?

Answer 53

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

Answer 54

- family history - NSAIDs - chronic stress

Answer 55

- 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

Answer 56

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

Answer 57

- 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

Answer 58

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

Answer 59

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)

Answer 60

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

Answer 61

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

Answer 62

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

Answer 63

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

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

- 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

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

- GOLD standard - CT - Xray - FBC

Answer 74

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

Answer 75

- less common 25% | - africa -> volvulus

Answer 76

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

Answer 77

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

Answer 78

- DRE - FBC - Xray - CT

Answer 79

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

Answer 80

Clinical picture mimicking obstruction but with no mechanical cause

Answer 81

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

Answer 82

Patients present with rapid and progressive abdominal distension and pain

Answer 83

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

Answer 84

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

Answer 85

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

Answer 86

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

Answer 87

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

Answer 88

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

Answer 89

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

Answer 90

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

Answer 91

- 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

Answer 92

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

Answer 93

- 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

Answer 94

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

Answer 95

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

Answer 96

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

Answer 97

- 45-65 yrs | - M=F

Answer 98

- constipation - diarrhoea - anal intercoruse - pregnancy

Answer 99

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

Answer 100

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

Answer 101

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

Answer 102

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

Answer 103

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

Answer 104

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

Answer 105

- MRI | - endoanal US

Answer 106

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

Answer 107

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

Answer 108

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

Answer 109

- perianal inspection

Answer 110

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

Answer 111

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

Answer 112

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)

Answer 113

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

Answer 114

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

Answer 115

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

Answer 116

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

Answer 117

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

Answer 118

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

Answer 119

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

Answer 120

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

Answer 121

``` 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

Answer 122

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

Answer 123

- 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

Answer 124

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

Answer 125

- >50 yrs | - sigmoid colon most frequent

Answer 126

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

Answer 127

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

Answer 128

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

Answer 129

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

Answer 130

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

Answer 131

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

Answer 132

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

Answer 133

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

Answer 134

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

Answer 135

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)

Answer 136

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

Answer 137

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

Answer 138

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

Answer 139

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

Answer 140

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

Answer 141

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

Answer 142

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) ```

Answer 143

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

Answer 144

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

Answer 145

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

Answer 146

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

Answer 147

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

Answer 148

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

Answer 149

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

Answer 150

- M>F - alcohol use - CKD - hereditary

Answer 151

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

Answer 152

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

Answer 153

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

Answer 154

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

Answer 155

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

Answer 156

- malaise - nausea - anorexia - maybe jaundice

Answer 157

- ascites - oedema - haematemesis - bruising - hepatomegaly

Answer 158

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

Answer 159

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

Answer 160

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

Answer 161

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

Answer 162

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

Answer 163

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

Answer 164

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

Answer 165

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

Answer 166

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

Answer 167

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

Answer 168

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)

Answer 169

- 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

Answer 170

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

Answer 171

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

Answer 172

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

Answer 173

- IV antibiotics | - ERCP - biliary drainage

Answer 174

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

Answer 175

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

Answer 176

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

Answer 177

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

Answer 178

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

Answer 179

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

Answer 180

Spread via the faeco-oral route

Answer 181

Shellfish - Travellers - Food handlers

Answer 182

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

Answer 183

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

Answer 184

``` 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)

Answer 185

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

Answer 186

- older men - common in UK - self limiting

Answer 187

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

Answer 188

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

Answer 189

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

Answer 190

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

Answer 191

- 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

Answer 192

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

Answer 193

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

Answer 194

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

Answer 195

common in eastern Europe

Answer 196

blood borne

Answer 197

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

Answer 198

SC PEGYLATED INTERFERON-ALPHA 2A:

Answer 199

- Egypt - IV drug users - rare vertical transmission

Answer 200

blood and blood products

Answer 201

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

Answer 202

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

Answer 203

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

Answer 204

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

Answer 205

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

Answer 206

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

Answer 207

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

Answer 208

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

Answer 209

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

Answer 210

- 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

Answer 211

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

Answer 212

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

Answer 213

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

Answer 214

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

Answer 215

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

Answer 216

- F>M - 40-50 yrs - immunological

Answer 217

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

Answer 218

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

Answer 219

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

Answer 220

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

Answer 221

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

Answer 222

ALCOHOL genetics immunological mechanisms

Answer 223

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

Answer 224

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

Answer 225

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

Answer 226

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

Answer 227

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

Answer 228

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

Answer 229

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

Answer 230

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

Answer 231

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

Answer 232

- 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

Answer 233

- Caucasians | - M>F

Answer 234

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

Answer 235

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

Answer 236

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

Answer 237

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

Answer 238

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

Answer 239

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

Answer 240

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

Answer 241

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

Answer 242

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

Answer 243

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

Answer 244

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

Answer 245

- Caucasians - family history chr 14 - autosomal recessive

Answer 246

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

Answer 247

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

Answer 248

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

Answer 249

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

Answer 250

accumulation of free fluid within the peritoneal cavity

Answer 251

- post op | - high sodium diet

Answer 252

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

Answer 253

- listened abdomen - mild abdo pain - respiratory distress

Answer 254

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

Answer 255

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

Answer 256

The inflammation of the peritoneum

Answer 257

- bacterial | - chemical; bile, old clotted blood

Answer 258

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

Answer 259

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

Answer 260

- antibiotics | - surgery

Answer 261

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

Answer 262

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

Answer 263

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

Answer 264

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

Answer 265

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

Answer 266

- surgical resection with combined chemotherapy and or radiotherapy

Answer 267

- barrets oesophagus - GORD - obesity

Answer 268

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

Answer 269

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

Answer 270

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

Answer 271

- M>F | - peak age 50-70

Answer 272

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

Answer 273

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

Answer 274

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

Answer 275

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

Answer 276

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

Answer 277

- coeliac disease | - crohns disease

Answer 278

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

Answer 279

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

Answer 280

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

Answer 281

abnormal growth of tissue projecting from the colonic | mucosa

Answer 282

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

Answer 283

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

Answer 284

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

Answer 285

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

Answer 286

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

Answer 287

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

Answer 288

- surgery | - endoscopic stenting radiotherapy & chemo

Answer 289

Common in China | - More common in MALES than females

Answer 290

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

Answer 291

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

Answer 292

- liver biopsy GOLD STANDARD - CT - USS

Answer 293

- surgery | - liver transplant

Answer 294

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

Answer 295

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

Answer 296

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

Answer 297

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

Answer 298

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

Answer 299

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

Answer 300

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

Answer 301

``` 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 ```

Answer 302

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

Answer 303

- surgery | - palliative therapy

Answer 304

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

Answer 305

- fever - vomiting - weigh loss - RUQ pain

Answer 306

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

Answer 307

- aspirate | - antibiotics - CO-AMOXICALV

Answer 308

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

Answer 309

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

Answer 310

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

Answer 311

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

GI&L Flashcards

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