GI & Liver Flashcards

Question

Describe the epidemiology of peptic ulcers?

Answer 1

* More common in elderly | * More common in developing countries – due to H. Pylori

Answer 2

- Duodenal ulcers most common (90%): o Relieved by eating o 2-3 times more common than gastric ulcers - Gastric ulcers – (50-80%): o Worsened by eating, also associated with NSAIDs/aspirin - Ulcers are a risk factor for gastric cancer due to chronic inflammation – gastric carcinoma and lymphoma

Answer 3

• Usually gastric mucosa is protected by a layer of mucin that is produced by gastric cells • Increased acidity overwhelms the protective mucin resulting in mucosal damage and ulceration • Ulcers result in gastritis (inflammation of gastric cells)

Answer 4

- H.Pylori– most common - NSAIDS e.g. aspirin - Mucosal Ischaemia - Increased acid - Bile reflux - Alcohol

Answer 5

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

Answer 6

o NSAIDS e.g. aspirin o Mucus secretion stimulated by prostaglandins o COX-1 needed for prostaglandin synthesis o NSAIDs inhibit COX-1 o No COX-1 = mucous isn’t secreted o Reduced mucosal defense --> mucosal damage

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

* Acquisition usually asymptomatic (but can cause nausea, vomiting and fever * Burning epigastric pain * Bloating * Vomiting * Haematemesis * Dyspepsia * Nausea * Flatulence

Answer 11

* Gastric ulcer pain often occurs when patient is hungry, eating and classically occurs at night, weight loss * Duodenal ulcer pain often occurs several hours after meals, weight gain, relieved by eating * Anorexia

Answer 12

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

Answer 13

- Endoscopy with biopsy o Biopsy urease test e.g. CLO test o Histology - Stool antigen test – for H. Pylori - Urea breath test - Blood test for IgG antibodies (can be positive for a year after treatment)

Answer 14

* Lifestyle management – reduce smoking, reduce stress, drink less * Stop NSAIDs • Antibiotics for H. Pylori - CAP o Clarithromycin o Amoxicillin o PPI e.g. omeprazole * Proton pump inhibitors e.g. lansoprazole and omeprazole * H2 antagonists e.g. cimetidine to reduce acid release * Surgery for complications

Answer 15

* Duodenal ulcers can grow deeper until it hits an artery (most commonly the gastroduodenal artery) --> massive haemorrhage --> shock * Perforation – requires immediate surgical consult * Obstruction * Peritonitis as acid enters peritoneum * Acute pancreatitis if ulcer reaches pancreas

Answer 16

- Gastritis is inflammation of the stomach lining that is associated with mucosal injury. - Gastropathy indicates epithelial cell damage and regeneration WITHOUT inflammation - commonest cause is mucosal damage associated with Aspirin/ NSAIDs

Answer 17

* H. Pylori infection – most common * Autoimmune gastritis – the cause of pernicious anaemia associated with antibodies to gastric parietal cells and IF * Viruses e.g. CMV and HSV * Duodenogastric reflux – whereby bile salts enter stomach and damage mucin protection resulting in gastritis * Crohn’s disease * Mucosal ischaemia * Increased acid * Aspirin and NSAIDs e.g. naproxen * Alcohol

Answer 18

- Affects the fundus and body of the stomach --> atrophic gastritis mistakenly destroys a special type of cell (parietal cells) in the stomach --> loss of parietal cells = intrinsic factor deficiency --> in pernicious anaemia (low RBCs due to low B12).

Answer 19

They inhibit prostaglandins (which stimulate mucus production) via the inhibition of cyclo-oxygenase resulting in less mucus production and therefore gastritis

Answer 20

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

Answer 21

* Epigastric pain * Nausea or recurrent upset stomach * Vomiting * Indigestion

Answer 22

* Loss of appetite * Abdominal bloating * Haematemesis

Answer 23

* Peptic ulcer disease * GORD * Non-ulcer dyspepsia * Gastric lymphoma * Gastric carcinoma

Answer 24

* Endoscopy * Biopsy and histology * H. Pylori urea breath test * H. Pylori stool antigen test

Answer 25

• CAP o Clarithromycin o Amoxicillin o PPI e.g. omeprazole * H2 antagonists e.g. ranitidine or cimetidine – reduce acid release/ Antacids * Prevention – give PPIs alongside NSAIDs – this also prevents bleeding from acute stress ulcers and gastritis often seen with ill patients – especially burn patients

Answer 26

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

Answer 27

* Coeliac disease * Tropical Sprue * Crohn’s * Parasitic infection - Before malabsorption is diagnosed, insufficient intake must be ruled out to ensure its actually malabsorption

Answer 28

* Insufficient intake- consider psychosocial cause * Defective intraluminal digestion - due to pancreatic insufficiency (pancreatitis) or defective bile secretion * Insufficient absorptive area - due to inflammation e.g. Crohn's * Lack of digestive enzymes - Disaccharidase deficiency (lactose intolerance) - Bacterial overgrowth – brush border damage • Defective epithelial transport o Abetalipoproteinemia o Primary bile acid malabsorption – mutations in bile acid transporter protein • Lymphatic obstruction - Lymphoma - TB

Answer 29

- Cystic fibrosis results in the blockage of the pancreatic duct due to excess mucus meaning enzymes fail to be released. - Whereas pancreatitis causes damage to most of the glandular pancreas meaning less or no enzymes are released

Answer 30

o Villi and microvilli produce massive SA to absorb nutrients o Gluten sensitive enteropathy (Coeliac Disease) - Villous trophy and crypt hyperplasia o Crohn’s – typically in terminal ileum - Inflammatory disease of bowel o Extensive surface parasitasion - E.g. Giardia Lamblia • Parasite eats food • Metronidazole for a week o Small intestinal resection or bypass - Procedure for morbid obesity - Crohn’s disease – coble stone mucosa --> can’t absorb anything - Infarcted small bowel

Answer 31

* Weight loss * Steatorrhea * Diarrhoea

Answer 32

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

Answer 33

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

Answer 34

- Ingestion of gluten stimulates immune system to attack small intestine --> (due to genetic susceptibility) = inflammation of mucosa of the upper small bowel - T-cell mediated autoimmune disease of the small bowel in which PROLAMIN (alcohol-soluble proteins in wheat, barley, rye and oats) intolerance causes VILLOUS ATROPHY + MALABSORPTION - Prolamin is a COMPONENT of GLUTEN PROTEIN - SUSPECT in ALL with DIARRHOEA, WEIGHT LOSS or ANAEMIA (especially if iron or B12 deficient)

Answer 35

• Gluten found in o Wheat o Barley o Rye

Answer 36

* Other autoimmune diseases – T1DM, Thyroid diseases, Sjogren’s * IgA deficiency * Breast feeding * Age of introduction into diet * Rotavirus infection in infancy increases risk

Answer 37

- 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 (40-60% risk in untreated patients leading to fracture risk) - Dermatitis hepetiformis - red raised patches, often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks

Answer 38

* Most common age for presentation is 4th to 6th decade * For every paediatric case diagnosed there are 9 adult cases * Affects males and females equally * Affects 1 in 100 individuals in European-derived populations – majority are undiagnosed * Presentation is at any age but typically presents infancy (after weaning on to gluten-containing foods) and in adults aged 40-49 • Increasing prevalence o Change in endoscopic techniques o Antibody screening o Increased awareness of spectrum of diversity in presentation of CD • Associated with other autoimmune conditions e.g. T1DM and thyrotoxicosis

Answer 39

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

Answer 40

* A-gliadin is the toxic portion of gluten and is resistant to proteases in the small intestinal lumen * Gliadin binds to secretory IgA in mucosal membrane * Gliadin-IgA is transcytosed to the lamina propria via HLA DQ2 and DQ8 * Gliadin binds to tissue transglutaminase (ttG) and is deaminated which increases its immunogenicity * Deaminated gliadin is taken up by macrophages and expressed on MHC II complex * T helper cells release inflammatory cytokines and stimulate B cells * This causes villous atrophy, crypt hyperplasia and intraepithelial lymphocyte infiltration --> reduced SA to absorb nutrients --> B12, folate and iron cannot be absorbed --> pernicious anaemia

Answer 41

- Should maintain gluten for at least 6 weeks before testing to get true results: 1) FBC: • Low Hb • Low B12 • Low ferritin 2) Duodenal biopsy is the gold standard for diagnosis: • See villous atrophy, crypt hyperplasia and increased intraepithelial white cell count - seen histologically • All reverse on gluten free diet 3) Serum antibody testing: * Indications include; persistent diarrhoea, folate or iron deficiency and a family history of coeliac disease or associated autoimmune disease * Most sensitive test (95% sensitive unless patient is IgA deficient)

Answer 42

* Lifelong gluten free diet i.e. no prolamins - use serum antibody testing for monitoring * Eliminate wheat, barley and rye - results in days/weeks * Dietitian review --> Correction of vitamin and mineral deficiencies e.g. B12, folate, iron, calcium and vitamin D * DEXA scan to monitor osteoporotic risk * Inform 10% risk in 1st degree relatives

Answer 43

- A few patients do not improve on a strict diet and are said to have non- responsive coeliac disease - Anaemia - Secondary lactose intolerance = T-cell lymphoma - IgA antibodies elevated - Vitamin deficiency - Osteoporosis

Answer 44

* Severe malabsorption (of two or more substances) accompanied by diarrhoea and malnutrition * Occurs in residents or visitors to tropical areas where the diseases in endemic – most of Asia, some Caribbean islands, Puerto Rico and parts of SA * Epidemics can break out in villages, affecting thousands at the same time

Answer 45

* Partial villous atrophy with malabsorption | * Onset is acute and occurs either a few days or many years after being in the tropics

Answer 46

- Cause is UNKNOWN but is likely to be infective because the disease occurs in epidemics and patients improve on antibiotics

Answer 47

* Diarrhoea | * Anorexia

Answer 48

* Weight loss * Severe malabsorption * Abdominal distension

Answer 49

* Bloods – anaemia due to malabsorption of B12, folate and iron (nutritional deficiency) * Jejunal biopsy – abnormal showing partial villous atrophy

Answer 50

* Leave region | * Folic acid daily and tetracycline antibiotic for up to 6 months

Answer 51

• Two major forms, these are both chronic autoimmune conditions: 1) Ulcerative colitis (UC) - which affects ONLY the COLON 2) Crohn’s disease (CD) - can affect ANY PART of the GI tract (mouth-anus) • IBD occurs when the mucosal immune system exerts an inappropriate response to luminal antigens, such as bacteria, which may enter the mucosa via a leaky epithelium

Answer 52

A 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) • Unlike in UC, there is unaffected bowel BETWEEN areas of active disease - these are SKIP LESIONS

Answer 53

- Highest incidence and prevalence in Northern Europe, UK and North America - F>M - Presents mostly at 20-40 - Smoking increases risk by 3-4 x - 1 in 5 patients with CD have a first-degree relative with the disease - Presentation mostly at 20-40 yrs - Lower incidence than UC per year

Answer 54

* Originates in mucosa and works through layers of bowel (mucosa, submucosa, muscularis propria + fat) * Affects any part of gut from mouth to anus – commonly terminal ileum and proximal colon • Macroscopically o Skip lesions o Cobblestone appearance due to ulcers and fissures in mucosa o Thickened and narrow • Microscopically o Transmural – affects all layers of bowels o Non-caseating granulomas (aggregations of epithelioid histiocytes) o Goblet cells

Answer 55

* Family history - mutation on NOD2 gene of chromosome 16 * Smoking * Female * Chronic stress * NSAIDs

Answer 56

* Blood in stool * Malabsorption * Mouth ulcers * Extra-intestinal features o Erythema nodosum o Anal fissures o Episcleritis ``` CHRISTMAS • Cobblestones • High temperature • Reduced lumen • Intestinal fistulae • Skip lesions • Transmural • Malabsorption • Abdominal pain • Submucosal fibrosis ```

Answer 57

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

Answer 58

• Alternative causes of diarrhoea should be excluded o Salmonella spp. o Giardia intestinalis o Rotavirus • Chronic Diarrhoea

Answer 59

* Tenderness of RIGHT ILIAC FOSSA * Colonoscopy – diagnostic * Biopsy * Barium enema * Stool sample – rules out infectious diseases • FBC o Raised ESR/CRP white cell count o Often low Hb due to anaemia • Faecal calprotectin – indicates IBD but not specific

Answer 60

* Oral corticosteroids e.g. budesonide and prednisolone * IV hydrocortisone in severe flare ups • Add anti-TNF antibodies e.g. Infliximab if no improvement o Has predisposition for TB – night sweats, haemoptysis (coughing up blood) and weight loss * Consider adding azathioprine or methotrexate to remain in remission if there are frequent exacerbations * Surgery (80%) – doesn’t cure disease

Answer 61

o Malabsorption: - Disease extent - Surgical resections o Obstruction: - Abscesses - Acute swelling - Chronic fibrosis o Perforation – acute abdomen o Fistula formation o Anal - Skin tags - Fissure - Fistula o Neoplasia – colorectal cancer - Systemic – amyloidosis (rare) - Resection at worst areas but can result in short bowel syndrome (leading to diarrhoea (since little colon to absorb fluids) and malabsorption lifelong)

Answer 62

* Relapsing and remitting inflammatory disorder of the COLONIC MUCOSA UP TO the ILEOCAECAL VALVE * Ulcers form along lumen of intestine * It may affect just the rectum - proctitis (50%) * It may affect the rectum and left colon - left-sided colitis (30%) * It may affect the entire colon (entire large bowel) UP TO the ILEOCAECAL VALVE - pancolitis/extensive colitis

Answer 63

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

Answer 64

* Remains in mucosa (does not go through full wall of bowel) * Only affects colon • Macroscopically o Continuous inflammation (no skip lesions) o Ulcers o Pseudo-polyps ``` • Microscopically o Mucosal inflammation o No granulomata o Depleted goblet cells o Increased crypt abscesses ``` • Paneth cells are involved in innate immunity and suggest an inflammatory condition when found in the descending colon.

Answer 65

* Family history * NSAIDs – associated with onset of IBD and flares of disease • Chronic stress and depression triggers flares • Smoking relieves UC

Answer 66

* LLQ abdominal pain * Fever * Diarrhoea with blood and mucus * Cramps

Answer 67

* Rectal tenesmus – incontinence, urgency, bleeding * Tender distended abdomen * Clubbing * Erythema nodusum ``` ULCERATIONS • Ulcers • Large intestine • Carcinoma – risk of • Extra-intestinal manifestations – uveitis, erythema nodosum, sclerosing cholangitis • Remnants of older ulcers - pseudo polyps • Abscesses in crypts • Toxic megacolon – risk of • Inflamed, red, granular mucosa • Originates at rectum • Neutrophil invasion • Stool is bloody and has mucous ```

Answer 68

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

Answer 69

* Colonoscopy - diagnostic * Biopsy – crypt abscesses * Barium enema • Bloods o FBC – raised ESR and CRP, low Hb o Test for pANCA – negative in Crohn’s o Iron deficiency anaemia * Faecal calprotectin * Stool sample – rule out infectious causes * CT/MRI * Abdominal X-ray

Answer 70

• Anti-inflammatory e.g. sulfasalazine – 5-aminosalicylic acid (5-ASA) absorbed in small intestine o Or mesalamine * Immunosuppressors – corticosteroids, azathioprine * Anti-TNF drugs - infliximab * Colectomy with ileo-anal anastamosis indicated in patients with severe UC not responding to treatment * Surgery – indicated for severe colitis that fails to respond to treatment

Answer 71

• Liver o Fatty change o Chronic pericholangitis o Sclerosing cholangitis • Colon o Blood loss o Toxic dilation o Colorectal cancer • Skin o Erythema nodosum o Pyoderma gangrenosum • Joints o Ankylosing spondylitis o Arthritis • Eyes o Iritis o Uveitis o Episcleritis

Answer 72

PRESENTATION AGE - Crohn's disease: 15-35 - Ulcerative colitis : Throughout lifespan SITE OF APPEARANCE - Crohn's disease: Mouth to anus - Ulcerative colitis: Colonic, rectal mucosa TYPE OF LESION - Crohn's disease: Transmural inflammation - Ulcerative colitis: Superficial ulcers MICROSCOPIC FINDINGS - Crohn's disease - Non-caseeating granulomas - Ulcerative colitis - crypt ulcers, abcesses CHARACTERISTIC PATTERN - Crohn's disease - skip lesions - Ulcerative colitis - continuous lesions CHARACTERISTIC APPEARANCE - Crohn's disease -Cobblestone pattern, creeping fat, string sign on barium x-rays - Ulcerative colitis - Loss of haustra on imaging (lead pipe appearance), friable mucosa CLINICAL PRESENTATION - Crohn's disease - right lower quadrant pain fistulas, phelgom - Ulcerative colitis - left lower quadrant pain, gross bleeding DISEASE MECHANISM - Crohn's disease - transmural inflammation along GI tract - Ulcerative colitis - destruction of colonic mucosa, submucosa TREATMENT - Crohn's disease - corticosteroids, azathioprine, metronidazol, infliximab, adalimumab - Ulcerative colitis - mesalamine, infliximab, surgical resection

Answer 73

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

Answer 74

* Age of onset <40 * F>M * Common in Western world – affects 1 in 5 * Symptoms are exacerbated by stress, food, gastroenteritis or menstruation

Answer 75

* Dysfunction in the brain-gut axis results in disorder of intestinal motility and/or enhances visceral sensitivity * Recurrent abdominal pain with NO inflammation * 3 types 1) BS-C – with constipation 2) IBS-D – with diarrhoea 3) IBS-M – with constipation and diarrhoea

Answer 76

* Psychosocial – stress, depression, anxiety * Psychological stress and trauma * GI infection - gastroenteritis * Sexual, physical or verbal abuse * Eating disorders

Answer 77

* Female * Stress * Gastroenteritis * Previous severe and long diarrhoea * High hypo-chondrial anxiety and neurotic score at time of initial illness

Answer 78

* Abdominal pain relieved by defecating or passing of wind * Bloating * Alternating bowel habits * Constipation * Diarrhoea

Answer 79

* Mucus in stools * Change in stool frequency * Change in stool consistency * Sensation of incomplete emptying * Urgency * Worsening symptoms after food

Answer 80

* Coeliac disease | * Lactose intolerance – especially in IBS-D, bile acid malabsorption, IBD or colorectal cancer

Answer 81

• Since there is nothing physical to be found, diagnosis made by ruling out the differentials • Bloods o FBC – for anaemia o ESR and CRP – biomarkers for inflammation (IBD) o Coeliac serology for EMA and tTG – if either positive --> high chance of coeliac disease * Faecal calprotectin – raised in IBD * Colonoscopy – to rule out IBD or colorectal cancer

Answer 82

• Lifestyle modification – fluids, avoid caffeinated drinks, alcohol and fizzy drinks, fibre (in wind and bloating NOT diarrhoea and bloating) • Treat symptoms o Pain/bloating – Buscopan o Constipation – laxative e.g. Senna o Diarrhoea – anti-motility e.g. Loperamide • If none of the above work - amitriptyline (tricyclic antidepressant)

Answer 83

If patient reports any of ABC: - A - Abdominal pain or discomfort - B - Bloating - C - Change in bowel habit

Answer 84

* Unexplained weight loss * PR bleed/blood in stool * Family history of bowel or ovarian cancer * Change in bowel habit and aged over 50 * Nocturnal symptoms * Rectal or abdominal mass * Anaemia * Raised inflammatory markers - IBD * If any found then refer to secondary care for further investigations

Answer 85

- IBS - Normal investigation results - IBD - Abnormal investigation results - IBS - Persistent/fluctuating symptoms - IBD - Persistent/fluctuating symptoms - IBS - Wouldn't really get fever - IBD - More likely to get fever - IBS - No symptoms outside GI tract - IBD - Symptoms outside GI tract - IBS - No blood in stool - IBD - Blood in stools - IBS - No Melena - IBD - Meleana - black poo, indicative of blood higher up in tract - Both = food triggers - IBS - No weight loss - IBD - Weight loss - IBS - No mouth ulcers - IBD - Mouth ulcers - IBS - Constipation more common - IBD - Constipation but less common than in IBS - IBS - Exacerbated by stress - IBD - Can also be exacerbated by stress - IBS - Bloating - IBD - Bloating much less common than in IBS - IBS can also mimic ovarian cancer in middle aged (50s) women.

Answer 86

* > 400species (around 100 trillion micro-organisms) * Predominantly anaerobes * The GI microbiome weighs more than your brains

Answer 87

* Gastric acid kills most swallowed pathogens * Bacteria are protective against luminal infection HOWEVER can also be pathogenic if in the wrong part of the peritoneum * The microbiome is protective against “against invaders” but is vulnerable to systemic antibiotics • Less gastric acid or broad-spectrum antibiotics --> increased risk of intra-luminal infection

Answer 88

* Abnormal passage of loose or liquid stool more than 3 times daily * Acute – lasts less than 2 weeks * Chronic – lasts more than 2 weeks

Answer 89

1) Sudden onset of watery bowel frequency associated with crampy abdominal pains and a fever = INFECTIVE CAUSE (proximal small bowel) 2) Bowel frequency with loose, mucoid, blood-stained stools = INFLAMMATORY CAUSE (colon) 3) Passage of pale, offensive stools that float often accompanied by a loss of appetite and weight loss = STEATORRHEA

Answer 90

1) Viral o Most cases caused by viruses e.g. rota/norovirus 2) Bacterial ``` o Campylobacter o Shigella o Salmonella o C.perfringens o S.aureus o B.cereus o E.coli o C.diff ``` o Parasites (e.g. giardia, cryptosporidium) 3) Children – rotavirus 4) Adults – norovirus, campylobacter ``` 5) Antibiotics – these can give rises to antibiotic induced C. Diff diarrhoea o Rule of C’s: - Clindamycin - Ciprofloxacin (quinolones) - Co-amoxiclav (penicillins) - Cephalosporins (particularly 2nd and 3rd generation) ``` 6) Infective o Intraluminal infection o Systemic infections e.g. sepsis, malaria 7) Non-infective ``` o Cancer o Chemical e.g. poisoning, sweeteners, side effects o IBS/malabsorption o Endocrine e.g. T4 o Radiation ```

Answer 91

• Immunosuppressed o Particularly to: - Cryptosporidium - Mycobacteria - Microsporidia - CMV - HSV

Answer 92

• HISTORY IS KEY o Onset/duration - Acute – viral/bacterial - Chronic – parasites and non-infectious o Family History o Characteristics of stool 1) Floating – fat content, malabsorption/coeliac 2) Blood or mucus – inflammatory, invasive infection, cancer 3) Watery small bowel infection o Food/drink - Dodgy takeaways – food poisoning - Meat/BBQs – campylobacter - Poultry – salmonella o Travel - No cholera in UK - Foreign travel? - Very common and self-limiting o Immunocompromised e.g. HIV, diabetes, chemo, transplant, steroids – crypto, CMV etc. o Unwell contacts – more likely to be infective o Fresh water/swimming – cryptosporidian, giardia o Animals - Reptiles – salmonella - Puppies – campylobacter o Medications – recent antibiotics - C diff. or side effects o Any neuro signs - Clostridium botunilum (descending weakness) - C. jejuni --> GBS 1-3 weeks after diarrhoeal episode (ascending weakness)

Answer 93

• Stool tests ``` o Stool culture o Faecal calprotectin o Faecal occult blood o Microscopy o Ova, cysts and parasites o Toxin detection ``` • Blood tests o FBC o Inflammatory markers (FBC/CRP) o Blood culture

Answer 94

* 2nd leading cause of death in children globally – after pneumonia * Highest prevalence in S. Asia and Africa

Answer 95

* Enterotoxigenic E.coli (30-70%) * Campylobacter (5-20%) * Shigella (5-20%) * Non-typhoidal Salmonella (5%) * V.parahaemolyticus (shellfish) * Viral (10-20%) ``` • Cholera o Vibrio cholerae o Contaminated food/water o Cholera toxin o Profuse watery “rice water” diarrhoea --> up to 20L a day o Vomiting o Rapid dehydration o Doxycycline and fluids ``` ``` • Parasites o Protozoal (5-10% more chronic) - Cyrpto - Giardia - Entamoeba ``` o Worms - Schistosomiasis - Strongyloides

Answer 96

* Foreign travel * PPI or H2 antagonist use * Crowded area * Poor hygiene

Answer 97

* Recurrent diarrhoea * Vomiting and nausea * Fever * Fatigue * Muscle pain * Steatorrhea

Answer 98

* Appendicitis * IBD * UTI * Coeliac Disease * Volvulus

Answer 99

``` • Diagnosis - 3 or more unformed stools per day plus one of the following: o Abdominal pain o Cramps o Nausea o Vomiting o Dysentery ``` • Blood – suggests bacteria o E. Coli and Shigella ALL cause bloody stools * Stool sample * If chronic, sigmoidoscopy and bloods

Answer 100

* Rehydration * Antibiotics – metronidazole or oral vancomycin * Barrier nursing – side room, gloves and apron • Fluids + electrolytes monitoring and replacement o E.g. oral rehydration sachets o IV replacement * Antiemetics – treat vomiting e.g. metoclopramide * Antimotility agents – NOT IN INFLAMMATORY DIARRHOEA

Answer 101

* Dehydration * Electrolyte imbalance * Renal failure * Immunocompromise * Severe abdominal pain

Answer 102

* Over 50 * Chronic diarrhoea * Weight loss * Blood in stool * FH cancer

Answer 103

* 3rd most common cancer worldwide * Usually adenocarcinoma • Majority occur in distal colon o More distal the cancer, the more visible blood and mucus will be * Majority of presentations >60 * M>F

Answer 104

* Increasing Age * Family history • Genetic predisposition o Familial adenomatous polyposis - Apc bound to GSK - Beta catenin binds apc complex in high levels of apc - In mutations, apc protein misfolded so can’t bind to beta catenin - Beta catenin able to move into nucleus --> endothelial proliferation --> adenoma o Hereditary non-polyposis colorectal cancer (HNPCC) - Normally two DNA protein repair genes - Some individuals born with just one which leaves them susceptible * Colorectal * Ulcerative

Answer 105

• Progression o Normal epithelium (prevention) --> adenoma (endoscopic resection) --> colorectal adenocarcinoma (surgical resection)--> metastatic colorectal adenocarcinoma (chemotherapy palliative care) * Nearly all are adenocarcinoma (+RECTAL) * Polypoid mass with ulceration * Spreads by direct infiltration through the bowel wall then spread to lymphatic and blood vessels and metastasise to liver and lung

Answer 106

* R0 – tumour completely excised locally * R1 – microscopic involvement of margin by tumour * R2 – macroscopic involvement of margin by tumour

Answer 107

* A – 95% 5 year survival, limited to muscularis mucosae (mucosa) * B - 75% 5 year survival, traverses bowel lining and into submucosa (not lymph) * C - 35% 5 year survival, involvement of regional lymph nodes * D - 25% 5 year survival – metastatic

Answer 108

``` • Right-sided carcinoma o Usually asymptomatic until they present with iron deficiency anaemia due to bleeding o May present with a mass o Weight loss o Abdominal pain ``` ``` • Left sided and sigmoid carcinoma o Change in bowel habit with blood and mucus in stools o Diarrhoea o Alternation constipation and diarrhoea o Thin/altered stool ``` • Rectal carcinoma o Rectal bleeding and mucus o When cancer grows, it will have thinner stools and tenesmus (cramping rectal pain) ``` • Emergency o Obstruction - Absolute constipation - Colicky abdominal pain - Abdominal distension - Vomiting (faeculent) ```

Answer 109

• Anorectal pathology o Haemorrhoids o Anal fissue o Anal prolapse • Colonic pathology o Diverticular disease o Irritable bowel disease (IBD) o Ischaemic colitis • Small intestine and stomach pathology o Massive upper GI bleed – haematochezia o Meckel’s diverticulum

Answer 110

• Colonoscopy – gold standard • Digital Rectal exam o 38% of colorectal cancers can be detected by DRE • Double contrast barium enema

Answer 111

* Surgery * Endoscopic stenting * Radiotherapy * Chemo

Answer 112

* 6th most common cancer worldwide * Squamous cell carcinoma occurs in middle third (40%) and upper third (15%) of the oesophagus • Adenocarcinomas occur in lower third of oesophagus and cardia of stomach and account for majority of oesophageal tumours (45%) * Presents mostly between 60-70 * More common in males

Answer 113

``` o High levels of alcohol consumption o Achalasia – disorder where oesophagus has reduced/no ability to do peristalsis and transport food down o Tobacco use o Obesity – since this increases reflux o Smoking o Low fruit and veg consumption ```

Answer 114

``` o GORD o Smoking o Obesity o Achalasia o Barrett’s oesophagus ```

Answer 115

* Oesophagus lined by squamous epithelium * Stomach lined by columnar glandular epithelium * Oesophageal epithelium undergoes metaplasia (change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type) to stomach epithelium * SCC in upper 2/3rds * Adenocarcinoma in lower 1/3rd

Answer 116

• Pain – due to impaction of food or infiltration of cancer into adjacent structures • Dysphagia – difficulty swallowing solids at first then fluids o If there is dysphagia to solids AND liquids from start this indicates benign disease

Answer 117

* Majority have no physical signs – detectable when advanced * Lymphadenopathy * Anorexia * Weight loss

Answer 118

* Oesophagoscopy with biopsy * Barium swallow – to see strictures * CT/MRI/PET for tumour staging

Answer 119

* Account for 1% of oesophageal tumours * Leiomyomas most common * Papillomas * Fibrovascular polyps * Haemangiomas * Lipomas

Answer 120

* Usually asymptomatic – usually found incidentally on barium swallowing * Dysphagia * Retrosternal pain * Food regurgitations * Recurrent chest infections

Answer 121

* Endoscopy * Barium swallowing * Biopsy

Answer 122

* Endoscopic removal | * Surgical of larger tumours

Answer 123

* 1% of all malignancies * Adenocarcinoma most common * Lymphomas (NHL) most frequently found in the ileum

Answer 124

* Family history * Coeliac Disease * Crohn’s Disease

Answer 125

* Abdominal pain * Diarrhoea * Weight loss

Answer 126

* Anorexia * Anaemia * Palpable mass

Answer 127

* Ultrasound * Endoscopic biopsy * CT/MRI scan

Answer 128

* Surgical resection | * Radiotherapy

Answer 129

* Falling incidence * Mainly affects Eastern Europe and Asia * Affects more males than females

Answer 130

o Unknown o Smoking o H/ Pylori increases risk at population level -->Increases risk of peptic ulcers --> gastric cancer • Affects more males than females

Answer 131

o Epigastric pain – constant and severe o Vomiting, nausea, anorexia o Weight loss o Dysphagia – if tumour is in fundus o Anaemia from occult blood loss o Liver metastasis --> jaundice

Answer 132

o Gastroscopy with biopsy o Endoscopic ultrasound o CT/MRI o PET scan

Answer 133

o Nutritional support | o Surgery and combination chemo

Answer 134

• Early o Can be classified as early gastric cancer even when it reaches lymph nodes o 90% 5 year survival rates • Late o 60% - 5 year survival rate

Answer 135

``` • CT/MRI liver • Biopsy • Raised AFP • Bloods o Clotting abnormalities o Deranged LFTs ```

Answer 136

* Surgical resection * Radiofrequency ablation * TACE, chemotherapy

Answer 137

* 99% of pancreatic cancer occurs in exocrine component of pancreas * UK incidence rising * More common in males * Typically presents >60 * Majority are adenocarcinoma and are of ductal origin

Answer 138

* Smoking * Excessive alcohol or coffee intake * Excessive use of aspirin * Diabetes * Chronic pancreatitis * Family history * Genetic mutations – presence of PRSS-1 mutation

Answer 139

* Originates in ductal epithelium and evolves from pre-malignant lesions to full-invasive cancer * 60% arise in pancreatic head * 25% arise in body * 15% arise in tail

Answer 140

* Anorexia * Weight loss * Acute pancreatitis • Body and tail of pancreas o Epigastric pain that radiates to back o Relieved by sitting forward • Head of pancreas o Painless jaundice o Weight loss

Answer 141

* Abdominal ultrasound or CT | * Biopsy

Answer 142

* Surgery | * Palliative therapy

Answer 143

Bacterial, Amoebic, and Hyatid

Answer 144

Faecal flora e.g.E.Coli, Klebsiella spp etc.

Answer 145

* Entamoeba histolytica * RUQ pain, fever, “PUO” * Seen on ultrasound or CT * Treatment = Antibiotics and drainage

Answer 146

- Echinococcus granulosa (Dog tapeworm) - Insidious RUQ pain, eosinophilia - Rupture --> anaphylactic shock - Albendazole and PAIR (drainage)

Answer 147

Arrest/blockage of onward propulsion of intestinal contents

Answer 148

Small bowel - 75% Large bowel - 25% o One of the common causes of hospital admission o True incidence not known - 5-20% emergency general surgical admission - US 12-16% surgical admission o Early prompt diagnosis and treatment has excellent outcomes o Mortality - Untreated strangulated obstruction – 100% - Strangulated small bowel treated >36 hours = 25% - Strangulated small bowel treated <36 hours =8% - Mechanical large bowel obstruction 20% - If perforated 40% - Non-mechanical (pseudo) obstruction – 15-30%

Answer 149

* Gut – mouth to anus * Intestinal obstruction – blockage to the lumen of gut o Commonly refers to blockage of intra-abdominal part of intestine

Answer 150

A twist/rotation of segment of bowel

Answer 151

o Abdominal structures sticking to one other - Bowel loops or omentum - Other solid organs - Abdominal wall

Answer 152

Part of the intestine slides into an adjacent part of the intestines (telescoping)--> one hollow structure into its distal hollow structure.

Answer 153

* According to site – large bowel/small bowel/gastric * Extent of luminal obstruction – partial/complete ``` • According to mechanism o Mechanical/true (intraluminal/extraluminal) o Paralytic (pseudo obstruction) - Failure of peristalsis - No mechanical obstruction ``` ``` • According to pathology o Simple o Closed loop o Strangulation o Intussusception ```

Answer 154

* Drugs, post op, trauma, intra-a sepsis * Unclear mechanism - Neural – increased SNS discharge - Toxins - Metabolic distension • Signs - Usually causes painless distension

Answer 155

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

Answer 156

o Tumours - Carcinoma - Lymphoma o Diaphragm disease - NSAIDs cause repeated ulceration then fibrosis o Gallstone ileus – rare form of small bowel obstruction caused by an impaction of a gallstone within the lumen o Meconium ileus – in neonates, content of bowel is sticky --> blockage

Answer 157

o Tumours o Crohn’s – inflammation, fibrosis and contraction o Diverticulitis – outpouchings in the sigmoid - Usually occurs in sigmoid colon - Diverticular pouchings form 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 can get inflamed or burst resulting in acute peritonitis and death o Hirschsprung’s – ganglion cells - Developmental abnormality where neonates born without complete innervation of colon to rectum - Dilated upper bowel - Ganglionic segment at sigmoid responsible for contraction of bowel - Aganglionic segments can’t contract --> bowel obstruction

Answer 158

o Tumours – disseminated malignancy of peritoneum - Ovarian cancer can spread into peritoneum o Adhesions – fibrosis after surgery - Post-surgery - Fibrous connections between loops of small bowel --> bowel becomes kinked - Corrected surgically o Volvulus – sigmoid colon has a “floppy” mesentery - Sigmoid colon can twist - Causes obstruction of the sigmoid - If there is ischaemia and infarction, sigmoid colon is resected

Answer 159

* Anorexia * Nausea ``` • Vomiting o Nature - Forceful - Regurgitation o Content - Bilious - Faeculant – can occur in small bowel, brewing for a long time - Coffee ground/altered blood ``` • Abdominal pain – mechanical o SOCRATES • Distension/swelling o More proximal less distension o Smaller the loop, lesser the swelling initially o Swelling – hernia --> obstruction • Altered bowel habits o Constipation – not moving bowels, can pass wind o Obstipation – can’t pass faeces or wind

Answer 160

* Tinkling bowel sounds | * Tympanic percussion

Answer 161

• 60-75% of intestinal obstruction

Answer 162

1) Adhesions o Usually secondary to previous abdominal surgery - Elective/emergency o Increased incidence - Pelvic surgery - Gynae surgery - Colorectal surgery o Can occur - As early as 3-4 weeks - Usually few years 2) Hernia – abnormal protrusion of an organ or tissue out of the body cavity in which it normally lies o Untreated can result in strangulation 3) Malignancy 4) Crohn’s

Answer 163

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

Answer 164

• Pain – initially colicky (starts and stops then diffuse) o Pain is higher in abdomen than in LBO * Vomiting following pain – occurs earlier in SBO compared to LBO * Nausea * Anorexia

Answer 165

* Obstipation - constipation with no passage of wind * Increased bowel sounds * Tympanic percussion * Tenderness – suggests strangulation * Less distension as compared to LBO (since more distal the obstruction, the greater the distension)

Answer 166

* Abdominal X-ray – shows central gas shadow that completely cross the lumen and no gas in large bowel * Abdominal CT * FBC

Answer 167

* Aggressive fluid resuscitation * Bowel decompression * Analgesia and anti-emetic * Antibiotics * Surgery

Answer 168

• Less common - ~ 25% of all intestinal obstruction • Acute presentation – on average 5 days of symptoms o Large bowel has a larger lumen as well as circular and longitudinal muscles --> the ability of large bowel to distend is much greater --> symptoms present slower and later than in SBO

Answer 169

* Colorectal malignancy – most common | * Volvulus (twist/rotation of segment of bowel)

Answer 170

* Colon proximal to obstruction dilates * Increased colonic pressure and decreased mesenteric blood flow --> mucosal oedema (transudation of fluid and electrolytes from lumen) * This can compromise the arterial blood supply and also cause mucosal ulceration --> full thickness necrosis and perforation • Colonic volvulus o Axis rotation based off mesentery and a 360˚ twist --> closed loop obstruction o Fluid and electrolytes shift into closed loops --> increased pressure and tension in the loop causing impaired colonic blood flow o Leads to ischaemia, necrosis and perforation of loop of bowel if untreated

Answer 171

* Abdominal pain – more constant than in SBO | * Vomiting – more faecal like

Answer 172

* Abdominal distension * Palpable mass – hernia, distended bowel loop or caecum * Constipation * Fullness/bloating

Answer 173

• Abdominal X-ray – peripheral gas shadows proximal to the blockage • DRE o Empty rectum o Hard stools o Blood * FBC – low Hb (sign of chronic occult blood loss) * CT/MRI

Answer 174

* Aggressive fluid resuscitation * Bowel decompression * Analgesia and anti-emetic * Antibiotics * Surgery

Answer 175

Protrusion of organ or tissue out of the body cavity it normally lies in.

Answer 176

1) Reducible hernia – can be pushed back into abdominal cavity with manual manoeuvring 2) Irreducible – cannot be pushed back in o Obstructed – intestine is obstructed within hernia due to pressure from edges of hernia – but blood flow is maintained o Incarcerated – contents of hernial sac are stuck inside by adhesions e.g. adhesions between the intestines and hernial sac 3) Strangulated – blood supply of the sac is cut off resulting in ischaemia o ± gangrene/perforation of hernial contents

Answer 177

• Muscle weakness o Age o Trauma ``` • Body strain o Constipation o Heavy lifting o Pregnancy o Chronic cough ```

Answer 178

Protrusion of abdominal cavity contents through inguinal canal

Answer 179

* Commonest type of hernia * More common in males * Two types – direct and indirect * Account for ~70% of all abdominal hernias * Most common in men over 40

Answer 180

* Male * Chronic cough * Constipation * Heavy weight lifting * Ascites

Answer 181

• The inguinal canal is a: o Short passage that extends medially and inferiorly through inferior part of abdominal wall o Extends from deep inguinal ring to superficial ring o Acts as a pathway by which structures can pass from abdominal wall to external genitalia o It is a potential weakness in abdominal wall and therefore common site of herniation

Answer 182

• Direct – less common (20%) o Protrudes directly into the inguinal canal o Medial to inferior epigastric vessels o Rarely strangulates • Indirect – more common (80%) o Protrudes through the deep inguinal ring o Lateral to inferior epigastric vessels o Can strangulate

Answer 183

• Usually asymptomatic – if painful then indicates strangulation

Answer 184

* Bulging – associated with coughing or straining (bowel movements, heavy lifting) * Appearance of lump

Answer 185

* Femoral hernia * Epididymitis * Testicular torsion * Groin abscess * Aneurysms * Hydrocele (the accumulation of serous fluid in a body sac). * Undescended testes

Answer 186

• Look for lump

Answer 187

* Medically – use of truss to contain and prevent further progression of hernia * Surgery

Answer 188

Bowel comes through the femoral canal below inguinal ligament

Answer 189

* Less common than inguinal hernia * More common in females * Occur in middle age and elderly

Answer 190

* Bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin * Likely to be irreducible and to strangulate due to the rigidity of the canal’s borders • The neck of the hernia is felt inferior and lateral to the pubic tubercle o Inguinal hernias are superior and medial to this point

Answer 191

* Inguinal hernia * Lipoma * Femoral aneurysm * Psoas abscess * Saphena varix – dilation of saphenous vein at junction of femoral vein in groin

Answer 192

* Surgical repair * Herniotomy – ligation and excision of sac/ the operation of cutting through a band of tissue that constricts a strangulated hernia.

Answer 193

Part of the stomach herniates through the oesophageal hiatus of diaphragm

Answer 194

• 30% of patients >50

Answer 195

• Obesity

Answer 196

• Sliding: o Oesophageal-gastric junction slides through the hiatus and lies above the diaphragm o No symptoms other than reflux symptoms • Rolling/Para-oesophageal: o Uncommon – gastric fundus rolls up through hiatus alongside the oesophagus o Therefore, the gastro-oesophageal junction remains below the level of the diaphragm o Treated via surgery

Answer 197

• Symptomatic GORD

Answer 198

* Barium swallow – confirms diagnosis | * Upper GI endoscopy

Answer 199

* Lose weight * Treat reflux symptoms * Surgery – to prevent strangulation

Answer 200

Ischemic colitis occurs when blood flow to part of the large intestine (colon) is temporarily reduced, usually due to constriction of the blood vessels supplying the colon or lower flow of blood through the vessels due to low pressures.

Answer 201

* Most commonly affects elderly | * Related to underlying atherosclerosis and vessel occlusion

Answer 202

* Occlusion of a branch of the superior mesenteric artery or inferior mesenteric artery * Results in a watershed area of the colon – most commonly at the splenic flexure

Answer 203

* Atherosclerosis * Thrombosis * Emboli * Decreased CO and arrhythmias * Vasculitis

Answer 204

* Contraceptive pill * Vasculitis * Thrombophilia

Answer 205

• LLQ abdominal pain

Answer 206

• Bloody diarrhoea

Answer 207

• Other causes of acute colitis e.g. IBD

Answer 208

``` • CT/MRI angiography • Stool analysis • Ultrasound and abdominal CT •Colonoscopy and biopsy – gold standard - Done after attack- Biopsy shows epithelial cell apoptosis ```

Answer 209

* Symptomatic management * Fluid replacement * Antibiotics – to reduce infection risks due to translocation of bacteria across possible dying gut wall * Surgery – for gangrene, perforation or stricture

Answer 210

- Acute mesenteric ischemia (AMI) is a syndrome caused by inadequate blood flow through the mesenteric vessels, resulting in Ischemia and eventual gangrene of the bowel wall. - Although relatively rare, it is a potentially life-threatening condition. - Broadly, AMI may be classified as either arterial or venous.

Answer 211

* >50 | * Almost always involves small bowel

Answer 212

* Superior mesenteric artery thrombosis – most common * Superior mesenteric artery embolism (e.g. due to AF) * Mesenteric vein thrombosis – common in younger patients with hypercoagulable states * Non-occlusive diseases

Answer 213

• Triad of o Acute severe abdominal pain o No abdominal signs o Rapid hypovolaemia resulting in shock – pale skin, weak rapid pulse, reduce urine output, confusion

Answer 214

* Laparotomy - diagnostic | * Bloods – shows metabolic acidosis and high lactate

Answer 215

* Surgery to remove dead bowel * Fluid resuscitation * Antibiotics – IV gentamicin and IV metronidazole * IV heparin to reduce clotting

Answer 216

* Inflammation of the appendix * Should be considered for all right sided pain if appendix has not already been removed. * Located at McBurney’s point which lies 2/3 of the way from umbilicus to the anterior superior iliac spine (ASIS)

Answer 217

* Most common surgical emergency * More common in males * Occurs at any age – highest incidence 10-20 years

Answer 218

* Occurs when the lumen of the appendix becomes obstructed * Intestinal lumen (including appendix) is always producing mucus and fluids to prevent pathogens from entering the blood stream and keep the tissue moist * When the appendix is obstructed, fluid and mucus build up increasing the pressure in the appendix causing it to expand and press on the afferent visceral nerve fibres nearby --> abdominal pain * Bacteria is now trapped and able to multiply resulting in invasion of gut organisms into the appendix wall * This leads to oedema, ischaemia, necrosis, perforation and inflammation

Answer 219

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

Answer 220

* Acute pain in umbilicus/Right iliac fossa – may originate in umbilical region then progress to RIF * Nausea * Vomiting * Fever

Answer 221

* Tender mass in RIF * Guarding * Rebound tenderness with palpation * Pyrexia

Answer 222

* Acute terminal ileitis due to Crohn’s * Ectopic pregnancy * UTI * Diverticulitis * Perforated ulcer * Food poisoning

Answer 223

• CT abdomen • Bloods o FBC – raised WBC count o Elevated CRP and ESR * Ultrasound – especially in women and children * Pregnancy test * Urinalysis

Answer 224

* Laparoscopic appendectomy | * Drainage of appendix abscesses

Answer 225

* If the appendix ruptures, infected and faecal matter will enter the peritoneum resulting in life threatening peritonitis with rebound tenderness * Appendix abscesses – can be on appendix or subphrenic (under diaphragm)

Answer 226

Generalised inflammation of the peritoneum (abdominal cavity)

Answer 227

Tensing of muscles to prevent movement of peritoneum

Answer 228

• Parietal o Covers the abdominal wall o Somatic innervation o Sensation is well localised • Visceral o On organs e.g. stomach, liver and colon o Autonomic innervation o Sensation is not well localised

Answer 229

• Foregut - Lower oseophagus to D2 (liver, spleen & gallbladder) - Site of autonomic pain - Epigastric • Midgut - D2 to 2/3 across transverse colon (majority of abdomen) - Site of autonomic pain - Periumbilical • Hindgut - Transverse colon to upper rectum - Site of autonomic pain - Hypogastric

Answer 230

* Approximately 370, 000 admissions annually in UK * Mortality of 15% * Resource intensive

Answer 231

• Can result from irritation of the peritoneum o Perforation of the appendix o Spontaneous bacterial peritonitis

Answer 232

• A – Appendicitis – umbilicus to RIF pain • E – Ectopic pregnancy – low abdominal pain, sudden onset, tachycardia, low BP • I – Infection with TB o Bacterial – most common - Gram-negative e.g. E. Coli and Klebsiella - Gram-positive staphylococcus e.g. S. Aureus * O – Obstruction – colicky pain, history of abdominal surgery * U – Ulcer – epigastric pain radiating to shoulder * Peritoneal dialysis

Answer 233

* Inflamed organ * Air – ulcers, stabbings * Pus * Faeces * Luminal contents – not faeces until it reaches colon * Blood – usually spleen

Answer 234

* Gastritis – epigastric pain * Cholecystitis – right hypochondrium, mid-clavicular line * Pancreatitis – midway between epigastric and umbilicus * Appendicitis – right iliac fossa * Diverticulitis – left iliac fossa

Answer 235

• Appendicitis

Answer 236

* Dull pain that becomes sharp | * Systemic symptoms and generally unwell

Answer 237

* Pain relieved by resting hands on abdomen – stops movement of peritoneum and therefore pain * Guarding/rebound tenderness * Absence of bowel sounds * Rigid abdomen * Pain worse on coughing or moving * Patient wants to lie still * Sepsis/septic shock – hypotension, tachycardia, oliguria, fever

Answer 238

• Bowel obstruction

Answer 239

* CT Scan * Clinical examination – rigid and guarding, laying still * Abdominal X-Ray – dilated bowel, flat fluid level, gas under diaphragm * Bloods – FBCs, U&Es, LFTs, clotting factors * Ascitic tap – high neutrophil count

Answer 240

* Broad spectrum antibiotics - metronidazole * Fluid resuscitation – IV fluids and electrolytes * Urinary catheter ``` • Surgery o Laparotomy i.e. big cut o Laparoscopy i.e. key-hole surgery o Treat problem - Patch hole - Remove organ/cause o Wash-out infection ```

Answer 241

• Sepsis – peritoneum is thin, has a large SA and is well drained by lymphatics o Suspect sepsis if BP is low

Answer 242

- SUDDEN inflammation and haemorrhaging of pancreas due to its own digestive enzymes (autodigestion) - Usually reversible

Answer 243

• Alcohol induced o Increases zymogen secretion from acinar cells while decreasing fluid and bicarbonate in the ducts --> thick and viscous pancreatic juice --> obstructs the pancreatic duct o Blocked duct causes pancreatic juices to become backed up which--> increases pressure and may distend the ducts o Zymogen granules may fuse with lysosomes which brings trypsinogen into contact with lysosomal enzymes converting it to trypsin --> digestive enzyme cascade activation and autodigestion of pancreas (acute pancreatitis) o Alcohol also stimulates cytokine release --> immune response --> neutrophils release superoxides and proteases • Gallstones o Become lodged in sphincter of Oddi which blocks release of pancreatic juices o Similar to alcohol pathology

Answer 244

I GET SMASHED * Idiopathic * Gall stones * Ethanol (alcohol) * Trauma – knife wound injury * Steroids * Mumps/malignancy * Autoimmune e.g. SLE * Scorpion stings * Hyperlipidaemia and hypercalcaemia * Endoscopic Retrograde Cholangiopancreatography * Drugs – azathioprine, metronidazole, tetracycline, furosemide

Answer 245

* Epigastric pain radiating to the back – relieved by sitting forwards * Nausea and vomiting

Answer 246

* Cullen’s sign – bruising around periumbilical region * Grey Turner’s sign – bruising on flanks * Tachycardia * Abdominal guarding and tenderness * Distension

Answer 247

• LFTs – inflammation of pancreas causes release of enzymes o Raised serum amylase o Raised serum lipase - Lipase to amylase >2 suggests alcoholic o Raised ALT and AST - Elevated ALT >150 suggests gallstones * CT abdomen – evidence inflammation, necrosis and pseudocyst * Abdominal X-ray – shows no psoas shadow (raised retroperitoneal fluid)

Answer 248

* NG tube * IV fluid and maintain electrolyte balance * Pain relief * May need bowel rest * Treat complications

Answer 249

* Acute Respiratory Distress Syndrome – leading cause of death * Sepsis * Pancreatic pseudocyst * Hypovolaemic shock from ruptured vessels * DIC

Answer 250

• Persistent inflammation due to structure changes such as fibrosis, atrophy and calcification - Generally irreversible

Answer 251

* With each bout of acute pancreatitis there is the potential for ductal dilatation and damage to pancreatic tissue * Stellate cells lay down fibrotic tissue which causes narrowing of ducts and acinar cell atrophy * In conditions like alcoholic acute pancreatitis, calcium deposits of various sizes can accumulate on plugs that form the ducts * Healthy tissue replaced by misshapen ducts, fibrosis and calcium deposits = chronic pancreatitis

Answer 252

* Repeated bouts of acute pancreatitis * Alcohol abuse * Cystic Fibrosis – main cause in children * Tumours * Pancreatic trauma – knife wounds

Answer 253

* Epigastric pain that radiates to back – may be linked to eating meals * Nausea * Vomiting

Answer 254

• Malabsorption due to endocrine dysfunction o Weight loss o Steatorrhea o Vitamin deficiency • Exocrine dysfunction o Diabetes Mellitus

Answer 255

``` • CT abdomen • Abdominal ultrasound • Abdominal X-ray – shows calcifications • ERCP/MRCP = x-ray + endoscope • Bloods o May be low lipase and amylase as there may not be enough healthy tissue to make the enzymes o Faeceal elastase ```

Answer 256

* Lifestyle modification – less alcohol, healthier diet, more exercise etc. * Pain control * Replace digestive enzymes and nutritional supplements * Insulin for diabetes

Answer 257

* The term used for pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the GB * The pain of stone-induced ductular obstruction is of sudden onset, severe but constant and has a crescendo characteristic * Pain is temporary and stops when gallstone dislodges

Answer 258

* May be present at any age but unusual <30 * Increasing prevalence with age * More common in females * More common in Scandinavians, S. Americans and Native North Americans * Less common in Asian and African groups * Most form in the GB * Present in 10-20% of population

Answer 259

o Cholesterol help in solution by detergent action of bile salts and phospholipids --> forms micelles and vesicles o Only form in bile which has an excess of cholesterol o The formation of cholesterol crystals and gallstones in lithogenic bile is promoted by factors that favour nucleation such as mucus and calcium o Gallstone formation further promoted by reduced GB motility and stasis

Answer 260

• Pigment gallstones o Consist of bilirubin polymers and calcium bilirubinate o Seen in patients with chronic haemolysis (e.g. hereditary spherocytosis and sickle cell disease) in which bilirubin production is increased and cirrhosis o Pigment stones may also form in bile ducts after surgery

Answer 261

* Majority of gallstones are asymptomatic * Once gallstones become symptomatic, there is a strong trend towards recurrent complications * Biliary or gallstone colic – sudden, severe but constant epigastric pain (may have a RUQ component and may radiate over right shoulder and scapular region) o Pain usually increases for ~15 mins, stays constant for a few hours then decreases once the stone has dislodged o Starts several hours after a meal o May be worse at night • N+V and sweating

Answer 262

* History – recurrent symptoms * Abdominal ultrasound * LFTs

Answer 263

• Ursodeoxycholic acid – decreases cholesterol • Gallbladder stones: o Laparoscopic cholecystectomy o Bile acid dissolution therapy (<1/3 success) ``` • Bile duct stones: o ERCP with sphincterotomy and: - Removal (basket or balloon) - Crushing (mechanical, laser) - Stent placement ``` • Surgery (large stones)

Answer 264

Inflammation of the gallbladder

Answer 265

* Large fatty meals stimulate CCK which signals bile release from GB * When the GB has a gallstone in it, the squeezing of the GB can get it lodged in the cystic duct * Bile stasis becomes a chemical irritant stimulates mucosa in wall to release mucus and inflammatory enzymes --> inflammation, distension and pressure build up * Bacteria can start to grow e.g. E. coli and invade into gallbladder wall --> peritonitis

Answer 266

• Gallstone impaction into the cystic duct or GB neck

Answer 267

* RUQ pain * Fever * Nausea and vomiting

Answer 268

* Murphy’s sign – tenderness that is worse on inspiration | * Muscle guarding

Answer 269

* Ultrasound of abdomen * FBC – high WBC count (leucocytosis) * LFTs – to exclude liver/bile duct pathology

Answer 270

* Laparoscopic cholecystectomy | * Analgesia and fluids if needed

Answer 271

• Peritonitis

Answer 272

Bacterial infection of the biliary tract as a result of infection.

Answer 273

* Fair = Northern European and Hispanic * Female * Fat - obese * Fertile = pregnancy, under 40

Answer 274

* Normally, bacteria can’t go up CBD as bile and pancreatic juices travel down and flush bacteria out * Obstruction of common bile duct --> stasis of bile --> invasion of bacteria from duodenum * High pressure on the CBD (due to the obstruction) can cause spaces between the cells do widen which allows the bacteria and the bile access to the blood stream --> bacteraemia and jaundice * Can be obstructed by stone, cancer, stricture, parasite (ascaris). - Also, infection can be introduced through intervention e.g. ERCP

Answer 275

• Infection of the biliary tree e.g. E. coli, Klebsiella, enterococcus (group D strep) o Most often secondary to common bile duct obstruction by gallstones – choledocholithiasis * Benign biliary strictures – often following biliary surgery, malignancy or associated chronic pancreatitis * Primary sclerosing cholangitis

Answer 276

• Charcot’s triad 1) Jaundice - Dark urine - Pale stools 2) RUQ pain 3) Fever

Answer 277

• Reynold’s Pentad – bacteraemia --> septic shock --> leaky vessels --> hypotension --> less blood to organs e.g. brain --> confusion ``` o Jaundice o RUQ pain o Fever o Shock – hypotension and tachycardia o Confusion ``` • Rigors

Answer 278

* Biliary colic: RUQ pain only | * Cholecystitis: RUQ pain and maybe fever

Answer 279

• Ultrasound abdomen • FBC o Raised WBCs o Raised ESR and CRP o Raised serum bilirubin (very high if bile duct obstruction) and serum alkaline phosphatase * ERCP * MRCP to locate stone * LFTs * CT

Answer 280

* IV antibiotics e.g. co-amoxiclav * Fluids * ERCP (endoscopic retrograde cholangiopancreatography) to image/stent/remove stone * Shockwave lithotripsy * If this fails --> laparoscopic/open cholecystectomy

Answer 281

• Glucose and fat metabolism • Detoxification and excretion o Bilirubin o Ammonia oDrugs/hormones/pollutants • Protein synthesis o Albumin o Clotting factors – Vitamin K • Defence against infection (Reticuloendothelial system)

Answer 282

• Acute: o Recovery o Liver failure • Chronic: o Cirrhosis – disorganisation and fibrous scarring o Liver failure - Varices – due to portal hypertension - Hepatoma

Answer 283

o Viral A, B, EBV o Alcohol o Drug o Vascular – ischaemia o Obstruction – usually bile o Congestion – from heart failure

Answer 284

o Alcohol o Viral B, C ``` o Autoimmune o Metabolic (excess iron - haemochromatosis, copper – Wilson’s) ```

Answer 285

``` o Malaise o Nausea o Anorexia o Jaundice o Confusion (rarer) o Bleeding (rarer) o Liver pain (rarer) – consider obstruction or malignancy ```

Answer 286

``` o Ascites o Oedema o Haematemesis (varices) – vomiting blood o Malaise o Anorexia o Wasting o Easy bruising o Itching o Erythema nodosum o Spider naevi o Hepatomegaly o Abnormal LFTs o Jaundice (rarer) o Confusion (rarer) ```

Answer 287

Jaundice – raised serum bilirubin (waste product of haemolysis)

Answer 288

- RBC degraded in the spleen after a lifetime of 120 days - RBC splits into Haem + globin - Haem oxygenase converts poryphrin ring (haem-iron) into BILLIVERDIN - BILLIVERDIN (green pigment) is converted into UNCONJUGATED BILLIRUBIN (lipid-soluble) (^occurs in the reticuloendothelial system in the speen/bone marrow/liver) - BILLIRUBIN travels to the liver in the blood stream - bound to albumin - Billirubin is then conjugated with glucoronic acid = CONGJUGATED BILLIRUBIN (water-soluble) - Conjugated billirubin is excreted by the liver into the bile (canaliculi membrane --> RHD/LHD--> CHD --> CBD --> Duodenum - In the ileum, colonic bacteria deconjugate and metabolises billirubin into UROBILINOGEN (lipid-soluble) - 90% of the urobilinogen continues into the large intestine where it reduced to stercobilinogen which is then acted upon by different colonic bacteria to form stercobilin (colours the faeces) and excreted through the rectum - The remaining 10% of the urobilinogen is reabsorbed into the blood, binds to albumin and travels back to the liver and then 5% goes to the kidneys where it is oxidised to urobilin to colour urine, the other 5% goes back to the duodenum by the bile duct (enterohepatic circulation)

Answer 289

1) Pre-hepatic 2) Hepatic 3) Post-hepatic

Answer 290

• Pre-hepatic – excess breakdown of Hb --> increases total unconjugated bilirubin o Increased unconjugated bilirubin o Normal stool and urine • Causes – more haemolysis - Malaria - Sickle cell anaemia - Foetal Hb in newborns

Answer 291

• Hepatic – failure of hepatocytes to take up, metabolise or excrete bilirubin o Increased unconjugated and conjugated bilirubin o Dark urine and normal/pale stools • Causes - Viral hepatitis - Drugs - Alcohol - Cirrhosis

Answer 292

• Hepatic – failure of hepatocytes to take up, metabolise or excrete bilirubin o Increased unconjugated and conjugated bilirubin o Dark urine and normal/pale stools o Causes - Viral hepatitis - Drugs - Alcohol - Cirrhosis

Answer 293

• Post-hepatic – obstruction in biliary system e.g. gallstone o Increased conjugated bilirubin o Dark urine and pale stools o Causes - Gallstones - Pancreatitis – head of pancreas blocks CBD

Answer 294

Answer 295

• History 1. Dark urine, pale stools, itching? 2. Symptoms - Biliary pain - Rigors – shivering - Abdomen swelling - Weight loss 3. Past history - Biliary disease/intervention - Malignancy - HF - Blood products - Autoimmune disease 4. Drug history – drugs/herbs started recently - Social history - Alcohol - Potential hepatitis contact due to i. Irregular sex ii. IVDU iii. Exotic travel iv. Certain foods c. Family history/system review – rarely helpful

Answer 296

* Liver enzymes - very high AST/ALT suggests liver disease (some exceptions) * Biliary obstruction – 90% have dilated intrahepatic bile ducts on ultrasound • Further imaging o CT o Magnetic resonance cholangiogram (MRCP) o Endoscopic retrograde cholangiogram (ERCP)

Answer 297

Chronic liver disease (CLD) is a progressive deterioration of liver functions for more than six months, which includes synthesis of clotting factors, other proteins, detoxification of harmful products of metabolism and excretion of bile.

Answer 298

o Alcohol o Non-alcoholic steatohepatitis (NASH) – form of advanced NAFLD o Viral Hep B, C o Immune - Autoimmune hepatitis - Primary biliary cirrhosis - Sclerosing cholangitis o Metabolic - Haemochomatosis – excess iron deposition due to high levels of hepcidin - Wilson’s – high copper absorption - alpha 1-antitrypsin deficiency o Vascular - Budd-Chiari – portal hypertension

Answer 299

o Past history of: - Alcohol problems - Biliary surgery - Autoimmune disease - Blood products o Social history – alcohol, sexual o Drugs – ALL o Family history

Answer 300

``` o Ascites o Oedema o Haematemesis (varices) – vomiting blood o Malaise o Anorexia o Wasting o Easy bruising o Itching o Palmar erythema o Spider naevi o Hepatomegaly ```

Answer 301

o Viral serology – Hep B surface antigen, Hep C antibody o Immunology - Autoantibodies • AMA, ANA, ASMA • Coeliac antibodies o Biochemistry - Iron studies - Copper studies • Caeruloplasmin • 24 hour urine copper - Alpha 1-antitrypsin level - Lipids, glucose o Radiological investigations – USS/CT/MRI

Answer 302

Inflammation of the liver

Answer 303

* Hep A, B ± D, C and E * Herpes virus e.g. HSV, VZV, EBV, CMV * Other viruses

Answer 304

* Spirochaetes e.g. leptospirosis * Mycobacteria e.g. TB * Parasites e.g. toxoplasma * Bacteria e.g. Coxiella (Q fever)

Answer 305

- Alcohol - Non-alcohol fatty liver disease - Drugs - Toxins/poisoning - Pregnancy - Autoimmune - Hereditary metabolic

Answer 306

``` • Acute o Can be asymptomatic o General malaise o Myalgia o Gastrointestinal upset o Abdominal pain ``` • Chronic o Can be asymptomatic/non-specific symptoms

Answer 307

• Acute o Jaundice (pale stools, dark urine) o Tender hepatomegaly o Raised AST, ALT (GGT, ALP) ± Bilirubin ``` • Chronic o ± signs of chronic liver disease - Clubbing - Palmar erythema - Dupuytren’s contracture - Spider naevi ``` o LFTs can be normal even in context of cirrhosis o Initially in cirrhotic patient, liver disease is compensated – liver function maintained (normal albumin and clotting) o Decompensated – jaundice, ascites, low albumin, coagulopathy, encephalopathy o Complications: Hepatocellular carcinoma (HCC); portal hypertension – varices, bleeding.

Answer 308

* Viral A, B, C, CMV, EBV * Drug-induced * Autoimmune * Alcoholic

Answer 309

A: - Faeco-oral normally with travel history - Contaminated food/water B: - Blood-borne - sex C: - Blood-borne - needles D: - Blood-borne, combines with B E: - Faeco-oral - Contaminated food/water - Endemic in UK - found in undercooked pork A: - RNA/ACUTE B: DNA / BOTH C: RNA/BOTH D: RNA/BOTH E: RNA/ACUTE Look at rhyme + summary!

Answer 310

- Autoimmune hepatitis is liver inflammation that occurs when your body's immune system turns against liver cells. - The exact cause of autoimmune hepatitis is unclear, but genetic and enviromental factors appear to interact over time in triggering the disease.

Answer 311

* Type 1 – anti-nuclear antibody (ANA), anti-smooth muscle antibody (ASMA) * Type 2 – anti-LKM-1 or anti-liver cytosolic-1 (anti-LC-1) antibodies * Liver biopsy

Answer 312

Immunosuppression – prednisolone ± azathioprine

Answer 313

- Cirrhosis is scarring (fibrosis) of the liver caused by long-term liver damage. - The scar tissue prevents the liver working properly. - It is an end stage of all progressive chronic liver diseases (such as hepatitis), which once fully developed is irreversible - It may be associated clinically with symptoms and signs of portal hypertension and liver failure - It's characterised by loss of normal hepatic architecture, nodular regeneration and bridging fibrosis

Answer 314

``` • Common o Chronic alcohol abuse o Non-alcoholic fatty liver disease o Hep B±D o Hep C ``` • Others o Primary biliary cirrhosis o Autoimmune hepatitis – presents as high ALT o Hereditary haemochromatosis (iron overload) o Wilson’s disease - excess copper stored in the liver o Alpha-Antitrypsin deficiency o Drugs e.g. amiodarone and methotrexate

Answer 315

* Chronic alcohol abuse * Hep B±C * Obesity * T2DM

Answer 316

* Chronic liver injury results in --> inflammation, matrix deposition, necrosis and angiogenesis --> 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) * Stellate cells release CYTOKINES that attract neutrophils and macrophages to the liver --> further inflammation and necrosis --> FIBROSIS * Results in severe reduction in liver function as fibrosis in non-functioning

Answer 317

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

Answer 318

When the liver can still function effectively and there are no (or few) noticeable clinical symptoms

Answer 319

- When the liver is damaged to the point that it cannot function adequately and overt clinical complications (such as jaundice, ascites, variceal haemorrhage and hepatic encephalopathy) are present. - Events causing decompensation include infection, portal vein thrombosis and surgery

Answer 320

• Compensated o Asymptomatic o Non-specific e.g. weight loss, weakness, fatigue • Decompensated o Jaundice o Pruritis o Abdominal pain – due to ascites

Answer 321

* Bruising * Leukonychia – white discolouration on nails due to hypoalbuminaemia * Clubbing of the fingers – no schamroth window * Palmar erythema * Spider naevi * Dupuytren’s contracture * Xanthelasma – yellow fat deposits under skin usually around eyelids * Ascites * Jaundice * Oedema – decreased albumin in blood

Answer 322

• Liver biopsy • LFTs – serum albumin and prothrombin time best indicators of liver function o Raised bilirubin, aspartate amino transferase (AST) and alanine aminotransferase (ALT) o Low albumin and long prothrombin = malfunction * Liver biochemistry * FBC – low platelets (due to loss of thrombopoteitin) * Transient elastography

Answer 323

• Treat underlying cause o Alcohol abstinence o Antivirals for Hep C o Spironolactone for ascites * Liver transplant * Good nutrition * 6-month ultrasound screening for hepatocellular carcinoma Decompensated = liver transplant/ Treat symptoms e.g. mannitol for hepatic encephalopathy

Answer 324

• Coagulopathy – fall in clotting factors II, VII, IX and X • Encephalopathy – liver flap (flapping tremor with wrist extended) and confusion/coma o When toxins e.g. ammonia make it into the brain and cause mental deficits * Thrombocytopenia * Hepatocellular carcinoma * Hypoalbuminaemia • Portal hypertension o Ascites o Oesophageal varices

Answer 325

1) Pre-hepatic – due to blockage of portal vein before liver o Portal vein thrombosis ``` 2) Intra-hepatic – resulting from distortion of liver architecture o Cirrhosis – most common cause o Schistosomiasis o Sarcoidosis o Congenital hepatic fibrosis ``` 3) Post-hepatic – due to venous blockage outside of liver o Budd-Chiari syndrome – hepatic vein obstruction by tumour or thrombosis o Right HF o Constrictive pericarditis o IVC obstruction

Answer 326

- Following liver injury and fibrogenesis (e.g. due to cirrhosis), the contraction of activated myofibroblasts (mediated by endothelin, NO and prostaglandins) contributes to INCREASED RESISTANCE TO BLOOD FLOW * Leads to portal hypertension --> splanchnic vasodilation -> drop in BP --> increased CO to compensate for BP --> salt and water retention to increase blood volume--> hyperdynamic circulation (increased portal flow) * --> formation of collaterals between portal and systemic systems e.g. lower oesophagus and gastric cardia

Answer 327

* Endothelin-1 production increased in cirrhosis --> more vasoconstriction * NO production reduces in cirrhosis --> less vasodilation * Reduced radius --> increases resistance --> higher pressure in portal system

Answer 328

* Often symptomatic | * GI bleeding from oesophageal or gastric varices

Answer 329

* Ascites * Hepatic encephalopathy * Splenomegaly * Oesophago-gastric varices

Answer 330

• Varices is a dilated vein at risk of rupture resulting in haemorrhage and can cause GI bleeding in the GI system

Answer 331

* Around 90% of patients with cirrhosis develop gastro-oesophageal varices over 10 years but only a third will bleed * Bleeding likely to occur in large varices or those with red signs at endoscopy and in severe lives disease * Tend to develop in lower oesophagus and gastric cardia

Answer 332

* At oesophago-gastric junction, rectum and anterior abdominal wall (via umbilical vein) the portal and systemic capillary beds meet * If portal hypertension is present, the blood takes the path of least resistance which is through the systemic circulation --> bypasses liver and into heart * Causes detoxification and nutrition issues * As portal pressure increases, it can cause a gastric-oesophageal varices to form and rupture --> massive haemorrhage

Answer 333

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

Answer 334

Same as portal hypertension. 1) Pre-hepatic – due to blockage of portal vein before liver o Portal vein thrombosis ``` 2) Intra-hepatic – resulting from distortion of liver architecture o Cirrhosis – most common cause o Schistosomiasis o Sarcoidosis o Congenital hepatic fibrosis ``` 3) Post-hepatic – due to venous blockage outside of liver o Budd-Chiari syndrome – hepatic vein obstruction by tumour or thrombosis o Right HF o Constrictive pericarditis o IVC obstruction

Answer 335

* Cirrhosis * Portal hypertension * Schistosomiasis infection * Alcoholism

Answer 336

* Haematemesis * Abdominal pain * Rectal bleeding

Answer 337

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

Answer 338

• Endoscopy

Answer 339

• Blood transfusion if anaemic • Medical o Beta blocker to reduce CO --> reduce portal pressure o Nitrate to cause vasodilation --> to reduce portal pressure o Terlipressin (ADH analogue) --> reduce portal pressure * Trans-jugular intrahepatic portoclaval shunt (TIPS) * Correct clotting abnormalities with vitamin K and platelet transfusion * Variceal banding – band put around varice using endoscopy

Answer 340

Autoimmune destruction of the bile ducts --> cirrhosis

Answer 341

* Women aged 40-50 constitute 90% of patients * More common in females * Typical presentation at 50

Answer 342

* Interlobar bile ducts are damaged by chronic autoimmune granulomatous inflammation resulting in bile leaking out into blood and other liver cells --> inflammation and bile stasis (similar symptoms to cholestasis and obstructive jaundice) * Advanced stage can lead to cirrhosis due to autoimmune attack and infiltration of bile

Answer 343

• Autoimmune

Answer 344

* Family history * Many UTIs * Smoking * Past pregnancy * Autoimmune disease

Answer 345

* Asymptomatic – discovered on routine examination or screening * Lethargy and fatigue * Hepatomegaly • Leakage of o Bile - Pruritis – itchy skin - Jaundice o Cholesterol - Pigmented Xanthelasma – yellow fat deposits under skin around eyelids - Xeropthalmia – dryness of conjunctiva and cornea - Corneal arcus * Joint pain and arthropathy * Variceal bleeding

Answer 346

* Autoimmune cholangitis | * Extrahepatic biliary obstruction

Answer 347

• Antibody tests o Presence of Anti-Mitochondrial Antibodies (AMA) o Raised serum IgM • LFTs o Raised ALP and GGT o Raised cholesterol * Ultrasound * Liver biopsy

Answer 348

* Ursodeoxycholic acid – reduces cholesterol absorption and improves bilirubin and aminotransferase levels * Cholestyramine – reduces cholesterol absorption * Bisphosphonates – for osteoporosis * Vitamin ADEK supplementation * Liver transplant

Answer 349

* Drinking a large amount of alcohol, even for just a few days, can lead to a build-up of fats in the liver. * This is called alcoholic fatty liver disease, and is the first stage of ARLD. * Fatty liver disease rarely causes any symptoms, but it's an important warning sign that you're drinking at a harmful level.

Answer 350

o Metabolism of alcohol produces fat in liver o Minimal with small amounts of alcohol but cells become swollen with fat (steatosis) with larger amounts • Fatty liver --> Alcoholic hepatitis --> alcoholic steatosis --> cirrhosis (Classically of the micronodular type but mixed patent also seen accompanying fatty change and evidence of pre-existing alcoholic hepatitis may be present) * Reduced NAD+ and increased NADH --> less oxidation of fat --> more fat synthesis --> accumulation of fat in hepatocytes * Increased ROS damages hepatocytes * Acetaldehyde damages liver cell membranes * Leads to inflammation and eventual cirrhosis

Answer 351

* Alcohol abuse * Genetic predisposition * Immunological mechanisms

Answer 352

* RUQ pain * Nausea * Vomiting * Diarrhoea

Answer 353

* Hepatomegaly * Ascites * Jaundice

Answer 354

• LFTs o GGT and ALP very raised o AST and ALT mildly raised – increased AST>ALT ratio (usually 2:1) • FBC o Thrombocytopenia – low plateletss o Hypoglycaemia – low blood sugar * Abdominal ultrasound * CT * MRI * Liver biopsy

Answer 355

• Alcohol abstinence – if alcohol intake stops then fat will disappear, and liver goes back to normal o Delirium tremens (withdrawal symptoms) commonly seen 12-48 hours after alcohol withdrawal - Seizures, insomnia, vomiting, headache, sweating, palpitations and tremulousness - Treated with diazepam ``` • IV thiamine – to prevent Wernicke-Korsakoff encephalopathy o Triad of - Confusion - Ataxia - Nystagmus ``` * Diet high in vitamins and proteins * Liver transplant

Answer 356

* Cirrhosis * Liver failure * Encephalopathy

Answer 357

- Non-alcoholic fatty liver disease (NAFLD) is the term for a range of conditions caused by a build-up of fat in the liver. - It's usually seen in people who are overweight or obese ---> Results from fat deposition in the liver --> affects individuals with metabolic syndromes

Answer 358

- Obesity (70%) - Diabetes (35-75%) - Hyperlipidaemia (20-80) - Hypertension - Hypertriglyceridemia

Answer 359

``` • Usually no symptoms; liver ache in 10% o Fatigue and malaise o RUQ pain o Jaundice o Hepatomegaly ```

Answer 360

o LFTs - Commonest cause of mildly elevated LFTs - Raised ALT and sometimes AST o Ultrasound o CT o MRI o Liver biopsy * Fat, sometimes with inflammation, fibrosis (NASH) * Need biopsy to distinguish NAFL from NASH * NASH: Important cause of “cryptogenic” cirrhosis * Still no effective drug treatments * Weight loss works - the more the better

Answer 361

* Liver failure occurs when the liver loses the ability to regenerate or repair so that decompensation occurs * Histologically there is multi-acinar necrosis involving a substantial part of liver * Acute hepatic failure – acute liver injury with encephalopathy and deranged coagulation (INR > 1.5) * Acute-on-chronic hepatic failure – liver failure as a result of decompensation of chronic liver disease

Answer 362

o Hepatic encephalopathy – confusion, coma, liver flap (asterixis – flapping tremor with wrist extended) and drowsiness - As liver fails, nitrogenous waste e.g. ammonia builds up in circulation and passes to brain --> permanent brain damage (ammonia is neurotoxic) - As astrocytes clear ammonia (involving conversion of glutamate to glutamine). Excess glutamine causes an osmotic imbalance and a shift of fluid into these cells --> cerebral oedema --> damage o Abnormal bleeding o Ascites o Jaundice

Answer 363

``` • Virus o Hep A, B(+D), E – rarely C o Cytomegalovirus o EBV o Herpes simplex virus ``` ``` • Drugs o Paracetamol – common cause o Alcohol o Anti-depressant – amitriptyline o NSAIDs o Ecstasy or cocaine o Antibiotics – Ciprofloxacin, doxycycline or erythromycin ``` * Hepatocellular carcinoma * Wilson’s disease or Alpha-1-anti-trypsin deficiency

Answer 364

* Fever | * Vomiting

Answer 365

* Jaundice * Ascites * Small liver * Hepatic encephalopathy * Fetor hepaticus – patient smells like pear drops * Bruising * Clubbing * Cerebral oedema

Answer 366

``` • Bloods o Hyperbilirubinemia o High serum ALT and AST o Low levels of coagulation factors and raising prothrombin time o Low glucose ``` * EEG – for grading encephalopathy * Ultrasound

Answer 367

* Treat cause e.g. in paracetamol poisoning give N-acetyl-cysteine * Signs of raised ICP – IV mannitol * Liver transplant

Answer 368

• Malnutrition • Coagulopathy o Impaired coagulation factor synthesis o Vitamin K deficiency (cholestasis) o Thrombocytopenia • Endocrine changes o Gynaecomastia o Impotence o Amenorrhoea • Hypoglycaemia

Answer 369

• Uncontrolled deposition of copper

Answer 370

Haemochromatosis is an inherited condition which results in too much iron being stored in the body. Your body doesn't have a way of getting rid of the iron overload, so if you have too much it gets deposited in the organs - particularly the liver, but at higher levels it can enter the heart, pancreas and other organs. * Genetic disorder * 90% have mutations in HFE gene: C282Y, H63D * Autosomal recessive; incomplete penetrance * Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas * Diagnosis suggested by raised ferritin and transferrin saturation, confirmed by HFE genotyping and liver biopsy • Cirrhosis o Present, risk of hepatocellular carcinoma o Not present and treated – normal life expectancy • Iron removal may lead to regression of fibrosis

Answer 371

- Abnormal accumulation of fluid within the abdominal cavity

Answer 372

* 10-20% survival 5-years from onset * Signifies other serious illness * Common post op

Answer 373

``` • High protein fluid (exudate) – extremely bad o Cloudy fluid o Low serum to ascites albumin gradient o Causes – peritoneal cause - Cancer - Sepsis - TB - Nephrotic syndrome ``` ``` • Low protein fluid (transudate) o Clear fluid o High serum to ascites albumin gradient (>11g/L) o Outflow problem (i.e. portal hypertension) o Decreased oncotic pressure o No issues with cell membrane o Causes: - Cirrhosis o Management - Treat underlying cause - Diet - Diuretic - Drainage ```

Answer 374

• Impaired blood outflow o Fluid cannot move forward through system e.g. due to a clot o Raised pressure and vessels causing fluid to leak out of vessels o Seen in - Cirrhosis i.e. portal hypertension - Budd-Chiari syndrome – occlusion of hepatic veins that drain liver - Cardiac failure - Constrictive pericarditis • Decreased oncotic pressure – low protein o With less protein e.g. albumin, there is an inability to pull fluid back into intravascular space o This fluid then accumulates in peritoneum o Seen in - Hypoalbuminaemia - Nephrotic syndrome - Malnutrition • Local inflammation e.g. peritonitis

Answer 375

* High sodium diet * Hepatocellular car inoma * Splanchnic vein thrombosis resulting in portal hypertension

Answer 376

* Severe pain – suspect bacterial peritonitis | * Abdominal swelling

Answer 377

* Shifting dullness – patient lies on back and percuss left flank (will sound dull), get them to life on side and percuss again (will sound resonant as fluid moved) * Abdominal distension * Protruding ascites * Presence of raised veins * Flank dullness * Fluid thrill * Bulging flanks

Answer 378

* Ascitic tap – culture, gram stain, cytology, protein * Ultrasound * Presence of fluid confirmed by demonstrating shifting dullness

Answer 379

* Treat underlying cause * Reduce sodium to help liver and reduce fluid * Diuretic – oral spironolactone (spares K+) ± Furosemide * Paracentesis (drain fluid)

Answer 380

• Spontaneous Bacterial Peritonitis – suspect in any ascitic patient that deteriorates o Bugs - E. Coli - Klebsiella - Enterococcus o Investigations - Ascitic tap – raised neutrophils o Management – cefotaxime o Prophylaxis – ciprofloxacin

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GI & Liver Flashcards

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