liver and GI Flashcards

Question

explain the different types of jaundice and the type of bilirubin that they present with

Answer 1

pre-hepatic jaundice - due to haemolysis; increased unconjugated bilirubin levels Hepatic jaundice - impaired liver function; elevated unconjugated and conjugated bilirubin post-hepatic jaundice - obstruction of bile flow from liver to intestine; accumulation of conjugated bilirubin in the bloodstream

Answer 2

haemolysis and gilbert's syndrome

Answer 3

pre-hepatic urine normal stools normal no itching normal liver tests post-hepatic urine dark stools pale maybe itching liver tests abnormal

Answer 4

post-hepatic/hepatic

Answer 5

A self-limiting pain in the RUQ/epigastrium associated with gallstones

Answer 6

Acute inflammation of the gallbladder, most commonly caused by gallstones

Answer 7

Infection of the biliary tree, commonly due to an obstructing stone in the common bile duct

Answer 8

Gallstones within the biliary tree

Answer 9

female age white caucasian, native americans and hispanic high cholesterol Extravascular haemolysis, haemolytic anaemia, sickle cell, hereditary spherocytosis Liver disease Rapid weight loss/prolonged fasting Diabetes Medications - eg Oestrogen HRT, ceftriaxone, octreotide Crohn's disease Rapid Weight Loss/Prolonged Fasting:

Answer 10

right upper quadrant radiating into right shoulder

Answer 11

Spontaneous bacterial peritonitis

Answer 12

Liver enzymes: AST/ALT Ultrasound: 90% have dilated intrahepatic bile ducts on ultrasound if the ducts are dilates you need further imaging: - CT - Magnetic resonance cholangioram MRCP - Endoscopic retrograde cholangiogram ERCP

Answer 13

Increased Ca Haemolysis Increased cholesterol Biliary stasis Infection

Answer 14

cholesterol stones --> vast majority of cases Black pigment stones --> due to too much billirubin brown pigment stones --> mixed stones

Answer 15

Localised RUQ pain worse after fatty meal

Answer 16

RUQ/Epigastric Pain - may radiate to right shoulder if diaphragm is irritated (phrenic nerve) Fever + rigors Nausea + Vomiting RUQ tenderness Murphy's Sign positive Occasionally mildly deranged LFTs - esp. If Mirizzi syndrome Raised inflammatory markers Ultrasound can show inflamed gallstones and pericholecystic fluid

Answer 17

Murphy's sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner's hand, Murphy's sign is positive.

Answer 18

Charcot's triad: 1. RUQ pain 2. Fever 3. Jaundice if sepsis is very severe Reynold's Pentad: Charcot's triad + Hypotension + confusion RUQ tenderness Raised inflammatory markers Raised bilirubin, ALT, ALP Duct dilation on ultrasound

Answer 19

in acute cholangitis you will have raised bilirubin, ALT and ALP as the biliary tree is inflamed, whereas in acute cholecystits you do not.

Answer 20

CT or MRCP

Answer 21

32-45% Antibiotics (Augmentin, Flucloxacillin, Erythromycin, Septrin, TB drugs) 15% CNS Drugs (Chlorpromazine, Carbamazepine Valproate, Paroxetine, 5% Immunosupressants 5-17% Analgesics/musculskeletal (Diclofenac…) 10% Gastrointestinal Drugs (PPIs…) 10% Dietary Supplements PARACETAMOL Statins

Answer 22

these are some of the liver function tests ALT = alanine aminotransferase --> important in protein breakdown - more specific for liver than AST AST - aspartate aminotransferase --> indicates protein metabolism and is not as specific as ALT ALP - alkaline phosphatase --> enzyme found specifically and bile duct in bone so indicates acute cholangitis GGT - gamma-glutamyl transferase --> enzyme found in bile duct cells; more specific than ALP

Answer 23

paracetamol is also known as acetaminophen There are 2 pathways for paracetamol metabolism: A most paracetamol is metabolised like this: 1) acetaminophen is conjugated with glucuronic acid 2) acetaminophen more hydrophilic now so easily excreted through urine B in case of OD or liver damage paracetamol is metabolised to a toxic compound which can further damage the liver 1) CYP2E1 converts acetaminophen to the intermediate NAPQI 2) NAPQI is toxic and causes hepatocyte damage

Answer 24

LFTs Viral testing FBC CRP ESR Drug screens CT Social and medical history are very important; any new changes in prescriptions or meds?

Answer 25

give N acetyl Cysteine supportive treatment for other complications of the OD: - coagulation factors - fluids, electrolytes - maintain acid-base balance - check for hypoglycaemia - check for encephalopathy

Answer 26

renal failure

Answer 27

Chronic liver disease is progressive liver dysfunction that if treated could still be reversed cirrhosis is the end result of chronic liver disease which couldn't be saved --> irreversible remodelling of the liver; irreversible liver damage

Answer 28

genetic disorder where you don’t produce antitrypsin so you have too much trypsin which just diugests proteins results in liver and lung damage

Answer 29

Wilson's disease is a rare genetic disorder characterized by the abnormal accumulation of copper in various tissues, particularly the liver, brain, and cornea of the eyes.

Answer 30

Hereditary hemochromatosis is a genetic disorder characterized by the excessive absorption and accumulation of iron in the body. Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas

Answer 31

weekly therapeutic phlebotomy --> kind of like dialysis for blood a certain amount of blood is withdrawn at regular intervals (usually weekly initially) to reduce iron levels.

Answer 32

excess fat deposition

Answer 33

decreased oncotic pressure cuz of no more albumin synthesis portal vein hypertension reduced blood flow to kidneys --> triggers RAAS and leads to water retention inflammation from cirrhosis increases blood vessel permeability

Answer 34

Coagulopathy - reducing clotting factor synthesis: evidence of bruising and deranged coagulation tests. Jaundice - impaired breakdown of bilirubin: yellow appearance of the skin and sclera Encephalopathy - poor detoxification of harmful substances: confusion Ascites - poor albumin synthesis and increased portal pressure due to scarring: accumulation of fluid in the abdominal cavity Gastrointestinal bleeding - increase portal pressure causing varices

Answer 35

Distended and engorged superficial epigastric veins around the umbilicus sign of chronic liver disease and portal hypertension

Answer 36

Red discolouration of palms especially over the hypothenar eminence High oestrogen causes vasodilation

Answer 37

Thickening of the palmar fascia; painless fixed flexion of fingers at the MCP joints (especially ring finger)

Answer 38

Appearance of white lines/dots in nails - sign of hypoalbuminaemia

Answer 39

Development of breast tissue in males - reduced hepatic clearance of androgens leads to peripheral conversion to oestrogen

Answer 40

Dilated capillary with central red papule and fine red lines extending radially - due to excess oestrogen - usually found in the distribution of the superior vena cava

Answer 41

liver biopsy

Answer 42

diuretics - spironolactone ± furosemide restrict water and sodium paracentesis + albumin Trans-jugular intrahepatic portosystemic shunt

Answer 43

give vit k and fresh frozen plasma

Answer 44

lactulose (decreases ammonia), antibiotics, and enemas (stops flora making NH3) Lactulose is an osmotic laxative which helps reduce ammonia

Answer 45

1) Fatty Liver: Accumulation of fat in liver cells (steatosis). 2) Alcoholic Hepatitis: Inflammation of the liver tissue. 3) Alcoholic Cirrhosis: Advanced scarring of the liver tissue; irreversible stage.

Answer 46

obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia. Drugs (NSAIDs, amiodarone)

Answer 47

faeco-oral pre- and post-exposure immunisation --> Inactivated hepatitis A virus Picorna virus RNA cholestasis (slowing of bile flow through the biliary system) pruritus significant jaundice dark urine and pale stools.

Answer 48

blood/sex pre- and post-exposure immunisation + sexual education and behavioral change (condoms) Hepadnavirus DNA Abdominal pain Fatigue Flu-like illness Pruritus (itching) Muscle and joint aches Nausea and vomiting Jaundice RUQ pain Malaise Myalgia

Answer 49

blood/sex blood donor screening + condoms Flavivirus RNA

Answer 50

blood/sex HBV (Hep B virus) immunisation + Condoms (Hep D requires Hep B for its replication → you can get Hep B vaccine to prevent Hep D) RNA Pegylated interferon alpha

Answer 51

faeco-oral clean drinking water RNA

Answer 52

1) Screen for other viral infections (e.g., HIV, hepatitis A, C and D) 2) Referral to gastroenterology, hepatology or infectious diseases 3) Avoid alcohol 4) Education about reducing transmission 5) informing potential at-risk contacts 6) Testing for complications (e.g., for cirrhosis and hepatocellular carcinoma) 7) Antiviral medication can be used to slow the progression of the disease and reduce infectivity 8) Liver transplantation for liver failure (fulminant hepatitis)

Answer 53

Estrogen is normally broken down in the liver, and its metabolites are excreted in bile. In liver diseases, this process is compromised, leading to elevated circulating levels of estrogen. reduced hepatic clearance of androgens leads to peripheral conversion to oestrogen

Answer 54

palmar erythema gynaecomastia spider naevi

Answer 55

antibiotic use --> disrupts the normal balance of the gut microbiota --> opportunity for C. difficile to proliferate and flourish.

Answer 56

proximal small bowel problem

Answer 57

BACTERIA vibrio cholerae E.coli bacillus cereus (rice) Clostridium perfringens (meats) Staph aureus VIRUSES rotavirus and norovirus

Answer 58

cooked meats

Answer 59

inflammatory cause - inflammatory bowel disease problem in colon possible colon cancer bacterial infection

Answer 60

shigella e coli salmonella clostridium difficile campylobacter jejuni

Answer 61

high fat content in stools malabsorption disease like coeliac or irritable bowel syndrome

Answer 62

rotavirus/norovirus

Answer 63

Occurs within 2 weeks of arrival in new country 3 or more unformed stools per day plus one of the following: Abdominal pain Cramps Nausea Vomiting Dysentery Caused by organisms such as enterotoxigenic e.coli, campylobacter, shigella, non-typhoidal salmonella, viral, protozoal, cholera

Answer 64

dark black, tarry feces that are associated with upper gastrointestinal bleeding

Answer 65

haematemesis - vomiting blood melaena - dark tarry stool coffee ground vomiting - With coffee ground emesis, the blood is not fresh or bright red. By the time your vomiting reflex was triggered, the blood had been in your GI tract long enough to begin to dry, congeal, and turn to a darker color.

Answer 66

Antibiotics - most patients die of sepsis because if they have a cirrhosed liver they are already immunocompromised and GI bacteria can translate to blood and to liver more easily Terlipressin - Terlipressin is a synthetic analog of vasopressin (antidiuretic hormone) that is used for its vasoconstrictive effects. When patient has esophageal bleeding you give terlipressin for vasoconstriction and because it will help the kidneys retain more water (avoid hypovolemia from bleed)

Answer 67

Glasgow-Blatchford score

Answer 68

Consider proton pump inhibitors.

Answer 69

esophageal varices peptic ulcers

Answer 70

the obstruction of the wall of the bowel --> obstruction is not in lumen, it is in the wall

Answer 71

obstruction of the intestinal lumen due to fibrous scarring from NSAIDS

Answer 72

Chron's disease diverticulitis tumours neural

Answer 73

sigmoid colon

Answer 74

adhesions volvulus tumours; peritoneal deposits

Answer 75

The Glasgow-Blatchford score is used at the initial presentation in suspected upper GI bleed. It estimates the risk of the patient having an upper GI bleed. A score above 0 indicates a high risk for an upper GI bleed. The NICE guidelines (updated 2016) suggest considering early discharge in patients with a score of 0. The easiest way to calculate the score is using an online calculator. It takes into account: Haemoglobin (falls in upper GI bleeding) Urea (rises in upper GI bleeding) Systolic blood pressure Heart rate Presence of melaena (black, tarry stools) Syncope (loss of consciousness) Liver disease Heart failure

Answer 76

Dehydration Electrolyte imbalance Renal failure Immune compromise Severe abdominal pain Cancer risk factors Over 50 Chronic diarrhoea Weight loss Blood in stool

Answer 77

fluids electrolyte monitoring and replacement antiemetics antimotility agents - not in inflammatory diarrhoea DO NOT give broad spectrum antibiotics

Answer 78

A chronic inflammatory disorder affecting any part of the GI tract from the mouth to the anus characterised by patchy, transmural inflammation of intestinal mucosa (transmural = layers that make up the wall of the intestine)

Answer 79

C cobblestone appearance R rosethorn ulcers O obstruction H Hyperplasia of lymph nodes N narrowing of lumen S skip lesions

Answer 80

genetic smoking western diets antibiotics contraceptives

Answer 81

distal ileum

Answer 82

Diarrhoea Abdominal pain Weight loss Fever Fatigue Intestinal complication - due to wall thickening, lumen narrowing and ulceration

Answer 83

Pyrexia Dehydration Angular stomatitis → inflammation of one or both corners of the mouth Aphthous ulcers → shallow and painful sores in the mouth Pallor → pale colour of skin; due to anaemia Tachycardia Hypotension Abdominal pain, mass and distension

Answer 84

chron's ulcerative colitis

Answer 85

Arthritis → inflammation in crohn's can extend beyond the gut leading to joint inflammation Erythema nodosum → painful red nodules under the skin - systemic inflammation Pyoderma Gangrenosum → rare skin condition characterised by painful, ulcerating skin lesions Episcleritis, Uveitis, Conjunctivitis – inflammation of the eyes’ episclera and uvea Aphthous Ulcers Fatty liver disease → Chronic inflammation associated with Crohn's disease can contribute to insulin resistance → can lead to increased hepatic lipogenesis, promoting the accumulation of fat in liver cells. Gallstones and kidney stones → chron’s affects formation of bile acid Pulmonary disease → also due to systemic inflammation Venous thrombosis → systemic inflammation triggers clotting cascade more readily Osteoporosis B12 deficiency Anaemia

Answer 86

endoscopy + biopsy of inflammation

Answer 87

FBC TFT LFT U&E CRP Faecal Calprotectin - very specific to IBD Endoscopy + biopsy --> GOLD STANDARD Colonoscopy Barium enema

Answer 88

Faecal Calprotectin

Answer 89

ENDOSCOPY + BIOPSY

Answer 90

oral corticosteroids: budesonide and prednisolone IV hydrocortisone in severe flareups Anti-TNF antibodies if no improvement: infliximab immunosuppressants if things get really bad: methotrexate or azathioprine

Answer 91

Infliximab

Answer 92

methotrexate

Answer 93

oral corticosteroids: BUDESONIDE AND PREDNISOLONE

Answer 94

colonoscopies because of increased risk of colorectal cancer

Answer 95

mucosal inflammation affecting the rectum and progressing proximally and continuously through the colon

Answer 96

ulcerative colitis

Answer 97

decreases risk

Answer 98

being jewish milk consumption bacterial microflora alteration NSAIDs

Answer 99

Potential abnormal immunological response to normal intestinal microflora

Answer 100

these are different presentations of ulcerative colitis proctitis in inflammation limited to the rectum left-sided disease is when the inflammation extends from rectum to sigmoid colon (on the left side of the body) pancolitis is when inflammation extends throughout the entire colon (from rectum to caecum)

Answer 101

Symptoms Bloody diarrhoea and rectal bleeding Acutely unwell - hypovolemic shock Abdominal pain Weight loss Fatigue Loose stools Tenesmus (constantly feeling like you need to poop even if your bowel is already empty) Signs Febrile Pale Dehydrated Abdominal tenderness Abdominal distension/mass Tachycardic, hypotensive

Answer 102

a group of inflammatory rheumatic diseases that primarily affect the joints of the spine (spondylo-) and may involve other joints as well would expect to see it in severe cases of ulcerative colitis

Answer 103

toxic megacolon

Answer 104

Thin colon wall can be perforated → release of bowel contents in abdominal cavity and sepsis Compromised blood flow to surrounding structures and to colon wall Can cause severe dehydration and electrolyte imbalance

Answer 105

TRUELOVE AND WITTS stool frequency bleeding pulse rate temperature

Answer 106

Routine bloods - FBC, TFT, LFT, U&E CRP Faecal Calprotectin ENDOSCOPY + BIOPSY Colonoscopy - asses colon and terminal ileum plus biopsy w/ PPV of 100% Sigmoidoscopy - alternative test Take care during acute flares as risk of perforation Abdominal X-Ray - observe dilatation of bowel and perforations. Dilatation present if (rule of 3s) Small bowel: diameter > 3cm Large bowel: diameter > 6cm Caecum: diameter > 9cm

Answer 107

UC - mucosa only Chron's - transmural (affects multiple layers - mucosa, submucosa, muscularis propria, serosa/adventitia (depending if you are intraperitoneal or retroperitoneal))

Answer 108

serosa - intra adventitia - retro

Answer 109

Diverticulitis is a condition characterized by inflammation or infection of small pouches (diverticula) that can develop along the walls of the colon (large intestine). These pouches, known as diverticula, are formed when weak spots in the colon wall give way under pressure, causing the mucosa to protrude through the submucosa and if very severe through the muscularis propria. if it fully goes through muscularis propria you get peritonitis

Answer 110

diverticulitis is infection of diveriticulum where diverticular disease is diverticulum with no infection yet

Answer 111

Increased fibre diet and bulk-forming laxatives eg ispaghula husk *Avoid stimulant laxative like Senna surgery if indicated

Answer 112

sigmoid colon

Answer 113

from stratified squamous to columnar

Answer 114

NAFL is just a simple fatty liver whereas NASH involves more liver damage (INFLAMMATION, FAT, HEPATOCELLULAR INJURY, FIBROSIS)

Answer 115

treat underlying cause and reduce risks (lose weight, exercise, smoking, control diabetes, LDL). Medication: pioglitazone, vitamin E, statins, ACEi.

Answer 116

a synthetic analog of vasopressin (antidiuretic hormone) that is used for its vasoconstrictive effects. When patient has esophageal bleeding you give terlipressin for vasoconstriction and because it will help the kidneys retain more water (avoid hypovolemia from bleed)

Answer 117

NSAID induced gastric ulcer

Answer 118

NSAIDs, anticoagulation or antiplatelet use peptic ulcers history

Answer 119

adhesions form previous abdominal, colorectal or pelvic surgeries hernias malignancies chron's disease

Answer 120

colorectal malignancy - most common volvulus

Answer 121

formation of strictures --> narrowing of the intestine

Answer 122

mechanical means due to hernias, adhesions, and malignancies Obstruction of the bowel 🡪 bowel distension above the block and results in increased fluid secretion into the distended bowel + swallowed air in small bowel More dilatation 🡪 decreased absorption and mucosal wall oedema Increased pressure with intramural vessels becoming compressed in distal intestine Untreated obstruction leads to Ischaemia Necrosis Perforation

Answer 123

Pain – initially colicky (starts and stops then diffuse) Pain is higher in abdomen than in LBO Vomiting following pain – occurs earlier in SBO compared to LBO Nausea Anorexia Obstipation - constipation with no passage of wind Increased bowel sounds Tympanic percussion --> where obstruction is the sound of percussion will be more resonant cuz of trapped air Tenderness – suggests strangulation Less distension as compared to LBO (since more distal the obstruction, the greater the distension)

Answer 124

Abdominal pain – more constant than in SBO Vomiting – more faecal like Acute presentation – on average 5 days of symptoms Abdominal distension Palpable mass – hernia, distended bowel loop or caecum Constipation Fullness/bloating

Answer 125

Large bowel has a larger lumen 🡪 the ability of large bowel to distend is much greater 🡪 symptoms present slower and later than in SBO

Answer 126

AXR CT (abdominal) FBC

Answer 127

AXR DRE - Digital rectal exam FBC CT/MRI

Answer 128

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

Answer 129

obstipation

Answer 130

PSC affects bile ducts inside and outside the liver PBC affects bile ducts inside of the liver PSC also is very common in IFD, whereas PBC is not to diagnose PSC you need Magnetic resonance cholangiopancreatography (MRCP) to diagnose PBC you can use blood tests which show elevated ALP PSC can't be treated PBC can be treated PSC increases your risk of colon cancer

Answer 131

two points of obstruction along the bowel - leading to a middle section sandwiched between two points of obstruction

Answer 132

Autoimmune T cell mediated inflammation of the mucosa of the small bowel, and malabsorption, following exposure to gluten

Answer 133

other autoimmune conditions IgA deficiency familial link

Answer 134

Gluten breaks down to gliadin which triggers the immune system to produce IgA autoantibodies such as anti-tissue transglutaminase (anti-tTG), and anti-endomysial (anti-EMA) which target the epithelial cells of the small bowel causing villous atrophy, crypt hyperplasia, intraepithelial lymphocytes. villous atrophy leads to malabsorption

Answer 135

duodenum and jejunum

Answer 136

anaemia --> malabsorption of Fe, B12, Folate steatorrhea and diarrhoea dermatitis herpetiformis abdominal pain fatigue and weakness

Answer 137

Angular stomatitis, mouth ulcers, weight loss, failure to thrive (in children), osteopenia (Ca2+ and Vit D malabsorption), bloating

Answer 138

Raised anti-tissue transglutaminase tTG antibodies raised anti-endomysial EMA antibodies Total IgA antibodies raised --> possible false negative for coeliac in IgA deficient patients as IgA will come back low)

Answer 139

Endoscopy and duodenal biopsy (villous atrophy, crypt hyperplasia, intraepithelial lymphocytes)

Answer 140

villous atrophy crypt hyperplasia intraepithelial lymphocytes

Answer 141

FBC --> Hb, iron, B12, folate DEXA bine scan genetic testing

Answer 142

IBD, IBS, lactose intolerance. Tropical sprue (chronic inflammation of bowel associated with travel. Jejunal biopsy = incomplete villous atrophy vs coeliac with complete atrophy)

Answer 143

gluten free diet replace vitamin deficiencies

Answer 144

Osteopenia, anaemia, malignancy (T cell lymphoma, NHL), vitamin deficiency

Answer 145

Inflammation of the stomach mucosal lining

Answer 146

autoimmune alcohol H. Pylori bacterial reflux NSAIDs stress

Answer 147

Alcohol increases gastric acid and irritates stomach.

Answer 148

NSAIDs inhibit COX which inhibits prostaglandin synthesis which decreases mucus protective barrier production.

Answer 149

Autoimmune gastritis attacks parietal cells and forms intrinsic factor antibodies which reduces B12 absorption.

Answer 150

Epigastric pain, nausea and vomiting, dyspepsia (indigestion), anorexia/loss of appetite

Answer 151

indigestion

Answer 152

1st line --> helicobacter pylori urea breath test + H. Pylori stool antigen test gold standard --> endoscopy and biopsy

Answer 153

triple therapy: PPI + 2 antibiotics for 7 days PPI: omeprazole antibiotics: amoxicillin 1g, clarithromycin 500mg. if penicillin allergy, swap amoxicillin for 400mg metronidazole

Answer 154

you stop consuming NSAID or alcohol PPI

Answer 155

PPI IM vit B12

Answer 156

Peptic ulcers Achlorhydria → low HCl in stomach bleeding and anaemia MALT lymphoma → Non-Hodgkin Mucosa-Associated Lymphoid Tissue Lymphoma gastric cancer

Answer 157

A break in the mucosal lining of the stomach or duodenum forming ulcers. 2 types: duodenal (most common) and gastric

Answer 158

H. Pylori, NSAIDS Zollinger Ellison syndrome → a condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid

Answer 159

NSAIDS and H. Pylori break down the gastric mucus barrier gastric acid then forms an ulceration in the lining

Answer 160

alcohol and caffein

Answer 161

lesser curvature of antrum

Answer 162

epigastric pain dyspepsia nausea vomiting haematemesis (if artery is perforated) melanea weight loss

Answer 163

H. Pylori urea breath test or stool antigen test, FBC (anaemia or high platelet count)

Answer 164

Endoscopy and biopsy (if red flags) – presence of ulcer

Answer 165

Oesophageal cancer, gastric cancer, GORD, biliary colic

Answer 166

stop NSAIDS/alcohol triple therapy for H pylori omeprazole (PPI) + 2 antibiotics (amoxicillin/metronidazole + clarithromycin)

Answer 167

Bleeding, perforation, gastric outflow obstruction, malignancy

Answer 168

swallowing difficulties

Answer 169

syndrome which causes oesophageal webs, dysphagia, glossitis, iron deficiency anaemia usually associated with precancerous oesophagus

Answer 170

squamous cell carcinoma --> upper 2/3 of oesophagus adenocarcinoma --> lower 1/3 of oesophagus

Answer 171

smoking alcohol achalasia hot foods and beverages plummer-vinson syndrome black and asian minority ethnicity

Answer 172

barret s oesophagus GORD obesity smoking hernias older age male caucasian

Answer 173

progressive dysphagia --> KEY PRESENTATION vomiting weight loss anorexia lymphadenopathy

Answer 174

hoarse voice odynophagia cough melaena heartburn

Answer 175

red flags are anaemia, loss of weight, anorexia, melanea, haematemesis, dysphagia and recent progressive symptoms. urgent 2 week endoscopy referral

Answer 176

Oesophagogastroduodenoscopy and biopsy (w/ barium swallow) CT/MRI of chest/abdomen (metastases and staging)

Answer 177

muscles of oesophageal tube which are right above the stomach are unable to relax; makes swallowing both liquids and solids difficult

Answer 178

Achalasia (not progressive dysphagia – difficulty swallowing both solids and liquids), oesophageal strictures, Barrett’s oesophagus

Answer 179

In achalasia, dysphagia usually occurs with both solid and liquid food, whereas in esophageal strictures, dysphagia typically occurs only with solid food and not liquids, until very late in the progression of the stricture. achalasia is a problem with the functioning of the oesophagus strictures are a problem with the structure of the oesophagus

Answer 180

surgical resection with adjuvant radiotherapy/chemotherapy. Palliative care

Answer 181

Leiomyomas = smooth muscle tumours in oesophageal wall They are slow growing and usually asymptomatic. Generally found by mistake in barium swallow

Answer 182

colorectal cancer

Answer 183

IBD sporadic mutations Hereditary: - Familial adenomatous polyposis - Hereditary nonpolyposis colorectal cancer

Answer 184

Familial adenomatous polyposis (FAP). Mutation in APC tumour suppressor gene causing high polyp formation → potential of cancer before age 40

Answer 185

hereditary nonpolyposis colorectal cancer. Mutation in DNA mismatch repair genes (genese which should identify mistakes in DNA and fix them)

Answer 186

Family history IBD - especially UC Age Diet - high in red/processed meat, low in fibre Obesity and sedentary lifestyle Smoking Alcohol Low fibre diet (butyrate) Genetics Diabetes mellitus

Answer 187

adenocarcinomas

Answer 188

liver and lungs

Answer 189

RIGHT: - from appendix and caecum to the first 2/3 of the transverse colon - usually asymptomatic until patient presents with iron deficiency anaemia from bleeding - weight loss - abdominal pain LEFT: - from last 1/3 of colon to anus - blood and mucus in stools - diarrhoea alternating with constipation - tenesmus --> specific for rectal carcinoma - thinner stools --> spoecific for rectal carcinoma

Answer 190

hepatomegaly jaundice lymphadenopathy

Answer 191

over 40yr + abdominal pain + unexplained weight loss over 50yr + unexplained rectal bleeding over 60yr + change in bowel habit/iron deficiency anaemia

Answer 192

Faecal Immunohistochemical Tests (FIT) digital rectal exam double contrast barium enema

Answer 193

colonoscopy and biopsy

Answer 194

IBS, IBD, haemorrhoids, anal fissure, anal prolaose, diverticulitis

Answer 195

surgical resection depending on affected area, chemotherapy (fluorouracil), radiotherapy

Answer 196

offer screening every 2 years between the ages of 60 and 74. We are gradually extending this age range, and people aged 56 are now being invited as part of this proces home testing kit --> faecal immunohistochemical test (FIT)

Answer 197

CT chest abdomen and pelvis --> look at metastasis and spread for staging

Answer 198

Duke stage

Answer 199

used for colon cancer A – cancer only in mucosa 95% 5 year survival B - cancer has gone through muscularis 75% 5 year survival C - spread to regional lymoh nodes 35% 5 year survival D - distal lymph node involvement and metastasis 25% 5 year survival

Answer 200

type 1 --> intestinal metaplasia/differentiated type 2 --> diffuse/undifferentiated; signet ring cells

Answer 201

east asian and eastern europe

Answer 202

H. Pylori, smoking, pernicious anaemia (chronic gastritis), mutations

Answer 203

type 1: intestinal; gland forming cells; differentiated type 2: diffuse; poorly differentiated cells, signet ring cells, linitis plastica (leather bottle appearance with thickened gastric wall)

Answer 204

linitis plastica (leather bottle appearance with thickened gastric wall)

Answer 205

Intestinal: male, older age, H. Pylori, chronic/atrophic gastritis Diffuse: female, younger age (<50), blood type A, genetic, H. Pylori

Answer 206

Virchow's node sister mary joseph node Severe epigastric pain dysphagia Metastatic signs --> jaundice → indicates liver mets Krukenberg tumour → ovaries Weight loss, vomiting, anorexia, epigastric pain, tired all the time

Answer 207

Dysphagia, melaena/haematemesis, anaemia

Answer 208

Gastroscopy with biopsy →2-week endoscopy referral if dysphagia or age>55 with upper abdo pain, reflux or dyspepsia Endoscopy ultrasound → shows depth of tumour invasion and nodal involvement CT/MRI of the chest and abdomen (Tumour Node staging and metastases) FBC (normal or anaemia)

Answer 209

Peptic ulcer disease, achalasia, oesophageal stricture

Answer 210

surgical resection (total or sub-total gastrectomy) + adjuvant radiotherapy/chemotherapy (fluorouracil/cisplatin)

Answer 211

colorectal cancer staging Looks at: T → tumour size and extent T1: Tumor in submucosa. T2: Tumor in muscularis propria (muscle layer). T3: Tumor in the serosa (outermost layer). T4: Tumor in adjacent structures N → involvement of nearby lymph nodes N0: No regional lymph node involvement. N1: Involvement of 1-3 regional lymph nodes. N2: Involvement of 4 or more regional lymph nodes M→ presence or absence of distant metastasis M0: No distant metastasis. M1: Distant metastasis present Prognosis after surgery R0 (Complete Resection): the entire tumor was successfully removed R1 (Microscopic Involvement): there is microscopic tumour left on the surgical margin R2 (Macroscopic Involvement): there is macroscopic (visible) tumour left on the surgical margin

Answer 212

Persistent chronic inflammation of the pancreas resulting in irreversible fibrosis and reduced function of the pancreas

Answer 213

Alcohol consumption Progression from acute pancreatitis Trauma Chronic kidney disease Cystic fibrosis Pancreatic cancer Hypertriglyceridemia

Answer 214

Alcohol, smoking, coeliac disease

Answer 215

Repeated bouts of acute pancreatitis can progress to chronic pancreatitis. With each bout of acute pancreatitis, there is ductal dilatation and damage to pancreatic tissue. Fibrotic tissue forms causing narrowing of ducts leading to stenosis.

Answer 216

Severe pain in epigastric region which can radiate to back Jaundice loss of exocrine function (no pancreatic enzymes secreted in GI tract, especially lipase) → steatorrhea loss of endocrine function (lack of insulin causing diabetes) signs of malabsorption

Answer 217

Fat soluble vitamin deficiency → ADEK

Answer 218

Faecal-elastase 1 → enzyme involved in fat digestion (low) faecal fat (high) pancreatic function tests (decreased function) → A combination of tests including amylase, lipase, glucose, and other markers to assess overall pancreatic function. Secretin-Stimulated Pancreatic Function Test: Measures pancreatic secretion in response to the hormone secretin, helping evaluate overall pancreatic function. ERCP for visualisation of ducts

Answer 219

X-ray/CT/MRI scan shows calcification of pancreas and dilated ducts

Answer 220

I GET SMASHED: Idiopathic Gallstones Ethanol (alcohol) Trauma Steroids Mumps Autoimmune Scorpion sting Hyperlipidaemia ERCP Drugs (diuretics)

Answer 221

1st line – control pain (analgesia, NSAIDs) and risk factors (less alcohol, less smoking, obesity) Replace pancreatic enzymes in deficiency (lipase), vitamin supplements. Insulin for diabetes. ECRP with stenting. Surgery to drain bile ducts

Answer 222

gallstones, alcohol, post-ERCP

Answer 223

pancreas releases exocrine enzymes which auto digest the pancreas.

Answer 224

Severe epigastric pain radiating to the back Vomiting abdominal tenderness Hypocalcaemia → The activated lipase, in particular, breaks down triglycerides (fats) into free fatty acids. These free fatty acids, in turn, bind to calcium ions in the bloodstream to form calcium soaps → less available free calcium in the blood

Answer 225

jaundice tachycardia Chvostek sign grey turner (flank bruising) Cullen sign (periumbilical bruising) signs of hypovolemia pleural effusion

Answer 226

cullen --> periumbilical bruising grey turner --> flank bruising

Answer 227

Dyspnoea, fever, nausea and vomiting, epigastric pain radiating to back

Answer 228

Serum amylase raised (3 times the upper limit level) FBC: leucocytosis (increase WBC count) with left shift (increase in immature WBCs) raised haematocrit → dehydration from vomiting (decreased plasma so more blood cells to plasma ratio) raised CRP Raised urea → kidney dysfunction, a potential complication of severe acute pancreatitis. low calcium Imaging: chest x-ray, abdominal USS (gallstones), CT scan (inflammation, necrosis, effusions)

Answer 229

Diagnosis needs 2 of 3: acute abdominal pain, elevated pancreatic enzymes (amylase/lipase), abnormal imaging

Answer 230

Serum lipase raised (3 times the upper limit level)

Answer 231

Glasgow score (severity of pancreatitis): PANCREAS mnemonic PaO2 low Age >55 Neutrophils raised Calcium low uRea raised Enzymes raised Albumin low Sugar raised

Answer 232

Abdominal aortic aneurysm, peptic ulcer disease, cholangitis, oesophageal spasm

Answer 233

1st line --> IV fluids, analgesia, nil by mouth, oxygen, antibiotics, electrolyte replacement. ERCP for gallstones, treat complications

Answer 234

Acute Respiratory Distress Syndrome – leading cause of death Sepsis Pancreatic pseudocyst Hypovolaemic shock from ruptured vessels DIC → coagulation factors released as inflammatory response → thrombosis Renal failure

Answer 235

Functional bowel disorder characterised by recurrent bouts of abdomen pain and abnormal bowel motility. No organic cause

Answer 236

More females, younger people

Answer 237

there is no cause

Answer 238

GI infections, previous severe and long-term diarrhoea, psychological (anxiety, depression, stress, trauma, abuse), eating disorders

Answer 239

IBS-C (constipation), IBS-D (diarrhoea), IBS-M (mixed, both D + C)

Answer 240

Abdominal pain, abnormal bowel motility, bloating, pain relieved by defaecation, altered stool form (diarrhoea, constipation), worse after eating, urgency, passage of mucus with stool

Answer 241

BY EXCLUSION Clinical diagnosis requires: a)abdominal pain + 2 of: - relieved by defaecation - altered stool form - altered bowel frequency. b) exclusion of: - infection (normal FBC, ESR/CRP) - IFD (Negative faecal calprotectin) - coeliac disease (no anti-TTG or anti-EMA) - Exclude cancer

Answer 242

1) Conservative: education, diet modification (small regular meals, increase fluids, avoid caffeine, low FODMAP diet, increase/decrease fibre for constipation/diarrhoea. FODMAP diet → a dietary approach designed to manage symptoms of IBS 2) Laxatives for constipation (senna, macrogol) Loperamide for diarrhoea Antispasmodics (buscopan, mebeverine) for pain and bloating 3) Severe IBS: tricyclic antidepressants (amitriptyline). Or SSRIs if they don’t work. Consider CBT FODMAPs = Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols → these are carbohydrates that can ferment in the gut and cause symptoms such as bloating, gas, abdominal pain, and altered bowel habits in some individuals. The low FODMAP diet involves restricting high-FODMAP foods for a specified period, followed by a structured reintroduction phase to identify specific triggers. Once trigger foods are identified, the diet can be personalized to include well-tolerated FODMAPs and avoid problematic ones.

Answer 243

key signs of acute cholangitis RUQ pain Jaundice Fever

Answer 244

key signs of very severe sepsis from acute cholangitis RUQ pain Jaundice Fever Confusion hypotension

Answer 245

Majority are adenocarcinoma of exocrine pancreas of ductal origin.

Answer 246

head of the pancreas or neck

Answer 247

Smoking, alcohol, diabetes, chronic pancreatitis, family history

Answer 248

Courvoisier sign = painless palpable gallbladder and jaundice → suggests that the jaundice is not due to gallstone but to obstruction pale stool and dark urine → high bilirubin that can’t be eliminated in poo Pruritis = itching to the elevated bilirubin in the blood Weight loss. Trousseau sign of malignancy = blood clots felt as small lumps under skin → indicates a hypercoagulable state which is often seen in malignancies

Answer 249

blood clots felt as small lumps under skin → indicates a hypercoagulable state which is often seen in malignancies

Answer 250

sign of pancreatic cancer painless palpable gallbladder and jaundice → suggests that the jaundice is not due to gallstone but to obstruction

Answer 251

1st line: Abdominal ultrasound + Pancreatic CT protocol (pancreatic mass) gold standard: biopsy

Answer 252

1st line – surgical resection (Whipple) Palliative therapy

Answer 253

Reflux of gastric contents into the stomach due to reduced pressure across the lower oesophageal sphincter causing inflammation of the oesophagus Decreased pressure across lower oesophageal sphincter makes it easier for gastric contents and acid to pass up into the oesophagus

Answer 254

Obesity, pregnancy, hiatal hernia, smoking, NSAIDs, caffeine, alcohol

Answer 255

Heartburn epigastric or retrosternal pain acid regurgitation (worse when lying down, related to meals, relieved by antacids) Dysphagia dyspepsia (indigestion) chronic cough, nocturnal asthma, laryngitis, dental erosion

Answer 256

dysphagia age >55 weight loss upper abdominal pain/reflux treatment-resistant dyspepsia nausea and vomiting low haemoglobin raised platelet count

Answer 257

go straight to PPI if no red flags if there are red flags: ENDOSCOPY

Answer 258

24-hour pH ambulatory monitor (pH <4 more than 4% of the time = abnormal)

Answer 259

oesophageal manometry --> catheter passed into the oesophagus and detects oesophageal and sphincter contractions

Answer 260

1. Conservative – stop smoking, stop alcohol, lose weight, eat smaller meals, avoid eating 3-4 hours before sleep, change sleeping position (more upright) 2. Medical – proton pump inhibitor (omeprazole, lansoprazole), H2 receptor antagonist (antihistamine which reduces stomach acid, e.g., ranitidine). Over-the-counter alginates (Gaviscon) for symptom relief 3. Surgery – Nissen fundoplication (tying the fundus of the stomach around the LOS to narrow it)

Answer 261

oesophageal adenocarcinoma

Answer 262

Tear of the oesophageal mucosal membrane due to sudden increases in intra-abdominal pressure

Answer 263

Forceful vomiting (alcoholism, bulimia), chronic coughing, weightlifting, hiatal hernia, retching

Answer 264

Haematemesis after retching Hx, melaena, hypovolemic shock (hypotension, dizziness), dysphagia. No Hx of liver disease or portal hypertension

Answer 265

2/3 of the distance between the umbilicus and the ASIS

Answer 266

most commonly due to obstruction of the lumen of the appendix by FAECOLITH (calcified faecal deposits), or infection and inflammation of the lymphoid tissue (LYMPHOID HYPERPLASIA, IBD) it can also be due to foreign bodies PATHOPHYSIO: Obstruction of the lumen of the appendix leads to stasis > bacterial overgrowth > inflammation. Obstruction leads to increased pressure in the appendix which can cause rupture.

Answer 267

Rovsing's Sign: palpation (pressing down) on the left lower quadrant of the abdomen causes pain in the right lower quadrant. Psoas Sign: Pain in the right lower quadrant is elicited when the patient extends the right hip against resistance or when the right hip is passively extended → The psoas is right next to the appendix Obturator Sign: Pain in the right lower quadrant is felt when the right hip is flexed and internally rotated. → the obturator is right next to the appendix Guarding: Involuntary tensing or contraction of the abdominal muscles in response to palpation or movement. Rebound Tenderness: Pain is experienced when pressure is released after palpating the abdomen → suggests peritoneal inflammation

Answer 268

sign of appendicitis palpation (pressing down) on the left lower quadrant of the abdomen causes pain in the right lower quadrant.

Answer 269

Abdominal CT with contrast

Answer 270

antibiotics and laparoscopic appendectomy

Answer 271

hepatic stellate cells

Answer 272

Pre-hepatic: portal vein obstruction (thrombus) Intrahepatic: cirrhosis, sarcoidosis, schistosomiasis Post-hepatic: right heart failure, constrictive pericarditis, Budd Chiari syndrome (hepatic vein obstruction)

Answer 273

freshwater parasite which affects liver, urinary bladder, intestines etc.

Answer 274

multisystem inflammatory disorder characterised by the formation of granulomas

Answer 275

Venous blood accumulates in the portal system, raising pressure above 5-10mmHg. This leads to the formation of portosystemic shunts where blood is directed away from the portal system and into systemic veins → liver receives less blood → reduced liver function (increased toxic products in the blood like ammonia which can cross BBB and cause hepatic encephalopathy).

Answer 276

oesophageal veins --> oesophageal varices paraumbilical veins

Answer 277

Ascites caput medusae → paraumbilical veins close when you are born and turn into ligaments but in the presence of portal hypertension they may reopen to offer an alternative pathway to bypass the liver GI bleeding from esophageal varices Haemoptysis melaena/hematochezia (passage of bright red blood through the rectum) Jaundice Pruritus hepatic encephalopathy (asterixis, altered consciousness, lethargy, seizure, coma) Gynecomastia Palmar erythema Spider naevi Splenomegaly

Answer 278

1st line Liver USS (nodules = cirrhosis), CT/MRI scan (ascites, cirrhosis, splenomegaly), endoscopy (oesophageal varices). Labs (FBC, LFT, serology may identify cause) gold standard Hepatic venous pressure gradient measurement (difference in pressure between IVC and portal vein)

Answer 279

paracentesis

Answer 280

Treat underlying disease → lifestyle modifications Beta blockers → to reduce portal pressure; they reduce HR so they reduce CO and the consequential pressure on the venous system Management of esophageal varices: sclerotherapy or endoscopic variceal ligation Diuretics Management of hepatic encephalopathy (lactulose, enemas, antibiotics) Transjugular intrahepatic portosystemic shunt

Answer 281

Hepatic encephalopathy, spontaneous bacterial peritonitis, Ascites, bleeding (oesophageal varices), caput medusae, diminished liver function, enlarged spleen

Answer 282

Alpha-fetoprotein → marker for liver cancer

Answer 283

Cirrhosis, congestive heart failure, peritonitis, malignancy, nephrotic syndrome

Answer 284

Excessive build-up of fluid in the peritoneal cavity. Poor liver function = low albumin = low blood oncotic pressure = fluid loss into the peritoneal cavity

Answer 285

Distended large abdomen, shifting dullness: percuss abdomen and observe dullness over fluid and resonance over air. Supine = central abdomen resonant as bowel floats, flanks dull as fluid collects. Lying on side = flank resonant as fluid moves to other side

Answer 286

1st line Shifting dullness on examination. WBC count Ascites tap: abdominal paracentesis → for protein measurement gold standard Abdominal ultrasound (fluid in peritoneal cavity)

Answer 287

Ascites tap: abdominal paracentesis → for protein measurement If Protein <25g/dL: Indicates a low protein concentration in the ascitic fluid. Typically associated with transudative ascites. Implies that there is not enough protein being synthesized by the liver. Possible causes: cirrhosis and heart failure If Protein >25g/dL: Indicates a higher protein concentration in the ascitic fluid. Typically associated with exudative ascites. Suggests that proteins, including inflammatory markers, have leaked from blood vessels into the peritoneal cavity due to increased permeability. Possible causes: nephrotic syndrome Peritonitis Malignancy TB

Answer 288

transudate is due to decreased oncotic pressure or increased hydrostatic pressure and results in plasma leaking in body cavities --> associated with portal hypertension, hypoalbuminea, heart failure exudate is due to inflammation which causes leaky capillaries so you get fluid full of proteins and vessel contents in body cavities --> associated with infections, cancers, inflammation, autoimmune conditions

Answer 289

Management of Ascites Fluid and salt restriction Diuretics: spironolactone ± furosemide (can be given together because spironolactone causes hyperkalemia and furosemide causes hypokalemia → they cancel each other out) Large-volume paracentesis Albumin Trans-jugular intrahepatic portosystemic shunt

Answer 290

spontaneous bacterial peritonitis

Answer 291

paracetamol OD N-acetylcysteine

Answer 292

Acute liver disease is most common cause Non-alcoholic fatty liver disease. Drugs: paracetamol, alcohol. Viral infection: hepatitis, Epstein Barr virus. Autoimmune hepatitis. Neoplastic: hepatocellular or metastatic carcinoma. Metabolic: Wilson’s disease, alpha 1 antitrypsin, haemochromatosis, NAFL. Vascular: Budd-Chiari syndrome → blockage of hepatic vein by a thrombus (hepatic vein thrombosis) which leads to liver congestion Congestive hepatopathy → Liver damage resulting from congestive heart failure

Answer 293

Chronic alcohol abuse, female, chronic hepatitis

Answer 294

Alcohol, obesity, T2DM, drugs, metabolic disease

Answer 295

decreased synthesis of albumin → lower oncotic pressure Portal hypertension → triggers vasodilation of splanchnic circulation (intestinal circulation) to redistribute blood away from liver → more fluid in abdominal vessels coupled with decreased oncotic pressure from decreased albumin Reduced blood flow to kidneys → activated RAAS → water retention Generalised inflammation increases blood vessel permeability

Answer 296

compensated, with some preserved liver function → asymptomatic decompensated which causes end-stage liver failure. → patient gets COAGULOPATHY, JAUNDICE, ENCEPHALOPATHY, ASCITES, UPPER GI BLEEDING

Answer 297

COAGULOPATHY, JAUNDICE, ENCEPHALOPATHY, ASCITES, UPPER GI BLEEDING

Answer 298

Jaundice Ascites → due to less albumin synthesis abnormal bleeding hepatic encephalopathy (confusion, altered mood, asterixis (liver flap), comatose) low serum albumin Hepatomegaly

Answer 299

Inflammation Fibrosis → reversible damage Cirrhosis → irreversible damage

Answer 300

Portal hypertension oesophageal varices (enlarged veins) caput medusae (cluster of swollen veins in abdomen) spider naevi palmar erythema Gynecomastia Clubbing fetor hepatis (sweet musty rotten egg garlic breath) → presence of certain sulfur-containing compounds that are produced in the intestines by bacteria due to impaired liver function; bacteria have to take over metabolism of ammonia Dupuytren’s contracture Malaise Nausea Vomiting abdominal pain Pruritis bleeding

Answer 301

LFTs (all raised): Bilirubin PT/INR serum AST + ALT AST/ALT Ratio AST/Platelet Ratio NH3 → liver should convert NH3 to urea GGT all raised → enzyme in liver and bile duct (inidcates inflammation of liver and bile) Serum albumin and glucose decreased. FBC: Anaemia Thrombocytopenia → liver helps make thrombopoietin leukopenia U&E: urea and creatinine raised → severe liver injury can impair blood flow to kidneys deranged electrolytes Bilirubin - hyperbilirubinemia in decompensated cirrhosis

Answer 302

thrombocytopenia

Answer 303

Liver biopsy (distortion of liver parenchyma)

Answer 304

blood cultures toxicology screen

Answer 305

1st line – prevent progression, lifestyle monitoring (less alcohol, reduce BMI) Antiviral therapy in viral hepatitis liver transplant (MELD score – model for end-stage liver disease. Assesses severity and transplant likelihood Manage complications: hepatic encephalopathy --> lactulose ascites --> diuretics bleeding --> vit K cerebral oedema --> mannitol Hyperglycaemia --> dextrose

Answer 306

dextrose + possible diabetes management

Answer 307

Malnutrition - increased use of muscle tissue as fuel (impaired glycogen storage and gluconeogenesis) + reduced protein available (form impaired liver metabolism) Portal Hypertension, Varices and Variceal Bleeding Ascites and Spontaneous Bacterial Peritonitis (SBP) Hepato-renal Syndrome Hepatic Encephalopathy Hepatocellular Carcinoma Hyponatraemia Cerebral oedema → mannitol AKI → acute kidney injury Acute-on-chronic liver failure Coagulopathy (Vit K def)

Answer 308

1st line – intensive care management, ABCDE, fluids analgesia. Assessment for liver transplant. Treat underlying causes and complications, e.g., paracetamol overdose with N-acetylcysteine

Answer 309

Vit K + FFP (fresh frozen plasma)

Answer 310

Alcoholic liver disease, non-alcoholic fatty liver disease, hepatitis B, hepatitis C

Answer 311

liver biopsy

Answer 312

Child-Pugh score Involves - bilirubin, albumin, INR, ascites, encephalopathy.

Answer 313

MELD score: model for end-stage liver disease. Gives 3 month mortality estimate and liver transplant advice

Answer 314

Pathogens enters body via GI → liver is first filter to infections → needs a lot of leukocytes so that it can eliminate the pathogens effectively liver patients have an impaired reticulo-endothelial function and reduced opsonic activity and leucocyte function

Answer 315

Chronic inflammatory liver disorder which causes a chronic relapsing hepatitis

Answer 316

PBC, PSC, Autoimmune hepatitis

Answer 317

Female, genetic predisposition, immune dysfunction, other autoimmune conditions, HLA loci → HLA-DR3/DR4

Answer 318

Type 1: occurs in adults, typically women. Type 2: occurs in children.

Answer 319

Anti-nuclear antibodies → Antibodies targeted against nuclear proteins and/or DNA anti-smooth muscle antibodies → Antibodies targeted against actin, tubulin and other proteins anti-soluble liver antigen

Answer 320

Anti-liver kidney microsomes-1. → Antibodies targeted against subcellular vesicles that are derived from the endoplasmic reticulum (ER). They contain various enzymes involved in drug metabolism and detoxification, particularly the cytochrome P450 enzymes. Anti-liver cytosol antigen type-1.

Answer 321

25% asymptomatic the rest present with either acute hepatitis or chronic liver disease rarely they can present directly with acute liver failure acute hep presentation: Jaundice RUQ pain Hepatomegaly Malaise fatigue fever chronic liver disease presentation: Non-specific features: anorexia, nausea, weight loss, amenorrhoea, arthralgia or arthritis, acne, unexplained fever Stigmata of chronic liver disease: hepatomegaly, splenomegaly, palmar erythema, spider naevi Complications of cirrhosis (i.e. decompensation): ascites, hepatic encephalopathy, jaundice, GI bleeding acute liver failure presentation: Jaundice + Confusion + Coagulopathy in absence underlying liver disease

Answer 322

Jaundice RUQ pain Hepatomegaly Malaise fatigue fever

Answer 323

Jaundice + Confusion + Coagulopathy in absence underlying liver disease

Answer 324

Primary biliary cirrhosis Primary sclerosing cholangitis Inflammatory bowel disease Coeliac disease Thyroiditis Rheumatoid arthritis Other connective tissue diseases

Answer 325

use of IAIHG scoring system it includes: 1) Gender: female more likely 2) ALP/AST ratio → indicator of cholestatic liver damage because ALP is marker for bile duct enzymes and bone whereas AST is general marker for liver damage and damage to other tissues. AST should generally be higher than ALP because it is in more tissue. If ALP is higher it indicates bile obstruction or primary biliary cholangitis. If the ratio is normal it simply excludes bile duct involvement 3) Serum immunoglobulins + Serum IgG → marker for the activation of the immune system and antibodies against liver; IgG is quite specific for liver antibodies 4) Antibodies: Type 1 autoimmune hepatitis (adult): ANA: antinuclear antibodies SMA: anti smooth muscle antibodies Type 2 (kid): LKM: anti liver-kidney microsomes 5) Drug use history 6) Average daily alcohol intake 7) Histological findings from liver biopsy → liver biopsy done with percutaneous or transjugular approach 8) Other autoimmune disease 9) AMA → antimitochondrial antibodies → highly specific for PBC 10) Hepatitis viral markers → to exclude viral hepatitis

Answer 326

1st line immunosuppression with corticosteroid and immunosuppressant prednisolone + azathioprine 2nd line liver transplant

Answer 327

hepatocellular carcinoma osteoporosis due to steroids: DEXA scan

Answer 328

autoimmune T-cell mediated attack of interlobular bile ducts which results in inflammation

Answer 329

PBC more common females PSC - males

Answer 330

Female, age 45-60, smoking, other autoimmune disease, rheumatoid diseases

Answer 331

cholesterol deposits in the skin (xanthelasma)

Answer 332

Immune system attacks small interlobular bile ducts in the liver which obstructs bile outflow causing cholestasis. Bile acids, bilirubin and cholesterol build up in the blood as they aren’t being excreted. Bile acids cause itching, bilirubin cause jaundice and cholesterol causes deposits in the skin (xanthelasma) and blood vessels. The back-pressure of the bile obstruction and overall disease process leads to fibrosis, cirrhosis, and liver failure.

Answer 333

Pruritis, fatigue, Jaundice, xanthelasma signs: Pale stools, signs of cirrhosis (hepatomegaly, ascites, spider naevi) symptoms: Abdominal pain, joint pain

Answer 334

1st line LFT bilirubin ALP ALT GGT albumin ultrasound gold standard: AMA --> anti-microbial antibodies

Answer 335

1st line: Ursodeoxycholic acid (bile acid analogue reduces intestinal absorption of cholesterol). Cholestyramine (bile acid sequestrant) for pruritis. Cholestyramine binds to bile acids in the intestine, forming complexes that are then excreted in the feces → decreases bile acid reabsorption → liver uses more cholesterol to synthesise new bile acids (less xanthelasma) + reduces bile acids overall and decreases itching Liver transplant if severe

Answer 336

Liver cirrhosis, portal hypertension, steatorrhea, osteoporosis, hypercholesterolaemia

Answer 337

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts, resulting in strictured ‘beaded’ appearance of bile ducts.

Answer 338

Male, aged 40-50, heavily associated with IBD especially ulcerative colitis

Answer 339

Inflammation of intrahepatic and extrahepatic bile ducts leads to fibrosis and stricturing. This obstructs bile flow causing cholestasis. The biliary strictures lead to build up of bile acids and bilirubin in the blood causing pruritus and jaundice. Ongoing strictures eventually lead to fibrosis, cirrhosis, and liver failure.

Answer 340

Pruritus, fatigue Charcot’s triad: RUQ abdominal pain, fever, jaundice hepatomegaly, IBD signs and symptoms

Answer 341

an acute infection of the bile ducts. In ascending cholangitis, bacteria from the intestines can ascend into the bile ducts, causing infection, inflammation, and obstruction. the three most key symptoms are from Charcot's triad: fever, RUQ pain, jaundice

Answer 342

1st line LFTs: raised bilirubin, ALP, AST and ALT, GGT. Decreased albumin. Serology: no antimicrobial antibodies (AMA), maybe pANCA antibodies gold standard MRCP (magnetic resonance cholangiopancreatography) – shows bile duct strictures or lesions MRCP is required for diagnosis!!!

Answer 343

cholestyramine for pruritus Liver transplant

Answer 344

Portal hypertension, cirrhosis, cholangiocarcinoma, colorectal cancer (risk from IBD), hepatic encephalopathy especially worried about cholangiocarcinoma and colorectal cancer

Answer 345

PBS PSC can't be treated

Answer 346

Metabolic liver disease with evidence of hepatic steatosis (fat build up) which is not a secondary cause of alcohol consumption. Stages: non-alcoholic steatosis, non-alcoholic steatohepatitis, fibrosis, cirrhosis

Answer 347

Metabolic syndrome: obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia

Answer 348

either asymptomatic or with very severe symptoms of liver failure hepatomegaly jaundice ascites RUQ pain absence of chronic alcohol consumption

Answer 349

1st line Deranged LFTs: increased PT/INR, low albumin, increased bilirubin, increased AST and ALT, increased GGT FBC: anaemia, thrombocytopenia. Lipid profile (raised LDL, cholesterol, triglyceride) Liver ultrasound (fatty infiltrates) gold standard Liver biopsy (steatosis, inflammation, fibrosis) Child Pugh score

Answer 350

1st line – treat underlying cause and reduce risks (lose weight, exercise, smoking, control diabetes, LDL). Medications: Pioglitazone → improves insulin sensitivity (improves fat levels in the blood which is a concern) vitamin E → excess fat can cause oxidative damage in NAFL, and vit E is an antioxidant Statins ACEi. end stage: liver transplant

Answer 351

Main cause of liver disease and failure

Answer 352

asymptomatic in early stages later: abdominal pain, hepatomegaly, jaundice, spider naevi (cluster of minute blood vessels under skin), alcohol dependency Palmar erythema, dupuytren’s contracture (fingers bend towards palm of hand), ascites, hepatic encephalopathy, caput medusae (enlarged superficial epigastric veins), bruising, asterixis (flapping tremor), gynecomastia

Answer 353

1st line: LFTS: Gamma-glutamyl transferase (raised), AST and ALT (transaminases - raised), AST:ALT (ratio>2), ALP (alkaline phosphatase - raised), bilirubin (raised), albumin (low), FBC: anaemia, thrombocytosis, high MCV gold standard: Liver biopsy: steatosis, inflammation, Mallory bodies

Answer 354

Mallory bodies

Answer 355

CAGE AUDIT

Answer 356

Completely stopping alcohol consumption. Give chlordiazepoxide for delirium tremens – alcohol withdrawal (tremors, agitation, ataxia, disorientation) Also: weight loss, stop smoking corticosteroids for alcoholic hepatitis (prednisolone) liver transplant if severe (must abstain from alcohol for 3 months first)

Answer 357

Wernicke-Korsakoff syndrome (thiamine deficiency), hepatic encephalopathy, renal failure, hepatocellular carcinoma, portal hypertension

Answer 358

haemochromatosis as a result of transfusions, hep B and C, NAFLD

Answer 359

mainly FAECES other ways include bleeding (sloughing of intestinal cells, menstruation etc.)

Answer 360

indicates past Hep A infection or vaccination IgM Antibodies: Early Infection Marker: IgM antibodies are often the first antibodies to appear in response to a new infection. The presence of IgM antibodies suggests an acute or recent infection. IgG Antibodies: Late Infection Marker: IgG antibodies usually appear later in the course of an infection. The presence of IgG antibodies, especially in the absence of IgM antibodies, may suggest a past or resolved infection. IgG antibodies can persist in the bloodstream for a more extended period, providing a marker of previous exposure or vaccination.

Answer 361

hepatic: Brain infection due to toxic metabolites (especially ammonia) not removed by the liver due to liver dysfunction can be due to liver cirrhosis and liver failure Wernicke's: it is specifically due to thiamine (vit B1) deficiency is due to excess alcohol, malnutrition or impaired absorption of thiamine

Answer 362

Thiamine deficiency impairs glucose metabolism, decreasing cellular energy. Brain is vulnerable to impaired glucose. Alcohol reduces thiamine by interfering with thiamine conversion to its active form, preventing absorption, causes cirrhosis which interferes with thiamine storage in liver

Answer 363

Ammonia is produced by intestinal bacteria when they break down proteins and is absorbed in the gut. Ammonia builds up in the blood in patients with cirrhosis because liver impairment prevents hepatocytes from metabolising ammonia into harmless waste products, and collateral vessels between the portal and systemic circulation mean that ammonia bypasses the liver and enters systemic circulation directly.

Answer 364

Reduced consciousness, confusion, stupor, coma, changes to personality mood and memory. Asterixis → clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements rigidity, hypokinesia.

Answer 365

investigations Blood ammonia raised, abnormal LFTs, EEG (decrease in brain wave frequency and amplitude), U&E (maybe hyponatraemia or hypokalaemia) management Laxatives (e.g., lactulose) promote excretion of ammonia from gut before it is absorbed. Antibiotics (e.g., rifaximin) reduce the number of intestinal bacteria which produce ammonia. Nutritional support, e.g., nasogastric feeding

Answer 366

Wernicke’s: confusion, apathy, difficulty concentrating, ophthalmoplegia weakness and paralysis of eye muscles, ataxia – difficulty with coordinated movement. Korsakoff: severe memory impairment (anterograde and retrograde), confabulation (creates stories to fill in memory gaps), behavioural changes

Answer 367

korsakoff syndrome

Answer 368

investigations: thiamine levels decreased, LFTs deranged, MRI degeneration of mammillary bodies management: IV thiamine infusion (pabrinex). Can be given with glucose, magnesium, and multivitamins

Answer 369

1st line Bloods, urine dipstick (rule out UTI), serum amylase + lipase (rule out pancreatitis), ECG if heart suspicion. Gold standard CT abdomen

Answer 370

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

Answer 371

severe malabsorption (of two or more substances) accompanied by diarrhoea and malnutrition usually happens to residents or visitors to tropical areas

Answer 372

Abd ultrasound

Answer 373

B most patients die of sepsis because if they have a cirrhosed liver they are already immunocompromised and GI bacteria can translate to blood and to liver more easily 1st line treatment is: terlipressin (vasoconstriction) + co-amoxiclav

Answer 374

10th costal cartilage

Answer 375

transpyloric plane: between left and right 9th costal cartilages crosses the pylorus of the stomach, the gallbladder, the pancreas and the hila of the kidney

Answer 376

between the right and left iliac crests

Answer 377

somatic T7-T11 subcostal nerve (T12) Iliohypogastric and ilioingunal nerve from L1

Answer 378

adrenal glands, aorta, kidneys, oesophagus, ureters, pancreas, duodenum, ascending and descending colon, rectum

Answer 379

umbilical arteries

Answer 380

oesophageal hiatus - T10 IVC - T8 Aorta - T12

Answer 381

oesophageal arteries from aorta + left gastric arteries drainage: left gastric vein azygous veins

Answer 382

SMA jejunal artery ileal artery ileocolic artery right colic middle colic IMA left colic artery --> anastomoses with the middle colic via marginal artery sigmoid artery superior rectal artery

Answer 383

spelling vein joins inferior mesenteric veins which then join the superior mesenteric and form the portal vein which breaks into smaller and smaller veins. all of the central veins then join into the hepatic vein which joins the IVC

Answer 384

parasympathetic: vagus sympathetic: T5-T9

Answer 385

1st half from the coeliac trunk (gastro-duodenal artery) and the second half from SMA (inferior pancreatico-duodenal artery) (this is because the duodenum has 2 embryological origins; first half is from the foregut and the second half is from the midgut)

Answer 386

Jejunum - lots of plicae circulares; ileum also has but much less Ileum - payer's patches (submucosal lymph nodes)

Answer 387

embryological remnant of the connection between the midgut and the yolk sac --> how the baby was fed (remnant of the vitelline duct)

Answer 388

haustra, taeniae coli, epiploic appendages

Answer 389

ligament between transverse colon and diaphragm at the splenic flexure

Answer 390

foregut sympathetic + visceral sensory- great splanchnic from T5-T9 parasympathetic - vagus midgut s + vs- lesser splanchnic T10-11 p - vagus hindgut s + vs - least T12 p - pelvic splanchnic S2-4

Answer 391

the entrance to the lesser sac; lies behind the portal triad and the lesser omentum

Answer 392

it is at the end of the falciform ligament inferior to the liver and it is the remnant of the umbilical vein

Answer 393

ductus venosus becomes the ligamentum venosum in the adult function of the ductus venosus is to shunt blood from umbilical vein straight to the IVC instead of through the liver because the umbilical vein carries very oxygenated blood from the mother --> you want to take that blood to systemic circulation and bypass the liver

Answer 394

gastroduodenal artery from coeliac trunk splits into the anterior and posterior superior pancreaticoduodenal arteries the SMA has the inferior anterior and posterior pancreatico-duodenal branches the splenic artery from the coeliac supplies the body of the pancreas

Answer 395

the circular muscle around the hepatopancreatic ampulla which leads to the major duodenal papilla

Answer 396

papilla = lump sphincter = muscle ampulla = opening

Answer 397

vomer ethmoid septal cartilage