GI Flashcards
What are 3 emergency causes of haematemesis in order of frequency?
Duodenal ulcer
Gastric ulcer
Oesophageal varices
What are 5 non-emergency causes of haematemesis?
Oesophagitis - reflux, bisphosphonates, toxins, Crohn’s, candida
Mallory-Weiss tear
Gastric carcinoma
5 important questions in haematemesis history
Timing, frequency, volume Smoking, alcohol Medical history Dyspepsia, dysphagia, odynophagia Steroids, NSAIDs, bisphosphonates, anticoagulants
Signs on haematemesis exam
Telangiectasia
Liver stigmata - jaundice, hepatosplenomegaly, spider naevi, ascites, palmar erythema
Epigastric tenderness (PUD, gastritis)
Investigations haematemesis
FBC - anaemia, low platelets if hypersplenism from portal hypertension (varices)
High urea:creatinine ratio = upper GI bleed
LFT - liver damage
Group and save and 4u crossmatched
OGD - immediately after resus if emergency, in 24h if not
CT abdo with IV contrast if endoscopy unremarkable or too unwell
Erect CXR for perforated ulcer - pneumoperitoneum
H pylori - PUD
ABG - hypoperfusion
What are the 2 scoring systems for upper GI bleed and what is it for?
Glasgow-Blatchford Bleeding score:
1. FBC - urea, Hb
2. Obs - pulse, systolic bp
3. Sx - melaena, syncope
4. Hx - known hepatic or cardiac failure
Associated with >risk of intervention need
Rockfall score - severity for GI bleed post-endoscopy
Resus for haematemesis
Transfuse blood, platelets, clotting factors according to local massive bleed protocol
Platelet transfusion if <50 and active bleeding
FFP if active and APTT>1.5
Prothrombin complex if activebleeding and warfarin
Recombinant factor VIIa if all else failed
Manage non-variceal upper GI bleed
Endoscopic: - Clips +- adrenaline - Or thermal coagulation with adrenaline - Or fibrin/thrombin with adrenaline PPI if stigmata of recent haemorrhage seen on endoscopy
Manage variceal upper GI bleed
Terlipressin until haemostats is achieved or 5d
Abx prophylaxis if suspected
Band ligation for oesophageal, and TIPS if not successful
Endoscopic injection if gastric, then TIPS if not successful
Long term B blockers
GI bleeding control and prevention if on anticoagulants
Continue low dose aspirin once haemostasis achieved
Stop NSAIDs during acute phase
Consider stopping clopidogrel - seek specialist advice
Likely causes of diarrhoea with blood and mucus
Inflammation - UC, radiation, bacterial, pseudomembranous colitis
Acute gastroenteritis - campylobacter, shigella, E. coli
Likely cause of pale and greasy stools
Malabsorption - SI disease, pancreatic insufficiency
- coeliac disease fhx
- alcohol
Likely cause of diarrhoea with nausea and vomiting
Enteritis, chronic pancreatitis
Likely cause of diarrhoea with joint pain, skin damage, uveitis
IBD
Hypomotility and malabsorption in bowels
Scleroderma
Jaundice and steatthoroea
Pancreatitis or pancreatic carcinoma
Important drug history in diarrhoea
Colchicine, metformin, digoxin = GI ADR
Purgatives
Broad spectrum abx (penicillin, cephalosporins) = C diff - pseudomembranous colitis
Important medical history in diarrhoea
Vagotomy in GI surgery = diarrhoea
GI resection = reduced motility and absorption
Radiotherapy on abdo/pelvis = GI ADR for years
Systemic conditions: DM - neuropathy, collagen, vascular disease
HIV = atypical infections ie cryptosporidium and CMV
Diarrhoea and dehydration on exam
Acute onset
IBD
VIP-oma - lose electrolyte-rich fluid in large quantities
Diarrhoea and pallor on exam
IBD/malignancy = blood loss
Anaemia of chronic disease
Iron and vit B/folate deficiency in malabsorption
Weight loss and diarrhoea
Malignancy or malabsorption
3 IBD findings on exam
Aphthous ulcers, pyoderma gangrenosum, uveitis
1 thyrotoxicosis finding on exam
Proptosis or exophthalmos
1 adrenal insufficiency finding on exam
Pigmentation
1 diabetes finding on exam
Peripheral neuropathy
Skin colour changes on GI exam for diarrhoea
Radiation enteritis
RIF mass on exam for diarrhoea
Crohn’s or caecel carcinoma
Diarrhoea and low urea
Malabsorption or malnutrition
Diarrhoea and high urea
Dehydrated or melaena
Urine dipstick for diarrhoea
5-hydroxyindoleacetic acid (5-HIAA) = metabolite of serotonin = carcinoid syndrome
LFT for diarrhoea
Pancreatic insufficiency or alcohol excess
Primary care investigations for diarrhoea
FBC (deficiencies - calcium, B12, folate, ferritin), coeliac screen (IgA tissue transglutaminase antibody (t-TGA) or IgA endomysial antibody (EMA)), U&E, LFT, thyroid, ESR, CRP, urine dipstick, stool culture
3 possible stool culture findings in diarrhoea
Ova and cysts in giardia - 3 specimens 2-3 days apart due to intermittent shedding
C diff if recent abx or nursing home resident
Viruses if immunosuppressed
Imaging for diarrhoea
Flexible sigmoidoscopy if <45y/o or colonoscopy if >45y/o, +- biopsy: mucosal inflammation, rectosigmoid carcinoma or polyps, melanosis coli in purgative abuse
Others:
Abdo x-ray for faecal impaction or megacolon (UC and very unwell)
Small bowel barium study/enema/colonoscopy if blood or anaemia - IBD
Duodenal biopsy if steatthorea and folate deficiency - coeliac
Breath test for bacterial overgrowth (H pylori) if steatthoea, low B12, normal folate
Red flag symptoms for diarrhoea
Unintentional or unexplained weight loss Rectal bleeding >6 weeks in >60y/o Abdominal or rectal mass Anaemia Raised inflammatory markers Family history or bowel or ovarian cancer
Diverticular disease - what is it and symptoms
Mucosal outpouchings in descending and sigmoid colon
Painless heavy self limiting bleeds
Haemorrhoids - what is it and symptoms
Enlarged vascular cushions in the anal canal
Cause mass and priorities
Fresh blood separate from stool
Painful when thrombosed
Malignancy symptoms with rectal bleeding
Other GI symptoms, weight loss
Family history
No focal anal symptoms
dark red blood mixed with stool
6 questions in rectal bleeding history
Pain - wake at night, increase or decrease with defecation
Mucus
Previous episodes
Haematemesis
Family history of cancer or IBD
Nature - colour, duration, frequency, relation to stool
Rectal bleeding examination findings and suggestions
General - anaemia, cachexia, lymphadenopathy
Mass = constipation from haemorrhoid with fissure
LIF tenderness +- guarding = inflammed diverticulae
Perianal lesions or skin tags = thrombosed haemorrhoids
Discharge = IBD or anorectal carcinoma
Increased tone and pain on DRE = fissure
Mass on DRE = rectal polyp or carcinoma
Investigations for rectal bleeding and indications
Proctoscopy for position of haemorrhoids or anal fissure
Rigid sigmoidoscopy for suspicious lesions 15-20cm from anal margin - carcinoma, IBD
Flexible sigmoidoscopy for left colon malignancy
Full colonoscopy and angiogram to identify bleeeding vessel +- arterial embolisation
Emergency OGD and CT angiogram if haemodynamically unstable
Others: FBC, U&E, LFT, coag, g&s, stool culture
Where is the cause of rectal bleeding likely to be depending where blood is in relation to stool?
Mixed and dark red = higher up - polyps, cancer, angiodysplasia, inflammatory
Separate from stool = low rectal +- mucus - anorectal carcinoma, diverticular disease, haemorrhoids, IBD
Spotting = haemorrhoids, anal tear
8 symptoms of IBS
LIF pain, relieved by passing wind and defecation Rectal dissatisfaction Distension and sensation of bloating with no obstruction Strain/urgency Symptoms worse after meals Mucus Pain Change in bowel habit
4 non-GI symptoms of IBS
Dysparaunia
Urinary symptoms
Fatigue
Anxiety and depression
Things to check in IBS history
No: weight loss, night symptoms, not acute onset, rectal bleeding, not >50y/o
3 IBS theories
Abnormal GI sensation or motility
Abnormal bowel flora
Altered GI serotonin signalling
Treat IBS: 4 advice and 4 medication
- Reassure and explain
- Try excluding certain foods
- Increase fibre and fluids if constipated
- Hypnotherapy, exercise and relaxation
- Anti-spasmodic - mebeverine
- Anti-motility - loperamide
- Laxative - bisacodyl
- Treat depression - TCA for pain
Blood supply to colon, 3 on each side
Right - ileocaecal, right colic, middle colic
Left - marginal, left colic, sigmoid arteries
What are the brought categories of causes of jaundice and what form is the bilirubin in for each?
Pre-hepatic = unconjugated Intra-hepatic = mixed Post-hepatic = conjugated
What is the process of heme breakdown and where is it done?
Spleen/macrophages: heme + heme oxygenase = biliverdin
+ biliverdin reductase = bilirubin (unconjugated and insoluble, bound to albumin)
Through sinusoids to hepatocytes in liver
Unconjugated bilirubin + glucuronic acid = conjugated bilirubin (water soluble)
Through biliary system into SI, + bacterial proteases = urobilinogen
90% = reduced to sterocobilinogen/oxidised to stercobilin = pigment in faeces
10% through portal vein to liver, then to kidney = urobilin (pigment) and to urine
What is the enterohepatic urobilinogen cycle?
Conjugated bilirubin is metabolised by bacterial proteasese to 90% urobilinogen reduced to stercobilin, oxidised to stercobilinogen which is the pigment in faeces
What happens to urobilinogen as a result of biliary obstruction?
Less conjugated bilirubin enters SI so lower levels of urobilin and stercobilin. Conjugated bilirubin enters blood stream and secreted by kidneys, so dark urine and pale stools
What are 2 main causes of dark urine and pale stools?
Cholestasis - less conjugated bilirubin enters SI
Reduced intestinal flora by broad spectrum abx - less conjugated bilirubin metabolised
What are 3 causes of reduced urobilinogen in urine?
Obstruction - reduce bilirubin in SI
Abx - reduced bacterial flora to metabolise bilirubin
Drugs that acidify urine ie ascorbic acid (vit c)
How are post-hepatic and hepatic causes of jaundice differentiated?
USS - dilated bile ducts = obstruction ie gall stones
What sign is seen on examination for haemolytic anaemia?
Haemosiderin deposits on lower legs
What localised conditions are associated with haemosiderin deposits? Name 4
Venous eczema
Venous ulcers
Dermatitis
DVT
Where is pre-hepatic jaundice caused?
Spleen and blood vessels
Name 4 causes of pre-hepatic jaundice and 2 causes of the main 2 categories
Immune
Burns
Infection
Mechanical
Transfusion
Haemolytic anaemia: thalassaemia, RBC membrane defects (spherocytosis)
Congenital hyperbilirubinaemia: Crigler-Najjar syndrome, Gilbert’s syndrome
Name 6 causes of intra-hepatic jaundice
Alcoholic liver disease Hepatobiliary carcinoma Hereditary haemochromatosis Hepatitis - viral, EBV, CMV, AI Intrahepatic cholestasis of pregnancy Drugs - paracetamol, amoxicillin, flucloxacilin, valproate, TB drugs, allopurinol
Where is post-hepatic jaundice caused? Name 4 locations
Biliary tree: L and R and common hepatic arteries, cystic duct, common bile duct, ampulla of vater
Name 2 intra-hepatic causes of post-hepatic jaundice
Cholangiocarcinoma
AI - PSC, PBC
Name 4 extra-hepatic causes of post-hepatic jaundice
Gall stones
Biliary stricture after lap chole
Chronic pancreatitis
Drugs causing cholestasis - Flucloxacillin, co-amoxicillin, steroids, nitrofurantoin
Relevant hepatitis hx (5)
Contact/area with A-E or EBV Risky behaviours - sharing needles, sex Seafood abroad Alcohol Farm/sewers = leptospirosis
Relevant jaundice PMH (2)
UC = PSC Cholecystectomy = stricture or bile duct stone
Relevant jaundice fx (3)
Congenital hyperbilirubinaemia
Wilson’s disease
A1 antitrypsin deficiency
What law is looked for on jaundice exam?
Courvoisier’s law: palpable gall bladder, non tender is not gall stones
Jaundice with acute distension (2)
Acute hepatitis
Hepatic vein thrombosis causing ascites
Jaundice with raised JVP and peripheral oedema
Heart failure = congested
Causes of generalised lymphadenopathy and jaundice (3)
EBV
CMV
Toxoplasmosis
5 signs of chronic liver disease
Palmar erythema Spider naevi Gynaecomastia Ascites Hepatosplenomegaly
Kaiser-Fleicher rings and jaundice
Wilson’s disease
Resp disease and jaundice
CF or a1 antitrypsin deficiency
Neuro signs and jaundice
Hepatolenticular degeneration in Wilson’s disease
AST:ALT raised
Viral hepatitis
AST:ALT >2
Alcoholic liver disease
Alkaline phosphatase raised
Biliary obstruction (or bone injury)
Gamma-GT raised
Biliary obstruction
What clotting study is abnormal in liver disease and why?
PT: vit K absorption reduced as it is fat soluble and there are fewer bile salts. Less factor 2, 7, 9, 10 (vit K dependent) so increased PT
FBC in alcoholic liver disease
MCV raised due to RBC damage (increased deposition of lipids and cholesterol on membrane surface, increasing size of RBC) - marrow toxicity, and B12/folate deficiency
Acute viral serology in liver screen
EBV, CMV, hepatitis A, B, C, E
Chronic viral serology in liver screen
Hep B, C
Acute non-infective markers in liver screen (4)
Anti-nuclear antibody - Sjogren’s, SLE, scleroderma
Paracetamol level
IgG subtypes increased in chronic active and alcoholic hepatitis and cirrhosis
Caeruloplasmin - carries copper, oxidises iron so it can be carried by transferrin, synthesised in liver - low in Wilson’s disease
Chronic non-infective markers in liver screen (5)
ANA (SLE, sjogren’s, scleroderma), AMA (PBC), Anti-SM (AI hepatitis)
Caerulosplasmin - low in Wilson’s disease
T-TGA - coeliac disease
Ferritin (increase) and transferrin (decrease) saturation - acute phase protein
A1 antitrypsin
Signs of Wilson’s disease (5)
Keyser-Fletcher rings Renal tubular acidosis Hyperparathyroid Infertility Cardiomyopathy
Imaging for jaundice
USS
MRCP if USS inconclusive or limited, or obstructive (dilated ducts)
Biopsy
Urine test for jaundice (3)
Low urobilinogen and raised bilirubin = obstruction
Low bilirubin = unconjugated (pre-hepatic cause)
Haemosiderin = haemolysis
Manage complications of liver failure (3)
Vit K, treat hypoglycaemia, FFP
Manage encephalopathy (decompensated liver failure)
Laxative
Neomycin/rifaximin - decrease ammonia producing bacteria in bowel
Obstructive jaundice management (surgery, med and symptoms)
ERCP, open surgery, cholecystectomy, bile duct stenting
Cholestyramine increases biliary drainage
Antihistamines for pruritis
Role of IgG
Secondary immune response - activates complement pathway: macrophages and neutrophils to phagocytosis, eosinophils and NK cells to extracellular targets
Internal body fluids, crosses placenta (Gestation)
Inhibited by staph a
Role of IgA
Most prevalent, produced in mucosae
Neutralises microorganisms in GI and resp tract
In breast milk
Role of IgM
Primary response (Meets), stays in circulation
Role of IgD
On B cells - antigen receptor
Role of IgE
Extracellular organisms - activates mast cells and basophils to release inflammatory mediators which attack parasitic worms
What is acute liver failure?
Massive hepatocyte necrosis
3 main causes of acute liver failure and survival rates
1) paracetemol toxicity 65%
2) idiosyncratic drug use 25%
3) acute hepatitis B 25%
Normal paracetamol metabolism
Mostly glucuronidation or sulfation, some with p450 to NAPQI, binds to glutathione to conjugate and makes cysteine and mercaptopuric acid conjugates
Paracetamol toxicity metabolism
Glutathione depleted (also in malnutrition) so more NAPQI which causes hepatocyte injury
Classification of acute liver failure?
From onset of jaundice to hepatic encephalopathy:
1) hyperacute <7d
2) acute 8-28d
3) subacute 29d-12w
Outcome of hyperacute liver failure
Cerebral oedema and RICP more likely
Spontaneous resolution more likely
Definition of acute liver failure (3)
Hepatic encephalopathy
Jaundice
Coagulopathy INR>1.5
Hepatic encephalopathy grading and purpose
Grade at presentation is prognostic
On consciousness and physical signs
1) sleep reversible, reduced awareness, short attention span
2) personality changes, lethargy, poor memory; asterexis
3) somnolence, disorientated, confusion; rigidity, clonus, hyper-reflexia, nystagmus
4) stupor and coma
Risk factors for acute liver failure (7)
>40y/o, female Pregnant Poor nutrition Paracetamol for chronic pain Drug/alcohol/substance abuse Chronic hep b
4 symptoms acute liver failure
Nausea and vomiting
Abdo pain
Malaise
Depression and suicidal ideation
4 signs of acute liver failure
Hepatomegaly (acute viral hepatitis, Budd-Chiari syndrome, CHF with congestion)
RUQ tenderness
Signs of cerebral oedema: abnormal pupillary reflexes, rigidity, decerebrate posturing
No signs of chronic liver disease - spider naevi, splenomegaly, ascites, palmar erythema
LFTs in Wilson’s disease
AST:ALT >2.2, alk phos:bilirubin <4
Role of U&E in acute liver failure
Renal failure predicts mortality - hepatomegaly syndrome, ATN, hypovolaemia
Correct K, phosphate and Mg
FBC in Wilson’s disease
Anaemia with Coombs test negative haemolysis
Role of ABG in acute liver failure
Paracetamol = metabolic acidosis, lactate increased = prognostic
Hepatitis viral serologies in acute liver failure - which ones?
Anti-A and E IgM
Anti-B core and surface IgM
Anti-C IgG
Imaging in acute liver failure
USS and Doppler for:
Hepatic vein thrombosis in Budd-Chiari
Nodularity in cirrhosis, or regeneration
Monitoring in acute liver failure (3)
Neuro status
Culture surveillance
Central venous pressure and pulmonary artery
Management of acute liver failure (6 points)
ICU as risk of rapid deterioration, sepsis, cerebral oedema, haemodynamic instability and renal failure
RICP: raise head, +- mannitol (requires good renal function or RRT)
RRT for optimal fluid management and electrolyte correction
Caution in IVi for fluid overload
Propofol and fentanyl as short half lives
Enteral nutrition
Manage acute liver failure due to paracetamol toxicity
NAC
Manage acute liver failure due to Budd-Chiari syndrome
Anticoagulation, hepatic vein stent or TIPS
Manage acute liver failure due to pregnancy
Caessarian
Manage acute liver failure due to AI hepatitis
If AST>10x or >5x with raised GGT = prednisolone
Manage acute liver failure due to Wilson’s disease
Plasmapheresis, continuous veno-venous haemofiltration
Contraindications to liver transplant (3)
Severe infection or septic shock
Extrahepatic malignancy
ARDS, severe cardiopulmonary disease or multi organ failure
Acute indications for liver transplant (3)
Post-operative
Trauma
Fulminant hepatic failure - paracetamol and others ie congenital biliary atresia in children
Chronic indications for liver transplant (5)
Cirrhosis due to alcoholism >6m abstinence Chronic hepatitis Hepatocellular carcinoma PSC PBC
Assessment for liver transplant score (2)
Child-Pugh score - determines severity and required treatment: Bilirubin Refractory ascites Albumin INR eNcephalopathy
MELD score - stratifies severity of end stage liver disease for transplant planning: Creatinine Sodium Bilirubin INR
Post-op treatment for liver transplant (4)
Cefuroxime
Metronidazole
PPI
Immunosuppression - methylprednisolone, ciclosporin, azathioprine, tacrolimus, monoclonal antibodies
Early complications of liver transplant
Bleeding, hypothermia
CVS - haemorrhage, vasodilation
Resp - TRALI, hypoxia, atelectasis, pleural effusion
Neuro - encephalopathy, cerebral oedema
Small for size - raised bilirubin, ascites, portal hypertension
Biliary leak
Biliary duct stricture
Hepatic artery thrombosis = fever and raised LFT
Portal vein thrombosis = ascites and renal failure
Late complications of liver transplant
Chronic rejection Renal failure Sepsis from immunosuppression Diabetes Post-transplant lymphoproliferative disease - EBV Disease recurrence
What is chronic liver disease?
Progressive destruction of liver parenchyma over >6m leading to fibrosis and cirrhosis
What are the 2 categories of hepatic encephalopathy?
Overt - defines decompensated liver failure
Covert -
- subtle neuropsychological signs, psychomotor slowness and difficulty with ADLs
- minimal and subclinical
- diagnose with psychometric testing
Sx of chronic liver disease for each region of body
Asterexis, Dupeytron’s contracture, palmar erythema, leuconychia Fatigue and encephalopathy Jaundice and fetor hepaticus Spider naevi and gynaecomastia Ascites, hepatomegaly and caput medusae Polyneuropathy
What is non-alcoholic fatty liver disease and what causes it?
Microvesicular steatosis, AST
Which hepatitis can cause chronic liver disease?
B, C, D
What is the most common cause of chronic liver disease?
Alcohol - 25% of cirrhosis
What questionnaire assesses drinking?
CAGE:
Do you ever think you should Cut down?
Do people Annoy you criticising your drinking?
Do you ever feel Guilty about how much you drink?
Do you ever need a drink as an Eye opener in the morning? To calm nerves or a hangover
Sx of alcoholic liver disease (3)
Nausea and vomiting
Abdo pain
Diarrhoea
Extrahepatic sx of alcoholic liver disease
Porphyria cutanea tarda Psychosocial - Wernicke-Korsakoff Malnutrition Cardiomyopathy, arrhythmia, HF Gastritis and erosions Proximal myopathy Peripheral neuropathy
What is Wernicke’s encephalopathy? (4)
Confusion
Nystagmus
Ataxia
Opthalmoplegia
What is Korsakoff’s psychosis?
Short term memory loss
How is alcohol broken down?
Oxidised by cytochrome p450 or by alcohol dehydrogenase to acetaldehyde
By acetaldehyde dehydrogenase to acetate
How is the liver damaged by alcohol breakdown?
NADPH becomes NADP and NADH becomes NAD, releasing free radicals which cause hepatocellular damage
What are the 3 features of alcoholic liver disease?
Fatty change
Hepatitis
Fibrosis with nodular regeneration
Describe the fatty change seen in alcoholic liver disease
Ethanol is metabolised to fatty acids, which accumulate and cause cell destruction
When is fatty change seen except alcoholism? (4)
Diabetes, obesity
Starvation
Pregnancy
Describe hepatitis in alcoholic liver disease
Polymorphonuclear leukocytes and Mallory bodies (hyaline) infiltrate (also in chronic active hepatitis)
What is Zieve syndrome?
Triad of alcoholic hepatitis/cirrhosis, hyperlipidaemia and haemolytic anaemia, with unconjugated bilirubin (jaundice) and abdo pain. Caused by alcohol withdrawal. Treat with abstinence
FBC in alcoholic liver disease (3)
Macrocytosis
Thrombocytopoenia - toxic to megakaryocytes
Leukocytosis
Further investigations for alcoholic liver disease
USS - macronodular, irregular margin, fatty change
Biopsy (trans jugular to minimise bleeding) - fatty change and cirrhosis
Manage alcoholic liver disease (4)
Abstinence increases 5y survival from 60-90%
Thiamine
Protein and calorie supplements
Withdrawal with benzodiazepines
What is haemochromatosis? Name 6 things it causes and investigation results
Excess iron absorption causing deposition in liver and organs
Cirrhosis Diabetes Heart failure Arrhythmia Hypogonadism Skin discolouration
Iron, ferritin and transferrin saturation increased, seen on biospy
What is the treatment for haemochromatosis? (2)
Regular venesection or desferrioxamine
What is Wilson’s Disease? Name 6 things it causes and investigation results
Autosomal recessive accumulation of copper
Neuropsychiatric - Parkinsonism Keyser-Fleicher rings Arrhythmia Cardiomyopathy Cirrhosis Renal tubular damage
Caeruloplasmin reduced, urinary copper increased
What is the treatment for Wilson’s disease?
Copper chelators - penicillamine
What is a1 antitrypsin deficiency and name 2 things it causes
A1-AT is a protease inhibitor which mediates inflammatory process. Deficiency causes excess breakdown of proteins in lungs and liver
Causes early onset basal lung emphysema and late onset cirrhosis
What are 5 genetic causes of chronic liver disease?
A1 antitrypsin deficiency CF Haemochromatosis Wilson’s disease Hereditary glycogen storage diseases
Who gets AI hepatitis and what is it associated with?
F>M, peaks in early 20s and perimenopausal
Associated with thyroiditis, psoriatic arthritis, AI haemolytic anaemia
What are 3 causes of AI hepatitis?
Primary sclerosing cholangitis
Primary biliary cirrhosis
AI hepatitis
Sx of primary biliary cirrhosis (6)
Pruritis Fatigue and lethargy Dark urine and pale stools Xanthelasma/xanthoma Bone disease from reduced vit D absorption Signs of chronic liver disease
Investigations for PBC (6)
LFT: alk phos + Cholesterol + AMA ++, ANA/antiSM + IgM + MRCP USS for focal lesion, thrombosis, external compression
Complications of PBC (4)
Renal tubular acidosis
Cirrhosis
Osteoporosis
Osteomalacia and coagulopathies
Treat PBC (4)
Cholestyramine for pruritis
Ursodeoxycholic acid
Vit A, D, E, K and calcium
Bisphosphonates
What is primary sclerosing cholangitis?
Inflammation and fibrosis of intra/extra hepatic biliary ducts
6 sx of PSC
IBD symptoms (linked to UC) Abdo pain, jaundice, pruritis Fatigue and weight loss Recurrent biliary infections Features of CLD Cirrhosis
Investigate PSC (4)
ANCA, AntiSM, ANA
LFT - high or normal
MRCP - bead like multiple strictures
Biopsy - progressive fibrous cholangitis
Complication of PSC
Cholangiocarcinoma
Treat PSC (6)
Ursodeoxycholic acid Cholestyramine Vitamins Antibiotics if bacterial cholangitis Stent/drain - balloon dilatation, sphincterotomy Liver transplant
Presentations of AI hepatitis (3)
CLD +- jaundice
Acute hepatitis with jaundice
AI - fever, rash, arthritis, malaise
Investigations for AI hepatitis (3)
LFT - raised bilirubin, ALT, IgG
FBC - normocytic normochromic anaemia, thrombocytopoenia, leucopoenia
Anti-SM antibodies
Treatment for AI hepatitis (2)
Corticosteroids induce remission
Azathioprine - antiproliferative immunosuppressant
Drugs which cause chronic liver disease and why (5)
Isoniazide - acute hepatitis
Methotrexate and amiodarone - cholestasis
Phenytoin and valproate - necrosis
Sarcoidosis and chronic liver disease, and treatment
Non-caseating granulomas, normally in lung, lymph nodes and skin
Treat with steroids and azathioprine
3 main areas of cirrhosis features
CLD stigmata
Endocrine
Neuro
Endocrine features of cirrhosis (5)
Loss of libido
Testicular atrophy, amenorrhoea
Parotid enlargement
Gynaecomastia
Cirrhosis investigations
LFT normal or all abnormal
Glucose high from pancreatic insufficiency
Dilutional hyponatraemia and albuminaemia
Raised PT
Macrocytic anaemia, B12/folate deficiency
Cirrhosis biomarker
A-fetoprotein for hepatocellular carcinoma
Secondary investigations for cirrhosis
USS - size, fatty change, fibrosis, carcinoma
Biopsy - macronodular = hepatitis B/C, micronodular = alcohol
Endoscopy for varicose - band or B blocker
4 complications of cirrhosis
Portal vein hypertension
Ascites
Encephalopathy
Hepatorenal syndrome
What causes hepatorenal syndrome?
Reduced intravascular volume activates RAAS, causing vasoconstriction of afferent arterioles, lowering GFR
Renal failure also from sepsis, diuretics or paracentesis reducing volume
What causes hepatic encephalopathy?
Toxic metabolites and ammonia from protein breakdown
What causes portal hypertension?
Collagen and fibrosis causes sinusoidal portal vascular resistance
Vasoactive substances from toxic metabolites ie nitric oxide cause vasodilation
Sodium retention causes increased plasma volume
How to treat vasodilation, increased plasma volume and varices in cirrhosis
Vasodilation - crystalloids and blood to replace intravascular volume; vasopressin analogue terlipressin to cause splachnic vasoconstriction and decrease portal flow
Plasma volume - spironolactone, loop diuretics, shunt (IJV, TIPS)
Varices - endoscopy and sclerotherapy, balloon tamponade, banding, TIPS, and B blockers
Cause of ascites in cirrhosis (2)
Vasoactive substances cause arterial vasodilatation - active RAAS - increase hydrostatic pressure - transudate
Hypoalbuminaemia decreases oncotic pressure
Sx and treatment of peritonitis
Nausea, abdo pain, fever, neutrophilia, clinical deterioration
Treat with fluroquinolone (ciprofloxacin)
How is iron absorbed?
Kept soluble by gastric acid, as ferrous and bound to gastroferrin. Binds to transferrin and undergoes endocytosis then is split, releasing iron into the blood where it is once again bound to transferrin
How are carbohydrates broken down in the intestine?
By a-amylase and bb enzymes to glucose
How is glucose absorbed?
Uses sodium gradient for active absorption using the SGLT1 cotransporter, into mucosal cells. Then diffuses through GLUT2 into ECF
How are fructose and lactose absorbed?
Through facilitated diffusion
What is in oral rehydration therapy and why?
Sodium and glucose - stimulates 2 osmotic gradients to increase water absorption
How is calcium absorbed?
Stimulated by PTH, uses vitamin D, to use Ca-ATPase pump for facilitated diffusion
How much calcium is absorbed compared to intake?
700mg absorbed of 6g consumed
How is B12 absorbed?
Binds to intrinsic factor to be absorbed in terminal ileum
What is absorbed in duodenum?
Water, HCO3- and iron
What is absorbed in jejunum?
Amino acids, fatty acids, carbs, vitamins, minerals, electrolytes and water
What is absorbed in large intestine?
Final water and salt
How much fluid is absorbed in SI?
14l to 1.5l
What happens when carbs are not absorbed?
Fermented by colonic bacteria to carbon dioxide, methane and hydrogen which causes bloating and distension
And fatty acids (acetate, lactate) which cause diarrhoea
What happens if fats are not absorbed? (2)
Trap fat soluble vitamins A, D, E, K - deficiency
Unabsorbed bile salts causes water secretion into colon which causes diarrhoea
How does bacteria cause malabsorbtion?
Overgrowth causes deconjugation and dehydroxylation of bile salts, decreasing fat absorption
What is the mechanism of coeliac disease?
Gluten-sensitive T cells cause inflammatory response causing mucosal villus atrophy in SI
Diagnosis of coeliac disease (4)
T-TGA Anti-EMA (endomysial antibody) Iron deficiency (microcytic anaemia) SI biopsy (D2) = villus atrophy, crypt hyperplasia, increased Intraepithelial cells
4 symptoms of coeliac disease
Failure to thrive
Anorexia
Apathy
Soft bulky clay-coloured offensive-smelling stools
8 signs of coeliac disease
Hypotonia Muscle wasting Pallor and sx of anaemia Abdo distension Glossitis Angular stomatitis Apthous ulcers Dermatitis herpatiformis
Skin condition associated with coeliac disease
Dermatitis herpatiformis - intense pruritic papulo-vesicular rash. Symmetrical on elbows, knees, shoulders, buttocks, scalp - extensors
Complications of coeliac disease
Intestinal lymphoma and other GI malignancies
Reduced fertility and amenorrhoea
Vit D and calcium deficiency causing osteomalacia/poenia/porosis