Phase 2a Rebecca Burger and Clare Greenwood The Peer Teaching Society is not liable for false or...

Phase 2a

Rebecca Burger and Clare Greenwood

GI 2- Liver and Friends

The Peer Teaching Society is not liable for false or misleading information…

• To cover key points on the– Pathophysiology– Presentation– Investigations– Management

• Of conditions of the liver, gall bladder, pancreas and some other random bits.

• Some topics we will not teach, but have created resources for you to use. These are at the end of the powerpoint for you to look at later.


aims

• We will cover: • Appendicitis• Biliary tract disease • Viral Hepatitis Cirrhosis, • portal HTN and varices• Primary biliary cirrhosis • Alcoholic liver disease• Metabolic causes of liver disease• liver failure • ascites • peritonitis• volvulus• GI cancers • Hernias• Infection


introduction


LIVER FUNCTION TESTSALANINE TRANSAMINASE (ALT): Stored in hepatocytes, released when they are damaged (e.g in hepatitis)

ASPARTATE AMINOTRANSFERASE (AST): Stored in hepatocytes, cardiac+skeletal myocytes, released when they’re damaged (less specific than ALT)

ALKALINE PHOSPHATASE (ALP) : found in lining of bile duct, raised in obstruction and intrahepatic cholestasis. Normally higher in children

ALBUMIN: Made by liver, low level can mean problem with liver

GAMMA GT: high level associated with heavy drinking

PROTHROMBIN TIME (PT): measures extrinsic coagulation pathway. Lengthened time suggestive of liver damage, vit K deficiency or warfarin dose


JAUNDICEBecomes visible when serum bilirubin is >35umol/L

PRE-HEPATIC: Anything that causes increased haemolysisGet increased unconjugated bilirubinCauses: Gilbert’s syndrome, thalassemia, trauma, haemolytic anaemia

HEPATIC: Hepatic damage reduces ability to metabolize bilirubinCauses: viral hepatitis, alcoholic liver disease, autoimmune hepatitis, drug-induced damage

POST-HEPATIC: Caused by obstruction of drainage into the biliary systemGet increased conjugated bilirubin, raised urinary bilirubin+reduced urobilinogen, raised ALPCauses: gallstones, biliary atresia, cholangiocarcinoma, pancreatitis, primary biliary cirrhosis


VIRAL HEPATITIS

Hepatitis A:- Most common viral hepatitis worldwide- Spread faeco-orally, or ingestion of contaminated food- Replicates in liver, then excreted through bile into faeces

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VIRAL HEPATITIS

Presentation:Non-specific malaise, nausea, anorexia1-2 weeks later, get jaundice, mild hepatosplenomegaly and transient rash

Investigations:Blood- jaundice causes raised serum bilirubin. Also see anti-HAV IgM

Treatment: generally nothing, mortality=0.1% due to fulminant hepatic necrosis. Majority recover completely within 3-6 weeks


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VIRAL HEPATITIS

Hepatitis B- Found worldwide, higher carrier rates in Africa, Middle and Far East- Can be transmitted vertically or horizontally- Damage occurs due to host immune response- Can become chronic


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VIRAL HEPATITISPresentation:Same as HAV, but more severe for acute episode

Investigations:Anti-HBc IgM is diagnostic

Treatment:Supportive treatmentIf acquired horizontally+there is acute episode, 99% clearance rateIf acquired vertically, not normally acute episode, and clearance rate is 10%4-10% get cirrhosis, chronic hepatitis, hepatocellular ca


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VIRAL HEPATITIS

Hepatitis C- Higher prevalence in Egypt- Transmitted by blood+blood products- Virus has rapidly changing envelope proteins


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VIRAL HEPATITISPresentation:Acute episode normally asymptomatic- 10% have mild flu+jaundice

Investigations:Acutely, may get raised serum AT1-8 weeks post infection, loo for HCV RNA

Treatment:Interferon prevents acute becoming chronicTreat chronic with antivirals- interferon ±telaprevir85-90% of asymptomatic get chronic liver disease, cirrhosis or hepatocellular Ca



METABOLIC LIVER DISEASE

Haemochromatosis:- Excessive iron deposition in organs- Causes fibrosis and organ failure- Genetic- inappropriately high intestinal iron absorption + erthyrophagocytosis- Normal body iron 3-4g



Presentation:bronze skin, hepatomegaly, diabetes M, pituitary dysfunction causing hypogonadism, cardiac failure

Investigations:serum iron >30umol/L, serum ferritin >500ug/L

Management:Mild- adjust diet- less iron, vit c + alcoholModerate- regular phlebotomy- 400ml every 1-2wks



Wilson’ Disease:- Faulty copper metabolism- Excess copper deposited in liver, basal ganglia and cornea- Autosomal recessive



Presentation:Hepatic problems, neurological problems, Kayser-Fleischer rings

Investigations:Urinary copper- >100-1000ug in 24hrs, genetic analysis

Management:Lifetime treatment with penicillamine



Alpha1-antitrypsin deficiency:- Abnormal protein production- Causes failed secretion of the protein, liver disease +emphysema- Autosomal recessive, gene prevalence 1 in 10 in N Europe



Presentation:Cirrhosis, chronic liver disease, respiratory problems

Investigations:Serum alpha1-antitrypsin- low

Management:Avoid smoking, manage complications

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ALCOHOLIC LIVER DISEASESteatosis:- Liver cells swollen, but not damaged- Reversible with abstinence - Continued damage causes fibrosis

Presentation:Normally asymptomatic, can get hepatomegaly

Investigation:LFTs- raised serum ATUSS/CT- fatty infiltration

Management:Abstinence until fat disappears


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ALCOHOLIC LIVER DISEASEAlcoholic hepatitis:- Get polymorphonuclear leukocyte infiltration, hepatocyte necrosis, Mallory bodies, and giant mitochondria

Presentation:Mild- moderate malaise± jaundiceSevere- abdominal pain, fever, jaundice, hepatosplenomegaly, ascites

InvestigationsLFTs- raised serum AST, ALT, AP+bilirubin, low serum albumin

ManagementSteroids, prophylaxis antifungals, supportive care, abstinence


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ALCOHOLIC LIVER DISEASEAlcoholic cirrhosis- Classically micronodular- Occurs with pre-existing steatosis+hepatitis

Presentation:May be relatively mild, with ascites, jaundice, telangiectas, finger clubbing and signs of alcohol dependency

Investigations:Same as before, also do biopsy

Management:Complete abstinence, supportive care, can only cure with liver transplant


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CIRRHOSIS

- Damage cause liver cell necrosis- Inflammatory response causes Stellate cell activation ---> fibrosis+ nodule formation- Leads to abnormal architecture---> impaired flow+function

Can be:- Micronodular: <3mm, liver uniformly involved- Macronodular: variably sized nodules

Causes:Alcohol, Hep B/C, NAFLD


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CIRRHOSISPresentation:Can be asymptomatic, get fatigue, abd pain, ascites, ankle swelling, pruritis, jaundice, spider naevi, gynaecomastia, hepatosplenomegaly, Duputren’s contracture, clubbing, testicular atrophy, purpura, loss of body hair

Investigations:Severity: LFTs, liver biochemistry, U&Es, serum creatinine, liver biopsy, USSType: viral markers, serum autoantibodies, serum Ig, ferritin, alpha1-antitrypsin

ManagementAlcohol abstinence


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QUESTIONS

• 22yr old girl. Presents with 2 month history of jaundice, malaise and abdominal pain. On examination, there is mild hepatomegaly, and on slit lamp examination there is a brown ring around both corneas

• On a 24hr urinary measurement, what would you expect to see elevated?

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• 65yr old woman presents with 2/52 hx of progressive jaundice, 10kg weight loss, palpable liver edge and a v high alkaline phosphatase

• Likely cause?• Ca head of pancreas• Cholangiocarcinoma• Cirrhosis• Liver mets

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• Contains:– Bile salts, Bile acids, Cholesterol, Pigment,

Bilirubin, Protein• Made in the liver hepatocytes,• Stored in the gallbladder• Release is stimulated by CCK


Bile

• Types of gallstone:• Mixed- 80% (calcium, pigment and cholesterol)• Cholesterol• Pure Pigment (asc haemolytic anaemia)

• Diagnosis:– 15% radiopaque on Xray, – Ultrasound better


Biliary Tract Disease- Gallstones

• Who?– Fat…………….. Associated with obesity– Forty……………Years peak incidence– Fertile………….Women of multiple pregnancies– Female



• Symptoms- only 30% symptomatic ever

• Pain, 1-2 hours after food, especially fatty food• ‘Colic’ as gallbladder contracts on stone

• Cholocystitis= gallstone blocks output of gallbladder by lodging in cystic duct

• ‘Strawberry gallbladder’’= cholesterolosis



• Obstruction at the neck of the gallbladder, causes inflammation• RUQ pain, vomiting, fever• Murphey’s sign +ve


Cholocystitis

• An infection caused by blockage of the common bile duct by a gallstone.

• (without infection= choledocholithiasis)

• Caused by – E.coli, Klebsiella sp, (gram –ve)– Enterococcus (gram +ve)


Ascending Cholangitis

• Charcot’s triad:–RUQ pain–Jaundice–Rigors


Ascending Cholangitis

• Cystic Duct Obstruction- can cause pancreatitis- enzyme release and autodigestion

• Infection- mucocoele/ empyema• Abscess- pus (= neutrophils, phagocytes and

bacteria) • Gall stone ileus (a hole made by the gallstone

pressing down on the 2nd part of the duodenum = cholecystoduodenal fistula)


Biliary Tract Disease- complications


PancreatitisACUTE CHRONIC

Gallstones Alcohol

Ethanol Autoimmune

Trauma Cystic FibrosisSteroidsMumpsAutoimmune: SLE, PANScorpion StingsHypercalcaemia, Hypothyroid, HyperlipidaemiaERCPDrugs- eg. azothioprine

• Typical history: central abdo pain radiates to the back, is relieved on sitting forwards

• Grey Turner’s sign (flank bruising)• Cullen’s sign (periumbilcal bruising)• Lipases => fat necrosis


Presentation

• Serum and urine amylase• Lipase• USS for gallstones

• APACHE score/ modified Glascow criteria

• Management: ERCP, cholecystectomy


Investigation

• Cause:– Primary (spontaneous): liver disease and ascites– Secondary: • bowel/ bladder perforation• Inflammation, infection or ischaemia of intra-

abdominal organs, eg. Appendicitis, pancreatitis• Peritoneal dialysis

• What Pathogen?Enterococci


Peritonitis

• Presentation– SYMPTOMS:• pain, tenderness, not wanting to move• Systemic: nausea, chills, rigors, weak

– SIGNS:• Lies very still• Guarding, rigidity• Rebound tenderness• Silent abdomen• (of fever- tachycardia, pyrexia etc)


Peritonitis

• Management:– Antibiotics


Peritonitis

• Classical presentation:

“ pain which started around the umbilicus but has now moved down into the right side, specifically to Mc Burney’s point (2/3 of the way between umbilicus and ASIS)


Appendicitis

• Classical Signs:– Rebound tenderness– Pain on percussion– McBurney’s point tenderness– Rovsing’s Sign: pushing in LLQ causes pain in RLQ– Dunphy Sign: coughing increases the pain– Markle Sign: dropping from toes to heels causes

pain to increase


Appendicitis

• A cause of bowel obstruction• Presents: – pain, – distension, – complete constipation (no faeces/ no flatus)– Nausea and vomiting– Increased resonance– TINKLING then ABSENT bowel sounds


Volvulus

Blood= Dysentry No Blood

ShigellaSalmonellaCampylobacterEscherichia ColiYersinia enterocoliticaClostridium difficileGiardia (traveller’s diarrhoea)Amoebiasis

Bacillus cereus (Reheated rice)Staphylococcus aureusVibrio chloerae (rice water stools)Escherichia ColiCampylobacter jejuniClostridium perfringens & difficile


Infections

• Salmonella– Poultry, eggs– Onset 12-48 hrs, resolves 3-6 days– Nausea, cramps, dysentry

• Shigella– Person-to-person spread, poor hygeine (eg. Nursery, care home)– Onset 24-48hrs, resolves 7-10 days– Frequent small volume stools, blood and mucus

• Giardia– Water bourne flagellate– Catch on holiday, often presents once you get home– Diarrhoea and malabsorption

• E. Coli– Cattle, sometimes food– Onset 12-48 hrs– Diarrhoea, abdominal pain, nausea, puerpera


Infections

• Caused by a protozoa • Tropics/ subtropics• Spread through the water• Often liver involvement• Dysentry, steatorrhoea


All About Amoebiasis

“A young man returns from holiday in Thailand and goes to his GP feeling unwell. He reports having unpleasant diarrhoea and feeling ‘off colour’ for 1wk.”

• 2 features that suggest this is not Norovirus?• Two features you see on stool microscopy?• Treatment?• 3 signs of hepatic amoebiasis abscess.• How to avoid catching this again?


Amoebiasis Question

An 80yo female, non-smoker, who drinks 10units alcohol/wk presents feeling unwell. She takes thiazides for HTN. She is diagnosed with ascending cholangitis.• 1) Name charcot’s triad:• 2) On investigation, she has gram negatives bacteria in her

blood. What are they likely to be?• 3) She has had epigastric discomfort for about a year, and now

acutely ill. What is the likely underlying cause and where (anatomically) is it now located?


Question:

A young man presents on a Friday night with severe abdominal pain radiating to the back which is relieved when he sits forward. He feels ill, is vomiting and areas of his abdomen look bruised.1) What do you think is going on?2) What test would you do and would you expect the result to

be higher or lower than normal?3) What do you think caused this?4) How could you confirm this?


Question:


Causes of abdominal pain

• Direct– Path: descends into posterior inguinal canal

» Does NOT follow the path of the testes» Medial to the inferior epigastric artery

– Who: elderly men• Indirect

– Path:follows the path of the testes» Lateral to the inferior epigastric artery

– Who: Males > females, young• Femoral

– Path: parietal peritoneum descends into femoral canal at the pubic tubercle

– Who: females


Hernias

• I recommend reading the lecture slides or the relevant bits in Underwood’s.

• The important bits are probably:–oesophageal cancer/ Barrett’s oesophagus, – The Amsterdam criteria for HNPCC

(“3,2,1,FAP)–Duke’s staging


GI Cancers

Phase 2a Rebecca Burger and Clare Greenwood The Peer Teaching Society is not liable for false or...

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