Liver And Friends Flashcards
Definitive treatment if symptomatic gallstones
Cholecystectomy
ERCP
Endoscopic retrograde cholangiopancreatography
Endoscope and X-Ray to look T the bile duct and pancreatic duct to search for and remove present gallstones
Presentation of pancreatitis
Epigastric pain radiating to the back
Vomiting
Pain may be relieved by leaning forward
Bile acid sequestrants
Bind to bile acids in the small intestine
Prevent their reabsorption into enterohepatic circulation
Reduction in bile acid levels causes hepatic conversion of LDL cholesterol to bile acids
Three biliary tract diseases
Gallstones (biliary colic)
Cholecystitis
Cholangitis
Distinguish between biliary colic, acute cholecystitis and ascending cholangitis using Charcot’s triad
Charcot’s triad: RUQ pain, fever, jaundice
Biliary colic: RUQ pain
Acute cholecystitis: RUQ pain, fever & increased WCC
Ascending cholangitis: RUQ pain, fever & increased WCC, Jaundice
Biliary colic pathophysiology
Gallstone blocks the cystic or common bile duct
Without signs of cystic inflammation
Components of bile
cholesterol, pigments and phospholipids
Types of gall stone
Cholesterol: excess production (obesity and fatty diets)
Pigment: (haemolytic anaemia)
Mixed: made of both of the above
Presentation of biliary colic
COLICKY RUQ PAIN
worse after eating large or FATTY meals (triggers gallbladder to contract AGAINST the blockage)
Five risk factors of gallstones
5 F's: Fat Fertile Forty Female FHx
Investigations for gallstones
Rule out:
- FBC & CRP: inflammatory response (cholecystitis)
- Amylase: pancreatitis can also give RUQ pain
- LFTs: raised ALP (bilirubin and ALT normal)
Diagnostic: ULTRASOUND
1) Stones
2) Gallbladder wall thickness (due to inflammation)
3) Duct dilation (distal blockage)
Gallstone differential diagnoses
RUQ pain: cholecystitis cholangitis IBD pancreatitis GORD peptic ulcers
Gallstone treatment
NSAIDs/analgesia
Cholecystectomy (optional to prevent recurrence)
Cholecystitis pathophysiology
Inflammation of the gallbladder wall (cholecyst-itis) usually caused by a stone blocking the duct causing bile to build up and distend the gallbladder
Presentation of cholecystitis
Generalised epigastric pain migrating to severe RUQ pain, fever
Pain associated with tenderness and guarding (inflamed gallbladder, local peritonitis)
Murphys sign
elicited in acute cholecystitis: ask patient to take in and hold a deep breath whilst palpating RUQ
positive = pain on inspiration when the gallbladder comes into contact with examiners hand
Ix cholecystitis
Positive Murphy’s sign
Inflammatory markers
Ultrasound (thick gallstone walls from inflammation)
Cholecystitis treatment
IV Abx
Heavy analgesia
IV fluids
Cholecystectomy (if needed)
Cholangitis
Bile DUCT inflammation caused by prolonged bile duct blockage
Bacteria can travel from the GI tract and not be flushed out with the bile, causing biliary tree infection
Jaundice: bile cannot enter the GI tract
Infection can travel to the pancreas as it shares the gallbladder ducts
Mortality: 5-10%
Cholangitis presentation
severe RUQ pain with fever and jaundice
may also present with:
sepsis
pancreatitis
Cholangitis investigations
FBC, LFTs, CRP: leukocytosis, raised ALP and bilirubin, raised CRP
Blood cultures/MC&S: for pathogen detection to use correct Ab
Ultrasound +/- ERCP (endoscopic retrograde cholangiopancreatography) = biliary tree contrast X-Ray
Cholangitis treatment
Treat SEPSIS
ERCP + stenting to mechanically clear the blockage
Surgery/cholecystectomy (if possible)
SEPSIS 6
- GIVE oxygen
- TAKE blood cultures
- GIVE IV Abx
- GIVE fluids
- TAKE lactate measurement
- TAKE urine output measurement
Causes of acute pancreatitis
I GET SMASHED Idiopathic Gallstones Ethanol Trauma Steroids Mumps Autoimmune (prevalent in Japan) Scorpion venom Hyperlipidaemia ERCP Drugs - NSAIDs, corticosteroids, ACEis
Two main causes of acute pancreatitis and the pathophysiology
GALLSTONES: BLOCKAGE of bile duct = back up of pancreatic juices
- change in luminal concentration causes calcium release inside pancreatic cells = activated trypsinogen early = AUTODIGESTION OF PANCREAS
ALCOHOL: CONTRACTS THE AMPULLA OF VATER obstructing bile clearance = calcium homeostasis disrupted = trypsinogen = AUTODIGESTION OF PANCREAS
Why does Grey Turner’s sign occur in acute pancreatitis
leaky and damaged pancreas = AUTODIGESTION to nearby structures = haemorrhage and Grey Turner’s sign (abdominal skin discolouration from retroperitoneal bleeding)
Why does hyperglycaemia occur in pancreatitis
disrupted insulin production
Acute pancreatitis presentation
SEVERE EPIGASTRIC PAIN RADIATING TO THE BACK
Anorexia, fever, jaundice, Grey Turner’s sign (flank bruising), N&V, tachycardia
Acute pancreatitis investigations
Serum amylase: raised
Urinalysis: raised urinary amylase
Serum lipase: raised (more specific than amylase)
CRP and FBC: raised CRP
Erect CXR: exclude gastroduodenal rupture
Abdo ultrasound, CT, MRI
Two scores used in acute pancreatitis
APACHE 2
Glasgow & Ranson
Acute pancreatitis treatment
Nil by Mouth (decrease pancreatic stimulation)
Analgesics
Prophylactic Abx
Treat gallstones if underlying cause
causes of chronic pancreatitis
CHRONIC ALCOHOL USE
Hereditary
Autoimmune
CKD
Presentation of chronic pancreatitis
EPIGASTRIC PAIN ‘BORING’ THROUGH THE BACK: worse after alcohol, better on leaning forward
Typical patient: 50 odd year old MALE with an appropriate SHx (drinking)
N&V, decreased appetite, malabsorption (painless weight loss)
Chronic pancreatitis investigations
Serum amylase and lipase: may be raised if enough cells remain to make them
Ultrasound abdo, CT, MRI
Treatment of chronic pancreatitis
Stop drinking Pancreatic enzyme supplements PPI to help digestion Insulin for DM Duct drainage
Haemochromatosis
inherited condition where IRON LEVELS build up in the body
Pathophysiology of haemochromatosis
mutation in autosomal recessive HFE gene (c6)
causes increased intestinal iron absorption
iron accumulates in liver, joints, pancreas, heart, skin, gonads
ORGAN DAMAGE: liver fibrosis, cirrhosis, HCC (hepatocellular carcinoma)
Presentation of haemochromatosis
Fatigue, arthralgia (joint stiffness), weakness
Hypogonadism e.g erectile dysfunction
Slate-grey skin (brownish/bronze)
Chronic liver disease, heart failure, arrythmias
haemochromatosis investigations
Bloods: iron study, LFTs
Genetic testing
GOLD STANDARD: liver biopsy
MRI: detects iron overload
Wilson’s disease
error of COPPER metabolism = copper deposition in organs, including liver, basal ganglia, cornea
Presentation of Wilson’s disease
KAYSER-FLEISCHER RING: copper in cornea (green/brown pigment at outer edge)
Psychiatric: depression, neurotic behavioural patterns
CNS: tremor, dysarthria, involuntary movements, dysphagia
Liver: hepatitis, cirrhosis
Wilson’s disease investigations
serum copper and ceruloplasmin reduced (but can be normal)
24 hour URINARY copper excretion HIGH
DIAGNOSTIC: LIVER BIOPSY
Wilson’s disease management
Avoid high copper foods (liver, chocolate, nuts, mushrooms, shellfish)
Chelating agent: PENICILLAMINE
Liver transplant
Ascites
Excessive buildup of fluid in the peritoneal cavity
Ascites pathophysiology
Poor liver function = low albumin = low blood oncotic pressure = fluid leaks out into peritoneal cavity
Main cause of ascites
Liver failure/cirrhosis
Presentation of ascites
LARGE DISTENDED ABDOMEN
Shifting dullness
- DULLNESS OVER FLUID
- RESONANCE OVER AIR
Ascites treatment
Low sodium diet
Diuretics: Spironolactone + Furosemide
Identify cause + treat accordingly
Peritonitis aetiology
- Primary
- Secondary
- Causative organisms
Primary: spontaneous bacterial infection, ascites
Secondary: perforation (bowel, appendix, peptic ulcer), gastritis, ectopic pregnancy
Most common causative organisms: S. Aureus, Klebsiella, E.coli
Presentation of peritonitis
Perforations: SUDDEN ONSET SEVERE ABDO PAIN with generalised shock/collapse
Secondary: gradual onset: generalised abdo pain»_space; localised severe pain (visceral»_space; parietal)
Rigid abdomen
Pyrexia, tachycardia, potential confusion, N&V
Guarding, rebound tenderness, rigidity, SILENT ABDO
Peritonitis investigations
Bloods: FBC & CRP, Amylase (pancreatitis), hCG (ruptured ectopic pregnancy)
Erect CXR for air below the diaphragm, AXR to exclude bowel obstruction, CT for abdo ischaemia
Ascitic tap and blood cultures: pathogen
Treatment of peritonitis
ABCDE
Find and treat underlying cause (e.g. may be surgery for perforated bowels)
IV fluids
IV Abx (broad spec»_space; specific)
Peritoneal lavage (clean the cavity surgically)
Hernias
protrusion of organ through defect in wall of its containing cavity
Hernia classifications
- Reducible (flattens when you lie down or push against it)
- Irreducible (loop of intestine becomes trapped and the bulge cannot flatten out) - requires immediate medical attention»_space; Obstructed (intestinal flow stopped)
-Strangulated (tightly trapped intestine causing blood supply to be cut off) > ischaemia > gangrene
Inguinal hernia
protrusion of abdominal contents through inguinal canal
presents superior and medial to pubic tubercle
- swelling in groin
- impulse
20% are direct (medial to inferior epigastric artery through a weakened area)
80% are indirect (lateral to inferior epigastric artery through deep inguinal ring)
Femoral hernia
bowel comes through femoral canal
Hiatus hernia
herniation of stomach through oesophageal aperture of diaphragm
Incisional hernia
hernia through surgical scar
Epigastric hernia
hernia through linea alba above umbilicus
Management of hernias
SURGERY
Risk factors for inguinal hernia
Male
Chronic cough
Heavy lifting
Past abdo surgery
Investigations for an inguinal or femoral hernia
Clinical diagnosis
USS/CT/MRI
Most likely classification in femoral hernia
Irreducible and strangulation (due to rigidity of canals borders)
Presentation of a femoral hernia
Mass in upper medial thigh
Neck of hernia is inferior and lateral to pubic tubercle
May be cough impulse
Types of hiatus hernia
Rolling: 20% - GOJ remains in abdo, part of fundus rolls up through hiatus, LOS
Sliding: 80% - GOJ and part of stomach slides up into chest, LOS less
Risk factors for hiatus hernia
Obesity Female Pregnancy Ascites Age
Hiatus hernia presentation
Heartburn/GORD
Dysphagia
Hiatus hernia investigation
CXR Barium swallow (oesophagogram) Endoscopy Oesophageal manometry
Functions of the liver
Oestrogen regulation Detoxification Carbohydrate metabolism Albumin production Clotting factor production Bilirubin regulation Immunity (Kupffer cells in reticuloendothelial system)
Pathophysiology of spider naevi and palmar erythema
Oestrogen dysregulation
Acute presentation of liver disease
Malaise
Nausea
Anorexia
Jaundice
Chronic presentation of liver disease
Ascites Oedema Pruritus Clubbing Palmar erythema Xanthelasma Spider naeivi Hepatomegaly Bleeding (haematemesis, bruising)
Causes of acute liver disease
Viral (Hep A, Hep B, EBV) Drugs Alcohol Vascular Obstruction Congestion
Causes of chronic liver disease
Alcohol
Viral (Hep B, Hep C)
Autoimmune
Metabolic (Iron, Copper)
Causes of liver failure
Toxins (Paracetamol, ALCOHOL - most common cause) Infection (viral HEPATITIS) Metabolic (Wilson's/A1AT) Autoimmune (PBC, PSC) Neoplastic (HCC) Vascular (Budd Chiari, ischaemia)
Signs of liver failure
Jaundice
Coagulopathy
Hepatic encephalopathy (altered mood, dyspraxia, asterixis)
Fetor hepaticus (sweet and musty breath/urine)
Characteristics of liver failure decompensation
Abnormal bleeding
Ascites
Hepatic encephalopathy
Jaundice
Investigations of liver failure
Clinical examination
Bloods (increased PT, increased AST/ALT, toxicology, FBC, U&E)
If ascites: peritoneal tap with MS&C
Management of liver failure
Conservative (fluids, analgesia)
Medical: treat complications
- Ascites: diuretics
- Bleeding: vitamin K
- Cerebral oedema: mannitol
- Encephalopathy: lactulose
- Sepsis: SEPSIS 6 (Abx)
- Hypoglycaemia: dextrose
Surgical: transplant
Hep A
Spread: faecal-oral (vowels = bowels) Virus: RNA Infection: acute + mild Test: Bloods show raised AST/ALT, raised IgG and IgM Management: supportive Vaccine available
Hep B
Spread: blood products + bodily fluids (unprotected sex)
Virus: DNA (the only DNA one)
Infection: can be severe
Test: Hep B serology
Management: pegylated interferon alpha 2a, tenofovir (inhibits viral replication)
Vaccine available
Hep C
Spread: blood products + bodily fluids (IVDU)
Virus: RNA
Infection: very slow progressing
Test: HCV RNA, Anti-HCV serology
Management: direct acting anti-virals, ribavirin, sufosbuvir
Hep D
Spread: blood products + bodily fluids Virus: RNA (requires Hep B) Infection: makes HBV worse, likely to progress to cirrhosis or HCC Test: HDV RNA, Anti-HDV Management: treat HBV
Hep E
Spread: faecal-oral (vowels = bowels) Virus: RNA Infection: normally mild Test: HVE RNA, Anti-HVE Management: supportive
- only really get symptoms if PREGNANT
Complications of hepatitis (B, C, D, E)
Cirrhosis
HCC
Hep B serology:
Vaccinated
HB core Ab: -ve
HB surface Ab: +ve
HB surface Ag: -ve
Hep B serology:
Previous HBV
HB core Ab: +ve
HB surface Ab: +ve
HB surface Ag: -ve
Hep B serology:
Chronic HBV
HB core Ab: +ve
HB surface Ab: -ve
HB surface Ag: +ve
IgM negative, IgG positive = chronic
Paracetamol metabolism and toxicity
- Glucuronidation = excretion
- Sulfation = excretion
- p450 > NAPQI [toxic] > NAPQI + glutathione = excretion
Overdose: too much toxic NAPQI without enough glutathione = liver damage
- nausea, vomiting, anorexia, RUQ pain
Treatment: activated charcoal, N-acetylcysteine
Non-alcoholic fatty liver disease (summary)
Healthy > Steatosis > Steatohepatitis > Fibrosis > Cirrhosis
Px: asymptomatic, nausea, vomiting, diarrhoea, hepatomegaly
Dx: biopsy (diagnostic), imaging
Tx: weight loss (reduce fat)
Alcoholic liver disease
Fatty liver > alcoholic hepatitis > cirrhosis
Ix:
- GGT high, AST and ALT mildly raised
- FBC: macrocytic anaemia
Calculation for units of alcohol
Strength (ABV) x volume (ml) / 1000 = units
Complications of alcoholic liver disease
Wernicke-Korsakoff encephalopathy (ataxia, confusion, nystagmus, memory; Tx: IV thiamine)
Acute/chronic pancreatitis
Mallory-Weiss tear
GGT (LFT)
Gamma-glutamyl transferase
Common causes of cirrhosis
Chronic alcohol abuse
NAFLD
Hepatitis (B & C)
Clinical Px of cirrhosis
Ascites Clubbing Palmar erythema Xanthelasma Spider naevi Hepatomegaly Peripheral oedema
Ix cirrhosis
Low platelets, high INR, low albumin
US + CT: hepatomegaly
Liver biopsy
Tx cirrhosis
Alcohol abstinence Good nutrition Liver transplantation Screen for HCC every 6 months (increased AFP) Symptoms e.g. spironolactone for ascites
Causes of portal hypertension
Prehepatic (portal vein thrombosis)
Intrahepatic (schistosomiasis, cirrhosis, Budd Chiari)
Post-hepatic (RH failure, IVC obstruction)
Pathophysiology of oesophageal varices
Portal hypertension pushes blood into surrounding vessels i.e. oesophageal varices
These are thin vessels and not meant to transport high pressure blood = easily ruptured
Rupture > haematemesis > digested blood > melaena
Tx oesophageal varices
Beta blocker (reduce CO > reduce portal HT)
Nitrate (reduce portal HT)
Terlipressin
Surgical: band ligation, TIPS shunt
Causes of prehepatic jaundice
Haemolytic anaemia = excessive red cell breakdown which overwhelms the liver’s ability to conjugate bilirubin = unconjugated hyperbilirubinaemia (jaundice)
Causes of hepatocellular jaundice
Liver failure Liver disease Hepatitis Iatrogenic (toxicity) Gilbert’s syndrome
Causes of post hepatic jaundice
Gallstones
Acute HBV infection serology
HB core Ab: +ve
HB surface Ab: -ve
HB surface Ag: +ve
IgM positive = acute
Blood results associated with alcoholic liver damage
Raised GGT
High AST:ALT ratio
Mallory bodies
Cholestatic picture
Dark urine
Pale stools
Complications of acute pancreatitis
ACUTE RENAL FAILURE (due to dehydration)
Sepsis
Acute respiratory syndrome
Chronic pancreatitis
Pancreatic cancer Px
tumour at head of pancreas
Painless obstructive jaundice
Steatthorea
RBC breakdown
Heme
Biliverdin
Bilirubin
Large intestine: Urobilinogen > Urobilin (urine) / Stercobilin (faeces)
What is ERCP?
Endoscopic retrograde cholangio-pancreatography
Primary biliary cholangitis
Intrahepatic ducts
Primary sclerosing cholangitis
Intra and extra hepatic ducts
Strong link with UC
Acute liver failure definition
Onset of less than 26 weeks duration and no previous liver disease
Medication used for delirium tremens/alcohol withdrawal
Chlordiazpoxide
IV B-vitamins
How does cirrhosis cause
1) Splenomegaly
2) Upper GI bleed
1) Portal hypertension
2) Oesophageal varices
