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Osha 2a > Liver and friends > Flashcards

Liver and friends Flashcards

1
Q

What is cholestasis?

A

blockage of bile flow

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2
Q

What is the difference between cholelithiasis and choledocholithiasis?

A
  • cholelithiasis: presence of gallstones
  • choledocholithiasis: gallstones in the bile duct
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3
Q

What is cholecystitis vs cholangitis?

A
  • cholecystitis: inflammation of the gallbladder
  • cholangitis: inflammation of the bile ducts
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4
Q

What is the pathophysiology behind primary biliary cirrhosis?

A
  • autoimmune condition of small bile ducts
  • intralobar ducts affected first
  • causes obstruction of bile outflow (cholestasis)
  • back pressure leads to fibrosis, cirrhosis and failure
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5
Q

What is the epidemiology behind primary biliary cirrhosis?

A
  • 90% cases occur in women
  • occurs in patients with other autoimmune diseases + rheumatoid conditions e.g. arthritis, systemic sclerosis
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6
Q

How does primary biliary cirrhosis present?

A
  • fatigue
  • pruritus (itching)
  • GI problems and abdominal pain
  • jaundice, pale stools
  • signs of cirrhosis/failure
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7
Q

What is the physiology behind the presentation of primary biliary cirrhosis?

A
  • bile acids, bilirubin and cholesterol are usually excreted through bile ducts but are obstructed and build up in blood
  • bile acids > itching
  • bilirubin > jaundice
  • cholesterol > xanthelasma
  • lack of bile acids in GI > GI disturbance, malabsorption and greasy, pale stools
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8
Q

How is primary biliary cirrhosis diagnosed?

A
  • LFTs: ALP raised, other liver enzymes and bilirubin later in disease
  • AMAs +ve in 95% cases
  • ESR and IgM raised
  • liver biopsy
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9
Q

How is primary biliary cirrhosis treated?

A
  • Ursodeoxycholic acid: reduces intestinal absorption of cholesterol
  • Colestyramine effective in 50% cases of pruritus
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10
Q

What is ascites?

A
  • fluid in the peritoneal cavity
  • inc pressure in portal system causes fluid to leak out of capillaries in liver and bowel
  • lower fluid sensed by kidneys > renin released > aldosterone release > fluid reabsorption > transudative (low protein content)
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11
Q

What are the signs, symptoms and investigations of ascites?

A
  • abdo distention
  • shifting dullness (fullness in flank)
  • fluid thrill
  • transudate low
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12
Q

How is ascites managed?

A
  • low sodium diet
  • anti aldosterone diuretic (spironolactone)
  • paracentesis
  • prophylactic antibiotics if bacterial
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13
Q

What is peritonitis and how is it caused?

A
  • inflammation of the peritoneum
  • caused by perforation of the GI tract, bacterial or surgery/trauma
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14
Q

How is peritonitis investigated and managed?

A
  • CXR, serum amylase to rule out pancreatitis, ultrasound/CT
  • IV fluids and electrolytes to reverse hypovolaemia
  • surgery to repair perforation
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15
Q

How does bacterial peritonitis present?

A
  • Can be asymptomatic so have a low threshold for ascitic fluid culture
  • Fever
  • Abdominal pain
  • Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
  • Ileus
  • Hypotension
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16
Q

What bacteria most commonly cause bacterial peritonitis and how is it treated?

A
  • Escherichia coli
  • Klebsiella pneumoniae
  • gram positive cocci e.g. staphylococcus or enterococcus
  • treated with cephalosporin e.g. cefotaxime
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17
Q

What is the difference between acute and chronic hepatitis?

A
  • hepatitis: inflammation of the liver
  • acute: lasting up to 6 months
  • chronic: lasting beyond 6 months
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18
Q

What is the presentation of acute hepatitis?

A
  • GI upset, abdo pain
  • jaundice, pale stools/dark urine
  • tender hepatomegaly
  • liver failure symptoms
  • raised transaminase (ALT+AST)
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19
Q

What are the viral causes of acute hepatitis?

A
  • hepatitis: A, B ± D, C, E
  • human herpes viruses e.g. HSV, EBV, CMV, VZV
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20
Q

What are the non-viral, infectious causes of acute hepatitis?

A
  • spirochetes
  • mycobacteria
  • bacteria
  • parasites
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21
Q

What are non-infection causes of hepatitis?

A
  • drugs
  • alcohol
  • Non-alcoholic fatty liver disease
  • Pregnancy
  • Autoimmune hepatitis
  • Hereditary metabolic causes
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22
Q

Where is hepatitis A found and how is it transmitted?

A
  • most common type of viral hepatitis worldwide
  • spreads through faeco-oral transmission: contaminated food and water
  • RNA virus
  • mostly in countries with lack of access to safe drinking water and lower socioeconomic backgrounds
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23
Q

How does Hepatitis A present and how is it treated?

A
  • incubation period of 2-4 weeks
  • cholestasis: pale stools, dark urine
  • 100% immunity after infection
  • managed by analgesia
  • self-limiting so cannot become chronic
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24
Q

What are the causes of hepatitis E and how is it transmitted?

A
  • faeco-oral transmission
  • G1+2: contaminated food and water, poor sanitation
  • G3+4: undercooked meat: mammalian zoonotic reservoir
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25
Q

Describe Hepatitis E

A
  • RNA virus
  • self-limiting acute hepatitis
  • risk of chronic infection from types G3+4 in immunocompromised patients
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26
Q

How is Hepatitis E managed?

A
  • acute: monitor for liver failure/fulminant hepatitis
  • chronic: reverse immunosuppression, treat with ribavirin
  • avoid undercooked meat
  • screen blood donors
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27
Q

What type of virus is Hep B and how is it transmitted?

A
  • DNA virus
  • transmitted by blood or bodily fluids
  • sharing needles/contaminated household products
  • vertical transmission
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28
Q

How does Hep B present?

A
  • incubation 30-180 days (mean 75)
  • monitor liver function
  • rarely get fulminant hepatitic failure
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29
Q

How can Hep B be prevented?

A
  • Antenatal screening (HBsAg)
  • screening and immunisation: followup testing for HBsAb
  • blood product screening
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30
Q

How is Hep B managed?

A
  • pegylated interferon-α 2a: weekly subcut injection
  • oral nucleoside analogues (inhibit viral replication): tenofovir, entecavir
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31
Q

What type of virus is Hepatitis D and how is it transmitted?

A
  • defective single stranded RNA virus
  • can only survive with Hep B
  • attaches itself to HbsAg to survive
  • transmitted by blood and bodily fluids
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32
Q

How is Hep D tested for and treated?

A
  • test for Hep D antibody, if +ve test for HDV RNA
  • treat with pegylated interferon α
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33
Q

What type of virus is Hep C and how is it transmitted?

A
  • RNA virus
  • becomes chronic in 75%
  • blood and bodily fluids
  • blood products, injecting drug use, iatrogenic
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34
Q

How is Hep C diagnosed and treated?

A
  • Hep C antibody then RNA screening
  • directly-acting antiviral therapy
  • lifestyle modification
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35
Q

Which types of hepatitis do PHE need to be notified of?

A
  • Hep A, B, C, D, E
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36
Q

Describe Type 1 autoimmune hepatitis

A
  • occurs in adults - typically women 40s/50s
  • fatigue, symptoms of liver disease
  • anti-LKM1 and anti-LC1 autoantibodies
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37
Q

Describe type 2 autoimmune hepatitis

A
  • occurs in children > teens-early 20
  • present with acute hepatitis, high transaminases, jaundice
  • ANA, anti-actin and anti-SLA/LP autoantibodies
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38
Q

How is autoimmune hepatitis diagnosed and treated?

A
  • liver biopsy
  • high dose steroids: prednisolone and immunosuppressants
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39
Q

What are the 3 steps in the progression of alcoholic liver disease?

A
  1. alcohol related fatty liver: drinking causes a buildup of fat which reverses after 2 weeks of sobriety
  2. alcoholic hepatitis: over a long period, alcohol causes inflammation in liver sites. also associated with binge drinking
  3. cirrhosis: liver is made up of more scar tissue than healthy tissue. Is irreversible
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40
Q

What are the signs of liver disease/cirrhosis?

A
  • jaundice
  • hepatomegaly
  • spider naevi
  • palmar erythema
  • bruising
  • ascites
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41
Q

What are the typical results of bloods in someone with alcoholic liver disease/cirrhosis?

A
  • FBC: raised MCV
  • LFTs: elevated ALT and AST. ALP in advanced stage. Low albumin and elevated bilirubin
  • Clotting: elevated PT
  • U&Es may be deranged
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42
Q

What are other investigations that can be done for alcoholic liver disease?

A
  • ultrasound
  • endoscopy
  • CT and MRI
  • liver biopsy
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43
Q

How is alcoholic liver disease managed?

A
  • stop drinking alcohol permanently
  • nutritional support and high protein diet
  • steroids in short term
  • refer for liver transplant if severe
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44
Q

What is Wernicke’s encephalopathy?

A
  • alcohol excess leads to thiamine (B1) deficiency
  • confusion, oculomotor disturbance and ataxia
  • leads to Korsakoff’s syndrome
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45
Q

What is non alcoholic fatty liver disease and how does it present?

A
  • chronic health condition
  • fat deposited in liver cells which can interfere with functioning
  • shares risk factors w CVD and diabetes
  • normally no symptoms and incidental findings then presents with liver failure symptoms
46
Q

What are the 4 stages of NAFLD?

A
  1. Non-alcoholic Fatty Liver Disease
  2. Non-Alcoholic Steatohepatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
47
Q

How is NAFLD managed?

A
  • weight loss
  • exercise
  • stop smoking
  • control diabetes, BP, cholesterol, avoid alcohol
  • possible treatment with Vit E or pioglitazone
48
Q

How is NAFLD investigated?

A
  • liver ultrasound
  • 1st line: enhanced liver fibrosis
  • 2nd line: NAFLD fibrosis score
  • 3rd line: Fibroscan
49
Q

Describe enhanced liver fibrosis testing

A
  • blood test
  • measures HA, PIIINP and TIMP-1
  • < 7.7 = none to mild fibrosis
  • ≤ 7.7 to 9.8 indicates mild fibrosis
  • ≥ 9.8 indicates severe fibrosis
50
Q

Describe NAFLD fibrosis score and fibroscan

A
  • if ELF unavailable
  • algorithm of age, BMI, liver enzymes, platelets, albumin
  • used to rule out fibrosis but not assess severity when present
  • fibroscan: measures stiffness
51
Q

What is primary sclerosing cholangitis?

A
  • bile duct inflammation
  • intrahepatic or extra hepatic ducts become structured and fibrotic
  • causes obstruction to bile flow out of liver and into intestines
  • leads to hepatitis, fibrosis and cirrhosis
52
Q

What are the causes and risk factors of primary sclerosing cholangitis?

A
  • genetic, autoimmune, intestinal microbiome and environmental factors
  • association with ulcerative colitis
  • male
  • aged 30-40
  • family history
53
Q

How does primary sclerosing cholangitis present?

A
  • jaundice
  • chronic upper right quadrant pain
  • pruritus
  • fatigue
  • hepatomegaly
54
Q

How is primary sclerosing cholangitis managed?

A
  • liver transplant
  • ERCP to dilate and stent strictures
  • Colestyramine
55
Q

How is primary sclerosing cholangitis diagnosed?

A
  • Gold: MRCP: magnetic resonance cholangiopancreatography
  • MRI of liver, bile ducts and pancreas
  • LFTs show cholestatic picture
  • ALP is most deranged
  • bilirubin, ALT and AST rise in more severe disease
56
Q

What is the serology of patients with primary sclerosing cholangitis?

A
  • AMA negative
  • HBVsAg and HCVAb negative
  • ANA, pANCA, SMA positive
57
Q

What are gallstones?

A
  • formation of hard stones in gallbladder
  • form from cholesterol, bile pigment, or mixed
  • lead to acute cholecystitis, acute cholangitis and pancreatitis
58
Q

What are the risk factors for gallstones?

A
  • 4 F’s
  • female, fat, fair, forty, (fertile)
59
Q

How do gallstones present?

A
  • may be asymptomatic
  • severe, colicky, epigastric or RUQ pain
  • triggered by meals, lasting 30 mins-8hrs
  • associated with nausea and vomiting
60
Q

How are gallstones diagnosed?

A
  • GOLD: ultrasound: duct dilation, stones, gallbladder wall thickness
61
Q

What is the pathophysiology and presentation of biliary colic?

A
  • occurs due to inc cholesterol, dec bile salts and biliary stasis
  • pain occurs when gallbladder contracts against stone lodged in neck of gallbladder
  • colicky RUQ pain
  • worse postprandially and after fatty meals
  • nausea and vomiting
62
Q

What is acute cholecystitis?

A
  • inflammation of the gallbladder caused by blockage of cystic duct preventing drainage
  • usually from gallstones
63
Q

How does acute cholecystitis present?

A
  • RUQ pain radiating around side and to right shoulder (due to diaphragmatic irritation)
  • pain on inspiration
  • fever, nausea, vomiting
  • tachycardia and tachypnoea
  • Murphy’s sign
  • raised inflammatory markers and wbc
64
Q

What is Murphy’s sign?

A
  • Place hand in RUQ and apply pressure
  • ask patient to breathe in
  • gallbladder moves downwards during inspiration and comes in contact with hand
  • stimulation of inflamed gallbladder results in acute pain and stopping of inspiration
65
Q

How is acute cholecystitis diagnosed?

A
  • abdo ultrasound
  • thickened gallbladder wall, stones/sludge and fluid around gallbladder
  • MRCP
66
Q

How is acute cholecystitis managed?

A
  • nil by mouth
  • IV fluids
  • antibiotics
  • NG tube
  • ERCP used to remove stones
  • cholecystectomy if more severe
67
Q

What is acute cholangitis?

A
  • infection and inflammation in the bile ducts
  • caused by obstruction or infection from ERCP
68
Q

Which organisms most commonly cause acute cholangitis?

A
  • E. coli
  • Klebsiella
  • Enterococcus
69
Q

How does acute cholangitis present?

A
  • Charcot’s triad: RUQ pain, fever, jaundice
70
Q

How is acute cholangitis diagnosed?

A
  • abdo ultrasound
  • CT
  • MRCP
  • endoscopic ultrasound
71
Q

How is acute cholangitis managed?

A
  • nil by mouth
  • IV fluids
  • blood cultures and IV antibiotics
72
Q

Describe pre-hepatic jaundice

A
  • occurs in excessive haemolysis causing inc bilirubin production
  • decreased liver uptake or conjugation > unconjugated bilirubin enters blood
  • water insoluble > doesn’t enter urine > hyperbilirubinaemia
  • newborns have reduced ability to remove bilirubin
  • leads to dark urine (on standing) and stools
73
Q

Describe hepatocellular jaundice

A
  • results from inability of liver to excrete or conjugate bilirubin due to tissue damage
  • hepatocyte damage and cholestasis
  • levels of conjugated and unconjugated bilirubin increase
  • causes are viral: CMV, EBV, hepatitis and cirrhosis
74
Q

Describe cholestatic jaundice

A
  • results from obstruction in the bile duct
  • liver can conjugate bilirubin but is unable to excrete it
  • conjugated bilirubin overspills into blood leading to conjugated hyperbilirubinaemia
  • leads to dark urine and pale stools
  • caused by gallstones, pancreatic cancer, PBC/PSC
75
Q

What is the pathophysiology behind jaundice?

A
  • yellow pigmentation of skin, sclera and mucosa
  • occurs due to inc plasma bilirubin >35µmol/l
  • normally, bilirubin is conjugated within the liver and excreted via bile. The majority of this is digested as urobilinogen and stercobilin
  • jaundice occurs when this is disrupted
76
Q

What are the causes of pancreatitis?

A

I - idiopathic
G - gallstones
E - ethanol (alcohol - is toxic > inflammation)
T - trauma
S - steroids
M - mumps
A - autoimmune
S - scorpion sting
H - hyperlipidaemia
E - ERCP
D - drugs (furosemide, thiazide diuretics, azathioprine)

77
Q

How do gallstones cause pancreatitis?

A
  • get trapped at ampulla of Vater
  • block flow of bile and pancreatic juice into duodenum
  • reflux of bile and prevention of pancreatic enzyme secretion > inflammation
78
Q

How does pancreatitis present?

A
  • severe epigastric pain radiating through to back
  • vomiting
  • abdo tenderness
  • systematically unwell
79
Q

How is pancreatitis investigated?

A
  • FBC, U&E, LFT, calcium, ABG
  • amylase raised >3x, lipase, CRP raised
  • Ultrasound, abdo CT
80
Q

What is the Glasgow score?

A
  • assesses pancreatitis severity
  • 0-1 = mild pancreatitis
  • 2 = moderate pancreatitis
  • 3+ = severe pancreatitis
81
Q

What factors are used to calculate the Glasgow score?

A
  • P – PaO2 < 8 KPa
  • A – Age > 55
  • N – Neutrophils (WBC > 15)
  • C – Calcium < 2
  • R – uRea >16
  • E – Enzymes (LDH > 600 or AST/ALT >200)
  • A – Albumin < 32
  • S – Sugar (Glucose >10)
82
Q

How is acute pancreatitis managed?

A
  • ABCDE resus
  • IV fluids and analgesia
  • nil by mouth
  • monitoring and treatment of complications
  • antibiotics if required
83
Q

What is liver cirrhosis?

A
  • Results from chronic inflammation and damage to liver cells
  • damage is replaced with scar tissue and nodules form
  • inc resistance causes portal hypertension
84
Q

What are the causes of cirrhosis?

A
  • Hep B + C
  • NAFLD
  • Alcoholic fatty liver disease
  • autoimmune hepatitis
  • PBC
85
Q

What is seen on the ultrasound of someone with liver cirrhosis?

A
  • nodularity of the surface
  • corkscrew appearance to the arteries to compensate for reduced portal flow
  • enlarged portal vein
  • ascites
  • splenomegaly
86
Q

How is cirrhosis managed?

A
  • ultrasound
  • endoscopy
  • high protein, low sodium diet
  • MELD score
  • possible transplant
87
Q

What are varices?

A
  • portal hypertension causes back pressure where the portal system anastomoses with the systemic venous system
  • causes swollen, torturous vessels
  • occur at: gastro-oesophageal, ileocaecal junctions, rectum, anterior abdo wall
88
Q

How are varices treated?

A
  • propanolol reduces portal htn by acting as non-selective β blocker
  • elastic band ligation
89
Q

What is high ALT/AST indicative of?

A
  • Alanine aminotransferase and aspartate aminotransferase
  • markers of hepatocellular injury
  • if ALT + AST slightly inc and ALP inc a lot = obstruction
  • ALT + AST high compared to ALP = hepatocellular injury
90
Q

What is ALP?

A
  • alkaline phosphatase
  • enzyme originating in the liver
  • raised ALP indicates biliary obstruction if present with RUQ pain and jaundice
  • can also be caused by liver + bone malignancy
91
Q

What is endoscopic retrograde cholangio-pancreatography (ERCP)?

A
  • inspiring endoscope down to sphincter of Oddi to clear stones in bile ducts
  • can take X-rays and diagnose pathology, clear stones, insert stents
  • can lead to cholangitis and pancreatitis
92
Q

What does HBsAg indicate?

A
  • Hep B surface antigen
  • active infection
93
Q

What does HBeAg indicate?

A
  • E antigen: marker of viral replication
  • indicates high infectivity
  • patient is in acute phase
  • if negative but HbeAb is positive then virus has stopped replicating
94
Q

What does HBcAb indicate?

A
  • hep B antibodies
  • can be used to distinguish acute, chronic and past infections
  • IgM: active infection
  • IgG: past infection where HBsAg is -ve
95
Q

What does HBsAB indicate?

A
  • past or current infection or vaccination
  • immune response to HBsAg
  • other viral markers needed
96
Q

What does HBV DNA show?

A
  • direct count of the viral load
97
Q

What is Wilson’s disease and what type of inheritance is it?

A
  • excessive accumulation of copper in body and tissues
  • caused by mutation on chromosome 13
  • autosomal recessive
98
Q

What are hepatic and psychiatric problems of Wilson’s?

A
  • Kayser-Fleischer rings
  • hepatitis and cirrhosis
  • ranging from depression to psychosis
  • haemolytic anaemia
  • renal tubular acidosis
  • osteopenia
99
Q

What neurological symptoms arise from Wilson’s?

A
  • dysarthria
  • dystonia
  • Parkinsonism: tremor, bradykinesia, rigidity
100
Q

How is Wilson’s diagnosed?

A
  • serum caeruloplasmin (protein that carries copper in the blood)
  • GOLD: liver biopsy
  • 24hr urine copper assay elevated
  • Kayser-Fleischer rings
101
Q

How is Wilson’s disease treated?

A
  • copper chelation
  • penicillamine
  • trietene
102
Q

What is haemochromatosis?

A
  • iron storage disorder resulting in excessive total body iron and iron deposition in tissues
  • mutations in human haemochromatosis protein (HFE)
  • autosomal recessive
103
Q

What are symptoms of haemochromatosis?

A
  • chronic tiredness
  • joint pain
  • pigmentation: bronze/slate-grey
  • hair loss
  • erectile dysfunction/ammenorrhoea
  • memory and mood disturbance
104
Q

How is haemochromatosis investigated?

A
  • high serum ferritin and high transferrin saturation
  • genetic testing
  • liver biopsy: Perl’s stain for Fe conc in parenchymal cells
105
Q

What is the management of haemochromatosis?

A
  • venesection
  • monitoring serum ferritin
  • avoid alcohol
  • genetic counselling
106
Q

What is α 1 antitrypsin deficiency?

A
  • abnormality in the gene for a protease inhibitor called α-1 antitrypsin
107
Q

What is the pathophysiology behind α 1 antitrypsin deficiency?

A
  • elastase secreted by neutrophils and digests connective tissue
  • A1AT produced in liver and inhibits elastase
  • coded for by chromosome 14
  • autosomal recessive defect
108
Q

How does A1AT affect the liver and lungs?

A
  • liver: A1AT is produced in the liver and the mutation can get trapped leading to cirrhosis and hepatocellular carcinoma
  • lungs: excess of enzymes attack connective tissue leading to bronchiectasis and emphysema
109
Q

How is A1AT diagnosed?

A
  • low serum α1AT
  • liver biopsy shows cirrhosis and acid Schiff positive globules
  • genetic testing
  • high res CT thorax
110
Q

How is A1AT managed?

A
  • stop smoking
  • symptomatic management
  • organ transplant

Osha 2a (15 decks)

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