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Osha 2a > Liver and friends > Flashcards

Liver and friends Flashcards

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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
Describe Hepatitis E
- RNA virus - self-limiting acute hepatitis - risk of chronic infection from types G3+4 in immunocompromised patients
26
How is Hepatitis E managed?
- acute: monitor for liver failure/fulminant hepatitis - chronic: reverse immunosuppression, treat with ribavirin - avoid undercooked meat - screen blood donors
27
What type of virus is Hep B and how is it transmitted?
- DNA virus - transmitted by blood or bodily fluids - sharing needles/contaminated household products - vertical transmission
28
How does Hep B present?
- incubation 30-180 days (mean 75) - monitor liver function - rarely get fulminant hepatitic failure
29
How can Hep B be prevented?
- Antenatal screening (HBsAg) - screening and immunisation: followup testing for HBsAb - blood product screening
30
How is Hep B managed?
- pegylated interferon-α 2a: weekly subcut injection - oral nucleoside analogues (inhibit viral replication): tenofovir, entecavir
31
What type of virus is Hepatitis D and how is it transmitted?
- defective single stranded RNA virus - can only survive with Hep B - attaches itself to HbsAg to survive - transmitted by blood and bodily fluids
32
How is Hep D tested for and treated?
- test for Hep D antibody, if +ve test for HDV RNA - treat with pegylated interferon α
33
What type of virus is Hep C and how is it transmitted?
- RNA virus - becomes chronic in 75% - blood and bodily fluids - blood products, injecting drug use, iatrogenic
34
How is Hep C diagnosed and treated?
- Hep C antibody then RNA screening - directly-acting antiviral therapy - lifestyle modification
35
Which types of hepatitis do PHE need to be notified of?
- Hep A, B, C, D, E
36
Describe Type 1 autoimmune hepatitis
- occurs in adults - typically women 40s/50s - fatigue, symptoms of liver disease - anti-LKM1 and anti-LC1 autoantibodies
37
Describe type 2 autoimmune hepatitis
- occurs in children > teens-early 20 - present with acute hepatitis, high transaminases, jaundice - ANA, anti-actin and anti-SLA/LP autoantibodies
38
How is autoimmune hepatitis diagnosed and treated?
- liver biopsy - high dose steroids: prednisolone and immunosuppressants
39
What are the 3 steps in the progression of alcoholic liver disease?
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
40
What are the signs of liver disease/cirrhosis?
- jaundice - hepatomegaly - spider naevi - palmar erythema - bruising - ascites
41
What are the typical results of bloods in someone with alcoholic liver disease/cirrhosis?
- 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
42
What are other investigations that can be done for alcoholic liver disease?
- ultrasound - endoscopy - CT and MRI - liver biopsy
43
How is alcoholic liver disease managed?
- stop drinking alcohol permanently - nutritional support and high protein diet - steroids in short term - refer for liver transplant if severe
44
What is Wernicke's encephalopathy?
- alcohol excess leads to thiamine (B1) deficiency - confusion, oculomotor disturbance and ataxia - leads to Korsakoff's syndrome
45
What is non alcoholic fatty liver disease and how does it present?
- 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
What are the 4 stages of NAFLD?
1. Non-alcoholic Fatty Liver Disease 2. Non-Alcoholic Steatohepatitis (NASH) 3. Fibrosis 4. Cirrhosis
47
How is NAFLD managed?
- weight loss - exercise - stop smoking - control diabetes, BP, cholesterol, avoid alcohol - possible treatment with Vit E or pioglitazone
48
How is NAFLD investigated?
- liver ultrasound - 1st line: enhanced liver fibrosis - 2nd line: NAFLD fibrosis score - 3rd line: Fibroscan
49
Describe enhanced liver fibrosis testing
- 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
Describe NAFLD fibrosis score and fibroscan
- 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
What is primary sclerosing cholangitis?
- 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
What are the causes and risk factors of primary sclerosing cholangitis?
- genetic, autoimmune, intestinal microbiome and environmental factors - association with ulcerative colitis - male - aged 30-40 - family history
53
How does primary sclerosing cholangitis present?
- jaundice - chronic upper right quadrant pain - pruritus - fatigue - hepatomegaly
54
How is primary sclerosing cholangitis managed?
- liver transplant - ERCP to dilate and stent strictures - Colestyramine
55
How is primary sclerosing cholangitis diagnosed?
- 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
What is the serology of patients with primary sclerosing cholangitis?
- AMA negative - HBVsAg and HCVAb negative - ANA, pANCA, SMA positive
57
What are gallstones?
- formation of hard stones in gallbladder - form from cholesterol, bile pigment, or mixed - lead to acute cholecystitis, acute cholangitis and pancreatitis
58
What are the risk factors for gallstones?
- 4 F's - female, fat, fair, forty, (fertile)
59
How do gallstones present?
- may be asymptomatic - severe, colicky, epigastric or RUQ pain - triggered by meals, lasting 30 mins-8hrs - associated with nausea and vomiting
60
How are gallstones diagnosed?
- GOLD: ultrasound: duct dilation, stones, gallbladder wall thickness
61
What is the pathophysiology and presentation of biliary colic?
- 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
What is acute cholecystitis?
- inflammation of the gallbladder caused by blockage of cystic duct preventing drainage - usually from gallstones
63
How does acute cholecystitis present?
- 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
What is Murphy's sign?
- 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
How is acute cholecystitis diagnosed?
- abdo ultrasound - thickened gallbladder wall, stones/sludge and fluid around gallbladder - MRCP
66
How is acute cholecystitis managed?
- nil by mouth - IV fluids - antibiotics - NG tube - ERCP used to remove stones - cholecystectomy if more severe
67
What is acute cholangitis?
- infection and inflammation in the bile ducts - caused by obstruction or infection from ERCP
68
Which organisms most commonly cause acute cholangitis?
- E. coli - Klebsiella - Enterococcus
69
How does acute cholangitis present?
- Charcot's triad: RUQ pain, fever, jaundice
70
How is acute cholangitis diagnosed?
- abdo ultrasound - CT - MRCP - endoscopic ultrasound
71
How is acute cholangitis managed?
- nil by mouth - IV fluids - blood cultures and IV antibiotics
72
Describe pre-hepatic jaundice
- 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
Describe hepatocellular jaundice
- 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
Describe cholestatic jaundice
- 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
What is the pathophysiology behind jaundice?
- 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
What are the causes of pancreatitis?
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
How do gallstones cause pancreatitis?
- 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
How does pancreatitis present?
- severe epigastric pain radiating through to back - vomiting - abdo tenderness - systematically unwell
79
How is pancreatitis investigated?
- FBC, U&E, LFT, calcium, ABG - amylase raised >3x, lipase, CRP raised - Ultrasound, abdo CT
80
What is the Glasgow score?
- assesses pancreatitis severity - 0-1 = mild pancreatitis - 2 = moderate pancreatitis - 3+ = severe pancreatitis
81
What factors are used to calculate the Glasgow score?
- 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
How is acute pancreatitis managed?
- ABCDE resus - IV fluids and analgesia - nil by mouth - monitoring and treatment of complications - antibiotics if required
83
What is liver cirrhosis?
- Results from chronic inflammation and damage to liver cells - damage is replaced with scar tissue and nodules form - inc resistance causes portal hypertension
84
What are the causes of cirrhosis?
- Hep B + C - NAFLD - Alcoholic fatty liver disease - autoimmune hepatitis - PBC
85
What is seen on the ultrasound of someone with liver cirrhosis?
- nodularity of the surface - corkscrew appearance to the arteries to compensate for reduced portal flow - enlarged portal vein - ascites - splenomegaly
86
How is cirrhosis managed?
- ultrasound - endoscopy - high protein, low sodium diet - MELD score - possible transplant
87
What are varices?
- 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
How are varices treated?
- propanolol reduces portal htn by acting as non-selective β blocker - elastic band ligation
89
What is high ALT/AST indicative of?
- 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
What is ALP?
- 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
What is endoscopic retrograde cholangio-pancreatography (ERCP)?
- 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
What does HBsAg indicate?
- Hep B surface antigen - active infection
93
What does HBeAg indicate?
- 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
What does HBcAb indicate?
- hep B antibodies - can be used to distinguish acute, chronic and past infections - IgM: active infection - IgG: past infection where HBsAg is -ve
95
What does HBsAB indicate?
- past or current infection or vaccination - immune response to HBsAg - other viral markers needed
96
What does HBV DNA show?
- direct count of the viral load
97
What is Wilson's disease and what type of inheritance is it?
- excessive accumulation of copper in body and tissues - caused by mutation on chromosome 13 - autosomal recessive
98
What are hepatic and psychiatric problems of Wilson's?
- Kayser-Fleischer rings - hepatitis and cirrhosis - ranging from depression to psychosis - haemolytic anaemia - renal tubular acidosis - osteopenia
99
What neurological symptoms arise from Wilson's?
- dysarthria - dystonia - Parkinsonism: tremor, bradykinesia, rigidity
100
How is Wilson's diagnosed?
- serum caeruloplasmin (protein that carries copper in the blood) - GOLD: liver biopsy - 24hr urine copper assay elevated - Kayser-Fleischer rings
101
How is Wilson's disease treated?
- copper chelation - penicillamine - trietene
102
What is haemochromatosis?
- iron storage disorder resulting in excessive total body iron and iron deposition in tissues - mutations in human haemochromatosis protein (HFE) - autosomal recessive
103
What are symptoms of haemochromatosis?
- chronic tiredness - joint pain - pigmentation: bronze/slate-grey - hair loss - erectile dysfunction/ammenorrhoea - memory and mood disturbance
104
How is haemochromatosis investigated?
- high serum ferritin and high transferrin saturation - genetic testing - liver biopsy: Perl's stain for Fe conc in parenchymal cells
105
What is the management of haemochromatosis?
- venesection - monitoring serum ferritin - avoid alcohol - genetic counselling
106
What is α 1 antitrypsin deficiency?
- abnormality in the gene for a protease inhibitor called α-1 antitrypsin
107
What is the pathophysiology behind α 1 antitrypsin deficiency?
- elastase secreted by neutrophils and digests connective tissue - A1AT produced in liver and inhibits elastase - coded for by chromosome 14 - autosomal recessive defect
108
How does A1AT affect the liver and lungs?
- 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
How is A1AT diagnosed?
- low serum α1AT - liver biopsy shows cirrhosis and acid Schiff positive globules - genetic testing - high res CT thorax
110
How is A1AT managed?
- stop smoking - symptomatic management - organ transplant

Osha 2a (15 decks)

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