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Phase 2a Green Conditions > Liver and friends > Flashcards

Liver and friends Flashcards

1
Q

What are the functions of the liver?

A
  • oestrogen regulation
  • detoxification
  • metabolises carbohydrates
  • albumin production
  • clotting factor production
  • bilirubin regulation
  • immunity → Kupffer cells in reticuloendothelial system
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2
Q

Acute presentation of liver failure

A
  • malaise
  • nausea
  • anorexia
  • jaundice

rare

  • confusion
  • bleeding
  • pain
  • hypoglycaemia
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3
Q

Chronic presentation of liver failure (11)

A
  • ascites
  • oedema
  • Dupuytren’s contracture
  • malaise
  • anorexia
  • clubbing
  • palmar erythema
  • xanthelasma
  • spider naevi
  • hepatomegaly
  • bleeding → haematemesis, easy bruising
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4
Q

Progression of chronic liver disease

A
  1. chronic liver condition
  2. liver damage
  3. liver symptoms
  4. liver cirrhosis if prolonged
  5. liver failure and higher risk of HCC
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5
Q

What bloods can be done to investigate liver failure?

A
  • liver function tests LFTs
  • liver hepatic enzymes
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6
Q

What can be measured in LFTs?

A
  • serum bilirubin
  • serum albumin
  • prothrombin time → INR

serum albumin and PT = best indicators of liver function

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7
Q

What can be measured in liver hepatic enzymes?

A

aminotransferases

  • leak into blood when hepatocytes are damaged
  • AST
  • ALT → more specific in disease

alkaline phosphate ALP
- raised in intra/extra hepatic cholestatic disease of any cause

gamma-glutamyl transferase GGT

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8
Q

What is liver failure?

A

liver loses its ability to repair and regenerate leading to decomposition

decomposition

  • hepatic encephalopathy
  • abnormal bleeding
  • ascites
  • jaundice
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9
Q

Causes of liver failure

A
  • infection → viral hepatitis
  • metabolic → Wilson’s, A1AT
  • autoimmune → PBC, PSC
  • neoplastic → HCC, metastatic disease
  • vascular → Budd Chiari, ischaemia
  • toxins → PCM, alcohol
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10
Q

Signs of liver failure

A
  • jaundice
  • coagulopathy
  • hepatic encephalopathy
  • fetor hepaticus = sweet and musty breath/urine
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11
Q

Investigations for liver failure

A

clinical examination

bloods

  • raised PT/AST/ALT
  • toxicology screen
  • FBC, U&E

if ascites present → peritoneal tap with M&C

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12
Q

Management of liver failure

A
  • fluids
  • supportive measures
  • treat complications
  • transplant
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13
Q

How do you treat the complications of liver failure?

A
  • ascites → diuretics
  • cerebral oedema → mannitol
  • bleeding → vitamin K
  • encephalopathy → lactulose
  • sepsis → sepsis 6, Abs
  • hypoglycaemia → dextrose
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14
Q

What is alcoholic liver disease

A

effect of long term excessive consumption on liver

  1. alcoholic related fatty liver
    - drinking leads to build up of fat in liver
    - reverses in 2 weeks if drinking stops
  2. alcoholic hepatitis
    - long term drinking → inflammation in liver sites
    - mild version is reversible
  3. cirrhosis
    - liver made of scar tissue
    - irreversible
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15
Q

Investigations for alcoholic liver disease

A
  • bloods
  • US/CT/MRI liver
  • endoscopy for varices
  • DIAGNOSTIC = liver biopsy
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16
Q

What blood results might you see in alcoholic liver disease

A
  • raised ALT/AST/PT
  • markedly raised GGT
  • raised ALP in later stages
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17
Q

Management of alcoholic liver disease

A
  • stop drinking
  • nutritional support
  • steroids improve short term outcomes
  • treat complications
  • transplant
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18
Q

What are the complications of alcoholic liver disease?

A
  • Wernicke-Korsakoff encephalopathy
  • acute/chronic pancreatitis
  • oesophageal varices
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19
Q

What is Wernicke-Korsakoff syndrome?

A
  • alcohol excess = B1 deficiency
  • presents with ataxia, confusion, nystagmus, memory impairment
  • treatment = IV thiamine, no alcohol
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20
Q

What is NAFLD?

A
  • non-alcoholic fatty liver disease
  • chronic metabolic syndrome relating to processing and storing energy
  • increases risk of heart disease, stroke, diabetes
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21
Q

Stages of NAFLD

A
  1. healthy
  2. steatosis
  3. steatohepatitis
  4. fibrosis
  5. cirrhosis
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22
Q

Risk factors for NAFLD (7)

A
  • obesity
  • poor diet, low activity
  • T2DM
  • high cholesterol
  • middle age onwards
  • smoking
  • high BP
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23
Q

Clinical presentation of NAFLD

A
  • asymptomatic
  • N,D&V
  • hepatomegaly
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24
Q

Investigations for NAFLD

A
  • US liver for steatosis
  • biopsy = DIAGNOSTIC

fibrosis

  1. enhanced liver fibrosis blood test
  2. NAFLD fibrosis score
  3. fibroscan
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25
Q

Management of NAFLD

A
  • weight loss
  • exercise
  • stop smoking
  • control diabetes, BP, cholesterol
  • avoid alcohol
  • treat fibrosis with vitE or pioglitazone
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26
Q

What investigations should be performed after abnormal LFTs

A
  • US liver
  • hepB and C serology
  • autoantibodies → autoimmune hep, PBC, PSC
  • immunoglobulins → autoimmune hep, PBC
  • caeruloplasmin → Wilson’s
  • A1AT levels
  • ferritin and transferrin saturation → hereditary haemochromatosis
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27
Q

What type of virus is hepA?

A

RNA

  • rarer
  • developing world
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28
Q

How is HepA transmitted?

A

faecal-oral transmission

  • contaminated food
  • fly vectors
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29
Q

Pathophysiology of HepA

A
  • acute infection
  • usually cleared by host immune system
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30
Q

Presentation of HepA

A
  • non specific symptoms → nausea, anorexia, malaise

after 1-2 weeks → liver symptoms

  • jaundice
  • hepatomegaly
  • skin rash
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31
Q

Investigations for HepA

A

LFTs

  • raised ALT, bilirubin
  • serology
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32
Q

Treatment for HepA

A
  • vaccine available
  • treatment often not required
  • generally supportive
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33
Q

Complications for HepA

A
  • rare
  • acute liver failure
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34
Q

What type of virus is HepB?

A

DNA

  • present worldwide
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35
Q

Pathophysiology of HepB

A
  • acute infection infects hepatocyte
  • usually cleared by cellular response

chronic HBV

  • if HBsAg >6 months
  • depends on age/immunocompetence
  • inflammation can last 10 years → cirrhosis
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36
Q

Presentation of HepB

A
  • similar acute infection
  • if chronic, then signs of cirrhosis → jaundice, pruritus etc
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37
Q

Investigations for HepB

A
  • LFTs, serology
    if Ag after 6 months, confirm chronic HBV
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38
Q

Treatment for HepB

A
  • vaccine available → at risk
  • antiviral treatment → tenofovir = pegylated interferon alpha 2a
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39
Q

Complications of HepB

A

if chronic, increased risk of cirrhosis, HCC

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40
Q

What type of virus is HepC

A

RNA

  • more common in UK
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41
Q

How is HepB transmitted?

A
  • blood products → IVDU
  • sexually → MSM
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42
Q

How is HepC transmitted?

A

blood/blood products → IVDU>sexually

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43
Q

Pathophysiology of HepC

A
  • acute infection often asymptomatic → allows progression to chronic
  • chronic HCV causes slowly progressive fibrosis
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44
Q

Presentation of HepC

A
  • acute = asymptomatic
  • later on = signs of chronic liver disease
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45
Q

Investigations for HepC

A
  • LFTs, serology
  • if Ag after 6 months, confirm chronic HCV
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46
Q

Treatment for HepC

A
  • revolutionising from interferon based regimens to directly acting antiviral agents
  • Ribavirin = expensive
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47
Q

Complications of HepC

A
  • chronic liver disease
  • HCC
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48
Q

What type of virus is HepD

A

RNA

49
Q

How is HepD transmitted?

A
  • blood borne
  • IVDU, sexually
50
Q

Pathophysiology of HepD

A
  • unable to replicate on its own
  • requires concurrent HBV infection
  • makes HepB more likely to progress to cirrhosis/HCC
51
Q

Presentation of HepD

A

indistinguishable from acute HBV infection

52
Q

Treatment for HepD

A

same as HBV

53
Q

Complications of HepD

A

cirrhosis, HCC

54
Q

What type of virus is HepE

A

RNA

  • common in UK
55
Q

How is HepE transmitted

A
  • faeco-oral transmission
  • undercooked meat
56
Q

Presentation of HepE

A
  • 95% asymptomatic
  • usually self-limiting
57
Q

Investigations for HepE

A

serology

58
Q

Treatment for HepE

A
  • often not required
  • supportive
59
Q

Complications of HepE

A
  • rare
  • can progress to cirrhosis in immunocompromised
60
Q

What is liver cirrhosis?

A
  • diffuse pathological process
  • fibrosis
  • conversion of normal liver to structurally abnormal nodules → regenerative nodules
  • final stage of any chronic liver disease
  • irreversible but significant recovery if underlying cause treated
61
Q

Causes of cirrhosis

A
  • alcohol abuse → alcoholic liver disease
  • NAFLD
  • hepatitis B, C
  • haemochromatosis
  • Wilson’s
  • A1AT deficiency
62
Q

Investigations for cirrhosis

A

DEFINITIVE DIAGNOSTIC = liver biopsy

blood tests

  • INR/PT high
  • LFTs
  • FBC → thrombocytopenia
  • serum electrolytes

US and CT → hepatomegaly

63
Q

Treatment for cirrhosis

A

same as chronic liver disease

conservative

  • fluids
  • alcohol abstinence
  • good nutrition

treat complications of liver failure

DEFINITIVE TREATMENT = liver transplant

64
Q

Complications of cirrhosis

A
  • ascites
  • portal HTN
  • varices
  • jaundice
  • coagulopathy
  • hypoalbuminaemia
  • portosystemic encephalopathy
65
Q

What is ascites?

A

fluid in the peritoneal cavity

66
Q

Why do you get ascites in cirrhosis

A
  • hypoalbuminaemia → reduced oncotic pressure
  • portal HTN → increased hydrostatic pressure
  • renal water retention → peripheral arterial vasodilation mediated by NO
67
Q

Causes of ascites

A

cirrhosis = commonest cause

4 basic mechanisms

  • peritonitis = more leaky
  • reduced capillary hydrostatic pressure
  • reduced colloid oncotic pressure
  • peritoneal lymphatic draining
68
Q

Types of ascites

A

transudate

  • <25 protein
  • portal HTN, budd chiari, low plasma protein, HF

exudate

  • >25 protein
  • peritonitis, peritoneal malignancy
69
Q

Presentation of ascites

A
  • shifting dullness
  • weight gain
  • abdominal distention
  • signs of liver disease
  • respiratory distress
70
Q

Investigations for ascites

A

DIAGNOSTIC = aspiration

  • albumin
  • neutrophil count
71
Q

Complications of ascites

A

spontaneous bacterial peritonitis SBP

  • infection of ascitic fluid
  • most common causes = E.coli then K.pneumoniae
72
Q

What is biliary colic?

A

temporary blockage of the cystic duct by gallstones

73
Q

What is bile made of?

A
  • cholesterol
  • pigments
  • phospholipids
74
Q

What are gallstones?

A

occur when there is a disturbance to the equilibrium of bile causing solid deposits

made of

  • cholesterol → excess production = obesity, fatty diet
  • pigment → haemolytic anaemia
  • mixed
75
Q

Risk factors of biliary colic

A

5 Fs

  • fat
  • female
  • forty
  • fair
  • fertile
76
Q

Presentation of biliary colic

A
  • classic colicky RUQ pain → worse after eating large/fatty meals
  • referred shoulder pain
  • N&V
77
Q

Investigations for biliary colic

A

rule out cholecystitis/cholangitis

DIAGNOSTIC = US

  1. stones
  2. gallbladder wall thickness
  3. duct dilation
78
Q

Treatment for biliary colic

A
  • NSAIDs/analgesia
  • optional lap cholecystectomy → gallstones often recur
79
Q

What is acute cholecystitis

A

inflammation of the gallbladder

80
Q

Pathophysiology of acute cholecystitis

A
  • gallstones block cystic ducts
  • buildup of bile → distends gallbladder
  • vascular supply may be reduced
  • inflammation
81
Q

Presentation of acute cholecystitis

A
  • generalised epigastric pain migrating to severe RUQ pain
  • signs of inflammation → fever/fatigue
  • pain associated with tenderness and guarding from inflamed gallbladder and local peritonitis
82
Q

Investigations for acute cholecystitis

A
  • positive murphy’s sign
  • inflammatory markers → FBC, CRP
  • US gallbladder → thick walls
83
Q

What is a positive murphy’s sign?

A
  • severe pain on deep inhalation with examiners hand pressed into RUQ
84
Q

Treatment for acute cholecystitis

A
  • Abs
  • early lap cholecystectomy (within 7 days) or wait 6 weeks
  • fluids and analgesia
85
Q

What is ascending cholangitis?

A
  • medical emergency
  • bacteria ascending through biliary tree → septicaemia
86
Q

What are the types of jaundice?

A

pre-hepatic

  • unconjugated bilirubin
  • cause = breakdown of RBCs → haemolytic anaemia

hepatic

  • unconjugated bilirubin
  • cause = hepatitis

post-hepatic

  • conjugated bilirubin → itching
  • causes = obstruction, stricture, cancer head of pancreas
87
Q

Presentation of ascending cholangitis

A
  • Charcot’s triad
  • Reynolds pentad
88
Q

What is Charcot’s triad?

A
  • RUQ pain
  • jaundice
  • fever and rigors
89
Q

What is Reynolds pentad

A
  • Charcot’s triad
  • confusion
  • septic shock
90
Q

Investigations for ascending cholangitis

A
  • amylase/lipase, LFTs, CRP, FBC
  • CT/US gallbladder
  • MRCP/ERCP
91
Q

Management of ascending cholangitis

A
  • aggressive fluid resuscitation
  • IV Abs → penicillins and aminoglycosides
  • pressor support
  • ERCP
  • cholecystectomy when better
92
Q

What is primary biliary cirrhosis

A
  • progressive autoimmune destruction of liver and biliary tree
  • leads to fibrosis then cirrhosis
  • AMA +ve against PDC-E2
93
Q

Risk factors for PBC

A
  • female
  • associated with autoimmune disease
94
Q

Presentation of PBC

A

very non-specific

  • fatigue
  • pruritus
  • liver failure symptoms if advanced
95
Q

Investigations for PBC

A
  • AMA
  • LFT → GGT/ALP raised
  • US gallbladder
  • biopsy
96
Q

Management of PBC

A

ursodeoxycholic acid to reduce cholestasis

97
Q

What is primary sclerosing cholangitis?

A

progressive sclerosis of biliary tree → chronic cholestasis and ESLD

98
Q

Causes of PSC

A
  • 80% associated with IBD → UC
  • p-ANCA and HLA association
  • exact mechanism unknown
99
Q

Diagnostic criteria of PSC

A
  • ALP >1.5x normal for >6 months
  • cholangiography → biliary strictures → beaded appearance
  • liver biopsy consistent with PSC
100
Q

Presentation of PSC

A
  • 50% asymptomatic until advanced
  • non specific pruritus and fatigue
  • may be diagnosed after presenting with ascending cholangitis
101
Q

Complications of PSC

A

predisposed to developing

  • HCC
  • cholangiocarcinoma
  • CRC
102
Q

Management of PSC

A
  • liver transplant
  • non known medical management
103
Q

What is acute pancreatitis

A
  • sudden inflammation of pancreas
  • leads to autodigestion of gland → reversible
104
Q

Presentation of acute pancreatitis

A
  • severe epigastric pain radiating to back
  • N&V
  • fever and chills
  • haemodynamic instability
  • retroperitoneal haemorrhage → Cullen’s and Grey Turner’s signs
105
Q

What is Cullen’s sign?

A

superficial oedema with bruising in the subcutaneous fatty tissue around the peri-umbilical region

106
Q

What is Grey Turner’s sign?

A

discolouration of the left flank associated with acute hemorrhagic pancreatitis

107
Q

Complications of acute pancreatitis

A
  • pancreatic pseudocyst
  • insulin dependent DM
  • ARDS and pleural effusion
  • DIC
108
Q

Causes of acute pancreatitis

A

I GET SMASHED
- idiopathic

  • gallstones
  • EtOH
  • trauma
  • steroids
  • mumps/malignancy
  • autoimmune
  • scorpion stings
  • hypertriglyceridaemia/hypercalcaemia
  • post ERCP
  • drugs → tobacco, thiazides
109
Q

Pathophysiology of acute pancreatitis

A

gallstones

  • blockage of bile duct → backup of pancreatic juices
  • change in luminal concentration causes Ca2+ release inside pancreatic cells
  • trypsinogen activated early → autodigestion

alcohol

  • contracts Ampulla of Vater
  • obstructs bile clearance
  • affects Ca2+ homeostasis
110
Q

What scoring systems are there for acute pancreatitis?

A
  • APACHE
  • Glasgow&Ranson
111
Q

Investigations for acute pancreatitis

A
  • raised amylase, lipase, CRP
  • erect chest xray
  • CT/US gallbladder
  • MRCP
112
Q

Management of acute pancreatitis

A
  • nil by mouth → bowel rest
  • aggressive fluid resuscitation
  • analgesia
  • Abs if necrotising pancreatitis
  • ITU/TPN if required
  • ERCP/surgery if required
  • treat underlying cause ie gallstones
113
Q

What is chronic pancreatitis?

A
  • long standing inflammation from irreversible damage to pancreas
  • can manifest as persistent pain and malabsorption in episodes
114
Q

Causes of chronic pancreatitis

A
  • generally caused by chronic alcohol abuse
  • CF
  • cancer
  • autoimmune
  • CKD
115
Q

Pathophysiology of chronic pancreatitis

A
  • obstruction of bicarbonate secretion in pancreatic lumen
  • early activation of trypsinogen and autodigestion
  • replaced by fibrosis
  • can be caused by CF/alcohol → increases trypsinogen activation
116
Q

Presentation of chronic pancreatitis

A
  • epigastric pain radiating to back → less than acute, better when leaning forward, worse with alcohol
  • N&V
  • steatorrhea
  • weight loss → malabsorption
  • insulin dependent DM
117
Q

Investigations for chronic pancreatitis

A
  • secretin stimulation test
  • CT, MRI, MRCP
118
Q

Management of chronic pancreatitis

A
  • creon
  • insulin
  • opioids
  • alcohol cessation
  • dietary modification
  • ERCP/surgery if required
119
Q

What is ERCP?

A

endoscopic retrograde cholangiopancreatography

Phase 2a Green Conditions (10 decks)

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