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Phase 2a Green Conditions > Liver and friends > Flashcards

Liver and friends Flashcards

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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
Management of NAFLD
- weight loss - exercise - stop smoking - control diabetes, BP, cholesterol - avoid alcohol - treat fibrosis with vitE or pioglitazone
26
What investigations should be performed after abnormal LFTs
- 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
27
What type of virus is hepA?
RNA - rarer - developing world
28
How is HepA transmitted?
faecal-oral transmission - contaminated food - fly vectors
29
Pathophysiology of HepA
- acute infection - usually cleared by host immune system
30
Presentation of HepA
- non specific symptoms → nausea, anorexia, malaise after 1-2 weeks → liver symptoms - jaundice - hepatomegaly - skin rash
31
Investigations for HepA
LFTs - raised ALT, bilirubin - serology
32
Treatment for HepA
- vaccine available - treatment often not required - generally supportive
33
Complications for HepA
- rare - acute liver failure
34
What type of virus is HepB?
DNA - present worldwide
35
Pathophysiology of HepB
- 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
36
Presentation of HepB
- similar acute infection - if chronic, then signs of cirrhosis → jaundice, pruritus etc
37
Investigations for HepB
- LFTs, serology if Ag after 6 months, confirm chronic HBV
38
Treatment for HepB
- vaccine available → at risk - antiviral treatment → tenofovir = pegylated interferon alpha 2a
39
Complications of HepB
if chronic, increased risk of cirrhosis, HCC
40
What type of virus is HepC
RNA - more common in UK
41
How is HepB transmitted?
- blood products → IVDU - sexually → MSM
42
How is HepC transmitted?
blood/blood products → IVDU\>sexually
43
Pathophysiology of HepC
- acute infection often asymptomatic → allows progression to chronic - chronic HCV causes slowly progressive fibrosis
44
Presentation of HepC
- acute = asymptomatic - later on = signs of chronic liver disease
45
Investigations for HepC
- LFTs, serology - if Ag after 6 months, confirm chronic HCV
46
Treatment for HepC
- revolutionising from interferon based regimens to directly acting antiviral agents - Ribavirin = expensive
47
Complications of HepC
- chronic liver disease - HCC
48
What type of virus is HepD
RNA
49
How is HepD transmitted?
- blood borne - IVDU, sexually
50
Pathophysiology of HepD
- unable to replicate on its own - requires concurrent HBV infection - makes HepB more likely to progress to cirrhosis/HCC
51
Presentation of HepD
indistinguishable from acute HBV infection
52
Treatment for HepD
same as HBV
53
Complications of HepD
cirrhosis, HCC
54
What type of virus is HepE
RNA - common in UK
55
How is HepE transmitted
- faeco-oral transmission - undercooked meat
56
Presentation of HepE
- 95% asymptomatic - usually self-limiting
57
Investigations for HepE
serology
58
Treatment for HepE
- often not required - supportive
59
Complications of HepE
- rare - can progress to cirrhosis in immunocompromised
60
What is liver cirrhosis?
- 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
Causes of cirrhosis
- alcohol abuse → alcoholic liver disease - NAFLD - hepatitis B, C - haemochromatosis - Wilson's - A1AT deficiency
62
Investigations for cirrhosis
DEFINITIVE DIAGNOSTIC = liver biopsy blood tests - INR/PT high - LFTs - FBC → thrombocytopenia - serum electrolytes US and CT → hepatomegaly
63
Treatment for cirrhosis
same as chronic liver disease conservative - fluids - alcohol abstinence - good nutrition treat complications of liver failure DEFINITIVE TREATMENT = liver transplant
64
Complications of cirrhosis
- ascites - portal HTN - varices - jaundice - coagulopathy - hypoalbuminaemia - portosystemic encephalopathy
65
What is ascites?
fluid in the peritoneal cavity
66
Why do you get ascites in cirrhosis
- hypoalbuminaemia → reduced oncotic pressure - portal HTN → increased hydrostatic pressure - renal water retention → peripheral arterial vasodilation mediated by NO
67
Causes of ascites
cirrhosis = commonest cause 4 basic mechanisms - peritonitis = more leaky - reduced capillary hydrostatic pressure - reduced colloid oncotic pressure - peritoneal lymphatic draining
68
Types of ascites
transudate - \<25 protein - portal HTN, budd chiari, low plasma protein, HF exudate - \>25 protein - peritonitis, peritoneal malignancy
69
Presentation of ascites
- shifting dullness - weight gain - abdominal distention - signs of liver disease - respiratory distress
70
Investigations for ascites
DIAGNOSTIC = aspiration - albumin - neutrophil count
71
Complications of ascites
spontaneous bacterial peritonitis SBP - infection of ascitic fluid - most common causes = E.coli then K.pneumoniae
72
What is biliary colic?
temporary blockage of the cystic duct by gallstones
73
What is bile made of?
- cholesterol - pigments - phospholipids
74
What are gallstones?
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
Risk factors of biliary colic
5 Fs - fat - female - forty - fair - fertile
76
Presentation of biliary colic
- classic colicky RUQ pain → worse after eating large/fatty meals - referred shoulder pain - N&V
77
Investigations for biliary colic
rule out cholecystitis/cholangitis DIAGNOSTIC = US 1. stones 2. gallbladder wall thickness 3. duct dilation
78
Treatment for biliary colic
- NSAIDs/analgesia - optional lap cholecystectomy → gallstones often recur
79
What is acute cholecystitis
inflammation of the gallbladder
80
Pathophysiology of acute cholecystitis
- gallstones block cystic ducts - buildup of bile → distends gallbladder - vascular supply may be reduced - inflammation
81
Presentation of acute cholecystitis
- 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
Investigations for acute cholecystitis
- positive murphy's sign - inflammatory markers → FBC, CRP - US gallbladder → thick walls
83
What is a positive murphy's sign?
- severe pain on deep inhalation with examiners hand pressed into RUQ
84
Treatment for acute cholecystitis
- Abs - early lap cholecystectomy (within 7 days) or wait 6 weeks - fluids and analgesia
85
What is ascending cholangitis?
- medical emergency - bacteria ascending through biliary tree → septicaemia
86
What are the types of jaundice?
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
Presentation of ascending cholangitis
- Charcot's triad - Reynolds pentad
88
What is Charcot's triad?
- RUQ pain - jaundice - fever and rigors
89
What is Reynolds pentad
- Charcot's triad - confusion - septic shock
90
Investigations for ascending cholangitis
- amylase/lipase, LFTs, CRP, FBC - CT/US gallbladder - MRCP/ERCP
91
Management of ascending cholangitis
- aggressive fluid resuscitation - IV Abs → penicillins and aminoglycosides - pressor support - ERCP - cholecystectomy when better
92
What is primary biliary cirrhosis
- progressive autoimmune destruction of liver and biliary tree - leads to fibrosis then cirrhosis - AMA +ve against PDC-E2
93
Risk factors for PBC
- female - associated with autoimmune disease
94
Presentation of PBC
very non-specific - fatigue - pruritus - liver failure symptoms if advanced
95
Investigations for PBC
- AMA - LFT → GGT/ALP raised - US gallbladder - biopsy
96
Management of PBC
ursodeoxycholic acid to reduce cholestasis
97
What is primary sclerosing cholangitis?
progressive sclerosis of biliary tree → chronic cholestasis and ESLD
98
Causes of PSC
- 80% associated with IBD → UC - p-ANCA and HLA association - exact mechanism unknown
99
Diagnostic criteria of PSC
- ALP \>1.5x normal for \>6 months - cholangiography → biliary strictures → beaded appearance - liver biopsy consistent with PSC
100
Presentation of PSC
- 50% asymptomatic until advanced - non specific pruritus and fatigue - may be diagnosed after presenting with ascending cholangitis
101
Complications of PSC
predisposed to developing - HCC - cholangiocarcinoma - CRC
102
Management of PSC
- liver transplant - non known medical management
103
What is acute pancreatitis
- sudden inflammation of pancreas - leads to autodigestion of gland → reversible
104
Presentation of acute pancreatitis
- severe epigastric pain radiating to back - N&V - fever and chills - haemodynamic instability - retroperitoneal haemorrhage → Cullen's and Grey Turner's signs
105
What is Cullen's sign?
superficial oedema with bruising in the subcutaneous fatty tissue around the peri-umbilical region
106
What is Grey Turner's sign?
discolouration of the left flank associated with acute hemorrhagic pancreatitis
107
Complications of acute pancreatitis
- pancreatic pseudocyst - insulin dependent DM - ARDS and pleural effusion - DIC
108
Causes of acute pancreatitis
I GET SMASHED - idiopathic - gallstones - EtOH - trauma - steroids - mumps/malignancy - autoimmune - scorpion stings - hypertriglyceridaemia/hypercalcaemia - post ERCP - drugs → tobacco, thiazides
109
Pathophysiology of acute pancreatitis
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
What scoring systems are there for acute pancreatitis?
- APACHE - Glasgow&Ranson
111
Investigations for acute pancreatitis
- raised amylase, lipase, CRP - erect chest xray - CT/US gallbladder - MRCP
112
Management of acute pancreatitis
- 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
What is chronic pancreatitis?
- long standing inflammation from irreversible damage to pancreas - can manifest as persistent pain and malabsorption in episodes
114
Causes of chronic pancreatitis
- generally caused by chronic alcohol abuse - CF - cancer - autoimmune - CKD
115
Pathophysiology of chronic pancreatitis
- 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
Presentation of chronic pancreatitis
- 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
Investigations for chronic pancreatitis
- secretin stimulation test - CT, MRI, MRCP
118
Management of chronic pancreatitis
- creon - insulin - opioids - alcohol cessation - dietary modification - ERCP/surgery if required
119
What is ERCP?
endoscopic retrograde cholangiopancreatography

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