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Phase 2A conditions > Liver conditions > Flashcards

Liver conditions Flashcards

1
Q

What does an increased ALT and AST indicate?

A

hepatocellular injury i.e. the liver is injured such as alcohol or hep B and C

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2
Q

What does an increase is ALP indicate?

A

cholestasis i.e. reduced or blocked bile flow

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3
Q

What is the classification of jaundice?

A

prehepatic or unconjugated: haemolysis
conjugated hepatic: hepatitis, ischaemia, neoplasm
conjugated post hepatic: gallstones in bile duct, stricture

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4
Q

What is liver failure?

A

Loss of the livers ability to regenerate and repair: destruction of hepatocytes, development of fibrosis, destruction of architecture

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5
Q

What is fulminant hepatic failure?

A

necrosis in substantial parts and encephalopathy

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6
Q

Why can liver failure present with encephalopathy?

A

ammonia in circulation stops krebs cycle in brain leading to cell death and oedema

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7
Q

What causes liver damage?

A

hepatitis A,B,D and E, cytomegalovirus, EBV, herpes simplex, paracetamol overdose, alcohol, Wilson’s disease, carcinoma

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8
Q

How does liver damage present?

A

abnormal bleeding, ascites, jaundice and encephalopathy (confusion, liver flap, coma), small liver, fetor hepaticus, cerebral oedema

  • acute: encephalopathy and INR below 1.5
  • chronic: bruising, clubbing and depuytren’s contracture (thick palm skin)
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9
Q

What are differentials of liver failure?

A

cerebral infarction, intoxication,

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10
Q

What test do you order for liver failure and what do you expect?

A

FBC: hyperbilirubinaemia, High AST and ALT, increased PTT, hyperglycaemia, high ammonia levels
EEG, ultrasound and cxr

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11
Q

How do you treat liver failure?

A

Treat cause

- IV mannitol if ICP rises
- IV vitamin K for coagulation
- Liver transplant
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12
Q

what do you give for a paracetamol overdose?

A

acetylcysteine

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13
Q

What is a hernia?

A

Profusion of an organ or part of an organ through a defect of the walls of its contained cavity

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14
Q

What is a reducible hernia?

A

can be pushed back

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15
Q

What is a irreducible hernia and what subtypes are there?

A

cannot be pushed back

- obstructed: blood flow maintained but intestine obstructed
- incarcerated: contents are stuck inside by adhesions
- strangulated: blood supply cut off, urged surgery
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16
Q

Give three examples of hernia’s?

A

inguinal hernia, hiatus hernia and incisional hernia

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17
Q

What is Budd Chair syndrome?

A

hepatic vein obstruction by thrombosis or tumour causing congestive ischaemia and hepatocyte damage

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18
Q

What is wilson’s disease?

A

Rare inherited disorder of biliary copper excretion with too much copper in the liver and CNS

autosomal recessive

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19
Q

How does wilsons disease present?

A

hepatic problems in children and CNS problems in adults, Kayser-Fleischer ring

24 hour urinary copper excretion is high, haemolysis and anaemia, basal ganglia and cerebellar degeneration

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20
Q

How do you treat wilson’s disease?

A

treat with life long chelating agent: penicillamine

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21
Q

How is hepatitis A transmitted?

A

from contaminated water and food through faecal-oral route

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22
Q

How does hepatitis A present?

A

Jaundice, dark urine and pale stool, hepatosplenomegaly and the jaundice lessens and illness ends
- IgM during acute infection, IgG as a memory (chronic or resolved) and HAV antibodies

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23
Q

How do you treat hep A?

A

Notifiable disease: usually self limiting and has an incubation of 2-6 weeks

Treat with supportive treatment, acid alcohol and motor liver function

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24
Q

Which type of hepatitis is similar to Hep A?

A

Hepatitis E

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25
Q

How is hepatitis B transmitted?

A

Blood borne and sexually

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26
Q

What antibody will you find in hep B?

A

HBsAg present and if longer than 6 months it means carrier status

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27
Q

How do you treat hep B?

A

Chronic treatment: SC pegylated interferon-alpha 2A or nucleoside analogues (tenofovir)

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28
Q

What is required for Hep D?

A

Hep B

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29
Q

What is common in drug users?

A

Hep C

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30
Q

How does portal hypertension occur?

A
  1. Contraction of activated myofibroblasts contribute to resistance in blood flow causing portal HTN
  2. that is counteracted by splancinc vasodilation resulting in a drop in BP.
  3. CO increases to compensate and salt/water is retained to cause higher blood volume and increased portal flow.
  4. This results in the formation of collaterals and varices
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31
Q

what is normal portal pressure?

A

5-8 mmHg

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32
Q

At what portal pressure will varices develop and bless?

A

Develop at above 10

Bleed at 12

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33
Q

What causes portal hypertension?

A

alcohol and viral cirrhosis are leading causes
pre hepatic: portal vein thrombosis
intrahepatic: cirrhosis, sarcoidosis
post-hepatic : IVC obstruction, pericarditis, HF

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34
Q

What causes varices?

A

portal hypertension

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35
Q

How does portal hypertension present?

A

often asymptomatic but can show splenomegaly or chronic liver disease features

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36
Q

How is portal hypertension managed?

A

Beta blockers i.e. propranolol

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37
Q

How do varices present?

A

present if they have ruptured: haematemesis, melaena (dark sticky faeces), abdominal pain, tachycardia, hypotension and pallor

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38
Q

How do you investigate varices?

A

endoscope

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39
Q

How do you treat varices?

A

treat by resuscitation, give vasopressin (IV terlipressin), correct clotting abnormalities and potentially give blood transfusion
surgery: banding, ballon tamponade or TIPS (shunt)

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40
Q

What is cirrhosis?

A

End stage of all progressive chronic liver disease

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41
Q

How does cirrhosis occur?

A
  • Hepatic stellate cells: release cytokines causing further inflammation and necrosis
  • Kupffer cells: secrete TNF beta which turns stellate to myofibroblasts, releasing collaged depositions
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42
Q

what are the two types of cirrhosis?

A

micro nodular (less than 3 mm) or macro nodular (varying size)

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43
Q

How does cirrhosis present?

A

leukonyctia (white nail discolouration), clubbing, palmar erythema, dupuytren’s contracture, ascites, ankle swelling and bruising

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44
Q

How do you investigate cirrhosis?

A

LFTs (best indicator is PTT or albumin) and liver biopsy (GS)

45
Q

What indicated hepatocellular carcinoma?

A

alpha faecalprotein

46
Q

What are complications of cirrhosis?

A

coagulopathy, encepathopathy, portal hypertension

47
Q

How do you treat cirrhosis?

A

alcohol abstinence, avoidance of NSAIDs, treat underlying causes

- liver transplant
- regular cancer screening
48
Q

What is non alcoholic fatty liver disease?

A

Fat accumulation in the liver unrelated to alcohol or viral causes

49
Q

what is the pathology of NAFLD?

A

Results from fat depositions in the liver but mechanism isn’t clear

  • Steatohepatitis (NASH): steatosis and inflammation, mallory denk bodies, increased neutrophils
    • chronic NASH causes stellar cells to lay down fibrotic tissue leading to cirrhosis
50
Q

What are RF for NAFLD?

A

50+, BMI over 28, diabetes, hyperlipidemia, HTN

essentially metabolic syndrome

51
Q

How does NAFLD present?

A

Even advanced stages can be asymptomatic but a small percentage experiences fatigue, malaise and liver ache

significant damage can cause hepatomegaly, RUQ pain, jaundice and ascites

52
Q

How tests do you order for NAFLD?

A

LFT (increased ALT rather than AST in alcoholic), Ultrasound and biopsy

53
Q

How do you treat NAFLD?

A

Steatosis and NASH are reversible by treating underlying cause

  • no effective drug treatment
54
Q

How does alcoholic liver disease occur?

A

Ethanol metabolism results in altered redox potential leading to hepatic accumulationn of FA, centrilobular necrosis and TNF alpha release from Kupffer cells

55
Q

what are the three stages of ALD?

A

Fatty liver, alcoholic hepatitis and cirrhosis

56
Q

What happens in the fatty liver stage?

A

cells swell with fat (steatosis) but no cell damage, stellate cells can become collagen producing leading to cirrhosis without hepatitis

57
Q

How does fatty liver present?

A

asymptomatic, vague abdominal symptoms, hepatomegaly

58
Q

What results would you expect in the fatty liver stage?

A

increased ALT and AST (more than ALT), CT shows fatty infiltration

59
Q

How do you treat alcoholic fatty liver?

A

can be reversed with alcohol cessation

60
Q

What happens in alcoholic hepatitis?

A

infiltration of leukocytes, hepatocyte necrosis, mallory bodies and giant mitochondria

61
Q

How does alcoholic hepatitis present?

A

jaundice and signs of chronic disease (ascites, clubbing, dupuytren’s contracture)
if severe may show pain and fever

62
Q

What do LFT show in alcoholic hepatitis?

A

increased ALT and AST (more than ALT), increased bilirubin and PTT

63
Q

how do you treat alcoholic hepatitis?

A

steroids and alcohol cessation

64
Q

How does alcoholic cirrhosis present?

A

chronic liver disease signs, features of alcohol dependency

65
Q

What type of cirrhosis is alcoholic cirrhosis?

A

micronodoular

66
Q

How do you treat cirrhosis?

A

avoid NSAIDS ad liver transplant

67
Q

Why would you give IV thiamine?

A

to prevent Wernicke-Korsakoff encephalopathy that can occur from alcohol withdrawal

68
Q

What is chronic pancreatites?

A

Progressive loss of exocrine tissue which is replaced by fibrosis

69
Q

What is the pathology of chronic pancreatitis?

A
  1. obstruction or reduction in bicarbonate secretion leads to alkaline pH and stabilises trypsinogen
  2. conversion into trypsin leads to tissue necrosis and eventual fibrosis
  • decrease in bicarbonate can be caused by functional defects in wall (CF or trauma)
  • obstruction can arise from protein deposits within duct (alcohol or increased intrahepatic enzyme activity)
70
Q

What causes chronic hepatitis?

A

LT alcohol excess, CKD, hereditary (trypsinogen gene defect or CF), autoimmune (IgG), trauma, recurrent acute pancreatitis

71
Q

What are RF for chronic pancreatitis?

A

alcohol, smoking, family history

72
Q

How does chronic pancreatitis present?

A

pigastric pain that is relived by sitting forward and can be exacerbated by alcohol, nausea, vomiting, anorexia

  • exocrine dysfunction (acinus and duct): malabsorption, diarrhoea, steatorrhea, protein deficieny
  • endocrine function: diabetes mellitus
73
Q

How do you confirm chronic pancreatitis

A

Ultrasound, serum amylase and lipase, faecal elastase, CT

74
Q

How do you manage chronic pancreatitis?

A
  • Manage with alcohol cessation and NSAIDs for pain

- treat associated symptoms

75
Q

What is acute pancreatitis?

A

Inflammation due to any injury

76
Q

How does acute pancreatitis occur and how does alcohol or gallstones help?

A

Premature activation of pancreatic enzymes leading to self-perpetuating inflammation, leaky vessels (oedema), destruction of blood vessels, destruction of islets of Langerhans and fat necrosis

Activation can occur through:
- gallstones: obstruction leads to build up, increase in calcium and therefore activation of trypsinogen which becomes trypsin

  • Alcohol: contraction of the ampulla of vader leads to obstruction and alcohol interferes with calcium homeostasis
77
Q

What causes acute pancreatitis?

A

IGETSMASHED: idiopathic, gallstones, ethanol, steroids, mumps, autoimmune, scorpion venom, hyperlipidemia, ERCP and drugs

78
Q

What are RF for acute pancreatitis?

A

middle aged, young men, gallstones, SLE, sjorgen’s

79
Q

How does chronic pancreatitis present?

A

Presents with epigastric pain that may be relieved by sitting forward, anorexia, N and V, tachycardia, fever and jaundice

  • Grey Turner sign (flank discolouration) and Cullen sign (bruising around umbilicus)
80
Q

What tests do you order for acute pancreatitis?

A

serum and urinary amylase, serum lipase, xray for gallstones

81
Q

What is a complication of acute pancreatitis?

A

systemic inflammatory response syndrome (SIRS)

presents with any 2 of: tachycardia 90+, tachypnea 20+, pyrexia over 38 and increased WCC

82
Q

How do you treat acute pancreatitis?

A

Treat with fluid resuscitation and nil by mouth

  • analgesia, catheter, antibiotics and potential drainage
  • assess severity with Glascow and Ranson (in 48 hours) or APACHE 2 (within 24 hours)
83
Q

What are two types of gallstones and how do you recognise them?

A

Cholesterol: 80% of stones, large and solitary, form from excess cholesterol that crystallises

Bile pigment: calcium, viable and irregular
- can be brown or black
(glass like)

84
Q

How are cholesterol stones formed?

A

excess cholesterol, decreased bile and phospholipids, reduced motility, crystalline promoting factors

85
Q

What causes gallstones?

A

obesity, rapid weight loss, diabetes, cirrhosis, contraceptive pill

86
Q

What are RF for gallstones?

A

female, fat, fertile and smoking

87
Q

How do gallstones present?

A

Majority are asymptomatic but can present with biliary colic

88
Q

What is biliary colic?

A

RUQ pain that is sudden and severe, can radiate to right shoulder

89
Q

How do you confirm gallstones?

A

ultrasound

90
Q

What are differentials of gallstones?

A

IBS, carcinoma, renal colic

91
Q

What are consequences of gallstones?

A

biliary colic, cholecystitis, mirizzi syndrome (hepatic duct obstruction due to pressure)

92
Q

How do you manage gallstones?

A

laparoscopic cholecystectomy if symptomatic

  • cholesterol stones can be dissolved by increased bile salts and statins
  • shock wave lithotripsy to fragment stones for passing
93
Q

What is cholecystitis?

A

Obstruction of gallbladder emptying leading to distention and inflammation

94
Q

What causes cholecystitis?

A

gallstones moving to common bile duct

95
Q

How does cholecystitis present?

A

fever, biliary colic and murphy’s sign (pain when taking in a deep breath and putting fingers on RUQ)

96
Q

How do you investigate cholecystitis and what do you expect to see?

A

FBC (increase WCC, bilirubin, ALP, ALT), abdominal ultrasound (stones and shrunken gallbladder)

97
Q

What are consequences of cholecystitis?

A

cholangitis, empyema (collection of pus) pancreatitis

98
Q

How do you treat cholecystitis?

A

nil by mouth, IV fluids, analgesia, IV antibiotics (cefuroxime) and cholecystectomy

99
Q

What is ascending cholangitis?

A

Infection of the biliary tree caused by bacteria ascending from duodenal junction

100
Q

What structures form the biliary tree?

A

pancreatic duct, cystic duct, common hepatic and common bile

101
Q

What causes ascending cholangitis?

A

gallstones, cancer of head of pancreas, biliary parasites and benign structure after surgery

102
Q

What are RF for ascending cholangitis?

A

over 50, gallstones

103
Q

How does ascending cholangitis present?

A

charcot’s triad: fever, jaundice, RUQ pain

dark urine, pale stool and itchy skin

104
Q

What tests do you order for ascending cholangitis and what do you expect?

A

Order FBC (increased bilirubin, increased ALP, ALT>AST) and trans abdominal ultrasound

  • MRI for pigmented stones
105
Q

What are consequences of ascending cholangitis?

A

Consequences include toxic cholangitis: pus in biliary tree, sepsis, hypotension and organ failure
- can present with reynolds pentad: charcot + sepsis and neurological changes

106
Q

How do you treat ascending cholangitis?

A

IV antibiotics (cefotaxime and metronidazole), biliary drainage and removal of stones

107
Q

What do gallbladder stones present with?

A

biliary colic, cholecystitis, mirizzi

108
Q

What do bile duct stones present with?

A

colic, pancreatitis, cholangitis, obstructive jaundice

Phase 2A conditions (7 decks)

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