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My Gastrointestinal > Liver disease > Flashcards

Liver disease Flashcards

1
Q

What happens in cirrhosis?

A
  • liver gets small and shrunken

- reduced liver blood flow, reduced metabolic function and reduced plasma proteins

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2
Q

What is happening if the oral dose of a drug is much higher than the IV dose?

A

first-pass metabolism in the liver

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3
Q

How is alcohol metbaolised?

A

by first-order until a set point then it is by zero order

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4
Q

What happens in liver disease with RAS?

A

there is an increase in renin

there is a decrease in the metabolism of aldosterone so there is secondary aldosteronism

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5
Q

What can happen to the kidneys in liver disease?

A
  • too much angiotensin 2 (vasoconstrictor), aldosterone, SNS and ADH
  • there is potassium loss, sodium retention and water retention
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6
Q

What are the consequences of moderate hepatic impairment?

A

gut oedema, liver and kidney congestion, gross oedema and ascites and CHF

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7
Q

Why are NSAIDs not used in liver disease?

A
  • get rid of renal prostaglandins
  • so harm kidneys and cause ulcers and bleeding
  • increase blood pressure
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8
Q

What must always be prescribed with an NSAID?

A

a PPI

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9
Q

What is the summary of drug metabolism?

A
  • phase 1 is P450 biotransformation

oxidation, reduction and hydrolysis

  • phase two is conjugation
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10
Q

How can paracetamol be dangerous?

A

can make a dangerous substance which is removed by out glutathione stores

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11
Q

What is the rule used to assess drug-induced liver disease severity?

A

Hy’s Rule

- uses ALT/AST and Bilirubin as parameters

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12
Q

What is the diuretic used in liver disease and how is this administered?

A
  • Spironolactone as it removes secondary aldosteronism

- 1kg/day weight loss of fluid is ideal

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13
Q

What is given to sedate patients with liver disease?

A

Phase 2 metabolised benzodiazepines eg Lorazepam

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14
Q

What are the features of Hep A?

A
  • faecal-oral spread
  • common in gay and IVDUs
  • acute not chronic
  • peak is in older children and young adults
  • confirmed by presence of IgM against Hep A
  • vaccine available
  • mild illness will usual full recovery
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15
Q

What are the features of Hep B?

A
  • sex, mother to child or by blood
  • chronic only if first exposure is in childhood
  • adults usually get acute
  • confirmed by presence of Hep B surface antigen (HBsAg)
  • carriers possible
  • antiviral therapy to those with liver inflammation and a high level of Hep B DNA
  • treat with vaccine, suppressive antivirals or peginterferon
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16
Q

What are the risk factors for Hep B?

A
  • people who live in affected areas
  • have multiple sexual partners
  • IVDUs
  • children of infected mothers
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17
Q

What are the features of Hep C?

A
  • no vaccine
  • transmission is blood or sex
  • test for antibody to virus then test for RNA by PCR
  • usually chronic
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18
Q

What are the features of Hep D?

A

only found with Hep B

makes acute or chronic Hep B worse

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19
Q

What are the features of Hep E?

A

Common in the tropics
Faecal-oral spread
More common than A
Caught from pigs
Genotypes in the tropics cause disease in pregnant women
No vaccine is available
Only chronic infection if there is an abnormal immune system

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20
Q

When is a viral infection classed as chronic?

A

over 6 months

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21
Q

Which Hep can spontaneously resolve?

A

Hep B not Hep C

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22
Q

What is the management of acute viral Hep?

A

monitoring for encephalopathy, resolution and vaccinate those at risk

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23
Q

What is the management of chronic viral Hep?

A

antivirals, vaccination, infection control, alcohol cessation and awareness and screening for hepatocellular carcinoma

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24
Q

Who is treated with antivirals?

A
  • chronic infection
  • inflammation is seen
  • if fit for treatment
  • HIV co-infection is difficult
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25
Q

What are the common antiviral and their sideffects?

A
  • infterferon alpha
  • peginterferon (flu symptoms)
  • ribavirin (anaemia)
  • sofosbuvir is active against all genotypes
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26
Q

What is compensated cirrhosis?

A

scarring in the liver without loss of normal functions such as metabolism and removal of toxins

27
Q

When does liver disease become chronic?

A

6 months

28
Q

What drug can cause cirrhosis?

A

methotrexate which is a treatment or rheumatoid arthritis and psoriasis

29
Q

What is numerically classed as portal hypertension?

A

5-8mmHg

30
Q

What are the clinical features of compensated cirrhosis?

A

normal from outside, found on imaging or labs, maybe portal hypertension, signs are spider naevi, clubbing, palmar erythema or none

31
Q

What are the clinical features of decompensated cirrhosis?

A

liver failure present, end stage liver disease, signs are jaundice, ascites, encephalopathy or bruising

32
Q

What are the complications of cirrhosis?

A

ascites, encephalopathy, variceal bleeding and liver failure

33
Q

What is ascites caused by?

A
  • increased number of vasodilators
  • enhanced sensitivity to these
  • resistance to vasoconstrictors
34
Q

What is the diagnosis and management of ascites?

A
  • diagnosis with shifting dullness
  • treat with spironolactone, paracentesis or TIPSS
  • stop drinking
  • sodium must be balanced
35
Q

What is the diagnosis and treatment of encephalopathy?

A
  • diagnosis is flap, neurology, ammonia

- treat with lactulose, Rifaxamin

36
Q

What is the treatments for oesophageal varices?

A
  • primary = beta blockers and ligation
  • acute = resuscitation, terlipressin, banding and TIPSS
  • emergency = balloon tamponade
  • secondary treatment = band ligation or beta blockers
37
Q

What are the main benign liver lesions?

A
  • haemangioma
  • focal nodular hyperplasia
  • hepatic adenoma
  • liver cysts
  • polycystic liver disease
  • abscess
38
Q

What are the main malignant liver lesions?

A
  • primary are hepatocellular carcinoma or cholangiocarcinoma

- metastases are common

39
Q

What are the features of haemangioma?

A 
common
females
single and small
asymptomatic
diagnosis is US, CTl, MRI
no treatment
40
Q

What are the features of focal nodular hyperplasia?

A
  • benign nodule of normal liver tissue
  • central scar with artery radiating branches to periphery
  • young middle aged females
  • asymptomatic
  • diagnosis is US, CT, MRI or FNA
  • no treatment
41
Q

What are the features of hepatic adenoma?

A
  • proliferation of normal hepatocytes
  • females
  • associated with contraceptive hormones and anabolic steroids,
  • asymptomatic or RUQ pain
  • present with rupture or haemorrhage
  • diagnosis is US, CT, MRI, stop hormones
  • weight loss for treatment and remove in males as malignancy is more common
42
Q

What are the types of liver cysts?

A 
simple
hydatid 
atypical
polycystic lesion
pyogenic/amoebic abscess
43
Q

What are the types of polycystic liver disease?

A

-Von Meyenburg complexes (benign cystic nodules)
-Polycystic liver disease
-Autosomal dominant PK disease
(treat with somatostatin)

44
Q

What are the features of liver abscesses?

A
  • high fever
  • leukocytosis
  • abdominal pain and complex liver lesion
  • treat with antibiotics, aspiration, echo then operation
45
Q

What is the epidemiology, aetiology and presentation of hepatocellular carcinoma?

A
  • men
  • most common primary cancer
  • risk factor is cirrhosis
  • presentation is abdo pain, RUQ, asymptomatic, worsening of chronic liver disease, cirrhosis signs, RUQ mass
46
Q

Where do hepatocellular carcinoma metastases move to?

A

liver, portal vein, pymph, lung, bone and brain

47
Q

What is the diagnosis and treatment of hepatocellular carcinoma?

A
  • AFP is high
  • liver transplant, can use RF ablation or chemoembolization
  • sorafenib
48
Q

What parts of the LFT are hepatocellular?

A

ALT and AST

49
Q

What parts of the LFT are cholestatic?

A

ALP
gGT
Bilirubin

50
Q

What does a raised ALT or AST say?

A

hepatocellular injury or hepatocellular necrosis

51
Q

What would the LFTs be in cholestasis?

A

very raised ALP, gGT and Bilirubin

raised or normal ALT

52
Q

What would the LFTs be in chronic hepatocellular damage?

A

normal or raised ALT, ALP, gGT and Bilirubin

53
Q

What would the LFTs be in acute hepatocellular damage?

A

very raised ALT
normal or raised ALP and gGT
raised Bilirubin

54
Q

What is acute liver disease?

A
  • rapid development of liver disease without any previous liver damage which is less than 6 months
  • causing encephalopathy and prolonged coagulation
55
Q

What are the true liver function tests?

A
  • Bilirubin
  • Albumin
  • Prothrombin time
56
Q

How does acute liver failure present?

A

jaundice, lethargy, nausea, anorexia, pain, itch, arthralgia and abnormal LFTs

57
Q

What are some of the main causes of acute liver disease?

A 
hepatitis
drugs
shock liver
cholangitis
alcohol 
malignancy
chronic liver disease
58
Q

What are some of the rarer causes of acute liver disease?

A

Budd Chiari, acute fatty liver of pregnancy or cholestasis of pregnancy

59
Q

What are the main investigations for acute liver disease?

A
  • HISTORY esp drug history
  • LFTs
  • prothrombin
  • examination
  • US including vascular
  • virology
  • investigations of chronic liver disease
60
Q

What is the treatment for acute liver disease?

A

rest up to 3 months, fluids, no alcohol, increase calories, observe for FHF

61
Q

What drugs can cause liver injury?

A

antibiotics (co-amox or fluclox), paracetamol, NSAIDs or statins

62
Q

What is fulminate hepatic failure?

A
  • a clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function
  • presents as an acute episode of severe liver dysfunction in a patient with a previous normal liver
63
Q

What is FHF caused by?

A

paracetamol, fulminant viral, drugs, HBV or non A-E

64
Q

What is the treatment for FHF?

A

supportive
fluids
renal replacement
transplant

My Gastrointestinal (18 decks)

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