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CSIM > Liver > Flashcards

Liver Flashcards

1
Q

NAFLD risk factors

A

T2DM, Metabolic syndrome, BMI >30, age, sedentary lifestyle

PCOS, OSA, hypothyroid, NSAIDs, tamoxifen, steroids, amiodarone

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2
Q

NAFLD

A

Excess triglycerides accumulate in liver causing steatosis often asymptomatic until late stages. Alcohol consumption of over 25ml ethanol daily excludes

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3
Q

Causes of cirrhosis

A 
Alcoholic liver disease - alcohol Hx
NAFLD - DM, obesity, HTN
Hep B/C - IVDU, transfusions, immigrants
Wilsons, Haemochromatosis - FHx
Drugs - paracetamol, methotrexate, steriods
AI conditions - PBC, PSC, AIH
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4
Q

PC chronic liver disease

A 
malaise, wt loss, lethargy
jaundice, oedema, puritis, encephalopathy, ascites 
abnormal LFTs, hepatosplenomegaly, 
? SOB/empysema - a1antitrypsin
bloody diarrhoea - PSC
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5
Q

Pathophysiology of liver failure

A

Steatosis - accumulation of fat in hepatocytes, altered fat metabolism leads to increased liver size
Steatohepatitis - accelerated by alcohol, HBV,HVC, obesity early fibrosis, disrupted architecture and angiogenesis
Cirrhosis - hyperplastic nodules, stellate cells prevent exchange, mass fibrotic tissue leads to impairment of function. Portal HTN, varices

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6
Q

Imaging in hepatology

A

USS - detect liver lesions and metastasis, dilated bile ducts and gallstones. Quick and non invasive. Can be used to guide biopsy and doppler to assess blood flow

CT - higher sensitivity shows focal liver lesions, contrast for vasculature

MRI - good for biliary tree imagine. MRCP is gold standard. No radiation but pt has to be well and able to lie still in claustrophobic environment for 30 mins

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7
Q

Indications for biopsy

A

chronic liver disease staging

post transplant rejection

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8
Q

Non invasive liver disease staging

A

AST:ALT > 0.8 indicative of advanced fibrosis
transient elastography
FIB-4 score

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9
Q

Fibrosis

A

Extravasation of blood components leads to haemostasis, vasodilation and increased permeability allow immune mediators to enter tissues clotting factors cleave fibrinogen to fibrin forming platelet plug. Active innate and fibroblast activation cause mass inflammation and cell recruitment. Matrix deposition, SM and collagen synthesis = repair. Repeated insults or failure to remove the irritant lead to fibrosis. This disrupts normal tissue architecture and impairs function

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10
Q

Primary biliary cholangitis

A

AI disease 40-60y/o women. Chronic progressive cholestatic liver disease

Destruction of small and medium intra hepatic ducts leading to disrupted bile flow. Bile irritates hepatic tissue leading to further inflammation and damage

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11
Q

PC PBC

A

asymptomatic
fatigue, itching due to bile salts
xanthomas - due to increased blood cholesterol
Coexisting AI conditions - Sjorgrens, arthropathy
Advanced liver disease

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12
Q

Inv PBC

A

AMA +ve, high IgM
increased ALP and GGT
USS to exclude reversible causes of binary obstruction
biopsy granulomatous deposits of inflammation around bile ducts

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13
Q

Complications and Mx PBC

A

Osteoporosis, hypercholestrolemia, HCC
Monitor yearly USS for HCC and osteoporosis
UDCA - ursodeoxycholic acid hydrophilic synthetic bile acid that improve cholestasis and LFT’s, reduces cholesterol uptake from gut to liver

Fibrates - reduce hypercholestrolemia, cholestryamine - reduce itch

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14
Q

AIH

A

Continual hepatocellular inflammation and necrosis. Genetic links with HLAD8, DR3. Environmental triggers ; Hep a,b,c, statins and nitrofurantoin

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15
Q

PC AIH

A

non specific fever, malaise, anorexia, arthralgia
1/3rd present with acute hepatitis - RUQ, fever
Acute liver failure

Links to other AI conditions - Graves, pernicious anaemia, Hashimotos, Sjogrens

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16
Q

Types of AIH

A

type 1 - 75% all ages ANA and AMSA +ve

type 2 - 15% 10:1 female to male ratio, presents in young adults, LKM1 +ve

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17
Q

Inv AIH

A

ANA, ASMA +ve
IgG, high ALT due to hepatocyte damage
biopsy shows widespread lymphocytic infiltrate

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18
Q

Mx AIH

A

Steroids + azathioprine to induce remission

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19
Q

Primary sclerosing cholangitis

A

Chronic condition that can progress to cirrhosis. Inflammation and fibrosis of the intra and extra hepatic ducts
90% of pt will suffer from IBD

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20
Q

PC PSC

A

fatigue, jaundice, puritis
can present acutely as ascending cholangitis
progressive leading to chronic liver disease

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21
Q

Inv PSC

A

pANCA +ve, high ALP
MRCP shows beading of bile ducts and annular strictures
biopsy - onion skin fibrosis. T cell mediated destruction leading to concentric rings of fibrosis.

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22
Q

Complications and Mx of PSC

A

increased risk of CRC and cholangiocarcinoma
replacement of fat soluble vitamins ADEK
stenting for strictures to prevent cholangitis
regular screening

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23
Q

Acute liver failure

A

PT increase 4-6 seconds ( INR >1.5)
hepatic enchalopathy
without pre-existing cirrhosis

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24
Q

Causes of acute liver failure

A 
hepatitis A,E,B
drugs - paracetamol, isoniazid, halothane, tetracycline, anti epileptics, statins, aspirin
Acute fatty liver of pregnancy 
excess alcohol 
budd chiari 
AI hepatitis
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25
Q

Stages of acute liver failure

A

hyper acute (0-7days) = early renal failure, not often ascites prolonged PT, low bilirubin. high risk of cerebral oedema

acute (8-28) = rare renal failure or ascites, marked coagulopathy

subacute = poor prognosis, cerebral oedema and prolonged PT rare. high bilirubin and risk of ascites

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26
Q

Paracetamol OD

A

widespread hepatocellular necrosis beginning centrally and spreading towards ports hepatis. Paracetamol metabolised via CYP450 to NAPQI. NAPQI is toxic and requires glutathione to break it down, in overdose glutathione is depleted.

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27
Q

Mx paracetamol OD

A

N-acetyl cystine @ presentation if paracetamol levels >100g/l

Pt @ high risk are those who are malnourished, and on enzyme inducing drugs

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28
Q

PC acute liver failure

A

jaundice, RUQ pain, ascites,
encephalopathy - asterixsis, apraxia
N/V, anorexia and malaise

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29
Q

Inv acute liver failure

A

increased PT, INR
high bilirubin, ALT often in 1000/s
?acidosis

paracetamol levels, U+e’s, ABG, ferritin, hep serology, AIH markers

MRI allows calculation of liver volume if below 1000ml = poor prognosis

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30
Q

Complications of acute liver failure

A

Coagulopathy - necrosis leads to inadequate synthesis of coagulation factors. progressive thrombocytopenia = increased risk of DIC or cerebral bleed

Renal failure - ATN or due to hyperdynamic circulation leading to hepatorenal syndrome

Infection risk - mass systemic inflammatory response leading to organ failure, reduce leukocyte function

Cardiac - high output state with peripheral vasodilation leads to hypotension, increased CO and adrenal insufficiency lead to reduced PR - ARDS/ pul oedema

Hypoglycaemia and hyperammonia

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31
Q

Pathogenesis of hepatic encephalopathy

A

cerebral vasomotor dysfunction leads to vasodilation of cerebral blood vessels to increase blood flow. SIRS = increased capillary permeability - cerebral oedema. Astrocytes swell converting excess ammonia to glutamine. Glutamine = osmotic effect drawing h20 into cells

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32
Q

PC encephalopathy

A

Personality changes, reduced GCS, asterixis, increased ICP - papilloedema, vomiting.

Grade I GCS 14-15 slurred speech, inverted sleep wake
Grade II = 11-13 drowsiness, confusion
Grade 3 = 8-11 somnolence, inability to perform tasks
Grade IV < 8 coma

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33
Q

Mx of increased ICP

A

20% mannitol, target Na+ <150, hypothermia, burr hole if due to bleed.

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34
Q

Urgent transplant for acute liver failure

A

i) Paracetamol = pH < 7.25 or all of the following PT >100, lactate >3.5, HE grade III/ IV
ii) Non paracetamol = PT >100 or 3/5 drug induced, 40+, jaundice 1 wk prior, bilirubin >300, PT >50

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35
Q

Mx acute liver failure

A

ITU - NAC stat for paracetamol OD, withdraw hepatic drugs . Glucose and vit K
prophylactic anti fungal and ABx
steroids for AIH

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36
Q

Causes of hepatic encephalopathy

A

GI bleed, renal failure, acute liver injury
diuretic use
constipation
infections

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37
Q

Mx hepatic encephalopathy

A

protect airway, treat underlying

lactulose to reduce generation of NH3 by gut bacteria by reducing gut transit time

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38
Q

HCC monitoring

A

@ risk pt get 6 monthly USS and aFP monitoring. These include hep B,C, alcoholic with cirrhosis, AI - PSC, haemochromatosis.

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39
Q

CT scans and HCC

A

Contrast used to identify tumor, should glow white on injection due to vascularisation and show venous washout due to extensive venous network

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40
Q

Prevention of HCC

A

1 - vaccinate HBV avoid alcohol

2 - venesect haemochromatosis pt, lose wt/control DM for NAFLD, abstain from alcohol cirrhotics

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41
Q

PC HCC

A

Hard to distinguish from CLD hence why screening is used.

wt loss, malaise, RUQ pain moving to back
jaundice - early in cholangiocarcioma
hepatomegaly +/- bruit

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42
Q

Childs Pugh

A

Used to assess grade of cirrhosis and risk of vatical bleed

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43
Q

Mx HCC

A

Dependent on scoring
A - carcinoma in situ, normal portal pressures resection
B-C early stages 3 nodules max possible transplant
D - palliative care

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44
Q

TACE

A

transarterial chemoembolisation aims to occlude main blood supply of tumour. Lesions must be <5cm for transplant

45
Q

Sofrafenib

A

tyrosine kinase inhibitor aims to prevent angiogenesis and growth.

46
Q

Oestrogenic stigmata of CLD

A

spider naevi - 5+ occur on upper trunk when compressed will blanche caused by high oestrogen. In distribution of SVC
palmar erythema - reddening of thenar and hypothenar eminence due to high oestrogen
gynecomastia - palpable glandular tissue esp around areolar
testicular atrophy

All due to impaired liver function reducing the catabolism of androstiendione leading to increased estradiol. (spironolactone can = due to inhibiting testosterone)

47
Q

Causes of acute decompensation

A

SBP, variceal bleed, alcoholic hepatitis, infection, constipation, dehydration, HCC, AKI, drug SE

48
Q

Clotting abnormalities in CLD

A

High PT - due to reduced production of fat soluble clothing factors can = easy bruising
thrombocytopenia - hypersplenism = increased platelet destruction, reduced production due to low production of TPO and myelosupression

49
Q

Wernickes encephalopathy

A

Triad of opthalmaplegia, confusion and ataxia due to B1 ( thiamine) deficiency

50
Q

Stigmata of portal HTN

A

Splenomegaly - abnormal congested blood flow leads to splenic pooling and enlargement. Can be due to increased function - sickle cell, SLE, sarcoid, myelodysplasis, mononucleosis

Ascites - pHTN and hypoalbuminemia leads to reduced oncotic and increased hydrostatic pressure forcing fluid into the peritoneal cavity. O/E - shifting dullness, bullying flanks, inverted umbilicus

Caput medusa, varices and haemorroids - due to hepatic congestion collateral veins are used to return blood to the IVC. Caput - engorged superficial epigastric veins

51
Q

SAAG

A

Serum ascites to albumin gradient
> 11g/l = portal hypertension - high hydrostatic
< 11g/l = nephrotic syndrome, TB, infections, peritoneal cancer

52
Q

SBP diagnosis

A

PMN cells > 250mm3

53
Q

leukconhyia

A

white nails due to hypoalbuminemia

54
Q

Follow up for pt with severe cirrhosis

A

HCC surveillance - USS and aFP 6 monthly
2 yearly endoscope for varies - propanolol for prevention
vit B and thiamine
treat osteoporosis
Ascites - poor prognosis approx 2 yr mortality fluid restrict low Na+ diet, diuretics if needed

55
Q

Metabolic syndrome

A

3/5 = HTN, hyperlipidemia, hypertriglyceridemia, low HDL, obesity +/- PCOS, acanthosis nigricans

56
Q

NAFLD pathogensis

A

Insulin resistance leads to reduced responsiveness and fat storage in the liver parenchyma. HDL secretion reduced and increased uptake and synthesis of fatty acids. Hepatocytes swell with fat globules = widespread steatosis, fat degradation due to free radicals leads to mass inflammation and stellate cells lay down fibrotic material

57
Q

Inv NAFLD

A

bright liver on USS
AST:ALT < 1
high lipid, triglyceride and low HDL levels

58
Q

Mx NAFLD

A

increase exercise, lose wt
control HTN, statins
dietician
DM - 1st lifestyle, 2nd - metformin, 3rd pioglitazone

59
Q

Hepatitis

A

Inflammation of the liver
acute <6 months
chronic 6months+ leads to fibrosis and cirrhosis

60
Q

Causes of hepatitis

A

Viral A-E, immunosuppressed - EBV,CMV, AI, alcoholic, drug induced, non alcoholic steatohepatitis

61
Q

PC acute hepatitis

A

prodromal - N/V, fatigue, headache, anorexia, fever
acute - RUQ pain, hepatomegaly, jaundice
recovery - resolution of LFT’s

62
Q

Inv hepatitis

A

Hepatitis serology,
IgG - AIH, IgM - PBC, IgA - alcoholic liver disease
AMA +e = PBC, ANA, ASMA +ve = AIH, p-anca = PSC

63
Q

Candidate for liver transplant

A

refractory ascites
frequent encephalopathy
HCC < 5cm

64
Q

Hepatitis E

A

type 1/2 = faecal oral in asia, middle east
type 3/4 = increasing incidence with undercooked meat esp pork seen in western world

single stranded RNA virus. 20% mortality for pregnant women in 3rd trimester

65
Q

Extrahepatic manifestations hep E

A

Guillan Barre, encephalitis, glomerulonephritis

66
Q

Chronic hep E

A

seen in immunocompromised pt approx 60% of transplant pt with acute hep E will develop chronic hep E. usually asymptomatic can progress to cirrhosis in 10% of pt
Mx - ribavarin

67
Q

Diagnosis of hep E

A

serum IgM high for 3-4wks, IgG peaks as IgM falls and remains for 4 years. Present in stool before blood

68
Q

Hepatitis B

A

Only 5% of adults develop chronic infection 20-40% of pt with chronic hep B will develop cirrhosis and HCC. Accounts for 50% of HCC

Blood bourne transmitted via sexual contact, transfusions, IVDU and perinatally

69
Q

Hep B transmission baby

A

90% develop chronic due to inability to clear infection

70
Q

Extrahepatic manifestation hep E

A

membraneous glomerulonephritis, polyarteritis nodosa, serum like sickness

71
Q

HBsAg

A

Antigen on surface of hep B virus indicates acute infection

72
Q

Anti-HBc

A

Presence indicates previous or ongoing hep B infection

73
Q

Mx chronic hep B

A

Tenofovir to reduce VL

6 monthly USS and aFP for HCC surveillance

74
Q

Anti-HBs

A

Immunity or vaccination

75
Q

Hepatitis C

A

80% of pt infected with hep C develop chronic infection. Of these 20% develop cirrhosis - this is accelerated 100x if alcohol abuse is coexistent.

76
Q

Extrahepatic manifestation hep C

A

Sjogrens syndrome, cryoglobulinaemia

77
Q

Transmission hep C

A

90% IVDU contamination of needles. HCV ab +ve

78
Q

Mx Hep C

A

direct acting antivirals + peg interferon

79
Q

Choleostatic drug injury (high bili/ALP)

A

steroids, COCP, co-amoxiclav, flucloxicillin,erthryomycin

80
Q

Hepatocellular drug injury (high ALT)

A

paracetamol, statins, methotrexate, valproate, rifampicin, NSAIDs, lisinopril, TCA’s, omeprazole

81
Q

Charcot’s triad

A

fever, RUQ pain and jaundice

82
Q

Pathogenesis of cirrhosis

A

Activation of stellate cells due to damage to hepatocytes leads to myelofibroblast proliferation. TGFb1 potentiates this and inhibits metalloproteinases to breakdown fibrotic tissue. These fibrotic bands disrupt the architecture of the liver reducing synthetic function and increasing the resistance to blood flow - portal HTN

83
Q

Mx Ascites

A

Na+ restricted diet, fluid restrict
spironolactone
Ascites drain
TIPPS shunting if severe - refractory ascites carries a prognosis of 6 months

84
Q

SBP PC

A

PC - abdo pain, fever often asymptomatic

Gram -ve ie e.coli, klebsiella. Ascites tap > 250mm3 diagnostic

Mx = IV co-amox/ oral ciprofloxacin

85
Q

Side effects of portal HTN

A

Severe pHTN leads to compensationery splanchnic dilation this splenic pooling reduces arterial volume so CO increases. Compensatory RAS activation leads to Na+ retention hence ascites. Peripheral vasoconstriction can precipitate hepatorenal syndrome.

86
Q

Hepatorenal syndrome

A

On the background of ascites in pt with severe cirrhosis. vasoconstriction of renal arteries and dilation off splanic vessels

87
Q

Type 1 Hepatorenal

A

2ndary to precipitate usually SBP, sepsis, peritonitis or GI bleed poor prognosis 50% at 1 month. Doubling of creatinine to over 221. Rapidly progressing may need terlipressin or ionotropes

88
Q

Type 2 Hepatorenal

A

Slowly progressive decline in renal function with refractory ascites creatine rises above 133. Prognosis 6 months without renal transplant

89
Q

Mx hepatorenal syndrome

A

look for infection/GI bleed as cause! stop nephrotoxic drugs
terlipressin 05mg QDS - acts to vasoconstrict splanchnic vessels
IV albumin

90
Q

Oesophageal varices

A

Collaterals from portoepiploic anastomoses develop particularly around L gastric vein. 50% of pt with cirrhosis have varices at diagnosis

91
Q

Primary prevention of varices

A

B-blockers 2/3 yearly endoscope

92
Q

Mx acute variceal bleed

A

ABCDE approach - protection of airway if needed.
Terlipressin
Band ligation/acid injection @ endoscopy
Antibiotics

93
Q

Secondary prevention

A

Endoscopic banding of varices
TIPS - transjugular intrahepatic portosystemic shunt
- This bypasses the liver reducing development of varies developing but can lead to hypoxic liver injury.

94
Q

Unconjugated hyperbilirubinemia

A

Gilberts, Criggler-Nijjar

Increased production - haemolysis

95
Q

Functions of the liver

A

Protein synthesis - Albumin -crucial to maintain oncotic pressure and to transport water insoluble substances such as hormones, fatty acids and drugs. Synthesis of all coagulation factors and complement

96
Q

Synthetic markers of liver function

A

PT, albumin, bilirubin

97
Q

Ultrasound Scan uses

A

Gallstones, hepatosplenmegly, HCC, Budd-Chairi, portal HTN, exclude post hepatic obstruction, NAFLD - bright fatty liver, guided biopsy

98
Q

Haemolytic Jaundice

A

Increased breakdown of RBC. raised unconjugated bilirubin, high urobilinogen . Due to causes of haemolytic anaemia - sickle cell, malaria, hypersplenism

99
Q

Investigation of a liver mass

A

If mass <1cm repeat USS in 4 months,

if >1cm an IV contrast CT scan/MRI scan

100
Q

ALT Rise

A 
1000 = ischemia, viral hepatitis, drugs
300-500 = AIH, chronic alcohol 
<300 = NAFLD, cirrhosis, wilsons, haemochromatosis
101
Q

AST:ALT

A

> 2 = alcoholic liver disease

102
Q

Gamma GT

A

Enzyme present in liver and other tissue.
Isolated ggt rise = alcohol or enzyme inducing drugs
- phenytoin, rifampicin, carbamazepine,

103
Q

ALP

A

Present in hepatic canalicular and sinusoids, bone and intestine.

Isolated ALP rise = bone disorders Pagets, bony mets, osteomalacia, fractures

Cholestasis = high ALP and ggt > AST and ALT

104
Q

Causes of cholestatic LFTS

A

Intrahepatic - PBC, PSC, drugs - erythromycin, flucloxicillin, COCP

Extrahepatic - gallstones, carcinoma head of pancreas

105
Q

Acute Hep B infection

A

HBsAg antiHBc +ve

106
Q

Chronic Hep B carriage

A

HBsAg antiHBc +ve

107
Q

Immunisation

A

anti-HBs +ve

108
Q

Immune from natural infection

A

antiHBs and antiHBc +ve

109
Q

High conjugated bilirubin

A

Blockage of bile outflow - gallstones, PBC, strictures, PSC and carcinoma of head of pancreas

Liver dysfunction - viruses (HBV, HCV), liver mets, cirrhosis

CSIM (12 decks)

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