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Liver Flashcards

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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
Stages of acute liver failure
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
26
Paracetamol OD
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.
27
Mx paracetamol OD
N-acetyl cystine @ presentation if paracetamol levels >100g/l Pt @ high risk are those who are malnourished, and on enzyme inducing drugs
28
PC acute liver failure
jaundice, RUQ pain, ascites, encephalopathy - asterixsis, apraxia N/V, anorexia and malaise
29
Inv acute liver failure
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
30
Complications of acute liver failure
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
31
Pathogenesis of hepatic encephalopathy
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
32
PC encephalopathy
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
33
Mx of increased ICP
20% mannitol, target Na+ <150, hypothermia, burr hole if due to bleed.
34
Urgent transplant for acute liver failure
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
35
Mx acute liver failure
ITU - NAC stat for paracetamol OD, withdraw hepatic drugs . Glucose and vit K prophylactic anti fungal and ABx steroids for AIH
36
Causes of hepatic encephalopathy
GI bleed, renal failure, acute liver injury diuretic use constipation infections
37
Mx hepatic encephalopathy
protect airway, treat underlying | lactulose to reduce generation of NH3 by gut bacteria by reducing gut transit time
38
HCC monitoring
@ risk pt get 6 monthly USS and aFP monitoring. These include hep B,C, alcoholic with cirrhosis, AI - PSC, haemochromatosis.
39
CT scans and HCC
Contrast used to identify tumor, should glow white on injection due to vascularisation and show venous washout due to extensive venous network
40
Prevention of HCC
1 - vaccinate HBV avoid alcohol | 2 - venesect haemochromatosis pt, lose wt/control DM for NAFLD, abstain from alcohol cirrhotics
41
PC HCC
Hard to distinguish from CLD hence why screening is used. wt loss, malaise, RUQ pain moving to back jaundice - early in cholangiocarcioma hepatomegaly +/- bruit
42
Childs Pugh
Used to assess grade of cirrhosis and risk of vatical bleed
43
Mx HCC
Dependent on scoring A - carcinoma in situ, normal portal pressures resection B-C early stages 3 nodules max possible transplant D - palliative care
44
TACE
transarterial chemoembolisation aims to occlude main blood supply of tumour. Lesions must be <5cm for transplant
45
Sofrafenib
tyrosine kinase inhibitor aims to prevent angiogenesis and growth.
46
Oestrogenic stigmata of CLD
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
Causes of acute decompensation
SBP, variceal bleed, alcoholic hepatitis, infection, constipation, dehydration, HCC, AKI, drug SE
48
Clotting abnormalities in CLD
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
Wernickes encephalopathy
Triad of opthalmaplegia, confusion and ataxia due to B1 ( thiamine) deficiency
50
Stigmata of portal HTN
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
SAAG
Serum ascites to albumin gradient > 11g/l = portal hypertension - high hydrostatic < 11g/l = nephrotic syndrome, TB, infections, peritoneal cancer
52
SBP diagnosis
PMN cells > 250mm3
53
leukconhyia
white nails due to hypoalbuminemia
54
Follow up for pt with severe cirrhosis
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
Metabolic syndrome
3/5 = HTN, hyperlipidemia, hypertriglyceridemia, low HDL, obesity +/- PCOS, acanthosis nigricans
56
NAFLD pathogensis
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
Inv NAFLD
bright liver on USS AST:ALT < 1 high lipid, triglyceride and low HDL levels
58
Mx NAFLD
increase exercise, lose wt control HTN, statins dietician DM - 1st lifestyle, 2nd - metformin, 3rd pioglitazone
59
Hepatitis
Inflammation of the liver acute <6 months chronic 6months+ leads to fibrosis and cirrhosis
60
Causes of hepatitis
Viral A-E, immunosuppressed - EBV,CMV, AI, alcoholic, drug induced, non alcoholic steatohepatitis
61
PC acute hepatitis
prodromal - N/V, fatigue, headache, anorexia, fever acute - RUQ pain, hepatomegaly, jaundice recovery - resolution of LFT's
62
Inv hepatitis
Hepatitis serology, IgG - AIH, IgM - PBC, IgA - alcoholic liver disease AMA +e = PBC, ANA, ASMA +ve = AIH, p-anca = PSC
63
Candidate for liver transplant
refractory ascites frequent encephalopathy HCC < 5cm
64
Hepatitis E
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
Extrahepatic manifestations hep E
Guillan Barre, encephalitis, glomerulonephritis
66
Chronic hep E
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
Diagnosis of hep E
serum IgM high for 3-4wks, IgG peaks as IgM falls and remains for 4 years. Present in stool before blood
68
Hepatitis B
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
Hep B transmission baby
90% develop chronic due to inability to clear infection
70
Extrahepatic manifestation hep E
membraneous glomerulonephritis, polyarteritis nodosa, serum like sickness
71
HBsAg
Antigen on surface of hep B virus indicates acute infection
72
Anti-HBc
Presence indicates previous or ongoing hep B infection
73
Mx chronic hep B
Tenofovir to reduce VL | 6 monthly USS and aFP for HCC surveillance
74
Anti-HBs
Immunity or vaccination
75
Hepatitis C
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
Extrahepatic manifestation hep C
Sjogrens syndrome, cryoglobulinaemia
77
Transmission hep C
90% IVDU contamination of needles. HCV ab +ve
78
Mx Hep C
direct acting antivirals + peg interferon
79
Choleostatic drug injury (high bili/ALP)
steroids, COCP, co-amoxiclav, flucloxicillin,erthryomycin
80
Hepatocellular drug injury (high ALT)
paracetamol, statins, methotrexate, valproate, rifampicin, NSAIDs, lisinopril, TCA's, omeprazole
81
Charcot's triad
fever, RUQ pain and jaundice
82
Pathogenesis of cirrhosis
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
Mx Ascites
Na+ restricted diet, fluid restrict spironolactone Ascites drain TIPPS shunting if severe - refractory ascites carries a prognosis of 6 months
84
SBP PC
PC - abdo pain, fever often asymptomatic Gram -ve ie e.coli, klebsiella. Ascites tap > 250mm3 diagnostic Mx = IV co-amox/ oral ciprofloxacin
85
Side effects of portal HTN
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
Hepatorenal syndrome
On the background of ascites in pt with severe cirrhosis. vasoconstriction of renal arteries and dilation off splanic vessels
87
Type 1 Hepatorenal
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
Type 2 Hepatorenal
Slowly progressive decline in renal function with refractory ascites creatine rises above 133. Prognosis 6 months without renal transplant
89
Mx hepatorenal syndrome
look for infection/GI bleed as cause! stop nephrotoxic drugs terlipressin 05mg QDS - acts to vasoconstrict splanchnic vessels IV albumin
90
Oesophageal varices
Collaterals from portoepiploic anastomoses develop particularly around L gastric vein. 50% of pt with cirrhosis have varices at diagnosis
91
Primary prevention of varices
B-blockers 2/3 yearly endoscope
92
Mx acute variceal bleed
ABCDE approach - protection of airway if needed. Terlipressin Band ligation/acid injection @ endoscopy Antibiotics
93
Secondary prevention
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
Unconjugated hyperbilirubinemia
Gilberts, Criggler-Nijjar | Increased production - haemolysis
95
Functions of the liver
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
Synthetic markers of liver function
PT, albumin, bilirubin
97
Ultrasound Scan uses
Gallstones, hepatosplenmegly, HCC, Budd-Chairi, portal HTN, exclude post hepatic obstruction, NAFLD - bright fatty liver, guided biopsy
98
Haemolytic Jaundice
Increased breakdown of RBC. raised unconjugated bilirubin, high urobilinogen . Due to causes of haemolytic anaemia - sickle cell, malaria, hypersplenism
99
Investigation of a liver mass
If mass <1cm repeat USS in 4 months, | if >1cm an IV contrast CT scan/MRI scan
100
ALT Rise
``` 1000 = ischemia, viral hepatitis, drugs 300-500 = AIH, chronic alcohol <300 = NAFLD, cirrhosis, wilsons, haemochromatosis ```
101
AST:ALT
> 2 = alcoholic liver disease
102
Gamma GT
Enzyme present in liver and other tissue. Isolated ggt rise = alcohol or enzyme inducing drugs - phenytoin, rifampicin, carbamazepine,
103
ALP
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
Causes of cholestatic LFTS
Intrahepatic - PBC, PSC, drugs - erythromycin, flucloxicillin, COCP Extrahepatic - gallstones, carcinoma head of pancreas
105
Acute Hep B infection
HBsAg antiHBc +ve
106
Chronic Hep B carriage
HBsAg antiHBc +ve
107
Immunisation
anti-HBs +ve
108
Immune from natural infection
antiHBs and antiHBc +ve
109
High conjugated bilirubin
Blockage of bile outflow - gallstones, PBC, strictures, PSC and carcinoma of head of pancreas Liver dysfunction - viruses (HBV, HCV), liver mets, cirrhosis

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