Liver Flashcards

1
Q

Anatomical vs functional division of liver

A

Anatomical divided by falciform ligament

Functional divided by inferior vena cava & gallbladder fossa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Couinaud segments of the liver
How are the segments divided?

A

Segment I: caudate lobe
Segments II to VIII clockwise

Each has their own independent vascular inflow, outflow, biliary drainage

Divided by split of portal vein transversely, right/middle/left hepatic veins sagittally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Liver blood supply

A

75% by hepatic portal vein (splenic vein + superior mesenteric vein)

25% by hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Functions of liver

A

1) Bile production
2) Metabolic functions - carbohydrate, lipid, protein, lactate
3) Clotting factor & protein synthesis
4) Vit D activation
5) Detoxification
6) Vitamin/mineral storage
7) Phagocytosis of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is portal hypertension?

A

Chronic increase in portal pressure due to mechanical obstruction of portal venous system

When hepatic venous pressure gradient >=6mmHg (normal 3-5)

Pressure gradient between portal vein and hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Portal vein formed by the union of the ___ and ___ at ___

A

splenic vein + superior mesenteric vein

behind the neck of pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of portal hypertension (divide into classifications)

A

1) Pre-sinusoidal
- splenomegaly -> increased splenic blood flow
- portal vein thrombosis
- splenic vein thrombosis

2) Sinusoidal
- CIRRHOSIS
- massive fatty change
- schistosomiasis
- Wilson’s disease, Caroli disease

3) Post-sinusoidal
- Hepatic vein thrombosis (Budd Chiari)
- Right heart failure, pericarditis
- IVC thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Budd Chiari syndrome?

A

Hepatic vein thrombosis that leads to post-sinusoidal portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do portosystemic shunts occur?

A

1) Oesophageal branch of azygos (S) + left gastric vein (P)

2) Inferior rectal (S) + superior rectal (P)

3) Superficial epigastric (S) + paraumbilical (P)

4) IVC (S) + left branch of portal vein (P)

5) Renal/Gonadal (S) + Colic (P)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complications of portal hypertension

A

Ascites

Portosystemic shunts - caput medusae, oesophageal varices

Portal hypertensive gastropathy - gastric mucosal friability & dilated blood vessels

Hepatic encephalopathy

Splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What diuretic is used in ascites? Why?

A

Spironolactone - aldosterone antagonist

Portal HTN -> splanchnic vasodilation -> less effective blood volume in abdomen -> hypoperfused kidneys -> RAAS releases aldosterone to increase salt and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is SAAG?

A

Serum-ascites albumin gradient - directly correlates w portal pressure

SAAG >=1.1g/dL have portal HTN causing ascites (all the prepostsinusoidal stuff)

SAAG <1.1g/dL, non-HTN causes of ascites (malignancy, infection, inflammation, chylous ascites, nephrotic syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CT scan liver lesion features (HCC, adenoma, FNH, haemangioma)

A

HCC: hypervascular enhancement on arterial phase, portal venous washout

Hepatic adenoma: hypervascular enhancement on arterial phase, iso/hypointense on portal venous phase

Focal nodular hyperplasia: early arterial enhancement w centrifugal filling, sustained enhancement in portal venous phase (CHARACTERISTIC CENTRAL SCAR)

Haemangioma: early peripheral nodular enhancement in arterial phase, centripetal filling in, follows blood pooling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most common benign liver tumour

A

Haemangioma - outgrowths of endothelium made of widened blood vessels

a/w with OCP, steroid, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can large haemangiomas cause?

A

Pain from liver capsule stretch, compression on surrounding structure

Rare: Kasabach-Merritt syndrome - consumptive coagulopathy -> thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you diagnose haemangioma?

A

NOOOO BIOPSY - HAEMORRHAGE

Ultrasound, CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is focal nodular hyperplasia?

A

2nd most common benign tumour

CT shows characteristic central stellate scar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are hepatic adenomas?

A

benign proliferation of hepatocytes - occurs in young females on OCP

Large lesions >5cm have high chance of rupture & haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Resection of hepatic adenomas indicated in

A

Large lesions >4-5cm
Symptomatic
Cannot rule out malignancy
Male gender - high risk of malignant transformation

20
Q

Hepatic cysts can be ___ or ___

A

Non-parasitic: simple liver cyst, PCLD, neoplastic cysts

Echinococcal cysts: most commonly Hydatid cyst (tapeworm)

21
Q

Most common primary hepatic cancers

A

Hepatocellular carcinoma (85%)
Intrahepatic cholangiocarcinoma (6%)

22
Q

HCC risk factors

A

1) Alcoholic cirrhosis
2) Non alcoholic cirrhosis
- hepatitis B, C
- NAFLD
- autoimmune: PBC, PSC
- metabolic: haemochromatosis, alpha1antitrypsin deficiency
- others: red meat, aflatoxins, diabetes, smoking, alcohol

23
Q

What is primary biliary cirrhosis?

A

Inflammation & destruction of intrahepatic bile ducts

more common in middle aged women presenting w pruritus

anti-mitochondrial antibodies present

24
Q

What is primary sclerosing cholangitis?

A

Inflammation & destruction of intra and extrahepatic bile ducts

More common in young men with IBD

25
Q

Pathogenesis of HCC

A

Chronic inflammatory process, ongoing hepatocellular damage w high cell regeneration, increased rates of genetic mutation -> accumulates & leads to carcinoma

26
Q

How to predict prognosis in pts with cirrhosis?

A

Model for End Stage Liver Disease (MELD) score

MELD score 15 = 6% mortality in 3 months

TIPSS: <14 good outcome, poor >24

27
Q

Signs & symptoms of HCC

A
  • Jaundice (5-10%)
  • Fever from central tumour necrosis
  • LOW, LOA
  • Budd-chiari syndrome -> ascites
  • Decompensated liver: hepatic encephalopathy, coagulopathy
  • Rupture -> peritonitis
  • Features of portal HTN
28
Q

What is hepatorenal syndrome?

A

Acute renal failure in pts with advanced liver disease from cirrhosis

Portal HTN + splanchnic arterial vasodilation -> reduce resistance -> “hypovolemia”

Kidneys hypoperfused -> RAAS activated and efferent arterioles constrict to improve GFR. Afferent arterioles also constrict -> kidneys hypoperfused

29
Q

How to diagnose HCC?

A

Triphasic CT
MRI - distinguish HCC from nodules in cirrhotic pts

30
Q

What is a biomarker used in HCC?

A

Alpha fetoprotein

No longer used officially in diagnosis, but a rise in AFP in those w cirrhosis should raise suspicion for HCC

31
Q

Child Pugh Score classifications

A

Class A: 5-6 points (better survival function), surgical mortality 10%

Class B: 7-9 points (still can resect), surgical mortality 20-30%

Class C: 10-15 (not for resection), surgical mortality 75-80%

Used to evaluate risk of portocaval shunting procedure in pts with portal HTN, also used for other procedures in cirrhotic pts

32
Q

Indocyanine green test is for?

A

Assessing adequacy of remaining liver function post resection

Percentage of ICG dye left after 15 mins should be <10%

33
Q

Hepatectomy of HCC in pts with cirrhotic liver has ____

A

high recurrence rates
cirrhosis = “field change” effect in the liver, new tumour can still develop in remnant liver

34
Q

Only Child’s __ and ___ can undergo liver resection

A

A, good B

Use indocyanine green to determine extent of resection

35
Q

Palliative therapies for HCC

A

1) Radiofrequency ablation
- destroy tissue with heat
2) Trans-arterial chemoembolisation
- selective intra-arterial administration of chemo agents + emoblise major tumour artery

36
Q

What are secondary liver malignancies?

A

Metastatic liver tumours with cells originating from cancer elsewhere

Most common: colorectal cancer
Others: neuroendocrine tumour from GIT/pancreas, other cancers

37
Q

Metastasis can be to the ___ or the ___. LFT changes in each? Jaundice in each?

A

liver parenchyma or porta-hepatis lymph nodes

Parenchyma LFT: deranged liver enzymes + obstruction

LN LFT: obstructive pattern (jaundice would present early)

38
Q

Presentation of liver abscess

A

-*Spiking fevers with chills (90%)
- Jaundice, hepatomegaly

39
Q

5 routes of infection for liver abscesses

A

1) Portal vein: from gut
2) Biliary tree: ascending infections
3) Hepatic artery: sepsis
4) Direct inoculation: trauma, iatrogenic
5) Adjacent organ infection

40
Q

Pyogenic liver abscess appearance on CT

A

Rim-enhancing lesion on triphasic scan
Irregular lesion w central necrosis, air-fluid levels, could be multiloculated

41
Q

How to treat pyogenic liver abscess

A

Empirical Abx: IV ceftriaxone + metronidazole

Drainage for >3cm (percutaneous or open)

42
Q

Common pyogenic abscess organisms

A

Klebsiella
E.coli
Proteus vulgaris
Strep faecalis, staph epidermidis

43
Q

Common amoebic abscess organisms

A

Entamoeba histolytica - faecal oral transmission, enters the gut and into the liver

44
Q

Diagnosis of amoebic abscess

A

CTAP - round lesion abutting liver capsule, WITHOUT rim enhancement (unlike pyogenic)

Serum antibody test for E.histolytica

45
Q

Treatment for amoebic abscess

A

metronidazole

needle aspiration not routinely done