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G.I. > Liver & Gall bladder > Flashcards

Liver & Gall bladder Flashcards

1
Q

Which veins make up the hepatic portal vein?

A
  1. Superior Mesenteric Vein
  2. Splenic Vein
  3. Inferior mesenteric
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2
Q

The portal vein carries outflow from?

A
  1. ) Spleen
  2. ) Oesophagus
  3. ) Stomach
  4. ) Pancreas
  5. ) Small and large intestine
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3
Q

How much blood does the hepatic portal vein supply to the liver?

A

75%

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4
Q

Hepatic Blood Flow

A
  1. Oxygenated blood from hepatic artery & nutrient-rich, deoxygenated blood from hepatic portal vein
  2. –> Liver sinusoids
  3. –> Central vein
  4. –> Hepatic vein
  5. –> IVC
  6. Right atrium
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5
Q

Portal-caval anastomoses

A

4 collateral pathways

  1. Esophageal and gastric venous plexus
  2. Umbilical vein from the left portal vein to the epigastric venous system
  3. Retroperitoneal collateral vessels
  4. Hemorrhoidal venous plexus
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6
Q

What may happen to the portal caval anastomoses?

A

In portal hypertension, the collateral vessels may become engorged, dilated or varicosed.

May rupture

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7
Q

Normal pressure of the portal vein system?

A

5-8 mmHg

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8
Q

PORTAL HYPERTENSION

A
  • Pressure above normal range of 5-8mmHg
  • Portal vein-hepatic vein pressure gradient greater than 5mmHg
  • Represents increase in hydrostatic pressure within portal vein and its tributaries
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9
Q

Portal Hypertension - Causes

  • Prehepatic
  • Intrahepatic
A
  1. Prehepatic -

Blockage of the portal vein before the liver, due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities

  1. Intrahepatic -

Due to distortion of the liver architecture
i. PRESINUSOIDAL - schistosomiasis; non cirrhotic portal hypertension

ii. POSTSINUSOIDAL - cirrhosis, alcoholic hepatitis, congenital hepatic fibrosis
3. Budd-Chiari and veno occlusive disease

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10
Q

Budd-Chiari syndrome

A

Thrombosis/Occlusion of the hepatic veins draining the liver

> Congenital webs
Thrombotic tendency, protein C or S deficiency

Clinical//

• Acute
– jaundice, tender hepatomegaly

• Chronic
– Ascites

Abdo pain, ascites and liver enlargement

Diagnosis//

– US of hepatic veins

Treatment//

    • Recanalisation
    • TIPSS
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11
Q

Wilson’s Disease

A
  • Disorder of copper metabolism
  • Loss of function or loss of protein mutations in CAERUOPLASMIN
  • Copper-binding protein, loss of copper regulation
  • massive tissue deposition of copper

Clinical //

  • Neurological (involuntary movements)
  • Hepatic (cirrhosis)
  • KAISER-FLEISCHER Rings
  • Basal ganglia degeneration
  • Dementia
  • Blue nails
  • Chromosome 13

Treatment//

copper chelation drugs - PENICILLAMINE
ZINC

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12
Q

Hepatic Carcinogenesis

A
  • Recurrent hepatocyte death
  • regeneration
  • cellular hyperplasia (recurrent DNA copying)

-INFLAMMATION
degranulation cell cycle control
DNA damage due to ROS & RNS

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13
Q

Cirrhosis

  • Compensated
  • Decompensated
A

i) Compensated

  • clinically normal
  • incidental finding
  • lab test/ imaging abnormality
  • Portal Hypertension may be present

ii) Decompensated

- Liver Failure
> acute on chronic 
---infection
---insult
---SIRS
> End-stage liver disease
--- insufficient hepatocytes
---"run out of liver"
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14
Q

What happens in the liver sinusoids?

A

Arterial and venous blood mixes

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15
Q

Route blood takes through the liver?

A

Hepatic artery and hepatic portal vein –> arterioles and venues –> sinusoids –> central vein of liver lobule –> branches of hepatic vein –> hepatic vein

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16
Q

Features of liver lobules

A
  • Hexagonal
  • Has a branch of hepatic vein at its centre (central vein)
  • Has a triad at each of its six corners with branches of hepatic portal vein, hepatic artery and bile duct
  • Cords of hepatocytes arranged as hepatic plates
  • BLOOD flows INWARDLY through sinusoids to the central vein
  • Bile flows OUTWARDLY through canaliculli to the bile duct
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17
Q

How are HEPATOCYTES arranged?

A

Arranged in between sinusoids in plates two cells thick

  • BASOLATERAL membrane faces the SPACE OF DISSE (extracellular gap between the latter and the endothelial cells that line the fenestrated sinusoids)
  • APICAL membrane of adjacent hepatocytes is grooved and forms the canaliculli
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18
Q

What do SINUSOIDAL SPACES contain?

A

> Endothelial cells
- form a fenestrated structure, allowing for free movement of solutes

> Kuppfer cells
- macrophages resident to the sinusoidal space, remove particulate matter and senescent erythrocytes

> Stellate (Ito) cells

  • within the space of Disse
  • important for vitamin A storage
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19
Q

Intrahepatic Bile System

A

Canaliculi -> terminal bile ductules -> perilobular ducts -> interlobular ducts -> septal ducts -> lobar ducts -> two hepatic ducts ->  the common hepatic duct

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20
Q

Bile production between meals

A

Stored and concentrated in the gall bladder (sphincter of Oddi closed)

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21
Q

Bile production DURING a meal

A
  • Chyme in duodenum stimulates gall bladder smooth muscle to contract
  • Sphincter of Oddi opens
  • Bile spurts into duodenum via cystic and common bile ducts
  • Digestion and absorption of fat
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22
Q

How does gall bladder contract, and the sphincter of oddi open?

A

CCK and vagal impulses

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23
Q

Bile from Bile Duct Cells

A

Alkaline, HCO3 rich

Between meals has an ionic composition

neutralisation of chyme

pH adjustment for enzyme action

mucosal protection

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24
Q

Bile from HEPATOCYTES

A 
> secreted into canaliculli
> Primary bile acids - CHOLIC and CHENODEOXYCHOLIC acids
> Water and electrolytes
> Lipids and phospholipids
> Cholesterol
> IgA
> Bilirubin
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25
Q

What effect can excess cholesterol relative to bile acids have?

A

Excess cholesterol may precipitate into micro crystals which aggregate into GALL STONES

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26
Q

What can be used to get rid of gall stones?

A

URSODEOXYCHOLIC ACID may be used to dissolve non-calcined cholesterol gall stones

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27
Q

Bilirubin

A

Breakdown product of the porphyrin component of Hb

Pigment rendering urine yellow and faeces brown

Causes JAUNDICE in excess

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28
Q

Enterohepatic Recycling

A

Only a small fraction of bile salts entering the duodenum is lost in the faeces

MOST is REABSORBED by active transport in the terminal ileum and undergoes enterohepatic recycling

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29
Q

Which drugs make use of this system?

A 
> RESINS
> Colestyramine, colestipol 
> Bind bile salts
> Prevent reabsorption
> Lower plasma cholesterol
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30
Q

Drug metabolism aims

A

> Convert parent drugs to more polar metabolites that are NOT readily absorbed by the kidneys –> excretion

> Convert drugs to metabolites that are usually less active than parent compound

> BUT, can be converted from inactive PRODRUGS to active compounds

> have unchanged activity

> possess a different type or spectrum of action (aspirin –> salicylic acid)

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31
Q

Drug Metabolism Phases

A

> Phase 1

  • makes drugs more polar, adds a chemically reactive group permitting conjugation
  • Oxidation
  • Reduction
  • Hydrolysis

> Phase 2

  • CONJUGATION
  • Adds an endogenous compound increasing polarity

> Not all drugs go through both phases, or can completely circumvent it before being excreted

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32
Q

Cytochrome P450 (CYP) Monooxygenases

A

> Mediate OXIDATION reactions (phase 1)
Located in the endoplasmic reticulum
Have distinct, but overlapping substrate specificities

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33
Q

What are the main gene families of CYP in the liver?

A

CYP1, 2 & 3

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34
Q

Monooxygenase P450 Cycle

A

> Drug enters cycle as drug substrate
Molecular oxygen provides 2 atoms of oxygen
One atom of oxygen is added to the drug to give the HYDROXYL PRODUCT
This leaves the cycle
the second oxygen combines with protons to form H2O

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35
Q

Phase 2 Reactions

A

> Usually result in inactive products
Conjugation of chemically reactive groups
Glucuronidation is a common reaction
Transfer of glucoronic acid –> electron-rich atoms
Bilirubin & adrenal corticosteroids

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36
Q

Hepatic Encephalopathy & Therapy

A

> Detoxification of NH3 to Urea does NOT occur in severe hepatic failure, blood NH3 levels rise resulting in coma

> Therapy - Lactulose, antibiotics (neomycin, rifaximin)

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37
Q

What does electrophoresis allow?

A

Separation of proteins by size

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38
Q

Functions of plasma proteins

A 
> maintenance of oncotic or colloid osmotic pressure (maintain BP)
> transport of hydrophobic substances
> pH buffering
> Enzymatic
> Immunity
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39
Q

alpha globulins

A

> transport lipoproteins, lipids, hormones and bilirubin
Cu2+
retinol binding protein (transports vitamin A)

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40
Q

Beta Globulins

A

> Transferrin (transports ferric ions in the body, Fe3+)

> Fibrinogen (inactive form of fibrin)

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41
Q

Albumin

A

> Most abundant plasma protein

  • small, negatively charged, water-soluble
  • main determinant of plasma oncotic pressure

> Liver synthesises about 14g/day

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42
Q

Which hormone stimulates albumin production?

A

Insulin

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43
Q

How is iron transported in the body?

A

> Transported as ferric ion, Fe3+

- bound to TRANSFERRIN in blood

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44
Q

How is iron STORED?

A

> In liver cells as Fe2+ bound to FERRITIN

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45
Q

How is COPPER transported in the blood?

A

> By Ceruloplasmin

deficiency of which causes Wilson’s disease

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46
Q

Steroid hormones and T3/T4 thyroid hormones are hydrophilic/hydrophobic?

A

HYDROPHOBIC

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47
Q

How is THYROXINE transported in the blood?

A

Bound to thyroid-binding globulin

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48
Q

How is CORTISOL transported in the blood?

A

Bound to cortisol-binding globulin

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49
Q

Lipoproteins
> core
> shell

A

> Core of cholesterol esters and tricgylcerides
Shell made up of polar lipids and phospholipids, APOPROTEINS

> Free cholesterol dispersed throughout
Fat transport between organs and tissues

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50
Q

Reverse cholesterol transport

A

> HDL
Removes excess cholesterol from cells
Liver is the only organ that can metabolise and excrete cholesterol

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51
Q

Cholesterol synthesis

A

Main site is the LIVER

Needs a lot of energy (36 ATP)

Using HMG-CoA reductase

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52
Q

HMG-Coa

A

> Catalyses the formation of MEVALONIC ACID
Rate limiting enzyme
Fasting stimulates activity and synthesis
Target for STATINS

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53
Q

Vitamin D

A

> Role in regulation of calcium and phosphorus metabolism
Most abundant form is vitamin D3
Derived from cholesterol

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54
Q

Where are corticosteroids synthesised?

A

Adrenal cortex

cholesterol derivative

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55
Q

Where are ANDROGENS synthesised?

A

Testis

cholesterol derivative

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56
Q

Where are ESTROGENS synthesised?

A

Ovary

cholesterol derivative

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57
Q

What is the main metabolic product of cholesterol?

A

BILE SALTS

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58
Q

Bile salt resins

A

Bind bile salts and inhibit reabsorption in the enterohepatic circulation

Increased bile salt excretion

Increased synthesis of bile salts

therefore, concentration of cholesterol in liver decreases

Number of LDL receptors of hepatic cells increases

Uptake of LDL cholesterol from plasma increases

–> lower plasma LDL

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59
Q

Wernicke-Korsakoff Syndrome

A

> Thiamine deficiency (vitamin b1)
Ataxia and confusion (Wernicke encephalopathy)
Memory impairment (Korsakoff syndrome)

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60
Q

Chronic Effects of ALCOHOL consumption

A 
•	G.I.
o	Stomach
o	Liver 
o	Pancreas
•	C.V.
o	Hypertension
o	Cardiomyopathy
o	M.I.
o	Stroke
•	C.N.S.
o	Neuropathies
o	Cerebellar degeneration
o	Dementia
o	Wernicke-Korsakoff’s syndrome 
♣	Thiamine deficiency
•	Hematologic
o	Anaemia
o	Bone marrow suppression
•	Musculoskeletal
o	Proximal myopathy 
•	Endocrine
•	Dermatologic
•	Reproductive
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61
Q

Solid liver lesions in older patients are more likely to be?

A

Malignant, in absence of liver disease

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62
Q

Solid liver lesions in chronic liver disease patients more likely to be?

A

Primary liver cancer

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63
Q

What is the most common solid liver tumour in NON CIRRHOTIC patients

A

HAEMANGIOMAS

64
Q

Focal liver lesions are normally found in what fashion?

A

Picked up incidentally on scans

65
Q

Benign Liver Lesions

A

> Haemangioma
Focal Nodular Hyperplasia
Adenoma
Liver cysts

66
Q

Malignant liver lesions

A
  1. Primary liver cancers
    - Hepatocellular carcinoma
    - Cholangiocarcinoma
    - -> Fibrolamellar carcinoma
    - -> hepatoblastoma
  2. Metastases
67
Q

Haemangioma

A
  • Commonest liver tumour
  • more females affected
  • Hypervascular
  • Single, small tumour
  • Well defined
  • Asymptomatic

Diagnosis
> US: echogenic spot
> CT: venous enhancement from periphery to centre
> MRI: High intensity area

Treatment
> no need for treatment
> not a premalignant pre cursor

68
Q

Focal Nodular Hyperplasia (FNH)

  • Features
  • Diagnosis
  • Treatment
A

> Benign nodule formation
Associated with Osler-Weber-Rendu and liver haemanagioma
Central scar containing a large artery, radiating branches to the periphery (HUB & SPOKE)
Hyperplastic response to abnormal arterial flow
More common in young/middle aged women
Asymptomatic, minimal pain

Diagnosis

> US: nodule with varying echogenicity
CT: hypervascular mass with central scar
MRI: Iso or hypo intense
FNA: normal hepatocytes and kupffer cells with central core

Treatment

> No treatment necessary

69
Q

What does FNA stand for?

A
  • Fine Needle Aspiration

- Used to get a sample and analyse cytology/histology

70
Q

Hepatic Adenoma

A

Clinical Features

  • Hormone related
  • Benign neoplasm composed of normal hepatocytes (no portal tract, central veins or bile ducts)
  • More common in women
  • Contraceptive hormones and anabolic steroids
  • Asymptomatic, may have RUQ pain
  • Found in RIGHT LOBE
  • May present with rupture, haemorrhage, or malignant transformation
  • Malignant transformation risk higher in males
  • Symptoms are size-related
  • Regression of tumour can occur if oral contraceptive is discontinued

Diagnosis

US: Filling defect
CT: Diffuse arterial enhancement
MRI: Hypo or hyper intense lesion
FNA: May be needed

Treatment

> Stop hormones, weight loss
Males (irrespective of size) : surgical excision
Females : imaging after 6months
<5cm or reducing in size - annual MRI
>5cm or increase in size - for surgical excision

71
Q

Simple liver CYST

A 
> Liquid collection lined by an epithelium
> no biliary tree communication
> Solitary
> Asymptomatic
> Symptoms related to
-intracystic haemorrhage
- infection
- rupture
- compression

Management

> no follow up necessary
if doubt, imaging 3-6 months
consider surgical intervention (huge cyst)

72
Q

Hydatid Cyst (caused by)

A
  • Echinoccocus granulises
  • due to ingestion of eggs of the tapeworm
  • not so common here
  • presentation of disseminated disease, erosion of cysts into adjacent structures
  • detection of anti-echinococcus antibodies

Management

> SURGERY

    • open cystectomy
    • pericystectomy, lobectomy

Risks - operative morbidity, anaphylaxis, dissemination of infection

73
Q

What medication would be used to treat parasites causing hydatid cysts?

A

Albendazole

74
Q

Polycystic Liver Disease (PLD)

A
  • Embryonic ductal plate malformation of the intrahepatic biliary tree
  • Numerous cysts throughout liver parenchyma
75
Q

What are the three types of PLD?

A
  1. Polycystic Liver Disease
  2. Von Meyenburg complexes
  3. Autosomal dominant poyscystic kidney disease
76
Q

Von Meyenburg Complex (VMC)

A

Type of polycystic liver disease

  • microhamartomas
  • benign cystic nodules throughout the liver
  • cystic bile duct malformations
  • silent during life, usually
  • incidental finding
77
Q

Polycystic Liver Disease (PCLD)

A
  • Liver function preserved, renal failure is rare
  • symtpoms depend on the size of the cysts
  • PCLD gene: PRKCSH and SEC63
78
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A
  • Renal failure due to polycystic kidneys and non-real extra-hepatic features
  • Potential massive hepatic enlargement
  • ADPKD genes - PKD1 and PKD2
79
Q

Polycystic Liver Disease - Management

A

C/O abdominal pain, abdominal distension, atypical symptoms due to voluminous cysts resulting in compression of adjacent tissue or failure of the affected organ

Conservative treatment is recommended to halt cyst growth to allow abdominal decompression and ameliorate symptoms

Invasive procedures are rarely required only in selective patient group with advanced PCLD, ADPKD or liver failure

  • Defenestration/aspiration
  • Liver transplantation

Pharmacological therapy by somatostatin analogues lead to beneficial outcome of PLD in terms of symptom relief and liver volume reduction

80
Q

Liver Abscess

A

Clinical Features//

  • High fever/septic
  • Leukocytosis
  • Abdo pain
  • Complex liver lesion

History//

abdo or biliary infection

Dental procedure

Management//

> Initial empiric broad spectrum antibiotics

> Aspiration/drainage percutaneously

> Echocardiogram

> Operation if no clinical improvement:

  • Open drainage
  • Resection

> 4 weeks antibiotic therapy with repeat imaging

81
Q

Hepatocellular Carcinoma (HCC)

  • Risk factors
  • Clinical Features
  • Metastases
  • Diagnosis
  • Prognosis
A

Risk Factors//

Cirrhosis from any cause:

  • Hep B
  • Hep C
  • Alcohol
  • Alfatoxin
  • Other

Clinical Features//

  • weight loss and RUQ pain (commenest)
  • Asymptomatic
  • Worsening of pre-existing chronic liver disease
  • Acute liver failure

o/e. Signs of cirrhosis; hard, enlarged RUQ mass.
Liver bruit

Metastases//

  • rest of liver
  • portal vein
  • lymph ndoes
  • lung
  • bone
  • brain

Diagnosis//

  • clinical presentation
  • elevated AFP
  • Ultrasound
  • Triphasic CT scan
  • MRI
  • Biopsy

Prognosis//

  • Tumour size
  • Extrahepatic spread –> worsens prognosis
  • Underlying liver disease
  • Patient performance status
  • Poor life expectancy
82
Q

What is Alfa fetoprotein?

A

> HCC tumour marker
values > 100ng/ml highly suggestive of HCC
Elevation seen in majority of patients
Larger the tumour –> more alfa fetoprotein
Small lesions may not cause a rise

83
Q

What is the diagnostic method of choice in hepatocellular carcinoma?

A

Imaging

84
Q

Hepatocellular Carcinoma - therapeutic options

A

> Liver transplant

  • BEST treatment
  • only if single tumour is less than 5cm in size or fewer than 3 tumours less than 3cm each

> Resection
- feasible for small tumours with preserved liver function

> Local ablation

  • for non-resectable pt
  • for pt with advanced liver cirrhosis
  • alcohol injection
  • radio frequency ablation
  • temporary measure

> Chemoembolisation

  • TACE
  • – Trans Arterial Chemo Embolisation
  • Inject chemo selectively in hepatic artery
  • then inject an embolic agent
  • for patients with early cirrhosis

> Systemic Therapies

  • Sorafenib
  • multikinase inhibitor of vascular endothelial gf receptor
85
Q

Fibro-Lamellar Carcinoma

A
  • Presents in young pt
  • AFP norma
  • Not related to cirrhosis
  • Stellate scar on CT, radial septa
  • SURGICAL RESECTION or TRANSPLANTATION
86
Q

Secondary Liver Metastases

A
  • Most common site for blood-born metastases
  • Common primaries: colon, breast , lung, stomach, pancreas, melanoma
  • Mild cholestatic picture (ALP) with preserved liver function
  • Dx imaging or FNA
  • Treatment depends on primary cancer
  • Resection or chemoembolisation is sometimes possible
87
Q

Conjugated Bilirubin

A

The bilirubin has been through the conjugation process within the liver by UDP glucuronosyltransferase

Water soluble

Therefore can be excreted by kidneys

88
Q

Unconjugated bilirubin

A

Has not yet been through the liver

NOT water soluble

Excess unconjugated bilirubin –> Crigler-Najjar Syndrome

89
Q

Crigler-Najjar Syndrome

A
  • Autosomal recessive
  • Jaundice in neonates and babies due to LACK/NONE of UDP– glucuronosyltransferase
  • Build up of unconjugated bilirubin
90
Q

What are the true LFTs?

A

Prothrombin Time (PT) & Albumin

91
Q

What are the liver enzymes?

A 
ALT
AST,
ALP, 
Bilirubin 
and GGT
92
Q

Signs of COMPENSATED CIRRHOSIS

A
  • Spider naevi
  • Palmar erythema
  • Clubbing
  • Gynaecomastia
  • Hepatomegaly
  • Splenomegaly
  • NONE
93
Q

Signs of Decompensated Cirrhosis

A
  • Jaundice
  • Ascites
  • Encephalopathy
  • Bruising
94
Q

Treatment of decompensated cirrhosis?

A
  • Remove or treat the underlying cause
  • Look for and treat infection

• NUTRITION
> energy intake of 35-40 kcal/kg)
> protein intake of 1.2-1.5g/kg

small frequent meals and snacks

• Vitamin and Mineral Requirements
> vitamin B supplementation
> Thiamine
> Calcium and vitamin D to counter osteoporosis

95
Q

COMPLICATIONS of Cirrhosis

A
  • Ascites
  • Encephalopathy
  • Variceal bleeding
  • Liver failure
96
Q

Ascites

A

> Accumulation of fluid in the peritoneal cavity

TREATMENT//

> Improve underlying liver disease

> Look for and treat infection

> NO NSAIDS

> Reduce salt intake , maintain nutrition

> Diuretics – SPIRONOLACTONE

> Paracentesis

  • – rapid relief
  • –risk of infection and encephalopathy
  • – hypovolaemia

> TIPSS
- stent within the liver

> Transplantation

abstain from alcohol.

97
Q

Diuretics for ascites

> new ascites
recurrent ascites

A

> Spironolactone, first line in new ascites
In recurrent use step-wise increments of spironolactone + LOOP diuretic

> Monitor U&Es

98
Q

Spontaneous Bacterial Peritonitis (SBP)

A

> Translocated bacterial peritonitis

Diagnosis//

  • tap of ascites and cell count
  • neutrophil count >250cells/mm^3

Treatment//

  • Urgent
  • Abx
  • Terlipressin
  • Maintain renal perfusion
  • HRS development (hepatorenal syndrome)
99
Q

Encephalopathy

> Cause
Diagnosis
Treatment

A
  • Microglial inflammation
  • Build up of ammonia

Diagnosis//

  • Liver flap
  • Confusion
  • any neurology

Treatment//

Look for cause and treat it

  • infection
  • metabolic
  • drugs
  • liver failure

> LACTULOSE
Maintain nutrition

> Consider TRANSPLANATION if spontaneous

100
Q

Varices

A 
> Increased portal pressure leading to formation of varices
> 1/3 bleed
> Decompensation
> Liver failure
> Death

Primary Prophylaxis//

  • Beta blockers -> propranolol, carvideolol
  • Variceal ligation

Secondary Prophylaxis//

  • variceal banding
  • beta blockers

Acute Variceal Bleeding//

  • resus
  • pharma therapy and timing
  • failed therapy –> TIPSS, transection

Ballon tamponade
Sclerotherapy

101
Q

Transplantation for liver disease

> UKELD score for transplantation

A 
> Event based
- ascites-resistant
> Liver function based
> Quality of life based
- itch, lethargy, spontaneous encephalopathy

> UKELD score
- 1 year mortality, score = 49

Patients with a UKELD score of ≥49 to be listed for elective transplant

Unless they have:

  • diuretic resistant ascites
  • hepatopulmonary syndrome
  • chronic hepatic encephalopathy
  • intractable pruritus
  • polycystic liver disease
  • familial amyloidosis
    > primary hyperlipidaemia
    > HCC
102
Q

Chronic Liver disease

  • Duration
  • Causes
A

> more than 6 months’ duration
progression –> cirrhosis
recurrent inflammation and repair with fibrosis and regeneration

Causes

  • Alcohol
  • NAFLD
  • Hep C
  • Primary biliary cirrhosis
  • Autoimmune hepatitis
  • Hepatitis B
  • Haemochromatosis = build-up of iron in the body
  • Primary Sclerosing Cholangitis
  • Wilsons disease
    o disorder of copper metabolism
  • Alpha-1 anti-trypsin deficiency
  • Budd chiari
    • occlusion of the hepatic veins
    • Methotrexate
103
Q

NAFLD

  • Pathogenesis
A
  • Associated with obesity
  • FATTY LIVER/STEATOHEPATITIS (NASH) in absence of other cause

Pathogenesis//

> 2 hit hypothesis

1st hit
excess fat accumulation

2nd hit

  • intrahepatic oxidative stress
  • Lipid per oxidation
  • TNF alpha, cytokine cascade
  • Lipopolysaccharide
  • Ischaemia-reperfusion injury

> ONE HIT

  • triglyceride benign
  • “Skinny” NASH
  • Hepatocytes can generate TNFa
  • OXIDATIVE STRESS

Diagnosis//

Elevated LFTs (around 100-150)

104
Q

What is NASH

A
  • Non Alcoholic Steatohepatitis
  • most severe form of NAFLD
  • maladaption to oxidative stress
105
Q

Management

> Simple steatosis
NASH

A 
Simple steatosis
> diagnosis by USS
> No liver outcomes
> Increased CV risk
> Treatment 
 -- weight loss and exercise

NASH
> diagnosis by Liver biopsy
> risk of progression to cirrhosis
> WEIGHT LOSS AND EXERCISE

106
Q

Primary Biliary Cirrhosis (Cholangitis) - PBC

A

> Mitochondrial Auto-antibodies (AMA antibodies)
More prevalent in older females

Symptoms

    • fatigue (tired all day)
    • itch without rash
    • xanthelasma and xanthomas
    • associated with high cholesterol

Diagnosis

> 2 of these 3

    • +AMA
    • Elevated ALP
    • Liver biopsy

Treatment

    • Urseodeoxycholic acid
    • Control the itch
  • tepid baths, transplant
107
Q

Autoimmune Hepatitis Type 1

What type of necrosis?

A
  • Adults
  • Antinuclear antibodies (ANA)
  • ASMA (anti-smooth muscle antibodies)
  • SLA severity (soluble liver antigen)
Associated with extra-hepatic manifestations
> thyroiditis
> Graves disease
> Chronic UC
> SLE
> Pernicious anaemia

Clinical Presentation

¥	Hepatomegaly
¥	Jaundice
¥	Stigmata of chronic liver disease
¥	Splenomegaly
¥	Elevated AST and ALT
¥	Elevated PT (prothrombin time)
¥	Non-specific symptoms: malaise, fatigue, lethargy, nausea, abdominal pain, anorexia

Diagnosis//

• Elevated AST and ALT
• Elevated IgG
* Presence of autoimmune antibodies

Histology//

> PIECEMEAL necrosis

Pathogenesis//

> Genetic predisposition + environemtanl agent

  • HLA-DR3 (SEVERE)
  • HLA-DR4 (late onset)
  • Drugs

Treatment//

  • corticosteroids
  • azathioprine
    • Prednisone + azathioprine
  • Prednisone – start at 30mg daily and taper down to 15mg at week 4, then maintain on 10mg daily until therapy endpoint
  • Azathioprine 50-100mg daily

Prognosis//

  • many will develop cirrhosis
  • oesophageal varices
  • spontaneous resolution
108
Q

Type 2 Autoimmnune Hepatitis

A

Children and young adults most affected

  • LKM 1
  • AMA
109
Q

Primary SCLEROSING cholangitis

A
  • Destructive disease of large and medium sized bile ducts
  • more MALE
  • recurrent CHOLANGITIS

Diagnosis//

  • imaging of biliary tree, ERCP

Treatment//

  • maintain bile flow
  • monitor for cholangiocarcinoma & colorectal cancer
  • Alcohol related
110
Q

Haemochromatosis

A
  • Genetic Iron Overload syndrome
  • Cirrhosis, cardiomyopathy, pancreatic failure
  • BRONZE diabetes

Treatment//

Venesection (removal of blood)

111
Q

Alpha-1 Anti-Trypsin Deficiency (A1AT)

A

> Genetic mutations in A1AT genes - variable phenotype

> Protein function lost
–> excess tryptic activity

Clinical//

  • Lung emphysema
  • Liver deposition of mutant protein, cell damage

Treatment//

• supportive management

112
Q

Methotrexate

A

> Drug used to treat rheumatoid arthritis and psoriasis

Dose dependent liver toxin –> progressive fibrosis

Clinical//

No signs
Monitor fibrosis

Treatment//

Discontinue the drug

113
Q

Cardiac Cirrhosis

A

> Secondary to high right heart pressures

  • incompetent tricuspid valve
  • congenital
  • rheumatic fever
  • constrictive pericarditis

Clinical//

ascites and liver impairment

Treatment//

Treat the cardiac condition

Decompensated right ventricular or biventricular heart failure causes transmission of elevated right atrial pressure to the liver via the inferior vena cava and hepatic veins. At a cellular level, venous congestion impedes efficient drainage of sinusoidal blood flow into terminal hepatic venules. Sinusoidal stasis results in accumulation of deoxygenated blood, parenchymal atrophy, necrosis, collagen deposition, and, ultimately, fibrosis.

114
Q

Hepatitis A

A

Transmission//

  • faecal-oral spread
  • poor hygiene/ overcrowding
  • Gay men and PWID

Clinical//

  • acute hepatitis
  • – no chronic infection
  • Older children/young adults

Labs//

  • clotted blood for serology
  • Hep A IgM

VACCINE

115
Q

Hepatitis E

A
  • More common in the tropics
  • Faecal-oral transmission
  • PREGNANT WOMEN

No vaccine

Some immunocompromised humans can become chronically infected

116
Q

Hepatitis D

A
  • Only found WITH hepatitis B virus
  • Exacerbates Hep B infection
  • SUPERINFECTION
117
Q

Hepatitis B

all markers

A

Transmission//

> Sex (multiple sexual partners)
Mother to child
Blood (PWID)
Chronic infection

HBsAg+ //

> Hepatitis B surface antigen present in blood of all infectious individuals

> indicates patietn is infected and infectious, more than 6 months = chronic

HBeAg//

> Hep B e-antigen usually also present in highly infectious individuals

Hep B DNA tests also used

HepBIgM//

recently infected cases

Anti-HBe//

> indicates low infectivity

Anti-HBs//

Immunity
due to vaccine or due to past infection.

Control//

> minimise exposure
vaccination of at-risk people
Post-exposure prophylaxis

Spontaneous cure is sometimes seen in chronic infection

118
Q

Hepatitis C

A

Transmission//

Similar to hep B - sex, blood, mother to child

less easily transmitted by sex than Hep B

Majority of cases - infection results in chronic infection

HepC antibody positive = past or active infection

HepC virus RNA//

positive = active infection
negative = past infection

there is NO vaccine

Once chronic infection has been established, spontaneous cure is not seen.

High levels of chronic hepatitis C

–> Chronic hepatitis –> cirrhosis -> cancer and/or liver failure –> death

119
Q

Time for a hepatitis infection to become cirrhosis?

A

> 20 years

120
Q

Time for a hepatitis infection to become cancerous? (Hepatocellular carcinoma)

A

> 30 years

121
Q

ACUTE viral hepatitis treatment

A
  • No antivirals given
  • Monitor for encephalopathy
  • Monitor for resolution
  • Notify public health
  • immunisation of contacts
  • test for other infections if at risk
  • vaccinate against other infections if at risk
122
Q

CHRONIC viral hepatitis management

A

ANTIVIRALS

  • genotype of Hep C important in deciding regime

> Vaccination
Infection Control
Decreased alcohol intake
HCC screening

123
Q

Acute Liver Disease

A
  • Rapid development of hepatic dysfunction without prior liver disease
  • any insult to the liver causing DAMAGE in a previously normal liver
  • <6 months duration

–> Encephalopathy and prolonged coagulation

124
Q

Clinical features of acute liver disease

A
  • [none]
  • jaundice
  • lethargy
  • nausea
  • anorexia
  • pain
  • itch
  • arthralgia
  • ABNORMAL LFTs
125
Q

Causes of Acute liver failure

A 
• Viral A,B,C,D,E,CMV EBV &amp;Toxoplasmosis
	• Drugs
	• Shock liver - massive hyper perfusion to the liver 
	• Cholangitis
	• Alcohol
	• Malignancy
	• Chronic Liver Disease
	• Ask about paracetamol
RARE
	•Budd Chiari
	•AFLP
	•Cholestatsis of Pregnancy
126
Q

Acute liver failure Investigations

A 
-	HISTORY
o	Symptoms
o	Duration
o	Drugs
     ♣	INCLUDING OTC
     ♣	Herbal (been known to cause liver damage)
     ♣	Food supplements
     ♣	Health food shop shite 
o	Possible toxins
o	Alcohol history 
-	LFTs
-	History and Examination
-	Ultra-sound
-	Virology 
-	Ix of chronic liver disease
-	RARELY – biopsy
127
Q

Acute Liver Failure TREATMENT

A
  • Rest
  • Fluids
  • Increase calories (35-40 kcal/kg/day & 1.2-1.5g protein/kg/day)
  • monitor and supplement electrolytes: K, PO4 and Mg
  • Hypoglycaemia
  • For itch - sodium bicarb bath, urso acid
  • Observation for FHF
128
Q

Paracetamol and the liver

A

Paracetamol overdose

It is converted to NAPQI by p4502E1

NAPQI is toxic.

Normally it is then converted to a non-toxic form by GLUTATHIONE.

But due to excess paracetamol, there is a depletion of glutathione

Leaving the toxic NAPQI.

Liver damage

129
Q

Drug-induced liver disease

A

> Antibiotics

  • -co-amoxiclav
    • flucloxacillin

> NSAIDs

> Fat burner or protein powders

> Nurofen and night nure (contain paracetamol)

Patients forget about some OTC medications that may potentially have paracetamol as an active ingredient.

130
Q

Fulminant Hepatic Failure (FHF)

A

> Severe and sudden onset
severe impairment of hepatic functions or severe necrosis of hepatocytes
JAUNDICE & ENCEPHALOPATHY in a patient with a previously normal liver

Complications//

  • hypoglycaemia
  • coagulopathy
  • circulatory failure
  • renal failure
  • infection
  • Cerebral oedema and raised ICP
131
Q

FHF causes

A

Common

>Paracetamol
>Fulminant viral
>Drugs
>HBV
>Non A-E

Rare

> AFLP (acute fatty liver of pregnancy)
> Mushrooms
> Malignancy
> Wilsons
> Budd Chiari
> HAV
132
Q

FHF Treatment

A

Supportive
> Inotropes and fluids
> renal replacement
> management of ICP

Transplantation
> life-long immunosuppression

133
Q

FHF assessment

A

Refer quickly

repeat bloods and double check

short window of opportunity

will drop grade of encephalopathy on transfer

NO HESITATION if you think this is FHF

134
Q

Grades of Encephalopathy

A

I Confusion

II Drowsiness. Liver flap

III Severe confusion and drowsiness. Liver flap

IV Coma

135
Q

Antiviral Treatment - Who to treat

A

> Chronic Infection
Risk of complications
– evidence of inflammation/fibrosis sought
– increased ALTs

> Fit for treatment

  • liver cancer is a contraindication
  • established cirrhosis is more difficult to treat
  • HIV co-infection more difficult to treat

> Patient Issues

  • side effects of antivirals
  • attitude to treatment
136
Q

The higher a chronic HBV patient’s starting HBV-DNA load, the…?

A

Greater the risk of cancer on follow up

137
Q

Interferon Alfa

A

Given as PEGINTERFERON - immune adjuvant

Side effects - flu like symptoms
Major - autoimmune disease, psychosis, thyroid disease

138
Q

Hepatitis B therapy

A

Option 1//

> Peginterferon alone
Try in HBsAg and HBeAg pos patients with compensated disease

Option 2//

>  suppressive antiviral drug 
> Advantage
--safer
-- increasing range available
> Disadvantage
--suppression not cure
--resistance can develop

leading to reduction in HBV DNA (suppression)

Loss of HBeAg (enduring suppression)

Loss of HBsAg (CURE)

Improved liver function

139
Q

Benefits of Chronic Hep C therapy

A
  • Response defined by loss of HCV RNA in blood sustained to 6 months after ned of therapy
  • Virological cure - SUSTAINED VIROLOGICAL RESPONSE (SVR)
  • SVR patients have improved liver function
140
Q

Types of Gallstones

A

> Cholesterol (pure yellow/ white)

> Pigment gallstones (black, excess bilirubin)

> Mixed (majority of gallstones)

> Primary bile duct stones (the stones themselves form within the bile ducts)

141
Q

Gallstones - the 5 Fs

&

other risk factors

A

> Fair (more common white people)

> Fat (BMI > 30)

> Female

> Forty (age)

> Fertile (pregnancy, children)

High fat diet
Hyperlipidaemia
Bile salt loss (Crohn's)
Dysmotility of GB
Prolonged fasting
Total parenteral nutrition
142
Q

Biliary Colic

A

> Stone impacts in cystic duct
Gradual crescendo of pain in RUQ
Radiates to back/shoulder
May last hours

Not “colicky” - it does not come and go, despite what the name suggests.
Majority of patients experience this gradual increase in pain and it remains a severe and constant pain for hours afterwards.

143
Q

Biliary colic - treatment

A

Pain killers, low fat diet
Lose weight

If recurrent episodes:

  • surgery
  • cholecystectomy

otherwise, if unfit

  • Ursodeoxycholic acid (dissolves non-calcified gall stones)
144
Q

Severe acute epigastric pain (differential)

A 
> Bilariy colic
> Peptic ulcer disease 
> Oesophageal spasm
> Myocardial infarction
> Acute pancreatitis
145
Q

Acute cholecystitis

A

> Inflammation in gall bladder (obstruction of cystic duct)

> Gall bladder becomes swollen and inflamed

146
Q

Acute cholecystitis - treatment

A
  • IV abx and IV fluids
  • Nil by mouth

Urgent cholecystectomy

147
Q

What is the diagnostic tool of choice for acute cholecystitis?

A

> Ultrasound scan ***

  • then

— CT, MRCP/ERCP, HIDA, EUS

148
Q

Complications of gallstones

A

Stones may migrate in common bile duct.

  • -> - Jaundice
    • cholangitis
    • acute pancreatitis (due to back pressure)

Gallstone ileum

149
Q

MRCP (magnetic resonance cholangiopancreatography)

A

> Itch, nausea, anorexia
Jaundice
Abnormal LFTs

150
Q

ERCP (can you remove stones?)

A

May be able to remove the stone there and then if it is small enough

Balloon ERCP
Dormia basket ERCP

151
Q

Acute Pancreatitis

A

> ALCOHOL/ gallstones
Autodigestion of peri-pancreatic tissues by activated enzymes

Cholecystectomy during INDEX admission

ERCP

ES = Endoscopic Sphincterectomy

152
Q

Gallstone Ileus

A

> Small bowel obstruction - gallstone impacted in distal ileum

> Fistula gallbladder + duodenum –> large gallstone passes into small intestine

> Moves down SB causing intermittent colic

> Present with distal SB obstruction

–>Ascites

dilatation

air in bile duct

153
Q

Gallstone Ileus - treatment

A

> Urgent laparotomy - Small bowel enterotomy to remove stone

> Interval cholecystectomy in 3 months

  • squeeze the stone out
154
Q

Cholangiocarcinoma

A

> Usually late presentation

    • jaundice
    • weight loss
    • anorexia
    • lethargy

> Lymph node metastases
20-30% peritoneal metastases

155
Q

Cholangiocarcinoma - diagnosis

A

> Duplex ultrasound

> Spiral CT/ ERCP/ PTC

> MRI

Types I - IV staging.

I - below confluence of hepatic ducts

II - confined to confluence

IIIa - extension into right hepatic duct

IIIb -extension into left hepatic duct

IV - extension into right and left hepatic duct

156
Q

Cholangiocarcinoma - treatment

Curative & palliative

A

Surgical resection.

Bile duct and liver resection.

Palliative//

Biliary stent

G.I. (20 decks)

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