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Phase 2 - Liver Flashcards

1
Q

What can acute and chronic liver injury lead on to?

A

Acute usually recovers but can lead on to liver failure

Chronic can lead to recovery but could also cause cirrhosis which can then lead to liver failure (including varices (usually oesophageal) and hepatoma)

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2
Q

What can cause acute liver injury

A
  • VIRAL infection (Hep A/B/E esp; EBV, CMV)
  • DRUGS (ALCOHOL, paracetamol)
  • VASCULAR (Budd-chiari syndrome - hepatic vein thrombosis)
  • Metabolic (Wilson’s, Haemochromatosis, A1ATD)
  • OBSTRUCTION (gallstone)
  • CONGESTION (e.g. from HF)
  • Pregnancy (increased metabolic demand)
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3
Q

What can cause chronic liver disease

A
  • ALCOHOL (common in inpatients)
  • VIRAL infection (esp Hep B/C)
  • AUTOIMMUNE
  • Metabolic (iron - haemachromatosis/copper - Wilson’s overload; A1ATD)
  • Ostruction/Congestion
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4
Q

Presentation of Acute liver injury

A
  • MALAISE
  • NAUSEA
  • Anorexia (potentially)
  • JAUNDICE (eventually)

Less common:

  • CONFUSION (ammonia in brain - encephalopathy)
  • BLEEDING (low clotting factors)
  • liver PAIN (consider obstruction/malignancy)
  • HYPOGLYCAEMIA (impaired gluconeogenesis/decreased insulin uptake)

Abnormal LFTs

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5
Q

Presentation of chronic liver injury

A
  • Congestion:
    • ASCITES (fluid backup/overload) -> hernia sometimes
    • Oedema
    • Haematemesis (VARICES - from portal HTN)
  • POOR ABSORPTION:
    • Malaise
    • Wasting/anorexia (poor absorption)
  • Easy bruising (low clotting) - vit K deficiency,
  • thrombocytopenia
  • SPIDER NAEVI (oestrogen)
  • Itching (bilrubin)
  • XANTHELASMA (fat deposits around eyes)
  • Hands:
    • CLUBBING
    • Dupuytren’s Contracture
    • Palmar erythema
  • Hepatomegaly (compensation)
  • Abnormal LFTs (normal if compensated)
  • Rarely jaundice/confusion (waste product accumulation)

(Hypoglycaemia, gynaecomastia, impotence, amenorrhoea - happens later)

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6
Q

Serum liver funtion tests (LFTs)

A

Bilirubin (normally unconjugated) - high

Albumin - low (or normal initially in acute) (but can also be low in infection/inflammation) - bad prognosis

Prothrombin time (sensitive - synthetic function) - increases

Cholestatic enzymes:
- alk phos - increased synthesis in intra/extrahepatic cholestatic disease (also - bone, intestine, placenta)
- gamma-GT (may leak into blood and so increase)

Hepatocellular enzymes:
Serum transaminases - (high - leak when liver damaged):
- ALT (only rises in liver disease)
- AST (also in - heart, muscle, kidney, brain)

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7
Q

What deficiency can also cause high prothrombin time

A

Vit K deficiency
- commonly occurs in biliary obstruction (Vit K need bile salts to absorb)

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8
Q

Types of jaundice

A

‘Pre-hepatic’ - unconjugated bilirubin

  • Haemolysis (too much made - not cleared quickly enough)
  • Gilberts (reduced UDP glucoronyl transferase activity)
    • Crigler-Najjar syndrome (still intrahepatic but NO UGT function at all) - v. rare

Intrahepatic (mixed conjugated + unconjugated)

  • Liver disease (hepatic level)
    *Hepatitis (don’t forget drugs, esp if acute)
    • Ischaemia/Congestion
    • Neoplasm

‘Cholestatic’ - conjugated

  • Bile duct obstruction (post hepatic)
    • Gallstone: common bile duct, Mirizzi
    • Stricture: MALIGNANCY, ischaemia, inflammation, PBC, PSC
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9
Q

Pre-heptic vs cholestatic jaundice

A

Pre-hepatic:
- NORMAL urine, stool and LFTs
- urine: neg bilirubin, increased urobilinogen
- NO ITCHING

Cholestatic:
- DARK URINE (because conjugated bilirubin is soluble in water so diffuses into blood)
- decreased urobilinogen, bilirubin is present in urine (diffused into blood before it could get to GI due to cholestasis)
- possibly PALE STOOL
- ABNORMAL LFTs
- MAYBE ITCHING

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10
Q

Symptoms of jaundice

A

Urine, stool, itching (varies depending on type)

Biliary pain - RUQ, radiates to shoulder
Rigors
Abdomen swelling
Weight loss

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11
Q

Potential sources of viral hepatitis

A

irregular sex (Hep B esp)
IV drug use (Hep C esp)
Exotic travel

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12
Q

Diagnosis/tests for Jaundice

A

LFTs: Very high AST/ALT suggest liver disease

  • ULTRASOUND (1st line): Biliary obstruction -> dialated INTRAhepatic bile ducts
  • CT if cancer suspicion
  • Magnetic resonance cholangiogram (- if intrahepatic suspision?)

Endoscopic retrograde cholangiogram (ERCP) - if stones in bile duct

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13
Q

Classification of bile stones

A

Bile pigment stones - more likely to be intrahepatic

Cholesterol - more likely from gallbladder (more common)

Mix of both

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14
Q

What is biliary colic

A

Pain from temporary obstruction of cystic/common bile duct by gall stone

Sudden onset, severe, CONSTANT, crescendo characteristic (worse in waves) - initially epigastric -> RUQ (related to peritoneal involvement) -> radiates to back (right shoulder/sub scapular region - unusual in colic)
- if severe -> possible nausea/vomiting

Associated with tenderness and muscle guarding/ridgity

Commonly affects mid-evening -> early morning

Related to increased fatty food consumption

NOT INFLAMMATORY

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15
Q

Causes/risk factors for gall stone

A
  • Obesity/rapid weight loss
    • diet: HIGH animal fat; LOW fibre
  • DM
  • FEMALE (esp caucasian)
  • Fertile (more kids = increased risk)
  • Contraceptive pill
  • Age
  • Liver cirrhosis
  • Smoking
  • NOT FAMILY HISTORY
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16
Q

Pathophysiology of cholesterol stone formation

A

If bile has relative EXCESS cholesterol (relative deficiency of bile pigments/phospholipids)
- cholesterol is held in solution (by detergent action of bile salts/phospholipids) -> forms micelles/vesicles -> crystalises IF cholesterol crystalising vs solubilising factors UNBALANCED

Typically forms large, solitary stones

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17
Q

Examples of when supersaturated (relative excess cholesterol) bile would be present

A

DM
High cholesterol diet (also decreases bile salt synthesis so further unbalanced)

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18
Q

Pathophysiology of bile pigment stones

A

2 types black and brown. Mainly composed of calcium.

Black:
- Composed of CALCIUM BILIRUBINATE, network of MUCIN GLYCOPROTINS that interlace with salts
- glass-like cross-sectional surface
- related to HAEMOLYTIC ANAEMIAS

Brown:
- Composed of CALCIUM SALTS (bicarbonate, bilirubinate and fatty acids)
- muddy: alternating brown/tan on cross-section
- ALMOST ALWAYS present with bile stasis/biliary infection
- common cause of recurrence after cholecystectomy

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19
Q

Presentation of gallstones

A
  • MAINLY ASYMPTOMATIC
  • symptoms linked to recurrence
  • BILIARY COLIC
  • Acute cholecystitis related symptoms (if stones obstruct gallbladder emptying)
    • RUQ pain radiating to RIGHT SHOULDER
    • Fatigue (inflam)
    • FEVER
    • Murphy’s sign (pain on inspiration when palpating right subcostal region)
  • Cholangitis (if stone blocks common bile duct)
    • RUQ pain radiating to R shoulder
    • FEVER + rigors
    • JAUNDICE (common bile duct blocked)
    • Murphy’s sign
    • May be septic: REYNOLD’S PENTAD (triad + confusion + hypotensive shock)
  • Pancreatitis if gallstones blocking drainage of pancreas

NOT ASSOCIATED WITH: fat intolerence, indegestion, bowel upset etc (vague upper gi symptoms)

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20
Q

Pathophysiology of acute cholecystitis

A
  • Gallbladder emptying blocked - usually by stones
  • Leads to increased gallbladder glandular secretion (compensation?) and distension (may compromise blood supply).
  • Retained bile -> TRANSMURAL inflammatory response (infection can occur secondarily to vascular/inflammatory events)
  • Inflammation can irritate parietal peritoneum -> local peritonitis (cause of localised RUQ pain)
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21
Q

What occurs in Mirizzi

A

Impacted stone in cystic duct/infundibulum of gallbladder -> extrinsic compression of common hepatic

Can present with cholestatic jaundice, biliar pain, cholecystitis.

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22
Q

Differential diagnosis for biliary colic

A

IBS/IBD, carcinoma on right side of colon, renal colic, pancreatitis, GORD, peptic ulcers

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23
Q

Differential diagnosis for acute cholecystitis

A

acute episode pancreatitis, peptic ulcer, pneumonia, intrahepatic abscess

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24
Q

Diagnosis of gallstones

A

1ST LINE - FBC + CRP:

  • raised WCC and CRP in inflammation (NOT COLIC)

LFTs:

  • raised alk phos in biliary COLIC
    • Serum transaminases (ALT normally higher than AST) also RAISED in CHOLESYSTITIS/cholangitis
    • Serum bilirubin also raised in CHOLANGITIS

Blood cultures/MC&S - for infections

ABDO ULTRASOUND (1st line imaging):

  • no major changes in bloods or images for biliary colic except STONES + duct dilation

Acute cholecystitis/cholingitis US:

  • thick walled, shrunken gallbladder (bile can’t enter from liver)
  • pericholecystic fluid (fluid around gallbladder)
  • STONES

MRCP (higher resolution but less accessible)

ERCP potentially for CHOLANGITIS

Contrast enhanced dynamic CT

  • excludes pancreatic carcinoma
  • EASIER TO SPOT PIGMENTED STONES in cholingitis
  • Amylase - Exclude Pancreatitis
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25
Q

What is Murphy’s sign

A

Pain on deep inspiration when 2 fingers placed in RUQ (push under ribs)

  • because diaphragm pushing down on gallbladder
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26
Q

Treatment for gallstones

A

LAPROSCOPIC CHOLECYSTECTOMY (GOLD for all SYMPTOMATIC gallstones - avoid in >80s)

  • try conservative FIRST
    • NSAIDs/ANALGESIA

If FEBRILE/SEPTIC need to treat INFECTION FIRST:

  • nil by mouth (can’t consume anything)
  • AGGRESSIVE FLUID RESUS (IV fluids)
  • Opiate analgesia
  • IV antibiotics (e.g. CEFUROXIME, CEFTRIAXONE)
  • Cholecystectomy after symptoms subside
  • ERCP if small stones at bottom of hepatic duct (involves sphinterectomy; use basket or balloon to remove; mechanical or laser to crush)
    put in stent (pigtail stent)))??

If pure/near-pure cholesterol stones:

  • STONE DISSOLUTION by increasing bile salt content
  • ORAL URSODEOXYCHOLIC ACID (UDCA)
  • can give statins (simvastatin) to lower cholesterol

Shock wave lithotripsy

  • shock wave fragments stones so they can be passed (only works if duct still patent)
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27
Q

What can cause ascending/acute cholingitis

A

Infection of biliary tree - usually secondary to PROLONGED common bile duct obstruction by stones

  • Bacteria CLIMB up from DUODENUM -> biliary tree infection + consolidation
    • SURGICAL EMERGANCY (sepsis = high mortality)

benign biliary STRICTURES from biliary SURGERY

CANCER of pancreas head compressing bile duct

PARASITES in Far East/Mediterranean

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28
Q

Treatment of cholingitis specifically

A
  • IV ANTIBIOTICS (e.g. CEFOTAXIME/METRONIDAZOLE) continued after drainage till SYMPTOM RESOLUTION
  • IV FLUIDS

Biliary drainage - Endoscopic Retrograde Cholangio-Pancreatography with sphincterotomy

  • basket or balloon to remove
  • mechanical or laser to crush
  • pigtail stent
  • UNSAFE FOR LARGE STONE -> REQUIRE SURGERY
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29
Q

Complication of gallstones

A
  • In the gallbladder & cystic duct:
  • Biliary colic
  • Acute cholecystitis
  • Empyema - gallbladder fills with pus
  • Carcinoma
  • Mirizzi’s syndrome - stone in gallbladder presses on bile duct casing jaundice
  • In bile ducts:
  • Obstructive jaundice
  • Cholangitis (inflammation of bile duct)
  • Pancreatitis
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30
Q

How can drugs cause liver injury

A

Disrupt intracellular Ca2+ homeostasis

Disrupt bile canalicular transport mechanisms

Induce apoptosis

Inhibit mitochondrial function -> prevents fatty acid metabolism -> acummulation of lactate and reactive oxygen species

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31
Q

When do most DILI occur

A

within 3 months/12 weeks of starting drug
- usually after at least 1 week

can occur weeks after stopping drug

usually resolves within 3 months of stopping drug but prolonged injury (over 6 months) -> long term damage

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32
Q

Which drugs DO NOT typically cause liver injury

A

Low dose aspirin
NSAIDs other than Diclofenac
HRT
Beta Blockers
ACE Inhibitors
Thiazides
Calcium channel blockers

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33
Q

How do you differentiate between hepatocellular and cholistatic injury based on LFTs

A

Hepatocellular:
- ALT >2 ULN, ALT/Alk Phos ratio >=5

Cholestatic:
- ALT >2, ratio <=2

Alk phos higher in cholestatic

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34
Q

Pathophysiology of paracetamol overdose

A

too much paracetamol over-saturates the Phase II reaction (glucoronidation and sulphate conjugation pathway -> Glucoronide + sulfate metabolites)

Normally if metabolised via phase 1 reaction (oxidation) makes reactive compund (NAPQI) which is made non-toxic by CONJUGATION with GLUTATHIONE (anti-oxident -> cystein conjugate)
- in over dose GLUCTATHIONE DEPLETES so INCREASED NAPQI

-> hepatotoxicity + kidney injury

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35
Q

Presentation + diagnosis of paracetamol overdose

A

First 24 hours - Usually asymptomatic then:

  • SUDDEN ONSET SEVERE RUQ pain
  • N + V
  • ANOREXIA
  • Jaundice
  • Confusion

LFTs show liver damage at 18 HOURS AFTER

  • RAISED ALT

72-96hrs after - PEAK ALT and Prothrombin time

Acute liver injury symptoms:

  • JAUNDICE AND ENCEPHALOPATHY
  • HYPOglycaemia (overdose inhibits gluconeogenesis)
  • Coagulation defects, electrolyte imbalances

Potential kidney injury from ACUTE TUBULAR NECROSIS:

  • METABOLIC ACIDOSIS (lactic acid)
  • Raised creatinine

DIAGNOSED on:

  • History
  • Raised ALT
  • Serum Paracetamol conc
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36
Q

Treatment for paracetamol overdose

A

ACTIVATED CHARCOAL - to prevent absorption in stomach (only works if given within 1 hour)

  • IV N-ACETYLCYSTEINE (give immediately - non-toxic form is a cystein conjugate so giving a cystine pushes it in that pathway)
    • replenishes cellular GLUTATHIONE
    • rash common side effect -> treat with CHLORPHENAMINE
    • don’t stop unless anaphylactoid
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37
Q

What is a serious complication of acute liver failure

A

Hepatic encephalopathy

Presents with CONFUSION, COMA or FLAPPING TREMOR (ASTERIXIS - flapping tremor with wrist extended)

Caused by build up of ammonia passing to brain (neurotoxic - halts Krebs cycle - irreparable/irriversible damage)

Also, astrocytes try to clear ammonia by converting glutamate to glutamine but EXCESS GLUTAMINE causes OSMOTIC SHIFT INTO CELLS -> CEREBRAL OEDEMA
(risk of oedema decreases the more delayed the onset of encephalopathy)

  • TREAT WITH IV MANNITOL or LACTULOSE - reduces ammonia)

Can also get Wernicke-Korsakoff syndrome - memory disorder due to B1 deficiency (thiamine) (damages neural/supporting cells)

  • ATAXIA, NYSTAGMUS
  • MEMORY IMPAIRMENT, confusion, behavioural changes
  • TREAT WITH IV THIAMINE
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38
Q

Causes of ascites

A

Local inflammation:
- pritonitis, PANCREATITIS
- TB
- Abdo CANCERS (esp OVARIAN)

Low Protein:
- NEPHROTIC syndrome (kidney disease), kidney failure

Flow stasis:
- CIRRHOSIS/chronic liver disease (MAIN)
- Budd-chiari (hepatic vein thrombosis), portal thrombosis
- HF, constrictive pericarditis

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39
Q

Investigations for ascites

A

SHIFTING DULLNESS exam (resonant at top when lying on back but dull at sides as bowels/gas floats; site of resonance changes to flank when on side)
- fluid wave/thrill (can feel tapping through fluid on other side of abdomen)

ASCITIC TAP/aspiration (peritoneocentesis - 10-20ml fluid)
- cytology (WCC) + cultures
- proteins + amylase

  • if TRANSUDATE (pushed out - increased hydrostatic pressure)
    - CLEAR fluid
    - <30g/L protein (LOW), Serum albumin-ascitic gradient <11g/L(SAAG - serum albumin-albumin in ascitic fluid)
  • if EXUDATE (leaks out due to inflammations)
    - CLOUDY
    - >=30g/L protein (HIGH), SAAG >= 11g/L

IMAGING:
- XR (worst sensitivity)
- US
- CT (best sensitivity)

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40
Q

Treatment for ascites

A

SODIUM/fluid restriction

SPIRONALACTONE (aldosterone antagonist) (furosimide works better on oedema - combined is effective but may contribute to kidney failure (electrolyte imbalance))

PARACENTESIS (draining); pleuric/indwelling drain (smaller volumes)

TIPS (transjugular intrahepatic portosystemic shunt)

Treat underlying cause:
Stop alcohol (usually not viable)
Liver transplant (esp if getting peritonitis)

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41
Q

Treatments for varices

A
  • TIPS - transjugular intrahepatic portosystemic shunt

stent connects portal veins to adjacent vessels with lower BP -> relives pressure in liver -> help stop fluid back up

INCREASED RISK OF ENCEPHALOPATHY (as blood bypasses liver) - give prophylaxis
- CONTRAINDICATED if multiple previous episodes of ENCEPHELOPATHY

  • VARICEAL BANDING - rubber band ligation if at risk of rupture
  • TERLIPRESSIN (vesopressin analogue -> SPLANCHNIC VASOCONSTRICTION)
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42
Q

Progression of AFLD from normal liver

A
  • Normal
  • Steatosis/fatty liver (smooth; fat-filled hepatocytocytes on cytology) - can be reversed
  • Alcoholic fibrosis with inflammation -> can progress to alcoholic hepatitis (talk about this if we get asked about stages of AFLD)
  • Cirrhosis (nodular - irreversible) - compensated or uncompensated
  • Hepatocellular carcinoma (HCC)
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43
Q

Risk factors for AFLD

A
  • Binge/chronic drinking
  • Obesity
  • Smoking
  • FEMALE sex
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44
Q

Presentation of AFLD

A

early - almost asymptomatic

more severe -> chronic liver failure/alcohol dependancy
- jaundice
- hepatomegally
- ascites
- spider naevi
- Hepatic encephalopathy (HE)
- palmar erythema, dupuytren contracture (painless, finger bent to palm, maybe cord in palm)
- easy bruising

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45
Q

Diagnosis of AFLD

A

FBC: macrocytic, non-megaloblastic anaemia

LFTs:

  • Raised AST/ALT
  • PARTICULARLY RAISED GGT (gamma-glutamyl transferase)
  • raised bilirubin
  • low albumin
  • raised prothrombin time (CLOTTING PROFILE)

Biopsy to confirm cirrhosis or hepatitis:

  • inflammation, necrosis
  • MALLORY BODIES (hyaline (from degeneration of connective tissue - looks darker) cytoplasmic inclusions in hepatocytes)
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46
Q

Treatment for AFLD

A

conservative:

  • STOP ALCOHOL
    • DiAZEPAM/LORZEPAM for Delireum tremens
  • lower fat diet, lower BMI
  • detox regiem

pharm:

  • short term steroids (only if necessary)
  • B1 (thiamine)/folate supplements
    • give prophylactically as alcohol prevents thiamine absorption in gut -> deficiency

(may give low/slow opiate analgaesia if viable)

surgical:

  • liver transplant if end-stage (only if abstains for 3 months; Lille score)

Treat complications e.g. ascites

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47
Q

Complications of AFLD

A
  • Pancreatitis (increased ethanol)
  • Encephalopathy
  • Ascites
  • ALCOHOL withdrawal - DELERIUM TREMENS
  • HCC
  • Mallory Weiss tear (lower oesophageal tear - violent coughing/vomiting)
  • Wernicke-Korsakoff syndrome (B1 deficiecy/alcohol withdrawal) - treat with IV B1 (thiamine)
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48
Q

Progression of NAFLD from normal liver

A

Normal
Hepatosteatosis (fatty liver - deposited in hepatocytes)
Non-alcoholisc steatohepatitis (NASH - fatty+fibrotic)
Fibrosis
Cirrhosis

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49
Q

Symptoms of NAFLD

A

Usually asymptomatic (picked up incidentally)

If severe - chronic liver failure symptoms

  • N+V
  • Diarrhoea
  • Hepatomegaly
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50
Q

Diagnosis of NAFLD

A

Deranged LFTs:

  • RAISED PT/INR and BILIRUBIN
  • LOW ALBUMIN
    - Enhanced Liver Fibrosis Test (if you suspect fibrosis)

1ST LINE : ULTRASOUND liver/abdomen (shows fatty liver)
CT/MRI

2nd line: Assess risk of fibrosis (non-invasive scoring system - FIB-4)

BIOPSY - DIAGNOSTIC

  • (may find Mallory bodies if biopsy done)
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51
Q

Treatment for NAFLD

A

Conservative + control risk factors

  • lower BMI/weight
  • EXERCISE
  • Stop SMOKING
  • avoid ALCOHOL
  • control risk factors - diabetes, HTN, cholesterol ( statins, metformin, ACE-I)
    • consider pioglitazone to improve insulin sensitivity

vitamin E can reduce fibrotic appearance (improves liver function)

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52
Q

Complications of NAFLD

A

HCC!

portal HTN, varices

encephalopathy

ascites

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53
Q

Risk factors for NAFLD

A

SAME AS CVD and DM:

  • hyperlipidaemia/HIGH CHOLESTEROL
  • OBESITY
    • Poor diet/low activity
    • HTN
    • T2DM - insulin resistence
  • MIDDLE AGE ONWARDS
  • SMOKING

Family history

Endocrine disorders
Drugs (NSAIDS, amioderone)
(- past bypass)

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54
Q

What can cause a sudden decline in patients with chronic liver disease

A

Constipation
Drugs
GI bleed
Infection
HYPO: natreamia, kalaemia, glycaemia
Alcohol withdrawal
Other (cardiac/intercranial)

ALWAYS DO ABCDE first

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55
Q

Why are liver patients vulnerable to infection

A
  • impaired reticulo-endothelial function
  • reduced opsonic activity (normally tag pathogens)
  • leucocyte function
  • permeable gut wall
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56
Q

What can cause renal failure secondary to liver failure

A

Drugs:
- Diuretics
- NSAIDS
- ACE Inhibitors
- Aminoglycosides (DON’T GIVE)
Infection
GI bleeding
Myoglobinuria (muscle brakdown -> too much in blood + urine)
Renal tract obstruction

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57
Q

Causes of coma in liver disease patients

A

Hepatic encephalopathy (ammonia)
- infection
- GI bleed
- constipation
- hypokalaemia
- drug (sedatives, analgesics)
Hyponatraemia / hypoglycaemia
Intracranial event

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58
Q

Bedside tests for encephalopathy

A

Serial 7’s
WORLD backwards
Animal counting in 1 minute
Draw 5 point star
Number connection test

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59
Q

Which investigations should you do for chronic liver disease

A

Viral serology - hepatitis B surface antigen, hepatitis C antibody, hep E IgG antibody, (EBV, CMV, hep A (IgM))

Immunology

  • autoantibodies
    - AMA, ANA, ASMA (smooth muscle)
    - coeliac antibodies
    • immunoglobulins

Biochemistry

    -	iron studies
-	copper studies	
    - 	caeruloplasmin (serum copper transport protein)			
    -	24 hr urine copper
-	α1-antitrypsin level
-	lipids, glucose

Radiological investigations - USS / CT / MRI

Biopsy if possible/required

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60
Q

Risk factors for autoimmune hepatitis

A
  • Female
  • Other autoimmune conditions (e.g. SLE)
  • Viral hep
  • HLA DR3/DR4 (also linked to T1DM)
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61
Q

Presentation of autoimmune liver disease

A

usually asymp

other wise - liver failure

COMPLICATION = Cirrhosis

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62
Q

Diagnosis/treatment of autoimmune liver disease

A

Raised IgG

Autoantibodies (not diagnostic):

  • Type ONE - OLDER women
    • Anti-nuclear (ANA)
    • Anti smooth muscle (ASMA)
    • Anti soluble Liver Antigen (Anti-SLA)
  • Type 2 - YOUNGER females (rarer)
    • Anti liver cytosol (ALC-1)
    • Anti liver kidney micrsomal (ALKM-1)

BIOPSY - diagnostic!

  • presence of plasma cells and other lymphocytes
  • INTERFACE HEPATITIS (affects hepatocytes around portal tracts); inflammation

TREAT WITH STEROIDS (prednisolone) + IMMUNOSUPPRESSANTS (AZATHIOPRINE)

  • or liver transplant
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63
Q

Risk factors for Primary Biliary cholangitis (PBC)

A

FEMALE
40-50 y/o
Other autoimmune/rheumatoid disease
Smoking

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64
Q

Pathophysiology of PBC

A

T cell mediated immune response causes intralobular (small, in lever) bile duct damage leading to:

  • Outflow obstruction (Cholestasis)
  • Chronic, GRANULOMATOUS INFLAMMATION

CHOLESTASIS -> back-pressure:

  • fibrosis
  • chirrhosis
  • portal HTN
  • infection
  • jaundice
  • reduced secretion of cholesterol via bile ducts causes it to build up in skin and blood vessels -> XANTHELASMA

Autonomic neuropathy -> correlates to fatigue

Autoantibodies are also present.

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65
Q

Presentation of PBC

A

usually asymp

  • early - PRURITIS + FATIGUE
  • GI disturbance/abdo pain
  • JAUNDICE
  • xanthelesma (yellow growths around eyelids - cholesterol deposits)/xanthoma
  • HEPATOMEGALY (+ other signs of CIRRHOSIS/FAILURE)

Complications:

  • cirrhosis -> HCC
  • MALABSORPTION of fats/ADEK (due to lack of bile) -> steaorrhoea, OSTEOMALACIA or OSTEOPOROSIS
  • coagulopathy (from vit K def)
  • Hypothyroid
  • Distal renal tubular acidosis (build up of acids)
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66
Q

Diagnosis of PBC

A
  • Deranged LFTs
    • ALP, GGT, BILIRUBIN RAISED;
  • ALBUMIN LOW
  • Rule out viral - check antibodies/antigens
  • SEROLOGY
    • ANTI MITOCHONDRIAL ANTIBODY (AMA) - most specific to PBC, (high specificity)
    • raised IgM
    • ANA present in 35%

USS - exclude extrahepatic cholestasis

BIOPSY - PORTAL TRACT LYMPHOCYTIC INFILTRATE + fibrosis
- granulomatous
- determines staging/diagnosis

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67
Q

Treatment for PBC

A

1ST LINE - URSDEOXYCHOLIC ACID (UDCA) lifelong

  • dampens immune; decreases cholestasis (it’s a bile acid analogue - slows down progression);
  • reduces portal pressure + varices - doesn’t reduce itching or fibrosis
  • reduces cholesterol absorption in gut -> less risk of xanthoma/CVD

CHOLESTYRAMINE for pruritis (RIFAMPICIN also, but can DAMAGE LIVER)

  • it’s a bile acid sequestrate that binds to bile acid to prevent absorption in gut (reduces pruritis)

Immunosuppressants (e.g. steroids) in some patients

ADEK vit supplement

Liver transplant

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68
Q

What is Charcot triad

A

shows BILE DUCT OBSTRUCTION

RUQ pain, fever, jaundice

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69
Q

Risk factors for Primary Sclerosing Cholangitis

A
  • MALE (atypical)
  • FHx
  • 30-40 y/o
  • UC (in 70%)
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70
Q

Pathophys of PSC

A
  • auto antibodies attack intra AND/OR extrahepatic bile ducts
  • Biliary tree becomes STRICTURED/FIBROTIC (lining stiffens)
    • OBSTRUCTION
  • chronic obstruction -> HEPATITIS, fibrosis, cirrhosis
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71
Q

Presentation + Complications of PSC

A

usually asymp

  • PRURITIS + FATIGUE
  • Chronic RUQ PAIN
  • Charcot triad (typically - JAUNDICE regardless)
  • Hepatosplenomegaly
  • IBD

COMPLICATIONS:

  • acute bacterial cholangitis
  • cholangiocarcinoma
  • colorectal cancer
  • CIRRHOSIS/FAILURE
  • BILIARY STRICTURES
  • FAT soluble VIT DEFEICIENCY
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72
Q

Diagnosis of PSC

A

Deranged LFTs

U&E, FBC

SEROLOGY

  • no viral,
  • no AMA,
  • USUALLY pANCA POSITIVE (anti neutrophil cytoplasmic - non-specific but present 94%)
  • ANA (77%)
  • aCL (anticardiolipin)

Biopsy - ONION SKIN fibrosis around ducts

GOLD STANDARD - MRCP (may show bile duct lesion/strictures - ERCP too invasive)

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73
Q

Treatment for PSC

A

Conservative:

  • Cholestyramine (pruritis)
  • ADEK vit supplement
  • monitor for complications
  • ERCP can dilate/stent strictures
  • consider liver TRANSPLANT

UDCA can also be used

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74
Q

Acute vs chronic hepatitis

A

Acute - less than 6 months
chronic - lasting >6 months

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75
Q

fulminant hepatitis

A

liver failure in acute hepatitis

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76
Q

Infectious causes of hepatitis

A

Viral:
- Hep A-E (B and D infect together - D can only infect with B, B can infect alone)
- Human herpes viruses (either in first case or on reactivation)
-Others like flu, covid etc can cause abnormal LFTs

Non-viral:
- Spirochaetes, e.g. leptospirosis, syphilis
- Mycobacteria, e.g. M. tuberculosis
- Bacteria, e.g. bartonella
- Parasites, e.g. toxoplasma

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77
Q

Infectious causes of chronic hep

A

Hep B+D (D can only infect alongside B, B can infect alone), C, (E)

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78
Q

signs and symptoms of acute hepatitis

A

Can be asymp
Non-specific (malaise, lethargy, myalgia)
GI upset, Abdo pain
Jaundice + pale stools/dark urine

Signs:
- Tender hepatomegaly, potentially jaundice
- signs of fulminant hepatitis (acute liver failure)
* bleeding, ascites, encephalopathy

Abnormal LFTs
- ALT/AST&raquo_space; GGT/ALP

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79
Q

Signs/symptoms of CHRONIC hepatitis

A

asymp/non-specific symptoms

Potentially signs of chronic liver disease:
- CLUBBING, palmar erythem, Dupuytren’s contracture, spider naevi etc.

LFTs normal if COMPENSATED.

DECOMPENSATED:
- coagulopathy, jaundice, low albumin, ascites (potentially spontaneous bacterial peritonitis), encephalopathy

complications: HCC, portal HTN -> bleeding

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80
Q

Hep A epidemiology/spread

A
  • FAECO-ORAL TRANSMISSION (fAEco = A/E)
  • contaminated food/drink (SHELLFISH)
  • linked to access to safe resources/socioeconomic indicators
    • Close contacts
    • Homelessness
  • typically in low income countries

in high income countries:

  • Travel
  • Sex (MSM)
  • Injecting drug use
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81
Q

Incubation period of Hep A

A

SHORT: 15-50 days (usually 14-28)
- incubation period normally lasts ~ 1-6m

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82
Q

Hep A presentation

A

USUALLY SYMPTOMATIC in adults:

  • PRODROMAL (no jaundice) - 1-2 weeks:
    * constituational symptoms e.g. FEVER, fatigue, NAUSEA, MALAISE
    * RUQ abdo PAIN
  • ICTERIC phase (jaundice) - few days - 1 week after pre-icteric starts - 3m:
    • JAUNDICE
    • dark urine, pale stools
    • pruritis

SELF-LIMITING - no chronic disease

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83
Q

Hep A immunity after infection

A

100% immunity

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84
Q

Diagnosis of Hep A

A

Acute Hep signs/symptoms

  • LFTs - RAISED ALT
  • RAISED total BILIRUBIN
  • SEROLOGY: Presence of anti-HAV antibody
    • IgM high if acute
    • IgG present shows Immunity

Can’t test IgG by itself so know past infection has occured if Total anti-HAV antibody is positive but IgM is negative.

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85
Q

Management of Hep A

A

SUPPORTIVE - anti-emetics, rest

Monitor liver function

FULMINANT HEP VERY RARELY
- consider liver transplant

Vaccines to close contacts within 1 week (or human normal immunoglobin within 14 days)

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86
Q

Primary preventation of Hep A

A

vaccines to high risk groups
- travels, MSM, injecting drug users

1 dose - immune for 12 months; 2 dose at 6-12 months - immune for at least 20 years

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87
Q

Epidemiology/spread of Hep E

A

FAECO-ORAL TRANSMISSION (fAEco = A/E)

4 genotypes:
- G 1/2: contaminated food/WATER
- G 3/4: UNDERCOOCKED meat from mammals (particularly PORK)

G3 most common in UK (endemic)

  • typically only ACUTE - usually SELF-LIMITING (chronic risk in immunocompromised with G3)

TRANSPLANT RECIPIENTS

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88
Q

Presentation of Hep E

A

Usually ASYMPTOMATIC

Extra-hepatic manifestations esp neurological (meningoencephalitis, Guillian-Barre etc - confusion, coma, muscle weakness/paralysis) - may be main presentation

More common but still rare fulminant hep
- esp G1/2 in pregnancy (esp 2/3 trimesters)

  • risk of CHRONIC in IMMUNOCOMPROMISED (G3/4 only)

Occassional acute-on-chronic liver failure (ie fulminant in someone who already had chronic) - high mortality

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89
Q

Who are at risk of HEV complications

A

Immunosupressed with G 3/4 -> more risk of chronic

Pregnant ppl (esp 2nd/3rd trimester) with G1/2 -> more risk of fulminant hep

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90
Q

Investigations for Hep E

A

SEROLOGY:
ACUTE - anti-HEV IgM + HEV RNA
Past infection - anti-HEV IgG

  • unreliable in immunocompromised

HEV RNA - measure/monitor in SERUM/STOOL
- if it persists for >6 months - chronic

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91
Q

Hep E management

A

ACUTE:

  • SUPPORTIVE (usually self limiting)
  • Monitor for liver failure
    • consider transplant or RIBAVIRIN (antiviral)

CHRONIC:

  • Reverse immunosuppression if possible
  • if HEV RNA persists - treat with RIBAVIRIN >= 3 months
  • (2nd line: pegylated interferon-a)
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92
Q

Preventation of Hep E

A
  • Avoid eating undercooked meats (especially if immunocompromised)
  • Screening of blood donors

(Vaccine available in China only (HEV 239 (Hecolin®) against HEV genotype 1)

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93
Q

Epidemiology/spread of hep B

A

Most common - BLOOD-BORNE (and bodily fluids)

  • MOTHER-TO-CHILD (usually during birth, can occasionally get in-utero transmission if mother acquires acute hep B in pregnancy) - VERTICAL

Horizontal:

  • SEXUAL
  • injecting drug use (SHARING NEEDLES)
  • iatrogenic/occupational (needles)
    • also DIALYSIS
  • household contact (esp siblings)
  • blood products (medical)
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94
Q

Hep B natural historypresentation in immunocompetent adult (presentation + complications)

A

Mostly SYMPTOMATIC with SPONTANEOUS RESOLUTION (tho genome stays in host so may reactivate if later immunocompromised)

  • PRODROMAL phase (1-2 weeks)
    • malaise, RUQ pain, N+V, Fever
  • ICTERIC phase: jaundice phase
    • usually few weeks; can last up to 6 months (longer than hep A)
    • JAUNDICE (with stool/urine change)
    • PRURITIS
    • ARTHRALGIA
    • ascites, encephalopathy, coagulopathy, hypoalbuminaemia, varcies/bleeding (typical more severe hepatic symptoms/signs)

<5% -> chronic HBV infection -> 25% progress to cirrhosis -> decompensation (might progress from chronic/cirrhosis to HCC)

  • some also get fulminant Hep
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95
Q

Hep B natural history in neonates/immunocompromised

A

MUCH MORE LIKELY TO BE CHRONIC

  • HCC, Cirrhosis
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96
Q

Investigations for Hep B

A

SEROLOGY:

Total anti- HB core antibody (IgM + IgG - again no specific IgG test) (Anti Hb C Ag)
- IgM if acute (at ~ sign as ALT)
- IgG - previous exposure/chronic

  • HB SURFACE ANTIGEN (Hb S Ag) - CURRENT infection (1st to become positive)
  • Anti Hb S Ag - indicates IMMUNITY/VACCINATION
    • 1-3 months after exposure

Hb E Ag = INFECTIVITY/viral REPLICATION (2nd)
Anti Hb E Ag = LOW activity/infectivity

HBV DNA - indicates viral load (2nd)

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97
Q

Hep B incubation period

A

30 - 180 days (mean 75)

98
Q

Management of Acute Hep B

A

SUPPORTIVE

monitor liver function

Fulminant very rare

  • treat with ORAL NUCLEOTIDE ANALOGUES (TENOFOVIR, ENTECAVIR)
  • pegylated interferon alpha 2a
  • consider liver transplant

vaccinate non-immune close contacts (provides surface antibody only)

99
Q

Why may someone have the anti-HB surface antibody but not anti-HB core IgG

A

They got the vaccine but never had Hep B

100
Q

what denotes high viral replication in Hep B

A

e-antigen (eAg)

if e-antibody (eAb) present suggests immune system is controlling infection

determines whether to treat someone with chronic Hep B or not

101
Q

Treatments for chronic Hep B

A

pegylated interferon-alpha 2a

  • weekly sub-cutaneous infection for 5 weeks

SIDE EFFECTS:

  • flu like symptoms, tired/weak, gi issues, skin reaction, hair thinning, insomnia
  • can stimulate autoimmune conditions (thyroid, T1DM)
  • lower blood count (cytopenia)
  • mental health issues

ORAL NUCLEOTIDE ANALOGUES
- TENOFOVIR DISOPROXIL FUMERATE
- ENTECAVIR

  • inhibit HBV DNA polymerase (and thus replication)
  • 1 tablet a day
  • high barrier to resistance
  • may be lifelong
  • MINIMAL SIDE EFFECTS BUT:
  • TDF needs RENAL MONITORING
    • it can cause a fanconi-like syndrome - loss of electrlytes and stuff through urine
102
Q

Hep B primary prevention

A

Antenatal screening (HBsAg)
- HBIG for baby at birth if high risk
- post exposure vaccines after birth
- tenofovir given to mother in pregnancy if high HBV DNA

Childhood immunisation

Immuninsation of healthcare workers and other at risk groups

Screening/immunisation of sexual/household contacts

Barrier contraception; PrEP (Tenofovir/Emtricitabine)

Universal screening of blood products

Sterile equipment/universal precautions in healthcare

103
Q

Side effects of pegylated interferon-alpha

A

Low blood count
Triggers autoimmune conditions
Hair thinning, skin/GI problems
Flu like symptoms
Mental health issues

104
Q

Side effect of TDF? What does TDF stand for

A

Tenofovir DIsoproxil Fumerate

a Fanconi-like syndrome - loss of eloctrolytes and stuff through urine

105
Q

When are the post birth-exposure vaccines given for Hep B

A

Within 24 hr of birth
At 4 weeks
At 8, 12, 16 weeks (as part of the hexavalent routine childhood immunisation)
At 1 year

106
Q

What factors make a baby high risk for Hep B resulting in them being given the HBIg

A

Mother has high e-antigen and/or high HBV DNA

Baby birth weight <1.5 kg

107
Q

When are the routine childhood vaccinations of Hep B administered

A

8, 12 and 16 weeks (as part of a hexavalent vaccine)

108
Q

Which medications are in PrEP

A

Tenofovir/Emtricitabine
(normally only used for HIV)

109
Q

What follow up should be done after Hep B vaccination for high risk contacts

A

Check vaccine response using anti-HB surface antibody and potentially offer a more immunogenic 2nd line vaccine if required

110
Q

What blood test is done as screening at every visit for chronic Hep B patients

A

Alpha-Feto Protein test - screens for development of primary liver cancer

111
Q

Epidemiology/spread of Hep D

A

BLOOD-BORNE/bodily fluids - same as hep B

  • Mother-to-child
  • INJECTING DRUG USE
  • BLOOD PRODUCTS
  • IATROGENIC
  • Sexual
  • Household contact
  • Occupational (tattoos, medical etc)
112
Q

Why can Hep D only infect alongside Hep B

A

Hep D is a defective RNA virus

Can only replicate in presence of/attached to HBsAg (also needs it for protection)

113
Q

Hep D + B coinfection natural history

A

More aggressive (often acute-on-chronic)

More likely to become chronic, cirrhotic and decompensated (accelerated progress to liver fibrosis)
- more likely to develop HCC

than in just Hep B infection

114
Q

Investigations for Hep D

A

Hep D antibody

if pos -> test for Hep D RNA

115
Q

Treatment for Hep D

A

Pegylated interferon-a - 48 weeks

Tenofovir or Entecavir (oral nucleotide analogues)

(buleviritide - blocks from entering hepatocytes - NOT YET approved by NICE)

116
Q

Transmission of Hep C

A

BLOOD-BORNE/bodily fluids

  • INJECTING DRUG USE!! (main)
  • Blood products
  • Iatrogenic
  • Mother-to-child
  • Household contact
  • Sexual
  • Occupational
    • Tattoos, piercings, medical etc.
117
Q

Hep C natural history in immunocompetent adults

A

ACUTE oft ASYMP - may have:

  • MALAISE, FEVER, Myalgia, Arthralgia, N+V, Diarrhoea

70% chance of becoming CHRONIC

  • Usual CHRONIC LIVER SIGNS

15-30% chance of becoming cirrhotic within 20 years

Most people are not good at making Hep C antibodies

118
Q

Hep C testing

A

FIRST test HCV IgG ANTIBODY to check for HCV EXPOSURE (may take 4-12 weeks to show up; might look -ve in immunocompromised - repeat downstream testing)

If positive -> HCV RNA to check for current infection - if positive, start treatment

Check HCV genotype to refine treatment (usually 1a, 1b, 3 - could potentially be any number to 6)

119
Q

Which methods used used for Hep C testing

A

Point of care testing is important (available for antibody test and RNA)

Dried blood spot test can be used for RNA/genotype

Venous (/capillary if bad veins) blood can be used for any of the above

120
Q

Importance of point of care testing in Hep C patients

A

Common in injecting drug users who can often be unwilling to engage with medical appointments

121
Q

Treatment for Hep C

A

NOT pegylated interferon-a - MENTAL HEALTH SIDE EFFECTS NOT WELL TOLERATED

DIRECTLY ACTING ANTIVIRAL (DAA) THERAPY
- NS3/4A protease inhibitors (-PREVIR)
- NS5A inhibitors (-ASVIR)
- NS5B inhibitors (-BUVIR)
Once daily tablets, 8-16 weeks
- may need to add RIBAVIRIN

122
Q

Which genotypes do Hep C DAA therapy act on

A

Elbasvir/Grazoprevir - only on G1 and G4
Glecaprevir/Pibretasvir - ALL (1-6)

Ledipasvir/Sofosbuvir - all but G3
Sofosbuvir/Velpatasvir - ALL (1-6)

Sofosbuvir/Velpatasvir/Voxilaprevir - ALL (1-6)

123
Q

Hep C Prevention

A

NO VACCINE (most people can’t make good immune response to it) - PREVIOUS INFECTION DOES NOT CONFER IMMUNITY

Screening blood products
Universal precautions when handling bodily fluids
Sterile equipment/safe disposal
- provision of sterile injecting equipment

Optiate addiction treatment

Treat/cure transmitters (e.g. IV drug users)

Safe sex (barrier contraception)

124
Q

Defense mechanisms of GI tract

A

Intestinal microflora - intere with/compete with pathogens (can produce antibacterials)

Gastric acid

Bile - antibacterial properties

125
Q

Define diarrhoea; acute, persistant, chronic

A

Passage of increased loose or watery stools (at least 3 times in 24 hours)

Acute - 14 days or less
Persistant - >14 but <30 days
Chronic > 30 days

Devided into watery vs bloody (Dysentery - often with fever/abdo pain)

126
Q

When is evaluation for acute diarrhoea warrented?

A

In individuals with:
- persistant fever
- bloody diarrhoea
- severe abdominal pain,
- symptoms of volume depletion (eg, dark or scant urine, symptoms of postural/orthostatic hypotension),
- history of inflammatory bowel disease,
- immunosuppression

127
Q

Causes of liver abscesses

A

PYOGENIC
- following biliary sepsis or haematogenous spread
- usually polymicrobial: enteric gram -ve and anaerobes

AMOEBIC:
- Entamoeba histolytica

128
Q

Symptoms/signs of liver abcesses

A

FEVER + RUQ PAIN
- nausea/vomiting
- malaise
- anorexia/weight loss

129
Q

Diagnosis of liver abscesses

A
  • Abdo CT or ultrasound
  • Blood cultures + E. histolytica serology
  • Aspiration and culture of the abscess material + E. histolytica molecular testing
130
Q

Treatment of liver abscesses

A

Drainage (surgical or imaging guided)
Antibiotics

131
Q

Causes of pancreatitis

A

I GET SMASHED

  • Idiopathic
  • GALLSTONES (>50% of acute cases)
  • ETHANOL (50% of chronic cases)
  • Trauma
  • STEROIDS
  • Mumps
  • Autoimmune
  • Scorpion/spider venom
  • HyperCALCAEMIA(/LIPIDAEMIA)
  • ERCP
  • Drugs (Azathioprine, NSAIDs, ACE-I)
132
Q

Pathophys of pancreatitis

A

2 main cuases: gall stones + alcohol

GALLSTONES OBSTRUCT pancreatic SECRETIONS (blocks ampulla of Vater)

  • Reflux of bile into pancreas
  • ACCUMULATION of DIGESTIVE ENZYMES in pancreas
  • Host defences (A1AT, PANCREATIC SECRETORY TRYPSIN INHIBITOR) OVERWHELMED
    -> AUTODIGESTION of gland + nearby structures
    -> INFLAMMATION + ENZYMES leak in BLOOD
    - Deranged pancreatic function e.g. insulin def

Alcohol = DIRECTLY TOXIC -> inflam

133
Q

Signs/symptoms of acute pancreatitis

A
  • SUDDEN SEVERE EPIGASTRIC PAIN RADIATING TO BACK (need to consider AAA for diff diagnose)
  • Nausea + vom
    (- Jaundice)
  • Pyrexia/chills
  • Tachycardia
  • Anorexia
  • Steatorrhoea (malabsorption)

Haemodynamic instability

  • GREY TURNERS sign (FLANK RETROPERITONEAL BLEEDING)
  • CULLEN sign (PERIUMBILICAL BLEEDING)
  • FOX sign (bruising around inguinal ligament)
134
Q

Diagnosis of acute pancreatitis

A

Characteristic signs/symptoms

Bloods:
- RAISED SERUM AMYLASE (gold)
- RAISED SERUM LIPASE (more specific than amylase)
- CRP raised

ABDO US (diagnostic for gallstones) - CT/MRI to see extent of damage

Need at least 2 of above to diagnose

Urinalysis - raised urine amylase

Also:
- standing CXR to EXCLUDE gastroduodenal PERFORATION (also has raised amylase/lipase)

135
Q

Pancreatic scoring systems

A
  • APACHE 2
    • assesses SEVERITY within 24HR
  • Glasgow + Rouson score
    • prediction of SEVERE attack only within 48HR

Glasgow can be remembered by PANCREAS:

  • P = PaO2 < 8KPa (partial Pa of O2 in blood)
  • A = Age > 55
  • N = Neutrophils (WBC > 15)
  • C = Calcium < 2
  • R = uRea > 16
  • E = Enzymes (LDH (lactate dehydrogenase) > 600 or AST/ALT > 200)
  • A = Albumin < 32
  • S = Sugar (Glucose > 10)

0-1 = mild
2 = moderate
3 or more = severe

136
Q

Treatment for acute pancreatitis

A

Assess severity with scoring

  • NIL BY MOUTH (decreased pancreatic stimulation)
  • IV FLUID
  • ANALGESIA (e.g. IV morphine)
  • Catheterise
  • Antibiotic prophylaxis
  • treat gall stones if present
  • treat any complications (e.g. endoscopic/percutaneous drainage of large collections)

careful monitoring

137
Q

Complication of acute pancreatitis

A

SIRS - SYSTEMIC INFLAMMATORY RESPONSE SYNDROME

has 2/more of following:
- TACHYCARDIA (>90 bpm)
-TACHYPNOEA (>20 resp rate)
- PYREXIA (>38 C)
- RAISED WCC

Can escalate to necrotising pancreatitis (autodigestion - v poor outcome)
- infections
- abscesses
- peripancreatic fluid collections
- pseudocyts up to 4wks after
- can progress to chronic pancreatitis

138
Q

Define chronic pancreatitis

A

3 MONTH history of PANCREATIC DETERIORATION

  • PERSISTANT IRREVERSIBLE pancreatic INFLAMMATION + FIBROSIS
  • Caused by CHANGES to pancreatic STRUCTURE
  • OBSTRUCTION of BICARB secretion into pancreatic lumen -> autodigestion -> fibrosis
139
Q

Causes of Chronic Pancreatitis

A
  • CHRONIC ALCOHOL (main)
  • CKD
  • CF (mucus gums up excretory ducts)
  • Trauma
  • RECURRENT acute pancreatitis
  • hereditary
  • autoimmune
  • idiopathic
140
Q

Symptoms of chronic pancreatitis

A

similar symps to acute but generally less intense/longer lasting

  • EPIGASTRIC PAIN boring through BACK
    • EXACERBATED by ALCOHOL
    • BETTER on LEANING FORWRDS
  • Nausea + vom
  • Exocrine dysfunction (e.g. steathorrhoea)
    • Steatorrhoea
    • Weight loss (malabsorp)
  • Endocrine dysfunction (e.g. DM)
    • INSULIN DEPENDANT DM

Strictures -> collections of bile + pancreatic juice -> abscesses + pseudocytes

141
Q

Diagnosis of chronic pancreatitis

A

Bloods:
- Amylase + lipase UNLIKELY TO BE HIGH IN SEVERE (not enough left to leak out/not enough cell remain to make)

typically DECREASED FEACAL ELASTASE (exocrine function marker)

Abdo US + CT (DIAGNOSTIC)
- detects pancreatic CALCIFICATION
- DILATED pancreatic DUCT

142
Q

Treatment for chronic pancreatitis

A
  • ALCOHOL CEASSATION
  • NASAIDs for Abdo PAIN
  • pancreatic supplements (enzymes, insulin etc.)
  • PPI to help digestion
  • ERCP or surgery as required
143
Q

Causes of portal hypertension

A

Pre-hepatic:
- PORTAL VEIN THROMBUS

Intrahepatic:
- CIRRHOSIS (main in uk)
- SCHISTOSOMIASIS

Post-hepatic:
- BUDD-CHIARI
- RIGHT HF
- Constrictive pericarditis (heart can fill properly - backs up)

144
Q

Pathophys of portal HTN

A

NORMAL: 5-8mmHg in PORTAL VEIN

Cirrhosis -> increased resistance
-> COMPENSATORY SPLANCHNIC DILATION + INCREASED CARDIAC OUTPUT
-> FLUID OVERLOAD in portal vein (>10mmHg = BAD, >12 = V. BAD)

-> COLLATERAL SHUNTING to (usually small) GASTROESOPHAGEAL veins -> OESOPHAGEAL VARICES (esp cardia + lower oes)

145
Q

Symptoms of portal HTN

A

usually asymp
- present with OESOPHAGEAL VARICEAL RUPTURE
- (90% with p htn have o.v. - 1/3 rupture)

146
Q

Types of peritonitis

A

Primary:
- ASCITES
- SPONTANEOUS BACTERIAL PERITONITIS (main)
- Primary pneumococcal peritonitis (typically as complication of nephrotic syndrome/cirrhosis)
- Familial Mediterranean fever (periodic + self-limiting)

Secondary - underlying cause e.g.
- BILE (chemical),
- TB
- malignancy

Acute or chronic

147
Q

Bacterial causes of peritonitis

A

G -ve:
- E. COLI
- KLEBSIELLA
(remember it as the sugary bacteria most likely to cause peritonitis)

G +ve:
- STREP + ENTEROCOCCI (most common g +ve)
- STAPH AUREUS

148
Q

Chemical causes of peritonitis

A
  • Bile
  • barium
  • Old clotted blood
  • Ruptured ectopic pregnancy
  • INTESTINAL PERFORATION

(ultimately get infected)

149
Q

Symptoms of peritonitis

A

SUDDEN ONSET SEVERE ABDO PAIN
-> collapse, septic shock, fever
- PAIN LESSENS WHEN RIGID - abdo guarding + rebound tenderness
(-> can DIFFERENTIATE FROM RENAL COLIC in this way as renal colic patients CAN’T LIE STILL)

  • POORLY LOCALISED (only visceral)
    -> WELL LOCALISED (more inflamed -> more press on parietal)
  • pelvic peritonitis -> tender rectal/vaginal exam

Usually ASCITES

150
Q

Diagnosis of peritonitis

A

Bloods:
- RAISED ESR/CRP, WCC
- U + E

  • ASCITIC TAP:
    -> NEUTROPHILIA
    -> CULTURES - causative organism

EXCLUDE:
- PREGNANCY (beta-hCG test)
- BOWEL OBS (ABDO XR)
- Urine dipstick (UTI)
- serum amylase (pancreatitis)

If ERECT CXR shows GAS UNDER DIAPHRAGM -> PERFORATED COLON

151
Q

Treatment of peritonitis

A

ABCDE

  • analgesia
  • IV FLUIDS + ANTIBIOTICS (e.g. CEFOTAXIME + METRONIDAZOLE)
  • URINARY CATHETER (to monitor fluid volume)
  • GI decopression (nasogastric drain)
  • Paracentesis

Surgery:
- PERITONEAL LAVAGE (surgical clean out)

(treat underlying cause when stable enough to do so)

152
Q

Complications of peritonitis

A

SEPTICEMIA if not treated early

Subphrenic/PELVIC ABSCESSES

Paralytic ILEUS

153
Q

Pathophys of haemochromotosis

A

AUTOSOMAL RECESSIVE
- mutation of HFE gene (chromosome 6) - codes for HFE protein (it competitively inhibits transferrin from binding to transferrin receptor 1 - this prevents transferrin from stimulating iron to enter the liver)

  • EXCESS IRON UPTAKE by TRANSFERRIN-1 receptor - INTO LIVER
  • REDUCED HEPCIDIN SYNTHESIS (regulates Fe homeostasis)

Iron accumulation (20-30g in body vs 3-4g normally)
- organ FIBROSIS - esp LIVER
(pancreas, kidney, heart, skin, ant pit. gland)

154
Q

Role of hepcidin

A

Protein that degrades ferroportin (iron exporter)
- REDUCES RELEASE OF IRON FROM STORAGE (in cells esp MACROPHAGES and ENTEROCYTES - duodenum)

155
Q

Amount of iron in body in haemochromatosis vs normally

A

20-30g

3-4g

156
Q

Symptoms of Haemochromatosis

A
  • Fatigue
  • JOINT PAIN (deposits)
  • HYPOGONADISM (due to pituitary damage)
  • SLATE GREY skin -> BRONZE
  • LIVER CIRRHOSIS Sx
  • OSTEOPOROSIS (increased iron = increased risk of resorption/formation imbalance)
  • HF
  • Irregular heartrate
  • Diabetes (pancreatic deposits)
157
Q

Triad of gross iron overload

A

BRONZE SKIN
HEPATOMEGALY
T2DM

158
Q

Diagnosis of haemochromatosis

A

IRON STUDIES:
- Raised seurm Fe
- RAISED FERRITIN
- RAISED TRANSFERRIN SAT
- Low TIBC

GENETIC TEST (HFE gene)

LIVER BIPOSY (extent of liver damage - Prussian ble stain)

159
Q

Treatment of haemochromatosis

A

1ST LINE: - VENESECTION (3-4 years, lifelong)

If contraindicated: DESFERRIOXAMINE (chelation)

+ lifestyle: low iron diet; avoid fruits

160
Q

RFx for haemochromatosis

A

family history
MALE
50s

(women less likely to have due to periods)

161
Q

Pathophys of WIlson’s disease

A

AUTOSOMAL RECESSIVE
- mutation of ATP7B copper binding protein (supposed to remove Cu from liver)

-> impaired COPPER BILIARY EXCRETION + normal transport via CAERULOPLASMIN
-> INCREASED Cu ACCUM in LIVER + CNS (basal ganglia) + other organs

162
Q

Symptoms of Wilson’s

A

HEPATIC - liver disease (JAUNDICE)

NEURO - PARKINSONISM (memory issues)

  • dystonia (muscle spasms/contractions)
  • dysarthria (difficulty speaking due to weakness in muscles involved in speech)

OPTHALMOLOGICAL - KEYSER FLEISHER RINGS (greenish brown copper rings in cornea) - pathogomonic

163
Q

Investigations for Wilson’s

A

Copper tests:
- LOW SERUM COPPER (most deposited in tissue)
- LOW CAERULOPLASMIN (gold???)

LIVER BIOPSY - if Dx UNCERTAIN (gold):
- RAISED COPPER; hepatitis

Brain MRI:
- cerebellar + basal ganglia degeneration

164
Q

Treatment for Wilson’s

A

1ST LINE:
- D-PENICILLAMINE (copper chelation - lifelong)
+ diet - avoid high Cu e.g. SHELLFISH, MUSHROOM

last resort -> consider liver transplant

165
Q

Pathophys of A1AT deficiency

A

Mutation of PROTEASE INHIBITOR (‘SERPINA-1’) gene (chromosome 14)

A1AT NORMALLY INHIBITS NEUTROPHIL ELASTASE (degrades elastic tissues)

In deficiency - high neutrophil elastase:
- LUNGS
-> ALVEOLAR COLLAPSE, air trapping + PANACINAR EMPHYSEMA (characteristic - lower lobes vs upper, all acinar involved uniformly - looks even more blobby)
- LIVER -> FIBROTIC -> CIRRHOSIS + HCC RISK

166
Q

function of liver with A1AT

A

Liver SYNTHESES A1AT
- damage -> even worse A1AT deficiency

167
Q

Symptoms of A1AT deficiency

A

COPD LIKE SYMPTOMS
- dyspnoea
- chronic cough
- sputum
- barrel chest

CHARACTERISTIC:
- YOUNG/MID AGE MALE - LITTLE/NO SMOKING Hx - COPD SYMPTOMS

Liver symptoms

168
Q

Diagnosis of A1AT deficiency

A
  • LOW SERUM A1AT (<20mmol/L)
  • BARREL CHEST (on examination)
    • CXR - hyper inflated lungs
  • CT - PANACINAR EMPHYSEMA
  • SPIROMETRY -> OBSTRUCTION (FEV:FVC <0.7)
  • GENETIC - PI mutation
169
Q

Treatment of A1AT deficiency

A

NO CURATIVE TREATMENT

  • smoking ceassastion
  • inhalres etc. for emphysema
  • Consider LIVER TRANSPLANT if in HEPATIC DECOMPENSATION
  • symptomatic managment
170
Q

Define ascites

A

Accumulation of excess serous fluid within peritoneal cavity

171
Q

What is a normal amount of peritoneal fluid in men and women

A

Men - negligible (baso none)

Women - up to 20 ML

(ascites can be up to 2L or so)

172
Q

Classification of Ascites (stages)

A
  • Stage 1: detectable only after careful examination / Ultrasound scan
    (Mild)
    ● Stage 2: easily detectable but of relatively small volume.
    ● Stage 3: obvious, not tense ascites. (moderate)
    ● Stage 4: tense ascites. (Large)
173
Q

Define transudate and exudate

A

Transudates - fluid with protein <25 g/L

Exudates - fluid with protein >25 g/L (cloudy)

174
Q

Transudate causes of Ascites

A

PORTAL HTN (thrombosis/cirrhosis)

HIGH CENTRAL VENOUS Pa - CONGESTIVE HF

LOW PLASMA PROTEIN conc:
- Malnutrition
- Nephrotic syndrome
- Protein losing enteropathy

175
Q

Exudate causes of ascites

A

MALIGNANCY
TB
PACREATIC ASCITES

Budd-Chiari syndrome

(inflammation or post hepatic congestion)

176
Q

Presentation of ascites

A

Abdo DISTENSION

Nausea, LOSS of APPETITE
CONSTIPATION
Cachexia - apparent wasting

PAIN/DISCOMFORT -> MALIGNANT

symptoms of underlying cause (oedema, jaundice)

may get UMBILICAL HERNIA

177
Q

Functions of peritoneum in health

A

Visceral lubrication

Fluid + particulate absorption

178
Q

Complications of PSC

A

Acute bacterial cholangitis,
Cholangiocarcinoma develops in 10-20% of cases,
Colorectal cancer,
Cirrhosis and liver failure,
Biliary strictures,
Fat soluble vitamin deficiencies

179
Q

What can liver look like on ultrasound

A
  • Larger in liver failure
  • cirrhosis can make it look smaller
  • can see nodules
180
Q

Marker for HCC

A

AFP

181
Q

Risk factors for A1AT deficiency

A
  • Family history
  • Male
  • SMOKING
    • Typical exam question would have male with copd-like symp but doesn’t smoke
182
Q

Pancreatic cancer pathophys

A
  • adenocarcinoma
  • Typically in HEAD of pancreas
    • can COMPRESS bile duct

THERE IS MORE, FILL THIS IN

183
Q

Tumour marker for pancreatic cancer

A

Ca 19-9

184
Q

Cholangiocarcinoma

A
185
Q

What is ALP particularly related to

A
  • Gallbladder
  • BONE
186
Q

How do you differentiate between high ALP biliary tree vs bony pathology

A

GGT (liver enzyme) will be present in liver pathology

187
Q

Functions of the Liver

A
  • Detoxification
  • Clotting factor production
  • Bilirubin regulation
  • METABOLISES CARBS
  • ALBUMIN production
  • IMMUNITY + Kupffer cells
  • OESTROGEN REGULATION
188
Q

What happens when Liver function goes wrong

A

Oestrogen regulation issues:

  • Gynaecomastia in men
  • Spider naevi
  • Palmar erythema

Detoxification issues

  • Hepatic encephalopathy

Carb metabolism:

  • HYPOGLYCAEMIA

Albumin production issues:

  • OEDEMA
  • LEUKONYCHIA (white nails)
  • ASCITES

Clotting issues:

  • Easy bleeding/bruising

Bilirubin issues:

  • Pruritis
  • Jaundice with stool/urine changes

Immunity issues:

  • Spontaneous bacterial infections

Reduced bile production -> reduced bile salts in lumen
- DECREASED absorption of bile salts/FAT SOLUBLE VIT

189
Q

Define Liver Failure

A

Liver LOSES ability to REPAIR and REGENARTE leading to DECOMPENSATION

(if compensated liver can still function and there are no/few noticible clinical symptoms)

190
Q

Presentation of Liver Failure

A

Same as acute injury

  • JAUNDICE
  • COAGULOPATHY
  • FETOR HEPATICUS (musty breath/urine due to retention of sulfur compounds)
  • Hepatic ENCEPHALOPATHY
    • Altered mood/dyspraxia
    • Liver flap/asterixis
191
Q

Investigations for Liver failure

A
  • Clinical exam
  • Ultrasound (can see nodules, blockages etc)
  • Bloods:
    • RAISED ALT/AST
    • RAISED PROTHROMBIN TIME
    • FBC + U&E
  • If ascites present - PERITONEAL TAP
    • Microscopy/culture
192
Q

Management of Liver failure

A
  • Conservative
    • ANALGESIA + FLUIDS
  • Treat complications!
    • Encephalopathy - LACTULOSE
    • Ascites - DIURETICS
    • Cerebral oedema - MANNITOL
    • Bleeding - VIT K
    • Sepsis - ANTIBIOTICS
    • Hypoglycaemia - DEXTROSE
  • Transplant
193
Q

Risk factors for Gallstones

A

5 Fs

  • FAT
  • FOURTY
  • FEMALE
  • FERTILE
  • Fair
194
Q

Charcot’s triad

A
  • RUQ pain
  • Fever
  • Jaundice (cholestatic)
195
Q

Reynold’s pentad

A
  • Charcot’s triad
    • RUQ pain
    • Fever
    • Jaundice
  • Sepsis/shock
  • confusion
196
Q

Define liver Cirrhosis

A

Result of CHRONIC INFLAM + DAMAGE to liver cells. Damaged liver cells replaced by FIBROSIS. NODULES of scar tissue form within liver.

Thought to be IRREVERSIBLE

197
Q

Causes of cirrhosis

A
  • AFLD
  • NAFLD
  • Hep B
  • Hep C

viral more common in developing, alcohol more common in developed

  • Haemochromatosis
  • Wilson’s disease
  • A1AT deficiency
198
Q

Presentation of cirrhosis

A

Similar to chronic liver disease/failure

Ascites, jaundice, hepatomegaly, splenomegaly, Spider Naevi, Palmar erythema, bruising, asterixis, caput medusae (vessels around umbilicus)

199
Q

Investigations for cirrhosis

A

FBC - thrombocytopenia, high INR, low albumin

US and CT - hepatomegaly

liver BIOPSY - diagnostic

200
Q

Complications of cirrhosis

A

Same as chronic liver failure

Ascites
Portal Hypertension
Varices/bleeding varices
hepatic encephalopathy
hepatocellular carcinoma
malnutrition
Jaundice
Coagulopathy
oedema - hypoalbuminemia

201
Q

Treatment of cirrhosis

A

Liver TRANSPLANT
Alcohol ABSTINENCE and good NUTRITION
Treat the COMPLICATIONS of liver failure

SCREEN for hepatocellular carcinoma every 6 months

  • Marker for HCC is AFP
202
Q

Define Pancreatic cancer

A

Typically ADENOCARCINOMA
Typically in HEAD OF PANCREAS

  • can compress bile ducts
203
Q

Risk factors for pancreatic cancer

A

Old age (60+),
smoking,
obesity,
T2DM,
FHx,
Chronic Pancreatitis

204
Q

Presentation of pancreatic cancer

A
  • Obstructive/Painless Jaundice, pale stools, dark urine, generalized itching (pruritus),
  • weight loss,
  • worsening of T2DM (or new onset)
  • Courvoisier’s Sign – palpable gallbladder + jaundice
  • Can get epigastric pain that radiates to back (body and tail cancer)
205
Q

Diagnosis of pancreatic cancer

A
  • Abdominal Ultrasound
  • CT of pancreas (identifies mass and helps with staging of cancer) – GOLD STANDARD
  • Tumour marker – Ca19-9 not diagnostic but helps with monitoring progression
206
Q

Treatment of pancreatic cancer

A
  • Surgery to remove tumour – Whipple procedure (pancreaticoduodenectomy + others)
  • Chemo/Radiotherapy
207
Q

Complications of pancreatic cancer

A

Poor prognosis as identified late, metastasis to liver, lungs etc.

208
Q

Causes/risk factors of HCC

A

Liver Cirrhosis due to:

  • Viral Hepatitis (B and C), Alcohol, NAFLD, other chronic liver diseases
209
Q

Pathophys of HCC

A

Arises from liver parencyma (not connective/supportive tissue i.e hepatocytes)

Metastesis to lymph nodes, lungs, (bones)

210
Q

Presentation of HCC

A

Liver specific:

  • Jaundice
  • Ascites
  • Pruritis
  • hepatic encephalopthy

Non-specific:

  • Weight loss
  • Fatigue
  • Weakness
  • N+V
211
Q

DIagnosis of HCC

A
  • 1ST LINE: Abdominal ULTRASOUND
  • CT to confirm (GOLD STANDARD)
  • Serum Alpha-Fetoprotein (AFP) = tumour MARKER for HCC
212
Q

Treatment of HCC

A

Poor Prognosis

  • Resection of Tumour
  • Liver Transplant (if isolated to the liver)
213
Q

Define cholangiocarcinoma

A

A cancer arising from the BILIARY TREE - usually ADENOCARCINOMA

214
Q

Causes/risk factors of cholangiocarcinoma

A
  • Liver Fluke infections
  • PSC
  • Chronic viral Hep B/C
  • Liver Chirrhosis
  • Biliary Cysts

RFx:
- older age
- smoking
- diabetes

215
Q

Presentation of Cholangiocarcinoma

A

Signs of cholestasis:

  • Jaundice, Pale Stools, Dark Urine, Pruritus + Courvoisier’s Sign (palpable/non-painful gallbladder)

Non-specific:

  • Weight Loss, Fatigue, Weakness, N+V
216
Q

Diagnosis of cholangiocarcinoma

A
  • 1st LINE – Abdominal Ultrasound and CT
  • ERCP – used to take biopsies/imaging - GOLD Standard
  • CA19-9 – Tumour marker for Cholangiocarcinoma/pancreatic
  • LFTs – raised bilirubin and ALP
217
Q

Treatment of cholangiocarcinoma

A
  • Surgical resection
  • ERCP -> place STENT (relieves symptoms)
218
Q

Time range types of liver failure

A
  • If you get encephalopathy within 7 days of jaundice = hyperacute
    • paracetamol, Hep A/E, Ischaemia
  • within 1-4 weeks = acute
    • Hep B, drugs
  • within 5-12 = subacute
    • Non-paracetamol

chronic
Acute-on-chronic

Fulminant is rapid, severe decline

219
Q

Classic 3 acute liver failure syigns

A

Jaundice
Coagulopathy
Encephalopathy

220
Q

Lemon yellow skin is charcteristic of what

A

Jaundice with anaemia (yellow mixed with pallor)
- pre hepatic jaundice

  • B12 deficiency
  • Haemolytic anaemia
221
Q

If AST is double ALT with GGT- suggests

A

AFLD

222
Q

If AST is less than ALT - suggests

A

NAFLD

223
Q

If ALT/AST ratio is really high - 4.5 - suggests

A

Metabolic disease

224
Q

PT/1.5 =

A

INR

225
Q

For liver hypocoagulopathy give

A

IV kit K

226
Q

Icteric meaning

A

Patient is jaundiced (skin, whites of eyes + mucous membranes)

227
Q

Stages of cirrhosis/failure

A

Compensated cirrhosis
- Stage 1 - no ascites, varices, encephalopathy - maybe jaundice
- stage 2 - varices, no asvites, mental state should still be fine, maybe jaundice
- stage 3 - ascites +/- varices, confusion/disorientation, jaundice
- stage 4 - bleeding +/- more severe ascites

228
Q

where does rbc breakdown occur

A

reticular endothelial cells - mainly in spleen
(small bit in liver + BM)

229
Q

how is unconjugated bilirubin transported in blood

A

attached to albumin - goes to liver

230
Q

Why does pre-hepatic jaundice not have urine/stool changes

A

Unconjugated bilirubin is not water soluble (while conjugated is) so it can’t be excreted in urine

231
Q

Gilbert’s syndrome

A

AUTOSOMAL RECESSIVE - affects UDP gene

Main cause of hereditary jaundice - esp in MALES

  • RFx: T1DM, males

Deficient/abnormal UGT (UDP-glucoronyltransferase) -> UNCONJUGATED HYPERBILIRUBINAEMIA

SYmp:
- 30% aSx
- Sudden onset Painless jaundice at young age

Relatively benign - usually ok without treatment

Crigler Najjar = more severe

  • jaundice w/ n+v
  • lethargy
232
Q

Choledocholilithiesis is what

A

Gall stones in the common bile duct

233
Q

Complication of Crigler Najjar syndrome

A

KERNICTERUS - can lead to death in childhood

  • bilirubin accumulation in BASAL GANGLIA of children causing severe neurological deficits
234
Q

Treatment of Crigler Najjar syndrome

A

Phototherapy - breaks down unconj bilirubin

235
Q

What would you see in Alcoholic HEPATITIS biopsy

A
  • Scarring/necrosis around central veins of liver
  • Mallory bodies
236
Q

Which enzymes are involved in alcohol metabolisation

A

Alcohol dehydrogenase (ADH) and mitochondrial aldehyde dehydrogenase (ALDH2) (not particularly needed to remember)

237
Q

Alcohol withdrawal symptoms (give time ranges)

A
  • 6-12 hrs after last drink - relatively mild symptoms of early withdrawal may begin, including headache, mild anxiety, insomnia, small tremors, and stomach upset
  • 12-24 - hallucinations
  • 24-48 - highest risk of seizures
  • 48-72 - delerium tremens
  • Within 24-72 hours, various symptoms may have peaked and begun to level off or resolve
238
Q

Pathophys of delerium tremens

A

downregulating gaba + upregulating excitatory systems because alcohol down-regulates excitatory pathways

In withdrawal -> alcohol down-regulation removed so double excitation

-> Delerium tremens, hallucinations etc

239
Q

Main drug treatment for alcohol withdrawal

A

IV CHLORDIAZEPOXIDE

or DIAZEPAM

240
Q

Cells responsible for liver fibrosis

A

Stellate cells

241
Q

What test is used to detect encephalopathy

A

Electroencephalogram (EEG)

242
Q

Mortality rate of of pancreatitis

A

25%

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