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Take 2: Electric Boogaloo > Phase 2 - Liver > Flashcards

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 failureChronic 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 prognosisProthrombin time (sensitive - synthetic function) - increasesCholestatic 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. rareIntrahepatic (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 ITCHINGCholestatic:- 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 shoulderRigorsAbdomen swellingWeight 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 intrahepaticCholesterol - 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 stoneSudden 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/vomitingAssociated with tenderness and muscle guarding/ridgityCommonly affects mid-evening -> early morningRelated to increased fatty food consumptionNOT 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 UNBALANCEDTypically forms large, solitary stones

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17
Q

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

A

DMHigh 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 ANAEMIASBrown:- 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 pancreasNOT 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 hepaticCan 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 CHOLANGITISBlood cultures/MC&S - for infectionsABDO ULTRASOUND (1st line imaging):- no major changes in bloods or images for biliary colic except STONES + duct dilationAcute cholecystitis/cholingitis US:- thick walled, shrunken gallbladder (bile can’t enter from liver)- pericholecystic fluid (fluid around gallbladder)- STONESMRCP (higher resolution but less accessible)ERCP potentially for CHOLANGITISContrast 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/ANALGESIAIf 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 cholesterolShock 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 SURGERYCANCER of pancreas head compressing bile ductPARASITES 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 FLUIDSBiliary 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+ homeostasisDisrupt bile canalicular transport mechanismsInduce apoptosisInhibit 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 weekcan occur weeks after stopping drugusually 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 aspirinNSAIDs other than DiclofenacHRTBeta BlockersACE InhibitorsThiazidesCalcium 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 >=5Cholestatic:- ALT >2, ratio <=2Alk 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- ConfusionLFTs show liver damage at 18 HOURS AFTER- RAISED ALT72-96hrs after - PEAK ALT and Prothrombin timeAcute liver injury symptoms:- JAUNDICE AND ENCEPHALOPATHY- HYPOglycaemia (overdose inhibits gluconeogenesis)- Coagulation defects, electrolyte imbalancesPotential kidney injury from ACUTE TUBULAR NECROSIS:- METABOLIC ACIDOSIS (lactic acid)- Raised creatinineDIAGNOSED 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 encephalopathyPresents 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 failureFlow 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/LIMAGING: - XR (worst sensitivity)- US- CT (best sensitivity)

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40
Q

Treatment for ascites

A

SODIUM/fluid restrictionSPIRONALACTONE (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 shuntstent connects portal veins to adjacent vessels with lower BP -> relives pressure in liver -> help stop fluid back upINCREASED 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 asymptomaticmore 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 anaemiaLFTs: - 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 regiempharm:- 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

NormalHepatosteatosis (fatty liver - deposited in hepatocytes)Non-alcoholisc steatohepatitis (NASH - fatty+fibrotic)FibrosisCirrhosis

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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/MRI2nd 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 sensitivityvitamin E can reduce fibrotic appearance (improves liver function)

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52
Q

Complications of NAFLD

A

HCC!portal HTN, varicesencephalopathyascites

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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- SMOKINGFamily historyEndocrine disordersDrugs (NSAIDS, amioderone)(- past bypass)

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54
Q

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

A

ConstipationDrugs GI bleedInfectionHYPO: natreamia, kalaemia, glycaemiaAlcohol withdrawalOther (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)InfectionGI bleedingMyoglobinuria (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 / hypoglycaemiaIntracranial event

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58
Q

Bedside tests for encephalopathy

A

Serial 7’sWORLD backwardsAnimal counting in 1 minuteDraw 5 point starNumber 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 - immunoglobulinsBiochemistry - iron studies - copper studies - caeruloplasmin (serum copper transport protein) - 24 hr urine copper - α1-antitrypsin level - lipids, glucoseRadiological investigations - USS / CT / MRIBiopsy 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 asympother wise - liver failureCOMPLICATION = Cirrhosis

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62
Q

Diagnosis/treatment of autoimmune liver disease

A

Raised IgGAutoantibodies (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); inflammationTREAT WITH STEROIDS (prednisolone) + IMMUNOSUPPRESSANTS (AZATHIOPRINE)- or liver transplant

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63
Q

Risk factors for Primary Biliary cholangitis (PBC)

A

FEMALE40-50 y/oOther autoimmune/rheumatoid diseaseSmoking

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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 INFLAMMATIONCHOLESTASIS -> 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 -> XANTHELASMAAutonomic neuropathy -> correlates to fatigueAutoantibodies 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 cholestasisBIOPSY - 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/CVDCHOLESTYRAMINE 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 patientsADEK vit supplementLiver transplant

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68
Q

What is Charcot triad

A

shows BILE DUCT OBSTRUCTIONRUQ 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- IBDCOMPLICATIONS:- 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 LFTsU&E, FBCSEROLOGY - no viral, - no AMA, - USUALLY pANCA POSITIVE (anti neutrophil cytoplasmic - non-specific but present 94%)- ANA (77%)- aCL (anticardiolipin)Biopsy - ONION SKIN fibrosis around ductsGOLD 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 TRANSPLANTUDCA can also be used

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74
Q

Acute vs chronic hepatitis

A

Acute - less than 6 monthschronic - 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 LFTsNon-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 asympNon-specific (malaise, lethargy, myalgia)GI upset, Abdo painJaundice + pale stools/dark urineSigns:- Tender hepatomegaly, potentially jaundice- signs of fulminant hepatitis (acute liver failure) * bleeding, ascites, encephalopathyAbnormal LFTs- ALT/AST&raquo_space; GGT/ALP

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79
Q

Signs/symptoms of CHRONIC hepatitis

A

asymp/non-specific symptomsPotentially 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), encephalopathycomplications: 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 countriesin 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 - pruritisSELF-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 ImmunityCan’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, restMonitor liver functionFULMINANT HEP VERY RARELY- consider liver transplantVaccines 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 users1 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 ASYMPTOMATICExtra-hepatic manifestations esp neurological (meningoencephalitis, Guillian-Barre etc - confusion, coma, muscle weakness/paralysis) - may be main presentationMore 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 chronicPregnant 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 RNAPast infection - anti-HEV IgG- unreliable in immunocompromisedHEV 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) - VERTICALHorizontal:- 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 exposureHb E Ag = INFECTIVITY/viral REPLICATION (2nd)Anti Hb E Ag = LOW activity/infectivityHBV 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

SUPPORTIVEmonitor liver functionFulminant very rare- treat with ORAL NUCLEOTIDE ANALOGUES (TENOFOVIR, ENTECAVIR)- pegylated interferon alpha 2a- consider liver transplantvaccinate 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 infectiondetermines 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 weeksSIDE 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 issuesORAL 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 DNAChildhood immunisationImmuninsation of healthcare workers and other at risk groupsScreening/immunisation of sexual/household contactsBarrier contraception; PrEP (Tenofovir/Emtricitabine)Universal screening of blood productsSterile equipment/universal precautions in healthcare

103
Q

Side effects of pegylated interferon-alpha

A

Low blood countTriggers autoimmune conditionsHair thinning, skin/GI problemsFlu like symptomsMental health issues

104
Q

Side effect of TDF? What does TDF stand for

A

Tenofovir DIsoproxil Fumeratea 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 birthAt 4 weeksAt 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 DNABaby 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 virusCan 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 HCCthan in just Hep B infection

114
Q

Investigations for Hep D

A

Hep D antibodyif pos -> test for Hep D RNA

115
Q

Treatment for Hep D

A

Pegylated interferon-a - 48 weeksTenofovir 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, Diarrhoea70% chance of becoming CHRONIC- Usual CHRONIC LIVER SIGNS15-30% chance of becoming cirrhotic within 20 yearsMost 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 treatmentCheck 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/genotypeVenous (/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 TOLERATEDDIRECTLY 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 G4Glecaprevir/Pibretasvir - ALL (1-6)Ledipasvir/Sofosbuvir - all but G3Sofosbuvir/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 IMMUNITYScreening blood productsUniversal precautions when handling bodily fluidsSterile equipment/safe disposal- provision of sterile injecting equipmentOptiate addiction treatmentTreat/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 acidBile - 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 lessPersistant - >14 but <30 daysChronic > 30 daysDevided 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 anaerobesAMOEBIC:- 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 + alcoholGALLSTONES 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 defAlcohol = 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/symptomsBloods:- RAISED SERUM AMYLASE (gold)- RAISED SERUM LIPASE (more specific than amylase)- CRP raisedABDO US (diagnostic for gallstones) - CT/MRI to see extent of damage_Need at least 2 of above to diagnose_Urinalysis - raised urine amylaseAlso:- 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 48HRGlasgow 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 = mild2 = moderate3 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 SYNDROMEhas 2/more of following:- TACHYCARDIA (>90 bpm)-TACHYPNOEA (>20 resp rate)- PYREXIA (>38 C)- RAISED WCCCan 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 DMStrictures -> 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 THROMBUSIntrahepatic:- CIRRHOSIS (main in uk)- SCHISTOSOMIASISPost-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 VEINCirrhosis -> 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- malignancyAcute 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 examUsually ASCITES

150
Q

Diagnosis of peritonitis

A

Bloods:- RAISED ESR/CRP, WCC- U + E- ASCITIC TAP: -> NEUTROPHILIA -> CULTURES - causative organismEXCLUDE:- 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)- ParacentesisSurgery:- PERITONEAL LAVAGE (surgical clean out)(treat underlying cause when stable enough to do so)

152
Q

Complications of peritonitis

A

SEPTICEMIA if not treated earlySubphrenic/PELVIC ABSCESSESParalytic 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

20-30g3-4g

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 SKINHEPATOMEGALYT2DM

158
Q

Diagnosis of haemochromatosis

A

IRON STUDIES:- Raised seurm Fe- RAISED FERRITIN- RAISED TRANSFERRIN SAT- Low TIBCGENETIC 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 historyMALE50s(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; hepatitisBrain 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, MUSHROOMlast 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 chestCHARACTERISTIC: - YOUNG/MID AGE MALE - LITTLE/NO SMOKING Hx - COPD SYMPTOMSLiver 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/LExudates - fluid with protein >25 g/L (cloudy)

174
Q

Transudate causes of Ascites

A

PORTAL HTN (thrombosis/cirrhosis)HIGH CENTRAL VENOUS Pa - CONGESTIVE HFLOW PLASMA PROTEIN conc:- Malnutrition- Nephrotic syndrome- Protein losing enteropathy

175
Q

Exudate causes of ascites

A

MALIGNANCYTBPACREATIC ASCITESBudd-Chiari syndrome(inflammation or post hepatic congestion)

176
Q

Presentation of ascites

A

Abdo DISTENSIONNausea, LOSS of APPETITECONSTIPATIONCachexia - apparent wastingPAIN/DISCOMFORT -> MALIGNANTsymptoms of underlying cause (oedema, jaundice)may get UMBILICAL HERNIA

177
Q

Functions of peritoneum in health

A

Visceral lubricationFluid + 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 ductTHERE IS MORE, FILL THIS IN
183
Q

Tumour marker for pancreatic cancer

A

Ca 19-9

184
Q

What is ALP particularly related to

A
  • Gallbladder- BONE
185
Q

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

A

GGT (liver enzyme) will be present in liver pathology

186
Q

Functions of the Liver

A
  • Detoxification- Clotting factor production- Bilirubin regulation- METABOLISES CARBS- ALBUMIN production- IMMUNITY + Kupffer cells- OESTROGEN REGULATION
187
Q

What happens when Liver function goes wrong

A

Oestrogen regulation issues:- Gynaecomastia in men- Spider naevi- Palmar erythemaDetoxification issues- Hepatic encephalopathyCarb metabolism:- HYPOGLYCAEMIAAlbumin production issues:- OEDEMA- LEUKONYCHIA (white nails)- ASCITESClotting issues:- Easy bleeding/bruisingBilirubin issues:- Pruritis- Jaundice with stool/urine changesImmunity issues:- Spontaneous bacterial infectionsReduced bile production -> reduced bile salts in lumen- DECREASED absorption of bile salts/FAT SOLUBLE VIT

188
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)

189
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

190
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
191
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
192
Q

Risk factors for Gallstones

A

5 Fs- FAT- FOURTY- FEMALE- FERTILE- Fair

193
Q

Charcot’s triad

A
  • RUQ pain- Fever- Jaundice (cholestatic)
194
Q

Reynold’s pentad

A
  • Charcot’s triad - RUQ pain - Fever - Jaundice- Sepsis/shock- confusion
195
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

196
Q

Causes of cirrhosis

A
  • AFLD- NAFLD- Hep B- Hep Cviral more common in developing, alcohol more common in developed- Haemochromatosis- Wilson’s disease- A1AT deficiency
197
Q

Presentation of cirrhosis

A

Similar to chronic liver disease/failureAscites, jaundice, hepatomegaly, splenomegaly, Spider Naevi, Palmar erythema, bruising, asterixis, caput medusae (vessels around umbilicus)

198
Q

Investigations for cirrhosis

A

FBC - thrombocytopenia, high INR, low albumin US and CT - hepatomegalyliver BIOPSY - diagnostic

199
Q

Complications of cirrhosis

A

Same as chronic liver failureAscites Portal Hypertension Varices/bleeding variceshepatic encephalopathyhepatocellular carcinoma malnutrition Jaundice Coagulopathy oedema - hypoalbuminemia

200
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

201
Q

Define Pancreatic cancer

A

Typically ADENOCARCINOMATypically in HEAD OF PANCREAS- can compress bile ducts

202
Q

Risk factors for pancreatic cancer

A

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

203
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)
204
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
205
Q

Treatment of pancreatic cancer

A
  • Surgery to remove tumour – Whipple procedure (pancreaticoduodenectomy + others)- Chemo/Radiotherapy
206
Q

Complications of pancreatic cancer

A

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

207
Q

Causes/risk factors of HCC

A

Liver Cirrhosis due to:- Viral Hepatitis (B and C), Alcohol, NAFLD, other chronic liver diseases

208
Q

Pathophys of HCC

A

Arises from liver parencyma (not connective/supportive tissue i.e hepatocytes)Metastesis to lymph nodes, lungs, (bones)

209
Q

Presentation of HCC

A

Liver specific:- Jaundice- Ascites- Pruritis- hepatic encephalopthyNon-specific:- Weight loss- Fatigue- Weakness- N+V

210
Q

DIagnosis of HCC

A
  • 1ST LINE: Abdominal ULTRASOUND - CT to confirm (GOLD STANDARD)- Serum Alpha-Fetoprotein (AFP) = tumour MARKER for HCC
211
Q

Treatment of HCC

A

Poor Prognosis - Resection of Tumour - Liver Transplant (if isolated to the liver)

212
Q

Define cholangiocarcinoma

A

A cancer arising from the BILIARY TREE - usually ADENOCARCINOMA

213
Q

Causes/risk factors of cholangiocarcinoma

A
  • Liver Fluke infections- PSC- Chronic viral Hep B/C- Liver Chirrhosis- Biliary CystsRFx:- older age- smoking- diabetes
214
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

215
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
216
Q

Treatment of cholangiocarcinoma

A
  • Surgical resection- ERCP -> place STENT (relieves symptoms)
217
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-paracetamolchronicAcute-on-chronicFulminant is rapid, severe decline
218
Q

Classic 3 acute liver failure syigns

A

Jaundice CoagulopathyEncephalopathy

219
Q

Lemon yellow skin is charcteristic of what

A

Jaundice with anaemia (yellow mixed with pallor)- pre hepatic jaundice- B12 deficiency- Haemolytic anaemia

220
Q

If AST is double ALT with GGT- suggests

A

AFLD

221
Q

If AST is less than ALT - suggests

A

NAFLD

222
Q

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

A

Metabolic disease

223
Q

PT/1.5 =

A

INR

224
Q

For liver hypocoagulopathy give

A

IV kit K

225
Q

Icteric meaning

A

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

226
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

227
Q

where does rbc breakdown occur

A

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

228
Q

how is unconjugated bilirubin transported in blood

A

attached to albumin - goes to liver

229
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

230
Q

Gilbert’s syndrome

A

AUTOSOMAL RECESSIVE - affects UDP geneMain cause of hereditary jaundice - esp in MALES- RFx: T1DM, malesDeficient/abnormal UGT (UDP-glucoronyltransferase) -> UNCONJUGATED HYPERBILIRUBINAEMIASYmp:- 30% aSx- Sudden onset Painless jaundice at young ageRelatively benign - usually ok without treatmentCrigler Najjar = more severe- jaundice w/ n+v- lethargy

231
Q

Choledocholilithiesis is what

A

Gall stones in the common bile duct

232
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

233
Q

Treatment of Crigler Najjar syndrome

A

Phototherapy - breaks down unconj bilirubin

234
Q

What would you see in Alcoholic HEPATITIS biopsy

A
  • Scarring/necrosis around central veins of liver - Mallory bodies
235
Q

Which enzymes are involved in alcohol metabolisation

A

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

236
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
237
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

238
Q

Main drug treatment for alcohol withdrawal

A

IV CHLORDIAZEPOXIDEor DIAZEPAM

239
Q

Cells responsible for liver fibrosis

A

Stellate cells

240
Q

What test is used to detect encephalopathy

A

Electroencephalogram (EEG)

241
Q

Mortality rate of of pancreatitis

A

25%

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