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h e p a t o l o g y Flashcards

1
Q

what are the causes of liver failure - acute vs chronic

A

chronic = cirrhosis
acute = Infection: Hep A/B, CMV, EBV, leptospirosis
 Toxin: EtOH, paracetamol, isoniazid, halothane
 Vasc: Budd-Chiari
 Other: Wilson’s, AIH
Obs - eclampsia, acute fatty liver of pregnancy

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2
Q

what are the signs of liver failure

A

Jaundice
 Oedema + ascites
 Bruising
 Encephalopathy= Aterixis, Constructional apraxia (5-pointed star)
 Fetor hepaticus
signs of cirrhosis or chronic liver disease

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3
Q

what investigations are required in liver failure

A 
 FBC: infection, GI bleed, ↓ MCV (EtOH)
 U+E = ↓U, ↑Cr: hepatorenal syndrome
 Urea synth in liver  poor test of renal function
 LFT
 AST:ALT > 2 = EtOH
 AST:ALT < 1 = Viral
Albumin: ↓ in chronic liver failure
PT: ↑ in acute liver failure
 Clotting: ↑INR
 Glucose
 ABG: metabolic acidosis
 Cause: Ferritin, α1AT, caeruloplasmin, Abs,
paracetamol levels
Microbiology
 Hep, CMV, EBV serology
 Blood and urine culture
 Ascites MCS + SAAG
Radiology
 CXR
 Abdo US + portal vein duplex
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4
Q

what is hepatorenal syndrome

A

dx of exclusion

renal failure in pt with advanced CLF

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5
Q

describe the pathophysiology of hepatorenal syndrome

A
  1. Cirrhosis → splanchnic arterial vasodilatation → effective circulatory volume → RAS activation → renal arterial vasoconstriction.
    Persistent underfilling of renal circulation → failure
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6
Q

how is liver failure managed

A

Manage in ITU
 Rx underlying cause: e.g. NAC in paracetamol OD
 Good nutrition: e.g. via NGT ̄c high carbs
 Thiamine supplements
 Prophylactic PPIs vs. stress ulcers

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7
Q

what clinical parameters require monitoring in liver failure

A

Fluids: urinary and central venous catheters  Bloods: daily FBC, U+E, LFT, INR
 Glucose: 1-4hrly + 10% dextrose IV 1L/12h

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8
Q

what are the complications of liver failure

A

 Bleeding: Vit K, platelets, FFP, blood
 Sepsis: tazocin (avoid gent: nephrotoxicity)
 Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt  Hypoglycaemia: regular BMs, IV glucose if <2mM
 Encephalopathy: avoid sedatives, lactulose ± enemas,
rifaximin
 Seizures: lorazepam
 Cerebral oedema: mannitol

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9
Q

what are the key points to remember when prescribing in liver failure

A

void: opiates, oral hypoglycaemics, Na-containing IVI  Warfarin effects ↑

 Hepatotoxic drugs: paracetamol, methotrexate,
isoniazid, salicylates, tetracycline

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10
Q

what are poor prognostic factors in liver failure

A 
Grade 3/4 hepatic encephalopathy
 Age >40yrs
 Albumin <30g/L
 ↑INR
 Drug-induced liver failure
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11
Q

what is cirrhosis

A

permenant scarring/ fibrosis of the liver parenchyma

leading to loss of elasticity of liver and impaired organ architecture

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12
Q

what are the common causes of cirrhosis

A

Chronic EtOH
 Chronic HCV (and HBV)
 NAFLD / NASH

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13
Q

what are other causes of cirrhosis

A

Genetic: Wilson’s, α1ATD, HH, CF
 AI: AH, PBC, PSC
 Drugs: Methotrexate, amiodarone, methyldopa,
INH
 Neoplasm: HCC, mets
 Vasc: Budd-Chiari, RHF, constrict. pericarditis

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14
Q

what are the HAND signs on examination seen in pt with cirrhosis

A 
Clubbing (± periostitis)
 Leuconychia (↓ albumin)
 Terry’s nails (white proximally, red distally)
 Palmer erythema
 Dupuytron’s contracture
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15
Q

what are the FACE signs on examination seen in pt with cirrhosis

A

Pallor: ACD
 Xanthelasma: PBC
 Parotid enlargement (esp. ̄c EtOH)

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16
Q

what are the TRUNK signs seen in cirrhosis on examination

A

Striae
 Hepatomegaly (may be small in late disease)
 Splenomegaly
 Dilated superficial veins (Caput medusa)
 Testicular atrophy

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17
Q

what are the complications associated with cirrhosis

A
  1. decompensation to hepatic failure
  2. SBP
  3. portal HTN
  4. increased risk of HCC
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18
Q

what are the signs of hepatic failure

A 
Jaundice (conjugated)
 Encephalopathy
 Hypoalbuminaemia → oedema + ascites
 Coagulopathy → bruising
 Hypoglycaemia
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19
Q

what Lx are required in cirrhosis

A 
 FBC: ↓WCC and ↓ plats indicate hypersplenism  ↑LFTs
 ↑INR
 ↓Albumin
Find Cause
 EtOH: ↑MCV, ↑GGT
 NASH: hyperlipidaemia, ↑ glucose
 Infection: Hep, CMV, EBV serology
 Genetic: Ferritin, α1AT, caeruloplasmin (↓ in Wilson’s)  Autoimmune: Abs (there is lots of cross-over)
 AIH: SMA, SLA, LKM, ANA  PBC: AMA
 PSC: ANCA, ANA
 Ig: ↑IgG – AIH, ↑IgM – PBC
 Ca: α-fetoprotein
Abdo US + PV Duplex

 Ascites Ascitic Tap + MCS
Liver biopsy

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20
Q

describe the general management of cirrhosis

A 
Good nutrition
EtOH abstinence: baclofen helps ↓ cravings Colestyramine for pruritus
Screening
 HCC: US and AFP
 Oesophageal varices: endoscopy
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21
Q

describe specific management of cirrhosis

A

HCV: Interferon-α
 PBC: Ursodeoxycholic acid
 Wilson’s: Penicillamine

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22
Q

what score is used to grade cirrhosis

A

child-pugh grading of cirrhosis

predicts risk of bleeding, mortality and need for Tx
 Graded A-C using severity of 5 factors
 Albumin
 Bilirubin
 Clotting
 Distension: Ascites
  Encephalopathy

score above 8 = significant risk for vatical bleeding

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23
Q

what are the causes of portal HTN

A

Pre-hepatic: portal vein thrombosis (e.g. pancreatitis)
 Hepatic: cirrhosis (80% in UK), schisto (commonest
worldwide), sarcoidosis.
post hepatic = Budd-chiari, RHF, constrictive pericarditis

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24
Q

what are the portosystemic anastomoses and their effect

A

oesophageal varices = Portal (left and short gastric veins), systemic (inferior oesophageal veins)

caput medusae = (portal) peri umbilical veins, systemic (superficial abdo wall veins)

haemorrhoids = (portal) superficial rectal veins, systemic (inferior and medial rectal veins)

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25
Q

describe the pathophysiology behind encephalopathy

A

↓ hepatic metabolic function
 Diversion of toxins from liver directly into systemic
system.
 Ammonia accumulates and pass to brain where
astrocytes clear it causing glutamate → glutamine
 ↑ glutamine → osmotic imbalance → cerebral oedema

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26
Q

describe how encephalopathy is graded

A

1: Confused – irritable, mild confusion, sleep inversion
 2: Drowsy – ↑ disorientated, slurred speech, asterixis
 3: Stupor – rousable, incoherence
 4: Coma – unrousable, ± extensor plantars

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27
Q

how do pt with encephalopathy present

A 
Asterixis, ataxia
 Confusion
 Dysarthria
 Constructional apraxia
 Seizures
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28
Q

what are the precipitant of encepatholopathy

A

HEPATICS

Haemorrhage: e.g. varices
 Electrolytes: ↓K, ↓Na
 Poisons: diuretics, sedatives, anaesthetics
 Alcohol
 Tumour: HCC
 Infection: SBP , pneumonia, UTI, HDV
 Constipation (commonest cause)
 Sugar (glucose) ↓: e.g. low calorie diet
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29
Q

what investigation required in encephalopathy

A

increased plasma NH4

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30
Q

how is encephalopathy managed

A

lactulose and PO4 enemas to reduce nitrogen forming bowel bacteria = 2-4 soft stool/ d

consider rifaximin PO to kill intestinal microflora

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31
Q

describe the sequelae of portal HTN

A

SAVE

Splenomegaly
 Ascites
 Varices
 Encephalopathy

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32
Q

what is ascites and what are the sx

A

Back-pressure → fluid exudation
 ↓ effective circulating volume → RAS activation
 (In cirrhosis: ↓ albumin → ↓ plasma oncotic pressure and aldosterone metabolism impaired)

Distension → abdominal discomfort and anorexia  Dyspnoea
 ↓ venous return

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33
Q

what is used to find ddx for ascites

A

Serum Ascites Albumin Gradient (SAGG)

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34
Q

what are the causes of SAAG grater than 1.1g/dL

A

SAAG ≥1.1g/dL = Portal HTN (97% accuracy)
 Pre-, hepatic and post
 Cirrhosis in 80%

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35
Q

what are the causes of SAAG less than 1.1g/dL

A

Other Causes
 Neoplasia: peritoneal or visceral (e.g. ovarian)  Inflammation: e.g. pancreatitis
 Nephrotic Syndrome
 Infection: TB peritonitis

36
Q

what ix are required in pt with ascites

A

Bloods: FBC, U+E, LFTs, INR, chronic hepatitis screen
 US: confirm ascites, liver echogenicity, PV duplex
 Ascitic tap
 MCS and AFB
 Cytology
 Chemistry: albumin, LDH, glucose, protein  SAAG = serum albumin – ascites albumin
 Liver biopsy

37
Q

how to manage pt with ascites

A

Daily wt. aiming for ≤0.5kg/d reduction
 Fluid restrict <1.5L/d and low Na diet
 Spironolactone + frusemide (if response poor)
 Therapeutic paracentesis ̄c albumin infusion (100ml 20% albumin /L drained)
 Respiratory compromise  Pain / discomfort
 Renal impairment
 Refractory: TIPSS

38
Q

SBP presents with

A

Pt. ̄c ascites and peritonitic abdomen

39
Q

most common pathogens causing SBP

A

E. coli, Klebsiella, Streps

40
Q

describe the management of SBP

A

Rx: Tazocin or cefotaxime until sensitivities known

 Prophylaxis: high recurrence  cipro long-term

41
Q

what are the systemic effects of alcoholism

A 
Hepatic
 Fatty liver → hepatitits → cirrhosis
 AST:ALT >2, ↑ GGT
GIT
 Gastritis, erosions
 PUD
 Varices
 Pancreatitis
 Carcinoma
CNS
 Poor memory / cognition
 Peripheral polyneuropathy (mainly sensory)
 Wernicke’s encephalopathy
 Confusion
 Ophthalmoplegia (nystagmus, LR palsy)  Ataxia
 Korsakoff’s: amnesia → confabulation
 Fits, falls
Heart
 Arrhythmias: e.g. AF
 Dilated cardiomyopathy
 ↑BP
Blood
 ↑MCV
 Folate deficiency → anaemia
42
Q

how is alcoholism dx

A 
CAGE
Cut down?
 Annoyed by people’s criticisms
 Guilty about drinking
 Eye opener?
43
Q

what are the sx and signs of etoh withdrawal

A

presenting 10-72h after last drink

signs = increased HR, reduced BP, tremor, confusion, fits, hallucinations esp formication

44
Q

how is alcohol withdrawal management

A

tapering regimen of chlordiazepoxide PO / lorazepam IM

 Thiamine

45
Q

describe the long term management of alcoholism

A

Group therapy or self-help (e.g. AA)
 Baclofen: ↓ cravings
 Acamprosate: ↓ cravings
 Disulfiram: aversion therapy

46
Q

how does alcoholic hepatitis present

A 
Anorexia
 D/V
 Tender hepatomegaly
 Ascites
 Severe: Jaundice, bleeding, encephalopathy
47
Q

what Ix are required in alcoholic hepatitis

A

 Bloods: ↑MCV, ↑GGT, AST:ALT>2
 Ascitic tap
 Abdo US + PV duplex

48
Q

management for alcoholic hepatitis

A 
Stop EtOH
 Rx withdrawal
 High dose B vitamins: Pabrinex
 Optimise nutrition
 Daily wt., LFT, U+E, INR
 Mx complications of failure
49
Q

what are the types of viral hepatitis, their spread and cause

A 
a = FO = seafood esp abroad
b = IV = blood, body fluids and babies - vertical 
c = IV = blood, less vertical 
d = iV dependen on prior HBV
e = FO in developing world
50
Q

what are the different phases of viral hepatitis and how each stage presents

A

pro dromal phase - seen particularly in HAV and BV. Flu-like, malaise, arthralgia, nausea

icteric phase - Hepatitis
 Abdo pain
 Hepatomegaly
 Cholestasis: dark urine, pale stools

chronic phase - Mainly HCV and childhood HBV

51
Q

Ix needed in viral hepatitis?

A

FBC, LFTs, clotting

 Hep A/B/C serology

52
Q

how do you managed viral hepatitis

A

supportive
 No EtOH
 Avoid hepatotoxic drugs (e.g. aspirin)

 Anti-viral = Indicated in chronic disease
 HBV: PEGinterferon
 HCV: PEGinterferon + ribavarin

53
Q

what is NAFLD

A

Cryptogenic cause of hepatitis and cirrhosis assoc. ̄c insulin resistance and the metabolic syndrome.

(NASH) is most extreme form and → cirrhosis

54
Q

Rx for NAFLD

A

Obesity
 HTN
 T2DM
 Hyperlipidaemia

55
Q

Presentation of NAFLD

A

Mostly asymptomatic

 Hepatomegaly and RUQ discomfort may be present.

56
Q

what is metabolic syndrome

A

Central obesity (↑ waist circumference) and two of:  ↑ Triglycerides
 ↓ HDL
 HTN
 Hyperglycaemia: DM

57
Q

Lx required in NAFLD

A

BMI
 Glucose, fasting lipids
 ↑ transaminases: AST:ALT <1  Liver biopsy

58
Q

Management for NAFLD

A

Lose wt.

 Control HTN, DM and lipids

59
Q

what is HH, describe the pathophysiology

A

hereditary haemochromatosis.

Inherited, multisystem disorder resulting from abnormal iron metabolism

 ↑ intestinal Fe absorption (↑ enterocyte DMT + ↓ hepatocyte hepcidin) → deposition in multiple organs.

60
Q

what are the clinical features of HH

A

iron MEALS

Myocardial
 Dilated cardiomyopathy  Arrhythmias

Endocrine
 Pancreas: DM
 Pituitary: hypogonadism → amenorrhoea, infertility
 Parathyroid: hypocalcaemia, osteoporosis

Arthritis
 2nd and 3rd MCP joints, knees and shoulders

Liver
 Chronic liver disease → cirrhosis → HCC
 Hepatomegaly

Skin = slate grey discolouration

61
Q

Lx in HH?

A

Bloods: ↑LFT, ↑ ferritin, ↑Fe, ↓TIBC, glucose, genotype
 X-ray: chondrocalcinosis
 ECG, ECHO
 Liver biopsy: Pearl’s stain to quantify Fe and severity
 MRI: can estimate iron loading

62
Q

how is HH managed

A 
Iron removal
 Venesection: aim for Hct <0.5
 Desferrioxamine is 2nd line
General
 Monitor DM
 Low Fe diet
Screening
 Se ferritin and genotype
 Screen 1st degree relatives
Transplant in cirrhosis
63
Q

prognosis of HH

A

enesection returns life expectancy to normal if non- cirrhotic and non-diabetic

 Cirrhotic patients have >10% chance of HCC

64
Q

describe the pathophysiology behind autoimmune hepatitis

A

Inflammatory disease of unknown cause characterised by Abs directed vs. hepatocyte surface antigens
 Predominantly young and middle-aged women

65
Q

prevention of AIH

A 
Teens and early 20s (25%)
 Constitutional: fatigue, fever, malaise 
 Cushingoid: hirsute, acne, striae
 Hepatitis
 HSM
 Fever
 Amenorrhoea
 Polyarthritis
 Pulmonary infiltration  Pleurisy
66
Q

lx in AIH

A 
↑LFTs
 ↑IgG
 Auto Abs: SMA, LKM, SLA, ANA
 ↓WCC and ↓plats = hypersplenism
 Liver biopsy
67
Q

management of AIH

A

Immunosuppression
 Prednisolone
 Azathioprine as steroid-sparer
 Liver transplant (disease may recur)

68
Q

how do you manage paracetamol overdose? Lx

A

NAC - N-acetyl cysteine acts as glutathione replacement

paracetamol levels in blood

69
Q

describe paracetamol overdose

A
  1. paracetamol is an antipyretic and analgesic. active ingredient is NAPQI
  2. NAPQI is toxic to liver if accumulates. oxidises hepatic enzymes and causes necrosis and apoptosis
  3. if overdose, reduction in glutathione which is used to neutralise the toxin.
70
Q

describe paracetomol overdose sx

A

bdominal pain, vomiting in first 24hrs

71
Q

what tool is used to assess malnutrition

A

MUST. nutritional tool. 1. calculate BMI. 2. calculate weight loss 3. establish acute disease effect and score. 4. overall risk of malnutrition. 5. use management guidelines to develop care plan.

72
Q

management based on MUST tool malnutrition

A

management = refer to dietician if high risk. low risk = no action. medium risk monitor. high risk = manage.

73
Q

options for nutritional support

A
  1. nutritional support = meal times should not be interrupted and high calorie options encouraged.
  2. some supplements = fortisips to give macro and micro minerals required
  3. unsafe swallow or non-functiong GI tract = NGT, PEG/RIG/PEGJ/RIGJ, parenteral nutrition.
74
Q

short term nutritional support and caution

A
  1. NGT short term for supplementary feeding or can be used on top pt usual oral intake. need to check pH prior to ensure tip in stomach and not in lungs and this can be used. this can be affected by PPI’s so a CXR may be required.
  2. NGT can be useful for pt with swallowing difficulty - decrease aspiration on food but pt can still aspirate on saliva.
75
Q

option for medium to long term nutritional support

A
  1. medium or long term feeding - requires puncturing the stomach. PEG, PEGJ, RIGJ, RIG.
  2. Parenteral nutrition = nutrition and fluids directly into pt veins. indicated if GIT not accessible or not working. given via PICC line (central line). risk of line sepsis and liver dysfunction.
76
Q

which drugs can cause a hepatocellular picture in drug induced liver disease

A 
paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin
77
Q

which drugs can cause a cholestatic picture in drug induced liver disease

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine

78
Q

GAMED antibodies in body

A

G = long life in body, years , and highest amount
A
M = produced in infection initially until IgG has been produced
E
D

79
Q

what are the 3 antigens of hepatitis B

A

surface antigen HBsAg
core antigen HBcAg
E antigen HBeAg

80
Q

what does HbsAg represent

A

HbsAg = s for sx
this is what the body wants ro get rid of

HBsAg vs IgG-HBsAg

81
Q

what does HBeAg represent

A

e = marker of viral replication

marker of infectibility or transmission

82
Q

how does body produce Ig against Hep b

A

it takes a while for IgG to be produced about 6 months

so body produces IgM’s and then IgG
Igm-HBCAg and later IgG HbcAg

83
Q

patient with hep b is cured when

A

IgG-HBsAg present

84
Q

if pt has HBsAG is present it means

A

current infection = acute to chronic

85
Q

if pt has IgG HBsAg present it means

A

you have won

either cured or vaccinated

86
Q

if IgG HBsAg is positive with positive IgG GBcAg it means

A

cured previous infection

87
Q

if IgG HBsAg is positive with negative IgG GBcAg it means

A

vaccinated

M E D (18 decks)

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