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Year 3 Medicine Block > GI: Liver disease > Flashcards

GI: Liver disease Flashcards

1
Q

Alcoholic liver disease has 3 stages of liver damage. What are they?

A
  1. Fatty liver (steatosis)
  2. Alcoholic hepatitis (inflammation and necrosis)
  3. Alcoholic liver cirrhosis
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2
Q

What risk factors may be present in a patient attending your clinic with alcoholic liver disease?

A

Prolonged heavy alcohol consumption
Hep C
Female

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3
Q

How may a patient with alcoholic liver disease present? (as if you were taking a Hx)

(Question made after talking to Reg in ward round about common presentations)

A

PC: Right upper quadrant abdominal pain. Sudden onset (as asymptomatic to start) Nauseous. Loss of appetite. Jaundice in eyes and skin. Haematemesis, jaundice.
PMH: previous admissions with alcohol related problem. Hepatitis C.
DH: previous use of diazepam, lorazepam, disulfiram, use of thiamine.
FH: alcohol misuse in family is a potential RF. Hepatitis in family.
SH: alcohol binging, live alone, smoker (occasionally).

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4
Q

What may you find on examination of a patient with alcoholic liver disease?

A

Hepatomegaly.
Obvious distension to abdomen - ascites.
Discomfort in RUQ.
Engorged para-umbilical veins
Splenomegaly
Jaundice of sclera and skin
Palmar erythema
Spider naevi i.e Cutaneous telangiectasia (trunk, face, UL)
Asterixis - i.e. liver flap
Caput medusae
Signs of malnutrition - wasting and anorexia
Confusion

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5
Q

What are functions of the liver?

A

Stores glycogen, releases glucose, absorbs fats, fat soluble vitamins and iron, makes cholesterol.

Bile salts dissolve dietary fats
Haemaglobin breakdown into bilirubin.
Produces most clotting factors
Has Kupfer cells to engulff antigens
Excretes drugs and breaks down alcohol
Produces important proteins - albumin and binding proteins

Nutrition/metabolic Bile salts
Protein synthesis
Clotting factors
Bilirubin
Detoxification
Immune function

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6
Q

How does acute liver disease contrast to chronic liver disease?

A

Acute = no pre-existing liver disease. Chronic = starts with acute liver disease which may be asymptomatic.

Acute = resolves in 6 months. Chronic = Ongoing beyond 6 months.

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7
Q

Which conditions can cause acute liver disease?

A

Hepatits A, E, cytomegalovirus, Epstein-Barr virus, Drug induced liver injury

if present - then need to look for acute liver failure

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8
Q

Which conditions can lead to chronic liver disease?

A

Most common: Alcoholic liver disease, non-alcoholic steatohepatitis, viral hepatitis (B+C)

Less common but important:
- in women = AI hepatitis, PBC
- in men = PSC associated to IBD
- younger men = haemochromatosis
- adolescents and young adults = Wilson’s disease and anti-LKM AI hepatitis

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9
Q

Which 3 conditions are part of autoimmune liver disease?

A

Primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis.

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10
Q

What are some causes of liver cirrhosis?

A

Alcohol.
Non-alcoholic fatty liver/non-alcoholic steatohepatitis
Hep B, Hep C
Alpha-1-antitrypsin deficiency,
Methotrexate use
Haemachromatosis
Wilson’s disease
PBC
PSC

Z2F said to remember common 4:
Alcoholic liver disease, NAFLD, Hep B, Hep C

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11
Q

How does liver cirrhosis present?

A

Asymptomatic with abnormal LFTs
Tiredness,
Itching
Arthralgia
Jaundice
Ascites
Upper GI bleed
Confusion or drowsy

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12
Q

What are RF for liver cirrhosis/disease?

A

Blood transfusion before 1990.
IVDU
Operations or vaccines with non-sterile equipment
Sexual exposure
Medications
Fix of liver disease
Obesity, metabolic syndrome
Alcohol
Foreign travel

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13
Q

Name 4 visible characteristics of chronic liver disease

A

Any from:

Spider nave, leukonychia, clubbing, Dupuytren’s contracture, parotid swelling, testicular atrophy, cachexia, para-umbilical vein engorgement, mild splenomegaly.

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14
Q

What are complications of liver cirrhosis?

A

Portal HTN
Splenomegaly
Oedema,
Ascites with shifting dullness,
R sided pleural effusion, hepatic flap aka asterisks, jaundice
Hepatorenal syndrome

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15
Q

A patient has liver cirrhosis. Over the phone, the radiologist says they have a R sided pleural effusion over 500ml. On their CXR, what typical sign may you see with this volume of effusion?

A

Hepatic hydrothorax

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16
Q

What is NAFLD, and how does this differ to NASH?

A

NAFLD = non-alcoholic fatty liver disease. This is where you get deposition of fat in the liver.

NASH = is where you have deposition of fat in the liver (aka accumulation of triglycerides in the hepatocytes) AND have inflammation present as a result of this = non-alcoholic steatohepatitis.

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17
Q

Risk factors of Non Alcoholic fatty liver disease?

A

DM, Obesity, Metabolic syndrome, Familial hyperlipidaemia

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18
Q

What may you prescribe to a patient at risk of non alcoholic liver disease?

A

Oral hypoglycaemic agents e.g. Pioglitazone
social prescription - walking, lifestyle modifications.

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19
Q

You are a foundation doctor working in a Gastroenterology rotation. A medical student presents the following history:

A 39-year-old man presents for the third time in 2 years with an intermittent productive cough and increasing dyspnoea on exertion. He has a 15 pack-year smoking history, reports thick, yellow phlegm at times. His medical history reveals mild intermittent asthma controlled with a salbutamol inhaler. His symptoms have persisted despite stopping smoking, with some attacks being unresponsive to salbutamol. Physical examination reveals a generally healthy-looking male apart from fatigue. He has hepatomegaly and ascites. Spirometry shows FEV1 of 40% of predicted value. I

What are your differentials and give reasoning why? Maximum of 3 so be selective !

A

Top differential = Alpha-1 antitrypsin deficiency - productive cough, cigarette smoker, hepatomegaly, ascites. A-1-antitrypsin= inherited, causes lung and liver problems. (Why is this relevant? Can cause inflammation and cirrhosis of liver!)

COPD - long period of smoking. Spirometry results.

Bronchiectasis - daily sputum.

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20
Q

Where can varices form as a result of portal hypertension?

A

Oesophageal
Anorectal
Umbilical

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21
Q

Describe the pathophysiology of hepatorenal syndrome. (Clue: this is the development of AKI in presence of cirrhosis - from GI module with Hannah Bonfield)

A
  1. Get portal hypertension
  2. This causes arterial vasodilation (splanchnic)
  3. This activates RAAS
  4. So get renal artery vasoconstriction = reduced blood flow to the kidney
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22
Q

Define decompensated liver disease

A

Liver disease = damage to the liver which affects structure. Structure becomes distorted and get nodules and fibrosis. Synthetic, metabolic and excretory functions are affected.

Decompensated = Liver damage is so advanced that organ can not function, and clinical complications (e.g. jaundice and ascites) are present that can not be overcome.

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23
Q

What does the Child-Pugh score assess?

A

Assess prognosis/severity of cirrhosis

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24
Q

What features are included in Child-Pugh score?

A

Bilirubin, albumin, INR, ascites, encephalopathy - see pg76 Z2F

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25
What is the MELD score used for?
Used every 6months in pts with compensated cirrhosis.. Helps guide referral for liver transplant and percentage estimated 3 month mortality.
26
Why may AST and ALT levels be normal in patient with liver cirrhosis?
Not enough healthy tissue to release elevated quantities of these enzymes, so appear normal
27
What is hepatitis?
Inflammation of the liver
28
What are causes of hepatitis?
Alcoholic hepatitis - alcohol NAFLD Viral hepatitis - viruses, CMV, EBV Autoimmune Drug induced
29
What things is it important to ask when taking a history from a patient with suspected liver disease?
Did they have any blood transfusions in the UK before 1990? IVDU? Operations and vaccinations, any with dubious sterility Sexual exposure Medications Fhx of liver disease, diabetes, IBD Obesity/other features of metabolic syndrome Alchohol (?dependency) Foreign travel
30
Acute vs Chronic liver disease
Acute: Resolves within 6 months Hep A,E, CMV, EBV Drug induced liver injury Chronic: Usually starts as acute- usually asymptomatic Still effects after 6 months Can lead to cirrhosis Alcohol Hep C Non-alcoholic steatohepatitis Autoimmune
31
What is the significance of ALT and ALP
ALT- released from hepatocytes ALP- released from the ducts
32
A patient has an ALT between 100-200, what are your differentials?
Non-alcoholic hepatitis Chronic viral hepatitis Autoimmune hepatitis Drug induced liver injury
33
A patient has an ALT>500, what are your ddx?
Viral Ischaemia Toxic- any drug but most commonly paracetamol Autoimmune
34
What are your ddx in patients with a higher ALP than ALT?
Cholestatic- dilated ducts: Gallstone Malignancy Non-dilated ducts: Alcoholic hep Cirrhosis due to PSC, PBC or Alcohol Drug induced liver injury e.g. antibiotics
35
What is the stepwise progression of alcoholic liver disease?
1) Alcohol relate fatty liver- reversible 2) Alcoholic hepatitis- if mild may be reversible 3) Alcoholic cirrhosis- where normal tissue replaced with scar tissue- not reversible, but can slow progression if stop drinking, however poor prognosis if keep drinking
36
What are some complications from alcohol consumption?
Increased risk of cancer Pancreatitis Alcoholic cirrhosis and complications from that Hepatocellular carcinoma Dependence and withdrawal Alcoholic liver cirrhosis
37
What are the causes for pancreatitis?
Idiopathic Gallstones Ethanol Trauma Steroids Mumps/malignancy Autoimmune Scorpion stings Hypertriglyridaemia/hypercalcaemia ERCP Drugs e.g. thiazides
38
What are the signs of liver disease?
Jaundice Sceleral icterus Bruising Ascites Palmar erythema Spider naevi Gynacomastia Hepatomegaly Caput medusa Flapping tremor (in decompensated)
39
What blood tests would you in a patient with suspected liver disease?
FBC- Increased MCV LFTs- Increased ALT and AST, increased ALP in cirrhosis, Increased bilirubin in cirrhosis, decreased albumin Coagulation Screening- Prothrombin time is increase U&Es to check for hepatorenal syndrome
40
What is hepatorenal syndrome?
Happens in cirrhosis Portal hypertension leads to back pressure of blood, leading to vasodilators being released This leads to arterial vasodilation which leads to a drop in pressure This leads to RAAS being activated and so you get vasoconstriction of the renal arteries, leading to reduced blood flow to the kidneys
41
What imaging would you use in a patient with liver disease?
USS- to detect any fatty changes and detect any changes related to cirrhosis Fibroscan- elasticity of the liver and measures the degree of cirrhosis CT/MRI- check for fatty infiltration, hepatocellular carcinoma, hepatosplenomegaly
42
When would a biopsy be indicated in a patient with liver disease?
When considering starting steroids
43
What is the general management in a patient with alcoholic liver disease?
* Alcohol abstinence + withdrawl treatment: IV diazepam 10mg (long acting), use short acting in older pts/ hepatic dysfunction * Weight reduction + smoking cessation * Thiamine (to prevent W-K) and high protein diet ( be aware of refeeding syndrome) * Influenza and pneummococcal vaccines * Treat complications of cirrhosis * Consider prophylatic abx in some pts to prevent SBP * Steroids- short term (1 month) in severe alcoholic hepatitis * Liver transplant, but patient has to be sober for 3-6 months
44
How does alcohol withdrawal present?
6-12hrs- craving, anxiety, sweats, headache 12-24hrs- hallucinations 24-48hrs-seizures- usually at 36hrs 48-72hrs- delirium tremens
45
What is the pathophysiology of delirium tremens?
In alcohol dependency GABA receptors gets upregulated and glutamate receptors gets down regulated, so when you stop, you have under functioning of GABA and over functioning of Glutamate leading to increased excitability, causing delirium tremens
46
What are the symptoms of delirium tremens?
Severe agitation Confusion Delirium and hallucinations Tachycardia hypertension hyperthermia Ataxia
47
How you manage alcohol withdrawal?
Chlordiazepoxide (benzo)- reducing regime 10-40mg, 1-4hrs depending on patients needs Pabrinex- high dose IV B vitamins and then followed by thiamine (oral) Lactulose- to remove ammonia
48
Why is thiamine so important to replace in alcohol dependency?
To prevent Wernicke-Korsakoff syndrome
49
What is Wernicke Korsakoff Syndrome?
Made up of Wernicke encephalopathy which comes first- confusion, oculomotor disturbances, ataxia- medical emergency Korsakoffs syndrome- comes after Anterograde and retrograde memory loss Behaviour changes Irreversible and patient needs to be institutional care
50
Characteristic findings in alcoholic hepatitis ?
AST/ALT ratio is 2:1 in alcoholic hepatitis e.g. AST - 790 ALT- 375 + Macrocytic anaemia (raised MCV) + Raised GGT Present: RUQ pain, jaundice, and signs of liver failure
51
What is liver cirrhosis?
Result of chronic inflammation of the liver--> scar tissue and nodules. Causes resistance in the vessels going to the liver, resulting in back pressure
52
What are the most common causes of liver cirrhosis?
Alcoholic liver disease Non-alcoholic liver disease Hep B Hep C
53
What are the less common causes of liver cirrhosis?
Autoimmune hepatits Primary biliary cirrhosis Haemochromatosis Wilsons disease Alpha-1-antitrypsin deficiency CF Drugs e.g. amiodarone, methotrexate and sodium valproate
54
What are the signs of liver cirrhosis?
Jaundice- due to high bilirubin Hepatomegaly - however may be smaller the more cirrhotic it gets Splenomegaly- due to portal hypertension Spider naevi Palmar erythema- caused by hyper dynamic circulation Gynaecomastia and testicular atrophy in males due to endocrine dysfunction Bruising- due to abnormal clotting Ascites Caput medusa-due to portal hypertension Flapping tremor
55
What investigations would you do for liver cirrhosis?
LFTs- often normal but in decompensated cirrhosis, they're often deranged Albumin- drop Prothrombin time- increases Both useful for synthetic function of the liver Hyponatraemia- fluid retention in severe disease Urea and creatinine become deranged in hepatorenal syndrome Further bloods can help establish the cause Alpha-fetoprotein- tumour marker for hepatocellular carcinoma, can be checked every 6 months in patients with cirrhosis as a screening tool
56
How do you interpret the results of the Enhanced liver fibrosis blood test?
<7.7 -none to mild fibrosis > or equal to7.7-9.8- moderate fibrosis > or equal to 9.8- severe fibrosis
57
What would an USS show in a pt with liver cirrhosis?
Nodularity of liver surface Corkscrew appearance to hepatic arteries Enlarged portal vein with reduced blood flow Ascites Splenomegaly
58
What does fibroscan measure?
Liver elasticity, therefore helps assess degree of cirrhosis Done every 2 years in high risk pts: Hep C Heavy alcohol drinkers Diagnosed alcoholic liver disease
59
What is the general management of liver cirrhosis?
USS and alpha-fetoprotein every 6 months to screen for heptocellular carcinoma Endoscopy every 3 years for pt with known varices High protein, low sodium diet MELD score every 6 months Consider liver transplant Manage complications
60
Why does liver cirrhosis relate to malnutrition
Increase use of muscle tissue as fuel and reduces amount of protein available in body for muscle growth . Disrupts ability of liver to store glucose as glycogen and release it when required = body using muscle tissue as fuel--> muscle wasting and weight loss
61
Management of malnutrition secondary to cirrhosis?
Meals every 2-3 hours Low Na diet-->minimise fluid retention High protein and high calorie diet Avoid alcohol
62
Sites of varices?
Gastro-oesophageal junction Ileocaecal junction Rectum Ant abdo wall via umbilical vein (caput medusa)
63
Treatment of stable varices?
Propranolol reduces protein hypertension by acting as a non-selective B blocker Elastic band ligation of varices Injection of sclerosant (less effective than band ligation)
64
What is TIPS?
Trans intra-hepatic portalsystemic shunt X-ray guided wire into jugular vein-->vena cava-->liver via hepatic vein. Connection between hepatic vein and portal vein and place stent--> relieves pressure in portal system When other treatments fail or bleeding cannot be controlled
65
What is ascites?
Fluid in peritoneal cavity Increased pressure in portal system forces fluid out into peritoneal cavity--> drop circulating volume--> reduced BP--> RAAS activated--> aldosterone leads to increased fluid and sodium reabsorption--> fluid and sodium overload
66
Management of ascites?
Anti-aldosterone diuretics--> Spironolactone Paracentesis if tense Low Na diet Prophylactic antibiotics agains SBP--> ciprofloxacin or norfloxacin in pts with less than 15g/L of protein Consider TIPS in refractory ascites Consider liver transplant in refractory ascites
67
Prophylatic antibiotic in liver cirrhosis against SBP?
ciprofloxacin or norfloxacin
68
Presentation of SBP?
Can be asymptomatic Fever Abdo pain Raised WCC, CRP, creatinine or metabolic acidosis Ileus hypotension
69
Most common organisms in SBP?
Escherichia Coli Klebsiella pneumoniae Gram positive cocci- staphylococcus or enterococcus
70
Management of SBP?
Ascitic culture before giving antibiotics IV cephalosporin e.g. cefotaxime
71
What is hepatic encephalopathy?
Build up of toxins that affect the brain e.g. ammonia
72
Why do you get build up of ammonia in liver cirrhosis?
Builds up due to liver unable to metabolise the ammonia and collateral vessels between portal and systemic circulation mean that the ammonia bypasses liver all together
73
Precipitating factors of hepatic encephalopathy?
Constipation Electrolyte disturbances Infection GI bleeding high protein diet Medications
74
Presentation of hepatic encephalopathy?
Reduced consciousness and confusion Chronically--> personality changes, memory and mood
75
Management of hepatic encephalopathy?
Laxatives e.g. lactulose, dose appropriately so patient has 2-3 motions a day Rifaximin- antibiotic--> reduces ammonia producing bacteria Nurtrional support
76
Investigations fo NAFLD?
1st line-Enhanced liver fibrosis blood test 2nd line- NAFLD fibrosis score 3rd line- Fibroscan
77
Management for NAFLD?
Weight loss Exercise Stop smoking Control of diabetes, BP and cholesterol Avoid alcohol
78
Presentation of hepatitis?
Asymptomatic or vague symptoms Abdominal pain Fatigue Pruritis Muscle and joint aches Nausea and vomitting Jaundice Fever (viral hepatits)
79
Epidemiology of Hep A?
Most common hep worldwide but relatively rare in UK
80
Transmission of Hep A?
Faecal oral route usually in contaminated water?
81
What type of virus is Hep A?
RNA
82
Presentation of Hep A?
Nausea, vomitting, jaundice and anorexia Cholestasis- dark urine and pale stools Moderate hepatomegaly
83
Management of Hep A?
Basic analgesia Resolves without treatment 1-3 months
84
Prevention of Hep A?
Vaccination and it is a notifiable disease
85
What type of virus is Hep B?
DNA
86
Transmission of Hep B?
Direct contact with blood or bodily fluids, sharing household items e.g. toothbrush Vertical transmission
87
Prognosis of Hep B?
Most people fully recover in 1-2 months 10-15% become chronic hepatitis B carriers--> virus DNA integrated into their own DNA
88
Viral markers and their relevance in Hep B?
Surface antigen (HBsAg)- active infection E Antigen (HBeAg)- marker of replication--> high infectivity Core antibodies (HBcAb)- past or current infection Surface antibody (HBsAb)- vaccination or past or correct infection Hep B virus DNA(HBV DNA)- direct count of viral load
89
How can Core antibodies in hep B determine past or current infection?
Look at IgM or IgG. IgM--> high in acute infection and low in chronic infection IgG--> past infection where HBsAg is negative
90
Outline the Hep B vaccine?
Inject HBsAg 3 doses at different intervals Check of HBsAb Included as past of UK routine
91
Management of Hep B?
Low threshold for screening at risk patients Screen for other blood borne viruses and other sexual transmitted disease Reder to GI/hepatology or infectious disease for specialist management Notify public health England Stop smoking and alcohol Education- transmission and at risk contacts Test for complications Antiviral medication to slow disease progression and reduce infectivity Liver transplant for end stage liver disease
92
What type of virus is Hep C?
RNA
93
Transmission of Hep C?
Blood and bodily fluids
94
Disease course of Hep C?
1 in 4--> full recovery 3 in 4--> chronic
95
Complications of Hep C?
Liver cirrhosis Hepatocellular carcinoma
96
How do you test for Hep C?
Hep C antibody screening test Hep C RNA testing used to confirm the diagnosis of Hep C, calculate viral load and assess for the individual genotype
97
Management of Hep C?
direct acting antivirals- tailored to specific genotype--> successful in over 90% patients, take 8-12 weeks Low threshold for screening at risk patients Screen for other blood borne viruses and other sexual transmitted disease Reder to GI/hepatology or infectious disease for specialist management Notify public health England Stop smoking and alcohol Education- transmission and at risk contacts Test for complications Liver transplant for end stage
98
What are the two types of Autoimmune hepatitis?
Type 1: occurs in adults Type 2: occurs in children
99
How does type 1 autoimmune hepatitis present? Who does it often affect?
Women around 40s-50s or around the menopause with fatigue and features of disease on examination
100
How does type 2 autoimmune hepatitis present?
Teenage years or early 20s with high transaminases and jaundice
101
Type 1 autoimmune hep antibodies?
Anti nuclease antibodies- ANA Anti- smooth muscle antibodies- Anti- actin Anti-soluble liver antigen- anti-SLA/LP
102
Type 2 autoimmune hep antibodies?
Anti-liver kidney microsomes-1 (anti-LKM1) Anti-liver cytosol antigen type 1 (Anti-LC1)
103
Parameters in MELD score?
A patient's bilirubin, creatinine, and the international normalized ratio (INR) to predict survival.
104
Define acute liver failure
Rapid onset of hepatocellular dysfunction. Leads to a variety of systemic complications.
105
Common causes of acute liver failure
Paracetamol overdose Alcohol Viral hepatitis - usually Hep A or Hep B Acute fatty liver of pregnanvy
106
Features of acute liver failure?
Jaundice Hypoalbuminaemia Hepatic encephalopathy Renal failure is common - hepatorenal syndrome
107
Investigations for acute liver failure (ALF) and why?
1) LFTs: would be raised: Bilirubin = Jaundice is a defining feature of acute liver failure - so look for hyperbilirubinaemia AST and ALT = high in paracetamol hepatotoxicity 2) INR = coagulopathy is a defining feature of ALF 3) U+Es = renal failure common in ALF 4) FBC - high WCC for infection.Thrombocytopenia common. Anaemia common 5) Cross match and G+S = may need blood transfusion 6) ABG = metabolic acidosis in paracetamol overdose
108
Immediate management for acute liver failure?
- Intensive care management - if hepatic encephalopathy is present plus the following if required: - liver transplant assessment - neurological status monitoring - blood glucose (every 1-2hrs), electrolytes (2x a day) and cultures monitoring. Correct if needed. - acetylcysteine if paracetamol overdose
109
Compare AST : ALT liver enzyme results in: 1. NAFLD 2. Alcoholic liver disease 3 Acute alcoholic hepatitis 4. Liver cirrhosis
1. NAFLD : ALT will be higher than AST 2. ALD: AST >2 x higher than ALT 3. Acute alcoholic hepatitis: AST>3 x higher than ALT 4. Cirrhosis: AST > 2.5 x higher than ALT In chronic hepatitis, you would expect AST to be 10x raised.
110
What are the parameters of the Child-Pugh Score ? the 5 things it look at ?
Bilirubin Albumin INR Ascites Hepatic Encephalopathy?
111
What are some risk factors for variceal haemorrhage?
High portal pressures (>12mmHg) Large varices Abnormal variceal wall at endoscopy (eg haematocystic spots) High Child-Pugh score
112
What are some complications of liver biopsy?
Shoulder tip pain Bowel perforation Renal laceration pnuemothorax billiary peritonitis
113
In what groups of people might liver biopsy be contraindicated and why?
High risk of bleeding in pts with: Large ascites Disordered platelets / clotting Not co-operative Severe cirrhosis WIth these ppl can do transjugular or laparoscopic routes
114
Treatment of chronic liver disease?
Remove underlying aetiology - e.g. stop drinking (if alcohol related), weight loss (if non-alcoholic liver steatohepatitis), antivirals (if hep B or hep C), venesection (if haemochromatosis)
115
Why is it important to treat chronic liver disease?
Prevent further liver damage and prevent progression to cirrhosis
116
Benefits of using a fibroscan for liver cirrhosis over other imaging?
Quicker More specific Can be performed in clinic room
117
What complications should you screen for in patients with liver cirrhosis? How would you screen for these?
- DEXA scan = screen for osteoporosis - USS of liver and AFP = screen for hepatocellular carcinoma
118
Pt has ascites. What investigation should be done for all pts with ascites?
Diagnostic ascitic tap (cell count and MC&S) - look for SBP.
119
Initial blood tests to do for cirrhosis and reasoning?
1) LFTs - albumin, bilirubin, liver enzymes = assess liver function 2) FBC - WCC look for infective cause, thrombocytopenia = chronic liver disease, Hb for anaemia = normocytic in Wilson's disease, oesophageal bleed or macrocytic if folate/b12 deficiency in alcohol excess 3)Urea and electrolytes to establish baseline renal function and to look for hepato-renal syndrome or any electrolyte abnormalities 4) INR - for coagulpathy 5) Others - autoantibodies - for AI hepatitis, alpha 1 antitrypsin, iron studies in haemochromatosis etc
120
What is the primary mechanism causing gynecomastia in liver cirrhosis?
Disordered metabolism of sex steroids, which leads to excess levels of oestrogen
121
What are the cardinal features of decompensation in liver disease?
Jaundice Ascites Hepatic flap Altered mental status
122
If a pt drinks around 2 litres of cider (ABV 5%) a day. How many units is that a week?
Alcohol units = volume (ml) * ABV / 1,000 2000 ml x 5% = 10,000 Divide this figure by 1,000 to get the number of units = 10,000/1,000 = 10 units/day 10 units/day x 7 days = 70 units
123
What LFT results would you expect in a patient with autoimmune hepatitis?
Raised ALT and bilirubin Normal/mildly raised ALP. May be IgG predominant hypergammaglobulinemia.
124
What are the drug causes of pancreatitis?
Azathioprine Sulfasalazine Valproate Statins ACE inhibitors Oral contraceptives
125
What is ischaemic hepatitis?
diffuse hepatic injury resulting from acute hypoperfusion (sometimes known as 'shock liver'). It is not an inflammatory process. It is diagnosed in the presence of an inciting event (e.g. a cardiac arrest) and marked increases in aminotransferase levels (exceeding 1000 international unit/L or 50 times the upper limit of normal).
126
When to suspect ischaemic hepatitis?
* if the ALT is high: exceeding 1000 international unit/L or 50 times the upper limit of normal).AND * the pt just had a cardiac arrest * low BP * Any acute hypoperfusion * Often, it will occur in conjunction with acute kidney injury (tubular necrosis) or other end-organ dysfunction.
127
How does alcoholic liver disease MOST COMMONLY present?
* Asymptomatic elevation of aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) in a person consuming alcohol in excess
128
What is important to remember in alchoholic liver disease when it comes to presentation?
* symptoms do not reflect severity
129
130
What is the CAGE questionnaire?
* screening tool for alcohol misuse and dependency * C-Have you ever felt you needed to CUT down on your drinking? * A: Have people ANNOYED you by criticising your drinking? * G: Have you ever felt GUILTY about drinking? * E: Have you ever felt you needed a drink first thing in the morning (EYE-OPENER) to steady your nerves or get rid of a hangover?
131
What signs may a person with early stage ALD present with?
Ascites Splenomegaly Venous collateral circulations.
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Complications of ascites?
* spontaneous infection of the fluid * development of abdominal hernias * difficulty in breathing * decreased food intake * progressive malnutrition * decreased physical activity with loss of muscular mass.
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What are some physical problems people with alcohol dependency face?
**may co-exist with ALD because of chronic alcohol use.** * Poor nutritional status * muscle wasting * peripheral neuropathy * dementia * cardiomyopathy
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# In bloods: What are markers of alcohol induced liver injury?
AST and ALT * AST and ALT can be normal in the absence of significant liver inflammation (a reassuring sign) or in advanced cirrhosis * the AST level is almost always elevated (usually above the ALT level). The classic ratio of AST/ALT >2 is seen in about 70% of cases * gamma-GT is frequently elevated in heavy drinking, but is not specific for alcohol use. It is helpful in identifying patterns of alcohol misuse.
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Blood results in ALD?
* Anaemia: multiple causes, including iron deficiency, gastrointestinal bleeding, folate deficiency, haemolysis, and hypersplenism. * Leukocytosis may be from an alcoholic hepatitis-related leukemoid reaction or an associated infection. * Thrombocytopenia may be secondary to alcohol-induced bone marrow suppression, folate deficiency, or hypersplenism. * A high MCV may also indicate liver disease. * Hyponatraemia is usually present in patients with advanced liver cirrhosis. * Hypokalaemia and hypophosphataemia are common causes of muscle weakness in ALD. * Hypomagnesaemia can cause persistent hypokalaemia and may predispose patients to seizures during alcohol withdrawal. * Hyperphosphataemia predicts poor recovery in advanced liver disease. * Prolonged prothrombin time (PT) and international normalised ratio (INR) indicate diminished hepatic synthetic function in advanced liver disease with cirrhosis or liver failure in patients with ALD. * high AST and ALT
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A pt presents with ?ALD what tests do you need to do to rule things out?
* Viral hepatitis serological panel (for hepatitis A, hepatitis B, hepatitis C) * Iron studies (for haemochromatosis) and copper studies (for Wilson's disease) * Anti-mitochondrial antibody (AMA) is used to test for co-existent primary biliary cirrhosis. * ANA (anti-nuclear antibody) and ASMA (anti-smooth muscle antibody) are used to rule out the presence of associated autoimmune hepatitis. * Alpha-1 antitrypsin
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A pt with ?ALD presents, what imaging would you do?
* Ultrasound should be performed among patients with harmful alcohol use, as it helps diagnose alcoholic fatty liver disease in patients with hepatic steatosis * Fibroscan for degree of cirhossis * CT/MRI: search for a tumour in patients with an elevated alpha-fetoprotein and high clinical suspicion of HCC whose ultrasound is negative.

Year 3 Medicine Block (56 decks)

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