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Phase 2A revision > liver to work on COPY > Flashcards

liver to work on COPY Flashcards

1
Q

Give 4 causes of hepatic jaundice

A
  1. Liver disease
  2. Hepatitis - viral, drug, immune, alcohol
  3. Ischaemia
  4. Neoplasm - HCC, mets
  5. Congestions - CCF
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2
Q

Give 3 causes of post-hepatic jaundice

A

Duct obstruction

  1. Gallstones
  2. Stricture - Malignancy, ischaemia, inflammatory
  3. Blocked stent
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3
Q

Give 3 symptoms of jaundice

A
  1. Biliary pain
  2. Rigors - indicate an obstructive cause
  3. Abdomen swelling
  4. Weight loss
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4
Q

which conditions can cause Gallstones

A
  1. Obesity and rapid weight loss
  2. DM
  3. Contraceptive pill
  4. Liver cirrhosis
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5
Q

Give 4 symptoms of gallstones

A

Most are asymptomatic

  1. Biliary colic (sudden RUQ pain radiating to the back and epigastrium +/- nausea/vomiting) - AFTER EATING FATTY MEALS
  2. Acute cholecystitis (gallbladder distension –> inflammation, necrosis, ischaemia)
  3. Obstructive jaundice
  4. Cholangitis
  5. Pancreatitis
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6
Q

Give 5 causes of acute liver disease

A
  1. Viral hepatitis
  2. Drug induced hepatitis
  3. Alcohol induced hepatitis
  4. Vascular - Budd-Chiari
  5. Obstruction
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7
Q

Give 5 causes of chronic liver disease

A
  1. Alcohol
  2. NAFLD
  3. Viral hepatitis (B,C,E)
  4. Autoimmune diseases
  5. Metabolic
  6. Vascular - Budd-Chairi
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8
Q

Give 5 signs of acute liver failure

A
  1. Jaundice
  2. Fetor hepaticus (smells like pears)
  3. Coagulopathy
  4. Asterixis - liver flap
  5. Malaise
  6. Lethargy
  7. Encephalopathy
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9
Q

Give 5 signs of chronic liver disease

A 
Ascites/Oedema
Gynaecomastia 
Dupuytren’s contracture
Malaise
Anorexia 
Jaundice/Pruritus
Clubbing/Leukonychia 
Palmar erythema
Xanthelasma
Spider Naevi/Caput Medusae
Hepatosplenomegaly
Bleeding - haematemesis, easy bruising
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10
Q

Give 4 complications of of liver failure

A
  1. Hepatic encephalopathy
  2. Abnormal bleeding
  3. Jaundice
  4. Ascites
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11
Q

What drugs should be avoided in liver failure?

A

Constipators
Oral hypoglycaemics
Warfarin has enhanced effects
Opiates

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12
Q

Give 4 signs of cirrhosis

A
  • ascites
  • clubbing
  • palmar erythema
  • xanthelasma
  • spider naevi
  • hepatomegaly
  • peripheral oedema
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13
Q

Give 4 complications of cirrhosis

A

Ascites
portal hypertension

  1. Decompensation
  2. SBP
  3. Increased risk of HCC
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14
Q

what is the clinical presentation of portal hypertension?

A
  • often asymptomatic
  • splenomegaly
  • spider naevi
  • GI bleeding
  • ascites
  • hepatic encephalopathy
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15
Q

Describe the pathophysiology of ascites

A
  1. Increased intra-hepatic resistance leads to portal hypertension –> ascites
  2. Systemic vasodilation leads to secretion of RAAS, NAd and ADH –> fluid retention
  3. Low serum albumin
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16
Q

Give 3 signs of ascites

A
  1. Distension
  2. Dyspnoea
  3. Shifting dullness on percussion
  4. Signs of liver failure
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17
Q

Describe the treatment for ascites

A
  1. Restrict sodium and fluids
  2. Diuretics - spirolactone
  3. Paracentesis
  4. Albumin replacement
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18
Q

Describe the effects of alcoholic liver disease

A
  1. Fatty liver –> hepatitis –> cirrhosis and fibrosis
  2. GIT –> gastritis, varices, peptic ulcers, pancreatitis , carcinoma
  3. CNS –> Degreased memory and cognition, wernicke’s encephalopathy
  4. Folate deficiency –> anaemia
  5. Reproduction –> testicular atrophy, reduced testosterone/progesterone
  6. Heart –> dilated cardiomyoapthy, arrhythmias
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19
Q

What distinctive feature is often seen on biopsy in people suffering form alcoholic liver disease?

A

Mallory bodies

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20
Q

How does alcoholic hepatitis present?

A 
Jaundice
Anorexia
Nausea and vomiting
Fever
Encephalopathy 
Cirrhosis 
Hepatomegaly
Ascites, bruising, clubbing
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21
Q

Give 3 infective causes of acute hepatitis

A
  1. Hepatitis A-E infections
  2. EBV
  3. CMV
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22
Q

Give 3 symptoms of acute hepatitis

A
  1. General malaise
  2. Myalgia
  3. GI upset
  4. Abdominal pain
  5. Raised AST, ALT
  6. +/- jaundice
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23
Q

Describe the natural history of HBV in 4 phases

A
  1. Immune tolerance phase
    - unimpeded viral replication
    - HBV DNA = high
  2. Immune clearance phase:
    - the immune system ‘wakes up’
    - liver inflammation
    - ALT = high
  3. Inactive HBV carrier phase
    - HBV DNA = low
    - ALT levels = normal
    - no liver inflammation
  4. Reactivation phase
    - ALT = intermittent
    - HBV DNA = intermittent
    - liver fibrosis
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24
Q

What are the potential consequences of chronic HBV infection?

A
  1. Cirrhosis
  2. HCC
  3. Decompensated cirrhosis
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25
Q

Give 3 side effects of alpha interferon treatment for HBV

A
  1. Myalgia
  2. Malaise
  3. Lethargy
  4. Thyroiditis
  5. Mental health problems
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26
Q

Give 2 HBV specific symptoms

A

Arthralgia

Urticaria (hives)

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27
Q

Give 3 causes of non-alcoholic fatty liver disease

A
  1. T2DM
  2. Obesity
  3. Hypertension
  4. Hyperlipidaemia
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28
Q

How do you manage NAFLD?

A

Lose weight
Control HTN,
DM and lipids

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29
Q

What is Budd-Chiari syndrome?

A

Hepatic vein occlusion –> ischaemia and hepatocyte damage –> liver failure or insidious cirrhosis

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30
Q

90% of people with haemochromatosis have a mutation in which gene?

A

HFE - chromosome 6

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31
Q

Give 4 signs of haemochromatosis

A
  • Fatigue, arthralgia, weakness
  • Hypogonadism – eg erectile dysfunction
  • SLATE-GREY SKIN (brownish/bronze)
  • Chronic liver disease, heart failure, arrythmias
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32
Q

Give 2 complications of haemochromatosis?

A

Liver cirrhosis –> failure/cancer

DM due to pancreatic depositions

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33
Q

Describe the pathophysiology of alpha 1 anti-trypsin deficiency?

A

● A mutation in the alpha-1-antitrypsin gene on chromosome 14 leads to reduced hepatic production of alpha-1-antitrypsin which normally inhibits the proteolytic enzyme, neutrophil elastase
● Deficiency results in emphysema, liver cirrhosis and hepatocellular carcinoma

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34
Q

How does Alpha 1 anti-trypsin deficiency present?

A

Liver disease in the young - cirrhosis, jaundice

Lung disease in the old (smokers) - emphysema

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35
Q

What is the treatment for Alpha 1 anti-trypsin deficiency?

A

● No treatment
● Treat complications such as liver disease
● Stop smoking
● Those with hepatic decompensation should be assessed for liver transplant
● Manage emphysema

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36
Q

How does Wilson’s disease present?

A

Children = liver disease - hepatitis, cirrhosis, fulminant liver failure

Adults = CNS problems, mood changes, and Kayser-Fleischer rings

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37
Q

What CNS changes are seen in a patient with Wilson’s disease?

A 
Tremor
Dysarthria 
Dyskinesia 
Ataxia
Parkinsonism 
Dementia 
Depression
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38
Q

What is the treatment for Wilson’s disease?

A

Lifetime treatment with penicillamine (chelating agent)
Low Cu diet - no liver, nuts, chocolate, mushrooms, shellfish
Liver transplant

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39
Q

How does autoimmune hepatitis present?

A 
Fatigue, fever, malaise 
Hepatitis 
Hepatosplenomegaly
Amenorrhoea 
Polyarthritis 
Pleurisy 
Lung infiltrates 
Glomuleronephritis
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40
Q

What diseases are associated with autoimmune hepatitis?

A 
Autoimmune thyroiditis 
DM
Pernicious anaemia
PSC
UC
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41
Q

What results would you see from the investigations of someone who you suspect has autoimmune hepatitis?

A

Raised LFTs - increased bilirubin, AST, ALT, ALP
Hypersplenism = low WCC and platelets
Autoantibodies = +ve ANA
Liver biopsy = mononuclear infiltrate

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42
Q

How is autoimmune hepatitis treated?

A

Prednisolone - immunosuppression

Liver transplant

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43
Q

What is primary biliary cirrhosis?

A

An autoimmune disease where intra-hepatic bile ducts are destructed by chronic granulomatous inflammation –> cholestatis (bile in liver) –> cirrhosis, fibrosis, portal hypertension

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44
Q

Give 3 disease associated with primary biliary cirrhosis

A
  1. Thyroiditis
  2. RA
  3. Coeliac disease
  4. Lung disease
    Other autoimmune diseases
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45
Q

Give 3 symptoms of primary biliary cirrhosis

A
  1. Pruritis
  2. Fatigue
  3. Hepatosplenomegaly
  4. Obstructive jaundice
  5. Cirrhosis and coagulopathy
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46
Q

What would investigations show in someone with primary biliary cirrhosis?

A

Bloods = LFT - GGT and ALP raised
Positive anti-mitochondrial antibody (AMA) = diagnostic
low albumin

Liver biopsy = epithelial disruption and lymphocyte infiltration

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47
Q

What is the treatment for primary biliary cirrhosis?

A

early stage = Ursodeoxycholic acid + steroids + Cholestyramine
ADEK vitamins

severe = Liver transplant

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48
Q

Describe the pathophysiology of primary sclerosing cholangitis

A

Inflammation of the bile duct –> stricture and hardening –> progressive obliterating fibrosis of bile duct branches –> cirrhosis –> liver failure

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49
Q

Give 3 causes of primary sclerosing cholangitis

A
  1. Primary = unknown causes
  2. Infection
  3. Thrombosis
  4. Iatrogenic trauma
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50
Q

Give 3 symptoms of primary sclerosing cholangitis

A
  1. Pruritus
  2. Charcot’s triad = fever with chills, RUQ pain, obstructive jaundice
  3. Cirrhosis
  4. Liver failure
  5. Fatigue
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51
Q

What would the investigations show in someone with primary sclerosing cholangitis?

A

Bloods = high ALP, bilirubin, pANCA
AMA negative
Imaging = ERCP and MRCP
Liver biopsy = fibrous and obliterative cholangitis

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52
Q

What is the treatment for primary sclerosing cholangitis?

A
  • Cholestyramine for pruritus
  • Ursodeoxycholic acid - may protect against colon cancer and improve LFT
  • ADEK vitamins
  • Liver transplant
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53
Q

What complications might occur due to primary sclerosing cholangitis?

A

Increased risk of bile duct, gallbladder, liver and colon cancer

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54
Q

Give 3 causes of ascending cholangitis?

A

Gallstone
Primary infection (Klebsiella, E. coli)
Strictures following surgery
Pancreases head malignancy

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55
Q

What other symptoms can present with Charcot’s triad with ascending cholangitis?

A

Reynolds pentad

  • Charcot’s triad (fever, RUQ pain, jaundice)
  • Hypotension
  • Confusion/altered mental state
56
Q

What investigations might you do in someone who you suspect might have ascending cholangitis?

A
  1. USS
  2. Blood tests - LFTS
  3. CT - excludes carcinoma
  4. ERCP - definitive investigation
57
Q

Describe the management of ascending cholangitis

A 
Fluid resuscitation 
Treat infection with broad spectrum antibiotics (cefotaxime, metronidazole)
ERCP to clear obstruction
Stenting 
Laparoscopic cholecystectomy
58
Q

What is the main difference between biliary colic and acute cholecystitis?

A

Acute cholecystitis has an inflammatory component

59
Q

What complications can occur due to acute ascending cholangitis?

A 
Sepsis
Biliary colic
Acute cholecystitis
Empyema
Carcinoma 
Pancreatitis
60
Q

Give 3 symptoms of peritonitis

A
  1. Abdominal pain and tenderness
  2. Nausea and vomiting
  3. Chills
  4. Rigors
  5. Fever
61
Q

Give 3 signs of peritonitis on an abdomen examination

A
  1. Guarding
  2. Rebound tenderness
  3. Rigidity
  4. Silent abdomen
  5. lying still
62
Q

What investigations might you do in someone who you suspect could have peritonitis?

A
  1. Blood tests: raised WCC, platelets, CRP, amylase, reduced blood count
  2. CXR: look for air under the diaphragm
  3. Abdominal x-ray: look for bowel obstruction
  4. CT: can show inflammation, ischaemia or cancer
  5. ECG: epigastric pain could be related to the heart
  6. B-HCG: a hormone secreted by pregnant ladies
63
Q

What is the management for peritonitis?

A
  1. ABCDE
  2. Treat the underlying cause - might be surgery if perforated bowel
  3. IV fluids
  4. IV antibiotics - first broad spectrum then specific
  5. peritoneal lavage (clean the cavity surgically)
64
Q

Give 5 potential complications of peritonitis

A
  1. Hypovolaemia
  2. Kidney failure
  3. Systemic sepsis
  4. Paralytic ileus
  5. Pulmonary atelectasis (lung collapse)
  6. Portal pyaemia (pus in portal vein)
65
Q

Name a bacteria that can cause spontaneous bacterial peritonitis

A
  1. E. coli

2. S. pneumoniae

66
Q

Describe the treatment for spontaneous bacterial peritonitis

A

Cefotaxime and metronidazole

67
Q

What is acute pancreatitis?

A

An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase)
the pancreas returns to functionally and structurallynormal after the episode
Occurs as isolated or recurrent attacks

68
Q

What are the causes of acute pancreatitis?

A 
I GET SMASHED – remember 
I = Idiopathic
G = Gallstones (60%)
E = Ethanol = alcohol (30%)
T = Trauma
S = Steroids
M = Mumps
A = Autoimmune
S = Scorpion venom
H = Hyperlipidaemia/ hypothermia/ high Ca
E = ERCP (endoscopic retrograde cholangiopancreatography) 
D = Drugs (furosemide, corticosteroid, NSAIDs, ACEi)
69
Q

which drugs can cause acute pancreatitis?

A

furosemide,
corticosteroid,
NSAIDs,
ACEi

70
Q

Give 4 symptoms of acute pancreatitis

A
  1. Severe epigastric pain that radiates to the back
  2. Anorexia
  3. Nausea, vomiting
  4. Signs of septic shock - fever, dehydration, hypotension, tachycardia
  5. Necrotising - umbilical (Cullens sign) vs flank (Grey Turners sign)
71
Q

What investigations are done on someone you think has acute pancreatitis?

A 
Raised serum amylase and lipase 
urinalysis - raised urinary amylase
Erect CXR 
Contrast CT 
MRI
72
Q

Describe the treatment for acute pancreatitis

A
  • analgesia
  • nil by mouth
  • IV fluids
  • prophylactic antibiotics
73
Q

Give 2 potential complications of acute pancreatitis

A
  1. Systemic inflammatory response syndrome
  2. Multiple organ dysfunction
  3. Pancreatic necrosis
  • hyperglycaemia
  • hypocalcaemia
  • renal failure
  • shock
74
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas leads to irreversible damage
- Progressive loss of exocrine pancreatic tissue which is replaced by fibrosis

75
Q

Describe the pathogenesis of chronic pancreatitis

A

Pancreatic duct obstruction leads to activation of pancreatic enzymes –> necrosis –> fibrosis

76
Q

Name 3 causes of chronic pancreatitis

A
  1. Excess alcohol - most common
  2. CKD
  3. Idiopathic
  4. Recurrent acute pancreatitis
  5. hereditary
  6. CF - all have it from birth
  7. autoimmune
  8. tropical
77
Q

What is the clinical presentation of chronic pancreatitis?

A
  1. Severe epigastric pain that radiate through to the back - worse after alcohol/meal and better on leaning forward
  2. Weight loss, malabsorption
  3. Nausea, vomiting
  4. Steatorrhea (lack of lipase)
  5. Exocrine/endocrine dysfunction (DM)
  6. jaundice
78
Q

A sign of chronic pancreatitis is exocrine dysfunction, what can be consequence of this?

A
  1. Malabsorption
  2. Weight loss
  3. Diarrhoea
  4. Steatorrhoea
79
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

A

IgG4

80
Q

How is autoimmune chronic pancreatitis treated?

A

Steroids

81
Q

What is the treatment for chronic pancreatitis?

A

Alcohol cessation
Analgesia (NSAIDs, tramadol)
Pancreatic enzyme (creon) and vitamin replacement
pancreatin + omeprazole
If DM = insulin
Surgery - local resection, for unremitting pain and duct draining

82
Q

What 2 enzymes, if raised, suggest pancreatitis?

A

LDH (lactate dehydrogenase) and AST

83
Q

Give 3 complications of chronic pancreatitis

A
  1. Diabetes
  2. Pseudocyst
  3. Biliary obstruction –> obstructive jaundice, cancer
84
Q

Name a drug that can cause drug induced liver injury

A
  1. Co-amoxiclav
  2. Flucloxacillin
  3. Erythromycin
  4. TB drugs
85
Q

Give 5 causes of diarrhoea infection

A
  1. Traveller’s diarrhoea
  2. Viral - (rotavirus/norovirus)
  3. Bacterial (E. coli)
  4. parasites (helminths, protozoa)
  5. Nosocomial (C. diff)
86
Q

Give 5 causes of non-diarrhoeal infection

A
  1. Gastritis/peptic ulcer disease (H. pylori)
  2. Acute cholecystitis
  3. Peritonitis
  4. Thyphois/paratyphoid
  5. Amoebic liver abscess
87
Q

What is the diagnostic criteria for travellers diarrhoea?

A

> 3 unformed stools per day and a least one of:
- abdominal pain
- cramps
- nausea
- vomiting
Occurs within 2 weeks (usually 3 days) of arrival in a new country

88
Q

give 3 causes of travellers diarrhoea

A
  1. Enterotoxigenic E. coli
  2. Norovirus
  3. Giardia
89
Q

Which type of E. coli can cause bloody diarrhoea and has a shiga like toxin?

A

Enterohaemorrhagic E.coli (EHEC)

90
Q

Give 5 symptoms of helminth infection

A
  1. Fever
  2. Eosinophilia
  3. Diarrhoea
  4. Cough
  5. Wheeze
91
Q

Why is c. diff infectious?

A

Spore forming bacteria (gram positive)

92
Q

Give 5 risk factors for c.diff infection

A
  1. Increasing age
  2. Comordities
  3. Antibiotic use
  4. PPI
  5. Long hospital admission
  6. NG tube feeding and GI surgery
  7. Immunocompromised - HIV, anti-caner drugs
93
Q

Name 5 antibiotics that can cause c. diff infection

A
  1. Ciprofloxacin (quinolones)
  2. Co-amoxiclav (penicillins)
  3. Clindamycin
  4. Cephlosporins
  5. Carbapenems

RULE OF C’s

94
Q

what is the clinical presentation of biliary colic?

A

● Recurrent episodes of severe and persistent pain in the upper abdomen which subsides after several hours
● Pain may radiate to right shoulder and suprascapular region
● Vomiting
● Normal examination

95
Q

what investigations should be undertaken for biliary colic?

A

● History and US showing gallstones
● Increases of serum alkaline phosphatase and bilirubin during an attack support the diagnosis of biliary pain
● Absence of inflammatory features differentiates this from acute cholecystitis

96
Q

what is the management of biliary colic?

A

● Analgesics and elective cholecystectomy
● Abnormal liver biochemistry or a dilated CBD on US is an indication for preoperative MRCP
● CBD stone removed at ERCP

97
Q

what is the clinical presentation of cholecystitis?

A
  • Generalised epigastric pain migrating to severe RUQ pain.
  • Signs of inflammation like a fever or fatigue.
  • Pain associated with tenderness and guarding from inflamed gallbladder and local peritonitis.

Tenderness worse on inspiration (Murphy’s sign)

98
Q

what are the investigations for cholecystitis?

A
  • Positive Murphy’s Sign = Severe pain on deep inhalation with examiners hand pressed into the RUQ.
  • Inflammatory markers - FBCs, CRP
  • Ultrasound: Thick gallstone walls from inflammation
99
Q

what is the management of cholecystitis?

A

• Antibiotics IV,
heavy analgesia,
IV fluids
an eventual Cholecystectomy if needed.

100
Q

what are the complications of cholecystitis?

A

● Empyema (pus)

● Perforation with peritonitis

101
Q

what is the pathophysiology of primary biliary cholangitis (primary biliary cirrhosis)?

A
  • Due to prolonged bile duct blockage, bile isn’t ‘flushing’ out the tubes so bacteria can climb up from the GI tract and cause biliary tree infection and consolidation.
  • This prevents bile entering the GI tract and causes jaundice.
  • 5-10% mortality and infection can affect the pancreas too since it shares ducts with the gallbladder.
102
Q

what is the clinical presentation of primary biliary cholangitis (primary biliary cirrhosis)?

A
  • Severe RUQ pain, with fever (rigors) AND jaundice.

* Patient may present as septic and/or have developed some level of pancreatitis.

103
Q

what are the investigations for primary biliary cholangitis (primary biliary cirrhosis)?

A

POSITIVE AMA
Raised ALP and Bilirubin, raised CRP
• Blood cultures/MC&S
• Ultrasound +/- ERCP

104
Q

what is the clinical presentation of ascending cholangitis?

A

RUQ pain, jaundice, & rigors (Charcot’s triad’)

105
Q

what is the treatment for ascending cholangitis?

A

Cefuroxime IV & Metronidazole IV/PR.

106
Q

what is primary sclerosing cholangitis?

A

a disease of the bile ducts that causes inflammation and obliterative fibrosis of bile ducts inside and/or outside of the liver.
- This pathological process impedes the flow of bile to the intestines and can ultimately lead to cirrhosis of the liver, liver failure, and bile duct and liver cancer

107
Q

what is the pathophysiology of portal hypertension?

A
  • Increased resistance to blood flow leads to portal hypertension causes splanchnic vasodilation
  • This results in a drop in BP
  • CO increases to compensate for BP resulting in salt and water retention
  • Hyperdynamic circulation/increased portal flow leads to the formation of collaterals between portal and systemic systems
108
Q

what is the treatment of GI varices?

A

● fluid resuscitation until haemodynamically stable
● If anaemic – blood transfusion
● Correct clotting abnormalities – vitamin K and platelet transfusion
● Vasopressin – IV terlipressin or octreotide
● Prophylactic antibiotics
● Variceal banding
● Balloon tamponade
● TIPS

109
Q

what is the prevention of varices?

A

o Nonselective B blockade – propranolol – reduced resting pulse and decrease portal pressure
o Variceal banding repeated to obliterate varices
o TIPSS
o Liver transplant

110
Q

what are the risk factors for developing ascites?

A
  • high sodium diet
  • HCC
  • splanchnic vein thrombosis causing portal hypertension
111
Q

what are the causes of ascites?

A 
● liver failure - cirrhosis
● Portal hypertension e.g. cirrhosis
● Hepatic outflow obstruction
● Budd-Chiari syndrome
● Peritonitis
● Pancreatitis
● Cardiac failure
● Constrictive pericarditis
112
Q

what investigations should be done for ascites?

A

● Diagnostic aspiration of 10-20ml of ascitic fluid
o Raised white cell count indicates bacterial peritonitis
o Gram stain and culture
o Cytology for malignant cells
o Amylase to exclude pancreatic ascites
● Protein measurement of ascitic fluid
o Transudate (low protein) - Portal hypertension, constrictive pericarditis, cardiac failure, Budd-Chiari syndrome
o Exudate (high protein) BAD!! - Malignancy, peritonitis, pancreatitis, peritoneal tuberculosis, nephrotic syndrome

113
Q

what is the management of ascites?

A
  • treat underlying cause
  • low sodium diet
  • spironolactone and furosemide
  • drain fluid - paracentesis
114
Q

what investigations are undertaken for chronic pancreatitis?

A
  • serum amylase and lipase - may be raised

- abdominal US, CT and MRI

115
Q

what is alpha 1 antitrypsin deficiency?

A
  • rare cause of cirrhosis
  • autosomal recessive condition
  • mutation of alpha-1-antitrypsin gene on chromosome 14
116
Q

what investigations are undertaken for gallstones?

A

FBC and CRP: Looking for signs of an inflammatory response - suggestive of cholecystitis
• LFTs: Raised ALP - Bilirubin and ALT usually normal.
• Amylase: Check for pancreatitis
• Ultrasound = diagnostic:
1.Stones
2.Gallbladder wall thickness (inflammation)
3.Duct dilation (suggests distal blockage)

117
Q

what are the side-effects of chelating agents?

A

skin rash,
fall in WCC, HB and platelets,
haematuria,
renal damage

118
Q

what are the investigations for wilsons disease?

A
  • Serum copper and ceruloplasmin reduced (but can be normal)
  • 24hr urinary copper excretion high
  • Liver biopsy – diagnostic
119
Q

what are the causes of peritonitis?

A

bacterial = most common

  • gram -ve coliforms - e.coli
  • gram +ve staphylococcus

chemical - bile, old clotted blood

120
Q

what is the clinical presentation of HAV?

A

nausea,
anorexia,
distaste for cigarettes
some become jaundiced - dark urine and pale stool

121
Q

what are the risk factors for non-alcoholic fatty liver disease?

A 
Obesity, 
diabetes, 
hyperlipidaemia, 
parental feeding, 
jejuno-ileal bypass, 
wilsons disease, 
drugs - Amiodarone, Tetracycline ,Methotrexate, Tetracycline
122
Q

which drugs increase the risk of developing non-alcoholic fatty liver disease?

A

Amiodarone, Tetracycline ,Methotrexate

123
Q

what are the clinical features of non-alcoholic fatty liver disease?

A

Usually no symptoms; liver ache in 10%

Fat, sometimes with inflammation & fibrosis

124
Q

what are the investigations for non-alcoholic fatty liver disease?

A

Fat, sometimes with inflammation & fibrosis

Need biopsy to distinguish NAFL from NASH

125
Q

what is the treatment for non-alcoholic fatty liver disease?

A

control risk factors, bariatric surgery - to treat obesity

126
Q

what are the clinical features of fatty liver?

A

o No symptoms or signs

o Vague abdominal symptoms are due to general effects of alcohol on the GI tract

127
Q

what are the investigations for fatty liver?

A

o Elevated MCV indicates heavy drinking
o Raised ALT and AST
o Ultrasound or CT/liver histology will demonstrate fatty infiltration

128
Q

what are the investigations for alcoholic hepatitis?

A

o FBC – leucocytosis, elevated MCV, thrombocytopenia
o Serum electrolytes abnormal – elevated serum creatinine
o Elevated AST, ALT, bilirubin, prothrombin time
o Microscopy and culture of blood, urine and ascites to search for infection
o Liver and biliary US used to identify obstruction

129
Q

what is the management for alcoholic hepatitis?

A

o Nutrition maintained with enteral feeding and vitamin supplements
o Steroids show short term benefit – reduce inflammation
o Infections treated and prevented

130
Q

what are the primary bile salts?

A

colic acid and chenodeoxycholic acid`

131
Q

what are the secondary bile salts?

A

deoxycholic acid and lithocholic acid

132
Q

what are the investigations for NAFLD?

A

1st line

  • enhanced liver fibrosis test (<7.7 = non-mild, >7.7-9.8 = moderate, >9.8 = severe)
  • LFTs - increased AST and ALT (AST:ALT ratio close to 1)
  • FBC - anaemia or thrombocytopenia

gold standard

  • liver US (diffuse fatty infiltration and abnormal echotexture)
  • liver biopsy (required for diagnosis)
133
Q

how can you tell the difference between NAFLD and alcoholic liver disease?

A

AST:ALT ratio

ratio close to 1 = NAFLD
2:1 ratio = alcoholic liver disease

134
Q

what are the symptoms of pre-hepatic jaundice?

A

pallor
fatigue
exertional dyspnoea

135
Q

what are the symptoms of intra-hepatic jaundice?

A

anorexia
fatigue
nausea
abdominal pain

136
Q

what are the symptoms of post-hepatic jaundice?

A 
pale stools
dark urine
pruritus
steatorrhea
RUQ pain
hepatomegaly
137
Q

what are the investigations for chronic pancreatitis?

A 
Secretin stimulation test
CT or MRI - pancreatic duct dilation, calcification, atrophy or pseudocysts
endoscopic ultrasound
Erect CXR
fecal elastase test - decreased elastase

Phase 2A revision (38 decks)

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