Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Medicine @ Lancaster Uni > 2.03 - Liver and Gallbladder diseases 🍻 > Flashcards

2.03 - Liver and Gallbladder diseases 🍻 Flashcards

1
Q

What is hepatitis?

A
  • General term relating to inflammation of the liver parenchyma
  • Characteristically show an increase in different liver enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the most common type of hepatitis?

A
  • Viral hepatitis is the most common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of virus is seen in Hep. A?

A
  • Picornavirus
  • Non- enveloped single-standed RNA virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the incubation period of Hep. A?

A
  • Hep. A has an incubation period of between 2-6 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is Hep. A spread?

A
  • Faecal-Oral route
  • Viral shedding occurs in the faeces at the same time as the onset of symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the epidemiology surrounding Hep. A?

A
  • Common worldwide
  • Often occurs in epidemics
  • Contracted through contaminated food and water
  • Notifiable Disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When should a Hep. A vaccination be given?

A
  • Before travel to high risk areas, such as:
  • Indian subcontinent
  • Africa
  • Central and South America
  • Far East
  • Eastern Europe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How long does a Hep. A vaccine provide protection for?

A
  • Provides immunity for 10 years
  • Considered life long
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is Hep. A often difficult to detect?

A
  • It is often asymptomatic and therefore many people never know they have the disease
  • They only find out if they have an acute exacerbation of the disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the common symptoms associated with Hep. A?

A
  • GI discomfort
  • Nausea
  • Anorexia
  • Flu-like symptoms
  • Rash
  • Pruritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the clinical signs associated with Hep. A?

A
  • Jaundice
  • RUQ tenderness
  • Hepatomegaly (85%)
  • Splenomegaly (10%)
  • Lymphadenopathy (5%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which groups are more at risk of contracting Hep. A?

A
  • Young people
  • Travellers to endemic areas
  • High risk sexual activity
  • Haematological disorders
  • Occupational risks
  • IV drug users
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the management plan for Hep. A?

A
  • As it is usually a self-limiting disease, management is often supportive rather than curative
  • Doesn’t require hospitalisation unless there is sever hepatic inpairment
  • Good hydration
  • Anti-nausea = Metoclopramide
  • Ant-itching = Chlorophenamine
  • Aim to reduce transmission
  • Plenty of rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pathologial process surounding the development of Hep. A?

A
  • Caused by the HAVirus
  • Typically acquired through ingestion
  • Virus replicates in the liver with this peaking at 10-12 days when the virus is present in the blood
  • This is then excreted via the biliary system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What investigations are undertaken in the diagnosis of Hep. A?

A
  • Hep. A IgM/IgA antibodies measured
  • Anti-HAV antibodies
  • Repeated liver serology tests
    LFT’s:
  • ALT/AST = significantly elevated
  • Bilirubin = moderate elevation
  • Prothrombin time = normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Do genetics play a role in Hep. A?

A
  • Underlying conditions can lead to increased susceptibilty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What type of virus is seen in Hep. B?

A
  • Enveloped DNA virus
  • Hepadnavirus
  • 42mm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the route of transmission seen in Hep. B?

A
  • Blood borne
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How long is the incubation period for Hep. B?

A
  • 6 weeks to 6 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms associated with Hep. B?

A
  • Fever
  • Malaise
  • Fatigue
  • Joint pain
  • Urticaria
  • Pale stools
  • Dark urine
  • Jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What clincal signs are seen in a patient with Hep. B?

A
  • Deranged LFT’s
  • HBsAG = Carrier if >6 months
  • Anti-HB’s imply immunity
  • Also test for HIV, HCV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the risk factors for the development of Hep. B?

A
  • IV drug use
  • Multiple sexual partners
  • Occupational exposure
  • Receiving regular blood products
  • Travel to high risk areas
  • Children born to mothers who are carriers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the management regime that is used for Hep. B?

A
  • Usually a self-limiting disease
  • Anti-virals in chronic cases, 48 week cause of interferons
  • Aim of treatment is to reduce the risk of complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What proportion of acute cases of Hep. B develop into chronic disease?

A
  • Around 10% develop into chronic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What type of virus causes Hep. C?

A
  • RNA
  • Enveloped RNA virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the incubation period for Hep. C?

A
  • Approximately 6/7 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the symptoms seen in a Hep. C infection?

A
  • Hep. C is largely asymptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the clincal signs seen in a Hep. C infection?

A
  • ALT>AST
  • HCV-DNA surface antigens
  • HIV, HBV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the possible at risk groups for a Hep. C infection?

A
  • Those who recieve regular blood products
  • IV drug use
  • Needlestick injury
  • Vertical through animals
  • Sexual transmission is rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is Hep. C transmitted?

A
  • It is a blood borne disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the management involved in the treatment of Hep. C?

A
  • Specialist assessment as only 30% have a self-limiting disease which does’t require treatment
  • If treatment is needed then interferon given for 3-6 months to reduce risk of chronicity
  • Chronic HCV is usually asymptomatic with diagnosis made 6 months following intial infection if not cleared
  • Anti-viral combo + monitoring is used to help track infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What type of virus causes Hep. D?

A
  • An incomplete RNA virus
  • Can co-exist with HBV
  • 36mm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the incubation period of Hep. D?

A
  • Around 90 days depending on viral load and other predetermining factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What symptoms are seen in a Hep. D infection?

A
  • The same symptoms as seen in HBV but the progression of these is usually acclerated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the signs seen in a patient presenting with a Hep. D infection?

A
  • Similar to HBV
  • If a superinfection of HBV + HDV then prognosis is bad
  • This can lead to fulminant liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is a complication of an acute HDV infection?

A
  • This can lead to a chronic HDV infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What type of managment is used in those with a Hep. D infection?

A
  • Mainly supportive
  • Interferon alpha if needed as otherwise can progress to chronic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What virus causes Hep. E?

A
  • Non-enveloped RNA virus
  • 27mm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the incubation period seen in Hep. E?

A
  • Approximately 10 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What symptoms are seen in someone with Hep. E?

A
  • Usually asymptomatic
  • Fatigue
  • Poor appetite
  • Stomach pain
  • Nausea
  • Jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What clincal signs are seen in someone with Hep. E?

A
  • HEVsAb’s
  • IgM/IgG
  • HEV-RNA via PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the risk factors for someone developing a Hep. E infection?

A
  • Same as HAV
  • Poor water sanitation and living conditions etc.
  • Raw pork is a notable causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What management regime is associated with the treatment of a HEV infection?

A
  • There is very little treatment needed
  • This is because Hep. E is a self-limiting disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is a possible complication of HEV?

A
  • In rare cases can lead to an acute fulminant liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the transmission route for Hep. E?

A
  • Faecal-oral
  • Zoonotic (Vertical)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Which hepatitis viruses are tranmitted via blood?

A
  • Hep. B
  • Hep. C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the different liver function tests available?

A
  • Albumin
  • Total protein
  • Direct bilirubin (Conjugated)
  • Total bilirubin
  • Prothrombin time
  • AST
  • ALT
  • ALP
    -GGT
  • Ammonia and urea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the pros of LFT’s?

A
  • Relatively cheap and available
  • Good for monitoring for change
  • If normal = no liver disease but may still be other associated pathologies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the cons of LFT’s?

A
  • Not hepato-specific
  • Cellular heterogenity
  • Differing sensitivities
  • Rarely definitive and requires clincial correlation
  • Overly-requested
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does a test for albumin show?

A
  • Assesses the livers ability to synthesise proteins
  • Important for maintenance of oncotic pressure
  • Liver disease/malnutrition -> Hypoalbuminaemia
  • If low = oedema/ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What does a test for total protein show?

A
  • Assesses the livers synthetic functions
  • An increase = an increase in Ig’s
  • Usually signifies infection of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What does a test for prothrombin time show?

A
  • Looks at the synthetic function of the liver by looking at the activity of vitamin K dependant clotting factors
  • Recorded as INR
  • Best marker for synthetic function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What does a test for total bilirubin show?

A
  • Assesses the possability of cholestasis
  • Jaundice apparent when levels are two times the upper limit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What does a test for direct (conjugated) bilirubin show?

A
  • Assess probability of cholestasis
  • Measures levels of conjugated bilirubin
  • Looks for post-hepatic causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What does a test for AST show?

A
  • AST = Aspartate aminotransferase
  • Indicator of hepatocellular injury
  • Non-specific to the liver
  • Found in hepatocyte mitochondria
  • Also found in cardiomyocytes, renal cells, myocytes and brain cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What does a test for ALT show?

A
  • ALT = Alanine transaminase
  • Indicator of hepatocellular injury
  • Specific to the liver
  • Released into the blood after injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What does a test for ALP show?

A
  • ALP = Alkaline Phosphatase
  • Increased in cholestatic liver disease
  • Biliary canaliculi component
  • Usually in bile, backs up into the blood after blockage
  • Can be raised in other conditions such as bone disease and mets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does a test for GGT show?

A
  • GGT = Gamma-glutamyl transferase
  • Found in bile canaliculi and hepatocytes
  • Raised levels seen in hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What does a test for ammonia/urea show?

A
  • Usually converted into urea when it can be excreted
  • In impaired function it can build-up
  • Crosses the blood-brain barrier -> neurotoxic effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What does an AST:ALT = >2 indicate?

A
  • Alcoholic liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What does an AST>ALT indicate?

A
  • Cirrhosis
  • Chronic hepatitis
  • Steatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What does an ALT>AST indicate?

A
  • Acute liver injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What two results are used alongside each other to check for acute liver abnormalities?

A
  • ALP and GGT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What other forms of specialist testing exist for the detection of liver diseases?

A
  • Liver biopsy
  • Viral serology
  • Immunoglobulins
  • Alpha-1 antitrypsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What does an abnormal IgA result show?

A
  • Alcoholic liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What does an abnormal IgG result show?

A
  • Autoimmune hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What does an abnormal IgM result show?

A
  • Primary biliary cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is jaundice?

A
  • Yellowing of the skin and sclera due to elevated levels of bilirubin in the blood due to hepatic impairment
  • Usually not noticeable till levels are greater than 34 micromols/L
69
Q

What enzyme helps to convert uncojugated bilirubin into conjugated bilirubin?

A
  • UGTIA1
70
Q

Which enzyme helps to prefer conjugated bilirubin for excretion?

A
  • MRP-2
71
Q

What are the three different ways in which urobilogen can be excreted?

A
  • Liver (Enterohepatic)
  • Kidneys (Urobilin)
  • Faeces (Urobilin/Sterobilin)
72
Q

What are the three different causes of jaundice?

A
  • Pre-hepatic
  • Hepatic
  • Post-hepatic
73
Q

What are some causes of pre-hepatic jaundice?

A
  • Major cause is haemolysis
    Can also occur in:
  • Sickle cell
  • Hereditary spherocytosis
  • Autoimmune haemolytic anaemia
  • Iatrogenic (Metallic heart valve)
74
Q

What are the characteristic features of pre-hepatic jaundice?

A
  • Anaemia
  • Unconjugated hyperbilirubinaemia
  • Markers of haemolysis
75
Q

What are some of the causes of hepatic jaundice?

A
  • Caused by either abnormal processing or abnormal excretion of bilirubin
76
Q

What is the result of impaired processing of bilirubin?

A
  • Unconjugated hyperbilirubinaemia
77
Q

What is the result of impaired excretion of bilirubin?

A
  • Conjugated hyperbilirubinaemia
78
Q

What is the hepatic cause of unconjugated hyperbilirubinaemia?

A
  • Reduced activity of UGTIAI or glucoronotransferase can lead to increase levels of uncojugated bilirubin
79
Q

What are the two causes of reduced/absent UGTIAI enzyme activity?

A
  • Inherited
  • Acquired
80
Q

What are some inherited causes of UGTIAI impairement?

A
  • Gilbert’s syndrome (10%-30% activity)
  • Crigler-Najjar syndrome 1 (absent)
  • Crigler-Najjar syndrome 2 (<10%)
81
Q

What are some acquired causes of UGTIAI impairment?

A
  • Hyperthyroidism
  • Ethinyl estradiol (Birth control)
  • Antibiotics
  • Antiretrovirals
82
Q

When does Gilbert’s syndrome typically occur?

A
  • Around the timing of puberty
83
Q

When does Crigler-Najjar syndrome typically occur?

A
  • Around the neonatal period
84
Q

What are some causes of conjugated hyperbilirubinaemia?

A
  • Hepatocellular injury
  • Infiltrative disorders
  • Malignancy
  • Inherited disorders
85
Q

What is cholestasis?

A
  • Poor bile flow through the biliary system
  • Essentially a cause of post hepatic jaundice
86
Q

What is a complication of cholestasis?

A
  • Leads to a build up of toxic substances which can cause hepatocelluar injury
87
Q

What is the principal mechanism of post-hepatic jaundice?

A
  • Biliary obstruction which prevents the outflow of bile
88
Q

What are some of the causes of post-hepatic jaundice?

A
  • Cholestatic liver disease
  • Gallstones
  • Malignancy
  • Parasitic infections
  • Mirizzi’s syndrome
89
Q

What are the characteristic features of post-hepatic jaundice?

A
  • Elevated conjugated bilirubin
  • Increase in cholestatic liver enzyme
  • Obstruction seen in imaging
90
Q

What are some associated symptoms of post-hepatic jaundice?

A
  • RUQ pain
  • Fever
  • Malaise
91
Q

What is the most common cause of acute liver failure which requires a liver transplant?

A
  • Paracetamol induced liver disease
92
Q

What are the two types of ingestion seen in a paracetamol overdose?

A
  • Acute - Potentially toxic dose in less than an hour (75mg/kg)
  • Staggered - Potentially toxic dose in less than 24hr (150mg/kg)
93
Q

Where is the primary site of paracetamol metabolism and what is it conjugated with?

A
  • Liver
  • Conjugated with glucouronide and sulfate
94
Q

How does a paracetamol overdose cause problems?

A
  • Usual metabolism pathway becomes overwhelmed meaning toxic compounds begin to build up
95
Q

What are some of the consequences of toxic compound buildup in the liver?

A
  • Hepatocellular injury
  • Zone 3 necrosis of hepatocytes
  • Liver impairment
96
Q

What is the primary intervention for the treatment of a paracetamol overdose?

A
  • N-acetylcysteine (NAC)
97
Q

What is the method of action of NAC?

A
  • It is a pre-cursor of glutathione which therefore increases availabilty of glutathione to bind to NAPQI
98
Q

What are symptoms of paracetamol induced liver disease?

A
  • Usually asymptomatic in the first 24 hours
  • Nausea + Vomiting
  • Weight loss
  • Malaise
  • Abdo pain
  • Confusion
99
Q

What are the signs of paracetamol induced liver disease?

A
  • Asterixis
  • Brusing
  • Jaundice
  • RUQ tenderness
  • Oliguria/Anuria
  • Tachycardia
  • Hypotension
  • Coma
100
Q

What are the three different stages of NAC administration?

A

1 - 150mg/kg over 1 hour
2 - 50mg/kg over 4 hours
3 - 100mg/kg over 16 hours

101
Q

What should be done if there is an anaphylactoid reaction to NAC?

A
  • Temporarily stop infusion
  • Consider antihistamine
  • Nebulised salbutamol
102
Q

What is Wernicke-Korsakoff syndrome?

A
  • A disease spectrum that causes two classical neurological syndromes because of thiamine (B1) deficiency
103
Q

What is Wernicke’s encephalopathy?

A
  • An acute encephalopathy characterised by confusion, ataxia, oculomotor dysfunction
104
Q

What is Korsakoff syndrome?

A
  • A chronic amnesic syndrome that is characterised by defects in both anterograde and retrograde memory
105
Q

What are the stages of diease that lead to Wernicke-Korsakoff syndrome?

A
  • Chronic alcoholism
  • Thiamine deficiency
  • Brain tissue ischaemia + cell death
106
Q

What are some symptoms that Wernicke’s can cause?

A
  • Confusion
  • Ataxia
  • Nystagmus
107
Q

What are some symptoms of Korsakoff syndrome?

A
  • Memory deficit
  • Confabulation
  • Poor insight
  • Global congnitive dysfunction -> Dementia
108
Q

What are some potential causes of Wernicke-Korsakoff syndrome?

A
  • Prolonged fasting/starving
  • Anorexia nervosa
  • Hyperemesis gravidarum
  • Systemic malignancy
  • Haemodialysis/Peritoneal dialysis
  • GI disease and malabsorption
109
Q

How can a thiamine deficiency be detected?

A
  • Erythrocyte thiamine transketolase activity before and after the addition of thiamine
110
Q

What is the main treatment option for Wernicke-Korsakoff syndrome?

A
  • Pabrinex IV (Vitamin replacement that includes B vitamins)
111
Q

What are the complications associated with Korsakoff’s syndrome?

A
  • Can lead to Korsakoff’s psychosis which is an irreversible amnesic disorder
112
Q

What is Wilson’s disease?

A
  • A disease caused by the excess accumulation of copper in the blood
113
Q

What does Wilson’s disease cause?

A
  • Can lead to multi-system failure due to excess accumulation and subsequent competitve binding
114
Q

What is the main aetiological cause of Wilson’s?

A
  • Mutation of ATP7B gene on ch.13
  • Autosomal recessive
115
Q

What are some clinical features of Wilson’s disease?

A
  • Kayer-Fleischer rings (Brownish rings on outside of iris)
  • Sunflower cataracts
  • Acute liver failure
  • Hepatitis
  • Cirrhosis
  • Haemolytic anaemia
  • Behavioural change
  • Basal ganglia signs
116
Q

What investigations can be used in the diagnosis of Wilson’s disease?

A
  • Serum caeruloplasmin
  • Serum copper
  • 24 hour urinary copper
  • Liver biopsy
  • MRI/CT head
  • Genetic testing
117
Q

What is Gilbert’s syndrome?

A
  • An autosomal recessive condition that causes abnormal bilirubin processing in the liver
118
Q

What is pathological process surrounding Gilbert’s syndrome?

A
  • Genetic defect in the promoter region of the gene that encodes for the UGT1A1 enzyme
119
Q

What are the clinical features seen in Gilbert’s syndrome?

A
  • Recurrent episodes of jaundice
  • Unconjugated hyperbilirubinaemia
120
Q

What is fatty liver disease?

A
  • Accumulation of fat within the liver
121
Q

What is the difference between steatosis and steatohepatitis?

A
  • Steatosis = Accumulation of fat within the liver
  • Steatohepatitis = Steatosis + inflammation
122
Q

What is the main cause of FLD?

A
  • Defective fatty acid metabolism due to various impairments such as insulin or mitochondrial damage
  • This leads to accumulation of trigylcerides/lipids in the hepatocytes
123
Q

What are the main risk factors associated with FLD?

A
  • Metabolic syndrome
  • T2DM
  • Dyslipidaemia
  • PCOS
  • Central obesity
  • Impaired glucose tolerance
  • Excess alcohol
124
Q

What are some clinical features associated with FLD?

A
  • RUQ pain
  • Fatigue
  • Malaise
  • Stigmata of liver disease
  • Jaundice/Ascites
  • Cirrhosis symptoms
125
Q

What investigation are used in FLD?

A
  • LFT’s - ALT raised first, then AST>ALT as progression seen
  • Ultrasound
  • Liver biopsy = Definitive
126
Q

What are the different management strategies used in FLD?

A
  • Alcohol related -> Abstinence
  • Low fat diet
  • Exercise
  • Gradual weight loss
127
Q

What is the prognosis associated with FLD?

A
  • Steatosis has good prognosis with abstinence and weight loss
  • Steatohepatitis = 12% of pts -> Cirrhosis in <8yrs
128
Q

What is alcoholic liver disease?

A
  • Disease/damage of the liver caused by excess alcohol consumption
129
Q

What are the three stages seen in alcoholic liver disease?

A
  1. Steatosis - Fat accumulation due to alcohol metbolism being prioritised
  2. Alcoholic hepatitis - Liver inflammation due to conjugation of acetylaldehyde which damages proteins
  3. Cirrhosis - Ethanol stimulates stellate cells to release collagen -> Fibrosis -> Cirrhosis
130
Q

What are the symptoms seen in alcoholic liver disease?

A
  • Ascites
  • HTN
  • Oesophageal varices
  • Portal HTN
  • Hepatic encephalopathy
  • Hepatorenal syndrome
131
Q

What are the metabolic signs seen in alcoholic liver disease?

A
  • Muscle wasting
  • Swollen abdomen
  • Red tongue
  • Dry, scaly,cracked skin
132
Q

What the endocrine signs seen in alcoholic liver disease?

A
  • Gynaecomastia
  • Testicular atrophy
  • Loss of body hair
  • Signs of ‘pseudo-cushings’ (red face, hump, striae)
133
Q

What are the facial/skin signs seen in alcoholic liver disease?

A
  • Parotid enlargement
  • Spider naevi
  • Easy bruising
  • Dupuytren’s contracture
134
Q

What are the neuromuscular signs seen in alcoholic liver disease?

A
  • Tremor
  • Memory loss
  • Cognitive impairment
  • Peripheral myopathy
  • Epilepsy
  • Wernicke-Korsakoff syndrome
135
Q

What are the cardiovascular signs seen in alcoholic liver disease?

A
  • Hypertension
  • Cardiomyopathy
  • Hyperdynamic circulation
136
Q

What are the bone signs seen in alcoholic liver disease?

A
  • Rib fractures on CXR
  • Spinal osteoporsis particularly seen in men
137
Q

What is the main cause of alcoholic liver disease?

A
  • Alcohol
138
Q

What are the lab findings seen in alcoholic liver disease?

A
  • Moderately elevated transaminases
  • AST/ALT ratio > 2
  • Elevated bilirubin
  • Elevated GGT
  • Elevated neutrophil count
  • Elevated INR
139
Q

What are the biopsy findings seen in alcoholic liver disease?

A
  • Steatosis
  • Neutrophil infiltration
  • Hepatocyte ballooning
  • Fibrosis
  • Cholestasis
  • Mallory-denk bodies (Eosinophilic accumulations of proteins) - No pathological role but a marker of ALD
140
Q

What are the management strategies used in alcoholic liver disease?

A
  • Alcohol withdrawl is definitive strategy
    Other options include:
  • Alcohol cessation
  • Hydration (Monitor renal function)
  • Albumin infusions
  • Adequate nutrition, possible NG tube, vitamin supplements
141
Q

What is pancreatitis?

A
  • Refers to inflammation of the pancreas which can either be acute or chronic
142
Q

What is the main cause of pancreatitis?

A
  • Abnormal release and activation of enzymes which cause the autodigestion of pancreatic tissue
  • Causing reduction in function of the pancreas which lowers its synthetic output
143
Q

What are the symptoms of pancreatitis?

A
  • Abdominal pain that radiates posteriorly
  • Nausea and vomiting
  • Anorexia
  • Diarrhoea
144
Q

What are the clincal signs associated with pancreatitis?

A
  • Abdominal tenderness
  • Abdominal distension
  • Tachycardia
  • Tachypnoea
  • Pyrexia
145
Q

What are the different possible causes of pancreatitis?

IGETSMASHED

A

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion bites
Hypercalcaemia
ERCP
Drugs

146
Q

What investigations should be conducted when pancreatitis is suspected?

A
  • FBC
  • Obs
  • ECG
  • Blood sugar
  • Amylase/Lipase
  • CRP
  • U&E
  • LFT’s
  • Ultrasound
147
Q

What is the management used for pancreatitis?

A
  • IV fluids
  • Analgesia
  • Nutritional support
148
Q

What are the two different types of gallstones?

A
  • Cholesterol (85%)
  • Pigment stones (15%, Calcium bilrubinate)
149
Q

What are the different conditions that can occur as the result of gallstones?

A
  • Biliary colic
  • Acute cholecystitis
  • Acute cholangitis
150
Q

What is biliary colic?

A
  • Self-limiting RUQ/Epigastrium pain associated with gallstones
151
Q

What is acute cholecystitis?

A
  • Refers to acute inflammation of the gallbladder, mostly caused by gallstones
152
Q

What blood results are seen in acute cholecystitis?

A
  • Raised WCC/CRP
  • Normal/mild increase in LFT’s
153
Q

What can be seen in an USS in acute cholecystitis?

A
  • Gallstones
  • Inflamed, thickened gallbladder
  • Pericholecystic fluid
154
Q

What is acute cholangitis?

A
  • Refers to infection of the biliary tree commonly caused by an obstructing stone in the common bile duct
155
Q

What blood test results are seen in acute cholangitis?

A
  • Raised WCC/CRP
  • Raised bilirubin, ALP and ALT
156
Q

What can be seen in an USS in acute cholangitis?

A
  • CBD stone (Not great sensitivity)
  • Duct dilation
157
Q

What is Charcot’s triad?

A
  • Fever
  • RUQ pain
  • Jaundice
158
Q

What are the main types of cells found in the liver?

A
  1. Hepatocytes - Functional cells
  2. Cholangiocytes - Epithelial cells that line bile ducts
  3. Stellate cells - Mesenchymal cells in space of Disse
  4. Kuppfer cells - Liver macrophages in the sinusoids
159
Q

What are the four main ligaments of the liver?

A
  1. Round (Teres) ligament - Remnant of umbilical veins
  2. Triangular - Attach to diaphragm at apex of liver
  3. Coronary - Attach to diaphragm
  4. Falciform - Seperates the right and left lobes
160
Q

What line seperates the caudate and quadrate lobes?

A
  • Cantlie’s line
  • Caudate is found above the quadrate
161
Q

From where does the liver develop embryologically?

A
  • Develops as a diverticulum at the junction between foregut and midgut
162
Q

At which week does the liver bud appear and where is it seen?

A
  • Appears at week 3
  • As an outgrowth of the endoderm layer on the ventral aspect
163
Q

What does the cranial aspect of the liver bud form?

A
  • Forms the left and right lobes of the liver
164
Q

What does the caudal aspect of the liver bud form?

A
  • Gallbladder
165
Q

What are the normal functions of the liver?

A
  1. Carb/Protein/Lipid metabolism
  2. Drug/hormone processing
  3. Excretion of bilirubin
  4. Synthesis of bile salts - For emulsification
  5. Storage - Glycogen, vit. A/B12/D/E/K
  6. Activation of vitamin D
166
Q

What is responsible for the innervation of the liver?

A
  • Hepatic nervous plexus
  • Sympathetic fibres from coeliac pelxus
  • Parasympathetic fibres from ant./pos. vagal trunks
167
Q

What two vessels supply the liver?

A
  • Hepatic artery
  • Hepatic portal vein
168
Q
A

Year 2 Medicine @ Lancaster Uni (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions