chronic liver disease Flashcards
1
Q
presentation of liver infection (5)
A
enlarged liver lymphadenopathy fever riggors general malaise
2
Q
enlarged smooth edged liver suggestive of
A
hepatitis
3
Q
infective causes of hepatomegaly (6)
A
- infectious mononucleosis
- viral hepatitis
- malaria
- amoebic
- hydatid cysts
- leishmaniasis
4
Q
cancers causing heptomegaly (4)
A
leukemia
lymphoma
hepatocellular carcinoma
5
Q
signs of liver cirrhosis (3)
A
jaundice
spider naevi
palmar erythema
6
Q
metabolic causes of liver disease (3)
A
Wilson’s syndrome
Haemochromatosis
acute porphyria
7
Q
3 drugs causing hepatitis
A
statins
amiodarone
macrolides
8
Q
2 main liver enzymes -released after hepatocellular injury
A
AST
ALT
9
Q
which liver enzyme is more specific for hepatic injury
A
ALT
10
Q
where can AST be found (3)
A
Skeletal and cardiac muscle
hepatocytes
RBCs
11
Q
ratio of AST and ALT increase in liver injury
A
1:1
12
Q
alcoholic liver disease ratio of AST to ALT
A
AST>ALT above 2:1
13
Q
ALP increased in
A
biliary tree obstruction -but not specific to liver
14
Q
where can ALP be found
A
liver
bone
placenta
15
Q
if ALP is raised from bone what will be normal
A
GGT
16
Q
3 tests for hepatic function (not liver enzyme tests)
A
serum albumin
serum bilirubin
PT/INR
17
Q
cholestatic pattern of liver enzymes
A
- marked increase ALP and GGT
- mild increase ALT and AST
18
Q
hepatic pattern of liver enzymes
A
- marked ALT and AST increase
- minimal to no ALP increase
19
Q
increase AST + ALT by several 100 = (3)
A
- chronic hepatitis
- alcohol induced hepatitis
- NAFLD
20
Q
increase AST and ALT by several 1000
A
acute viral heptitis
21
Q
increase AST and ALT by >10,000 (2)
A
- toxin related paracetamol (paracetamol)
- liver ischaemia
22
Q
5 manifestations of liver disease
A
- coagulopathy
- ascites
- hepatorenal syndrome
- variceal bleeding
- hepatic encephalopathy
23
Q
what substances accumulation causes hepatic encephalopathy
A
ammonia
24
Q
what happens to ammonia in the brain
A
absorbed and removed by astrocyte brain cells
25
how do the astrocyte cells metabolise ammonia
via converting glutamate to glutamine to metabolise the ammonia
26
what does increasing glutamine stores do to brain cells
causes osmotic pressure changes and causing water movement into the brain causing cerebral oedema
27
mental state changes in hepatic encephalopathy (5)
- forgetfulness
- confusion
- irritability
- inverted sleep pattern
- personality change
28
LFTs hepatic encephalopathy
increased AST, ALT, albumin, bilirubin, PT,
29
management of hepatic encephalopathy (5)
- lactulose
- antibiotics
- increased protein and kcal diet
- BCAA and protein supplements
- transplant
30
pathology of variceal bleeding
fibrosis compresses veins and arteries--> portal hypertension --> high pressure in collateral circulation --> veins in lower oesophagus dilated and prominent --> more prone to damage from coughing/ eating etc --> hematemesis
31
hepatorenal synrome=
rapid deterioration in renal function with cirrhosis or fluminant liver failure
32
when does hepatorenal syndrome often occur
sudden insult to the liver -infection of GI bleed
33
what happens causing renal hypotension
cirrhosis causes release of NO, prostaglandins and other vasoactive substances causing splanchnic vasodilation
34
what does hypotension in the kidneys trigger
RAS - further hypoperfusion of the kidneys -kidney failure
35
hepatorenal syndrome 1=
- rapid deterioration circulation and renal function -
- terlipressin resists hypovolemia
- may need haemodialysis
- median survival <2 weeks
36
hepatorenal syndrome 2 =
- steady deterioration
- may need TIPS
- 6 months median survival
37
medical management of hepatorenal syndrome
terlipressin
octreotide
midodrine
38
surgical management of hepatorenal syndrome
liver transplant +/- kidney transplant
39
ascites pathology
portal hypertension causing splanchnic vasodilation --> hypoperfusion of kidneys +RAS --> Na+ reabsorption + aldosterone --> fluid retention
40
aldosterone released from
zona glomerulosa of adrenal gland
41
what in liver failure contributes to ascites formation
less albumin formation decreasing osmotic pressure
42
causes of ascites
portal hypertension
hypoalbuminemia
malignancies
infections
43
complications of ascites (3)
bacterial peritonitis
hepatorenal syndrome
thrombosis
44
3 clinical features of ascites
abdominal swelling
SOB
weight gain
45
what does serum ascites albumin gradient (SAAG) determine
if ascitic fluid is due to portal hypertension
46
SAAG >1.1=
ascites due to portal hypertension
47
SAAG <1.1 =
etiology other than portal hypertension -nephrotic syndrome, cancer
48
investigations of an ascitic tap
```
albumin measurement
neutrophil count
amylase
culture
cytology
```
49
2 effects of decreased thrombopoietin synthesis
thrombocytopenia
| portal hypertension
50
hepatitis acute symptomatic disease (4)
Hep A
Hep B
Hep B+D
Hep E
51
possible hepatitis chronic disease
Hep B
Hep B+D
Hep C
52
transmission route of Hep A
fecal oral route
53
recovery from Hep A
99%
54
diagnosis of Hep A
high ALT + bilirubin
55
symptoms of Hep A
jaundice
epigastric pain
nausea
dark urine/ pale stools
56
Hep B transmission route
```
blood-blood
sexual
unsterile needle
vertical
tattooing and body piercing
```
57
Hep B more prevalent in
health care workers
58
if Hep B not treated can lead to
HCC
59
HBsAg=
antigen present of outside of virus
60
HBsAg antibodies without antigens=
non-infected immunity
61
HBcAg=
core antigen
62
HBcAg indicates
active viral replication and infection
63
Hep C infection presentation
remains asymptomatic and develops into chronic disease
64
Hep C spread=
blood-blood contact
65
test for Hep C
Anti-HCV antibody test
66
if anti-HCV positive next step =
HCV polymerase chain reaction -positive in chronic infection
67
most common cause of viral hepatitis worldwide=
Hep E
68
host of Hep E=
pig
69
most cases of Hep E=
asymptomatic
70
range of disease in NAFLD
steatosis
steatohepatitis
fibrosis
cirrhosis
71
what causes NAFLD
fatty deposits in the liver unrelated to alcohol or viral cause
72
metabolic syndrome = 3 of the following (5)
```
obesity
hypertension
diabetes
hypertriglyceridemia
hyperlididemia
```
73
what factor is a major contributor to NAFLD
insulin resistance
74
macroscopic view of liver in NAFLD
large
soft
yellow
greasy
75
clinical features of NAFLD -My hepatocytes no more fast food
- micro/ macrovesicular steatosis
- hepatocyte balloon degeneration with necrosis and apoptosis
- neutrophil rich inflammation
- mallory denk bodies
- fibrosis
76
complications of NAFLD
cirrhosis
| HCC
77
LFTs of NAFLD
ALT> AST
78
liver cirrhosis =
end stage liver damage by disruption of normal hepatic parenchyma by bands of fibrosis and nodules
79
inflammatory changes in cirrhosis=
TGF-beta sub-endothelial fibrosis from stellate cells
80
where are stellate cells
beneath endothelial cells lining sinusoids
81
causes of cirrhosis (7)
-alcoholic liver disease
-NAFLD
-Chronic hep A and C
-PBC and PSC
-haemochromatosis and wilsons disease
alpha-1 antitrypsin
-cystic fibrosis
82
why do you get palmar erythema
hyperestrinism since liver removes estrogen from blood
83
compensated cirrhosis classical presentation (3)
fatigue
weight loss
weakness
84
decompensated cirrhosis presentation (6)
```
confusion
ascites
edema
pruritis
hematemesis
melena
```
85
what score can predict mortality and survival in liver disease
Child-pugh score -A BEAP
86
Child-pugh score=
```
Albumin
Bilirubin
Encephalopathy
Ascites
PT (INR)
```
87
liver failure=
development of coagulopathy and encephalopathy
88
hemochromatosis=
excess iron in body which deposits in tissues
89
primary hemochromatosis =
autosomall recessive defect -HFE gene
90
secondary hemochromatosis (3)
chronic transfusions
CLD
ineffective erythropoiesis
91
when does hemochromatosis present
late adulthood 30-50 years old
92
classical triad of disease from hemochromatosis
- micronodular cirrhosis
- diabetes mellitus
- bronze skin
93
complications of hemochromatosis
```
HCC
cirrhosis
CHF
cardiac arrhythmia's
thyroid dysfunction
sepsis
```
94
treatment of hemochromatosis
venesect
| avoid iron rich food
95
Wilsons disease=
increased copper from
- lack of copper transport into bile
- lack of copper incorporation into ceruloplasmin
- decreased ceruloplasmin secertion into blood
96
when does wilsons disease usually present
<30 years old
97
neurological changes of wilsons (4)
- change in behaviour
- dementia
- chorea
- parkinsonian symptoms
98
eye change in wilsons
kayser-fleischer rings in descemet membrane of cornea
99
skin changes in wilsons (3)
- blue lunulae in nails
- grey skin
- hypermobile joints
100
complications of wilsons (7)
```
HCC
Coombs
arthritis
neurological deficits
psychiatric problems
amino aciduria
nephrocalcinosis
```
101
management of wilsons (6)
- avoid copper
- lifelong D-penicillamine
- anticholinergics, GABA antagonist
- antiepileptics
- lactulose
- liver transplant
102
A1 anti-trypsin deficiency =
defect in protease inhibitor
103
consequence of a1 anti-trypsin deficiency
emphysema and liver
104
when does a1 anti-trypsin present
30-40
105
symptoms of panacinar emphysema
SOB
wheezing
cough
106
three systems affected with PiZZ genotype of a1 anti-trypsin deficiency
lungs
liver disease
skin disease
107
what is affected by the PiSZ genotype of a1 anti-trypsin deficiency
predisposed to lung disease
108
management of a1 anti-trypsin (3)
- quit smoking
- IV augmentation via infusion of pooled human a1 antiprotease
- transplant
