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Met 3A > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What are the symptoms of acute/chronic liver disease?

A

asymptomatic

cholestatic - jaundice, pruritis, pale stools/dark urine

systemic - cachectic, fatigue, fever, xanthelasma, parotid enlargement, spider naevi, organomegaly, clubbing, Dupuytren’s contracture, telangiectasis

decompensation - ascites, distension, dizzy, drowsy, disorientated, hepatic flap, bleeding

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2
Q

What is Wilson’s disease?

A 
dysregulated Cu2+ 
autosomal recessive - ATP7B
excess copper deposits - especially in liver and brain
affects younger ages
presents similar to ALF + cirrhosis
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3
Q

What is haemochromatosis?

A

excess iron absorption in gut –> particularly effects, liver, heart, and endocrine glands

TF saturation and raised ferritin

affects M>W

primary = genetic cause/iatrogenic - autosomal recessive - HFE
secondary = from another disease/cause
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4
Q

How does alcohol lead to liver disease?

A

Metabolic –> alcohol, obesity, insulin resistance –> fat deposits

Inflammatory –> translation of lipid signal in inflammation - chemo/cytokines –> scarring + fibrosis

Genetic –> disturbance of lipid metabolism –> steatosis
PNPLA3
TM6SF2
MBOAT7

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5
Q

What is the AUDIT score?

A

= Alcohol Use Disorders Indentification Test

There are 3 sections:
hazardous alcohol use
symptoms of dependance
harmful alcohol use

10 questions - ?/40
>20 means concerning alcohol dependence
16-19 indicates hazardous use
8-15 indicates mild intervention required

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6
Q

What is Alcohol Withdrawal Syndrome?

A

onset of a set of symptoms after last drink

6-36hrs = headache, tremor, anorexia, palpitations, anxiety

6-48hrs = seizures

12-48hrs = alcoholic hallucinosis

48-96hrs = delirium tremens

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7
Q

How do you treat alcohol withdrawal syndrome?

A

chlordiazepoxide (benzodiazepine)

lorazepam if cirrhosed liver

if severe delirium tremens –> haloperidol

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8
Q

Define alcoholic hepatitis

A

recent onset of jaundice +/- ascites w/ ongoing alcohol abuse

presents with additional fever, raised WCC, platelets and AST

will show steatosis, hepatocyte ballooning and inflammatory infiltrate on biopsy

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9
Q

How is alcohol hepatitis managed?

A 
sepsis treatment
NG feed
steroids 
liver transplant
alcohol abstinence
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10
Q

What is NAFLD?

A

= Non-alcoholic fatty liver disease

caused by:
hepatic triglyceride accumulation –> FFA released –> oxidative stress –> inflammatory mediators –> inflammatory cascade –> progressive fibrosis –> cirrhosis

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11
Q

What is NASH?

A

= non-alcoholic steatohepatitis

a stage of NAFLD

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12
Q

How does NAFLD present?

A

abdnormal LFTs - ALT/AST >1, persistent transaminitis
fatigue
RUQ pain
hepatomegaly

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13
Q

What are the risk factors for NAFLD?

A 
obesity
T2DM
hyperglyceridemia
hypertension
metabolic syndrome
CVS complications
TPN
haemochromatosis
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14
Q

Which drugs can increase the risk of NAFLD?

A

steroids
amiodarone
methotrexate

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15
Q

How is NAFLD diagnosed?

A 
exclusion of other causes + 
metabolic syndrome =
impaired glucose tolerance
central obesity
raised LDLs but low HDLs
hypertension

liver bx + fibroscan

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16
Q

How is NAFLD treated?

A

weight loss

treat metabolic factors eg statins, antihypertensives

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17
Q

Describe the 5 types of viral hepatitis

A

Hep A - RNA - FO route - can be vaccinated

Hep B - DNA - hepadnavirus - parenteral (28-160 incubation days) - vaccine

Hep C - RNA - flavivirus - parenteral (15-150 incubation days)

Hep D - RNA - parenteral - protected via HBV vaccine

Hep E - RNA - FO route

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18
Q

What can happen as a result of an acute HBV infection?

A

Futuminant hepatitis
acute hepatitis
recovery
chronicity –> chronic hepatitis –> cirrhosis

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19
Q

What do these mean?

a. HBs Ag
b. HBs Ab
c. HBc Ab
d. HBe Ag
e. HBe Ab

A

a. HBV surface AntiGen - raised = active infection
b. HBV surface AntiBody - raised = immunisation
c. HBV core AntiBody -
d. HBV E AntiGen - raised = high infectivity
e. HBV E AntiBody - past infection/latent

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20
Q

Where does hep B and hep C most commonly affect?

A

B - S. America, Africa, Middle East

C - Central Asia, Africa, S. America

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21
Q

How is Hep B treated?

A

aim is to decrease viral replication

nucleoside/tide analogues (RTi)
eg entercovir or tenofovir

PEG-IFN

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22
Q

How is Hep C diagnosed?

A 
HCV IgG +ve
HCV RNA
Genotype 1-6
LFTs
HCC screen - US + AFP (alpha feto-protein)
Bx or fibroscan
23
Q

How is Hep C treated?

A

curable!
8-12 weeks

combinations of these drugs depending on genotype + stage of fibrosis:
Harvoni
Vierkirax + exvira
Zepatier
Epclusa
Mariviret
24
Q

How is haemochromatosis diagnosed and treated?

A

fibroscan or bx –> ferriscan of liver

treatment = venesection or Fe chelation therapy

25
Q

How is Wilson’s disease diagnosed?

A 
low caer
raised urinary Cu2+
liver bx
MRI brain
Kaiser-Fleischer rings
movement + psychiatric disorders - due to copper deposits in basal ganglia
26
Q

How is Wilson’s treated?

A

Cu chelation therapy

eventually need liver transplant

27
Q

How is HCC screened for and diagnosed? What is its main RF?

A

AFP test every 6 months for those with known cirrhosis

diagnosed with CT + MRI

28
Q

How do you treat HCC?

A

Curative:
surgical resection
transplant
RFA

Palliative:
TACE - transcatheter arterial chemoembolisation 
SIRT - selective internal radiotherapy
RFA - radiofrequency ablation 
Sorafenib - protein kinase inhibitor
29
Q

How do you test for HBV?

A

Screen:
HBcAb - previous infection
HBsAg - active infection

If +ve:
HBeAg - how infective?
HBV DNA - viral load

If solely HBsAb –> vaccinated

30
Q

What is Autoimmune Hepatitis?

A

auto-antibodies made attack hepatic cells –> interface inflammation

F>M 3:1

associations: autoimmune thyroid, coeliac, vitiligo

31
Q

How is AIH diagnosed?

A

raised ALT
auto-antibodies present - SM, ANA, LKM, ALSA
raised IgG
liver Bx

32
Q

How is AIH treated?

A

high dose steroids –> prednisolone, budesonide
immunomodulators –> azathioprine
Liver transplant if nothing helps

33
Q

What are some clinical features of CLD?

A

systemic:
weight loss
muscle loss
fatigue

cholestatic:
jaundice
pruritus
pale stools/dark urine
 otherwise asymptomatic until decompensation
34
Q

What are the features of decompensated liver disease?

A 
jaundice
fluid retention - low albumin 
drowsiness/confusion/hepatic flap - ammonia build up
GI bleed - varices
sepsis
splenomegaly - pancytopenia
35
Q

What are signs of compensated liver disease?

A 
xanthelasmata
parotid enlargement
spider naevi
palpable liver
clubbing
dupuytren's contracture
pigmented ulcers
gynacomastia 
palmar erythema
36
Q

How do you treat a variceal bleed?

A 
ABCDE
Abx
Terlipressin
Endoscopy - banding/glue
TIPSS = Transjugular intrahepatic portosystemic shunt

banding + beta-blockers to prevent recurrence

37
Q

How does liver disease lead to ascites?

A

low protein production –> low albumin –> low oncotic pressure –> fluid leaves vessles –> ascites

potal hypertension –> splanchnic vasodilation –> decreased effective circulating volume –> upregulation of RAAS –> renal Na+ avidity –> ascites

38
Q

Spontaneous bacterial peritonitis can occur when ascites is present? How is it diagnosed and treated?

A

WCC >250
neutrophils
gram -ve rods - E.Coli most common
jaundice

IV abx (cefotaxime) + human albumin solution (HAS)

39
Q

How is ascites treated?

A 
low sodium diet
paracentesis
diuretics - spironolactone or furosemide
TIPSS
liver transplant
40
Q

What is hepatorenal syndrome?

A

renal failure in the setting of cirrhosis + hepatic circulatory dysfunction

type 1 = precipitant eg AIH
type 2 = progressive

41
Q

How is HRS treated?

A

HAS + terlipressin + liver transplant

42
Q

What is hepatic encephalopathy?

A 
= altered level of consciousness due to liver failure and accumulation of ammonia 
graded I (mild confusion) --> IV (comatose)
precipitants inc:
constipation
sepsis
GI bleeding
drugs - opioids, diuretics, BDZs
dehydration
PVT
43
Q

How is hepatic encephalopathy diagnosed and treated?

A

hepatic flap + confusion
serum ammonia
EEG

Treat precipitants
lactulose –> flush out NH4+
Rifaximin
liver transplant

44
Q

How can you tell the difference between hepatic and obstructive jaundice?

A

hepatic will have normal looking stool + splenomegaly

whereas obstructive will have pale stools + no splenomegaly

45
Q

What are these Liver Function enzymes?

a. ALT
b. AST
c. ALP
d. GGT

A

a. alanine aminotransferase - specific to liver
b. aspartate aminotransferase - mitochondrial enzyme released from heart/muscle/kidney/liver
c. alkaline phosphatase - bile cannicular + sinusoidal membranes + bones + placenta
d. gamma-glutamyl transpeptidase - hepatocellular - raised in cholestasis + alcohol

46
Q

If a person tests positive for ____, they most likely have?

a. AMA, M2M, IgM
b. ANA, SMA, SLA, IgG
c. ANCA
d. IgA

A

a. Primary Biliary Cholangitis
b. AIH
c. Primary Sclerosing Cholangitis
d. ALD

47
Q

What does TIPSS do?

A

decreases portal system pressure

embolises recurrent varices

48
Q

What is Primary Biliary Cholangitis (PBC)?

A

small bile duct destruction
F>M 9:1
>40 yrs

49
Q

What are the S&S of PBC? How is it diagnosed?

A

xantholasmata
jaundice
pruritis
fatigue

raised ALP + GGT
presence of AMA + M2
fibroscan —> ductopenia
grannuloma on bx

50
Q

How is PBC treated?

A

1st line = ursodeoxycholic acid (UDCA)
–> thins bile and makes it flow easier

2nd line = obeticholic acid if that doesn’t work

for itching - cholestyramine or rifampicin

51
Q

What is Primary Sclerosing Cholangitis (PSC)?

A

= chronic inflammation and scarring of the bile ducts (in particular, the large bile ducts)

M>F 2:1
>20yrs
65% have an IBD
increased risk of cancer - cholangiocarcinoma + colorectal

52
Q

What are the symptoms of PSC?

A

xantholasmata
jaundice
pruritis
fatigue

53
Q

How is PSC treated?

A

no treatment
ERCP for strictures
liver transplant

Met 3A (19 decks)

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