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2a RRS > liver liver > Flashcards

liver liver Flashcards

1
Q

what are the 3 progressive stages of alcoholic liver disease

A

fatty liver disease
alchololic hepatitis
alcholic cirrhosis

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2
Q

what happens in fatty liver disease

A

metabolism of alchohol to fat

accumulates in cells - steatosis

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3
Q

what occures in alcoholic hep

A

infiltration by polymorphonuclear leucocytes (look for mallory bodies and giant mitochondria)
and hepatocyte necrosis occurs
inflamation

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4
Q

what is alcoholic cirrhosis

A

micronodular type - regenerative

mixed pattern seen with fatty changes

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5
Q

Cfs of fatty liver disease

A

asympt.

vague abdo symptoms assos w alcohol consumption

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6
Q

CFs of alcoholic hep

A

mild to mod ill health - mild jaundice
chronic Liver symptoms ==> hepatic enceph
ascites
easy bruising

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7
Q

CFs of alcoholic cirrhosis

A 
signs of chronic L disease
jaundice
ascites
high fever
clubbing
abdo pain
hepatomegaly
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8
Q

3 warning signs of severe alcoholic liver disease

A

coagulopathy
jaundice
encephalopathy

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9
Q

Dx of fatty liver disease

A

mild abnormalities on LFT
increased ALT (increased AST to ALT ratio)
ALP increase
y-GT increase

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10
Q

Dx of alcoholic hep bloods

A 
elevated PTT (thrombocytopenia)
elevated serum bilirubin
increase AST
increase WCC
macrocytic anaemia
low serum albumin
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11
Q

Dx of alcoholic hep not bloods

A

histology - mallory bodies and giant mitochondria
perivenular fibrosis
leucocyte infiltraion

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12
Q

Mx of alcoholic liver disease

A

stop drinking - in fatty liver this is reversible
alcoholic hep - pre cirrhotic
treat withdrawals with diazepam (tremor,sweats,arrythmia)
supplements - protein for encephalopathy
steroids - supress imune system
ALCOHOLIC CIRRHOSIS - liver transplant

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13
Q

how do you predict alcoholic hep prognosis

A

Maddrey score

glasgow score

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14
Q

chronic liver disease symptoms

A 
pruitus
anorexia
malaise
fatigue
fever
weakness
R hypochondriac pain(liver distension)
abdo distension
fetor hepaticus (ammonia breath)
haematemesis / dysphagia (oesophogeal varices)
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15
Q

chronic liver disease sign

A 
Ascites
Anorexia
Atrophy of testicles
Asterix
Bruising
Clubbing
Colour of nails (leukonychia)
Dyspagia (varices)
Erythema (palmor)
Encephalopathy (confusion)
Fetor hepaticus (Fishy ammonia breath)
(G)
Hepatomegaly
Increased unconj bilirubin -->
Jaundice

AAAABCCDEEF(G)HIJ

spider naevi
splenomegaly (portal HTN)
periph oedema

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16
Q

Causes of chronic L disease

A 
cirrhosis
hep B C D
Non alc fatty liver 
Metabolic (wilsons, haemchromatosis, alpha 1 antitrypsin defic)
Biliary tract diseases n stones
autoimmune hep
Drugs (methotrexate, paracetabol OD)
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17
Q

what is wilsons disease

A

autosomal recessive genetic defect (in ATP7B) causing a XS of COPPER deposited in tissues (liver, basal ganglia and cornea)

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18
Q

what causes wilsons disease

A

ATP7B defect meaning cannot bind Cu to apoceryloplasmin turning it into ceryloplasmin (Cu carrying protein)
Rest is packaged into vesicles - exocytosed into the bile for excretion
This cannot occur so Cu builds up - free radicals - and spills out into intestinal space - blood stream - deposits in tissues

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19
Q

where does copper deposit in wilsons

A

liver
cornea
basal ganglia

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20
Q

Presentation of Wilsons disease in children

A

hepatic probs - hepatitis
cirrhosis
fulimant liver failure

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21
Q

presentation of wilsons in teens n adults

A

CNS problems - Cu deposits in the basal ganglia = PARKINSONISM - tremor, rigidity
cerebral cortex = changing mood and mem loss
dementia
ataxia
dysarthia

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22
Q

Signs of Wilsons

A

ascites
tremor
Kayser - Fleischer rings in cornea

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23
Q

what is seen on examination with a slit lamp in Wilsons

A

Kayser-Fleischer rings

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24
Q

Dx of Wilsons

A 
bloods - low serum Copper, lowe serum ceryloplasmin
24hr urinary Cu excretion high
LFT - elevated 
MRI - basal ganglia and cerbella degen
slit lamp = KAYSER - FLEISCHER RINGS
LIVER BIOPSY - increased hepatic Cu
(DNA test?)
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25
Q

Mx of Wilsons

A

penicillamine (binds free Cu = chelation)
Zinc (prevents Cu absorption) (slow onset)
Sever? - Liver transplant

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26
Q

what is alpha 1 - antitrypsin deficiency

A

autosomal recessive - causes liver cirrhosis and emphesema in adults
defect in alpha 1 - antitryspin protease inhibitor so elastase over activity (not inhibited)

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27
Q

what does alpha 1 AT do

A

its a protease inhibitor that inhibits the activity of elastase that breaks down elastin

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28
Q

consequence of too much elastase in A1AT defic

A

elastin in walls of alveoli broken down causing emphysema - dyspnoea

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29
Q

consequences in liver of alpha1AT defic

A

misfolded = gets stuck in endoplasmic reticulum of the liver = builds up = hepatocyte death = liver cirrhosis

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30
Q

Dx of alpha 1 AT defic

A

serum alpha 1 A low

Liver biopsy

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31
Q

Tx of alpha1 antitrypsin

A

IV alpha1AT
supportive - dont smoke
liver cirrosis tx
tranplant if req

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32
Q

Presentation of A1AT defic

A

SOB
dyspnoea
cirrhosis symptoms - portal HTN - varices, jaundice

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33
Q

what is hereditary haemochromatosis

A

XS iron depostited in organs leading to fibrosis and organ failure
autosomal recessive HFE gene mutation decreasing hepcidin production

34
Q

what does hepcidin do

A

controls Fe absorbtion

synthesised in the liver

35
Q

how does hereditary haemochromatosis result in XS iron absorption

A

HFE gene mutation so decreased hepcidin gene expression = less hepcidin sythesised so doesnt do neg feedback on Fe levels == increase in iron absorption == XS taken up by the liver

36
Q

what is a consequence of increased uptake of iron in the liver

A

over long period causes fibrosis due to free radical production and thus cellular damage

37
Q

Cfs of hereditaryhaemochromatosis

A

liver = cirrhosis (jaundice, ascites), increased cancer risk
pancreas = type 1 diabetes (beta islet cell damage)
skin = bronze (melanin depostition)
heart = deposits in myocardium = cardiomyopathy
joints = degenerative joint disease
Jack Lost His Point and Shoot

38
Q

acronym for hered haemochromatosis

A 
Jack Lost His Point and Shoot
J- Joint = arthralgia
L- Liver = hepatomegaly
H - heart - cardiomyopathy
P - pancreas (T1DM) and pituitary (hypogonadism) 
&; - erectile dysfuntion
S - skin - bronzed
39
Q

what is a complication of haematochromatosis

A

Liver cirrhosis = increased risk of hepatocarcinoma

bronze diabetes = bronze skin, hepatomegaly, DM

40
Q

Dx of haematochromatosis

A 
increased ferritin (stores iron in cells)
and transferrin (careful as increase in inflam)
liver biopsy = perls stain blue
genetic testing - HFE genotype
total iron binding capactiy
41
Q

Mx of haematochromatosis

A

venesection - life long - weekly
anual monitoring
Hep A and B vaccine
DEFERIOXAMINE = iron chelation

42
Q

what is secondary haemochromatosis cause by and how prevented

A

too many blood transufions = prevented by chelation

DEFERIOXAMINE

43
Q

haemochromatosis management disease modifying drug

A

DEFERIOXAMINE = iron chelation

44
Q

functions of the liver

A

Protein synthesis and metabolism- albumin, carrier proteins and coag factors, hepcidin and ferratins
Lipid and glucose metabolism
hormone and drug inactivation- converts to hydrophillic
conjugation of bilirubin to be excreted
bile synthesis
Immune function- consumes antigens
activation of Vit D

45
Q

Breakdown of RBCs

A

Haemoglobin in macrophage in spleen liver or bonemarrow- splits into globin (get reused) and haem.
haem broken into Fe and porphyrin which becomes unconj bilirubin (water insol so binds to albumin in blood) and leaves to liver = gets conjugated (now water sol) and is secreted into bile where it becomes urobiliogen (via enterohepatic circulation - kidneys - urine) or sterobillin (stools)

46
Q

causes of pre hepatic jaundice and what see

A

Haemolytic- increased turnover= increased unconjugated bilirubin. liver functional so there is no bilirubin in urine just very dark urine due to increased urobiliogen

Cx= haemolytic anaemia, ineffective haematopoeisis
spherocytosis

47
Q

causes of intrahepatic jaundice

A

failure of bile secretion
Cx= autoimmune cholangitis, viral hep, alcoholic hep, cirrhosis
pale stools dark urine itching

48
Q

causes of extra hepatic jaundice

A

biliary drainage interference - pale stools dark urine
as no urobilinogen (and thus sternobilin) and itching
Cx= common duct stones
carcinoma
biliary stricture
sclerosing cholangitis
pancreatic pseudocyst

49
Q

complications of liver failure

A 
encephalopathy 
jaundice 
Ascites - spontanous bacterial peritonitis 
sepsis 
portal hypertension - varices 
renal failure 
Hepatiocell carcinoma
50
Q

Management of liver cirrhosis

A

diet, stop alcohol and reduced NSAIDS and Salt to minimum
Screen every 3-6 months via ultrasound and Alpha fetoprotien for H
treat prutius by- colestyramine
put on transplant list if decompensated

51
Q

Penicillamine SE and what used for

A

used as copper chelation in Wilsons disease

S/E = skin rashes, hematuria, renal damage

52
Q

what is liver cirrhosis

A

non specific disease, is an end stage of all progressive chronic liver diseases, which once fully developed is irreversible.
liver architecture is diffusely abnormal so interferes with blood flow

53
Q

histologically what is liver cirrhosis

A

Histologically, loss of normal hepatic architecture with bridging and nodular regeneration

54
Q

What cells are involved in liver cirrhosis

A

stellate and kuffer cells get activated

55
Q

pathophysiology of the stellate cells in liver cirrhosis

A

activated by cell injury = stellate cells release cytokines that produce collagen = fibrosis (TGF-beta)
the cytokines then attract neutrophils n macrophages = further inflam and necrosis
fibrosis of space of diss = loss of fenestrations impairing L function.
Fibrosis compresses BVs = portal hypertension = fluid OUT into peritoneal cavity = ASCITES

56
Q

pathophysiology of the kupffer cells in liver cirrhosis

A

phagocytose nectotic and apoptic cells - secrete pro inflam mediators - increase myofibroblasts - fibrosis and scarring

57
Q

2 types of liver cirrhois nodules and causes of each

A

micro and macronodular
micro = alcohol, biliary tract disease
macro = chronic hepatitis

58
Q

2x types of cirrosis

A

decompensated

compensated

59
Q

what is decompensated cirrhosis

A

cannot function adequately - extensive fibrosis

60
Q

CFs of decomp cirrhosis

A 
jaundice
clubbin
ascites
easy bruising
hepatic encephalopathy
leuconychia (low albumin = white nails)
61
Q

Cfs of compensated cirrhposis

A

non specific - weight loss and fatigue

62
Q

what is comp cirrhosis

A

still functioning effectivinly - asympt

some fibrosis

63
Q

causes of liver cirrhosis

A 
XS alcohol consumption
prolonged viral (hep B and C)
autoimmune Hep
wilsons
alpha 1 antitrypsin defic
primary biliary cirrhosis
64
Q

how does fibrosis cause ascites

A

portal hypertension causing fluid to accumulate in peritoneal cavity (down pressure gradient)

65
Q

how does fibrosis lead to hepatorenal failure

A

portal hypertension causing incresae in pressure so a portosystemic shunt

66
Q

why is splenomegaly a complication of cirhosis

A

portal hypertenion due to fibrosis causes back up of blood in spleen

67
Q

why CNS effected in cirrhosis

A

HEPATIC ENCEPHALOPATHY
portal hypertenion due to fibrosis of liver, blood diverted and liver function decreased
less detoxification so ammonia not metabolized (toxic) - depostis in brain =
asterix
confusion
coma

68
Q

in liver cirrhosis what causes parma erythema and spider naevi

A

failing liver function = less oestrogen metablozied therfore increase in blood

69
Q

Dx of liver cirrhosis

A

livery biopsy
bloods - LFT (low albumin, long PTT)
biochem - AST and ALT increased
imaging - size texture, blood flow changes etc

70
Q

Mx of liver cirrhosis

A

no alcholo

avoid NSAIDs and Aspirins = precip GI bleeds or renal impairment

71
Q

what is portal hypertension an effect of

A

cirrhosis

72
Q

what makes up the portal vein

A

splenic and SMV

73
Q

What does portal hypertension cause

A

dilation of vessels causes collaterals to form. if these form in gastoesophageal junction they are called varices

74
Q

presentation of gastroesophageal varices bursting

A

Haematesis and Melaena

hypovolemic shock

75
Q

causes of portal hypertension

A

prehepatic- congenital abnormality, portal vein thrombosis
hepatic- cirrhosis(commonest), sarcoidosis, schistosomiasis (cause = flatworms)
post hepatic- RIGHT sided heart failure, IVC obstruction, contrictive pericarditis

76
Q

Cfs of portal hypertension

A 
GI bleed secondary to haemorrages = haematesis and melaena
ascites
jaundice
thrombocytopenia
anaemia
leukopenia
77
Q

management of active gastroesophageal varices bleed

A

stabilise- IV plasma or blood transfusion, treat shock, prophylaxis antibiotics
endoscopy to confirm this was variceal bleed
injection scleroptherapy or variceal banding to stop hleeding

78
Q

what are varices

A

abnormally dilated vessel - usually in venouse stystem

79
Q

what causes varices to form

A

portal HTN - activates myofibrobalsts to contract (NO, endothelin and prstaglandin mediated). increases resistance to blood flow hence opening portosystemic anastomoses.
Na retention due to splanchnic vasodilatoin.
blood flow redirected to lower p areas so collateral circ develops - distended BV and thing walled = bleed

80
Q

Cfs of varices bleed

A

signs = anaemia and liver disease
haematemesis
abdo pain
dysphagia

2a RRS (26 decks)

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