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Liver Problem Flashcards

0
Q

What is jaundice?

What is the earliest sign of jaundice and why?

A

Yellow discolouration of skin

Scleral icterus = yellow discolouration of ie = Sclera has high affinity for Bilirubin

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1
Q

A serum BilRubin level of what leads to jaundice

A

> 2.5 mg/dL

Increase UCB +/or increase CB

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2
Q

Grt

A

Ffs

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3
Q

Give the type of hyperbilirubinaemia
Whether there is BiliRubin or UBG in Urine
@extravascular haemolysis or ineffective erythropoiesis

Explain the disorder

A

CB BM macrophage consume RBC) – >

XS UCB i.e.
more UCB made>Liver ability to conjugate UCB

– >XS UCB @blood – >

XS CB at bile therefore increased p(pigmented gallstone) Cos will deconjugate again– >

XS Billy Rubin + duodenum = XS urobilinogen – >

XS resorbed into blood + filtered @kidney – >

Dark urine due to XS urobilin

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4
Q

Give the type of hyperbilirubinaemia
Whether there is BiliRubin or UBG in Urine
@physiological jaundice of newborn

Explain how a newborn Can become jaundiced

A

CB

Increased you see B @blood = fat-soluble therefore can’t go to urine– >

Kernicterus = fat-soluble UCB deposit @brain = Basal ganglia = Neuro deficit + death

Phototherapy – >(Convert fat-soluble UCB – >
water-soluble UCB) – >UCB leak out into your

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5
Q

Give the type of hyperbilirubinaemia
Whether there is BiliRubin or UBG in Urine
@Gilbert syndrome

Explain Gilbert syndrome

A

Genetically mildly low AR UGT conjugating activity
+
decreased Bilirubin uptake
– > increased UCB

Patient metabolises less BUT
UCB amount metabolised = amount made

@Stress + fasting UCB made >UCB metabolised = jaundice

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6
Q

Give the type of hyperbilirubinaemia
Whether there is BiliRubin or UBG in Urine
@crigler-najjar syndrome

Explain crigler-najjar syndrome

A

Absence of UGT – > Very high UCB – >
Kernicterus + jaundice

Type II = less severe: phenobarbital – >increased liver enzyme synthesis

BASICCALLY The same as Gilberts syndrome but worse

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7
Q

Explain Dublin Johnson+ Rotor syndrome

A

Rare autosomal recessive = deficient canalicular transport protein

@Hepatocyte: UCB – >CB – >exported from Canalicular Transport Protein into canaliculi To go to the duodenum

But due to Decreased CTP = CB build up @hepatocyte – >leak into blood – >conjugated hyperbilirubinaemia– >

PITCH BLACK LIVER (rotor syndrome limit isn’t black but it’s exactly the same process)

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8
Q

Explain biliary tract obstruction leads to jaundice

A

Gallstones, pancreatic carcinoma,
Parasites/liver fluke, cholangiocarcinoma– >

Obstruction – >

  1. CB leak into blood
  2. Bile Salts/acids leak into blood– >Deposit @skin
    – >Pruritus
  3. Cholesterol leak = hypercholesterolaemia
    – >xanthoma

– > bile not in bowel =
pale stools, steatorrhea, malabsorption of fat-soluble vitamins ADEK, dark urine due to blood CB increase = water-soluble = BilRubinuria = dark

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9
Q

Give the type of hyperbilirubinaemia
Whether there is BiliRubin or UBG in Urine
@hepatitis virus

Explain viral hepatitis

A

CB = 20 to 50% = mixed
Increased bilirubin + UBG @Urine

Virus cause inflammation – >
disrupt Hepatocyte (increase UCB)
 \+ 
Disrupt Small bile ductule 
(increased CB = Water-soluble – >Leak into urine = dark urine) – >
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10
Q

In Viral hepatitis what we know about urobilinogen?

A

Can’t conjugate much UCB due to virus damage
+
CB leaks into blood due to damaged small bile ductules
– >

Less CB go into duodenum – >

Urine/urobilinogen = normal/decreased

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11
Q

Three phases of hepatitis?

A
  1. Prodrome (don’t like cigs/alcohol, serum transaminases increase, atypical lymphocytosis )
  2. Jaundice =
    increase urine bilirubin
    +
    increase urine UBG
  3. Recovery = Jaundice resolves
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12
Q

@Acute hepatitis how long the symptoms last for. And which to areas of the liver are inflamed?

A

> 6 months

Two areas = inflammation =
portal tract
+
hepatocytes between lobules (Inflammatory infiltrate between cells )

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13
Q

As chronic hepatitis what is there a risk of occurring?
How long do symptoms last for?
Where does inflammatorily reactions occur?

A

Risk of cirrhosis
Symptoms >6 months

Involve portal tracts = inflammatory reaction

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14
Q

Explain in terms of immunology what happens to virally infected cell?

A

So in fact with virus – > Present antigen + MHC 1 – >

CD8+ recognise MHC1 – >Cytotoxic killing of hepatocyte = apoptosis

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15
Q

Viral hepatitis occurs due to which viruses usually?

A

Usually hepatitis virus

Could be due to EBV/CMV

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16
Q

Transmission, carrier, incubation, HCC risk

Of hep A+E

A

Faecal oral
A = @ travellers
E = Contaminated water + undercooked seafood

Not Carrier, short incubation, no HCC risk

Virus replicates @liver + shed in faecal matter
2 wks before symptoms + 1 wk after symptoms

Sarah IgM = infection = active
Serum IgG = 
person protected/
Had prior infection/
immunised (only for hep A)
A = asymptomatic + acute
E = 
enteric + 
expectant mums = 
(fulminant hepatitis = liver failure + massive necrosis) + epidemic
17
Q

Transmission, carrier, incubation, HCC risk
Of hep B

What does HbeAG/HBV
signify?

A

Parenteral = piercing of skin/mucus membranes
– Maternal – fetal Childbirth
– Sex – IV drug use

Yes carrier, long incubation,
yes HCC risk = integrates into genome = oncogenic

Acute, window, resolved, chronic, immunisation
(Look in book For detail - draw the table it will help )

18
Q

Transmission, carrier, incubation, HCC risk

Of hep C

A

Parenteral = piercing of skin/mucus membranes
– Maternal – fetal Childbirth
– Sex – IV drug use

Yes, long, yes due to inflammation

Chronic, Carcinoma, cirrhosis, carrier

@Infection: increase Hep C virus RNA
@Recovery: decrease Hep C virus RNA
@chronic: PERSISTENT increase RNA

19
Q

Transmission, carrier, incubation, HCC risk

Of hep D

A

Parenteral = piercing of skin/mucus membranes
– Maternal – fetal Childbirth
– Sex – IV drug use

Yes, long, yes due to inflammation

(Pre-existing hep B infection – > get hep D later)
= superinfection - more severe than coinfection. Short incubation

Get hep B + get hep D Both together– >
= Coinfection - long incubation

20
Q

What is liver cirrhosis?

A

End-stage liver damage due to:

bands of irreversible diffuse fibrosis of liver
+
formation of regenerative nodules

21
Q

Where are stellate cells located and
What Does it produce
what effect does this create in terms of cirrhosis?

A

Stellate cell = beneath endothelial cells that line sinew sides

Stellate cell makes TGF beta – >fibrosis

22
Q

Explain how Regenerative nodules are formed

A

Injuries to hepatocytes reaction – >regenerative nodules

23
Q

Histologically what do we see At regenerative nodules?

A

– Lack portal triad + sinusoids -> lose architecture

– Get bands of fibrosis

  • Compress sinusoids + Central venues– >
    Intrasinusoidal HTN +
    decrease functional sinusoids +
    increase hydrostatic pressure @ portal vein
24
Causes of liver cirrhosis?
Alcoholic liver disease Metabolic diseases – haemochromatosis, off one antitrypsin deficiency, Wilsons disease, galactosaemia Autoimmune disease – primary biliary cirrhosis, autoimmune hep Postnecrotic cirrhosis = hep B+C
25
Explain the five clinical features of cirrhosis
1.(intradinusoidal HTN) + (anastomoses between PV tributaries + art. system) – >resistance to intrahepatic bloodflow = Portal HTN – >all organs draining to portal system = ⬆️ hydrostatic pressure – > Ascites at peritoneal cavity, congestive splenomegaly (hyperactive + consume RECs + placements = cytopenias = hypersplenism) , Portosystemic shunt cos blood can't get through liver (oesophageal varices, haemorrhoids, caput medusae = periumbilical venous collaterals), Hepatorenal syndrome (chronic liver disease e.g. psoriasis – >loss of renal autoregulation – >intense renal vasoconstriction – >reversible renal failure without parenchymal disease = ⬆️ blood urea nitrogen + creatNNNiNNNe. Treat equals dialysis liver transplants albumin. ⬇️ protein synthesis – > (hypoalbuminaemia= ⬇️ oncotic pressure– > ascites) (Coagulopathy = ⬇️ epoxide reductase – > ⬆️ PT + PTT ⬇️ prot C + S = Hyper-coagulable ⬇️ Coag factors = bleeding diathesis) Decreased in detoxification – >⬆️ aromatic AA (turn into false NM) + ⬆️ Serum NH3 (Cos of ⬇️ urea cycle) = Hepatic encephalopathy= Increase protein @diet/GI bleed – >bacterial conversion of urea to ammonia, alkalosis, portosystemic shunts, sedatives– > Mental status change, asterixis , Coma, somnolence Decreased liver oestrogen degradation + androstnedione – > XS oestrogens symptoms – >gynaecomastia, impotence, female hair distribution, spider telangiectasia, palmar erythema Increased oestrogen – >increased sex hormone binding protein synthesis – >increased binding of free testosterone – >decreased free testosterone – >decreased libido – >erectile dysfunction ⬇️ conjugating ability –> jaundice
26
Hepatic encephalopathy treatment? What are the three liver changes due to alcohol consumption XS?
Rifaximin+Lactulose = ⬆️NH4+ production 1. Hepatic steatosis - Macrovesicular fatty change = reversible with cessation Tender hepatomegaly without fever/neutrophil it can leucocytosis 2. Alcoholic hepatitis = direct chemical injury by acetaldehyde to Hepatocyte by alcohol = binge drinking long term - Swollen, - necrotic, - Mallory bodies = intracytoplasmic eosinophilic inclusion of damaged keratin filaments, - Stimulation of collagen synthesis around Central venues = perivenular fibrosis AST >LT = AST = @mitochondria + alcohol = mitochondrial poison. AST preferentially increases + alcohol-based damage. Painful hepatomegaly fever neutrophil leukocytosis ascites hepatic encephalopathy 3.alcoholic cirrhosis = final + irreversible Associated with obesity = diagnosis of exclusion i.e. make sure patients not abusing alcohol ALT >AST
27
What is non-alcoholic fatty liver disease associated with? What are the three liver changes? Liver enzymes? how does N-AFL disease leads to cirrhosis ?
Associated with obesity = diagnosis of exclusion make sure patients not abusing alcohol Hepatic steatosis, hepatitis, cirrhosis ALT >AST Insulin resistance – >fatty infiltration of hepatocytes – > cellular ballooning – > necrosis – >cirrhosis/HCC
28
Explain how XS body Fe2 plus leads to organ damage I.e. haemochromatosis?
XS body Fe2+ – >deposit @ tissues = FR generation = haemosiderosis – > organ damage = haemochromatosis because in disease caused by the Fe2+ deposition
29
Explain the pathogenesis of primary haemochromatosis
Normally the IntraSite takes up all iron from the gut but Entress I will will hold onto iron and want to pass it off unless there is a need via the transporter. At primary haemochromatosis due to C282Y/H63D mutation+HFE gene assoc with HLAA3 whatever comes into the IntraSite directly goes into the blood – >haemosiderosis – >haemochromatosis
30
What is secondary haemochromatosis due to? | Symptoms?
Due to blood transfusion complication RBC = 120 days – >Fe2+ recycled I.e. can't get rid of it – >haemosiderosis (build up) – >haemochromatosis (damaged tissue) Bronze skin Micronodular cirrhosis = Prussian blue stain Due to Haemosiderosis Secondary diabetes mellitus = bronze pancreas Cardiac arrhythmias Testicular atrophy
31
Explain the labwork of haemochromatosis Treatment haemochromatosis What cancer is there a risk of
High ferratin – >low TiBC Fe2+ plus leaks out – >serum Fp2 plus = high – >high percentage saturation ``` Phlebotomy = remove rbc – > low Fe2+ Chelation = deferoxamine deferasirox ``` Hepatocellular carcinoma
32
What is the defect in Wilsons disease? | what two things unable to happen due to this mutation?
Autosomal recessive defect = ATP7B gene @ ATP mediated hepatocyte copper transport system @chromosome 13 – Can't put copper into bile – Can't incorporate copper into ceruloplasmin (Molecule that carries copy into blood)
33
As a result of Not being able to put copy into bile What happened as a result of this? What is there a high risk of developing due to Wilsons disease?
Copper builds up in hepatocyte – >leak into Serum – > deposit @tissue – >copper-mediated hydroxyl FR's – >tissue damage Hepatocellular carcinoma
34
Lab results Wilsons disease?
Increased copper Decreased serum Ceruloplasmin cos Can't put copper in ceruloplasmin Increased copper @live a biopsy because can't put copper into bile
35
What is reye syndrome? | Symptoms?
Fulminant liver failure + encephalopathy In child with - Viral illness = varicella + flu B - Takes ASPIRIN Coma, vommit, Mitochondrial damage of hepatocytes Hypoglycaemia + hepatomegaly
36
Explain hepatic encephalopathy What increases ammonia production What decreases ammonia removal
Cirrhosis – >portosystemic shunt – >decrease the money metabolism – >neurocyte issues = asterixis, arousal decreased, coma Increase ammonia production = Increased protein diet GI bleed Constipation + infection Decrease ammonia removal = Diuretics, renal failure Bypassed hepatic bloodflow after transjugular intrahepatic portosystemic shunt
37
Give an example of a rare benign liver tumour? What a medication is this tumour often related to? Despite being but nine what is there a fear of happening?
Hepatic Adenoma Associated with OCPs/anabolic steroids Stop OCP – >regress HA There is a fear of rupture of HA as HA = subcapsular – >intraperitoneal haemorrhage especially @ Pregnancy (High oestrogen)
38
Give an example of a common benign liver tumour that occurs in people aged 30 to 50? What is contraindicated in these people?
Cavaness haemangioma Don't do biopsy due to risk of haemorrhage
39
Give a tumour associated with – Chloride – Arsenic – Vinyl Given its origin?
Angiosarcoma Origin = endothelial malignant tumour
40
Which one is more common metastasis to the liver or primary liver tumours? Where are the most common sources?
Metastasis to liver Colon Pancreas lung breast
41
What is the most common primary malignant tumour in the liver in adults? What two things can cause HCC? Prognosis? Serum tumour marker?
Hepatocellular carcinoma 1. chronic hep B + C 2. Cirrhosis = alpha-1 antitrypsin Wilsons Haemochromatosis Ai disease aspergillus = grains – >aflatoxins –> p53 mutations Non-alcoholic fatty liver disease

GI Liver (11 decks)

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