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GI Liver > Liver Problem > Flashcards

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
Q

Causes of liver cirrhosis?

A

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
Q

Explain the five clinical features of cirrhosis

A

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
Q

Hepatic encephalopathy treatment?

What are the three liver changes due to alcohol consumption XS?

A

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
Q

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 ?

A

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
Q

Explain how XS body Fe2 plus leads to organ damage I.e. haemochromatosis?

A

XS body Fe2+ – >deposit @ tissues = FR generation = haemosiderosis – >
organ damage = haemochromatosis because in disease caused by the Fe2+ deposition

29
Q

Explain the pathogenesis of primary haemochromatosis

A

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
Q

What is secondary haemochromatosis due to?

Symptoms?

A

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
Q

Explain the labwork of haemochromatosis
Treatment haemochromatosis
What cancer is there a risk of

A

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
Q

What is the defect in Wilsons disease?

what two things unable to happen due to this mutation?

A

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
Q

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?

A

Copper builds up in hepatocyte – >leak into Serum
– > deposit @tissue – >copper-mediated hydroxyl FR’s – >tissue damage

Hepatocellular carcinoma

34
Q

Lab results Wilsons disease?

A

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
Q

What is reye syndrome?

Symptoms?

A

Fulminant liver failure + encephalopathy
In child with
- Viral illness = varicella + flu B
- Takes ASPIRIN

Coma, vommit,
Mitochondrial damage of hepatocytes
Hypoglycaemia + hepatomegaly

36
Q

Explain hepatic encephalopathy
What increases ammonia production
What decreases ammonia removal

A

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
Q

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?

A

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
Q

Give an example of a common benign liver tumour that occurs in people aged 30 to 50?
What is contraindicated in these people?

A

Cavaness haemangioma

Don’t do biopsy due to risk of haemorrhage

39
Q

Give a tumour associated with
– Chloride
– Arsenic
– Vinyl

Given its origin?

A

Angiosarcoma

Origin = endothelial malignant tumour

40
Q

Which one is more common metastasis to the liver or primary liver tumours?

Where are the most common sources?

A

Metastasis to liver

Colon Pancreas lung breast

41
Q

What is the most common primary malignant tumour in the liver in adults?
What two things can cause HCC?
Prognosis?
Serum tumour marker?

A

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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