68 - jaundice, 69 enlarged liver Flashcards Preview

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Flashcards in 68 - jaundice, 69 enlarged liver Deck (31)
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1
Q

Causes of jaundice

A

Pre-hepatic: haemolytic anaemias, Gilbert’s syndrome, malaria

Hepatic: hepatitis, chronic alcoholism, cirrhosis, hepatic necrosis,

Post-hepatic: pancreatic cancer, pregnancy, pancreatitis, cysts, parasites

2
Q

What is the function of bile acids?

A

produced by liver to emulsify fats and help excrete bilirubin

Bile Aids absorption of fat soluable vitamins A,D,E and K

3
Q

Lack of bile ->

A

steatorrhea and vitamin deficiencies. ADEK

4
Q

Risk of what with neonatal jaundice

A

kernicterus

5
Q

Which type of bilirubin can cross blood brain barrier

A

unconjugated

6
Q

What can kernicterus -> ?

A

permanent athetoid cerebral palsy and other neurological problems (and death!)

7
Q

Ix in neonatal jaundice

A

Full blood count and grouping

Urine culture

Transcutaneous bilirubinometer

Serum bilirubin (always in less than 24 hours)

Direct antiglobulin test (DAT): Also known as the direct Coombs’ test; this test is used to detect antibodies or complement proteins that are bound to the surface of red blood cells. Positive test indicates immune mediated haemolytic anemia.

Indirect screens maternal blood for IgG antibodies.

8
Q

Mx of severe neonatal jaundice

A

Phototherapy: baby gets a sunlamp. UV light breaks down bilirubin. Check blood levels every 8 hours. Ensure baby is naked.

Treat underlying cause (iv immunoglobulin if blood group incompatibility)

Exchange transfusions: dangerous. Babies blood volume is replaced entirely.

9
Q

Why is physiological jaundice common? How long does it often last?

A

Due to under compensating hepatic enzymes, shorter life of fetal blood cells and lack of enteric bacteria.

Lasts about two weeks.

10
Q

What is cause of rhesus disease

A

mother is Rh –ve and foetus is +ve.

Maternal antibodies (IgG) are produced against the Rh group, accumulating with successive pregnancies (very rare in firstborns).

11
Q

Basic prevention of rhesus disease

A

IM injection of Anti-D for Rh or blood transfusions for ABO (rarely needed)

12
Q

Risk of what with Rhesus in preg?

A

hydrops fetalis - very poor prognosis

13
Q

What is biliary atresia? when does it present?
What happens?
mx?

A

Rare malformation of the bile ducts.
Jaundice after 1st week of life

Cirrhosis and portal hypertension develop

Poor prognosis, even with surgical treatment there is high risk of morbidity and mortality. Usually requires liver transplant.

14
Q

Hep A
Transmission?
prognosis?

A

faecal-oral infection producing mild self-limiting disease. Avoid poorly prepared food.

Most recover after 2/12.

15
Q

Hep B
Transmission?
prognosis?
Complications?

A

Blood borne.

15% produce antibodies which do not overcome the infection, leading to chronic illness. Of these 65% respond to treatment.

Causes cancer and cirrhosis.

16
Q

Hep C
Transmission?
prognosis?

A

Blood borne.

Leads to chronic hepatitis and cirrhosis but usually clinically silent for decades. Viral levels may be lowered by treatment.

17
Q

Hepatitis vaccines?

A

Vaccine available to prevent A, lasts 10 years

B vaccine: 3 injections lasting a lifetime offered to those at risk: MSM, healthcare and sex workers, IVDU, travellers.

No vaccines available for other hepatitis viruses.

18
Q

what is haemochromatosi

A

AR condition leading to excess iron absorption by small bowel. Iron is deposited through body, damaging organs.

19
Q

triad of haemochromatosis

A

bronzed skin, diabetes and cirrhosis.

20
Q

Dx of haemochromatosis

A

transferrin and ferritin testing. Organ biopsy may be necessary.

21
Q

Mx haemochromatosis

A

chelation therapy (desferrioxamine mesilate) and venesection.

22
Q

What is gilberts? what happens?

A

Common liver disease producing elevated bile levels in bloodstream and thus jaundice particularly during stress.
Reduced glucuronyltransferase, enzyme responsible for conjugating bilirubin.
Clinically harmless.

23
Q

Name 4 things the liver does

A

Bile digestion

Drug metabolism (cytochrome p450) and hormone breakdown

Glycogenesis and glycogenolysis. Gluconeogenesis

Protein metabolism: albumin, clotting factors, angiotensinogen

Lipogenesis and cholesterol synthesis

Storage: glycogen, vitamins, monocytes, metals.

Toxin removal

24
Q

Bar liver what causes decrease in Albumin?
AST?
ALT ?
ALP?

A

Albumin: also decreased in nephrotic syndrome

AST: also indicates cardiac and muscular damage

ALT: usually higher than AST in liver disease. Also indicates muscular damage

ALP: if ratio of ALP raised over AST then the problem may be in the biliary disease. Also raised in Paget’s

25
Q

What does raised GT indicate?

A

steatohepatitis

-fatty alcohol liver

26
Q

Which LFT is thought to be most sensitive to acute liver damage

A

PT

27
Q
Hep antibodies 
What doi they mean if positive? 
HBsAg
Anti-HBc
Anti-HBs

If all negative?

A

HBsAg indicates present infection if positive.

Anti-HBc indicates past and present infection. Takes longer to alter than HBsAg

Anti-HBs indicates immunity to Hep B if positive. Thus, if it is the only positive, indicates vaccination.

IgM anti-HBc indicates acute infection if positive.

Thus, all negative indicates Hep B susceptible.

28
Q

Causes of hepatocellular carcinoma

A

by alcoholism, chronic hepatitis (infectious or for any other reason), haemochromatosis, alpha1 anti-trypsin defiency

29
Q

Sx of hepatocellular carcinoma

A

: jaundice, oedema, bleeding and bruising, loss of appetite, weight loss, fatigue, vomiting and nausea.

30
Q

Screening of those at risk of hepatocellular carcinoma includes?

A

US

Alpha-fetoprotein biomarker and CT with three phase contrast.

31
Q

Mx of hepatocellular Ca

A

Surgical resection and transplantation. Chemo and radiotherapy usually reserved for palliative treatment or those awaiting a transplant.

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