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3A week 3 - the liver > jaundice > Flashcards

jaundice Flashcards

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1
Q

what is jaundice

A

the clinical manifestation of biochemical hyperbilirubinemia, detected by the change of skin colour and sclera

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2
Q

what is icterus

A

jaundice e.g. the sclera can be icteral

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3
Q

where is juandice normally first noticable

A

in the sclera - get them to look down as it usually accumulates above the pupil

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4
Q

what is eryptosis

A

apoptosis of erythrocytes - erythrocyte shrinkage, blebbing, and phospholipid scrambling of the cell membrane

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5
Q

what is ferrous converted to by ROS in erythrocyte damage

A

ferric iron

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6
Q

what happens to the glycolytic enzymes in RBCs as they age

A

decreases

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7
Q

examples of markers for macrophage digestion of senescent RBCs (5)

A
  1. reduced glycolytic enzyme
  2. loss of membrane
  3. neoantigen appearance
  4. exposure of membrane phosphadtidylserine
  5. desaialyation of surface proteins
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8
Q

what are heinz bodies

A

inclusions of irreversibly denatured hemoglobin attached to the erythrocyte cell membrane -> indicative of oxidative injury

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9
Q

what is white pulp

A

the lymphatic tissue of the spleen -> trebecular arteries are surrounded by it in the spleen

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10
Q

how do red blood cells go from the radial arteries to the veins (spleen)

A

they must leave the radial arteries and traverse the red pulp to reach the veins

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11
Q

what are howell-jolly bodies

A

inclusions of nuclear chromatin remnants -> indicate spleen damage

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12
Q

what are siderocytes

A

RBCs containing granules of iron that are not part of the cell’s haemoglobin

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13
Q

what are pappenheimer bodies

A

inclusion bodies formed by phagosomes that have been engulfing excessive amounts of iron

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14
Q

how does the spleen remove old rbcs (3)

A
  1. in order to reach the vein, rbcs must squeeze through gaps in the bv wall
  2. ages rbcs loose their membrane elasticity and become trapped in the red pulp as they cannot squeeze through
  3. they are engulfed by macrophages
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15
Q

in macrophages what are the main haemaglobin breakdown steps (3)

A

Hb -> Heam + Fe -> globin + porphyrin -> bilirubin

  1. Hb -> haem +Fe
  2. haem -> globin + prophyrin
  3. porphyrin -> bilirbin
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16
Q

what is the reaction that ALA dehydrogenase is used in (haem synthesis)

A

2ALA –(ALA dehydrogenase)–> porphobilinogen (PBG)

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17
Q

what is the last main step in haem synthesis

A

protophorphyrin IX + Fe2+ –(ferrochelatase)–> haem

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18
Q

what is the intermediate compound in the haem breakdown pathway that gives bile its colour

A

biliverdin

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19
Q

what enzyme is used in the formation of biliverdin

A

haem oxygenase (there are 2 forms of the enzyme)

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20
Q

what enzyme is used in the conversion of biliverdin to bilirubin

A

biliverdin reducatse

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21
Q

what are the 2 forms of the biliverdin reducatse gene (BLVR) and which is predominant

A

BLVRA -> forms biliverdin IXa
BLVRB -> forms biliverdin IXβ
biliverdin IXβ is the predominant form

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22
Q

what type of bilirubin is produced in the macrophage

A

unconjugated bilirubin or indirect bilirubin (non water soluble)

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23
Q

what can unconjugated bilirubin bind to and for what reason

A

it can binds to albumen -> allows for it to be carried in the blood

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24
Q

where cant unconjugated bilirubin appear

A

in the urinw

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25
where is unconjugated bilirubin taken up
by the hepatocytes
26
where does bilirubin conjugation occur
in the liver (hepatocytes)
27
what enzyme is key in bilirubin conjugation
UDP glucuronyl transferase
28
what is bilirubin conjugated to
glucaronic acid
29
where is conjugated bilirubin secreted into from the liver
the bile
30
what is conjugated bilirubin broken down into in the bowel(3)
1. urobilinogen 2. unconjugated bilirubin 3. stercobilin (majority)
31
what breaks down conjugated bilirubin into urobilinogen
the bacteria
32
what happens to urobilinogen after the bowel
it is soluble so it taken up into the kidneys to be excreted
33
what happens to unconjugated bilirubin after the bowel
it enters teh eneterohepatic circulation to be retaken up by the liver
34
what happens to stercobilin after the bowel
is its egested in the faeces -> it is what turns faeces brown
35
what does pale faeces indicate
no conjugated bilirubin the bowel -> biliary or pancreatic problem
36
what receptor is key in transporting UC bilirubin into the hepatocytes
OATP1
37
what is gilbert syndrome
an autosomal recessive condition where the liver in unable to process bilirubin properly
38
what transmemebrane protein is implicated in gilberts syndrome
UGTA1
39
how does conjugated bilirubin enter the GI tract
carried in bile and travels through the ampulla of vater into the duodenum
40
what is hepatocyte hopping
while the majority of conjugated bilirubin is transported into the bile, some is effluxed back into the sinusoid (via MRP3) which is then taken up by neighbouring cells, this is then excreted further up into the bile duct
41
why does hepatocyte hopping occur
to stop overwhelming the cannicular system
42
what 4 bacteria are responsible for the bibirubin -> urobilinogen reduction
1. Clostridium ramosum 2. Clostridium perfringens 3. Clostridium difficile 4. Bacteroides fragilis
43
what happens to the urobilinogen in the intestines (3)
1. turned into stercobilin 2. enters the enterohepatic circulation to be transported back to the liver 3. deposited in the kidneys to be oxidised to urobilin (yellow pigment seen in urine)
44
what are the 3 types of jaundice
1. pre hepatic 2. hepatic 3. post hepatic /obstructive
45
what is pre hepatic jaundice
increase in the blood of UNconjugated bilirubin -> build up and failure to conjugate bilirubin leading to build up of UC bilirubin in the blood
46
what urine/faeces change is seen w pre hepatic jaundice
none -> UC bilirubin is not soluble but any bilirubin that manages to be conjugated will be excreted
47
3 causes of pre-hepatic jaundice
1. increased red cell break down -> too much bilirubin is being delivered to the liver and it can conjugate it all 2. large hameatoma (lots of rbcs broken down again) 3. failure of hepatic conjugation e.g. genetic condition
48
what blood results indicate pre-hepatic jaundice due to haemolytic process
raised reticulocytes; raised LDH; low Hb
49
what are the 2 types of haemolysis
intravascular; extravascular
50
examples of autoimmune intravascular haemolysis (3)
1. acute haemolytic transfucton reaction e.g. incompatible ABO group 2. warm autoimmune haemolysis 3. cold autoimmune haemolysis
51
exampls of autoimmune extravascular haemolysis (4)
1. warm autoimmune haemolysis 2. cold autoimmune haemolysis 3. haemolytic disease of the foetus and newborn (RhD incompatibility) 4. delayed haemolytic transfusion reaction (atypical cell antibodies from prior transfusion)
52
where is the mutation in gilberts syndrome
the gene promoter box (TATA box) -> less transport protein produced -> less conjugation of bilirubin
53
what is crigler najjar syndrome
an autosomal recessive inherited disorder that leads to congenital non-hemolytic jaundice -> caused by an absence or profoundly decreased level of the enzyme UDP-glucuronosyltransferase due to a genetic defect in the UGT1A1 gene
54
how does crigler nijjar (T1) syndrome present
shortly after birth with kernicterus
55
crigler nijjar (T1) syndrome mgx (2)
1. photo therapy -> changes the bilirubin structure so that it becomes soluble 2. liver transplant
56
how does UC bilirubin build up cause kernicterus
due to the non-polar nature of UC bilirubin, it can easily cross the BBB and destroy neurons in the brain
57
what is breast milk jaundice
a common and benign cause of jaundice in newborns who are primarily breast milk fed -> may inhibit UGT1A1 protein leading to lack of bilirubin conjugation substitution w formula milk leads to rapid recovery
58
what is hepatic jaundice
jaundice that occurs when liver disease affects the ability to both conjugate and secrete bilirubin
59
5 underlying causes for hepatic jaundice
1. acute liver injury 2. acute liver failure 3. chronic liver disease 4. cirrhosis decompensation 5. acute on chronic liver faliure
60
what kind of bilirubin is elevated in hepatic jaundice
a mixture of UC and conjugated bilirubin
61
what may the urine of a hepatic jaundice pt look like
dark urine and pale stool -> conjugated bilirubin is excreted into the urine (as goes into the blood but not GI tract) but wont enter the bowel
62
what is dubin johnson syndrome
an autosomal recessive condition in which the MRP2 protien is mutated and so bilirubin cannot be excreted into the bile => conjugated bilirubin enters the blood stream instead (leads to dark urine, pale faeces)
63
what is the appearance of the liver in dubin-johnson syndrome
liver appears black as NA excretion from the liver is also impaired which causes the liver to turn black
64
what is rotor syndrome
an autosomal recessive condition where hepatocyte hopping is impaired meaning that bilirubin entering the blood cant reenter the hepatocytes => excreted in the urine
65
what is post-hepatic jaundice
jaundice that occurs due to disruption preventing the bile and the bilirubin inside it from draining out of the gallbladder and into the digestive system -> usually due to an obstruction e.g. tumour, gallstones
66
what LFT are raised in post-hepatic jaundice
ALP, GGT
67
causes of post hepatic jaundice (5)
1. Common bile duct stone 2. Cholangitis 3. Bile duct strictures (PSC) 4. Malignancy 5. Pancreatitis
68
what test is useful when determing what type of jaundice is present
split bilirubin -> shows levels of UC and C bilirubin
69
post hepatic jaundice urine and faeces change
pale stool, dark urine
70
how does bilirubin enter the blood stream in post hepatic jaundice
the cholangiocytes become "leaky" and the bilirubin moves into the bloodstream; hepatocytes also excrete this directly into the blood
71
why does pruritis occur in post hepatic jaundice
due to build up of bile acids as they are not being excreted

3A week 3 - the liver (9 decks)

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