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1Principles of Biomedicine - MD1 > 126 > Flashcards

126 Flashcards

1
Q

Epo signalling

A

Binds to a blast cell.

Through Janus kinase 2 (Jak2), signals.

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2
Q

Process of erythropoiesis
1
2
3

A

1) Proerythroblast
2) Polychromatic erythrocytes
3) Erythrocytes

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3
Q

Outcome of erythrocytes having no nucleus or mitochondria

A

Obligate anaerobes. Make lactate continuously.

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4
Q

How quickly do blast cells mature to erythrocytes?

A

~7 days

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5
Q

Rate at which RBCs are made in adults

A

~2 million per second

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6
Q

Where is EPO synthesised?

A

Kidney

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7
Q

Epo function

A

Erythropoietin (Epo) is required
for survival, proliferation and
differentiation of committed
erythroid progenitor cells.

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8
Q

Met-haemoglobin

A

Hb with Fe3+ (Fe2+ has been oxidised).

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9
Q

How is RBC lifespan determined?

A

Give chromium 51 to random sample of RBCs, infuse.
Over ~120 days the label is removed.
120 days is the maximum lifespan. Many things can shorten lifespan.

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10
Q

Vitamin B12 role in RBC maturation

A

Methylation step in haemoglobin synthesis

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11
Q

What happens when a RBC has ~15% met-Hb?

A

Macrophages in spleen, liver, red bone marrow phagocytoses RBC

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12
Q

What converts haeme to biliverdin?

A

Haem oxygenase

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13
Q

Where does the Fe from metabolised Hb go?

A

Stored in transferrin, which goes to the liver.

Transfered to ferritin.

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14
Q

Spleen microscopic structure

A

White pulp - Immune cells

Red pulp -  is a system of blood vessels
arranged to facilitate removal of old or
damaged red blood cells from the
circulation. The removal is performed by
macrophages.
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15
Q 
Mononuclear phagocyte system of the spleen
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2
3
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6
A

1) Performed by monocytes/macrophages in spleen, lymph nodes. Also by Kupfer cells in the liver.
2) Formation of new RBCs and WBCs (in embryo).
3) Destruction of old RBCs and WBCs.
4) Formation of antibody
5) Formation of plasma proteins.
6) Formation of bile pigments.

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16
Q

Examples of altered surface molecules on RBCs that macrophages can recognise

A

Exposure of phosphatidyl serine, reduced content of sialic acid anchored to glycophorin.

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17
Q

Surface protein on RBCs that determine immunogenicity

A

Carbohydrates (neuraminic acid, also called sialic acid) attached to glycophorin.

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18
Q

How does the body determine age of RBCs?

A

Neuraminidase in body slowly cleaves off sialic acid while RBC circulates. After maximum 120 days, enough has been removed for macrophages to phagocytose RBC.

As the RBC ages, more phosphatidylserine flips to the outer
side of the membrane. Eventually it reaches equilibrium, and this is a signal for destruction.

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19
Q

Causes of haemolysis
1
2
3

A

1) External attack on RBC (EG: strep, enterococcus)
2) Parasitic haemolysis (EG: malaria)
3) Congenital or genetic factors

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20
Q

Haptoglobin

A

Plasma protein that binds haemoglobin (repurposed serine protease).
Cleaves tetrameric structure of Hb, binds to it.
This signals to a macrophage to phagocytose Hb-Hp.

21
Q

What happens when haptoglobin is depleted?

A

Get Hb in the urine, as haptoglobin isn’t degrading Hb

22
Q

What to suspect when there is low haptoglobin?

A

Haemolytic anaemia, as this depletes haptoglobin

23
Q

Protein that carries haeme to liver

A

Hemopexin

24
Q

Why does haeme need to be removed from the blood?

A

It is neurotoxic

25
Q

Role of hemopexin

A

Takes up free haeme in blood, transfers it to the liver

26
Q

Signs of haemolytic anaemia

A

Low haemopexin, haptoglobin

27
Q 
Consequences of haemolysis
1
2
3
4
A
  • Unconjugated (indirect) hyperbilirubinemia. Jaundice occurs when the conversion of Hb to bilirubin exceeds the liver’s capacity to conjugate and excrete bilirubin.
  • Increased stercobilin (brown) in the stool and urobilinogen in the urine.
  • Sometimes cholelithiasis (gall stones from bile acids).
  • Reticulocytosis when the bone marrow responds to the excess loss ofRBCs by accelerating production and release of RBCs
28
Q

Signs and symptoms of haemolysis

A

Pallor, fatigue, dizziness, possible hypotension.

If very severe, haemolytic crisis.

29
Q

Haemolytic crisis

A

It may be accompanied by chills, fever, pain in the back and abdomen, prostration, and shock. Severe hemolysis can cause jaundice and splenomegaly. Hemoglobinuria causes red or reddish-brown urine.

30
Q

Endogenous production of carbon monoxide

A

When haeme is broken down, NADPH and O2 react with products to form Fe3+, CO and NADPH

31
Q

Enzyme that converts biliverdin to bilirubin

A

Biliverdin reductase

32
Q 
Timeline of bruises
1
2
3
4
5
A

1) First presentation is reddish as the blood is trapped in interstitial tissue.
2) 1 -2 days: bruise turns bluish-purple or even blackish (deoxy and met-Hb).
3) 5 -10 days: bruise turns greenish or yellowish (biliverdin).
4) 10 -14 days: yellowish-brown or light brown (bilirubin).
5) >14 days the bruise fades away

33
Q

What can serum albumin bind?

A

Highly-hydrophobic bilirubin

34
Q

What happens to bilirubin after it has been formed?

A

Released from organ that formed it.
Binds serum albumin in the blood.
Transferred to the liver

35
Q

What happens to bilirubin in the liver?

A

Bilirubin UDP-transferase makes bilirubin more hydrophilic by conjugating to a hydrophilic gluconurate.

It can be excreted by the kidneys.

36
Q

cMOAT

A

Canalicular multispecific organic anion transporter.

Actively transports bilirubin diclucuronide into the liver canaliculi.

37
Q

Syndrome from cMOAT deficiency

A

Dubin-Johnson syndrome

38
Q

Dubin-Johnson syndrome

A

Failure to export dihydropurinides into bile.
Can lead to hyperbilirubinaemia, but this is normally asymptomatic.
Dihydropurinides are non-toxic, so not really dangerous.

39
Q

Name for syndrome with deficiency in UDP gluconyltransferase 1 family

A

Crigler-Najjar syndrome

40
Q

Crigler-Najjar syndrome

A

In Crigler-Najjar patients the transferase is either inactive (type I) or severely reduced (type II). Bilirubin cannot be excreted into the bile and remains in the blood. The high plasma level of unconjugated bilirubin presents as persistent jaundice.

Some patients exhibit kernicterus (bilirubin encephalopathy and brain damage) due to bilirubin toxicity. Kernicterus can produce hypotonia, lethargy, deafness and oculomotor palsy.

41
Q

Treatment of Crigler-Najjar syndrome

A

Must begin early to protect brain
Children given 10-12 hours treatment/day.
Exposed to blue light (phototherapy).

42
Q

How does phototherapy work for Crigler-Najjar syndrome?
1
2
3

A

Some of the double-bonds in bilirubin isomerize cis/trans when exposed to light.

The Z,Z-isomer flips to E,Z and E,E-isomers and bilirubin becomes more soluble.

E,E form is more soluble, can be excreted.

43
Q

Proportion of bile that bile salts are

A

~4.4%. Higher in haemolysis.

44
Q

Enterohepatic urobilinogen cycle

A

Resorption of uribilinogen in gut and excretion by kidney.

Conjugated bilirubin is secreted in bile into gut.
Bacterial enzymes convert conjugated bilirubin into urobilinogen, 90% of which is excreted in faeces. The rest is taken up by the portal vein, and 9% of this is excreted again in bile. 1% enters blood, is excreted by the kidneys.

45
Q

What is the most common cause of low urobilinogen?

A

Gallstone blocking bile duct.

46
Q

What can increased urobilinogen in urine mean?

A

Increased values indicate RBC breakdown (haemolytic

disease), hematoma, poisoning and liver cirrhosis.

47
Q

Urobilin

A

Urobilinogen slowly converts to urobilin in the presence of O2.

48
Q

Major colourant of faeces

A

Stercobilin, which is deep red-brown.

1Principles of Biomedicine - MD1 (157 decks)

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