The Erythrocyte Membrane Flashcards

1
Q

describe the erythrocyte membrane’s unique qualities, and how their function effects their structure

A

Erythrocytes are unique as the plasma membrane is their only structural component and therefore has to carry out all of its antigenic, transport and mechanical needs.
In order to carry out these demands the membrane must be highly flexible whilst very strong
The erythrocyte achieves this by the interaction of its membrane lipid bilayer and the protein cytoskeleton

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2
Q

what are the 4 functions of the erythrocyte membrane

A
  • To provide a hydrophobic barrier between the contents of the erythrocyte and the plasma
  • To maintain the biconcave shape of the red cell. 
  • To regulate intracellular cation concentration
  • To act as a communication tool so that the cell and its environment can interact - this is achieved by membrane surface receptors.
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3
Q

what does the red cell membrane consists of?

A
  • Proteins~50%
  • Lipids~40%
  • Carbohydrates~10%
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4
Q

describe lipids in the erythrocyte membrane:
what does it consist of?
what are their functions?

A

The lipid bilayer consists of:
• Phospholipids
• Sphingolipids
• Cholesterol
It provides hydrophobic (waterproof) coating
It is also important in protecting the intact RBC cell from destruction by macrophages:
• Cholesterol is distributed equally on both surfaces. The phospholipids are different over the 2 surfaces -Probably so that those phospholipids recognised by macrophages are on the inner surface of the cell so they don’t get recognised whilst the cell is healthy
• To allow the cell to move freely through the microvasculature
The membrane cholesterol lies between the two layers of the lipid bilayer.
The function of cholesterol in the membrane is to determine membrane surface area and fluidity: an increase in membrane cholesterol leads to an increased surface area and decreased deformability.

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5
Q

describe carbohydrates in the erythrocyte membrane

A

Carbohydrates (oligosaccharides) occur only on the external surface of the red cell, where they cover the surface of the erythrocytes.
They are linked to Glycoproteins, such as glycophorin, and glycolipids.

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6
Q

describe proteins and their function in the erythrocyte membrane

A

These are either:
• Peripheral (temporary attached to membrane)
• Integral or Intrinsic (penetrating the lipid bilayer.)
More than 50 transmembrane proteins are known
These are to
• transport molecules into and out of the cell
• adhere erythrocytes to other cells
• to communicate between erythrocytes and other cells and tissues

Integral proteins (e.g glycophorin) have internal, external and transmembrane domains E.g. Erythrocyte anion channel (Cl-,HCO3-)
•	hydrophobic domain traverses the membrane (responsible for Cl-,HCO3-exchange
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7
Q

describe the protein cytoskeleton in the erythrocyte membrane

A

Peripheral membrane proteins interact to form a cytoskeleton:
This forms a tough flexible framework for the lipid bilayer- it maintains deformability, flexibility and durability of the red blood cell. This allows the cells to squeeze through capillaries that are less than half their own diameter.They also allow the erythrocyte to return to its original shape once it is in wider capillaries

It maintains the biconcave shape of cells

This in turn maintains the high surface area allowing maximal O2 exchange

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8
Q

describe erythrocyte membrane disorders (general description not specific conditions)

  • what should it be like
  • what happens if its not right
A

It is essential that erythrocytes maintain membrane organisation and stability so that the biconcave shape is maintained, to allow the erythrocyte to optimally carry out its functions Any mutations or deformities in the membrane and skeletal proteins that cause changes in the cell shape cause:
Decreased membrane surface area decreased ability to transport O2
Decreased erythrocyte life span Resultant haemolytic anaemia

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9
Q

describe Hereditary Spherocytosis

A

Common inherited haemolytic anaemia
Caused by genetic defect in cytoskeletal proteins leading to defective anchoring of the cytoskeleton to the membrane.
Defects can be in
1. ankyrin
2. Spectrin
3. Band 3 or
4. Protein 4.2
Ankyrin deficiency is the most common cause of HS in Northern European populations
Clinical characterisations are haemolytic anaemia, jaundice, splenomegaly (enlarged spleen)
Erythrocytes are smaller, rounder, and more fragile than normal

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10
Q

describe Hereditary elliptocytosis

A

Relatively common disorder worldwide (esp malarial areas) causing presence of elliptically- shaped RBCs.
Often asymptomatic but some present anaemia 
Unstable membrane with characteristic shape and membrane fragmentation
Severity of disease related to decrease in membrane stability

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11
Q

describe Hereditary ovalocytosis

A

Again common in malaria endemic areas.
Characterised by oval-shaped RBCs(ovalocytes)
Only present as heterozygotes as homozygote thought to be fatal
RBC membrane is very rigid

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12
Q

describe A, B, O blood grouping

A

There are 4 blood groups A, B, AB and O
The blood groups can be explained by the presence or absence of two enzymes which add sugar residues to proteins and lipids on the surface of erythrocyte membranes
• Type O individuals lack both of these enzymes. 
• An AB person has both.
• Types A and B have one or the other.

Type A people have A-antigens in their bodies but B- antibodies so any B-antigens entering the body are recognised as ‘foreign’ and antibodies will attack them.
Type B (rare) people have B-antigens and A- antibodies.
Type AB blood has both A- and B-antigens and are universal recipients
Type O blood has only H protein (A- and B-antigens are produced from genes that modify the H protein), and no antigens to A or B substance, People with type O blood are universal donors.

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13
Q

describe Rheu’s blood grouping

A

This was named after the monkeys in which it was found 
There is a positive and negative group
Rhesus negative blood can be given to anyone
Rhesus positive blood can only be given to Rh+ve people
But antibodies to Rhesus antigens do not develop until after 1st exposure after this any further exposure to Rh+ve blood will lead to severe side effects
85% UK population are Rh +ve

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14
Q

describe haemolytic disease of the newborn

A

Caused by a Rh-ve mother carrying a Rh+ve baby
If the 1st pregnancy is ‘normal’ then the birth will proceed normally
On birth the mother is likely to come into contact with the baby’s blood and develop antibodies against the Rh+ve. These antibodies remain in the mother’s blood.
Future pregnancies will be at risk with antibodies from the mother crossing the placenta and attacking the feotus’ RBCs
The feotus develops HDN – jaundice, enlarged liver and spleen, anaemia
Very rare (1:1000 births) as preventable disease:
Antibodies, which bind to Rh+ve proteins entering the mothers body effectively hiding them from the mother’s immune system, are given at 28wks and after birth of a Rh+ve baby

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15
Q

what are the challenges of blood transfusion

A
  1. Supply – after donation blood can only be kept 35 days at certain times of the year (Christmas and summer) supply is very low. In each bag of blood there are 2x1012 RBCs, we use 2 million bags of blood a year.
  2. Infections – have got into the supply in the past e.g. variant CJD and HIV
  3. Cost – 3% NHS budget
  4. Cross matching – not all blood can be given to all people. In the
    UK type A blood Rh+ve is very common but can only be given to A and AB positive individuals. Type O –ve can be given to anyone but only 7% of population have this type so hard to supply
  5. Time – in an emergency blood must be cross matched before transfusion
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