2. Haemoglobin and RBCs Flashcards
what does the RBC not have
Nucleus
Mitochondria,
Ribosomes
benefits of giv ing these up
- Efficient and stable – nothing unnecessary
- Room for haemoglobin
- Unattractive to infecting organisms
downsides of giving these things up
No nucleus: No capacity for to making mRNA – no new protein
No Mitochondria no TCA cycle – limits the capacity to generate ATP or reducing power - vulnerable
No Ribosomes no translation of mRNA no protein synthesis
Cant self repair or go through apoptosis due to lack of protein synth + mitochond (needs to be removed by spleen)
key parts of the RBC memb
alpha spectrin
ankyrin
what can shortage of spectrin cause
eliptical shape
if cells cant apoptosis or self repair, then what happens to prevent toxicity
temporary fixing of the membrane
why is RBC damage toxic
Hb leakage is highly toxic = aggregates and blocks kidneys
what can fibrin strands formed by sepsis cause
acts like cheese wire
slices RBCs
how does cell repair after slicing damage
forms vacules
vacuole will pop but reseal
cytoskeleton forms and seals the membrane
what are these slicing damaged cells called
keratocytes
what forms after damage repair caused by diffuse damage
spherocytes
what does defect in memb prtoeins e.g. enykrin cause
hereditary spherocytosis
hereditary spherocytosis
- unstable cell memb
- lotsa spherocytes
- anaemia due to breakdown of RBCs
- mild jaundice and gall stones (due to release of RBCs)
- enlarged spleen
2 things that allow the sigmoid curve
haem = O2 binding element
globin= surrounding protein element
what kind of structure does haem have
porphyrin
what do the 2 remaining interaction sites in Fe allow
fixing the molecule to the globin protein
and binding the O2
if hb was single chained, what type of O2 release would it be
hyperbolic
O2 only released in sever hypoxia
loose and tight conform of globin
- loose binds o2 tightly
- tight gives up O2 easily
factors that influence tight and relaxed conforms of globin molecules
pH
CO2
metabolic products
why does foetal Hb have higher affinity for O2
doesnt bind 2,3 DPG
so the HbF can compete with mothers Hb, and win
so O2 goes from mum to foetus
2 stages of malaria development you shoud know
trophozoites
schizonts
when did malaria start affecting humans
10,000 yrs ago during agriculture and stuff
but RBC was fully evolved by this time
how is malaria able to survive
is protected from immune system in RBC
and metabolises the Hb for energy
4 things that can provide protection from malaria
- Sickle cell
- beta thalassaemia
- G6PD deficiency
- Hb C (mild form of sickle cell)
what ishow does a RBC produce reducing power (NADPH)
via hexose monophosphate shunt
what is an essential component of hexose monophosphate shuint
G6PD
how does G6PD deficiency provide malarial protection
- high oxidative stress and the cell cant deal with it (not enough reducing power)
- so RBC destroyed
- It is thought that if malaria parasites invade a cell with G6PD deficiency then oxidation occurs leading to early destruction of the infected cell.
