haem side quest Flashcards
sites of haematopoiesis from foetus to adult
starts in embryonic yolk sac –> moves to foetal liver and spleen
bone marrow takes over from 6 months gestation
after birth red marrow grad replaced by yellow marrow
ago 20+ haematopoeisis conc in axial skeleton and articular ends of femoral and humerus bones
lifespand of normal RBC
120 days
earliest morphological red cell precursor and morphology
proerythroblast
- high nuclear : cytoplasmic ratio
- prominent nucleoli
- blue cytoplasm (RNA present)
from proerythroblast to reticulocyte
as mature = SMALLER , more condensed chromatin, loose nucleoli, cytoplasmic changes (blue—> pink)
EVENTUALLY nucleus extruded = reticulocyte
reticulocyte –> erythrocyte
retic = retain some ribosomal RNA to make haemoglobin
lost 1-2 days after enter peripheral circulation = erythrocyte
factors affacting erythropoeisis - epo
-made kidneys
- lack of = profound reticulocytopaenia –> seen in renal failure
- excessive ep = normal response to hypoxia or result of pathology (epo secreting tumours)
- hypoxia inducible factor = production increases when hypoxic / impaired gas exchange / increased tissue demand for O2 –> HIF stims kidney to make epo
maturation factors eg and pathology cause
B12 + folate = component in DNA synthesis –> causes megaloblastic anaemia
Androgens + thryoxine = stim affect on erythropoiesis
Copper and pyridoxine = key comppenet of iron incorp in haem –> sideroblastic anaemia
4 examples of microcytic anaemia
- IDA
- Thallassaemias
- Inflammatory anaemia
- Sideroblastic anaemia
8 examples of normocytic anaemia
- inflammatory anaemia
- acute bleeding
- marrow disease
- renal anaemia
- haemolysis
- myeloma
- sequestration
- dilutional
iced bannanas mixed really hard makes smooth discharge
8 examples of macrocytic causes
- B12/folate
- reticulocytosis
- pregnancy
- liver
- hypothyroid
6.MDS - drugs e.g. axaithroprine
- alcohol
BORED RABBITS PLAY LIKE HYPNOTISED MONKEYS DOING ADDERRALL
What are spherocytes on blood film and what do they suggest
small rbc without area of central pallor –> have lost their membrane without losing the cytosol
in haemolysis:
immune mediated
- autoimmune haemolytic anaemia
- transfusion reaction / disease of newbron/ ABO incombat
congenital = hereditary spherocytosis
Direct red cell damage:
- burns / drowning / snake venom / clostricum perfigens
what are shistocytes and what do they suggest on blood film
FRAGMENTS OF RBC
TTP / haemolytic uraemic Sx , DIC
pregnancy related –> HELLP / preeclampsia / valvular haemolysis / HTN emeregency
drug induced
systemic malignancy
stem cell transplant
what are degmacyte (bite/blister/ghost cells) and what do they indicate
Removal of denaturated hemoglobin inclusions (Heinz bodies) by splenic macrophages
results in one or more semicircular punches on the cell margin resembling bite marks
Indicate oxidative haemolysis:
- G6PD deficiency
- Drugs –> sulphasalzine
what are target cells and what do they suggest on blood film
increased staining resulting from redundant RBC membrane in relation to its cytoplasm
(means excess cell membrane in relation to cytoplasm)
suggests = haemoglobinopathies
what is agglutination seen on a blood film and what does it suggest
red blood cells clump together, forming aggregates
suggests:
cold haemagglutinin disease / paroxysmal cold haemoglobinuria
tests to do when you think patient is haemolysing
- blood film
- see diff morphologies depending on cause - bilirubin
- should be unconjugated cos prehepatic cuase - haptoglobin
- protein that binds to free haemoglobin so then can be removed by reticuloendothelial system –> will be low if haemolysing as its all used up! - LDH
- sensitive bu nonspecific for haemolysis (can be raised in number of conditions)
what conditions raised LDH
haemolysis / acute MI / lymphoma / liver disease /
basic any condition assoc w tissue damage/ high cell turnover
what are the steps in Ix ?haemolysis?
1 = is the patient haemolysing?
2 = is it immune mediated?
3 = any Hx to explain this?
how to test if haemolysis is immune mediated
direct coombs test
in immune mediated haemolysis what is relevant Hx to ask?
prev exposure to blood products / ati-d immune globulin / Sx of LRTI ? could be Sx of mycoplasma pneumonia!!!
and drugs –> penicillins / cephalosporins / diclofenac / methydopa
in nonimmune mediated haemolysis what are key Hx points?
personal and FHx of
membrane defects –> hereditary spherocytosis / eliptocytosis
enzymopathies –> G6PD / pyruvate kinase defiecny
thalassemias / haemoglobinopathies
what can nonimmune haemolysis be further divided into (2 categories)
- congenital
- acquired
what is the key regulator of iron homeostasis and how does it work
HEPCIDIN
binds to iron transport protein ferroportin –> causes it to be internalised and degraded
ferroportin found on eneterocytes and all organs which act as iron stores (liver / BM / splenic macrophages)
action hepcidin –> reduce enteric iron absorption + promote sequestration into body compartments
when is hepcidin transcription rates increased
inflamm states or when serum iron high (like overload
when is hepcidin transcription rates reduced
IDA over when increased epo / hypoxia
body iron distrubtuion
stored in liver / BM / splenic macrophages
signif amount also circulates as haem in Hb
