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Haematology > red cells > Flashcards

red cells Flashcards

1
Q

substances require for production

A 
iron copper cobalt manganese
B12 folic acid thiamine Vit B6 CE
aminoacids
Erythropoietin, GM-CSF
Thyroxine, androgen
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2
Q

Red cell breakdown

A 
occurs in the reticuloendothelial system
macropahges in spleen liver lymph nodes
120 days
Globin
AA reutilised
Haem
Iron recycled
Haem- biliverdin- bilirubin
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3
Q

genetic defects

A

in red cell membrane
in metabolic pathways
in haemoglobin

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4
Q

skeletal proteins

A

responsible for maintaining red cell shape and deformability

defects can lead to increased cell destruction

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5
Q

most common membrane disorder

A 
hereditary spherocytosis
autosomal dominant
defects in 5 different structural proteins
-Ankyrin
-Alpha Spectrin
-Beta Spectrin
-Band 3
-Protein 4.2
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6
Q

clinical presentation

A 
anaemia
jaundice
splenomegaly
pigment gallstones
treatment
folic acid
transfusion
splenectomy
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7
Q

rare membrane disorders

A

hereditary elliptocytosis

hereditary pyropoikilocytosis

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8
Q

red cell enzymes

A

glycolysis
provides energy
Pentose Phosphate shunt
-protects from oxidative damage

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9
Q

Glucose 6 phosphate deficiency

A 
commones disesse cusing enzymopathy in the world
Oxidative damage
confers protection against malaria
X Linked
affects males
female carriers
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10
Q

G6PD defieciency

A 
blister/ bite cells
clinical features
variable anaemia
neonatal jaundice
splenomegaly
pigment gallstones
drug broad bean or infection precipated jaundice and anaemia
\: intravascular hemolysis
if sick red cell count can be infected
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11
Q

pyruvate kinase deficiency

A 
reduced ATP
increased 2 3 DPG
anaemia
jaundice
gallstone
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12
Q

4 alpha genes

A

chromosome 16 ( 2 from one parent)

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13
Q

2 Beta genes

A

chromosome 11

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14
Q

normal adult

A

HbA -97
Hb A2 -2
Hb F -1

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15
Q

sickle cell disease

A

point mutation in beta chain Glu replaced by Val
crystal form through deoxygenation tension
hemolysis
coagulation activation
dysregulation of vasomotor tone by vasodilator mediators
->
vaso- occlusion

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16
Q

presentation

A 
stroke, brain
sickling in lungs,
bone
early childhood sickling in spleen
auto infarction- hyposplenic
Bone pain presentation
abnormal spleen immunity low
high red cell turnover, parvovirus severe anaemia requiring transfusion
sequestraion crises- enlarged liver spleen
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17
Q

painful crisis

A 
severe pain
often requires opiates
	-Analgesia should be given within 30 mins of presentation 
	-Effective analgesia by 1hour
	- Avoid pethidine
Hydration
Oxygen
Consider antibiotics
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18
Q

management

A 
Life long prophylaxis
Vaccination
Penicillin (and malarial) prophylaxis	
Folic acid
Acute Events
Hydration 
Oxygenation
Prompt treatment of infection
Analgaesia
Opiates
NSAIDs
 - Blood transfusion
19
Q

disease modifying drugs

A

hydroxycarbamide

20
Q

blood transfusion

A

episodic or chronic
alloimmunisation
iron overload

21
Q

thalassemia

A

reduced or absent globin chain

mutations or deletions

22
Q

beta thalassaemia major

A 
severe anaemia
-presents at 3-6 months
expansion of ineffective bone marrow
bony deformities
splenomegaly
growth retardation
23
Q

chronic transfusion

A

iron overloading

death in 2nd or 3rd decades due to heart/ liver/ endocrine failure if iron loading not treated

24
Q

beta thalassemia ajor treatment

A

iron chelation therapy

bone marrow transplant

25
Q

defects in haem synthesis

A

defects in mitochondrial
causes sideroblastic anaemia
defects in cytoplasmic result in porphyrias

26
Q

factors affecting normal range

A 
age
sex
ethnic origin
time of day
time of analysis
27
Q

clinical features

A 
feel tired
pallor
breathlessness
swelling of ankles
dizziness
chest pain
28
Q

morphological description

A

hypochromic microcytic, normochromic normocytic
macrocytic
red cell indices
blood film

29
Q

hypochromic microcytic

A

serum ferritin

30
Q

normochromic normocytic

A

reticulocyte count

31
Q

macrocytic

A

B 12/folate

bone marrow

32
Q

serum ferritin

A 
low
iron deficiency
normal increased
thalassaemia
secondary anaemia
sideroblastic anaemia
33
Q

iron metabolism

A

absorbed iron bound to mucosal ferritin and sloughed off or transported
transported across the basement membrane by ferroportin

Then - bound to transferrin in plasma

Stored as Ferritin - mainly in liver

34
Q

role of hepcidin

A

Iron absorbed in duodenum - Fe2+ > Fe3+
Transported from enterocytes and macrophages by ferroportin
Transported in plasma bound to transferrin
Stored in cells as ferritin
hepcidin synthesised in hepatocytes in response to ↑iron levels and inflammation – blocks ferroportin so reduces intestinal iron absorption and mobilisation from reticuloendothelial cells

35
Q

reticulocyte count

A 
increased 
Acute blood loss
Haemolysis
normal/low
Secondary anaemia
Hypoplasia
Marrow infiltration
36
Q

secondary anaemia

A 
70% normochromic normocytic
30% hypochromic microcytic
Defective iron utilisation
increased hepcidin in inflammation
frritin often eleveated
37
Q

acquired (HA)

A

autoimmune hemolytic anaemia
mechanical valve
PreEclampsia T/ HUS/ TTP

38
Q

cogenital

A 
Hereditary spherocytosis (HS)
Enzyme deficiency (G6PD deficiency)
Haemoglobinopathy (HbSS)
39
Q

Acquired

A

immune- extravascular

non immune- mostly intravascular

40
Q

immune haemolysis

A 
warm auto antibody
autoimmune drugs CLL
cold autoantibody
CHAD
infections
lymphoma
Alloantibody
transfusion reaction
41
Q

Schistocytes

A

bad

42
Q

haematinics

A

B12/folate

ferritin in microcytic

43
Q

megaloblastic

A

B12 deficiency

Folate deficiency

Haematology (16 decks)

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