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haematology > haemolysis > Flashcards

haemolysis Flashcards

1
Q

haemolysis?

A

premature red cell destruction

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2
Q

why particularly susceptible to damage?

A

biconcave shape limited metabolic reserve (rely exclusively on glucose metabolism for energy), can’t generate new proteins once in the circulation

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3
Q

compensated haemolysis?

A

increased red cell destruction compensated by increased red cell production i.e. Hb maintained

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4
Q

haemolytic anaemia

A

increased rate of red cell destruction exceeding bone marrow capacity for red cell production i.e. Hb falls

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5
Q

consequences of haemolysis?

A 
erythroid hyperplasia (increased bone marrow red cell production)
excess red cell breakdown products e.g. bilirubin
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6
Q

rely on detecting therefore the breakdown products of red cells and the increased red cell production

A

y

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7
Q

bone marrow response to haemolysis?

A

reticulocytosis and erythroid hyperplasia

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8
Q

are reticulocytes nucleated?

A

NO

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9
Q

why would a blood film in a patient with haemolysis have polychromasia?

A

ribosomal DNA in reticulocytes have RNA that shows blue ray appearance

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10
Q

are reticulocytes diagnostic of hs?

A

no, they are a response to bleeding, iron therapy and iron deficiency anaemia

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11
Q

supravital stain?

A

supravital stain staining ribosomal RNA

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12
Q

automated reticulocyte counting

A

ribosomal RNA is labelled with a flourochrome and fluorescent cells are counted

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13
Q

bone marrow erythroid hyperplasia

A

.

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14
Q

extravascular hs occurs in ?

A

liver and spleen

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15
Q

intravascular?

A

cells destroyed within the circulation

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16
Q

which is commoner - intra or extravascular?

A

extra

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17
Q

what sort of signs of extravascular would you get?

A

hyperplasia at sites of destruction i.e. splenomegaly or hepatomegaly

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18
Q

normal products are in excess

A

.

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19
Q

intravascular haemolysis

A

red cells destroyed in circulation, spilling their contents

20
Q

4 things you see?

A

haemoglobinaemia, methaemalbuminaemia, haemoglobinuria (pink urine, turns black on standing, haemosiderinuria

21
Q

what is methaemalbumin?

A

methaem binds to albumin

22
Q

these are ABNORMAL products

A

intravascular homeless may be life threatening

23
Q

when would you get intravascular haemolysis?

A

ABO incompatible blood transfusion, G6PD deficiency, malaria, PNH, PCH (rare)

24
Q

extravascular ?

A

all other causes of haemolysis

25
Q

investigations?

A

FBC, reticulocyte count, serum unconjugated bilirubin, serum haptoglobins, urinary urobilinogen

26
Q

what does haptoglobin bind?

A

free haemoglobin

27
Q

blood film might show?

A 
mechanical damage (red cell fragments)
oxidative stress (Heinz bodies)
Others i.e. sickle cell disease
28
Q

premature destruction of normal red blood cells. autoimmune haemolysis?

A

warm IgG - idiopathic, autoimmune disorders, lymphoproliferative disorders, drugs, infection

29
Q

cold IgM?

A

idiopathic, infections, lymphoproliferative disorders

30
Q

what does direct coombs test identify?

A

antibody bound to own red cells

31
Q

alloimmune haemolysis?

A

Immediate IgM - predominantly intravascular

delayed IgI - predominantly extravascular

32
Q

passive transfer of the antibody

A

haemolytic disease of the newborn

rhd, abo incompatibility, others eg anti kell

33
Q

haemolytic transfusion reaction iMMediate Mintravascular. delayed Gextravascular

A

.

34
Q

mechanical red cell destruction

A

DIC, haemolytic uraemic syndome, TTP, leaking heart calve, infections ie malaria

35
Q

mechanical damage caused - valve related - red cell fragmentation.

A

MAHA - microangiopathic haemolytic anaemia

36
Q

in burns related homeless

A

microspherocytes, red cells are sheared as they pass through damaged capillaries. only seen in severe burns

37
Q

membrane defects are all very rare

A

ziev’s syndrome, vitamin e deficiency, PNH

38
Q

zieves syndrome

A

haemolysis, alcoholic liver disease, hyperlipidaemia

39
Q

anaemia, polychromatc macrocytes, irregularly contracted cells?

A

zieves syndrome

40
Q

hereditary spherocytosis?

A

pheric red blood cells which are destroyed in the spllen

41
Q

what would you see in spherocytosis

A

splenomegaly

42
Q

g6pd deficiency -

A

no glutathione, no atp. haemolysis

43
Q

g6pd deficiency - failure to cope with oxidative stress

A

y

44
Q

dapsone therapy can cause keratocyte and irregularly contracted cell

A

in beta thalassaemia major, get bony deformities of chronic erythroid hyperplasia and marrow cavity expansion

45
Q

why can g6pd deficiency cause intravascular haemolysis

A

involved in production of NADPH, which i.e. needed for glutathione production

haematology (20 decks)

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