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Flashcards in Blood Films Deck (20)
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1
Q

Blood Film Characteristics of Iron Deficiency Anaemia

A

Microcytic (small)

Hypochromic (pale)

Central pallor –> defect in chain synthesis (iron-deficiency or thalassaemia)

Poikilocytes (abnormally shaped = tear-drop)

Anisopoikilocytosis (aniso=size, poikilo=shape) –> variation in size and shape

Elliptocyte

2
Q

Basophilic Stippling

A

Aggregated ribosomal material (inclusion bodies)
Many dots

beta-thalassaemia trait
Sideroblastic anaemia
Alcoholism
Lead poisoning

3
Q

Hyper-segmented Nuetrophils

A

> 5 lobes

B12 deficiency
Folate deficiency
Drugs

4
Q

Target cells

A

Codocytes: high surface area: volume ratio

Hyposplenism
Thalassaemia
Iron deficiency
Liver disease

5
Q

Howell-Jolly Bodies

A

Nuclear remnants in red cell (Single large dot)

Hyposplenism
Spleen should remove these cells

6
Q

Causes of Hyposplenism

A

Absent spleen - trauma or therapeutic

Poorly-functioning
SIC Spleen

Sickle cell
Inflammatory Bowel disease
Coeliac
SLE

7
Q

Leukoerythroblastic Changes

A

Aniopoikilocytosis
Nucleated RBCs
Immature myeloid cells

8
Q

MAHA

A

Red cell fragments

Low platelets

9
Q

Reactive lymphocytosis

A

Modest Lymphocytosis

> 3.5x109/l

Mature cells

Could be
EBV viral infection
early CLL

10
Q

Primary lymphocytosis

A
Chronic Lymphocytic
leukaemia
Excess lymphocytes
smear cells /Small lymphocytes (CLL or NHL)
All mature

OR

Acute lymphoblastic
leukaemia
Excess lymphocytes
All immature

11
Q

Cell Markers

A

CD19 = B cell

CD19 TDT –> Acute lymphoblastic leukaemia

CD19 FMC7 –> Mature B cell

12
Q

Blood Group and Save

A

Forward Testing
Take patient’s RBCs and add to Anti-A and Anti-B reagents

Reverse Testing
Take patient’s serum and add to known RBC types

Stay afloat –> agglutinated cells
Pass to bottom –> no agglutination

Antibody screen on patient’s plasma
Use 2 or 3 reagent red cells containing all the important red cell antigens between them – blood from others with all 20 antibodies known in there.

Test with patient’s blood

Screen by incubating the patient’s plasma and screening cells using IAT** technique

13
Q

Maximum Surgical Blood Ordering Schedule (MSBOS)

A

in ELECTIVE SURGERY:

GROUP AND SCREEN before operation: then if no antibodies present, do not cross-match blood, but just save sample in the fridge
If unexpected need for blood, can provide it within 10 minutes (by Electronic Issue, as no antibodies present)

ALWAYS CROSSMATCH UP FRONT IF RBC ANTIBODIES PRESENT

14
Q

Acute Transfusion Reaction <24 Hours

A

Wrong blood: Acute haemolytic (ABO incompatible)
Restless (sense of impending doom), chest/ loin pain (don’t get pain with bacterial infection but the rest of the symptoms are similar), fever, vomiting, flushing, collapse, haemoglobinuria (later, should not be waited for –> dark red urine);
↓BP & ↑HR (shock), ↑Temp

Bacterial contamination
Symptoms/Signs
Restless, fever, vomiting, flushing, collapse.
↓BP & ↑HR (shock), ↑Temp
Presents in a similar way to “wrong ABO blood” minus the pain

Allergic Transfusion reactions
Mild urticarial or itchy rash sometimes with a wheeze. Sometimes periorbital oedema.
Common in atopic and with FFP

Severe anaphylaxis
BP & ↑HR (shock),
very breathless with wheeze,
often laryngeal &/or facial oedema
Infection (bacterial contam) very similar in appearance to ABO incompatibility
Occurs particularly in IgA deficiency as patients have made Abs against IgA that they lack

Febrile non-haemolytic – have to separate from infection
Rise in temperature of 1C, chills, rigors

Respiratory
Transfusion associated circulatory overload (TACO) – too much fluid
Acute lung injury (TRALI) – transfusion related acute lung injury
Very similar, SOB, ↓O2 sats, ↑HR, ↑BP BUT in TACO JVP is raised
In TRALI, it is not

15
Q

Delayed Transfusion Reaction >24 Hours

A

Delayed Haemolytic Transfusion Reaction
Red cell antibodies - IgG mediated
You get a delayed haemolysis (5-10 days later)
Extravascular haemolysis
Jaundice
Haemolysis tests: Increase bilirubin, Decreased Hb, Increased reticulocytes
Haemoglobinuria over few days

Transfusion Transmitted Infections
Malaria
vCJD
Viral infection

Transfusion Associated Graft-Versus-Host Disease
Prevent: irradiate blood components for very immunosuppressed; or patietns having HLA matched components

Post Transfusion Purpura
Purpura appears 7-10 days after transfusion of blood or platelets and usually resolves in 1 to 4 weeks but can cause life threatening bleeding
Affects HPA -1a negative patients - previously immunised by pregnancy or transfusion
Due to an anti-platelet antibody in patient
Exposure during pregnancy to a fetal platelet antigen patient doesn’t have
Incoming transfusion of antigen positive platelets,
BUT not only donor platelets destroyed, patient’s own original platelets destroyed
Next time give HPA matched platelets
Mx infusion of IVIG

Immune-modulation
Possible increased rate of infections post-op
Increased recurrence of cancers in patients who have blood transfusion - conflicting studies – uncertain

Iron overload – blood has lots of iron (more than 100 units transferred)
Mx: desferioxamine

16
Q

Haemolytic Disease of the Newborn (AND Fetus)

A

Mechanism of RhD sensitisation during the first pregnancy (OR Blood Transfusion) –> fetal red cell destruction during the second pregnancy with an RhD positive fetus

Only IgG antibodies can cross the placenta.

If mother has high levels of IgG antibody - it can destroy fetal red cells, if they are positive for the corresponding antigen

Fetal anaemia (haemolytic)

Haemolytic disease of newborn (anaemia plus high bilirubin - which builds up after birth as no longer removed by placenta)

If severe can cause severe anaemia
Compensate by increased cardiac output –> heart failure
Hydrops fetalis usually stems from fetal anemia, when the heart needs to pump a much greater volume of blood to deliver the same amount of oxygen
Hydrops fetalis is a condition in the fetus characterized by an accumulation of fluid, or edema, in at least two fetal compartments.
Bilirubin dealt with by placenta until delivery
Immature liver of fetus can’t deal with bilirubin, it builds up and crosses the blood brain barrier and causes Kernicterus (Syndrome of hyperextension and neurological damage, and sometimes death)

17
Q

Hydrops fetalis

A

Hydrops fetalis usually stems from fetal anemia, when the heart needs to pump a much greater volume of blood to deliver the same amount of oxygen

Hydrops fetalis is a condition in the fetus characterized by an accumulation of fluid, or edema, in at least two fetal compartments.

18
Q

Kernicterus

A

Syndrome of hyperextension and neurological damage, and sometimes death

19
Q

Anti-D

A

RhD positive (fetal) red cells get coated with anti-D Ig and then they get removed by the mother’s reticuloendothelial system (spleen) before they can sensitise the mother to produce anti-D antibodies

Must give IM anti-D injection within 72 hours of the ‘sensitising event’:
spontaneous miscarriages if surgical evacuation needed and therapeutic terminations
amniocentesis and chorionic villous sampling
abdominal trauma (falls and car accidents)
external cephalic version (turning the fetus)
stillbirth or intrauterine death

20
Q

Doses of anti-D

A

Kleihauer test –> fetal haemoglobin
Gives volume of cells in maternal circulation

At least 250 iu - for events before 20 weeks of pregnancy

At least 500 iu - for events any time after 20 weeks of pregnancy (including delivery)

Sometimes a larger dose is needed for larger bleeds–> Kleihauer test is always done if > 20 weeks and at delivery

125 iu can prevent sensitisation from a 1mL FMH

So : 500 iu covers up to 4mL fetal red cells
1250 iu covers up to 10mL
1500 iu covers up to12mL