Blood Films Flashcards
Blood Film Characteristics of Iron Deficiency Anaemia
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
Basophilic Stippling
Aggregated ribosomal material (inclusion bodies)
Many dots
beta-thalassaemia trait
Sideroblastic anaemia
Alcoholism
Lead poisoning
Hyper-segmented Nuetrophils
> 5 lobes
B12 deficiency
Folate deficiency
Drugs
Target cells
Codocytes: high surface area: volume ratio
Hyposplenism
Thalassaemia
Iron deficiency
Liver disease
Howell-Jolly Bodies
Nuclear remnants in red cell (Single large dot)
Hyposplenism
Spleen should remove these cells
Causes of Hyposplenism
Absent spleen - trauma or therapeutic
Poorly-functioning
SIC Spleen
Sickle cell
Inflammatory Bowel disease
Coeliac
SLE
Leukoerythroblastic Changes
Aniopoikilocytosis
Nucleated RBCs
Immature myeloid cells
MAHA
Red cell fragments
Low platelets
Reactive lymphocytosis
Modest Lymphocytosis
> 3.5x109/l
Mature cells
Could be
EBV viral infection
early CLL
Primary lymphocytosis
Chronic Lymphocytic leukaemia Excess lymphocytes smear cells /Small lymphocytes (CLL or NHL) All mature
OR
Acute lymphoblastic
leukaemia
Excess lymphocytes
All immature
Cell Markers
CD19 = B cell
CD19 TDT –> Acute lymphoblastic leukaemia
CD19 FMC7 –> Mature B cell
Blood Group and Save
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
Maximum Surgical Blood Ordering Schedule (MSBOS)
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
Acute Transfusion Reaction <24 Hours
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
Delayed Transfusion Reaction >24 Hours
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
Haemolytic Disease of the Newborn (AND Fetus)
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)
