Anaemia Flashcards
1
Q
What is a normal reticulocyte count?
A
1-2%
2
Q
What happens to the reticulocyte account in anaemia in a properly functioning marrow?
A
Increases to >3%
= Good marrow response
If <3% = poor marrow response
3
Q
List causes of microcytic anaemia
A
Fe deficiency anaemia
Thalassemia (disorder of globin synthesis)
Anaemia of chronic disease (impaired iron metabolism)
Sideroblastic anaemia (disorder of haem synthesis)
Lead poisoning (disorder of haem synthesis)
4
Q
Hb is made up of haem (… +…) + globin
A
Haem = iron + protoporphyrin
5
Q
List causes of normocytic anaemia
A
Blood loss Haemolysis Anaemia of chronic disease Renal failure/anaemia BM failure - infiltration, chemo/drug-induced
6
Q
List causes of macrocytic anaemia
A
B12 (megaloblastic) Folate (megaloblastic) ETOH (B12 deficiency, liver disease, BM suppression) Multiple myeloma MDS Hypothyroidism Liver disease Drugs - MTX, azathioprine, cyclophosphamide, chemotherapy, allopurinol, erythromycin, PPI, OCP, hydroxyurea, trimethoprim
7
Q
Where is iron absorbed?
A
Duodenum
8
Q
Iron is consumed in two forms. What are they?
A
Haem (meat)
Non-haem (vegetables)
9
Q
What happens to your platelets in iron deficiency?
A
Raised platelets
10
Q
List causes if iron deficiency
A
Blood loss
Low iron intake (vegetarians)
Reduced absorption - IBD, coeliac, bariatric surgery, H.pylori
Increased demand - pregnancy, lactation, puberty
Paroxysmal nocturnal haemoglobinuria (rare)
11
Q
List clinical features of Fe deficiency
A
Features of anaemia
Kilonychia (spoon-shaped nails)
Pica (chew on things classically ice)
12
Q
How long to wait before checking response to IV iron?
A
6 weeks
13
Q
In what diseases would you consider a higher iron target?
A
Renal failure
Heart failure
14
Q
How does the MCV compare in thalassemia and iron deficiency?
A
MCV is often much longer in thalassemia
15
Q
What do you the following parameters reflect: Serum iron Transferrin/total iron binding capacity Tf sat Ferritin
A
Serum iron - this can fluctuate with food, time of day
Transferrin/total iron binding capacity - measure of transferrin molecules (made by liver) in the blood
Tf sat - % of transferring molecules that are bound to iron
Ferritin - iron stored in macrophages or liver
16
Q
What is DMT1, haem carrier protein-1 (HCP-1) and ferroportin?
A
DMT 1 transports non-haem iron (Fe2+; vegetable) from gut lumen to enterocyte
HCP-1 transports haem iron (meat) from gut lumen to enterocyte
Ferroportin transports Fe2+ from enterocyte to blood
17
Q
What’s hepcidin?
A
Expressed mostly in the liver (small amounts in muscle, intestine, lungs etc)
1) Binds to ferroportin and stops iron from going from enterocyte to circulation (traps iron within enterocyte)
2) Traps iron in macrophages
3) Suppresses EPO production
Goal is to prevent bacteria from accessing iron
18
Q
What happens to hepcidin in these situations?
High iron =
Hypoxia =
Inflammation =
Erythropoiesis =
Chronic haemolytic anaemia or thalassemia =
Haemachromatosis =
A
High iron = high hepcidin
Hypoxia = low hepcidin (want more RBCs to be produced so need more iron)
Inflammation = high hepcidin (reduce amount of iron available to bacteria)
Erythropoiesis = low hepcidin
Chronic haemolytic anaemia or thalassemia –> Fe overload = low hepcidin (inappropriate –> worsens iron overload)
Haemachromatosis = low hepcidin (inappropriate)
19
Q
How to differentiate between iron deficiency anaemia and anaemia of chronic disease?
A
Serum iron - both low
Transferrin/TIBC - high + low
Tf sat - both low
Serum ferritin - low + normal/high
20
Q
What is sideroblastic anaemia?
A
Anaemia due to defective protoporphyrin synthesis
- Reduced protoporphyrin –> reduced haem –> reduced Hb –> microcytic anaemia
21
Q
How do you get sideroblastic anaemia?
A
Congenital
Acquired - ETOH, lead poisoning, Vitamin B6 deficiency (isoniazid in TB)
22
Q
What is your iron status like in sideroblastic anaemia?
A
Fe overloaded state
Because the problem is you don’t have enough protoporphyrin!
Iron + protoporphyrin = haem
23
Q
Hb consists of 2 pairs of globin chains. Pair of alpha chains and pair of non-alpha chains (these are …)
A
Adult: beta chains
Baby: Gamma chains
24
Q
What are the 2 types of thalassemia?
A
𝛼- and 𝛽-thalassemia
25
```
What happens in 𝛼-thalassemia?
A) 1 gene deletion
B) 2 gene deletion
C) 3 gene deletion
D) 4 gene deletin
```
A) asymptomatic
B) mild anaemia with raised RBC count
C) severe anaemia; 𝛽 chains form tetramers (Hb) that damage RBCs
D) hydrops fetalis (lethal in utero); 𝛾 chains form tetramers (Hb Barts) that damage RBCs
26
𝛽-thalassemia
Two 𝛽 genes are present on chromosome 11; mutations result in absent (𝛽0) or diminished (𝛽+) production of the 𝛽-globin chain.
What happens in 𝛽-thalassemia minor?
𝛽/𝛽+
Mildest form of disease
Asymptomatic with raised RBC
Hb electrophoresis shows slightly decreased HbA and increased HbA2 (𝛼2𝛿2) and HbF (𝛼2𝛾2).
27
What are the normal types of Hb?
HbF (𝛼2𝛾2) - foetal
HbA (𝛼2𝛽2) - adult
HbA2 (𝛼2𝛿2) - small portion of adult Hb
28
𝛽-thalassemia
Two 𝛽 genes are present on chromosome 11; mutations result in absent (𝛽0) or diminished (𝛽+) production of the 𝛽-globin chain.
What are the complications of 𝛽-thalassemia major?
𝛽0/𝛽0
Most severe form of disease
1) Severe anaemia within a few months of life (HbF at birth is temporarily protective)
- Unpaired 𝛼 chains precipitate and damage RBC membrane, resulting in ineffective erythropoiesis and extravascular haemolysis (by spleen)
2) Massive erythroid hyperplasia/extramedullary haematopoiesis
3) Iron overload
4) Cholecystitis (increased RBC turnover --> increased unconjugated bilirubin)
5) Unusual VTEs (thrombophilia especially those post splenectomy)
6) High output heart failure, pulmonary hypertension
Above can also happen in thalassemia intermedia (wide spectrum from asymptomatic to almost transfusion dependent
29
What is massive erythroid hyperplasia in 𝛽-thalassemia major?
Expansion of haematopoiesis into the skull (reactive bone formation leads to 'crewcut' appearance on xray and facial bones ('chipmunk facies')
Extramedullary haematopoiesis with hepatosplenomegaly, paraspinal mass (can cause nerve compression and paraplegia/quadraplegia)
Risk of aplastic crisis with parvovirus B19 infection of erythroid precursors
30
Electrophoresis in 𝛽-thalassemia major?
Electrophoresis shows HbA2 and HbF with little or no HbA
31
In 𝛽-thalassemia, what do 𝛽0 and 𝛽+ mean?
𝛽0 absent production of beta chain
| 𝛽+ reduced production of beta chain
32
Explain how HbS is formed in sickle cell disease
A single amino acid change replaces normal glutamic acid (hydrophilic) with valine (hydrophobic)
= Abnormal 𝛽 chain of haemoglobin
= Results in HbS
33
How does HbS cause problems?
HbS polymerises when deoxygenated --> polymers aggregate into needle like structures --> distorts RBC shape --> difficulty manoeuvring through vasculature --> damage to RBC membrane
"Sickling" is reversible
34
What causes HbS to sickle or precipitates sickle cell crisis?
```
Hypoxia
Hypo/hyperthermia
Altitude
Acidosis
Pregnancy
Fever
Sepsis
```
Cells sickle --> blocks vasculature --> causes inflammation
35
What protects HbS from sickling?
HbF
High HbF at birth protects HbS from sickling (presents only after 6 months of age). Taking hydroxyurea produces more HbF.
36
List complications of sickle cell disease
Almost every organ can be affected
- Anaemia
- Jaundice with unconjugated bilirubin --> bilirubin gallstones
- Chipmunk facies, frontal bossing
- Hepatosplenomegaly
- Pain crisis from infarction
- Infarction of organs including bone, spleen/shruken fibrotic spleen/autosplenectomy, MI/ACS, kidneys/renal papillary necrosis, lungs/acute chest syndrome, stroke, dactylitis
- Infections (hyposplenism)
- Leg ulcers
37
What are the consequences of autosplenectomy in sickle cell disease?
Infection with encapsulated organisms such as strep pneumoniae, haemophilus influenzae (most common cause of death in children)
Increased risk of salmonella typhi osteomyelitis (usually staph aureus in normal people)
38
How does acute chest syndrome present in sickle cell disease?
- Chest pain, SOB, lung infiltrates
- Often precipitated by pneumonia
- Most common cause of death in adults
39
What's the difference between sickle cell trait and sickle cell disease?
Trait: presence of one mutated and one normal 𝛽 chain, results in <50% HbS in RBCs
Disease: presence of 2 mutated 𝛽 chains, resulting in >90% HbS in RBCs
40
Do people with sickle cell trait have symptoms?
Generally asymptomatic
No anaemia
RBCs with <50% HbS do not sickle in vivo except in renal medulla (extreme hypoxia and hypertonicity of the medulla can cause sickling --> microinfarction --> microscopic haematuria --> inability to concentrate urine)
41
What do you expect to see on blood film in sickle cell disease?
```
Target cells (dehydrated cells due to damaged RBC membranes)
Sickle cells
```
Not seen in sickle cell trait
42
What do you expect to see on electrophoresis in sickle cell disease/trait?
Disease - >90% HbS, 8% HbF, 2% HbA2 (no HbA)
| Trait - 43% HbS, 55% HbA, 2% HbA2
43
Inheriting the thalassemia gene mutation is protective against ...
Malaria
44
What is Haemoglobin E?
Structurally abnormal hb
| Behaves like a 𝛽-thalassemia mutation
45
List some lab screening tests for thalassemia
FBC + blood flim
- Microcytic, hypochromic anaemia
- Target cells
- Nucleated RBCs (when made in abnormal location such as liver, spleen, they escape too early and retain nucleus)
Iron studies - iron overload
Hb electrophoresis - shows HbA, HbF, little HbA2
Sickle solubility test
Genetic testing
46
What's high performance liquid chromatography?
Similar to Hb electrophoresis
Can identify different Hb molecules
E.g. shows that the patient has elevated HbA2
However can't tell which type of 𝛽-thalassemia (e.g. 𝛽+/𝛽0, 𝛽0/𝛽0), and is normal in alpha thalassemia carriers (need genetic testing)
47
Rx for 𝛽-thalassemia major (𝛽0/𝛽0)
1) Transfusion dependent
2) Iron chelation (for iron overload)
3) Consider splenectomy
48
Complications of iron overload
- Excessive melanin skin pigmentation (bronze diabetes)
- Hypothyroidism
- Hypoparathyroidism
- Pulmonary hypertension and embolism
- Cardiomyopathy (major cause of death)
- Arrhythmias
- Venous thrombosis
- Haemosiderosis and cirrhosis of liver
- Diabetes (beta cell destruction)
- Delayed puberty
- Osteoporosis
- Testicular or ovarian failure
- Splenomegaly
49
How to assess iron overload? (transfusion dependent thalassemia)
1) Serum ferritin - useful for frequent monitoring
2) MRI to measure iron concentration in liver and heart
- Very high iron concentration correlates with liver fibrosis/liver function abnormalities, and heart failure
50
What are some available iron chelation thearpies?
Desferrioxamine (DFO)
Deferiprone (DFP)
Deferasirox (DFX)
51
Whats HbH disease?
HbH has extremely high O2 affinity --> doesn't unload oxygen to tissue
Hence it is an ineffective carrier of oxygen
52
Where is folate absorbed?
Jejunum
53
Is it more common to be folate or B12 deficient?
Folate deficiency is more common as we have minimal body stores. Can develop within months.
B12 deficiency takes years to develop due to large stores B12 in the liver
54
Where do we get folate from?
Vegetables and fruits
55
Causes of folate deficiency
Poor diet (alcoholics, elderly)
Increased demand (pregnancy, haemolysis, chronic inflammatory state such as cancer)
Folate antagonist e.g. MTX, trimethoprim
B12 deficiency disrupts folate uptake into cells (but increases serum folate)
56
How is vitamin B12 absorbed?
Dietary vitamin B12 is bound to animal-derived protein
Salivary amylase liberates vitamin B12, which is then bound to R-binder (salivary gland)
Carried to stomach
Pancreatic proteases in the duodenum detach vitamin B12 from R binder
Vitamin B12 binds intrinsic factor (gastric parietal cells) in the small bowel
Vitamin B12-intrinsic factor complex gets absorbed in the terminal ileum --> portal blood system
57
Where is vitamin B12 absorbed?
Terminal Ileum
58
Causes of Vitamin B12 deficiency
1) Pernicious anaemia (most common)
- Autoimmune destruction of gastric parietal cells --> intrinsic factor deficiency
- Intrinsic factor (IF) ab = very specific
- Parietal cell ab = very sensitive
2) Poor diet (rare)
- Vegans, alcoholics, underlying haemolytic anaemia
3) Crohn's
Inflammation of ileum
4) Small bowel resection or gastrectomy
5) Pancreatic insufficiency
6) Infection - tropical sprue, tapeworm
59
Clinical findings of Vitamin B12 deficiency
1) Glossitis, angular stomatitis
2) Subacute combined degeneration of the spinal cord
- Affects posterior (dorsal column tract) and lateral (corticospinal tract)
- Poor proprioception and vibration (symmetrical neuropathy LL > UL) and spastic paresis
- May be reversible
3) Neural tube defects (spina bifida)
4) Increased melanin/pigmentation
60
Lab findings in vitamin B12 deficiency
Low serum B12
Film: Macrocytic anaemia, hypersegmented neutrophils, oval macrocytes (RBC), low reticulocytes, pancytopenia (if severe)
BM: megaloblastic change
Positive haemolysis screen
Holo-transcobalamin II - measures the amount of B12 bound to transcobalamin (available to tissues)
61
Clinical findings of folate deficiency
```
Diarrhoea, LOA, LOW
Weakness
Sore tongue
Headaches
Palpitations
Irritability
Infertility
Infants with neural tube defects
Signs of anaemia
```
62
Lab findings in folate deficiency
Low serum folate (variable depending on recent intake)
Low red cell folate (>95% folate is in RBC; best assessment of long term stores; less variable)
Film: Macrocytic anaemia, hypersegmented neutrophils, oval macrocytes (RBC), low reticulocytes, pancytopenia (if severe)
BM: megaloblastic change
63
How to reverse methotrexate toxicity?
Leucovorin (folinic acid)
| To reverse folate deficiency caused by dehydro-folate-reductase inhibition caused by MTX
64
Where are RBCs destroyed in extravascular haemolysis and intravascular haemolysis?
Extravascular: reticuloendothelial system (macrophages of the spleen, liver, lymph nodes)
Intravascular: within the blood vessels
65
What's in a haemolysis screen?
```
Bilirubin
Haptoglobin
Reticulocyte count
LDH
Blood flim
Direct Coombs test - measures level of immunoglobulins stuck onto red cells; positive in autoimmune haemolysis
```
Do urinary haemosiderin if suspecting intravascular
66
What 3 things indicate haemolysis?
Increased red cell breakdown or free Hb
Damaged red cells
Compensatory erythropoiesis
67
In haemolysis, list evidence of red cell breakdown
Hyperbilirubinemia
Reduced haptoglobin
```
Intravascular haemolysis
Raised plasma Hb
Haemoglobinuria
Urinary haemosiderin
Methaemalbuminaemia
```
68
In haemolysis, list examples of damaged red cells
Spherocytosis (increased osmotic fragility)
Fragmented and contracted cells (TTP)
Sickled cells
69
In haemolysis, list examples of compensatory erythropoiesis
Reticulocyte >3%
| Erythroid hyperplasia of marrow
70
What are spherocytes (in hereditary spherocytosis)?
Defect in cytoskeleton of RBC membrane
These RBCs are round instead of donut shaped
Less able to manoeuvre through splenic sinusoids and are consumed by splenic macrophages
Increased osmotic fragility (lyses in hypertonic saline)
71
List clinical features of hereditary spherocytosis
Jaundice (RBCs --> unconjugated bilirubin)
Gallstones
Splenomegaly
Leg ulcers
Haemolytic "crisis" (often in the presence of infection)
Aplastic crisis (parvovirus B19 infection)
72
Where does the haemolysis occur in hereditary spherocytosis?
Extravascular (spleen)
73
Rx: hereditary spherocytosis
Splenectomy (problem is not with the spherocytes but with the destruction of the spherocyte by the spleen)
74
How is hereditary spherocytosis diagnosed?
Blood film: spherocytes
Negative DAT/direct coombs test
Flow cytometry
75
How to manage chronic sickle cell disease?
- Transfusions or RBC exchange (replace sickle cells with normal RBCs; target HbS <30%)
- Hydroxyurea - boost HbF which is protective against sickle cell
- Immunisation (from hyposplenism)
- Folic acid (need it to make RBCs)
- Consider BM transplant
Novel therapy - crizanlizumab (prevent pain crisis), gene therapy
76
How to manage acute sickle cell crisis?
- Aggressive hydration
- Analgesia
- Treat infection
- If severe may require red cell exchange
77
When is hydroxyurea indicated in sickle cell disease?
Adults with ≥3 pain crisis/year
Adults with sickle cell-associated pain that interferes with ADLs/QOL
History of recurrent or severe ACS
All Children >9 months old
78
Which antibodies are involved in immune haemolytic anaemia?
IgG - extravascular haemolysis
IgM - intravascular haemolysis
79
How to diagnose immune haemolytic anaemia?
Coombs (DAT) test - can be direct or indirect
- Positive DAT does not = haemolysis
Evidence of haemolysis
80
What's the difference between direct and indirect Coombs test?
Direct looks at the presence of ab or complement on RBCs
Indirect looks at the presence of ab in the serum
81
What are the 2 main types/syndromes of autoimmune haemolytic anaemia?
Warm AIHA >85%
| Cold agglutinin haemolysis <15%
82
List some secondary causes of autoimmune haemolytic anaemia
```
Lymphoproliferative disorders
Other malignancy
Infection
CT disease e.g. SLE
Drug induced or associated
```
83
What is warm autoimmune haemolytic anaemia?
Warm temperature --> IgG binds RBCs --> RBCs are consumed by splenic macrophages --> spherocytes (membranes are removed bit by bit)
Extravascular haemolysis
84
What is warm autoimmune haemolytic anaemia associated with?
SLE (most common cause)
CLL
Drugs classically penicillin and cephalosporin
Viruses
85
How to treat warm autoimmune haemolytic anaemia?
Transfusion if Hb <70
Steroids (pred 1mg/kg)
DVT prophylaxis
2nd line
IVIG (spleen eats this instead of RBCs = buys time)
Rituximab (takes time to work so can use IVIG in the mean time; probably consider this prior to splenectomy)
Splenectomy (removes source of ab)
```
Refractory
Cyclosporine
High dose cyclophophamide
Mycophenolate mofetil
Danazol
```
86
What is cold agglutinin/autoimmune haemolytic anaemia?
Cold temperature --> IgM binds RBCs --> binds complement --> activates complement --> intravascular haemolysis
Intravascular
87
What is cold agglutinin/autoimmune haemolytic anaemia associated with?
Mycoplasma pneumoniae
EBV/CMV
Lymphoma
Idiopathic
88
How to treat cold agglutinin/autoimmune haemolytic anaemia?
Often not significant enough to treat
Keep warm
Rituximab
Steroids (if mixed cold/warm antibodies)
89
What happens to RBCs in G6PD deficiency?
G6PD deficiency makes RBCs susceptible to oxidative stress --> oxidative stress --> intravascular haemolysis
90
How do you get G6PD deficiency?
Inherited
| X linked recessive disorder
91
What precipitates haemolysis in G6PD deficiency?
Oxidative stress
| Causes include infections, drugs (e.g. sulphur drugs, dapsone) and fava beans
92
How does G6PD deficiency present?
Haemoglobinuria
Back pain (Hb is nephrotoxic)
Hours after exposure to oxidative stress
93
What do you see on blood flim in G6PD deficiency after an episode of oxidative haemolysis?
Bite cells
94
What are heinz bodies and bite cells?
In G6PD deficiency
Oxidative stress precipitates clumps of damaged Hb within the RBCs (Heinz bodies). These Heinz bodies are removed by splenic macrophages, resulting in bite cells
They are evidence of oxidative injury
95
What happens to the small vessels in microangiopathic haemolytic anaemia (MAHA)?
Get platelet microthrombi formation (consume platelets) --> RBCs are "sheared" as they pass through the microthrombi --> haemolytic anaemia
96
What are the disorders associated with microangiopathic haemolytic anaemia (MAHA)?
Hint: 2 groups
2 groups
Group 1 - platelet microthrombi --> sheer stress
1) TTP
- large uncleaved VWF --> Platelet microthrombi
2) HUS
- Drugs/infection cause endothelial damage --> platelet microthrombi
3) DIC
4) HELLP/pre-eclampsia
Group 2 - mechanical haemolysis
5) Prosthetic heart valves
6) Severe aortic stenosis (calcified)
97
What are the clinical findings of TTP/HUS?
MEDICAL EMERGENCY
Thrombocytopenia
AKI (microthrombi formation in the renal vessels)
Neurological abnormalities (microthrombi formation in the vessels of the CNS)
Fever
Microangiopathic haemolytic anaemia
Bleeding/bruising
98
What abnormal lab findings do you expect in microangiopathic haemolytic anaemia (MAHA)?
Think FBC, blood film, BM
Low platelets
Low Hb
Blood film: schistocytes (red cell fragments), polychromasia (multicoloured RBCs; suggests RBCs being released prematurely from BM)
Evidence of haemolysis
BM: lots of megakaryocytes (to try and make more platelets)
99
Rx microangiopathic haemolytic anaemia (MAHA)
Plasmapharesis (to remove autoantibodies)
| Corticosteroids
100
Pathogenesis of TTP
Large uncleaved VWF molecules (should normally be cleaved by ADAMTS13 which are being attacked by autoantibodies) --> catch platelets --> platelet microthrombi --> shear RBCs --> haemolysis --> end organ damage
101
How to diagnose TTP?
Clinical and ADAMTS 13 <10%
| Exclude STEC infection (shiga toxin producing ecoli)
102
How to manage TTP?
```
Medical emergency
Apharesis (remove whole blood from the patient, separate the blood into individual component so that one particular component can be removed)
FFP
Steroids
Rituximab
(Caplacizumab - not available in Aust)
```
Assess with LDH and platelet count
103
What are the disorders associated with TTP/HUS/MAHA?
```
Idiopathic
Familial
Complement induced MAHA - Rx eculizumab
Infection (ecoli, HIV) - diarrhoea associated HUS
SLE
Pregnancy/post-partum
Chemotherapy
Drugs - quinine, cyclosporin
BM transplant
```
104
How does paroxysmal nocturnal haemoglobinuria result in haemolytic anaemia and haemoglobinuria?
GPI anchors decay accelerating factor (DAF) to RBCs
Absent GPI --> absent DAF --> RBCs susceptible to complement damage --> intravascular haemolysis of RBC, WBC, platelets --> haemaglobinemia + haemaglobinuria + haemosiderinuria (days later)
105
What time of the day does paroxysmal nocturnal haemoglobinuria occur?
During sleep --> shallow breathing --> mild respiratory acidosis --> activates complement --> haemolysis
106
What are the complications of paroxysmal nocturnal haemoglobinuria?
1) Venous thrombosis in unusual places
Destroyed platelets --> release cytoplasmic content --> thrombosis
Main cause of death
2) Iron deficiency anaemia (due to chronic loss of Hb in the urine)
3) Acute myeloid leukaemia - 10%
- Problem in the myeloid stem cell which results in absent GPI in the first place
107
How to diagnose paroxysmal nocturnal haemoglobinuria?
Flow cytometry to detect lack of CD59 (DAF) on blood cells and CD16 on neutrophils
108
Rx for paroxysmal nocturnal haemoglobinuria
Eculizumab
| - Ab against complement
109
What disease do you see spur cells/acanthrocytes (RBCs with spike like projections)?
End stage liver disease
110
How do you get anaemia in ESKD?
Lack of EPO
Iron sequestration in anaemia of chronic disease
Iron, B12, folate deficiency
111
What's the Hb target in GI bleed?
80
But transfuse anyway if haemodynamically unstable
Aim 80-100 in IHD
112
What's the Hb target in variceal bleed?
70
But transfuse anyway if haemodynamically unstable
Aim 80-100 in IHD
113
```
List the antigen on RBC, ab in serum and compatible blood for each of the following:
A) Blood group A
B) Blood group B
C) Blood group AB
D) Blood group O
```
A)
A
B, AB
A, O
B)
B,
A, AB
B, O
C)
A, B
Nil
AB, A, B, O
D)
Nil
A, B
O only
114
Which blood is the universal plasma (contains no antibodies)?
AB
| Not O
115
What is the ratio of plasma to red cells to platelets used in massive transfusion?
Start with 1:1:1
i.e. RCs 4 units: FFP 4 units: plat one pool
Next pack add in cyoprecipitate 8-10 units
Check coags regularly to look for trends if not using TEG/ROTEM
116
How is recombinant factor VIIa used in massive transfusion?
Enhances thrombin generation on already activated platelets
Turns off bleeding in 15 minutes!
Very $$$$, not used frequently
Effective, well tolerated
117
List examples of adverse transfusion reactions
Allergy
Febrile non-haemolytic transfusion reaction
Fluid overload
TRALI
Delayed haemolytic transfusion reaction
Infection - hepatitis, HIV, bacterial infection
ABO incompatibility
