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HaemOverview Flashcards

1
Q

How long does a full cross match take?

A

60 minutes

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2
Q

Emergency alternatives to full X-match and timeframes?

A

Group O (immediate):
Rh + or - can be given
Immediate transfusion reactions do not occur due to Rh compatibility
Woman of childbearing age = avoid Rh+

Type-specific (2 minutes):
ABO and Rh only
Good for military and civilian mass casualty events

Type-specific + abbreviate x-match (30 mins):
ABO/Rh + unexpected antibiodies

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3
Q

Define massive transfusion

A

50% blood vol within 4 hours
OR
>1 blood volume in 24 hours

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4
Q

PRBC:FFP:Plt ratio in MTP?

A

≤ 2:1:1

Reduces mortality

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5
Q

Risk of FVII use?

A

1% develop thrombosis
No evidence it improves survival in trauma

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6
Q

TXA trials findings?

A

CRASH2 -> decreased 28 day mortality with TXA

PATCH (2023) -> Given prehospital: Decreased early death from haemorrhage (24hrs: 14 vs 9%) but no significant difference at 6 months.
Also increased survival with poor neurological outcome in the head injury arm

Give it in hospital
Pre-hospital -> PATCH author conclusions = no evidence
High loss to follow up of PATCH - 13%!

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7
Q

TXA in coronary artery surgery?

A

Reduced blood product requirments
BUT
increased post-operative seizures

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8
Q

What’s the definition of a febrile non-haemolytic blood transfusion reaction?

A

Increase of 1 or more degrees 0-6hrs post transfusion

one of most common with transfusion (1 in 300)

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9
Q

Steps if a patient develops fever during transfusion?

A

Stop transfusion
Send unit and new group and hold
Direct and indirect coombs test

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10
Q

What are the most serious transfusion reactions?

A

ABO incompatibility = immediate haemolysis when recipients antibodies recognise donor red blood cells. Proportional to amount of blood received

Graft vs host (immunocompromised) - need irradiated blood cells

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11
Q

What are the two brands of warfarin?

A

Coumadin and marevan

They are NOT bioequivalent!

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12
Q

Warfarin action and how to start

A

Inhibits Vit-K dependent clotting factors II, VII, IX, X (extrinsic)

Initially blocks protein C and S so need LMWH coverage first 5 days and 48 hours after the INR is in therapeutic range

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13
Q

Warfarin bleeding events

A

Greatest risk first 3 months

Strongest risk factor >70

50% of bleeding episodes occur with INR <4

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14
Q

Why is oral vit K preferred over IV?

A

Anaphylactoid reactions with IV vit K -> aim for oral first where possible

Low risk of bleeding with INR >9 = 2.5-5mg oral vit K or 1-2mg IV vit K

Want to use a lower dose to prevent subtherapeutic/anticoagulation resistance if required again (if the patient isn’t actively bleeding)

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15
Q

Only approved thrombolytic in stroke?

A

Alteplase
0.9mg/kg max 90mg
Over 1 hour (10% bolused in first minute)

NNT for functional improvment = 1 in 10
NNT for ICH = 1 in 20
NNT to kill someone as a side effect = 1 in 200

Tenecteplase has reduced systemic bleeding in AMI

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16
Q

What’s the most common manifestation of sickle cell?

A

Vasocclusive crisis

Baseline anaemia 60-90 oft present!

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17
Q

What are cmmon precipitants of vasoocclusive crisis in SCD?

A

Hypoxia
Dehydration
Infections
Cold weather
Stress

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18
Q

Treatment of vasocclusive crisis?

A

Oxygen (if sats <95%)
NSAIDS +/- opiates
Abx (incr susceptibility to encapsulated organisms)

Hydroxyurea can reduce the frequency and severity of crisis

In severe cases -> exchange transfusion

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19
Q

What are three organ specific complications of sickle cell disease?

Other than pneumonia

A

Pulmonary infarct

Aplastic crisis: often precipitated by parvovirus B19 - usually 7-10 days self limiting

Acute splenic sequestration: life threatening anaemia, rapid splenomegaly and high retics -> Rx = volume resus, aggressive transfusion support with leucodeplete blood matched for Rh and Kell antigens

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20
Q

What are the causes of palpable petechia/purpura?

A

Vasculitis
Subacute bacterial endocarditis
SLE
Rheumatoid arthritis

21
Q

Hallmarks of ITP

A

Autoimmune destruction of platelets

Flat petechiae/purpura

Reduced, large platelets on peripheral blood smear

22
Q

Serious bleeding is common in children with ITP?

A

False

It is rare!

23
Q

Proportion of ITP that resolves within 2-3 months in children?

A

80%

Adults rarely remits without treatment and often not with treatment either!

24
Q

Treatment for ITP?

A

Mild = expectant

Mucous bleeding = initial 4mg/kg/day of pred

Serious bleeding/procedural intervention = IVIg

Life-threatening/intracranial bleeding = only time to give platelets

All children with ITP need to have activity restriction while they have thrombocytopaenia and avoid NSAIDs

25
How do you differentiate bleeding secondary to a platelet disorder from coagulation deficiency?
Platelets = petechiae/mucosal Coag deficiency = ecchymosis / haemarthrosis / retroperitoneal / ICH
26
Haemophilias?
A (aight) = F8 deficiency B = christmas = IX Both prolong aPPT (intrinsic) but normal PT ## Footnote Clinically indistinguishable
27
How is fever defined in cancer patients?
Single oral temp ≥ 38.3 OR >38 x 2 OR Axillary temp ≥ 38
28
What % of fevers in cancer patients have an infectious origin?
70%
29
When is the neutrophil nadir post chemo?
5-10 days
30
What are the majority of organisms in febrile neutropaenia?
85% bacterial Gram positive (most common): Staph aureus Staph epidermidis (not a contaminant in neutropaenia) Gram negative: E. Coli Pseudomonas aeruginosa Klebsiella
31
Do you need to always remove indwelling vascular catheters in suspected infections?
No! Only when: Tunnel infection Persistent bacteraemia despite Rx Atypical mycobacteria/candidaemia Add vanc for line infections
32
What is tumour lysis syndrome and why and when does it occur?
Metabolic crisis due to massive apoptosis Most common in haematological malignancies Precipitated by rapid tumour growth and chemotherapy Malignant cells have x4 the amount of phosphate of normal cells
33
What are the most common electrolyte abnormalities in TLS and how are they treated?
Hyperkalaemia (treated as per normal) Hyperuricaemia Hyperphosphataemia Hypocalcaemia ## Footnote Main Rx is: 1. Aggressive fluid rehydration 2. Only give calcium in life-threatening scenarios e.g. arryhtmia/seizures because the calcium can cause metastatic precipitation of calcium phosphate 3. Allopurinol (-ve synth of new uric acid) -> effect in 48 hrs 4. Haemodialysis if not responding Fluid resus increases renal blow flow to clear the uric acid but also prevents uric and CaPO4 precipitation in the distal nephrons
34
Most common symptoms of malignant spinal cord compression?
Pain (90%) Motor deficit (80%) Sensory deficit (70%) Spinchter/autonomic dysfunction (50%)
35
What are the three mechanisms malignancy causes hypercalcaemia?
1. Parathyroid hormone related protein production (80%) -> particularly SCLC 2. Metastatic bone destruction 3. Vitamin D anaolgue production
36
Why doesn't the absolute calcium level necessarily correlate with the degree of symptoms?
Often related to acuity of the rise
37
What's the treament of hypercalcaemia and why?
1. IV fluids -> vol expansion (calcium produces osmotic diuresis causing profound dehydration) 2. Pamidronate IV (must rehydrate first to prevent calcium complex deposition in the kidneys) -> cotraindicated if CrCl <30ml/min Calcitonin +/- glucocorticoids ## Footnote In patients with pre-exisiting CCF or renal failure can consider using furosemide to avoid fluid overload but be cautious
38
What's the most common cancer in children?
Acute leukaemia! Of these:) A.L.L (75%) AML (25%) ## Footnote Present in a similar way with secondary bone marrow failure due to replacement by malignant cells: Bone pain (typically not tender to palpate unless periosteal) Anaemia/thrombocytopaenia WBC can be high/low/normal! AML (less likely ALL) causes: DIC particularly in newly diagnosed Extramedullary involvement e.g. ginigval hyperplasia/subcut nodule/chloromas (mass of blasts)
39
Most common ED complications of acute leukaemia?
1. Bleeding: thrombocytopaenia/chemo/DIC 2. Tumour lysis syndrome 3. Hyperleucocytosis syndrome 4. Sepsis (functional neutropaenia even if count is normal) ## Footnote some AML blasts release a procoagulant tissue factor than cause life-threatening consumptive coagulopathy
40
AML treatment?
May be asked to initiate cytarabine in ED
41
What is hyperleukocytosis and assoc risk factors?
WBC > 100 !! Risk factors: <1 yo Male M4/5 leukaemia Philadelphia chromosome
42
What complications occur with hyperleukocytosis?
1. Leukostasis (mortality 40%): blast mediated microvascular obstruction to lung and CNS -> hypoxaemia/resp failure/seizure/stroke 2. Tumour lysis syndrome 3. DIC 4. ICH (especially if plts <20)
43
What is the treatment of hyperleukocytosis syndrome?
1. Aggressive IV hydration 2. Hydroxyurea 100mg/kg BD 3. AVOID red cells and diuretics (can increase viscosity) 4. Platelets (if <20) - they do not increase viscosity 5. 2 unit phlebotomy with IV saline replacement can be temporising
44
What is the most common paediatric solid organ cancer?
Brain tumours Also second most common cancer after acute leukaemia in children
45
Most common type of metastatic childhood brain cancer
Medulloblastoma
46
Proportion of kids who have headaches prior to presenting with brain cancer?
2/3 Reflective of background numbers of headaches in kids though : /
47
Of children presenting with headache and brain tumour what % had neurological findings?
98%! ## Footnote Seizures Vomiting Positional headache Cushing's triad: HTN | bradycardia | cheyne stokes breathing Opthalmoplegia Papilloedema Asymmetric motor/sens/reflex exam Ataxia Macrocephaly (toddlers/infants)
48
Most common malignant abdo tumour in kids and age group?
<5 yo Wilms (renal) + neuroblastoma ## Footnote Wilms peak 2-3 years old
49
What proportion of primary neuroblastoma occur in the abdomen?
2/3 ## Footnote Neuroblastoma = most common extracranial solid tumour in children Oftern present with constitutional symptoms. Sometimes periorbital ecchymosis/proptosis resembling raccoon eyes from periorbital metastases

Haematology (8 decks)

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