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CP3 Medicine > Haematology 2 > Flashcards

Haematology 2 Flashcards

1
Q

What investigations are done for myeloma?

A

FBC: normochromic, normocytic anemia, leucopenia
Blood film: roleaux formation
ESR: raised
U&Es: often deranged
calcium: raised
ALP: normal
Serum/urine electrophoresis: paraprotein monoclonal band seen

Urine Bence-Jones protein: positive
Free immunoglobulin light chains present in the urine the precipitate and then disappear again on heating the urine

Skeletal XR: punched out lytic lesions e.g. pepper pot skull

Bone marrow biopsy: increased clonal plasma cells >10%
If under 10% then the disease may be termed ‘monoclonal gammopathy of uncertain significance’: MGUS

CT of body

B – Bence–Jones protein (request urine electrophoresis)
L – Serum‑free Light‑chain assay
I – Serum Immunoglobulins
P – Serum Protein electrophoresis
Bone marrow biopsy is necessary to confirm the diagnosis of myeloma and get more information on the disease.

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2
Q

What is the management for myeloma?

A

Supportive therapy
Chemotherapy - bortezomid, thalidomide, dexamethasone
Radiotherapy
Bone marrow stem cell transplants used if <70 as this allows higher dose chemotherapy

Patients require venous thromboembolism prophylaxis with aspirin or low molecular weight heparin whilst on certain chemotherapy regimes (e.g. thialidomide) as there is a higher risk of developing a thrombus.

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3
Q

What are the complications of myeloma?

A

Hypercalcaemia, spinal cord compression, hyperviscosity and acute renal failure

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4
Q

What is the prognosis for myeloma?

A

Original myeloma cell is very resistant so oftenrmeturns
median survival is 3-4 years
death is usually from renal failure or infection

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5
Q

What are lymphomas?

A

Malignant proliferation of lymphocytes, which most commonly accumulate in peripheral lymph nodes, but ca accumulate in teh peripheral blood or infiltrate organs

Most are derived from B cells

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6
Q

What proportion of lymphomas are Hodgkin’s lymphomas?

How are they differentiated?

A

1 in 5 or 20-25% are Hodgkin’s lymphoma

characterised by Reed-Sternburg cells: Binucleate ‘mirror cells’ on biopsy

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7
Q

What is the largest peak of incidence of Hodgkin’s lymphomas?

A

Bimodal: As young adults (20-35)

A second peak in 50-70 year olds

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8
Q

What are the risk factors for Hodkin’s lymphomas?

A 
Male
family history
HIV
EBV
autoimmune condition such as SLE
obese
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9
Q

What are the symptoms of Hodkin’s lymphoma?

A

B symptoms:
fever, weight loss, profuse night sweats

Alcohol - lymph node pain
mediastinal LN can have mass effects (SVC / bronchial obstruction or effects of direct extension (pleural effusion)

Fatigue
Itching
Cough
Shortness of breath
Abdominal pain
Recurrent infections
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10
Q

What is Non-Hodgkin’s lymphoma?

A

Includes all lymphomas without the presence of Reed-Sternberg cells
Peak incidence is 70 years

Either high grade: divide rapidly, typically present with rapid onset lymphadenopathy

or

Low grade tumours: divide slowly, typically present more insidiously and thus tend to be widely disseminated at diagnosis, often incurable

Burkitt lymphoma
MALT lymphoma
Diffuse large B cell lymphoma (most common)

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11
Q

What are the symptoms of Non-Hodgkin’s lymphoma?

A

extra Nodal disease: 75% have superficial lymphadenopathy at presentation, can affect the oropharynx, skin, CNS, gut or lung

B symptoms: weight loss indicates disseminated disease

Bone marrow failure

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12
Q

What investigations can be done for Non-Hodgkin’s lymphoma?

A

FBC, film, ESR, LFTs, U&Es, LDH, Ca2+

lymph node dissection biopsy if possible
Image guided biopsy, laparotomy, mediastinoscopy

Staging CT

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13
Q

What is the management of Non-Hodgkin’s lymphoma?

A

chemotherapy, radiotherapy or chemo-radiotherapy

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14
Q

What is the prognosis for non-hodgkin’s lymphoma?

A

Poor prognostic signs are age >60 at presentation, disseminated disease and raised LDH

Survival = very variable

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15
Q

How is staging of lymphomas done?

A

Ann Arbor
Stage 1: Confined to one region of lymph nodes.
Stage 2: In more than one region but on the same side of the diaphragm (either above or below).
Stage 3: Affects lymph nodes both above and below the diaphragm.
Stage 4: Widespread involvement including non-lymphatic organs such as the lungs or liver.

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16
Q

What are myeloproliferative disorders?

A

These conditions occur due to uncontrolled proliferation of a single type of stem cell. They are considered a type of bone marrow cancer.

The three myeloproliferative disorders to remember are:

Primary myelofibrosis - haematopoeic stem cell
Polycythaemia vera - erythroid cells
Essential thrombocythaemia - megakaryocyte (platelet precursor)

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17
Q

What is essential thrombocythaemia

A

Clonal proliferation of megakaryocytes leading to persistently raised platelets which is often asymptomatic

The platelets have abnormal function, thus the most common presentation is with microvascular obstruction

Other symptoms may be related to bleeding or aterial / venous thrombosis

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18
Q

What is PCV?

A

Polycythemia vera
Malignant proliferation of a clone derived from one pluripotent marrow cell - Excess production of RBCs, WBCs and platelets lead to serum hyperviscosity and thrombotic complications

Diagnosed by increased red cell mass, or investigation for a JAK2 mutation

Often asymptomatic, or presents in patients >60 with arterial or venous thrombosis

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19
Q

What are the other rarer presentations of PCV?

A

Vague hyperviscosity symptoms: headache, dizziness, tinnitus, facial plethora, erythromelalgia, splenomegaly
gout - due to increased cell turnover

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20
Q

What’s the management of polycythaemia vera?

A

Venesection can be used to keep the haemoglobin in the normal range. This is the first line treatment.

Aspirin can be used to reduce the risk of developing blood clots (thrombus formation).

Chemotherapy can be used to control the disease

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21
Q

What are the key differentials to rule out in primary PCV?

A

Hypoxia and renal disease

In these secondary polycythaemia syndromes, only the red cell count is raised

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22
Q

What is primary myelofibrosis?

A

proliferation of the cell line leads to fibrosis of the bone marrow (replaced with scar tissue)

This is in response to cytokines that are released from the proliferating cells: fibroblast growth factor.

This fibrosis affects the production of blood cells and can lead to anaemia and low white blood cells (leukopenia).

Due to fibrosis, (haematopoiesis) starts to happen in other areas such as the liver and spleen.

This is known as extramedullary haematopoiesis and can lead to hepatomegaly and splenomegaly (most common presentation)

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23
Q

What are the symptoms of primary myelofibrosis?

A

B symptoms

Anaemia (except in polycythaemia)
Splenomegaly (abdominal pain)
Portal hypertension (ascites, varices and abdominal pain)
Low platelets (bleeding and petechiae)
Thrombosis is common in polycythaemia and thrombocythaemia
Raised red blood cells (thrombosis and red face)
Low white blood cells (infections)

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24
Q

How might disease course of Essential Thrombocythaemia and PCV change?

A

Essential Thrombocythaemia

and PCV both may progress to myelofibrosis or AML, but risk of this is relatively rare

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25
Q

What is aplastic anaemia?

A

Rare stem cell disorder leading to pancytopenia and hypo plastic marrow

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26
Q

What is the cause of aplastic anaemia?

A

Most commonly autoimmune (triggered by drugs, viruses or irradiation but can be inherited (Fanconi anaemia)

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27
Q

How Is diagnosis of aplastic anaemia done?

A

Bone marrow biopsy

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28
Q

How is aplastic anaemia managed?

A

Blood product transfusion and immunosuppression in autoimmune conditions

In younger patients, allogenic bone marrow transplant may be curative

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29
Q

What prevents platelet adhesion in homeostatic conditions?

primary haemostasis

A

PGI2 and NO prevent platelet adhesion

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30
Q

Describe the process of primary haemostasis

A
  1. If there is endothelial damage, there is exposed collagen and von Willebrand factor which leads to platelet adhesion
  2. Platelet adhesion leads to degranulation of the platelets, releasing ADP
  3. Platelets also synthesise the prostaglandin thromboxane A2 (TXA2) which causes both vasoconstriction and further aggregation
  4. Receptors on the platelet surface then activate the coagulation cascade, which generates fibrin to form a fibrin/platelet thrombus
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31
Q

What is the action of aspirin?

A

Low dose (75mg) aspire inhibits cyclo-oxygenase, preventing conversion of arachadonic acid to endoperoxides such as Pg12 or Txa2

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32
Q

How does aspirin affect Txa2 but not Pgi2?

A

Nuclei of endothelial cells are quickly able too secrete mRNA for PGI2 production

the anucleate platelets cannot form TXA2, so levels decrease until new platelets are formed in approximately 7 days

Low doses of aspirin every 24-48 hours thus decrease synthesis of TXA2 without massively affecting PGI2 production

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33
Q

What is the function of clopidogrel?

A

Can be used as an alternative to aspirin, or an adjunct

Works as an ADP receptor antagonist, thus preventing glycoprotein expression and platelet aggregation

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34
Q

What is the cause of immune thrombocytopenia?

A

Reduced platelet production in the bone marrow, or excessive peripheral destruction of platelets

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35
Q

What conditions cause reduced production of platelets?

A

Aplastic anaemia
Marrow infiltration
Marrow suppression

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36
Q

What conditions cause excess destruction of platelets?

A 
ITP 
other immune causes: SLE, CLL, viruses
TTP
HUS
Sequestration: hypersplenism
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37
Q

What is the presentation of immune thrombocytopenia?

A

Bruising / purpura of the skin

Epistaxis / haemorrhage

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38
Q

When does ITP arise in children / adults?

A

In children, usually acute and self-limiting, following a virus or immunisation

In adults. usually less acute, classically in women with other autoimmune disorders

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39
Q

What investigations are done for ITP?

A

FBC - thrombocytopenia
Bone marrow examination: not in children normally. but normal/increased megakaryocytes numbers found - otherwise normal

Platelet autoantibodies: positive in 70% patients but does not confirm diagnosis

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40
Q

What is the management for ITP?

A

Children are not usually treated
If clinically necessary, they may be treated with prednisolone or IVIG.
Chronic thrombocytopenia = rare and requires specialist management

In adults, corticosteroids = first line
IVIG if rapid rise in platelets is required
Splenectomy may be second line

Platelet transfusions are reserved for extreme haemorrhage

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41
Q

What lab tests are used to test the clotting system?

A

PT
INR
APTT
TT

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42
Q

What does PT test?

A

The extrinsic pathway - by addition of a tissue factor substitute to the patient’s plasma

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43
Q

What conditions cause prolonged PT?

A

Liver disease, or if the patient is on warfarin

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44
Q

What does INR test?

A

Ratio of a patient’s PT to a normal control whilst using an international reference preparation (standardises laboratories worldwide)

0.9-1.1 = normal range
Used for warfarin testing

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45
Q

What does APTT entail?

A

Add-on of a surface activator to the plasma

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46
Q

What does APTT test?

A

Intrinsic pathway

Monitoring for unfractionated heparin

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47
Q

What is thrombin time?

A

Addition of thrombin to the patient’s plasma

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48
Q

What causes prolonged thrombin time

A

Prolonged with fibrinogen deficiency or abnormal function or inhibitors such as heparin

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49
Q

Where are clotting factors synthesised?

A

the liver

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50
Q

What is factor 1?

A

Fibrinogen

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51
Q

What is factor II

A

Prothrombin (so thrombin is IIa)

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52
Q

What is the end result of the intrinsic / extrinsic pathways?

A

Both lead to a common pathway that leads to production of fibrin and thus a thrombus can be formed

53
Q

Where is Vitamin K found?

A

Leafy green vegetables, dairy products and soya beans

54
Q

Which clotting factors is vitamin K a necessary co-factor for?

A

2, 7, 9, 10

55
Q

What is the result of vitamin K deficiency?

A

Clotting factor deficiencies –> increased PT and haemorrhage

56
Q

What can vitamin K deficiencies arise from ?

A

Malabsorptive conditions (fat soluble, cholestatic jaundice or antibiotics

57
Q

DRAW OUT THE CLOTTING CASCADE

A

wot r u waiting for, go draw

58
Q

What are the inhibitors of coagulation?

A

Anti-thrombin III: serine protease inhibitor, potentiated by heparin

Activated Protein C (APC): also generated by vitamin K, and activated by thrombin

59
Q

How does APC act?

A

Acts with the co-factor protein S to induce fibrinolysis

Destroys factor V and VIII, reducing further thrombin generation and also inhibits stabilisation of the fibrin clot

60
Q

How does fibrinolysis occur?

A

Plasminogen is converted to plasmin by tissue plasminogen activator (t-PA_

Many mediators including thrombin and APC stimulate the release of t-PA

Plasmin is a serine protease that breaks down fibrinogen and fibrin into fibrin degradation products e.g. D-dimer

61
Q

What does D-dimer presence in the plasma indicate?

A

D-dimers = fibrinolysis degredation products: significant thrombus breakdown in the body

62
Q

What is Haemophilia A?

A

Factor VIII deficiency
Xlinked recessive
BUT high rate of new mutations

63
Q

What is Haemophilia B?

A

Factor IX deficiency

X linked recessive

64
Q

What are the clinical features of haemophilia?

A

Major bleeds following minor trauma
Recurrent haemoarthroses leading to crippling arthropathies
Compartment syndrome / nerve palsies can develop due to pressure effects

65
Q

How Is diagnoses of haemophilia done?

A

Raised APTT

Low factor VIII / IX on assays

66
Q

What is the management of haemophilia?

A

Avoid NSAIDs and IM injections
Minor bleeding - compression and elevation, desmopressin raises factor VIII levels and may be sufficient

Major bleeding (e.g. haemoarthrosis): infusion of recombinant factor VIII / IX to raise factor levels to 50% of normal

Life threatening bleeds - raise to 100% of normal

67
Q

What are the other causes of factor deficiency?

A

vWD, liver disease, DIC, vitamin K deficiency or anticoagulant drugs

Most common inherited disorder = VWD

68
Q

What is von willebrand’s disease?

A

Absence of vWF or presence of abnormally functioning vWF due to autosomal dominant condition

Gives symptoms of platelet type disorder: epistaxis, menorrhagia, with haemoarthrosis rare in vWF

69
Q

What is the mode of inheritance of von willebrand’s disease?

A

Autosomal recessive: cormpleteabsence of detectable vWF (20%)

Autosomal dominant: less severe depletion of vWF (80%)

70
Q

Which tests are changed in Vwd?

A

APTT is increased but INR and platelets are within normal limits

71
Q

What is the management of vwd?

A

Desmopressin can be used to stimulates the release of VWF
VWF can be infused
Factor VIII is often infused along with plasma-derived VWF

Women with VWD that suffer from heavy periods can be managed by a combination of:

Tranexamic acid
Mefanamic acid
Norethisterone
Combined oral contraceptive pill
Mirena coil
72
Q

What history points should be covered when investigating a bleeding disorder?

A

site of bleed - muscle/joint bleeds: coagulation issues
purpura, epistaxis, menorrhagia, GI haemorrhage: platelet issue / vWd
recurrent bleeds at one site: ?local endothelial abnormality

Duration of hx / fh: congenital/acquired

seriousness

surgical hx - bleeding that starts immediately after is suggestive of platelet issue

PMH: renal/liver failure

Drug hx: Anticoagulation, steroids, NSAIDs

73
Q

How should patient with ?bleeding disorder be examined?

A

Skin: bruises, purpura, telangiectasia
Joints: any evidence of haemoarthrosis
Abdomen: splenomegaly, evidence of hepatic dysfunction

74
Q

What is warfarin?

A

Vitamin K antagonist
Inhibits the enzyme responsible for regenerating ‘active’ vitamin K, thus producing an anti-coagulativestate analogous to vitamin K deficiency

75
Q

How long does warfarin take to have an effect?

A

up to 5 days
has an initial prothrombotic effect so should always be combined with a heparin agent until INR is within the Therapeutic range

76
Q

In which patients is warfarin contra-indicated in?

A

Peptic ulcer disease
bleeding disorders
severe hypertension
pregnancy

77
Q

What are the target INRs for prophylactic use of warfarin?

A

Single DVT/PE: 2-3
AF: 2-3
Recurrent DVT/PE: 3-4
Prosthetic metal heart valves: 3-4

78
Q

How is warfarin initiated?

A

Loading dose given with INR measured on alternate dats and dose titrated according to INR

79
Q

Name three NOACS commonly used?

A

Dabigatran, Apixaban and rivaroxaban

80
Q

How do NOACs work?

A

Apixaban and rivaroxaban = competitive factor Xa antagonists
Dabigatran = reversible competitive antagonist of thrombin (IIa)

81
Q

What are the advantages of NOACs?

A

Rapid onset of coagulation effects
more predictable pharmacokinetics
lower potential for clinically important interactions with food, lifestyle and other drugs

No need for routine coagulaitonmonitoring

82
Q

What are the disadvantages of NOACs?

A

?Increased risk of GI bleed

NO antidotes

83
Q

How should over anticoagulation be managed in a patient taking warfarin?

A

INR measurement:
If 4.6-6 - reduce dose of warfarin / omit dose, restart when INR <5

If 6-8: stop warfarin, restart when INR<5

If >8: with no bleed / minor bleed, stop warfarin and give vitamin K

Also give 0.5-2mg oral vitamin K if risk factors for bleeding

If major bleed, stop warfarin, give 5-10mg vitamin K IV plus octaplex (Prothrombin complex concentrate) or FFP according to local guidelines

84
Q

Give an example of a LMWH?

A

Exoxaparin (SC)

85
Q

How do LMWH work?

A 
Inactivate Xa (but not thrombin)
no lab monitoring required, but if requited, then anti Xa levels used

Can accumulate in renal failure - lower dose prophylactically

86
Q

What is the purpose of UFH?

A

If high risk of bleeding - anticoagulation can be terminated rapidly

In CKD

87
Q

What is the mode of action of UFH?

A

Potentiates anti-thrombin III

Increases its ability to inhibit thrombin, factor Xa and IXa

88
Q

How is UFH monitored?

A

APTT

should be checked at 6 hours, aiming for APTT of 1.5-2.5

89
Q

What are the side effects of UFH?

A

Common to both LMWH and UFH but less common in LMWH

Bleeding e.g. GI, operative site, intracranial
heparin induced thrombocytopenia (HIT)
Osteoporosis with long term use
Hyperkalaemia

90
Q

What are the contraindications for heparin?

A

bleeding disorders, platelets <60x10^9, previous HIT, peptic ulcer

91
Q

How should overanticoagulaiton with heparins be treated?

A

Stop infusion

Give protamine sulphate

92
Q

How is thrombolysis achieved?

A

Streptokinase: purified fraction of filtrate obtained from haemolytic streptococci

Alteplase - recombinant tissue type plasminogen activator, leading to increased plasminogen activation and fibronlysis

93
Q

What are the contra-indications to thrombolysis?

A 
Active bleeding: any sign of cerebral haemorrhage in stroke
suspected aortic dissection in ACS 
Severe hypertension (>200/120)
Recent head trauma
recent surgery 
Pregnancy or recent delivery 
severe liver disease / oesophageal varices 
Prolonged /traumatic CPR
94
Q

What is thrombophilia?

A

Inherited / acquired coagulopathy, predisposing to thrombosis, usually venous

95
Q

What are the causes of thrombophilia?

A

Inherited: APC resistance, factor V Leiden mutation
Antithrombin III deficiency
Prothrombin gene mutation

Acquired: APL syndrome

96
Q

What are the indications for screening for thrombophilia?

A

Arterial thrombosis <50
Venous thrombosis <40 with no risk factors
Familial VTE
Recurrent unexplained VTE
Unusual site of thrombosis e.g. mesenteric or portal vein thrombosis
Recurrent fetal loss

97
Q

What investigations can be done for thrombophilia?

A

FBC
clotting
fibrinogen concentration +/- APC resistance test
lupus anticoagulant / anti-cardiolipin antibodies
Antithrombin and protein C/S assays for deficiency
Factor V Leiden mutation PCR if APC resistance test = positive

PCR for prothrombin gene mutation

98
Q

What is DIC?

A

Systemic activation of of the coagulation pathways, leading to extensive intravascular coagulation and fibrin clot development

There is thrombotic occlusion of the arterial microvasculature

Depletion of clotting factors + consumption of platelets = ++HAEMORRAHAGE

Organ failure ensues

99
Q

What are the causes of DIC?

A 
Infection 
Trauma
Malignancy 
Obstetric complications (amniotic fluid emboli, pre-eclampsia) 
Severe liver failure
Tissue destruction (pancreatitis/burns)
Toxic / immunogenic stimuli
100
Q

What are the clinical features of DIC?

A

Bruising
Excessive bleeding from any site: e.g. venipuncture wounds
renal failure

101
Q

What are the investigations for DIC

A

Low platelets, low fibrinogen
Raised PT and APTT
Raised D dimer
Blood film: broken RBCs (schistocytes)

102
Q

What is the treatment for DIC?

A

Treat the cause
Aggressive resuscitation, replacing platelets, coagulation factors (FFP) and fibrinogen (cryoprecipitate)

Protein C: reduces mortality in multi-organ failure / severe sepsis

103
Q

How are blood groups determined?

A

By antigens on the surface of red cells, with the ABO / rhesus groups the 2 major blood groups

104
Q

Describe the ABO system

A

Red cells either A, B, AB or O
named according to surface antigens

Carry IgM antibodies against any antigen that they do not carry.
O blood group contains anti-A and anti-B antibodies

AB = both A and B antigens
AB group blood will not carry any anti-A or anti-B antibodies

105
Q

Describe the rhesus system?

A

RBC either show the rhesus D antigen or not (+ve or -ve)
If a rhesus negative individual Is exposed to rhesus positive blood products, they can develop IgG antibodies directed against the rhesus D antigen

If exposed AGAIN, there will be haemolysis

106
Q

What are the principles of cross matching blood?

A

Blood grouping: ABO and RhD groups of the patient are determined
Antibody screening: patient serum/plasma screened for atypical antibodies that would cause significant haemolysis of transfused cells

Tested using at least 2 group O donors expressing a wide range of antigens

107
Q

What is the indirect agglutination test?

A

Donor RBCs added to patient’s serum, then Coomb’s reagent is added, agglutination indicates that the patients serum has antibodies for the donor RBCs
This test is always performed pre-transfusion

108
Q

What is the direct agglutination test?

A

Patient’s ‘washed’ RBCs are added to Coomb’s reagent and if they agglutinate, that indicates that there is an autoimmune haemolytic process occurring with the RBCs coated with immunoglobulins

‘Coomb’s test’

109
Q

Which blood products need to be cross matched?

A

ALL except platelets

110
Q

What is a group and save?

A

Antibody screen performed to confirm negative so appropriate blood can be made available
undergoing elective surgery where transfusion not expected

111
Q

What is the massive transfusion protocol?

A

2 Units of O negative blood to be made available immediately

Blood of the same ABO / rhesus group will be available in 10-15 minutes

fully cross-matched blood will be available within 45 minutes

112
Q

When are packed red cells given?

A

Given with crystalloids/colloids in acute blood loss

113
Q

When are platelet concentrates given?

A

TO treat bleeding in severe thrombocytopenia or prophylactically in patients with bone marrow failure

114
Q

When is FFP given?

A

Contains all the coagulation factors present in fresh plasma, so is used mainly for replacement of coagulation factors in acquired deficiencies e.g. liver disease, TTP, warfarin overdose where vitamin K would be too slow

115
Q

What is cryoprecipitate and when is it given?

A

FFP without supernatant,

Highly concentrated fibrinogen
useful in conditions such as DIC where the fibrinogen is very low

116
Q

What are factor VII and IX concentrates used for?

A

Specific factor concentrates, used in haemophilia / vWD

117
Q

What is albumin used for?

A

In severe hypoalbuminaemia where the patient is overloaded and resistant to diuretics

118
Q

What is IVIG used for?

A

Either normal / specific to prevent infections in hypogammaglobulinaemia or other conditions such as ITP

119
Q

What kind of transfusion reactions can patients get?

A

Acute haemolytic reaction

Allergy/anaphylaxis

Bacterial contamination

Transfusion-related acute lung injury

Non-haemolytic febrile transfusion reaction

Fluid overload

120
Q

What are the symptoms of acute haemolytic reaction?

A

agitation, raised temperature, low BP, abdominal/chest pain, or signs of DIC

121
Q

How should an acute haemolytic reaction be monitored?

A

STOP transfusion

A-E resuscitation, give 0.9% saline

122
Q

How should allergic transfusion reaction be monitored?

A

If simple allergy (urticaria/itch), slow/stop and give chloramphenamine

If anaphylaxis, stop and treat as such

123
Q

What are the symptoms of ?bacterial contamination reaction

A

sepsis and rigors

124
Q

How should bacterial contamination reaction be monitored?

A

Stop transfusion

Start sepsis protocol, sending the blood unit to the lab as well as cultures from the patient

125
Q

What is TRALI?

A

Transfusion related acute lung injury

ARDS due to antibodies in the donor plasma, suggested by dyspnoea and CXR white out

126
Q

What are the symptoms of non-haemolytic febrile transfusion reaction?

A

Shivering and fever usually 0.5-1 hour after starting transfusion

Slow the transfusion, administer antipyretic and monitor closely

127
Q

How should fluid overload be managed?

A

Slow or stop transfusion
Give oxygen and a diuretic
If the patient is not hypovolaemic, it is often standard practice to co-prescribe furosemide to prevent overload

Consider exchange transfusion

128
Q

Which blood bottle is used for cross match?

A

PINK

129
Q

What are the important principles of requesting blood products?

A

Ensure a blood sample has been taken
Consent the patient for transfusion

Benefits/indications
Risks of infection: HIV 3 million, HBV 2/100,000
Non-infectious risks: transfusion reactions
Right to refuse e.g. Jehovah’s witnesses

Specific form

CP3 Medicine (19 decks)

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