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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
What is aplastic anaemia?
Rare stem cell disorder leading to pancytopenia and hypo plastic marrow
26
What is the cause of aplastic anaemia?
Most commonly autoimmune (triggered by drugs, viruses or irradiation but can be inherited (Fanconi anaemia)
27
How Is diagnosis of aplastic anaemia done?
Bone marrow biopsy
28
How is aplastic anaemia managed?
Blood product transfusion and immunosuppression in autoimmune conditions In younger patients, allogenic bone marrow transplant may be curative
29
What prevents platelet adhesion in homeostatic conditions? | primary haemostasis
PGI2 and NO prevent platelet adhesion
30
Describe the process of primary haemostasis
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
31
What is the action of aspirin?
Low dose (75mg) aspire inhibits cyclo-oxygenase, preventing conversion of arachadonic acid to endoperoxides such as Pg12 or Txa2
32
How does aspirin affect Txa2 but not Pgi2?
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
33
What is the function of clopidogrel?
Can be used as an alternative to aspirin, or an adjunct Works as an ADP receptor antagonist, thus preventing glycoprotein expression and platelet aggregation
34
What is the cause of immune thrombocytopenia?
Reduced platelet production in the bone marrow, or excessive peripheral destruction of platelets
35
What conditions cause reduced production of platelets?
Aplastic anaemia Marrow infiltration Marrow suppression
36
What conditions cause excess destruction of platelets?
``` ITP other immune causes: SLE, CLL, viruses TTP HUS Sequestration: hypersplenism ```
37
What is the presentation of immune thrombocytopenia?
Bruising / purpura of the skin | Epistaxis / haemorrhage
38
When does ITP arise in children / adults?
In children, usually acute and self-limiting, following a virus or immunisation In adults. usually less acute, classically in women with other autoimmune disorders
39
What investigations are done for ITP?
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
40
What is the management for ITP?
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
41
What lab tests are used to test the clotting system?
PT INR APTT TT
42
What does PT test?
The extrinsic pathway - by addition of a tissue factor substitute to the patient's plasma
43
What conditions cause prolonged PT?
Liver disease, or if the patient is on warfarin
44
What does INR test?
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
45
What does APTT entail?
Add-on of a surface activator to the plasma
46
What does APTT test?
Intrinsic pathway | Monitoring for unfractionated heparin
47
What is thrombin time?
Addition of thrombin to the patient's plasma
48
What causes prolonged thrombin time
Prolonged with fibrinogen deficiency or abnormal function or inhibitors such as heparin
49
Where are clotting factors synthesised?
the liver
50
What is factor 1?
Fibrinogen
51
What is factor II
Prothrombin (so thrombin is IIa)
52
What is the end result of the intrinsic / extrinsic pathways?
Both lead to a common pathway that leads to production of fibrin and thus a thrombus can be formed
53
Where is Vitamin K found?
Leafy green vegetables, dairy products and soya beans
54
Which clotting factors is vitamin K a necessary co-factor for?
2, 7, 9, 10
55
What is the result of vitamin K deficiency?
Clotting factor deficiencies --> increased PT and haemorrhage
56
What can vitamin K deficiencies arise from ?
Malabsorptive conditions (fat soluble, cholestatic jaundice or antibiotics
57
DRAW OUT THE CLOTTING CASCADE
wot r u waiting for, go draw
58
What are the inhibitors of coagulation?
Anti-thrombin III: serine protease inhibitor, potentiated by heparin Activated Protein C (APC): also generated by vitamin K, and activated by thrombin
59
How does APC act?
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
How does fibrinolysis occur?
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
What does D-dimer presence in the plasma indicate?
D-dimers = fibrinolysis degredation products: significant thrombus breakdown in the body
62
What is Haemophilia A?
Factor VIII deficiency Xlinked recessive BUT high rate of new mutations
63
What is Haemophilia B?
Factor IX deficiency | X linked recessive
64
What are the clinical features of haemophilia?
Major bleeds following minor trauma Recurrent haemoarthroses leading to crippling arthropathies Compartment syndrome / nerve palsies can develop due to pressure effects
65
How Is diagnoses of haemophilia done?
Raised APTT Low factor VIII / IX on assays
66
What is the management of haemophilia?
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
What are the other causes of factor deficiency?
vWD, liver disease, DIC, vitamin K deficiency or anticoagulant drugs Most common inherited disorder = VWD
68
What is von willebrand's disease?
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
What is the mode of inheritance of von willebrand's disease?
Autosomal recessive: cormpleteabsence of detectable vWF (20%) Autosomal dominant: less severe depletion of vWF (80%)
70
Which tests are changed in Vwd?
APTT is increased but INR and platelets are within normal limits
71
What is the management of vwd?
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
What history points should be covered when investigating a bleeding disorder?
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
How should patient with ?bleeding disorder be examined?
Skin: bruises, purpura, telangiectasia Joints: any evidence of haemoarthrosis Abdomen: splenomegaly, evidence of hepatic dysfunction
74
What is warfarin?
Vitamin K antagonist Inhibits the enzyme responsible for regenerating 'active' vitamin K, thus producing an anti-coagulativestate analogous to vitamin K deficiency
75
How long does warfarin take to have an effect?
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
In which patients is warfarin contra-indicated in?
Peptic ulcer disease bleeding disorders severe hypertension pregnancy
77
What are the target INRs for prophylactic use of warfarin?
Single DVT/PE: 2-3 AF: 2-3 Recurrent DVT/PE: 3-4 Prosthetic metal heart valves: 3-4
78
How is warfarin initiated?
Loading dose given with INR measured on alternate dats and dose titrated according to INR
79
Name three NOACS commonly used?
Dabigatran, Apixaban and rivaroxaban
80
How do NOACs work?
Apixaban and rivaroxaban = competitive factor Xa antagonists Dabigatran = reversible competitive antagonist of thrombin (IIa)
81
What are the advantages of NOACs?
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
What are the disadvantages of NOACs?
?Increased risk of GI bleed NO antidotes
83
How should over anticoagulation be managed in a patient taking warfarin?
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
Give an example of a LMWH?
Exoxaparin (SC)
85
How do LMWH work?
``` 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
What is the purpose of UFH?
If high risk of bleeding - anticoagulation can be terminated rapidly In CKD
87
What is the mode of action of UFH?
Potentiates anti-thrombin III | Increases its ability to inhibit thrombin, factor Xa and IXa
88
How is UFH monitored?
APTT | should be checked at 6 hours, aiming for APTT of 1.5-2.5
89
What are the side effects of UFH?
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
What are the contraindications for heparin?
bleeding disorders, platelets <60x10^9, previous HIT, peptic ulcer
91
How should overanticoagulaiton with heparins be treated?
Stop infusion | Give protamine sulphate
92
How is thrombolysis achieved?
Streptokinase: purified fraction of filtrate obtained from haemolytic streptococci Alteplase - recombinant tissue type plasminogen activator, leading to increased plasminogen activation and fibronlysis
93
What are the contra-indications to thrombolysis?
``` 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
What is thrombophilia?
Inherited / acquired coagulopathy, predisposing to thrombosis, usually venous
95
What are the causes of thrombophilia?
Inherited: APC resistance, factor V Leiden mutation Antithrombin III deficiency Prothrombin gene mutation Acquired: APL syndrome
96
What are the indications for screening for thrombophilia?
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
What investigations can be done for thrombophilia?
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
What is DIC?
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
What are the causes of DIC?
``` Infection Trauma Malignancy Obstetric complications (amniotic fluid emboli, pre-eclampsia) Severe liver failure Tissue destruction (pancreatitis/burns) Toxic / immunogenic stimuli ```
100
What are the clinical features of DIC?
Bruising Excessive bleeding from any site: e.g. venipuncture wounds renal failure
101
What are the investigations for DIC
Low platelets, low fibrinogen Raised PT and APTT Raised D dimer Blood film: broken RBCs (schistocytes)
102
What is the treatment for DIC?
Treat the cause Aggressive resuscitation, replacing platelets, coagulation factors (FFP) and fibrinogen (cryoprecipitate) Protein C: reduces mortality in multi-organ failure / severe sepsis
103
How are blood groups determined?
By antigens on the surface of red cells, with the ABO / rhesus groups the 2 major blood groups
104
Describe the ABO system
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
Describe the rhesus system?
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
What are the principles of cross matching blood?
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
What is the indirect agglutination test?
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
What is the direct agglutination test?
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
Which blood products need to be cross matched?
ALL except platelets
110
What is a group and save?
Antibody screen performed to confirm negative so appropriate blood can be made available undergoing elective surgery where transfusion not expected
111
What is the massive transfusion protocol?
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
When are packed red cells given?
Given with crystalloids/colloids in acute blood loss
113
When are platelet concentrates given?
TO treat bleeding in severe thrombocytopenia or prophylactically in patients with bone marrow failure
114
When is FFP given?
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
What is cryoprecipitate and when is it given?
FFP without supernatant, Highly concentrated fibrinogen useful in conditions such as DIC where the fibrinogen is very low
116
What are factor VII and IX concentrates used for?
Specific factor concentrates, used in haemophilia / vWD
117
What is albumin used for?
In severe hypoalbuminaemia where the patient is overloaded and resistant to diuretics
118
What is IVIG used for?
Either normal / specific to prevent infections in hypogammaglobulinaemia or other conditions such as ITP
119
What kind of transfusion reactions can patients get?
Acute haemolytic reaction Allergy/anaphylaxis Bacterial contamination Transfusion-related acute lung injury Non-haemolytic febrile transfusion reaction Fluid overload
120
What are the symptoms of acute haemolytic reaction?
agitation, raised temperature, low BP, abdominal/chest pain, or signs of DIC
121
How should an acute haemolytic reaction be monitored?
STOP transfusion | A-E resuscitation, give 0.9% saline
122
How should allergic transfusion reaction be monitored?
If simple allergy (urticaria/itch), slow/stop and give chloramphenamine If anaphylaxis, stop and treat as such
123
What are the symptoms of ?bacterial contamination reaction
sepsis and rigors
124
How should bacterial contamination reaction be monitored?
Stop transfusion | Start sepsis protocol, sending the blood unit to the lab as well as cultures from the patient
125
What is TRALI?
Transfusion related acute lung injury | ARDS due to antibodies in the donor plasma, suggested by dyspnoea and CXR white out
126
What are the symptoms of non-haemolytic febrile transfusion reaction?
Shivering and fever usually 0.5-1 hour after starting transfusion Slow the transfusion, administer antipyretic and monitor closely
127
How should fluid overload be managed?
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
Which blood bottle is used for cross match?
PINK
129
What are the important principles of requesting blood products?
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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