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Conditions + definitions > Haem 2 > Flashcards

Haem 2 Flashcards

1
Q

What are the elements of haemostasis?

A

Primary haemostasis
Blood coagulation
Fibrynolysis

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2
Q

What are the features of primary haemostasis?

A

Vasoconstriction
Platelet adhesion
Platelet aggregation

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3
Q

What constitutes coagulation?

A

Insoluble fibrin formation

Fibrin cross-linking

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4
Q

What is Fibrynolysis?

A

Turning plasminogen into plasmin

Which converts fibrin into fibrinogen/fibrin degrading products

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5
Q

What are the types of thrombosis?

A

Arterial
Venous
Microvascular

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6
Q

What is an arterial thrombus?

A

White clot - made of platelets and fibrin
Results in ischeamia and infarction
Secondary to atherosclerosis

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7
Q

What are the risk factors for arterial thrombosis?

A 
Age
Smoking
Sedentary lifestyle
Hypertension
Diabetes mellitus
Obesity
Hypercholesterolaemia
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8
Q

How do you manage arterial thrombosis?

A 
Primary prevention
>(lifestyle/risk factor modifications)
Acute presentation
>Thrombolysis
>Antiplatelet/anticoagulant drugs
Secondary prevention
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9
Q

What is a venous thrombosis?

A

‘Red thrombus’~fibrin and red cells
Results in back pressure
Principally due to stasis and hypercoagulability

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10
Q

What are the risk factors of venous thrombosis?

A 
Stasis/hypercoaguability
Increasing age
Pregnancy/HRT
Surgery
Obesity etc
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11
Q

What systems are used to predict venous thrombosis?

A

Wells score

Geneva score

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12
Q

What are the types of anticoagulants?

A

LMWH (heparin)
Coumarins (warfarin)
NOACs

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13
Q

What is heritable thrombophilia?

A

Inherited predisposition to venous thrombosis

Commonly caused by defect in prothrombin or Factor V leiden

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14
Q

What is microvascular thrombus?

A

Platelets and/or fibrin
Results in diffuse ischaemia
Principally in Disseminated Intravascular Coagulation

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15
Q

What is DIC (Disseminated intravascular coagulation)?

A 
Diffuse systemic coagulation activation
Occurs in:
>Septicaemia
>Malignancy
>eclampsia
Causes tissue ischaemia
>Gangrene
>organ failure
Consumption of platelets and clotting factors leading to bleeding
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16
Q

What are the important parts of a bleeding history?

A

Do they have a bleeding disorder?
How severe is the bleeding?
How appropriate is the bleeding?
Pattern of bleeding

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17
Q

How do you discern the pattern of bleeding?

A 
Platelet type 
>Mucosal
>Epistaxis
>Purpura
>Menorrhagia
>GI

Coagulation Factor >Articular
>Muscle Haematoma
>CNS

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18
Q

What are the features of haemophilia?

A 
X-linked so only males
Haemarthrosis
Muscle haematoma
CNS bleeding
Retroperitoneal bleeding
Post surgical bleeding
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19
Q

What are the complications of haemophilia?

A

Synovitis
Chronic Haemophilic Arthropathy
Neurovascular compression (compartment syndromes)
Other sequelae of bleeding (Stroke)

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20
Q

How do you diagnose haemophilia?

A 
Clinical
Prolonged APTT
Normal PT
Reduced FVIII or FIX
Genetic analysis
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21
Q

How do you treat haemophilia?

A 
Coagulation factor replacement  FVIII/IX
Now almost entirely recombinant products
DDAVP
Tranexamic Acid
Emphasis on prophylaxis in severe haemophilia
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22
Q

What is von Willebrand disease?

A 
Common (1 in 200)
Variable severity
Autosomal
Platelet Type bleeding (mucosal)
Quantitative and qualitative abnormalities of vWF
3 types, in order of severity
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23
Q

How do you treat von willebrand disease?

A

vWF concentrate or DDAVP
Tranexamic Acid
Topical applications
OCP

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24
Q

What bleeding disorders can you acquire?

A 
Thrombocytopenia
Liver failure
Renal failure
DIC
Drugs related
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25
Q

What causes thrombocytopenia?

A

Decreased production
>Marrow failure
>Aplasia
>Infiltration

Increased consumption
>Immune ITP
>Non immune DIC
>Hypersplenism

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26
Q

What is the presentation of thrombocytopenia?

A

Petechia
Ecchymosis
Mucosal Bleeding
Rare CNS bleeding

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27
Q

What bleeding abnormalities does liver failure lead to?

A

Factor I, II, V, VII, VIII, IX, X, XI all affected
Prolonged PT, APTT Reduced Fibrinogen

Cholestasis -
>Vit K dept factor deficiency
»(Factor II, VII, IX, X.)

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28
Q

How do you correct bleeding abnormalities in liver failure?

A

Replacement FFP

Vitamin K

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29
Q

What cells make up myeloid malignancies?

A

Red
Platelets
Granulocytes
Monocytes

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30
Q

What cells make up lymphoid malignancies?

A

B-cells

T-cells

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31
Q

What is the difference between leukaemia and lymphoma?

A

Leukaemia generally starts in the bone marrow

Lymphoma is cancerous lymph nodes/lymph tissue

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32
Q

What are the acute leukaemias?

A

Acute lymphoblastic leukaemia (ALL)

Acute Myeloid Leukaemia (AML)

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33
Q

What are the chronic leukaemias?

A

Chronic myeloid leukaemia (CML)

Chronic lymphocytic leukaemia (CLL)

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34
Q

What are the malignant lymphomas?

A 
Non-Hodgkin lymphoma (NHL)
Hodgkin lymphoma (HL)
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35
Q

What are the groups of haematological disease?

A 
Acute Leukaemias
Chronic Leukaemias
Multiple myeloma
Myelodysplastic syndromes (MDS)
The chronic myeloprolifertive diseases (biologically malignant)
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36
Q

What is the difference between acute and chronic leukaemia?

A

Acute - leukaemic cells don’t differentiate, whereas chronic they can
Acute is failure of bone marrow, chronic has proliferation without bone marrow failure
Acute rapidly fatal if untreated but good prognosis
Chronic is potentially curable, but often only few year survival

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37
Q

What are the complications of bone marrow failure?

A

Anaemia

  • Thrombocytopenic bleeding (Purpura and mucosal membrane bleeding)
  • Infection because of neutropenia (predominantly bacterial and fungal)
38
Q

How can lymphoma present?

A 
Nodal disease (lymphadenopathy)
Extranodal disease
Systemic symptoms
>Fever
>Drenching sweats
>Weight loss
>Prutitis
>Fatigue
39
Q

What causes Lymphadenopathy?

A

Localised and painful:

Bacterial infection in draining site

40
Q

What causes Localised and painless Lymphadenopathy?

A

Rare infections, catch scratch fever, TB
Metastatic carcinoma from draining site- hard
Lymphoma-rubbery
Reactive, no cause identified

41
Q

What causes Generalised and painful/tender Lymphadenopathy?

A

Viral infections, EBV, CMV, hepatitis, HIV

42
Q

What causes Generalised and painless Lymphadenopathy?

A 
Lymphoma
Leukaemia
Connective tissue diseases, sarcoidosis
Reactive, no cause identified
Drugs
43
Q

What are the clinical features of multiple myeloma?

A 
Bone pain
Hyperviscosity syndrome
Bleeding tendency
Amyloidosis
Anaemia
Renal failure
Recurrent infections
44
Q

What is an antibody?

A

An immunoglobulin produced by B cells
Made up of 2 heavy chains and 2 light chains
5 types of heavy chain

45
Q

What are the types of heavy chain?

A 
IgG
IgA
IgM
IgD
IgE
46
Q

What is the structure of an immunoglobulin?

A

Y shaped
> part of y is fab region which determines target binding
| part of Y is Fc region which is the subclass

47
Q

What is a paraprotein?

A

monoclonal immunoglobulin present in blood or urine

When present shows proliferation of B lymphocyte somwhere in body

48
Q

What immunoglobulin tests are available?

A

Total immunoglobulin (by subclass)
Electrophoresis
Immunofixation
Light chains

49
Q

What immunoglobulins are present in myeloma + lymphoma?

A 
Lymphoma 
>IgM 
Myeloma
>IgG
>IgA
50
Q

What is meyloma?

A

Neoplastic disorder of plasma cells, resulting (usually) in excessive production of a single type of immunoglobulin (paraprotein)
More common in black population

51
Q

What are the features of myeloma?

A 
bone disease
>lytic bone lesions
>pathological fractures
>cord compression
>hypercalcaemia
bone marrow failure esp. anaemia
infections
52
Q

What complications can arise from raised paraprotein?

A

Renal failure
Hyperviscosity
Hypogammaglobinaemia
Amyloidosis

53
Q

How do you diagnose myeloma?

A

Excess plasma cells in bone marow (greater than 10%)

54
Q

How do you treat meyloma?

A 
Chemo (proteasome inhibs)
Bisphosphonate therapy (zoledronic acid)
Radiotherapy
Steroids
Autologous stem cell transplant
55
Q

What is the function of the different immune cells?

A

Neutrophils – bacterial & fungal infection
Monocytes – fungal infection
Eosinophils – parasitic infections
T lymphocytes – fungal & viral infection, PJP
B lymphocytes – bacterial infection

56
Q

How do you reduce risk of sepsis in haematological malignancy?

A 
Prophylaxis
Growth factors e.g. G-CSF
Stem cell rescue/transplant
Protective environment e.g. laminar flow rooms
Intravenous immunoglobulin replacement
Vaccination - never live
57
Q

What is the prophylaxis of reducing sepsis risk?

A

Antibiotics (ciprofloxacin)
Anti-fungal (fluconazole or itraconazole)
Anti-viral (aciclovir)
PJP (co-trimoxazole)

58
Q

What are the common gram positive causative agents?

A

Staphylococci - MRSSA/MRSA, coagulase negative

Streptococci viridans

59
Q

What are the common gram negative causative agents?

A

Escherichia coli
Klebsiella spp : ESBL
Pseudomonas aeruginosa

60
Q

How does neutropenic sepsis present?

A 
Fever with no localising signs
	Single reading of >38.50C or 380C on two readings one hour apart
Rigors
Chest infection/ pneumonia
Skin sepsis - cellulitis
Urinary tract infection
Septic shock
61
Q

What is sepsis 6?

A

Give
Administer high flow oxygen
Give appropriate IV antibiotics within ONE hour
Start IV fluid resuscitation

Take
Assess/measure urine output
Take blood cultures, other cultures, consider source control
Measure serum lactate concentration

62
Q

How do you manage neutropenic sepsis?

A

Broad spectrum IV antibiotics
+ vancomycin if gram positive
No response after 72 hours add antifungal

63
Q

What are the myeloid malignancies?

A

Acute Myeloid Leukaemia (AML)
Chronic Myeloid Leukaemia (CML)
Myelodysplastic Syndromes (MDS)
Myeloproliferative Neoplasms (MPN)

64
Q

What are the clinical features of AML?

A

Anaemia
Thrombocytopenic bleeding
Infection

65
Q

How do you treat AML?

A

Supportive
Amto-leukaemic therapy
Allogenic stem cell transplantation
All-trans retinoic acid + arsenic trixoide (in APL)
Some targeted treatments becoming available

66
Q

How does CML present?

A 
Anaemia
 Splenomegaly, often massive
 Weight loss
 Hyperleukostasis - Fundal haemorrhage and venous congestion, altered consciousness, respiratory failure.
Gout
67
Q

What are the lab results in CML?

A

High (very sometimes) WCC
High platlets
Anaemia
Blood film shows all stages of white cell differentiation with increased basophils
Bone marrow is hypercellular
Bone marrow and blood cells contain the Philadelphia chromosome - t(9;22)

68
Q

How do you treat CML?

A 
Tyrokinase ihibitors
>Imatinib (Glivec)
> Dasatinib (Sprycel)
>Nilotinib  (Tasigna)
>Busitinib
> Ponatinib
69
Q

What are myelodysplastic syndromes?

A

Acquired clonal disorders of the bone marrow
Commonly seen in old age
Present as macrocytic anaemia and pancytopenia
They are pre-leukaemic
They are fatal as a result of progression to bone marrow failure or AML
Treatment is supportive or stem cell transplantation for the few young patients

70
Q

What are the myelodysplastic syndromes?

A 
Polycythaemia  Vera (PV)
Essential Thrombocythaemia (ET)
Idiopathic Myelofibrosis (IM)
71
Q

What mutations are present in myelodysplastic syndromes?

A

All can have JAK2V617F

CALR can also be affected in ET

72
Q

What are the features of polycythaemia vera?

A 
Headaches
Itch
Vascular occlusion
Thrombosis
TIA/stroke
Splenomegaly
73
Q

What are the lab features of polythaemia vera?

A 
A raised haemoglobin concentration 
Raise haematocrit.
 A tendency to have a raised WCC 
Raised platelet count
 A raised uric acid
 A true increase in red cell mass when the blood volume is measured
74
Q

How do you treat PRV?

A

Venesection to keep haemocrit down
Aspirin
Hydroxcarbamide

75
Q

What is essential thrombocythaemia?

A

Myeloproliferative disease with predominant feature of raised platelet count
Symptoms of arterial and venous thromboses, digital ischaemia, gout, headache
Mild splenomegaly

Can progress to myelofibrosis or AML

76
Q

How do you treat ET?

A

Treated with aspirin and hydroxycarbamide or anagrelide

77
Q

What are the types of lymphoma?

A

Hodkins

Non-hodgkins (split into high/low grade)

78
Q

What is acute lymphoblastic leukaemia (ALL)?

A

Neoplastic disorder of lymphoblasts
Diagnosed by > 20% lymphoblasts present in bone marrow
Present with 2-3 week history of bone marrow failure or bone/joint pain
>Bone marrow failure +/- raised white cell count
>Bone pain, infection, sweats

79
Q

How do you treat ALL?

A 
Induction chemotherapy to obtain remission
Consolidation therapy
CNS directed treatment
Maintenance treatment for 18 months
Stem cell transplantation (if high risk)
Newer therapies emerging -
80
Q

What are the newer treatments for ALL?

A

Bispecifc T-cell engagers (BiTe molecules) – e.g. Blinatumumab
CAR (chimeric antigen receptor T-cells)

81
Q

What are the poorer risk factors for ALL?

A 
Increasing age
Increased white cell count
Immunophenotype (more primitive forms)
Cytogenetics/molecular genetics
t(9;22); t(4;11)
Slow/poor response to treatment
82
Q

How does CLL present?

A 
Often assymptomatic at presentation
Frequent findings:
>Bone marrow failure (anaemia, thrombocytopenia)
>Lymphadenopathy 
>Splenomegaly (30%) 
>Fever and sweats (< 25%)

Less common findings:
>Hepatomegaly
>Infections
>weight loss

83
Q

What are the indications for treatment in CLL?

A 
Progressive bone marrow failure
Massive lymphadenopathy 
Progressive splenomegaly
Lymphocyte doubling time <6 months or >50% increase over 2 months
Systemic symptoms
Autoimmune cytopenias
84
Q

How do you treat CLL?

A

Cytotoxic chemotherapy e.g. fludarabine, bendamustine
Monoclonal antibodies e.g. Rituximab, obinutuzamab
Novel agents

85
Q

What are the novel agents for CLL?

A

Bruton tyrosine kinase inhibitor eg ibrutinib
PI3K inhibitor eg idelalisib
BCL-2 inhibitor eg venetoclax

86
Q

What indicates poor prognosis in CLL?

A 
Advanced disease (Binet stage B or C)
Atypical lymphocyte morphology
Rapid lymphocyte doubling time (<12 mth)
CD 38+ expression
Loss/mutation p53; del 11q23 (ATM gene)
Unmutated IgVH gene status
87
Q

How do lymphomas present?

A

lymphadenopathy/hepatosplenomegaly
Extranodal disease
“B symptoms”
bone marrow involvement

88
Q

What is hodgkin’s lymphoma assciated with?

A

association with Epstein Barr virus;

familial and geographical clustering

89
Q

How do you treat hodgkin’s lymphoma?

A 
Combination chemotherapy (ABVD)
\+/- radiotherapy
Monoclonal antibodies (anti-CD30)
Immunotherapy (checkpoint inhibitors)
Use of PET scan to assess response to treatment and to limit use of radiotherapy
90
Q

How do you treat non’hodgkin’s lymphoma?

A

typically anti-CD20 monoclonal antibody

+ chemo

Conditions + definitions (68 decks)

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