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Phase 4 > Haematology final one plz > Flashcards

Haematology final one plz Flashcards

1
Q

Contrast HUS and TTP:

A

HUS:

  • bloody diarrhoea
  • Microangiopathic haemolytic anaemia
  • thrombocytopenia
  • kidney failure

TTP:

  • no diarrhoea
  • Microangiopathic haemolytic anaemia
  • Thrombocytopenia
  • Kidney failure
  • CNS involvement
  • Fever
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2
Q

How does an amniotic embolism cause DIC?

A

Releases tissue factor which triggers the extrinsic pathway

Tissue factor is the triggering factor

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3
Q

What are some of the causes of DIC?

A

Sepsis

Obstetric complications
- especially amniotic embolisms

Acute pancreatitis

Haematological malignancy
- AML -M3

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4
Q

What is found in cryoprecipitate?

A

Von- Williebrand
Factor VIII
Fibrinogen

Useful for:

  • Haemophilia A
  • DIC
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5
Q

How is DIC management:

A
  • *treat the underlying cause
  • *contact haematology
  • FFP
  • platelets
  • Cryoprecipitate (fibrinogen, von-Williebrand, VIII)
    +/-
  • Heparin if coagulating
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6
Q

Which drug can cause haemolytic anaemia which is associated with coeliac disease?

A

Dapsone

- used for dermatitis herpatoformis

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7
Q

What is the diagnostic criteria for tumour lysis syndrome and how is it managed?

A

Clinical:

  • AKI
  • Cardiac arrhythmias
  • Confusion/ weakness - hypocalcaemia
  • Muscle cramps

Bloods;

  • Hypocalcaemia
  • Hyperuricemia
  • Hyperphosphatemia
  • Hyperkalaemia
Treatment: 
- IV fluids 
- Frusemide
- Calcium gluconate (both replenish Ca2+ and protects for K+) 
- Phosphate binders 
- Rasburicase (anti- uricaemic) 
\+/- 
- Haemodialysis
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8
Q

In heparin induced thrombocytopenia - what would you expect the bleeding to be like?

A

There is a paradoxical increased risk of thrombosis

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9
Q

If requesting blood for a pregnant female - what do you ask for?

A

CMV - negative RBCs

*this is also required if neonate transfusion

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10
Q

What is the test to diagnose hereditary spherocytosis?

A

EMA binding test

Autosomal dominant

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11
Q

How is tranexamic acid delivered during an emergency?

A

IV bolus
followed by
IV infusion

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12
Q

Outline the major causes of Polycythaemia:

A

Polycythaemia Ruba Vera
- haematological malignancy

Relative polycythaemia

Secondary to COPD, high altitude

EPO producing tumour
- renal cell carcinoma

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13
Q

What are some of the signs of polycythaemia Ruba vera and list some complications:

A

Facial plethora
Itching
Headaches
Itchiness

Complications:

  • Budd Chiari
  • Stroke
  • Cavernous sinus thrombosis
  • Malignant transformation into AML
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14
Q

How would you manage a patient bleeding who has haemophilia A and those with haemophilia B?

A

Haemophilia A:

  • Desmopressin
  • Recombinant Factor VIII (can cause antibodies to them)
  • Cryoprecipitate (contains VIII)

Haemophilia B:

  • Recombinant IX
  • FFP
  • Prothrombin Complex Concentrate
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15
Q

In the setting of acute haemolytic reaction what two major bloods do you want? what else should should be done?

A

Two Major bloods:
Cross match
- repeat

Direct Coombs test

Other bloods:

  • coagulation
  • U&Es

Keep unit of blood and sent to haematology
Check all details

IV fluids and flush

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16
Q

If someone has Raised MCV anaemia with hypothyroidism - what may be causing the raised MCV?

A

Pernicious anaemia

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17
Q

What is the kidney disorder that can occur in sickle cell disease leading to AKI?

A

Renal Papillary necrosis
- due to ischemia

Avascular necrosis can also occur in the bone

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18
Q

Who get Hodgkin’s lymphoma? and What are the diagnostic investigations and what is the treatment?

A

Young people
Elderly
- bimodal disruption

Investigations: 
Bloods: 
- FBC 
- Blood film 
- LDH *prognosticator 
- HIV serology

CXR
ST for staging (Ann Arborr)

Lymph node biopsy *Reid Steinberg cells seen
Bone marrow aspiration with trephine

Treatment:

  • radiotherapy
  • Chemotherapy (ABVD)
  • Autologous Stem cell transplant
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19
Q

What is the most common type of Hodgkin’s lymphoma? and what are some risk factors?

A

Nodular Sclerosing

Risk factors:

  • EBV
  • HIV
  • Sarcoidosis
  • Family history
20
Q

What is the common translocation in CML? and what other leukaemia can this be present in and what does it suggest?

A

Philadelphia chromosome
- 9:22

It can also be associated with ALL which is a poor prognostic factor

21
Q

What are the stages of CML?

A

Chronic phase

Accelerated phase

Blast phase

22
Q

What would you expect to see on the blood film of CLL?

A

Smudge cells

23
Q

What are the three phases of chemotherapy?

A

Remission induction
Remission consolidation
Remission Maintenance

24
Q

How are leukaemia’s classified?

A

Morphology

Immunological

Cytogenetics

25
Q

What are the poor prognostic factors for ALL?

A 
Age <2 years, >10 years 
9:22 translocation 
High B and T cell count 
Male sex 
>20 WCC
26
Q

Name the notable causes for a massive splenomegaly:

A

Malaria

Myelofibrosis

CML

27
Q

What is the immunological agent that can cure CML and how does it work?

A

Imatinib

BCR- ABL Tyrosine kinase inhibitor

28
Q

What cells may you see on a blood film of someone with iron deficiency anaemia?

A

Anisocytosis - changes in cell sizes and shapes

Piokilocytosis
- irregular shaped

29
Q

What are the clinical features of iron deficiency anaemia?

A

Symptoms:

  • dizziness
  • Palpitation
  • Dyspnoea
  • Reduced energy
  • Headaches
  • restless leg

Signs:

  • Angulitis stomatitis
  • atrophic glossitis
  • Koilonychia
  • Pale
  • Oesophageal webs
30
Q

What are the iron supplements that can be given?

When giving IV Iron supplementation what is an important aspect to be aware of?

A

Ferrous Fumarate

Ferrous gluconate

IV Iron will not cause a haematological response any quicker than PO, but does replenish iron stores slightly quicker.

31
Q

If there is folate deficiency - what must you check before treating?

A

Must check B12 levels

- can worsen sub-acute combined spinal cord degeneration if not

32
Q

What type of haemolysis is Hereditary spherocytosis and how is it managed long term?

A

Autosomal dominant.

Extravascular.

Diagnosed:
- EMA binding

Management:

  • folate replacement
  • Splenectomy

**can be a cause of haemolytic jaundice and splenomegaly

33
Q

What are the general causes of aplastic anaemia?

A

Primary:
- idiopathic/ genetic related

Secondary:
- Virus induced - parvovirus B19

Iatrogenic: (including radiation)

Management:

  • Blood transfusions
  • Neutropenic sepsis management

<40 years:
- allogenic stem cell transplant

> 40 years:
- Anti-thymocyte drugs

34
Q

What is the intervention done which removes plasma from the blood?

A

Plasmapheresis

*look at spelling!!

35
Q

What tests should you order in multiple myeloma to establish an increase in paraprotein, and what test to distinguish exactly what it is?

A

Electrophoresis of the plasma:

  • establishes high M protein
  • is quantitative

Immunofixation of plasma:

  • establish the type (IgG, IgM, Kappa, lamda)
  • is Qualitative
36
Q

What do bands on a blood film suggest?

A

The suggest granulocytes at different stages of maturation.

Very suggestive of CML as multiple neutrophils etc will be at different stages.

37
Q

What is a D-Dimer?

A

Fibrin Degradation products

38
Q

High light all the clinical signs/ symptoms you may see with someone who has myeloma:

A

Amaurosis Fagux
- high ESR

Bruising/ easy bleeding

Pathological fractures

Confusion

Constipation

Carpal tunnel
- secondary amyloidosis

Nephritis

  • Amyloidosis
  • tubular acidosis
  • Direct toxicity of paraproteins
  • NSAID use

Infections

39
Q

What test is needed for the confirmation of myeloma?

A

Bone marrow aspiration

>10% blast cells

40
Q

What is needed for a diagnosis of myeloma?

A

Blast cells >10% in bone marrow

Evidence of paraproteins
- in urine
or
- Blood

Evidence of CRAB

41
Q

What is the treatment for myeloma?

A

Cancer:

  • chemotherapy
  • autologous stem cell transplant

Anaemia:

  • Blood transfusions
  • EPO

Infections:

  • Prophylactic antibiotics
  • Immunoglobulin transfusions

Bones:

  • Bisphosphonates
  • Analgesia
  • Radiotherapy
  • Vertebroplasty/ Kyphoplasty

Anti-thrombotic prevention
- risk of DVTs is high

Prognosis:

  • smouldering disease
  • 5 years - 50%
42
Q

How should warfarin overdose be managed?

A

INR 5-8: with hold and start again when <5

INR >8: Withhold. IV vitamin K. Contact haematology

Any major bleed/ Intracranial bleed: Stop warfarin, IV vitamin K, Prothrombin complex concentrate

*prothrombin complex concentrate contains factors:
- II, V, IX, X
all which warfarin inhibits

43
Q

What are you differentials for myeloma?

A

Monoclonal gammopathy of undetermined significance

Waldenstrom’s macroglobinaemia

Amyloidosis

Hodgkin’s

44
Q

What clinical test can be done to help establish a DVT?

A

Dorsiflexion of the affected limp will often produce significant pain

45
Q

Where does a P.E typically originate from?

A

Iliofemoral

Phase 4 (49 decks)

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