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Phase 2a Yellow Conditions > Haematology > Flashcards

Haematology Flashcards

1
Q

Pathophysiology of TTP

A
  1. dysfunctional vWF cleaving protease
  2. can’t break clumps of vWF into useful monomers
    3 microvascular clots form
  3. problem with primary haemostasis
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2
Q

Presentation of TTP

A
  • fatigue
  • fever
  • jaundice
  • petechiae
  • purpura
  • neurological deficit
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3
Q

Investigations for TTP

A

FBC

  • raised WCC
  • low Hb, platelets

blood smear → schistocytes

other → raised bilirubin, creatinine

normal clotting

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4
Q

Treatment of TTP

A
  • plasma exchange
  • IV methylprednisolone
  • monoclonal Abs
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5
Q

Pathophysiology of ITP

A
  • autoimmune
  • IgG destruction of GpIIb/IIIa
  • platelets cannot activate
  • problem with primary haemostasis
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6
Q

Presentation of ITP

A

same as TPP

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7
Q

Investigations for ITP

A
  • FBC → raised WCC, low Hb and platelets
  • clotting normal
  • blood smear normal
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8
Q

Treatment of ITP

A
  • steroids
  • IV IgG
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9
Q

What is haemophilia

A

A

  • factor VIII deficiency (intrinsic)
  • secondary haemostasis
  • X linked recessive

B
- factor IX deficiency (intrinsic)

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10
Q

Presentation of haemophilia

A

soft tissue bleeding pattern → into muscles, joints, haematoma formation

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11
Q

Investigations for haemophilia

A
  • APTT long
  • PT may be normal
  • genetic testing
  • factor VIII/IX testing
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12
Q

Treatment for haemophilia

A
  • recombinant factor VIII or IX
  • depends on type
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13
Q

What is Von Willebrand’s disease?

A
  • defect in quantity or quality of vWF
  • many subtypes
  • varied inheritance
  • primary haemostasis disorder
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14
Q

What is the most common type of Von Willebrand’s disease?

A
  • type 1
  • autosomal dominant
  • quantitative disease
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15
Q

Presentation of Von Willebrand’s disease

A

mucocutaneous bleeding

  • epistaxis
  • GI bleeds
  • menorrhagia
  • easy bruising
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16
Q

Investigations for Von Willebrand’s disease

A
  • plasma vWF
  • APTT can be prolonged if FVIII low
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17
Q

How does Von Willebrand’s disease cause factor VIII deficiency?

A
  • vWF protects FVIII from liver protein C destruction
  • FVIII deficiency occurs is vWF affected
18
Q

Treatment for Von Willebrand’s disease

A
  • type 1 responds to desmopressin
  • tranexamic acid → reduces acute bleeding
19
Q

What is G6PD?

A
  • glucose-6-phosphate dehydrogenase
  • role in pentose sugar metabolism
  • protects RBCs from damage
20
Q

What is G6PD deficiency?

A

RBCs exposed to more oxidative stress → haemolysis

21
Q

Risk factors for G6PD deficiency

A
  • X linked
  • west africa, middle east, asia
22
Q

Presentation of G6PD deficiency

A
  • haemolytic anaemia
  • splenomegaly
23
Q

Investigations for G6PD deficiency

A

bloods

  • anaemia
  • increased LDH and reticulocytes → markers of haemolysis

blood smear → Heinz bodies

24
Q

Treatment for G6PD deficiency

A
  • blood transfusion
  • stop exacerbating drugs
25
Q

What is antiphospholipid syndrome?

A
  • type of inherited thrombophilia
  • AP antibodies bind to cell surfaces
26
Q

Risk factors for antiphospholipid syndrome

A
  • SLE
  • females
  • diabetes
  • HTN
  • obesity
27
Q

Presentation of antiphospholipid syndrome

A
  • unexplained thrombosis
  • recurrent miscarriage
  • Livedo reticularis

CLOT

28
Q

What is polycythaemia?

A
  • high concentration of erythrocytes in the blood
  • 2 types → absolute and relative
29
Q

What is relative polycythaemia?

A
  • normal number of erythrocytes
  • reduction in plasma

causes
- obesity
- dehydration
- excessive alcohol

30
Q

What is absolute polycythaemia?

A
  • increased number of erythrocytes
  • 2 types → primary and secondary
31
Q

What is primary polycythaemia?

A
  • abnormality in the bone marrow
  • AKA polycythaemia vera
32
Q

What is secondary polycythaemia?

A
  • disease outside bone marrow causing overstimulation of bone marrow

causes
- COPD
- sleep apnoea
- PKD
- renal artery stenosis
- kidney cancer

33
Q

Features of polycythaemia vera

A
  • myeloproliferative neoplasm
  • most people have JAK2 mutation
  • affected bone marrow can also produce excessive platelets, WBCs
34
Q

Presentation of polycythaemia vera

A
  • headaches
  • dizziness
  • fatigue
  • blurred vision
  • red skin → hand, face, feet
  • HTN
  • itching esp after conact with warm water
  • hepatosplenomegaly
35
Q

Diagnosis of polycythaemia vera

A
  • FBC → raised Hb, haematocrit, WCC, platelets
  • genetic testing
  • serum erythropoietin → decreased (raised/normal in other polycythaemias)
36
Q

Management of polycythaemia vera

A
  • venesection
  • low dose aspirin daily
  • hydroxycarbamide → if high risk of thrombus
37
Q

What is pernicious anaemia?

A
  • lack of intrinsic factor
  • usually produced by parietal cells in stomach
  • allows B12 absorption in terminal ileum
  • low B12 = B12 deficiency macrocytic anaemia
38
Q

What is malaria?

A
  • parasitic infection Plasmodium
  • spread by female mosquito
  • most common in Africa
39
Q

What are the species of Plasmodium?

A
  • p.falciparum → most common
  • p.vivax
  • p.ovale
  • p.malariae → least common
40
Q

Signs and symptoms of malaria

A

non-specific symptoms
- fever, chills
- headache
- cough
- splenomegaly

severe disease in p.falciparum
- SOB
- fits and hypovolaemia
- AKI and nephrotic syndrome

41
Q

Investigations for malaria

A
  • travel history
  • thick and thin blood smears → 3 over 48hrs
  • rapid diagnostic tests → detect parasitic antigens
  • PCR
  • bloods
  • chest xray
  • lumbar puncture
42
Q

Treatment for malaria

A

A
non-falciparum malaria
- chloroquine

falciparum malaria
- oral quinine sulphate
- IV quinine dihydrochloride for severe disease

do not treat those with G6PD deficiency

Phase 2a Yellow Conditions (12 decks)

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