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J3 > Bloed > Flashcards

Bloed Flashcards

1
Q

What does an increased reticulocyte count suggest?

A

1) haemolytic anaemia
2) blood loss

The bone marrow is working hard to replace the lost cells and is releasing immature cells

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2
Q

Name 3 causes of microcytic anaemia

A

“SIT”

Sideroblastic anaemia
Iron deficiency anaemia
Thalassaemias

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3
Q

Name 3 causes of normocytic anaemia

A

acute blood loss
anaemia of chronic disease
sickle cell anaemia

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4
Q

Name 4 causes of macrocytic anaemia

A

remember: FAT RBC

F = folate deficiency
A = alcohol
T = thyroid (hypothyroidism)
R = reticulocytosis
B = B12 deficiency
C = cytotoxic drugs
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5
Q

Name 3 causes of IDA

A

Chronic blood loss (menstrual, GI (high urea))
Malabsorption (coeliac’s disease, gastrectomy)
Increased demand (pregnancy, growth)

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6
Q

What lab results would you expect in haemolytic anaemia?

A

elevated unconjugated bilirubin
elevated LDH (from RBC)
increased reticulocyte count

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7
Q

What would you check in iron studies?

A

Iron
transferrin
total iron binding capacity
ferritin

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8
Q

Name the haematinics

A

B12
folate
ferritin

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9
Q

What is polycythaemia?

A

Increased concentration of Hb within the blood

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10
Q

What are causes of polycythaemia?

A

Relative polycythaemia: (decreased plasma volume)
-acute dehydration

Absolute polycythaemia: (increased RBC mass)

  • polycythaemia ruba vera (primary)
  • raised EPO or chronic hypoxia (secondary)
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11
Q

Causes of thrombocytopaenia

A

1) decreased production
- bone marrow failure
- aplastic anaemia
- megaloblastic anaymia

2) increased destruction/consumption:
- DIC/TTP/HUS
- ITP
- SLE/CLL
- drug induced

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12
Q

WBC differential

A

determines the number of polymorphs, lymphocytes and monocytes in the total WCC

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13
Q

Which conditions cause hypochromic microcytic RBC?

A

poorly haemoglobinised and small (reduced MCH/MCV)

1) IDA
2) ACD
3) thalassaemia

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14
Q

MCV

A

mean corpuscular volume = RBC size

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15
Q

MCH

A

Mean corpuscular Hb content

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16
Q

Reticulocytes

A

Immature RBC
Usually <2% of RBC
No nucleus but some persisting RNA

polychromatic appearance on blood film

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17
Q

Name two conditions in which you would see spherocytes

A

AIHA

hereditary spherocytosis

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18
Q

Howell-Jolly bodies

A

nuclear fragments in RBC

Seen in hyposplenic patients

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19
Q

In which condition would you see macrocytes?

A

Large RBC (increased MCV)

B12/folate deficiency
hepatic disease
hypothyroidism

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20
Q

What is anisopoiklocytosis and when would you see it?

A

variation in size (anisocytosis) and shape (poiklocytosis) of RBC.

Seen in B12/folate deficiency

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21
Q

When would you see RBC fragmentation?

A

In mechanical haemolytic anaemias (e.g. prosthetic valve malfunction)

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22
Q

When would the direct coombs test be positive?

A

test to detect the presence of an antibody on the RBC surface

positive in AIHA and HDN

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23
Q

What are leukaemic blasts and when would you expect to see them?

A

abnormal primitive blast cells that are found in the bone marrow and sometimes the peripheral blood.

Seen in acute leukaemia and poor prognosis myelodysplastic syndromes

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24
Q

What are myelodysplastic syndromes?

A

Characterised by dysplasia and ineffective haemopoieisis in 1 or more of the myeloid cells.

Characterised by progressive bone marrow failure. Peesent with fatigue/infections/bleeding.

May be associated with monosomy 7 (loss of a chromosome)

Can progress to secondary AML

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25
Q

Myeloproliferative disorders

A

Describes proliferation of cells in the bone marrow with normal (non-dysplastic) appearance.

CML
Polycythaemia Vera
Essential thrombocythaemia
Myelofibrosis

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26
Q

Myeloma

A

malignant prolfieration of plasma cells in the bone marrow

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27
Q

What kind of disorder is myeloma?

A

a lymphoproliferatice disease

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28
Q

What is PT and what does it assess?

A

Prothrombin time

Test of the extrinsic pathway of coagulation

Sensitive to warfarin

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29
Q

What is INR?

A

International normalised ratio

Measure of warfarin activity

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30
Q

What is PTT?

A

= APTT

Partial thromboplastin time

Measure of the intrinsic pathway of coagulation

Sensitive to IV heparin

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31
Q

What is a group and screen?

A

determines ABO and Rh group

Screens plasma for immune RBC antibodies

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32
Q

What are packed RBC?

A

units of blood from which plasma has been removed

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33
Q

What is cryoprecipitate?

A

prepared from donated plasma

rich in factor VIII and fibrinogen

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34
Q

What is the indirect coombs test?

A

a test used to detect the presence of RBC antibodies in plasma.

Forms the basis of the Cross match and the antibody screen in group and screen.

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35
Q

Which cells are derived from lymphoid progenitor cells?

A

B cells
T cells
NK cells

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36
Q

where is EPO mainly produced?

A

peritubular interstitial cells of the kidneys

Liver in newborns (less sensitive than the kidneys to hypoxia, so newborns have a smaller EPO response)

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37
Q

Where is TPO produced?

A

the liver

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38
Q

Which cytokines stimulate WBC formation?

A

IL-7 stimulates lymphoid progenitor cell line (7 upside down is like an L)

IL-3 stimulates myeloid cell line (3 on its side looks like an m)

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39
Q

What is anaemia?

A

Haemoglobin concentration below the reference range for age and sex

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40
Q

What is pernicious anaemia?

A

Insufficient haemopoieisis due to an inability of parietal cells to produce intrinsic factor, which is required for B12 absorption

Antibody against intrinsic factor

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41
Q

What is aplastic anaemia?

A

Rare condition in which there is destruction of red bone marrow and haematopoeitic stem cells.

Causes pancytopaenia = anaemia + leukopaenia + thrombocytopaenia

Caused by toxins, gamma radiation and drugs.

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42
Q

Signs and symptoms of anaemia

A

SOB
pallor
fatigue

jaundice in haemolytic forms

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43
Q

Where are HSC found?

A

Bone marrow
Umbilical cord blood
peripheral blood after stimulation with G-CSF

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44
Q

What are bone marrow stromal cells and what is their role?

A

Macrophages, fibroblasts, fat cells, endothelial cells and reticulum cels

Stromal cells form the bone marrow microenvironment that supports developing HSC. They have adhesion molecules which retain developing cells in the bone marrow

They secrete extracellular matrix molecules (collagen, fibronectin, laminin and proteoglycans) and growth factors.

Provides the requirements of the stem cell for growth and division

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45
Q

Clonal HSC disorders

A

haematological malignancies arising from a single ancestral cell

NB: in contrast, nonmalignant proliferations are polyclonal

46
Q

Name 3 myeloproliferative disorders

A

1) polycythaemia ruba vera (PRV)
2) Essential thrombocytosis
3) myelofibrosis - marrow filled with fibrous tissue, so liver and spleen take over blood cell production

Can transform into AML

47
Q

Essential thrombocytosis

A

overproduction of platelets

Associated with Jak2 and calreticulin mutations

Clumps of platelets seen in peripheral blood

Platelets produced are non-functional, so haemorrhage may occur

Treat with aspirin and mild chemotherapy (severe cases)

Can use JAK2 inhibitors (ruxolitinib)

48
Q

Refractory anaemia

A

Group of anaemic conditions not associated with any other disease; characterised by a frequently advanced anaemia that can only be successfully treated by blood transfusions.

Associated with monosomy 7

may have excess blasts (risk of progressing to CML)

49
Q

Fanconi anaemia

A

Most common inherited form of aplastic anaemia. Causes pancytopaenia.

Autosomal recessive. faulty FANC gene

Much of the bone marrow becomes replaced by fat.

Other abnormalities:

  • cafe au lait spots
  • hearing loss
  • micropthalmia
  • GI/GU malformations

Requires allogeneic SCT

50
Q

What are the main indications for SCT?

A

relapsed Hodgkin’s disease
non-Hodgkins lymphoma
Myeloma

51
Q

What does increased serum ferritin suggest?

A

Can suggest iron overload

However, ferritin is an acute phase reactant, so it will be elevated in tissue inflammation/infection damage as well. (IDA can occur with normal serum ferritin in the presence of tissue inflammation)

Therefore elevated ferritin does not necessarily suggest iron overload

52
Q

What is latent IDA?

A

low serum ferritin and normal haemoglobin

Erythroblasts take what iron is available in stores to maintain normal Hb levels

53
Q

Clinical presentation of IDA

A

koilonychia
atrophic glossitis (pale, smooth, painless tongue)
Angular stomaitis

54
Q

Anaemia of chronic disease

A

Form of anaemia seen in chronic infection, chronic immune activation and malignancy

Normal or increased iron stores but decreased amounts in serum. Inflammation can prevent the body from using stored iron (failure of iron utilisation)

Low iron
Low TIBC
N/increased ferritin
increased ESR
N/low MCV/MCH
55
Q

What form of anaemia is associated with a painful tongue and subacute demyelination of the spinal cord?

A

vitamin B12/folate deficiency = megaloblastic anaemia

Bilateral peripheral neuropathy
mild jaundice
megaloblastic anaemia

56
Q

Haemolytic anaemia

A

anaemia related to reduced RBC lifespan
no blood loss
no haematinic deficiency

57
Q

What are the lab findings in compensated haemolytic anaemia?

A

normal Hb
elevated reticulocyte count
elevated unconjugated bilirubin

58
Q

Congenital haemolytic anaemias

A

1) abnormalities of RBC membrane = hereditary spherocytosis (AD)
2) haemoglobinopathies
3) abnormalities of RBC enzymes = Pyruvate Kinase Deficiency Anaemia (AR) or G6P dehydrogenase deficiency (XLR)

59
Q

Causes of acquired haemolytic anaemia

A

1) autoimmune - warm AIHA (IgG) / cold AIHA (IgM)
2) isoimmune - haemolytic disease of the newborn
3) fragmentation - haemolytic uraemic syndrome or valve malfunction

60
Q

Cold AIHA (autoimmune hemolytic anemia)

A

IgM autoantibody

Causes RBC agglutination

Seen in infections (e.g. mycoplasma)

Difficult to treat. Keep warm.

61
Q

Warm AIHA (autoimmune hemolytic anemia)

A

more common than cold AIHA

IgG autoantibody

seen in context of other autoimmune diseases - SLE, RA.

May be drug-induced.

Stop causative drugs and give steroids / immunosuppressants. Splenectomy if all else fails

62
Q

Mechanisms of Drug Induced AIHA

A

1) acting as a hapten - binds to RBC and stimulates antibody formation
2) immune complex formation - antibodies form to drug and RBC are caught in the crossfire
3) autoimmune - drug can stimulate immune system to attack RBC (rare)

63
Q

Name 3 inherited bleeding disorders

A

1) haemophilia (A = factor VIII, B = factor IX)
2) von Willebrand disease
3) severe platelet disorders

64
Q

Name 3 acquired bleeding disorders

A

1) DIC
2) coagulopathy in liver disease (alcohol)/vitamin K deficiency
3) complication of warfarin therapy

65
Q

Name 3 inherited thrombotic disorders

A

1) thrombophilia
2) Factor V Leiden
3) prothrombin gene mutation

66
Q

Name an acquired thrombotic disorder

A

1) antiphospholipid syndrome

67
Q

What does mucocutaneous bleeding suggest?

A

platelet disorder

68
Q

What does bleeding into a potential space (e.g. haemarthrosis) suggest?

A

Coagulation defect

69
Q

What does easy bruising since childhood suggest?

A

an inherited cause of the bleeding disorder

70
Q

What are the functions of von Willebrand factor?

A

1) facilitated platelet adhesion and aggregation (binds collagen and platelet glycoproteins)
2) prolongs half-life of factor VIII

71
Q

What lab findings would you expect in DIC?

A 
prolonged PT
prolonged APTT
schistocytes on blood film
thrombocytopaenia
elevated d-dimer
72
Q

Treatment of DIC

A

aggressively treat underlying cause

Give FFP and platelets

73
Q

Bleeding complications with warfarin

A

increased risk of brain haemorrhage (elevated INR)

74
Q

Management of elevated INR

A

Stop warfarin (if life-threatening bleeding) or reduce dose

Give Vitamin K (oral takes 24 hours, IV takes 6 hours)

Give coagulation factors II, VII, IX and X -> Beriplex (takes 20 minutes)

75
Q

What is the effect of Desmopressin (DDVAP) in management of bleeding disorders?

A

increases the concentration of von willebrand factor and factor VIII

76
Q

What lab results would you expect for factor VII deficiency?

A

prolonged PT, normal APTT

77
Q

What lab results would you expect for a factor XII deficiency?

A

Normal PT, prolonged APTT

78
Q

What lab results would you expect for haemophilia?

A

Normal PT, prolonged APTT

79
Q

What lab results would you expect for von willebrand’s disease?

A

Normal PT, prolonged APTT (vWF prevents degradation of factor VIII)

80
Q

What is PT and how is it assessed?

A

Prothrombin time, assesses the function of the extrinsic pathway

Add Thromboplastin to patient’s plasmin and add calcium. Measure time to clot

NB: INR = standardised form of PT

81
Q

What is aPTT and how is it assessed?

A

Activated partial thromboplastin time (APTT) assesses the function of the intrinsic pathway.

Add:
Patient’s plasma
Contact factor 
Phospholipid 
Calcium

Measure time to clot

82
Q

What is TCT and how is it assessed?

A

Thrombin Clotting Time (TCT)

Measurement of conversion of fibrinogen to fibrin clot. Indicates how much functioning fibrinogen is in the patient’s blood (common pathway)

Add excess thrombin

83
Q

What is the impact of Lupus anticoagulant on the coagulation screen?

A

Causes prolonged APPT

84
Q

Which drug provides immediate but short-acting anticoagulant effects?

A

heparin

85
Q

which anticoagulant drug is safe to use in pregnancy?

A

heparin

86
Q

Mechanism of action of warfarin

A

Blocks reduction of vitamin K, which is required as a cofactor for the synthesis of factors II, VII, IX and X

Results in decreased prothrombin levels

NB: has delayed onset and offset. Therefore NOT used for immediate anticoagulation or short term thromboprophylaxis

87
Q

Which drug would you use for immediate anticoagulation or short term thromboprophylaxis?

A

Heparin. DOACs are also active immediately

Must start with heparin therapy before initiating warfarin (because of the delayed onset of warfarin as the existing pool of functional clotting factors has to be replaced by dysfunctional factors)

88
Q

Which bacteria is Streptokinase isolated from?

A

group C haemolytic streptococci bacteria

Causes systemic plasmin activation

89
Q

Uses of Fibrinolytics

A 
used IV or intra-arterially to treat:
o	Venous thrombosis
o	Myocardial infarction (within 12h)
o	Thrombotic stroke (within 4.5h)
o	massive PE
90
Q

Mechanism of action: Clopidogrel

A

blocks platelet ADP receptor, preventing aggregation

91
Q

Mechanism of action: aspirin

A

irreversibly inhibits COX in platelets. This prevents production of thromboxane A2, preventing platelet activation/aggregation

92
Q

Mechanism of action: Dipyridamole

A

prevents platelet activation/aggregation by increasing cAMP, thereby reducing responsiveness to ADP stimulation

93
Q

What are the risks of splenectomy?

A

infection with encapsulated microorganisms:

  • streptococcus pneumoniae
  • haemophilus influezae
  • neisseria meningitidis
94
Q

What prophylactic measures should be taken with splenectomy?

A

vaccination
prophylactic antibiotic therapy (penicillin V)
carry a splenectomy card

95
Q

What is immunophenotyping and why is it done?

A

used to determine cell nature (lymphoid vs myeloid)
Done using monoclonal antibodies to surface or intracellular markers.

done on blood/bone marrow samples

methods:

1) flow cytometry
2) immunocytochemistry

96
Q

Causes of pancytopaenia

A

1) bone marrow failure
2) hypersplenism
3) peripheral consumption of blood cells

97
Q

When would you find normal blast cells in peripheral blood?

A

cancer metastases to bone
severe infection

radiotherapy for cervical cancer can cause bone marrow scarring

98
Q

What is leucoerythroblastic anaemia?

A

anaemia due to a space occupying lesion of the bone marrow

99
Q

What investigations would you perform in a patient with suspected acute leukaemia?

A

FBC/blood film

bone marrow examination:

  • microscopy
  • immunophenotyping
  • cytogenetics to check for a chromosomal translocation
100
Q

What is a bone marrow transplant?

A

transplantation of multipotent HSC (from bone marrow/peripheral blood/umbilical cord blood)

A means of replacing malignant cells with normal stem cells

the patient must be conditioned before (put into full remission)

101
Q

Idiopathic thrombocytopaenic purpura

A

isolated thrombocytopaenia
purpuric rash and tendency to bleed
diagnosis of exclusion (e.g. not secondary to SLE/RA)

no splenomegaly –> splenomegaly excludes a diagnosis of ITP

102
Q

Infectious mononucleosis

A

caused by EBV

fever, sore throat, cervical lymphadenopathy, fatigue

atypical mononuclear cells

do NOT give amoxicillin - will cause a rash. Give penicillin V instead

103
Q

How do you test for infectious mononucleosis?

A

Monospot test (IM produces heterophile antibodies)

104
Q

does lupus anticoagulant predispose to thrombosis or bleeding?

A

in vitro - anticoagulant effect. Prolongs APTT (not corrected by addition of normal plasma)
in vivo - thrombotic tendency

105
Q

What system is used to stage lymphoma?

A

Ann-Arbor

106
Q

What are the stages of Ann-Arbor for lymphoma?

A

Stage I - single group of lymph nodes
Stage II - more than one group of lymph nodes on the same side of the diaphragm
Stage III - groups of lymph nodes affected on both sides of the diaphragm (includes spleen)
Stage IV - extranodal involvement

A - no B symptoms
B - B symptoms

107
Q

What kind of lymphoma is seen more often in older patients?

A

Non-Hodgkin’s Lymphoma

108
Q

Give 4 examples of intravascular haemolysis

A

1) RBC fragmentation syndromes
2) ABO incompatible blood transfusion
3) cold type AIHA
4) malaria

109
Q

What are the main laboratory findings in intravascular haemolysis?

A
  • Anaemia, reticulocytosis and raised unconjugated bilirubin
  • Haemoglobinaemia and haemoglobinuria
  • Haemosiderinuria

free Hb saturates plasma haptoglobin (a binding protein).
Excess free Hb in the plasma is filtered at
the glomerulus leading to haemoglobinuria.

The renal tubules reabsorb some Hb from the urine.
This is broken down to form haemosiderin which can also appear in the urine.

110
Q

What type of haemolysis is caused by warm AIHA?

A

Extravascular

The IgG attaches to the red cell antigen and damages the RBC membrane. The damaged RBCs become
spherocytic and are phagocytosed by the RES, particularly the spleen.

111
Q

Which unusual sites can be infiltrated in ALL?

A

CSF and testicles

112
Q

D-dimer

A

fibrin degradation product

o a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis

o elevated D-dimer levels = due to high fibrinolytic activity

NB: high d-dimer level common in patients who abuse alcohol (poor clearance of activated coagulation factors)

J3 (18 decks)

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