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AA Y4 Finals cards NE > Haematology > Flashcards

Haematology Flashcards

1
Q

A high MCV indicates the problem is where?

A

A problem with the maturation of RBCs

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2
Q

Where is iron absorbed?

A

The duodenum

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3
Q

In primary haemostasis, what do the platelets bind to?

What clotting factor helps them do this?

A

Platelets bind to sub endothelial collagen, which is exposed due to vessel damage

von willebrand factor helps them do this

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4
Q

Where are the clothing factors for secondary haemostasis produced?

Why is this relevant?

A

The liver

Patients with liver damage will have prolonged PTT

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5
Q

which clotting factors are vit K dependant?

A

2,7,9 and 10

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6
Q

which clotting factors are involved in the intrinsic pathway?

A

CFs 8, 9, 11 & 12

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7
Q

What is the end product when the intrinsic and extrinsic pathways converge?

A

factor Xa

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8
Q

What is the main role of plasmin?

A

to break down fibrin molecules in fibrinolysis

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9
Q

what complex is responsible in the extrinsic pathway of secondary haemostasis?

A

Tissue factor binding to and activating factor 7

Ie - the “TF- 7” complex is most important

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10
Q

compare what clotting factors are inhibited in LMWH and warfarin?

A

Warfarin: 2, 7, 9, 10

LMWH: factor Xa

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11
Q

Which 2 things is PT used to assess for?

A

Liver function

monitor warfarin
(vit K antagonist, so stops production of CFs 2,7,9 and 10- factor 7 is essential in the extrinsic pathway)

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12
Q

compare tests used to assess heparin and warfarin therapy?

A

Warfarin: PT

Heparin: APTT

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13
Q

what is the PT measuring?

A

The extrinsic pathway of 2ndary haemostasis

IE : TF-7

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14
Q

What pathway is the activatedPTT measuring?

A

The intrinsic 2ndary haemostasis pathway

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15
Q

which pathway is factor X activated in?

A

the common pathway

This pathway is the one that actually produces the thrombin

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16
Q

Which pathway does the thrombin time (TT) measure?

A

The common pathway

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17
Q

What is the role of protein C/S?

A

Control haemostasis

they are found on the surface of platelets and are activated by binding to thrombin and inhibiting factors 5&8

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18
Q

Which haemostasis is typically affected in vascular disorders?

How does this present clinically?

A

Primary haemostasis

Patients present with epistaxis, purpura, easy bruising, mucosal bleeding

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19
Q

Deficiency of what vitamin can cause a platelet deficiency?

A

Vit B12 deficiency

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20
Q

Name 3 drugs that cause bone marrow suppression and subsequent platelet disorders?

A

chemotherapy, radiotherapy, methotrexate

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21
Q

Which drugs cause increased use or destruction of platelets?

A

Heparin, penicillin, furosemide, digoxin, valproate

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22
Q

What is the underlying cause of idiopathic thrombocytopenic purpura?

A

an autoimmune condition where antibodies attack platelets

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23
Q

How is idiopathic thrombocytopenic purpura managed?

A

Kids: self limiting

Adults: self limiting unless severe - in which case, oral prednisolone

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24
Q

How is thrombotic thrombycytopenic purpura (TTP) different from idiopathic thrombocytopenic purpura (ITP)?

A

TTP is an emergency

in TTP, there is a defect in the enzyme used to cleave the vWB factor

This results in clumps of platelets sticking together in vessels and thrombosing

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25
Q

How does TTP present?

A

Thrombocytopenia and microangiopathic haemolytic anaemia

fever, mucosal bleeding, fluctuating CNS signs, AKI with haematuria

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26
Q

Describe the Hb, LDH, bilirubin and coagulation tests in TTP?

A

Low Hb
High LDH
High bilirubin
Normal coagualtion

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27
Q

What is seen on blood film in TTP?

A

Schistocytes

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28
Q

How is TTP managed?

A

plasmaphoresis
steroids and immunoglobulin
splenectomy

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29
Q

What does haemolytic anaemia syndrome occur secondary to?

What age are patients usually?

A

occurs secondary to E.Coli

most commonly affects children

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30
Q

what is released in haemolytic anaemic syndrome?

A

VTEC

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31
Q

in VWB disease, what class of drugs should be avoided? why?

A

NSAIDs

The can cause platelet abnormalities

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32
Q

How is VWF disease managed?

A

Mild: desmopressin

Severe haemorrhage: VWF concentrates

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33
Q

Describe the aPTT and bleeding time in someone with VWF disease?

A

Both APTT and VWF increased

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34
Q

How is haemophilia passed onto offspring?

A

X Linked

Only males will be affected, females will be carriers

if mum has it:
50% chance son will be symptomatic
50% daughter will be a carrier

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35
Q

which clotting factors are affected in haemophilia type A and B?

which is more common?

A

Type A: factor 8 deficiency (more common)

Type B: factor 9 deficiency

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36
Q

describe a long term complication of haemophilia

A

arthritis

repetitive haemarthrosis causes inflammation and scar tissue in the joints, which can lead to OA

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37
Q

how is APTT affected in haemophilia

A

there is an isolated increase in APTT but none of the other clotting tests

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38
Q

in alcoholic liver disease, which LFTs are abnormal?

A

GGT and AST

“wASTed”

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39
Q

What is warfarins MOA?

A

Vit K reductase inhibitor

It stops Vit K from being reduced into its active form, hence stopping production of clotting factors 2,7,9&10

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40
Q

in vit K deficiency, which is more pronounced; the increase in PTT or aPTT time?

A

increase in PTT is more pronounced

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41
Q

How is bleeding time affected by vit K deficiency?

A

Bleeding time remains unaffected; bleeding time is a reflection of primary homeostasis- none clotting factors 2,7,9&10 are involved in this

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42
Q

What is the underlying cause of DIC?

A

a widespread release of procoagulant material results in multiple thrombi in the body and uses up all the clotting factors

fibrinolysis is activated to break the clots down, resulting in increased bleeding

the clotting factors have already been used up, so haemorrhage ensues

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43
Q

Which blood test can be used in DIC to give a reflection of fibrin degradation products

which differential can this be used to discount?

A

D Dimers

Used to discount liver disease

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44
Q

Name 5 causes of DIC

A
  1. trauma, burns, surgery
  2. sepsis
  3. ABO mismatch: haemolytic transfusion reaction
  4. obstetric complications (pre-eclampsia, abruption)
  5. Malignancy
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45
Q

How are PTT, aPTT and TT affected in DIC?

A

All are raised

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46
Q

what does heparin bind to and potentiate?

A

anti-thrombin 3

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47
Q

which CFs does LMWH inhibit?

A

CF Xa only

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48
Q

How is heparin and LMWH excreted?

A

renal excretion

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49
Q

what can be used to reverse heparin?

A

protamine sulphate

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50
Q

prior to surgery, when should heparin/LMWH be stopped?

A

the evening before surgery

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51
Q

when is fondaparinux preferred to LMWH?

A

in ACS (unstable angina and NSTEMI)

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52
Q

Give 2 indications for warfarin therapy?

A

VTE

stroke

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53
Q

describe early features of haemachromatosis

A

occurs in a middle aged man with:

fatigue
arthralgia
weakness

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54
Q

Describe late features of heamachromatosis

A

slate grey skin, liver failure, diabetes

‘they are known as bronzed diabetics’

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55
Q

How is heamachromatosis managed ?

A

Regular venesection

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56
Q

Describe iron studies in haemachromatosis?

A

High: iron, ferritin, transferrin saturation

Low: iron binding capacity

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57
Q

What Hb level warrants an acute transfusion?

A

Hb<70

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58
Q

Name 4 causes of microcytic anaemia?

A 
"TAILS" 
Thalassemia - affects globin chains 
Anaemia of chronic disease 
Iron deficiency - most common 
Lead poisoning - affects porphyrin 
Sideroblastic anaemia
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59
Q

What is the underlying cause of microcytic anaemia?

A

reduced haemoglobin production

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60
Q

Give 4 specific signs of iron deficiency

A

Nails: koilonychias (nail spooning)

Mouth: angular stomatitis, atrophic glossitis

Throat: post cricoid webs (Plummer vinson syndrome in PM woman)

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61
Q

How does the body try to compensate for iron deficiency?

How can this be picked up on a test?

A

High total iron binding capacity

the body tries to compensate for the lack of iron by increasing transferrin and therefore the iron carrying capacity of blood

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62
Q

Name 4 presenting symptoms of anaemia

A

exertional SOB
palpitations
general fatigue
syncope

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63
Q

Name 2 specific signs of iron deficiency anaemia seen on FBC

A
  1. pencil poikilocytosis - abnromally shaped RBCs

2. target cells

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64
Q

in suspected iron def anaemia, what should always be screened for? why?

A

Coeliac disease

occurs in the colon, where iron is absorbed from
can be the cause of malabsorption

also colon cancer in old men

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65
Q

what constitutes iron replacement therapy?

A

ferrous fumerate or sulphate 200mg TDS

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66
Q

What needs to be done for ALL men who present with an iron deficiency anaemia?

A

urgent OGD and colonoscopy

could be colorectal cancer

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67
Q

describe 4 causes of sideroblastic anaemia? (its rare)

A

primary: X linked condition

secondary:
chemotherapy, lead poisoning, anti-TB drugs

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68
Q

which cause of microcytic anaemia is associated with ineffective erythropoiesis and problems with the porphyrin ring?

A

Sideroblastic anaemiea

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69
Q

describe total iron binding capacity in cases of sideroblastic anaemia?

A

it is normal… lack of iron isn’t the problem

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70
Q

describe the presentation of thalassemias?

what differentiates them from anaemias?

A

they present as microcytic anaemias

BUT- unlike anaemias, they have normal iron levels

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71
Q

what is the underlying problem in thalassemia?

A

defective production of porphyrin rings

Porphyrin is an essential component of Hb production

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72
Q

In an adult, name the components that make up a haemoglobin molecule?

A

Haem:

  • Fe2+
  • porphyrin ring

globin

  • 2 alpha chains
  • 2 beta chains
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73
Q

what mutation causes alpha thalassemia?

where does this mutation occur?

A

a deletion on chromosome 16

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74
Q

How does alpha thalassemia present?

A

It depends on how many copies of the alpha gene have been affected.

each person has 4 copies of the gene- symptoms experienced will depend on how many of the 4 are affected

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75
Q

describe α+ thalassemia trait?

what are the clinical manifestations?

A

1/4 copies of the gene have been deleted

asymptomatic

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76
Q

describe α0 thalassemia trait?

what are the clinical manifestations

A

2/4 copies of the gene have been deleted

clinical: asymptomatic, mild anaemia, hypochromic RBCs and Heinz bodies

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77
Q

What are Heinz bodies and why do they occur?

A

they are accumulations of tetramers of B globin chains

the lack of production of alpha chains in alpha thalassemia means the beta chains have nothing to bind to… they accumulate and are known as heinz bodies

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78
Q

what is HbH disease (or α Thalassemia)?

A

When 3/4 genes have been deleted

called HbH disease due to the increased production of abnormal Hb chains

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79
Q

describe symptoms of HbH disease

A

highly variable
general symptoms of anaemia
symptoms of chronic haemolysis: jaundice, leg ulcers, hepatosplenomegaly
growth retardation, iron overload, gallstones

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80
Q

How is HbH managed?

A

depends on severity

mild: folic acid supplementation
moderate: intermittent transfusion
severe: regular transfusions and splenectomy if severe

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81
Q

what is Hb barts hydrops fetalis?

A

when all 4/4 copies of the gene are deleted

there is no functional alpha chains

results in intra uterine death

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82
Q

compare the types of mutations seen in alpha and beta thalassemias and also on which chromosomes

A

alpha: deletion on chromosome 16
beta: point mutation on chromosome 11

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83
Q

what do Β+ and β0 denote?

A

B+ - reduced production of beta chains

B0- absent production of beta chains

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84
Q

which type of beta thalassemia a patient has is based on clinical severity rather than how many genes are affected.

name the 3 forms of B thalassemia

A
  1. B thalassemia trait - asymp or mild anaemia
  2. B thalassemia intermedia - occasional transfusions but not reliant
  3. B thalassemia major - dependant on transfusions
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85
Q

In B thalassemia major in infants, describe HbF levels

A

HbF is very high- as HbF is made from 2 alpha and 2 gamma chains, it is not dependant on the dysfunctional beta chains.

therefore, levels of HbF are very high to compensate

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86
Q

what is the main cause of megaloblastic macrocytic anaemia?

A

Vit B12 and folate deficiency

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87
Q

which will the body become deficient in 1st; B12 or folate?

A

Folate

the body store of folate is much smaller than that of B12

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88
Q

what is the underlying cause of megaloblastic macrocytic anaemia?

A

impaired DNA synthesis and nuclear maturation

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89
Q

name a complication in the nervous system that can occur in B12 deficiency

A

subacute combined degeneration of the cord

degeneration of the corticospinal tract and DCML pathways

loss of pain, fine touch and proprioception

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90
Q

why should folate not be given without also giving B12?

A

failing to provide B12 may precipitate or worsen subacute combined degeneration of the cord

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91
Q

what differentiates a megaloblastic anaemia from a non-megaloblastic anaemia?

A

megaloblastic anaemias show hypersegmented neutrophils

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92
Q

in macrocytosis, why are the RBCs larger than they should be?

A

there is defective nuclear maturation and DNA synthesis, so RBCs don’t divide as they properly should

this results in growth without division prior to nuclear expulsion

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93
Q

compare absorption sites of vit B12 and folate

A

vit B12 - absorbed in terminal ileum

Folate - absorbed in the duodenum

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94
Q

in addition to vit B12 deficiency, what can pernicious anaemia also present with?

A

a peripheral neuropathy

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95
Q

compare the sensitivities and specificities of anti-gastric parietal cell and anti-intrinsic factor

A

anti gastric parietal cell - sensitive but not specific

anti-intrinsic factor- specific but not as sensitive

anti-intrinsic is still used as the antibody of choice to diagnose pernicious anaemias

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96
Q

what can be seen on bone marrow biopsy in patients with low B12/folate

A

megaloblasts

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97
Q

give 4 causes of non-megaloblastic macrocytosis.

what makes marrow failure as a cause different from the other 4?

A
  1. pregnancy
  2. alcohol abuse
  3. liver disease- target cells on blood film
  4. hypothyroidism

marrow failure causing non-megaloblastic macrycytosis will always result in anaemia

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98
Q

describe what is going on in spurious macrocytosis/ reticulocytosis?

A

reticulocytosis describes increased volumes of circulating reticulocytes due to increased red cell production

the reticulocytes appear larger than normal RBCs and therefore increase MCV

99
Q

name 4 situations when spurious macrocytosis is seen

A
  1. haemorrhage
  2. haemolysis
  3. treatment of anaemia
  4. thalassemia (this will cause reticulocytosis but not macrocytosis)
100
Q

where does extravascular haemolysis occur? (2 places)

A

the spleen

the liver

101
Q

name the 3 hallmarks of extravascular haemolysis

A
  1. splenomegaly
  2. raised unconjugated bilirubin
  3. urobilinogen
102
Q

name signs of intravascular haemolysis

A

increased lactate dehydrogenase
schistocytes
decreased haptoglobins
haemoglobinuria

103
Q

name 4 causes of extravascular haemolysis

“SHAT”

A

Sickle cell disease
Heredity spherocytosis
Autoimmune haemolytic anemia
Thalassemia

104
Q

name causes of intravascular haemolysis

A 
ABO mismatch 
severe malaria 
microanggiopathic haemolytic anemia 
G6PD deficiency
drug induced
105
Q

what is an important component to ask about in haemolysis consultations

A

any recent foreign travel

106
Q

What is a Coombs test used for?

A

to detect antibodies that attack the surface of RBCs

ie- an AI cause of haemolysis

107
Q

what is the difference between hot and cold autoimmune haemolytic anaemias?

A

hot: antibodies bind and cause haemolysis at room temperature
cold: antibodies bind and cause hamolysis when exposed to the cold

108
Q

cold autoimmune haemolysis can occur secondary to what?

A

lymphoma, leukemia, IgM

109
Q

What does a G6PD deficiency result in?

A

results in reduced NADPH production which means that cells cannot handle oxidative stress

the cells are unable to produce glutathione

110
Q

what happens to RBCs with G6PD deficiency when they are exposed to oxidative stress?

A

the red cells undergo intravascular haemolysis

111
Q

IN G6PD deficiency, the rapid onset jaundice and anaemia occurs after exposure to what 4 main things?

A
  1. henna
  2. drugs: aspirin
  3. acute illness
  4. broad beans
112
Q

on blood film, what is most likely diagnosis if there is presence of hienz bodies and bite and blister cells?

A

G6PD deficiency

113
Q

How is G6PD deficiency diagnosed?

A

Enzyme assay- shows reduced G6PD

114
Q

what is the most likely diagnosis in a young child with a FHx of splenectomy who has jaundice, splenomegaly, mild anaemia and failure to thrive?

A

Hereditary spheocytosis

115
Q

what is the problem in hereditary sperocytosis?

A

RBCs are too spherical in shape

results in sequestration in the spleen and extravascular heamolysis

116
Q

what test diagnoses hereditary spherocytosis

A

EMA binding test

117
Q

what is the underlying cause of anaemia of chronic disease?

A

develops in diseases associated with chronic inflammation

118
Q

How can CKD cause anaemia of chronic disease?

what kind of anaemia will this cause?

A

reduced EPO production, so reduced RBC

normocytic, normochromic

119
Q

what will be high and what will be low in anaemia of chronic disease?

A

High: ferritin

Low: iron, TIBC

this differs from iron deficiency anaemia, where ferritin levels will also be LOW

in anaemia of chronic disease, the body is trying to ‘hide’ the iron from the disease process to deny it nutrition

120
Q

what is a lymphoma?

A

a malignant proliferation of lymphocytes that accumulate in lymph nodes

cause lymphadenopathy and can infiltrate other tissues

121
Q

describe the itch felt in lymphoma

A

an itch without a rash

122
Q

what causes painless and persistent, soft, rubbery lymphadenopathy?

A

lymphoma

123
Q

what is the diagnostic investigation in lymphoma

A

excisional node biopsy

124
Q

what are malignant proliferations of B cells known as

A

Hodgkin’s lymphoma

they make up around 10% of lymphomas

125
Q

what cell is pathognomic for Hodgkin’s lymphoma?

A

reed steenberg cell

126
Q

what 3 things indicate a poor prognosis for Hodgkins lymphoma?

A

fever, night sweats and weight loss

127
Q

what is the differentiating feature for Hodgkin’s lymphoma

A

lymph node painful on drinking alcohol

128
Q

what is the most common type of Hodgkin’s lymphoma?

A

nodular sclerosing

129
Q

name 4 risk factors for Hodgkin’s lymphoma?

A
  1. family history
  2. post-transplant
  3. EBV
  4. western population
130
Q

who is typically affected by Hodgkins lymphoma?

A

young adults (15-30) or old adults

131
Q

how is Hodgkins lymphoma managed

A

managed with curative intent

chemotherapy +/- radiotherapy +/- anti CD30

132
Q

what are 2 side effects of chemotherapy used to treat HL?

A

bone marrow suppression

risk of AML

133
Q

name the 4 chemotherapy drugs used to treat HL?

ABVD

A

Adriamycin
Bleomycin
Vincristine
Dacarbazine

134
Q

what are any lymphomas that are not reed steenberg positive known as?

A

Non-hodgkins lymphoma

135
Q

what is the most common type of NHL?

A

B cell NHL

NHL can be B cell or T cell in nature

136
Q

what are the greatest risk factors for a NHL?

A

immunosuppression

infection (HIV, EBV, malaria)

137
Q

how are B cell proliferations in NHL identified?

A

CD20+ antigen expression

138
Q

is extra nodal disease more common in NHL or HL?

A

NHL

139
Q

compare the grade of NHL in follicular types with mantle types?

A

Follicular NHL: low grade

Mantle NHL: high grade

140
Q

who is burkitt’s NHL most commonly seen in?

A

African children who are EBV +ive

141
Q

what is waldeyers ring in NHL?

what does it cause?

A

a ring of lymphoid tissue found in the throat

causes difficulty breathing

142
Q

typically, what age of patient does NHL tend to affect?

A

typically affects older people

in comparison to HL which can affect 15-30 year olds

143
Q

is NHL curative?

what does this mean clinically for patients?

A

no - management can only induce remission, it will never be cured

patients will tend to have a chronic relapse- remitting course

144
Q

in NHL, is high grade or low grade more likely to respond to chemotherapy?

A

High grade - tends to be associated with longer periods of remission

145
Q

what is rituximab?

A

an anti CD 20 monoclonal antibody

146
Q

compare the prognosis of high and low grade NHL?

A

low grade has a better prognosis

high grade has a poorer prognosis but a higher cure rate

147
Q

which type of NHL shows as a “starry sky” on lymph node biopsy?

A

Burkitts lymphoma

148
Q

how many cell lines are involved in each leukemia?

what does this mean in terms of mutations?

A

just the one

there is malignant monoclonal expansion of a single cell line

this means the entire population stems from the same stem cell and are associated with the same mutations

149
Q

what 4 factors is leukaemia classification based on?

A
  1. onset: acute or chronic
  2. immunophenotyping: antigen expressed
  3. cell lineage: lymphoid or myeloid
  4. cytogenetics: mutations present in the cells
150
Q

what is the difference in definition between acute and chronic leukaemia?

A

difference is if the cells dividing are matured or not…

acute leukaemia: uncontrolled proliferation of immature WBCs

chronic leukaemia: uncontrolled proliferation of partially mature WBCs

151
Q

what is the most common childhood cancer?

A

Acute lymphocytic leukaemia (ALL)

affects 2-8 year olds

152
Q

which acute leukaemia is described as a malignant proliferation of B or T cells that results in arrested maturation and uncontrolled proliferation of immature precursor cells (called blasts) within the bone marrow?

A

acute lymphocytic leukaemia

153
Q

what are the 2 main risk factors for acute lymphocytic leukaemia

A

downs syndrome

irradiation (especially in pregnancy)

154
Q

name the 4 main sites of infiltration in ALL?

A

CNS
Lymph nodes
Tesits
Liver/spleen

155
Q

describe symptoms in ALL that occur secondary to marrow failure

A
  1. anaemia- normocytic, normochromic
  2. thrombocytopenia: purpura, easy bruising, mucosal bleeding
  3. leukopenia: not feeling well, recurrent infections (throat and ear)
156
Q

what is strange about WCC in ALL?

A

there appears to be a leukocytosis (high WCC)

although there appears to be a high WCC, the cells are non-functioning

along with the low neutrophils, this makes patients susceptible to infection

157
Q

what is seen on blood film and bone marrow biopsy in ALL?

A

> 20% blasts

158
Q

why may a CT head be indicated in ALL?

A

to look for infiltration in the head

they may cause palsies or CNS infiltration

159
Q

how is ALL managed?

what is the cure rate

A

managed with curative intent with long duration chemotherapy (2/3 years)

cure rate >90% in children

160
Q

compare the cell lines involved in ALL vs acute myeloid leukaemia

A

ALL: B or T cell lineage

AML: myeloid cell lineage

161
Q

AML can occur secondary to chemotherapy treatment for other malignancies.

In particular, which chemotherapy drugs are most likely to cause this?

A

cyclophosphamide

mephalin

162
Q

name the main differentiating feature in terms of infiltration in ALL vs AML?

A

AML has no CNS infiltration, ALL does

163
Q

compare the age of patients in ALL vs AML?

A

ALL - kids

AML - adults, more common in males

164
Q

In AML, what are diagnostic on blood film and marrow biopsy?

A

Auer rods

165
Q

how is AML managed?

give a side effect caused by this treatment

A

intense chemotherapy given

complete marrow suppression

166
Q

what is the most common type of leukaemia in adults?

A

chronic lymphocytic leukemia

167
Q

which type of cells are almost always involved in chronic lymphocytic leukaemia?

A

almost always B cells involved

they escape apoptosis and undergo cell cycle arrest in G0/G1

168
Q

which 2 things is CLL associated with

A
  1. autoimmune haemolytic anaemia

2. idiopathic thrombocytopenic purpura

169
Q

what are B symptoms

A

they are systemic symptoms seen in leukemias and lymphomas

night sweats, fever and weight loss

170
Q

how can CLL sometimes present

A

asymptomatic… may be an incidental finding on FBC

171
Q

what can be seen on FBC in CLL?

A

normocytic, normochromic anemia
low neutrophils and platelets
high WCC
smudge cells/smear cells seen

172
Q

in terms of management, which leukaemia tends to follow the rule of 1/3rds?

A

CLL

1/3 dont progress
1/3 will progress over time
1/3 are actively progressing at presentation

173
Q

how are those that are actively progressing in CLL managed?

A

chemotherapy +/- stem cell transplant

174
Q

what is the pathognomonic mutation in chronic myeloid leukaemia?

A

philadelphia chromosome 9;22

175
Q

which leukaemia can cause gout? why?

how is this reflected in blood tests?

A

chronic myeloid leukaemia

due to increased red cell turnover

high urate

176
Q

why may patients with CML present with abdominal pain and bloating?

A

massive splenomegaly

177
Q

what is 1st line management of CML?

A

tyrosine kinase inhibitors (imatinib)

they are not curative but completely control the disease

178
Q

which virus can precipitate an aplastic crisis?

A

Parovirus B19

179
Q

What happens to HbS cells when they are deoxygenated?

A

the HbS polymerises and distorts the shape of the RBC

180
Q

what autosomal pattern is sickle cell?

A

autosomal recessive

181
Q

name 6 causes for polymerisation in sickle cell disease

A 
hypoxia 
infection
stress and fatigue 
dehydration 
acidosis 
cold exposure
182
Q

name 2 consequences of RBC polymerisation in sickle cell disease

A
  1. small vessel occlusion

2. sequestration of distorted RBCs in liver and spleen, leading to extravascular haemolysis

183
Q

explain the difference in HbS concentration in HbS trait and disease?

which is homozygous and which is heterozygous?

A

sickle cell trait: HbS makes up <50% of total Hb concentration

sickle cell disease: HbS makes up the majority of Hb concentration

sickle cell trait= heterozygous

sickle cell disease= homozygous

184
Q

how is sickle cell disease diagnosed?

A

haemoglobin electrophoresis

185
Q

why is sickle cell disease more common in African populations

A

the sickle cell trait offers some protection against malaria

186
Q

name the 3 crises that can occur in sickle cell crises

A

aplastic crisis
sequestration crisis
vaso-occlusive crisis

187
Q

which sickle cell crisis causes temporary bone marrow failure

A

aplastic crisis - causes sudden onset marrow failure due to infection with parvovirus B19

188
Q

which patients is sequestration crisis most common in?

A

usually children - they have not undergone splenic atrophy

189
Q

when is a vaso occlusive crisis considered severe?

A

when the chest is involved or the is neurological involvement (ie- seizures, strokes)

190
Q

in patients with sickle cell, which vaccination is given every 5 years?

A

pneumococcal

191
Q

in patients with recurrent sickle cell crisis, what can be given?

How does it work?

A

hydroxyurea (hydroxycarbamide)

it increases the production of HbF, which dilutes out the HbS and reduces severity of crisis

192
Q

which type of sepsis is a common complication of chemotherapy?

A

neutropenic sepsis

193
Q

what are the antibiotics of choice in neutropenic sepsis?

when should they be started?

A

tazobactam and piperacillin

start them ASAP, dont wait for FBC

194
Q

what is the name of the group of disorders that continually activate the JAK 2 pathway?

A

chronic myeloproliferative disorders

195
Q

what does constant activation of the JAK 2 pathway result in clinically?

A

normally, JAK 2 is only activated when additional blood cell production is required

in chronic myeloproliferative disorders, it is constantly switched on, meaning there is an increase in blood cell production (which type of blood cell depends on the specific disorder)

196
Q

what is the most common meyloproliferative disorder?

in which blood cell is there an excessive production of?

A

polycythemia vera

excessive production of RBCs

197
Q

which 2 cancers can cause secondary polycythemia vera due to reduced EPO production

A

hepatic or renal cancers

198
Q

name symptoms of polycythemia vera

A
  1. hyper viscosity: venous or arterial thrombosis, lethargy, confusion, headache/TIAs, visual disturbance
  2. splenomegaly: abdominal pain and distension
  3. diagnostic: itch after a warm shower or bath (due to excessively activated basophils)
199
Q

what can be seen on marrow biopsy in polycythemia vera

A

erythroid hyperplasia

200
Q

what is 1st line management in polycythemia vera?

what is 2nd and 3rd line?

A

1st: venesection

2nd and 3rd: aspirin and hydroxyurea

201
Q

what type of blood cell is increased in essential thrombocytopenia?

A

platelets (>450)

202
Q

what does essential thrombocytopenia result in?

A

thrombosis OR

bleeding (due to utilisation of all VWF)

203
Q

how can essential thrombocytopenia present?

A 
thrombosis (DVT/PE/TIA) 
stroke
recurrent miscarriages 
digital ischemia 
episodic swelling, erythema and shooting pains in the limbs
204
Q

what is seen on marrow biopsy in essential thrombocytopenia?

A

hypercellular with megakaryocytes

205
Q

which myeloproliferative disorder presents with bone marrow fibrosis and splenomegaly?

A

primary myelofibrosis

it is the rarest and most severe myeloproliferative disorder

splenomegaly due to extramedullary haematopoesis

206
Q

why is there splenomegaly and hepatomegaly in a patient with myelofibrosis

A

they have bone marrow failure and pancytopenia

so the haematopoesis must occur extramedullary, in the liver and spleen

207
Q

which myeloproliferative disorder presents similar to lymphoma?

A

primary myelofibrosis

presents with :
B symtoms (fever, night sweats and weight loss)
fatigue
symptoms of marrow failure

208
Q

what can be seen on blood film in primary myelofibrosis?

A

leukoerythroblastosis and tear shaped RBCs

209
Q

what is the most common cause of inherited thrombophillia?

A

factor 5 leiden

210
Q

what does factor 5 Leiden cause?

A

protein C resistance

this predisposes to thrombophillia

211
Q

in antibody production, which has a higher production rate? heavy chains or light chains?

what does this mean?

A

light chains have a higher production rate

means there are some free circulating light chains in the body

212
Q

what is the difference between polyclonal and monoclonal expansion?

A

polyclonal expansion is a normal response to infection. there is an expansion of a variety of B cell populations

monoclonal expansion= paraprotein disease.
there is expansion of a single B cell population, resulting in a single antibody produced

213
Q

what can be seen on blood film in paraprotein disease?

A

Roulex formation

214
Q

name 5 causes of paraprotein disease?

A 
monoclonal gammopathy of undetermined significance (MGUS)
myeloma 
amyloidosis 
B cell lymphoma 
chronić lymphocytic leukemia
215
Q

what is the definition of multiple myeloma

A

an malignant proliferation of B cells within the bone marrow

216
Q

how are multiple myelomas classified?

A

based on the antibody and type of light chain produced

217
Q

in multiple myeloma, what local effects on the bone does increased release of antibodies and light chains have

A

increased breakdown of bone to form osteolytic lesions - results in hypercalcemia

infiltration of the marrow- resulting in bone marrow failure

218
Q

name 2 effects increased production of antibody and light chain have in multiple myeloma

A

increased viscosity

immunosuppression- reduced production of effective antibodies

increased viscosity can cause a stroke

219
Q

in multiple myeloma, where do light chains become deposited?

what does this cause?

A

light chains deposited in the kidney

this causes a cast nephropathy and a decline in renal function

220
Q

what does CRABBI stand for in multiple myeloma?

A 
Calcium (up) 
Renal (impaired) 
Anaemia (marrow failure) 
Bleeding 
Bones (increased breakdown) 
Infection
221
Q

in multiple myeloma, where is the bone pain usually felt

A

the back- it can cause pathological crush fractures

222
Q

who should myeloma always be considered in

A

patients >50 with an AKI and hypercalcaemia or anaemia

223
Q

what type of anaemia would be seen in multiple myeloma

A

normochromic normocytic anaemia

224
Q

what would be seen on urine electrophoresis in multiple myeloma

A

bence jones protein

225
Q

how is multiple myeloma managed?

A

not curative- its a relapsing, remitting disease

younger patients get stem cell transplant

226
Q

what is monoclonal gammopathy of unknown significance?

A

a paraproteinemia without any pathological consequences

there is no evidence of myeloma
no bone pain, infections, marrow failure

227
Q

what is the diagnostic finding of amyloid light chain amyloidosis?

A

apple green bifringence with Congo red stain

228
Q

how is amyloid light chain amyloidosis managed?

A

effectively no treatment- will die within a couple of years of diagnosis

229
Q

which type of paraprotein disease will cause a raised IgM on electrophoresis?

A

waldenstroms macroglobinaemia

main pathological outcome of this is IgM mediated hyper viscosity

230
Q

what is the one inherited cause of pancytopenia

how is it inherited?

A

fanconi anaemia

autosomal recessive

231
Q

what type of leukaemia can fanconi anaemia predispose to?

A

acute myeloid leukaemia

232
Q

in a transfusion reaction, what sign in a patient would you find most concerning?

A

hypotension

233
Q

what is the diagnostic test for sickle cell disease?

A

haemoglobin electrophoresis

234
Q

which GI condition classically causes a B12 deficiency?

why?

A

crohns disease causes B12 deficiency

due to terminal ileal disease impairing V12 absorption

235
Q

what is the most common cause of an isolated thrombocytopenia?

A

ITP

236
Q

describe the differences in symptoms between transfusion associated cardiac overload (TACO) and transfusion related acute lung injury (TRALI)?

A

TACO: hypertensive, raised JVP, afebrile, S3 present

TRALI: hypotensive, pyrexia, normal/unchanged JVP

237
Q

what is the 1st line tx for transfusion associated circulatory overload?

A

furosemide

TACO can be prevented in the 1st instance by giving prophylactic diuretics to high risk patients

238
Q

which medication can be used to reduce the incidence of complications of sickle cell disease?

A

hydroxycarbamide

239
Q

what is the main way to differentiate between a sequestration crisis and a haemolytic crisis?

A

both cause anaemia and increased reticulocytosis

haemolytic crisis is rarer, and would present with pain and jaundice

sequestration crisis is more common and patients are often asymptomatic

240
Q

in myeloma, only in which conditions is alkaline phosphate usually raised?

A

usually only elevated in metastatic disease

Ca is raised in all myelomas, Alk phos and phosphate normal unless mets

241
Q

what finding is DIC associated with on blood film?

A

schistocytes

242
Q

which fluroquinone is a common cause of haemolysis in patients with G6PD deficiency?

A

ciprofloxacin

243
Q

which is the only type of leukemia that causes a massive splenomegaly?

A

chronic myeloid leukaemia

AA Y4 Finals cards NE (40 decks)

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