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FLASH FINALS > Haematology > Flashcards

Haematology Flashcards

1
Q

Primary haemostasis sequence

A

Vessel damage -> exposes sub-endothelial collagen - platelets bind via VWF (via Glycoprotein 1b)

Following that: activation of platelets, release of ADP and TXA2 which stimulate platelet aggregation and form the plug

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2
Q

Causes of failure (primary haemostasis)

A

Vascular factors
Low or absent VWF
Low or absent platelets

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3
Q

Vitamin K dependent clotting factors

A

2,7,9,10 All produced in the liver

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4
Q

Secondary haemostasis =

A

production of fibrin to form more stable clot.

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5
Q

Extrinsic pathway (most important in the production of fibrin) measured time

A

PROTHROMBIN TIME (PTT)

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6
Q

Intrinsic pathway (important in amplifying the response) measured time:

A

ACTIVATED PARTIAL PROTHROMBIN TIME (aPTT)

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7
Q

Failure of intrinsic pathway can cause:

A

Bleeding into muscles and joints

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8
Q

Common pathway (forms THROMBIN) measured time:

A

Thrombin time (TT)

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9
Q

Anticoagulant proteins

A

Tissue factor inhibitor
Anti-thrombin 3
Protein C/S (inhibit factors 5&8)

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10
Q

What do vascular disorders typically present as failure of : primary or secondary hemostasis (and how do they present?)

A

Primary: (bleeding, purpura, mucosal bleeding)

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11
Q

Hereditary Haemorrhagic Telangiectasia (HHT)

A

Autosomal dominant condition.
Telangiectasia throughout body, especially on fingers, nose and surface of organs
Px. as upper GI bleed

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12
Q

Scurvy bleeding ?

A

Peri-follicular

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13
Q

Bruising syndrome px?

A

Tingling in arms and legs followed by painful easy bruising

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14
Q

Normal platelet count

A

150-400

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15
Q

Causes of decreased production of platelets

A 
Anything that results in marrow suppression: 
Myelofibrosis
Myelodysplasia
Aplastic anaemia
Leukaemia etc.
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16
Q

Myelosuppressive drugs (2 therapies, 1 drug)

A

Chemotherapy, radiotherapy, Methotrexate

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17
Q

Causes of increased destruction or use of platelets - conditions

A

ITP, TTP, HUS, DIC
Autoimmune: SLE, APLS
Hypersplensism: CCF, Cirrhosis, SLE

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18
Q

Drug causes of increased destruction or use of platelets? -

A

Heparin, antibiotics (penicillin), sulphonamides, furosemide, digoxin, valproate

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19
Q

ITP px./ mx.

A

AI condition with antibodies against platelets
Bloods: bleeding time increased
Platelets low
Bone marrow biopsy: increased megakaryocytes

Epistaxis, menorrhagia, easy bruising

Mx. Only if severe;

1) steroids
2) splenectomy
3) Azathioprine

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20
Q

TTP - haematological emergency px. mx.

A

Fever, AKI, Mucosal bleeding, fluctuating consciousness.

Blood film: Schistocytes

Mx. Plasmapheresis
Steroids + Ig
Normal coagulation

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21
Q

Abnormal platelets - bloods
Coagulation
Platelet count
Bleeding time

A

Coagulation: normal.
Platelet count: normal.
Bleeding time: increased

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22
Q

Von Willebrand disease (autosomaml dominant condition) bloods:

A

Coagulation: increased aPTT, bleeding time.
Serum: low VWF, low factor 8. (VWF needed for factor 8)

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23
Q

VWB disease mx.

A

Mild: Desmopressin

Severe haemorrhage: VWF concentrates

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24
Q

What medication class should be avoided in VWBD

A

NSAIDS

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25
Q

Haemophilia A/B chromosome

which is more common

A

8/9

A

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26
Q

Haemophillia blood results

A

Coagulation: isolated increase in aPTT
Serum: low factor 9 or 8

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27
Q

Haemophillia Mx:

A

General: AVOID NSAIDS, IM injections

Active bleeding = active infusions

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28
Q

Disseminated intravascular coagulation px.

A

MIXEd thrombosis and coagulation defect.
Thrombosis: multi-organ failure
Bleeding: large widespread bruising
oozing blood from mouth nose and cannulation sites

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29
Q

DIC causes:

A

Sepsis, trauma burns and surgery, ABO mismatch, Obstetric causes: Pre-eclampsia, abruption.

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30
Q 
DIC bloods: 
•D Dimers:  
•Platelets:
•Bleeding time: 
•PTT, APTT, TT:
A

D Dimers: high.
Platelets: low.
Bleeding time: increased.
PTT, APTT, TT: increased

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31
Q 
Summary - causative pathologies for: 
Increased bleeding time: 
•	Prolonged PTT: 
•	Prolonged APTT: 
•	Prolonged TT: 
•	Increased everything:
A

Increased bleeding time: platelet issues.
- Prolonged PTT: liver disease / warfarin.
- Prolonged APTT: haemophillia, VWD, heparin.
- Prolonged TT: heparin, advanced liver disease.
Increased everything: DIC.

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32
Q

Heparin MoA

A

POTENTIATES antithrombin 3

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33
Q

Clotting factors targeted by potentiated ATIII depend on type of heparin
Unfractioned:
LMWH:

A

UF: inhibits 2,9,10,11,12
LMWH inhibits 10a only

Renal excretion

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34
Q

Heparin which is more markedly increased : aPTT or PT

A

aPTT

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35
Q

Monitoring LMWH/UF Heparin

A

NONE REQUIRED

UFH: aPTT

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36
Q

Heparin complications

and long term..

A 
Bleeding
HYPERKALAEMIA
Heparin induced thrombocytopenia
LONG term:
OSTEOPOROSIS
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37
Q

Heparin reversal drug:

A

Protamine sulphate (stopping alone is usually enough however)

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38
Q

Fundoparinex:
Target:
Route:
Indications:

A

Inhibits factor 10
S/C injection also
Generally same as LMWH but preferred for anti-coagulation in ACS.
Lower risk of HIT

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39
Q

Warfarin: inhibits?

A

Vit K reductase which inhibits the production of factors 2,7,9,10

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40
Q

Warfarin effects on coagulation:

A

Increased aPTT and PT, PT more profound than aPTT

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41
Q

CIs for Warfarin

A 
Pregnancy 
Non-thromboembolic strokes
Severe uncontrolled hypertension. 
Severe liver or renal disease 
Peptic ulcer disease or GI bleeds.
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42
Q

Drugs that potentiate warfarin:

A 
Alcohol 
Omeprazole
Erythromycin 
Ciprofloxacin 
Valproate
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43
Q

Drugs that reduce warfarin effects:

A

Phenytoin
Carbamazepine
Rifampicin
(these are all P450 inducers)

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44
Q

Warfarin: Medical Potentiators/inhibitors

A

Potentiate: febrile illness
hyperthyroidism, cardiac failure, liver/renal disease

Inhibitors: pregnancy, hypothyroidism

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45
Q 
Warfarin reversal 
INR >5, <6 
INR 6-8
INR > 8 w/little bleeding 
INR > 8 w/severe bleeding
A

INR >5, <6: Reduce dose
INR 6-8 w/little bleeding: Stop warfarin - restart at < 5
INR > 8 w/ little bleeding: Stop warfarin, oral vit K. restart <5
INR > 8 w/severe bleeding - Stop warfarin, Prothrombin complex concentrate. Beriplex FFP if available, IV vit K

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46
Q

Do NOACs require monitoring

A

NO

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47
Q

Virchow’s triad

A

Stasis
Hypercoagulability
Vessel wall damage

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48
Q

Neutrophillia causes:

A

Acute inflammation/infection/haemorrhage, pregnancy, drugs: steroids (due to reducing marginization - the process in which neutrophils leave the blood.

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49
Q

Neutropenia causes

A

Aplastic anaemia, pancytopenia, drugs: carbimazole and clozapine

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50
Q

Eosinophils raised in ?

A

Churg-strauss, atopy, PARASITIC INFECTIONS, HODGKINS

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51
Q

Monocytes - (circulate for a couple days before entering tissues and becoming macrophages) raised in?

A

Chronic bacterial infections, SLE, RA, lymphoma, leakaemia

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52
Q

lymphocytes - raised in?

A

infection, malignancy, hyposplenism

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53
Q

How much iron is stored in the body (grams)

A

4 g

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54
Q

Female normal Hb:

Pregnant female Hb:

A

> 120

>110

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55
Q

What is haematocrit a measure of?

A

how much of the volume of blood is RBCs - expressed as a percentage.

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56
Q

At what Hb do you transfuse a pt.

A

> 70

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57
Q

What are microcytic hypochromic anaemias caused by:

A

REDUCED HAEMOGLOBIN PRODUCTION

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58
Q

Causes of reduced Hb
Haem group:
Porphyrin ring:
Globin chains:

A

Haem group: Iron deficiency, anaemia of chronic disease
Porphyrin ring: Sideroblastic anaemia
lead poisoning
Globin chains: pyridoxine responsive anaemia

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59
Q

Management of iron deficiency anaemia:

Screen for?

A

Iron replacement - 200mg ferrous sulphate or fumerate TDS.

Coeliac disease

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60
Q

How long should treatment be given, minimum

A

3 months

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61
Q

How long should treatment be given after correction minimum

A

3 months

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62
Q

When to refer for OGD/colonoscopy in IDA

A

Iron deficiency anaemia W/ dyspepsia
ALL MEN with unexplained IDA.
IDA with rectal bleeding or symptoms of CRC
ALL WOMEN NOT MENSTRUATING and iron deficient
IDA not responding to treatment.

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63
Q 
Sideroblastic anaemia (Xlinked condition or 2ry to chemo,lead poisoning or anti-TB drugs) - 
part of Hb it affects?
A

Porphyrin ring

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64
Q

When should sideroblastic anaemia be considered a diagnosis
Iron studies:
Mx:

A

When microcytic anaemia does not respond to treatment
HIGH IRON FERRITIN AND TRANSFERRIN . Normal TIBC
Treat cause, regular blood transfusions

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65
Q

Thalassaemia effect on Hb production

A

Defective production of globin chains.

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66
Q

a-globin gene chromosome

A

16

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67
Q

α+ thalassemia trait:

A

1/4 copies of gene deleted - asymptomatic

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68
Q

α0 thalassemia trait

Key finding on blood film

A

2/4 copies of gene deleted
Clinical: asymptomatic
FBC: mild anaemia
Blood film: HEINZ BODIES

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69
Q

α Thalassemia (HbH disease)

px

A

3/4 copies lost. Causes increased production of HbH (abnormal haemoglobin)
Iron: normal or increased

General symptoms of anemia.
Symptoms of chronic haemolysis: jaundice, leg ulcers, hepatosplenomegaly.
Others: growth retardation, gallstones, iron overload

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70
Q

Diagnostic test for HbH

A

HPLC - high performance liquid chromatography.

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71
Q

Mx.

A

Folic acid supplementation -> to support increased erythropoiesis.
Mild: intermittent transfusion
Severe: regular transfusion

72
Q

Hb Barts - hydrops fetalis

A

4/4 copies lost

No functional alpla Hb = intra-uterine death

73
Q

β Thalassemia chromosome

A

11

74
Q

B chain only present in HbA, therefore:

A

Reduced HbA production and compensatory increases in other Hb

75
Q

β thalassemia intermedia
thalassemia intermedia is the less severe form of clinically apparent B thalassemia most likely type to be misdiagnosed as IDA

px.
mx.

A

Mild/moderate anaemia +/- splenomegaly

Intermittent transfusions

76
Q 
β Thalassemia major
When does it present 
Ix findings 
FBC: Hb? MCV?
HPLC?

Skull XR: hair on end sign

A

First year of life (failure to thrive, severe anaemia.

HPLC: Very high: HbF.
• High: HbA2.
• Low HbA.

Skull XR: hair on end sign

77
Q

β Thalassemia major Mx.

A

Life long transfusions
Folate supplementation.
- Life long transfusions + Iron chelators -> Deferiprone +/- splenectomy.

-> The main mortality is caused by iron overload from chronic transfusions.

78
Q

Sickle cell pathophysiology

A

Point mutation in codon 6 of B globin gene -> alters structure of Hb -> Hbs. Hbs polymerises if exposed to low oxygen for prolonged periods. This distorts the red cell, damaging the RBC membrane.

79
Q

Precipitants of sickle crisis?

A 
Hypoxia 
Dehydration 
Infection 
Cold exposure
Stress/fatigue
80
Q

Mx. Sickle crisis

A 
Opiate analgesia
hydration 
rest 
oxygen 
(Antibiotics if evidence of infection)
81
Q

Long term Mx. Sickle cell

A

Hyposplenism -> reduce risk of infection, prophylactic penicillin. VACCINATION: pneumococcus,meningococcus, haemophilus
Folic acid supplementation (increased turnover so increased demand)

82
Q

Macrocytosis threshold (MCV)

A

> 100

83
Q

Causes of megaloblastic macrocytic anaemia

A

Vit. B12 and FOLATE DEFICIENCY

84
Q

B12 -> absorbed? via? how long does body store last

A

Absorbed in terminal ileum via intrinsic factor

Store = 2-4 years

85
Q

Folate -> absorbed? how long does body store last

A

Absorbed in the duodenum, a lot smaller store than B12 meaning that folate will become deficient first.

86
Q

Pernicious anaemia -> describe? Auto-antibodies?

A

AUTOIMMUNE ATROPHIC GASTRITIS with reduction OF HCL and INTRINSIC FACTOR. m/c in women in their 40s with other AI conditions.
Anti-parietal cell = sensitive but not specific
Anti-intrinsic factor = specific but not sensitive

87
Q

Common autoimmune condition that can cause B12 deficiency

A

Coeliac disease

88
Q

Acute px of B12 def.

A

SUBACUTE DEGENERATION OF THE SPINAL CORD.

Degeneration of CST and dorsal column.

89
Q

Mx. B12/folate deficiency

A

ID and Tx. underlying cause:
FOLATE: 5mg for 4 months
B12: IM B12 COBALAMIN initially on alternate days then 3 monthly if appropriate.
RULE: folate should not be given ALONE due to failure to provide B12 causing/worsening SACD

90
Q

Causes of non-megaloblastic macrocytosis

All cause an increase in RBC size by altering the red cell membrane.

A

ALCOHOL
pregnancy
HYPOthyroidism
Liver disease

91
Q

What is Reticulocytosis?

A

An increased number of circulating reticulocytes due to increased production of RBCs.

92
Q

When is reticulocytosis seen

A

Haemolysis
Haemorrhage
Treatment of anaemia
Thalassemia (reticulocytosis but not macrocytosis)

93
Q

Haemolysis = breakdown of RBCs before how many days

Bone marrow response =

A

120

Erythroid hyperplasia/reticulocytosis

94
Q

What is extra-vascular haemolysis hallmarked by:
(EV haemolysis occurs in liver and spleen mainly)
Can be physiological or pathological

A

Hepatoplenomegaly
Unconjugated bilirubin
Urobilinogen

95
Q

Intra-vascular haemolysis - always pathological

Hallmarked by?

A 
Schistocytes
Increased LDH
Decreased Haptogglobins 
Haemoglobinaemia/ methealbuminaemia 
haemosidenuria
96
Q

Causes of EV and IV Haemolysis

A

EV = Thalassaemia, sickle cell disease, hereditary spherocytosis, AI haemolytic anaemia

Intravascular: Drug induced, ABO mismatch, G6PD deficiency, severe malaria, MAHA

97
Q

Acquired haemolytic anaemia causes

A

Infection: malaria

Drug-induced, autoimmune haemolytic anaemia.

98
Q

Drug induced haemolytic anaemia
COOMBS postive
COOMBS negative

A

COOMBS positive: Penicillin, cephalosporin

COOMBS negative: rituximab

99
Q

Microangiopathic haemolytic anaemia:
Intravascular haemolysis due to mechanical disruption of RBCs leading to their fibrosis and release of extracellular components
CAUSES?

A

DIC, pre-eclampsia, TTP, HUS

100
Q

Autoimmune haemolytic anaemia

classified by hot and cold (based on temperature at which the ABs bind) Mx.

A

Management:
HOT =Steroids +/- splenectomy
COLD = keep warm, CHLORAMBUCIL

101
Q

Hereditary haemolytic anaemias: (3)

A

G6PD deficiency
Hereditary spherocytosis
Haemoglobinopathies: thalassaemia, sickle cell

102
Q

G6PD def. inheritance

A

X-linked

103
Q

G6PD Presentation = rapid onset jaundice/ anaemia after exposure to
On blood film:

A

Acute illness
Broad beans
Drugs: ASPIRIN
HENNA

Heinz bodies, bite cells

104
Q

Hereditary spherpocytosis Px: YOUNG child with family history of splenectomy w/ jaundice, splenomegaly, mild anaemia
Blood film?

A

Spherocytes

Mx. Splenectomy

105
Q

Haemolytic disease RBC blood picture

A

Polychromatic (colourful) macrocytosis with high reticulocytes

106
Q

Pancytopenia : Fanconi anaemia inheritance

A

Autosomal recessive

107
Q

Fanconi syndrome px.

A

Short stature

missing limbs/radii

108
Q

Which cancer is Fanconi syndrome assoc. with an increase in?

A

Acute Myeloid Leukaemia

109
Q

Aplastic anaemia - group of conditions where there is damage to bone marrow that results in instability of stem cells to generate cells.
Normochromic normocytic anaemia
Causes:

A

Irradiation
Infection: parvovirus B19
Drugs: chloramphenicol, carbamazepine, cytotoxics

110
Q

Aplastic anaemia mx:

A

Identify and treat underlying cause +/- splenectomy: supportive treatment: red cell/ platelet transfusion
Infection prophylaxis.

111
Q

Paraprotein diseases examples:

Blood film:

A 
Myeloma 
MGUS 
amyloidosis 
B cell lymphoma 
Chronic lymphocytic anaemia 
Waldenstroms Macroglobinaemia

Roulex formation

112
Q

Multiple myeloma: Malignant proliferation of B cells within the bone marrow. Px?

Myeloma should always be considered in AKI if patient is greater than 50 or has anaemia or hypercalcemia

A

As direct effect on bone: bone pain, usually back, osteoporosis and pathological fractures

Hypercalcaemia: bones,groans, moans, psychiatric undertones

Aplastic anaemia: anaemia, bleeding, bruising, recurrent infections.

Renal impairment: AKI or CKD

Hyperviscosity: reduced vision and cognition

113
Q 
Ix. 
Blood film: 
Serum electrophoresis:
urine electrophoresis: 
skeletal survey:
A

Blood film: Rouleaux formation
Serum electrophoresis: paraprotein
urine electrophoresis: BENCE JONES PROTEIN
skeletal survey: PEPPERPOT SKULL VERTEBRAL COLLAPSE.

114
Q

Myeloma prognostic investigation:

A

B2 microglobin

115
Q

Myeloma management:

A

Active tx. - immunosupression and chemotherapy
Dexamethasone
Melphalin
Thaidomide/lenalidomide

116
Q

MGUS - monoclonal gammopathy of unknown significance
defined as less than X paraprotein?
Is there evidence of myeloma or end-organ damage
Can this progress to myeloma

A

X < 30g
Bone marrow plasma cells <10%
No
Yes

117
Q 
Amyloidosis px: 
Kidney 
Liver
GI 
Heart 
Nerves 
Skin
A 
Nephrotic syndrome 
Hepatomegaly
Macroglossia, malabsorption 
Restrictive cardiomyopathy
autonomic and peripheral neuropathy 
peri-orbital purpura = characteristic
118
Q

Amyloidosis diagnostic finding.

Mx.

A

Apple green birefringence with congo red stain

essentially none and pt. tend to die in a few years

119
Q

What are B cell symptoms

A

Fever
Wt. loss
Night sweats

120
Q

Waldenstroms macroglobinaemia:
what antibody does it concern ?
Main pathological outcome ?
Mx.

A

IgM
IgM mediated hyperviscosity
Chemotherapy: Chlorambucil
Hyperviscosity: Leucophoresis and plasmapharesis

121
Q 
Leukaemia classification based on?
Onset: 
Cell lineage: 
Immunophenotyping:
Cytogenics:
A

Onset: acute or chronic
Cell lineage: lymphoid or myeloid
Immunophenotyping: antigen expressed
Cytogenics: mutations present in the cells

122
Q 
Acute lymphoid leukaemia: 
most common cancer in what age group? 
main risk factors: 
Px?
Examination:
A

CHILDREN (2-8)
Downs syndrome, irradiation (esp. during pregnancy)
Px: Anaemia, thrombocytopenia (easy bruising), Leukopenia (recurrent infections, not feeling well)
Hepatosplenomegaly, lymphadenopathy, orchidomegaly

123
Q 
Acute lymphoid leukaemia ix:
Bloods
Blood film
Bone marrow biopsy
additional investigations?
A

bloods: normocytic normochromic, neutropenia, leukocytosis (although WCC Is high, they are NON- functioning)

> 20% blasts
20% blasts
Immunophenotyping/cytogenetics
CT CAP/ head - look for infiltration

124
Q

ALL Mx:

A

Curative intent with long term chemotherapy.

Cure rate = 90% in children

125
Q

Acute Myeloid leukaemia features similar infiltration of tissues outside of the bone marrow as ALL (skin, gums, lymph nodes, liver and spleen) with one exception - what is it?

A

NO CNS INFILTRATION

126
Q

Key finding in ALL marrow biopsy

A

AUER RODS

127
Q

ALL Mx:

A 
Intense chemotherapy regimen
5 cycles given one week apart
common drugs: Daunorubicin cytrabine 
stem cell transplant -> 
APL ALTRA transretinoic acid - pretty much curative
128
Q

Chronic Lymphocytic leukaemia:

Associations?

A

Autoimmune haemolytic anaemia

ITP

129
Q

CLL occurs almost exclusively in which age group

Most common leukaemia in adults.

A

> 50 years

130
Q

CLL investigations:
Bloods:
Electrophoresis:
immunophenotyping:

A

Normochromic normocytic anaemia
low neutrophils, platelets
high WCC -> lymphocytes

hypoggammaglobinaemia
CD19/20

131
Q

CLL rule of 1/3rds

A

1/3 don’t progress
1/3 will progress with time
1/3 actively progressing at presentation

132
Q

CLL mx:

A

Not actively progressing: observation
actively progressing: Chemotherapy: cyclophosphamide, Fludarabine
+/- stem cell transplant

133
Q

Chronic Myeloid Leukaemia: pathognominic mutation:

A

Philadelphia chromosome 9:22 results in a abnormal tyrosine kinase

134
Q

CML presents as a slow onset of

A

Weight loss, fatigue, fever and night sweats
Gout -> increased red cell turnover
Abdominal pain/ bloating -> massive splenomegaly

135
Q

CML Ix: marrow biopsy

A

Hyper cellular marrow

136
Q

CML Mx:

A

TYROSINE KINASE INHIBITORS: IMATINIB

does not cure disease but completely controls it.

137
Q 
Lymphoma general investigations: 
Bloods: 
Diagnostic: 
Immunological:
Imaging:
A

Bloods: FBC, LDH, blood film.
Diagnostic = Excisional lymph node biopsy
immunological: cytogenics, immunophenotyping
imaging: CXR, CTCAP, PET, CT - PET CT is best for staging and for assessing treatment response in HL.

138
Q

Hodgkins lymphoma: percentage of of lymphomas

A

10%

139
Q

Pathognomonic CD30+ cell of Hodgkins lymphoma:

A

Reed sternberg cell

140
Q

Differentiating feature of HL (apparently)

A

Lymph node pain on DRINKING ALCOHOL

141
Q

Mx Hodgkins Lymphoma.

A 
CURATIVE INTENT w/ chemotherapy +/- radio +/- anti-CD30
ABVD:
o	A Adriamycin.
o	B Bleomycin. 
o	V Vincristine. 
o	D Dacarbazine.
142
Q

Hodgkins lymphoma: CD..antigen?

Non-Hodgkins lymphoma (NHL) CD..?

A 
HL = CD30 
NHL = CD20
143
Q

Types of NHL.

A

Burkitts
Follicular
Mantle

144
Q

Key facts:
Burkitts:
Follicular:
Mantle:

A

Burkitts Usually seen in African children who are EBV +.
Typically presents as a large tumour on face.

Follicular: High grade B cell lymphoma.
Mantle: Low grade B cell lymphoma

145
Q

Extra nodal disease is more common in NHL: examples?

A
  • CNS.
  • Spleen: splenomegaly.
  • Marrow: marrow failure.
  • Skin: popular rash, usually T cell.
  • Waldeyers ring: difficulty breathing.
146
Q

Mx. NHL:

A

Non-curative and serves to induce remission only -> chronic relapsing-remitting course.

RCHOP: 
Rituximab - anti-CD20 monoclonal antibody 
Cyclophosphamide 
Hydroxyduanorubicin
O - Vincristine 
P - Prednisolone
147
Q 
Lymphoma lymph nodes = 
Tender? 
Consistency? 
Surface? 
Inflammation? 
Tethered?
A 
Non-tender, 
rubbery and soft
smooth
no inflammation 
not tethered
148
Q 
Causes of hypersplenism: 
Infective 
Inflammatory 
Congestion 
Haematological
A

Infective: malaria, leishmaniasis,EBV
Inflammatory: rheumatoid, SLE
Congestion: heart failure, liver cirrhosis
Haematological: lymphoma, leukaemia, myeloproliferative disorders, thalassaemia, spherocytosis

149
Q

Felty’s syndrome (3)
sequestration of blood cells in the spleen
Mx?

A

Rheumatoid arthritis, splenomegaly and LOW WCC

treat cause +/- splenectomy

150
Q 
Myeloproliferative disorders: 
RBC:
WCC:
Platelets:
FIbroblasts:
A

Polycythaemia rubra vera
Chronic myeloid leukaemia
Essential thrombocythaemia
Myelofibrosis

151
Q

Myeloproliferative disorder diagnosis when there is no reactive cause for:

A

splenomegaly or thrombosis +/-
high granulocytes
high platelets
high Hb

152
Q

Polycythaemia rubra vera
An increase in red cell mass described as
Absolute:
Relative:

A

Absolute: increased red cell mass from increased red cell production - hallmarked by an increase in packed cell volume.
Primary = PRV
Secondary: COPD smoking, increased EPO production (renal and hepatic carcinoma)
Relative = increase in red cell mass due to plasma volume depletion -> no increase in red cell volume is seen: caused by alcohol, obesity, dehydration

153
Q

PRV mutation

A

JAK-2 (results in loss of auto-inhibtion and stimulation of RBC in absence of stimuli)

154
Q

Diagnostic PRV; Itch when?

A

Itch after warm shower +/- eryhtromelalgia

155
Q

Mx. PRV ?

A

Reduce risk of thrombosis:
low risk = venesection + aspirin
high risk: hydroxycarbamide + aspirin (>60 y/o or previous thrombosis)

156
Q

Essential thrombocythaemia: platelets >?

A

> 450

157
Q

Causes of Thrombocythaemia:

clonal proliferation of MEGAKARYOCYTES

A

bleeding, infection, malignancy, trauma/surgery, splenectomy and hyposplensim

158
Q

Thrombocythaemia mutations

A

JAK2 or CALR

159
Q

Thrombocythaemia Mx.

A

Low risk = aspirin

High risk = aspirin + hydroxycarbamide

160
Q

Myelofibrosis blood film finding:

A

Leukoerythroblastosis and TEAR DROP SHAPED RBC

161
Q

Myelofibrosis management:

A

Supportive (allopurinol if hyperuricaemic

active treatment + bone marrow transplant or Ruxolitinib (JAK 2 inhibitor)

162
Q

Blood transfusions What diseases are all donations screened for?
unable to screen for?

A

Malignancy, HIV, hepatitis, syphillis, HTLV

CJD

163
Q

Red cells
shelf life:
once out of fridge needs to be transfused within?

A

35 days

4 hours

164
Q

Platelets:
Shelf life:
Once out storage use by?

A

5 days

1 hour

165
Q 
FFP 
Stored at? 
For up to?
Use within?
Use in: DIC and warfarin overdose.
A

-30 degrees
2 years
4 hours

166
Q

Cryopreciptate: factors?

A

8/9 VWF, fibrinogen

167
Q

Anti-D uses:

A

Antepartum haemorrhage/ prophylaxis of rhesus negative mother

168
Q

PT complex

A

Used in vitamin K deficiency -
warfarin
liver disease

169
Q

Acute haemolytic transfusion reaction mediated by Ig?

Causes severe hypotension, DIC, AKI and shock

A

IgM

170
Q

Delayed haemolytic reaction (5-10 days after transfusion)

m/c in pts. with previous transfusions Px.

A

Jaundice, sudden drop in Hb and AKI

171
Q

White cell complications: febrile, non haeolytic px.

A

Fever, rigors

172
Q

White cell complications: TRALI (transfusion related lung injury).
SOB, Cough, tachypnoea, bilateral crepitations
CXR?
Mx.

A

CXR = white out

Mx. stop transfusion, high flow oxygen, admit to ITU.

173
Q

Anaphylaxis
ABCDE
Adrenaline dose
hydrocortisone dose chloramphenamine dose

A

Adrenaline 0.5 ml 1:1000 IM
Hydrocortisone - 200mg IV
Chloramphenamine - 10 mg IV

174
Q

Frequent transfusions: iron overload - minimised by?

A

Iron chelators: Deferiprone

175
Q

Splenectomy pts. which organism are they still vulnerable to despite anti-biotic prophylaxis:

A

Haemophilus influenzae

FLASH FINALS (34 decks)

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