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Year 3 Conditions - Jan > Haem > Flashcards

Haem Flashcards

1
Q

Microcytic anaemia

A

MCV < 80

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2
Q

Aetiology Microcytic anaemia

A

Defects in haem synthesis

  • Iron deficiency
  • Anaemia of Chronic disease

Defects in globin synthesis –> Thalassemia

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3
Q

Anaemia symptoms

A 
o	Tiredness
o	Lethargy 
o	Malaise 
o	Dyspnoea
o	Pallor
o	Palpitations 
o	Exacerbation of ischaemic conditions (e.g. angina, intermittent claudication)
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4
Q

Anaemia signs

A

Pallor
Brittle hair and nails
Koilonychia (if severe)

Glossitis
Angular Stomatitis

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5
Q

Anaemia investigations

A

Bloods

Iron studies

Blood film

CRP and ESR (for ACD)

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6
Q

Microcytic anaemia management

A

Oral iron supplements
Sideroblastic anaemia - treat teh cause
Lead poisoning - remove the source and dimercaprol

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7
Q

Normocytic anaemia

A

MCV 80-100

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8
Q

Aetiology normocytic anaemia

A

Acute blood loss

Failure of RBC production

  • Bone marrow failure
  • Bone marrow infiltration
  • Renal failure - abnormal erythopoeitic drive
  • Hypothyroidism
  • VIT B2/6 deficiency

Increase in plasma vol

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9
Q

Macrocytic anaemia

A

> 100 MCV

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10
Q

Aetiology macrocytic anaemia

A

Oftn from abnormal haemopoeisis

Megaloblastic - delay in maturation of nucleus whilt cytoplasm growns

  • Vit B12/folate deficiency
    • Dec absorption
      - ie (pernicious anaemia)
    • Inc demand

Non-megaloblastic

  • Alcohol excess
  • Multiple myeloma
  • Hypothyroidism
  • Aplastic anaemia
  • Haemolysis
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11
Q

Pernicious anaemia

A

AI conditon causing severe lack of IF

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12
Q

Perncisious anaemia signs

A

Mild jaundice
Glossitis
Angular stomatitis
Weight loss

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13
Q

B12 deficiency signs

A

Peripheral neuropathy
Ataxia
Optic atrophy
Positive Babinski’s

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14
Q

Test for pernicious anaemia

A

Schilling Test

B12 absorbed when given with intrinsic factor

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15
Q

Management for macrocytic anaemia

A

Pernicious anaemia
- IM hydroxycobalamin

B12 deficiency - dietary supplemants

Folate deficiency
- Folic acid

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16
Q

Haemolytic anaemia

A

Premature erythrocute breakdown causing shortened cerythrocyte life span with anaemia

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17
Q

Aetiology haemolytic anaemia

A

Hereditary

  • Membrane defects (hereditary spherocytosis)
  • Metabolic defects (G6PD, Pyruvate kinase defi)
  • Haemoglobinopathies (SCA, THala)

Acquired

  • Autoimmune
  • Drugs (eg. penicillin)
  • Trauma –> microangiopathic haemolytic anaemia
  • Infection (malaria, sepsis)
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18
Q

Haemolytic anaemia Sx

A

Jaundice
Haematuria
Dark urine

Pallor
Hepatosplenomegaly

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19
Q

Direct Coomb’s test

A

Autoimmune haemolytic anaemia

Identifies erythrocytes coated with Abs

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20
Q

Haemolytic Uraemic Syndrome

A

Traid of:

Microangiopathic haemolytic anaemia
Acute renal failure
Thrombocytopaenia

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21
Q

Two forms of Haemolytic Uraemic Syndrome

A

D+ - diarrhoea associated

D- –> no prodromal illness identified

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22
Q

HUS vs TTP

A

HUS overlaps with TTP, but TPP has additonal below Sx:

Fever
Fluctuating CNS signs

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23
Q

Pathophysiology HUS

A

Toxin = endothelial damage = platelet activation
Release of large vWF and activation of platelets & clotting cascade
Fibrin deposition in small cells = microthrombi & clots.
Blood smashing into clots = haemolysis –> schistocytes
Damaged RBC clog vessels
= Acute renal failure

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24
Q

Pathophyisology TTP

A

Defieincy of protease cleaves vWF –> platelet aggregation & fibrin deposition

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25
Q

Causes of HUS & TTP

A

Infection –> E.COLI O157
- Shigella

Drugs

  • COCP
  • Ciclosporin
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26
Q

HUS & TTP Sx

A

Abdominal colic
Wattery diarrhoea with bloodstains

Oliguria/anuria
Haematuria

Slight jaundice
Generalised oedema
Abdo tenderness

(in TTP;

Weakness
Reduced vision
Fits
Reduced consciousness)

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27
Q

Ix HUS/TTP

A

FBC

U&Es

  • High urea and creatinine
  • High K+ and low Na+

Clotting

LFTs

Blood film

Stool samples

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28
Q

Immune Thrombocytopenic Purpura (ITP)

A

Syndrome, immune destruction of platelets

Acute seen in children
Chronic in adults

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29
Q

Aetiology ITP

A

Idiopathic

Maybe:

  • Infection
  • AI
  • malignancies
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30
Q

Sx ITP

A

MEME

Mucosal bleeding
Easy bruising
Menorrhagia
Epistaxis

Visible petechiae

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31
Q

Aplastic anaemia

A

Stem cell disorder –> diminished haematopoietic precursors in bone marrow and pancytopaenia

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32
Q

AETIOLOGY aplastic anaemia

A

AI triggered by drugs, viral infeciton or iiradiation

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33
Q

Aplastic anaemia Sx

A

Anaemia signs

Thrombocytopaenia signs

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34
Q

Risk factors for all leukaemias

A 
Radiation exposure
Previous chemotherapy 
Benzene exposure 
Tobacco
FHx
White male
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35
Q

Skin signs with AML

A

Leukaemia cutis
Sweet’s sydnroome
Pyoderma gangrenosum

Gingival enlargement (gum enlargement)

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36
Q

Major cause of CML

A

Philadelphia chromosome
TRANSLOCATION 9–> 22
BCR-ABL (a tyrosine kinase)

37
Q

Leukaemia - why cant it disseminate quickly>

A

Exists as leukaemic cells not solid tumour, .>. replaces normal bone marrow cells in circulation quickly.

38
Q

ALL aetiology

A

Lymphoblasts undergo malignancy

RISK FACTORS:
Radiation
Genetic (Down’s, Neurofibromatosis 1, Fanconi’s)

HAPPEN IN CHILDREN OFTEN

39
Q

ALL SX

A

Bone Marrow failure:
Anaemia
Bleeding
Infections

Organ infiltration:
Tender bones
Enlarged nodes
Mediastinal compresssion
Meningeal involvement (headache, visual disturbances, nausea)
40
Q

AML Risk Factors

A

Ionising radiation
Cancer therapy
Chemotherapy

MOSt COMMON ACUTE LEAUKAEMIA IN ADULTS

41
Q

AML SX

A

Bone marrow failure:
ANaemia
Bleeding
Opportunistic infecitons

Tissue infiltration:
GUm swelling/bleeding
CNS involvement

42
Q

AML vs ALL

A

Differentiate using blood film

Myeloblasts vs Lymphoblasts

Myelobasts have AUER Rods

43
Q

ALL & AML Bone marrow biopsy

A

> 20% blast cells

44
Q

CLL aetiology

A

Chromosomal changes

Trisomy 12
11q and 13q deletions

45
Q

CLL epi

A

OLD WHITE MALES

46
Q

CLL investigations

A

Bloods

Blood film
- Smudge cells

47
Q

CML aetiology

A

PHILADELPHIA CHROMOSOME
- Transolcation between 9 & 22 (fusion BCR-ABL gene)

Fusion gene enhances tyrosine kinase activity and drives cell replication

48
Q

CML main sign

A

Splenomegaly

49
Q

Hodgkin’s lymphoma risk factors

A

EBV - main one

SLE

50
Q

Hodgkin’s lymphoma Sx & Signs

A

Painless enlarging mass
- often in neck

Mediastinal lymph ndoe involvement = bronchial/SVC obstruction

51
Q

Hodgkin’s lymphoms Ix

A

Bloods

Lymph node biopsy –> REED-STERNBERG CELLS

52
Q

Staging of lymphomas

A

Ann-Arbour staging

o I = single lymph node region
o II = 2+ lymph node regions on one side of the diaphragm
o III = lymph node regions on both sides of the diaphragm
o IV = extranodal involvement e.g. liver/bone marrow

o Each stage is either A/B +/- subscript A/E
o A = absence of B symptoms except pruritis
o B = presence of B symptoms – worse prognosis
o E = localised extranodal extension
o S = involvement of spleen

53
Q

Non-Hodgkin Lymhpoma

A

Any lymphoma without REED-STERNBERG cells

Can be B cell or T cell derived

54
Q

Non-Hodgkin lymphoma Risk factors

A

EBV/Burkitt’s lymphoma

o	Radiotherapy 
o	Immunosuppressive agents 
o	Chemotherapy 
o	HIV, HBV, HCV
Connective tissue disease (e.g. SLE)
55
Q

Entranodal disease in Non-Hodgking’s

A

Skin
Oropharynx
Gut
Small bowel

56
Q

Non-Hodgkin’s organ involvement Sx

A 
Skin rashes - mycosis fungoides 
Headache
Sore throat
Abdo discomrt 
testicular swelling
57
Q

Multiple myeloma

A

Proliferation of plasma cells

= bone lesions and production of monoclonal Ig

58
Q

Multiple myeloma Sx

A

CRAB

Calcium high
Renal impairment
Anaemia
Bone pain & lesions

59
Q

Diagnosis of myeloma

A
  • High suspicion if bone/back pain that is not improving
  • Diagnostic criteria:
    1. Monoclonal protein band in serum/urine electrophoresis
    2. High plasma cells on marrow biopsy
    3. Evidence of end-organ damage from myeloma e.g. hypercalcaemia/renal insufficiency/anaemia
    4. Bone lesions – x-rays
60
Q

Multiple myeloma blood film

A

Rouleaux formation (suggests high protein)

61
Q

Multiple myeloma urine electrophoresis

A

Serum paraprotein

Bence-Jones proteins

62
Q

Myelodysplasia

A

Marrow failure characterised by chronic pancytopaenia

63
Q

Myelodysplasia aetiology

A 
Maybe primary (intrinsic bone marrow prob)
Chemo/radio therapy
64
Q

Myelodysplasia signs and Sx

A 
o	Anaemia (pallor, cardiac flow murmur)
o	Neutropaenia (infections)
o	Thrombocytopaenia (purpura or ecchymoses) 
o	Gum hypertrophy 
o     Lymphadenopathy
o	Spleen NOT enlarged (except in CMML)
65
Q

Myelofibrosis

A

• Disorder of haematopoietic stem cells characterised by progressive bone marrow fibrosis associated with extramedullary haematopoiesis and splenomegaly

66
Q

Myelofibrosis Ix

A

Bloods

Blood film
- tear drop poikilocyte red cell

Bone marrow aspirate or biopsy
- aspirate often unsuccessful due to fibrosis

67
Q

DIC

A

Disorder of clotting cascade

Acute form where clots build up and = depletion of platelets and clotting factors

68
Q

Aetiology DIC

A

Infection - Gram -ve sepsis

Obstetric Complications - missed miscarriage etc

Malignancy

  • Acute promyelocytic leukaemia - ACUTE DIC
  • Lung, breast & GI malignancy - Chronic DIC
69
Q

HAEMOPHILIA A

A

Deficiency in Factor 8

70
Q

Haemophilia B

A

Deficiency in factor 9

71
Q

Haemophilia C

A

Deficiency in Factor 11

72
Q

Haemophilia Sx

A

Bleeding into muscles or joints

Haemarthroses
Muscle haematomas

73
Q

Haemophilia Ix

A

Clotting screen (high APTT)

74
Q

vWf 3 roles

A

Bring platelets into contact with exposed subendothelium

Make platelets bind to each other

Bind to factor 8, protecting it from destruction in circulation

75
Q

vW disease Sx

A 
Easy bruising 
Epistaxis 
Menorrhagia
Haematochezia
Haematuria
76
Q

vW disease Ix

A

APTT - High
Favtor 8 - low
vWF Ag - Low in Type 1 & 3, normal in2

77
Q

Antiphospholipid syndrome

A

Presence of antiphospholipid antibodies (APL) in plasma, venous and arteria thromboses

78
Q

APL syndrome Sx

A

Causes Clots

Coagulation defects
Livedo reticularis - swelling of venules due to clots
Obstetric - recurrent miscarriages
Thromocytopaenia

79
Q

Polycythaemia Sx

A

Due to hyperviscosity

Headaches
Dyspnoea 
Tinnitus 
Blurred vision 
Pruritis after hot bath 
Burning sensation in fingers and toes

Red ruddy complxion
Conjunctival suffusion

80
Q

Sickle Cell Anaemia

A

HbSS

81
Q

Sicle Cell train

A

HbS (one copy)

82
Q

Factors that precipitate sickling

A

I HAD

Infeciton
Dehydration
Hypoxia
Acidosis

83
Q

Sickle cell disease Sx

A

Vaso-occlusion/infarction Sx

  • Autosplenectomy (splenic atrophy)
    • inc risk of encapsulated organism infeciton
  • Abdo pain (mesent isch)
  • Bones –> dactylitits
  • Myalgia & arthralgia
  • CNS –> fits & strokes, cognitive defects
84
Q

Sickle cell Sequestration crisis Sx

A

Occurs due to pooling of red cells in various organs

Liver -> anaemia exacerbation

Lungs –> acute chest

  • Breathlessness
  • Cough
  • Pain
  • Fever

Corposa cavernosa
- Painful erection
Impotence

ENlarged spleen

85
Q

Sickle cell disease management acute (painful crises)

A 
O2
IV fluids
Strong analgesia
Abs
Cross match

Infection prophylaxis - Penicillin

Hydroxyurea/hydroxycarbamide - if frequent crisis

86
Q

Thalassemia

A

Reduced globin chain synth

87
Q

Alpha thalassemia types

A
  • 4 gene deletion = Haemoglobin Barts Hydrops Fetalis (intrauterine death)
  • 3 gene deletion = Haemoglobin H microcytic hypochromic anaemia and splenomegaly
  • 2 gene deletion = Alpha 0 thalassemia microcytic hypochromic red cells, NO ANAEMIA
  • 1 gene deletion = Alpha+ thalassemia microcytic hypochromic red cells, NO ANAEMIA
88
Q

Beta Thalassemia Types

A

Major –> little or no beta-chain synth

Intermedia - mild defect due to variety of causes (eg. co-inheritance of beta-thalassemia train with another haemoglobinopathy)

Train –. asymptomatic

89
Q

Thalassemia Sx

A

Beta thalassemia major

  • Severe anaemia
  • Presents at 3-6 mnths
    • HbF to HbA change
  • Pallor
  • Malaise
  • SoB
    Mild jaundice
    Hepatosplenomegaly

Year 3 Conditions - Jan (9 decks)

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