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Gen Med and Surg - C.U > Haematology > Flashcards

Haematology Flashcards

1
Q

What causes urticaria?

A

IgE reacting with foreign material

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2
Q

Approaching urticaria reaction to blood transfusion

A

Slow transfusion rate and give antihistamine

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3
Q

Approaching anaphylactic reaction to blood transfusion

A 
ABCDE 
Stop infusion 
Oxygen 
IM adrenaline 
IV hydrocortisone 
IV fluids
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4
Q

Microcytic anaemia causes

Stop Those Incy Little Cells

A 
Sideroblastic 
Thalasaemia 
Iron deficiency 
Lead poisoning 
Chronic disease
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5
Q

Normocytic anaemia causes

Medium Red Blood Cells

A

Marrow failure
Renal failure
Blood loss
Chronic disease

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6
Q

Macrocytic anaemia causes

FAT RBCs

A 
Folate deficiency 
Alcohol 
Thaimine deficiency 
Reticulocytosis 
B12 deficiency
Cytotoxic drugs and Cirrhosis  
Smoking
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7
Q

Symptoms of anaemia

A 
Lethargy 
Headaches 
SOB 
Palpitations 
Angina
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8
Q

Blood tests in anaemia

A 
FBC
U&E
LFTs
CRP 
Blood film 
Haematimics
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9
Q

Further tests in anaemia

A

BMB

GI endoscopy

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10
Q

Three causes of iron deficiency anaemia

A

Lack of intake
Malabs
Loss

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11
Q

Causes of lack of iron intake

A

Diet

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12
Q

Causes of malabsorption of iron

A

Coeliac disease

Gastrectomy

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13
Q

Causes of iron loss

A

GI bleed - upper / lower - Ca / Inflam / Infection / Ulcer

Menstruation

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14
Q

Specific clinical signs of iron deficiency anaemia

A

Spooning of nails
Angular stomatitis
Glossitis

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15
Q

Side effects of iron therapy

A

Black stools, change in bowel habits, abdo pain, nausea

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16
Q

Iron replacement therapy - aim for rise in Hn

A

2g/dl every 3 weeks

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17
Q

3 causes of B12 deficiency anaemia

A

Lack of intake - diet

Malabsorption - pernicious anaemia, gastrectomy

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18
Q

Neurological complications of B12 deficiency

A

Subacute combined degeneration of the cord - weakness, ataxia and paraplegia

Peripheral neuropathy

Parasthesia

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19
Q

Treatment of B12 deficiency

A

Injections of B12 - will not fix the cord degeneration

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20
Q

4 cause of folate deficiency

A

Increased requirement - preganancy
Insufficient intake - diet
Malabsorption - crohns, coeliac
Drugs - methotrexate

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21
Q

Extra tests if suspect folate deficiency

A

Jejunal biopsy - look for coeliac disease

BM aspirate

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22
Q

What does folate deficiency often come with?

A

Vit B12 deficiency

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23
Q

Where are RBC destroyed extravascularly in haemolytic anaemia (4)

A

Spleen
Marrow
Liver
Phagocytes

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24
Q

Two classifications of reticulocytosis

A

Intravascular and extravascular

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25
Q

3 types of cellular defects causing haemolytic anaemia

A

Metabolic - pyruvate kinase
Cell membrane - hereditary spherocytosis
Hb dysfunction - thalassaemia, sickle cell

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26
Q

Immune causes of haemolytic anaemia (2)

A

autoimmune

drug induced

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27
Q

Non immune causes of heamolytic anaemia

A 
heart valves 
DIC
Drugs 
Toxins 
Infections 
Renal / Liver disease
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28
Q

target cell may indicate

A

thalassaemia

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29
Q

Heiz bodies are

A

fragments of Hb

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30
Q

Clinical features of haemolytic anaemia (5)

A 
Splenomegaly 
Jaundice 
Dark urine
Pallor 
Pigment gallstones
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31
Q

Hereditary spherocytosis inheritance type

A

autosomal dominant

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32
Q

Thalassaemia inheritance type

A

autosomal recessive

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33
Q

How many genes affected in hydrop fatalis?

A

4

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34
Q

How long does beta thalassaemia major take to become symptomatic from birth? and why does it take that long?

A

3-6 months as the fetal Hb is no longer made

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35
Q

What can be currative in beta thalassaemia?

A

bone marrow transplant

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36
Q

main way thalassaemia is treated?

A

blood transfusions

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37
Q

inheritance of sickle cell

A

autosomal recessive

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38
Q

4 types of sick cell crisis

A

Vaso occlusive
Aplastic
Haemolytic
Visceral sequestration

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39
Q

Blood test in suspected sick cell crisis

A 
RBC
U&E
LFTs 
Bilirubin 
LDH 
ABG
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40
Q

Bed side tests in suspected sick cell crisis

A

Urine analysis
Sputum analysis
Blood culture

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41
Q

Further test in sickle cell crisis

A

Blood film

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42
Q

Acute treatment of sick cell crisis

A 
ABCDE 
Fluids 
Pain relief 
Antibiotics if infection 
\+/- blood transfusion
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43
Q

Prevention of a sickcell crisis

A

Vaccinations
Penicillin
Avoid triggers

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44
Q

Test to detect antibodies again RBC

A

Indirect Coombs

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45
Q

In Acute thrombocytopenic purpura what do the autoantibodies target?

A

antigens on platelet surface

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46
Q

Clinical features of Acute thrombocytopenic purpura

A

Epistaxis
Brusing under the skin
Menorrhagia
Gingivitis

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47
Q

At what platelet level should Acute thrombocytopenic purpura be treated?

A

<30

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48
Q

How should Acute thrombocytopenic purpura be treated?

A

Steroids and immunoglobulin infusion

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49
Q

Haemophilia A is due to a deficiency in?

Haemophilia B is due to a deficiency in?

A

factor 8

factor 9

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50
Q

In haemophilia - blood result

APTT
PT
vWF

A

elongated

normal

normal

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51
Q

Treatment of:

Haemophilia A
Haemophilia B

A

desmopressin and factor 8

factor 9

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52
Q

vWD - blood results

APTT

PT

Factor 8

vW factor

A

Elongated

Normal

reduced

decreased

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53
Q

Treatment of VWD

A

vWF concentrate
vasopressin infusions
cyroprecipitate
FFP

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54
Q

DIC =

A

pathological activation of coagulation

results in bleeding and microvascular thrombosis

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55
Q

Causes of DIC

A 
Infection 
Malignancy 
Obstetrics 
Anaphylaxis 
Liver disease
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56
Q

Blood results in DIC

APTT

PT

TT

Fibrinogen

A

Raised

Raised

Raised

Lower

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57
Q

Why is there bleeding in DIC ?

A

Depletion of platelets and clotting factors due to lots of clots being made systemically

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58
Q

DVT

For those likely to have a DVT (Wells >2), what test should be done?

For those unlikely to have a DVT (Wells >2), what test should be done?

A

Duplex scan

D dimer

59
Q

Minimum length of anticoagultant treatment after DVT

A

3 months

6 months if unprovoked

60
Q

Primary causes of thrombophilia

A

Protein S/ C deficiency
Antithrombin III deficiency
Factor V leiden

61
Q

Secondary causes of thrombophilia

A 
Malignancy 
Immobility 
Major surgery 
OCP 
Smoking 
Pregnancy 
APS
62
Q

Two types of lymphoma

A

Non hodgkins lymphoma

Hodgkins lymphoma

63
Q

3 places lymphadenopathy can be found in lymphoma

A

Cervical
Axilla
Inguinal

64
Q

Types of cells found in Hodgkins lymphoma

A

Reed-Sternberg cell

65
Q

Which virus is associated with Hodgkins lymphoma

66
Q

Main presentation of NHL

A

Painless lymphadenopathy

67
Q

Leukaemia pathophysiology

A

Increase in no. of non functional haemopoietic blood cells produced by bone marrow

68
Q

Action of leukaemia cells on the bone marrow

A

Suppress production of normal cells

69
Q

Common leukaemia in children

70
Q

Symptoms in leukaemia due to BM supression

A

Anaemia
Bruising / bleeding
Susceptible to infections

71
Q

White blood cells raised in CLL

A

lymphocytes

72
Q

WBC cells raised in CML

A

Neutrophils and metamyelocytes

73
Q

ALL predominant cell type

A

immature lymphoblastic cells

74
Q

Chromosomal defect associated with ALL

A

Philidelphia

75
Q

Pathology of CLL

A

Uncontrolled poliferation and accumulation of mature non-functional peripheral lymphocytes

76
Q

What is seen on a CLL film

A

Smudge cells (mature lymphocytes which are fragile)

77
Q

Which WBC cells are class as “myeloid”

A

Eosinophils, neutrophils and basophils

78
Q

In AML what do the blasts infiltrate

A

Mainly bone marrow

Also liver, spleen, skin and gums

79
Q

Main causes of AML

A 
Radiation 
Chemo 
Transformation from myelodysplastic syndromes 
Down's syndrome 
Fanconi anaemia
80
Q

Presentation of AML

A

Splenomegaly
Hepatomegaly
Lymphadenopathy
Bone pain

81
Q

Type of anaemia in AML

A

Normocytic and normochromic

82
Q

Blood test results in AML

RBC 
WBC 
Platelets 
Urate 
LDH 
Calcium
A

Decreased

Decreased (increase blasts)

Platelets - decrease

Urate / LDH / Calcium - increase

83
Q

Other tests than bloods in AML

A

Blood film

Bone marrow

Cytogenic / molecular analysis

84
Q

CML =

A

chronic accumulation of basophils, eosinophls and neutrophils

85
Q

CML can transform to?

A

AML - 60%

ALL - 60%

86
Q

90% with CML have?

A

Philadelphia chromosome

87
Q

Blood test results in CML

FBC 
WBC
Platelets 
Urate
LDH
Vit B12
A 
Decrease 
Increase
Increase 
Increase
Increase 
Increase
88
Q

other tests than blood tests in CML

A

Bone marrow

89
Q

Main lifelong treatment in CML

90
Q

Paraproteinaemias =

A

presence of monoclonal immunoglobulins in the blood

91
Q

Bence jones =

A

monoclonal light chains

92
Q

Paraproteins can be three things

A

Whole immunoglobulins
Heavy chains
Light chains (bence jones)

93
Q

Light chains can be found in?

A

the urine (filtered out by the kidneys)

94
Q

Multiple myeloma =

A

malignant proliferation of plasma cells of the bone marrow.

95
Q

What do the multiple myeloma cells release?

As a result what is suppressed?

A

monoclonal immunoglobulins

normal immunoglobulin function suppressed

96
Q

Presentation of patients with multiple myeloma

A 
gets regular infections 
pathological fractures 
renal failure 
hyperviscosity symptoms - epistaxis, visual disturbances, headaches and confusion 
hypercalcaemia 
pancytopenia 
SCC?
97
Q

how is bone weakened in multiple myeloma

A

neoplastic cells produce osteoclastic activating factors, increases osteoclast activity, weakening bone

98
Q

What is found on blood film in multiple myeloma

A

rouleaux formation

99
Q

Other tests in multiple myeloma

A

electrophoresis - monoclonal paraprotein band

bone marrow - can qualify the paraprotein

100
Q

What is found on x-ray in multiple myeloma

A

pepper pot skull - osteolytic lesions in skull

101
Q

treatment for myeloma

A

Supportive

  • bisphosphonates
  • AB
  • pain relief
  • watch out for cord compression
  • plasmapheresis
  • chemo
  • radio for bone pain
102
Q

how to treat hyperviscosity in myeloma

A

plasmapheresis

103
Q

myelopoliferative disorders =

A

overproduction of one or more of the early cell lines in the bone marrow

104
Q

essential thrombocytosis =

A

increase in the number of platelets

often abnormal platelets so don’t work properly

105
Q

Clinical features of thrombocytosis

A

Asymptomatic

BUT

  • VTE
  • Bleeding - esp GI
  • Bruising
  • CV symptoms
  • weight loss
  • puritis
  • sweats
106
Q

Causes of secondary thrombocytosis

A

Iron deficiency
Chronic bleeding
trauma
Inflammation

107
Q

Polycythaemia =

A

increase in RBCs in the blood

108
Q

cause of primary polycythaemia =

A

Due to a malignant myelopoliferative disorder

109
Q

another name for primary polycythaemia =

A

polycythaemia rubra vers

110
Q

cause of secondary polycythaemia =

A

increased erythropoietin production

  • chronic hypoxia - lung / heart disease, high altitude
  • inappropriate erythropoietin production - renal / lung disease
111
Q

Presentation of polycythaemia ruba vera

A 
erythemaa 
facial plethora 
tiredness 
gout 
arterial / venous occulsive event 
hyperviscosity symptoms
112
Q

mutation in 92% of polycythaemia ruba vera

113
Q

Blood test results in PRV

Hb 
Packed cell vol 
RBC 
WBC 
Platelets
A

All increased

114
Q

tests in PRV

A

FBC
ABG
CXR
Renal US

115
Q

Treatment of PRV

A

Venesection
Aspirin
Reduce risk factors for arterial / venous thromboembolism

116
Q

myelofibrosis

A

fibrosis of the marrow due to hyperplasia of megakaryocytes (platelet precursor). leads to bone marrow failure.

117
Q

what typically causes purpura?

A

low platelets

118
Q

Two differentials to investigate in children with purpura?

A

meningococcal septicaemia or acute lymphoblastic leukaemia

119
Q

Henoch-schonlein purpura is what type of vasculitis?

A

IgA mediated small vessel vasculitis

120
Q

Hb level for transfusion in most patients

A

< 70 g/L

aim (70 - 90)

121
Q

Hb level for patients with ACS

A

< 80

aim (80 - 100)

122
Q

Platelet transfusion should be

given?

A

Patient is actively bleeding and thrombocytopenia < 30 x10(9)/ L

123
Q

What is in the first blood pack in the massive haemorrhage protocol

A

4 x blood

4 x FFP

124
Q

products to be given in initial ressus of a major haemorrhage

A

1:1

FFP and blood

125
Q

Non urgent blood transfusion given over?

126
Q

When should observations be done on a patient who’s having a blood transfusion?

A

0, 15mins and 30 mins

127
Q

Factor V leiden =

A

activated protein c resistance - Factor V is inactivated much more slowly by protein C

128
Q

Treatment of venous reflux disease

A

Conservative - compression stockings

Surgical - ligation and striping

129
Q

Virchow’s triad

A

Venous stasis
Hypercoagulation
Vascular injury

130
Q

Thrombotic risk reduces peri surgery

A

compression stockings
early mobalisation
LMWH

131
Q

define varicose viens

A

dilated subcut vein with reversed blood flow

132
Q

Risk factors for venous valve reflux

A

FH
Pregnancy
Obesity
Occupation

133
Q

Cause of lipodermatosclerosis

A

chronic venous hypertension leads to subcut fat becoming fibrotic

134
Q

saphina varix =

A

dilation of saphenous vein at its junction with the femoral vein in the groin

135
Q

What does heparin activate and what does it inhibit?

A

Antithrombin III

Forms a complex that inhibits thrombin, factors Xa, IXa, Xia and XIIa

136
Q

What does LMWH activate and what does it inhibit?

A

Antithrombin III

Factor Xa only

137
Q

Monitor

1) heparin with?
2) LMWH with?

A

Activated partial thromboplastin time (APTT)

Anti-Factor Xa (although routine monitoring is not required)

138
Q

How often are Vit B12 injections given?

A

every 3 months

139
Q

Venous thromoboembolism - length of warfarin treatment

A

provoked (e.g. recent surgery): 3 months

unprovoked: 6 months

140
Q

antidote for dabigatran

A

Idarucizumab is a reversal agent for dabigatran

141
Q

Types of Hodgkins Lymphoma

A

Nodular schlerosing - most common, “fibrotic bands” present

Lymphocyte rich - Reed-Steinburg cells and small lymphocytes

Mixed cellularity - Reed-Steinburg cells, mixed infiltrate

142
Q

Investigations in Lymphoma

A

FBC
Blood film
Chest x-ray
Lymph node BIOPSY

143
Q

Follow up investigations in unprovoked DVT

A

May be concerned about cancer

  • Full hx and physical
  • chest x-ray
  • set of bloods including calcium

Consider Abdo-pelvis CT (and mammogram in women) if >40

If concerned about thrombophillia ie first degree relative with unprovoked DVT/PE too - could check for this then as well

144
Q

Wells score in PE meaning a CTPA is done straight away

Gen Med and Surg - C.U (16 decks)

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