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My Phase 2a Medicine > Haematological Conditions > Flashcards

Haematological Conditions Flashcards

1
Q

What is polycythaemia?

A

=increased haemoglobin, PCV and red blood cell count

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2
Q

What is is PCV?

A

Packed Cell Volume = proportion of blood made up from red blood cells

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3
Q

What is primary polycythaemia?

A

Increase in red blood cells is due to a problem with red blood cell production

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4
Q

What are the causes of primary polycythaemia?

A
  • genetic mutation in EPO receptor (EPO triggers RBC production)
  • mutation in hypoxia-sensing pathway (hypoxia triggers RBC production)
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5
Q

What are the symptoms of polycythaemia?

A
  • tiredness
  • itching
  • vertigo
  • headache
  • visual disturbance
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6
Q

What are the complications of polycythaemia?

A
  • thrombosis
  • haemorrhage
  • gout
  • peptic ulceration
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7
Q

How is polycythaemia diagnoses?

A
  • measure haemoglobin

- investigate presence of genetic mutations

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8
Q

How is polycythaemia managed?

A
  • chemotherapy
  • low dose aspirin (reduce risk of thrombosis)
  • venesections (regular removal of blood)
  • anagrelide (inhibits megakaryocyte differentiation)
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9
Q

What is secondary polycythaemia?

A

increase in RBC due to an underlying condition

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10
Q

What are the causes of secondary polycythaemia?

A 
appropriate increase in EPO
-high altitude
-chronic lung disease
-cardiovascular disease
-smoking
inappropriate increase in EPO
-renal disease
-adrenal tumour
-hepatocellular carcinoma
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11
Q

What is relative polycythaemia?

A

decrease in plasma volume causes a relatively high proportion of RBC/haematocrit

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12
Q

What are the causes of relative polycythaemia?

A
  • smoking
  • high alcohol
  • obesity
  • high blood pressure
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13
Q

What are bleeding disorders? Give examples

A

Conditions affecting coagulation of blood

  • thrombocytopenia
  • thromobocytosis
  • platelet function disorders
  • Haemophilia
  • Von Willebrand’s disease
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14
Q

What is thrombocytopenia?

A

=low platelet number in the blood

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15
Q

What are the causes of thrombocytopenia?

A 
reduced platelet production
-bone marrow failure
-myeloma
-drugs
excessive peripheral platelet production
-immune
-auto-immune
-drugs
-post-transfusions
sequestration into an enlarged spleen
-splenomegaly
-hypersplenism
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16
Q

What are the symptoms of thrombocytopenia?

A
  • excessive/easy bruising
  • superficial bleeding into skin = purpura
  • prolonged bleeding from cuts
  • bleeding from gums/nose
  • blood in urine or stools
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17
Q

How is thrombocytopenia managed?

A

treat underlying condition

platelet transfusion

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18
Q

What is immune thrombocytopenic purpura?

A

immune system destroys platelets, causing superficial bleeding under the skin

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19
Q

How is immune thrombocytopenic purpura managed?

A
  • corticosteroids
  • IV immunoglobulins
  • splenectomy
  • platelet transfusion
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20
Q

What is thrombotic thrombocytopenic purpura?

A

Clotting in small blood vessels results in low platelet count in the blood

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21
Q

What are the symptoms of thrombotic thrombocytopenic purpura?

A
  • florid purpura
  • fever
  • haemolytic anaemia
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22
Q

How is thrombotic thrombocytopenic purpura managed?

A
  • corticosteroid

- plasma exchange

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23
Q

What are platelet function disorders?

A

inherited or acquired conditions where platelets are dysfunctional

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24
Q

Give some examples of acquired platelet function disorder

A
  • renal or liver disease
  • drug use
  • myeloproliferative disorders
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25
Q

Give some examples of congenital platelet function disorders

A
  • glanzmann’s thromboasthenia =abnormality in genes encoding for glycoproteins IIb/IIIa
  • bernard-soullier syndrome =abnormality in genes for glycoprotein IIb/IIIa
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26
Q

What are the symptoms of platelet function disorders?

A
  • easy bruising
  • bleeding
  • thrombosis
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27
Q

How are platelet function disorders managed?

A
  • platelet transfusion

- dialysis

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28
Q

What is thrombocytosis?

A

too many platelets in the blood

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29
Q

What are the causes of thrombocytosis?

A
  • splenectomy
  • malignancy
  • inflammatory disorders
  • major surgery
  • myeloproliferative disorders
  • iron deficiency
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30
Q

What are the symptoms of thrombocytosis?

A
  • usually asymptomatic
  • headaches
  • weakness/numbness
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31
Q

How is thrombocytosis managed?

A

treat the underlying cause

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32
Q

What are the complications of thrombocytosis?

A

Increased risk of thrombosis formation, leading to increased risk of MI and stroke

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33
Q

What are inherited coagulation disorders?

A

=genetic condition which results in impaired coagulation

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34
Q

What are is haemophilia?

A

x-linked condition where there is a deficiency in a clotting factor

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35
Q

What is the difference between haemophilia A and B?

A

Haemophilia A factor VIII (8) is deficiency. Haemophilia B factor IX (9) is deficient

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36
Q

What are the symptoms of haemophilia?

A
  • easy bruising
  • excessive bleeding
  • bleeding gums
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37
Q

How is haemophilia managed?

A

Replacement of the deficient clotting factor

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38
Q

What is Von Willebrand’s disease?

A

deficiency in VWG causing platelet dysfunction

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39
Q

What are the symptoms of Von Willebrand’s disease?

A
  • excessive bleeding
  • epistaxis (nose bleed due to damage of blood vessels in the nasal mucosa)
  • menorrhagia (abnormally heavy periods)
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40
Q

How is Von Willebrand’s disease managed?

A
  • desmopressin (increases conc of VMWF and factor 8)
  • tranexamic acid (prevents enzymes from breaking down blood clots)
  • VWF concentrate
  • avoid aspirin and anti-inflammatory drugs
  • manage menorrhagia with contraception
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41
Q

What are acquired coagulation disorders?

A

conditions which are not genetic which cause impaired coagulation

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42
Q

Name 3 acquired coagulation disorder?

A
  • vitamin k deficiency
  • liver disease
  • disseminated intravascular coagulation (DIC)
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43
Q

How does vitamin K deficiency impair coagulation

A

vitamin K is essential for the production of factors 2, 7, 9 ,10

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44
Q

What are the causes of vitamin K deficiency?

A
  • inadequate storage
  • malabsorption
  • anticoagulants which act as vitamin K antagonisists
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45
Q

How does liver disease impair coagulation?

A
  • reduced coagulation factor synthesis
  • thrombocytopenia
  • vitamin K deficiency
  • functional abnormalities in platelets and fibrinogen
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46
Q

What is disseminated intravascular coagulation?

A

activation of the coagulation cascade results in the lots of small intravascular thrombi and a depletion in coagulation factors

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47
Q

What are the causes of disseminated intravascular coagulation?

A
  • malignancy
  • septicaemia
  • haemolytic transfusion reaction
  • liver disease
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48
Q

What are the symptoms of disseminated intravascular coagulation?

A
  • acutely ill
  • range from no bleeding to widespread haemorrhage depending on the severity
  • thrombotic events
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49
Q

How is disseminated intravascular coagulation managed?

A
  • treat the underlying cause
  • platelet transfusion
  • anti-coagulant e.g. heparin
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50
Q

What is lymphoma?

A

malignancy of the lymphoid tissue

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51
Q

What is the difference between Hodgkin’s and non-Hodgkin’s lymphoma?

A

Hodkin’s lymphoma contains Reed-Sternberg cells which are not found in non-Hodgkin’s lymphoma

52
Q

What are the clinical feature of Hodgkin’s lymphoma?

A
  • painless cervical lymphadenopathy
  • mediastinal lymphadenopathy
  • hepato/splenoegaly
53
Q

How is Hodgkin’s lymphoma managed?

A

chemotherapy

54
Q

What are the 2 types of non-Hodgkins lymphoma?

A
  • B cell lymphoma (80%)

- T cell lymphoma (20%)

55
Q

What are the symptoms of B cell lymphoma?

A

painless lymphadenopathy at 1 site

56
Q

How is B cell lymphoma managed?

A
  • radiotherapy

- chemo/immunotherapy

57
Q

What are the symptoms of T cell lymphoma?

A
  • inflammatory disease
  • fever
  • electrolyte abnormalities
58
Q

How is T cell lymphoma managed?

A

chemotherapy

59
Q

What is primary extranodal lymphoma?

A

malignancy of lymphoid tissue which originated outside the lymph nodes

60
Q

What is Malaria?

A

parasitic infection caused by the Plasmodium parasite which is transmitted via female Anopheles mosquitos

61
Q

What parasites cause malaria?

A

Plasmodium

  • falciparum
  • vivax
  • ovale
  • malariae
62
Q

What is the vector for the malaria parasite?

A

Female Anopheles mosquito

63
Q

Describe the parasitology of malaria.

A
  • infected mosquito bites human
  • sporozites transferred from the saliva into human blood
  • sporoxites accumulate in the heaptocytes of the liver
  • hepatocytes bursts and merorzoites are released into the blood
  • merozoites invade RBC
  • meorzoites replicate
  • RBC burst and merozoites are released into the blood
  • gamaetocytes alose prodcued in the RBC
  • gametocytes taken up by a non-infected mosquito when bitten
64
Q

Which species of Plasmodium have a latent period in malaria?

A

P. vivax and P.ovale.

Some sporozites remain dormant in the liver and can reactivated to cause malaria long after infection

65
Q

What are the clinical features of malaria?

A
  • fever
  • malaise
  • headaches
  • vomitting
  • diarrhoea
66
Q

What symptoms occur in severe complicated malaria and what species of parasite causes this?

A

Plasmodium falciparum

  • impaired consciousness
  • convulsions
  • shock
  • hypogylcaemia
  • death
67
Q

How is malaria diagnosed?

A
  • blood films (thick and thin)

- rapid diagnostic test (identifies antigen - useful when microscopy not available)

68
Q

How is malaria treated?

A
  • chloroquine (unless P. falciparum as resistance has developed)
  • IV antimalarials (quinine and artesunate)
69
Q

How is malaria prevented?

A
  • reduce breeding sites (standing water)
  • long-lasting insecticide treated nets
  • insecticide spray
  • chemoprophylaxis (medicine to people at risk)
70
Q

What is viremia?

A

viral infection of the blood

71
Q

What is fungemia?

A

fungal infection of the blood

72
Q

What is septicaemia?

A

infection of the blood stream

73
Q

What are the causes of septicaemia?

A
  • bacteria infection enters the blood (bacteraemia)

- UTI, lung infection, kidney infection, abdominal infection spreads

74
Q

What are the clinical features of septicaemia?

A
  • chills
  • fever
  • clammy pale skin
  • hyperventilation
  • tachycardia
  • confusion
  • nausea/vomiting
  • dec urine volume
  • inadequate blood flow (septic shock)
75
Q

How is septicaemia diagnoses?

A

medical history of infection

test body fluids

76
Q

How is septicaemia managed?

A
  • antibiotic (if bacterial)
  • IV fluids
  • oxygen
77
Q

What is Sepsis?

A

life threatening organ dysfunction caused by dysregulated host response to infection

78
Q

How many deaths occur due to sepsis in the UK per year?

A

> 44,000

79
Q

What are the clinical feature of mild and severe sepsis?

A 
mild
RR: 21-24 (high)
BP: 91-100 (low)
HR: 91-130 (high)
severe
RR: >24
BP: <90
HR: >120
80
Q

How is sepsis managed?

A
  • assess risk using HR, BP, RR
  • antibiotics
  • IV fluids
  • oxygen
  • AKI
  • blood tests
81
Q

What is myeloma?

A

malignant disease of the bone marrow plasma cells

82
Q

Explain the pathogenesis of myeloma.

A
  • clonal expansion of abnormally proliferating plasma cells
  • increased production of paraproteins (IgG/A)
  • organ dysfunction
  • bone destruction (due to infiltration with plasma cells)
83
Q

What are the symptoms of myeloma?

A
  • bone pain
  • anemia symptoms (fatigue, faintness, headache, dyspnoea)
  • recurrent infections
  • renal failure symptoms (confusion, oedema, dec urine)
  • hypercalcaemia symptoms (nausea, vomiting, loss of appetite, inc thirst, weakness, muscle pain, disorientation)
84
Q

How is myeloma diagnosed?

A
  • FBC (anaemia, neutropenia)
  • increased Ca
  • bone marrow biopsy (inc plasma cell)
  • monoclonal protein band in serum from paraprotein
  • bone lesions on x-ray
85
Q

How is myeloma managed?

A
  • analgesia for bone pain
  • bisphosphates
  • treat anaemia (EPO, blood transfusion)
  • antibiotics for infection
  • treat renal failure (fluid and dialysis)
  • chemotherapy (may need stem cell transplant after)
86
Q

What are the complications of myeloma?

A
  • hypercalcaemia
  • spinal cord compression
  • hyperviscosity
  • acute renal injury
87
Q

What is leukaemia?

A

Cancer originating from blood-forming tissue normally in the bone marrow

88
Q

What are the 4 common types of leukaemia?

A

Aute lymphoblastic
Acute myeloid
Chronic lymphocytic
Chronic myeloid

89
Q

What is acute lymphoblastic leukaemia?

A

Malignancy of the lymphoid cells (B and T cells)

90
Q

What is the clinical presentation of acute lymphoblastic leukaemia?

A
  • bone marrow failure (anaemia, infection, bleeding)

- tissue infiltration (hepatomegaly, splenomegaly, lymphadenopathy, bone pain)

91
Q

How is acute lymphoblastic leukaemia treated?

A
  • blood/platelet transfusion
  • IV antibiotics for infections
  • chemotherapy (multi-drug and multi-phase)
  • bone marrow transplant
  • subcutaneous port system of Hickman’s line
92
Q

Whats is acute myeloid leukaemia?

A

malignancy of myeloid cells (progenitors of granulocytes and monocytes -RBC, neutrophils etc)

93
Q

What is the clinical presentation of acute myeloid leukaemia?

A
  • marrow failure (anaemia, infection, bleeding)

- tissue infiltration (hepatomegaly, splenomegaly, gum hypertrophy, bone pain)

94
Q

How is acute myeloid leukaemia treated?

A
  • blood/platelet transfusion
  • chemotherapy (intensive and long)
  • bone marrow transplant
  • subcutaneous port or Hickmans line
95
Q

What is chronic myeloid leykaemia?

A

slow developing malignancy of the myeloid cells (cells which form granulocytes and monocytes)

96
Q

What is the clinical presentation of chronic myeloid leukaeia?

A
  • weight loss
  • tiredness
  • fever
  • marrow failure (anaemia, infection, bleeding)
  • hepatomegaly
  • splenoegaly
97
Q

How is chronic myeloid leukaemia treated?

A
  • imatinib (tyrosine kinase inhibitor)
  • chemotherapy
  • bone marrow transplant
98
Q

What is chronic lymphocytic leukaemia?

A

slow developing malignancy of lymphoid cells (precursors of lymphocytes)

99
Q

What is the clinical presentation of chronic lymphocytic leukaemia?

A
  • lymphadenopathy
  • weight loss
  • fever
  • infections
  • anaemia
  • splenomegaly
  • hepatomegaly
100
Q

How is chronic lymphocytic anaemia treated?

A
  • platelet/blood transfusion
  • radiation therapy
  • chemotherapy
  • stem cell transplant
  • targeted therapy (monoclonal antibodies, tyrosine kinase inhibitors
101
Q

What is thrombosis?

A

formation of a solid mass of blood constituents which forms in the circulation of a living organism

102
Q

What is thromboembolism?

A

Obstruction of a blood vessel due to a thrombus breaking off from its original site and being transported to another part of the circulation where it gets stuck

103
Q

How is a thrombus formed?

A

-damaged to the endothelium
-platelets adhere to the exposed collagen
-platelets are activated and release granules
platelets aggregate
-coagulation cascade activated
-fibrinogen converted to fibrin
-fibrin mesh forms

104
Q

What the symptoms of a thrombus?

A

Aysmptomatic unless significantly reduces blood flow

  • swelling
  • redness
  • pain
  • throbbing
  • ischaemia
105
Q

What are the complications of thrombosis?

A
  • myocardial infarction (chest pain, short of breath)
  • stroke (weakness on one side, slurred speech)
  • limb ischaemia (pain, discoloured, cold)
106
Q

How is thrombosis managed?

A
  • decrease risk factors (smoking, hyperlipidemia)
  • anti-platelet drugs (aspirin)
  • anti-coagulants (warfarin)
  • thrombolytic therapy (medication to breakdown of thrombus e.g. streptokinase)
  • emeboletomy (surgical removal of thrombus)
107
Q

What is deep vein thrombosis (DVT)?

A

thrombus which form in a deep vein, commonly in the legs

108
Q

What are the risk factors for DVT?

A
  • surgery

- hospitilisation

109
Q

What are the clinical features of DVT?

A
  • pain in calf
  • swelling and redness
  • engorged superficial veins
  • ankle oedema
  • cyanotic discolouration
110
Q

How is DVT managed?

A
  • anticoagulants (warfarin, heparin)
  • mobilise (after anticoagulant given)
  • wear elastic stocking
  • thrombolytic therapy (streptokinase)
111
Q

What are the risk factors for thrombosis?

A
  • smoking
  • hyperlipidemia
  • hypertension
  • diabetes mellitus
  • lack of exercise
112
Q

What is anaemia?

A

insufficient haemoglobin in the blood

113
Q

Name 4 types of anaemia

A
  • hypochromic microcytic
  • normochromic normocytic
  • macrocytic
  • haemolytic
114
Q

What is hypochromic microcytic anaemia?

A

RBC have a love Hb content and low MCV (small RBCS)

115
Q

What are the causes of hypochromic microcytic anaemia?

A
  • iron deficiency

- anaemia of chronic disease (occurs alongside a chronic disease)

116
Q

What is normochromic normocytic anaemia?

A

red blood cells have a normal MCV and Hb content

117
Q

What is macrocytic anaemia?

A

RBC have a high MCV

118
Q

What is megaloblastic anaemia?

A

large immature RBC synthesised in a small quantity

119
Q

What is the cause of megaloblastic anaemia?

A

Impaired DNA synthesis commonly due to B12/folate deficiency

120
Q

What is haemolytic anaemia?

A

increased destruction of RBC - may be due to an inherited, immune or auto-immune condition

121
Q

What is sickle cell anaemia?

A

genetic mutation causes the production of abnormal red blood cells - results in impaired passage and reduced lifespan of RBC

122
Q

How is sickle cell anaemia treated?

A
  • blood transfusion
  • stem cell transplant
  • analgesia
  • hydroxycarbamide?
123
Q

What is sickle cell anaemia?

A

genetic mutation causes the production of abnormal red blood cells - results in impaired passage and reduced lifespan of RBC

124
Q

How is sickle cell anaemia treated?

A
  • blood transfusion
  • stem cell transplant
  • analgesia
  • hydroxycarbamide (chemotherapy)
125
Q

What is haemolytic disease of the newborn?

A

mother produces antibodies to the rhesus antigen on the fetal RBC which cross the placenta and causes lysis of the RBC

My Phase 2a Medicine (5 decks)

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