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Phase 2a flashcards (Alec's) > Haematology > Flashcards

Haematology Flashcards

1
Q

What is key to look at in a FBC and what do they indicate?

A
  • RBC (anaemias)
  • Neutrophils (bacterial infection)
  • Lymphocytes (chronic infection)
  • Platelets (clotting ability)
  • Eosinophils (parasitic infection)
  • Monocytes (myelodysplastic syndromes)
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2
Q

What is a normal number of RBCs for men and women?

A

Men = 4.0 - 5.9 x 10^12 / litre

Women = 3.8 - 5.2 x 10^12 / litre

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3
Q

How is blood clotting measured (3 ways)

A
  • Prothrombin time (PT)
  • Activated partial thrombo-plastin time (APTT)
  • Bleeding/ thrombin time (TT)
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4
Q

What is prothrombin time a measure of and how long is it?

A

Extrinsic pathway (10 - 13.5 seconds)

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5
Q

What is INR

A

Patient PT / standard PT time

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6
Q

What is activated partial thrombo-plastin time a measure of and how long is it?

A

Intrinsic pathway (35 - 45 seconds)

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7
Q

What is thrombin time a measure of?

A

Fibrinogen –> fibrin (12 - 14 seconds)

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8
Q

What does mean corpuscular volume (MCV) measure?

A

Average size of your RBCs

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9
Q

What is anaemia?

A

Low levels of haemoglobin in the blood

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10
Q

What is a low haemoglobin level in grams per litre?

A

Males = <130 g/l

Females = <120 g/l

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11
Q

What are the 3 classes of anaemia?

A
  • Microcytic
  • Normocytic
  • Macrocytic
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12
Q

What is the normal MCV value?

A

Normocytic = 80-95

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13
Q

What are the general symptoms of anaemia (5)?

A
  • Fatigue
  • Pallor
  • Tachycardia
  • Raised respiratory rate
  • Dysponea (exertional)
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14
Q

What are two types of haemolysis?

A
  • Intravascular (contents released into BVs)
  • Extravascular (@spleen mostly)
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15
Q

What is the most common cause of anaemia worldwide?

A

Iron deficiency anaemia

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16
Q

What are 4 causes of microcytic anaemia?

A
  • Fe deficiency anaemia
  • Thalassaemia
  • Sideroblastic anaemia
  • Lead poisoning
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17
Q

What is Fe deficiency anaemia?

A

Low haemoglobin levels due to non-inherrited Fe deficiency

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18
Q

Where is iron absorbed in the gut?

A

Duodenum + proximal jegunum

Iron first, bro

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19
Q

What causes iron deficiency (4)?

A
  • Malnutrition
  • Malabsorption (coeliacs, IBD)
  • Menorrhagia (heavy periods)
  • GI bleeding (cancer, ulcers)
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20
Q

What medications can interfere with the absorption of iron?

A

Medications that alter stomach pH as stomach acid is required to keep iron in a soluble form (e.g. PPIs)

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21
Q

What does iron circulate bound to?

A

Transferrin

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22
Q

What is iron stored bound to?

A

Ferritin

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23
Q

Why does Fe deficiency cause microcytic anaemia?

A

Not enough iron to fatten up RBCs

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24
Q

What are the specific symtpoms of Fe deficent anaemia?

A
  • Koilonychia (spoon shaped nails)
  • Angular stomatitis (ulcers at mouth corners)
  • Atrophic glossitis (white texture on tounge)
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25
Q

How is Fe deficiency anaemia investigated (3)?

A
  • FBC = microcytic anaemia
  • Fe studies
  • Blood film
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26
Q

What do Fe studies show in Fe deficient anaemia? (4)

A
  • Low ferritin
  • Low Fe
  • High transferrin
  • Low transferrin saturation/ total iron binding capacity (TIBC)
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27
Q

What does the blood film show in Fe defficient anaemia (3)?

A
  • Hypochromic RBC (as low haemoglobin)
  • Target cells (dark RBC due to high SA/V ratio)
  • Howell jolly bodies (nucleated RBCs)
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28
Q

Who is given an endoscopy for Fe deficient anaemia?

A

Over 60s

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29
Q

How is Fe deficient anaemia treated?

A

Oral Fe (ferrous sulphate)

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30
Q

What is thalassaemia?

A

Change in the genes that code for the proteins that make up haemoglobin (2 alpha, 2 beta chains), microcytic

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31
Q

What are the two types of thalassaemia?

A
  • Alpha
  • Beta
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32
Q

Which chromosome is affected in alpha thalassaemia?

A

16

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33
Q

What are the 4 chains found in haemoglobin?

A
  • Alpha
  • Beta
  • Gamma
  • Delta
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34
Q

What is found in feta haemoglobin?

A

2 alpha, 2 gamma

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35
Q

What is HbH?

A

4 Beta chains

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36
Q

What types of thalassaemia alpha are there?

A

Ranging from 1 to 4 gene deletions, increasing in severity (more HbH = more severe)

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37
Q

What is Hb A2

A

2 alpha, 2 delta chains

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38
Q

What are the types of Beta thalassaemia?

A

Thalassaemia minor, intermedia and major

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39
Q

What is thalassaemia minor?

A

1 abnormal, 1 normal Beta gene OR 1 deletion, 1 normal Beta gene

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40
Q

What is thalassaemia intermedia?

A

2 defective genes OR 1 defective, 1 deletion gene

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41
Q

What is thalassaemia major?

A

2 deletion beta genes

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42
Q

What haemoglobin levels does thalassaemia increase?

A
  • HbA2 (in beta)
  • HbF (in beta)
  • HbH (in alpha)
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43
Q

What are the specific signs/ symptoms of thalassaemia (2)?

A
  • Chipmunk facies (look like chipmunk)
  • Hepatosplenomegally (increased destruction of RBCs)
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44
Q

How is thalassaemia investigated (2)?

A
  • FBC/ blood film
  • Hb electrophoresis (diagnostic - shows Hb type proportions)
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45
Q

What would be abnormal on FBC and Blood film in thalassaemia (3)?

A
  • Hypochromic RBCs
  • Target cells (microcytic)
  • High reticulocytes (fast RBC turnover)
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46
Q

How is thalassaemia treated (3)?

A
  • Supportive
  • Stem cell bone marrow transplant (definitive)
  • Transfusion (+ chelation)
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47
Q

What supportive treatments are given for thalassaemia (4)?

A
  • Iron chelaction (reduce iron levels)
  • Transfusions
  • Folate
  • Splenectomy
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48
Q

What is Sideroblastic anaemia?

A

Genetic problem, mitochondria not able to synthesis Hb properly

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49
Q

What are iron levels like in sideroblastic anaemia?

A

High

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50
Q

What are the normocytic haemolytic anaemias?

A
  • Sickle cell
  • Hereditary spherocytosis
  • G6PDH deficiency
  • Malaria
  • Autoimmune haemolytic
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51
Q

What are the normocytic non haemolytic anaemias

A
  • CKD
  • Aplastic anaemia
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52
Q

What is sickle cell disease?

A

Autosomal recessive condition that affects the beta chains of haemoglobin

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53
Q

What is Hb S made of?

A

2 Alpha chains, 2 mutated B chains

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54
Q

What nucleotides are different in sickle cell disease?

A

GAG –> GTG on 6th codon of beta globulin (glutamate –> valine)

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55
Q

What is the result of this mutation in sickle cell disease?

A

RBCs become sickle shaped under stressed conditions

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56
Q

What are some examples of conditions that stress RBCs in sickle cell disease (5)?

A
  • Dehydration
  • Hypoxia
  • Infection
  • Cold temp
  • Acidosis
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57
Q

Specific symptoms/ signs of sickle cell disease (2)?

A
  • Pre hepatic jaundice (lots of RBCs killed)
  • Painful limbs (RBCs getting stuck)
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58
Q

Complications of sickle cell anaemia (3)?

A
  • Splenic sequestration (spleen jammed up by sickle RBCs)
  • Vaso-occlusive crisis (cappilaries jammed –> ischemia)
  • Acute chest crisis (vaso-occlusion of pul vessels)
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59
Q

Investigations for Sickle cell disease (2)

A
  • Blood film + FBC
  • Hb electrophoresis (diagnostic)
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60
Q

What would blood film + FBC show in sickle cell disease (3)?

A
  • High reticulocytes
  • Sickle RBCs
  • Howell Jolly bodies (nucleated RBCs)
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61
Q

How are acute sickle cell attacks treated (4)?

A
  • Fluids
  • Analgesia (NSAIDs)
  • O2
  • (Antibiotics)
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62
Q

How is sickle cell treated long term (5)?

A
  • Hydroxycarbomide = hydroxyurea (reduce DNA synthesis)
  • Folic acid supplements
  • Transfusion
  • Fe chelation
  • BM transplant (last resort)
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63
Q

What drug is used for Fe chelation?

A

Desferrioxamine

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64
Q

What is G6PDH deficiency?

A

Glucose-6-phosphate dehydrogenase deficiency allows ROS to damage RBCs

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65
Q

How does G6PDH protect agains ROS

A

G6PDH involved with glutathione synthesis, glutathione protects against ROS by reacting with them

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66
Q

How is G6PDH deficiency inherrited?

A

X-linked recessive

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67
Q

What would precipitate symptoms in those with G6PDH deficiency?

A

Things that increase ROS e.g. smoking, fava bean consumption, certain medications

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68
Q

What sort of haemolysis occurs in G6PDH deficiency?

A

Intravascular

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69
Q

What is present within the blood of people with G6PDH deficiency (blood film, 2)?

A
  • Heinz bodies (damaged/ denatures Hb by ROS)
  • Bite cells (chunks taken out as denatured Hb removed by spleen)
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70
Q

How is G6PDH deficiency treated?

A
  • Blood transfusions
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71
Q

What is hereditary spherocytosis?

A

Deficiency in structural membrane protein spectrin

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72
Q

How is hereditary spherocytosis inherrited?

A

Autosomal dominant

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73
Q

What change in shape does hereditary spherocytosis cause?

A

RBC become spherical + rigid

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74
Q

What is a result and complication of these spherical RBCs in hereditary spherocytosis?

A

Increased splenic recycling, RBCs get stuck in capillaries –> splenomegally, autosplenectomy

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75
Q

What are some specific symptoms of hereditary spherocytosis?

A
  • Neonatal jaundice
  • Splenomegally
  • Gall stones
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76
Q

Why are gall stones common in some anaemias?

A

Low iron levels –> bile supersaturation, increasing the risk of gall stones

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77
Q

How is hereditary spherocytosis diagnosed (2)?

A
  • Blood film = spherocytes
  • Coombs -ve (therefore not AHA)
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78
Q

How is hereditary spherocytosis treated?

A

Splenectomy

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79
Q

What age is a splenectomy usually done after?

A

6 years (due to risk of sepsis)

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80
Q

How is neonatal jaundice treated?

A

Phototherapy (expose skin to UV) - helps liver break down bilirubin

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81
Q

What is a complication of neonatal jaundice?

A

Kernicterus - Collection of bilirubin in basal ganglia –> death

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82
Q

What is autoimmune haemolytic anaemia?

A

Abs bind to RBC –> haemolysis

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83
Q

How is autoimmune haemolytic anaemia tested for?

A

Direct Coombs test (tests for auto RBC Abs)

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84
Q

How does CKD cause anaemia?

A

Low production of erythropoetin

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85
Q

What is aplastic anaemia?

A

Pancytopenia (all 3 blood componenets low in levels) bone marrow fails to make haemopoeitic stem cells

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86
Q

What causes aplastic anaemia?

A
  • Idiopathic
  • Congenital
  • Infection (maybe)
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87
Q

How is aplastic anaemia diagnosed?

A

Bone marrow biopsy (hypocellularity)

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88
Q

What are the types of Megaloblastic macrocytic anaemia?

A
  • B-12 deficiency
  • Folate deficiency
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89
Q

What are the types of non-megaloblastic macrocytic anaemia?

A
  • Hypothyroidism
  • Alcohol excess
  • Liver disease
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90
Q

What is the difference between megaloblastic and non-megaloblastic macrocytic anaemia?

A

Megaloblastic is to do with deficiency/ impairment of utilisation of B12/ folate

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91
Q

What is B12 needed for?

A

RBCs DNA to mature and condense

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92
Q

What are 3 causes of vitamin B12 deficiency?

A
  • Malnutrition
  • Pernicious anaemia
  • Absorption problems (e.g. crohns)
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93
Q

What cells produce intrinsic factor?

A

Parietal cells

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94
Q

What is pernicious anaemia?

A

Autoimmune response against parietal cells or intrinsic factor

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95
Q

What does B12 attach to in the saliva and protect it from the stomach acid and transports it around the blood?

A

Transcobalamin 1

(Cobalamin = Vit B12)

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96
Q

Where is B12 absorbed in the gut?

A

Distal ileum

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97
Q

What are the specific symptoms of B12 deficiency (3)?

A
  • Yellow skin (high bilirubin)
  • Angular stomatits + glossitis
  • Neurological symtpoms
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98
Q

What causes neurological symptoms in B12 deficiency?

A

Low B12 –> demyelination

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99
Q

What sort of neurological symptoms occur with Vit B12 deficiency (2)?

A
  • Symmetrical paraesthesia
  • Muscle weekness
    Lots of other stuff
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100
Q

How is vit B12 deficiency diagnosed (2)?

A
  • Blood film
  • Low serum B12
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101
Q

What would the blood film in vit B12 deficiency show (2)?

A
  • Macrocytic RBCs
  • Megaloblasts
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102
Q

What is a megaloblast?

A

Large, nucleated RBC precursor

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103
Q

How is pernicious anaemia diagnosed?

A

Anti IF/ parietal cell antibodies present

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104
Q

How is vitamin B12 deficiency treated (2)?

A
  • Oral B12 supplements (cyanocobalamin)
  • Pernicious anaemia = IM hydroxocobalamin (synthetic B12)
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105
Q

What are the causes of folate deficiency anaemia (4)?

A
  • Malnutrition/ absorption
  • Alcohol
  • Dihydrofolate reductase inhibitors
  • Pregnancy
106
Q

What is the function of folate?

A

DNA synthesis

107
Q

What are the specific symptoms of folate deficiency?

A

Angular stomatits + glossitis

108
Q

How is folate deficiency diagnosed (2)?

A
  • Macrocytic megaloblasts (on blood film)
  • Low serum folate
109
Q

How is folate deficiency treated?

A

Folate supplements

Pregnancy = folate for first 12 weeks

110
Q

What is immportant to do in people with folate and B12 deficiency?

A

Treat B12 deficiency first

111
Q

Why does B12 deficiency need to be treated before folate deficiency?

A

Folate depletes B12 further causing demyelination (subacute degeneration of the cord)

112
Q

How long does folate deficiency and B12 deficiency take to develop?

A
  • B12 deficiency = years
  • Folate deficiency = months
113
Q

How does alcoholism cause macrocytic anaemia?

A

Damages precursors to RBCs so not as many and larger ones produced

114
Q

How does hypothyroidism cause macrocytic anaemia?

A

Interferes with erythropoetin

115
Q

What is leukaemia?

A

Mutation in the precursor to WBCs in the bone marrow

116
Q

What does this mutation seen in leukaemia cause?

A

Proliferation of this progenitor cell and overproduction of the cell it differentiates to

117
Q

What types of cells can leukaemia affect?

A
  • Myeloid (precursors to granulocytes + monocytes)
  • Lymphoid (precursor to lymphocytes)
118
Q

How else can leukaemias be classified reguarding how quickly they develop?

A
  • Chronic = slow (usually larger genetic mutation)
  • Acute = fast (usually smaller genetic mutation)
119
Q

What are the 4 types of leukaemia?

A
  • Acute myeloid leukaemia
  • Chronic myeloid leukaemia
  • Acute lymphoid (lymphoblastic) leukaemia
  • Chronic lymphoid (lymphocytic) leukaemia
120
Q

What are general symptoms/ signs of leukaemia (7)?

A
  • Bone pain
  • Bleeding
  • Infection
  • Pancytopenia
  • Fatigue
  • Hepatosplenomegally
  • Petechiae
121
Q

What are petechiae?

A

Red spots on skin - sign of bleeding

122
Q

What investigations are usually done in people suspected of leukaemia?

A
  • FBC + blood film
  • BM biopsy
123
Q

What is AML associated with?

A
  • Down syndrome
  • Radiation exposure
124
Q

What is the prognosis in AML?

A

Very severe 20% 3 year survival. Treatment ASAP

125
Q

What is a specific symptom of AML?

A

Gum infiltration (big puffy gums)

126
Q

How is AML diagnosed?

A
  • Blood studies myeloperoxidase +ve and Auer rods
  • BM biopsy = >20% myeloid blasts
127
Q

What are auer rods?

A

Collection of myeloperoxidase in neutrophils

128
Q

How is AML treated?

A
  • Chemo
  • BM transplant = last resort
129
Q

What can occur from chemotherapy if tumour killed too quickly?

A

Tumour lysis syndrome

130
Q

What is tumour lysis syndrome?

A

Death of tumour cells quickly releases uric acid

131
Q

What is a complication of tumour lysis syndrome?

A

Accumulation of uric acid crystals in kidneys –> AKI

132
Q

How is tumour lysis syndrome treated?

A

Allopurinol (reduce uric acid levels)

133
Q

What are the three phases of CML?

A
  • Chronic
  • Accelorated
  • Blast
134
Q

How long does the chronic phase typically last?

135
Q

What mutation often causes CML?

A

Translocation between chromosome 9 and 22; t(9:22)

136
Q

What is this mutation known as in CML?

A

Philadelphia chromosome

137
Q

Which two genes join together in the philadelphia chromosome?

A

BCR-ABL gene fusion

138
Q

What does the philadelphia chromosome result in being irreversibly turned on?

A

Tyrosine kinase

139
Q

What effect does tyrosine kinase have on cells?

A

Increases cell proliferation

140
Q

What percent myeloblasts cells are the three phases of CML

A
  • Chronic = <10%
  • Accelerated = 10-19%
  • Blast crisis = >20%
141
Q

How is CML diagnosed?

A
  • High myeloblast cell percent in blood
  • High BM biopsy myeloblast cell proportion
  • Philadelphia chromosme genetic test
142
Q

How is CML treated?

A
  • Chemo
  • Tyrosine kinase inhibtors
143
Q

What is an example of a tyrosine kinase inhibitor?

144
Q

What can CML progress to?

145
Q

What mutation usually causes ALL?

A

Mutation in B cells

146
Q

What translocation often occurs in ALL?

147
Q

How is ALL diagnosed?

A
  • Blood film = high lymphoblasts
  • BM biopsy = >20% lymphoblasts (diagnostic)
148
Q

What is present in lymphoblasts in ALL?

A

Terminal deoxynucleotidyl transferase (TdT)

149
Q

How is ALL treated?

A
  • Chemo
  • Allopurinol
150
Q

What cell does CLL usually affect?

151
Q

How is CLL diagnosed?

A

Blood film = smudge cells present (fragile lymphocytes damaged in filmed preperation)

152
Q

What is low in the blood in CLL?

A

Hypogammaglobulinaemia - B cells proliferate but dont differentiate to plasma cellsand produce IgG

153
Q

How is CLL treated?

A
  • Chemo
  • Allopurinol
154
Q

What is a complication of CLL?

A

B cells transform to more agressive lymphoma and accumulate in lymph node

155
Q

What is the transformation of CLL to a more agressive lymphoma known as?

A

Richter transformation

156
Q

What is the most common leukaemia in adults and affects older people?

157
Q

What is the most common leukaemia in children?

158
Q

What is the most common acute adult leukaemia?

159
Q

What can CML progress to?

160
Q

What is a lymphoma?

A

Cancer of lymphocytes (T and B cells or NK cells) that collect in lymph nodes

161
Q

How are lymphoma classified (2 ways)?

A
  • Hodgkin/ non hodgkin
  • Grade (low, high, very high)
162
Q

What cell is found in hodgkin lymphoma?

A

Reed sternberg cell

163
Q

What are typical symptoms of Lymphoma?

A
  • Fever
  • Night sweats
  • Unintentional weight loss
  • Lymphadenopathy
164
Q

What are the B symptoms?

A
  • Night sweats
  • Unintentional weight loss
  • Fever

(systemic affects of lymphoma)

165
Q

What cell is most commonly affected in lymphoma?

166
Q

What age groups does hodgkin lymphoma usually present?

A

2 peaks
* Teens
* Elderly

167
Q

What have Lymphoma been associated with?

A
  • Viruses - HIV, EBV, helicobactor pylori
  • Autoimmune - SLE, Sjogrens
168
Q

How is hodgkins affected by alcohol?

A

Hodgkins is painful after alcohol

169
Q

How is hodgkins investigated?

A
  • Bloods - low Hb, high ESR
  • BM biopsy (diagnositic)
  • Imaging - stage the tumour
170
Q

What is a pop corn cell?

A

Variant of reed sternberg cells found in some hodgkin lymphoma

171
Q

What is used to stage lymphomas?

A

Ann Arbour staging (1-4)

172
Q

What are stages 1-4 of Ann Arbour?

A
  1. Single lymph node.
  2. Multiple lymph nodes on same diaphragm side.
  3. Lymph nodes on both diaphragm sides.
  4. Extranodal organ spread.
173
Q

What chemo is used to treat hodgkin lymphoma (3)?

A
  • Adriamycin
  • Bleomycin
  • Vinblastine
174
Q

What are some side effects of this chemotherapy (3)?

A
  • Alopecia
  • N+V
  • BM failure + infection
175
Q

What are people on chemotherapy at risk of?

A

Febrile neutropenia

176
Q

What is febrile neutropenia?

A

Infection when immune system surpressed by chemo

177
Q

How is non-hodgkin lymphoma graded?

A
  • Low
  • High
  • Very high
178
Q

What is an example of a low grade lymphoma?

A

Follicular lymphoma

179
Q

What is an example of a high grade lymphoma?

A

Diffuse B cell lymphoma

180
Q

What is an example of a very high grade lymphoma?

A

Burkitts lymphoma

181
Q

How does burkitts lymphoma present?

A

Differently in different areas of the world

E.g. in africa = large swollen jaw

182
Q

How is non-hodgkin lymphoma diagnosed?

A
  • Blood tests/ films
  • BM biopsy (diagnostic)
  • Imaging to stage
183
Q

What chemo is used for non-hodgkin lymphoma (2)?

A
  • Rituximab - targets CD20 (on B cells)
  • Cyclophosphamide
184
Q

What else is used to treat lymphoma as well as chemotherapy?

A

Radiotherapy

185
Q

How can lymphomas affect the skin?

A
  • Mycosis fungoides (NHL)
  • Skin excoriations (HL)
186
Q

What is myeloma?

A

Cancer of plasma cells (activated B-cells) that cause rapid uncontrollable monoclonal division

187
Q

What are the 3 types of myeloma?

A
  • Monoclonal gammopathy of undetermined significance
  • Multiple myeloma
  • Smouldering myeloma
188
Q

What is the most commonly affected Ig in myeloma?

189
Q

What are 2 risk factors for myeloma?

A
  • Old >70
  • Afro-caribbean
190
Q

What effect do plasma cells have on bone?

A

Release cytokines that surpress osteoblasts and increase osteoclasts activity - this degrades bone

191
Q

What are 4 symptoms/ features of myeloma?

A
  • Hypercalaemia
  • Renal disease
  • Anaemia (pancytopenia)
  • Bone lesions
192
Q

What can the high number of proteins (Igs) in myeloma result in?

A

Hyperviscosity

193
Q

What can hyperviscosity cause?

A
  • Easy bleeding/bruising
  • Decreased blood supply
  • Heart failure
194
Q

What causes renal impairment in myeloma?

A
  • Hypercalaemia decreases renal function
  • High Igs levels blocks BVs and can deposit in the nephrons
195
Q

What is Ig deposition in the kidneys known as?

A

Kappa deposition

196
Q

How is suspected myeloma initially investigated (1 test, 4 results)?

A

Blood tests:
* Pancytopenia
* Raised Ca
* Raised ESR
* Raised plasma viscosity

197
Q

How is myeloma tested for (2)?

A
  • Bence jones proteins in urine
  • Serum protein electrophoresis
198
Q

What is a bence jones protein?

A

Monoclonal light Ig chain found in urine

199
Q

What would serum protein electrophoresis show?

A

‘M’ spike (monoclonal Ig spike)

200
Q

How can a myeloma diagnosis be confirmed?

A

Bone marrow biopsy >10% plasma cells

201
Q

What imaging is done for myeloma?

A

Bone imaging to check for lesions (X-ray, mri or ct)

202
Q

How is myeloma treated?

A
  • Chemo
  • Bisphosphinates
  • Dialysis
  • Stem cell transplant
203
Q

How do bisphosphonates work and give an example?

A

Surpress osteoclasts

Alendronate

204
Q

What is monoclonal gammopathy of undetermined significance (MGUS)?

A

Excess monoclonal antibody, but no other symptoms of myeloma (<10% plasma cells in BM biopsy)

205
Q

What can MGUS progress to?

A

Smouldering myeloma

206
Q

What is smouldering myeloma called when there is excessive IgM specifically?

A

Waldenstroms macroglobulinaemia

207
Q

What are 2 myeloproliferative disorders?

A
  • Polycythaemia
  • Thrombocythaemia
208
Q

What are 2 types of polycythaemia?

A
  • Primary (polycythaemia vera)
  • Secondary
209
Q

What can cause secondary polycythaemia (3 things)?

A
  • Hypoxia
  • Dehydration
  • High levels of EPO
210
Q

What mutation usually causes polycythaemia vera?

A

JAK2 V617 mutation

211
Q

Signs/ symptoms of polycythaemia vera (5)?

A
  • Itching + numbness in limbs (due to cytokine production)
  • Red puffy face
  • Blurred vision
  • Hepatosplenomegally
  • Hyperviscosity
212
Q

How is polycythaemia vera investigated (2)?

A
  • FBC = High RBC, WBC, Platelets
  • Genetic testing = JAK2 V617 positive
213
Q

How is polycythaemia vera treated (3)?

A
  • Venesection (remove blood - 1 pint)
  • Aspirin (reduce clot risk)
  • Chemo (hydroxyurea)
214
Q

What can polycythaemia vera cause in the bone marrow?

A

Myelofibrosis (BM replaced with scar tissue due to cytokines)

215
Q

What conditions affect the coagulation cascade (3)?

A
  • Haemophilia A/B
  • Von willebrand factor disease
  • Disseminated intravascular coagulopathy
216
Q

How is haemophilia A/B inherited?

A

X linked recessive

217
Q

What clotting factors do haemophilia A and B affect?

218
Q

What are the signs/ symptoms of haemophilia?

A
  • Easy bleeding + bruising
  • Haemarthrosis (bleeding into joints)
219
Q

What would happen to PT and APTT?

A
  • PT is normal as extrinsic pathway unaffected
  • APTT high as intrinsic pathway slow
220
Q

How can Haemophilia be diagnosed?

A
  • Coagulation factor assay (F8/9 low)
  • Genetic testing
221
Q

How is haemophilia treated?

A

IV factor 8/9

222
Q

What should be given with factor 8?

A

Desmopressin - helps synthesis + release of VWF from endothelial cells

223
Q

What is the function of VWF?

A
  • Prevents the breakdown of factor 8
  • Helps platelets adhere to damaged endothelium
224
Q

How is VWF disease inherited?

A

Autosomal dominant

225
Q

What are the signs/ symptoms of VWF disease?

A

Easy bleeding/ bruising

226
Q

How is VWF disease diagnosed?

A
  • Family history/ genetic testing
  • APTT high PT normal
    No definitive test for diagnosis
227
Q

How is VWF disease treated?

A
  • VWF infusion
  • Desmopressin (stimulate release of VWF)
228
Q

What causes disseminated intravascular coagulopathy (DIC)?

A

Overactivation of the clotting cascade e.g.:
* Trauma
* Sepsis

229
Q

How is DIC treated (2)?

A
  • Clotting factor, fibrinogen replacement
  • Platelet, RBC transfusion
230
Q

What is a normal platelet count?

A

150-450 x 10^9 / l

231
Q

What is thrombocytopenia?

A

Low platelets in the blood

232
Q

What are the two main types of thrombocytopenia?

A
  • Thrombotic thrombocytopenic purpura
  • Immune thrombocytopenic purpura
233
Q

What Ig class causes ITP?

234
Q

What are some causes/ risk factors fro ITP (3)?

A
  • Recent viral infection
  • Other autoimmune conditions
  • Heparin induced thrombocytopenia (HIT)
235
Q

How is ITP diagnosed (2)?

A
  • Thrombocytopenia
  • High bone marrow megakaryoblasts (biopsy)
236
Q

How is ITP treated (3)?

A
  1. Prednisolone (steroid)
  2. IV IgG (surprises IgG production)
  3. Splenectomy
237
Q

How is ITP paradoxical?

A

There are low platelets, however the IgGs that attach to the platelets activate the clotting cascade causing more unusual blood clots.

238
Q

What causes TTP?

A

Tiny blood clots forming through small blood vessels using up the platelets

239
Q

What gene causes TTP?

A

ADAMTS13 gene problem

240
Q

What does a deficiency in ADAMTS13 protein cause?

A

vWF not inactivated this causes over expression of vWF –> lots of platelet adhesion and activation –> low platelet levels systemically

241
Q

What are the symptoms of thrombocytopenia (3)?

A
  • Purpuric rash
  • Easy bleeding + menorrhagia
  • AKI, haemolytic anaemia, neurological symptoms
242
Q

How is TTP diagnosed (3)?

A
  • Thrombocytopenia
  • Schistocytes (fragmented RBCs)
  • Microangiopathic haemolytic anaemia
243
Q

How is TTP treated (3)?

A
  • Plasmapheresis (removes proteins that damage ADAMTS13)
  • Prednisolone (steroid)
  • Rituximab (monoclonal antibody agains B cells)
244
Q

What 4 parasites cause malaria?

A
  • Plasmodium falciparum
  • Plasmodium ovale
  • Plasmodium vivax
  • Plasmodium malariae
245
Q

What is the most common and deadly type of malaria?

A

Plasmodium falciparum

246
Q

Describe how malaria replicates (5 steps).

A
  • Sporozoites in mosquito saliva enter blood
  • Multiply in hepatocytes as merozoites
  • Divide in RBC: meroxoites –> trophozoites –> shizont –> new merozoites
  • RBCs replicate, plasmodium spill out
247
Q

What are the symptoms/ signs of malaria (4)?

A
  • Fever
  • Anaemia
  • Hepatosplenomegaly
  • Blackwater Fever (RBCs burst releasing haemoglobin into blood + urine)
248
Q

How is malaria diagnosed (2 things)?

A

Blood film
* Thick film - identifies malaria
* Thin film - identifies species

249
Q

How is malaria treated (3)?

A
  • Quinine + doxycycline (Abx)
  • Artesunate (IV) - If severe
250
Q

What can EBV put you at greater risk of?

A

Lots of types of cancer e.g. lymphoma (Hodgkins and Burkitts)

251
Q

How is EBV spread?

A

Via saliva/ bodily fluids

252
Q

How is EBV diagnosed?

A
  • Antibody blood test
  • A-typical lymphocytes on blood film
253
Q

How is HIV spread (3)?

A
  • Blood contact
  • Sexual contact
  • Mother to child
254
Q

Give 4 risk factors for HIV?

A
  • IV drug users
  • Unprotected anal sex
  • Paid sex workers
  • High prevalence countries
255
Q

What are the two types of HIV and which is most common and most virulent?

A
  • HIV-1 (most common, most virulent)
  • HIV-2
256
Q

How does HIV cause infection (5)?

A
  • Enters CD4+ (TH cells) via gp120
  • Endocytoses RNA + enzymes
  • Reverse transcriptase RNA –> DNA
  • Integrase - viral DNA inserted into hosts
  • Protein synthesis + takes control of CSM
257
Q

What are the 4 stages of HIV?

A
  1. Infection - dip in CD4+
  2. Clinical latency (can last years)
  3. Symptomatic phase
  4. AIDS
258
Q

What are the symptoms of HIV (4)?

A
  • Fever
  • Opportunistic infections
  • Weight loss
  • Night sweats
259
Q

What defines AIDS?

A

CD4+ < 200 / ml

260
Q

How is HIV diagnosed?

A

ELISA (enzyme linked immunosorbent assay)
Tests for anti HIV Ig (P24 Ab)

261
Q

How is HIV treated?

A

HAART (highly active antiretroviral therapy)

Phase 2a flashcards (Alec's) (13 decks)

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