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ALS > Block 4 > Flashcards

Block 4 Flashcards

1
Q

what are the functions of blood? (2)

A
  • transportation - supplies O2 and nutrients to tissues
  • regulation - body temp, maintain pH and osmotic pressure
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2
Q

how much blood does an average adult have?

A
  • 5 litres
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3
Q

what are the components of blood? (2)

A
  • 55% liquid - plasma
  • 45% formed elements - RBCs, WBCs and platelets
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4
Q

what are the components of plasma? (3)

A
  • 92% water
  • 7% proteins
  • 1% other
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5
Q

what are the components of formed elements?

A
  • 99% RBCs
  • 1% WBCs and platelets
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6
Q

what is haematopoiesis?

A

blood cell formation

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7
Q

where does haematopoiesis start?

A
  • yolk sac
  • bone marrow in adults
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8
Q

where does haematopoiesis occur in adults?

A
  • long bones
  • flat bones in later life
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9
Q

what does a long term haematopoietic stem cell differentiate into?

A

short term haematopoietic stem cell

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10
Q

what does a short term haematopoietic stem cell differentiate into?

A
  • multipotent progenitor
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11
Q

what can a multipotent progenitor cell differentiate into? (2)

A
  • common myeloid progenitor
  • common lymphoid progenitor
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12
Q

what can a common myeloid progenitor cell differentiate into? (3)

A
  • megakaryote
  • erythrocytes
  • granulocyte/macrophage
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13
Q

what can a granulocyte/macrophage cell differentiate into? (5)

A
  • mast cell
  • basophil
  • neutrophil
  • eosphil
  • monocyte
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14
Q

what does a megakaryocytic differentiate into?

A
  • thrombocytes
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15
Q

what can a common lymphoid progenitor cell differentiate into? (4)

A
  • dendritic cell
  • natural killer cell
  • B-cells
  • T-cells
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16
Q

what does a B-cell differentiate into?

A

plasma cell

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17
Q

what does a monocyte differentiate into? (2)

A
  • macrophage
  • dendritic cell
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18
Q

what are the 7 stages of erythropoiesis?

A
  • hemocytoblast
  • proerythroblast
  • early erythroblast
  • late erythroblast
  • normoblast
  • reticulocyte
  • erythrocyte
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19
Q

what is erythropoiesis?

A
  • red blood cell formation
  • occurs in bone marrow
  • regulated by EPO binding to erythropoietin receptors on progenitor cells
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20
Q

what is the role of haemoglobin?

A
  • O2 binding
  • transport
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21
Q

how long do RBCs live for?

A

120 days

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22
Q

what removes RBCs?

A

spleen macrophages

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23
Q

what is iron transported by?

A

transferrin

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24
Q

where is iron transported to for new RBCs ?

A

bone marrow

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25
Q

what is the role of platelets? (3)

A
  • maintaining blood volume
  • bind to endothelial cells in blood vessels to prevent blood loss
  • become activated during tissue damage
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26
Q

what % of platelets are stored?

A

30%

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27
Q

where are platelets stored?

A

spleen

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28
Q

how long do platelets live for?

A

7-10 days

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29
Q

what is the role of leucocytes (WBCs)?

A

mediate protective effects of blood through regeneration of the inflammatory process

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30
Q

what are the 5 signs of inflammation?

A
  • pain
  • redness
  • heat
  • swelling
  • loss of function
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31
Q

what % of neutrophils make up WBCs?

A

60-70%

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32
Q

what % of eosinophils make up WBCs?

A

2-5%

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33
Q

what % of basophils make up WBCs?

A

0.2%

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34
Q

what % of monocytes make up WBCs?

A

2-10%

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35
Q

what % of natural killer cells make up WBCs?

A

15%

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36
Q

what % of lymphocytes make up WBCs?

A

20%-40%

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37
Q

what is the lifespan of neutrophils?

A

18hrs

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38
Q

what is the lifespan of eosinophils?

A

2-5 days

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39
Q

what is the lifespan of basophils?

A

1-2 days

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40
Q

what is the lifespan of monocytes?

A

1-7 days

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41
Q

what is the lifespan of natural killer cells?

A

14 days

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42
Q

what is the lifespan of lymphocytes?

A

weeks-years

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43
Q

what role do neutrophils play in the immune system?

A

phagocytosis

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44
Q

what role do eosinophils play in the immune system?

A

phagocytosis

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45
Q

what role do basophils play in the immune system?

A

allergic reaction

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46
Q

what role do monocytes play in the immune system?

A
  • phagocytosis
  • differentiate to become macrophages in tissue
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47
Q

what role do natural killer cells play in the immune system?

A

killing virally infected cells

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48
Q

what is anaemia?

A
  • reduction of RBCs
    or
  • decreased amount of haemoglobin in RBCs
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49
Q

what is the consequence of anaemia?

A
  • reduced level of O2 delivered to tissues
  • causing weakness, tiredness, inability to exercise and SOB
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50
Q

what are the signs of anaemia? (5)

A
  • pallor
  • tachycardia (100bpm+)
  • glossitis (swollen tongue)
  • koilonchia (spoon nails)
  • dark urine
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51
Q

how does EPO regulate erythrocytes? (3)

A
  • juxtatubular intestinal cells of the renal cortex produce 90% of the EPO
  • sense O2 levels through oxygen-dependant prolyl-hydroxylase
  • regulates transcription factor for EPO HIF-1 (alpha).
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52
Q

describe the negative feedback system of EPO (5)

A
  • hypoxia (low o2)
  • increased HIF detected and increases EPO production
  • this increases erythrocyte production
  • decrease in hypoxia
  • decrease HIF therefore decreased EPO production
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53
Q

name two types of conditions that affect erythropoiesis

A
  • Pure Red Cell Aplasia (PRCA) - only affects erythropoiesis
  • Pancytopenia - affects RBC and other cell types (WBC, platelets)
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54
Q

name an example of PRCA

A
  • diamond-blackfan anemia
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55
Q

what is haemolytic anaemia?

A

premature destruction of erythrocytes either by extrinsic or intrinsic mechanisms

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56
Q

what causes haemolytic anaemia?

A

bone marrow is unable to match production to the destruction of new RBCs

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57
Q

what are the two causes of haemolytic anaemia?

A
  • RBCs destroyed by external processes e.g. drugs, toxins, infection
  • something is intrinsically wrong e.g. damage, abnormal haem, destruction
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58
Q

what is an extrinsic cause of haemolytic anaemia?

A
  • Auto-immune Haemolytic Anemia (AIHA)
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59
Q

what is Auto-immune Haemolytic Anemia (AIHA)?

A

patients own immune system recognises own erythrocytes as foreign and destroy them

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60
Q

what can cause Auto-immune Haemolytic Anemia (AIHA)?

A
  • lymphoproliferative disorders
  • drug induced - bind to the surface of RBCs to act as antigen
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61
Q

how is Auto-immune Haemolytic Anemia (AIHA) diagnosed?

A

on a blood film
- schisocytes - fragments of RBCs
- polychromatic - blue tint of RBCs
- spherocytes - different sizes

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62
Q

what is haemoglobinpathies?

A
  • autosomal co-dominant genetic defects
  • causing abnormal structure of the global chains of the haem molecule
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63
Q

give two examples of haemoglobinpathies

A
  • sickle cell anaemia
  • sideroblastic anaemia
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64
Q

what happens in iron deficiency anaemia?

A

absence of iron means not enough o2 is absorbed

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65
Q

what can be two causes of iron deficiency anaemia?

A
  • malnutrition
  • malabsorption
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66
Q

how is iron deficiency anaemia diagnosed?

A

on a blood film
- hypochromic - pale
- microcytes - small

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67
Q

what is sideroblastic anaemia?

A

this is not from a lack of iron, but failure to be incorporated into haem in erythrocyte precursor cells

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68
Q

what forms in sideroblastic anaemia?

A
  • failure of incorporation of iron forms iron-rich mitochondria that surrounds the nucleus as granules
  • called sideroblasts
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69
Q

what is the type of anaemia as a result of a low MCV?

A

microcytic

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70
Q

what is the type of anaemia as a result of a normal MCV?

A

normocytic

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71
Q

what is the type of anaemia as a result of a high MCV?

A

macrocytic

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72
Q

what can cause anaemia with low MCV and a low RBC level?

A
  • iron-deficiency
  • lead poisoning
  • sideroblastic
  • chronic inflammation
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73
Q

what can cause anaemia with low MCV and a high RBC level?

A

thalassemias

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74
Q

what can cause anaemia with a normal MCV level?

A
  • haemolytic anaemias
  • bone marrow disorders
  • acute blood loss
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75
Q

what can cause anaemia with a high MCV level? (4)

A
  • vit B12 deficiency
  • folate acid deficiency
  • liver disease
  • hypothyroidism
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76
Q

what are the 4 blood groups?

A
  • A
  • AB
  • B
  • O
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77
Q

what are A and B antigens?

A

carbohydrates present on red cell membranes

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78
Q

how are blood groups determined?

A
  • by one gene on chromosome 9
  • three variants can be inherited from out parents
  • Ia, Ib or I
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79
Q

which blood groups are dominant and recessive?

A
  • Ia, Ib are co-dominant
  • I is recessive to both Ia and Ib
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80
Q

what type of antibodies does a person with blood group A possess?

A

anti-B

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81
Q

what type of antibodies does a person with blood group B possess?

A

anti-A

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82
Q

what type of antibodies does a person with blood group AB possess?

A

no antibodies

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83
Q

what type of antibodies does a person with blood group O possess?

A
  • anti-A
  • anti-B
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84
Q

what is the process of Rhesus disease? (4)

A
  • Father is Rh+ and mother is Rh-. Mother is carrying a Rh+ baby.
  • When pregnant with the first child the Rh antigens from foetus enters the mothers blood during delivery
  • mother produces Rh antibodies in response to the fetal Rh antigens (sensitisation)
  • when mother becomes pregnant again with Rh+ foetus, antibodies will cross the placenta and damage fetal red blood cells
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85
Q

what % of the population are RhD-?

A

15%

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86
Q

what are the symptoms of rhesus disease?

A

range from mild anaemia to miscarriage

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87
Q

what are the treatments for rhesus disease?

A
  • prophylaxis anti-D therapy - bind and neutralise any Rh+ cells preventing development of maternal antibodies
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88
Q

what DNA changes occurs in sickle cell anaemia?

A

GAG to GTG
changes DNA base to Valine

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89
Q

what affect does sickle cell anaemia have?

A

alters Hb affinity for o2

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90
Q

Describe the genetic make up of sickle cell disease/ traits/ no disease?(3)

A

HbAA = no disease
HbAS = SC trait
HbSS = SC disease

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91
Q

what are the chances of inheriting sickle cell anaemia?

A
  • both parents are carrying the gene - 25% will have and 25% will NOT have and 50% they would be a carrier
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92
Q

Which ethnicity is sickle cell anaemia most present?

A

African/Caribbean

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93
Q

Why is sickle cell anaemia most present in African/Caribbeans?

A
  • sickle cell correlates with malaria
  • HbAS provides protection from dying of malaria (selective advantage)
  • HbSS gains worse outcome for malaria
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94
Q

what are the treatments of sickle cell anaemia?(6)

A
  • prophylaxis
  • bone marrow/stem cell transplants
  • prevention
  • education
  • management
  • NHS services
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95
Q

how has immunology been important? (4)

A
  • vaccinations for infectious diseases
  • transplantation
  • cancer vaccines
  • immunotherapies
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96
Q

where is the site of haematopoiesis?

A
  • foetal life - week 4 of development in the Yolk sac
  • before birth - liver
  • adult life - bone marrow in pelvis, sternum, vertebrae
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97
Q

what are the types of lymphoid tissue?

A
  • primary
  • secondary
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98
Q

what is a primary lymphoid tissue?

A
  • sites where lymphocytes differentiate to express antigen receptors
  • e.g. thymus (T-cells) and bone marrow (B-cells)
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99
Q

what is a secondary lymphoid tissue?

A

specialised sites for turning on the acquired immune response
- e.g. lymph nodes, speen, MALT, GALT, NALT

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100
Q

what is the lymphatic system?

A

a drainage system in fluid balance, returning to the blood

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101
Q

how much lymphatic fluid is lost per day?

A

3L/day

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102
Q

what are lymph capillaries?

A
  • ‘closed tubes’
  • walls contain overlapping endothelial cells that respond to fluid pressure
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103
Q

what are the two types of lymphatics?

A
  • superficial lymphatics - follows superficial veins e.g. axillary, inguinal, neck where they drain into deep lymphatics
  • deep lymphatics - follows main vessels e.g. pre-aortic and post-aortic
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104
Q

what are lymph nodes?

A
  • meeting place for cells of the immune system to expose the antigen
  • filters lymphatics
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105
Q

what is the role of the spleen?

A
  • directs immune responses to antigens in the blood
  • clearance of RBCs
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106
Q

what are the two pulps in the spleen?

A
  • red-pulp - clearing RBCs
  • white pulp - ‘lymph nodes’
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107
Q

why do we have innate immunity? (4)

A
  • prevent pathogen establishment
  • limit pathogen multiplication
  • provides protection from early death
  • instructs nature of acquired immune response after infection
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108
Q

what are the three pathways in the complement system?

A
  • classical
  • lectin
  • alternative
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109
Q

what do all three complement pathways produce?

A

C3

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110
Q

what does C3 split into?

A
  • C3a
  • C3b
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111
Q

what is the role of C3a?

A
  • enhances inflammation
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112
Q

what is the role of C3b?

A
  • opsonisation
  • lysis of cell membrane (attack complex)
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113
Q

how does the classical pathway work?

A
  • activated when antibodies bind to antigen of pathogen
  • C1q, C1s, C1r binds to antibody
  • forms C4b2a - C3 convertase
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114
Q

how does the lectin pathway work?

A
  • activated when proteins bind to carbohydrates
  • mannose binds to MASP-1 and MASP-2
  • forms C4b2a - C3 convertase
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115
Q

what does C4b2a activate?

A

C3 protein

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116
Q

what does the C3 do?

A

split to form C3a and C3b

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117
Q

how does the alternative pathway work?

A
  • C3b binds on the surface of the pathogen
  • forms C3Bb - C3 convertase
  • enhances classical and lectin pathway
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118
Q

describe the common pathway?

A
  • C3 convertase activates C3
  • C3 splits to C3a and C3b
  • C3b binds to C4b2a complex to form C4b2a3b - C5 convertase
  • C5 convertase activates C5 to split into C5a and C5b
  • C5a - enhances inflammation
  • C5b - iniaties membrane attack complex which causes the cell to self destruct
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119
Q

how are pathogens identified?

A

Pattern recognition receptors identify pathogens by recognising “pathogen associated molecular patterns” (PAMPs)

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120
Q

what do PAMPs trigger?

A

phagocytosis

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121
Q

how do PAMPs trigger phagocytosis? (4)

A
  • attachment by PAMPs
  • forms phagosome
  • granule fusion and killing
  • release of microbial products
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122
Q

what do phagocytes release during phagocytosis?

A
  • activates NADPH oxidase during respiratory burst
  • releases toxic oxygen radicals
  • these directly damage microbial membranes and activate microbial enzymes
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123
Q

what is the role of the phagocytes in adaptive immunity? (4)

A
  • antigen degradation
  • antigen processing
  • antigen presentation - MHCII
  • antigen presentation - MHCI
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124
Q

what is the role of the phagocytes in innate immunity? (3)

A
  • pathogen killing
  • pathogen processing
  • pathogen presentation
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125
Q

what do neutrophils contain? (3)

A
  • chromatin
  • granule proteins
  • pathogen presentation
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126
Q

what are the features of HSC-derived monocytes and macrophages? (3)

A
  • varied differentiation pathways
  • long-lived
  • host cells for pathogens
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127
Q

what are macrophages in the liver called?

A

kupfer cells

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128
Q

what is the role of kupfer cells? (3)

A
  • respond to environment
  • transcription factors
  • forms and functions in different tissue
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129
Q

what are dendritic cells?

A

phagocytes specialised for interacting with lymphocytes

130
Q

what are the features of dendritic cells? (3)

A
  • activated in innate immunity
  • innate immune response
  • sedentary or migratory
131
Q

how do macrophages travel from blood to tissue? (5)

A
  • cytokines produced by macrophages cause blood vessels nearby to dilate
  • leukocytes move to periphery of blood vessel because of increased expression of adhesion molecules
  • monocyte binds adhesion molecules on endothelium near sites of infection and gets chemokine signal
  • monocyte migrates into the surrounding tissue
  • monocyte differentiates into macrophage and migrates to the site of infection
132
Q

what are cytokines and chemokines?

A

hormones of the immune system that allow communication between immune/non-immune cells

133
Q

what are the features of cytokine/chemokine regulation?

A
  • short acting
  • released in polar fashion at ‘synapses’
  • recognised on target cells by specific receptors
  • receptor expression highly regulated to control duration of response
134
Q

what are the role of steroids?

A

block the function of cytokines/chemokines

135
Q

give an example of a steroid?

A

prednisone

136
Q

at what temperature are RBCs stored and for how long?

A
  • 4 degrees
  • 35 days
137
Q

at what temperature are platelets stored and for how long?

A
  • 22 degrees
  • 5 days
138
Q

at what temperature is frozen plasma stored and for how long?

A
  • 30 degrees
  • 24 months
139
Q

what did the Blood Safety and Quality Regulations (2005) advise? (4)

A
  • all units must be traced and records maintained for at least a period of 30 years
  • quality systems must be in place to monitor adverse events
  • haemoviliance - review safety of transfusion
  • training and education of all staff
140
Q

what are the prices of blood components? (2)

A
  • red cells - £160/unit
  • platelets - £250/unit
141
Q

why is transfusion of RBCs used?

A

increase oxygen delivery capacity of the blood when anaemia contributes to inadequate oxygen delivery to tissues

142
Q

what makes up the total volume of one blood unit?

A
  • 20ml plasma
  • the rest saline
  • 250-350mL/unit
143
Q

why is transfusion of platelets used?

A

for prevention and treatment of haemorrhage in patients with thrombocytopenia or platelet function defects

144
Q

why is transfusion of fresh frozen plasma used?

A

for single clotting factor deficiencies

145
Q

how many bags is one dose of fresh frozen plasma?

A

4 bags = 1L = 1 dose

146
Q

why is transfusion of cryoprecipitate used?

A

for low fibrigin levels (<1.5)

147
Q

how many bags is one dose of cryoprecipitate?

A

2 bags = 1 dose

148
Q

what blood group is the universal recipients?

A

AB

149
Q

what blood group is the universal donors?

A

O

150
Q

what happens if you transfuse the wrong blood group to a patient? (2)

A
  • antibody is capable of destroying incompatible red cells by complement activation
  • leads to immediate intravascular haemolysis
151
Q

what are the factors to consider when transfusing? (4)

A
  • risks
  • limited supply
  • cost
  • transfusion thresholds
152
Q

what does patient blood management and NICE standards emphasise the use of? (5)

A
  • single units of transfusion of RBCs in non-bleeding patients
  • point of care testing - aids decision making
  • anaemia management
  • management of abnormal haemostasis
  • adherence to indication codes
153
Q

how can we reduce transfusion errors? (2)

A
  • use bedside checklist (9 points)
  • have patient identification already labelled
154
Q

what are the types of transfusion reactions?

A
  • F - febrile
  • H - haemolytic
  • A - allergic
  • T - transfusion associated circulatory overload (TACO)
155
Q

what is haemostasis?

A

a physiological state, maintain fluid blood flow within the vasculature

156
Q

what is thrombosis?

A
  • pathological manifestation of haemostasis
  • causes restriction/blockage of blood vessel leading to hypoxia
157
Q

what are the three stages of haemostasis?

A
  1. vascular spasm
  2. platelet plug formation
  3. coagulation
158
Q

what happens in the vascular spasm stage?

A

damaged blood vessels constrict, reducing blood flow in the damaged area

159
Q

what happens in the platelet plug formation stage?

A

platelets bind to the damaged vessel wall and form a platelet plug (primary heamostasis)

160
Q

what happens in the coagulation stage?

A

stable clot forms by converting fibrinogen to fibrin (secondary haemostasis)

161
Q

what happens in primary haemostasis?

A

platelet adhesion

162
Q

what are the stages of primary haemostasis? (4)

A
  • vessels damaged, platelets ‘tether’ to the sub endothelium
  • blood ‘rolls’ platelet along subendotheium, promoting more GPIb/vWF associations. Leads to firmer adhesion
  • firmer adhesion innitiates platelet activation, results in granule release
  • conformational change leads to stronger adhesions and further activations
163
Q

which factors in the coagulation cascade are vitamin K dependant?

A

2, 7, 9, 10

164
Q

which factors are in the intrinsic pathway?

A

12, 11, 9, 8

165
Q

which factors are in the extrinsic pathway

A

7, 3

166
Q

which factor starts the common pathway?

A

10

167
Q

what is needed to form factor 2?

A
  • prothrombin
  • factor 5 and Ca2+
168
Q

what is needed to form factor 1?

A
  • fibrinogen
  • thrombin
169
Q

what is the name for factor 2?

A

thrombin

170
Q

what is the name for factor 1?

A

fibrin

171
Q

which factors does heparin act on?

A

10, 2 (thrombin)

172
Q

which factor does LMWH act on?

A

10

173
Q

what is the antidote for warfarin?

A

vit k

174
Q

what is the antidote for heparin and LMWH?

A

protamine sulphate

175
Q

which lab test measures the intrinsic pathway?

A

partial thromboplastin time (PTT)

176
Q

which lab test measures the extrinsic pathway?

A

prothrombin time (PT)

177
Q

which factors does PTT measure?

A

7, 11, 8

178
Q

which factors does PT measure?

A

7, 10, 5, 2

179
Q

what are the 4 types of lab tests used for coagulation?

A
  • platelet aggregometry
  • coagulometer
  • prothrombin time
  • partial thromboplastin time
180
Q

how does platelet aggregometry work? (3)

A
  • shines light through platelet solution
  • add agglutination agonist
  • measure coagulation via light absorption
181
Q

how does coagulometery work? (3)

A
  • plasma added to spinning machine
  • metal ball stones when coagulated plasma forms
  • recorded via magnets and timer
182
Q

what are the possible conditions from a prolonged PT and a normal PTT? (3)

A
  • liver disease
  • decreased Vit K
  • decreased/defective factor 7
183
Q

what are the possible conditions from a normal PT and a prolonged PTT? (2)

A
  • vWF disease
  • lupus anticoagulant
184
Q

what are the possible conditions from a prolonged PT and a prolonged PTT? (2)

A
  • liver disease
  • intravascular coagulation
185
Q

what are the possible conditions from a normal PT and a normal PTT? (3)

A
  • decreased platelet function
  • thrombocytopenia
  • weak collagen
186
Q

what is thrombocytopenia?

A

a condition of low circulating platelets

187
Q

what is primary thrombocytopenia?

A

occurs spontaneously for an unknown reason

188
Q

what % of primary thrombocytopenia cases are found in plasma?

A

60%

189
Q

what is the name given to when antibodies are found in plasma?

A

Immune Thrombocytopenia (ITP)

190
Q

What are cleared in ITP?

A
  • IgG coated platelets
  • by splenic macrophages or kupfer cells
191
Q

what is a symptom for mild ITP?

A

petechia (small haemorrhages)

192
Q

what are symptoms for severe ITP?

A
  • extensive haematomas
  • cerebral haemorrhages
193
Q

what is Glanzmann’s Thrombasthenia?

A

lack of platelet aggregation

194
Q

how is Glanzmann’s Thrombasthenia acquired?

A

autosmal recessive

195
Q

what does Glanzmann’s Thrombasthenia affect?

A

changes function of GPIIb or GPIIIa

196
Q

what is haemophilia?

A

bleeding disorder by changes in proteins

197
Q

how is haemophilia acquired?

A
  • recessive sex linked X-chromosome
  • affects men
198
Q

what are the two types of haemophilia?

A

A and B

199
Q

how common is haemophilia A?

A

1 in 5,000 males

200
Q

what is deficient in haemophilia A?

A

FVIII

201
Q

how common is haemophilia B?

A

rare, 1 in 30,000 males

202
Q

what is deficient in haemophilia B?

A

FIX

203
Q

name two anti-platelet drugs

A
  • aspirin
  • clopidogrel
204
Q

how does aspirin work?

A
  • inhibits platelet cyclo oxygenate
  • a key enzyme in thromboxane A2 (TXA2)
  • TXA2 triggers platelet activation and aggregation
  • aspirin blocks this by inhibiting its mediator
  • lasts for 7-10 days
205
Q

what is aspirin effective against?

A
  • ischemic stroke
  • chronic stable angina
  • prevention of MI (65+)
  • unstable angina
  • acute/previous MI
206
Q

what are two side effects of aspirin?

A
  • GI bleeding
  • hemorrhagic strokes
207
Q

what are aspirins dosage levels?

A
  • low dose - 81mg/day
  • high dose - 325mg/day
208
Q

how does clopidogrel work?

A
  • stops ADP binding to the ADP receptor
  • ADP is released by platelets to activate other platelets
  • broken down in the liver before it has an effect (prodrug)
209
Q

what are ADP receptor agonists effective against?

A
  • prevents blockage of coronary arterial stents
  • reduce thrombotic events in patient with a history of MI, stroke
210
Q

what is the mutation for poor metabolism of Clopidogrel?

A

CYP2C19

211
Q

what is used in patients with the CYP2C19 mutation?

A

-ADP antagonist drugs
- prosugreal and ticagrelor

212
Q

what are the side effects of ADP agonist drugs? (2)

A
  • bleeding
  • Thrombotic Thrombocytpoenic Purpura (TTP)
213
Q

what are anticoagulants?

A
  • drugs that reduce fibrin
214
Q

what are the two mechanisms of anticoagulants?

A
  • inhibit synthesis of clotting factors
  • inhibit activity of clotting factors
215
Q

what are the two ways anticoagulants can work?

A
  • direct thrombin
  • direct factor Xa
216
Q

what is heparin?

A

heterogenous natural polysaccharide

217
Q

how does unfractionated heparin (UFH) work? (5)

A
  • UFH binds to anti-thrombin
  • causes conformational change
  • increases binding affinity for FXa and thrombin
  • UFH and AT form a ternary structure with thrombin
  • leads to inactivation
218
Q

what is the similarity and differences between UFH and LMWH?

A
  • same pentassacharide complex
  • only inactivates Factor Xa
  • LMWH cannot form a ternary structure
219
Q

what type of drug is warfarin?

A

vitamin K antagonist

220
Q

which coagulation factors are reliant on vit K?

A

7, 9, 10

221
Q

how does warfarin work?

A
  • blocks reformation of KH2 from its oxidised form
  • decreases clotting
222
Q

what are the side effects of warfarin? (2)

A
  • bleeding
  • foetal haemorrhage
223
Q

what is type 1 hypersensitivity?

A

allergy

224
Q

what is type 2 hypersensitivity?

A

antibody-antigen

225
Q

what is type 3 hypersensitivity?

A

immune complexes

226
Q

what is type 4 hypersensitivity?

A

delayed response

227
Q

how does type 1 hypersensitivity work?

A
  • resting mast cells contains granules with histamine (inflammatory mediators)
  • antigen cross links bind to IgE
  • releases granule contents
228
Q

what are allergens?

A

small proteins which cause allergy

229
Q

what type of response do allergens produce?

A

Th2 response

230
Q

when does an allergy only occur?

A
  • only occurs as a result from repeated exposures that generate an IgE mediated immune response
231
Q

what is atropy?

A

Predisposition for IgE mediated immune response

232
Q

what are the three stages of type 1 hypersensitivity?

A
  1. sensitisation
  2. immediate reaction
  3. late phase response
233
Q

what happens in the immediate reaction?(2)

A
  • allergies recognised by mast cell
  • triggers degranulation response
234
Q

give examples of mast cell mediators? (6)

A
  • histamine
  • enzymes
  • leukotrines
  • cytokines
  • Th2 cytokines
  • prostaglandins
235
Q

what happens in the late phase response? (2)

A
  • migration of eosinophils which release peroxidase and other mediators
  • cause further tissue damage
236
Q

what are the types of sensitivity? (2)

A
  • skin - redness, inflammed, itching
  • airway - sneezing, rhinitis, wheezing, asthma
237
Q

what are the two types of allergic rhinitis?

A
  • seasonal - grass pollen
  • perennial - indoor pollen
238
Q

what are the treatments for allergic rhinitis? (4)

A
  • reduced exposure
  • intranasal corticosteroids
  • anti-histamines
  • immunotherapy
239
Q

what are the treatments for asthma? (4)

A
  • reliever inhalers - salbutamol
  • preventative inhalers - corticosteroids
  • leukotrine receptor antagonists
  • theophyllines
240
Q

what is eczema?

A

allergic reaction of the skin

241
Q

what are the treatments for eczema?

A
  • reduce scratching
  • moisturising
  • topical corticosteroids
242
Q

what is urticaria?

A
  • allergic reaction of the skin
243
Q

what are the treatments for urticaria? (5)

A
  • trigger avoidance
  • anti-histamine
  • corticosteroids
  • ciclosporin
  • anti IgE therapy
244
Q

what is anaphylaxis?

A

systemic reaction to an allergen via exposure routr

245
Q

what happens in anaphylaxis?

A

rapid prostaglandin and leukotriene synthesis

246
Q

how does anaphylaxis occur? (4)

A
  1. vasodilation and increased pemeability
  2. fluid enters extravascular space
  3. fall in blood pressure
  4. results in bronchiole constriction, odema and shock
247
Q

what is the two main anti-bodies found in type 2 reactions?

A

IgG or IgM

248
Q

what are the two ways type 2 hypersensitivity acts by?

A
  • antibody dependant
  • complement dependant
249
Q

how is sensitisation prevented in Rhesus disease? (2)

A
  • Routine Antenatal Anti-D prophylaxis (RAADP)
  • anti-D antibodies neutralises any D+ RBC that the mother is exposed to
250
Q

what is Drug Induced Haemolytic Anaemia?

A
  • binding of a drug triggers an immune response
  • the drug is called ‘hapten’
251
Q

what happens in Goodpasture Syndrome? (3)

A
  • IgG antibodies recognise collagen within the kidney basement membrane
  • IgG binds to kidney basement membrane
  • leads to complement activation
252
Q

what are the treatments for Goodpasture Syndrome?

A
  • oral immunosuppressants
  • plasmapheresis
253
Q

what is Myasthenia Gravis?

A
  • antibodies block Act at the neuromuscular junction
  • prevents nerve impulse transmission
254
Q

what is the main symptom in Myasthenia Gravis?

A
  • muscle weakness
  • particularly in eyes and face
255
Q

what are the treatments for Myasthenia Gravis?

A
  • pyridostigmine - blocks Acetylcholinesterase
  • corticosteroids
  • immunosuppressants
  • thymectomy - removal of thyroid
256
Q

what happens in Grave’s Disease? (2)

A
  • antibodies bind the Thyroid hormone receptor
  • causes receptor activation and increased thyroid hormone production
257
Q

what are the treatments for Grave’s Disease? (3)

A
  • thionamides
  • radioactive iodine therapy
  • surgery
258
Q

what antibodies are involved in antagonism?

A
  • IgG4
  • IgG1
259
Q

what antibody is involved in signalling?

A

IgG

260
Q

what antibodies are involved in complement dependant?(4)

A
  • IgG1
  • IgG2
  • IgG3
  • IgM
261
Q

what antibodies are involved in antibody dependant?

A
  • IgG1
  • IgG3
262
Q

what is the main antibody found in type 3 hypersensitivity?

A

IgG

263
Q

how does type 3 hypersensitivity work?

A
  • antigen-antibody complexes deposit in tissues
  • causes damage by complement activation or phagocytes
264
Q

what causes type 3 hypersensitivity?

A
  • infectious antibodies - hep B
  • environmental antibodies - fungal spores
  • autoantigens - DNA
265
Q

What happens to the antibody level in type 3 hypersensitivity?

A

as antibody level increases, larger complexes form

266
Q

what is altruism?

A

the regard for others as principle of action

267
Q

how many pints of blood does an individual have?

A

10

268
Q

how many pints of blood do the NHS need per day?

A

5,000

269
Q

what are the top 5 demands for blood?

A
  • general surgery - 23%
  • general medicine - 15%
  • cardiothoracic surgery - 13%
  • orthopaedics - 11%
  • blood diseases - 9%
270
Q

what are the risks of transfusion? (2)

A
  • wrong blood group given to patients
  • infections
271
Q

how many units and new donors are needed in the NHS each year?

A
  • 1.4 million units
  • 135,000 donors
272
Q

what is the case against a market for blood? (4)

A

Richard Titmus argued (1970)…
- market represses altruism
- erodes the sense of community
- sanctions profits in hospitals and clinics
- increases blood supply from poor, unskilled and unemployed

273
Q

what is the case for a market of blood? (3)

A

Cooper and Culver argued…
- supply can be increased by removing obstacles to donors
- offering financial rewards on the basis of blood donated
- other alternatives cant offer the same quality, safety and quantity

274
Q

what is the opt in/opt out system? (2)

A
  • until 2020, people registered to be on the organ donor register
  • from may 2020, all adults considered organ donors unless they opt out to
275
Q

what are the alternatives to transplantation?

A
  • mechanical maintenance for kidneys
276
Q

what has been done to increase the supply of organs? (4)

A
  • transplant co-ordinates
  • DVLA nudges
  • financial incentives
  • replace opt in with opt out
277
Q

which country is the only country where organ trade is legal?

A

iran

278
Q

should we allow a market for used body parts? (2)

A
  • yes it would increase supply
  • no it would attract ‘transplant tourism’ could be risky for donor and recipient without a market
279
Q

what did Rottenberg (1971) argue?

A

“Each has property rights in his own body”

280
Q

what is polycythemia?

A

excess of RBCs in circulation

281
Q

what is essential thrombocythemia?

A

excess of platelets

282
Q

what is idiopathic myelofibrosis? (2)

A
  • too few RBCs
  • too many platelets and WBC
283
Q

give three examples of myeloproliferative disorders?

A
  • polycythemia vera
  • essential thrombocythemia
  • idiopathic myelofibrosis
284
Q

what is primary polycythemia?

A
  • genetically controlled excess of RBCs
285
Q

what are the clinical signs of polycythemia? (8)

A
  • breathing difficulties
  • dizziness
  • excessive bleeding
  • splenomegaly
  • headache
  • itchiness
  • SOB
  • phlebitis
286
Q

what is mutated in polycythemia ruby vera (PV)?

A
  • JAK2V617
  • increase in RBC production
287
Q

what is secondary polycythemia?

A

high RBC that is promoted by RBC development

288
Q

what can cause secondary polycythemia? (3)

A
  • hypoxia - due to COPD
  • EPO secreting tumours, carcinoma
  • neonatal polycthemia - maternal RBC transfusion
289
Q

what is relative polycythemia?

A

RBCs normal but reduced plasma volume e.g. vomitting, dehydration

290
Q

what are clinical signs of essential thrombocythaemia? (3)

A
  • asymptomatic
  • hemorrhage
  • progress to lueukemia
291
Q

what is a JAK kinase?

A
  • JAK2 gene is a member of a family of 4 kinases
  • protein attaches to intracellular portion of receptors
  • this inmates phosphorylation events to initiate transcription
292
Q

what happens in a JAK mutation?

A

mutation of the auto-inhibitory domain makes JAK2 active in the absence of ligand binding

293
Q

what is an example of primary immunodeficiency disease?

A

Chronic granulomatous disease

294
Q

what is an example of secondary immunodeficiency disease?

A

HIV/Aids

295
Q

what is Chronic granulomatous disease?

A

genetic disorder affecting how phagocytes kill bacteria, fungi and parasites

296
Q

what are the clinical signs of chronic granulomatous disease? (4)

A
  • impetigo
  • skin and rectal abscesses
  • presence of granulomas
  • reoccur ant pneumonia
297
Q

what is HIV/Aids?

A
  • a retroviral infection leading to loss of CD4+ T cells
  • Aids - diagnosed with stage 3 HIV
298
Q

what is a normal CD4+ count?

A

500-1500/mm3

299
Q

what is an example of too many T-cells?

A

acute lymphoblastic leukaemia of B and T cells

300
Q

what is an example of too little T-cells?

A

insufficient T or B cell response to recognise and kill pathogens

301
Q

what is auto-inflammation?

A

prolong, unwanted innate immunity

302
Q

what is auto-immunity?

A

loss/failure/non-self recognition

303
Q

what are some therapeutic interventions in autoimmune and auto-inflammatory diseases? (3)

A
  1. cytokine therapies
  2. reducing lymphocyte activation
  3. killing the cause of diease
304
Q

what can acute inflammation be driven by? (4)

A
  • infections
  • trauma and foreign bodies
  • chemical, physical, endogenous agents leading to cell death
  • allergies
305
Q

what are two types of mediators of autoimmunity?

A
  • preformed mediators
  • synthesised mediators
306
Q

what are examples of preformed mediators?

A
  • platelets - seretonin + histamine
  • basophils - histamine
307
Q

what are examples of synthesised mediators?

A
  • leukocytes - leukotrines, prostaglandins
  • macrophages - nitric oxide, cytokines
308
Q

what is the liver a major source of? (2)

A
  • mediators e.g. Factor XII
  • complement factors
309
Q

what can cause chronic inflammation? (3)

A
  • persisting infections
  • chronic exogenous/endogenous toxicity
  • chronic immune reactions
310
Q

what is the link between acute ad chronic inflammation?

A
  • invading microbes leads to acute response leads to resolution.
  • Failed resolution leads to chronic inflammation
311
Q

what enzymes do NSAIDS target?

A

COX1 and COX2

312
Q

what do membrane phospholipids get converted to?

A

arachidonic acid

313
Q

what can arachidonic acid convert into?

A
  • leukotrienes lipoxins - anti-inflammatory
  • PGG2 - prostaglandins by COX enzyme
314
Q

what role does prostacyclin (PGI2) have?

A

antiplatelets

315
Q

what is the difference between COX1 and COX 2?

A
  • COX1 - constitutive = ON all of the time
  • COX2 - inducible = switched ON/OFF e.g. during inflammation
316
Q

what is the main feature of Aspirin?

A

the only NSAID to irreversibly inactivate both COX1 and COX2

317
Q

what is aspirins mechanism of action?

A
  • affects COX2
  • performs an incomplete reaction resulting in lipoxin generations
  • hydrophobic channel allows arachidonic acid to bind at the site
  • aspirin acetyles and binds to position 529 to block AA from accessing active site
318
Q

what is the difference between aspirin and ibuprofen?

A
  • aspirin is irreversible
  • ibuprofen is reversible
  • ibuprofen blocks the activity of aspirin - blocks anti platelet effect
319
Q

what are aspirins side effects? (6)

A
  • GI issues
  • bleeding
  • vomitting
  • heart burn
  • ringing in ear
  • swelling of eyes
320
Q

what is the name of the drugs that only target COX2?

A

Coxibs
- Withdrawn because of safety and side effects

321
Q

what is the mechanism for glucocorticoids?

A
  • passes through cell membrane since it is lipid soluble
  • receptors binds inside the cell (Hsp90) travels to the nucleus
  • drive anti-inflammatory response

ALS (10 decks)

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