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Year 1 IMS > Blood > Flashcards

Blood Flashcards

1
Q

How much blood do we have in our body?

A

5L

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2
Q

What are the phagocytic leucocytes?

A

1) Neutrophils
2) Eosinophils
3) Monocytes/macrophages

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3
Q

What are the non-phagocytic leucocytes?

A

1) Lymphocytes

2) Basophils

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4
Q

What is the appearance of a neutrophil?

A

Multilobed nucleus

Blue Granules

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5
Q

What is the appearance of basophils?

A

Nucleus obscured by highly granular dark staining cytoplasm

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6
Q

What is the appearance of eosinophils?

A

Bi lobed nucleus
Pink cytoplasmic granules
‘Tomato wearing sunglasses’

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7
Q

What is the appearance of monocytes and macrophages?

A

Granular (blue) cytoplasm containing white vacuoles

Nucleus has a characteristic kidney shape

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8
Q

What is the appearance of lymphocytes?

A

Large nucleus
Very little cytoplasm
Dense purple nuclei, poorly stained cytoplasm

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9
Q

How do neutrophils protect against pathogens and how long do they survive?

A

Granules contain proteolytic enzymes - break down ingested material
Non specific as dont recognise specific pathogens
Mobile, phagocytic and chemotactic (respond to chemo attractants)
Defence against bacteria and fungi
Survive for 8-10 hours make up 50-70% of leucocytes

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10
Q

How do basophils protect against pathogens and how long do they survive?

A

Basophils circulate in blood, migrate to tissues and become mast cells
Mast cells possess receptors and when they get a signal spill there granular contents into peripheral blood
Survive 1-5 days, 0-1% of leucocytes

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11
Q

How do eosinophils protect against pathogens and how long do they survive?

A

Circulate in blood and migrate to tissues where they defend against parasitic infections - certain cytokines (chemicals that affect cell division/production of immune cells) stimulate increased production of eosinophils
Survive circulating in the blood for 4-5 hours and live in tissue for 8-12 days

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12
Q

How do monocytes and macrophages protect against pathogens and how long do they survive?

A

Monocytes circulate in the blood until they migrate to tissues and become macrophages
Ingest pathogenic material, can kill intracellular organisms and are also professional APC’s
Survive circulating in the blood for 1-3 days but have a long tissue life span

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13
Q

What is the life span of lymphocytes?

A

Years

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14
Q

What is the appearance of plasma cells?

A

Granular ‘clock faced nuclei’

Basophilic cytoplasm

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15
Q

Whats the appearance of platelets and whats there lifespan?

A

No nucleus, small, blue staining

Lifespan of 20 days

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16
Q

What are platelets made from?

A

Fragments of megakaryocytes that bud off in the bone marrow before entering the blood

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17
Q

What is the most abundant protein in the blood?

A

Albumin

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18
Q

What is the difference between serum and plasma?

A 
Serum = plasma - clotting factors
Plasma = serum + clotting factors (+clotting inhibitor)
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19
Q

How do you extract serum/plasma from the blood?

A

Using a centrifuge

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20
Q

What happens when incompatible groups of blood are mixed and when does this present a problem?

A

Ab react with Ag on the surface of the new RBC’s causing haemolysis
This presents a problem for pregnancy and transfusion

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21
Q

What are the 2 main classifications of blood groups?

A

1) ABO

2) Rh

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22
Q

How is your ABO blood group classified?

A 
Based on a carbohydrate present in the RBC membrane
A = Ag A
B = Ag B
AB = Ag A and AgB
O = no Ag
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23
Q

Which ABO blood group is considered a universal donor and a universal recipient?

A

Universal donor = O
It has no Ag for you to have Ab against
Universal recipient = AB
Blood contains Ag for neither A nor B

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24
Q

Why, in terms of compatibility must you considered blood type when doing a plasma transfusion (not containing RBC’s)?

A

Because plasma contains Ab so must make sure plasma transfused doesn’t contain Ab to your RBC’s

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25
Q

What are the components of an acute haemolytic reaction (which occurs when incompatible blood is transfused)?

A

1) Haemolysis
2) Hypotension to keep up with haemolysis
3) Kidney failure - must excrete haem and iron products from haemolysis - haemoglobinuria (free Hb in urine)
4) Systemic symptoms (fever and chills)
5) Pain in lumbar region (loins and lower back)
6) Constricting pain in chest
7) Heat sensation in transfused vein
8) DIC (disseminated intravascular coagulation)

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26
Q

How is youre Rhesus blood group classified?

A

Based on a transmembrane protein (ion channel) in RBC membrane called D antigen
Rh+ is with the Ag
Rh- is without the Ag

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27
Q

When does haemolytic disease of the newborn occur?

A

During pregnancy of a Rh+ child to a Rh- woman

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28
Q

Why does haemolytic disease of the newborn tend to present in second pregnancies?

A

1) Sensitisation - mixing of mothers and foetus blood during birth of the first child which triggers an immune response
2) In future pregnancies, Ab are able to cross the placenta and cause haemolysis in the Rh+ foetus and thus potentially lethal aneamia in the foetus

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29
Q

How can haemolytic disease of the new born be prevented?

A

Prevention with intramuscular Rh IgG (Ab that mop up Ag) injections at 28,34 and 72 hours after delivery (passive immunity) - can do an intrauterine injection if necessary

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30
Q

What colour do RBC’s and eosinophil granules stain?

A

Pink/red

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31
Q

What colour do DNA and RNA stain?

A

Blue/purple

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32
Q

What colour do platelets and other granules (other than eosinophil granules) stain?

A

Blue/purple

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33
Q

What are the 2 main processes involved in stemming bleeding?

A

1) Vasoconstriction (peptides/hormones lead to the contraction of smooth muscle cells in the vessel wall eg.
- Thromboxane (produced by platelets)
- Vasopressin (produced by anterior pituitary)
- Angiotensin 2 (precursor produced by liver)
- Serotonin (secreted by activated platelets)
2) Haemostasis
- Primary haemostasis: platelet activation and agregation
- Secondary haemostasis: coagulation pathway activation

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34
Q

What is a thrombocyte?

A

Another name for platelets

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35
Q

What 2 types of granules do platelets contain?

A

Alpha granules and dense granules

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36
Q

What is the shape change that platelets undergo when they are activated and what is it?

A

Pseudopodia
Little extensions from the membrane
Stretch and bind together and from a platelet plug

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37
Q

What structures/substances/enzymes are found within platelets?

A

Mitochondria: source of ADP for activation
Glycogen: source of energy
Canicular system (invaginations): increased surface area for activation
COX1 and TX synthase: leads to production of thromboxane

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38
Q

What role does thromboxane have in activating platelets?

A

Auto activation loop

Activated platelets produce thromboxane which further activates other platelets

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39
Q

What type of molecules are ADP and Thromboxane (TxA2)?

A

Autocrine molecules (secreted by platelets and activate platelets)

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40
Q

What is the ligand for aIIB1 and GPVI receptors and what are they involved in?

A

Collagen (important for adhesion)

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41
Q

What is the ligand for PAR-1, PAR-4 receptors and what kind of receptors are they and what are they involved in?

A

GPCR’s
Ligand is Thrombin
Involved in activation

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42
Q

What is the ligand for P2Y1 and P2Y12 receptors and what kind of receptors are they?

A

GPCR’s
ADP
Involved in activation

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43
Q

What is the ligand for the TP receptor, what kind of receptor is it and what is it involved in?

A

GPCR
Ligand is thromboxane (TXA2)
Involved in activation

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44
Q

What does the aIIIbB3 receptor bind and what is it important for?

A

Binds fibrinogen and VWF
Important for aggregation
Platelets in close proximity are able to bind to eachother via fibrinogen and VWF

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45
Q

From what granules in the platelet is ADP released?

A

Dense granules

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46
Q

What occurs to get the inactivated platelets to bind at the site of injury?

A

1) No injury - platelet circulate
2) Subendothelial matrix is rich in collagen, when an injury occurs to the endothelium this collagen is exposed and binds to receptors on the platelets activating them aswell as binding platelets at the sight of injury
3) Activated platelets release thromboxane and serotonin which cause local vasoconstriction
4) VWF present in the blood can bind platelets and collagen, fibrinogen binds inbetween platelets all helping to strengthen the platelet plug (once a2B3 receptor is activated)
5) Activated platelets also release ADP, thrombin and thromboxane which serve to recruit and activate other platelets

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47
Q

Although platelets can aggregate and change shape, aggregation is still reversible until what occurs?

A

Release of granules

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48
Q

What does the word limited in ‘limited proteolysis’ refer to?

A

The fact that the proteolysis is specific, one type of protein: one cut

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49
Q

What is the difference between the intrinsic and extrinsic coagulation pathways?

A

Intrinsic - Nothing needs to be added to the blood, coagulation is triggered by factor FXII within the blood coming into contact with a negative surface eg. glass
Extrinsic - Need to add something to the blood in order to activate it to coagulate eg. tissue factor

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50
Q

Which organ is rich in tissue factor and how could you explain that?

A

Brain - tissue factor triggers the extrinsic coagulation cascade - this is the last place you want internal beeding!

51
Q

Where is tissue factor located and how does it trigger coagulation?

A

Located in the endothelium of blood vessels, damage to blood vessels will lead to exposure of TF in the blood, TF is found on the membranes of perivascular cells (smooth muscle cells and fibroblasts)
FVII autoactivates when bound to TF
This plays a role in thrombosis, when a plaque ruptures lots of TF released

52
Q

What factor are haemophilia A sufferers deficient in?

A

FVIII

53
Q

What factor are haemophilia B sufferers deficient in?

A

FIX

54
Q

What factors are involved in the consolidation pathway?

A

Thrombane activates:

FV, FVIII, FXI, FXIII

55
Q

What co factor is needed to convert prothrombin to thrombin?

A

Ca2+

56
Q

What additional substance needs to be present with FXIIIa to form transglutaminase cross links in fibrin clot?

A

Ca2+

57
Q

What is hereditary angiodema?

A

Recurrent episodes of severe oedema in various parts of the body
Types, 1,2 and 3 (type 1 = most common)
Caused by lack of complex blood proteins

58
Q

What is Leukopenia?

A

Reduction in the number of WBC’s in the blood

59
Q

What is thrombocytopenia?

A

Deficiency in platelets - leads to slow clotting time

60
Q

What is infectious mononucleosis?

A

Glandual fever: prolonged lassitude (weariness/lack of energy), viral, swelling of lymph glands

61
Q

What is disseminated intravascular coagulation?

A

Widespread activation of the clotting cascade, lots of small clots form, but this consumes platelets and clotting factors, disrupt normal clotting so bleeding can occur

62
Q

What is factor V leiden?

A

inherited thrombophilia - increased tendency to form blood clots

63
Q

What is thrombocythaemia and what can it cause?

A

High platelet levels, can cause thrombosis

64
Q

What is hypercoagulability?

A

Inhibitor deficiencies mean increased risk of thrombosis

65
Q

HTLV-1 (a retrovirus) has been associated with what cancer?

A

Leukaemia

66
Q

Burkitt’s lymphoma is associated with what kind of genetic mutation?

A

Translocation

67
Q

How are haematological malignancies classified?

A 
According to blood cell lineage:
1) MYELOID neoplasm
or 2) LYMPHOID neoplasm
According to location:
1) In the blood = LEUKAEMIA
2) In the lymph nodes = LYMPHOMA
Also according to time:
ACUTE (blasts)
CHRONIC (years - mature cells)
68
Q

What are myeloproliferative disorders?

A

Bone marrow makes too many WBC’s or RBC’s or platelets

Slow growing blood cancers which often remain stable or progress quite slowly

69
Q

What is myelofibrosis?

A

Increased megakaryocytes - intense bone marrow fibrosis

70
Q

What is the philadelphia chromosome?

A

Abnormal small chromosome found in leucocytes of sufferers of leukaemia

71
Q

What is polycythaemia?

A

Increased RBC’s - increase in Hb conc, packed cell volume and red cell count

72
Q

What kind of blood cell is increased in chronic myeloid leukaemia?

A

Granulocytes

73
Q

What happens in leukaemia?

A

1) Accumulation of WBC in the bone marrow and peripheral blood
2) RBC count decreased, platelet count decreased and WBC in the blood increases (abnormal cells though)
3) Leads to bone marrow failure in advanced disease, meaning WBC levels fall

74
Q

What are the blood symptoms in leukaemia?

A

1) Blood hyperviscosity due to white cells, causing respiratory or neurological symtoms
2) Infection if white cells fall (bone marrow failure)
3) Tiredness/anaemia
4) Bleeding (platelet count decreased)
5) Bone pain in children

75
Q

What happens in lymphoma?

A

T or B lymphocyte neoplasia
Non hodgkin/hodgkin (characterised by reed-steinberg cell - generally originate from B cells which become enlarged and multinucleated or have a bilobed nucleus and have lost the ability to make antibodies

76
Q

What type of growth factor is involved in the haemapoiesis of myeloid cells including RBCs?

A

Colony stimulating factors

77
Q

What type of growth factor is involved in the haemapoiesis of lymphocytes and natural killer cells (the lymphoid line)?

A

Lymphokines

78
Q

What is the role of Epo (erythropoietin) in haemapoesis and where is it produced?

A

Stimulates the formation of bust forming units which form RBCs
Produced by interstitial fibroblasts in the kidneys
Renal failure can lead to anaemia

79
Q

How is the production of Epo by the kidney controlled?

A

By negative feedback

high RBCs inhibits the production of Epo by the kidney

80
Q

What kind of anaemia does iron deficiency lead to and what happens to the RBCs produced?

A 
Microcytic anaemia (pale and small RBCs due to reduced Hb 
Hypochromic (less Hb in each RBC)
Increased anisocytosis (variation in size) and poikilocytosis (variation in shape) - some may be elongated (pencil cells)
81
Q

Why does VitB12 (or folate) deficiency lead to anaemia?

A

Vit B12 and folate involved in DNA replication. Deficiency in either causes problems with mitosis of proerythroblast

82
Q

What kind of anaemia is caused by Vit B12 or folate deficiency?

A

Megaloblastic or macrocytic anaemia (large RBCs)
Includes the formation of macroovalocytes (enlarged oval shaped RBCs) and also may lead to hypersegmented neutrophils (due to disordered nuclear maturation

83
Q

What kind of anaemia does blood loss lead to?

A

Normocytic anaemia (no abnormalities in production)

84
Q

What are the possible causes of folate deficiency?

A

1) Poor nutrition
2) Alcoholism
3) Malabsorption
4) Certain drugs (sedatives, certain Abx and anti-epileptics)

85
Q

Haemolytic syndrome in the new born is an immune cause of aquired haemolytic anaemia, what are the non immune causes?

A

1) Drug induced
2) Snake venom
3) Mechanical (heart valves)
4) Infections, malaria, septicaemia

86
Q

What are the 3 problems in inherited haemolytic anaemia?

A

1) RBC cytoskeleton defects
Mutations in alpha or beta spectrin = hereditary spherocytosis
2) RBC enzyme defects
G6PD deficiency, involved in NADPH metabolism
3) Hb defects
Sickle cells diease

87
Q

Where are the Hb alpha and beta gene clusters?

A

Alpha - chromosome 16

Beta - chromosome 11

88
Q

What are the 3 types of Hb present in adults?

A

1) HbA (alpha2beta2)
2) HbA2 (alpha2delta2)
3) HbF (alpha2gamma2)

89
Q

What kind of Hb is found in the foetus?

A

HbF

90
Q

What happens in alpha thalassaemia?

A

Generally large deletions of alpha globin genes

  • a/aa and a-/a- = mild
  • a/– = severe
  • -/– = fatal
91
Q

What is beta thalassaemia?

A

Point mutations in the beta-globin gene

If both alleles are affected patient has HbF = beta thalassaemia major

92
Q

What are the major components in a venous thrombus?

A

Fibrin

Erythrocytes

93
Q

What are the 3 points of the triangle on Virchows triangle and what do they define?

A

1) Circulatory stasis
2) Endothelial injury
3) Hypercoaguability state
Define the 3 factors that contribute to thrombosis

94
Q

What are the 4 natural inhibitors of coagulation and what do they do?

A

1) Antithrombin (AT) - direct inhibitor of thrombin, FXa and FIXa
2) Tissue factor pathway inhibitor (TFPI) - direct inhibitor of FVII/TF complex and FXa
3) Activated protein C (aPC)
Proteolytically inactivates FVa and FVIIIa (aPC is a Vit K dependent serine protease, only cuts active forms of the factors
4) Protein S (PS) - cofactor for aPC in the inactivation of FVa/FVIIIa

95
Q

What is idiopathic venous thrombosis and what is it generally caused by?

A

Venous thrombosis without any clear cause
Factor V leidens
Deficiency in natural inhibitors of coagulation

96
Q

What is the mechanism behind Factor V leiden?

A

Inherited protein C resistance
Substitution mutation in FV gene which increases the risk of DVT
(Cuts FV at 3 arginine bases, one of these arginine bases is replaced by glutamine)

97
Q

What is fibrinolysis?

A

Physiological system which helps to break down fibrin when its not needed

98
Q

Which enzyme breaks down the fibrin clot?

A

Plasmin

99
Q

What enzymes are involved in activating plasminogen to plasmin?

A

tPA and uPA
tPA is secreted by endothelial cells
uPA is important in pregnancy

100
Q

What substance enhances conversion of plasminogen to plasmin and what does this ensure?

A

Enhanced by fibrin - this ensures fibrin degradation only occurs at the right place

101
Q

PAI-1, alpha 2 antiplasmin, TAF1 are all fibrinolytic drugs, what are there targets?

A

PAI-1 (plasmin activation inhibitor 1) binds to tPA active site
Alpha2antiplasmin - direct inhibitor of plasmin
TAF1 inhibits the enhancement of conversion of plasminogen to plasmin by fibrin

102
Q

What is the main component of arterial thrombus?

A

Platelets

103
Q

What is the process of plaque formation?

A

1) Plaque forms between tunica media and endothelium
2) Accumulation of foam cells in core (macrophages which have eaten lots of fat)
3) Foam cells produce TF
4) TF, collagen and LPA accumulate in the core
5) Cap of plaque is prone to rupture
6) LPA, and collagen activate platelets
7) TF activates coagulation cascade

104
Q

How can disseminated intravascular coagulation be caused?

A

By infection
Sepsis, as a consequence of the infection blood cells expose TF on there membranes
TF activates the coagulation cascade
Microvascular clots
Consumes clotting factors and platelets which leads to bleeding
Get thrombosis and bleeding at the same time
If treatment is ineffective, multiple organ failure occurs

105
Q

What are the vit K dependent clotting factors?

A

FVII, FIX and FX, Protein C and Protein S

106
Q

How are FVII, FIX and FX vitamin K dependent?

A

1) These clotting factors undergo post translational modification of Glu to gamma-carboxyglutamic acid (Gla) in a Vitamin K dependent reaction
2) Gla binds to activated clotting factors (negatively charged phospholipids) via Ca2+
3) This increases the catalytic efficiency of the limited proteolysis dramatically (so much so it needs this to work)

107
Q

What enzyme is inhibited by warfarin and what effect does this have?

A

VKOR, cant regenerate Vit K after it has converted 1 Glu to Gla

108
Q

What is the cause of Vitamin K deficiency?

A

Fat malabsorption
May occur in alcoholic liver cirrhosis
May occur in newborn infants
Can occur due to oral anticoagulant over dosage

109
Q

How are haemophilia A and B inherited?

A

Sex linked (X-linked recessive)

110
Q

What stage of thrombin generation is affected in haemophilia A and B?

A

Consolidation phase

111
Q

What is the clinical presentation of haemophilia?

A

Bleeding in knees joints and muscles

112
Q

What are the 2 different standard coagulation assays and what deficiencies are they prolonged in?

A

1) PROTHROMBIN TIME (PT)
Uses TF as a trigger
Measures factors in the extrinsic pathway
Prolonged in FVII deficiency
Used in INR monitoring of oral anticoagulants
2) ACTIVATED PARTIAL THROMBOPLASTIN TIME (APTT)
Uses silica as a trigger
Measures factors in intrinsic pathway
Prolonged in FVIII, FIX, FXI and FXII deficiency
-Both are sensitive to deficiencies in the common pathway

113
Q

What is the possible prophylactic treatment for haemophilia?

A

Recombinant or plasma factor concentrates

NB. patient may develop an inhibitor against factor concentrates after prolonged treatment

114
Q

What is Von Willebrand disease and what are the different types?

A

Deficiency in vWF
1) Type 1: heterozygous disease (autosomal dominant) - commonest and most mild type, reduced level in blood
2) Type 2: functional deficiency (autosomal dominant) - milder than type 3 but more severe than type 1
3) Type 3: complete deficiency (autosomal recessive)
severe
4) Platelet type: mutation in GP1 (receptor for vWF) called pseudo wVF as its clinical presentation is similar to von willebrand disease

115
Q

Other than its involvement in platelet adhesion and aggregation what else does vWF do?

A

Stabilises FVIII, without it have less FVIII available

116
Q

Where is vWF produced?

A

Produced by endothelial cells and packaged in weibel palade bodies
Also produced by megakaryocytes
Upon stimulation the endothelial cells will secrete it

117
Q

What does the drug desmopressin do in the treatment of vW disease?

A

Releases wVF from the weibel palade bodies in endothelial cells

118
Q

What is thrombasthenia?

A

dysfunctioning platelets

119
Q

CAMT (congenital amegakaryocytic thrombocytopenia) and Fanconi’s anaemia causes of?

A

Fanconi’s anaemia is involved in haematological malignancy and bone marrow failure
Both causes of thrombocytopaenia

120
Q

Glanzmann thrombasthenia and Bernard-Soulier syndrome are causes of what?

A

Thrombasthenia

121
Q

Is the bleeding in thrombocytopenia or thrombasthenia more severe than in haemophilia?

A

Less severe

122
Q

What is the treatment for thrombocytopenia/thrombasthenia?

A

Focuses on the underlying cause

1) Corticosterois in ITP
2) Platelet transfusions
3) Splenectomy (immune suppression)

123
Q

Immune thrombocytopenic purpura (ITP) is a cause of what?

A

Thrombocytopenia

Year 1 IMS (14 decks)

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