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IMS > Topic 9 - Blood > Flashcards

Topic 9 - Blood Flashcards

1
Q

What is an artery?

A

Brings blood (generally oxygenated) to the heart from the organs and tissues

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2
Q

What is a vein?

A

Returns blood (generally deoxygenated) from the organs and tissues to the heart

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3
Q

What happens to the blood in one pump of the heart?

A
  • Deoxygenated blood from tissues/organs travels through the Vena Cava into the right atrium.
  • Right ventricle pumps the blood through the pulmonary artery to the lungs.
  • Valves prevent backflow.
  • Reoxygenated blood travels from the lungs to the left atrium through the pulmonary vein.
  • Left ventricle pumps blood via the Aorta to the tissues and organs.
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4
Q

What are the functions of the blood?

A
  • Hydration of tissues and organs
  • Delivery of oxygen to tissues and organs
  • Provision of nutrients to tissues and organs
  • Fight infection: innate and adaptive responses
  • Regulation of body temperature and pH
  • Distribution of endocrine hormones
  • Prevent it’s own (blood) loss
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5
Q

Which WBCs contribute to immune response to allergic reactions?

A
  • Eosinophils

- Basophils

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6
Q

What are endocrine hormones?

A

They are secreted directly to the blood stream.

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7
Q

What are exocrine hormones?

A

They are secreted through ducts opening on to an epithelium rather than directly into the blood.

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8
Q

How does blood prevent it’s own loss?

A
  • Platelets (small anucleate cells that clump together)

- Blood coagulation pathway (through the formation of thrombin a fibrin clot is formed)

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9
Q

What is the common progenitor cell that all blood cells are derived from?

A

The multipotential haematopoietic stem cell

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10
Q

What are the two major lineages of blood cells?

A
  • Myeloid

- Lymphoid

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11
Q

Which two blood cells can be found in body tissues?

A
  • Mast cells

- Macrophages

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12
Q

Which 5 blood cells are found in the blood marrow?

A
  • Hemocytoblast (stem cell)
  • Common myeloid progenitor
  • Megakaryocyte
  • Myeloblast
  • Common lymphoid progenitor
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13
Q

Which 11 blood cells can be found within blood specifically?

A
  • Platelets
  • Basophil
  • Neutrophil
  • Eosinophil
  • Monocyte
  • Natural killer cell (large granular lymphocyte)
  • Small lymphocyte
  • T lymphocyte
  • B lymphocyte
  • Plasma cell
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14
Q

How can plasma be separated from blood cells?

A

Centrifugation

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15
Q

What volume of blood is blood plasma?

A

55%

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16
Q

What are the 3 most abundant blood plasma proteins?

A
  • Albumin
  • Immunoglobulins
  • Fibrinogen
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17
Q

What is blood serum?

A

Plasma without the clotting factors

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18
Q

What percentage of blood is taken up by RBC?

A

45%

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19
Q

What occurs if incompatible blood groups are mixed?

A

Antibodies in the plasma reacts with antigens on the RBC membrane, causing haemolysis.
Potential complication during blood transfusion/pregnancy.

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20
Q

What is the ABO blood group?

A

Based on the carbohydrate antigen present on the RBC membrane. A, AB, B and O types.

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21
Q

Which ABO blood type is a universal donor?

A

O

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22
Q

Which ABO blood type is a universal acceptor?

A

AB

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23
Q

What are the main symptoms of an acute hemolytic reaction?

A
  • Hypotension
  • Kidney failure
  • Bleeding
  • Chills/Fever
  • Hemoglobinuria
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24
Q

What is Hemoglobinuria?

A

Haemoglobin in the urine due to erythrocyte lysis

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25
Q

What is the Rhesus blood group?

A

Based on the ion-channel antigen (D-antigen) on the RBC membrane

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26
Q

When does haemolytic disease occur during pregnancy?

A

Rh- (no D-antigen) woman and a Rh+ fetus (D-antigen).
During birth some foetal blood enters mothers system causing an immune response. In a following pregnancy the immune response will be much larger and will attack the foetus.

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27
Q

How can haemolytic syndrome in a foetus be treated?

A

Intramuscular injection of mother with Rh antibody at 28 weeks, 34 weeks and within 72 hours after delivery. Intrauterine transfusion via umbilical cord may be necessary.

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28
Q

What are the diseases of blood plasma?

A
  • Bleeding
  • Thrombosis
  • Hereditary angioedema
  • Complement deficiency
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29
Q

What are the diseases of the blood cells?

A
  • Haematological malignancies
  • Sickle cell anemia
  • Thalassaemia
  • Haemoglobinopathies
  • Leukopenia
  • Thorombocytopenia
  • Infectious mononucleosis
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30
Q

What are haemoglobinopaties?

A

Genetic defect that results in abnormal structure of one of the globin chains of the hemoglobin molecule. eg. Thalassaemia and Sickle cell anemia

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31
Q

What are diseases affecting the platelets called?

A

Thrombocytopaenias

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32
Q

What is a leukopenia?

A

A decrease in the number of leukocytes found in the blood, which places individuals at increased risk of infection.

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33
Q

What may cause bleeding?

A
  • Acute injury
  • Chronic disease
  • Low platelet count
  • Coagulation deficiencies
  • Vitamin K deficiency
  • Drugs
  • Liver disease
  • Infection/sepsis
  • Aneurysm repture
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34
Q

Which drugs can cause bleeding?

A
  • Aspirin
  • Warfarin
  • Heparin
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35
Q

What is the ultimate killer in heart disease and stroke?

A

Thrombosis

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36
Q

What are the causes of thrombosis?

A
  • Atherosclerosis
  • Cancer
  • Immobilisation
  • Surgery
  • Hypercoagulability
  • Thrombocythaemia
  • Factor V Leiden
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37
Q

Why does hypercoagulability occur?

A

Inhibitor deficiencies - PC, PS, AT

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38
Q

What is atherosclerosis?

A

A disease in which plaque builds up inside your arteries

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39
Q

What is neoplasia?

A

Uncontrolled cell growth. May be benign/malignant (therefore not necessarily cancer)

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40
Q

Which two classes of genes are implicated in neoplasia?

A

Tumour suppressor genes

Oncogenes

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41
Q

What are oncogenes?

A

Genes directly causative of cancer – includes growth factors and their receptors, DNA binding proteins

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42
Q

What are tumour suppressor genes?

A

Loss of suppressor activity leads to cancer.

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43
Q

What initiates cancer?

A
  • point mutations (UV, radiation, carcinogens)
  • chromosome translocation
  • viral genes
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44
Q

Which retrovirus is associated with leukemia?

A

Human T-Lymphotropic Virus (HTLV-1)

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45
Q

What is an example of a cancer caused by chromosomal translocation?

A

Burkitt’s Lymphoma

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46
Q

How are haemotological malignancies classified?

A

Blood cell lineage (myeloid neoplasm/lymphoid neoplasm)

Location (leukemia - blood/lymphoma - lymph nodes)

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47
Q

What cells are the precursors of platelets?

A

Megakaryocytes

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48
Q

What are Myeloproliferative disorders?

A

A group of slow-growing blood cancers in which the bone marrow makes too many abnormal red blood cells, white blood cells, or platelets, which accumulate in the blood

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49
Q

What are some myeloproliferative disorders?

A
  • Myeloid neoplasia
  • Polycythaemia (^ RBC)
  • Thrombocythaemia (^ platelets)
  • Myelofibrosis (^ megakaryocyte)
  • Chronic myeloid leukemia (^ granulocytes)
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50
Q

What does leukemia result in?

A

Accumulation of WBC in the bone marrow and blood, bone marrow failure.
Decrease in RBC, platelets and eventually WBC themselves in advanced disease.
-blood hyperviscosity
-infection
-tiredness/anemia
-bleeding
-bone pain in children

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51
Q

What is lymphoma?

A

T or B lymphocyte neoplasia - affecting the lymph nodes

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52
Q

What are the typed of lymphoma?

A

Non-Hodgkin and Hodgkin

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53
Q

How is Hodgkin lymphoma characterised?

A

By Reed-Sternberg cells

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54
Q

Where do Reed-Sternberg cells originate?

A

B lymphocytes, which become enlarged and are multinucleate or have a bilobed nucleus.

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55
Q

What is anemia?

A

Loss of oxygen delivery

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56
Q

What are the haemoglobin levels in anemia?

A

<13.5 g/dl (men)

<11.2 g/dl (women)

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57
Q

What are the symptoms of anemia?

A
  • Tiredness
  • Pallor
  • Fainting
  • Tachycardia
  • Shortness of breath
58
Q

What is tachycardia?

A

A heart rate that exceeds the normal resting rate. In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults.

59
Q

What is anemia caused by?

A
  • RBC or haemoglobin production abnormalities

- RBC destruction abnormalities

60
Q

What are Colony Stimulating Factors involved in?

A

Haemopoiesis of myeloid cells including RBCs.

61
Q

What are lymphokines involved in?

A

Haemopoiesis of lymphocytes and NK cells.

62
Q

What are two examples of growth factors?

A

Epo and Thpo

63
Q

How is Epo produced?

A

By interstitial fibroblasts in the kidney as an endocrine hormone

64
Q

What are the causes of an iron deficiency?

A
  • Diet induced
  • Blood loss (acute or chronic)
  • Infection (hookworm)
  • Growth spurts (children), Pregnancy
65
Q

What is distinctive of RBC in hypochromic microcytic anemia?

A
  • Smaller cells with increased zone of central pallor
  • Increased anisocytosis
  • Increased poikilocytosis
  • Some RBC become elongated
66
Q

What is anisocytosis?

A

A medical term meaning that a patient’s red blood cells are of unequal size. This is commonly found in anemia and other blood conditions.

67
Q

What is poikilocytosis?

A

Variation in cell shape.

68
Q

What are Vitamin 12 and Folate involved in?

A

DNA replication

69
Q

What does a deficiency in either Vitamin 12 or Folate cause?

A
  • Issues with mitosis of the proerythroblast

- Causing megaloblastic or macrocytic anemia (large RBCs)

70
Q

What causes Vitamin 12 deficiency?

A

Reduced absorption

71
Q

What causes Folate deficiency?

A
  • Poor nutrition
  • Alcoholism
  • Malabsorption
  • Certain drugs (barbiturates, antibiotics and anti-epileptics)
72
Q

What is a barbiturate?

A

A drug that acts as a central nervous system depressant, and can therefore produce a wide spectrum of effects, from mild sedation to death.

73
Q

What does megaloblastic anemia lead to?

A
  • Abnormally large RBCs
  • Macroovalocytes
  • Hypersegmented Neutrophils
74
Q

When does chronic blood loss cause anemia?

A

When the volume of blood lost exceeds the capability for haematopoiesis of bone marrow

75
Q

What kind of anemia does blood loss lead to?

A

Normocytic anemia (no RBC abnormalities)

76
Q

What does growth factor Epo do?

A

Stimulates haemopoiesis of stem cells into erythrocytes (BFU production) in the bone marrow

77
Q

What causes haemolytic anemia?

A
  • Increased RBC destruction
  • RBC lifespan decreases from 120 to 20 days
  • Bone marrow unable to replace sufficient number of RBCs
  • Acquired/Inherited
78
Q

What are the two types of acquired haemolytic anemia?

A
  • Immune

- Non-immune

79
Q

How is acquired immune haemolytic anemia caused?

A
  • Haemolytic syndrome in newborn (Rh)
  • Autoantibodies
  • Complement
80
Q

How is acquired non-immune haemolytic anemia caused?

A
  • Drug-induced
  • Snake venom
  • Mechanical (heart valves)
  • Infections (malaria, septicaemia)
81
Q

What are the causes of inherited haemolytic anemia? (most haemolytic anemias are inherited)

A
  • RBC cytoskeletal defects (mutations in alpha or bate spectrin)
  • RBC enzyme defects (G6PD deficiency in NADPH metabolism)
  • Haemoglobin defects (thalassaemia/sickle cell)
82
Q

What do mutations in alpha or beta spectrin cause?

A

Hereditary spherocytosis

83
Q

What is spherocytosis?

A

The presence in the blood of spherocytes, i.e erythrocytes (red blood cells) that are sphere-shaped rather than bi-concave disk shaped as normal. Spherocytes are found in all hemolytic anemias to some degree.

84
Q

What is the cause of sickle cell disease?

A
  • Mutation in the Hb beta globin gene (Glu 6 -> Val)

- Polymerisation of Hb, distorting RBCs

85
Q

What are the effects of sickle cell disease?

A
  • ‘Sickling’ of RBCs
  • Sickle cell crisis due to blockage of microvasculature
  • Heterozygosity confers protection against malaria
  • Increased infection risk
86
Q

What is a sickle cell crisis?

A

Pain that can begin suddenly and last several hours to several days. It happens when sickled red blood cells block small blood vessels that carry blood to your bones.

87
Q

Which haemoblobin genes are found on which chromosomes?

A
  • Two alpha genes on chr 16

- One beta gene on chr 11

88
Q

What are the main haemoglobins in adults?

A
  • HbA (alpha2beta2)
  • HbA2 (alpha2delta2)
  • HbF (alpha2gamma2)
89
Q

What causes alpha thalassaemia?

A

Generally large deletions of the alpha-globin

90
Q

What causes beta thalassaemia?

A

Point mutations in the beta-globin gene

91
Q

What is haemostasis?

A

Arrest of blood flow

92
Q

What is the function of haemostasis?

A

To prevent severe blood loss after injury

93
Q

Why is bleeding a significant cause of mortality?

A
  • Trauma
  • Aneurysm rupture
  • Infection/Drugs
  • Haemophilia
94
Q

What are the main two processes involved in the stemming of bleeding?

A
  • Vasoconstriction (peptides/hormones lead to contraction of smooth muscle cells in the vessel walls)
  • Haemostasis (primary and secondary)
95
Q

What peptides/hormones lead to vasoconstriction?

A
  • Thromboxane
  • Serotonin
  • Angiotensin
  • Vasopressin
96
Q

What is thromboxane produced by?

A

Activated platelets

97
Q

What is serotonin secreted by?

A

Activated platelets

but produced by enterochromaffin cells, mostly in the GI tract

98
Q

What is primary haemostasis?

A

Platelet activation and aggregation

99
Q

What is secondary haemostasis?

A

Coagulation pathway activation

100
Q

What is the precursor or angiotensin?

A

Angiotensinogen (produced by the liver)

101
Q

What is the platelet mechanism of haemostasis?

A
  • Primary haemostatic response
  • Platelets activated by thrombin & collagen
  • Activated platelets change shape
  • Activated platelets aggregate to form coagulum
  • Platelet response alone is insufficient to stem bleed
102
Q

What is pseudopodia?

A

A temporary protrusion of the surface of an amoeboid cell for movement and feeding

103
Q

What is the coagulation mechanism of haemostasis?

A
  • Secondary haemostasis response
  • Involves cascade of proteolytic enzymes in the plasma that activate one another
  • Activated by a tissue factor or contact activation
  • Produces fibrin clot network
  • Coagulation response alone insufficient to stem bleed
104
Q

What are proteolytic enzymes?

A

Essential regulators and modulators of the inflammatory response

105
Q

What categories of coagulation factors are there?

A
  • Serine proteases (enzymes)

- Co-factors

106
Q

How do coagulation factors usually circulate in the plasma?

A

As an inactive pro-enzyme

107
Q

What catalyses the conversion of fibrinogen to fibrin?

A

Thrombin

108
Q

Which coagulation factors are serine proteases?

A 
FVIIa
FIXa
FXa
FXIa
thrombin
trypsin
109
Q

Which coagulation factors are co-factors?

A

Tissue factor
FVa
FVIIIa

110
Q

What is proteolysis?

A

A protein is cut into smaller fragments, usually by hydrolysis of peptide bonds

111
Q

How does proteolysis by digestive enzymes differ from proteolysis by coagulation factors?

A

Digestive: produces many small fragments from many proteins
Coagulation: more specific - one protein, one cut

112
Q

What is the principle of limited proteolysis and enhancement of trigger?

A

Small amount of trigger via intermediates leads to a larger amount of product

113
Q

What are the advantages of a cascading enzymatic pathway?

A
  • Allows for a small trigger to produce a larger amount of product
  • Allows foe acceleration of the response
114
Q

What are some examples of cascading enzymatic pathways?

A
  • Coagulation pathway
  • Complement pathway
  • Signalling pathways
115
Q

How is coagulation triggered?

A
  • Exposure of the blood to tissue factor
  • TF is transmembrane protein expressed on perivascular cells
  • After injury clotting factor FVII from the blood binds to TF expressed on the membranes of perivascular cells
  • FVII self activates
  • FVIIa proteolytically cleaves and activates FX
  • FXa converts prothrombin to thrombin
  • Thrombin converts fibrinogen to fibrin
116
Q

What are perivascular cells?

A

Situated or occurring around a blood vessel.

117
Q

What additional reactions to consolidate thrombin generation occur in coagulation?

A
  • Activation of FIX to TF/FVIIa
  • FIXa converts FX to FXa
  • Activation of FXI, FVIII and FV by thrombin
  • FVIIIa and FVa act as co-factors to FIXa and FXa respectivelly
118
Q

What does a FIX deficiency cause?

A

Haemophilia B

119
Q

What does a FVIII deficiency cause?

A

Haemophilia A

120
Q

What can the deficiency of FIX/FVIII/FV lead to?

A

Severe spontaneous bleeding

121
Q

What can a deficiency of vWF lead to?

A

Moderate to severe bleeding

122
Q

What can a deficiency of FXI lead to?

A

Mild bleeding

123
Q

Which three pathways can the coagulation system be divided into?

A
  • Extrinsic
  • Intrinsic
  • Common pathway
124
Q

What is the extrinsic coagulation pathway triggered by?

A

TF

125
Q

What is the intrinsic coagulation pathway triggered by?

A

Negatively charged surfaces (Silica, polyphosphates released by platelets and misfolded proteins)

126
Q

Which blood clotting complexes are vitamin K dependent?

A

TF/FVIIa
FIXa/FVIIIa
FXa/FVa

127
Q

How do vitamin K dependent clotting factor complexes bind to platelet surface?

A

Via Ca2+

128
Q

What is FXIII?

A

A transglutaminase activated by thrombin that cross-links fibrin to stabilise the fibrin network and increase its resistance to fibrinolysis.

129
Q

What can a deficiency in FXIII lead to?

A
  • Severe and spontaneous bleeding
  • Miscarriage in pregnancy
  • Poor wound-healing
130
Q

How does fibrin help to protect against infection?

A

Forms fibrin film with fibres behind the film, stops microbes getting in

131
Q

What is the structure of a platelet?

A
  • Smallest blood cell (2-3 micrometers diameter)
  • No nucleus
  • Contain alpha-granules and dense granules
  • Lifespan 5-9 days
  • Produced by megakaryotes
132
Q

What do alpha granules contain?

A
  • Fibrinogen
  • FV
  • vWF
  • Growth factors
133
Q

What do dense granules contain?

A
  • ADP/ATP
  • Serotonin
  • Calcium
  • Polyphosphate
134
Q

How do platelets become activated?

A

Through signalling through ligand-receptor (eg. collagen) interactions.
Adrenaline activates platelets so that during fight or flight if injured your blood clots.

135
Q

What is the process of primary haemostasis?

A
  1. Resting platelets circulate
  2. Vascular injury damages endothelium and exposes sub-endothelial collagen
  3. Platelets bind to collagen via GPVI and alpa-2-beta-1, also vie GPI and vWF. Platelets activate
  4. Platelets release ADP and thromboxane that further activate them though binding P2Y and TP receptors respectively
  5. Alpha-llb-beta-3 is activated
  6. AllbB3 binds fibrinogen and von Willebrand factor, which assist in platelet aggregation and holding the platelet plug together
136
Q

Which platelet receptor is involved in initial adherence of platelets to collagen?

A

GPVI/a2b1

137
Q

Which process is targeted by aspirin?

A

Thromboxane synthesis

138
Q

What is spontaneous bleeding?

A

No obvious cause, but due to coagulopathy, or other disease

139
Q

What is induced bleeding?

A

From trauma, surgery

external

140
Q

What are some examples of internal major bleeding?

A
  • haemophilia (joint/muscle)
  • aneurysm rupture
  • drug-induced
  • gastro-intestinal
141
Q

What are examples of minor bleeds?

A
  • Normal bruises
  • menorhaggia
  • epistaxis

IMS (13 decks)

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