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Medicine Year 2 > IIH > Flashcards

IIH Flashcards

1
Q

What are the stages of Erythropoesis that occur in the bone marrow?

A

Stem Cell -> Proerythroblast -> Early Erythroblast -> Late Erythroblast -> Normublast -> Reticulocyte

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2
Q

How long does the reticulocyte remain in the bone marrow before moving into the blood stream?

A

~3 days

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3
Q

What occurs in the Early Erythroblast?

A

Ribsosome synthesis

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4
Q

What occurs in the Late Erythroblast?

A

Haemoglobin Accumulation

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5
Q

At what stage in Erythropoesis does the cell lose its nucleus?

A

From Nomublast to Reticulocyte

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6
Q

After how long does a Reticulocyte become an Erythrocyte?

A

1-2 days in the bloodstream

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7
Q

How long is the life cycle of an erythrocyte?

A

~120 days

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8
Q

Where and how are old erythrocytes broken down?

A

In the spleen, liver and bone by macrophages

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9
Q

What happens to the haemoglobin that is produced when erythrocytes are broken down in the spleen?

A

It is further broken down to heme and globin
The Globin is broken down to amino acids
The heme is broken down to bilirubin and Fe2+

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10
Q

What happens to the amino acids produced by breakdown of erythrocytes?

A

They return to the bone marrow, via the blood stream, to be reused for erythropoesis

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11
Q

What happens to Fe2+ produced by the breakdown of erythrocytes?

A

It is converted to Fe3+ and bound to transferrin by hepatocytes so it can return to the bone marrow

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12
Q

What is the Hb range for anaemia?

A

Hb <130 g/L (men)

Hb <120 g/L (women)

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13
Q

What does the term clot refer to?

A

An intravascular thrombus

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14
Q

What is haemostasis?

A

The process that results from the stopping of bleeding following blood vessel injury

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15
Q

What does a haemostasic response involve normally?

A

Complex interactions between activated plasma clotting factors and platelets at the site of injury.

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16
Q

How are platelets produced?

A

They are produced by megakaryocytes in the bone marrow

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17
Q

What is the normal lifespan of a platelet?

A

8-12 days

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18
Q

What is the initial response to damaged endothelium?

A

Transient local vasoconstriction in order to reduce blood loss

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19
Q

What is the structure of a clot surrounding damaged endothelial tissue?

A

The inner shell consists of a dense inner core made up of fully activated platelets
This is surrounded by an outer shell of partially activated loosely packed platelets

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20
Q

What are the three main types of granules contained within platelets?

A

Dense granules - contain mediators of platelet activation such as serotonin, atp and calcium
Alpha granules - contain a number of clotting factors including FV, FVIII, fibrinogen, von Willebrand factor
Glycogen granules - provide the energy source for platelet reactions

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21
Q

Which are the two most important platelet glycoprotein receptors and what do they do?

A

GP1b - attaches to von Willebrand factor to form the initial tethering of the platelets
GPIIb/IIIa - is activated after tethering and expresses vWF which causes further platelets to tether and begins to form the clot

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22
Q

What are the inhibitors of coagulation?

A

Tissue factor pathway inhibitor (TFPI)
Antithrombin
Protein C
Protein S

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23
Q

What are two platelet inhibitors?

A

Prostacyclin

Nitric Oxide

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24
Q

What initially activates platelets at damaged endothelium?

A

ADP released from damaged blood vessel endothelial cells. Along with exposed collagen and thrombin

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25
Q

How are blood coagulation factors synthesised and released?

A

They are synthesised in the liver and released into the circulation in inactive precursor forms

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26
Q

What vitamin is required for synthesising some of growth factors and which growth factors are these?

A

Vitamin K is required to synthesise prothrombin (factor II) F VII, IX and X

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27
Q

Which factors are cofactors in the coagulation cascade and for which factors?

A

FV is a cofactor for activated FX

FVIII is a cofactor for activated FIX

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28
Q

What two forms do naive T cells differentiate into?

A

CD4 t cell which differentiates to a t helper cell

CD8 t cell which differentiates to a cytotoxic t cell

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29
Q

What cell do the CD4 and CD8 t cell receptors have affinity for? and what is the result of these being bound to?

A

CD4 t cell receptors have affinity for the MHC I receptor with epitope attached which is found on normal cells. This causes the t cell to be activated into a cytotoxic t cell.
CD8 t cell receptors have affinity for the MHC II receptor with epitope attached which is found in antigen presenting cells such as macrophages. This causes the t cell to be activated to a t helper cell.

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30
Q

What are the three main functions of complement proteins?

A

Opsonisation
Forming membrane attack complexes
Enhance Inflammation

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31
Q

What is opsonisation?

A

Coating of the surface of pathogens in complement proteins

Macrophages have complement receptors so this allows pathogens to be engulfed more easily

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32
Q

What is a membrane attack complex?

A

The process by which a group of complement proteins make a hole in a pathogens cell membrane causing lysis

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33
Q

Where are comlement proteins produced and how do they move around the body?

A

Complement proteins are produced in the liver and circulate in the bloodstream in an inactive form.
They become activated when they meet a pathogen

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34
Q

What are the three types of complement activation pathways?

A

Classical pathway
Alternative pathway
Lectin pathway

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35
Q

What is the ultimate step of all three complement activation pathways?

A

They all lead to the generation of C3 convertase.

This breaks down C3 to C3a and C3b

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36
Q

What are the functions of C3a and C3b

A

C3a acts to enhance inflammation

C3b acts to enhance opsonisation and cause the formation of membrane attack complexes

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37
Q

What is the classical pathway of complement protein activation?

A

Recognition of an antigen-antibody complex.

A complex protein binds to the Fc portion of the antibody and activates the production of C3 convertase.

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38
Q

What is the Lectin binding pathway of complement protein activation?

A

Acute phase proteins are released by the liver in response to interleukins in the bloodstream from local tissue macrophages.
Manose binding Lectin (MBL) binds to mannose and causes the production of C3 convertase

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39
Q

Which complement proteins are fundamental for enhancing inflammation?

A

C3a and C5a

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40
Q

What factors need to be present to allow macrophages to engulf opsonised pathogens?

A

C3b must opsonise the pathogens surface and C5a must also be present.
Macrophage has both a C5a receptor and a CR1 receptor that binds to C3b on the pathogens surface

41
Q

How is a membrane attack complex formed?

A

C3b can activate C5 convertase which causes the cleavage of C5 to C5a and C5b. C5a enhances inflammation and C5b combines with other complement proteins to form membrane attack complexes

42
Q

What are the two types of inflammatory mediators?

A

Plasma inflammatory mediators- complement proteins and kinins
Cell mediated inflammatory mediators - histamine and cytokines

43
Q

How does vasodilation and increased vascular permeability occur as a result of a pathogen entering the tissue?

A

PAMP (pathogen associated molecular patterns) sections on the pathogens surface are recognised by PRR (pattern recognition receptors) on histamine molecules.
This stimulates the release of histamine and aracodonic acid metabolites (leukotrienes and prostaglandins). These all increase vascular permeability.

44
Q

What is the result of a macrophage in the tissue fluid binding to a PAMP?

A

This causes the macrophage to release cytokines such as TNFalpha (tissue necrosis factor) and Interleukin-1. These will have local effects of inflammation and tissue repair by stimulating fibroblast activity. They have the systemic effects of fever and leukocytosis (Accumulation of white blood cells)

45
Q

Wha happens to monocytes when they move from the blood stream into the tissues?

A

They then become known as macrophages

46
Q

Where are PAMPs found on pathogens?

A

They can be found as part of the cell wall, in the flagella of a bacteria or even in the DNA or RNA of the pathogen

47
Q

What happens when a PRR binds to a PAMP

A

This causes activation of the innate immune system through complement cascade and other methods

48
Q

Where are PRRs found on immune cells?

A

Extracellularly on the cell surface
Intracellularly within the cell
Secreted as markers

49
Q

What is the process by which a progenitor t cell becomes a naive t cell?

A

Somatic recombination, this consists of the progenitor t cell receiving a unique t cell receptor to become a naive t cell

50
Q

Where will naive t cells migrate once they have matured in the thymus?

A

Migrate to the lymph nodes

51
Q

What is the process whereby a progenitor b cell becomes a naive b cell?

A

Somatic recombination

This leads to the b cell gaining a unique antibody

52
Q

What causes activation of a Naive t cell and what does it differentiate into?

A 
It is activated by the T cell receptor binding to an MHC class 2 with part of an antigen bound to it. This is typically from a dendritic cell.
This causes the t cell to differentiate into either a cytotoxic t cell of a T helper cell.
53
Q

What do mature B cells differentiate into and how does this happen?

A

They differentiate into plasma cells, This occur through either binding of antigen to the b cells immunoglobulin receptor or through binding of a helper t cell to its MHC class 2 receptor with processed antigen

54
Q

In general what are the two types of T cells and what receptor types do they bind?

A

CD4 T-cells are activated to form T helper cells through binding to antigen presenting MHC class 2 receptors

CD8 T-cells are activated to form cytotoxic T-cells through binding to antigen presenting MHC class 1 receptors

55
Q

What receptors allow a naive CD8 T cell to proliferate and differentiate and how does this happen?

A 
The T-cell receptor binds to an antigen presenting MHC class 1 receptor (for example on a dendritic cell) with the CD8. The Naive CD8 T-cell also has a CD28 receptor that must bind to the B7 receptor on the dendritic cell.
This causes the Naive CD8 T-cell to produce IL-2 which binds to interleukin 2 receptors on the cell surface. This causes proliferation and differentiation into killer cells or memory cells.
56
Q

What is aplastic anaemia?

A

When a reduction in the number of pluripotent stem cells in the bone marrow causes anaemia through reduction in all the major cell lines: red cells, white cells and platelets

57
Q

What is pernicious anaemia?

A

This results from an autoimmune attack on the parietal cells of the stomach. This results in a lack of production of intrinsic factors which is essential for vitamin B12 absorption. Vitamin B12 is required for normal haematopoesis and without it abnormally large red cells are produced. This can result in a macrocytic anaemia.
It can also result from an autoimmune attack on the intrinsic factor or the intrinsic factor receptors in the small intestine.

58
Q

What is iron deficiency anaemia?

A

A lack or intake, increased loss or increased demand of iron which results in not enough iron being present for normal erythropoesis. This results in macrocytic anaemia.

59
Q

What are causes of microcytic anaemia?

A

Most common - iron deficieny
Thalassemia - hereditary, results in abnormal haemoglobin production
Sideroblastic anaemia - marrow produces ringed sideroblasts instead of healthy red cells
Chronic disease (not common) - Increased inflammatory IL-6 causes reduced ferroportin so iron is not as available to the bone marrow.

60
Q

What are causes of normocytic anaemia?

A

Chronic disease - Increased inflammatory IL-6 causes reduced ferroportin so iron is not as available to the bone marrow.
Acute bleeding
Everything else

61
Q

What are the causes of macrocytic anaemia?

A

B12/folate deficiency
haemolysis
drugs
alcoholism

62
Q

What are the main advantages and disadvantages of the innate immune system?

A

Advantages: Immediate, doesn’t require prior exposure
Disadvantages: limited number of receptors for specific structures on pathogens, non-specific

63
Q

What are the main advantages and disadvantages of the adaptive immune system?

A

Advantages:allows recognition of a large range of pathogens, memory cells created so can respond more rapidly to subsequent infections.
Disadvantages: Slow to react to initial infections if not previously encountered (1-2 weeks)

64
Q

What is the basic structure of an antibody?

A

Immunoglobulin molecule with identical pairs of heavy and light chains (2 heavy, 2 light)

65
Q

What are the different classes of antibody and how are they classed?

A

Classes are coded by the constant region of the heavy chain. IgG has gamma heavy chains, IgA has alpha heavy chains, IgM has mu heavy chains, IgD has delta heavy chains and IgE has epsilon heavy chains.

66
Q

What are the two types of immunoglobulin light chains?

A

kappa or lambda

67
Q

What are the heavy and light immunoglobulin chains made up of?

A

Both are made up of immunoglobulin domains which are globular chains of amino acids.
The light chains contain two domains, one constant and one variable.
The heavy chain contains four to five domains with one variable and majority of the rest constant.

68
Q

What do the constant domains of the antibody determine?

A

The function of the antibody

69
Q

What is the purpose of the fc region of an antibody?

A

Critical for the effector function of the antibody (activating classical complement pathway)

70
Q

What is the purpose of the fab region of an antibody?

A

It has an antigen binding site that varies between b cells

the fab region is identical for both arms

71
Q

What is the purpose of the hinge region of the antigen?

A

Hinge region at bottom of each arm on an antibody, allows the arms to move so both antigenic binding sites can be used.

72
Q

What are the primary and secondary lymph organs?

A

Primary are the bone marrow and the thymus

Secondary are the spleen and lymph nodes

73
Q

How do B cell immunoglobulins signal to the B cell when an antigen is bound?

A

There are associated molecules next to the antibodies on the cell membrane that transmit signals when the antibody has bound to something.
There are also CD21 molecules which receive activated C3 which enhance the signalling

74
Q

Lecture 24: The immune system in early life

A

L24

75
Q

How long is the adaptive immune system immune for after birth?

A

It remains immature for a year after birth. Lymphocyte levels are their highest just after birth and decrease throughout childhood to reach adult levels

76
Q

What kind of antibodies predominate in a neonate and how does it receive antibodies for its first months of life?

A

The predominant immunoglobulin is IgM and the infant receives maternal antibodies through the placenta to protect it after it is born.

77
Q

What is a transplacental infection and how can it occur?

A

Whilst the placenta provides a barrier to infection for the foetus it is not perfect and sometimes viruses can breach it to reach the foetus, examples are rubella and herpes

78
Q

What is congenital rubella and what medical problems can it cause?

A

It is a virus that can be passed from the mother to the foetus most likely in the first trimester of pregnancy. The virus causes congenital abnormalities in the foetus mainly including:
Sensorineural deafness (58% of babies)
Eye disease e.g. Retinopathy (43% of babies)
Congenital heart problems (50% of babies)

79
Q

If a mother gets rubella in the first trimester of pregnancy what are the chances of her baby having congenital rubella?

A

50%

80
Q

Which antibody is transferred across the placenta from mother to foetus and what is its purpose?

A

The IgG antibody crosses the placenta to protect the child in its first 3 to 6 months against infections. IgA and IgM do not cross the placenta

81
Q

What is the disadvantage of Transplacental IgG transfer from mother to foetus? Give examples of conditions

A

It can potentially lead to the transfer of IgG mediated autoimmune disease, examples include:
Myesthenia gravis where the antibody blocks the acetylcholinesterase receptor
RO positive antibodies (antinuclear antibodies) that are seen in lupus. This can cause neonatal heart block as the anti nuclear antibodies attack the nerve conduction fibres

82
Q

What is myasthenia gravis?

A

An autoimmune disease in which IgG antibodies block the acetylcholinesterase receptor. This prevents the breakdown of acetylcholine and therefore affects muscle contractions due to effecting the neuromuscular junction.

83
Q

What is Leukocyte adhesion deficiency (LAD)?

A

An autosomal recessive condition that results in a defect in the surface integrin protein on neutrophils. These proteins are required to allow neutrophils to tether to the endothelial walls and migrate to the sites of infection. This is because without the integrin protein then the neutrophils cant bind to ICAM 1 on the endothelial surface.
Characterised by increased numbers of neutrophils in blood and lack of puss at sites of infection

84
Q

What is common variable immunodeficiency (CVID)?

A

An immune disorder characterised by recurrent infections and low antibody levels. It can develop later in life even if an individual has been born normal. Number of causes some genetic, ultimately end up with lowered antibody levels.

85
Q

What is the principle method of innate immune system recognising pathogens?

A

Each innate immune cell carries an array of recognition molecules that can recognise molecular patterns seen on pathogens

86
Q

What is the principle method of innate immune system recognising pathogens?

A

Each innate immune cell carries an array of recognition molecules that can recognise molecular patterns seen on pathogens

87
Q

What are granulocytes?

A

neutrophils, eosinophils and basophils

88
Q

What are the two broad lineages that hematopoietic stem cells can differentiate into?

A

Myeloid lineage - erythrocytes, platelets, granulocytes, monocytes, macrophages and dendritic cells
Lymphoid lineage- T and B lymphocytes, NK cells

89
Q

Where does haematopoiesis occur in the foetus?

A

Definitive HSCs begin to appear in the aorta-gonad-mesonephros (AGM) before migrating to the foetal liver and then to the bone marrow.

90
Q

What is the difference between red and yellow marrow?

A

Red marrow is where haemotopoiesis occurs and is associated with a rich blood supply
Yellow marrow is just fat cells and no active haematopoiesis occurs here.

91
Q

What do haematopoietic stem cells require to develop and differentiate?

A

Intrinsic factors i.e. lineage-determining transcription factors and their epigenetic regulation
Extrinsic regulators i.e. soluable growth factors

92
Q

What protein regulates platelet production and where is it produced?

A

Thrombopoietin is mainly produced by the liver

93
Q

How are platelets produced?

A

They bud off megakaryocytes which form from megakaryoblasts. 2000-3000 platelets are formed from each megakaryocyte.

94
Q

What regulates granulocyte production?

A

Granulocytes (neutrophils, eosinophils and basophils) production is regulated by G-CSF (Granulocyte colony-stimulating factor) glycoprotein.

95
Q

What is the main stimulus for epo production?

A

The main stimulus is hypoxia.

96
Q

What are haematopoietic growth factors and where are they produced?

A

HGFs are soluable regulators for survival, proliferation and differation of primitive hematopoietic stem cells. They are produced in the bone marrow stroma.

97
Q

What is thromabopoietin mainly used to treat?

A

Immune thrombocytopenia

98
Q

What are the difference between leukaemias and lymphomas?

A

leukaemias are cancers of haematopoietic cells which arise in the marrow and spread to the blood and lymph nodes.
Lymphomas are cancers of the cells in the lymph nodes and spleen that can then spread to the bone marrow.

99
Q

What do these types of leukaemia stand for?

A

AML-acute myeloid leukaemia
CML-Chronic myeloid leukaemia
ALL-Acute lymphocytic leukaemia
CLL- Chronic lymphocytic leukaemia

Medicine Year 2 (6 decks)

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