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Foundations 3 > IIH > Flashcards

IIH Flashcards

1
Q

Where are the circulating blood cells formed? What is this process called

A
  • Bone marrow

- Haematopoiesis

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2
Q

What is the lifespan of granulocytes?

Mostly consists of neutrophils, some basophil and eosinophil

A

Less than 48 hours

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3
Q

What is the lifespan of erythrocyte?

A

120 days

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4
Q

What is the lifespan of platelets?

A

7-10 days

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5
Q

What is the lifespan of monocytes?

A

Days to weeks depending on differentiation. Some macrophages in tissue can last years.

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6
Q

What is the lifespan of lymphocytes?

A

Days to years depending on whether naive or memory

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7
Q

What are the progenitor cells of the blood cell line?

A

Haematopoietic stem cell

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8
Q

What are the properties possessed by haematopoietic stem cell?

A
  • Mostly in quiescent (non-dividing) state
  • Capacity to self renew
  • Multipotent
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9
Q

What are the 2 lineages to which haematopoietic stem cells can divide into and name all the cells that can be formed from these lineages?

A
  1. Myeloid
    - Erythrocytes and platelets
    - Neutrophils, basophils /mast cells, eosinophil
    - Monocytes and macrophages
    - Dendritic cell
  2. Lymphoid
    - T and B cells
    - NK cell
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10
Q

What produces platelets? How many platelets can one of it produce?

A

Megakaryocytes. 2000-3000

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11
Q

What tests can be done to identify cell types in the laboratory?

A
  1. Full blood count
  2. Immunophenotyping: Specific proteins or cell markers that are found on the cell surface or inside the cell.
  3. Microscopic examination
  4. Genetic testing
  5. Functional assays to identify early lineage cells. (Functional activity of the cell)
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12
Q

What is an important immunophenotypic marker for a subset of marrow cells that include haematopoietic stem cells?

A

CD34

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13
Q

When is there an increase in haematopoietic stem cell?

A
  • Marrow recovering from damage inflicted by cytotoxic drugs

- Administration of Granulocyte-Colony Stimulating Factor. (G-CSF)

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14
Q

What is the use of G-CSF?

A

Mobilisation of stem cells into blood for harvesting for Haematopoietic Stem Cell transplants.

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15
Q

How do you differentiate Haematopoietic Stem Cell from rest of the cells in a blood culture for stem cell transplant?

A

Use CD34 marker

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16
Q

Where are the 4 regions in which haematopoiesis progresses to take place in a foetus? What day post-fertilisation does haematopoiesis starts to occur?

A
  1. Extra-embryonic Yolk Sac
  2. Aorta-gonad-mesonephros
  3. Foetal liver
  4. Bone marrow
    Day 17
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17
Q

What are the 2 regions in the bone marrow and what is their specific functions?

A

Red - Rich in blood supply, found only in axial skeleton and contains 30-70% haematopoietic stem cells. Rest is fat.
Yellow - No active haematopoiesis so just fat cells present.

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18
Q

Can haematopoiesis occur in an adult liver and spleen? If yes, what conditions does it occur in?

A

Yes it can when the bone marrow is compromised eg in untreated thalassaemia and myelofibrosis

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19
Q

What are the possible options for a haematopoietic stem cell to become or not?

A
  • Quiescence
  • Self-renewal
  • Differentiation
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20
Q

What are the fate choices for a progenitor cell?

A
  • Proliferate
  • Lineage commitment
  • Terminal differentiation
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21
Q

What do haematopoietic stem cells require to develop and differentiate?

A
  • Intrinsic factors: Transcription factors and epigenetic regulation
  • Extrinsic factors: Cellular and soluble growth factors
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22
Q

What are the cellular elements provided by the bone marrow stroma?

A
  • Fat cells
  • Fibrocytes
  • Extracellular matrix
  • Sinusoids
  • Reticular fibrocytes form the adventitial surfaces of the vascular sinuses, extend cytoplasmic projections and form lattice on which blood cells are found.
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23
Q

How can one demonstrate the lattice formed by extended cytoplasmic projections of the reticular fibrocytes?

A

Reticulin stains of marrow sections

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24
Q

Where is the sample of bone marrow taken from?

A

Iliac crest

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25
Q

What are the 2 ways in which bone marrow biopsy can be performed?

A
  • Aspiration: Cells in the syringe

- Trephine: Removal of 1-2cm of bone marrow

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26
Q

What regulates the production of platelets? Where is this regulator produced?

A

Thrombopoietin produced in the liver

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27
Q

How long does a platelet transfusion usually last? How does this differ with transfusion in someone with immune thrombocytopenia?

A
  • 1 to 5 days
  • Immune thrombocytopenia only a few hours because autoantibodies against platelets rapidly destroy them and spleen clearance works alongside.
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28
Q

What regulates the production of

a) Granulocyte
b) Monocyte

A

a) G-CSF

b) GM-CSF

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29
Q

What is the difference between mature granulocyte and monocytes?

A

Mature granulocytes have lost chromation, segmented nuclei and cannot proliferate whereas monocytes are able to divide but have unusual proliferatin.

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30
Q

What regulates erythrocytes? Where is this produced? What is its stimulus?

A

Erythropoietin produced in the kidney (Peritubular fibrocytes of kidney cortex). Hypoxia

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31
Q

What can stain neutrophil lineage?

A

Myeloperoxidase (MPO)

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32
Q

What is the maturation steps of an erythrocyte?

A
  1. Pre-normoblast (Pre-erythrocyte)
  2. Normoblast
    - Nucleus becomes more condensed and then extruded
    - Cytoplasm contains more haemoglobin
  3. Reticulocyte - Spend 1-2 days in bone marrow then circulate for another 1-2 days before terminally differentiating. It has no nucleus but still able to synthesise haemaglobin and contain some ribosomal RNA.
  4. Erythrocyte
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33
Q

What is the longevity of red blood cells from a transfusion?

A

1 month

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34
Q

What nutritional factors are needed for erythropoiesis to occur?

A
  • Iron
  • Folate
  • B12
  • B6,Vitamin C, E, cobalt, manganese and amino acids
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35
Q

What hormonal deficiencies can affect erythropoiesis?

A
  • Hypothyroidism

- Lack of androgens

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36
Q

If normoblasts are present in a full blood count, what does it suggest?

A

Haemolytic anaemia as there is an increased stress for erythropoiesis

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37
Q

In what circumstances are erythropoietin recombinant given?

A
  • Renal failure
  • Anaemia due to malignant diseases receiving chemo/radiotherapy
  • Patients donating their own blood prior to a surgery: Jehovah’s Witness alternative for transfusion
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38
Q

What are the possible side effects of EPO recombinant?

A
  • Hypertension
  • Thrombosis
  • Thrombophlebitis (Inflammation of wall of vein: Usually in the leg)
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39
Q

When is G-CSF used in treatment?

A
  • Neutropenic patients prevention of infection especially in those who have undergone chemotherapy or congenital neutropenia
  • Mobilisation of stem cells for haematopoietic stem cell transplant
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40
Q

When is thrombopoietin used?

A
  • Immune thrombocytopenia
  • Myelodysplasia (bone marrow does not make enough healthy cells)
  • Post chemotherapy
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41
Q

When do blood cancers arise?

A

When the balance between progenitor proliferation and differentiation is altered

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42
Q

What can cause blood cancers to arise?

A
  • Genetic abnormality

- Viral infection: Epstein Barr can cause Burkitt’s lymphoma

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43
Q

What is the difference between leukaemia and lymphoma?

A
  • Leukaemia is the cancer in the bone marrow that can spread to the lymph nodes and secondary lymphoid organs
  • Lymphoma is the cancer of the lymph nodes or secondary lymphoid organs that spread to the bone marrow
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44
Q

How are blood cancers differentiated?

A
  • Lymphoid (T-B cells) or myeloid lineage
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45
Q

How can once classify leukaemias?

A

AML- Acute Myeloblast Leukaemia
CML- Chronic Myeloid Leukaemia
ALL- Acute Lymphoblastic Leukaemia
CLL- Chronic Lymphocytic Leukaemia

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46
Q

What is the function of neutrophils?

A

Engulf and destroy bacteria via phagocytosis

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47
Q

What is the most likely cause of death of someone with neutropenia?

A

Bacterial infection not treated with antibiotics

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48
Q

What is the function of eosinophils?

A

Parasite infections

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49
Q

What are the functions of monocytes?

A

Phagocytic to engulf and destroy dead cells, bacterial, protozoa and fungi.

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50
Q

What is the parameter that suggests anaemia in men and women in g/L?

A

Men <130

Women <120

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51
Q

What are the structures of a red blood cell?

A
  • Biconcave in shape
  • No nucleus
  • 7 micrometer
  • Consists of haemoglobin
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52
Q

What makes up the haemoglobin?

A
  • Haem group

- 4 polypeptide chains 2 alpha and 2 beta

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53
Q

How does adult and foetal Hb differ?

A

Adult: 2 alpha and 2 beta
Foetal: 2 alpha and 2 gamma

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54
Q

Why does foetal blood contain gamma instead of beta?

A

2,3-DPG shifts curve to the right for more oxygen dissociation to occur. 2,3-DPG binds to beta so if there is no Beta, it is not influenced by 2,3-DPG and so foetal Hb curve more left shifted so it is less ready to give up oxygen.

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55
Q

What causes a left shift in Hb curve? Name condition/normal phenomena in which this is seen

A
  • Decreased carbon dioxide
  • Decreased hydrogen ions
  • Decreased 2,3-DPG
  • Decreased temperature
    Seen in foetal blood
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56
Q

What causes a right shift in the Hb curve? Name condition/normal phenomena in which this is seen.

A
  • Increased carbon dioxide
  • Increased hydrogen ions
  • Increased temperature
  • Increase 2,3-DPG
    Seen in sickle cell anaemia and methaemoglobin
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57
Q

What can cause a failure of haem synthesis?

A
  • Porphyria: Inherited metabolic disorder due to slower production of haem.
  • Sideroblastic anaemia: Abnormally nucleated erythroblasts with granules of iron accumulated on the mitochondria
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58
Q

What are the signs of porphyria?

A

Sensitivity in light, acute attacks

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59
Q

How is anaemia defined?

A
  • Lack of blood

- Reduction of haemoglobin, red blood cell count or haemoglobin

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60
Q

What is normal Hb levels in pregnant women? Why is there an apparent anaemia?

A

> 110g/L. In pregnant women, the plasma volume increases so there is a decreased haematocrit.

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61
Q

In an acute major blood loss, when will anaemia become apparent?

A

After 24 hours

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62
Q

What is a haematocrit?

A

Fraction of RBC/FBC

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63
Q

What are the symptoms of anaemia?

A
  • Fatigue
  • Drowsiness
  • Headaches
  • Palpitations
  • Shortness of breath
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64
Q

What are the signs of anaemia?

A
  • Tachycardia
  • Angular stomatitis
  • Koilonychia: Spooning of the nails
  • Pallor mucous membranes and conjunctiva
  • Flow murmur
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65
Q

What 2 ways can be used to classify anaemia?

A
  • Size of red blood cell (Macro, normo or microcytic)

- Cause of anaemia (Reduced RBC, Poor function, Increased loss or destruction)

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66
Q

What causes a normocytic anaemia with an increased loss of red blood cell?

A

Acute blood loss/ Anaemia of chronic disease (can cause result in microcytic anaemia)

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67
Q

What causes a microcytic anaemia with an increased loss of red blood cell?

A

Iron deficiency anaemia

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68
Q

What are the causes of Iron Deficiency Anaemia?

A
  • Dietary
  • Chronic blood loss
  • Menstruation
  • Gastritis/ulcer of the GIT
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69
Q

What can cause a macrocytic anaemia with a reduced production of red cells?

A

B12/folate deficiency. Pernicious anaemia due to a loss of IF which is needed for B12 reabsorption at the terminal ileum.

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70
Q

What causes a microcytic anaemia with a poor function of red blood cells?

A

Thalassaemia: Autosomal recessive condition due to abnormal production of polypeptide
Sickle cell anaemia

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71
Q

What causes macrocytic anaemia with an increased destruction of RBC?

A
  1. Haemolytic anaemia which is an autoimmune condition that produces autoantibody against body’s own RBC.
  2. Hereditary Spherocytosis: Autosomal dominant
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72
Q

How can you differentiate haemolytic anaemia and hereditary sphrecytosis?

A

Coomb’s test- detection of antibodies against RBC’s. + for thalassaemia

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73
Q

How does one treat thalassaemia?

A

Transfusion

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74
Q

Problem associated with transfusion? What is used to fix the problem?

A

Iron overload can corrected using deferoxamine which binds iron to aluminium.

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75
Q

What is the problem in hereditary spherocytosis?

A

Red blood cells are sphere shaped due to a defect in the outer layer. So, red cells are broken rapidly by the liver leading to a splenomegaly.

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76
Q

What does haemostasis mean?

A

Process that results in the stopping of bleeding following a vessel injury

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77
Q

What is the membrane of the platelet made up of?

A
  • Phospholipid bilayer

- Glycoprotein receptors GPIb/IIb/IIIa

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78
Q

What is the cytoplasm of the platelet made up of?

A
  • Actin and myosin fibrils which interact after platelet activation to enable platelet to change shape.
  • Storage granules either dense, alpha granules or glycogen.
  • Dense granules contain mediators of platelet activation such as serotonin, ADP, catecholamines, calcium
  • Alpha granules contain clotting factors
  • Glycogen granules used as an energy source
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79
Q

What are the sequence of events following blood vessel injury?

A
  1. Localised vasoconstriction at the site of the injury.
  2. Platelet adhesion to the sub-endothelial collagen of damaged blood vessel.
  3. Activation of coagulation cascade
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80
Q

How does platelet adhesion to the sub-endothelial collagen of damaged blood vessel?

A
  • It is mediated by vWF adherence to platelet membrane on the GPIb.
  • This causes GPIIb/IIIa to adhere as well making the bond stronger.
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81
Q

What happens once the platelets adhere to the sub-endothelial collagen of the damaged blood vessel?

A

Platelet aggregation activation occurs where damaged blood endothelium releases ADP and when exposed to collagen or thrombin activates platelet metabolic pathways. This contributes to a thrombus formation.

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82
Q

What is the complication of liver failure?

A

Bleeding because liver is an important coagulation factor synthesiser.

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83
Q

What happens after thrombus is formed?

A

Fibrinolytic degradation of clot

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84
Q

Explain the platelet coagulation cascade?

A 
Tissue factor (TF) activates VIIa which activates V which is paired with X. Xa then activates prothrombin to thrombin which then activates fibrinogen to fibrin which forms a mash of a stable plug. Thrombin also activates plasminogen into plasmin and factor XIII. Plasmin and factor 13 work together to break the cross-link.
XIIa-> XIa-> IXa +VIIIa-> Xa+V
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85
Q

What is calcium needed for?

A

Phospholipid binding of clotting factors.

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86
Q

What is an example of a tissue factor?

A

Thromboplastin

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87
Q

What causes haemophilia A?

A

Clotting factor VIII deficiency

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88
Q

What causes haemophilia B?

A

Clotting factor IX deficiency

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89
Q

What happens in von Willebrand Disease?

A
  • No vWF released to bind to GPIb and cause platelet adhesion to the sub-endothelial collagen of the damaged blood vessel.
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90
Q

What causes the Bernard-Soulier syndrome?

A

Deficiency in the GPIb in the platelet membrane

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91
Q

What causes Glanzmann’s Thrombasthenia?

A

Deficiency in GPIIb/IIIa

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92
Q

What is the most common cause of acquired thrombocytopenia?

A
  • Autoimmune destruction

- Bone marrow failure

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93
Q

What can cause the acquired deficiency of clotting factors?

A
  • Liver disease

- Vitamin K deficiency

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94
Q

What clears the fibrin degradation products?

A

Cleared by the reticulo-endothelial system

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95
Q

When does the blood vessel repair process occur and what happens during this repair process?

A

Occurs simultaneously with the fibrolysis. Blood vessel smooth muscle and endothelial cells undergo cell division and multiply until the breach of the vessel is closed

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96
Q

What factor plays a major role in the vessel repair process?

A

Platelet derived growth factor.

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97
Q

What are the anticoagulant mechanisms in place to prevent coagulation activation proceeding as far as thrombus formation?

A
  • Anti-thrombin
  • Protein C system
  • Presence of natural heparins on the endothelial cell surface
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98
Q

How does the anti-thrombin mechanism function?

A

Inactivated thrombin and factors IX,X,XI

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99
Q

How does the Protein C system work?

A
  • Free thrombin binds to Thrombomodulin (TM).
  • This allows protein C to bind adjacent to it.
  • Protein C is cleaved into its activated form.
  • Activated protein C forms a complex with its cofactors protein S and inactive FV.
  • Enzymatically degrades factor V and VIII.
  • Significant suppression of coagulation activation and restricts the thrombus to the site of the injury.
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100
Q

How does natural heparin work as an anti-coagulant?

A
  • Binds to the endothelial cell surface to enhance the anticoagulant activity of anti-thrombin
  • Synthesis and release of a platelet inhibitory prostaglandin called prostacyclin.
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101
Q

What are the main consequences of occlusion of arterial or venous blood?

A
  • Myocardial infarction

- Cerebrovascular stroke

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102
Q

What do you call the conditions that predispose to thrombosis?

A

Thrombophilias

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103
Q

What are the 3 hereditary thrombophilia states?

A
  • Factor V Leiden mutation.
  • Protein C, S and AT deficiency, mutation in prothrombin gene
  • Elevation in the circulating levels of the amino acid homocysteine associated with arterial and venous thrombosis
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104
Q

What happens in a factor V Leiden mutation?

A
  • Impaired protein C cofactor activity

- When active form, resistant to neutralisation by protein C

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105
Q

What causes acquired thrombophilia states?

A
  • Malignancy
  • Lupus anticoagulant
  • Surgery
  • Long haul flights
  • Myeloproliferative disorders
  • Prolonged periods of immobility
  • Pregnancy
  • Smoking
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106
Q

What is the lupus anticoagulant?

A

Autoantibody that causes prolongation of the phospholipid- based in vitro coagulation tests

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107
Q

What does lupus anticoagulant present with?

A
  • Recurrent thrombosis

- Recurrent miscarriage

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108
Q

What are the 2 most common coagulation tests?

A
  • Prothrombin time (PT)

- Activated Partial thromboplastin time (APTT)

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109
Q

What are Prothrombin Time and Activated Partial Thromboplastin Time used for?

A
  • Investigation of bruising or bleeding
  • Monitoring warfarin
  • Monitoring IV Heparin
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110
Q

What does an isolated prolongation of the Prothrombin Time indicate?

A

Factor VII deficiency

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111
Q

What causes factor VII deficiency?

A
  • Hereditary
  • Mild liver disease
  • Mild Vitamin K deficiency
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112
Q

If APTT returns to normal it indicates a?

A

Clotting factor deficiency (Factor 8,9,11,12)

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113
Q

If APTT fails to correct, is shows?

A

Presence of an inhibitor such as lupus anticoagulant or factor 8 antibodies

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114
Q

If both PT and APTT are prolonged, what does that mean?

A
  • Single factor deficiency in common pathway so factor 10,5, prothrombin or fibrinogen
  • Multiple factor deficiency due to liver disease, Vitamin K, warfarin therapy, DIC, Dilutional Coagulopathy
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115
Q

What function does vWF serve for Factor VIII?

A

Acts as a carrier protein

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116
Q

Where is vWF synthesised?

A

Blood vessel endothelial cells and megakaryocytes

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117
Q

How does the analyser that measures full blood count work?

A
  • Laser light shined on each cell

- Degree of scattering is measured

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118
Q

What does side and forward scatter show?

A

Size and granularity of cell

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119
Q

What does mean cell Hb concentration show?

A

Concentration of haemoglobin and can deduce if normochromic, hyperchromic or hypochromic

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120
Q

When can hypochromic be seen?

A

Microcytic anaemia

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121
Q

When can hyperchromic be seen?

A

Sickle cell anaemia

Hereditary spherocytosis

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122
Q

When can normochromic be seen?

A

Macrocytic anaemia

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123
Q

When can mean cell Hb concentration be artificially high?

A

Agglutination

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124
Q

What happens in polycythaemia?

A

Increased number of red blood cells produced. This increases haematocrit and blood viscosity and thus more prone to thrombosis.

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125
Q

What are the primary and secondary causes of polycythaemia?

A 
Primary 
- JAK2 mutation
- Malignancy in bone marrow
Secondary
- Living in higher altitudes
- EPO injections increase red blood cell number
- Chronic hypoxia due to COPD
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126
Q

If precursor to WBC is present in blood, what does it suggest?

A

Sepsis

Leukaemia

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127
Q

What is the difference between neutrophil and lymphocyte count between adults and children?

A

Adults have more neutrophils than lymphocytes. Opposite is true for children

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128
Q

What does high neutrophil count suggest?

A

Infection

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129
Q

What causes a variation in neutrophil count?

A
  • Age
  • Gender
  • Pregnancy
  • Race
  • Physiological status
  • Exercs=use
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130
Q

What causes neutrophilia (Increased neutrophil number)?

A

Corticosteroids as they suppress inflammation

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131
Q

What causes neutropenia based on inherited, acquired, reduced production and increased destruction?

A 
Inherited + Reduced production
- Congenital
- Cyclical
Inherited + Increased destruction
- Autoimmune neutropenia due to SLE or Evan's syndrome
Acquired+ Reduced production
- Blood cancer
- Aplastic anaemia
- B12/folate deficiency
- Drugs such as carbimazole (treat hyperthyroidism)
- Viral infection
Acquired + Increased destruction
- Chemotherapy
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132
Q

What controls the production of lymphocytes?

A

Growth factors

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133
Q

What causes the expansion of lymphocytes?

A

Antigen driven production

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134
Q

How does sequesteration of lymphocytes occur?

A
  • In secondary lymphoid tissue

- Maintain reserves outside of cells

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135
Q

How does the apoptosis of lymphocytes occur?

A
  • Ligation of death receptors via Fas expressed by cytotoxic T cells.
  • Deprivation of growth and survival factors
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136
Q

What do cells undergoing apoptosis go through?

A
  • Cell shrinkage
  • Chromatin condensation
  • Chromatin marginalisation
  • Plasma membrane blebbing
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137
Q

What causes lymphocytosis?

A
  • Reactive to overcome infection

- Clonal due to malignancy

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138
Q

What is the neoplasm during development?

A

Leukaemia of T/B cell

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139
Q

What is the neoplasm in matured lymphocytes?

A

Chronic lymphocytic leukaemia/lymphomas

- Hodgkin and non-hodgkin lymphomas

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140
Q

What causes lymphopenia?

A

Inherited: Recurrent severe bacterial, viral, fungal infection SCID (absence of T cells)
Acquired: Immunosuppresants used in inflammatory disease and cancer

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141
Q

What causes an increased and decreased monocyte count?

A

Increased
- Leukaemia, infection and Epstein Barr Virus
Decreased
- GATA2 mutation, marrow infiltration

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142
Q

What causes increased and decreased basophil count?

A

Increased
- Infection, hypothyroidism, myeloid malignancy
Decreased
- Hyperthyroidism, steroids

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143
Q

What causes increased and decreased eosinophil count?

A

Increased
- Parasitic infection, Allergic condition, Hypereosinophilic syndrome
Decreased
- Alcohol, steroid

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144
Q

What can cause thrombocytopenia?

A
  • Underproduction
  • Increased destruction
  • Sequestration
  • Abnormal platelet function
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145
Q

What causes thrombocytopenia due to underproduction?

A
  • Infection
  • Vitamin B12/folate deficiency
  • Infiltration of marrow
  • Aplastic anaemia
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146
Q

What is the management for thrombocytopenia due to underproduction of platelets?

A
  • TPO recombinant
  • Platelet transfusion
  • Treat underlying condition
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147
Q

What causes thrombocytopenia due to increased platelet destruction?

A
  • Immune thrombocytopenic purpura
  • SLE
  • HIV/Hep C
  • Heparin induced thrombocytopenia
  • Post-transfusion purpura
  • DIC
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148
Q

What are the managements available for increased platelet destruction?

A

Splenectomy

Steroids

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149
Q

What are the causes of sequestration?

A

Hypersplenism due to cirrhosis, infection, malignancy

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150
Q

What are the causes of abnormal platelet function?

A

Inherited: vWF, Bernard Soulier, Glanzmann’s
Acquired: Aspirin, liver disease, autoimmune, severe iron or folate deficiency

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151
Q

What are the features of a prion?

A
  • No nucleic acid

- Smaller than virus

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152
Q

What is a consequence of a prion infection?

A

Fatal neurodegenerative disease

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153
Q

What are the 2 disease that causes neuronal function loss?

A
  • Bovine Spongiform Encephalopathy

- Variant Creutzfeldt- Jakob disease (vJCD)

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154
Q

What causes the neuronal function loss in bovine spongiform and varian Creutzfeldt Jakob disease?

A

Misfolding of protein that incorporated into brain tissue to form amyloid fibres which aggregate and cause progressive degeneration

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155
Q

Why are prions difficult to eradicate?

A
  • Heat and disinfectant resistant
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156
Q

What is the difference between PrPsc and PrPc?

A

PrPc is normal whereas PrPsc is infectious

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157
Q

What is the common structure of all viruses?

A
  • Either DNA/RNA genetic material
  • Capsid
  • Has neuraminidase (N) and haemagglutinine (H)
  • Only reproduce within the host cell
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158
Q

What disease does Varicella Zoster Virus (VZV) cause?

A
  • Chicken pox, adaptive immunity remains but T-cells decrease with age so re-exposure in old age can cause Shingles
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159
Q

What does Shingles affect?

A

Affects nerve root ganglia and can be debilitating for elderly.

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160
Q

What is the bacterial pyramid made up of?

A
  • Obligate pathogens that are always pathogenic
  • Opportunistic pathogens that are only pathogenic when affects someone with a suppressed immune system or based on location
  • Commensals that pose no threat
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161
Q

What is a bacterial unit typically made up of?

A
  • Plasmid
  • Nucleoid
  • Fimbriae/pilli
  • Cell wall made up of proteoglycan
  • Ribosomes
  • Flagella
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162
Q

How are bacteria classified?

A
  • Gram +/-
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163
Q

What features discriminate between gram +/-?

A
  • Gram + has thick peptidoglycan wall, lipotechnoic acid and purple stain
  • Gram - has a thin peptidoglycan wall, lipopolysaccharide and pink strain.
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164
Q

What is the immune irritant for gram + and gram -?

A
  • Gram +: Septic cshock

- Gram -: Sepsis

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165
Q

What are the bacterial products that cause disease?

A
  • Toxins
  • Lipopolysaccharide structure
  • Flagella
  • Fimbriae
  • Extracellular polysaccharide
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166
Q

What feature does the Lipopolysaccharide has?

A

O- antigen which is released upon lysis and is toxic

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167
Q

What causes bacteria to move through flagella?

A

Chemotaxis

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168
Q

What does the pilli/fimbrae do?

A

Attach to host cells example in UTI attach to Ureter

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169
Q

What are the features of fungi?

A
  • Multicellular
  • Chitin cell wall
  • Contains mitochondria, golgi apparatus, ER
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170
Q

What is an ex of a fungal infection?

A

Athletes foot due to candida infection

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171
Q

What is the ideal environment for fungal infection?

A
  • Moist
  • Slightly acidic
  • Can grow with or without light
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172
Q

What are the anti-fungal drugs available

A
  • Amphotericin B

- Azole

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173
Q

Is bacteria a prokaryote or eukaryote?

A

Prokaryote

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174
Q

What are the 5 things a bacteria needs to do to cause disease?

A
  • Attach to host
  • Invade the host
  • Nutrient acquisition
  • Immune evasion
  • Cause damage
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175
Q

How does the bacteria attach to the host?

A

Fimbriae or pilli used to attach and their own uptake into pathways to allow intracellular survival rather than killing.

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176
Q

What system does the bacteria use to invade the host?

A

Type 3 secretion system to promote invasion

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177
Q

How does the bacteria acquire nutrients?

A

It consists of siderophores that can scavenge for iron from host proteins

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178
Q

How does the bacteria evade hosts immune system?

A
  • Inhibit apoptosis by inhibiting phagocytosis, antigen presentation and inappropriate T-cell activation.
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179
Q

What are the 2 ways in which bacteria can cause damage?

A
  • Direct using toxins

- Indirect via over-activation of inflammation

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180
Q

What happens in Group A streptococci and acute rheumatic fever?

A

Antibodies to streptococcal proteins cross react with heart, lung and kidney

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181
Q

What is the consequence of staphylococcus aureus toxin?

A

Toxic shock syndrome

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182
Q

What is the target of Beta lactam antibiotics?

A

Bacterial cell wall

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183
Q

Examples of beta lactam antibiotics

A

Penicillin, cephalosporin, carbapenems and monobactams

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184
Q

What site does antibiotics like tetracycline and aminoglycoside act on?

A

Bacterial ribosome

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185
Q

What is the action of penicillin on the bacterial wall?

A

Inhibits enzymes that make the crosslinks in the peptidoglycan polymer found in the bacterial cell wall

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186
Q

What initially caused the resistance to penicillin?

A

Beta lactam ring was broken by an enzyme released by the staphylococcus.

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187
Q

What is different to cause MRSA?

A

MRSA strain produced a different beta lactam target enzyme to synthesise its cell wall called penicillin binding protein 2A

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188
Q

How can MRSA be treated?

A

Using toxic and not very effective vancomycin.

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189
Q

How did Ampicillin cause resistance in E.coli?

A

Beta Lactamase TEM is transferable between different gram negative bacteria by means of plasmids. Plasmids are double stranded DNA.

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190
Q

What causes the spread of antibiotic resistance?

A
  • Existence of megacities
  • Poor public health with poor infrastructure and unclean water/poor sewage disposal
  • Extensive use of antibiotics
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191
Q

How do we combat antibiotic resistance?

A
  • Use less antibiotics
  • Antibiotic stewardship
  • Restriction and changes in animal husbandry
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192
Q

Why are viruses called obligate?

A

No metabolic activity outside the host cell as it is not alive.

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193
Q

How are viruses classified?

A

6 Classification

  • Double stranded DNA
  • Single stranded DNA
  • Double stranded RNA
    • Sense RNA v
    • Antisense RNA
  • RNA reverse transcriptase
  • DNA reverse transcribing virus
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194
Q

What is the viral life cycle?

A
  1. Entry
  2. Replicate
  3. Assemble
  4. Release
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195
Q

What is needed for virus to enter?

A

Virus requires a specific target protein

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196
Q

Where does flu virus bind to and in what species can it bind to?

A

Sialic acid. Bind to pigs, birds and humans

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197
Q

What happens during the replication stage of the virus?

A
  • Virus begins to take control of cell synthesis in order to synthesise viral components
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198
Q

What does it require to take control of the cell’s synthesis?

A
  • Essential replication factors
  • Subunits that assemble new capsids
  • Copies of viral genome
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199
Q

What are the 2 ways in which virus can be released?

A
  1. Cell lysis

2. Budding

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200
Q

What virus uses cell lysis method? How does it work?

A

Non-enveloped virus destroys the target cell and has a high replication rate

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201
Q

How does budding work?

A
  • Intracellular vesicle or surface release over an extended period of time
  • Leads to a chronic infection
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202
Q

What does tropism mean?

A

Virus infects cells by binding to a specific receptor on the surface and it is organ/species specific

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203
Q

What receptor does HIV bind to? Which cells are these receptors found on?

A

CD4 and CCR5

CD4 T-cells and macrophages

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204
Q

How is the Herpes Simplex Virus different to HIV?

A

HSV invades immune system then becomes quiescent by residing in the nucleus of the host cell and not producing any proteins. However, it produces a spectrum of microRNA’s that can act to control the host cell. It is not recognised by the immune system as protein needed for immune recognition

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Perfectly
205
Q

What are the 4 types of infection graphs? Give an example of virus for each type of infection.

A
  1. Acute infection - Rhinovirus/influenza
  2. Persistent smouldering - Lymphocytic choriomeningitis
  3. Latent, persistent - Herpes Simplex Virus
  4. Persistent, slow - HIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

Why is there always a prodormal response to a virus?

A
  • Release of an interferon response that is predictive, prescriptive and universal.
  • About 300 genes stimulated by this response
  • Causes innate system to switch on the prodormal response.
207
Q

What type of virus is Influenze?

A

Segmented RNA virus where all genomes are not in one piece

208
Q

What is the difference between positive sense RNA and negative antisense RNA?

A

Negative antisense is genetically more diverse than positive sense RNA.

209
Q

How many RNA segments does segmented RNA virus has? What do they mean?

A

7-8.
1-6 is for encoding 1 protein
7-8 2 small proteins

210
Q

What are the proteins on the viral surface? What are their function?

A
  1. Haemagglutinin - Binds to sialic acid and responsible for haemagluttination (Clumping together of red blood cells)
  2. Neuraminidase - Release of virus from host cell
211
Q

What are the strategies of flu virus to avoid host cell’s immune system over long periods of time?

A
  1. Segmented virus rapid mutation could lead to reassortment between 2 strains if they infect same cell which can lead to an antigenic shift. New strain
  2. Virus’s dominant antigents H and N change over time due to selective pressure and this changes accumulates and causes an antigenic drift.
212
Q

What are the treatments available against influenza virus?

A
  1. Anti-influenza drug: Amantadine- no longer used due to 92% resistance
  2. Vaccination
213
Q

What is an antigenic sin?

A

Immunological memory for previous infection is stimulated by a virus that is of slightly different version of that virus so inappropriate antibody response produced

214
Q

What actually kills you from a viral infection?

A

Bacterial infection as viral infection causes inflammation and promotes conditions in which bacteria can thrive in

215
Q

What type of a virus is HIV?

A

RNA reverse transcriptase

216
Q

What is special about HIV that it escapes the immune system?

A

Adaptive immune system takes about 1-2 weeks to produce antibodies however the HIV virus rapidly mutates that it has enough antigenic drift to escape the antibodies.

217
Q

What is the life cycle of a HIV virus?

A
  1. Entry and attachment to host cell
  2. RNA to DNA conversion and incorporation into host’s genome
  3. Genome replication and protein expression
  4. Assemble
  5. Release of mature virions from infected cell
218
Q

What is essential for HIV maturation?

A

Cleavage of p55 into a series of smaller proteins p24, p17, p7, p2

219
Q

What are the 3 genes that HIV encodes?

A
  1. Capsid
  2. Envelope
  3. Polymerase
220
Q

What type of Infection is HIV?

A

Persistent slow

221
Q

What does the 2 separate curves on the HIV infection graph show?

A

1st - Establishment of infection where prodormal effects seen as there are high levels of virus in the blood. Transient loss of CD4 T-cells. Neutralising antibodies and CD8 T-cells reduce this to a set point where viral load is more stable.
2nd - Higher viral loads and a slow decline in CD4 T-cells and patient becomes increasingly immunodeficient

222
Q

What are the 3 current treatments available for HIV?

A
  1. Reverse transcriptase inhibitor - Nucleoside, non-nucleoside
  2. Protease inhibitors
  3. Highly Active Anti-Retroviral Therapy (HAART)
223
Q

What type of virus is Herpes Simplex Virus?

A

Double stranded DNA virus

224
Q

What cells does Herpes Simplex Virus pre-dominantly affect?

A

Cytotoxic CD8 T-cell and CD4 T-cell

225
Q

What is the only Herpes vaccine available?

A

HHV3- Varicella Zoster Virus

226
Q

What are the 5 types of Herpes human virus?

A

HHV1,2 - Produce cold sores/genital sores
HHV3 - Itchy rash of spots which turn into fluid-filled blisters
HHV1,2,3 - Same group because have reactivate periodically and infect neurons
HHV4 - Epstein Barr virus
HHV5 - Cytomegalovirus

227
Q

What are the effects of EBV? which cells does it effect?

A

B-cells and give mild form of lymphoma. Usually T-cells kill these transformed B-cells so more prevalent in someone lacking T-cells
Childhood - Asymptomatic
Puberty - Glandular fever, infect epithelial cells of the back of the throat from which it can be shed via saliva.

228
Q

Describe the effects of cytomegalovirus and which cells they affect?

A

Affect a diverse number of cells - Lung, liver, endothelium, myeloid cells.

  • Need CD4/CD8 T-cell to counteract it.
  • When T-cell fail due to extreme age, immunosuppressive infection, transplantation
  • Patients can obtain varies viral disease: Hepatitis, phenumonitis, retinitis, colitis
229
Q

What are the 3 types of barriers?

A
  • Mechanical
  • Chemical
  • Microbiological - Normal flora
230
Q

What defect in barrier immunity can result in an increased susceptibility to infection

A
  • Cystic fibrosis
  • Asthma
  • Congenital defects of cilia
231
Q

What are the consequences of lung infections?

A
  • Scarring
  • Dilatation
  • Distortion of bronchi
232
Q

What factors form the mechanical barrier?

A
  1. Constant flow - Stagnant flow promotes infection liking environment
  2. Cilia - Sweeps away trapped particle
  3. Epithelial cells form tight junctions
233
Q

What factors form the chemical barrier?

A
  1. Mucous
  2. Acidic environment
  3. Enzymes
  4. Bile acid
234
Q

What factors form the microbiological barrier?

A

Commensal bacterial that prevents invasion of pathogenic bacteria

235
Q

What causes a loss of normal flora?

A
  1. Antibiotics

2. Excessive use of antiseptic solutions

236
Q

What is the function of a dendritic cell?

A

Take up pathogen and express antigen to T-cells.

237
Q

How does Langerhan cells function?

A

If there is a local tissue injury, langerhan cells found on the surface of the skin take up antigen via pinocytosis. Recognise antigen via PAMPS-PRR. Engulf via phagocytosis.

238
Q

What are the 2 class of cells involved in phagocytosis?

A
  1. Monocytes/macrophages - Slow replicating bacteria

2. Neutrophil - Most important. Eosinophil - Parasitic infection. Basophil - Least important

239
Q

Where are macrophages found?

A
  1. Tissue surface
  2. Serous cavities
  3. Sinusoidal: Kupffer cells
  4. Spleen
240
Q

Where are mast cells found?

A

Lies in all the tissues

241
Q

What is the action of mast cells?

A

When there is a tissue damage, release chemical mediators such as histamine, Kallikrein which activates bradykinin, tryptase, heparin and then can lead to vasodilation of blood vessels.

242
Q

What is the function of NK cells?

A
  • Not antigen specific but will kill all cells that do not express MHC molecules such as virus infected and tumour cells.
243
Q

What occurs in a TLR mechanism?

A

Toll-like receptor binds to PAMS which uses Myd88, IRAK and TRAF to trigger a cascade signal within the cell and activates genes in nuclei to upregulate inflammatory cytokines

244
Q

What will happen if there is a genetic defect in IRAK or Myd88?

A

No innate response because cascade not activated and cannot upregulate inflammatory cytokines. So recurrent infection wth no prodormal effects seen.

245
Q

What are the 3 pathways in which complement can be activated?

A
  1. Classical pathway - Antibody present from previous infection binds to antigen and activates complement.
  2. Alternative - PAMP binds to PRR and surface of the bacteria contains C3 convertase which converts soluble C3 into insoluble C3b and C3a. C3b opsonises the pathogen.C3a activates mast cells degranulation.
  3. Lectin Binding pathway - C3b binds to macrophage which releases IL-1B, IL-6 and TNFa. Act on liver to produce CRP (acute phase proteins). CRP Mannose binding lectin are TLR that can detect bacterial cell wall components and their interaction causes an amplified effect of alternative pathway
246
Q

What is the function of complement?

A
  1. C3b causes opsonisation of pathogen
  2. C3a causes mast cell degranulation
  3. C5/ C3b bind to macrophage releases IL-8 which causes neutrophil chemotaxis
  4. C5 activates C5-9 activates MAC which is a pore that causes cell lysis.
247
Q

What complement tests are usually done?

A
  • C3
  • C4
  • C1esterase inhibitor
248
Q

What is the hereditary cause of low C4?

A

Hereditary angiodema - C1 esterase inhibitor blocks C1 and initiates bradykinin pathway which increases intravascular permeability and causes swelling.

249
Q

What effects seen if no C4 present?

A

Recurrent infection of encapsulated bacteria such as pneumococcus.

250
Q

What is the acquired cause of low C4?

A

Complex diseases

  • Lupus
  • ANCA postive vasculitis
  • Cryoglobulinaemia
  • Rheumatoid vasculitis
251
Q

What are the causes of inherited C3 deficiency?

A

C3, Factor H, I deficiency

252
Q

What happens to someone with a C3 deficiency?

A

Neisseria meningitides meningitis

253
Q

What is the acquired cause of C3 deficiency?

A
  • Post streptococcal glomerulonephritis
254
Q

What is the life course of neutrophils in the absence of an infection?

A

Circulate around the blood for 12-16 hours and then they are removed by macrophage in the liver, spleen and bone marrow.

255
Q

What happens to neutrophils when an infection is present?

A

Rapidly released in or to phagocytose and kill invading bacterial and fungal pathogens

256
Q

What happens to neutrophil levels of patients who are undergoing cancer treatment? How are they protected from infection?

A

Neutropenia. Given prophylactic antibiotic and measures to avoid exposure to infection is taken. There is no point giving neutrophils via transfusion because their life span is less than 48 hours.

257
Q

What are the steps towards transendothelial neutrophil migration?

A
  1. Rolling - Carbohydrate chain on neutrophil binds to the selectin on the activated endothelium. Not strongly bound so rolling occurs.
  2. Triggering - IL8 receptor on neutrophil binds to IL-8 on the activated endothelium which activates integrin.
  3. Firm Adhesion - Integrin binds to ICAM on the activated endothelial surface to form a firm adhesion and shape of neutrophil can change.
  4. Extravasation of neutrophil and once in the tissue it will follow IL-8 chemotaxis to reach the site of injury
258
Q

What is the function of Fc receptors on neutrophils?

A

Fc receptors are receptors for immunoglobulin. It allows them to bind and phagocytose pathogens that have been opsonised in specific antibodies in affected tissues.

259
Q

How is complement activated in a primary infection? How is this different in a secondary infection?

A

Primary - Rely on complement receptors whereas in secondary can use classical pathway and Fc receptors.

260
Q

What are the phagocyte killing mechanisms?

A
  1. Toxic reactive oxygen such as superoxide anions, hydrogen peroxide, nitrogen oxide
  2. Nitrogen species
  3. Exposure to granule contents which contain antimicrobial mediators.
261
Q

How is a superoxide generated?

A
  • Generated by a multi component membrane associated enzyme called phagocyte oxidase.
  • Transient increase in oxygen consumption: Respiratory burst
262
Q

What are the 2 ways in which neutrophils can die?

A

Apoptosis or necrosis

263
Q

How does neutrophil apoptosis occur?

A

Apoptotic ligands on surface of neutrophils bind to apoptotic receptors on macrophage. Macrophage enguld the neutrophils and safely dispose their toxic products within the macrophage so no inflammatory response.

264
Q

How does neutrophil necrosis occur?

A

When there is an overwhelming pathogen in immune system, very large number of neutrophils present so macrophage cannot be used to kill all the neutrophils so they lyse and release their toxic substances into the environment causing further damage. Could lead to pus and abscess formation

265
Q

What are the visual characteristics of an inflammation? What causes them?

A
  1. Swelling- Increased vascular permeability
  2. Redness - Vasodilation
  3. Heat - Cytokines
  4. Pain- Mediators such as histamine
266
Q

What are the characteristics of an innate immune defence?

A
  • Fast response
  • No memory
  • Low specificity
  • Generic response
  • PAMP recognised by PRR
267
Q

What cells are responsible for recognising threat?

A
  1. Monocytes/macrophages
  2. Dendritic cells
  3. Mast cells- Sentinels
268
Q

What cells are responsible for killing?

A
  1. Phagocytes: Neutrophils and macrophages

2. Granucocytes

269
Q

What are the proteins of the innate system? Functions for each protein

A
  1. Acute phase proteins needed for opsonisation or presenting pathogens. CRP
  2. Cytokines needed for chemotaxis or modulating cell activity
  3. Complement needed for opsonisation, neutrophil chemotaxis, MAC, mast cell degranulation
270
Q

What are the examples if acute phase cytokines?

A

IL- 1, IL-6, TNFa

271
Q

What is anti-TNFa used for?

A

Inflammatory bowel disease and rheumatoid arthritis

272
Q

What are anti-IL1/6 drugs used for?

A

Rheumatoid arthritis

273
Q

What happens when there is an overproduction of TNFalpha and IL-1?

A

Can cause septic. Increased amounts produced when infection cannot be cleared, massive vasodilation, drops blood pressure, increase heart rate, inadequate oxygen supply to tissue resulting in necrosis and multi-organ failure.

274
Q

What are the outcomes of an acute inflammation?

A
  • Complete healing
  • Scar formation
  • Abscess
  • Granuloma
  • Chronic inflammation
275
Q

When does chronic inflammation occur?

A

Acute phase cannot be resolved due to persistent injury/infection, prolonged toxic agent exposure, autoimmune disease.

276
Q

What are the effects of chronic inflammation?

A
  • Tissue destruction by inflammatory cells
  • Cellular infiltration granulomas
  • Attempts to repair results in fibrosis and angiogenesis.
277
Q

What are the anti-inflammatory cytokines?

A

TNF-Beta and IL-10

278
Q

What is the function of CRP?

A
  • Pathogen recognition molecule

- Opsonises pathogens and activates classical complement cascade.

279
Q

What is ESR?

A

Rate at which erythrocytes settle out of unclotted blood in one hour.

280
Q

Is the normal ESR low or high?

A

Low because red blood cells are negatively charged so repel against one another.

281
Q

What happens in the presence of acute phase proteins?

A

Red blood cells lose their negative charge so there is an increased agglutination leading to increased ESR.

282
Q

What are the characteristics of an adaptive immune system?

A
  • Highly specific recognition towards different pathogen

- Memory response build

283
Q

What are antigens?

A

Molecules that induce an immune response through the activation of antigen specific lymphocytes.

284
Q

What are the 3 groups of molecules that work together to recognise an antigen for the adaptive immune system?

A
  • MHC
  • T cells
  • B cells
285
Q

How do B and T cell achieve specificity? How does B cell goes one step further?

A

Both have gene rearrangement but B cells also undergo hypermutation.

286
Q

What type of molecules do T-cells recognise? How is that done?

A

Short peptide sequences from antigen and not whole antigen. Antigen presenting cells need to take up and process antigen and present on surface through MHC molecules it to T-cells

287
Q

What type of molecules do B cells recognise?

A

Whole antigen through their B cell receptor

288
Q

What do terminally differentiated B-cells produce?

A

Antibodies/Immunoglobulin.

289
Q

Can B cells present antigens to T-cells?

A

Yes very effectively

290
Q

What is the difference between MHC I/II

A

MHC I recognises endogenous proteins whereas MHC II recognise exogenous protein.

291
Q

Where are MHC I cells found?

A

All cells except neurones

292
Q

Where is the MHC molecule produced and name the 2 chaperone proteins? Why are these proteins needed

A

Ribosomes. Calnexin and Calreticulin. MHC molecules are unstable before it has bound protein.

293
Q

Explain the process of MHC 1 and T-cell interaction.

A
  • Endogenous protein broken down by proteosome. Some amino acids recycled but longer peptides ender the ER via TAP protein.
  • Endogenous protein loaded onto MHC I.
  • CD8 cytotoxic T-cell specific to the antigen interacts with the MHC I on infected cell surface.
  • Induces cell apoptosis
  • Macrophage consumes the cell later.
294
Q

What protein retains a pool of MHC I in the ER? Why is this necessary?

A

Tapasin. Needed to cause a rapid increase in surface peptide/MHC complex following a peptide binding.

295
Q

What cells express MHC II?

A

Antigen presenting cells - Dendritic cells, B cells, Macrophages/monocytes

296
Q

Explain the process of MHC II and T-cell activation

A
  1. APC uptake of exogenous protein, phagocytose into smaller peptide molecules.
  2. Comes into contact with MHC II peptide binds to it.
  3. When in contact with antigen specific CD4 T-cell, t-cell becomes activated
  4. Cytokine environment polarizes T-cell to become a specific effector cell
  5. Activates T helper cell
  6. Activates B cell
297
Q

What is the downside of MHC polymorphism?

A

Histocompatibility match needed during transplant

298
Q

What constitutes a typical immunoglobulin molecule?

A
  • Heavy and light chain formed by disulphide bond

- Hinge region

299
Q

What enzyme can digest the hinge region? What is the yield?

A

Papain. 2 Fab and 1 Fc region

300
Q

What is the function of Fab and Fc?

A

Fab- Antigen binding sites

Fc- Antigen-Antibody complex formation

301
Q

What is the need for signalling molecules such as CD19 in B-cells?

A

Short cytoplasmic tail so accessory molecule needed to relay signal from the outside to the inside of the cell when antigen is bound.

302
Q

Where is the variable region concentrated on the immunoglobulin?

A

Antigen binding site- Complement Determining Region

303
Q

What are the constant domains for light and heavy chain?

A
  1. Light chain - kappa/Lambda

2. Heavy chain - IgM,IgG, IgA, IgE, IgD

304
Q

Describe a T-cell receptor

A
  • 2 non identical Ig polypeptide chains
  • Either be Alpha+ Beta or Gamma+Delta
  • Linked by disulphide bond
  • Has constant and variable regions
  • CD3 signalling molecule
  • Most peripheral alpha+beta T-cells have CD4/8 wither their T-cell receptor
305
Q

What is the process of gene rearrangement to produce more specific antibodies and T-cell receptors?

A

Somatic recombination

306
Q

What are the 2 enzymes needed for somatic recombination?

A

RAG 1/2

307
Q

What condition will one have if they have no RAG1/2 enzymes?

A

SCID - No B/T cells

Need bone marrow transplantation

308
Q

What is the difference in gene rearrangement between heavy and light chain?

A

Heavy - VDJ regions

Light - VJ

309
Q

How does somatic recombination occur?

A
  1. Combine DJ segment to heavy chain
  2. Add V segment to DJ for heavy chain.
  3. Once mRNA for V/C segments synthesised, they are spliced and translated.
  4. Similar process occurs for light chain but only containing V/J segments for the variable regions.
310
Q

How can one add additional diversity to somatic recombination? Is there anything different with an immunoglobulin?

A
  • Terminal deoxynucleotidyl transferase (TdT)- Add nucleotides to the junctional site
  • Ig also uses somatic hypermutation
311
Q

Are genes on both chromosomes used during somatic recombination?

A

No prevented by a process of alleic exclusion so every cell only expresses heavy and light chains from one parental chromosome.

312
Q

What are the classes and subclasses of Ig?

A

4-IgG, 2-IgA, IgD, IgE, IgM

313
Q

Can one antibody have both kappa and lambda light chain?

A

No only has one type of light chain.

314
Q

What is the structure of IgM? Function? Problem?

A

Pentameric so stable molecule as it has 10 identical epitopes and only loses binding when all 10 fail. Too large to cross the placenta

315
Q

Describe the structure of IgA and function.

A
  1. Produced by plasma cells as a dimer
  2. Attach to poly Ig on basal surface of epithelial cells
  3. Transported to the apical surface and receptor is cleaved to release IgA dimer via transcytosis.
316
Q

What is the structure of IgD?

A

Expressed as a transmembrane receptor molecule on the surface of mature lymphocytes

317
Q

What are the function of the antibodies?

A
  1. Antibody Dependent Cell mediated Cytotoxicity (ADCC)
  2. Complement activation
  3. Direct cell activation by Fc receptors
  4. Neutralisation
  5. Opsonisation
  6. Precipitation
318
Q

How does opsonisation occur?

A
  • Antigen binds to antibody which causes opsonisation as antigen is marked
  • Easier for phagocyte to identify and initiate phagocytosis
  • Activates C3b/C4b
319
Q

How does neutralisation occur?

A
  • Antibody binds to antigen to prevent antigen bind to receptor on the cell that could allow toxins, viruses and bacteria to gain access.
  • Antibody can also neutralise virus by binding to their envelope proteins that allow docking and entry into their putative host cell.
320
Q

How does antibody cause precipitation?

A
  • Antigen molecule interacts with several Ig molecules to form an immune complex.
  • If it is a large protein with different epitopes, many Ig specific are produced and they form a large complex with multivalent antigens which can result in a precipitation or agglutination
  • Fc receptor directs phagocytosis
321
Q

How is complement activated?

A

1 IgM or 2 IgG molecules activate C3b, C5a, C3a, MAC

322
Q

How direct cellular activation occurs? Give an example

A

Fc receptor has the ability to trigger specific functions. In IgE, Fc receptor triggers mast cell degranulation through FcEr1 (E- epsilon) in allergic reactions.

323
Q

How does Antibody Dependent Cell mediated Cytotoxicity occurs? What is the need to ADCC?

A
  1. Antibody binds to antigen creates an opsonisation which then activates the effector cell to lyse the target cell.
  2. Fc receptor of antibody recognised by Fc of effector cell such as NK cells that release interferon which then recruits phagocytes and cytotoxic granules containing granzymes and perforin.
  3. Apoptosis of cell occurs.
    ADCC important to contain infected or mutated cells
324
Q

How are monoclonal antibodies produced?

A
  1. Antibody secreting cell is fused with an immortal cell such as a myeloma cell.
  2. Transferred to a medium to proliferate
  3. Hybridomas that secrete antibodies are selected and cloned.
325
Q

What is tolerance?

A

Process of neutralising or eliminating self-reactive lymphocytes

326
Q

Where does central tolerance take place?

A

B-cells: Bone marrow

T-cells: Thymus

327
Q

When is thymus at its largest? What happens throughout adulthood?

A

Most active and largest during neonatal to adolescence. From then onwards, the size of thymus shrinks and replaced with adipose tissue.

328
Q

Where does T-cell development occur?

A

Precursor T-cell leave the bone marrow and enter the thymus where T-cells mature.

329
Q

What cells can be found in the thymus?

A
  1. Thymic stromal cells
    - Cortical epithelial
    - Medullary epithelial
    - Dendritic cells
  2. Thymocytes
330
Q

Which layer of the thymus are the immature and mature thermocytes present in?

A

Immature - Cortex

Mature- Medulla

331
Q

How are T-cell receptors generated?

A

Somatic recombination (Heavy DJ then VDJ, mRNA splicing translation for V/C same for light VJ) RAG1/2. Tdt

332
Q

Where does positive selection of T-cells occur?

A

Cortex. If MHC recognised, then positively selected, if not then death by neglect. If MHC II expressed, they lose CD8 and vice versa for MHC I.

333
Q

What is present in the boundary of the cortex and medulla?

A

Macrophage to prevent damaged or dying cells to enter the medulla.

334
Q

What happens in the medulla of the thymus?

A

Presence of the AIRE gene which exposes maturing thymocytes to organ specific genes prior to its release into the circulation. If thymocytes bind too strongly to the MHC molecule, apoptosis is induced due to negative selection. This is mediated by dendritic cells.

335
Q

What are the strategies for peripheral tolerance for T cells?

A
  1. Ignorance (Immune privilege) - Ex: Eye and testes
    - Suppression of immune responses by cytokines
    - Active deletion of reactive cells
    - Programmed cell death by apoptosis- Phagocytic clearance so no expression of fragments of apoptotic cells on MHC molecules and they are invisible to the immune system
  2. Treg- Suppresses self-reacting T cells from causing damage. TF: FoxP3.
  3. Inappropriate antigen presentation: Although self antigen are recognised by the T-cell receptor but no danger signals such as costimulatory factor and cytokines received so T cell cannot be activated into an effector cell. If there is an infection at the same time, chances of autoimmunity is higher cause there is a permanent danger signal.
  4. Capacity of T-cells to regulate themselves. CD28 postive acceleration and CTLA4 provides a brake.
336
Q

How is B-cell tolerance developed?

A
  1. Released from bone marrow, if exposed to antigen and they react to it before reaching secondary lymphoid organs- They will either be deleted or inactivated
337
Q

What is the major source of B-cell tolerance?

A

Lack of T-cell help as they are needed for somatic hypermutation to occur where a specific high affinity antibody is released.

338
Q

What are the genetic cause problems with thymus?

A
  • DiGeorge Syndrome

- FoxN1 deficiency in Man

339
Q

What is the natural cause of problems with thymus?

A

Old age due to thymus atrophy

340
Q

What happens if there is a FoxP3 deficiency in man?

A

Treg deficiency, autoimmunity, IPEX

341
Q

What happens if there is an AIRE deficiency in man?

A

APECED, autoimmunity

342
Q

What are the subtypes of CD4 T-cell?

A
  • Th1
  • Th2
  • Th17
  • Tfh
  • Treg
343
Q

What are the functions of primary, secondary and third signal when peptide/MHC complex binds to T-cell Receptor?

A

Primary - Binding of T-cell receptor to MHC/Peptide complex with good affinity
Secondary - Co-stimulatory molecules for T-cell proliferation (CD28)
Tertiary- Cytokines secreted by dendritic cell and local microenvironment directs T-cell differentiation by upregulating a specific and lineage defining transcription factor.

344
Q

How do cytotoxic CD8 T-cells function to kill the pathogen?

A
  • Release granzyme and perforin to punch holes and digest the target cell.
  • FasL/Fas apoptotic signal pathways to kill susceptible Fas expressing target cells.
345
Q

What is the TF of Th 1?

A

T-bet

346
Q

What cytokines trigger Th1 differentiation?

A

IL-12 and amplified by IFN-gamma

347
Q

What does Th1 do?

A

Secrete IFN-gamma

348
Q

What is the function of IFN-gamma?

A

Activate macrophage

349
Q

What is the result of an activated macrophage?

A
  1. Increase co-stimulatory expression
  2. Maturation of phagolysosome
  3. Upregulation of MHC
  4. Nitric oxide production
350
Q

What is the cytokine for Th2 differentiation?

A

IL-4

351
Q

What is the TF for Th2?

A

GATA-3

352
Q

What is released by Th2?

A

IL-4,5,13

353
Q

What is the function of Th2?

A

Immunity against parasitic (Helminth) infections

354
Q

What is the function of the IL-4,5,13?

A
  • Promotes class switching to IgE

- Alternative macrophage differentiation programme compared to Th1

355
Q

What causes allergic diseases?

A

Imbalance between Th1: Th2

356
Q

What cytokines needed to differentiate into Th17?

A

IL-1B, IL-6, TGF-B.

357
Q

What is the TF for Th17?

A

RORyt

358
Q

What is the function of Th17?

A

Releases IL-17 needed to increase neutrophil, recruitment, protect against bacteria and fungi, control barrier function of epithelium

359
Q

What happens when RORyt cannot be produced?

A

HyperIgE syndrome as there is a switch from Th17 to Th2.

360
Q

What are the symptoms of HyperIgE syndrome?

A
  • Cold funny abscesses

- Eczema like rashes

361
Q

What diseases have an association with Th17?

A

Inflammatory bowel and autoimmune such as psoriasis and multiple sclerosis

362
Q

What is the function of Tfh?

A

Expresses CXCR5 which allow migration towards B-cell areas to enable somatic hypermutation of B-cell

363
Q

What is TF for Tfh?

A

Bcl-6

364
Q

What is the TF for Treg?

A

FoxP3

365
Q

What disease is caused due to Treg deficiency?

A

I: Immune dysfunction
P: Polyendocrinopathy
E: Enteropathy
X: X-linked

366
Q

What are the main secondary lymphoid organs?

A
  • Spleen

- Lymph node

367
Q

Can maternal lymphocytes cross the foetal circulation?

A

No they are barred as foetus could have paternal HLA

368
Q

What are the 2 regions in the spleen?

A

Red and white pulp

369
Q

What is the function of the red pulp?

A

Sinusoids lined with macrophages with slow flowing blood. Using phagocytosis, bacteria, fungi and parasite are engulfed

370
Q

When is the red pulp more effective?

A

Pathogen is opsonised

371
Q

What is the function of the white pulp?

A

Region where B and T cells collaborate to produce high affinity antibodies

372
Q

What happens to the antibodies produced in the white pulp?

A

They enter the red pulp to opsonise the bacteria so that they are attract phagocytes

373
Q

What is the downside of antibodies produced in the spleen?

A

Autoantibodies against red blood cells and platelets can be produced leading to anaemia and thrombocytopenia

374
Q

What is the treatment for autoantibodies produced causing anaemia and thrombocytopenia?

A

Splenectomy

375
Q

What is the problem with splenectomy?

A

Higher risk of Streptococcal infection

376
Q

What are the measures taken after a splenectomy

A
  • Vaccination

- Antibiotics for prophylaxis

377
Q

Describe the primary antibody response

A
  • T-cells are primed when they interact with antigen presenting cells that have taken up and processed pathogen and loaded onto MHC II.
  • B-cells bind foreign proteins on their receptor. They tend travel towards primed T-cells in the secondary lymphoid organs via afferent lymph.
  • If T-cell is specific to the antigen on the B-cells then it will offer help for B-cells to proliferate and differentiate into plasma cells that will secrete antibodies.
  • If antibodies are of low affinity, it will be phagocytosed by macrophages in the red pulp of spleen or medulla of the lymph node.
  • If T-cell is not specific to foreign particle and no help offered, B-cell enters efferent lymph to re-enter circulation.
378
Q

What gene is needed for lymph node organisation?

A

Lymphotoxin Beta Receptor Gene (LTBR)

379
Q

What is the function of the AID gene?

A
  1. Somatic hypermutation of B-cells

2. Class switching from IgM or IgD to IgG,A/E

380
Q

What is the difference between follicular dendritic cell and T zone dendritic cell?

A

Follicular dendritic cell traps antigen whereas T-zone dendritic cell takes up and processes antigen into peptide

381
Q

What happens to antibodies produced from somatic hypermutation that are same/have less affinity?

A

Apoptotic via FasL/Fas system then engulfed and cleared by macrophages.

382
Q

What happens to antibodies that have high affinity?

A

Bind to either Tfh or FDC and then differentiates to form either a memory or plasma cell. It also undergoes class switching

383
Q

Which region of the lymph node does somatic hypermutation occur?

A

Dark zone of the germinal centre

384
Q

Where does IgA function at?

A

Mucosal surfaces against invading pathogens

385
Q

What is one at risk of if IgA deficient?

A

Increased risk of autoimmune and inflammatoy gut

386
Q

What is the most important immunoglobulin? Why?

A

IgG. Focuses on dominant antigens on the surface of the pathogens

387
Q

What is the problem encountered by IgG due to focusing on dominant antigens?

A

Pathogens may change their surface coat and become invisible to the immune system.

388
Q

What are the characteristics of IgG?

A
  • Small
  • High affinity and specificity
  • Longer half life because recycled after phagocytosis
  • Can be transferred across placenta
389
Q

What happens if a previous infection occurs again?

A
  • Memory T and B cells present and react quickly
  • Produce primed T-cells rapidly
  • Produce IgG and IgA rapidly as well
  • CD4 T-cells and B cells collaborate to coordinate T-cell dependent antibody responses that overwhelm the intruder.
390
Q

What happens to an individual with OXO40 deficiency?

A

No memory cells developed

391
Q

What is a cause of hyposplenism?

A

Sickle Cell anaemia because of recurrent splenic infarction

392
Q

What are the natural antibodies?

A

IgM production antigen indepenent, not undergone somatic hypermutation and no class switching

393
Q

What is the importance of natural antibodies?

A

Providing resistance to common pathogen in the first 48 hours of infection as they are variable and not specific.

394
Q

What B-cells produce natural antibodies? Where are they found?

A

B1 cells. Found in peritoneal and pleural cavities

395
Q

B1 cells derived from common lineage of macrophage. How can this be proven?

A

B1 cells still help macrophages by promoting opsonisation in phagocytes

396
Q

What are TI-1 antibodies?

A
  • Evoked by components of bacterial or viral cell wall that co-operate with either complement of BCR
  • Low affinity but fast
397
Q

What are TI-2 antibodies?

A

Encapsulate bacteria evades the immune system but breaks down into bits of polysaccharide which can conjugate to proteins to generate peptides that evoke T cell help for B-cells specific to that.

398
Q

What causes the prodromal effects?

A

Interferons released by the innate system which can only be signalled via a limited repertoire of intracellular protein such as Myd88, TRIF, TIRAP, TRAM which then activate about 300 Interferon Stimulated Gene.

399
Q

What does the antiviral response stimulated by the Interferon Stimulated Gene do?

A
  • Limit growth of pathogen

- Clear infection without the help of adaptive immunity

400
Q

What is the interferon bystander effect?

A
  • Interferons signal through Myd88, TRAM, TIRAP, TRIF intracellularly
  • Stimulates gene expression
  • Production of more interferons which can bind to the receptor of the surface of the cell and the cells surrounding it
  • This will put those cells into an anti-viral state.
401
Q

Which MHC pathways do viruses use?

A

MHC 1

402
Q

What is the importance of NK cells in viral infection?

A

Viruses shown to inhibit peptide presentation by down modulating MHC 1. This activates NK cell.

403
Q

What are the ways viral infection activates NK cell?

A
  1. Release of interferon gamma which stimulates ISG’s which render cells less susceptible to infection
  2. Cytolytic granules released to target MHC 1 null cell for destruction and death receptor mediated cytolysis
  3. Respond to variety of stress proteins produced by infected cells
  4. Migrate along IL-12 gradient towards infected cells responding to PAMP.
404
Q

How does CD8 T-cells kill infected cells?

A
  1. Granzyme and perforin

2. FasL/Fas death receptor apoptosis

405
Q

How does Antibody Directed Cell Cytotoxicity(ADCC) occurs in NK cells?

A
  • NK cells have Fc portion (FcyRIII) which bind to Fc on the IgG bound on the surface of the infected cell
  • This then activates NK cell to kill the cell.
406
Q

What function of antibodies are most capable of killing a viral infection?

A

Antibodies against surface proteins/neutralisation

407
Q

What happens in the case of dengue when ADCC goes wrong?

A
  • On first exposure, dengue replicates in dendritic cell and stimulates prodromal response
  • Neutralising antibodies for that serotype of dengue is produced
  • On the second exposure, non-neutralising antibodies Fc used to bind to FcyRIII on the NK cell
  • This enables enhanced viral delivery to target cells
  • They attain a Dengue Haemorrhagic Fever which has a high mortality.
408
Q

What is autoimmunity?

A

Failure of self-tolerance

409
Q

How is central tolerance maintained for T and B cell?

A

T-cell : positive and negative selection in the thymus

B-cell: If respond to antigen in the circulation while going towards secondary lymphoid organs, apoptosis occurs

410
Q

How is peripheral tolerance maintained for T and B cell?

A 
T-Cell
- Anergy
- Ignorance
- Treg
B-cell
- Lack of T cell help in order to secrete high affinity antibodies
411
Q

Why does the eye, testes and brain have an immune privilege?

A

To prevent scarring

412
Q

What happens when there is a penetrating injury to the eye?

A

Immune system becomes aware of the previously hidden antigen. Can lead to sympathetic opthalmia where a contralateral eye that was not affected involved in severe immune response which can lead to total blindness

413
Q

What is the treatment for sympathetic opthalmia?

A

Steroid, Immunosuppressants

414
Q

How does cell anergy or death occurs?

A

When there is a peptide bound to the APC but no co-stimulatory or cytokines released to activate T-cell completely so response does not occur and cell dies

415
Q

What if the body has an infection and a self peptide is presented?

A

Co-stimulatory and cytokines received as danger signals present so T-cell activated

416
Q

What happens to Treg in patients with rheumatoid arthritis?

A

Levels are normal but function is impaired so does not suppress antibodies against self peptide

417
Q

In what 5 ways does T-cell intolerance cause disease? Give a disease example for each.

A
  1. Opsonisation - Haemolytic anaemia
  2. Immune complexes - Glomerulonephritis
  3. Complement dependent lysis - Paroxysmal Cold Haematuria
  4. Receptor blockade - Myasthaenia Gravis, Pernicious Anaemia
  5. Receptor stimulation- Grave’s disease
418
Q

What is Hashimoto’s?

A
  • Autoimmune condition producing antibodies against TSH

- Low T3/T4 levels

419
Q

What is Grave’s disease?

A
  • Antibodies that stimulate increase of thyroid stimulating immunoglobulin which mimics TSH to increase thyroid levels
420
Q

What is Goodpasture’s syndrome?

A

Type IV collagen antibodies against the capillary basement membrane of the Glomerulus/lung alveoli

  • Destruction of these structures
  • Can lead to haemophysis/haematuria
421
Q

What is the antibody in RA?

A

Rheumatoid factor: Antibodies against Fc receptor of IgG

Anti-Cyclic Citrullinated Peptide (Anti-CCP)

422
Q

What are the characteristics of an ideal vaccine?

A
  1. Safe
  2. High efficacy
  3. Cost-effective
  4. Stable so can be used in extreme climate
  5. Easy to administer
  6. Long term protection
423
Q

What are the different types of vaccination and give examples?

A
  1. Whole vaccine
    - Attenuated: VZV, MMR, BCG, yellow fever
    - Dead: Pertussis, Rabies
  2. Subunit of microorganism
    - Polysaccaride: Pneumococcus, meningococcus
    - Inactivated toxin: Diptheria toxoid, tetanus
    - Recombinant protein: HPV, Hep B
    - Conjugated vaccine polysaccharide+inactivated toxin
424
Q

How does a conjugate vaccine work?

A
  1. Polysaccharide+Inactivated toxin
  2. B-cell specific for capsular polysaccharide binds the conjugate vaccine with its surface Ig.
  3. Complex is pinocytosed then fused with antigen presenting endosome.
  4. Diphteria toxoid processed into peptide that is presented to T-cell.
  5. T-cell offers help to B-cell which enables B-cell to produce specific antibodies against capsuled polysaccharide
425
Q

What are adjuvants?

A

Substance that enhances the immunogenicity of substances mixed with it

426
Q

What adjuvants are used in vaccines?

A
  1. Soluble antigen converted into particulate matter: Alum
  2. Oil in water+dead myobacteria
  3. Toll receptor agonists: Tumour vaccination
427
Q

How can flu vaccine cause anaphylaxis?

A

Ovalbumin (egg) present in flu vaccination as viral vaccines are created within hen eggs. People who are allergic to eggs could have anaphylaxis.

428
Q

What factors affect herd immunity?

A
  • Coverage rates
  • Susceptibility
  • Vaccine effectiveness
  • Force of transmission
  • Crowding
  • Nasopharyngeal carriage
429
Q

What is passive immunity treatment?

A

Transferring pre-formed antibodies into a person who does not need to produce these elements themselves and are protected immediately

430
Q

When are passive immunity used?

A
  • Maternal IgG transfer to foetal blood to protect foetus in the first 6 months after birth
  • Individuals without B cells- immunoglobulin administered intravenously
  • Provide protection against specific microbes in patients with immunodeficiency or particular risk
431
Q

Where can bacteria be found intracellularly?

A
  • Cytoplasm

- Vacuole

432
Q

What are the advantages of intracellular bacterial?

A
  • Obtain nutrients supply continuously

- Protected from the extracellular microcide

433
Q

What is the disadvantage of intracellular bacteria?

A

Need to evade the innate immune system’s killing phagocytically.

434
Q

In what ways can intracellular microbial pathogens be killed?

A
  • Reactive oxygen species
  • Nitric oxide toxic
  • Enzymes: Lysozyme breaks down the wall of gram + bacteria
  • pH: Acidic pH.
  • Antimicrobial peptides
  • Competitors such as Lactoferrin or B12.
435
Q

Give an example of a bacteria that resides in a restricted vacuole.

A

Myobacterium tuberculosis

436
Q

How is the bacteria in a restricted vacuole killed?

A
  • Bacteria though resides in the vacuole still releases metabolic and surface proteins which traffic to the lysosome to be degraded.
  • Loaded onto MHC II
  • When in contact with CD4+ T-cell, T-cell receptor binds to antigen, CD40 co-stimulator received and IL-12 cytokine released which differentiates T-cell into a Th1.
  • Th1 releases IFNy which activates macrophage which then upregulates MHC, nitric oxide,co-stimulatory cytokines and promote phagocytosis,
437
Q

Give an example of bacteria that resides in the cytoplasm.

A

L.monocytogenes

438
Q

How is the bacteria in the cytoplasm killed?

A
  • Proteosomes degrade proteins in the cytoplasm.
  • Enters ER via TAP protein
  • Loaded onto MHC I.
  • Recognised by specific CD8 T-cell
  • Death either via granzyme+perforin/ FasL/Fas induced apoptosis.
439
Q

What gram bacteria is myobacterium tuberculosis?

A

Gram positive

440
Q

What gives myobacterium tuberculosis the advantage?

A

Complex lipid cell envelope

441
Q

What are the advantages of a complex lipid cell envelope?

A
  • Longevity
  • Drug permeability
  • Host response modulation
  • Pathogenesis: Tissue damage
442
Q

Why are granulomas form in TB?

A

As a final attempt to wall off the chronic irritant

443
Q

What layers make up the granuloma of TB?

A
  1. Layer of T-cells both CD4/8
  2. Layer of fibrolasts or collagen to isolate it
  3. Presence of tissue necrosis inside the macrophage mass
444
Q

When are granulomas visible on a X-ray?

A

Calcium deposition which calcifies the granulomas make it visible on X-ray.

445
Q

What is Delayed Type Hypersensitivity (DTH) reaction?

A
  • When someone has pre-exposure to an infection, they develop memory cells against it
  • When re-exposed to it, undesirable reaction due to extent of recall produced by cell-mediated immunity which can be from mildly irritating to tissue damaging.
446
Q

What test can be done to diagnose TB aside from an X-ray?

A

Skin test (Mantoux test)

447
Q

How does the skin test show positive TB?

A
  • Inject intradermally a crude protein extract of myobacterium tuberculosis called tuberculin
  • Taken up by tissue macrophage and immature dendritic cells
  • They become activated and travel to the lymph node where a strong memory T-cell response elicited in TB infected individual
  • Th1 effector cells migrate to the site of injection and show an inflammation response
  • Induration (increased fibrous tissue) seen 24-48 hours later.
448
Q

What can the bacteria produce to inhibit the effect of superoxide killing?

A

Superoxide dismutase- Converts superoxide to hydrogen peroxide
Catalase - Converts hydrogen peroxide into water

449
Q

Why does maternal IgG gets transferred across the placenta to the foetus?

A

So that foetus is protected from infection for the first 6 months. Foetus adaptive immune system is immature and has a high number of naive lymphocytes (IgM) which do not respond well to antigen.

450
Q

Why are there still cases of congenital Rubella even though vaccination is offered?

A
  • Coverage rate is not 100%

- Mothers who fail to respond the vaccination

451
Q

When is the most dangerous period for a mum to contract Rubella?

A

First trimester of pregnancy

452
Q

What are the medical problems seen in a foetus whose mum contracted Rubella?

A
  • Sensorineural deafness
  • Heart problems
  • Eye disease including retinopathy, cataract and microphthalmia.
453
Q

What is the downside of placental IgG transfer? 2 conditions that foetus can get

A
  1. Neonatal myasthaenia gravis (acetylcholinesterase receptor blocker)
  2. Neonatal heartblock in RO positive (destroys nerve conduction fibres) SLE patients
454
Q

Why is IgG at its lowest point in the course of birth till 1 years old?

A
  • Maternal IgG is catabolised
  • Infant building its own repertoire of IgG
  • Hypogammaglobulinaemia
455
Q

What happens if there is a delay in infant developing IgG?

A

Transient Hypogammaglobulinaemia of Infancy

456
Q

What actions were taken when there was an increase in Pertussis (Whooping cough) in the first months of life?

A
  • Infant cannot be vaccinated in the first 2 months

- Mother’s were given vaccination so maternal IgG via placental transfer entered foetus

457
Q

Why is breast feeding important?

A
  • Protect against early infection
  • IgA antibodies
  • Bactericidal proteins such as lactoferrin
  • Cytokines help boost infant’s immune system to respond better to vaccine and infections.
458
Q

What method is used to overcome immaturity of the infant’s immune system?

A

Conjugate vaccines rather than polysaccharide to elicit T-cell help.

459
Q

What mechanisms used to evade maternal immune system?

A
  1. Placenta acts as a physical barrier
  2. Trophoblasts disguises itself from the immune system
  3. Placental suppressor factors released
  4. Paternal genes regressed.
460
Q

What happens to the immune cells to evade maternal immune system?

A
  • Increased Treg to suppress immune action
  • Increased T-cell activation threshold due to anti-inflammatory cytokines
  • Inhibitory molecules released by trophoblast to reduce Cytotoxic T-cell activity
  • Low T-cell influx due to reduced decidual expression of chemokines
  • Immune regulatory cells are increased by anti-inflammatory APC’s in decidual or uterine lining
461
Q

What is Rhesus Incompatibility?

A

If mother is Rhesus -, then during childbirth, foetus + will enter into maternal circulation and antibodies will be produced against it. (IgG). If mother pregnant will second child who is also Rhesus +, antibodies can cross the placenta to attack foetal erythrocytes

462
Q

What is the DiGeorge syndrome?

A

Absence of thymus due to a defect in pharyngeal pouch development

463
Q

How does ageing affect the cytokines?

A
  • Increases pro-inflammatory cytokines (IL-1B, IL-6, TNF-alpha)
  • Decreases anti-inflammatory cytokines (IL-10, TNF-Beta
464
Q

How does ageing affect the neutrophils?

A
  • No change in numbers
  • Decrease ability for chemotaxis, phagocytosis and cytotoxic effects
  • Affects gram + more than gram -
465
Q

How does ageing affect mast cell, eosinophils and basophils?

A

Decrease degranulation

466
Q

How does ageing affect dendritic cells?

A
  • Decrease ability to phagocytose antigen

- Decrease ability to present peptide to obtain T-cell help

467
Q

How does ageing affect NK Cells?

A
  • Increase in numbers
  • Decrease in cytotoxicity
  • Decrease in telomere length
  • Decrease in proliferation in response to IL-2.
468
Q

How does ageing affect monocyte and macrophages?

A
  • Increase in numbers
  • Reduces phagocytosis
  • Reduces ROS generation
469
Q

How does ageing affect T-cells?

A
  • Increase in memory T-cells but decrease in naive T-cells
  • Decrease in co-stimulatory expression
  • Decrease in telomere length
  • Decreased production
470
Q

How does ageing affect B-cells?

A
  • Decrease in naive but increase in memory B-cells
  • Decrease in telomere length
  • No T-cell help so cannot make high affinity antibodies
  • High chance of developing autoantibodies
471
Q

Why is vaccinating an ageing population a problem?

A
  • Thymus atrophy so unable to produce new T-cells

- Decrease in adaptive immunity due to lack of T-cell help for B-cells to produce high affinity antibodies.

472
Q

How is autoimmunity developed in ageing population?

A
  • Decrease T-reg function decreases peripheral tolerance
  • T cells replace NK cell receptor so cannot kill cells that down regulate MHC.
  • Increased autoantibodies
473
Q

What are the causes of inflammageing?

A
  • Increase in adipose tissue
  • Decrease in sex hormones
  • Asymptomatic infections
  • Macrophages
474
Q

What can an immunodiagnostic test measure?

A
  • Protein presence/quantitiy
  • Autoantibodies
  • Cell numbers, phenotype and function
475
Q

What antibody is produced in SLE?

A

Anti-nuclear antibodies which are antibodies against double stranded DNA.

476
Q

What does the dilution concentration of anti-nuclear antibody show? Also what does the pattern of ANA show?

A
  • The higher the dilution concentration, the more likely it is SLE if the person is not old, symptomatic and high strength of antibody
  • If homogenous pattern seen then the whole cell is stained whereas if speckled then less specific.
477
Q

What is a good ELISA test?

A

Test for coeliac disease where antibodies against transglutaminase tissue is produced.

478
Q

When can there be a false negative for a coeliac disease test?

A
  • If person is IgA deficient then even thought they have it, it will not show up.
479
Q

What are the primary quantitative causes of neutropenia?

A
  • Cyclic and congenita neutropenia
480
Q

What are the secondary quantitative causes of neutropenia?

A
  • Chemotherapy
  • Autoimmune
  • Leukaemia
481
Q

What are the primary qualitative causes of neutropenia?

A
  • Neutrophil killing defect

- Neutrophil migration defect

482
Q

What is an example of a disease caused by the inability of neutrophils to kill?

A

Chronic granulomatous disease

483
Q

What is Chronic Granulomatous disease?

A

Inability to produce an oxidative burst

484
Q

What occurs when there is a neutrophil migration defect?

A
  • Leukocyte Adhesion Deficiency
  • Deficiency in the integrin so tight adhesion to cause extravasation does not occur as cannot bind to ICAM.
  • No pus/abscess formation
  • Neutrophil count is abnormally high
485
Q

What can cause primary B-cell deficiency?

A
  1. Inability to produce B-cells
  2. Inability to educate B-cells
  3. Failure to Class Switch
486
Q

What can cause an inability to produce B-cells?

A
  • Absence of B-cell tyrosine kinase
  • Failure of B-cell lymphopoiesis
  • X-linked agammaglobulinaemia
487
Q

What can result in the failure of B-cells to educate?

A

When there is a T-cell defect so B and T-cells cannot co-operate in the germinal centre due to either

1) DiGeorge’s Syndrome
2) SCID

488
Q

What could cause a failure to class switch?

A
  • Defective CD40 ligand expressed by T-cells

- Germinal centres do not form

489
Q

What is the secondary cause of B-cell deficiency?

A
  • Myeloma
  • Chronic Lymphocytic Leukaemia
  • Iatrogenic: Autoimmune antibodies
490
Q

What are the clinical manifestations of a B-cell deficiency?

A
  • Recurrent respiratory tract infections

- Common pathogens pneumococcus, haemophilus influenza B

491
Q

What are the primary causes of T-cell deficiency?

A
  • DiGeorge’s syndrome

- SCID

492
Q

What are the secondary causes of T-cell deficiency?

A
  • Immunosuppression
  • HIV (attacks CD4 T-cells)
  • Lymphoid malignancy
493
Q

What is hypersensitivity?

A

Uncontrolled reactions of the immune system that can be detrimental to the host.

494
Q

What does hypersensitive reactions target?

A

Not an antigen but more inoculous substances like pollen, animal proteins and they are called allergens

495
Q

How many types of hypersensitivity are there?

A

4
I: IgE mediated mast cell degranulation
II: IgG autoantibodies causing direct damage
III: IgG/antigen complex damage
IV: Delayed Hypersensitivity T-cell mediated

496
Q

Give an example for each type of hypersensitivity.

A

I: Food, pollen, hayfever, nuts
II: Myasthenia Gravis, Goodpasture’s syndrome
III: SLE, cryoglobulinaemia, glomerulonephritis, vasculitis
IV: Contact dermatitis, delayed drug reaction

497
Q

What is the difference between Type I and IV hypersensitivity?

A 
Type 1
- Fast
- Life threatening
- Patient able to tell exact cause of it
Type IV
- Occurs more than 4 hours after exposure usually 24-48 hours
- Patient unable to tell what caused it
- Not life threatening
498
Q

How does contact dermatitis develop?

A
  • Pre-exposure resulted in T-cell to develop against the antigen.
  • On second exposure, it takes time for T-cells to travel to the site of exposure
499
Q

If symptoms developed similar to type IV hypersensitivity but concluded as it isn’t it, what other options are there?

A
  • Food intolerance
  • Irritant response
  • Delayed drug reaction
500
Q

How does one develop allergy on first exposure?

A

No symptoms of allergic reaction noticed however allergen causes T-cell stimulation to become Th2 effector cells due to release of IL-4 and then Th2 releases IL-4,5,13. IL-5,13 needed for class switching to IgE. On re-exposure allergic response is observed.

501
Q

What are the genetic factors that can predispose someone to produce IgE?

A
  • FcER1, IL-5,13
502
Q

Does environment affects someone ability to be allergic to a substance?

A

Hygiene hypothesis, if less exposed to bacteria, virus and fungi, more likely to experience an allergic reaction

503
Q

How does an allergic response take place?

A
  • Antigen binds to the IgE antibody specific to it
  • Antibody antigen complex forms a cross linking to the FcER1 on the effector cells which are either mast cell,s eosiniphils or basophils
  • This will cause the effector cells to degranulate
  • Effector cells releases substances that cause the allergic reaction.
504
Q

What are the 2 types of substances released by the effector cells?

A
  • Pre-formed mediators

- Late mediators

505
Q

What are the pre-formed mediators?

A

Histamine, Kallikrein, Heparin, Serotonin

506
Q

What are the late phase mediators?

A

Prostaglandin, leukotrienes, cytokines

507
Q

How are late-phase mediators release prevented in anaphylaxis?

A

Steroid/anti-histamine given

508
Q

What is anaphylaxis?

A

Severe life threatening allergic reaction

509
Q

What are the treatments available for anaphylaxis?

A
  • Intramuscular adrenaline injection

- Steroid/Anti-histamine

510
Q

What are the signs of anaphylaxis?

A
  • Stridor due to laryngeal oedema and mouth swelling
  • Wheeze due to bronchoconstriction
  • Blood pressure drop
  • Increase in HR
  • Increase Cardiac arrest risk
  • Incontinence, diarrhoea, swelling of the abdomen
  • Urticaria (hives), angiodema
  • Confusion
511
Q

How does IgE antibodies aid in anti-helminth immunity?

A
  • IgE antigen complex forms cross links with FcER1 on effector cells especially eosinophil which is needed for the elimination of parasitic infection.
512
Q

What substances released from eosinophils kills the parasite?

A

Preformed mediators: Major Basic Protein- Strong alkali so highly toxic to parasites
Contents of granules constitutes of ribosomes, peroxidase, ribonucleases kill the helminth
Reactive oxygen and nitric ocide

513
Q

How is helminth eradicated once its been killed?

A

IL-13 causes goblet cell hyperplasia and mucous production, stimulates contraction of the gut smooth muscle to facilitate elimination.

514
Q

What antimicrobial agents that a antibiotic can target? Name antibiotic example for each.

A
  1. Cell wall - Beta lactams so penicillin, cephalosporin, carbapenem, monobactams
  2. Ribosomes - Tetracyclines, aminoglycosides
  3. DNA gyrase - Ciproflaxacin
  4. Folic acid syntheses- Sulphonamides, trimethoprim

Foundations 3 (8 decks)

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