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B4W3 > THE BLOOD AND BODY DEFENCES > Flashcards

THE BLOOD AND BODY DEFENCES Flashcards

1
Q

What are myeloproliferative neoplasms?

A

a group of rare blood cancers in which excess red blood cells, white blood cells or platelets are produced in the bone marrow

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2
Q

what is polycythaemia?

A

an excess of red blood cells in the circulation

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3
Q

what are the clinical signs of polycythaemia?

A

breathing difficulties, excessive bleeding, splenomegaly, red colouring, symptoms of phlebitis

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4
Q

what are the symptoms of polycythaemia?

A

fatigue, dizziness, increased sweating, blurred vision, headache, itchiness (especially after a hot shower)

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5
Q

what is itchiness caused by in polycythaemia?

A

increases basophils and mast cells which release histamine- histamine makes the skin itch

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6
Q

what are the 2 main types of polycythaemia?

A

primary and secondary

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7
Q

what is the main type of primary polycythaemia?

A

polycythaemia rubra vera

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8
Q

what is the cause of primary polycthaemia?

A

its a familial congenital version due to the enhanced responsiveness to EPO caused by mutations in the EPO receptor

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9
Q

what is the cause of secondary polycythaemia?

A

caused by conditions that promotes RBC development by overstimulating the normal bone marrow e.g. hypoxia in COPD stimulates this or EPO-secreting tumours

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10
Q

what is the cause of polycythaemia rubra vera?

A

A mutation in JAK2 that stops the domain having an auto-inhibitory function the kinase is always on even in the absence of EPO

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11
Q

polycythaemia rubra vera can lead to myelofibrosis and acute leukaemia. what are these conditions?

A

myelofibrosis is when RBCs dry out and forms fibrous scar tissue in the bone marrow so it loses its function- can lead to anaemia
leukaemia is a blood cancer caused by a rise in WBC

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12
Q

what is essential thrombocythemia? what are the implications?

A

an excess of platelets

can increase risk of blood clots and increase risk of bleeding

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13
Q

why would thrombocythaemia carry an increased risk of bleeding?

A

because all the vWF is used up forming clots so when it is actually needed, there isn’t much available

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14
Q

what are the clinical signs of thrombocythaemia?

A

frequently asymptomatic
haemorrhages, thrombosis
can occasionally lead to leukaemia and Myelofibrosis

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15
Q

what is thrombocythaemia caused by?

A

a mutation in JAK2 so its stimulated even when thrombopoietin isn’t present

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16
Q

what is myelofibrosis?

A

when bone marrow gets replaced with connective tissue (fibrosis) so bone marrow cannot produce blood cells efficiently

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17
Q

what are the 2 types of myelofibrosis? how do these differ?

A

primary- mutation in JAK 2

secondary- develops from conditions like polycythaemia and thrombocythaemia

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18
Q

what are the clinical signs of myelofibrosis?

A

splenomegaly, bone marrow fibrosis, anaemia, thrombocythaemia, thrombocytopenia, variable WBC

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19
Q

name 3 myeloproliferative neoplasms?

A

polycythaemia
essential thrombocythaemia
myelofibrosis

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20
Q

what is a kinase?

A

An enzyme that catalyses the transfer of phosphate groups from high-energy, phosphate-donating molecules to specific substrates

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21
Q

what is EPO?

A

erythropoietin, a cytokine that allows cells to go down a transcriptional pathway to allow the production of myeloid cells

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22
Q

what are the domains of JAK2?

A

one is the 3d structure that interacts with cytokine receptors, one allows kinase activity, one helps form the conformation and stability of the molecule and one is the auto inhibitory domain

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23
Q

what does the auto-inhibitory domain of JAK2 do?

A

it keeps the kinase inactive until there’s an appropriate interaction and signal through the receptor

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24
Q

what is the JAK2 mutation called?

A

V617F

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25
Q

what is type 1 hypersensitivity?

A

an allergic reaction provoked by re-exposure t an allergen e.g. anaphylaxis

26
Q

why are IgE levels in the blood low?

A

because most is bound to mast cells

27
Q

describe the sensitisation step of type 1 hypersensitivity immune response?

A

at first exposure the allergen is picked up by an APC and is processed and expressed on its cell surface. APC presents this to Th cells which then activates B cells. B cells proliferate and undergo isotype switching to produce IgE on their surfaces. B cells release IgE which mast cells pick up and present. IgE also binds to basophil surfaces

28
Q

describe the response at second exposure in a type 1 hypersensitivity immune response?

A

on subsequent exposure, the IgE on mast cells recognise the allergen and the allergen will crosslink the IgE molecules to activate the mast cell to degranulate and release histamine

29
Q

what is the effect of mast cells releasing histamine?

A

increased vascular permeability and vasodilation to cause oedema to local tissues

30
Q

what is the “late phase”?

A

About 50% of the time, the allergic reaction progresses into a “late phase.” This late phase occurs about four to six hours after the exposure.

31
Q

what is synthesised in the late phase of type 1 hypersensitisation?

A

leukotrienes, prostaglandins, eosinophil chemotaxis factor-anaphylaxis

32
Q

what do leukotrienes do in type 1 hypersensitivity?

A

cause increased vascular permeability and bronchoconstriction

33
Q

what do prostaglandins do in a type 1 hyper sensitisation reaction?

A

cause bronchoconstriction

34
Q

what do eosinophil chemotaxis factor-anaphylaxis (ECF-A) do?

A

attracts eosinophils to tissues immediately

35
Q

what is systemic anaphlaxis?

A

when you have mast cells that have been primed with IgE all throughout the body so you get inflammation all throughout the body

36
Q

what effects does histamine have on the GI tract?

A

increased fluid secretion and increased peristalsis so we get expulsion of GI tract contents via diarrhoea or vomiting

37
Q

what effects does histamine have on the airway?

A

decreased diameter and increased mucus secretion so we get expulsion of airway contents via coughing and phlegm

38
Q

what effects does histamine have on blood vessels?

A

increased blood flow and permeability so we get oedema, inflammation and increased lymph flow

39
Q

describe what happens in type 2 hypersensitivity

A

antigens on cells are picked up, processed and presented by an APC which travels to the lymph node and activates Th cells which then activate B cells.B cells then become plasma cells and undergo isotype switching to form IgG and IgM molecules which can then activate the complement (inflammatory mediators increased, opsonisation for phagocytes, membrane attack complex and activation of NK cells to kill cells, can disrupt cell function)

40
Q

what are examples of type 2 hypersensitivity?

A

rhesus disease, penicillin allergy, chronic urticaria

41
Q

describe the process of producing immune complexes in type 3 hypersensitivity?

A

soluble antigens are picked up by circulating B cells and macrophages. the APC will process and express the antigen on its surface. the APC will travel to lymphoid tissue and present the antigen to Th cells which will then activate B cells (3 steps). these can differentiate into plasma cells and undergo class switching where we change from IgM to IgG. the IgG bind to soluble antigens (different from those bound to cells in type 2) and form chains of antibodies and antigens to form immune complexes.

42
Q

how are immune complexes normally cleared?

A

macrophages in the spleen and liver

43
Q

what happens if immune complexes are not cleared?

A

they deposit into various tissues where they induce complement activation to promote the inflammatory response

44
Q

what can type 3 hypersensitivity cause?

A

blotchy skin, arthritis, vasculitis, nephritis (depends on where immune complexes deposit)

45
Q

describe the process of a type 4 hyper sensitisation immune response?

A

a soluble or cell-associated antigen binds to APC, is processed and presented. at lymphoid tissues, the APC presents the antigen to T cells. this activates the T helper cell or cytotoxic T lymphocyte. T cells release cytokines which act on the vascular endothelium. proliferation has to occur so this is known as the delayed response. DOESNT REQUIRE ANTIBODIES

46
Q

what are examples of type 4 hypersensitivity immune responses?

A

contact dermatitis, chronic asthma, tuberculin reaction

47
Q

what are the 2 types of immunodeficiency? how do they vary?

A

primary- has a genetic cause and usually arises in infancy

secondary- caused by another disease and arises later in life

48
Q

what is chronic granulomatous disease?

A

a genetic disorder affecting how phagocytes kill microbes.

49
Q

what are the clinical signs of chronic granulomatous disease?

A

impetigo, skin and rectal abscesses, chronic lymphadenopathy recurrent pneumonia

50
Q

what is a granuloma?

A

a way of containing an area of microbial infection to prevent it from spreading

51
Q

why do we see the formation of granulomas in chronic granulomatous disease?

A

as it shows the microbe can’t be eliminated so the cell is trying to contain it

52
Q

what’s an example of a secondary immunodeficiency?

A

HIV/AIDS

53
Q

what is autoimmunity?

A

when the body starts to target self-proteins or tissues

54
Q

what is auto inflammation?

A

When innate immune cells become activated, due to dysregulated secretion of pro-inflammatory cytokines and consequent damage to host tissues which activates innate immune cells

55
Q

what is auto reactivity?

A

exhibiting an immune response against the body’s own antigens

56
Q

what are the 4 mechanisms of induction of autoimmunity by infection?

A

molecular mimicry, protein changes, super antigens and bystander activation

57
Q

what is molecular mimicry?

A

when a pathogen expresses a molecule which is very similar to a host molecule so phagocytic cells recognise the pathogen but cannot distinguish between it and the host cell

58
Q

what are super antigens?

A

antigens that can activate T cells without the presence of all 3 signals- they excessively activate the immune system

59
Q

what is bystander activation?

A

the activation of a T cell which is independent of specific T-cell receptor stimulation.

60
Q

what are the 3 ways in which we can therapeutically intervene in auto inflammatory and autoimmune diseases?

A

cytokine therapy (e.g. anti-TNF)
reducing lymphocyte activation (e.g. steroids blocking receptors)
killing the disease-causing cells (e.g. anti-B cell antibodies)

61
Q

what is the problem with anti-B cell antibodies?

A

it kills helpful B cells as well as diseased ones

B4W3 (7 decks)

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