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PHYSIOLOGY PRIMARY > immunology > Flashcards

immunology Flashcards

1
Q

Categorise different types of white blood cell..

A

myeloid
- neutrophils - most abundant
- macrophages / monocytes
- basophils
- eosinophils

lymphoid
- NK cells
- lymphocytes

(monocytes also differentiate into dendritic cells)

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2
Q

which cells are granulocytes?

A

basophils
eosinophils
neutrophils

appear granular under microscope

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3
Q

can you name any tissue specialised macrophages?

A

Kupfer cells
microglial cells
alveolar macrophages

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4
Q

what is the difference between the innate and adaptive immunity?

A

Innate immunity
- fast acting
- present from birth
- non specific
- includes protective barriers, immune cells (neutrophils, macrophages, mast cells, eosinophils etc), complement system and acute phase response

adaptive immunity
- slower to develop
- relies on previous exposure and history
- very specific to antigen / infection
- memory exists
- includes T and B lymphocytes

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5
Q

Describe the components of the innate immune system

A

1st line defences
- skin
- mucus membranes - macrophages, goblet cells, cilia, IgA.
- stomach acid
- tears
- lysozyme in saliva and teers
- coughing/ sneezing

cellular responses
- macrophages and neutrophils mostly

complement system

acute phase response proteins

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6
Q

what are acute phase proteins?
name some acute phase response proteins..

A

group of proteins produced by the liver in response to inflammation / infection

The acute phase response is a response by the liver to produce such proteins but also downregulate others over to aid inflammatory process.

CRP acts as an opsonin and activates complement and macrophages

fibrinogen to help wound healing

ferritin reduces iron available for bacteria.

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7
Q

what is a cytokine?

A

small protein molecule involved in signalling immune response and inflammation.

often released by immune cells and act on other components to activate / proliferate them.

major ones IL1, TNFa, IL6, IFNg

e.g. IL1 induces fever
IL6 & TNFa can stimulate acute phase response

their roles are a lot more complex than this

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8
Q

what role does the arachidonic pathway have in inflammation?

A

tissue injury causes injury to phospholipid membrane which promotes phospholipase A2. Increases production of arachidonic acid and thus prostaglandins and leukotrienes

leukotrienes acts to increase permeability/ vasodilation, chemotaxis, bronchospasm

prostaglandins - pain , vascular permeability, chemotaxis

i.e. both promote inflammation and regulate immune response.

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9
Q

what is the role of the complement system?

A

25 plasma proteins produced by the liver and circulate in blood stream

when activated, biochemical cascade causes activation and amplification and production of membrane attack complex

can be activated in 3 ways =
classical pathway = C3 convertase activated by Ag-Ab complex
alternative pathway = C3 convertase activated via microbial surface
lectin pathway = activated by mannin binding protein which is bound to bacterial carbohydrates

once activated
C3 convertase cleaves C3 to C3a andC3b
this results in positive feedback and other complement activation.

overall roles
- inflammation - cause mast cell degran
- opsoniation - C3b coats microbes
- membrane attack complex - C5-C9 - produces holes in bacterial wall and cell lysis
- chemotaxis

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10
Q

what is inflammation?

A

The immediate non specific response to injury to promote destruction of harmful substances and healing

consists of 4 cardinal features
- rubor - redness - from vasodilation
- calor - heat - as above
- dolor - pain - prostaglandins and other mediators have receptors on nerve ending. protects from further damage
- tumour - swelling - increased permeability and migration of cells (chemotaxis)

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11
Q

describe the process involved in inflammation…

A
  1. tissue damage stimulates process e.g. arachidonic pathway or cytokines
  2. hyperaemia - vasodilation and increased permeability.
  3. exudation - fluid, complement, cytokines leak out into tissue - swelling and pain
  4. emigration - white cells migrate via chemotaxis.

many mediators involved and very complex interactions.

e.g. histamine and leukotrienes increase capillary permeability and chemotaxis
prostaglandins also do this + cause pain.

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12
Q

what is SIRS response?

A

systemic inflammatory response syndrome

life threatening condition related to deregulated host response to inflammation/infection.

characterised by
temp >38/<36
tachycardia >90
Tachypnoea >20 or PaCO2 <4.3
WCC >12 or <4

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13
Q

describe the immune response to exogenous pathogens..

A

exogenous pathogens first come into contact with barriers

if they pass these barriers they are next exposed to phagocytes (e.g. macrophages)

phagocytosis occurs and pathogen is destroyed via ROS and hydrolytic enzymes

fragments of this pathogen are combined with MHC class II and presented on the surface of the cell.

the cells move to lymph nodes where T cells reside and the specific TCR that is complementary to the antigen/MHC II complex is selected and activated. This will be a T helper cell (as it is exogenous)

This results in clonal expansion

meanwhile B cells also phagocytose and present on MHC II

when B cells and T cells with complementary MHC II and TCR meet it results in activation of B cell to plasma cell. Also relies on co-receptor activation.

plasma cells can now secrete antibodies to help clear exogenous pathogen

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14
Q

what cells are antigen presenting cells?

A

macrophages
dendritic cells
monocytes

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15
Q

can you describe the process of phagocytosis?

A

foreign material detected via its antigen

binds surface receptors of phagocytes

triggers endo cytosis

the pathogen is endocytosed into a vesivle

this is now called a phagosome.

the phagosome combines with a lysosome and is exposed to ROS

causes breakdown of material inside

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16
Q

what are MHC molecules?

A

Major histocompatibility complex
group of glycoproteins texpressed on cell surface in combination with self antigen.

thus acts as markers for recognition by immune system.

MHC I present on all cells - for presenting self antigen and protecting from immune destruction
MHC II present on immune cells and for presenting exogenous antigen

17
Q

how are virally infected cells detected and cleared by immunity?

A

virally infected cells will express MHC class I
however they will expose viral peptides on these.

MHC Class I + viral peptide is presented to T cells and promotes production of CD8 cytotoxic T cells

Type 1 T helper cells will also be activated which promote the CD8 cells.

cytotoxic T cells put holes in infected cells via perforins

18
Q

can you explain the roles of the different lymphocytes in adaptive immunity..

A

can be categorised into B and T cells
T cells have further category of CD8 cytotoxic and CD4 helper T cells.

CD4 helper T cells can be further divided into
Th1 = help CD8 for intracellular infections e.g. viruses
Th2 = help B cells for exogenous pathogens e.g. bacteria.

19
Q

what is the thymus gland?

A

gland present in the upper anterior portion of the chest behind the sternum

larger during child hood whilst T cell maturation occurring

atrophies in adulthood

20
Q

what is an antigen?

A

An antigen is any substance that can be recognized by the immune system and trigger an immune response.

can be protein, glycoprotein, lipisaccharide etc

can be endogenous or exogenous or may be self antigen triggering autoimmunity.

21
Q

what is a B and T cell receptor?

A

integral membrane proteins that have a constant region that is integrated in the phospholipid bilayer and a variable region which is specific for a certain type of antigen.
collectively all the T and B cells are able to detect a vast range of antigens.

The antibody is a soluble version of a BCR

22
Q

what are the different forms of immunological memory?

A

active or passive

passive = lasts few days to months. from acquiring antibodies e.g. baby across placenta/ breast milk.

active = immunity produced by activation of adaptive immune system and formation of memory B and T cells which can produce antibodies on repeated exposure to the same pathogen. long lived.

23
Q

can you draw and describe the structure of an antibody

A

peptide molecules consisting of 2 light chains and 2 heavy chains joined by disulphide bonds.

they come together to form a constant region and variable region for contact with various antigen.

the heavy chain determines the class of Ab e.g. IgA, M etc

24
Q

what are the functions of antibodies

A

antibodies have variable region capable of recognising and binding antigen

opsonisation - constant portion binds leukocytes and helps them to phagocytose

neutralisation - stops bacteria dividing and making toxins

agglutination - clumps bacteria together, makes phagocytosis more efficient

activate classical complement pathway

25
Q

what different types of antibody do you know?

A

IgA - mostly in body fluids and mucosal areas e.g. saliva, tears, gut, respiratory. helps as first line defence preventing colonisation.

IgM - exist as a monomer - star shaped 5 together - found in blood stream helps to remove bacteria and activate complement

IgG - provides most Ab based immunity. most abundant antibodies.circulates blood waiting to coat microbes. can cross placenta

IgE - binds pathogen, stimulates mast cell degranulation. invovled in allergy

IgD - less defined function

26
Q

what are the 4 main classes of hypersensitivity?

A

type 1 - IgE mediated. Causes mast cell degranulation, inflammation & bronchoconstriction. immediate response and is the mechanism of allergy and anaphylaxis

type 2 - antibody mediated (IgG/M) e.g. antibodies which bind self antigen and trigger tissue destruction e.g. by complement activation, phagocytosis, cytotoxicity. E.g. myasthenia gravis, rheumatic fever. this occurs within minutes to hours

type 3 - immune complex mediated (IgG/M) - antigen-Ab complexes circulate and deposit in tissues causing inflammation e.g. RA, SLE. This takes hours.

type 4 - T cell mediated. E.g. T1DM, TB. this is delayed and can take over 1 month.

(More recently group 5 has been created for antibodies against receptors. this would take myasthenia gravis out of class 2. also Graves would be in class 5).

27
Q

can you describe the mechanism behind anaphylaxis..

A

sensitising event:
- exposure to antigen - triggers immune response, B cells activated, IgE produced specific to that antigen.
- these IgE bind surface of mast cells and basophils

next exposure
- antigen binds IgE
- triggers mast cell degranulation
- histamine and other mediators released
- histamine causes vasodilation and bronchospasm.

28
Q

can you tell me about immunodeficiency …

A

immunodeficiency encompasses a collection of diseases whereby there is an impairment of the immune system.

This can be further categorised into specific forms of deficiency or whether the deficiency is primary or secondary.

primary immunodeficiency = genetic disorders that result in impaired immunity e.g. Severe combined immunodeficiency disease (SCID) where there is both T and B cell dysfunctions. DiGeoge is another primary immunodeficiency disorder with defects in T cell function. Others can be as specific as antibody deficiencies.

secondary immunodeficiency are those acquired. with the major one being HIV. others may be from prolonged steroid use or due to leukaemia

29
Q

how is the immune system affected by anaesthesia?

A

can be divided into physical and chemical factors

physical:
disruption of physiochemical barriers - cannulas, incision of surgery, ET tubes bipass mucocilary escalator

hypothermia - depresses immunity

chemical:
exposure to allergens e.g. anaphylaxis risk

stress response to surgery releases cortisol - depresses immunity

volatiles and opioids have also been shown to impair immune dysfunction

on the other hand TIVA has shown to be better in cancer patients and reduces reoccurance.

30
Q

what specific roles does skin have in innate immunity?

A

physical barrier
chemical barrier - slightly acidic due to sweat, antimicrobial peptides
commensal microbes - inhibit growth of others through competition
langerhan cells - specialised dendritic cells.

PHYSIOLOGY PRIMARY (17 decks)

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