3. Adaptive Immunity Flashcards

Question

CNS dysfunction

Answer 1

``` Systemic inflammation • Hypoxemia • Hypotension • Haemorrhage • Medications such as sedatives and analgesics ```

Answer 2

– possible source of infection – factors that increase risk of sepsis = same factors for everything other disorders and infections – any indications of clinical concern, such as new onset abnormalities of behaviour, circulation or respiration

Answer 3

Extremes of age • Impaired immune systems because of illness or drugs, including people being treated for cancer with chemotherapy (suspect neutropenic sepsis) • Recent surgery, or other invasive procedures • Breach of skin integrity (e.g. cuts, burns, blisters or skin infections) • IVDU • Indwelling lines or catheters. • Women who are pregnant, have given birth or had a termination of pregnancy or miscarriage in the last 6 weeks, • Neonates

Answer 4

``` • Assess – Temperature – Heart rate – Respiratory rate – Blood pressure – Level of consciousness – Oxygen saturation ```

Answer 5

* Score all assessments listed above from 0 –3 * Higher score = worse case of sepsis ---> body goes to overcompensate that’s why most levels of bp, pulse, heart rate go higher but then body can't do enough so it decompensates and goes lower = big problem • Focus on the simple things – look at the patient, check their general levels, observe them

Answer 6

``` • Immediate action required ○ Quick action of antibiotics and oxygen into patient – increase succces ○ Early identification and treatment • Inform senior doctor for review • Send urgent investigations • Complete Sepsis Six Bundle ```

Answer 7

Titrate oxygen to a saturation target of 94% = Airways • Take blood cultures. = circulation • Administer empiric intravenous antibiotics. • Measure serum lactate and send full blood count. = platelets • Start intravenous fluid resuscitation. • Commence accurate urine output measurement. Investigations • Lactate – hypoxic injuries = more lactate , anaerobic respiration • Full blood count - platelets

Answer 8

``` • carry out a venous blood test for the following: – blood gas including glucose and lactate measurement – blood culture – full blood count – C-reactive protein – urea and electrolytes – creatinine – clotting screen ```

Answer 9

---> start treatment whilst monitoring – give the best guess of what the causative thing is • give a broad-spectrum antimicrobial at the maximum recommended dose without delay (within 1 hour of identifying that they meet any high risk criteria in an acute hospital setting) • Monitor people physiological parameters

Answer 10

Ensure mechanisms are in place to deliver antibiotics fast • Take microbiological samples before prescribing an antimicrobial (where possible) • If meningococcal disease is specifically suspected (fever and purpuric rash) – parenteral benzyl penicillin in community settings – intravenous ceftriaxone in hospital settings.

Answer 11

Oxygen keep it > 94% • Give oxygen to target saturation of 94–98% ○ Sigmoidal curve levels off at 94% - oxygen dissociation • 88–92% for those at risk of hypercapnic respiratory failure

Answer 12

* Rash – non blanching (do not disapear under pressure) | * Peripheral sinosis, ischaemia

Answer 13

---> Adaptive immunity is the process by which a specific immune response is elicited Adaptive immune system gives innate immune system focus

Answer 14

* Neutrophil * Macrophage * Eiosinophil * Dendritic cell * Natural killer cell * Mast cell Innate immune system --> myeloid cells, mature systemically in tissues

Answer 15

* Helper T cell * Cytotoxic T cell * B cell – antibody producing cells * Natural killer cell Adapative immune system --> lymp, lymphoid system

Answer 16

---> primary cells * Mature in the Thymus – hence T cells * Originate as haematopoietic stem cells (HSCs) in the bone marrow. * In the thymus they are screened for their ability to recognise ‘self’ antigens. Those that do are directed towards apoptosis.

Answer 17

○ Every T cell has a T cell receptor = CD3 on surface of every T cell but every CD3 receptor is different as they all recognise different potential antigens ○ Each T cell has its own CD3 receptor • Self tolerance – CD3 receptors should never revognise self

Answer 18

* Differentiate between what is self and not self * It uses signposts on each cell. These are known as MHC I and MHC II. • MHC complexes are tissue antigens which display proteins which are being made within that cell. ○ This allows the immune system to determine if it’s observing “self” or “non-self”. ○ This is critical for T cell tolerance.

Answer 19

• MHC I interacts with CD8 on cytotoxic T cells. - self antigens made within host cell ○ This can be important for cancer cell detection and clearance as well as virally infected cells.- self cells are hijacked by virus to produce things that are not self – Present on all nucleated cells. (not red blood cells as there is no nucleus)

Answer 20

• MHC II interacts with CD4 on helper T cells. - foreign antigens from phagocyte on antigen presenting cells ○ This displays antigens which have been processed by antigen presenting cells and leads to an antibody response.

Answer 21

``` CD25 = receptor for an interleukine IL2 = growth factor for T cells ```

Answer 22

• cortical region at top (cortex) = where t cells differentiate into either CD4 or CD8 ○ CD4 interacts with MHCII ○ CD8 interacts with MHC1 • Medulla region – medullary epithelial cells, if the cd8 or CD4 interacts with self cells on MHC1/2 they are targeted for apotosis as they will target self cells which is damaging

Answer 23

1. Lymphoid progenitor cell enters the outer cortex of the thymus. 2. T cell which don’t express CD4 or CD8 (double negative; DN) go migrate through the thymus. 3. Expression of CD4 and CD8 leads to a double positive (DP) cell. 4. DP cell interacts with cortical epithelial cell where it recognises either MHC I or MHC II. 5. Lack of interaction leads to cell death by neglect. 6. Depending on MHC class interaction, cells will become committed to the CD4 or CD8 lineage. 7. CD4 and CD8 cells pass into the medulla. Here, they interact with dendritic cells displaying “self” antigen. Recognition leads to cell death.

Answer 24

Antigen presentation is a two-step process which occurs in the lymph node* CD4 cells: • APC finds T cell with complementary receptor • If complementary receptor is found, cell and T cell form together with CD4 and MHCII • Activates T cell ---> make sure T cell receptor is completely complimentary to MHCII by using secondary signal • If it is not complementary it would activate wrong b cell and produce wrong antibodies

Answer 25

1. Presentation of the antigen by an antigen presenting cell (macrophage, dendritic cell, professional antigen presenting cells) to T cells. 2. Helper T cells activate B cells expressing a specific B cell receptor (Ig) for the antigen.

Answer 26

- exogenous 1. APC picks up an antigen 2. Activate MHCII 3. Present receptor of pathogen on MHCII receptor

Answer 27

– endogenous 1. Normal somatic cell produces proteins 2. Puts them onto MHCI 3. Only recognised by CD8 t cells when the proteins on self cells aren't familiar (virus or mutation in cell that alters proteins)

Answer 28

T cells have specific receptors on their surface – one T cell recognises one antigen (lock and key cell)

Answer 29

'---> Process of gene rearrangement whereby variable, diverse and joining regions are rearranged in different combination to produce a vast range of unique receptors. • Recombination of 3 gene elements to give a huge array of protein outputs

Answer 30

* Germline seqments , V, D , J anc constant regions at end = give antigen recognition * D and J recombination – splice some diverse and joining regions, reorganise * V to DJ recombination * Recombine all regions to give more simple focused, spliced transcript Mediated by VDJ recombinase – which does splicing and joining together to give transcript

Answer 31

• B cells, like T cells, have receptors which are specific to a single antigen. • B cell receptor is essentially an immunoglobulin = sereted to vecome soluble effector • B cells will encounter the antigen on their own, but this isn’t sufficient to activate the B cell. ○ Instead, the B cell internalises the antigen and then presents it on MHC II. • Primed (activated) T cells secrete more IL2 (T cell growth factor… remember CD25 It’s the IL2 receptor!) • IL2 growth factor causing expansion of the population of T cells which recognised the antigen. • Primed T cells then encounter B cells. If they come across a B cell displaying the antigen that theyrecognise, they bind to it causing activation of B cell

Answer 32

``` • Progenitor lymphoid cell • Differentiates into progenitor b cell Somatic recombination (VDJ) recombination • Differentiate into immature b cell with receptor to recognise one specific antigen • Leave bone marrow to become = naïve b cell (that hasn't met an antigen yet from T cell) ```

Answer 33

* Dark zone | * Light zone

Answer 34

• Clonal expansion – rapid expansion of b cells in dark zone

Answer 35

T Cells carry bacteria migrate to lymph, leave captured antigens for b cells to pick up and recognise with b cell receptor (mature b cell) • Enter dark zone and activate b cells • Clonal expansion – rapid expansion of b cells in dark zone • B cells internalise antigen • In light zone B cells are screened to make sure that they don't recognise self antigens • If b cells don't recognise self antigens – they are released as plasma cells

Answer 36

Plasma cells – secrete immunoglobulins into plasma (systenic release of antibody) • Plasma cells produce antibodies • They are effector cells

Answer 37

IgD IgM IgG

Answer 38

IgD = b cell receptor, membrane bound, sits on membrane

Answer 39

IgmM= mainly produced by infanats/ children • Very sticky but only some specificty to target antigen – off tagret effects may stick to something it is not supposed to • Produced in first days of immune response in adults

Answer 40

IgG = most common effective form of antibody • Very highly specific, very sticky • Only produced in any large quanity aboove age 6 • Vaccines in children – used to kick start igG production

Answer 41

Class switching = must occur for appropriate antiboidy production • B cells first produce igm • Switch to produce igG

Answer 42

* Each antibody can capture 2 antigens – fragment antigen binding region at top of antigen * Fragment crystallisation region on bottom

Answer 43

--->• An opsonin is a molecule which can attach to an antigen on the surface of a bacteria (or virally infected cell). It acts as a beacon for phagocytes which will come in and ‘eat’ the pathogen. • Binding of opsonin allows neutrophil to internalsie antibody antigen complex

Answer 44

– Complement proteins (innate immunity) | – Antibodies (immunoglobulins, Ig; adaptive immunity)

Answer 45

IgG can further activate compliment when bound to antigen

Answer 46

• C3 opsonising complement protein * This leads to internalisation of the pathogen which has been coated in antibody. * The macrophage produces reactive oxygen species to destroy the pathogen

Answer 47

----> Complement can “punch holes” in the cell membrane of the pathogen leading to death. • Phagocytes such as macrophages and neutrophils have Fc receptors on their surface which bind to the Fc region of an antibody which has formed a complex with an antigen.

Answer 48

• Once T and B cells have encountered an antigen for the first time and are prompted to proliferate,- clonal expansion - some will be become effector cells which combat the infection. ○ Others don’t proliferate and reside predominantly in the spleen (45% of memory B cells) and some in the circulation awaiting a second encounter with their specific antigen. - some wait in the lymph as memory population ○ A second challenge from the same pathogen with unaltered antigens elicits a much swifter immune response as mature effector memory cells are already present. ○ These just need to be instructed to proliferate and migrate out of the lymph node

Answer 49

Immunological memory is the foundation principle of immunity which allows vaccination to work Vaccines Information in the grid ---> therapeutic way of manipulating function of immunological memory

Answer 50

* Bind to things that are abnormal on cells | * Secret enzymes liker perforin (perforate cell) and granzymes (effect capsins which lead to apoptosis)

Answer 51

These cells directly have an effect on thwat they are are targeting • Recognise cells infected by virus – that are producing viral proteins that are put on MHC1 • There is now a not self protein on MHCI as it is a viral protein • CD8 binds to and anchors cytotoxic t cell to MCHi • Complementary to antigen – 2 step verification system ○ The still have a two-step verification system in place and won’t induce apoptosis without interaction of Fas ligand (FasL) on the T cell surface with Fas on the surface of the infected cell • Cytotoxic t cell marks cells for apoptosis – cell death

Answer 52

3 things in: antibiotics, oxygen fluids | 3 things out: lactate, urine output blood culture.,.

3. Adaptive Immunity Flashcards

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