immunology 1 Flashcards
In the treatment of anaphylaxis, you can repeat adrenaline every 5 minutes
a. true
b. false
a.true
contact dermatitis is what type of hypersensitivty reaction
delayed type hypersensitivity reactions (Type IV)
skin patch test
After 48 hours, the patches are removed and any skin reactions are assessed. A positive reaction typically presents as redness and swelling at the site where the allergen was applied.
when do type 1 hypersensitivity reactions occur
immediately IgE mediated
first-line treatment for anaphylaxis.
adult dose is 500 micrograms (0.5ml of 1:1000 adrenaline) given into the anterolateral thigh. IM administration provides rapid absorption but is safer than the intravenous route.
given IM
Refractory anaphylaxis is defined as respiratory and/or cardiovascular problems persisting despite 2 doses of IM adrenaline
a. true
b. false
a. true
initiate IV adrenaline infusion
treatment of refractory anaphylaxis
IV adrenaline (under expert guidance)
+ IV fluid bolus
most commonly utilised test for confirming a diagnosis of anaphylaxis
Serum mast cell tryptase
Elevated levels indicate mast cell degranulation, which occurs in immunoglobulin E (IgE)-mediated type 1 hypersensitivity reactions. These reactions are responsible for anaphylaxis and its associated clinical manifestations.
Skin prick testing is testing for immediate urticaria formation (i.e. a type I hypersensitivity reaction).
a. true
b.false
a. true
Skin prick testing is testing for immediate urticaria formation (i.e. a type I hypersensitivity reaction).
Skin patch testing is looking for delayed onset dermatitis (I.e. a type IV hypersensitivity reaction).
a. true
b.false
a.true
anaphylaxis is what type of hypersensitivity response
type 1 -
treatment for anaphylaxis
oxygen - 15l/m and nebulised salbutamol
**IM adrenaline 10mcg/kg or EPIPen (junior 150mcg) if out of hospital
**
gain IV access and fluid resus if needed (20ml/kg 0.9% saline)
where do myeloid cells mature
within the bone marrow
where do b-lymphocytes mature
within the bone marrow
and then migrate to secondary lymphoid organs where they differienitate
where do t-lymphocytes mature
migrate to the thymus to mature
migrate to secondary lymphoid organs where they differienitate further
physical barriers
skin
mucosa
chemical barriers
HCL in stomach
lysozymes in sweat , tears,
lactic acid in the vagina
tasked with the immediate response to infection - its actions begin at the site
innate immune system
which cells activate the innate immune system
macrophages (recognise pathogen and activate)
role of dendritic cells
pick up antigens and present antigen on their surface membrane - and transport to site of B and T cells (LNs and MALT) to facilitate immune response
MALT- mucosa associated lymphoid tissue
pathogens can directly activate the complement system
a. true
b. false
a. true
via lectin pathway and alternative pathway
what effects do cytokines have
released by macrophages
-> vasodilation
-> increased vascular permeability
-> mast cell degranulation
-> activate clotting system
-> activate kinin system
interlukins are released during acute phase reaction with pathogen
a. true
b. false
a. true
what are major histocompaibility complexes 1
cell surface proteins which are vital for presentation of both antigens and self-markers to the immune system
MHC-1 are present on the surface of ALL nucleated cells (and platelets - exception)
will signal something is wrong if host cell is damaged -> can be destroyed
MHC-2 is present were?
only on antigen presenting cells
-> dendritic cells
-> macrophages
-> b-cells
present to T-cells
what are the parts of the innate immune system
Physical barriers: Skin, mucous membranes, and other physical structures that prevent pathogen entry.
Phagocytes: White blood cells like neutrophils and macrophages that engulf and digest foreign particles or pathogens.
Natural killer (NK) cells: Cells that can destroy infected or cancerous cells.
Inflammation: A response to infection or injury that helps to isolate pathogens and promote healing.
Complement system: Proteins that enhance the ability of antibodies and phagocytes to clear pathogens.
There are two types of adaptive immunity:
- humeral immunity (mediated by B cells)
- cell-mediated (mediated by T-cells)
explain humeral immunity (mediated by B-cells)
B cells are responsible for producing antibodies, which are proteins that specifically recognize and bind to antigens on pathogens, marking them for destruction.
Antibodies can neutralize toxins, prevent pathogens from entering cells, and enhance phagocytosis.
Memory B cells are produced after an infection or vaccination, which can provide long-lasting immunity.
explain cell-mediated immunity (t-cells)
T cells are responsible for directly killing infected cells or activating other immune cells.
Helper T cells (CD4+) coordinate the immune response by stimulating B cells, macrophages, and cytotoxic T cells.
Cytotoxic T cells (CD8+) directly destroy infected cells by recognizing specific antigens presented on the cell’s surface.
Memory T cells are also formed after an infection and can provide long-term immunity.
type of immunity that is immediate, nonspecific, and does not change over time.
innate immune system
T cells (CD4+)
Helper T cells (CD4+) coordinate the immune response by stimulating B cells, macrophages, and cytotoxic T cells.
T cells (CD8+)
Cytotoxic T cells (CD8+) directly destroy infected cells by recognizing specific antigens presented on the cell’s surface.
CD8+ cyctoxic killer t-cells role?
bind to infected cells (when antigens are bound to MCH-1)
release perforin - which makes a hole in the membrane of the infected cells and enzymes result in its destruction
CD4+ t-helper cells role?
Th1, Th2, Th12, tfh
recognise antigens bound to MHC-2
therse activate other immune cells
and sitmulate B-cells to differieniate into plasma cells to produce antibodys
Th1 role
(T-helper cell 1)
activates macrophages
Th2
activates eosinophils
Th-17
activates neutrophils
Tfh
stimulate b-cells
where do B cells get made and where do they mature
both in the bone marrow
b-cells differientiate into?
plasma cells
-> produce antibodys
GAMED
first antibody to be produce
IgM
antibody found in the mucus membranes (respiratory , GI, urogenital tract)
IgA
(mucosal associated lymphod tissue - MALT)
mucus , salvia, tears and breast milk contain IgA
antibody involved in parasite immune responses
IgE
transient hypogammaglobulinema of the infancy occurs when?
< 4
slow to synthesize **IgG **
(huge dip when maternal IgG runs out between 3-6 months)
slow to synthesize **IgG **
(huge dip when maternal IgG runs out between 3-6 months)
transient hypogammaglobulinema of the infancy
XL brutons disease
mutation in B-> burtons tyrosine kinase gene -
< 4 - X linked (boys)
no B-lymphocytes*** -> no plasma cells -> no antibodies
B -> no B cells
no immunoglobulins of ALL classes
hyper IgM syndrome
IgM is the 1st antibody to be produced but cannot class switch
-> high IgM but low IgG and IgA
mutation in CD40 gene (switching gene)
most common primary antibody deficiency
common variable immune deficiency
-> recurrent chest infections and low antibody levels
-> autoimmune disroders
disagnosed once adult usually
‘Selective IgA deficiency’ is a condition commonly associated with?
coeliac disease
undetectable or low serum IgA - with normal IgG and IgM
when is G-CSF injections given
to those undergoing chemo to prevent neutropenia
- is a protein that stimulates bone marrow to produce WBCs and stem cells
causes of acquired neutropenia
cytotoxic drugs
leukaemia
aplastic anaemia
infections
leucocyte adhesion deficiency
leukocytes dont adhere to the enodthelial cells and cant get into tissues
delay in umbilical cord sloughing is associated with
leucocyte adhesion deficiency
deficiency associated with angioedema is linked to what complement
hereditory angioedema deficiency of C1
chronic granulomatous disease occurs when
lackof NADPH oxidase reduces the ability of the phagocytes to produce reactive oxygen species
phagocytes engulf but cannot destroy the pathgogens via phagocytosis
x-linked, penumonitis reoccurs , granulomas
what cells are low in di-george syndrome
CD3
CATCH 22 for digeorge
C- congenital heart disease
A- abnormal faces
T- thymic hypoplasia (thymus is abnormal and does not produce normal CD3 levels)
C- cleft palate
H - hypocalcaemia
22p 11.2 deletion
t-cells affeceted because thymus
Wiskott-aldrich syndrome is dysfunction of? and triad of symptoms
combined B and T cell dysfunction
- recurrent bacterial infections
- eczema
- thrombocytonpania - bleeding
most important allele in minising risk of graft rejection in renal transplant
HLA - DR
describe type 4 sensitivity - time to respond and cell mediated by
Delayed 24-72 hours for reaction
T-cell mediated
how is type 4 sensitivty tested for
skin patch
-> exposure to anitgen for period of time results in contact dermatitis
-> mantoux TB
-> biopsy is rare
how does type 4 reaction occur
dendritic cells present antigens /delivered to CD4+ cells
-> become t helper cells -> cytokines -> macrophages recruited -> proinflammatory cytokines -> localised inflammation
contact dermatitis what kind of sensitivity reaction
4
what is humerol immunity
ChatGPT said:
the aspect of the adaptive immune response that is mediated by antibodies (also called immunoglobulins, Ig). These antibodies are produced by B cells, a type of white blood cell, and are responsible for defending the body against extracellular pathogens like bacteria, viruses, and toxins.
-> b cell activation
Activated B cells differentiate into plasma cells, which produce large quantities of antibodies specific to that antigen.
a. true
b. false
a. true
where is IgA found
Found in mucosal areas (e.g., respiratory and gastrointestinal tracts), provides protection against infections in these areas.
where is IgG found
The most abundant antibody in blood and extracellular fluid, responsible for long-term immunity and protection.
