case 5, itching to get better.docx

8/10/2019 Case 5, itching to get better.docx

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Case 5: Itching to get better.6th November

1. What is an allergen?

Any substance which causes an allergic reaction. Allergens are environmental antigens which provoke a type 1

hypersensitivity reaction. Atopic individuals have a genetic predisposition to development of type 1 hypersensitivity. In

their case harmless antigens stimulate an Ig-E response inappropriately which leads to the allergic reaction.

2.

What is histamine?Histamine (C5H9N3) is released from mast cells and basophils in an allergic reaction. It is made by removing a CO2

molecule from the amino acid histidine with the enzyme L-histidine decarboxylase. It is then inactivated by other

enzymes and stored in granules in mast and basophil cells.

Histamine binds to histamine receptors of which there are 4 types H1- H4, all of which are members of the G protein-

coupled family of receptors. H1receptors are found on most cells but predominantly on smooth muscle, the CNS and

vascular endothelial cells. Binding to H1brings around most of the effects associated with histamine release including

contraction of intestinal and bronchial smooth muscle, increased venule permeability and increased mucus secretion. H2

receptors are bound to adenylate cyclise via another protein and receptor activation stimulates cAMP production and

increases the concentration of Ca2+

Binding of histamine to H2receptors increases vasopermeability and vasodilatation,

stimulates exocrine glands and increases the production of stomach acid. When histamine binds to H 2 receptors a

negative feedback loop is established and degranulation is suppressed. H3 receptors are found in the nervous system

(mainly the CNS). They act as receptors for histamine when it is functioning as a neurotransmitter for histaminergic

neurons. Activation of the receptor leads to inhibition of histamine and cAMP formation, neurotransmitter release and

induction of sleepiness. H4 receptors are highly expressed in bone marrow and white blood cells and regulates

neutrophil release from bone marrow. They are also found in the colon, liver, lung, small intestine, spleen, testes,

thymus, tonsils, and trachea. They mediate chemotaxic signaling from mast cells by decreasing cAMP levels. Inhibition of

H4 receptors can be used to treat allergies and atopic asthma as if the mast cells cant release their cytokines,

lymphocytes dontflock to the area so no inflammatory response is brought about.

Itching caused by histamine is thought to be due to H1 and H4 receptors being stimulated by histamine. H3 antagonists

have the reverse effect and relieve the itching sensation. When histamine and H1 bind, phospholipase C is activated

which increases the amount of Ca2+ in the unmyelinated sensory neurons which causes an action potential to the brain.Activation of H4 receptors also increases Ca2+ levels in the cell. As it exists in sensory neurons an action potential is

triggered. Itch receptors are only found in the epidermis and dermis, mostly in the stratum basale.

3. What is antihistamine?

Antihistamines are also called H1 antagoniststhey counteract the physiological effects of histamine. This is achieved by

competing for the receptors. They suppress the vasodilatation, itching and scratching caused by histamine release.

4. How is histamine involved in the immune response?

Histamine release causes the inflammatory response and constriction of smooth muscle. Its release causes

vasodilatation, increased capillary permeability, increased blood flow to the area and glandular hypersecretion (more

mucus). It is involved in inhibition of lectin- or antigen-induced proliferation of T cells, release of cytokines from T cells,

the induction of cytoxic T cells, cytolysis by mature cytoxic T cells, B cell differentiation, lysozyme enzyme release in

neutrophils, IgE-mediated histamine release from basophils, and in chemotaxic effects on neutrophils and eosinophils.

These actions can be blocked by H2 antagonists. Many of these effects on leukocyte function are inhibitory and can be

seen as anti-inflammatory actions, which can limit antibody hypersensitivity. However, H1 effects of histamine on blood

vessels and skin encourage inflammation and occur during hypersensitivity reactions.

Degranulation occurs when IgE bound to Fc receptors is cross linked by an allergenic antigen. Tyrosine kinase cascade

reactions are initiated which leads to IP3 and DAG production along with Ca2+ being released from the ER. This is

needed to move the granules to the cell membrane where SNARG proteins on the granule and membrane fuse, causing

exocytosis
http://en.wikipedia.org/wiki/Neutrophilhttp://en.wikipedia.org/wiki/Neutrophil


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5. What is Ig-E?

An antibody produced in the lungs, skin and mucosa. Normally makes up 0.05% of serum antibody levels but it is still

capable of providing a very strong response. IgE binds very tightly to Fc receptors on basophils, mast cells and

neutrophils before interacting with antigen. As a result of its binding to basophils and mast cells, IgE is involved in

allergic reactions. Binding of the allergen to the IgE on the cells results in the release of histamine and heparin granules.

IgE levels also rise in parasitic diseases, measuring IgE levels is helpful in diagnosing parasitic infections. Eosinophils have

Fc receptors for IgE and binding of eosinophils to IgE-coated helminths results in killing of the parasite.

Atopic individuals have up to 10x more IgE in their blood which leads to more degranulation of histamine, even when

there is only a small amount of antigen present. Mast cells are primed for histamine release from their long term IgE Fc

interaction.

Somatic rearrangement of antibodies (V (D) J rearrangement) involves the rearrangement of DNA in somatic cells so the

recombined genes are not passes between generations. Therefore each individual has their own unique Ig repertoire.

The process is regulated by enzymes. Exons are rearranged by cleaving the DNA before transcription which leads to a

variety of light and heavy chains being formed.

Somatic hypermutations occur commonly (1x10-3

mutations per base pair per generation). Individual nucleotides are

substituted altering the specificity of the antibody. It is more common in IgG and IgA than in IgM antibodies and affects

the heavy chain more than the light chain.

Type Description

IgAFound inmucosal areas, such as thegut,respiratory tract andurogenital tract,and prevents

colonization bypathogens.Also found in saliva, tears, and breast milk.

IgDFunctions mainly as an antigen receptor on B cells that have not been exposed to antigens. It has

been shown to activate basophils and mast cells to produce antimicrobial factors.

IgEBinds toallergens and triggershistamine release frommast cells andbasophils,and is involved in

allergy.Also protects againstparasitic worms.

IgGIn its four forms, provides the majority of antibody-based immunity against invading pathogens. The

only antibody capable of crossing the placenta to give passive immunity to fetus.

IgMExpressed on the surface of B cells and in a secreted form with very high avidity. Eliminates

pathogens in the early stages of B cell mediated (humoral) immunity before there is sufficient IgG.
http://en.wikipedia.org/wiki/IgAhttp://en.wikipedia.org/wiki/IgAhttp://en.wikipedia.org/wiki/Mucosalhttp://en.wikipedia.org/wiki/Gut_(zoology)http://en.wikipedia.org/wiki/Respiratory_tracthttp://en.wikipedia.org/wiki/Urogenital_tracthttp://en.wikipedia.org/wiki/Pathogenhttp://en.wikipedia.org/wiki/IgDhttp://en.wikipedia.org/wiki/IgDhttp://en.wikipedia.org/wiki/IgEhttp://en.wikipedia.org/wiki/IgEhttp://en.wikipedia.org/wiki/Allergenshttp://en.wikipedia.org/wiki/Histaminehttp://en.wikipedia.org/wiki/Mast_cellshttp://en.wikipedia.org/wiki/Basophilhttp://en.wikipedia.org/wiki/Allergyhttp://en.wikipedia.org/wiki/Parasitic_wormhttp://en.wikipedia.org/wiki/IgGhttp://en.wikipedia.org/wiki/IgMhttp://en.wikipedia.org/wiki/IgMhttp://en.wikipedia.org/wiki/IgMhttp://en.wikipedia.org/wiki/IgGhttp://en.wikipedia.org/wiki/Parasitic_wormhttp://en.wikipedia.org/wiki/Allergyhttp://en.wikipedia.org/wiki/Basophilhttp://en.wikipedia.org/wiki/Mast_cellshttp://en.wikipedia.org/wiki/Histaminehttp://en.wikipedia.org/wiki/Allergenshttp://en.wikipedia.org/wiki/IgEhttp://en.wikipedia.org/wiki/IgDhttp://en.wikipedia.org/wiki/Pathogenhttp://en.wikipedia.org/wiki/Urogenital_tracthttp://en.wikipedia.org/wiki/Respiratory_tracthttp://en.wikipedia.org/wiki/Gut_(zoology)http://en.wikipedia.org/wiki/Mucosalhttp://en.wikipedia.org/wiki/IgA


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9. What are corticosteroids?

Steroids produced in the adrenal cortex from cholesterol to regulate inflammation, carbohydrate

metabolism and blood electrolyte levels. Glucocorticoids control glucose metabolism and

mineralocorticoids influence toe mineral/ H2O balance. They can be

administered as tablets, topically as a cream, by inhalation of a powder or

injected intravenously.

Mechanism: they diffuse through plasma membrane to intracellular receptors

where a hormone-receptor complex is formed, this then enters the

nucleus and interacts with glucocorticoid response elements (withtranscription factors transcription rate is raised or lowered which

changes the metabolic rate. This process takes around an hour from the time of administration. In the

inflammatory response, the glucocorticoid response element causes the production of the enzyme

phospholipase A2which makes arachidonic acid. This is essential for formation of inflammatory mediators such

as histamine.

10. What are emollients?

Substances to soften and soothe the skin. They are often found as ingredients in moisturisers. They relieve

dryness and itching of the skin. Emollients should be applied several times a day during a flare or daily when

not flared up. Apply after any topical steroids as if the other way around the steroid wont be absorbed.

Mechanisms: Occlusion total air and water barrier. Oil layer on surface of skin reduces water loss whichincreases the water content in the stratum corneum. Humectants attract water molecules from the

surroundings by containing hydrophilic groups. Needs to soak into dermis in order to work. Lubricants reduce

friction between the skin and clothing so less epithelium is lost.

11. What is Staphylococcus aureus?

A gram positive, catalase positive (converts H2O2to H2O and O2 distinguishes

staph aureus from enterococci and streptococci), spherical bacteria which is

commonly found on the skin and inside the nose.

If Staph is resistant to methicillin, MRSA is the result. It is resistant as it

produces lactamase which leaves the lactam ring found in all penicillins.

Therefore MRSA must be treated with antibiotics which do not contain the lactam ring, such as vancomycin (a glycopeptides antibiotic). However

vancomycin use is limited to prevent widespread resistance developing. VRSA is

a strain of Staph aureus already resistant to vancomycin.

12. What is a secondary infection of the skin?

One which sets in during/ immediately after treatment for another infection/

disease. E.g. if taking antibiotics the immune system is suppressed so its

easier for other bacteria to take hold.

In atopic dermatitis patients are more susceptible to secondary staph

infections. Staph is usually resistant to penicillins so oxacillin or flucoxacillin

can be used to treat the infection. In secondary Staphylococcal infections,

the bacteria enters the epidermis through a wound boils and scalded skin

syndrome appear. In severe infections staphylococcal endocarditis

(infection of heart valves) and pneumonia may occur.

13. What is interferon?

A glycoprotein secreted into interstitial fluid by lymphocytes in the presence of cells infected with a virus. This

allows 2 enzymes to be produced, 1 which reduces mRNA translation, the other degrades both host and viral

mRNA. It is part of the innate immune system.
http://en.wikipedia.org/wiki/File:Cortisol2.svghttp://en.wikipedia.org/wiki/File:Cortisol2.svghttp://en.wikipedia.org/wiki/File:Cortisol2.svghttp://en.wikipedia.org/wiki/File:Cortisol2.svghttp://en.wikipedia.org/wiki/File:Cortisol2.svghttp://en.wikipedia.org/wiki/File:Cortisol2.svghttp://en.wikipedia.org/wiki/File:Cortisol2.svghttp://en.wikipedia.org/wiki/File:Cortisol2.svg


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14. What is innate immunity?

The innate immune system is non-specific and responds immediately to pathogenic invasion.

It includes phagocytosis, natural killer cells, stomach acid, the cough reflex, digestive enzymes, skin, mucosa and

lysozyme. It usually works in pattern recognition it recognises non self proteins on cell membranes. If the same antigen

enters the body a second time the response will be exactly the same the innate system has no antigenic memory.

Natural Killer Cells (NKCs) are large granular leukocytes which induce apoptosis in APCs. The granules in the cytoplasm

contain special proteins such as perforin and proteases known as granzymes. Upon release in close proximity to a cell

slated for killing, perforin forms pores in the cell membrane of the target cell through which the granzymes and

associated molecules can enter, inducing apoptosis. The NKC is unaffected by this process.

Lysozyme is an enzyme responsible for breaking down the polysaccharide walls of gram positive bacteria. Children fed

infant formula lacking lysozyme in their diet have three times the rate of diarrheal disease. Since lysozyme is a natural

form of protection from pathogens like Salmonella, E. coli, and Pseudomonas, a deficiency due to infant formula feeding

can lead to increased incidence of disease. Whereas the skin is a protective barrier due to its dryness and acidity, the

conjunctiva (membrane covering the eye) is, instead, protected by secreted enzymes, mainly lysozyme and defensin.

However, when these protective barriers fail,conjunctivitis results.

Phagocytosis is a form of endocytosis in which a pathogen is ingested by a leukocyte. The plasma membrane expands

around the particulate material to form large vesicles called phagosomes (10-20times larger than endosome). Only

specialized cells are capable of phagocytosis, whereas endocytosis is carried out by virtually all cells. Once particulate

matter is ingested into phagosomes, the phagosomes fuse with lysosomes and the ingested material is then digested bya process similar to that seen in endocytosis. The so-called "professional phagocytes" include: monocytes &

macrophages, neutrophils, and dendritic cells. There are a few other cells which can be induced to become phagocytic

under certain circumstances (i.e. during intense inflammation); both fibroblasts and epithelial cells are known as "non-

professional" phagocytes.
http://en.wikipedia.org/wiki/Conjunctivahttp://en.wikipedia.org/wiki/Defensinhttp://en.wikipedia.org/wiki/Conjunctivitishttp://en.wikipedia.org/wiki/Conjunctivitishttp://en.wikipedia.org/wiki/Defensinhttp://en.wikipedia.org/wiki/Conjunctiva


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15. What is the adaptive immune system?

It recognises and eliminates specific antigens and members of the same species will have different responses depending

on their personal antibody profile. Immunological memory leads to a heightened response if a second infection occurs,

lifelong immunity can be gained after the first exposure to an antigen. Non-self cells are recognised. Immunity must be

acquired as there isnt physically enough room to have lymphocytes able to make the millions of different types of

antibody that we may, but most likely wont, need during our lifetime.

Humoral response occurs in the blood (B cells), the cell mediated response occurs around infected tissues (T cells).

Antibodies evolved to be able to activate the compliment system (see above), activate phagocytes and to be able to bind

to specific antigens.

Activation of lymphocytes:

The B or T cell encounters their antigen and their behaviour changes form non-dividing to proliferative. This means they

can produce large amounts of antibody or cytokine to help repel the pathogen.

T cells need to see their antigen on the class I MHC molecule.

Lymphocytes: B lymphocytes mature in the bone marrow. They each have a unique antigen receptor on their surface.

When a naive b call encounters its antigen for the first time it rapidly divides to form plasma and memory B cells.

T lymphocytes mature in the thymus gland. During the maturation process they have a T cell receptor appear on their

membranes. T helper cells have the CD4 glycoprotein receptor whilst cytoxic T cells have the CD8 receptor. T cells

recognise antigens when theyre bound to MHC proteins. When they recognise their specific antigen on the MHC

molecule they proliferate rapidly and differentiate into memory and effector cells.Some C3b coated pathogens may bind to macrophages but not be phagocytised. However in the presence of antigens

the pathogen will be taken in and digested as antibody receptors will cross link on the phagocyte. Antibodies are made

by B cells which have differentiated into plasma cells their sole job is to produce large amounts of a specific antibody

to treat the current infection.

Primary infections: when a lymphocyte binds to a

complimentary antigen for the first time, clonal

proliferation occurs. B cells differentiate into plasma cells

and memory cells the plasma cells produce the antibody

to the specific antigen encountered whilst the memory cells

go into storage. They are able to stimulate production of

the antibody much faster should a second infection by the

same organism occur. It may take several days for

significant levels of the antibody to appear in the blood on

the first infection but only a matter of hours in subsequent

infections. The secondary response is of much greater

magnitude as well as being much faster.

Cell mediated immunity: T cells recognise antigens on the

surface of a body cell when bound to the MHC class II

receptors. They then produce cytokines which attract

macrophages, B lymphocytes and dendrites to the antigen

presenting cell. They contain enzymes which digest the APC. Some fragments combine with human leukocyte antigenand are presented on the surface of cell making it recognisable as infected to cytoxic T cells. The T Cthen attaches to the

class I MHC complex and releases interferon which induces apoptosis.


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Maturation of specialised cells in the immune system


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16. What are hypersensitivity reactions?

Type 1 (IgE mediated hypersensitivity): The response is induced by allergens and causes a humoral antibody response.

Plasma cells secrete IgE which binds to Fc receptors on mast/ basophil cells. If there is a second exposure to the antigen,

cross links form between cell bound IgE which causes degranulation of the mast cells and basophils. Histamine, heparin,

prostaglandins and various leukotrines are released. Can be systemic (-> anaphylaxis) or localised (acute inflammation).

Inflammation occurs at a late phase after eosinophils, neutrophils and T H2 build up. Eosinophils bind to the antibody

coated antigen which causes them to release inflammatory mediators.

Type 2 (antibody mediated cytoxic hypersensitivity): antibodies bound to surface antigens activate the complement

system which causes pores to form in the pathogenic cell membrane. The antibodies produced by the immune response

bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self"

antigen, innately part of the patient's cells) or extrinsic (absorbed onto the cells during exposure to some foreign

antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages anddendritic cells

which act as APCs, which causes aB cell to differentiate into a plasma cell which produces antibodies against the foreign

antigen. IgG and IgM antibodies bind to these foreign antigens to form complexes which activate the complement

system which kills cells presenting foreign antigens. Mediators of acute inflammation are generated at the site and MAC

cause celllysis and death. The reaction takes hours to a day.

Another form of type II hypersensitivity isantibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting

the foreign antigen are tagged with IgG or IgM antibodies. These tagged cells are then recognised by natural killer (NK)

cells and macrophages (recognized by the IgG which is bound via the Fc receptors to the effector cell surface receptor)which in turn kill these tagged cells.

Type 3 (immune-complex mediated hypersensitivity): high IgG and IgM antigen levels lead to cross links forming

antibody complexes forming. Tissue damage occurs as cytoxic cells produce lytic enzymes. Soluble antigens which arent

bound to a cell surface bind to antibodies forming free complexes in the blood. Macrophages are very effective at

phagocytising larger complexes but smaller complexes often evade the system. They insert themselves into to cell walls

of blood vessels and joints, inducing an inflammatory response. The complement system is activated which attracts

neutrophils to the area. Lytic enzymes are released with the purpose of digesting the immune complexes however some

tissue damage is inevitable. The process can take hours, days or weeks to develop.

Type 4 (delayed T cell mediated hypersensitivity): CD8 and CD4 cells recognize antigen in a complex with either type 1 or

2 MHC. The APCs in this case are macrophages which secrete Interleukin-12, which stimulates the proliferation of

further CD4 T cells. CD4 T cells secrete Interleukin-2 and interferon gamma, which induces the release of other

cytokines, regulating the immune response. Activated CD8 cells destroy APCs on contact, whilst macrophages produce

hydrolyticenzymes and, on presentation with certain intracellular pathogens, transform into multinucleatedgiant cells.

It usually occurs 24-72 hours after exposure to the antigen.

17. How does breast milk aid development of the immune system?

Contains IgA and other molecules to prevent infection. Provides the infant with a form of passive immunity and is

essential in maintaining infant health. Macrophages and neutrophils are secreted for bacterial defence and E coli

antibodies are passes to the infant to prevent fatal diarrhoea. Milk also contains lysozyme to kill bacteria. If a formula

supplement is used instead of breast milk the infant will have a weakened immune system and will be more likely to

develop allergies and infections. Breast milk is essential whilst the infant builds up their own immune system and B cell

collection. Memory and plasma B cells require an initial antigen exposure before they form so it takes time for the infant

to build up immunity to common environmental antigens.
http://en.wikipedia.org/wiki/Macrophagehttp://en.wikipedia.org/wiki/Dendritic_cellhttp://en.wikipedia.org/wiki/B_cellhttp://en.wikipedia.org/wiki/IgGhttp://en.wikipedia.org/wiki/IgMhttp://en.wikipedia.org/wiki/Complement_membrane_attack_complexhttp://en.wikipedia.org/wiki/Lysishttp://en.wikipedia.org/wiki/Antibody-dependent_cell-mediated_cytotoxicityhttp://en.wikipedia.org/wiki/Major_histocompatibility_complexhttp://en.wikipedia.org/wiki/Interleukin_2http://en.wikipedia.org/wiki/Interferonhttp://en.wikipedia.org/wiki/Hydrolytic_enzymehttp://en.wikipedia.org/wiki/Enzymehttp://en.wikipedia.org/wiki/Giant_cellhttp://en.wikipedia.org/wiki/Giant_cellhttp://en.wikipedia.org/wiki/Enzymehttp://en.wikipedia.org/wiki/Hydrolytic_enzymehttp://en.wikipedia.org/wiki/Interferonhttp://en.wikipedia.org/wiki/Interleukin_2http://en.wikipedia.org/wiki/Major_histocompatibility_complexhttp://en.wikipedia.org/wiki/Antibody-dependent_cell-mediated_cytotoxicityhttp://en.wikipedia.org/wiki/Lysishttp://en.wikipedia.org/wiki/Complement_membrane_attack_complexhttp://en.wikipedia.org/wiki/IgMhttp://en.wikipedia.org/wiki/IgGhttp://en.wikipedia.org/wiki/B_cellhttp://en.wikipedia.org/wiki/Dendritic_cellhttp://en.wikipedia.org/wiki/Macrophage


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18. What is allergy testing?

Process: A microscopic amount of anallergen is introduced to a patient's skin by various means. If an immune-response

is seen in the form of a rash, Urticaria, or in extreme cases anaphylaxis, it can be concluded that the patient has a

hypersensitivity (orallergy)to thatallergen.Further testing can be done to identify the particular allergen. As a control,

known antigens such as histamine are injected. You expect to find a wheal here; if not all negative results are

interpreted as falsely negative.

Scratch test - very commonly used as an allergen test. A similar test involving injecting the allergen is also used, but is

not quite as common due to increased likelihood of infection and general ineffectiveness by comparison. There are

other methods available to test forallergy.Some allergies are identified in a few minutes but others may take several

days depending on the hypersensitivity reaction occurring. In all cases a positive results will show by the skin becoming

raised, red and feeling itchy. A negative test does not mean that the subject is not allergic; simply that either the right

concentration was not used or the body failed to elicit a response.

Prick test - a few drops of the purified allergen are gently pricked on to the skin surface, usually the forearm. This test is

usually done in order to identify allergies to pet dander,dust, pollen, foods or dust mites. Intradermal injections are

done by injecting a small amount of allergen just beneath the skin surface. The test is done to assess allergies to drugs

likepenicillin or bee venom.

Patch test - a large patch which has different allergens on it is applied onto the skin, usually on the back. The allergens

on the patch include latex, medications, preservatives, hair dyes, fragrances, resins and various metals. When a patch is

applied the subject should avoid bathing or exercise for at least 48 hours.Skin end point titration (SET)uses an intradermal injection of allergens of increasing concentrations to measure allergic

response. To prevent a severe allergic reaction, the test is started with a very dilute solution. After 10 minutes, the

injection site is measured to look for growth of wheal, a small swelling of the skin. Two millimeters of growth in 10

minutes is considered positive. If 2 mm of growth is noted, then a second injection at a higher concentration is given to

confirm the response. The end point is the concentration of antigen that causes an increase in the size of the wheal

followed by confirmatory whealing. If the wheal grows larger than 13 mm, then no further injection are given since this

is considered a major reaction.

19. What is Urticaria?

A rash with pale red, itchy bumps usually caused by allergens/ Causes wheals (raised skin with red base). Trigger is

usually allergic with high levels of inflammatory mediators (histamine) which causes the leakage of interstitial fluid from

capillaries. Treated with histamine antagonists.

20. What is angiodema?

Swelling of the dermis, subcutaneous tissue,mucosa and submucosal tissue. Can he allergic, hereditary (autosomal dominant) or

a side effect of medication (ACE inhibitors for high BP). Tue skin swells and it itchy and painful. Urticaria often occurs simultaneously,

except in hereditary angiodema. Treat with antihistamines and avoiding the allergen.

21. What is ichthyosis vulgaris?

An autosomal dominant skin disorder resulting in dry scaly skin. Affects 1/250. Usually develops between 3 months and 5 years.

Symptoms usually fade by puberty but become more severe in old age.

22. Duties of a doctor as a teacher and a learner?

GMC guidelines: Keep professional knowledge and skills up to date.

Drs should be actively involved in teaching, training, appraising and assessing other Drs and students

When involved in teaching Drs should have the correct skills attitudes and practices

Should have knowledge of new laws, codes of practice, treatment guidelines and developments in particular speciality

23. Protocol for involving students in consultations?

Student must be supervised at all times when with patient

Confidentiality most patients realise medical training requires access to patients so will give consent. If trainees are

part of the team treating the patient they are allowed access to records and personal info. If they are not treating the

patient, anonymised data should be supplied or patients consent should be gained before showing the student.

Students shouldnt discuss anything they see or hear with anyone other than their clinical tutor.

Consentask permission for the student to observe the consultation and respect the patients decision. Dont assume

the patient will be comfortable talking openly in front of the studentmay not divulge full information.
http://en.wikipedia.org/wiki/Allergenhttp://en.wikipedia.org/wiki/Rashhttp://en.wikipedia.org/wiki/Urticariahttp://en.wikipedia.org/wiki/Anaphylaxishttp://en.wikipedia.org/wiki/Hypersensitivityhttp://en.wikipedia.org/wiki/Allergyhttp://en.wikipedia.org/wiki/Allergenhttp://en.wikipedia.org/wiki/Allergyhttp://en.wikipedia.org/wiki/Danderhttp://en.wikipedia.org/wiki/Pollenhttp://en.wikipedia.org/wiki/Penicillinhttp://en.wikipedia.org/wiki/Penicillinhttp://en.wikipedia.org/wiki/Pollenhttp://en.wikipedia.org/wiki/Danderhttp://en.wikipedia.org/wiki/Allergyhttp://en.wikipedia.org/wiki/Allergenhttp://en.wikipedia.org/wiki/Allergyhttp://en.wikipedia.org/wiki/Hypersensitivityhttp://en.wikipedia.org/wiki/Anaphylaxishttp://en.wikipedia.org/wiki/Urticariahttp://en.wikipedia.org/wiki/Rashhttp://en.wikipedia.org/wiki/Allergen


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Lecture notescase 5

Autoimmune disease incidence has gone up (MS, type 1 diabetes, rheumatoid arthritis, atherosclerosis,

alzeimhers, Parkinsonsdisease, certain cancers)

Infection

1. Entry to bodyskin, mucosa, mucus secretions, gut bacteria, stomach acid normal barriers

2. Replication and spreading of bacteria within body

3. Disease symptoms

4. Exit from the body and infection of other individuals

Innate

Viral infections within cells lead to interferon production acts on cells for protection and antiviral response

Natural killer cells recognise injected cells and kill them without being damaged in the process. Stops viral replication

Specific

Lymphocytes migrate to lymph nodes

Spleen removes old red blood cells

Antigens are usually proteins but can also be carbohydrates, lipids or DNA

Antibodies recognise part of the antigen

CD8 T cells kill virally infected cells

MHC is a protein complex on the surface of cells which binds to antigen fragments. Reacts with CD8 cells

Memory B cells provide a bigger, faster response to secondary infections

Biological barriers

Skin functions: protection (keratin, innate immune system, physical barrier)

Thermoregulation (capillaries, sweat glands, erector pili muscles for hairs)

Immunological (inflammation, infection control)

Skin epidermis is acidic and dryinhospitable to bacteria. Resident flora includes Staphylococcus (epidermidis and aureus) and

streptococci.

Skin dermis contains fibroblasts, lymphocytes, adipocytes, mast cells, macrophages, nerves, lymphatics, connective tissue,

Pacinian corpuscles, Merkel cells, Meisseners corpuscles, deep and superficial vascular plexuses.


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Defence against infection

0-4 hours after infection: immediate response, preformed immunological mediators

4-96 hours after infection: innate cells recruited

>96 hours after infection: adaptive acquired immune response

The pathogen enters the blood/fluid and encounters a naive B cell (with a very small cytoplasm) with a specific antibody. The B

cell is then activated in the lymph nodes where it differentiates into memory and plasma cells. Plasma cells have a much larger

cytoplasm with lots of endoplasmic reticulum for synthesising the specific antibody required.

Antibodies and immunoglobulin are the same thing. They have 3 heavy and 2 light chains with a variable region for antigens to

attach to. Neutrophils recognise the Fc region at the base of the heavy chains and engulf the pathogen.

In DiGeorge syndrome yo9u have normal IgM and love IgG levels. T cells dont mature as the thymus is absent -> no IgG

produced. IgM production in the B cells is unaffected.

CD8kills virally infected cells

CD4, TH1activate macrophages

CD4, TH2activates B cells -> IgM produced.

Dendritic cells take pathogens to lymph nodes where they present antigens on their surface. Digested pathogen fragments

attach to the MHC class II protein which is then recognised by TH2 cells in order to activate B cells.

Opsonition is essential for neutrophil phagocytosis

CD8 recognises MHC class I.

CD8 cells are activated by MHC I on dendritic cells. They kill by apoptosis. They recognise the pathogen, puncture a hole in its

membrane and release granules into the affected cell. The infected cell dies whilst the CD8 is unaffected.

Normally lysosomes digest phagosomes. TH activated by interferon causes macrophages to digest the pathogen in the

phagosomes.

case 5, itching to get better.docx

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