autoimmune

7/17/2019 Autoimmune

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Autoimmune system 2009

XI/Immune system/Himawati Adiapsari/SMA Negeri Mojoagung/2011| 1

H ND OUT

Lesson : BiologyClass : XI GradesTopic : Immune systems

Duration : 90 MinutesSubtopics : Immune system disorderGoal : To understand the functions of the immune system disorder Teacher : Himawati Adiapsari

Immune system disorders vary from the unserious one, such as allergic, to the more seriousones, such as organ transplant rejection, immunodeficiency, and autoimmune disease.

Allergies

Allergies are exacgerated(hypersensitive) responses to certain antigens called allergens. TheMost common allergies involve antibodies of the IgE.Hay fever for instance, occurs when plasma cellssecrete IgE antibodies specific for antigens on the surface of pollen grains. Some of these antibodiesattach by their base to mast cells in connective tissues. Latter, when pollen grains again enter the body,the attach to the antigen binding sites og IgE on the surface of the mast cell. Interaction with the largepollen grains cross-links adjacent IgE molecules, including the mast cell to release histamine and otherinflammatory agent from granules(vesicles), a process called degranulation. Recall that histamine causedilatation and increased permeability of small blood vessels. Such vascular changes lead to typicalallergiy symptoms: sneezing, runny nose, tearing eyes, and smooth muscle contractions that can resultin breathing difficulty. Drugs called antihistamine diminish allergy symptoms (and imflamation) by

blocking receptors for histamine.

(Source: Chambells 7 th )

Reaksi Fotoalergik from Bramida

Urtikaria





Autoimmune

In some people, the immune system turns against particular molecules of the body., causingautoimmune disease . This loss of tolerance can take some many forms. In systemic lupus

erythematosus , commonly called lupus, the immune system generates antibodies against histones andDNA released by the normal breakdown of body cells. These self-reactive antibodies cause skin rashes,lever, arthritis and kidney dysfunction. Another antibody-mediated autoimmune disease, rheumatoid

arthritis , leads to damage and painful inflammation of cartilage and bone of joints (Figure 1 ).

Type 1 diabetes mellitus , the insulin-producing beta cells of the pancreas are the target of theautoimmune cytotoxic T cells. The most common chronic neurogical disorder in developed countries iaan autoimmune disease – multiple sclerosis . In the disease, T cells infiltrate the central nervous system,leading to destruction of the myelin sheath of that surrounds parts of many neurons

Gender, genetics, and environment influence susceptibility to autoimmune disorders. Forexample, members of certain families show an increased susceptibility to particular autoimmunedisorders. In addition, many autoimmune diseases afflict females more often than males. Women aretwo to three times as likely as men to suffer from multiple sclerosis and rheumatoid arthritis and ninetimes more likely to develop lupus. There has been substantial progress in the field of autoimmunity.For example, we now know that regulatory T cells ordinarily help prevent attack by any self-reactivelymphocytes that remain functional in adults. Nevertheless, much remains to be learned about theseoften-devasting disorders.

The immune system normally distinguishes self from non-self. Some lymphocytes are capable ofreacting against self, but these are generally suppressed. Autoimmune diseases occur when there issome interrupyion of the normal control process, allowing lymphocytes to escape from suppression, orwhen there is an alteration in some body tissue so that it is no longer recognized as self. The exactmechanisms behind autoimmune malfunctions are not fully understood but pathogens or drugs mayplay a role in triggering an autoimmune response in some one who already has genetic predisposition.The reaction are similar to those that occur in allergies, except that in autoimmune disorders thehypersensitivity responses is to the body itself, rather than to an outside substance.





Multiple sclerosis

MS is a progressive immflamatory disease of the central nervus system in which scalteredpatches of myelin in the brain and spinal cord are destroyed. Myelin is the fatty connective tissue

sheath surrounding conducting axons and its destruction result in the symptoms of MS: numbness,tingling, muscle weakness, and paralysis.

MS usually start early and adult life andthe disease is charecterised by a patchy pattern ofdisabilities, often with dramatic unpredictableimprovements. There is a genetic component tothe disease, as relativies of affected people areeight times more likely to contract the disease.

Exertion, Stress and Immune System

Many forms of exertion and stress influence immune system function. Consider, for example,susceptibility to the common cold and other infections of the upper respiratory tract, Moderate exercise

improves immune system function and significantly reduces the ris of these infections. In contrast,exercise to the point of exhaustion leads to more frequent infections and to more severe symptoms.Studies of marathons runners support the conclusion of the exercise intensity is the critical variable.Such runners get sick lessoften than their more sedentary peers during training, a time of moderateexertion, but a marked increase in illness in the period immediately following the grueling race itself.Similarly psychological stress has been shown to disrupt immune system regulation by altering theinterplay of the hormonal nervous, and immune systems.

Immunodeficiency Diseases

A didsorder in which the ability of an immune system protect against pathogens is defective orabsent is called immunodeficiency. An inborn immunodeficiency results from a genetic or developmentaldefect in the immune systems. An acquired immunodeficiency develops later in life following exposureto chemcical or biological agents. Whatever its cause and nature, an immunodeficiency can lead tofrequent and recurrent infections and increased susceptibility to sertain cancers.

Lupus Eritematosus Sistemik ( Bhs. Indonesia)

LES (Lupus Eritematosus Systemik) adalah penyakit peradangan kronik multisistem ygdihubungkan dg ketidaknormalan sistem imun. SLE berpengaruh pd kulit, persendian & membran

serosa (pleura, perikardium), jantung, ginjal, sistem hematologi & neurologi (Lewis et al, 2004)Penyakit autoimun yang melibatkan berbagai organ dengan manifestasi klinis yang bervariasidari yang ringan sampai berat .





Pada keadaan awal, sering sekali sukar dikenal sebagai LES, karena manifestasinya sering tidak terjadibersamaan. Sampai saat ini penyebab LES belum diketahui ada dugaan faktor genetik, infeksi danlingkungan ikut berperan pada patofisiologi LES

Reaksi sistem imun terhadap antigen jaringan sendiri. Antigen tersebut disebut autoantigen

sedang antibodi yang dibentuk disebut autoantibody.Dibagi 2 kelompok:Kelompok ringan : panas , artritis, perikarditis ringan, efusi pleura / perikard ringan, kelelahan

dan sakit kepala.Kelompok berat : Termasuk pada kelompok ini ialah : efusi pleura dan perikard masif, penyakit

ginjal, anemia hemolitik, trombositopenia, lupus serebral, vaskulitis akut,miokarditis, lupus pneumonitis dan perdarahan paru.

Tanda dan gejala Keluhan umum adalah demam, penurunan BB, arthralgia,

kelemahan yang berlebihan. Dermatologi Lesi pembuluh darah di kulit dapat timbul di semua lokasi,

namun paling sering di area kulit yang terpapar sinarmatahari. Reaksi kulit yang berat dapat terjadi pada orangyang fotosensitif

Tanda rash kupu2 didaerah pipi, melewati area hidung dialami oleh 50% pasien dg SLE Ulser pada mulut atau membran nasopharing tjd lebih dari ½ pasien dg SLE. Umum terjadi: gatal pd kulit kepala & rambut rontok, kebotakan (alopesia) dengan atau tanpa

lesi pada kulit kepala.

Rambut dapat tumbuh kembali selama masa penyembuhan, tapi kehilangan rambut dapatmenjadi permanen di sekitar lesi.

Kulit kepala menjadi kering, bersisik & atrofi.

Refference

Biggs,Alton et.all. Biology, The Dynamics of life. Teacher Wraparound Edition. Mc GrawHill,Glencoe.Columbus. 2004. P: 183 -200.

Cambell et. all . Biology. 8 th ed. Pearson Benjamin Cumming. San Francisco. 2008. P: 106 – 109; 933 - 936

Jones,Mary et. All. Biology, As Level and A Level. Second edition. Cambridge University Press. 2007.

P: 124-141

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