PENGENALAN TERHADAP

IMUNOLOGI
DAN
PENYAKIT IMUNOLOGI
RANDANAN BANDASO

H0W ANIMAL
BECOMES IMMUNE
NATURAL AND ARTIFICIAL

IMMUNOLOGY

PENYAKIT IMUNOLOGI
PENYAKIT YANG DITIMBULKAN
RESPONS IMUNOLOGI DAN
GANGGUAN SISTEM IMUNOLOGI

INFECTION

IMMUNITY

INSEPERABLE

NATURAL RESISTENCE
ANATOMIC BARRIER
PHAGOCYTOSIS
COMPLEMENT
NUTRTIONAL
HORMONAL
GENETIC

BAKTERI,VIRUS, PARASITES

INFECTION UN COMMON

HOST DEFENCE
LOCAL
SYSTEMIC
NONSPECIFC
HUMORAL
CELLULAR

SISTEM PERTAHANAN TUBUH

DUNIA INI PENUH DENGAN
MIKROORGANISME YANG MEMBAHAYAKAN
KITA
KARENA ITU SEJAK LAHIR MANUSIA
DIPERLANGKAPI DENGAN SISTEM
KEKEBALAN
KADANG-KADANG SISTEM KEKEBALAN INI
TIDAK BERJALAN DENGAN BAIK

KEJADIAN 1:26-27-28
26. Berfirmanlah Allah: Baiklah kita
menjadikan manusia menurut gambar
dan rupa Kita..
27. Maka Allah menciptakan manusia itu
menurut gambarNya, menurut gambar
Allah diciptakanNya dia; laki-laki dan
perempuan.
28. Beranak cuculah dan bertambah
banyak.

NONSPESIFIK IMMUNITY
BODY SURFACE
DISCHARGE MICROORGANISM
FROM THE BODY
LOCAL PRODUCTION OF CHEMICAL
ANTIMICROBES
BACTERIAL INTERFERENCE
LACTOBACILLUS

BODY SURFACE
MICROORGANISME TO PRODUCE
INFECTION SLIP TO BARRIER
SURFACE DEFENCES
THIKNES OF EPITHELIAL IS DIFFER
NONSPECIPIC

DISCHARGE
OF MICROORGANISME
FROM THE BODY
MUCOCILIARY ESCALATOR OF THE RESPIRATORY
TRACT OROPHARYNX COUGHED OR
SWALLOWED
DESQUAMATION OF EPITHELIAL CELL REMOVED
LARGE AMOUNT OF BACTERIA
DEFECATION ELIMINATE 10.000 000 000 000 /DAY
URINATION ELIMINATE BACTERIAL COLONIZING
IN URETHRAL EPITHELIUM RETENTION OF URINE
ENHANCE THE RISK OF INFECTION
SALIVATION, LACRIMATION, SNEEZING DISPLACE
POTENTIALLY INFECTIVE MICROORGANISME

MAN
OBSERVED
RECOVERY FROM INFECTION
IMMUN

JENNER : VACCINATION OF SMALL FOX

SUCCESFULL APLICATION OF OBSERVATION

HISTORY OF IMUNOLOGY
ZAMAN PURBA : SEMBUH DRI PNYKT SULIT KENA PENYAKIT ITU
SEB.MASEHI : VARIOLATION (AMBIL KEROPENG CACAR)

1798 EDWARD YENNER : COWPOX VACCINATION

1880 LOUIS PASTEUR: ATTENUATED VACCINES

1900 KARL LANDSTEINER ABO

1975 MILSTEINAND KOHLER
MNCLNL ANTIBODI

NOBEL PRIZE WINNERS

IN IMUNOLOGY
1901 1984

11 NOBEL PRIZE
WINNER.
1901 EMIL VON BEHRING SERUM
THERAPY.
1984 KOHLER AND MILSTEIN
MONOCLONAL ANTIBODIES

SISTEM IMMUNITAS
SISTEM IMUNITAS
ORGAN IMUNITAS:
SUM-SUM TULANG
THYMUS
GALT =GUT ASSOCIATET LY.TIS.
MALT = MUCOSA -BURSA FABRICUS

SEL-SEL SISTEM IMUN

LIMFOSIT T
LIMFOSIT B
MAKROFAG
SEL DENDRITIC DAN LANGERHANS
NATURAL KILLER CELL (SEL
PEMBUNUH ALAMIAH)

SISTEM IMUNITAS
KOMPLEMEN

SUM-SUM TLG

SEL T

THYMUS

SEL B

BURSA
FABRICUS
GALT
MALT

KILLER CELL
MAKROPHAG

INFEKSI

GANGGUAN GIZI

A
M
S
A
L
P
NEO

SEBAB
MANUSIA
SAKIT

K
I
L
O
B
A
ET

GANGGUAN SISTEM IMUN

DEGE
NERA
TI

GE
NE
TIK

REAKSI
BERLEBIHAN

HYPERSENSITIVITAS

PENIMBUNAN IG

AMYLOIDOSIS

RESPONSE IMUN

DEF.IMUN

AUTOIMUN

RESPONS IMUN SEPERTI PEDANG BERMATA DUA

BISA MERUGIKAN/BERBAHAYA

SANGAT BERMANFAAT

HYPERSENSITIVITAS:
1.TIPE 1 (TIPE ANAFILAKTIK)
2.TIPE 2 (TIPE SITOTOKSIK)
3.TIPE 3 (IMUNOKOMPLEKS)
4.TIPE 4 (CELL-MEDIATED)

REAKSI TIPE 1:
SISTEMIK
TERJADI SESUDAH
PEMBERIAN PROTEIN ASING

LOKAL

ATOPIC ALERGY

SIFAT-SIFAT REAKSI TIPE 1

REAKSI IMUNOLOGIK YANG CEPAT
TERJADI DALAM BEBERAPA MENIT
SESUDAH KOMBINASI ANTIGEN DAN
ANTIBODI
ANTIBODI MELEKAT PADA MAST CELL
DAN BASOFIL
PADA INDIVIDU YANG SUDAH SENSITASI
SEBELUMNYA

SIFAT REAKSI TIPE 1

ANTIGEN:
PROTEIN ASING (ANTISERA)
HORMONES , ENZYMES
POLYSACHARIDES ,OBAT.
BERATNYA REAKSI TERGANTUNG LEVEL
SENSITASI
BESARNYA SCHOK DOSE BISA KECIL
SEKALI
BISA MEMBAWA KEMATIAN

LOCAL ANAPHYLAXIS
DISEBUT JUGA ATOPIC ALLERGY
10% DARI PENDUDUK
ALLERGENS:
SERBUK BUNGA DEBU RUMAH
BULU BINATANG IKAN
RIWAYAT KELUARGA 50%
SERUM IgE LEBIH TINGGI

LOCAL REACTION
SKIN CONTACT ANTIGEN
URTICARIA
GASTROINTESTINAL INGESTION
DIARHEA
LUNG INHALATION
BRONCHOCONTRICTION
NOSE INHALATION RHINITIS

ALLERGEN

REAKSI

GATAL
TERSUMBAT
KELUAR CAIRAN
BERSIN

RHINITIS ALLERGICA

SYSTEMIC REACTION
PARENTRAL ADMINISTRATION
WITHIN MINUTES ITCHING AND
URTICARIA RESPIRATORY
DIFFICULTY VOMITING,
ABDOMINAL CRAMPS DIARHEA
SYSTEMIC
VASODELATATIONCIRCLATORY
COLLAPSE DEATH

KONTAK PERTAMA :

SENSITASI---PRODUKSI IgE

PELEPASAN MEDIATOR

Antigen
SIGNALS SITOKIN
SIGNALS UTK
AKTIVASI
PHOSPHOLIPASE A2

PHOSPHOLIPASEA2

Ige
Signal
Granules

ACTIVE PHOSPHOLIPASEA2

MEMBRAN
PHOSPHOLIPID

Degranulation

MEDIATOR
PRIMARY MEDIATOR:
DALAM GRANULA MAST CELL
SECONDARY MEDIATOR:
LIPID MEDIATOR
CYTOKINES

PRIMARY MEDIATOR
BIOGENIC AMINES:
HISTAMINE: KONTRAKSI
OTOT POLOS, SEKRESI NASAL,
BRONCHIAL.LAMBUNG MENINGGI ADENOSINE
MENINGKATKAN MEDIATOR MAST CELL,
MENGHAMBAT AGREGASI PLATELET
CHEMOTACTIC
ENZYMES
PROTEOGLYCANS

SECONDARY MEDIATOR
LEUKOTRIENES LEUK.C4 DAN D4
VASOAKTIF/SMOGENIC. LEUK.B4
CHEMOTACTIC KUAT UTK EOS,NEUT
DAN MONOCYTE
PROSTAGLANDIN
PROST.D2
BRONCHOSPSM+ MUCUS
SECR.

SECONDARY MEDIATOR
PAF
PLATELET AGREGATION,
RELEASE HIST-->BRONCHOSPA
VASODELATATION
CYTOKINES
TNF
IL1,IL3,IL4,IL5.IL6

SITOKIN YANG MENGATUR REAKSI TIPE1

SINTESIS IgE
IL4,IL5,IL6->PRODUK
TH2--> SUBSET CD4 IFGAMMA
-->PRODUK TH1 DOWN REGULATE.
MAST CELL GROWTHIL3,IL4
EOS. GROWTH AND ACTIVATION . IL5
DARI TH2

ANAPHYLACTOID

CYTOKINES (IL8)
CODEINE,MORPHINS
MELLITIN (IN BEE VENOM)
PHYSICAL STIMULI:
HEAT,COLD, SUNLIGHT
STRES ? LIHAT MERTUA SESAK !

HYPERSENSITIVITAS II
TERJADI OK ADANYA ANTIBODI
TERHADAP ANTIGEN PADA
PERMUKAAN SEL ATAU KOMPONEN
JARINGAN
ANTIGEN:
INTRINSIK
EXOGEN

HIPERSENSITIVITAS TIPE 2
COMPLEMENT- DEPENDENT
REACTIONS (REAKSI TERGANTUNG
KOMPLEMEN)
ANTIBODY- DEPENDENT CELL
MEDIATED CYTOXICITY
ANTIBODI MEDIATED CELLULAR
DYSFUNCTION

JENIS REAKSI (1):

1.COMPLEMENT DEPENDENT
REACTION:
ANTIBODI + ANTIGEN ---->
AKTIVASI KOMPONEN ---->
MEMBRANE ATTACK KOMPLEX
FIKSASI ANTIBODI ATAU COMPL
C3B--> OPSONISASI.

JENIS REAKSI (2):

ANTIBODY DEPENDENT CELL
MEDIATED CYTOXITY (ADCC)-->
TIDAK BUTUH PHAGOCYTOSIS.
LYSIS DILAKUKAN OLEH
MONOSIT, EOS, NEUT YANG
PUNYA FC RESEPTOR.

KLINIK TIPE II
REAKSI TRANSFUSI
ERYTHROBLASTOSIS FOETALIS
AHA (AUTOIMMUNE HEMOLYTIC
ANAEMIA)
DRUG REACTION
MYASTHENIA GRAVIS DAN GRAVE
DISEASE

REAKSI TIPE II
A. Complement dependent

Target cell
Opsonic adherence
and phagocytosis

AF
AR
SY

ACETHYLCHOLINE

MYASTHENIA GRAVIS
TUBUH MEMBUAT
ANTIBODI
TERHADAP RESEPTOR
ACTH
OTOT

DIPECAH
ACETHYLCHOLINESTRASE

ANTIBODY
TO
TSH RECEPTOR
EXCESS
PRODUCTION
THYROID
HORMONE
TSH
RECEPTOR

THYROID CELLS

TYPE II HYPERSENSITIVITY GRAVES DISEASE

AYAH
(DD,Dd)

ERYTHROBLASTOSIS
(IBU MEMBUAT
ANTIBODI THD ANAK)

IBU
(dd)

ANAK I
(Dd)
Rhesus+

LAHIR HIDUP
ANAK BERIKUT
LAHIR MATI
(SEL DARAH MERAH
LYSIS)

REAKSI TIPE III

DIINDUKSI KOMPLEKS ANTIGENANTIBODI YANG MENYEBABKAN
KERUSAKAN JARINGAN, SEBAGAI
AKIBAT KEMAMPUANNYA UNTUK
MENGAKTIFKAN MEDIATOR SERUM
TERUTAMA KOMPLEMEN.

HYPERSENSITIVITAS (TIPE III)

SISTEMIK .
SYSTEMIC IMMUNE COMPLEX
DISEASE

LOKAL.
LOCAL IMMUNE COMPLEX
DISEASE (ARTHUS REACTION)

REAKSI TIPE 3
ANTIGEN : EXOGEN-ENDOGEN
LOKAL ATAU SISTEMIK
TIGA PHASE:
1.PEMBENTUKAN AGAB
KOMPLEKS DLM SIRKULASI
2.DEPOSISI AG-AB KOMPLEKS
3.REAKSI INFLAMASI
TEMPAT PENIMBUNAN AG-AB KOMP
GINJAL, SENDI, KULIT, JANTUNG,
P.DARAH KECIL.

REAKSI TIPE III

FASE 1

B CELL

ENDOTHEL

ANTIGEN-AB
COMPLEX

PLASMA
CELL

FREE ANTIBODY

AG-AB COMP

PHASE 2
MAST CELL

PHASE 3 :COMPL.MEDIATED IMFL.

COMPLMNT

PLATELET
AGREGATE

PMN

DEG.FIBRINOID
LYSOSOME

IMMUNE COMPLEX VASCULITIS

TYPE IV HYPERSENSITIVITY
(CELL MEDIATED)

DELAYED TYPE HYPERSENSITIVITY

TRANSPLANT REJECTION
MECHANISM INVOLVED IN REJECTION
METHODS OF INCREASING GRAFT
SURVIVAL
TRANSPLANTATION OF OTHER SOLID
ORGANS
TRANSPLANTATION OF
HEMOTOPOETIC CELLS

REAKSI TIPE IV
DIINDUKSI SEL T YANG SUDAH
DISENSITASI
2 TIPE: KLASIK: CD4+ TCELL
DIRECT CYTOTOXITY--> CD8+
TCELL.
M.TBC,VIRUSES, FUNGI, PROTOZOA
DAN PARASIT

REAKSI TIPE4 KLASIK

REAKSI TUBERKULIN
PROTEIN LIPOPOLYSACHARIDE
(M.TBC).
SENSITASI 8-12 JAM INDURASI,
MAKSIMAL 24-72 JAM.
PROSES TERJADINYA:
CD4+TCELLS--> KONTAK ANTIGEN -->
TH1 CELL.

REAKSI TIPE 4 (DIRECT)

CD8+TCELLS KILLS
ANTIGENBEARING TARGETCELL
DISEBUT CYTOTOXIC T
LYMPHOCYTE (CTLs)
CTLs BERPERAN PADA: GRAFT
REJECTION RESISTENSI THD
VIRUS TUMOR IMMUNITY

PROSES PEMBENTUKAN
GRANULOMA

LYMPHOCYT

MACROPHAGE

SITOKIN PADA REAKSI TIPE4

MACROPHAGE SERANG M.TBC

MACROPHAGE HASILKAN IL12
IL12-->CD4TCELLS --TH1 CELLS.
TH1 CELLS -> IFN GAMMA ----->AKTIFKAN
--> MACROPHAGE -->
FIBROSIS.
IL2--AUTOCRINE/PARACRINE
TNF ALPHA DAN LIMFOTOXIN-->
VASODELATASI, ADHESION,
CHEMOTACTIC

SKEMA
PENGHANCURAN
GRAFT

ACUTE CELLULAR REJECTION

OF RENAL
ALLOGRAFT
MANIFEST BY
A DIFFUSE
MONONUCLEAR
CELL
INFILTRATE AND
INTERTITIAL
EDEMA

MONONUCLEAR

REAKSI PENOLAKAN
TRANSPLANTASI
GINJAL SECARA
HUMORAL

INTIMA MENEBAL
PERADANGAN
ACUTE VASCULITIS
INTIMA MARKEDLY
THICKENED AND
INFLAMED

AUTOIMMUNE DISEASES

IMMUNOLOGIC TOLERANCE
MECHANISM
SISTEMIK
ORGAN TUNGGAL

PENYAKIT AUTOIMUNE:
PENYAKIT KARENA RESPONSE IMUN
TERHADAP DIRI SENDIRI
KRITERIA: 1.ADANYA REAKSI
AUTOIMUN. 2.SECARA KLINIK
MAUPUN EXP
DAPAT DIBUKTIKAN
BUKAN
REAKSI AKIBAT
KERUSAKAN
JARINGAN. 3.TIDAK
ADANYA PENY.PENYAKIT LAIN.

MEKANISME AUTOIMUN:
HILANGNYA TOLERANCE
MODIFIKASI MOLEKUL
KOMPLEKS
SELF AG.<-->OBAT ATAU M.ORG.
MOLECULAR MIMICRY
POLYCLONAL LYMPHOCYTE
ACTIVATIVATION
IMBALANCE SUPRESSOR-HELPER T
CELL FUNCTION
SEQUESTERED ANTIGEN

SKEMA KEMUNGKINAN MEKANISME TOLERANSI

A.CLONAL DELETION

B.CLONAL ANERGY

C.SUPRESSION

IMMUNOKOMPETENT
CELLS
KENAL
TIDAK DIKENAL
TIDAK ADA REAKSI

AHA

TERJADI REAKSI

LYSIS

ANTI INSULIN RECEPTOR

INSULIN
RESISTENT
DIABETES

INSULIN RECEPTOR

YUVENILE INSULIN DEPENDENT DIABETES

ANTI INSULIN
ANTI ISLET CELLS

ISLET CELLS OF LANGERHANS

PRODUKSI INSULIN

LUPUS
ERYTHEMATOSUS

CONCENTRIC
PERIARTERIAL
FIBROSIS
IN
THE SPLEEN

LUPUS NEPHRITIS DGN FOCAL NEKROSIS PD JAM 11 DAN 14

SYSTEMIC SCLEROSIS :
.Thinning epidermis .No appendages .Dense collagen

ADVANCE SYSTEMIC SCLEROSIS. A CLAW LIKE FLEXION DEFORMITY

INFERTIL
AB THD
SPERMATOZOA

ANTIGEN KONTAK
IMMUNOKOMPETENT
CELLS

SPERMATOZOA
(SEQUESTER
ANTIGEN

RUSAK

SEQUESTER
ANTIGEN
TIDAK DIKENAL

RUSAK

IMMUNOCOMPETENT CELLS

SURFACE
ANTIGEN
DIKENAL

HASHIMOTO THYROIDITIS

ANTIBODI

PARIETAL CELLS

RESORBSI VI B12

ANAEMIA
PERNICIOSA

ANTIMELANOSIT

VITILIGO

MELANOSIT

M E L A N I N

RHEUMATOID ARTHRITIS
IS A SYSTEMIC, CHRONIC INFLAMATORY
DISEASE AFFECTING MULTIPLE TISSUE
BUT PRINCIPALLY ATTACKING THE
JOINTS TO PRODUCE NONSUPPURATIVE
PROLIFERATIVE SYNOVITIS THAT
FREQUENTLY PROGRESSES TO
DESTROY ARTICULAR CARTILAGE AND
UNDERLYING BONE WITH RESULTING
DISABLING ARTHRITIS

EXTRA ARTICULAR
INVOLMENT OF R.A.
SKIN
HEART
BLOOD VESSELS
MUSCLES
SKIN
LUNGS
RESEMBLE SLE OR SCLERODERMA

R.A.
PREVALENCE 1%
3-5 X MORE COMMON IN WOMAN
PEAK INCIDENCE SCOND
FOURTH DECADE OF LIFE
NO AGE IS IMMUNE

PATHOGENESIS
OF CHRONIC SYNOVITIS
SYNOVIAL CELL HYPERPLASIA
DENSE PERIVASCULER INFLAMATORY CELLS
INCREASED VASCULARITY DUE O
ANGIOGENESIS
NEUTROPHYL AND ORGANIZING FIBRIN IN THE
SURFACE
INCREASED OSTEOCLAST ACTIVITY
FORMATION OF PANNUS
FIBROSIS AND CALCIFICATION
PERMANENT ANKYLOSIS

PENYAKIT IMUNODEFISIENSI
PRIMER: AGAMMAGLOBINEMIA OF
BRUTON.
DIGEORGES SYNDROME SEVERE COMBINED
IMMUNODEFICIENCY DISEASE (SCID)
KERUSAKAN PADA B,T,STEM CELL, KOMPLEMEN.
SEKUNDER:
AIDS, MALNUTRISI, AGING,
IMMUNOSUPRESSIVE-RADIASI

IMUNODEFISIENSI PRIMER:
X LINKED AGAMMA GLOBINAEMIA OF
BRUTON
ISOLATED IgA DEFISIENCY
DI GEORGE SYNDROME
SWISS TYPE AGAMMAGLOBINAEMIA
SEVERE COMBINED ID (SCID)
WISKOT ALDRICH SYNDROME
GENETIC DEFICIENCY OF THE COMPLEMENT
SYSTEM.

BRUTON DISEASE:

TIDAK ADA IG DI SERUM

X LINKED TERBATAS PADA PRIA
INFEKSI MULAI PADA UMUR 8-9 BLN
INFEKSI PALING SERING ADALAH
INFEKSI PYOGENIK STAPH,HAEMP)
CONJUNCTIVITIS, PHARINGITIS, OM,
BRONCHITIS, P.MONIA, INF.KULIT
DLM DRH DAN KEL.LYMPHE SEL B
TIDAK ADA.

DI GEORGES SYNDROME
T CELL DEFICIENCY
THYMUS DAN PARATHYROID TIDAK
BERKEMBANG
KEKEBALAN SELLULER HILANG
RENTAN INF.JAMUR DAN VIRUS
TETANY

SWISS TYPE A
GAMMAGLOBINAEMIA (SCID)
KOMB DEF.SEL T DAN SEL B
INFEKSI REKURENS:
CANDIDA, PNEMOCYTIS CARINI,
PSEUDOMONASVIRUS DAN
BAKTERI.
MATI DALAM TAHUN I, BILA TIDAK
TRANSPLANTASI SUM-SUM TULANG

IMMUNODEFISIENSI DENGAN
TROMBOSITOPENI DAN EKSEMA
THROMBOYTOPENIA, ECZEMA
RENTAN INFEKSI REKUREN--> KEMATIAN
AWAL.
DEFEK IMUNOLOGIK SULIT DITERANGKAN
DEPLESI LIMFOSIT PADA DARAH PERIFER
DAN KEL.LIMPHE.
IgM RENDAH, IgG NORMAL, IgA DAN IgE
MENINGGI

AIDS
DITEMUKAN PERTAMA KALI JUNI 1981
DI LOS ANGELES AS
IMMUNOSUPRESSION
OPPORTUNISTIC INFECTION
SECONDARY NEOPLASM NEUROLOGIC
MANISFESTATION
1993
300.000 KASUS POSITIF
PHENOMENA GUNUNG ES
AFRICA PALING BANYAK

EPIDEMIOLOGI
1994 ----> 163 NEGARA
FIVE HIGH RISK GROUPS: HOMOSEXUAL
AND BISEXUAL MAN
INTRAVENOUS
DRUG ABUSER
HEMOPHILIAC
RECIPIENT OFBLD AND B.CMPNENT.
HETEROSEXUAL CONTACT WITH
OTHER HIGH RISK GROUP.

ETIOLOGI:
A HUMAN RETROVIRUS FELINE IV,
SIMIAN IV, VISNA VIRUS OF SHEEP.
LONG INCUBATION PERIODE --> FATAL
OUTCOME
TROPISM FOR HAEMOTOPOETIC AND
NERVOUS SYSTEM
ABILITY TO CAUSE IMMUNOSUPRESSION
CYTOPHATIC EFFECT IN VITRO

HIV VIRION

HIV INFECTION

CLINICAL LATENCY

CLINICAL SYMPTOMS

IMMUNOPATHOGENESIS OF HIV INFECTION

CD4+T CELLS AND MACROPHAGES ARE THE MAYOR TARGET OF HIV
INFECTION OF THESE TWO CELLS LEAD A MARKED LOSS OF CD4+TCELL
DISSEMINATION OF HIV TO VARIOUS TISSUE ESPECIALLY THE CNS

DECREASED:
RESPONSE TO SOLUBLE ANTIGEN
LYMPHOKINE SECRETION

HIV

DIMINISHED CYTOTOXIC ABILITY

DECREASED CHEMOTAXIS
REDUCED IL1 SECRETION
POOR ANTIGEN PRESENTATION

MACROPHAGE

DEPRESED
IG PRODUCTION
IN RESPONSE
TO NEW ANTIGEN

DECREASED SPECIFIC
CYTOTOXITY
DECREASE KILLING
OF TUMOR CELL

HIV INFECTION
FORMATION OF
GIANT CELL
IN
THE BRAIN

TYPICAL COURSE OF HIV INFECTION

AMYLOIDOSIS
SUBS.PROTEIN ABNORMAL
YANG DIDEPOSISI DIANTARA
SEL PADA BERBAGAI
JARINGAN DAN ORGAN,
DENGAN GEJALA KLINIK
YANG BERVARIASI

AMILOID:
95% FIBRIL PROTEIN
05% P COMPONENT, GLYCOPROT
AMILOID PROTEIN (15):AL
(AMYLOID LIGHT CHAIN) DARI
PLASMA CELL --> Ig LIGHTCHAIN
AA (AMYLOID ASSOCIATED)
PROTEIN DISINTESIS DI HATI

DEPOSITS
OF AMILOID

AMYLOIDOSIS

DEPOSITS OF
AMYLOID

AMYLOIDOSIS
OBSERVED BY POLARISING
MICROSCOPE

AMYLOIDOSIS OF THE KIDNEY. THE GLOMERULAR

ARCHITECTURE IS ALMOST TOTALLY OBLITERATED
BY MASSIVE ACCUMULATION OF AMYLOID

AMYLOIDOSIS
OF AGING
IN THE HEART
AMYLOID

MYOCARDIAL
FIBERS

the

Selamat Belajar
end SEMOGA SUKSES