11.Jejas Dan Adaptasi

8/12/2019 11.Jejas Dan Adaptasi

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INJURY AND ADAPTATION

PROCESSES

Department of Anatomic Pathology

Fac. of Medicine Gadjah Mada University


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DEFINITION

Pathology is a discipline bridging clinical practiceand basic sciences

Identify changes in cells and tissues morphology

diagnoses and therapy

Focus of pathology:

etiology ( cause )

pathogenesis

pathways by which morphologic changes occurs


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DEFINISI

Patologi adalah menjembatani disiplin praktek klinis dan

ilmu dasar

Identifikasi perubahan dalam jaringan sel dan morfologi -

diagnosis dan terapi

Fokus patologi:etiologi (penyebab)

patogenesis

jalur dimana terjadi perubahan morfologi


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CELLULAR RESPONSES AGAINST INJURY

Cells

Cellular adaptations

Physiologic stresses/ pathologic stimuli

Adaptive responses:atrophy, hypertrophy, hyperplasia, metaplasia

Cellular injury

Adaptive capability is exceeded

Reversible injury Irreversible injury

Dies: apoptosis and necrosis


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Causes of cellular injury :

HypoxiaPhysical agents

Chemicals and drugs

Microbiologic agents

Immunologic agentsGenetic defects

Nutritional imbalances

Aging


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Hipoksia

Agen fisik

Bahan kimia dan obat-obatan

Microbiologic agenKekebalan agen

Cacat genetik

Ketidakseimbangan giziPenuaan


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Hipoksia

Menghilangkan / kehilangan suplai darah

Penyempitan / penyumbatan pembuluh darah

Mengurangi pasokan oksigenKegagalan respirasi cardio -

Jantung

Penyakit paru-paru

Berkurang / hilangnya daya oksigenHbCO stabil CO

Efek: tergantung pada derajat stres


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DRUGS AND CHEMICAL SUBSTANCES

Toxic agentcellular deathtissue death

Non toxic agent: glucosahigh osmotic pressure

cellular injury

Specific target of chemical substance:

absorption, transportation, metabolism, excretion

-barbituratliver damage due to degradation/metabolism process

- mercurichlorida stomach(absorption), colon

and kidney ( excretion)


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NARKOBA DAN KIMIA ZAT

Beracun agen jaringan seluler mati-

mati

Non toxic agent: glucosa - tekanan

osmotik tinggi cedera selular

Sasaran spesifik zat kimia:

penyerapan, transportasi,

metabolisme, ekskresi

- Barbiturat kerusakan hati akibat

degradasi / proses metabolisme- mercurichlorida perut

(penyerapan), kolon dan ginjal

(ekskresi)


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Microbiologic agents Virus:

Cytolytic/cytophaticcellular death

Oncogenic ->>> proliferation -- neoplasm

Bacterie Exotoxin

Endotoxin

Lecitinasedamage of cell membrane Hemolysin -> hemolysis

Fungi actinomycosis

- Parasite- Amoeba, malaria, toxoplasm

Worm Filaria dll


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Microbiologic agen

Virus:

Cytolytic / cytophatic kematian sel

Onkogenik ->>> proliferasi - neoplasma

Bacterie

Eksotoksin

EndotoksinLecitinase kerusakan membran sel

Hemolysin -> hemolisis

Jamur

actinomycosis

Parasit

Amuba, malaria, toxoplasmCacing

Filaria dll


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Physical agent:

Cold

vasoconstrictionblood supply burn ulcer cardiac arytmia


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Fisik agen

Dingin

vasokonstriksi aliran darah


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Immunologic reaction

anaphylactic reaction

Genetic defects

Defect congenital

Hemoglobin S of sickle cell anemia

Nutritional imbalances Protein calorie insufficiency, obesity

Atherosclerosis

Aging

acumulation of subletal injury -> decreased of

cellular responses


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Reaksi kekebalan

reaksi anafilaksis

Cacat genetik

Cacat bawaanHemoglobin S dari anemia sel sabit

Ketidakseimbangan gizi

Kekurangan kalori protein, obesitas

AterosklerosisPenuaan

acumulation dari cedera subletal -> penurunan

dari tanggapan selular


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Mechanisms of cell injury

Most forms of cell injury to ultimate cell death have

proved difficult to dissect, because:

* not all of injuries invariably fatal

* it is difficult to distinguish the primary target of

injury from any secondary ripple effects

* no precise cut-off point to establish cause and effect


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Sebagian besar bentuk cedera sel utama

kematian sel memiliki

terbukti sulit untuk membedah, karena:

* Tidak semua luka selalu fatal

* Sulit untuk membedakan target utama

cedera dari setiap sekunder efek riak

* Tidak tepat cut-off point untuk menentukan

sebab dan akibat


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There are a number of generalizations

The cellular responses to injurious depends on the typeof injury, its duration, and its severity

The consequences of injury are also dependent on the

typeof cell, its current status, and its adaptability Four intracellular systems are vulnerable:

1.cell membrane integrity

2. aerobic respiration

3. protein synthesis

4. the integrity of genetic aparatus

. Oxygen , oxygen derived free radicals and failure ofintracellular calcium homeostasis


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Tanggapan selular untuk merugikan tergantung pada

jenis cedera, dengan durasi, dan tingkat keparahan

Konsekuensi dari cedera juga tergantung pada jenis sel,

status saat ini, dan kemampuan beradaptasi

Empat sistem intraselular yang rentan:1. integritas membran sel

2. respirasi aerobik

3. sintesis protein

4. integritas aparatus genetik. Oksigen, oksigen radikal bebas yang berasal dan

kegagalan homeostasis kalsium intraselular


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Irreversible cell injury


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Mechanisms of irreversible injury: Inability to reverse mitochondrial dysfunction causing

marked ATP depletion

Development of profound disturbances in membranefunction

Several biochemical mechanisms may contribute tomembrane damage:

1. Loss of membrane phospholipids 2. Mitochondrial dysfunction

3. Cytoskeleton abnormalities

4. reactive oxygen species 5. Lipid breakdown products

6. Loss of intracellular amino acids


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Mekanisme dari cedera ireversibel:

Ketidakmampuan untuk membalikkan disfungsi

mitokondria menyebabkan ATP ditandai penipisan

Pengembangan mendalam gangguan dalam fungsi

membranBeberapa mekanisme biokimia dapat menyebabkan

kerusakan membran:

1. Hilangnya fosfolipid membran

2. Disfungsi mitokondria3. Sitoskeleton kelainan

4. spesies oksigen reaktif

5. Produk pemecahan lipid

6. Kehilangan asam amino intraselular


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Oxygen free radicals: Superokside : O2

-

Hidrogenperoksida : H2 O2 Ion hidroksil : OH *

Hydrogen peroxide

O2-+ O 2- + 2 H +SOD

H 2O2 + O2 Superoksid { O2

-} + enzym ( xanthine oxidase,cytochrome P-450, dll )

Hidroksil [OH *]- water hydrolysis due to ion radiation

H2O H* + OH*

- Fenton reaction:

Fe+++ H2 O2 --- Fe+++ + OH * + OH - Haber-Weiss reaction:

H2 O2 + O2- ---OH * + OH + O2

Free radical injuced cell injury


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Chemicals injury

Mercuri chloride + sulfidril of cellular membrane

Cyanide --- destruction of mitochondria

CCl4 -- CCL3--- ( lipid peroxydase) fatty changes

Acetaminophen [ tylenol ) : toxic metabolite to theliver


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Chemicals cedera

Mercuri klorida + sulfidril dari membran

selular

--- Penghancuran sianida mitokondriaCCl4 - CCL3 --- (lipid peroxydase) - lemak

perubahan

Acetaminophen [Tylenol): metabolitberacun ke hati


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Sub-lethal injury [ reversible injury] Hydropic change = cellu lar swel ling, hydropic change

Cellular edema : pale , vacuolated and edema ofcytoplasms

Causa: toxic agent, hypoxia

Reversible

irreversible, in a persistent causa( mola hidatido sa,

adamantinoma )Microscopic

membrane = blebbing, blunt ing

ME :

mikrovilli = distortion

mitokondria = fosfolipid amrof mass , clumpingRE = dilatation, disagregation of polisom

nuclear= disintegration of fibriler element


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Sub-mematikan cedera [dibalik cedera]

Hidropik perubahan = selular pembengkakan, perubahan hidropik

Seluler edema: pucat, edema vacuolated dan cytoplasms

Causa: beracun agen, hipoksia

Reversibel

ireversibel, dalam sebuah gigih causa (mola hidatidosa,adamantinoma)

Mikroskopis

membran = blebbing, menumpulkan

ME:

mikrovilli = distorsimitokondria = fosfolipid amrof massa, penggumpalan

RE = dilatasi, disagregation dari polisom

nuklir = disintegrasi fibriler elemen


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Hydropic change


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Hydropic change in liver tissue


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Hydropic change in hydatid mole


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Musin degeneration / accumulation


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Hialin degeneration of the uterus tumor


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Intracell accumulations :

Accumulation of normal cellular materials:

water, lipid, protein dan charbohydrat

Accumulation of abnormal materials:

exogenous and endogenous materials ---

Mineral , metabolism metabolite

Pigmen


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Intracell akumulasi:

Akumulasi bahan seluler normal:

air, lemak, protein dan charbohydratAkumulasi bahan abnormal:

eksogen dan endogen bahan ---

Mineral, metabolisme metabolitPigmen


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Fatty accumulation, Fatty change:

Fatty drops accumulation due to abnormal of ribosomes function

>> liver

Causa : Hypoxia, alcohol

Microscopic:

Fatty drops - vacuola nuclear expanded to

the one side of the cell Reversible : mild- moderate grade

Irreversible : severe grade


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Lemak akumulasi, perubahan Fatty:

Tetes akumulasi lemak

karena abnormal fungsi ribosom

>> Hati

Causa: Hipoksia, alkohol

Mikroskopis:Lemak tetes - vacuola - nuklir diperluas ke satu sisi sel

Reversibel: ringan-sedang kelas

Ireversibel: kelas berat


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Fatty changes

Fatty accumulation of the liver normal liver tissue


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Pigment carbon in the lung tissue

Lung tissue


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Bilirubin pigment in the skin and sclera of the eye


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Lipofuchsin pigmen ( wear tear pigmen )


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Calcification

Calsium accumulation in the organ/ tissues Dhystrophic calcification:

Locally Calcification in nonviable/ dying tissue

Lithopedion, arteriosclerosis, calcification in

neoplastic processes, necrosis

- metastatic calcification:

Calcification in disturbance of calcium metabolism

Hyper parathyroid hormone, destruction of bone

tissue ( plasmacytoma ), vit. D related disorder, renal

failure


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Pengapuran

Calsium akumulasi pada organ / jaringan

Dhystrophic kalsifikasi:

Pengapuran lokal di nonviable / sekarat jaringan

Lithopedion, arteriosclerosis, kalsifikasi dalam prosesneoplastik, nekrosis

- Kalsifikasi metastatik:

Pengapuran dalam gangguan metabolisme kalsium

Hyper paratiroid hormon, kerusakan jaringan tulang(plasmacytoma), vit. D terkait disorder, gagal ginjal


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Disthropic calcification


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Calcification in breast cancer

N i


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Necrosis: Morphological changes in the cellular death

Type of necrosis:

enzymatic dygestionliquifaction necrosis

protein denaturationcoagulative necrosis

Microscopic : nuclear picnosis, caryorexis, cariolysis


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Necrosis:

Morfologis perubahan dalam kematian

selular

Jenis Nekrosis:dygestion enzimatik liquifaction nekrosis

denaturasi protein nekrosis coagulative

Mikroskopis: picnosis nuklir, caryorexis,

cariolysis


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Necrotic tissue

Necrosis:


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Necrosis:

Coagulative necrosis

Liquefaction necrosis

Caseous necrosis

fat necrosis Fibrinoid necrosis

gangrenous necrosis


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Coagulative necrosis liquefaction necrosis


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Fat necrosis


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Caseous necrosis


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Apoptosis:

Programmed cell death

- Destruction of cells during embriogenesis:

implantation, organogenesis

- homeostasis mechanism: normal cells

population- Protection : immunologic reaction

- Ageing processes


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Apoptosis:

Kematian sel terprogram

- Penghancuran sel selama

embriogenesis: implantasi, organogenesis- Mekanisme homeostasis: populasi sel-

sel normal

- Perlindungan: reaksi kekebalan- Penuaan proses


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Regulation of cell death


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Morphology of apoptosis:

Cellular shrinkage , denses organella

Condensation of chromatin, chromatin

aggregation, nuclear fragmented

apoptotic bodies

Phagocytosis of apoptotic bodiesbymacrophages / cellular nearby


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Morfologi apoptosis:Cellular penyusutan, denses organella

Kondensasi kromatin, kromatin agregasi,

terfragmentasi nuklirapoptotic tubuh

Apoptotic fagositosis dari badan oleh

makrofag / seluler di dekatnya


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Adaptation processes:Hypertrophy

Hyperplasia

Atrophy

Metaplsi

Dysplasi


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Morfologi apoptosis:Cellular penyusutan, denses organella

Kondensasi kromatin, kromatin agregasi,

terfragmentasi nuklirapoptotic tubuh

Apoptotic fagositosis dari badan oleh

makrofag / seluler di dekatnya

H l i


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HyperplasiaIncrease of cells number in an organ/ tissue

In an active DNA-synthesizing cells or cells mitoses

Physiologic hyperplasi

hormonal hyperplasi:

Glandular breast proliferation ( puberty,

pregnancy) Uterus in pregnancy

Compensatoir hyperplasi

Partial hepatectomy

Pathologic hyperplasi:

Endometrial hyperplasi ( hormonal )

growth factor effect on targetcells


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Peningkatan jumlah sel dalam suatu organ / jaringanDalam aktif sintesis DNA sel atau mitosis sel

Fisiologis hyperplasi

hormon hyperplasi:

Kelenjar payudara proliferasi (pubertas, kehamilan)Kehamilan rahim

Compensatoir hyperplasi

Partial hepatectomy

Patologis hyperplasi:

Endometrium hyperplasi (hormonal)

efek faktor pertumbuhan sel-sel sasaran


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Endometrial hyperplasi

endometrium

miometrium

H t h


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Hypertrophy

Increase in the size of cells - increase in the size oftissue / organ

No new cells

Increase of cellular syntesis ( not edema )

Hypertrophy :

physiologic: uterus / breast during pregnancy ( hormonalstimulation )

pathologic: muscular enlargement of the heart / sceletalmuscle ( >>> functional demand )


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Peningkatan ukuran sel - peningkatanukuran jaringan / organ

Tidak ada sel-sel baru

Kenaikan syntesis selular (tidak edema)

Hipertrofi:

fisiologis: rahim / payudara selamakehamilan (hormon stimulasi)

patologis: pembesaran otot jantung /

sceletal otot (>>> fungsional permintaan)
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Hyperthropy of the heart

At h
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Atrophy

Shrinkage in the size of cells by loss of substancesPhysiologic atrophy:

- embryogenic structure: thyroglossal duct

- decreased of uterus/ breast size after parturition

Pathologic atrophy:1. Decreased workload / disuse atrophy

2. loss of inervation

3. diminished blood suply

4. inadequate nutrition

5. loss of endocrine stimulation6. ageing process

7. pressure


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Penyusutan dalam ukuran sel oleh hilangnya zatFisiologis atrofi:

- Embryogenic struktur: thyroglossal saluran

- Penurunan dari rahim / ukuran payudara setelah

kelahiranPatologis atrofi:

1. Penurunan beban kerja / tidak digunakan atrofi

2. kehilangan inervation

3. SUPLY darah berkurang

4. nutrisi yang tidak mencukupi

5. hilangnya stimulasi endokrin

6. proses penuaan

7. tekanan


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Testis atrophy Kidney atrophy

Metaplasi


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Metaplasi

Reversible changes in which one adult celltype is replaced by another adult cell type

Exp: - columner epithel squamous epithel

( heavy smoker , chronic cervicitis)- Squamous ep --- columner ep

( Barrets esophagus )

- columner ep --- apocrine ep( fibrocystic changes of the breast )

- connective tissue metaplasia


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Reversibel perubahan di mana satu tipesel dewasa digantikan oleh jenis sel

dewasa lain

Exp: - columner epithel - epithel squamous(Perokok berat, cervicitis kronis)

- Skuamosa ep ep --- columner

(Barrets kerongkongan)- Apokrin --- columner ep ep

(fibrokistik perubahan dari payudara)

- Metaplasia jaringan ikat


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Barets esophagus ( squamous cell --- glandular cells )


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Apocrine metaplasia of the breast

Dysplasi


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Dysplasi

mild moderate severeBasal cell pro 1/3 2/3- all

liferation

Maturity yes / no yes / no noMitosis no/ mild moderate many

Cells atypi mild moderate severe


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