t s str u c tu r e

a n g e d o n i m e
h i c h i s c h ca u s e o f so
C e l l w u n c tio n b e
l og y ) a n d f
(morph o
c t o r a g e n t
in j u r y e ff e

Sel yang me
ngalami pe
(morfologi) rubahan str
dan fungsi uktur
injuri atau a akibat peng
gen a r uh
REAKSI SEL TERHADAP STIMULUS
 hipertrofi

ADAPTATION
artrofi

REVERSIBLE INJURY
Jejas reversible

IRREVERSIBLE INJURY
Jejas irreversible
Cellular condition between normal condition and fully stress cell. Cellular
adaptation begin by some mechanism, many adaptive response, involve up
regulation or down regulation specific cellular receptor . Example , surface
cell receptor which is involve on take LDL (low density lipoprotein)

Kondisi selular antara kondisi normal sel dan sel terluka yang stres
berlebihan . Adaptasi selular didahului dengan beberapa mekanisme,
beberapa respon adaptif, melibatkan up regulation dan down regulation
reseptor selular spesifik . Misalnya, reseptor permukaan sel yang terlibat
pada pengambilan LDL (low density lipoprotein)
 Adaptasi Sel Hypertrophy (hipertrofi)
Cell size larger cause organ size larger too
(penambahan ukuran sel menyebabkan
penambahan ukuran organ)

CELL ADAPTATION

Atrophy (Artrofi)
Shrink of cell that loosing of cell substance
(pengerutan ukuran sel dgn hilangnya
substansi sel)
Gelembung Myelin figure

Sel bengkak
ER bengkak
Kromatin Ribosom
menggumpal lepas

Autofagi Mitokondria
bengkak
Small
densities
1. Changed of plasma membrane (perubahan plasma membran)
Swollen (pembengkakan)
Microvillic distortion (distorsi mikrovili)
Loosening of cell binding (longgarnya perekatan antar sel)

2. Mitochondrial changed (perubahan mitokondria)

swollen (bengkak)
amorf density rich of phospolipid (munculnya amorf densitas kaya akan
fosfolipid)

3. Reticulum Endoplasmic dilatation (dilatasi RE)

destroyed of ribosom (ribosom rusak)
polisom disociation (disosiasi polisom)

4. Nuclear changed (perubahan nuclear)

disagregation of granular and fibrilar element (disagregasi unsur
granular dan fibrilar )
 Lisosom
bocor Defek membran

Nukleus Myelin figure

piknotis
ER lisis

Mitokondria
bengkak

Large densities
NECROSIS

Necrosis show the sequence of morphologic changed which is following the

cell death on live tissues. Description of necrosis morphology is result of two
important process in which happen at the same time :

1. cell enzymatic digestion

2. denaturation of protein

JEJAS IRREVERSIBLE

Necrosis menunjukkan perubahan morfologi yang diikuti kematian sel di jaringan

yang masih hidup. Penggambaran morfologi nekrosis menghasilkan dua proses
penting dimana terjadi di waktu yang sama

1. digesi enzimatik sel

2. denaturasi protein
 1. Primarily found in Kidneys,
heaart and adrenal glands
(ditemukan terutama pada
ginjal, jantung dan kelenjar
adrenal)

2. Protein denaturation and increased intracellular level of Ca ( denaturasi

protein dan kenaikan kandungan Ca dalam sel )
 This necrosis comes after
ischemic events in stroke
(nekrosis terjadi setelah
iskemik pada stroke)

Neurons and glial cells of

the brain die and are rich in
digestive enzymes
( neuron dan glial sel pada
otak mati dan kaya akan
enzim digestif)

Hydrolytic enzymes causes brain tissues to become soft and liquefy – sometimes
walled off and form cysts ( hidrolisis enzim menebabkan jaringan otak menjadi
lembut dan mencair)
Found in Tuberculous Combination of coagulative and
pulmonary infection (terletak liquefactive necrosis (kombinasi
pada infeksi tuberkulus paru- dari koagulatif dan liqueaktif
paru) nekrosis)
Action of lipases – break down fats to FA and glycerols (akibat dari lipase,
gangguan lemak dan gliserol)

Common in Breast, pancreas, and other abdominal organs (terjadi pada dada,
pankreas dan organ bagian abdominalis lain)
Clinical term (temperatur klinis)

Dry vs. wet gangren (gangren kering dan gangren basah)

Apoptosis is programmed death cell, it means it is active self destruction of
normal and pathologic tissues . Apoptosis happens in pathologic and
physiologic situation. And its different from necrosis

Apoptosis adalah kematian sel terprogam, jadi merupakan kematian yang

“bunuh diri” bukan “pembunuhan sel” . Terjadi pada situasi fisiologi dan
patologi . Dan Apoptosis berbeda dengan nekrosis.
Programmed cellular death – found mostly to occur during development of
embryo (kematian sel terprogam seringkali terjadi pada embrio)

Mechanism – specific signaling chemicals send message to cells

programmed to die ( mekanisme, spesifik sinyal komponen mengirim
pesan ke sel untuk kematian terprogram)

While necrosis usually effects all cells in an area apoptosis effects

(nekrosis biasanya menmberikan efek kepada semua sel yang ada di
daerah terinfeksi apoptosis)
1. Signaling (pemberian sinyal)

apoptosis can be triggered by many signal which is

happen from intrinsik programmed event, decrease of growth
factor, interaction of ligan and specific receptor, and other injury
agent .

2. Control and Integration (kontrol dan integrasi)

this is completed by specific protein that is relation death

signal and end eksekusi program (dilengkapi dengan protein
spesifik yang meghubungkan sinyal kematian dengan program
eksekusi akhir)
3. Execution (eksekusi)

this end way signed by activation many catabolic cytosolic

enzyme (jalur ini ditandai dengan aktivasi sejumlah enzim katabolik
sitosolik)

4. Lifting up death cell (Mengangkat kematian sel)

apoptosis cell and their fragments have sign molecule on

the surface, it is for take and loose by cell around or fagosite easily.
(sel apopttotik dan fragmennya memiliki molekul penanda pada
permukaannya, untuk memudahkan pengambilan dan pelepasan
oleh sel di sekitarnya atau fagosit )
Feature Necrosis Apoptosis

Cell size Enlarged (swelling) Reduce (shrinkage)

Nucleus Pyknosis, karyorrhexis, Fragmentation into

karyolisis nucleusome size fragments

Plasma membrane disrupted Intact, altered structure

Cellular contents Enzymatic digestion, Intact, release in apoptotic

leakage bodies

Adjacent inflammation Frequent no

Physiologic or pathologic Always Pathologic Often, but not always

role physiologic
Aging is progressive accumulation of subletal injurious events that
disturbing cell function and caused death of cell. (Penuaan sel
(aging) merupakan akumulasi progresif cedera subletal yang
mengganggu fungsi sel dan dapat menimbulkan kematian sel).

Aging theory sure that aging process caused by genetic

programming that have determined. Research prove that normal
adult human fibroblast on the cell have certain range life of time.
Fibroblast stop to split and growing old after some replication on
the certain number. (Teori penuaan sel berpegang bahwa
proses penuaan sel terjadi kerena pemrograman genetik yang
telah ditetapkan. Penelitian membuktikan bahwa fibroblas
manusia dewasa normal pada kultur sel memiliki rentang masa
hidup tertentu. Fibroblas berhenti membelah dan menua
setelaah beberapa kali penggandaan sejumlah tertentu.)