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PROSES RADANG, PROSES RADANG, PROSES RADANG, PROSES RADANG, INFEKSI, PEMULIHAN INFEKSI, PEMULIHAN INFEKSI, PEMULIHAN INFEKSI, PEMULIHAN

JARINGAN DAN JARINGAN DAN JARINGAN DAN JARINGAN DAN DEGENERASI DEGENERASI DEGENERASI DEGENERASI

DEPARTEMEN PATOLOGI ANATOMIDEPARTEMEN PATOLOGI ANATOMIDEPARTEMEN PATOLOGI ANATOMIDEPARTEMEN PATOLOGI ANATOMI

FK FK FK FK ---- USU MedanUSU MedanUSU MedanUSU Medan

2008200820082008

DEGENERASI

� Terjadi perubahan morfologik (dalam sel / dalam zat antar sel) akibat gangguan metabolisme pada sel

Penyebab : jejas non-fatal

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Sifat degenerasi : • Ringan (reversibel)

• Berat (irreversibel) � Nekrosis

The sequential ultrastructural changes seen in necrosis (left) & apoptosis (right).

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Degenerasi Infiltrasi

Adanya jejas pada sel

Perubahan metabolisme

Adanya perubahan metabolisme

Jejas pada sel

Degenerasi & infiltrasi

Dapat terjadi gangguan yang bersifat biokimia/

biomolekuler

DEGENERASI

Sering disertai pengendapan zat-zat :

� Lemak

� Amiloid

� Lipoid (zat yang menyerupai lemak)

Degenerasi :

� D. Albumin

� D. Hidropik

(D.vakuoler)

� D. Hyalin

� D. zenker/ waxy deg.

� Deg / infiltrasi

glikogen

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DEGENERASI HIDROPIK(Degenerasi vakuoler)

� Edema intraseluler menonjol (> deg. bengkak keruh)

� Kerusakan tampak lebih berat

� Sediaan :

� Kuretage cavum uteri ( abortus imminens) � perdarahan hebat

� Hasil Kuretage (makroskopis): � Gelembung jernih � Ø bervariasi

� Diagnosa : Mola hidatidosa

Macroscopis (Hydatidiform Mole)� a mass of tissue with grape-like swollen villi

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Complete mole. All villi are markedly swollen.

Macroscopis (Hydatidiform Mole)

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Normal Villi The 1st trimester (7-8 weeks)(20X)

Microscopis (Hydatidiform Mole)

Avascular

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Complete mole showing large villi with stromal edema & markedtrophoblastic proliferation.

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Radang : reaksi jaringan hidup terhadap semua bentuk jejas (injury)

Rubor

Calor

Tumor

Dolor

Functio laesa

Akut

Kronik

Mikroskopis:

Infiltrasi sel-sel radang akut (PMN)

Vasodilatasi

Oedema

Mikroskopis:

Infiltrasi sel-sel radang kronik (MN)

Proliferasi jaringan fibroblast

Neovaskularisasi

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A B

ED

C

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ACUTE INFLAMATION

GROSS :

REDNESS (RUBOR)

HEAT (CALOR)

SWELLING (TUMOR)

PAIN (DOLOR)

LOSS OF FUNCTION (FUNCTIO LAESA)

ACUTE INFLAMATION

MICROSCOPIC :

Hyperaemia

Exudation

Emigration of Leucocytes

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Hyperaemia

Micro-vascular changes

(Lewis’s Triple Response) :

• Flush � Dull red line (capilar dilatation)

• Flare � Bright red (artery dilatation)

• Wheal

� Protein fluid � interstitial (wheal)

� Fluid ↑� dilution of toxin

� Protein ↑ :

- Globulin � antibodies

- Fibrin � to limit spread bacterial

� Wound healing

Exudation

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- Chemical Mediator

� Endothelial Damage

↑ Permeabilitas

Exudation (Mechanism)

Protein Passage :

� PMN & MN

� Pass (amoeboid)

Emigration of leucocytes

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1. Peradangan serosaDitandai : extravasasi cairan ↑ protein ↓ selSebagian besar peradangan akut bermula sebagai bentuk serosa

2. Peradangan fibrinosaDitandai : eksudasi plasma ↑ fibrinogen

3. Peradangan purulenDitandai : keluarnya neutrofil & pembentukan pus.

4. Peradangan pseudomembranosa

Gambaran Histologis Bentuk-Bentuk Makroskopik Peradangan :

Fig. 11.127. Outer aspect of appendix involved by acute inflammation.A thick purulent coating is seen together with marked hyperemia of the serosa.

Hyperemia (serosa)

Purulent

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Acute appendicitis with massive inflammatory infiltrate, extensive ulceration,and hemorrhage. An island of heavily inflamed residual mucosa is seen in the center.

Radang Kronik

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� WOUND HEALING

� COMPLICATIONS : - CONTRACTURE

- GRANULATION

- KELOID

- FIBROSIS

� REGENERATION

� SPECIAL SITUATION.

HEALING

� PRIMARY HEALING :

- CLEAN EXISED WOUND

- GOOD POSITION (PALNED SURG.INCIS)

� IMMEDIATELY: - BLOOD CLOT

� 2-3 HOURS : - INFLAMATION (+)

- MILD HYPERAEMIA

- FEW POLYMORPHS

WOUND HEALING

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� 2-3 DAYS : - MACROPHAGE � REMO-

VING CLOT

- FIBROBLASTIC

� 10-14 DAYS : - SCAB LOOSE

- EPITHELIAL COVERING.

- FIROUS UNION

WOUND HEALING

� WEEKS : - SCAR TISSUE SLIGHLY

HYPERAEMIA

- GOOD FIBROUS UNION

� MONTHS – YEAR:

- DEVASCULARISATION

- COLLAGEN(-) ENZYME

- SCAR MINIMAL.

WOUND HEALING

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� LOSS OF TISSUE >>

� NECROSIS (+)

� INFECTION (+)

� EARLY : BLOOD & FIBRIN CLOT (+)

ACUTE INFL. CELLS (+)

� FEW DAYS : - EPITH.PROLIFERATION

- NEW CAPILARY

- MACROPHAGE

- PMN, FIBROBLAST

SECONDARY HEALING

� 1 WEEK : - SURFACE DEBRIS (-)

- FIBROBLASTS >>

- EPITH.PROLIF’TION

- CAPILARY >>

- GRANULATION

SECONDARY HEALING

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� 2 WEEKS : - EPITH.COVERING COMPL

- TRANSVERS COLLAGEN

- DECREASED CAPILARY

- FEW CELLS

� MONTH : - FULL EPITH.COVERING

- SURFACE DEPRETION (< )

- THICK COLLAGEN SCAR

- VASCULAR ( < )

SECONDARY HEALING