bbs ii slide proses radang infeksi pemulihan jaringan dan degenerasi
3/28/2011
1
DEGENERASI
Terjadi perubahan morfologik (dalam sel / dalam zat antar sel) akibat gangguan metabolisme pada sel
(2)
2
Sifat degenerasi :
• Ringan (reversibel)
• Berat (irreversibel) Nekrosis
The sequential ultrastructural changes seen in necrosis (left)& apoptosis (right).
(3)
3/28/2011
3
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
(4)
4
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)
(5)
3/28/2011
5 Complete mole. All villi are markedly swollen.
(6)
6
Normal Villi
The 1sttrimester (7-8 weeks)(20X)
(7)
3/28/2011
7 Complete mole showing large villi with stromal edema & marked
(8)
8 ! " # $ %
& '
! " # % $ " "
(9)
3/28/2011
9 )
(10)
10
ACUTE INFLAMATION
GROSS :
REDNESS (RUBOR)
HEAT (CALOR)
SWELLING (TUMOR)
PAIN (DOLOR)
LOSS OF FUNCTION (FUNCTIO LAESA)
ACUTE INFLAMATION
MICROSCOPIC :
Hyperaemia
Exudation
(11)
3/28/2011
11
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
(12)
12 -Chemical Mediator
Endothelial Damage
Permeabilitas
Exudation (Mechanism)
Protein Passage :
PMN & MN
Pass (amoeboid)
(13)
3/28/2011
13
+, $
- (
.
/, $ "
"
0, $
" 1 ,
2, $
3 4 ) #)
$
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
(14)
14
Acute appendicitis with massive inflammatory infiltrate, extensive ulceration,
and hemorrhage. An island of heavily inflamed residual mucosa is seen in the center.
(15)
3/28/2011
15 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
(16)
16 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.
(17)
3/28/2011
17 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
(18)
18 2 WEEKS : - EPITH.COVERING COMPL
- TRANSVERS COLLAGEN - DECREASED CAPILARY - FEW CELLS
MONTH : - FULL EPITH.COVERING - SURFACE DEPRETION (< ) - THICK COLLAGEN SCAR - VASCULAR ( < )
(1)
13
+, $
- ( .
/, $ "
"
0, $
" 1 ,
2, $
3 4 ) #)
$
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
(2)
Acute appendicitis with massive inflammatory infiltrate, extensive ulceration,
and hemorrhage. An island of heavily inflamed residual mucosa is seen in the center.
(3)
15
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
(4)
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.
(5)
17
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
(6)
2 WEEKS : - EPITH.COVERING COMPL - TRANSVERS COLLAGEN - DECREASED CAPILARY - FEW CELLS
MONTH : - FULL EPITH.COVERING - SURFACE DEPRETION (< ) - THICK COLLAGEN SCAR - VASCULAR ( < )