deskrpsi lesi mikros -a.ppt

7/24/2019 deskrpsi lesi mikros -a.ppt

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I. DEGENERASI DAN NEKROSIS

• 1. Degenerasi melemak

• 2. Degenerasi hidropik

• 3. Degenerasi hyalin• 4. Sel nekrosis

• 5. Autolosis post mortum

• 6. Apoptosis• 7. Inclusion odies



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MEMBUAT DIAGNOSA

MORFOLOGIS

1 SEVERITY

2 DISTRIBUTION

3 DURATION

4 LESION TYPE

5 TISSUE INVOLVED

1 NAMA ORGAN

2 TIPE LESI

3 DURASI

4 DISTRIBUSI

5 DERAJAT

KEHEBATAN



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MEMBUAT DIGNOSA

MORFOLOGISS!"!#!#I$%

DIS$#I&'$I()

D'#A$I() *!SI() $%+! $ISS'!I)"(*"!D

S!"!#! ,%+(+*ASIA -!#!&!**I

S!"!#! +!#I*(&'*A# A-'$! A$$% D!/!) *I"!#

S!"!#! 0'*$I(-A* -,#()I- $'&!#-'*('S ,!+A$I$IS

0(D!#A$! 0'*$I(-A* A-'$! )!-#($I- ,!+A$I$IS

0I*D (-A* S'&A-'$! $'0(# SI)

S!"!#! DI'S! -,#()I- $'0(# "'*"A"A/I)A



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Degenerasi melemak pada hepar



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degenerasi hidropik



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aryorrheis lymphocytes lien.



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Sel nekrosis piknosis



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Degenerasi hyalin



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Apoptosis cytoarchitecture ,! stain



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II. Kalsifkasi danPigmentasi

• 1. anthrakosis

• 2. hemosiderosis

• 3. melanosis• 4. Icterus

• 5. kalsiikasi metastatik



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Anthrakosis pigmen karon pada septa al8eoli



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III. Bentuk – bentuk

nekrosis

• 1. nekrosis koagulasi

• 2. nekrosis li9ue9kti

• 3. nekrosis caseosa

• 4. at necrosis



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)ekrosis koagulasi



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)ekosis

koagulasi



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D. Gangguanemodinamik !

sirkulasi• 1. ongesti hiperemia

• 2. +erdarahan hemoragi

• 3. (edema

• 4. $hromus

• 5. Inark



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Arterial thromi lapisan

gelap platelet irin

lapisan terang.

&ercampur dengan eritrosit

dan leukosit dalam lapisan

:ahn.



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INFARK



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". bentuk radang ! eksudates in

a#ut in$amasi

• 1. radang irinous serous akut• 2. radang catarrhal

• 3. radang purrulent suppurati8e

• 4. ulcera

&entuk radang kronis ;

1. #adang granulomatous caseosa

G. BENTUK_-BENTUK RADANG.



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1

2 3

4 56

7

<

Gambarkan bentuk sel radang dalam jaringan :

Sel radang !lim!r"!nuklear #mn$ :

Sel radang mononuklear 1 SD 7 ;



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!udation microscopic in acute inlammation



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!udation microscopic in acute inlammation.

Seen here is 8asodilation =ith eudation that

has led to an outpouring o luid =ith irin into

the al8eolar spaces along =ith +0)>s.



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A -hronic inlammation in the

lung sho=ing all three

characteristic histologic

eatures; 1 collection ochronic inlammatory

cells ? 2 destruction o

parenchyma normal al8eoli are

replaced y spaces lined y

cuoidal epithelium

arrowheads), and 3replacement y connecti8e

tissue irosis arrows).

B, &y contrast in acute

inlammation o the lung acute

ronchopneumonianeutrophils ill the al8eolar

spaces and lood 8essels are

congested.



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#adang serousirinous



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0ild acute dius katharrha pn



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0oderate dius suacute suppurati8e pneumonia



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0$-)0- -)'' 0,& N#%) %(% ('%#&8 )*&-)* #90*(%0)

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)(,) *((8) ER; ),*#:'($0- )%0-&'&< =K;

-)(%0,) >0,($)< LDH; '(-%(%) *)*#8),($)< RNP; 0#,&-')#:#%)0,

=#(8&'(%0) (,* '0+&).(-%0) ,)-#$0$ A; K0*,) 0,.(-% )900%0,8 -#(8&'(%0) ,)-#$0$; ?0% '#$$ #.

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.0'')* ?0% ?0%) -)''$ (,* -)''&'( *)0$; -)(%0,8 ( ),(' ($-)$$ %(% #'0%)(%)$ %) ,#('

(-0%)-%&)



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,ere are t=o pulmonary granulomas. /ranulomatous inlammation

typically consists o mitures o cells including epithelioid

macrophages giant cells lymphocytes plasma cells and

irolasts. $here may e8en e some neutrophils.



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B(0,; ':#-%0- :)0($-&'( -&..0,8



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'l

ulcer



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'lceraulcer

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