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PRAKTIKUM PA

BLOK 3.08
KARDIOVASKULER
ATHEROSKLEROSIS
Bitangcor,C.
Atherosclerosis.
2013
International Journal for Research and
Investigation on Atherosclerosis and
Related Diseases, 2011
library.med.utah.edu/WebPath
Limfo
Neovaskularis Nekrosit
asi sis

Lipid – laden makrofag /


kolesterol foam cell

ekstraseluler

Otot polos Jaringan ikat

library.med.utah.edu/WebPath
Neovaskularis
asi

Lipid – laden makrofag / Limfo


kolesterol
Jaringan ikat foam cell sit
ekstraseluler

microscopyu.com
TROMBOANGIITIS OBLITERANS
Sun, X. et al. Pathogenesis of thromboangiitis obliterans: Gene polymorphism and
immunoregulation of human vascular endothelial cells.
Piazza, G. Thromboangiitis Obliterans. CIRCULATIONAHA. 2010;121:1858-1861
Babb, F.P. Thromboangiitis Obliterans (Buerger Disease). 2017
A, Typical subacute thrombotic occlusion of the right digital artery in a
37-year-old male smoker with Buerger’s disease (H&E, ×64).
B, High-power view of area a in A demonstrating the digital artery with
cellular arterial thrombus (t) and remarkable inflammation in the intima
(i) (H&E, ×400).
C, High-power view of area v in A demonstrating the adjacent digital
vein with phlebitis (H&E, ×400). n, Nerve.

thoracickey.com/thromboangiitis-obliterans-buergers-disease
A, Microphotograph of a chronic-stage lesion of Buerger’s disease, with recanalized
arterial thrombus and striking intimal thickening (H&E, ×200). The internal elastic
lamina (arrowheads) and the architecture of the vascular wall are well preserved.
B, The same vessel stained with elastic van Gieson (×200).

thoracickey.com/thromboangiitis-obliterans-buergers-disease
Neutrophil
s

Limfosit

Fibroblast

Sel Datia tipe


http://peir.path.uab.edu
TROMBOFLEBITIS
Ghazal F. Ain Sham University
pathophys.org
pathophys.org
Hawbaker, S. Venous Thromboembolism
in the Cancer Population: Pathology,
Risk, and Prevention. J Adv Pract
Oncol. 2012. 3:23–33
www.massgeneral.org http://peir.path.uab.edu
Ghazal F. Ain Sham University
Organizing DVT

http://peir.path.uab.edu
HEMANGIOMA KAVERNOSA
Haggstrom, A. et al. Patterns of Infantile Hemangiomas: New Clues to Hemangioma Pathogenesis
and Embryonic Facial Development . AAP. 2013. 696-704
Figure 1: Involvement of the β-adrenergic system in the pathogenesis of infantile hemangiomas (IHs).
Hypoxia is likely to induce an increase in local norepinephrine (NE) levels that predominantly activates β2-
ARs. The β2-adrenergic signaling cascade induces the adenyl cyclase/cAMP pathway that, in turn, activates
several kinases and the downstream phosphorylation of transcription factors (TFs) are able to induce the
production of angiogenic factors, such as vascular endothelial growth factor (VEGF) and stromal cell-derived
factor-1α (SDF-1α), and matrix metalloproteases (MMPs). Hypoxia may also directly activate TFs, such as
hypoxia-inducible factor 1. PKA also activates the endothelial isoform of nitric oxide synthase (eNOS)
resulting in increased nitric oxide (NO) production. The activation of these multiple signals results in the
induction of vasodilation, angiogenesis, and in antiapoptotic effects. In addition, SDF-1α mobilizes and
homes hemangioma stem cells, thus promoting vasculogenesis. The role of β3-ARs in hemangioma
endothelial cells is debated. The gray dashed double-headed arrow indicates a possible cross-talk between
β2- and β3-ARs. AC, adenylyl cyclase; Gs, stimulatory G protein; MAPK, mitogen-activated protein kinase..
Satish, V. et al. Capillary Hemangioma in Maxillary Anterior Region: A Case Report. Jaypee Journals. 2013. 144-147
Hemangioma
kapiler

Hemangioma
kavernosa
Webpathology.com
Terimakasih

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