PATOLOGI KARDIOVASKULER Flashcards

1
Q

pada kondisi normal, endotel butuh

A

laminar flow
growth factor
adhesi stabil dan baik yang berada dibawah membran basal

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2
Q

respon endotel saat injury

A

trombosis dan vasokontriksi

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3
Q

pemicu aktivasi endotel

A

virus, bakteri
lipid
hipoksia
sitokin proinflamasi

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4
Q

bentuk respon endotel

A

berubah bentuk
produksi sitokin dan kemokin, gf, faktor prokoagulan, ekspresi molekul adhesi

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5
Q

lama respon dibagi menjadi 2 yaitu

A

rapid dan late

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6
Q

akibat paparan injury terus terusan

A

kerusakan endotel-vasodilatasi
peningkatan radikal bebas o2
hiperkoagulasi state

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7
Q

akibat paparan injury yang terus terusan

A

trombosis
lesi vaskuler
atherosklerosis

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8
Q

fungsi otot polos

A

repair vaskuler

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9
Q

cara otot polos repair vaskuler

A

migrasi dan proliferasi
upregulasi matriks ekstraseluler
elaborasi growth factor
memediasi vasodilatasi dan vasokontriksi

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10
Q

lokasi atherosklerosis

A

coronary
carotid
perifersl

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11
Q

perbedaan atherosklerosis dengan thromboangiitis obliterans

A

atherosklerosis: atheroma + fibrosis
tromboangiitis obliterans: trobosis+ fibrosis

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12
Q

mikroskopis dari atherosklerosis

A

tampak foams cell, jaringan fibrous pada tunisa intima, neovaskularisasi, nekrosis

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13
Q

perbedaan aterosklerosis dan non aterosklerosis

A

atero: terjadi peningkatan tunica intima ( bagian dalamnya terdapat foam cell, fibrosis)
non atero: terjadi obliterasi lumen, dinding masih intak

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14
Q

karakteristik tromboangiitis obliterans

A

trombosis vaskuler
infiltrasi sel inflamasi sekitar trombus dan adventitia
fibrosis intima dan media
perubahan internal elastic layer

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15
Q

patof tromboangiitis obliteras

A
  1. plak/deposit nikotin di vena/arteri
  2. eNOS turun, NO turun, disfungsi endotel, trombosis, vasokontriksi. hipersensitivitas thdp tobaco dlm rokok
  3. inflamasi arteri/vena ukuran kecil-sedang
  4. a. inflamasi factor migrasi ke vena/arteri yang terinflamasi> terbentuk mikroabses> oklusi lumen trombotic
    b. arter/vena ekstremitas menebal> platelet terdeposisi dalam arteri/vena menebal> oklusi fibrinoid
  5. sirkulasi darah terganggu
  6. iskemik, cidera, nekrosis
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16
Q

3 fase patologi dari tromboangiitis obliterans

A

akut: oklusi, inflamasi trombus terbentuk di vena/arteri distal
mikroabses dan sel inflamasi muncul
elastic internal lamina intak
elastic eksternal alami gangguan
sub akut : vaskular vibrosis
progresif organisasi inflamasi trombus
kronik: sel inflamasi hilang
organisasi trombus dan fibrosis tetap berlangsung

17
Q

gejala khas buerger disease

A

SCRAPS
Segmental trombus vaskuler
Claudiation
Raynauld phenomenom
Assosiated with smoking
pain even rest
superficial nodular phlebitis

18
Q

Patof atherosklerosis

A

Endhotel injury&raquo_space; permeabilitas meningkat»adhesi monosit dan leukosit&raquo_space; aktivasi makrofag dan msc&raquo_space;membentuk foam cell»deposit lemak, fibrosis, msc>terbentuk necrotic core dan fibrous cap

19
Q

6 macam progresivitas atherosklerosis

A
  1. Initial lesion: terlihat normal, tapi sudah terbentuk foam cell dan aktivasi makrofag
  2. Fatty streak: akumulasi lemak di intraseluler
  3. Intermediet: akumulasi lemak smp ekstraseluler
  4. Atheroma: terbentuk akumulasi lipid intra dan ekstra sel&raquo_space;lipid core
  5. Fibrousatheroma: cores + fibrotic layers
  6. Complicated lesion: surface defect, hematoma hemorrhage, trombosis
20
Q

3 prinsip komponen atherosklerosis:

A
  1. Cell: makrofag, limfosit T, smc
  2. ECM: kolagen, elastin fibers, proteoglikans
  3. Intra dan ekstrasel lipid
21
Q

Tampakan mikro hemangioma kavernosa

A

Vena dilatasi bentuk kaverna bersepta
Dilapisi selapis endotel monomorf
Berisi eritrosit di lumen