Difference between revisions of "Vascular disease"

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(→‎See also: +fibromuscular dysplasia)
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Image: [http://library.med.utah.edu/WebPath/ATHHTML/ATH022.html Hyperplastic arteriolosclerosis (utah.edu)].
Image: [http://library.med.utah.edu/WebPath/ATHHTML/ATH022.html Hyperplastic arteriolosclerosis (utah.edu)].
==Fibromuscular dysplasia==
===General===
Etiology:
*Unknown, possibly genetic.
Gender:
*Women > men.
===Gross/radiologic===
*Segmental - thinning and thickening.<ref name=pmid11579971/>
Classical locations:<ref name=pmid11579971/>
*Renal artery - leading to [[hypertension]].
*Carotid artery.
===Microscopic===
Features:<ref name=pmid11579971>{{Cite journal  | last1 = Hata | first1 = D. | title = Fibromuscular dysplasia. | journal = Intern Med | volume = 40 | issue = 9 | pages = 978-9 | month = Sep | year = 2001 | doi =  | PMID = 11579971 | URL = http://www.journalarchive.jst.go.jp/jnlpdf.php?cdjournal=internalmedicine1992&cdvol=40&noissue=9&startpage=978&lang=en&from=jnlabstract }}</ref>
*Smooth muscle hyperplasia.
*Elastic fibre fragmentation.
===Stains===
*[[Elastic trichrome]] or [[Movat stain]] - to demonstrate elastic fibre fragmentation.


==See also==
==See also==

Revision as of 14:54, 18 December 2011

The article covers vascular disease, i.e. diseases of blood vessels. Vasculitides are covered in a separate article called vasculitides.

Normal blood vessels

Comparing arteries and veins:[1]

Feature Artery Vein
Internal elastic lamina prominent/thick, usu. complete thin & incomplete
External elastic lamina present, thick absent
Shape circular / lumen wide open collapsed
Wall thickness thick thin

Great vessels

When things go wrong here, you see a cardiac surgeon.

Atherosclerosis

General

Clinical risk factors:

  • Age.
  • Blood pressure - modifiable (antihypertensives).
  • Cholesterol - modifiable (statins, diet).
  • Diabetes mellitus - modifiable (hypoglycemic medications, diet, lifestyle).
  • Smoking - modifiable (cessation).
  • Family history.

Microscopic

Features:

  • Intimal hyperplasia.
  • Lipid deposition.
  • Foamy macrophages within intima & media.
  • Cholesterol clefts
  • Luminal narrowing.

Image:

Notes:

  • Considered "complex" if any of the following are present:[2]
    • Calcifications.
    • Thrombosis.
    • Haemorrhage.

Aortic dissection

General

Associations

Heritable:[3]

Others:

Classification

Two classification exist:

  • DeBakey.
  • Stanford.

Stanford dissection classification:[5]

  • Type A - aortic root to the left subclavian artery.
    • Considered a surgical emergency.
  • Type B - distal to (left) subclavian artery.
    • Generally, treated conservatively.

Microscopic

See: cystic medial degeneration.

Cystic medial degeneration

General

  • AKA cystic medial necrosis.[6]
    • Often not cystic and not necrotic.

Microscopic

Features:[7][8]

  • Basophilic ground substance in the media (seen on Movat's stain).
  • Disruption of the elastic lamina (seen on elastic trichrome stain).
  • +/-Focal necrosis.

Images:

Medial calcific sclerosis

  • AKA Moenckeberg medial calcific sclerosis, calcific medial sclerosis of Monckeberg, and Monckeberg's arteriosclerosis.

General

  • Usually of no clinical consequence.

Microscopic

Features:[9]

  • Medial calcification (purple irregular stuff -- calcium phosphate).

Note:

  • Lumen unaffected.

Images:

Hyperplastic arteriolosclerosis

General

Microscopic

Features:[9]

  • Onion-skin appearance of intima & media due to:
    • Intimal hyperplasia.
    • Smooth muscle hyperplasia.

Image: Hyperplastic arteriolosclerosis (utah.edu).

Fibromuscular dysplasia

General

Etiology:

  • Unknown, possibly genetic.

Gender:

  • Women > men.

Gross/radiologic

  • Segmental - thinning and thickening.[11]

Classical locations:[11]

Microscopic

Features:[11]

  • Smooth muscle hyperplasia.
  • Elastic fibre fragmentation.

Stains

See also

References

  1. URL: http://www.lab.anhb.uwa.edu.au/mb140/corepages/vascular/vascular.htm. Accessed on: 13 January 2011.
  2. Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 4. ISBN 978-1416002741.
  3. Gleason TG (2005). "Heritable disorders predisposing to aortic dissection". Semin. Thorac. Cardiovasc. Surg. 17 (3): 274-81. doi:10.1053/j.semtcvs.2005.06.001. PMID 16253833.
  4. Loeys BL, Schwarze U, Holm T, et al (August 2006). "Aneurysm syndromes caused by mutations in the TGF-beta receptor". N. Engl. J. Med. 355 (8): 788-98. doi:10.1056/NEJMoa055695. PMID 16928994. http://content.nejm.org/cgi/content/full/355/8/788.
  5. Finkelmeier BA (September 1997). "Dissection of the aorta: a clinical update". J Vasc Nurs 15 (3): 88-93. PMID 9362838.
  6. URL: http://emedicine.medscape.com/article/756835-overview. Accessed on: 12 August 2010.
  7. URL: http://emedicine.medscape.com/article/756835-overview. Accessed on: 12 August 2010.
  8. Ha HI, Seo JB, Lee SH, et al. (2007). "Imaging of Marfan syndrome: multisystemic manifestations". Radiographics 27 (4): 989–1004. doi:10.1148/rg.274065171. PMID 17620463. http://radiographics.rsna.org/content/27/4/989.full.
  9. 9.0 9.1 Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 7. ISBN 978-1416002741.
  10. URL: http://library.med.utah.edu/WebPath/IMMHTML/IMM028.html. Accessed on: 11 May 2011.
  11. 11.0 11.1 11.2 Hata, D. (Sep 2001). "Fibromuscular dysplasia.". Intern Med 40 (9): 978-9. PMID 11579971.