Difference between revisions of "Vascular disease"
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===Microscopic=== | ===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> | 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. | *Smooth muscle hyperplasia - '''key feature'''. | ||
*Elastic fibre fragmentation. | *Elastic fibre fragmentation. | ||
*Luminal narrowing. | |||
Image: | |||
*[http://www.brown.edu/Courses/Digital_Path/systemic_path/cardio/fibromuscular-dysplasia.html FMD (brown.edu)]. | |||
===Stains=== | ===Stains=== | ||
Revision as of 15:03, 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
- Coronary artery atherosclerosis -> myocardial infarction +/-coronary thrombosis.
- Peripheral artery atherosclerosis -> peripheral vascular disease -> amputations.
- Carotid artery atherosclerosis -> thrombotic stroke.
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]
- Marfan's syndrome.
- Loeys-Dietz syndrome.[4]
- Marfan-like syndrome.
- Ehlers-Danlos syndrome.
- Bicuspid aortic valve.
Others:
- Tertiary syphilis.
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
Cystic medial degeneration
General
Microscopic
- Basophilic ground substance in the media (seen on Movat's stain).
- Disruption of the elastic lamina (seen on elastic trichrome stain).
- +/-Focal necrosis.
Images:
- www:
- WC:
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
- Hyperplasia = proliferation of cells.
- Associated with:[10]
- Malignant hypertension.
- Scleroderma.
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]
- Renal artery - leading to hypertension.
- Carotid artery.
Microscopic
Features:[11]
- Smooth muscle hyperplasia - key feature.
- Elastic fibre fragmentation.
- Luminal narrowing.
Image:
Stains
- Elastic trichrome or Movat stain - to demonstrate elastic fibre fragmentation.
See also
References
- ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/corepages/vascular/vascular.htm. Accessed on: 13 January 2011.
- ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 4. ISBN 978-1416002741.
- ↑ 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.
- ↑ 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.
- ↑ Finkelmeier BA (September 1997). "Dissection of the aorta: a clinical update". J Vasc Nurs 15 (3): 88-93. PMID 9362838.
- ↑ URL: http://emedicine.medscape.com/article/756835-overview. Accessed on: 12 August 2010.
- ↑ URL: http://emedicine.medscape.com/article/756835-overview. Accessed on: 12 August 2010.
- ↑ 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.
- ↑ 9.0 9.1 Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 7. ISBN 978-1416002741.
- ↑ URL: http://library.med.utah.edu/WebPath/IMMHTML/IMM028.html. Accessed on: 11 May 2011.
- ↑ 11.0 11.1 11.2 Hata, D. (Sep 2001). "Fibromuscular dysplasia.". Intern Med 40 (9): 978-9. PMID 11579971.