Chapter 11
Blood Vessels
1.
Where in the circulation is the principal point of resistance to flow? Where does vascular
leakage preferentially occur? What is the process of remodeling existing arteries called?
Arterioles
From postcapillary venules
Arteriogenesis
2.
What is fibromuscular dysplasia? Why worry about it?
Congenital, focal thickening of medium-large arteries like renal, carotid, splanchnic, or
vertebral
Renal vascular hypertension and aneurysms
3.
When does a neointima form? What cells make it up?
Thickening occurs after basicaly any injury
Smooth muscle cells, either from circulating precursors or the tunica media
4.
What causes hypertension? What are two named single gene mutations that can cause
hypertension?
95% of the time it is essential hypertension, which is idiopathic
Liddle syndrome: ENaC mutation causes excess reabsorption
mutations like 11B-hydroxylase and 17a-hydroxylase cause too much aldosterone to be
released
5.
What are the morphologic signs of benign hypertension and malignant hypertension?
Hyaline arteriosclerosis
Fibrinoid necrosis, onion skinning
6.
What is Monckeberg medial sclerosis?
Insignificant calcifications in the arteries of people under 50, which sometimes turn to bone
7. What is the most significant risk factor for atherosclerosis? What is another risk factor and
simple marker for inflammation? What other risk substance that may be increased by deficient
folate or vitamin B12?
Family history
C-reactive protein
Homocystine is bad at high levels
8.
What are foam cells? Who gets fatty streaks?
Eaters of oxidized LDL in the intima, derived from macrophages and smooth muscle cells
Just about everybody by childhood
9.
Where do atherosclerotic plaques like to form?
Abdominal aorta, coronary arteris, popliteal arteries, internal carotids, then circle of Willis
10. When does stable angina occur? What makes a plaque vulnerable? What time of day do MIs
tend to occur?
At the point of critical stenosis: ~70% occlusion
Thin fibrous cap, can be due to excess MMP activity or insufficient TIMPs
Sympathetic circadian periodicity causes most MIs in the morning between 6 and noon
11. What are three genetic conditions that can cause aneurysms? What are two familiar causes of
infectious (mycotic) aneurysm? What are the two major causes of aneurysm?
Marfan, Loeys-Dietz (TGF-β receptor mutation), and Ehlers-Danlos
Syphilis in the aorta, Salmonella in the AA
atherosclerosis and Hypertension
12. What is the major risk factor for dissection? Others? What is the most frequent preexisting
histology?
hypertension
i. unlike aneurysm, the medial fibrosis of atherosclerosis inhibits tear propogation
the three genetic disorders above, vitamin C deficiency, copper metabolic defects
most commonly aneurysms arise from no distinct lesion
i. otherwise, cystic degeneration of the tunica media
13. How does the DeBakey classification correspond to dissection type? Clinical presentation?
DeBakey I and II = type A = proximal lesions
DeBakey III = type B = begin distal to subclavian artery
tamponade, aortic insufficiency, MI, compression of spinal arteries=> transverse myelitis;
death occurs if it ruptures
Other Junk
14. What are the three mechanisms of noninfectious vasculitis?
Immune complex deposition: drug hypersensitivity or viral protein + antibody
i. E.g. hepatitis B
Antineutrophil cytoplasmic antibodies: ANCAs may react with cytokine-activated cells to
cause direct injury to the endothelium or further activate neutrophils
Anti-endothelial cell antibodies
15. What general category of vasculitis is associated with ANCAs? What do PR3 ANCAs correspond
to? What 2 diseases do MPO-ANCAs (old name is P-ANCAs) correspond to?
Small-vessel
Wegner granulomatosis
Microscopic polyangiitis and Churg-Strauss syndrome
16. Why is giant cell (temporal) arteritis an emergency? How do affected arteries appear (2)?
It can cause permanent blindness
Segments of intimal thickening that constrict the vessels
Large to small arteries undergo granulomatous inflammation that leads to elastic lamina
fragmentation
17. What do you call a granulomatous vasculitis of medium and larger arteries, which causes
peripheral weakening of the pulses and ocular disturbances? How is this differentiated from
giant cell aortitis?
Takayasu arteritis (“pulseless disease”)
i. Principally transmural fibrous aortic thickening, especially the arch
ii. Not mentioned above are neurologic disturbances, MI, pulmonary HTN, and
systemic HTN
If age of patient greater than 50 = giant cell aortitis; age less than 50 = Takayasu
18. What do you call vasculitis of young adults involving small to medium sized arteries in the renal
and visceral vessels? What infection is associated in 30% of cases? Describe its morphology.
Polyarteritis nodosa
Chronic Hepatitis B; immune complexes are deposited
Two coexisting stages:
i. Transmural inflammation with fibrinoid necrosis
ii. Fibrous thickening of the vessel walls
19. What disease is going to cause MIs and aneurysms in children? What are its other (actually more
common) signs? What disease does it resemble under a low-power microscope?
Kawasaki disease; caused by anti-endothelial antibodies
i. Affects large-medium-small arteries, but especially coronary arteries
Fever, oral erosions, edema of hands and feet, erythema of palms and soles, and
desquamation
Polyarteritis nodosa
20. How can the small vessel vasculitises be differentiated based on clinical signs?
Microscopic polyangiitis: no asthma, no granulomas
Wegener granulomatosis: no asthma
Churg-Strauss: +asthma, +granulomas, and +eosinophilia
21. What disease resmbles polyarteritis nodosa, but only in small vessels and capillaries? What are
its other signs?
Microscopic polyangiitis: like PAN, but all lesions are of the same stage
Necrotizing glomerulonephritis and pulmonary capillitis are most common
Many organ systems can be involved: hemoptysis, hematuria, proteinuria, bowel
pain/bleeding, muscle pain, palpable cutaneous purpura, brain involvement
22. What is Churg-Strauss syndrome? What signs are associated? What marker is seen in ~half of
cases?
Small-vessel necrotizing vasculitis, associated with asthma, allergies, cardiomyopathy, GI
bleeds, glomerulosclerosis, hypereosinophilia, and necrotizing extravascular granulomas
MPO-ANCAs
23. What triad makes up Wegener Granulomatosis (3)? What marker is almost always present?
Necrotizing granulomas of the upper respiratory tract
Necrotizing intravascular granulomas in small-medium vessels, mostly affecting lungs
Necrotizing glomerulonephritis in the kidneys
PR3-ANCAs
[a “W” has three upward facing tips/sideways 3]
24. What disease causes segmental thrombosing inflammation of small-medium arteries (especially
tibial and radial arteries)? What is the risk factor? What are some associated clinical signs?
Thromboangiitis obliterans (Buerger disease)
Smoking
Raynaud phenomenon, instep claudication, chronic ulcerations of extremities, and pain
25. What is the consequence of varicose veins?
Stasis dermatitis
[think: Winston scratching his varicose ulcer in 1984]
26. What two fungi species often cause vasculitis?
Mucor and Aspergillus
Makes you prone to mycotic aneurysm
27. What is the pattern of Raynaud’s phenomenon? What conditions can cause secondary
Raynaud’s phenomenon?
Proximal=> distal: red, white, & blue
SLE, scleroderma, Buerger disease, or atherosclerosis
28. Besides the Deep Veins, where can thromboses arise? What is a funny cause of
hypercoagulability?
Dural sinuses and veins in the skull, periprostatic venous plexus, and pelvic venous plexus in
females
Neoplasia—remember the Trousseau sign (migratory thrombophlebitis)?
29. What causes inferior vena caval syndrome?
Neoplasms like hepatocellular carinoma or renal cell carcinoma
Thrombus from lower extremities that propogates upward
30. What disease causes primary lymphedema? When does lymphangitis occur?
Milroy disease causes lymphatic agenesis or hypoplasia, resulting in lymphedema
infection
31. What kind of hemangioma does not spontaneously regress? What disease are they associated
with? What kind often appears after trauma or pregnancy? What is a cystic hygroma?
Cavernous;
i. occur in the CNS (brain stem, cerebellum, and retina) in Von Hippel-Lindau
disease, which has similar pancreatic and liver neoplasms
Pyogenic granuloma (called “granuloma gravidarum” or pregnancy tumor; form in gingiva in
pregancy)
Cavernous lymphangioma; common in Turner syndrome
32. What is a glomus tumor? What is Sturge-Weber syndrome? What is another name for
hereditary hemorrhagic telangiectasia?
Painful tumor arising around or under the fingernails; from thermoregulator specialized
smooth muscle cells
Congenital syndrome associated with Facial port wine nevi, mental retardation, angiomatous
masses in the meninges, and hemiplegia
[think of a nevus in the shape of a retarded sturgeon]
Osler-Weber-Rendu disease; the dangers are nose, GI, and urinary bleeding
33. What hormone can cause formation of spider angiomas?
Estrogen—pregnancy and cirrhosis
34. What two microbes cause bacillary angiomatosis?
Bartonella henselae (cat scratch disease) and B. quintana (trench fever), usually in an
immunocompromised host
=> vascular proliferation in the form of raised red papules and nodules or subcutaneous
masses
35. What can Kaposi sarcoma help you diagnose? What does it look like? Who gets chronic KS?
Which version is the most common tumor in central Africa? What is the causative agent?
AIDS
Multiple red-purple plaques in distal extremities which spread from the distal extremities
inward and increase in number
Ashkenazi Jews or Mediterraneans
Lymphadenopathic KS, associated with Burkitt lymphoma
Human Herpes Virus 8 (KSHV), a gamma herpesvirus
36. What vascular tumor occurs around big veins? What malignant tumor occurs around capillaries
and venules?
Epitheliod hemangioendothelioma
Hemangiopericytoma
37. What toxins cause angiosarcoma in the liver? What is another cause of angiosarcoma
elsewhere? What is interesting about the histology of angiosarcoma?
Arsenic, thorotrast, and polyvinyl chloride (actually the vinyl chloride monomer)
Lymphedema, especially that which occurs after mastectomy
All degrees of differentiation can be seen, as well as endothelial origin
38. What needs to be given during angioplasty and stenting? Why are left internal mammary artery
grafts better than autologous saphenous vein?
Antiplatelet agents
More likely to remain patent
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