Vascular Diseases - Jarzembowski Flashcards
Distinguish between a true and false aneurysm.
Which are symmetric: Saccular or fusiform aneurysms?
True aneurysms involve ballooning of all three vessel wall layers. False involves a defect in one or more and leads to mural hematoma.
Fusiform are symmetric.
According to Pathoma, all dissections (and aneurysms) require two things: High stress and wall weakness. What usually constitutes these two criteria?
High stress = Mostly happen in aorta, where pressure is highest.
Wall weakness = Hypertension (causing cystic medial degeneration) or inherited connective tissue disease.
In addition to Marfan syndrome, another connective tissue disease known as _____ can promote aneurysm formation because of defective synthesis of type ___ collagen.
Ehler-Danlos, III.
What role do MMPs and TIMPs play in aneurysm formation?
MMPs degrade connective tissue, TIMPs inhibit MMP action.
How does hypertension cause medial degeneration?
How does atherosclerosis cause medial degeneration?
Which of these more typically affects the abdominal aorta?
Hypertension compresses the vasa vasorum, causing ischemia of the tunica media in large vessels (actually hyaline arteriolosclerosis).
Atherosclerosis builds plaques that inhibit oxygen diffusion, causing ischemia of the tunica media in medium vessels (no vasa vasorum present)
Abdominal: Atherosclerosis
Besides HTN and atherosclerosis, what are some other, rarer causes of aneurysms?
Congenital defects (eg Berry), infections (eg mycotic, syphilis), trauma, and other vasculites.
What is the most common aortic aneurysm?
Which demographics are at highest risk?
How does it present?
Abdomanal Aortic Aneurysm, AAA.
Older men who smoke and have hypertension. Or some combination thereof.
A pulsatile abdominal mass that grows over time.
What are some of the complications of AAAs?
How are they treated?
Rupture is the most serious. May cause impingement of nearby structures (ureter, renal/mesenteric/spinal arteries). May form thrombi/emboli.
If large, must be treated agressively with stenting or open repair.
What is the classic cause of thoracic aortic aneurysms? (hint: Not just hypertension)
What are some of its complications?
Syphilis!
Mediastinal encroachment (can compress trachea, esophagus, recurrent laryngeal nerve), aortic dilation & insufficiency, and aortic rupture.
Who are at highest risk of aortic dissections?
What exactly occurs, and where?
Those with hypertension (“40-60yrs of age”), or with connective tissue disorders.
A tear in the tunica intima (usually within first 10cm of ascending aorta) allows blood to penetrate and rupture the tunica media, forming a false lumen.
Where does aortic dissection usually progress?
What are some complications of aortic dissection?
Usually anterograde (“out”).
Blood may “reenter” and form a double-barreled lumen (google it). If dissection occurs retrograde, cardiac tamponade may result. Can also rupture pleurally/peritoneally.
What is the classic presentation of an aortic dissection?
Distinguish between a type A and B dissection.
Tearing/stabbing, 10 out of 10 pain in the anterior chest that radiates to the back.
A: Starts proximal to the aortic arch. B: Starts distal to the arch.
What are the three etiologies of vasculitis?
Immune-mediated, infectious, or idiopathic.
What are ANCAs?
What are the signifiances of PR3-ANCAs and MPO-ANCAs?
ANCA: Anti-neutrophil cytoplasmic antibody, targeted against something in neutrophil granules.
PR3: A proteinase. ANCA+ in Wegner’s Granulomatosis.
MPO: Myeloperoxidase. ANCA+ in Microscopic Polyangiitis and Churg-Strauss Syndrome.
Describe how infections can contribute to vasculitis.
Which vasculites have unknown etiologies?
Either by direct invasion of the vessel wall, or by triggering an autoimmune reaction.
Unknown: Giant cell arteritis, Takayasu Arteritis, Polyarteritis Nodosa (all large/medium)
