Path: disease of blood vessels Flashcards
1
Q
Congenital anomalies of blood vessels (benign) 1
A
- Vascular malformations: birthmarks, due to errors in vascular morphogenesis (benign), has normal cell turnover/growth
- Capillary malformations (nevus simplex and flammeus): malformed dilated blood vessels that are not cancerous and appear as blotches of red or purple (will involute)
2
Q
Congenital anomalies of blood vessels (benign) 2
A
- Nevus simplex (blanching): single or multiple blanchable pink-red patches, often found on nape of neck and btwn eyes, usually spontaneously disappear
- Nevus flammeus (port-wine stain): usually on head/neck and likes the V1-V3 dermatomes, change from pink to red to purple and do not disappear
3
Q
Hemangiomas of infancy
A
- Bening vascular tumors (non blanching) often on head and neck, looks like red macule that slowly grows over first few months
- 2 phases: first is rapid growth and proliferation over 6-12 mo, then slow involution over several years
- Most follow benign course
4
Q
Venous and arteriovenous malformations
A
- Venous: soft compressible blue masses, pain common and may have venous stasis leading to localized coagulopathy
- AVM: usually in brain but can also be in head and neck, may hemorrhage or lead to seizures, headache or progressive neurological deficit
- AVMs may decrease TPR and lead to increase in SV and CO, which can cause cardiac failure
5
Q
Coarctation of aorta (CoA)
A
- Congenital narrowing of the aorta arising at level of ductus arteriosus/ligamentum arteriosum
- May occur w/ other defects, such as bicuspid Ao valve, Ao stenosis and IV septal defect, berry aneurysms
- 2 types: preductal (infantile) which is more severe (lethal) and less common, and postductal (adult) which is more common and less severe
6
Q
Pre vs postductal coarctations
A
- Preductal: narrowing of aorta is proximal to ductus arteriosus, which remains patent and results in cyanosis of lower half of the body and eventual heart failure
- Postductal: clinically it depends on the degree of narrowing, but the narrowing is distal to the ligamentum arteriosus
- Typically there is hypertension in upper body and weak pulses/hypotension in lower extremities w/ potential ischemia
- Often will see intercostal arteries enlarged which causes erosion of the undersurface of the ribs which causes characteristic x ray findings (rib notching)
7
Q
Hereditary hemorrhagic telangiectasia
A
- Manifests later in life, no Sx at birth
- AVM apparent after birth (incl plum AVM), recurrent epitaxis, mucocutaneous and GI telangiectasias develop progressively w/ age
- Fe deficiency anemia due to hemorrhage
- Dx requirements: epitaxis, telangiectasias, visceral lesions, family Hx
- Commonly associated w/ 2 genes
8
Q
Arteriosclerosis
A
- 3 forms of artery hardening
- Atherosclerosis
- Monckeberg arteriosclerosis
- Arteriolosclerosis
9
Q
Atherosclerosis
A
- Presence of fatty plaque within intima of elastic and muscular arteries
- Can lead to major consequences: aneurysm, MI, CVA, gangrene, etc
- Prominent around site of branching b/c of turbulence
- Fibrous cap overlying soft, necrotic lipid core containing foam cells, lymphocytes, cholesterol crystals
- May have neovascularization of the plaque from the vasa vasorum
10
Q
Complicated atherosclerotic lesions
A
- Focal erosions or rupture of fibrous cap leading to thrombus formation
- Hemorrhage
- Aneurysmal dilation
- Calcification
11
Q
Formation of atheromas
A
- Fatty streaks are precursor, leading to a chronic inflammation of the intima and fibroproliferative process
- Endothelial injury is trigger of inflammation (HTN, hyperlipidemia, DM, smoking)
- Injury is followed by endothelial dysfxn, lowered expression of vasodilatory molecules, increased constriction and pro-inflammatory markers unregulated
- LDL is oxidized and consumed by macs and VSMCs to become foam cells, leading to T cell activation
- VSMCs migrate to surface of intima and contribute to formation of fibrous cap
12
Q
Monckenberg Arteriosclerosis
A
- Ring-like calcifications within the media of muscular arteries
- Ca not associated w/ any inflammation, intima and adventitia unaffected
- Does not narrow the lumen
13
Q
Arteriosclerosis
A
- Arteriosclerotic changes in small arteries and arterioles
- Associated w/ HTN and DM
14
Q
Aneurysms
A
- Pathologic dilation of a blood vessel or wall of the heart
- True vs false lumen: true is where normal blood flow is, false is where stagnant blood flow, often clot, is due to rupture of the intimal and medial layers and blood collecting in adventitia
- Different formations of aneurysms: saccular (spherical dilation), berry (CoW), fusiform (symmetrical dilation of full vessel circumference)
15
Q
Subtypes of aneurysms
A
- Abdominal Ao aneurysms (AAA): most common, usually due to advanced atherosclerosis
- Other causes of AAA: medial degeneration
- AAAs are usually below renal arteries and above ilial bifurcation
- Mycotic aneurysms: infection of vessel wall, usually due to septic embolus from infective endocarditis
- Syphilitic aneurysm: during tertiary syphilis, lesions usually in ascending/thoracic aorta
- Causes arteritis of vasa vasorum leading to ischemia, necrosis of media, dilation of aortic root, and secondary aortic valve incompetence
16
Q
Aortic dissection (AD)
A
- Tear in intima and media leads to blood entering a new false lumen
- Blood pools btwn outer 1/3rd and inner 2/3rds of media, usually in descending (type B) or ascending Ao, or both (type A)
- Rupture of Ao leads to massive hemorrhage
- Blood in false lumen can reenter the true lumen thru a second distal tear (double-barreled)
- Ao regurg, MI, cardiac tamponade (blood in pericardium) and other infarctions are common complications
