blood vessels Flashcards
Aneurysm
- localized abnormal dilation of a blood vessel or the heart
- over time due to underlying defect in the media of the vessel
Arteriovenous malformations (AVM):
arteries →veins without intervening capillaries
–Tangle, worm-like vascular channels with prominent pulsatile arteriovenous shunting with high blood flow
-Large or multiple AVMs may lead to high output cardiac failure
Fibromuscular dysplasia:
-focal irregular thickening in medium & large muscular arteries (renal, carotid, splanchnic, & vertebral vessels)
–Usually developmental defect, but can arise from trauma etc
-young women
Berry aneurysms
Circle of Willis, AD polycystic kidney dz
–“the worst headache I’ve ever had”
-2% of pop
-90% near major branch points of ant circulation
-diameter 10>mm= 50% risk of bleeding per year
-1/3 rupture due to increase intracranial pressure (stool,orgasm)
-25-50% die w/ 1st rupture
-repeat bleeding common
most common cause of subarachnoid hemorrhage
is rupture of saccular(berry) aneurysm
where do mycotic aneurysms arise from?
(1) embolization of a septic embolus, usually as a complication of infective endocarditis
(2) an extension of an adjacent suppurative process
(3) circulating organisms directly infecting the arterial wall
- rare
what do arteriovenous malformations result from?
–can result from rupture of an arterial aneurysm into the adjacent vein
–penetrating injuries that pierce arteries & veins
–or from inflammatory necrosis of adjacent vessels
-can be surgically generated for hemodialysis
what BP is associated with increased risk of atherosclerosis
diastolic >80mmHg
systolic>139mmHg
secondary HTN
5%
- underlies renal or adrenal disease
- Primary aldosteronism, Cushing syndrome, or pheochromacytoma
- HTN due to renal artery stenosis caused by increased renin
- bruit heard
essential HTN
- idiopathic
- 90-95%
- increases with age and african americans
- Cardiac hypertrophy & heart failure (hypertensive heart dz, HHD), multi-infarct dementia, & renal failure
what do untreated HTN patients die from?
half (½) die of ischemic heart dz (IHD) or congestive heart failure, another third (⅓)die of stroke
malignant HTN
5% rapid ↑BP → death within 1-2 years
Systolic > 200mmHg, diastolic > 120mmHg
–Severe HTN, renal failure, retinal hemorrhages & exudates +/-papilledema
–Often superimposed on pre-existing benign HTN
what is blood pressure a function of?
cardiac output & peripheral vascular resistance, (genetics and environment)
cardiac output
- heart rate X stroke vol
- influenced by blood volume which is regulated by renal sodium
vascular resistance
regulated at level of arterioles;
influenced by neural & hormonal inputs
what are some humoral blood vessel constrictors
- angiotensin II
- catecholamines
- thromboxane
- leukotrienes
- endothelin
what are some blood vessel dilators
- prostaglandins
- NO
- kinins
what are neural blood vessel dilators
-beta-adrenergic
what are neural blood vessel constrictors
-alpha-adrenergic
what is HTN a risk factor for?
Atherosclerosis, CHF, & renal failure
what can HTN cause?
cardiac hypertrophy &heart failure (hypertensive heart disease),multi-infarct dementia, aortic dissection (discussed later in this chapter), &renal failure
what does untreated HTN lead to?
roughly ½ of HTN patients die of ischemic heart disease (IHD) or congestive heart failure (CHF); and another ⅓ die of stroke
what type of HTN is seen in most patients?
Essential HTN 90-95% of cases
what does sustained HTN require?
participation by kidney
Hyaline arteriolosclerosis:
-↑smooth muscle matrix synthesis
-plasma protein leakage
Homogeneou spink (hyaline) thickening of the vessel wall, →luminal narrowing
nephrosclerosisdue to chronic HTN
diffuse impairment of renal blood supply &glomerular scarring
Hyperplastic arteriolosclerosis:
-severe hypertension
Smooth muscle cells form concentric lamellations (“onionskinning”)→ luminal narrowing
malignant hypertension,
- laminations
- fibrinoid deposits
- necrotizing arteriolitis (esp in kidney)
what are two types of ateriolosclerosis
1) hyaline
2) hyperplastic
Mönckeberg medial sclerosis:
> 50yo
calcification of muscular arteries,
internal elastic membrane involved,
no narrowing of lumen,
no clinical significance
what is most frequent & clinically important pattern of Atherosclerosis
“gruel” & “hardening”,
Atheroma
Raised lesion with a soft grumous core of lipid covered by a fibrous cap
what can happen to atherosclerotic plaque?
1) obstruct blood flow
2) rupture and lead to thrombosis
3) increase diffusion distance leading to weakening of wall and aneurysm
what is the morphology of atherosclerotic plaque?
1) fibrous cap
2) necrotic center with foam cells and cholesterol crystals
what are nonmodifiable risk factors for atherosclerosis
1) genetic abnormalities
2) family history
3) increasing age (risk of MI increase 5X between 40 and 60)
4) male gender
what are modifiable risk factors for atherosclerosis
1) hyperlipidemia
2) hypertension
3) smoking
4) diabetes (incidence MI 2x higher)
5) inflammation
what are major contributors to atherosclerosis
1) age
2) hypercholesterolemia
3) metabolic syndrome
what protein predicts cardiovascular risk?
C reactive protein (CRP)
what cytokines are released during atherosclerosis inflammation
1) IL-1
- recruits macrophages and T lymphocytes
what GF are implicated in smooth muscle cell proliferation
1) PDGF
2) fibroblast growth factor
3) TGF-alpha
what are common site of atheromatous plaques in decreasing order of frequency/severity
Abdominal aorta Coronary arteries Popliteal arteries Internal carotid arteries Circle of Willis
Complications of atherosclerotic plaques
1) rupture and ulceration leading to thrombosis
2) hemorrhage
3) embolism
4) aneurysm
what are consequences of atherosclerosis
1) stenosis of lumen= ischemia
2) acute plaque change (thrombus, hemorrhage)
what is critical stenosis of lumen?
approx 70% occluded
what can cause fibrous cap on plaque to rupture?
things that decrease collagen synthesis
1) changes in BP
2) vasoconstriction
what can emboli be composed of?
may be composed of fat droplets, nitrogen bubbles, atherosclerotic debris(cholesterol emboli), tumor fragments, bone marrow, or even foreign bodies
what are 3 clinical complications of atherosclerosis
1) aneurysms and hemorrhage
2) occlusion by thrombus
3) critical stenosis
Aneurysm
“localized abnormal dilation of a blood vessel, or the heart, that may be congenital or acquired”
“True” aneurysm:
an intact(but thinned) muscular wall at the site of dilation
“False” aneurysm (pseudo-aneurysm):
efectthrough the wall of the vessel, or heart, communicatingwith an extravascular hematoma that freely communicates with the intravascular space (“pulsating hematoma”)
arterial dissection
arises when blood enters a defect in the arterial wall & tunnels between its layers
can can a aneurysm occur?
Ananeurysm may occur whenever the connective tissue of the vascular wall is weakened
what are 3 causes of aneurysm?
1) defective vascular wall CT (marfan and fibrillin)
2) net degradation of vascular wall CT (atherosclerosis increases MMP)
3) weakening of vascular wall by ischemia (atherosclerosis (inner media), hypertension (outer media) , and tertiary syphillis
Tertiary syphilis
ischemia of outer media (thoracic aorta)
Obliterative endarteritis
(characteristic of late-stage syphilis) shows a predilection for small vessels, including those of the vasa vasorum of the thoracic aorta.
-leads to aneurysmal dilation which sometimes involves aortic valve annulus (aortic valve regurg)
Cystic medial degeneration
Loss of vascular wall elastic tissue,or ineffective elastin synthesis
-disrupted and disorganized elastin filaments and increased proteoglycans
what is Cystic medial degeneration final common pathway of?
ischemic medial damage and Marfan syndrome
what are the 2 most common causes of aortic aneurysm?
1) HTN
2) atherosclerosis
what is abdominal aortic aneurysms (AAA) typically due to?
atherosclerosis
where do AAA typically occur?
- below renal arteries
- often involve common iliac arteries
what are AAA most frequent in?
- men
- smokers
- 6th decade of life
characterizations of AAA
- severe atherosclerosis of aorta
- covered with mural thrombus
- may be detected as pulsating mass in abdomen
- lines of zhan
complications of AAA
- Rupture and hemorrhage
- Occlusion of branching arteries and downstream ischemia
- Embolism
- Impingement on another structure
what causes thoracic aortic aneurysm?
hypertension,or less commonly congenital defect in connective tissue synthesis(Marfan)
marfan syndrome
- autosomal dominant
- defective synthesis of fibrillin
- abberrant TGF-beta activity weakens elastic tissue
clinical presentation of thoracic aortic aneurysm due to
- Impingement
a) Lower respiratory tree
b) Esophagus
c) Recurrent laryngeal nerves - Aortic valvular insufficiency
- Rupture
aortic dissection
-occurs when blood enters defect in intima and travels through a tissue plane within layers of the aortic media
who does aortic dissection occur in?
1) hypertensive males 40-60
2) younger patients with CT disorders (marfans)
what is primary risk factor for aortic dissection?
HTN
classic presentation of aortic dissection
- severe chest pain begins ant and radiates to back between scapulae.
- moves downward as progresses
- can be confused with AMI
what can aortic dissection cause?
1) massive hemorrhage
2) cardiac tamponade
3) double barreled aorta->can become chronic dissections
where do aortic dissections commonly occur?
ascending aorta within 10cm of aortic valve
in aortic dissections how does blood enter aortic wall?
- intimal tear
- some degree of cystic medial degeneration
type A dissections
- more common
- associated with higher morbidity and mortality
- COD=rupture
type A dissections treatment
- antihypertensive therapy
- surgical repair
vasculitis
inflammation of vessles
consitutional symptoms of vasculitis
-fever, malaise, arthralgia’s, myalgias
where does vasculitis occur?
more often arterioles, capillaries & venules affected (a few vasculitides tend to affect only one vessel type or location)
Non-infectious versus Infectious vasculitis
–Immune mediated inflammation vs direct invasion by infectious pathogens
how is immune mediated vasculitis treated?
immunosuppression
Major cause of noninfectious vasculitis
immune response (local or systemic)
Immune complex mediated vasculitis
autoantibody production and formation of immune complezxes
-deposition of ag-ab complexes in vascular walls
where is Immune complex mediated vasculitis seen?
1) systemic immunologic disease (SLE)
2) drug hypersensitivity
3) secondary exposure to infectious agent (PAN)
varicose veins
abnormal dilation of veins with valvular incompentence secondary to sustained intraluminal pressure
-embolism from thrombi of superficial LE veins RARE
esophageal varices
-portal hypertension
hemorrhoids
Dilation of the venous plexus at the anorectal junction
thrombophlebitis
venous thrombosis and inflammation
-almost always involved deep veins of legs
single most imp factor for developing DVT in LE
prolonged activity/immobilization
what may increase risk of DVT
systemic hypercoagulability
what is most serous consequence of DVT
pulmonary embolism
Migratory thrombophlebitis (Trousseausign):
- patients with cancer= hypercoagulability as paraneoplastic syndrome
- seen in mucin producing adenocarcinomas
- adenocarcinomas of lung ovary and pancreas
SVC syndrome
- bronchogenic carcinoma, mediastinal lymphoma, or aortic aneurysm
- marked dilation of the veins of the head, neck, and arms with cyanosis
- Pulmonary vessels can also be compressed →respiratory distress
IVC syndrome
- neoplasms or thrombosis of the hepatic, renal, or lower extremity veins that propagates cephalad
- Hepatocellular Carcinoma (HCC) and Renal Cell Carcinoma (RCC):occlude IVC into right atrium
- lower extremity edema, distention of the superficial collateral veins of the lower abdomen
- renal vein involvement → massive proteinuria
Lymphangitis
acute inflammation & spread of bacterial infection into lymphatics (group A β-hemolytic streptococci most common agent)
–
Red, painful subcutaneous streaks (inflamed lymphatics) & painful enlargement of draining LN (lymphadenitis)
–
Can progress to cellulitis & focal abscesses; or bacteremia & sepsis
Primary Lymphedema:
isolated congenital defect, of familial Milroy disease (lymphatic agenesis or hypoplasia)
Secondary or obstructive lymphedema:
blockage of previously normal lymphatic
•Malignant tumor, surgical procedures (radical mastectomy with axillary node dissection), post-irradiation fibrosis, filariasis, post inflammatory thrombosis or scarring
peau d’orange(orange peel):
skin overlying breast cancer, draining lymphatics clogged
benign tumors
-vascular channels filled with RBC, monolayer of normal appearing endothelial cells
malignant tumors
- cellular
- proliferative
- cytologic atypia
- don’t form well organized vessels
- confirmed with CD31 of vWF
Ectasia
any local dilation of a structure
Telangiectasia
a permanent dilation of preexisting small vessels (capillaries, venules, and arterioles) that form a discrete redlesion—usually in the skin or mucous membranes. These can be congenital or acquired andare not true neoplasms;some of them are malformations and others are hamartomas
nevus flammeus
(“birthmark”) most common form of vascular ectasia;light pink to deep purpleflat lesion on the head or neck composed of dilated vessels. Most ultimately regress spontaneously.
port wine stain:
special form of nevus flammeus. Grow during childhood, thicken the skin surface, and do not fade with time. Such lesions in the distribution of the trigeminal nerve are associated with the Sturge-Weber syndrome
Sturge-Weber syndrome (aka:encephalotrigeminal angiomatosis)
This uncommon congenital disorder is associated with facial port wine nevi, ipsilateral venous angiomas in the cortical leptomeninges, mental retardation, seizures, hemiplegia, and skull radio-opacities.
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease):
- autosomal dominant disorder
- mutations in genes that encode components of the TGF-β signaling pathway. The telangiectasias are
- malformations composed of dilated capillaries and veins that are present at birth.
- skin and oral mucous membranes, as well as in the respiratory, gastrointestinal, and urinary tracts.
- The lesions can spontaneously
what is used for small bore grafts
- saphenous vein (50% patency at 10 yrs)
- internal mammary arteries (90 % patency 10 yrs)
Giant cell (temporal) arteritis & aortitis
- branches of carotid artery
- older patients (>50)
- females
- chronic T cell mediated (mostly CD4) inflmation of arteries in head (especially temporal a’s
- temporal artery may be painful to palpation
- double vision or involvement of ophthalmic artery may lead to vision loss (50% patients
- granulomatous inflammation w/multinucleated giant cells
Takayasu arteritis
- aortic arch
- Pulmonary artery (involved in ½the cases),coronary & renal arteries may be involved
- -younger (<50)
- Japanese but now global
- females
- Ocular disturbances & marked weakening of pulses of the upper extremities (pulseless disease)
- weak pulse and low BP in UE
- Granulomatous
Polyarteritis nodosa (PAN)
Renal vessels Heart Liver GI Tract *pulmonary vessels are spared Clascially young adult -HTN -abdominal pain and bloody stools -myalgias -peripheral neuritis -renal involvement=mortality -1/3 of patients= chronic hep B -immune complex mediated
Kawasaki disease
-coronary arteries
Infants and small children( 80%≤4years)
-erythema of thec onjunctiva, oral mucosa, palms and soles; desquamative rash
-cervical LN enlargement= mucocutaneous lymph node syndrome
-aneurysms->thrombosis or rupture->MI
TX= IVIg and aspirin
Microscopic polyangiitis
Necrotizing vasculitis involving arterioles,capillaries and venules
-renal glomeruli and lung capillaries most commonly affected (90%=necrotizing glomerulonephritis)
palpable cuteanous purpura
**fragmented PMN
*granulomas are absent
Churg-strauss syndrome (allergic granulomatosis and angiitis)
*resembles PAN or microscopic polyangiits w/ addition of granulomas and eosinophils
Behcet disease
Classic triad: •Aphthous ulcers of the oral cavity •Genital ulcers •Uveitis (eye inflammation) -associated with HLA-B51 Tx= immunosuppression with steroid or TNF antagonist
Granulomatosis with polyangiitis (formerly known as Wegener granulomatosis)
- upper and lower resp tract and kidneys
- -males
- avg age= 40
- T cell mediated due to innocuous inhaled microbial or environmental agent
- PR3-ANCA
- granulomas w/central necrosis and vasculitis
- giant cells
Thromboangiitis obliterans (Buergerdisease)
- small and medium arteries
- tibial and renal arteries
- heavy smokers
- <35 yrs old
- israeli, Indian subcontinent and japanese
- chronic ulcerations can cause gangrene
- raynaud phenomenon
- leg pain with exercise
- instep foot pain with exercise
- superficial nodular phlebitis
- severe pain even @ rest
- extremity ulcerations
- gangrene
Raynaud phenomenon
Small arteries and arterioles (fingers and toes) (red, white, blue)
primary raynaud
- cold or emotion
- symmetric
- young women
- benign
secondary raynaud
- component of another arterial disease (SLE, scleroderma etc)
- asymmetric
- worsens with time
