Peripheral Vascular Disease I and II Flashcards
peripheral artery disease (PAD)
when blood flow to the extremities is blocked, usually due to atherosclerosis of the vessels
types of PAD
claudication
rest pain
tissue loss
claudication
muscle pain, called intermittent claudication
typically comes on with exercise and is relieved with rest
rest pain
as atherosclerosis progresses and blockage becomes more severe, pain may occur in the feet even when at rest
rest pain occurs because the arteries of the leg can no longer deliver adequate blood flwo to the feet, even at rest
generally worsens when the legs are elevated, such as wehn lying in bed at night
relieve may occur only when the feet are dangled
two drugs that are accepted treatment for claudication
cilostazol and pentoxifylline
cilostazol is much more effective
chronic changes in skeletal muscle histology
honeycomb pattern
increased adipose
increased inflammatory cells
increased angular fibers
decreased type III fibers
decreased gastroc strength - cross-sectional area
treatment for CAD
medication
exercise
risk factor modification and management
bypass surgery
endovascular interventions
emerging CAD therapies
gene therapy - VDGF165, VEGF121, hepatocyte growth factor (HGF), fibroblast growth factor 1 (FGF-1)
stem cell therapy - bone marrow, peripheral blood
acute mesenteric ischemia
caused by decreased intestinal blood flow that can be caused by a number of mechanisms
results in ischemia and subsequent reperfusion damage that may progress to the development of mucosal injury, tissue necrosis, and metabolic acidosis
intestinal blood supply
celiac axis
superior mesenteric artery
inferior mesenteric artery
types of acute mesenteric ischemia
embolic disease
thrombolic disease
nonocclusive mesenteric ischemia
venous thrombosis
embolic disease
embolus tends to lodge in SMA distal to middle colic artery
this preserves the proximal jejunum and transverse colon
doesn’t go into the celiac because of the angle of the vessels
etiology of embolic disease
atrial tachyarrhythmia
MI
cardiomyopathy
heart defects
cardiac tumors
endocarditis
aortic mural thrombus
thrombotic disease
atherosclerosis
hypercoagulable state
etiology of nonocclusive mesenteric ischemia
caused by vasospasm
atherosclerosis is frequent
low flow states
hypovolemia
vasoconstrictors
vasoactive agents
aortic insufficiency
liver failure
cardiopulmonary bypass
venous thrombosis
superior mesenteric vein is the most common
sometimes the inferior mesenteric vein and portal vein
characterized by edema, hemorrhage, and sloughing
etiology of venous thrombosis
hypercoagulable state
malignancy
trauma
abdominal surgery
hepatic failure
pancreatitis
oral contraceptives
clinical presentation of embolic and thrombotic acute mesenteric ischemia
sudden pain out of proportion to exam
gut emptying
nausea
vomiting
diarrhea
clinical presentation of embolic and thrombotic chronic mesenteric ischemia
post prandial pain
weight loss
food fear
clincial presentation of NOMI and MVT
slower course
usually critically ill, hospitalized, intubated
abdominal pain
nausea and vomiting
bloody stool
dehydration
fluid shifts
diagnosis of MAD
laboratory studies
x-ray
ultrasound
CTA
MRA
contrast angiography is the gold standard
management of embolic MAD
early diagnosis
SMA embolectomy
anticoagulation
bowel resection
second look
management of thrombotic MAD
early diagnosis
SMA/CA bypass (venous)
anticoagulation
bowel resection
second look
management of NMI
correct underlying problem
systemic vasodilator infusion
catheter directed vasodilator infusion
management of venous thrombosis
resuscitation
anticoagulation
laparotomy if periotneal signs
? thrombolytic therapy
carotid artery disease plaque anatomy
commonly occurs at bifurcations
typically thickest at bulb and extends 2 cm
occurs along lateral wall of the carotid artery
pathophysiology of stroke
embolism of overlying thrombus
embolism of plaque fragment
low flow through post stenotic segment
clinical presentation of carotid stenosis
asymptomatic
transient ischemic attack (TIA)
stroke
diagnosis of carotid stenosis
carotid duplex - imaging, velicity measurements
MRA
CTA
contrast angiography
treatment of carotid artery disease
medical therapy - antiplatelet (aspirin and clopidogrel)
surgical therapy - carotid enarterectome (CEA) or carotid artery stenting (CAS)
etiology of aortic dissection
dissection of blood between and along the laminar planes of the media, with formation of a blood-filled channel within the aortic wall
the inciting incident is usually related to severe hypertension
type A dissections
very life-treatening and usually require emergent surgical treatment
dissection may affect aortic valve, causing sudden valvular incompetence and death
rupture into the pericardium and sudden death is not unusual
50-60 years of age
type B dissections
begin and remain distal to the left subclavian artery
less life-treatening as the heart is not involved
branches of the arota may be occluded, causing symptoms such as paraplegia, renal failure, valvular hypertension, bowel gangrene, or leg ischemia
if not life-threatening, management involves medical rather than surgical treatment
60-70 years of age
pathophysiology of aortic dissection
Hyptertension
medial degeneration - deterioration of medial collagen and elastin, loss of vascular smooth muscle cells
intimal thickening - fibrosis, calcifications, fatty acid deposition
adventitial fibrosis - obstruct small intramural vasa vasorum
inherited connective tissue disorders
association with cocaine use
circadian pattern
presentation of aortic dissection
severe excruciating pain in the anterior chest and back
malperfusion syndrome:
stroek
intestinal ischemia
lower extremity ischemia
paralysis
cardiac tamponade/coronary ostia compromise
hypotension/shock
treatment of type A aortic dissection
emergency surgery
treatment of type B aortic dissection
no ischemic complications - medical therapy
ischemic complications - surgery
rupture - surgery
abdominal aortic aneurysms
enlargement of the arterial diameter, usually 1.5 times the adjacent normal arterial diameter or more
shapes are either fusiform or saccular
95% are below the renal arteries
rupture of aortic aneurysms is usually posterior and to the left
types of aortic aneurysms based on location
infrarenal
juxtarenal
pararenal
suprarenal
pathophysiology of aneurysms
inflammation
disruption of conective tissue architecture with loss of elastin
medial thinning
inflammation leading to aneurysm
inflammatory cells
release of cytokines
activate MMPs
degradation of collagen and elastin
matrix metalloproeinases
zinc-dependent enzymes
secreted as zymogens
degrade collagen, elasin, and gelatin
sources of MMP
vascular smooth muscle cells
fibroblasts
inflammatory cells
endothelial cell surrounding the vaso vasorum
MMP-2
72kDa gelatinase A
substrates - type IV collagen, gelatin, elastin
elevated in small, stable aneurysms
not elevated in normal aorta or occlusive disease
MMP-9
92kDa gelatinase B
main substrate is elastin
elevated in large, rapidly expanding aneurysms
tissue and circulating levels of MMP-9 correlate with aneurysm size
medial thinning
increased SMC apoptosis (3-fold)
decreased SMC density
impaired SMC proliferation
protective factors of abdominal aortic aneurysm
female sex
black race
diabetes mellitus
etiology of abdominal aortic aneurysm
atherosclerosis is the predominant cause
Marfan syndrome
fibrillin-1 defect
main structural component in elastin-associated microfibrils
Type IV Ehlers-Danlos syndrome
type III procollagen defect
clinical presentation of abdominal aortic aneurysms
asymptomatic
distal emboli
rupture
How big does an aneurysm have to be to risk surgery
5.5 cm - benefits outweight risks at this point
diagnosis of abdominal aortic aneurysm
asymptomatic
physical exam
plain x-ray
CT scan
rupture
treatment of abdominal aortic aneurysms
open repair
endovascular repair
size is not a limitation
proximal “landing zone” at least 15mm
proximal neck angulation <60 degrees
delivered by bilateral transfemoral route
limited by tortuous, calcified, small iliacs
concomitant aneurysms limit use
indications for repair
large (>5.5 cm)
rapid expansion of >0.5 cm/year
rupture
symptomatic
other arterial aneurysms
subclavian
femoral
popliteal
hand
