peripheral vascular disease pathophy Flashcards
peripheral effects of atherosclerosis
intermittent claudication
critical leg ischemia
where can you see PAD
1) aortoiliac
2) superficial fem
3) tibial
risk factors of PAD
1) diabetes (4x)
2) smoking
3) lipid
4) HTN
PAD HAS 6X INCR RISK OF CV DEATH
symptoms of PAD
intermittent claudication
NO SX AT REST, ONLY WITH EXERCISE
1) cramp
2) calf fatigue
why do you only have sx with exercise in intermittent claudication
because decr blood flow with exercise (insufficient supply and increased demand)
symptoms of PAD
ischemic rest pain/ischemic ulcers
SX AT REST AND EXERCISE
1) pain in distal foot/heel worse with leg elev, improved by depedency and dangle foot
2) distal ulcers on toes/heel
why do you have sx with exercise and rest in ischemic ulcers of PAD
decr blood flow with exercise and rest
signs of PAD
1) decr/absent pulses
2) bruit (abd/femo)
3) muscle atrophy
4) critical leg ischemia
what is critical leg ischemia
pallor of foot when raised
dependent rubor
what are important measures of arterial stenosis
1) radius of stenosis (Q = r^4)
2) length of stneosis
___ incr at higher flow velocities
hemodynamic severity
hemodynamic severity incr at ___
higher flow velocities
more turbulent flow
develop high resistant collaterals, high oxid stress
Factors that affect arterial hemodynamics
1) perfusion pressure
2) blood viscosity
3) arterial stenosis
4) flow velocity
a
a
what is the ankle-brachial index (ABI)
ABI = ankle SBP/arm SBP
if < 0.90 = PAD (occlusion/stenosis)
if 0.90 - 1.00 = atherosclerosis
normal = 1.10
why treat claudication?
1) prevent MI, stroke, vascular death
2) incr limb sx, exercise performance, and QOL
3) heal ulcers, decr limb loss
how to treat claudication?
1) surgery/angioplasty
2) exercise training incr muscle metab
3) drugs (cilostazol)
what is arterial aneurysm
expansion of ALL 3 ARTERIAL LAYERS
normal sizes of aorta in adult
3 cm at root
2.5 cm mid-descending thoracic
2 cm at infra renal
what is cut-off size for AAA
diameter > 3cm
or
50% incr in size relative to proximal normal
mechanism behind anerusym formation
1) weak aortic wall (decr elastin/collagen)
2) inflammation (B/T lymphocytes, mac, cytokine, autoantigen
3) proteolytic enzyme of collagen(incr MMP2/9)
4) stress (HTN, turbulent blood flow, mural thrombus)
WHAT DO YOU DO WITH CONTAINED RUPTURED AAA
GO TO CATH LAB
a
a
AAA risk factors
1) age
2) gender (male more)
3) smoking
4) FHx
incr aortic diameter, incr risk of ___
AAA
clinical present of AAA
70% asymptomatic before sudden death
30% abdominal discomfort or severe radiating pain to back
how to dx AAA
1) XR
2) US
3) CT- can see prox/distal AAA,
4) MRI
5) arteriography (may miss)
which imaging test can miss AAA
arteriography because VIEWS LUMEN NOT ARTERIAL WALL
how to perform endovascular infrarenal aortic repair?
1) put in device into graft
2) assemble in body and put seals below the renal
3) internal iliac and hypogastric preserved b/c blood to pelvis
a
a
mechanism of aortic dissection
1) primary intimal tear
or
2) rupture of vasa vasorum (microcirculation of exterior wall)
risk factor for aortic dissection
1) HTN (cocaine)
2) Marfan/ Ehlers-Danlos
3) bicuspid aortic valve
4) coarctation
5) pregnancy
6) aortitis
7) surgery/arterial cath
8) trauma
clinical manifest of aortic dissection
SEVERE, TEARING PAIN
with aortic dissection, disruption of arterial circulation can cause ___ (5)
1) stroke (carotid)
2) syncope (vertebral)
3) MI (coronaries)
4) intestinal ischemia (mesenteric)
5) renal failure (renal)
how to medically treat aortic dissection
1) control change in pressure- beta blockers)
2) control BP - nitroprusside, ACE inhib, Ca2+ channel blocker
3) control pain (narocotics)
what is assoc with chronic type A dissection
aortic regurg
what is assoc with acute B dissection
rupture
organ ischemia
marfan’s
predisposing patients of venous thromboembolic disease without prophylaxis
1) hip surgery
2) paralytic stroke
3) MI
typical story of VTE
1) female student fly to Europe
2) 24 hr later, tender swollen right calf worse with standing
3) treated with LMWH hep and 6 month of warfarin
4) 2 year later, chronically swollen right calf
2 types of acute venous thromboembolism
1) DVT
2) PE
stages of chronic VTE (4)
1) swelling
2) visible collaterals
3) stasis dermatitis
4) ulceration
mechanism of thrombophilia
1) incr thrombin or 2) incr platelet activ/aggreg or 3) fibrinolytic inhibition
risk factors for severe thrombophilia
homozygous protein C deficiency
RARE
risk factors for mild thrombophilia
heterozygous factor V leiden
COMMON
risk factor for acquired thrombophilia
infection
inflammatory
estrogens
COMMON
how to treat thrombophilai parenterally?
1) heparin/LMWH
2) fondaparinaux
3) dabigatran, argatroban (thrombin inhib)
how to treat thrombophilia orally
1) warfarin
2) dabigatrain
3) rivagoxaban/apixaban (factor Xa inhib)
compare indirect vs. direct factor Xa inhib
administration
indirect = parenteral
direct = oral
compare indirect vs. direct factor Xa inhib
cofactor?
indirect = yes, requires AT
direct = no cofactor
compare indirect vs. direct factor Xa inhib
PF4?
indirect = bind PF4
direct = no bind PF4, no risk fo HIT
compare indirect vs. direct factor Xa inhib
what does it inhib
indirect = free factor Xa inhib only
dirct = free factor Xa and factor Xa in prothrombinase (BETTER)
RISK FACTORS FOR VTE?
1) hypercoag state
2) venous trauma
3) stasis
VTE puts you at risk for ___
post phlebitic syndrome
what does he have?
68 y/o male
H/o revasc for angina in 2009
2011 –> left calf cramp with walking relieved with rest
smoker, LDL high, diabetes
right carotid bruit
absent femoral/pedal pulses left leg
limb claudication
