17209813
A 63 year old smoker with leg pain
- Claudication
- Muscle pain on mild exertion
- Relieved by a short period of rest
- differential diagnosis
- Musculoskeletal
- Arthritis
- Chronic
compartment
syndrome
- Muscle strain
- Medial tibial stress syndrome
- Arthritis
- Neurologic
- Nerve root
compression
- Peripheral
neuropathy
- Spinal stenosis
- Nerve entrapment
- Nerve root
compression
- Vascular
- Peripheral Vascular Disease
- Circulation disorder due to
narrowing or blockage of
blood vessels.
- Earliest sign
- Pain in the calf muscles.
- increases with exercise
and subsides with rest
- increases with exercise
and subsides with rest
- Pain in the calf muscles.
- Fontaine Stages
- Stage 1: Asymptomatic.
- Stage 2: Intermittent claudication.
- Stage 3: Rest Pain.
- Stage 4: Ischemic Ulcers or Gangrene.
- Stage 1: Asymptomatic.
- Causes
- Atherosclerosis
- Pathogenesis of Atherosclerosis
- 1- Endothelial injury
- induced by mechanical,
metabolic, and other
adverse influences.
- 2- This will result
in Endothelial
dysfunction
- Leading to leukocyte
adhesion and increased
permeability to lipids,
so lipid accumulation.
- 3- Accumulation and
attachment of
platelets to the
vessel wall
- platelets degranulate,
releasing growth factors and
permeability factors, and
also help recruit monocytes.
- 4- The monocytes
will be activated
into
macrophages
- 5- Smooth
muscle cell
recruitment
- due to factors released from
activated platelets,
macrophages, and vascular
wall cells.
- 6- Oxidation of
lipids deposited
in the stroma
- macrophages
releasing reactive
free oxygen
radicals
- 7- Uptake of oxidized lipids
into the cytoplasm of
macrophages and smooth
muscle cells results in the
formation of foam cells.
- 8- Foam cells die and
release cell debris,
enzymes, and lipids that
form the semiliquid core of
atheromas.
- 9- Smooth muscle cells change
their phenotype and become
collagen-producing cells that
form the capsule of atheroma.
- 9- Smooth muscle cells change
their phenotype and become
collagen-producing cells that
form the capsule of atheroma.
- 8- Foam cells die and
release cell debris,
enzymes, and lipids that
form the semiliquid core of
atheromas.
- macrophages
releasing reactive
free oxygen
radicals
- due to factors released from
activated platelets,
macrophages, and vascular
wall cells.
- 5- Smooth
muscle cell
recruitment
- platelets degranulate,
releasing growth factors and
permeability factors, and
also help recruit monocytes.
- Leading to leukocyte
adhesion and increased
permeability to lipids,
so lipid accumulation.
- induced by mechanical,
metabolic, and other
adverse influences.
- 1- Endothelial injury
- Pathogenesis of Atherosclerosis
- Injury to the arms or legs
- Irregular anatomy of
muscles or ligaments
- Infections
- CAD
- Atherosclerosis
- Risk Factors
- Complications
- Amputation
- Poor wound healing
- Restricted mobility due to pain or discomfort
- Severe pain in the affected extremity
- Stroke
- Amputation
- Investigations
- Imaging
- Duplex US
- Anatomic
information
- Vessel wall, intraluminal obstructive lesions,
perivascular compressive structures
- Vessel wall, intraluminal obstructive lesions,
perivascular compressive structures
- Anatomic
information
- MR
- 3D
- CT
- DSA
- 2D
- Radiation
- 2D
- Duplex US
- Physical Exam
- Ankle-Brachial Index
- Ankle-Brachial Index
- Blood tests
- Complete blood count
- Blood urea nitrogen,creatinine, and electrolyte studies
- lipid profile
- coagulation tests
- Complete blood count
- Imaging
- Management
- Medication
- Surgical
procedures
- Peripheral
artery bypass
surgery
- Atherosclerosis
endarterectomy
- Peripheral
artery bypass
surgery
- Interventional
procedures
- Angioplasty
- Stenting
- atherectomy
- Angioplasty
- Medication
- Circulation disorder due to
narrowing or blockage of
blood vessels.
- Deep venous
thrombosis
- Signs and symptoms
- - Asymmetrical edema\ erythema in the
affected leg\ warmth in the affected leg\
Asymmetrical calf swelling \
Asymmetrical localized pain
- - Asymmetrical edema\ erythema in the
affected leg\ warmth in the affected leg\
Asymmetrical calf swelling \
Asymmetrical localized pain
- Causes
- Virchow’s triad
- venous stasis
- post operation, long flights, car
trips and pregnancy
- clotting factor adhesion and activation
of coagulation cascade
- post operation, long flights, car
trips and pregnancy
- Hypercoagulability
- genetic defects \ surgeries \
certain medications like OCP
- genetic defects \ surgeries \
certain medications like OCP
- Endothelial damage
- infections, chronic inflammation or toxins like tobacco.
- exposes the tissue factor and collagen
- infections, chronic inflammation or toxins like tobacco.
- venous stasis
- Virchow’s triad
- Complications
- Pulmonary embolism
- Post thrombotic syndrome
- Pulmonary embolism
- Investigations
- Full blood count\ D-dimer lab
test\ Liver function test\ Urea
and creatinine\ INR\ APTT\
Venous duplex ultrasound\
Venography\ Chest imaging.
- Full blood count\ D-dimer lab
test\ Liver function test\ Urea
and creatinine\ INR\ APTT\
Venous duplex ultrasound\
Venography\ Chest imaging.
- Signs and symptoms
- Politeal
artery
entrapment
- Vasculitis
- Clinical features
- Fever, arthralgia,
myalgia, malaise
- Fever, arthralgia,
myalgia, malaise
- Types
- Large
Vessel
Vasculitis
- Temporal (Giant Cell) Arteritis
- Granulomatous vasculitis that classically involves branches of the carotid artery
- Most common form of vasculitis in older adults (> 50 years); usually
affects females
- Presents as headache (temporal artery involvement),
visual disturbances (ophthalmic artery involvement), and
jaw claudication. Flu-like symptoms with joint and
muscle pain (polymyalgia rheumatica) are often present.
ESR is elevated.
- Biopsy reveals inflamed vessel wall with giant cells and intimal fibrosis
- Granulomatous vasculitis that classically involves branches of the carotid artery
- Takayasu Arteritis
- Granulomatous vasculitis
that classically involves the
aortic arch at branch points
- Presents in adults < 50 years old
(classically, young Asian females) as
visual and neurologic symptoms with
a weak or absent pulse in the upper
extremity ('pulseless disease'). ESR is
elevated
- Granulomatous vasculitis
that classically involves the
aortic arch at branch points
- Temporal (Giant Cell) Arteritis
- Medium
Vessel
Vasculitis
- Polyarteritis
Nodosa
- Necrotizing vasculitis
involving multiple
organs; lungs are
spared
- Classically presents in young adults as
hypertension (renal artery involvement),
abdominal pain with melena (mesenteric
artery involvement), neurologic disturbances,
and skin lesions.
- Associated
with serum
HBsAg
- Necrotizing vasculitis
involving multiple
organs; lungs are
spared
- Kawasaki Disease
- Classically
affects Asian
children < 4
years old
- Presents with nonspecific signs
including fever, conjunctivitis,
erythematous rash of palms and
soles, and enlarged cervical lymph
nodes
- Coronary artery
involvement
- Classically
affects Asian
children < 4
years old
- Buerger Disease
- Necrotizing vasculitis
involving digits
- Presents with ulceration,
gangrene, and
autoamputation of fingers
and toes; Raynaud
phenomenon is often
present
- Highly associated with
heavy smoking
- Necrotizing vasculitis
involving digits
- Polyarteritis
Nodosa
- Small Vessel Vasculitis
- Henoch-Schonlein Purpura
- Vasculitis due to IgA
immune complex
deposition; most common
vasculitis in children
- Presents with palpable
purpura on buttocks and
legs, GI pain and bleeding,
and hematuria (IgA
nephropathy); usually occurs
following an upper
respiratory tract infection
- Disease is
self-limited, but
may recur
- Vasculitis due to IgA
immune complex
deposition; most common
vasculitis in children
- Henoch-Schonlein Purpura
- Large
Vessel
Vasculitis
- Clinical features
- Chronic venous insufficiency
- Causes
- DVT
- Phlebitis
- Congenital defects
- Complication of varicose veins
- When venous valves become
incompetent they tend to place extra
pressure on more distal valves,
which may also become
incompetent.
- This condition produces dilated tortuous superficial veins
- signs and symptoms
- Obvious dark blue or purple
veins\ Spider veins\ Veins that
appear to be bulging and
twisted\ Heavy feeling in legs\
Burning, throbbing muscle
cramping in lower legs\ Pain
worsened after standing for long
time\ Itchiness and redness
around veins
- Obvious dark blue or purple
veins\ Spider veins\ Veins that
appear to be bulging and
twisted\ Heavy feeling in legs\
Burning, throbbing muscle
cramping in lower legs\ Pain
worsened after standing for long
time\ Itchiness and redness
around veins
- signs and symptoms
- This condition produces dilated tortuous superficial veins
- When venous valves become
incompetent they tend to place extra
pressure on more distal valves,
which may also become
incompetent.
- DVT
- Lead to blood stagnation in
lower extremity
- start to cause inflammatory
reaction in the vessels and
surrounding tissue which lead
to fibrosis and ulcers called
venous stasis ulcers. Other
symptoms include,
hyperpigmentation of the skin,
pruritis, varicose veins, pain and
a lot of edema
- start to cause inflammatory
reaction in the vessels and
surrounding tissue which lead
to fibrosis and ulcers called
venous stasis ulcers. Other
symptoms include,
hyperpigmentation of the skin,
pruritis, varicose veins, pain and
a lot of edema
- Causes
- Peripheral Vascular Disease
- Musculoskeletal
- Muscle pain on mild exertion
- History of Diabetes and Hypertension
Anexos de mídia
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