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31 Cards in this Set

  • Front
  • Back
There are three general category classifications of vascular dz. What are they?
- Arteriosclerosis (of which there is athero/ ateriolosclerosis and Monckeberg's calcific sclerosis)
- Inflammatory (vasculitis)
- Congenital anomalies (berry aneurysms, arteriovenous fistulas, fibromuscular dysplasia)
Match atherosclerosis, arteriolosclerosis and Monckeberg's medial calcific sclerosis to its general findings.

1. Have chunky calcification in the wall of the vessel
No obstruction of the vessel lumen, so is more benign
2. Wil see yellow plaques grossly inside the vessel, Patchy involvements, Vessels are NOT completely obstructed
3. Microscopic findings, Thickening (see pink donuts) due to hyaline or amyloid narrow the lumen of the vessel
1. Monckeberg's medial calcific sclerosis
2. Atherosclerosis
3. Arteriolosclerosis
Recall the layers (in to out) of large arteries.
Recall the layers (in to out) of large arteries.
1. Intima lined by endothelial cells
2. Internal eslatic lamina
3. Media containing smooth muscle cells
4. External elastic lamina
5. Adventitia with vasa vasorum
1. Intima lined by endothelial cells
2. Internal eslatic lamina
3. Media containing smooth muscle cells
4. External elastic lamina
5. Adventitia with vasa vasorum
Atherosclerosis is hardening of the arteries. The five most common vessels involved are...
1. abdominal aorta (AAA)
2. coronary artery (MI)
3. popliteal artery (PVD)
4. descending thoracic
5. internal carotid (stroke)

6. (just for funsies) is Circle of Willis
What are the
a. major nonmodifiable (4)
b. potentially controllable (5)
risk factors for artherosclerosis?
Major nonmodifiable:
- increased age
- male gender
- family history
- genetic abnormalities

Potentially controllable
- hyperlipidemia
- HTN
- cigarette smoking
- diabetes
- C- reactive protein

Other lesser, uncertain nonquantitated risks:
- obesity
- physical inactivity
- stress
- postmenopausal
Describe the pathogenesis of atherosclerosis formation.
Chronic injury (HTN, smoking, toxins) that help the lipoproteins accumulate inside the vessel lumen.  For the lipoproteins to accumulate inside the vessel, you need to have a lot of cholesterol (hyperlipidemia), especially of the LDL kind.  Once the lipid
Chronic injury (HTN, smoking, toxins) that help the lipoproteins accumulate inside the vessel lumen. For the lipoproteins to accumulate inside the vessel, you need to have a lot of cholesterol (hyperlipidemia), especially of the LDL kind. Once the lipids get inside, they are eventually eaten up by macrophages. But, keep in mind the chronic endothelial injury also attracts monocyte and platelets to adhere to epithelium. Once you get all the lipoproteins inside, you get activation of factors and macrophages and you get smooth muscle proliferation and extracellular muscle synthesis. So you end up with cholesterol, fat and macrophages inside of your vessel (that’d make up the plaque).
What is this?
What is this?
Cholesterol clefts! The pink (just pink - no nuclei) is necrotic tissue.
True or False:
Fatty streaks are the precursor to plaques.
Most likely true.

Basically, fatty streaks are macrophages in the intima.
What differentiates a plaque from being "vulnerable" to "stable"?
The more fibrous cap on the lipid core, the more stable the plaque.
The more fibrous cap on the lipid core, the more stable the plaque.
There are two subdivies of arteriolosclerosis:
[ hyaline / hyperplastic ] arteriolosclerosis which are very leaky, breakable and hemorrhage easily and is commonly associated with diabetes and looks like pink donuts ;
[ hyaline / hyperplastic ] which are associated with malignant HTN and has multiple layers and looks like an onion
hyaline : pink donuts, associated with daibetes. Leakage of plasma proteins, excessive extracellular matrix production.


hyperplastic: looks like an onion, associated with HTN. Lamellar re-duplication of intimal smooth muscle cells
____________ is a vascular dilation due to weakened wall. Indicates structural weakness, inflammatory process and/or trauma.
aneurysms

significance: is can lead to rupture, thrombosis and embolism, erosionor compression of adjacent structures
Aneurysms in various areas can indicate different things.
A. Ascending aorta aneurysm (plus plasma cells) =
B. Lower abdominal aorta aneurysm =
C. Mid abdominal area =

pickin' s: atherosclerosis, mycotic, tertiary syphillis
A. Ascending aorta aneurysm (plus plasma cells) = tertiary syphillis
B. Lower abdominal aorta aneurysm = due to atherosclerosis
C. Mid abdominal area = mycotic
What is the classic "rupture triad" for an abdominal aortic aneurysm?
- abrupt onset of severe back pain
- hypotension
- pulsative mass
A ______________ is entry of blood into aortic wall through an intimal tear, causing wall to split
A "dissecting aneurysm"

Risk factors: age, hypertension, CT disorder (Marfan syndrome, Ehler-Danlos syndrome) and/or cystic medial degeneration
What are the symptoms of a Type A aortic dissection?
Sudden pain in chest and in between scapulae.  
Note: Type A is more dangerous, so needs surgical intervention immediately!!
Sudden pain in chest and in between scapulae.
Note: Type A is more dangerous, so needs surgical intervention immediately!!
Vasculitis is inflammation of vessels. Match the following with their description.

1. has association w/ polymyalgia rheumatica
60y/o, ERS=60,Tx=60mg prednisone
2. Wherever it occurs, you get necrotizing inflammation in the vessels which can manifest as muscle weakness or pain commonly. Most commonly in renal arteries.
3. Pediatrics. 2-4 yrs old. Have strawberry tongue, peeling of red lips, skin on fingers. Thrombosis too. So treatment would be IV Ig and aspirin. Most common cause of acquired coronary diseases in pediatrics population!
4. involvement of upper respiratory tract (patient will have sinusitis and simultaneously blood in urine or coughing blood). Know that both upper respiratory tract and kidney involvement occurs with this.

Giant cell temporal arteritis, Kawasaki disease, Polyarteritis nodosa, Wegener granulomatosis
1. has association w/ polymyalgia rheumatica
60y/o, ERS=60,Tx=60mg prednisone = GIANT CELL TEMPORAL ARTERITIS
2. Wherever it occurs, you get necrotizing inflammation in the vessels which can manifest as muscle weakness or pain commonly. Most commonly in renal arteries. = POLYARTERITIS NODOSA
3. Pediatrics. 2-4 yrs old. Have strawberry tongue, peeling of red lips, skin on fingers. Thrombosis too. So treatment would be IV Ig and aspirin. Most common cause of acquired coronary diseases in pediatrics population! = KAWASAKI DISEASE
4. involvement of upper respiratory tract (patient will have sinusitis and simultaneously blood in urine or coughing blood). Know that both upper respiratory tract and kidney involvement occurs with this. = WEGENER GRANULOMATOSIS
What vasculitis is described?
Involves intermediate and small arteries, sometimes veins, usually of the lower extremities. Usually in young adults, before age 35. Strong association with heavy cigarette smoking. Occlusive thromboses with microabscesses.

A. Giant cell (temporal) arteritis
B. Polyarteritis nodosa
C. Thromboangiitis obliterans
C. Thromoangiitis obliterans / aka Buerger's Disease
What are some atherosclerotic risk factors? (4)
HTN, cigarette smoking, diabetes and hyperlipidemia
What are noninvasive laboratory assessments to discern whether an occlusive disease is present?
- Duplex study (Doppler probe analysis that looks at flow characteristics + B-mode ultrasound imaging)
- ABI, ankle to brachial index. (Blood pressure measured at both R and L ankels AND R and L arms. Systolic BP of ankle is compared to systolic BP of arm. The lower the ABI, the more severe the loewr extremity arterial insufficiency.
- Angiography
Regarding the ABI index, or ankle to brachial index, an assessment of whether occlusive dz is present, the lower the ABI the worse. Claudication likely occurs with ABIs < ______, lower extremity and ischemic rest pain in patients with ABIs < ____ and ischemic gangrene with ABIs < _____.
claudication < 0.75
ischemic rest pains < 0.4
ischemic gangrene < 0.25
Lower extremity peripheral arterial disease (PAD) can remain asymptomatic if mild, or may manifest with what three things?
Claudication, rest pain, or tissue loss!

Claudication: cramping lower extremity pain precipitated by walking. Patient knows they can walk a certain distance (ex. 1 block) before they cramp and need to rest for a few minutes. Usually calves or thighs cramp.
Rest pain: aching pain in the forefoot that is alleviated by dangling foot. Also, commonly rest pains wake people up in the night.
Tissue loss: includes things like non-healing ulcers or gangrenous extremities.
True or False:
Although intermittent claudication can be debilitating, it is not strongly predictive of limb loss; less than 5% of claudicators will develop limb threatening ischemia over five years.
TRUE

Hence, treatment for intermittent claudication is for lifestyle improvement in most circumstances. Treatment is conservative with risk factor modifications (esp smoking cessation) and a regular walking program. Cilostazo, a PDE inhibitor is effective at palliating claudication symptoms and occasionally improving ABIs. Refractory debilitating claudication can be treated with loewr extremity revascularization including angioplasty and bypass surgery.
Which of the following is FALSE about ischemic rest pain?
A. Carries a high risk for subsequent limb loss
B. Usually presents burning in character
C. If a patient has a palpable pedal pulse, pain in their foot at rest is likely NOT ischemic rest pain
D. All are true
FALSE IS B!! This is more indicative of diabetic neuroptahy. Ischemic rest pain is more like an aching forefoot pain.
What are the three indications for lower extremity revascularization procedures to be done?
- rest pain(carries a high risk for subsequent limb loss)
- gangrene (including non-healing ulcers or recurrent wounds/infections)
- disabling claudication
Patients presenting with ACUTE loewr extremity ischemia (secondary to acute arterila embolus versus in-situ thrombosis of native occlusive disease) present with the classic 5P's....
pulselessness
pain
poikilothermia (temp varies widely)
pallor
paralysis

urgent arteriography is necessary to differentiate embolus versus acute thrombosis atop baseline occlusive dz. Treatment for former is catheter embolectomy and anticoag whereas for latter it is systemic anticoag with directed thrombolysis or surgical thrombectomy
An aneurysm is defined as...
a localized idlation in artery diameter to 1.5 times the normal expected diameter
What is FALSE about abdominal aortic aneurysms?
A. presenting symptoms are usually back pain, hypertension, and a palpable pulsatile mass
B. 4:1 male to female ratio of occurence
C. 40% are associated with iliac artery aneurysms
D. mostly found in patients with atherosclerosis
E. radiologic imaging is critical for diagnosing an AAA; abdominal ultrasonography is the most commonly used screening modality or, if suspected ruptured, then CT scan
FALSE! A. presenting symptoms are usually back pain, hypertension, and a palpable pulsatile mass - instead of hypertension should be HYPOtension!!!
The risk of AAA rupture increases rapidly with a 5-year rupture rate of 25%-41% if the aneurysm is how wide?
5cm in diameter

Average growth rate is 0.5cm per year. For those under 5cm, a nonoperative approach to AAAs below 5 cm in size presumes patients will receive treatment for risk factors, particularly hypertension.
[ Iliac / Popliteal ] aneurysms are the most common peripheral aneurysm and rarely rupture but have a moderate risk of thrombosing (thus high limb loss rate) or embolizing.
Popliteal aneurysm
What is the first most common peripheral artery aneurysm?
Popliteal aneurysms.

Second most common is femoral artery aneurysm (presents with groin pain and palpable mass (femoral bruit) and posisble ecchymosis in context of an acute pseudoaneurysm.
Patients presenting with carotid artery occlusive dz can be symptomatic or asymptomatic. If symptomatic, usually present with....
focal sided neurological deficit (ex. unilateral limb weakness or parasthesias, aphasia, dysphaia, amaurosis fugax) that can resolve in 24 hours or not.