Flashcards in Blood Vessel and Lymphatic Disorders Deck (69):
A 60 y/o male smoker presents with a 6 month history of impotence along with calf, thigh, and buttocks claudication. The femoralsare not palpable. Angiogram is shown. This man has a (an):
need pic, aorto iliac artery is occluded
Treatment for artery occlusion
1. Smoking cessation and BP control
2. ASA and/or clopidogrel(Prevents MI, CVA , etc).
3. Cilostazol(Pletal/phosphodiesterase type 3 inhibitor –inhibits platelet aggregation and dilates vessels) 100 mg BID
4. Pentoxifylline(Trental/phosphodiesterase inhibitor with antihemorrheologicactivities) 400 mg TID
6. Statin (rosuvastatin40 mg daily)
8. Axillo-femoral bypass; Aorto-fem bypass
9. Intermittent calf compression. Angiogenesis with injection of mononuclear cells.`
aspirin thromboxane a2
Cilostazol Pentoxifylline kep 5amp from going to camp
P2Y12 signalling modulates thrombin generation
ADP feedback loop
A 60 y/o diabetic male presents with cramping pain in both calves with walking2-4 blocks. The femoral arterial pulses seem somewhat diminished in the groin, the left popliteal and left pedal pulses are diminished. The right pedal pulses are absent. The Ankle/Brachial index is 0.5 on the left and 0.1 on the right. There is no hair on the right toes and the patient has dependent rubor on the right. The patient most likely has severe occlusion of the
higher the blockage the sooner you will
Ankle/Brachial index normal is
If the profunduswere involved, the claudication would
occur much earlier
what artery would be the source of collateral network in pt with superficial femoral blocked
with profundus you could only walk
with superficial femoral you can walk
under what conditions would it have been possible to have a more normal ABI on the right (ie.8 or .9) and still have poor circulation?
When the vessels are calcified*as in diabetics. This does not allow
practical use of ABI and thus one must resort to wave form analysis.
failed reading with cuff
Osler’s sign or maneuver?
of calcified vessels.
Treatment of superficial and common femoral and popliteal stenosis
•1. structured walking program
•2. Fem-pop bypass*
*absolute indication for surgery –rest pain and non-healing ulceration
A 55 year old man is seen for progressive bilateral leg and calf pain
with ambulation and relief with sitting down in a chair. History is positive for hypertension and the patient is on an ACE inhibitor. Physical examination reveals an S4. Present BP is 130/60. He has a “simian gait” and complains of worse pain with extension of his back and improvement with bending forward. Calves are tender.
Pedal pulses are questionably diminished. Which test will most likely be positive?
Progressive narrowing of the spinal canal may occur alone or in combination with acute
disc herniations. Lumbar spinal stenosis (LSS) remains the leading preoperative diagnosis
for adults older than 65 years who undergo spine surgery.
atrial kick from unrelaxed ventricle (ventricle is stiff so it makes noise going in)
bc hypertensive heart disease
why are pedal pulses diminished
bc dorsalis pedis may not be where it belongs
spinal stenosis may look like peripheral vascular disease but it gets better when
nerve pain from compression
Lumbar spinal stenosis
Absence of pain or improvement of symptoms when seated assists in ruling in LSS. Patients with significant lumbar spinal canal narrowing report pain, weakness, and numbness in the legs while walking. Compressed nerve roots become ischemic due to stenosis. This is the hallmark of neurogenic claudication. The pain is relieved when the patient flexes the spine by, for example, leaning on shopping carts or sitting. Flexion increases canal size. The most common nerve affected is the L5, with associated weakness of extensor hallucislongus. Neurogenic claudication pain is exacerbated by standing erect and downhill ambulation and is alleviated with sitting, squatting, and lumbar flexion.
Lumbar spinal stenosis Neurogenic claudication pain is exacerbated by
standing erect and downhill ambulation
Lumbar spinal stenosis Neurogenic claudication pain is alleviated with
sitting, squatting, and lumbar flexion.
Tibial and pedal artery occlusion A 45 y/o diabetic presents with burning, dorsal foot pain that is relieved by getting up or dangling the foot. How do you know this is not diabetic neuropathy? How is the diagnosis made? What is the treatment?
relieved by dangling
Vein bypass to distal tibial or pedal arteries. (sometimes vessels cant take the pressure and they rupture when distal)
A 35 y/o male from south Africa presents with sudden onset painin the right lower extremity. The leg is pale, weak, and numb. The pedal pulses are absent and the foot is cold. The heart rhythm is irregular. What has happened?
Acute arterial occlusion of a limb
neuropathy bc no blood is getting down there
arteries feeding nerve are blocked and so you get numb
afib, he has thrown a clot
Acute arterial occlusion of a limb
A. 50% of cardiac emboli go to the legs.
B. With loss of light touch, surgery should be done immediately.
C. Before revascularization, NaHCO3should be administered. (lactic acidosis from hypoxia)
D. Cause is sometimes due to thrombosis.
E. Pedal pulse are not palpable.
6 Ps of acute arterial occlusion
Paresthesias (most concerned about this one)
Poikilothermia* (irregular temp, ice cold)
A 58 y/o hypertensive, diabetic, female presents with dizziness, diploplia, dysphagia, dysarthria, dysmetria, and ataxia of 50 minutes duration. The patient is having which type of an event?
dizziness, diploplia, dysphagia, dysarthria, dysmetria, and ataxia
The Dsof VB TIAs
brainstem function having to do with these things
The Lateral Medullary Syndrome
with occlusion of vertebral or PICA = the Ds plus numbness in contralateral arm or leg and ipsilateral face, with Horner’s
whalenberg or lateral medullary syndrom
Carotid Territory TIA
Aphasias, unilateral weakness or numbness, and amaurosis fugax (sudden loss of vision in one eye, everything is unilateral)
The Lateral Medullary Syndrome with occlusion
of vertebral or PICA
not asking this...
ringing in the right ear, dizziness and right facial pain. There is nystagmus on right lateral gaze. There is right perceptive deafness. Intention tremor is present on the right with falling to the right with Romberg position. There is loss of pain and temperature over the right face and opposite trunk and extremities with ptosis of the right eye
and constriction of the right pupil..
left you would get expressive or receptive
A 45 y/o hyperlipidemic, diabetic female has had abdominal pain lasting for 2 hours after meals for the past 3 years. She has had a 20 lb weight loss over the past 6 months related to fear of eating. She presents suddenly with periumbilical pain, but no significant clinical abdominal findings except for bloating. The patient has a (an)
marker for this is palpation and no pain and they are complaining about it
pain after meals from no blood while trying to digest
mesenteric occlusion treatment
•Angioplasty and stent versus aorto-celiac or superior mesenteric bypass
rt iliac to sma sephanous graft
lt iliac to ima sephanous graft
A 65 y/o female with a history of polycythemia and frequent phlebotomies presents with abdominal pain and swelling. Two months ago she had an episode of amaurosis fugax and two weeks ago, she had left sided numbness that lasted for 10 minutes. She has been having abdominal pain after meals for the past 6 months. Hbis 18 gm with WBC of 13,000 and platelets of 350,000. Exam shows abdominal enlargement with dullness to percussion in the flanks. A CT angiogram is performed and shows portal vein thrombosis. What is most unusual in this patient?
blood clots on both sides and clotting in venous and arterial system
Portal vein thrombosis
Basis of a red clot
fibrinogen forms and red cells get caught
Caused by multiple thrombophilic* and /or
hypofibrinolytic** factors, mostly inherited. Also
due to acquired risk factors (pregnancy, BCPs,
high dose steroids, immobilization, surgery,
and foreign bodies in the blood stream/catheters
Basis of a white clot
aterial side due to platelet aggregation
Caused by smoking,
DM, cholesterol emboli.
What causes arterial and venous clotting?
said wont be on test
Heparin induced thrombocytopenia (HIT)
Paroxysmal Nocturnal Hemoglobinuria(PNH)
Myeloproliferative disease (especially JAK 2)
Anti Phospholipid Antibody Syndrome (APLAS)
Anti Cardiolipin Antibody Syndrome (ACLA)
Thromboangitis obliterans (Buerger’sdisease: vasculitis of arteries and veins).
Nephrotic syndrome (antithrombinIII, protein S and C deficiency).
Right to left shunt
Popliteal artery aneurysm
•USPFTS: One time screening (for AAA) of 65-75 y/o males who have ever smoked. Insufficient evidence for women.
•Truly significant at 5-6 cm. (when you ahve to operate)
•Thrombosis in aortic aneurysms -no anticoagulation
•Do coronary surgery prior to aneurysm repair.
What is the treatment for an aortic aneurysm?
•Labetolol20 mg over 2 min IV (want to drop bp), then 40 -80 mg q 10 min
•Esmolol0.5 mg/kg IV
•Nitroprusside50 mg in 1000 D5 at 0.5 mL/min
•Surgical repair or endovascular graft (older pts)
A tall, thin 35 y/o male presents for a flight physical to renew his license for Delta. During the exam he is found to have a 3/6 diastolic decresendo murmur at the base, with a 2/6 systolic murmur at the apex that lengthens with standing and shortens with handgrip. History is positive for a prior pneumothorax. Which would be an additional finding in this patient?
on the test
problem with collagen tissue so proglem at valve rings
Aortic root dilation
as it dialated it went down to the ring
diastolic decresendo murmur at the base
systolic murmur at the apex that lengthens with standing and shortens with handgrip
Which is associated with a dissecting aortic aneurysm?
dissection into the intima
sharp intense chest pain
inferior wall mi
gets close to right coronary artery and you get an infaction in the inferior wall
4-5 % of people have arteries going to spinal cord so you get paraplegia
Can also see dissection in
pregnancy, bicuspid aortic valve, and coarctation.
Know the symptoms of a dissecting ascending thoracic aortic aneurysm
versus a descending thoracic aortic aneurysm as given in Lange’s CMDT!
What is the medical treatment for an expanding or dissecting aortic aneurysm?
What produces mediastinal widening?
not on test
•Artifact –patient rotated
•Mediastinal Mass –T and B cell lymphoma, teratoma, thyroid, thymus = 4 Ts
•Vessels –aortic aneurysm
Peripheral Artery Aneurysms
•An easily palpable popliteal pulse may well be an aneurysm which can present with loss of distal pulse with acute leg or foot pain
•Popliteal aneurysms account for 70% of peripheral arterial aneurysms –risk include thrombosis and embolization.
•In treatment, surgery is indicated for peripheral embolization, > 2cm or a mural thrombus. Often can be conservative if light touch remains in tact
Which of the following predisposes to thrombophlebitis?
Hypercoagulability (lack of fibrinolysis protein cs and antithrombin deficiencies)
This patient had presented with a post-phlebiticsyndrome involving the left leg. The clot in the left iliac vein was related to pressure from the
right iliac artery is crossing over left iliac vein, sets up clots in people
iliac clot occurs on the left side, called may ferners syndrome
May –Thurnersyndrome: may account for 30%
of all venous events in the US each year.
A 59 y/o male with pancreatic cancer presents with a two week history of a swollen left leg with calf tenderness. Physical exam shows a superficial phlebitis of the left arm. The cause of these findings is most likely:
Armand Trousseau who diagnosed himself with gastric cancer. Involves mucin(glycans) producing epithelial cancers that activate platelet and leukocyte (P and L) selectins(CD62/glycoproteins or cell adhesion molecules/CAMs) that lead to platelet rich microthrombi(seen most often in adenocarcinoma of the lung).
Thrombogenic cancers: gastric, esophageal, lung, pancreas, renal, ovarian, AML, non-Hodgkins lymphoma*.
adenocarcinomas you activate and l selectins so they get more sticky and you get a clot
need to know this
History of trauma, pregnancy, and varicose veins
Superficial, irregular margins
Ruddy, beefy (bc artery is good), fibrinous, granulation
Moderate to heavy exudate
Cap refilling -
need to know
History of smoking, rest pain claudication
Site of pressure
Deep, “punched out” with sharp borders
Bed pale grey or yellow
Dry necrotic base with eschar
Pale,hair loss, cold feet, atrophic skin, no pulses
Cap filling >4-5 sec.
History of numbness
Common in DM
Cap refilling normal
ABI = normal
firm ridge and callous around it
Chronic leg ulcers
Autoimmune diseases (Felty’s)
Septic Superficial Thrombophlebitis
don't worry about
•Vancomycin15 mg/kg IV q 12 hrs
•Ceftriaxone 1 gm IV q 24 hrs
Phlegmasia Cerulean Dolens*
Literally inflammatory (edematous), blue, and painful, ie. painful, sky blue and inflamed!
Due to primary venous insufficiency with secondary arterial
insufficiency (not so in AF where emboli cause primary arterial occlusion and pallor occurs).
Most common cause is cancer, though may be obesity, old age, immobilization, or other procoagulantconditions (Factor V Leiden, etc)
so much venous insufficiency the leg swells up and blocks the artery, can tell primary problem is venous bc it is edematous and purple not white
goes with cancers
Phlegmasia alba dolens
is white one so it is an artery problem
Phlegmasia Cerulean Dolens*
3. Evaluate for cancer
A 64 y/o male with lung cancer presents with dizziness, blurred vision and headache. Physical exam shows flushed faciesand dilated neck veins. This patient has developed
vena cava obstruction
Non small cell lung cancer is the most common cause of
vena cava syndrome* followed by small cell and then lymphoma . Pancoastssyndrome is more often d
Causes of SVC obstruction
Chronic fibrotic mediastinitis(reaction to
DVT from arm veins
Aortic arch aneurysm
mroe swelling in face in morning bc gravity helps to drain
What causes lymphedema and what are its characteristics
partial agenesis of lymphatics
pitting edema without ulcers, varicose veins or stasis pigmentation
stewart treves syndrome
milroys disease 1892
–(described in a missionary from India)
–congenital lymphedema with break in the VEGFR 3 gene (know this (the gene controls lymphogenesis)
stewart treves syndrome
wont ask this
looks like lymphadema
actually a hemangiosarcoma rather than a lymphangiosarcoma due to local immunodeficiency (possibly radiation contributes)