BV and Lymphatics Flashcards
A 60 y/o male smoker presents with a 6 month history of impotence along with calf, thigh, and buttocks claudication. The femorals are not palpable.
Aorto-iliac occlusion
**Location of occlusion is important
Claudication
Pain caused by too little blood flow
Leriche’s syndrome
Aorto-iliac occlusion disease
Claudication, impotence, no femoral pulses
Treatment of occlusion disease
Stop smoking and BP control ASA, clopidogrel (anti-platelet) Cilostazol (inhibit platelet aggregation and dilate vessels) Pentoxifylline (antihemorrheological - change blood and vessel properties) Ramipril Statin (Rosuvastatin) Stent Bypass Calf compression, angiogenesis
Dose of Cilostazol for occlusion disease
100 mg BID
Dose of Pentoxifylline for occlusion disease
400 mg BID
Reasoning for Ramipril use
Imbalance of NO and Ang II -> increase oxygen-free radicals -> increase adhesion molecules -> inflammatory response in vessels (increase SM proliferation and ECM production)
Protease Inhibitor antiplatelet drugs
Cilostazol and Pentoxifylline
Inhibit CAMP to 5’AMP
Decrease intracellular calcium
ASA mechanism
Decrease TXA2 levels
GP IIb/IIIa inhibitors
Decrease fibrinogen cross linking and direct binding
Thienopyridines
Block ADP feedback loop
P2Y12 signaling
Modulates thrombin generation
ADP feedback loop
A 60 y/o diabetic male presents with cramping pain in both calves with walking 2-4 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:
Superficial femoral
Provides branches to lower leg
Dependent rubor
Diminished circulation to extremity -> turns red when standing, will blanch when elevated
Block in profunda femoris
Claudication will occur earlier and higher on leg
Under what conditions would it have been possible to have a more normal ABI on the right (.8 or .9) and still have poor circulation?
DM - falsely high BP due to calcified vessels
Osler’s Sign
Pseudohypertension due to calcified vessels
Can you use ABI in diabetics with calcified vessels?
No, use wave form analysis instead
Occlusion will demonstrate diminished wave forms
Most potent predictor stent thrombosis
Calcification
Treatment for popliteal or femoral stenosis
Bypass
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.
Spinal stenosis
Can present like peripheral vascular disease
Imaging to detect spinal stenosis
Lumbar MRI
Simian gate
Waddling - not due to claudication
Improvement of back back with bending forward
Spinal stenosis
S4 heart sound
Strong atrial contraction into non-compliant ventricle
S4 seen frequently in patients with
DM and HTN
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.
DM neuropathy vs Tibial/pedal occlusion
Occlusion feels relief of burning and pain by dangling the foot
Diagnose occlusion with
MRA - magnetic resonant angiography
Dorsalis pedis can sometimes be difficult to palpate even in normal patient but tibialis should always be present
A 35 y/o male from south Africa presents with sudden onset pain in 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.
A fib from thrown clot
A fib -> mural thrombi in left atria -> travels through arterial system -> stroke or leg clot
50% of cardiac emboli go to
Legs
Can also go to brain
Loss of light touch with arterial occlusion implies
Surgery should be immediate
Before revascularization what should be administered?
NaHCO3
6 Ps of acute arterial occlusion
Pain Pallor Paralysis Paresthesias Pulselessness Poikilothermia (irregular temperature regulation)
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?
Vertebro-basilar TIA
The Ds of VB TIA
**Dizziness Diploplia Dysphagia Dysarthria Dysmetria
TIA vs Stroke
TIA < 24 hrs
Lateral Medullary Syndrome
Occlusion of vertebral or PICA Ds Numbness in contralateral arm and leg Numbness in ipsilateral face Horner's syndrome (CN 5)
Other LMS with Occlusion of vertebral or PICA symptoms
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.
Areas of medulla effected by LMS
Vestibular nerve
Restiform body
Ambiguous nucleus
Spinal tract of trigeminal nerve
Carotid territory TIA
Aphasias, unilateral weakness or numbness, and amaurosis fugax
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.
Mesenteric occlusion
Treatment for mesenteric occlusion
Angioplasty and stent
Bypass
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 (TIA). She has been having abdominal pain after meals (abdominal angina) for the past 6 months. Hb is 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?
Portal vein thrombosis
BOTH venous and arterial involvement
Red clot
Stasis clot on venous side
Caused by multiple thrombophilic and /or
Hypofibrinolytic factors, mostly inherited. Also
due to acquired risk factors.
Inherited thrombophilic factors of red clot
Factor V Leiden, Prothrombin G20210A, ACLA
Inherited hypofibrinolytic factors of red clot
4G/5G polymorphism of the plasminogen activator inhibitor-1 gene (PAI-1)
Acquired risk factors of red clot
pregnancy, BCPs, high dose steroids, immobilization, surgery, and foreign bodies in the blood stream/catheters
White clot
Arterial side
Starts with platelet aggravation
Causes of white clot
Caused by smoking, hypertension, hyperlipidemia, DM, cholesterol emboli
What causes both arterial and venous clotting
**Heparin induced thrombocytopenia (HIT)
Paroxysmal Nocturnal Hemoglobinuria (PNH)
*Myeloproliferative disease (especially JAK 2)
Polycythemia vera – like in this case
Anti Phospholipid Antibody Syndrome (APLAS)
Anti Cardiolipin Antibody Syndrome (ACLA)
Hyperhomocysteinemia
Thromboangitis obliterans (Buerger’s disease: vasculitis of arteries and veins).
Nephrotic syndrome (antithrombin III, protein S and C deficiency).
Right to left shunt
Popliteal artery aneurysm
Key causes of both arterial and venous clotting to remember
HIT
Polycythemia vera
Thrombangitis obliterans (Buerger’s)
Nephrotic syndome
Significant AAA
Greater than 5-6 cm
Do you give anticoagulant for thrombosis in AAA?
No - increase risk of rupture
Coronary surgery and AAA
Look at coronary arteries with AAA is detected
Coronary surgery before AAA repair to insure proper perfusion of heart during procedure
Use of B blocker with AAA
Reduce pressure to reduce incidence of tearing
Treatment for AAA
Labetolol 20 mg over 2 min IV, then 40 -80 mg q 10 min
Esmolol 0.5 mg/kg IV
Nitroprusside 50 mg in 1000 D5 at 0.5 mL/min
Surgical repair or endovascular graft
A tall, thin 35 y/o male is found to have aortic insufficiency, mitral valve prolapse. History is positive for a prior pneumothorax.
Aortic root dilation
Marfans
Spontaneous pneumothorax
Tall slender individuals
Marfans
Aortic insufficiency murmur
Diastolic decresendo murmur at the base
Mitral prolapse
Systolic murmur at the apex that lengthens with standing and shortens with handgrip
Squatting decreases murmur
Increasing volume with increased afterload or increased venous return decreases the murmur
Dissecting aorta involves dissection of:
Media
Dissecting aortic aneurysm presents with:
Sharp tearing chest pain
Inferior MI (RCA nearby)
Diastolic murmur
Dissecting aortic aneurysm associated with:
HTN (cause)
Paraplegia (descending aorta dissection cuts off supply to vertebral arteries supplying spinal cord)
Dissection also associated with
Pregnancy, bicuspid aortic valve, and coarctation
Expanding/dissection aortic aneurysm treatment
Beta blocker
Surgery for Type A
Surgery for Type B effecting perfusion to extremeties etc.
Surgery for AA greater than 5-6 cm
Ascending aortic dissection
More chest pain
Upper extremities may be hypotensive
Descending aortic dissection
More back and abdominal pain
Paraplegia
Mediastinal widening
Artifact – patient rotated
Mediastinal Mass – T and B cell lymphoma, teratoma, thyroid, thymus = 4 Ts
Vessels – aortic aneurysm
Anthrax
70% Peripheral artery aneurysms
Popliteal artery
Can present with loss of distal pulse with acute leg or foot pain
Risk with peripheral artery aneurysms
Thrombosis, embolization
Surgery indication for peripheral artery aneurysm when:
Peripheral embolization, > 2cm in size, or a mural thrombus
Surgery on peripheral artery aneurysm can be conservative when
Light touch sensation is still present
Predisposition to thrombophlebitis
Trauma
Virchow’s triad
Increased risk of thrombus
Blood (hypercoagulability)
Flow (stasis)
Vessels (trauma)
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:
Cancer - systemic hypercoagulability
Trousseau’s Syndrome
Cancers produce P and L selectins (glycoproteins and adhesion molecules) -> platelet rich microthrombi
Metastatic cells are sticky and move through blood making little clots
Thrombogenic cancers
**Adenocarcinoma of lung
Gastric, esophageal, lung, pancreas, renal, ovarian, AML, non-Hodgkins lymphoma
Manifestations of cancer associated thrombogenic cancers
Plegmasia cerulean dolens, DIC, TTP, marantic endo, superficial migratory thrombophlebitis,
and arterial thrombosis
Absence of glycoproteins
Bleeding disorders
72 y/o male with a traumatic ulcer on his ankle most likely has:
Venous insufficiency
Venous ulcer
History of trauma, pregnancy, and varicose veins Medial malleolus Superficial, irregular margins Ruddy, beefy, fibrinous, granulation Edema Dermatitis Lipodermatosclerosis –indurated Hyperpigmentation Moderate to heavy exudate Cap refilling - < 3 sec (Normal) ABI = 0.9 or greater
Key findings of venous ulcer
History of trauma On medial malleolus Irregular borders, beefy, red Edema Indurated Hyperpigmentation Exudate
Arterial ulcer
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 Lateral Pale, hair loss, cold feet, atrophic skin, no pulses Cap filling >4-5 sec ABI = 0.5 or less
Key findings of arterial ulcer
Claudication Site of pressure Sharp borders Grey or yellow Hair loss, cold feet, no pulses
Neuropathic ulcer
History of *numbness Common in *DM Pressure site Variable depth Surrounding *callus Cap refilling normal ABI = normal
Diabetic foot infections
More likely with positive probe to bone test, ulcer duration > 30 days, trauma , PVD, peripheral neuropathy, and RI
Chronic leg ulcers associated with
PAD
Venous insufficiency
DM
Autoimmune diseases (Felty’s)
SS anemia
Erythema induratum/nodular
vasculitis/panniculitis
Fungal infectionSeptic Superficial Thrombophlebitis
Venous thrombosis associated with inflammation in the setting of bacteremia
Septic Superficial Thrombophlebitis treatment
Vancomycin 15 mg/kg IV q 12 hrs
Ceftriaxone 1 gm IV q 24 hrs
Phlegmasia Cerulean Dolens
Literally inflammatory (edematous), blue, and painful
Due to primary venous insufficiency with secondary arterial
insufficiency
Causes of Phlegmasia Cerulean Dolens
**Cancer
Obesity, old age, immobilization, or other procoagulant conditions (Factor V Leiden)
Phlegmasia Cerulean Dolens also causes
Hypovolemic shock
Massive fluid loss with decreased BP, or even vasodilatory shock from inflammatory mediators
Phlegmasia Alba Dolens
Tissue not cyanotic and blue
Colateral veins allowing some drainage so that tissue ischemia does not occur
Phlegmasia Cerulean Dolens treatment
Fluids
Anticoagulation
Investigate cancer
A 64 y/o male with lung cancer presents with dizziness, blurred vision and headache. Physical exam shows flushed facies and dilated neck veins.
Vena cava obstruction (superior)
Causes of SVC obstruction
Cancer Chronic fibrotic mediastinitis (reaction to Histoplasmosis antigen, can happen with TB as well) DVT from arm veins Aortic arch aneurysm Constrictive pericarditis
Most common cause of SVC obstruction due to cancer
Non small cell lung cancer
Followed by small cell and lymphoma
Pancoasts syndrome due to
NSCLC (especially squamous and adenocarcinoma)
Is edema better in AM or PM
PM
Better venous flow with muscle use
A 35 y/o black female presents with malaise, anorexia, sweating, chills, fever and throbbing pain in the left arm. There is warmth at the left antecubital fossa and a faint red streak is discovered over the dorsal left hand. The left axillary nodes are swollen. She denies any bites.
Cat scratch fever
Cat-born diseases
Saliva:
Bartonella henselae, Pasteurella multocida, Rabies, Capnocytophagia, Tularemia
(**Gm Neg intracellular bacteria)
Fecal:
Toxoplasma gondii, Cryptosporidium, Salmonella, Campylobacter, Ancyclostoma braziliense (Hookworm), Toxacara cati (Round worm)
Aerosol:
Coxiella burnetti
Tick or flea bites:
Lyme disease, Ehrlichiosis, Babesiosis, Yersinia pestis
Urine:
Leptospirosis
Direct contact:
Sporothrix schenckii, Microsporum canis (Ringworm)
Lymphedema
Pitting edema without ulcers, varicose veins or stasis pigmentation
Fibroses
Milroy’s disease
Congenital lymphedema with break in the VEGFR 3 gene
Stewart-Treves syndrome
Actually a hemangiosarcoma rather than a lymphangiosarcoma due to local immunodeficiency
