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Clinical Medicine 3 > Lecture 9 (Vascular Disorders)-Exam 3 > Flashcards

Lecture 9 (Vascular Disorders)-Exam 3 Flashcards

1
Q

General characterisitcs

What is an aortic aneurysm?
* What is the most common cause? other causes?

A
  • An aortic aneurysm is a weakness in subsequent dilation of the vessel wall, usually caused by a genetic defect or atherosclerotic damage to the vessel intima
  • Atherosclerosis is the most common cause, although some exist as congenital defects or as a result of vasculitis, trauma, Marfan syndrome, or Ehlers-danlos syndrome
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2
Q

Aortic Aneurysm:
* What is the clasic picture?
* Where does it most commonly occur?
* AAA most commonly occur where?
* Left untreated, what is the mortality rate?

A
  • Males are 8 times more likely to have an aneurysm; The classic picture is an elderly male smoker with coronary artery disease, HTN and a pulsatile abdominal mass
  • Aneurysms occurs most frequently in the abdominal aorta (90%), and thoracic aorta (10%)
  • AAA most commonly occur infrarenally
  • Left untreated, the mortality rate for rupture is above 90%
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3
Q

Clinical features of AAA
* Present with that?
* What happens in about 25% of patients? Why?

A
  • AAA Maybe asymptomatic or present as a pulsatile abdominal mass, sometimes accompanied by abdominal or back pain
  • Renal or lower extremity occlusive disease is present in about 25% of patients
    * This Is related to atherosclerotic disease
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4
Q

Clinical features of AA:
* Thoracic aortic aneurysms may be what? Why?
* AAA rupture causes what? Is this an issue?

A

Thoracic aortic aneurysms may be symptomatic or cause substernal, back, or neck pain; Dyspnea, stridor, and cough; Dysphasia; Hoarseness; Or symptoms of SVC syndrome
* This is related to the mass effect of the aneurysm

AAA rupture causes severe back pain, abdominal, or flank pain and hypotension or shock
* This is a surgical emergency which requires a very morbid open repair in most cases

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5
Q

Dx studies of AAA
* What does the USPSTF recommend?
* What is the inital imaging study of choice? Whatelse can you use to further evaluation?

A
  • The USPSTF recommends one-time screening for abdominal aortic aneurysm by ultrasonography in men ages 65 to 75 years who have ever smoked
  • Ultrasound is the initial imaging study of choice, CT scan is the test of choice for thoracic aneurysms and for further evaluation of patients with known AAA
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6
Q

What is the gold standard test for AA?

A

Computed tomography angiography (CTA) is considered the gold standard for diagnosing an aortic aneurysm, whether it’s thoracic or aortic

  • A note on this, some references will just mention angiography as the gold standard, this can be misleading that’s what it really should say is CT angiography.
  • The last thing you want to do is stick a catheter into a thin walled blown out aortic aneurysm and risk rupture
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7
Q

What are the different types of AAA?

A
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8
Q
A
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9
Q

Fill in the covered part?

A
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10
Q

What is the only effective txt of AAA?
* Who will decide the decisions?
* Generally thoracic aortic aneurysms require what?
* Five year survival after repair is what?

A

The Only effective treatment is endovascular or open surgery repair
* This decision will be made by the surgical team, vascular surgeons often have the capabilities to perform either endovascular or open repair
* Generally thoracic aortic aneurysms require cardiothoracic surgeons to repair, especially when the root is involved
* Five year survival after repair is greater than 60%

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11
Q

Fill in for aortic dissection?

A
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12
Q

aortic dissection
* What is it? What does it result in?

A

Aortic dissection is due to the separation of the layers of the aortic vessel wall
* A tear in the intimal layer results in the progression of the dissection (either proximal or retrograde) chiefly due to the entry of blood in between the intima and media

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13
Q

aortic dissection
* An acute aortic dissection is associated with what?
* Patients with what have a slightly better prognosis?
* Major risk factors include what?(4)

A
  • An acute aortic dissection is associated with very high mortality; the majority die even before reaching the emergency department
  • Patients with a chronic aortic dissection (more than two weeks) have a slightly better prognosis.
  • Major risk factors include hypertension, severe increase in blood pressure acutely (e.g., strenuous weight-lifting and use of sympathomimetic agents such as cocaine, ecstasy, or energy drinks), connective tissue disorders, atherosclerosis
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14
Q

What is the stanford criteria?

A
  • Type A involves the ascending aorta, regardless of the site of the primary intimal tear. Type A dissection is defined as a dissection proximal to the brachiocephalic artery.
  • Type B aortic dissection originating distal to the left subclavian artery and involving only descending aorta.
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15
Q

What is the debakey criteria?

A

The DeBakey classification is based upon the site of origin of the dissection.
* Type 1 originates in the ascending aorta and to at least the aortic arch.
* Type 2 originates in and is limited to the ascending aorta.
* Type 3 begins in the descending aorta and extends distally above the diaphragm (type 3a) or below the diaphragm (type 3b).

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16
Q

Clinical features of AD
* What is very common? What indicates a rupture?
* What should raise a suspicion of AAD?

A
  • Hypertension is very common in AAD; if the patient presents with hypotension then this is a grave sign most likely indicating a rupture.
  • A difference of more than 20mmHg in blood pressure between the arms should raise suspicion of AAD.
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17
Q

What are sxs of AD?(6)

A
  • Wide pulse pressure
  • Aortic insufficiency
  • Syncope
  • Altered mental status
  • Loss of peripheral pulses
  • Horner syndrome
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18
Q

What is this?
* Patients will present with a history of hypertension, diabetes, and coronary artery disease presents to the emergency department with severe, tearing, knife-like back pain. Stating that the pain started approximately 30 minutes ago, and felt lightheaded and dizzy ever since its onset.

A

aortic dissection

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19
Q

Dx studies of AD:
* What is sensitive for dx?
* What is gold standard?
* What does a CXR show?

A
  • CT scan is sensitive for the diagnosis of aortic dissection, can be performed quickly, and allows for rapid intervention. It is the most appropriate first-line diagnostic modality.
  • MRI angiography is the gold standard for evaluation, though this is rarely used in clinical practice as CT is much quicker and highly sensitive
  • CXR “widened mediastinum”
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20
Q

Treatment AD:
* What is the txt perioperatively for type A?

A

Tight HR and BP control perioperatively in case of type A
* Goal SBP…enough to perfuse the brain, think SBP 90-100
* HR goal 60-80, less shear force

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21
Q

Txt of AD
* How do you txt stanford type A? What does it involve?

A
  • Stanford Type A dissections should be managed surgically in the first instance under the care of a cardiothoracic surgery.
  • The surgery involves removal of the ascending aorta (with or without the arch) and replacement with synthetic graft. If the dissection has damaged the suspensory apparatus of the aortic valve, this will also require repair
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22
Q

Txt of AD:
* What do you need to do if any additional branches of aortic arch are involved?

A
  • Anyadditional branches of the aortic archthat are involved will require reimplanation into the graft (i.e. brachiocephalic artery, left common carotid artery, left subclavian artery), with long Type A dissections involving the descending and possibly abdominal aorta may require staged procedures.
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23
Q

txt of AD
* Uncomplicated Type B dissections arebest managed how? What is the aim of the therapy?

A

best managed medically, with good survival rates.
* First line treatment is management of hypertension with intravenous beta blockers (labetalol) (or calcium channel blockers assecond line therapy).
* The aim of this therapy is to rapidly lower the systolic pressure, pulse pressure, and pulse rate to minimize stress of the dissection and limited further propagation

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24
Q

Txt of AD
* In the acute setting, what is not recommended? Why?
* Surgical intervention in Type B dissections is only warranted in who?

A
  • In the acute setting, endovascular repair is not recommended due to the risk of retrograde dissection, thereforemedical management remains gold standard.
  • Surgical intervention in Type B dissections is only warranted in the presence of certaincomplications, such as rupture, renal, visceral or limb ischaemia, refectory pain, or uncontrollable hypertension
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25
Q

Txt of AD:
* Type B dissections can go on to bewhat?
* The most common complication of chronic disease is what?
* These present further surgical problems, with what?

A
  • Type B dissections can go on to bechronic, with continued leakage into the dissection, even if a stent has been placed.
  • The most common complication of chronic disease is theformation of an aneurysm.
  • These present further surgical problems, withendovascular repairoffering a better survival chance
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26
Q

Arterial embolism/thrombosis
* Caused by what?
* Can be where?
* Arterial thrombosis is most commonly caused by what?

A
  • Caused by a sudden arterial occlusion
  • Can truly be anywhere, brain, coronary artery, kidney, spleen, gut
  • Arterial thrombosis is most commonly caused by atherosclerosis
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27
Q

how is embolus is different than thrombosis

A
  • Thrombosis think atherosclerosis, slow narrowing of blood vessel to occlusion
  • Embolus, acute and blood clot comes from elsewhere
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28
Q

What plays a significant role in the pathophysiology of thrombosis?

A

Virchow’s triad (ie, endothelial damage, hypercoagulability, and venous or arterial blood stasis)

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29
Q

What happens/ the pathway if damage to vessel wall?

A
  • Damage to the vessel wall leads to the production of pro-inflammatory cytokines, increased expression of tissue factor, proliferation of adhesion molecules, and enhanced platelet activation.
  • Inflammation is a normal body reaction to unwanted stimuli such as foreign pathogens or infection and endothelial damage, whether acute (eg, trauma or surgery) or chronic (underlying inflammatory disorders or peripheral vascular disease).
  • The activation of the leucocytes and endothelial cells causes the formation of adhesion molecules, which will eventually initiate clot formation.
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30
Q

What in the body prevents the formation of thrombosis?

A

The body’s endogenous anticoagulants, such as proteins C and S and antithrombin III, prevent the formation of thrombosis

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31
Q

What are the clinical features of Arterial embolism/thrombosis?

A
  • Acute limb ischemia
  • Remember the 5P’s of arterial emboli: Pain, Pallor, Pulselessness, Paresthesia, Poikilothermia
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32
Q

Arterial embolism/thrombosis
* What is the gold stand for diagnosis?
* What else can you do?

A

Angiography is considered the gold standard for diagnosis
* ECG (looking for MI, AFib)
* Echocardiogram (+/- ) looking for clot, MI, valve vegetation
* Consider hypercoagulable workup as well

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33
Q

Arterial embolism/thrombosis
* What is the treatment?
* If limb-threatening, what do you do?

A
  • Anticoagulate with IV heparin (bolus followed by constant infusion)
  • If limb-threatening, call the vascular surgeon for angioplasty, graft, bypass or endarterectomy
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34
Q

Arterial embolism/thrombosis
* Most often, following revasc of a limb, they will require what?
* Treatment more in line w/ what?

A
  • Most often, following revasc of a limb, they will require ANTIPLATELET and sometimes DUAL ANTI-PLATELET medicine though there are no consensus guidelines, and this will be determined on an individual basis
  • Treatment more in line w/ CAD treatment
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35
Q

How does Arterial embolism/thrombosis event different from VTE?

A

This differs from VENOTHROMBOTIC EVENTS (VTE)
* Guidelines now suggest the use of direct oral anticoagulants (DOACs) over vitamin K antagonists (ie, warfarin) for most VTE conditions. The DOACs most commonly used are dabigatran, apixaban, edoxaban and rivaroxaban.

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36
Q
A
37
Q

What is Arteriovenous malformation?

A

Arteriovenous malformationis an abnormal connection between arteries and veins, bypassing the capillary system, usually in the brain or spine, but also the lungs

38
Q

Arteriovenous malformation
* What are the sxs of brain?

A

Brain: epilepsy, neurologic deficits, and severe sudden onset headache indicate subarachnoid hemorrhage
* In a brain AVM, blood passes directly from the arteries to the veins via tangled vessels. This disrupts the typical process of how blood circulates through the brain.

39
Q

Arteriovenous malformation
* What are the sxs of spine, and lungs?

A
  • Spine: sensory disturbances, muscle weakness, and paralysis
  • Lungs: Usually asymptomatic, may cause SOB or hemoptysis
40
Q

What is the cause of brain AVMs?

A

The cause of brain AVMs is yet unknown, however, it is possibly multifactorial; apparently both genetic mutation and angiogenic stimulation (the physiological process of formation of new blood vessels from pre-existing vessels) playing roles in AVM development

41
Q

Clinical features of AVM:
* Depends on what?
* Often what?
* Unfortunately will sometimes present after what?

A

Really will depend on the location of the AVM
* Will often be asymptomatic, found incidentally on diagnostics
* Unfortunately, will sometimes present after rupture
* 41-79% present w/ intracranial hemorrhage

42
Q

Brain AVM:
* What is gold standard for dx? What are other options?

A

Diagnosed by angiography (gold standard), CTscan, orMRI

43
Q

AVM treatment:
* Invasive management is recommended for who?
* Who should get medical management?

A

Invasive management is recommended for younger patients with the presence of one or more of the high-risk features for an AVM rupture, whereas in the case of older individuals with no high-risk features, the usual best treatment is medical management

44
Q

AVM treatment:
* In some patients, what management can be the only thing required?
* What is the mainstay treatment/ cure patients?
* What are alternatives and can also be useful in surgery?

A
  • In these particular patients, anticonvulsants for seizure control and pertinent analgesia for headaches may be the only management required
  • Surgical excision — Open microsurgical excision is the mainstay of treatment and offers the cure for patients considered to be at high risk of hemorrhage.
  • Radiotherapy and endovascular embolization are not only useful alternatives to surgical treatment in patients at high risk for surgical therapy but can also be useful adjuncts to the main surgical management
45
Q
  • What does DVT usually involve?
  • What should you remember?
  • This is a major problem accounting for most cases of what?
A
  • DVT usually involves the lower limb venous system, with clot formation originating in a deep calf vein and propagating proximally
  • Remember Virchow’s Triad!
  • This is a major problem accounting for most cases of pulmonary embolism
46
Q

DVT:
* What are deep veins?
* What are the lower and upper extremity ones?

A

The veins that lie beneath the muscular fascia and drain the lower extremity muscles are the deep veins
* Lower extremity: Fem, popliteal, peroneal, AT, PT, fibular
* Upper extremity: Brachial, radial, ulnar, sublclavian, axillary

47
Q

DVT clinical features:
* Unilateral what?
* What sign is present?

A
  • Unilateral (ASYMMETRICAL) swelling of the lower extremity (or upper)
  • Homan sign: discomfort behind the knee on forced dorsiflexion of the foot
48
Q

DVT:
* What does the history show?
* What does the physical examination show?

A

History
* Pain (50% of patients)
* Redness
* Swelling (70% of patients)
* Prolonged period of immobility

Physical Examination
* Limb edema may be unilateral or bilateral if the thrombus extends to pelvic veins (rare)
* Red and hot skin with dilated veins
* Tenderness

49
Q

DVT:
* What is the first line test?
* What can be used to rule out low risk DVT patients? What else can you use?

A

Venous duplex ultrasoundis the first-line imaging test

D-dimer- a negative D-dimer will rule out DVT in low-risk patients
* (very sensitive but not very specific)
* Coagulation profile
* Wells score

50
Q

What is the wells score?

A
51
Q

What is the gold standard of DVT?

A

Venography is considered GOLD STANDARD (rarely used in practice)

52
Q

Treatment of DVT:
* What should be given immediately?
* Following initial anticoagulation for the first 5 to 10 days, patients with VTE require what?

A
  • Immediateanticoagulation⇒ LMW heparin or fondaparinux, or the oral factor Xa inhibitors
  • Following initial anticoagulation for the first 5 to 10 days, patients with VTE require therapy for a more prolonged period.
53
Q

DVT txt:
* What are the options for long term anticoagulation?
* Long-term anticoagulant therapy is administered for a finite time beyond the initial period, usuallyhow long?
* Recurrent DVTrequireswhat?

A
  • Options forlong-term anticoagulationinclude oral anticoagulants (ie, factor Xa inhibitors, direct thrombin inhibitors, and warfarin)
  • Long-term anticoagulant therapy is administered for a finite time beyond the initial period, usuallythree to six months, andoccasionally up to 12 months
  • Recurrent DVTrequireslifetime anticoagulation
54
Q

What do you give to a patient who are intolerant of systemic AC?

A

IVC filter

55
Q

Giant cell arteritis (GCA)
* What is it?

A

Giant cell arteritis (GCA) is a chronic inflammatory vasculitis that predominantly affects large- and medium-sized arteries

56
Q

Giant cell arteritis (GCA)
* What branches does it commonly affect?
* The granulomatous nature of GCA contributes to what?

A
  • Commonly involves the cranial branches of the carotid arteries.
  • The granulomatous nature of GCA contributes to the loss of vascular smooth muscle cells and elastic fibers, potentially leading to aneurysm formation and vascular remodeling. Intimal hyperplasia and lumen occlusion contribute to ischemic complications.
57
Q

Giant cell arteritis (GCA)
* The defining pathogenic feature of GCA is what?
* What characterizes GCA?

A
  • The defining pathogenic feature of GCA is the inflammation of medium- and large-sized arteries arising from the aortic arch.
  • Dysregulation in both the innate and adaptive immune systems characterizes GCA. GCA’s pathophysiology revolves around the body’s improper reaction to vascular endothelial injury
58
Q

Giant cell arteritis (GCA)
* What is the rule?

A

The rule of 50 for temporal arteritis
* Age greater than 50
* ESR greater than 50
* Steroids greater than 50 (will start patient typically on 60 mg of prednisone)

59
Q

Giant cell arteritis (GCA)
* Idiopathic +/- autoimmune viral infectioncauses what?
* Vasculitis affects what arteries (4)?

A
  • Idiopathic +/- autoimmune viral infectioncauses monocyte activation and inflammatory cytokine production, inflammation, and tissue destruction, resulting in symptoms
  • Vasculitis affects extracranial branches of the carotid artery: temporal artery, occipital artery, ophthalmic artery, posterior ciliary artery (TOOP)
60
Q

Giant cell arteritis (GCA)
* What is the primary complaint? How it is described as?
* What are classically ascribed to patients with underlying cranial GCA?

A
  • A new headache is a primary complaint in nearly two-thirds of patients with typical GCA.Classically described as a temporal headache associated with scalp tenderness, the headache can be frontal, occipital, unilateral, or generalized. The headache may wax, wane, worsen, or subside before treatment begins.
  • Enlargement, nodular swelling, tenderness, and loss of pulse of the temporal artery, either unilateral or bilateral, are classically ascribed to patients with underlying cranial GCA. The absence of any physical temporal artery findings modestly decreases the likelihood of GCA
  • New Headache
  • scalp tenderness
  • swelling/ tenderness of temporal a.
  • jaw claudication
  • visual involvement
61
Q

GCA:
* What is jaw claudication?
* What is visual involvement?

A
  • Jaw claudication: Jaw claudication, occurring in nearly 50% of patients with GCA, manifests as pain or fatigue in the mandible and occasionally the tongue, triggered by chewing, and typically subsides upon cessation of chewing.
  • Visual involvement:Approximately 20% to 30% of the patients experience visual disturbances. GCA-associated visual loss can be transient or permanent. Transient visual changes typically present as an abrupt partial field defect or as if a curtain covers the field of vision of 1 eye. Permanent vision loss, most often resulting from anterior ischemic optic neuropathy, is painless and sudden, and it can be unilateral, bilateral, partial, or complete
62
Q

GCA DX:
* What will be high?
* What are other inflam markers that might be high?
* What is the gold standard dx?
* What are other options?

A
  • ESR will be elevated
  • Other inflammatory markers, CRP, also likely elevated
  • Gold standard diagnosis is temporal artery biopsy
  • Ultrasound other option, less sensitive though Bilateral halo signs of the temporal arteries arehighly specific for GCA.
63
Q

GCA:
* What is the txt?

A
  • Treatment includes high-dose prednisone taper
  • If suspicion is high, don’t wait for biopsy given risk for blindness
  • Note: closely associated w/ polymyalgia rheumatica (PMR), headache will be you differentiator
64
Q

Peripheral artery disease
* What is it?
* This typically reduces blood flow to what? What does this cause?
* Patients with peripheral arterial disease (PAD) have what?

A
  • Peripheral arterial disease (PAD) is a circulatory problem causing a reduced blood flow through the arteries
  • This typically reduces blood flow to the extremities manifesting as thigh or calf pain during walking or exertion. CLAUDICATION
  • Patients with peripheral arterial disease (PAD) have decreased lower extremity arterial perfusion which is commonly referred to as “poor circulation.”
65
Q

PAD:
* In most cases of PAD, atherosclerotic plaques causes what?
* Many patients with PAD have either what?

A
  • In most cases of PAD, atherosclerotic plaques narrow the arterial flow lumen which restricts blood flow to the distal extremity.
  • Many patients with PAD have either no symptoms or atypical complaints that do not strictly conform to the definition of claudication. Others may develop limb-threatening compromise of blood flow, necessitating emergent surgery.
66
Q

What are the risk factors of PAD?(8)

A
67
Q

What age does PAD mostly affect? Gender?

A
  • PAD affects over 200 million adults worldwide and the incidence of PAD increases to as high as 20% in people over the age of 70.
  • Equally effects men and women
68
Q

PAD:
* The most characteristic symptom of PAD is what?
* Patients with severe PAD can develop what?

A
  • The most characteristic symptom of PAD is claudication which is a pain in the lower extremity muscles brought on by walking and relieved with rest.
  • Patients with severe PAD can develop ischemic rest pain.
69
Q

PAD:
* They sometimes cannot sleep due to what? What can help with the pain?

A

They sometimes cannot sleep due to the pain and often dangle their lower leg over the side of the bed in an attempt to relieve their discomfort. The slight increase in blood flow due to gravity temporarily diminishes the otherwise intractable pain.

70
Q

PAD:
* What are some sxs?
* Ulcers are what?

A
  • Lower extremity loss of hair, brittle nails, pallor, cyanosis, claudication, hypothermia
  • Ulcers are pale to black, well-circumscribed and painful, located laterally and distally
71
Q

Dx of PAD:
* What can be used and why? (2)
* What is gold standard?

A
72
Q

How do you calculate ABI?

A
73
Q

What is the txt of PAD?

A

Definitive treatment is arterial bypass
* Medical treatment: Antiplatelets, anti-lipids, manage risk factors, cilostazol Aspirin, Plavix

74
Q

Phlebitis/thrombophlebitis
* What is the etiology?
* What is Superficial thrombophlebits ?
* Phlebitis has no what?

A
  • Etiology: Spontaneous or after trauma, or IV/PICC lines
  • Superficial thrombophlebitis is an inflammatory disorder of superficial veins with coexistent venous thrombosis.
  • Phlebitis, no thrombus
75
Q

Phlebitis/thrombophlebitis
* What does it usually affect?
* What may increase the risk?

A
  • It usually affects lower limbs, particularly the great saphenous vein (60% to 80%) or the small/short saphenous vein (10% to 20%)
  • A hypercoagulable state, prolonged immobilization, or vessel wall trauma may increase the risk of SVT. Superficial thrombophlebitis accounts for 5.4% of the adjusted population attributable risk for initial DVT or PE
76
Q

Phlebitis/thrombophlebitis
* What is the presentation?

A

Presentation: Dull pain, erythema, induration of vein,palpable cord

77
Q

What is this?
* Vignette: a 49-year-old male who is being evaluated for pain and swelling of his right lower extremity. He noticed his calf appears red and denies any trauma to the affected area. A week prior to presentation, he was on a plane for over 13 hours. Medical history is significant for venous insufficiency. On physical exam, there is erythema on the posterior calf and tenderness along the course of a superficial vein. A duplex ultrasound demonstrates impaired blood flow and incompressibility of a superficial vein.

A

Phlebitis/thrombophlebitis

78
Q

Phlebitis/thrombophlebitis
* What is gold standard?

A

Venous duplex ultrasound is the gold standard for diagnosis- noncompressible SUPERVICIAL vein with clot and vein wall thickening

79
Q

Phlebitis/thrombophlebitis
* How do you tx it?

A

Treat phlebitis with elevation, warm or cool compresses, NSAIDs
* May treat thrombophlebitis (phlebitis + thrombosis) w/ AC

Antibiotics are useful only with clear infection.

80
Q

Varicose veins
* Who does this affect more?
* What are risk factors?
* What is the main mechanism?

A
  • Approximately 15% of adults, particularly women who have been pregnant, developed varicose veins.
  • Other risk factors include obesity, family history, prolonged sitting or standing, history of phlebitis
  • The main mechanisms are superficial venous insufficiency and valvular incompetence; Inherited defects in the vein walls or valves also play a role
81
Q

Varicose veins
* What can you usually see?
* Varicosities may be what?
* What may may develop in severe or prolonged disease?

A
  • Dilated, tortuous veins develop superficially in the lower extremities, particularly in the distribution of the great saphenous vein. Smaller blue-green, flat reticular veins; Telangiectasias and spider veins are further evidence of venous dysfunction
  • Varicosities may be asymptomatic or associated with aching and fatigue
  • Chronic distal edema, abnormal pigmentation, fibrosis, atrophy, skin ulceration may develop in severe or prolonged disease
82
Q

Varicose veins
* How do you dx?
* What can be used?

A
  • Diagnosis is clinical- visual inspection of the leg in a dependent position usually confirms the presence of varicosities
  • Duplex ultrasonography may be used in preoperative planning in the event a patient is planning to have their varicose veins treated
83
Q

Varicose veins
* What is the txt?

A

Compression therapy, leg elevation, wound care, sclerotherapy, and surgery.

84
Q

Venous insufficiency
* What is it?
* CVI encompasses several pathological changes that cause what?
* the primary underlying mechanism is believed to be what?

A
  • Chronic venous insufficiency (CVI) is a condition in which the flow of superficial or deep venous blood is impaired, causing venous hypertension.
  • CVI encompasses several pathological changes (eg, lower extremity edema, skin trophic changes, and discomfort) that result secondary to venous hypertension
  • Though the exact etiology of CVI is unclear, the primary underlying mechanism is believed to be valvular reflux.

An estimated 10% to 35% of adults have CVI in the US, with 4% of adults aged 65 years or older developing venous ulcers

85
Q

What are the Risk factors for CVI?

A
86
Q

What are the clinical features of CVI?

A
  • Edema, atrophic, shiny skin, brawny induration, stasis dermatitis, brown hyperpigmentation, varicosities, ulcers above the medial malleolus
  • Although there can be variations in presentation among patients, certain features are more prevalent, including telangiectasias, reticular veins, varicose veins, pain, cramping, itching, prickling, and throbbing sensation
87
Q

CVI
* What is the gold standard? What else can be used?

A
  • When evaluating CVI, color duplex ultrasound is considered the gold standard. ABI, Trendelenburg tests also used
  • Assessing the competency of the valves of the examined veins
88
Q

txt of CVI
* What do you do for skin changes?
* How do you treat ulceration?

A

Sclerotherapy, vein stripping, compression hose
* Skin changes (“stasis dermatitis”) respond to topical dermatologic agents
* Midpotency topical steroids

Venous ulceration is treated with a combination of ulcer wound management and compression therapy (stockings, bandaging systems).

Clinical Medicine 3 (27 decks)

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