CVS Week 11 Flash Quiz Flashcards
(30 cards)
Define Peripheral Vascular Disease (PVD) and Acute Limb Ischemia (ALI).
PVD: A general term for diseases of blood vessels outside the heart and brain. [cite: 1] ALI: A sudden decrease in limb perfusion, usually threatening limb viability. [cite: 1]
What are the causes and clinical manifestations of Acute Limb Ischemia (ALI)?
Causes of ALI often include embolism or thrombosis. [cite: 1] Clinical manifestations of ALI include the ‘6 Ps’: Pain, Pallor, Pulselessness, Paresthesia, Paralysis, and Poikilothermia (coldness). [cite: 1]
How is Acute Limb Ischemia (ALI) diagnosed and managed?
Diagnosis of ALI involves clinical assessment, Doppler ultrasound, and angiography. [cite: 2] Management requires urgent revascularization, such as embolectomy, thrombolysis, or bypass surgery. [cite: 2]
What are the causes and clinical manifestations of chronic lower limb ischemia?
The most common cause of chronic lower limb ischemia is atherosclerosis. [cite: 3] Clinical manifestations include intermittent claudication, rest pain, non-healing ulcers, and gangrene. [cite: 3]
How is chronic limb ischemia diagnosed and managed?
Diagnosis of chronic limb ischemia involves ankle-brachial index (ABI), Doppler ultrasound, and angiography. [cite: 4] Management includes lifestyle modification, pharmacotherapy (e.g., antiplatelets), and revascularization (e.g., angioplasty, bypass surgery). [cite: 4]
Define Aortic Dissection (AD) and discuss its epidemiology.
AD is defined as a tear in the inner layer (intima) of the aorta, leading to blood flowing between the layers of the aortic wall, separating them. [cite: 6] It is a relatively rare but life-threatening condition. [cite: 6]
Enumerate the risk factors for Aortic Dissection (AD) and discuss the role of cystic medial degeneration.
Risk factors for AD include hypertension, Marfan syndrome, Ehlers-Danlos syndrome, bicuspid aortic valve, and coarctation of the aorta. [cite: 6] Cystic medial degeneration plays a role by weakening the aortic wall’s middle layer (media) due to loss of smooth muscle cells and elastic fibers, predisposing to dissection. [cite: 6]
Explain the Stanford and DeBakey classifications of Aortic Dissection (AD).
The Stanford classification for AD includes Type A (involves the ascending aorta, regardless of the primary tear site) and Type B (involves only the descending aorta, distal to the left subclavian artery). [cite: 7] The DeBakey classification includes Type I (originates in the ascending aorta and extends to the descending aorta), Type II (originates and is confined to the ascending aorta), and Type III (originates in the descending aorta and extends distally). [cite: 7]
Describe the clinical manifestations of Aortic Dissection (AD).
Clinical manifestations of AD typically include sudden onset of severe, tearing or “ripping” chest or back pain. [cite: 8] The pain may migrate. [cite: 8] Other symptoms can vary depending on affected branches, such as neurological deficits, limb ischemia, or acute aortic regurgitation. [cite: 8]
How are Aortic Dissection (AD) diagnosed and managed?
Diagnosis of AD primarily relies on CT angiography (CTA) as the gold standard, along with MRI and transesophageal echocardiography (TEE). [cite: 8] Management for Type A AD is a surgical emergency (open repair). [cite: 8] For Type B AD, medical management (blood pressure control) is often the initial approach, with surgery or endovascular repair reserved for complications. [cite: 8]
Define an aneurysm and discuss its epidemiology.
An aneurysm is defined as a localized abnormal dilation of a blood vessel or the heart. [cite: 10] Abdominal aortic aneurysms (AAAs) are more common, especially in older men with atherosclerosis. [cite: 10]
Discuss the classification and pathogenesis of aortic aneurysm.
Aneurysms can be classified as true aneurysms (involve all three layers of the arterial wall; saccular or fusiform) or false aneurysms/pseudoaneurysms (hematoma outside the arterial wall communicating with the lumen). [cite: 10] Pathogenesis involves weakening of the arterial wall due to atherosclerosis, genetic disorders (e.g., Marfan), infection, or inflammation. [cite: 10]
Describe the clinical manifestations and diagnosis of aortic aneurysm.
Aortic aneurysms are often asymptomatic until rupture. [cite: 11] When symptomatic, they may present as a pulsatile abdominal mass, back pain, or symptoms related to compression. [cite: 11] Rupture causes severe pain, hypotension, and shock. [cite: 11] Diagnosis is commonly made using ultrasound, CT scan, or MRI. [cite: 11]
How is an aortic aneurysm managed?
Management of aneurysms varies: small, asymptomatic aneurysms are monitored with imaging and risk factor control. [cite: 11] Larger or symptomatic aneurysms typically require surgical repair (open or endovascular aneurysm repair - EVAR). [cite: 11] Ruptured aneurysms necessitate emergency surgical repair. [cite: 11]
Define varicose veins.
Varicose veins are defined as dilated, tortuous superficial veins, typically in the legs, resulting from incompetent valves. [cite: 12]
Discuss the pathogenesis and clinical manifestations of varicose veins.
The pathogenesis of varicose veins involves valvular incompetence leading to retrograde blood flow, increased venous pressure, and vein dilation. [cite: 12] Clinical manifestations include visible bulging veins, aching, heaviness, itching, swelling, and skin changes (hyperpigmentation, lipodermatosclerosis). [cite: 12]
What are suitable investigations and diagnostic findings for varicose veins?
Suitable investigations for varicose veins include clinical examination and duplex ultrasound (to assess valve competence and rule out DVT). [cite: 12] Diagnostic findings on duplex ultrasound include reflux and dilated superficial veins. [cite: 12]
Outline the management, prognosis, and complications of varicose veins.
Management of varicose veins can include conservative measures (compression stockings, elevation), sclerotherapy, endovenous ablation (laser or radiofrequency), and surgical ligation and stripping. [cite: 13] The prognosis is generally good with treatment, but recurrence is possible. [cite: 13] Complications include superficial thrombophlebitis, bleeding, skin changes, and venous ulcers. [cite: 13]
Discuss the pathogenesis and clinical manifestations of Deep Venous Thrombosis (DVT).
The pathogenesis of DVT is described by Virchow’s Triad: venous stasis, endothelial injury, and hypercoagulability. [cite: 14] Clinical manifestations include unilateral leg swelling, pain, tenderness, warmth, redness, and sometimes a positive Homan’s sign. [cite: 14]
What are suitable investigations and diagnostic findings for DVT?
Suitable investigations for DVT include D-dimer (useful for ruling out DVT) and compression ultrasonography (gold standard for diagnosis). [cite: 14] Diagnostic findings on ultrasound include non-compressible vein segments and the presence of thrombus. [cite: 14]
Outline the management, prognosis, and complications of DVT.
Management of DVT typically involves anticoagulation, with thrombolysis in selected cases, and IVC filters as an option. [cite: 15] Prognosis is good with timely treatment, but there’s a risk of post-thrombotic syndrome and recurrence. [cite: 15] Complications include pulmonary embolism (most serious) and post-thrombotic syndrome (chronic leg pain, swelling, skin changes). [cite: 15]
Define chronic venous insufficiency.
Chronic venous insufficiency (CVI) is defined as a condition resulting from damaged venous valves, leading to impaired venous return and chronic venous hypertension in the lower limbs. [cite: 16]
Discuss the pathogenesis and clinical manifestations of chronic venous insufficiency.
The pathogenesis of CVI often follows DVT or primary venous valve incompetence, leading to venous reflux and sustained elevation of venous pressure. [cite: 16] Clinical manifestations include edema, pain, itching, skin changes (stasis dermatitis, hyperpigmentation, lipodermatosclerosis), and venous ulcers (typically medial malleolus). [cite: 16]
What are suitable investigations and diagnostic findings for chronic venous insufficiency?
Suitable investigations for CVI include clinical examination and duplex ultrasound (to assess venous reflux and obstruction). [cite: 16] Diagnostic findings on ultrasound include evidence of venous reflux and/or obstruction. [cite: 16]
