Flashcards in 226 - Varicose Veins Deck (23):
What causes peripheral vascular disease?
atherosclerotic stenosis/occlusion of large/medium arteries. BP at ankle should be higher than in arm but lower in disease. blood flow cant increase on exertion causing claudication. In later stages resting blood flow reduce and ischaemia causes ulcers. lIvedo reticulares purple discolouration due to stagnation of blood
*risks - smoking, diabetes, HTN, hyperlipidaemia, FH, sedentary lifestyle
what are the differences between arterial and venous ulcers?
arterial over bony prominances venous gaiter region
art smaller, more painful and demarcated
art punched out ven superficial
art necrotic centre, ven granulating centre
ven exuadative and hyperpigmented which art blanched
what are the 5ps of peripheral vascular disease?
how is the ankle-brachial pressure index measured (ABPI)?
ratio of ankle BP to brachial BP. normal >1 mild 0.9-0.7 mod 0.7-0.5 and severe rest pain
what would be expected in a patient with peripheral vascular disease on doppler pulse studies?
*normal is triphasic waveform
what treatment is available for AVD?
*surgical - balloon dilatation, stenting, bypass
what causes venous hypertension?
*valvular incompetence - reflux occurs leading to a column of uninterupted blood forming in veins and incr. venous pressure
what are signs of venous HTN?
*varicose veins - dilated torturous superficial veins with dull ache on standing still/sitting made better by elevation
*Lipodermatosclerosis - scarring of skin and fat with brown smooth tightened skin and pain
*venous eczema (stasis dermatitis) - fibrin activation on skin, ischaemia and immune cells causing inflammation and fibrosis due to chronic venous oedema. Erythema and hyperpigmentation and scaling
what tests are there for venous HTN?
*Trendelenburg test - leg elevated to empty superficial veins, sapheno-femoral junction occluded, pt stands _slowfilling= problem at SF junction, fast filling=incompetent perforators
*venous refill time - calf muscle pump used to empty veins, pt stands ,time for varocosities to refill
what treatment options are available for venous HTN?
*graduated compression bandaging - PVD must be excluded first
-sclerotherapy (foram - STD)
-endovenous laser treatment
what are the different types of chronic lymphoedema?
*lymphoedema - inadequate drainage, normal cap filtration, incr. protein conc.
*lymphovenous oedema - venous system pathology, incr. cap filtration
*dependency oedema - immobile limbs, decr. venous return, inc cap filtration
what are the 2 pathways for microcirculation?
*terminal arteriole>capillary>post capillary venule
*arteriole>AV anastamosis>larger venules
what do terminal arteries do?
supply bunch of cap and carry out vasomotion to produce intermittent flow of blood
what happens to post capillary venules in inflammation?
become incr permeable causing leakage of plasma into interstitium and swelling/heat
what do arterio-venous anastomoses do?
only in some cap beds in skin extremities. open at high body temps>lower resistance and incr blood flow to skin and heat loss
how does diffusional permeability vary along a capillary?
more permeable at venous end of cap and more reabsorption.
what is the diffusion rate in a capillary dependent on?
*permeability of cap wall
*surface area of cap wall
*conc gradient across wall
how do lipid soluble molecules and hydrophilic molecules pass through capillary walls?
*highly permeable to lipid soluble molecules and anaesthetics - transcellular and diffusion through extracellur pathways
*less permeable to hydrophilic molecules as must diffuse through pores and permeability depends on molecule size
what are the 3 types of capillaries?
*continous capillaries - skin, lungs, connective tissue, muscle, CNS - single layer of epithelial cells with small pores in intracellular clefts - discontinuous tight junctions
*fenestrated capillaries - areas of high fluid filtration out of caps eg kidneys, glands, intestinal mucosa - endothelium with pores and basement membrane highly permeable
*sinusoids - areas of high cellular exchange - eg spleen, liver, bone marrow - endothelium with large gaps and discontinuous basement membrane
what carries out molecular sifting in extracellular pathways?
glycocalyx - layer of -ve charged carbohydrate covering endothelium that binds plasma proteins to form an exclusion zone and makes pores smaller
what prevents the accumulation of fluid in the interstitium?
*vasomotion - intermittent flow reduces ave pressure in cap and incr absorption
*lymphatic drainage - large junctions so easy movement of fluid. Muscle contraction and valves push fluid through. relaxation allows less P and more fluid sucked in
what causes excess fluid in interstitial space (oedema)?
cap filtration rate > lymphatic drainage rate
cap filtration rate=LpS[(Pc-Pi) - sigma(PIpl - PIi)]
*incr in cap filtration rate due to high hydrostatic P in capillaries (heart failure) and low plasma oncotic P due to decr. plasma protein conc (malabsorption, malnutrition, liver failure)
*decr in lymphatic drainage due to cancer damage in lymph nodes, surgical damage, filariasis (roundworm infect lymphatics)