vascular - podiatry Flashcards
risk factors of PAD
smoking, hypertension, dyslipidaemia, DM, Male gender, CVD, elevated plasma hmyocysteine levels, sedentary lifestyle, age, family Hx of PAD, other known forms of atherosclerosis
clinical signs and symptoms of PAD
anhydrotic skin, minimal hair growth, IC, general thickening of the nail (onychauxis) pulslessness, temperature
reasons for Anhidrotic skin
not meeting metabolic demands of the dermal structures(arterial insufficiency) , fungal infections like tinea pedis, non- enzymatic glycosilation, surgery affecting the sweat response.
diabetes and PAD together
higher incidence of lower leg arterial involvement, greater severity of disease process, likelihood of distal ishemic ulcers and gangrene and higher chance of amputation
anhydrtoc skin appearance
dry, flaky skin affecting the dorm or plantar surfaces and extending up the leg
causes of onychauxis
damage to mnail matrix - trauma form single blow of micro trauma from footwear, Fingal nail infection, systemic disturbance like PAD(impaired arterial insufficiency), also due to ageing and
what is intermittent claudication
transient ischemic muscle pain occurring due to exercise. when increased exercise demands metabolites, by products accumulate activating pain receptors therefore inducing pain symptoms. reduction of exercise, reduces metabolic demand therefore reducing pain.
clinical features of Intermittent claudication
cramp like pain and tiredness. (at muscle compartment that is affected) can be at buttock-thigh-calf (aortoilliac), calf + plantar (femoropopliteal) plantar (infrapopliteal)
characteristic of pain between compartment syndrome and IC, venous congestion
ic: cramp like, tiredness, tightness
compartment+ venous congestion: tightness, bursting pain
location of discomfort (IC vs spinal stenosis)
IC - buttock, hip, thick, calf, plantar foot
Spinal - buttock, hip and thigh
further diagnosis of extent of PAD process
duplex scan - provides info on location and extent of arterial disease and type of lesion present
what is critical limb ischemia
the End stage of PAD where peripheral flow is reduced to the point at which a Pt has chronic ishemia rest pain.
what is rest pain
persistent pain at night due to nerve ishemia leading to ishemic neuropathy. occurs when legs are elevated. gravity assists decrease of pain.
what does Rest pain indicate
two haemodynamically significant arterial blocks in series
clinical features of rest pain
tearing, pulling agonising discomfort often with burning throbbing and tingling
further diagnosis for rest pain nada IC
vascular screening from GP - duplex ultrasound
ishaemic ulcers
wounds caused by lack of arterial flow to the capillary bed. causing tissue damage that is unable to repair as a result
signs and symptoms of ischemic ulcers
usaully brown, yellow or black. slight depression and borders look like they have been punched out. incase of infection - surrounding tissue (erythemous) commonly found at apex. extremely painful
rest pain Vs. night cramps
rest pain - tingling, throbbing, burning discomfort. (at plantar foot)
night cramps - at calf muscles, due to neurological hyper excitability.
what is gangrene
necrotic tissue repressenting end stage arterial insufficiency. affects distal extremities first.
possible causes for gangrene
atherosclerosis, Myocardial infarction, embolism or valvular heart disease
dry vs wet gangrene
dry - possible due to ishemia
wet/moist - bacterial infection
what may venous hypertension cause
pain, swelling oedema, skin changes and ulcerations
risk factors with chronic venous insufficiency
age, gender, family history, varicose vein, obesity, varicosities, pregnancy, phlebitis, previous leg injury
risk factors for CVD
smoking, overweight, diabetes, genes, depression, age, diet, sedentary lifestyle, cholesterol, ethnicity
risk factors of atherosclerosis
hyperlydidemia, lifestyle, hypertension, smoking, genetics
what is the difference between thrombosis and embolism
thrombosis - blot in the blood vessel
embolis.- clot that moves
aneurism - when it bulges out
what are lipoproteins
combination of lipids (fat) and proteins
what is PAD
pathology in the arteries due to obstruction in the blood flow
management of PAD
- if impacting on life - consider revascularisation, arteriography e.g.g
- if non- lifestyle limiting - exercise and pharmacotherapy
surgical - endarectomy, vascular bypass, infrainguinal bypass (fem pop bypass is most common
chronic limb threatening schema management
- best treated with surgical revascularisation, however if surgery is precluded may be managed with long term pharmacotherapy
what is the difference between intermittent claudication and neurogenic claudication
IC. -relieved by rest (shop window to shop window) - indicator for significant PAD, causes by atherosclerosis
NC - relief with sitting down and bending forward , reported back pain on sneezing, coughing and pain in bed, causes by spinal stenosis
neurogenic claudication
lumbrosacral narrowing of vertebral canal, causing compression of intraspinal neuromuscular structures
Ddx for Intermittent claudication
neurogenic claudication (spinal stenosis) arthritis, venous congestion, compartment syndrome
what is a typical PAD exercise program (diabetes lecture)
warm up 10 min intensity to mild and moderate claudication/pain duration - 45 -50 min cool down 10 min 3-5 times a week
what is acute limb schema
rapid, sudden decrease in limb perfusion, may appear as first manifestation of vascular disease
normally ude to embolism or thrombus.
(occur over hours or days
bilateral comparison.
presentation signs for acute limb ischaemia (6)
pain, perishably cold, pallor, parasthesia, pulseless, paralysis
diagnostic testing for acute lime ischemia
doppler and vascular imaging
clinical presentation of chronic critical limb ischemia
Pt history, ischemic rest pain, severe pain with intermittent sharp exacberated affecting digits and dorm , disturbed demo, heightened sensitivity to compression, presence of gangrene or ulceration. pain starts distally. “ tooth ache type pain”
Ddx for chronic critical limb ischemia
diabetic sensorimotor neuropathy
nerve root compression
what helps allow normal venous flow
- valves (they stop back flow
- negative pressure (in deep veins that produce vacuum suction abilities to help bring flow up)
- phasic flow (wave-like, movement of the diaphragm through breathing motion helps move blood up)
- muscle pump
what occurs at the arteriole end
filtration occurs allowing fluid to be resorbed at the venue end minus what is removed by the lymphatic system
what are varicose veins + risk factors
dilated, elongated and tortuous vessels. most commonly at saphenous vein. valves fail and back flow on blood occurs.
clinical presentation - pain at end of the day
risk factors - hormone (female) age, genetics, obesity, long periods of standing
risk factors of CVI (chronic venous insufficiency)
age, gender, history (family) of varicose veins, obesity, pregnancy, phlebitis and previous leg injury
venous hypertension
results from high venous flow in peripherals
secondary varicose veins occur from…
DVT, INCOMPETENT DEEP VEIN VALVES, obstruction, (thrombus), pregnancy
pathogenesis of varicose veins
the dilated elongated vessels occurs from venous hypertension which occurs from the incompetence of htecperforating veins (unrestricted back flow from deep to superficial veins
what is venous oedema
swelling of soft tissue/ fluid accumulation > interstitial fluid that is protein poos and has low viscosity
found in peri-malleolar region
difference between protein rich and poor
protein rich likes to be organised so with lymphedema you won’t see any pitting, and organised, becomes stiff and woody
protein rich - oedema changes throughout the day
what is haemosyderin
pigmentation of iron rich pigments that are caused through breakdown of red blood cells and may occur in various tissues throughout the body due to both localised and systemic causes. release of haemoglobin turning to haemosiderin. this is a sign for an underlying venous pathology (CVI)
what is venous stasis dermatitis
eczematous process which occurs in the lower legs as a result of insufficient venous return. pruritic, erythemtous plaques on lower leg
venous stasis dermatitis treatment
corticosteroids however beware of skin atrophy
lipodermatosclerosis
skin changes due to inflammation of subcutaneous adipose tissue of the lower leg for Pt with long term CVI. dermis and subcutaneous tissue becoming indurated and fibroses with the lack of pitting oedema; skin becomes atrophic, loses sweat glands and hair follicles
atrophie Blanche
smooth ivory white atrophic plaques of sclerosis, fibrotic with low blood flow and may contain talangiectasias. Pt have CVI
telangiectasia
broken or dilated small superficial blood vessels (spider veins)
usually asymptomatic but may be a sign go underlying health issue
venous ulceration
high levels of exudate, gaiter area, usually superficial but can be deep,
management of varicose veins
compression, surgery, ablation (injection of sclerosant - destroying the vein and laser ablation)
complicaitons - DVT, bruising,
venous thrombosis (DVT) pathogenesis
virchows triad
- vessel wall injury (due to trauma)
- stasis of blood (due to prolong still movement can cause thrombus formation
- abnormal tendency for blood to coagulate
what is DVT
a thrombosis in the deep veins of the leg
if Patient comes n with a red, hot swollen leg - suspect this
associated with Stasis!
CLINICAL PRESENTATION OF DVT
general - swelling (unitlateral), erythema over tissues, high fever, dilation of superficial vessels in a supine
calf - mild calf soreness and renderness
minimal ankle swelling
femoral/iliac DVT: grossly swollen, painful, white leg (due to extensive oedema under skin
diagnosis of DVT
venous duplex is best method
pharmacological treatment for DVT involves:
heparin first 7-10 dys(blood thinner) warfarin (blood thinner - anticoagulant) 5-7 days after hep, then continue for 1-2 months
complications of DVT
recurrence, varicose veins, talangiectasias, purpuric colouration, oedema, eczema, haemosiderosis, atrophic blanche, atrophic skin, fibrosis and induration, venous ulceration
management for venous hypertension
elevation, exercise, compression (maintain venous drainage,
pharmacological :
- emollients and topical steroids and antibiotics antiseptics, wound dressings
- skin grafts
pharm: - pentoxifylline, diuretics, antibiotics, stanozolol
what is lymphedema
swelling of a body part (usually limb due to due to accumulation of fluid from obstructed flow of the imvompotence.
it is protein rich
congenital primary lymphedema include:
congenita - onset before 1yrs
praecox - from one to 35 yrs
tarda - 35+
treatment of Lymphedema
no cure, more so management strategies like manual lymph drainage,
elevation, protection of limb, compression,
pharm: antibiotics
goals for treatment
improve cosmoses, preserve skin integrity, soften subcutaneous tissue decrease limb size, avoid contracture of the involved limb
patient and family education
goals for treatment for lymphedema
improve cosmoses, preserve skin integrity, soften subcutaneous tissue decrease limb size, avoid contracture of the involved limb
patient and family education
