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Podiatry vascular > vascular - podiatry > Flashcards

vascular - podiatry Flashcards

1
Q

risk factors of PAD

A

smoking, hypertension, dyslipidaemia, DM, Male gender, CVD, elevated plasma hmyocysteine levels, sedentary lifestyle, age, family Hx of PAD, other known forms of atherosclerosis

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2
Q

clinical signs and symptoms of PAD

A

anhydrotic skin, minimal hair growth, IC, general thickening of the nail (onychauxis) pulslessness, temperature

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3
Q

reasons for Anhidrotic skin

A

not meeting metabolic demands of the dermal structures(arterial insufficiency) , fungal infections like tinea pedis, non- enzymatic glycosilation, surgery affecting the sweat response.

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4
Q

diabetes and PAD together

A

higher incidence of lower leg arterial involvement, greater severity of disease process, likelihood of distal ishemic ulcers and gangrene and higher chance of amputation

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5
Q

anhydrtoc skin appearance

A

dry, flaky skin affecting the dorm or plantar surfaces and extending up the leg

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6
Q

causes of onychauxis

A

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

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7
Q

what is intermittent claudication

A

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.

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8
Q

clinical features of Intermittent claudication

A

cramp like pain and tiredness. (at muscle compartment that is affected) can be at buttock-thigh-calf (aortoilliac), calf + plantar (femoropopliteal) plantar (infrapopliteal)

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9
Q

characteristic of pain between compartment syndrome and IC, venous congestion

A

ic: cramp like, tiredness, tightness

compartment+ venous congestion: tightness, bursting pain

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10
Q

location of discomfort (IC vs spinal stenosis)

A

IC - buttock, hip, thick, calf, plantar foot

Spinal - buttock, hip and thigh

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11
Q

further diagnosis of extent of PAD process

A

duplex scan - provides info on location and extent of arterial disease and type of lesion present

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12
Q

what is critical limb ischemia

A

the End stage of PAD where peripheral flow is reduced to the point at which a Pt has chronic ishemia rest pain.

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13
Q

what is rest pain

A

persistent pain at night due to nerve ishemia leading to ishemic neuropathy. occurs when legs are elevated. gravity assists decrease of pain.

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14
Q

what does Rest pain indicate

A

two haemodynamically significant arterial blocks in series

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15
Q

clinical features of rest pain

A

tearing, pulling agonising discomfort often with burning throbbing and tingling

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16
Q

further diagnosis for rest pain nada IC

A

vascular screening from GP - duplex ultrasound

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17
Q

ishaemic ulcers

A

wounds caused by lack of arterial flow to the capillary bed. causing tissue damage that is unable to repair as a result

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18
Q

signs and symptoms of ischemic ulcers

A

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

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19
Q

rest pain Vs. night cramps

A

rest pain - tingling, throbbing, burning discomfort. (at plantar foot)
night cramps - at calf muscles, due to neurological hyper excitability.

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20
Q

what is gangrene

A

necrotic tissue repressenting end stage arterial insufficiency. affects distal extremities first.

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21
Q

possible causes for gangrene

A

atherosclerosis, Myocardial infarction, embolism or valvular heart disease

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22
Q

dry vs wet gangrene

A

dry - possible due to ishemia

wet/moist - bacterial infection

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23
Q

what may venous hypertension cause

A

pain, swelling oedema, skin changes and ulcerations

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24
Q

risk factors with chronic venous insufficiency

A

age, gender, family history, varicose vein, obesity, varicosities, pregnancy, phlebitis, previous leg injury

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25
Q

risk factors for CVD

A

smoking, overweight, diabetes, genes, depression, age, diet, sedentary lifestyle, cholesterol, ethnicity

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26
Q

risk factors of atherosclerosis

A

hyperlydidemia, lifestyle, hypertension, smoking, genetics

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27
Q

what is the difference between thrombosis and embolism

A

thrombosis - blot in the blood vessel
embolis.- clot that moves
aneurism - when it bulges out

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28
Q

what are lipoproteins

A

combination of lipids (fat) and proteins

29
Q

what is PAD

A

pathology in the arteries due to obstruction in the blood flow

30
Q

management of PAD

A
  • 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
31
Q

chronic limb threatening schema management

A
  • best treated with surgical revascularisation, however if surgery is precluded may be managed with long term pharmacotherapy
32
Q

what is the difference between intermittent claudication and neurogenic claudication

A

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

33
Q

neurogenic claudication

A

lumbrosacral narrowing of vertebral canal, causing compression of intraspinal neuromuscular structures

34
Q

Ddx for Intermittent claudication

A

neurogenic claudication (spinal stenosis) arthritis, venous congestion, compartment syndrome

35
Q

what is a typical PAD exercise program (diabetes lecture)

A 
warm up 10 min
intensity to mild and moderate claudication/pain
duration - 45 -50 min
cool down 10 min
3-5 times a week
36
Q

what is acute limb schema

A

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.

37
Q

presentation signs for acute limb ischaemia (6)

A

pain, perishably cold, pallor, parasthesia, pulseless, paralysis

38
Q

diagnostic testing for acute lime ischemia

A

doppler and vascular imaging

39
Q

clinical presentation of chronic critical limb ischemia

A

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”

40
Q

Ddx for chronic critical limb ischemia

A

diabetic sensorimotor neuropathy

nerve root compression

41
Q

what helps allow normal venous flow

A
  • 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
42
Q

what occurs at the arteriole end

A

filtration occurs allowing fluid to be resorbed at the venue end minus what is removed by the lymphatic system

43
Q

what are varicose veins + risk factors

A

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

44
Q

risk factors of CVI (chronic venous insufficiency)

A

age, gender, history (family) of varicose veins, obesity, pregnancy, phlebitis and previous leg injury

45
Q

venous hypertension

A

results from high venous flow in peripherals

46
Q

secondary varicose veins occur from…

A

DVT, INCOMPETENT DEEP VEIN VALVES, obstruction, (thrombus), pregnancy

47
Q

pathogenesis of varicose veins

A

the dilated elongated vessels occurs from venous hypertension which occurs from the incompetence of htecperforating veins (unrestricted back flow from deep to superficial veins

48
Q

what is venous oedema

A

swelling of soft tissue/ fluid accumulation > interstitial fluid that is protein poos and has low viscosity
found in peri-malleolar region

49
Q

difference between protein rich and poor

A

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

50
Q

what is haemosyderin

A

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)

51
Q

what is venous stasis dermatitis

A

eczematous process which occurs in the lower legs as a result of insufficient venous return. pruritic, erythemtous plaques on lower leg

52
Q

venous stasis dermatitis treatment

A

corticosteroids however beware of skin atrophy

53
Q

lipodermatosclerosis

A

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

54
Q

atrophie Blanche

A

smooth ivory white atrophic plaques of sclerosis, fibrotic with low blood flow and may contain talangiectasias. Pt have CVI

55
Q

telangiectasia

A

broken or dilated small superficial blood vessels (spider veins)
usually asymptomatic but may be a sign go underlying health issue

56
Q

venous ulceration

A

high levels of exudate, gaiter area, usually superficial but can be deep,

57
Q

management of varicose veins

A

compression, surgery, ablation (injection of sclerosant - destroying the vein and laser ablation)
complicaitons - DVT, bruising,

58
Q 
venous thrombosis (DVT)
pathogenesis
A

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
59
Q

what is DVT

A

a thrombosis in the deep veins of the leg
if Patient comes n with a red, hot swollen leg - suspect this
associated with Stasis!

60
Q

CLINICAL PRESENTATION OF DVT

A

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

61
Q

diagnosis of DVT

A

venous duplex is best method

62
Q

pharmacological treatment for DVT involves:

A

heparin first 7-10 dys(blood thinner) warfarin (blood thinner - anticoagulant) 5-7 days after hep, then continue for 1-2 months

63
Q

complications of DVT

A

recurrence, varicose veins, talangiectasias, purpuric colouration, oedema, eczema, haemosiderosis, atrophic blanche, atrophic skin, fibrosis and induration, venous ulceration

64
Q

management for venous hypertension

A

elevation, exercise, compression (maintain venous drainage,
pharmacological :
- emollients and topical steroids and antibiotics antiseptics, wound dressings
- skin grafts
pharm: - pentoxifylline, diuretics, antibiotics, stanozolol

65
Q

what is lymphedema

A

swelling of a body part (usually limb due to due to accumulation of fluid from obstructed flow of the imvompotence.
it is protein rich

66
Q

congenital primary lymphedema include:

A

congenita - onset before 1yrs
praecox - from one to 35 yrs
tarda - 35+

67
Q

treatment of Lymphedema

A

no cure, more so management strategies like manual lymph drainage,
elevation, protection of limb, compression,
pharm: antibiotics

68
Q

goals for treatment

A

improve cosmoses, preserve skin integrity, soften subcutaneous tissue decrease limb size, avoid contracture of the involved limb
patient and family education

69
Q

goals for treatment for lymphedema

A

improve cosmoses, preserve skin integrity, soften subcutaneous tissue decrease limb size, avoid contracture of the involved limb
patient and family education

Podiatry vascular (2 decks)

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