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3101 manuals > Vascular manual > Flashcards

Vascular manual Flashcards

1
Q

What are we assessing with a doppler?

A

arterial blood flow, audio and waveform

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2
Q

What are the risk factors of PAD?

A

Smoking, HTN, hyperlipidaemia, DM, CVD, revious surgery on arterial system, elevated plasma homocysteine levels, low physical activity

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3
Q

what is homocysteine?

A

an amino acid, promotes the formation of oxidized LDL, endothelial dysfunctionad nthe proliferation of vascular smooth muscle cells.

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4
Q

What are symptoms of PAD?

A

Cramp-like pain, tightness, tiredness, impotency, rest pain

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5
Q

symptoms related to CVI?

A

tingling, aching, burning pain, cramp-like pain, sensation of swelling, throbbing, heaviness, itching skin, restless, leg tiredness and fatigue?

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6
Q

how might you differ intermittent claudication from CVI?

A

timing of the symptoms (CVI may get worse with heat and as the day progresses)

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7
Q

How does a doppler work?

A

emitting ultrasonic sound waves which are reflected of moving erythrocytes.

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8
Q

what are some things to consider before performing a doppler waveform assment?

A

pt should be supine for 10minutes prior
aquasonic gel
probe held at a 45degree angle

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9
Q

when assessing the sound of the waveform what are we listening for?

A

phases, volume, clarity

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10
Q

describe a triphasic waveform?

A

forward, back, forward

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11
Q

What is the third phase of the wave form representing?

A

The final forward flow in later diastole produced by elastic recoil of the artery.

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12
Q

What is the initial upsweep of a wave form?

A

systole, as the blood is ejected from the heart

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13
Q

Describe the second phase of a triphasic waveform?

A

Period of reverse flow due to high resistance in the arteriolar network.

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14
Q

What measurement is used for the velocity rate?

A

seconds per centimeter

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15
Q

What is the dicrotic notch?

A

the point that reverse flow commences

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16
Q

what is missing in a biphasic waveform?

A

loss of the late diastole forward flow

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17
Q

what are some of the causes of a biphasic waveform?

A

age related changes, atherosclerosis, diminished elasticity and compliance of the artery wall.

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18
Q

what is missing in a monophasic waveform?

A

both the early and later diastolic phases are absent

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19
Q

what are the reasons for loss of waveform?

A

an artery with significant stenosis will have no clear diastolic or systolic phases.

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20
Q

who do we perform an ABI on?

A

anyone 50+ who smokes and or DM and pts with risk factors present, all adults 65yrs and over.

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21
Q

what is the goal of an ABI?

A

determine if overall blood flow to the foot is adequate (quantifying)

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22
Q

what should a patient avoid when performing a vascular assessment?

A

pt supine for 10 mins, caffine, smoking and exercise for at least 1 hour

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23
Q

where do we take a brachial pressure?

A

cubital fossa

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24
Q

how long should you inflate cuff when taking a pressure reading?

A

until the pulse is obliterated +20mmHg

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25
Q

what rate do we release the cuff?

A

2mmHg per second

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26
Q

When do we take our brachial pressure reading?

A

the point at which the SOUND returns is the systolic pressure

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27
Q

when interpreting an ABI when is pathology diagnoses?

A

ABI 0.5-0.9 inclusive

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28
Q

what is the diagnosis of an ABI 0.91-0.99

A

“borderline”

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29
Q

What is the interpretation of an ABI of 1.3-1.4?

A

suggests significant calcification, unreliable results

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30
Q

Interpretation of an ABI of 0.40-0.80

A

intermittent claudication

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31
Q

what does it mean to have a pathological artery?

A

significant atherosclerosis and therefore PAD

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32
Q

what is the cut off for cuff inflation considered MAC?

A

260mmHG

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33
Q

when the ankle pressure is greater than 75mmHg above the brachial what is the interpretation?

A

medial arterial calcification

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34
Q

what is medial arterial calcification?

A

focal calcification of the middle layer of the arterial wall as a result of increased expression of bone morphogenetic protein

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35
Q

Recommended action for consecutive ABI less than 0.80

A

referral for Duplex scan and vascular surgeon via GP

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36
Q

recommended action for an ABI 0.50-0.90

A

repeated in 3months. if similar results in 3months initiate intensive risk factor modification.

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37
Q

recommended action for an incommpressible artery (greater than 75mmHg over brachial)?

A

reassessed in 3months to confirm diagnosis of MAC. refer on.

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38
Q

what are the risks associated with medial arterial calcification

A

macro and micro vascular complications

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39
Q

what are some of the associations between DM and vascular problems?

A

autonomic neuropathy leading to increased arteriovenous shunting leading to decreased skin perfusion, predisposing tissue to hypoxia and necrosis and sensorimotor dysfunction

40
Q

what are the advantages of a TBI?

A

potentially more specific and sensitive than an ABI if the presence of peripheral neuropathy and MAC. occlusions distal to the ankle

41
Q

how does a PPG work?

A

infrared light emitted onto the skin, the amount of light absorbed depends on the volume of blood in the skin

42
Q

following inflation of the digital cuff at what point is the toe pressure taken?

A

when small regular upstrokes appear to the nearest 2mmHg

43
Q

what is reactive hyperaemia?

A

transient increase in blood flw that occurs following a period of ischemia

44
Q

what should a toe pressure be in relation to a brachial?

A

70% of the highest brachial

45
Q

what is the management plan for TBI less than 0.75 with risk factors?

A

rescreen in one year

46
Q

what is the management plan for a TBI of less than 0.75

A

rescreen in 6months

47
Q

what is the management plan for a TBI 0.3-0.5

A

rescreen in 3months if still present refer to GP

48
Q

What is the management plan of a TBI less than 0.3

A

referal to GP for a duplex ultrasound and referral to a vascular surgeon.

49
Q

What do we consider a waveform and signs and symptoms when interpreting a TBI?

A

there is currently limited literature available on TBI with PAD therefore should be interpreted with other signs and symptoms

50
Q

what is PAD?

A

those entities which result in obstruction to to blood flow in the arteries

51
Q

what is involved in screening for PAD?

A

history, including risk factors, signs and symptoms, clinical observation and non-invasive vascular testing.

52
Q

why might a patient with PAD have hypohydrotic skin?

A

metabolic demands of the dermal structures not being met.

53
Q

DDX for dry flakey skin?

A

autonomic neuropathy causing sudomotor dysfunction, tinea pedia, previous sugery

54
Q

implications of vascular insufficiency on hair growth?

A

inadequate supply of nutrients to the hair follicle resulting in the hair being released and the follicle dies.

55
Q

how can reduced peripheral blood flow affect the nails

A

damage to the nail matrix resulting in general thickening of the nails

56
Q

breifly describe intermittent claudication?

A

transient ischaemic muscle pain occurs during exercise.

57
Q

describe the pathophysiology of intermittent claudication?

A

when stenosis occurs the vessel has uneven lumen size due to plaque build up and the amount of blood able to pass is limited and the metabolic demands of the muscle are not met.

58
Q

why is intermittent claudication painful?

A

pain is felt when the accumulation of metabolic by-product within the muscle is at a high enough concentration to activate pain receptors.

59
Q

what are the clinical signs and symptoms of Intermittent claudication?

A

aching, cramp-like pain and tirendess of the muscle compartment (typically calf muscles)

60
Q

in the presence of normal ABI where intermittent claudication is suspected what should you do?

A

perform a post excercise ABI following 50 toe raises. PAD is indicated if there is a drop in the ABI post-excerise

61
Q

gold standard for intermittent claudication?

A

referral for a duplex ultrasound

62
Q

what is the benefit of Duplex ultrasound?

A

provides information about the location and extend of arterial disease and type of lesions present

63
Q

what is rest pain?

A

rest pain is persistent pain caused by nerve ischaemia and usually indicates two haemodynamically significant arterial blocks in series.

64
Q

what causes ischemic ulceration?

A

lack of arterial flow to the capillary bed.

65
Q

what might an ischemic ulcer look like?

A

base is usually brown, grey, yellow or black.
does not bleed, punched out borders.
very painful

66
Q

What is gangrene?

A

tissue death - end stage arterial insufficiency

67
Q

what is the cause of secondary venous insufficiency?

A

result of an acquired condition, most commonly reflux of blood into the superficial venous system

68
Q

what causes vein wall changes?

A

hypertrophy of the vein wall with increased collagen content, together with disruption of smooth muscle cells and elastin fibres.

69
Q

what is the roll of type III collagen?

A

increases ability of tissue to tolerate pressure

70
Q

what are the major clinical features of venous insufficiency?

A

oedema, dilated veins, leg pain and cutaneous changes.

71
Q

what are the types of oedema?

A

venous and lymph

72
Q

what is low viscosity, protein-poor interstitial fluid resulting from increased capillary filtration that cannot be accommodated by normal lymphatic system?

A

venous oedema

73
Q

what is excess protein-rich interstitial fluid within the skin and subcutaneous tissue resulting from lymphatic dysfunction??

A

Lymphoedema

74
Q

breifly describe how CHF might lead to oedema?

A

the rate of fluid entering the tissue is greater than the ability of the lymphatic system to return fluid to the vascular system

75
Q

what type of oedema will you see with left ventricular failure?

A

pulmonary oedema

76
Q

what type of oedema will you see wit hright ventricular failure?

A

peripheral oedema

77
Q

what are some of the causes of oedema?

A

CHF, pulmonary hypertension, medication, DVT, pregnancy, obesity, lymphoedema, venous insufficency

78
Q

how do we determine the cause of oedema?

A

pt history, duration of swelling, pain, medications review, distribution of oedema

79
Q

what are variscosities

A

tortuous, dilated, lengthened vessel caused by increased internal vessel pressure

80
Q

veins most commonly affected by variscosities?

A

saphenous

81
Q

risk factors for varicose veins

A

female, age, genetics, obesity, standing occupation

82
Q

what are telangiectasias?

A

permanent dilation of pre-existion blood vessels, where the blood remains confined in the vasculature.

83
Q

describe the most common cause of telangiectasias?

A

venous hypertension from valvular incompetence or variscosities

84
Q

what are haemosidering deposits?

A

yellow-to-brown iron-rich pigments that are caused through the breakdown fo the red blood cells

85
Q

breifly describe venous stasis dermatitis

A

eczematous process that occurs as a result of insufficient venous return. chronic inflammatory skin reaction associated with venous pooling.

86
Q

how does venous stasis dermatitis present?

A

erythematous pruritic plauques on the leg.

87
Q

how do you treat venous stasis dermatitis?

A

topical steroids is often used but may lead to cutaneous atrophy increasing the risk of venous ulceration

88
Q

what is lipodermatosclerosis?

A

acute inflammatory skin change due to inflammation of subcutansoue adipose tissue

89
Q

what are the characteristics of lipodermatosclerosis?

A

dermis and subcutaneous tissue becoming hardened and fibrosed with lack of pitting oedema, skin becomes atrophic, loss of sweat glands and hair follicles, variable pigmentation.

90
Q

what happens in chronic lipodermatosclerosis?

A

alters the shape of the leg - inverted champagne bottle

91
Q

what is atrophie blanche?

A

smooth ivory-white atrophic plaques of sclerosis. Typically fibrotic with low blood flow and may contain telangiectasias

92
Q

what is cellulitis?

A

diffuse, acute bacterial infection of the skin and subcutaneous tissue

93
Q

breifly describe venous ulceration

A

superficial ulceration, breakdown of the cutaneous and subcutaneous tissue. usually in the gaiter region

94
Q

management of CVI?

A

compression stockings, surgical treatment

95
Q

signs and symptoms of autonomic neuropathy

A

vascular disturbance (arteriorvenous shunting), thermoregulation, sudomotor dysfunction.

3101 manuals (2 decks)

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