Venous Insufficiency Flashcards

1
Q

Diagnosis

A

Identification of the underlying pathophys of the wound is critical to development and implementation of a POC

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2
Q

Artery vs. Vein

A

Size of muscular wall is large in arteries!
Arterial system is a resistance system with more pressure in it
Veins have smaller vascular wall so less pressure associated with it

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3
Q

Vein has what

A

valves - so blood moves in one direction only

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4
Q

Elastin a vs. vein

A

the larger the artery, the more recoil the artery will have
veins have elastin but not as much as arteries
so arteries have blood flow into them, they contract, and as blood moves away, the elastic contracts and allows for maintenance of normal pressure on the arteries - this is less true for the veins

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5
Q

Endothelial cells (inside - lumina)

A

they respond to shear stress
blood flow through the a and v is a shear force
They respond to inc in flow pressures by releasing inflammatory mediators that produce localized ifnlammation in the local areas - happens more in artery side because more pressure there
Endothelial cells also release growth factors

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6
Q

Epidermis vascularization

A

NONE!!! no vascularization within it

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7
Q

Basement membrane does wht

A

reduce friction between epidermis and dermis

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8
Q

Beneath the basement membrane is what

A
Plexus
moves into basement membrane 
Another one between the dermis and the adipose tissue 
Another layer within subQ tissue
Each of these is larger as you go deeper
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9
Q

Deep veins

A

Run along with arteries that share their name - might be more than one vein that runs along with it
Contained in the same sheath as the artery
Deep veins are thinner and less muscular than the superficial veins - they have less pressure associated with them than the superficial veins do
Because they are so deep though they have a little more pressure related to soft tissue around them

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10
Q

LE venous anatomry - deep veins

A
Anterior tibial vein
Posterior tibial vein
Peroneal vein
Popliteal vein
Femoral vein
Deep femoral vein
Common femoral vein
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11
Q

Perforating veins do what

A

connect superficial veins to deep veins

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12
Q

Perforating vein - venous insufficiency theory

A

Thought is that it might be an issue with the valve not getting the blood to the superficial?

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13
Q

Superficial veins of LE

A

Great saphenous vein

Small saphenous vein

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14
Q

What happens in the ankle are

A

The blood moves directly into the deep veins and from the deep veins it moves into the superficial veins which then fills the saphenous veins and then perforating veins and then deep veins further up
This is why we often see venous insufficieicny in the medial ankle region

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15
Q

Venous insufficiency ulcers

A

Chronic condition
Insidious
Venous hypertension exists!!! - this is the primary cause!

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16
Q

Theories of venous insufficiency ulcers

A

Fibrin cuff theory of ulcer development
White blood cell trapping
Growth factor trapping (this is outlier of the theories)

17
Q

Theories of venous insufficiency ulcers - Fibrin cuff

A

Constant venous hypertension causes widening of capillary pores
This allows large molecules like fibrinogen to move through
Fibrin accumulates around the vascular walls and within the interstitial spaces
Mechanical barrier is built
This is an older theory

18
Q

Theories of venous insufficiency ulcers - Growth factor trapping

A

The cuff traps growth factors into its matrix decreasing its availability (of growth factors to health insult to tissue)

19
Q

Theories of venous insufficiency ulcers - White blood cell trapping AKA ischemia reperfusion injury

A

Cycling venous pressure allow an accumulation of WBCs in the capillaries
Localized ischemia occurs secondary to dec flow
WBC become activated and release lytic enzymes - other infalmmatory cytokines activate

20
Q

Skin characteristics in a CVI ulcer

A

1 Hyperprofileration of the epidermis
2 Thickening of the dermis with the dermal epidermal junction becoming convoluted
3 Dermal tissue changes may impair keratinocyte migration
All of this leads to - Lipodermatosclerosis (sclerosis, skin, fat)

21
Q

Lipodermatosclerosis

A

Heardening (sclerosis) of the skin

A form of panniculitis/inflammation of the SubQ tissue

22
Q

Risk factors

A
Calf muscle pump failure (weak, sustained standing)
Vein dysfunction - varicosities 
Age over 65 
Diabetes Mellitus
Trauma
23
Q

Differential diagnosis

A

Ischemic ulcer

Diabetic (neuropathic) ulcer

24
Q

Clinical classification - CO - class

A

No visible or palpable signs of venous disease

25
Q

Clinical classification - C6 - class

A

Skin changes are defined above with active ulceration

26
Q

Clinical classification - S - clinical presentation class

A

symptomatic - but not seeing the classic venous signs

27
Q

Clinical classification - A

A

asymtomatic

28
Q

E - etiological classification

A
Ec = congenital 
Ep = primary
Es = secondary (postthrombotic)
En = no venous causes identified
29
Q

Anatomic classification

A
As = superficial veins
Ap = perforator veins
Ad = deep veins
An = no venous location identified
30
Q

Pathophysiologic classifciation

A

Pr = reflux
Po = obstruction
Pr, O = reflux and obstruction
Pn = no venous pathophys identifiable

31
Q

Venous insufficiency ulcers -c haracterisitcs

A
1 hemosiderin deposits 
2 lipodermatosclerosis
3 generally on medial aspect of leg above medial malleolus
4 loss of subQ fat
5 dry skin surrounding wound
6 shallow wound
7 irregular wound margins
8 moderate to severe exudate
9 mild pain
10 red round bed may have fibrous yellow or white slough
32
Q

Venous insufficiency ulcers - general tx guidelines

A
1 infection prevention, measures needed
2 dec risk of trauma
3 LE exercises
4 promote healing - edema control, compression, dressing to control exxudate)
5 clean and moisturize skin
6 pt education regarding life long care
33
Q

Venous insufficiency ulcers - general tx guidelines - dressing that control exudate

A

usual semipermeable semiocclusive