Chap 55-56 CVI General Considerations Flashcards Preview

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Flashcards in Chap 55-56 CVI General Considerations Deck (40):
1

what conditions contribute to venous pathology?

valvular incompetence of the deep or superficial veins

perforator incompetence

venous obstruction

muscle pump dysfunction

2

what does normal venous pressure do with exercise?

resting venous pressure drops with exercise >50%

returns to normal but takes >20sec

3

What are primary and secondary cause of valve dysfunction?

preexisting weakness in vessel or leaflets

secondary to direct injury superficial phlebitis
excessive venous distention from hormonal effects or high pressure

4

How does high venous pressure enter the superficial system?

failure of valves located at junctions b/w deep and superficial

failure of valves in communicating perforator

5

What are the most common tributaries with reflux?

saphenous
small saphenous
both

6

What are obstructive causes of reflux?

venous thrombosis

destruction of valves from DVT

compression (May-thurner)

7

What is the genetic inheritance of VV?

autosomal dominant with variable penetrance

8

How does microangiopathy occur?

hemo changes in large veins are transmitted to microcirculation

microvalve dysfunction

9

What are features of microangiopathy?

elongation, dilatation, tortuosity of capillary beds

thickening of BM with increased collagen and elastic fibbers

endothelial damage

increased pericapillary edema with 'halo' formation

10

what happens to the capillary once microangiopathy has started?

increase permeability and high venous pressure

accumulation of fluid, macromolecules and extravasated red blood cells in the interstitial

fragmentation and destruction of microlymphatics (impairs drainage)

11

What mechanisms have been postulated for devel of microangiopathy?

fibrin cuff formation (accumulation of fluid in pericapillary sapce)
this impairs fibrinolysis, increase diffusion barrier, inhibit repair process and maintain inflame process

WBC trapping in capillaries with activation of leuks and inflammation

growth factor activation (unavailable for healing)

12

What are skin changes in CVI?

edema

corona phlebectatia

hyper pigmentation from hemosiderin deposition

lipodermatosclerosis with scarring and thickening of the skin

atrophie blanche

13

what is lipodermatosclerosis?

inflammation of the fat under the epidermis

get fat necrosis

causes tapering at ankles

14

What is atrophie blanche?

smooth, ivory-white plaque stippled with telangiectases and is surrounded by hyper-pigmentation

15

What is the character of the edema associated with CVI?

initially pitting
then brawny and resistant to pitting

16

What is corona phlebectatica?

fan shaped appearance of intradermal veins on the ankle (inframalleolar ankle flare)
advanced disease

17

What is the Brodie-trendelenburg test?

distinguish deep and superficial

supine
elevate leg to empty vein
tourniquet over superficial veins
upright

with superficial reflux, release of tourniquet with have rapid filling of superficial veins

with deep reflow the superficial veins will fill despite tourniquet

normal will take >20sec to fill with removal of trouniquet

18

What is the C in the CEAP classification?

clinical
C0 no visible signs
C1 telangiectasia/reticular veins
C2 varicose veins
C3 edema
C4 changes in skin and sub cut
A pigmentation/eczema
B lipodermatosclerosis/atrophie blanche
C5 healed ulcer
C6 active ulcer

19

What is the E in the CEAP classification?

etiology

Ec congenital (KTS)
Ep primary
Es secondary (DVT)
En no venous cause

20

What is the A in the CEAP classification?

Anatomic
As superficial
Ad deep
Ap perforator
An no venous location

21

What is the P in the CEAP classification?

Pathophys

Pr reflux
Po obstruction
Pr,o reflux and obstruction
Pn no venous patho

22

What is the best test a diagnosing CVI?

duplex
phtoplethmysmography

23

What is the best test a determining severity for CVI?

air plethysmography

24

What is the best test for determining anatomy for CVI?

venogram

25

What is the best test for assessing hem significance?

APG
foot pressure

26

What is the venous filling index?

APG
90% of the venous volume divided by the time required to 90% of the venous volume (once upright)
2ml/s normal
>4ml/s abnormal

27

What are invasive/non-invasive methods of measuring CVI?

NI

DUS
PPG
APG
CTV
MRV

invasive
plebogram
Ambulatory venous P
IVUS

28

What is early treatment recommendation for venous ulcer?

compression 30-40
wound care
ablation superficial vein

29

What are exercise recommendations for CVI?

regular moderate
vigorous can worsen
leg elevation when resting

30

What are the classes for compression therapy?

class 1--15mmHg
class 2--20-30mmHg
class 3 30-40mmHg
class 4--40-50mmHG
>60 unsafe

31

What did the REACTIV trial show for C2-3 dz?

2 yr symptom relief, satisfaction, QoL
better with surgery (saph ligation)
sclero better then conservative

Surgery most cost efficient followed by sclera

32

How does compression work?

opposes reflux induced VHTN
improves muscle pump
improved microcirculation

33

What are some adjuncts for compression therapy?

circAid garment
Unna boot
layered elastic and non-elastic compression bandage
IPC (good if edema)

34

What is the evidence in compression?

improves healing times
decreases recurrence

35

What is evidence for compression in C6 dz?

ssurgery plus compression ;pwer recurrence then compression alone

36

What is the role of diuretics in CVI?

unclear

37

What is the role of zinc in CVI?

MA
no benefit

38

What is the role of fibrinolytics in CVI?

no proven benefit

39

What is the role of pentoxifylline in CVI?

evidence of benefit in combo with compression

40

List the tributaries at the saphenofemoral junction.

inferior epigastric
superficial circumflex
lateral accessory saphenous
deep external pudedal
superficial external pudendal
medial accessory saphenous