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Flashcards in 3: aortic and peripheral vascular disease Deck (54)
1

give me some epidemiology facts about aortic dissection

5-10/1million
most lethal condition
males 2-3x more
50-70 y/o (except collagen shit, congenital shit, pregnancy, coarctation, turner syndrome, trauma)

2

risk factors for aortic dissection

hypertension 67%
collagen disorders (marfan's 1/3 develop dissection)
pregnancy (half under 40 y/o)
congenital heart defects

3

aortic dissection pathophysiology

medial degeneration (loss of smooth mm. and elastic fibers)
repeated flexion of aorta
hydrodynamic stress on intima

*not aneurysmal!!

4

DeBakey classifications of aortic dissection

type I - asc/arch/desc
type II - ascending only
type IIIa - descending, above diaphragm
type IIIb - descending, below diaphragm

5

aortic dissection presentation

tearing, ripping, knife-like pain
migrating pain (radiates to back)
vasovagal symtoms
neuro deficits, syncope in some

6

aortic dissection physical exam

general - apprehensive, sense of impending doom
tachycardia
cool clammy skin
BP disconnect (central vs. peripheral)
murmur - suggesting aortic regurgitation
signs of tamponade (friction rub, JVD, pulsus paradoxus, muffled heart tones)

7

diagnostic tests ordered in aortic dissection

labs
EKG
imaging - CXR
-echo/TEE!
CT scan
aortography

8

treatment for type A aortic dissections

surgical repair
-resect original tear
-graft blood to true lumen
-operative mortality 7%

9

treatment for type B aortic dissections

medical management
-BP control (B blockers, 15-20% mortality)

surgical management if:
-increasing pain
-HTN
-major branch occlusion

10

epidemiology of abdominal aortic aneurysm (AAA)

degenerative process of aging (nonspecific)
65-70 y/o

11

risk factors for AAA

age more than 65
PAD
FH
other arterial aneurysms

12

AAA natural history

progressive enlargement leading to rupture and fatal hemorrhage
-majority die before getting to hospital
-average growth rate 0.2-0.5 cm/y
-most ruptures more than 5 cm (but may rupture earlier)

13

presentation of unruptured AAA

abdominal pain, back or flank pain
gradual onset/vague/dull quality (colicky)

14

presentation of ruptured AAA

pain
hypotension
pulsatile abdominal mass

15

AAA physical exam

HALLMARK: pulsatile, expansile abdominal mass***
abdominal bruits
pulses often maintained
early findings of thromboembolic events suggest proximal source (blue toes)

16

AAA diagnostic testing

stable: duplex screening
acute symptoms: bedside DUS to conform to surgery
-presence of AAA
-free fluid in abdomen

17

asymptomatic management of AAA

serial DUS until >4.0 or symptoms
patient education

18

symptomatic management of AAA

surgical repair
-endovascular
-open techniques

19

PAD/atherosclerosis pathophysiology

large/medium arteries
basic lesion - fibrofatty plaque + raised lesion w/i intima
progression - plaques increase in size and thickness
ultimately compromise arterial flow

20

atherosclerosis risk factors

cigarettes
diabetes
hypercholesterolemia
HTN

21

presentations of PAD

-thromboembolic
-symptoms of claudication
-"my leg fell off"

22

describe arterial insufficiency

-symptoms worsen with ambulation
-elevation worsens
-weak/absent pulses
-compression worsens
-lack of oxygenated blood to tissues

23

describe venous insufficiency

-symptoms improve with ambulation
-elevation helps
-normal pulses
-compression helps
-excess of deoxygenated blood pooling in tissues

24

diagnostic work up for arterial insufficiency

segmental arterial pressure study
-cuff arms + 3 or 4 on limbs
-couple DUS with actual BP measurement
-compares limbs
-identifies level of lesion

ABI
-less than 0.7 significant disease
-less than 0.5 rest pain is common

angiogram
-allows for surgical planning (open vs. endovascular)

25

emergent surgical management of PAD

-acute thrombosis - plaque disruption, thrombophilia
-intractable rest pain due to ischemia
-gangrenous limbs

26

expectant management of PAD

claudication mild symtpoms
-anti-platelet therapy
-compression therapy
-follow symptoms and restudy if symptoms worsen
-encourage cessation of smoking

27

does PAD or venous insufficiency affect more people?

venous insufficiency

28

complication of venous insufficiency

stasis ulcers

29

what is the 3rd most common cause of death among hospitalized patients?

fatal PE

30

what symptoms do patients who survive DVT +/- PE get?

chronic pain and swelling

31

which gender gets venous insufficiency more?

females to males 3:1

32

musculovenous pump: what happens to blood during muscle relaxation?

blood is drawn inward through perforating veins

superficial veins act as collecting system

33

describe the superficial venous system

vessels relatively more fragile
values are less well developed
lack of structural support from superficial tissue

34

physical findings in venous insufficiency

venulectasia/telangiectasia
combined tributary and small vessel disease
hyperpigmentation (chronic venous pressure - hemosiderin)
eczematoid dermatitis
atrophie blanche
corona phlebectatica
stasis dermatitis
lipodermatosclerosis (sclerosing panniculitis)
superficial thrombophlebitis
stasis ulceration
recurrent stasis ulcer

35

what is eczematoid dermatitis?

inflammation typically adjacent to a bulbous tributary

36

what is atrophie blanche?

inflammation and scarring leading to plaques of skin without pigment

37

what is corona phlebectatica?

red flare around a lesion that is a pre-cursor to stasis ulceration

38

what is stasis dermatitis?

heavy inflammatory changes in a gaiter area bilaterally in a patient with bilateral saphenous vein reflux - pre ulcerous condition

39

what is lipodermatosclerosis/sclerosing panniculitis?

painful inflammatory lesions that are firm and contracted - pre ulcerous

40

what is superficial thrombophlebitis?

firm palpable cords over superficial varices
overlying inflammation
common to see seasonal patterns

41

what is stasis ulceration?

end stage venous disease representing true urgency for control of venous condition

42

primary causes of varicose veins

hereditary
hormonal
pregnancy
gravity

43

secondary causes of varicose veins

obesity
trauma
gravity
occupations requiring prolonged sitting or standing

44

what are varicose veins a problem?

they can lead to complications from chronic venous HTN, similar to other chronic diseases that go unchecked

45

symptoms of varicose veins

pain
heaviness
intensification
cramping

46

complications of varicose veins

superficial phlebitis (SVT)
DVT
venous stasis dermatitis/ulceration
bleeding
chronic pain syndrome

47

when is venous evaluation indicated?

presence of advanced disease
quality of life impairment
unexplained leg pain +/- swelling

48

ways to evaluate veins

hand held doppler (fairly high false (+); intersaphenous v.)
detailed venous mapping

49

what treatment options are best?

depends, but generally speaking, lesser invasive therapies offer less pain and less down-time

50

what is thrombophilia

imbalance b/w clot formation and dissolution

virchow's triad: injury, stasis, inherited/acquired changes

51

when do you consider thrombophilia?

young patient with VTE
recurrent idiopathic thrombosis
unusual site of thrombosis
family history of VTE/multiple miscarriages
heparin resistance
warfarin induced skin necrosis

52

causes of thrombophilia: hereditary, loss of fxn

antithrombin deficiency
protein C and S deficiency

53

causes of thrombophilia: hereditary, gain of fxn

APC/factor V leiden mutation
prothrombin gene mutation
factor elevations
hyperhomocysteinemia

54

causes of thrombophilia: acquired

anti-PLA syndrome
HIT
malignancy