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ICM > 3: aortic and peripheral vascular disease > Flashcards

3: aortic and peripheral vascular disease Flashcards

1
Q

give me some epidemiology facts about aortic dissection

A

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

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2
Q

risk factors for aortic dissection

A

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

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3
Q

aortic dissection pathophysiology

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

*not aneurysmal!!

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4
Q

DeBakey classifications of aortic dissection

A

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

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5
Q

aortic dissection presentation

A

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

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6
Q

aortic dissection physical exam

A

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)

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7
Q

diagnostic tests ordered in aortic dissection

A 
labs 
EKG 
imaging - CXR 
              -echo/TEE! 
CT scan 
aortography
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8
Q

treatment for type A aortic dissections

A

surgical repair

  • resect original tear
  • graft blood to true lumen
  • operative mortality 7%
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9
Q

treatment for type B aortic dissections

A

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

surgical management if:

  • increasing pain
  • HTN
  • major branch occlusion
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10
Q

epidemiology of abdominal aortic aneurysm (AAA)

A

degenerative process of aging (nonspecific)

65-70 y/o

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11
Q

risk factors for AAA

A

age more than 65
PAD
FH
other arterial aneurysms

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12
Q

AAA natural history

A

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)
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13
Q

presentation of unruptured AAA

A

abdominal pain, back or flank pain

gradual onset/vague/dull quality (colicky)

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14
Q

presentation of ruptured AAA

A

pain
hypotension
pulsatile abdominal mass

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15
Q

AAA physical exam

A

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

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16
Q

AAA diagnostic testing

A

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

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17
Q

asymptomatic management of AAA

A

serial DUS until >4.0 or symptoms

patient education

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18
Q

symptomatic management of AAA

A

surgical repair

  • endovascular
  • open techniques
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19
Q

PAD/atherosclerosis pathophysiology

A

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

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20
Q

atherosclerosis risk factors

A

cigarettes
diabetes
hypercholesterolemia
HTN

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21
Q

presentations of PAD

A
  • thromboembolic
  • symptoms of claudication
  • “my leg fell off”
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22
Q

describe arterial insufficiency

A
  • symptoms worsen with ambulation
  • elevation worsens
  • weak/absent pulses
  • compression worsens
  • lack of oxygenated blood to tissues
23
Q

describe venous insufficiency

A
  • symptoms improve with ambulation
  • elevation helps
  • normal pulses
  • compression helps
  • excess of deoxygenated blood pooling in tissues
24
Q

diagnostic work up for arterial insufficiency

A

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
Q

emergent surgical management of PAD

A
  • acute thrombosis - plaque disruption, thrombophilia
  • intractable rest pain due to ischemia
  • gangrenous limbs
26
Q

expectant management of PAD

A

claudication mild symtpoms

  • anti-platelet therapy
  • compression therapy
  • follow symptoms and restudy if symptoms worsen
  • encourage cessation of smoking
27
Q

does PAD or venous insufficiency affect more people?

A

venous insufficiency

28
Q

complication of venous insufficiency

A

stasis ulcers

29
Q

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

A

fatal PE

30
Q

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

A

chronic pain and swelling

31
Q

which gender gets venous insufficiency more?

A

females to males 3:1

32
Q

musculovenous pump: what happens to blood during muscle relaxation?

A

blood is drawn inward through perforating veins

superficial veins act as collecting system

33
Q

describe the superficial venous system

A

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

34
Q

physical findings in venous insufficiency

A

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
Q

what is eczematoid dermatitis?

A

inflammation typically adjacent to a bulbous tributary

36
Q

what is atrophie blanche?

A

inflammation and scarring leading to plaques of skin without pigment

37
Q

what is corona phlebectatica?

A

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

38
Q

what is stasis dermatitis?

A

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

39
Q

what is lipodermatosclerosis/sclerosing panniculitis?

A

painful inflammatory lesions that are firm and contracted - pre ulcerous

40
Q

what is superficial thrombophlebitis?

A

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

41
Q

what is stasis ulceration?

A

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

42
Q

primary causes of varicose veins

A

hereditary
hormonal
pregnancy
gravity

43
Q

secondary causes of varicose veins

A

obesity
trauma
gravity
occupations requiring prolonged sitting or standing

44
Q

what are varicose veins a problem?

A

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

45
Q

symptoms of varicose veins

A

pain
heaviness
intensification
cramping

46
Q

complications of varicose veins

A 
superficial phlebitis (SVT) 
DVT 
venous stasis dermatitis/ulceration 
bleeding 
chronic pain syndrome
47
Q

when is venous evaluation indicated?

A

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

48
Q

ways to evaluate veins

A

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

49
Q

what treatment options are best?

A

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

50
Q

what is thrombophilia

A

imbalance b/w clot formation and dissolution

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

51
Q

when do you consider thrombophilia?

A 
young patient with VTE 
recurrent idiopathic thrombosis 
unusual site of thrombosis 
family history of VTE/multiple miscarriages 
heparin resistance 
warfarin induced skin necrosis
52
Q

causes of thrombophilia: hereditary, loss of fxn

A

antithrombin deficiency

protein C and S deficiency

53
Q

causes of thrombophilia: hereditary, gain of fxn

A

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

54
Q

causes of thrombophilia: acquired

A

anti-PLA syndrome
HIT
malignancy

ICM (26 decks)

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