vascular disease: disease of aorta, PVD Flashcards Preview

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Flashcards in vascular disease: disease of aorta, PVD Deck (81):
1

normal artery from the inside out

-single layer of endothelial cells in subendothelial connective tissue
-separated from the media by the dense elastic membrane called the internal elastic lamina
-smooth muscle cells in layers of media lamina
-surrounded by its Lamina Adventitia

2

vascular lumen

channel for fluid transport

3

intima

thin columnar ring of active endothelial cells on a dense and "pliable" basement membrane the internal elastic lumen

4

media lamina

layers of smooth muscle cells in a metabolically active ECM composed of elastin, collagen and glycosoaminoglycans (where action happens)

5

adventitia

supportive fibrous tissue with nerves and blood vessels (vasovasorum)

6

Vasa vasorum

-in large and medium arteries
coursing into the outer one half to two thirds of media

7

large and medium arteries have

1. Vasa vasorum
2. well defined external elastic lamina,
3. (external to media is) Adventitia: consisting of connective tissue with nerve fibers and vasa vasorum

8

veins

-low pressure systems
-have thin walls

9

large veins have

intimal
media
adventitial layers

10

medium sized veins

less adventitia

11

venules have

progressively less adventitia

12

post capillary venules

less adventitia (the least)

13

capillary compensition

endothelial cell
encircling pericytes, but NO MEDIA
thin walled
slow flow
function gas exchange (insufficient over great distances)
nutrient exchange

14

highest density of capillaries

metabolically highly active tissues (like myocardium)

15

artery function

nutrients
oxygen
immuno-chemicals and cells for healing and growth
pharmacologic agents

16

all arterial diseases result from?

altered architecture
altered function

17

atherosclerosis

affects elastic and muscular arteries
-in large and medium sized arteries

18

HTN

affects small muscular arteries and arterioles

19

vasculitides

affects vessels of variable

20

tunica intima

-endothelial linning and connective tissue
-beneath connective tissue-> internal elastic lamina

21

tunica media

circumferential smooth muscle
external elastic lamina

22

tunica adventitia

connective tissue fibers

23

aortic dissection

-structural weakness of vessel wall
-loss of smooth muscle cells or insufficient extracellular matrix
-blood enters walls and separates the various layers
-causes rupture and/or obstruction of vessels branching off the aorta

24

aortic aneurysm

-dilations of blood vessels (abnormal bulge in vessel)
-involves entire thickness of wall
-causes rupture, thrombosis and embolization
-can predispose to dissection
-loss of smooth muscle cells or insufficient extracellular matrix
-causes: ischemia, genetic defect, defective matrix remodeling, trauma

25

LaPlace's law

a principle of physics that the tension on the wall of a sphere is the product of:
1. pressure times the radius of chamber
2. and tension is inversely related to thickness of wall

26

common causes of aortic aneurysms

atherosclerosis (arch and abd)
HTN
cystic medial degeneration
infectious such as TB, shyphilitic, staph, strep
rheumatic aortitis
trauma
congenital defects
marfan syndrome, ehler's danlos syndrome
pregnancy (3rd trimester)

27

diagnosis of aortic aneurysm

-radiograph: widened mediastinum, shift of midline structures (like trachea)
-echo or TEE good for ascending or descending (not in arch)

28

presentation of ascending thoracic aortic aneurysm

-discovered accidentally
-usually asymptomatic
-occasional chest pain
-compression of local structures
-AR

29

complications from ascending thoracic aortic aneurysm

1. chronic AR:
-LV dysfunction
-CHF
2. dissection
3.. rupture

30

therapy of ascending thoracic aortic aneurysm

control HTN
beta-blockers
serial imaging to assess for progression
surgery

31

descending thoracic aortic aneurysms

usually associated with atherosclerosis
chronic aortic dissection
surgery

32

abdominal aortic aneurysm

-manifestation of atherosclerosis
-high risk of concurrent CAD

33

risk factors for abdominal aortic aneurysm

smoking is the strongest
family history aneurysm
HTN
dyslipidemia, diabetes, age, male sex

34

clinical manifestations of abdominal aortic aneurysm

often asymptomatic
back/flank or abdominal pain (expanding, inflamed, leaking)
LE claudication
distal embolization

35

complications abdominal aortic aneurysm

peripheral embolization of adherent thrombus
rupture risk strongly related to size and rate of expansion
indications for surgery
-diameter >5.5 cm
-expansion rate: >1 cm year
-symptoms
treat vascular risk factors and assess for underlying CAD

36

aortic dissection risk factors

-long standing arterial HTN
-smoking, dyslipidemia, cocaine/crack
-connective tissue disorders
-hereditary vascular conditions: Marfans, Ehler's-Danlos, bicuspid aortic valve, coarctation of aorta
-vascular inflammation: giant cell arteritis, takayasu, Behcet;s disease, syphilis
-deceleration trauma
-iatrogenic factors: catheters/instrument intervention, valvular/aortic surgery, graft anastomosis, side of cross-clamping the aorta

37

pathophysiology of aortic dissection

-intimal tear leads to penetration of blood within the aortic wall
-false lumen forms separating layers of aortic wall

38

aortic dissection: De Bakey, type I

originates in ascending aorta, propagating at least to the aortic arch and often beyond it distally

39

aortic dissection: De Bakey, type II

originates in and as confident to the ascending aorta

40

aortic dissection: De Bakey, type III

originates in descending aorta and extends distally down the aorta, (rarely retrograde)

41

aortic dissection: standford type A

always involves the proximal aorta
-all dissection involving the ascending aorta

42

aortic dissection: standford type B

NO proximal involvement at all
-descending aorta dissection only
-all dissection not involving the ascending aorta

43

Type A common presenting symptoms

-none
-pain, numbness, TIA, stroke
-symptoms: related compression of adjacent tissue such as chest pain, dyspnea, hoarseness, dysphagia, CHF (ascending aorta), aortic insufficiency, head and neck swelling

44

complications of type A dissection

-aortic rupture
-cerebral ischemia
-pericardial tamponade
-acute aortic regurg. leading to pulmonary edema and cardiogenic shock
-coronary insufficiency

45

complications from acute type A dissection

-rupture of pericardium, pleura, peritoneal cavity
-disruption of aortic annulus
-extension into great arteries of neck or the coronaries, causing vascular obstruction and ischemic consequences like MI or stroke or spinal vascular disruption

46

clinical presentation: aortic dissection

-abrupt onset of severe pain in chest or back
-ripping, tearing or migrating pain
-focal neurologic deficits if dissection extends into cerebral vessels
-syncope

47

physical exam of aortic dissection

-unequal upper extremity BP's
-tachycardia
-pulse deficits
-focal neurologic deficits
-aortic insufficiency (acute)
-evidence of pericardial tamponade

48

imaging for aortic dissection

CT scanning
TEE
MRI
aortography

49

therapy for acute aortic dissection

establish beta-blockers
CCB
vasodilators
adequate analgesia
low threshold for intubation if unstable

50

type A dissection initial treatment

-surgery
*aortic rupture, pericardial tamponade, cardiogenic shock, cerebral/coronary insufficiency
*valve sparing surgery if NO pathological changes to aortic cusps (if normal size aortic root)
-stabilization with IV access and monitoring and anti-hypertensives therapy
-mortality is very high patient presents with hemorrhage or evidence of distal ischemia (CVA)
-immediate ICU admission

51

type B dissection: unstable

-impending rupture
-propagation with compromise of downstream vasculature
-unrelieved pain
-treatment: same as Type A

52

type B dissection: is stable and uncomplicated

-control blood pressure and cardiac contractility
-beta blockers
-ACE-I, ARB's, CCB
-monitor every 6-12 months

53

acute aortic dissection therapy for Type B

beta blockers
surgery
IRAD

54

chronic aortic occlusion

-progressive narrowing of distal aorta
-ASPVD
-in renals or iliac
Sx: claudication of low back, butt and impotence (or none)
PE: absent pulse obstruction, bruit, skin/hair changes, redness on dependency

55

acute aortic occlusion

-distal aorta-> MEDICAL EMERGENCY
-pre-existing narrowing with plaque and rupture
-acute ischemia of lower extremities
-pain with rest
-pallor
-absent pulse
-DX: aortography
TX: stabilize for surgery or thrombectomy or revascularization

56

aortitis

-can cause or aneurysms and dissection
-complications depend on locations and severity of underlying mechanism of the disease process

57

rheumatic causes of aortitis

-endarteritis of vasovasorum
-location affected: ascending thoracic aorta most common
-associated with:
rheumatoid arthritis
AS
psoriatic
reiter's syndrome
relapsing polychondrits
IBS

58

takayasu's arteritis

-young asian women
-inflammatory process
-often the arch and ascending aorta
-can cause obstruction
-acute and chronic phase
-no therapy

59

tertiary syphilus

-15-30 years past primary disease
-proximal aorta and root to arch, saccular or fusiform shape
-calcified ascending aortic aneurysm is classic
-PCN, excision and repair treatment

60

giant cell arteritis

-older woman more than men
-large medium size vessels
-aortitis with aortic insufficiency and associated with PMR and obstruction of medium size vessels of the body

61

Buerger's disease

-young male smoker
-no TX except stop smoking

62

aortic coarctation

-strong associaton with bicuspid aortic valve
*aortic aneurysm and dissection, VSD, berry aneurysm of circle wills, premature CAD
-pressure gradient across obstruction (>15-20 mmHg, considered significant)

63

clinical manifestations of aortic coarctation

asymptomatic
HTN
arm, leg, pulse differential
leg fatigue
bicuspid aortic valve
cerebral hemorrhage

64

diagnosis of aortic coarctation

physical exam
ECG with evidence of LVH
chest radiograph
echo
cardiac MRI
contrast aortography with invasive hemodynamics

65

TX aortic coarctation

surgery
percutaneous stenting

66

acute PAD results from

Embolic sources:
-atrial fib.
-MI
-ventricular aneurysm
-cardiomyopathy
-infectious sources
-prosthetic heart valves
-atrial myxoma

67

acute PAD is

a medical emergency

68

important to identify PAD

-surrogate marker for coronary artery disease

69

chronic PAD of LE

-occlusive arterial disease
-atherosclerosis
-risks rise from AODM, dyslipidemia, HTN, smokers
-high association with cerebral vascular and heart disease

70

chronic PAD sites

-stenotic or occlusive segmental lesions
-large and medium sized arteries
-plaques, calcification, thinning media, destruction of muscle and elastic fibers, fragmentation of internal elastic lamina and thrombi of platelets and fibrin
- sites-> femoral and popliteal, tibial and perineal, abdominal and iliac

71

hallmarks of LE PAD disease

-claudication
-reproducible sx-> effort, location, examination

72

spectrum of LE arterial disease

asymptomatic
claudication
rest pain
numbness, tingling, lack sensation
ulceration and gangrene

73

claudication

-Sx occur one joint level distal to the point of obstruction
-cramping, pain or weakness in a muscle group that occurs after a reproducible amount of effort

74

signs of chronic PAD

-decreased or absent pulses distal to obstruction
-bruits heard over narrowed artery
-muscle atrophy and weakness with exercise
-skin texture(thin and shiny) and color changes (cool, pale, blue) and hair loss

75

ankle to brachial index (ABI)

-Pros: quick stethoscope and BP cuff
-Cons: gives no info on disease level (ABI artificially elevated in calcified vessels in diabetes)

76

how to ABI

-patient must be lying down
-measure systolic and diastolic BP on right and left arms
-higher systolic reading of left and right arm is used in the assessment
-pressure in each foot posterior tibial artery and dorsalis pedis artery are measured with higher of the two values used as the ABI for that leg
-ABI is calculated by dividing the systolic blood pressure at the ankle by systolic blood pressure in arm
-average each of systolic BP

77

management of PAD therapy

-supportive measures: care of feet, compression hose, protective shoes
-non-operative intervention: life style changes, exercise, no smoking, diet management
-pharmacologic: control BP, treat AODM, cholesterol
-no help with most vasodilators, heparin or alpha-blockers or CCB
-trental may help
-surgery and possibly thrombolytics for acute disease

78

Consequences of DVT

PE
Death
Chronic venous stasis: leg swelling, heat, redness, pain, cyanosis due to stasis, ulcers
Calf pain with weight bearing

79

Consequences of SVT

Heaviness of limb
Pain
Severe swelling
Ulcerations
Cosmetic dis figuration

80

Diagnosis of PVD: deep vein type

History and physical exam
D-dimmer (sensitive)
Duplex venous ultrasound and direct visualization with non-compression of the vein

81

Treatments

Thrombolytics
Avoid weight bearing
Anticoagulants
Support hose
Treat underlying condition (if one)