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ICM-Cardio > vascular disease: disease of aorta, PVD > Flashcards

vascular disease: disease of aorta, PVD Flashcards

1
Q

normal artery from the inside out

A
  • 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
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2
Q

vascular lumen

A

channel for fluid transport

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3
Q

intima

A

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

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4
Q

media lamina

A

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

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5
Q

adventitia

A

supportive fibrous tissue with nerves and blood vessels (vasovasorum)

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6
Q

Vasa vasorum

A

-in large and medium arteries

coursing into the outer one half to two thirds of media

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7
Q

large and medium arteries have

A
  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
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8
Q

veins

A
  • low pressure systems

- have thin walls

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9
Q

large veins have

A

intimal
media
adventitial layers

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10
Q

medium sized veins

A

less adventitia

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11
Q

venules have

A

progressively less adventitia

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12
Q

post capillary venules

A

less adventitia (the least)

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13
Q

capillary compensition

A 
endothelial cell
encircling pericytes, but NO MEDIA
thin walled
slow flow
function gas exchange (insufficient over great distances)
nutrient exchange
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14
Q

highest density of capillaries

A

metabolically highly active tissues (like myocardium)

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15
Q

artery function

A

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

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16
Q

all arterial diseases result from?

A

altered architecture

altered function

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17
Q

atherosclerosis

A

affects elastic and muscular arteries

-in large and medium sized arteries

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18
Q

HTN

A

affects small muscular arteries and arterioles

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19
Q

vasculitides

A

affects vessels of variable

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20
Q

tunica intima

A
  • endothelial linning and connective tissue

- beneath connective tissue-> internal elastic lamina

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21
Q

tunica media

A

circumferential smooth muscle

external elastic lamina

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22
Q

tunica adventitia

A

connective tissue fibers

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23
Q

aortic dissection

A
  • 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
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24
Q

aortic aneurysm

A
  • 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
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25
Q

LaPlace’s law

A

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
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26
Q

common causes of aortic aneurysms

A 
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)
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27
Q

diagnosis of aortic aneurysm

A
  • radiograph: widened mediastinum, shift of midline structures (like trachea)
  • echo or TEE good for ascending or descending (not in arch)
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28
Q

presentation of ascending thoracic aortic aneurysm

A
  • discovered accidentally
  • usually asymptomatic
  • occasional chest pain
  • compression of local structures
  • AR
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29
Q

complications from ascending thoracic aortic aneurysm

A
  1. chronic AR:
    - LV dysfunction
    - CHF
  2. dissection
  3. . rupture
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30
Q

therapy of ascending thoracic aortic aneurysm

A

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

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31
Q

descending thoracic aortic aneurysms

A

usually associated with atherosclerosis
chronic aortic dissection
surgery

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32
Q

abdominal aortic aneurysm

A
  • manifestation of atherosclerosis

- high risk of concurrent CAD

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33
Q

risk factors for abdominal aortic aneurysm

A

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

34
Q

clinical manifestations of abdominal aortic aneurysm

A

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

35
Q

complications abdominal aortic aneurysm

A

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
Q

aortic dissection risk factors

A
  • 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
Q

pathophysiology of aortic dissection

A
  • intimal tear leads to penetration of blood within the aortic wall
  • false lumen forms separating layers of aortic wall
38
Q

aortic dissection: De Bakey, type I

A

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

39
Q

aortic dissection: De Bakey, type II

A

originates in and as confident to the ascending aorta

40
Q

aortic dissection: De Bakey, type III

A

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

41
Q

aortic dissection: standford type A

A

always involves the proximal aorta

-all dissection involving the ascending aorta

42
Q

aortic dissection: standford type B

A

NO proximal involvement at all

  • descending aorta dissection only
  • all dissection not involving the ascending aorta
43
Q

Type A common presenting symptoms

A
  • 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
Q

complications of type A dissection

A
  • aortic rupture
  • cerebral ischemia
  • pericardial tamponade
  • acute aortic regurg. leading to pulmonary edema and cardiogenic shock
  • coronary insufficiency
45
Q

complications from acute type A dissection

A
  • 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
Q

clinical presentation: aortic dissection

A
  • 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
Q

physical exam of aortic dissection

A
  • unequal upper extremity BP’s
  • tachycardia
  • pulse deficits
  • focal neurologic deficits
  • aortic insufficiency (acute)
  • evidence of pericardial tamponade
48
Q

imaging for aortic dissection

A

CT scanning
TEE
MRI
aortography

49
Q

therapy for acute aortic dissection

A 
establish beta-blockers
CCB
vasodilators
adequate analgesia
low threshold for intubation if unstable
50
Q

type A dissection initial treatment

A
  • 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
Q

type B dissection: unstable

A
  • impending rupture
  • propagation with compromise of downstream vasculature
  • unrelieved pain
  • treatment: same as Type A
52
Q

type B dissection: is stable and uncomplicated

A
  • control blood pressure and cardiac contractility
  • beta blockers
  • ACE-I, ARB’s, CCB
  • monitor every 6-12 months
53
Q

acute aortic dissection therapy for Type B

A

beta blockers
surgery
IRAD

54
Q

chronic aortic occlusion

A

-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
Q

acute aortic occlusion

A

-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
Q

aortitis

A
  • can cause or aneurysms and dissection

- complications depend on locations and severity of underlying mechanism of the disease process

57
Q

rheumatic causes of aortitis

A

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

58
Q

takayasu’s arteritis

A
  • young asian women
  • inflammatory process
  • often the arch and ascending aorta
  • can cause obstruction
  • acute and chronic phase
  • no therapy
59
Q

tertiary syphilus

A
  • 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
Q

giant cell arteritis

A
  • 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
Q

Buerger’s disease

A
  • young male smoker

- no TX except stop smoking

62
Q

aortic coarctation

A
  • 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
Q

clinical manifestations of aortic coarctation

A 
asymptomatic 
HTN
arm, leg, pulse differential
leg fatigue
bicuspid aortic valve 
cerebral hemorrhage
64
Q

diagnosis of aortic coarctation

A 
physical exam
ECG with evidence of LVH
chest radiograph
echo
cardiac MRI
contrast aortography with invasive hemodynamics
65
Q

TX aortic coarctation

A

surgery

percutaneous stenting

66
Q

acute PAD results from

A

Embolic sources:

  • atrial fib.
  • MI
  • ventricular aneurysm
  • cardiomyopathy
  • infectious sources
  • prosthetic heart valves
  • atrial myxoma
67
Q

acute PAD is

A

a medical emergency

68
Q

important to identify PAD

A

-surrogate marker for coronary artery disease

69
Q

chronic PAD of LE

A
  • occlusive arterial disease
  • atherosclerosis
  • risks rise from AODM, dyslipidemia, HTN, smokers
  • high association with cerebral vascular and heart disease
70
Q

chronic PAD sites

A
  • 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
Q

hallmarks of LE PAD disease

A
  • claudication

- reproducible sx-> effort, location, examination

72
Q

spectrum of LE arterial disease

A 
asymptomatic
claudication
rest pain
numbness, tingling, lack sensation
ulceration and gangrene
73
Q

claudication

A
  • 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
Q

signs of chronic PAD

A
  • 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
Q

ankle to brachial index (ABI)

A
  • Pros: quick stethoscope and BP cuff

- Cons: gives no info on disease level (ABI artificially elevated in calcified vessels in diabetes)

76
Q

how to ABI

A
  • 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
Q

management of PAD therapy

A
  • 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
Q

Consequences of DVT

A

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

79
Q

Consequences of SVT

A 
Heaviness of limb
Pain
Severe swelling
Ulcerations
Cosmetic dis figuration
80
Q

Diagnosis of PVD: deep vein type

A

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

81
Q

Treatments

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

ICM-Cardio (21 decks)

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