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CPR Fall 2019 Test 1 > blood vessels > Flashcards

blood vessels Flashcards

1
Q

Aneurysm

A
  • localized abnormal dilation of a blood vessel or the heart

- over time due to underlying defect in the media of the vessel

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2
Q

Arteriovenous malformations (AVM):

A

arteries →veins without intervening capillaries

–Tangle, worm-like vascular channels with prominent pulsatile arteriovenous shunting with high blood flow
-Large or multiple AVMs may lead to high output cardiac failure

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3
Q

Fibromuscular dysplasia:

A

-focal irregular thickening in medium & large muscular arteries (renal, carotid, splanchnic, & vertebral vessels)
–Usually developmental defect, but can arise from trauma etc
-young women

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4
Q

Berry aneurysms

A

Circle of Willis, AD polycystic kidney dz
–“the worst headache I’ve ever had”
-2% of pop
-90% near major branch points of ant circulation
-diameter 10>mm= 50% risk of bleeding per year
-1/3 rupture due to increase intracranial pressure (stool,orgasm)
-25-50% die w/ 1st rupture
-repeat bleeding common

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5
Q

most common cause of subarachnoid hemorrhage

A

is rupture of saccular(berry) aneurysm

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6
Q

where do mycotic aneurysms arise from?

A

(1) embolization of a septic embolus, usually as a complication of infective endocarditis
(2) an extension of an adjacent suppurative process

(3) circulating organisms directly infecting the arterial wall
- rare

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7
Q

what do arteriovenous malformations result from?

A

–can result from rupture of an arterial aneurysm into the adjacent vein
–penetrating injuries that pierce arteries & veins
–or from inflammatory necrosis of adjacent vessels
-can be surgically generated for hemodialysis

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8
Q

what BP is associated with increased risk of atherosclerosis

A

diastolic >80mmHg

systolic>139mmHg

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9
Q

secondary HTN

A

5%

  • underlies renal or adrenal disease
  • Primary aldosteronism, Cushing syndrome, or pheochromacytoma
  • HTN due to renal artery stenosis caused by increased renin
  • bruit heard
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10
Q

essential HTN

A
  • idiopathic
  • 90-95%
  • increases with age and african americans
  • Cardiac hypertrophy & heart failure (hypertensive heart dz, HHD), multi-infarct dementia, & renal failure
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11
Q

what do untreated HTN patients die from?

A

half (½) die of ischemic heart dz (IHD) or congestive heart failure, another third (⅓)die of stroke

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12
Q

malignant HTN

A

5% rapid ↑BP → death within 1-2 years

Systolic > 200mmHg, diastolic > 120mmHg

–Severe HTN, renal failure, retinal hemorrhages & exudates +/-papilledema
–Often superimposed on pre-existing benign HTN

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13
Q

what is blood pressure a function of?

A

cardiac output & peripheral vascular resistance, (genetics and environment)

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14
Q

cardiac output

A
  • heart rate X stroke vol

- influenced by blood volume which is regulated by renal sodium

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15
Q

vascular resistance

A

regulated at level of arterioles;

influenced by neural & hormonal inputs

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16
Q

what are some humoral blood vessel constrictors

A
  • angiotensin II
  • catecholamines
  • thromboxane
  • leukotrienes
  • endothelin
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17
Q

what are some blood vessel dilators

A
  • prostaglandins
  • NO
  • kinins
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18
Q

what are neural blood vessel dilators

A

-beta-adrenergic

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19
Q

what are neural blood vessel constrictors

A

-alpha-adrenergic

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20
Q

what is HTN a risk factor for?

A

Atherosclerosis, CHF, & renal failure

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21
Q

what can HTN cause?

A

cardiac hypertrophy &heart failure (hypertensive heart disease),multi-infarct dementia, aortic dissection (discussed later in this chapter), &renal failure

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22
Q

what does untreated HTN lead to?

A

roughly ½ of HTN patients die of ischemic heart disease (IHD) or congestive heart failure (CHF); and another ⅓ die of stroke

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23
Q

what type of HTN is seen in most patients?

A

Essential HTN 90-95% of cases

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24
Q

what does sustained HTN require?

A

participation by kidney

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25
Q

Hyaline arteriolosclerosis:

A

-↑smooth muscle matrix synthesis
-plasma protein leakage
Homogeneou spink (hyaline) thickening of the vessel wall, →luminal narrowing

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26
Q

nephrosclerosisdue to chronic HTN

A

diffuse impairment of renal blood supply &glomerular scarring

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27
Q

Hyperplastic arteriolosclerosis:

A

-severe hypertension

Smooth muscle cells form concentric lamellations (“onionskinning”)→ luminal narrowing

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28
Q

malignant hypertension,

A
  • laminations
  • fibrinoid deposits
  • necrotizing arteriolitis (esp in kidney)
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29
Q

what are two types of ateriolosclerosis

A

1) hyaline

2) hyperplastic

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30
Q

Mönckeberg medial sclerosis:

A

> 50yo
calcification of muscular arteries,

internal elastic membrane involved,

no narrowing of lumen,

no clinical significance

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31
Q

what is most frequent & clinically important pattern of Atherosclerosis

A

“gruel” & “hardening”,

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32
Q

Atheroma

A

Raised lesion with a soft grumous core of lipid covered by a fibrous cap

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33
Q

what can happen to atherosclerotic plaque?

A

1) obstruct blood flow
2) rupture and lead to thrombosis
3) increase diffusion distance leading to weakening of wall and aneurysm

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34
Q

what is the morphology of atherosclerotic plaque?

A

1) fibrous cap

2) necrotic center with foam cells and cholesterol crystals

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35
Q

what are nonmodifiable risk factors for atherosclerosis

A

1) genetic abnormalities
2) family history
3) increasing age (risk of MI increase 5X between 40 and 60)
4) male gender

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36
Q

what are modifiable risk factors for atherosclerosis

A

1) hyperlipidemia
2) hypertension
3) smoking
4) diabetes (incidence MI 2x higher)
5) inflammation

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37
Q

what are major contributors to atherosclerosis

A

1) age
2) hypercholesterolemia
3) metabolic syndrome

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38
Q

what protein predicts cardiovascular risk?

A

C reactive protein (CRP)

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39
Q

what cytokines are released during atherosclerosis inflammation

A

1) IL-1

- recruits macrophages and T lymphocytes

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40
Q

what GF are implicated in smooth muscle cell proliferation

A

1) PDGF
2) fibroblast growth factor
3) TGF-alpha

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41
Q

what are common site of atheromatous plaques in decreasing order of frequency/severity

A 
Abdominal aorta
Coronary arteries
Popliteal arteries
Internal carotid arteries
Circle of Willis
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42
Q

Complications of atherosclerotic plaques

A

1) rupture and ulceration leading to thrombosis
2) hemorrhage
3) embolism
4) aneurysm

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43
Q

what are consequences of atherosclerosis

A

1) stenosis of lumen= ischemia

2) acute plaque change (thrombus, hemorrhage)

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44
Q

what is critical stenosis of lumen?

A

approx 70% occluded

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45
Q

what can cause fibrous cap on plaque to rupture?

A

things that decrease collagen synthesis

1) changes in BP
2) vasoconstriction

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46
Q

what can emboli be composed of?

A

may be composed of fat droplets, nitrogen bubbles, atherosclerotic debris(cholesterol emboli), tumor fragments, bone marrow, or even foreign bodies

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47
Q

what are 3 clinical complications of atherosclerosis

A

1) aneurysms and hemorrhage
2) occlusion by thrombus
3) critical stenosis

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48
Q

Aneurysm

A

“localized abnormal dilation of a blood vessel, or the heart, that may be congenital or acquired”

49
Q

“True” aneurysm:

A

an intact(but thinned) muscular wall at the site of dilation

50
Q

“False” aneurysm (pseudo-aneurysm):

A

efectthrough the wall of the vessel, or heart, communicatingwith an extravascular hematoma that freely communicates with the intravascular space (“pulsating hematoma”)

51
Q

arterial dissection

A

arises when blood enters a defect in the arterial wall & tunnels between its layers

52
Q

can can a aneurysm occur?

A

Ananeurysm may occur whenever the connective tissue of the vascular wall is weakened

53
Q

what are 3 causes of aneurysm?

A

1) defective vascular wall CT (marfan and fibrillin)
2) net degradation of vascular wall CT (atherosclerosis increases MMP)
3) weakening of vascular wall by ischemia (atherosclerosis (inner media), hypertension (outer media) , and tertiary syphillis

54
Q

Tertiary syphilis

A

ischemia of outer media (thoracic aorta)

55
Q

Obliterative endarteritis

A

(characteristic of late-stage syphilis) shows a predilection for small vessels, including those of the vasa vasorum of the thoracic aorta.
-leads to aneurysmal dilation which sometimes involves aortic valve annulus (aortic valve regurg)

56
Q

Cystic medial degeneration

A

Loss of vascular wall elastic tissue,or ineffective elastin synthesis
-disrupted and disorganized elastin filaments and increased proteoglycans

57
Q

what is Cystic medial degeneration final common pathway of?

A

ischemic medial damage and Marfan syndrome

58
Q

what are the 2 most common causes of aortic aneurysm?

A

1) HTN

2) atherosclerosis

59
Q

what is abdominal aortic aneurysms (AAA) typically due to?

A

atherosclerosis

60
Q

where do AAA typically occur?

A
  • below renal arteries

- often involve common iliac arteries

61
Q

what are AAA most frequent in?

A
  • men
  • smokers
  • 6th decade of life
62
Q

characterizations of AAA

A
  • severe atherosclerosis of aorta
  • covered with mural thrombus
  • may be detected as pulsating mass in abdomen
  • lines of zhan
63
Q

complications of AAA

A
  • Rupture and hemorrhage
  • Occlusion of branching arteries and downstream ischemia
  • Embolism
  • Impingement on another structure
64
Q

what causes thoracic aortic aneurysm?

A

hypertension,or less commonly congenital defect in connective tissue synthesis(Marfan)

65
Q

marfan syndrome

A
  • autosomal dominant
  • defective synthesis of fibrillin
  • abberrant TGF-beta activity weakens elastic tissue
66
Q

clinical presentation of thoracic aortic aneurysm due to

A
  • Impingement
    a) Lower respiratory tree
    b) Esophagus
    c) Recurrent laryngeal nerves
  • Aortic valvular insufficiency
  • Rupture
67
Q

aortic dissection

A

-occurs when blood enters defect in intima and travels through a tissue plane within layers of the aortic media

68
Q

who does aortic dissection occur in?

A

1) hypertensive males 40-60

2) younger patients with CT disorders (marfans)

69
Q

what is primary risk factor for aortic dissection?

A

HTN

70
Q

classic presentation of aortic dissection

A
  • severe chest pain begins ant and radiates to back between scapulae.
  • moves downward as progresses
  • can be confused with AMI
71
Q

what can aortic dissection cause?

A

1) massive hemorrhage
2) cardiac tamponade
3) double barreled aorta->can become chronic dissections

72
Q

where do aortic dissections commonly occur?

A

ascending aorta within 10cm of aortic valve

73
Q

in aortic dissections how does blood enter aortic wall?

A
  • intimal tear

- some degree of cystic medial degeneration

74
Q

type A dissections

A
  • more common
  • associated with higher morbidity and mortality
  • COD=rupture
75
Q

type A dissections treatment

A
  • antihypertensive therapy

- surgical repair

76
Q

vasculitis

A

inflammation of vessles

77
Q

consitutional symptoms of vasculitis

A

-fever, malaise, arthralgia’s, myalgias

78
Q

where does vasculitis occur?

A

more often arterioles, capillaries & venules affected (a few vasculitides tend to affect only one vessel type or location)

79
Q

Non-infectious versus Infectious vasculitis

A

–Immune mediated inflammation vs direct invasion by infectious pathogens

80
Q

how is immune mediated vasculitis treated?

A

immunosuppression

81
Q

Major cause of noninfectious vasculitis

A

immune response (local or systemic)

82
Q

Immune complex mediated vasculitis

A

autoantibody production and formation of immune complezxes

-deposition of ag-ab complexes in vascular walls

83
Q

where is Immune complex mediated vasculitis seen?

A

1) systemic immunologic disease (SLE)
2) drug hypersensitivity
3) secondary exposure to infectious agent (PAN)

84
Q

varicose veins

A

abnormal dilation of veins with valvular incompentence secondary to sustained intraluminal pressure
-embolism from thrombi of superficial LE veins RARE

85
Q

esophageal varices

A

-portal hypertension

86
Q

hemorrhoids

A

Dilation of the venous plexus at the anorectal junction

87
Q

thrombophlebitis

A

venous thrombosis and inflammation

-almost always involved deep veins of legs

88
Q

single most imp factor for developing DVT in LE

A

prolonged activity/immobilization

89
Q

what may increase risk of DVT

A

systemic hypercoagulability

90
Q

what is most serous consequence of DVT

A

pulmonary embolism

91
Q

Migratory thrombophlebitis (Trousseausign):

A
  • patients with cancer= hypercoagulability as paraneoplastic syndrome
  • seen in mucin producing adenocarcinomas
  • adenocarcinomas of lung ovary and pancreas
92
Q

SVC syndrome

A
  • bronchogenic carcinoma, mediastinal lymphoma, or aortic aneurysm
  • marked dilation of the veins of the head, neck, and arms with cyanosis
  • Pulmonary vessels can also be compressed →respiratory distress
93
Q

IVC syndrome

A
  • neoplasms or thrombosis of the hepatic, renal, or lower extremity veins that propagates cephalad
  • Hepatocellular Carcinoma (HCC) and Renal Cell Carcinoma (RCC):occlude IVC into right atrium
  • lower extremity edema, distention of the superficial collateral veins of the lower abdomen
  • renal vein involvement → massive proteinuria
94
Q

Lymphangitis

A

acute inflammation & spread of bacterial infection into lymphatics (group A β-hemolytic streptococci most common agent)
–
Red, painful subcutaneous streaks (inflamed lymphatics) & painful enlargement of draining LN (lymphadenitis)
–
Can progress to cellulitis & focal abscesses; or bacteremia & sepsis

95
Q

Primary Lymphedema:

A

isolated congenital defect, of familial Milroy disease (lymphatic agenesis or hypoplasia)

96
Q

Secondary or obstructive lymphedema:

A

blockage of previously normal lymphatic
•Malignant tumor, surgical procedures (radical mastectomy with axillary node dissection), post-irradiation fibrosis, filariasis, post inflammatory thrombosis or scarring

97
Q

peau d’orange(orange peel):

A

skin overlying breast cancer, draining lymphatics clogged

98
Q

benign tumors

A

-vascular channels filled with RBC, monolayer of normal appearing endothelial cells

99
Q

malignant tumors

A
  • cellular
  • proliferative
  • cytologic atypia
  • don’t form well organized vessels
  • confirmed with CD31 of vWF
100
Q

Ectasia

A

any local dilation of a structure

101
Q

Telangiectasia

A

a permanent dilation of preexisting small vessels (capillaries, venules, and arterioles) that form a discrete redlesion—usually in the skin or mucous membranes. These can be congenital or acquired andare not true neoplasms;some of them are malformations and others are hamartomas

102
Q

nevus flammeus

A

(“birthmark”) most common form of vascular ectasia;light pink to deep purpleflat lesion on the head or neck composed of dilated vessels. Most ultimately regress spontaneously.

103
Q

port wine stain:

A

special form of nevus flammeus. Grow during childhood, thicken the skin surface, and do not fade with time. Such lesions in the distribution of the trigeminal nerve are associated with the Sturge-Weber syndrome

104
Q

Sturge-Weber syndrome (aka:encephalotrigeminal angiomatosis)

A

This uncommon congenital disorder is associated with facial port wine nevi, ipsilateral venous angiomas in the cortical leptomeninges, mental retardation, seizures, hemiplegia, and skull radio-opacities.

105
Q

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease):

A
  • autosomal dominant disorder
  • mutations in genes that encode components of the TGF-β signaling pathway. The telangiectasias are
  • malformations composed of dilated capillaries and veins that are present at birth.
  • skin and oral mucous membranes, as well as in the respiratory, gastrointestinal, and urinary tracts.
  • The lesions can spontaneously
106
Q

what is used for small bore grafts

A
  • saphenous vein (50% patency at 10 yrs)

- internal mammary arteries (90 % patency 10 yrs)

107
Q

Giant cell (temporal) arteritis & aortitis

A
  • branches of carotid artery
  • older patients (>50)
  • females
  • chronic T cell mediated (mostly CD4) inflmation of arteries in head (especially temporal a’s
  • temporal artery may be painful to palpation
  • double vision or involvement of ophthalmic artery may lead to vision loss (50% patients
  • granulomatous inflammation w/multinucleated giant cells
108
Q

Takayasu arteritis

A
  • aortic arch
  • Pulmonary artery (involved in ½the cases),coronary & renal arteries may be involved
  • -younger (<50)
  • Japanese but now global
  • females
  • Ocular disturbances & marked weakening of pulses of the upper extremities (pulseless disease)
  • weak pulse and low BP in UE
  • Granulomatous
109
Q

Polyarteritis nodosa (PAN)

A 
Renal vessels
Heart
Liver
GI Tract 
*pulmonary vessels are spared 
Clascially young adult 
-HTN
-abdominal pain and bloody stools
-myalgias
-peripheral neuritis 
-renal involvement=mortality
-1/3 of patients= chronic hep B 
-immune complex mediated
110
Q

Kawasaki disease

A

-coronary arteries
Infants and small children( 80%≤4years)
-erythema of thec onjunctiva, oral mucosa, palms and soles; desquamative rash
-cervical LN enlargement= mucocutaneous lymph node syndrome
-aneurysms->thrombosis or rupture->MI

TX= IVIg and aspirin

111
Q

Microscopic polyangiitis

A

Necrotizing vasculitis involving arterioles,capillaries and venules

-renal glomeruli and lung capillaries most commonly affected (90%=necrotizing glomerulonephritis)

palpable cuteanous purpura
**fragmented PMN

*granulomas are absent

112
Q

Churg-strauss syndrome (allergic granulomatosis and angiitis)

A

*resembles PAN or microscopic polyangiits w/ addition of granulomas and eosinophils

113
Q

Behcet disease

A 
Classic triad:
•Aphthous ulcers of the oral cavity
•Genital ulcers
•Uveitis (eye inflammation) 
-associated with HLA-B51
Tx= immunosuppression with steroid or TNF antagonist
114
Q

Granulomatosis with polyangiitis (formerly known as Wegener granulomatosis)

A
  • upper and lower resp tract and kidneys
  • -males
  • avg age= 40
  • T cell mediated due to innocuous inhaled microbial or environmental agent
  • PR3-ANCA
  • granulomas w/central necrosis and vasculitis
  • giant cells
115
Q

Thromboangiitis obliterans (Buergerdisease)

A
  • small and medium arteries
  • tibial and renal arteries
  • heavy smokers
  • <35 yrs old
  • israeli, Indian subcontinent and japanese
  • chronic ulcerations can cause gangrene
  • raynaud phenomenon
  • leg pain with exercise
  • instep foot pain with exercise
  • superficial nodular phlebitis
  • severe pain even @ rest
  • extremity ulcerations
  • gangrene
116
Q

Raynaud phenomenon

A

Small arteries and arterioles (fingers and toes) (red, white, blue)

117
Q

primary raynaud

A
  • cold or emotion
  • symmetric
  • young women
  • benign
118
Q

secondary raynaud

A
  • component of another arterial disease (SLE, scleroderma etc)
  • asymmetric
  • worsens with time

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