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Patho 1 > Chap 11- Blood Vessels > Flashcards

Chap 11- Blood Vessels Flashcards

1
Q

what are blood vessels made of?

A
  • endothelial cells
  • smooth muscle cells
  • connective tissue
  • proportion of three are what make vessels different
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2
Q

what are the three layers of blood vessels?

A
  • tunica intima
  • tunica media
  • tunica adventicia
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3
Q

what is the tunica intima?

A
  • inner most layer of vessels
  • single layer of endothelial cells
  • connective tissue
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4
Q

what is the tunica media?

A
  • middle layer of blood vessels
  • made of mostly smooth muscle
  • also has elastic fibers
  • this layer small in veins and large in arteries
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5
Q

what is the tunica adventicia?

A
  • outermost layer of blood vessels
  • loose connective tissue
  • nerve fibers
  • vasa vasorum
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6
Q

what is the vasa vasorum?

A
  • “vessels of vessels”

- tiny vessels on outside of blood vessels

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7
Q

Large arteries

A
  • elastic arteries
  • tunica intima has high elastin fibers
  • allows for pulsating motion
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8
Q

medium sized arteries

A
  • muscular arteries
  • consist of smaller branches of aorta
  • mainly made of smooth muscle
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9
Q

capillaries

A
  • only have endothelial cell lining

- main site of gas exchange

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10
Q

veins

A
  • small, medium, and large veins
  • “blood reservoir”
  • under lower BP than arteries
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11
Q

basal endothelial cells state

A
  • normal BP
  • laminar flow
  • stable growth factors
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12
Q

activated endothelial state

A
  • turbulent flow
  • HTN
  • cytokines
  • cigarette smoke
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13
Q

what is the function of vascular smooth muscle cells?

A
  • migrate and proliferate
  • release cytokines and growth factors
  • synthesize and remodel ECM
  • cause vasoconstriction and vasodilation
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14
Q

what are the types of congenital vascular diseases?

A
  • developmental aneurysms
  • arteriovenous fistulas
  • fibromuscular dysplasia
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15
Q

aneurysm

A
  • weakening of blood vessels, they bulge out

- occurs in cerebral tissue

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16
Q

arteriovenous fistulas

A
  • abnormal connections between artery and vein
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17
Q

fibromuscular dysplasia

A
  • abnormal cellular growth in medium and large muscular arteries
  • results in stenosis and aneurysm
  • blood vessels lose integrity
  • “string of pearls”
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18
Q

blood pressure

A
  • determined by cardiac output and peripheral vascular resistance
  • influenced by genetic and environmental factors
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19
Q

cardiac output

A
  • amount of blood pumped by heart with each beat

- determined by myocardium contractility, HR, and blood volume

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20
Q

peripheral resistance

A
  • diameter of blood vessels

- determine by humoral and neural factors

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21
Q

vasodilators

A
  • NO

- Prostaglandins

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22
Q

vasoconstrictors

A
  • angiotensin II
  • endothelin
  • catecholamines
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23
Q

what are the neural factors that cause vasoconstriction?

A

alpha-adrenergic

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24
Q

what are the neural factors that cause vasodilation?

A

beta-adrenergic

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25
Q

atrial natriuretic peptide (ANP)

A
  • released from heart (atrium) in response to blood volume increase
  • causes vasodilation and sodium excretion
  • result is decrease BP
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26
Q

Renin

A
  • released from kidneys
  • in response to low BP
  • converts angiotensinogen -> angiotensin I -> angiotensin II
  • vasoconstriction and aldosterone production
  • aldosterone production retains Na in body
  • result is increased BP
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27
Q

what is HTN classified as?

A

140/90 mmHg

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28
Q

what can HTN cause?

A
  • significant vessel and end-organ damage

- major risk factor for coronary heart disease, CVA, heart and renal failure, aortic dissection

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29
Q

what is essential HTN?

A
  • 90-95% of all HTN

- idiopathic

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30
Q

what is secondary HTN?

A
  • direct cause of other diseases
  • renal diseases
  • endocrine diseases
  • cardiovascular diseases
  • neurologic stress
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31
Q

what is the most important cause of HTN?

A

sodium levels* and vascular resistence

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32
Q

What are the broad categories of vascular diseases?

A
  • stenosis

- aneurysm

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33
Q

what are the main causes of stenosis?

A
  • progressive narrowing- is a long process

- precipitous narrowing- i.e. blood clot formation, thrombosis

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34
Q

arteriosclerosis

A
  • arterial wall thickening and loss of elasticity, hardening of vessel
  • classified as arteriolosclerosis or atherosclerosis
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35
Q

arteriolosclerosis

A

hardening of small arteries due to ischemia

36
Q

atherosclerosis

A
  • hardening and narrowing of medium and large arteries
  • most frequent and clinically important
  • characterized by elevated intimal-based plaques
37
Q

what makes up an atherosclerotic plaque?

A
  • fibrous cap
  • possibly necrotic center
  • cholesterol crystals
  • foam cells
  • proliferating smooth muscle cells
  • inflammatory cells
  • increased ECM
38
Q

normal vessel response to vascular injury

A
  • endothelial cell loss or dysfunction -> SMC growth -> ECM synthesis and thickening of vascular wall
  • development of neointima
39
Q

what is neointima?

A
  • thickening of intimal layer via SMC recruitment/ proliferation and ECM production
40
Q

non-modifiable atherosclerosis risk factors

A
  • genetics
  • family history**
  • increasing age
  • male
41
Q

modifiable atherosclerosis risk factors

A
  • hyperlipidemia **
  • HTN **
  • cigarette smoking
  • diabetes
  • c-reactive proteins
42
Q

why is hyperlipidemia associated with atherosclerosis?

A

increased LDL and decreased HDL

43
Q

pathogenesis of atherosclerosis

A
  • endothelial injury/dysfunction
  • accumulation of lipoproteins
  • platelet adhesion
  • monocyte adhesion to endothelium
  • lipid accumulation
  • SMC recruitment
  • SMC proliferation and ECM production
44
Q

common cuases of endothelial cell injury

A
  • hemodynamic distrubances

- hyperlipidemia

45
Q

where do plaques characteristically develop?

A

at vascular branch points due to increased turbulent flow

46
Q

lipoproteins

A
  • lipids carried in blood by piggybacking on proteins
  • chylomicrons
  • VLDL
  • LDL
  • HDL
  • proportion of lipid to protein determines different types
47
Q

why is chronic hyperlipidemia bad?

A
  • contributes to atherosclerosis because of chronic inflammation
  • increases local ROS production and causes mitochondrial/membrane damage
  • oxidized lipoproteins are toxic to endothelial cells, SMC, and macrophages
  • sitm release of GF, Cytokinds, chemokines
48
Q

what are vulnerable plaques?

A
  • larger areas of foam cells and lipids
  • thin fibrous caps
  • a lot of inflammatory cells
49
Q

what are stable plaques?

A
  • smaller area of foam cells and lipids
  • thick fibrous cap
  • few inflammatory cells
50
Q

atherosclerotic plaque outcomes

A
  • rupture, ulceration, erosion
  • hemorrhage
  • atheroembolism
  • aneurysm formation
51
Q

pre-clinical phase of atherosclerosis

A
  • usually occurs at young age

- have fatty streak that accumulates

52
Q

clinical phase of atherosclerosis

A
  • vulnerable plaque is formed
  • can lead to aneurysm and rupture
  • occlusion by thrombosis
  • critical stenosis- 90% of diameter occluded
53
Q

thrombus

A

forms over disrupted plaque or contents of atherosclerotic plaque can embolize and obstruct downstream vessels

54
Q

thrombin

A

an activator of smooth muscle cell so it leads to atherosclerotic growth

55
Q

true aneurysm

A

all three vessel layers are weakened

56
Q

false aneurysm

A
  • extravascular hematoma that feely communicates with intravascular space
  • part of vessel wall has been lost
  • loss of endothelial cells
57
Q

dissection

A
  • occurs when blood enters arterial wall (intima layer)
  • blood goes through layers and dissects them
  • different from false aneuyrsm
58
Q

pathogenesis of aneurysm

A
  • inadequate/abnormal CT synthesis
  • excessive collaged degradation by inflammation
  • loss/change in SMC due to medial ischemia
59
Q

types of aortic aneurysm

A
  • abdominal

- thoracic

60
Q

abdominal aortic aneurysm

A
  • assoc with atherosclerosis
  • usually occurs in middle aged male smokers over 50
  • inflammatory infiltrates in atherosclerotic lesions produce proteolytic enzymes -> ECM degradation
  • mostly asymptomatic
61
Q

clinical features of AAA

A
  • rupture into peritoneal cavity with massive hemorrhage
  • occlusion of branch vessel
  • atheroembolism
  • compression of adjacent structures
62
Q

thoracic aortic aneurysm

A
  • associated with HTN
63
Q

clinical features of thoracic aortic aneurysm

A
  • respiratory or feeding difficulty
  • persistent cough
  • pain
  • cardiac abnormalities
  • aortic dissection/ rupture
64
Q

aortic dissection

A
  • dissects media and enters aortic wall
  • form blood filled channel
  • often leads to rupture causing sudden death
  • usually HTN men between 40-60 or young individuals with CT defects
65
Q

aortic dissection pathogenesis

A
  • assoc with HTN
  • HTN causes medial degeneration and loss of SMC/ disorganized matrix
  • etiology unknown
66
Q

aortic dissection clinical features

A
  • excruciating pain that starts in chest and radiates to back
  • sometimes confused with MI
  • death is usually result
67
Q

vasculitis

A
  • blood vessel wall inflammation
  • two types: non-infectious or infectious
  • non-infectious is immune-mediated inflammation
68
Q

immune complex associated vasculitis

A
  • non-infectious
  • antigen- antibody complex deposited in blood vessels, causes inflammation
  • ANCA formed
69
Q

Antineutrophile cytoplasmic anitbodies (ANCA)

A
  • directly activate neutrophils and cause release of proteolytic enzymes and ROS
  • found in serum of pt who have certain vasculitis
70
Q

Giant cell arteritis

A
  • aka temporal arteritis
  • noninfectious vasculitis
  • usually happens in elderly
  • focal granulomatous inflammation of large or medium cranial arteries
  • T cell-mediated immune response
  • facial pain and head ache, flu like symptoms
71
Q

polyarteritis nodosa (PAN)

A
  • systemic disease characterized by inflammation of vessels and necrosis
  • mainly affects kidney
  • pathogenesis associated with Hep B
  • clinical features releated to organ involved
72
Q

Granulomatosis with polyangitis

A
  • GPA, aka wegner granulomatosis
  • characterized by triad
  • T- cell hypersensitivity
  • ANCA present in most patients
73
Q

what is the triad of GPA?

A
  • necrotizing granulomas of upper and/or lower respiratory tract
  • necrotizing or granulomatous vasculitis of vessels in lungs and upper airway
  • glomerulonephritis
74
Q

clinical features of GPA

A
  • men older than 40 more common
  • persistent pneumonitis
  • chronic sinusitis
  • renal disease
75
Q

raynaud phenomenon

A
  • excessive vasoconstriction of fingers and toes
  • can lead to necrosis
  • characterized by red, white, and blue fingers/toes
76
Q

primary raynaud phenomenon

A
  • 3-5% of population
  • usually young women
  • increase in alpha 2 adrenergic response in digits
77
Q

secondary raynaud phenomenon

A
  • vascular insufficiency due to arterial narrowing caused by other conditions
  • pathogensis depends on underlying insult to physiology
78
Q

Varicose veins of extremities

A
  • dilated and twisting of veins due to chronically elevated pressure that weakens vessel walls
  • valves do not function properly
  • stasis, congestion, persistent edma and pain are normal, embolism is rare
79
Q

esophageal varices

A
  • portal vein HTN due to liver cirrhosis causes blood to go back to veins in GI
  • rupture can cause massive GI hemorrhage
80
Q

hemorrhoids

A
  • varicose veins
  • can be result of prolonged pelvic vascular congestion at anorectal junction
  • can ulcerate and bleed or thrombose
81
Q

thrombophlebitis and phlebothrombosis

A
  • venous thrombosis and inflammation
  • usually DVT
  • caused by prolonged immobilization
  • first clinical manifestation is usually a pulmonary embolism
82
Q

Lymphangitis

A
  • spread of accute inflammation into lymphatics
  • usually from acute infection of streptococcus pyogenes
  • can be caused by surgery
  • some anatomic abnormalities can also cause obstruction of lymphatic channels
83
Q

clinical manifestations of lymphangitis

A
  • painful red streaks
  • enlarged lymph nodes
  • neutrophils and macrophages in lymphatics
  • sepsis
84
Q

lymphedema

A
  • lymphatic vessels overwhelmed, extracellular fluid builds up
  • primary or secondary lymphedema
  • chronic edema can result in orange peel skin
85
Q

hemangioma

A
  • benign tumor of vascular endothelial cells
  • usually in kids
  • caused by hypoxia
  • most common one- capillary hemangioma
  • pathogenesis unknown
86
Q

kaposi sarcoma

A
  • associated with AIDS patients
  • vascular neoplasm
  • caused by HHV-8
  • coinfection of HHV-8 and HIV
  • transmitted sexually, oral secretions, and cutaneous contact
  • usually asymptomatic
87
Q

angiosarcoma

A
  • malignant tumor
  • high grade vascular neoplasm
  • usually in liver
  • linked to carcinogenic exposure
  • genetic mutations if Kras2 and TP53 genes
  • aggressive and metastasize anywhere
  • liver failure common

Patho 1 (12 decks)

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