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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
atrial natriuretic peptide (ANP)
- released from heart (atrium) in response to blood volume increase - causes vasodilation and sodium excretion - result is decrease BP
26
Renin
- 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
27
what is HTN classified as?
140/90 mmHg
28
what can HTN cause?
- significant vessel and end-organ damage | - major risk factor for coronary heart disease, CVA, heart and renal failure, aortic dissection
29
what is essential HTN?
- 90-95% of all HTN | - idiopathic
30
what is secondary HTN?
- direct cause of other diseases - renal diseases - endocrine diseases - cardiovascular diseases - neurologic stress
31
what is the most important cause of HTN?
sodium levels* and vascular resistence
32
What are the broad categories of vascular diseases?
- stenosis | - aneurysm
33
what are the main causes of stenosis?
- progressive narrowing- is a long process | - precipitous narrowing- i.e. blood clot formation, thrombosis
34
arteriosclerosis
- arterial wall thickening and loss of elasticity, hardening of vessel - classified as arteriolosclerosis or atherosclerosis
35
arteriolosclerosis
hardening of small arteries due to ischemia
36
atherosclerosis
- hardening and narrowing of medium and large arteries - most frequent and clinically important - characterized by elevated intimal-based plaques
37
what makes up an atherosclerotic plaque?
- fibrous cap - possibly necrotic center - cholesterol crystals - foam cells - proliferating smooth muscle cells - inflammatory cells - increased ECM
38
normal vessel response to vascular injury
- endothelial cell loss or dysfunction -> SMC growth -> ECM synthesis and thickening of vascular wall - development of neointima
39
what is neointima?
- thickening of intimal layer via SMC recruitment/ proliferation and ECM production
40
non-modifiable atherosclerosis risk factors
- genetics - family history** - increasing age - male
41
modifiable atherosclerosis risk factors
- hyperlipidemia ** - HTN ** - cigarette smoking - diabetes - c-reactive proteins
42
why is hyperlipidemia associated with atherosclerosis?
increased LDL and decreased HDL
43
pathogenesis of atherosclerosis
- endothelial injury/dysfunction - accumulation of lipoproteins - platelet adhesion - monocyte adhesion to endothelium - lipid accumulation - SMC recruitment - SMC proliferation and ECM production
44
common cuases of endothelial cell injury
- hemodynamic distrubances | - hyperlipidemia
45
where do plaques characteristically develop?
at vascular branch points due to increased turbulent flow
46
lipoproteins
- lipids carried in blood by piggybacking on proteins - chylomicrons - VLDL - LDL - HDL - proportion of lipid to protein determines different types
47
why is chronic hyperlipidemia bad?
- 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
what are vulnerable plaques?
- larger areas of foam cells and lipids - thin fibrous caps - a lot of inflammatory cells
49
what are stable plaques?
- smaller area of foam cells and lipids - thick fibrous cap - few inflammatory cells
50
atherosclerotic plaque outcomes
- rupture, ulceration, erosion - hemorrhage - atheroembolism - aneurysm formation
51
pre-clinical phase of atherosclerosis
- usually occurs at young age | - have fatty streak that accumulates
52
clinical phase of atherosclerosis
- vulnerable plaque is formed - can lead to aneurysm and rupture - occlusion by thrombosis - critical stenosis- 90% of diameter occluded
53
thrombus
forms over disrupted plaque or contents of atherosclerotic plaque can embolize and obstruct downstream vessels
54
thrombin
an activator of smooth muscle cell so it leads to atherosclerotic growth
55
true aneurysm
all three vessel layers are weakened
56
false aneurysm
- extravascular hematoma that feely communicates with intravascular space - part of vessel wall has been lost - loss of endothelial cells
57
dissection
- occurs when blood enters arterial wall (intima layer) - blood goes through layers and dissects them - different from false aneuyrsm
58
pathogenesis of aneurysm
- inadequate/abnormal CT synthesis - excessive collaged degradation by inflammation - loss/change in SMC due to medial ischemia
59
types of aortic aneurysm
- abdominal | - thoracic
60
abdominal aortic aneurysm
- 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
clinical features of AAA
- rupture into peritoneal cavity with massive hemorrhage - occlusion of branch vessel - atheroembolism - compression of adjacent structures
62
thoracic aortic aneurysm
- associated with HTN
63
clinical features of thoracic aortic aneurysm
- respiratory or feeding difficulty - persistent cough - pain - cardiac abnormalities - aortic dissection/ rupture
64
aortic dissection
- 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
aortic dissection pathogenesis
- assoc with HTN - HTN causes medial degeneration and loss of SMC/ disorganized matrix - etiology unknown
66
aortic dissection clinical features
- excruciating pain that starts in chest and radiates to back - sometimes confused with MI - death is usually result
67
vasculitis
- blood vessel wall inflammation - two types: non-infectious or infectious - non-infectious is immune-mediated inflammation
68
immune complex associated vasculitis
- non-infectious - antigen- antibody complex deposited in blood vessels, causes inflammation - ANCA formed
69
Antineutrophile cytoplasmic anitbodies (ANCA)
- directly activate neutrophils and cause release of proteolytic enzymes and ROS - found in serum of pt who have certain vasculitis
70
Giant cell arteritis
- 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
polyarteritis nodosa (PAN)
- systemic disease characterized by inflammation of vessels and necrosis - mainly affects kidney - pathogenesis associated with Hep B - clinical features releated to organ involved
72
Granulomatosis with polyangitis
- GPA, aka wegner granulomatosis - characterized by triad - T- cell hypersensitivity - ANCA present in most patients
73
what is the triad of GPA?
- necrotizing granulomas of upper and/or lower respiratory tract - necrotizing or granulomatous vasculitis of vessels in lungs and upper airway - glomerulonephritis
74
clinical features of GPA
- men older than 40 more common - persistent pneumonitis - chronic sinusitis - renal disease
75
raynaud phenomenon
- excessive vasoconstriction of fingers and toes - can lead to necrosis - characterized by red, white, and blue fingers/toes
76
primary raynaud phenomenon
- 3-5% of population - usually young women - increase in alpha 2 adrenergic response in digits
77
secondary raynaud phenomenon
- vascular insufficiency due to arterial narrowing caused by other conditions - pathogensis depends on underlying insult to physiology
78
Varicose veins of extremities
- 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
esophageal varices
- portal vein HTN due to liver cirrhosis causes blood to go back to veins in GI - rupture can cause massive GI hemorrhage
80
hemorrhoids
- varicose veins - can be result of prolonged pelvic vascular congestion at anorectal junction - can ulcerate and bleed or thrombose
81
thrombophlebitis and phlebothrombosis
- venous thrombosis and inflammation - usually DVT - caused by prolonged immobilization - first clinical manifestation is usually a pulmonary embolism
82
Lymphangitis
- 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
clinical manifestations of lymphangitis
- painful red streaks - enlarged lymph nodes - neutrophils and macrophages in lymphatics - sepsis
84
lymphedema
- lymphatic vessels overwhelmed, extracellular fluid builds up - primary or secondary lymphedema - chronic edema can result in orange peel skin
85
hemangioma
- benign tumor of vascular endothelial cells - usually in kids - caused by hypoxia - most common one- capillary hemangioma - pathogenesis unknown
86
kaposi sarcoma
- 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
angiosarcoma
- 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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