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Pathology > 3.1a Blood Vessels 1 > Flashcards

3.1a Blood Vessels 1 Flashcards

0
Q

What are the three types of capillaries based on endothelium? Describe each in terms of basal lamina and endothelial lining.

A
  1. Continuous: (basal lamina) complete, (endothelium) continuous
  2. Discontinuous: incomplete, fenestrated
  3. Fenestrated: complete, fenestrated
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1
Q
  1. Roughly the size of RBCs (7-8 microns)
  2. (+) thin endothelium
  3. (+) thin basement membrane
  4. Conducive for transport of oxygen and nutrients (slow flow + Hugh surface area)
A

Capillaries

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2
Q

(+) thinner muscular wall
(+) poorly defined internal elastic membrane
For soft tissue support

A

Veins

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3
Q
  1. Follow the course of arteries
  2. Smaller
  3. Thinner walls than veins
  4. Play a role in immunity and removing excessive fluid in interstitial space
A

Lymphatics

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4
Q

Enumerate the layers of arteries (3) and describe each one.

A
  1. Intima: endothelial lining + sub endothelial collagen
  2. Media: internal and external elastic lamina + elastic/smooth ms.
  3. Adventitia: vasa vasorum
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5
Q

Types of arteries (3). Give examples.

A
  1. Large/elastic (aorta, carotids)
  2. Medium/muscular/distributing (renal, cerebral, coronary)
  3. Small/arterioles (<2mm in diameter)
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6
Q

Give examples of diseases specific to artery size (2)

A
  1. Atheroma (large)

2. Hyaline atherosclerosis (small end arterioles)

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7
Q

Give examples of diseases that affect a specific arterial layer (3)

A
  1. Atherosclerosis (intima)
  2. Vasculitis (media)
  3. Syphilitic arteritis (adventitia)
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8
Q

Give examples of large elastic arteries (4)

A
  1. Aorta and its main branches
  2. Pulmonary arteries
  3. Common carotids
  4. Iliac artery
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9
Q

This type of arteries are

  1. Rich in elastic fibers
  2. (+) elastic recoil for blood distribution
  3. Prominent internal and external elastic lamina
A

Large/Elastic arteries

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10
Q

Give examples of medium/muscular arteries (3)

A
  1. Other branches of the aorta
  2. Coronary artery
  3. Renal artery
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11
Q

This type of artery are:

  1. Elastic fibers are limited to the external and internal elastic lamina
  2. For vasoconstriction and vasodilation
A

Medium/muscular arteries

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12
Q

This type of artery is:

  1. <20-100 microns
  2. For regulation of arterial BP and distribution of blood flownvia capillaries
  3. Possess important properties of endothelial cells
A

Small arteries

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13
Q
  1. These are the innermost lining of blood vessels

2. Elongated, polygonal cells with pinocytic vesicles

A

Endothelial cells

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14
Q

Function of endothelial cells

A

Induces of prevents thrombosis and inflammation (normal integrity = separation of circulating blood from vessel walls)

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15
Q

Endothelial cells are positive for which markers? (3)

A
  1. Endothelial markers CD31
  2. Hemophilic markers
  3. Weibel-Palade bodies (storage organelle of vWF)
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16
Q
  1. Maintains homeostasis and permeability
  2. Elaboration of pro- and anti- thrombotic factors
  3. ECM production
  4. Modulate blood flow and vascular tone
  5. Regulate inflammation and immunity
  6. Regulate growth of other cells
  7. Oxidize LDL
A

Endothelium

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17
Q

What substances modulate vasoconstriction?

A
  1. Endothelin

2. ACE

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18
Q

What modulates vasodilation?

A
  1. NO/EDRF

2. Prostacyclin

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19
Q

What substances stimulate growth of other cells? (3)

A
  1. PDGF
  2. CSF
  3. FGF
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20
Q

What substances inhibit growth of other cells? (2)

A
  1. Heparin

2. TGF-B

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21
Q

What are the functions of vascular smooth muscle? (5)

A
  1. Moderates vascular tone
  2. Synthesis of collagen, elastin, proteoglycans
  3. Elaboration of GF, inhibitors, cytokines
  4. Migratory and proliferative activity
  5. Contractile function
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22
Q
  1. An acute endothelial cell loss or chronic endothelial injury/dysfunction
  2. Potentially reversible changes in the functional state of endothelial cells that occur in response to environmental stimuli
A

Vascular injury

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23
Q

What are neo-intima?

A

Abnormally functioning endothelial cells formed from irritation of endothelial cells

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24
Q

Give examples of activators of neo-intimal formation (8)

A 
Cytokines
Bacterial products
Lipid
Hemodynamics stress
Viruses
Complements
Hypoxia
Glycosylation end products
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25
Q

What is intimal thickening?

A

Exaggerated endothelial healing resulting from endothelial injury
The formation of neo-intima

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26
Q

What are the steps in intimal thickening? (3)

A
  1. Smooth muscle migration
  2. Intimal cells proliferation
  3. Synthesis of ECM
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27
Q
  1. Hardening of arteries
  2. Fibrosis of the wall leading to hardening
  3. Generic term for: arterial wall thickening, loss of elasticity
A

ARTERIOsclerosis

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28
Q

Types of arteriosclerosis (4)

A
  1. Atherosclerosis
  2. Monckeberg’s medial calcific sclerosis
  3. Hyaline arteriosclerosis
  4. Hyperplastic arteriosclerosis
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29
Q

This is a negative correlate for atherosclerosis.
Is protects by transporting/mobilizing circulating lipid–> remove it from circulation–>put it in storage area (liver or adipose cell)

Hint: good cholesterol

A

HDL

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30
Q

What is the basic lesion on atherosclerosis?

A

Atheroma or fibro-fatty plaque (focal intimal plaque with central core of lipid, fibrous cap) –> eccentric thickening of blood vessel wall

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31
Q

Atherosclerosis affects

  1. ELASTIC arteries (aorta and its main branches, iliac)
  2. Large, medium-sized muscular artery (coronary, renal, popliteal)

EXCEPT

A

Pulmonary artery

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32
Q

What area the (3) components of atherosclerosis?

A
  1. Cells: smooth ms, macrophages, leukocytes
  2. Connective tissue ECM: collagen, elastic fibers, proteoglycans (surrounds and covers lipids)
  3. Intra- and extra cellular lipids: cholesterol, cholesterol esters
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33
Q

Diseases associate with atherosclerosis (4)

A
  1. IHD
  2. Cerebro-vascular accident (CVA): thrombosis, hemorrhage, cerebral embolism
  3. Infarction of extremities: deposits of atheroma–>obstruction to blood flow–>gangrene
  4. Abdominal aortic aneurysm: atheromatous deposits are heaviest in abdominal aorta –>dilatation
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34
Q

Major controllable risk factors of atherosclerosis

A
  1. Hyperlipidemia/diet
  2. Cigarette smoking
  3. HPN: –> production of neo-intima
  4. DM: abnormalities in CHO metabolism
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35
Q

Major non-modifiable risk factors of atherosclerosis (4)

A
  1. Male
  2. Age: increases from 40-60 years old
  3. Genetic abnormalities: familiar hypercholesterolemia
  4. Familial history
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36
Q

What hormone has been found to have a protective mechanism to the development of atherosclerosis due to its antilipid profit?

A

Estrogen

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37
Q

Pathogenesis of atherosclerosis (4)

A
  1. Response to injury hypothesis
    - -> endothelial dysfunction, smooth ms migration (media to intima), proliferation
  2. Organization and growth of thrombi
  3. Monoclonal hypothesis
  4. Infection: herpes virus, CMV, chlamydia pneumoniae have been detected in atherosclerotic plaques
    - ->local immune response –> can contribute to local prothrombotic state
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38
Q

It is the cornerstone of response-to-injury hypothesis due to HPN, irradiation, chemical toxins, immune complex deposition, turbulence flow –> intimal thickening

A

Endothelial injury

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39
Q

What underlies human atherosclerosis?

A

Endothelial dysfunction

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40
Q

Name important causes of endothelial dysfunction (2)

A
  1. Hemodynamic disturbances

2. Hypercholesterolemia

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41
Q

What is the role of lipids in atherosclerosis? (3)

A
  1. Impairs endothelial function: produces superoxide and O2 free radical
  2. Lipid accumulation at site of injury
  3. Oxidized form of LDL
    - -> formation of foam cells (macrophages)
    - -> increase adhesion of monocytes
    - -> increase chemotaxis to circulation of monocytes
    - -> stimulate GF release
    - -> inhibits mobility of macrophages
    - -> endotheliotoxic
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42
Q

What is the role of macrophages in atherosclerosis? (3)

A
  1. Produce IL-1, cytokines, TNF –> adhesion of leukocytes
  2. Secrete toxins (which aid in oxidation of LDL)
  3. Secrete GF –> smooth ms proliferation, production of ECF
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43
Q

What is the role of smooth muscle in atherosclerosis?

A

Intimal cell proliferation and ECMA deposition convert a fatty streak into a mature atheroma

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44
Q

What is the earliest lesion in atherosclerosis?

A

Fatty streak

45
Q

Enumerate the events in atherogenesis (7)

A
  1. Chronic endothelial injury
  2. Isudation of LP into vessel wall
  3. Adhesion/migration of blood and tissue monocytes to intima, transformation to macrophages/foam cells
  4. Platelet adhesion to injured site
  5. Intimal migration of smooth ms
  6. Proliferation of smooth ms, elaboration of ECM
  7. Lipid accumulation
46
Q
  1. Flat yellow spots/streaks of discoloration found on intimal/linear marks on endothelium of aorta
  2. Collection of foam cells (lipid filled macrophages) with T-lymphocytes and extracellular lipids
A

Fatty streak

47
Q
  1. It consists of a central core of lipid covered by whit fibrous cap
  2. Cause local flow disturbances –> increased susceptibility to plaque formation
  3. Predilection to be found in LARGE VESSELS
    Lower abdominal aorta > coronary arteries > popliteal arteries > ICAs > vessels of Circle of Willis
  4. It cannot be seen in pulmonary arteries or arterioles
A

Basic lesion of atherosclerosis

48
Q

What are the (3) components of the basic lesion in atherosclerosis?

A
  1. Cells
  2. Connective tissue ECM
  3. Intra and extracellular lipids
49
Q

What are the (5) complicate lesions found in atherosclerosis?

A
  1. Calcification: secondary calcification of basic lesion
  2. Rupture/ulceration/erosion: induces thrombosis
  3. Hemorrhage into a plaque: rupture of fibrous cap or thin walled vessels in area of neovascularization –> intraplaque hemorrhage
  4. Cholesterol embolization: plaque rupture –> discharge of atherosclerotic debris into bloodstream –> microemboli
  5. Thrombosis: can have complete obstruction and occlusion to blood flow
50
Q

What is Mockenberg’s medial sclerosis?

A

Calcific deposits in the MEDIA of MEDIUM-SIZED muscular arteries (uterine a., testicular a., arteries of intestines)

51
Q
  1. “Disease of aging”
  2. Does not produce obstruction
  3. Prone to develop secondary atherosclerosis
A

Mockenberg’s medial sclerosis

52
Q

Name (2) major complications of Mockenberg’s medial sclerosis due to increased pulse pressure

A
  1. Kidney damage

2. Heart damage

53
Q

Common sites of Mockenberg’s medial sclerosis

A

Extremities (arteries of upper and lower limbs)

54
Q

(+) homogenous pink hyaline thickening

(+) positive PAS stain

It’s risk factors include aging, HPN, DM

(+) luminal narrowing

(+) nephrosclerosis due to chronic HPN –> impairment in renal blood supply –> glomerular scarring

(+) excessive ECM production

A

Hyaline atherosclerosis

55
Q

Hitopathology or hyaline atherosclerosis (2)

A
  1. Narrowing of lumen

2. Thickening and hyalinization of walls

56
Q

Another name for hyaline arteriolonephrosclerosis

A

Benign nephrosclerosis

57
Q

Histopathology of hyaline arteriolonephrosclerosis

A

Narrowing of lumen –> focal ischemia

Thickening and hyalinization of walls

58
Q

Symptoms of hyaline arteriolonephrosclerosis (4)

A
  1. Uremia
  2. Renal insufficiency
  3. Moderate reductions in renal plasma flow with normal/slightly reduced GFR
  4. Mild proteinuria
59
Q

Pathophysiology or hyaline arteriolonephrosclerosis (2)

A
  1. Medial and intimal thickening (response to hemodynamics changes, genetic defects)
  2. Hyaline deposition (caused by extravasation if plasma proteins, increased deposition of basement membrane matrix)
60
Q
  1. Concentric proliferation if the intimal and smooth muscle cells of an arteriole
  2. “Onion-skin arteriole”
  3. Progressive narrowing of lumen
A

Hyperplastic arteriosclerosis

61
Q

Hyperplastic arteriosclerosis causes which diseases? (4)

A

Malignant HPN
Pulmonary HPN
Scleroderma
Hemolytic-uremic syndrome

62
Q

This manifests the ff:

  1. HPN
  2. Fibrinoid deposits
  3. Vessel wall necrosis
  4. Onion-skin lesions
  5. Concentric thickening of walls (media)
  6. Reduplicated thickened basement membrane
  7. Concentric lamination of intima and medial cells forming onion skin appearance
A

Hyperplastic arteriosclerosis

63
Q

Clinically significant HPN (BP)

A

Sustained systolic pressures > 139 mmHg

Sustained diastolic pressures > 89 mmHg

64
Q

Mechanisms of HPN (3)

A
  1. Reduced renal sodium excretion - key initiating event in essential HPN
  2. Vasoconstrictive influences –> may cause thickening and rigidity of vessels
  3. Environmental factors
65
Q

Pathogens is of renovascular HPN (5 steps)

A

Renal stenosis – decreased renal outflow – induce renin secretion – increase sodium reabsorption

66
Q

What is one of the most common causes of secondary HPN?

A

Primary aldosteronism

67
Q
  1. Systolic pressure >200 mmHg
  2. Diastolic pressure >120 mmHg
  3. Renal failure
  4. Retinal hemorrhages
A

Malignant HPN/Hypertensive Emergency

68
Q

What causes of secondary hypertension?

A

Renal diseases

69
Q

BP = (____)(____)

A

BP = (CO)(PVR)

70
Q

CO is dependent on what?

A

Blood volume, which is influenced by sodium homeostasis and aldosterone

71
Q

PVR is determined at the level of what?

A

Arterioles

72
Q

Name (2) vasoconstrictors

A
  1. Angiotensin II

2. Catecholamines

73
Q

What increases the reabsorption of sodium and water if distal tubular and collecting ducts via aldosterone to increase BP?

A

Angiotensin II

74
Q

Name (2) cardiac factors in HPN

A
  1. Rate

2. Contraction

75
Q

Name (2) neural factors in HPN

A
  1. Alpha adrenergic (constriction)

2. Beta adrenergic (dilation)

76
Q

Name (2) vasodilators in HPN

A
  1. AntiHPN substances: PG and NO

2. Kinins: bradykinin and kallidin

77
Q

HPN usually affects which organs?

A

End organs

78
Q

Name complications of HPN (3)

A
  1. Ischemia: MI, CNS, Kidney, eye are damaged
  2. Aneurysm/Rupture: weakening of blood vessels –> dilatation, CNS, aorta
  3. Myocardial hypertrophy: LVH, Cardiac failure
79
Q

Which organs are affected by HPN (5)

A
  1. Blood vessels
  2. Heart
  3. Kidneys
  4. Eyes
  5. Brain
80
Q

Effects of HPN on blood vessels (4)

A
  1. Atherosclerosis
  2. Arteriosclerosis
  3. Thickened with concentric onion skinning
  4. Narrowing of lumen
81
Q

Effects of HPN on heart (3)

A
  1. LVH
  2. Ischemia
  3. Infarction
82
Q

Effects of HPN on kidney (3)

A
  1. Ischemia
  2. Infarction
  3. Nephrosclerosis
83
Q

Effects of HPN on eyes (1)

A

Retinopathy

84
Q

Effects of HPN on brain (3)

A
  1. Ischemia
  2. Infarction
  3. Hemorrhages
85
Q

What are the special features of cerebral blood vessels? (3)

A
  1. Thin walled
  2. End arteries
  3. Congenital aneurysms
86
Q

Gross manifestation of kidney damage secondary to benign nephrosclerosis

A

Leathery granularity due to minute scarring

87
Q

Gross manifestation of retinal retinopathy

A

Cotton wool flecks

88
Q

These are localized abnormal dilatation of the blood vessels or heart

A

Aneurysms

89
Q

What is a true aneurysm?

A
  1. Blood vessel is intact and attenuated or

2. Ventricular wall of heart is thin

90
Q

Give examples of true aneurysms (3)

A
  1. Atherosclerotic aneurysm
  2. Syphilitic aneurysm
  3. Congenital aneurysm
91
Q

Want is a false aneurysm?

A

A defect in the vascular wall which causes extravascular hematoma that communicates with intravascular space

92
Q

Give examples of false aneurysms (2)

A
  1. Ventricular rupture

2. Leak at suture of vascular graft

93
Q

What are the types of aneurysms according to shape? (3)

A
  1. Saccular aneurysm
  2. Fusiform aneurysm
  3. Berry aneurysm
94
Q

Type of aneurysm that is:

  1. Spherical OUTPOUCHING involving one portion of the vessel wall
  2. 5-20cm in diameter
  3. Would most likely contain a thrombus
A

Saccular aneurysm

95
Q

Type of aneurysm that is:

  1. Sausage-like, elongated
  2. Involves diffuse, circumferential DILATATION of a long vascular segment
  3. Usually affects LARGE arteries (aortic arch, abdominal aorta, iliac arteries)
A

Fusiform aneurysm

96
Q

Type of aneurysm that is:

1. Small, spherical, congenital RUPTURE which can cause subarachnoid hemorrhage

A

Berry aneurysm

97
Q

What are the types of aneurysms according to etiology? (4)

A
  1. Atherosclerotic aneurysm
  2. Syphilitic aneurysm
  3. My optic aneurysm
  4. Dissing aneurysm/dissection
98
Q

Type of aneurysm that weakens the vascular wall

A

Atherosclerotic aneurysm

99
Q

Type of aneurysm that

  1. Occurs in thoracic aorta or aortic arch
  2. Involves vasa vasorum –> weakening of aorta because of complications from tertiary syphilis
A

Syphilitic aneurysm

100
Q

Type of aneurysm that is caused by infection of blood vessels

A

Mycotic aneurysm

101
Q

Type of aneurysm where blood vessel walls are separated by columns of blood

A

Dissecting aneurysm

102
Q

Pathogenesis of aneurysms (4)

A
  1. Arteriosclerosis –> destruction of media –> focal weakening of wall –> dilatation
  2. Familial cases, genetic defects in connective tissue
    (Intrinsic quality of vascular wall CT is poor)
  3. Inflammatory infiltrates (disrupts balance of collagen degradation and synthesis)
  4. Loss of smooth muscle cells
103
Q

What are the complications of abdominal aortic aneurysm? (5)

A
  1. Rupture
  2. Occlusion
  3. Embolism
  4. Impingement of adjacent vessels
  5. Pseudo-tumor
104
Q

Gross feature of abdominal aortic aneurysm

A

Fusiform dilatation

105
Q

Histologic feature of abdominal aortic aneurysm (2)

A
  1. Severe complicated atherosclerosis

2. Adventitia is fibrotic with chronic inflammation

106
Q

A ruptured aneurysm has a high mortality due to?

A

Hypovolemic shock

107
Q

It is a complication of tertiary syphilis with obliteration endarteritis of vasa vasorum

A

Syphilitic aneurysm

108
Q

Pathological features of syphilitic aneurysm (6)

A
  1. Involves aortic arch
  2. Tree-barking of aorta
  3. Superimposed atherosclerosis
  4. Secondary AV regurgitation and dilatation
  5. LV hypertrophy
  6. Obliterative endarteritis of vasa vasorum
109
Q

Is is the:

  1. Splitting of MEDIAL layer of aorta by dissecting hematoma
  2. Not associated with marked dilatation
  3. HPN is usually the antecedent
  4. Associated with Marfan syndrome or arterial cannulation
A

Aortic dissecting

110
Q

Pathophysiology of aortic dissection (4)

A
  1. HPN (can enhance hematoma progression)
  2. Intimal tear (often precedes dissection)
  3. Cystic medial degeneration (CMD)
  4. Exact trigger is unknown
111
Q

Morphology of aortic dissection (4)

A
  1. Intimal tear
  2. Medial cleavage
  3. Double-barreled aorta
  4. Cystic medial degeneration or necrosis

Pathology (10 decks)

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