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Pathology > Chapter 11- Blood Vessels > Flashcards

Chapter 11- Blood Vessels Flashcards

1
Q

What are the two mechanisms of vascular pathology?

A
  1. Stenosis/obstruction

2. Weakening of vessel walls

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2
Q

What are the three layers of blood vessels?

A
  1. Intima
  2. Media
  3. Adventitia
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3
Q

What separates the layers of the vessels?

A

Elastic lamina (internal and external)

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4
Q

What is the vaso vasorum?

A

Arterioles that supply the outer vessel

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5
Q

Where is the vasa vasorum found?

A

In the adventitia

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6
Q

How do arteries and vessels differ?

A

Arteries are made up of well organized, concentric layers of smooth muscle (thicker wall)

Veins are thin walled and contain less organized muscle

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7
Q

What are the three types of arteries?

A
  1. Large/elastic
  2. Medium/muscular
  3. Small and arterioles
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8
Q

What layer do capillaries lack?

A

Media

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9
Q

What vessels are a common place of inflammation?

A

Post capillary venules

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10
Q

What are berry aneurysms?

A

Congenital weaknesses in cerebral vessels

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11
Q

What are arteriovenous fistulas?

A

Abnormal artery-vein communication

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12
Q

What is fibromuscular dysplasia?

A

Focal irregular thickening and attenuation of the arterial wall (alternating thick and thin areas due to hyperplasia and fibrosis)

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13
Q

What is endothelial dysfunction?

A

Altered phenotype that affects vasoreactivity

Induced a thrombogenic surface

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14
Q

What is the vascular wall response to injury?

A
  1. Endothelial cell’s are activates (thrombotic state)
  2. Vascular smooth muscle is recruited to the intima (thickening)
  3. Stenosis due to intimal thickening
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15
Q

What is the stereotyped response to injury in vessel walls?

A

Stenosis

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16
Q

What defines hypertension?

A

Diastolic pressure >89mmHg

Systolic pressure >139mmHg

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17
Q

What is hypertension a risk for?

A

Coronary heart disease

Heart/renal failure

Aortic dissection

Atherosclerosis

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18
Q

What is blood pressure a function of?

A

Cardiac output and peripheral vascular resistance

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19
Q

What is cardiac output a function of?

A

Stroke volume and heart rate

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20
Q

What is peripheral resistance regulated by?

A

Arterioles

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21
Q

How is BP regulated when there is volume overload?

A

ANP secretion causes vasodilation and sodium excretion (water follows)

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22
Q

How does high BP provide positive feedback resulting in maintenance of the hypertension?

A

Stenosis acts on kidney

Renin is released which activates angiotensin II

Vascular contraction, aldosterone secretion and sodium reabsorption increase BP

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23
Q

What is hyaline arteriosclerosis?

A

Reduced vessel flexibility due to hyaline thickening

Luminal thickening, plasma and protein leakage

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24
Q

What is hyperplastic arteriosclerosis?

A

Concentric lamina thickening (onion skin) with luminal narrowing

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25
Q

What are common causes of secondary hypertension?

A

Renovascular hypertension (renal artery stenosis)

Single gene disorders affecting aldosterone metabolism

Conn’s syndrome (primary hyperaldosteronism)

Liddel syndrome (affects proteins that influence sodium reabsorption)

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26
Q

What is arteriosclerosis?

A

Artery hardening- wall thickening and loss of elasticity

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27
Q

What is Monckeberg medical sclerosis?

A

Calcification of muscular artery walls

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28
Q

Does Monckeberg medial sclerosis affect the lumen?

A

No

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29
Q

How does atherosclerosis contribute to arteriosclerosis?

A

Causes hardening

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30
Q

What increases the risk of developing atherosclerosis?

A 
Cholesterol
Smoking 
Hypertension
LDL receptor mutations
Age 
Obesity
Sex
Inflammation
Hyperhomocystinemia
Metabolic syndrome
Factors affecting hemostasis
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31
Q

What is the pathogenesis of atherosclerosis?

A

Endothelial injury causes the accumulation of lipoproteins which triggers inflammation

Monocytes migrate in and engulf the lipids releasing cytokines

GF drives smooth muscle proliferation and ECM deposition producing a plaque

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32
Q

What is an atheromatous plaque?

A

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

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33
Q

How to plaques contribute to vessel pathology?

A

Obstruction

Rupture

Increase diffusion distance from lumen to media

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34
Q

What is the necrotic core of an atheromatous plaque made out of?

A

Lipid, debris from dead cells, foam cells, fibrin, thrombus, plasma proteins

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35
Q

What percentage of occlusion results in critical stenosis?

A

70%

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36
Q

What arteries are most commonly involved in atherosclerosis?

A

Heart, brain, kidneys and lower extremities

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37
Q

What are the two kinds of plaques?

A
  1. Vulnerable- thin fibrous cap (rupture likely)

2. Stable- thick layer of smooth muscle cells

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38
Q

What are aneurysms?

A

Dilation did the heart or blood vessels that involve the entire wall thickness

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39
Q

What are the types of aneurysms?

A
  1. True- saccular (one side) or fusiform (both sides)

2. False- rupture (held together by extravascular tissue)

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40
Q

What conditions can predispose someone to aneurysm?

A

Marfan syndrome

Inflammation (MMPs)

Cystic medial degeneration

Atherosclerosis (ischemia)

Systemic hypertension (ischemia)

Mycotic aneurism

41
Q

Where does abdominal aortic aneurysm occur?

A

Below the renal arteries and above the bifurcation of the aorta

42
Q

What are the characteristics of abdominal aortic aneurysms?

A

Atherosclerosis common

Male smokers over 50

Mural thrombi

Asymptomatic

Risk of rupture related to size

43
Q

Why can abdominal aortic aneurysms affect the renal and superior/inferior mesenteric arteries?

A

Less collateral flow

44
Q

What are the characteristics of thoracic aortic aneurysms?

A

Respiratory difficulties

Difficulty swallowing

Persistent cough

Hypertension/cardiac disease

Rupture

45
Q

What causes syphilitic aneurysms?

A

Aortic valvular incompetence

46
Q

What is an aortic dissection?

A

Tear in the intima, leading to separation of the layers, blood pools and travels within the wall

47
Q

What increases risk of developing aortic dissection?

A

Hypertensive males 40-60

Younger people with connective tissue defects

Trauma

Complications from arterial cannulation

Pregnancy

48
Q

When is aortic dissection uncommon?

A

Atherosclerosis or conditions with medial scarring

49
Q

What are the direction of movement of spontaneous dissections?

A

Retrograde (toward heart)

Anterograde (into great arteries)

50
Q

What can retrograde dissection cause?

A

Coronary compression or hemopericardium with tamponade

51
Q

What is chronic dissection?

A

Vessel re-enters the lumen causing a double barrelled aorta

52
Q

What are the types of spontaneous dissections?

A

A- 10cm from aortic valve

B- distal (usually to subclavian)

53
Q

What type of spontaneous dissection is more common and dangerous?

A

A

54
Q

What is vasculitis?

A

Vessel wall inflammation

55
Q

What are the most common causes of vasculitis?

A

Inflammation and infection

56
Q

How is vasculitis often diagnosed?

A

Blood tests for specific markers

57
Q

What are the types of vasculitis?

A

Noninfectious

Giant cell (temporal) arteritis

Takayasu arteritis

Polyarteritis nodosa

Kawasaki disease

Microscopic polyangitis

Churg-Strauss syndrome

Bechet disease

Granulomatosis with polyangitis

Thromboangitis obliterans

Infectious vasculitis

58
Q

What can noninfectious vasculitis be caused by?

A

Immune complex deposition

Anti-neutrophil cytoplasmic Abs

Anti-endothelial cell Abs

Autoreactive T-cells

59
Q

What population is giant cell arteritis common in?

A

The elderly

60
Q

What is a consequence of giant cell arteritis?

A

Fibrosis with medial scarring and luminal narrowing can cause blindness

61
Q

What are the characteristics of Takayasu arteritis?

A

Granulomatous vasculitis of medium-large arteries

Thickening of aortic arch

Weakening of upper extremity pulse

62
Q

What is Takayasu arteritis known as?

A

Pulseless disease

63
Q

What is Takayasu disease in people over 50?

A

Giant cell arteritis

64
Q

What is polyarteritis nodosa?

A

Segmental transmural necrotizing vasculitis of small-medium arteries in young adults

65
Q

What is Kawasaki disease?

A

Medium-large vessel arteritis

Febrile illness of children

66
Q

What is Kawasaki disease also known as?

A

Mucocutaneous lymph node syndrome

67
Q

What is microscopic polyangitis?

A

Necrotizing vasculitis affecting capillaries, small arterioles and venules

68
Q

What is Churg-Strauss syndrome?

A

Small vessel necrotizing vasculitis with eosinophilic infiltrates

69
Q

What is Bechet disease?

A

Small-medium vessel neutrophilic vasculitis

70
Q

Why is the Bechet disease triad?

A

Recurrent oral apthous ulcers

Genital ulcers

Uveitis

71
Q

What is granulomatosis with polyangitis?

A

Necrotizing vasculitis of small-medium vessels

72
Q

What is granulomatosis with polyangitis also known as?

A

Wegener granulomatosis

73
Q

What is the granulomatosis with polyangitis triad?

A

Upper airway (mostly)

Necrotizing granulomas in upper and respiratory tracts

Glomerulonephritis

74
Q

What is thromboangitis obliterans?

A

Segmental, thrombosing, acute and chronic inflammation of medium-small arteries

75
Q

What is thromboangitis obliterans also known as?

A

Buerger disease

76
Q

What are two disorders of blood vessel hyperreactivity?

A
  1. Raynaud’s phenomenon- exaggerated vasoconstriction of arteries in extremities
  2. Myocardial vessel vasospasm- excessive coronary artery constriction
77
Q

What can cause myocardial vessel vasospasm?

A

Vasoactive mediators

Increased thyroid hormone

AutoAbs

78
Q

What are varicose veins?

A

Superficial lower extremity veins that are dilated and tortuous

79
Q

What are complication of varicose veins?

A

Stasis dermatitis

Ulcerations

Haemorrhoids

80
Q

What causes esophageal varicies?

A

Portal vein hypertension increased flow to gastroesophageal veins

81
Q

What is thrombophlebitis/phlebothrombosis?

A

Venous thrombosis and inflammation

82
Q

What are superior/inferior vena cava syndromes?

A

Neoplasms compressing/invading the respective vessel

83
Q

What are the clinical differences between superior and inferior vena cava syndromes?

A

Superior- dilation of head, neck and arm veins

Inferior- lower extremity edema, distension of superficial collateral veins of lower abdomen

84
Q

What is lymphangitis?

A

Inflammation dues to infection spreading through lymphatics

85
Q

What is lymphedema?

A

Lymphatic obstruction and dilation with increased interstitial fluid

86
Q

What is fluid from lymphatics called?

A

Chylous ascites

Chylothorax

Chylopericardium

87
Q

What are the different types of benign vascular tumours and their characteristics?

A

Vascular ectasias- local vessel dilation

Hemangiomas- pediatric

Lymphangioma

Glomus tumour- from modified smooth muscle cells of the glomus body

Bacillary angiomatosis- proliferation from opportunistic infection

88
Q

What are the forms of vascular ectasias?

A

Nevus flammeus (port wine stain)- dermal vessel dilation

Spider telangiectasias

Hereditary hemorrhagic telangiectasia/Osler-Weber-Rendu disease

89
Q

What are the four forms of hemangiomas?

A
  1. Capillary- skin and mucous membranes
  2. Cavernous- deep structures
  3. Juvenile (“strawberry”)
  4. Pyogenic granuloma- ulcerated polypoid variant of capillary, resemble proud flesh
90
Q

What are the types of lympangiomas?

A
  1. Capillary- blister-like blend

2. Cavernous/cystic hygromas- neck/axilla of children

91
Q

What are the types of borderline tumours?

A
  1. Kaposi sarcoma (HHV8)

2. Hemangioendotheliomas

92
Q

What are the forms of Kaposi sarcoma?

A
  1. Chronic/classic/European
  2. Lymphadenopathic/African/endemic
  3. Transplant associated
  4. AIDS associated
93
Q

What are the types of malignant tumours?

A

Angiosarcoma

Hemangiopericytoma

94
Q

What are pericytes?

A

Contractile cell’s that wrap around endothelial cell’s in capillaries and venules

95
Q

What interventions are possible when vascular pathologies are encountered?

A

Endovascular stenting

Vascular replacement

96
Q

What areas do better with vascular replacement?

A

Large diameter vessels in high flow locations

97
Q

What are complications of stents?

A

Thrombosis and intimal thickening

98
Q

What are the two possible sites for graft harvesting?

A
  1. Saphenous vein

2. Internal mammary artery (better outcome but less to use and atherosclerosis may be apparent)

Pathology (25 decks)

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