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23 General Pathology > 8 - Blood Vessels > Flashcards

8 - Blood Vessels Flashcards

1
Q

what are basic constituents of BV

A
  1. endothelial cells
  2. smooth muscle cells
  3. variety of extracellular matrix
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2
Q

what are the concentric layers of arteries and veins (in to out)

A
  1. tunica intima
  2. tunica media
  3. tunica externa
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3
Q

what is a single layer of endothelial cells attached to BM and thin underlying layer of ECM

A

intima

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4
Q

what contains smooth muscle cells and ECM

A

tunia media

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5
Q

what has LCT and can also contain nerve fibers

A

tunica adventitia

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6
Q

what is thicker: arterial walls or their corresponding veins

A

arterial walls

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7
Q

what does atherosclerosis mainly affect

A

elastic and muscular arteries

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8
Q

what does hypertension affect

A

small muscular arteries and arterioles

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9
Q

what does vasculitis affect

A

only vessels of a certain caliper

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10
Q

what causes the blood vessel lumen to decrease

A
  1. narrow artery w/ inflammation
  2. occluded artery with inflammation and scarring
  3. aneurysm
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11
Q

what is responsible for more morbidty and mortality than any other category of human diseases

A

vascular path

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12
Q

vascular pathology mainly involves arteries or veins?

A

arteries (venous disorders are not inconsequential tho)

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13
Q

2 principal mechanisms that underlie vascular disease

A
  1. narrowing (stenosis) or complete obstruction of vessel lumina
  2. weakening of vessel walls
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14
Q

what results in inadequate organ perfusion and can lead to dysfunction or tissue death

A

hypotension

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15
Q

what can cause end organ damage and is one of the major risk factors for atherosclerosis

A

hypertension

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16
Q

what is the BP of patients with clinically significant hypertension

A

> 120/>80

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17
Q

what is the cause of hypertension

A

largely unknown so called essential hypertension

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18
Q

what is secondary hypertension

A

10% of patients resulting from underlying renal or adrenal disease, renal artery stenosis, or other identifiable cause

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19
Q

Multifactorial disorder resulting from the cumulative effects of multiple genetic polymorphism and interacting environmental factors

A

hypertension

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20
Q

does the prevalence and vulnerability of hypertension complications increase w age

A

yes

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21
Q

is hypertension asymptomatic until late in its course

A

yes

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22
Q

what happens if hypertension is untreated

A
  1. 1/2 die of ischemic heart disease or congestive heart failure
  2. 1/3 die of stroke
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23
Q

what is malignant hypertension

A

5% patients show rapidly risking BP that if left untreated leads to death within 1-2 years

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24
Q

what is the BP of severe pressure elevation

A

> 200/>120

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25
Q

what characterizes malignant hypertension

A
  1. severe pressure elevations
  2. renal failure
  3. retinal hemorrhages and exudates with or w/o papiledema
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26
Q

Essential hypertension accounts for what percent of cases

A

90-95% of all cases

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27
Q

secondary hypertension accounts for what percent of cases

A

5-10% of all cases

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28
Q

what diseases can result in secondary hypertension

A
  1. renal
  2. endocrine
  3. CVD
  4. neurologic
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29
Q

blood pressure is determined by ___ and ___

A

vascular resistance and cardiac output

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30
Q

how is vascular resistance regulated

A

Vascular resistance is regulated at the level of the arterioles, influenced by neural and hormonal outputs

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31
Q

how is cardiac output determined

A

Cardiac output is determined by heart rate and stroke volume, which is strongly influenced by blood volume; blood volume in turn is regulated mainly by sodium excretion and absorption

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32
Q

what is a major regulator of BP and is secreted by kidneys in response to decreased BP in afferent arterioles

A

renin

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33
Q

renin pathway

A

renin -> cleaves angiotensinogen to angiotensin I -> produces angiotensin II -> regulates BP by increasing vascular SMC tone and by increasing adrenal aldosterone secretion -> increase renal sodium resorption

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34
Q

vascular pathology in hypertension:

[accelerates or decelerates] atherogenesis
causes [formative or degenerative] changes in walls of large and medium arteries that can lead to both aortic dissection and cerebrovascular hemorrhage

A

accelerates; degenerative

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35
Q

what is the hardening of arteries, generic term for arterial wall thickening and loss of elasticity

A

arteriosclerosis

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36
Q

what are the general patterns of arteriosclerosis? what does it affect?

A
  1. arteriolosclerosis - small vessels
  2. Monckeberg medial sclerosis - middle layer
  3. fibromuscular intimal hyperplasia - inner layer
  4. atherosclerosis - medium and large vessels
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37
Q

Arterioles show homogenous, pink hyaline thickening with associated luminal narrowing; these changes reflect both plasma protein leakage across injured epithelial cells and increased smooth muscle cell matrix synthesis in response to the chronic hemodynamics pressure of HT. what is this

A

hyaline arterioslcerosis

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38
Q

vessels of older patients frequently exhibit hyaline AS, it is most generalized and severe in patients with ___ and ___

A

hypertension and DM

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39
Q

hyperplastic AS occurs in what

A

severe HT

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40
Q

what has vessels that exhibit concentric laminated (“onion skin”) thickening of walls with luminal narrowing. Laminations consist of SM cells with thickened, reduplicated BM

A

hyperplastic arteriolosclerosis

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41
Q

when is hyperplastic AS accompanied by fibrinoid deposits and vessel wall necrosis

A

malignant HT

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42
Q

what is characterized by calcifications of medial walls of MUSCULAR arteries

A

monckeberg medial sclerosis

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43
Q

who is affected by monkceberg medial sclerosis

A

adults > 50

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44
Q

do calcifications enroach vessel luman in Monckebeg Medial Sclerosis? are they clinically significant?

A

do not encroach and are not clinically significant

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45
Q

what is this:

  1. Occurs in muscular arteries larger than arterioles
  2. It is driven by inflammation or by mechanical injury
  3. Can be considered a healing process
A

fibromuscular intimal hyperplasia

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46
Q

what is an intimal based lesion composed of fibrous capsule and an atheromatous core

A

atherosclerosis

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47
Q

what are present in the plaque of atherosclerosis

A

The constituents of the plaque include smooth muscle
cells, extracellular matrix, inflammatory cells,
calcifications, lipids, and necrotic debris

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48
Q

in atherosclerosis, do plaques develop and grow quickly or slowly

A

slowly over decades

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49
Q

atherosclerosis is driven by interplay of __ and ___

A

vessel wall injury and inflammation

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50
Q

what can produce symptoms related to chronic ischemia by narrowing vessel lumsn

A

stable plaques

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51
Q

what can produce fatal ischemic complications related to acute plaque rupture and embolism

A

unstable plaques

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52
Q

atherosclerosis underlies the pathogenesis of what diseases

A
  1. coronary
  2. cerebral
  3. preipheral vascular disease
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53
Q

nonmodifiable risk factors for atheroscelrosis

A
  1. genetic abnormalities
  2. family history
  3. increasing age
  4. male gender
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54
Q

what are modifiable risks for atherosclerosis

A
  1. hyperlipidemia
  2. hypertension
  3. cigarette smoking
  4. diabetes
  5. inflammation
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55
Q

major consequences of atherosclerotic diseases

A
  1. myocardial infarction (heart attack)
  2. cerebral infarction (stroke)
  3. aortic aneurysm
  4. peripheral vascular disease (gangrene of legs)
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56
Q

what are the major targets of atherosclerotic diseases

A
  1. large ELASTIC arteries (aorta, carotid, and iliac arteries)
  2. large-and medium-sized MUSCULAR arteries (coronary and popliteal arteries)
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57
Q

atherosclerotic plaques progress from ___ to a ___ leading to either erosion or rupture of thin-capped fibroatheroma

A

fatty streak to classic atheroma

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58
Q

how do atheromas cycle

A

between healing, thrombosis and finally to blockage of the concerned artery

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59
Q

T/F: there could be multiple cycles of healing and rupture of atherosclerotic plaques before an artery is blocked

A

TRUE

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60
Q

what do atherosclerotic plaque consist of

A

extracellular lipid particles, foam cells, and debris that have accumulated in the intima of arterial wall and form a lipid or necrotic core

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61
Q

what is the core of atherosclerotic plaque surrounded by? covered by?

A

surrounded by layer of collagen-rich matrix and smooth muscle cells

covered by endothelial cells called fibrous cap

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62
Q

what is a localized abnormal dilation of BV or heart that may be congenital or acquired

A

aneurysm

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63
Q

what aneurysm involves all layers of intact arterial wall of thinned ventricular wall of the heart

A

true aneurysm

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64
Q

what aneurysm is a defect in the vascular wall leading to extravascular hematoma that freely communicates with intravascular space “pulsating hematoma”

A

false aneurysm (pseudoaneurysm)

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65
Q

what are the 2 most important causes of aortic aneurysms

A
  1. atherosclerosis
  2. hypertension
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66
Q

who has aneurysms

A

men over 50 and smokers

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67
Q

aneurysm complicates are related to what

A
  1. rupture
  2. thrombosis
  3. embolism
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68
Q

what occurs when blood separates the laminar planes of the media to form a blood-filled channel within the aortic

A

dissections

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69
Q

aortic dissections are generally associated with what

A

aortic dilation

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70
Q

it can be disatrous if dissections rupture thru what

A

thru adventitia and hemorrhage into adjacent spaces

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71
Q

who has aortic dissections

A
  1. men aged 40-60 years with antecedent hypertension (MOSTLY)
  2. younger patients with syndromic diseaes affecting aorta (Marfan syndrome)
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72
Q

an aortic dissection may lead to ___ ; such a massive amount of hemorrhage can lead to cardiac tamponade

A

hemopericardium when blood dissects thru media proximally

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73
Q

what is a general term for vessel wall inflammation and is frequently associated w/ systemic manifestations and organ dysfunction

A

vasculitis

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74
Q

what are 2 pathogenic mechanisms of vasculitis

A
  1. immune-mediated inflammation (sterile)
  2. direct invasion of vessel wall by infectious pathogens (insterile)
75
Q

what is the chronic, classically granulomatous inflammation of large-
to small-sized arteries that principally affect arteries in the head (T-cell immune response)

A

giant cell (temporal) arteritis (GCA)

76
Q

what is the most common form of vasuclitis among elderly adults

A

GCA (temporal)

77
Q

what vessels are involved in GCA

A

opthalmic, vertebral, and aorta

78
Q

are temporal arteries vulnerable in GCA?

A

no but name is in disorder because they are the most readily biopsied in making the diagnosis

79
Q

symptoms of GCA

A
  1. vague and constructional
  2. facial pain and headache
  3. most intense along course of superficial temporal artery which is painful to palpation
80
Q

GCA diagnosis is based on what

A

biopsy and histologic confirmation

81
Q

is GCA extremely focal within an artery

A

YES!

82
Q

adequate biopsy of GCA requires what

A

1 cm segment

83
Q

treatment of GCA

A

corticosteroids and anti-TNF therapies

84
Q

what vasculitis can cause lingual necrosis

A

GCA (temporal)

85
Q

what is takayasu arteritis also called

A

pulseless disease

86
Q

what is granulomatous vasculitis of large- and medium- sized arteries characterized principally by ocular disturbances and marked weakness of pulses in the upper extremities

A

Takayasu arteritis (pulseless disease)

87
Q

what is the transmural fibrous thickneing of aorta-particularly of the aortic arch and great vessels resulting in severe luminal narrowing

A

Takayasu arteritis (pulseless disease)

88
Q

what age of ppl with takayasu arteritis

A

under age 50

89
Q

what shares the same clinical and histologic features of GCA except for age?

A

Takayasu Arteritis

90
Q

what is the likely etiology of takayasu arteritis

A

autoimmune

91
Q

what disease:

Initial symptoms are usually nonspecific (fatigue, weight-loss, fever); with progression, vascular features dominate (reduced BP and weaker pulses in the upper extremities, ocular disturbances and total blindness, and neurological deficits

A

takayasu arteritis

92
Q

takayasu arteritis involves what portion of the aorta? what does this leads to?

A

distal aorta leading to claudication of the legs

93
Q

pulmonary artery involvement in takayasu arteritis leads to what

A

pulmonary hypertension

94
Q

renal artery involvement in takayasu leads to what

A

systemic hypertension in 1/2 of patients

95
Q

takayasu arteritis is mainly [lower extremities OR upper and head]

A

lower extremities

96
Q

GCA is mainly [lower extremities OR upper and head]

A

upper and head

97
Q

Systemic vasculitis of small- or medium-sized muscular arteries that typically affect renal and visceral vessels but SPARES PULMONARY CIRCULATION

A

polyarteritis nodosa (PAN)

98
Q

clinical manifestation of PAN result from what

A

ischemia and infarction of affected tissues and organs

99
Q

PAN is often associated with what

A

transmural necrotizing inflammation often w/ superimposed aneurysms and thrombosis

100
Q

what age does PAN o ccur

A

young adults (younger than 50)

101
Q

is PAN requently remitting and episodic with short symptom-free intervals?

A

NO!! PAN is frequently remitting and episodic with LONG symptom free intervals

102
Q

what has a typical presentation of rapidly developing HT due to renal artery involvement, abdominal pain and bloody stools caused by vascular GI lesions, diffuse myalgia, and peripheral neuritis

A

PAN

103
Q

what is the major cause of PAN mortality

A

renal involvementi

104
Q

is untreated PAN fatal

A

yes

105
Q

immunosuppression of PAN can yield remission in ___% cases

A

90%

106
Q

what is an acute, febrile, usually self-limiting illness of infancy and childhood associated w/ large to medium sized vessel arteritis

A

kawasaki disease

107
Q

who gets kawasaki disease

A

80% <4 years old

108
Q

clinical significance of kawasaki disease stems from what

A

invovlement of coronary arteries

109
Q

in ___ people, a variety of infectious agents (mostly viral) have been positioned to trigger kawasaki

A

genetically susceptible people

110
Q

what disease:

Presents with conjunctival and oral erythema; blistering edema of hands and feet; erythema of palms and soles; desquamative rash; cervical LN enlargement

A

Kawasaki disease

111
Q

20% of untreated patients with kawasaki disease develop waht

A

cardiovascular signs and symptoms resulting in asymptomatic coronary arteritis, to giant coronary artery aneurysms

112
Q

aneurysms associated w/ Kawasaki disease are associated with what

A
  1. rupture
  2. thrombosis
  3. MI
  4. sudden death
113
Q

kawasaki disease tx

A

IV immunoglobulin therapy and aspirin

114
Q

granulomatosis with polyangitis was previously called what

A

Wegner granulomatosis

115
Q

granulomatosis w/ polyangitis (GPA) is a necrotizing vasculitis characterized by what

A
  1. acute necrotizing granulomas of upper or lower respiratory tract
  2. necrotizing granulomatous vasculitis of small to medium size vessels (PROMINENT IN LUNGS)
  3. glomerulonephritis
116
Q

who has GPA

A

> males, average age of 40 years

117
Q

what are classic features of GPA

A
  1. bilateral pneumonitis (w/ nodular and cavitary lesions) (MAIN)
  2. chronic sinusitis
  3. mucosal ulceration of nasopharynx
  4. renal disease
  5. (also: rashes, myalgia, articular involvement, neuritis, and fever)
118
Q

if GPA is untreated, what happens

A

disease become rapidly fatal w/ 80% mortality within 1 year

119
Q

what are the most fatal of noninfectious vasculitis

A

PAN and GPA

120
Q

what features strawberry gingivitis

A

GPA

121
Q

what disease:

Characterized by segmental, thrombosing, acute and chronic inflammation of medium- and small-sized arteries, especially the tibial and radial arteries, that often lead to vascular insufficiencies, typically of the extremities

A

thromboangiitis obliterans (Buerger disease)

122
Q

thromboangiitis obliterans is also called what

A

buerger disease

123
Q

who has buerger disease

A

heavy cigarettes smokers usually before the age of 35

people who smoking really like eating burgers

124
Q

early manifestations of buerger disease

A
  1. Raynaud phenomenon
  2. instep foot pain (induced by exercise)
  3. superficial nodular phlebitis
125
Q

Buerger disease has vascular insufficiences that are acocmpanied by what? why?

A

accompanied by severe pain (even at rest) due to neural involvement

126
Q

chronic extremity ulcerations of Buerger disease can progress over time to become what

A

frank gangrene

127
Q

can smoking abstinence in early stage of Buerger disease prevent further attacks

A

yes

128
Q

once Buerger disease is established, will smoking abstience help?

A

no - vascular lesions no longer respond to abstience

129
Q

what causes infectious vasculitis

A

direct invasion of infectious agents (usually bacteria or fungi)

130
Q

what species of bacteria or fungi cause infectious vasculitis

A
  1. Aspergillus
  2. Mucor
131
Q

is infectious vasculitis invasion mostly local or systemic?

A

localized tissue invasion (bacterial pneumonia)

132
Q

less commonly, how does infectious vasculitis spread

A

hematogenous spread of microorganisms during septicemia or embolization from infective endocarditis

133
Q

in what vasculitis are vessels weakend and culminate in mycotic aneurysms or thrombosis and dowards infarction

A

infectious vasculitis

134
Q

what results from exaggerated vasoconstriction of arteries and arterioles in response to cold or emotion

A

raynaud phenomenon

135
Q

what does Raynaund Phenomenon affect

A

extremities (fingers and toes)
occasionally nose, earlobes, or lips

136
Q

restricted blood flow in raynaud’s induces what

A

paroxysmal pallor and cyanosis

137
Q

color changes in raynaud

A

whte -> blue -> red

138
Q

who does primary raynaud phenomenon affect? where?

A

> in young women; occurs symmetrically in the extremities; severity and extend of involvement does not progress

139
Q

what does secondary raynaud phenomenon refer to

A

vascular insufficienes (unkown cause) due to arterial disease cuased by other entities (SLE, scleroderma, Buerger, or atherosclerosis= BASS)

140
Q

is primary or secondary raynaud symetric?

A

primary is symmetric
secondary is asymmetric

141
Q

T/F: 10% of patient with Raynaud Phenomenon manifest an underlying disorder

A

TRUE

142
Q

what is another name for thrombophlebitis

A

phlebothrombosis

143
Q

what are abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure with vessel dilation and incompetence of venous valves

A

varicose veins

144
Q

what veins are commonly involved in varicose veins? why?

A

superficial veins of upper and lower legs bc venous pressure by prolonged dependent pressure

145
Q

who gets varicose veins

A

20% men and 1/3 of women

146
Q

what increases risk of varicose veins

A

obesity

147
Q

incompetence of venous valves due to variicose veins lead to what

A

stasis, congestion, edema, pain and thrombosis

148
Q

what occurs from chronic venous congestion and poor vascular draininage leading to congestion dermatitis and ulceration

A

secondary tissue ischemia (in relation to varicose veins)

149
Q

what are the 3 causes of esophageal varices

A
  1. liver cirrhosis
  2. portal vein thrombosis
  3. hepatic vein thrombosis
150
Q

portal HT leadgs to opening of portosystemic shunt that increases blood flow to what structures? what does this form?

A
  1. gastroesophageal junction -> forms esophageal varices
  2. rectum -> forms hemorhoids
  3. periumbilical veins of abdominal walls -> forms Caput medusa
151
Q

___ are the most important varices since their rupture can lead to massive (fatal) upper GI hemorrhage (aka the most problematic)

A

esophageal varices

152
Q

what relieves the high BP in the portal vein that often occurs in the setting of liver cirrhosis

A

portosystemic shunt

153
Q

___ allows blood flowing into the liver from the portal vein to flow through the ___ directly into the hepatic vein, the vein that drains blood out of the liver to the vena cava and then immediately into the heart.

A

portosystemic shunt; portosystemic shunt

154
Q

are deep vein thrombosis most of the cases?

A

yes! 90%

155
Q

decreased blood flow in the setting of prolonged immobilization is the most common cause of what

A

lower extremity deep vein thrombosis

156
Q

examples of things that cause thrombophlebitis/phlebothrombosis

A

extended bed rest, sitting during long airplane, automobile excusions

157
Q

risk factors of thrombophlebitis and phlebothromobsis

A

pregnangy, oral contraceptive use, obesity, CHF and malignancy

158
Q

diferent between thromblophlebitis and phlebothrombosis

A

thrombophlebitis = clot AND inflammation
phlebothrombosis = clot only NOT inflammation

159
Q

what is a serious complication of DVT resulting from detachment or fragmentation of venous thrombi

A

pulmonary embolism

160
Q

what represents acute inflmmation caused by spread of bacterial infection into lymphatics

A

lymphangitis

161
Q

what is the most common agent of lymphangitis

A

group A beta-hemolytic streptococcu

162
Q

what happens to affected lymphatics in lymphangitis

A

lymphatics are dilated and filled w exudate of neutrophils and monocytes

163
Q

manifestations of lymphangitis

A

Manifested as red, painful subcutaneous streaks with
painful enlargement of the draining lymph nodes
(lymphangitis)

164
Q

what is build-up of fluid in soft tissues when the lymph system is damaged or blocked

A

lymphedema

165
Q

secondary causes of lymphedema

A

Tumors
Surgical procedures
Post radiation fibrosis
Filariasis
Post inflammatory thrombosis or scarring

166
Q

what are benign neoplasmic vascular tumors

A
  1. hemangioma
  2. lymphangioma
167
Q

what are immediate grade neoplasmic vascular tumors

A

kaposi sarcoma

168
Q

what are malignant neoplastic vascular tumors

A

angiosarcoma

169
Q

what is a very common benign tumor composed of blood filled vessels. It is 7% of all benign tumors of infancy and childhood. most are present at birth and initially increase in size but eventually regress spontanteously

A

hemangioma

170
Q

where are hemangioma lesions

A

typically on head and neck and thoracic skin, but can also arise internally

1/3 of internal lesions are in LIVER

171
Q

is malignant transofmration of hemangioma common?

A

NO! rare

172
Q

what is a benign tumor of lymphatic vessels

A

llymphangioma

173
Q

what i a cystic lymphangioma most commonly occuring in head and neck and axilla of an infant

A

cystic hygroma

174
Q

what is the most common intraoral site of lymphangioma

A

tongue

175
Q

what is malignant neoplasm of endothelial cells caused by human herpesvirus 8 (HHV 8; AKA KS herpesvirus)

A

kaposi sarcoma

176
Q

kaposi sarcoma is common in patients with what

A

AIDS

177
Q

4 classical presentations of Kaposi sarcoma

A
  1. classic
  2. endemic (african)
  3. epidemic (AIDS related)
  4. iatrogenic (transplant associated)
178
Q

what are the 3 stages of kaposi sarcoma

A

patches (red-purple macules), raised plaques and eventually nodular lesions

179
Q

what is angiosarcoma? who gets it?

A

Malignant neoplasm of endothelial cells
>older males and females

180
Q

where does angiosarcoma occur

A

Can occur at any site; > in skin, breast, and liver
Can also arise in the setting of lymphedema (in
ipsilateral upper extremity several years after radical
mastectomy for breast Ca

181
Q

what is angiosarcoma induced by

A

radiation

182
Q

is angiosarcoma locally invasive and can readily metastasize

A

yes

183
Q

what is the survival rate of angiosarcoma

A

5 year ~30%

23 General Pathology (24 decks)

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