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Pathology II PCC > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

Vascular disease most commonly involves what vessels?

A

arteries

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2
Q

Which type of narrowing/obstruction of the lumen of vessels with vascular disease is gradual? which is rapid?

A

gradual: atherosclerosis rapid: thromboembolism

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3
Q

what are the two general types of vascular disease?

A
  1. narrowing/obstruction of the lumen 2. weakening of vessel wall
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4
Q

what is arteriosclerosis?

A

hardening of arteries

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5
Q

what is atherosclerosis a subset of?

A

arteriosclerosis

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6
Q

what is an aneurysm?

A

dilation of a vascular wall

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7
Q

what is a thrombus? a common example of one?

A

BLOOD CLOT in a vessel. Ex: deep vein thrombosis (blood clot in leg, thigh, pelvis)

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8
Q

what is a varicosity?

A

dilation of a vein

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9
Q

What is the layers of the vascular structures throughout the CVS and what theyre made of?

A
  1. tunica intima: endothelia cells, internal elastic lamina 2. tunica media: smooth muscles, external elastic lamina 3. adventitia: CT, nerves, vessels
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10
Q

what supplies blood to the interior vascular wall (aka the tunica intima & inner portion of the tunica media) of the CVS?

A

diffusion of blood from the lumen

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11
Q

what supplies blood to the exterior vascular wall (aka outer tunica media & adventitia) of the CVS?

A

vasa vasorum

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12
Q

what is the vascular pathway?

A

Large elastic arteries –> medium muscular arteries –> small arteries –> arterioles –> capillary beds –> postcapillary venules –> collecting venules –> progressively larger veins

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13
Q

what in the vascular pathway controls blood pressure?

A

arterioles

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14
Q

what are postcapillary venules involved with?

A

edema and leukocyte diapedesis

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15
Q

where in the vascular pathway does gas exchange occur?

A

capillary beds

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16
Q

T/F: All vessels may spread disease?

A

true

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17
Q

which vascular structure is more prone to metastatic invasion?

A

veins

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18
Q

which vascular structures have valves?

A

veins

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19
Q

what vessels drain interstitial fluid?

A

lymphatic vessels

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20
Q

what’s another name for lymph nodes?

A

lymph follicles

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21
Q

what vessels are lined with endothelial cells?

A

ALL vessels

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22
Q

what is the MAIN feature of the lining of vessels? the other features?

A

main: non-thrombogenic interface other: regulates vasoreactivity & cell growth

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23
Q

what is endothelial activation? what’s it caused by?

A

pro-inflammatory response to trauma in vessels. caused by vascular lesions (HTN, diabetes, irradiation, infxn), thrombosis, atherosclerosis

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24
Q

are vascular anomalies typically symptomatic?

A

nope, most relevant during surgery

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25
Q

what are the three types of congenital vascular anomalies?

A
  1. berry aneurysms 2. arteriovenous fistula 3. fibromuscular dysplasia
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26
Q

what is a berry aneurysm?

A

dilation of CEREBRAL vessels rupture –> subdural hemorrhage

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27
Q

what is an arteriovenous fistula?

A

connection of arterial & venous systems, bypass capillaries

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28
Q

what is fibromuscular dysplasia?

A

local thickening of medium/lg artery walls –>ischemia non-atherosclerotic, non-inflammatory MC in young adult females

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29
Q

what population is fibromuscular dysplasia MC in?

A

young adult females

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30
Q

what is hypotension and its side effects?

A

<90/60 decreased perfusion, dysfunction

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31
Q

what is hypertension and its side effects?

A

> or equal to 140/80 damages vessels/organs atherosclerosis, hypertensive retinopathy

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32
Q

what determines blood pressure regulation?

A
  1. cardiac output (HR + stroke volume) 2. vascular resistance
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33
Q

what controls vascular tone & blood volume? (3 things)

A
  1. kidneys: sodium, renin-angiotensin system 2. adrenals: aldosterone 3. Heart: atrial natriuretic peptide (associated w stretching)
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34
Q

what happens, physiologically, when blood pressure increases?

A

stretches heart –> ANP is released 1. reduced sodium resorption 2. vasodilation

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35
Q

what happens, physiologically, when blood pressure decreases?

A

renin-angiotensin system kicks in 1. sodium resorption 2. vasoconstriction

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36
Q

what are 3 medicines used to control blood pressure?

A

ACE (angiotensin-converting enzyme) inhibitors, Angiotensin II receptor blockers diuretics (water pills)

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37
Q

what is the outlook for untreated patients with HTN?

A

50% die of ischemic heart disease (MI) or congestive heart failure (CHF) 1/3 will die of stroke

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38
Q

what’s the prevalence of HTN in the US?

A

25% of US adults

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39
Q

what is known as the ‘silent killer’?

A

insidious, asymptomatic HTN

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40
Q

T/F: is HTN MC idiopathic?

A

T: 95% idiopathic ‘essential HTN’ Increased vascular resistance, decreased sodium excretion

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41
Q

what race is most likely to be hypertensive?

A

african american

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42
Q

if you decrease your BP, you decrease your risk of what three conditions?

A

ischemic heart disease, congestive heart failure & stroke

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43
Q

what is malignant HTN? its prevalence? its symptoms?

A

>200/120 5% of all HTN cases lethal within 1-2 years causes: renal failure & retinal hemorrhage (papilledema)

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44
Q

what is the non-specific response of vascular walls to injury?

A
  1. endothelial injury/dysfxn 2. smooth muscle cell recruitment 3. growth of smooth muscle cell & ECM 4. irreversible intimal thickening (vessel stenosis)**
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45
Q

what happens to vessel walls with aging?

A

tunica intima thickens and becomes harder rarely clinically significant

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46
Q
A

dystrophic calcification

Mönckenberg medial sclerosis

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47
Q
A

Fibromuscular dysplasia

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48
Q
A

Hyaline arteriolosclerosis

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49
Q
A

Hyperplastic arteriolosclerosis

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50
Q
A

Malignant Hypertension: papilledema

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51
Q
A

polyarteritis nodosa

52
Q
A

strawberry tongue

Kawasaki disease

53
Q
A

Thromboangiitis obliterans
Buerger disease

54
Q

what causes hyaline arteriolosclerosis? what happens to the arteries?

A

benign HTN –> chronic hemodynamic stress

prolonged DM

luminal narrowing

pink hyaline

increased ECM

55
Q

what causes hyperplastic arteriolosclerosis?

A

severe HTN

luminal narrowing –> onionskin appearance

kidneys are most sensitive

56
Q

what is arteriolosclerosis?

A

arteriosclerosis of small arteries/arterioles

possible ischemic injury (HTN, diabetes)

57
Q

what are the different types of arteriosclerosis?

A

arteriolosclerosis

Monckenberg medial sclerosis

atherosclerosis

58
Q

what is Monckenberg medial sclerosis?

A

calcium within arteries –> tunica media

dystrophic calcification

no stenosis

NOT clinically significant

MC > 50 years old = ELDERLY

59
Q

details about atherosclerosis

A

atheroma/plaque

STENOSIS

rupture

thrombosis

Heart, brain, GI, kidneys, legs

60
Q

T/F: 99% of arteriosclerosis is atherosclerosis?

A

True

61
Q
A

dystrophic calcification

Monckenberg medial sclerosis

62
Q

What is the #1 cause of morbidity & mortality in US?

A

Atherosclerosis

CAD, MI, carotid atherosclerosis, stroke

63
Q

what are atheromas? why are they important?

A

associated with atherosclerosis

  1. plaque build up on the inside of artery walls, protrude into the lumen, decrease flow, block diffusion of blood to the middle of the blood vessel
  2. prone to rupture –> massive thrombosis
  3. weakens tunica media –> risk for aneurysm
64
Q

what are foam cells?

A

fat-laden macrophages

associated with atheromatous plaque

65
Q

how much occlusion must occur for there to be coronary artery disease?

A

70% occlusion of coronary arteries

66
Q

what is the ‘response to injury’ hypothesis?

A

chronic endothelial injury –> inflammation –> atherosclerosis

67
Q

at what areas, branch points or straight-aways, is atherosclerosis most likely to occur? why?

A

branch points because there’s more turbulence

68
Q

does dyslipidemia cause atherosclerosis?

A

yes, it is increased cholesterol

69
Q

does atherosclerosis weaken the vessel wall?

A

yes, and if the wall ruptures, it is a thrombosis

70
Q

which plaque is more likely to rupture, one with a thick fibrous cap or thin fibrous cap?

A

thin fibrous cap

71
Q

true aneurysm vs. false aneurysm

A

true: all 3 layers of a vessel, heart wall
false: defect in a vascular wall; extravascular hematoma

72
Q

what is a dissection?

A

blood enters the arterial wall

dissects layers of the vessel

hematoma

73
Q

where do abdominal aortic aneurysm’s occur most commonly?

A

located between the renal & common iliac arteries

74
Q

what part of the vessel degenerates and dies with abdominal aortic aneurysms?

A

ECM and tunica media

75
Q

which gender is more likely to acquire an AAA?

A

men

76
Q

is an AAA a contraindication for adjusting?

A

yes

77
Q

percentages for likelihood of an AAA rupturing depending upon their size:

< or equal to 4 cm :

4-5 cm:

5-6 cm:

>6 cm:

A

< or equal to 4 cm: very rare

4-5 cm: 1% per year

5-6 cm: 11% per year

>6 cm: 25% per year

78
Q

what percent of ruptured AAA are fatal?

A

50%

79
Q

what’s the smallest an AAA can be?

A

5 cm or larger is an AAA

80
Q

what is an aortic dissection?

A

blood splays apart the laminar planes of the media to form a blood-filled channel inside the aortic wall

81
Q

what is the major risk factors for aortic dissections?

A

HTN*** 90% of cases

older males (40-60)

adolescents with CT disorders (marfan, Ehlers-Danlos, Wilson)

82
Q

what unlikely condition helps protect against aortic dissections?

A

atherosclerosis

83
Q

symptoms of an aortic dissection

A

sudden & severe tearing or stabbing pain in the

anterior chest, projects posterior and radiates inferior

84
Q

what is the most common & most severe type of aortic dissection? were does it occur? what is the other type?

A

most common & severe: Type A/proximal/DeBakey I & II– ascending aorta

other type: Type B/distal/DeBakey III – distal to left subclavian A

85
Q

what is vasculitis and in what vessels is it most common?

A

inflammation of the vascular wall, local vessel destruction

MC in small arteries

86
Q
A

Aortic dissection types

First and Second: Type A/Proximal = most common & severe

third: Type B/distal

87
Q

what are the three causes of vasculitis?

A
  1. infectious: vascular invasion = Hep B
  2. non-infectious: immune mediated, ADRs = SLE, penicillin
  3. etc: irradiation, trauma
88
Q

what is the most common vasculitis in older adults (>50 years)?

A

giant cell arteritis/temporal arteritis

89
Q

what arteries are involved in giant cell arteritis?

A
  1. temporal artery

2. ophthalmic artery: 50%, involves EYES (diplopia & permanent blindness)

  1. vertebral artery & aorta
90
Q

what kind of inflammation is found with giant cell arteritis/temporal arteritis?

A

granulomatous inflammation

91
Q

what is hypothesized to cause giant cell arteritis, polyarteritis nodosa and takayasu arteritis?

A

autoimmune hypothesis

92
Q

granulomatous vasculitis is aka

A

takayasu arteritis

93
Q

what arteries are affected in takayasu arteritis/granulomatous vasculitis?

A

aortic arch

branches off the aortic arch

94
Q

what is known as the ‘pulseless disease’?

A

takayasu arteritis

radial & carotid arteries

95
Q

what sense does takayasu arteritis affect?

A

eyesight

96
Q

what age group does granulomatous vasculitis affect?

A

<50 years***

97
Q

what arteries does polyarteritis nodosa affect?

A

system-wide small & medium-sized arteriesa

98
Q

what arteries avoid damage with polyarteritis nodosa?

A

pulmonary arteries

99
Q

what causes polyarteritis nodosa?

A

1/3: chronic hep B viral infection

2/3: idiopathic, autoimmune hypothesis

100
Q

what age group is affected by polyarteritis nodosa? what are the symptoms?

A

MC in young adults

symptoms: episodic, diffuse myalgia & peripheral neuritis, end-organ damage

renal A: rapid increase in blood pressure

G.I. A: abdominal pain, bloody stools

101
Q

what is the pediatric vasculitis?

A

Kawasaki disease; 80% <4 years

102
Q

what percentage of Kawasaki disease has cardiovascular involvement?

A

20%

103
Q

what determines the prognosis of Kawasaki disease?

A

the severity of CAD, if present

no CAD = full recovery

>50% of aneurysms resolve within 2 years

104
Q

what is the ‘hallmark’ of Kawasaki disease?

A

acute/persistant fever that doesn’t respond to ibuprofen or acetaminophen

105
Q

what vasculitis is hypothesized to be a type IV hypersensitivity?

A

Kawasaki disease

106
Q

what is the main sign of Kawasaki disease? how is it treated?

A

sign: strawberry tongue

Tx: aspirin, steroids, CABG (coronary artery bypass graft)

107
Q

what type of vasculitis is a type II hypersensitivity?

A

Wegener granulomatosis, necrotising vasculitis

108
Q

what organs does Wegeners granulomatosis effect? what changes occur?

A

kidneys and upper & lower respiratory tracts

  1. granulomas
  2. systemic vasculitis – small & medium arteries
  3. glomerulonephritis
109
Q

what population is effected by Wegners granulomatosis?

A

middle age males

110
Q

what is the prognosis for untreated Wegener granulomatosis?

A

lethal after 1 year (80%)

111
Q

What is effected with Thromboangiitis obliterans/Buerger disease?

A

medium-sized arteries

feet (tibial A) & hands (radial A)

112
Q

who is effected by thromboangiitis obliterans/Buerger disease?

A

Heavy tobacco smokers

Males, 25-35 years

113
Q

signs/symptoms of Buerger disease?

A

pain at rest

Raynaud phenomenon

Vascular claudication (pain that goes away after you stop moving)

ulcerations & gangrene

**woman on the video**

114
Q

what is Raynaud phenomenon? who does it occur in? primary v. secondary?

A

exaggerated arteriole vasoconsriction

MC in females

primary: cold & emotional
secondary: atherosclerosis, Buerger disease, lupus, scleroderma

115
Q

What three diseases make up 90% of venous diseases?

A
  1. varicose veins
  2. phlebothrombosis: NO previous inflammation

3. thrombophlebitis: Follows inflammation

116
Q

Details about Thrombophlebitis

A

DVTs = 90% of all cases

localized cyanosis or erythema

117
Q

what cancers are associated with superior vena cava syndrome? inferior vena cava syndrome?

A

SVC syndrome: bronchogenic carcinoma & mediastinal lymphoma

IVC syndrome: hepatocellular carcinoma & renal cell carcinoma

118
Q

primary vs. secondary lymphadema

A

primary: congenital lymphatic abnormalities; milroy disease, hypoplasia/agenesis of lymph vessels
secondary: obstruction of previously normal lymph vessels; neoplasia, infection, thrombosis, fibrosis

119
Q

what are 2 signs of chronic lymphedema?

A

Peau d’orange

brawny induration (hardening of skin)

120
Q

are vascular tumors most commonly malignant or benign?

A

benign

121
Q

details about hemangiomas

A

common benign

increase in local capillary growth

superficial tissues

enlarge after birth –> most self-resolve by age 7

122
Q

details about kaposi sarcoma

A

malignancy of lymphatic endothelial cells

HHV-8

defining disease of AIDS

MC in lower extremity

123
Q

details about angiosarcoma

A

malignant endothelial neoplasia

extremely variable

if anaplastic –> poor prognosis

MC older adults

widely spread –> MC skin, breast, liver

long latency period

124
Q

what 2 vessels are commonly used for vascular grafts?

A
  1. great saphenous vein: 50% at 10 years
  2. internal mammary artery: 90% at 10 years
125
Q

what is the most common type of arteriolosclerosis?

A

hyaline

126
Q

what is the MC arteriosclerosis?

A

atherosclerosis

Pathology II PCC (7 decks)

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