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System Pathology I -- Roecker > Exam 3: Sec. 4: Vascular Pathologies Pt1 > Flashcards

Exam 3: Sec. 4: Vascular Pathologies Pt1 Flashcards

1
Q

What are more common and cause more serious/clinically significant signs/symptoms, venous pathologies or arterial pathologies?

A

arterial pathologies

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2
Q

What are the two main mechanisms that vascular pathologies involve?

A
  1. Narrowing or Obstruction of the lumen

2. Weakening of the Vessel wall

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3
Q

What are the two ways that Narrowing or Obstruction of the lumen may occur?

A
  1. Gradual = atherosclerosis or thickening of tunica intima after prolonged injury
  2. Rapid = Thromboembolism
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4
Q

How may Weakening of the vessel wall occur?

A

following a congenital defect–> may be ass. with CT disorder

Dilation –> aneurysm
Rupture–> dissection

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5
Q

What is the thickening and hardening of the walls of the arteries?

A

Arteriosclerosis

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6
Q

What is a form of arteriosclerosis whereas the hardening of the arterial walls is the result of atherosclerotic plaque deposition?

A

Atherosclerosis

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7
Q

What is a tear along the inside of an artery called?

A

dissection

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8
Q

What is a blood clot that forms within the vascular lumen, which impeded blood flow?

A

Thrombus

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9
Q

What is the similar organization along all arteries and veins?

A

tunica intima
tunica media
tunica adventitia

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10
Q

When it comes to the three layers or vessels, describe the difference b/w arteries and veins.

A

arteries have thick of tunica media (smooth muscle)

veins have relatively thin layers of smooth musculature, AND contain valves

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11
Q

Why are arterial walls thicker than the walls of veins?

A

to accomodate pulsation and higher BP

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12
Q

What are small arteries that are the primary sites for blood pressure regulation and what does it ultimately regulate?

A

arterioles

via vasodilation or vasoconstriction –> regulates peripheral resistance

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13
Q

T/F. Veins are thin-walled vessels that hold larger volumes of blood than arteries, but are more easily compromised, dilated, and invaded by inf. microbes or tumors

A

True

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14
Q

What are examples of large elastic arteries?

A
  • aorta
  • vessels branching from aortic arch
  • iliac arteries
  • pulmonary arteries
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15
Q

What are examples of medium-sized muscular arteries?

A

coronary arteries, renal arteries

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16
Q

What are examples of small arteries and arterioles?

A

various small arteries throughout body which are located just before body’s many capillary beds

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17
Q

How do small or thin-walled vessels get their nutrient supply?

A

nutrients and oxygen may diffuse from w/in arterial lumen to entire vascular wall

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18
Q

How do thick-walled arteries, such as large and medium-sized arteries get their nutrient supply?

A

Tunia intima and inner 1/2 of tunica media–> diffusion from blood w/in lumen

Outter 1/2 of tunica media and tunica adventitia–> nutrients delivered from vasa vasorum

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19
Q

What cells make up the inner lining of all blood vessels and lymphatic vessels?

A

Endothelial cells

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20
Q

How are endothelial cells organized?

A

single-layer that creates a “non-thrombogenic blood-tissue interface”

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21
Q

What three things are endothelia cells involved in?

A

modulating - intravascular inflammatory responses

  • assist in regrowth and repair of injured smooth muscle cells w/in tunica media
  • secrete vasoactive substances (NO, Endothelin)
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22
Q

What are the vasoactive substance that endothelial cells release? How do they affect the vessel?

A

Nitric oxide–> potent vasodilator

Endothelin–> potent vasoconstrictor

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23
Q

What do we call when the endothelial lining is injured or irritate and an inflammatory response is initiated?

A

endothelial activation

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24
Q

What may cause endotheial activation?

A
  • microbial infs
  • hypoxia
  • hemodynamic stress
  • diabetes mellitus
  • inflam. cytokines
  • high cholesterol levels
  • activated compliment system
  • chemicals from tobacoo smoke
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25
Q

What are the three more common or unique vascular congenital anomilies we are focusing on?

A
  1. Saccular Aneurysm
  2. Arteriovenous (AV) Fistula
  3. Fibromuscular Dysplasia
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26
Q

What are the most common form of cerebrovascular malformation?

A

intracranial Saccular Aneurysm (“berry” aneurysms)

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27
Q

Where are saccular aneurysm most likely to develop?

A

branch points on Circle of Willis

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28
Q

What are saccular aneurysms at risk of doing and causing what?

A

rupturing and causing a subaracnoid hemorrhage–> “thunderclap” HA

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29
Q

What are patients that develop saccular aneurysms believe to have? What other disease is ass.?

A

born w/ congenitally weak spots w/in tunica media of intracranial vessels

ass. with Polycystic kidney disease

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30
Q

What is an Arteriovenous (AV) Fistula?

A

fistula = abnormal connection b/w medium-to-large artery and vein and blood bypasses the related capillaries

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31
Q

How does one acquire an Arteriovenous Fistula?

A
  • may be congenital vascuarl anomalies

- may be traumatically acquired from a penetrating injury

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32
Q

What is a lethal complication of large Arteriovenous (AV) Fistulas?

A

High-Output Heart Failure

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33
Q

What is High-Output Heart Failure?

A
  • -> occurs when large volumes of oxygenated arterial blood is returned to the heart and lungs
  • bypassing capillaries causes HR to increase
  • sets up positive feedback loop–> eventually causing heart to fail
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34
Q

What condition is when the tunica media and tunica intima of medium-sized arteries become overgrown, due to hyperplasia and fibrosis?

A

Fibromuscular Dysplasia

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35
Q

Where is the most common place for Fibromuscular Dysplasia to occur? What percent of all cases does this occur in? What may it stimulate?

A

MC renal artery –> 75%

may stimulate–> Renovascular hypertension

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36
Q

What features and symptoms to inds with Fibromuscular Dysplasia have?

A 
--most asymptomatic
But may have:
- HA
- light-headedness
- vertigo
- transient neurological deficits
- unexplanted HTN
37
Q

What age is Fibromuscular Dysplasia MC discovered in?

A

MC in young women (reproductive age)

38
Q

What is a relatively rare form of HTN that develops following ischemia to a kidney?

A

Renovascular Hypertension

39
Q

How does Renovascular Hypertension develop from a kidney detecting hypoxia?

A

reduced blood supply activated
“renin-angiotensin-aldosterone system (RAAS)”–> retain Na+ and water and increase total blood volume
- arterioles vasocontrict
= BP rises

40
Q

What will the managment of Renovascular Hypertension from Fibromuscular dysplasia involve?

A
  • surgical correction
  • antihypertensive meds
  • even removal of involved kidney
41
Q

What is the term for regulating blood pressure w/in a narrow range of what is normal ?

A

normotension

42
Q

What is BP the result of?

What is CO the resutl of?

A

BP = CO x PVR (peripheral vascular resistance)

CO = HR x SV

43
Q

How is the peripheral vascular resistance primarily regulated?

A

by body’s arterioles

44
Q

What other factors influence the blood pressure regulation?

A
  • heart
  • kidneys
  • lungs
  • adrenal glands
45
Q

What is low blood pressure known as? What is it defined as?

A

hypotension = BP that is less than 90/60 mm Hg

46
Q

What is a hypotension a feature of all forms of?

47
Q

What is high blood pressure known as?

A

Hypertension (HTN)

48
Q

What BP does High BP Stage 1 begin at?

A

at or above 130/80 mm Hg

49
Q

What BP is:

  1. Normal
  2. Elevated
  3. High BP Stage 1
  4. High BP Stage 2
  5. Hypertensive Crisis
A
  1. less than 120/80
  2. 120/ less than 80
  3. at or above 130/80
  4. at or above 140/90
  5. at or above 180/120
50
Q

How is the myocardium involved in BP regulation? Stimulus? Response? Effect?

A 
Stimulus = increase BP
Response = secrete ANP (atrial natriuretic peptide)
Effect = increase exretion of Na+/H2O (reduce BP), and vasodilation
51
Q

How are the kidneys involved in BP regulation? Stimulus? Response? Effect?

A 
Stimulus = low BP
Response = secrete renin (actiavte RAAS)
Effect = Renin interacts with liver
52
Q

How is the liver involved in BP regulation? Stimulus? Response? Effect?

A 
Stimulus = exposed to renin
Response = renin cleaves angiotensinogen to angiotension I
Effect = angiotension I interacts with lungs
53
Q

How are the lungs involved in BP regulation? Stimulus? Response? Effect?

A 
Stimulus = exposure to angiotensin I
Response = ACE enzyme converts angiotensin I into II
Effect = angiotensin II interacts w/ adrenal galnds and stimulates vasocontriction
54
Q

How are the Adrenal Glands involved in BP regulation? Stimulus? Response? Effect?

A 
Stimulus = Exposure to angiotensin II
Response = secrete aldosterone
Effect = cause kidney to increase Na+/H2O resorption which increases blood vol.
55
Q

What are the genetic risk factor to developing HTN?

A
  • having family history
  • identical twin with HTN
  • being African American
  • inds. with Polycystic Kidney disease
56
Q

What are env. risk ractors for HTN?

A
  • psychological stress
  • obesity
  • physical inactivity
  • consumption of high salt diet
  • drinking too much alc
  • diabetes mellitus
  • smoking tobacco
57
Q

What is referred to as the “silent killer”? Why?

A

Hypertensive Vascular Disease (HTN, high BP, HBP)

– b/c patients are most likely asymptomatic for many years as condition progresses

58
Q

What will about 50% of inds with prolonged HTN suffer from?

What will about 33% suffer?

A

lethal ischemic heart disease (i.e. MI, CHF)

lethal cerebral infarction

59
Q

What conditions are associated with HTN?

A
  • atherosclerosis
  • coronary artery disease
  • CHF
  • cardiac hypertrophy
  • Cerebral infarction
  • aortic dissection
  • renal failure
  • arteriolosclerosis
  • MI
  • vascular dementia
  • Primary brain parenchymal hemmorrhage
  • HTN retinopathy
60
Q

What represents ~90% of all cases of HTN?

A 
Essential HTN (Primary HTN or idopathic HTN) 
--age-related
61
Q

What is Essential Hypertension?

A

cases of HTN that are NOT attributable to any other known pathology
–age-related disease

62
Q

What is the term for a known cause of HTN? What may it develop following?

A

Renovascular Hypertension

  • -May Develop following:
  • any form of renovascular disease
    • fibromuscular dysplasia
    • polyarteritis nodosa (involve renal artery)
63
Q

What is a rare form of HTN involving extreme elevations in BP (>180/120 mm Hg) and end organ damage? What percent of all HTN does it represent?

A

Malignant Hypertension

~1%

64
Q

What organs are most likely to be damaged by Malignant HTN?

A
  • CNS
  • cardiovascular system
  • renal system
65
Q

What may Malignant HTN cause?

A
  • cerebral infarction
  • cerebral edema
  • intracranial hemorrhages
66
Q

What is a component of Malignant HTN that involves the swelling of optic disc and indicates presence of increased ICP?

A

Papilledema

67
Q

What does Malignant HTN frequently manifest with?

A
  • retinal hemorrhages

- kidney damage

68
Q

What is an adrenal gland tumor that may cause episodic spikes in BP?

A

Pheochromocytoma

– a neuroendorine tumor composed of abnormal chromaffin cells that secrete catecholamines

69
Q

What does the circulating catecholamines from Pheochromocytoma cause episodic features of?

A
  • HBP
  • HA
  • tremors
  • sweating
  • tachycardia
  • temporary cardiac arrhythmias
70
Q

What episodes of HBP from Pheochromocytoma are a risk factor for what?

A

HTN-related conditions such as:

  • MI
  • cerebral infarction
  • renal failure
71
Q

What percentage of cases is Pheochromocytoma malignant in? Can it be cured?

A

~10% and may be cured following surgical removal

72
Q

What are some things that can cause injury to the tunica intima?

A
  • mechanical trauma
  • immunological injury
  • hemodynamic stressors (prolonged HTN or turbulent blood flow)
  • septic inf
  • toxic expsure (tobacco, oxidized lipids)
73
Q

What is the nonspecific response the vascular wall has to all forms of injury?

A
  • thickening of the tunica intimal (internal thickening) –> narrows intravascular lumen–> inhibits blood flow through involved vessel
  • -> cause sig. vascular stenosis, end-organ damage, and inhibited vasoreactivity
74
Q

T/F. After vascular wall injury and thicking of the tunica intima, the body can heal and the vessel can go back to normal.

A

False– usually the damage is irreversible and is unlikely to return to pre-injured state

75
Q

T/F. Arteriosclerosis does not suggest a cause of the hardening and is purely descriptive.

A

True

= hardening of arterial wall and loss of elasticity

76
Q

What are the three main causes of arterioslcerosis?

A
  1. Arteriolosclerosis
  2. Monckenberg Medial Sclerosis
  3. Atherosclerosis
77
Q

What is a form of arteriosclerosis that is specifically describing a hardening of the small arterioles?

A

Arteriolosclerosis

78
Q

What is Arteriolosclerosis typically the result of?

A
  • HTN

- diabetes mellitus

79
Q

What are two distinct forms of arteriolosclerosis that we talk about?

A
  1. Hyaline arteriolosclerosis

2. Hyperplastic arteriolosclerosis

80
Q

What develops following prolonged period of low-level hypertension (benign HTN) or diabetes mellitus and produces a homogenous “pink” thickening detected upon cross section?

A

Hyaline arteriolosclerosis

81
Q

What does Hyaline arteriolosclerosis cause? What is it characteristically ass. with?

A

significant stenosis of involved arterioles

ass. w/ kidney damage and kidney failure

82
Q

What type of arteriolosclerosis develops following periods of severe blood pressure elevation (malignant HTN)?

A

Hyperplastic arteriolosclerosis

83
Q

What is characteristic to Hyperplastic arteriolosclerosis that is detectable on a cross section?

A

produces a layered or “onion skin” thickening

84
Q

What does Hyperplastic arteriolosclerosis cause? What is it characteristically ass. with?

A

vascular stenosis

ass. wth kidney damage and kidney failure

(same as Hyaline arteriolosclerosis)

85
Q

What is a form of arteriosclerosis that characteristically involves the deposition of calcium ions w/in the tunica media of medium-to-large arteries?

A

Monckeberg Medial Sclerosis

Monckenberg’s arteriosclerosis, Monckenberg’s sclerosis, medial calcific sclerosis

86
Q

What age group is Monckeberg Medial Sclerosis limited to?

A

older adults, beginning at age 50

87
Q

T/F. Monckeberg Medial Sclerosis causes vascular stenosis and clinically significant features.

A

FALSE– it does NOT produce vascular stenosis and it does NOT cause clinically sig. features

88
Q

How is Monckeberg Medial Sclerosis usually detected?

A

incidental finding that appears on advance imaging (mammography or X-ray)

89
Q

What causes the vast majority of all cases of arteriosclerosis? (the MC cause)

A

Atherosclerosis (info in neck deck of notecards)

System Pathology I -- Roecker (14 decks)

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