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System Pathology I -- Roecker > Exam 3: Sec. 4: Vascular Pathologies Pt2 > Flashcards

Exam 3: Sec. 4: Vascular Pathologies Pt2 Flashcards

1
Q

What is atherosclerosis defined as?

A

the presence of athersclerotic plaques, formally known as atheromas, that develop within the tunica intima and cause stensosis of the vascular lumen

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2
Q

About how many deaths in the U.S. is atherosclerosis ass. with?

A

about half!!

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3
Q

What diseases does the vascular stensosis caused by atherosclerosis lay at the core of?

A
  • coronary artery disease
  • heart attack
  • cerebral vascular disease
  • stroke
  • peripheral vascular disease
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4
Q

How do atherosclerotic plaques effect nutrients getting to the vessel?

A

reduce the diffusion to the inner half of the tunica media

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5
Q

What do atherosclerotic plaques increase the risk of?

A

aneurysms and vascular disruption/hemorrhage

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6
Q

What is the combination of macrophages and lipids w/in an atheroma known as?

A

foam cells

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7
Q

What happens if an atherosclerotic plaque ruptures?

A

the foam cells and other debris combine with circulating blood and cause vascular occlusion, via formation of excessive thromboemboli

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8
Q

What do we call atherosclerotic plaques that are ass. with greater levels of inflam. and have a thinner outer fibrous cap?

A

vulnerable plaques–> are more prone to rupturing

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9
Q

What do vulnerable plaques contain greater amounts of?

A
  • macrophages
  • lymphocytes
  • degradative matrix metalloproteinases (MMPs)
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10
Q

What is the MC cause of Myocardial infarction?

A

ruptured atherosclerotic plaque

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11
Q

When atherosclerotic plaques rupture, what may they be referred to as?

A

“erosion”, “ulceration”, “fissuring”, of a plaque or even “acute plaque change”

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12
Q

What represents atheromas with lower levels of inflammation and are less prone to rupturing?

A

stable plaques

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13
Q

What is coronary artery disease defined as?

A

70% occlusion or coronary arteries

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14
Q

When it comes to the Epidemiology of Atherosclerosis, what areas of the world have higher rates of atherosclerosis, what areas have lower rates?

A

higher–> U.S.–> due to exposure to Standard American Diet

lower–> Japan

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15
Q

What is the Standard American Diet?

A 
(SAD) 
High levels of:
- processes meat
- red meat
- fried foods
- high fat
- refined grains
- high sugar drinks
- high-fructose corn sytrup
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16
Q

Where are rates of atherosclerosis highest in the world? What age group?

A

among Americans–> over 70 years of age have sig. levels of atheroslcerosis w/in larger-to-medium sized arteries

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17
Q

How are the risk factors for atherosclerosis commonly classified?

A
  1. Inherent/ non-modifiable (constitutional)

2. modifiable

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18
Q

What are some constitutional risk factors (non-modifiable) for atherosclerosis?

A
  • family history
  • familial hypercholesterolemia
  • over age 40
  • male sex
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19
Q

Describe the risk of atherosclerosis of males and females.

A

males have higher risk earlier in life than females, and it increases gradually from there

females risk approaches that of males when they are postmenopausal

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20
Q

What are some Modifiable Risk factors for atherosclerosis?

A
  • consumption of omega-3 FAs = good
  • regular physical exercise
  • consume 1-2 alc drinks per day

Increases risk:

  • hypercholesteremia (major risk factor)
  • consumption of trans fats
  • prolonged HTN
  • smoking tobacco
  • systemic inflam.
  • metabolic syndrome
  • diabetes mellitus
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21
Q

What are all risk factors for atherosclerotic plaque formation thought to contribute to?

A

development of atherosclerosis via “response-to-injury” hypothesis

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22
Q

What do the various risk factors of atherosclerosis cause?

A
  • *endothelial injury
  • inflam.
  • thickening of tunica intima
  • accumulation of foam cells, cellular debris, lipids
  • dytrophic calcification
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23
Q

Can hemodynamic stressors contribute to atheroma formation?

A

yes–> include turbulent blood flow at site of previous site of atheroma, branch points, or structural irregularities on inside of vessel wall

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24
Q

What four clinical consequences is Atherosclerosis ass. with?

A
  1. Cardiovascular complications
  2. Metabolic Syndrome
  3. Peripheral Vascular Disease
  4. Aneurysms
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25
Q

What are the three most clinically significant consequences of atherosclerosis?

A
  • coronary artery disease
  • MI
  • CHF
  • -also cerebral infarction
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26
Q

What are the top 3 risk factors for M.I.? What is ones risk if they have 2 or them? What about 3 of them?

A
  1. Hyperlipidemia
  2. HTN
  3. Smoking
  • -any 2 = 4-fold increase
  • -any 3 = 7-fold increase
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27
Q

By what fold does having a history of diabetes mellitus increase ones risk of of a myocardial infarction?

A

2 fold

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28
Q

What do most cardiovascular complications from atherosclerosis involve?

A

a ruptured atheroma and a sudden occlusion of blood vessels supplying heart or brain

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29
Q

What is an occlusion of 70% of more of a vessel’s cross-sectional space known as?

A

critical stenosis

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30
Q

What is the point at which coronary artery disease begins to cause angina pectoris (chest pain)?

A

at critical stenosis (70% occlusion)

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31
Q

What may critical stenosis of the arteries supplying the brain cause?

A

TIAs (transient ischemia attacks)

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32
Q

What is Metabolic Syndrome?

A

(previously Syndrome X)
- combination of separate conditions that occur together and increase ones risk of developing cardiovascular disease and type 2 diabetes mellitus

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33
Q

What are the 5 criteria that one must have 3 of to be diagnoses with Metabolic Syndrome?

A
  1. Central (visceral) obesity
  2. Hypertension
  3. Dyslipidemia
  4. Insulin resistance
  5. Pro-inflammatory state (hypercoagulability)
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34
Q

What is a generic term for disease processes that affect the vessels of the “periphery”, which are not vessels supplying heart and brain?

A

Peripheral Vascular Disease

–vessels usually in extremities or other organs

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35
Q

What most likely causes Peripheral Vascular Disease?

A

atherosclerotic narrowing–> cause peripheral ischemia

rarely from embolism or prolonged spasm

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36
Q

What are the risk factors for Peripheral Vascular Disease? What are the the most sig. ones in the U.S.?

A

same as atherosclerosis

in U.S.–> smoking and diabetes mellitus

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37
Q

What vessels are most likely to develop Peripheral Vascular Disease? What is the painful cramping sensation that may develop called? What worsens the cramping?

A

vessels of lower extremities

claudication (vascular claudication)–> exercise worsens it

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38
Q

How may Peripheral Vascular Disease manifest?

A
  • claudication
  • pale discoloration
  • gangrenous necrosis in severe cases
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39
Q

What is the treatment for Peripheral Vascular Disease?

A

lifestyle modifications, such as:

  • smoking cessation
  • strict glucose control among diabetics
  • regular physical activity
  • improved dietary choices

–rarely surgical angioplasty and bypass grafts may be needed

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40
Q

What is a congenital or acquired localized dilation of an arterial wall called?

A

an aneurysm

“ballooning” of the arterial wall

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41
Q

How will an aneurysm affect the vessel wall?

A
  • increase tension on dilated/weakened wall–> risk of vascular rupture and hemorrhage
  • site for vascular stasis or turbulance
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42
Q

What layers of the vessels wall do the majority of aneurysms involve? What are they referred to as?

A

all 3 layers (tunica intima, media, adventitia)

= “true” aneurisms

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43
Q

Rarely, an aneurysm may allow blood to escape and form a dilated hematoma that is only 1 or 2 vascular layers, when this occurs what do we call it?

A

“false” aneurysm

or a pseudoaneurysm

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44
Q

What are the two MOST significant risk factors for developing an aneurysm? What are other causes?

A
  1. atherosclerosis
  2. hyperextension
  • physical trauma, vasculitis, congenital defects
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45
Q

What two CT conditions may cause inherent weakness in arterial wall?

A
  1. Marfan syndrome–>weakened ECM risk of aortic aneurysm–> aortic arch or thoracic aorta
  2. Ehlers-Danlos syndromes–> irreg. collagen
46
Q

What other conditions is ass. with intracranial saccular aneurysms?

A

polycystic kidney disease

47
Q

Where are aneurysms that develop following the formation of atherosclerotic plaques most likely to occur?

A

lower abdominal aorta or common iliac arteries

48
Q

Who is as risk of developing a AAA/ triple A (abdominal aortic aneurysm)?

A

Caucasian males older adults (above 50 yrs) with history of HTN, smoking tobacco, and ahve abdominal aortic atherosclerosis

family history

49
Q

Where are Abdominal Aortic Aneurysms most likely located?

A

inf. to origin of renal arteries and sup. to iliac bifurcation

50
Q

What is the diagnostic criteria for a Triple A?

A

must be 50% dilated, is ~5cm in diameter

use musculoskeletal ultrasound

51
Q 
What is the risk of an AAA rupturing that is:
<4cm?
4-6cm?
5-6cm? 
>6cm?
A 
<4cm = rare
4-5cm = 1% each year
5-6cm = 11% chance each year
>6cm = 25% change
52
Q

What percentage of AA that rupture are lethal?

A

1/2!!!

53
Q

Surgery on a AA will decrease the risk of rupture to what percent?

A

5% chance

54
Q

A Triple A takes up space, what may this impact?

A
  • obstruction of one or both ureters

- pressure on arteries and cause ischemia

55
Q

What are aneurysms that develop following prolonged HTN and are most likely to occur in thoracic region of aorta? Inds. with what condition are at an increased risk of developing them?

A

Thoracic Aortic Aneurysms

inds. with Marfan Syndrome

56
Q

Most cases of an Arterial dissection occur in the presence of what, aka what is the MC risk factor for developing an arotic dissection?**

A

90% cases occur in presence of HTN

57
Q

What occurs when blood tears apart the laminar planes of the tunica media and forms a blood-filled channel w/in the wall of the involved artery?

A

Arterial dissection (aka vascular dissection)

58
Q

How does an Arterial Dissection manifest?

A
  • sudden onset

- cause sharp “tearing” or “stabbing” sensation in area of dissection

59
Q

What are the consequences of an Arterial Dissection? (4)

A
  • continued enlargement of dissection through tunica adventitia
  • severe hemorrhage
  • creation of vascular flap that occludes vascular lumen and cause ischemic injury
  • thrombosis created by turbulent blood at site of dissection
60
Q

T/F. The pain from an Arterial Dissection is widespread.

A

False– it is well-localized to area of dissection

61
Q

Where do thoracic dissections typically occur? What do they cause and what may they mimic?

A
  • near aortic arch and may cause anterior chest pain
  • mimic heart attack
  • pain may project posteriorly b/w scapulae
62
Q

Where do most Arterial Dissections occur?

A

in thoracic aorta, w/in 10 cm of the heart

63
Q

How are Arterial Dissections typically described?

A

1 - 5 cm tears that have “sharp” or “jagged” edgges

64
Q

What are the two primary classifications for describing thoracic aortic dissections?

A
  1. Type A (proximal dissections)

2. Type B (distal dissections)

65
Q

Which type of thoracic aortic dissection is more common and more serious, why?

A

Type A, b/c it occurs w/in ascending aorta region of aortic arch and is serious due to their proximity to aortic valve and tissues of the heart

66
Q

Which way do Type A thoracic aortic dissections enlarge?

A

toward the heart and may cause blood to accumulate w/in pericardial sac –> may cause lethal pericardial tamponade or lethal disruption of aorta form heart

67
Q

What do we call it when a Type A thoracic aortic dissections creates a lethal disruption of the aorta from the heart?

A

“disruption of the aortic valvular apparatus”

68
Q

Where does a Type B thoracic aortic dissection occur?

A

(= distal dissections)
- occur distal to left subclavian artery

–less common and less life-threatening b/c less likely to involve aortic valve and cardiac tissues

69
Q

What sex and age are at a greater risk of developing an aortic dissection?

A

males b/w 40-60

younger inds–> if have Marfacn syndrome, Ehlers-Danlos syndrome, or Wilson disease

70
Q

Patients that present with sudden, severe and/or sustained neck pain, HAs, or vertigo should be evaluated for what?

A

potential cervical artery dissection

71
Q

What are the warning signs of a Dissection or Stroke?

A 
"5 Ds and 3 Ns"
D- diplopia
D- dizziness
D- drop attacks (sudden fall)
D- dysarthria
D- dysphagia
N- numbness
N- nausea
N- nystagmus
72
Q

What is a life-threatening condition that develops following the accumulation of fluid w/in pericardial space?

A

Pericardial tamponade (aka cardiac tamponade)

73
Q

For pericardial tamponade, when fluid accumulates w/in the pericardial space, what is progressively lost?

A

ventricular filling is progessively lost–> may progress to cardiogenic shock and death

74
Q

What will patients with pericardial tamponade present with a sudden onset of?

A
  • dyspnea
  • tachycardia
  • tachypnea
  • severely reduced cardiac output
  • confusion or altere consciousness
  • cyanotic, cold, or “clammy” extremities
75
Q

What is the treatment for pericardial tamponade?

A

it is a medical emergency is an “Echo” is needed to visualize the heart and urgent drainage of the excessive fluid is necessary for survival

76
Q

What disease causes abnormal copper metabolism and makes it difficult for body to excrete copper so it accumulates at toxic levels? How does one get it?

A

Wilson Disease

  • autosomal recessive disorder
  • mutation in ATP7B gene
77
Q

What does cellular injury form copper accumulation relate to?

A

excessive oxidative stress that results from Fenton reaction

78
Q

What are the most characteristic locations for copper to accumulate in inds. with Wilson Disease?

A
  • liver
  • brain
  • iris of eyes
79
Q

What occurs when copper accumulates in the liver from Wilson Disease?

A

fatty change = steatosis
inflamed = hepatitis
–together = steatohepatitis

liver may become cirrhotic and liver failure may occur

80
Q

When occurs when copper accumulates in the brain from Wilson Disease?

A

Neuropsychiatric features develop:

  • parkinsonism
  • dysarthria
  • astaxia
  • lack of facial expressions
  • clumsiness
  • poor coordination
  • spasticity
  • seizures
81
Q

What is Kayser-Fleischer rings ass. with in 90% of cases of what disease?

A

Wilson Disease

  • when Copper accumulates in iris of the eye
  • greenish-to-gold colored rings form
82
Q

How many people are affected by Wilson Disease? How many are carriers for the mutated gene in the U.S.?

A

1 in 30,000

1 in 90 ppl in U.S. carry gene mutation

83
Q

When do the features of Wilson Disease manifest?

A

variable, but: b/w ages 6-40

84
Q

What are the initial features of Wilson Disease?

A

related to hepatic dysfunction or onset of neuropsychiatric features

85
Q

What is the generic term for inflammation of the vessel wall?

A

vasculitis

86
Q

What may vasculitis result from?

A
  1. Infectious
  2. Immune-mediated
  3. traumatic stimuli—physical or chemical injury
87
Q

Which type of hypersensitivity causes vasculitis?

A

Type III

88
Q

What are some examples of infections that may cause vasculitis?

A
  • Hepatitis B (HBV) inf.

- Syphilis

89
Q

What are some immune-mediated conditions that may cause vasculitis?

A
  • SLE (lupus)
  • PAN (polyarteritis nodosa)
  • ADRs
90
Q

What are some physcial or chemical injuries that can cause vasculitis?

A
  • ionizing radiation
  • mechanical trauma
  • toxic exposures
91
Q

What are the general features for how vasculitis will manifest?

A

indicative of inflammation:

  • fever
  • malaise
  • myalgia
  • arthritis
92
Q

What is a systemic autoimmune vasculitis that affects the small-to-large sized arteries in the head and neck of ELDERLY inds (over 50)?

A

Temporal Arteritis

93
Q

What is the most common form of vasculitis in adults and has has a prevalence of 1 in 500 inds age 50 or older?

A

Temporal Arteritis

94
Q

What arteries are involved usually in Temporal Arteritis?

A
  1. temporal artery
  2. ophthalmic artery (50%)
  3. vertebral artery and aorta
95
Q

How does Temporal Arteritis manifest?

A

chronic inflammation; T-cell involvement (Type IV hyper.) reaction

  • causes granulomas (aka “giant cells”)
96
Q

When the aorta is involved with Temporal Arteritis, what is it renamed as? Who is it MC among?

A

giant cell aortitis

MC among elderly females

97
Q

What are the clinical features of Temporal Arteritis?

A
  • HA
  • facial pain over superficial temporal artery
  • ophthalmic involved–> cause diplopia and possibly complete vision loss
98
Q

What type of autoimmune vasculitis causes chronic inflammation and granulomatous inflammation usually in younger (<50 years) inds.?

A

Takayasu Arteritis

99
Q

What condition is referred to as “pulseless disease”? Why?

A

Takayasu Arteritis
- b/c causes destructive narrowing of medium-to-large arteries of aortic arch and arteries brancing from aortic arch–> distribute to radial artery and carotid artery = common places to measure pulse

100
Q

About 1/2 of all patients with Takayasu Arteritis have what artery involvement?

A

pulmonary artery involvement

101
Q

What are the clinical features of Takayasu Arteritis?

A
  • reduced upper extremity BP
  • upper extrem. weakness
  • reduced/absent radial or carotid pulses
  • visual disturbances
  • fatigue, fever, weigh tloss
102
Q

What age group is spared from Takayasu Arteritis? Who is MC diagnosed?

A

the elderly

age 30 and most (80%) are females

103
Q

T/F. Takayasu Arteritis is a common condition.

A

False– it is rare at 1 in 200,000 inds

  • MC among Asian and Indian descent
104
Q

What is a systemic autoimmune vasculitis that results from a type III hypersentivitiy reaction and immune complex deposition into artery walls?

A

Polyarteritis Nodosa (PAN)

105
Q

Arteries of what organs are most likely to be involved with Polyarteritis Nodosa (PAN)?

A
  • kidney*,
  • heart*
  • liver
  • GI tract
106
Q

Uniquely, what arteries are NEVER involved in Polyarteritis Nodosa (PAN)?

A

pulmonary arteries

107
Q

What fraction of cases of Polyarteritis Nodosa (PAN) are related to patients with chronic hepatitis B viral infections (HBV)?

A

1/3

2/3 are auto-immune related

–all Type III hypersensitivity

108
Q

What condition causes patchy areas of fibrinoid necrosis to form w/in vessel walls and mutliple small aneurysms along affect vessel referred to as a “rosary sign”?

A

Polyarteritis Nodosa (PAN)

109
Q

What are the clinical features of Polyarteritis Nodosa (PAN)?

A

episodic and widely varied:

  • fever, malaise, weight loss
  • renal artery involved–> rapid elevation in BP due to renovascular HTN
  • GI involed–> abd pain and blood in stool
  • purple skin lesions (purpua)
  • motor defects
  • tissue atrophy and ulcerations
110
Q

What can untreated Polyarteritis Nodosa (PAN) lead to?

A

typically is FATAL from kidney failure or a M.I.

111
Q

What age is most likely to develop Polyarteritis Nodosa (PAN)?

A

young adults…but has be Dx in all ages

~4-100,000 inds

System Pathology I -- Roecker (14 decks)

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