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Systemic Pathology > Vascular Pathology > Flashcards

Vascular Pathology Flashcards

1
Q

What is Vasculitis ?

A

Inflammation of a blood vessel wall (artery/vein)

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2
Q

What does Vasculitis cause?

A

Inflammation weakens the blood vessel —> causes aneurysm
Causes fibrosis of vessel wall and reduces lumen size —> can cause Ischemia

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3
Q

What are the layers of blood vessels?

A

Intima, Media, Adventitia

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4
Q

Tunica Intima

A

Keeps the blood flowing smoothly- Regulates blood pressure, prevents blood clots and keeps toxins out of your body

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5
Q

Media

A

SMOOTH MUSCLE
Contains elastic fibres that keep blood flowing in one direction

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6
Q

Adventitia

A

CONNECTIVE TISSUE
Helps delivers oxygen and nutrients from your blood to your cells and helps remove waste

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7
Q

What is the etiology of Vasculitis

A

Unknown

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8
Q

Is Vasculitis infectious

A

No

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9
Q

What are the non specific symptoms of Vasculitis ?

A

Fever, Fatigue, Weight Loss, Myalgia (This shows an inflammation is occurring)

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10
Q

Symptoms of organ ischemia due to:

A
  • Thrombus Formation (damage of endothelium which exposes tissue factor and collagen that stimulates clot formation)
  • Reduced lumen size (injury and healing of vessel wall causes fibrosis that reduces lumen size of the vessel)
    Aneurysm- Inflammation and necrosis of vessel wall weakens it leading to aneurysm
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11
Q

What does Large Vessel Arteritis affect?

A

Aorta and it’s major branches

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12
Q

What does Medium Vessel Arteritis affect?

A

Muscular arteries that supplies organs (renal artery, coronary artery)

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13
Q

What does Small Vessel Artery affect?

A

Arterioles, Capillaries and Venules

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14
Q

What are the 2 diseases of Large Vessel Vasculitis

A

-Temporal GIANT CELL Arteritis
-Takayasu Arteritis (PULSELESS DISEASE)

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15
Q

What are the 3 diseases of Medium Vessel Vasculitis?

A

-Polyarteritis Nodosa
-Kawasaki Disease
-Buerger Disease

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16
Q

What are the 4 diseases of Small Vessel Vasculitis ?

A

-Wegner Granulomatosis
-Microscopic Polyangitis
-Churg Strauss
-Henoch Schonlein

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17
Q

Who is usually affected by Temporal Giant Cell Arteritis

A

Vasculitis of old people (avg age 72)- Usually affects females

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18
Q

What is the classic location of Temporal Giant Cell Arteritis?

A

Branches of carotid artery

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19
Q

Old people with new onset of headache

A

Vasculitis of Temporal Artery

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20
Q

Visual Disturbance

A

Vasculitis of Opthalmic Artery

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21
Q

Jaw Claudication

A

Vasculitis of Arteries of Jaw

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22
Q

What would you expect the ESR to be for a patient with temporal giant cell arteritis

A

Elevated > 100

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23
Q

What clinical feature is Polymyalgia with flu like symptoms associated with ?

A

Temporal Giant Cell Arteritis

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24
Q

How is Temporal Arteritis diagnosed?

A

Vessel Biopsy- should see an inflamed vessel wall with giant cells and Intimal fibrosis

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25
Q

How is the vessel affected for temporal arteritis?

A

Segmentally so a long segment is taken out for biopsy

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26
Q

How do we treat temporal arteritis ?

A

Corticosteroids- Treat asap because risk of blindness due to involvement of ophthalmic artery

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27
Q

Who is affected by Takayasu Arteritis?

A

Mainly adults >50. Classic Pt is young Asian female

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28
Q

What disease affects aortic arch at branch point?

A

Takayasu Arteritis

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29
Q

What clinical findings do we see with Takayasu Arteritis?

A

-Visual and neurologic symptoms
-Weak or absent pulse in upper extremity (therefore disease called pulseless disease)
-ESR is elevated, vasculitis is granulomatous
-Treat with corticosteroids

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30
Q

What type of Medium Vessel Arteritis is a necrotising Vasculitis that affects vessels in many organs EXCEPT the lungs

A

Polyarteritis Nodosa

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31
Q

What are the clinical findings of Polyarteritis Nodosa?

A

Classic pt is young adults
Symptoms depend on vessel involved-
-Renal artery involvement cause hypertension
-Mesenteric arteries - abdominal pain with melena
-CNS arteries - neurologic disturbances
-Skin lesions

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32
Q

What chemical is associated with Polyarteritis Nodosa

A

Serum HbsAg

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33
Q

What is the pearl on string appearance of Polyarteritis Nodosa?

A

Early character of disease is that it creates
fibrinoid necrosis that makes the vessel lumen wide (as dead vessel is weak, aneurysms occur). Late character of disease is that it creates thick fibrosis that narrows the lumen. Therefore imaging gives a “string-of-pearl” appearance with alternate thick and thin sections.

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34
Q

How can we treat Polyarteritis Nodosa?

A

Corticosteroids & Cyclophosphamide
Fatal if not treated

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35
Q

Classic Pt is Asian child under 4

A

Kawasaki Disease

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36
Q

What is the clinical presentation of Kawasaki Disease?

A
  • Very non specific viral like infection
    -Fever>5 days
    -Shrieking irritability - extremely irritable kid
    -Conjunctivitis sparring area right next to iris
    -Erythematous rash of palms and soles and any mucocutaenous membrane (ex - strawberry tongue)
    -Enlarged cervical lymph nodes
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37
Q

What artery is affected with Kawasaki Disease

A

Coronary Artery

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38
Q

What are the complications of Kawasaki Disease?

A

Thrombosis with MI- Due to endothelial damage and exposure of collagen and tissue factor
Aneurysm with rupture

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39
Q

What is the treatment of Kawasaki Disease?

A

Aspirin- Prevents Thrombosis (Antiplatelet drug- Prevents formation of thromboxans A2)
IVIG (Intravenous Immunoglobulin)

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40
Q

Why can we not give kids aspirin when they have a viral disease?

A

As they can get Rye Syndrome- Encephalopathy and massive liver necrosis

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41
Q

What is Buerger Disease

A

Necrotising Vasculitis involving digits. Presents with ulceration, gangrene and auto amputation of fingers and toes

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42
Q

What can Buerger Disease be associated with?

A

Raynaud Phenomenon- Pale to blue to red colour change in digits due to exposure to cold. Pale and blue colour is due to vasopasm; red is due to return of circulation

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43
Q

What can Buerger Disease also be associated with?

A

Smoking- Smoking cessation = treatment

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44
Q

What 3 diseases can lead to RPGN?

A

Wegner Granulomatosis, Microscopic Polyangitis, Chug-Strauss

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45
Q

Wegner Granulomatosis is …

A

C-ANCA +

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46
Q

What affects Nasopharynx, Lungs and Kidney?

A

Wegner Granulomatosis

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47
Q

What is the treatment of Wegner Granulomatosis?

A

Cyclophosphamide and Corticosteroids
Relapse common

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48
Q

Microscopic Polyangitis is…

A

P-ANCA +

49
Q

What affects lungs, kidney and other organs?

A

Microscopic Polyangitis

50
Q

What is the treatment of Microscopic Polyangitis?

A

Cyclophosphamide and Corticosteroids
Relapse is common

51
Q

Churg Strauss is …

A

P-ANCA+

52
Q

Affects multiple organs including lungs and heart

A

Churg Strauss

53
Q

What causes Palpable purpura in buttocks pathogenic?

A

Henoch Schonlein Palpura

54
Q

Henoch Schonlein Palpura is shown after a

A

Upper respiratory infection

55
Q

How can we treat Henoch Schonlein Palpura?

A

With steroids

56
Q

What affects middle aged males

A

Wegner Granulomatosis

57
Q

Presentation of Wegner Granulomatosis?

A

Sinusitis or Nasopharyngeal Ulceration
Hemoptysis with bilateral modular lung infiltrates
Hematuria due to RPGN
Serum C-ANCA level correlates with disease

58
Q

How can we diagnose Wegner Granulomatosis?

A

Pt. Is C-ANCA +
A biopsy would show large necrotising granuloma with adjacent necrotising vasculitis

59
Q

How can we treat Wegner Granulomatosis?

A

Cyclophosphamide and Corticosteroids

60
Q

Does Microscopic Polyangitis involve Nasopharyngeal?

A

No

61
Q

Serum P-ANCA is associated with

A

Microscopic Polyangitis

62
Q

In C-ANCA, anticytoplasmic antibodies mainly target

A

Cytoplasm away from Nucleus

63
Q

In P-ANCA, anticytoplasmic antibodies mainly target

A

Cytoplasm in Perinuclear area

64
Q

What 3 features distinguish Microscopic Polyangitis from Churg Strauss?

A

Necrotising granulomatous vasculitis with eosinophils.
Involves multiple organs, especially lungs and heart.
Asthma and peripheral eosinophila.

65
Q

Churg Strauss

A

• Necrotizing granulomas with eosinophils present
• Peripheral eosinophila and asthma present
• Involves heart and lung
• P-ANCA correlate with disease activity

66
Q

What Vasculitis is due to IgA immune complex deposition and most common in children?

A

Henoch-Schonlein Purpura

67
Q

Presentation of Henoch-Schonlein Purpura?

A

-Palpable Purpura on buttocks and legs
-GI Involvement (GI Pain and Bleeding)
-IgA nephropathy leads to Hematuria
-Usually after an upper respiratory infection (The infection generates IgA as IgA protects mucosal site. Too much IgA causes deposition and disease)

68
Q

How is Henoch-Purpura treated?

A

Self-Limited
Treat with steroids if severe

69
Q

What is Hypertension?

A

Increase in blood pressure

70
Q

What are 2 types of hypertension?

A

Pulmonary
Systemic

71
Q

What is the finding for systemic HTN?

A

BP > 140/90

72
Q

What is the etiology for primary HTN?

A

We don’t know

73
Q

Risk factors for primary HTN

A

Age
Race
Obesity
Stress
High Salt Diet
Lack of Physical Activity

74
Q

How does high sodium cause HTN?

A

-Systolic BP is a function of stroke volume
-Diastolic BP is a function of total peripheral resistance
-Sodium increases blood volume and peripheral resistance so increases both systolic and diastolic

75
Q

How does renal artery stenosis cause secondary HTN?

A

Low blood flow to juxtaglomerular apparatus causes release of renin.
Renin converts angiotensin to angiotensin I
Angiotensin I is converted to Angiotensin II by ACE in lung endothelium

76
Q

Angiotensin II increases BP by 2 ways:

A
  • Powerful vasoconstrictor (increases diastolic BP)
  • Stimulates adrenal medulla to secrete aldosterone (it increases sodium reabsorption and potassium excretion from DCT. Water follows sodium and nobody will have more water- increases systolic BP
77
Q

Clinical presentation of Renal Artery Stenosis

A

Atrophy of the stenoses kidney
Increases blood renin

78
Q

Important causes of RAS

A

Atherosclerosis
Fibromuscular Dysplasia

79
Q

What is benign HTN?

A

Mild/Moderate increase in BP
Clinically silent
Vessels and organs are damaged over time

80
Q

What is malignant HTN?

A

Severe increase in BP 200/120 mm Hg
Can arise from pre-existing benign HTN
Pt. Presents with acute end organ damage

81
Q

What is arteriosclerosis?

A

Hardening of arterial wall

82
Q

Atherosclerosis

A

Thickening of intima due to plaque (occurs in medium and large sized vessels)

83
Q

Arteriosclerosis

A

Thickening of small vessels

84
Q

Hyaline Arteriolosclerosis leads to

A

Diabetes, Benign HTN

85
Q

Hyper-plastic Arteriolosclerosis leads to

A

Malignant HTN

86
Q

What is mockenberg medial sclerosis

A

When media is calcified but doesn’t affect lumen size

87
Q

Histology of Artherosclerosis?

A

Intimal plaque that obstructs blood flow, contains necrotic lipid core with a fibromuscular wall

88
Q

4 most common sites for Artherosclerosis

A

Abdominal aorta
Coronary arteries
Popliteal artery
Internal carotid artery

89
Q

Modifiable key risk factors for Atherosclerosis

A

HTN
Hypercholesteremia
Smoking
Diabetes

90
Q

Non-Modifiable Key risk factors for Artherosclerosis?

A

Age
Gender
Genetics

91
Q

Pathogenesis of Atherosclerosis

A

-Intima is damaged –> lipids gets between intima and media –>lipid is oxidized and then
phagocytozed by macrophage –> this makes fatty streak. Fatty streak is seen as early as
teenagers.
-Inflammation, healing and increased deposition of lipid occurs. A fibromuscular cap occurs due to
inflammation and healing

92
Q

What are complications of Atherosclerosis

A

Asymptomatic until occlusion is >70%

93
Q

Stenosis of medium sized vessels

A

Peripheral vascular disease (popliteal A)
Angina (coronary A)
Ischemia bowel disease (mesenteric A)

94
Q

Plaque rupture with thrombosis

A

MI (coronary A)
Stroke (MCA)

95
Q

Plaque rupture with embolisation

A

Results in Artherosclerotic emboli (hallmark is cholesterol cleft in emboli)

96
Q

Aneurysm due to weak wall

A

Atrophic ballooning of the wall

97
Q

Arteriolosclerosis

A

Narrowing of small Arterioles

98
Q

Causes of Arteriolosclerosis

A

Deposition of hyaline or hyperplastic media

99
Q

What is hyaline Arteriolosclerosis

A

Proteins leaking into vessel wall causes vascular thickening
Seen as pink hyaline in microscopy

100
Q

What are 2 causes of Hyaline Arteriolosclerosis?

A

Benign HTN- High pressure forces protein into the vessel wall
Diabetes- Non enzymatic glycosides ion of basement membrane makes vessel wall leaky and protein leaks in. This is how diabetes can cause nephrotic syndrome

101
Q

What is key consequence of hyaline Arteriolosclerosis?

A

Reduced vessel diameter leads to end organ ischemia
Classically produces glomerular scarring which progresses to chronic renal failure

102
Q

What is Hyperplastic Arteriolosclerosis

A

Vessel wall thickens due to hyperplasia of smooth muscle
Onion skin like appearance

103
Q

What causes hyperplastic arteriosclerosis

A

Malignant HTN which leads to acute renal failure and fibrinoid necrosis of vessel

104
Q

Consequences of hyperplastic arteriosclerosis

A

-Reduced vessel diameter leads to end organ ischemia
- Malignant HTN may lead to fibrinoid necrosis of vessel wall (another cause of fibrinoid necrosis is
vasculitis)
- Classically causes ARF with ‘flea-bitten’ appearance - flea-bitten necrosis is due to pin point
hemorrhages (HY)

105
Q

Aortic Dissection

A

Blood leaks into the media through a break in Intima and it rips the media in half

106
Q

What 2 things are needed for aortic dissection?

A

Stress
Pre-existing weakness of media

107
Q

How does HTN weaken media and lead to aortic dissection?

A

Leads to hyaline Arteriolosclerosis of vaso vasorum. Media weakens due to low supply of blood

108
Q

What is the most common cause of aortic dissection

A

HTN

109
Q

What connective tissue disorders can lead to dissection?

A
  • Marfan syndrome - mutation in fibrillin-1 protein. Fibrillin is the base on which elastic fibers are
    laid down. Media has lots of elastic fibers
  • Ehlers-Danlos syndrome - mutation in collagen or proteins that interact with collagen
110
Q

Clinical picture of aortic dissection?

A
  • Presents with tearing chest pain that radiates to the back
  • Most common cause of death is cardiac tamponade. Other causes include aorta bursting open and
    obstruction of arteries that branch off aorta.
111
Q

2 classic locations of Aneurysm

A

Thoracic and Abdominal aneurysm

112
Q

Classic cause of thoracic aneurysm

A
  • Tertiary syphilis- syphilis is end arteritis disease. It affects vaso vasorum and poor blood supply
    weakens aortic wall. Weak vessel wall leads to aneurysm
  • Tree bark appearance of aorta is classic finding - as vaso vasorum is affected, poor blood supply leads to fibrosis and scarring
113
Q

Complications of thoracic aneurysm

A
  • Aortic insufficiency (HY) - as aorta dilates, the valves are pulled apart and can’t close well
  • Compression of mediastinal structures
  • Thrombosis in wall of aneurysm due to disruption in laminar blood flow. It can embolize.
114
Q

Common site of abdominal aortic aneurysm

A

Below the renal arteries and above aortic bifurcation

115
Q

Presentation of AAA

A

60 year old male smoker with HTN
Pulsatile abdominal mass that grows with time

116
Q

Complications of AAA

A

Rupture especially when < 5cm in diameter
Presents with triad of hypotension, pulsatile abdominal pain, and flank pain

117
Q

What is a hemangioma?

A

Benign tumour compromised of blood vessels
Present at birth- regresses during childhood
Involves skin and liver
If pressed it would blanch

118
Q

What is a Angiosarcoma?

A

Malignant proliferation of endothelial cells
Highly aggressive

119
Q

What is Kaposi Sarcoma

A

Will NOT blanch
Low grade malignant proliferation of endothelial cells
HHV-8 virus that drives the tumour
Presents as purple patches, plaques/nodules on skin
Involves visceral organ

Systemic Pathology (2 decks)

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