Circulation Part 2 > Vasculities- Bricks > Flashcards

Vasculities- Bricks Flashcards

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1
Q

Vasculitis is _

A

Vasculitis is inflammation of the blood vessel walls stimulated by activation of the immune system
* It often manifests in predisposed individuals after an environmental trigger

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2
Q

Vasculities can arise as primary conditions or they can be secondary to conditions such as:

A

Vasculities can arise as primary conditions or they can be secondary to conditions such as hepatitis C, rheumatoid arthritis, lupus

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3
Q

What are some of the consequences of untreated vasculitis?

A

If left untreated, vasculitis can lead to
* Tissue ischemia
* Organ necrosis
* Aneurysms

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4
Q

Some general findings of vasculitides include _

A

Some general findings of vasculitides include fever, malaise, elevated ESR and CRP

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5
Q

Large vessel vasculitis includes _ and _

A

Large vessel vasculitis includes Giant Cell arteris and Takayasu arteritis

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6
Q

Giant cell arteritis most commonly affects _

A

Giant cell arteritis most commonly affects carotid artery branches

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7
Q

Takayasu arteritis involves _ and _

A

Takayasu arteritis involves aortic arch and proximal great vessels
* Including subclavian, carotid, mesenteric, renal arteries
* Sometimes called pulseless disease

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8
Q

A patient with new-onset unilateral severe headache in the context of systemic illness may have _

A

A patient with new-onset unilateral severe headache in the context of systemic illness may have Giant Cell arteritis
* Left untreated, this can progress to blindness

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9
Q

Medium vessel vasculitis includes _ and _

A

Medium vessel vasculitis includes polyarteritis nodosa (PAN) and Kawasaki disease

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10
Q

_ is a medium vessel systemic vasculitis that generally involves skin, renal, and visceral vesssels but spares the lungs

A

PAN is a medium vessel systemic vasculitis that generally involves skin, renal, and visceral vesssels but spares the lungs

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10
Q

The leading cause of chest pain in children comes from _

A

The leading cause of chest pain in children comes from Kawasaki disease
* Most often seen in young children

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11
Q

Small vessel vasculitis causes _ , _ , and _ disease but may involve other organs too; patients sometimes have _ or _ skin findings

A

Small vessel vasculitis causes renal , lung , and skin disease but may involve other organs too; patients sometimes have petechiae or palpable purpura skin findings

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12
Q

5 types of small vessel vasculitis

A
  1. Granulomatosis with polyangiitis (GPA)
  2. Eosinophilic granulomatosis with polyangiitis (EGPA)
  3. IgA vasculitis
  4. Microscopic polyangiitis (MPA)
  5. Anti-glomerular basement membrane disease (anti GBM)
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13
Q

The mechanism behind vasculitides involve _

A

The mechanism behind vasculitides involve immune complex deposition and the presence of:
* Antineutrophil cytoplasmic antibodies (ANCAs)
* Anti-endothelial cell antibodies
* Autoreactive T cells

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14
Q

ANCAs are _

A

ANCAs are a group of antibodies directed against components of neutrophils, monocyte lysosomes, endothelial cells
* The exact role of ANCAs in the pathogenesis of vasculitis is unknown but they are thought to mediate damage through the activation of neutrophils –> which then release proteolytic enzymes and reactive oxygen species

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15
Q

C-ANCAs are _ and they target _

A

C-ANCAs are cytoplasmic ANCAs and they target proteinase 3, a component of neutrophil azurophilic granules

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16
Q

P-ANCAs are _ and they target _

A

P-ANCAs are perinuclear ANCAs and they target myeloperoxidase
* Recall that myeloperoxidase is found in lysosomal granules and forms ROS

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17
Q

Name the histologic features of vasculitis

A

Histologic features of vasculitis include:
* Infiltration of WBC fibrinoid necrosis
* Granuloma formation

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18
Q

Fibrinoid necrosis is a type of tissue death seen when _

A

Fibrinoid necrosis is a type of tissue death seen when antigens and antibodies are deposited in vessel walls –> mediates vessel wall destruction

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19
Q

Fibrinoid necrosis is seen in _ and _ vasculitis

A

Fibrinoid necrosis is seen in PAN and SLE vasculitis

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20
Q

Granulomas are characteristic of four types of vasculitides:

A

Granulomas are characteristic of four types of vasculitides:
1. GCA
2. Takayasu arteritis
3. GPA
4. EGPA

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21
Q

Giant cell arteritis (GCA) classically affects _ population

A

Giant cell arteritis (GCA) classically affects older females (50+)

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22
Q

GCA commonly affects _ arteries; it may also involve the vertebral and opthalamic arteries and cause blindness

A

GCA commonly affects temporal arteries; it may also involve the vertebral and opthalamic arteries and cause blindness
* The branches of the ophthalamic artery that arise from the internal carotid artery are at risk

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23
Q

GCA has a strong associated with an inflammatory condition called _ that causes diffuse pain and stiffness of the shoulders, neck, and hips

A

GCA has a strong associated with an inflammatory condition called polymyalgia rheumatica (PMR) that causes diffuse pain and stiffness of the shoulders, neck, and hips

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24
Giant cell arteritis can be characterized by _ on histology; however it is not required for diagnosis
Giant cell arteritis can be characterized by **multinucleated giant cells** on histology; however it is not required for diagnosis
25
The definitive diagnosis for giant cell arteritis is _
The definitive diagnosis for giant cell arteritis is **temporal artery biopsy** * In patients with high suspicion, start treatment right away without biopsy to avoid vision loss ## Footnote Halo seen on doppler ultrasound
26
Treatment for giant cell arteritis is _
Treatment for giant cell arteritis is **high-dose corticosteroids** like prednisone
27
The classic population affected by Takayasu arteritis is _
The classic population affected by Takayasu arteritis is **younger females of Asian descent** * Age of onset 10-40
28
Takayasu arteritis presents with _ symptoms
Takayasu arteritis presents with generalized symptoms as well as **arthralgias, myalgias, claudication, limb pain**
29
The histology of Takayasu is similar to GCA, showing arterial wall inflammation of _ cells
The histology of Takayasu is similar to GCA, showing arterial wall inflammation of **CD4, CD8, histocytes, macrophages, plasma cells**
30
_ is a complication of Takayasu that occurs because of proximal narrowing of the subclavian artery --> retrograde blood flow into the vertebral artery causes syncope, dizziness, and neuro deficits
**Subclavian steal syndrome** is a complication of Takayasu that occurs because of proximal narrowing of the subclavian artery --> retrograde blood flow into the vertebral artery causes syncope, dizziness, and neuro deficits * Essentially we take blood flow from the brain to perfuse the arm --> causes lightheadedness
31
Another complication of Takayasu is vasculitis of the _ arteries which can consequently activate RAAS
Another complication of Takayasu is vasculitis of the **renal arteries** which can consequently activate RAAS * Renovascular hypertension
32
Patient presents with a bruit of the subclavian or abdominal aorta and has a difference in systolic blood pressure between the arms; this might be _
Patient presents with a bruit of the subclavian or abdominal aorta and has a difference in systolic blood pressure between the arms; this might be **Takayasu arteritis**
33
Treatment for Takayasu arteritis is _
Treatment for Takayasu arteritis is **corticosteroids**
34
Explain the process of immune complex deposition of vasculitis
Immune complexes deposit in the walls of vessels --> *activates complement* --> recruits neutrophils --> neutrophils release lysosomal enzymes which damage the vessel wall * This occurs in PAN and IgA
35
The body develops antibodies against components of neutrophils, monocyte lysosomes, and endothelial cells called _
The body develops antibodies against components of neutrophils, monocyte lysosomes, and endothelial cells called **anti-neutrophil cytoplasmic antibodies (ANCAs)**
36
How are ANCAs involved in immune-mediated vasculities?
ANCAs **activate neutrophils --> release proteolytic enzymes and ROS** --> this ends up injuring the vasculature
37
C-ANCA targets _ in the PMN azurophilic granules
C-ANCA targets **proteinase 3** in the PMN azurophilic granules
38
P-ANCA targets _ in the lysosomal granules
P-ANCA targets **myeloperoxidase** in the lysosomal granules
39
We can also have some anti-endothelial cell antibodies involved in _ types of vasculitis
Anti-endothelial cell antibodies: * GPA * Kawasaki disease * Takayasu arteritis
40
Autoreactive T cells can also trigger vascular injury via _
Autoreactive T cells can also trigger vascular injury via **cytokine production --> macrophage activation --. B cell activation --> antibody formation against SM and endothelial cells**
41
The deposition of Ag:Ab complex in the vessel wall leads to a special kind of necrosis called _
The deposition of Ag:Ab complex in the vessel wall leads to a special kind of necrosis called **fibrinoid necrosis**
42
Two defining features of vasculitis include _ and _
Two defining features of vasculitis include **inflammatory WBCs** and **fibrinoid necrosis**
43
Granulomas are nodules of _ and _ cells; they are characteristic of:
Granulomas are nodules of **macrophages** and **giant cells**; they are characteristic of: * GCA * Takayasu arteritis * GPA * EGPA
44
Patient presents with a *focal* granulmona formation and has impaired vision
Patient presents with a *focal* granulmona formation and has impaired vision --> **giant cell arteritis**
45
Two stages of takayasu
*Recall that it is caused by granulomatous inflammation of med-large arteries* 1. **Inflammatory phase** fever, fatigue, weight loss 2. **Stenosis effects** decreased pulses, claudication
46
The best definitive way to diagnose giant cell arteritis is _
The best definitive way to diagnose giant cell arteritis is **biopsy**
47
We can detect Takayasu arteritis via _ imaging
We can detect Takayasu arteritis via **MR angio or CT angio**
48
Kawasaki disease is idiopathic? or may be caused by _
Kawasaki disease is idiopathic? or may be caused by **incidental infection with nonspecific immune system activation** --> systemic necrotizing vasculitis in small-medium vessels
49
How does Kawasaki disease present?
Kawasaki presents with "crash and burn" * Conjunctivitis * Rash * Adenopathy * Strawberry tongue * Hand and foot * Fever for 5 days
50
The danger of kawasaki disease is that about 70% of cases involve the _ arteries
The danger of kawasaki disease is that about 70% of cases involve the **coronary arteries** --> can lead to aneurysm
51
We treat kawasaki disease with _ and _
We treat kawasaki disease with **IVIG** and **aspirin**
52
The medium vessel vasculitis that affects adults (middle aged) is _
The medium vessel vasculitis that affects adults (middle aged) is **Polyarteritis Nodosa** * Affects more males than females
53
Explain the pathogenesis of PAN
PAN is idiopathic --> **type 3 immune response** --> necrotizing inflammation of the vessel wall --> **fibrinoid necrosis** --> thrombosis --> infarct
54
In about 30% of PAN cases, the causative antigen is _
In about 30% of PAN cases, the causative antigen is **Hepatitis B**
55
Classically, PAN affects most organ systems but spares the _
Classically, PAN affects most organ systems but **spares the lungs**
56
The complications of PAN include _
The complications of PAN include **renal failure, MI, stroke**
57
The classic population affected by GPA (granulomatosis with polyangiitis) is _
The classic population affected by GPA (granulomatosis with polyangiitis) is **white middle aged men**
58
Importantly, the pathogenesis of GPA involves _
Importantly, the pathogenesis of GPA involves **c-ANCA**
59
The triad of symptoms in GPA include:
1. **Respiratory tract**- saddle nose deformity 2. **Lung**- infiltrates or cavities causing dyspnea, hemoptysis 3. **Kidney disease**- nephritic syndrome and possible glomerulonephritis
60
GPA may present with _ skin findings
GPA may present with **petechia, pupuric skin lesions**
61
Eosinophilic granulomatosis with polyangiitis (EGPA) typically present in _ population
Eosinophilic granulomatosis with polyangiitis (EGPA) typically present in **adults aged 40-50**
62
Some of the EGPA cases will be positive for _
Some of the EGPA cases will be positive for **p-ANCA** (30-40%)
63
Three stages of progression in EGPA
1. **Allergic rhinitis/ asthma**- or may be sinusitis, nasal polyps 2. **Eosinophilic stage**- high eosinophil count; the lungs and the GI tract are involved --> we have weight loss, fever, malaise, GI bleeding, abdominal pain 3. **Vasculitic stage**- severe blood vessel inflammation --> ischemia to the GI system and heart
64
How does IgA vasculitis normally present?
IgA vasculitis most commonly occurs in **children following a URI** --> IgA immune complexes, fibrin, and complement deposits in small blood vessels
65
Clinical presentations of IgA vasculitis
IgA vasculitis presents as: * Abdominal pain * Arthritis * Glomerulonephritis * Petechiae/ purpura (on the bum)
66
How do we treat IgA vasculitis?
IgA vasculitis is *usually self-limiting*; in severe cases of renal disease we can treat with corticosteroids
67
Microscopic polyangiitis is another small vessel vasculitis that is associated with _
Microscopic polyangiitis is another small vessel vasculitis that is associated with **p-ANCA**
68
MPA can affect multiple organs but the classic triad includes _ , _ , and _
MPA can affect multiple organs but the classic triad includes **lungs** , **kidneys** , and **skin** * Lungs- hemoptysis * Kidneys- hematuria, proteinuria, hypertension * Skin- palpable purpura
69
Mixed cryoglobulinemia syndrome occurs when _
Mixed cryoglobulinemia syndrome occurs when **Ig precipitates at cold temperatures and affects the small vessels**
70
The most common associated pathogen with mixed cryoglobulinemia syndrome is _
The most common associated pathogen with mixed cryoglobulinemia syndrome is **hepatitis C** * HBV * HIV * Bacteria * Fungi * SLE * RA
71
Mixed cryoglobulinemia syndrome presents with many of the same symptoms as the other small vessel vasculitides; however, the classic triad is _
Mixed cryoglobulinemia syndrome presents with many of the same symptoms as the other small vessel vasculitides; however, the classic triad is 1. **Arthralgias** 2. **Palpable purpura** 3. **Weakness** Other symptoms: peripheral neuropathy, liver disease, renal disease, raynauds
72
Goodpasture's syndrome is another name for _
Goodpasture's syndrome is another name for **anti-glomerular basement membrane disease** * Caused by autoantibodies directed against collagen epitopes in the **kidney and lung glomerular/alveolar basement membranes** * Associated with declining renal function and pulmonary hemorrhage
73
Describe the pathophysiology of thromboangiitis obliterans
**Thromboangiitis obliterans** involves acute inflammation of the small-medium arteries of distal limbs --> thombosis --> infarcts --> raynauds, gangrene, etc * **Most commonly caused by smoking!**
74
The classic population to be affected by thromboangiitis obliterans is _
The classic population to be affected by thromboangiitis obliterans is **30-50 year old male who smokes**
75
Raynauds can occur as a primary or secondary phenomenon; it is ultimately a _ in the skin
Raynauds can occur as a primary or secondary phenomenon; it is ultimately a **arterial/arteriolar vasospasm** in the skin * Fingers, toes
76
Raynauds is most classically associated with _
Raynauds is most classically associated with **SLE, scleroderma**
77
How does raynauds present?
Finger transition from pallor --> blue --> red * cold, paresthesia, pain
78
We can treat Raynaud with _ , _ , _
We can treat Raynaud with **Ca2+ channel blockers, alpha blockers, vasodilators**
Circulation Part 2
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