Vascular diseases Flashcards
(541 cards)
1
Q
What does Peripheral Vascular Disease (PVD) refer to?
A
A chronic condition involving the narrowing, blockage, or spasm of blood vessels outside the heart and brain
2
Q
What is the most common cause of Peripheral Vascular Disease (PVD)?
A
Atherosclerosis
3
Q
What are other possible causes of Peripheral Vascular Disease (PVD)?
A
- Thromboembolism
- Vasculitis
- Fibromuscular dysplasia
4
Q
Which areas of the body are most commonly affected by PVD?
A
Lower extremities
5
Q
What is intermittent claudication?
A
Leg pain on exertion relieved by rest
6
Q
List some symptoms associated with Peripheral Vascular Disease (PVD).
A
- Intermittent claudication
- Rest pain
- Non-healing ulcers
- Gangrene
7
Q
What other diseases are associated with Peripheral Vascular Disease (PVD)?
A
- Coronary artery disease
- Cerebrovascular disease
8
Q
What is Acute Limb Ischemia (ALI)?
A
A sudden decrease in limb perfusion that threatens the viability of the limb
9
Q
What are common causes of Acute Limb Ischemia (ALI)?
A
- Embolus
- Thrombosis of a diseased artery
- Trauma
10
Q
Why is Acute Limb Ischemia (ALI) considered a vascular emergency?
A
It can lead to tissue necrosis and limb loss if not treated promptly
11
Q
What is the typical onset time for Acute Limb Ischemia (ALI)?
A
Within hours to days
12
Q
What are the 6 Ps of Acute Limb Ischemia (ALI)?
A
- Pain
- Pallor
- Pulselessness
- Paresthesia
- Paralysis
- Poikilothermia
13
Q
What urgent treatments are required for Acute Limb Ischemia (ALI)?
A
- Thrombectomy
- Thrombolysis
- Bypass
14
Q
What is the most common cause of arterial occlusion?
A
Embolism; often cardiac (e.g., atrial fibrillation, mural thrombus, prosthetic valve)
15
Q
What is thrombosis in situ?
A
Acute thrombosis superimposed on a pre-existing atherosclerotic plaque
16
Q
What causes arterial injury from trauma?
A
Fracture, dislocation, penetrating trauma, or iatrogenic (e.g., catheterization)
17
Q
What is arterial dissection?
A
Intimal tear leads to occlusion of flow (e.g., aortic dissection extending into limb arteries)
18
Q
What is a popliteal artery aneurysm?
A
Can thrombose or embolize distally
19
Q
What is vasculitis?
A
Inflammatory damage to vessels may cause thrombosis
20
Q
What are hypercoagulable states?
A
Cancer, antiphospholipid syndrome, inherited thrombophilias
21
Q
What are iatrogenic causes of arterial occlusion?
A
Post-surgical or catheter-based interventions (e.g., arterial cannulation, stenting)
22
Q
What does sudden, severe limb pain indicate?
A
Ischemia
23
Q
What does pallor indicate?
A
Pale or mottled appearance from lack of perfusion
24
Q
What does pulselessness mean?
A
Absence of distal pulses on palpation or Doppler
25
What is paresthesia?
Numbness or tingling from ischemic nerve injury
26
What does paralysis indicate?
Weakness or inability to move limb; a late and ominous sign
27
What is poikilothermia?
Coolness of the limb; temperature matches environment (cold limb)
28
What additional findings may occur with ischemia?
Skin changes: mottling, cyanosis, delayed capillary refill; Muscle tenderness: due to ischemic injury; Demarcation line: may appear if necrosis develops
29
What factors affect the severity and reversibility of ischemia?
Time to intervention
30
What do neurological signs like paresthesia and paralysis suggest?
Advanced ischemia and may indicate irreversible damage
31
What are the '6 Ps' to look for in Acute Limb Ischemia?
Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia
## Footnote
These signs are critical in the clinical assessment of limb ischemia.
32
Why is the time of onset crucial in Acute Limb Ischemia?
Limb viability deteriorates rapidly
## Footnote
Timely intervention is essential to prevent irreversible damage.
33
What is assessed to evaluate the severity of Acute Limb Ischemia?
Neurologic status (sensory/motor loss)
## Footnote
This helps in determining the urgency of intervention.
34
What is the purpose of Bedside Doppler Ultrasound in diagnosing ALI?
To assess presence or absence of pulses
## Footnote
It provides an audible signal over the artery and distinguishes between arterial and venous signals.
35
What imaging modality is considered the gold standard for ALI?
Digital Subtraction Angiography (DSA)
## Footnote
It is used during catheter-directed intervention.
36
What is the first immediate measure in managing Acute Limb Ischemia?
Anticoagulation
## Footnote
Typically involves IV Heparin bolus followed by infusion.
37
What are the management categories for limb viability in ALI?
I – Viable
IIa – Threatened (mild)
IIb – Threatened (severe)
III – Irreversible
## Footnote
Each category has specific management strategies.
38
What is indicated for a Category I limb in ALI?
Urgent work-up, non-emergent revascularization
## Footnote
No sensory/motor loss and audible Doppler pulses are present.
39
What is the management for a Category IIb limb in ALI?
Immediate revascularization
## Footnote
This is necessary due to sensory/motor deficit and immediate threat.
40
What management is indicated for Category III limbs?
Amputation
## Footnote
Revascularization is not viable for limbs with profound anesthesia/paralysis.
41
What is catheter-directed thrombolysis used for?
For embolic/thrombotic occlusions in viable or marginally threatened limbs
## Footnote
It is a specific intervention aimed at restoring blood flow.
42
What is the emerging technique for removing clots in ALI?
Percutaneous mechanical thrombectomy
## Footnote
This method allows for clot removal without open surgery.
43
What should be monitored for after revascularization?
Reperfusion injury: compartment syndrome, acidosis, hyperkalemia, renal failure
## Footnote
These complications can arise following successful revascularization.
44
What is the transition of anticoagulation after revascularization?
From heparin to warfarin or DOAC
## Footnote
This ensures continued prevention of thrombus formation.
45
Fill in the blank: ALI is a _______.
vascular emergency
## Footnote
Immediate management is critical to limb survival.
46
What are the '6 Ps' to look for in Acute Limb Ischemia?
Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia
## Footnote
These signs are critical in the clinical assessment of limb ischemia.
47
Why is the time of onset crucial in Acute Limb Ischemia?
Limb viability deteriorates rapidly
## Footnote
Timely intervention is essential to prevent irreversible damage.
48
What is assessed to evaluate the severity of Acute Limb Ischemia?
Neurologic status (sensory/motor loss)
## Footnote
This helps in determining the urgency of intervention.
49
What is the purpose of Bedside Doppler Ultrasound in diagnosing ALI?
To assess presence or absence of pulses
## Footnote
It provides an audible signal over the artery and distinguishes between arterial and venous signals.
50
What imaging modality is considered the gold standard for ALI?
Digital Subtraction Angiography (DSA)
## Footnote
It is used during catheter-directed intervention.
51
What is the first immediate measure in managing Acute Limb Ischemia?
Anticoagulation
## Footnote
Typically involves IV Heparin bolus followed by infusion.
52
What are the management categories for limb viability in ALI?
I – Viable
IIa – Threatened (mild)
IIb – Threatened (severe)
III – Irreversible
## Footnote
Each category has specific management strategies.
53
What is indicated for a Category I limb in ALI?
Urgent work-up, non-emergent revascularization
## Footnote
No sensory/motor loss and audible Doppler pulses are present.
54
What is the management for a Category IIb limb in ALI?
Immediate revascularization
## Footnote
This is necessary due to sensory/motor deficit and immediate threat.
55
What management is indicated for Category III limbs?
Amputation
## Footnote
Revascularization is not viable for limbs with profound anesthesia/paralysis.
56
What is catheter-directed thrombolysis used for?
For embolic/thrombotic occlusions in viable or marginally threatened limbs
## Footnote
It is a specific intervention aimed at restoring blood flow.
57
What is the emerging technique for removing clots in ALI?
Percutaneous mechanical thrombectomy
## Footnote
This method allows for clot removal without open surgery.
58
What should be monitored for after revascularization?
Reperfusion injury: compartment syndrome, acidosis, hyperkalemia, renal failure
## Footnote
These complications can arise following successful revascularization.
59
What is the transition of anticoagulation after revascularization?
From heparin to warfarin or DOAC
## Footnote
This ensures continued prevention of thrombus formation.
60
Fill in the blank: ALI is a _______.
vascular emergency
## Footnote
Immediate management is critical to limb survival.
61
What is the most common cause of chronic lower limb ischemia?
Atherosclerosis
## Footnote
A progressive plaque buildup that narrows large and medium arteries
62
Name a factor that accelerates atherosclerosis and contributes to microvascular disease.
Diabetes Mellitus
## Footnote
It is a significant risk factor for vascular complications.
63
What is considered a major modifiable risk factor for chronic lower limb ischemia?
Smoking
## Footnote
Smoking causes endothelial damage, which worsens vascular health.
64
How does hypertension contribute to chronic lower limb ischemia?
Damages vascular endothelium and promotes atherosclerosis
## Footnote
Hypertension is a significant risk factor for vascular diseases.
65
What role does hyperlipidemia play in chronic lower limb ischemia?
Promotes plaque formation
## Footnote
High levels of lipids in the blood contribute to arterial blockages.
66
Which condition is associated with vascular calcification and atherosclerosis?
Chronic kidney disease
## Footnote
This condition can worsen vascular health over time.
67
What is vasculitis, and how does it relate to chronic lower limb ischemia?
Inflammatory arterial damage
## Footnote
Conditions like Takayasu arteritis and Buerger’s disease can cause ischemia.
68
How can radiation therapy affect the arteries?
Causes fibrosis and narrowing of vessels
## Footnote
This can lead to reduced blood flow and ischemia.
69
What is fibromuscular dysplasia, and who does it mainly affect?
A rare condition affecting young females that leads to arterial narrowing
## Footnote
It can cause ischemic symptoms in this demographic.
70
Define intermittent claudication.
Cramping leg pain on exertion, relieved by rest
## Footnote
This is a common symptom of chronic lower limb ischemia.
71
What does rest pain indicate in the context of chronic lower limb ischemia?
Indicates critical limb ischemia
## Footnote
Occurs at night or when the limb is elevated.
72
What are the signs of decreased or absent pulses in chronic lower limb ischemia?
On palpation of femoral, popliteal, dorsalis pedis, or posterior tibial pulse
## Footnote
This indicates reduced blood flow to the limb.
73
What does a cool, pale limb signify?
Reduced blood flow
## Footnote
This is a physical manifestation of ischemia.
74
What causes muscle atrophy in chronic lower limb ischemia?
Chronic hypoperfusion leads to disuse and wasting
## Footnote
Reduced blood supply affects muscle health.
75
What trophic changes can occur due to poor perfusion?
Hair loss and thin skin
## Footnote
These changes are indicative of chronic ischemia.
76
What changes can occur in toenails due to long-term ischemia?
Brittle or thick toenails
## Footnote
This is a symptom of chronic lower limb ischemia.
77
What is a non-healing ulcer, and where is it commonly found?
Ulcers especially over pressure points like heels or toes
## Footnote
They are a serious complication of chronic ischemia.
78
What is gangrene, and when does it occur in chronic lower limb ischemia?
Late sign of tissue death, may be wet (infected) or dry
## Footnote
It indicates severe ischemic damage.
79
What is the purpose of Fontaine Staging?
Helpful in grading severity of chronic ischemia
## Footnote
It provides a systematic approach to assess ischemia.
80
What are the clinical features of Stage I in Fontaine Staging?
Asymptomatic
## Footnote
No symptoms are present in this initial stage.
81
What distinguishes Stage IIa from Stage IIb in Fontaine Staging?
Stage IIa has mild claudication (walking >200 meters), Stage IIb has moderate to severe claudication (<200 meters)
## Footnote
This classification helps assess the severity of symptoms.
82
What characterizes Stage III in Fontaine Staging?
Rest pain
## Footnote
This indicates a more severe level of ischemia.
83
What are the manifestations of Stage IV in Fontaine Staging?
Ulceration or gangrene
## Footnote
This stage indicates critical limb ischemia with severe complications.
84
What is the most common cause of chronic lower limb ischemia?
Atherosclerosis
## Footnote
A progressive plaque buildup that narrows large and medium arteries
85
Name a factor that accelerates atherosclerosis and contributes to microvascular disease.
Diabetes Mellitus
## Footnote
It is a significant risk factor for vascular complications.
86
What is considered a major modifiable risk factor for chronic lower limb ischemia?
Smoking
## Footnote
Smoking causes endothelial damage, which worsens vascular health.
87
How does hypertension contribute to chronic lower limb ischemia?
Damages vascular endothelium and promotes atherosclerosis
## Footnote
Hypertension is a significant risk factor for vascular diseases.
88
What role does hyperlipidemia play in chronic lower limb ischemia?
Promotes plaque formation
## Footnote
High levels of lipids in the blood contribute to arterial blockages.
89
Which condition is associated with vascular calcification and atherosclerosis?
Chronic kidney disease
## Footnote
This condition can worsen vascular health over time.
90
What is vasculitis, and how does it relate to chronic lower limb ischemia?
Inflammatory arterial damage
## Footnote
Conditions like Takayasu arteritis and Buerger’s disease can cause ischemia.
91
How can radiation therapy affect the arteries?
Causes fibrosis and narrowing of vessels
## Footnote
This can lead to reduced blood flow and ischemia.
92
What is fibromuscular dysplasia, and who does it mainly affect?
A rare condition affecting young females that leads to arterial narrowing
## Footnote
It can cause ischemic symptoms in this demographic.
93
Define intermittent claudication.
Cramping leg pain on exertion, relieved by rest
## Footnote
This is a common symptom of chronic lower limb ischemia.
94
What does rest pain indicate in the context of chronic lower limb ischemia?
Indicates critical limb ischemia
## Footnote
Occurs at night or when the limb is elevated.
95
What are the signs of decreased or absent pulses in chronic lower limb ischemia?
On palpation of femoral, popliteal, dorsalis pedis, or posterior tibial pulse
## Footnote
This indicates reduced blood flow to the limb.
96
What does a cool, pale limb signify?
Reduced blood flow
## Footnote
This is a physical manifestation of ischemia.
97
What causes muscle atrophy in chronic lower limb ischemia?
Chronic hypoperfusion leads to disuse and wasting
## Footnote
Reduced blood supply affects muscle health.
98
What trophic changes can occur due to poor perfusion?
Hair loss and thin skin
## Footnote
These changes are indicative of chronic ischemia.
99
What changes can occur in toenails due to long-term ischemia?
Brittle or thick toenails
## Footnote
This is a symptom of chronic lower limb ischemia.
100
What is a non-healing ulcer, and where is it commonly found?
Ulcers especially over pressure points like heels or toes
## Footnote
They are a serious complication of chronic ischemia.
101
What is gangrene, and when does it occur in chronic lower limb ischemia?
Late sign of tissue death, may be wet (infected) or dry
## Footnote
It indicates severe ischemic damage.
102
What is the purpose of Fontaine Staging?
Helpful in grading severity of chronic ischemia
## Footnote
It provides a systematic approach to assess ischemia.
103
What are the clinical features of Stage I in Fontaine Staging?
Asymptomatic
## Footnote
No symptoms are present in this initial stage.
104
What distinguishes Stage IIa from Stage IIb in Fontaine Staging?
Stage IIa has mild claudication (walking >200 meters), Stage IIb has moderate to severe claudication (<200 meters)
## Footnote
This classification helps assess the severity of symptoms.
105
What characterizes Stage III in Fontaine Staging?
Rest pain
## Footnote
This indicates a more severe level of ischemia.
106
What are the manifestations of Stage IV in Fontaine Staging?
Ulceration or gangrene
## Footnote
This stage indicates critical limb ischemia with severe complications.
107
What is chronic limb ischemia?
A progressive condition marked by reduced blood flow to the lower extremities over time.
## Footnote
It often leads to symptoms like intermittent claudication and rest pain.
108
What are classic symptoms of chronic limb ischemia?
Intermittent claudication and rest pain.
## Footnote
Intermittent claudication is exertional leg pain relieved by rest.
109
What cardiovascular risk factors are commonly associated with chronic limb ischemia?
* Smoking
* Diabetes
* Hypertension
* Hyperlipidemia
* Chronic kidney disease
110
What is involved in the pulse assessment during physical examination?
Careful palpation of peripheral pulses: femoral, popliteal, dorsalis pedis, and posterior tibial arteries.
## Footnote
Diminished or absent pulses raise suspicion for arterial narrowing.
111
What skin and trophic changes are indicative of poor perfusion?
* Pallor
* Coolness
* Hair loss
* Nonhealing ulcers
112
What is functional assessment in the context of chronic limb ischemia?
Documentation of walking distances and the impact of claudication on daily activities to help stage the disease.
113
What are the Fontaine stages of clinical staging for chronic limb ischemia?
* Stage I: Asymptomatic
* Stage IIa: Claudication (mild)
* Stage IIb: Claudication (moderate-severe)
* Stage III: Rest pain
* Stage IV: Presence of ulcers or gangrene
114
What is the Ankle-Brachial Index (ABI)?
A simple, cost-effective screening tool that compares systolic blood pressures in the ankle and arm.
## Footnote
An ABI less than 0.90 suggests peripheral arterial disease.
115
What does Duplex Ultrasound evaluate in chronic limb ischemia?
Visualizes arterial flow, determines the location and extent of stenosis, and estimates blood flow velocity.
116
What is CT Angiography (CTA) used for?
Offers detailed anatomical views of arterial lesions, calcifications, and collateral networks.
117
What is the advantage of Magnetic Resonance Angiography (MRA)?
Provides high-resolution images without ionizing radiation.
118
What is Digital Subtraction Angiography (DSA)?
The gold standard for delineating vascular anatomy, especially when planning revascularization procedures.
## Footnote
DSA also allows for simultaneous therapeutic intervention.
119
What are the key components of conservative management for chronic limb ischemia?
* Lifestyle Modifications
* Pharmacotherapy
120
What lifestyle modifications are recommended for chronic limb ischemia?
* Smoking cessation
* Exercise therapy
* Optimizing diet
121
What pharmacotherapy is generally recommended for chronic limb ischemia?
* Antiplatelet therapy (low-dose aspirin or clopidogrel)
* Statins
* Antihypertensive medications
* Diabetic control
122
When is revascularization considered for chronic limb ischemia?
When symptoms significantly impair quality of life or when there is evidence of tissue loss.
123
What are the two main approaches to revascularization?
* Endovascular revascularization
* Surgical revascularization
124
What procedures are included in endovascular revascularization?
* Angioplasty and stenting
* Atherectomy
125
What is involved in surgical revascularization?
* Bypass surgery
* Endarterectomy
126
What is the importance of wound care in chronic limb ischemia management?
Critical for promoting healing and preventing infection in patients with ulcers or tissue loss.
127
What role does pain management play in chronic limb ischemia?
May be required for patients with rest pain; optimizing perfusion usually improves symptoms.
128
What is the purpose of long-term surveillance in chronic limb ischemia management?
Regular follow-up with noninvasive vascular studies helps monitor for re-stenosis or progression of disease.
129
What is aortic dissection?
A life-threatening condition involving a tear in the intimal layer of the aortic wall, allowing blood to enter the media and create a false lumen.
130
What are the potential consequences of aortic dissection?
Rupture, ischemia of organs, aortic valve insufficiency.
131
What is the incidence of aortic dissection?
Approximately 3–5 cases per 100,000 person-years.
132
Which age group is most commonly affected by aortic dissection?
Adults aged 60–80 years.
133
Which gender is more commonly affected by aortic dissection?
Males (male-to-female ratio ~2:1).
134
What happens to mortality rates in untreated aortic dissection?
Mortality increases 1% per hour after symptom onset.
135
What is the most important modifiable risk factor for aortic dissection?
Chronic hypertension.
136
Name a connective tissue disorder that is a risk factor for aortic dissection.
Marfan syndrome or Ehlers-Danlos syndrome.
137
What are some additional risk factors for aortic dissection? (List at least two)
* Bicuspid aortic valve or coarctation of the aorta
* Aortic aneurysm
* Iatrogenic causes (e.g., catheterization, cardiac surgery)
* Pregnancy (particularly in the third trimester)
* Cocaine or stimulant use.
138
What classification system is used for aortic dissection?
Stanford classification.
139
What is Stanford Type A aortic dissection?
Involves the ascending aorta (with or without descending aorta involvement); more common and more dangerous.
140
What is Stanford Type B aortic dissection?
Involves the descending aorta only (distal to left subclavian).
141
What is the most common risk factor for aortic dissection?
Hypertension
## Footnote
Chronic pressure damages intima and media
142
Name two connective tissue disorders that affect collagen and elastin.
* Marfan syndrome
* Ehlers-Danlos syndrome (type IV)
## Footnote
These disorders can increase the risk of aortic dissection.
143
What congenital heart diseases are associated with aortic dissection?
* Bicuspid aortic valve
* Coarctation of the aorta
## Footnote
These conditions can predispose individuals to aortic dissection.
144
How do aortic aneurysms affect the risk of dissection?
Aortic aneurysms increase the risk due to wall dilation
## Footnote
The dilation weakens the aortic wall, making it more susceptible.
145
What is an iatrogenic risk factor for aortic dissection?
Aortic instrumentation (e.g., catheterization, surgery)
## Footnote
Medical procedures can inadvertently damage the aorta.
146
What type of trauma can cause intimal tears leading to aortic dissection?
Deceleration injuries
## Footnote
These injuries can cause significant stress on the aortic wall.
147
Name two inflammatory conditions that are risk factors for aortic dissection.
* Giant cell arteritis
* Takayasu arteritis
## Footnote
Vasculitis can weaken the aortic wall.
148
During which trimester of pregnancy is the risk of aortic dissection particularly increased?
Third trimester
## Footnote
Hormonal changes weaken connective tissue during this period.
149
Which substances can cause sudden blood pressure surges that may lead to aortic dissection?
* Cocaine
* Amphetamines
## Footnote
Stimulant use can dramatically increase blood pressure.
150
What role does family history play in aortic dissection?
Genetic predisposition in familial thoracic aortic disease
## Footnote
A family history can indicate an increased risk.
151
What age range is more commonly affected by aortic dissection?
60–80 years
## Footnote
Older age is a significant risk factor.
152
Which sex is more commonly affected by aortic dissection?
Males
## Footnote
There is a higher incidence of aortic dissection in males.
153
What is cystic medial degeneration (CMD)?
A histopathological hallmark of aortic wall weakening characterized by:
* Loss of smooth muscle cells
* Fragmentation of elastic fibers
* Accumulation of basophilic ground substance (mucin) in the tunica media
* Formation of cyst-like spaces devoid of structural support
## Footnote
CMD is crucial in the context of aortic dissection.
154
Why is cystic medial degeneration important in aortic dissection?
* Weakens the media, the main load-bearing layer
* Makes it vulnerable to intimal tearing
* Facilitates propagation of the dissection plane once blood enters
## Footnote
The structural integrity of the aorta is compromised by CMD.
155
In which conditions is cystic medial degeneration especially prevalent?
* Marfan syndrome
* Ehlers-Danlos syndrome
* Age-related degeneration
* Hypertensive patients with chronic medial stress
## Footnote
These conditions are associated with increased risk of CMD.
156
What is the most common risk factor for aortic dissection?
Hypertension
## Footnote
Chronic pressure damages intima and media
157
Name two connective tissue disorders that affect collagen and elastin.
* Marfan syndrome
* Ehlers-Danlos syndrome (type IV)
## Footnote
These disorders can increase the risk of aortic dissection.
158
What congenital heart diseases are associated with aortic dissection?
* Bicuspid aortic valve
* Coarctation of the aorta
## Footnote
These conditions can predispose individuals to aortic dissection.
159
How do aortic aneurysms affect the risk of dissection?
Aortic aneurysms increase the risk due to wall dilation
## Footnote
The dilation weakens the aortic wall, making it more susceptible.
160
What is an iatrogenic risk factor for aortic dissection?
Aortic instrumentation (e.g., catheterization, surgery)
## Footnote
Medical procedures can inadvertently damage the aorta.
161
What type of trauma can cause intimal tears leading to aortic dissection?
Deceleration injuries
## Footnote
These injuries can cause significant stress on the aortic wall.
162
Name two inflammatory conditions that are risk factors for aortic dissection.
* Giant cell arteritis
* Takayasu arteritis
## Footnote
Vasculitis can weaken the aortic wall.
163
During which trimester of pregnancy is the risk of aortic dissection particularly increased?
Third trimester
## Footnote
Hormonal changes weaken connective tissue during this period.
164
Which substances can cause sudden blood pressure surges that may lead to aortic dissection?
* Cocaine
* Amphetamines
## Footnote
Stimulant use can dramatically increase blood pressure.
165
What role does family history play in aortic dissection?
Genetic predisposition in familial thoracic aortic disease
## Footnote
A family history can indicate an increased risk.
166
What age range is more commonly affected by aortic dissection?
60–80 years
## Footnote
Older age is a significant risk factor.
167
Which sex is more commonly affected by aortic dissection?
Males
## Footnote
There is a higher incidence of aortic dissection in males.
168
What is cystic medial degeneration (CMD)?
A histopathological hallmark of aortic wall weakening characterized by:
* Loss of smooth muscle cells
* Fragmentation of elastic fibers
* Accumulation of basophilic ground substance (mucin) in the tunica media
* Formation of cyst-like spaces devoid of structural support
## Footnote
CMD is crucial in the context of aortic dissection.
169
Why is cystic medial degeneration important in aortic dissection?
* Weakens the media, the main load-bearing layer
* Makes it vulnerable to intimal tearing
* Facilitates propagation of the dissection plane once blood enters
## Footnote
The structural integrity of the aorta is compromised by CMD.
170
In which conditions is cystic medial degeneration especially prevalent?
* Marfan syndrome
* Ehlers-Danlos syndrome
* Age-related degeneration
* Hypertensive patients with chronic medial stress
## Footnote
These conditions are associated with increased risk of CMD.
171
What classification involves the Ascending Aorta?
Stanford A and DeBakey I and II
## Footnote
Stanford A and DeBakey I and II classifications involve the Ascending Aorta.
172
What is the origin of Stanford A classification?
Ascending aorta
## Footnote
Stanford A originates from the Ascending aorta.
173
What is the extent of Stanford A classification?
May extend distally
## Footnote
Stanford A may extend distally beyond the initial origin.
174
What is the typical management for Stanford A classification?
Surgical
## Footnote
Stanford A typically requires surgical management.
175
Does Stanford B classification involve the Ascending Aorta?
No
## Footnote
Stanford B does not involve the Ascending Aorta.
176
What is the origin of Stanford B classification?
Descending aorta
## Footnote
Stanford B originates from the Descending aorta.
177
What is the extent of Stanford B classification?
Distal to left subclavian artery
## Footnote
Stanford B extends distal to the left subclavian artery.
178
What is the typical management for Stanford B classification?
Medical ± Endovascular
## Footnote
Stanford B is typically managed medically or with endovascular techniques.
179
What classification involves the Ascending Aorta and extends to the Descending Aorta?
DeBakey I
## Footnote
DeBakey I classification involves both Ascending and Descending Aorta.
180
What is the origin of DeBakey I classification?
Ascending aorta
## Footnote
DeBakey I originates from the Ascending aorta.
181
What is the typical management for DeBakey I classification?
Surgical
## Footnote
DeBakey I requires surgical management.
182
What classification involves the Ascending Aorta but only extends to the Ascending Aorta?
DeBakey II
## Footnote
DeBakey II classification involves only the Ascending Aorta.
183
What is the typical management for DeBakey II classification?
Surgical
## Footnote
DeBakey II typically requires surgical management.
184
Does DeBakey III classification involve the Ascending Aorta?
No
## Footnote
DeBakey III does not involve the Ascending Aorta.
185
What is the origin of DeBakey III classification?
Descending aorta
## Footnote
DeBakey III originates from the Descending aorta.
186
What are the extents of DeBakey III classification?
Limited (IIIa) or extends (IIIb)
## Footnote
DeBakey III can be limited (IIIa) or extend (IIIb).
187
What is the typical management for DeBakey III classification?
Medical ± Endovascular
## Footnote
DeBakey III is typically managed medically or with endovascular techniques.
188
What factors determine the symptoms and signs of aortic dissection?
Location of the dissection, extent of involvement, complications
## Footnote
Examples of complications include tamponade and ischemia.
189
What is the most common symptom of aortic dissection?
Sudden, severe chest pain
## Footnote
Described as 'tearing' or 'ripping', often radiates to the back.
190
What does pain migration in aortic dissection indicate?
Pain may shift as the dissection progresses along the aorta.
191
What does hypotension suggest in the context of aortic dissection?
Tamponade or rupture.
192
What symptom may result from tamponade, stroke, or vagal response in aortic dissection?
Syncope.
193
What feeling is commonly associated with severe cardiovascular catastrophes, including aortic dissection?
Sense of impending doom.
194
What is a characteristic manifestation of Stanford Type A aortic dissection?
Anterior chest pain
## Footnote
Caused by dissection of the ascending aorta.
195
What causes aortic regurgitation in Stanford Type A aortic dissection?
Extension into aortic valve leading to early diastolic murmur.
196
What is a possible consequence of cardiac tamponade in Stanford Type A aortic dissection?
Hemopericardium from rupture into pericardial space.
197
What can occur if the dissection extends into the carotid arteries?
Stroke or altered consciousness.
198
What is a possible cause of myocardial infarction in Stanford Type A aortic dissection?
Occlusion of coronary arteries, especially RCA.
199
What is a manifestation of Stanford Type B aortic dissection?
Interscapular or back pain
## Footnote
Caused by dissection of the descending thoracic aorta.
200
What can abdominal pain in Stanford Type B aortic dissection indicate?
Extension into abdominal aorta or mesenteric ischemia.
201
What is a possible consequence of obstruction of iliac or femoral arteries in Stanford Type B aortic dissection?
Lower limb ischemia.
202
What can compromise spinal arteries leading to paraplegia in aortic dissection?
Compromise of the artery of Adamkiewicz.
203
What may indicate renal failure or hematuria in Stanford Type B aortic dissection?
Extension into renal arteries.
204
What sign may indicate dissection involving the subclavian artery?
Unequal blood pressure in arms.
205
What does pulse deficit indicate during examination of aortic dissection?
Asymmetric or absent pulses in limbs.
206
What new murmur might be heard in aortic dissection and what does it indicate?
New murmur (early diastolic) indicating aortic regurgitation from aortic valve involvement.
207
What could cause hypotension/shock in a patient with aortic dissection?
Cardiac tamponade, massive blood loss, or rupture.
208
What is a critical indicator of aortic dissection in patients?
Sudden, severe “tearing” chest or back pain, pulse deficits or BP differences between limbs, history of hypertension, Marfan syndrome, bicuspid aortic valve
## Footnote
High index of suspicion is essential in these cases.
209
What is the purpose of an ECG in suspected aortic dissection?
To rule out myocardial infarction (MI)
## Footnote
ECG usually shows normal or nonspecific changes in aortic dissection.
210
What can a chest X-ray reveal in cases of aortic dissection?
Widened mediastinum, pleural effusion (especially left-sided)
## Footnote
These findings can be indicative of aortic dissection.
211
What does an elevated D-dimer indicate in aortic dissection?
May be elevated but is not specific; useful for low-risk exclusion
## Footnote
D-dimer levels can help in determining risk but are not definitive.
212
What is the first-line imaging technique for aortic dissection?
CT Angiography (CTA)
## Footnote
CTA is quick, widely available, and provides excellent detail.
213
When is Transesophageal Echo (TEE) particularly useful?
In unstable patients or at bedside (especially in ICU or intraoperatively)
## Footnote
TEE provides critical information in emergency situations.
214
What is the most sensitive imaging method for aortic dissection?
MRI Angiography
## Footnote
However, it is time-consuming and rarely used in emergencies.
215
What was historically the gold standard for imaging aortic dissection?
Aortography
## Footnote
It is now rarely used except during interventions.
216
What are the initial emergency management steps for all patients with aortic dissection?
ICU Admission, hemodynamic stabilization, pain control, oxygen, fluids, and monitoring
## Footnote
These steps are critical for managing aortic dissection.
217
What medications are used for hemodynamic stabilization in aortic dissection?
IV β-blockers (e.g., labetalol, esmolol), IV vasodilators (e.g., nitroprusside)
## Footnote
These medications help reduce heart rate and shear stress.
218
What are the target goals for heart rate and systolic blood pressure in aortic dissection management?
HR: <60 bpm, SBP: 100–120 mmHg
## Footnote
These targets help in stabilizing the patient.
219
What type of surgical intervention is required for Stanford Type A aortic dissection?
Urgent surgical repair: replace ascending aorta ± aortic valve
## Footnote
Type A dissections are critical and require prompt surgical intervention.
220
What is the initial management approach for Stanford Type B aortic dissection?
Initial medical management unless complications arise
## Footnote
Complications may necessitate endovascular repair (TEVAR) or surgery.
221
What are the preferred long-term management strategies for aortic dissection?
Lifelong blood pressure control, surveillance imaging, avoid heavy lifting and contact sports, genetic screening
## Footnote
These strategies help prevent complications and monitor patient health.
222
What complications should be monitored in patients with aortic dissection?
Cardiac tamponade, aortic regurgitation, stroke or MI, renal failure, limb or visceral ischemia, rupture
## Footnote
These complications can have serious consequences and require vigilant monitoring.
223
Fill in the blank: The preferred medication for blood pressure control in long-term management of aortic dissection is _______.
β-blockers
## Footnote
β-blockers are recommended for lifelong blood pressure control.
224
What is the definition of an aneurysm?
A localized, abnormal dilation of a blood vessel wall that exceeds 50% of the vessel's normal diameter
## Footnote
Occurs due to structural weakness in the vascular wall and can affect arteries or veins
225
What are the three layers involved in a true aneurysm?
Intima, media, adventitia
## Footnote
A true aneurysm involves all three layers of the vessel wall
226
What is a false aneurysm (pseudoaneurysm)?
Blood escapes the vessel but is contained by surrounding tissues or adventitia
## Footnote
Often post-traumatic or post-surgical
227
Define a saccular aneurysm.
Outpouching on one side of the vessel
## Footnote
Characterized by a localized bulge
228
What is a fusiform aneurysm?
Circumferential, symmetrical dilation of the vessel
## Footnote
Involves a uniform expansion around the entire circumference
229
What characterizes a dissecting aneurysm?
Blood dissects between layers of the vessel wall
## Footnote
Commonly occurs in the aorta
230
What is the most common type of true aneurysm?
Abdominal Aortic Aneurysm (AAA)
## Footnote
Prevalence is ~4–8% in men over 65 years
231
What are the main risk factors for Abdominal Aortic Aneurysm (AAA)?
* Age > 60
* Male sex
* Smoking
* Hypertension
* Atherosclerosis
* Family history
## Footnote
Smoking is noted as the strongest modifiable risk factor
232
What conditions are associated with Thoracic Aortic Aneurysm (TAA)?
* Hypertension
* Connective tissue disorders (e.g., Marfan, Ehlers-Danlos)
* Bicuspid aortic valve
* Syphilitic aortitis
* Trauma or dissection
## Footnote
TAA is less common than AAA
233
Where do cerebral (Berry) aneurysms typically occur?
At arterial branch points in the Circle of Willis
## Footnote
Prevalence is ~1–2% of the population and often asymptomatic
234
What are the risk factors for cerebral (Berry) aneurysms?
* Hypertension
* Smoking
* Polycystic kidney disease
* Family history
## Footnote
These factors increase the likelihood of developing cerebral aneurysms
235
Which arteries are most commonly involved in peripheral aneurysms?
Femoral and popliteal arteries
## Footnote
Often associated with other aneurysms, especially AAA
236
True or False: Aneurysms can be asymptomatic until rupture or thrombosis.
True
## Footnote
This emphasizes the importance of monitoring and screening
237
What is recommended for screening for AAA?
Recommended in men >65 years who have ever smoked
## Footnote
This guideline aims to catch potential aneurysms early
238
Fill in the blank: The risk of aneurysms increases with _______.
age, hypertension, and smoking
## Footnote
These factors are critical in assessing an individual's risk
239
What is the definition of a saccular aneurysm?
Localized outpouching involving only a portion of the vessel wall, often spherical and asymmetric.
## Footnote
Common in cerebral (berry) aneurysms.
240
What characterizes a fusiform aneurysm?
Uniform, circumferential dilation of a long segment of the vessel, typical of abdominal aortic aneurysms (AAA).
## Footnote
This type of aneurysm affects the vessel uniformly along its length.
241
What occurs in a dissecting aneurysm?
Blood enters the vessel wall and splits its layers, most commonly affecting the aorta (aortic dissection).
## Footnote
This condition can lead to serious complications if not managed properly.
242
What is a true aneurysm?
Involves all three layers of the arterial wall: intima, media, and adventitia (e.g., AAA, TAA).
## Footnote
True aneurysms maintain the structural integrity of the vessel wall.
243
What defines a false aneurysm (pseudoaneurysm)?
Disruption of the vessel wall with blood contained by surrounding tissue; no intact vessel wall, often from trauma or catheterization.
## Footnote
This type of aneurysm does not involve all layers of the arterial wall.
244
What is a mycotic aneurysm?
Result of infection of the vessel wall, commonly bacterial or fungal; can be saccular and prone to rupture.
## Footnote
Mycotic aneurysms often require aggressive treatment due to their infectious nature.
245
What is a common cause of atherosclerotic aneurysms?
Atherosclerosis.
## Footnote
Atherosclerosis is a buildup of fats, cholesterol, and other substances in and on the artery walls.
246
Name two congenital conditions that can lead to aneurysms.
* Marfan syndrome
* Ehlers-Danlos syndrome
## Footnote
These conditions affect connective tissue and can lead to vascular abnormalities.
247
What are some examples of infectious causes of aneurysms?
* Infective endocarditis
* Tuberculosis (TB)
* Fungal infections
## Footnote
Infections can weaken the vessel wall, leading to aneurysm formation.
248
What types of conditions fall under inflammatory/vasculitic causes of aneurysms?
* Takayasu arteritis
* Giant cell arteritis
* Behçet’s disease
## Footnote
These conditions involve chronic inflammation of blood vessels.
249
What can cause traumatic aneurysms?
Blunt trauma or iatrogenic injury.
## Footnote
Iatrogenic injuries may occur during medical procedures.
250
What characterizes degenerative aneurysms?
Age-related weakening of the vessel wall.
## Footnote
These aneurysms often develop in older adults due to natural wear and tear.
251
What does idiopathic mean in the context of aneurysms?
No identifiable cause.
## Footnote
Idiopathic aneurysms can be challenging to manage due to the lack of known risk factors.
252
What are the two main types of aortic aneurysms?
* Abdominal aortic aneurysm (AAA)
* Thoracic aortic aneurysm (TAA)
## Footnote
AAA is the most common type, while TAA can occur in various locations of the aorta.
253
Where are cerebral aneurysms commonly found?
At the Circle of Willis, often termed berry aneurysms.
## Footnote
These aneurysms are particularly prone to rupture.
254
List three examples of peripheral aneurysms.
* Popliteal artery
* Femoral artery
* Carotid artery
## Footnote
Peripheral aneurysms can lead to complications depending on their location.
255
What are visceral artery aneurysms?
Aneurysms in the splenic, hepatic, renal, and mesenteric arteries.
## Footnote
These aneurysms can affect blood flow to vital organs.
256
Fill in the blank: Aneurysms can be classified based on _______.
[morphology, pathological structure, etiology, anatomical location]
257
True or False: Fusiform aneurysms involve localized outpouching.
False.
## Footnote
Fusiform aneurysms involve uniform dilation, not localized outpouching.
258
What are the four main classification types of aneurysms?
* Morphology
* Wall involvement
* Cause
* Location
## Footnote
Each classification type helps guide diagnosis and management.
259
What are the potential presentations of aortic aneurysms?
Silent for years, incidental discovery, symptoms due to expansion, compression of nearby structures, embolization, or rupture.
260
What is a common finding in Abdominal Aortic Aneurysm (AAA)?
Pulsatile abdominal mass.
261
What type of pain may indicate expansion in AAA?
Dull, steady, or gnawing abdominal or lower back pain.
262
What serious condition can result from AAA rupture?
Sudden, severe abdominal or back pain, hypotension, syncope, and possibly death.
263
What symptom is associated with Thoracic Aortic Aneurysm (TAA)?
Chest pain that is pressure-like or tearing.
264
What can compression of the trachea or bronchi in TAA lead to?
Cough, dyspnea, stridor.
265
What symptom can result from esophageal compression in TAA?
Dysphagia.
266
What is a rare symptom of TAA due to recurrent laryngeal nerve compression?
Hoarseness.
267
What condition may occur if the aneurysm involves the aortic root?
Aortic regurgitation.
268
What is superior vena cava syndrome and how is it related to TAA?
Facial swelling and distended neck veins; it is a rare complication.
269
What are the major imaging modalities used for diagnosing aortic aneurysms?
Abdominal ultrasound, CT angiography (CTA), MRI/MRA, chest X-ray, echocardiography (TTE and TEE).
270
What is the role of abdominal ultrasound in AAA diagnosis?
First-line for screening and diagnosis; quick, non-invasive, and cost-effective.
271
Which imaging modality is most accurate for assessing size and shape of aneurysms?
CT angiography (CTA).
272
What is an alternative to CTA for patients with contrast allergy or kidney dysfunction?
MRI/MRA.
273
What can a chest X-ray show in cases of TAA?
Widened mediastinum.
274
What is the role of echocardiography in TAA diagnosis?
TTE can detect proximal TAA; TEE is better for thoracic aorta.
275
What laboratory investigations are used in the context of aortic aneurysms?
Assess complications or underlying conditions; no lab test can confirm aneurysm.
276
What is the screening recommendation for men aged 65–75 who have ever smoked?
One-time abdominal ultrasound.
277
What is recommended for first-degree relatives of someone with AAA?
Consider early screening.
278
What is the primary focus of aneurysm management?
Preventing rupture, controlling risk factors, repairing the aneurysm when indicated
279
What factors determine the treatment for aneurysms?
Type, location, size, growth rate, presence of symptoms or complications
280
What is the goal of monitoring in aneurysm management?
Prevent rupture
281
What strategies are used to manage risk factors for aneurysms?
* Control BP
* Stop smoking
* Manage lipids
282
What underlying causes should be treated in aneurysm management?
* Genetic disorders
* Infectious disorders
* Inflammatory disorders
283
What are the indications for surgical or endovascular intervention?
Repair when necessary
284
What is the target blood pressure for managing aneurysms?
<130/80 mmHg (especially in TAA)
285
Which medications are used for blood pressure control in aneurysm management?
* β-blockers
* ACE inhibitors
286
What is the strongest modifiable risk factor for AAA?
Smoking cessation
287
What is the purpose of lipid management in aneurysm treatment?
To reduce vascular inflammation
288
How often should AAA measuring 3.0–3.9 cm be imaged?
Every 3 years
289
What is the imaging frequency for AAA measuring 4.0–4.9 cm?
Every 12 months
290
What is the recommended imaging frequency for AAA measuring 5.0–5.4 cm?
Every 6 months
291
What is the imaging recommendation for TAA less than 5.5 cm?
Annual CT/MRI (varies based on cause)
292
What diameter warrants elective repair for AAA in men?
Diameter ≥5.5 cm
293
What diameter warrants elective repair for AAA in women?
Diameter ≥5.0 cm
294
What is the threshold for rapid growth in AAA that indicates repair?
>0.5 cm in 6 months
295
When should a cerebral (berry) aneurysm be repaired?
* Symptomatic
* >7 mm
* High-risk location (e.g., posterior circulation)
296
What are the indications for repairing peripheral aneurysms?
If symptomatic, enlarging, or thrombotic
297
What is open surgical repair?
Aneurysm is replaced with a synthetic graft
298
What is the main characteristic of endovascular aneurysm repair (EVAR / TEVAR)?
Stent graft inserted via femoral artery under imaging guidance
299
Which repair method is more invasive and has a higher perioperative risk?
Open surgical repair
300
What is the immediate management for a ruptured aneurysm?
IV fluids, blood products
301
What is required for urgent management of a ruptured aneurysm?
Urgent imaging (if stable)
302
What type of repair is needed for a ruptured aneurysm?
Emergency surgical or endovascular repair
303
True or False: Mortality is low despite treatment of ruptured AAA or TAA.
False
304
What should be monitored in aneurysm management?
Ultrasound/CT/MRI based on location and size
305
What is important for follow-up after aneurysm repair?
Lifelong surveillance post-repair (especially after EVAR)
306
What are varicose veins?
Dilated, tortuous, and elongated superficial veins most commonly found in the lower limbs due to chronic venous insufficiency.
307
Which veins are most commonly affected by varicose veins?
Great and small saphenous veins.
308
What causes varicose veins?
Failure of venous valves, leading to blood pooling and increased venous pressure.
309
How do varicose veins typically appear?
Visible, bulging, twisted veins.
310
What symptoms are often associated with varicose veins?
Leg discomfort or heaviness.
311
What is the clinical significance of varicose veins?
May be cosmetic or symptomatic.
312
What complications can arise from varicose veins?
Edema, skin changes (e.g. hyperpigmentation, eczema), and venous ulcers.
313
What is the goal of investigation for varicose veins?
To confirm the diagnosis, assess venous valve function, and determine the extent of reflux and venous obstruction.
314
What does visible dilated, tortuous veins suggest?
Superficial varicosities.
315
What does the Trendelenburg test assess?
Superficial valve incompetence.
316
What does the percussion test (Schwartz test) detect?
Transmitted impulse from tapping the vein.
317
What is checked during manual palpation in a clinical examination?
Tenderness, suggestive of thrombophlebitis.
318
Why should the physical exam be done with the patient standing?
Gravity reveals venous dilation.
319
What is the gold standard investigation for varicose veins?
Duplex Ultrasound.
320
What does B-mode (gray scale) in Duplex Ultrasound visualize?
Anatomy of veins.
321
What does Color Doppler in Duplex Ultrasound show?
Direction and velocity of flow.
322
What does Spectral Doppler confirm?
Reflux (flow reversal >0.5 sec on valsalva).
323
What are the findings of Duplex Ultrasound in varicose veins?
* Incompetent valves in saphenous veins or perforators
* Venous reflux with reversal of flow
* Can detect deep venous thrombosis (DVT) or obstruction.
324
What does Photoplethysmography (PPG) measure?
Venous refill time; helps assess venous insufficiency.
325
When is Venography used?
Invasive; used only when noninvasive imaging is inconclusive.
326
What is the purpose of MR or CT venography?
Used when pelvic or abdominal vein involvement is suspected.
327
What findings suggestive of varicose veins can be observed during a clinical exam?
* Visible varicosities
* Skin changes
* Positive Trendelenburg test.
328
What findings can Duplex ultrasound reveal?
* Valve incompetence
* Venous reflux (>0.5 sec)
* Vein diameter increase.
329
What does a decreased venous refill time indicate?
Venous insufficiency.
330
What can Venography visualize?
Abnormal venous structure (rare use).
331
What is the primary aim of management for varicose veins?
To relieve symptoms, prevent progression, and treat complications
## Footnote
Management includes conservative measures, minimally invasive procedures, and surgery when indicated.
332
What are conservative measures in the management of varicose veins?
Strategies include:
* Compression therapy
* Leg elevation
* Exercise
* Weight loss
* Avoid prolonged standing/sitting
## Footnote
Conservative measures are considered first-line treatment.
333
What is the purpose of compression therapy in varicose veins management?
To improve venous return and relieve symptoms and edema
## Footnote
Graduated compression stockings are most effective.
334
How does leg elevation help in managing varicose veins?
It reduces venous pressure by elevating legs above heart level
## Footnote
Recommended several times daily.
335
What role does exercise play in the management of varicose veins?
Regular walking improves calf muscle pump function.
336
Why is weight loss beneficial for patients with varicose veins?
It is especially beneficial in obese patients.
337
What are the indications for interventional management of varicose veins?
Indications include:
* Symptomatic varicose veins not responding to conservative measures
* Complications (ulcers, bleeding, thrombophlebitis)
* Cosmetic concerns (in selected cases)
338
What is endovenous thermal ablation?
A first-line intervention using heat to close the vein
## Footnote
It can be performed using laser or radiofrequency.
339
Describe sclerotherapy.
Injection of sclerosant causes vein fibrosis and closure; best for small veins.
340
What is surgical ligation and stripping?
Removal of long segments of vein; less common now due to minimally invasive options.
341
What is ambulatory phlebectomy?
Microextraction of superficial veins via tiny skin incisions.
342
What is the prognosis for varicose veins?
Generally good in most uncomplicated cases with proper management
## Footnote
Recurrence risk is 20–30% even after intervention.
343
What worsens the prognosis of varicose veins?
Prognosis worsens if complications like ulcers or thrombophlebitis develop.
344
What is chronic venous insufficiency (CVI)?
Longstanding venous hypertension leading to edema, skin changes, and ulceration.
345
What is venous stasis dermatitis?
Itchy, inflamed skin due to blood pooling.
346
What causes hyperpigmentation in varicose vein complications?
Hemosiderin deposition in skin causes brown discoloration.
347
What is lipodermatosclerosis?
Fibrosis and thickening of subcutaneous tissue.
348
Where do venous ulcers typically occur?
Typically at the medial malleolus; they are painful and slow to heal.
349
What is superficial thrombophlebitis?
Clotting and inflammation of superficial veins; may be tender and red.
350
What complication can arise from trauma to engorged veins?
Significant bleeding may occur.
351
What is the general management approach for varicose veins?
Start with conservative measures; escalate to ablation, sclerotherapy, or surgery if needed.
352
What are the common complications of varicose veins?
Complications include:
* Chronic venous insufficiency (CVI)
* Ulcers
* Skin changes
* Thrombophlebitis
* Bleeding.
353
What is the goal of investigating suspected DVT?
To confirm the diagnosis, assess the extent of thrombosis, and evaluate for complications like pulmonary embolism (PE)
## Footnote
This involves a combination of clinical scoring systems, imaging, and laboratory testing.
354
What is the Wells Score used for?
To assess clinical probability of DVT
## Footnote
A score of ≥2 indicates DVT is likely, while a score of <2 indicates it is unlikely.
355
List three factors that contribute +1 point in the Wells Criteria for DVT.
* Active cancer (treatment within 6 months or palliative)
* Paralysis, paresis, or recent plaster immobilization
* Recently bedridden >3 days or major surgery <12 weeks
356
What does a score of <2 on the Wells Score indicate?
DVT unlikely
357
What is the role of D-dimer in laboratory testing for DVT?
High sensitivity, low specificity
## Footnote
A negative D-dimer in low-risk patients excludes DVT, while a positive result or moderate/high risk requires imaging.
358
What is considered the gold standard imaging test for DVT?
Compression Ultrasound
359
What does a non-compressible vein in Duplex Compression Ultrasound confirm?
Thrombus
360
What sensitivity does Duplex Compression Ultrasound have for proximal DVT?
>95%
361
When is CT or MR Venography used?
For cases with pelvic/central DVT or equivocal ultrasound
362
What is the indication for a thrombophilia screen?
Young patients with unprovoked DVT or family history
363
What tests are included in baseline labs before anticoagulation?
CBC, coagulation panel
364
What should be done if PE is suspected?
Perform ECG and CXR
365
What is the first step in the diagnostic pathway for DVT?
Calculate Wells score
366
What is the next step if the Wells score indicates low risk?
D-dimer testing
367
What should be done if the initial ultrasound is negative but suspicion remains high?
Repeat scan in 5–7 days
368
Fill in the blank: A score of ≥2 on the Wells Score indicates _______.
DVT likely
369
True or False: Contrast venography is now the first-line imaging test for DVT.
False
370
What is Deep Vein Thrombosis (DVT)?
Formation of a blood clot within a deep vein, most commonly in the lower limbs
## Footnote
Major component of venous thromboembolism (VTE), which includes DVT and pulmonary embolism (PE)
371
What are the three primary factors in Virchow’s Triad for the pathogenesis of DVT?
* Venous stasis
* Endothelial injury
* Hypercoagulability
## Footnote
These factors lead to the formation of a thrombus.
372
What mechanism is associated with venous stasis in DVT?
Reduced blood flow promotes clot formation
## Footnote
Causes include prolonged immobility, surgery, and paralysis.
373
What is the effect of endothelial injury in DVT?
Injury to vein wall activates coagulation cascade
## Footnote
Causes include trauma, surgery, and central venous catheters.
374
What does hypercoagulability refer to in the context of DVT?
Increased clotting tendency
## Footnote
Can be inherited (e.g. Factor V Leiden) or acquired (e.g. cancer, pregnancy).
375
Where do thrombi most commonly form in DVT?
In the deep veins of the calf or thigh (e.g. femoral, popliteal)
## Footnote
Thrombi may propagate proximally.
376
What serious condition can arise from DVT if a thrombus embolizes?
Pulmonary embolism (PE)
## Footnote
This can be life-threatening.
377
What is the most common symptom of DVT?
Swelling
## Footnote
Caused by venous outflow obstruction.
378
What are some common signs and symptoms of DVT?
* Pain or tenderness in calf or thigh
* Erythema and warmth
* Dilated superficial veins
* Positive Homan’s sign (rarely used)
## Footnote
Symptoms are usually unilateral.
379
What are the red flags suggesting pulmonary embolism (PE) in a patient with suspected DVT?
* Sudden onset dyspnea
* Pleuritic chest pain
* Hemoptysis
* Tachycardia
## Footnote
Immediate consideration of PE is necessary if respiratory symptoms are present.
380
What is phlegmasia alba dolens?
Painful white leg due to massive DVT with arterial spasm
## Footnote
This is a less common presentation of DVT.
381
What is phlegmasia cerulea dolens?
Painful cyanotic leg, associated with venous gangrene risk
## Footnote
This is another less common presentation of DVT.
382
What are the primary goals of DVT treatment?
* Prevent clot extension
* Reduce risk of pulmonary embolism (PE)
* Minimize recurrence
* Prevent long-term complications like post-thrombotic syndrome (PTS)
## Footnote
These goals are essential for effective DVT management.
383
What is the mainstay of DVT treatment?
Anticoagulation
## Footnote
Anticoagulation therapy is crucial in the management of DVT.
384
What is the first-line medication for initial therapy in DVT, especially in cancer patients?
Low-molecular-weight heparin (LMWH)
## Footnote
LMWH is preferred due to its effectiveness and safety profile.
385
When is unfractionated heparin (UFH) used in DVT treatment?
When rapid reversal is needed (e.g., surgery or high bleeding risk)
## Footnote
UFH is often used in acute settings.
386
Name three direct oral anticoagulants (DOACs) used in DVT treatment.
* Rivaroxaban
* Apixaban
* Dabigatran
## Footnote
DOACs are preferred in most patients due to their ease of use.
387
What is the required INR monitoring medication in DVT treatment?
Warfarin (vitamin K antagonist)
## Footnote
Warfarin is used in certain populations, including those with mechanical heart valves.
388
What is the recommended duration of therapy for provoked DVT?
3 months
## Footnote
Duration may vary based on individual circumstances.
389
What is the recommended duration of therapy for unprovoked DVT?
≥3–6 months; consider indefinite if low bleeding risk
## Footnote
Extended therapy may be necessary based on risk factors.
390
What role do compression stockings play in DVT management?
Prevent post-thrombotic syndrome; wear for at least 2 years if symptoms persist
## Footnote
Compression stockings are a key supportive measure.
391
What is encouraged once anticoagulation is initiated?
Early ambulation
## Footnote
Early mobilization helps reduce complications associated with DVT.
392
What is the role of leg elevation in DVT management?
Reduces swelling and discomfort
## Footnote
Elevation can provide symptomatic relief.
393
When is an IVC filter considered in DVT treatment?
In patients with contraindications to anticoagulation or recurrent VTE despite anticoagulation
## Footnote
IVC filters are used in specific clinical situations.
394
What is the prognosis for most patients with prompt DVT treatment?
Most patients recover without serious complications
## Footnote
Early intervention significantly improves outcomes.
395
What is the risk of pulmonary embolism (PE) if DVT is untreated?
30–50% risk
## Footnote
Anticoagulation significantly reduces this risk.
396
What factors increase the risk of DVT recurrence?
* Unprovoked DVT
* Thrombophilia
## Footnote
Certain conditions predispose individuals to recurrent events.
397
What are the long-term outcomes for DVT if treated early?
Good; monitor for post-thrombotic syndrome
## Footnote
Early treatment is crucial for favorable long-term results.
398
What is the most serious complication of DVT?
Pulmonary embolism (PE)
## Footnote
PE occurs when a clot migrates to the pulmonary arteries.
399
What are the symptoms of post-thrombotic syndrome (PTS)?
* Chronic leg pain
* Swelling
* Heaviness
* Skin changes
* Ulcers due to valve damage
## Footnote
PTS can significantly impact a patient's quality of life.
400
What can occur if risk factors for DVT persist or treatment is inadequate?
Recurrent DVT
## Footnote
Continuous risk factor management is essential.
401
What condition can be secondary to chronic venous insufficiency due to DVT?
Venous ulcers
## Footnote
These ulcers can be difficult to manage and may require extensive treatment.
402
What is phlegmasia cerulea dolens?
Massive DVT with compromised arterial inflow → risk of gangrene
## Footnote
This is a rare but serious condition associated with DVT.
403
What are key points in the management of DVT?
* Anticoagulation (DOACs or heparin/warfarin)
* Compression stockings
* Early mobilization
## Footnote
These strategies are fundamental to effective DVT management.
404
What is the prognosis for untreated DVT?
Poor due to PE or PTS
## Footnote
Without treatment, the risks of complications increase significantly.
405
What are common complications of DVT?
* Pulmonary embolism (PE)
* Post-thrombotic syndrome (PTS)
* Recurrent DVT
* Chronic venous insufficiency
## Footnote
Understanding these complications is critical for patient education and management.
406
What is Chronic Venous Insufficiency (CVI)?
A condition in which the veins in the legs are unable to return blood effectively to the heart due to valvular incompetence, venous obstruction, or venous hypertension
## Footnote
This leads to blood pooling (stasis) in the lower extremities, causing a range of chronic symptoms and skin changes.
407
What is venous reflux?
Failure of venous valves allows backward flow of blood
## Footnote
This is one of the key characteristics of Chronic Venous Insufficiency.
408
What is venous hypertension?
Sustained high pressure in the venous system, especially during standing
## Footnote
This condition is a significant factor in Chronic Venous Insufficiency.
409
List some progressive symptoms of Chronic Venous Insufficiency.
* Edema
* Pain
* Skin changes (e.g., hyperpigmentation, eczema)
* Venous ulcers (in severe cases)
## Footnote
These symptoms can worsen over time if the condition is not managed.
410
What are common causes of Chronic Venous Insufficiency?
* Previous deep vein thrombosis (DVT)
* Varicose veins
* Congenital valve defects
* Obesity
* Prolonged standing/sedentary lifestyle
## Footnote
These factors can contribute to the development of CVI.
411
True or False: Chronic Venous Insufficiency can lead to venous ulcers.
True
## Footnote
Venous ulcers are a severe complication associated with Chronic Venous Insufficiency.
412
Fill in the blank: Chronic Venous Insufficiency leads to blood _______ in the lower extremities.
pooling
## Footnote
This pooling is referred to as stasis.
413
What is Chronic Venous Insufficiency (CVI)?
A long-term condition where venous blood does not return effectively from the lower limbs to the heart, leading to venous stasis, inflammation, and tissue damage.
414
What typically causes Chronic Venous Insufficiency?
Prolonged venous hypertension due to:
* Valvular incompetence
* Venous obstruction
* Previous deep vein thrombosis (DVT)
415
What is the first step in the mechanism of CVI?
Venous Valve Incompetence
416
What happens when venous valves fail in CVI?
Retrograde flow (reflux) occurs.
417
What is the effect of reflux on venous pressure?
Increases pressure in the superficial and deep veins, especially during standing.
418
What are the consequences of venous hypertension on capillaries?
Causes capillary dilation, increased permeability, and plasma protein leakage.
419
What does capillary leakage lead to?
Edema and release of inflammatory mediators.
420
What chronic changes occur due to inflammation in CVI?
Endothelial dysfunction, skin fibrosis, and pigmentation.
421
What causes hyperpigmentation in CVI?
Hemosiderin deposition from RBC breakdown.
422
What are the early symptoms of CVI?
Worse with prolonged standing and improve with leg elevation:
* Leg heaviness/aching
* Swelling (edema)
* Leg fatigue/cramping
423
Describe the advanced signs of CVI.
Include:
* Hyperpigmentation
* Venous eczema (stasis dermatitis)
* Lipodermatosclerosis
* Venous ulcers
* Atrophie blanche
424
What is lipodermatosclerosis?
Thickened, fibrotic skin with a 'champagne bottle' appearance.
425
What are venous ulcers?
Shallow, irregularly shaped ulcers near the medial malleolus; painful and slow to heal.
426
Fill in the blank: The pathogenesis of CVI involves valve failure leading to ______, which results in venous hypertension.
venous reflux
427
True or False: Symptoms of CVI typically improve with leg elevation.
True
428
What is the description of hyperpigmentation in CVI?
Brown discoloration from hemosiderin, especially over the medial malleolus.
429
What are the key findings in the late stages of CVI?
Include:
* Hyperpigmentation
* Eczema
* Ulcers
* Lipodermatosclerosis
430
What is the role of leukocyte activation and cytokine release in CVI?
They contribute to chronic inflammation and tissue damage.
431
What is the goal of investigating CVI?
The goal is to:
* Confirm the diagnosis
* Assess the extent of venous reflux or obstruction
* Rule out deep vein thrombosis (DVT) or other causes of leg swelling
## Footnote
CVI stands for Chronic Venous Insufficiency.
432
What are the key features assessed during a clinical history for CVI?
Key features include:
* Leg heaviness
* Aching
* Swelling
* Skin changes
* Symptoms worse with standing
## Footnote
These symptoms are indicative of venous problems.
433
What findings are looked for during the inspection phase of a physical examination for CVI?
Findings include:
* Varicose veins
* Edema
* Hyperpigmentation
* Ulcers (medial malleolus)
## Footnote
Medial malleolus ulcers are common in CVI.
434
What does palpation reveal during a physical examination for CVI?
Palpation may reveal:
* Pitting edema
* Warmth
* Tenderness if thrombophlebitis is present
## Footnote
Pitting edema indicates fluid retention.
435
What is the purpose of the Trendelenburg test in CVI assessment?
The Trendelenburg test is used to assess superficial venous valve competence
## Footnote
This test helps in determining valve function.
436
What is the gold standard for diagnosing CVI?
Duplex Ultrasonography is the gold standard
## Footnote
It provides detailed information about venous anatomy and blood flow.
437
What does B-mode imaging in Duplex Ultrasonography show?
B-mode imaging shows the anatomy of superficial and deep veins
## Footnote
It is essential for visualizing the structure of veins.
438
What does Color Doppler in Duplex Ultrasonography visualize?
Color Doppler visualizes flow direction and velocity
## Footnote
This helps in assessing blood flow dynamics.
439
What does Spectral Doppler confirm during Duplex Ultrasonography?
Spectral Doppler confirms reflux >0.5 seconds during Valsalva or after distal compression
## Footnote
This indicates valve incompetence.
440
What is the purpose of Photoplethysmography (PPG) in CVI assessment?
PPG evaluates venous refill time; shortened refill suggests reflux
## Footnote
It is a non-invasive method to assess venous function.
441
What does Air Plethysmography measure?
Air Plethysmography measures overall venous function
## Footnote
It is less commonly used compared to other methods.
442
What is Venography and when is it used?
Venography is an invasive test used when duplex findings are unclear
## Footnote
It provides detailed images of veins.
443
When is MRI or CT Venography used?
MRI or CT Venography is used for pelvic or iliac vein obstruction or preoperative planning
## Footnote
These imaging techniques provide detailed cross-sectional images of veins.
444
What is the role of D-dimer testing in CVI?
D-dimer is used to rule out acute DVT if clinically suspected
## Footnote
Elevated levels can indicate thrombosis.
445
What is the purpose of the Ankle-brachial index (ABI) in CVI assessment?
ABI is used to rule out peripheral arterial disease before compression therapy
## Footnote
It compares blood pressure in the ankle with blood pressure in the arm.
446
What is a key finding in clinical examination for CVI?
Key findings include:
* Edema
* Pigmentation
* Ulcers
* Varicose veins
## Footnote
These findings help in diagnosing CVI.
447
What does Duplex ultrasound reveal in CVI?
Key findings include:
* Venous reflux >0.5 sec
* Vein dilation
* Rules out DVT
## Footnote
These findings are crucial for diagnosis.
448
What does a shortened refill time in PPG indicate?
A shortened refill time suggests reflux
## Footnote
It reflects impaired venous function.
449
What does a normal Ankle-brachial index (ABI) indicate?
An ABI >0.9 is normal; <0.9 suggests coexisting arterial disease
## Footnote
This helps differentiate between venous and arterial issues.
450
What are the goals of managing Chronic Venous Insufficiency (CVI)?
Improve venous return, reduce symptoms and swelling, promote ulcer healing, prevent disease progression and recurrence
451
What is the mainstay of treatment for CVI?
Compression therapy
452
What is the purpose of graduated compression stockings in CVI management?
Improve venous return and reduce edema
453
How should legs be positioned to reduce venous pressure?
Elevate legs above heart level several times daily
454
What type of exercise is beneficial for improving venous pump function?
Walking and calf muscle exercises
455
What lifestyle change can help reduce venous pressure in obese patients?
Weight loss
456
What type of skin care is recommended for CVI?
Emollients to prevent dryness; topical corticosteroids for stasis dermatitis
457
What are the components of wound care if ulcers are present in CVI?
Dressings, debridement, infection control, and moist wound healing principles
458
What are venoactive agents used for in pharmacologic therapy for CVI?
May reduce symptoms and improve venous tone
459
When are antibiotics used in the management of CVI?
Only if there is secondary infection of ulcers
460
What is the purpose of topical corticosteroids in CVI treatment?
For venous eczema or inflammation
461
What is the purpose of endovenous ablation in CVI treatment?
To close incompetent veins using laser or radiofrequency
462
What is sclerotherapy used for in CVI management?
Injection of sclerosant to obliterate varicose veins
463
What is surgical vein stripping?
Removal of long segments of diseased vein
464
What is the purpose of venous stenting in CVI?
For iliac vein compression or obstruction
465
What is the prognosis for mild-to-moderate CVI?
Good with conservative treatment and lifestyle modification
466
What is the prognosis for severe CVI with ulcers?
Requires long-term care and has high recurrence risk
467
What increases the recurrence risk of CVI?
Not modifying risk factors such as obesity and inactivity
468
How can quality of life be affected by consistent management of CVI?
Can significantly improve
469
What is a common complication of CVI?
Venous ulceration
470
What is stasis dermatitis?
Red, itchy, scaly skin due to inflammation
471
What is lipodermatosclerosis?
Chronic fibrosis of subcutaneous tissue leading to 'inverted champagne bottle' leg
472
What causes hemosiderin deposition in CVI?
Brownish skin discoloration from red blood cell breakdown
473
What infections are patients with CVI at risk for?
Cellulitis or ulcer infection, especially if ulcers are chronic
474
What is the risk of venous thrombosis in CVI?
Risk of superficial or deep vein thrombosis due to venous stasis
475
What are key points in the management of CVI?
Compression, elevation, exercise, wound care, endovenous procedures
476
What is the prognosis for ulcerated or recurrent cases of CVI?
Guarded
477
What complications can arise from CVI?
Ulcers, eczema, lipodermatosclerosis, infection, thrombosis
478
What is vasculitis?
A group of disorders characterized by inflammation and necrosis of blood vessel walls
479
What are the potential consequences of vasculitis?
* Compromised blood flow
* Tissue ischemia or infarction
* Aneurysm formation or vessel rupture
480
What types of blood vessels can be affected by vasculitis?
Arteries, veins, or capillaries of any size
481
What are the two main categories of vasculitis based on etiology?
* Primary (idiopathic/autoimmune)
* Secondary to infections, malignancy, or drugs
482
How is vasculitis classified based on the size of affected vessels?
* Large-vessel vasculitis (e.g. Giant cell arteritis)
* Medium-vessel vasculitis (e.g. Polyarteritis nodosa)
* Small-vessel vasculitis (e.g. ANCA-associated vasculitis)
483
True or False: Vasculitis can only affect large blood vessels.
False
484
Fill in the blank: Vasculitis can lead to _______ of blood vessel walls.
inflammation and necrosis
485
What is vasculitis?
Inflammation and damage to blood vessels caused by non-infectious or infectious mechanisms
486
What are the consequences of vasculitis?
Vessel wall injury, luminal narrowing or thrombosis, ischemic damage to downstream tissues
487
What is Non-Infectious Vasculitis?
Vasculitis caused by dysregulated immune responses, including autoimmunity and immune complex deposition
488
What triggers Immune Complex–Mediated Vasculitis?
Circulating antigen-antibody complexes deposit in vessel walls leading to complement activation and neutrophilic inflammation
489
Name an example of Immune Complex–Mediated Vasculitis.
Henoch-Schönlein purpura (IgA vasculitis)
490
What are ANCA-Associated Vasculitides characterized by?
Activation of neutrophils by anti-neutrophil cytoplasmic antibodies (ANCAs) resulting in vessel wall injury
491
List examples of ANCA-Associated Vasculitis.
* GPA (Granulomatosis with polyangiitis) – c-ANCA/PR3
* MPA (Microscopic polyangiitis) – p-ANCA/MPO
* EGPA (Eosinophilic granulomatosis with polyangiitis) – p-ANCA/MPO
492
What is Cell-Mediated (Granulomatous) Vasculitis?
T-cell–mediated immune responses lead to macrophage activation and granuloma formation
493
Give an example of Cell-Mediated Vasculitis.
Giant cell arteritis
494
What is Autoimmune-Associated Vasculitis?
Vasculitis seen in systemic autoimmune diseases leading to secondary vasculitis
495
List systemic autoimmune diseases associated with Autoimmune-Associated Vasculitis.
* Systemic lupus erythematosus (SLE)
* Rheumatoid arthritis
* Sjogren’s syndrome
496
What characterizes Infectious Vasculitis?
Infectious agents directly damaging the vessel wall or triggering immune-mediated injury
497
What occurs during Direct Invasion of the Vessel Wall?
Bacteria, viruses, or fungi invade and cause septic vasculitis or mycotic aneurysms
498
Name common pathogens involved in Infectious Vasculitis.
* Aspergillus
* Mucor
* Treponema pallidum (syphilis)
499
What triggers Immune Response to Infection in vasculitis?
Infections may trigger immune complex formation or molecular mimicry
500
Give an example of a virus that can lead to secondary vasculitis.
Hepatitis B virus in polyarteritis nodosa (PAN)
501
What factors influence the clinical presentation of vasculitis?
Type and size of vessel involved, organ systems affected, speed of disease progression
## Footnote
These factors determine the variability in symptoms among patients with vasculitis.
502
What are common constitutional symptoms of vasculitis?
* Fever
* Fatigue, malaise
* Weight loss
* Arthralgia or arthritis
* Myalgia
* Night sweats
## Footnote
These symptoms reflect the underlying inflammatory process associated with vasculitis.
503
What is the typical presentation of fever in vasculitis?
Low-grade or intermittent
## Footnote
Fever is often one of the early signs of vasculitis.
504
What does palpable purpura indicate in the context of vasculitis?
Non-blanching, raised lesions typically on lower limbs
## Footnote
Palpable purpura is a common cutaneous manifestation, especially in small-vessel vasculitis.
505
What is livedo reticularis?
Mottled, net-like discoloration of skin
## Footnote
This is a cutaneous manifestation seen in vasculitis.
506
What are the neurological symptoms associated with vasculitis?
* Mononeuritis multiplex
* Peripheral neuropathy
* Stroke or seizures
## Footnote
These symptoms can arise from large-vessel or CNS vasculitis.
507
What symptom is indicative of pulmonary capillaritis in vasculitis?
Hemoptysis
## Footnote
This can occur in conditions like GPA or MPA.
508
What are the cardiac manifestations of vasculitis?
* Chest pain
* Pericarditis
* Heart failure
## Footnote
These symptoms can arise from coronary arteritis or other forms of vasculitis.
509
What renal symptoms are associated with vasculitis?
* Hematuria
* Proteinuria
* Hypertension
## Footnote
These are often related to glomerulonephritis and renal ischemia.
510
What gastrointestinal complications can arise from vasculitis?
* Abdominal pain
* GI bleeding
* Bowel perforation
## Footnote
These complications can be severe and life-threatening.
511
What ocular symptoms may occur in vasculitis?
* Vision changes/blindness
* Scleritis or uveitis
## Footnote
These symptoms are particularly associated with giant cell arteritis and ANCA-associated vasculitis.
512
Fill in the blank: Night sweats are a common _______ symptom of vasculitis.
systemic
## Footnote
This symptom reflects the inflammatory process in vasculitis.
513
True or False: Weight loss in vasculitis is usually intentional.
False
## Footnote
Weight loss is often unintentional and may be significant.
514
What is a potential severe complication of gastrointestinal involvement in vasculitis?
Bowel perforation
## Footnote
This is a life-threatening complication that can occur in severe cases.
515
What is required for diagnosing vasculitis?
A combination of clinical suspicion, laboratory evaluation, imaging, and often biopsy to confirm vessel wall inflammation.
516
What are the purposes of obtaining a detailed history in clinical evaluation?
Assess systemic symptoms (fever, weight loss), organ involvement, triggers (e.g., infection, drugs).
517
What physical exam findings may indicate vasculitis?
Skin lesions, neurologic deficits, bruits, asymmetric pulses, ulcers.
518
What findings support the diagnosis of vasculitis in laboratory tests?
↑ ESR, CRP (non-specific but support diagnosis).
519
What autoantibodies are associated with vasculitis?
* c-ANCA (PR3, GPA)
* p-ANCA (MPO, MPA/EGPA)
* ANA, anti-dsDNA (lupus-associated vasculitis)
* Rheumatoid factor (RF)
* Complement levels (low in immune complex vasculitis).
520
What does urinalysis reveal in renal involvement of vasculitis?
Hematuria, proteinuria.
521
What laboratory tests are monitored to assess systemic impact and treatment safety?
CBC, LFTs, renal function.
522
What laboratory tests screen for infectious-associated vasculitis?
Cryoglobulins, Hep B/C serology.
523
What imaging modalities are used for detecting large and medium vessel inflammation?
CT/MR angiography.
524
What is the purpose of a PET scan in vasculitis diagnosis?
Assess vessel inflammation in large-vessel vasculitis.
525
What imaging findings might suggest pulmonary involvement in vasculitis?
Pulmonary nodules, infiltrates, hemorrhage (GPA, MPA).
526
What is the gold standard for diagnosing vasculitis?
Biopsy.
527
What types of biopsies are used for specific vasculitis diagnoses?
* Skin biopsy for palpable purpura or nodules
* Temporal artery biopsy for giant cell arteritis
* Kidney biopsy for glomerulonephritis in ANCA-associated vasculitis
* Lung biopsy for alveolar hemorrhage or nodules.
528
What factors influence the management of vasculitis?
* Type of vasculitis
* Severity and organs involved
* Presence of infection or malignancy
* Autoimmune vs infectious origin.
529
What is the purpose of removing triggers in vasculitis management?
Stop offending drug; treat infection (e.g., HBV in PAN).
530
What is the mainstay of initial treatment for vasculitis?
Glucocorticoids (e.g., prednisone).
531
Which drug is used for severe or life-threatening vasculitis?
Cyclophosphamide.
532
What is used for maintenance therapy in vasculitis?
Azathioprine or methotrexate.
533
What alternative therapy is used for ANCA vasculitis?
Rituximab.
534
What is plasmapheresis used for in vasculitis treatment?
Severe ANCA-associated disease with renal involvement or pulmonary hemorrhage.
535
What supportive care strategy is important for patients with renal involvement?
Blood pressure control.
536
What prophylaxis is recommended for patients on high-dose steroids and cyclophosphamide?
Antibiotic prophylaxis for Pneumocystis jirovecii.
537
What factors impact the prognosis of vasculitis?
* Early diagnosis and treatment
* Severe organ involvement
* ANCA positivity
* Infectious cause identified and treated.
538
What is a key action in the initial therapy for vasculitis?
Steroids ± cyclophosphamide or rituximab.
539
What is the main focus of maintenance therapy in vasculitis?
Azathioprine, methotrexate, or rituximab.
540
In infectious cases of vasculitis, what is crucial for management?
Treat underlying infection + supportive care.
541
What should be monitored in patients with vasculitis?
Relapse, medication toxicity, organ damage.
