Vascular Disease Flashcards
(85 cards)
1
Q
Blood Flow in The Arterial & Venous System depends on?
A disturbance disrupts?
3
A
Depends on a system of
- patent blood vessels and
- adequate perfusion pressure
A disturbance disrupts:
- The delivery of oxygen and nutrients
- The removal of waste products
- The return of blood to the heart
2
Q
Effects of Blood Vessel Disease Physiology
Arterial disorders? 2
Venous disorders? 2
A
Arterial disorders
- Decreased blood flow to the tissues
- Impaired delivery of oxygen and nutrients
Venous disorders
- Interference with the outflow of blood from the capillaries
- Interference with removal of tissue wastes and return of blood to the heart
3
Q
- Pathologic changes in the vessel wall are? 2
- Raynaud’ phenomenon is caused how? (printzmentals, MI)
- Abnormal vessel dilation problems? 2
- Tumors or edema cause what?
A
- Atherosclerosis and vasculitis
- Acute vessel obstruction due to thrombus, embolus or vasospasm
- Arterial aneurysms (weakeningof the wall) or varicose veins
- Compression of blood vessels by extravascular forces
4
Q
Arteriosclerosis
three types?
A
- Atherosclerosis
- Moenckeberg medial calcific sclerosis
- Arteriolosclerosis
5
Q
Describe what the following are:
- Atherosclerosis
- Moenckeberg medial calcific sclerosis
- Arteriolosclerosis
A
Atherosclerosis
-Plaque buildup made up of fat, cholesterol, or calcium
Moenckeberg medial calcific sclerosis
- Calcium deposits in the muscular middle layer (Tunica Media)
- Poorer diagnosis
Arteriolosclerosis
-Vessel wall thickening and luminal narrowing in the small arteries and arterioles
6
Q
Common Features of arteriosclerosis?
3
A
- Stiffening of arterial vessels
- Thickening of the arterial wall
- Degenerative nature of the disease
7
Q
Arteriosclerosis 2 vs Atherosclerosis
A
Arteriosclerosis:
- Thickening and hardening of arterial walls.
- Loss of elasticity of medium or large vessels.
Atherosclerosis:
Specific form of arteriosclerosis caused by build up of fatty plaques and cholesterol in the arteries.
8
Q
Major complications of atherosclerosis
4
A
- Ischemic heart disease
- Stroke (Carotid Arterial Disease)
- Aneurysm
- Peripheral vascular disease
9
Q
Atherosclerosis develops in response to what?
What can this cause?
6
A
vascular injury and involves inflammation and vessel remodeling
- Hypercholesterolemia
- Diabetes
- Smoking
- Hypertension
- Obesity
- Family history of early heart disease
10
Q
Clinical Presentation of Atherosclerosis
- Cardiac? 2
- Arteries in arms and legs? 1
- Kidneys? 1
- Genitals? 1
- Neurologic? 4
A
Cardiac:
- Chest pain/pressure (angina)
- Sudden numbness or weakness in arms or legs, difficulty speaking or slurred speech, or drooping muscles in your face.
Arteries in arms and legs
1. Leg pain when walking(intermittent claudication)
Kidneys
1. High blood pressure or kidney failure
Genitals:
1. Difficulties with sex or erectile dysfunction in men
Neurologic:
- Sudden numbness or weakness in arms or legs
- Difficulty speaking or slurred speech
- Drooping muscles in face
- TIA (Transient ischemic attack) may progress to a stroke
11
Q
What can cause paralyzing strokes?
A
- Vascular disease can block the carotid arteries to the brain and cause paralyzing strokes.
12
Q
- Whats a TIA?
- Whats it caused by?
- How do you want to work this up? 3
- What do we send them home on? 2
A
- Transient episode of neurologic dysfunction caused
- by loss of blood flow either focal brain, spinal cord or retinal without infarction (tissue death)
- US and listen for carotid
- EKG for AFIB
- TE
- Statin
- Aspirin
13
Q
How can a TIA present? 3
When does it usually resolve?
A stroke lasting more than 24 hours is usually what?
A
Can present as a
- transient hemispheric event or 2. monocular blindness (amaurosis fugax),
- aphasia, slurred speech (dysarthria) and mental confusion.
Usually resolves in 24 hours.
Stroke >24 hrs and usually an embolus
14
Q
Carotids Evaluation 4
(whats our first step test?)
(whats the gold standard?)
A
- Physical Exam
- Duplex(go to right away)
50% in symptomatic & 80% in asymptomatic require intervention
At least one other to confirm - MRA (Magnetic Resonance Angiography)
- CTA (Computed Tomography Angiography)
- Angiography (gold standard, but risks are stroke or bleeding plus high cost)- absolute diagnosis
15
Q
Asymptomatic patients with CAS (Carotid Arterial Stenosis) >___% will benefit from surgery assuming the surgeon has complication rate
A
80
2
prophylactic
16
Q
- Rheumatic Fever is what?
- Whats it believed to be caused by?
- Usually develops how often after Group A strep?
- Usually appears in what kind of population?
A
- Inflammatory disease following
Streptococcus pyogenes infection i.e. Strep pharyngitis. - Believed to be caused by antibody cross-reactivity.
- two to four weeks
- Usually appears in children between the ages of 6 and 15 with only 20% of first time attacks occurring in adults.
17
Q
Major Manifestations of Rheumatic Fever
5
A
- Migratory arthritis (predominantly involving the large joints)
- Carditis and valvulitis (eg pancarditis)
- Central nervous system involvement
- Erythema marginatum
- Sydenham’s chorea (rapid movements without purpose of the face and arms occurring late in the disease
18
Q
Carditis and valvulitis (eg pancarditis) will present how (from rheumatic fever?
3
A
- Myocarditis which can manifest as congestive heart failure with shortness of breath
- Pericarditis with a rub
- New heart murmur
19
Q
Minor Criteria for rheumatic fever?
6
A
- Fever of 100.8-102.0
- Arthralgia: Joint pain without swelling
- Elevated ESR or C reactive protein
- Leukocytosis
- ECG showing features of heart block such as prolonged PR interval. (Cannot be included if carditis is present as a major symptom)
- Previous episode of rheumatic fever
20
Q
Modified Jones Criteria For Diagnosis
of Rheumatic Fever
2
What are the exceptions?
2
A
- Two major criteria
- One major criteria plus two minor criteria.
Exceptions:
- Chorea
- Indolent carditis
21
Q
Treatment of Rheumatic Fever
3
A
Anti-inflammatory
- Aspirin (ASA)
- NSAID’s
- -Ibuprofen for moderate to severe inflammatory reaction
- -Corticosteroids - Antibiotics
22
Q
Treatment of heart failure with rheumatic fever?
4
What do you have to be careful with in Reye’s syndrome?
What antibiotics would we use? 2
A
Heart failure:
1. Ace inhibitors 2. Diuretics 3. Beta Blockers 4. Corticosteroids
Be careful in children as ASA associated with Reye’s Syndrome
Risks, benefits and alternative treatments must always be considered
- Penicillin or Clarithromycin or
- Zpack
23
Q
Disorders of the aorta include:
2
A
- Aneurysms (bulges) in weak areas of its walls
2. Dissection (separation of the layers of it’s wall)
24
Q
- Aneurysms (bulges) in weak areas of its walls can develop where?
- 90% of aortic aneurysms develop where?
- WHats the most common cause?
- Can develop in the arteries where?
A
- Can develop anywhere along the aorta
- 90% of aortic aneurysms develop in the abdominal aorta
- Most common cause is atherosclerosis
- Can develop in the arteries at the back of the knee (popliteal arteries)
25
What is Dissection?
Inner lining of the aortic wall tears
| Artery wall deteriorates and usually associated with high blood pressure (separation of the layers of it’s wall)
26
Describe the onset of Aortic Aneurysm/Dissection
These disorders can be immediately fatal, but they usually take years to develop.
27
Thoracic Aortic Aneurysm (TAA)
May be secondary to what?
2
May be secondary to collagen vascular diseases
1. Marfan’s Syndrome 2. Ehlers- Danlos Syndrome
28
Thoracoabdominal
Describe Traumatic occur at ligamentum arteriosum? 2 (where does it develop and how?)
Crawford Classification of Thoracoabdominal TA/AA: where does it commonly develop? 4
1. Just beyond the Left subclavian artery
2. From rapid deceleration accidents (MVA’s & Falls)
- I (L) subclavian to renal arteries
- II (L) subclavian to iliac bifurcation
- III Midthoracic to infrarenal
- IV Distal thoracic to infrarenal
29
Thoracic Aortic Aneurysms
Clinical presentation? 5
If we see these symptoms what should we do?
Most present how?
Clinical Presentation/Treatment
Symptomatic can have any/all of the following symptoms:
1. Sub sternal, back or abdominal pain
2. Dyspnea, stridor, or brassy cough (trachea pressure)
3. Dysphagia (Pressure on esophagus)
4. Hoarseness (Pressure on recurrent laryngeal nerve)
5. Neck and arm edema from SVC compression
Start Beta Blockers and call surgeon
Most are asymptomatic
30
Abdominal Aortic Aneurysms AAA:
1. Most originate where?
2. What has decreased mortality?
3. Half of newly detected aneurysms are how big and 2/3 will need what?
1. >90% Originate BELOW the renal arteries
2. ROUTINE U/S screening of high-risk groups has decreased mortality by 53%
3. Half of all newly detected aneurysms are less than 5cm and 2/3 will eventually require surgical repair
31
Screening For AAA
1. How should we screen?
2. Who should we screen? 2
1. Abdominal ultrasonography is a highly sensitive and specific screening test for AAA
2. One-time screening recommended in men ages 65-75 who have ever smoked.
2. One-time screening for men ages 65-75 who have never smoked but who have a first degree relative who required repair of an AAA or died of ruptured AAA
32
Clinical Presentation of AAA:
Asymptomatic? 3
Symptomatic? 2
Asymptomatic
1. Picked up on routine physical exam with prominent aortic pulsation and/or lateralization
2. Incidental finds on CT scan or US
3. 25% will also have LE occlusive disease
Symptomatic
1. Midabdominal or lower back pain with prominent aortic pulsations
2. Aneurysms that produce symptoms are at increased risk for rupture
33
Arterial Embolism/Thrombosis:
1. Whats an embolism?
2. Classified by substance. Name the 7 embolisms classifications.
3. Whats thrombosis?
1. Embolism: Sudden interruption of blood flow to an organ or body part due to embolus adhering to the wall of an artery blocking the flow of blood.
1. Thromboembolism: embolism of thrombus (blood clot)
2. Cholesterol embolism: embolism of cholesterol often from atherosclerotic plaque inside a vessel
3. Fat embolism: embolism of bone fracture or fat droplets
4. Air embolism: embolism of air bubbles
5. Septic embolism: embolism of bacteria containing pus
6. Tissue embolism: embolism of small fragments of tissue.
7. Foreign body embolism: foreign materials such as talc and other small objects
3. Thrombosis: formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood.
34
Sites of Embolization
| 7
Bifurcations
1. Femoral – 40%
2. Aortic – 10-15%
3. Iliac – 15%
4. Popliteal – 10%
5. Upper extremities – 10%
6. Cerebral – 10-15%
7. Mesenteric/visceral – 5%
35
Arterial Embolic Disease:
History: What do we specifically want to ask for 2 and what are positive signs and symtpoms?
2
1. The onset and duration of symptoms
2. Pain
1. Sudden onset – embolic
2. Long standing before acute event - thrombotic
36
Risk Factors for atherosclerotic heart disease
6
1. Hypercholesterolemia
2. Diabetes
3. Smoking
4. Hypertension
5. Obesity
6. Family history of early heart disease
37
Clinical Presentation of Arterial Embolic Disease
6
6 P’s of acute limb ischemia (KNOW THESE!!!!)
1. Pain
2. Pallor: extreme or unnatural paleness
3. Pulselessness
4. Paresthesia: sensation such as burning, prickling, itching or tingling
5. Paraparesis (paralysis): muscle weakness allowing limited movement
6. Poikilothermia: variation of body temperature regionally
38
Arterial Embolic Disease:
Imaging
Why would we do this? 4
Arteriography
1. Pt with viable limb
2. Evaluate the anatomy
3. Operative planning –target vessel
4. Therapeutic – thrombolysis, angioplasty
39
Arterial Embolic Disease
Management
1. Who should be sent straight to arteriography?
2. Whats the first thing we should do? WHat meds and why?
3. Whats our next option?
4. Alternative therapy to surgery?
1. Pt with threatened extremity should not delay revascularization & arteriography may be done intra-operatively
2. Rapid systemic anticoagulation
- Heparin bolus/continuous drip
- Prevent propagation of thrombus, distal thrombosis, venous thrombosis
3. Surgery – Embolectomy
4. Several trials have demonstrated that thrombolytic therapy is a safe and effective alternative to surgery in appropriately selected patients
40
Disorders of The Venous Circulation: What do they cause?
Why are these patients predisposed to clot formation?
Types of disorders? 3
1. Produce congestion of the affected tissues
2. Predispose to clot formation because of stagnation of flow and activation of the clotting system
Types of disorders
1. Varicose Veins
2. Thrombophlebitis
3. There are also veno-occlusive disorders (VOD)
41
1. Describe varicose veins
| 2. Describe Thrombophlebitis
1. Enlarged tortuous veins usually on the leg but can occur elsewhere
2. “Vein Inflammation”
42
Disorders of The Venous Circulation,
Thrombophlebitis:
Formation of a venous clot depends on the presence of at least one of Virchow’s triad factors. What are they?
1. Venous stasis
2. Injury to vessel wall
3. Hypercoagulable state
43
What is venous stasis?
Risk factors for this? 4
Alterations in normal blood flow
1. Prolonged immobility
2. Long plane or car ride
3. Bed bound during hospitalization
4. Varicose veins
44
1. Venous Stasis (AKA Venous Insufficiency) is pooling blood in the leg which begins where?
2. What kind of pain? (when is it the worst?)
3. What are often present?
4. Skin changes? 4
1. ankle and calf
2. Dull, aching discomfort
Worse at end of day and improves with elevation
3. Often varicosities are present
4. Skin changes
- Stasis dermatitis
- Brownish pigmentation
- Brawny induration – LDS lipodermatosclerosis
- Skin is thin, shiny, atrophic and cyanotic
45
Venous Stasis:
DDX?
Treatment? 4
Skin treatment? 2
1. CHF/Renal Disease:
2. Lymphedema: No varicosities
Treatment
1. Limit standing
2. Intermittent elevation of legs during day
3. Daily use of Thigh-high compression stockings
4. Regular exercise
Skin treatment is
1. protection and
2. lubrication
46
Venous Stasis:
1. Lyphedema doesn't respond to what?
2. Edema is more prominant where?
3. What will CHF/Renal disease look like?
1. Doesn’t respond to elevation
2. Edema more prominent in dorsum of foot
3. Bilateral edema
47
```
Thrombophlebitis
Virchow’s Triad shows
Endothelial injury or vessel wall injury.
Vessel piercings and damages from:
3
```
1. Bacteria
2. Monocytes in chronic inflammation
3. Biomaterials of implants/devices
48
1. What causes Hypercoagulability?
| 2. Specifically? due to a deficiency of what?
1. Alterations in the constitution of blood
2. Hyperviscosity
Deficiency of:
Antithrombin III, protein C or S deficiency
Leiden V factor
49
What else could cause hypercoacgulability besides hyperviscosity (Deficiency of
Antithrombin III, protein C or S deficiency
Leiden V factor)? 9
1. Nephrotic syndrome
2. Changes after severe trauma or burn
3. Disseminated cancer
4. Late pregnancy and delivery
5. Race
6. Advanced age
7. Cigarette smoking
8. Hormonal contraceptives
9. Obesity
50
Thrombophlebitis
Virchow’s Triad:
What are the hemodynamic changes caused by?2
1. Sheer stress
| 2. Hypertension
51
Disorders of The Venous Circulation/Thrombophlebitis (Pathophysiology):
1. Thrombi usually form where?
2. Alternatively, what else can clots form from?
3. What are clots formed from?
1. Thrombi usually form at the venous cusps of deep veins where altered or static blood flow causes clot formation
2. Alternatively, clots form from intimal defects
3. Clots are composed from fibrin, red cells and platelets and cause partial/complete obstruction of vein
52
1. Describe Superficial Thrombophlebitis?
2. What are characteristic findings? 3
3. MIld cases can be treated how? 3
4. Severe cases are treated how? 4
5. When would we use antibiotics?
1. Thrombosis can occur in any superficial vein primarily the saphenous vein and it’s tributaries
2.
- Local pain,
- erythema and
- tenderness are characteristic findings
3. Mild cases can be treated with -cold compresses,
- analgesia and
- elastic supports
4. Severe cases can be debilitating and should be managed by
- bed rest,
- elevation of extremity,
- support stockings and
- analgesia
5. Antibiotics are useful in septic thrombophlebitis
53
1. What is Buerger’s Disease
Thromboangiitis Obliterans?
2. Strongly associated with what?
3. 2/3 of patients have what with this?
1. Recurring progressive inflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet.
2. Strongly associated with use of tobacco products primarily from smoking, but also from smokeless tobacco.
3. Two thirds of patients with severe periodontal disease
54
Buerger’s Disease
Thromboangiitis Obliterans
Pathopysiology?
3 theorized causes
1. Tobacco may trigger an immune response in susceptible
2. Tobacco may unmask a clotting defect
3. Inflammatory reaction of the vessel wall which eventually leads to vasculitis and ischemic changes in distal parts of limbs
55
Buerger’s Disease
Thromboangiitis Obliterans Labs?
5
1. CBC with differential
2. Chemistry panel
3. Immunologic panel
4. Complete hypercoagulability screen
5. Toxicology panel
56
Buerger’s Disease
Thromboangiitis Obliterans Labs.
--Chemistry panel to include? 5
-- Immunologic panel to include? 2
--Complete hypercoagulability screen to include what? 6
--Toxicology panel to include? 3
1. FBS,
2. LFT,
3. renal function
4. Urinalysis
5. ESR & CRP
1. ANA,
2. RF
1. coagulation tests,
2. antiphosholipid antibodies,
3. anticardiolipin antibodies,
4. protein C & S,
5. Antithrombin III,
6. factor V Leiden
1. cocaine,
2. amphetamines,
3. cannabis
57
```
Buerger’s Disease
Thromboangiitis Obliterans
Diagnosis:
1. Age?
2. Current or present use of?
3. Presence of?
4. Exclusion of?
5. Consistent ___________ findings in what?
6. What the only means to establish definitive diagnosis?
-How often do we do this?
```
1. Typically between 20-40 yo male
2. Current or recent use of tobacco
3. Presence of distal extremity ischemia
4. Exclusion of other
- autoimmune diseases
- Hypercoagulable states
- diabetes by lab tests
- proximal source of emboli by echocardiography and arteriography
5. Consistent arteriographic findings in the clinically involved and non involved limbs
6. Biopsy rarely done but only means to establish definitive diagnosis
58
Buerger’s Disease
Thromboangiitis Obliterans
Treatment
3
1. Smoking Cessation!!!
2. CONSIDER Calcium channel blockers to manage vasospasm
Nifedipine,
Amlodipine
Nicardipine
3. Hyperbaric chamber
59
1. What is Peripheral Arterial Disease (PAD)?
2. Increases risk of cardiac disease by how much?
3. Plaque formation predominates where? 3
PAD is occlusive arterial disease primarily of the lower extremities
2. 250%
3.
- Aortic bifurcation
- Tibial trifurcation
- Femoral artery at adductor hiatus
60
PAD occurs when:
1. MOst commonly
2. Where else can it develop
1. Most commonly seen when the arteries of your legs become hardened and clogged and reduce the flow of blood to your legs and feet.
2. However, PAD can also develop in the arteries that carry blood from your heart to your head, arms, kidneys and stomach
Just like clogged arteries in your heart, clogged arteries in your legs raises your risk for having a heart attack or stroke.
61
PAD can affect your quality of life: How so?
How can you help this?
Nearly everyone who has P.A.D, even those that do not report leg symptoms suffers from an impaired ability to walk as fast or as far as they could with P.A.D.
will build collaterals for exercise so when we reperfuse them they have to exercise
62
1. What does PAD result in?
| 2. Peripheral arterial disease may be described as what two kinds?
1. Peripheral arterial disease results in reduced blood flow in the arteries of the trunk, arms and legs
2. Occulsive or Functional
63
1. Occlusive PAD is due to?
2. Functional PAD is due to?
3. There is also Raynaud’s disease which is a condition in which are?
1. Occlusive PAD is due to structural changes that narrow or block arteries and often results from atherosclerosis
2. Functional is usually due to a sudden, temporary narrowing (spasm)
3. small arteries (arterioles), usually in fingers or toes, constrict more tightly in response to cold or stress
Distinct syndrome and is NOT ALWAYS due to PAD
64
Three distinct patterns of disease
1. Type I: affects 10-15% of patients? 2
Most common in younger pts?
2. Type II: affects 25% of patients?
- afeects what?
3. Type III: most common (60-70% of patients)?
- What kind of disease?
- Affects what? 5
```
Type I: affects 10-15% of patients
1. Limited to
-aorta
-common iliacs
Most common in younger patients (40-55)
Heavy smokers and/or hyperlipidemia
```
Type II: affects 25% of patients
1. Affects the
- aorta,
- common
- external iliacs
Type III: most common (60-70% of patients)
1. Multilevel disease
2. Affects
- aorta
- iliac
- femoral
- popliteal
- tibial
65
Type II and III have typical risk factors of atherosclerosis?
5
1. older
2. male
3. DM
4. HTN and
5. higher incidence of CV disease and CAD
66
LE- Peripheral Arterial Disease
Clinical Presentation
4
1. Erectile dysfunction (iliac disease)
2. Claudication
3. Gangrene
4. Leriche’s Syndrome (triad)
67
LE- Peripheral Arterial Disease:
Ischemic Rest Pain= Pain in the absence of exertion
1. Described as what kind of pain?
2. Relieved by what?
1. Usually described as nocturnal pain across the dorsum of the foot and metatarsal heads
2. Usually relieved by placing feet in dependent position
(at this point its pretty difficult to treat)
68
Leriche’s Syndrome (triad)
| 3
1. ED
2. Caludication
3. absent or descreased pulses
69
LE -Peripheral Arterial Disease
Clinical Presentation
6
1. Temperature
2. Hair loss
3. Pallor
4. Nail hypertrophy
5. Ulcer
6. Gangrene
70
Diagnostics for LE -Peripheral Arterial Disease
| Diagnosis? 3
1. ABI (Ankle Brachial Index) most useful in assessing situation
2. Gadolinium-enhanced MRA is used in evaluation of LE occlusive disease (Does NOT require contrast and MANY of these patients have renal insufficiency)
3. X-rays and CT
71
ABI (Ankle Brachial Index) most useful in assessing situation
--Name the 3 levels.
--How do we calculate it?
--Who is ABI not reliable in?
1. Normal ABI = 1.0 or greater
2. ABI less than 0.8 is diagnostic of claudication
3. ABI
72
What are X-rays and CTs used to rule out in LE -Peripheral Arterial Disease?
are used to R/O osteomyelitis in patients with non-healing ulcers
73
LE -Peripheral Arterial Disease
Diagnosis
NOninvasive procedures? 6
Invasive procedures? 2
High likelihood in pts with what disease?
NonInvasive:
1. ABI’s
2. Segmental limb pressures
- -Measured a the ankle, below the knee and mid thigh
3. Limb plethysmography
4. Exercise testing
- -Performed in vascular lab
5. Doppler & duplex ultrasound
6. MR angiography
Invasive
1. Contrast arteriography
2. CT angiography
High likelihood pt with renal disease
74
Three approaches for treating P.A.D:
3
The overall goals of treatment
3
1. Lifestyle changes
2. Taking medication
3. In some cases, special procedure or surgery
1. Reduce symptoms
2. Improve quality of life and mobility
3. Prevent heart attack, stroke, and amputation
75
LE -Peripheral Arterial Disease
Treatment
4
Whats the bottom line for treatment of PAD?
1. Tobacco cessation critical!!!
2. Anti-platelet agent- aspirin 81mg
3. Cilostazol (100mg BID)
4. Supervised walking program has increased distance by 150% in 6 months
BOTTOM LINE: Due to CAD, patients with claudication have a 50% 5-year survival
76
What is Cilostazol (100mg BID)?
(what does it do? 2)
IF TOLERATED, what are the results?
1. a phosphodiesterase inhibitor
2.
- Impairs platelet aggregation
- Increases calcium mediated vasodilation
3. IF TOLERATED, has improved 2/3 of patients
77
Whats Vasculitis?
Can be classified how? 4
Group of disorders that destroy blood vessels by inflammation.
Can be classified by the
1. cause,
2. the location,
3. the type of vessel or
4. the size of vessel
78
Classification by the size of vessel
- Large vessel? 2
- Medium vessel? 3
- Small vessel? 2
1. Takayaus arteritis,
2. Temporal arteritis
1. Buerger’s disease,
2. Kawasaki disease,
3. Polyarteritis nodosa
1. Henoch-Schonlein purpura,
2. Behcets syndrome
79
Possible Vasculitis Symptoms
| 8
1. General symptoms: Fever, weight loss
2. Skin: Palpable purpura
3. Muscle and joints: Myalgia, arthralgia or arthritis
4. Nervous system: headache, stroke, tinnitus, reduced visual acuities
5. Heart and arteries: MI, HTN, gangrene
6. Respiratory tract: Nose bleeds, bloody cough, lung infiltrates
7. GI tract: Abdominal pain, bloody stool, perforations
8. Kidneys: Glomerulonephritis
80
Vasculitis Diagnosis
| 6
1. ESR
2. CRP
3. Anemia
4. Increased WBC and eosinophilia
5. Biopsy of involved organ or tissue is definitive
6. Angiogram as an alternate to biopsy
81
Vasculitis Treatment?
| 3
1. Corticosteroids (Prednisone)
2. Possibly immune suppression drugs
3. Possibly antibiotics
82
IN what diseases will your ESR and SED levels be elevated?
| 3
1. infection,
2. cancer,
3. rheum diseases
83
1. What is Giant – Cell Arteritis
Temporal Arteritis?
2. Whats the most serious complication?
3. Woman >men by a ratio of 2:1
Presentation?
9
Inflammatory disease of blood vessels most commonly involving large and medium arteries of the head predominantly the external carotid artery.
Most serious complication is permanent blindness
1. Bruits
2. Fever
3. Headache
4. Sensitivity of the scalp
5. Jaw claudication
6. Tongue claudication
7. Acute visual loss or reduced visual acuity
8. Diplopia (double vision)
9. Acute tinnitus
84
How would we start treating temporal arteritis?
| 3
1. SED
2. IV steriods high dose (Treatment is high dose prednisone to prevent blindness)
prevent blindness
3. Biopsy at the end of that maybe
85
Giant – Cell Arteritis
Temporal Arteritis
PE? 4
Labs? 4
Gold standard for diagnosis?
1. Palpation of the head reveals prominent temporal arteries with or without pulsation
2. Temporal area may be tender
3. Decreased pulses may be found through out the body
4. Evidence of ischemia may be noted on fundal exam
1. LFT’s, increased ALP- alkaline phosphatase
2. ESR can be >60
3. CRP commonly elevated
4. Platelets may be elevated
Biopsy
