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Vascular diseases Flashcards

1
Q

Where can disturbances in blood flow occur?

A
  • depends on system of patent blood vessels and adequate perfusion pressure
  • disturbance disrupts:
    delivery of O2 and nutrients
  • removal of waste products
  • return of blood to the heart
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2
Q

What occurs in arterial disorders?

A
  • decreased blood flow to the tissue, impaired O2 and nutrient delivery
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3
Q

What occurs in venous disorders?

A
  • interference with outflow of blood from capillaries

- interference with removal of tissue wastes and return of blood to heart

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4
Q

What are the factors that contribute to disturbance in blood flow?

A
  • pathologic changes in vessel wall: atherosclerosis and vasculitis
  • acute vessel obstruction due to thrombus, embolus, MI, or vasospasm (prinzmetals angina) - raynauds phenomenon
  • abnormal vessel dilation: atretial aneurysms or varicose veins (valve disorder)
  • compression of blood vessels by extravascular forces: edema or tumors
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5
Q

Basic constituents of blood vessels?

A
  • tunica intima: innermost layer and lines the lumen
  • tunica media: middle layer, smooth muscle and elastic fibers, responsible for vasodilation and constriction
  • tunica adventitia: most superficial, dense irregular basement membrane, collagen fibers for strength
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6
Q

Process of platelet aggregation?

A
  • platelets circulate in close proximity to vascular walls
  • they don’t interact with endothelial cells which provide natural resistance to thrombosis
  • may adhere in many inflammatory states
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7
Q

3 types of arteriosclerosis?

A
  • atherosclerosis: plaque buildup of fat, cholesterol, or calcium
  • moenckenberg medial calficific sclerosis: calcium deposits in muscular mdidle layer (tunica media), poorer dx
  • arteriosclerosis: vessel wall thickening and luminal narrowing in small arteries and arterioles
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8
Q

common features of arteriosclerosis?

A
  • stiffening of arterial vessels (HTN, widens pulse pressure - lose elasticity)
  • thickening of arterial wall
  • degenerative nature of the disease
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9
Q

difference b/t arterioscleroiss and atherosclerosis?

A
  • arteriosclerosis: thickening and hardening of arterial walls
  • loss of elasticity of medium or large vessels (lead to an aneurysm)
  • atherosclerosis: specific form of arteriosclerosis caused by build up of fatty plaques and cholesterol in the arteries (have fatty streaks at age of 9)
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10
Q

Major complications of atherosclerosis, risk factors?

A
  • responsible for 50% of all deaths in developed world
  • major complications:
    ischemic heart disease
    stroke (CAD)
    aneurysm
    PVD
  • develops in response to vascular injury and involves inflammation and vessel remodeling
  • RFs:
    hypercholesterolemia
    diabetes
    smoking
    HTN
    obesity
    family hx of early heart disease
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11
Q

clinical presentation of atherosclerosis?

A
  • cardiac: CP/pressure (angina)
  • sudden numbness or weakness in arms or legs, difficulty speaking or slurred speech, or drooping muscle in your face
  • arteries in arms and legs: leg pain when walking (intermittent claudication)
  • kidneys: High BP or kidney failure
  • genitals: ED
  • neuro: sudden numbness or weakness in arms or legs
  • difficulty speaking or slurred speech
    drooping muscles n face, TIA may progress to stroke
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12
Q

What is Carotid artery disease? What can this cause?

A
  • vascular disease can block the carotid arteries to the brain and cause paralyzing strokes
  • stroke is 3rd leading cause of death in US and the leading cause of perm diability among older Americans
  • more than $50 billion spent annually on care of stroke pts
  • without Afib, 90% come from ICA, the ICA is one of main arteries that feeds eyes and parts of the cerebral hemispheres
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13
Q

What is a TIA?

A
  • transient episode of neuro dysfunction caused by loss of blood flow either focal brain, spinal cord or retinal without infarction (tissue death)
  • called mini strokes
  • can cause same sxs assoc with strokes
  • can present as transient hemispheric event or monocular blindness (amaurosis fugax), aphasia, slurred speech (dysarthria) and mental confusion
  • usually resolves in 24 hrs, stroke is more than 24 hrs and usually there is an embolus
  • you want to aggressively tx a TIA
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14
Q

Carotids eval?

A
  • PE (bruits)
  • duplex: 50% in sx and 80% in asx require intervention, at least one other to confirm
  • MRA
  • CTA
  • angiography: gold std but risks are stroke or bleeding pluse high cost (not really worth it)
  • only 10% of stroke pts have had TIA prior
  • asx bruits are present in 5% of pop over 50, bruits are not dx of sig stenosis (only 23% have more than 50% stenosis)
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15
Q

When do you tx pts with carotid occlusion?

A
  • asx pts with CAS of more than 80% will benefit from surgery assuming teh surgeon has complication rate of less than 2%, prophylactic operation
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16
Q

What is rheumatic fever?

A
  • inflamm disease following strep pyogenes - strep pharyngitis
  • believed to be caused by ab cross reactivity
  • usually develops 2-4 weeks after a group A strep infection
  • usually appears in children b/t ages of 6 and 15 with only 20% of first time attacks occurring in adults
  • named because of similarity in presentation to rhematism
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17
Q

Major manifestations of rheumatic fever?

A
  • migratory arthritis: predom involving large joints
  • carditis and valvulitis (pancarditis): myocarditis which can manifest as CHF with SOB
    pericarditis with a rub, new heart murmur
  • CNS involvement
  • erythema marginatum
  • sydenham’s chorea (rapid movements withou purpose of the face and arms occurring late in the disease)
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18
Q

Minor criteria for dx Rheumatic fever?

A
  • fever of: 100.8-102
  • arthralgia: joint pain without swelling
  • elev ESR or CRP
  • leukocytosis
  • EKG showing heart block such as prolong PR interval (can’t be included if carditis present as major sx)
  • previous episode of rheumatic fever
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19
Q

Modified Jones criteria for dx of rheumatic fever?

A
  • 2 major criteria
  • one major + 2 minor
  • exceptions:
    chorea
    indolent carditis
    (these are auto considered dx)
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20
Q

Tx of rheumatic fever?

A
  • anti-inflamm: ASA - be careful in children - Reyes
  • NSAIDs: ibuprofen for moderate to severe inflammatory reaction, corticosteroids
  • abx
  • PCN or clarithro or Zpack
  • HF:
    ACEI, diuretics, BBs, corticosteroids (inflammation - pericarditis)
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21
Q

What is an aortic aneurysm?

A
  • bulges in weak areas of the aorta’s wall
  • it can develop anywhere along the aorta (90% develop in abdominal aorta, most common cause is atherosclerosis), can develop in arteries at back of kneew (popliteal arteries)
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22
Q

What is an aortic dissection?

A
  • separation of the layers of its walls
  • inner lining of aortic wall tears
  • artery wall detiorates and usually asscd with high BP
  • both dissection and aneurysm can be immediately fatal, but they usually take years to develop
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23
Q

What kind of conditions do you see TAAs in?

A
  • less than 10% of aortic aneurysms
  • may be secondary to collagen vascular diseases:
    marfans or ehlers-danlos syndrome
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24
Q

Thoracoabdominal aneurysms? Classification?

A
  • traumatic occur at ligamentum arteriosum - just beyond the left subclavian artery, occurs from from rapid deceleration accidents (MVAs, and Falls)
  • TAAA:
    I (L) subclavian to renal arteries
    II (L) subclavian to iliac bifurcation
    III: midthoracic to infrarenal
    IV: distal thoracic to infrarenal
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25
Q

Clinical presentation/tx of TAAs?

A
  • most are asx
  • sx can have all of the following sxs:
    substernal, back or abd pain
    dyspnea, stridor or brassy cough (trachea pressure), dysphagia (pressure on esophagus), hoarseness (pressure on recurrent laryngeal nerve), neck and arm edema from SVC compression
    ** start BBs and call a surgeon
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26
Q

Characteristics of AAA, who is it common in?

A
  • 10th leading cause of death in men over 50
  • over 90% originate below renal arteries
  • present in 5-8% of men older than 65 and incidence has 3x in past 30 years
  • routine U/S screening of high risk groups has decreased mortality by 53%, half of all newly detected aneurysms are less than 5 cm and 2/3 will eventually need surgical repair
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27
Q

screening for AAA?

A
  • abdominal US is highly sensitive and specific screening test for AAA
  • one time screening recommended in men ages 65-75 who have ever smoked
  • one time screening for men 65-75 who have never smoked but who have first degree relative who required repair of an AAA or died of ruptured AAA
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28
Q

Clinical presentation of AAA

A

asx: picked up on routine PE with prominent aortic pulsation and or lateralization
- incidental finds on CT scan or US
25% will also have LE occlusive disease

sx: midabdominal or lower back pain with prominent aortic pulsations
anurysms that produce sxs are at increased risk for rupture
(when pt complains of lower back pain: aneurysms, mets, or prostate)

29
Q

What is an arterila embolism/thrombosis? how is it classified?

A
  • embolism: sudden interruption of blood flow to an organ or body part due to embolus adhering to wall of an artery blocking the flow of blood
  • classified by substance:
    *thromboembolism - blood clot
  • fat embolism: bone fracture or fat droplets
    *septic: embolism of bacteria containing pus
    *air: embolism of air bubbles
    tissue: embolism of small fragments of tissue
    FB embolism: foreign materials such as talc and other small objects
30
Q

Sites of embolization?

A
  • bifurcations:
    femoral - 40%
    aortic - 10-15%
    iliac- 15%

popliteal: 10%
upper extremities: 10%
cerebral: 10-15%
mesenteric/visceral: 5%

31
Q

Onset and duration of sxs of arterial emboli?

A
  • pain: sudden onset = embolic

- long standing before acute event= thrombotic

32
Q

RFs for atherosclerotic heart disease?

A
  • hypercholesterolemia
  • diabetes
  • smoking
  • HTN
  • obesity
  • family hx of early heart disease
33
Q

Clinical presentation of arterial embolic disease?

A
  • 6 Ps of acute limb ischemia:
  • pain
  • pallor: extreme or unnatural paleness
  • pulselessness
  • paresthesia: sensation such as burning, prickling, itching or tingling
  • paraparesis (paralysis): muscle weakness allowing limited movement
  • poikilothermia: variation of body temp regionally: cold
34
Q

Imaging dx - in arterial embolic disease?

A 
- ateriography:
Pt with viable limb
evaluate the anatomy
operative planning - target vessel
therapeutic: thrombolysis, angioplasty
35
Q

Management for arterial embolic disease?

A
  • pt with threatened extremity shouldn’t delay revascularization and arteriography may be done intraoperatively
  • rapid systemic anticoag: heparin bolus/continuous drip, prevent propagation of thrombus, distal thrombosis, venous thrombosis
  • surgery: embolectomy
  • several trials have demonstrated that thrombolytic therapy is safe and effective alt to surgery in approp selected pts
36
Q

What is occuring in venous circulation disorders?

A
  • produced congestion of affected tissues

- predispose to clot formation because of stagnation of flow and activation of clotting system

37
Q

Types of venous disorders?

A
  • varicose veins: enlarged tortuous veins usually in legs (valve issue - bulging, backflow)
  • thrombophlebitis: vein inflammation
  • there are also veno-occlusive disorders (VOD)
38
Q

Formation of venous clot depends on the presence of at least 1 of virchow’s triad factors. What are these? lead to thrombophlebitis

A
  • venous stasis
  • injury to vessel wall (inflammation, smoking)
  • hypercoagulable state (factor 5 leiden def, lupus)
39
Q

What are the components of venous stasis?

A 
- alterations in normal blood flow:
prolonged immobility
long plane or car ride
bed bound during hosp
varicose veins
40
Q

Presentation of venous stasis (venous insufficiency)

A
  • progressive edema of leg which begins at ankle and calf
  • dull aching discomfort
  • worse at end of day and improves with elevation
  • often varicosities are present
  • skin changes:
    stasis dermatitis
    brownish pigmentation: breakdown of hemoglobin: iron is being deposited in the skin
    brawny induration: LDS - lipodermatosclerosis
    skin is thin, shiny, atrophic, and cyanotic
41
Q

DDx of venous stasis?

A
  • CHF/renal disease: bilateral edema

- lymphedema: won’t respond to elevation: edema is more prominent in dorsum of foot, no varicosities

42
Q

tx of venous stasis?

A
  • limit standing
  • intermittent elevation of legs during the day
  • daily use of thigh high compression stockings
  • regular exercise
  • skin tx: protection and lubrication
43
Q

virchow’s triad: endothelial injury or vessel wall injury comoponents?

A
  • vessel piercings and damages from:
    bacteria
    monocytes in chronic inflammation biomaterials of implants/devices
44
Q

virchow’s triad: hypercoagulability components?

A

alterations in constitution of blood:

  • hyperviscosity - def of antithrombin III, protein C or S def, Leiden 5 factor
  • nephrotic syndrome
  • changes after severe trauma or burn
  • disseminated cancer (malignancy)
  • late preg and delivery
  • race
  • advanced age
  • cigaretted smoking
  • hormonal contraceptives
  • obesity
45
Q

What hemodynamic changes occur that impact venous circulation?

A
  • sheer stress

- HTN

46
Q

Pathophys of thrombophlebitis?

A
  • thrombi usually form at venous cusps of deep veins where altered or static blood flow causes clot formation
  • alt: clots form from intimal defects
  • clots are composed from fibrin, red cells, and platelets and cause partial/complete obstruction of vein
47
Q

What is superficial thrombophlebitis?

A
  • thrombosis can occur in any superficial vein primarily in saphenous vein and its tributaries
  • local pain, erythema, and tenderness are characteristic findings
  • mild cases can be tx with cold compresses, analgesia, and elastic supports
  • severe cases can be debilitatiing and should be managed by bed rest, elevation of extremity, support stockings and analgesia
  • abx are useful in septic thrombophlebitis
48
Q

What is Buerger’s disease (or thromboangiitis obliterans)?

A
  • recurring progressive inflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet
  • strongly assoc with use of tobacco products primarily smoking but from smokeless tobacco also
  • 2/3 of pts with severe periodontal disease
49
Q

Pathophys of buergers disease?

A
  • mechanisms still largely unknown but smoking and tobaccos consumption are major factors assoc with it
  • tobacco may trigger an immune response in susceptible
  • tobacco may unmask clotting defect
  • inflam reaction of vessel wall which eventually leads to vasculitis and ischemic changes in distal parts of the limbs
50
Q

Labs for dx Buergers disease?

A
  • CBC with diff
  • chem panel to include FBS, LFT, renal fxn
  • urinalysis
  • ESR and CRP
  • immunologic panel to include ANA, RF
  • complete hypercoag screen to include coag tests, antiphosph abs, anticardiolipin abs, protein C and S, antithrombin III, factor V Leiden
  • toxicology panel to include cocaine, amphetamines, cannabis
51
Q

Dx buergers disease?

A
  • typically b/t 20-40 male
  • current or recent tobacco use
  • presence of distal extremitiy ischemia
  • exclusion of other autoimmune diseases, hypercoag states and diabetes by lab tests
  • exclusion of proximal source of emboli by echo and arteriography
  • consistent arteriographic findings in clinically involved and noninvolved limbs
  • bx rarely done but only means to est definitive dx
52
Q

tx of buergers disease?

A
  • smoking cessation
  • consider CCB to manage vasospasm: nifedipine, amlodipine, nicardipine
  • hyperbaric chamber
53
Q

What is PAD? most common plaque formation areas?

A
  • occlusive arterial disease primarily of lower extremities
  • affects 8-12 mill Americans
  • impt cause of disability
  • increases risk of major cardiac event by 250%!!!!
  • plaque formation predominates at:
    aortic bifurcation
    tibial trifurcation
    femoral artery at adductor hiatus
54
Q

When does PAD occur?

A
  • most commonly seen when arteries in legs become hardened and clogged and reduce flow of blood to legs and feet
  • PAD can also develop in arteries that carry blood from heart to head, arms kidneys, stomach
  • just like clogged arteries in the heart - clogged arteries in legs raises your risk for having a HA or stroke
  • nearly everyone with PAD even those who don’t report leg sxs suffers from an impaired ability to walk as fast or as far as they could compared to when they didn’t have PAD
  • you can lower your risk of PAD: exercise
55
Q

Pathophys of PAD? Different types?

A
  • results in reduced blood flow in arteries of the trunk, arms and legs
  • disorders affecting arteries that supply the brain are considered separately as CVD
  • PAD: may be described as occlusive or functional:
    occlusive PAD is due to structural changes that narrow or block arteries and often results from atherosclerosis
  • functional is usually due to a sudden temporary narrowing (spasm)
  • there is also Raynaud’s disease: condition in which small arteries (arterioles) usually in fingers or toes, constrict more tightly in response to cold or stress
    distinct syndrome and isn’t alway due to PAD
56
Q

describe rayndauds?

A
  • fingertips of hand turn blue - vasospasm in rxn to cold

- can be assoc with scleroderma

57
Q

3 distinct patterns of PAD?

A
  • type 1: affects 10-15%, limited to aorta and common iliac, most common in younger pts (40-55)
    heavy smokers and or hyperlipidemia
  • type II: affects 25% of pts: affects aorta, common and external iliacs
    Type III: most common (60-70%)
    multilevel disease, affects aorta, iliac, femoral, popliteal, and tibial
  • type II and III have typical RFs of atherosclerosis: older, male, DM, HTN and higher incidence of CV disease and CAD
58
Q

Clinical presentation of PAD in LE?

A
  • ED (iliac disease)
  • claudication
  • gangrene
  • leriche’s syndrome (triad): ED, claudication, decreased pulses
  • ischemic rest pain = pain in absence of exertion
    usually described as nocturnal pain across dorsum of foot and metatarsal heads, usually relieved by placing feet in dependent position (severe PAD)
  • temp: cold
  • hair loss
  • pallor
  • nail hypertrophy
  • ulcer (slow healing)
  • gangrene:
    dry: non infected black eschar
    wet: tissue maceration and purulence
    bacteria- fail to thrive, most likely due to poor flow or emboli
59
Q

Dx of PAD in LEs?

A
  • ABI: most useful in assessing situation:
    normal = 1 or greater
    ABI less than 0.8 is dx of claudication
    abi is systolic B/P at ankle divided by systolic B/P in arm
    ABI less than 0.4: usually have rest pain and non healing ulcers
  • segmental limb pressures: measured at ankle, below the knee and mid thigh
  • limb plethysmography
  • exercise testing: performed in vascular lab
  • doppler and duplex US
  • Gadolinium enhanced MRA: used in eval of LE occlusive disease (doesn’t require contrast and many of these pts have renal insufficiency)
  • CXRs and CT are used to R/O osteomyelitis in pts with non healing ulcers
  • invasive:
    contrast arteriography
    CT angiography
  • high likelihood pt with renal disease
60
Q

ABI signifcant numbers?

A
  • comparison of ankle pressure to brachial SBP
  • reproducible, useful for long term surveillance
  • normal: 0.85-1.2
  • claudicants: 0.5-0.7
  • critical ischemia less than 0.4
  • may be falsely elevated in calcified vessels (DM pts)
61
Q

Tx of PAD? overall goals of tx?

A
  • 3 approaches:
    lifestyle changes: tobacco cessation, supervised walking program has increased distance by 150% in 6 months
    taking meds: aspirin 81 mg, cilostzol (100 mg BID) - phosphodiesterase inhibitor: impairs platelet aggregation, increases calcium mediated vasodilation, if tolerated: has improved 2/3 pts
    in some cases: special procedure or surgery

overall goals:
reduce sxs, improve quality of life, and mobility, prevent heart attack, stroke and amputation

62
Q

Pts with claudication have what kind of 5 year survival %?

A
  • due to CAD - 50% 5 yr survival

- tx all risk factors

63
Q

What is vasculitis?

A
  • group of disorders that destroy blood vessels by inflammation
  • can be classified by the cause, location, the type of vessel or the size of the vessel:
    by size -
    large vessel: takayaus arteritis, temporal arteritis
    medium: Buergers disease, kawasaki disease, polyarteritis nodosa
    small vessel: henoch-schonlein purpuram behcets syndrome
64
Q

What are some possible sxs of vasculitis?

A
  • general: fever, wt loss
  • skin: palpable purpura
  • muscle and joints: myalgia, arthralgia, or arthritis
  • nervous system: HA, stroke, tinnitus, reduced visual acuities
  • Heart and arteries: MI, HTN, and gangrene
  • respiratory tract: nose bleeds, bloody cough, and lung infiltrates
  • GI tract: abdominal pain, bloody stool, perforations
  • kidneys: glomerulonephritis
65
Q

Vasculitis dx? tx?

A
  • ESR
  • CRP
  • anemia
  • increased WBC and eosinophilia
  • bx of involved organ or tissue is definitive
  • angiogram as an alternate to bx
  • tx:
    corticosteroids (prednisone)
    possibly immune suppression drugs
    possible abx
66
Q

What is Giant Cell arteritis? presentation?

A
  • inflamm disease of blood vessels most commonly involving large and medium arteries of the head predom the external carotid artery
  • most serious complication: perm blindness
  • women more likely to get it than men (2:1)
  • presentation:
    bruits
    fever
    HA
    sensitivity of the scalp
    jaw claudication****
    tongue claudication
    acute visual loss or reduced visual acuity
    diplopia
    acute tinnitus
67
Q

PE - Giant cell arteritis? labs?

A
  • palpation of head reveals prominent temporal arteries with or w/o pulsation
  • temporal area may be tender
  • decreased pulses may be found through out body
  • evidence of ischemia may be noted on fundal exam
labs:
LFTs: increased ALP
ESR can be greater than 60
CRP: commonly elev
platelets: can be elevated
bx: gold std for dx!!!!
- tx is high dose prednisone to prevent blindness
68
Q

What is impt to remember with vascular disease?

A
  • pt education!!!!

- risk modification

Cardiology (20 decks)

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