Vascular Disease Flashcards

1
Q

Definition/age risk

Peripheral artery disease

A
  • Sclerotic plaque buildup in arteries
  • Incidence increases with age
  • Results in ↓ blood flow to extremities
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2
Q

4 stages

PAD Stages

A
  1. Reduced pulses
  2. Intermittent claudication
  3. Pain even when resting
  4. Ulcers
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3
Q

PAD clinical findings

A
  • Leg ischemia + pain d/t cramp in calf w/exercise that is relieved by rest
  • Many asymptomatic > 50yrs (masked b/c low activity level)
  • Atypical leg pain
  • Calf claudication, buttock + hip → A/w weakness while walking in hip + thigh; foot (night)
  • Critical limb ischemia (RARE)
  • ↓ muscle endurance
  • Relieved by hanging feet over edge of bed or walking around
  • Ischemic neuropathic pain - throbbing, burning w/severe shoot pain up limb
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4
Q

PAD objective findings

A
  • Abnormal LE pulse exam (femoral)
  • KNOWN atherosclerosis @ other sites (coronary, carotid, renal artery)
  • Poor wound healing
  • UNL cool extremity
  • Prolonged venous filling
  • Mm atrophy, skin is shiny
  • Hypertrophic nails
  • Absence of hair not predictr
  • Buerger test
  • Foot pallow w/leg elevation
  • Dusky red flush spreading proximally to toes
  • Bruit
  • Wait to examine them if cold out
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5
Q

Who are you most worried about to have this?

PAD indications

A
  • Patients > 70
  • Age 50-69 w/hx of smoking or DM
  • Suggestive s/s of leg pain w/exertion or ischemic pain at rest
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6
Q

PAD diagnostics
GOLD STANDARD

A
  • ABI (ankle brachial index) < 0.9% in either leg = DEFINITIVE
  • Normal: ankle BP > brachial BP
  • Ask about
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7
Q

PAD exam questions; what to ask about their symptoms

A
  • Exertional leg s/s, other LE s/s
  • Impaired walking function
  • Poor wound healing in LEs
  • P! at rest in LEs or feet; does it occur recumbent or upright
  • Abd p! after eating, associated w/wt loss
  • 1st degree relative w/AAA
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8
Q

PAD Differentials

A
  • Dependent on location
  • Buttock + hip: aortoiliac disease
  • Thigh: aortoiliac or common femoral artery
  • Upper 2/3rds of calf: superficial femoral artery
  • Lower 1/3rd of calf: superficial femoral artery
  • Foot claudication: tibial or peroneal artery
    DVT, MSK disorders, spinal stenosis (pseudo claudication), nocturnal leg cramps, neurogenic (neurospinal disc disease, spinal stenosis, tumor) or neuropathic causes (DM, EtOH)
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9
Q

PAD
pharmaclogic txs

A
  • Aspirin, clopidogrel, or BOTH for high risk
  • Antiplatelets
  • Lipid lowering meds to protect against CAD + stroke → slow PAD progression
  • Aggressive tx w/renal artery site
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10
Q

PAD
Nonpharmacologic txs

A
  • BP control management
  • Lifestyle changes
  • Tobacco cessation
  • Daily exercise
  • Low fat diet
  • HLD, DM, HTN control
  • Compression socks
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11
Q

PAD
Risk factors

A

Similar Risk factors to coronary atherosclerosis (a/w eaerly onset)
* HLD
* Smoking
* HTN
* Diabetes
* Non-hispanic blacks
* Low renal function
* Metabolic syndrome dx (obesity, hypercholesterolemia, HTN, insulin resistance → higher PAD risk)

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12
Q

PAD management
referral indications

A
  • Vascular surgery referral
  • Visits Q3months
  • Refer if patient has: severe claudication, rest pain, ulcer, infected ulcer or cellulitis, gangrene
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13
Q

Definition/pathology

Venous insufficiency

A
  • Venous HTN = high venous pressure fomr reflux or obstruction
  • Telangiectasis + rectangular veins → Varicose veins → Chronic venous insufficiency
  • Varicose veins → ankle/leg edema → Stasis dermatitis → Venous stasis ulcer
  • Varicose veins = there’s backwash other way
  • Telangiectasis: dialted veins
Telangiectasis
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14
Q

Venous insufficiency clinical findings

A
  • Telangiectasis s/s
  • Burning, swelling, throbbing, cramping, aching, heaviness, restless legs, leg fatigue
  • Pain relieved by walking + elevation
  • Pain relieved with warmth + compression
  • S/s can improve then worsen
  • DVT almost always symptomatic w/heaviness, aching, soreness
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15
Q

Venous insufficiency objective findings

A
  • Chronic Venous disease
  • Abnormal reticular veins 1st → incompetent perforators + truncal varicosities later
  • Varicose Veins
  • LE edema, pitting
  • Skin discoloration, hyperpigmentatino
  • Venous dermatitis
  • Cellulitis - not frequently
  • Normal veins visibly distended on footm ankle, popliteal fossa - not normal finding
  • Non-healing ulcer
  • Dilated vein
  • Darkening of skin on medial side of ankle or lower leg
  • Lipodermatosclerosis (fibrosing dermatitis of SQ)
  • Skin changes on lateral ankle → trauma or arterial insuff
Varicose veins
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16
Q

Venous insufficiency Diagnostics

A
  • Clinical - C1-C6; C6 most severe s/s
  • Staged by: Etiology, Anatomy, Patho
  • Help to DX type and severity
  • Imaging
  • U/S → Superficial vs deep vein insufficiency → Candidate for venous ablation
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17
Q

Venous insufficiency differentials

A
  • Basal Cell Carcinoma
  • Cellulitis
  • Contact dermatitis
  • Dermatological manifestations of cardiac or renal disease
  • Erisepelas
  • Squamous cell carcinoma
  • Traumatic ulcers
  • Stasis dermatitis
  • Varicose veins
  • Spider veins
  • Generalized essential telangiectasia
  • Klippel-Trenaunay-Weber Syndrome
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18
Q

Venous insufficiency phamacological txs

A
  • Topical agents
  • Emollients
  • Avoid topical abx and steroids unless necessary d/t rxns
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19
Q

Venous insufficiency nonpharm txs

A
  • Compression stockings, up to GII, or if severe, GIII
  • higher grade stockings hard to put on
  • Elevation
  • Exercise
  • Ulcer wound management w/dressings
  • Unna’s boot
Venous ulcer
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20
Q

Venous insufficiency risk factors

A
  • Age
  • Female
  • Pregnancy
  • FMHx of varicose veins
  • Obesity
  • Previous leg injury
  • Prolonged standing or sitting
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21
Q

Venous insufficiency complications

A
  • Superficial thrombophlebitis
  • VTE + deep DVT
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22
Q

Treatment for LE telangiectasis, reticular veins + small varicose veins

A
  • Sclerotherapy
  • Laser
  • Endovenous ablation
  • Endoscopic
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23
Q

Patient education Venous insufficiency

A
  • Need regular visits w/PCP for teaching of warning signs of worsening disease or DVT
  • Chronic management
  • Refer to vein clinic for further therapy
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24
Q

Definition

Deep Venous Thrombosis (DVT)

A
  • Presence of thrombus in one of deep veins+ accompanying inflammation response
  • Varicose veins
  • Incidence increases w/age; rare < 40
  • M:W 1.2:1
  • Can have upper extremity DVT
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25
Q

DVT clinical findings

A
  • Inflammatory s/s
    • Virchow’s Triad
    • Venous stasis
    • Endothelial injury
    • Hypercoagulability
  • Pain in limb that’s worse w/motion, walking of dependency
  • Relieved by rest + elevation
  • 50% have no s/s at all
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26
Q

DVT OBJ findings

A

PE systems
* Cardiac: Heart sounds
* Respiratory: crackles
* Extremities: nails, hair distribution, pulses, warmth/edema

  • SOB
  • UNL edema
  • Calf tenderness; if circumference of one calf 3cm+ > other - must r./o DVT
  • Superficial phlebitis (heat, redness, tenderness over superficial vein) - DVT
  • Dusky cyanosis if DVT extensive
  • HOMAN’S SIGN NOT RELIABLE
27
Q

DVT diagnostic GOLD STANDARD

A
  • 1st line: Duplex U/S over blood vessels +D dimer
28
Q

DVT differentials

A
  • Superficial phlebitis, cellulitis, ruptered baker’s cyst (behind knee)
  • Strained mm
  • Malignant neoplasm
  • Mm strain
  • Lyphedema
  • Achilles tendonitis
  • Arthritis
29
Q

DVT pharm txs

A
  • NSAIDs
  • Direct PO coagulants (Fondaparinux) Atrixa
  • LMW heparin
  • Warfarin contraindicted in pregnant persons INR blood draws; see pt Q2wks for draw
30
Q

DVT nonpharm txs

A
  • Compression therapy
    • support stockings
  • Maintain consistent diet while on warfarin
  • Sit in aisle seat on plane + do calf exercises
  • Seek care if having SOB or chest pain
31
Q

DVT patient education

A
  • Still encourage patient t walk - calf will pump + work against gravity to return blood to heart while upright all day
32
Q

DVT Risk Factors

A
  • Recent ortho surgery, knee replacement
  • Plane ride > 6hrs
  • Pregnancy
  • Malignancy
  • Major trauma
  • New onset paralysis
  • Hx of FMHxof DVT
  • CHF
  • Nephrotic syndrome
  • Taking OCPs/other estrogen
33
Q

DVT F/U

A
  • See patient w/in one week of ER discharge to monitor anticoagulation therapy
  • Eval warning signs of bleeding
34
Q

Definition, population

Cellulitis

A
  • Result of bacterial entry via breaches in skin barrier
  • Comminly missDX
  • Can be seen in LE edema
  • Common middle and older aged adults
  • Common in warmer months in non-tropical areas
  • Involves deeper dermis + SQ fats
35
Q

Cellulitis common bacterial pathogens

A
  • Beta hemolytic strep
  • Group A strep or Strep pyogenes
  • S. aureus
36
Q

Cellulitis clinical findings

A
  • Skin redness, edema, warmth
  • Skin abscess - collection of pus w/in dermis or SQ space, not well-defined
  • Petechiae +/or hemorrhage in erythematous skin
  • Superficial bullae
37
Q

Eryseipelas

A
  • Common in young children + older adults
  • Unilateral
38
Q

Cellulitis common sites

A
  • Extremities: most common
  • Hands (hospital)
  • Face (erysipelas)
  • Around eyes
  • Neck: uncommon
  • Breast (beta hemolytic)
  • Abdominal wall (surgical site infxn)
  • Genitalia (DX fournier gangrene, necrotizing fasciitis of perineum → MED E!)
39
Q

Cellulitis objective findings

A
  • Fever + other systemic manifestations of infxn
  • UNL
40
Q

Cellulitis diagnostics

A

Nonspecific lab findings
* Leukocytosis
* Elevated inflammation markers: ESR, CRP
* Labs usually not required
* Pts w/drainable abcess should undergo incision + drainage
* DX based on clinical manifestations

41
Q

When to culture for cellulitis?

A
  • Severe local infection (extensive cellulitis)
  • Systemic infxn signs (e.g. fever)
  • Hx of recurrent or multiple abscesses
  • Failure of initial abx therapy
  • Extremes of age (young infants/ older adults)
  • Presence of underlying comorbidities (lymphedema, malignancy, neutropenia, immunodeficiency, splenectomy, diabetes)
  • Special exposures (animal bite, water-associated injury)
  • Presence of indication for prophylaxis against infective endocarditis
  • Community patterns of S. aureus susceptibility are unknown or rapidly changing
42
Q

Cellulitis pharm txs

A
  • Abx therapy
  • Selection of empiric abx therapy based on determining most likely pathogen
    • Should always cover beta-hemolytic streptococci + MSSA
    • Systemic signs of toxicity
    • Cellulitis w/purulent drainage or exudate
    • immunocomp
    • presence of RFs for MRSA infxn
  • PO abx regiments
    • Dicloxacillin, Cephalexin, Cefadroxil
  • 5-6d therapy appropriate for pts w/uncomplicated cellulitis whose infxn improved
  • Extension of abx therapy (to 14d) may be warranted in setting of
    • severe infxn
    • slow response to therapy
    • Immunosuppression
    • 48-72 hours check-in to make sure the therapy is working
43
Q

Cellulitis nonpharm txs

A
  • Management of exacerbating conditions incl. point of entry infxn
  • Manage exacerbating conditions + any points of entry for microorganisms
  • Elevation + edema management
  • Skin management
44
Q

Cellulitis pharm contraindications

A
  • No NSAIDs corcorticosteroids
  • No topical abx d/t involvement in layers below dermis
  • Hyperbaric oxygen – no evidence for effectiveness
45
Q

Cellulitis predisposing factors

A
  • Skin barrier disruption d/t trauma (i.e. abrasion, penetrating wound, pressure ulcer, venous leg ulcer, insect bite, injection drug use)
  • Skin inflamm (i.e. eczema, radiation therapy, psoriasis)
  • Edema → impaired lymphatic drainage
  • Edema → venous insufficiency
  • Obesity
  • Immunosupp(i.e. DM or HIV infxn)
  • Skin breaks betwn toes (“toe web intertrigo”); clinically inapparent
  • Pre-existing skin infxn (i.e. tinea pedis, impetigo, varicella)
  • Prior saphenous vein harvesting for coronary artery bypass graft surgery
  • Close contact w/persons infected w/or carrying MRSA
46
Q

Cellulitis vs erysipelas vs Abscess

A
47
Q

Definition, prevalence M vs. W

Abdominal Aortic aneurysm

A
  • Aortic enlargement w/diameter of 3cm or <
  • Defect in tunica intima
  • Develops from degeneration of arterial media + elastic tissues
  • Prevalence increases w/age
  • Uncommon in persons <50yo
  • Less common in women, but more likely to rupture in women
48
Q

AAA clinical findings

A
  • Usually asymptomatic (incidental)
    Classic symptoms
  • HoTN
  • Shooting abd or back p!
  • Pulsatile abd mass
    **Be mindful of atypical presentations + attentive to new-onset, nonspecific back or abdominal p! in pts at risk of AAA
  • Clinically silent (screening allows to ID cases early on)
49
Q

AAA Objective findings

A
    • PE w/palpation only moderately sensitive
  • Pulsatile mass around level of umbilicus – most common
  • Abd auscultation à bruit
    * Pay attention on abd exam for screening
  • As aneurysms increase in size → expand at greater rate + risk of rupture increases
50
Q

AAA Diagnostics

A
  • Abd U/S
  • Abd CT
  • Possible plain radiography if aneurysm has calcified
  • Image more frequently as they get bigger
  • Stay on surveillance schedule for imaging + refer when appropriate
51
Q

AAA nonpharm txs

A
  • EVAR (endovascular aneurysm repair) good results
  • Open repair – also good results but not as good as EVAR
52
Q

AAA Risk factors

A
  • > 65
  • Male
  • Smoking hx
  • > 100 cigarettes over pt’s lifetime
    Other risk factors
  • FMHx of AAA
  • CAV, CVD
  • HTN
  • PAD
  • Hx prior to MI
  • Other aneurysms in vascular bed
    Reduced risk associated with
  • DM, Hispanic,, Black race
53
Q

Definition, M vs. W, prevalence, common site

Carotid artery stenosis

A
  • Presence of atherosclerotic narrowing of extracranial internal carotid artery
  • Tends to happen at bifurcation of carotid artery
  • Prevalence low in gen pop
  • Incidence increases w/age
  • M > W
54
Q

Carotid artery stenosis clinical findings

A
  • Often asymptomatic
  • Risk equivalent of coronary heart disease
  • Neurologic s/s sudden in onset
  • Transient ischemic attack
  • Transient monocular blindness = amaurosis fugax
  • Vertigo + syncope not generally caused by UNL carotid disease
55
Q

Carotid artery stenosis objective findings (PE)

A
  • Visual exam
  • Auscultation for carotid bruits during PE
  • bruits better indicator of general atherosclerotic dx than of stroke risk
  • Stroke risk markers
    • Progression
    • Detection of embolism
    • Carotid plaque burden + morphology
    • Reduced cerebrovascular reserve
    • Presence of silent embolic infarcts
    • U/S ID microembolization
56
Q

Carotid artery stenosis
diagnostics

A
  • Order imaging
  • Carotid duplex U/S – 1st line
    • Do not do routinely
  • Magnetic resonance angiography
  • CT angiography
  • Cerebral angiography – GOLD STANDARD but inappropriate for screening due to invasive nature…
    • Know these screenings
57
Q

Carotid artery stenosis pharm + nonpharm tx

A
  • Antiplatelet agents
  • HTN/DM tx
  • Healthy lifestyle changes
  • Revascularization w/ carotid endarterectomy medically stable
  • Revascularization w/ asymptomatic carotid stenosis who have very HI stroke risk, along w/intensive medical management
  • Carotid stenting
    – greater risk of stroke + death
  • Risk of MI greater w/carotid endarterectomy
58
Q

Carotid stenosis Stroke risk indications

A

STROKE RISK!
* Asymptomatic carotid stenosis considered risk equivalent of coronary heart disease
* Marker for INC risk for MI + death

59
Q

Do you screen for carotid artery stenosis in asymptomatic patients and why?

A

Do not screen in asymptomatic persons w/imaging tests
- no valid markers in asymptomatic pts who would benefit from revascularization

60
Q

Meds for patients with beta-lactam allergies: cellulitis tx

A
  • Oral antibiotic regimen – if no indication for parental abx consider
    ** TMP-SMX (Bactrim)
    Linezolid
    Clindamycin**
    MRSA:
  • Amoxicillin plus doxycycline
  • TMP-SMX has activity against both Streptococcus and S. aureus, including MRSA. Doxycycline provides coverage for S. aureus, including MRSA; amoxicillin is added to it for streptococcal coverage.
61
Q

When to screen for AAA?

A
  • AAA < 3cm DO NOT SCREEN
  • AAA 3-3.9cm → U/S q2-3yrs or q3yrs
  • AAA 4-5.4cm: Q6-12mos OR 4-4.4cm Q2yrs; 4.5-5.4cm Q1yr
  • AAA 5-5.4cm → Surgical consult
62
Q

Erysipelas pharm tx

A

Can be usually managed by PO abx
* Penicillin V potassium
* Amoxicillin
* Cephalexin
* Cefadroxil

63
Q

Venous Wound ulcers and management

from book

A
  • located on the medial lower leg, above the medial malleolus
  • granulation tissue or fibrinous material over the surface, with moderate to heavy exudate and minimal pain
  • hemosiderin pigmentation, edema, and lipodermatosclerosis
    *
64
Q

Arterial wound ulcer and management

A
  • occur most often on the lower extremity distal to the area of impaired perfusion
  • painful and dry, have well-demarcated edges, and can be very deep with exposed support structures
    • borders are often punched out with surrounding callus; the ulcer base varies on the basis of arte- rial perfusion. With good perfusion, they have red granulation; poorly perfused ulcers are often drier, with flattened pale gran- ulation or black eschar, warranting further vascular evaluation
  • limb is traditionally thin, cool, pale or hyperemic, hairless, and shiny as a result of decreased perfusion