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
2
Q
4 stages
PAD Stages
A
- Reduced pulses
- Intermittent claudication
- Pain even when resting
- Ulcers
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
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
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
6
Q
PAD diagnostics
GOLD STANDARD
A
- ABI (ankle brachial index) < 0.9% in either leg = DEFINITIVE
- Normal: ankle BP > brachial BP
- Ask about
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
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)
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
10
Q
PAD
Nonpharmacologic txs
A
- BP control management
- Lifestyle changes
- Tobacco cessation
- Daily exercise
- Low fat diet
- HLD, DM, HTN control
- Compression socks
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)
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
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
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
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
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
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
18
Q
Venous insufficiency phamacological txs
A
- Topical agents
- Emollients
- Avoid topical abx and steroids unless necessary d/t rxns
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
20
Q
Venous insufficiency risk factors
A
- Age
- Female
- Pregnancy
- FMHx of varicose veins
- Obesity
- Previous leg injury
- Prolonged standing or sitting
21
Q
Venous insufficiency complications
A
- Superficial thrombophlebitis
- VTE + deep DVT
22
Q
Treatment for LE telangiectasis, reticular veins + small varicose veins
A
- Sclerotherapy
- Laser
- Endovenous ablation
- Endoscopic
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
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
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
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
