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Nur 3010 exams > structural, infectious, and inflammatory cardiac ds + PVD > Flashcards

structural, infectious, and inflammatory cardiac ds + PVD Flashcards

1
Q

review: blood flow through heart

A

R atrium -> tricuspid valve -> R vent -> pulmonary valve -> pulmonary arteries -> pulmonary veins -> left atrium -> mitral valve -> L vent -> aortic valve

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2
Q

iclicker: which valve has the highest contractility, pressure, power house of the heart

A

L vent

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3
Q

risk factors for valve ds (5)

A
  • HTN (LT)
  • older age
  • smoking
  • diabetes (uncontrolled)
  • rheumatic fever/infectious endocarditis
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4
Q

assessment findings of valve ds. (5)

A
  • murmurs (systolic murmur, swooshing sound)
  • extra heart sounds (s3,s4)
  • dysrhythmias
  • dyspnea (depending on back flow of blood -> stenosis)
  • fatigue/syncope (mobilizing floor moving forward, cause by decreased cardiac output)
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5
Q

diagnostics of valve ds. (3)

A
  • ECG: L vent hypertrophy
  • CXR: shows pulmonary infiltrates
  • ECHO: GOLDEN STANDARD shows valve shape, function, and mood, main for diagnosis of valve ds., can tell regurgitation/stenosis
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6
Q

iclicker: enlarged L ventricle causes what valve disorder

A
  • aortic stenosis d/t overflow of L ventricle -> increased resistance -> hypertrophy
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7
Q

enlarged L atria causes what valve ds

A
  • mitral stenosis
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8
Q

enlarged R vent causes what valve ds.

A
  • pulmonic stenosis
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9
Q

enlarged R atria causes what valve ds.

A
  • tricuspid stenosis
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10
Q

types of valvular ds. (7)

A
  • valve prolapse
  • regurgitation
  • stenosis
    SPECIFIC DISORDERS:
  • mitral valve prolapse/mitral regurg
  • mitral stenosis
  • aortic regurg
  • aortic stenosis
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11
Q

what is valve prolapse

A
  • stretching of atrioventricular valve leaflet into the atrium during diastole
  • back flow of blood into systole from diastole
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12
Q

what is stenosis

A

valve does not OPEN completely, blood flow through valve is REDUCED
- decreased outflow = increased resistance to get more blood flow through

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13
Q

what is regurgitation

A

valve does not CLOSE properly, BLOOD BACKFLOW through valves

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14
Q

iclicker: if mitral stenosis, which chamber would increase in pressure

A
  • L atrium
  • can’t move forward? MOVE BACKWARDS
  • if aortic stenosis -> issues in L ventricle
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15
Q

what occurs during aortic stenosis (3)

A
  • valve is stenosed (constricted)
  • increased pressure in L ven
  • hypertrophy d/t vent needing more muscle mass to eject blood through stenosed valve
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16
Q

what occurs during mitral regurgitation (3)

A
  • back flow of blood
  • increased pressure in L atrium
  • risk factor for AFIB
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17
Q

nursing mgmt for valve ds (7)

A
  • patient education
  • monitor VS trends (dyspnea)
  • monitor for complications: HF, dysrhythmias, dizziness, syncope
  • med schedule: education (unit repair valve)
  • daily weights: monitor for weight gain (fluid retention)
  • plan activity w. rest periods
  • sleep with HOB elevated (orthopnea)
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18
Q

medical therapy for mitral regurg (2)/stenosis (2) and aortic regurg (1)/stenosis (2)

A

mitral regurg
- fluid congestion -> diuretics
- afterload reduction -> ACE, ARBs, Vasodilators (use BP to reduce afterload demand to make easier to move flood forward)
mitral stenosis
- can form clots
- tx: anticoags -> reduce clot formation (warfarin)
aortic regurg
- tx: control BP to promote forward BF
aortic stenosis
- tx: repair valve w/ stent, surgically
- not much can be done medically

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19
Q

types of surgical mgmt (2)

A

1) valvuloplasty (repair of valve)
- commissurotomy (break apart valve leaflets)
- balloon valvuloplasty (insert Cath intro valve space, inflate, break leaflets apart)

2) valve replacement (percutaneous approach, similar to cardiac Cath)
- mechanical valves: clicking noise upon auscultation, risk: clots
- tissue valve: bioprothesis (Xenograft: different animals, homograft: cadavers, autografts: tissue from self)

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20
Q

transaortic vave replacement (TAVR)

A
  • most common way to replace aortic valve
  • Cath into femoral and when reach stenosed area -> inflate Cath to deploy new valve
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21
Q

nursing mgmt for valvuloplast & valve replacement (3)

A

balloon valvuloplasty
- monitor for HF and emboli
- assess heart sounds every 4 hours
- same care as after cardiac catheterization: lay flat, homeostasis, assess entry site

surgical valvuloplasty or valve replacements
- focus on HEMODYNAMIC STABILITY & recovery from anesthesia
- frequent assessments w/ attention to neurologic, respiratory, and cardiovascular systems

patient education
- anticoagulant therapy: mechanical valve (on anticoags for rest of life), xenograft (aspirin for risk mitigation)
- prevention of infective endocarditis: diseased valve
- follow up: valves can degrade overtime (also have systemic ds if valve ds overall)
- repeat ECHO

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22
Q

post valve replacement med regimens (2)

A

anticoagulations
- mechanical valves: lifelong anticoags w/ Coumadin (vit. k antagonist), INR goal: 2.5-3.0 (therapeutic range), if eat vitamin K: need to stay consistent
- bioprosthetic valves (xenograft): daily baby ASA

prophylaxis
- if going under major dental work (scaling, root planing, NOT ROUTINE) = prophylactic abx treatment before recommended
- indicated for: valve ds., congenital heart defects (repaired, unrepaired), cardiac transplant with valve regurg

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23
Q

iclicker: loud diastolic murmur over R upper sternum border can be heard where? which valve?

A
  • aortic heart sound
  • surgery is treatment
  • assessment is important!
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24
Q

what is cardiomyopathy (what, can lead to, etiology, types)

A
  • what: disease of myocardium resulting in impaired cardiac output (not contracting as it should)
  • can lead to: HF, sudden death, dysrhythmias
  • etiology: primary or secondary (HTN, valve ds)
  • types (3): dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restrictive/constrictive cardiomyopathy (RCM)
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25
Q

dilated cardiomyopathy (DCM) (fact, what, manifestation, s/sx, diagnostics, tx)

A
  • most common cardiomyopathy w/ long standing HTN
  • what: dilation of vent w/o hypertrophy and systolic dysfunction (balloon out chamber -> not as efficient)
  • manifestation: low CO w/ subsequent pulmonary congestion (activates SNS (HR), RAAS (BP)
  • s/sx: pulmonary edema, peripheral edema, restlessness/agitation, angina, syncope (chamber: AV valve regurg - mitral, narrowed pulse pressure, S3/murmur -> blood smacking dilated ventricular wall)
  • diagnostics: CXR (enlarged heart), ECHO (EF, valve function), angiography (if caused by MI or cardiac Cath), BNP (high d/t vent stretch, immobilization of fluid)
  • tx: (manage BP) ACE inhibitors, beta blockers/ca channel blockers, digoxin (inotropic, increased contractility), diuretics (fluid overload) (tip: ABCDD)
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26
Q

restrictive cardiomyopathy (what, manifestation, etiology, s/sx, diagnostics, tx)

A
  • what: restrictive/hard walls which don’t pump effectively - inadequate diastolic filling (can’t fully relax, decreased pump efficiently)
  • manifestation: less blood in = less CO
  • etiology: familial, protein deposition (amyloidosis), sarcoidosis (collagen deposition ds., leads to scaring d/t damage of myocardium)
  • s/sx: pulmonary edema, peripheral edema, restless/agitation, angina, syncope
  • diagnostics: CXR (normal w/ congestion at times d/t no dilation, hypertrophy), ECHO (normal EF w/ some wall motion abnormalities)
  • tx: prevention (primary), transplant
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27
Q

hypertrophic cardiomyopathy (what, manifestation, s/sx, diagnostics, tx)

A
  • what: thickened walls s/d to increased demand (HTN, CAD - risk factors)
  • in peds: rare, deadly, GENETIC
  • manifestation: low CO, subsequent demand for O2 d/t hypertrophic muscle, increases strain on already hypertrophied myocardium
  • s/sx: often asymptomatic unless under strain -> SOB
  • diagnostics: CXR (normal, mildly enlarged in severe cases), ECHO (septal thickening walls)
  • tx: beta blockers, ca channel blockers (myocardial relaxation) OR excision of hypertrophic muscle (surgery, peds, too much muscle)
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28
Q

L vent hypertrophy issues?

A
  • thickened ventricular septum -> increased O2 demand -> decreased efficient pump
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29
Q

HOCM (hypertrophic obstructive cardiomyopathy) (5)

A
  • deadly in peds
  • vents enlarged but can’t see on ECHO or XRAY or BP
  • bulges -> no BF d/t HOCM -> sudden death
  • not often caught
  • dangerous
  • tx: sugerical removement
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30
Q

patient education for cardiomyopathy (5)

A
  • diet: low Na, low FAT
  • rest periods with activity
  • exercise with appropriate rest periods
  • stop smoking and alcohol
  • stress reduction
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31
Q

nursing assessment of cardiomyopathy (6 + physical assessment)

A
  • hx (predisposing facors (PMH), family history)
  • chest pain
  • ROS: presence of orthopnea, syncope (distal extremities, pulmonary)
  • review of diet: Na reduction, vitamin supplements
  • psychosocial history: impact on family, stressors, depression

physical assessment:
- VS pulse pressure
- pulsus paradoxus (deep breath causes BP/HR to change)
- weight gain/loss
- PMI, murmurs
- S3/S4
- pulmonary auscultation for crackles (indicates congestion)
- JVD
- edema

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32
Q

potential complications of cardiomyopathy (6)

A
  • HF
  • ventricular dysrhythmias (vtach, fib)
  • atrial dysrhythmias (afib, aflutter)
  • cardiac conduction defects
  • pulmonary or cerebral embolism
  • valvular dysfunction
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33
Q

inflammatory diseases of the heart (5)

A
  • all 3 layers may be affected by infectious process (have to specify which)
  • diseases named by later of the heart that is affected
  • diagnosis made by patient symptoms and ECHO
  • management for all infectious diseases is PREVENTION (GOAL)
  • IV abx are necessary once infection has developed in the heart
34
Q

types inflammatory diseases of heart (4)

A
  • rheumatic endocarditis
  • infection endocarditis
  • pericarditis
  • myocarditis
35
Q

what is rheumatic endocarditis (who, what, tx)

A
  • occurs in school age children post GROUP A BETA HEMOLYTIC STREPTOCOCCAL PHARYNGITIS
  • need to promptly recognize & treat strep throat to prevent rheumatic fever
  • tx: abx OR naturally can treat, but can spread to endocardium, causing autoimmune inflammation of endocardium/valves (s/sx: HF)
36
Q

what infective endocarditis (what, who, goal)

A
  • bacteria in blood (not specific to strept)
  • develops in people with prosthetic heart valves or structural cardiac defects, IV drug abuser, debilitating diseases, indwelling catheters, prolonged IV therapy
  • goal: remove all lines asap to prevent bacterial buildup
  • right sided valve disease = indwelling lines/IV abuse
37
Q

rheumatic endocarditis (s/sx, diagnostics, tx)

A

s/sx: HF s/d rheumatic endocarditis
- tachycardia
- cardiomegaly
- friction rub (velcro pull apart)
- chest pain
- murmurs
- rash (abrasive skin
- cough

diagnostics:
- throat swab (active strept infection)
- ASO (anti-strptolysin) titer: tests of antibodies in blood (kidney disease)

tx:
- abx
- potential repair or replacement of valves

38
Q

infective endocarditis (s/sx, diagnostics, tx)

A

infective is way sicker than rheumatic, bizarre ds. presentation, active bacteriamia

sx: systemic, general bacteriemia
- fever
- flu like sx
- murmurs
- petechia (unusual rashes)
- splinter hemorrhages (under nail beds)
- roth spots (lesions in retina)
- laneway lesions (painful red lesions on palm and soles)
- Osler nodes (painful red lesions on hands and feet)
- anemia and hemolysis

diagnosis:
- blood cultures
- echo

tx:
- abx (lots)
- possible valve replacement if necessary
- prophylaxis (prophylactic abx: high risk dental procedures w/ abnormal heart valves)
- stop IV drugs

39
Q

pericarditis (3)

A
  • inflammation of pericardium
  • many causes
  • potential complications: pericardial effusion, cardiac tamponade
40
Q

myocarditis (3)

A
  • inflammatory process involving myocardium
  • most common pathogens involved in myocarditis tend to be VIRAL (endocarditis = bacterial)
  • complications: cardiomyopathy, HF (inability to move blood where it needs to go)
41
Q

pericarditis (causes (5), s/sx (5), diagnostics (3), tx (4))

A

causes:
- uremia: chest pain manifestations, renal failure, increased nitrogenous products
- viral infection: very common
- MI
- autoimmune diseases
- cancer

s/sx:
- pericardial effusion/cardiac tamponade (diminished heart sounds, low BP, JVD)
- constriction of pericardium (fibrosis of pericardium) (hard to diagnose w/o ECHO)
- fever
- chest apin (worse = breathing; better = leaning forward, heart moves away from inflammation)
- friction rub

diagnostics:
- ECG changes (electrical alternans: fluid filled sac around heart, causing it to swing back and forth, complex QRS)
- CXR
- ECHO

treatment:
- pain relief
- treat cause (underlying)
- colchicine (inhibits neutrophil migration, reduce = affects pericarditis)
- sx: pericardiocentesis, percardiectomy

42
Q

myocarditis (risk factors (4), s/sx (7), diagnosis (2), tx (3))

A
  • inflamed muscle tissue

risk factors:
- younger pt.
- (primary)post viral: coxsacki/parvovirus/covid
- bacterial: Lyme ds., rheumatic fever
- lupus

s/sx:
- cardiogenic shock (inflamed muscle stops working, pump fail) -> death
- chest pain (left sternal/retrosternal, nonpleuritic, non-positional if isolated to myocardium)
- fever
- fatigue
- arrhythmias/tachycardia (unexplained apart from fever)
- syncope
- CHF sx (dyspnea, orthopnea, PND, peripheral edema)

diagnosis:
- ECG supports patient presentation
- elevated trops (look @ hx. as well)

tx:
- supportive, eliminate cause if possible
- not much we can do for patient
- self limiting!!

43
Q

clinical manifestations for inflammatory concerns (5 overall, alert) + diagnostics (12))

A
  • fever
  • new heart murmur; friction rub at left lower sternal border (pericarditis)
  • osler nodes, janeway lesions, Roth spots, splinter hemorrhages in nail beds (rheumatic)
  • overall: cardiomegaly, HF, tachycardia, splenomegaly (rheumatic)
  • ALERT sx: fatigue, dyspnea, syncope, palpitations, chest pain (myocarditis) (decrease CO)

diagnostic tools:
- blood cultures (inflammatory issues, MAIN, outlier of all)
- ECHO (heart function)
- CBC
- rheumatoid factors
- ESR (inflammatory marker, sedimentation rate)
- CRP
- urinalysis
- ECG
- cardiac catheterization (diagnostic pressures in heart)
- CMR imaging
- TEE
- CT scan

44
Q

prevention of inflammatory diseases of heart (5)

A
  • antibiotic prophylaxis BEFORE certain procedures (major dental work w/ valve ds)
  • ongoing oral hygiene (pt. who can’t help themselves)
  • meticulous care should be taken in patients “at risk” who have catheters
  • catheters should be removed ASA no longer indicated (post op)
  • immunizations (when recommended)
45
Q

review: describe the vascular system

A
  • consists of two interdependent systems (R side -> pulmonary, L side -> systemic)

-arteries/arterioles
- capillaries
- veins and venules
- lymphatic vessels (move fluid back and forth, separate)

46
Q

functions of vascular system (4)

A
  • circulatory needs of tissues (supply blood, o2, electrolytes, ATP, glucose, etc.)
  • augments BP/hemodynamic resistance as we move blood from aorta -> fingers
  • capillary filtration and reabsorption
  • peripheral vascular regulating mechanisms
47
Q

physiologic changes of vascular system (3)

A
  • pump failure (issues with blood supply)
  • alterations in blood and lymphatic vessels
  • results in: circulatory insufficiency of the extremities
48
Q

gero considerations of vascular system (2)

A
  • aging produces changes in walls of blood vessels that affect transport of oxygen and nutrients to tissues
  • changes cause vessels to stiffen and results in: more contriction (increased peripheral resistance, impaired blood flow, increased left ventricular workload)
49
Q

assessment of vascular system (5)

A

health hx:
- intermittent claudication (calf pain, ischemia muscle)
- “rest pain”
- location of pain

physical assessment:
- skin (cool, pale, pallor, rumor, loss of hair, brittle nails, dry or scaling skin, atrophy, ulcerations
- pulses (DP/PT, good temp, pulse, hair on toes = good sign)

50
Q

diagnostic evaluation of vascular system (2)

A

doppler US flow studies:
- ankle brachial index (ABI): ankle BP/ARM BO P = ABI (use systolic of each)
- ankle BP higher than arm BP due to gravity dependence

continuous wave doppler US:
- detects blood flow, combined with computation of ankle or arm pressure
- characterize nature of peripheral vascular disease
- easy to identify
- recognize flow of blood

TIP: if ABI <1% = PAD

51
Q

diagnostic evaluation of peripheral vascular disease (7)

A
  • exercise testing: walk until intermittent claudication occurs
  • duplex ultrasonography: venous obstructions/clots
  • computed tomography scanning: assess lymphatic collections
  • angiography: changes in BF
  • magnetic resonance angiography
  • contract phlebography (venography)
  • lymphoscintigraphy: radioactive isotope -> lymph node -> look for accumulation in body
52
Q

arterial disorders (types) (8)

A
  • arteriosclerosis and atherosclerosis
  • peripheral arterial occlusive disease (PVD)
  • upper extremity arterial occlusive disease (PVD)
  • aortiliac disease (PVD)
  • aneurysms (thoracic, abdominal, other)
  • dissecting aorta
  • arterial embolism, arterial thrombosis
  • Raynaud phenomenon and other acrosyndromes
53
Q

arterioscleosis (3)

A
  • occurs with age
  • hardening of arteries
  • diffuse process where by the muscle fibers and the endothelial lining of the walls of small arteries and arterioles become thickened
54
Q

atherosclerosis (4)

A
  • global hardening, age factor
  • different process, affecting intimate of large and medium sized arteries
  • accumulation of lipids, calcium, blood components, carbohydrates, fibrous tissue on the intimal layer of the artery
  • atheroma or plaques
55
Q

common sites of atherosclerotic lesions (3)

A
  • common carotid
  • left common iliac
  • popliteal artery
56
Q

risk factors for atherosclerosis and PAD (modifiable) (9)

A
  • presence/absense of nicotine, smoking
  • diet
  • HTN
  • diabetes
  • obesity S/D to increased estrogen
  • stress
  • sedentary lifestyle
  • C-reactive protein (predicts inflammatory disease)
  • hyperhomocysteinemia (inflammatory marker)
57
Q

risk factors for atherosclerosis and PAD (unmodifiable) (3)

A
  • age
  • gender
  • familial predisposition/genetics
58
Q

Peripheral arterial Disease (hallmark, etiology, s/sx)

A
  • hallmark sx: intermittent claudication described as aching, cramping, inducing fatigue or weakness (LE cals)
  • occurs w/ some degree of exercise or activity
  • relief w/ REST
  • pain: associated w/ critical ischemia of distal extremity, described as persistent, aching, boring (rest pain)
  • ischemic rest pain worse at night, wakes patient up (d/t no gravity help w/ BF, dangling relieves pain)
59
Q

pharmacologic therapy PAD (5)

A
  • pentoxifylline (trental): vasodilator of peripherals
  • cilostazol (pletal): vasodilator, platelet inhibitor
  • aspirin (PAI): around atheromas
  • clopidogrel (plavix) (PAI): around atheromas
  • stains (decrease global risk atherosclerosis)
60
Q

assessment with PAD (8)

A
  • health hx
  • meds
  • risk factors
  • s/sx of arterial insufficiency
  • claudication, rest pain
  • color changes
  • weak/absent pulses
  • skin changes/ skin breakdown
61
Q

how to improve peripheral circulation (8)

A
  • exercises and activity: walking, graded isometric exercises (walk on stairs, flex motion)
  • positioning strategies: HOB elevated
  • temperature: effects of heat (vasodilation, increase BF), cold (vasoconstriction, decrease BF)
  • smoking cessation
  • control BP ,glucose
  • stress reduction
  • interventional angioplasty (distal arteries, stens and/or arterial grafts)
  • same preventative drugs as high risk MI/CAD (stain, BP control)
62
Q

aneurysms (what, classified, common, types)

A
  • localized sac or dilation formed at weak point in wall of artery (dilation)
  • classified by its shape or form
  • most common forms: saccular, fusiform
  • saccular: projects from only one side of the vessel
  • fusiform: when entire arterial segment becomes dilated

TIP: dangerous!! monitor, critical, make sure NO RUPTURE

63
Q

Raynaud’s disease (what, manifestations, triggers, tx.)

A
  • intermittent arterail vaso-occlusion, of fingertips or toes
  • associated with other underlying disease (scleroderma)
  • manifestations: sudden vasoconstriction results in color changes, numbness, tingling, burning pain (pain in cold temp)
  • episodes: brought on by trigger: cold or stress
  • occurs most frequently in young women
  • tx: protect from cold and other triggers, avoid injury to hands and fingers, gloves
64
Q

venous disorder (types, 4)

A
  • venous thromboemolism
  • chronic venous insufficiency/postthrombotic syndrome
  • leg ulcers
  • varicose veins
65
Q

venous thromboembolism’s (patho, RF, manifestation)

A
  • pathophysiology
  • risk factors (3): venous stasis, hyper coagulability, endothelial damage
  • manifestations: destruction of valves, venous obstruction, redness, warmth
66
Q

what are the risk factors of thromboemolisms (3)

A
  • venous stasis: age <65 years, hospitalization/bedrest, HF, varicosities (calf muscles act like pump to circulate blood to IVC)
  • hyper coagulability (heparin, aspirin): (S/D) obesity, factor V deficiency, cancer, septicemia, pregnancy, post surgery, estrogen
  • endothelial damage (access to vein): central catheters, surgery/trauma, infection
67
Q

manifestations of thromboembolism (3)

A
  • destruction of valves: varicosities, venous ulcers
  • venous obstruction: edema, fluid staus
  • redness, warmth: unilateral
68
Q

medical management of thromboembolism (4)

A
  • thrombectomy (rare): suck out clots
  • anticoagulation: direct factor Xa inhibitors (DOACs) (Xarelto, eliquis) (only on forever if afib)
  • endovascular umbrella filters: vena cava filters
  • thrombolytics (Tpa, alteplase): dissolves clots, used for unstable pulmonary embolisms
69
Q

preventative measures for thromboembolism (5)

A
  • application of graduated compression stockings
  • pneumatic compression devise (SCDs)
  • early ambulation: KEY
  • subq: heparin, LMWH
  • lifestyle changes: weight loss, smoking cessation, regular exercise
70
Q

varicose veins (what, prevention (5)

A
  • engorged veins, valves don’t function appropriately

prevention:
- avoid activities that cause venous stasis (wear socks that are too tight at the top or that leave marks on skin, crossing the legs at the thighs, sitting or standing for long periods)
- elevate legs 3-6 in higher than heart level
- encourage to walk 30 minutes each day if there are no contraindications
- wear graduated compression stockings
- overweight patient should be encouraged to begin weight reduction plans

71
Q

arterial symptoms of ulcers (7)

A
  • prevents BF to extremity
  • dependent positioning reduces pain (elevation WORSENS pain)
  • pain: sharp, worse at night, “rest pain”
  • intermittent claudication
  • extremity: cool to touch, thin/dry/hairless skin, rubor w/ dangle
  • diminished/absent pulses
  • ulcers: end of toes, dorsal of feet, lateral malleoulus (ankle), scant drainage, pale or black, punched appearance
72
Q

venous symptoms of ulcers (6)

A
  • elevation ALLEVIATES pain
  • worse when standing, sitting for long periods
  • pain: heavy, dull, throbbing
  • extremity: thick/tough skin, warm skin, brownish color, swelling
  • pulses: present (unless lots of edema)
  • ulcers: medial part of lower legs, swollen, lots of drainage, granulation present, shallow with irregular borders (higher on leg)
73
Q

medical management of leg ulcers (5)

A
  • anti-infective therapy depends on infecting agent (broad growth inhibitors - silver/honey/impregnanted dressing) -> abx
  • compression therapy/compression dressings for venous wounds (leg wraps that prevent accumulation venous fluid)
  • wound debridement for arterial: sx, mechanical (enzymatic, autolytic), larval therapy
  • dressings: occlusive (moist and warm sterile saline)
  • other: irrigation (cleansing w/ sterile salone or approved agent), hyperbaric O2 (send someone to hyper O2 chamber), negative pressure wound vacs
74
Q

treatment options of leg ulcers (5)

A
  • compression dressings for wound management
  • left on for up to 7 days at a time
  • consistent wound therapy
  • keep elevated
  • med honey
75
Q

potential complications with ulcers (6)

A

infection:
- abx
- difficult to differentiate cellulitis and vascular disease (infection can mask problem)
- few ulcers are clinically infected but positive for bacterial colonization

gangrene:
- necrosis and subsequent surgical emergency
- amputation
- XR of foot

76
Q

nutritional recommendations for ulcers (6)

A
  • protein
  • vitamin C and A
  • iron
  • zinc
  • avoiding sodium
  • many patients with peripheral vascular disease are older adults. particular considerations should be given to their iron intake bc many older people are anemic
77
Q

lymphatic disorders (3)

A
  • lymphangitis: inflammation/infection of lymphatic channels (tract, red streak down leg)
  • lymphadenitis: inflammation/infection of lymph nodes
  • lymphedema: tissue swelling r/t obstruction of lymphatic flow (primary: congenital OR secondary: acquired obstruction s/d cancer, mastectomy patients, compressive sleeve)
78
Q

cellulitis (s/sx, tx, nursing mgmt)

A
  • tissue infection
    -s/sx: localized swelling or redness, fever, chills, sweating
  • tx: oral abx initially, then IV abx (iv first only if: necrotizing fasciitis, 50% or more of extremities, on face)
  • nursing mgmt: elevate affected area, warm moist packs to site every 2-4 hours, educate regarding prevention of recurrence, reinforce education about skin and foot care, trace border of inflammation (for improvements or worsening)
79
Q

necrotizing fascitis (what, sx., targets, who)

A
  • exacerbation of cellulitis, prevents BF -> need to be removed
  • sx. of medical emergency
  • primarily affects limbs and perineum
  • immunosuppressed/PAD are at HIGHEST RISK
80
Q

review: labs to precipitate afib

A

potassium, magnesium
A1C
lipid panel
CMP: electrolytes

81
Q

review: when it hypertensive crisis an emergency

A
  • target organ damage

Nur 3010 exams (13 decks)

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