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What is endocarditis
infection of endocardium or valves of heart
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When does rheumatic heart disease occur?
- occurs after strep infection
- carditis can cause permanent valve damage, CHF
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What is one of the main causes of death in the first year of life?
congenital heart disease
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What are the risk factors for congenital heart disease
- genetic disorders (down's, trisomys, etc)
- maternal diabetes
- alcohol consumption
- exposure to environmental toxins
- family hx
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What happens in acyanotic?
- increased pulmonary flow
- obstruction of flow to heart
- blood to body is oxygenated
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what happens in cyanotic
- decreased pulmonary flow
- mixed blood flow
- blood going to body has venous (deoxygenated) component
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what do you see with CHD/CHF
- the tachys
- decreased cap refill
- weak peripheral pusles
- pallor
- decreased urine output
- weakness
- restlessness (hard to breathe)
- edema (peripheral, periorbital, ascites)
- neck vein distention
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How do we care for CHD/CHF
- improve cardiac function
- remove fluid and sodium buildup
- decrease cardiac demnad
- improve O2
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How do we improve cardiac function
administer meds (digoxin most common, also ACE inhibitors)
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How do we remove fluid and sodium buildup
- med therapy (diuretics, potassium supplement depending on diuretic choice)
- possibly fluid and sodium restriction
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how do we decrease cardiac demand
bed rest, positioning, treat infection, may have anti-anxiety meds ordered
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How do you treat endocarditis?
with high dose antibiotic therapy for 2-8 weeks
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what do we see with rheumatic fever
- chest pain
- joint pain
- new murmurs
- muscle weakness
- nontender swelling over bony prominences
- erythema to trunk and extremities
- positive throat culture
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What are we going to do with rheumatic fever
- med therapy (penicillin the drug of choice, anti-inflammatory meds)
- family support
- education (likelihood of relapse)
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how is kawasaki disease caused?
etiology is unknown
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how do we dx kawasaki disease
by clinical findings and lab results, not by diagnostic tests
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what do we see with kawasaki disease
- high, persistent fever
- edema, erythema or peeling of skin on palms and soles
- bilateral conjunctival inflammation w/o exudate
- erythema of lips
- oropharyngeal reddening
- strawberry tongue
- cervical lymphadenopathy
- polymorphous rash
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What are the 3 phase of kawasaki disease
acute phase, subacute phase and convalescent phase
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What do we see with the acute phase of kawasaki disease
- abrupt onset of high fever
- fever unresponsive to antibiotics and antipyretics
- very irritable
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what do we see with the subacute phase of kawasaki disease
- resolution of the fever
- lasts until all clinical signs disappear
- child at greatest risk for coronary artery aneurysms in this phase
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what do we see with the convalescent phase of kawasaki disease
- all clinical signs resolved
- lab values have not returned to normal
- phase complete when lab values return to normal (usually 6-8 weeks after onset)
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what are the long term complications of kawasaki disease
- coronary artery aneurysms
- myocardial infarction
- myocardial ischemia
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what is the therapeutic management of kawasaki disease
- gamma globulin infusion
- high-dose aspirin therapy
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what is the prognosis of kawasaki disease
- with early dx and treatment, full recovery anticipated
- death primarily associated with cardaic damage (primarily thrombosis)
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What are we going to do for kawasaki disease
- monitor cardiac status carefully
- strict I/O
- daily weights
- assess for CHF
- monitor during gamma-globulin infusion
- treatment of symptoms
- family support/education
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what is sickle cell anemia?
- hemoglobin disorder
- autosomal recessive disorder
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what do we see with sickle cell anemia
- swelling of hands and feet
- pain (can be generalized, specific, often in joints)
- can have chest pain
- pallor
- can have respiratory difficulty, high levels of anxiety
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what are we going to do for sickle cell anemia?
- pain management (PCA, steriod therapy)
- possible O2 therapy
- adequate hydration
- blood tranfusion
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what are we looking at in a cardiac-focused physical assessment
- skin color
- hair distribution
- cap refill
- edema
- temp
- pulses
- BP
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Who has the highest rates of HTN
- older adults
- african-americans
- lower socioeconomic classes
- lower education levels
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what are some risk factors for atherosclerosis
- diabetes
- smoking
- HTN
- obesity
- hyperlipidemia
- phlebitis
- surgery
- autoimmune diseases
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What are we going to see with arterial disorders
- intermittent claudation
- several different kinds of pain
- localized skin temp changes
- different skin colors in certain regions
- edema?
- wound healing issues
- diminished pulses distal to the occlusion
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what is virchow's triad
- venous stasis - blood not moving
- hypercoagulability - blood clots alot
- injury to venous walls
- (at least 2 of 3 need to be present for thrombus formation)
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what are we going to see with superficial venous disorders
- redness
- warmth
- tenderness
- induration
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what are we going to see with deeper thrombophlebitis
- may be asymptomatic
- unilateral leg swelling
- pain
- rednesss/warmth of leg
- dilated veins
- low-grade fever
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what is the key nursing goal with thrombophlebitis
- prevention
- other goals include early detection, prevention of extension or spread, and prevention of further formation
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what are we going to do for venous disorders
- assess and document
- encourage ambulation
- active ROM
- SCDs or ted hose
- anticoagulant therapy
- monitor for PE
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what are common anticoagulants
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what lab tests are performed to determine need or efficacy of anticoagulant therapy
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what is the antagonist for coumadin
vitamin K
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what is the antagonist for heparin
protamine sulfate
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