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exam 2 Flashcards

1
Q

what is hypertension

A
  • common and manageable chronic condition
  • major risk factor for other severe medical disorders
  • leads to increased risk of premature morbidity and morality
  • > 130/>80
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2
Q

risk factors for HTN

A
  • cigarette smoking
  • obesity
  • physical inactivity
  • excessive alcohol use
  • diet
  • stress
  • dyslipidemia
  • diabetes
  • microalbuminuria or GFR <60mL/min
  • age
  • family hx of premature CVD in males below 55 and females younger than 65
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3
Q

BP =

A

CO x PVR
- mechanisms that involve increased CO, increased PVR, or both will overall increase BP
- anything that increases HR or circulating volume will increase BP
- anything that increases PVR, like angiotensin II will increase BP

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4
Q

increased sodium intake causes

A

increased sodium fluid retention increasing stroke volume and BP

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5
Q

renin-angiotensin-aldosterone system (RAAS) causes

A
  • excess angiotensin II resulting in vasoconstriction and increased BP
  • excess angiotensin also resulting in increased aldosterone
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6
Q

aldosterone causes

A
  • sodium and water retention resulting in increased stroke volume and BP
  • enhanced K+ secretion causing low K+
  • low K+ increases vasoconstriction through closure of K+ channels
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7
Q

sympathetic nervous system causes

A
  • vasoconstriction reuslting in increased peripheral vascular resistance and increased BP
  • ## can increase HR
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8
Q

essential hypertension

A
  • family hx
  • african americans
  • hyperlipidemia
  • smoking
  • older than 60 or postmenopausal
  • excessive sodium and caffeine intake
  • overweight/obesity
  • physical inactivity
  • excessive alcohol intake
  • low K+, Ca+, or Mg
  • excessive and continuous stress
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9
Q

secondary hypertension

A
  • kidney disease
  • primary aldosteronism
  • pheocromocytoma
  • cushing disease
  • coarctation of aorta
  • brain tumors
  • encephalitis
  • pregnancy
  • drugs: estrogen, glucocorticoids, mineralocorticoids, sympathomimetics
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10
Q

out of office and office BP elevated =

A

sustained HTN

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11
Q

out of office high and office BP normal =

A

masked HTN

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12
Q

out of office BP normal and office BP high =

A

white coat HTN

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13
Q

out of office BP normal and office BP normal =

A

normal BP

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14
Q

elevated BP

A

120-29/<80 mmHg

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15
Q

stage 1 HTN

A

130-139/80-89 mmHg

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16
Q

stage 2 HTN

A

140+/90+ mmHg

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17
Q

hypertensive crisis

A

> 180/>120

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18
Q

hypertensive urgency

A

DBP >=120mmHg w/ no s/s of organ damage

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19
Q

hypertensive emergency

A

DBP >120mmHg w/ evidence of organ damage

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20
Q

renal findings if TOD present

A
  • proteinuria
  • elevated BUN and creatinine
  • decreased eGFR
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21
Q

endocrine findings if TOD present

A
  • elevated Na+
  • elevated K+
  • elevated TSH
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22
Q

metabolic findings if TOD present

A
  • fasting blood glucose >100mg/dL
  • LDL, triglycerides
  • low HDL
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23
Q

other tests for TOD

A
  • left ventricular hypertrophy
  • low hematocrit
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24
Q

treatment for HTN

A
  • based on severity
  • goal: deccrease BP readings and minimize or prevent end-organ damage
  • first step: life style changes
  • second step: medications
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25
Q

DASH diet

A
  • 6-8 servings of grains/day
  • 4-5 servings of fruits/day
  • 4-5 servings of veggies/day
  • low-fat or nonfat dairy servings 2-3/day
  • lean meats, fish, or poultry servings 6 or fewer/day
  • nut, seeds, legumes servings 4-5/week
  • fats and oils servings 2-3/day
  • sweets 5 or fewer/wk
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26
Q

assessment of HTN

A
  • cardiac
  • renal
  • neuro
  • visual acuity
  • vascular
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27
Q

nursing interventions and teaching for HTN

A
  • administer meds
  • initiate DASH diet
  • promote adherance to meds and lifestyle changes
  • educate on how to take BP
  • s/s of complications
  • overall stress management
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28
Q

complications of HTN

A
  • coronary artery disease
  • stroke
  • hypertensive crisis
  • peripheral vascular disease
  • end organ damage: HF, KF
  • retinal damage
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29
Q

hypertensive crisis info

A
  • include urgency and emergency
  • both are severly elevated BP
  • emergency = s/s of organ damage
  • acute and life threatening emergency: SBP >180, DBP >120
  • requires immediate treatment
  • monitor neuro and renal status
  • strict I&Os
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30
Q

function of vascular system

A
  • supply adequate circulation of blood to body tissues
  • ensure adequate capillary exchange between blood plasma, interstitial fluid, and tissue cells
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31
Q

atherosclerosis

A
  • plaque formation, typically from cholesterol, on interior of vessel wall
  • arteriosclerosis often used interchangeably BUT not the same (arterio= genetic term)
  • describeds thickening/hardening of arterial wall associated w/ aging
  • increases stiffness of artery wall and decreases elasticity of vessel
  • comprised of 3 possible path process (medial calcific sclerossis or calcium deposits, arteriolar sclerosis or thickening of smaller arterioles, or atherosclerosis or LDL build up on arterial wall
  • primary cause of many vascualr disorders
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32
Q

risk factors of atherosclerosis

A
  • starts in childhood and increases w/ age
  • elevated LDL or HDL
  • elevated triglycerides
  • HTN
  • diabtetes
  • smoking
  • family hx
  • sedentary lifestyle
  • males or postmenopausal women
  • black and hispanic people have increased incidence of smoking, diabetes, and HTN
  • whites have high abnormal serum lipids
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33
Q

pathophysiology of atherosclerosis

A
  • disease in which LDL builds up on arterial walls
  • slow developing complex disorder
  • begins from vessel damage causing inflammation leading to accumulation of atherosclerotic plaque, once inflamed fatty streaks appear on lining of artery
  • lipids become deposited on arterial wall thickening arterial wall and decreases internal diameter of artery
  • causes decreased BF and O2 to affected tissues
  • plaques may rupture and cause blood clots to form and block blood flow entirely
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34
Q

clinical manifestations of atherosclerosis

A
  • little to no s/s
  • progresses as the vessel narrowing becomes critical; pt typically ends up in ER for MI, unstable angina, sudden cardiac arrest, stroke, or death
  • depends on location and degree of severity of atherosclerotic disease
  • frequently manifests as chest pain (angina), SOB, fatigue, arrythmias
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35
Q

carotid cartery atherosclerosis can lead to

A

stroke

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36
Q

cardiac artery atherosclerosis can lead to

A

MI or cardiac arrest

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37
Q

peripheral artery atherosclerosis can lead to

A

pain and reduced functionality of extremities
can cause gangrene (death of body tissue r/t lack of blood flow and oxygenation

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38
Q

medical management of atherosclerosis

A
  • identify and control risk factors for development
  • med management and decrease lipid levels
  • anticoagulants to prevent clot formation
  • diabetes management
  • encourage modification of dietary habits, smoking, exercise, stress levels/relief techniques
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39
Q

surgical management atherosclerosis

A

reserved for irreversible manifestations of atherosclerosis

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40
Q

assessment and analysis of atherosclerosis

A
  • manifestations vary based on arteries involved
  • complete pt hx and cardiovascular assessment
  • assess BP in both arms
  • palpate pulses at all major sites in body (note differences at any/all locations
  • auscultate for bruits
  • lab values, fasting lipid profile, triglyceride levels, homocysteine, glyc
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41
Q

nursing diagnoses/problem list for atherosclerosis

A
  • risk for ineffective tissue perfusion
  • pain r/t decreased BF
  • activity intolerance/fatigue
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42
Q

nursing interventions for atherosclerosis

A
  • assessments
  • administer meds or management of HTN and lipids
  • BP management
  • lifestyle changes
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43
Q

evaluation of outcomes for atherosclerosis

A
  • well managed through diet, activity, and stress management
  • smoking cessation
  • evaluate severity and/or resolution of symptoms
  • pt’s will be monitored through follow up care with providers as lifelong treatment
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44
Q

epidemiology of PAD

A
  • affects >230 million
  • significant morbidity, mortality, and alterations in quality of life
  • atherosclerosis is MAIN contributor to PAD
  • risk factors of atherosclerosis are also risk factor of PAD
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45
Q

pathophysiology of PAD

A
  • progressive and chronic condition
  • blood flow through large peripheral arteries is obstructred causing partial or total occlusion
  • caused by combo of atherosclerosis, inflammation, stenosis, embolus, or thrombus
  • deprives lower extremities of oxygen and nutrients
  • causes ischemia, necrosis, and cell death
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46
Q

clinical manifestations of PAD

A
  • most often seen as atypical lower extremity pain or intermittent claudication (muscle pain occurring during exercise)
  • described as ache, cramp, numbness, or sense of fatigue
  • most often in calf
  • typically relieved by rest
  • limited or painful joints, ulcerated or cold extremities, painful stretching
  • limits exercise ability and QOL
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47
Q

stage 1 PAD

A
  • no claudication/pain
  • bruit may be heard
  • pedal pulses are decreased or absent
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48
Q

stage II PAD (claudication)

A
  • muscle pain, burning, and cramping experienced w/ exercise and relieved by rest
  • pain is reproducible with same amount of exercise
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49
Q

stage III (rest)

A
  • pain at rest
  • often awakens pt at night
  • numbness and burning in distal portions of extremity
  • relieved by putting extremity in dependent position
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50
Q

stave IV PAD (necrosis/gangrene)

A
  • ulcers and blackened tissue in toes, forefoot, or heel
  • gangrenous odor may be present
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51
Q

diagnosis of PAD

A
  • complete vascular assessment (pulses, auscultation of femoral bruits, inspection of legs and feet)
  • all physical assessment findings must be confirmed w/ diagnostics
  • ankle-brachial index (doppler probe to compare BP at ankle to brachial artery, ankle should be higher)
  • plethysomography (evaluates arterial flow to lower extremities done through pulse volume measurements and tracings)
  • anatomical imaging reserved for highly syptomatic patients who need to undergo surgery (duplex u/s, CTA, MRA, invasive angiography)
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52
Q

ABI values

A

> 1.30 - noncompressible arteries
- 1-1.29 = normal
- 0.91-0.99 = borderline
- 0.41-0.9 = mild to moderate
- 0-0.4= severe PAD

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53
Q

goals of PAD treatment

A
  • provide relief of symptoms and improve QOL
  • prevent progression of arterial disease
  • prevent cardiovascular complications
  • provide further education about disease
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54
Q

treatment of PAD

A
  • first line: nonpharmacological interventions
  • weight loss, smoking cessation, exercise, adherance to low fat diet
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55
Q

medications for PAD

A
  • target risk factors that may profress the atherosclerotic process
  • antihypertensives
  • antiplatelets
  • statins
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56
Q

nonsurgical interventions for PAD

A
  • positioning and promotion of vasodilation (legs in dependent position)
  • exercise
  • percutaneous transluminal angioplasty (helps improve arterial BF by inserting cannula into occluded artery placing a stent to open up artery
  • laser-assisted angioplasty (cannula inserted into occluded artery and laser probe heat vaporizes blockage in smaller occlusions and vessels)
  • rotational atherectomy (hard, calcified lesions to remove plaque by breaking it into small peices)
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57
Q

surgical interventions for PAD

A
  • when clients have severe pain at rest or claudication interfering with ability to perform ADLs
  • revascularization through surgical bypass graft placement to byspass BF and use autogenous grafts
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58
Q

complications of PAD

A
  • critcal limb ischemia
  • acute limb ischemia
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59
Q

critical limb ischemia

A
  • sustained and severe decrease in arterial blood flow
  • leads to chronic ischemia, pain at rest, ulceration, gangrene
  • present after long term PAD
  • prognosis generally poor
  • further risk of infection, cellulitis, and tissue breakdown
  • requires revascularization surgery with about 40% needed limb amputation within 6 months
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60
Q

acute limb ischemia

A
  • sudden decrease in blood flow to extermity
  • acutely thretens tissue viability
  • may be first presenting symptoms of PAD
  • may be caused by acute event
  • most common cause = embolus
  • more common in lower extremities
  • manigested by severe pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia (six P’s)
  • requires immediate intervention to preserve tissue and save limb
  • anticoag and potential revascularization treatment
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61
Q

assessment and analysis of PAD

A
  • clinical manifestations vary with affected tissue
  • bilateral BP
  • palpate all pulses in both legs
  • visual assessment of feet and legs
  • temperature of bilateral lower extremities
  • assess pain and s/s of infection in lower extremities
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62
Q

nursing diagnoses/problem list in PAD

A
  • ineffective peripheral tissue perfusion
  • risk for impaired skin integrity
  • chronic pain
  • bleeding risk
  • risk for unstable blood pressure
  • impaired mobility
  • risk for infection
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63
Q

nursing interventions for PAD

A
  • assess client
  • admin meds
  • properly position patient to help w/ tissue perfusion
  • independent positioning to help w/ BF
  • inspect feet daily and report skin changes
  • report chest discomfort or neuro changes
  • lifestyle changes; DASH diet, limit alc, smoking cessation, moderate exercise
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64
Q

evaluating outcomes of PAD

A
  • symptoms relief
  • pain free and able to participate in normal activites
  • decreased progression of illness
  • improved QOL
  • adherance to lifestyle changes and med regimen
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65
Q

carotid artery disease epidemiology

A
  • common atherosclerotic vascular disease
  • typically begins developing in 40s
  • prevalence increases w/ age
  • higher incidence in males and white and native american populations
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66
Q

risk factors for carotid artery disease

A
  • smoking
  • HTN
  • diabetes
  • dyslipidemia
  • sedentary lifestyle
  • obesity
  • poor stress management
  • age <75
  • male gender
  • hx of CAD
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67
Q

pathophysiology of carotid artery disease

A
  • vessel wall thickening plaque formation and progressive narrowing of carotid arteries
  • plaque disruption and thrombus formation is possible
  • stenosis is most significant at carotid bifurcation
  • severity based on vessel lumen diameter
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68
Q

clinical manifestations of carotid artery disease

A
  • asymptomatic until vessel lumen is obstructed to point of causing cerebral perfusion impairment
  • bruit will be present past obstruction at bifurcations
    -s/s of transiet ischemic attack (sudden weakness, dizziness or loss of coordination, difficulty talking, facial drop on one side, sudden vision problems, sudden and severe headache
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69
Q

diagnosis of carotid artery disease

A
  • physical assessment, noninvasive procedures, and occasionally invasive procedures
  • conventional carotid angiography is invasive procedure that is the gold standard for diagnosis of severity of external carotid artery stenosis
  • done through catheterization of femoral artery and use of contrast dye to visualize the blockages
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70
Q

noninvasive tests for carotid artery disease

A
  • carotid duplex u/s
  • MRA
  • MRI
  • CTA
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71
Q

treatment of carotid artery disease

A
  • depends on severity of occlusion and whether the patient is symptomatic or asymptomatic
  • asymptomatic patients w/o hx of stroke or TIA: optimal medical therapy which is a combo of lifestyle change and medications (antiplatelets, antihypertesnives, statins, etc.)
  • surgical intervention is controversial due to complications
  • symptomatic patients who present w/ TIA or stroke include OMT and surgical management
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72
Q

surgical management of carotid artery disease

A
  • procedures for revascularization
  • carotid endarterectomy (CEA): removal of plaque to improve BF and prevent stroke w/ med management of antiplatets, hypertesnives, and statins
  • carotid artery stenting (CAS): in combination w/ carotid angioplasty where stent is placed to open artery requiring lifelong aspiring
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73
Q

CEA postop priorities

A
  • tight BP monitoring
  • neuro assessments
  • bleeding prevention
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74
Q

CAS post op priorites

A
  • frequent VS monitoring
  • neuro assessments
  • access site monitoring
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75
Q

assessment and analysis of carotid artery disease

A
  • typically asymptomatic until lumen is obstructing cerebral BF
  • symptoms of stroke may appear
  • auscultate carotid arteries for bruits
  • vital monitoring (!BP!)
  • neuro assessments
  • stroke hx or s/s of stroke
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76
Q

nursing diagnosis for carotid artery disease

A
  • risk of poor tissue perfusion
  • risk for injury
  • anxiety
  • risk for bleeding
  • risk for fluctuations in BP and HR
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77
Q

nursing interventions for carotid artery disease

A
  • post op monitoring of RR, SpO2, presence of stridor or tracheal deviation, vitals, cranial nerves and renal function
  • admin meds as ordered
  • manage diabetes and maintain glucose levels
  • postop: keep BP within ordered parameters, maintain neutral head alignment, encourage fluids
  • educate on s/s of stroke
  • lifestyle changes, DASH, exercise, smoking cessation, limitation of alcohol
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78
Q

evaluating care outcomes of carotid artery disease

A
  • educated on risk factor modifications
  • compliance of medication regimen
  • adherence to lifestyle changes
  • goal of no clinical manifestations of stroke
  • no post-op complications of pain, swelling, or bleeding
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79
Q

epidemiology of aneursyms

A
  • common in men
  • common in white people
  • common in those with atherosclerosis
  • thoracic aortic aneurysms (TAAs) more common in men 40-70yo
  • non-modifiable risks: family hx, advanced age, male sex, genetic abnormalities, known CAD, Marfan’s syndrome
  • modifiable risks: smoking, high cholesterol, HTN
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80
Q

causes of aneurysms

A
  • atherosclerosis
  • chronic inflammation (aortitis)
  • blunt trauma
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81
Q

pathophysiology of aneurysms

A
  • permanent localized dilation of an artery that forms when middle layer of artery is weakned
  • causes stretching in artery walls increasing tension
  • can occur in ascending, descending (thoracic), or abdominal aorta
  • all 3 layers are weak
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82
Q

medical management of aneruysms

A
  • imaging to detect aortic dilation
  • CT scan w/ IV contrast is gold standard
  • abdominal u/s or transthroacic echocardiography
  • cardiac MRI
  • ECG to rule out MI
  • meds: focus on reducing growth and preventing complications, aggresive HTN management, antibiotic to prevent infections, statins to reduce atherosclerosis and growth
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83
Q

surgical management of aortic aneurysms

A
  • determined by size, location, and presence of symptoms
  • surgery is only effective in preventing AAA rupture and anuerysm related death
  • most commonly a resection and repair (aneurysmectomy)
  • risk of bleeding, infection, MI, renal failure, and graft occlusion
  • endovascular aneurysm repair is less invasive w/ less risk
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84
Q

aneurysmectomy

A

aneurysm is excised and graft is applied

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85
Q

endovascular aortic repair (EVAR)

A

placement and attachement of sutureless aortic graft prosthesis across aneurysm

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86
Q

aortic dissection

A
  • caused by sudden tear in aortic intima creating a false lumen in artea
  • life threatening emergency due to loss of circulation to major arteries
  • s/s: sudden, severe, persistent pain in anterior chest or back, pain extends to shoulders, epigastric area, or abdomen, desrcibed as “ripping” or tearing, diaphoresis, n/v, faintness, tachycardia, BP different in LUE than RUE
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87
Q

aneurysm rupture

A
  • life threatening
  • leads to sudden and extreme blood loss
  • s/s similar to dissection w/ LOC and hypovolemic shock
  • death rate about 80%
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88
Q

assessment and analysis of anerysms

A
  • assessments
  • vitals specifically for hypotension and tachycardia for concern of rupture
  • neuro assessment
  • pain presence and severity
  • peripheral pulses, skin color, temp
  • peripheral sensation and motor response
  • gentle abdominal auscultation and palpation
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89
Q

nursing diagnosis for aneurysms

A
  • risk for ineffective peripheral tissue perfusion
  • acute pain
  • fear
  • risk for bleeding, decrease CO, and hypovolemic shock
  • risk for fluctuations in BP
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90
Q

nursing interventions for aneurysms

A
  • assessments
  • admin meds as ordered
  • admin stool softners
  • reduce stress
  • educate on s/s of aneurysm complications
  • marfan’s syndrome: encoruage to do regular screening and call HCP w/ new onset of s/s
  • strict treatment regimen: med compliance, weight reduction, smoking cessation, regular exercise, avoid crossing or eelvating legs, reduce stress
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91
Q

evaluating care outcomes of anerysms

A
  • compliance w/ perscribed therapy
  • BP and HR WNL
  • strong peripheral pulses
  • normal skin color and texture
  • no complaints of abdmoinal, back, or chest pain
  • no complaints of wheezing or SOB
  • no complaints of dysphagia or hoarsness
  • normal neuro assessment
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92
Q

epidemiology of DVT

A
  • 1/1000 per year
  • 0.5-7/1000 pregnancies
  • can detach from site of formation and become mobile in blood stream leading to PE or MI
  • risk increases w/ prolonged bedrest, venous stasis, surgery, increased age, active cancer w/ or w/o chemo, varicose vevins, prior VTE, pregnancy, postpartum, oral contraceptive use, hormone therapy, surgery, trauma, covid-19
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93
Q

pathophysiology of DVT

A
  • virchow’s triad= factors implicated in formation of VTE
  • decreased BF rate or statsis of BF
  • damage to vessel wall or endothelial cell injury
  • increased tendency for blood to clot (hypercoaguability)
  • more common in lower extremities and creates environment for clotting
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94
Q

clinical manifestations of DVT

A
  • clot can cause complete or partial blockage of circulation in vein
  • pain, swelling, tenderness, discoloration or redness, warmth
  • Homan’s sign= calf pain elicited by dorsiflexion of foot
  • ^ can indicate presence of DVT but is not diagnostic
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95
Q

diagnosis of DVT

A
  • pretest probability
  • d-dimer (if high, clot is present)
  • compression u/s (CUD) to visualize thrombi and ID if unstable or floating
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96
Q

prevention of DVT

A
  • early ambualtion
  • VTE prophylaxis (LMWH, compression stokcings
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97
Q

meds for DVT

A
  • anticoag w/ LMWH or heparin
  • long term anticoags w/ warfarin or eliquis or apixiban
  • thrombolytic agent only used as VERY LAST resort
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98
Q

surgical management of DVT

A
  • rarely used unless massive occlusion not responding to treatment
  • must be recent
  • thrombectomy
  • less invasive= ballon angioplasty
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99
Q

coplications of DVT

A
  • PE: SOB, decreased SpO2, tachycardia, hypotension, sweating, sharp chest pain, hemoptysis, increased PVR, incerased workload on heart, deceased O2 on lung
  • post-thrombotic syndrome: chronic disorder ranging from limb swelling and discomfort to sever leg pain, intractable edema, irreversible skin changes and leg ulcers
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100
Q

assessments for DVT

A
  • vitals w/ o2
  • extremity assessment for pain, tenderness, warmth, redness, or swelling
  • compare R and L calf, thigh, or arm
  • gentle palpation to insepction for induration
  • D-dimer test
  • lab values: INR, PT/aPTT, H/H
  • assess for s/s of bleeding
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101
Q

nursing diagnosis for DVT

A
  • ineffective peripheral tissue perfusion
  • acute pain
  • risk for impaired physical mobility
  • risk for bleeding
  • impaired gas exchange
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102
Q

nursing interventions for DVT

A
  • assessment
  • early ambulation
  • leg elevation
  • compression stockings
  • avoid use of SCDs
  • encourage adeuqate fluid intake
  • admin meds
  • educate of prevention: ambulation, fluids, avoid constricting clothing, avoid long periods of sitting/car rides/ planes
  • educate on s/s of bleeding
  • educate on lab compliance
  • safety precautions when taking anticoags
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103
Q

evaluating care outcomes for DVT

A
  • compliance w/ prescribed anticoagulants
  • stable vs and O2 sat
  • decreased extremity pain, tenderness, or swelling
  • prevention activities and maintenance of active and healthy lifestyle
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104
Q

chronic venous insuffiency risk factors

A
  • obesity
  • smoking
  • sedentary lifestyle
  • increased age
  • prolonged standing
  • previous LE trauma or thrombosis
  • HTN
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105
Q

pathohypsiology of CVI

A
  • superficial and deep veins of peripheral venous system consist of one-way bicuspid valves
  • most likely caused by congenital factors, hormones, prolonged standing, thrombosis, or non-thrombotic events
  • DVT is usually results in deep vein incompetence
  • valves become damaged and venous pressure increases, blood reutnr from lower extremities is obstructured leading to arterial perfusion impairment, lower extremity edema, skin ulcers
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106
Q

clinical manifestations of CVI

A
  • lower extermity pain and edema
  • dilated veins
  • skin changes: capillary walls thicken causing breakdown of RBCs, brown skin, tissues and cells will necrose, fibrous tissue begins to develop in subq fat
  • ulcer formation
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107
Q

diagnosis of CVI

A
  • rule out other causes
  • ID clinical changes, dialted vessels, skin changes, and ulcers-
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108
Q

treatment of CVI

A
  • compression and avoiding prolonged standing
  • compression stockings
  • basic skin care
  • wound care
  • exercise w/ walking and ankle flexion increasing venous return
    leg elevation
  • adequate nutrition
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109
Q

meds for CVI

A
  • cellulitis development so may need antibiotics
  • wound care
  • aspirin and steroids
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110
Q

surgical management of CVI

A
  • varicose vein treatment
  • complicated, infected wounds may need debridement to remove necrotic tissues
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111
Q

complications of CVI

A
  • leg discoloration
  • dilated veins
  • edema
  • leg pain
  • ulcers
  • cellulitis
  • sepsis
  • limb amputation
  • DVT or PE
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112
Q

assessment of CVI

A
  • clinical manifestations
  • vs and O2
  • monitor extermities for edema, dilated vessels, skin discoloration, pain, warmth, redness, or ulcer formation
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113
Q

nursing diagnosis for CVI

A
  • risk for infection
  • risk for ulcer formation
  • impaired mobility
  • pain
  • edema of extermities
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114
Q

nursing interventions for CVI

A
  • provide skin care and apply dressings
  • compression therapy
  • elevation of extremities
  • encourage ambulation
  • admin meds as ordered
  • education on compression therapy, skin care, exercise, elevation, and nutrition
  • educate on importance of avoiding prolonged standing
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115
Q

evaluating care outcomes for CVI

A
  • demonstrating adgerence to treatment regimen
  • demonstrate decreased leg swelling, vein dilation, and ulcer formation
  • increased exercise tolerance and elevation of legs when resting
  • compliant with compression therapy, skin care, and nutrition
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116
Q

epidemiology of HF

A
  • prevalent in 6.5 million people over age 20
  • high mortality rate
  • more common in those: over 65, african americans, previous heart attacks, obesity
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117
Q

risk factors for HF

A
  • CAD
  • HTN
  • DM
  • metabolic syndrome
  • obesity
  • smoking
  • high Na+
  • sleep apnea
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118
Q

common conditions causing HF

A
  • valvular dysfunction
  • cardiomyopathies
  • infections and inflammatory heart disorders
  • dysrythmias
  • anemia
  • thyroid disease
  • cardiotoxic substance exposure (alcohol, chemo, drugs)
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119
Q

less common conditions causing HF

A
  • respiratory conditions
  • pulmonary artery HTN
  • COPD
  • interstitial lung disease
  • obstructive sleep apnea
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120
Q

pathophysiology of HF

A
  • progressive disease characterized by myocardial cell dysfunction and decreased CO
  • frank-starling law: increased blood in ventricles cause increased contracility of ventricle
  • constant demands of myocardial muscles
  • weakned heart muscles and inability to contract efficiently
  • compensatory mechanisms kick in
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121
Q

compensatory mechanisms

A
  • SNS
  • ventricular remodeling
  • neurohormonal responses (RAAS, BNP)
  • all short term compensation
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122
Q

ventricular remodeling

A
  • causes fibrosis, cardiomyocyte loss, cardiomyocyte hypertrophy, and electrophysical changes
  • ^ leads to impaired contractility, LV dilation, and wall thinning leading to HF
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123
Q

HF w/ reduced EF

A
  • weakened heart contraction
  • EF 40% or less
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124
Q

HF w/ preserved EF

A
  • EF maintained above 50%
  • ventricles have impaired ability to fill
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125
Q

normal EF

A

55-70%

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126
Q

AHA HF

A

a- no risk factors but s/s
b- no s/s but elevated heart pressures or BNP
c- current or past s/s of HF
d- marked signs that interfere w/ daily life

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127
Q

NYHA HF

A

I: no s/s w/ physical activity
II: mild s/s w/ ordinary activies
III: marked limitation w/ activity but comfortable at rest
IV: severe limitation

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128
Q

clinical manifestations of HF

A
  • acute: sudden onset and immediate interventions
  • chronic: basline set of symptoms, limitations are relatively stable w/ treatment and self-management
  • fatigue
  • weight gain
  • tachycardia
  • hypotension or hypertesnion
  • heart murmurs related to valve dysfunction
  • S3 may be present
  • S4 common in chronic heart failure
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129
Q

s/s of right sided HF

A
  • fatigue
  • increased peripheral venous pressure
  • enlarged liver or spleen
  • distended jugular veins
  • anorexia or GI distress
  • swelling in hands and fingers
  • dependent edema
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130
Q

s/s of left sided HF

A
  • dyspnea
  • orthopnea
  • bendopnea
  • edema
  • fatigue
  • crackles on auscultation
  • poor skin color and delayed cap refill
  • weak pulses
  • cool skin temp on extremities
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131
Q

heart failure progression

A
  • L HF can lead to R HF
  • heart may be initally affected in its entireity
  • s/s become less clear
  • can have exacerbations: hypotension, cool extremities, decreased/no output, poor decreasing mentation
  • +S3 and 4
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132
Q

diagnosis of HF

A
  • imaging to rule out other problems and cause
  • imaging: xray, echo, CT, MRI, ECG, nuclear imaging
  • labs: cardiac biomarkers, serum electrolytes, CBC, urinalysis, glucose levels, fasting lipids, LFTs, renal function tests
  • biomarkers: BNP and n-terminal pro B-type natiuretic peptides, troponins
  • nuclear imaging
  • stress test
  • coronary angiography
  • exercise testing
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133
Q

medical management of HF

A
  • medications most often used for HF w/ reduced EF
  • for HF w/o reduced EF treatment of underlying cause, BP control, diuretic and s/s management
  • goal: reduce risk factors, manipulation of critical component of CO- preload, afterload, and contractility
  • successful management: slows disease progression, prevents complications, reduces morbidity and mortality, improves QOL
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134
Q

risk factor management for HF

A
  • BP and glucose control
  • weight loss
  • optimizing serum lipids
  • smoking cessation
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135
Q

meds that impact preload

A

diuretics

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136
Q

meds that reduce afterload

A

ACE inhibitors
ARBs
ARNIs

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137
Q

meds to affect contractility

A

postive inotropic agents (digoxin)

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138
Q

management of HF exacerbation

A
  • IV meds for quick and effective management
  • goal to decrease preload and afterload and increase contractility
  • vasodilators
  • IV inotropic and inodilators
  • requires VS monitoring: frequent BP/HR, cardiac monitoring and rhythm assessment
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139
Q

furosemide and morphine

A

can cause hypotension
BP monitoring frequently
LOC monitoring
K+ monitoring
UO monitoring
fall precautions
CNS depression

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140
Q

device and surgical interventions

A
  • implantation of ICD for dysrhythmia control and ventricular resynchronization
  • intra-aortic balloon pump
  • ventricular assist device
  • valve replacement
  • heart transplant
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141
Q

self management of HF

A
  • s/s monitoring
  • daily weights
  • med adherance
  • lifestyle changes (weight, Na+, prevention of cardiac cachexia)
  • participation in cardiac rehab
142
Q

older adult considerations of HF

A
  • more common w/ aging
  • often have 5+ comorbidites
  • reduced self-management ability
  • decline in renal function w/ age
  • potential poor nutritional status and risk of dehydration
143
Q

complications of heart failure

A
  • pulmonary edema
  • dysrhythmias r/t heart muscle enlargement and catecholamine release
  • renal failure r/t decreased BF to kidneys
144
Q

pulmonary edema

A
  • acute complication of HF
  • accumulation of fluid in interstitial and alveolar spaces of lungs
  • s/s: SOB, low spO2, pink/frothy sputum, orthopnea, bendopnea, tachycardia, chest pain, anxiety/fear
145
Q

treatment for pulmonary edema

A
  • supplemental O2
  • initiation of higher dose or IV diuretics
  • respiratory support: CPAP, BiPAP, intubation w/ mechanical ventilation
146
Q

assessment for HF

A
  • v/s
  • breath sounds for congestion
  • cardiac monitoring
  • skin color and temp changes
  • peripheral pulse changes and cap refill time
  • dry persistent cough r/t meds
  • activity tolerance/intolerance
  • changes in urine output
  • daily weights
  • lab data trends
  • mental health screenings
  • social support-
147
Q

nursing diagnosis HF

A
  • impaired oxygenation r/t fluid build up in lungs
  • decreased CO related to altered preload, afterload, and contractility
  • ineffective peripheral perfusion r/t decreased CO
  • electrolyte imbalances
  • fatigue
148
Q

nursing interventions for HF

A
  • assessments
  • O2 therapy
  • HOB elevation
  • med administration
  • dietary restrictions
  • medication management
  • maintain activity as toelrated
  • diet teaching
  • daily weights
  • cardiac rehab
  • s/s of worsening HF
  • immunization
149
Q

evaluating care for HF

A
  • reduce stress
  • fluid status and salt intake monitoring
  • successful implementation of treatment plan
  • frequent assessment, pt education, and self-management
  • reduced dyspnea and fatigue
  • ability to actively participate in ADLs
  • reduced hospitalizations
150
Q

GI system is responsible for

A
  • digestion
  • metabolism
  • excretion/elimination
151
Q

proper functioning of GI system is essential to ensure

A

proper nutrition

152
Q

where does reabsorption of fluids and electrolytes primarily occur

A

large intestine

153
Q

enzymes that digest carbohydrates

A

amylase

154
Q

enzyme that digests fats

A

lipase

155
Q

secretion of digestive enzymes are controlled by waht body system

A

endocrine

156
Q

gastric motility (peristalsis) is controlled by which body system

A

neurological

157
Q

3 major accessory organs of GI tract

A
  • liver
  • gallbladder
  • pancreas
158
Q

funciton of liver

A
  • detox
  • metabolize and absorb
  • secretes and produces prothrombin
159
Q

gallbladder function

A

storing and secretion of bile (needed to digest fat)

160
Q

complications of gallbladder can cause

A
  • difficult digesting fats
  • infection
  • gallstones
  • diarrhea due to increased fats
  • dehydration and electrolyte loss
161
Q

pancreas function

A

produces insulin and amylase and lipase to digest food and manage blood sugar levels

162
Q

complications of pancreas can cause

A
  • hyperglycemia
  • diabetes
  • malnutrition
163
Q

transformation of waste from a semiliquid state to formed stool occurs in

A

large intestine

164
Q

abnormal albumin levels indicate

A

malnutrition
normal range: 3.7-5.1

164
Q

components of large intestine

A
  1. ascending
  2. transverse
  3. descending
  4. sigmoid
165
Q

prealbumin levels indicate

A

more specific malnutirtion
<12

166
Q

transferrin

A

refers to how iron is transporting
M= 215-365 F- 250-350
if abnormal = hepatic damage

167
Q

GI health hx

A
  • diet
  • nutrition
  • oral health
  • preventative health
  • weight changes
  • appetite changes
  • stool changes
  • pain
  • social hx
  • medical hx
  • surgical hx
168
Q

GI labs

A
  • CBC
  • CMP (electrolytes, LFTs, bilirubin, albumin, total protein, glucose)
  • prealbumin
  • transferrin
  • lipase
  • prothrombin time (PT)
  • UA
  • stool culture
  • c-diff
  • ova and parasite
  • fecal fat analysis
  • fecal occult blood test (FOBT)
  • fecal imunochemical test (FIT-DNA)
169
Q

abdominal xray

A
  • abdominal pain
  • prep: remove jewelry and other metal that may obscure images, assess for pregnancy, empty bladder
  • positioning may increase pain
170
Q

abdominal ultrasound

A
  • can detect any structural abnormalities of underlying abdominal cavity
  • preferred method when patient cannot receive contrast dye
171
Q

barium studies

A
  • series of timed x rays using fluoroscopy to examine integrity and patency of GI tract after given barium (radiographic opaque liquid)
  • preop: explain procedure, ensure diet of clear liquids to NPO is ordered, administer laxatives or enema night before, respiratory assessment, administer barium contrast (TIMING!!!)
  • postop: assess for return of gag reflex (maintain NPO until it returns), monitor VS, monitor I&Os, respiratory assessment, education on resumption of diet, meds, and activity, increase fluid intake to increase elimination of barium
172
Q

withhold food and drinks for ____ before a barium swallow

A

4-8hrs prior

173
Q

stools should appear what color after barium enema

A

gray or chalky white for 24-72hrs postop

174
Q

endoscopy

A
  • general term used to describe procedure in which a fiberoptic scope is use to visualize GI tract, patients are sedated during procedure
  • common tests: esophagogastroduodenoscopy (EGD), colonscopy, sigmoidoscopy
175
Q

preop implications for endoscopy

A
  • perform focused physical assessment
  • assess mouth/oral cavity for loose teeth or dentures
  • ensure patient has been NPO for instructed time
  • ensure consent has been completed, signed, and witnessed
  • hold anticoagulants and aspirin as ordered
  • bowel prep as ordered
176
Q

postop implications for endoscopy

A
  • assess for return of gag reflex (maintain NPO until return)
  • monitor vitals
  • hold anticoags and aspirin as ordered
  • assess for s/s of perforation
177
Q

preop EGD

A
  • informed consent
  • NPO 6-8 hrs before test
  • avoid anticoags and NSAIDs several days before
  • local anesthetic before scope is inserted
  • positioned on left side to facilitate saliva drainage and provide easy acess
  • airway patency is monitored and pulse ox is used
  • emergency equipment readily available
178
Q

postop EGD

A
  • monitor vitals
  • gag reflex assessment
  • monitor for perforation (pain, bleeding, difficulty swallowing, elevated temp)
  • maintain bed rest and keep side rails raised
  • lozenges, saline gargles, oral analgesics
179
Q

esophageal perforation

A
  • excruciating retrosternal pain
  • dysphagia
  • sever hypotension
  • surgical emergency (>24hrs increases mortality rate)
  • preop care: NPO, IVF, antibiotics, prepare for surgery
180
Q

bowel prep

A

use of golytely, dulcolax, or miralax to flush out stool
stool output should be yellow and clear like urine when ready

181
Q

postop colonoscopy

A
  • do not allow pt to take anything by mouth until sedation wears off
  • take vitals q15-30min until alert
  • keep pt in left lateral position until passing of flatus
  • keep top side rails up until pt alert
  • assess for rectal bleeding or severe pain
  • remind pt fullness and cramping expected
  • assess for signs of perforation (severe abdominal pain, guarding, fever)
  • assess for hypovolemic shock (dizziness, light-headedness, decreased BP, tachycardia, pallor, altered LOC
  • refrain from activities requiring heavy focus
182
Q

hiatal hernia

A

upper part of stomach protrudes through diaphragm into chest cavity
caused be weakening of diaphragm muscle or increased abdominal pressure

183
Q

risk factors of hiatal hernia

A
  • western countries residence
  • obesity
  • pregnancy
  • smoking
184
Q

clinical manifestations of hiatal hernia

A
  • often asymptomatic
  • bowel sounds over chest (peristalsis)
  • fullness, feel like food gest “stuck”
185
Q

causes of hiatal hernia

A
  • birth defects
  • muscle weakness
  • trauma to diaphragm
  • previous abdominal surgeries
  • high abdominal pressure
186
Q

type I hiatal hernia

A
  • sliding
  • lower esophagus and stomach ascend through hiatus
187
Q

type II hiatal hernia

A
  • paraesophageal hernia
  • fundus migrate into throacic cavity parallel to esophagous
188
Q

type III hiatal hernia

A

both GEJ and porition of stomach migrate into cavity

189
Q

type IV hiatal hernia

A
  • stomach and other parts of GI tract protrude into chest
190
Q

diagnosis of hiatal hernia

A
  • upper GI xray
  • barium swallow
  • EGD
  • CT
191
Q

medical management of hiatal hernia

A
  • meds: avoid meds that delay gastric emptying (anticholinergics), neutralize stomach acid (antacids), treat reflux using PPI or H2RAs
  • surgical repair: gastropexy (pull stomach back through diaphragm and create new esophagogastric junction to prevent slipping), nissen fundoplication (recreate LES pressure by wrapping fundus of stomach around esophagus in abdomen, GOLD STANDARD)
192
Q

hiatal hernia assessments

A
  • breathlessness
  • suffocation feeling
  • chest pain
  • palpitations
  • dysphagia
  • clinical manifestations of GERD or heartburn
  • n/v
  • belching
  • h/h
193
Q

nursing actions for hiatal hernia

A
  • administerd meds
  • HOB >30 after meals
  • avoid straining
  • small frequent meals
  • do not recline for 2hrs after eating
  • elevate HOB 4-8 in at night
  • lose weight
  • meds
  • refrain from tight clothes
  • post-op selfcare
  • when to seek immediate HCP attnetion
194
Q

GERD

A

acid reflux from stomach into esophagous when LES is weak or relaxes inappropriately

195
Q

signs of GERD

A
  • dyspepsia
  • regurgitation
  • water brash
  • dental caries
  • dysphagia
  • odynophagia
  • globus
  • pharyngitis
  • coughing
  • hoarseness
  • chest pain
  • heartburn (pyrosis)
  • epigastric pain
  • generalized abdominal pain
  • flatulence
  • nausea
196
Q

diagnosis of GERD

A
  • pH testing of regurgitation
  • PPI trial
  • esophageal manometry or motility testing
197
Q

medical management of GERD

A
  • surgery (nissen fundoplication, linx0
  • avoid meds that decrease gastric emptying (anticholinergics)
  • meds: antiacids, H2RAs, PPIs, prokinetics
198
Q

complications of GERD

A
  • dental erosion
  • pharynx or esophageal ulcers
  • laryngeal damage
  • esophageal strictures
  • adenocarcinoma
  • pulmonary issues
199
Q

MRI is not indicated after which surgery

A

linx

200
Q

GERD assessments

A
  • assess for clinical manifestations
  • monitor for aspiration pneumonia, chronic cough, hoarseness, nocturnal wheezing, adult onset asthma, laryngitis, pharyngitis, bronchitis w/ regurgiation
  • pH of gastric aspirate
201
Q

GERD actions

A
  • meds
  • HOB elevated at least 6-12 inches
  • small, frequent meals
  • avoid smoking and alcohol
  • avoid NSAIDs and aspirin
  • do not recline 2hrs after eating
  • elevated HOB 4-8 in/night
  • lose weight
  • meds
  • do not wear constricting clothing
202
Q

gastritis

A
  • inflammation of lining of stomach
  • can be acute occuring suddenly and often resolving quickly or it can be chronic, persisting longer periods of time
203
Q

signs of gastritis

A
  • abdominal discomfort
  • anorexia, nausea, vomtiing
  • headache
  • hiccuping
  • reflux or dyspepsia
204
Q

causes of gastritis

A
  • erosive: ASA, NSAIDs, corticosteroids, ETOH, gastric radiation
  • nonerosive: H. pylori
  • ingestion of strong acid or alkali (mucosa becomes gangrenous and perforates)
  • during acute illness
  • trigger foods
  • viral infection
  • food poisoning
205
Q

gastritis diagnosis

A
  • abomdinal xray
  • endoscopy
  • biopsy
  • CBC (H/H)
  • urea breath test
  • stool for occult blood
206
Q

medical management of gastritis

A
  • treat underlying cause and symptoms
  • GI rest (NPO, slowly advance)
  • eliminate irritating foods
  • bland diet
  • small frequent meals
  • vomiting (fluid replacement)
  • PPIs, H2RAs, antacids, antibiotics, vitamin b12
  • quit smoking
  • ensure water is clean
  • surgery: vagotomy, gastrectomy, pyloroplasty
207
Q

assessments for gastritis

A
  • vitals
  • I&Os
  • key features
  • respiratory assessent
  • labs: pH of aspirate (stomach = 1.5-2.0, esophagous = 6.0-7.0), H. pylori, electrolytes
208
Q

actions for gastritis

A
  • diet mod
  • NPO than advance
  • no caffeine, aclohol, spicy, irritating, or highly seasoned foods
  • administer IVF
  • monitor I&Os
  • admin meds as ordered
  • reduce stress
  • no NSAIDs
  • no smoking
  • releve pain
209
Q

education for gastritis

A

call doctor if:
- s/s don’t improve in 24-72hrs,
- unable to keep food or meds down
- blood in stool or vomit
- take all meds as prescribed
- follow up with HCP

210
Q

gastroenteritis

A
  • condition characterized by inflammation of stomach and intestines
  • commonly called the stomach flu
  • commonly caused by viral or bacterial infections, parasitic infections, ingestion of toxins, adverse effects of antibiotics
  • inflammatory response leads to increased permeability of intestinal lining allowing fluid to leak in intestinal lumen causing diarrhea
  • usually self-limiting
211
Q

gastroenteritis prevention

A
  • good hygeine
  • hand hygeine
  • avoid contaminated food and water
212
Q

gastroenteritis s/s

A
  • diarrhea
  • nausea
  • vomiting
  • anorexia
  • abdominal distention
  • discomfort
  • dehydration
  • hyperactive bowel sounds
  • decreased BP
213
Q

diagnosis of gastroenteritis

A
  • stool testing to find caustive organism
    (acute watery diarrhea = viral, subacute or chronic watery diarrhea = parasitic, acute inflammatory diarrhea w.o blood or wbcs = bacterial, acute inflammatory diarrhea w./ blood.= c. diff, diarrhea w/ gross blood = dysentery, shigellosis, e. coli, r/o UC)
  • blood cultures
  • stool for ova and parasite
214
Q

medical management of gastroenteritis

A
  • supportive treatment
  • oral or IV rehydration
  • antidiarrheal agents except c. diff
  • oral bismuth subsalicylate
  • antibiotics
  • antiemetics
  • diet (clear liquids, slowly introduce bland and easy to digest foods)
215
Q

gastroenteritis assessment

A
  • patient hx (severity of diarrhea, dehydration, onset, frequency, quantity, duration of diarrhea, vomiting)
  • recent travel hx, eating hx
  • I&Os
  • weight loss
  • VS w/ orthostatic
  • abdominal distention
  • bowel sounds and elimination patterns
  • labs: electrolytes, BUN/CR
  • perineal skin
  • s/s of dehydration
  • pain
216
Q

gastroenterititis actions

A
  • hand hygeine
  • IVF
  • admin medications
  • clear liquids oral rehydrations
  • promote rest
  • VTE prophylaxis
  • perineal care
  • oral care
  • diet mods
  • preventative measure (sanitation of food and water when traveling, proper food prep)
217
Q

peptic ulcer disease

A
  • ulceractions and erosions in lower esophagous, stomach or duodenum
  • results from imbalance between protective factors that line GI tract and damging effects of stomach acid and digestive enzymes
218
Q

2 types of PUD

A
  • gastric ulcers
  • duodenal ulers
219
Q

manifestations of PUD

A
  • dull gnawing pain or burning in epigastric area or back
  • n/v
  • constipation
  • diarrhea
  • bleeding
  • gastric: pain after eating, hematemesis (fresh blood in stool)
  • duodenal: pain 2-3hrs after eating, melena (black tarry stool)
  • perforation: sudden onset of sever sharp pain that travels to shoulder, extreme abomdinal tenderness, rigid abdomen, n/v, hypotension, tachycardia
220
Q

diagnosis of PUD

A
  • physical exam
  • upper GI study
  • endoscopy w/ biopsy
  • h. pylori testing
  • CBC
  • stool for occult blood
221
Q

medical management of PUD

A
  • meds
  • avoidance of NSAIDs and ASA
  • smoking cessation
  • diet mod (NPO if GI bleed)
  • surgery
222
Q

meds for PUD

A
  • PPI
  • antiulcer (misoprostol)
  • antacids
  • antibiotics
223
Q

complications of PUD

A
  • GI bleed: sudden severe pain w/o warning, sudden weakness, dizziness, cold, pale mosit skin, passage of loose tarry stool or coffee ground emesis
  • penetration: intense persistent pain
  • perforation: peritonitis causes sudden intense epigastric pain, release of GI content into peritoneum
  • obstruction: early satiety, epigastric fullness, gastric reflux, weight loss, abomdinal pain
224
Q

dumping syndrome

A
  • rapid emptying of gastric contents into small intestine occuring after gastric resection
  • 30 minutes after eating
  • nausea
  • vomiting
  • feelings of fullness and cramping
  • diarrhea
  • palpitations and tachycardia
  • perspiration
  • weakness and dizzines
  • borborygmi (loud gurgling)
225
Q

PUD assessments

A
  • hx: risk factors, use of NSAIDs or ASA, alcohol, tobacco, diet, and eating pattern
  • general appearance
  • vitals
  • weight
  • abdominal exam including shape and contour
  • bowel sounds and tenderness to palpations
  • presence of obvious or occult blood in emesis and stool
  • inspection of skin turgor and oral mucous mebmranes
  • pain
  • labs: emesis and feces for occult blood, electrolytes, BUN/Cr, CBC, peritoneal fluid culture
226
Q

PUD actions

A
  • maintain IV infusions
  • admin blood
  • admin meds
  • assist w/ gastric lavage for bleeding, irrigate NG tube with room temp water as rodered
  • prep for endoscopy or surgery
  • document and report anorexia,fullness, nausea, vomiting, or s/s of dumping syndrome
  • take meds as ordered
  • avoid eating within 2hrs of bed
  • avoid risks
227
Q

constipation

A
  • symptom, not a disease
  • fewer than 3 BM/wk or hard, dry, small and difficult to pass stools
  • complications: vasovagal, impaction, hemorrhoids, fissures, rectal prolapse, perforation (surgery w/ colostomy)
  • treatment: underlying cause, exercise, increase fiber and fluid, laxatives and/or enema, assess for impaction, privacy to use bathroom, NPO until n/v resolves and has BM, education on diet, fluids, exercise, and importance of defecating when urge is felt
228
Q

hemorrhoids

A
  • swollen or dilated veins in anorectal area
  • can be internal or external
  • medical treatment is symptom management and surgical removal
229
Q

nursing care of hemorrhoids

A
  • assess for prescence of hemorrhoids and s/s of bleeding
  • risk for altered bowel elimination due to pain
  • local analgesics/anesthetics
  • astringents
  • corticosteroids
  • protectants/emollients
  • provide cold packs and sitz baths
  • avoid straining (administer laxatives and increase fiber and fluids)
  • apply local moist heat
  • education
230
Q

hernias

A
  • ingunial, femoral, umbilical, or ventral
  • intestine protrudes through abdominal opening
  • reducible, incarcerated, or strangulated
  • cause: pressure on abdomen, weakened structures post-op, straining, lifting heavy objects, sudden twists, pulls or muscle strain, weight gain, chronic cough
  • s/s: buldge in abdomen or groin
  • tx: reduction or surgical repair (hernia repair or bowel resection)
  • AVOID COUGHING, STRAINING, AND LIFTING POST-OP
231
Q

nursing care of hernia

A
  • identify presence of hernia
  • preop and post op
  • treat pain
  • assess for complications (strangulation, surgical site infection, bowel obstruction)
  • education
232
Q

peritonitis

A
  • inflammation of peritoneum
  • bacterial infection from leakage of GI tract contents from a perforation, surgery, trauma, or peritoneal dialysis
233
Q

s/s of peritonitis

A
  • rigid board like abdomen
  • abdominal pain (can refer to shoulder or chest)
  • distended abdomen
  • n/v
  • anorexia
  • diminished bowel sounds
  • inability to pass gas or stool
  • high fever
  • tachycardia
  • dehydration
  • rebound tenderness
  • decreased urine output
  • hiccups
  • possible compromised respiratory status
234
Q

intestinal obstruction

A
  • blockage that prevents normal flow of intestinal contents through intestinal tract
  • SBO - most common
  • LBO
  • causes: surgery, hernia volvulus, intussusception, tumor/mass, adhesions, strictures, diverticular disease, paralytic ileus
235
Q

neurogenic/functional obstruction

A
  • dysfunction of nervous system affecting peristalsis (i.e., paralytic ileus, spinal cord injury/paralysis, multiple sclerosis)
  • paralytic ileus: temporary paralysis of normal intestineal movement commonly from surgery taht involves intestine manipulation
236
Q

obstruction complications

A
  • perfusion to intestinal segment can be compromised causing: ischmemia leading to necrosis, or rupture or perforation causing peritonitis and septic shock/death
237
Q

small bowel obstruction signs

A
  • abdominal discomfort or pain accompained by visible peristaltic waves in upper and middle abdomen
  • upper or epigastric abdominal distention
  • nasuea and early vomiting (may contain fecal material)
  • obstipation
  • severe fluid and electrolyte imbalances
  • metabolic aklakosis (not always)
238
Q

large bowel obstruction signs

A
  • intermittent lower abdominal cramping
  • lower abdominal distention
  • minimal or no vomiting
  • obstipation or ribbon-like stools
  • no major fluid and electrolyte imbalances
  • metabolic acidosis (not always)
239
Q

management of intestinal obstruction

A

bowel decompression w/ NGT up to 3 days
- NPO w/ IVF
- antiemetics
- electrolyte replacement
- TPN

gastrografin - GI contrast media to dislodge, break up, and flush out partial obstruction
- administer via NGT, clamp for 2-4hrs, then abdominal xrays- if dye is in large intestine, obstruction should resolve w/o surgical intervention

surgery: hernia repair, lysis of adhesions, bowel resection

240
Q

nursing care for intestinal obstruction

A
  • monitor vitals (BP and HR!) for fluid balance monitoring
  • assess abdomen 2x/day for bowel sounds, distention, and passage of flatus
  • monitor fluid and electrolyte balance status include lab values
  • manage NGT: monitor drainage, ensure tube patency, check tube placement, irrigate tube as perscribed, maintain NPO, provide frequent mouth and nares care, maintain pt in semi-fowlers position
  • give analgesics for pain
  • maintain IV therapy for fluid and electrolyte replacement
  • give alvimopan as prescribed for patients w/ post-op ileus
  • maintain parenteral nutrition if prescribed
241
Q

NGT q4hrs

A
  • assess placement, suction, patency, and output
  • assess for presence of bowel sounds and flatus
  • assess for nasal pressure injury
242
Q

inflammatory bowel idsease

A
  • exact cause unknown
  • inflammatory condition impacting GI tract causing chronic inflammation and intestinal mucosal damage
  • exacerbations and remissions
  • impaired ability to absorb nutrients due to diarrhea leading to weight loss
  • umbrella term for 2 disease: crohn’s and ulcerative colitis
243
Q

chron’s disease

A
  • inflammation of GI tract wall that extends through all layers, most commonly distal ileum and ascending colon
  • crypt inflammation and abscesses will develop into ulcers taht deeped and become separated by edematous patches creating cobble stone apperance
  • fistuals, fissures, and abscesses form leading to postential perforation and peritonitis
  • diseased segments of bowel are adjoined by areas of normal bowel tissue
244
Q

ulcerative colitis

A
  • inflammation and ulceration of colon and rectal mucosa
  • begins in rectum and progresses through colon (continuous pattern)
245
Q

ulcerative collitis features

A
  • begins in rectum an proceeds in a continuous manner toward cecum
  • 15-25 and 55-65 age of diagnosis
  • 10-20 liquid bloody stools per day
  • complications: hemorrhage, nutritional deficiencies
  • 20-40% need surgery
246
Q

chron’s disease features

A
  • most often in terminal ileum with patchy involvement through all layers of bowel
  • 15-40 yr age of onset
  • 5-6 soft, loose stools per day, non bloody
  • fistuals and nutritional deficiencies common
  • 75% need surgery
247
Q

symptoms of inflammatory bowel disease

A
  • abdominal cramping, LLQ pain
  • severe bloody, purulent, mucousy diarrhea
  • tenesmus (painful and constant need to empty bowel)
  • bleeding causing anemia (pallor, fatigue)
  • anorexia (malnutrition, weight loss)
  • vomiting (dehydration, electrolyte imbalances)
  • fever
248
Q

mild UC

A
  • <4 stools/day w/ or w/o blood
  • asymptomatic
249
Q

moderate UC

A

> 4 stools/day w/ or w/o blood
mild abdominal pain
mild intermittent nausea
increased CRP or ESR

250
Q

severe UC

A

> 6 bloody stools/day
fever
tachycardia
anemia
abdominal pain
increased CSR and/or ESR

251
Q

fulminant UC

A

> 10 bloody stools/day
increasing symptoms
anemia may need transfusion
colonic distention

252
Q

complications of UC + chrons

A
  • hemorrhage/perforation: lower GI bleeding results from erosion of bowel wall
  • abscess formation: localized pockets of infection develop in ulcerated bowel lining
  • toxic megacolon: massive dilation of colon and colonic ileus that can lead to gangrene and peritonitis
  • intestinal malabsorption
  • non mechanical bowel obstruction: obstruction results from toxic megacolon or cancer
  • fistulas: in chron’s, inflammation is transmural, fistuals can occur anywhere but usually track between the bowel and bladder, resulting in pyuria and fecaluria
  • colorectal cancer: patients w/ UC w/ a hx of longer than 10 years have high risk for colorectal cancer
  • extraintestinal complications: arthritis, hepatic and biliary disease (especially cholelithiasis), oral and skin lesions and ocular disorders such as iritis
  • osteoporosis: common in chron’s
253
Q

medical management of inflammatory bowel disease

A
  • physical rest
  • treat inflammation
  • treat infection
  • correct malnutrition (bowel rest and TPN, fluid and electrolyte management, nutrition)
  • alleviate stress
  • symptom relief
  • complementary and alternative therapies to improve QOL (stress reduction, fear, self-esteem, depression, anxiety)
  • surgery: colectomy w/ ostomy temp or permanent
254
Q

nursing managment of inflammatory bowel disease

A
  • vitals
  • daily weights
  • I&Os
  • fluid and electrolyte status (IVF, electrolyte replacement)
  • nutritional intake (NPO during flare, TPN, advance from NPO to clear to low fiber)
  • assess bowel sounds
  • monitor for tenderness, cramping, s/s of perforation, peritonitis, hemorrhage, obstruction
  • stool frequency and characteristics
  • rest
  • skin care
  • administer meds as perscribed (salicylate compounds, corticosteroids, immunosuppresants, antidiarrheals, pain meds)
  • education: low fiber, high protein, vitamin and iron supplements, small frequent meals, foods to avoid, smoking cessation, meds, followups, colonscopy
255
Q

diverticular disease

A
  • small bulging pouches that form in lining of colon
  • susceptible to complications like inflammation (diverticulitis), bleeding, or perforation
  • diverticulosis: presence of non-inflammed diverticula
  • diverticulitis: inflammation and infection of diverticula
256
Q

symptoms of diverticulosis

A
  • none
  • hx: chronic constipation, bowel irregularity, nausea, anorexia, bloating, distentions
257
Q

symptom of diverticulitis

A
  • acute onsent of abdominal cramping LLQ
  • constipation or diarrhea
  • bloating, distention
  • anorexia
  • flatulence
  • n/v
  • fever
  • leukocytosis
  • rectal bleeding
  • if abscess present: tenderness, palpable mass
258
Q

complications of diverticulitis

A
  • hemorrhage
  • fistula
  • inflammaiton
  • abcess
  • perforation
  • bowel obstruction
  • bleeding
259
Q

uncomplicated diverticulitis management

A
  • outpt
  • rest
  • diet (oral fluids, low fiber and low fat)
  • anitbiotics
  • pain meds
260
Q

diverticulitis w/ complication management

A
  • hospitalization
  • NPO
  • IVF
  • NGT
  • antibiotics
  • pain meds
  • antiemetics
  • surgery: colon resection, ostomy
  • discharge education
261
Q

stomas

A
  • surgically created fecal diversion to abdominal wall via stoma
  • permanent or temporary
  • ileostomy (small intestine)
  • colostomy (colon)
262
Q

reporting of stoma

A
  • stoma ischemia and necrosis (dark red, purplish, or black color, dry)
  • continuous heavy bleeding
  • mucocutaneous separation (breakdown of suture line securing stoma to abdominal wall)
263
Q

stool consistency based on ostomy

A

ileostomy - liquid to semi-liquid
ascending colostomy - semiliquid
transverse colostomy - semiliquid to semiformed
descending colostomy - semiformed
sigmoid colostomy - formed stool

264
Q

appendicitis

A
  • inflammation of appendix
  • when appendix becomes inflammed or infected
  • can cause perforation or rupture within 24 hrs, gangrene after 24-36hrs, peritonitis and/or sepsis
265
Q

s/s of appendicitis

A
  • vague periumbilical pain progressing to RLQ
  • rebound tenderness, abdominal rigidity
  • anorexia
  • n/v
  • fever
  • abdominal distention
  • leukocytosis
  • constipation or diarrhea
266
Q

diagnosis of appendicties

A
  • clinical presentation
  • u/s
  • CT scan
267
Q

medical management

A

7-10 day antibiotics but may still need surgery

268
Q

surgical management

A

appendectomy

269
Q

appendicitis assessments

A
  • vitals
  • intake and output
  • pain
  • rebound tenderness
  • WBCs
270
Q

actions for appendicitis

A
  • keep NPO
  • admin IVF
  • prepare pt for OR
  • provide comfort
  • position supine w. HOB elevated
  • advance diet as tolerated
  • NO LAXATIVES OR ENEMAs
  • NO APPLICATION OF HEAT
271
Q

teaching for appendicitis

A
  • TCDB
  • incentive spirometer
  • early ambulation
  • take full course of antibiotics
  • wound care
272
Q

abdominal trauma

A
  • blunt or pentrating trauma between diaphragm and pelvis
  • spleen and liver most common
  • causes: MVA, stabbing, GSW, fall, asault, contact sports
  • complications: peritonitis, hemorrhage, shock
  • diagnosis: lab studies, xray, CT scan, diagnostic peritoneal lavage, FAST exam
273
Q

signs of abdominal trauma

A
  • bruising
  • penetrating injuries
  • abrasions
  • lacerations
  • discolorations
  • asymmetry
  • cullen’s sign: ecchymosis around umbilicus
  • turner’s sign: ecchymosis around flank
274
Q

medical management of abdominal trauma

A
  • dependent on nature of injury
  • large bore IV
  • fluid resuscitation
  • NG tube
  • surgery: exploratory laparotomy
275
Q

nursing assessments for abdominal trauma

A
  • ABCDE (airway, breathing, circulation, disability (neuro), exposure
  • vitals: tachycardia and tachypnea
  • LOC
  • area of injury
  • clinical manifestations
  • bowel sounds
  • CBC
  • serum electrolytes
  • urinarlysis (hematuria)
276
Q

hypovolemic shock signs

A
  • restlessness
  • anxiety
  • cool clammy skin
  • confusion
  • weakness
  • pale color
  • tachypnea
  • tachycardia
  • hypotension
277
Q

nursing actions for abdominal trauma

A
  • admin o2
  • insert large bore IVs
  • draw labs
  • collect UA
  • insert catheter
  • do not remove object protruding from wound
  • control bleeding
  • admin antibiotics
  • keep family informed about pt condition
278
Q

diagnostics for hepatic and biliary disorders

A
  • ALT
  • AST
  • alkaline phosphatase
  • GGT
  • LDH
  • bilirubin direct and indirect
  • albumin
  • amonnia
  • coags
  • platelets
279
Q

liver biopsy

A
  • used to diagnosis conditions
  • tissue samples are removed from liver and checked under a microscope fro signs of damage or disease, cancer cells or other abnormal cells in liver
  • can tell how liver is functioning
280
Q

preop steps for liver biopsy

A
  • informed consent
  • withhold fluid and food for 8-12hrs before procedure
  • perform baseline assessment
  • assess results of coags and blood type and x
  • teach about postop care and need to hold breath after expiration when needle is isnerted
  • administer sedative as prescribed
  • note client is placed in supine or left lateral during procedure to allow right side exposure
281
Q

if client’s coags and platelets are prolonged and low…

A
  • must notify HCP
  • you may admin platelets, vitamin K, FFP, thrombopoietin agonists, prothrombin complex, and cryoprecipitate
282
Q

postop liver biopsy

A
  • assess vitals
  • monitor site for bleeding
  • monitor for peritonitis
  • maintain bed rest for 12-14hrs
  • place client on right side w/ pillow under costal margin for 2 hrs to decrease the risk of bleeding, and instruct the client to avoid coughing and straining
  • instruct client to avoid havy lifting and strenous exercise for 1wk and to avoid coughing or straining which may cause increased intra-abdominal pressure
  • notify the HCP if dyspnea, cyanosis, or restlessness occurs as these are signs of pneumothorax
283
Q

liver function

A
  • blood storage
  • blood filtration
  • production of bile
  • synthesis of clotting factors (prothrombin and factors II, VII, IX, and X)
  • removal of clotting factors to prevent clotting
  • metabolism of carbs, fats, protein
  • detox blood
  • storage area for vitamins A,D, E, K, and iron
284
Q

hepatic dysfunction

A

occurs when liver is no longer able to perform usual function
caused by: hepatitis, cirrhosis, trauma, or cancer

285
Q

manifestations of liver dysfunction

A
  • thrombocytopenia causing bleeding gums, tachycardia, petechiae, 150k> platelets
  • distended, large abdomen feeling tight w/ abdominal discomfort, lack of appetite, and SOB
  • jaundice: yellowing of skin due to high levels of bilirubin in blood caused by bile duct obstruction, liver dysfunction, and colecystisis
  • esophageal varicies: dilated veins in lining of lower esophagous caused by portal HTN from cirrhosis, portal vein thrombosis, right-sided HF, and schistosmiasis
  • hepatic encephalopathy
286
Q

nursing interventions for esophageal varicies

A
  • monitor vs
  • elevated HOB
  • monitor orthostatic hypotension
  • monitor lung sounds for signs of distress
  • administer o2 as prescribed
  • monitor LOC
  • maintain NPO
  • admin fluids IV as prescribed to restore fluid volume and electrolyte imbalances
  • monitor I&Os
  • monitor h/h and coags
  • administer blood transfusions or clotting factors
  • assist NGT insertion or balloon tamponade
  • prepare to assist with meds to induce vasoconstriction and reduce bleeding
  • instruct patient to avoid activites causing vasovagal responses
  • prepare client for endoscopic procedures or surgical procedures as prescribed
287
Q

hepatic encephalopathy

A
  • life threatening condition
  • liver dysfunction causes impaired ability to metabolize toxic substances like ammonia causing brain dysfunction
  • s/s: insomnia, hypersomnia, mood changes, confusion, coma, asterixis
288
Q

hepatitis

A
  • inflammation of liver leading to dysfunction
  • impairs liver’s ability to fxn in detoxifying body of substances production of proteins and clotting factors ability to store vitamins, fats, and sugars
  • results in jaundice, fatigue, nausea, vomiting, abdominal pain, fever, dark urine, light colored stool
  • caused by a virus, bacteria, or exposure to meds, chronic alcohol use or toxins
  • vital: A,B, and C
  • transmission: blood, body fluid exposure (sex, needles, etc.), stool, fecal-oral contamination
289
Q

hepatitis A

A
  • fecal-oral contaminated water or food
  • sources include feces and contaminated water or food
  • 2-7wk incubation epriod
  • acute ilness
  • vaccine available
  • symptom management is treatment
290
Q

hepatitis B

A
  • percutaneous or mucosal blood, body fluids, needles, and sharps is how disease is transmitted
  • 2-5mo incubation period
  • acute and chronic
  • vaccine available
  • interferon and antivirals for treatment
291
Q

hepatitis C

A
  • percutaneous or mucosal blood, body fluids, needles, and sharps is form of transmission
  • 1wk-several months for incubation period
  • acute and chronic condition
  • no vaccine
  • interferon and antivirals
292
Q

treatment for hepatitis C

A
  • direct acting antivirals
  • interferon
293
Q

herpatitis s/s

A
  • preicteric stage: jaundice, flu-like symptoms, anorexia, n/v, diarrhea, pain, elevated bilirubin and enzyme levels
  • icteric stage: jaundice, elevated bilirubin, dark urine, clay colored stools, pruritis, decrease in preicteric phase, fatigue, abdominal pain
  • posticteric: resolution of jaundice, urine and stool return to normal, energy increases,p ain subsides, minimal GI s/s, bilirubin and enzymes WNL
294
Q

hepatitis A prevention

A
  • avoid contaminated food
  • treat municipal water supplies
  • screening of food handlers
  • preexposure prophylaxis w/ immune globulin for travelers
  • vaccine
295
Q

hepatitis B prevention

A
  • hand hygeine
  • HBV vaccine
  • needle precautions
  • avoiding unprotected contact with body fluids of infected persons
  • blood donor screening
  • testing on women who are pregnant
296
Q

treatment of hepatitis B

A
  • antivirals
  • interferon
  • vaccine required for some
  • mild: rest, adequate fluids and nutrition
  • chronic: monitor liver function
297
Q

hepatitis C prevention

A
  • good handwashing
  • blood donor screening
  • needle precautions
  • avoid unprotected sex w. infected persons
298
Q

treatment of hepatitis C

A

direct acting antivirals for 8-24wks, ongoing monitoring viral load and LFTs
interferon
transplant

299
Q

symptoms of hepatitis A

A
  • pain in right side of abdomen
  • fever
  • jaundice
  • digestion problems
  • dark urine
  • feeling weak
  • vomiting
  • nausea
300
Q

symptoms of hepatitis B

A
  • jaundice
  • encephalopathy
  • ascites
  • palmar erythema
  • violation of blood clotting
  • edema
  • bleeding from esophagus and stomach
  • itching of skin
301
Q

symptoms of hepatitis C

A
  • jaundice
  • ascites
  • nausea
  • bruising and bleeding
  • intoxication
  • asthenia
  • joint pain
  • lack of appeitie
302
Q

therapy for hepatitis

A
  • rest and low level exercise
  • diet: low fat, high fruits veggies, and grains, small frequent meals, alcohol reduction, vitamin A, D, E, and K supplements
  • fluids
  • avoid acetaminophen
  • med: direct acting antivirals, antiemetics, sofosbuvir, nucleoside and nucleotide analogs
303
Q

nursing assessments for hepatitis

A
  • vs
  • labs- LFTs, bilirubin, ammonia
  • skin- color and sclera
  • nutritional intake, daily weight, I&Os
  • observe stools for color, consistency, amount and frequency
  • s/s of complications: change in LOC, ascites, edema, dehydration, respiratory problems, myalgia, arthralgia, s/p transplant (assess for rejection)
303
Q

nursing management for hepatitis

A
  • allow client to rest
  • administer antipruritic meds
  • admin antiemetics
  • admin meds for HBV suppression
  • administer direct acting antivirals
  • provide balanced diet as tolerated
  • encourage small, frequent meals, admin IV nutrition if needed
  • provide adeuqate fluids
  • monitor I&Os and electrolyte balance
  • private room for HAV if client exhibits poor hygeine or has bowel incontinence
  • provide range of motion exercises to minimize risk of blood clots
  • standard precautions!!!!
303
Q

patient education for hepatitis

A
  • handwashing
  • do not share bathrooms
  • individual washcloths, towels, drinking and eating utensils, toothbrushes, razors, etc.
  • cannot prep food for family
  • client should avoid alcohol and OTCs
  • increase activity gradually
  • small frequent high carb low fat meals
  • cannot donate blood
  • crowds should be avoided
  • medicalert bracelet
  • inform HCP
  • med adherance
303
Q

cirrhosis

A
  • condition where healthy liver tissue is replaced by scar tissue affecting liver ability to function
  • liver damage: over time from various factors like alcohol, viral hepatitis infections, fatty liver disease, or other causes the liver to be damaged
  • scar tissue formation: in response to damage, liver tries to heal itself by forming scar tissue which gradually replaces healthy liver tissue
  • impaired liver fxn: as more scar tissue forms, livers ability to perform its vital fxn’s, like detox, protein synthesis, and bile production is impaired
303
Q

diagnosis of cirrhosis

A
  • US
  • CT
  • EGD
  • biliary tract obstruction (percutaneous transhepatic portal angiography, or perc. transhepatic cholangiography
303
Q

signs of cirrhosis

A
  • SOB
  • jaundice
  • pruritis
  • increased risk of bleeding: nosebleeds, easy bruising, bleeding gums, thrombocytopenia, PTT
  • changes in LOC (elevated ammonia levels, hyponatremia)
  • chanegs in motor fxn (asterixis)
  • increased abdominal girth
  • abdominal pain and bloating
  • hemorrhids
  • fatigue
  • weight loss
304
Q

clinical presentation of cirrhosis

A
  • ascites
  • GI varicies
  • bleeding
  • vitamin K deficiency causing poor clotting ability
  • hepatic encephalopathy
  • infection and peritonitis
305
Q

complications of cirrhosis

A
  • portal HTN
  • hepatic encephalopathy
  • spontaneous bacterial peritonitis
  • heptorenal syndrome
  • liver cancer
  • coagulopathy
  • malnutrition
  • liver failure
306
Q

medical management of cirrhosis

A
  • increase Na+ and water excetion (restrct <2g/day of sodium)
  • admin diuretics
  • treat ascites: routine paracentesis, peritoneovenous shunt
  • treat portal HTN (vasoactives)
  • treat hepatic encephalopathy: eat small meals to prevent protein loading, rifaximin, or neomycin, lactulose
  • manage bleeding (banding of varicies, beta blockers, baloon tamponade
  • correct fluid and electrolyte imbalances
  • tranjuglar intrahepatic protosystemic shunt
  • liver transplant
307
Q

nursing management of cirrhosis

A
  • assess for anorexia, n/v, ascites
  • measure girth
  • assess for muscle wasting and poor nutrition
  • assess color of urine
  • assess stools
  • assess respiratory status
  • complete physical
  • assess for prescence of jaundice
  • ask client about itching
  • assess for melean or hematemeis
  • assess client for bleeding and esophageal and GI varicies
  • assess symptoms of hepatorenal syndrome: decrease UO and decreased urine sodium and increased levels of BUN/CR
  • monitor for hepatic encephalopathy
  • assess for a sweet musty odor on client’s breath
  • VS
    -petechiae, bruising, bleeding gums, nosebleeds
  • I&Os, daily weights
  • spider angiomas
  • palmar erythema
308
Q

nursing actions

A
  • nutritional/fluid and electrolytes (diet, high cal low protein, restrict sodium intake and fluid intake, enteral or parenteral nutrition, IVF)
  • meds: antipruritic, diuretics, beta blockers, lactulose, antibiotics, vitamin supplements: K, A, C, B, complex, folic acid, thiamine
  • electrolyte replacements
  • octreotide
  • treat pruritis
  • elevate HOB breathing
  • promote rest
  • test stool for occult blood
  • reorient as needed
  • safety measures to prevent injury
  • administer blood products
  • avoid meds like opioids or sedatives, barbiutrates, any hepatotoxic meds
  • assist with paracentesis, prep for shunting or TIPS procedure
309
Q

patient education for cirrhosis

A
  • teach client experiencing pruitis to sue knuckles to rub itchy areas
  • teach client ot not drink alcohol
  • avoid straining for bowel movements, sneezing, vomiting
  • assist client to quit alcohol
  • sodium restriction
  • read foods labels
  • instruct client on intake of high cals and nutritional supplement
  • instruct client on when to call HCP
  • need for care with hygeine, soft toothbrushes, careful flossing, electric razors
310
Q

paracentesis preop

A
  • ensure understanding of procedure
  • obtain vs
  • obtain weight
  • assist client to void and empty bladder
  • measure abdominal girth
  • position client upright
311
Q

postop paracentesis

A
  • assess HCP in comfort and support
  • apply dressing to puncture site for bleeding
  • monitor for hematuria, caused by bladder trauma
  • monitor vs for BP and HR
  • monitor for LOC
  • measure abdominal girth and weight
  • monitor for hypovolemia and electrolyte loss
  • measure amount of fluid removed and description of it
  • label and send fluid to lab
  • document event and client response
  • instruct HCP if urine becomes bloody, pink or red
312
Q

gallbladder disease

A
  • prescence of stones in gallbladder or common bile duct
  • cholelithiasis
  • coldedocolithiasis
313
Q

cholilithiasis

A
  • supersaturation of bile with cholesterol occurs causing colesterol to precipitate into stones
  • protein, bile salts, and calcium precipitate into stones
  • conditions like pregnancy, obstructive lesions, or inflammation of biliary system and immobility decrease flow increasing risk
  • gallstones frequently stay in gallbladder but may move to ducts causing obstruciton and pain
314
Q

s/s of cholelithiasis

A
  • biliary colic
  • severe rapidly intensifying pain
  • localized to upper right or central abdomen
  • triggered at night after fatty meal
315
Q

diagnosis of cholelithiasis

A
  • abdominal ultrasound
  • endoscopic ultrasound
  • endoscopic retrograde cholangiopancreatography
316
Q

cholesystitis

A
  • can occur as acute or chronic
  • acute is inflammation resulting from obstruction from biliary sludge or gallstones
  • chronic disease is caused when wall of gallbladder becomes scarred and itssues become fibrotic, causing a shrunken gallbladder and decreased function
  • gallbladder becomes swollen and contains pus
  • can occur in absence of gallstones
317
Q

signs of cholecystitis

A
  • indigestions, belching, flatulence after high fat foods
  • pain in RUQ, epigastric pain radiating to right shoulder, between shoulder blades
  • gaurding, rigidity, bebound tenderness
  • hypoactive bowels
  • tachycardia
  • s/s of dehydration
318
Q

cholecystitis medical management

A
  • NPO
  • manage pain
  • antibiotics
  • maintain fluids and electrolytes
  • IVF
  • antiemetics
  • NGT if n/v severe
  • transhepatic biliary catheter
  • lithotripsy
  • ERCP
  • cholecystectomy
  • gallstone dissolution therapy (bile acids (ursodiol)
  • low fat diet
  • fat soluble vitamins
319
Q

nursing interventions for cholecystitis postop

A
  • monitor vs
  • abdominal assessment: distention, bowel sounds, murphy’s sign (taking a deep breath and palpating, if pain occurs on inspiration and palpation it is +)
  • maintain NPO
  • I&Os
  • administer antibiotics, antiemetics, analgesics
  • NGT if ordered
  • prep client for nonsurgical and surgical procedures as ordered
320
Q

patient education for cholecystitis

A
  • keep dressing on for 24hrs after procedure
  • don’t take shower for 48hrs or get incision wet
  • pain meds instruction, constipation, prevention
  • activity level; walk w/i a week, driving, working, light lifting <10lbs, no driving while on narcotics
  • s/s of infection or jaundice
  • postop care of t-tube (monitor drainage
  • clincial manifestations of infection, obstruction, jaundice, color of urine and stool
321
Q

pancreatitis

A

acute: occurs suddenly as one attack or can be recurrent with resolutions
chronic: continual inflammation and destruction of pancreas with scar tissue replacing pancreatic tissue

322
Q

causes of acute pancreatitis

A
  • trauma
  • pancreatic obstruction (tumors, cysts, abscess)
  • metabolic problems
  • renal involvement
  • familial inherited pancreatitis
  • penetrating gastric or duodenal ulcers causing peritonitis
  • viral infections such as coxsckievirus B and HIV
  • alcoholism
  • toxicities of drugs like opiates, sulfonamides, thiaxides, steroids, and oral contraceptives
  • cigarette smoking and tobacco use
  • CF
  • gallstones
323
Q

signs of acute pancreatitis

A
  • low grade fever
  • hypovolemia (tachycarida, hypotension)
  • hypoxia (restlessness, anxiety)
  • abdominal pain (sudden onset, midepigastric or LUQ, radiation to back, aggravated by fatty meal, alcohol, or lying flat)
  • abdominal distention
  • n/v
  • hiccups
  • indigestions
  • absent or decerased bowel sounds
  • jaundice
  • cullen’s sign: bruising around umbilical site
  • turner’s sign: bruising around flank
  • eleavted WBC, lipase, and amylase
  • monitor for hypocalcemia (Chvostek’s sign (hyperexcittability of masseter muscle/cheek), Trousseau’s sign (hand pulls inward), tetany, and laryngospasm)
  • pleural effusion
  • ARDS
  • MODS
324
Q

complications of pancreatitis

A
  • pancreatic infection leading to shock
  • hemorrhage (necrotizing hemorrhagic pancreatitis)
  • acute kidney failure
  • paralytic ileus
  • hypovolemic shock
  • pleural effusion
  • ARDs
  • atelectasis
  • penumonia
  • multiorgan system failure
  • disseminated ivtravascular coagulation (DIC)
  • type 2 diabetes mellitus
325
Q

nursing management of acute panceratitis

A
  • vitals (tachycardia, hypotension, increased RR, decreased O2, fever)
  • NPO
  • monitor lipase and amylase levels
  • abdominal assessment
  • monitor stool color
  • daily weight I&Os
  • assess for s/s of hypocalcemia, tetany
  • NG tube if vomiting, has biliary obstruction or paralytic ileus
  • administer parenteral nutrition for severe nutritional deficiency
  • prolonged NPO status remains - NJ tube
  • admin opiod analgesics for pain
  • admin anticholinergics to decrease secretions
  • histamin blocks, pancreatic enzymes, and antibiotics
  • observe for changes in LOC related to alcohol withdrawal, hypoxia, or sepsis
326
Q

education for pancreatitis

A
  • diet mods
  • avoid alcohol and smoking
  • follow ups
  • notify HCP if acute abdominal pain, jaundice, clay-colored stools, or dark-colored urine develops
327
Q

chronic pancreatitis signs

A
  • constant severe upper abdominal and back pain
  • vomiting
  • steatorrhea, foul smelling stools
  • clay colored stools
  • malnutrition
  • anorexia
  • weight loss
  • jaundice
  • ascites
  • elevated serum glucose
  • elevated amylase, lipase, serum bilirubin, and alkaline phosphatase
328
Q

nursing management of chronic pancreatitis

A
  • VS: pain increasing HR, RR, BP
  • abdominal assessment, look for cullen or turner signs
  • assess sclera
  • assess stool
  • monitor labs
  • pain management
  • IVF
  • electrolyte replacement
  • pancreatic enzyme replacement. (PERT- do not chew)
  • nutritional support
  • glucose management
  • GI prophylaxis
  • avoid alcohol and irritating food/beverages, limit fat, avoid heavy meals, small high calorie snacks, follow up
329
Q

BMI scale

A
  • underweight <18.5
  • normal 18.5-24.9
  • overweight 25.0-29.9
  • obesity (class 1) 30-34.9
  • obesity (class 2) 35-39.9
  • extreme obesity (class 3) >40
330
Q

obesity increases risk for

A
  • type 2 DM
  • CVD
  • stroke
  • OSA
  • cancer
  • end stage renal disease
  • psych episodes
  • incerased prescriptions for pain
331
Q

bariatrics

A

medical specialty that focuses on causes, prevntion, and treatment of obesity

332
Q

treatments for obesity

A
  • weight loss therapy
  • diet therapy
  • physical activity
  • behavioral therapy
  • medications
  • bariatric surgery
333
Q

orlistat (alli)

A

inhibits pancreatic lipase reducing dietary fat absorption

334
Q

lorcaserin (belviq)

A

affects chemicals in brain regulating appetite and increase feeling of fullness after eating

335
Q

pentermine/topiramate-extended release (Qsymia)

A

phentermine supressess appetite causing weight loss, decreased appetitie, an enhanced satiety

336
Q

bupropion-naltrexone (contrave)

A

can raise BP, antidepressant

337
Q

liraflutide (saxenda)

A

glucagon like peptide reception agonist to slow gastric emptying dosage titrated up weekly

338
Q

restrictive surgery

A

weight loss by reduced gastric capcity adjustable gastric banding, sleeve gastrectomy

339
Q

malabsorptive surgery

A

no longer commonly preformed
induces weight loss through decreased nutrient absorption, jejunoileal bypass and biliopancreatic diversion

340
Q

combination surgery

A

induces weight loss through restriction also creating component of malabsorption Roux-en-Y gatric bypass

341
Q

complications of bariatric surgery

A
  • mortality rates steadily declined
  • PE
    -infection
    -anastomosis leak
  • band slippage
  • obstruction
  • hernia
  • esophageal erosion
  • ulcers
  • acid reflux
  • vitamin deficiency
  • osteoporosis
  • anemia
  • dumping syndrome
342
Q

nursing management of bariattric surgery

A
  • impaired breathing
  • atelectasis and pneumonia
  • increased risk VTE
  • increased risk pressure injury
  • risk for skin infetions
  • immobility
  • anastomosis leak (life threatening complication causing tachycardia, fever, hypotension, and abdominal pain)
  • bleeding
  • peritonitis
  • intestinal obstruction
  • dehydration
  • electrolyte imbalance related to vomiting
  • malnutrition
343
Q

nursing assessments for obesity/bariatric surgery

A
  • VS
  • o2 sat
  • electrolytes
  • daily weight
  • skin assessment
  • incisions and drains
  • pain
344
Q

nursing management for obese

A
  • obtain appropriate sized equipments
  • elevate HOB
  • VTE prevention
  • use mobility devices
  • turn and position
  • skin care
  • do not reposition NG tube
  • monitor NG tube for patency
  • introduce clear liquids as ordered
  • emotional support
  • teaching: post op lifting restrictions, diet (clear liquids advancing to pureed and then solid foods, PROTEIN!!!), signs to report to HCP, follow up
345
Q
A

med surg (3 decks)

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