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Adults 1 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

manifestations of hypokalemia

A

weak irregular pulse, orthostatic hypotension, confusion, lethargy, coma, decreased motility (decreased bowels sounds), nausea, vomiting, skeletal muscle weakness, decreased deep tendon reflex, parasthesias, shallow resp., EKG changes

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1
Q

causes of hypokalemia

A

potassium loss (d/t meds, increased aldosterone, vomiting, diarrhea, NG tube prolonged suction, diaphoresis, impaired K reabsorption (kidney disease)), inadequate potassium intake, movement from ECF to ICF (alkalosis, hyperinsulinism), dilution of serum potassium (water intox., IVF with potassium deficient sol.)

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2
Q

EKG changes with hypokalemia

A

ST depressions, shallow flat or inverted T wave, prominent U wave

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3
Q

management of hypokalemia

A

monitor heart rhythms (cardiac monitor, focused cardiac assess.), assess resp., GI, and renal (urine output, BUN, creatinine), monitor electrolytes, hold potassium-wasting meds, replenish potassium (potassium rich food)

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4
Q

replenishing hypokalemia

A

levels 2.5-3.5 supplement orally, less than 2.5 supplement IV

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5
Q

causes of hyperkalemia

A

excess K intake (food, meds, or IV sol.), decreased K excretion (K sparing meds, NSAIDs, ACEI, renal disease, adrenal insufficiency), movement for ICF to EXC (tissue damage, acidosis, hyperuricemia, hypercatabolism)

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6
Q

manifestations of hyperkalemia

A

slow irregular pulse, dysrhythmias, hypotension, weakened skeletal muscles, increased motility, hyperactive B.S., diarrhea, muscle spasms, cramping, parasthesias, profound weakness and paralysis in extrem. at late and lethal levels

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7
Q

EKG changes of hyperkalemia

A

peaked T waves, flat P waves, widened QRS complex, Prolonged PR interval

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8
Q

management of hyperkalemia

A

limit/discontinue intake of K, increase excretion (potassium wasting diuretics, kayexalate for renal impairment, IV hypertonic glucose with insulin, IV calcium to prevent myocardial excitability, monitor K levels, assess cardiac function continuously

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9
Q

causes of hypocalcemia

A

inadequate oral intake (alcoholism), malabsorption (lactose intol., celiac disease/crohns disease, inadequate vit. D intake, ESRD), increased excretion (renal disease, diarrhea, wound drainage-especially GI), decreased ionized fraction of calcium (chelate or binding meds, acute pancreatitis, hypophosphatemia, removal/drainage of parathyroid glands)

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10
Q

manifestations of hypocalcemia

A

bradycardia, hypotension, diminished pulses, irritable skeletal muscles (twitching, cramp, tetany, seizure), decreased resp., paresthesias, hyperctive deep tendon reflex, anxiety, irritability, increased GI motility, hyperactive BS, cramping, diarrhea, positive trosseau’s and chvosteks

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11
Q

EKG changes with hypocalcemia

A

prolongs SR and QT

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12
Q

management of hypocalcemia

A

replenish Calcium (IV Slowly), increase vit. that increase absorption (vit D, aluminum hydroxide to reduce Phosph, have 10% cal. gluconate available for acute deficit), reduce environmental stim., seizure precautions, monitor EKG for changes (especially w/ IV calcium), educate calcium rich foods

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13
Q

trosseaus sign

A

carpal spasm induced by inflation of BP cuff

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14
Q

chvosteks sign

A

contraction of facial muscles in response to light tap over facial nerve in front of ear

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15
Q

isotonic dehydration

A

equal loss of water and electrolytes; decreased circulating blood causing inadequate tissue perfusion

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16
Q

hypertonic dehydration

A

water loss > electrolyte loss (causing hypernatremia); fluid moves from intracellular into plasma (cells shrink) d/t alterations in plasma electrolytes

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17
Q

hypotonic dehydration

A

electrolyte loss > water loss (causing hyponatremia); fluid moves from plasma and interstitial space into cells (cells swell) d/t fluid shifting between compartments and decreasing plasma volume

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18
Q

fluid volume deficit manifestations of lab findings

A

increased serum osmolarity, increased hematocrit, increased BUN, increased serum sodium, increases urine Specific gravity

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19
Q

fluid volume deficit management

A

oral rehydration/ IV: isotonic dehydration rehydrate with isotonic fluids, hypertonic dehydration with hypotonic, hypotonic dehydration with hypertonic

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20
Q

fluid volume deficit manifestations of assessment

A

weak/thready/diminished pulse, decreased BP/ortho., flat neck veins, decreased RR/dyspnea, lethargy/coma, muscle weakness, fever, decreased urine output, decreased skin turgor, dry mouth, diminished bowel sounds, constipation, thirst

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21
Q

process of stroke

A

cerebral anoxia- lack of O2 to the brain which can cause cell damage, cerebral infarction- death of brain tissue from lack of O2/blood supply, cerebral edema- brain swelling (compensatory mechanism that can damage the brain further due to increased ICP), cerebral dysfunction- portion of brain that lost function d/t death

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22
Q

2 types of stroke

A

hemorrhagic or ischemic

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23
Q

2 types of ischemic strokes

A

thrombotic or embolic

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24
Q

manifestations of ischemic stroke

A

sudden severe headache; weakness/numbness; difficulty speaking/understanding speech; loss of balance/difficulty walking/dizziness; confusion/altered LOC; dysphagia; facial droop to one side

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25
Q

manifestations of hemorrhagic stroke

A

sudden severe headache (worst headache of pt life); weakness/numbness; N/V; difficulty speaking/understanding speech; vision problems; loss of balance/difficulty walking/dizziness; confusion/altered LOC; seizures

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26
Q

nursing intervention of acute phase of stroke

A

maintain airway, supplemental O2, neuro exam- monitor ICP within first 72 hours, elevate HOB and place pt on side to prevent aspiration, foley catheter, fluid and electrolyte admin., medication admin., quiet environment, seizure precautions

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27
Q

nursing interventions of post acute phase of stroke

A

position 2 hours on unaffected side and 20 minutes on affected side, antiembolism stockings, ROM exercises, eval. gag reflex and ability to swallow, NPO to begin and advance as tolerated

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28
Q

what is a seizure

A

abnormal, sudden, excessive discharge of electrical activity in the brain

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29
Q

3 main types of seizures

A

focal onset- localized to one area of brain, generalized onset- more wide spread brain activity, unknown onset

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30
Q

6 types of seizures

A

tonic-clonic (gen), absence (gen.), myoclonic, atonic/akinetic, simple partial (focal), complex partial (focal)

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31
Q

general stroke symptoms

A

sudden weakness, numbness, difficulty speaking, loss of coordination

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32
Q

non-modifiable risk factors for stroke

A

age, gender (males higher risk), ethnicity (african americans higher risk), genetics

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33
Q

modifiable risk factors for stroke

A

HTN, atherosclerosis, Afib, anticoag therapy, stress, obesity, oral contraceptives, DM

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34
Q

primary cause of stroke

A

HTN

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35
Q

embolic ischemic stroke

A

clot/debris that travels to brain; sudden severe symptoms; less common warning signs; pt remains conscious but complains of headache

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36
Q

thrombotic ischemic stroke

A

build up of plaque in artery in brain; gradual onset compared to other strokes; no decrease in LOC in first 24 hours; s/s progressively worsen as infarction and edema occurs

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37
Q

common stroke assessment findings

A

agnosia, apraxia/dyspraxia, hemianopsia, neglect syndrome, proprioception alterations, aphasia

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38
Q

agnosia

A

inability to recognise familiar objects/people

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39
Q

apraxia/dyspraxia

A

loss of ability to carry out skilled movements or gestures

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40
Q

meds used to prevent strokes

A

anticoag therapy, antiplatelet, antihypertensive, dyslipidemia

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41
Q

acute stroke management

A

CT without contrast to identify if hemorrhagic or ischemic; if ischemic then use thrombolytic therapy

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42
Q

window for administering thrombolytic therapy

A

3.5-4 hours after onset of altered status

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43
Q

epilepsy

A

disorder characterized by chronic seizure activity; indicates CNS or brain irritation

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44
Q

causes of seizures

A

genetics, tumors, trauma, circulatory or metabolic disorders, toxicity, infection

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45
Q

status epilecticus

A

rapid succession of epilectic spasms without intervals of consciousness; can occur with any type of seizure

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46
Q

what is the danger of seizures?

A

can cause brain damage

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47
Q

tonic/clonic seizures

A

may begin with aura; tonic phase consist of stiffening/rigidity of muscles in arms or legs for 10-20 sec followed by LOC; clonic phase consist of hyperventilation and rapid jerking of extrem. lasting 30 seconds; may lose control of bladder during clonic phase; postictal phase may take hours to recover

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48
Q

when to seek medical treatment for seizures

A

if seizure lasts longer than 5 min

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49
Q

myoclonic seizure

A

minor/brief generalized jerking or stiffening of extremities; can cause pt to fall to ground; pt is aware of the event

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50
Q

atonic seizures

A

sudden loss of muscle tone causing person to drop/fall to ground; both sides of brain usually affected; can happen to part or entire body; lasts less than 15 sec; pt not completely aware of event

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51
Q

simple seizure

A

occurs in one area of brain on one side; motor and sensory symptoms localized to specific area; pt remains conscious; rarely lasts longer than 1 hour; may experience aura

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52
Q

complex seizure

A

most common seizure in adults; consist of blank stare (usually involves temporal lobe); periods of altered behavior that pt is unaware of; lasts longer than 1 minute; pt loses consciousness for a second

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53
Q

nursing assessment of seizure

A

seizure HX, type of seizure, what happened before/during/after; were there prodromal signs/aura; loss of bladder? LOC?; details of postictal state

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54
Q

phases of seizure

A

prodromal phase, aura phase, ictal phase, postictal phase

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55
Q

nursing interventions for seizure

A

note time/duration; assess behavior at beginning/middle/end; lower pt to ground; support ABCs; remain with pt but do not restrain; remove tight clothing; note type of seizure; monitor incontinence; admin IV meds; monitor vitals; reorient pt

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56
Q

myasthenia gravis

A

chronic progressive neuromuscular disease characterized by severe weakness and abnormal fatigue of voluntary muscles; interruption of transmission of nerve impulses at myoneural junction

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57
Q

causes of myasthenia gravis

A

insufficient secretion of acetylcholine; excessive secretion of cholinesterase; unresponsiveness of muscle fibers to acetylcholine

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58
Q

what is the role of acetylcholine neurotransmitter

A

muscle contraction and movement

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59
Q

what is the role of cholinesterase

A

destruction of acetylcholine

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60
Q

assessment of myasthenia gravis

A

weakness, fatigue, difficulty with chewing and swallowing, dysphagia, diplopia, weak/hoarse voice, difficulty breathing, ptosis

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61
Q

nursing interventions for myasthenia gravis

A

monitoring of respiratory, swallowing, cough reflex, speech, muscle strength, myasthenic or cholinergic crisis; educate pt to wear medic alert, sit up when eating, conservation of muscle strength

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62
Q

treatment of myasthenia gravis

A

admin anticholinesterase meds which relieve muscle weakness by blocking acetylcholine breakdown at neuromuscular junction

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63
Q

myasthenic crisis

A

acute exacerbation of disease that is caused by rapid progression of disease, infection, too little meds, fatigue, or stress

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64
Q

manifestations of myasthenic crisis

A

tachycardia, tachypnea, HTN, dyspnea, cyanosis, incontinence, absent cough/swallow reflex

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65
Q

nursing interventions for myasthenic crisis

A

assess for symptoms, increase anticholinesterase meds as prescribed

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66
Q

osteoarthritis

A

breakdown of articular cartilage leading to damage of bone; osteophytes form in joint space that cause narrowing and decreased movement in joints; causes progressive degeneration

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67
Q

risk factors for developing osteoarthritis

A

old age, female, obesity, labor intensive occupations, sports

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68
Q

manifestations of osteoarthritis

A

pain when moving under stress that is relieved by stress; hard and bony stiff joints; morning stiffness for about 30 minutes; often impacts weight bearing joints like hips knees c-spine and l-spine

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69
Q

2 types of bony growths in osteoarthritis

A

heberden- distal; bouchard-proximal

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70
Q

assessment of osteoarthritis

A

joint crepitus; effusion d/t inflammation; non-systemic; x-ray + for decreased joint space and osteophyte formation; subchondral bones may appear thick

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71
Q

does osteoarthritis appear bilaterally?

A

no but it can

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72
Q

management of osteoarthritis

A

decrease pain and stiffness, maintain/improve mobility, exercise to preserve joint, weight loss, OT/PT, orthotics and walking devices, NSAIDs/steroids, arthroplasty in severe cases

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73
Q

osteoporosis

A

bone resorption (osteoclast) > bone formation (osteoblast); causing thinning of bone

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74
Q

osteoporosis can lead to…

A

compression FX of T and L spine, FX of hips, FX of wrists; increased FX risk

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75
Q

risk factors for developing osteoporosis

A

small frame, female, ethnicity, aromatase inhibitor use, nutritional factors, autoimmune diseases, steroid use, immobility, diabetes

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76
Q

typical age range for onset of osteoporosis

A

men- 60 to 70
women- 50 to 60

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77
Q

manifestations of osteoporosis

A

low bone mineral density on DEXA scan, rounding of upper back (aka dowager humps), osteoporotic FX; otherwise can be asymptomatic

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78
Q

assessment of osteoporosis

A

X-ray + for radiolucency if significant demineralization (dark area indicative of low density); dual energy xray (DEXA) provides bone mineral density

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79
Q

prevention of osteoporosis

A

balanced diet rich in calcium and vitamin D, regular weight bearing exercises (20-30 per day)

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80
Q

why weight training for osteoporosis prevention

A

stimulates bone mineral density

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81
Q

management of osteoporosis

A

pharmacological therapy to improve bone density via bisphosphenates or alendronate; hip FX managed with replacement; compression FX managed conservatively

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82
Q

osteoporosis nursing interventions

A

educate pt on how to prevent worsening, pain management, improve bowel elimination to avoid FX, injury prevention

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83
Q

osteomalacia

A

inadequate mineralization of bone caused by Vitamin D deficiency; leads to soft and weakened bones

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84
Q

causes of osteomalacia

A

failure to absorb calcium; excessive calcium loss; GI disorders; liver disease; kidney disease; renal insufficiency; hyperparathyroidism; malnutrition

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85
Q

assessment of osteomalacia

A

X-ray + for general demineralization; X-ray can show compression FX; labs show low Ca, low Phosp, elevated alkaline phosphatase; bone biopsy shows increased osteoid

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86
Q

what is osteoid

A

demineralized cartilaginous bone matrix; aka pre-bone

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87
Q

management of osteomalacia

A

treat underlying cause f possible; Vitamin D, calcium supplements, sun exposure; if kidney disease is issue then admin of activated Vitamin D med; if dietary is cause then recommend change; severe deformities may warrant braces

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88
Q

why low calcium and low phosphorus in osteomalacia

A

bone is unable to mineralize

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89
Q

why elevated phosphatase in osteomalacia

A

increased bone turnover

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90
Q

septic arthritis

A

infection of joint; mortality for ingle infected joint is 11%

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91
Q

risk factors for developing septic arthritis

A

older age, diabetes, rheumatoid arthritis, skin infection, alcoholism, HX of joint surgery, IV drug use

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92
Q

manifestations of septic arthritis

A

warm, painful, swollen joint; decreased ROM; chills, fever, leukocytosis; half of all cases localized to knee

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93
Q

assessment of septic arthritis

A

infectious workup; aspirations, examination, and culture of synovial fluid (will be purulent pus); CT/MRI and bone scan

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94
Q

septic arthritis management

A

primary broad spectrum antibiotic, aspirate synovial fluid periodically (therapeutic aspiration), splinting, pain relief, progressive ROM, potential for joint fibrosis, monitor for reoccurrence

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95
Q

nursing interventions for septic arthritis

A

pain relief; improve physical mobility; control infection promote home, community, transitional care

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96
Q

3 types of fractures

A

closes or simple, open or compound/complex, intra-articular

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97
Q

avulsion FX

A

fx where fragment of one has been pulled away by tendon and its attachment

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98
Q

comminuted FX

A

fx where bone has splintered into severe fragments

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99
Q

compression FX

A

fx where bone has become compressed (common or vertebrae)

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100
Q

depressed FX

A

fx where fragments are driven inward (commonly seen in skull)

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101
Q

epiphyseal FX

A

fx through epiphysis

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102
Q

greenstick FX

A

fx where one side is broken and other is bent (common in children)

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103
Q

impacted FX

A

fx where bone fragment is driven into another bone fragment

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104
Q

oblique FX

A

fx occurring at angle across bone; ess stable than transverse FX

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105
Q

open FX/ compound FX

A

fx where bone is protruding through skin or mucous membrane; damage to skin or mucous membrane; increased risk for infection

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106
Q

pathologic FX

A

fx that occurs through area of diseased bone; can occur with or without trauma; ex. osteoporosis or bone cyst

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107
Q

simple FX

A

fx that remains contained in skin; no disruption of skin integrity

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108
Q

spiral FX

A

fx that twists around the bone shaft

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109
Q

stress FX

A

fx resulting from repeated loading of bone and muscle

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110
Q

transverse FX

A

fx that is straight across bone shaft

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111
Q

manifestations of bone FX

A

loss of function, shortening, crepitus, edema, deformity, ecchymosis

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112
Q

assessment of FX

A

health HX, comorbidities, vital signs, respiratory status, LOC, s/s of shock, neurovascular assessment of extremity, bowel/bladder elimination, bowel sounds, I/Os if hip FX, skin condition, anxiety and coping

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113
Q

management of FX

A

immediate immobilization, cover open wounds, FX reduction and then immobilize if needed

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114
Q

3 types of FX reduction

A

closed reduction- manual traction; open reduction- surgical intervention; delayed reduction- waiting for pt to stabilize prior to intervention

115
Q

2 types of immobilizations

A

external fixation- casts and bandages; internal fixation- plates and screws

116
Q

nursing interventions of FX

A

elevate, monitor for neurovascular compromise (5 Ps), monitoring for normal elimination, isometric muscle exercises, encourage ADLs and independence, pain management, pt education, wound care

117
Q

risk factors for FX healing

A

over 40 years of age, corticosteroid use, NSAID use, avascular necrosis, bone loss, tobacco use, comorbidities, local trauma, inadequate immobilization, malalignment, premature weight bearing, infection, local malignancy

118
Q

acute FX complications

A

shock, fat embolism, compartment syndrome, DVT, PE, DIC, infection loss of bladder control in hip FX, hemorrhage

119
Q

chronic FX complications

A

delayed union of bone, malunion of bone, AVN of bone, complex regional pain syndrome (CRPS), heterotrophic ossification (benign bone growth in atypical location)

120
Q

5 Ps of neurovascular assessment

A

pain, pulse, pallor, parasthesia, paralysis

121
Q

assessment of casts, splints, braces

A

assess injury, treat lacerations and wounds, assess neurovascular status (5 Ps)

122
Q

complications associated with casts, splints, braces

A

pressure injuries, disuse syndrome (muscle weakness/wasting and joint stiffness), acute compartment syndrome

123
Q

compartment syndrome

A

increased pressure within compartment that impairs blood flow and compromised tissue viability

124
Q

management of compartment syndrome

A

fasciotomy

125
Q

hypertension classifications

A

primary- unknown cause; secondary- caused by another factor and need to target underlying cause; malignant- HTN crisis

126
Q

interventions for HTN prior to medications

A

lifestyle modification for 1-3 months such as reducing alcohol, sugar, sodium, fat, stress, and increasing exercise

127
Q

causes of primary HTN

A

aging, family HX, African American race, sedentary lifestyle, smoking, alcohol, HLD

128
Q

causes of secondary HTN

A

results from other conditions like CV disorders, renal disease, endocrine diseases, pregnancy, meds, sleep apnea

129
Q

assessment for HTN

A

History: family HX, current meds, perception of diseases; Signs and symptoms: dietary pattern, headache, visual changes, neurological assessment, lab tests; Physical exam: obtain 2 BP on both arms when supine and then standing, compare to prior, assess weight, assess for JVD, HR, dysrhythmias, S3, enlarged heart on Xray

130
Q

common end organ damage from HTN

A

cerebrovascular damage, vasculopathy, heart disease, nephropathy

131
Q

cerebrovascular damage resulting from HTN

A

acute HTN encephalopathy (confusion), stroke, vascular dementia, retinopathy

132
Q

vasculopathy from HTN

A

atherosclerosis, aortic aneurysm

133
Q

heart disease from HTN

A

left ventricular hypertrophy, coronary artery disease, MI, HF, atrial fibrillation

134
Q

nephropathy from HTN

A

proteinuria, renal failure

135
Q

non-pharmacological interventions for HTN

A

weight reduction, sodium reduction (less than 2g/day), reduce alcohol and caffeine, exercise, smoking cessation, stress reduction, monitor BP

136
Q

older adult considerations HTN

A

isolated systolic HTN d/t age related loss of elasticity of carotid and aorta; hard to treat due to low DBP; medication issues because of failure to remember, polypharm, expensive, orthostatic hypotension

137
Q

HTN urgency

A

BP > 180/120 with no evidence of end-organ damage; pharmacological interventions used to normalize BP within 24-48 hours

138
Q

coronary artery disease

A

narrowing or obstruction of 1 or more coronary arteries due to atherosclerosis; leads to inadequate perfusion and oxygenation of myocardial tissue

139
Q

effects of coronary artery disease can lead to

A

HTN, angina, dysrhythmias, MI, heart failure, death

140
Q

collateral circulation

A

vascular system is generated around the obstruction to bypass and perfuse; takes ~ 10 years to form

141
Q

modifiable ris factors for CAD

A

BMI>30, DM, HTN, alcohol use, high LDL and low HDL, tobacco use

142
Q

non-modifiable risk factors for CAD

A

65 years and older, family HX, genetic predisposition

143
Q

manifestations of CAD

A

early on is asymptomatic, chest pain, dyspnea, syncope, cough/hemoptysis, palpitations, excessive fatigue

144
Q

diagnosing CAD

A

EKG: ischemia = depression and infarction = elevation; Lipids: elevated cholesterol, stress tests, cardiac cath

145
Q

cardiac cathertirzation

A

angiogram used to diagnose CAD; injected dye into arteries to identify atherosclerotic plaques blocking off blood flow (plaques do not illuminate)

146
Q

treatment for CAD

A

tobacco cessation, manage HTN, low cal, low sodium, low fat, low cholesterol, increased dietary fiber, control Dm, reduce stress, reduce alcohol, pharmacological management

147
Q

lymphedema

A

increase in lymph due to obstruction of a vessel; can be primary or secondary (d/t other condition)

148
Q

treatment of lymphedema

A

ambulatory compression stockings, manual drainage, physiotherapy, skin care

149
Q

TIA or transient ischemic attack

A

temporary neurologic deficit resulting from temporary blood flow impairment; seen as a warning sign for potential impending stroke; requires medical attention to rule out infarction

150
Q

manifestations of TIA

A

transient/short-lived symptoms; same as ischemic stroke: weakness/numbness; difficulty speaking/understanding speech; vision problems; difficulty walking/loss of balance/dizziness; facial droop to one side

151
Q

tuberculosis

A

highly contagious communicable disease caused by M. tuberculosis; airborne; exudative response causes nonspecific pneumonitis and granulomas in lung tissue; onset is insidious and pt are unaware until disease is advanced

152
Q

risk factors for developing tuberculosis

A

elderly, <5 years of age, unpasteurized milk if cow is infected, homeless, low socioeconomic group, minorities, refugees, frequent contact with untreated/undiagnosed individual, crowded living areas, malnutrition, immune dysfunction, alcohol abuse/IV drug use

153
Q

causes of tuberculosis

A

bacteria forms tubercle lesion and immune system encapsulates tubercle leaving scar; if no encapsulation then bacteria can enter lymph and cause inflammatory response called granulomatous inflammation leading to primary lesions forming

154
Q

active phase of tuberculosis

A

infection causes necrosis and cavitation in lesions that can rupture and spread necrotic tissue damaging various parts of the body; need xray to confirm because a recent BCG vaccine can cause positive PPD/mantioux test

155
Q

manifestations of tuberculosis

A

may be asymptomatic in primary phase, fatigue, lethargy, anorexia, weight loss, low grade fever, chills, night sweats, persistent cough (can be blood streaked but usually dry), chest tightness, dull aching chest pain with cough

156
Q

testing for tuberculosis

A

chest xray may show cessation and inflammation, advanced may show partial obstruction of bronchus from endobronchial disease (wheezing and dyspnea present), TB skin test (positive result does not mean active), quantiferon TB gold test (sensitive and rapid blood test), sputum culture for confirmation

157
Q

managing tuberculosis

A

goal is to prevent transmission, reduce symptoms, prevent progression; risk of transmission decreases after 2-3 weeks of treatment; treatment for up to 12 months; educate importance on medication compliance; well balanced diet; sputum culture every 2-3 weeks until 3 negative tests consecutively

158
Q

emphysema

A

air sacs enlarged and damaged causing hyperinflation and breathlessness; pink puffer; barrel chest

159
Q

atelectasis

A

collapse of alveoli; can be acute or chronic; occurs as result of ventilation; can be caused by reduced ventilation or obstruction; at high risk for developing when post op

160
Q

clinical manifestations of COPD

A

cough, exertional dyspnea, wheezing/crackles, sputum production, weight loss, barrel chest, accessory muscle use, prolonged expiration, orthopnea, cardiac dysrhythmias, congestion/hyperinflation of chest xray, ABG show acidosis and hypoxemia, decreased capacity of pulmonary function test

161
Q

management of COPD

A

monitor vital signs, admin O2, fowlers position and leaning forward, respiratory treatments chest physiotherapy, educate on tripod breathing and pursed lip, bronchodilators, corticosteroids, mucolytics, antibiotics, high calcium and high protein diet, 2-3L fluid, suction as needed

162
Q

causes of atelectasis

A

foreign body, tumor/growth, altered breathing patterns, retained secretions, pain, prolonged supine position, increased abdominal pressure, reduced lung volumes from muscular/neurological disorders, surgery

163
Q

manifestations of atelectasis

A

dyspnea, cough, sputum production, hypoxemia, decreased breath sounds, crackles, respiratory distress, tachycardia, tachypnea, pleural pain, central cyanosis

164
Q

prevention of atelectasis

A

frequent turning, early ambulation, lung volume expansion maneuvers like deep breathing and coughing and incentive spirometers, positive end respiratory pressure (PEEP), CPAP

165
Q

diabetes mellitus

A

chronic disorder of impaired carbohydrate, protein, and lipid metabolism; primarily carbohydrate; deficiency of insulin results in hyperglycemia

166
Q

sub categories of DM

A

Type 1, Type 2, and metabolic syndrome (pre-diabetes)

167
Q

complications of DM

A

microvascular complications, macrovascular complications, reduced healing causing increased risk of infection

168
Q

type I DM

A

nearly absolute deficiency of insulin due to autoimmune primary beta cell destruction (negligible insulin); if insulin is not given then fat is metabolized for energy causing DKA; genetic

169
Q

type II DM

A

relative lack of insulin or resistance t the action of insulin; insulin is sufficient to stabilize fat and protein metabolism but not carbohydrate; develops over time

170
Q

metabolic syndrome

A

coexisting risk factors for developing type II diabetes; risk factors include abdominal obesity, hyperglycemia, HTN, high triglyceride levels, low HDL

171
Q

assessment of DM

A

polyuria, polydipsia, polyphagia, hyperglycemia, weight loss, blurred vision, slow wound healing, vaginal infections, weakness/parasthesias, signs of inadequate circulation of feet, signs of accelerated atherosclerosis

172
Q

A1C diagnostic for diabetes

A

> 6.5

173
Q

primary intervention for type II DM

A

exercise, diet, and lifestyle; if not working after 6 months than oral hypoglycemics and maybe insulin prescribed

174
Q

only oral hypoglycemic not contraindicated in

A

SGLT-2 inhibitors

175
Q

dawn phenomenon

A

hyperglycemia on morning awakening resulting from excessive release of GH and cortisol early in morning; treatment is increase in insulin dose or change in administration timing

176
Q

somogyi effect

A

normal/elevated glucose at bedtime, hypoglycemia around 2am causing increase in production of counterregulatory hormones; blood glucose rebounds by 7am in response to counterregulatory hormones and pt is hyperglycemic; treat with decreased insulin and or having large bedtime snack

177
Q

hypoglycemia

A

<70 mg/dL or rapid drop from elevated level; caused by too much insulin, too much oral hypoglycemic, too little food, or too much exercise

178
Q

signs and symptoms of hypoglycemia

A

cold, clammy, headache, lethargy, AMS, hungry, tachycardia, jittery, angry

179
Q

assessment of hypoglycemia

A

mild is 40-70: fully awake with neurogenic symptoms like tremors, palpitations, sweating, hunger; moderate is 20-39: s/s of worsening hypoglycemia like dizziness, drowsiness, and weakness; severe is <20: severe neuroglycopenic symptoms like delirium, seizure, coma, and death

180
Q

hypoglycemia interventions

A

check BGL, 15/15 rule- if symptomatic or below 70mg/dL give 15 gram of simple carbs (4oz juice), recheck BGL in 15 min and administer another 15g, if still below 70 after 45 g sugar admin 15-50 ml of 50% dextrose or 1mg glucagon; pt should then eat snack

181
Q

DKA

A

life threatening complication of type I that can occur with severe insulin deficiency; too much breaking down of fats producing ketones which are acidic; hyperkalemia can be seen (H into cell and K out into blood stream)

182
Q

assessment of DKA

A

precipitated by infection, stress, inadequate insulin, or can be sudden; glucose >300 Cr > 1.5, urine has ketones, K elevated with acidosis, ABG show acidotic, dehydrated, polydipsia, polyuria, weight loss, dry skin, sunken eyes, lethargy, coma

183
Q

Interventions for DKA

A

restore blood volume, IV insulin with infusion of NS or 1/2 NS with dextrose added; monitor K and correct imbalances in electrolyte; cardiac monitoring if needed

184
Q

HHS- hyperosmolar hyperglycemic syndrome

A

extreme hyperglycemia without ketosis/acidosis; more often inn Type II diabetes; enough insulin is present to prevent breakdown of fts for energy (no ketosis); need to have neurological side effects present

185
Q

assessment of HHS

A

gradual onset precipitated by infection, stressors, poor fluid intake; neurological symptoms from altered CNS function; dehydration and electrolyte imbalance from high glucose displacing electrolytes; polyuria, polydipsia, weight loss, sunken eyes, dry skin, lethargy, coma; glucose >800, hypokalemia, hyponatremia, elevated creatinine, negative urine ketones; ABD does not show acidosis

186
Q

diabetes insipidus

A

hyposecretion of ADH by posterior pituitary (too little ADH is reabsorbed); kidney fails to reabsorb water; Central DI is decreased ADH production; Nephrogenic DI is adequate ADH production but kidneys do not respond appropriately (very rare)

187
Q

assessment of diabetes insipidus

A

large amount of dilute urine; polydipsia, dehydration, inability to concentrate urine, low urine specific gravity; fatigue and muscle weakness; headache; postural hypotension that may cause vascular collapse; tachycardia

188
Q

intervention for DI

A

monitor VS, neuro status, cardio status, fluids, electrolytes, IOs, weight; maintain adequate fluid intake with IV hypotonic saline to replace urinary loss; avoid diuresing foods and liquids; vasopressin if indicated; ensure safe environment; pt education on prescribed meds

189
Q

addisons disease

A

aka primary adrenal insufficiency; causes hyposecretion of adrenal cortex hormones like glucocorticoids(cortisol), mineralocorticoids (aldosterone), and androgens; commonly caused by autoimmune destruction; requires lifelong replacement of glucocorticoids; fatal if left untreated

190
Q

addisons disease loss of glucocorticoids

A

leads to decreased vascular tone, decreased vascular response to catecholamines, decreased gluconeogenesis

191
Q

addisons disease loss of mineralocorticoids

A

leads to dehydration, hypotension, hyponatremia, hyperkalemia

192
Q

adrenal insufficiency assessment

A

lethargy, fatigue, muscle weakness, GI disturbances, weight loss, menstrual changes, impotence in men, electrolyte imbalance (hyponatremia, hyperkalemia, hypocalcemia), hypoglycemia, hypotension, hyperpigmentation of skin

193
Q

interventions for adrenal insufficiency

A

monitor VS, weights, IOs; labs- WBCs, glucose, potassium, sodium, calcium; admin prescribed glucocorticoids and/or mineralocorticoids, monitor for s/s of addisonian crisis

194
Q

addisonian crisis

A

medical emergency caused by acute adrenal insufficiency; caused by stress, infection trauma, surgery, or abrupt withdrawal of supplemental corticosteroids

195
Q

assessment of addisonian crisis

A

can result in hyponatremia, hyperkalemia, hypoglycemia, severe headache, abdominal pain, weakness, irritability, confusion, severe hypotension, evidence of shock

196
Q

interventions for addisonian crisis

A

admin of IV glucocorticoids, fluids, and electrolytes; monitor VS, neuro status, IOs, labs; oral glucocorticoids and mineralocorticoids following resolution

197
Q

cushings syndrome

A

metabolic disorder causing chronic excessive production of cortisol d/t increased ACTH from pituitary; iatrogenic- cortisol coming from adrenal cortex resulting from prolonged admin of high dose glucocorticoids; can be caused by ACTH secreting tumors

198
Q

cushings syndrome assessment

A

generalized muscle weakness and wasting, moon face, buffalo hump, truncal obesity with thin extrem., weight gain, hirsutism (masculinity in women), electrolyte imbalance (hypernatremia, hypokalemia, hypocalcemia), hyperglycemia, HTN, fragile skin, easy bruising, red/purple striation on abdomen and thighs

199
Q

cushings syndrome interventions

A

monitor VS, weight, IOs; monitor labs- WBC, glucose, sodium, potassium; chemotherapeutic agents for inoperable adrenal tumors, removal of pituitary, adrenalectomy d/t adrenal adenoma; increased glucocorticoid during stress for those with lifelong therapy; assess for post op thrombus formation, medic alert bracelet

200
Q

hypothyroidism

A

hyposecretion of thyroid hormones; decreased rate of body metabolism; T4 is ow and TSH is high

201
Q

primary hypothyroidism

A

source of dysfunction is the thyroid gland that cannot produce necessary amount of hormones

202
Q

secondary hypothyroidism

A

thyroid is not being stimulated by pituitary gland to produce hormones; anterior pituitary not releasing TSH

203
Q

assessment of hypothyroidism

A

lethargy, fatigue, weakness, muscle aches, parasthesias, cold intolerance, weight gain, dry skin/hair, hair loss, bradycardia, constipation, myxedema (edema around eyes and face), forgetfulness, menstrual disturbances, goiter, cardiac enlargement

204
Q

hypothyroidism interventions

A

monitor VS, admin thyroid replacement as prescribed, assess for constipation, educate pt on therapy compliance, monitor for signs of hypo/hyperthyroidism, encourage low cal low cholesterol low sat fat die, include fiber, plenty of fluids for constipation, provide warm environment, avoid sedating meds d/t increases sensitivity and increased sedation effects (may cause myxedema coma)

205
Q

mxedema coma

A

rare but serious disorder caused by low thyroid hormone production; can be precipitated by illness, withdrawal of thyroid meds, anesthesia, surgery, hypothermia, sedatives

206
Q

myxedema assessment

A

hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, gen edema, resp fail, coma

207
Q

myxedema interventions

A

maintain patent airway, asp. precautions, IV fluids, levothyroxine IV, glucose IV, corticosteroids, assess temp/blood pressure/mental status/ electrolytes/glucose, keep pt warm

208
Q

hypoparathyroidism

A

hyposecretion of parathyroid hormone by parathyroid gland; can occur following thyroidectomy that removes parathyroid tissue

209
Q

hypoparathyroidism assessment

A

hypocalcemia, hyperphosphatemia, numbness/tingling in face, muscle cramps in extrem., abdominal cramping, + trosseaus or + chvosteks, signs of overt tetany, hypotension, anxiety, irritability, depression

210
Q

CATS for signs of hypocalcemia

A

convulsions, arrhythmias, tetany, stridor and spasms

211
Q

hypoparathyroidism interventions

A

monitor VS, monitor for hypocalcemia and tetany, seizure precautions, emergency trach set O2 and suction at bed, increase calcium intake (calcium gluconate IV, high calcium low phos diet, vit d supps), admin phosphate binding agents to excrete via GI, encourage medic alert bracelet

212
Q

cholecystitis

A

inflammation of the gallbladder; acute or chronic; majority of acute cases are calculous cholecystitis

213
Q

acalculous cholecystitis

A

inflammation without obstruction by gallstones

214
Q

manifestations of cholecystitis

A

pain, tenderness, rigidity of RUQ; may radiate to midsternal area or right shoulder; accompanied by N/V if acute

215
Q

jaundice types

A

pre-hepatic- excessive breakdown of RBC overwhelms liver ability to process bilirubin; hepatic- livers impaired ability to process bilirubin, occurs in hepatitis cirrhosis and drug induced liver injury; post-hepatic- obstructive, blocked bile flow from liver to intestine that commonly occurs with gallstones tumors and bile duct disorders

216
Q

signs and symptoms of jaundice

A

yellowing of skin/eyes, dark urine d/t excess bilirubin excretion, pale/clay colored stool d/t lack of bilirubin in GI tract, pruritis; may include symptoms of hepatomegaly, splenomegaly, abd pain, fatigue/weakness, cognitive changes, and bleeding

217
Q

ascites manifestations

A

increased abdominal girth, rapid weight gain, SOB

218
Q

ascites nursing interventions

A

negative sodium balance to reduce fluid retention (2g), administration of diuretics and monitoring fluid/electrolyte balance, prepare for paracentesis (up to 5-6L removed)

219
Q

transjugular intrahepatic portosystemic shunt

A

cannula threaded through portal vein by transjugular route and placed between portal circulation and hepatic vein; decreases sodium retention and prevents recurrence of fluid accumulation that would result in ascites

220
Q

hepatic encephalopathy

A

accumulation of ammonia and other toxic metabolites in blood d/t hepatic insufficiency and portosystemic shunting; early signs are mental changes and motor disturbances; late signs are constructional ataxia, asterixis and fetor hepaticus

221
Q

assessment of hepatic encephalopathy

A

EEG, changes in LOC, potential seizures, fetor hepaticus, monitor fluid electrolyte and ammonia levels

222
Q

4 stages of hepatic encephalopathy

A
  1. normal level of consciousness with periods of lethargy and euphoria, reversal of day night sleep patterns; 2. increased drowsiness disorientation, inappropriate behavior, mood swings, and agitation; 3. stuporous, difficult to rouse, sleeps most of time, marked confusion, incoherent speech; 4. comatose, may not respond to painful stimuli
223
Q

managing hepatic encephalopathy

A

eliminate precipitating cause, lactulose to reduce serum ammonia, IV glucose to minimize protein catabolism, protein restriction, reduction of ammonia from GI tract via suction enema and oral antibx, discontinue sedatives analgesics and tranquilizers, monitor or treat complications/infections

224
Q

hepatic encephalopathy interventions

A

assess LOC changes, IOs, bodyweight, VS q4, serial daily ammonia levels and electrolytes, restricted dietary protein, GI tract suctioning, administer lactulose, monitor therapeutic response, monitor resp. status

225
Q

hepatic cirrhosis

A

alcoholic: scar tissue characteristically surrounding portal areas; post-necrotic: broad bands of scar tissue; biliary: scarring occurs in the liver around bile ducts; hemochromatosis related; NAFLD/NASH related

226
Q

compensated cirrhosis

A

ankle edema, firm and enlarged liver, intermittent mild fever, palmar erythema, splenomegaly, vascular spiders, vague morning indigestion

227
Q

uncompensated cirrhosis

A

ascites, clubbing of fingers, continuous fever, epistaxis, hypotension, jaundice, muscle wasting, purpura

228
Q

cirrhosis interventions

A

promote rest, improve nutrition, provide skin care, reduce risk of injury, monitor/manage potential complications

229
Q

cirrhosis complications

A

bleeding/hemorrhage, hepatic encephalopathy, fluid volume excess

230
Q

hepatitis A

A

spread via poor hand hygiene; oral-fecal route; incubates in 2-6 weeks; ill ness last 4-8 weeks; acute only, doe not progress to chronic disease

231
Q

s/s of hepatitis A

A

asymptomatic, GI s/s, jaundice, dark urine, joint pain, fever, fatigue

232
Q

managing hepatitis A

A

prevention via handwashing, vaccine, immunoglobulin for contacts to provide passive immunity; bed rest during acute, nutritional support

233
Q

hepatitis B

A

transmitted via blood, saliva, vaginal secretions; is sexually transmitted; transmitted to infant at time of birth; acute and chronic result in cirrhosis and liver cancer; incubation is 1-6 months; risk factors are healthcare workers, birth, tattoo, IV drug use

234
Q

signs and symptoms of hepatitis B

A

flu like symptoms, arthralgias, jaundice, dark urine

235
Q

hepatitis B diagnostic

A

+HBsAG/ anti-HBs

236
Q

managing hepatitis B

A

chronic meds: alpha interferon (subq) and antiviral agents (oral entecavir ETV + tenofovir TDF), bed rest, nutritional support, hand hygiene, vaccine of those at high risk, vaccination of infants; passive immunity for those exposed, standard precautions and infection control measures, screening of blood/blood products

237
Q

hepatitis C

A

transmitted via IV drug use, sex, and blood transfusions prior to 1992; most common bloodborne infection; 1/3 cause liver cancer (need transplant), incubates in 15-160 days, can be acute or chronic, risk factors are healthcare workers IV drug users and multiple sexual partners

238
Q

diagnostic for hepatitis C

A

anti-HCV (chronic)

239
Q

signs and symptoms of hepatitis C

A

flu like symptoms, jaundice, dark urine

240
Q

managing hepatitis C

A

antiviral meds like DAA, avoid alcohol, prevention via public health programs to decrease needle sharing, screening blood supply, safety needles for healthcare workers

241
Q

hepatitis

A

viral- systemic viral infection causing necrosis and inflammation of liver cells with characteristic symptoms and cellular/biochemical changes; A/E: fecal-oral route; B/C: bloodborne; D: only people with B are at risk; nonviral- d/t drugs and medications

242
Q

ascites

A

caused by portal HTN which increases capillary pressure and causes obstruction of venous blood flow; failure to metabolize aldosterone causing increasing fluid and sodium retention and intravascular fluid; decreased albumin synthesis causing decreased serum oncotic pressure; movement of albumin causes fluid shifts to peritoneal cavity; vasodilation of splanchnic circulation

243
Q

GERD

A

backflow of gastric and duodenal contents into the esophagus; caused by incompetent lower esophageal sphincter, pyloric stenosis, motility disorder

244
Q

GERD assessment

A

heartburn, cough, regurgitation, dysphagia, laryngitis, chest pain (may mimic MI); obtain HX and info about diet

245
Q

GERD interventions

A

avoid food triggers, GERD friendly diet- smaller more frequent meals high in fiber alkaline and fluids, elevate HOB and encourage sitting up for 30 min following meal, medications- proton pump inhibitors and H2 receptor blockers, monitor for aspiration

246
Q

peptic ulcer disease

A

ulceration in mucosal wall of stomach, pylorus, duodenum, or esophagus in portion accessible to gastric secretions; erosion can extend through muscle to peritoneum; usually occurs alone and in people aged 30-60

247
Q

interventions for peptic ulcer disease

A

monitor VS for signs of bleeding, small frequent bland meals, H2 receptor agonist or PPI to decrease gastric acid secretion, antacids to neutralize secretions, mucosal barrier protectants 1 hr before meal, prostaglandins for protecting and antisecretory actions, avoid alcohol caffeine chocolate smoking NSAIDs

248
Q

peptic ulcer disease surgical interventions

A

gastroduodenostomy/billroth I- partial gastrectomy and remaining segment connected to duodenum; gastrojejunostomy/billroth II- partial gastrectomy and remaining segment is connected to jejunum; total gastrectomy- removal of the stomach and attach esophagus to jejunum or duodenum; pyloroplasty- enlargement of pylorus to prevent/decrease pyloric obstructing increasing gastric emptying

249
Q

dumping syndrome

A

rapid emptying of gastric contents into the small intestine following a gastric resection

250
Q

constipation

A

less than 3 bowel movements per week; caused by surgery, chronic laxative, immobility, diet, ignoring urge, lack of exercise

251
Q

TPN

A

continuous administration over 24 hours or cyclical overnight through central vein/PICC; must infuse via pump; admin D10W when TPN runs dry and waiting for new bag; watch for sclerosis, phlebitis, swelling; monitor glucose

252
Q

when discontinuing TPN

A

need evaluation by nutritionist; gradually decrease flow for 1-2 hours while increasing oral intake; change IV dressing after removal until healed; encourage PO nutrition; record IO, weight, lab results of electrolytes and glucose levels

253
Q

pancreatitis

A

self-digestion by pancreatic enzymes; gallstone obstruct flow of pancreatic juice activating the enzymes; enzyme act. leads to vasodilation, increased permeability, necrosis, erosion, hemorrhage

254
Q

causes of pancreatitis

A

infections, mumps complications, trauma, peptic ulcers, vascular issues, HLD, hypercalcemia, alcohol, tobacco, hereditary

255
Q

interstitial edematous pancreatitis

A

mild common form characterized by gland enlargement due to edema; minimal organ dysfunction that resolves in 6 months; risk of shock, fluid electrolyte imbalance, sepsis

256
Q

necrotizing pancreatitis

A

severe rare form with tissue necrosis in or around pancreas; enzymes damage blood vessels leading to bleeding and thrombosis; necrosis may extend retroperitoneal; can cause organ failure

257
Q

acute pancreatitis assessment

A

severe abdominal pain that radiates to back that is aggravated by meals and unrelieved by antacids; abdominal guarding; rigid abdomen if peritonitis, bruising in flank (turners sign) or umbilicus (Cullens sign); n/v, fever, jaundice; hypotension, tachycardia, cyanosis, cold skin, resp. distress, hypoxia, AKI, hypocalcemia, hyperglycemia, coag issues

258
Q

chronic pancreatitis manifestation

A

recurring severe abdominal pain and back pain, attacks become more frequent severe and longer, weight loss d/t decreased intake and malabsorption, frothy foul smelling diarrhea, calcification of gland and formation of calcium stones

259
Q

diagnosing acute pancreatitis

A

2 of 3 following- upper abdominal pain hx, amylase/lipase elevation, typical imaging

260
Q

oncological diagnosis

A

consists of review of systems, PE, labs, biopsies, imaging

261
Q

bleeding precautions

A

thrombocytopenia d/t chemotherapy: <50k increased risk for bleeding, <10k increased risk for spontaneous bleeding; concern for prolonged bleeding; soft toothbrush; no flossing; no razors; hold blood thinners; low threshold for fall precautions

262
Q

HIV- human immunodeficiency virus

A

virus that targets cells with CD4+ receptors; transmission via blood, blood products, semen, vaginal secretions, mother to child through breast milk and amniotic fluid

263
Q

AIDS- acquired immunodeficiency syndrome

A

chronic viral condition caused by human immunodeficiency virus; manifested by opportunistic infections and unusual malignancy; incubation can be 10+ years; may not be symptomatic until late in the infection

264
Q

assessment for HIV/AIDS patient

A

malaise, fatigue, flu like symptoms, anorexia, weight loss, lymphadenopathy >3 months, leukopenia, diarrhea, night sweats, opportunistic infections, kaposi’s sarcoma

265
Q

HIV stages of infection

A

stage 0- early, lab detectable, seroconversion, 2-12 weeks; stage 1 primary infection- CD4+ >= 500, HIV specific antibodies, flu like symptoms; stage 2 clinical latency- CD4+ 200-499 cells/mm3, asymptomatic, can still transmit, no opportunistic infections; stage 3 symptomatic infection- CD4+ <200, high viral load, opportunistic infections

266
Q

diagnostic testing for HIV

A

antigen/antibody early as 2 weeks, HIV antibodies early as 2.5 weeks (rapid testing), Nucleic acid (RNA of virus in blood), CD4 count 500-1500is normal for non HIV (determines med therapy), plasma HIV RNA determines staging and progression

267
Q

kaposi sarcoma

A

skinlike cancer present in individuals with HIV; most often males 60-70; elliptical-shaped cutaneous lesions; can be present on skin, anal cavity, mucosal membraneof GI tract (mouth to anus)

268
Q

HIV neurological changes

A

HIV associated neurocognitive disorder (HAND)- subcortical neurodegenerative disease affecting 20% of those with HIV (changes in language, memory, problem solving and, psychomotor skill), peripheral neuropathy, HIV encephalopathy

269
Q

rheumatoid arthritis

A

chronic systemic inflammatory disease, leads to destruction of connective tissue and synovial membrane within joints; exacerbated by stress and fatigue

270
Q

pathology of RA

A

synovitis, pannus, joint disappears, bony ankylosis

271
Q

manifestations of RA

A

years 20-60, can affect joints bilaterally, inflammation/tenderness/stiffness of joints, joint deformities, muscle atrophy, decreased ROM, spongy soft joints on palpation, constitutional symptoms like low grade fever fatigue weakness anorexia weightloss

272
Q

diagnostic testing for RA

A

elevated ESR and/or CRP, positive rheumatoid factor, joint deterioration on imaging, synovial tissue biopsy shows inflammation

273
Q

treatment for RA

A

NSAIDs to decrease inflammation, steroids, DMARDs (disease modifying anti-rheumatic drugs), biological response modifiers, surgery

274
Q

nursing interventions for RA

A

increase mobility with ROM, pain management, self care by assisting with ADLs, decrease fatigue via monitoring for anemia and prescribing meds, assisting in disturbed body image

275
Q

chemotherapy side effects

A

cytopenias, N/V/D, mucositis, alopecia, renal dysfunction, cardiotoxicity, infertility, neurotoxicity, fatigue, neutropenia

276
Q

immunotherapy side effects

A

flu-like symptoms, hypersensitivity reaction, congestion, infection, capillary leak syndrome, pulmonary edema, myalgias, hypotension

277
Q

neutropenic precautions

A

hand washing, washing fruits and vegetables, avoid bodies of water, gloves if gardening, avoid pet waste, dont share cups/utensils

278
Q

sensory impairments in older adults

A

visual changes- cataracts, macular degenerations, glaucoma; auditory- presbycusis, tinnitus, earwax accumulation; cognitive changes- slower processing speed, short term memory changes, decreased multitasking ability

279
Q

cataracts

A

clouding of the lense

280
Q

macular degeneration

A

deterioration of the central portion of the retinag

281
Q

glaucoma

A

increased intraocular pressure causing optic nerve damage and vision loss

282
Q

nursing interventions for older adult vision losses

A

ensure adequate lighting, assistive magnifiers, regular eye exams

283
Q

nursing interventions for auditory changes in older adults

A

regular hearing checks, regular cleanings, use low pitched clear speech, encourage hearing aid use

284
Q

presbycusis

A

age related hearing loss usually to high frequency

285
Q

bone health in older adults

A

decreased bone density; more susceptible to FX

286
Q

integumentary changes in older adults

A

fragile skin more susceptible to temp changes, decrease subcutaneous fat

Adults 1 (10 decks)

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