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adults exam 1 > management for COPD > Flashcards

management for COPD Flashcards

1
Q

COPD is characterized by

A

airflow limitation that is not fully reversible and is slowly progressive, airflow limitation on exhalation

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2
Q

pathophysiology of COPD

A

airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases; the inflammation occurs in primal and peripheral airways (if main airways are squeezed shut, the peripheral airways won’t get air)

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3
Q

risk factors for COPD

A

smoking (any kinds), 2nd hand smoke, increased age, job exposure, air pollution, genetics

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4
Q

complications of COPD

A

hypoxia, respiratory acidosis, infections, narrowing of airways, HF, cardiac dysrhythmias, decreased quality of life, death (because CO2 levels are so high it can shut off brain)

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5
Q

respiratory acidosis is what

A

high PaCO2

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6
Q

3 primary symptoms of COPD

A

chronic cough, sputum production, dyspnea (others are weight loss, DOE, use of accessory muscles)

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7
Q

assessments and diagnosis for COPD

A

health hx, IS, ABGs, chest x ray, pulmonary function tests

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8
Q

bronchitis is AKA

A

big blue bloater, bronchiole tubes are inflamed (chronic inflammation and edema/ hypertrophy & hypersecretion of mucus glands)

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9
Q

how to diagnosis bronchitis

A

cough with daily sputum production, at least 3 months/ year for 2 consecutive years

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10
Q

common characteristics of chronic bronchitis

A

used pursed lip breathing, stocky build, use of accessory muscles, fluid retention, side effects of steroid use (only give steroids when in exacerbation)

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11
Q

signs of chronic bronchitis

A

cyanotic, recurrent cough and increased sputum production, hypoxia, hypercapnia, acidosis, increased RR, exertion dyspnea, clubbing, edematous, increased incident in smokers, cardiac enlargement, cor pulmonale

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12
Q

what is cor pulmonale

A

a condition that causes the right side of the heart to fail

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13
Q

why do you try not to give steroids for COPD

A

the do decrease inflammation but they increase glucose, increase risk of infection, increase risk of fractures, makes skin thin, increase gastric acid (pain & burning in stomach), they shut down adrenal cortex so they don’t make any steroids anymore making people diabetic

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14
Q

after using steroid inhaler what will you do

A

rinse out mouth

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15
Q

emphysema

A

impaired oxygen and carbon dioxide exchange; destruction of the walls of over distended alveoli, progresses slowly for years

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16
Q

breakdown of alveolar walls in emphysema lead to

A

increase in dead space (the more dead space the less air er can get into the lungs leading to hypoxemia), no gas exchange can occur, CO2 elimination is impaired leading to hypercapnia & respiratory acidosis, leading to over inflation of alveoli and air trapping

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17
Q

emphysema AKA

A

pink puffer; gets flushed

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18
Q

common characteristics of emphysema

A

thin appearance, increased RR to maintain adequate oxygen levels, accessory muscle use, barrel shaped chest, purse lipped breathing

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19
Q

signs of emphysema

A

dyspnea, purse lip breathing, orthopneic, barrel chest, prolonged expiratory time, speaks in jerky sentences, anxious, use accessory muscles, thin, leads to right sided HF, ineffective cough, sleep sitting up

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20
Q

pulmonary function tests

A

deep breaths, blow out as hard as you can and they will measure that

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21
Q

how to reduce risk of COPD

A

stop smoking, eat smaller meals (high protein:source of energy, high fat, low carbohydrate), bronchodilators, costicosteriods, hydrate, surgery, pulmonary rehab

22
Q

why do you want low carb for COPD

A

because CO2 is a waste product of carbohydrates and if you already have a lot of CO2 you will increase your CO2 level even more which is what you don’t want

23
Q

what are pulmonary rehabs for COPD

A

breathing exercise, activity pacing, self care activities, physical conditioning, coping mechanism, oxygen

24
Q

what is asthma

A

chronic inflammatory disease of the airways -> airway hyper-responsiveness (each time you cough, they react more)-> mucosal edema -> increase mucus production -> cough, chest tightness, wheezing, & dyspnea

25
Q

bronchospasm are part of

A

asthma but are usually reversible end not permanent lung changes

26
Q

when an asthma attack occurs initially what do you see

A

hypoxia -> hyperventilation -> respiratory alkalosis

27
Q

later in an asthma attack what do you see

A

increased CO2 -> respiratory acidosis -> respiratory failure

28
Q

in an asthma attack what cells are the first to attack

A

neutrophils

29
Q

characteristics of asthma

A

mast cells, macrophages, neutrophils, eosinophils, T lymphocytes play role in inflammation

30
Q

trigger of asthma

A

allergens, medications, upper respiratory infections, GERD, strong odors, hormone levels (in females), exercise, stress, cold air, laughing

31
Q

3 most common clinical manifestations of asthma

A

cough, dyspnea, wheezing

32
Q

other symptoms of asthma

A

anxiety, chest tightness, prolonged expiration, diaphoresis, hypoxemia, tachycardia, tachypnea, widened pulse pressure

33
Q

diagnostics for asthma

A

forced expiratory volume (FEV1), forced vital capacity, PFTs

34
Q

forced expiratory volume

A

the amount of air expired after one, two, three seconds of forced vital capacity

35
Q

FVC

A

the amount of air forced out of lungs after the greatest exhalation

36
Q

albuterol is a

A

sympathomimetic; first shake, use spacer (not always), breath in slowly

37
Q

nebulizer vs inhaler

A

nebulizer you can combine meds/ inhaler has a meter to tell how much med to take or took

38
Q

after breathing after asthma attack what should happen

A

breath sounds from wheezing to clear, activity tolerance should increase, RR should decrease after breathing treatment

39
Q

complications of asthma

A

status asthmatics, respiratory failure, pneumonia, atelectasis, hypoxemia

40
Q

status asthmatics

A

very bad; asthma attack that does not respond to normal treatment, not able to get airways reversed, lasts longer than a normal asthma attack, go into respiratory alkalosis then acidosis then respiratory failure

41
Q

dyspnea management: nonpharmacological

A

cool air on face, strengthen respiratory muscles thru exercise, improve nutrition to improve muscle mass, positioning, pursed lip & diaphragmatic breathing, oxygen therapy

42
Q

dyspnea management: pharmacological

A

bronchodilators, opioids (not always for pain, but they will decrease RR to slow HR), anxiolytics

43
Q

most effective inhaled costicosteriods for asthma and COPD

A

fluticasone, budesonide, flunisolide

44
Q

anticholinergics for asthma and COPD

A

ipratropium (dry up secretions; no spit, no shit, no pee, no see(no tears))

45
Q

short acting bronchodilator for all (rescue) for asthma and COPD

A

beta 2 adrenergic agonists, albuterol, levalbuteral (does not increase HR as much as albuterol)

46
Q

long acting B2 adrenergic agonist (maintenance or prevention) for asthma and COPD

A

salmeterol, formoterol

47
Q

combo meds for asthma and COPD

A

fluticasone- salmeterol/ budesonide- formoterol

48
Q

leukotriene modifers for asthma and COPD

A

montelukast (black box warning for nueropsychiatric symptoms, suicidal thoughts)/ not a dilator but it does prevent restricting

49
Q

immunomodulators for asthma and COPD

A

IgE-inhibiting IgG monoclonal antibody (omalizumab): decreases immune system; higher risk for infections & cancers

50
Q

nursing interventions for all types of COPD

A

O2 management & respiratory therapy, conserve your engird, exercise promotion, dyspnea assessments, medications, administer fluids, cough enhancement, breathing exercising (pursed lip/ abd & diaphragm), anxiety reduction (but not hypoxia), nutritional balance

adults exam 1 (9 decks)

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