TOPIC 3 - asthma, COPD, CF Flashcards

1
Q

manifestations of oxygen toxicity

A

non productive cough, substernal chest pain, GI upset, dyspnea
compliancy decreases = crackles, hypoxemia, atelectasis, pulmonary edema

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2
Q

interventions for oxygen toxicity

A

use lowest level of O2 to treat condition, monitor vitals and respiratory assessment

request ABGs when declining

notify MD if PaO2 is greater than 90

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3
Q

hypoxic drive

A

when PaCO2 increases gradually over time to 60-65, the CO2 receptors no longer function and do not stimulate breathing

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4
Q

interventions for hypoxic drive

A

use lowest level of O2 (1-3L) with venturi mask
hyperventilation occurs in the first 30 minutes of O2 therapy

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5
Q

oxygen toxicity is defined by

A

O2 level greater than 50% for more than 24-48 hours

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6
Q

pathophysiology of asthma

A

reversible airway obstruction from bronchial smooth muscle contraction, vascular congestion, tenacious mucus, and mucosal edema

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7
Q

triggers for asthma

A

inflammatory - allergies, resp infection, work
irritants - temp change, exercise, strong odors, stress, cold air
others - meds, tobacco, gastric reflux, pollutants, food additives

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8
Q

symptoms related to asthma

A

labored breathing, wheezing, sleep problems, chest pain, frequent coughing, allergies, common cold, feeling tired

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9
Q

mild asthma attack interventions

A

prompt relief with inhaled SABA such as albuterol - take 2 to 4 puffs every 20 min

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10
Q

moderate to severe asthma attack interventions

A

may require ED visit, relief from SABA, oral systemic corticosteroids (oral if moderate, IV if severe), ipratropium, IV magnesium

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11
Q

forced vital capacity

A

amount of air that can be quickly and forcefully exhaled after maximum inspiration

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12
Q

stepwise approach for managing asthma

A

1 - quick relief : albuterol, Proventil, Ventolin
2 - flovent
3 - flovent and LABA

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13
Q

controller vs reliever meds

A

controller - daily meds for persistent asthma, long term control, anti-inflammatory

reliever/quick relief - bronchodilators, used PRN and preventative, oral corticosteroid bursts

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14
Q

long term control anti- inflammatory meds

A

corticosteroids (inhaled = flovent diskus or HFA) (oral = prednisone)

leukotriene modifiers (montelukast)

anti-IgE (omalizumab)

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15
Q

long term bronchodilators

A

long acting inhaled B2 agonist (salmeterol)
long acting oral B2 agonist (albuterol)
methylxanthines (theophylline)

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16
Q

quick relief bronchodilators

A

short acting inhaled B2 agonist (albuterol)
anticholinergics inhaled (ipratropium)

17
Q

quick relief anti-inflammatory drugs

A

systemic corticosteroids (prednisone)

18
Q

COPD

A

characterized by persistent airflow limitation that is usually progressive
associated with enhanced chronic inflammatory response in the airways and lungs

19
Q

interventions for COPD

A

Improve gas exchange & airway clearance
Administer O2
Facilitate deep breathing & coughing to remove secretions
Encourage hydration 2-3L/d
Chest physiotherapy
Prevent or treat infections
Administer bronchodilators, corticosteroids
Small volume nebulizer (SVN), Inhalers
Patient education
Improve nutrition
Improve sleep
Stop smoking

20
Q

pathophysiology of COPD

A

hyperplasia of goblet cells - increasing production of mucus
reduced airway diameter - difficulty clearing secretions
loss of ciliary activity
abnormal dilation of distal air space with destruction of alveolar walls
loss of elastic recoil and airflow obstruction

21
Q

risk factors for COPD

A

cigarette smoking
environmental exposure
occupational chemical and dusts
air pollution
infections: recurring RTI in childhood, TB
genetics
A1 antitrypsin deficiency

22
Q

signs and symptoms of COPD

A

chronic cough with sputum
cyanosis of mucosal membranes
barrel chest
increased resting resp rate
use of accessory muscles
shallow breathing
pursing lips during expiration

EXACERBATING SYMPTOMS
worsening dyspnea
chest tightness
malaise
fatigue
decreased exercise tolerance

23
Q

complications of COPD

A

cor pulmonale
acute exacerbations
acute respiratory failure

24
Q

goals of managing COPD

A

to alleviate breathlessness and other respiratory symptoms that affect daily activities;

to prevent and reduce the frequency and severity of acute exacerbations;

to minimize disease progression and reduce the risk of morbidity/mortality;

to optimally manage comorbidities (if present) to reduce exacerbations and COPD symptoms related to comorbidities.

25
Q

O2 sat goals for COPD

A

above 90%

26
Q

complications of O2 therapy

A

combustion - do not smoke
CO2 narcosis - assess mental status and VS before starting
O2 toxicity - high concentrations can result in severe inflammatory response resulting in severe pulmonary edema and hypoxemia

27
Q

interventions for nutritional therapy of COPD

A

Rest for 30 minutes before eating and use a bronchodilator before meals

Avoid exercise and treatments 1 hour before and after meals

Ensure O2 therapy is in use during eating

Encourage activity during the day to stimulate appetite (e.g., walking or getting out of be during the day)

If underweight, supply with protein and calories, moderate carbohydrate and fats
5-6 small meals a day

28
Q

chronic bronchitis

A

the presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is an independent disease that may precede or follow the development of airflow limitation.

29
Q

emphysema

A

is the destruction of the alveoli and is a pathologic term that explains only one of several structural abnormalities in COPD patients.

30
Q

chronic bronchitis

A

inflammation of the bronchi and bronchioles caused by exposure to irritants, especially cigarette smoke.

The irritant triggers inflammation, vasodilation, mucosal edema, congestion, and bronchospasm.

Bronchitis effects only the airway, not the alveoli. Bronchial walls thicken and impair airflow.

This thickening along with mucous blocks some of the smaller airways and narrows larger ones.

Mucous provides a breeding ground for organisms and leads to chronic inflammation.

31
Q

ABG labs of chronic bronchitis

A

PaO2 levels decrease and arterial carbon dioxide level increases

32
Q

emphysema

A

Loss of lung elasticity and hyperinflation of the lung. These changes result in dyspnea and need for an increased respiratory rate.

The hyper inflated lung flattens the diaphram, weakening the effectiveness of the muscle. These patients need to then use more accessory muscles in the neck, chest wall, and abdomen to inhale and exhale. This increased workload increases the need for oxygen, making the patient have ‘air hunger’ sensation.

33
Q

cystic fibrosis

A

autosomal recessive disease

transport of Na and Cl in and out of epithelial cells
negative impact to lungs, GI tract, reproductive tract, and kidneys

34
Q

meconium ileus

A

bowel obstruction that occurs when themeconiumin your child’s intestine is even thicker and stickier than normalmeconium, creating a blockage in a part of the small intestine called the ileum. Most infants withmeconium ileushave CF

35
Q

med therapy for relieving obstruction

A

Aerosol and nebulization treatments to dilate airways, liquefy mucus and facilitate clearance

CPT (postural drainage with percussion and vibration)

Expiratory techniques: PEP devices (Flutter device)

O2 therapy in severe disease

36
Q

med therapy for controlling infection

A

long course of antibiotics

37
Q

med therapy for pancreatic insufficiency

A

Enzyme replacement: (Pancreaze, Creon, Ultresa) before each meal and snack

Vitamin supplement: (A, D, E, and K)

Diet: Adequate fat, calories, protein, and vitamins. Added salt with sweating is excessive

Diabetes: administer insulin

38
Q

complications of CF

A

Cystic Fibrosis Renal Disease
Bone disease
Sinus disease
Pancreas & Liver disease
Pneumothorax
Respiratory failure
Pulmonary hypertension