NP614 Test 5 - Sheet1 Flashcards
(300 cards)
1
Q
Objective signs of dying and death
A
Elusive, depending on pt’s diagnosis
2
Q
Question to help you think of pallative care differently
A
WOuld you be surprised if this pt died in the next 6 months to 1 yr?
3
Q
Key concept of pallative care
A
Replace models of cure vs palliation with one that uses pallative strategies that are concurrent with disease-modifying treatments. Treatment should begin long before death is imminent
4
Q
Goal of pallative care
A
Prevent and relieve suffering and to support the best possible quality of life for pts and their families, regardless of the stage of their disease or the need of other therapies.
5
Q
First step of pallative care
A
Understand the pts preferences and help identify goals of care that may change as the disesase progresses
6
Q
Elements of “Five Wishes” advanced directives
A
The person to make care decisions when I can’t. The kind of medical treatment I want or do not want. How comfortable I want to be. How I want people to treat me. What I want my loved ones to know.
7
Q
Cachexia
A
A state of general malnutrition marked by weight loss, malnutrition, weakness, and emaciation. Usually marked by an equal loss of fat, muscle, and bone mineral content.
8
Q
Causes of anorexia
A
Second most common symptom in cancer pts. Includes situational coping, unrelated illness, treatment side effects, anxiety, and depression. With advanced dementia is a marker of the traensition to end-stage disease.
9
Q
Realistic goals of nutritional intake in pallative care
A
Focus on improving quality of life with preferred foods, giving them foods previously restricted, no glucose monitoring, restraining from use of cholester-lowering agents. Can use appetitie stimulants
10
Q
Characteristics of anxiety
A
Insomnia, headache, SOA, weakenss, chest pain, palpitaitons, sensation of butterflies in stomach, urinary frequency, pallor, restlessness, tremor, and sweating
11
Q
Difference between anxiety and fear
A
Fear has a definable quality or cause. Anxiety is a sense of deep unease
12
Q
PCP consideration of high-risk populations regarding HIV
A
Act as a case finder and be thinking of the possibility of HIV when caring for pts with unusual symptoms or are high-risk
13
Q
Important role of PCP regarding education of HIV
A
Education to teens, women, and infected individuals regarding primary and secondary prevention
14
Q
Treatment of anxiety
A
Pharmacologic interventions and removal of specific problem if possible.
15
Q
Characteristics of delirium
A
Sudden changes in mental status, a mental status that waxes and wanes, a reduced attention span, and hyperactivity or hypoactivity. Common in pts iwth advanced disease. Often worsens in late afternoon or at night. May signal impending death.
16
Q
Diagnostics of delirium
A
Should only be taken if resutls are likely to change pt management
17
Q
Opiod medications less likely to cause delirium
A
Fentanyl, hydromorphone, and oxycodone
18
Q
Medications to avoid in pt with delirium
A
Benzodiazepines can result in paradoxical effects and worsen symptoms
19
Q
Most important assessment criterion of dyspnea
A
The patient’s self-reporting
20
Q
Management of the “death rattle”
A
Scopolamine patches - 1.5 mg transdermal, atropine 1% ophthalmic drops used SL
21
Q
Ceiling doses of opiods
A
There are none
22
Q
Goal of pallative sedation
A
Alleviate the suffering caused by the unrelieved symptoms
23
Q
Types of preventable cancers
A
Those associated with lifestyle factors - smoking, obesity. Those associated with infectious agents - Hep B, HPD
24
Q
Types of skin cancers
A
Nonmelanomatous (NMSCs) - such as basal cell carcinoma (BCC) and squamous cell (SCC) and malanomatous - such as malignant melanoma (MM)
25
Most common form of skin cancer
Basal cell
26
Reasons skin cancer rates have increased
Increased sun exposure and depletion of protective ozone layer
27
Risks of skin cancers
Acute sunburns, second-degree burn before 18, Fair-skinned men and women > 65, atypical moles, and those with more than 50 nevi. Hereditary component.
28
Warning signs of skin cancer
An open sore that does not heal for 3 weeks; a spot or sore that burns, itches, stings, crusts or bleeds; and any mole or spot that changes in size or texture, develops irregular borders, or appears pearly or translucent or multicolored.
29
Characteristics of basal cell carcinomas
Raised, shiny appearance, often with pearly borders
30
Characteristics of squamous cell carcinoma
Roughened, scaling area that does not heal and bleeds readily when scraped.
31
Keratinization of skin cancers
Can lead to a heaped-up appearance that flakes
32
ABCDEs of skin cancers
Asymmetry, border, color, diameter, and elevation
33
Most definitive diagnostic test of skin cancers
Punch or shave biospy techniques
34
Treatment of skin cancers
BCC - electrodesiccation and curretage. SCC - total excision
35
Types of lung cancers
Small cell (SCLC) and non-small cell (NSCLC)
36
Risk factors for lung cancers
Tobacco use, environmental and occupational exposures, radon, radiation, low socioeconomic status, decreased education, certain racial minorities, genetic predisposition, prior lung disease, dietary factors, and decreased physical activity.
37
Lung cancers and smoking
Related to degree of exposure of dialy use of tobacco, pack-year history, extent of inhalation, use of filtered vs unfiltered, age that began smoking.
38
Common symptoms of lung cancer
Cough. Dyspnea, hoarseness, hemoptysis, chest pain, wheezing, stridor, frequent URIs, dysphagia, superior vena cava syndrome, phrenic nerve paralysis, pleural effusion, pericardial effusion, anorexia, weight loss, and upper extremity pain or edema.
39
Primary immunodeficiencies
Congenital and most arise from single-gee defects. Must appear by age 6. The early the immunodeficiency presents, the more severe the underlying disease
40
Secondary immunodeficiencies
Influenced by genetics, but outside or environmental factors cause these diseases more often. Ex - T helper cells being destroyed by HIV infection
41
Divisions of the immune system
Innate system - skin, mucus, immune cells, cytokines. Adaptive system - evolutionary B and T cells (humoral immunity) and cell-mediated immunity
42
Treatment goals of pt with primary immunodeficiency
Minimize occurrence of infections and their impact on overall health of individuals. Replace defective components of immune system by passive transfer or transplantation when possible.
43
Antibiotic use and primary immunodeficiency patients
Provider should use. May need to be more aggressive and prolonged and always attempts to narrow antibiotic based on C&S results
44
Whole blood transfusions and immunodeficient patients
Contraindicated because donor blood may contain lymphocytes that could induce a grave-vs-host rejection
45
Lymphadenopathy
Lymph nodes that have enlarged or changed in consistency. Should be between 0.5 and 2.5 cm.
46
Lymphadenitis
Tender, warm, erythematous nodes. Indicates infection at the drainage terminal of the lymph system.
47
Generalized lymphadenopathy
Three or more disparate node enlargements
48
Function of lymph nodes
Provide filtration of foreign substances through the action of lymphocytes, monocytes, and macrophages.
49
Why do lymph nodes swell?
In response to an antigen.
50
Key factors to consider in pt with lymphadenopathy
Age of pt, location of swollen glands, adn associated symptoms.
51
Most suspicious sizes of enlarged lymph nodes
1.0 and 2.25 cm
52
Characteristics of lymph nodes to assess
Size, distribution, degree or flactuance, firmness, matted or shoddy quality, mobility or morbality, tenederness adn nontenderness.
53
Primary lymphadema
Congenital malformations
54
Secondary lymphadema
Tramatic injury resulting from cancer obstruction, irradiation, recent infeciton, or surgery
55
AIDS defining conditions
Decline in functional capacity of the immune system where the person begins to suffer from complications of the immune dysfunction and seldom occurs until the CD4 T-cells drop below 200 cels/mm3.
56
PHI
Primary HIV infection - the time after infection but before the infected person has established a comprehensive immunologic response to infection. A latent period.
57
Opportunistic infections that can occur when CD4 counts are higher than 200
Rare - lymphomas (cervical and anal carcinoma). TB. Shingles, severe psoriasis, severe pneumococcal, recurrent oral and vaginal candidiasis, oral hairy leukoplakia, and ITP.
58
Common opportunistic infections that begin to occur when CD4 counts fall below 200`
Pneumocystis jiroveci pneumonia (PCP), Kaposi's sarcoma, cryptococcal meningitis, and esophageal candidiasis.
59
Opportunistic infections that occur when CD4 counts fall below 50
Toxoplasma encephalitis, disseminated Mycobacterium avium-intracellulare complex infection, cytomegalovirus retinitis, progressive multifocal leukoencephalopathy, AIDS dementia, CNS lymphoma, and AIDS wasting syndrome
60
ELISA and Western blot testing
Used to diagnose HIV. If +ELISA, Western blot will be used to confirm. -ELISA, no Western blot.
61
Management of HIV infections
Highly active antiretroviral therapy (HAART) when indicated, attention to med adherence, prevention of opportunistic infections, appropriate immunization, close monitoring for HIV complications, management of comorbid conditions, and minimizing behaviors that result in HIV transmission.
62
Result of correctly used HAARTs (Highly active antiretroviral therapy)
Can convert HIV infection from a progressive and inevitably fatal disease to a chronic disease with potentially normal life expectancy
63
Result of poorly used HAARTs (highly active antiretroviral therapy)
Can result in viral resistance to all antivirals and consequently untreatable progressive disease.
64
Theoretical benefit of treatment of primary HIV infection
This may minimize early immunologic damage and allow development of a more robust immunologic response to HIV, resulting in better immunologic control.
65
An absolute indication for HAART
Pregnant women to prevent mother-to-child transmission. Can reduce transmission from 25% to 2%.
66
Short term goal of HAART
Suppress viral replication to such a degree that there is no detectable HIV in peripheral blood. Can occur within 6 months
67
Most important predictor of life expectancy in HIV patient
The patient's ability to tolerate and maintain a high level of adherence to antiviral drugs.
68
Lab monitoring while taking antiviral medications
Fasting lipid profile at baseline and every 1-3 months after any change in medications. May also cause insulin resistance.
69
Lipodystrophy
Refers to a change from baseline in the relative proportion of fat and can occur anywhere in the body. Can not be reversed
70
Drug interactions of antivirals and other medications
Numerous!
71
Low dose CT versus chest x-ray to diagnose lung ca
Shows to detect more nodules and lung cancers, including early-stage cancers
72
What to do for pt exposed <72 hrs to potentially infected fluids of person known to be infected with HIV that represents a substantial risk for transmission
28 day course of highly active antiretroviral therapy as soon as possible after exposure
73
What to do for pt exposured <72 hrs to body fluids of person unknown with HIV that represents a substancial risk of transmission
No recommendation for prophylaxis
74
What to do for pt exposure > 72 hrs to fluids with no substantial risk for HIV
No recommendation for prophylaxis
75
Routine HIV screening
Routine for all pts ages 13-64. All being treated for TB. All pts seeking treatment for STIs and during each visit for a new complaint.
76
Repeat HIV screening
Annual test of all high-risk persons - IV drug users and their sex partners, persons who exchange sex for money or drugs, those with more than one sex partner since last HIV test. Before initiating a new sex partner. Any person exposed occupationally.
77
Testing CD4
Baseline and repeat every 3-6 months for stable pts. Repeat if inconsistent with clinical picture. Used for HIV staging and prognosis. Helps guide initiation of ART.
78
Quantitative plasms HIV RNA (HIV Viral load)
Perform at baseline. Also 2-8 weeks after initiation or change in ART then every 4-8 weeks until viral load is suppressed. Stable - every 3-4 months. Used to monitor effect of ART
79
USPSTF HIV screening recommendation
Grade A - for adolescents and adults 15-65. Those younger or older who are at increased risk. All pregnant women including those in labor who are untested and whose HIV status is unknown.
80
Pre-test and post-test counselling for pt undergoing HIV testing
Education should be "front-loaded". Positive results may be too overwhelming. Negative results may be too relieved to liste.
81
Behavior risks that increase risk of HIV
Substance abuse. Sharing contaminated injection equipment. Drug use, ETOH use. Drug addicts often trade unsafe sex for drugs or money.
82
Four main strategies for prevention of HIV
Incorporate HIV testing as a routine part of care in traditional medical settings. Implement new models for diagnosing HIV infectious outside medical settings. Prevent new infections by working with people diagnosed with HIV and their partners. Further decrease mother-to-child HIV transmission.
83
What improves resistance rates of HIV
Education about potential resistance improves adherence to therapy
84
How does HIV cause AIDS
HIV infects and destroys the T-helper cell also known as CD4. When CD4 cells are destroyed, the body loses its ability to fight off infections
85
What do CD4 cells do
They direct and coordinate other cells in the immune system to battle infections.
86
When do HIV pts become diagnosed with AIDS
When they develop an opportunistic infection
87
What is the viral load
A measure of the quantity of HIV in a drop of the pt's blood and is usually measured in copies/mL. The higher the viral load, the faster CD4 cells are destroyed.
88
Treatment with antivirals immediately after the primary HIV infection (PHI)
Some evidence that early treatment may favorably influence subsequent course of disease
89
What tests to order for HIV pt
CD4, viral load. CBC. CMP. Toxoplasmosis, CMV IgG, PRP, Hep AB&C, screening for other STI: oral, rectal, urethral GC adn urethral Chlamydia
90
Benefits of antiretrovial therapy related to HIV
Reduced morbidity and mortality. Immune system recovery
91
Drawbacks to antiretroviral therapy
Toxicities, lifestyle changes, potential for developing resistance
92
Key considerations of initiating antiretroviral therapy
Symptoms and opportunistic infections, CD4 count, HIV viral load, anticipated adherence - patient readiness
93
When to ideally initiate antiretroviral therapy
Before the CD4 count drops below 200 cells/mm3 and before clinical symptoms develop.
94
What to do if CD4 level is below 200 in HIV+ pt
Antiretroviral therapy should be initiated as soon as pt is ready to start
95
What does the viral load in a HIV+ pt indicate
Predicts the slope of CD4 decline and may help determine when to start antiretroviral therapy
96
Predictors of poor adherence to meds for HIV
Active ETOH or substance abuse. Depressed moood. Lack of preceived efficacy of ART. Lack of advanced disease. Concern over side effects. Regimen complexity.
97
Factors associated with higher adherence to meds for HIV
Twice-daily or once-daily regimens. Belif in own ability to adhere to regimen. Not living alone. History of opportunistic infection or advanced HIV disease. Belief in efficacy or ARTs. Belief that non-adherence will lead to viral resistance.
98
St. John's Wort and HIV drugs
Has significant interations with many antiretroviral agents.
99
HIV and Hep C
HIV accelerates the course of Hep C. Avoid ETOH. Treatment can be helpful, even curative, and deserves consideration.
100
Health care maintenance of HIV pt
Vaccines - Hep A&B, pneumonia, flu, tetanus, pap smears, cancer screenings, cholesterol screening, PPDs, STI screening
101
High risk pts for lung ca screening
Category 1 - those 55-74 with at least a 30 pck/year history of smoking and smoking cessation less than 15 years. Category 2B - those at least 50 with a 20 or more pack/year and 1 additional risk factor
102
Lung nodules more than 8 mm at baseline
CT should be considered with biopsy or excision when results suspicious for lung CA
103
Solid endobronchial nodules
Reexamined at 1 month with low-dose CT, immediately after vigorous coughing. If still present in 1 month, bronchoscopy should be performed
104
Staging of cancer using TNM
T - primary tumor; N - node; M - metastasis.
105
Consequences of excessive and chronic cough
Anxiety, fatigue, insomnia, myalgia, dysphonia, perspiration, urinary incontinence, syncope, rib fractures, and depression. Can be a symptom of underlying disase.
106
Timing of acute cough
Less than 3 weeks
107
Timing of subacute cough
3 weeks to 8 weeks
108
Timing of chronic cough
Persists past 8 weeks
109
When should a cough be investigated
When it has persisted past 3 weeks and has failed initial treatment
110
Causes of subacute cough
Generally due to bacterial sinusitis or asthma, and sometimes URIs
111
Post-infectious cough
A cough that follows a viral or virus-like infection. Lasts no longer tha 8 weeks, chest x-rays are normal, and cough eventually resolves without intervention.
112
Most common causes of chronic cough in adults
Upper airway cough syndrome (previously called postnasal drip syndrome), asthma, and GERD. Called the pathogenic triad.
113
Cough indicative of chronic bronchitis
Lasts for 3 consecutive months for more than 2 consecutive years
114
Cough indicative of GERD
Sudden cough in the supine position associated with sour taste in mouth
115
Cough consistent with upper airway and sinusitis
Constant clearing of the throat and thick mucus production, especially on rising from bed
116
Assessment of HIV+ pt with cough
A chest x-ray and O2 saturation should be obtained earlier in the assessment
117
Causes of upper airway cough syndrome
Viral URI, perennial rhinitis, irritants, drugs, vasomotor response, and chronic sinusitis.
118
One of the worst signs of worsening asthma
Chronic cough
119
Older patient, cough, and asthma
May present with cough and no wheezing
120
Cough-variant asthma
Characterized by a dry, nocturnal cough and associated with a drop in early morning peak flows.
121
Most accurate way to assess degree and reversibility of obstruction related to asthma
Spirometry, which is forced expiratory volume in 1 sec (FEV1).
122
FEV1 less than 80% and strong response to beta 2 agonist bronchodilators
Strongly suggestive of asthma
123
Most important risk factor for cough and sputum production in COPD patients
Cigarette smoking
124
Spirometry that reveals an airway obstruction that is not responsive to inhaled bronchodilators
Suggestive of chronic bronchitis or smoker's cough
125
Most effective therapeutic intervention of cough
Smoking cessation and occurs within 8 weeks
126
Bronchiectasis
Associated with overproduction of secretions. Often accompanied by fever, hemoptysis, and weight loss. Chest x-ray shows increased thickening of bronchial wall, in lower lobes of advanced disease.
127
Sputum of bronchiectasis
If left standing will separate into three layers - frothy top, serous middle, and purulent bottom layers
128
Management of cough
Either antitussive (prevent, control, or eliminate) or protussive (make cough more productive)
129
When is antitussive treatment indicated for cough
When cough serves no purpose, such as clearing airway. Directed at aggravating factors
130
When is protussive treatment indicated for cough
For patients whom coughing serves a useful function - such as cystif fibrosis.
131
Length of cough after ACE inhibitors are stopped
Should resolve within 1-4 weeks, but may last 3 months
132
Emperical therapy of cough
Appropritae when there is a reasonable suspicion of a specific diagnosis
133
Treatment of cough in asthma patients
Use an inhaled beta2 agonists, inhaled corticosteroids, or inhaled NSAIDs, and occassionally oral steroids
134
Treatment of upper airway cough caused by sinusitis
Oral decongestants, nasal steroids, and possibly but not necessarily antibiotics. Antibiotics with purulent nasal drainage and sinus tenderness.
135
Treatment of cough associated with chronic bronchitis
Smoking cessation, ipratropium bromide inhaler, beta2 agonist inhaler. Antibiotics when purulent sputum - use 7-10 day course.
136
Common complications of coughing
Costochondritis or hemoptysis
137
Airflow limitations of COPD
Caused by a combo of both small airway disease and parenchymal destruction. Used to describe chronic bronchitis and emphysema
138
Definition of COPD
A chronic, persistent cough or sputum production for 3 consecutive months each year for 2 consecutive years, with periodic acute exacerbations during which the symptoms worsen.
139
Pathologic features of COPD
Inflammation of the cells lining the bronchial wall, hyperplasia of the mucous glands, and narrowing of the small airways.
140
Emphysema
Permanent and abnormal enlargement of any part of the air spaces distal to the terminal bronchioles. Involves destruction of the alveolar walls without fibrosis.
141
Risks for COPD
Genetic, behavioral, socioeconomic, and environmental factors. Cigarettes adn regular exposure to a dusty environment are two major external factors. Overcrowded living conditions with frequent exposure to viral infections, poorly ventilated homes, inadequate nutrition, exposure to passive cigarette smoking, adn suboptimum care for childhood respiratory infections, and air pollution from burning of wood.
142
Advanced COPD and smoking
In advanced stages, degeneration of the lung function will probably continue even with smoking cessation.
143
Diagnosis of COPD
Requires a thorough patient history, physical exam, and diagnostic testing
144
Most common presenting symptom of COPD
Dyspnea on exertion. Usually develops late in the course of the disease, when irreversible changes may have already occurred.
145
Physical findings in early onset COPD
May often be normal
146
Physical findings in advanced stages of COPD
Those resulting from hyperinflation, tobacco stains on fingers, and occassionally clubbing of fingernales, increase in AP diameter of chest and intercostal spaces, abnormal retractions during inspiration. Abd breathing. Forward-sitting posture with hands on knees.
147
Characteristic physical finding of late COPD
Pursed-lip breathing with prolonged expirations.
148
Importance of early detection of COPD
Important for decreasing the associated morbidity and mortality
149
When to consider COPD
Any pt with dyspnea, chronic cough, sputum production, and a history of exposure to risk factors of disease, such as smoking and occupational exposure
150
Forced expiratory timing to diagnose COPD
A time of 6 seconds or more.
151
"Gold standard" of diagnosis and assessment of COPD
Spirometry because it is the more reproducible, standardized, and objective way of measuring airflow limitation. FVC, FEV1, and FEV1/FVC ratio are primary spirometric measurements used
152
Spirometric indications of COPD
A post-bronchodilator FEV1/FVC of less than 0.70 and FEV1 of less than 80%
153
Stage I - Mild COPD
Mild airflow limitation (FEV1/FVC 80%) and usually, but not always chronic cough and sputum production. The individual may or may not be aware of abnormal lung function
154
Stage II - Moderate COPD
Worsening airflow limitations (50% <80% predicted) and usually a progression of symptoms, with shortness of breath developing with exertion
155
Stage III - Severe COPD
Further worsening of airflow limitations (30% <50% predicted
156
Stage IV - Very severe COPD
Severe airflow limitations (FEV1 <50% predicted plus chronic respiratory failure. Quality of life is very impaired and exacerbations may be life-threatening
157
Blood gas and COPD
Measurements are necessary to assess and manage pts during exacerbations and when O2 therapy is indicated.
158
Features that may help distinguish COPD from other common pulmonary diseases
Likely midlife onset, long hx of smoking and slowly progressing symptoms
159
Goals of treatment of COPD
Reverse or reduce airflow obstruction; to control cough and secretions; to prevent and eliminate infection; and to control complications, including polycythemia, hypoxemia, and right-sided heart failure.
160
Medicare criteria for 24-hr supplementation of oxygen
PaO2 of 55 mm Hg or less and an O2 sat of 88% while on room air.
161
Indications of oxygen desaturation during sleep
Daytime hypoxemia (PaO2 <55 mmHg), Hct greater than 50-55%, morning headaches, daytime sleepiness, and poor exercise tolerance.
162
First choice of medication for patient with nonasthmatic COPD
Anticholinergics, but are less effective than beta2-adrenergic agonists. First-line maintenance therapy for COPD patients.
163
Treatment choice for patients with intermittent COPD symptoms
Short-acting beta2-adrenergic agonists
164
How anticholinergics work
Decreased stimulation to the cholinergic nerves of the bronchial smooth muscles lessens bronchoconstriction. The nerves are plentiful in the proximal airways and these are the ones influenced by COPD. They are slower onset, but prolonged and intense
165
How beta2-adrenergic agonists work
Cause bronchial smooth muscle dilation and can also improve mucociliary clearance.
166
Major side effects of beta2-adrenergic agonists
Tachycardia and tremor.
167
Beta2-adrenergic agonists and older patients
Toxicity and drug-drug interactions must be avoided, especially in those with co-existing heart disease
168
Combination anticholinergic and short-acting beta2 agonists and COPD
Shown to reduce exacerbations, to lower cost, and to improve lung function and quality of life
169
Theophylline
Considered 3rd line agent in treatment of COPD because it's bronchodilatory effect is limited and its therapeutic range is narrow.
170
Corticosteroid use and COPD
Improve airflow and gas exchange and management is discouraged secondary to unfavorable benefit-to-risk ratio
171
Complications of corticosteroids
Skin damage, cataracts, diabetes, obesity, peptic ulcer disease, osteoporosis, and secondary infection. Oral meds can be used to treat acute exacerbations by using a tapering course.
172
Complication of rapid corticosteroid tapers
Rebound bronchospasm
173
Reducing risk of oral candidiasis with corticosteroid use
Rinse mouth with water or mouthwash after every use or by using a spacer
174
Inhaled glucocorticosteroids and bronchodilators
More effective than when used individually and improves lung function and reduces exacerbations. But increases pneumonia and does not significantly effect mortality.
175
Mucoactive agents and COPD
Not typically recommended in COPD. Decreases viscosity and adhesiveness of sputum and facilitates expectoration. Increasing oral hydration does not thin secretions.
176
Use of antibiotics in COPD
Do not use unless infection present. First-line is broad-spectrum
177
Principle goals of pulmonary rehab
Reduce symptoms, to improve quality of life, and to increase physical and emotional participation in everyday activities. Highly individualized to meet needs of each pt.
178
Exercise training and COPD
Improve pt's exercise tolerance and symptoms of dyspnea and fatigue
179
Immunizations and COPD
Yearly flu and prophylaxis of pneumococcal
180
Lung volume reduction surgery (LVRS)
One surgery for COPD. Improves elastic recoil and diaphragmatic function by reducing hyperinflation.
181
Lung transplantation and COPD
Surgery to correct disease and will improve quality and functional capacity of life.
182
Symptoms of theophylline toxicity
GI symptoms, tremors, headache, or tachycardia. Corticosteroids and diuretics use may cause hyperglycemia, hypokalemia, and azotemia.
183
Other complications of COPD
Sleep disorders (nocturnal O2 desaturation), acute respiratory failure, and cor pulmonale
184
Cor pulmonale
Severe complication of COPD and is right ventricular enlargemnt, hypertrophy, or dialtion secondary to lung disease
185
Symptoms of cor pulmonale
Peripheral edema, JVD, and a congested liver
186
The most common sleep-related breathing disorder
Obstructive sleep apnea (OSA)
187
The physiologic derangement of obstructive sleep apnea
Repetitive upper airway narrowing or closure, which occurs during sleep, leading to increased efforts to breathe, finally ending with a brief CNS arousal to reestablish patency of the upper airway. This leads to sleep fragmentation and poor-quality sleep
188
Upper airway resistance syndrome (UARS)
Increased resistance due to narrowing in the upper airway, which causes the individual to increase respiratory efforts to maintain airflow. Tidal airflow remains essentially the same, but increased respiratory efforts still may lead to CNS arousals and has many of the same consequences of OSA
189
Central sleep apnea (CSA)
Less common. Altered CNS respiratory drive, the pt does not receive the usual metabolic feedback during sleep to drive breathing. Repetitive cycles characterized by cessation of airflow. Causes fragmented sleep
190
Characteristics of OSA and UARS
Loud, disruptive snoring, with or without witnessed apneas, nocturnal gasping, or choking. Frank daytime sleepiness, daytime fatigue adn tiredness, vague depressive symptoms. Nocturia is frequent.
191
Most common risk factors of OSA
Obesity; more common in men; use of ETOH, opiates, or muscle relaxants such as benzos; heart disease; HTN; stroke; crowded oropharynx
192
Complication of untreated OSA
Independent cause of systemic hypertension, cardiac disease, and stroke
193
Characteristics of central sleep apnea (CSA)
Partners report pauses in breathing which may or may not be followed by a period of more rapid breathing. History of snoring. Daytime fatigue.
194
Risk factors of central sleep apnea (CSA)
Decompensated congestive heart failure and use of opiods, particularily long-acting meds such as methadone.
195
Standard test to diagnose OSA, UARS, and other sleep-related breathing disorders
Overnight polysomnography (PSG)
196
Management of OSA and UARS
Nasal continuous positive airway pressure (nCAP). Weight loss may be helpful. Custom-fit dental appliances.
197
Goal of treatment of COPD
Now aimed at immediately relieving and reducing the impact of symptoms, as well as reducing the risk of future adverse health events such as exacerbations
198
Making a clinical diagnosis of COPD
Should be considered in any pt with dyspnea, chronic cough or sputum production, and a history of exposure to risk factors for the disease. Spirometry is required to make the diagnosis in this clinical context.
199
Assessment of COPD
Based on pts symptoms, risk of exacerbations, the severity of the spirometric abnormality, and identification of comorbidities.
200
COPD exacerbation
An acute event characterized by a worsening of a pt's respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication.
201
COPD
Defined by abnormal permanent enlargement of pulmonary air spaces accompanied by destruction of alveolar walls, without fibrosis. Actually is two diseases - emphysema and chronic bronchitis
202
Emphysema definition
A progresive disease characterized by airflow limitations that are not fully reversible.
203
Etiology of COPD
Most often in those over 40 with a history of smoking (current or former), Smoking is common cause. Environmental factors. Genetic factors - alpha1 antitrypsin or AAA deficiency
204
Alpha1-antitrypsin
A protease inhibitor produced by the liver that acts in the lungs
205
Symptoms of COPD
Not acute. Constant coughing or "smoker's cough"; SOA doing normal activities; excess sputum; not being able to take a deep breath; wheezing; changing daily activities because loss of air
206
Spirometry and COPD
Determines severity and distinguishes from asthma
207
Diagnosis of COPD based on spirometry
FEV1/FVC <0.7 (post-bronchodilator). Encourage smoking cessation
208
COPD on x-ray
Lungs are hyperextended - extend past 7th intercostal space. Lungs also look darker. Loss of normal shape of hemidiaphragm - flatten out. Narrowing of diameter of heart
209
Ordering home oxygen
Spirometry needs to be retested every 60-90 days. Walking the patient around the office may produce a more valid indication of respiratory status when testing for eligibility
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Interstitial lung disease
Restrictive lung disease or parenchymal lung disease
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Characteristics of restrictive lung disease
Fibrosis in the lungs alveoli and small airways. Alveolar walls thicken, portions of the pulmonary capillary bed are destroyed, and increased elastic connective tissue holds small airways open. While exhalation is rapid with increased FEV1, it is difficult for pt to inhale. Low tidal capacity and fall in vital capacity.
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Causes of restrictive lung disease
Idiopathic pulmonary fibrosis sarcoidosis, histiocytosis, pulmonary manifestations of systemic rheumatic disorders (RA, SLE, scleroderma, ankylosing spondylitis), fibrosis induced by drugs, other inherited disorders and occupational exposure (asbestosis, coal, silicosis). Also severe kyphosis.
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First signs of restrictive lung disease
Breathlessness and dry cougn
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Diagnosis of restrictive lung diseases
Tough. Ask about environmental and occupational factors, hobbies, legal and illegal drug use, arthritis, and risk factors for diseases that affect immune system. First, obtain chest x-ray, then PFT, ultimately CT and biopsy. Refer to pulmonologist
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Treatment of restrictive lung diseases
Steroids for flares. Oxygen and transplant are possibilities.
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Most important risk factor for obstructive sleep apnea
Obesity, male gender (until about age 50); postmenopausal state; upper airway anatomic obstruction; African-American, Asain, or Hispanic ethnicity; being a football player secondary to large neck circumference
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Pathophysiology of obstructive sleep apnea - most comon etiology
Area just behind the soft palate and tongue. The soft palate, tongue, and uvula can all occlude the airway.
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CNS effects of obstructive sleep apnea
Cognitive impairment; motor vehicle accidents (doubles risk); and impaired quality of life
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Cardiovascular effects of obstructive sleep apnea
Systemic HTN; pulmonary HTN; nocturnal arrhythmias; coronary artery disease; TIA/stroke
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Metabolic effects of obstructive sleep apnea
Insulin resistance
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Cause of HTN
Sleep apnea - from JNC 7
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Cardiac conditions associated with obstructive sleep apnea
A-fib; CHF; stroke; ischemic events (MI); and death
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Patient history in which to suspect obstructive sleep apnea
Snoring; unrefreshing sleep (nonspecific) /daytime sleepiness; witnessed apneas; insomnia; restless sleep; snoring; morning headaches; nocturia; dry mouth/ sore throat/ sinus and nasal congestion; family history; mood, memory, and learning problems
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Causes of sleepiness other than obstructive sleep apnea
Most common is not getting enough sleep. Depression. Medication side effects. Obesity. Chronic illness especially diabetes
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Witnessed apnea
The most robust historical, predictor of sleep apnea, in men. Self-reported apneas do not have the same value.
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Presentation of women with sleep apnea
Present with insomnia; depression; have thyroid disease; report nightmares, palpitations, and hallucinations; have comorbid restless leg syndrome. More likely to report symptoms that will have they referred to psychiatrist. Less likely to have snoring and witnessed apnea.
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Physical findings in obstructive sleep apnea
Obesity is best predictor. Neck circumference is a surrogate for central obesity - >17 in men, > 16 in women. HTN - loss of morning dip in BP is an early sign. Narrowed oropharynx.
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What is monitored during polysomnography (PSG) - sleep study
Airflow - thermistry, ETCO2, nasal pressure. SaO2. Respiratory movement/effort. ECG. EMG. EOG. Leg movements. Typically done in sleep centers, but are now doing them portable in pt's own home.
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Definitions of apnea and hypopneas
Decrease in airflow or chest wall movement to an amplitude smaller than approximately 25% (apnea) or 70% (hypopnea) of baseline. At least 10 seconds. Associated with oxyhemoglobin desaturation of 4% or greater as compared with baseline.
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Apnea + hypopnea index (AHI)
Apneas + hypopneas divided by total sleep time in hrs
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Respiratory disturbance index (RDI)
Apnea + hypopneas index, more or less
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Sleep-distordered breathing (SDB)
What you would say when you are not sure what you are including. May include snoring, RERA's, oxygen desaturation, and who know what!
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CMS's definition of obstructive sleep apnea (OSA)
AHI >15 or AHI >5 with HTN, stroke, sleepiness, ischemic heart disease, insomnia, or mood disorders
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Treatment of OSA
Behavioral, positive pressure, oral appliances, surgical, drugs, and oxygen
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Behavioral treatments of OSA
Weight loss of maybe 10% may be enough to cure, lateral decubitus sleeping position, smoking cessation, avoidance of muscle relaxants, and avoidance of sleep deprivation
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Treatment of OSA via positive pressure
It splints the entire airway from nose to alveoli
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How long to use CPAP each night
Minimum of 4 hrs a night
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Effectiveness of nasal CPAP
Decreases sleepiness; improves quality of life; improves cognitive function; and decreases hospitalizations and health care costs. Decreases MVCs, HTN, mortality and cardiac risk. Improves glucose control. Reverses impotence. But the patient has to use it!
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Adverse complaints of CPAP use
Rhinorrhea, nasal congestion or dryness, epistaxis, skin abrasions/rashes, chest discomfort, claustrophobia, aerophagy, sinus discomfort
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Predictors of CPAP compliance
Severity of symptoms; preceived benefit; degree of sleep fragmentation; higher educational status; hypoxemia; supportive bed partner; and higher pressure levels
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Predictors of CPAP non-compliance
Referral by ENT physician; cigarette smoking; male; mild symptoms; prior palatal surgery; being a mouth breather; and mood disturbance
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Strategies to improve CPAP compliance
Education/ support/ reinforcement (most important); humidification; attention to patient-machine interface; bilevel pressure (not really supportive); and nasal steroids (no real evidence)
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Oral appliances - Second line treatment for OSA
Shown to reduce apnea + hypopnea index, improve BP and O2 in people with apnea. Not as good as CPAP, but better than surgery.
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Surgery - treatment for OSA
Variety. Most studied is uvulopalatopharyngoplasty (UPPP). Nose procedures. Oral surgery. Sommoplasty. Variable results. Success with UPPP is 50%. Relapse is common.
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Drugs to treat OSA
Nasal steroids are very common. Not a lot of supportive data.
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GOLD standards criteria to consider COPD
In any patient who has dyspnea, chronic cough or sputum production and/or a history of exposure to risk factors for the disease
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Early diagnostic changes indicitive of COPD on x-ray
Negative chest x-ray with flattening of the diaghram
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JNC BP goal
140/90
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Consideration of unexplained weight loss in an elderly patient
Must think about cancer. Is always concerning.
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TSH, CBC and look for anemia, stools for occult, and lung CT
Tests for older patient with COPD
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Test to obtain in pt with COPD
PFTs with and without bronchodilation to confirm diagnosis of COPD
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Test required to make diagnosis of COPD
Spirometry. The presence of post-bronchodilator FEV1/FVC <0.70 confirms the presence of airflow limitation and thus of COPD
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Bronchodilator use and PFT testing
Must hold for 4 hours prior to PFT testing
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Onset of asthma versus COPD
Asthma 40
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Family history of asthma and COPD
Asthma - usually. COPD - no
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Prominence of cough in asthma versus COPD
Asthma - nocturnal, post - exercise. COPD - early am
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History of atopy in asthma and COPD
Asthma - often. COPD - no
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Bronchidilator reversibility in asthma and COPD
Asthma - complete / nearly so. COPD - partial
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Steroid resonsiveness of asthma and COPD
Asthma - strong. COPD - weak
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Progressive deterioration of asthma and COPD
Asthma - uncommon. COPD - typical
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Anticholinergic responsivity of asthma and COPD
Asthma - beta-agonists better. COPD - best first-line treatment
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Beta-agonist responsivity in asthma and COPD
Asthma - very good. COPD - anticholinergics are better
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Purulent sputum in asthma and COPD
Asthma - uncommon. COPD - typical
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Smoking history in asthma and COPD
Asthma - variable. COPD - essentially always
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Spirometry
Measures the ratio of the forced expiratory volume in the first second to the forced vital capacity (FEV1/FVC) and this measurement is the most sensitive and specific test for detecting obstruction of airflow in the lungs
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Predicted values of spirometry
The normal results that your doctor would expect for people with the same height, weight, age, and sex as you
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Measured values of spirometry
Your results in comparison with normal or predicted values. For example - if you only blow out half the amount of air that would normally be predicted, the measured value of your vital capacity (VC) would be 50%. If your total lung capacity (TLC) is exactly what would be predicted, the measured value is 100%.
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FVC
Forceful exhalation of all the air from the lung. Measure of lung volume and is usually reduced in diseases that cause the lungs to be smaller. Such processes are generally termed restrictive and include disorders of the lung parenchyma, such as pulmonary fibrosis, neuromuscular disease, pleural effusion, or hyperinflated due to emphysema, not considered a reliable indictor of total lung capacity.
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Number of measurements taken of FVC
Usually given 3 tries to perform test.
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FEV1
How much can the pt exhale in 1 second. Most widely used to measure the mecanical properties of the lungs. In normal persons, it accounts for the greatest part of the exhaled volume for the spirometric maneuver and reflects properties of the large and medium sized airways. It occurs at about 75-85% of the FVC. Reducing the FEV1/FVC below the lower limit of normal indicates airflow limitation.
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FEV1 in obstructive lung diseases
Is reduced to the FVC
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FEV1 in restrictive lung diseases
FVC and total lung capacity are all reduced. The ratio is normal or even higher.
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Diagnosis of COPD with spirometry
FEV1 < than 70% or 0.70
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Spirometry of asthma
FVC and total lung capacity are all reduced. The ratio is normal or even higher.
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Mild COPD
FEV1/FVC 80%. Reduce risk factors - immunizations. Add short-acting bronchodilators as needed
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Moderate COPD - stage II
FEV1/FVC <50%. Reduce risk factors - immunizations. Short-acting bronchodilators PRN. Add regular treatment with one or more long-acting bronchodilators. Rehabilitation
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Severe COPD - stage III
FEV1/FVC 30%. Reduce risk factors - immunization. Short-acting bronchodilators PRN. Regular treatment with one or more long-acting bronchodilators. Rehab. Add inhaled glucocorticosteroids if repeated exacerbations.
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Very severe OPD - stage IV
FEV1/FVC < 30% plus chronic respiratory failure. Reduce risks. Short-acting bronchodilators PRN. Regular long-acting bronchodilators. Add inhaled glucocortisoids. Add long-term O2 if chronic respiratory failure. Consider surgery.
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Beta 2 agonists
Albuterol - work by relaxing the beta receptors in the muscles around the airways. Short-term. Work best in asthma
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Anticholinergic agents
Muscarinic receptors such as atrovent or Spriva or Tudorza - work by acting on the muscarinic receptors located on smooth muscle cells and submucosal glands that leads to reduction in smooth muscle contraction and mucus secretion producing bronchidilation.
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Use of steroids in lung diseases
Should be used late in the game. Add to quality of life, but do not add to improvement in lung function. Actually increase the risk of pneumonia.
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1st drug to use in COPD
Short-acting beta2-adrenergic, such as combovent agonists
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When is steroid use good for COPD
When exacerbations and then the FEV1 is very low <50%. Should be used sparingly.
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Common presentation of COPD
Professive dyspnea. Decreased exercise tolerance. Cough. Sputum production. Usually slow onset, but progressive with exacerbations. Long smoking history. Airflow is limited and only partially reversible. Associated with inflammatory response triggers. Must consider in ANY pt who smokes and has pulmonary complaints. May occur in those with chronic exposure to second-hand smoke.
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Importance of early diagnosis of COPD
To reduce mild symptoms and slow the progression of the disease
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Use of terms emphysema and chronic bronchitis
Declining in use due to their lack of specificity and overlapping descriptions. COPD is accepted term for both
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Target intervention for COPD
Smoking cessation
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Beta blockers and COPD
Theory has changed in use of beta blockers. Now, BB use with COPD pts is acceptable.
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Oral steroids and COPD exacerbation
Non tapered for a week; but a taper is more typically done, to avoid rebound bronchospasm.
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Treatment of COPD exacerbations
Look for exacerbations - steroids and antibiotic if purulent sputum and increased dyspnea and sputum volume. Chose 1st or 2nd line antibioitcs.
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Treatment of repeated exacerbations
Max out the bronchodilators; if FEV1 <50% predicted start inhaled corticosteroids.
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Oxygen therapy and COPD
Prescribe if pulse ox 88% on room air, rest, or with walking. Use for 15 hours a day.
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Polycythemia and COPD
Consider with pt taking ASA. Can be used to justify prescription of O2
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Depression and COPD
Be on alert for symptoms
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Management of COPD
Reduce symptoms, improve quality of life, remain active for as long as possible. Education, education, education!
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Smoking cessation and COPD
Motivational interviewing, have a variety of suggestions for pt; be a coach. Ask and chart at every visit. Assess for other inhaled irritants and discuss use of masks if exposed to dirty environments - mowing grass
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Vaccinations for COPD
Influenza, pneumococcal pneumonia
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Oral corticosteroid use
Not recommended with COPD
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Antibiotic of choice in COPD exacerbation
Azithromax because broad-spectrum
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Prescription of oxygen and COPD
At stage IV and when SaO2 < 88%. Goal is SaO1 at rest of > 90%.
