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Comps - Mod 3 > NP614 Test 5 - Sheet1 > Flashcards

NP614 Test 5 - Sheet1 Flashcards

1
Q

Objective signs of dying and death

A

Elusive, depending on pt’s diagnosis

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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?

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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

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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.

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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

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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.

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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.

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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.

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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

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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

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11
Q

Difference between anxiety and fear

A

Fear has a definable quality or cause. Anxiety is a sense of deep unease

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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

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13
Q

Important role of PCP regarding education of HIV

A

Education to teens, women, and infected individuals regarding primary and secondary prevention

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14
Q

Treatment of anxiety

A

Pharmacologic interventions and removal of specific problem if possible.

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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.

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16
Q

Diagnostics of delirium

A

Should only be taken if resutls are likely to change pt management

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17
Q

Opiod medications less likely to cause delirium

A

Fentanyl, hydromorphone, and oxycodone

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18
Q

Medications to avoid in pt with delirium

A

Benzodiazepines can result in paradoxical effects and worsen symptoms

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19
Q

Most important assessment criterion of dyspnea

A

The patient’s self-reporting

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20
Q

Management of the “death rattle”

A

Scopolamine patches - 1.5 mg transdermal, atropine 1% ophthalmic drops used SL

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21
Q

Ceiling doses of opiods

A

There are none

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22
Q

Goal of pallative sedation

A

Alleviate the suffering caused by the unrelieved symptoms

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23
Q

Types of preventable cancers

A

Those associated with lifestyle factors - smoking, obesity. Those associated with infectious agents - Hep B, HPD

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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)

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25
Q

Most common form of skin cancer

A

Basal cell

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26
Q

Reasons skin cancer rates have increased

A

Increased sun exposure and depletion of protective ozone layer

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27
Q

Risks of skin cancers

A

Acute sunburns, second-degree burn before 18, Fair-skinned men and women > 65, atypical moles, and those with more than 50 nevi. Hereditary component.

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28
Q

Warning signs of skin cancer

A

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.

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29
Q

Characteristics of basal cell carcinomas

A

Raised, shiny appearance, often with pearly borders

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30
Q

Characteristics of squamous cell carcinoma

A

Roughened, scaling area that does not heal and bleeds readily when scraped.

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31
Q

Keratinization of skin cancers

A

Can lead to a heaped-up appearance that flakes

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32
Q

ABCDEs of skin cancers

A

Asymmetry, border, color, diameter, and elevation

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33
Q

Most definitive diagnostic test of skin cancers

A

Punch or shave biospy techniques

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34
Q

Treatment of skin cancers

A

BCC - electrodesiccation and curretage. SCC - total excision

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35
Q

Types of lung cancers

A

Small cell (SCLC) and non-small cell (NSCLC)

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36
Q

Risk factors for lung cancers

A

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.

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37
Q

Lung cancers and smoking

A

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.

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38
Q

Common symptoms of lung cancer

A

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.

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39
Q

Primary immunodeficiencies

A

Congenital and most arise from single-gee defects. Must appear by age 6. The early the immunodeficiency presents, the more severe the underlying disease

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40
Q

Secondary immunodeficiencies

A

Influenced by genetics, but outside or environmental factors cause these diseases more often. Ex - T helper cells being destroyed by HIV infection

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41
Q

Divisions of the immune system

A

Innate system - skin, mucus, immune cells, cytokines. Adaptive system - evolutionary B and T cells (humoral immunity) and cell-mediated immunity

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42
Q

Treatment goals of pt with primary immunodeficiency

A

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.

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43
Q

Antibiotic use and primary immunodeficiency patients

A

Provider should use. May need to be more aggressive and prolonged and always attempts to narrow antibiotic based on C&S results

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44
Q

Whole blood transfusions and immunodeficient patients

A

Contraindicated because donor blood may contain lymphocytes that could induce a grave-vs-host rejection

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45
Q

Lymphadenopathy

A

Lymph nodes that have enlarged or changed in consistency. Should be between 0.5 and 2.5 cm.

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46
Q

Lymphadenitis

A

Tender, warm, erythematous nodes. Indicates infection at the drainage terminal of the lymph system.

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47
Q

Generalized lymphadenopathy

A

Three or more disparate node enlargements

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48
Q

Function of lymph nodes

A

Provide filtration of foreign substances through the action of lymphocytes, monocytes, and macrophages.

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49
Q

Why do lymph nodes swell?

A

In response to an antigen.

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50
Q

Key factors to consider in pt with lymphadenopathy

A

Age of pt, location of swollen glands, adn associated symptoms.

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51
Q

Most suspicious sizes of enlarged lymph nodes

A

1.0 and 2.25 cm

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52
Q

Characteristics of lymph nodes to assess

A

Size, distribution, degree or flactuance, firmness, matted or shoddy quality, mobility or morbality, tenederness adn nontenderness.

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53
Q

Primary lymphadema

A

Congenital malformations

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54
Q

Secondary lymphadema

A

Tramatic injury resulting from cancer obstruction, irradiation, recent infeciton, or surgery

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55
Q

AIDS defining conditions

A

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.

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56
Q

PHI

A

Primary HIV infection - the time after infection but before the infected person has established a comprehensive immunologic response to infection. A latent period.

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57
Q

Opportunistic infections that can occur when CD4 counts are higher than 200

A

Rare - lymphomas (cervical and anal carcinoma). TB. Shingles, severe psoriasis, severe pneumococcal, recurrent oral and vaginal candidiasis, oral hairy leukoplakia, and ITP.

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58
Q

Common opportunistic infections that begin to occur when CD4 counts fall below 200`

A

Pneumocystis jiroveci pneumonia (PCP), Kaposi’s sarcoma, cryptococcal meningitis, and esophageal candidiasis.

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59
Q

Opportunistic infections that occur when CD4 counts fall below 50

A

Toxoplasma encephalitis, disseminated Mycobacterium avium-intracellulare complex infection, cytomegalovirus retinitis, progressive multifocal leukoencephalopathy, AIDS dementia, CNS lymphoma, and AIDS wasting syndrome

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60
Q

ELISA and Western blot testing

A

Used to diagnose HIV. If +ELISA, Western blot will be used to confirm. -ELISA, no Western blot.

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61
Q

Management of HIV infections

A

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.

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62
Q

Result of correctly used HAARTs (Highly active antiretroviral therapy)

A

Can convert HIV infection from a progressive and inevitably fatal disease to a chronic disease with potentially normal life expectancy

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63
Q

Result of poorly used HAARTs (highly active antiretroviral therapy)

A

Can result in viral resistance to all antivirals and consequently untreatable progressive disease.

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64
Q

Theoretical benefit of treatment of primary HIV infection

A

This may minimize early immunologic damage and allow development of a more robust immunologic response to HIV, resulting in better immunologic control.

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65
Q

An absolute indication for HAART

A

Pregnant women to prevent mother-to-child transmission. Can reduce transmission from 25% to 2%.

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66
Q

Short term goal of HAART

A

Suppress viral replication to such a degree that there is no detectable HIV in peripheral blood. Can occur within 6 months

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67
Q

Most important predictor of life expectancy in HIV patient

A

The patient’s ability to tolerate and maintain a high level of adherence to antiviral drugs.

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68
Q

Lab monitoring while taking antiviral medications

A

Fasting lipid profile at baseline and every 1-3 months after any change in medications. May also cause insulin resistance.

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69
Q

Lipodystrophy

A

Refers to a change from baseline in the relative proportion of fat and can occur anywhere in the body. Can not be reversed

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70
Q

Drug interactions of antivirals and other medications

A

Numerous!

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71
Q

Low dose CT versus chest x-ray to diagnose lung ca

A

Shows to detect more nodules and lung cancers, including early-stage cancers

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72
Q

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

A

28 day course of highly active antiretroviral therapy as soon as possible after exposure

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73
Q

What to do for pt exposured <72 hrs to body fluids of person unknown with HIV that represents a substancial risk of transmission

A

No recommendation for prophylaxis

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74
Q

What to do for pt exposure > 72 hrs to fluids with no substantial risk for HIV

A

No recommendation for prophylaxis

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75
Q

Routine HIV screening

A

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.

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76
Q

Repeat HIV screening

A

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.

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77
Q

Testing CD4

A

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.

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78
Q

Quantitative plasms HIV RNA (HIV Viral load)

A

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

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79
Q

USPSTF HIV screening recommendation

A

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.

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80
Q

Pre-test and post-test counselling for pt undergoing HIV testing

A

Education should be “front-loaded”. Positive results may be too overwhelming. Negative results may be too relieved to liste.

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81
Q

Behavior risks that increase risk of HIV

A

Substance abuse. Sharing contaminated injection equipment. Drug use, ETOH use. Drug addicts often trade unsafe sex for drugs or money.

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82
Q

Four main strategies for prevention of HIV

A

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.

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83
Q

What improves resistance rates of HIV

A

Education about potential resistance improves adherence to therapy

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84
Q

How does HIV cause AIDS

A

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

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85
Q

What do CD4 cells do

A

They direct and coordinate other cells in the immune system to battle infections.

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86
Q

When do HIV pts become diagnosed with AIDS

A

When they develop an opportunistic infection

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87
Q

What is the viral load

A

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.

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88
Q

Treatment with antivirals immediately after the primary HIV infection (PHI)

A

Some evidence that early treatment may favorably influence subsequent course of disease

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89
Q

What tests to order for HIV pt

A

CD4, viral load. CBC. CMP. Toxoplasmosis, CMV IgG, PRP, Hep AB&C, screening for other STI: oral, rectal, urethral GC adn urethral Chlamydia

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90
Q

Benefits of antiretrovial therapy related to HIV

A

Reduced morbidity and mortality. Immune system recovery

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91
Q

Drawbacks to antiretroviral therapy

A

Toxicities, lifestyle changes, potential for developing resistance

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92
Q

Key considerations of initiating antiretroviral therapy

A

Symptoms and opportunistic infections, CD4 count, HIV viral load, anticipated adherence - patient readiness

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93
Q

When to ideally initiate antiretroviral therapy

A

Before the CD4 count drops below 200 cells/mm3 and before clinical symptoms develop.

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94
Q

What to do if CD4 level is below 200 in HIV+ pt

A

Antiretroviral therapy should be initiated as soon as pt is ready to start

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95
Q

What does the viral load in a HIV+ pt indicate

A

Predicts the slope of CD4 decline and may help determine when to start antiretroviral therapy

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96
Q

Predictors of poor adherence to meds for HIV

A

Active ETOH or substance abuse. Depressed moood. Lack of preceived efficacy of ART. Lack of advanced disease. Concern over side effects. Regimen complexity.

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97
Q

Factors associated with higher adherence to meds for HIV

A

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.

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98
Q

St. John’s Wort and HIV drugs

A

Has significant interations with many antiretroviral agents.

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99
Q

HIV and Hep C

A

HIV accelerates the course of Hep C. Avoid ETOH. Treatment can be helpful, even curative, and deserves consideration.

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100
Q

Health care maintenance of HIV pt

A

Vaccines - Hep A&B, pneumonia, flu, tetanus, pap smears, cancer screenings, cholesterol screening, PPDs, STI screening

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101
Q

High risk pts for lung ca screening

A

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

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102
Q

Lung nodules more than 8 mm at baseline

A

CT should be considered with biopsy or excision when results suspicious for lung CA

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103
Q

Solid endobronchial nodules

A

Reexamined at 1 month with low-dose CT, immediately after vigorous coughing. If still present in 1 month, bronchoscopy should be performed

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104
Q

Staging of cancer using TNM

A

T - primary tumor; N - node; M - metastasis.

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105
Q

Consequences of excessive and chronic cough

A

Anxiety, fatigue, insomnia, myalgia, dysphonia, perspiration, urinary incontinence, syncope, rib fractures, and depression. Can be a symptom of underlying disase.

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106
Q

Timing of acute cough

A

Less than 3 weeks

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107
Q

Timing of subacute cough

A

3 weeks to 8 weeks

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108
Q

Timing of chronic cough

A

Persists past 8 weeks

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109
Q

When should a cough be investigated

A

When it has persisted past 3 weeks and has failed initial treatment

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110
Q

Causes of subacute cough

A

Generally due to bacterial sinusitis or asthma, and sometimes URIs

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111
Q

Post-infectious cough

A

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.

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112
Q

Most common causes of chronic cough in adults

A

Upper airway cough syndrome (previously called postnasal drip syndrome), asthma, and GERD. Called the pathogenic triad.

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113
Q

Cough indicative of chronic bronchitis

A

Lasts for 3 consecutive months for more than 2 consecutive years

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114
Q

Cough indicative of GERD

A

Sudden cough in the supine position associated with sour taste in mouth

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115
Q

Cough consistent with upper airway and sinusitis

A

Constant clearing of the throat and thick mucus production, especially on rising from bed

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116
Q

Assessment of HIV+ pt with cough

A

A chest x-ray and O2 saturation should be obtained earlier in the assessment

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117
Q

Causes of upper airway cough syndrome

A

Viral URI, perennial rhinitis, irritants, drugs, vasomotor response, and chronic sinusitis.

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118
Q

One of the worst signs of worsening asthma

A

Chronic cough

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119
Q

Older patient, cough, and asthma

A

May present with cough and no wheezing

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120
Q

Cough-variant asthma

A

Characterized by a dry, nocturnal cough and associated with a drop in early morning peak flows.

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121
Q

Most accurate way to assess degree and reversibility of obstruction related to asthma

A

Spirometry, which is forced expiratory volume in 1 sec (FEV1).

122
Q

FEV1 less than 80% and strong response to beta 2 agonist bronchodilators

A

Strongly suggestive of asthma

123
Q

Most important risk factor for cough and sputum production in COPD patients

A

Cigarette smoking

124
Q

Spirometry that reveals an airway obstruction that is not responsive to inhaled bronchodilators

A

Suggestive of chronic bronchitis or smoker’s cough

125
Q

Most effective therapeutic intervention of cough

A

Smoking cessation and occurs within 8 weeks

126
Q

Bronchiectasis

A

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
Q

Sputum of bronchiectasis

A

If left standing will separate into three layers - frothy top, serous middle, and purulent bottom layers

128
Q

Management of cough

A

Either antitussive (prevent, control, or eliminate) or protussive (make cough more productive)

129
Q

When is antitussive treatment indicated for cough

A

When cough serves no purpose, such as clearing airway. Directed at aggravating factors

130
Q

When is protussive treatment indicated for cough

A

For patients whom coughing serves a useful function - such as cystif fibrosis.

131
Q

Length of cough after ACE inhibitors are stopped

A

Should resolve within 1-4 weeks, but may last 3 months

132
Q

Emperical therapy of cough

A

Appropritae when there is a reasonable suspicion of a specific diagnosis

133
Q

Treatment of cough in asthma patients

A

Use an inhaled beta2 agonists, inhaled corticosteroids, or inhaled NSAIDs, and occassionally oral steroids

134
Q

Treatment of upper airway cough caused by sinusitis

A

Oral decongestants, nasal steroids, and possibly but not necessarily antibiotics. Antibiotics with purulent nasal drainage and sinus tenderness.

135
Q

Treatment of cough associated with chronic bronchitis

A

Smoking cessation, ipratropium bromide inhaler, beta2 agonist inhaler. Antibiotics when purulent sputum - use 7-10 day course.

136
Q

Common complications of coughing

A

Costochondritis or hemoptysis

137
Q

Airflow limitations of COPD

A

Caused by a combo of both small airway disease and parenchymal destruction. Used to describe chronic bronchitis and emphysema

138
Q

Definition of COPD

A

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
Q

Pathologic features of COPD

A

Inflammation of the cells lining the bronchial wall, hyperplasia of the mucous glands, and narrowing of the small airways.

140
Q

Emphysema

A

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
Q

Risks for COPD

A

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
Q

Advanced COPD and smoking

A

In advanced stages, degeneration of the lung function will probably continue even with smoking cessation.

143
Q

Diagnosis of COPD

A

Requires a thorough patient history, physical exam, and diagnostic testing

144
Q

Most common presenting symptom of COPD

A

Dyspnea on exertion. Usually develops late in the course of the disease, when irreversible changes may have already occurred.

145
Q

Physical findings in early onset COPD

A

May often be normal

146
Q

Physical findings in advanced stages of COPD

A

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
Q

Characteristic physical finding of late COPD

A

Pursed-lip breathing with prolonged expirations.

148
Q

Importance of early detection of COPD

A

Important for decreasing the associated morbidity and mortality

149
Q

When to consider COPD

A

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
Q

Forced expiratory timing to diagnose COPD

A

A time of 6 seconds or more.

151
Q

“Gold standard” of diagnosis and assessment of COPD

A

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
Q

Spirometric indications of COPD

A

A post-bronchodilator FEV1/FVC of less than 0.70 and FEV1 of less than 80%

153
Q

Stage I - Mild COPD

A

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
Q

Stage II - Moderate COPD

A

Worsening airflow limitations (50% <80% predicted) and usually a progression of symptoms, with shortness of breath developing with exertion

155
Q

Stage III - Severe COPD

A

Further worsening of airflow limitations (30% <50% predicted

156
Q

Stage IV - Very severe COPD

A

Severe airflow limitations (FEV1 <50% predicted plus chronic respiratory failure. Quality of life is very impaired and exacerbations may be life-threatening

157
Q

Blood gas and COPD

A

Measurements are necessary to assess and manage pts during exacerbations and when O2 therapy is indicated.

158
Q

Features that may help distinguish COPD from other common pulmonary diseases

A

Likely midlife onset, long hx of smoking and slowly progressing symptoms

159
Q

Goals of treatment of COPD

A

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
Q

Medicare criteria for 24-hr supplementation of oxygen

A

PaO2 of 55 mm Hg or less and an O2 sat of 88% while on room air.

161
Q

Indications of oxygen desaturation during sleep

A

Daytime hypoxemia (PaO2 <55 mmHg), Hct greater than 50-55%, morning headaches, daytime sleepiness, and poor exercise tolerance.

162
Q

First choice of medication for patient with nonasthmatic COPD

A

Anticholinergics, but are less effective than beta2-adrenergic agonists. First-line maintenance therapy for COPD patients.

163
Q

Treatment choice for patients with intermittent COPD symptoms

A

Short-acting beta2-adrenergic agonists

164
Q

How anticholinergics work

A

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
Q

How beta2-adrenergic agonists work

A

Cause bronchial smooth muscle dilation and can also improve mucociliary clearance.

166
Q

Major side effects of beta2-adrenergic agonists

A

Tachycardia and tremor.

167
Q

Beta2-adrenergic agonists and older patients

A

Toxicity and drug-drug interactions must be avoided, especially in those with co-existing heart disease

168
Q

Combination anticholinergic and short-acting beta2 agonists and COPD

A

Shown to reduce exacerbations, to lower cost, and to improve lung function and quality of life

169
Q

Theophylline

A

Considered 3rd line agent in treatment of COPD because it’s bronchodilatory effect is limited and its therapeutic range is narrow.

170
Q

Corticosteroid use and COPD

A

Improve airflow and gas exchange and management is discouraged secondary to unfavorable benefit-to-risk ratio

171
Q

Complications of corticosteroids

A

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
Q

Complication of rapid corticosteroid tapers

A

Rebound bronchospasm

173
Q

Reducing risk of oral candidiasis with corticosteroid use

A

Rinse mouth with water or mouthwash after every use or by using a spacer

174
Q

Inhaled glucocorticosteroids and bronchodilators

A

More effective than when used individually and improves lung function and reduces exacerbations. But increases pneumonia and does not significantly effect mortality.

175
Q

Mucoactive agents and COPD

A

Not typically recommended in COPD. Decreases viscosity and adhesiveness of sputum and facilitates expectoration. Increasing oral hydration does not thin secretions.

176
Q

Use of antibiotics in COPD

A

Do not use unless infection present. First-line is broad-spectrum

177
Q

Principle goals of pulmonary rehab

A

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
Q

Exercise training and COPD

A

Improve pt’s exercise tolerance and symptoms of dyspnea and fatigue

179
Q

Immunizations and COPD

A

Yearly flu and prophylaxis of pneumococcal

180
Q

Lung volume reduction surgery (LVRS)

A

One surgery for COPD. Improves elastic recoil and diaphragmatic function by reducing hyperinflation.

181
Q

Lung transplantation and COPD

A

Surgery to correct disease and will improve quality and functional capacity of life.

182
Q

Symptoms of theophylline toxicity

A

GI symptoms, tremors, headache, or tachycardia. Corticosteroids and diuretics use may cause hyperglycemia, hypokalemia, and azotemia.

183
Q

Other complications of COPD

A

Sleep disorders (nocturnal O2 desaturation), acute respiratory failure, and cor pulmonale

184
Q

Cor pulmonale

A

Severe complication of COPD and is right ventricular enlargemnt, hypertrophy, or dialtion secondary to lung disease

185
Q

Symptoms of cor pulmonale

A

Peripheral edema, JVD, and a congested liver

186
Q

The most common sleep-related breathing disorder

A

Obstructive sleep apnea (OSA)

187
Q

The physiologic derangement of obstructive sleep apnea

A

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
Q

Upper airway resistance syndrome (UARS)

A

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
Q

Central sleep apnea (CSA)

A

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
Q

Characteristics of OSA and UARS

A

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
Q

Most common risk factors of OSA

A

Obesity; more common in men; use of ETOH, opiates, or muscle relaxants such as benzos; heart disease; HTN; stroke; crowded oropharynx

192
Q

Complication of untreated OSA

A

Independent cause of systemic hypertension, cardiac disease, and stroke

193
Q

Characteristics of central sleep apnea (CSA)

A

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
Q

Risk factors of central sleep apnea (CSA)

A

Decompensated congestive heart failure and use of opiods, particularily long-acting meds such as methadone.

195
Q

Standard test to diagnose OSA, UARS, and other sleep-related breathing disorders

A

Overnight polysomnography (PSG)

196
Q

Management of OSA and UARS

A

Nasal continuous positive airway pressure (nCAP). Weight loss may be helpful. Custom-fit dental appliances.

197
Q

Goal of treatment of COPD

A

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
Q

Making a clinical diagnosis of COPD

A

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
Q

Assessment of COPD

A

Based on pts symptoms, risk of exacerbations, the severity of the spirometric abnormality, and identification of comorbidities.

200
Q

COPD exacerbation

A

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
Q

COPD

A

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
Q

Emphysema definition

A

A progresive disease characterized by airflow limitations that are not fully reversible.

203
Q

Etiology of COPD

A

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
Q

Alpha1-antitrypsin

A

A protease inhibitor produced by the liver that acts in the lungs

205
Q

Symptoms of COPD

A

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
Q

Spirometry and COPD

A

Determines severity and distinguishes from asthma

207
Q

Diagnosis of COPD based on spirometry

A

FEV1/FVC <0.7 (post-bronchodilator). Encourage smoking cessation

208
Q

COPD on x-ray

A

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
Q

Ordering home oxygen

A

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

210
Q

Interstitial lung disease

A

Restrictive lung disease or parenchymal lung disease

211
Q

Characteristics of restrictive lung disease

A

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.

212
Q

Causes of restrictive lung disease

A

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.

213
Q

First signs of restrictive lung disease

A

Breathlessness and dry cougn

214
Q

Diagnosis of restrictive lung diseases

A

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

215
Q

Treatment of restrictive lung diseases

A

Steroids for flares. Oxygen and transplant are possibilities.

216
Q

Most important risk factor for obstructive sleep apnea

A

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

217
Q

Pathophysiology of obstructive sleep apnea - most comon etiology

A

Area just behind the soft palate and tongue. The soft palate, tongue, and uvula can all occlude the airway.

218
Q

CNS effects of obstructive sleep apnea

A

Cognitive impairment; motor vehicle accidents (doubles risk); and impaired quality of life

219
Q

Cardiovascular effects of obstructive sleep apnea

A

Systemic HTN; pulmonary HTN; nocturnal arrhythmias; coronary artery disease; TIA/stroke

220
Q

Metabolic effects of obstructive sleep apnea

A

Insulin resistance

221
Q

Cause of HTN

A

Sleep apnea - from JNC 7

222
Q

Cardiac conditions associated with obstructive sleep apnea

A

A-fib; CHF; stroke; ischemic events (MI); and death

223
Q

Patient history in which to suspect obstructive sleep apnea

A

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

224
Q

Causes of sleepiness other than obstructive sleep apnea

A

Most common is not getting enough sleep. Depression. Medication side effects. Obesity. Chronic illness especially diabetes

225
Q

Witnessed apnea

A

The most robust historical, predictor of sleep apnea, in men. Self-reported apneas do not have the same value.

226
Q

Presentation of women with sleep apnea

A

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.

227
Q

Physical findings in obstructive sleep apnea

A

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.

228
Q

What is monitored during polysomnography (PSG) - sleep study

A

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.

229
Q

Definitions of apnea and hypopneas

A

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.

230
Q

Apnea + hypopnea index (AHI)

A

Apneas + hypopneas divided by total sleep time in hrs

231
Q

Respiratory disturbance index (RDI)

A

Apnea + hypopneas index, more or less

232
Q

Sleep-distordered breathing (SDB)

A

What you would say when you are not sure what you are including. May include snoring, RERA’s, oxygen desaturation, and who know what!

233
Q

CMS’s definition of obstructive sleep apnea (OSA)

A

AHI >15 or AHI >5 with HTN, stroke, sleepiness, ischemic heart disease, insomnia, or mood disorders

234
Q

Treatment of OSA

A

Behavioral, positive pressure, oral appliances, surgical, drugs, and oxygen

235
Q

Behavioral treatments of OSA

A

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

236
Q

Treatment of OSA via positive pressure

A

It splints the entire airway from nose to alveoli

237
Q

How long to use CPAP each night

A

Minimum of 4 hrs a night

238
Q

Effectiveness of nasal CPAP

A

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!

239
Q

Adverse complaints of CPAP use

A

Rhinorrhea, nasal congestion or dryness, epistaxis, skin abrasions/rashes, chest discomfort, claustrophobia, aerophagy, sinus discomfort

240
Q

Predictors of CPAP compliance

A

Severity of symptoms; preceived benefit; degree of sleep fragmentation; higher educational status; hypoxemia; supportive bed partner; and higher pressure levels

241
Q

Predictors of CPAP non-compliance

A

Referral by ENT physician; cigarette smoking; male; mild symptoms; prior palatal surgery; being a mouth breather; and mood disturbance

242
Q

Strategies to improve CPAP compliance

A

Education/ support/ reinforcement (most important); humidification; attention to patient-machine interface; bilevel pressure (not really supportive); and nasal steroids (no real evidence)

243
Q

Oral appliances - Second line treatment for OSA

A

Shown to reduce apnea + hypopnea index, improve BP and O2 in people with apnea. Not as good as CPAP, but better than surgery.

244
Q

Surgery - treatment for OSA

A

Variety. Most studied is uvulopalatopharyngoplasty (UPPP). Nose procedures. Oral surgery. Sommoplasty. Variable results. Success with UPPP is 50%. Relapse is common.

245
Q

Drugs to treat OSA

A

Nasal steroids are very common. Not a lot of supportive data.

246
Q

GOLD standards criteria to consider COPD

A

In any patient who has dyspnea, chronic cough or sputum production and/or a history of exposure to risk factors for the disease

247
Q

Early diagnostic changes indicitive of COPD on x-ray

A

Negative chest x-ray with flattening of the diaghram

248
Q

JNC BP goal

A

140/90

249
Q

Consideration of unexplained weight loss in an elderly patient

A

Must think about cancer. Is always concerning.

250
Q

TSH, CBC and look for anemia, stools for occult, and lung CT

A

Tests for older patient with COPD

251
Q

Test to obtain in pt with COPD

A

PFTs with and without bronchodilation to confirm diagnosis of COPD

252
Q

Test required to make diagnosis of COPD

A

Spirometry. The presence of post-bronchodilator FEV1/FVC <0.70 confirms the presence of airflow limitation and thus of COPD

253
Q

Bronchodilator use and PFT testing

A

Must hold for 4 hours prior to PFT testing

254
Q

Onset of asthma versus COPD

A

Asthma 40

255
Q

Family history of asthma and COPD

A

Asthma - usually. COPD - no

256
Q

Prominence of cough in asthma versus COPD

A

Asthma - nocturnal, post - exercise. COPD - early am

257
Q

History of atopy in asthma and COPD

A

Asthma - often. COPD - no

258
Q

Bronchidilator reversibility in asthma and COPD

A

Asthma - complete / nearly so. COPD - partial

259
Q

Steroid resonsiveness of asthma and COPD

A

Asthma - strong. COPD - weak

260
Q

Progressive deterioration of asthma and COPD

A

Asthma - uncommon. COPD - typical

261
Q

Anticholinergic responsivity of asthma and COPD

A

Asthma - beta-agonists better. COPD - best first-line treatment

262
Q

Beta-agonist responsivity in asthma and COPD

A

Asthma - very good. COPD - anticholinergics are better

263
Q

Purulent sputum in asthma and COPD

A

Asthma - uncommon. COPD - typical

264
Q

Smoking history in asthma and COPD

A

Asthma - variable. COPD - essentially always

265
Q

Spirometry

A

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

266
Q

Predicted values of spirometry

A

The normal results that your doctor would expect for people with the same height, weight, age, and sex as you

267
Q

Measured values of spirometry

A

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%.

268
Q

FVC

A

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.

269
Q

Number of measurements taken of FVC

A

Usually given 3 tries to perform test.

270
Q

FEV1

A

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.

271
Q

FEV1 in obstructive lung diseases

A

Is reduced to the FVC

272
Q

FEV1 in restrictive lung diseases

A

FVC and total lung capacity are all reduced. The ratio is normal or even higher.

273
Q

Diagnosis of COPD with spirometry

A

FEV1 < than 70% or 0.70

274
Q

Spirometry of asthma

A

FVC and total lung capacity are all reduced. The ratio is normal or even higher.

275
Q

Mild COPD

A

FEV1/FVC 80%. Reduce risk factors - immunizations. Add short-acting bronchodilators as needed

276
Q

Moderate COPD - stage II

A

FEV1/FVC <50%. Reduce risk factors - immunizations. Short-acting bronchodilators PRN. Add regular treatment with one or more long-acting bronchodilators. Rehabilitation

277
Q

Severe COPD - stage III

A

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.

278
Q

Very severe OPD - stage IV

A

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.

279
Q

Beta 2 agonists

A

Albuterol - work by relaxing the beta receptors in the muscles around the airways. Short-term. Work best in asthma

280
Q

Anticholinergic agents

A

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.

281
Q

Use of steroids in lung diseases

A

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.

282
Q

1st drug to use in COPD

A

Short-acting beta2-adrenergic, such as combovent agonists

283
Q

When is steroid use good for COPD

A

When exacerbations and then the FEV1 is very low <50%. Should be used sparingly.

284
Q

Common presentation of COPD

A

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.

285
Q

Importance of early diagnosis of COPD

A

To reduce mild symptoms and slow the progression of the disease

286
Q

Use of terms emphysema and chronic bronchitis

A

Declining in use due to their lack of specificity and overlapping descriptions. COPD is accepted term for both

287
Q

Target intervention for COPD

A

Smoking cessation

288
Q

Beta blockers and COPD

A

Theory has changed in use of beta blockers. Now, BB use with COPD pts is acceptable.

289
Q

Oral steroids and COPD exacerbation

A

Non tapered for a week; but a taper is more typically done, to avoid rebound bronchospasm.

290
Q

Treatment of COPD exacerbations

A

Look for exacerbations - steroids and antibiotic if purulent sputum and increased dyspnea and sputum volume. Chose 1st or 2nd line antibioitcs.

291
Q

Treatment of repeated exacerbations

A

Max out the bronchodilators; if FEV1 <50% predicted start inhaled corticosteroids.

292
Q

Oxygen therapy and COPD

A

Prescribe if pulse ox 88% on room air, rest, or with walking. Use for 15 hours a day.

293
Q

Polycythemia and COPD

A

Consider with pt taking ASA. Can be used to justify prescription of O2

294
Q

Depression and COPD

A

Be on alert for symptoms

295
Q

Management of COPD

A

Reduce symptoms, improve quality of life, remain active for as long as possible. Education, education, education!

296
Q

Smoking cessation and COPD

A

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

297
Q

Vaccinations for COPD

A

Influenza, pneumococcal pneumonia

298
Q

Oral corticosteroid use

A

Not recommended with COPD

299
Q

Antibiotic of choice in COPD exacerbation

A

Azithromax because broad-spectrum

300
Q

Prescription of oxygen and COPD

A

At stage IV and when SaO2 < 88%. Goal is SaO1 at rest of > 90%.

Comps - Mod 3 (5 decks)

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