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Complex Health I > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Parkinson’s disease is a

A

chronic, terminal/fatal disease

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2
Q

Dopamine levels are __________ and acetylcholine levels are __________ in patients with Parkinson’s disease.

A

low; high

Acetylcholine levels are normal, but in relation to dopamine levels they are considered high.

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3
Q

What is the cause of Parkinson’s disease?

A

The cause is unknown. There could be a genetic or environmental factor.

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4
Q

What are secondary causes of Parkinson’s disease?

A

Antipsychotic drugs, tumor, or trauma (pseudo Parkinson sx)

Antipsychotic drugs drop dopamine levels; taking pts off meds will stop sx

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5
Q

Parkinson’s disease affects motor, cognitive, and ADL function.

True or false?

A

True

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6
Q

Parkinson’s disease are at an increased risk for falls and injury?

True or false?

A

True

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7
Q

Symptoms of Parkinson’s disease

A

-mask-like, blank expression
-pill rolling tremors (occurs most often at rest)
-loss of normal arm swing while walking
-shuffling, propulsive gait
-muscle rigidity (increased resistance to passive movement)
-cog wheel, jerky slow movement
-bradykinesia
-drooling

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8
Q

Risk factors for Parkinson’s disease

A

Onset between 40-70yo, male, possible predisposition, exposure to toxins/antipsychotic meds

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9
Q

Brain autopsy of patient with Parkinson’s disease reveals

A

lewy bodies and neuronal loss in the substania nigra

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10
Q

How is Parkinson’s disease diagnosed?

A

Providers diagnose by ruling out other diseases

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11
Q

Stages of Parkinson’s disease

A

Stage 1 through 5
Stage 1 is mild
Stage 5 is completely dependent

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12
Q

Medications used to treat Parkinson’s disease increase dopamine and decrease acetylcholine.

True or false

A

True

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13
Q

Dopaminergics

A

Trigger dopamine receptors to function

Ex: Levodopa-carbidopa

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14
Q

What does Levodopa do? What does Carbidopa do?

A

Levodopa is converted into dopamine. Carbidopa is used to decrease breakdown and help levodopa cross blood brain barrier.

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15
Q

How long do dopaminergics work? What is the next step?

A

Dopaminergics stop working after 5 years of use. Start addressing acetylcholine levels.

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16
Q

What medication is used to treat tremors in pts with Parkinson’s diease?

A

Triexphenidyl/Benztropine

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17
Q

What side effects should you look out for with Triexphenidyl/Benxtropine?

A

Monitor for dry mouth, constipation, urinary retention, and possible confusion.

Triexphenidyl/Benztropine has DRYING effects.

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18
Q

What Catechol-O-methyltransferase (COMT) inhibitors is taken with Levodopa and why?

A

Entacapone

Only taken w/ Levodopa to decrease the breakdown of Levodopa.

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19
Q

MAO-B inhibitors are last resort because they interact w/everything. Increases dopamine. What foods should the patient avoid?

A

Foods with tyramine

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20
Q

Pts with Parkinson’s disease take antivirals to stimulate the release of dopamine and prevent its reuptake. What is a common antiviral taken by these pts?

A

Amantadine

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21
Q

What procedures are completed when PD pts do not respond to meds?

A

Ablative procedures (thalamotomy, pallidotomy), deep brain stimulation, and cell transplantation

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22
Q

Possible complications for PD pts & nursing care

A

Aspiration pneumonia
-Swallowing precautions, diet per speech therapy, maintain weight, high protein supplements

Altered cognition/mobility
-Provide safe environment
-PD pts require more time to complete tasks (walking, answering questions)

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23
Q

Huntington’s disease is a

A

Chronic, terminal/fatal disease

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24
Q

Is there a cure for Huntington’s disease?

A

no

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25
Q

Is Huntington’s disease hereditary?

A

yes, autosomal dominant

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26
Q

Risk factors for Huntington’s disease

A

genetics, Caucasian, 30-50yo (male or female)

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27
Q

This disease has an imbalance of dopamine, GABA, and glutamate from the basal ganglia.

A

Huntington’s disease

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28
Q

The earlier the sx associated with Huntington’s disease present; the more severe the disease is. Death will be sooner.

True or false

A

True

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29
Q

How quickly can juvenile sx cause death in HD?

A

within 10 years

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30
Q

Symptoms of Huntington’s disease

A

-progressive dementia, personality changes, mood swings, depression
-slurred speech, difficulty swallowing, weight loss
-Choreiform movements (uncontrolled, rapid movements/unsteady gait when sitting still)

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31
Q

Diagnostic testing for Huntington’s disease

A

Genetic testing, CT for frontal horn enlargement, MRI, and PET scan

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32
Q

Is there any neuroprotective/neurorestorative treatment available for Huntington’s disease?

A

No. Only supportive and symptomatic treatments.

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33
Q

Medications used for Huntington’s disease

A

-Tetrabenazine to suppress involuntary chorea movements. S/E include new or worsening depression, drowsiness, nausea, restlessness
-Other antipsychotics for psych sx

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34
Q

Possible complications for HD pts & nursing care

A

Complications: Decisional conflict r/t having children, aspiration pneumonia, altered cognition and mobility

Nursing care: Suicide prevention, encourage planning for residential and EOL care

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35
Q

Amyotrophic Lateral Sclerosis/ALS is also known as

A

Lou Gehrig’s Disease

Stephen Hawking had this disease.

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36
Q

ALS is a

A

chronic, progressive neurodegenerative disease

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37
Q

Is there a cure for ALS?

A

No

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38
Q

Is ALS fatal?

A

Yes. Most die within 3-5 years from start of sx.

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39
Q

ALS targets the CNS and brain. There is a loss of

A

voluntary movement control and weakness

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40
Q

What causes ALS?

A

the cause is unknown

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41
Q

Risk factors for ALS

A

more common in men, 40-60yo

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42
Q

Symptoms of ALS

A

Causes progressive muscle weakness and wasting. Clients lose the ability to speak, eat, and eventually breathe (paralysis of respiratory muscles).

Muscle atrophy, muscle weakness, dysarthria (uncoordinated speech), and dysphagia (difficulty swallowing)

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43
Q

What medications do ALS pts take & why?

A

Riluzole to decrease GABA and
Edaravone to reduce oxidative stress

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44
Q

ALS complications

A

Death anxiety r/t impending progressive loss of function leading to death

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45
Q

Nursing care for ALS pts

A

Palliative care for symptom management
Ex: Home health, EOL care

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46
Q

Multiple Sclerosis/MS is a

A

chronic, progressive, neurodegenerative disease

Autoimmune inflammatory as well

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47
Q

Is there a cure for Multiple Sclerosis/MS?

A

no

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48
Q

Do pts with Multiple Sclerosis/MS have a shorter lifespan?

A

No. They have a normal lifespan.

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49
Q

Risk factors for Multiple Sclerosis/MS

A

Women 2x greater risk than men, 20-50yo, whites of northern European ancestry

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50
Q

Disease that targets the brain & spinal cord (myelin sheath). Demyelination of white matter leads to decreased flow of nerve impulses.

A

Multiple Sclerosis/MS

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51
Q

Symptoms of Multiple Sclerosis/MS

A

-intention tremors
-fatigue
-diplopia
-Uthoff’s sign
-Nystagmus
-tinnitus
-decreased sexual function
-gait changes
-muscle spasticity

Over time can lead to tetraplegia (quadriplegia)

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52
Q

What causes Multiple Sclerosis/MS?

A

the cause is unknown

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53
Q

What can make Multiple Sclerosis/MS symptoms to worsen?

A

Symptoms worsen in extreme heat & cold, stress, infection, fatigue, and pregnancy

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54
Q

What medications do MS pts take?

A

-Interferon beta 1a and beta 1b (Causes flu like sx)
-Baclofen, dantrolene, diazepam (muscle relaxants)
-Medical marijuana to decrease pain, stiffness, and spasticity
-Dalfampridine to improve walking/gait
-Dexamethasone is a steroid to manage relapses (Increased risk of infection)

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55
Q

Why should MS pts avoid fatigue and overheating?

A

To minimize exacerbations

-If exacerbations are minimized, pt can live a relatively normal life
-w/ every exacerbation, MS gets worse

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56
Q

What does CSF of MS pts reveal?

A

CSF reveals elevated protein levels & slight increase in WBCs

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57
Q

What does a MRI of MS pts reveal?

A

MRI reveals plaques of the brain and spine

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58
Q

Evoke potential testing for MS pts

A

Give stimulation and see if sense is decreased

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59
Q

What is the cause of migraines?

A

Many triggers including genetics

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60
Q

Patho of migraines

A

Cerebral artery vasodilation –> prostaglandins released –> brain tissue inflammation

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61
Q

Symptoms of migraines

A
  • Photophobia and phonophobia (sensitivity to sounds)
  • Nausea and vomiting
  • Stress and anxiety
  • Unilateral pain, often behind one eye or ear
  • Health history and family history for headache patterns
  • Alterations in ADLs for 4-72 hr
  • Manifestations that are similar with each headache
62
Q

Three types of migraines

A

Migraine w/aura (classic migraine)
Migraine w/o aura (common migraine)
Atypical migraine

63
Q
  • Prodromal stage: Aware it’s coming, irritated, food cravings, depressed
  • Aura stage: minutes to hours, n & t of face, mouth, acute confusion, vision problems (light flashes, bright spots)
  • Second stage: Severe, throbbing, incapacitating HA
  • Third stage (4-72hr): Dull HA
  • Recovery: Pain & Aura subsiding, increased muscle spasms & myalgia
  • Older adult: Visual Migraine, Aura w/o pain
A

Migraine w/aura (classic migraine)

64
Q
  • Pain is aggravated by physical activity.
  • Unilateral, pulsating pain.
  • One or more manifestations present: photophobia, phonophobia, N/V
  • Persists for 4-72 hr. Often occurs in early AM, during stress, or with premenstrual tension or fluid retention.
A

Migraine w/o auro (common migraine)

65
Q
  • Status migrainous: >72hrs
  • Migrainous infarction: Neuro sx for > 7 days, imaging may show ischemic infarct.
  • Unclassified: Does not fit other criteria
A

Atypical migraine

66
Q

Risk factors of migraines

A

All ages, women affected more than men. May be associated with other conditions like colds, allergies, stress, low BS, or muscle tension.
Migraine sufferers are at r/f stroke & epilepsy.

67
Q

What are preventative options for migraines?

A

-NSAIDS
-Beta Blockers-Take even when asymptomatic for prevention to prevent vascular changes.
-Botox

68
Q

Migraine abortive therapy options during aura or soon after aura begins

A

-NSAIDS (ibuprofen), Tylenol (acetaminophen),
-Antiemetics: Reglan (metoclopramide)

For Severe migraines
-Triptans: produce vasoconstrictive effect
Imitrix (sumatriptan) contraindicated in heart disease
-Ergotamine preparations with caffeine: vasoconstriction & decreases inflammation

69
Q

Complications & nursing care for migraines

A
  • Focus on pain mgmt during HA (dark environment, HIB elevated, meds)
  • HA diary for patterns & triggers
  • Trigger avoidance
  • Avoid foods with tyramine (pickles, caffeine, beer, wine, ages cheese, artificial sweeteners) & foods with MSG
  • Manage anger & conflict
  • Avoid glare & flickering lights
  • Adequate sleep/rest
  • Avoid environmental triggers like odors, perfumes, & tobacco smoke
  • Yoga, meditation, exercise, acupuncture, external trigeminal nerve stimulator (wearable head band that stimulates branches associated with HA (not to be used for >20min/day)
70
Q

Systemic Lupus Erythematosus (SLE) is a

A

chronic, progressive autoimmune disorder

71
Q

Lupus exacerbations accelerate

A

organ damage

72
Q

What is the cause of Lupus?

A

Genetic susceptibility not clearly identified. Triggers include infection, injury, drugs, hormones, and exposure to environmental substances, esp. UV light.

73
Q

Most common cause of death in Lupus pts

A

CKD and CV impairment

74
Q

Symptoms of Lupus

A

Onset of sx is slow. Avg time from initial mild sx to actual dx is 6 years.

  • Chronic fatigue
  • Recurrent fevers with unknown origin
  • Persistent joint & muscle pain, swelling, tenderness, weakness
  • Alopecia
  • Blurred vision
  • Pleuritic pain, pericarditis (pericardial friction rub)
  • Anorexia/weight loss, anemia
  • Depression
  • Butterfly rash
  • Raynaud’s phenomenon
75
Q

Risk factors of Lupus

A
  • Present in women (30-44yo initial dx) 10x more frequently than men
  • Incidence declines in females following menopause which suggests estrogen (childbearing years) as a trigger
  • African Americans compared to whites in 8:1
76
Q

Labs and diagnostics of Lupus

A
  • Skin Biopsy – used in dx. Lupus cells & cellular inflammation is seen.
  • Antinuclear antibodies (ANAs) - (+) titers in 95% of clients
  • ESR – inflammatory biomarker, elevated
  • BUN/Creat – Increased with kidney involvement
  • UA – protein, casts, & RBCs (kidney involvment)
  • CBC – pancytopenia
77
Q

Medications for Lupus pts

A
  • NSAIDs: used to reduce inflammation/pain. Contraindicated with kidney disease.
  • Corticosteroids: prednisone used for inflammation & immunosuppression. Monitor fluid status for fluid retention, HTN, impaired kidney function. Do not stop abruptly, must taper dosage. Risk for fracture. Watch for hyperglycemia.
  • Immunosuppressant agents: DMARDs (methotrexate), belimumab, azathioprine. Monitor for infection secondary to immunosuppression. Monitor liver enzymes (AST/ALT)
  • Antimalarial: hydroxychloroquine used to suppress synovitis, fever, & fatigue.
78
Q

Education to provide to Lupus pts

A
  • Wear a wide‐brimmed hat, long‐sleeve shirt, and long pants when outdoors.
  • Avoid UV and prolonged sun exposure. Use sunscreen when outside and exposed to sunlight.
  • Use mild protein shampoo and avoid harsh hair treatments.
  • Use steroid creams for skin rash.
  • Report peripheral and periorbital edema promptly.
  • Report evidence of infection related to immunosuppression.
  • Avoid crowds and individuals who are sick, because illness can precipitate an exacerbation.
  • Understand the risks of pregnancy with lupus and treatment medications.
79
Q

Obstructive Sleep Apnea is defined as

A

Breathing stops during sleep for greater than 10 seconds and at least 5 times/hr

80
Q

Apnea leads to __________ gas exchange (hypoxemia), __________ blood CO2 levels (hypercapnia), __________ pH causing the sleeper to wake up & correct obstruction. Cycle repeats throughout the night.

A

Apnea leads to decreased gas exchange (hypoxemia), increased blood CO2 levels (hypercapnia), decreased pH causing the sleeper to wake up & correct obstruction. Cycle repeats throughout the night.

81
Q

What is the cause of OSA?

A

Upper airway obstruction by the soft palate or tongue

82
Q

Expected OSA findings

A

-snoring
-excessive daytime sleepiness
-inability to concentrate
-irritability
-bedwetting or excessive urination at night
-reduced sex drive
-fatigue
-depression
-pharyngeal edema
-Chronic OSA: increased risk of HTN, stroke, cognitive deficits, weight gain, DM, pulmonary and CV disease

83
Q

OSA risk factors

A

obesity, large uvula, short neck, smoking, enlarged tonsils or adenoids, oropharyngeal edema

84
Q

Diagnostics for OSA

A

-STOP Bang Sleep Apnea questionnaire
-Pulmonary function tests (PFTs)
-Overnight sleep study (Polysomnography)

85
Q

Meds for OSA

A

Modafinil

Not the first line of therapy. Promotes daytime wakefulness. Does not treat OSA cause. May also help pts with narcolepsy.

86
Q

Surgical management of OSA

A

Adenoidectomy, uvulectomy, or uvulopalatopharyngoplasty

Severe cases may need trach

87
Q

Non-surgical management of OSA

A

Change of sleep position, weight loss, decrease alcohol use, positive pressure ventilation, avoiding sedating meds, breathing machines

88
Q

Bilevel airway pressure - More pressure when breathing in, less pressure when breathing out

A

BiPAP

89
Q

Continuous positive airway pressure - constant airflow

A

CPAP

90
Q

Auto titrating positive airway pressure - algorithmic control

A

APAP

91
Q

Intermittent and reversible airflow obstruction. Affects airways only, not alveoli. Inflammation and bronchconstriction.

A

asthma

92
Q

What triggers asthma symptoms?

A

allergens, cold air, dry air, airborne particles, ASA/NSAIDs, exercise, and food w/ MSG

93
Q

Asthma symptoms

A

-audible wheeze, increased respiratory rate, SOB
-Increased cough
-Use of accessory muscles
-Barrel chest
-Long breathing cycle
-Cyanosis
-Hypoxemia
-CO2 retention
-Increased mucus

94
Q

Emergent, life threatening situation for pts with asthma. Symptoms do not respond to usual treatment in 30 minutes.

A

Status asthmaticus

95
Q

Asthma risk factors

A

genetic, environmental

96
Q

Labs for asthma

A

ABG’s- low PAO2, low PACO2 initially, & increased PACO2 later in attack

97
Q

Diagnostics for asthma

A

Pulmonary function tests (PFTs)
Forced vital capacity (FVC)
Forced expiratory volume in first second (FEV1)
Peak expiratory flow rate (PEFR)

98
Q

Asthma meds

A

Bronchodilators: Short-Acting Beta2 Agonists (SABA) & Long-Acting Beta2 Agonists (LABA), Cholinergic Antagonists, Anti-inflammatories, Corticosteroids, Cromone, and Leukotriene Modifier

99
Q

Cause bronchodilation through relaxing bronchiolar smooth muscle by binding to and activating pulmonary beta2 receptors

A

bronchodilators- SABA and LABA

100
Q

Bronchodilator that primary use is a fast-acting reliever (RESCUE) drug to be used either during an asthma attack or just before engaging in activity that triggers an attack

A

Short-Acting Beta2 Agonist (SABA)

Ex: albuterol and levalbuterol

101
Q

Albuterol pt teaching

A

Carry drug with them at all times because it can stop or reduce life-threatening bronchoconstriction

102
Q

Levalbuterol pt teaching

A

-Monitor heart rate because excessive use causes tachycardia
-Teach pt technique for using the MDI or DPI

103
Q

Bronchodilator that causes bronchodilation through relaxing bronchiolar smooth muscle by binding to and activating pulmonary beta2 receptors. Onset of action is slow with long duration. Primary use is PREVENTION of an asthma attack.

A

Long-Acting Beta2 Agonist (LABA)

Ex: Salmeterol

104
Q

Salmeterol pt teaching

A

Do not use as a reliever drug

105
Q

Spacers are helpful for what pts?

A

children, confused, elderly, and disabled pts

106
Q

Causes bronchodilation by inhibiting the parasympathetic nervous system, allowing the sympathetic system to dominate, releasing norepinephrine that activates beta2 receptors. The purpose is to both relieve & prevent asthma and improve gas exchange.

A

Cholinergic Antagonists

Ex: ipratropium and tiotropium

107
Q

Tiotropium pt teaching

A

Increase daily fluid intake because the drugs cause mouth dryness

108
Q

Disrupt production pathways of inflammatory mediators. The main purpose is to prevent an asthma attack caused by inflammation or allergies (controller drug).

A

Corticosteroids

Ex: Fluticasone, Beclomethasone, Budesonide, and Prednisone

109
Q

Fluticasone, Beclomethasone, & Budesonide (MDI inhaled drug) pt teaching

A

Drug daily even when no symptoms are present, good oral care & check for lesions

110
Q

Prednisone pt teaching

A

Increases risk of infection, do not suddenly stop the drug for any reason

111
Q

Blocks the leukotriene receptor, preventing the inflammatory mediator from stimulating inflammation. Purpose is to prevent asthma attack triggered by inflammation or allergens.

A

Leukotriene Modifier

112
Q

MDI

A

Metered dose inhaler

113
Q

DPI

A

Dry powder inhaler

114
Q

Management of asthma - step wise method used for prescribing

A

ASTHMA

Adrenergics (Beta2 Agonists)
Steroids
Theophylline
Hydration (IV)
Mask O2
Anticolinergics

115
Q

Ace inhibitors can cause

A

angioedema

116
Q

Also called atopic allergy, hay fever, most common type

1st exposure –> T lymphocytes tell B lymphocytes to create IgE specific to allergen –> Mast cells (tissue) basophils (blood stream) have IgE receptors with lots of IgE attached —> allergen binds to IgE –> causes degranulation (allergic cascade)

A

Patho of allergies

117
Q

Allergies Type I

A

Hay fever, allergic asthma, anaphylaxis, angioedema

118
Q

What causes allergies?

A

Excessive production of immunoglobulin E (IgE) antibody class

119
Q

Allergens are contracted by

A

inhalation, ingestion, or injection

120
Q

Symptoms of allergies

A

Sneezing, runny nose, & red, watery, itchy eyes

Can be seasonal

121
Q

Are allergies genetic?

A

yes

122
Q

Allergy labs

A

ABG’s

123
Q

Allergy diagnostics

A

Skin prick test (SPT), Intradermal skin test, Blood tests, Physician supervised challenge tests, Patch tests

124
Q

Allergy Meds

A
  • Supportive therapy – no nasal washing!
  • Complementary and alternative therapy - vitamin C, zinc
  • Steroids - Used for anti-inflammatory effect and act to decrease edema in the bronchial airways and decrease mucus secretion.
  • leukotriene inhibitors – Montelukast (Singulair)
  • Antihistamines – Diphenhydramine (Benadryl)
  • Eye decongestants
  • Decongestants – Avoid use of nasal decongestant sprays regularly because they can cause a rebound effect.
  • Bronchodilators
  • Anti-inflammatories
  • Antipyretics
  • Mast cell stabilizers
125
Q

Allergy procedures

A

Immunotherapy- Allergy Shots: Subcutaneous injection of low amount of allergens, then gradual increased amount.

126
Q

Allergy complications

A

Angioedema & Anaphylaxis can be fatal - Potential for airway obstruction as a result of mucosal swelling & anxiety as a result of cerebral hypoxia and threat of death.

Uticaria (hives)

127
Q

What causes Tuberculosis/TB?

A

Mycobacterium tuberculosis - Airborne droplets inhaled

128
Q

Is TB contagious?

A

Only with symptoms

129
Q

TB Risk Factors

A
  • Frequent contact with untreated person
  • Immunocompromised
  • Living in crowded areas
  • Older homeless adults
  • IVDU or ETOH abusers
  • Lower socioeconomic status
  • Foreign immigrants
130
Q

TB disease course and findings (sx)

A

Most common bacterial infection worldwide
Airborne, May be infected with bacillus, but not have active TB, slow onset
* Persistent cough, mucopurulent sputum, blood streaks (hemoptysis)
* Progressive fatigue, lethargy
* Nausea, anorexia, and/or unintended weight loss
* Irregular menses
* Low-grade fever, night sweats, chills

131
Q

Symptom screening - at this time, do you have any of these symptoms?
1. Coughing for more than 2-3 weeks?
2. Coughing up blood?
3. Weight loss of more than 10 pounds for no known reason?
4. Fever of 100 degrees Fahrenheit for over 2 weeks?
5. Unusual of heavy sweating at night?
6. Unusual weakness or extreme fatigue?

A

Standard screening questions for TB

132
Q

TB Labs & Diagnostics

A

-NAA test - secretions
-Sputum culture
-BCG vaccine & chest Xray - think about Yule
-Tuberculin (Mantoux) test - skin test
-Blood analysis - QuantiFERON-TB Gold (what I had for the program)

133
Q

TB Meds

A

Combination drug therapy w/ strict adherence!

Isoniazid- kills actively growing mycobacteria & inhibits growth
Take on empty stomach, avoid alcohol, liver toxicity

Rifampin- kills slower growing organisms
Orange-reddish staining of skin, urine, and other secretions. Contact lenses will become permanently stained. Reduces effectiveness of oral contraceptives.

Pyrazinamide- can effectively kill organisms residing within very acidic environment
Makes gout worse, photosensitivity, and increases risk of sunburn

Ethambutol- inhibits bacterial RNA synthesis, thus suppressing bacterial growth
Can cause optic neuritis

134
Q

Nursing Care for TB pts

A

-Promote airway clearance by increasing fluids, using incentive spirometer, TCBD
-Decrease drug resistance and infection spread
-Airborne precautions in hospital
-No airborne precautions at home; but family should be tested
-Drug compliance is very important
-Improve nutrition
-Manage fatigue and anxiety

135
Q

COPD is the name we use for a person w/

A

emphysema and bronchitis

136
Q

Chronic inflammation of the bronchi & bronchioles

A

chronic bronchitis

137
Q

Decreased lung elasticity and hyperinflation of the lung

A

emphysema

138
Q

What causes COPD?

A

smoking

139
Q

COPD Risk factors

A

-genetic/environmental
-smoking
-asthma (12x risk for COPD)
-AAT deficiency (gene is recessive)

140
Q

Sx of COPD

A

-easily fatigued
-frequent respiratory infections
-use of accessory muscles
-orthopneic
-thin in appearance
-Cor Pulmonale (R sided heart failure)
-wheezing
-pursed lip breathing
-chronic cough
-barrel chest
-dyspnea
-prolonged expiratory time
-clubbing

141
Q

COPD Labs

A

-ABGs
-sputum samples
-CBC
- hemoglobin and hematocrit
-serum electrolytes
-serum AAT (rule out genetic disorder)

142
Q

COPD Diagnostics

A

PFTs
Chest X-ray

143
Q

COPD Meds

A

Same as asthma
-beta adrenergic agents
-cholinergic antagonists
-methylxanthines
-corticosteroids
-NSAIDs
-mucolytics

144
Q

COPD Procedures

A

-lung reduction surgery
-lung transplant surgery (rare)

145
Q

COPD complications

A

hypoxemia and acidosis

146
Q

Nicotine replacement options to help with smoking cessation

A

skin patches, gum, lozenges, inhaler, nasal spray, varenicline (Chantix), and bupropion

147
Q

Varenicline (Chantix) will decrease cravings. Should be taken with a full glass of water. Side effects include

A

hallucinations, manic behavior, impaired judgement, nausea, and abnormal dreams

148
Q

Patient & Family Education- Smoking Cessation

A

-Make a list of the reasons why you want to stop smoking
-Set a date and keep it
-Ask for help
-Consult your health care provider about nicotine replacement therapy
-Remove ashtrays and lighters
-Reward yourself w/ money you save from not smoking
-Avoid places that might tempt you to smoke
-Find activities that keep your hands busy
-Take five deep breaths when you feel the urge to smoke
-Keep plenty of healthy, low-calorie snacks
-Drink at least 8 glasses of water each day
-Begin an exercise program
-Don’t beat yourself up for backsliding
-Think of each day w/o tobacco as a major accomplishment

149
Q

Diaphragmatic or Abdominal Breathing

A

-Lie on your back w/ knees bent. If you can not lie comfortably, sit in a chair.
-Place your hands or book on your abdomen to create resistance
-Begin breathing from your abdomen while keeping chest still.

150
Q

Pursed Lip Breathing

A

-Close your mouth and breathe in through your nose
-Purse your lips as you would to whistle. Breathe out slowly through your mouth w/o puffing your cheeks. Spend at least twice the amount of time it took to breath in.
-Use abdominal muscles to squeeze every bit of air out you can

151
Q

What is a vibratory positive expiratory pressure device used for in COPD pts?

A

It is used to help pts remove airway secretions.

Complex Health I (53 decks)

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