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153 Cards in this Set
- Front
- Back
Opioid Analgesics |
-Use to treat moderate to sever pain -Attach to opiate receptors in CNS -Change perception of an response to pain -Agonist, agonist-antagonists, antagonists |
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Opioid Agonists |
-Morphine (prototype) -Fentanyl (Duragesic) -Meperidine (Demerol) -Codeine -Oxycodone (OxyContin) -Hydromorphone (Dilaudid) |
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Expected Action of Opioid Agonists |
-Acts on opiate receptors: mu, kappa, delta -Activation of mu receptors produces analgesia, respiratory depression, euphoria, sedation -Activation of kappa receptors produces analgesia, sedation, decreased GI motility |
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Therapeutic use |
-Relief of moderate to secure pain -Sedation -Reduction of bowel motility -Cough suppression (codeine) |
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Routes |
-Morphine: PO, SQ, IM, IV, rectal, epidural, intrathecal -Fentanyl: IV, IM, transmucosal, transdermal -meperidine: PO, SQ, IM, IV -Codeine: PO, SQ, IM, IV -Hydromorphone: PO, SQ, IV -Oxycodone: PO, rectal -Methadone: PO, SQ, IM |
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Adverse effects: |
-Respiratory depression- very important to watch for -Constipation: VERY COMMON -Orthostatic hypotension -Urinary retention -Cough suppression -Sedation: ALSO VERY COMMON -Biliary colic: Do NOT give morphine to people with biliary colic or history of same -Nausea/ vomiting: give anti-emetic -Opioid OD triad: coma, resp dep, pinpoint pupils |
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Contraindications |
-Morphine: biliary tract surgery: other opioids can be used -Premature infants: suppresses respiration -Meperidine: kidney failure- can cause toxicity and seizures -Caution! -Pts with respiratory probs -Pregnant, laboring (inhibits uterine contractions, neonatal respiratory suppression) -Extreme obesity (prolonged effects) -IBD (ileus, megacolon) -Enlarged prostate (urinary retention) -Hepatic or renal disease |
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Interactions |
-CNS depressants: additive effect -Anticholinergic agents: increase urinary retention and constipation -Antihypertensives: additive effect -Meperidine: use with MAO inhibitors can cause hyperpyrexic coma |
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Nursing considerations |
-Monitor VS (especially RR & BP) If RR <12, hold -Assess pain level regularly -Follow controlled substance procedures: 2 nurse check -Administer IV slowly- over 2-5 min -Be sure opioid antidote [naloxone (Narcan)], and resuscitation equipment are available -Cancer puts should have scheduled round the clock dosing -Those discontinuing PCA put and transitioning to PO meds should have adequate PCA dosing until PO med is effective |
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Educating the pt |
-Teach -Don't increase dose w/o provider order -Don't discontinue med abruptly: withdrawal -If using PCA pump, teach pt is to pus -Teach that lockout makes OD impossible -Teach to use button before painful activities -Transdermal fentanyl takes several hours to achieve full effect |
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Evaluation |
-Pt should experience relief of moderate to severe pain -Cough suppression -Resolution of diarrhea |
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Opioid Agonist/antagonists |
-Butorphanol (Stadol)- prototype -Nalbupine (Nubain) -Buprenorphine (Buprenex) -Pentazocine (Talwin) |
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Opioid agonist/antagonist |
-Act as antagonist on mu, agonists on kappa, except buprenorphine (Buprenex) which is the opposite -Lower potential for abuse -Less respiratory depression -Less analgesic effect -Used for moderate to severe pain, treatment of opioid dependence (buprenorphine), anesthesia, relief of labor pain (butorphanol) -All can be administered IV, some IM, SL, SQ, epidural |
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Adverse effects |
-Abstinence syndrome is used for treatment of opiate addiction and if sill using opioid treatment of opiate addiction and if still using opioid agonist -Abdoiminal pain, fever, anxiety -Do not give these to people who may be opioid dependent -Sedation, res dep -Dizziness, headache Caution: history of MI, kidney/liver disease, res dep, head injury, opioid dependence, |
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Interaction |
-CNS depressants: addictive effect -Opioid agonists: antagonize and reduce effects of opioid |
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Client teaching |
same as for agonist |
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Evaluation |
improvement of symptoms |
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Opioid Antagonists |
-Naloxon (narcan) MOST COMMON -Naltrexone (ReVia, Vivitrol), methylnaltrexone (Relistor) |
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Method of action |
Competes with opioids for opioid receptors |
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Use |
Antidote for opioid OD or adverse effects (ResDep, severe constipation |
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Route |
IV, IM, SQ, PO Iv is most common More than one dose may need to be given: half-life of opioid may exceed half-life of nolaxone Watch for return of pain, res deep, hypertension, tachycardia, nausea/vomiting |
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Adjuvants |
-Adjuvant meds for pain used with a primary pain med, usually an opioid agonist, to increase pain control without increasing does of opioid -Enhance effects of opioids -Not a sub for opioids -From several different classes of drug -Trycyclic antidepressants (amitriptyline-Elavil) depression and neuropathic pain -Anticonvulsants (carbamazepine-Tegretol; gabapentin (Neurotin) neuropathic pain -CNS stimulants (methylphenidate-Ritalin) augment analgesia and decrease sedation -Antihistamines (hydroxyzine-Vitaril) decrease nausea, anxiety, insomnia -Glucocorticoids (dexamethasone-Decadron )decrease intracranial pressure an spinal cord pressure pain -Bisphosphonates (etidronate-Didronel) decrease bone pain -NSAIDS (ibuprophen-Motrin) decrease inflammation |
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Upper respiratory tract |
resident flora |
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Lower respiratory tract |
sterile |
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Purpose of the Respiratory System |
-The upper resp system warms and filters air -Lungs- gas exchange -Lungs deliver o2 to and expels co2 from the cells |
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Upper Resp tract |
Nose
Sinuses and nasal passages Pharynx tonsils Adenoids Larynx (epiglottis, glottis, vocal cords, cartilages) Trachea |
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Oropharynx |
Common passage for air and food Epiglottis: protects opening into larynx Closes over glottis at swallowing to prevent aspiration; leaf-shaped flap made of elastic cartilage covered with mucous membrane; attached to the entrance of the larynx; located behind the tongue at the top of the larynx; Function is to seal off the windpipe during eating; helps with some aspects of sound production in certain languages |
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Larynx |
two pairs of vocal chords |
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Trachea |
C-shaped rings of cartilage Lined by pseudo stratified ciliated epithelium |
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The purpose of the cilia (fine hairs) is to move the mucus (secreted continuously by goblet cells) back to the larynx |
True |
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Nasopharynx |
pharyngeal tonsils in posterior wall |
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Palatine tonsils |
lymphoid tissue in posterior portion of the oral cavity |
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Nasal cavity |
Warming and moistening of air Foreign material trapped by mucous secretions |
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Lungs |
enclosed within the thoracic cage Ventilation occurs with movement of the walls of thoracic cage and its floor (diaphragm) Inspiration requires energy, but expiration is passive. The left lung has an upper and lower lobe. The right lung has upper, middle, and lower lobes |
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Pleura |
the serous lining of the thoracic cavity (parietal pleura) and lungs (visceral pleura) This pleural fluid allows of rest movement between the two |
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Mediastinumm |
contains the heart, thymus, aorta, vena cava, and esophagus |
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Bronchi & Bronchioles |
lined with cells covered with cilia Bronchioles lead to the alveolar ducts and sacs and then the alveoli where the gas exchange takes place |
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Lower Respiratory Tract |
Bronchial tree (continuous branching) -Trachea branching into: right and left bronchi secondary bronchi bronchioles alveolar ducts alveoli: lined by simple epithelium Type 1: structure (epithelial cells) Type 2: surfactant to reduce surface tension and maintain inflation Alveoli are the end-point for inspired air & the Site of gas exchange |
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Type 2 alveoli |
secrete surfactant (phospholipid sticky substance that lines the surface and reduce surface tension and maintain inflation of alveoli) premature babies have very little surfactant |
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Respiration |
the process of gas exchange between atmospheric air and the blood at the alveoli, and between the blood cells and the cells of the body via perfusion in the capillaries Exchange of gasses occurs because of differences in partial pressures Oxygen diffuses from the air into the blood at the alveoli to to be transported to the cells of the body Carbon dioxide diffuses form the blood into the air at the alveoli to be removed from the body |
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Pulmonary bronchial circulation |
-Facilitates gas exchange -Delivers nutrients to lung tissue -Acts as a reservoir for left ventricle -Serves as filtering system that removes clots, air, & other debris from circulation |
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Bronchial circulation |
-Entire cardiac output from right ventricle goes into lungs -Pulmonary circulation has lower pressure and resistance than the systemic circulation -Increased delivery of blood to the lungs does not normally increase the mean pulmonary artery pressure -Every segment bronchus, bronchioles has an accompanying artery -Form a net of pulmonary capillaries around the alveolus -Capillary wall and thin basement membrane frequently fuses with basement membrane of alveolar septum -Gas exchange occurs across this membrane with normal perfusion -Any disorder that thickens the membrane impairs gas exchange |
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Pulmonary vein |
-Each pulmonary vein drains several pulmonary capillaries -Leave the lungs at the hila where it enters the left atrium -Pulmonary veins have no valves -Not all capillaries drain into their own venous system, some empty into pulmonary vein (Contribut to normal venous mixture of oxygenated vs. de-oxygenated blood) |
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Pulmonary capillaries around alveolus |
If there is good airflow to the alveoli, the blood flow will be good. The blood flow proficiency matching the airflow to the area. If the airflow to a particular area of the lung is restricted, the body will not send as much blood flow to the area. Ventilation will also adjust to circulatory changes of the lungs. IF blood flow is decrease to an area of the bronchioles, the bronchiole will constrict and allow less airflow to the area. |
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Lymphatic system |
-Deep and superficial lymphatic capillaries -Fluid and alveolar macrophages migrate from the alveoli to the terminal bronchioles, where they enter lymphatic system and are drained. |
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Ventilation |
-The thoracic cavity is an airtight chamber -Inspiration: contration of the diaphragm -Expiration: with relaxation, the diaphragm moves up and intrathoracic pressure increases; elastic recoil of the lungs -Inspiration normally is 1/3 of the respiratory cycle an expiration is 2/3 |
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Mechanics of breathing |
-Major accessory muscles -Elastic properties -Resistance to airflow |
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Major & Accessory muscles |
-Inspiration: Diaphragm: contraction creates neg. pressure External intercostal: contraction increases anterior-posterior diameter Accessory: Sternocleidomastoid: enlarge AP diameter of thorax Scalene muscles: do not work as efficiently as diaphragm Expiration: no major muscles; passive -abdominal and internal intercostal muscles assist |
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Surfactant |
-Lowers surface tension by coating the air-liquid interface of alveoli -Easier to inflate at low lung volumes (after expiration) than at higher volumes (after inspiration) -Keeps alveoli free of fluid -Plays role in inhibiting foreign pathogens |
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If surfactant is not produced in adequate amounts |
Alveolar surface tension increases, causing alveolar collapse, decreased lung expansion, increased work of breathing, severe gas-exchange abnormalities |
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Elastic Properties of Lungs/ Chest Wall |
-Elastin fivers in alveolar walls and surrounding the small airways and pulmonary capillaries -Elastic coil is tendency of lungs to return to the resting state after inspiration |
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Compliance |
-The measure of lung an chest wall distensibility -Defined as volume change per unit of pressure change -Increased compliance indicates that the lungs or chest walls abnormally easy to inflate an has lost some elastic recoil -Decrease indicates that the lungs or chest wall is abnormally stiff or difficult to inflate |
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Airway Resistance |
-Determined by length, radium, and cross-sectional area of the airways -Density, viscosity, and velocity of the gas -Bronchoconstriction increases airway resistance Stimulation of parasympathetic receptors in bronchial smooth muscle an by numerous irritants and inflammatory mediators -Airway resistance increased by edema of bronchial mucosa and by airway obstruction such as mucus, tumors, or foreign bodies -Bronchodialation: caused by B2-Adrenergic receptor stimulation |
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Work of Breathing |
-Determined by muscular effort (and therefore O2 and energy) required for ventilation -Work of breathing increases significantly in diseased that disrupt the equilibrium between forces exerted by the lung and chest wall -Lung compliance decreases, chest wall compliance decrease, airways are obstructed -Increase in work of breathing can result in marked increase in O2 consumption and inability to maintain ventilation |
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Tidal volume (TV) |
The amount of air exchanged with quiet inspiration and expiration Amount of air entering lungs with each normal breath 500 mL |
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Residual Volume (RV) |
volume of air remaining in lungs after max respiration 1200 mL |
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Vital Capacity (VC) |
Maximal amount of air that can be moved in and out of the lungs with a single force inspiration and expiration Maximal amount of air expire following a maximal inspiration 4600 mL |
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Total lung capacity (TLC) |
Total volume of air in the lungs after maximal inspiration 5800 mL |
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Inspiratory reserve (IRV) |
Max amount of air that can be inhaled in excess of normal quiet inspiration 300 mL |
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Expiratory Reserve (ERV) |
Max volume of air expired following a passive expiration 1100 mL |
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Ventilation/ PerfusionRe |
-Gas exchange depends on approximately even distribution of gas (ventilation) and blood (perfusion) -Greatest vol of pulmonary blood flow normally will occur in the gravity-dependent areas of the lung -Body position effects the distribution of pulmonary blood flow -Relationship between ventilation and perfusion is expressed as a ratio: ventilation-perfusion ration (V/Q) (The amount by which perfusion exceeds ventilation under normal conditions is 0.8. |
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PO2 |
partial pressure of o2 |
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PCO2 |
partial pressure of carbon dioxide |
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Ventilation |
-Process of inspiration and expiration -Airflow depends on pressure gradient (Boyle's law) -Air always moves from high to low pressure -Atmospheric pressure is higher than alveoli pressure- Inspiration: air moves form atmosphere into lungs -Pressure in alveoli is higher than atmosphere: Expiration: air moves form lungs into atmosphere |
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Oxygen trasport |
-Small amount dissolves in plasma -Remainder binds to hemoglobin Partial pressure of o2 molecules in alveolar gas is much greater than that in capillary blood which promotes rapid diffusion down the concentration gradient form alveolus not the capillary |
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Determinants of Arterial Oxygenation |
-As o2 diffuses, it dissolves in plasma -Exerts pressure (partial pressure of o2 in arterial blood (PAO2) -As PAO2 increases, o2 moves from plasma into RBCs; binds with hemoglobin -O2 continues to bind with hemoglobin until the hemoglobin-binding sites are filled or saturated -O2 continues to diffuse across the membrane, pressures equalize: Eliminate the pressure gradient across the membrane, thus diffusion stops. |
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Oxyhemoglobin association and dissociation |
-Binding of o2 to hemoglobin in lungs is called oxyhemoglobin or saturation of O2 -O2 released form hemoglobin in the body tissue at the cellular level is called desaturation -When polled on graph, it is called oxyhemoglobin dissociation curve |
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Hypercapnia |
-Carbon dioxide levels in the blood increase -Carbon dioxide easily diffuses not CSF -Lowers PH and stimulates respiratory center -Increased rate and depth of respirations (Hyperventilation) -Caused respiratory acidosis- Nervous system depression |
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Hypoxemia |
-Decrease in Oxygen -Chemoreceptors respond -Importan control mechanism in individuals with chronic lung disease- Move to hypoxic drive |
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Hypoxia |
Respiratory and metabolic acidosis (deficient tissue oxygenation) |
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Hypoxic Drive |
In some individuals, such as those withCOPD, due to chronic increased CO2 levels, the chemoreceptors are no longerstimulated by elevated levels of CO2. It’s at that high level all the time, so the receptors “ignore” thelevels. We call these people CO2 retainers, and you’ll see elevated CO2 levelson their labs.In these people, the drive forrespiration becomes hypoxia. As CO2increased, O2 decreases. When there is asignificant decrease in O2 levels (hypoxia), the receptors are stimulated. This causes an increase in respirations,removal of CO2 and increase of O2. Respirations then decrease.We must be very careful in administeringoxygen to people with a hypoxic drive, because that increased O2 level willsuppress their breathing drive. They canactually stop breathing altogether if they receive too high a dose of O2. That is why it is very very important toadminister the prescribed rate of oxygen to those who have a hypoxic drive. |
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Hypocapnia |
Cause by low carbon dioxide concentration (low partial pressure of carbon dioxide) in blood May be caused by hyperventilation (excessive amounts of carbon dioxide expired Causes respiratory ALKALOSIS |
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Carbon Dioxide Transport |
Three Ways -Dissolved in plasma (PCO2) -As bicarbonate [CO2 is a gaseous waste product frommetabolism. The blood carries carbon dioxide to your lungs, where it isexhaled. More than 90% of carbon dioxide in your blood exists in the form ofbicarbonate (HCO3).] -Carbamino compounds (includes binding to hemoglobin) [Carbaminocompounds are any carbamic acidderivative formed by the combination of carbon dioxide with a free amino groupto form an N-carboxygroup, -NH-COOH, as in hemoglobin forming carbaminohemoglobin.] |
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Spirometry |
Pulmonary Function Test (PFT) -Tests pulmonary volumes and airflow times |
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Arterial blood gas determination |
Checks o2, co2, bicarbonate, serum pH |
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Oximetry |
Measures O2 saturation |
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Exercise tolerance testing |
For puts with chronic pulmonary disease |
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Radiography |
-Helpful in evaluating tumors -Evaluate infections |
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Bronchoscopy |
-perform biopsy -Check site of lesion or bleeding |
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Culture and sensitivity tests |
-Sputum testing for presence of pathogens -Determine antimicrobial sensitivity of pathogen |
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Common Cold (Infectious Rhinitis) |
-Viral infection of upper Res tract -Rhinovirus, adenovirus, parainfluenza virus, coronavirus -More than 200 -Spread through res droplets directly inhaled or speed by secretions on hands or contaminated objects |
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Symptoms of Common Cold |
-Mucous meds of nose and pharynx red and swollen, increased secretions, nasal congestion, copious watery discharge, sore throat, headache, slight fever, malaise-May spread to cause pharyngitis, laryngitis, acute bronchitis
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Treatment of Common Cold |
-Treatment is symptomatic, acetaminophen for fever and headache and decongestants (vasoconstrictors) to reduce the edema and congestion -Antihistamines reduce secretions but may cause excessive drying of tissues and cough -Humidifiers |
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Sinusitis |
-Usually a bacterial infection secondary to a cold or an allergy that has obstructed the drainage of one or more of the paranasal sinuses into the nasal cavity -pneumococci, streptococci, Haemophilus influenzae |
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Symptoms of Sinusitis |
-As exudate accumulates, pressure builds up inside sinus cavity, causing severe pain in the facial bone -Nasal congestion, fever, sore throat |
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Diagnosis of Sinusitis |
Radiograph or transillumination |
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Treatment of Sinusitis |
-Decongestants and analgesics until the sinuses are draining well -Antibiotics |
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Laryngotracheobronchitis (Croup) |
-Common viral infection -Particularly in children between 1 and 2 -Adults may also contract laryngitis, tracheitis, bronchitis -Parainfluenza virus, adenoviruses |
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Symptoms of Croup |
-Begins as an upper res condition with nasal congestion and cough
-Young: larynx and subglottic area become inflamed with swelling and exudate, leading to obstruction and a characteristic barking cough, hoarse voice, inspiratory stridor -Becomes more severe at night |
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Treatment of Croup
|
-Cool, moisturized air from shower or humidifier -Infection is self-limited -Full recovery in several days -Some children with allergic tendencies, smooth muscle spasm may exacerbate the obstruction, requiring additional medical treatment |
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Epiglottitis |
-Acute infection -H. influenzae type B -Common in children 3-7, has been increasing in adults - |
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Symptoms of Epiglottis |
-Swelling of the larynx, supraglottic area, and epiglottis -Appears as a round, red ball obstructing the airway -Onset is rapid, fever, sore throat -Child refuses to swallow -Drooling -Inspiratory stridor -Child appears anxious, pale, assumes sitting position (tripod) with mouth open, struggling to breathe -CAUTION is required during laryngeal exam to prevent reflex spasm and total obstruction of the airway |
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Treatment of Epiglottis |
Oxygen Antimicrobial therapy -Intubation or tracheotomy if necessary |
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Influenza (Flu) |
-Viral infection -May affect upper and lower res tracts -3 groups: Type A: most prevalent Type B & C -Mutate constantly: preventing effect immune defense for prolonged time periods -Intubation period is 1-4 days (2) -2-3 weeks before immunity develops |
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Symptoms of Influenza |
-Sudden, acute onset with fever, marked fatigue, and aching pains in the body -May cause viral pneumonia- death |
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Treatment of Influenza |
-Symptomatic and supportive unless bacterial infection occurs -amantadine (Symmetrel, Endantadine), zanamivir (Relenza inhaler) osletamivir (Tamaflu) taken by adults in the first 2 days, may reduce symptoms and duration and risk of infecting others |
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Scarlet Fever |
-Upper respiratory infection -Cause by group A B-hemolytic streptococcus (Streptococcus pyogenes) -Incubation period is 1-2 days |
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Symptoms and Treatment of Scarlet Fever
|
-Begin with fever and sore throat
Chills, vomiting, abdominal pain, malaise -Strawberry tongue: caused by the exotoxin produced by the bacteria -Fine rash on the chest, neck, groin, thighs Once a serious childhood disease, now generally treatable with antibiotics |
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Bronchodialation |
results when sympathetic stimulation relaxes the smooth muscle, dilating or enlarging the bronchioles |
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Primary control centers for breathing |
Inspiratory center in the medulla controls the basic rhythm by stimulating the phrenic nerves to the diaphragm and the intercostal nerves to the external intercostal muscles Expiratory center in the medulla functions when forced expiration is required Pons: coordinate inspiration, expiration, and intervals for each |
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Chemoreceptors |
sense changes in the levels of carbon dioxide, hydrogen ions, an do2 in blood or cerebrospinal fluid |
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central chemoreceptors |
medulla -respond quickly to slight elevations in Pco2 (from a normal 40 to 43 mmHg) or to a decrease in pH of cerebrospinal fluid |
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peripheral chemoreceptors |
located in carotid bodies at the bifurcation of the common carotid arteries in the aortic body in the aortic arch -sensitive to decrease o2 levels in arterial blood as well as to low pH |
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Hypoxic drive |
"In a normal person it is the carbon dioxide in the blood that triggers the urge to breath. In a person with compromised gas exchange (COPD, chronic bronchitis) the body gets used to the high levels of CO2 and so no urge to breathe. For these individuals, it is the lowered oxygen level that triggers the urge to take a breath." It is important for these pts to always remain slightly hypoxic and not be given excessive amounts of o2 at any time. |
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Hypercapnia |
Carbon dioxide leves in the blood increase -the gas easily diffuses into the cerebrospinal fluid, lowering pH, and stimulating the respiratory center, resealing in increased rate and depth of respirations (hyperventilation) -causes resp acidosis which depresses the nervous system |
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Hypocapnia |
(low Pco2) -May be caused by hyperventilation after excessive amounts of carbon dioxide has been expired -Causes resp alkalosis |
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Gas exchange or external respiration |
the flow of gases between the alveolar air and the blood in the pulmonary circulation |
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Pao2 |
partial pressure of o2 in arterial blood
|
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Factors affecting diffusion of gasses
|
-Thickness of resp membrane: fluid accumulates in the alveoli or interstitial tissue, diffusion of o2 is impaired -Normally, pressure in pulmonary circulation is low. -Extra fluid may impede blood flow through the pulmonary capillaries and increase surface tension in the alveoli, restricting lung expansion -Total surface area for diffusion and thickness of alveolar membranes (part of the alveolar wall is destroyed with emphysema & fibrosis) |
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Va/Q |
ventilation-perfussion ratio An auto-regulatory mechanism in the lungs can adjust ventilation and blood flow in an attempt to produce a good match. Ex: If Po2 is low, vasoconstriction occurs, shunting the blood to areas in the lungs where ventilation is better. If airflow is good, the pulmonary arterioles dilate to maximize gas exchange |
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Spirometry-pulmonary function testing (PFT) |
test pulmonary volumes, measuring volume and airflow times |
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Arterial blood gas determinations |
used to check oxygen, carbon dioxide, and bicarbonate levels, serum pH |
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Oximeters |
O2 saturation |
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Exercise tolerance testing |
testing is useful in pts with chronic pulmonary disease of ridings s and monitoring of pt's progress |
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Radiography
|
evaluating tumors or infections such as pneumonia or TB |
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Bronchoscopy |
used in performing a biopsy or unchecking for the site of a lesion or bleeding |
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Culture and sensitivity tests on exudates from upper res tract or sputum specimens |
identify pathogens and assist in determining therapy |
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Sneezing |
a reflex response to irritant in the upper resp tract -assists in removing the irritant -associated with inflammation or foreign material in the nasal passages |
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Coughing |
-may result form irritation caused by a nasal discharge dripping into the oropharynx or from inflammation or foreign material in the lower res tract or form inhaled irritants (tobacco) -Cough reflex is controlled by a center in the medulla -Consists of coordinated actions that inspire air and then close the glottis and vocal cords then forceful expiration |
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Yellowish-green, cloudy thick |
bacterial infection |
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Rusty, dark colored |
pneumococcal pneumonia |
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Large amount of purulent (pus) with foul odor |
bronchiectasis |
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Thick, tenacious (sticky)
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asthma, cystic fibrosis Blood tinged: chronic cough and irritation that causes rupture of superficial capillaries, may be sign of a tumor or TB |
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Hemoptoysis
|
blood tinged (bright red0 frothy -pulmonary edema |
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Eupnea |
normal breathing rate 10-18 regular, effortless |
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Kussmaul
|
deep, rapid "air hunger" typical of a state of acidosis or may follow strenuous exercise |
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Labored respirations prolonged inspiration or expiration times |
obstruction of airways |
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Wheezing or whistling |
obstruction in the small airways |
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Stridor |
high-pitched crowing usually indicates upper airway obstruction |
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Rales
|
light bubblier cracking sounds associated with serous secretions |
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Rhonchi
|
deeper and harsher sounds resulting from thicker mucus |
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Absence of breath sounds
|
indicates nonaeration or collapse of a lung (atelectasis) |
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Dyspnea |
subjective feeling of discomfort that occurs when a person feels unable to inhale enough air -breathlessness, or shortness of breath |
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Severe dyspnea |
flaring of nostrils use of accessory muscles reaction of muscles between or above the ribs |
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Orthopnea |
dyspnea that occurs when a person is lying down Pulmonary congestion: when blood pools in the lungs |
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Paroxysmal nocturnal dyspnea |
sudden acute type of dyspnea common in pots with left-sided congestive heart failure |
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Cyanosis |
bluish coloring of the skin and muses membranes that results from large amounts of unoxygenated hemoglobin in the blood -May occur in pots with cardiovascular disease or respiratory disease -Not a reliable indicator of hypoxia |
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Pleural pain |
results from inflammation infection of the parietal pleura -cyclic pain that increases as the inflamed membrane is stretched with inspiration or coughing |
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Friction rub |
may be heard -soft sound produced as the rough membranes move against each other Pleural inflammation may be caused by lobar pneumonia or lung infarction |
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Clubbed fingers |
sometimes toes result from chronic hypoxia associated with respiratory or cardiovascular disease -painless, firm, fibrotic enlargement at the end of the digit |
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Hypoxemia |
inadequate o2 in the blood (Pao2) |
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hypoxia |
inadequate o2 supply to the cells a. deficit of RBCs or hemoglobin levels that are too low for adequate o2 transport b. Circulatory impairment, which may lead to decreased cardiac output from the heart to the lungs or the systemic circulation c. Excessive release of o2 from RBCs if circulation is sluggish through the system or is partially obstructed by vascular disease d. Impaired respiratory function, including inadequate ventilation, inhalation of o2-deficient air, or impaired diffusion e. Carbon monoxide poisoning |
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Respiratory acidoses |
-more common -results from impaired expiration -high Pco2 -low serum pH |
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Respiratory alkalosis |
-occurs when the RR is increased -Usually because of acute anxiety or excessive intake of aspirin |
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Boyle's Law |
As the size of the thoracic cavity decreases, the pressure inside the cavity increases. |
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Sequence of events of inspiration and expiration |
1. Normal quiet inspiration begins with contraction of the diaphragm and the external intercostal muscles 2. Diaphragm flattens and descends, increased the length of the thoracic cavity 4. External intercostal muscles raise the ribs and sternum up and outward, increasing the transverse and anteroposterior diameters of the thorax 5. As the ribs and diaphragm move, the attached parietal pleura pulls the adhering visceral pleura an lungs long with it. 6. As the visceral pleura moves outward, the elastic lungs expand with it, resealing in a decrease in air pressure inside the lungs. 7. At this point, atmospheric pressure is greater than intra-alveolar pressure, so air flows form atmosphere to alveoli. (Breathing requires physical effort and cellular energy) 8. During normal expiration, the diaphragm and external intercostal muscles relax, leading to a decrease in thoracic size. 9. This decrease, combined with the natural elastic recoil of the alveoli, results in increased intra-alveolar pressure (greater than atmospheric pressure) 10. Therefore air flows out of the alveoli into the atmosphere. Quiet expiration is a PASSIVE process and does not require cell energy. |
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Dead space |
refers to the passageways or areas where gas exchange cannot take place -space first filled by newly inspired air -increased by obstruction in the passageways or collapse of alveoli |
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Pharyngitis (Strep Throat) |
-Viral or bacterial infection of the pharynx -Group A B-hemolytic Streptococci pharyngitis physical findings: Erythema, swelling, or exudates of the tonsils or pharynx Temp of 38.3C 100.9F or higher Tender anterior cervical nodes Absence of conjunctivitis, cough, an rhinorrhea, which are symptoms that may suggest viral illness Treated best with penicillin or erythromycin antibiotics |
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Type A H1Ni Influenza |
-This virus contains genes form pig, bird, and human flu strains
-Usually affects children and teens younger than 20 years -Healthy young adults also at high risk -High mortality rate caused by acute respiratory syndrome Pulmonary edema Pneumonia Requires ICU care |
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Allergic Rhinitis Hay Fever |
-Allergic reaction in nasal mucosa -Sneezing, copious watery nasal secretions, itching -Eyes: frequently red, watery, pruritic -Often seasonal, plant pollens, molds, dust Mechanism: IgE bound to mast cells; release of histamine mediators -Antigen is often called the allergen. Specific allergen ca be a pollen, food, chemical, plant, drug |
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Allergic Rhinitis Treatment |
Antihistamines -taken PO and bought without prescription -May cause drowsiness -Antihistamine nasal sprays work well- need prescription Corticosteroids: -Nasal corticosteroid sprays are most effective treatment -Work best when use nonstop, but they can also be helpful when used for shorter periods of time -Generally safe for children and adults -Many brands available: no prescription Decongestants: -Helpful in reducing symptoms such as nasal stuffiness -Do not use nasal decongestants for more than 3 days (Remove allergen when possible) |
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Anaphylaxis |
-Systemic hypersensitivity reaction resulting in decrease BP, airway obstruction, and severe hypoxia -Common causes: latex, insect stings, nuts, penicillin -Reaction occurs within minutes |
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Anaphylaxis Treatment |
-Epinephrine injection (EpiPen) -Stimulates sympathetic nervous system which causes vasoconstriction; increases rate and strength of heartbeat; increases BP; relaxes bronchial smooth muscle which opens airway -Administer o2 and antihistamine (IM if possible) -Call 911 -Treat of shock; CPR if warranted |