Download Exam One Solutions: Respiratory Conditions and more Exams Nursing in PDF only on Docsity!
NURS 3525 - EXAM ONE - Combined With Complete Solutions
Allergic Rhinitis Inflammation of the nasal mucosa, usually due to a specific allergen Seasonal Rhinitis During spring and fall due to pollen from trees, flowers, weeds, or grasses Perennial Rhinitis Present throughout the year caused by environmental allergens such as dust mites, animal dander, cockroaches, fungi, mold Episodic, intermittent, & persistent What are the types of rhinitis? Episodic Rhinitis Symptoms related to intermittent exposure to allergen not typically present in usual environment Intermittent rhinitis Symptoms present < 4 days/week or < 4 weeks/year Persistent rhinitis Symptoms present > 4 days/week or > 4 weeks/year
Sneezing, watery, itchy eyes and nose, ↓ sense of smell, and thin, watery nasal discharge leading to 𝖳 mucus production and congestion What are the clinical manifestations of allergic rhinitis? Nasal turbinates pale, boggy, swollen What are the physical assessments for allergic rhinitis? HA, stuffy nose, nasal congestion, 𝖳 sinus pressure. Nasal polyps, postnasal drip results in cough + hoarseness What are the clinical manifestations of chronic exposure to allergens? Avoid triggers of allergic reactions What is the nonpharmacologic management of allergic rhinitis? ↓ inflammation, reduce nasal symptoms, minimize complications, maximize QOL What is the pharmacologic goal for allergic rhinitis? H1-antihistamines (Benadryl, Claritin, allegra), decongestants (pseudoephedrine, afrin), leukotriene receptor antagonists (LTRAs) What are some examples of oral medications for allergic rhinitis? Antihistamines, anticholinergics, corticosteroids, mast-cell stabilizers, decongestants What are some examples of intranasal medications for allergic rhinitis? Allergy shots What are some examples of immunotherapy for allergic rhinitis?
Acute bronchitis, sinusitis, otitis media, tonsilitis, pneumonia. Antibiotics do not treat viruses What are the possible complications of URIs?? 𝖳 fever, swollen glands, severe sinus + ear pain, worsening symptoms What do we look for during URIs to prevent complications?? Viral. Classified in 4 serotypes A,B,C,D. A/B significant to humans, A most common + virulent virus. What is the etymology of influenza? B/t humans through infected droplets, inhalation of aerosolized particles, and in a lesser extent through direct contact with contaminated surfaces How is influenza contagious? Abrupt onset, chills, fever, generalized myalgia, HA, cough, sore throat, fatigue What are the clinical manifestations of influenza? Gradual vs. abrupt onset, no fever vs. fever, no HA vs. HA, slight vs. severe myalgia, occasional vs. usual fatigue What are the manifestations of the common cold vs. influenza? Bronchitis, pneumonia, acute respiratory failure and acute respiratory distress syndrome (ARDS) What are the complications of influenza? Cultures done via nose + throat can identify causative agents. Rapid test screens for A/B, can get false positive What diagnostics are used in a Pt. w/influenza?
Prevention: flu vaccine. + relief of symptoms What is the management plan for influenza? Inactivated flu vaccine - Trivalent Protects against 3 different types of flu virus (2-type A, 1 - type B) Inactivated flu vaccine - Quadrivalent Quadrivalent: Protects against 4 different types of flu virus (2-type A, 2 - type B) Inactivated flu vaccine Given by injection, approved for use in people >6 months, should not be used for those with serious allergy or reaction to previous vaccine, Guillain-Barre syndrome. Most common side effects: injection site reactions such as pain, redness, swelling Live-attenuated flu vaccine Made from weakened influenza virus, given as intranasal into both nostrils, approved for healthy people ages 2 - 49, should not be used in pregnant woman or woman who could become pregnant. Adverse effects are rare and may resemble mild flu with runny nose, nasal congestion, cough, HA doi: Can be viral or bacterial What is the etiology of sinusitis?? Nasal polyps, foreign bodies, deviated septum, or tumors obstruct mucus drainage What 𝖳 the risk of sinusitis?? Acute, subacute, recurrent acute, or chronic
anterior 90% of nosebleeds occur in the part of the nasal cavity, they are easy to visualize, can be self-treated and usually stops spontaneously Posterior bleeds occur more often in older adults with other health problems, since they are closer to the throat, it is hard to determine how much blood is lost, may require medical treatment Trauma, low humidity, URIs, allergies, sinusitis, foreign bodies, chemical irritants, overuse of decongestant nasal sprays, facial or nasal surgery, anatomic malformation, tumors, medications or conditions that prolong bleeding time What are causes of epistaxis? Aspirin, NSAIDs, warfarin, other anticoagulant drug What medications prolong bleeding time?
- Place the patient in a sitting position, leaning slightly forward with head tilted forward.
- Apply direct pressure by pinching the entire soft lower part of the nose (nostrils) together for 5 to 15 minutes.
- If bleeding doesn't stop after 15 minutes, go to emergency. What is the Tx plan for a Pt. with epistaxis? Place pledget (nasal tampon) impregnated with anesthetic solution, and/or vasoconstrictive agent into nasal cavity, or absorbable materials How do you Tx anterior epistaxis? Oxidized cellulose (surgical) Gelatin foam (Gelfoam)
Gelatin thrombin combination (Floseal) What are some examples of absorbable materials? Packable: CompresseD nasal sponges, epistaxis balloons, nasal sling arterial embolism How do you manage a posterior epistaxis? Pneumonia Acute infection of the lung parenchyma Inflammatory response = neutrophils attracted, release of inflammatory mediators, accumulation of fibrinous exudates, RBCs, bacteria → Alveoli fill with fluid+debris (consolidation)/increased production of mucus (airway obstruction) → decreased gas exchange → Resolution of infection: macrophages in alveoli ingest+remove debris, normal lung tissue restored, gas exchange returns to normal. Explain the brief pathophysiology of pneumonia CAP: Community-acquired pneumonia Acute infection of the lung in patients who have not been hospitalized or resided in long-term care facilities within 14 days of symptom onset HAP: Hospital-acquired pneumonia or nosocomial pneumonia Pneumonia in a non-intubated patient that begins 48 hours or longer after admission to hospital and was not present on admission. VAP: Ventilator-associated pneumonia A subtype of HAP, refers to pneumonia that occurs more than 48 hours after endotracheal intubation
Pneumonia chest X-ray Reveals characteristics of the infecting pathogen may also reveal pleural effusion Pneumonia bronchoscopy with bronchial washings or thoracentesis Obtains cell and fluid samples from patients not responding to initial therapy Pneumonia arterial blood gas (ABG) Reveals hypoxemia, hypercapnia, acidosis Leukocytosis Bacterial pneumonia WBC > 15 , Sputum sample for pneumonia Culture and gram stain to identify organism before starting antibiotics Blood cultures for pneumonia Done for the seriously ill with pneumonia Labs for pneumonia C-reactive protein (CRP), procalcitonin, interleukin 6 No signs of hypoxia, normal breathing pattern, clear breath sounds, normal chest x-ray, normal WBC, no complications What is the goal for pneumonia management? Supply oxygen, help perfusion, relieve obstruction, early mobilization, control infection and nutrition, relieve cough, fever, and pain with medicine What do we do for a Pt with pneumonia?
Complications: sepsis, pleural effusion, pleurisy, acute respiratory failure What do we monitor for with a Pt with pneumonia? Chronic obstructive pulmonary disease (COPD) Progressive lung disease characterized by persistent airflow limitation Chronic bronchitis Presence of cough and sputum production for at least 3 months in each of 2 consecutive years Emphysema The destruction of alveoli without fibrosis COPD Previous definitions included chronic bronchitis and emphysema. Each condition features , but neither by itself is. Smoking, infection, asthma, air pollution, occupational chemicals and dust, aging, genetics, alpha- 1 antitrypsin deficiency What are risk factors for COPD? Noxious particles & gases → inflammation of central airways, peripheral airway remodeling, parenchymal destruction, pulmonary vascular changes → COPD pathology Describe the brief pathophysiology of COPD Mild (GOLD 1), moderate (GOLD 2), severe (GOLD 3), very severe (GOLD 4) How is COPD classified? Develops slowly over time, chronic cough with sputum production, dyspnea, ↓ breath
COPD nutrition therapy Lung volume reduction surgery, bullectomy Surgical therapy for COPD Health promotion, acute care, ambulatory care, rehabilitation, activity, psychosocial, sexuality, sleep, end of life What is the management plan for a Pt diagnosed with COPD? Vaccinations, follow medication regimen, stop smoking, hand hygiene, avoid sick, exercise Health promotion for COPD Monitor regularly indications of respiratory function, monitor AP, collaborate w/interprofessional team members: respiratory therapist, dietitian, physical therapist, social worker Acute care for COPD Pt teaching + understanding. Teach to understand early exacerbations Ambulatory care for COPD Exercise training, smoking cessation, nutrition cancelling, more teaching
Rehabilitation for COPD Conserve energy, assistive devices, alternate ADL methods, rest periods, regular exercise + strength training Activity for COPD Anger, denial, depression. Support groups + therapy should be encouraged Psychosocial for COPD ↓ dyspnea during intimacy Sexuality for COPD Assess for sleep apnea, difficulty sleeping related to dyspnea Sleep for COPD Consider palliative care + hospice End of life for COPD Relieve symptoms, able to do ADLs, increased exercise tolerance, no COPD r/t complications, slowing of disease process, improved QOL What is the goal of care for COPD? Impaired respiratory function, activity intolerance, nutritionally compromised, ineffective coping What is the clinical problem of COPD?
Volume of blood pumped by each ventricle in one minute CO = SV x HR What is the cardiac output formula? 4 - 8 L/min What is normal range for CO when at rest? CO 𝖳 What happens if HR 𝖳? CO ↓ What happens to CO if HR ↓? HoTN, cool, clammy, cyanotic or modeled skin, ↓ pulse, S/SX of altered mental status, etc. What are some S/S of ↓ CO? Preload, contractility, afterload What does SV depend on? Preload The volume of blood distending the ventricles at the end of diastole before pulling Contractility The "force" with which the heart contracts
Afterload Peripheral resistance ↓ Preload: dehydration, stiff atria 𝖳 Preload: excess fluid What would 𝖳 vs. ↓ a state of preload? Clear blood vessels vs. atherosclerosis plaque or obstruction What does afterload depend on? CO x SVR What is the equation for BP? Blood pressure Measure of force exerted by blood against the walls of the arterial system 120/ What is considered normal BP? 𝖳 Risk of stroke, confusion, HA, convulsions What is the impact on the brain with HTN? 𝖳 Risk of hypertensive retinopathy What is the effect on the eyes with HTN? 𝖳 Risk for MI + HF
Renin + aldosterone How does the renal system regulate BP? Renin is secreted by kidneys & converts Angiotensin I to Angiotensin II (potent vasoconstrictor) How does Renin help regulate BP? 𝖳 BP What is the effect of angiotensin on BP? Aldosterone secretion = Na+ & fluid retention How does aldosterone help regulate BP? 𝖳 BP What is the effect of aldosterone on BP? <120/<80 mmHg What is normal BP range - systolic/diastolic? 120 - 129/<80 mmHg What is elevated BP range - systolic/diastolic? 130 - 139 or 80 - 89 mmHg What is high (Stage 1 HTN) BP range - systolic/diastolic? 140> or 90> mmHg
What is high (Stage 2 HTN) BP range - systolic/diastolic? Primary HTN Elevated BP without identified cause (many contributing factors) Weight, smoking, age, family history, etc. (FILL IN FROM BOOK) What are contributing factors of HTN Secondary HTN Elevated BP with a specific cause Cirrhosis, endocrine disorders, neurologic disorders, preeclampsia, renal disease, etc. (FILL IN FROM BOOK) What are causes of secondary HTN? "Silent killer" What is HTN known as? From effects on blood vessels in various organs & tissues What are the secondary symptoms caused by with HTN? Fatigue, dizziness, palpitations, angina, SOB What are secondary symptoms of HTN? Target organ damage What are the complications of HTN?
