NLE Respiratory Nursing — Upper & Lower Respiratory InfectionsSummary

URTIs include infections of the sinuses, pharynx, and upper airway structures above the vocal cords. Common conditions include sinusitis, pharyngitis, and acute rhinitis. Sinusitis is inflammation of paranasal sinuses most often viral in origin; bacterial superinfection is suspected when symptoms persist beyond 10 days or worsen after initial improvement, presenting with facial pain/pressure (worse on forward bending), purulent nasal discharge, and post-nasal drip. Pharyngitis ('sore throat') is primarily viral, but Group A beta-haemolytic streptococcus (GABHS) is the critical bacterial pathogen to identify because untreated infection leads to acute rheumatic fever and acute glomerulonephritis—sequelae that have lifelong consequences. Classic strep clues include sudden onset, fever, tonsillar exudate, tender anterior cervical nodes, and conspicuous absence of cough.

An acute systemic viral illness caused by influenza A or B viruses, characterized by abrupt onset of high fever, myalgia, headache, dry cough, and profound fatigue—more severe systemic symptoms than the common cold. The hallmark is the abruptness and severity of malaise. Complications include viral or secondary bacterial pneumonia, particularly in high-risk groups: elderly, pregnant women, immunocompromised individuals, and those with chronic underlying diseases (diabetes, heart disease, COPD). Antivirals (neuraminidase inhibitors such as oseltamivir) are most effective when initiated within 48 hours of symptom onset; otherwise, management is supportive (fluids, rest, antipyretics). Prevention through annual influenza vaccination is recommended for high-risk populations, with respiratory/droplet precautions and rigorous hand hygiene.

Inflammation of the bronchi, most commonly viral and self-limiting, often following an upper respiratory infection. The hallmark symptom is a persistent cough that initially is dry then becomes productive, lasting up to 3 weeks, frequently accompanied by low-grade fever and chest discomfort/tracheitis pain. Unlike pneumonia, bronchitis does not cause consolidation of alveolar tissue; therefore, chest X-ray findings are typically normal or show only mild bronchial thickening. Management is primarily supportive: hydration (to thin secretions), rest, humidification, and antipyretics/analgesics. Antibiotics are NOT indicated in the vast majority of cases because the condition is viral; inappropriate antibiotic use drives antimicrobial resistance—a key public health concern in the Philippines.

CAP is infection of the lung parenchyma causing inflammation and consolidation of alveoli with exudate, which impairs gas exchange and produces hypoxemia. The most common bacterial cause is Streptococcus pneumoniae; other significant pathogens include atypical organisms (Mycoplasma, Chlamydia, Legionella). Pathophysiology: inhaled pathogens reach the alveoli and trigger an acute inflammatory response; alveoli fill with exudate containing fibrin, red blood cells, and white blood cells (consolidation), reducing surface area for gas exchange. Consolidated lung tissue transmits sound differently on examination—hence increased tactile fremitus, dullness to percussion, bronchial breath sounds, and crackles over the affected area. Clinical presentation: fever with chills, productive cough with purulent or rust-colored sputum (classic for pneumococcal pneumonia), pleuritic chest pain, dyspnoea, and tachypnoea. ATYPICAL presentation in elderly: confusion, lethargy, weakness, and falls may be the only signs with blunted fever response—a critically important high-yield NLE point.

HAP/VAP occurs >48 hours after hospital admission or intubation respectively, caused by organisms different from CAP—often more resistant Gram-negative bacilli (Pseudomonas aeruginosa, Acinetobacter) and methicillin-resistant Staphylococcus aureus (MRSA). Risk factors include prolonged intubation, supine positioning, sedation, gastric colonization, aspiration, and impaired host defenses. Diagnosis may be more subtle than CAP; chest X-ray findings can lag behind clinical deterioration. Management requires broader spectrum antibiotics pending culture results, with frequent reassessment. Prevention is paramount: elevate head of bed 30–45 degrees, minimize sedation, provide oral care with chlorhexidine, remove nasogastric tube when no longer needed, and implement stress ulcer prophylaxis.

Pneumonia resulting from inhalation of gastric contents or oropharyngeal secretions containing anaerobic bacteria. High-risk populations: patients with impaired swallowing (stroke, neuromuscular disease), decreased level of consciousness (sedation, head injury, seizure), nasogastric tube feedings, and the elderly. Pathophysiology involves both a chemical injury (gastric acid-induced inflammation) and bacterial infection by anaerobic flora from the oral cavity. Clinical presentation is similar to CAP but often indolent; aspiration is often silent, and symptoms may develop over hours to days. Diagnosis requires a high clinical suspicion combined with risk factor assessment; chest X-ray typically shows infiltrates in dependent lung zones (right lower lobe when supine, left lower when upright).

TB is caused by Mycobacterium tuberculosis, an acid-fast bacillus (AFB) transmitted by airborne droplet nuclei when an infected person coughs, sneezes, or speaks. The Philippines carries one of the world's highest TB burdens, making TB a cornerstone of NLE content. Pathophysiology involves primary infection (usually asymptomatic in immunocompetent individuals) where bacilli lodge in the alveoli; the immune system typically walls them off into a granuloma (the Ghon complex), producing latent TB infection (LTBI)—the person is infected but not infectious and asymptomatic, with a positive tuberculin skin test (TST). Active (pulmonary) TB develops when granulomas rupture and bacilli replicate, causing tissue destruction and often cavitation in the upper lung lobes. This can occur years/decades after initial infection, usually triggered by immunosuppression (HIV/AIDS, diabetes, malnutrition, corticosteroid use, advanced age). Extrapulmonary TB can affect lymph nodes (TB lymphadenitis), bone (Pott's disease of the spine), meninges (TB meningitis), kidneys, and other organs.

Active pulmonary TB classically presents with a chronic productive cough lasting ≥2 weeks (this is the key screening trigger in Philippine TB programs), low-grade afternoon fever, night sweats (often drenching, requiring change of bedclothes), unexplained weight loss, fatigue, anorexia, and hemoptysis (blood-streaked sputum). Onset is typically insidious over weeks to months. Patients often appear chronically ill and cachectic. Extrapulmonary TB presents differently depending on the organ involved: TB lymphadenitis causes painless lymph node swelling; Pott's disease presents with back pain and potential paralysis; TB meningitis manifests as subacute meningitis with headache, neck stiffness, and altered consciousness.

The Philippine National TB Control Program employs a tiered diagnostic approach with GeneXpert MTB/RIF as the first-line/primary diagnostic test for presumptive TB. GeneXpert is a rapid molecular test that detects Mycobacterium tuberculosis AND rifampicin resistance simultaneously in approximately 2 hours, with high sensitivity and specificity. This represents a paradigm shift from sputum smear microscopy (DSSM—Direct Sputum Smear Microscopy) being the traditional first test; microscopy is still used for treatment monitoring and in resource-limited settings. Chest X-ray showing upper-lobe infiltrates/cavitation supports the diagnosis but is not confirmatory alone and is not required to initiate treatment if GeneXpert is positive. The tuberculin skin test (Mantoux test/PPD—purified protein derivative) is performed intradermally; read at 48–72 hours by measuring induration (not redness) in millimeters. Induration ≥5 mm is considered positive in HIV+ individuals; ≥10 mm in close contacts and those with clinical symptoms; ≥15 mm in general population. TST indicates TB infection/exposure but does NOT differentiate LTBI from active TB; it can remain positive after successful treatment and is positive in BCG-vaccinated individuals, limiting its specificity in the Philippines where BCG vaccination is routine.

DOTS (Directly Observed Therapy, Short-course) is the backbone of the Philippine NTP and the global TB control strategy. Core principle: a trained treatment partner (family member, community health worker, or health facility staff) directly observes the patient swallowing every dose of anti-TB medication to ensure adherence. This is non-negotiable because incomplete treatment is the leading cause of treatment failure and the development of multidrug-resistant TB (MDR-TB). TB diagnosis and all anti-TB drugs are provided free through government health facilities under the NTP. Standard first-line treatment for drug-susceptible TB is 6 months total: an intensive phase of 2 months with FOUR drugs (RIPE) followed by a continuation phase of 4 months with TWO drugs (RH—rifampicin + isoniazid). The RIPE acronym stands for: Rifampicin, Isoniazid, Pyrazinamide, Ethambutol. Dosing is weight-based and ideally given as a fixed-dose combination (FDC) tablet to simplify regimen adherence. All TB drugs must be taken together as a single daily dose on an empty stomach (30 minutes before food or 2 hours after) for optimal absorption.

Rifampicin is a rifamycin antibiotic with potent bactericidal activity against M. tuberculosis. Standard dose: approximately 10 mg/kg body weight per day, typically 450–600 mg once daily. Mechanism: inhibits bacterial RNA polymerase, preventing transcription. Signature clinical effect that amazes patients: rifampicin metabolites turn all body fluids orange-red, including urine, sweat, tears, saliva, and semen. Patients must be forewarned or they will panic thinking they are bleeding internally. This discoloration is harmless and resolves when the drug is discontinued. Rifampicin is hepatotoxic and is a potent cytochrome P450 enzyme inducer—it markedly reduces the plasma concentration of many drugs including oral contraceptives, warfarin, azathioprine, and dapsone. Women using oral contraceptives must be counseled to use an additional contraceptive method (barrier method preferred) or consider a non-hormonal method because breakthrough pregnancy on OCP + rifampicin is common. Rifampicin may also cause rifampicin-induced immune reconstitution inflammatory syndrome (IRIS) in HIV-coinfected patients as immune function recovers.

Isoniazid (INH) is a prodrug that is converted to an active form by catalase in M. tuberculosis; it inhibits mycolic acid synthesis, essential for the mycobacterial cell wall. Standard dose: approximately 5 mg/kg body weight per day, typically 300 mg once daily. Signature toxicity: peripheral neuropathy (affecting sensory and motor nerves, especially in the lower extremities), manifesting as paresthesias, numbness, and potentially foot drop if severe. Neuropathy is preventable by administering pyridoxine (vitamin B6) 25–50 mg daily with each dose of isoniazid. This is a critical exam point: any patient receiving isoniazid MUST receive pyridoxine to prevent neuropathy. Isoniazid is also hepatotoxic and is associated with drug-induced lupus-like syndrome (rare) and optic neuritis (rare but must distinguish from ethambutol's optic neuritis). Isoniazid also causes drug interactions by inhibiting metabolism of phenytoin and warfarin, potentially elevating their levels.

Pyrazinamide (PZA) is converted to its active form (pyrazinoic acid) by the enzyme pyrazinamidase in M. tuberculosis; this active form accumulates inside the bacterium and disrupts membrane function and inhibits fatty acid synthesis. Standard dose: approximately 25 mg/kg body weight per day, typically 1500–2000 mg depending on weight. Signature toxicity: hyperuricemia (elevated serum uric acid), which can precipitate acute gout attacks manifesting as sudden-onset joint pain, swelling, and erythema, often in the big toe. Patients with history of gout require close monitoring. Manage by ensuring adequate hydration (promote urine output to clear uric acid) and teaching avoidance of purine-rich foods. Allopurinol is NOT routinely given during TB treatment but may be considered if gout develops. Pyrazinamide is also hepatotoxic. Rarely, PZA may cause cutaneous hyperuricemia-like reactions. Unlike older regimens, pyrazinamide allowed shortening TB treatment from 9 months to 6 months, a major public health advancement.

Ethambutol (EMB) inhibits arabinosyl transferases, enzymes essential for mycobacterial cell wall synthesis. Standard dose: approximately 15 mg/kg body weight per day, typically 1200–1600 mg once daily depending on weight. Signature toxicity: optic neuritis—inflammation of the optic nerve causing decreased visual acuity, blurred vision, and red-green color blindness (the patient may not see the red dot on the traffic signal or may confuse red with green). Optic neuritis is dose-dependent and usually reversible if ethambutol is discontinued promptly upon symptom recognition, but delayed recognition can lead to permanent vision loss. Baseline visual acuity testing and Ishihara color plate testing should be performed before initiating ethambutol and periodically during treatment. Patients MUST be counseled to report ANY visual changes immediately (blurred vision, dimmed vision, color vision changes)—this is a critical safety teaching point. Ethambutol is generally well-tolerated otherwise; hyperuricemia can occur but is less significant than with pyrazinamide.

Rifampicin, isoniazid, and pyrazinamide are all hepatotoxic—they can cause hepatitis with elevation of liver transaminases (AST, ALT), hyperbilirubinemia, and clinical hepatitis with jaundice, dark urine, pale stools, right-upper-quadrant pain, nausea, and vomiting. Hepatotoxicity risk is elevated in patients with pre-existing liver disease, heavy alcohol use, HIV/AIDS, and concurrent use of other hepatotoxic medications. Philippine NTP protocols typically include baseline liver function tests (LFTs) before initiating TB treatment; repeat LFTs are performed if symptoms develop. Patients must AVOID ALCOHOL during TB treatment because alcohol potentiates hepatotoxic effects and increases risk of hepatitis. Clinical teaching emphasizes reporting jaundice, darkening of urine, abdominal pain, or persistent nausea immediately. Most hepatotoxicity is reversible if the drugs are discontinued early upon recognition.

Standard treatment for drug-susceptible TB consists of two phases: (1) Intensive Phase: 2 months of RIPE (4 drugs daily), during which bacterial load decreases dramatically and the patient becomes non-infectious. After the intensive phase, sputum smear microscopy should become negative (if initially positive). (2) Continuation Phase: 4 months of RH (2 drugs daily—rifampicin + isoniazid). Total duration = 6 months. During the intensive phase, clinical improvement is usually evident within 2 weeks (fever resolves, cough improves, appetite returns). By 2–3 weeks of effective therapy, if clinical response is evident and sputum smear converts to negative, the patient is generally considered non-infectious and can be managed in outpatient settings (though isolation precautions may continue per institutional policy). A patient is considered to have completed successful treatment after 6 months of adherent therapy with clinical resolution and bacteriological cure (sputum smear remains negative). Default or incomplete treatment leads to treatment failure and MDR-TB development.

Latent TB infection (LTBI) represents the state where M. tuberculosis bacilli are present in the body, usually walled off in granulomas, but the person is asymptomatic, has no clinical or radiological signs of TB disease, and is NOT infectious (cannot transmit TB to others). LTBI is identified by a positive tuberculin skin test (TST) with induration ≥5–15 mm depending on risk factors, OR positive interferon-gamma release assay (IGRA, such as QuantiFERON-TB), in the absence of symptoms or radiological evidence of active TB. The lifetime risk of LTBI progressing to active TB is approximately 5–10% overall but is much higher (up to 50%) in HIV+ individuals. In the Philippines, LTBI preventive therapy is recommended for high-risk groups: HIV+ patients, close contacts of active TB patients (especially children), healthcare workers, and patients with comorbidities like diabetes. The standard preventive regimen is isoniazid monotherapy (300 mg daily) for 6 months, though shorter regimens (3 months INH + rifampicin) are emerging. Preventive therapy reduces TB progression risk by ~90%.

TB is transmitted via airborne droplet nuclei (particles <5 micrometers) that remain suspended in air for hours; they are generated when an infected person coughs, sneezes, or speaks. Infection control requires AIRBORNE PRECAUTIONS, not droplet precautions—this distinction is critical and is a classic NLE distractor. Airborne precautions include: (1) Negative-pressure isolation room with 6–12 air changes per hour vented to the outside; (2) High-efficiency particulate air (HEPA) filtration; (3) N95 respirator for all staff entering the room (surgical masks are inadequate for TB); (4) Surgical mask on the patient during transport outside the room; (5) Hand hygiene before and after patient contact. Patients with active pulmonary TB receiving effective treatment (clinical improvement, reduced cough) for approximately 2–3 weeks are generally considered non-infectious, but isolation precautions may continue per institutional protocols. Once sputum smear microscopy converts to negative and clinical improvement is evident, outpatient management is appropriate. Patients must understand the importance of covering their mouth when coughing, disposing of sputum-contaminated tissues in closed containers, and ensuring good ventilation in their home environment.

Contact investigation is a cornerstone of TB control in the Philippines. Close contacts of active TB patients (household members, frequent visitors, coworkers in close proximity) have a significantly elevated risk of TB infection and progression. The NTP mandates that contacts be screened with TST (or IGRA) and clinically evaluated for symptoms of active TB. Those with positive TST and no evidence of active disease (LTBI) require preventive therapy. Children <5 years old who are household contacts should receive preventive therapy regardless of TST status because of their high risk of progression to severe TB (TB meningitis, miliary TB). Healthcare workers routinely exposed to TB patients should be screened annually and offered preventive therapy if TST converts. Community health nurses play a vital role in contact tracing, ensuring close contacts are identified and evaluated, and supporting their adherence to preventive therapy. BCG vaccination (Bacille Calmette-Guérin) is part of the Philippine Expanded Program on Immunization (EPI); it is given at birth and provides some protection against TB, especially miliary TB and TB meningitis in children.

Using NANDA-I taxonomy and Maslow's hierarchy of needs to organize nursing care for respiratory infections: PHYSIOLOGICAL NEEDS (lowest level, highest priority): (1) Impaired gas exchange related to lung consolidation/inflammation—prioritized in pneumonia and severe TB because it is life-threatening; interventions include oxygen therapy, positioning (high-Fowler's), deep breathing/coughing, and adequate hydration to loosen secretions. (2) Ineffective airway clearance related to excessive mucus production/cough—addressed through airway suctioning, humidification, and chest physiotherapy. (3) Ineffective breathing pattern related to dyspnoea—managed through positioning, breathing exercises, and anxiety reduction. (4) Imbalanced nutrition: less than body requirements related to anorexia, dysphagia (TB), and increased metabolic demands—supported through nutritious diet, small frequent meals, and nutritional supplements. SAFETY NEEDS: (1) Risk for infection related to airborne transmission (TB)—managed through strict airborne precautions, DOTS, and contact investigation. (2) Risk for deficient fluid volume related to fever and insensible losses—prevented through adequate hydration. LOVE & BELONGING/ESTEEM NEEDS: (1) Social isolation related to respiratory isolation precautions—addressed through therapeutic communication, family involvement, and explaining the temporary nature of isolation. (2) Disturbed self-image related to isolation, weight loss (TB), chronic illness—supported through encouragement and psychosocial counseling. SELF-ACTUALIZATION (lowest priority): (1) Deficient knowledge related to disease process, treatment regimen, and prevention—addressed through patient education.

In acute respiratory infections (pneumonia, severe TB), maintaining a patent airway and adequate oxygenation is the top nursing priority. Specific interventions include: (1) Position the patient in HIGH-FOWLER'S (45–90 degrees) or sitting upright to maximize lung expansion and reduce the work of breathing. A patient with severe respiratory distress may prefer orthopnea (sitting upright, leaning forward on a table). (2) Administer supplemental oxygen to maintain SpO2 ≥90% (target may be higher depending on underlying disease and institutional protocol); use pulse oximetry for continuous monitoring. Start with low-flow oxygen (nasal cannula 2–4 L/min) and titrate based on response. (3) Encourage DEEP BREATHING AND COUGHING every 1–2 hours; teach the patient to splint the chest with a pillow when coughing to reduce pleuritic pain. (4) Perform or assist with incentive spirometry to promote maximum inspiration and prevent atelectasis. (5) Perform chest PHYSIOTHERAPY (percussion, vibration, postural drainage) to mobilize secretions, especially in patients with excessive sputum production. (6) Suction the airway (via mouth or endotracheal tube if intubated) as needed based on physical signs (rattling, elevated RR, agitation). (7) Ensure ADEQUATE HYDRATION (2–3 L/day unless contraindicated by cardiac or renal disease) because fluids thin secretions and reduce their viscosity, facilitating clearance. Monitor intake and output. (8) Use a HUMIDIFIER or cool mist to prevent drying of respiratory secretions. (9) CLUSTER CARE and minimize unnecessary activities to allow rest and energy conservation, reducing oxygen demand. (10) Monitor vital signs continuously: rising respiratory rate, falling oxygen saturation, increased use of accessory muscles, nasal flaring, or altered mental status (hypoxia-induced confusion) are signs of deterioration requiring immediate intervention.

Community-acquired pneumonia (CAP) treatment depends on severity and comorbidities. FIRST-LINE AGENTS for CAP: (1) Amoxicillin 500 mg orally three times daily (or high-dose for severe disease) is the traditional first choice for CAP when S. pneumoniae is suspected, provided the patient is not penicillin-allergic. It has excellent lung penetration and covers the most common pathogen. (2) MACROLIDES (azithromycin 500 mg on day 1, then 250 mg daily for 4 more days; or clarithromycin) are used as monotherapy in mild-to-moderate CAP or in combination with a beta-lactam for severe disease or atypical coverage. Macrolides also cover Mycoplasma and Chlamydia. Side effect: GI upset (nausea, diarrhea), and QT prolongation (monitor ECG in elderly or those with cardiac disease). (3) RESPIRATORY FLUOROQUINOLONES (levofloxacin 500–750 mg daily or moxifloxacin 400 mg daily) provide broad-spectrum coverage including atypical organisms and are suitable for severe CAP, especially in the elderly with comorbidities. CAUTION: fluoroquinolones carry FDA warnings for tendon rupture (Achilles tendon most common), increased risk in elderly and those on concurrent corticosteroids; also risk of QT prolongation and hyperglycemia/hypoglycemia in diabetics. More severe cases (hospitalized patients) may require a combination: amoxicillin-clavulanate (beta-lactam + beta-lactamase inhibitor) plus macrolide, or a respiratory fluoroquinolone alone. TREATMENT DURATION: typically 5–7 days for mild-to-moderate CAP; up to 10–14 days for severe pneumonia. Success is judged by resolution of fever, improvement in cough, normalization of vital signs, and clear lung fields on exam/X-ray.

Pneumonia complications include: (1) Pleural effusion—accumulation of fluid between visceral and parietal pleura, detected by dullness to percussion, decreased breath sounds, and confirmed by chest X-ray or ultrasound. May resolve with antibiotics or require thoracentesis (pleural tap) for diagnosis/therapy. (2) Empyema—infected pleural fluid (indicated by positive culture), requiring drainage (chest tube) in addition to antibiotics. (3) Sepsis/septic shock—systemic inflammatory response with hemodynamic instability (hypotension, tachycardia, altered mental status); requires aggressive fluid resuscitation, vasopressors, and intensive care. (4) Respiratory failure/ARDS (Acute Respiratory Distress Syndrome)—severe hypoxemia unresponsive to high-flow oxygen, requiring mechanical ventilation. (5) Atelectasis—collapse of a lung segment due to mucus plugging; prevented by deep breathing, coughing, and chest physiotherapy. (6) Lung abscess—localized collection of pus within lung tissue; may require drainage or prolonged antibiotics. Red flags requiring immediate escalation: SpO2 <90% despite oxygen therapy, respiratory rate >30, use of accessory muscles, stridor, inability to speak in full sentences, hemoptysis, altered mental status, signs of sepsis (hypotension, fever, tachycardia), or worsening despite antibiotics.

Sinusitis management: Most cases (viral) resolve with supportive care: saline nasal irrigation 2–3 times daily (using a neti pot or spray), steam inhalation (hot shower), decongestants (pseudoephedrine 30–60 mg every 4–6 hours, max 240 mg/day) to relieve congestion, and analgesics (paracetamol or ibuprofen) for facial pain. Antibiotics (amoxicillin, amoxicillin-clavulanate) are reserved for confirmed/suspected bacterial sinusitis—indicated if symptoms persist beyond 10 days or worsen after initial improvement, or if patient has severe symptoms (fever >39°C, severe facial pain). Treatment duration: 5–7 days. Patient teaching: avoid smoking and secondhand smoke, maintain hydration, humidify indoor air, and practice hand hygiene to prevent spread. Pharyngitis (sore throat) management: Viral pharyngitis (most common) is managed supportively: throat lozenges, warm salt-water gargles (1/2 teaspoon salt in 250 mL warm water), fluids, rest, and analgesics. Antibiotics are NOT indicated for viral pharyngitis. Group A beta-hemolytic streptococcal (GABHS/strep) pharyngitis requires a complete antibiotic course: Penicillin V 250 mg orally 4 times daily × 10 days (or Penicillin G benzathine 1.2 million units IM as a single dose) OR Amoxicillin 500 mg orally 3 times daily × 10 days. For penicillin-allergy: Azithromycin 500 mg on day 1, then 250 mg daily × 4 days, OR Cephalexin 500 mg 4 times daily × 10 days (if not anaphylaxis-level PCN allergy). The rationale for completing the full 10-day course is PREVENTION OF ACUTE RHEUMATIC FEVER (ARF) and acute post-streptococcal glomerulonephritis—these are serious sequelae that can cause permanent heart and kidney damage. Many patients stop antibiotics after 2–3 days when symptoms resolve but before the infection is fully eradicated; this incomplete treatment is the primary reason rheumatic fever develops in susceptible individuals.

Influenza (Flu) Prevention: Annual influenza vaccination is the cornerstone of prevention, recommended for all high-risk groups (elderly ≥65 years, pregnant women, those with chronic lung/heart/metabolic disease, healthcare workers, and immunocompromised individuals). Vaccination provides partial protection and reduces disease severity. Other preventive measures: respiratory hygiene/cough etiquette (cover mouth when coughing/sneezing), hand hygiene, avoid touching face, maintain distance from ill persons, and ensure good indoor ventilation. Influenza Management: Antiviral therapy is most effective when started within 48 hours of symptom onset. Oseltamivir (Tamiflu) 75 mg orally twice daily × 5 days reduces symptom duration by 1–2 days and reduces risk of complications in high-risk groups. Outside the 48-hour window, treatment is supportive: rest, hydration, antipyretics (paracetamol, ibuprofen), and decongestants if needed. Monitor for complications (secondary bacterial pneumonia). Acute Bronchitis Prevention & Management: Prevention includes smoking cessation, avoiding air pollution/irritants, hand hygiene, and avoiding close contact with ill persons. Management is supportive because >90% of cases are viral: rest, hydration, cough suppressants (dextromethorphan) if cough is dry and interferes with sleep, and analgesics. Expectorants (guaifenesin) may help loosen secretions in productive cough. Inhaled corticosteroids or bronchodilators may be considered if airway obstruction is present. Antibiotics are NOT indicated unless secondary bacterial infection is suspected (which is rare). Most coughs resolve within 3 weeks; a persistent cough lasting >3 weeks warrants further investigation (possible TB, asthma, ACE inhibitor use, or postnasal drip).