Patho

Exam 3 key things

• Understand Definitions & Relationships – Know what each term means and how it connects to others in the same category.

• Distinguish Similar Terms – For conditions like types of asthma or pneumonia, understand their differences.

• Recognize Causes & Effects – For diseases, identify causes, symptoms, and potential complications.

• Know Diagnostic & Treatment Methods – Some terms relate to diagnosis (e.g., Barrett esophagus) or treatments (e.g., LAIV for flu).

• Review Pathophysiology – Understand underlying mechanisms, especially for major conditions like COPD or hepatitis.

Chapter 30 Outline

Respiratory Tract Infections – upper (nose, pharynx, larynx) & lower (trachea, bronchi, bronchioles & alveoli); signs/symptoms depend on function of structure, severity of infection, age and general health status

• viruses are most common cause of respiratory infections; damage bronchial epithelium, obstruct airway, lead to secondary bacterial infections

Common cold - viral infection of upper respiratory tract; most common respiratory infection; begins with dryness/stuffiness

➡ excessive nasal secretions & lacrimation; muco

us membranes are red/swollen/bathed in secretions; usually

self-limited & resolves in 7 days

• caused by a variety of viral agents:

1- rhinoviruses – prevalent in early fall/late spring,

2-respiratory syncytial virus – winter & spring months

3- adenovirus – winter & spring

4- coronavirus – winter & spring

5- parainfluenza virus –

• respiratory syncytial virus & parainfluenza virus are most common in children <3 years old

• rhinovirus most common source of colds in 5-40 yr olds; over 100 serotypes known; acquire lifetime immunity to an individual serotype

• children are major reservoir of cold viruses; fingers are greatest source of spread; nasal mucosa & conjunctiva of eyes are most common portals of entry for the virus; highly contagious period = first 3 days, incubation period = 5 days; aerosol spreading is not as important as spread by fingers ➡ importance of hand-washing; rest & antipyretic drugs used (antibiotics aren’t effective against viral agents)

Rhinosinusitis – sinusitis; develops when upper respiratory infection or allergic rhinitis narrows the ostia and obstructs flow of mucus

• acute rhinosinusitis can be of viral, bacterial, or mixed origin & can last from 5-7 days (bacterial) or up to 4 weeks (bacterial)

• recurrent acute rhinusinusitis = 4+ episodes within 1 yr

• subacute rhinosinusitis = lasts from 4 wks to less than 1 yr

• chronic rhinosinusitis = lasts beyond 12 weeks

• acute bacterial rhinosinusitis – due to Haemophilus influenza

or Streptococcus pneumoniae

• chronic rhinosinusitus– due to anaerobes Peptostreptococcus, Fusobacterium & Prevotella with or without aerobes such as Streptococcus or Staphylococcus species

• immunocompromised individuals can have infections with gram- negative bacteria & fungi as well

• manifestations = facial pain, headache, purulent nasal discharge, decreased sense of smell, fever

• chronic rhinosinusitis = fullness in ears, hoarseness, postnasal drip, cough, unpleasant breath, loss of taste & smell

• for diagnosis – sinusitis headache is usually worse when bending forward, coughing or sneezing

• treatment = antibiotics, decongestants, mucolytic agents

Influenza– viral infection that kills 36,000/yr in US during nonpandemic yea

rs; A,B,C types

• highest infection rates among children; highest rates of serious

illness/death among 65+ year olds

• type A–affects humans, pigs, horses & birds; major cause of epidemics & pandemics

• subtype hemagglutinin (HA)– attachment protein that aids viral entry

• subtype neuroaminidase (NA)– aids viral replication & release from host cell

• contagious nature of Type A reflects its ability to develop new HA & NA subtypes (e.g., H1,H2...; N1,N2,...) ➡ antigenic shift

• types B & C don’t exhibit antigenic shift

• transmission by aerosol or direct contact; inhaling as few as 3 particles can cause an infection!

• young children are most likely to become infected & spread infection- incubation period = 1-4 days; contagious period remains through 5+ days after symptom onset (children can be infectious longer >10 days)

• can result in three types of infection:

1-upper respiratory infection (rhinotracheitis)

2-viral pneumonia

3-respiratory viral infection followed by a bacterial infection

• virus targets/kills mucus- secreting, ciliated epithelial cells leaving holes in basal cell membrane & allowing ECF to escape ➡ runny nose

• lower respiratory tract involvement includes damage to bronchial & alveolar cells ➡ increased bacterial adhesion to epithelial cells ➡ pneumonia

• symptoms = chills, fever, aching, headache, watery nasal discharge, nonproductive cough, sore throat

• characterized by rapid onset of symptoms

• viral pneumonia is common complication in elderly & individuals with cardiopulmonary diseases

• secondary complications include: sinusitis, otitis media, bronchitis, & bacterial pneumonia (S. pneumoniae, S. aureus, H. influenza, Moraxella catarrhalis)

• treatment – try to limit infection to upper respiratory tract; rest (decreases oxygen demand & respiratory rate), keep warm (maintain respiratory epithelium at temperature slightly above viral replication optimum), drink fluids (prevents dehydration of epithelial lining)

• aspirin should be avoided in children (Reyes syndrome – fatty liver & encephalitis)

• 1st generation antiviral drugs (amantadine, rimantadine) – effective against influenza A but not B; prevent uncoating of viral RNA ➡ prevents replication

• 2nd generation antiviral drugs (zanamivir, oseltamivir)–NA inhibitors, effective against influenza A & B

-effective antiviral therapy should begin within 30hrs of symptom onset - immunization (must be changed yearly due to changes in virus - 1°prevention strategy; involves trivalent inactivated influenza vaccine (TIIV) and newer live, attenuated influenza vaccine (LAIV)

Pneumonias –classified according to agent causing infection (typical, atypical), infection distribution (lobar pneumonia, bronchopneumonia) and setting (community or hospital)

• typical pneumonias –caused by bacteria that multiply extracellularly in alveoli & cause inflammation & fluid exudation into alveoli air spaces

• atypical pneumonias–caused by viral and mycoplasma infections of the alveolar septum & lung interstitium

• lobar pneumonia – infection found contained within a part or all of a lung lobe

• bronchopneumonia –patchy infection involving more than one lobe

• community-acquired pneumonia – infection begins in an individual outside of a hospital or nursing home setting ; most common causes are S.pneumoniae (1st ), H. pneumoniae, S. aureus & gram-negative bacilli; less common are M. catarrhalis , Klebsiella pneumoniae, Neisseria meningitides, Legionella sp., Mycoplasma pneumoniae, and Chlamydia pneumoniae are atypical agents found in 20-40% of cases; viral causes include influenza virus, respiratory syncytial virus, adenovirus, & parainfluenza virus

• hospital- acquired pneumonia – noscomial pneumonia; lower respiratory tract infection that was not present or incubating upon hospital admission;second most common cause of hospital-acquired infections, has a mortality rate of 20-50%; most hospital infections are bacterial (Pseudomonas aeruginosa, S. aureus, Enterobacter sp. Klebsiella sp., Escherichia coli, & Serratia) ; many have acquired antibiotic resistance

• pneumonia in immunocompromised persons – compromised hosts are without many of the functioning defenses that protect us from morbidity & mortality when exposed to infective agents; includes persons with HIV, bone marrow/organ transplantation, cancers, & those on corticosteroid or other immunosuppressant drugs; infections can be caused by any bacterial or viral agent commonly associated with pneumonia + Aspergillus & Candida (fungal agents)

• acute bacterial (typical) pneumonias – important cause of morbidity & mortality among elderly; organisms causing disease are usually present in the respiratory tract and don’t cause a problem until they become more virulent, represent a large inoculum or host defenses are impaired; often classified according to causative agent:

• S. pneumoniae pneumonia –most common bacterial pneumonia; 90 serotypes with distinct capsule polysaccharides; can be prevented through immunization (23- valent pneumococcal vaccine, contains 23 different capsular types); multidrug- resistant strains are known

• Legionnaires disease– caused by Legionella pneumophila found in warm, standing water; risk is greatest among smokers, people with chronic diseases or impaired cell -mediated immunity

• primary atypical pneumonias – patchy inflammatory changes of lungs confined to alveolar septum & pulmonary interstitium; most common agent is Mycoplasma pneumoniae, although viral agents are also common; course of infection is variable & it can assume epidemic status (pandemics of 1915 & 1918)

Tuberculosis – caused by Mycobacterium tuberculosis, resistant to destruction, can persist in necrotic & calcified lesions for prolonged periods & reinstate growth

• contracted/spread by inhaling my cobacterium- containing droplet nuclei that circulate in air

• cell-mediated response walls off bacteria (within a granulomatous lesion called a Ghon focus) & prevents active tuberculosis; persons with impaired cell - mediated immunity are more likely to develop active tuberculosis upon infection

• positive TB skin test result means person has been infected with organism and has mounted a cell -mediated immune response; it does not mean that person has active tuberculosis

• primary tuberculosis – develops in individuals previously unexposed/ unsensitized; usually clinically & radiologically silent; most go on to develop latent infection with T cells & macrophages surrounding organisms in granulomas that limit their spread; persons with decreased cell-mediated immunity can develop progressive primary tuberculosis with lung tissue destruction & spread to multiple sites

• secondary tuberculosis – reinfection or reactivation of a previously healed primary lesion; usually localized at apex of upper lobes of lung

• treatment –requires long -term antimycobacterial therapy (6-12 months)

Fungal infections – classified as: superficial, subcutaneous, deep-seated, & opportunistic pathogenic fungi; deep-seated highly -virulent dimorphic fungi have the ability to invade deep tissues & cause systemic diseases

• Histoplasma capsulatum  (histoplasmosis), Coccidioides immitis ( coccidioidomycosis), Blastommyces dermatitidis ( blastomycosis) produce pulmonary infections that resemble TB; can produce lung damage and can spread to other organs

Lung Cancer – leading cause of death in men & women in the US; smoking causes genetic changes that convert normal bronchial cells to cancer cells; lung cancer also associated with exposure to asbestos, arsenic, chromium, nickel & vinyl chloride

• 95% of primary lung cancers arise from bronchial epithelium

(bronchiogenic carcinoma); remaining 5% are a miscellaneous group of multiple origin

• bronchiogenic carcinomas – aggressive, locally invasive, metastatic tumors that arise from epithelial lining of bronchi; subdivided into 4 major categories:

1 - squamous - cell carcinoma–25-40%; mostly in male smokers;

originates in central bronchi & is amen able to early detection;

metastasis outside the thorax occurs later than in other bronchiogenic cancers

2 - adenocarcinoma – 25-40%; most common type found in US; most common form found in women & nonsmokers; more peripheral in location & associated with areas of scarring

3 - small- cell carcinoma– 20-25%, distinctive small, round -oval cells that grow in clusters; strong association with cigarette smoking; highly malignant; 70% have undergone metastases at time of diagnosis; brain involvement common

4 - large -cell car cinoma – 10-15%; large polygonal cells; tend to occur at lung periphery; poor prognosis because of early spread

• lung cancers cause nonspecific symptoms such as anorexia, weight loss & paraneoplastic syndromes involving endocrine, neurologic, & hematologic dysfunction

• treatments include surgery, irradiation, & chemotherapy

Respiratory disorders in children –

Lung development – 5 stages of development: embryonic

➡ glandular ➡ canicular ➡ saccular ➡ alveolar periods; 1 st

three stages involve development of air conducting pathways, last two phases involve gas exchange sites; lung development is

incomplete at birth & alveoli continue to increase in number until age 5

Alterations in breathing patterns -

• most lung diseases in young children result in decreased lung compliance & signs of restrictive lung disease; breathing is faster & respiratory excursions are shallow

• expiratory grunt – when child tries to raise the functional residual capacity by closing the glottis at the end of expiration

• nasal flaring – method used by infants to take in more air; reduces nasal resistance & maintains airway patency (open)

• inspiratory retractions – pulling in the soft tissue surrounding the cartilaginous & bony thorax is seen when the airway is obstructed

• extrathoracic airway obstruction (nose, pharynx, larynx, upper trachea)– produces turbulence of airflow & an audible inspiratory crowing sound, stridor

• intrathoracic airway obstruction ( bronchi & bronchioles) –produces audible wheezing or whistling sound

Respiratory disorders in the neonate –

• respiratory distress syndrome (RDS) – hyaline membrane disease; common respiratory disease in premature infants

• pulmonary immaturity & lack of enough surfactant (reduces surface tension in alveoli, reduces pressure needed to inflate & keep alveoli open) ➡ alveolar collapse

• type II alveolar cells that produce surfactant do not start working until 25-28 weeks gestation

• infants of diabetic mothers are more prone to RDS because insulin inhibits surfactant production; corticosteroids can promote type II alveolar cell development and surfactant synthesis

• bronchopulmonary dysplasia (BPD) – chronic pulmonary disease that develops in premature infants who were treated with mechanical ventilation

Respiratory infections in children–

• upper (viral croup, laryngotracheobronchitis ; spasmodic croup & epiglottitis) and lower (acute bronchiolitis) airway infections are common in infancy & childhood

• croup or acute laryngotracheobronchitis – viral infection that affects larynx, trachea & bronchi; parainfluenza virus accounts for 75% of cases; commonly seen in children 3 mo. –5 yrs; usually follows a cold, observe stridor & a wet, barking cough; symptoms lessen with moist air

• spasmodic croup – may be of allergic origin; usually occurs at night

• epiglottitis - life- threatening supraglottic infection that may cause airway obstruction & asphyxia; sudden onset, child sits with mouth open & chin thrust forward; can be caused by Haemophilus influenzae type B, Streptococcus pyrogenes, S. pneumoniae, & S. aureus

• bronchiolitis –caused by respiratory syncytial virus; most commonly seen in children under 2 yrs; observe breathlessness, rapid/shallow breathing, wheezing, cough and inspiratory retraction