Pulmonary Flashcards
(29 cards)
function of alveolar type I cells
function of alveolar type II cells
type I : responsible for gas exchange, large squamous cells usually a single cell layer thick.
type II : produced surfactant which covers the surface of alveoli, small and cuboidal. more abundant. Surfactant reduces surface tension of on the alveoli increasing elasticity; prevents alveoli from collapsing
The process of breathing is largely ______ and controlled by ____?
involuntary, controlled by medulla oblongata
describe the inspiration phase of breathing
expiration?
neural process - nerve impulses travel from brain to diaphragm which contracts, lower, and flatten to draw air INTO the lungs. Intercostal muscles are contracting to lift the ribs up and out.
expiration phase is passive once the diaphragm relaxes and goes to og position. increase intrapulmonary pressure and decrease thoracic volume -> forcing air out of lungs.
Infective Rhinitis
clinical manifestation?
dx/tx?
usually caused by viruses RHINOvirus (any other virus too). organism invades epithelial lining of nasal mucosa -> infected cells release chemokines/cytokines -> immune system and inflammation activation. Runny nose, nasal discharge, mucus production.
dx: based off signs and symptoms. dx of i.R is when there is NOT a local or focused complaint like sore throat, or infection on ONE anatomic location.
purulence and fever may be bacterial but can be present with viral infections
tx: symptomatic treatment, OTC, can lead to secondary infections. pneumonia, otitis media etc.
Rhinosinusitis
most common causes?
patho?
acute/subacute/chronic/recurrent
CM?
most commonly caused by viruses. also by allergies, barotrauma. Bacterial includes streptococcus pneumoniae or haemophilus influenzae.
patho: inflammation and increased mucus prevents the outflow of nasal secretions -> infection proliferates and damages the ciliated linin in the sinus.
acute 4 wks, subacute 4-12 wks, chronic 12+ wks. Recurrent is several attacks within a year
CM: pressure in the sinus cavity, facial/bone pain, headache. coughing or sudden movements exacerbates pain. lying or leaning forward = pain in frontal sinus. standing worsens maxillary sinus pain. Retro-orbital pressure or eye pain may indicate ethmoid sinusitis.
what are the 3 common pharyngitis?
Viral pharyngitis (most common)
Infectious Mononucleosis
bacterial pharyngitis
Infectious Mononucleosis
common cause?
CM?
Dx/Tx
Epstein-Barr Virus. Usually asymptomatic in children, mild symptoms in adults. Virus can remain in-active and reactivates during immunocompromised states.
CM: EBV and Cytomegalovirus (CMV) usually asymptomatic, incubates 4-6 weeks. fever, myalgia, sore throat, fatigue. Physical exam = lymphadenopathy, exudative pharyngitis.
spleenoMEGALY and hepatoMEGALY common with EBV
dx: monospot blood test, CVC will show increase bands, wbc.
tx: symptom management. Oral glucocorticoids for enlarged tonsils or airway obstruction concern.
Bacterial Pharyngitis
common cause?
CM?
dx/tx?
Streptococcus pyogenes; bacteria
CM: acute sudden sore throat, painful swallowing. Tonsillar erythema / hypertrophy / and exudates (sometimes).
petechiae on palate = strawberry tongue.
dx: throat swab, culture. Treat with antibiotics. Penicillin or amoxicillin.
GABHS (strep beta-hemolytic) is self limiting but antibx can shorten the length of disease.E
Epiglottitis
CM?
Dx/Tx?
rapid CM in children but slowly in adults. upper airway obstruction + high fever, sore throat, MUFFLED VOICE, dysphagia. inspiratory stridor , retractions.
dx: throat should NOT be examined risk for laryngospasm
tx: maintain airway, O2, xray, ABG, Neck on xray lateral view may have a THRUMBPRINT sign.
Peritonsillar Abscess
CM?
Dx/Tx?
CM: sore throat, dysphagia, drooling, odynophagia (painful swallowing). Trismus (jaw locking). UNILATERAL (rarely bilateral) swelling of tonsil with exudate, uvula displacement, soft palate asymmetry.
dx: CT neck w/ contrast.
tx: stabilize airway if needed, IV antibx, pain control. I&D abscess.
Laryngotracheitis (croup)
CM?
Dx/Tx
affects the larynx and trachea -> edema to subglottic area. The edema develops rapidly leading to narrowing airway/ obstruction.
CM: usually begins with URI, hoarseness; seal-like BARKING cough, inspiratory stridor, cyanosis.
dx: physical assessment, CBC, xray
tx: croup is self limiting, but corticosteroids decrease edema, humidified O2. Aerosolized-epinephrine. HELIOX (mix of helium and O2) decreases airway resistance.
Difference between type A, b, C influenza? (who it affects)
influenza A continuously goes through antigenic changes; commonly found in aquatic birds without causing them harm. But it can jump species to pigs, chicken.
B - usually regional, more mild, primarily human.
C - sporadic cases, usually minor, it is antigenically stable, humans/pigs/dogs
Pneumonia
patho
CM
inflammation of the lung parenchyma, where gas transfer occurs (includes bronchioles, alveolar ducts, and alveoli). Once inflammation gets bad enough, the exudate/cell debris accumulate in alveoli and bronchioles impairing gas exchange. -> consolidation.
Community Acquired pneumonia
Hospital acquired pneumonia
Atypical pneumonia
Legionnaires disease
Aspiration Pneumonia
Middle East respiratory syndrome
CAP - usually gram positive bacterial; acquired within the community itself.
HAP - introduction of pathogen from not cleaning hands to ETT tubes. Ventilator associated pneumonia within 48hrs of intubation
Atypical pneumonia - when pathogens do not respond to usual antibiotics including legionella pneumophilia
Legionnaires - pneumonia caused by legionella pneumophilia; warm moist environment. acquired by inhaling small water droplets.
Aspiration - gag reflex is impaired or secondary to nasogastric tube placement. inflammation caused by irritants in the lung tissue causing increased mucus production -> atelectasis.
Middle east - same coronavirus family, camel -to-human transmission. and human to human.
Patho of TB
- Inhalation of TB bacteria
You breathe in droplets from someone with active TB (e.g., coughing).
The bacteria reach the alveoli in the lungs.
- Immune system responds
White blood cells (especially macrophages) try to eat the bacteria.
But TB bacteria are sneaky—they hide and multiply inside the macrophages.
- Granuloma formation (tubercle)
The immune system walls off the infected area.
Forms a granuloma: a tight group of immune cells trying to trap the TB.
Inside the granuloma, the bacteria go dormant—they stay alive but inactive.
This is called Latent TB (no symptoms, not contagious).
- Active TB (when granuloma breaks down)
If the immune system weakens (e.g., HIV, malnutrition, stress), the granuloma breaks.
Bacteria escape and multiply.
This causes lung tissue destruction, cavities, and chronic inflammation.
Asthma patho early response
Exposure to allergen (trigger):
Examples: pollen, dust mites, animal dander, mold.
Immune system overreacts:
The body treats harmless things like they’re dangerous invaders.
IgE antibodies are produced against the allergen.
Mast cells release chemicals:
Especially histamine and leukotrienes.
These cause:
Bronchoconstriction (airways tighten)
Inflammation
Mucus production
Narrowed airways = asthma attack:
Hard to breathe out (especially).
Classic asthma symptoms occur:
Wheezing
Shortness of breath
Coughing
Chest tightness
Asthma Late response
after initial hypersensitivity response. Neutrophils, lymphocytes and eosinophils release same mediators like in the acute phase.
alveolar hyperinflation -> air trapping, unable to clear mucus causing mucus plugs. without treatment it progresses to fibrosis, hypertrophy of smooth muscle. “airway remodeling”
Pathogenesis of COPD
CM?
caused by smoking or inhaling irritants. inflammation from wbc primarily CD4+ and eosinophils -> fibrosis, small airway damage.
usually there is balance between protease and antiprotease; keeps lung tissue from being destroyed. but during inflammation increase destructive protease. -> alveoli turn large and irregular pockets called BULLAE -> limited gas exchange
elastic fibers and surfactant destroyed -> alveoli cant keep open causing airway to collapse during expiration -> trapping gas -> hyperinflation -> hypercapnia and hypoxemia.
CM: dyspnea, hypoxemia -> increase erythropoietin -> secondary polycythemia; clubbing fingers, cyanosis, and dyspnea. Fatigue, weight loss. COPD triggered by stimuli and impaired pulmonary defense leading to infection.
Pathogenesis of sleep apnea? OSA and CSA
CM?
Dx/Tx
OSA is obstruction at the soft palate/nasopharynx or tongue. decrease size of upper airway -> more resistance. Enlarged tongue, tonsils or oral structures (usually occurs with obesity)
CSA not as common; brain is sending signals to inhibit respirations rather than excite -> cessation or decreased airflow. Cheyne-stokes respirations (deep and fast breathing then followed by decrease and slow or absent breathing)
CM: habitual snoring, periods of silence with apnea. Breath holding. not good sleep with daytime sleepiness, fatigue, poor concentration and irritability.
dx: sleep study (polysomnography), 5 or more obstructive respiratory events per 1 hr of sleep WITH one or more comorbidity like diabetes, HF, stroke, Afib etc.
OR 15 or more events within 1 hr REGARDLESS of comorbidities.
Pathology of Cystic Fibrosis
CM
changes to the cells that produce mucus, sweat, and saliva -> number of goblet cells increase (even in digestive system) -> more mucus production -> secretions are more thick. Cilia cant clear the excess mucus.
neutrophils release oxidants damaging the lungs. N elastase damages elastin, inflammation, and stimulates MORE mucus secretion. IgG is destroyed by neutrophil elastase -> damaged immune system.
Pseudomonas aeruginosa is common with CF because stagnant mucus is perfect for it to grow.
CM: declining lung function starting at early childhood. Meconium ileus (blockage of small intestine by meconium). baby’s skin tastes salty.
thick sputum, dyspnea, fatigue, digital clubbing, wheezing.
dx: sweat analysis - sweat chloride concentration greater than 60mmol/L is diagnostic. check chromosome 7 mutation if suspected false negative sweat test or if siblings are carriers.
Stage and treatment per stage of non small cell lung cancer
I
II
III
IV
stage I - invaded lung tissue but NOT lymph nodes. Surgery
Stage II - spread to neighboring lymph nodes or chest wall. Surgery, radiation, chemo
Stage IIIA - spread from lung to lymph nodes in CENTER of chest. combined chemo and rad. surgery is depending on results after tx.
Stage IIIB - cancer spread locally like heart, blood vessels, trachea, esophagus (all within chest)
Stage IV cancer spread to other parts of body like liver, bones or brain. Chemo, immunotherapy, supportive care
Small cell lung cancer limited stage vs extensive stage
limited: cancer confined to one lung and to neighboring lymph nodes
extensive: spread beyond one lung and nearby lymph nodes. more than one lung, more remote lymph nodes or other organs.
is there normally fluid in the pleural cavity and why? where from?
20ml of lymphatic fluid is portioned out to the pleural cavity to lubricate the lungs due to constant movement. however pleural effusions occur when it is not drained or there is excess pleural fluid.
CM of pneumothorax
sudden chest pain over affected lung, tightness , dypsnea. diminished breath sounds over affected lung. Asymmetrical chest rise.
deviated trachea and mediastinal shift, hypotension
