6 respiratory Flashcards
When does cyanosis occur
When 5 g of Hb is desaturated (normal amounts is 15g/dl)
Clubbed fingers
Distorted angle of nail bed from cardiopulmonary insufficiences
Rhinitis
Most common resp infection with 100+ variations (rhinovrus, adenovirus, parainfluenza, coronavirus)
Spread hand contamination to nasal mucosa or conjunctiva
1-2 days or 1-2 weeks
Nasal congestion, rhinorrhea, throat pain, sneezing, cough, malaise, mild fever and prone to secondary infections -need antibiotics
Influenza overview
A,B, C
A has HA and NA surface antigens, by changing subtype it avoid preeixsting specific immunity
Infection spread via droplets
Influenza targets which cells
Mucous-secreting and endothelial in URT, leaving holes for ECF to escape
Influenza spread
Starts in URT(7-10 days), can spread to LRT where it can causes bronchial and alveolar cells to shed to single cell-thick basal layer.
High mortality rate if it spreads and turns to pneumonia
Clinical manifestations of influenza
Sudden onset Fever/chills/malaise Myalgia/headache Nasal discharge, sore throat, cough Secondary bacterial pneumonia
Sinusitis Rhinosinusitis
Obstruction of ostia (drain paranasal sinuses)
Impairs mucociliary clearance in nasal cavity
Self limiting in 5-7 days
Acute bacterial may last longer than 10
Etiology of sinusitis rhinosinusitis
Viral infections Allergies Nasal polyps Barometric changes Swimming/diving Abuse of nasal decongestants
Manifestations of sinusitis rhinosinusitis
Facial pain, positional changes in facial pain
Sense of face fullness
Headache (worse with movement)
Nose discharge, postnasal drip, cough, sneeze
Fever
Bacterial usually presents unilaterally
Diptheria
Bacterial infection of tonsils and nasopharynx
Highly contagious
Produces toxins which can result in HF and paralysis
Vaccine present (but is on the rise)
Epiglottitis overview
Bacterial, from haemophilus influenza, most common in children under 3
Epiglottitis presentation
Sudden loss of voice and hoarseness
Throat pain with swallowing and excessive drooling
Edema/redness of epiglottis and surrounding inflamed pharyngeal mucosa
Narrowing of airways
Cherry red epiglottis
Middle resp syndromes for peds
Epiglottits croup pertussis
Croup
Acute, can be life threatening
Viral, kids under 3
From parainfluenza virus
Inflammation of mucous membranes superior to larynx
Marked by spasm of vocal cord resulting in resp stridor (barking cough)
Pertussis
Highly contagious bacterial disease
All ages now (before vaccines more common in kids)
Can cause permanent disability/death in infants
Similar to common cold, 10-12 later cough starts, lasts 6 weeks
Lower resp infections
Bronchiolitis
Pneumonia
Legionnaire’s
TB
Bronchiolitis
Bronchi, bronchioles but not alveoli
Childhood, from respiratory syncytial virus (RSV)
Invades epithelial cells causing cell death and desquamation
Incites inflam response
Edema of small airways and desquam (exfoliation) causes obstruction
Wheezing, low grade fever, SOB
Pneumonia
Infection of lung from bacteria, fungi, viruses, protozoan or parasites
Acute or secondary
Most causative microorganisms found in oropharynx
70% is streptococcus pneumonia
Types of pneumonia based off these 4 days (First 3 most important)
Causative agent
Anatomical location
Pathophysiological changes
Epidemiological data
Bronchopneumonia
Begins in bronchial, migrates to alveoli, has multiple bacteria to cause it, insidious onset
Scattered diffuse patches of infection on both lungs
Lobar pneumonia
Infection localized one or more lobes, often lower lobes
Consolidation present, caused by strept pneuomniae, has a sudden and acute onset
Interstitial pneumonia
Infection in interstitial tissue of lungs in patches and all throughout
Viral or mycoplasma with variable onset
Etiology of pneumonia
Upper resp flora or extraneous pathogens not normally associated with body, causative agents can be inhaled, aspirated, or spread by blood
Patho of pneumonia
Pathogens hit lungs, normally controlled by cough, mucociliary clearance, phagocytosis and inflammation
In susceptible that pathogen can multiply, release toxins, and stimulate full scale inflam and immune response
Pneumonia endotoxins
Damage bronchial mucous and alveolocapillary membranes
Patho of pneumonia part two
Inflammation and edema cause acini and terminal bronchioles to fill with infection debris and exude, leading to V/Q abnormalities
Consolidation filled with inflamm response (solid mass)
Staph can cause lung necrosis
Complications of pneumonia
Pleuritis - inflammation can extend to pleural surface, cause pleural effusion
Abscess - Pus inside bronchi destroy walls and causes bronchial dilation
Chronic lung disease - Parenchyma destruction and fibrosis transform lung to honeycomb like structure which is unresponsive to treatment
Clinical manifestations of pneumonia
Fever, chills, malaise productive or dry cough,
Pleural pain
Impaired gas exchanged (SOB, tachypnea)
Exudate and tissue destruction can cause blood-tinged sputum or hemoptysis
Consolidation causes crackles or ronchi
Primary atypical pneumonia
Interstital from viral or mycoplasma
Variabe onset, little exudate, unproductive cough
Variable fever, headache, myalgia
Pneumocystis carinii pneumonia
Atypical, opportunistic infection in pts with immune suppresion (AIDs, preemies)
From fungi (protozoa)
Inhaled it attaches to alveolar wall causing necrosis and diffuse interstitial inflammation
Onset is difficult breathing and unproductive cough
Legionnaire’s disease
From legionella pneumophila
Resides in cytoplasm of pulm macrophages
Thrives in warm and moist spots
Untreated causes massive consolidation and necrosis of parenchyma, associated with high mortality
TB caused by
Mycobacterium tuberculosis
Airborne droplet transmission, can affect systems other than lungs
Other names for TB
Phthisis pulmonalis, consumption
Pathophysiology of TB
Inhaled myobacterium tb lodge in lung periphery (upper lobes) where it may migrate to lymph
Progression is dependant on the individual (high or low resistance)
Delayed hypersensitivity reaction
TB test (manteaux test)
High resistance pts with TB
Primary infection, neutrophils and macrophages migrate to site of inflamm, engulf bacilli, seal off the colonies and form granulamatous lesions called tubercle
Tissue after TB is walled off
Infected tissue in tubercle die, forming cheese-like material (caseation necrosis) collagen scar tissue grows around tubercle, completing isolating (ghon complex)
Tb can remain dormant for life in this form
Secondary infection of TB
Active infection from
Decreased immunity, new invasion, or bacilli escaping ghon complex where it spreads to apex causing lobular pneumonia
Granulmoas lead to cavitation
Destruction of lung tissue, erosion of bronchi and blood supply, causes hemoptysis
TB low resistance
Initial contact progresses to cavitation
S&S of TB
Primary is asymptomatic
Secondary or active has insidious onset
First anorexia, malaise, fatigue, weight loss
Afternoon-low grade fever and night sweats
Prolonged severe productive cough purulent (with pus) with blood
Complications of TB
Miliary TB - widespread seeding of bacteria in lungs or other organs (formation of small granulomas)
Pneumonia/pleuritis
Extrapulmonary in larynx, GI, etc from swallowing infected sputum
Obstructive pulmonary diseases
Bronchiectasis Chronic bronchitis Emphysema Asthma Cystic Fibrosis Characterized by difficult expiration (more force is required or lung emptying is slower)
COPD is
Chronic bronchitis and emphysema
Bronchiectasis
Permanent dilation of bronchi, usually localized
From persistent inflamm inside airways or obstruction of airways by neoplasm/foreign bodies, CF.
Most common complication of chronic bronchitis
Causes of bronchiectasis
Dilation from enzymes released in inflammatory response, lungs break down garb and can’t clear it.
Stagnated material causes spread of infection
Chronic bronchitis
20X greater in smoker
Inflammation from irritants or infection
Chronic bronchitis defintion
Hypersecretion of mucous and chronic productive cough that continues for 3 months in two consecutive years
Patho of chronic bronchitis
Irritants increase mucous production and # goblet cells which means bacteria more likely to become embedded in it
Ciliary function impaired, reducing mucous clearing.
Increases chance of infection
More patho of chronic bronchitis
Thickening/inflammation of bronchial walls from
edema
accumulation of inflamm cells
bronchial smooth musce hypertrophy
causing airway obstruction
Airway collapse early in expiration trapping gas in distal portions of lung, eventually leading to V/Q mismatch, hypovetn and hyopxemia
Clinical manifestations of chronic bronchitis
Blue bloaters
Decreased exercise tolerane
SOB, productive cough, evidence of airway obstruction using spirometry
Hypoxemia with exertion
Copious sputum, some wheezing, prone to pulm infections
More clinical manifestations of chronic bronchitis
Airway obstruction results in decreased alveolar ventilation and increased PaCO2
Hypoxemia (leads to polycythemia, cyanosis and pulm hypertension cor pulmonale
Hypoxic drive develops
Emphysema
Abnormal and permanent enlargement of gas exchange airways (acini), and destruction of alveolar walls without obvious fibrosis
Obstruction is result of lung tissue changes rather than mucous and inflamm
Loss of elastic recoil is reason for air flow limitations
Alpha1 antityrpsin
A protein which inhibits the activity of proteases (destructive enzymes like neutrophils, bacteria)
1-2% of emphysema is caused by a lack of this. Emphysema develops early in life
Smoking and emphysema
Excessive accumulation of neutrophils in lung parenchyma, and decreases alpha1-antitrypsin activity
Certain bacteria can also cause emphysema by release of proteases
Acinus
Refers to any cluster of cells that resembles a many lobed “berry”
Parenchyma
Functional tissue of an organ
Protease
Any enzyme that performs proteolysis (catabolism by hydrolysis of peptide bonds)
COPD cardiac effects
Alveolar breakdown, eliminates portions of pulm cap beds, increases volume of acinus which reduces elastic recoil
Increased residual volume, diminished caliber of bronchioles and additional narrowing possible from inflam responses
Two forms of emphysema
Centriacinar and panacinar
Centriacinar emphysema
Centrilobular.
Widening of airpsace in center of lobule, involves resp bronchioles mostly and is most common form
Panacinar
Panlobular emphysema
Involves all the airspace distal to terminal bronchioles
Blue bloaters
Chronic bronchitis
Pink puffers are emphysema
Clinical manifestations of emphysema
Pink puffers
Dyspnea with exertion which eventually is continuous dyspnea
No cough, little sputum, home O2
Thin pts, tachypnea, prolonged expiration, accessory muscle use, increased AP diameter
Tripoders, hyperressonance on percussion
Definition of asthma
Periodic severe but reversible bronchial obstruction from hypersensitive or hyperresponsive airways
Dyspnea, chest tightness, wheezing, sputum production, cough
Prevalence of asthma
8.5% of Canadians over aged 12
13% of children
80% of deaths could be prevented by education, 50% die before arrival to hospital
Asthma classifications
Education and TX plans, based on severity, correlates better with management and outcomes
Also based on etiology (intrinsic and extrinsic)
Asthma by education and treatment plans
Very mild, mild, moderation, moderately severe, severe
Based on clinical manifestations and peak flow
Emphasis on fact relieve bronhospasm is no longer PRIMARY treatment
Three s’s of asthma
Swelling (inflammation) from increased camp perm and mucosal edema
Secretions - mucous plug formation
Spasm - inflamm mediators constrict broncial smooth muscle, cause wheezing and prolonged expiration
Extrinisc asthma
Allergic asthma
Onset commonly in children
Intrinsic asthma
non allergic
Onset common in adulthood
Many pts have combo of two
Over 20 genes identified in susceptibility and patho
Common triggers of asthma
Allergens, lung irritants, weather, upper resp infections, physical exertion, excitement/emotional stress, ASA, NSAIDs, beta blockers
Extrinsic asthma
Type I hypersensitivity
Distinguished by mast cell activation, eosinphil infiltration and epithelial sloughing
Triggered by environmental antigens
Extrinsic asthma initial encounter
Stimulates plasma cells to produce antigen specific IgE antibodies that bind to mast cells
Important mediators of extrinsic allergies
Histamine, bradykinin, leukotriens, chemotactic factors, prostaglandins, thomboxane A2, platelet-activating factor
Reaction of extrinsic asthma
Eosinophils produce
- a major basic protein that stops ciliary beating
- disrupts mucosal integrity
- causes damage and sloughing of epithelial cells
Causes bronchospasm, bronchial inflammation occurs
Reaction can also stimulate branches of vagus nerve which causes reflex bronchoconstriction
Second stage (late) of asthmatic reaction
Result of significant allergen exposure
Inital response is 15min to 3 hours, 40% of patients then experience further obstruction in 4-12 hours which is more severe
Caused by chemotaxis from inflamm cells invade airways promoting further inflamm and hyper responsiveness
Precipitators of intrinsic
Resp infections Drugs (asa, b antagonists) environmental irritants Cold, dry air, exercise, stress GERD 75% of pts with asthma have GERD Bronchospasm may be due to imbalance of parasympa and sympa nervous system Increased parasympa causes constriction
Exacerbation of intrinsic asthma patho
3’s lead to hyperinflation of pts chest
Pressures in lung increases, more pressure needed to move air in and expiration is slowed resulting in air trapping and lung hyperinflation
Needs more inspiratory muscle force, evidenced by dyspnea, tachycardia, accessory muscle use
Air trapping in asthma
Areas with poor ventilation will retain CO2 (PaCO2 70-80mmHg)
Can cause spontaneous pneumo, pneumomediastinum, subq epmhysema
Pneumomediastinum
Presence of air or other gas in mediastinum
Cardiovascular effects of asthma
Increased negative pleural pressures needed on inspiration cause CV stress
LV must pump blood from negative intrathoracic pressure to systemic circulation leading to fall in BP during inspiration (pulsus paradoxus) and narrowing BPs
Status asthmaticus
Bronchospasms not relieved by normal measures 5-10X normal work of breathing Air trapping becomes severe Pulsus paradoxus Prone to pneumothorax
Status asthma manifestations
Hypoxia Decreased exp flow and volume Fatigue from work of breathing Decreased pH PaCO2 up to 70mmHg Silent chest
CNS effects of asthma
Anxiety and confusion from hypoxia
Tired and obtunded
Skin signs of asthma
Peripheral/central cyanosis
Diaphoresis
Breathing signs in asthma
Tachypnea Accessory muscle use Intercostal and supraclav retractions Increased work of breathing Chest expansion (assess for equal bilat)
Wheezes and sats in asthma
Silent chest may in severe exacerbation
90% O2 means PO2 of 60mmHg in alveoli
Oxyhemoglobin curve shifts
Speech and cough in asthma
Speech is a good indicator of improving/worsening
Cough is white, thick sputum but may be non-productive
Labured spasms caused by irritation/constriction of airways
Cardiac asthma (merck manual)
Bronchospasms with hyperventilation
May be indistuingishable from other asthma
Induced by LV failure (intrinsic)
Cystic fibrosis
Fatal disorder of secretory glands of mucous and sweat
Creates thick/concentrated secretions
Affects mainly children
In adults it may be mild, and due to CS gene not being as faulty
Effects resp, GI, skin and repoductive
