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6 respiratory Flashcards

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1
Q

When does cyanosis occur

A

When 5 g of Hb is desaturated (normal amounts is 15g/dl)

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2
Q

Clubbed fingers

A

Distorted angle of nail bed from cardiopulmonary insufficiences

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3
Q

Rhinitis

A

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

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4
Q

Influenza overview

A

A,B, C
A has HA and NA surface antigens, by changing subtype it avoid preeixsting specific immunity
Infection spread via droplets

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5
Q

Influenza targets which cells

A

Mucous-secreting and endothelial in URT, leaving holes for ECF to escape

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6
Q

Influenza spread

A

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

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7
Q

Clinical manifestations of influenza

A 
Sudden onset
Fever/chills/malaise
Myalgia/headache
Nasal discharge, sore throat, cough 
Secondary bacterial pneumonia
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8
Q

Sinusitis Rhinosinusitis

A

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

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9
Q

Etiology of sinusitis rhinosinusitis

A 
Viral infections
Allergies
Nasal polyps
Barometric changes
Swimming/diving
Abuse of nasal decongestants
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10
Q

Manifestations of sinusitis rhinosinusitis

A

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

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11
Q

Diptheria

A

Bacterial infection of tonsils and nasopharynx
Highly contagious
Produces toxins which can result in HF and paralysis
Vaccine present (but is on the rise)

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12
Q

Epiglottitis overview

A

Bacterial, from haemophilus influenza, most common in children under 3

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13
Q

Epiglottitis presentation

A

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

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14
Q

Middle resp syndromes for peds

A

Epiglottits croup pertussis

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15
Q

Croup

A

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)

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16
Q

Pertussis

A

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

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17
Q

Lower resp infections

A

Bronchiolitis
Pneumonia
Legionnaire’s
TB

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18
Q

Bronchiolitis

A

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

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19
Q

Pneumonia

A

Infection of lung from bacteria, fungi, viruses, protozoan or parasites
Acute or secondary
Most causative microorganisms found in oropharynx
70% is streptococcus pneumonia

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20
Q

Types of pneumonia based off these 4 days (First 3 most important)

A

Causative agent
Anatomical location
Pathophysiological changes
Epidemiological data

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21
Q

Bronchopneumonia

A

Begins in bronchial, migrates to alveoli, has multiple bacteria to cause it, insidious onset
Scattered diffuse patches of infection on both lungs

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22
Q

Lobar pneumonia

A

Infection localized one or more lobes, often lower lobes

Consolidation present, caused by strept pneuomniae, has a sudden and acute onset

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23
Q

Interstitial pneumonia

A

Infection in interstitial tissue of lungs in patches and all throughout
Viral or mycoplasma with variable onset

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24
Q

Etiology of pneumonia

A

Upper resp flora or extraneous pathogens not normally associated with body, causative agents can be inhaled, aspirated, or spread by blood

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25
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
26
Pneumonia endotoxins
Damage bronchial mucous and alveolocapillary membranes
27
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
28
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
29
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
30
Primary atypical pneumonia
Interstital from viral or mycoplasma Variabe onset, little exudate, unproductive cough Variable fever, headache, myalgia
31
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
32
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
33
TB caused by
Mycobacterium tuberculosis | Airborne droplet transmission, can affect systems other than lungs
34
Other names for TB
Phthisis pulmonalis, consumption
35
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)
36
Delayed hypersensitivity reaction
TB test (manteaux test)
37
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
38
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
39
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
40
TB low resistance
Initial contact progresses to cavitation
41
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
42
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
43
Obstructive pulmonary diseases
``` Bronchiectasis Chronic bronchitis Emphysema Asthma Cystic Fibrosis Characterized by difficult expiration (more force is required or lung emptying is slower) ```
44
COPD is
Chronic bronchitis and emphysema
45
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
46
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
47
Chronic bronchitis
20X greater in smoker | Inflammation from irritants or infection
48
Chronic bronchitis defintion
Hypersecretion of mucous and chronic productive cough that continues for 3 months in two consecutive years
49
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
50
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
51
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
52
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
53
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
54
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
55
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
56
Acinus
Refers to any cluster of cells that resembles a many lobed "berry"
57
Parenchyma
Functional tissue of an organ
58
Protease
Any enzyme that performs proteolysis (catabolism by hydrolysis of peptide bonds)
59
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
60
Two forms of emphysema
Centriacinar and panacinar
61
Centriacinar emphysema
Centrilobular. | Widening of airpsace in center of lobule, involves resp bronchioles mostly and is most common form
62
Panacinar
Panlobular emphysema | Involves all the airspace distal to terminal bronchioles
63
Blue bloaters
Chronic bronchitis | Pink puffers are emphysema
64
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
65
Definition of asthma
Periodic severe but reversible bronchial obstruction from hypersensitive or hyperresponsive airways Dyspnea, chest tightness, wheezing, sputum production, cough
66
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
67
Asthma classifications
Education and TX plans, based on severity, correlates better with management and outcomes Also based on etiology (intrinsic and extrinsic)
68
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
69
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
70
Extrinisc asthma
Allergic asthma | Onset commonly in children
71
Intrinsic asthma
non allergic Onset common in adulthood Many pts have combo of two Over 20 genes identified in susceptibility and patho
72
Common triggers of asthma
Allergens, lung irritants, weather, upper resp infections, physical exertion, excitement/emotional stress, ASA, NSAIDs, beta blockers
73
Extrinsic asthma
Type I hypersensitivity Distinguished by mast cell activation, eosinphil infiltration and epithelial sloughing Triggered by environmental antigens
74
Extrinsic asthma initial encounter
Stimulates plasma cells to produce antigen specific IgE antibodies that bind to mast cells
75
Important mediators of extrinsic allergies
Histamine, bradykinin, leukotriens, chemotactic factors, prostaglandins, thomboxane A2, platelet-activating factor
76
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
77
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
78
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 ```
79
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
80
Air trapping in asthma
Areas with poor ventilation will retain CO2 (PaCO2 70-80mmHg) Can cause spontaneous pneumo, pneumomediastinum, subq epmhysema
81
Pneumomediastinum
Presence of air or other gas in mediastinum
82
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
83
Status asthmaticus
``` Bronchospasms not relieved by normal measures 5-10X normal work of breathing Air trapping becomes severe Pulsus paradoxus Prone to pneumothorax ```
84
Status asthma manifestations
``` Hypoxia Decreased exp flow and volume Fatigue from work of breathing Decreased pH PaCO2 up to 70mmHg Silent chest ```
85
CNS effects of asthma
Anxiety and confusion from hypoxia | Tired and obtunded
86
Skin signs of asthma
Peripheral/central cyanosis | Diaphoresis
87
Breathing signs in asthma
``` Tachypnea Accessory muscle use Intercostal and supraclav retractions Increased work of breathing Chest expansion (assess for equal bilat) ```
88
Wheezes and sats in asthma
Silent chest may in severe exacerbation 90% O2 means PO2 of 60mmHg in alveoli Oxyhemoglobin curve shifts
89
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
90
Cardiac asthma (merck manual)
Bronchospasms with hyperventilation May be indistuingishable from other asthma Induced by LV failure (intrinsic)
91
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

Pathology (24 decks)

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