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Pathology > 6 respiratory > Flashcards

6 respiratory Flashcards

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
Q

Patho of pneumonia

A

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

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26
Q

Pneumonia endotoxins

A

Damage bronchial mucous and alveolocapillary membranes

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27
Q

Patho of pneumonia part two

A

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

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28
Q

Complications of pneumonia

A

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

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29
Q

Clinical manifestations of pneumonia

A

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

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30
Q

Primary atypical pneumonia

A

Interstital from viral or mycoplasma
Variabe onset, little exudate, unproductive cough
Variable fever, headache, myalgia

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31
Q

Pneumocystis carinii pneumonia

A

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

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32
Q

Legionnaire’s disease

A

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

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33
Q

TB caused by

A

Mycobacterium tuberculosis

Airborne droplet transmission, can affect systems other than lungs

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34
Q

Other names for TB

A

Phthisis pulmonalis, consumption

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35
Q

Pathophysiology of TB

A

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)

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36
Q

Delayed hypersensitivity reaction

A

TB test (manteaux test)

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37
Q

High resistance pts with TB

A

Primary infection, neutrophils and macrophages migrate to site of inflamm, engulf bacilli, seal off the colonies and form granulamatous lesions called tubercle

38
Q

Tissue after TB is walled off

A

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
Q

Secondary infection of TB

A

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
Q

TB low resistance

A

Initial contact progresses to cavitation

41
Q

S&S of TB

A

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
Q

Complications of TB

A

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
Q

Obstructive pulmonary diseases

A 
Bronchiectasis
Chronic bronchitis
Emphysema
Asthma
Cystic Fibrosis
Characterized by difficult expiration (more force is required or lung emptying is slower)
44
Q

COPD is

A

Chronic bronchitis and emphysema

45
Q

Bronchiectasis

A

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
Q

Causes of bronchiectasis

A

Dilation from enzymes released in inflammatory response, lungs break down garb and can’t clear it.
Stagnated material causes spread of infection

47
Q

Chronic bronchitis

A

20X greater in smoker

Inflammation from irritants or infection

48
Q

Chronic bronchitis defintion

A

Hypersecretion of mucous and chronic productive cough that continues for 3 months in two consecutive years

49
Q

Patho of chronic bronchitis

A

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
Q

More patho of chronic bronchitis

A

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
Q

Clinical manifestations of chronic bronchitis

A

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
Q

More clinical manifestations of chronic bronchitis

A

Airway obstruction results in decreased alveolar ventilation and increased PaCO2
Hypoxemia (leads to polycythemia, cyanosis and pulm hypertension cor pulmonale
Hypoxic drive develops

53
Q

Emphysema

A

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
Q

Alpha1 antityrpsin

A

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
Q

Smoking and emphysema

A

Excessive accumulation of neutrophils in lung parenchyma, and decreases alpha1-antitrypsin activity
Certain bacteria can also cause emphysema by release of proteases

56
Q

Acinus

A

Refers to any cluster of cells that resembles a many lobed “berry”

57
Q

Parenchyma

A

Functional tissue of an organ

58
Q

Protease

A

Any enzyme that performs proteolysis (catabolism by hydrolysis of peptide bonds)

59
Q

COPD cardiac effects

A

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
Q

Two forms of emphysema

A

Centriacinar and panacinar

61
Q

Centriacinar emphysema

A

Centrilobular.

Widening of airpsace in center of lobule, involves resp bronchioles mostly and is most common form

62
Q

Panacinar

A

Panlobular emphysema

Involves all the airspace distal to terminal bronchioles

63
Q

Blue bloaters

A

Chronic bronchitis

Pink puffers are emphysema

64
Q

Clinical manifestations of emphysema

A

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
Q

Definition of asthma

A

Periodic severe but reversible bronchial obstruction from hypersensitive or hyperresponsive airways
Dyspnea, chest tightness, wheezing, sputum production, cough

66
Q

Prevalence of asthma

A

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
Q

Asthma classifications

A

Education and TX plans, based on severity, correlates better with management and outcomes
Also based on etiology (intrinsic and extrinsic)

68
Q

Asthma by education and treatment plans

A

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
Q

Three s’s of asthma

A

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
Q

Extrinisc asthma

A

Allergic asthma

Onset commonly in children

71
Q

Intrinsic asthma

A

non allergic
Onset common in adulthood
Many pts have combo of two
Over 20 genes identified in susceptibility and patho

72
Q

Common triggers of asthma

A

Allergens, lung irritants, weather, upper resp infections, physical exertion, excitement/emotional stress, ASA, NSAIDs, beta blockers

73
Q

Extrinsic asthma

A

Type I hypersensitivity
Distinguished by mast cell activation, eosinphil infiltration and epithelial sloughing
Triggered by environmental antigens

74
Q

Extrinsic asthma initial encounter

A

Stimulates plasma cells to produce antigen specific IgE antibodies that bind to mast cells

75
Q

Important mediators of extrinsic allergies

A

Histamine, bradykinin, leukotriens, chemotactic factors, prostaglandins, thomboxane A2, platelet-activating factor

76
Q

Reaction of extrinsic asthma

A

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
Q

Second stage (late) of asthmatic reaction

A

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
Q

Precipitators of intrinsic

A 
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
Q

Exacerbation of intrinsic asthma patho

A

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
Q

Air trapping in asthma

A

Areas with poor ventilation will retain CO2 (PaCO2 70-80mmHg)
Can cause spontaneous pneumo, pneumomediastinum, subq epmhysema

81
Q

Pneumomediastinum

A

Presence of air or other gas in mediastinum

82
Q

Cardiovascular effects of asthma

A

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
Q

Status asthmaticus

A 
Bronchospasms not relieved by normal measures
5-10X normal work of breathing
Air trapping becomes severe
Pulsus paradoxus
Prone to pneumothorax
84
Q

Status asthma manifestations

A 
Hypoxia
Decreased exp flow and volume
Fatigue from work of breathing
Decreased pH
PaCO2 up to 70mmHg
Silent chest
85
Q

CNS effects of asthma

A

Anxiety and confusion from hypoxia

Tired and obtunded

86
Q

Skin signs of asthma

A

Peripheral/central cyanosis

Diaphoresis

87
Q

Breathing signs in asthma

A 
Tachypnea
Accessory muscle use
Intercostal and supraclav retractions
Increased work of breathing
Chest expansion (assess for equal bilat)
88
Q

Wheezes and sats in asthma

A

Silent chest may in severe exacerbation
90% O2 means PO2 of 60mmHg in alveoli
Oxyhemoglobin curve shifts

89
Q

Speech and cough in asthma

A

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
Q

Cardiac asthma (merck manual)

A

Bronchospasms with hyperventilation
May be indistuingishable from other asthma
Induced by LV failure (intrinsic)

91
Q

Cystic fibrosis

A

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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