Chap 15- The Lungs Flashcards
1
Q
divisions of the respiratory system
A
- air conducting
- gas exchange
2
Q
air conducting system
A
- delivers air
- nose
- mouth
- trachea
- bronchi
- bronchioles
3
Q
gas exchange
A
- swaps gases between air and blood
- alveoli and capillaries
4
Q
what protects the respiratory system from harmful inhaled particles?
A
- mucus
- cilia
- immune cells in lungs- especially macrophages
- capillaries in nose warms and humidify air
5
Q
what is the V/Q ratio?
A
- ventilation/ perfusion ratio
- normal ventilation= 4L per min
- normal perfusion = 5L per min
- normal V/Q ratio =0.8
- depends on alveolar and capillary surface area and thickness
6
Q
gas transportation
A
- carried by Hb
- once at target, Hb releases gases
- affected by pH and temperature
7
Q
what does Hb increased affinity for oxygen mean?
A
- does not release oxygen
- O2 partial pressure curve moves to the left
8
Q
what does Hb decreased affinity for oxygen mean?
A
- does not bind oxygen
- O2 partial pressure curve moves to the right
9
Q
what is surfactant?
A
- lipoprotein
- coats wall of alveoli
- prevents them from collapsing (reduces surface tension)
10
Q
lung compliance is due to
A
- elasticity
- recoil
- surfactant
- negative pressure system
11
Q
how is breathing controlled?
A
- by the medulla oblongata
- have chemoreceptors and stretch receptors
12
Q
obstructive lung disease
A
- FEV1/FVC <0.7
- partial or complete obstruction of airway
- increases resistance to airflow
13
Q
restrictive lung disease
A
- FEV1/FVC is normal or >0.7
- lungs cannot expand to full capacity
14
Q
what is FEV1
A
forced expiratory volume in 1 second of FVC
15
Q
what is FVC
A
- forced vital capacity
- how much air you can expire after maximum inspiration
16
Q
what does the FEV1/FVC ratio tell us?
A
- how much air you can expire within one second
- differentiates between obstructive vs. restrictive lung diseases
17
Q
what two diseases make up COPD
A
chronic bronchitis and emphysema
18
Q
emphysema
A
- irreversible enlargement of airspace distal to terminal bronchiole
- have destruction of alveolar walls
- small airway fibrosis -> airflow obstruction
19
Q
what makes up the acinus?
A
respiratory bronchiole, alveolar duct, alveolus
20
Q
how do you classify emphysema?
A
- centriacinar
- panacinar
- distal acinar
- irregular
21
Q
centriacinar
A
proximal part of acinus affected
22
Q
panacinar
A
entire acinus affected
23
Q
distal acinar
A
distal portion of acinus affected
24
Q
pathogenesis of emphysema
A
- inflammatory mediators and leukocytes induce structural changes
- proteases are released from inflammatory and epithelial cells-> CT break down, these pts dont have antiproteases
- ROS causes alveolar damage and inflammation
- infection can worsen sx
25
clinical features of emphysema
- asymptomatic until 1/3 of lung parenchyma is damaged
- dyspnea, cough, wheezing
- weight loss
- "pink puffers"
- hyperinflated lungs
- heart is covered by hyperinflated lungs
26
chronic bronchitis
- persistent cough with sputum production for at least 3 months in at least 2 consecutive years
- common in smokers and people exposed to air pollution
27
clinical features of bronchitis
- persistent cough producing sputum
- asymptomatic for many years
- dyspnea on exertion
- hypercappnia
- hypoxemia
- mild cyanosis -> "blue bloaters"
28
pathogenesis of chronic bronchitis
- smoking destroys cilia in lungs
- excessive mucus not propelled out of lungs
- muscle layer of bronchus undergoes hypertrophy
- excess mucus and hypertrophy cause obstruction
29
asthma
- chronic disorder of conducting airways
- caused by hypersensitivity especially of bronchus
- divided into early phase and late phase
30
clinical features of asthma
- recurrent episodes of bronchospasm
- wheezing, breathlessness
- chest tightness
- cough
31
types of asthma
- atopic asthma- allergic asthma
- non-atopic asthma
- drug induced i.e. aspirin
- occupational
32
what does the airway in asthmatic pts look like?
- increased number of glands
- hypertrophy of SMC
- a lot of immune cells especially macrophages and eosinophils
- thickening of basement membrane
- mucus secretion
33
early phase asthma pathogenesis
- allergen processed by T helper 2 cells
- causes stimulation of mucus secretiong glands
- stimulates antibody producing B cells to produce IgE
- eosinophils are recruited
- IgE binds to mast cells
34
late phase asthma pathogenesis
- next exposure to antigen, IgE antibodies bind to antigen
- causes degranulation of mast cells
- mast cells release histamines and cytokines
- causes sx of asthma
- mucus production, vasodilation, stimulation of vagal receptors -> bronchoconstriction
- eosinophils are recruited which recruit other immune cells
35
status asthmaticus
- life threatening asthma attack that isn't responsive to treatment
- can cause respiratory alkalosis and respiratory failure
36
diagnosis of status asthmaticus
- increased airflow obstruction
- difficulty with exhalation
- peripheral blood eosinophilia
- sputum with eosinophils, curschmann spirals, and charcot-leyden cristals
37
what are curschmann spirals?
- dead and desquammated epithelial cells
| - found in status asthmaticus
38
what are charcot-leyden crystals?
- dead eosinophils release contents- lysophospholipase
- appears as crystals
- seen in status asthmaticus
39
bronchiectasis
- destruction of SMC and elastic tissue in bronchus
| - uncommon due to antibiotics
40
clinical course of bronchiectasis
- severe persistent cough
- foul smelling sometimes bloody sputum
- dyspnea and orthopnea
- massive hemoptysis
- cyanosis
41
complications of bronchiectasis
- cor pulmonlae
- brain abscess
- amyloidosis
42
what is amyloidosis?
- cytokines stimulate liver to secrete a lot of abnormal proteins
- depsitited into multiple tissues
43
pneumoconiosis
- non-neoplastic lung restriction due to inhalation of mineral dusts
- usually from work exposure
- small particles and soluble in blood are most dangerous
44
what does pneumoconiosis development depend on?
- amount of dust retained
- size, shape, buoyancy of particles
- particle solubility and phsyiochemical reactivity
- other irritant exposure i.e. smoking
45
pathogenesis of pneumoconiosis
- inhaled particles gather in lungs
- engulfed by macrophages
- macrophages release toxic factors -> lung injury and fibrogenic factors
- fibroblasts recruited -> fibrosis
- neutrophils recruited -> inflammation
46
clinical symptoms of pneumconiosis
- course takes 20-30 years
- cough
- dyspnea
- respiratory failure
- cor pulmonale
- pleural plaques
47
sarcoidosis
- granulomatous disease, unclear origin
- dx of exclusion
- usually affects bilateral hiler lymphadenopathy or lungs, then eyes and skin
- sx are vague and nonspecific
48
pathogenesis of sarcoidosis
- inappropriate expansion of CD4+ cells
- release of IL-2 and INF-gamma which causes macrophage activation
- TNF release
- more T cells and macrophages recruited -> granuloma
49
pulmonary embolism
- important cause of morbidity and mortality in bedridden patients
- occurs in pts with hyper coagulable conditions
50
pathogenesis of pulmonary embolism
- have respiratory compromise: blood doesnt get past where clot is so alveoli get filled up with blood -> infarction
- have hemodynamic compromise: blood backs up from clot -> RHF
51
clinical symptoms of pulmonary embolism
- very similar to MI
- chest pain, dyspnea, tachypnea
- fever
- cough
- hemoptysis
- fibrinous pleuritis -> pleural friction rub
52
pulmonary hypertension
- mean PAP > 25 mmHg at rest
- happen in conditions that increase pulmonary HF, pulmonary vascular resistance, or left heart resistance
- see an increase in endothelin and decrease in NO
53
secondary causes of pulmonary HTN
- chronic obstructive/ interstitial lung disease
- congenital or acquired heart disease
- recurrent thromboemboli
- autoimmune diseases
- obstructive sleep apnea
54
pulmonary edema
- leakage of excess interstitial fluid which accumulates in alveolar spaces
- pulmonary edema -> heavy wet lungs
55
what are the sx of pulmonary edema
- difficulty breathing** (orthopnea, paroxysmal nocturnal dyspnea)
- coughing up blood
- sweating
- anxiety
- pale skin
56
what are the reasons for fluid to accumulate in the lungs?
- increased hydrostatic pressure (cardiogenic)
| - increased capillary permeability (non-cardiogenic)
57
what is the most common cause of pulmonary edema?
left sided heart failure
58
atelectasis
- incomplete expansion of the lung or collapse of inflated lung
- insufficient functioning of lung in either case
59
what is the mediastinum
- area between the two lungs
| - occupied by heart, blood vessels, trachea, and esophagus
60
resorptive atelectasis
- excessive secretion -> obstruction of airway
- air is resorbed from dependent alveoli which collapse
- mediastinum shifts towards affected lung
- i.e. asthma, chronic bronchitis, foreign bodies
61
compression atelectasis
- something compressing the lungs
- accumulation of significant volumes of fluid, tumor, or air within pleural cavity
- medinastium shifts away from affected lung
62
contraction atelectasis
- extensive fibrosis prevents lung expansion
- is irreversible
- can happen in pneumoconiosis
63
acute lung injury
- abrupt onset of significant hypoxemia and bilateral pulmonary infiltrates
- non-cardiogenic
- inflammation causes increased vascular permeability, edema, and epithelial cell death
- diffuse alveolar damage
64
acute respiratory distress syndrome
severe acute lung injury
65
clinical features of ARDS
- dyspnea
- tachypnea
- cyanosis
- hypoxemia
- respiratory failure
- ventilation/perfusion mismatch -> respiratory acidosis
- less surfactant -> stuff lungs
66
pleural effusion
- movement of fluid into the layers of pleura
| - common manifestation in both primary and secondary pleural diseases
67
accumulation of fluid in pleural effusion is due to the following reasons
- increased hydrostatic pressure
- increased vascular permeability
- increased intrapleural negative pressure
- decreased osmotic pressure
- decreased lymphatic drainage
68
empyema
pleural fluid becomes infected
69
intrinsic causes of pleural effusion
- malignancy
- infection
- autoimmune
- causes increased permeability and protein rich fluid
70
extrinsic causes of pleural effision
- heart failure
- kidney failure
- liver failure
- see transudate effusion
71
pneumonia
- any infection of lung parenchyma
72
factors that impair defense mechanisms of the lungs and cause pneumonia
- loss/suppression of cough reflex
- injury to cilia
- accumulation of secretions
- immunodeficiency
- pulmonary congestion and edeam
73
what is the most common type of pneumonia and its cause
- community acquired pneumonia
| - due to streptococcus pneumoniae aka pneumococcus
74
stages of pneumonia
- infection
- edema
- red hepatization
- gray hepatization
- resolution
75
what is red hepatization?
- congestion in lungs causes leakage of blood cells into alveoli
- appears red and firm
- happens 2-3 days after edema
76
what is gray hepatization?
- RBC break open and lyse
- other inflammatory infiltrate accumulates
- lungs are gray and firm
- happens 2-3 days after red hepatization
77
what are the clinical sx of pneumonia?
- fever, shaking, chills
- cough with sputum
- pleuritis
- good prognosis generally
- death can occur if infection spreads to other organs
78
influenza virus
- type A is most problematic
- affects humans, pigs, horses, and birds
- two different antigens- hemagglutin and neuramidase
79
hemagglutin
- attach virus to target
| - H1-3
80
neuraminidase
- releases newly formed virions budding from infected cells
| - N1 an N2
81
antigenic shift
- causes pandemics
| - antigens on virus replaced through recombination with animal viruses
82
antigenic drift
- causes epidemics of flu
- spontaneous mutation that alter epitopes on virus
- still resemble other flu viruses so have partial immunity
83
pathogenesis of influenza
- pneumocytes infected and inhibit Na channels
- causes electrolyte imabalce and water shift
- alveolar edema
- virus hijacks cells -> cell death
- before cells die they recruit other inflammatory cells -> inflammation
84
lung cancer
- most frequently diagnosed cancer in the world
- most common cause of cancer mortality
- largely due to cardiogenic effects of cigarettes
- most are due to metastasis of other cancers
85
small cell carcinoma
- exclusively found in smokers
| - very aggressive
86
squamous cell carinoma
- happens close to hilum
| - central location in lungs
87
adenocarcinoma
happens in periphery of lungs
88
causes of lung cancer
- tobacco smoke
- industrial hazards
- air pollution
- molecular genetics
89
main symptoms of lung cancer
- persistent dry cough that doesn't go away in four weeks
| - hemoptysis
