3a Pulmonary diseases Flashcards
1
Q
respiration
A
gas exchange
2
Q
ventilation
A
moving air in and out
3
Q
clara cells
A
not ciliated, anti-inflamm, detoxify gases, regenerates-more ciliated or clara cells.
4
Q
type 1 aveolar cell
A
structure
5
Q
type ll aveolar cells
A
secrete surfactant
6
Q
surfactant
A
lipoprotein that keeps alveoli open even after exhaling
7
Q
Branching of the respiratory tree
A
conducting airways –> respiratory unit
trachea–>segmental bronchi-bronchioles
–>alveolar ducts
8
Q
visceral pleura
A
covers surface of lung
9
Q
parietal pleura
A
covers inner thoracic wall
10
Q
pleural cavity
A
-potiential space filled with fluid
-reduces friction
-allows adherence
11
Q
lungs naturally want to
A
recoil (collapse )
12
Q
Negative intrapleural pressure
A
keeps outside of lungs adhered to inside of thoracic wall
13
Q
lung pressures help
A
expand when breathing in
14
Q
ventilation requires
A
muscle contraction
15
Q
inhalation _____thoracic cavity
A
expands
16
Q
increased volume
A
decreased pressure –>air flows IN
17
Q
exhalation_____thoracic cavity
A
reduces
18
Q
decreased volume
A
increased pressure –> pushes air OUT
19
Q
physical factors influencing pulmonary ventilation
A
-airway resistance
-alveolar surface tension
-lung compliance
20
Q
Airway resistance
A
-normally low due to highly branched bronchioles (increased area)
-increased by smooth muscle contraction, excess mucus, inflamm
21
Q
Aleveolar surface tension
A
normally low due to surfactant. (without surfactant think blowing up a balloon)
22
Q
lung compliance
A
ability of lungs to stretch
-normally high: diminished by scarring in lung, stiffness of thoracic cage
23
Q
Flow=
A
change in pressure (P)/Resistance (R)
24
Q
gas exchange occurs in
A
alveoli
25
gas exchange facilitated by
proximity of air and blood
26
alveoli kept dry by
-absorption into capillaries
-extensive lymphatic drainage
27
Perfusion
blood flow to any organ
28
Ventilation-perfusion
V/Q air flow needs to match blood flow
29
hypoxemia
=low oxygen in blood
30
Gas diffusion is driven by
partial pressure gradients, high --> low
31
Oxyhemoglobin dissociation
dropping of O2 from hemoglobin protein
32
hemoglobin reversibly binds to
O2 (uptake in lungs, release in tissues)
33
illiness and changes in altitude
can decrease PO2
34
as long as PO2 >______ minimal consequence on O2 saturation of Hb
70 mm Hg
35
tidal volume
volume of exhaled air after normal inspiration
36
expiratory reserve volume
extra volume after exhaling
37
Respiratory rate (f)=
breaths per min, resting=12-18 breaths/mins
38
minute volume (Ve)=
volume of air moved per min
influenced by respiratory rate and tidal volume
39
Minute Volume
Ve=f x Vt (breath rate x tidal volume)
40
FEV1=
forced expiratory volume in 1 second
41
FVC=
Forced vital capacity
42
Ratio of ___is clinically important
FEV1: FVC
43
Sputum
mucus that is coughed up
44
Hemoptysis
bloody sputum
45
Tachypnea
rapid breathing
46
bradypnea
slow breathing
47
Hyperpnea
deep breathing, can be rapid or not
48
Dyspnea
feeling breathless (any breathing rate or pattern)
49
Hypercapnia
increased CO2 concentration
50
Hypoxemia
reduced oxygenation
51
cyanosis
manifestation of hypoxemia
-bluish color from reduced or de-saturated hemoglobin
52
clubbing
bulbous enlargement of tips of fingers caused by chronic hypoxemia
53
Pneumothorax
presence of air/gas in pleural space
54
atelectasis
collapse of lung
55
pleural effussion
presence of fluid in pleural space
56
respiratory failure
inadequate gas exchange-organ failure of lungs
57
Spirometry
-measures forced expiration
forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1)
58
Flow rate
=change in volume/time
means how much air
59
Spirometry can distinguish between ___and____
obstructive and restrictive diseases
60
Arterial blood gas analysis
measures Pa O2 and CO2
provides info abt ventilation-perfusion
can indicate acidosis/alkalosis
61
Chest radiograph
imaging airways and alveoli
can reveal emboli, tumors, other obstructions
62
obstructive lung disease
airways obstructed, air trapped in lungs after full expiration
-air in just fine, but cant get it out as well
63
Restrictive lung dx
lungs are unable to expand normally. stiffness of lung tissue or chest wall decreases compliance
-not as much air in or out (still normal flow rate)
64
FEV1: FVC ratio in restrictive
ratio normal
FVC decreased
65
FEV1: FVC ratio in obstructive
ration decreased
FCV normal
66
Types of obstructive lung dx
emphysema
asthma
chronic bronchitis
bronchiectasis
67
Types of restrictive lung dx
autoimmune
idopathic
work-related
drug-related
68
Infectious lung dx
Pneumonia
69
Neoplastic lung dx
small cell lung carcinoma
non-small cell lung carcinoma
70
Chronic obstructive pulmonary disorder (COPD) main 2 types
CHRONIC BRONCHITIS
EMPHYSEMA
71
COPD is
-progressive airflow limitation
-associated w/ inflamm response of lung to noxious particles/gases
72
COPD characterized by
-labored breathing ( wheezing, dyspnea)
-V/Q mismatch
-decreased FEV1 (cant push out air in 1 min)
73
most common COPD diseases
asthma, chronic bronchitis, emphysema
74
COPD risk factors/causes
SMOKING (accounts for 80% of cases) / vaping
-occupational inhalation: irritants, vapors, fumes
-air pollution
-genetics - mutation for emphysema
75
patho of COPD
-chronic irritant exposure=recruitment of mo, neutrophils, lymphocytes
-progressive damage to lungs and airways from: inflammation--> oxidative stress-->ECM degen --> Apoptosis
-systemic effects: -->muscle wasting: exercise intolerance, hypoxia, inflamm cytokines
-osteoporosis: inflamm cytokines--> increases osteoclast activity (breaks bones)
corticosteriods--> decrease osteoblast (builds bone) number
-renal dysfunction: decr in GFR
76
Chronic bronchitis, 2 defining characteristics:
-hypersecretion of mucus
-chronic productive cough
77
chronic bronchitis manifests as
decr in exercise tolerance
decr FEV 1 indicating obstruction
decr alveolar ventilation (V/Q mismatch)
incr Pa CO2
hypoxemia and cyanosis
78
Chronic bronchitis Pathogenesis
-inhaled irritant cause inflammation
--> prolonged inflammation causes:
1. Bronchial edema
2. Hypertrophy/ hyperplasia of goblet cells
-thick mucus difficult to clear b/c of impaired ciliary fxn
-incr risk of pulm infection
-infection add to airway damage
3. Airway SM proliferation
-bronchioles progressively obstructed, leads to air trapping
79
Emphysema
abnormal perm enlargement of alveoli
-destruction of alveolar walls
-elastin broken down, replaced with fibrotic tissue
-loss of elastic recoil--> limits airflow
dyspnea on exertion, progresses to dyspnea at rest
80
Primary emphysema
genetic defect in a1-antitrypsin
81
secondary emphysema
smoking
environmental/occupational exposures
-childhood respiratory tract infections
82
alpha 1 antitrypsin
-enzyme produced by lives
-protects lung tissue from proteases
-deficiency in genetically inherited
-makes lungs vulnerable to damage-especially from activated immune cells
-contributes to COPD in non-smokers
83
Emphysema - pathogenesis
breakdown of alveolar walls by:
-imbalance of proteases/ anti-proteases
-oxidative stress
-apoptosis of structural cells
Alveolar destruction leads to
-loss of lung surface area--> impaired gas exchanges
-sig V/Q mismatch
-hypoxemia
-hypercapnia
large spaces bullae of trapped air
-leads to hyperextension of chest (barrel chest)
-incr work of breathing
84
TX of CB and emphysema
-lifestyle changes: smoking cessation, diet, pulmonary rehab (breathing exercises)
-supp O2 mechanical ventilation (for hypoxemia/hypercapnia)
85
inhaled meds to improve lung fxn
to relax airway: bronchodilators, anticholinergics, beta-agonists
anti-inflamm: corticosteroids, phosphodiesterase-4 inhibitor (PDE4)
86
Fibrosis
-restrictive lung dx
excessive amounts of fibrotic or connective tissue in lungs: -stiffness of lung tissue, decrease in compliance and volume (lungs cannot fully expand)
-hyperoxemia/hypercapnia
result of prolonged lung injury: -drug-related (chemo). environmental (inhalants, viral infect), autoimmune (SLE, RA), idopathic
87
Fibrosis risk factors/causes
primarily the result of environmental exposure
-tobacco smoking and vaping
-toxins/particles usually seen in industrial and manufacturing: ammonia, sulfur dioxide, chlorine, silica, asbestos, cement, talc
88
fibrosis patho
-inhaled particles damage airway epithelium, cilia and alveoli-persisent damage followed by impaired healing
results in: inflammation. incr mucus production, mucosal and pulm edema, hypoxemia
if exposure cont, so will damage
-chronic inflamm
-alveolar/airway remodeling--> collagen and fibronectin, fueled by GF secertion
89
fibrosis tx
for acute exposures: supplemtnal O2, mechanical ventilation, support of CV system
-ONLY TX for progressive damage is to limit exposure
90
danger in supplementing O2
-too much leads to oxygen toxicity, can exacerbate inflamm
-severe inflamm from oxygen-derived free radicals
91
Bronchiolitis obliterans
-late stage fibrotic process
-inflammation and SM proliferation narrow airways
-also seen after lung transplantation sometimes
92
"popcorn lung" dx
bronchiolotis obliterans
--> artificial butter flavor chemical (diacetyl) was responsible
-also attributed to electronic cigs --> flavored nic contains airway irritants
93
Tx for Bronchiolitis obliterans
-similar to bronchitis and emphysema
-corticosteroids
-immunosuppressants
94
Pneumonia
infection of lower resp tract
-6th leading cause of death in US
-Very common in healthcare setting
95
Types of pneumonia
-community-acquired (typical or atypical)
-nosocomial
-aspiration
-necrotizing
-chronic (usually due to TB)
96
Pneumonia risk factors
-age (very old or very young)
-compromised immunity
-underlying cardiac, lung, renal dx
-residence in a health facility-->nosocomial
-smoking
-alcoholism
97
pneumonia causes
microorganisms:
-bacteria- staph, strep, pseudomonas
-virus-influenza, covid
-fungi
-parasites
-protozoa
98
pneumonia pathogenesis
1. aspiration of microorganism (strep)
2. congestion- attraction of neutrophils, release of inflamm mediators--> formation of serous exudate
3.red hepatization- lobe is firm and red, filled with neutrophils, RBCs fibrous exudate
4. gray hepatization: RBCs lysed, fibrous exudate remains
5. resolution: mo ingest and remove dead neutrophils and bacteria
99
pneumonia dx
chest x-ray
-pleural effusion
-extent of infection
breathing impairment
-dyspnea, tachypnea, cough
-inspiratory crackles--> consolidation
-cultures of resp secretions, blood, elevated leukocytes -WBC
100
Pneumonia tx
-ventilation to correct: hypoxemia, V/Q mismatch
-Adequate hydration
-drug tx depends on source of infection
bacterial; abx
viral: supportive therapy
fungal: antifungal
101
Pulmonary embolism
occulsion of pulm artery or its branches
-typically results of thromboembolism originating from legs
102
Pulmonary embolism risk factors/causes
anything that promotes blood clotting
-venous status: immobilization, heart failure
-hypercoagulability; inherited coagulation disorder, hormonal therapy/oral contraceptives, pregnancy
-endothelial injury
-genetic defects
103
pulmonary embolism pathogen
1. thromboembolism lodges in pulmonary circulation
2. release of neurohumoral substances-serotonin, ang ll, histamine, Epi, NE
3. release of inflammatory mediators- leukotrienes, thromboxanes
widespread vasoconstriction --> rasies pulmonary artery pressure
104
in pulm embolism lack of blood flow causes:
V/Q mismatch, hypoxemia
decrease in surfactant production
atelectasis (collapse of alveoli)
105
if embolism does not causes infarction___
-clot is dissolved by fibrinolytic system
-lung fxn returns to normal
106
if embolism does cause infarction____
affected lung area will shrink and develop scar tissue
107
pulm embolism dx is by___
CT angiography
108
pulm embolism pt typically presents with:
sudden chest pain
-dyspnea
-trachycardia
-hyperventilation
-unexplained anxiety
109
pulm embolism tx
-ideal tx is prevention: lowering risk factors, anticoagulation therapy-meds
immediate tx: supplemental O2, anticoagulants, thrombolytics
110
pulmonary hypertension
-mean pulm artery pressure > 25mm Hg at rest
-caused by narrowing and constriction of pulm vessels
-usually not detected until dx is very advanced
-tends to be masked by CV dx or other pulm dx
111
pulm htn risk factors/causes
-any dx that causes chronic hypoxemia-COPD
-idiopathic: endothelial dysfunction
-familial: caused by mutated gene, bone morphogenic protein receptor type ll (BMPR2) is inactivated
-normally suppresses VSMC proliferation
-tissue remodeling
112
pulm htn patho
incr production of vasoconstrictors
incr production of vasodilators
-release of growth factors--> proliferation of ECs, SMCs, fibroblasts
-Results in narrow vessels and abnormal vasoconstriction: incre in resistance to pulm artery blood flow and incr in workload of RV--> RV dilated: cor pulmonale
113
cor pulmonale
when RV remodels gets enlarged dilates
114
pulm htn tx
supplemental O2
diuretics, decrease blood volume
-anticoagulants and prostacyclin analogs inhibit platelet activation
-endothelin receptor antagonists and phosphodiesterase-5 inhibitors are (vasodilators)
115
pulm htn is irreversible once___
arterial smooth muscle started remodeling
116
to dx pulm htn
right-sided heart catheterization; get inside to measure pressure
117
hypoxemia is reduced Pa O2 caused by
ventilation-perfusion mismatch, decreased oxygen content of inspired gas, hypoventilation
