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Pathophys > 3a Pulmonary diseases > Flashcards

3a Pulmonary diseases Flashcards

1
Q

respiration

A

gas exchange

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2
Q

ventilation

A

moving air in and out

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3
Q

clara cells

A

not ciliated, anti-inflamm, detoxify gases, regenerates-more ciliated or clara cells.

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4
Q

type 1 aveolar cell

A

structure

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5
Q

type ll aveolar cells

A

secrete surfactant

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6
Q

surfactant

A

lipoprotein that keeps alveoli open even after exhaling

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7
Q

Branching of the respiratory tree

A

conducting airways –> respiratory unit
trachea–>segmental bronchi-bronchioles
–>alveolar ducts

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8
Q

visceral pleura

A

covers surface of lung

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9
Q

parietal pleura

A

covers inner thoracic wall

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10
Q

pleural cavity

A

-potiential space filled with fluid
-reduces friction
-allows adherence

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11
Q

lungs naturally want to

A

recoil (collapse )

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12
Q

Negative intrapleural pressure

A

keeps outside of lungs adhered to inside of thoracic wall

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13
Q

lung pressures help

A

expand when breathing in

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14
Q

ventilation requires

A

muscle contraction

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15
Q

inhalation _____thoracic cavity

A

expands

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16
Q

increased volume

A

decreased pressure –>air flows IN

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17
Q

exhalation_____thoracic cavity

A

reduces

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18
Q

decreased volume

A

increased pressure –> pushes air OUT

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19
Q

physical factors influencing pulmonary ventilation

A

-airway resistance
-alveolar surface tension
-lung compliance

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20
Q

Airway resistance

A

-normally low due to highly branched bronchioles (increased area)
-increased by smooth muscle contraction, excess mucus, inflamm

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21
Q

Aleveolar surface tension

A

normally low due to surfactant. (without surfactant think blowing up a balloon)

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22
Q

lung compliance

A

ability of lungs to stretch
-normally high: diminished by scarring in lung, stiffness of thoracic cage

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23
Q

Flow=

A

change in pressure (P)/Resistance (R)

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24
Q

gas exchange occurs in

A

alveoli

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25
Q

gas exchange facilitated by

A

proximity of air and blood

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26
Q

alveoli kept dry by

A

-absorption into capillaries
-extensive lymphatic drainage

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27
Q

Perfusion

A

blood flow to any organ

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28
Q

Ventilation-perfusion

A

V/Q air flow needs to match blood flow

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29
Q

hypoxemia

A

=low oxygen in blood

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30
Q

Gas diffusion is driven by

A

partial pressure gradients, high –> low

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31
Q

Oxyhemoglobin dissociation

A

dropping of O2 from hemoglobin protein

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32
Q

hemoglobin reversibly binds to

A

O2 (uptake in lungs, release in tissues)

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33
Q

illiness and changes in altitude

A

can decrease PO2

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34
Q

as long as PO2 >______ minimal consequence on O2 saturation of Hb

A

70 mm Hg

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35
Q

tidal volume

A

volume of exhaled air after normal inspiration

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36
Q

expiratory reserve volume

A

extra volume after exhaling

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37
Q

Respiratory rate (f)=

A

breaths per min, resting=12-18 breaths/mins

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38
Q

minute volume (Ve)=

A

volume of air moved per min
influenced by respiratory rate and tidal volume

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39
Q

Minute Volume

A

Ve=f x Vt (breath rate x tidal volume)

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40
Q

FEV1=

A

forced expiratory volume in 1 second

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41
Q

FVC=

A

Forced vital capacity

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42
Q

Ratio of ___is clinically important

A

FEV1: FVC

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43
Q

Sputum

A

mucus that is coughed up

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44
Q

Hemoptysis

A

bloody sputum

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45
Q

Tachypnea

A

rapid breathing

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46
Q

bradypnea

A

slow breathing

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47
Q

Hyperpnea

A

deep breathing, can be rapid or not

48
Q

Dyspnea

A

feeling breathless (any breathing rate or pattern)

49
Q

Hypercapnia

A

increased CO2 concentration

50
Q

Hypoxemia

A

reduced oxygenation

51
Q

cyanosis

A

manifestation of hypoxemia
-bluish color from reduced or de-saturated hemoglobin

52
Q

clubbing

A

bulbous enlargement of tips of fingers caused by chronic hypoxemia

53
Q

Pneumothorax

A

presence of air/gas in pleural space

54
Q

atelectasis

A

collapse of lung

55
Q

pleural effussion

A

presence of fluid in pleural space

56
Q

respiratory failure

A

inadequate gas exchange-organ failure of lungs

57
Q

Spirometry

A

-measures forced expiration
forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1)

58
Q

Flow rate

A

=change in volume/time
means how much air

59
Q

Spirometry can distinguish between ___and____

A

obstructive and restrictive diseases

60
Q

Arterial blood gas analysis

A

measures Pa O2 and CO2
provides info abt ventilation-perfusion
can indicate acidosis/alkalosis

61
Q

Chest radiograph

A

imaging airways and alveoli
can reveal emboli, tumors, other obstructions

62
Q

obstructive lung disease

A

airways obstructed, air trapped in lungs after full expiration
-air in just fine, but cant get it out as well

63
Q

Restrictive lung dx

A

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
Q

FEV1: FVC ratio in restrictive

A

ratio normal
FVC decreased

65
Q

FEV1: FVC ratio in obstructive

A

ration decreased
FCV normal

66
Q

Types of obstructive lung dx

A

emphysema
asthma
chronic bronchitis
bronchiectasis

67
Q

Types of restrictive lung dx

A

autoimmune
idopathic
work-related
drug-related

68
Q

Infectious lung dx

A

Pneumonia

69
Q

Neoplastic lung dx

A

small cell lung carcinoma
non-small cell lung carcinoma

70
Q

Chronic obstructive pulmonary disorder (COPD) main 2 types

A

CHRONIC BRONCHITIS
EMPHYSEMA

71
Q

COPD is

A

-progressive airflow limitation
-associated w/ inflamm response of lung to noxious particles/gases

72
Q

COPD characterized by

A

-labored breathing ( wheezing, dyspnea)
-V/Q mismatch
-decreased FEV1 (cant push out air in 1 min)

73
Q

most common COPD diseases

A

asthma, chronic bronchitis, emphysema

74
Q

COPD risk factors/causes

A

SMOKING (accounts for 80% of cases) / vaping
-occupational inhalation: irritants, vapors, fumes
-air pollution
-genetics - mutation for emphysema

75
Q

patho of COPD

A

-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
Q

Chronic bronchitis, 2 defining characteristics:

A

-hypersecretion of mucus
-chronic productive cough

77
Q

chronic bronchitis manifests as

A

decr in exercise tolerance
decr FEV 1 indicating obstruction
decr alveolar ventilation (V/Q mismatch)
incr Pa CO2
hypoxemia and cyanosis

78
Q

Chronic bronchitis Pathogenesis

A

-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
Q

Emphysema

A

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
Q

Primary emphysema

A

genetic defect in a1-antitrypsin

81
Q

secondary emphysema

A

smoking
environmental/occupational exposures
-childhood respiratory tract infections

82
Q

alpha 1 antitrypsin

A

-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
Q

Emphysema - pathogenesis

A

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
Q

TX of CB and emphysema

A

-lifestyle changes: smoking cessation, diet, pulmonary rehab (breathing exercises)
-supp O2 mechanical ventilation (for hypoxemia/hypercapnia)

85
Q

inhaled meds to improve lung fxn

A

to relax airway: bronchodilators, anticholinergics, beta-agonists
anti-inflamm: corticosteroids, phosphodiesterase-4 inhibitor (PDE4)

86
Q

Fibrosis

A

-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
Q

Fibrosis risk factors/causes

A

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
Q

fibrosis patho

A

-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
Q

fibrosis tx

A

for acute exposures: supplemtnal O2, mechanical ventilation, support of CV system
-ONLY TX for progressive damage is to limit exposure

90
Q

danger in supplementing O2

A

-too much leads to oxygen toxicity, can exacerbate inflamm
-severe inflamm from oxygen-derived free radicals

91
Q

Bronchiolitis obliterans

A

-late stage fibrotic process
-inflammation and SM proliferation narrow airways
-also seen after lung transplantation sometimes

92
Q

“popcorn lung” dx

A

bronchiolotis obliterans
–> artificial butter flavor chemical (diacetyl) was responsible
-also attributed to electronic cigs –> flavored nic contains airway irritants

93
Q

Tx for Bronchiolitis obliterans

A

-similar to bronchitis and emphysema
-corticosteroids
-immunosuppressants

94
Q

Pneumonia

A

infection of lower resp tract
-6th leading cause of death in US
-Very common in healthcare setting

95
Q

Types of pneumonia

A

-community-acquired (typical or atypical)
-nosocomial
-aspiration
-necrotizing
-chronic (usually due to TB)

96
Q

Pneumonia risk factors

A

-age (very old or very young)
-compromised immunity
-underlying cardiac, lung, renal dx
-residence in a health facility–>nosocomial
-smoking
-alcoholism

97
Q

pneumonia causes

A

microorganisms:
-bacteria- staph, strep, pseudomonas
-virus-influenza, covid
-fungi
-parasites
-protozoa

98
Q

pneumonia pathogenesis

A
  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
  3. gray hepatization: RBCs lysed, fibrous exudate remains
  4. resolution: mo ingest and remove dead neutrophils and bacteria
99
Q

pneumonia dx

A

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
Q

Pneumonia tx

A

-ventilation to correct: hypoxemia, V/Q mismatch
-Adequate hydration
-drug tx depends on source of infection
bacterial; abx
viral: supportive therapy
fungal: antifungal

101
Q

Pulmonary embolism

A

occulsion of pulm artery or its branches
-typically results of thromboembolism originating from legs

102
Q

Pulmonary embolism risk factors/causes

A

anything that promotes blood clotting
-venous status: immobilization, heart failure
-hypercoagulability; inherited coagulation disorder, hormonal therapy/oral contraceptives, pregnancy
-endothelial injury
-genetic defects

103
Q

pulmonary embolism pathogen

A
  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
Q

in pulm embolism lack of blood flow causes:

A

V/Q mismatch, hypoxemia
decrease in surfactant production
atelectasis (collapse of alveoli)

105
Q

if embolism does not causes infarction___

A

-clot is dissolved by fibrinolytic system
-lung fxn returns to normal

106
Q

if embolism does cause infarction____

A

affected lung area will shrink and develop scar tissue

107
Q

pulm embolism dx is by___

A

CT angiography

108
Q

pulm embolism pt typically presents with:

A

sudden chest pain
-dyspnea
-trachycardia
-hyperventilation
-unexplained anxiety

109
Q

pulm embolism tx

A

-ideal tx is prevention: lowering risk factors, anticoagulation therapy-meds
immediate tx: supplemental O2, anticoagulants, thrombolytics

110
Q

pulmonary hypertension

A

-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
Q

pulm htn risk factors/causes

A

-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
Q

pulm htn patho

A

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
Q

cor pulmonale

A

when RV remodels gets enlarged dilates

114
Q

pulm htn tx

A

supplemental O2
diuretics, decrease blood volume
-anticoagulants and prostacyclin analogs inhibit platelet activation
-endothelin receptor antagonists and phosphodiesterase-5 inhibitors are (vasodilators)

115
Q

pulm htn is irreversible once___

A

arterial smooth muscle started remodeling

116
Q

to dx pulm htn

A

right-sided heart catheterization; get inside to measure pressure

117
Q

hypoxemia is reduced Pa O2 caused by

A

ventilation-perfusion mismatch, decreased oxygen content of inspired gas, hypoventilation

Pathophys (11 decks)

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