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Patho 1 > Chap 15- The Lungs > Flashcards

Chap 15- The Lungs Flashcards

1
Q

divisions of the respiratory system

A
  • air conducting

- gas exchange

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2
Q

air conducting system

A
  • delivers air
  • nose
  • mouth
  • trachea
  • bronchi
  • bronchioles
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3
Q

gas exchange

A
  • swaps gases between air and blood

- alveoli and capillaries

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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
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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
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6
Q

gas transportation

A
  • carried by Hb
  • once at target, Hb releases gases
  • affected by pH and temperature
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7
Q

what does Hb increased affinity for oxygen mean?

A
  • does not release oxygen

- O2 partial pressure curve moves to the left

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8
Q

what does Hb decreased affinity for oxygen mean?

A
  • does not bind oxygen

- O2 partial pressure curve moves to the right

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9
Q

what is surfactant?

A
  • lipoprotein
  • coats wall of alveoli
  • prevents them from collapsing (reduces surface tension)
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10
Q

lung compliance is due to

A
  • elasticity
  • recoil
  • surfactant
  • negative pressure system
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11
Q

how is breathing controlled?

A
  • by the medulla oblongata

- have chemoreceptors and stretch receptors

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12
Q

obstructive lung disease

A
  • FEV1/FVC <0.7
  • partial or complete obstruction of airway
  • increases resistance to airflow
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13
Q

restrictive lung disease

A
  • FEV1/FVC is normal or >0.7

- lungs cannot expand to full capacity

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14
Q

what is FEV1

A

forced expiratory volume in 1 second of FVC

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15
Q

what is FVC

A
  • forced vital capacity

- how much air you can expire after maximum inspiration

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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

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17
Q

what two diseases make up COPD

A

chronic bronchitis and emphysema

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18
Q

emphysema

A
  • irreversible enlargement of airspace distal to terminal bronchiole
  • have destruction of alveolar walls
  • small airway fibrosis -> airflow obstruction
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19
Q

what makes up the acinus?

A

respiratory bronchiole, alveolar duct, alveolus

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20
Q

how do you classify emphysema?

A
  • centriacinar
  • panacinar
  • distal acinar
  • irregular
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21
Q

centriacinar

A

proximal part of acinus affected

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22
Q

panacinar

A

entire acinus affected

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23
Q

distal acinar

A

distal portion of acinus affected

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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
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25
Q

clinical features of emphysema

A
  • asymptomatic until 1/3 of lung parenchyma is damaged
  • dyspnea, cough, wheezing
  • weight loss
  • “pink puffers”
  • hyperinflated lungs
  • heart is covered by hyperinflated lungs
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26
Q

chronic bronchitis

A
  • 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
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27
Q

clinical features of bronchitis

A
  • persistent cough producing sputum
  • asymptomatic for many years
  • dyspnea on exertion
  • hypercappnia
  • hypoxemia
  • mild cyanosis -> “blue bloaters”
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28
Q

pathogenesis of chronic bronchitis

A
  • smoking destroys cilia in lungs
  • excessive mucus not propelled out of lungs
  • muscle layer of bronchus undergoes hypertrophy
  • excess mucus and hypertrophy cause obstruction
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29
Q

asthma

A
  • chronic disorder of conducting airways
  • caused by hypersensitivity especially of bronchus
  • divided into early phase and late phase
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30
Q

clinical features of asthma

A
  • recurrent episodes of bronchospasm
  • wheezing, breathlessness
  • chest tightness
  • cough
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31
Q

types of asthma

A
  • atopic asthma- allergic asthma
  • non-atopic asthma
  • drug induced i.e. aspirin
  • occupational
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32
Q

what does the airway in asthmatic pts look like?

A
  • increased number of glands
  • hypertrophy of SMC
  • a lot of immune cells especially macrophages and eosinophils
  • thickening of basement membrane
  • mucus secretion
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33
Q

early phase asthma pathogenesis

A
  • 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
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34
Q

late phase asthma pathogenesis

A
  • 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
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35
Q

status asthmaticus

A
  • life threatening asthma attack that isn’t responsive to treatment
  • can cause respiratory alkalosis and respiratory failure
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36
Q

diagnosis of status asthmaticus

A
  • increased airflow obstruction
  • difficulty with exhalation
  • peripheral blood eosinophilia
  • sputum with eosinophils, curschmann spirals, and charcot-leyden cristals
37
Q

what are curschmann spirals?

A
  • dead and desquammated epithelial cells

- found in status asthmaticus

38
Q

what are charcot-leyden crystals?

A
  • dead eosinophils release contents- lysophospholipase
  • appears as crystals
  • seen in status asthmaticus
39
Q

bronchiectasis

A
  • destruction of SMC and elastic tissue in bronchus

- uncommon due to antibiotics

40
Q

clinical course of bronchiectasis

A
  • severe persistent cough
  • foul smelling sometimes bloody sputum
  • dyspnea and orthopnea
  • massive hemoptysis
  • cyanosis
41
Q

complications of bronchiectasis

A
  • cor pulmonlae
  • brain abscess
  • amyloidosis
42
Q

what is amyloidosis?

A
  • cytokines stimulate liver to secrete a lot of abnormal proteins
  • depsitited into multiple tissues
43
Q

pneumoconiosis

A
  • non-neoplastic lung restriction due to inhalation of mineral dusts
  • usually from work exposure
  • small particles and soluble in blood are most dangerous
44
Q

what does pneumoconiosis development depend on?

A
  • amount of dust retained
  • size, shape, buoyancy of particles
  • particle solubility and phsyiochemical reactivity
  • other irritant exposure i.e. smoking
45
Q

pathogenesis of pneumoconiosis

A
  • inhaled particles gather in lungs
  • engulfed by macrophages
  • macrophages release toxic factors -> lung injury and fibrogenic factors
  • fibroblasts recruited -> fibrosis
  • neutrophils recruited -> inflammation
46
Q

clinical symptoms of pneumconiosis

A
  • course takes 20-30 years
  • cough
  • dyspnea
  • respiratory failure
  • cor pulmonale
  • pleural plaques
47
Q

sarcoidosis

A
  • granulomatous disease, unclear origin
  • dx of exclusion
  • usually affects bilateral hiler lymphadenopathy or lungs, then eyes and skin
  • sx are vague and nonspecific
48
Q

pathogenesis of sarcoidosis

A
  • 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
Q

pulmonary embolism

A
  • important cause of morbidity and mortality in bedridden patients
  • occurs in pts with hyper coagulable conditions
50
Q

pathogenesis of pulmonary embolism

A
  • 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
Q

clinical symptoms of pulmonary embolism

A
  • very similar to MI
  • chest pain, dyspnea, tachypnea
  • fever
  • cough
  • hemoptysis
  • fibrinous pleuritis -> pleural friction rub
52
Q

pulmonary hypertension

A
  • 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
Q

secondary causes of pulmonary HTN

A
  • chronic obstructive/ interstitial lung disease
  • congenital or acquired heart disease
  • recurrent thromboemboli
  • autoimmune diseases
  • obstructive sleep apnea
54
Q

pulmonary edema

A
  • leakage of excess interstitial fluid which accumulates in alveolar spaces
  • pulmonary edema -> heavy wet lungs
55
Q

what are the sx of pulmonary edema

A
  • difficulty breathing** (orthopnea, paroxysmal nocturnal dyspnea)
  • coughing up blood
  • sweating
  • anxiety
  • pale skin
56
Q

what are the reasons for fluid to accumulate in the lungs?

A
  • increased hydrostatic pressure (cardiogenic)

- increased capillary permeability (non-cardiogenic)

57
Q

what is the most common cause of pulmonary edema?

A

left sided heart failure

58
Q

atelectasis

A
  • incomplete expansion of the lung or collapse of inflated lung
  • insufficient functioning of lung in either case
59
Q

what is the mediastinum

A
  • area between the two lungs

- occupied by heart, blood vessels, trachea, and esophagus

60
Q

resorptive atelectasis

A
  • 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
Q

compression atelectasis

A
  • something compressing the lungs
  • accumulation of significant volumes of fluid, tumor, or air within pleural cavity
  • medinastium shifts away from affected lung
62
Q

contraction atelectasis

A
  • extensive fibrosis prevents lung expansion
  • is irreversible
  • can happen in pneumoconiosis
63
Q

acute lung injury

A
  • 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
Q

acute respiratory distress syndrome

A

severe acute lung injury

65
Q

clinical features of ARDS

A
  • dyspnea
  • tachypnea
  • cyanosis
  • hypoxemia
  • respiratory failure
  • ventilation/perfusion mismatch -> respiratory acidosis
  • less surfactant -> stuff lungs
66
Q

pleural effusion

A
  • movement of fluid into the layers of pleura

- common manifestation in both primary and secondary pleural diseases

67
Q

accumulation of fluid in pleural effusion is due to the following reasons

A
  • increased hydrostatic pressure
  • increased vascular permeability
  • increased intrapleural negative pressure
  • decreased osmotic pressure
  • decreased lymphatic drainage
68
Q

empyema

A

pleural fluid becomes infected

69
Q

intrinsic causes of pleural effusion

A
  • malignancy
  • infection
  • autoimmune
  • causes increased permeability and protein rich fluid
70
Q

extrinsic causes of pleural effision

A
  • heart failure
  • kidney failure
  • liver failure
  • see transudate effusion
71
Q

pneumonia

A
  • any infection of lung parenchyma
72
Q

factors that impair defense mechanisms of the lungs and cause pneumonia

A
  • loss/suppression of cough reflex
  • injury to cilia
  • accumulation of secretions
  • immunodeficiency
  • pulmonary congestion and edeam
73
Q

what is the most common type of pneumonia and its cause

A
  • community acquired pneumonia

- due to streptococcus pneumoniae aka pneumococcus

74
Q

stages of pneumonia

A
  • infection
  • edema
  • red hepatization
  • gray hepatization
  • resolution
75
Q

what is red hepatization?

A
  • congestion in lungs causes leakage of blood cells into alveoli
  • appears red and firm
  • happens 2-3 days after edema
76
Q

what is gray hepatization?

A
  • RBC break open and lyse
  • other inflammatory infiltrate accumulates
  • lungs are gray and firm
  • happens 2-3 days after red hepatization
77
Q

what are the clinical sx of pneumonia?

A
  • fever, shaking, chills
  • cough with sputum
  • pleuritis
  • good prognosis generally
  • death can occur if infection spreads to other organs
78
Q

influenza virus

A
  • type A is most problematic
  • affects humans, pigs, horses, and birds
  • two different antigens- hemagglutin and neuramidase
79
Q

hemagglutin

A
  • attach virus to target

- H1-3

80
Q

neuraminidase

A
  • releases newly formed virions budding from infected cells

- N1 an N2

81
Q

antigenic shift

A
  • causes pandemics

- antigens on virus replaced through recombination with animal viruses

82
Q

antigenic drift

A
  • causes epidemics of flu
  • spontaneous mutation that alter epitopes on virus
  • still resemble other flu viruses so have partial immunity
83
Q

pathogenesis of influenza

A
  • 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
Q

lung cancer

A
  • 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
Q

small cell carcinoma

A
  • exclusively found in smokers

- very aggressive

86
Q

squamous cell carinoma

A
  • happens close to hilum

- central location in lungs

87
Q

adenocarcinoma

A

happens in periphery of lungs

88
Q

causes of lung cancer

A
  • tobacco smoke
  • industrial hazards
  • air pollution
  • molecular genetics
89
Q

main symptoms of lung cancer

A
  • persistent dry cough that doesn’t go away in four weeks

- hemoptysis

Patho 1 (12 decks)

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