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patho 300 exam 2 > pulmonary function > Flashcards

pulmonary function Flashcards

1
Q

central respiratory center

A

controls the rate of breathing

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2
Q

central chemoreceptors

A

sensitive to changes in PaCO2 and pH

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3
Q

peripheral chemoreceptors

A

located in the carotid and aortic bodies

sensitive to changes in PaO2 and PaCO2

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4
Q

anatomic “dead space”

A

all of the airways that do not contain alveoli for gas exhange

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5
Q

alveolar “dead space”

A

alevoli that are filled with air, but gas exchange is not occuring

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6
Q

airway resistance determined by:

A

length of the tube
radius of the tube
viscosity (thickness) of substance flowing through the tube

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7
Q

what is consistent in the airway regarding resistance

A

lenth and viscosity is constant so changes in the radius is primary force influcencing resistance

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8
Q

a change in airway radius results in

A

a fourfold. hange in airway constriction

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9
Q

types of change that can alter airway radius

A

bronchoconstriction

inflammation (swelling)

mucus production

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10
Q

tissue resistance is influenced by the balance of what two factors?

A

compliance and elastance

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11
Q

compliance

A

ease of inflation of alveoli

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12
Q

elastance

A

ease of alveolar recoil

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13
Q

la places law

A

smaller spheres are more difficult to inflate

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14
Q

surfactant

A

mixture of proteins and phospholipids

secreted by Type 2 alveolar cells

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15
Q

what does surfactant do?

A

reduce surface tension = helpping them inflate

prevent water from coming into the alveoli

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16
Q

what happens if we have surfactant deficiency?

A

decreases the compliance of the alvoli (more difficult to inflate)

would allow water from the interstitial space to enter then alveoli

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17
Q

ventilation (V) and perfusion (Q) relationship
(dont need to know but know the ups and downs)

A

normal pulmonary perfusion=5 lpm

normal alveolar ventilation=4 lpm

normal V/Q ration=0.8-0.9

4lpm alveolar ventilations
———————————— = 0.8
5lpm pulmonary perfusion

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18
Q

low V/Q ratio

(vascular shunt)

A

Perfusion without Ventilation

problems with pumonary ventilation (inadequate oxygen in the alveoli)

(most pulmonary disorders are from this)

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19
Q

high V/Q ratio

(alveolar dead space)

A

ventilation without perfusion

problem with pulmonary perfusion

blood flow through pulmonary vasculature is inadequate

(pulmonary cascular defects)

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20
Q

how chronic elevation of paCO2 levels in a pt with chronic lung disease can cause a “resetting” of the homeostatic set point of the central chemoreceptors for CO2

A

↑paCO2 and normal pH is (compensated respiratory acidosis) so we have the secondary monitors (peripheral chemoreceptors)

paO2 becomes main indicator because paCO2 is always elevated

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21
Q

why use caution when administering oxygen to pt with chronic lung disease

A

they are sensitive to oxygen

may cause them to stop breathing

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22
Q

hypoxia induced pulmonary vasoconstriction
(alveolar oxygen issue)

A

local ↓ in alveolar oxygenation leads to a responsive vasocontriction

this increases resistance and decreases blood flow through pulmonary vessels

this increases the work load of the right side of the heart and can lead to right sided heart failure

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23
Q

work of beathing

A

amount of energy expended to support ventilations

pt with pulmonary disease have ↑ work of breathing

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24
Q

if there is not enough energy to perform work of breathing what happens

A

respiratory failure

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25
Q

forced expiratory volume (FEV)

A

volume of air expired in the first second of FVC (full volume capacity or full inspiration)

(this measures airway resistance)

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26
Q

what do we do if FEV is low?

A

give bronchodilator med

check PFT again

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27
Q

Peak Expiratory Flow Rate (PEFR)

A

measure how fast you breath out (measuring degree of airway resistance to the outflow of air)

same as FEV but it is the rate of flow not a volume of air exhaled

use a peak flow meter to measure the resistance

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28
Q

hypoxemia

A

decreased O2 level in arterial blood

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29
Q

hypoxia

A

decreased O2 in tissues

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30
Q

hypercarbia (hypercapnea)

A

increased CO2 in arterial blood

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31
Q

acute respiratory failure
Lab values

A

ABG values:
primarily hypoxemic : paO2 50mmHg or less

Primarily hypercarbic: paCO2 50 or more (with ↓ pH)

These pt will need to be oxygenated

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32
Q

Upper respiratory tract infections

A

Common cold

Rhinosinusitis (rhinitis and sinusitis)

Laryngitis

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33
Q

Upper and lower respirator tract infection

A

Influenza

Effects both upper and lower

We worry about it getting lower

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34
Q

Lower respiratory tract infection

A

Acute bronchitis (bronchi)

Bronchiolitis (bronchioles)

Pneumonia (alveoli)

Tuberculosis

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35
Q

Pneumonia

A

Causes: bacteria, viral, fungi

Agent depends where the pneumonia was acquires

Hospital or community acquired pnemonia

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36
Q

Lobar pneumonia
Where got it
Where located
Xray

A

Usually HAI

Infection within a lobe of the lung

Appears on xray as consolidation of a lobe

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37
Q

Bronchopneumonia

Where got it
Where located
Xray

A

Usually community aquired

Infection spread throughout the lungs
*particularly where the bronchioles connect to avloli

Appears on xray as patchy areas throughout

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38
Q

Pluritis (pleurisy)

A

Pluritis and Pleuritic pain may occur with pneumonia
*sharp stabbing pain on inspiration

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39
Q

Typical pattern of pneumonia

A

Infection within alvoli

Most bacterial

Neutrophil response

40
Q

Atypical pattern pneumonia

A

Infection within interstitial spaces

Most viral

Lymphocyte response

41
Q

Stages of bacterial pneumonia

A

Edema

Red hepatization

Grey hepatization

Resolution

42
Q

Edema

(Stage of bacterial pneumonia)

A

Frothy, pink sputum

43
Q

Red hepatization

(Stage of bacterial pneumonia)

A

Consolidation of alveoli with RBCs, neutrophils

Rust colored sputum (may be present in both red and grey hepatization)

44
Q

Grey hepatization

(Stage of bacterial pneumonia)

A

Immune process production of fibrin and immune molecules

45
Q

Tuberculosis

A

Cause : mycobacterium tuberculosis

Resistant to destruction alvolar macrophages (infects the macrophages)

Tb induce a Type IV cell-mediated hypersensitivity response

46
Q

TB Type IV cell mediated hypersensitivity response

A

Results in production of t cytotoxic cells specific for the TB organism

47
Q

TB healing

A

Healing by granuloma formation

Ghon Foci/ Ghon Complex

Tb is walled off in granuloma

48
Q

Fungal resp tract infections

A

Most common in immune compromised persons
*opportunistic infections

Usually persent as lower resp infections but its really not

Very serious and difficult to cure

49
Q

Malignancies of the resp tract

A

Laryngeal cancer

Lung cancer (bronchogenic carcinoma)

Tobacco is a common cause

50
Q

Pulmonary disorders in children

A

Airways are small

Since their radius is already small then small changes to the radius can rapidly lead to resistance of their air flow

Airway obstructions are a common issue

51
Q

Serious resp tract infection in children

A

Acute bronchitis

Acute laryngotracheobrhonchitis (Croup)
*barkey cough

Bronchiolitis
*more severe in children due to small airways

Epiglotitis

52
Q

Epiglotitis in children

A

Inflammation of the epiglottis

Can cause complete obstruction of airway

May need intubation

53
Q

Neonatal respiratory distress syndrome

(Hyaline membrane disease) HMD

A

Pink membranes that form in the alveoli

Cause: developmental deficiency of surfactant (born too early)
*Type II alvolar cells too immature to produce enough surfactant

Most common in preterm newborn infants

54
Q

Bronchopulmonary dysplasia

A

Iatrogenic type of chronic lung disease
*began due to treatment

Occurs in infants treated with mechanical ventilation for congential pulmonary problems
*pressure of ventilations damages cell

The dysplastic changes cause scarring and fibrosis of airway and pulmonary tissue

55
Q

Classification of lung disorders

A

Disorders of lung inflation

Obstructive lung disorders

Interstitial lung disorders

Pulmonary vascular disorders

56
Q

Disorders of lung inflation

A

Aspiration
Atelectasis
Pulmonary edeam
Pleural disorders:
-pnemothorax
-pleural effusion
-pleuritis (pleurisy)
Flail chest
Acute lung injury and acute respiratory distress syndrome (ARDS)

57
Q

Aspiration

A

Inhalation of foreign substances into the lungs

Risks of aspiration:
-Airway obstruction prevent gas exchange

-Aspiration pneumonia

(aspiration into right mainstem bronchus is more common due to anatomy)

58
Q

High risk population for aspiration

A

-young children

-person who conditions that disrupt the ability to protect airway
*swallowing dysfunction neuro problems
*⬇️ level of consciousness

59
Q

Atelectasis

A

Compression atelectasis :
something outside lungs push against the alvoli and prevent them from inflating

Absorption atelectasis:
Alveoli reabsorb air causing atelectasis

60
Q

Pulmonary edema

A

Fluid into alveoli
Due to :
-increased capillary hydrostatic pressure in pulmonary capillaries due to left sided HF

S/s:
Frothy pink sputum
Crackles possibly

61
Q

Pleural disorder: pneumothorax

A

Air in pleural space due to:

-External trama to chest

-Internal pulmonary injury:
*chronic lung disease
*iatrogenic consequences of mechanical ventilation

62
Q

Spontaneous pneumothorax occurs particularly in?

A

Newborn infants (pressure of first breaths)

Marfan syndrome (connective tissues weakened)

63
Q

2 presentations of pneumothorax

A

Communicating pneumothorax (open)
*can get air in and out

Tension pneumothorax
*only have air coming in not out

64
Q

Pleural effusion
Types

A

Liquid in lungs

Transudative pleural effusion (serous fluid)
*due to HF

Exudative pleural effusion (infectious/inflammatory exudate) (most common)
*empyema

Chylothroax (lymphatic fluid)

Hemothroax (blood)

65
Q

Pleuritis (plurisy)
(Other pleural abnormalities)

A

Inflammation within pleural space

Characteristic pattern of sharp/stabbing inspiratory pain (pleuritic pain)

66
Q

Flail chest

A

Chest injury with fracture of a segment of ribs

Paradoxical (opposite) free floating movement

Rib segment moves in when chest moves out

Creates high risk for pneumothroax

67
Q

Acute respiratory distress syndrome (ARDS)

A

Severe hypoxemia

ARDS is secondary to various critical illnesses or injury

Severe inflammatory response with widespread destruction of alveoli

Too much stuff in alveoli and decreased surfactant

68
Q

Neonatal RDS

A

Primary developmental deficiency of surfactant so you can treat with surfactant

Preterm infants

69
Q

Obstructive pulmonary disorders

A

Obstruction to the outflow of air during expiration

Asthma (bronchial asthma)
Chronic obstructive pulmonary disease (COPD)
*chronic obstructive bronchitis
*emphysema
Cystic fibrosis
Bronchiectasis

70
Q

Asthma (bronchial asthma)

A

Reactive airway disease (RAD)

No cure but can reverse symptoms (makes it unique)

S/s:
Edema
Mucus secretion
Bronchoconstriction

71
Q

Characteristics of asthma

A

Chronic inflammatory disorder

⬆️ bronchial hyperresponsiveness to “triggers”

Difficulty with expiration

S/s:
Wheezing, breathlessness, chest tightness, coughing
Common at night or early morning

72
Q

Pathophysiology of asthma
Small airway
Inflammation leads to

A

Small airway especially affected:
⬆️ smooth muscle
Little supporting cartilage

Airway inflammation leads to:
Edema
Mucus plug
Airway hyperresponsiveness
Bronchospasm
Hyperexpansion of alveoli

73
Q

Airtrapping in asthma

A

Breathing:
Inspiratory phase is active
Expiratory phase is passive

Air can enter alveoli when airway is dilated with inspiration bc its active and using muscles
BUT
Air gets trapped when it relaxes on expiration bc no muscles being used

74
Q

Triggers of asthma symptoms

A

Allergic vs non allergic triggers
(Early vs late response)

Extrinsic vs intrinsic triggers
(Extrinsic: external origin)
(Intrinsic: internal origin (stress)

Childhood vs adult onset

75
Q

Immune responses in allergic asthma

A

Early phase:
Degranulation of mast cells with IgE
Causes release of inflammatory mediators

Late phase:
Leukocyte responses with more inflammatory cytokines

76
Q

Clinical manifestation of asthma

A

Cough
Expiratory wheezing (may be absent)
Chest tightness
⬆️ work of breathing with fatigue
⬇️ peak expiratory flow rate (PEFR)
⬇️ forced expiratory volume in 1 second (FEV1)
Chest xray usually normal

77
Q

Chronic obstructive pulmonary disease (COPD)

A

Two different disorders but may occur seperately
*chronic bronchitis
*emphysema

Neither are reversible or curable

78
Q

Pathophysilogy of chronic bronchitis

A

Inflamed and swollen airway with increased mucus secretion

Narrowed ariway with mucus plugs cause air trapping like asthma

79
Q

Clinical manifestation of chronic bronchitis

A

Excessive bronchial secretions=airway obstruction

SOB with decreased exercise tolerance

Cyanosis, hypoxemia and hypercapnea

Polycythemia due to simulation of erythropoiesis due to hypoxia

May develop right sided HF (cor pulmonale) with peripheral edema

80
Q

Pathophysiology of emphysema

A

Destruction of alveoli and supportive tissue

Distortion of small airways (causes air trapping)

Two types of emphysema:
Centriacinar
Panacinar

81
Q

Centriacinar emphysema

A

Occurs in smokers

Alveolar damage is due to continued exposure to toxins

Affects central bronchioles

82
Q

Panacinar emphysema

A

Due to inherited deficiency of the enzyme Alpha 1 Antitrypsin (genetic)

distal alveoli affected first

Alpha 1 Antitrypsin opposes the action of proteolytic enzymes within lungs

Without opposing proteolytic enzymes we have destruction of alveolar tissue

83
Q

Clincial manifestagtion of emphysema

A

-Dyspnea

-Increased work of breathing with accessory muscle use (over compensation so s/s are late)

-barrel chest due to air trapping

-pursed lip breathing

-weight loss (unique)

84
Q

Chronic bronchitis vs emphysema

A

Chronic bronchitis: blue bloaters
Difficulty breathing and decreased O2
Turn blue

Emphysema: pink puffers
Fast breathing turn red

85
Q

Cystic fibrosis

Obstructive pulmonary disorder

A

Autosomal recessive mutation on long arm (q) chr 7

Chloride transport issue causing production of mucus thats thick and dehydrated

Causes airway obstruction due to the mucus

86
Q

Bronchiectasis

A

Permanent dilation of bronchi due to chronic airway damage

Destruction of bronchial muscle and supportive lung tissue

Due to several chronic lung diseases
(not a disease entity on its own)

87
Q

Interstitial lung disorders

A

Causes:
Occupational and environmental inhalants

Side effect to drug

Immunologic lung diseases
*sarcoidosis: multisystem immune disorder (formation of granulomas in the lung)

88
Q

Interstitial lung disorder

Case model

A

Pulmonary fibrosiss
Idiopathic pulmonary fibrosis
(fibrous tissue between alveoli effects ventilation)

Idiopathic=dont know what caused it

89
Q

Pulmonary vascular disorders

A

Perfusion issue 🚮

Issue primary of decreased perfusion

Problem with the Adequacy of flow of blood to lungs

High V/Q ratio disorders

90
Q

Pulmonary vascular disorders
Case models

A

Pulmonary embolism

Pulmonary hypertension

Cor pulmonale

91
Q

Pulmonary embolism
(Pulmonary vascular disorders)

A

Fragment travels to lung

Can originate from:
A clot (DVT)
Air (iv therapy
Fat (ortho injury exposing fat)
Amniotic fluid in pregnancy

92
Q

Pulmonary hypertension
(Pulmonary vascular disorders)

A

Elevated BP in main pulmonary artery

Primary and secondary pulmonary hypertension

93
Q

Pulmonary hypertension
(Pulmonary vascular disorders)

Primary HTN

A

Fatal due to no tx

Increase resistance to blood flow due to narrowing in pulmonary artery

Idiopathic condition

94
Q

Pulmonary hypertension
(Pulmonary vascular disorders)

Secondary HTN

A

1)Secondary to pulmonary disorders which causes decreased alveolar oxygen

2)hypoxia induced pulmonary vasoconstriction

3)increase resistance to blood flow thru pulmonary vessels

4)secondary elevation of BP in main pulmonary artery

95
Q

Cor pulmonale
(Pulmonary vascular disorders)

A

Right sided HF secondary to pulmonary disease

Lung disease produces hypoxia induced pulmonary vasoconstriction leads to:
1. Increased resistance in pulmonary vessels
2. increased BP in main pulmonary artery
3. increased workload on the right side of heart
4. right sided HF

patho 300 exam 2 (6 decks)

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