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Anatomy and Phyisology > HLTH respiratory review > Flashcards

HLTH respiratory review Flashcards

1
Q

4 bones forming sinuses in the nasal cavity

A

frontal, ethmoid, sphenoid, and maxillary

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2
Q

upper respiratory tract mucosa epithelium

A

pseudostratified columnar with cilia with mucus secreting goblet cells

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3
Q

how does smoking change the respiratory mucosa?

A

replaces pseudostratified columnar with simple squamous and impairs the function of cilia

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4
Q

what leads to mouth breathing?

A

inflamed pharyngeal tonsils

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5
Q

palatine tonsils

A

are lymphoid tissue in the posterior portion of the oral cavity

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6
Q

natural flora in the respiratory tract

A

upper tract has natural flora but lungs are sterile

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7
Q

right vs left bronchi

A

the right is larger and straighter

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8
Q

how does the epithelium change throughout the respiratory tract?

A

upper is pseudostratified columnar, then simple columnar, then simple cuboidal near the terminal bronchioles

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9
Q

function of surfactant

A

reduces surface tension and prevents collapse of the alveoli during expiration

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10
Q

lobes in right and left lungs

A

right has 3, left has 2

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11
Q

structure of ribs (false vs true)

A

first 7 are true and attach to the sternum, next 3 are attached to the 7th ribs and are false, and last 2 are attached to the vertebrae and are floating

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12
Q

boyle’s law

A

as the size of the thoracic cavity decreases, the pressure inside increases (hence air will move out)

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13
Q

quiet inspiration

A

involves contraction of the diaphragm and the external intercostal muscles

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14
Q

quiet expiration

A

muscles relax and this process is passive, requiring no cellular energy

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15
Q

forced inspiration

A

requires additional energy and muscular activity by accessory muscles

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16
Q

forced expiration

A

requires additional energy and the abdominals contract

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17
Q

compliance

A

refers to the ability of the lungs to expand and depends on the elasticity of the tissues

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18
Q

tidal volume

A

amount of air entering lungs with each normal breath

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19
Q

residual volume

A

amount of air remaining in the lungs after forced expiration

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20
Q

inspiratory reserve

A

maximum amount of air that can be inhaled past normal quiet inspiration

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21
Q

expiratory reserve

A

maximum amount of air that can be expired following a passive expiration

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22
Q

vital capacity

A

maximum amount of air expired following a maximal inspiration

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23
Q

total lung capacity

A

is the total volume of air in the lungs after maximal inspiration

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24
Q

central chemoreceptors

A

respond to an increase in PaCO2 or a decrease in pH

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25
Q

peripheral chemoreceptors

A

respond to decreased oxygen levels in the blood

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26
Q

hypercapnia

A

refers to high CO2 levels

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27
Q

how does respiration change with high CO2 levels?

A

respirations increase in both rate and depth

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28
Q

dalton’s law

A

each gas in a mixture moves according to its own partial pressure gradient and is independent of other gases

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29
Q

how much of O2 is released from hemoglobin in the blood?

A

25%

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30
Q

what does CO2 attach to in hemoglobin?

A

an amino acid, making it carbaminohemoglobin

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31
Q

ratio of bicarbonate to carbonic acid

A

20:1

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32
Q

sneezing

A

is a response to irritation in the upper respiratory tract

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33
Q

coughing

A

is a result of nasal dripping into the oropharynx or irritation of the lower respiratory tract

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34
Q

productive cough

A

refers to removing irritating materials from the lower respiratory tract

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35
Q

yellow-green sputum

A

indicates bacterial infection

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36
Q

rusty or dark coloured sputum

A

is a sign of pneumococcal pneumonia

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37
Q

pus-containing sputum

A

indicates bronchiectasis

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38
Q

thick and sticky sputum

A

can indicates cystic fibrosis or asthma

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39
Q

hemoptysis

A

is blood containing sputum that is associated with pulmonary edema

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40
Q

eupnea meaning and rate

A

refers to breathing rate and normal is 10-18 per minute

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41
Q

kussmaul respirations

A

are deep, ‘air hungry’ respirations and are associated with acidosis or strenuous exercise

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42
Q

labored respirations

A

are often associated with airway obstruction

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43
Q

wheezing

A

can indicate obstruction in the small airways

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44
Q

stridor

A

is a high pitched crow sound and is associated with obstruction in the upper airways

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45
Q

rales

A

light, bubbly or crackling sounds associated with serous secretions

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46
Q

rhonchi

A

are deeper and harsher sounds associated with thick mucus

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47
Q

absence of breath sounds meaning

A

can indicate a collapsed lung (atelectasis)

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48
Q

dyspnea

A

refers to discomfort and trouble breathing

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49
Q

severe dyspnea signs

A

nostril flaring, use of accessory muscles, and retraction of muscles above the ribs

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50
Q

pleural pain

A

results from irritation or inflammation of the parietal pleura

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51
Q

why does hypoxia lead to acidosis?

A

because of anaerobic metabolism that leads to production of lactic acid

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52
Q

surface tension meaning

A

the ability for fluid to reduce its surface area by forming droplets

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53
Q

most common pathogen causing the common cold

A

rhinovirus

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54
Q

common cold

A

is a viral infection of the upper respiratory tract which is spread by respiratory droplets

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55
Q

secondary infections of the common cold

A

pharyngitis, laryngitis, or acute bronchitis and usually are caused by microorganisms invading necrotic mucus membranes

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56
Q

sinusitis

A

is usually a secondary bacterial infection to a cold or allergies, in which one or more of the paranasal sinuses is obstructed

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57
Q

causative organisms for sinusitis

A

pneumococci, streptococci, or Haemophilus influenza, as well as fungi or viruses

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58
Q

signs of sinusitis

A

pressure in the sinus cavities causes pain and headache, nasal congestion, fever, and sore throat

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59
Q

laryngotracheobronchitis

A

is a common viral infection in young children aged 3 months to 3 years which begins as an upper respiratory infection

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60
Q

signs of laryngotracheobronchitis

A

nasal congestion, cough, barking cough, hoarse voice, and inspiratory stridor

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61
Q

epiglottis causative organism

A

haemophilus influenzae type B

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62
Q

epiglottis signs

A

swelling of the epiglottis and larynx, appearing as a red ball, fever, sore throat, difficulty swallowing, drooling, and inspiratory stridor

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63
Q

influenza

A

aka flu which is a viral infection of the upper and lower respiratory tracts and has 3 types

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64
Q

flu vs cold

A

flu has a more acute onset, along with fever, fatigue, and aches

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65
Q

causative organism in scarlet fever

A

A β-hemolytic streptococcus (Streptococcus pyogenes)

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66
Q

scarlet fever

A

is a bacterial upper respiratory tract infection

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67
Q

signs of scarlet fever

A

fever, sore throat, chills, vomiting, abdominal pain, strawberry tongue, and rash

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68
Q

bronchiolitis

A

lower respiratory tract viral infection common in young children aged 2 to 12 months, causing inflammation and necrosis in the small bronchioles

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69
Q

causative agent of bronchiolitis

A

respiratory syncytial virus (RSV), a myxovirus

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70
Q

signs of bronchiolitis

A

wheezing, dyspnea, rapid and shallow respirations, cough, rales, chest retractions, and fever

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71
Q

pneumonia

A

may develop as a primary acute infection or secondary to aspiration or inflammation in the lungs when cilia are impaired and may be caused by a bacteria, virus, or fungi

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72
Q

common pneumonia-nosocomial infectious agents

A

often are gram-negative bacteria like klebsiella pneumoniae or pseudomonas aeruginosa

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73
Q

lobar pneumonia causative agent

A

S. pneumoniae

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74
Q

lobar pneumonia

A

begins as congestion in the alveolar walls, followed by accumulation of a solid mass called consolidation, causing rusty coloured sputum; gas exchange is impaired and infection may spread to involve the pleura

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75
Q

signs of lobar pneumonia

A

acute onset, fever, chills, dyspnea, tachypnea, tachycardia, rales, rusty coloured sputum, and productive cough

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76
Q

consolidation

A

is present in lobar pneumonia and involves the accumulation of neutrophils, fibrin, and RBCs that form a solid mass in the alveolar exudate

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77
Q

complications of lobar pneumonia

A

hypoxia can lead to metabolic acidosis, dehydration can occur, and infection may spread to the pleura

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78
Q

bronchopneumonia

A

involves a diffuse pattern of spreading in the lower lobes, beginning in the bronchial mucosa and spreading to the alveoli and pooled secretions in the lungs are common, impairing gas exchange

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79
Q

signs of bronchopneumonia

A

gradual onset with fever, cough, rales, and productive cough with yellow-green sputum

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80
Q

Legionnaires’ disease

A

a type of bacterial pneumonia that often in spread in spas and nosominal areas due to preference for warm and moist environments and resides in macrophages in its host

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81
Q

causative organism for legionnaires’ disease

A

gram-negative bacterium, Legionella pneumophila

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82
Q

primary atypical pneumonia

A

is atypical because it involves interstitial inflammation and is caused by a virus or mycoplasma

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83
Q

causative agent of primary atypical pneumonia

A

mycoplasma pneumoniae which is a small bacteria that lacks a cell wall or influenza A, B, an adenovirus, or RSV

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84
Q

mycoplasmal pneumonia

A

is common in older children and young adults and is transmitted by aerosol

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85
Q

viral pneumonia

A

infection begins in the upper tract mucosa and descends to involve the lungs, in which exudate is diffuse, with little forming in the lungs

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86
Q

signs of viral pneumonia

A

unproductive cough, hoarseness, sore throat, headache, and fever

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87
Q

pneumocystis carinii pneumonia

A

is an atypical pneumonia common in AIDS patients that causes necrosis, diffuse intestinal inflammation, and damage to alveoli

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88
Q

signs of pneumocystis carinii pneumonia

A

unproductive cough and difficulty breathing

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89
Q

unique characteristics of COVID

A

rapid and firm attachment to lung cells and cytokine storm

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90
Q

COVID virus

A

enveloped, ss, positive-sense RNA virus

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91
Q

SARS

A

severe acute respiratory syndrome that occured in 2003, causing flu-like symptoms, dry cough, marked dyspnea, and hypoxia

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92
Q

SARS causative agent

A

SARS CoV which is an RNA associated coronavirus

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93
Q

tuberculosis

A

bacterial infection associated with poverty and homelessness affecting the lungs and is caused by mycobacterium tuberculosis

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94
Q

Mycobacterium

A

is a slow growing bacillus this is resistant to drying and disinfectants due to cell wall and can live in dried sputum for weeks

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95
Q

TB primary infection

A

is when the bacteria enters the lungs and is engulfed by macrophages, causing a local inflammatory reaction often in the upper lungs and the formation of granulomas

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96
Q

granuloma

A

lymphocytes and macrophages cluster together at the site of inflammation and surround the pathogen which may still be alive

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97
Q

tubercle

A

refers to a granuloma with an alive mycobacterium, causing cessation necrosis to develop and cheesy necrosis in the centre

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98
Q

Ghon complexes

A

tubercle/granuloma complexes in the lungs and lymph nodes

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99
Q

miliary or extrapulmonary TB

A

is a rapidly progressive form in which multiple granulomas affect the lungs, spread into the circulation, and affect other organs and tissues; common in children and those who are immunocompromised

100
Q

secondary infection of TB

A

occurs years later when the bacillus escapes the granuloma when the individual is immunocompromised, causing cavitation

101
Q

cavitation

A

is the formation of a large opening in the lung caused by secondary TB, eroding the bronchi and vessels, causing the spread of the infection to other areas

102
Q

signs of secondary TB

A

anorexia, malaise, fever, fatigue, weight loss, prolonged cough that gets worse and often is productive, and purulent sputum that often contains blood

103
Q

causative organism for histoplasmosis

A

histoplasma capsulatum which is a fungus

104
Q

histoplasmosis

A

fungal infection common in AIDS patients in which the pathogen is found inside macrophages, in which this presents similarly to TB (primary and secondary stage which involves granulomas and cavitation)

105
Q

signs of histoplasmosis

A

cough, fever, fatigue, and night sweats

106
Q

anthrax

A

is a bacterial infection of the skin, respiratory tract, and GI tract in humans and cattle

107
Q

causative agent for anthrax

A

is a gram-positive bacillus that forms white-greyish spores

108
Q

signs of skin anthrax

A

blisters that may itch, swelling, and painless open skin sore with black centre often on the face, neck, arms, or hands

109
Q

signs of respiratory anthrax

A

fever, chills, chest discomfort, shortness of breath, cough, headache, sweats, and body aches

110
Q

GI form of anthrax

A

fever and chills, neck swelling, sore throat, painful swallowing, hoarseness, nausea, vomiting, headache, and fainting

111
Q

is what infection may a child take a sitting/tripod position?

A

epiglottis

112
Q

cystic fibrosis

A

is an autosomal recessive inherited disorder due to a genetic mutation on the CFTR gene on the 7th chromosome, causing a defect in exocrine glands that produce abnormally thick mucus, affecting the lungs and pancreas

113
Q

how does CF affect the lungs?

A

mucus obstructs airflow in the bronchioles, causing air trapping and damage to the bronchial walls, and providing excellent conditions for infection; eventually right-sided CHF will develop

114
Q

meconium ileus

A

refers to the small intestine being blocked by mucus at birth in infants with CF

115
Q

how does CF affect the digestive tract?

A

meconium ileus is present at birth, pancreatic secretions are blocked, bile ducts may be blocked, and a result malabsorption, malnutrition, and dehydration develop

116
Q

how are the salivary glands affected by CF?

A

secretions are abnormally high in NaCl and mucus may block the submaxillary and sublingual glands

117
Q

how are the sweat glands affected by CF?

A

abnormally high concentrations of NaCl

118
Q

how is reproduction affected by CF?

A

mucus may obstruct the vas deferens or the cervix, causing infertility

119
Q

signs of cystic fibrosis

A

meconium ileus at birth, salty skin, steatorrhea, distended abdomen, chronic cough, failure to gain weight, and fatigue

120
Q

usual cause of death in CF

A

respiratory failure or right sided CHF (cor pulmonale)

121
Q

lung cancer

A

leading cause of cancer deaths and third most common cancer; common for primary and secondary tumors, and benign tumors are rare here; 2 groups small cell and non-small cell

122
Q

small cell lung cancer

A

cells are small and round, the cancer spreads rapidly, often is associated with smoking, is resistant to chemo, and mortality is higher

123
Q

non-small cell lung cancer

A

cells are larger, the spread is less, and the cells are responsive to chemo

124
Q

subtypes of NSCLC

A

adenocarcinoma, squamous cell carcinoma, and large cell carcinoma

125
Q

most common type of malignant lung cancer

A

bronchogenic carcinoma

126
Q

squamous cell carcinoma

A

usually develops from the epithelium of a bronchi near the hilum and projects into the airway

127
Q

what types of lung cancer are harder to detect?

A

bronchoalveolar cell carcinomas and adenocarcinomas

128
Q

small cet/oat cell carcinoma

A

are located near a major bronchus usually in the middle of the lung and metastasize early on

129
Q

mesothelioma

A

associated with asbestos and is usually fatal

130
Q

how do the lungs change with cancer?

A

first metaplasia and cilia damage (often due to smoking), and then dysplasia/ cancer in situ develops

131
Q

common sites for metastasized lung cancer?

A

brain, bone, and liver

132
Q

paraneoplastic syndrome of bronchogenic carcinoma

A

the tumors secretes hormone like substances like adrenocorticotropic hormone and ADH; this can lead to blood and muscle difficulties

133
Q

effects of tumors in the lungs

A

obstruction, inflammation, effusion, systemic effects, and paraneoplastic syndrome

134
Q

risk factors for developing lung cancer

A

snoking, secondhand smoke, genetic factors, chronic obstructive pulmonary disease, and occupational exposure to carcinogens like silica or asbestos

135
Q

early signs of lung cancer

A

persistent cough, dyspnea, or wheezing, hemoptysis, pleural effusion, chest pain, and hoarseness

136
Q

aspiration

A

involves the passage of fluid, vomit, drugs, or other foreign material into the trachea and lungs, commonly leading to obstruction and/or inflammation

137
Q

ball-valve effect

A

can occur with aspiration when inspiration passes past the obstruction, however, expiration is blocked, leading to a buildup of pressure distal to the obstruction

138
Q

aspirated liquids

A

disperse into several bronchi and cause inflammation, leading to increased secretions and narrowed airways, and in some cases the alveoli are affected

139
Q

aspiration pneumonia or chemical aspiration

A

can be due to inflammation of the alveoli due to aspirated liquids, predisposing to infection

140
Q

common causes of aspiration

A

children being children, lying down, post-operative, congenital abnormalities like cleft palate, or a complication of the gag reflex

141
Q

signs of aspiration

A

coughing and choking, stridor and hoarseness if upper airway is obstructed, wheezing, tachycardia, tachypnea, nasal flaring, hypoxia, and cardiac arrest

142
Q

sleep apnea

A

is a result of pharyngeal tissues collapsing during sleep, leading to repeated, momentary cessation of breathing

143
Q

complications of sleep apnea

A

pulmonary hypertension, type 2 diabetes, right sided CHF, stroke, erectile dysfunction, and depression

144
Q

treatment for sleep apnea

A

CPAP (continuous positive airway pump)

145
Q

asthma

A

involves periodic episodes of severe and reversible bronchoconstriction in those with hypersensitive airways

146
Q

extrinsic asthma

A

involves acute episodes that are triggered by a type I hypersensitivity reaction to an inhaled allergen and is often genetic

147
Q

intrinsic asthma

A

develops in adults and is when other types of stimuli (not allergens) target the airways and may be due to infections, exposure to cold, exercise, aspirin, or cigarette smoke

148
Q

three changes of the respiratory tract during an asthma attack

A

inflammation of the mucosa, constriction of the bronchioles, and increased secretion of thick mucus

149
Q

what antibody is reacted with in extrinsic asthma?

A

IgE

150
Q

what chemical mediators are released during extrinsic asthma?

A

histamine, kinins, and prostaglandins

151
Q

second stage of extrinsic asthma attack

A

eosinophils release additional chemical mediators such as leukotrienes, resulting in prolonged inflammation, constriction, and mucosa damage

152
Q

air trapping

A

can occur with asthma when air passes into the area distal to the obstruction but only some is expired; this leads to increased residual volume and potential collapse of a bronchial wall

153
Q

status asthmaticus

A

is a persistent asthma attack that does not respond to therapy, and may be fatal leading to hypoxia, acidosis, cardiac arrhythmias, and a depressed nervous system

154
Q

chronic asthma

A

aka COLD; frequent attacks cause the bronchial walls to thicken and fibrous tissue develops

155
Q

causes of asthma

A

often are genetic are related to family history of asthma, eczema, and hay fever; may also be caused by a viral infection, sedentary lifestyle, and increased exposure to allergens

156
Q

signs of an asthma attack

A

coughing, wheezing, dyspnea, inability to speak tightness in chest, labored breathing, thick mucus, tachycardia, hypoxia, and initial respiratory alkalosis, followed by respiratory acidosis

157
Q

pulsus paradoxus

A

refers to the pulse differing on expiration and inspiration and is a sign of asthma attack

158
Q

function of the mutated protein in CF

A

is helps to transport chloride into the cell

159
Q

chronic obstructive pulmonary disease

A

is a group of chronic respiratory disorders that are characterized by progressive tissue destruction and obstruction of airways

160
Q

types of COPD

A

emphysema, chronic bronchitis, and chronic asthma

161
Q

complications of COPD

A

respiratory failure (due to right sided CHF or cor pulmonale), hypoxia, or hypercapnia

162
Q

emphysema

A

involves the destruction of alveolar walls and septae, leading to large, permanently inflamed alveoli spaces

163
Q

cause of emphysema

A

can be due to a defect of alpha1-antitrypsin, genetic, and cigarette smoking

164
Q

alpha1-antitrypsin

A

is a protein present in body tissues and fluids and inhibits the activity of proteases (released during inflammation and can cause tissue damage)

165
Q

changes in the lungs during emphysema

A

the breakdown of the alveolar wall, fibrosis and thickening of walls, and difficulty with breathing develops

166
Q

effects of the breakdown of alveolar walls

A

decreased surface area, decreased pulmonary capillaries, and loss of elastic fibres

167
Q

blebs or bullae

A

are air filled spaces present in emphysema

168
Q

complications of emphysema

A

pneumothorax, hypercapnia, hypoxia, increased risk for infection, pulmonary hypertension, cor pulmonale, and secondary polycythemia

169
Q

signs of emphysema

A

dyspnea, barrel chest, hyperventilation with prolonged expiration, clubbed fingers, anorexia, and fatigue

170
Q

chronic bronchitis

A

irreversible and progressive changes in the bronchi due to irritation from smoking or exposure to pollution

171
Q

how do the bronchi change with chronic bronchitis?

A

mucosa is inflamed and swollen, hypertrophy and hyperplasia of the mucus gland, increased secretions, and fibrosis and thickening of walls

172
Q

pink buffer

A

is used to characterize emphysema and includes signs of dyspnea, hyperventilation, and overinflation

173
Q

blue bloater

A

is used to characterize chronic bronchitis and includes signs of lower oxygen levels, cyanosis, and edema

174
Q

signs of chronic bronchitis

A

constant productive cough, tachypnea and shortness of breath, thick secretions, cyanosis, secondary polycythemia, weight loss, and cor pulmonale signs

175
Q

bronchiectasis causes

A

is a secondary problem that develops in those with CF or COPD, more specifically from childhood infections, aspiration, or a weakness in the bronchial wall

176
Q

bronchiectasis

A

is a dilation and widening of the bronchial walls that arise from recurrent inflammation and infection, causing fluid to accumulate and cause frequent infections

177
Q

how do the bronchial walls change in bronchiectasis?

A

walls dilate, loss of cilia, metaplasia, fibrosis, and progressive obstruction

178
Q

signs of bronchiectasis

A

chronic cough, excessive amounts of purulent sputum, rales, foul breath, dyspnea, hemoptysis, and anemia

179
Q

restrictive lung disorders

A

refers to a group of disorders in which expansion is impaired and total lung capacity is reduced and includes two groups (chest wall limits expansion or tissues limit expansion)

180
Q

causes of restrictive lung disorders due to chest wall limiting expansion

A

kyphosis, scoliosis, MD, ALS, poliomyelitis, or botulism

181
Q

causes of restrictive lung disorders due to tissue damage

A

pulmonary fibrosis and occupational diseases due to inhaled particles

182
Q

pneumoconiosis

A

are chronic restrictive lung disorders resulting from long-term toxic inhaled particles such as asbestos in which normal defences such as cilia and mucus are damaged

183
Q

pathophysiology of pneumoconiosis

A

inflammation and fibrosis develop, in which tissues are progressively damaged, alveoli become nonfunctional, and infections are common, contributing to the damage

184
Q

signs of pneumoconiosis

A

dyspnea, cough, and increasing effort for respiration

185
Q

pulmonary edema

A

refers to fluid collecting in the alveoli and interstitial area, interfering with gas exchange and lung expansion

186
Q

causes of pulmonary edema

A

inflammation that increases capillary permeability, decreased osmotic pressure in capillaries (kidney or liver disease), and pulmonary hypertension (left sided CHF or sleep apnea)

187
Q

mild pulmonary edema signs

A

cough, rales, and orthopnea

188
Q

severe pulmonary edema signs

A

hemoptysis, frothy and bloody sputum, labored breathing, hypoxia, cyanosis, and may lead to paroxysmal nocturnal dyspnea

189
Q

pulmonary embolus

A

is a blood clot or other mass that obstructs the pulmonary artery or a branch of it (often from the lower limbs), blocking the flow of blood through the lung tissues

190
Q

effect of large pulmonary embolus

A

effect the cardiovascular system and may cause right-sided CHF and decreased CO and vasoconstriction occurs as a reflex mechanism, in which sudden death may occur as a result

191
Q

causes of pulmonary embolus

A

embolus in the leg veins, many as a result of phlebothrombosis or thrombophlebitis which can be due to childbirth, CHF, dehydration, cancer, and increased coagulability of the blood; can also be due to fat emboli, vegetations from endocarditis in the right side of the heart, and amniotic fluid emboli from placenta tears

192
Q

signs of a small pulmonary embolus

A

cough, chest pain, and dyspnea

193
Q

signs of a large pulmonary embolus

A

chest pain, tachypnea, dyspnea, hemoptysis, fever, and sympathetic response due to hypoxia

194
Q

signs of an massive pulmonary embolus

A

severe crushing chest pain, low BP, rapid weak pulse, and loss of consciousness

195
Q

signs of a fat emboli

A

rash, neurologic dysfunction, and acute respiratory distress

196
Q

atelectasis

A

is the collapse or non aeration of a lung often due to a secondary condition, leading to decreased gas exchange and hypoxia

197
Q

what happens to the lungs during atelectasis?

A

the alveoli collapse, ventilation and perfusion are compromised, and O2 diffusion is greatly impaired (CO2 diffusion is only slightly impaired because this gas diffuses easier)

198
Q

obstructive or resorption atelectasis

A

occurs as a result of mucus or a tumor in which air is not replaced distal to the obstruction

199
Q

compression atelectasis

A

occurs as a result of a mass compressing the lung, in which air is preventing from entering that part of the lung; adhesion between the pleural membranes may also be impaired

200
Q

increased surface tension atelectasis

A

can result due to pulmonary edema or respiratory distress syndrome, in which expansion is impaired

201
Q

contraction atelectasis

A

is due to fibrosis tissue in the lungs which may lead to collapse

202
Q

postoperative atelectasis

A

often is due to abdominal surgery and can be due to pain preventing expansion, supine position, decreased cough effort, and slow and shallow respirations due to anesthesia and analgesics

203
Q

signs of atelectasis

A

can cause dyspnea, increased HR and respiratory rate, and asymmetrical chest expansion (due to the unaffected lung overinflating)

204
Q

pleural effusion

A

is an accumulation of fluid between the pleural membranes and may be accompanied by pleurisy

205
Q

pleurisy

A

aka pleuritis and is when the pleural membranes are inflamed, rough and swollen; may accompany pleural effusion

206
Q

where are fluids from the pleural cavity drained by?

A

the lymphatics

207
Q

complications of pleural effusion

A

can impair expansion of the lungs, can cause atelectasis, reduced venous return, and a shift of the trachea/mediastinum towards the unaffected side

208
Q

transudate effusion

A

aka hydrothorax and is water in the pleural cavity often due to increased hydrostatic pressure or decreased osmotic pressure of the vessels, leading to a shift of fluid into this potential space

209
Q

exudative effusions

A

are often due to inflammation or tumors, in which the fluid contains WBCs and proteins

210
Q

hemothorax effusions

A

is blood in the pleural cavity often the result of surgery, trauma, or cancer

211
Q

empyema

A

refers to pus in an area in the body, often in the pleural cavity and is associated with infection

212
Q

signs of pleural effusion

A

dyspnea, chest pain, increased HR and respiratory rate, tracheal deviation, and absence of breath sounds over the affected area

213
Q

pneumothorax

A

refers to air in the pleural cavity, preventing expansion and leading to atelectasis

214
Q

hydropneumothorax

A

refers to both air and fluid in the pleural cavity, but more fluid

215
Q

3 types of pneumothorax

A

closed, open, and tension

216
Q

closed pneumothorax

A

refers to air entering the pleural cavity from an opening directly in the internal airways or visceral pleura, not through the chest wall

217
Q

simple or spontaneous pneumothorax

A

occurs when a tear on the surface of the lung allows air to escape from inside the lung or bronchi into the pleural cavity; as the lung collapses, it conceals the leak

218
Q

secondary pneumothorax

A

is associated with respiratory conditions causing a rupture of an emphysematous bleb or erosion by a tumor to cause cavitation through the visceral pleura

219
Q

open pneumothorax

A

refers to an opening in the chest wall allowing atmospheric air to enter the cavity and can be a result of trauma or surgery

220
Q

sucking wound

A

refers to a large opening in the chest wall causing a sucking sound due to air moving in and out

221
Q

tension pneumothorax

A

can result from either open or closed damaged, but is unique and serious because it creates a one-way valve effect, whereas on inspiration the opening grows but closes on expiration, leading to increased pressure with each inspiration and compressing the other lung

222
Q

complications of tension pneumothorax

A

the unaffected lung and inferior vena cava are compressed, leading to hypoxia and respiratory distress

223
Q

general signs of pneumothorax

A

dyspnea, chest pain, atelectasis, cough, reduced breath sounds over the affected area, hypotension, and mediastinal shift

224
Q

flail chest

A

refers to fractures of the thorax, causing potential bleeding, edema, and atelectasis; this also causes opposite movements of the lungs on expiration and inspiration

225
Q

flail chest inspiration

A

the broken section of ribs moves inward rather than outward, limiting expansion, and compression from the affected side leads to stale and new air entering in the unaffected side

226
Q

flail chest expiration

A

affected side is pushed outward and air from the affected side moves into the unaffected side

227
Q

mediastinal flutter

A

occurs with flail chest when the mediastinum is pushed to and fro with breathing; this creates pressure on the inferior vena cava and impairs venous return to the heart

228
Q

infant respiratory distress syndrome

A

refers to inadequate maturation of the lungs and surfactant before birth, leading to impaired alveolar expansion and atelectasis, as well as increased capillary alveolar permeability and thus increased fluid in the intestinal area

229
Q

hyaline membrane

A

refers to increased alveolar capillary permeability in IRDS, causing fluid and proteins to lead into the interstitial area, further impairing gas exchange

230
Q

complications of infant respiratory distress syndrome

A

increased effort to breathe leads to anaerobic metabolism, lactic acid, and thus acidosis; this triggers vasoconstriction and impairs cell metabolism, further impairing the production of surfactant

231
Q

causes of infant respiratory distress syndrome

A

often is due to premature birth, but also is more common in males and those who has a C-section

232
Q

early signs of infant respiratory distress syndrome

A

60+ per minute respirations, flaring nostrils, subcostal and intercostal retraction, rales, and low body temperature

233
Q

prolonged signs of infant respiratory distress syndrome

A

rapid and shallow respirations, expiratory grunt, frothy sputum, cyanosis, hypoxia, and decreasing BP

234
Q

adult respiratory distress syndrome

A

is a restrictive lung disorder due to alveolar or pulmonary capillary damage, leading to pulmonary edema and decreased surfactant production; this impairs respiration and gas exchange and may cause microthrombi to form

235
Q

long term damage from adult respiratory distress syndrome

A

necrosis and fibrosis in the lungs

236
Q

complications of adult respiratory distress syndrome

A

fibrosis and necrosis in the lungs, CHF, and pneumonia

237
Q

causes of adult respiratory distress syndrome

A

prolonged shock, inhalation of irritating particles, viral infections, toxins, fat emboli, aspirations, and lung trauma

238
Q

signs of adult respiratory distress syndrome

A

dyspnea, restlessness, rapid and shallow respirations, increased heart rate, rales, cyanosis, and productive cough with frothy sputum

239
Q

acute respiratory failure

A

is the result of many pulmonary disorders and is present when PaO2 is less than 50 mm Hg or PaCO2 is greater than 50 mm Hg, and serum pH is decreasing

240
Q

normal PaO2 and PaCO2 values

A

80 - 100 for O2 and 35 - 45 for CO2

241
Q

respiratory insufficiency

A

refers to an interim state when blood gases are abnormal but cell function can continue

242
Q

conditions that may lead to acute respiratory failure

A

chronic conditions like emphysema, chronic disorders combined with acute ones like pneumonia, CNS depression by narcotics, chest trauma, asthma, pulmonary embolism, or disorders like ALS or myasthenia gravis

243
Q

signs of acute respiratory failure

A

rapid, shallow and laboured respirations, headache, tachycardia, hypoxia, hypercapnia, lethargy and confusion

244
Q

when may the mediastinum shift towards the affected side?

A

atelectasis

245
Q

when may the mediastinum shift towards the uneffected side?

A

pleural effusion

246
Q

inspiration and expiration with an open pneumothorax

A

on inspiration, the mediastinum moves towards the unaffected side and on expiration is moves back towards the affected side

247
Q

glottis

A

is the true vocal cords (lower ones) and the space between them

Anatomy and Phyisology (94 decks)

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