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Patho: Nursing > exam 2- respiratory > Flashcards

exam 2- respiratory Flashcards

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1
Q

pulmonary space

A

the whole pulmonary cavity (largest)

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2
Q

pleural space

A

a “potential” space between the 2 vicera (chest wall and lungs)(middle)

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3
Q

pulmonary interstitial space

A

a “potential” space between the cap mem and the alveolar mem. (smallest)

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4
Q

what do you not want in the pulm. interstitial space

A

water/fluid

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5
Q

why did they call it surfactant

A

surface
active
agent

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6
Q

what is surfactant

A

substance (lipoprotein) produced by the alveoli

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7
Q

what is the purpose of surfactant

A

reduces the surface tension and allows the alveoli to stay open for gas exchange

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8
Q

what do the pulmonary capillaries of alveolar and cap membrane form

A

a network around each alveolus so dense that an almost continuous sheet of blood covers the alveoli

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9
Q

how many blood cells can move through ta pulm capp at a time

A

one, they must move in a single file line

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10
Q

each RBC stays in cap bed for how long and how many alveoli does it exchange with

A

1 second

2-3 alveoli exchange

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11
Q

normal ventilation stimulates what in the alveoli

A

surfactant replacement

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12
Q

what happens to the alveoli when a person hyperventilates

A

leads to alveolar collapse (atelectasis)

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13
Q

normal alveolar unit

A

normal ventilation

normal perfusion

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14
Q

dead space unit

A

(pulmonary emboli)
normal ventilation
NO perfusion

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15
Q

shunt unit

A

NO ventilation
no perfusion
(tumor or fluid blocking the air from reaching alveoli)

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16
Q

silent unit

A

NO ventilation

NO perfusion

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17
Q

ventilation

A

movement of atmospheric air into the alveoli

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18
Q

diffusion

A

movement of o2 across alveolar walls into pulm caps

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19
Q

perfusion

A

movement of o2 to and into the cells (tissues)

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20
Q

each rbc has how many HG

A

300

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21
Q

how many o2 molecules can one HG carry

A

4

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22
Q

how many o3 molecules can one RBC carry

A

1,200

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23
Q

what are the 7 steps required to transfer O2 from environmental air into cells

A

ventilation of lungs
transport of o2 from alveoli into plasma
co2 out
circulation of blood
diffusion of o2 from cap into intersitital fluid
diffusion into cells
diffusion of o2 into mitochondria where it synths ATP

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24
Q

if any of the 7 steps of air to cells is interrupted, what happens

A

tissue becomes hypoxic

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25
Q

hypoxemia

A

decreased oxygenated of the arterial blood

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26
Q

hypoxia

A

decreased o2 levels of the cells

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27
Q

why might hypoxia be localized

A

a blood clot, where the person doesn’t need to be hypoxemic generalized

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28
Q

what are the four major etiologies of hypoxia

A

reduced transfer of O2 from alveolar (atmospheric) air to blood (hypoxemia)

decreased HgB concentration

decreased inspired O2

Ichemia

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29
Q

what are etiologies of reduced transfer of 02 from alveolar air to blood

A

hypoventilation
impaired transport of O2 across alveolar membrane
ventilation perfusion mismatch

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30
Q

hypoventilation:

A

decreased rate and or depressed depth of respirations

risk for those who have undergone anethesia

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31
Q

what two things can impaire transport of 02 across alveolar membrane causing the diffusion capaity of alveolar membrane to be affected

A

drug overdose
general anesthesia
chest and abdominal pain (surgery or trauma)
surface area available (fluid)
thickened membrane (pulmonary fibrosis)
intestinal space issues (fluid, infection)

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32
Q

what is ventilation perfusion mismatch

A

ventilation (air into alveoli) and perfusion (pulmonary cap blood flow) normally match but respiratory disease lead to mismatch

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33
Q

what are the etiologies for decreased HGB concentration

A

anemia

CO poisoning

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34
Q

what is/causes anemia

A

blood loss
decreased production of RBC’s
decreased iron intake

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35
Q

what is CO poisoning

A

Co combines with HGB at same site as O2 and blocks sites for O2
HGB likes CO better than O2

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36
Q

what are the etiologies for decreased inspired O2

A

breathing high altitude air

breathing air from which o2 has been removed (fire)

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37
Q

what are the etiologies of ischemia

A

decreased blood flow to tissue

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38
Q

why would blood flow decrease to tissues

A

vasoconstriction
obstruction in BV
decreased cardiac ouput

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39
Q

what causes local or regional ischemia

A

vasoconstriction
blocking
(ie atherosclerosis of iliac arteries leading to decreased blood flow to legs)

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40
Q

what causes general systemic ischemia

A

decreased perfusion of o2 to tissues caused by heart not pumping enough

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41
Q

why does hypovolemic shock lead to ischemia

A

loss of blood volume = lack of blood= lack of O2 perf

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42
Q

what are the manifestations of hypoxia

A

decreases SaO2, pO2
increased pCO2
decreased pH (respiratory acidosis)

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43
Q

what are the early signs of hypoxia

A

confusion
lethargy
increased HR
change in behavior

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44
Q

what are the middle signs of hypoxia

A

dyspnea (sob)
decreased urine output
prolonged cap refill

45
Q

what are the late signs of hypoxia

A

decreased BP

cyanosis at lips tounge

46
Q

what is atelectasis

A

collapse of alveoli

47
Q

what are three patho of atelectasis

A

compression atelectasis
absorption atelectasis
decreased surfactant production

48
Q

what is compression atelectasisq

A

external pressure usually caused by tumor or fluid pressing on alveoli

49
Q

what is absorption atelectasis

A

in alveoli, internal obstruction usually caused by secretions in alveoli

50
Q

what causes decreased surfactant production leading to atelectasis

A

premi babies
anesthesia
prolonged mechanical ventilation

51
Q

what are the clinical manifestations of atelectasis

A 
crackles (rales)
decreased breath sounds
dyspnea
cough
fever
decreased pO2, SaO2
increased pCO2
52
Q

what is pleural effusion

A

collection of fluid in pleural space

53
Q

what are the etiologies for pleural effusion

A

transudate (hydrothorax)
exudate
pus (empymea)
blood (hemothorax)

54
Q

what is transudate (hydrothorax) in pleural effusion

A

water accumulation usually under viceral pleura (cardiac/liver/kidney disease)

55
Q

what is exudate in pleural effusion

A

fluid is high in proteins from infection or malignancy

56
Q

what is pus from in pleural effusion

A

infection

57
Q

what is blood from in pleural effusion

A

trauma, thoracic surgery

58
Q

what are the clinical manifestations of pleural effusion

A

atelectasis because of fluid displaceing lung tissue

dyspnea
chest pain during respiration
mediastinal shift

59
Q

what is pneumothorax

A

the presence of air in pleural space

60
Q

what are the etiologies of pneumothorax

A

fractured ribs
rupured bleb (copd)
thoractomy
spontaneous

61
Q

why do the etiologies cause a pneumothorax

A

air enters pleural space… negative pressure in pleural space is destroyed, lung collapses

62
Q

what are the clinical manifestations of pneumothorax

A

dyspnea
chest pain on breath movts
no breath sounds on effected lung
hypoxia

63
Q

tension pneumothorax

A

life threatining

64
Q

what are the etiologies of tension pneumothorax

A

usually from trauma
air enters pleural space on inspiration but cannot escape on expiration
wound acts as a one way valve so air continues to build up in pleural space

65
Q

what are the clinical manifestations of tension pneumothorax

A

hypoxia
SOB
medistinal shift
decreased BP because of shift in great BV’s

66
Q

pneumonia

A

acute infection in lungs (tissue) caused by bacteria, virus, fungus

67
Q

what is the etiology of pneumonia

A

lower respiratory tract infection caused by streptococcus (pneumococcal) pneumonia

68
Q

what are the two types of pneumonia

A

community acquired

nosocomical (hospital aquried–bacteria ventilator associated– cant cough)

69
Q

what is the patho chain for pneumonia

A 
aspiration of microb (respiratory droplets)
inflammatory response
alveoli fill with exudate
phagocytosis in alveoli
resolution of inflection
70
Q

what are the clinical manifestations of pneumonia (6)

A 
fever
chest pain
increased RR
rusty, brown, yellow colored sputum
increased WBC
chest x-ray "infiltrates"
71
Q

pulmonary emboli

A

occulsion of a pulmonary artery by an emoblus

72
Q

what are the four types of emboli in pulmonary emboli

A

blood clot (thrombus from deep calf)
tissue frag
fat emboli (break in large bone)
air bubble

73
Q

what are the etiologies of pulmonary emboli

A

venous statis
vessel injury (trauma, surgery)
history of prior embolus/thrombus

74
Q

what is venous statis

A

etiology of PE
blood that doesnt move much
(bedrest, obesity, HF, central venous cath)

75
Q

what is the patho chain of PE

A

thrombus(clot) formation
dislodgement of thrombus (becomes emboli)
occlusion of part of pulmonary artery
(can go from this point)

76
Q

what are the three different chains after occlusion of pulm artery in pulmonary emboli

A 
.. increase in pulm artery pressure
right ventricular failure
severe shock
sudden death.\
....
resolution of clot resulting in absorbed/dissolved or scar tissue from death of tissue in lung
77
Q

what are the clinical man of PE (7)

A 
depends on severity of PE
breathing is silent (dyspnea)
fever
cough (bloody)
tach
chest pain
hypoxemia
78
Q

what is acute respiratory failure

A

inadequate gas exchange to meet tissue oxidation needs at rest
not an actual disease- its a term used to anything demo decreased gas exchange at rest

79
Q

acute respiratory failure can be applied to any respiratory disorder if it meets what?

A

pO2 less than 50 mmhg (norm >80)

pCO2 more than 50 mmhg (norm 35-45)

80
Q

what are the clinical manifestations of acute respiratory failure

A

depends on specific etiology

81
Q

acute heart failure leading to pulmonary edema (flash)

A

accumulation of fluid in the pulmonary interstitial sapce and INTO alveoli

82
Q

what are the etiologies of acute HF leading to plash pulm edema (4)

A

left v. heart failure (most common)
mitral stenosis- fluid backs up in pulm inter space
alveolar-cap damage
volume overload

83
Q

what is the path chain for acute HF leading to plash pulm edema

A 
increase in pulm cap hydrostatis pressure
fluid into pulm interstitial space
fluid into alveoli
dilutes surfactants
atelectasis
84
Q

what are the clinical manifestations of acute HF leading to flash pulm edema (7)

A 
dsypnea sob- 
orthopnea
paroxymal noturnal dyspnea
crackles
rhonchi
hemoptysis
hypoxia
85
Q

what is orthopnea

A

sob/dyspnea that occurs when laying flat

86
Q

what is paroxysmal noturnal dyspnea

A

sob attack when asleep

a sensation athat wakes a person up

87
Q

what is hemoptysis

A

pink frothy sputum

88
Q

tuberculosis

A

infection caused by mycobacterium tuberculosis bac

89
Q

what is the patho chain of TB

A 
tb transmitted via airborne droplets
inhailed into lung and tb X's
inflammation (neurtophils/macrophages)
tubercle lesion
necrosis of infected tissue
either becomes dormant or active tb
90
Q

what are the clinical manifestations of TB

A 
fatigue
weight loss
night sweats
low grade fever
cough (non productive at first, tons (purulent) later (late sign)
91
Q

how do you diagnos TB

A

TB skin test
if positive
must have all: +skin test, +sputum culture, + CXR

92
Q

who get neg TB skin tests

A

those never exposed and those who were exposed but not infected

93
Q

who gets positive TB skin tests

A

active TB

dormant Tb

94
Q

what is COPT

A

obstruction of air flow— difficult expiration

95
Q

chronic broncitis

A

hypersecretion of muccus and chronic cough (3 mo during winter at least 2 consec. years

96
Q

what is the etiology of chronic bronchitis

A

chronic inhailed irritation

cigs, air pollution and infections

97
Q

what is the patho chain of chronic bronchitis

A 
irritants
increase in thick mucus in lungs
decrease in cillary function
decrease of mucus clearance
increase in infection risk
inflamed and THICK bronchial walls
airway obstruction (esp on expiration)
98
Q

what are the two major things with chronic bronchitis

A

mucus build up

thickened bronchial walls

99
Q

what kind of pts are usually chronic bronchitis

A

chubby pts

100
Q

what are the clinical manifestations of chronic bronchitis (7)

A 
wheezing
dyspnea
productive cough (tons of muccus)
decreased exercise tolerance
repeated resp infection (yellow green, rusty)
hypoxia with resp acidosis
cyanosis
101
Q

emphysema

A

destruction of alveolar walls - loss of elastic recoil

obstruction is from changes in lung tissue rather than muccus production and inflam

102
Q

what are the etiologies of emphysema

A

cig smoking

alpha antitrypsis deficincy- prevents lung tissue from breaking down

103
Q

what is the patho chain of emphysema

A 
irritants
alveolar destruction
increase air in alveoli (air trapping)
collapse of small airways
decrease alveolar diffusing surface area
decrease gas exchange (o2 and co2)
104
Q

what kind of pt are those with emphysema

A

thin pts

105
Q

what are the clinical manifestations of emphysema

A 
dyspnea on exp
hypoxia with resp acidosis
cyanosis
no cough- little sputum
increased anterior-posterior lateral diameter(barrel chest)
freqquent resp infections
106
Q

pursed lip breathing with what

A

emphysema

107
Q

chronic b and emph

A

occure together a lot cuz of cigs

108
Q

which two chronic resp issues contribute to COPD

A

chronic bronchitis

and emphysemia

Patho: Nursing (4 decks)

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