Pulm Flashcards
1
Q
When are lungs ready
- lecithin/ sphingomyelin ratio
- sphingomyelin
- lecithin
- phosphatidylglycerol
- cortisol
A
- is 2:1
- too much means that nervous system is still myelinating
- is modified surfactant; increases sharply by 30 wks
- break down product of surfactant; increases at 36 wks
- steroids stimulate the production of surfactant by inducing enzymes for surfactant enzymes -> beclomethasone or betamethasone
2
Q
Amniotic Fluid
- function
- maintenance
- cycle-> what is required
- prolonged oligohydraminos: causes; caused by
- polyhydraminos: caused by
A
- lung dev, shock absorber, protection from atmospheric pressure
- by mom until 4 months, after that by baby
- baby swallows amniotic fluid, absorbed by fetal GI tract, excreted by fetal urinary sxs, back into amniotic space; GI integrity and NM integrity
- pulm hypoplasia; caused by baby being unable to urinate
- baby cannot swallow or digest fluid
3
Q
Polyhydraminos caused by
- Riley- Day syndrome
- Werdnig - Hoffman syndrome
- Esophageal atresia
- Duodenal atresia
A
- inherited disorder affecting dev and function of body’s nerves
- AR; spinal atrophy -> degenration of ant horns of spinal cord; symmetrical weakness and wasting of voluntary muscles
- vomit after 1st feeding
- double bubble sign
4
Q
Oligohydraminos caused by
- renal agenesis
- renal obstruction
A
- kidney dont form
- kidneys blocked from secreting urine
5
Q
Oligohydraminos leads to
- potter syndrome
- prune belly syndrome
- drugs to help
A
- born w/o abd musculature, fetus unable to urinate in utero bc unable to to create adequate pressure; self cath
- carbachol and bethanechol -> treat auto neuropathy in early stages by acting at parasympathetics to stimulate muscarinic receptors
6
Q
Diaphragmatic Hernia
- leads to
- development of diaphragm
- premature birth
- ant defect
- sequelae
- dx
- tx
A
- pulm hypoplasia
- ant aspect of abdomen to posterior aspect
- causes posterior hernia (bochtalek defect)
- morgaani defect
- intestines push into thoracic cavity and cause pulm hypoplasia
- fetal US, with bowel sounds in thoracic cavity on auscultation
- surgical repair
7
Q
Muscles of respiration
- normal inhalation
- forced inhalation
- normal expiration
- forced expiration
A
- external and internal intercostals -> rib elevation and diaphragm -> descends to increase thoracic cavity size
- sternocleidomastoid -> sternum elevation, scalenes -> upper rib elevation, pec minor -> elevated 3rd - 5th rib
- passive
- internal intercostals -> push ribs down, abdominal -> pull ribs down, compresses abd contst to push diaphragm up, quad lumborum -> pull last rib down
8
Q
Muscles of respiration
- normal inhalation
- forced inhalation
- normal expiration
- forced expiration
A
- external and internal intercostals -> rib elevation and diaphragm -> descends to increase thoracic cavity size
- sternocleidomastoid -> sternum elevation, scalenes -> upper rib elevation, pec minor -> elevated 3rd - 5th rib
- passive
- internal intercostals -> push ribs down, abdominal -> pull ribs down, compresses abd contents to push diaphragm up, quad lumborum -> pull last rib down
9
Q
Pulm Circulation
- how does it work
- also called
- blood flow
- kind of system
A
- from right ventricle, to lungs, into left atria
- right sided circulation
- same rate as in systemic system
- low pressure, low O2
10
Q
Pleural borders
- midclavicular
- mid axillary
- paravertebral
A
- Both: 7th rib
- R: Upper border 10, L: lower border of 10
- both: 12th rib
11
Q
Tracheobronchial tree
- trachea divides into
- difference in sides
- diff in lobes
- cartilage
- SM
A
- 2 mainstem bronchi at carina
- right is shorter, wider and more vertical
- right has 3, left has 2
- trachea has c chaped cartilage rings and become o shaped in bronchioles
- In bronchi
12
Q
Tracheobronchial tree
- trachea divides into
- difference in sides
- diff in lobes
- cartilage
- SM
- narrowings
A
- 2 mainstem bronchi at carina
- right is shorter, wider and more vertical
- right has 3, left has 2
- trachea has c chaped cartilage rings and become o shaped in bronchioles
- In bronchi
- 1st -> glottis, 2nd -> midway down bc of compression by aortic arch, 3rd -> carina
13
Q
Cell types in lungs
- trachea
- bronchi
- bronchioles
- resp bronchioles
- alveolar ducts
- alveolar sacs
A
- cilia, SM, and cartilage
- cilia, SM, some cartilage
cilia, SM, no cartilage - some cilia, some SM
- some SM
- some SM
14
Q
Airway
- upper
- lower
A
- lips to glottis
- glottis to alveoli
15
Q
Airway
- upper
- lower
- 10-15 um
- 2.5-10 um
- activated macophages
- penumoconioses
- pt is upright
- pt is supine
- lying on right side
- lying on left side
A
- lips to glottis
- glottis to alveoli
- trapped in upper tract
- enters trachea and bronchi, cleared by mucociliary elevator
- activated by dust particles -> will release cytokines and induce inflammation to injure alveoli
- platelet derived growth growth factor and IGF released causing fibroblast proliferation and formation of collagen fibrosis w/ recurring injury
- will aspirate to RLL,
- posterior segment of RUL or apical segment of RLL,
- middle segment of RLL or posterior segment of RUL
- will go to lingula
16
Q
Epi of resp tract
- nose, paranasal sinuses, nasopharynx, larynx and bronchi
- bronchioles
- terminal bronchioles
- resp bronchioles
- alveoli
- other layer
- specific on cilia
A
- psudostratified ciliated columnar epi
- ciliated columnar
- columnar OR cuboidal, ciliated -> transition
- ciliated cuboidal
- simple squamous
- mucus
- only beat towards pharynx
17
Q
Pneumocytes
- types 1: function
- type 2: function
- lamellar bodies
- what happens w/o surfactant
- goblet cell function
A
- gas exchange
- produce surfactant -> can become type 1 with damage
- look like stack of coins, contain surfactant
- atelectasis -> alevolar collapse
- produce mucus
18
Q
Pneumocytes
- types 1: function
- type 2: function
- lamellar bodies
- what happens w/o surfactant
- goblet cell function
A
- gas exchange
- produce surfactant -> can become type 1 with damage
- look like stack of coins, contain surfactant
- atelectasis -> alevolar collapse
19
Q
Other cells
- goblet
- club
A
- produce mucus
- Clara cells, produce GAGs -> protect bronchial lining and conjugate IgA
20
Q
Other cells
- goblet
- club
A
- produce mucus
- Clara cells, produce GAGs -> protect bronchial lining and conjugate IgA to activate them
21
Q
Other cells
- goblet
- club
- SM: location, leads to
A
- produce mucus
- Clara cells, produce GAGs -> protect bronchial lining and conjugate IgA to activate them
- most prominent in medium sized bronchioles, constriction causes asthma attacks
22
Q
Lung volumes
- anatomical dead space
- total ventilation
- tidal vol
- inspiratory reserve
- expiratory reserve
- vital capacity
- residual volume
- functional residual capacity
A
- areas that cannot exchange O2
- vol dead space + volume of alveoli
- normal breathing
- max amount can inhale
- max amount you can exhale
- max inhale to max exhlae
- amount of air that cannot be expired and just remains in lungs
- expiratory reserve vol + residual vol
23
Q
What happens at high altitude?
A
- concentration of )2 is lower so cannot get in enough O2 creating a chronic resp alkalosis
24
Q
Diffusion of O2 across alveolar wall
A
- pulm surfactant -> alveolar epi -> alveolar insterstium -> capillary endothelium -> plasma -> RBC -> Hemoglobin
25
Q
What happens during exercies
- HR
- CO
- respiration
- partial pressures
- venous blood
- pH of venous blood
A
- increase
- increases
- increase
- unaffected
- exercising muscles extract more O2 -> so venous blood has less O2
- oH f venous blood is more acidic bc of increased CO2
26
Q
Ventilation
- minute
- alveolar
- hypoxemia
A
- amount air entering in 1 min; tidal vol * RR
- amount of air participating in gas exchange in 1 min; (tidal vol- deade space) * RR
27
Q
Hypoxemia
- CNS response
- Pulm vasc response
- Systemic vasc response
A
- peripheral arterial chemoreceptors send neural imuplses to CNS resp centers -> increase RR to blow off CO2
- pulm vasc will vasoconstrict in areas that are low with O2 and send blood to places with higher amount of O2
- vasodilate to get more blood to area and increase O2 in area
28
Q
Alveolar diffusion
- how long is gas exchange
- perfusion limited
- diffusion limited
A
- 2.5 seconds
- rate at which gas is transported away from alveoli is limited by rate of blood flow
- gas exchange is limited by diffusion process; no O2 at alveoli or hard to get O2 across alveoli into blood
29
Q
V/Q ratio
- what is it
- ideal
- normal
- 4 causes of hypoxemia
A
- ventilation/ perfusion
- 0.95
- .80 - 1.2
- alveolar hypoventilation (not breathing) , ventilation perfusion mismatch (PE), diffusion impairment (preventing O2 from diffusin across alveolar membrane), right to left shunt
30
Q
Comparison between airway pressure and atmospheri pressure
- inspiration
- at end of deep breath
- expiration
- At functional capactiy
A
- Patm»Pa; bc airway pressure is neg
- Patm= Pa; no net movement of air
- Patm<
31
Q
Zones of ventialtion- perfusion
- zone 1
- zone 2
- zone 3
A
- apex; pressure from alveoli> pressure in artery –> ventilation is greater than perfusion
- hilum; pressure from artery> pressure from alveoli–> majority of gas echange occurs
- base; pressure artery> pressure from vein > pressure from alveoli –> better perfusion than ventilation -> this is where inflammation occurs bc of the perfusion
32
Q
O2 dissociation curve
- oxometer
- normal measurement
- right shift: what causes it, what happens
- left shift
A
- measure PaO2 w/o having to get blood gas
- pa O2 of 60 = oximeter at 90%
- caused by increase in temp (increased metabolism), acidity (increased metabolism -> lactic acidosis) or 2-3 BPG; increased offloading of O2/ decreased affinity of hemoglobin for O2; oximeter will now need to be above 85 to be at 60 paO2
- caused by decrease in temp, acidity or 2-3 BPG; decreased offloading O2; increased affinity for hemoglobin; oximeter needs to be at 95 in order to be at PaO2 of 60
33
Q
A- a gradient
- what is it
- equation
- normal
- how is it determined
A
- diff between p)2 in alveoli vs artery
- PA O2 - PaO2
- not exceed 10-15
- arterial PO2 is calculated via arterial blood gas; alveoli P O@ calculated via 150- (PaCO2/.8)
34
Q
Cerebral blood flow regulator
- hypercapnia
- severe hypoxemia
A
- see vasodilation of cerebral vasc
- pO2 has to be lower than 50 to affect cerebral blood flow
35
Q
Neuro Control of respiration
- aortic body: location, function, how
- carotid body: location, function, how
- low O2: what level does it have to be at
- pons: what does it do, what centers are in charge
- medulla: what does it do, innervation, blood supply
A
- arch of aorta, measure pCO2 and pO2, transmits through vagus to brain stem
- bifurcation of internal and external carotid, measure pO2, pCP2, H+, transmits through glosspharygeal n to brainstem
- if arterial pO2 is less than 60 will activate peripheral chemoreceptors which activated medulla and ventriallation is increased; no affect on central chemoreceptors
- responds to environment -> and modifies medulla w/ apneusti center (detects hypoxia and stimulates inspiration) and pneumotactic center (detects hypercapnia and stimulate exhalation)
- responsible for breathing, CN 9, 10, 11, 12; anterior spinal, PICA, and vertebral
