Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/92

Click to flip

92 Cards in this Set

  • Front
  • Back
what is the only muscle the abducts (opens) the vocal cords?
posterior cricoarytenoid
what nerve innervates the larynx
recurrent laryngeal n
cricothyroid innervated by
supoerior laryngeal n.
which cartilidge in the larynx is the only fully circular one?
cricoid
where would you cut for choking victm
cricoid cartilidge
the recurrent laryngeal n loops under what structure on L and R
L-aorta
R-subclavian
what type of cartilage is in epiglottis
elasic
epithelium of true vocal folds is
stratified squamous nonkeratizined
what is the difference between the take off of L adn R primary bronchi
L is longer
primary-
secondary-
tertiary-
lung
lobe
segment
carina is
bifurcation of trachea - if enlarged --> cancer staging
cartilage ends with
bronchioles
goblet cells
produce mucous
brush cells
sensory receptors (cough reflex)
topography:
Angle of Lewis
Horizontal fissure
pleural space
T4/5
4th/5th ICS
8-10ICS
relationship of L R pul a to bronchi
L over
R in front
# of lobes on L?R?
L-8 R-10
at what level does cartilage dissapear
bronchioles
epithelium of false vc
PSCC
epithelium of true vc
stratified squamous non-ker
alveolar pores of Kohn do
help with reexpansion and collateral ventilation
major difference between L/R hila
L-pul a in front
R-pul a on top
where does lower left lobe drain
right superior tracheobronchial nodes
what are the 5 stages of lung development
embyronic
pseudoglandular
cannalicular
saccular
alveolar
embryonic
4-5 weeks
formation of lung bud
congenital abnormalities associated with embryonic period
esophageal atresea, fistulas --> polyhydramnios
Shh and Gli2/Gli3
for lung formation in embryonic period
Nkx2.1
for branching in embryonic period
pseudoglandular
5-17 weeks (branching)
steps of the mesenchymal-epithelial interactions
1)epithelial cell proliferation and elongatoin FGF-10 indcuces BMP4 and epithelial cells grow
2) tips stop (Shh BMP4, TGF-b block FGF10)
3) branching new foci of FGF10 at edges allows branching
congenital abnormality associated with pseudoglandular phase
congential cystic adenomatoid malformation (variable cysts in branchign)
when does the diaphram develop
4-12 weeks
congenital abn associated with deve of diaphram
congenital diaphragmatic hernia
what happens in cannalicular phase?
acinar formation, epithelial cell differenceiation, dev of capillary bed, thinning of mesenchyme
16-26
type 2 cells form
saccular phase
24-36 weeks
alveolar phase
32-postnatal
secondary septation
capillary remodeling
role of glucocorticoids in embryology
decrease fibroblast proliferation and condense septal intersititum
ENHANCE SURFACTANT SYNTHESIS
Hyaline membrane disease
ground-glass appearance
tachypnea, retraction, nasal flaring, grunting, cyanosis
born 24-26 weeks (end of cannalciluar phase)
what is the composition of surfactant
80% phospholipid DPPC
8% neutral lipids
12% protein
Fick's law
V=(A/T) Dg (pA-pB)
limits to diffusion effect o2 or co2 more
o2 more
perfusion limits o2 or co2 more
o2 and co2
ventilation limits o2 or co2 more
co2
alveolar ventilation eq
VA=K*Vco2/pAco2
(pAco2 usually used interchangeably with paco2)
how will excercise and anemia affect calculated diffusing capacity in CO test
exercise makes high and anemia makes low (increased flow and decreased RBCs)
what causes a right shift in Hb saturation curve, what are the axis, and what happens to O2 affinity and P50
decreased O2 affinity
increased p50
%hb sat. v. pO2
dec pH
inc CO2
inc temp
inc 2,3 DPG
how to calculate o2 content
[Hb] * 1.34 * % sat + (0.003ml/dl/mmHg* pO2)
carboxyHb is
Hb with CO
respiratory acidosis (acute and compen)
inc pCO2 (above 40) low pH
inc pCO2 (above 40) compensated pH
Henderson-Hasselbach eq
pH=6.1 + log [HCO3]/(0.03*pCO2)
when A-a pO2 difference is > than --> abn
20mmHg
high V/Q
top part of lungs
interferes most with CO2
acts like dead space
low V/Q
bottom of lungs
interferes most with O2
acts like shunt
effect of shunt on pO2
major drop bc the new oxygen content/O2 capacity --> percent saturation that --> low pO2
calculations with blood mixtures use
O2 content
calculations with diffusions use
partial pressure
alveolar gas equation
pAO2=FO2(pB-pH2O)-(PaCO2/R)
percent shunt =
(CiO2-CaO2)/(CiO2-CvO2)
CiO2 is using alveolar pO2
physiological dead space eq:
Vd/Vt=(pACO2-pECO2)/pACO2
effects of cut below upper third of pons through vagus?
long inspiratory spasms with brief expiratroy efforts (apneusis)
cut blocks an inhibitory influence on inspiration
effects of cut below the pons
unstable rhythm that can give way to gasping with long expiratory pauses and brief inspirations
PONS important in STABILZATION AND COORDINATION
inspiratory neurons located
rostral area of medulla
expiratory neurons located
caudal area of medulla
restrictions --> breathing pattern
shallow, frequent
obstructions --> breathing patterns
slow, deep
Hering Breuer reflex
senses
travels in
senses stretch (extent and changes (some adapt, some dont)
runs in vagus
limits respiratory excursion to safe size
cut --> deeper, slower
Irrants -> breathing reflex
travels in
vagus
cough, broncho-constriction, mucus secretion, fast shallow breathing
juxta-capillary receptors
travel in
vagus
stimulated by certain substances
--> slow or stoped breathing followed by fast and shallow breathing
play role in dyspnea
how can 100% O2 --> apnea
barbiturate poisoning or hypercapnia where O2 drive is only thing keeping respiration going
which more potent central or peripheral
central
central respond to
CO2
peripheral respond to
most, especially O2
carotid receptors
signal in CN IX and vagus
response time shorter than central
key role to check O2
respond to nicotine
barbiturates and opiates depress breathing through
central
central
sense CSF, CO2
slow
adapts
cheyne stokes
mild hypoxia --> deep breathes with intermittent pause
high altitudes sleep/kidney failure
biot's breathing
more abrupt cheyne-stoeks, with brain damage, high CSF pressure
Kussmaul
metabolic acidosis with for ex, diabetes mellitus
PAO2 (alveolar gas eq) relatd to PACO2
PAO2 - PIO2 - PACO2/R
high altitidue shift Hb curve?
right bc of increased 23DPG
p increase _ per 10m
1 atm
hypoxic hypoxia
low pO2 of arterial blood
anemic hypoxia
low pO2 bc of decreased Hb
stagnant hypoxia
low pO2 bc of reduced blood flow
histotoxic hypoxia
cells cant make use of normal O2
type II cells form in which phase
canalicular
alveoli first appear in which stage
saccular
functional type 1 and 2 in
saccular
what gene upregulates elastin, myofibroblast differentiation, and secondary septum formation in alveolar phase
PDGF-A
Bronchopulmonary dysplasia
A disease of <1000g, 24-26 wk infants
results from inflammation and scarring of the lung
often bc preme or mechanical ventilation
how does ERV IRV change from standing to supine?
ERV goes down, IRV goes up
how does FRC and VC change with restrictve? obstructive?
r:both decrease
o: FRC up, VC down