pulmonary anatomy + physiology Flashcards

1
Q

most common type of tracheoesophageal anomaly

A

esophageal atresia with distal tracheoesophageal fistula

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2
Q

“gastric bubble” on CXR

NG tube stuck in blind pouch of esophagus

A

esophageal atresia with distal tracheoesophageal fistula

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3
Q

ciliated columnar epithelium

A

trachea

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4
Q

tracheal epithelium of smokers

A

metaplasia: columnar cells → squamous epithelium (no cilia - can’t mobilize sputum - get chronic bronchititis)
opposite of distal esophagus metaplasia in BE: squamous → columnar with goblet cells

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5
Q
nonfunctional cilia in:
respiratory tract
sinuses
eustachian tubes
fallopian tubes
flagella of sperm
chronic infections
infertility 
hearing loss
A

Kartagener syndrome: primary ciliary dyskinesia

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6
Q

defective dynein arm (need for moving along microtubule)→ nonfunctional cilia

A

Kartagener syndrome: primary ciliary dyskinesia

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7
Q

associated with situs inversus reversal of circulatory system + viscera (50%)

A

Kartagener syndrome: primary ciliary dyskinesia

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8
Q

divides thorax from abdominal cavity

A

diaphragm

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9
Q

4 embryological structures that form the diaphgragm

A

septum transversum
pleuroperitoneal membranes
dorsal mesentary of esophagus
abdominal wall

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10
Q

congenital defect in pleuroperitoneal membrane → abdominal contents in pleural cavity → lung hypoplasia
usually occur on left side
associated with polyhydramnios

A

congenital diaphragmatic hernia

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11
Q

flattened abdomen
cyanosis
inability to breath

A

congenital diaphragmatic hernia

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12
Q

innervated by phrenic nerve (C3 C4 C5)

A

diaphragm

C3 C4 C5 keeps diaphragm alive

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13
Q

neck or shoulder pain can suggest

A

irritated diaphragm (affecting phrenic nerves): referred pain due to:
gallbladder disease
splenic rupture

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14
Q

structures that perforate the diaphgragm:
T8
T10
T12

A

I 8 10 EGGS AAT 12
T8: IVC
T10: esophagus, vagus
T12: aorta, azygous vein, thoracic duct

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15
Q

cells that line alveoli

responsible for gas exchange

A

pneumocytes

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16
Q

simple squamous epithelial cells
>97% alveolar surface
GAS EXCHANGE
susceptible to toxic insults (can’t replicate)

A

type I pneumocyte

17
Q

larger
cuboidal
located at alvelar septal junction
cover 3% alveolar surface
secrete SURFACTANT: dipalmitoyl phosphatidylcholine
REPLICATE after lung damage: precursor to type I and type II cells

A

type II pneumocyte

18
Q

↓ alveolar surface tension → more compliant (stay open)→ prevent atelectasis (alveolar collapse)

A

surfactant

19
Q

sample of amniotic fluid of premature baby

lecithin:sphingomyelin ratio >2.0 suggests

A

fetal lung maturity (type II pneumocytes are making enough surfactant)

20
Q

to enhance fetal lung maturity, give mom

A

corticosteroids: matures type II pneumocytes

21
Q

DOC for altitude sickness

A

acetazolamide

22
Q

rapid ascent to high altitude
begins few hours to 2 days after ascent
headache
fatigue
acute cerebral edema due to hypoxia-induced vasodDILATION
acute pulmonary edema: hypoxia causes vasoCONSTRICTION (↑ cap pressure → transudate of fluid into lungs)

A

acute mountain sickness

23
Q

visual black out occurs at what + G force

A

4-6 G
force pulling blood into abdomen + legs
insufficient blood return to heart
insufficient pumping of blood to brain

24
Q

G force achieved during spacecraft liftoff

A

8-9 G

need to be in semi reclined position on take-off

25
Q

occurs when diver breathing compressed air for hour at 120 feet (extreme depths for too long)
nitrogen dissolves into neural membrane →↓ neuronal excitability → diver becomes jovial/careless → drowsy →
loss of strength + coordination

A

nitrogen narcosis (not decompression sickness)

26
Q

at depth: high pressure → nitrogen gas dissolves into blood

surfacing: ↓ pressure → nitrogen escapes solution → formation of bubbles that can occlude vessels

A

decompression sickness (bends or Caisson Disease)

27
Q

joint/muscle pain in arms + legs
neuro sx: dizzy, paralysis, syncope
“the chokes”: air bubbles occlude lung capillaries → SOB, pulmonary edema, death

A

decompression sickness

28
Q

prevention of decompression sickness

A

surface slowly

allow nitrogen to be eliminated through lungs by expiration

29
Q

treatment of decompression sickness

A

hyperbaric O2 therapy (high pressure room):

convert nitrogen from gaseous state to dissolved state so it can be exhaled by lungs

30
Q

use of hyperbaric O2 therapy

A

decompression sickness
arterial gas emboli
CO monoxide poisoning
gas gangrene due to clostridium perfringens (anerobe) or osteomyelitis: increase O2 to part of area