Severson: Normal and Abnormal Respiratory System Flashcards

1
Q

Where does the laryngotracheal groove and diverticulum develop?

A

The Laryngotracheal groove develops from the VENTRAL WALL of the PRIMITIVE PHARYNX (caudal to the 4th pair of pharyngeal pouches).

It DEEPENS to form the RESPIRATORY DIVERTICULUM.

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2
Q

What germ layer contributes to the epithelial lining and glands of the larynx?

A

ENDODERM

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3
Q

What germ layer contributes to the supporting wall (CT, cartilage and smooth muscle)?

A

Splanchnic mesenchyme of the forgegut

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4
Q

What is the purpose of the tracheoesophageal folds and septum?

A

They divide the cranial part of the foregut into a LARYNGOTRACHEAL TUBE.(primordium of the larynx, trachea, bronchi and lungs) and a DORSAL PORTION (primordium of the oropharynx and esophagus).

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5
Q

What branchial arch cartilages contribute to the laryngeal cartilages?

A

4th and 6th pharyngeal arches

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6
Q

What cells form the cartilagenous tissue?

A

MESENCHYME from neural crest cells

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7
Q

What branchial arches give rise to the laryngeal muscles?

A

MYOBLASTS from the 4th and 6th pharyngeal arches

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8
Q

What nerves innervate the laryngeal muscles?

A

vagus nerve

superior laryngeal and the recurrent laryngeal

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9
Q

What germ layers contribute to the laryngotracheal tube?

A

Endoderm

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10
Q

What germ layer gives rise to the trachebronchial glands?

A

ingrowth of surface epithelium of ENDODERMAL ORIGIN

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11
Q

What germ layer gives rise to the supporting walls?

A

Cartilage, CT and muscles are derived from SPLANCHNIC MESODERM

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12
Q

What tissue forms the visceral and parietal pleura?

A

visceral- spanchnic mesoderm

parietal- somatic mesoderm

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13
Q

What developmental defect has occurred when a tracheoesophageal fistula is present?

A

An abnormal communication between the TRACHEA and the ESOPHAGUS

*most common anomaly of the lower RT

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14
Q

What is esophageal atresia?

What is it associated with?

A

An abnormal partitioning of hte TRACHEOESOPHAGEAL SEPTUM producing an abnormal communication between the trachea and the esophagus.

fistula

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15
Q

When would gastric secretions possible cause pneumonitis?

A

When food or gastric contents enter lungs>

pneumonitis

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16
Q

When would lipid pneumonia occur?

A

?

17
Q

When and why does polyhyraminos occur?

A

Amniotic fluid accumulates (polyhydramnios) because amniotic fluid cannot pass to the stomach and intestines for absorption and subsequent transfer via the placenta to the mother’s blood.

18
Q

How do the bronchi and lungs develop?

A

Laryngotracheal groove —> respiratory diverticulum —> tracheal bud —>
primary bronchial buds —> secondary bronchial buds —> segmental branches

19
Q

What is the usual cause of lung hypoplasia?

A

Usually associated with congenital diaphragmatic hernia.

20
Q

How many oligohydraminos cause lung hypoplasia?

A

Oligohydramnios= an insufficient amount of amniotic fluid

Causes pulmonary hypoplasia by allowing the uterine wall to compress the fetal thorax.

21
Q

Why does renal agenesis contribute to oligohydraminos?

A

Bilateral renal agenesis causes oligohydramnios because lack of urine production reduces the amount of amniotic fluid.

22
Q

What is potter’s syndrome?

A

Pulmonary hypoplasia and bilateral renal agenesis.

23
Q

At what week of development are type I and II alveolar cells evident in the developing lung?

A

26 weeks

24
Q

What is the earliest developmental period that respiration is possible?

A

16-26 weeks

Respiration is possible because of developing alveoli

25
Q

What are type I alveolar cells?

A

Squamous epithelium of endodermal origin

Pneumocytes

26
Q

What cells produce surfactant?

A

Type II alveolar cells

At about 20 weeks but doesn’t become sufficient until 26-28 weeks and continues to increase towards the end of preganancy.

27
Q

What is surfactant?

A

Surfactant serves to lower surface tension at the air-alveolar interface.

Maternal glucocorticoid (β-methasone) treatment during pregnancy accelerates fetal lung development and surfactant production.

28
Q

How is the amniotic fluid removed from the lung at birth?

A

Removal of fluid occurs :

(1) through the mouth and nose by pressure on the thorax during delivery
(2) into the pulmonary capillaries, and
(3) into the lymphatics.

Aeration at birth is the rapid replacement of intra-alveolar fluid by air. The lung fluid is derived from amniotic fluid, the lung tissue itself, and from secretions by the tracheal and bronchial glands.

29
Q

What is responsible for the occurrence of respiratory distress syndrome (hyaline membrane disease)?

A

Caused by a deficiency of surfactant

30
Q

Why is there a protein rich fibrin rich exudate in the alveolar space?

A

Injury to the alveolar wall results in a protein-rich, fibrin-rich exudation derived from the injured pulmonary epithelium and circulating blood substance.

31
Q

Who is likely to develop respiratory distress syndrome?

A

Respiratory distress syndrome accounts for 20% of all infant deaths in the newborn period.

32
Q

What morphological features of the lung accounts for death in newborns w/ respiratory distress syndrome?

A

Protein rich, fibrin rich esxudate is located in the alveolar spaces and forms a hyaline membrane (result is respiratory distress syndrome).

33
Q

How do the lungs of a stillborn and live infant differ?

A

Newborn lungs: contain air and float in water.

Stillborn infant’s lungs: firm and sink when placed in water because they contain fluid, not air.

34
Q

Why do the lungs of stillborn infants sink in water?

A

They contain fluid NOT air.

35
Q

Where do congenital diaphragmatic hernias usually occur?

A

diaphgram

36
Q

What developmental anomaly is responsible for congenital diaphgragmatic hernias?

A

Failure of the diaphragm to close completely during development