w6 histology Flashcards

1
Q

where does the elastin lie

A

lamina propria

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2
Q

PT presents with crushing’s like symptoms from ectopic ACTH secrection. Where is the likely source?

A

Tumor can cause crushing’s like symptoms, ACTH secrection in the respiratory epithelium

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3
Q

there is a mutation in the serous secretions of the submucousal glands. What layer is most likely disturbed?

if the patient was not able to create glycoproteins what layer would be distrubed

A

Sol layer

gel layer

  • Gel layer: Mucous layer derived from goblet cells and mucous portion of submucosal glands; Viscous, lubricating properties due to mucins(hydrophilic glycoproteins that are hydrated to form mucus)
  • Sol layer: Watery, periciliarylayer derived from serous portion of submucosalglands
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4
Q

a male patient presents to the infertility clinic with infertility issues and has a long history of chronic respiratory infections. what is likely the source of his problem?

A

Primary ciliary dyskinesia (or Immotile Cilia Syndrome) from a dyein mutation

if the patient also presented with: (1) dextrocardia with or without situsinversus, (2) chronic sinusitis, and (3) bronchiectasis = •Kartagener’ssyndrome:

situs invertus is only some times because the beating of the cillia determines the orientation in embryology

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5
Q

compare and contrast COPD from metaplasia

A

metaplasia

Goblet cell hyperplasia increased cell number; increased mucous secretions protect surface from physical stress & mucosal irritants

Basal cell hyperplasia indicates stem cell proliferation and differentiation to replace cells that are damaged

Squamous cell metaplasia offers better protection against increased airflow that may be associated with “smoker’s cough”, bronchiectasis

COPD

hypertrophy of glands in trachea and bronchi

goblet cell hyperplasia extending into small bronhioles

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6
Q

where are the stem cells within the lung

A

basal cells

type II pneumocytes (can diff into type 1 so more plastic)

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7
Q

patient presents with edema contained to the superficial lamina propria, what is this called?

A

a Cyst or Reinke’s edema

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8
Q

what area of the submucousa is subject to changes with age

A

the hyaline cartilage in the anterior and lateral edges can essify with age

Posterior wall contains trachealissmooth muscle, fibroelastic ligamentconnecting ends of rings

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9
Q

what is the smooth muscle called in the trachea and in the bronchus

A

trachealis and muscularis

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10
Q

is this an extrapulmonary or intrapulmonary artery and how do you know

A

extrapulmonary because it has complete rings of cartilage while intrapulmonary cartilage has discontinous rings

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11
Q

a baby is born with a lung that is not working, what is likely the problem

A

Congenital neonatal emphysema

Congenital absence of bronchial cartilage formation

air can enter but cannot exit

cartilage rings help prevent collapsing of bronchi during exhalation

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12
Q

differentiate between restrictive and obstructive lung diseases

A

obstructive–> cant get air out (dysnea and wheezing)

restrictive–> cant get air in

Restrictive lung diseases decrease the lung volume and the compliance

Obstructive lung diseases increase the lung volume and the compliance

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13
Q

patient presents with signs of COPD how can we quickly estimate the pathology

A

Reid Index to analyze the gland hypertrophy

Ratio of seromucous gland acini to wall from epithelial basement membrane to inner surface the cartilage (A/B);normal value is 0.4; measurements of > 0.55 seen in many patients with chronic bronchitis

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14
Q

what conditions present with wheezing

A

Asthma, emphysema, and chronic bronchitis (COPD)

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15
Q

where do goblet cells stop

A

brionchiole, none in terminal bronchiole

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16
Q

what is the source of problems in asthma

A

bronchioles

Parasympatheticstimulation of muscarinic receptors causes bronchiolar smooth muscle contraction and stimulates submucosal gland secretion

Sympatheticstimulation of β-2 receptors causes bronchiolar smooth muscle relaxation(e.g., during exercise)

17
Q

patient presents with pneumonia, what was the likely source through which this spread

A

pores of kohn

These openings serve to equalize pressure and increase collateral ventilation of air. If obstructive disease blocks normal airflow to distal regions, undamaged alveoli aerated by the blockage airway can still communicate, to a limited extent, with the airways of an adjacent lobule or acinus.

A disadvantage is that these small openings can also serve as avenues of dissemination of infections.

18
Q

what does an oxygen molecule have to diffuse through to get to the blood vessel

A

Type 1 pneumocyte (occluden junctions- tight junctions), BM (type 4 collagen) and endothelial

19
Q

what occurs in pulmonary edema

A

Increase in capillary, hydrostatic pressure or inflammation increases fluid exiting capillaries, exceeds lymphatic drainage capacity tight junctions between pneumocytes initially confine fluid to interstitium, if not resolved fluid eventually seeps into alveolar lumen

20
Q

what makes up the interalvelar septa

A

Contained within thick segment connective tissue are reticular fibers (type III collagen) that supports the connective tissue and elastic fibers prividing recoil properties to the interalvelarsepta.

21
Q

differentiate Centriacinar Emphysema and Panacinar Emphysema

A

Centriacinar Emphysema is usually confined to an area and is the result of smoking wherare panacinar is usually entire area arising from a1 antitrypsin deficiency. Both have excess elastase degredation

22
Q

what is an acini

A

portions of lung consisting of a terminal bronchiole and the respiratory airways it aerates.

23
Q

outline what happens in emphysema

A

macrophages –> neurophils –> elastase –> overwhelms the protective effect of a1 antitrypsin and neutralize the basal cells

LOSS OF RECOIL

ØIrreversible distention of respiratory airways (i.e., loss of recoil, elasticity, elastance)

24
Q

what cells produce surfactant

how do you measure it in amnotic fluid

what is the pathogenesis of neonatal respiratory distress syndrome

A

type II cells and club cells non-ciliated bronchiolar cells

type II cells –> Dipalmitoylphosphotidylcholineaccounts for almost all surface-tension reducing properties of surfactant

a phosphotidylcholine: sphingomyelin ratio lower than 2:1 and the absenceof phosphatidyl glycerol = not developed

•Pathogenesis: lack of surfactant production by type II pneumocytes→ increased surface tension→ collapse of smaller alveoli and dilation of alveolar ducts and respiratory bronchioles → stretch damages the epithelium and vasculature→ deposition of intraluminal fibrin and platelet aggregation (eosinophilic staining = “hyaline membrane”)

25
Q

you detect high CC16 what is it an indicator of

A

Damaged terminal bronchioles

CC16 is a Clara cell protein of 16 kilodaltons. Damaged terminal bronchioles, and therefore damaged Clara cells, would decrease the concentration of CC16 in bronchial lavage fluid. Conversely, leakage of CC16 across the air-blood barrier would increase CC16 in serum and indicate the integrity of the airway walls are damaged.

26
Q

22-year-old man with a two-year history of cigarette smoking presents to the otolaryngologist after developing a change in his voice. Laryngoscopy shows edema of the true vocal fold (see picture). A biopsy would show edematous fluid has collected in Reinke’s space, which is a thin strip of connective tissue between the stratified squamous epithelium and the vocal ligament. Which of the following best identifies Reinke’s space in the attached photomicrograph of a true vocal cord?

A

B

•True vocal cord: stratified squamous epithelium (protective), Reinke’sspace, elastic cone, skeletal muscle (vocalis)