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CCDB > respiratory - histology > Flashcards

respiratory - histology Flashcards

1
Q

most distal part of conducting portion?

A

terminal brochioles

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2
Q

bronchial tree?

A

not the extrapulmonary (not in lungs), or the respiratory portion (gas exchange)

the INTRApulmonary - including bronchiles

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3
Q

respiratory portion - starts where?

A

respiratory bronchioles - alvelos ducts, sac, alveoli

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4
Q

where does gas exchange occur?

A

alveoli

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5
Q

how does gas exchange occur?

A

close assocation betw alveolar spaces and pulm caps

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6
Q

what do mucus gland do in respir system

A

condition air - moisten, warm, clean - that’s why there is so much of it along the resp tract

within mucosa and submucosa
serous and mucosal

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7
Q

hallmark of lamina propria in nasal cavity? SWELL

A

rich vascular plexus - swell bodies

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8
Q

stuffy nose?

A

swelling of lamina propria of nasal mucosa / edema

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9
Q

sense of smell occurs in which region of NASAL cavity? what cells responsible?

A

olfactory region of nasal cavity

Neurons BIPOLAR

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10
Q

What cells can regenerate smell sensation - olfactory perception?

A

basal cells - these are basal stem cells

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11
Q

What do supporting cells do in olfactory system?

A

secrete odorant binding proteins - OBPs that transport odorant chemical to receptors present on plasma membrance of cilia of olfactory vesicles

fucntion like neuroglial cells of CNS - “sustenacular cells”

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12
Q

Olfactory glands? in olfactory mucosa

A

Bowman’s glands - serous secretions dischage to surface of olfactory epitheliaum, where provide solvent for chemical odorants - constant flow of fluid helps to clean and remove odorants allowing continually new odorants to appear

nerve fibers and GLANDS in this area key - in lamina propria

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13
Q

what expect to find in olfactory mucosa?

A

Bowman’s glands and neurons

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14
Q

Respi epith?

A

ciliated psuedostratified columnar w/ goblet cells - if not this then stratified squam (non-keritainzed ?) where direct air is present ?

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15
Q

Chronic sinusitis caused by what subcell structure not functioning?

A

cilia sweeps mucus

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16
Q

phonation shaped by which structure in head and neck? what type of cells cover?

A

vocal folds - control flow of air passing through larynx, vibrate to produce sound - injury or inflmamation to vocal folds may change phonation

Stratified squamous protects because lots of direct air

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17
Q

What structure protects trachae?

A

15 - 20 cartilagenous rings from larynx to sternal angle

c shaped area bridged by smooth muscles

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18
Q

The function of the pulmonary brush cell

A

is obscure. … Many cells throughout the body have developed “microvillous” appendages for various tasks, including sensing fluid flow (through renal distal tubules), absorption, chemosensing, or as a repair process for ciliated epithelial cells after injury.

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19
Q

endocrine function of respiratory cells?

A

small granule cells - secrete seritonen, calcintonen, variety of other things - don’t think people know what they really do

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20
Q

What membrane becomes thicker in smoker’s respiratory system?

A

basement membrane of mucosa

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21
Q

how many segmental bronchi arise from right primary bronchus?

A

10 in right, 8 in left

primary bronchi enter at hilum, split to

3 lobar bronchi on right, 2 on left, (secondary bronchi)

each secondary bronchus supplies one lobe of lung - 5 lobes in total

then divide into tertiary bronchi

18 in total bronchopulmonary segments

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22
Q

bronchopulmonary segments?

A

18 in total

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23
Q

What do Clara cells do?

A

secrete surfactant, and can repopulate respiratory bronchioles following injury

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24
Q

Where do Clara cells first appear in bronchial tree?

A

terminal bronchioles

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25
Q

olfactory epithelium?

A

non-motile cilia - bi polar nerve cells in roof of nasal cavity

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26
Q

Bowman gland?

A

lie in lamina propria beneath elpith. produce water secretion moistening olfactory surface

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27
Q

terminal bronchioles? Clara

A

most distal conduction portion - no gas exchange, two types cells - secretory (CLARA and ciliated -

no cartilage

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28
Q

Trachea?

A

thick basment membrane - pseudostratified ciliated columnar

c shape cartiaged, smooth muscle (trachealis) extends between c tips

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29
Q

REspirataory bronchiles

A

gas exchange can occur here - some alveoli interrupt their walls - simple cuboidal lining w/ Clara and ciliated cells -

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30
Q

asthma?

A

constriction of smooth muscles in bronchioles, makes expiration difficult - mucus settles in, inflammatory cells invade bronchiolar walls

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31
Q

What do alveolar macrophages secrete?

A

ELASTASE

normally a1-antitrypsic, a serum protein w. elastase, proteccts lung

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32
Q

emphysema (hereditary) treated w? lack of ELASTICity is issue - barrel chest

A

recombinant a1-antitrypsin which has antielastase activity

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33
Q

interstitial pulmonary fibrosis?

A

asbestosis - in walls of bronchioles, ducts and alveoli

may turn to mesotheliosma - CANCER

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34
Q

barrel chest?

A

emphasyma - lack of elastiicty - antitrypsin

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35
Q

pregnant? glucocorticoids?

A

stimulate surfactact

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36
Q

surfactant? type 2

A

Pulmonary surfactant is a mixture of lipids and proteins which is secreted by the epithelial type II cells into the alveolar space. Its main function is to reduce the surface tension at the air/liquid interface in the lung.

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37
Q

Bowman’s glands - Bow Wow! - in lamina propria

A

(aka olfactory glands, glands of Bowman) are situated in the olfactory mucosa, beneath the olfactory epithelium, in the lamina propria, a connective tissue also containing fibroblasts, blood vessels, and bundles of fine axons from the olfactory neurons.

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38
Q

NOLTBBT - conducting system

muscles to lining - all reducing in size to get way down to thin membrane for gas exchange

A

nasal, oral, larynx, trachea, bronchi, bronchiloes, terminating bronchioles

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39
Q

respiratory portion? RDSA

A

respiratory bronchioles, alv ducts, sacs, alveoli

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40
Q

kulchitsky cells (peptides) ? basal STEM STEM

A

Trachea - kulchitsky secrete peptides, basal maybe w/ nerves

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41
Q

trachea lamina propria?

A

collagen and elastic

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42
Q

traechilis muscle

A

bridges C shaped cartilage rings -

submucosa has seromucous glands

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43
Q

c shaped cartilage is where in 4 layers -

A

adventitia to muscular - that’s where the traechilis muscle is

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44
Q

respiratory epithelium?

A

ciliated psuedostratified w/ goblet

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45
Q

bronchi has what kind of plates?

A

cartilage plates in ADVENTITIA - and muscular layer prominent CIRCULAR Layers smooth muscle

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46
Q

Bronchioles - Clara

A

clara - nonciliated - surfactn secreting, cell protein P450

Clara cells express high levels of cytochrome P450 monooxygenases (specialized in metabolism of toxins), making them susceptible to toxicant-induced injury and death.

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47
Q

Terminal bronchioles - switch type of lining , Clara

A

ciliated simple cuboidal, reduced circular m

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48
Q

respiratory bronchiles

A

ciliated simple cuboidal, Clara, ALVEOLI open into walls - so some gas exchange

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49
Q

alveolar ducts - muscle knobs

A

simple squamous - collagen, elastic

muscle layer - smooth knobs

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50
Q

Alveoli - type 1, type 2 - no muscles in alveoli

macrophages

pores of KOHN

A

type 1 most common - no mitotic capacity

type 2 - secrete surfactant, stored as lamellar bodies,

MITOTIC,

at junction of Interalveolar spetae and bulge in to air space

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51
Q

What does Hyperplasia type II pneumocytes tell you?

A

alveolar injury and repair

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52
Q

what do alveolar macrophages do? DUST cells

A

migrate around, picking up DUST, bacteria, degraded surfactant

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53
Q

pores of KOHN - pressure, bypasses in disease

A

equalize pressure within alveoli - important role in obstructive lung disease bypassing aerate alveoli distal to blockage

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54
Q

what is surfactant made of?

A

cholesterol 50%, elasticity of lung - LAPLASE law - collapsing force

large alveoli have a low collapse force

small have high collapse force and are difficult to keep open

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55
Q

Blood air barrier - fick’s law

A

surfactant, type 2 pneumotycte basement membrane, capillary

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56
Q

Fick’s law BAB - blood air barrier

A

thicker barrier, less oxygen can pass through

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57
Q

Air flow law - Poiseuille Law? dramatic reduction

air flow RESISTANCE

A

reduced by 2, resistance goes up to 16 - factor of 8

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58
Q

Sympathetic? opens or closes?

A

OPENS - reduces resistance

B2 adrenergic - albuterol, PGE2

parasympathetic stim - closes them down - bronchoconstrictors

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59
Q

Infant respiratory distress syndrome ? RDS

A

deficiency of surfactant - thyroxine and cortisol can help increase production

repeated gasping can further damage alveoloar lining - hyaline membrane disease

60
Q

Emphysema - pink puffers, thin, barrel chest -
increased breathing rate -

2 types

A

widening of air spaces
two types

panacinar emphy (antitrypsin deficiency - enzymes destroy walls of alveoli - air spaces widen distal to terminal bronchilles

cetriaacicnar (SMOking) - alveoli fine, but spaces in respiratory bronchioles are widened

61
Q

Chronic bronchitis - smoking - blue bloater

A

excessive mucus produced, sputum, bronchi inflamed - hypertrophy of mucous glands

62
Q

Asthma - smooth muscle hyperactivity - in bronchi and bronchiloes - increased mucus, edema

A

Eosinophils within bronchila wall - To be Continued - from High yield histo

63
Q

no cartialge in ?

A

bronchioles

64
Q

vagus nerve?

A

decreases lumen - parasympathetic

65
Q

sympathetic - RELAX

A

expand lumen

66
Q

terminal bronchioles

A

simple cuboidal change

67
Q

club cells - CLARA

A

in terminal bronchiol - NO Globlet,

surfactant P450 - enzyme - detoxifies

68
Q

P450 - enzyme - detoxifies

A

when inhaled, this is where this clara’s it - cleans it! has to clean here - before enters respiratory zone

69
Q

vascular system?

WHAT called when doesn’t go cap - arttery - cap venous? or whatever it is supposed to do?

A

blood comes into pulmonary capilaries - where gas exchange is done - carried back to heart - via pulmonary vein

Thru HILEM

70
Q

muscle fibers vs elastic arrangement - concentric vs. longitudinal

A

elastic longitudinal,

smooth concentric

surrounding terminal bronchioles

71
Q

pores of kohn - blockage help

A

connect adjacent alveoli - if blocked - can get around this problem

continuous ventilation

72
Q

bronchi - make up

cartilage platelike - no c shape

A

m concentric,

elastic longitudinal

serous/mucous - submucosa

BALT -

Hyaline cart - no longer in C shape - smaller plates

ONLY in Trachea see C shape

73
Q

BALT - in mucosa

A

esp in lamina propria -

epith, lamina propri, muscul

submucosa

cartilage

adventitia

Bundles of smooth muscle in BRonchus

74
Q

bronchioles - no cartilage, no glands in submucosa

A

scattered goblet in initial segments - but thinning out into Clara Cells

75
Q

bronchioles - no cartilage, no glands in submucosa

scattered goblet proximal

A

scattered goblet in initial segments - but thinning out into Clara Cells

simple ciliated columnar change to simple cuboidal ciliated -
towards end - cilia and nonciliated - turn to CLARA cells

76
Q

Clara CLUB cells - can mitose

A

basally located nucleus, RER, golgi - granules

surfactant secrete
also secrete
secretoglobin -

Transport CHLORIDE

P450 - increase number to pollutants-

secrete mucus

secrete antiinflamation CCSP - protect airway from infection

77
Q

Vaping?

A

damages cilia? - inhibits mucus clearance - decreases chloride

78
Q

Resp zone

respi bronchioles

no more clara cells? when do clara stop?

A

respiratory - no cilia - becomes low cuboidal non-ciliated to eventually simple squamous

walls have alveoli

elastic CT and smooth muscles still present

79
Q

alveolar ducts, sacs -

A

gas exchange -

80
Q

type 1 pneumocytes

A

in alveolar ducts,

81
Q

alveoli

A

from alveolar ducts,

300 million alveoli - packed tightly - separated by interalveolar septum

82
Q

blood air barrier

A

attachement of type 1 pneu w/ pulm capillaries - FUSION

83
Q

type 2 also connects with alveloili

A

produces surfactant

cuboidal

84
Q

interavular septum? compartments

A

type 1

has alveolar pore in system - can get around problem -

macrophages in septum and lumen

elastic fibers - helps w/ recoiling

blood air barrier

85
Q

blood air barrier

FUSED basal lamina

carbon dioxide passes into alveoli, oxygen into RBCs that are coming thru lumen

A

share basal lamina - alveoli and endo cells of capillary

common basal lamina
between type 1 pneu and pulmoney endo cells

86
Q

Type 2 make the surfactant

A

and the surfactant lays on the type 1 - reduces surface tension - and prevent alveoli COLLAPSE

87
Q

interstitium see?

A

collagen, reticular, elastic fibers

fibroblasts, mast cells,

contractile cells

capillary endothelial, type 1, type 2,

alveolar macrophages - in lumen and in septum

88
Q

capillary endo cells?

A

simple squ - very thin

numerous PINOCYTOTIC vesicles

tight junctions.

89
Q

non - resp functions?

ACE???? angiotensin secreated here!!!!

A

break down serotinin
transform ACE - angiotensin 1 to II

inactivate bbradykinin

90
Q

Type 1 - no mitosis, if injury?

A

type 2 has to replace -

type 1 97% of lung surface

91
Q

Angiotensin -

A

is a peptide hormone that causes vasoconstriction and an increase in blood pressure. It is part of the renin–angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys.

92
Q

type 2 - sprinkled around, cuboidal

A

lamellar bodies - store lipids!

93
Q

lamellar bodies? components of surfactant!

A

stores lipids that make up surfactact

94
Q

surfactant?

A

cholesterol, dppc, proteins -

95
Q

club cells surfactant?

A

secrete - but different kind

96
Q

neonatal respi distress syndrome

A

lack of surfactant - after 35 week - secrete

corticosteriods - stim secrete

diabetic mothers - insulin higher risk of developing hyaline membrane disease

if surfactant coat low or non-existent - surface tension goes up - FIBRIN form a hyaline membrane, leads to Carbon dioxide retention

97
Q

newborn, lack of surfactant

A

causes lungs to collapse - because surfactant keeps alveoli shape open-

98
Q

alveolar macrophages ?

A

in septa, and walls of alveolar spaces -

and Free in under surfactant

irregular in shape, show ruffles, lamellipodia -

phagocytose - antigens, etc

99
Q

Dust cells

A

macrophages - shuttling around - can move from septa to lumen -

100
Q

lots of dust cells in whom?

A

smokers -

101
Q

heart failure cells?

A

alveolar macrophages - in congestive heart failure

lungs become congested with blood - RBC into alveoli

Heart failure cells are siderophages generated in the alveoli of patients with left heart failure or chronic pulmonary edema, when the high pulmonary blood pressure causes red cells to pass through the vascular wall. Siderophages are not specific of heart failure.

102
Q

outside of lungs - pleura

A

mesothelium,

103
Q

disorders of tracheobronchial tree?

A

chemical toxins,

bacteria -

104
Q

squamous metaplasis?

A

prolonged damage to area

-

105
Q

Chronic bronchitis -

A

wall is thickened

106
Q

asthma?

COPD

A

constriction do to muscle contraction VISCID mucus

EMPHYsema

COPD - 3

107
Q

Asthma - IGE - mast cells

A

hypersecretion of mucus - charcot leyden crystals??

vasoconstriction

hypertrophy of smooth m

mucous plug formed - charcto leyden crystal

108
Q

severe asmtha changing in med sized airways -

A

thickening of smooth musces, hypertrophy

hypertrophy of golbet cells

increase vasculaaroity, etc

109
Q

treatments of asthma?

A

it is inflammatory disease - bronchial hyperactivity, …

early asmtha reposen

mast cells activitates

later - eosinolphils and lympocytes plug -

bronchodilators help - widen LUMEN

110
Q

beta receptor agonist

A

beta 2 selective

theophylline

muscarinic receptor blockers - (to stop constriction)

cromolyn and nedocromil - prevent degranulation of Mast cells - loewr histamine release

corticostiods - inhibits WBCs

others listed -

111
Q

What causes bronchoconstrictors -

A

inhibit these things

112
Q

prosto glandins PGE2

A

will relax

113
Q

Cystin fibrosis -

A

recessive genetic disease -

reduces chorine

reduces mucus clearnace

mucus GEL Matrix - clara cells

if defective - chloride decreases viscosity of mucous

114
Q

Chloride roll?

A

decrease viscosity of mucus

that is supposed to be secreted into lumen

115
Q

thicken mucus -

A

neutrophils can’t move because of thick mucus layer, bacteria proliferates!

116
Q

Elastaste and emphysema

A

normal -

elastic fibers in interalveolar space -

macrophages increased

neutrophils release elastase to degrade elastic fibers

but in alpha 1 antitrypsin in liver - neutralizes elastase - prevents destrcution of elastic fibers

117
Q

BUT if neutrophils and macrophages are too many

A

too much elastase released - degrading elastic fibers - especially if already decrease in alpha 1 antitrypsin levels decreased !

so Elastic fibers decreased -

leads to emphysema

can’t recoil

SO air space grows - SMOKING

118
Q

industrial lung diseases?

A

coal miners

excess collagen - thickinging of walls of alveoli - decrease in gas exchange, forms lung fibrosis
FIBERS

119
Q

what secretes chloride?

A

x

120
Q

macrophages are supposed to degrade asobestosis,

A

??

121
Q

lung tumors?

A

excessive stimulation to cells

metaplasia
displastic

122
Q

What secretes IgA?

A

plasma cells

123
Q

ability to phonate?

A

vibration between reinke’s space (lamina propria) and true vocal cords (aka FOLDS)

124
Q

Reinke’s edema?

A

laryngitis? inability to speak -

viral infection
trauma
severe coughing

125
Q

stiumulation of Sympathetic Nervous System for air spaces in lungs?

A

stiumulate by Sympth - prohibits contraction by Parasympathetics - which would cause contraction

Contraction decreases lumen

126
Q

What does vein from lung have?

A

oxygenated blood to heart

127
Q

What structures pass through the hilum of the lung?

A

The hilum of the lung is the point of entry for the root of the lung, which includes the bronchi, the pulmonary arteries, and the pulmonary veins. A pleural sleeve is created around these structures, where the pleura reflects, changing from visceral to parietal.

128
Q

two types of arteries in lungs?

A

pulmonary - deoxyg blood

bronchial - oxyg blood to lung tissue, etc

Both left and right bronchial arteries usually travel behind the trachea and main-stem bronchi before entering the lung via the hila

129
Q

Where do bronchial arteries drain?

A

Bronchial vessels usually originate from the aorta or intercostal arteries, entering the lung at the hilum, branching at the mainstem bronchus to supply the lower trachea, extrapulmonary airways, and supporting structures; this fraction of the bronchial vasculature drains into the right heart via systemic veins.

130
Q

Clara cells - where are granules vs nucleus?

can migrate to replenish alveolar epith cells - alveolar bronchiolization

can regenerate bonchiolar epithelium and alveloar epithelia~~

A

nucleus at base - grans on top

NON CILIATED, cuboidal

131
Q

clara cells CLEARS the air

A

P450 - goes up when more pollution - detoxifies

surfactant

132
Q

types of capillary at air blood barrier?

A

continuous, with many pinocytitic vesicles

tight junctions

133
Q

type 2 - where store surfactant?

A

lamellaar bodies

134
Q

where see mast cells?

A

DUST cells - if pick up too much bad stuff, can fibrose -

- silicosis

135
Q

where see mast cells?

dust cells - ruffled, lying under the surfactant

A

DUST cells - if pick up too much silica, can fibrose -
- silicosis -

release chemical alveolitis - which creates fibrosis of lungs

136
Q

Hyaline membrane disease in infants?

A

not enough surfactact - week 35,

respiratory distress syndrome -

fibrin type of hyalin released by newborns - hence hyaline membrane disease

137
Q

where do dust cells go when have antigen to report to T cells?

A

through bronchi, to upper airway psarynx (via cilia) where they are swallowed in saliva~~~

138
Q

congestive heart failure?

alveolar macrophage

A

lungs become congested with blood - RBC pass into alveola - where phagocytosed by macrophages - “heart failure cells) when present in lungs and sputum

high pulmonary pressure pushes RBCs through wall

139
Q

disorders of tracheobronchila tree?

A

mucosa can die if damaged by chemical agent, virus, bacteria

turns into squamous epithelium -

repeated damage - chronic bronchitis -

bronchila

140
Q

disorders of tracheobronchila tree?

A

mucosa can die if damaged by chemical agent, virus, bacteria

turns into squamous epithelium -

repeated damage - chronic bronchitis -

bronchial wall thickens - by increase in numbers and activity of seromucous glands - thickening muscle layer - commonly associated with ASTHMA -

severe bronchoconstriction due to bronchial smooth muscle contrcaiont and production of mucus - and EMPHYSEM - where alveloar walls are destroyed -

combo of all three - chronic obstruction pulmonary disease

141
Q

What is COPD - 3

A

chronic bronchitis (bronchial wall thickens)

asthma (bronchoconstrictuion)

emphysema (alveolar walls are destroyed

142
Q

charcot leyden crystals

A

Charcot–Leyden crystals are microscopic crystals composed of eosinophil protein galectin-10 found in people who have allergic diseases such as asthma or parasitic infections such as parasitic pneumonia or ascariasis.

143
Q

asthma - what happens?

A

inhale allergen

IgE receptors on MAST cells - degranulation, histamines chemoattraction of EOSINOPHILS

increased permeability of blood vessels, smooth muscle constrcition, hyper secretion of mucus by goblet cells

Th2 cells secrete IL 13 - airway tightening and ups mucus production, TH@ cells secrete IL 5 - essential for maturation of eoisinphils

inflammatory cells and Chacot- Leyden crystals

144
Q

asthma causes changes in lungs

A

medium airways - mucous cell hyperplasia an hyper secretion, smooth muscles increase

increased vascularity

deposition of subepithelial collagen

145
Q

Emphysema - chronic lung disease

neutrophils come to fix problem, release elastase - too much and antitrypsin is overwhelmed, elastase takes over and destroys elasticity of alveloa

A

enlarged air space in brochiloles with destructin of interalveolar wall - SMOKING

smoking or other stimulus - increases macrophages, which secrete chemoattractants calling for neutorphils, which come and release elastase - serum ANTITRYPSIN neutralizes elastase and prevents it destructive oeffect on wall

persistent stiumulus of neutrophils and macrophages =

eventually antitrypsin levels decrease and elastase destroys elastic fibers - damaged fibers can’t recoil when stretched -

146
Q

what does chronic smoking do to respiratory lining?

A

changes it into stratified squamous - the initial step

CCDB (13 decks)

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