respiratory - histology Flashcards
most distal part of conducting portion?
terminal brochioles
bronchial tree?
not the extrapulmonary (not in lungs), or the respiratory portion (gas exchange)
the INTRApulmonary - including bronchiles
respiratory portion - starts where?
respiratory bronchioles - alvelos ducts, sac, alveoli
where does gas exchange occur?
alveoli
how does gas exchange occur?
close assocation betw alveolar spaces and pulm caps
what do mucus gland do in respir system
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
hallmark of lamina propria in nasal cavity? SWELL
rich vascular plexus - swell bodies
stuffy nose?
swelling of lamina propria of nasal mucosa / edema
sense of smell occurs in which region of NASAL cavity? what cells responsible?
olfactory region of nasal cavity
Neurons BIPOLAR
What cells can regenerate smell sensation - olfactory perception?
basal cells - these are basal stem cells
What do supporting cells do in olfactory system?
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”
Olfactory glands? in olfactory mucosa
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
what expect to find in olfactory mucosa?
Bowman’s glands and neurons
Respi epith?
ciliated psuedostratified columnar w/ goblet cells - if not this then stratified squam (non-keritainzed ?) where direct air is present ?
Chronic sinusitis caused by what subcell structure not functioning?
cilia sweeps mucus
phonation shaped by which structure in head and neck? what type of cells cover?
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
What structure protects trachae?
15 - 20 cartilagenous rings from larynx to sternal angle
c shaped area bridged by smooth muscles
The function of the pulmonary brush cell
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.
endocrine function of respiratory cells?
small granule cells - secrete seritonen, calcintonen, variety of other things - don’t think people know what they really do
What membrane becomes thicker in smoker’s respiratory system?
basement membrane of mucosa
how many segmental bronchi arise from right primary bronchus?
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
bronchopulmonary segments?
18 in total
What do Clara cells do?
secrete surfactant, and can repopulate respiratory bronchioles following injury
Where do Clara cells first appear in bronchial tree?
terminal bronchioles
olfactory epithelium?
non-motile cilia - bi polar nerve cells in roof of nasal cavity
Bowman gland?
lie in lamina propria beneath elpith. produce water secretion moistening olfactory surface
terminal bronchioles? Clara
most distal conduction portion - no gas exchange, two types cells - secretory (CLARA and ciliated -
no cartilage
Trachea?
thick basment membrane - pseudostratified ciliated columnar
c shape cartiaged, smooth muscle (trachealis) extends between c tips
REspirataory bronchiles
gas exchange can occur here - some alveoli interrupt their walls - simple cuboidal lining w/ Clara and ciliated cells -
asthma?
constriction of smooth muscles in bronchioles, makes expiration difficult - mucus settles in, inflammatory cells invade bronchiolar walls
What do alveolar macrophages secrete?
ELASTASE
normally a1-antitrypsic, a serum protein w. elastase, proteccts lung
emphysema (hereditary) treated w? lack of ELASTICity is issue - barrel chest
recombinant a1-antitrypsin which has antielastase activity
interstitial pulmonary fibrosis?
asbestosis - in walls of bronchioles, ducts and alveoli
may turn to mesotheliosma - CANCER
barrel chest?
emphasyma - lack of elastiicty - antitrypsin
pregnant? glucocorticoids?
stimulate surfactact
surfactant? type 2
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.
Bowman’s glands - Bow Wow! - in lamina propria
(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.
NOLTBBT - conducting system
muscles to lining - all reducing in size to get way down to thin membrane for gas exchange
nasal, oral, larynx, trachea, bronchi, bronchiloes, terminating bronchioles
respiratory portion? RDSA
respiratory bronchioles, alv ducts, sacs, alveoli
kulchitsky cells (peptides) ? basal STEM STEM
Trachea - kulchitsky secrete peptides, basal maybe w/ nerves
trachea lamina propria?
collagen and elastic
traechilis muscle
bridges C shaped cartilage rings -
submucosa has seromucous glands
c shaped cartilage is where in 4 layers -
adventitia to muscular - that’s where the traechilis muscle is
respiratory epithelium?
ciliated psuedostratified w/ goblet
bronchi has what kind of plates?
cartilage plates in ADVENTITIA - and muscular layer prominent CIRCULAR Layers smooth muscle
Bronchioles - Clara
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.
Terminal bronchioles - switch type of lining , Clara
ciliated simple cuboidal, reduced circular m
respiratory bronchiles
ciliated simple cuboidal, Clara, ALVEOLI open into walls - so some gas exchange
alveolar ducts - muscle knobs
simple squamous - collagen, elastic
muscle layer - smooth knobs
Alveoli - type 1, type 2 - no muscles in alveoli
macrophages
pores of KOHN
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
What does Hyperplasia type II pneumocytes tell you?
alveolar injury and repair
what do alveolar macrophages do? DUST cells
migrate around, picking up DUST, bacteria, degraded surfactant
pores of KOHN - pressure, bypasses in disease
equalize pressure within alveoli - important role in obstructive lung disease bypassing aerate alveoli distal to blockage
what is surfactant made of?
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
Blood air barrier - fick’s law
surfactant, type 2 pneumotycte basement membrane, capillary
Fick’s law BAB - blood air barrier
thicker barrier, less oxygen can pass through
Air flow law - Poiseuille Law? dramatic reduction
air flow RESISTANCE
reduced by 2, resistance goes up to 16 - factor of 8
Sympathetic? opens or closes?
OPENS - reduces resistance
B2 adrenergic - albuterol, PGE2
parasympathetic stim - closes them down - bronchoconstrictors
Infant respiratory distress syndrome ? RDS
deficiency of surfactant - thyroxine and cortisol can help increase production
repeated gasping can further damage alveoloar lining - hyaline membrane disease
Emphysema - pink puffers, thin, barrel chest -
increased breathing rate -
2 types
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
Chronic bronchitis - smoking - blue bloater
excessive mucus produced, sputum, bronchi inflamed - hypertrophy of mucous glands
Asthma - smooth muscle hyperactivity - in bronchi and bronchiloes - increased mucus, edema
Eosinophils within bronchila wall - To be Continued - from High yield histo
no cartialge in ?
bronchioles
vagus nerve?
decreases lumen - parasympathetic
sympathetic - RELAX
expand lumen
terminal bronchioles
simple cuboidal change
club cells - CLARA
in terminal bronchiol - NO Globlet,
surfactant P450 - enzyme - detoxifies
P450 - enzyme - detoxifies
when inhaled, this is where this clara’s it - cleans it! has to clean here - before enters respiratory zone
vascular system?
WHAT called when doesn’t go cap - arttery - cap venous? or whatever it is supposed to do?
blood comes into pulmonary capilaries - where gas exchange is done - carried back to heart - via pulmonary vein
Thru HILEM
muscle fibers vs elastic arrangement - concentric vs. longitudinal
elastic longitudinal,
smooth concentric
surrounding terminal bronchioles
pores of kohn - blockage help
connect adjacent alveoli - if blocked - can get around this problem
continuous ventilation
bronchi - make up
cartilage platelike - no c shape
m concentric,
elastic longitudinal
serous/mucous - submucosa
BALT -
Hyaline cart - no longer in C shape - smaller plates
ONLY in Trachea see C shape
BALT - in mucosa
esp in lamina propria -
epith, lamina propri, muscul
submucosa
cartilage
adventitia
Bundles of smooth muscle in BRonchus
bronchioles - no cartilage, no glands in submucosa
scattered goblet in initial segments - but thinning out into Clara Cells
bronchioles - no cartilage, no glands in submucosa
scattered goblet proximal
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
Clara CLUB cells - can mitose
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
Vaping?
damages cilia? - inhibits mucus clearance - decreases chloride
Resp zone
respi bronchioles
no more clara cells? when do clara stop?
respiratory - no cilia - becomes low cuboidal non-ciliated to eventually simple squamous
walls have alveoli
elastic CT and smooth muscles still present
alveolar ducts, sacs -
gas exchange -
type 1 pneumocytes
in alveolar ducts,
alveoli
from alveolar ducts,
300 million alveoli - packed tightly - separated by interalveolar septum
blood air barrier
attachement of type 1 pneu w/ pulm capillaries - FUSION
type 2 also connects with alveloili
produces surfactant
cuboidal
interavular septum? compartments
type 1
has alveolar pore in system - can get around problem -
macrophages in septum and lumen
elastic fibers - helps w/ recoiling
blood air barrier
blood air barrier
FUSED basal lamina
carbon dioxide passes into alveoli, oxygen into RBCs that are coming thru lumen
share basal lamina - alveoli and endo cells of capillary
common basal lamina
between type 1 pneu and pulmoney endo cells
Type 2 make the surfactant
and the surfactant lays on the type 1 - reduces surface tension - and prevent alveoli COLLAPSE
interstitium see?
collagen, reticular, elastic fibers
fibroblasts, mast cells,
contractile cells
capillary endothelial, type 1, type 2,
alveolar macrophages - in lumen and in septum
capillary endo cells?
simple squ - very thin
numerous PINOCYTOTIC vesicles
tight junctions.
non - resp functions?
ACE???? angiotensin secreated here!!!!
break down serotinin
transform ACE - angiotensin 1 to II
inactivate bbradykinin
Type 1 - no mitosis, if injury?
type 2 has to replace -
type 1 97% of lung surface
Angiotensin -
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.
type 2 - sprinkled around, cuboidal
lamellar bodies - store lipids!
lamellar bodies? components of surfactant!
stores lipids that make up surfactact
surfactant?
cholesterol, dppc, proteins -
club cells surfactant?
secrete - but different kind
neonatal respi distress syndrome
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
newborn, lack of surfactant
causes lungs to collapse - because surfactant keeps alveoli shape open-
alveolar macrophages ?
in septa, and walls of alveolar spaces -
and Free in under surfactant
irregular in shape, show ruffles, lamellipodia -
phagocytose - antigens, etc
Dust cells
macrophages - shuttling around - can move from septa to lumen -
lots of dust cells in whom?
smokers -
heart failure cells?
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.
outside of lungs - pleura
mesothelium,
disorders of tracheobronchial tree?
chemical toxins,
bacteria -
squamous metaplasis?
prolonged damage to area
-
Chronic bronchitis -
wall is thickened
asthma?
COPD
constriction do to muscle contraction VISCID mucus
EMPHYsema
COPD - 3
Asthma - IGE - mast cells
hypersecretion of mucus - charcot leyden crystals??
vasoconstriction
hypertrophy of smooth m
mucous plug formed - charcto leyden crystal
severe asmtha changing in med sized airways -
thickening of smooth musces, hypertrophy
hypertrophy of golbet cells
increase vasculaaroity, etc
treatments of asthma?
it is inflammatory disease - bronchial hyperactivity, …
early asmtha reposen
mast cells activitates
later - eosinolphils and lympocytes plug -
bronchodilators help - widen LUMEN
beta receptor agonist
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 -
What causes bronchoconstrictors -
inhibit these things
prosto glandins PGE2
will relax
Cystin fibrosis -
recessive genetic disease -
reduces chorine
reduces mucus clearnace
mucus GEL Matrix - clara cells
if defective - chloride decreases viscosity of mucous
Chloride roll?
decrease viscosity of mucus
that is supposed to be secreted into lumen
thicken mucus -
neutrophils can’t move because of thick mucus layer, bacteria proliferates!
Elastaste and emphysema
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
BUT if neutrophils and macrophages are too many
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
industrial lung diseases?
coal miners
excess collagen - thickinging of walls of alveoli - decrease in gas exchange, forms lung fibrosis
FIBERS
what secretes chloride?
x
macrophages are supposed to degrade asobestosis,
??
lung tumors?
excessive stimulation to cells
metaplasia
displastic
What secretes IgA?
plasma cells
ability to phonate?
vibration between reinke’s space (lamina propria) and true vocal cords (aka FOLDS)
Reinke’s edema?
laryngitis? inability to speak -
viral infection
trauma
severe coughing
stiumulation of Sympathetic Nervous System for air spaces in lungs?
stiumulate by Sympth - prohibits contraction by Parasympathetics - which would cause contraction
Contraction decreases lumen
What does vein from lung have?
oxygenated blood to heart
What structures pass through the hilum of the lung?
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.
two types of arteries in lungs?
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
Where do bronchial arteries drain?
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.
Clara cells - where are granules vs nucleus?
can migrate to replenish alveolar epith cells - alveolar bronchiolization
can regenerate bonchiolar epithelium and alveloar epithelia~~
nucleus at base - grans on top
NON CILIATED, cuboidal
clara cells CLEARS the air
P450 - goes up when more pollution - detoxifies
surfactant
types of capillary at air blood barrier?
continuous, with many pinocytitic vesicles
tight junctions
type 2 - where store surfactant?
lamellaar bodies
where see mast cells?
DUST cells - if pick up too much bad stuff, can fibrose -
- silicosis
where see mast cells?
dust cells - ruffled, lying under the surfactant
DUST cells - if pick up too much silica, can fibrose -
- silicosis -
release chemical alveolitis - which creates fibrosis of lungs
Hyaline membrane disease in infants?
not enough surfactact - week 35,
respiratory distress syndrome -
fibrin type of hyalin released by newborns - hence hyaline membrane disease
where do dust cells go when have antigen to report to T cells?
through bronchi, to upper airway psarynx (via cilia) where they are swallowed in saliva~~~
congestive heart failure?
alveolar macrophage
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
disorders of tracheobronchila tree?
mucosa can die if damaged by chemical agent, virus, bacteria
turns into squamous epithelium -
repeated damage - chronic bronchitis -
bronchila
disorders of tracheobronchila tree?
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
What is COPD - 3
chronic bronchitis (bronchial wall thickens)
asthma (bronchoconstrictuion)
emphysema (alveolar walls are destroyed
charcot leyden crystals
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.
asthma - what happens?
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
asthma causes changes in lungs
medium airways - mucous cell hyperplasia an hyper secretion, smooth muscles increase
increased vascularity
deposition of subepithelial collagen
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
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 -
what does chronic smoking do to respiratory lining?
changes it into stratified squamous - the initial step
