HISTOLOGY OF RESPIRATORY SYSTEM (HISTOFISIOLOGY)

YAN EFFENDI HASJIM, DAHKYAN EFFENDI HASJIM, DAHK

SRIWIJAYA UNIVERSITY, FACULTY OF MEDICINEDEPARTEMENT OF HISTOLOGY

2015

RESPIRATION

1. Breathing / Ventilation (Movement of air in and out of the lungs ) 2. External Respiration (Exchange of O2 in the inspired air for carbon

dioxide in the blood)

3. Transport of Gases (Conveyance of O2 and CO2 to and from the cells)

4. Internal Respiration (Exchange of CO2 for O2 in the vicinity of the cells )

providing O2 to and eliminating CO2 from the cells of the body.

RESPIRATORY SYSTEM

HISTOPHYSIOLOGY:

• PROVIDING OXYGEN (O2) TO, AND ELIMINATING CARBON DIOXIDE (CO2) FROM CELLS:

1. CONDUCTION AIR FROM AND TO ALVEOLAR

2. EXCHANGE GASES O2 - ALVEOLUS AIR & CO2 IN CAPILLARIES BLOOD (EXTERNAL RESPITATION)

• CORRELATION TO CARDIOVASCULAR SYSTEM

COMPONENTS

1. CONDUCTION PORTION

2. RESPIRATORY PORTION

CONDUCTION PORTION 1. Nose2. Pharynx3. Larynx4. Trachea5. Bronchi6. Branchioles

RESPIRATORY PORTION1. Respiratory bronchioles2. Alveolar duct3. Alveolar sacc4. Alveoli

CONDUCTION PORTION

NOSE

Concha

Concha

Concha

HISTOPHYSIOLOGY

PROTECTION AND CONDITIONINGA OF RESPIRATION AIR PHYSIOLOGIC

FILTER, WARM, HUMIDIFIES THE INHALED AIR AND PERCEPTION OF ODORS

ANTERIOR ASFECT OF NASAL CAVITY

• SEPTUM NASI (CARTILAGO & BONY)

• ANTERIORLY, NARIS (NOSTRIL), POSTERIORLY NASOPHARYNX, (CHOANA)

• NARES, VESTIBULE, • SKIN AND VIBRISSAE (FILTER

LARGE DUST PARTICLE) • DERMIS : SEBACEOUS AND SWEET

GLANDS (MOISTEN)

• NASAL CONCHAE,

SUPERIOR, MIDDLE, INFERIOR NASAL CONCHAE AIR SIRCULATION (HARM)

MUCOSA OF NASAL CAVITY

• EPITEHLIUM– VESTIBULI, EPIDERMIS FILTER– OLFACTORY REGION (OLFACTORY EPITHELIUM)

PERCEPTION OF ODORS– PSEUDOSTRAFIED CILIATED COLLUMNAR

EPITHELIUM (RESPIRATORY EPITHELIUM : CILLIATED, GOBLET CELLS, SEROUS GLANDS) CLEANING

• LAMINA PROPRIA, SUBEPITHELIAL CONNECTIVE TISSUE– RICHLY VASCULARIZED, (>> CONCHA AND

SEPTUM NASAL, LARGE ARTERIAL PLEXUS AND VENOUS SINUSES HARM

– SEROMUCOUS GLANDS MOISTEN– LYMPHOID ELEMENT >> (LN, MASTOCYTES,

PLASMATOCYTES) ANTIBODIES (IgA, IgE, IgG) DEFENSE

• HUMAN OLFACORY MUCOSA • OLFACTORY CILIA (Ci)• CONECTIVE TISSUE: BOWMAN’S GLANDS,

BASAL CELL (BC), OLFACTORY CELL (OC), LAMINA PROPRIA (LP).

OLFACTORY EPITHELIUM

OLVACTORY GLAND (BOWMAN), SECRETES CONTAINING ODORANT-BINDING PROTEIN (OBP)

ODORANT-OBP COMPLEX TO RECEPTOR ON SURFACE CILIUM

ODORANT MOLEKUL BOUND TO OBP

OLFACTORY CELL (BIPOLAR NEURON)

DENDRITE

MODIFIED CILIUM

AXON

BASAL LAMINA

CLINICAL CORRELATIONS

NASAL BLEEDING (EPISTAXIS)

• KIESSELBACH’S AREA (ANTEROINFERIOR OF NASAL SEPTUM)• ANASTOMOSIS ARTERIAL (SUPPLY OF NASAL MUCOSA)

CLINICAL CORRELATIONS

• BLOOD FLOW TO VENOUS SINUSES LAMINA PROPRIA PROTECTE NASAL MUCOSA FROM DEHYDRATION.

• VENOUS SINUSES ENGORGED WITH BLOOD REDUCTING FLOW OF AIR THROUG, SEEPAGE OF PLASMA SINUSES + SEROMUCOUS SECRETION OF GLANDS REHYDRATE THE MUCOSA EVERY HALF HOUR

• SNEEZE REFLEX, REMOVE CHEMICAL IRRITANS AND PARTICULATE FROM NASAL CAVITY SUDDEN EXPULSION OF AIR CLEARS THE NASAL OF IRRITANT

PHARYNX

• CHOANE TO OPENING OF LARYNX• CONTINUOUS CAVITY: 3 REGIONS:

(1) NASOPHARYNX (SUPERIOR)(2) OROPHARYNX (MIDDLE) (3) LARYNGEAL PHARYNX (INFERIOR)

• NASOPHARYNX : RESPIRATORY EPITHELIUM, ORAL - LARYNGEAL PHARYNX , STRATIFIED SQUAMOUS EPITHELIUM

• LAMINA PROPRIA, LOOSE TO DENCE, IRREGULAR, VASCULARIZED CONNECTIVE TISSUE, SEROMUCOUS GLANDS AND LYMPHOID ELEMENT.

• POSTERIOR ASPECT OF NASOPHARYNX, PHARYNGEAL TONSIL (UNENCAPSULATED COLLECTION OF LYMPHOID TISSUE)

LARYNX

• IRREGULAR TUBE AND STRUCTURALLY MOST COMPLEX

• PROJECTS FROM LARYNX: – EPIGLOTTIS – 2 PAIRS FOLD (VESTIBULAR

FOLD/FALSE VOCAL CORD & VOCAL FOLD/TRUE VOCAL CORD)

FOR PHONATION • MUCOSA OF LARYNX TWO PAIRS FOLD (BY

NARROW CLEF LARYNGEAL VENTRICLE) : – 1). VESTIBULAR VOCAL FOLD/ FALSE VOCAL FOLD

(SUPERIOR) – 2). VOCAL FOLD/ TRUE VOCAL CORD (INFERIOR)

• VESTIBULAR FOLD, IMMOVABLE, • VOCAL FOLD, PRODUCES AND MODULATED

SOUND• ADULT, MALE LARGER THAN FEMALE VOICES

DEEPER THEN WOMEN

HISTOLOGICALLY1) VOICE BOX, PHONATION 2) SWALLING PREVENTING OF FOOD AND FLUIDS INTO

RESPIRATORY SYSTEM

LARYNX

1. MUCOSA

PSEUDOSTRATIFIED CILIATED COLLUMNAR, TRANSPORTING MUCUS + PARTICULATE TO MOUTH (EXCEPT, SUPERIOR EPIGLOTTIS AND VOCAL FOLD)

LAMINA PROPRIA, – LOOSE CONNECTIVE TISSUE , SEROMUCOUS GLANDS,

ADIPOSES CELLS, LYMPHOID ELEMENTS (LN), BLOOD VESSEL, SOME MUSCLE

– CARTILAGES HYALIN – PERICHONDRIUM

2. SUBMUCOSA (VOCAL FOLD, ABSENT),

3. ADVENTITIA,

RELATIF THIN, CONNECTIVE TISSUE, ADIPOSE, BLOOD VESSEL

STRUCTURE LARYNX

• VOCAL CORD AT JUNCTION OF NONCORNIFIED STRATIFIED SQUAMOUS AND RESPIRATORY EPITHELIUM

• SUBMUCOSA, DEEP SKELETAL MUSCLES FIBERS

VESTIBULAR FOLD / FALSE FOLD, (UPPER)• RESPIRATORY EPITHELIUM• LAMINA PROPRIA : SEROMUCOUS GLANDS >> MAINTAIN MOISTURE

VOCAL FOLD /TRUE VOCAL CORD (LOWER)• STRATIFIED SQUAMOUS EPITHELIUM (EXCEPT),

ABERATION (THE RAPIDLY MOVING AIR STERAM AND PHYSICAL CONTACT BETWEEN VOCAL FOLD)

LANGERHANS CELL IMMUNOLOGICAL FUNCTION.• LAMINA PROPRIA: SEROMUCOUS GLANDS << TO

MAINTAIN MOISTURE, LUBRICATION DURING FRICTION.

• VOCALIS MUSCLES, REGULATE TENS OF FOLD & LIGAMNET (DISTANCE AND SHAPE OF TRUE VOCAL FOLDS DURING PHONATION SOUND OF DIFFERENTS FREQUENSCIES)

• VOCALIS LIGAMENT STRUCTURAL SUPPORT).

EPIGLOTTIS

• PROJECTS FROM LARYNX, EXTEND TO PHARYNX, 2 SURFACE (LINGUAL AND LARYNGAEL SURFACE)

• A JUNCTION RESPIRATORY AND GASTROINTESTINAL TRUCTS

• GUARDS THE AIRWAY ENTRANCE FROM FOREIGN MATERIALS, FOOD DURING SWALLOWING.

HISTOLOGICAL FEATURE

• EPITHELUM

– LINGUAL & APICAL LARYNGEAL SURFACE : NON-KERATINIZED STRATIFIED SQUAMOUS ,

– TRANSITION INTO RESPIRATION EPITHELIUM (LARYNGEAL SIDE)

• SUBEPITHELIUM: MIXED GLANDS

• LAMINA PROPRIA: – ELASTIC CARTILAGO – TUBULOACINAR MUCOUS, SEROUS, OR

MIXED GLANDS

CLINICAL CORRELATIONS

LARYNGITIS

• INFLAMATION OF LARYNGEAL TISSUES, INCLUDING VOCAL FOLD

SOUND HOARSE (CAN ONLY WHISPER)• CHEMICAL IRRITANS / PARTICULATE MATTER IN UPPER AIR PASSAGES, TRACHEA

OR BRONCHI,

COUGHT REFLEX

• EXPLOSIVE RUSH OF AIR TO REMOVE THE IRRITANT

• BEGINS WITH INHALATION LARGE VOLUME OF AIR AND CLOSURE EPIGLOTTIS AND GLOTTIS (ABDUCTIVE VOCAL FOLDS),

• FOLLOWED BY POWERFUL CONTRACTION MUSCLES FOR FORCED EXPIRATION (INTERCOSTAL AND ABDOMINAL MUSCLES).

• SUDDEN OPENING GLOTTIS AND EPIGLOTTIS GENERATES A RUSH OF AIR, VELOCITY CAN EXCEED 100 MILES PER HOUR, REMOVING IRRITAN WITH AN ENOMEROU FORCE

.

TRACHEA

• TRACHEALIS MUSCLE, CONTRACTION CONNTRICTION OF LUMEN, DISLOGING OF FOREIGN MATERIAL (OR MUCUS OR OTHER IRRITANS) FROM THE LARYNX BY COUGHING.

• CILIA MOVE THE MUCOUS NASOPHARYNX• MICROVILLI (NERVE ENDINGS) , SENSORY ROLE• MONITOR O2-CO2 LEVEL IN LUMEN (DNES / KULCHITSKY CELLS)

10 - 12 HORSESHOE-SHAPED HYALIN CARTILAGE RINGS (C-RINGS), • OPEN POSTERIORLY, CONNECTED BY

SMOOTH MUSCLE (TRACHEALIS MUSCLE),

• ROUNDED ANTERIORLY AND FLATTENED POSTERIORLY

• PERICHONDRIUMS IS CONNECTED BY FIBROELASTIC CONNECTIVE TISSUE FLEXIBILITY , AND ELONGATION DURING INSPIRATION

HISTOLOGICALLY

1. MUCOSA

• RESPIRATORY EPITHELIUM , (IRRITATION, CHRONIC COUGH. MAY CHANGE TO ANOTHER TYPE)– BASEMENT MEMBRANE THICKEST. – BEATING OF CILLIA DIRECT TOWARD

OROPHARYNX (EXPECTORANS OR SWALLOWING) CIGARETE SMOKE ARE CILIOTOXIC.

– SIX CELL TYPE: GOBLET, CILIATED AND NONCILIATED COLLUMNAR CELLS AND BASAL CELLS (90% POPULATION) BRUSH CELLS, SEROUS, DIFFUSE NEUROENDOCRINE SYSTEM (DNES) CELLS.

• LAMINA PROPRIA, LOOS CONNECTIVE TISSUE

mucinogen, (aqueous environment

mucin)

cilia and microvilli move the mucus nasopharynx

stem cells

microvilli (nerve endings) sensory roleapical granules

(serous fluid)

monitor O2-CO2 levels in lumen.

1. GOBLET CELLSs 30% 2. CILIATED COLLUMNAR CELLS 30%. 3. SHORT BASAL CELLS 30%. 4. BRUSH CELLS 3%.5. SEROUS CELLS 3%6. DNES, KULCHIITSKY CELLS, 3% to

4%.

2. SUBMUCOSA

• DENCE, IRREGULAR FIBROELASTIC CON.TIS. • MUCOUS & SEROMUCOUS GLANSDS (SHORT

DUCT OPEN TO SURFACE)• LYMPHOID ELEMENT • RICH BLOOD AND LYMPH SUPPLY

3. FIBROCARTILAGE LAYER/ADVETITIA • CONNECTIVE TISSUE BIND TRACHEA TO

ADJESENT STRUCTURES, LARGE BLOOD VESSEL, NERVES AND LYMPHATICS .

• SERIES ELASTIC(16-20) of C-SHAPED CARTILAGE RINGS PREVENT COLLAPSE . PERICHONDRIUM MERGES WITH SUBMUCOSA AND ADVENTITIA

• OPEN END POSTERIORLY, CLOSED BY TRANSVERSE BAND OF SMOOTH MUSCLE (TRACHEAL MUSCLE). INCREASEES INTRA THORACIC PRESSURE DURING COUGHING

• BETWEEN THE RINGS, FIBROELASTIC CONNECTIVE TISSUE

Ciliated CellCiliated Cell

Watery (sol)Watery (sol)phasephase

from serousfrom serousglandsglands

Duct ofDuct ofserousserousglandgland

GobletGobletcellcell

MucousMucousphasephase

TRACHEATRACHEA

DNES / SMALL-GRANULE / KULCHITSKY CELLS (3% -4%).

• PROCESSES (LONG, SLENDER) EXTEND INTO LUMEN, • SYNAPTIC SENSORY NERVE ENDING PULMONARY NEUROEPITHELIAL BODIES• GRANULES (amines, peptides, acetylcholine, and adenosine triphosphate). • HYPOXIA CONDITIONS :

• CONNECTIVE TISSUE SPACES OF LAMINA PROPRIA (PARACRINE) LOCAL EFFECTS REGULATING PERFUSION

• OR ENTER VASCULAR (HORMONS). GENERALIZED EFFECTS EFFERENT NERVE FIBERS RESPIRATORY REGULATORS IN MEDULLA OBLONGATA

MONITOR O2-CO2 LEVEL

CLINICAL CORRELATIONS

• chronically exposed to irritants (cigarette smoke) REVERSIBLE METAPLASIA goblet cells >> relative to ciliated.

• REDUCTED NUMBER OF CILLIA retards the rate of mucus elimination, in congestion.

• NCREASE SIZE OF SEROMUCOUS GLDS (gland lamina propria + submucosa) a more copious secretion.

• A few months after elimination of the pollutants, the cell ratio returns to normal (1:1) and the seromucous glands revert to their previous size.

1. primary bronchi (extrapulmonary bronchi)

2. secondary & tertiary bronchi (intrapulmonary bronchi)

3. bronchioles,

4. terminal bronchioles,

5. respiratory bronchioles

BRONCHIAL TREE

• TRACHEA

• 2 MAIN / PRIMARY BRONCHI

• RIGHT PRIMARY BRONCHI WIDER, SHOTER, MORE VERTICAL, 3 SCUNDARY BRONCHI /LOBAR BRONCHI (SUPERIOR, MIDLE INFERIOR)

• LEFT PRIMARY BRONCHI DIVIDES 2 SECUNDARY BRONCHI (SUPERIOR AND INFERIOR LOBE)

• SECUNDARY BRONCHI TERTIARY BRONCHI (SEGMENTAL BRONCHI)

• BRONCHIOLES TERMINAL BRONCHIOLES

• RESPIRATORY BRONCHIALES ALVEOLAR DUCTS, ALVEOLAR SAC ALVEOLUS (BASIC ANATOMICAL UNIT EXCHANGE GAS)

BRONCHIAL TREE

1. PROGRESSIVELY DECREASE– SIZE, AMOUNT, CONTINUITY OF CARTILAGE

LACK– NUMBER OF GLANDS LACK– NUMBER OF GOBLET CELLS LACK

– TYPE AND HEIGHT OF EPITHELIUM CELLS RESPIRATORY EPITHELIUM SIMPLE CUBOID NONCILIATED

PROGRESSIVE CHANGES OF STRUCTURE

2. PROGRESSIVELY INCREASE– SMOOTH MUSCLE AND ELASTIC

TISSUE (WITH RESPECT TO THICKNESS OF WALL)

– CLARA CELLS REPLACE GOBLET CELLS

EpitheliuEpitheliumm

Goblet CellsGoblet Cells GlandsGlands CartilageCartilage

CiliatedCiliatedpseudostpseudostrat.rat.columnacolumnarr

CiliatedCiliatedsimplesimplecolumnarcolumnar

AbundantAbundant

ScatteredScattered

NoneNone

PresentPresent

FewFew

None

C-ringsC-rings

PlatesPlates

NoneNone

1. CARTILAGE HYALIN• PRIM. BRONCHI : IRREGULAR INCOMPLETE RING • SCUNDARY BRONCHI : FEW ISLANDS • BRONCHIOLE DISAPEAR

2. SMOOTH MUSCLES• UPPER BRONCHI CONTINUOUS LAYER• DISTAL PORTIAN LESS ABUDANT AND MORE

LOOSELY ORGANIZED• BRONCHIOLUS >> ABUDANT COMPONENT OF

WALL

3. EPITHELIUM, GREAT CHANGES, GRADUAL • BRONCHI = TRACHEA • TO TERMINAL BRONCHIOLI GREAT CHANGE

GRADUALY– HEIGHT GRADUALI DECREASE– BRONCHIOLI SIMPLE CILIATED CUBOIDAL – TERMINAL BRONCHIOLI, LOW CUBOID NON

CILIA

4. GOBLET CELLS AND GLAND• DIMINISH IN NUMBER, PRESENT BEFORE

TERMINAL BRONCHIOLI• BRONCHIOLI: GOBLET CELLS (-), REPLACE BY

CLARA CELLS

• PRIMARY (PRINCIPAL, EXSTERNAL) BRONCHI: – QUITE SIMILAR TRACHEA– CARTILAGO RINGS FLATTENED IRREGULAR,

SPIRAL BANDS SMOOTH MUSCLE COMPLETE ENCYRCLE LUMEN

• SECUNDARY BRONHI (LOBAR BRONCHI)– SIMILAR PRIMARY, EXCEPT CARTILAGE FEW

IRREGULAR ISLANDS.

• TERTIARY/SEGEMENTAL BRONCHI – IDENTICAL SCUNDARY BRONCHI, BUT DECRESE

IN DIAMETER, CARTILAGE SOME ISLAND

BRONCHUS

• DISTINGUIS FROM BRONCHI :

1. EPITHELIUM GRADUAL, SIMPLE CILIATED COLLUNAR SIMPLE CILIATED LOWER, AND THEN LOSSE CILIA

2. DIMINISHING NUMBERS GOBLET, AND THEN LOSSE (GOBLETS LOOSE AFTER LOOSE CILIA EPITHEL)

3. LACK OF CARTILAGE AND GLANDS

BRONCHIOLE

• less than 0.5 mm in diameter• CHARATERIZED BY

– SIMPLE CILIATED CUBOIDAL EPITHELIUM, – NO GOBLET, SMOOTH MUSCLE – (ELIMINATION GOBLET BEFORE CILIA OF

CELLS, IMPORTANT TO PREVENTING FROM DROWNING IN OWN MUCUS)

– CLARA CELLS ,CUBOID DOME SHAPEED CILIA, • BRANCHIOLE 2- MORE RESPIRATORY

BRONCHIOLES (RESPIRATORY PORTION)

TERMINAL BRONCHIOLE

RESPIRATORY PORTION

• STRUCTURE = TERMINAL BRONCHIOLES, + ALVEOLI

• LOW SIMPLE CUBOID, INERRUPTED BY ALVEOLAR (SIMPLE SQUAMOUS EPITHELIUM)

• THIN SPIRALING CONTINUES SMOOTH MUSCLE AND ELASTIC FIBERS

• TERMINATES IN ALVEOLAR DUCTS, ALVEOLAR SACS, AND ALVEOLI

RESPIRATORY BRONCHIOLE

ALVEOLAR DUCTS & ALVEOLAR SACS

ALVEOLAR DUCTS • WALLS FORMED BY PULMONARY

SACS + ALVEOLI + SEPTA CONECTIVE TISSUE, COVERED BY FEW BRONCHIOLAR EPITHELIAL

• SMOOTH MUSCLE IN SEPTA

ALVEOLAR SACS• WALL CLOSELY WITH ALVEOLY• NO SMOOTH MUSCLE, BUT HAVE

ELASTIC AND COLLAGEN FIBERS

• PRIMARY STRUCTURAL AND FUNCTIONAL UNIT OF RESPIRATORY SYSTEM

• SMALL AIR SPACE (0.002mm3), TOTAL NUMER APPROXIMATE 300 MILLION (SPONGE-LIKE CONSISTENCY) LARGE INTERNAL SURFACE AREA (DIFFUSION GAS EXCHANGE) , 140 M2 (SINGLE TENNIS COURT)

• Elastic and collagen fibers , between the capillaries support, – collagen fibres wall firmness, – elastic fibres permit expansion and

contraction during breathing.

PULMONARY ALVEOLUS

• OXYGEN RELATIVE LOW SOLUBILITY , RATE DIFFUSION OF OXYGEN: – VERY THIN WALLS OF THE ALVEOLI. THIN FLAT

CELLS (TYPE I CELLS), – NUMEROUS CAPILLARIES

• ELASTIC AND COLLAGEN FIBERS , WEAVING BETWEEN CAPILLARIES SUPPORT .

• A, A respiratory bronchiole, alveolar sac, alveolar pore, and alveoli. • B, Interalveolar septum. • C, Carbon dioxide uptake from body tissues by erythrocytes and plasma. • D, Carbon dioxide release by erythrocytes and plasma in the lung.

SRUCTURE ALVEOLUS

• SIMPLE SQUAMOUS EPITHELIUM

– SQUAMOUS TYPE I >>, MOST EFFICIENT GAS EXCHANGE

– CUBOID TYPE II (SURFACTANT), > LARGE, PALE, <

• INTERALVEOLAR SEPTUM

– SMALLEST AMOUNT RETICULAR AND ELASTIC CONNECTIVE TISSUE,

– NUMEROUS CAPILLARIES (VASCULAR MESHWORK BETWEEN ALVEOLI)

– SEPTAL CELLS, AND ALVEOAR MACROPHAGES (THE “DUST” CELLS)

– ALVEOLAR PORES

• Type I Pneumocytes (type I alveolar cells and squamous alveolar cells).

• LIKE MESOTHELIUM • 10% POPULATION, 95% ACCUPY SURFACE • ALVEOLAR PORES • LATERAL, JUCTION ATTACHEMENT PREVENTING

SEEPAGE EXTRACELLULAR FLUID INTO LUMEN

• Type II Pneumocytes (great alveolar cells, septal cells, and type II alveolar cells)

• 12% POPULATION, ONLY ACCUPACY 5%• CUBOID, INTERSPACED

• MICROVILLI SHORT, APICAL

• CHARASTERISTIC CYTOSOMES SECRETED ONTO LUMEN CONTRIBUTE TO PULMONARY SURFACTANT

ALVEOLAR MACROPHAGE

• directly exposed to any inhaled dust or bacteria • Phagocyte bacteria : acid phosphatase, glucuronidase , and lysozym

substantially higer than macrophages others from peritoneal cavity• Sigaretes smokers, cytoplasm crowded with undigestivble residues • persons with heart disease, pulmonary congesion, contan many

vacuoles filled Hemosiderin (extravasated erythrocytes and degedration of hemoglobin

• free cells migrating over its luminar surface• original,

• transformation of exfoliated epithelial cell, (not from the general mononuclear phagocyte system)

• from stem cells in the bone marrow and transported in the blood as monocyte

• Enter the interstitium of lung transformed into macrophage migrate into lumen of alveoli

• Type II cells (GRANULAR PNEOMOCYTE),

– surfactant, a COATING film of fatty substances

– to lowering of alveolar surface tension. (NO collapse).

• AlveolaR MACROPHAGE (DUST CELLS),

– on internal surfaces alveoli, alveolar ducts, and bronchioles.

– engulf foreign particles (dust, bacteria, carbon particles, and blood cells from injuries).

ALVEOLUSALVEOLUS

Type IType I

TypeType II II

capillarycapillary

Septum:Septum:

macrophagemacrophage

Reticular &Reticular &elastic fiberselastic fibers

ALVEOLUSALVEOLUS

RBCsRBCs

CLINICAL CORRELATIONS

• The smooth muscle layers of bronchioles are controlled by the parasympathetic nervous system.

• Normally, the smooth muscle contract at the end of expiration and relax during inspiration.

• In asthma, prolonged contraction during expiration; difficulty in expelling air from their lungs.

• Steroids and β2-agonists relax bronchiolar smooth muscle (to relieve asthmatic attacks).

CLARA CELLS

• CUBOID ROUNDED APEX (DOME SHAPED), MICROCILIA, • GLYCOGEN GRANULES, APICAL FEW SECRETORY GRANULES (MAY BE

SEROUS SECRETORY CELLS SUBSTITUTING MUCUS GOBLET CELLS• SHORT PROCESSES INTERCELLULAR SPACE• DISTRIBUTED FROM BRONCHI TO DISTAL BRONCHIOLES (50% CELLS

POLPULASION EPITHEL TERMINAL BRONCHIOLI)• FUNCTION ? • BRONCHIOLI: ABCENSE GOBLET CELLS ABUDANCE CLARA CELL

– in bronchioles a need for a proteinaceous lining layer to ensure the potency of these minute tubes < 0,4mm in diameter

RESPIRATORY DISEASES

1. Emphysema

2. Asthma

3. Respiratory distress syndrome (Hyaline membrane disease)

EMPHYSEMA

• ELASTASE OF NEUTROPHYL DESTRUCTION OF ELASTIC FIBERS CHANGE WALLS STRUCTURE GREAT ENLARGEMENT OF AIR SPACE DISTAL TO TERMINAL BRONCHIOLES INEFFICIENCY GASEOUS EXCHANGE

• IN EARLY PHASES , LEAKAGE FLUID FROM CAPILLARIES INTERSTITIAL EDEMAI AND ACCUMULATION FLUID IN ALVEOLI

• ENVIRONMENTAL FACTOR (CIGARETE SMOKING, IR POLUTION).

• INDIVIDUALS, LACK NORMAL BLOOD LEVEL OF ALPHA-AMTITRYPSIN (INHIBITOER OF VARIOUS PROTEASES, INCLUDING ELASTASE)

• Microscopically: the loss of alveolar walls destruction alveolar walls and overinflation Remaining airspaces are dilated.

EMPHYSEMAEMPHYSEMA

SmokingSmoking

Increased elastase from neutrophilsIncreased elastase from neutrophils

Elastic damage in alveolar wallElastic damage in alveolar wall

Wall destruction & alveolar enlargementWall destruction & alveolar enlargement

Respiratorybronchiole

Destruction of alveolar wallsDestruction of alveolar walls& overinflation& overinflation

Alveolus

EmphysemaEmphysema

ASTHMA BRONCHIALE

• ALLERGIES STRONGLY LINGKED TO ASTHMA & OTHER RESPIRATORY DISEASE (chronic sinusitis, middle ear infections, nasal polyps)

• REQUIRE POWERFUL MEDICATION TO CONTROL SYMPTOMS

• ASSOCIATED WITH MAST (LIKE HISTAMIN), EOINOPHYLS, T-LYMPHOCYTES (ALLERGY & INFLAMATION)

• PHYSIOLOGICALLY REVERSIBLE OBSTRUCTION • PATHOLOGICALLY OVERDEVELOPED MUCUS

GLANDS, SCARRING & INFLAMATION (THICKENING OF AIR WAY) AND BRONCHOCONSTRICTION

Obstruction of the lumen of the bronchiole by mucoid exudate, goblet cell metaplasia, epithelial basement membrane thickening and severe inflammation of bronchiole.

Respiratory distress syndrome (Hyaline membrane disease)

• At birth, the infant's lungs expand upon the first intake of breath, and the presence of pulmonary surfactant permits the alveoli to remain patent.

• Immature infants (born before 7 months of gestation) have not as yet produced / inadequate supply surfactant potentially fatal respiratory distress of the newborn.

• Therapy: a combination of synthetic surfactant and glucocorticoid. (synthetic surfactant to reduce surface tension, glucocorticoids stimulate type II pneumocytes to produce surfactant)

• Measurment of amount surfactant in amniotic fluid assess the degree of maturity of lungs in he fetus

• THORACIC CAVITY • SEROUS MEMBRANE, SIMPLE SQUAMOUS EROUS EPITHELIUM• SUBSEROUS CONNECTIVE TISSUE

• >> CAPILLARIES AND LYMPHATICS • <, NERVES IN PARIETAL PLEURA (branches of phrenic and intercostal

nerves), Nerves to visceral pleura are branches of vagus and the sympathetic nerves that supply the bronchi

• PLEURA :– visceral pleura : pleura covers and adheres to the lung, – parietal pleura : adheres to the walls of the thoracic cavity. – pleural cavity : space between visceral and parietal pleura

• SLIGHT SEROUS FLUID (by serous membranes) NERALY FRICTIONLESS THIN LAYER OF CONNECTIVE TISSUE (fibroblast, collagen fibers and several layers of elastic fibers)

PLEURA