pathologies of lung,respiratory disorders

1. THE LUNG BY
DOCTER.PUGAZHENTHI RAVICHANDAR

3. INTRODUCTION:
• the respiratory system is an outgrowth
from ventral wall of foregut.
• the right bronchus is more vertical than left
bronchu and directly lies in an line of
trachea.
• the foreign material such as
vomits,blood,foreign substance tend to
enter right lung more than left lung.

4. • branching of bronchi forms
bronchioles(lacks cartillage and
submucous glands as in brnochi).
• branching of bronchioles forms terminal
bronchioles which are less than 2mm in
diameter.
• the distal part of terminal bronchioles is
called acinus(spherical in structure withb
an diameter of 7mm)
• the vocal cards are lined by stratified
squamous epithelium

5. • cells of alveoli
type 1: they forms structure of wall of alveoli.
type2:they secrecte surfactants

6. • the trachea and bronchi contains
numerous goblet cells and submucosal
gland.
• the average pair of human lungs contains
700 million pairs of alveoli.
• each alveoli is wrapped with capillaries in
which 75% areas of alveoli.
• normal alveoli has an average diameter
200 mm of diameter which can increase
during inhalation.

8. • alveolar epithelium- plate like cells (TYPE
1 PNEUMOCYTES-covering 95% of
alveolar surface) and round(type 2
pneumocytes-synthesise surfactants and
contains lamellar bodies which is involved
in the repair of alveolar epithelium and has
the ability to regenerate type 1
pneumocytes)
• alveolar macrophages-loosely attached to
alveolar spaces that are derived from
mononuclear phagocyte system.

9. STRUCTURE OF ALVEOLAR WALLS
• capillary ENDOTHELIUM- has
anastomising network of capillaries.
• BASEMENT MEMBRANE: the basement
membranes of endothelium and
epithelium are fused together at thinner
portions except in the thicker portions they
separated by an space is called
pulmonary intersistium or intersistial
space.

10. • the larynx,trachea
and bronchioles are
lined by ciliated
columnar epithelium.
• the bronchial mucosa
contains
neurosecrectory cells
such as
calcitonin,serotonin,g
astrin releasing
peptide(bombesin)

12. • the alveolar walls has
numerous pores is
called pores of kohn
which allows the
passage of exudates
and bacteria within
the adjacent alveoli.

13. • tracheal and bronchial anamolies such as
atresia(congenital absence or closure of a
normal body opening or tubular
structure),stenosis(an abnormal narrowing
or contraction of a body passage or
opening;),tracheoesophageal fistula(A
Fistula is a permanent abnormal
passageway between two organs in the
body or between an organ and the exterior
of the body).

15. • pulmonary vascular
anamolies

16. • congenital lobar over inflation
(emphysema)

17. CONGENITAL ANAMOLIES
• hypoplasia of lungs-the defective
development of both lungs in which one
lung is more affected than the others thats
results in decreased weight and volume of
the lung.

18. EMPHYSEMA LUNGS

21. • foregut cysts arises from
the ABNORMAL
detachement of primitive
foregut that are located in
hilum or middle
mediastinum.
• these cysts may be
bronchogenic (most
common), esophageal
and enetric
• the foregut cysts are
lined by cilliated
psedostratified columnar
epithelium.

24. • the walls of the foregut cysts contains
bronchial glands,cartillage and smooth
muscles.
• pulmonarys sequesteration is defined as
the continous mass of lung tissuses
without normal connections to the airways
system.
• extralobular sequesterations refers to the
abnormal lesions in infants whichs occurs
external to lungs such as thorax or
mediastinum.

27. • intralobular
sequesterations
occurs within the
lungs due to
bronchiectasis or
infection occuring in
older childrens.

28. ATELECTASIS
• it is the incomplete expansion of the lungs or collapse
over inflated lungs which produces airless area in lung
parenchyma.
• it is divided into 3 types
1) resorption atelectasis- an complete obstruction of the
airways which leads to resorption(loss of substances by
lysis or physiologic means) of oxygen without
impairement of blood flow to the affected alveolar walls.it
is caused by excessive secrection of mucus or
exudates(a fluid with a high content of protein and
cellular debris that has escaped from blood vessels and
has been deposited in tissues or on tissue surfaces,
usually as a result of inflammation) within the smaller
bronchi .causes:
asthma.bronchitis,bronchiostasis,bronchial neoplasm,

30. 2) COMPRSSION
ATELECTASIS-OCCURS
when the pleural cavity is
partially or completely
filled with
fluid,exudates,tumor,bloo
d or air or in
pneumothorax( when the
air pressure threatens the
functions of the lungs and
mediastinum and major
vessels.

31. 3) contraction atelectasis- local or
generalized fibrotic changes in the lung or
pleura

34. HEMODYNAMIC PULMONARY EDEMA
• the main hemodynamic cause is left sided
congestive heart failure as a result
pulmonary congestion and edema occurs
in lung .lungs are heavy and wet.
• fluids accumulates in the lower lobe of the
lungs bcoz hydrostatic pressure is greater
in these areas
• histologically alveolar capillaries are
engorged and intra-alveolar granular b
pink stains can be seen

37. • hemisideren laden
macrophages is
called heart failure
cells are present.
• pulmonary congestion
is always seen in
mitral stenosis.

38. • the fibrosis and thickening of
the alveolar cause lungs to
become sloggy,firm and brown
is called brown induration
which impairs normal
respiratory functions and
predisposes to infections

39. 2) EDEMA CAUSED BY
MICROVASCULAR INJURY
– due to injuries to capillaries
of the alveolar septa.
– the edema results from
primary injuries to vascular
endothelium or alveolar
epithelial cells which
results in leakage of fluids
and proteins into
intersistial cells(the
interstitium (the tissue and
space around the air sacs
of the lungs).[2] It concerns
alveolar epithelium,
pulmonary capillary
endothelium, basement
membrane, perivascular
and perilymphatic tissues)
and then into alveoli .
– in pneumonia the edema
remains localized and
oftens manifests to
infections.

40. • The oxygen supply of the cells is depended on
pulmonary ventilation, lungs perfusion, on
exchange of respiratory gases and on capacity
of blood to transport the oxygen
• Oxygen is transported from the environment to
the tissues by the following sequence:
• 1. convectional( transmitting)transport till alveoli
(ventilation), 2.Diffusion from alveoli to
pulmonary capillaries, 3.
Convectional( transmitting) transport of airs by
blood to tissue capillaries. 4. Diffusion(high
concentaction to low concentraction) from
capillaries to tissues.
Respiratory system disorders

43. • The main mechanisms of respiratory failure are
the disturbances of ventilation, lungs perfusion,
diffusion or their combinations.
• Ventilation, perfusion and exchange of the
respiratory gases in the lungs are the primary
functions of the cardiopulmonary system.
• Ventilation includes the mechanics of inspiration
and the providing of atmospheric air to the
alveoli, and the mechanics of expiration during
which the air with decreased oxygen and
increased carbon dioxide levels is expired.

44. • The exchange of respiratory gases
depends also on the integrity, thickness
and area of the alveolar membrane(the
site of the gas exchange) ,relative gradient
of gases and their solubility on both sides
of the membrane,the affinity of
hemoglobin to oxygen, and on the
distribution of ventilation and perfusion(the
blood flow enabling the oxygen transport
between alveoli and blood).

46. Pulmonary ventilation and its disorders
• Ventilation(lung ventilation is gas exchange between
atmospheric and alveolar air) of the lungs is a
complex of processes ensuring the transport of air
into the lungs and the expiration of air enriched in
carbon dioxide with low oxygen content.
• During inspiration the thoracic cavity enlarges due to
the contraction of the respiratory muscles. The
inspiration is an active process which depends on
several factors. The expiration is a passive process,
depending on relaxation of inspiratory muscles. The
elastic properties of chest and lungs are important
factors.

47. PULMONARY EDEMA
• it can results from
hemodynamic
disturbances or direct
injury to
microvasculature
which results in
crease in capillary
permeability.

48. • central neural system (respiratory centers
located in medulla oblongata and pons),
sensitive and motoric peripheral nerves,
upper respiratory airways, and lungs are
involved. Lung ventilation disorder takes
place at any of their dysfunction which
decreases at central neural system
impairment causes brain blood vessels
sclerosis and spasm, hemorrhage, brain
compression, intoxications).

49. • Respiratory failure is a syndrome of
inadequate gas exchange due to
dysfunction of one or more essential
components of the respiratory system:
1)CNS or Brain Stem
2)Chest wall (including pleura and
diaphragm)
3) Airways and Alveoli
4) capillary units of Pulmonary circulation
5) Peripheral motoric and sensitive Nerves

50. Respiratory dysfunction related
with the respiratory center
disorders
1)Respiratory centers located in medulla oblongata and pons
(Pneumotaxic center) – provide the certain depth, rate and
rhythm of respirationit depends on CO2 density and PH of
blood.The excitation of respiratory center decreases
at central neural system impairment causes brain
blood vessels sclerosis and spasm, hemorrhage,
brain compression, intoxications).
2)They permanently receive impulses from upper
neural systems – (brain bark, hypothalamus) and
peripheral chemo-, baro-, mechano-, and thermo
receptors

51. • at High temperature respiration gets
frequent as well as certain hormones (e.g.
adrenalin and progesterone) increases
lung ventilation.
• The excitation of respiratory center and
lung ventilation is depended on CO2
density and PH of blood.
• The excitation of respiratory center and
consequently lung ventilation decreases at
central neural system impairment causes
brain blood vessels sclerosis and spasm,
hemorrhage, brain compression,
intoxications).

52. • Chemoreceptors involved in respiratory
regulation react mainly on oxygen density
decrease in blood; In this case ventilation
is increased.
• Vegetative neural system is very
important: by symphathetic prevalence
bronches are dilated, and excess
parasympathetic impulses cause
bronchospasm.
• at inspiration alveoli are stretched,
sensitive receptors are irritated that
reflectively causes expiration (Hering–
Breuer reflex).

53. at inflammation acid exudates increase sensitivity of stretching receptors
and inspiration ends earlier – therefore superficial respiration develops.

54. Ventilation disorders related with
Chest wall dysfunctions (including
pleura and diaphragm).
1)Obstruction in upper respiratory ways
cause respiratory failure of obstructive
type (foreign body, tumor, laryngospasm.
2)Lower respiratory ways obstruction (e.g.
bronches or bronchioles obstruction with
vomited masses, water, and mucus.) also
cause obstructive type of respiratory
failure.

55. 2)Ventilation disorders at lung respiratory
surface decrease are characterized by
severe decrease of external respiration of
restrictive type.
• The lung stretching capacity decrease
restricts alveoli’s ability to enlarge that can
be met at pneumonia, pulmonary
circulation congestion, at emphysema,
fibrosis, some toxic impairments.
• surfactants decreases surface tension in
the alveolis.

56. • Forms of ventilation disorders are:
hyperventilation, hypoventilation.
• Physiologic or compensative
hyperventilation (e.g. at exercise) is an
organism’s reaction to excessive demand
for oxygen and is being stopped when the
cause is eliminated.

57. • Pathologic hyperventilation develops at
respiratory centre excitation during brain
and its membranes’ inflammation.
• Prolonged and severe hyperventilation
causes hypocapnia (deficiency of carbon
di oxide in blood) and alkalosis that
inhibits respiratory centre and cause
hypoventilation.

58. Respiration act changes-types of
breathing
• Normally a man breathes without any
effort paying no attention to the process;
this condition is called respiratory comfort
- eupnoea.
• Bradypnoea is a rare breathing. This reflex
– decreasing breathing rate may be
observed at increased arterial pressure
(reflex from the baroreceptors of aortic
arch and carotidal sinus), at
hyperoxia(tissues and organs are exposed
to excess supply of oxygen)

59. • Polipnoea or tachipnoea is frequent
superficial respiration. Tachipnoea occurs
when there is increased stimulation of
pneomotaxic centres(medulla oblongata
and pons) or excessive inactivation of their
inhibiting factors.
• Hyperpnoea or deep and frequent
breathing develops e.g. at mountain
disease because of oxygen partial
pressure decrease. At this time excess
CO2 is eliminated that cause
hypocapnia(decrease of co2 in the body),
alkalosis, and rarely stopping of breathing.
• Apnea is an absence of breathing.

60. • Dyspnea is a
ventilation disorder
together with feeling
of breathing difficulty.
• it's of two types
1) Inspirational
(prolonged inspiration
phase) and
2)expirational dyspnoea
(expiration process
disorder)

61. –Periodic breathing – it is a breath rhythm
disorder when breaths are separated by
intervals of apnea.
• Cheyne-Stokes respirations occurs in response
to hypercapnia in the respiratory system. The
cycle starts with a smooth increase, in the rate
and depth of respirations followed by a gradual
smooth decrease, in the rate and depth of
respirations ending in a short period of apnea
that can last from 15 to 60 seconds. causes; any
condition that slows the blood flow to the brain
stem because it slows impulses sending
information to the respiratory center,An injury of
the brain above the brain stem,CNS dysfunction,
cardiac failure with low cardiac output, sleep,
hypoxia, hypocapnia.

62. • Biots’ Breathing is irregular respirations with
irregular periods of apnea. There is no cyclic
nature to them as in Cheyne-Stokes breathing.
causes: It may be seen with respiratory depression
and brain damage at the level of the medulla.
Kussmaul respirations, or hyperpnoea, are deep,
rapid respiration with no end-expiratory pause
and indicate the body is trying to compensate for
severe metabolic acidosis .
They have an increased rate and no expiratory
pause. In other words there is no stopping
between inhaling and exhaling.
It is seen in profound metabolic acidosis, i.e.
diabetic ketoacidosis.