RESPIRATORY

SYSTEM
By: Muhammad Afkar Bin Haji Ishak
Content
1) Pneumonia (Streptococcus pneumonia) )
10
Respiratory Malignancies
2)
Pulmonary Tuberculosis
3) Upper Respiratory Tract Infection
4) Bronchial Asthma

5)
Emphysema
6) Chronic Bronchitis

7) Bronchiectasis

8) Pulmonary Embolism
9)
Respiratory Failure
 Pneumonia
-
→ infected lung parenchyma -
inflamed lungs
•

commonly caused by i STREPTOCOCCUS PNEUMONIAE

> Necrotising Pneumoniae

✓ Cavitation & destruction

lung parenchyma
← of
Lobar Pneumoniae Types of pneumonia
lobar consolidation d It
↳ Interstitial Pneumoniae
|
•

exudates from infection clots

•
Invasion of lung interstitium

Broncho pneumoniae
•
patchy consolidations spread
via airways throughout the
lungs

Possiblecausativettgents ( based on CXR )

lobar -
S .

pneumonia ,
Klebsiella , Haemophilus Influenza ,
Gram - ve bacteria

patchy -
Atypical ,
viral , legionella

Interstitial -
Viral
,
Pneumocystic Pneumonia , Legionella
↳ by
pneumocystis jirovecii (fungus)
:

(antony (lung abscess) - Anaerobes ,

Klebsiella , Tuberculosis, S aureus , .

Fungi

staph anaerobes, Klebsiella

Large Effusion - .

Impaired Respiratory Tract Defence

originated from hospital -
antedecent viral resp . tract disease
µ -

impaired mucous secretion / cilia action

Nosocomial ← risk factors →
-
Immunocompromised
↳ Mechanical ventilation ,
-
Age

tracheotomy
↳ Prolonged hospital stay
↳ comatose / stroke

CIinicalmanifestation-Atypn.cat Pneumonia
→ Fever
: •
Milder Sx
Nonproductive cough
•

→ chills
Flu-like No focal infiltration on AIR
symptoms
•
→

•
Extra pulmonary manifestation .
 ÑH0GENE Examination
streptowccuspneumom.ae • VITAL SIGNS

tachypneaytrespiratoryrale-4.HR
-

* congestion
① -
Fever more 0
,
circulate ]
* 4
stages of stage
Normal BP&HR
↳
-

PNEUMONlA_
• PERCUSSION
dullness
}
-

on side of inflammation, pus , exudates

abscess / effusion ✗ abscess
③ f* ②
↳
*
• AUSCULTATION • broncho constriction
redhepatisation

)
-

crackles on inspire
• fibrous blood neutrophil exudates
groom +ve wheeze
→
fibrin pleural ✗ lung
on the
exprn
diplom
-

on ,

surface → rough pleural surface

-
Pleural rub
rub together
④

[
* • CXR inflammation
+
10bar / interstitial pattern purulent exudate forms
- :

(green ) +
blood :X
haemolytic liquid)
dense
agar
-
area

optodnin sensitive ClinicalManifestations_ • OTHER

/Q
/
-
V mismatch " " " → alveoli but 0
,
doesn't
1) abrupt onset w/ single rigor
diffuse

Wheveisthewuteofmfeehon?_
into it → plasma 0,4
Intra
pulmonary shunting
-

+
tissue
hypoxia
2)
① endogenous spread from colonised bloody sputum Investigation
nasopharynx 3)
pleuntic chest
pain
.

microscopy • staining
to distal sites
or
oropharynx Pneumococcal pneumonia
pathogenesis ( pathophysiology )
→

② person to person -

spread through infectious droplets .

→ gramtvedipiowai

culture ( sheep blood ) → green pigments

③ colonisation children their contact
is
highest in & Infection
+
→ macrophages
Iv →
vasodilation
Iv optoc.hn sensitivity
agar
>
susceptible
4-hemolysis)
ILL thermo regulator)9 9 vascular
inflammatory Permeability
Prostaglandin CPGEZ)9 Treatment
•

mediators
to
t t penicillin cell wall inhibitor
*
FEVER transudate
-

synthesis
:( colonisation
-
\ 9 set point bacteria + exudates
temp µ
& + blood + neutrophils exudate vancomycin • inhibits synthesis of bacterial cell
to + -

migration
µ µ
geffn.am ,
wall phospholipid
cold sensation
pruning edema •
cell wall inhibitor + resistant to
Tissue I
µ +
-
-

'" "" M "

destruction
-

( HILLS
* -
obstruction LUNG
consolation
Prevention
i.
Phagocytic µ
-
survival stimulates cough vaccine
centre in medulla
* •
23 valent
-

pneumococcal polysaccharide ( PP5V-23; > ZY10)

x x
• 13 -
valent conjugated pneumococcal vaccine (pcv -13,4410)
productive cough HAEMOPTYSIS
- recommended for :

All children
Lzylo
complication Adults at risk for disease (immunocompromised)
*
• Bacteremia → valvular heart disease
others :
• Extra pulmonary manifestation Meningitis :
,
otitis mediate
sinusitis Haemophilus Influenza vaccine (HIB)
 Manton✗ test → subcutaneous injection of

pulmonary-hiberculos.is É
PPD tuberculin

POSITNE_ ,
if • skin induration > 10mm post 48hr5 U

causative agent Mycobacterium

: Tuberculosis (AFB)
+
.

• Blister formation É
↳
respiratory droplets ,
inhalation .

www.dsen
staining NEGATNÉ
G-lycolipidlipoarabi.no if induration < 10mm

§
virulence factor : mannan ,

( possibly BLEinaon.wea-enedmmuesy.tn )
PATH0GENL continues to

* Lowenstein Jensen agar progress

sputum culture :-, -

µ
,µm ,
manifestation
→ AFB in serpentine cord

CLINICALMANIFESTATON-ly.in/-er1eUkin
12

Management
±
Histopathology ✓

- -

used to
←
Taplin
DIAG-NOSTICFEATURES-suppresshy.gg -
↳ Loss of

appetite .

Distinguish Sx : 1) Loss of weight .

GhonFo÷ Ranke's complex

is Night sweat
iris Night fever

w) whitish sputum → haemoptys.is

tvocalfremitus & vocal resonance
V)

dlt parenchymal consolidation

a
TB →
granulomas → caseous necrosis → fibrosis
PREVENTlON_
?⃝
 Upperkespiratoy-ra-tnfe.tn Influent
virulence factor
Pharyngitis
:

Diphtheria Gram -
ve
capsular polysaccharides
Cocco bacilli
✗ Gram tire cocci
→ Gramtve ↳
Prevention
, ,

Club shaped bacilli

arranged chains Haemophilus Influenzae
-

in

( flora
of respiratory tract ) Hib ( Haemophilus Influenzae
type B) Vaccination .

Streptococcus Pyogenes
-

usually in infant &

elderly
( flora of throat ✗ skin)
Corynebacterium diphten.ae -

main cause of otitis media,

(flora of & "" "
respiratory system
B- haemohgsisj
sinusitis &
meningitis in

bactrian sensitive children

exotoxin
-
-

virulence factor :
F
- -

virulence factor : toxins &

enzymes
main
pathology :
pseudo membrane formation

symptoms : -
→ sore throat Prevention
→
lymphadenopathy vaccination w/ diphtheria toxoid
the like SX
( ppt ) →
→
diphtheria pertussis
-

, ,
tetanus

chronic infection can cause :

-

↳ rheumatic fever

↳ glomerulonephritis
 Pathogenesis Histopathology
Bronchialtslhmapostinih.at sensitization ,

APC presents antigen to

chronic TH2W
inflammatory disease
*
a
-

triggered by a variety of stimuli

the bronchospasm ? It -13

what
triggers IT4 1LT
-

Respiratory Infections f t t
Environmental irritants
stimulates activates stimulate
mucus
•
hypertrophy / hyperplasia of smooth
gland
-

B- cells eosinophils production

muscle cells & Subepithdial mucus .

Drugs ( Aspirin ) Iv
y
• 9 submucosal glands ✗ airway vasculanty
-

Stress exercise , cold air, etc TIGE releases factors

Management
. .

,
that damage bronchial tissue
+
CLASSlFKATl0N_ bmdstofc.recept.rs
on mastitis Anti -

asthmatic
0
Atopic Asthma (Allergen sensitization) I
to
exposure
re
-

type hypersensitivity ( IgE mediated)

/
allergenstimulates
masted degranulation
triggered by environmental allergens
-

to
" SHORT TERM LONG-TERM LONG-TERM
- tree
family history releasing granule contents ✗
cytokines RELIEVER RELIEVER CONTROLLER
Diagnosed w/ skin test / RASTA clinicalmanifestation ( ↳ sodium ↳ long acting
-

identify allergen >

Bzagonist Bz agonist
)
↳ chromogty.cat
.

(acute onset, short duration

Non Atopic Asthma (Allergen sensitization) "" " " (salmeterol
-

o " M0
Corticosteroids
-

Productive "

cough [ non-productive
,

/ hyper irritability of
d 1- bronchial tree
wheeze & > (> ↳ Leukotriene " hated )

viral infection (
eg rhinovirus , parainfluenza)
-
S0B Anticholinergic Receptor
" ""
""

↳ Methylxantine
.

" tremulous
Iv
-

chest tightness Antagonist

↳ pectus
caunatum
viral induced inflammation
-
-

Findings of trapping I barrel chest

air >

µ percussion

MechanismofAchon_
resonance
p×_
affected resp mucosa .

FBC → eosinophilia
I
+ threshold
ofsubepithelialvagallungfxtest-fFVC.EU;FEY/Frc ratio

receptors to irritants
TFRC(f- residual capacity)
.

→ ✗

Asthma
Broncho dilator
Challenge Test
•
Drug-induced → relieved SX
post
-

administration

aspirin sputum → eosinophils

inhibits cyclooxygenase pathway
w/ sparing of lipoxygenase pathway
+
tleukotrienes ( broncho constrictors ) Charcot -

leyden crystals
curschmann spirals
 ^"""[
""" """""""
*
cigarette smoking &
Permanent destruction of the
genetic predisposition
-

airspace distal to the terminal µ

bronchioles
jeutnph.IS ✗ lymphocytes
accompanied bythe

destruction of their wall,

tinflammationlNO.MO.to)
↳ monocytes
restricted to the
1
annus

tcytokines /protease/ oxidants -

Aetiology to
* smoking Clinicalfeatures
* 9- antitrypsin deficiency hereditary protease anti protease imbalance
-

Age L40-6OY/ ) o I be caused

can by inflammation
→ or
congenital "
occupational 4- AT deficiency
-

exposure → xeiastase-xre.co
a'Yrtrapped
by oxidants
&
↳ inhibited
&
Type Oztree radicals
Complications
1) Centriacinar
destruction of bronchioles
( CENTRIACINAR)
-

alw cigarette smoking

OR
dilation that affects respiratory bronchioles
- -

destruction of bronchioles alveolar

,

ducts alveoli CPANACINAR)

⇒ Panacinar
Diagnosis
-
alwa antitrypsin ( anti elastase) deficiency
-

initial distention of the alveolus & alveolar duct Pathology •

Physical examination
bronchioles
which
eventually affects respiratory
-
alveolar damage
I
testify & over -

inflation
Lab
or
Investigations
-
bullae (air pockets)
Voluminous'
lungs
-
-

enlarged airspace
loss of alveolar walls
Both FEV,&FVCt
-

- No fibrosis .

OBSTRUCTIVE

FEVIIVFVC remains slight change

,
.

RESTRICTIVE
 chwnicBronchih.sc/inicaIManifestation- Diagnosis
-
Persistent cough with sputum production
23 months in aHeast2 consecutive yrs .

Aetiology
-

Smoking
-
Recurrent bronchial infection

Pathogenesis
smoking pollutants irritants

Management
, ,

+ +
inflammation
hypertrophy / hyperplasia of ( to ,macw.NO )
bronchial mucous
gland Iv
Iv mucus
+
fhmucous production inflammation / fibrosis
Iv Iv
bronchial obstruction bronchioles narrow
Iv Iv
chronic obstructive bronchitis airflow
obstruction

Pathology

oedematousohyperemic mucosa

-
epithelium squamous metaplasia
- Goblet cells hyperplasia ✗ metaplasia
-
mucus gland hypertrophy
-

smooth muscle cell hyperplasia

-
inflammation ⇒ wall fibrosis
 Bronchiectasis Pathology
Predisposingtrs
-

→ dilated
airways;
permanent abnormal dilation of bronchi
-

& bronchioles dlt muscle may become

✗ elastic tissue
cystic
destruction from chronic necrotizing
infection

Pathogenesis dilated bronchus w/

-

necrotizing inflammation
obstruction
Clinicalfeatures with destruction of wall
infections > -

active chronic inflammation

> " →
COUGH -

epithelial desquamation
inflammation → Fever ✓
squamous metaplasia
-

→ copious foul smelling purulent sputum -

fibrosis ✗
scarring
destruction of → Dyspnoea
wall Management
amnion →
cyanosis
production \ -

stop smoking
necrotizing wall -

hydrate to avoid mucus

buildup .

Complications -

Physiotherapy
Antibiotics
for mucus clearance

during flare ups

-

or L -

permanent dilation •
Haemorrhage -
Broncho dilators
copious purulent sputum -

Lung abscess
v
•

Septic emboli
mucous stasis
•
2° amyloidosis
1
Respiratory failure
•

Recurrent infection
•
(or
pulmonate
lablnvestigati-COPDC.umma-n.se
Pathogenesis

Principlesofmanagement
1) smoking cessation

Bronchodilator
2) Drug Therapy →
→ steroids
→ Antibiotics
→
Muwlytics
3) 02 therapy →
give slowly for chronic
bronchitis ( hypoxic drive)

4) Nutritional Support
Giant bullet my
5) Surgery →

→
Lung Volume Reduction Surgery
→
Lung Transplant
 pulmonaryt-m-bo.sn CIMicalmanifestati-Differentialdiagnosismorphi.to
-
gy
T -

wedge shaped
-

When blood clots multiple or thrombi - dark solid areas

migrate from the systemic circulation to -

Fibrin exudates

the pulmonary vasculature -75% at the lower

lobes

Pathophysiology ✗
Consequence
- loss of normal
architecture

Virchow's Triad :
-

Coagulation necrosis
Thrombus
→
Pathophysiology w/ signs symptoms
Endothelial insane
RBC filed alveolar
-

✗
]
- -

Alteration of flow formation

spaces
Hypercoagu /ability
- .

Emboli detached &

✓ flows in bloodstream

occlusion of arteries
pulmonary
depending on emboli size

Large Medium small 60 -80%1 -

large emboli at main

t t t vessels
main
pulmonary medium sized small
arteries
sized
"" " " "
pulmonary
arteries occlusion
artery occlusion
l
-

occurs at the bifurcation

t t
* heart failure
-

clinically silent
collapse
-

pulmonary haemorrhage
R|SKFA#RS
Cvs
-

multiple emboli overtime

pulmonary infarction ( rare,
-

Saddle emboli
-

µ
-

alternative bronchial blood

( in pulmonary bifurcation PP1Y)
pulmonary hypertension
,

sudden death )
-

Hypoxic death
+
(or pulmonate
pathway of emboli

at lower limb :
at Upper Limb :

Great Saphenous "

Basilic v -

t t
Popliteal v. Subclavian V .

I
Femoral v. Brachitouphah.cn Any 1) prevent thrombi from worsening

mgyyygygyggyyg.my
External # iacv .
1 2) prevent formation of new thrombus

t Superior vena cava

common iliac v.
↳ "

Typesofpulmonaryembotismtlu.NU
A) heart

-
Thromboembolism
-
Fat embolism
- Air embolism
- Amniotic embolism
-

Septic embolism
-

Malignancy
-
Blood clot disorder
-

Blood-borne parasite
 Respiratory Chest wall functions musculoskeletal
cIinicaIPresentation_ Treatment
◦ -

•
Muscles -

myasthenia gravis
◦
Hypoxia
a
syndrome of inadequate gaseous exchange
cyanosis (
-

> 59% deoxygenated Hb) →

supportive therapy
.

Guillain →
- -
Barre syndrome
muscle dystophies CNS confusion /
-
→
depression
-

02 supplementation
types -
myopathies
oxygenation failure →
Respiratory distress mechanical ventilation
Rupture diaphragm
-

→ -

ECMO
1) Path Dyspnoea
*
< 60
mmHg
-

•
Skeletal *
Tachypnoea ( Bronchodilator)
2) Paco, > 60 mmHg Calw hypoxia) -
Fractures *
Accessory muscle
_

Drugs
usage
↳ ventilation failure -
TUMOUR
COMPONENTS THAT AFFECT
-

Kypho scoliosis ◦
Hypercapnoea ( Paco ≥
> 45mm
Hg)
→
Lung transplantation
REs0N9RAT0RYe • pleura
→ CNS confusion /
depression
◦
Nervous Control -

pneumothorax
→ warm &
dry peripheries
chemo
-

Hydrothorax / haemothorax → bounding pulse

receptor regulation of breathing with
-

central
→ Pypsnoea
modification
◦ Alveolar dysfunctions
•
Centrally
CNS depression
Pulmonary fibrosis, interstitial lung diseases
Investigation
- •

drugs
→ • Asthma
→ infection • Bronchitis 1) determine whether the patient has
Emphysema respiratory failure by :
central
sleep
•
→
apnoea
•
Atelectasis
•
Peripherally •
Alveolar flooding -

pulse oximetry
oedema
-
Nervous conduction defect
→
Pulmonary _

capnography
→ Pneumonia
Arterial Blood
ARDS / acute lung gas
-

conduction
Disruption of nervous → injury
•

Trauma cervical spinal injury

possible causes by
→
2) determine the
-

myelitis
Pulmonary
Transverse
→ ◦
circulation .

◦
Bed side
clinical examination
Pulmonary
-

• embolus
◦
Airway Passages -
peak expiratory flow rate ( PEFR)
Obstruction • V/Q mismatch bronchos
•

copy
-

-
Extrinsic compression • Shunts
Shock
→ Tumour
Trauma strangulation
•
◦
Laboratory
cardio
Genie
→
-

→ obstructive sleep apnoea

→ -
culture sensitivity
& -
bacterial

Intrinsic
→ septicaemia
-

Immunological tests
lung volume flow rate)
compression
-

test (
Hypovolemic Lung function
-

→
collapse of structure -
trachea malaria → ,

→ Tumour
→ oedema of mucosa
-

burns , infection
, epiglottis
°
Imaging
-

Luminal obstruction
-
CXR
-

CT scan
→
Foreign -
MRI
→
Passages disruption
• Trauma - transection - Ultrasound
-

Radioisotopescan
 Squamous Cell Carcinoma
Respiratoryma-ignan.es
•

Clinicalmanifeslation staging
→
•
rapid growth
•
well -10 poorly differentiated SCC
• keratin & desmosomes
present
↳ Cough LOW
, ,
chest pain
, dyspnoea

Respiratory Neoplasm Haemoptysis

↳
↳ 4 tumour cells)
sputum production ( contain
↳ Focal atelectasis , bronchiectasis, abscess
emphysema ,
pulmonary
← Vena cava
UPPER LOWER intra parenchymal mass
↳
Superior syndrome
•
cauliflower like
Neuritis
-

↳ Pericarditis
↳ Nasopharyngeal ↳ Squamous cell
•
Fung ate into bronchial lumen
spread
,

• Extension to
pleura ✗ LN → distant ↳ Horner 's
↳ syndrome
↳ Laryngeal Adenocarcinoma
( ADH ACTH PT1-1RP)
↳ Para neoplastic syndrome , ,

↳ small cell carcinoma

↳ Hoarseness ( recurrent laryngeal nerve )
↳ Large cell carcinoma
Adenocarcinoma
Nasopharyngeal carcinoma Riskfactors
☐
•

→ • well differentiated
Tobacco
Glandular elements
smoking
• •
→ Keratin
•
icing squamous cell carcinoma • Mucin -

producing gland cells

keratin
non
icing squamous cell carcinoma Industrial Hazards
• -

• undifferentiated
• Basaloid Squamous cell carcinoma •
Air pollution
c-
intra parenchymal mass
cauliflower like
Molecular
genetics
• -

•
Fung ate into bronchial lumen

Can be
• Extension to
pleura &LN→ distant spread
proliferative
••
,
ulcerative or infiltrate've
✓
complicahondeftec.to
Small cell Carcinoma Pathogenesis -

→
Clinicalmanifestation Multistep in which
process gradually accruing sequential
•
" "
• Classic oat cell
genetic & cellular
↳ nasal Sx : bleeding ,
obstruction and , discharge • small blue ,
oral + round cells , changes result in invasive tumour
↳ Ear scant
moulding
Sx :
infection deafness and tinnitus
,
cytoplasm ,
nuclear
format on
↳ Headaches Dense core neuro
secretory granule
• -

↳ cervical LN enlargement ↳ driven by genetic / epigenetic damage dlt chronic

↳ related to Epstein-Barr Virus ( EBV )
to tobacco
exposure carcinogens .

o
Laryngeal Carcinoma Arise
~ ↳
oncogenes
-
activated point mutation gene
via
,
⑧ in
major bronchi or

alw alcohol ✗ asbestos

smoking
amplification or chromosomal
periphery of the lung
-

, in

L Most
•
squamous cell carcinoma
•
malignant
rearrangements
Metastasize
• Presence of keratin pearl
•
widely
Massive tumour • Derived from neuroendocrine
giant cells
•

↳ Tumour inactivated
by lossof
cells of the bronchial
epithelial
suppressor gene
Lablnvestigafions
-

inn
,

Carcinoma parental allele &

☐
Large cell one

•
supraglottic glottis ,
✗
subglottic mutation / abberant
lesions
→ •
Anaplastic large polygonal
, ,
cells
with vesicular nuclei
enlarged ulcerated &
methylation of target
• Lesions are ,

fun
gating • Giant cell carcinoma Clear cell
,
carcinoma ,

spindle cell carcinoma

suppressor gene the

Management
in

Clinicalmanifestation remaining allele .

↳ Dysphonia / aphonia L At
↳
Dysphagia / Dyspnea •
cauliflower like -
intra parenchymal mass

↳
•
Fung ate into bronchial lumen
Aspirated ,
blood -

tinged sputum • Extension to

pleura & LN → distant spread
↳
Fatigue ,
weakness , cachexia
↳ Pain
↳ Halitosis
Good Luck
Guys !!!

µ
see
year 3-
you in
-
201 I. patient ( pursed lips ) 202¢
has emphysema 1 .

Streptococcus pneumonia
Pathogenesis
source Infectious droplet
>
*
'

cigarette smoking & :

> Fat embolism /

a w pelvic & long
genetic predisposition
/ airborne
bone fracture
M0T :
.

↓
Is
↑utnPʰ'
.

lymphocytes
↑ inflammation ( NO
, MQLO) V. Factor ÷
↳ monocytes
↓
↑
cytokines / protease/ oxidants
↓ *

Asthma colonization
:

protease anti protease imbalance

-

migration

↓ can be caused by inflammation

deficiency
Tissue
congenital
-
-
.

- _
or
destruction
× , AT
-

*
↳ inhibited oxidants & Phagocytic
by
:

↓ 02 free radicals
survival

destruction of bronchioles
*
-

( CENTRIACINAR)
-
OR -

destruction of bronchioles alveolar

,
*
duct & alveoli CPANACINAR )

2 .

4.
Tachypnea
Infection
Myocardial
→ macrophages vasodilation
↑ plasma CO2 -7 stimulation → ↑HR ↓ ↓ ↓
ILL thermo regulator)↑ inflammatory
↑ vascular

Exertionat Dyspnea Prostaglandin CPGEZ)↑ mediators

permeability
↓
↓ ↓
¥ᵈ
" transudate
✓ / Q mismatch → hypoxia ✗ hypercapnoea → excessive stimulation
\ ↑
temp set point bacteria
+ " " d-'
+ exudates
neutrophils
↓
exudate
↓
of respiratory centre
↓ ↓
cold sensation
↑ mucus edema
↓
↓ ↓
CHILLS obstruction LUNG
-
↓ CONSOLIDATION
Barrel chest stimulates cough
-

centre in medulla

↓ Lung elastic recoil ↑ total

lung capacity
→ ←
✓- Productive cough HAEMOPTYSIS

trapped lungs hyper inflated lungs ( barrel chest)

-
→ air in →

3. FVC Total amount of 5

exhaled
complications
:
air
forcefully
'

after deep inspiration Bacteremia → valvular heart disease

FEVI Total amount of air exhaled with force

:
breath at 1 in one second .
◦ Extra pulmonary manifestation Meningitis :
,
otitis media &
sinusitis

FE4 reduced dlt the airway inflammation causing obstruction on

the 6 allwall synthesis inhibitor

air
escaping lungs
.
.

4. 37.5L Itis used to determined whether the 7 Prevention

, patient is .

obstructive vaccine
experiencing a restrictive or
lung disease .

•
23 valent
-

pneumococcal polysaccharide ( PP5V-23,244)

• 13 -
valent conjugated pneumococcal vaccine (pcv -13 ; < Zylo)
recommended for :

All children <

ZY10
Adults at risk for disease (immunocompromised)

others :

(Pathogenesis )
Haemophilus Influenza vaccine CHIB)
 Small cell Carcinoma
201£
0
1 .

" "
• classic oat cell
• small blue ,
oval to round cells ,

scant
cytoplasm ,
nuclear
moulding
Dense core neuro
secretory granule
• -

~
⑧ Arise in
major bronchi or

in periphery of the lung

Most
•
malignant
Metastasize
•
widely
• Derived from neuroendocrine
cells of the bronchial
epithelial
lining

≥
haemoptysis : due to tumour obstruction
on
airway → stimulate
cough centre @ medulla
-
→
haomoptys is

cachexia tumour :
produces cytokines macrophages ,

TNFX & It -1 → ↑ protein catabolism

produces
↓ fat & ↑
fatty acid mobilisation
→
synthesis

clubbing :
MegaKay ◦ cyle undergo fragmentation
within
pulmonary capillaries →
platelets produced
→
bypass lung capillary network → enters systemic
circulation →
impacts fingertip circulation →
platelet aggregation MegaKay ◦ cyle clumping
&

→ PDGF & VEGF ↑ → ↑ blood flow

✗ connective tissue clubbed
" "
• classic oat cell
• small blue ,
oval to round cells ,

scant
cytoplasm ,
nuclear
moulding
Dense core neuro
secretory granule
• -