PULMONARY DISORDERS

"
RLD PERRY
"
"

COPD OBER

/
_ _

" "" "" " "" "" " "" " """" "" """" """"
" "
-
problem i EXPIRATION -

problem i INSPIRATION

① CYSTIC FIBROSIS ① ATELACTAS15

② ASTHMA ② PNEUMONIA
③ BRONCHIESTASIS
"

③ TUBERCULOSIS
"
APT 41' sa Bra
④ EMPHYSEMA ④ PULMONARY EDEMA
⑤ CHRONIC BRONCHITIS ⑤ PULMONARY EMBOLISM
⑥ PLEURAL EFFUSION
⑦ PNEUMOTHORAX
"
"
Come And BE chronic

⑧ SARS (severe Acute Respiratory syndrome)

⑨ BRONCHOGENIC CARCINOMA

(GENERALPAH0PHYnowI
STIMULANT / IRRITANT changes in
↓ lung tissue and pleura dlt :

fluid build-up in pleura or alveoli

inflammation of airways
•

↓ inflammation
•
chronic
•
tumor ; emboli
↓ • alveolar affectation

↓ dec mechanical compliance of lungs

narrowing
= obstruction of airways .

↓ ↓
destruction of alveolar { bronchial walls ↓ dec lung
.
expansion
↓ ↓
↑ mucus production et retention Hypoxia dlt low Oz in tissues

① chronic cough ① dyspnea / SOB

② flattened diaphragm ② irritating dry , ,
non -

productive cough
③ cyanosis ⑤ wasted , ab ⑧ thin / weak appearance
④ digital clubbing VC air that be Maxtipp Max INSP

{
:

④
can

⑧ barrel chest
↓ IRV amt.cn
: : air that can be INSP 1510⑧ INSP
TLC : air contained in
lungs 15 Max INSP
(4) A) problem e- ANSPI RATION
dlt deficient lung expansion
 COPD
Kandi nag
Anastomoses →
nag Hemoptysis
-

① CYSTIC FIBROSIS "

② ASTHMA
hypersensitivity ③ BRONCHIESTAgyg
• :
"

description Honeycomb lungs

"ʰᵈ¥ • description : chronic inflammatory
-

condition w/ e •
description : irreversible
"
DILATION "

of the mainstem bronchi / bronchioles

,

•
etiology detector
:
CTFR gene causes WIDESPREAD BRONCHOSPASM / constriction) •
etiology repeated epithelial
:
wall infections
damagewetdltsecretions
:

↳ ix. regulation of ↳ accumulation of mucus and

Na et Cl entry •
etiology :
exposure to stimuli /dust , pollen)
↳ 5 this there is an
,

↑ mucus production

pathophysiology :
•
pathophysiology : •

pathophysiology :

Naetcl channels BRONCHO SPASM recurrent difficulty stagnation

A) abnormal CTFR gene stimuli inflammatory INFECTIONS
→
i
→
of mucus

regulated
→
not →
constriction pulmonary walls
expelling mum,
→ are
response - -

post surgery
-
in

membrane Na et Cl ions narrowing of thickening et ANATOMOSES

pulmonary
↓
permeability ←
cannot enter cells ↓ pulmonary airways ←
epithelial wall damage
↓ un bronchial , ← £
ycells
✓ dehydrated
pulmonary blood vessels
↳ coughing of blood occurs when
wall damage
↑ Production
are

/ Hemoptysis)
→
of the anastomoses is damaged hallmark
Na) ←

]
( µ, * 11ms mucus
mucus

lung obstruction ←
plugging 4

• SYMPTOMS :
• SYMPTOMS : • SYMPTOMS :

① Honeycomb lungs 1. TRIAD : ① Wheezing ← dltbnnchoconshiitim ① HEMOPTYSIS ← hallmark

② Coughing marmot
Salty sweats
"
Sweat Test ↑
"
② Na et Cl ② wet
←

production cough / font smelling)

:
mucus

③↑ appetite but poor ③ Dyspnea ③ purulent sputum / pus filled )

weight gain -

④ bulky font , smelting stools II. Others : tachypnea

use of awning mm .
For breathing
knrschmann 's spirals -
twisted mucus characteristic
 COPD
ati Issues
④ EMPHYSEMA air avg.ff.ir
tapping "
respiratory bronchioles ⑤ CHRONIC BRONCHITIS
:{ alveolar ducts
↳

•
description distention
:
-
of respiratory zone alveolar sacs •
description cough that
: lasts for 3 months only
alveoli but is observed for 2 consecutive
years
•
etiology :

""
① ohmic exposure to environmental irritants initio
② nicotine *
mainly affects MAINSTEM BRONCHI → bronchioles
③ AAT deficiency
↳ protein that protects lung tissues
↳ collagen
↳persuasion
etiology prolonged exposure to irritants
• : →
of mucus
•

pathophysiology : •

pathophysiology :

chronic soft time time chronic ① scarring of bronchial lining

inflammation
→ → PMm9eᵈ exposure
inflammation
]
destruction remodeling to irritants → →
② ↑ bronchial wall thickness

NARROWING ←
loss of
←
destruction of
<
③ hypertrophy of mucus glands
elasticity ELASTIN
C > air tapping → orerdistention
a- alveoli structure
→ pathologic
dead spaces Hypoxemia ←
obstruction of airflow
reduced airway clearance ←
↳Perseeretion
of mucus
↓
* the structures are ↳ overdistended alveoli d /t mums
will no longer
STRETCHED beyond undergo
⑨ respiration
their normal
dimensions

• SYMPTOMS :
• SYMPTOMS :

" " " "

① Pink puffers _ a) pink skin upon SOB ① Blue Bloaters

-
d /t A) peripheral cyanosis et edema @ LE
L lips
, fingertips
② Prominent / hypertrophied production larger built i A) BLOATING
}
accessory mm .

dit ↑ TNF :
② A)
A) thin /asthenic -
asthenia
A) barrel chest
weight-loss ③ A) ⑨ ventricular hypertrophy
-

( unintentional wt loss)
-
-
cachexia .

③ Tripod position dit difficulty breathing ④ pooling of blood

A) i

"

④ Hyperinflated
"

lungs ⇐ air tapping

⑤ small heart / lungs appear larger) ✓ ④ chest lung size ; diaphragm shape
;

⑥ flattened diaphragm
RLD
↓ dei alveolar
"
lung collapse /alveoli )
"

① ATELACTAS15
" "E"
dit
}
is
: → .

① Primary / compressive)
expansion deflated

/symptoms :
asymmetric chest expansion ② Secondary ( obstructive) -
mk

TYPES :
① Bacterial strep pneumonia lmk)
② PNEUMONIA
}
:

:
inflammation of alveoli dlt infection ② Viral

/symptoms chin!;
:
' ther ③ Aspiration
chest pain
④ Hospital Acquired "
""
ai
③ TUBERCULOSIS : inflammatory condition of the
lungs dlt MYOBAUTERIUMTUBERCUUAE -

① PHASE I infection flu likes×

|8YMPJMg
: -

2 PHAGES :

② PHASE II flu-like sx ; ↓ weight ; hemoptyris ;

: it> night sweats
""
↑M
④ PULMONARY EDEMA : ↑ fluid build up in -

lungs dlt alveolar capillary permi ability

-
pressure aosaiahedi ⑥ eat
↳
|Ñ) ① A) crackles It] crackles
:

② sputum pink et frothy :

⑤ PULMONARY EMBOLISM :
HI dihoged thrombus occlusion necrosis
to pulmonary a- mutation
= →

acute
migrates
!!!
pain
KIMANI ?cough
,
:

inflammation of pleural wall

⑥ PLEURAL EFFUSION
"
Plcuritis
"

}
:
out pleural +mid accumulation P tube insertion @
-

sharp dull pain

|sYMPT0M ↳ 8- 9th 1cg
,

: A) pleural rub 1+1 pleural rub

doorstop breathing

⑦ PNEUMOTHORAX :
gas /air inside pleural space → bln parietal d- visceral pleura

}
p tube insertion @
-

/symptoms
sharp Pain
: 2- 3rd Ics
breathing
doorstop

⑧ SARS (severe Acute Respiratory Syndrome) :

coronavirus
fever is one throat
|sYMPT0M -

.
myalgia ; lethargy
dry cough
causing airway obstruction
⑨ BRONCHOGENIC CARCINOMA :
"
lung cancer
"
:
malignant tumor = compression of lung tissue
thorough
lgympyom.CI
types : ① small cell Fatal
: unexplained wt loss .

(4) ←

hemoptyris ② Oat cell

hoarseness
③ squamosalI ← MIC
 .am/. . . m. . . .
11 . ANCIWARY PROCEDURES 111 .
PT ASSESSMENT
① chest x-ray ① General Appearance
a. Body Type / Posture / Appearance
② pulmonary function test b. Evaluation of neck mm activity
: .

hypertrophy of accessory
③ ECG (for pulmonary edema)
mm .

C. Evaluation of chest symmetry

or

congenital defects
from f) Peons EXCAVATUM
IV. TREATMENT programme eins CAMMITUM
' "

ÑAT : ① provide
ongoing secretion removal ② Breathing : PATTERNS / SOUNDS
-

dyspnea _
crackles /rates) : att secretions
② promote SELF MANAGEMENT
- " -
tachYpnea wheeze airway obstruction

Breathing
_
:

-
bradYpne9 stridor ↑ pitch wheeze
via
µWE
-
:

Apnea ↓ pitch /
wheeze snore like
-

Cheyne stokes
A. MEDICAL
-

-
Biot 's
cessation most important intervention
① smoking
←

broncho dilators
② medications :

steroids ③ Auscultation
anti histamine
④ Tracheal Position
-

ventolin / albulerol

③ Oz fat should be maintained ⑤ GMWT

B. PT TREATMENT

① AROME
②
strengthening ex .
-

high resistance low reps ,

⑤ Breathing ex 12-3 reps)

a.
Diaphragmatic breathing
↑ intra bronchial Pressure
b. Pursed lip -

breathing :

c. Segmental breathing
8-10 gulps
d. Glossopharyngeal breathing :

:
* air

more" clear
③ Double tough : 1st 1 secretions ) → 2nd / airways)
;
④ Postural Drainage :
20-30 mins

}
3 manual techniques : > UPPER LOBE
APICAL :/ can back
a. percussion
• SITTING
[posterior : lean forward

supine *memoir
b. vibration
-
•

c.
shaking > LOWER LOBE
""

÷:
Trendelenbnrg
:(÷:÷÷} "¥yin9Tp%%
POSTERIOR : prone

LATERAL
'