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CHEST
Anatomy
N.B.: to find a certain rib: Midclavicular line (MCL).
Find angle of Lewis 2 rib.
nd
Anterior axillary line (AAL):
Find last rib from the back 12th passes through anterior axillary
rib. fold.
Find apex of scapula 7th rib. Midaxillary line (MAL) خطططط خياططططة
القميص
N.B.: the rib is followed by its space Posterior axillary line (PAL):
downwards. passes through posterior axillary
fold.
N.B.: Vertical lines: Scapular line (SL): passes
Midline (ML). through apex of scapula.
Parasternal line (PSL). Paravertebral line (PVL):
midway between ML and SL.
Oblique fissure:
o Starts from T2
o Move parallel to medial border of scapula (while patient rising his arms
up) till MAL at 5th rib.
o Move forwards and medially till MCL at 6th rib.
NB:
o T2: below T1 below C 7 to get its process tell the patient to flex his
neck; it will be the most prominent.
o When the examiner asks you to examine lower lobe examine back.
o Lateral view of right lung is the best to see the 3 lobes.
o To ML at 4th rib
Kronigs Isthmus:
o Apex apex of lung
o Base 4 pints:
1. Sterno-clavicular junction.
2. Spine of C 7.
3. Junction between lateral 1/3 and medial 2/3 of clavicle.
4. Junction between lateral 2/3 and medial 1/3 of spine of scapula.
NB:
Right lung Left lung
Upper lobe: Apical Apical
Anterior Anterior
Posterior Posterior
Superior lingular
Inferior lingular
Middle lobe: Medial No middle lobe
Lateral
Lower lobe: Apical basal Apical basal
Anterior basal Anterior basal
Posterior basal Posterior basal
Lateral basal Lateral basal
Mediastinum:
o Upper: presented by trachea, affected by lesions to upper ½ of lung.
o Lower: presented by cardiac apex, affected by lesions to lower ½ of
lung.
Histology
o Trachea main bronchus lobar bronchus bronchioles respiratory
bronchioles alveoli.
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Monomolecular layer is responsible for sliding and adhesion between the 2 pleural
layers.
For you: Capacity of thoracic cage is 5 liters while capacity of lungs is 1 liter. In
spite of that, there are impressions for ribs on lung surface. This is explained as
follow:
At birth capacities are equal.
During life, hard tissue grows faster than soft tissue. Monomolecular layer of pleura
pulls thoracic cage inwards and lungs out wards making both of them stretched and
making capacity of both 2.5 liters.
After death, when we dissect they have their real capacities.
Physiology
Respiration is controlled by:
1) Chemical control:
a) Inspiration ↑ O2 -- R.C. Expiration.
b) Expiration ↑ CO2 ++ R.C. Inspiration.
Inspiratory Expiratory
Active Passive
Need muscle contraction Depends on recoil tendency
Homogenous air flow 80% of air in 1st 1/3 time
20% of air in last 2/3 time
Pathology
Bronchial Diseases:
o Bronchitis o B.A.
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o Bronchiectasis o Bronchopneumonia
o Bronchogenic
carcinoma+bronchial edema
Pulmonary diseases:
diseases
o Consolidation o Lung fibrosis
o Emphysema o Lung collapse
o Cavitations
Pleural diseases:
diseases
o Pleurisy
o Pleural effusion
o pneumothorax
Bronchitis:
• Inflammation of bronchial mucosa: edema+ hypersecretion generalized
narrowing in proximal bronchi.
• It is chronic if occurs for 3 months in 2 successive years.
• Chronic bronchitis is usually associated with emphysema together called
COPD (chronic obstructive pulmonary disease) or COLD (chronic obstructive
lung disease) or COAD (chronic obstructive airway disease).
• May be associated with B.A or bronchiectasis.
N.B:
- Cilia spill mucous and distribute it.
- Ciliary dysfunction mucus accumulation COPD, and
predisposes to infection destruction of bronchial wall become
thin:
o Dilatation (bilateral and basal [anaerobic
infection])
o Surrounded by consolidation, fibrosis and
collapse.
o Filled with pus ( suppurative lung syndrome)
and blood ( bronchiectasis sicca hemorrhagica)
Bronchial Asthma:
• On 1st exposure to antigen formation of IgE without Ag-Ab reaction.
• On 2nd exposure Ag-Ab component fixation degradation of mast cells
liberation of chemical mediators distal bronchi: bronchospasm, edema
in mucosa and hypersecretion generalized narrowing of peripheral
airways.
N.B: Generalized narrowing in B.A. is more severe than in bronchitis due to
broncho-spasm and distal bronchi have been already narrower.
• Course:
o During attack: severe dyspnea, wheezy chest
o In between attacks: complete free.
Chronic bronchitis
B.A.
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Consolidation:
Alveoli are filled with fluid, cellular exudates and fibrin.
Causes:
o Pneumonia (broncho-, lobar-)
o Bronchiectasis
o Around lung abscess.
Emphysema:
Compensatory
Localized due to partial obstruction
As part of COPD
Mechanism:
Inhaled micro-organisms contain lipase to digest fat, amylase to digest CHO,
protease (α1 trypsin) to digest proteins, but α1 trypsin of micro-organism is
inhibited by α1 anti-trypsin. Smoking decreased synthesis of α1 anti-
trypsin, and accumulation of monocytes containing α1 trypsin leading to loss
of recoil tendency hyperinflation (emphysema).
NB: smokers suffer from emphysema and chronic bronchitis.
COPD:
Type A:
o Emphysema > chronic bronchitis.
o Pink puffer المريض أحمر وينافخ
o Inflation rupture of interalveolar septa decreased surface of gas
exchange
Decreased O2, increased CO2 stimulation of R.C. wash
CO2, increased O2 pinkish.
Tachycardia puffer.
Type B:
o Bronchiectasis > emphysema.
o Blue bloater المريض منفوخ وأزرق
o Breathing is difficult due to bronchitis cyanosis blue.
o Acidosis due to increased H2CO3 increased H+ acidic urine +
increased Na+ reabsorption together with its iso-osmotic water
bloater.
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Cavitations:
Filled:
o Cyst
o Abscess:
Pyogenic
T.B.
Amebic
Empty: old abscess.
Lung fibrosis: narrowing.
Lung collapse:
Compressive:
o Pleural effusion
o Pneumothorax
Obstructive:
o With obstructive main bronchus:
Tumor
F.B.
Fibrosis
o With patent main bronchus:
Hypersection.
Pneumothorax:
A. Closed: forced cough rupture of alveoli into cavity. If
emphysematous rupture of emphysematous bullae more serious
condition.
B. Open:
Trauma:
• Stab wound
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C. Tension pneumothorax:
Cause: stab wound at angle, where the 2 holes not opposing
each other.
In inspiration: air enters inside pleural cavity.
In expiration: air is trapped as 2 holes not opposing each other
+ve pressure.
NB: Closed regressive course: air is absorbed.
Open stationary course: air ↔
Tension progressive course: treatment by making open
pneumothorax.
D. Hydropneumothorax.
Local Examination
1) Inspection:
a) Skin:
i) Dilated veins:
(1) SVO, commonest, due to tumor, thrombus.
(2) IVO.
ii) Scar: right and left thoracotomy: in lobectomy or pleurectomy.
b) Chest Wall:
i) Shape:
NB: For inspecting shape, look from foot side while patient lying on flat bed
and watch carefully right and left antero-posterior length.
(1) Symmetrical:
(a) Elliptical: antero-posterior: Transverse =5:7 (normal shape).
(b) Barrel shaped= permanent inspiratory position:
Antero-posterior≥Transverse ≈ 1:1
Wide subcostal angle.
Horizontal ribs.
Wide intercostal spaces.
Cause: hyperinflated chest (clinical term), e.g.: Emphyema which
is pathological term.
(c) Pigeon chest=Pecten Cranium:
Causes:
Hard tissue: Rickets, osteomalacia.
Soft tissue: severe precordial bulge (RVE), hyperinflation as
COPD since childhood.
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NB: to say: this is a ricketic chest, must be there one of two signs:
Harrison sulcus + rosary beads.
Harrison Sulcus:
- In healed rickets
- Diaphragm originates from lower ribs. In inspiration, diaphragm
pulls cartilaginous parts inwards forming a sulcus at costal margin,
even in healed rickets.
Rosary beads:
- Normally costal cartilage proliferates from adjacent to bone then
ossifies.
- Here, growth of cartilage without ossification masses in vertical
lines.
- When patient recovers atrophy of them.
If severe:
Disturbs anatomy of:
• Heart H.F.
• Lung R.F.
Press on the R.V. picture of constrictive pericarditis.
(e) Flat (alar) chest: For examination: only mentioned with pulmonary
T.B.
(f) Kyphosis: if severe, it disturbs anatomy of heartH.F., Lung
R.F.
(2) Asymmetrical Chest:
ii) Movement:
(1) Type:
In males, diaphragm is dominant abdominothoracic breathing.
In females, intercostals muscles are dominant thoracoabdominal
breathing.
Bradypnea Tachypnea
Pontine hemorrhage +
H as CO2 cannot
Increased intracranial cross BBB
pressure ↓R.C. CO2 + H2O H2CO3 ↑R.C.
Barbiturate toxicity HCO3-+H+
Morphine Acidosis and
Severe hypoxia stimulation of R.C.
Acidosis:
- Metabolic hyperventilation (rapid+deep)
In:
Diabetic ketoacidosis
Uremia
Excessive acid intake (salycylate poisoning)
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N.B.: In herpes zoster, in the first 24 hours no signs, only severe pain, so patient go
to internist doctor not to dermatologist.
o Rules:
- Comparative
- By the same hand
- Tips of fingers directed laterally
- Sites:
• Supramamary, mammary, inframammary
• Upper, middle, lower axillary.
• Supra-, inrascapular on both sides, interscapular.
- Each time tall patient to say أربعة أربعة
o ↑↑ TVF:
- Consolidation:
o Pneumonia
o Bronchiectasis
o Around lung abscess
- Lung cavity: large, superficial, empty, connected to a bronchus.
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g) Palpable Rhonchi:
o Rules: as TVF but ask patient to take deep breath.
o Causes:
o Bronchitis
o B.A.
o Fibrosis
o F.B.
o Tumor
o Secretions (air way obstruction).
h) Pulsation: see inspection + cardiology.
i) Expansion:
i) Apical يامنّيل Method:
ii) Basal: o Take skin fold medially.
(1) Anterior (infrasternal). o Ask patient to breath.
(2) Posterior (interscapular). o Notice widening.
3) Percussion:
o Rules:
Comparative
From up downwards
Horizontal pleximeter in intercostal spaces, nut horizontal or vertical
in paravertebral.
Light percussion except the back heavy.
o Sites:
Lungs:
Apex:
o Vertical pleximeter from behind patient.
o Normally resonant.
o Causes of dullness:
- apical fibrosis
- apical collapse
- apical tumor (Pancoast tumor)
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