6patologi respirasi
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Erna SulistyowatiBagian Patologi PPD Unisma
I. The Upper Respiratory Tract & Ear : • Upper resp tract infections• Epiglottitis• Wegener’s granulomatosis• Allergic reactions• Paranasal & aural polyps• Nasal & aural papillomas• Laryngeal papillomatosis• Squamous cell carcinomas• Lethal midline granuloma• Otitis media• Otosclerosis
II. The Lung
. Bronchial asthma . Pulmonary edema
. Pneumonia . Pulmonary embolism
. Emphysema . Diffuse alveolar damage
. COPD . Hyaline mambrane disease
. Atelectasis . Pneumoconiosis
. Pneumothorax . Sarcoidosis
. Pleural effusion . Bronchogenic carcinoma
. Mesothelioma
I. UPPER RESPIRATORY TRACT INFECTION
Viral nasal cavity & paranasal sinuses = common cold
- mucosa edematous - infilt acute/ chronic inflamatory cells
(2nd inf bacterial : increase in neutrophils)
- excess fluid production
LARYNGOTRACHEOBRONCHITISCx : influenza virus, respiratory syncytial virus,rhinovirus
EPIGLOTTITIS
- viral airway obstruction
- Corynebacterium diphtheriae pseudomembrane in pharynx
Candidosis Epiglotitis
Acute Epiglotitis
Wegener’s granulomatosis- unknown cause- involves : URT, lungs, kidneys- characterized : vasculitis, granulomatous inflamation rhinorrhea, sinusitis, & malaisehistol : necrotizing granulomas, multinucleated giant cells,
chronic vasculitis.
ALLERGIC REACTIONS- edema, eosinophilic infiltration- rhinorrhea and stuffy nose- larynx may be narrowed
INFLAMATORY POLYPS of the nasal cavity & paranasal sinuses- represent polypoid areas of edema & inflamation, with eosinophilic infiltrate.
Ex : infection or allergy
Nasal Polyps
Other benign conditions :
Blockage of the outflow of the paranasal sinuses can lead to a MUCOCELE
LARYNGEAL CYST arises similarly through the obstruction of the draining duct of mucous glands of the larynx resulting in hoarseness
LARYNGEAL NODULE or SINGERS’ NODE is related to chronic trauma of the vocal cords. This nodules vary in histologic appearance depending on their stage of development from edema through fibrosis.
TUMORSA. BENIGN
Benign Squamous Papilloma (BSP) nasal cavity & paranasal sinuses
o Inverted papilloma : is a polypoid growth has invagination of squamous epithel lateral nasal wall & paranasal sinuses, HPV is implicated
o Laryngeal papillomatosis : consists of BSP, seen most often in children, at times obstruct the larynx
o Nasopharyngeal Juvenile Angiofibroma
- profound epistaxis complicates the picture
- may destroy adjacent structures
Histol : BSP consist of fibrous tissue & blood vessels
B. MALIGNANT1. Squamous Cell Carcinoma (SCC) is the most common
- may occur on the nose, nasal cavity, nasopharynx, and larynx
- association with smokingNASOPHARYNGEAL Ca (NPC)
Anaplastic NPC - squamous origin - China >>, EBV related - often become evident owing to metastases Obstructions late in the course of the disease
Transtional Cell CaLymphoepithelioma : poorly diff. SCC from URT area
which has metastasized to a regional lymph nodesLARYNGEAL SCC
- in smokers hoarseness -on true vocalcords & anterior commissure
Histol : leukoplakia to thickening, nodularity, ulceration & infiltration
2. Lethal Midline Granuloma ( Polymorphic reticulosis )is characterized by respiratory tract ulcerating & necrotizing lesions
3. Extramedullary plasmacytomas URT : the nasal cavity, nasopharynx, paranasal
sinuseshistol : plasma cell proliferation
eventually develop multiple myeloma4. Olfactory neuroblastoma/ Esthesioneuroblastoma
- is derived from the olfactory mucosa - produces a polypoid mass- neural crest origin- histol : variable appearance- present with rhinorrhea, epistaxis, obstruction of the
nasal passages- recurrences & metastases are common
II. EARINFLAMATION
•Otitis externa bacterial inflamation
Pseudomonas aeruginosa destructive
•Otitis media (Acute = OMA ; chronic = OMC ; purulenta = OMP)
- in the middle ear, usually related to blockage to the eustachian tube
- cx : H. influenzae, Strep. Pyogenes, Strep. pneumoniae- pain, erythema, bulging of the tympanic membrane
ruptur ear drainage
•Otosclerosisis a process of bone resorption & replacement by fibrous
tissue, which is later replace by immature bone- autosomal dominant abnormality- causes hearing loss in the young & middle aged
TUMORS
A. BENIGN
* Squamous papilloma* Schwannoma ( n. VIII = acoustic neurinoma )
- hearing loss, vertigo & ringing in the ears
- Tx : surgical removal
* Meningioma pressure effect
* Chemodectomas = Nonchromaffin paragangliomas,
Glomus jugulare tumor
- n. VIII hearing loss
B. MALIGNANT
SCC - of the external ear related sun exposure
- of the auditory canal are agressive
II. THE LUNGCONGENITAL DISORDERS* Benign pulmonary cyst
- in the peripheral lung, < 5cm, lined by respiratory epithelium
- no symptoms, occasionally become infected * Pulmonary sequestrations
a portion of lung receives a blood supply directly from the aorta & has no connection to the rest of the lung
- intrapulmonary : a mass of tissue in a lower lobe,
which may become infected
- extrapulmonary : is found outside the lung
above/below diagphragm, in the mediastinum
* Cystic adenomatoid malformation* Esophageal atresia* 1-antitrypsin deficiency
1-antitrypsin deficiency- is a biochemical deficiency of a protease inhibitor- The phenotype PiZZ has markedly seru level ofhepatic origin enzyme, may result in panacinar emphysema
The Lungare ingeniously constructed to carry out their cardinal function, the exchange of gases between inspired air and the bloodAlveolar wall :- capillary endothelium- basement membrane (yellow)- alveolar epithelium :
-Type I pneumocyte- Type II pneumocyte
- alveolar macrophages- pores of Kohn
INFLAMATORY CONDITIONSBRONCHITIS
a. Acute bronchitis- usually a viral URT infection,
- bacterial superinfection may be present
b. Chronic bronchitis- chronic cough productive sputum due to excessive mucus production
- histol : hyperplasia of the mucous glangs, mucous cells - is due to chronic irritation or infection, especially from smoking
BRONCHIAL ASTHMAThe patient has repeated episodes of bronchospasm with expiratory
wheezing & cough.Alergic (extrinsic) :
- 50% of cases of asthma - begins in young adult, history of allergic rhinitis, elevated Ig E levels-antigens presipitating : pollens, animal dander, molds
b. Nonallergic (intrinsic)
- no identifiable offending antigen, Ig E levels are normal
- starts in later adulthood
c. Occupational asthma ( dusts, gases, fumes)
d. Exercise, Viral Infection, aspirin ingestion may induce asthma attacks
- bronchospasm occurs with edema of bronchial & bronchiolar walls
- thick mucus production
e. Continuing attack which can lead to death is Status asthmaticus
ASTHMA ALLERGIC
BRONCHIECTASIS
is an irreversible dilatation of bronchi & bronchioles with an accompaniying infection marked by sputum production.
Ex : damaging acute infection
bronchial obstruction ( foreign object, tumor, mucus )
congenital/ hereditary conditions : congenital bronchiectasis
cystic fibrosis, immune deficiency
immotile cilia
asymptomatic, or may have : cough, foul-smelling sputum production,
fever, recurrent pulmonary infection
gross : the lower lobes are usually involved, bronchi & bronchioles are dilated & extend nearly to the visceral pleura, contain mucopurulent material
histol : ulcerated mucosa, acute/ chronic inflammation in the wall
destruction & fibrosis of the smooth muscle & elastic tissue
Tx : supportive & antibiotics
Bronchiectasis
Sinusitis
Situs inversus
There is a defect in ciliary motility, associated with structural abnormalities of cilia.
Males : tend to be infertile, owing to ineffective mobility of the sperm tail.
Inherited – autosomal recessive
Kartagener syndrome :
EMPHYSEMA
EMPHYSEMA
BRONCHIOLITIS OBLITERANS-ORGANIZING PNEUMONIA( BOOP)
-occurs as a result of several insult such as :
viral and bacterial infections
diffuse interstitial pneumonia
autoimmune disease, graft-versus-host reaction in bone marrow transpl.
inhaled toxins & extrinsic allergies
- clinically : cough & dyspnea with or without fever & wheezing
bronchioles are narrowed & inflamed,
contain a plug of fibrous tissue within the lumen
- Tx : Steroids is helpful
3. Gangguan vaskuler paru
Kongesti & edema paru
Adult Respiratory Distress Syndrome = ARDS (Diffuse Alveolar Damage)
NRDS (Newborn Resp. Distress Syndrome)
Emboli, perdarahan, dan infark
Hypertensi pulmonal and sklerosis vaskular
Pulmonary congestion & Edema
Pulmonary embolism, hemorrhage & infarction
Occlusions of the pulmonary arteries by blood clot are almost always embolic in origin.
Large vessel in situ thromboses are rare, develop only in the presence of :
* pulmonary hypertension
* pulmonary atherosclerosis
* heart failure
Pulmonary emboli
thrombi in the deep veins of the leg ( >95%)
Total occlusion in the great vessels fatal
sudden death
Pulmonary infarct : macroscopic
Pulmonary infarct : histology
Hipertensi &sklerosis vaskuler paru
ARDS = adult respiratory distress syndrome
diffuse alveolar damage
shock lung
acute alveolar injury
traumatic wet lung
Terjadi akibat cedera akut pada alveolus.
: cedera sel transudasi cairan kedlm alveolus&edema paru, fibrin menutupi epitel yg rusak.
NRDS = newborn respiratory distress syndrome
penyakit membran hialin
Terjadi akibat kurangnya pembentukan surfaktan paru oleh pneumosit tipe II, paru gagal mengembang, alveolus kolaps, cedera epitel fibrin
: a syndrome caused by diffuse alveolar capillary damage.
Characterized clinically :The rapid onset of severe life-threatening respiratory insufficiencyCyanosisSevere arterial hypoxemia :
* that is refractory to oxygen therapy* that may progress to extrapulmonary
multisystem organ failure.
ARDS
ARDS
Morphology ARDS
Acute edematous stage :* lungs are heavy, firm, red,and boggy
* congestion, interstitial & intra-alveolar edema, and inflamation
* fibrin deposition
= alveolar hyaline membranes
Resolution : is unusual
Organization of the fibrin exudate, with resultant
intra-alveolar fibrosis :* proliferation of interstitial cells & deposition of collagen
thickening of the alveolar septa ensues
Superimposed bronchopneumonia fatal cases
ARDS
Histologic feature of ARDS :
Clinical course ARDS Usually hospitalizedProfound dyspnea & tachypneaCyanosis, Hypoxemia, & respiratory failure, X-ray : diffuse bilateral infiltrates.
If unresponsive to O2 therapy respiratory acidosis
THERAPY :* difficult, frequently fatal
* Oxygen toxicity high concentrations of O2
* resorption of the edema fluid* reexpansion of ateletatic area.
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