patologi respirasi

7/29/2019 patologi respirasi

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RESPIRATORY

PATHOLOGY

BLOK IV KBK

FK-UMI


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LUNG DISEASE

INFECTION

NON INFECTION TUBERCULOSIS


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LUNG DISEASE

INFECTION

- BRONCHITIS

- BRONCHIOLITIS- PNEUMONIA

* BRONCHO PNEUMONIA

* LOBAR PNEUMONIA SPECIAL PNEUMONIA


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BRONCHITIS

ACUTE : SPREAD ACUTE

LARYNGOTRACHEO

BRONCHITIS (CROUP)

SEVERE (CHILD)

ETIO : RSV, H. INFL, STREP.

PNEUMONIA

CLINIC : COUGH, PURULENT,

SPUTUM


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BRONCHITIS

CHRONIC: - ACUTA CHRONICA

- COUGH > 3 MONTH /

2 YRS

ETIO : SMOKER, POLUTION, INF.STR. PNEMONIA, H. INFLUENZAE,

RSV, ADENOVIRUS

CLINIC : MAN

HYPERCAPNIA,HYPOXCEMIA, CYANOSIS ( BLUE

BLOATERS ) EMPHYSEMA


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PNEUMONIA

ALVEOLAR INFLAMMATION

HIGH PROTEIN EXUDATE

PMN,LYMPHOCYTE &MACROPHAGE INFILTRATION

LOBAR &

BRONCHOPNEUMONIA


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PNEUMONIA

CLINIC : - PRIMAIR

- SECUNDARY

ETIO :

- BACTERIAL

* STREP. PNEUMONIA

* STAPH. AUREUS

* M. TUBERCULOSA, ETC

- VIRAL * INFLUENZAE, MEASLESS

- YEAST* CRYPTOCOCCUS,

CANDIDA, ASPERGILLUS


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PNEUMONIA

ETIO : OTHERS PNEUMOCYSTISCARINII, MYCOPLASMA, ASPIRA-

TION, LIPID & EOSINIPHYLIC

HOST REACTION :

- FIBROUS

- SUPURATIVE

ANATOMIC :

- BRONCHOPNEUMONIA

- PNEUMONIA LOBARIS


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BRONCHOPNEUMONIA

CONSOLIDATION PLAQUE

BRONCHIOLUS & BRONCHUS

AROUND ALVEOLI

INFANT & OLD & WEAKNESS

PATIENT ( CA, CARDIAC FAILURE,

CHRONIC KIDNEY FAILURE, TRAUMA-

TIC CEREBROVASCULAR), ACUTE

BRONCHITIS, CHRONIC OBSTR. RESP.TRACT,OR CYSTIC FIBROSIS & POST

OP.


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BRONCHOPNEUMONIA

- LESION :

- FOCAL (CENTRE OFRESPIRATORY TRACT) / PLAQUE

- BILATERAL ( BASAL )

- AUSCULTATION CREPITATION

- ETIO :- Staphylococcus

- Streptococcus

- H. influenzae- Coliform, Yeast

- HP :- ACUTE INFLAMMATION + EXUDATE


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LOBAR PNEUMONIA

ALL OF LOBUS

INFANT & OLD PATIENT WOMEN

90 % STREP. PNEUMONIA

(PNEUMOCOCCUS)

CLINIC COUGH RUSHTY SPUTUM

FEBRIS (40OC), INSPIRATION

PAIN, BRONCH ASPIRATION KLEBSIELLA OLD, DM, ALKOHOLIC


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PNEUMONIA (STADIUM)

CONGESTION :

- I 24 HRS

- EXUDATE (PROTEIN)

ALVEOLI SPACE

- OEDEMA PULMONAL

- RED COLOUR


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RED HEPATISATION

- > 24 HRS DAYS

- ACCUMULATION

(LYMPHOCYTE, MACROPHAGE) ALVEOLAR

- EXTRAVASATION RED CELLS

- FIBRINOUS EXUDATE

(PLEURAL)

- GAS (-) , CONSOLIDATION(HEPAR)


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GRAY HEPATISATION

- FEW DAYS (STAD II)

- FIBRINE (ACCUMULATION)- WHITE & RED CELLS (LYSIS)

- DARK GRAY


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RESOLUTION :

- 8 10 DAYS UNTREATED

- EXUDATE & INFILTRATION

DEBRIS (ABSORB)

- ALVEOLUS WALL (N)

- ALL OF CASE RECOVERY


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PNEUMONIA NON INFECTION

ASPIRATION

- LIQUID / FOOD

CONSOLIDATION

INFLAMMATION (SECONDAIRY)- RISK FACTOR : POST OP, COMA,

STUPOR, LARYNX CA, ETC

- LESION : POSITION !!


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LIPID PNEUMONIA

- ENDOGENOBSTRUCTION

(MACROPHAGE GIANT

CELL)

- EXOGEN

PARAFFIN LIQUID

INTERSTITIAL FIBROSIS


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EOSINIPHYLIC PNEUMONIA

- EOSINOPHYL >

INTERSTITIAL & ALVEOLI(ASTHMA, ASPERGILLUS,

MICROPHYLARIA),

LOEFFLER SYNDROME(IDIOPATIC)


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TUBERCULOSIS

ETIO : M. TUBERCULOSE

LOC : - LUNG >>

- ETC

CLINIC : - VARIATION

- DYSPNOE

- LOSS BODY WEIGH

- FEBRIS - DISTRESS

- SWEATING - COUGH


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TYPE : - PRIMAIR

- SECUNDAIR

- MILIER

DX CLINICAL SIGN

LAB : - SPUTUM - MANTOUX

- BLOOD

RADIOLOGY

IMMUNISATION BCG


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PRIMAIR :

- FIRST CONTACT

- PRIMAIR LESION (GHON

LESION) + REG.

LYMPHNODE (GHONCOMPLEX)

- FIBROCALCIFICATION,

BACIL (+)


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SECUNDAIR :

- REACTIVATION (PRIMAIR)

- LOC APEX ( +/- BILATERAL )

- FIBROCALCIFICATION


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MILIER

- PRIMAIR / SECUNDAIR

- IMMUNITY >,

- POLUTION

STREP. PNEUMONIAH. INFLUENZAE &

VIRAL SEVERE

HYPERCAPNIA, HYPOXIA &

CYANOSIS (BLUE BLOATERS)


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EMPHYSEMA

ALVEOLUS DILATATION +ELASTICITY (


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OTHER FORM

- BULOSA EMPHYSEMA

- INTERSTITIAL EMPHYSEMA

- SENILE EMPHYSEMA CLINIC :

- DYSPNOE

- COUGH

- SPUTUM


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ASTHMA

BRONCHUS IRRITABLE (+)

BRONCHUS SPASM MUCOUS (>>)OBSTRUCTIONDYSPNOE

TYPE : - ATOPIC

- NON ATOPIC- ASPIRINE INDUCED

- OCCUPATIONAL

- ALLERGIC (ASPERGILLUS)


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ATOPIC ASTHMA

ENVIRONMENT MATERIAL

HYPERSENSIVITY

REACTIONBRONCHUS

CONSTRICTION

TACHYPNOE, DYSPNOE

STATUS ASTHMATICUS

DEAD


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NON ATOPIC ASTHMA

T. RESP. INFECTION

CHRONIC BRONCHITIS

ALLERGEN TEST (-)

LOCAL IRRITATION

BRONCHUS CONSTRICTION


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ASPIRINE INDUCED ASTHMA

MECHANISM (?)

+/- PROSTAGLANDINE

DECREASE / LEUKORINE

INCREASE RESP. TR.

IRRITABLE

RHINITIS, NASAL POLYPS,

URTICARIA (+)


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OCCUPATIONAL ASTHMA

REACTIVE HYPERSENSIVITY(ALLERGEN)

DYSPNOE

COUGH (CHRONIC)ALLERGEN :

- WOOD

- CHEMICAL- ETC


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ASPERGILLUS BRONCHITIS ALLERGY

SPORA ASPERGILLUS

FUMIGATUS HYPERSEN-

SITIVITAS REAC DYSPNOE

MUCOUS GLOBULE

ASPERGILLUS HYPAE (+)


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BROCHIECTASIS

ETIO :

- BRONCHUS OBSTRUCTION

- INFECTION (SEVERE)

- CONGENITAL () + BLOOD


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CLINIC :

- LOBUS INFERIOR + INFECTION

- CLUBBING FINGER

COMPLICATION

PNEUMONIA, EMPIEMA,

SEPTICAEMIA, MENINGITIS,

ABSCESS METASTASIS(CEREBRAL), AMYLOID (+)


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PNEUMOCONIOSIS

DUST: INORGANIC / ORGANIC

TISSUE REACTION :

- MILD

- FIBROUS

- ALLERGIC

- NEOPLASTIC


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COAL WORKERS

PNEUMOCONIOSIS

SILICOSIS

ASBESTOSIS

HYPERSENSITIVITY


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CARCINOMA OF THE LUNG

Squamous cell.

Adenocarcinoma.

Large Cell Undifferentiated

Carcinoma.

Small Cell Undifferentiated

(Oat Cell) Carcinoma.


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PLEURA

EFFUSION

NEOPLASMS OF THE PLEURA


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PLEURAL EFFUSION

A collection of fluid in the

pleural cavity.

Transudate Low specific

gravity, low protein concentrat,and lack of inflammatory cells.

Exudates : specific gravity over

1.015, a protein level of over 1.5g/dL, and many inflammatory

cells.


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Empyema : Bacterial infection

commonly produces a frankly

purulent exudate.

Hemorrhagic exudates occur inmalignant effusions, TB, uremia,

and pulmonary infarction.

Cytologic examination ofeffusion sediment malignant

neoplasia .


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CHYLOTHORAX

Chylothorax : Secific kind of pleural

effusion characterized by

accumulation of chyle in the pleural

cavity. Chyle : Milky fluid of high fat content

that is normally present in the

thoracic duct.

Evidence of an abnormalcommunication between the thoracic

duct and the pleura.


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Neoplasms of the Pleura

Primary Mesothelial Neoplasm.

Secondary Pleural Neoplasms.


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Primary Mesothelial Neoplasm

Benign Fibrous Mesothelioma.

Malignant mesothelioma.

Rare neoplasm strongly related

etiologically to asbestos exposure;many cases have occurred in World

War II shipyard workers.

There is a long lag period (as long as

40 years) between asbestos

exposure and tumor development.


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Secondary Pleural Neoplasms

Direct involvement of the pleura

by lung carcinoma is the most

common secondary pleural

neoplasm. Metastases from distant sites

the breast, colon, kidney, and

thyroid.

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