Pathology Flashcards

1
Q

Second name of neonatal respiratory distress syndrome

A

Hyaline membrane disease

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2
Q

Neonatal respiratory distress syndrome

A

Respiratory distress
Refractory to oxygen therapy in newborn
Due to hyaline membranes formation in alveoli because of immaturity of lungs with surfactant deficiency

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3
Q

First symptoms of neonatal respiratory distress syndrome

A
Resuscitation at birth 
within 30 minutes :
dyspnea 
tachypnea 
expiratory grunts
 cyanosis 
crepitations in the lungs
 ground glass opacity over the lungs on x-rays
Apneic spells
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4
Q

Neonatal respiratory distress syndrome incidence

A

60% incidence when born before 28 weeks

30% incidents one born between week 28 and 34

Less than 5% chance is one born After week 34

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5
Q

Risk factors of Neonatal respiratory distress syndrome

A

Prematurity (born before week 36)

Maternal diabetes

Planned c section

Male gender

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6
Q

Neonatal respiratory distress syndrome pathogenesis

A
Prematurity 
Low surfactants 
High surface tension in alveoli
Atelectasis
 Uneven Perfusion and hypoventilation 
Hypoxemia and CO2 retention
Acidosis 
vicious cycle because acidosis decreases surfactant release
Pulmonary Hypoperfusion 
endothelial and epithelial cell damage 
exudation  of plasma into alveoli 
Fibrosis necrosis and Hyaline membrane 
increased gradient rate 
hypoxemia and co2 retention 
vicious cycle
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7
Q

Type of cell that produce surfactant

A

Type 2 pneumocyte

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8
Q

Surfactant regulation

A

Corticosteroid induce production

Insulin repress production

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9
Q

MacroMorphology of neonate respiratory distress syndrome

A

Lungs look airless, solid, reddish purple,sink in water

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10
Q

Microscopic morphology of respiratory distress syndrome

A

Atelectatic Aleve alveoli alveoli
necrotic debris in alveolar duct in terminal bronchiole
Eosinophilic hyaline membrane ( in respiratory bronchiole, alveoli , alveolar ducts

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11
Q

What are hyaline membranes

A

Fibrin with necrotic type 2 pneumocytes , RBC, rare neutrophils , macrophages

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12
Q

Prevention of neonatal respiratory distress syndrome

A

Delay labor
antenatal steroids to mother
surfactants to very young fetuses

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13
Q

Neonatal respiratory distress syndrome treatment

A

Oxygen

exogenous surfactants

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14
Q

Neonatal respiratory distress syndrome complications

A
Retrolental fibroplasia 
broncopulmonary dysplasia due to oxygen toxicity
patent ductus arteriosus 
intraventricular hemorrhage 
necrotizing enterocolitis
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15
Q

Why are male neonate more prone to respiratory distress syndrome

A

Estrogen influence lung developments

Lower rates of alveolar sodium transport channels than in female => fluid accumulation and less gas exchange

Female develop surfactant earlier

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16
Q

Why do diabetic mothers have higher chances of having a neonate with respiratory distress syndrome

A

Higher chances of pre-terms baby

Inadequate use of glycogen for surfactant Synthesis

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17
Q

Coryza

A

Infectious rhinitis - common cold

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18
Q

Coryza cause

A

Virus ( adeno, rhino, RSV, echo)

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19
Q

Most common virus in coryza

A

Rhino virus

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20
Q

Coryza characteristics

A

Acute inflammation
Catarrhal
Mucus hyper secretion
Loss of epithelial cells

Bacterial secondary inflammation

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21
Q

Atopic rhinitis (hay fever / allergic rhinitis) causes

A

Sensitization to house dust mites proteins plants pollen fungi animal allergens
IGE mediated

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22
Q

Atopic rhinitis pathogenesis

A
Mast cells release histamine: 
 Mucosal edema 
nasal obstruction 
redness 
watery rinorhea
 goblet cells hyperplasia 
thickened basement membrane 
inflammatory exudate with many eosinophils
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23
Q

Chronic rhinitis

A

Sequel to recurrent acute/allergic rhinitis
Superimposed bacterial infection
Mixed inflammatory exudate
Can extend into sinuses

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24
Q

Nasal polyps cause

A

Chronic inflammation or type 1 hypersensitivity or asthma

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25
Nasal polyps morphology
Soft rounds or elongated masses pale gray brown 0.5 to 2 cm
26
Nasal polyps site
Middle turbinate
27
Nasal polyp histology
Surface epithelium with meta plasia | Allergic type have lot of eosinophils
28
Nasal polyp complications
Loss of smell | Frequent infections
29
Acute sinusitis
Acute inflammation of sinuses
30
Cause of acute sinusitis
Acute /chronic rhinitis with edema and sinus Ostia blockage
31
Bacteria in secondary infection in acute sinusitis
Staph aureus H influenza Pneumococcus Strep pyogenes
32
Acute sinusitis complications
Empyema
33
Chronic sinusitis
Failure to resolve acute sinusitis
34
Origin of severe form of chronic sinusitis
Fungal origin
35
Necrotizing nasal lesions
Acute fungal infection
36
Necrotizing nasal lesions Morphology
Granulomatosis - Polyangitis (wegeners granulomatosis) giant cell granulomas of lungs Polyarteritis renal damage Extranodal T cell then lymphoma in elderly
37
Pharyngitis and tonsillitis
Non-specific inflammation of needs a pharynx
38
Common causes of pharyngitis and tonsillitis
Mostly viral | sometimes bacterial
39
Characteristics of pharyngitis and tonsillitis
Red Oedematous mucosa Enlarged tonsils and lymph node
40
Of what bacteria is pharyngitis and translate is an important sequelae
B haemolytic strep( pyogenes)
41
Benign tumors of nose Sinuses nasopharynx larynx
Hemangiomas squamous papillomas juvenile angiofibroma
42
Juvenile angiofibroma
Benign tumor of nasopharynx in childhood almost exclusive to male Vascular and epistaxis
43
Malignant tumor of nose nasopharynx pharynx sinuses
``` Squamous cell carcinoma Adenocarcinoma (common in wood workers) lymphoma sarcomas Olfactory neuroblastoma Nasopharyngeal carcinoma ```
44
Naso pharyngeal carcinoma incidence
Twice in males Peak at 10-20 and 6th decade
45
Causes of nasal pharyngeal carcinoma
Hereditary Age EBV diet
46
Acute epiglotitis causes
RSV H influenza B streptococcus
47
A cute epiglottis presentation
Respiratory obstruction by edema | dyspnea worse in supine position
48
Managements of acute epiglottitis
Emergency so may require tracheostomy
49
Acute Laryngotracheo bronchitis
Gradual onset of cough stridor croupy cough
50
Benign tumors of larynx and trachea
``` Squamous papilloma (Single in adults and multiple in children) polypoid mass on true vocal cord ```
51
Causes of benign tumors of larynx in trachea
Hpv6 /11
52
Presentation of benign tumors of larynx and trachea
Hoarse voice | Bleeding
53
Laryngeal fibroma
Vocal cords polyp | Covered by epithelium with a core of myxomatous connective or dense fibrocollagenous tissue
54
Causes of laryngeal fibroma
Common in singers smokers and in Myxedema
55
Malignant tumors of larynx and trachea
Squamous cell carcinoma of larynx ( commonest neoplasm of larynx)
56
Origin of squamous cell carcinoma of larynx
Squamous epithelium a vocal cords
57
cause of squamous cell carcinoma larynx
``` Smoking excess alcohol previous irradiation zinc and vitamin a deficiency asbestos HPV infection ```
58
Squamous cell carcinoma of larynx incidence
Higher in male Chronic smokers
59
Morphology of squamous cell carcinoma of larynx
Severe dysplasia carcinoma in situ metastasis to cervical notes Blood borne metastasis to lungs liver bones keratinizing and non-keratinizing squamous carcinoma & spindle cell
60
Factors affecting local defense in respiratory tract
Suppression of cough reflex like in coma or anesthesia Ciliary defects Mucus disorders acquired or congenital hypogammaglobulinemia ( low IgA) Immunosuppression depressed alveolar macrophage function pulmonary edema with fluid accumulation in alveoli
61
Specific infections of LRT
Bronchitis Bronchiolitis Pneumonia Lung abscess
62
Acute bronchitis
Acute inflammation of bronchi
63
Acute bronchitis causes
Viruses - RSV Pollutants SO2 Smoke
64
Acute bronchitis presentation
``` Cough Dyspnoea Tachypnoea Sputum production May have laryngotracheobronchitis and lungs issues ```
65
What disease superimposed with chronic obstructive airway disease
Acute bronchitis
66
Bronchiolitis
Inflammation of bronchioles
67
Cause of bronchiolitis
Viral disease in children (RSV)
68
Bronchiolitis presentation
Dyspnoea Tachypnoea Resolve in few days Rarely bronchopneumonia
69
Pneumonia
Inflammation affecting lungs parenchyma | Exudate formation leading to consolidation of lung tissue
70
Clinical classification of pneumonia
community acquired acute pneumonia Health care associated pneumonia Hospital acquired pneumonia Aspiration pneumonia Chronic pneumonia Necrotizing pneumonia and lung abscess Pneumonia in immunecompromised Host
71
Anatomic classification of pneumonia
Bronchopneumonia : patchy consolidation of lungs 3-4cm , common at autopsy Lobar pneumonia : acute bacterial infection by droplets acquired by community , diffuse consolidation of one or more lobes or segments by fibrinosuppurative exudate , accompanied by pleural reaction with fibrin deposition
72
Causes of lobar pneumonia
90-95% : strep pneumonia type 1,3,7,2 Klebsiella pneumoniae Staph aureus H influenza Pseudomonas Proteus
73
Causes of bronchopneumonia
``` Staph Strep Pneumococci H influenza Pseudomonas ```
74
Pneumonia pathogenesis
Impaired defense mechanism by virulent organisms Lobar pneumonia -> extensive exudate -> organism spread rapidly through pores of kohn too other alveoli Bronchopneumonia involve bronchiole and spread to adjacent alveoli
75
Lobar pneumonia morphological stages
Congestion (lung heavy , red, Vascular engorgement intra-Alveolar fluid With few neutrophils and many bacteria Red hepatization (the lung firm red, airless , liver like consistency, many RBC and neutrophils, breaks when firm gentle pressure instead of regaining shape ) Grey hepatization ( lung firm, gray brown, dry surface, progressive disintegration of RBC, fibrinosuppurative exudate ) Resolution ( consolidated exudate progressively digested by enzymes, resorted by macrophages or coughed up, inflammation resolution)
76
Pneumonia complications
``` Local: Lung abscess solid fibrotic lung Pleural effusion Empyema thoracis ``` ``` Systemic: Bacteraemic dissemination Meningitis Pericarditis kidney or splenic abscess septicemia ```
77
Symptoms of pneumonia
``` Fever (5days, and drops 2 days after antibiotics) cough sputum production chest pain due to pleural reaction dullness bronchial breathing ```
78
X-ray findings of pneumonia
Opaque Well delineated lobe in lobar pneumonia Focal opacities in bronchopneumonia
79
Community acquired viral pneumonia
Acute febrile respiratory disease with Patchy inflammatory changes in Lungs confined to the alveolar septa and pulmonary interstitium
80
Causes of Community acquired viral pneumonia
``` Viruses influenza RSV Varicella adenovirus rubeola CMV SARS Coxiella burnetti chlamydia mycoplasma ```
81
Community acquired viral pneumonia morphology
Lung subcrepitant, patchy, unilateral or bilateral no reaction at pleura Septa widens by edema mononuclear cells and very few neutrophils Alveoli mostly free of exudates Few cases with exudate and hyaline membrane
82
Community acquired viral pneumonia symptoms
``` Severe cold cough fever headache muscle aches leg pains ```
83
Pneumonia in the immunocompromised
Due to opportunistic infections In debilitating disease, therapy for organ transplants , tumors , irradiation
84
Pneumonia in the immunocompromised presentation
Fever short breath cough
85
Immunocompromised pneumonia x rays
``` Lung infiltrates focal infiltrate ( with CMV, P Carinii, aspergillus, cryptococcus, tb, rubeola, drug run, malignancy ) ``` Diffuse infiltrate ( gram neg bacilli, stap aureus, aspergillus, candida, cryptococcus, Nucor, p caring, legionella, malignancy )
86
Aspiration pneumonia
Inflammation and consolidation of the lung went fluids or foods is aspirated into lung
87
Risk factors of lung aspiration
``` Sedition alcohol abuse operations Coma stupor laryngeal carcinoma severe debilitation ```
88
What part of the lung will be affected if you aspirate something when laying on the back
Lower lobe
89
What part of the lung will be affected if you aspirate something when laying on the side
Upper lobe
90
Endogenous Lipid pneumonia
Airway obstruction by distal collection of foamy macrophages and giant cells
91
Exogenous lipid pneumonia
Aspiration of lipid rich material like paraffin oil in nasal drops, palm oil when given to children to Treats Toxicity, Vacuoles of lipids from foreign body giant cells in lung
92
Lung abscess
Local suppurative process in the lung with necrosis of lung tissue
93
Predisposition to lung abscess
``` Oral pharyngeal surgery or disease sinobronchial infection dental sepsis bronchiectasis complications of pneumonia ```
94
Causes of lung abscess
Potentially any organism usually Aero and anaerobic strep, staph aureus, gram neg organism 60% of cases => fusobacterium, peptococcus
95
Introduction of organisms to form lung abscess
Aspiration of infected material from mouth and pharynx Primary bacterial or fungal infection of lung Septic embolism Neoplasia Direct penetrating injuries cryptogenic
96
Lung abscess morphology
Size goes from micro to macro | Any parts of the lung can be affected
97
What side of the long is more affected by lung abscess
Right side because more aspiration
98
Lung abscess x ray
Air fluid level
99
In what case of lung abscess can you get gangrene of the lung
Super imposed saprophytic infection ( large fetid green black area)
100
Lung abscess clinical presentation
Fever | cough with copious sputum (foul smelling and bloody or purulent)
101
Lung abscess complications
Metastatic abscesses in the brain ,kidney ,spleen , and finally pleura (risk of empyema) malignancy in 15% of cases
102
2 groups of obstructive airway disease
Localised (mechanical factors like tumors, foreign body) Diffuse (COPD)
103
Chronic obstructive pulmonary disease
Group of disease which presents with dyspnea increased resistance to air flow reduce expiratory capacity Diffuse reversible or irreversible abnormalities in bronchi or bronchioles Respiratory improvements chronic airflow limitation Reduce vital capacity , FEV1/FVC ratio under 0.7
104
Types of COPD
``` Chronic bronchitis emphysema bronchiectasis bronchial asthma bronchiolitis ```
105
Chronic bronchitis
Defined clinically with persistent productive cough each day for at least three months of the year over 2 consecutive years
106
In which population do you see the most chronic bronchitis
Smokers | Inhabitants of urban smug laden cities (so2, no2, dusts....)
107
Types of chronic bronchitis
Simple chronic bronchitis ( Early disease, cough, little sputum, no physiologic obstruction) chronic asthmatic bronchitis ( Bronchospasm and intermittent wheezing) chronic emphysematous bronchitis ( emphysema added)
108
Incidence of chronic bronchitis
Both sexes affected most common in in the middle age
109
Risk factors of chronic bronchitis
``` Smoking (about 90% of patients ) air pollutants (about 20 to 40% of patients ) artificial fibers coolant occupational fumes like welding ```
110
Chronic bronchitis pathogenesis
Tissue damage by irritants inflammation large airways have hypersecretion due to enlarged mucus glands Small airways like bronchi and bronchioles have goblet cell hyperplasia Secondary infection of mucus more damage and hypersecretion airway obstruction
111
How does cigarette smoking predisposes to infection
Interfere with ciliary action damage airway epithelium Inhibit ability of bronchial and alveolar leukocytes to clear bacteria
112
Chronic bronchitis macro appearance
``` Hyperemia swelling of mucous membranes mucus cast in bronchi and bronchiole mucus secretions in bronchi and bronchioles Frank pus collection in bronchi ```
113
Histology of chronic bronchitis
Mucus glands enlargement Mucus hypersecretion increased diameter of acini of glands increased proportion of mucus to serous cell Goblets cell hyperplasia In bronchi and bronchioles Bronchial narrowing and obstruction Squamous metaplasia with dysplasia in bronchial epithelium
114
Reid index
Ratio Of the thickness of mucus glands layer to the thickness of bronchial wall
115
Normal reid index
0.36 to 0.41
116
Reid index in Chronic bronchitis
0.44 to 0.79 | Increases in proportion to severity and duration of disease
117
Bronchial mirroring and obstruction due to in chronic bronchitis :
``` Mucus secretion and plugging increased goblet cell hyperplasia Inflammation with exudate accumulation of pigmented alveolar macrophages in clusters fibrosis of the wall of the bronchioles obliteration of bronchioles ```
118
Blue bloater
Classic patience with long-standing chronic bronchitis and obstructive features Long history of chronic of recurrence airway insufficiency and recurrent chest infections
119
Blue bloater incidence
Male between 40 to 45-year-old
120
Symptoms of blue bloater
Progressive dyspnoea | cyanosis
121
Blue bloater x ray
Increased lung markings | large heart outline
122
Blue bloater pathogenesis
Failure of oxygenation in alveoli Central Cyanosis with low alveolar oxygen pressure and increased alveolar co2 Ventilation perfusion imbalance pulmonary hypertension with right heart changes right heart failure which is a cause of death recurrent infections respiratory impairments coma death
123
Emphysema
Permanent abnormal enlargement of any part of the respiratory acinus ,destruction of the elastin in the wall, no obvious fibrosis
124
Where is emphysema common
Advanced countries
125
Population more at risk of emphysema
Female African-American
126
Most important risk factor of emphysema
Heavy cigarette smoking and urban dwelling
127
Four types of emphysema
Centriacinar ( 95%) Panacinar Distal acinar Irregular
128
Centriacinar (centrilobular)
Respiratory bronchioles at center of lobules affected Distal acinus and alveoli spared Inflammation in terminal and respiratory bronchioles Affects more upper part of lungs Males heavy smoker and coal miners most affected
129
Panacinar emphysema
Entire acinus from respiratory bronchiole to alveolar sacs uniformly Commoner in lower zones, anterior margins 70-80% idiopathic Associated with alpha1 anti trypsin deficiency
130
Paraseptal
Affect distal acinus Most striking Adjacent to pleura , along lobular connective tissue septa and margins of lobules Adjacent to areas of fibrosis, scarring, atelectasis More severe in upper half of lungs May be responsible for pneumothorax
131
Irregular emphysema
``` Acinus irregularly involved Invariably associated with scarring Wall adjacent to scar is destroyed Asymptomatic Post inflammatory Post tuberculosis Pneumoconiosis ```
132
Pathogenesis of emphysema
Inflammation done by inflammatory mediators, oxidant antioxidants (mice studies on NRF2 gene inactivation ) protease anti protease(a1 deficiency homozygotes develop emphysema especially in smokers )
133
Emphysema morphology
``` Voluminous lungs Cardiac shadow covered Higher lung weight Large blebs or bullae Dilated alveoli Abnormally large alveoli Large pore of kohn Floating alveolar sept ```
134
Clinical feature of emphysema
Classic => Pink puffer (patient is thin, tachypneoa, pink skim, prolonged expiration) 70-75yo male with no chronic bronchitis but pure emphysema Early onset of dyspnoea - steadily progressive Weight loss Barrel Chest (trapping of air in lungs due to destruction of alveoli ) Hyperventilation Late stage => reduced PAO2 , pulmonary hypertension, cor pulmonale, death
135
Causes of death in emphysema
Corpulmonale Pneumothorax with lung collapse Respiratory acidosis ->coma-> death
136
Other forms of emphysema
Compensatory emphysema Obstructive overinflation Bullous emphysema Interstitial emphysema
137
Compensatory emphysema
Loss of lung substance leading to dilatation with no alveoli destruction (pneumomectomy)
138
Obstructive over inflation
Lung expand due to trapped air Obstruction by tumor or FB Collateral air passages - pore of kohn, bronchioalveolar canals of lambert supply air to distant parts. Can compress normal part of lung => emergency
139
Bullous emphysema
Large bleb or bullae distended with air ( usually near subpleural, apex, tb scars ) If rupture -> pneumothorax
140
Interstitial emphysema
Air into connective tissue strong of lung, mediastinum, or subcutaneous tissue Air enter by alveolar tear from emphysema, congenital dx, chest wound, fractures , whooping cough, bronchitis, Crackling sensation under hands
141
Bronchiectasis
Chronic necrotizing infections of bronchi and bronchioles | Abnormal permanent dilatation of airways
142
Bronchiectasis presentation
Recurrent chest infections Fever Productive Cough of Foul smelling purulent sputum (sometimes bloody)
143
Bronchiectasis etiology
Bronchial obstruction Necrotizing pneumonia Congenital or hereditary conditions Idiopathic
144
Type of bronchial obstruction leading to bronchiectasis
Focal : foreign body, tumor, lymphadenopathy, mucus impact ion, Diffuse : obstructive airway disease, bronchial asthma, chronic bronchitis
145
Type of Necrotizing pneumonia leading to bronchiectasis
Tb Staph Mixed infections Post whooping cough , measles, influenza
146
Types of congenital or hereditarily conditions leading to bronchiectasis
( defect in development of bronchi) Cystic fibrosis Immunodeficiency Kartagener s syndrome : immobile cilia syndrome
147
Bronchiectasis pathogenesis
Obstruction atelectasis bronchial wall inflammation and secretion reversible dilatation of bronchi Persistence of obstruction / secondary infection Inflammation Destruction of wall Permanent dilatation Extensive bronchiolar damage Endobrinchial obliteration Atelectasis distal to obliterated area Extensive bronchial damage Bronchiectasis
148
Cystic fibrosis
Squamous metaplasia Impaired mucociliary action Infection and necrosis of walls Bronchiectasis
149
Kartageners syndrome
Ciliary motility defect due to structural abnormalities Poor bacterial clearance -> infection in sinus and bronchi Bronchiectasis Sinusitis and situs inversus ( poor cell motility in embryogenesis)
150
MacroMorphology of bronchiectasis
Lower lobes bilaterally Unilateral in FB or tumors Almost vertical air ways Severe in distal bronchi and bronchioles => dilated 4x normal Dilatation can be cylindroid, fusiform or saccukar Gross examination -> dilated bronchi seen through pleural surface as cysts
151
Micro morphology of bronchiectasis
``` Acute or chronic inflammation Ulceration of mucosa Squamous metaplasia of epithelium Abscess due to necrosis Fibrosis in peribronchial and peribronchiolar tissue ```
152
Clinical presentation of bronchiectasis
``` Persistent cough Foul smelling sputum sometimes bloody F3ver Dyspnoea Cyanosis ```
153
Bronchiectasis complications
Cor pulmonale Lung abscess Metastatic micro abscesses in brain kidney
154
Bronchial asthma
Chronic relapsing inflammatory disease of conducting airways Hyperreactive airways Inflammation of bronchial walls Increased mucus secretion
155
Bronchial asthma presentation
Wheezing ( due to acute reversible increase in resistance to airflow in small airways so more respiratory effort) Dyspnoea Chest tightness Cough triggered by bronchospasm
156
Classification of bronchial asthma
Atopic asthma => extrinsic, allergic, IgE mediated, allergen sensitization Non atopic asthma => intrinsic, no evidence of allergen sensitization
157
Stimuli of bronchial asthma
``` Respiratory infection Cold air Exercise Exposure to irritants ( smoke, fumes, smog) Stress , emotional state’s DRugs like opiates, aspirin Food allergens ```
158
Features of atopic asthma
``` Most common type Classic igE Mediated hypersensitivity rxn Begins in childhood Triggers domestic environmental Positive FHA OF ASTHMS ```
159
Features of non atooc asthma
No evidence of allergen sensitization Less FH positive for asthma Common triggers => respiratory infection and environmental pollutants
160
Classification asthma
Seasonal Exercise induced Drug induced Occupational Asthmatic bronchitis in smokers
161
Drug induced asthma (aspirin)
Not common Recurrent rhinitis and nasal polyps React excessively to nsaids Inhibition of Cox so less prostaglandin E2 and more leukotrienes b4-e4
162
Occipqtional asthma
Triggered by fumes (epoxy resins, plastics) gases (toluene), organic and chemical dusts ( wood cotton platinum) other chemicals ( formaldehyde, penicillin)
163
Pathogenesis of asthma
Exaggerated TH2 and IGE respond to environment antigen Sensitization ( 1st exposure allergen, th2 release IL4 &5, IL4 stimulates B cells which stimulates plasma cells for IgE which bind mast cells, IL5 recruits eosinophils for activation ) Reexposure - immediate or late ( immediate => allergenbinds IgE on mast cells , mast cell release granules, cytokines release too )
164
Immediate asthma phase response
Bronchoconstriction Increased mucus production Vasodilation Increased vascular permeability White cells recruitment
165
Late phase of asthma response
``` 4-8h later Mediated by white cells Release cytokines , leucotrienes, PAF, eosinophils cationic protein, Epithelial damage Airway constriction ```
166
Action of leucotrienes
Prolonged bronchoconstriction | Increase vascular permeability
167
Acetylcholine action
Bronchoconstriction
168
Histamine action
Bronchoconstriction
169
Prostaglandin D2 action
Bronchoconstriction | Vasodilation
170
PAF action
Platelet aggregation | Release histamine and serotonin
171
MacroMorphology of asthma
Over distended Lung Small areas atelectasis Occlusion of bronchioles by thick mucus plugs
172
Micro morphology of asthma
Thick tenacious layer of mucus to form plugs Curschmann spiral Numerous eosinophils Collections of crystalloids with eosinophils membrane protein (Charcot leyden crystals ) Lot of goblet cells in epithelium Basement membrane more thick Edema and inflammation infiltrate in bronchial wall Increased size of submucosal glands Hypertrophy of bronchial wall Emphysematous changes and bronchitis
173
Clinical features of asthma
Attack last several hours Coughing When severe -> impaired respiratory function -> cyanosis -> death
174
Cause of airway obstruction in asthma
Bronchial contraction Bronchial mucosal increased thickness Mucus and exudate retention in lumen
175
Asthma diagnosis
History Examination-> resp difficulty, decreased air entry , wheezing Test Increased eosinophils in blood Increased eosinophils, curschmann, spiral, Charcot Leyden crystals in sputum
176
Diagnosis of type of asthma
Increased IgE serum | Positive skin allergen test , RAST TEST
177
Diffuse interstitial lung disease
Group of lung disease with chronic diffuse involvement of the connective tissue of the lungs Especially the most peripheral and delicate interstitium in alveolar walls
178
Interstitium in diffuse interstitial lung diseases
Basement membrane of endothelial and epithelial cells Collagen Elastic fibers Proteoglycans Fibroblasts Mast cells Histiocytes Monocytes
179
Do we know most causes of diffuse interstitial lung diseases
No mostly idiopathic
180
Lung diseases with restrictive effect but non obstructive
Diffuse interstitial lung disease
181
Changes in the lung due to diffuse interstitial lung disea3e
Thick wall =< less o2 diffusion across wall Decreased lung volume Decreased lung compliance
182
Diffuse interstitial lung disease presentation
Dyspnoea Tachypnoea Cyanosis No wheezing
183
Diffuse interstitial lung diseases x ray
Diffuse infiltration lay small granules , irregular lines, ground glass shadows
184
Complications of diffuse interstitial lung disease
Pulmonary hypertension Right heart failure With cor pulmonale Honey comb lung due to scarring and destruction
185
Classification of diffuse interstitial lung disease based on....
Known etiology Not known etiology
186
Diffuse interstitial disease with known etiology
``` Pneumoconiosis Ionizing radiation Following ARDS Drug busulfan Bleomycin Beryllosis Hypersensitivity pneumonitis ```
187
Diffuse interstitial disease with unknown etiology
``` Collagen vascular disease Goodpastures syndrome Idiopathic pulmonary fibrosis Idiopathic hemosiderosis Sarcoidosis Wegeners granulomatosis ```
188
Pneumoconiosis
Non neoplasticism lung reaction to inhalation of mineral dusts, organic dusts, chemical fumes, vapor
189
Types of pneumoconiosis based on mineral dusts involved
``` Coal - Anthracosis Asbestos - abestosis Silica- silicosis Beryllium- beryllosis Iron oxide - siderosis Barium sulphate - baritosis Tin oxide - stannosis ```
190
Types of pneumoconiosis based on organic dusts involved
Moldy hay: farmers lung Bagase: bagassosis Bird droppings: bird breeders lung
191
Types of pneumoconiosis based on fumes and vapors involved o
No2 So2. Benzene Insecticide
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Type of reaction to dust and fumes
Inert ( simple, coal worker pneumoconiosis Fibrosis ( progressive fibrosis , asbestosis, silicosis) Allergy ( extrinsic allergy alveolitis Neoplasm (=mesothelioma, bronchogenic
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Pneumoconiosis pathogenesis
Dust retained in lung Small dust (1-5mm) can get into alveoli Large dust trapped early Dust particles phagocytosed by alveolar macrophages and go to hilar lymph nodes
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Particularity with asbestos fibers
Even tho long (8mm) , very thin so can get into alveoli
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Coal workers pneumoconiosis
Inhalation of coal dust leading to Asymptomatic anthracosis Simple CWP => macular or nodular CWP Complicated CWP=> progressive massive fibrosis
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Macular CWP
Local aggregate of dust laden macrophages in and around Bronchioles, arterioles, veins, lymphatic, hilar lymph nodes No significant scarring Mild emphysema due to smoking
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Nodular CWP
Small nodules with more extensive macular lesions No fibrosis No functional difficulty
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Complicated CWP
``` Extensive fibrosis Large fibrotic nodules Compromised lung function Possible central liquefaction in nodules Mid and upper zones of lungs 10% of simple CWP lead to complications Pulmonary dysfunction Pulmonary hypertension Cor pulmonale ```
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Silicosis
Inhalation of crystalline silicon dioxide Slowly progressive nodular fibrosing pneumoconiosis Particles phagocytized by macrophages in alveoli but not destroyed Release of fibrogenic mediators(TNF, cytokines, IL-1, fibronectin, lipid mediators, free radicals ) Toxic injury due to SiOH denature membrane proteins and damage lipid membranes
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Commonest occupational disease
Silicosis
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Morphology of silicosis
At first => tiny dispersed nodules in upper zone Nodules becomes hard fibrous scars , few cells, some with central cavitation Eggshell calcification of lymph nodes Progressive massive fibrosis occurs
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Histology of silicosis
Nodular lesions with layers of collagen with dense collagenous capsule Silica particles seen under polarized light
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Can silicosis reactivate Tb
Yes
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Association between silicosis and cancer
Increased risk of cancer by 2
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Disease caused by asbestos
Crystalline Hydrated silicates that form fibers which can cause - localized fibrous plaques - pleural effusions - parenchyma interstitial fibrosis (asbestosis ) - bronchogenic carcinoma - mesothelioma - laryngeal and extra pulmonary cancer
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Type of asbestos
Serpentine - curly and flexible (chrysolite) Amphibole - straight stiff brittle fibers ( crocidolite, amosite, tremsolite)
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Most case of asbestosis due to what type of asbestos
Amphiboles
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Asbestosis pathogenesis
``` React with lung macrophages and epithelial cells Release of fibrogenic mediators Diffuse interstitial lung disease No nodules Starts in lower lobes and extend ```
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Asbestos morphology
Diffuse pulmonary interstitial fibrosis Asbestos bodies - golden brown beaded rods with asbestos fibers coated with iron and proteinaceous material Ferruginous bodies - inorganic particles coated with iron Pleural plaques of dense collagen with calcium - most common manifestation Pleural effusion - not common Diffuse pleural fibrosis - rare Bronchogenic carcinoma -5x Mesothelioma - 1000x
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Sarcoidosis
Systemic disease Idiopathic Non caseating Naked granulomas Bilateral hilar lymphadenopathy + lung involvement -90% cases Eyes lesions ( iridocyclitis, corneal opacities, glaucoma, blindness) Skin, salivary glands, spleen, liver
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Incidence of sarcoidosis
Male more than females | Blacks mostly
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Sarcoidosis pathogenesis
``` Unknown antigen poorly degradable type 4 reaction Granuloma formation High CD4 + lymphocytes in lung High soluble IL2 receptors in serum and lung ```
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Sarcoidosis morphology
Non caseating granulomas Laminated concretions of calcium and shaumann bodies Stellate inclusion bodies in giant cells cytoplasm => asteroid bodies ``` Activated alveolar macrophages , class II HLA expression , APC activity Oligoclonal T cell proliferation in lung ```
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Sarcoidosis presentation
``` Dyspnoea Cough Chest pain Haemoptysis Fatigue Weight loss Fever Anorexia Night sweats ```
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Effective treatment of sarcoidosis
Steroids
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Pulmonary vascular diseases
``` Pulmonary congestion and edema Adult respiratory distress syndrome Pulmonary embolism Pulmonary Hemorrhage Pulmonary Infarction Pulmonary hypertension Cor pulmonale ```
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Adult respiratory distress syndrome (diffuse alveolar damage)
Rapid onset of severe life threatening respiratory insuffiency, cyanosis , severe arterial hypoxemia Refractory to O2 therapy Associated with severe pulmonary edema
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X ray of adult respiratory distress syndrome
Diffuse alveolar infiltrate | Hyaline membrane in alveoli
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Pulmonary embolism hemorrhage infarction epidemiology
200,000 death per year in US High incidence in autopsy Common in Ghana
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Etiology of pulmonary embolism hemorrhage infarction
Pulmonary arterial occlusion (generally thromboembolism, mostly coming from legs deep veins) Large vessel thrombosis rare Pulmonary hypertension Pulmonary atherosclerosis Congestive cardiac failure
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Risk factor of pulmonary embolism hemorrhage infarction
``` Cardiac disease Cancer Immobilization over Long time Hypercoagulable states Indwelling central venous lines Post op Pregnancy Post party’s ```
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PAthogenesis of pulmonary embolism hemorrhage infarction
Fragmented thrombi of DVT Carried through veins Channels into right atrium Gets into pulmonary arterial vascular use Causes : Respiratory compromise - non perfused segment Hemodynamics compromise - increased pulmonary resistance due to obstruction
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Severity of pulmonary embolism hemorrhage infarction depends on
Extent of arterial obstruction Size of occluded vessel Number of emboli Status of CVS
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Morphology of pulmonary embolism hemorrhage infarction
If large embolus => sudden death by blocking blood flow to lung and causing acute cor pulmonale Small emboli => infarction if circulation inadequate , common in lower lobes, wedge shaped ( blocked artery tap apex, base at periphery with pleura with fibrinosuppurative exudate ) , red brown raised area, heals by fibrosis => if circulation adequate , pulmonary hemorrhage , no infarct Tiny microembolism (shower emboli) => asymptomatic, over time may cause reduced cross sectional area, high vascular resistance , pulmonary hypertension
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Pulmonary hypertension
Normal pulmonary pressure is 1/8 systemic blood pressure | Pulmonary hypertension is 1/4 systemic blood pressure
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Pulmonary hypertension causes
Cardio pulmonary disease with increased blood flow and/or pressure Increased pulmonary vascular resistance Left heart resistance to blood flow Secondary pulmonary hypertension Idiopathic Chronic obstructive airway disease (emphysema) Chronic interstitial Lung disease Congenital or acquired heart disease (Mitral stenosis, increased left atrial pressure, pulmonary venous congestion, increased pulmonary artery pressure ) Recurrent shower embolism Vasospam (bush tea, anti obesity appetite suppressor)
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Pulmonary hypertension morphology
Vascular lesions Atheromatous plaques in pul artery Medial hypertrophy and intimate fibrosis with pinpoint channels in small arteries and arterioles
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How is it determined if surgery of lung is required in pul HT
Biopsy
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Wegener granulomas
Systemic vasculitis affecting upper respiratory tract, lung, kidneys, liver, and skin
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Wegener granuloma morphology
Necrotizing granuloma of nose Giant cell granuloma of lungs Polyarteritis Renal damage
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Wegeners granuloma histology
Vasculitis affecting small arteries Necrosis Fibrinoid deposition in the wall Thrombosis of vessel Granuloma with central necrosis (caseated like) Cellular infiltrate with macrophages eosinophils neutrophils Kidney have segmental glomerulonephritis
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More common type of primary tumors of the lungs
Malignant type more common than benign
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Are all secondary tumors of lungs malignant..
Yes
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Most commo type of lung tumor
Secondary
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Types of malignant primary tumor of lungs
Bronchogenic (90-95%) Neuroendocrine (carcinoid) Mensenchymal tumors Lymphomas
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Major diagnosed cancer worldwide and most common cause of cancer mortality
Bronchogenic carcinoma
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Population more affected by bronchogenic carcinoma
Male more than female Smokers Age 40-70 peak at 50-60
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Bronchogenic carcinoma etiology
Tobacco smoking (80% of the cancer patients ) Rise with amount of smoking , especially tobacco smoking Passive smoking Smokeless tobacco (women more susceptible to carcinogen in tobacco ) Genetic susceptibility cytp450 Industrial hazard (asbestos, coal, nickel, hematite, arsenic, chronium, uranium, mustard gas, vinyl chloride) Air pollutant (increase risk in susceptible people, chronic irritation, inflammation and repair , Genetics - cyt P450 polymorphism
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Amount of carcinogens in smoke
1200 known
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Impact of smoking on bronchial mucosa
Squamous metaplasia to dysplasia to squamous ca
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Type of bronchiogenic carcinoma
Adenocarcinoma -40%, females Squamous cell ca 20% male smokers Small cell ca 14% Large cell ca 3% Other 25%
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Common mixed cancer seen in bronchogenic carcinoma
Small cel ca with squamous cell ca Squamous cell with adenocarcinoma
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Bronchogenic cell ca morphology of ADC
In peripheral lung ADC Central hilar region. SCC Atypical adenomatous hyperplasia ADC if in Situ becomes invasive ADC can grow like acinar, lepidic, papillary, solid
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Bronchogenic cell ca morphology of SCC
Sq metaplasia leads to dysplasia leads to ca in situ leads to invasive SCC Patterns: Fungating mass in lumen Infiltrative in peribronchial tissue and mediastinum Cauliflower intraoarenchymal mass ``` Greg white color Firm to hard Focal hemorrhages Necrosis May have cavity ```
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Bronchogenic carcinoma presentation
``` Cough Weight loss Chest pain Dyspnoea S ```
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Bronchogenic carcinoma lab test
Sputum cytology tumor cells Pleural effusion cytology FNA fine needle aspiration cytology
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Bronchogenic ca complication s
Emphysema - tumor partial obstruction; Lobar colllapse Pneumonia Lung absces Severe suppurative Ulcerative bronchitis Lipid pneumonia from obstruction Cellular lipid accumulation SVC syndrome - venous congestion that can lead to circulatory collapse Malignant pericarditis , pleurisy, effusions , cardiac tamponadd Bronchiectasis Hornets syndrome ( sympathetic ganglia involved leading to enoohtalmos, ptosis, miosis, anhidrosis) Pancoasts tumor ( apical tumor invading cervical neural plexus , pain in ulnar nerve causing horners syndrome ) Rib destruction Diaphgram paralysis Dysphasia Hoarseness Hypertrophic pulmonary osteodystrophy
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Main site of spread of lung carcinoma
Lymph metastasis to trachea, bronchial m mediastinal lymph node Blood borne metastasis to adrenal mostly and then liver and finally brain and bone
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Metastatic lung tumors morphology
Discrete nodules over lungs mostly on periphery Peribronchial and peribascular infiltrate in connective tissue septa Subpleural lymph outlined in lymphangitis carcinomatosa Diffuse in apparent intro lymphatic dissemination
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Metastatic lung tumor treatment
Surgical excision Radiation Chemotherapy
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Metastatic lung tumor prognosis
Poor | E5YS - 5%/