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Respiratory Module > Pathology > Flashcards

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
Q

Nasal polyps morphology

A

Soft
rounds or elongated masses
pale gray brown
0.5 to 2 cm

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26
Q

Nasal polyps site

A

Middle turbinate

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27
Q

Nasal polyp histology

A

Surface epithelium with meta plasia

Allergic type have lot of eosinophils

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28
Q

Nasal polyp complications

A

Loss of smell

Frequent infections

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29
Q

Acute sinusitis

A

Acute inflammation of sinuses

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30
Q

Cause of acute sinusitis

A

Acute /chronic rhinitis with edema and sinus Ostia blockage

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31
Q

Bacteria in secondary infection in acute sinusitis

A

Staph aureus
H influenza
Pneumococcus
Strep pyogenes

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32
Q

Acute sinusitis complications

A

Empyema

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33
Q

Chronic sinusitis

A

Failure to resolve acute sinusitis

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34
Q

Origin of severe form of chronic sinusitis

A

Fungal origin

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35
Q

Necrotizing nasal lesions

A

Acute fungal infection

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36
Q

Necrotizing nasal lesions Morphology

A

Granulomatosis - Polyangitis (wegeners granulomatosis)
giant cell granulomas of lungs
Polyarteritis
renal damage
Extranodal T cell then lymphoma in elderly

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37
Q

Pharyngitis and tonsillitis

A

Non-specific inflammation of needs a pharynx

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38
Q

Common causes of pharyngitis and tonsillitis

A

Mostly viral

sometimes bacterial

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39
Q

Characteristics of pharyngitis and tonsillitis

A

Red
Oedematous mucosa
Enlarged tonsils and lymph node

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40
Q

Of what bacteria is pharyngitis and translate is an important sequelae

A

B haemolytic strep( pyogenes)

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41
Q

Benign tumors of nose Sinuses nasopharynx larynx

A

Hemangiomas
squamous papillomas
juvenile angiofibroma

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42
Q

Juvenile angiofibroma

A

Benign tumor of nasopharynx in childhood almost exclusive to male

Vascular and epistaxis

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43
Q

Malignant tumor of nose nasopharynx pharynx sinuses

A 
Squamous cell carcinoma 
Adenocarcinoma (common in wood workers)
lymphoma 
sarcomas 
Olfactory neuroblastoma
Nasopharyngeal carcinoma
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44
Q

Naso pharyngeal carcinoma incidence

A

Twice in males

Peak at 10-20 and 6th decade

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45
Q

Causes of nasal pharyngeal carcinoma

A

Hereditary
Age
EBV
diet

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46
Q

Acute epiglotitis causes

A

RSV
H influenza B
streptococcus

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47
Q

A cute epiglottis presentation

A

Respiratory obstruction by edema

dyspnea worse in supine position

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48
Q

Managements of acute epiglottitis

A

Emergency so may require tracheostomy

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49
Q

Acute Laryngotracheo bronchitis

A

Gradual onset of cough
stridor
croupy cough

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50
Q

Benign tumors of larynx and trachea

A 
Squamous papilloma (Single in adults and multiple in children)
polypoid mass on true vocal cord
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51
Q

Causes of benign tumors of larynx in trachea

A

Hpv6 /11

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52
Q

Presentation of benign tumors of larynx and trachea

A

Hoarse voice

Bleeding

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53
Q

Laryngeal fibroma

A

Vocal cords polyp

Covered by epithelium with a core of myxomatous connective or dense fibrocollagenous tissue

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54
Q

Causes of laryngeal fibroma

A

Common in singers smokers and in Myxedema

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55
Q

Malignant tumors of larynx and trachea

A

Squamous cell carcinoma of larynx ( commonest neoplasm of larynx)

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56
Q

Origin of squamous cell carcinoma of larynx

A

Squamous epithelium a vocal cords

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57
Q

cause of squamous cell carcinoma larynx

A 
Smoking 
excess alcohol 
previous irradiation 
zinc and vitamin a deficiency 
asbestos 
 HPV infection
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58
Q

Squamous cell carcinoma of larynx incidence

A

Higher in male Chronic smokers

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59
Q

Morphology of squamous cell carcinoma of larynx

A

Severe dysplasia
carcinoma in situ
metastasis to cervical notes
Blood borne metastasis to lungs liver bones
keratinizing and non-keratinizing squamous carcinoma & spindle cell

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60
Q

Factors affecting local defense in respiratory tract

A

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

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61
Q

Specific infections of LRT

A

Bronchitis
Bronchiolitis
Pneumonia
Lung abscess

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62
Q

Acute bronchitis

A

Acute inflammation of bronchi

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63
Q

Acute bronchitis causes

A

Viruses - RSV
Pollutants
SO2
Smoke

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64
Q

Acute bronchitis presentation

A 
Cough
Dyspnoea
Tachypnoea 
Sputum production  
May have laryngotracheobronchitis and lungs issues
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65
Q

What disease superimposed with chronic obstructive airway disease

A

Acute bronchitis

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66
Q

Bronchiolitis

A

Inflammation of bronchioles

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67
Q

Cause of bronchiolitis

A

Viral disease in children (RSV)

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68
Q

Bronchiolitis presentation

A

Dyspnoea
Tachypnoea
Resolve in few days
Rarely bronchopneumonia

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69
Q

Pneumonia

A

Inflammation affecting lungs parenchyma

Exudate formation leading to consolidation of lung tissue

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70
Q

Clinical classification of pneumonia

A

community acquired acute pneumonia

Health care associated pneumonia

Hospital acquired pneumonia

Aspiration pneumonia

Chronic pneumonia

Necrotizing pneumonia and lung abscess

Pneumonia in immunecompromised Host

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71
Q

Anatomic classification of pneumonia

A

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

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72
Q

Causes of lobar pneumonia

A

90-95% : strep pneumonia type 1,3,7,2

Klebsiella pneumoniae

Staph aureus

H influenza

Pseudomonas

Proteus

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73
Q

Causes of bronchopneumonia

A 
Staph
Strep
Pneumococci
H influenza
Pseudomonas
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74
Q

Pneumonia pathogenesis

A

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

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75
Q

Lobar pneumonia morphological stages

A

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)

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76
Q

Pneumonia complications

A 
Local:
Lung abscess 
 solid fibrotic lung
Pleural effusion 
Empyema thoracis 
Systemic:
Bacteraemic dissemination 
Meningitis 
Pericarditis 
kidney or splenic abscess 
septicemia
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77
Q

Symptoms of pneumonia

A 
Fever (5days, and drops 2 days after antibiotics)
 cough 
sputum production 
chest pain due to pleural reaction 
dullness
 bronchial breathing
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78
Q

X-ray findings of pneumonia

A

Opaque Well delineated lobe in lobar pneumonia

Focal opacities in bronchopneumonia

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79
Q

Community acquired viral pneumonia

A

Acute febrile respiratory disease with Patchy inflammatory changes in Lungs
confined to the alveolar septa and pulmonary interstitium

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80
Q

Causes of Community acquired viral pneumonia

A 
Viruses
 influenza 
RSV 
Varicella  
adenovirus
 rubeola 
CMV
SARS 
Coxiella burnetti
 chlamydia 
mycoplasma
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81
Q

Community acquired viral pneumonia morphology

A

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

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82
Q

Community acquired viral pneumonia symptoms

A 
Severe cold
 cough
 fever 
headache 
muscle aches
 leg pains
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83
Q

Pneumonia in the immunocompromised

A

Due to opportunistic infections In debilitating disease, therapy for organ transplants , tumors , irradiation

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84
Q

Pneumonia in the immunocompromised presentation

A

Fever
short breath
cough

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85
Q

Immunocompromised pneumonia x rays

A 
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 )

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86
Q

Aspiration pneumonia

A

Inflammation and consolidation of the lung went fluids or foods is aspirated into lung

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87
Q

Risk factors of lung aspiration

A 
Sedition 
alcohol abuse 
operations
Coma
stupor 
laryngeal carcinoma 
severe debilitation
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88
Q

What part of the lung will be affected if you aspirate something when laying on the back

A

Lower lobe

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89
Q

What part of the lung will be affected if you aspirate something when laying on the side

A

Upper lobe

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90
Q

Endogenous Lipid pneumonia

A

Airway obstruction by distal collection of foamy macrophages and giant cells

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91
Q

Exogenous lipid pneumonia

A

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

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92
Q

Lung abscess

A

Local suppurative process in the lung with necrosis of lung tissue

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93
Q

Predisposition to lung abscess

A 
Oral pharyngeal surgery or disease 
sinobronchial infection 
dental sepsis 
bronchiectasis 
complications of pneumonia
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94
Q

Causes of lung abscess

A

Potentially any organism usually Aero and anaerobic strep, staph aureus, gram neg organism

60% of cases => fusobacterium, peptococcus

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95
Q

Introduction of organisms to form lung abscess

A

Aspiration of infected material from mouth and pharynx
Primary bacterial or fungal infection of lung
Septic embolism
Neoplasia
Direct penetrating injuries
cryptogenic

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96
Q

Lung abscess morphology

A

Size goes from micro to macro

Any parts of the lung can be affected

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97
Q

What side of the long is more affected by lung abscess

A

Right side because more aspiration

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98
Q

Lung abscess x ray

A

Air fluid level

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99
Q

In what case of lung abscess can you get gangrene of the lung

A

Super imposed saprophytic infection ( large fetid green black area)

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100
Q

Lung abscess clinical presentation

A

Fever

cough with copious sputum (foul smelling and bloody or purulent)

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101
Q

Lung abscess complications

A

Metastatic abscesses in the brain ,kidney ,spleen , and finally pleura (risk of empyema)
malignancy in 15% of cases

102
Q

2 groups of obstructive airway disease

A

Localised (mechanical factors like tumors, foreign body)

Diffuse (COPD)

103
Q

Chronic obstructive pulmonary disease

A

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
Q

Types of COPD

A 
Chronic bronchitis 
emphysema 
bronchiectasis 
bronchial asthma 
bronchiolitis
105
Q

Chronic bronchitis

A

Defined clinically with persistent productive cough each day for at least three months of the year over 2 consecutive years

106
Q

In which population do you see the most chronic bronchitis

A

Smokers

Inhabitants of urban smug laden cities (so2, no2, dusts….)

107
Q

Types of chronic bronchitis

A

Simple chronic bronchitis ( Early disease, cough, little sputum, no physiologic obstruction)

chronic asthmatic bronchitis ( Bronchospasm and intermittent wheezing)

chronic emphysematous bronchitis ( emphysema added)

108
Q

Incidence of chronic bronchitis

A

Both sexes affected

most common in in the middle age

109
Q

Risk factors of chronic bronchitis

A 
Smoking (about 90% of patients )
air pollutants (about 20 to 40% of patients )
artificial fibers 
coolant 
occupational fumes like welding
110
Q

Chronic bronchitis pathogenesis

A

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
Q

How does cigarette smoking predisposes to infection

A

Interfere with ciliary action
damage airway epithelium
Inhibit ability of bronchial and alveolar leukocytes to clear bacteria

112
Q

Chronic bronchitis macro appearance

A 
Hyperemia 
swelling of mucous membranes 
mucus cast in bronchi and bronchiole 
mucus secretions in bronchi and bronchioles 
Frank pus collection in bronchi
113
Q

Histology of chronic bronchitis

A

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
Q

Reid index

A

Ratio Of the thickness of mucus glands layer to the thickness of bronchial wall

115
Q

Normal reid index

A

0.36 to 0.41

116
Q

Reid index in Chronic bronchitis

A

0.44 to 0.79

Increases in proportion to severity and duration of disease

117
Q

Bronchial mirroring and obstruction due to in chronic bronchitis :

A 
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
Q

Blue bloater

A

Classic patience with long-standing chronic bronchitis and obstructive features
Long history of chronic of recurrence airway insufficiency and recurrent chest infections

119
Q

Blue bloater incidence

A

Male between 40 to 45-year-old

120
Q

Symptoms of blue bloater

A

Progressive dyspnoea

cyanosis

121
Q

Blue bloater x ray

A

Increased lung markings

large heart outline

122
Q

Blue bloater pathogenesis

A

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
Q

Emphysema

A

Permanent abnormal enlargement of any part of the respiratory acinus ,destruction of the elastin in the wall, no obvious fibrosis

124
Q

Where is emphysema common

A

Advanced countries

125
Q

Population more at risk of emphysema

A

Female African-American

126
Q

Most important risk factor of emphysema

A

Heavy cigarette smoking and urban dwelling

127
Q

Four types of emphysema

A

Centriacinar ( 95%)

Panacinar

Distal acinar

Irregular

128
Q

Centriacinar (centrilobular)

A

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
Q

Panacinar emphysema

A

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
Q

Paraseptal

A

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
Q

Irregular emphysema

A 
Acinus irregularly involved 
Invariably associated with scarring 
Wall adjacent to scar is destroyed 
Asymptomatic
Post inflammatory 
Post tuberculosis 
Pneumoconiosis
132
Q

Pathogenesis of emphysema

A

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
Q

Emphysema morphology

A 
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
Q

Clinical feature of emphysema

A

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
Q

Causes of death in emphysema

A

Corpulmonale
Pneumothorax with lung collapse
Respiratory acidosis ->coma-> death

136
Q

Other forms of emphysema

A

Compensatory emphysema
Obstructive overinflation
Bullous emphysema
Interstitial emphysema

137
Q

Compensatory emphysema

A

Loss of lung substance leading to dilatation with no alveoli destruction (pneumomectomy)

138
Q

Obstructive over inflation

A

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
Q

Bullous emphysema

A

Large bleb or bullae distended with air ( usually near subpleural, apex, tb scars )
If rupture -> pneumothorax

140
Q

Interstitial emphysema

A

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
Q

Bronchiectasis

A

Chronic necrotizing infections of bronchi and bronchioles

Abnormal permanent dilatation of airways

142
Q

Bronchiectasis presentation

A

Recurrent chest infections
Fever
Productive Cough of Foul smelling purulent sputum (sometimes bloody)

143
Q

Bronchiectasis etiology

A

Bronchial obstruction
Necrotizing pneumonia
Congenital or hereditary conditions
Idiopathic

144
Q

Type of bronchial obstruction leading to bronchiectasis

A

Focal : foreign body, tumor, lymphadenopathy, mucus impact ion,

Diffuse : obstructive airway disease, bronchial asthma, chronic bronchitis

145
Q

Type of Necrotizing pneumonia leading to bronchiectasis

A

Tb
Staph
Mixed infections
Post whooping cough , measles, influenza

146
Q

Types of congenital or hereditarily conditions leading to bronchiectasis

A

( defect in development of bronchi)
Cystic fibrosis
Immunodeficiency
Kartagener s syndrome : immobile cilia syndrome

147
Q

Bronchiectasis pathogenesis

A

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
Q

Cystic fibrosis

A

Squamous metaplasia
Impaired mucociliary action
Infection and necrosis of walls
Bronchiectasis

149
Q

Kartageners syndrome

A

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
Q

MacroMorphology of bronchiectasis

A

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
Q

Micro morphology of bronchiectasis

A 
Acute or chronic inflammation 
Ulceration of mucosa 
Squamous metaplasia of epithelium
Abscess due to necrosis 
Fibrosis in peribronchial and peribronchiolar tissue
152
Q

Clinical presentation of bronchiectasis

A 
Persistent cough
Foul smelling sputum sometimes bloody
F3ver
Dyspnoea 
Cyanosis
153
Q

Bronchiectasis complications

A

Cor pulmonale
Lung abscess
Metastatic micro abscesses in brain kidney

154
Q

Bronchial asthma

A

Chronic relapsing inflammatory disease of conducting airways
Hyperreactive airways
Inflammation of bronchial walls
Increased mucus secretion

155
Q

Bronchial asthma presentation

A

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
Q

Classification of bronchial asthma

A

Atopic asthma => extrinsic, allergic, IgE mediated, allergen sensitization

Non atopic asthma => intrinsic, no evidence of allergen sensitization

157
Q

Stimuli of bronchial asthma

A 
Respiratory infection 
Cold air
Exercise
Exposure to irritants ( smoke, fumes, smog) 
Stress , emotional state’s
DRugs like opiates, aspirin 
Food allergens
158
Q

Features of atopic asthma

A 
Most common type 
Classic igE Mediated hypersensitivity rxn 
Begins in childhood
Triggers domestic environmental 
Positive FHA OF ASTHMS
159
Q

Features of non atooc asthma

A

No evidence of allergen sensitization
Less FH positive for asthma
Common triggers => respiratory infection and environmental pollutants

160
Q

Classification asthma

A

Seasonal

Exercise induced

Drug induced

Occupational

Asthmatic bronchitis in smokers

161
Q

Drug induced asthma (aspirin)

A

Not common
Recurrent rhinitis and nasal polyps
React excessively to nsaids
Inhibition of Cox so less prostaglandin E2 and more leukotrienes b4-e4

162
Q

Occipqtional asthma

A

Triggered by fumes (epoxy resins, plastics) gases (toluene), organic and chemical dusts ( wood cotton platinum) other chemicals ( formaldehyde, penicillin)

163
Q

Pathogenesis of asthma

A

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
Q

Immediate asthma phase response

A

Bronchoconstriction

Increased mucus production

Vasodilation

Increased vascular permeability

White cells recruitment

165
Q

Late phase of asthma response

A 
4-8h later 
Mediated by white cells 
Release cytokines , leucotrienes, PAF, eosinophils cationic protein, 
Epithelial damage 
Airway constriction
166
Q

Action of leucotrienes

A

Prolonged bronchoconstriction

Increase vascular permeability

167
Q

Acetylcholine action

A

Bronchoconstriction

168
Q

Histamine action

A

Bronchoconstriction

169
Q

Prostaglandin D2 action

A

Bronchoconstriction

Vasodilation

170
Q

PAF action

A

Platelet aggregation

Release histamine and serotonin

171
Q

MacroMorphology of asthma

A

Over distended Lung
Small areas atelectasis
Occlusion of bronchioles by thick mucus plugs

172
Q

Micro morphology of asthma

A

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
Q

Clinical features of asthma

A

Attack last several hours

Coughing

When severe -> impaired respiratory function -> cyanosis -> death

174
Q

Cause of airway obstruction in asthma

A

Bronchial contraction
Bronchial mucosal increased thickness
Mucus and exudate retention in lumen

175
Q

Asthma diagnosis

A

History
Examination-> resp difficulty, decreased air entry , wheezing

Test
Increased eosinophils in blood
Increased eosinophils, curschmann, spiral, Charcot Leyden crystals in sputum

176
Q

Diagnosis of type of asthma

A

Increased IgE serum

Positive skin allergen test , RAST TEST

177
Q

Diffuse interstitial lung disease

A

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
Q

Interstitium in diffuse interstitial lung diseases

A

Basement membrane of endothelial and epithelial cells

Collagen

Elastic fibers

Proteoglycans

Fibroblasts

Mast cells

Histiocytes

Monocytes

179
Q

Do we know most causes of diffuse interstitial lung diseases

A

No mostly idiopathic

180
Q

Lung diseases with restrictive effect but non obstructive

A

Diffuse interstitial lung disease

181
Q

Changes in the lung due to diffuse interstitial lung disea3e

A

Thick wall =< less o2 diffusion across wall

Decreased lung volume

Decreased lung compliance

182
Q

Diffuse interstitial lung disease presentation

A

Dyspnoea
Tachypnoea
Cyanosis
No wheezing

183
Q

Diffuse interstitial lung diseases x ray

A

Diffuse infiltration lay small granules , irregular lines, ground glass shadows

184
Q

Complications of diffuse interstitial lung disease

A

Pulmonary hypertension
Right heart failure With cor pulmonale
Honey comb lung due to scarring and destruction

185
Q

Classification of diffuse interstitial lung disease based on….

A

Known etiology

Not known etiology

186
Q

Diffuse interstitial disease with known etiology

A 
Pneumoconiosis 
Ionizing radiation
Following ARDS
Drug busulfan
Bleomycin
Beryllosis 
Hypersensitivity pneumonitis
187
Q

Diffuse interstitial disease with unknown etiology

A 
Collagen vascular disease
Goodpastures syndrome 
Idiopathic pulmonary fibrosis 
Idiopathic hemosiderosis 
Sarcoidosis 
Wegeners granulomatosis
188
Q

Pneumoconiosis

A

Non neoplasticism lung reaction to inhalation of mineral dusts, organic dusts, chemical fumes, vapor

189
Q

Types of pneumoconiosis based on mineral dusts involved

A 
Coal - Anthracosis
Asbestos - abestosis 
Silica- silicosis
Beryllium- beryllosis 
Iron oxide - siderosis 
Barium sulphate - baritosis 
Tin oxide - stannosis
190
Q

Types of pneumoconiosis based on organic dusts involved

A

Moldy hay: farmers lung
Bagase: bagassosis
Bird droppings: bird breeders lung

191
Q

Types of pneumoconiosis based on fumes and vapors involved o

A

No2
So2.
Benzene
Insecticide

192
Q

Type of reaction to dust and fumes

A

Inert ( simple, coal worker pneumoconiosis
Fibrosis ( progressive fibrosis , asbestosis, silicosis)
Allergy ( extrinsic allergy alveolitis
Neoplasm (=mesothelioma, bronchogenic

193
Q

Pneumoconiosis pathogenesis

A

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

194
Q

Particularity with asbestos fibers

A

Even tho long (8mm) , very thin so can get into alveoli

195
Q

Coal workers pneumoconiosis

A

Inhalation of coal dust leading to
Asymptomatic anthracosis
Simple CWP => macular or nodular CWP
Complicated CWP=> progressive massive fibrosis

196
Q

Macular CWP

A

Local aggregate of dust laden macrophages in and around
Bronchioles, arterioles, veins, lymphatic, hilar lymph nodes

No significant scarring

Mild emphysema due to smoking

197
Q

Nodular CWP

A

Small nodules with more extensive macular lesions
No fibrosis
No functional difficulty

198
Q

Complicated CWP

A 
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
199
Q

Silicosis

A

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

200
Q

Commonest occupational disease

201
Q

Morphology of silicosis

A

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

202
Q

Histology of silicosis

A

Nodular lesions with layers of collagen with dense collagenous capsule

Silica particles seen under polarized light

203
Q

Can silicosis reactivate Tb

204
Q

Association between silicosis and cancer

A

Increased risk of cancer by 2

205
Q

Disease caused by asbestos

A

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
206
Q

Type of asbestos

A

Serpentine - curly and flexible (chrysolite)

Amphibole - straight stiff brittle fibers ( crocidolite, amosite, tremsolite)

207
Q

Most case of asbestosis due to what type of asbestos

A

Amphiboles

208
Q

Asbestosis pathogenesis

A 
React with lung macrophages and epithelial cells 
Release of fibrogenic mediators 
Diffuse interstitial lung disease
No nodules 
Starts in lower lobes and extend
209
Q

Asbestos morphology

A

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

210
Q

Sarcoidosis

A

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

211
Q

Incidence of sarcoidosis

A

Male more than females

Blacks mostly

212
Q

Sarcoidosis pathogenesis

A 
Unknown antigen poorly degradable
 type 4 reaction 
Granuloma formation 
High CD4 + lymphocytes in lung 
High soluble IL2 receptors in serum and lung
213
Q

Sarcoidosis morphology

A

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
214
Q

Sarcoidosis presentation

A 
Dyspnoea 
Cough 
Chest pain
Haemoptysis
Fatigue 
Weight loss
Fever
Anorexia 
Night sweats
215
Q

Effective treatment of sarcoidosis

216
Q

Pulmonary vascular diseases

A 
Pulmonary congestion and edema 
Adult respiratory distress syndrome 
Pulmonary embolism 
Pulmonary Hemorrhage 
Pulmonary Infarction 
Pulmonary hypertension 
Cor pulmonale
217
Q

Adult respiratory distress syndrome (diffuse alveolar damage)

A

Rapid onset of severe life threatening respiratory insuffiency, cyanosis , severe arterial hypoxemia
Refractory to O2 therapy
Associated with severe pulmonary edema

218
Q

X ray of adult respiratory distress syndrome

A

Diffuse alveolar infiltrate

Hyaline membrane in alveoli

219
Q

Pulmonary embolism hemorrhage infarction epidemiology

A

200,000 death per year in US
High incidence in autopsy
Common in Ghana

220
Q

Etiology of pulmonary embolism hemorrhage infarction

A

Pulmonary arterial occlusion (generally thromboembolism, mostly coming from legs deep veins)

Large vessel thrombosis rare

Pulmonary hypertension
Pulmonary atherosclerosis
Congestive cardiac failure

221
Q

Risk factor of pulmonary embolism hemorrhage infarction

A 
Cardiac disease
Cancer
Immobilization over Long time
Hypercoagulable states
Indwelling central venous lines 
Post op 
Pregnancy 
Post party’s
222
Q

PAthogenesis of pulmonary embolism hemorrhage infarction

A

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

223
Q

Severity of pulmonary embolism hemorrhage infarction depends on

A

Extent of arterial obstruction
Size of occluded vessel
Number of emboli
Status of CVS

224
Q

Morphology of pulmonary embolism hemorrhage infarction

A

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

225
Q

Pulmonary hypertension

A

Normal pulmonary pressure is 1/8 systemic blood pressure

Pulmonary hypertension is 1/4 systemic blood pressure

226
Q

Pulmonary hypertension causes

A

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)

227
Q

Pulmonary hypertension morphology

A

Vascular lesions
Atheromatous plaques in pul artery
Medial hypertrophy and intimate fibrosis with pinpoint channels in small arteries and arterioles

228
Q

How is it determined if surgery of lung is required in pul HT

229
Q

Wegener granulomas

A

Systemic vasculitis affecting upper respiratory tract, lung, kidneys, liver, and skin

230
Q

Wegener granuloma morphology

A

Necrotizing granuloma of nose
Giant cell granuloma of lungs
Polyarteritis
Renal damage

231
Q

Wegeners granuloma histology

A

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

232
Q

More common type of primary tumors of the lungs

A

Malignant type more common than benign

233
Q

Are all secondary tumors of lungs malignant..

234
Q

Most commo type of lung tumor

235
Q

Types of malignant primary tumor of lungs

A

Bronchogenic (90-95%)

Neuroendocrine (carcinoid)

Mensenchymal tumors

Lymphomas

236
Q

Major diagnosed cancer worldwide and most common cause of cancer mortality

A

Bronchogenic carcinoma

237
Q

Population more affected by bronchogenic carcinoma

A

Male more than female
Smokers
Age 40-70 peak at 50-60

238
Q

Bronchogenic carcinoma etiology

A

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

239
Q

Amount of carcinogens in smoke

A

1200 known

240
Q

Impact of smoking on bronchial mucosa

A

Squamous metaplasia to dysplasia to squamous ca

241
Q

Type of bronchiogenic carcinoma

A

Adenocarcinoma -40%, females

Squamous cell ca 20% male smokers
Small cell ca 14%

Large cell ca 3%

Other 25%

242
Q

Common mixed cancer seen in bronchogenic carcinoma

A

Small cel ca with squamous cell ca

Squamous cell with adenocarcinoma

243
Q

Bronchogenic cell ca morphology of ADC

A

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

244
Q

Bronchogenic cell ca morphology of SCC

A

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
245
Q

Bronchogenic carcinoma presentation

A 
Cough 
Weight loss
Chest pain 
Dyspnoea
S
246
Q

Bronchogenic carcinoma lab test

A

Sputum cytology tumor cells
Pleural effusion cytology
FNA fine needle aspiration cytology

247
Q

Bronchogenic ca complication s

A

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

248
Q

Main site of spread of lung carcinoma

A

Lymph metastasis to trachea, bronchial m mediastinal lymph node

Blood borne metastasis to adrenal mostly and then liver and finally brain and bone

249
Q

Metastatic lung tumors morphology

A

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

250
Q

Metastatic lung tumor treatment

A

Surgical excision

Radiation

Chemotherapy

251
Q

Metastatic lung tumor prognosis

A

Poor

E5YS - 5%/

Respiratory Module (5 decks)

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