Respiratory l Flashcards

1
Q

casue of Acute rhinitis

A

Aka the common cold, it is caused by allergies or A viral infection (adenoviruses)

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2
Q

Clinical picture of Acute rhinitis

A

1) runny nose
2)sneezing
3) nasal congestions
4) mild soar throat

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3
Q

Pathogenesis of allergic rhinitis

A

*IgE immune l reaction
*association with mucosal and submucosal mast cells
*increase in Eosinophils in peripheral blood and nasal discharge

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4
Q

Bacteria causing bacterial infection of acute rhinitis

A

Staphylococci, streptococci, H.Influenza

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5
Q

*fibrous scarring
*atrophy of the epithelium and mucous glands
* decreases vascularity

Are the micro-/macroscopic features of what respiratory condition?

A

Acute rhinitis caused by bacterial infection

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6
Q

__________ is a common condition characterised by inflammation and swelling of the sinuses for at least 12 weeks, despite treatment attempts

A

Chronic sinusitis, aka chronic rhinosinusitis

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7
Q

Epidemiology of chronic sinusitis

A

Young and middle-aged adults

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8
Q

Cause of chronic sinusitis

A
  • Infection or
  • nasal polyps in the sinusis, or
  • deviated nasal septum
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9
Q

Pathogenesis of chronic sinusitis

A

Obstruction of drainage outlets from the sinuses —> accumulation of mucous secretions or exudate

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10
Q

Signs and symptoms of chronic sinusitis

A

1)thick discoloured discharge from the nose
2) nasal obstruction congestion (nasal inflammation)
3) pains tenderness and swelling around the eyes, cheeks, nose/forehead
4) reduced sense of smell and taste(adults), cough (children)

Other sings and symptoms:
1)fatigue
2)ear pain
3) aching in the upper jaw and teeth
4)sore throat
5)bad breath
6)Nausea
7) cough that might worsen at night

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11
Q

State the difference between Acute vs chronic sinusitis

A

*similar signs and symptoms
However, fever is a common sign of acute sinusitis but not chronic sinusitis

Acute sinusitis: a temporary infection of the sinuses, often associated with a cold
Chronic sinusitis: the signs and symptoms often last longer and cause more fatigue

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12
Q

————— acute inflammation of the larynx

A

Laryngitis

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13
Q

Cause of laryngitis

A

Inhalations of irritants, allergic reactions, bacteria, viruses, voice overuse

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14
Q

Clinical manifestations of laryngitis

A

Hoarseness—-> due to inflammation and Oedema of the vocal cords

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15
Q

What are the 2 uncommon forms of laryngitis?

A

1) tuberculous laryngitis ( caused by active Tbc; infected sputum is coughed up)
2) diphtheritic laryngitis

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16
Q

Pathogenesis of diphtheritic Laryngitis : Inhalation of ——————- —>implantation on the upper-airways’ mucosa—> release of exotoxin —> necrosis of the epithelium—> dense fibrino-purulent exudate

A

Corynebacterium diphtheriae

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17
Q

Clinical features of Diphtheritic Laryngitis

A

tonsils and pahrynx:
–> sore throat, low fever, malaise (restlessness), dysphagia
–> “Bull neck” (p.18) due to swelling and inflammation of the lymph nodes (lymphadenopathy)

larynx:
–> Hoarsness (loss of voice/ sever respiratory tract obstruction)

skin:
pain, tenderness and erythema —> ulcers with sharply defined borders and browinish-grey membrane (see p.20)

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18
Q

Complications of Diphtheritic Laryngitis

A

1) Myocarditis and peripheral neuropathy –> absorption of bacterial exotoxins

2) obstruction of major airways –> sloughing and aspiration of pseudo-membrane

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19
Q

——–: Acute inflammation of the epiglottis

A

Acute Epiglottits

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20
Q

Epidemiology of Acute Epiglottitis

A

young children

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21
Q

Cause of Acute Epiglottitis

A

Haemophilus influenzae (H. influenzae)

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22
Q

clinical features of Acute Epiglottits

A

pain and airway obstruction

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23
Q

prognosis of Acute Epiglottitis

A

Failure to appreciate the need to maintain
an open airway for a child → Life-threatening
condition with fatal consequences

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24
Q

Croup?

A

Aka Acute Laryngotracheobronchitis
–> inflammation of the larynx, trachea and epiglottis

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25
Q

casue (virus) of Croup in children

A

1) Parainfluenza Virus (most common)
2) Respiratory Syncytial Virus

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26
Q

clinical picture of Croup

A
  • Harsh, persistent cough
  • Inspiratory stridor (noisy high-pitched sound with breathing, caused by blockage or narrowing in the upper airway)
    -restlessness
  • increased respiratory rate
  • supra-sternal retraction
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27
Q

Complications of Croup

A
  • Occasionally, laryngeal inflammatory reaction →Prominent airway narrowing → Respiratory failure
  • Secondary bacterial infection (Staphylococci, Streptococci, H. influenzae) of upper respiratory tract
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28
Q

————–: Nosebleed, which can range from a trickle to a strong flow

A

Epistaxis

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29
Q

The 2 types of Epistaxis

A

1) Anterior (most common) : originates in the Kiesselbach’s plexus (vessels in the antero-inferior septum)
2) posterior [less common, but more serious]; Associated with atherosclerosis or bleeding disorders
–> (originates in the posterior septum overlying the vomer bone, or laterally on the inferior or middle turbinate)

p.26

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30
Q

cause of Epistaxis

A

1) drying of nasal mucosa
2) local trauma (casued by nose picking or blowing)
3) less common: coagulopathy, arteriosclerosis, local infections, foreign bodies, septal perforation

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31
Q

What are the signs of Epistaxis that must be given particular attention for?

A

1) bleeding not stopped by direct pressure
2) Use of anticoagulant drugs
3) miltiple recurrences, with no clear cause
4) signs of Hypovolemia (loss of body fluid) and heamorrhagic shock
5) cutaneous signs of a bleeding disorder

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32
Q

————– : Tissue injury caused by a pressure related change in body compartment gas volume

A

Barotruama

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33
Q

Affected organs in Barotrauma

A

lungs, ears, sinusis, GI tract, etc.

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34
Q

risk factors of Barotrauma

A

(those interfering with eq. of pressure)
1) sinus congestions
2) infection
3) Eustachian tube blockage
4) structural anomaly

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35
Q

pathogenesis of Barotrauma

A

Entrapment of air or other gas within
the lungs → Over-inflation of them → Pulmonary barotrauma

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36
Q

Symptoms of Barotruama

A

1) ear pain
2) hearing loss
3) sinus pain
4) vertigo
5) abdominal pain
6) alveolar rupture and pneumothorax (collapsed lungs) –> Dyspnoea and loss of consciousness
7) Epistaxis

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37
Q

diagnosis of Barotrauma

A

 Clinical evaluation
 Imaging tests

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38
Q

treatment of Barotrauma

A

case 1 : life threatening conditions like Alveolar and GI rupture
a. Abnormal vital signs –> high flow 100% O2
b. respiratory failure –> endotracheal intubation

case 2: Nurologic symptoms:
–> recompression chamber

case 3: pneumothorax
–> chest decompression with a large bore needle ( 2nd intercostal space, mid-clavicular line) and subsequent thoracostomy

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39
Q

Laryngeal/Pharyngeal Obstruction: Blockage of upper airway, occurs when the (upper/lower ?) breathing passages become ————- or ———— → Impairment of breathing

A

upper, narrowed, blocked

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40
Q

parts affected as a result of Laryngeal/Pharyngeal Obstruction

A

trachea, larynx and pharynx

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41
Q

causes of laryngeal/pharyngeal obstruction

A

1) allergic reactions to various agents and substances
2) fire or burns from breathing in smoke
3) chemical burns and reactions
4) Epiglottitis
5) injury or infection of the upper airways
6) laryngeal cancer
7) peritonsillar or retropharyngeal abscess

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42
Q

symptoms of Laryngeal/Pharyngeal Obstruction

A

1) choking
2) unusual breathing sounds: wheesing, Crowing, whistling
3) loss of consciousness
4) confusion and panic
5) Cyanosis
6) difficulty in breathing and gasping air
7) agitation or fidgeting

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43
Q

exams and tests for Laryngeal/Pharyngeal Obstruction

A

*X-ray
*bronchoscopy
*laryngoscopy

physical examination:
–> decreased breath sounds in the lungs
–> Rapid, shallow, or slowed breathing

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44
Q

treatment for Laryngeal/Pharyngeal Obstruction

A

1) endotracheal intubation
2) Tracheostomy or cricothyrotomy (p.39)
3) removal of stacked objects with special instruments

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45
Q

Inhalation of a foreign object into the nose, mouth, or lower respiratory tract → Stuck within the respiratory system → Breathing problems or choking caused by →
—————— and —————–

A

Inflammation and infection

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46
Q

epidemiology of inhalation of Forgein body

A

Mostly children, 1-3 years old

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47
Q

causes of forgein body related conditions

A

Certain foods (e.g. nuts, seeds, popcorn) and
small objects (e.g. buttons, beads) → Partial or total airway blockage

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48
Q

symptoms of inhalation of a foreign body

A
  • Patients with complete airway obstruction require immediate medical attention and typically are aphonic (loss of voice) and unable to breath

*Patients who are coughing, gagging, and vocalising have partial obstruction

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49
Q

management of inhalation of a foreign body

A

Use of the Heimlich manoeuvre has improved the mortality rate of patients with complete airway obstruction, but use of it in patients with partial obstruction may produce complete obstruction

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50
Q

epidemiology of nasal Papilloma

A
  • Most common benign neoplasm of nasal cavity and paranasal sinuses
  • Male, 50-60 years
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51
Q

clinical features of nasal papilloma

A

1) nasal obstruction
2) Epistaxis

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52
Q

what are the 2 types of nasal papilloma

A

1) Exophytic: Grows outward from epithelial surface; Lateral walls

2) Endophytic: Grows inward into tissues in finger-likeprojections from a superficial site of origin; Nasaldiaphragm

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53
Q

*Cylindrical epithelium of airway tract with increase in the number of cellular rows
*Squamous metaplasia of cylindrical epithelium
*Resemblance to transitional (cell) epithelium

Are the microscopic features of what nasal carcinoma?

A

nasal papilloma

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54
Q

epidemiology of nasal angiofibroma

A

Rare, prominent vascularised lesion

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55
Q

clinical manifestaions of nasal angiofibroma

A

Mainly with epistaxis

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56
Q

localisation of nasal angiofibroma

A

In the posterior nasal wall of adolescent
males

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57
Q

microscopic findings of nasal Angiofibroma

A

Numerous blood vessels in a marked fibrotic matrix

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58
Q

prognosis of nasal Angiofibroma

A

Histologically benign, but locally aggressive

59
Q

epidemiology of nasal Squamous cell Carcinoma

A

Most frequent malignant nasal tumour

*All types of differentiation (well-, moderately- and poorly-differentiated tumours)

60
Q
  • Large, eosinophilic and polygonal cells
  • Cells are layered in an architectural pattern that looks like squamous cell epithelium
    *Frequently, keratin production (in the centre of agroup of epithelial cells with a whorled appearance;This type of keratin is known as “keratin pearl”)

Are the microscopic feature of which nasal carcinoma?

A

squamous cell carcinoma

61
Q

undifferentiated Nasopharyngeal Carcinoma is aka?

A

Lymphoepithelioma

62
Q

epidemiology of Nasopharyngeal Carcinoma

A

Common in Southeast Asia and
East Africa

63
Q

cause of Nasopharyngeal Carcinoma

A

Epstein-Barr virus

64
Q

localisation of nasopharyngeal carcinoma

A

Pharyngeal fossa of Rosenmülle

65
Q

*Tumours composed of sheets or large bands of large undifferentiated cells that also contain a population of non-neoplastic small (predominantly T) lymphocytes

  • Tumour cells with vesicular nuclei and prominent cytoplasm
    *No signs of keratinisation

Are the microscopic features of which Carcinoma?

A

Nasopharyngeal Carcinoma

66
Q

Epidemiology of Nasal Adenocarcinoma

A

5% of malignant tumours of the nose
and throat

67
Q
  • Intestinal-Type Adenocarcinoma (Neoplastic
    intestinal glands resembling Colonic Adeno-Ca)
  • Non-Intestinal Type Adenocarcinoma
  • Salivary gland-like Carcinomas (Adenoid Cystic Carcinoma)

Are the microscopic classifications of which Nasal Carcinoma?

A

Adenocarcinoma

68
Q

Olfactory Neuroblastoma is aka?

A

Aesthesioneuroblastoma

69
Q

epidemiology of Olfactory Neuroblastoma

A

Usually, older male patients (paediatric tumours:
adrenals/abdomen of infants and young children)

70
Q

*Small round blue cells in a neurofibrillary matrix
*Characteristic Flexner-Wintersteiner rosettes

Are the microscopic features of which carcinoma?

A

Olfactory Neuroblastoma

71
Q

Immunohistochemistry of nasopharyngeal carcinoma

A

[+] PANCKs, CK-8, -18, -19, ΕΜΑ, B-, T-cell, LCA and EBV (EBER in-situ hybridisation)

72
Q

immunohistochemistry of Olfactory Neuroblastoma

A

Positivity for: Chromogranin,
ACTH, Neurofilament (NF), Neuron Specific Enolase(NSE), S-100 and Cytokeratins (CKs)

73
Q

localisation of nasal (extramedullary) Plasmacytoma

A

Upper airway tract –> Most common
extra-medullary site

*Either as a regional manifestation of Multiple
Myeloma or as a primary lesion

74
Q

*Sub-mucosal localisation
*Airway tract obstruction
*Ulceration and haemorrhage

Are the macroscopic features of which nasal carcinoma?

A

Extramedullary Plasmacytoma

75
Q

*Diffuse cellular population
*Round to ovoid cells
*“Cart-wheel” chromatin
*Basophilic cytoplasm

Are the microscopic findings of which nasal carcinoma?

A

extramedullary Plasmacytoma

76
Q

immunohistochemistry of Extramedullary Plasmacytoma

A

–> Positivity in one of the light
chains (κ, λ) and in one
immunoglobulin (IgG, IgM)
–>Positive staining for: CD38,
CD79A, CD138, VS38c

77
Q

————— : Aggressive mesenchymal malignancy of skeletal muscle origin

A

Embryonal Rhabdomyosarcoma

78
Q

epidemiology of Embryonal Rhabdomyosarcoma

A
  • Most common soft tissue sarcoma of childhood and adolescence
  • Approximately 87% of patients <15 years
79
Q

localisation of Embryonal Rhabdomyosarcoma

A

Occurrence in any anatomic site, although
mostly in the head, neck or genitourinary tract

80
Q
  • Small, round blue cell tumour
  • Cells with high cytologic variability (representing several stages of skeletal muscle morphogenesis):
    • Appearance of highly differentiated
      neoplasms containing rhabdomyoblasts
      with large amounts of eosinophilic
      cytoplasm and cross striations, or
    • More commonly, the appearance of poorly
      differentiated tumour cells
      *Elongated pleomorphic tumour cells
      *Centrally located hyperchromatic nuclei
  • Variable nuclear pleomorphism
  • Loose, myxoid or cellular collagenous stroma
  • High mitotic index
    *Prominent nucleoli

Are the microscopic features of which Nasal Carcinoma?

A

Embryonal RHabdomyosarcoma

81
Q

clinical features of Embryonal Rhabdomyosarcoma

A

*Expanding mass → Pain and symptoms related to the compression of nearby structures
*Metastases
→ Pain in the bones
→ Anaemia, thrombocytopenia, and
neutropenia
→ Difficulty with respiration due to lung
nodules or pleural effusion

82
Q

prognosis of Embryonal Rhabdomyosarcoma

A

*Metastatic tumours: 5-year survival rate less
than 30%
* Confined disease treated with combined
surgery, radiation and chemotherapy: 5-year
survival rate of over 80%

83
Q

pathogensis of squamous cell carcinoma of the Oropharynx

A

–> Association with high risk HPV (Type 16, ~80% of cases)
–> Most frequent tumour in this location (mainly in palatine and lingual tonsils)

84
Q

histopathology of squamous cell carcinoma of the Oropharynx : (Non-kretanising/kreatinising) squamous cell carcinoma with ————– morphology

A

Non-Kreatinsing, Basaloid (p. 84)

85
Q

epidemiology of squamous cell carcinoma of the oropharynx related to HPV(+) cases

A

*young patients
*Non-smokers
*higher stage at presentation, with cervical lymph nodal metastases
*better prognosis than HPV(-) cases [association wiht tobacco and alcohol abuse)

86
Q

what are tumours of the larynx ka?

A

Vocal Cord Nodule or Singer’s Nodule

87
Q

cause of vocal cord nodule tumours

A

1) Chronic irritation (e.g. excessive use
of the voice)
2) heavy cigarette smoking

88
Q

vocal cord nodule tumors are localised to the [TURE/FALSE?] vocal cords?

A

TRUE vocal cords

89
Q

Epidemiology of squamous papilloma of the larynx

A
  • Benign neoplasm; Rarely becomes malignant
  • Association with low-risk HPV-6 and -11
    *Centered around true vocal cords
    *Multiple lesions (in children and adolescents) → Extension into the trachea and bronchi → Airway obstruction [Juvenile laryngeal papillomatosis]
90
Q

epidemiology of squamous cell carcinoma of the larynx

A

*Most common malignant tumour of the larynx
*Men >40 years

91
Q

predisposing factors of squamous cell carcinoma of the larynx

A
  • Combination of cigarette smoking and alcoholism
  • NO association to HPV infection
92
Q

clinical picture of squamous cell carcinoma of the larynx

A

Persistent hoarseness

93
Q

Epidemiology of Glottic Carcinoma

A

–> carcinoma in the larynx
–> originates from the true vocal cords
–> most common and best prognosis

94
Q

epidemiology of supra- and subglottic carcinomas (of the larynx)

A

less common and worse prognosis (compared to glottic carcinoma )

95
Q

give exmaples of Infectious, Immunologic and Inflammatory Disorders of the Upper Airways:

A

 Acute Rhinitis
 Sinusitis (Acute and Chronic)
 Laryngitis (e.g. viral, bacterial, diphtheritic)
 Acute Epiglottitis
 Acute Laryngotracheobronchitis (Croup)

96
Q

list a few Traumatic and Mechanical Disorders of the Upper Airways:

A

 Epistaxis
 Barotrauma
 Laryngeal/Pharyngeal Obstruction
 Tracheomalacia
 Foreign Body

97
Q

—————— : Lesions of congenital origin derived from the primitive foregut

A

Bronchogenic Cysts

98
Q

Epidemiology of Bronchogenic cysts

A

–> most common primary cysts of the mediastinum
–> Majority of the cysts are in the mediastinum
the rest –> lung parenchyma :15-20%

99
Q

describe what is observed in an imaging study of Bronchogenic cysts

A

–> uni-locular, non-calcified masses
–> sphearical or oval, with smooth outlines

100
Q

(DD) Differential Diagnosis of Bronchogenic cysts

A

Lung abscess, Tbc, infected bullas, neoplasms, etc.

101
Q

macroscopic features:

  • Uni-locular cyst (cyst with a single sac)
  • Content: Clear fluid, haemorrhagic secretions or air

Are the features of what respiratory condition?

A

Bronchogenic cysts

102
Q

microscopic features
* Cyst’s internal lining: Columnar ciliated epithelium
* Cyst’s wall: Cartilage and bronchial mucous glands

A

Bronchogenic cysts

103
Q

clinical features of bronchogenic cysts

A
  • Cough
  • Fever
  • Pain
  • Dyspnoea
  • Tracheobronchial compression and lung infections (in children; because of the soft tracheo-bronchial tree)
104
Q

complications of Bronchogenic cysts

A
  • Infections (in cysts with bronchial communications)
  • Rapture of cyst into trachea, pleural or pericardial cavity
  • Pneumothorax, accompanied by pleuritis
105
Q

what are the 2 Most common congenital malformations of the lower respiratory tract?

A
  • Congenital Cystic Adenomatoid Malformation [CCAM]
    (= congenital pulmonary airway malformation)
  • Broncho-Pulmonary Sequestration [BPS]
106
Q

localization of Broncho-Pulmonary Sequestation

A

1) Intralobar:
–>Observed within the lung
–>Without own pleura

2) Extralobar:
–> Completely covered with pleura
–>May be extrathoracic; 10% subdiaphragmatic, left side

3) Both intra- and extralobar:
–> Solid, well-circumscribed and echogenic masses (US), similar to Type 3 CCAM (Bronchial/alveolar)

107
Q

types of congenital Diaphragmatic Hernia

A
  1. Postero-lateral Bochdalek-type (70%)
  2. Anterior Morgagni-type (27%)
  3. Central septum transversum-type (2-3%)
  • CDH defects range from small subcentimeter defects to complete diaphragmatic agenesis
  • Bochdalek hernias: Left side (85%); Right side (13%); Bilateral (2%)
108
Q

Pathogenesis of CCAM & BPS

A
  • Abnormalities that occur during the branching and proliferation of the bronchial structures
  • Abnormal proliferation of tissues, airway obstruction, dysplasia and metaplasia of the normal tissue
109
Q

Congenital Cystic Adenomatoid Malformation [CCAM] classification, based on presumed site of development of the malformation:

A

0 = Tracheo-bronchial
1 = Bronchial/bronchiolar
2 = Bronchiolar
3 = Bronchiolar/alveolar
4 = Distal acinar

110
Q

Pathogenesis of Congenital Diaphragmatic Hernia

A
  1. Result from a non-fusion of different parts of the diaphragm (failed fusion) → Herniation of
    abdominal contents into the thorax →
    Compression and dysgenesis of the lungs
  2. Abnormal lung development → Results in
    abnormal diaphragmatic development
  3. Failure of the pleuro-peritoneal fold to fuse with the post-hepatic mesenchyme
111
Q

Diagnosis of Congenital Diaphragmatic Hernia

A

1) Ultrasound:
–> Assessment of the extent of herniation and
associated mediastinal shift
–> Inadequate to identify a herniated liver because of its comparable echogenicity to the fetal lung
–>Doppler US: Assessment of blood flow to the ipsilateral lung, which closely parallels lung development

2) MRI:
–> Provides detail of the herniated viscera
–> Allows for precise measurements for prognostic calculation

112
Q

What are the 2 factors that determineine the severity of CDH?

A

1) liver position:
–> Foetuses with the liver up in the chest –> More severe form of CDH and lower survival rate

2) Lung-to-Head Ratio or LHR:
–> Numeric estimate of the size of the foetal lungs, based on measurement of the amount of visible lung; High LHR values >1.0 –> Better outcomes

*LHR: luteinizing hormone receptor

113
Q

Immotile Cilia Syndrome is aka?

A

Primary Ciliary Dyskinesia, Kartagener Syn.

114
Q

Cause of Immotile cilia syn.

A

Mutations in the:
1) DNAI1 [Dynein Axonemal Intermediate chain1] &
2) DNAH5 [Dynein Axonemal Heavy
chain 5] –> 30% of cases; Autosomal recessive
inheritance

115
Q

Immotile cilia syn is charcterised by:

A

a. Chronic respiratory tract infections
b. Abnormally positioned internal organs
c. Infertility

116
Q

Signs and symptoms caused by immotile cilia syn.?

A

1) Babies–> Breathing problems at birth

2) Early childhood –> Frequent respiratory tract infections → Bronchiectasis

3) 50% of patients–> Situs inversus totalis (mirror-image reversus)

4) 12% of patients –> Heterotaxy syndrome or situs ambiguus –> Structurally abnormal or improperly positioned organs (heart, liver, intestines, spleen).
- May also be accompanied by asplenia or polysplenia

5) Infertility (males: due to flagella dysfunction of sperms; females: due to abnormal cilia in the
fallopian tubes)

117
Q

Treatment of Abnormal cilia syndrome

A

1) Antibiotics –> Infections (caused commonly by Hemophilus influenzae or Staphylococcus aureus)
2) Inhaled bronchodilators, mucolytics, and chest physiotherapy –> Obstructive lung disease/ bronchiectasis
3) Surgical care: Tympanostomy tubes → Reduction of recurrent infections and conductive hearing loss

118
Q

causes of pulmonary embolisim

A

1) Venous thrombosis (lower extermities or pelvis)
2) fat
3) amniotic fluid
4) clumps of tumour cells or bone marrow

119
Q

Risk factors of Pulmonary embolism

A

1) Stasis of blood flow (prolonged bed rest or immobilisation)
2) Hypercoagulable states
3) Use of Oral contraceptives

120
Q

clinical findings of Pulmonary embolism

A

1) Saddle embolus:
*A sudden increase in Pulmonary Artery pressure
*Acute right ventricular strain → Sudden death

2) Pulmonary infarction:
*Sudden onset of dyspnoea and tachypnoea
*Pleuritic chest pain
*Friction rub
*Effusion
*Expiratory wheezing

121
Q

laboratory findings of Pulmonary embolism

A

1) Respiratory alkalosis (arterial PCO2 <33 mmHg)
2) PaO2 <80 mmHg (90% of cases)
3) Increase in A(lveolar)-a(rterial) gradient (100% of cases)
4) Increase in D-dimers
5) Positive D-dimers
* Good sensitivity (85-98%)
* Poor specificity

122
Q

Diagnostic tests of Pulmonary embolism

A

1) Chest X-ray
–>Elevation of ipsilateral hemi-diaphragm
–>Pleural effusion (haemorrhagic)
–>Westermark’s sign of peripheral oligaemia
–>Fleischner’s sign of “amputated” pulmonary artery
–> Hampton hump (wedge-shaped area of
consolidation)

2) Abnormal Perfusion Radionuclide Scan
–>Ventilation scan: Normal
–>Perfusion scan: Abnormal
–>Pulmonary angiogram: Gold standard
confirmatory test

123
Q
  • Red-blue raised wedge-shaped area that extends to the pleural surface
  • Majority are located in the lower lobes (Perfusion > Ventilation)
    *Fibrinous exudate on pleural surface
    *Haemorrhagic pleural effusion

Are the macro-/micro scopic features of what kind of embolism?

A

Pulmonary embolism

124
Q

Epidemiology of primary pulmonary hypertension

A
  • Rare with Unknown aetiology; Genetic predisposition
  • NO heart or lung disease
  • Vascular hyper-reactivity with smooth muscle proliferation
125
Q

Hisologic picture of primary pulmonary hypertension

A

Characteristic plexiform lesions

126
Q

Epi of secondary pulmonary hypertension

A

More common than primary

127
Q

pathogenesis of Secondary pulmonary hypertension

A
  • Endothelial cell dysfunction
    –>Loss of vasodilators (e.g. NO)
    –> Increase in vasoconstrictors (e.g. Endothelin)
    *Hypoxaemia & Respiratory Acidosis → Pulmonary arteries vasoconstriction → Smooth muscle
    hyperplasia and hypertrophy
128
Q

causes of secondary pulmonary hypertension

A

1) Chronic hypoxaemia (e.g. Chronic lung disease)
2) Chronic respiratory acidosis (e.g. Chronic bronchitis)
3) Loss of pulmonary vasculature → Workload for remaining vessels (e.g. Emphysema, recurrent pulmonary emboli)
4) Left-to-right cardiac shunts → Volume overloading pulmonary vasculature
5) Left-sided valvular disease (e.g. Mitral stenosis) → Backup of blood into pulmonary veins → Venous hypertension

129
Q

Histopathology

1) Atherosclerotic changes of main pulmonary arteries (Result of ↑ pressure to endothelium → Endothelial injury)
2) proliferation of myo- intimal and smooth muscle cells

Are the features of what condition?

A

Secondary Pulmonary Hypertension

130
Q

pathogenesis of pulmonary oedema

A
  1. Due to alterations in Starling forces (transudate)
    * Increased hydrostatic pressure in pulmonary
    capillaries
    –>Left-sided heart failure
    –>Volume overload
    –> Mitral stenosis
    *Decreased oncotic pressure
    —>Nephrotic syndrome
    —>Cirrhosis
  2. Due to micro-vascular or alveolar injury (exudate) –> Increased alveolar capillary permeability
    ▪ Infections (e.g. sepsis, pneumonia)
    ▪ Aspiration (e.g. drowning, gastric contents)
    ▪ Drugs (e.g. heroin)
    ▪ High altitude
    ▪ Acute Respiratory Distress Syndrome (ARDS)
131
Q

causes of Adult Respiratory Distress Syndrome
(ARDS)

A

Shock, sepsis, trauma, uraemia, aspiration of
gastric contents, acute pancreatitis, inhalation of chemical irritants, oxygen toxicity, heroin, bleomycin, etc

132
Q

pathogenesis of Adult Respiratory Distress Syndrome (ARDS)

A

Damage to alveolar capillary endothelium and alveolar epithelium (Diffuse alveolar damage) → ↑ in alveolar capillary permeability → Leakage of protein-rich fluid into alveoli

133
Q

pathogenic factors of Adult Respiratory Distress Syndrome?

A
  • Neutrophils → Release of substances, toxic to
    alveolar wall
  • Activation of coagulation cascade → Micro-emboli
  • Oxygen-derived free radicals → Oxygen toxicity
134
Q

clinical features of Adult Respiratory Distress Syndrome (ARDS)

A

Impairment of respiratory gas exchange → Severe hypoxia

135
Q

Histopathologic pictures of Adult Respiratory Distress Syndrome (ARDS)

A

Formation of intra-alveolar hyaline membranes (fibrin and cellular debris)

136
Q

cause of Neonatal Respiratory
Distress Syndrome (NRDS)

A

Deficiency of surfactant, due to immaturity

137
Q

clinical features of Neonatal Respiratory
Distress Syndrome (NRDS)

A

1) Dyspnoea
2) Cyanosis
3) Tachypnoea

138
Q

what are the advantages of surfactants in Neonatal Respiratory Distress Syndrome? where are they secreted from ?

A

1) Reduces surface tension within the lung →
Facilitates expansion during inspiration and
prevents atelectasis during expiration
2) Secreted by type II pneumocytes

138
Q

predisposing factors of Neonatal Respiratory
Distress Syndrome (NRDS)

A

1) Prematurity
2) Maternal Diabetes Mellitus
3) Birth by caesarian section

138
Q

Macro-/Microscopic findings:
*Heavy lungs, with alternating areas of atelectasis and alveolar or alveolar-ductal dilatation
*Engorgement of small pulmonary vessels
*Leakage of blood products into the alveoli →
Formation of intra-alveolar hyaline membranes
(fibrin and cellular debris)

Are the features of what respiratory syndrome?

A

Neonatal Respiratory Distress Syndrome (NRDS)

139
Q

complications of Neonatal Respiratory
Distress Syndrome (NRDS)

A

1) Broncho-Pulmonary Dysplasia: Result of treatment with high-concentration oxygen and mechanical ventilation
2) Patent ductus arteriosus: Due to immaturity and hypoxia
3) Intra-ventricular brain haemorrhage
4) Necrotising Enterocolitis: Fulminant inflammation of the small and large intestines

140
Q

❖ Interstitial fibrosis
❖ Inadequate alveolar development

Are the Histopathologic features of which respiratory syndrome ?

A

Broncho-Pulmonary Dysplasia

141
Q

————- :Collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma

A

Acquired Atelectasis

142
Q

Acquired atelectasis, divided into:

A

1) Resorption (or Obstruction) Atelectasis
2) Compression Atelectasis
3) Contraction Atelectasis