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Respi > respi patho > Flashcards

respi patho Flashcards

1
Q

defences against infection in lungs (3)

A
  • large microbes trapped in mucus -> transported to throat by ciliary action -> swallowed
  • cough reflex
  • smaller organisms phagocytosed by alveolar macrophage/if enter bloodstream, will incite immune response
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2
Q

which parts of the aiway is sterile

A
  • anywhere below the vocal chords (ie LOWER RESPIRATORY TRACT) -> due to defence mechanisms
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3
Q

main causative organism of acute URTI

A

viral infection

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4
Q

pathology of rhinitis (2)

A

INFECTIVE (mostly viral) -> surface epithelial cells necrosis -> exudation of fluid and mucous and swelling -> nasal obstruction
ALLERGIC -> hypersensitive to environmental agent, mast cell degranulation etc -> produce exudate and mucosal edema -> if antigenic stimulus persists, mucosa becomes swollen and polypoid -> formation of nasal polyps

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5
Q

which parts of the sinus is affected in sinusitis

A
  • inflammation of the paranasal sinus linings of ANTERIOR GROUP of sinuses (maxillary, ethmoid and frontal sinuses)
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6
Q

complication of sinusitis

A
  • mucosal edema (edema build up in mucosa forming a small lump) -> impair drainage of secretion -> secondary bacterial infection
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7
Q

clinical presentation of acute laryngitis and pharyngitis (3)

A
  • sore throat (supraglottic)
  • hoarseness (glottic)
  • cough and tracheal soreness (subglottic)
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8
Q

acute laryngitis and pharyngitis is usually caused by:

A

viral infection

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9
Q

why is acute laryngitis and pharyngitis dangerous in young children

A
  • children have small airways that are easy to collapse, mucosal & submucosal edema can cause airway obstruction easily
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10
Q

describe breathing sound in children with acute pharyngitis/ laryngitis

A

stridor
stridor + cough = coup

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11
Q

predisposing factor to chronic laryngitis + pathogenesis

A
  • heavy smokers
  • chronic irritation of epithelium cause squamous metaplasia
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12
Q

chronic laryngitis increases risk of:

A

dysplasia and squamous cell carcinoma

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13
Q

most common laryngeal carcinoma & location

A

SQUAMOUS CELL CARCINOMA (95%)
- mostly GLOTTIC (can be supraglottic/ subglottic)

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14
Q

risk factors for squamous cell carcinoma of LARYNX

A
  • Smoking (alw associated with SCC)
  • Alcoholism
  • Asbestos
  • Chronic laryngitis
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15
Q

describe benign lesions of the larynx (2)

A
  • singer’s nodules -> stress vocal chords too much; cause HOARSENESS
  • laryngeal papilloma/ squamous papilloma -> due to HPV INFECTION
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16
Q

patient presents with facial edema and bronchospasm

A

allergic pharyngolaryngeal edema
- life threatening Type I hypersensitivity

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17
Q

types of nasopharyngeal carcinoma (3)

A
  • keratinizing NPC
  • differentiated nonkeratinizing NPC
  • UNDIFFERENTIATED NONKERATINIZING NPC (most common!!! 95% of NPCs)
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18
Q

main risk factors for keratinizing NPC (nasopharyngeal carcinoma) (2)

A
  • EBV INFECTION (at nasopharyngeal epithelium) at young age -> presents as infectious mononucleosis
  • family history -> esp SOUTHERN CHINESE
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19
Q

NPC clinical presentations

A
  • hearing loss, tinnitus
  • diplopia
  • nasal obstruction
  • cervical lymph node metastasis
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20
Q

what tests are recommended for people with fam history of NPC? (2)

A
  • EBV IgA antibody -> IgA usually precedes tumour development by a few years
  • nasoendoscopy
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21
Q

inhaling hot toxic fumes in a fire cause:

A

acute toxic laryngitis

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22
Q

three types of atelectasis and their causes (3)

A
  • Resorption -> obstruction of alveoli, O2 in alveoli resorbed thus alveoli collapses
  • Compression -> by pleural effusion/ haemothorax/ pneumothorax
  • Contraction -> lung fibrosis cause loss of surfactant -> alveoli collapse
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23
Q

what does atelectasis predispose a patient to

A
  • INFECTION due to mucus trapping
  • and hypoxia
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24
Q

bronchiolitis pathogenesis

A
  • inflammation of airway diameter <2mm (BRONCHIOLES)
  • macrophage infiltrate airways, cause SCARRING & NARROWING -> obstruction of airway
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25
Q

bronchitis vs bronchiolitis (2)

A
  • difference in region infected (bronchi vs bronchiole)
  • bronchitis have MUCUS production (hyperplasia of mucus glands are seen in CHRONIC bronchitis)
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26
Q

causative organism for bronchitis/ bronchiolitis

A

VIRUSES
- eg influenza tracheobronchitis, respiratory syncitial virus (RSV) bronchiolitis

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27
Q

broncho pneumonia pathogenesis & complications

A
  • bronchi infected -> spread to bronchioles & alveoli

complication: lung abscess

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28
Q

lobar pneumonia pathogenesis & complications

A
  • Organisms begin infection from bronchioles & alveolar space (does not start from bronchi)

complication: bacteremia

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29
Q

common organism in lobar pneumonia

A

S pneumonia, Klebsiella

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30
Q

aspiration pneumonia pathogenesis & complication

A
  • swelling or aninfectionof the lungs/ large airwaysdue tounconscious/ impaired swallowing

complication: lung abscess

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31
Q

aspiration pneumonia causative organisms

A

causative organisms: oropharyngeal bacteria, anaerobes

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32
Q

IMAGING: pneumonia

A
  • basically opaque white block (usually at bottom of lung), no pulmonary vessels
  • differentiate from pleural effusion: pneumonia still HAS costophrenic angle
  • differentiate from mass: pneumonia has poorly defined margins
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33
Q

what is lung abscess

A

localized area of suppurative necrosis, usually forming large cavities

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34
Q

what causes lung abscess (6)

A
  • broncho pneumonia
  • aspiration pneumonia
  • septic emboli (eg Staph aureus)
  • trauma
  • bronchiectasis -> bronchial obstruction -> accumulate mucus -> infection & necrosis
  • pulmonary infarction -> necrosis
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35
Q

complications of lung abscess (4)

A
  • Empyema (rupture into pleura)
  • Bronchopleural fistula
  • Haemorrhage from erosion into pulmonary vessel
  • Septicaemia
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36
Q

lung abscess vs empyema

A
  • lung abscess involves LUNG PARENCHYMA
  • empyema involves PLEURAL SPACE
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37
Q

lung abscess contains mainly?

A

neutrophils

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38
Q

atypical pneumonia causative organisms

A
  • Mycoplasma (#1), legionella, chlamydia, rickettsia
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39
Q

IMAGING & presentation: atypical pneumonia

A
  • absence of consolidation on Xray due to minimal airspace exudate
  • interstitial inflammation (pneumonitis) thus increase interstitial markings in Xray

presentation:
- symptoms of pneumonia

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40
Q

what type of hypersensitivity is hypersensitivity pneumonitis

A
  • Acute exposure –> type III hyper sensitivity response –> respiratory 4-8 hours after exposure
  • Repeated exposure -> sensitisation and type IV hypersensitivity reaction –> insidious development of dyspnoea and pulmonary fibrosis in a patient that has not experienced acute symptoms
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41
Q

IMAGING: pneumonitis

A

pneumonitis:
- inflammatory disease dominated by interstitial inflammation -> increase interstitial markings in Xray

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42
Q

TB histo presentations (3)

A
  • Granuloma (epithelioid histiocytes surrounding area of central caseous necrosis)
  • Multinucleated giant cells
  • Lymphocytes
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43
Q

risk factors for TB

A
  • poverty, crowded, endemic areas
  • immunocompromised: diabetes, HIV
  • alcoholic
  • chronic lung diseases
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44
Q

complications of pri TB (uncommon)

A

progresses with severe pneumonia & dissemination
- continuing enlargement of the caseating granulomas in the lymph nodes
- spread occurs by the enlarging nodes eroding either
1) through wall of a bronchus (tuberculous bronchopneumonia) 2) into a thin-walled blood vessel (miliary TB)

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45
Q

primary vs secondary TB

A
  • lymph node involvement more evident in pri TB -> secondary TB immune cells immediately activated to contain infection
  • secondary TB found at apex of lung in CXR, pri TB at lymph nodes
  • secondary TB cause increase tissue destruction (greater immune response)
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46
Q

complications of secondary TB

A

Vigorous immune response:
healing of apical lesion -> leave central area of caseous necrotic material (may contain bacteria) surrounded by dense collagenous wall -> calcifies (fibrocaseous TB)
* If immune response weakens and still have bacteria -> reactivated fibrocaseous tuberculosis

Poor immune response:
progressive enlargement of apical lesion -> continued destruction of lung tissue
* Bigger lesion -> increase risk of erosion into blood vessels or airways

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47
Q

IMAGING: secondary TB

A
  • TB always found at APEX of lungs (highest pO2)
  • little lymph node involvement (granuloma is contained in CXR) as immune system recognises and contains it
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48
Q

IMAGING: miliary TB

A
  • millet seed appearance (many white spots all over lung)
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49
Q

bronchiectasis pathogenesis

A

permanent abnormal dilation of main bronchi -> cycle of inflammation, mucus secretion, infection, airway dilation/destruction

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50
Q

bronchiectasis clinical presentations (3)

A
  • recurrent infection
  • hemoptysis
  • mucopurulent sputum production lasting months to years
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51
Q

predisposing factors to bronchiectasis (2)

A

Drainage secretion obstruction
- cystic fibrosis
- immotile cilia syndrome

Recurrent and persistent infection

52
Q

complications of bronchiectasis

A
  • cor pulmonale
  • lung abscess
  • systemic amyloidosis
  • pyemia (pus bacteria released into blood) causing brain abscess
53
Q

obstructive vs restrictive lung disease - differences (4)

A

FEV1/FVC
- obstructive (<0.7-0.8)
- restrictive (>0.7-0.8)

Lung capacity
- obstructive: normal capacity
- restrictive: lowered capacity

Expiratory flow rate
- obstructive: reduced
- restrictive: normal

Pathogenesis
- obstructive: airway blockage
- restrictive: parenchymal

54
Q

obstructive lung diseases - causes (3)

A
  • obstructive sleep apnea
  • asthma
  • COPD
55
Q

risk factor for OSA (obstructive sleep apnea)

A
  • men, obese
56
Q

asthma pathogenesis

A
  • triggered by atopic (allergen)/ non atopic agents (non allergen, eg cold)
  • affects BRONCHI (mucus produced)
57
Q

3 immediate effects of asthma on bronchi

A
  • hypertrophy of smooth muscle
  • hypersecretion of mucus + mucosal edema
  • bronchial mucosa infiltrated with eosinophils, mast cells, lymphoid cells, macrophage
58
Q

status asthmaticus

A

acute severe asthma -> cannot be treated by inhalers/steroids, cause respiratory failure

59
Q

COPD characteristics (3)

A
  • emphysema
  • chronic bronchitis -> cough with sputum (mucus hyper secretion) + narrowing of airway
  • bronchiolitis -> airway scarring
60
Q

causes of emphysema (3)

A
  • SMOKING -> inhibit a1-antitrypsin -> protease protease inhibitor imbalance -> protease cause tissue destruction
  • CONGENITAL a1-antitrypsin deficiency
  • pneumoconiosis
61
Q

complications of emphysema (3)

A
  • Cor pulmonale
  • Respiratory failure
  • Pneumothorax
  • Peptic ulcer
62
Q

barrel chest is a sign of:

A

emphysema

63
Q

IMAGING: emphysema

A
  • too many posterior ribs visible
  • compressed diaphragm on both sides
64
Q

difference between COPD vs asthma (2)

A
  • COPD is IRREVERSIBLE (bronchospasm/constriction in asthma reversible)
  • COPD is PROGRESSIVE (asthma is recurrent acute attacks)
65
Q

restrictive lung diseases - causes (2)

A
  • interstitial edema
  • fibrosis of alveoli (diffuse parenchymal lung disease)
66
Q

cause of interstitial edema in restrictive lung diseases (1)

A

acute stage of ARDS (acute respiratory distress syndrome) - fluid accumulation in alveoli due to systemic sepsis/ severe trauma or burn/ inhalation of toxic fume
-> damage to alveolar capillary endothelium OR alveolar lining cell

67
Q

characteristics of diffuse parenchymal lung disease (4)

A
  • widespread INFLAMMATION in interstitium
  • reduced lung COMPLIANCE
  • EDEMA and FIBROSIS
  • alveolar wall thickening -> reduced gas exchange
68
Q

main causes of parenchymal lung disease

A
  • IDIOPATHIC (most common)
  • late organisation phase of ARDS (2nd most common)
  • pneumoconiosis (inhale dust - eg silica/ coal dust/ asbestos)
  • end stage pulmonary fibrosis
69
Q

histological patterns of reaction in lung parenchymal damage (7)

A

Alveoli
- Haemorrhage
- Fibrin exudation -> form hyaline membrane
- Macrophage accumulation
- Fibrosis

Interstitium:
- Edema
- Inflammation
- Fibrosis

70
Q

ARDS pathogenesis

A

acute phase -> fluid accumulation in alveoli and damaged secondary to other reasons

late organisation phase -> regeneration of Type II alveolar lining cells and hyaline membrane with fibrosis + inflammation and fibrosis of interstitium -> HONEYCOMB LUNG -> death by RESPI & CARDIAC failure

71
Q

predisposing factor to pneumoconiosis

A
  • occupational exposure
  • smoking (worsens condition)
72
Q

forms of lung cancer (2)

A
  • small cell carcinoma (20%)
  • non small cell carcinoma (squamous cell carcinoma + adenocarcinoma)
73
Q

cause of small cell carcinoma + prognosis

A
  • SMOKING
  • poor prognosis -> central, rapid growth
74
Q

main feature of squamous cell carcinoma (1)

A

central cavitation

75
Q

main cause of squamous cell carcinoma (1)

A
  • SMOKING
    *more common in MALES
76
Q

is adenocarcinoma related to smoking or gender?

A

NO, NO (present in both genders equally)

77
Q

IMAGING: minimally invasive adenocarcinoma (vs other lung carcinoma)

A
  • NO MASS, similar to consolidation as cancer spreads along alveolar septa,
  • other lung carcinoma -> mass
78
Q

how does lung cancer spread (4)

A
  • Local -> lung, pleura, mediastinal structures, chest wall
  • Lymphatic -> lymph nodes (mediastinum, neck, others)
  • Transcoelomic (across the peritoneal cavity) -> pleural and pericardial effusions
  • Haematogenous
79
Q

paraneoplastic syndromes of lung cancer

A
  • SIADH (syndrome of inappropriate ADH secretion)
  • Cushing’s syndrome (Excessive ACTH Secretion, EAS)
  • Hypercalcaemia (PTHrp)
80
Q

pleural diseases (6)

A
  • haemothorax (blood)
  • pneumothorax (air)
  • pleural effusion (fluid - pus/ edema)
  • chylothorax (chyle from thoracic duct)
  • pleurisy (pleural inflammation, neutrophils predominate)
  • cancer
81
Q

causes of pneumothorax (3)

A
  • spontaneous (primary [thin young men/ rupture of congenital sub pleural apical bleb] & secondary [rupture of emphysematous bulla/ asthmatics])
  • traumatic
  • iatrogenic (caused by medical examination)
82
Q

IMAGING: open/ closed pneumothorax

A
  • smaller lung (wrapped by air) in Xray
  • diaphragm depressed
83
Q

IMAGING: tension pneumothorax

A
  • smaller lung (wrapped by air) in Xray
  • diaphragm depressed
  • shift in mediastinum position (bilateral tension pneumothorax may not show mediastinum shift)
84
Q

describe the fluid in pleural effusion (2)

A

EXUDATE [high protein] - eg empyema (pus in pleura) from pneumonia; haemothorax from rib fracture
TRANSUDATE [low protein] - eg pulmonary edema, HF

85
Q

IMAGING: pleural effusion

A
  • NO COSTOPHRENIC ANGLE, with meniscus
  • opacity at base of lung
86
Q

what is predominantly found in pleurisy

A
  • pleura inflammation -> neutrophil predominate
87
Q

types of pleural cancer (2)

A
  • 2ndary metastatic carcinoma (most common)
  • malignant mesothelioma (pri tumour) -> due to ASBESTOS exposure
88
Q

why is lungs/ liver a common site of metastasis from other cancers

A
  • end capillary bed
89
Q

anterior mediastinum mass likely diagnosis

A

thymoma

90
Q

what is thymoma associated with

A

myasthenia gravis

91
Q

middle mediastinum mass likely diagnosis

A

enlarged hilar lymph nodes (due to sacoidosis, lung cancer, TB etc)

92
Q

posterior mediastinum mass likely diagnosis

A

schwannoma (nerve sheath tumour)

93
Q

causes of lung granulomas (4)

A
  • infection (eg TB/ fungal infection)
  • foreign matter (pneumoconiosis, hypersensitivity pneumonitis)
  • unknown causes (sarcoidosis) -> characterised by nonnecrotising granulomas in many tissues and organs
  • wegener’s granulomatosis
94
Q

predisposing factor of sarcoidosis (race related, my fav disease)

A
  • rare in chinese
  • common in caucasians, black, indian
95
Q

neonatal diseases

A
  • developmental anomalies -> bronchial atresia/ bronchogenic cysts/ bronchopulmonary sequestration
  • neonatal respiratory distress syndrome
  • immotile cilia syndrome (abnormal cilia structure/ unable to beat coordinately)
  • cystic fibrosis
96
Q

what is bronchial atresia

A

obstruction of bronchial segment

97
Q

what is bronchogenic cyst

A

accessory bronchial buds that become sealed off from airway

98
Q

what is bronchopulmonary sequestration

A

lung tissue with blood supply but no respiratory function (not connected to bronchial tree)

99
Q

neonatal respiratory distress syndrome pathogenesis

A
  • deficiency in lung surfactant (usually premature birth) causing alveolar collapse
    **AKA hyaline membrane disease
100
Q

effects of neonatal respiratory distress syndrome on lungs (3)

A
  • Hypoxia
  • Damage to endothelial and alveolar lining cells
  • Fibrin exudation (forms hyaline membrane)
101
Q

cystic fibrosis pathogenesis

A
  • autosomal recessive
  • abnormal viscous mucus -> builds up in lungs, pancreas, and other organs
  • predispose to repeat infections and BRONCHIECTASIS
102
Q

lung diseases secondary to systemic diseases/ lung diseases causing systemic disease (5)

A
  • pulmonary edema due to LH failure
  • pulmonary arterial hypertension
  • cor pulmonale
  • pulmonary emboli
  • pulmonary vasculitis
103
Q

causes of pulmonary hypertension (4)

A
  • LH failure
  • pulmonary emboli
  • L to R shunt (ASD/ VSD/ PFO-patent foramen ovale)
  • chronic lung disease (loss of capillaries + hypoxic vasoconstriction of arteries)
104
Q

consequence of ARTERIAL hypertension

A
  • TUNICA MEDIA hypertrophy + INTIMA proliferation -> narrowing -> FURTHER INCREASE in PRESSURE
105
Q

cor pulmonale

A
  • RHF secondary to primary lung disease (lung disorder causes HTN)
106
Q

physiological outcomes of pulmonary emboli (4)

A
  1. Circulatory collapse (BIG EMBOLI -> sudden cardiac death, heart cannot pump)
  2. Infarction (INTERMEDIATE emboli; RARE! -> only 10% of the cases bc bronchial artery supply still exists, lung is dual blood supply!)
  3. Pulmonary hypertension (RECURRENT, SMALL thromboemboli -> reduce pulmonary vasculature)
  4. V/Q mismatch (regardless of emboli size, as long as blood supply is cut off)
107
Q

pathogenesis of pulmonary vasculitis

A
  • inflammatory destruction of blood vessels
  • cause bleeding into lungs -> HEMOPTYSIS
108
Q

2 diseases with prominent lung manifestations

A
  • Wegener granulomatosis -> affect nose, lungs, kidneys
  • ChurgStrauss syndrome -> infiltration of many organs by EOSINOPHILS; pt usually has asthma
109
Q

types of respiratory failure (3)

A
  • Type 1
  • Type 2
  • COPD induced (pink puffers vs blue bloaters)
110
Q

effects of respi failure (3)

A
  • breathlessness (air hunger) -> due to hypoxia
  • polycythemia (increase EPO production due to hypoxia)
  • pulmonary arterial HTN (due to hypoxic vasoconstriction) -> secondary RH strain
111
Q

what is type 1 respiratory failure & treatment

A
  • hypoxaemia, NO hypercapnia (only some areas gas exchange affected, CO2 retention insignificant) -> alveolar capillary gas exchange affected, ventilation normal (eg pulm emolism/ pus in alveoli/ lung collapse/ fibrosis)
  • can cause cyanosis

treatment
- give high pO2

112
Q

what is type 2 respiratory failure

A
  • hypoxaemia + hypercapnia
  • poor ventilation -> cannot remove CO2
113
Q

which 2 ways can type 1 respi failure lead to type 2 respi failure

A
  1. exhaustion or insufficient oxygen supply to the brain -> ventilation problems -> hypercapnia
  2. progression of disease (more of lung being affected) or exhausted -> compensatory measures (hyperventilation, tachycardia) fail -> hypercapnia
114
Q

cause of pink puffers

A
  • EMPHYSEMA

presentations
- hyperventilation due to less SA for gas exchange; use of accessory breathing muscles
- pink complexion
- barrel chest due to emphysema, flattened diaphragm on CXR

115
Q

cause & presentation of blue bloaters

A
  • CHRONIC BRONCHITIS
  • hypoxemia + hypercapnia
  • capillaries & alveoli undamaged but air CANNOT enter -> V/Q mismatch (no ventilation) -> deoxygenated blood
  • R heart pumps harder to perfuse lungs better (but in vain) -> RH failure

Presentations
- cyanosis (deox blood around body) + overweight
- wheezing & crackles (bronchitis)
- elevated haemoglobin

116
Q

what happens in chronic blue bloaters

A
  • hypercapnia & hypoxemia tolerance increases -> dulls CO2 breathing reflex (FATAL)
117
Q

what must be carefully given to blue bloaters

A
  • oxygen -> dulling of CO2 driven breathing effect -> giving too much O2 can cause further decrease in ventilation rate -> O2 levels normal but CO2 builds up as breathing rate too slow to clear it -> acidosis
118
Q

blue bloaters/ pink puffers treatment (4)

A

1) treat cause (eg infection)
2) give O2 (controlled in blue bloaters)
3) bronchodilators
4) assist ventilation (if necessary)

119
Q

IMAGING: cardiac failure (4)

A
  • cardiomegaly >0.55
  • prominent interstitial markings (due to pulmonary edema) -> BAT WING appearance due to bilateral perihilar lung shadowing
  • consolidations
  • no costophrenic angle -> pleural effusion
120
Q

IMAGING: causes of mass on Xray (3)

A
  • granuloma
  • primary lung carcinoma
  • secondary metastases
121
Q

IMAGING: posterior CXR vs anterior CXR

A
  • PXR -> clavicle points sharply downwards
  • CXR -> apex heart at 5th rib
122
Q

IMAGING: supine vs upright CXR

A
  • upright -> presence of gastric bubble
  • supine -> no gastric bubble (CXR taken when person lying down, fluid fills entire gastric surface)
123
Q

combination vaccines given in childhood to combat against 5 microbes (5)

A

Diphtheriae
Tetanus
Pertusis
Polio
Haemophilus influenzae

124
Q

viral pathogens that can cause pneumonia (5)

A
  • influenza
  • adenoviruses
  • rhinoviruses
  • paramyxoviruses
  • SARS/ coronavirus infections
125
Q

lung diseases associated with asbestos (4)

A

Larynx
1. squamous cell carcinoma of larynx

Pleura
1. pleural plaque (benign areas of thickened tissue that form in the pleura or lung lining
2. malignant mesothelioma (pleural cancer)

Lung
1. progressive chronic lung fibrosis (abestosis) - parenchymal lung disease

Respi (2 decks)

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