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m2 CA2 > respi patho > Flashcards

respi patho Flashcards

1
Q
  • Infective rhinitis is _____ in origin and _____ ______ of surface epithelial cells results in _______ of ______ and ______ from the damaged surface
  • submucosal oedema produces _______ and _______ ________
  • viral infection of URT may spread to _____
A
  • Infective rhinitis is viral in origin and viral necrosis of surface epithelial cells results in exudation of fluid and mucus from the damaged surface
  • submucosal oedema produces swelling and nasal polyps
  • viral infection of URT may spread to LRT
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2
Q

What is the microscopy of nasal polyps?

A

localised outgrowths of lamina propria due to accumulation of oedema fluid, inflammation and fibroblast proliferation

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3
Q

what are the benign tumours of the nose and paranasal sinus?

A
  • squamous papilloma of the nasal vestibule
  • sinonasal papilloma aka schneiderian papilloma
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4
Q

what are the malignant tumours of the nose and paranasal sinuses?

A
  • squamous cell carcinoma (most common)
  • adenocarcinoma
  • transitional cell carcinoma
  • malignant melanoma
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5
Q

what is juvenile angiofibroma?

A
  • rare tumour in male adolescent
  • benign, grows rapidly
  • frequently ulcerates and present with bleeding
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6
Q

what is observed in non-keratinizing nasopharyngeal carcinoma?

A

tumour is poorly differentiated and intermingled lymphocytes among carcinoma cells

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7
Q

what is observed in keratinizing nasopharyngeal carcinoma?

A

intercellular bodies
bright pink cytoplasm
keratin formation

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8
Q

what are the main risk factors for NPC?

A
  • ebv infection at young age
  • salt preserved food
  • family history
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9
Q

what are the symptoms of NPC?

A

tumour is an obstruction to eustachian tube -> secretory otitis media -> hearing loss and tinnitus

  • increased diplopia due to invasion of 6th cranial nerve
  • increased nasal obstruction
  • increased metastasis to cervical lymph nodes
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10
Q

for epstein barr virus, infection in ______ is more symptomatic. what are the symptoms?

A

adolescents;
infectious mononucleosis and glandular fever

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11
Q

what does EBV infect?

A

nasopharyngeal epithelium and tonsillar b lymphocytes

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12
Q

EBV can lead to…

A

NPC

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13
Q

what is the link between EBV and NPC?

A

patients with NPC will have elevated antibody titres against EBV viral antigens

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14
Q

which childhood diseases have been largely eradicated by vaccination?

A

diphtheria and measles

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15
Q

what is respiratory failure? what are the main symptoms?

A

inadequate gas exchange due to dysfunction of one or more essential components of the respiratory system -> inability to maintain O2 and CO2 levels at normal levels

main symptoms: breathlessness, consequences of hypoxia

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16
Q

long-standing hypoxia results in:

A
  • pulmonary hypertension and secondary right heart strain
  • polycythaemia due to stimulation of erythropoietin release from kidney
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17
Q

what is type 1 respiratory failure?

A

hypoxaemia without hypercapnia

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18
Q

what is type 2 respiratory failure?

A

hypoxaemia with hypercapnia

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19
Q

pulmonary oedema is caused by?

A

pulmonary capillary congestion due to left heart failure

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20
Q

what occurs during pulmonary oedema?

A
  • increased fluid in alveolar wall will lead to increased fluid in alveolar spaces
  • capillary rupture will lead to leakage of RBCs into interstitium -> RBCs will be phagocytosed by alveolar macrophages aka heart failure cells aka hemosiderin ladden macrophages in alveolar spaces
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21
Q

what are some causes of pulmonary hypertension?

A
  1. secondary to left heart disease
  2. left to right shunts
  3. chronic lung disease
  4. sequelae of pulmonary emboli
  5. unknown cause
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22
Q

sustained increased pulmonary arterial pressure will lead to…

A
  • irreversible structural changes in pulmonary arteries
  • medial hypertrophy in muscular arteries -> narrowing/occlusion -> reduced CSA -> further increases pressure
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23
Q

what is cor pulmonale?

A
  • heart failure secondary to lung disease
  • long term need to pump at higher pressures eventually causes right heart to fail
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24
Q

what is atelectasis?

A

collapse of lungs
(inadequate lung expansion -> loss of lung volume)

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25
Q

causes of atelectasis

A
  1. resorption atelectasis: airway obstruction
  2. compression atelectasis: air or fluid in pleural space with compression of lung
  3. contraction atelectasis: scarring of lung; loss of normal surfactant
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26
Q

what is pneumonia

A

infective inflammation

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27
Q

what is seen on x-ray in pneumonia?

A

consolidation of lung (filling of air spaces by inflammatory exudate)

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28
Q

what is pneumonitis?

A

inflammatory disease dominated by interstitial inflammation

29
Q

community acquired pneumonia is caused by gram _____ bacteria

A

positive;
eg. strep pneumonia, haemophilus influenzae, mycoplasma, legionella, m. tuberculosis

30
Q

hospital acquired pneumonia is caused by gram ______ bacteria

A

negative;
eg. klebsiella, e. coli, pseudomonads

31
Q

if TB enters blood, patient develops?

A

miliary TB

32
Q

in primary TB, following inhalation, infection and necrosis occurs at?

A

periphery of the lung, just beneath the pleura (ghon focus)

33
Q

in primary TB, bacteria conveyed to local lymph nodes will cause lymph nodes to…

A

lymph nodes will enlarge through granulomatous inflammation and caseation

34
Q

in primary TB, when area of caseation heals, what remains?

A

small calcified nodules left

35
Q

primary TB occurs in

A

unsensitised host

36
Q

how does the spread of TB occur in the host?

A

spread occurs by enlarging nodes eroding through the wall of a bronchus or into a thin-walled vessel

37
Q

secondary TB occurs in

A

previously exposed, sensitised people

38
Q

in secondary TB, the infection occurs at

A

apex of the lungs (usually)

39
Q

what happens during secondary TB?

A
  • rapid mobilisation of defence reaction at site of entry and increased tissue destruction
  • little lymph node involvement
  • apical lesion (assmann focus) begins as central area of necrosis surrounded by granulomas
  • destruction of lung tissue along with bacteria -> CAVITATION
40
Q

outcome of secondary TB

A
  • apical lesion heals, leaving a central area of caseous necrotic material surrounded by thick dense collagenous wall which often calcifies
  • latent TB can spread infection in immunocompromised patients
41
Q

what is atypical pneumonia?

A

marked infiltration of alveolar interstitium by chronic inflammatory cells caused by infection by mycoplasma, chlamydia, rickettsia

42
Q

atypical pneumonia has symptoms of pneumonia but…

A

absence of consolidation on x-ray

43
Q

bronchiectasis is…

A
  • permanent abnormal dilation of main bronchi -> problems of drainage of secretions + persistent infection
  • dilated airways, purulent secretions, chronic inflammation of wall with loss of normal epithelium
  • haemoptysis and phlegm
44
Q

2 main factors that predispose to bronchiectasis

A
  1. interference with drainage of secretions
    eg) obstruction to proximal airway, abnormality in viscosity of mucus, immotile cilia syndrome
  2. recurrent and persistent infection
45
Q

complications of bronchiectasis

A
  1. chronic suppuration +/- lung abscess
  2. haematogenous spread of infection
  3. secondary amyloidosis
46
Q

some examples of lung disease in children

A
  • bronchial atresia
  • bronchogenic cysts
  • bronchopulmonary sequestration
  • neonatal respiratory distress syndrome (lack of surfactant in lungs -> increase surface tension -> reduce compliance of lungs -> alveoli collapse)
  • immotile cilia syndrome
  • cystic fibrosis (production of abnormally viscous mucus that can’t be cleared)
47
Q

asthma

A
  • chronic disease of bronchioles
  • bronchospasm + excessive production of mucus
  • atopic (allergy) vs non-atopic (hypersensitive)
  • treatment: decrease chronic inflammation (preventative) + decrease bronchospasm (therapeutic)
48
Q

structural changes observed in asthma

A
  1. hyperactivity and hypertrophy of smooth muscle of bronchus
  2. hypersecretion of mucus
  3. mucosal oedema
  4. infiltration of bronchial mucosa by eosinophils, macrophages, mast cells, lymphoid cells
  5. deposition of collagen beneath bronchial epithelium
49
Q

what are the 3 main pathologies in COPD?

A

emphysema
chronic bronchitis
bronchiolitis

50
Q

what is emphysema?

A
  • permanent dilatation of airspaces distal to terminal bronchioles with destruction of tissue in absence of scarring
  • destruction of alveolar wall leads to loss of elastic recoil of lungs -> reduce lung compliance -> reduce gas exchange capacity
51
Q

pathogenesis of emphysema in smokers

A

cigarette smoke:
-> inhibit protease inhibitor which potentiates tissue damage
-> contains abundant radicals which cause tissue damage
=> destruction of alveolar wall

52
Q

in chronic bronchitis, what is being produced? for how long?

A

cough productive of sputum on most days for 3 months of a year for at least 2 successive years
-> airway obstruction due to luminal narrowing + mucus plugging results in alveolar hypoventilation

53
Q

what is bronchiolitis?

A
  • inflammation of airways <2mm in diameter
  • macrophages and lymphoid cells infiltrate airway wall -> scarring and narrowing of airways -> loss of function of lungs distal to the affected bronchioles
54
Q

pink puffers

A
  • pink complexion, obvious breathing effort
  • emphysema: patient compensates for less lung surface area by hyperventilating
55
Q

blue bloaters

A
  • normal lung capacity but poor ventilation -> hypoxaemia + hypercapnia
  • chronic bronchitis/bronchiolitis
  • ventilation perfusion mismatch
  • breathing reflex is only driven by O2 levels due to years of hypercapnia
56
Q

diffuse parenchymal lung disease is a… and results in… due to ___ in acute cases and ___ in chronic cases

A

diffuse parenchymal lung disease is a widespread interstitial inflammation and results in reduced lung compliance due to oedema in acute cases and fibrosis of alveolar wall in chronic cases

57
Q

what are the main histological patterns of reaction in lung following diffuse parenchymal lung disease?

A
  1. haemorrhage and fibrin exudation into alveoli
  2. oedema and inflammation in interstitium
  3. macrophage accumulation in alveolar spaces
  4. fibrosis in interstitium or alveolar spaces
58
Q

what is acute respiratory distress syndrome?

A
  • acute form of diffuse parenchymal lung disease
  • diffuse alveolar and capillary damage
59
Q

what are some of the most common causes of ARDS?

A

systemic sepsis, severe trauma, inhalation of toxic fumes

60
Q

what are the phases of ARDS?

A
  1. acute exudative phase
    - interstitial oedema and high protein exudation
    (fibrin rich fluid + necrotic epithelial cells = hyaline membranes)
  2. late organisation phase
    - regeneration of type II alveolar lining cells
    - organisation of hyaline membranes with fibrosis
61
Q

causes of granuloma in lung

A
  • infection
  • foreign material
  • unknown)&
62
Q

what is sarcoidosis?

A
  • non-necrotising and numerous granulomas formed
  • no caseous necrosis
  • no multinucleated giant cell
63
Q

what are the types of lung cancer?

A
  • small cell carcinoma
  • non- small cell carcinoma
    -> squamous cell carcinoma
    -> adenocarcinoma
64
Q

how can lung cancer spread?

A

local
lymphatic
transcoelomic
haematogenous

65
Q

squamous cell carcinoma

A
  • commoner in males
  • associated with smoking
  • central cavitation
  • presence of keratinization
66
Q

adenocarcinoma

A
  • equal gender incidence
  • not associated with smoking
67
Q

small cell carcinoma

A
  • rapid rate of growth and metastasis
  • high association with smoking
  • tumour cells show neuroendocrine differentiation
  • poor prognosis
68
Q

metastatic tumour

A
  • usually blood borne spread
  • cannon ball metastasis
69
Q

pleura is lined by ____ cells with constant generation of fluid from parietal pleura and resorption from visceral pleura

A

mesothelial cells

m2 CA2 (22 decks)

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