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Respiratory Flashcards

1
Q

Factors affecting pulmonary function

A

Airway resistance
Alveolar surface tension
Lung compliance

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2
Q

Resistance in air flow greatest in?

A

Medium-sized bronchi

Resistance in smaller bronchioles plays a major role in disease - more vulnerable to obstruction

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3
Q

Surfactant reduces surface tension in water and is secreted by…

A

Type II alveolar epithelial cells

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4
Q

Infant respiratory distress syndrome

A

Premature babies don’t have surfactant and can’t reinflate lungs at the end of expiration

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5
Q

Lung compliance affected by:

A

Alveolar surface tension
Distensibility of lungs/thoracic cage

(Extent to which lung volume will expand for a given increase in transpulmonary pressure)

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6
Q

Alveolar damage –> loss of alveolar surface –> cells lost due to disease and infection –> less surface area –>

A

Increased compliance (lungs bigger as seen in COPD and emphysema)

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7
Q

Bronchial smooth muscle, which innervation predominates

A

Parasympathetic

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8
Q

Parasympathetic innervation of bronchial smooth muscle?

A 
Vagus nerve 
Ach 
M3 receptor 
Mild to moderate Bronchoconstriction
Mucus secretion 
Vasodilation 
G protein coupled pathway --> phospholipase C --> catalysed formation of IP3 from PIP3 --> ca release from SR
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9
Q

Sympathetic innervation

A

Adrenaline and noradrenaline from adrenal medulla
B2 receptors
Bronchodilator
Vasculature control is important

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10
Q

Pathology features of asthma

A 
Increased mucus secretion 
Glandular hyperplasia 
Smooth muscle hypertrophy 
Inflammatory exudate (mononuclear cells mainly t helper lymphocytes, eosinophils, neutrophils) 
Charcot Leyden crystals 
Crushmann's spirals 
Shedding on respiratory epithelium 
Foci of squamous metaplasia sometimes
Mucus-laden goblet cells 
Hyperinflation of alveoli 
Bronchial wall thickened, congested, oedematous
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11
Q

Histology of respiratory system

A

Pseudostratified ciliated columnar epithelium with goblet cells

Nasal cavity - olfactory pseudostratified ciliated with sustentacular cells

Trachea - discontinuous cartilage as well with goblet cells and basal cells

Bronchus - occasional glandular tissue

Bronchioles - no cartilage, Clara cells (?), occasional glandular tissue, simple cuboidal

Gas exchange surface - simple squamous

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12
Q

Asthma acute vs late reaction?

A

Acute - smooth muscle hyper reactivity (targeted by CNS drugs)
Late - inflammation, excess mucus and injury (targeted by corticosteroids)

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13
Q

Mechanism of action of methylxanthines

A

Theophylline
Long term treatment (maintainence) of asthma/COPD
Non-selective adenosine receptor antagonist (a1, a2, a3)
Inhibits phosphodiesterase
Effects include bronchial smooth muscle relaxation, anti inflammatory effects, increased diaphragm contractility, CNS stimulation
Narrow therapeutic ratio so limited use
Broken down by CYP1A2

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14
Q

Beta adrenergic agonists - Mechanism of action of SABAs

A

B2 adrenergic agonist
Salbutamol
Increase cAMP –> activates PKA –> reduced availability of ca –> relaxation and bronchodilation
Alveolar epithelium - increased Na channels –> increased mucociliary clearance
Slight anti-inflamm
Tachycardia (and lost sensitivity to beta1 stimulation)
Tremor (b2 on sk muscle)

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15
Q

Mechanism of action - LABAs

A 
Salmeterol 
Efometerol
Maintainence
B2 agonist 
No significant tolerance on long term
Should be used in conjunction with corticosteroids
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16
Q

Anticholinergics - mechanism of action

A 
Ipratropium (non-selective)
Tiotropium (m1 and m3) 
Inhibit primarily M3 receptor 
Some M2 antag activity 
Blocks vagal tone and reflexes 
Dry mucosal secretions (reduced secretion and increased clearance) 
Maintainence treatment
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17
Q

Corticosteroids?

A 
Oral pred 
Inhaled budesonide 
Injected hydrocortisone 
Reduced inflamm activity 
Decreased lung micro vascular permeability, decreased oedema 
Up regulated Beta adrenergic receptors 
Maintainence and acute 
Decreased mucus secretion 
AEs: oral thrush and horse voice, bronchospasm etc
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18
Q

Cromolyns?

A

Cromoglycate
Inhibit release of inflammatory mediators from mast cells
Mast cell stabiliser
Maintainence
Protection against exercise induced asthma

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19
Q

Leukotrine receptor antagonists:

A

Montelukast
Inhibits CysLT receptor - prevents LTD4
AEs : hypersensitivity reactions, headaches , abd pain, diarrhoea, churg-Strauss syndrome.

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20
Q

Management of cough and cough promotion

A

Antitussives eg codeine

Expectorants eg k+ citrate, ammonium salts
Mucolytics eg bromhexine
Acetylcysteine

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21
Q

Omalizumab

A

Binds to free IgE decreasing cell bound IgE
Decreased receptor expression
Decrease mediator release
Decreased allergic inflamm and exacerbation of asthma

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22
Q

Drug delivery devices

A

Metered aerosol/ auto inhaler
Spacer
Dry powder devices
Nebulisers

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23
Q

Productive cough
Airway inflammation
What disease could this be?

A

Chronic bronchitis

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24
Q

Alveolar wAll destruction
Overinflation
What disease?

25
A respiratory until is called a
Acinus Respiratory bronchiole Alveolar duct Alveolar sac Alveolus
26
What are heart failure cells?
Alveolar macrophages become laden with brown-black hemosiderin due to breakdown of RBCs from engorged capillaries
27
What features are required to diagnose chronic bronchitis
Persistent productive cough for at least 3 consecutive months over 2 consecutive years Persistent obstruction and largely irreversible due to mucus and airway thickening due to chronic inflammation
28
Can asthma be drug induced
``` Yes. Aspirin Inhibits cox but not LPO(?) So increased leukotrines Increased spasms ```
29
Atopic asthma
``` Childhood onset Gene on chromosome 5q Assoc with type 1 IgE hypersensitivity Urticaria Hay fever Eczema ``` Rhinitis Positive RAST
30
Restrictive lung disease divided into :
``` Alveolar Interstitial Pleural Neuromuscular Thoracic cage/ extrinsic eg obesity ```
31
How to differentiate extrinsic vs intrinsic causes of restrictive lung disease
DLCO test | Normal = extrinsic, ie chest wall, pleural, neuromuscular
32
Some causes of lung cancer
``` Smoking Radon exposure Asbestos Environmental tobacco smoke Other toxin exposure Pollution Tar (in ciggies) ```
33
Most common area for lung cancer
Main bronchi and subdivisions
34
Presentation of bronchial carcinoma
Localised: cough, sputum, haemoptysis, SOB General: weight loss, fever, fatigue Metastasis
35
Classification of lung cancer
``` Small cell carcinoma Non small cell carcinoma: - squamous cell - adenocarcinoma - large cell - other ```
36
Small cell carcinoma usually arises from
Epithelial cells of centrally located bronchi Commonest cause is smoking and tends to spread widely early Very bad prognosis
37
Increased adenocarcinoma thought to be due to
Shift to filtered cigarettes Lowered incidence of squamous cell carcinoma
38
Subtypes of adenocarcinoma
Lepidic - line the alveolar lining with no architecture disruption and no invasion Acinar - glandular formation Papillary - true fibrovascular cores lined by tumour cells replacing alveolar lining, psammoma bodies? Micropapillary - Ill defined projection/tufting with no fibrovascular cores Solid - solid sheets and nests of tumour Invasive mucinous Lepidic - best prognosis Micropapillary and solid - more aggressive EGFR and ALK mutations?
39
Common mutations in adenocarcinoma
1. KRAS 2. EGFR 3. ALK
40
Most common type of lung cancer
Adenocarcinoma 40% Best prognosis
41
Large cell carcinomas : some are
Poorly differentiated adenocarcinoma or squamous cell Large cell Neuroendocrine tumours
42
Sequence of molecular changes for lung cancer
Inactivation of putative tumour suppressor genes (on chromosome 3p) TP53 mutations or activation of KRAS oncogene Additional mutations Sometimes EGFR mutation EGFR and K-RAS EML4-ALK tyrosine kinase fusion genes and c-MET tyrosine kinase gene amplifications Targeted with tyrosine kinase inhibitors
43
How can some specific genetic pleomorphisms involving the P450 genes cause lung cancer
P-450 monooxygenase enzyme system needed for metabolic activation of some procarcinogens into carcinogens
44
Pathology of lung cancer
Small mucosal lesions firm and white-grey May arise as intraluminal, invade bronchial mucosa, or form large bulky masses pushing into adjacent lung perenchyma Some large masses --> cavitation secondary to central necrosis or develop focal areas of haemorrhage May extend to pleura, invade pleural cavity and spread to intrathoracic structures Lymphatic or haematogenous route for further spread
45
Well differentiated squamous cell cancers can show
Keratin pearls | Intracellular bridges
46
Putative precursor for adenocarcinoma thought to be
Atypical adenomatous hyperplasia (AAH) - focus of epithelial proliferation composed of cuboidal or low-columnar cells
47
K-RAS mutation can
Enable cells to escape normal checkpoint mechanisms and proliferate without end
48
Lung carcinomas presentation
Chronic cough and expectoration Hoarseness Chest pain Superior Vena cava syndrome Pericardial or pleural effusion Persistent segmental atelectasis or pneumonitis Spread to brain (neuro symptoms), liver(hepatomegaly) or bones (pain)
49
Hallmark of asthma
Hyperrresponsiveness of airway to stimuli Paroxysmal and reversible Chronic bronchial inflammation with eosinophils Sm hypertrophy and hyper reactivity Increased mucus secretion (mucus plugs)
50
Non atopic asthma
Adult type No allergen sensitisation (negative RAST) Respiratory infections Humoral and cellular mediators are the same
51
Types of asthma
Atopic Non atopic Occupational Drug induced
52
RAST
Serum radioallergosorbent test - present of IgE antibodies specific to panel of radiolabelled antigens Skin test - wheal and flare reaction
53
Repeated bouts of inflammation leads to (asthma)
Remodelling of airways
54
In asthma what interleukins are involved?
IL-4 --> attracts IgE B cells IL-5 --> attracts mast cells which degranulate after attachment of IgE antibody to IgE Fc receptor on mast cell IL-13 induces more mucus production Interleukins released from Th2 cells Th2 activated by APC/dendritic cell after recognising antigen
55
Small cell lung carcinomas
Appear as pale gray centrally located masses with extension into lung parenchyma and early lymph node involvement (Hilar and mediastinal) Cells - round to fusiform shape, scant cytoplasm and finely granular chromatin Necrosis invariably present Fragile cells --> Crush artifact Often express variety to nehroendocrine markers and may result in paraneoplastic syndromes Rarely assoc with genetic abnormality (KRAS if that)
56
Paraneoplastic syndrome assoc with lung cancer
Hypercalcemia (path-r peptide- most often with squamous cell neoplasms) Cushing Syndrome (ACTH) Inappropriate ADH secretion Neuromuscular syndromes incl peripheral neuropathy Clubbing of fingers and hypertrophic pulmonary osteomyopathy Coagulation abnormalities incl nonbacterial endocarditis and DIC Secretion of calcitonin and other ectopic hormones documented
57
Carcinoid tumours
Do we need to know this lol
58
Squamous cell carcinoma
???? Idk
59
Blood values used to determine the cause of acidosis and alkalosis?
pH: <7.35 = acidosis >7.45 = alkalosis pCO2: >45mmHg = resp cause <35mmHg = resp compensation Bicarbonate: <22mEq/L = metabolic acidosis >26mEq/L = metabolic alkalosis

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