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STUDY FOR BARRIERS > Respiratory > Flashcards

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?

A

Emphysema

25
Q

A respiratory until is called a

A

Acinus

Respiratory bronchiole
Alveolar duct
Alveolar sac
Alveolus

26
Q

What are heart failure cells?

A

Alveolar macrophages become laden with brown-black hemosiderin due to breakdown of RBCs from engorged capillaries

27
Q

What features are required to diagnose chronic bronchitis

A

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
Q

Can asthma be drug induced

A 
Yes. 
Aspirin 
Inhibits cox but not LPO(?) 
So increased leukotrines
Increased spasms
29
Q

Atopic asthma

A 
Childhood onset 
Gene on chromosome 5q 
Assoc with type 1 IgE hypersensitivity 
Urticaria
Hay fever 
Eczema

Rhinitis

Positive RAST

30
Q

Restrictive lung disease divided into :

A 
Alveolar 
Interstitial 
Pleural
Neuromuscular
Thoracic cage/ extrinsic eg obesity
31
Q

How to differentiate extrinsic vs intrinsic causes of restrictive lung disease

A

DLCO test

Normal = extrinsic, ie chest wall, pleural, neuromuscular

32
Q

Some causes of lung cancer

A 
Smoking 
Radon exposure 
Asbestos 
Environmental tobacco smoke
Other toxin exposure 
Pollution 
Tar (in ciggies)
33
Q

Most common area for lung cancer

A

Main bronchi and subdivisions

34
Q

Presentation of bronchial carcinoma

A

Localised: cough, sputum, haemoptysis, SOB
General: weight loss, fever, fatigue
Metastasis

35
Q

Classification of lung cancer

A 
Small cell carcinoma 
Non small cell carcinoma: 
- squamous cell
- adenocarcinoma 
- large cell 
- other
36
Q

Small cell carcinoma usually arises from

A

Epithelial cells of centrally located bronchi

Commonest cause is smoking and tends to spread widely early

Very bad prognosis

37
Q

Increased adenocarcinoma thought to be due to

A

Shift to filtered cigarettes

Lowered incidence of squamous cell carcinoma

38
Q

Subtypes of adenocarcinoma

A

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
Q

Common mutations in adenocarcinoma

A
  1. KRAS
  2. EGFR
  3. ALK
40
Q

Most common type of lung cancer

A

Adenocarcinoma
40%
Best prognosis

41
Q

Large cell carcinomas : some are

A

Poorly differentiated adenocarcinoma or squamous cell

Large cell Neuroendocrine tumours

42
Q

Sequence of molecular changes for lung cancer

A

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
Q

How can some specific genetic pleomorphisms involving the P450 genes cause lung cancer

A

P-450 monooxygenase enzyme system needed for metabolic activation of some procarcinogens into carcinogens

44
Q

Pathology of lung cancer

A

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
Q

Well differentiated squamous cell cancers can show

A

Keratin pearls

Intracellular bridges

46
Q

Putative precursor for adenocarcinoma thought to be

A

Atypical adenomatous hyperplasia (AAH) - focus of epithelial proliferation composed of cuboidal or low-columnar cells

47
Q

K-RAS mutation can

A

Enable cells to escape normal checkpoint mechanisms and proliferate without end

48
Q

Lung carcinomas presentation

A

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
Q

Hallmark of asthma

A

Hyperrresponsiveness of airway to stimuli
Paroxysmal and reversible
Chronic bronchial inflammation with eosinophils
Sm hypertrophy and hyper reactivity
Increased mucus secretion (mucus plugs)

50
Q

Non atopic asthma

A

Adult type
No allergen sensitisation (negative RAST)
Respiratory infections
Humoral and cellular mediators are the same

51
Q

Types of asthma

A

Atopic
Non atopic
Occupational
Drug induced

52
Q

RAST

A

Serum radioallergosorbent test - present of IgE antibodies specific to panel of radiolabelled antigens

Skin test - wheal and flare reaction

53
Q

Repeated bouts of inflammation leads to (asthma)

A

Remodelling of airways

54
Q

In asthma what interleukins are involved?

A

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
Q

Small cell lung carcinomas

A

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
Q

Paraneoplastic syndrome assoc with lung cancer

A

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
Q

Carcinoid tumours

A

Do we need to know this lol

58
Q

Squamous cell carcinoma

A

???? Idk

59
Q

Blood values used to determine the cause of acidosis and alkalosis?

A

pH:
<7.35 = acidosis
>7.45 = alkalosis

pCO2:
>45mmHg = resp cause
<35mmHg = resp compensation

Bicarbonate:
<22mEq/L = metabolic acidosis
>26mEq/L = metabolic alkalosis

STUDY FOR BARRIERS (11 decks)

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