block 5- the respiratory tract Flashcards

1
Q

what are the functions of the respiratory tract

A

Primary function: Gas exchange (O₂ in, CO₂ out).

Other functions:
pH regulation (via CO₂ levels)
Blood pressure regulation (angiotensin-converting enzyme)
Vocalization (air through vocal cords)
Olfaction (smell)
Protection (against dehydration, temp changes, pathogens)

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2
Q

what are the two divisions of the respiratory tract based on structure

A

Upper Respiratory System: Nose → Pharynx
Shared with the digestive tract.

Lower Respiratory System: Larynx → Lungs
Air passage only.

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3
Q

what are the functional divisions of the respiratory tract

A

Conducting Zone (air conduction, no gas exchange):
Nose, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles.

Respiratory Zone (site of gas exchange):
Respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli.

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4
Q

the respiratory epithelium and adaptations

A

Conducting Zone: Pseudostratified ciliated columnar epithelium with goblet cells (mucus production & clearance to keep airway clean and prevent pathogens from entering).

Stratified squamous epithelium in oropharynx & laryngopharynx (abrasion resistance agaisnt food).

Respiratory Zone: Simple squamous epithelium (minimizes gas exchange distance).

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5
Q

functions of nose and nasal cavity

A

Functions: Warms, moistens, filters air; detects smells; modifies speech.

nose:
- hairs on the inside filter particles before they reach the lower respiratory tract
- held open by bones and cartiliage

nasal cavity:
- connected to paranasal sinuses
- 3 conchae projecting from lateral wall (bones)
- air passing through has to go through the meatus( each conchae has a passageway)

nasal conchae function:
(turbinates): Spin air, trap particles, humidify air.

meatus function:
increases surface area for contact with mucosa

Blood supply: Warms air but prone to nosebleeds.

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6
Q
A
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6
Q

the pharynx

throat

A
  • air moves from nasal cavity to here
  • are muscular tubes transmitting air and food

3 regions:
1. Nasopharynx: Respiratory epithelium, nasal cavity to uvula
2.Oropharynx: stratified squamous from uvulva to epiglottis
3.Laryngopharynx: Stratified squamous, from epiglottis to oesophagus
Soft palate & epiglottis prevent food entering nasal cavity/larynx.

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7
Q

the larynx

voicebox

A
  • passageway connecting the pharynx with the trachea

functions:
Air passage, sound production as air crosses the vocal folds, closes airway when swallowing.

formed from cartiliage:
the 3 singular ->
Epiglottis: Prevents food entry.
Thyroid (Adam’s apple).
Cricoid: Complete ring, landmark for emergency airway.

3 paired:
Arytenoids: Adjust vocal cord tension.
Cuneiform
corniculate

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8
Q

trachea

windpipe

A
  • air moves from larynx to windpipe

-12cm tube, C-shaped cartilage rings keep it open.
- lined with epithelium

- Bifurcates into left and right primary bronchi at carina which each go to the lungs carina = cartiliagious ridges separating the bronchi 

The tracheal bifurcation is the point at which the trachea divides into, and is continuous with, the two main bronchi.

Right bronchus: Wider & more vertical (higher risk of obstruction).

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9
Q

describe the bronchial tree

A
  1. Primary bronchi → Left & right, cartilage rings.
  2. Secondary (Lobar) bronchi → 2 left, 3 right cartiliage plates
  3. Tertiary (Segmental) bronchi → Cartilage plates one to each lung segment
  4. Bronchioles → No cartilage, smooth muscle walls.
  5. Terminal bronchioles → End of conducting zone, simple cuboidal epithelium
  6. Respiratory bronchioles → Start of respiratory zone.
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10
Q

alveoli and gas exchange

A

alveoli structure: Clusters forming alveolar sacs (~500 million in lungs). -> create a large surface area for gas exchange

gas exchange:
occurs by diffusion across alveolar and capillary walls = Respiratory epithelium

Cell Types:
Type I cells: Gas exchange (simple squamous).
Type II cells: Secrete surfactant (reduces alveolar surface tension).

Capillary network: Surrounds alveoli, facilitates diffusion.

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11
Q

the lungs and pleura

A
  • lungs separated by the mediastinum

Right lung: 3 lobes (divided into superior, middle and inferior by horizontal +oblique fissures).
Left lung: 2 lobes (superior + inferior by oblique fissure) + cardiac notch.

Pleura membrane:
Parietal layer: Lines thoracic wall.
Visceral layer: Covers lungs.
Pleural fluid: Reduces friction, adheres lungs to chest wall, found in pleural cavities

things that enter and leave lungs (hilum):
- bronchi, pulmoneary arteries and veins, lymphatics, nerves

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12
Q

thoracic cage

A
  • composed of the Ribs, sternum, vertebrae T1-T12

-function: protects organs & aids respiration + breathing
- attatchment site for muscles of respiration

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13
Q

inspiration and expiration in respiration

A
  • Air moves into lungs when pressure inside lungs (alveolar pressure) is less than atmospheric pressure

Inspiration (Active - drawing air in):
Diaphragm contracts & flattens → Increases thoracic volume.
External intercostal muscles elevate ribs (bucket & pump-handle movement).

Expiration (Passive):
Diaphragm relaxes, lungs recoil, thoracic volume decreases → Air expelled.

Forced Expiration: Abdominal muscles & internal intercostals pull ribs down.

Accessory Muscles: Arms, shoulders used in labored breathing (hands on knees when out of breathe)

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14
Q

diaphragm

A
  • is the main muscle of respiration
  • separates the thorax from the abdomen
  • supplied by the phrenic nerve originating from C3, 4 and 5
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15
Q

the intercostal muscles

A

= lie between the ribs in the intercostal spaces

  • 3 muscle layers:
  • External intercostal (downwards and forwards)
  • Internal intercostal (downwards and backwards)
  • Innermost intercostal
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16
Q

respiration simplified for understanding

A
  • Inspiration thoracic cavity expands –> lung expands -> interpulmonary pressure decreases = draws air in
    • Expiration decrease in volume of thoracic cavity -> lung contracts -> interpulmonary pressure increases = air expelled
    • Inspiration requires energy – muscle contraction
    • Expiration is passive–elastic recoil
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17
Q

what is meant by bucket handle and pump handle movements

A

Contraction of the external intercostals raises the lateral part of the ribs, causing a bucket handle motion that increases the transverse diameter of the thorax. The vertebrosternal ribs also follow a pump handle motion, which raises the sternum and increases the anterior-posterior dimensions of the thorax.

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18
Q

describe the mechanisms of breathing

purpose, process and partial pressures

A

Breathing purpose: Bring in oxygen (O₂) and remove carbon dioxide (CO₂).
Ventilation: Movement of air in and out of the lungs, maintaining blood homeostasis (O₂, CO₂, and pH).

Partial Pressure (P₀₂, PCO₂):
At rest: P₀₂ = 100 mmHg, PCO₂ = 40 mmHg.
Minimal changes occur during exercise except in extreme cases.

Breathing Process:
Inspiration (Active): Diaphragm contracts, external intercostals lift ribs.
Expiration:
Quiet breathing: Passive, due to elastic recoil.
Strenuous breathing: Active, involving abdominal and internal intercostal muscles.

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19
Q

what is partial pressure?

A

-the pressure that the gas exerts in a certain environment

MmHg of mercury or torr, are units of measurement and are used interchangeably

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20
Q

ventilation

A

= The process of moving air in and out of the lungs to facilitate gas exchange

At Rest: ~6L per minute (tidal volume × respiratory rate).
During Exercise: Increases to maintain blood gas homeostasis.
Extreme Exercise: Minor changes in P₀₂ and PCO₂, but ventilation significantly increases.

Ventilation and Partial Pressure:

Alveolar P₀₂ = ~102 mmHg
Alveolar PCO₂ = ~40 mmHg
Gas moves down its pressure gradient (O₂ into blood, CO₂ out).

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21
Q

the flow of air movement into the lungs sequence

A
  1. nasal cavities
  2. pharynx
  3. larynx
  4. trachea
  5. bronchi (same function as trachea)
  6. lungs
  7. alveoli
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22
Q

describe active inspiration and expiration in terms of strenuous breathing

A

inspiration: ACTIVE
Greater contraction of diaphragm (1cm quiet breathing up to 10cm during strenuous breathing) and external intercostals.
Inspiratory accessory muscles active, e.g., sternocleidomastoid, alae nasi, genioglossus.

Expiration: ACTIVE
Abdominal muscles (rectus abdominus, internal oblique, external oblique and transversus abdominus
Internal intercostal muscles oppose external intercostals by pushing ribs down
and inwards.

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23
Q

the pressure and volume change key terms

A

Ppl (Pleural Pressure) – Pressure in the pleural cavity (always negative to keep lungs expanded).

Pel (Elastic Recoil Pressure) – Force exerted by the lung tissue wanting to collapse.

PA (Alveolar Pressure) – Pressure inside the alveoli.

PL (Transpulmonary Pressure) – Difference between alveolar pressure and pleural pressure, keeps lungs open.

PB(Barometric Pressure) – Atmospheric pressure outside the body.

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24
Q

breathing cycle step 1- beginning of inspiration

A
  1. no airflow as alveolar pressure and barometric pressure = 0
  2. inspiratory muscles contract -> (diaphragm, external intercostals), expanding thoracic cavity
  3. pleural pressure becomes more negative, pulling lungs outwards
  4. transpulmonary pressure increases, helping expand alveoli
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25
Q

breathing cycle step 2 - air flows in

A
  1. alveolar pressure becomes negative, below barometric pressure
  2. air moves into the alveoli from high pressure (atmosphere) to low pressure (lungs)
  3. lung volume increases
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26
Q

breathing cycle step 3- end of inspiration

no air flow

A
  1. muscles stop contracting
  2. alveolar pressure = barometric pressure, stopping airflow
  3. maximum lung volume reached
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27
Q

breathing cycle step 4- beginning of expiration

air moves out

A
  1. Thoracic volume decreases as inspiratory muscles relax.
  2. pleural pressure and transpulmonary pressure return to pre-inspiration values
  3. Elastic recoil of the lungs compresses air inside alveoli.
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28
Q

breathing cycle step 5- air flows out

A
  1. alveolar pressure becomes positive
  2. air flows out of lungs due to pressure gradients
  3. lung volume decreases
29
Q

key concept of breathing

A

Breathing is driven by pressure changes:

Air moves in when alveolar pressure is lower than atmospheric pressure.
Air moves out when alveolar pressure is higher than atmospheric pressure.

30
Q

what are the functional components of the airway system

A
  1. Upper Airways:
    Functions: Humidify, Warm, Filter air before reaching the lungs.
    Lined by ciliated columnar epithelium with mucus-producing goblet cells.
    Cilia move trapped particles out of airways.
  2. Respiratory Tree:
    -Conducting Airways (Trachea, Bronchi, Non-respiratory bronchioles):
    No gas exchange, forms anatomic dead space (~150ml).
    -Respiratory Airways (Respiratory bronchioles, alveolar ducts, alveoli):
    Gas exchange occurs here.
    Total volume: ~2500ml.

3.Alveoli (Gas Exchange Units):
~300-400 million in adults.
Type 1 cells (97% surface area) = Gas exchange.
Type 2 cells (3% surface area) = Surfactant production (reduces surface tension).
Alveolar macrophages remove debris.

31
Q

what is the respiratory tree

A

=composed of the trachea, the bronchi, and the bronchioles that transport air from the environment to the lungs for gas exchange.

from trachea -> bronchi -> non-respiratory bronchioles -> respiratory bronchioles -> alveolar duct….Each division results in an increase in number, a decrease in diameter and an increase in surface area.

32
Q

gas exchange in the lung

Blood circulation

A
  1. Pulmonary Circulation:
    Brings deoxygenated blood from heart to lungs.
    Returns oxygenated blood to heart for systemic circulation.
    Low resistance, high compliance system.
  2. bronchial circulation:
    - brings oxygenated blood to lung parenchyma via bronchiole artery

Alveolar-Capillary Network:
Thin walls (0.5mm) & large surface area (~100m²) optimize diffusion (gas exchange)
O₂ enters blood, CO₂ leaves blood following pressure gradients.
02 -> alveoli to capillary
co2 -> capillary to alveoli

Gas Gradients:
Pulmonary Circuit: O₂ into blood, CO₂ out.
Systemic Circuit: O₂ out of blood, CO₂ in.
- pressure gradient for 02 is larger than for C02 as CO2 is more diffusible.

33
Q

inspiration and expiration in quite breathing

A

inspiration is an active process
expiration is passive

34
Q

by what mechanism does gas move throughout the respiratory system

35
Q

characteristics of gas transport for breathing to occur optimally

A
  • large surface area
  • large partial pressure gradients
  • gases with advantageous diffusion properties
  • Specialised mechanisms for transporting O2 and CO2 between lungs and tissues
36
Q

the two forms of oxygen transport in the blood

A

Forms of Oxygen in Blood:
1. Dissolved: Small amount, but clinically measured as PaO2.
2. Bound to Hemoglobin (Hb): Major form, carried in red blood cells. Hb binds 4 O2 molecules per molecule.

37
Q

dissolved o2

A

-Proportional to partial pressure (PaO2).
-For example, at 100 mmHg PO2, 0.3 ml of O2 per 100 ml of blood.
-Insufficient on its own for body needs, hence the need for Hb. (not enough dissolved in blood for daily requirements)

38
Q

describe role and structure of haemoglobin

A

-Four heme groups (iron-containing) attached to globin protein (two α and β chains).
-280 million Hb molecules per RBC.
- each molecule can transport 4 oxygens

39
Q

explain the oxyhemoglobin dissociation curve

A

-Shows the relationship between PO2 and Hb saturation.
-Flat portion (100-60 mmHg): Little change in saturation.
-Steep portion (below 60 mmHg): Large release of O2 into tissues, with only a small change in PO2
- 02 binding to Hb is reversible
- when saturation is high -> lots of 02 is being transported by haemoglobin

40
Q

explain oxygen saturation

A

-oxygen saturation (SaO2) = amount of O2 bound to Hb.
- 100% saturation = all haem groups of Hb full saturated with 02

-Hb can carry 1.39 ml of O2 per gram of Hb.
- normal blood has ~ 150g of Hb/ L of blood
- the 02 capacity is: 150 x 1.39 = 208ml of 02/L of blood
- when we add the dissolved components~ 3mls/L of blood
- therefore the total 02 capacity = 211ml 02/L of blood

  • much more can be carried by haemoglobin than is dissolved in the blood
41
Q

describe the forms of c02 in the blood and amount that is produced

A
  1. 7% dissolved in plasma
  2. 23% bound to hemoglobin (carbaminohemoglobin)
  3. 70% converted to bicarbonate (HCO3-)
  • 200ml of C02 produced per minute
42
Q

what is the respiratory exchange ratio

A

= Ratio of expired CO2 to O2 uptake

In normal conditions, respiratory exchange ratio = 0.8 (80 CO2 to 100 O2).
- 80 molecules CO2 expired by lung for every 100 molecules of O2 entering.

43
Q

bicarbonate buffering in co2

A
  • the co2 that is converted to H2CO3 occurs in red blood cells
  • happens by the enzyme carbonic anhydrase
  • the bicarbonate ions dissociate into H+ and HC03-
  • the HC03- moves out of RBC in exchange for Cl- moving into it

-in systemic capillaries, CO2 produced by tissues is converted to HCO3-.
-In pulmonary capillaries, the reverse happens to expel CO2 into alveoli
-Critical for maintaining blood pH and acid-base balance.

44
Q

what is the function and location of chemoreceptors

A

Function: detect changes in the surrounding environment
in respiratory systems they detect changes in PO2, PCO2 and pH in the blood

Location: Peripheral (aortic arch, carotid sinuses) and central (brainstem).

45
Q

the location, response and pathway of peripheral chemoreceptors

A

Location: small vascularised bodies in aortic bodies and carotid bodies.

Response:
-Sensitive to low O2 (hypoxia).
-Stimulate increased ventilation when PO2 drops below 60 mmHg. (trying to get more oxygen into body)
-Also respond to elevated CO2.(main role in breathing)

Pathway:
-Signals sent to nucleus tractus solitarius (NTS) in the medulla via the glossopharyngeal and vagus nerves.
-Increases ventilation to restore PO2.

46
Q

location, response and pathway of central chemoreceptors

A

Location: clusters of neurones in the brainstem (medulla).

Response:
-Sensitive to increased PCO2 (hypercapnia) and decreased pH.
-Small changes in PCO2 result in significant changes in ventilation.
-Plays a major role in moment-to-moment control of breathing.
- a slight deviation above or below 40mmHg of PCO2 at resting -> instant changes in breathing

Pathway:
Stimulated by elevated CO2 → signals processed in NTS → increased ventilation.

47
Q

describe mechanoreceptors location, function and response

A

Function: Detect mechanical changes like lung inflation and chest wall movement. (more generally- pressure, movement and touch)

Location: Throughout the respiratory tree.

Response:
-During inspiration, lung inflation activates mechanoreceptors.
-Information sent to the NTS in brainstem via the vagus nerve.
-Adjustments in ventilation occur based on lung and chest movement.

48
Q

explain the integration of information in the brainstem

A
  1. NTS- receives information from mechanoreceptors and chemoreceptors
  2. this information is processed in brainstem by respiratory neurones
  3. clusters of respiratory neurones in brainstem generate the rhythm of breathing
  4. the rhythmic signal is sent to the respiratory muscles
49
Q

describe the respiratory neurones in the brainstem

A

Primary Respiratory Centers:
Pontine Respiratory Group: Regulates transitions between inhalation and exhalation.
Ventral Respiratory Group: Includes inspiratory and expiratory neurons, involved in the basic rhythm of breathing.

Firing Patterns:
-Respiratory neurons fire continuously, but their activity is modulated based on input from peripheral and central chemoreceptors and mechanoreceptors.

Integration:
-Input from NTS (medulla) coordinates the breathing cycle, adjusting for environmental and metabolic changes.

50
Q

explain the output from brainstem to respiratory muscles

signals sent down spinal cord

A
  • brainstem neurones produce rhythmic output
  • rhythmic neural signals sent to spinal cord
  • phrenic nerve exits spinal cord at cervical spinal cord level 3-5
  • phrenic nerve innervates diaphragm
  • nerves exiting thoracic spinal cord innervate intercostal muscles
51
Q

what is the function of the lung

A
  • to oxygenate blood
  • they do this by bringing inspired air into close contact with oxygen poor blood in the pulmonary capillaries to promote efficient gas exchange.
  • the trachea conducts inhaled air into the lungs
  • bronchia distribute air within the lungs
52
Q

how is airway function controlled

A

It is regulated by centers in the brain, CNS, and spinal cord, coordinating afferent (sensory) and efferent (motor) pathways to regulate musculature, blood vessels, and glands in the airways.

53
Q

what is the role of afferent and efferent nerves in airway control?

A

Afferent nerves send sensory information from the lungs to the CNS (e.g., breathing patterns, cough, and airway tone).

Efferent nerves receive signals from the CNS to regulate muscle contractions and gland secretion in the lungs.

54
Q

How do chemoreceptors and nocireceptors affect airway function?

afferent

A

=They respond to chemicals, inflammatory mediators, and physical stimuli (e.g., cold air), affecting breathing patterns.

  • these are sensed when we take air in
55
Q

What are the roles of parasympathetic and sympathetic nerves in airway function?

A

Parasympathetic nerves cause bronchoconstriction and mucus secretion in upper airways (via acetylcholine action on M3 muscarinic receptors).

Sympathetic nerves do not directly innervate airway smooth muscle but act indirectly through the release of noradrenaline. They influence blood vessels and glands and regulate β2 receptors in the airway smooth muscle.

  • noradrenaline produced in adrenal glands and distributed by blood circulation and reaching the B2 receptors in the airway smooth muscle
56
Q

What are NANC nerves and their role in airway function?

A

Non-adrenergic, non-cholinergic (NANC) nerves:

-Inhibitory NANC: Release NO and VIP to relax airway smooth muscle.

-Excitatory NANC: Release tachykinins (substance P, neurokinin A), causing neuro-inflammation.

57
Q

how is mucus secretion regulated?

A

-Mucus secretion is increased by parasympathetic stimulation, inflammatory mediatoes and chemical/physical stimuli and reduced by sympathetic stimulation.

-Goblet cells secrete mucus as a protective layer in the airways against pathogens or particles.

58
Q

What is asthma and what are the structural changes associated with it?

A

=is an obstructive lung disease characterized by chronic inflammation and acute exacerbations (asthma attacks).

The airways in asthma undergo structural changes:
1. Airway narrowing: Due to inflammation and smooth muscle constriction, leading to a smaller lumen.
2. Hypersecretion of mucus: Contributes to further narrowing and obstruction.
3. Edema: Fluid accumulation in the airway tissues causes further damage.
4. epithelial damage
5. infiltration of inflammatory cells
6. oedema (liquid accumulation in airway)
7. smooth muscle cell hypertrophy/hyperplasia + contraction

59
Q

what triggers asthma symptoms?

A

Asthma can be triggered by allergens (e.g., pet dander, dust mites), respiratory infections, exercise, pollutants, cold air, stress, and even some medications like NSAIDs.
- also some genetic factors

60
Q

what is bronchial hyper-reactivity?

A

=refers to abnormal sensitivity of the airways to a wide range of stimuli, causing excessive bronchoconstriction and inflammation.

  • e.g irritants, allergens, changes in air temperature
61
Q

What role does spirometry play in asthma diagnosis?

A

Spirometry measures the airflow that can be expelled from the lungs, helping diagnose obstruction and assess the severity of asthma

62
Q

What are the two main types of drug therapy for asthma?

A

Bronchodilators (relievers) - Relax airway muscles to ease breathing. - blue inhaler

Anti-inflammatory agents (preventers) - Reduce inflammation and prevent asthma attacks. - brown inhaler

63
Q

How do bronchodilators work in asthma management?

A
  1. B2-agonists (e.g., Salbutamol) -> increasing cAMP levels, which leads to bronchodilation and muscle relaxation, short acting
  2. muscarinic antagonists (e.g., ipratropium) -> short acting non-selective (M1,2,3)
  3. methylxanthines (e.g., theophylline) -> increase cAMP by inhibiting phosphodiesterase
  • we want to keep cyclic AMP levels high
  • the main aim is bronchodilation
64
Q

How do anti-inflammatory agents help in asthma management?

A

These drugs (e.g., glucocorticoids) prevent chronic inflammation by blocking inflammatory processes, reducing cytokine release, and limiting tissue damage.

  • they inhibit the production of prostanoids, cytokines and leukotrienes
  • administered by inhalers and frequently used alongside long acting B2-adrenoceptor agonists
65
Q

What are monoclonal antibodies and their role in asthma treatment?

A

Monoclonal antibodies target IgE or other mediators to prevent them from binding to mast cells, reducing allergic reactions and severe asthma symptoms.

66
Q

Why are glucocorticoids used in asthma therapy?

A

Glucocorticoids reduce inflammation and control the progression of chronic asthma by inhibiting the production of pro-inflammatory proteins and cytokines, though they can have side effects if used long-term like immune suppression.

67
Q

bronchodilator examples

A

Beta-2 Agonists (e.g., Salbutamol): These drugs increase cAMP levels, leading to smooth muscle relaxation and bronchodilation.

Muscarinic Receptor Antagonists: Prevent acetylcholine from causing bronchoconstriction via M3 receptors.

68
Q

what are the two phases of asthma

A
  1. immediate phase
    - bronchospasm (use drugs to target this)
    - fast onset after contact with stimuli
    - activation of mast cells
  2. late phase
    - airway inflammation and hyper-reactivity
    - onset after hours of immediate phase
    - progressive inflammatory response
    - infiltration and activation of Th2 cells and eosinophils
    - use drugs to target the inflammatory response
69
Q

other drugs to treat asthma - biologics

A
  • consist of monoclonal antibodies that target either IgE antibodies or other mediators of the inflammatory response
  • can treat severe asthma
  • they reduce the inflammatory effects mediated by mast cells, eosinophils or basophils
  • given by injection or drip
  • only used in severe cases when nothing else is working