GEP (Life support) Week 1 Flashcards

1
Q

What are the subparts of the pharynx?

A

-Nasopharynx
-Oropharynx
-Laryngopharynx

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2
Q

Where is the larynx located and what is its role?

A

The larynx is below the vocal cord and above the trachea.

It Mediates the crossover of digestive and respiratory passageways
Voice production

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3
Q

How many ribs do we have and how are they catogarised?

A

-We have 12 pair of ribs
-1-7 are true ribs that articulate to the sternum directly
-8-10 are flase ribs that articulate to the sternum by joining with other ribs coastal cartilage.
-11-12 are floating ribs, and they do not attach to the sternum.

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4
Q

What is the Pleura and how is it divided?

A

The pleura is a double memebrane covering the lungs and thorax that is divided into visceral and parietal.

Viscerel: This covers the surface of the lungs ( this is innervated by the pulmonary plexus and is only has a strech sensation).

Parietal: Covers the inside of the thorax (this is innervated by phrenic and intercostal nerve and can sense pain).

The space inbetween is also know as the intrapleural space (pleural cavity), this is a thin film of serous fluid.

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5
Q

How many lobes does the lung have?

A

Right lobe: 3 lobes and 2 fissures
Left lobe: 2 lobes and 1 fissure

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6
Q

Describe the histology of the lungs?

A

The lungs have:
Ciliated pseudostratified columnar cells (lines the epithelium of the lungs)
Mucous secreting goblet cells
Basal cells (Basal cells are the stem cells or progenitors of the airway epithelium )

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7
Q

Describe the lung vasculature?

A

Pulmonary circulation (for gas exchange):
-For each lobe there is 1 pulmonary artery which carries deoxygenated blood and 2 pulmonary vein which carries oxygenated blood (2A and 4V in total for both lungs).

Systematic Circulation (supplying the tissue):
-Bronchial arteries: supplies bronchi, lung roots, visceral pleura, supporting lung tissue
Bronchial Veins: Right bronchial vein –> Azygous vein
Left bronchial vein –> Hemiazygous vein

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8
Q

Describe the innervation of the lungs?

A

Parasympathetic (derived from the vagus nerve):
-This stimulates the seceretion from bronchial glands.
-This stimulates the contraction of bronchial smooth muslce
-Vasodilation of pulmonary vessels

Sympathetic (derived from the sympathetic trunk):
-Stimulates the relaxation of the bronchial smooth muscle
-Vasoconstriction of pulmonary vessels

Visceral afferent:
-Pain impulses to sensory ganglion of vagus nerve

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9
Q

Identify Hila anatomical regions

A
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10
Q

Outline the key landmarks in the throax vertebre

A
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11
Q

Describe the anatomy of breathing

A

Inspiration
External intercostals contract, raising the ribcage upwards and outwards
Diaphragm contracts and flattens, displacing digestive organs below
Increases intrapulmonary volume and decreases the intrapulmonary pressure below atmospheric pressure
Air is then drawn into the lungs down its pressure gradient from higher atmospheric pressure to lower intrapulmonary pressure

**Expiration **
External intercostal relax, which lowers the ribcage
Diaphragm relaxes and moves upwards
This decreases intrapulmonary pressure above atmospheric pressure
Air is drawn out of the lungs down its pressure gradient, from higher intrapulmonary pressure to low atmospheric pressure

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12
Q

What is a GPCRs and its mechanism?

A

GPCRs is also known as G protien coupled receptors
-The structure is where 1 protien is embedded in the membrane. There is 7 transmembrane region, N-terminal extracellular binding domain, C-terminal G-protein binding domain.

Mechanism
-Ligand binds to the N-terminal
-Induces a conformational chain in the GPCR
-Exposes the alpha subunit protein
Once exposed, the alpha subunit will swap its bound GDP for GTP
-Binding of the GTP to the alpha subunit causes it to detach from the GPCR
The beta and the gamma units remain bound
-Detached alpha subunit will then activate enzymes that produce secondary messengers inside the cell
-When not in use, the alpha subunit converts GTP back to GDP
This is it utilising its intrinsic GTPase activity
-Alpha GDP complex reforms with beta and gamma subunits again

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13
Q

Describe the different subunits of GPCRs?

A
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14
Q

Describe Ligand gated ion channels?

A

**Ligand gated ion channel **
Binding of a ligand to an extracellular site induces a conformational change in the protein subunits
Channels open and allow ions to move in/out of the cell

Response time = milliseconds
Example = Nicotinic ACh receptors

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15
Q

Describe a Receptor Tyrosine Kinase ?

A

Receptor Tyrosine Kinase
Ligand binds to extracellular binding domain
Activates the intracellular G protein
Intracellular RTK monomers then phosphorylate tyrosine residues on eachother
Phosphorylated monomers then induce an intracellular enzyme/proteins

Response time = hours
Example = Cytokine and insulin receptors

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16
Q

Describe a Nuclear Receptor?

A

Nuclear Receptors (Corticosteroids)
Lipophilic ligand passes through the plasma membrane and binds to a cytosolic receptor
HR complex translocates to the nuclease, where it binds to a Hormone Response Element (HRE) on the DNA
Receptor complex acts as a transcription factor and induces a desired response

Response time is longer
Example = steroid hormones

17
Q

Define Asthma and the triggers for an asthma attack?

A

Asthma is a type 1 hypersensitivity reaction of the airway leading to inflammation and reversible bronchoconstriction.

18
Q

What is the atopic triad

A

Eczema
Asthma
Allergic Rhinitis

19
Q

What are the risk factors of Asthma

A

Risk Factors
Family history
Exposure to tobacco smoke
Maternal factors
Antenatal viral infection
Maternal smoking
Low birth weight
Obesity
Respiratory infections in infancy

20
Q

What are the differential diagnosis of asthma?

A
21
Q

Briefly describe the epidemiology of asthma

A

Asthma affects more than 300 million people worldwide

In the UK, ~12% people have been diagnosed with asthma, although some have grown out of it (NICE, 2023)
5.4 million people currently receiving treatment

3 people per day die from asthma (1400 deaths in England & Wales in 2018; including 20 children under 14)

Childhood asthma more common in boys, adult asthma more common in women

22
Q

Describe the aetiology of asthma

A

Interplay between genetic and environmental factors

FHx not necessary for development of asthma - indicates importance and impact of environmental triggers

Acute effects include bronchoconstriction:
Wheeze
Cough
↑ Vascular permeability

Airway remodelling occurs as consequence of chronic inflammation

23
Q

What are the clinical signs and symptoms of asthma?

A

Symptoms:
Shortness of breath
Productive cough
Tight chest
Wheeze

Symptoms typically worse during the night or in the morning

Signs
Expiratory wheeze
Hyperinflation
Hyper-resonant on percussion
Tachypnoea
Silent chest (severe)

24
Q

Describe the pathophysiology of asthma (sensitisation)

A
25
Q

What is the pathophysiology of asthma on re-exposure

A
26
Q

How does the inflammatory mediators work and causes signs and symptoms?

A
27
Q

What are the investigations for Asthma and daignosing asthma?

A

-Peak Flow - highest of 3 readings. Results decrease in an asthma attack
-Respiratory exam
-Bloods - ABG, FBC, U&E’s, Serum IgE
-Chest X ray
Special Tests:
Sputum culture
Spirometry
Fractional exhaled nitric oxide (FENO)
Bronchodilator reversibility test (BDR)
Direct bronchial challenge test

28
Q

what would an asthmatic ABG look like?

A

Mild asthma: high PH and low paCo2
Moderate asthma: type 1 resp failure
Severe Asthma: type 2 resp failure + low PH and low bicarbonate

29
Q

Describe the different sounds on auscultation of respiratory conditions

A
30
Q

What is FEV1 and FVC

A

FEV1: air forced from lungs in 1 sec
FVC: air that is forced out of the lungs after deepest breath possible

In obstruction: FEV1 is low, FVC is normal and the FEV1/FVC ration is low (less than 80%)

31
Q

What is the management of Asthma?

A
32
Q

What is the management of asthma continued

A

**Conservative: **Avoid triggers like pets, smoke etc
Medical:
Salbutamol reliever
SABA
>3 times a week = poorly controlled & needs further medication
Low dose ICS - usually beclomethasone
LABA - usually salmeterol

If still poorly controlled:
Stop LABA (if no response)
Increasing ICS to medium dose
Adding leukotriene receptor antagonist (LRTA)

If STILL poorly controlled:
High dose ICS
LRTA (Leukotriene Receptor Antagonists, like montelukast)
LAMA (long acting muscurenic antagonist)

33
Q

What is the management of emergency asthma

A

O: Oxygen
S: Salbutamol through nebuliser
H: Hydrocortisone/prednisolone
I: Ipatropium bromide through a nebuliser
T: Theophylline/Aminophylline through IV and needs monitoring
M: Magnesium sulphate
E: Escalate it to ICU if there is no improvement

If all else fails, you can have surgery, known as bronchial thermoplasty where radio waves are heat up and reduce the amount of thickened smooth muslce on the inside of the wall of the airways

34
Q

What is type 1 and type 2 respiratory failure?

A

Exists when pO2 <8kPa
Type I (hypoxic) – pCO2 <6.5kPa
VQ mismatch
Increased resp rate leads to a fall in pCO2
Caused by alveolar hypoventilation, low atmospheric pressure/fraction of inspired oxygen (Eg. high altitudes), diffusion defect (fluid in the lungs, eg. Pneumonia), ventilation/perfusion mismatch and right-left shunt
Type II (hypercapnic) - pCO2 >6.5kPa
Ventilatory failure
Insufficient to excrete CO2 being produced by tissues
Caused by respiratory pump failure (Obstruction eg. COPD) and increased CO2 production