Respiratory Flashcards
What are the functions of the nose?
Warm inspired air
increase humidity of the air
filter function
defence (cilia take inhaled particles backwards to be swallowed)
What are turbinates?
Structures inside of the nose that increase the surface area of the nasal cavity. They are an outpouching of bone lined with epithelium.
*Superior meatus:
Olfactory epithelium
Cribriform plate
Sphenoid sinus
- Middle meatus
Sinus openings - Inferior meatus
nasolacrimal duct
Describe the paranasal sinuses
We have four pairs of sinuses:
Frontal
Maxillary
Ethmoid
Sphenoid bones
They are arranged in pairs.
Evagination of the mucous membrane from the nasal cavity.
Describe the frontal sinuses
Within the frontal bones
They have a midline septum that is not in the actual midline of the body.
They go over the orbit and across the superciliary arch (where most people’s eyebrows are).
They are supplied by the opthalmic division of the V cranial nerve. The trigeminal nerve innervates sensory components of the sinus.
Describe the maxillary sinuses
Located within the body of the maxilla
They have a pyramidal shape:
* Base of the pyramid is the lateral wall of the nose
* Apex is the zygomatic process of the maxilla.
* Roof - floor of the orbit.
* Floor - alveolar process
The maxillary sinus opens into the middle meatus through the hiatus semilunaris. This allows the fluid in the sinus to drain back into the nasal cavity.
Describe the ethmoid sinuses
Located between the eyes.
Composed of a labyrinth of air cells.
They drain into by the semilunar hiatus into the middle meatus.
Nerve supply - opthalmic and maxillary divisions of V cranial nerve.
Describe the sphenoid sinuses
It is a small sinus that
It is inferior to the optic canal, dura and pituitary gland.
Empties into the sphenoethmoidal recess, lateral to the attachment of the nasal septum.
Innervated by the opthalmic V.
It is close to the carotid artery, the III, IV, V and VI cranial nerves.
Medial to the cavernous sinus.
What is the phraynx?
Links the back of the nose to the larynx.
What is the larynx?
It is a very complicated valve.
Prevents liquids and food from entering the lung.
Has a rigid structure - comprised of cartilage. Multiple muscles involved.
The arytenoid cartilages rotate on the cricoid cartilage to change the vocal cords.
The cartilages in the larynx are the following:
*Single:
Epiglottis x1
Thyroid x1
Cricoid x1
*double:
Cuneiform x2
Corniculate x2
Arytenoid x2
How is the larynx innervated?
Innervated by the 2 branches of the vagus (X) nerve:
*Superior laryngeal nerve. The internal branch is sensory.
The external branch supplies the cricothyroid muscle.
*Recurrent laryngeal nerve innervates all muscles bar the cricothyroid. The L and R recurrent laryngeal nerves are different.
How are the lungs arranged in the thoracic cavity?
ML can’t be seen poseriorly.
What are the differences between the right and left main bronchi?
The carina is the point at which the split occurs.
The right main bronchus is more vertical and shorter. (1-2.5cm long).
The L main bronchus is longer and more curved as it must avoid the heart and the aortic arch (5cm long).
What is the lower respiratory airway structure?
The main airways are as follows:
Trachea.
main bronchi.
lobar bronchi.
segmental bronchi.
respiratory bronchi.
terminal bronchiole.
alveolar ducts and alveoli.
What are the branches in the segmental bronchi?
(dont really need to know lol)
In the right lung:
Upper lobe - apical, anterior and posterior
Middle lobe - medial and lateral
Lower lobe - apical, anterior, posterior, medial, lateral
In the left lung:
Upper love - apico-posterior, anterior
Lingu
How does the structure of the lung tubes change?
They slowly become more adapted for gas exchange.
What is the acinus?
It is a functional unit running out from the terminal bronchiole. The system that starts at the respiratory bronchiole and terminates at the alveoli is called an acinus, and it is functionally characterized by having the ability to both conduct air as well as enable gas exchange.
What are the pleura?
2 layers of mesodermal origin, each a single cell layer, that are continuous with each other.
Visceral - applied to lung surface. Has only autonomic innervation.
parietal - applied to internal chest wall. Has pain sensation.
fluid between
How does the neutrophil help with host defence in the lung?
It is part of the innate immune system.
They have multiple functions:
1. Receptors identify the threats. They recognise bacterial structures like cell walls, lipids, peptides. Also host mediators (cytokines, lipids) and other host molecules.
- Activation.
- Adhesion.
- Migration/ chemotaxis. They can quickly identify the site where the threat is, and efficiently deal with it.
- Phagocytosis.
- Bacterial killing
- Apoptosis (programmed cell death).
What is inflammation?
Vasodilation leading to exudation of plasma, including antibodies.
It causes the activation of biochemical cascades.
It encourages the migration of blood leukocytes into the tissues - mainly neutrophils but also some monocytes.
How can inflammation be bad?
Repeated inflammation can lead to the death of alveolar cells, through various mechanisms.
What is ARDS?
Acute respiratory distress syndrome.
A buildup of fluid, immune cells, and other stuff in the alveoli in the lungs.
Also causes thickening of the alveolar walls.
How is inflammation initiated?
Initiated by epithelial production of hydrogen peroxide, which damages and releases cellular contents.
This stimulates other cells to create cytokines and chemokines, which recruit inflammatory cells causing a cascade in inflammation.
It is amplified by specialist tissue resident macrophages.
These include alveolar macrophages (lung), Kupffer cells (liver), histiocytes (skin and bone) and dendritic cells.
These deal with low level threats and coordinate signalling.
They respond to:
* PAMPs (pathogen associated molecular patterns)
* DAMPs (damage associated molecular patterns).
What are the patterns on pathogens?
Signalling receptors:
Toll-like receptors (TLRs)
Nod-like receptors (NLRs)
Endocytic receptors (phagocytic receptors):
Mannose receptors
Glucan receptors
Scavenger cells
What are the alveolar macrophages?
They colonise the lung during foetal development.
Macrophage plasticity:
Macrophages can change their behaviour (phenotype) depending on their environment.
They adapt to the individual threat.
They can also heal surrounding tissues once the threat is gone.
Describe neutrophil structure.
They contain granules:
Primary granules contain myeloperoxidase, elactase, cathepsins, defensins. These can damage cells but help in killing baceria.
Secondary granules contain new receptors for the cell surface and other enzymes useful for killing bacteria (lysozymes, collagenase).
Some neutrophils are adhered to the endothelium, but most travel in circulation.
How are neutrophils removed?
They take up bacteria and digest them.
They release chemicals that damage tissues. They must be removed, so they undergo apoptosis.
The key effector proteins are cut up by proteases within the cell. The cell is recognised as being apoptotic, so it can be taken up by macrophages.
Describe (2) neutrophil activation?
Called stimulus response coupling.
The amount of neutrophils produced must be appropriate to the size of the threat.
This is done by pathways involving calcium, phospholipases, protein kinases and G proteins.
Describe (3) neutrophil adhesion
They initially are flowing in the blood.
In the blood, they will be ‘captured’ by an activated piece of endothelium through a process between selectin molecules on the endothelium and neutrophil. This causes the neutrophil to roll across the endothelium.
They then interact with integrins, which capture the neutrophils fully, causing them to go stationary. They then squeeze between endothelial cells, out of the blood vessels.
How to neutrophils do phagocytosis (5)?
Membrane pinching creates a phagosome, inside of which is the pathogen. They then undergo a war.
How do neutrophils kill bacteria? (7)
Happens within the phagosome.
The pathogen is killed by enzyme release.
ROS (reactive oxygen species) is generated by NADPH oxidase complex.
What is Pouiseuille’s law?
Determining flow through a tube
How do we determine pressure across circulation?
Principles of V=IR
Pressure across circuit = CO x resistance
Pressure across pulmonary circulation:
mPAP - PAWP = CO x PVR
mPAP - mean pulmonary arterial pressure
PAWP - pulmonary arterial wedge pressure, which is left atrial pressure
CO - cardiac output
PVR - pulmonary vascular resistance.
How does the pulmonary arterial pressure stay constant during exercise?
mPAP is stable
CO significantly increases.
Resistance must fall to accommodate this.
This is done by recruiting more capillaries and using them.
Capillary vessels can also be distended.
What are the two main causes of hypoxaemia?
Type I and type II respiratory failure.
Both involve a pO2 < 8kPA.
Type I:
pCO2 < 6kPA (normal levels)
Type II:
pCO2 > 6 kPA (abnormally high level)
These are caused, generally, by 4 main things:
* Hypoventilation
* Diffusion impairment
* shunting
* V/Q mismatch
How does hypoventilation cause hypoxaemia?
Causes type II respiratory failure. Means alveoli cannot be ventilated properly.
Can be caused by problems with skin, muscular weakness, bones.
Can also be caused by things that control the breathing - drugs that reduce the respiratory drive.
How can diffusion impairment cause respiratory failure?
gaseous diffusion:
- Alveoli may be filled with fluid (pulmonary oedema).
Membrane diffusion:
- Interstitial fibrosis
Blood diffusion:
- If you are anaemic, less oxygen can get round the body.
What is VQ mismatch, and how does it cause hypoxaemia?
V/Q mismatch
V= ventilation
Q = perfusion.
If the blood flow and air flow are not matched properly, not enough oxygen may be transferred.
If the V/Q ratio is too high/ too low, exchange is ineffecient.
What is shunting?
Blood flows into the lungs but no gas exchange occurs.
For example:
- Complete lobar collapse.
Eisenmenger’s syndrome causes blood to flow into the RV from LV as pressure in LV is higher. This damages the small pulmonary arteries, remodelling the vessels. They respond by becoming narrower, increasing resistance and pressure. This build in pressure can lead RV pressure to be higher than LV pressure. Deoxygenated blood then flows into the LV, and into systemic circulation. Oxygen saturation is lower.
What are the host defences in the lungs?
Intrinsic: always present
Physical and chemical defences: apoptosis, autopahgy, RNA silencing, antiviral proteins.
Innate defence: induced by infection
Macrophages, NK cells, cytokines
Adaptive immunity: tailored to a pathogen
T cells and B cells.
What is the function of mucus?
It is a viscoelastic gel containing water, carbohydrates, proteins and lipids.
Secreted by goblet cells and the submucosal glands.
Protects the epithelium from foreign material and from fluid loss.
Mucociliary clearance (rhythmic beating of cilia) and air flow moves mucus from the lower respiratory tract into the pharynx.
What is a cough?
An expulsive reflex (voluntary or involuntary) that protects the lungs and respiratory passages from foreign bodies.
Causes:
- Irritants (smoke, fumes, dusts)
- Diseased conditions (COPD, tumours)
- Infections (influenza)
Motor and sensory innervation causes the cough reflex.
What is a sneeze?
Involuntary expulsion of air containing irritants from the nose.
Causes:
- Irritation of nasal mucosa.
- Excess fluid in airway
Receptors in the upper respiratory tract detect particulates in the nose. Sensory neurones register this. CNS. Motor neurones - sneeze. Irritant is expelled.
What molecules are secrete
- Antiproteases (pathogens may use proteases to invade the epithelium).
- Anti-fungal proteins
- Anti-microbial proteins (focus bacterial pathogens).
- Antiviral proteins
- Opsins are involved in completement pathways.
These are produced by different epithelial cells. Different classes of cells produce many types of chemicals and proteins.
How does the airway exhibit functional plasticity?
The respiratory epithelium can essentially complete a complete repair. The basal cell is the fundamental cell, from which other cells differentiate.
Metaplasia is where there is a reversible differentiation from one cell type to another. Some of the epithelium in smokers can be removed and replaced.
Why are ventilation as perfusion important for gas exchange?
Ventilation - maintaining conc gradient for diffusion of gases in the air.
perfusion - maintaining conc gradient for diffusion of gases in the blood.
Ventilation and prefusion must be matched to ensure efficient exchange.
What is alveolar dead space?
It is the volume of air not contributing to ventilation.
For two reasons:
1) not all inspired air reaches alveoli
2) not all alveoli are perfused with blood.
What is typical blood pressure?
Systemic: less than 120/80 mmHg
Pulmonary: 24/10 mmHg
What is unique about the arteries in the lungs?
The broncho-vascular artery runs parallel with an airway, not a vein (as is typical).
How efficient is gas exchange?
25% through the alveolar capillaries, haemoglobin is fully saturated.
Alveolar perfusion also depends on pulmonary arterial and venous pressure, as well as alveolar pressure.
What is the alveolar gas equation?
R = respiratory quotient (ratio of CO2 vol released / vol O2 absorbed. Assume standard = 0.8)
PAO2 = alveolar partial pressure of O2 (same with CO2).
PaO2 = arterial partial pressure of O2 (same with CO2). Can be measured in both CO2 (by pH) and O2 (by HCO3-).
PiO2 = pressure of inspired oxygen
FiO2 = fraction of inspired oxygen
VA = alveolar ventilation
VCO2 = CO2 production.
CO2 elimination:
PaCO2 = kVCO2 / VA
normally PaCO2 = 4-6 kPa.
PAO2= PiO2 - (PaCO2 / R)
What are some causes of high CO2?
(high PaCO2)
PaCO2 = kVCO2 / VA
CO2 is carried in the blood in 3 ways:
1. bound to haemoglobin.
2. Plasma dissolved.
3. As carbonic acid.
- VA reduced; reduced minute ventilation.
- VA reduced; increased dead space ventilation by rapid shallow breathing.
- VA reduced; increased dead space by ventilation/ perfusion (V/Q) mismatching.
- High CO2 production.
How is blood acidity managed?
Maintaining pH of the blood.
It can change CO2 under predominant respiratory control (rapid change).
It can change HCO3- under predominant renal control (slower change).
In order to keep pH at 7.4, the log ratio in the HH eqution must equal 1.3.
If PaCO2 rises (due to resp failure), HCO3- must rise to compensate (done by the renal compensatory mechanism).
What are the four main acid-base disorders?
Respiratory acidosis: increased PaCO2, decreased pH, mild increased HCO3- (where CO2 retention leads to increased carbonic acid dissociation). To compensate, there is increased renal H+ excretion and bicarbonate retention.
Respiratory alkalosis: decreased PaCO2, increased pH, mild decreased HCO3- (CO2 depletion due to hyperventilation). Increases renal bicarbonate loss.
Metabolic acidosis: reduced bicarbonate and decreased pH. Body compensates by hyperventilation to increase CO2 excretion.
Metabolic alkalosis: increased bicarbonate and increased pH (many causes, like alkali ingestion or GI acid loss (ie by vomitting)). Body compensates by hypoventilation and renal bicarbonate excretion.
What are some measurements in lung physiology?
TV (tidal volume): vol inhaled and exhaled during a normal breath.
TLC: total lung capacity (typically 5.9L)
VC (vital capacity): vol of lungs after max air exhaled foracbly - small vol remains to prevent lung collapse).
Residual volume (RV): alveolar dead space, ~1.2L.
ERV (expiratory reserve): the vol of air that can be exhaled after a normal tidal expiration ~1.2L.
Inspirational Capacity (IV): the vol that can be inhaled after a normal tidal expiration ~3.5L.
FRC: functional residual capacity: total vol of air in lungs after tidal expiration
FEVI = forced expiratory volume in one second. 80% of vital capacity in healthy person.
FVC = forced vital capacity (the amount of air that can be forcably exhaled from the lungs. Does not include alveolar dead space. TLC does). Ie max air exhaled after max vol inhaled using max force.
PEF (peak air flow): max velocity of air during FVC. In a healthy person, velocity should decrease linearly after PEF.
FVC = TLC - RV
Note:
FEV1/FVC > 0.8, ordinarily.
What is the use of a spirometer?
Measures PEF. Readings in L/min.
In airway obstruction: reduced airflow leading to hyperinflation, decreasing FEV1 but increasing RV & TLC. FVC remains similar, ratio of FEV1/FVC reduced to below 0.7. ‘Scalloped’ flow loop. E.g.: COPD, asthma
In airway restriction: reduced compliance of lungs, reducing both FEV1 and FVC. Ratio remains the same but all other parameters reduced (VC, IC, EC. E.g.: pulmonary fibrosis
What are ways of measuring lung vol?
Expiratory procedure only measure VC, not RV.
Other methods are required to measure RV and TLC.
These are gas dilution and body box.
How can gas dilution measure lung volume?
Measures TLC.
Ask the patient to breathe in a known conc of gas.
The change in conc of the gas after being breathed back out is a function of the volume of the lungs.
May not work if a section of the lung isn’t being ventilated.
What are the 7 layers of gas exhange?
- Fluid lining alveolus
- Layer of epithelial cells – type I pneumocytes
- Basement membrane of type I cells
- Interstitial space
- Basement membrane
- Endothelia
- Erythrocyte
How does the total body plethysmography?
Patients are locked into a box and are (often) asked to pant/ hyperventilate).
Oscillations in the pressure in the box allow measures of lung volume.
Summarise control of breathing
Where are the peripheral chemoreceptors for breathing?
In the carotid bodies:
- At the bifurcation of the common carotid.
- IX cranial nerve afferents
In the aortic bodies:
- Ascending aorta
- Vagal (X) nerve afferents.
Describe lung function trajectories
How can CF be classified by genotype?
Class I: no functional CFTR protein is made (e.g. G542X)
Class II: CFTR protein is made but it is mis-folded (e.g. F508del). The F508del is the most common mutation. Affects 80-90% of patients.
Class III: CFTR protein is formed into a channel but it does not open properly (e.g. G551D)
Class IV: CFTR protein is formed into a channel but chloride ions do not cross the channel properly (e.g. R347P)
Class V: CFTR protein is not made in sufficient quantities (e.g. A455E)
Class VI: CFTR protein with decreased cell surface stability (e.g. 120del123)
Class II and III are the main ones. Make sure you can remember them.
Show normal barometric pressures at increased altitudes.
Describe the oxygen dissociation curve
Shifts to the right with decreased pH/
Describe high altitude pulmonary oedema (HAPE).
Symptoms are cough, shortness of breath.
Caused by a rapid ascent to over 8000ft.
Indicated by cough, frothy sputum and breathlessness.
DESCENT IS PRIMARY TREATMENT
Treatments include:
- O2
- Gamow bag
- Steroids
- Ca2+ blockers
-Sildenafil
What are the stages of lung development?
Embryonic - 0-5 weeks
Pseudoglandular - 5-17 weeks
Cannalicular - 16-25 weeks
Alevolar - 25 weeks to term.
What is tracheoesophageal fistula?
Where the trachea and the oesophagus become attached.
How does blood pressure change at birth?
Before birth, R heart pressure is higher.
Rapid switch to L heart high pressure system, R low.
What is Laplace’s Law?
Larger alveoli may preferentially open as smaller alveoli preferentially shut with a given surface tension. Surface tension is essential for keeping smaller alveoli patant.
