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2nd Year - systems 2 > Systems 2 - Respiratory > Flashcards

Systems 2 - Respiratory Flashcards

1
Q

Respiration definition

A

-O2 from atmosphere delivered to cells of body -enables cells to produce energy by oxidative reactions -the by-product, CO2, is removed to atmosphere

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2
Q

Trachea structural features - Cartilage

A

Supporting C circles of hyaline cartilage

Provide structure

Incomplete ring, so bolus can pass through oesophagus in swallowing

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3
Q

Trachea structural features - Cells

A

Pseudostratified ciliated epithelium

Goblet cells for mucus production

-> Together, mucociliary escalator to beat mucus to back of throat where it can be swallowed, goes to acidic stomach

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4
Q

Bronchioles structural features

A

No cartilage, patency maintained by connective and elastic tissue’s radial traction of lung

Lots of smooth muscle, for bronchoconstriction/dilation

Diameter > 1mm

Ciliated simple columnar epithelium in conducting (= terminal) bronchioles

Ciliated simple cuboidal epithelium in respiratory bronchioles

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5
Q

Alveoli structural features

A

Walls 0.5μm thick, only simple squamous eptheilium

Large surface area, mainly filled with capillaries for gas exchange

4 cell types- type I and II pneumocytes, alveolar macrophages and red blood cells

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6
Q

Cells in alveoli

A

TYPE I PNEUMOCYTES

  • large, flat surface for gas exchange
  • 90% of SA of alveoli
  • tight junctions
  • cell wall fused to capillary endothelium

TYPE II PNEUMOCYTES

  • secrete surfactant to reduce surface tension
  • only produced after 24 weeks gestation, so ‘respiratory distress of the newborn’ if premature

ALVEOLAR MACROPHAGES
- to mop up foreign tissue present

RED BLOOD CELLS

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7
Q

Functions of the airway

A

Primary

  • conducting zone to deliver air to site of gaseous exchange
  • respiratory zone to carry out gaseous exchange

Secondary

  • humidify and warm air
  • protect against particulates and infection

As the diameter of individual airways decreases, SA for gas exchange increases

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8
Q

Measurement of Functional Residual Capacity

A

Fill spirometer bell and tubing with 10% Helium (He doesn’t dissolve in body tissues but stays in gas filled spaces of lungs)

C₁ x V₁ = C₂ x (V₁ + V₂)

1 = conc/volume of He in spirometer and tubing before equilibration
C₂ = conc of He in new increased volume (V₂ also)
V₂ = volume of air in lungs

Therefore FRC = (Volume in spirometer x ([He} at start - [He} at end)) / [He} at end

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9
Q

Residual volume

A

Residual Volume = Functional residual capacity - End residual volume

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10
Q

Anatomical dead space

A

The volume of gas in collecting airways (so not taking part in gas exchange)

Measured using Fowler’s method:

  • subject inhales single breath of 100% O₂
  • expires breath into nitrogen meter
  • initial air has 0% nitrogen as is from dead space air just breathed in
  • then nitrogen content rises as alveolar air mixes
  • draw line down curve to get approx. 2.2 ml/kg nitrogen
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11
Q

Physiological dead space

A

The total volume of gas in the system not taking part in gas exchange.

Measured using Bohr method:

  • measure first air expired (dead space) for CO₂ conc
  • measure last air expired (alveolar) for CO₂ conc

Volume dead space/Tidal volume = Fraction alveolar CO₂-Fraction expired CO₂/Fraction alveolar CO₂

Approx 165ml is dead space, 1/3 of tidal volume

Pulmonary embolism increases dead space - more ventilation without perfusion

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12
Q

Estimated dead space (ml)

A

2.2 x body weight (kg)

Usually approx 165ml, 1/3 of tidal volume

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13
Q

Minute volume

A

Volume of gas breathed in or out per minute

Minute volume = Tidal volume x frequency

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14
Q

Alveolar ventilation

A

(Vt-Vd) x frequency

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15
Q

Fraction of alveolar CO₂

A

Fraction of alveolar CO₂ ∝ Rate of production of CO₂ / Alveolar ventilation

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16
Q

Correcting volume for different conditions

A

V₂ = V₁ x T₂/T₁ x P₁/P₂

To correct for pressure and temperature

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17
Q

Pressures in lung lining

A

Lung pulls into centre due to elastic recoil

Chest walls pulls out due to elastic recoil

-> Pleural sac in between therefore has negative intrapleural pressure

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18
Q

Boyle’s law

A

Pressure ∝ 1/Volume
for a given quantity of gas in a container.

(Pressure is inversely proportional to Volume. Also written PV=K where K is a constant.)

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19
Q

Process of inspiration

A

Diaphragm flattens and moves down

Contraction of external intercostal muscles so ribs move up and out

  • > increased volume in thoracic cavity
  • > decrease in alveolar pressure
  • > air moves in until alveolar pressure = atmospheric pressure
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20
Q

Process of expiration

A

Passive expiration in normal quiet breathing:
lungs recoil, decrease in lung volume, increase in alveolar pressure

In forceful expiration, abdominal muscles and internal intercostals contract

At FRC, recoil of lungs is balanced with recoil of chest walls, so only need forceful expiration past FRC.

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21
Q

Pneumothorax

A

Air in thorax, usually from trauma when chest wall is damaged

Chest wall becomes separated from lung, so -> collapsed lung (will appear on CXR as mediastinal shift away and absent vascular markings)

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22
Q

Work of breathing

A

30% for airway resistance

65% for compliance (elasticity of lung)

5% functional resistance

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23
Q

Airway resistance

A

Determines flow of gas through system

Q= ΔP/R

Flow = change in pressure/resistance

Upper airways have most resistance, smallest airways have low resistance, as they have the greatest total cross sectional area

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24
Q

Pouiselle’s law, airway resistance

A

Resistance of tube = (8 x viscosity x length) / π x radius⁴

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25
Q

To measure airway resistance

A

Airway resistance = FEV₁/FVC

= Forced expiratory volume in one second / forced vital capacity

Should equal or exceed 80% in a healthy person

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26
Q

Vitalograph

A

Breathe out as hard and fast as possible into machine

-> Produces curved graph of volume over time

FEV₁ can be found by 1s along up to volume

FVC is plateau point at maximum volume

-> Then can find FEV₁/FVC, so airway resistance

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27
Q

Peak expiratory flow

A

Can be found by steepest point of vitalograph (first section)

Changes with age and height, but should be approx 420ml for women, 600ml for men

If less than 80% of expected PEF -> amber
If less than 50% -> red, probable airway resistance

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28
Q

Airway resistance decreased by

A

Sympathetic nervous system activity, altering smooth muscle tone, dilation of airways

Increased lung volume, pulling open airways by radial traction

Increased CO₂ concentration

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29
Q

Pathophysiological changes to increase airway resistance

A

ASTHMA - increased constriction of smooth muscle in bronchioles, increased mucus secretion, inflammation

COPD

  • Bronchitis - Increased mucus, inflammation
  • Emphysema - Decreased pulmonary tissue, so decreased radial traction, airway collapse, decreased elastic recoil of lungs, INCREASED FRC as airway size increases, but airway more collapsible, harder to hold open

PULMONARY OEDEMA - eg left sided heart failure

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30
Q

COPD diagnosis (ratio)

A

Obstructive, so decreased rate at which air can leave the lungs

Lower FEV₁/FVC ratio

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31
Q

Compliance

A

A measure of the elasticity of the lungs, the ease with which they can be inflated

Compliance = Change in lung volume (ΔV) that results from a given change in transpulmonary pressure (Pressure in alveoli - interpleural pressure)

Compliance = ΔV/ΔP

With increased compliance, there will be an increased change in lung volume for a given increase in transpulmonary pressure.

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32
Q

Pressure-Volume curve

A

As pressure around the lung rises (becomes for negative), lung volume increases

Different inward and outward tracks (to do with surface tension)

Can measure intrapleural pressure by putting balloon in oesophagus. Oesophagus is floppy so exposed to pressures in thorax.

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33
Q

Regional effect of gravity on lung ventilation

A

Higher pressure at top of lung than at bottom -> so more distended at top

Different regions of lung work at different points in the compliance curve

-> so more ventilation at bottom than at top of lung

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34
Q

Compliance depends on

A

Elasticity of lungs

  • elastic fibres in connective tissue exert force opposing lung expansion
  • a build up of collagen stiffens lung

Surface tension of fluid lining alveoli
- traction between liquid molecules pulls alveoli closed

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35
Q

Law of Laplace, relevance to alveolar filling

A

P = 2T/r

Air pressure inside alveolus = 2 x surface tension / alveolus radius

Therefore if small and large alveoli had the same surface tension, small alveoli would not fill as they would have higher pressure, and would collapse into larger alveoli, creating an unstable structure.

Surfactant stops this, stabilises the structures by decreasing surface tension

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36
Q

Surfactant

A

Phospholipid

Produced by type II pneumocytes

Decreases surface tension - more surfactant in smaller alveoli, so equal pressure in large and small alveoli.

Increases the compliance of the lungs, decreasing the work of breathing

If born premature (pre 24 weeks), deficient surfactant so newborn respiratory distress syndrome.

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37
Q

Factors increasing compliance

A

Emphysema - increases lung volume

Ageing

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38
Q

Factors decreasing compliance

A

Fibrosis - decreases lung volume

Surfactant deficiency

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39
Q

Restrictive lung disease

A

Decreases FRC

eg fibrosing alveolitis - increased collagen in lung, so thickened membrane, stiffer lung, harder to increase volume

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40
Q

Pulmonary circulation

A

Same volume pumped from left and right ventricles

  • but lower pressure in pulmonary system
  • so must have decreased resistance

Higher bp in bottom of lung than top, as more ventilation here

Due to low pressure pulmonary artery, gravitates to bottom of lung

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41
Q

Anatomical shunt

A

Deoxygenated blood added to systemic circulation

~2% in health, increased in pathology (eg if lung not ventilated)

Intrapulmonary - some capillary pathways don’t go in via alveoli
Deep bronchial veins - to supply lung tissue
Thebesian circulation - to supply cardiac tissue

All drain into pulmonary vein or left heart, already deoxygenated

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42
Q

Calculation of shunt

A

Qs / Qt = (CcO₂ - CaO₂) / (CcO₂ - CvO₂)

Blood flow through shunt/total blood flow = (Pulmonary capillary O₂ content - arterial O₂ content) / (Pulmonary capillary O₂ content - venous O₂ content)

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43
Q

Shunt and dead space

A

Neither take part in gas exchange

SHUNT- blood flow but no O₂

DEAD SPACE- ventilated but no blood flow

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44
Q

Hypoxic vasoconstriction

A

Decreased PAO₂ -> local vasoconstriction, diverting blood away from poorly ventilated alveoli

Beneficial, helps ventilation as perfusion matching important in foetus.
Bad when large areas of lung have low PAO₂, eg at altitude or in chronic hypoxic lung disease.

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45
Q

Calculating partial pressures of gas

A

DRY GAS:
Pgas = Ptotal x Fgas

SATURATED:
Pgas = (Ptotal - Ph₂o) x Fgas

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46
Q

Henry’s law, volume of dissolved gas

A

Volume of dissolved gas = volume of blood x stability of gas x Pgas

Pgas is measured at the equilibrium of tendency of gas to leave vs tendency to enter liquid.

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47
Q

Rate of diffusion of gases influencing factors

A

Rate is proportional to

  • size of concentration gradient
  • surface area of membrane
  • permeability of membrane to particular substance
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48
Q

Clinical test for diffusing capacity

A
  • one breath of 0.3% CO
  • hold for 10s
  • measure CO conc in expired air
  • determine how much CO has diffused into lung, giving volume of CO transferred in ml/min/mmHg of alveolar partial pressure

Typically around 25ml/min/mmHg Lower than this indicates problem with gas exchange

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49
Q

Ventilation-Perfusion ratio

A

VA/Q = ventilation per unit blood flow

More blood flow and ventilation at the bottom of the lung, where there is the lowest VA/Q (not ideal)

If you block ventilation, VA/Q decreases, as composition of venous blood = arterial blood

If you block blood flow, VA/Q increases, as composition of expired gas = inspired gas

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50
Q

Expenditure of O₂

A

Breathe in 150mmHg O₂ in air

Decreases in alveoli, added to dead space, humidified V/Q inequalities and diffusion

Shunt in arteries

Loss to tissues

Venous blood 40mmHg

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51
Q

Alveolar-Arterial difference

A

PAO₂ > PaO₂ due to physiological shunts

PAO₂ calculated with alveolar gas equation, PaO2 measured in sample of arterial blood

Can be used in differentiating causes of hypoxia

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52
Q

Alveolar gas equation

A

PAO₂ = PIO₂ - PAO₂/RQ

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53
Q

Cause of hypoxia differentiation - High Altitude

A

Low PAO₂

Low PaO₂

Normal A-a difference

O₂ therapy beneficial

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54
Q

Cause of hypoxia differentiation - Hypoventilation

A

Low PAO₂

Low PaO₂

Normal A-a difference

O₂ therapy beneficial

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55
Q

Cause of hypoxia differentiation - VQ mismatch

A

Normal PAO₂

Low PaO₂

Increased A-a difference

O₂ therapy beneficial

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56
Q

Cause of hypoxia differentiation - Shunt

A

Normal PAO₂

Low PaO₂

Increased A-a difference

O₂ therapy limited benefts

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57
Q

Cause of hypoxia differentiation - Diffusion defect

A

Normal PAO₂

Low PaO₂

Increased A-a difference

O₂ therapy beneficial

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58
Q

CO₂ output

A

CO₂ output = (Volume expired x Fraction expired CO₂) - Volume inspired x Fraction inspired CO₂)

Usually around 200ml of CO₂ at rest

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59
Q

O₂ uptake

A

O₂ uptake = (Volume inspired x Fraction inspired O₂) - (Volume expired x Fraction expired O₂)

Usually around 250ml of O₂ at rest

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60
Q

Measuring O₂ consumption with a spirometer

A
  • drum filled with 100% O₂
  • soda lime used to remove CO₂ from exhaled air

-> can measure the rate of loss of O₂, rate of consumption

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61
Q

Respiratory quotient

A

RQ= CO₂ output / O₂ uptake

Should be 0.8 under resting conditions (200/250)

Changes with substrate:
0.7 Fat
0.8 Protein
1 Carbohydrate

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62
Q

Carriage of O₂ in the blood

A

Each 100ml of arterial blood is approx 20ml O₂

In solution and with haemoglobin

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63
Q

O₂ in solution

A

PO₂ relatively high (PaO₂ = 100mmHg)

BUT O₂ not very soluble (0.003ml O₂/100ml blood/mmHg PO₂) -> at PO₂ of 100mmHg, 100mls of blood contains 0.3ml of O₂ in solution

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64
Q

O₂ with haemoglobin

A

Majority of O₂ carried this way

Hb has 4 interlinked polypeptide chains (2 alpha, 2 beta)
Each chain binds to a haem group, which each contain Fe²⁺
Each haem group binds one O₂ molecule, so one Hb has four O₂s

Foetal haemoglobin has a lower PO₂, so an increased affinity for O₂ due to different polypeptides.

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65
Q

Reversible binding of O₂

A

High PO₂, binding
Becomes oxyhaemoglobin, and then diffuses down concentration gradient to tissues with low PO₂

Low PO₂, release

Deoxyhaemoglobin is dark purple, oxyhaemoglobin is bright red

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66
Q

Oxygen content of blood calculation

A

O₂ content = ([Hb} x 1.34 x % saturation) + (PO₂ x 0.003)) ml O₂/100ml blood

In arterial blood, around 20ml O₂/100ml blood

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67
Q

PaO₂ SaO₂ CaO₂

A

Partial pressure of O₂ dissolved in blood, mmHg

Percentage saturation of Hb with O₂, %, sigmoidal relationship to PaO₂

Total volume of O₂ contained per unit volume blood, ml/100ml

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68
Q

Oxyhaemoglobin dissociation curve

A

Sigmoidal

Binding O₂ increases the affinity to bind another, due to conformational change in the molecule

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69
Q

Affinity of haemoglobin for O₂

A

Sigmoidal curve shifts

To left - increase affinity, O₂ loaded more easily (foetal)

To right - decrease affinity, O₂ unloaded more easily

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70
Q

Factors decreasing haemoglobin’s affinity for O₂

A

SHIFT TO RIGHT

Increase in temperature
Decrease pH (more acidic)
Increase CO₂
Increase in 2,3-DPG (produced in erythrocytes in glycolysis, increases when Hb O₂ is low)

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71
Q

Oxygen delivery to systemic tissues

A

Rate of delivery > rate of O₂ consumption (gives safety margin)

Oxygen delivery = Q x CaO₂ (rate of flow x oxygen content of arterial blood)

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72
Q

Hypoxaemia (hypoxic hypoxia)

A

Low arterial PO₂, so decreased saturation of Hb, decreased O₂ content

Caused by

  • decreased inspired PO₂
  • hypoventilation
  • impaired diffusion
  • V/Q inequality, shunt

Decreased arterial PO₂, decreased venous PO₂, cyanosis possible

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73
Q

Ischaemic hypoxia

A

Decreased perfusion of tissues (inadequate blood flow)

Caused by

  • cardiac failure
  • arterial or venous obstruction

Normal arterial PO₂, decreased venous PO₂, cyanosis possible

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74
Q

Anaemic hypoxia

A

Decreased O₂ binding capacity

Caused by

  • anaemia
  • abnormal Hb eg in CO poisoning

Normal arterial PO₂, decreased venous PO₂, cyanosis unlikely

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75
Q

Histotoxic hypoxia

A

Impairment of respiratory enzymes

Caused by
- cyanide poisoning

Normal PO₂, increased venous PO₂, cyanosis unlikely

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76
Q

Signs and symptoms of acute hypoxia

A

SIGNS:

  • ataxia (loss of motor control)
  • convulsions
  • confusion
  • tachycardia
  • sweating
  • coma

SYMPTOMS:

  • euphoria
  • fatigue
  • headaches
  • light-headedness
  • tunnel vision
  • anorexia
  • irritability
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77
Q

Carriage of CO₂ in the blood - in solution

A

PCO₂ relatively low (40mmHg in alveoli)

BUT 20 x more soluble than O₂

-> at PCO₂ of 40mmHg, 100mls blood has 2.4 ml of CO₂ in solution

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78
Q

Carriage of CO₂ in the blood - as bicarbonate

A

CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻

First stage is SLOW, accelerated by carbonic anhydrase, which is only found in RBCs so reaction mainly occurs here.

CO₂ in plasma diffuses to RBCs, becomes H⁺ + HCO₃⁻

H⁺ causes Hb to release O₂, which diffuses out to plasma, HCO₃⁻ diffuses straight to plasma

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79
Q

Effects of Haemoglobin buffering H⁺

A

Hb binds to H⁺, so buffers it, causing:

  • stops free [H⁺] rising too much in blood
  • decreases affinity of Hb for O₂, so O₂ is released where CO₂ is present, at site of respiration
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80
Q

Carriage of CO₂ in the blood - as carbamino compounds

A

Protein with NH₂ group + CO₂ ↔ Protein with COO⁻ group + H⁺

Mainly in RBCs, where Hb provides rich source of NH₂ groups via 4 polypeptide chains with amines

Hb buffers H⁺

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81
Q

Haldone effect

A

Increasing PO₂ decreases the amount of CO₂ carried in blood

But much more CO₂ is in blood than O₂, as it has many different ways of being carried and is more soluble

82
Q

Hypercapnia signs and symptoms

A
  • vasodilatation
  • bounding pulse
  • papilloedema (swelling of optic disc in eye)
  • flapping tremor
  • depressed conscious level
  • respiratory acidosis and decreased cardiac contractility
83
Q

Acid base implications of CO₂

A

CO₂ is a volatile acid, becomes H⁺

Eliminated by ventilation

Changes in PaCO₂ alter pH of blood

Blood is slightly alkaline, especially in veins

84
Q

Respiratory acidosis

A

More H⁺ due to more CO₂, so more HCO₃⁻ to compensate from kidney (->long term changes in pH)

Caused by alveolar hypoventilation or chronic condition eg asthma, COPD, pneumonia, sleep apnea

85
Q

Acidosis symptoms

A
  • headache, sleepiness, confusion, loss of consciousness, coma
  • seizures, weakness
  • diarrhoea
  • shortness of breath, coughing
  • arrythmia, increased heart rate
  • nausea, vomiting
86
Q

Generation of respiratory rhythym

A

Inspiratory neurones stimulate motorneurones of phrenic (diaphragm, C3-C5) and external intercostal (T1-T11), causing contraction of inspiratory muscles

Ventilation is regulated intrinsically by O₂, CO₂ and pH in lungs, overriding voluntary control

87
Q

Brain controlling respiration

A

Medulla is centre for basic control of respiration, produces respiratory drive

Pons regulates the medulla- pneumotaxic centre and apneustic centre
Pneumotaxic centre is stimulated by apneustic centre and outflow from inspiratory neurones
Apneustic centre is tonic stimulation of inspiration, inhibited by pulmonary stretch receptors and by pneumotaxic centre

-> Together they facilitate transition between inspiration and expiration (inspiration inhibits inspiratory drive)

88
Q

Central hypoventilation syndrome, Ondine’s curse

A

Respiratory control centre stops working, so when unconscious there is no respiratory drive and no breathing

Requires ventilator before sleeping

89
Q

Central chemoreceptors (medulla)

A

Beneath ventral surface of medulla, near exit of cranial nerves 9 and 10 (glossopharyngeal and vagus)

Anatomically separate from medullary respiratory centre

Minute to minute control of ventilation

Surrounded by brain extracellular fluid

Respond to [H⁺] in CSF Blood brain barrier protects, as H⁺ cannot cross, CO₂ can

CO₂ becomes H⁺ and bicarbonate in CSF

-> Increased H⁺ increases ventilation drive

90
Q

Peripheral chemoreceptors (carotid bodies and aortic bodies)

A
  • Carotid bodies at bifurcation of common carotid arteries (where blood goes to brain) - most important
  • Aortic bodies (where blood goes to system)

Respond to decreased arterial PO₂ and pH, and responds to increased arterial PCO₂

Without these receptors, lose ventilatory response to hypoxia

High blood flow here, small arterial-venous O₂ difference in spite of high metabolic rate

Carotid body info via glossopharyngeal to medulla Aortic body info via vagus to medulla

91
Q

Effects of arterial PO₂ on ventilation

A

Normal resting level of O₂ sits of plateau, so small changes will not bring about a change in ventilation

Normal resting level of CO₂ on steep part of curve, so small changes in CO₂ bring a marked change in ventilation

Therefore minute to minute ventilation mainly driven by CO₂ and not O₂

92
Q

Central chemoreceptors

A

In ventral medulla

Responds to changes in pH

Insensitive to hypoxia

93
Q

Peripheral chemoreceptors

A

In aortic and carotid bodies

Responds to changes in arterial PO₂, pH and PCO₂

94
Q

Lung stretch receptors

A

Within smooth muscle of walls of airways

Lung inflation increases frequency of impulses in vagal afferents, increasing expiratory time and decreasing breathing rate

95
Q

Irritant receptors

A

Between airway epithelial cells

Smoke, dust, cold air etc trigger vagal afferents

Causes bronchoconstriction, increasing breathing frequency

96
Q

Type I respiratory failure

A

Hypoxic hypoxia (hypoxaemia), without hypercapnia = Lung failure

Caused by
- decreased inspired PO₂
- shunt
- V/Q mismatch
- impaired diffusion
eg altitude, congenital cyanotic disease, fibrosis, pulmonary embolus

97
Q

Type II respiratory failure

A

Hypoxaemia AND hypercapnia = Pump failure

Caused by
- CNS or PNS disease
- chest wall or upper airway problems
eg stroke, opiate overdose, myasthenia gravis, burns, laryngospasm, oedema

98
Q

Normal physiological values - Respiration rate, O₂ saturation, PaO₂, PaCO₂

A

Respiration rate - 12-20pm

O₂ saturation - 96-100%

PaO₂ - 80-105 mmHg

PaCO₂ - 35-45 mmHg

99
Q

Bronchopneumonia

A

Areas of patchy tan-yellow consolidation (dense material)

Remaining lung shows pulmonary congestion, dark red

Alveoli filled with neutrophilic exudate

TYPICAL BACTERIA
- Staph aureus, Klebsiella, E coli, Pseudomonas

CXR

  • diffuse, patchy shadowing
  • loss of sharp borders; blunted costophrenic angle and heart borders
100
Q

Lobar Pneumonia

A

Consolidation of entire lobe

TYPICAL BACTERIA
- Streptococcus pneumoniae (95%)

CXR
- white patch of increased opacity bordering fissures, better defined than in bronchopneumonia

101
Q

Viral Pneumonia

A

Interstitial lymphocytic inflitrates, no alveolar exudate

CAUSES - influenza A and B, parainfluenza, adenovirus, metapneumovirus

  • respiratory syncitial virus (in children)
  • cytomegalovirus (if immunocompromised)
102
Q

Sinusitis

A

CAUSES
- mainly viral - Streptococcus pneumoniae, Haemophilius influenzae, Moraxella catarrhalis

TREATMENT

  • antibiotics only in severe or prolonged infections more than 5 days SIGNS
  • facial view X ray shows fluid, meniscus in sinus (but rarely X ray)
103
Q

Asthma

A

Starts in childhood normally, 1/10 children, 1/20 adults

Increased risk with family history and allergies

Typical triad of asthma, eczema and allergic rhinitis

Histology - see submucosa widened by smooth muscle hypertrophy, oedema, inflammation (mainly eosinophils)

104
Q

COPD

A

Persistent productive cough for more than 3 months over 2 years

5% worldwide population

SMOKING

SEE
- black carbon deposits in lung
- inflammation in lung
> bronchitis (inflammation and narrowing of small airways
> more chronic inflammatory cells in submucosa, neutrophils and macrophages
> breakdown of lung issue (emphysema), loss of alveolar walls

Damage is cumulative and permanent

105
Q

Lung cancer

A

Carcinoma, from epithelial cells

Histology - nests of polygonal cells with pink cytoplasm, distinct cell borders

Two classes, small-cell and non-small-cell lung carcinoma, important for predicting outcome

CXR

  • mass
  • widening of mediastinum
  • collapse (atelectasis)
  • consolidation
  • pleural effusion
106
Q

Pharyngitis

A

VIRAL

  • 80%
  • adenovirus / infectious mononucleiosis / common cold

BACTERIAL

  • 20%
  • group A beta haemolytic streptococcus / Haemolytic influenza / Streptococcus pneumoniae
107
Q

Influenza

A

Type A most common, also B and C

RNA viruses

Seasonal variation

Pandemics (eg bird/swine flu)

CONTAGIOUS - airbourne, direct contact, surface contact

108
Q

LRTI

A

Lower Respiratory Tract Infection

Any infection of respiratory tract from vocal chords downwards
Should be sterile here!

Colonisers are often from URT, eg Haemophilius influenzae, Streptococcus pneumoniae

Antibiotic therapy will affect URT also

109
Q

LRTI sequence of events

A

Abnormal flora in LRT

  • > paralysis of cilia
  • > excessive volume or viscosity of mucus
  • > failure to protect LRT
  • > failure to cough up debris from larger airways
  • > loss of swallow reflex
110
Q

Chronic bronchitis

A

Antibiotic therapy if two of

  • increased breathlessness
  • increased sputum volume
  • increased sputum purulence (mucky/different)

—–> problems with diagnosis, normal exacerbations of COPD will cause (first two) even without infection, purulence is main indicator

TREATMENT

  • 1st - Beta lactam - amoxicillin, acts on cell wall
  • 2nd - tetracycline, acts on ribosomes
  • 3rd - macrolide, acts on ribosomes
111
Q

Community acquired pneumonia

A

CAP

More common in winter

2 x more in men than women

More in elderly

112
Q

Symptoms of CAP

A
  • acute LRTI symptoms (cough and one other)
  • new focal chest signs on examination
  • one or more systemic features (sweating, fever, shivers, aches and pains, temp above 38°C
  • no other explanation for illness

–> treat with antibiotics

113
Q

CRB score for mortality risk assessment in CAP

A

One point for each of:
Confusion
Raised resp rate (30+pm)
Blood pressure low (less than 90/60)
aged 65+

0- low risk, home treatment
1/2- moderate, consider hospital referral
3+ -high risk, urgent hospital admission

114
Q

Main pathogens causing CAP

A

In GP

  • Streptococcus pneumoniae
  • Haemophilius influenzae
  • Viruses

In hospital
- more atypical bugs, chlamydophila pneumoniae and mycoplasmia pneumoniae

115
Q

Streptococcus pneumoniae (PNEUMOCOCCUS) causing CAP

A

Gram +ve diplococcus

Colonises URT in 10% adults

Alpha haemolytic - produces enzymes that haemolyse RBCs by producing hydrogen peroxide -> green

Can be commensal, virulence potential

More than 90 recognised serotypes

Encapsulated -> lobar and bronchopneumonia

Vaccines in childhood and the elderly (eg PVC 13 covers 13 serotypes)

116
Q

Haemophilius influenzae causing CAP

A

Gram -ve

Capsulated and uncapsulated strains

Mainly in lung disease and smokers

20% B lactamase positive, so make enzyme that degrade B lactam antibiotics, the usual 1st line treatment

117
Q

Atypical pneumonia causing CAP

A

Atypical pathogens

  • mycoplasma pneumoniae
  • legionella pneumophilia
  • chlamydophilia pneumoniae
  • chlamydophilia psittaci

Insidious onset usually, comes on slowly with few symptoms

Classically; non-productive cough, fever, headache, chest radiograph more abnormal than clinical assessment suggests

Often sub-clinical, many cases go undiagnosed

118
Q

Mycoplasma pneumoniae causing atypical CAP

A

No peptidoglycan cell wall

Resistant to B lactam antibiotics

Primary cause of atypical pneumonia (~15%)

119
Q

Legionella pneumophilia causing atypical CAP

A

= Legionnaire’s disease

Lives and multiplies inside macrophages, so hard to target

Often from aircon units/after trip abroad

Causes severe pneumonia, high mortality rate

120
Q

Chlamydophilia pneumoniae and Chlamydophilia psittaci causing atypical CAP

A

Obligate intracellular parasite (only in cell)

Chlamydophilia pneumoniae usually self-limiting and mild

Chlamydophilia psittaci can cause severe pneumonia, associated with bird contact

121
Q

General investigations on hospital admission for CAP

A

Full history and examination

Oxygen saturations, arterial blood gases, bp, temp
CXR
Urea and electrolytes (added to CRB, now CURB)
CRP
Full blood count
Liver function test

122
Q

Low severity CAP treat with:

A

5 day course single antibiotic, amoxicillin usually

Extend course if symptoms not improved in 3 days

123
Q

Moderate severity CAP treat with:

A

7-10 day course of antibiotics

Dual treatment with amoxicillin and macrolide

124
Q

High severity CAP treat with:

A

7-10 day course of antibiotics

Dual treatment with B lactamase stable B lactam and macrolide

Need broader therapy if hospital acquired! (atypical)

125
Q

Lung abscess

A

Pus, mainly neutrophils

Caused by

  • aspiration of GI content into lungs
  • periodontal disease
  • septic emboli
  • bacteraemias

To treat

  • drain abscess
  • CXR and CT
  • blood cultures
  • culture aspiration fluid
  • antibiotics 4-6 weeks
126
Q

Cystic Fibrosis newborn screening

A

At 5 days old, heel-prick test in home

Confirm with sweat test around 2 months old, and DNA testing

127
Q

Complications in baby with CF

A

Pancreatic insufficiency - faecal elastase low

Pulmonary infection
- flexible fibreoptic bronchoscopy used if recurrent cough - avoided as is invasive, requires general anaesthetic

Fat soluble vitamin deficiency - yearly blood tests to check, low E -> anaemia, low A and D -> vision and bone problems long term, low clotting factors

128
Q

Additional complications in adults

A

CF diabetes

CF bone disease

Fertility/pregnancy complications

Genetic counselling needed, psychological problems

GI/liver problems

129
Q

What is Cystic Fibrosis?

A

Affects exocrine glands of liver, lungs, pancreas, intestines
-> progressive disability due to multisystem failure

Autosomal recessive inheritance, mutations in CFTR on chromosome 7, leading to defective ion transport

130
Q

Symptoms / signs of CF in an infant

A
  • Meconium ileus (apparent in newborns) = acute intestinal obstruction, bilious vomiting, abdominal distension —-> requires medical and surgical assistance: enema, laporotomy, resection
  • Failure to thrive
  • Thin, fretful, feeding doesn’t satisfy
  • Steatorrhoea
  • Persistent moist cough
  • Clubbing
131
Q

Symptoms / signs of CF in an older child

A
  • Loose, smelly stool
  • Recurrent chest infections, pneumonia
  • Chest deformity (Harrison’s sign, chest falling in)
  • Clubbing
132
Q

Symptoms / signs of CF in an adult

A

May be classical presentation, or no features

  • Pancreatitis
  • Sinusitis, recurrent
  • Male infertility (absence of vas deferens, azoospermia,(can still father children if sperm collected from testes))

If non classical, lower degree of morbidity and treatment burden

133
Q

Management of cystic fibrosis

A
  • Hospital visits every 6-8 weeks, with large multidisciplinary team
  • Prophylactic antibiotics
  • Fat soluble vitamins (ADEK)
  • Twice daily physiotherapy
  • Inhalers, nebulisers
  • Mucolytics
  • Steroids
  • Pulmonary lobectomy in established and severe bronchiectasis, persistent infection
134
Q

Improved survival rate of CF in current age due to:

A
  • Nebulisers to assist airway clearance
  • Nebulised and IV antibiotics
  • Avoidance of BMI less than 19
  • Physiotherapy
135
Q

Genetics of CF

A
  • 1/25 carry faulty CFTR gene in UK
  • 1/4 chance of passing on if both parents carriers

Different ways of non-functioning CFTR gene:
I - defective protein production
II - misfolded protein, eg ΔF508 (91%)
III - non-regulated protein, eg G551D
IV - not conducted, eg R117H

136
Q

Pathology of intestine in CF

A
  • Meconium ileus - failure of newborn infant to pass meconium, causing plugging of internal ileum
  • Distal Intestinal Obstructive Syndrome (DIOS)
  • Constipation
  • Rectal prolapse, volvulus, intussusception, atresia

No villi or microvilli in ileum, many crypts secreting mucus in colon

Decreased hydration of tube

  • 1) ion transport defect
  • 2) different properties of mucus, stickier, more acidic
  • 3) acid affects microbiota, so abnormal flora in intestine
137
Q

Pathology of pancreas in CF

A

Mucus accumulates in small ducts

  • > flattening and atrophy of epithelia
  • > duct plugging and obstruction
  • > dilatation of ducts and acini
  • > fibrosis
  • > exocrine pancreas replaced by adipose tissue, so islets of langerhans in wrong environment, develop CF diabetes
138
Q

Pathology of lung and URT in CF

A

Failure of lung defence mechanisms

  • > persistent bacterial infections, excessive inflammation, airway destruction
  • > bronchiectasis

Mucus plugged airways - due to goblet cell hyperplasia and disrupted function of cilia

139
Q

Pathology of liver in CF

A

Biliary duct epithelial cells affected, not hepatocytes

  • plugging of intrahepatic bile ducts by thick bile
  • chronic inflammation and fibrosis
  • hepatomegaly
  • focal biliary cirrhosis
  • multilobar cirrhosis
140
Q

Other CF pathologies

A

Sinusitis
Nasal polyps
Salty sweat
Congenital bilateral absence of vas deferens
Osteoporosis
Rheumatic disease
Clubbing of distal phalanges

141
Q

Chloride movements drive salt and water secretion (CFTR1)

A

Cystic Fibrosis Transmembrane Conuctance Regulator

  • 2 membrane-spanning domains
  • 2 nucleotide-binding domains (ATP needed)
  • 1 regulatory domain (PKA, requires phosphorylation)
142
Q

Normal CFTR action

A

CFTR is Cl⁻ channel in apical membrane

1) Cl⁻ travels into cell
2) Causes water and Na⁺ to follow paracellularly into lumen
3) Cl⁻ moves through cell to CFTR
3) 2 nucleotide binding domains receive ATP, cause 2 membrane spanning domains to come together, making a channel
4) Cl⁻ out of cell into lumen

143
Q

Faulty CFTR action

A

Cl⁻ can travel into cell as normal

But faulty CFTR means cannot exit cell

Therefore no Na⁺ or H₂O out

144
Q

ΔF508

A

Class II mutation

Deletion in F508

91% of CFTR mutations causing CF

CFTR protein is made but not transported to golgi or apical membrane

145
Q

G551D

A

Class III mutation

6% of CFTR mutations causing CF

Protein is made and delivered to apical surface, but behaves abnormally - gate doesn’t open often enough, though pathway for ion movement is normal

146
Q

Therapy pathways for CF

A

Current therapies

  • Airway clearance bronchodilators, mucolytics
  • Antibiotics
  • Anti-inflammatory agents
  • Lung transplant (at bronchiectasis stage)

New therapies (target earlier in pathogenesis pathway)

  • Gene therapy
  • CFTR potentiators and correctors
  • CFTR bypass therapy (other way for chloride to leave cell)
147
Q

Characteristics of asthma

A
  • wheeze
  • cough
  • outflow obstruction
  • chest tightness
  • dyspnoea
  • airway hyper-responsiveness
  • inflammation of lungs
148
Q

Triggers of asthma

A
  • respiratory infections
  • exercise/breathing cold air
  • exposure to allergens (pollen, moulds, dust mites, pollution, pets, tobacco smoke)
149
Q

Prevalence of asthma

A

IgE levels genetically influenced, 50% more asthma in black people

Higher in city dwellers

150
Q

Pathology of allergens triggering asthma (Pathology 1) - ALLERGENS

A

Allergens trigger T cells

  • > generate B-cell activating cytokines
  • > IgE production
  • > induces expression of IgE receptors (Fc) on mast cells and macrophages
151
Q

Pathology of acute phase in asthma (Pathology 2) - IgE RECEPTORS EXPRESSED

A
  • > mediators released from macrophages/mast cells (eg histamine, leukotrines, cytokines, neurokinins, platelet activating factor, prostaglandins
  • > promote bronchoconstriction
  • > acute asthma attack
  • > attracts T cells, neutrophils, platelets, monocytes, which release more spasmogens and inflammogens
  • > exacerbates bronchoconstriction and triggers inflammation
152
Q

Pathology of late phase in asthma (Pathology 3) - BRONCHOCONSTRICTION AND INFLAMMATION

A
  • > progressive inflammation
  • > influx of TH2 lymphocytes
  • > activation of eosinophils releasing toxic proteins
  • > PGE₂ from smooth muscle increases permeability of blood vessels
  • > oedema
  • > damage and loss of epithelium
  • > bronchial hyperactivity, increased irritant receptor accessibility
  • > subepithelial cell fibrosis
  • > hypertrophy and hyperplasia of SMCs
153
Q

Asthma drugs - β₂ agonists - effects and mechanisms

A

Bronchodilators

  • > bronchodilatation
  • > inhibits release of histamine and other inflammatory mediators
  • > reduce vascular permeability and mucosal oedema

Mechanism

  • activates β₂ adrenoreceptor
  • increases intracellular cAMP
  • activates K⁺ channel
  • activates Na⁺/K⁺ ATPase
  • decreases Ca²⁺ dependent coupling of actin and myosin

-> inhibits cholinergic transmission, smooth muscle relaxation

154
Q

Asthma drugs - β₂ agonists - drugs

A

Short acting, use as needed:
Salbutamol
Terbutaline

Longer acting, use twice daily if chronic asthma where glucocorticoid therapy inadequate:
Salmeterol
Formoterol

Non-selective β agonists, IV, in severe asthma:
Isoprenaline
Adrenaline

155
Q

Asthma drugs - Xanthine drugs

A

Bronchodilators

Used in addition to steroids in patients non-responsive to β₂ agonists, in acute severe asthma

Mechanism unclear

Theophylline
Aminophyline

Very narrow therapeutic window - careful!

Theophylline is metabolised by liver, half life dependent on liver function

156
Q

Asthma drugs - muscarinic receptor antagonists

A

Bronchodilators

Inhibit M3 receptors, so less smooth muscle contraction and secretion
May also inhibit M2 so reduced effectiveness

Inhibit mucus secretion

Used as adjunct to β₂ agonists or to relieve bronchospasm

Ipratropium bromide
Tiotropium

157
Q

Asthma drugs - cysteinyl leukotrine antagonists

A

Anti-inflammatory, acting on 5-lipo-oxygenase pathway

Zileutin inhibits arachidonic acid -> leukotrines

Montelukast inhibits leukotrines effects (so decreases bronchoconstriction, oedema, inflammation, chemoattraction)

158
Q

Asthma drugs - glucocorticoids

A

Anti-inflammatory
Immunosuppressive

Decreases IL3 synthesis, decreases cytokine production

  • so decreases microvascular permeability
  • so relaxes bronchial muscle by increasing β₂ adrenoreceptor levels, increasing G protein expression

Inhaled glucocorticoids are first line where symptoms persist despite 2x daily inhaler

159
Q

Asthma drugs - glucocorticoids - drugs

A

Inhaled:
Fluticasone
Budesonide
Beclometasone dipropionate (BDP)

Systemic, for severe asthma:
Prednisolone
Prednisone - needs to be converted in liver to active form, so good in pregnancy
Hydrocortisone

160
Q

Asthma drugs - other anti-inflammatory drugs

A

Cromoglicate
Nedocromil

161
Q

Asthma drugs - histamine receptor antagonists

A

= antihistamines

Fexofenadine
Cetrizine

162
Q

Management of asthma

A

1) Mild disease - control with short acting bronchodilator as needed
2) If needed more than 1x daily - add inhaled glucocorticoid
3) If still uncontrolled - add longer acting bronchodilator
4) If still uncontrolled - go to maximum dose of glucocorticoid and add theophylline/montelukast 5) If still uncontrolled - go to oral glucocorticoid

163
Q

Status asthmaticus

A

= severe acute asthma

Needs emergent hospitalisation, treat with oxygen, nebulised salbutamol, IV hydrocortisone, IV salbutamol

164
Q

OSHIT! Asthma attack

A

Oxygen

Salbutamol

Hydrocortisone

Ipratropium

Theophylline

(! Magnesium)

165
Q

Allergic emergency - anaphylaxis

A

= food allergy

Treat with adrenaline, oxygen, anti-histamine, hydrocortisone

166
Q

Allergic emergency - angio-oedema

A

= intermittent focal swelling of skin

Aspirin worsens

Treat with leukotriene antagonists

167
Q

COPD symptom progression

A

Morning cough in winter -> chronic cough -> URTI/bronchitis -> progressive breathlessness -> pulmonary hypertension, heart failure

168
Q

COPD pathogenesis

A
  • small airway fibrosis, bronchitis
  • destruction of alveoli/elastic fibres = emphysema, promoted by protease release due to inflammatory response

—> impaired gas transfer and chronic inflammation

169
Q

COPD treatment

A

STOP SMOKING

Immunise against infection

Long acting bronchodilators - modest benefit, no effect on inflammation (steroids ineffective)

Long term oxygen therapy

170
Q

COPD cough

A

Protective reflex to remove foreign material/secretions

Productive, removes sputum from lungs. If dry cough, commonly seen if on ACE inhibitors.

Cough suppression only if a dry painful cough- anti-tussives

171
Q

COPD drugs - Anti-tussives

A

OPIOIDS: analgesics act on cough centre in brain (Codeine, dextromethorphan, pholcodine, morphine)

DEMULCENTS: for cough originating above larynx, forms protective coating over irritated pharyngeal mucosa, syrups of lozenges (natural)

LOCAL ANAESTHETICS: inhibit cough reflex, only used eg before bronchoscopy

172
Q

COPD drugs - Expectorants

A

Decrease bronchial secretion viscosity, so easier to cough out.
Adequate hydration more important!

Guafenesin, iodides (eg potassium iodide, iodinated glycerol, to break up bronchial secretions)

173
Q

COPD drugs - Decongestants

A

α receptor agonists

  • > vasoconstriction of nasal blood vessels
  • > reduce nasal mucosa volume
  • > open airways

Used topically for short term relief

Short acting

  • oxymetazoline
  • hydrochloride

Long acting
- pseudoephedrine

174
Q

Symptoms of tuberculosis

A

Chronic cough
Sputum production
Appetite loss
Weight loss
Fever
Night sweats
Haemoptysis

175
Q

Mycobacterium tuberculosis

A

Gram +ve

Obligatory aerobe

Slow growing

-> intracellular infection

176
Q

Epidemiology of tuberculosis

A

1.7 billion affected, 1.6 million deaths annually

But infection≠disease (presence of mycobacteria≠clinical manifestation)

177
Q

Risk factors for tuberculosis

A

HOST FACTORS
Proximity, duration of contact
Age
Immune status, malnutrition, diabetes

ENVIRONMENTAL FACTORS
Crowding, poor ventilation
Smoking, alcohol, occupation

178
Q

Primary tuberculosis: 0-3 weeks

A

Asymptomatic

or

Fever, malaise, tiny fibrocalcific nodule at site of infection

Bacteria enter macrophages by endocytosis

  • > prevent phagosome-lysosome fusion
  • > inhibit lysosome acidification
  • > lipopolysaccharide inhibits IFN-γ
179
Q

Primary tuberculosis: 4-6 weeks

A
  • TH1 response activates macrophages to become bactericidal
  • TH1 release IFN-γ, stimulating macrophages to form phagolysosome complex to contain infection
  • TH1 stimulate formation of granulomas by triggering macrophages -> epitheloid histiocytes
180
Q

Granuloma

A

In tuberculosis

Mycobacterium tuberculosis and necrotic infected macrophages are at the core

T and B cells surround

Fibrous border at outside to prevent rupture

181
Q

TB progression

A

Primary infection -> Primary complex ->

1) Healed lesion (scar)
2) Progressive primary TB -> miliary TB (haematogenous spread)
3) Latent lesions - - -> if reactivated become secondary TB -> miliary TB - - -> cavitary TB if immune system compromised, can NOW be spread via cough etc

182
Q

Miliary TB

A

Every organ in body will have nodules- kidney, testes, liver, spleen, lymph nodes etc

183
Q

Epidemiology of asthma

A

Earlier onset indicative of more severe asthma

Exposure to smoking/pollutants during early years is significant (some countries higher risks)

184
Q

Early/late/persistent asthma

A

TRANSIENT EARLY WHEEZERS

  • peak age 0-3 years, usually with viral infection
  • gone by age 6

NON-ATOPIC WHEEZERS
- age 4-5

IgE ASSOCIATED WHEEZE
- increasing wheeze prevalence throughout early years

185
Q

Hygiene hypothesis

A

Decreasing exposure to microbes increases hygiene, increases allergies and asthma

Good to have infections early in life!

Upregulates TH1, downregulates TH2

186
Q

Small cell lung carcinoma

A

12-15% cases

Aggressive - 5% 5 year survival

Usually bilateral, so inoperable

187
Q

Non-small cell lung carcinoma

A

80-85% cases

Good prognosis - 75% 5 year survival

Presents earlier, so can be operable

188
Q

Risk factors for lung cancer

A

Smoking
Age - 45-75 mainly
Occupational factors
Genetic (influence)
Diet - dietary fat increases chemically induced pulmonary tumours
Prior respiratory disease - asthma, emphysema etc - as chronic immune stimulation leads to random pro-oncogenic mutations
Gender - more common in men
Socioeconomic class - more in lower

189
Q

Embryology of lower respiratory tract

A

Endoderm - ventral growth from foregut to -> respiratory epithelium

Mesoderm -> lung tissue (parenchyma), muscular diaphragm, pleural cavities

190
Q

Embryonic period - week 4-8

A

Future trachea evaginates from foregut -> oesophagus and trachea

Lung buds become lung shaped and primary bronchi form

191
Q

Tracheoesophageal fistula

A

Can be blind-ended oesophagus, communication between, etc

Baby vomits milk, risk of aspiration

Foetus cannot practise breathing or swallowing, fluid around baby is a marker

192
Q

Pseudoglandular period - week 5-17

A

Conducting airways branch

Epithelia become tall columnar and cuboidal

By week 8, all segmental bronchi formed

193
Q

Canalicular period - week 16-26

A

Epithelia differentiate so respiratory bronchioles formed - distinction between gas exchange vs conducting airways

Canalisation of lung parenchyma by capillaries

194
Q

Surfactant deficiency

A

= Infant respiratory distress syndrome

Airsacs collapse on expiration as increased surface tension
So more energy required for breathing

Need to give exogenous surfactant to reduce mortality and pulmonary air leaks (pneumothorax)

195
Q

Saccular period - week 24-38

A

Terminal sacs form (primitive alveoli), associated with blood vessels

Cuboidal cells flatten, become type 1 pneumocytes

Vascular tree increases in length and diameter

Type II pneumocytes produce surfactant

196
Q

Alveolar period - week 36-8years

A

Terminal saccules replaced by mature alveoli

Only 16% alveolar cells present at birth, process continues

197
Q

Pleural cavities - inc congenital diaphragmatic hernia

A

Derived from mesoderm

Single body space separated into three cavities - pleural, pericardial, peritoneal

Diaphragm develops via pleuroperitoneal separation

If incorrectly forms, congenital diaphragmatic hernia - gut contents pushes up into chest, baby can’t breathe properly

198
Q

Embryology of nasal cavity

A

Formed from frontonasal prominence

Nasal placode appears at WEEK 4

Cavity is formed from 5 facial prominences

  • 2 medial
  • 2 lateral
  • 1 frontal
  • -> cleft/lip palate if incomplete as face forms from side to midline
199
Q

Embryology of larynx

A

Pharyngeal arches from

  • the core of mesoderm -> cartilage, muscle, connective tissue
  • inner endoderm -> epithelial lining 4-6 pharyngeal arches make larynx

Each pharyngeal arch is associated with a specific cranial nerve (10 for larynx)

–> if orifice doesn’t open, fatal, miscarriage at 12 weeks as lung needs to develop

200
Q

Spirometer graph

A

2nd Year - systems 2 (7 decks)

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