MGEM2013

Question 1

Hypoventilation syndromes & CCHS

Describe & explain the basis of Congenital Central Hypoventilation Syndrome (CCHS), signs & symptoms
.
understand rationale for treatments

Answer 1

genetic basis: autosomal dominant, repeat mutations in paired-like homebox 2B (PHOX2B) gene on short arm of chromosome 4. Most cases due to Increased polyalanine repeat mutations (PARM) & some due to non-polyalanine repeat mutations (NPARM) in Exon 3 of PHOX2B gene. Cause autonomic NS dysregulation, more mutations=more severe dysfunction
.
sign & symptoms: Voluntary breathing is intact when awake, BUT Automatic breathing is absent during sleep=obstructive sleep apnea, increased PaCO2, very reduced tidal volume, shallow breathing. May also have multi-systemic effects, eg, dysregulated BP during sleep (CVS), seizure/delayed development (neurological), impaired basal temp & metabolic control, blood glucose dysregulation, GI Hirschsprung’s disease=constipation, poor eye sight, neural crest tumours/cancer
.
* portable positive pressure ventilators via tracheostomy for home ventilation for younger children <8yrs.
* Young adult need more ventilation so use Mechanical ventilation & noninvasive intermittent positive pressure ventilation via face masks
* diaphragm pacing during sleep - electrical impulses transmit to phrenic nerve electrodes
* Bronchoscopy performed every 12-24 months to allow for diagnosis of granulomas due to high risk of cancer =malignant tumours

Question 2

Hypoventilation syndromes & CCHS

Compare the characteristics of CCHS (Congenital Central Hypoventilation Syndrome) with other hypoventilation syndrome subtypes concerning sleep-related breathing

Answer 2

Obesity hypoventilation syndrome: also display Obstructive sleep apnea (=breathing stop/disrupted) & Hypercapnia(high CO2 in arterial blood), but also Body mass index >30 kg/m2 where thick neck folds put weight on trachea
.
other Sleep-related hypoventilation not due to genetics, can due to medical disorder (pulmonary vessels, lung parenchyma, neurological disorders) OR pharmacological influence, patient too sensitive to Narcotics, sedatives, anaesthetics, depressants, muscle relaxants, opioid intake
.
Late-onset central hypoventilation not due to genetics but due to respiratory illness OR Hypothalamic dysfunction, eg due to disease/impaired circulation to brainstem/hypothalamus

Question 3

initiation of breathing

compare & contrast the roles of dorsal respiratory group & ventral respiratory group?

Answer 3

Some neurones in the VRG cause inspiration and some cause expiration. DRG neuron ONLY cause inspiration
.
VRG has no role in the basic rhythmical oscillations/initiation of breathing whereas DRG has (DRG drive movement & timing)
.
VRG Inactive in normal, quiet breathing but
DRG is active
.
VRG Involved in active breathing e.g. greater than normal ventilation & forced expiration that increases with exercise, dyspnoea, lung disease, stress
.
DRG in nucleus tractus solitarius; VRG in nucleus ambiguus & nucleus retroambiguus

Question 4

initiation of breathing

Describe, at a basic level, the neurogenic basis of breathing
.
==which nucleus of pneumotaxic centre signal to DRG to finely tune respiratory rate & pattern?

Answer 4

Pneumotaxic centre sends continual inhibitory impulses to inhibit apneustic centre (in lower pons) & DRG (in medulla)
.
Kolliker-Fuse nucleus finely tunes the respiratory rate & breathing pattern (amplitude & duration) by signaling to DRG.
. pneumotaxic signals inhibit activity of phrenic nerve
.
DRG neurons in nucleus tractus solitarius in medulla are thought to be inherently rhythmic
.
DRG send repetitive ‘ramped’ bursts of inspiratory neuronal action potentials to (inspiratory muscles like) diaphragm & external intercostal muscles for 2 secs on (inspire) then 3 sec off (inspiratory AP inhibited by pneumotaxic centre to allow expiration by elastic recoil of lungs & thoracic cage in normal quiet breathing) =5 sec respiratory cycle if 12 breaths/min. Ramped AP firing =gradual increase in signal strength to ensure steady increase in lung volume rather than inspiratory gasps.
.
When the respiratory drive for increased pulmonary ventilation becomes greater than normal, eg during heavy exercise/forced expiration, VRG also contribute extra respiratory drive

Question 5

regulation of breathing mechanisms?

Answer 5

Vagal & glossopharyngeal nerves’ sensory termination at nucleus tractus solitarius, so also modulates activity in DRG. They transmit sensory info from peripheral chemoreceptors; baroreceptors; receptors in liver, pancreas, and multiple parts of GI tract; & several types of receptors in lungs.
.

Question 6

initiation of breathing

what are the roles of the dorsal respiratory group, ventral respiratory group, the apneustic centre & the pneumotaxic centre?
.
explain consequences of injury to the latter? on the respiratory phase

Answer 6

DRG:
Drives movements & timing=initiate breathing. Output to inspiratory muscles=external intercostal muscle
.
Active during inspiration - neurons cause inspiration ONLY - repetitive ‘ramped’ bursts of inspiratory neuronal action potentials for 2 secs on (inspire) then 3 sec off (allow expiration) =5 sec respiratory cycle if 12 breaths/min. Allows steady increase in lung volume rather than inspiratory gasps.
.
Neurones located in nucleus tractus solitarius
.
VRG:
Either side of the medulla, anterior and lateral to the DRG, main role=forced expiration
.
Located in nucleus ambiguus & nucleus retroambiguus - neurons can cause BOTH inspiration & expiration
.
Pre-Bötzinger complex(=central pattern generator) exact location unsure. May also responsible 4 initiation of breathing
.
Inactive in normal, quiet breathing as
DRG is active & expiration is passive.
Involved in active breathing e.g. greater than normal ventilation & increased forced expiration e.g. voluntary forced exhalation activity increases with exercise, dyspnoea, lung disease, stress
.
apneustic centre is excitatory and it stimulate DRG to prolong inspiration =delay OFF signal to smooths/modulate breathing cycle so breathing in and out isn’t abrupt =smooth transition betwn inspire & exspire
.
Inhibited by stretch receptors at max inspiration or by pneumotaxic centre
.
it prolong inspiration for long deep breaths by stimulating DRG & VRG to increase tidal volume i.e. delays the ‘off signal
.
When it’s damaged though, this transition is lost and the cycle becomes very abrupt as you’ll be gasping because inspiratory neurones are mainly excited. Injuries to the Section of brainstem immediately above apneustic centre gives prolonged inspiratory gasps interrupted by transient expiratory efforts =apneusis/apneustic breathing??? resp cycle becomes abrupt
.
pneumotaxic centre is inhibitory and stops the lungs from overinflating by shorting the duration of the inhalation i.e. it helps you to breathe out. When it’s more active/the signal is stronger, the rate of breathing is faster (due to amplitude & duration of inspiration are reduced). This protective control is taken away if the centre is damaged, E.g. upper pons damage (head injury/cerebral stroke/ischemia to pons) - where duration of inspiration increases (to 5sec/more) so amplitude/volume of inspiration increase= lose protection against overinflation
.
Pneumotaxic centre sends continual inhibitory impulses to inhibit apneustic centre (in lower pons) & DRG (in medulla) so inhibit activity of phrenic nerves (C3-5) which innervate diaphragm
.
Kolliker-Fuse nucleus finely tunes the respiratory rate & breathing pattern (amplitude & duration) by signaling to DRG

Question 7

which centre stops the lungs becoming too full/overinflating by shortening the duration of inhalation. When that centre is more active, the breathing rate becomes ?
.
when what centre is damaged, the respiration cycle is abrupt?

Answer 7

[pneumotaxic centre] stops the lungs becoming too full by [shortening the duration of inhalation] . When it’s more active, the breathing rate is [faster] The two centres are very different. For example, when the [apneustic centre] is damaged, the respiration cycle is [abrupt]
.
The pneumotaxic centre is inhibitory and stops the lungs from becoming too full by shorting the duration of the inhalation i.e. it helps you to breathe out. When it’s more active, the rate of breathing is faster (due to breathing amplitude & duration are reduced). This protective control is taken away if the centre is damaged so, inspiration gets bigger!

On the other hand, the apneustic centre is excitatory and smooths your breathing cycle so breathing in and out isn’t abrupt. When it’s damaged though, this transition is lost and the cycle becomes very abrupt as you’ll be gasping because inspiratory neurones are mainly excited.

Question 8

pneumotaxic & apneustic centre found where?
excitatory OR inhibitory?

Answer 8

apneustic centre is found in the lower pons & excitatory
.
pneumotaxic in upper pons, inhibitory effect on apneustic centre & dorsal respiratory group (DRG)

Question 9

resp failure & VQ mismatch

Describe alveolar-blood gas diffusion & partial pressures for O2 & CO2 exchange (in both mmHg & kPa in exam)

both mmHg & kPa units will appear in exam

Answer 9

Normal arterial values?????
PaO2 = 11-15 kPa; ~90-113 mmHg
PaCO2 = 4.6-6.4 kPa; ~33-46 mmHg
.
alveolar air: pO2 =105mmHg/14kPa (reduced from atmospheric due to 37 degreebody temp, water vapour added in conducting zone)
pCO2 =40mmHg/5.3kPa
.
atmospheric air: pO2 =~159mmHg/21kPa
pCO2 =0.3mmHg/0.04kPa
.
arterial blood paO2 (lowercase a) in reality ~85-100mmHg (11.3-13.3kPa) although theoretically should be same as alveolar pAO2 (uppercase A) after diffusion & equilibrium. So O2 diffuse into arterial blood down O2 partial pressure gradient (105->~95mmHg), CO2 out of blood then out to atmosphere down CO2 partial pressure gradient (vein45mmHg/6kPa->alveoli40mmHg/5.3kPa->0.3mmHg)

Question 10

Why alveolar O2 partial pressure differ from arterial O2 partial pressure?

Answer 10

In health, PAO2 (~105mmHg/14kPa) & PaO2 (~85-100mmHg/11.3-13.3kPa) differ slightly (approx. < 15 mmHg) after equilibration as not all the pulmonary blood goes to the alveoli. Also some arterial and venous blood also mix in our bodies causing the PaO2 to fall slightly
Both these states are shunts

Examples:
Some veins bypass the lungs and empty directly into the arterial circulation.
Some bronchial veins drain into pulmonary veins
Coronary venous blood drains into the left ventricle
Thebesian veins of the left cardiac ventricle drain into the right ventricle

Question 11

resp failure & VQ mismatch

Describe factors that influence gas exchange in health (including exercise) & in disease states
.
* Influential factors (Fick’s principle)
* Ventilation-perfusion VQ matching

Answer 11

1. factors affecting diffusion rate: (Fick’s law)
   * gas solubility
   * gas molecular weight - heavier & less soluble gas=slower diffusion (except CO2 which is heavier but more soluble, diffuse faster than O2)
   .
   * alveolar surface area –eg, decrease in disease Emphysema (permanent loss), Pneumonia (inflammatory consolidation), so slower diffusion
   .
   * partial pressure gradient –eg increase due to Increased metabolism in exercises or if given 100% O2, so faster diffusion; Altitude decreases rate of diffusion
   .
   * air-blood barrier/alveolar wall thickened –eg, due to alveolar wall covered by pus/thickened pneumocytes, in diseases eg, pulmonary fibrosis (chronic RF), oedema (acute RF), asbestosis, pneumonia

.
. 2. hypoventilation - hypercapnia -Type 2 resp failure
.
. 3. shunts - blood go through lung but no gas exchange due to alveoli filled with pus, tumour, oedema, blood, or atlectasis
.
. 4. VQ mismatch

Question 12

resp failure & VQ mismatch

Explain the effect of gravity on Ventilation and Perfusion & the VQ ratios from lung apex to base

Answer 12

Gravity causes a mismatch of regional ventilation & perfusion at the base & apex of the lungs
.
Due to effects of gravity, zone 3 (lung base below heart, higher BP due to weight of lungs due to gravity) has very distended arteries and veins & small/shrivelled alveoli, so V < Q; lower V/Q ratio. Always normal blood flow due to (hydrostatic pressure & weight of blood), local alveolar capillary BP > alveolar air pressure throughout entire cardiac cycle
.

zone 2 V=Q; intermittent blood flow because during diastole, blood pressure drop below alveolar air pressure so no blood flow. ONLY in systole blood flows
.

zone 1 (lung apex above heart with lower BP) has narrower vessels & very distended alveoli. V>Q; higher V/Q ratio. Narrow/closed alveolar capillaries due to alveolar air pressure > BP of capillary in alveolar walls, (capillaries compressed by alveolar air pressure from outsides) so no blood flow. ONLY Occurs Under Abnormal Conditions, e.g. upright person breathing against positive air pressure so intra-alveolar air pressure is greater than normal with normal pulmonary systolic BP, OR pulmonary systolic arterial pressure is exceedingly low after severe blood loss. In health, lung apex has compressed alveoli??? due to less pressure gradient as apex has less negative intrapleural pressure
.
At the apex, where the lungs are overventilated relative to blood flow, V > Q, the PaO2 is higher than base, but PaCO2 is lower.
.
PaO2 at base of the lungs is lower because the blood is not fully oxygenated as a result of V < Q, underventilation relative to blood flow

Question 13

resp failure & VQ mismatch

Explain how VQ is controlled & the effect of increased & decreased VQ matching on partial pressures

Answer 13

When V > Q, ppO2 increase, local pulmonary arterioles dilate, vascular resistance decrease, perfusion/blood flow increase & ppCO2 decrease, local bronchioles constrict, airway resistance increase, ventilation reduce
.
When V < Q, ppO2 decrease, local pulmonary arterioles constrict, vascular resistance increase, perfusion reduce & ppCO2 increase, local bronchioles dilate, airway resistance decrease, ventilation increase
.

When the V/Q ratio is low, the partial pressures approach that of mixed venous blood. When the V/Q ratio is high, the partial pressure is close to inspired
.

At the apex, where the lungs are overventilated relative to blood flow, V > Q, the PaO2 is higher than base, but PaCO2 is lower.
.
PaO2 at base of the lungs is lower because the blood is not fully oxygenated as a result of V < Q, underventilation relative to blood flow

Question 14

Resp failure & VQ mismatch

Compare pulmonary & systemic circulation characteristics

Answer 14

Pulmonary arterioles constrict to low PaO2 (hypoxia) to reduce flow & redirect blood to better perfused areas. Vasodilate when PaO2 increase
.
whereas in systemic circulation, systemic arteriole vasodilate when low PaO2 & vasoconstrict when PaO2 increase

Question 15

resp failure & VQ mismatch

Define Respiratory Failure
.
describe main causes & explain clinical examples arising from these causes

Answer 15

Definition: A failure to maintain adequate gas exchange and is characterised by abnormal arterial blood gas partial pressures
.
type 1: hypoxaemia (< 8kPa) & normal/low CO2
* impaired gas exchange, dyspnoea (breathless), irritable, tachycardia, may develop arrythmia, cyanosis (bluish skin, more O2 unloaded from haemoglobin to be used so more deoxy-haemoglobin in blood)

type 2: hypoxaemia & hypercapnia (>6kPa)
* headache (due to CO2 retention), drowsy, confusion, peripheries shaking tremor (eg hand), warm fingers (as CO2 is a good vasodilator)

.
main causes:
a) alveolar hypoventilation due to not enough O2 to breathe in or insufficient lungs pump activity (=impaired lung mechanics, eg ribs/diaphragm broken, airways blocked). Type 2 respiratory failure
* reduction in minute ventilation characteristically shows an increase in PaCO2 - (minute ventilation=breath volume 0.5L x 12 breath frequency=6L/min so may due to change in tidal volume or frequency of breath)
* increased proportion of physiological dead space (=alveoli) as CO2 can’t be removed/exchanged from alveoli out of body
.

b) diffusion deficit eg thickened alveolar wall
.
c) shunts, blood bypass lungs so not oxygenated, venous blood mixing with oxygenated blood so pO2 reduce
* Extra-pulmonary shunt –Mainly paediatric cardiac causes e.g. ductus arteriosus. This usually reverses.
* intra-pulmonary shunt
blood is transported through lungs without taking part in gas exchange. Commonly due to alveolar filling (pus, oedema, blood, tumour) & atelectasis. Giving 100% oxygen does ‘not’ correct pure shunt hypoxia, it increase pO2 but tissues mostly use O2 bound to haemoglobin, not dissolved O2 in blood (or because 100% oxygen cant enter blood perfusing consolidated/collapsed alveoli)

.
d) ventilation–perfusion (VQ) mismatch =local effect on 1 place in lungs, not affect everywhere in lungs, most common cause type 1 respiratory failure
.

8kPa=60mmHg
6kPa=45mmHg

Question 16

SAQ

Explain the shape of the oxyhaemoglobin curve & compare the effects of the changes in patients – one with a fever and one with carboxyhaemoglobin

Question 17

SAQ

Explain, with reference to sources of resistances to breathing, what pulmonary surfactant is and 3 important benefits it conveys on breathing.

Question 18

A patient is diagnosed with hereditary neuropathy type II following lack of sensation in their hands and feet. They are told breathing difficulties may arise.
.
Which nuclei would be responsible for any breathing abnormality in this case?

a.Kolliker-Fuse nucleus
b.Nucleus parabrachialis medialis
c.Nucleus tractus solitaris
d.Nucleus retroambiguus
e.Nucleus retrofacialis

Answer 18

c. Nucleus tractus solitaris

Question 19

A man having respiratory complaints is breathlessness when walking up a slight hill. What is their MRC breathless score?

Answer 19

score 1

0 – strenuous exercise;
1 – hurrying or walking up a slight hill;
2- walking slower than others of same age or stopping for a breath at own pace on the flat ground;
3 – stopping after a few Minutes or 150 m;
4- too breathless to leave the house or when dressing/undressing

Question 20

control of breathing

J receptors are stimulated in a patient causing rapid shallow breathing. Which patient condition would directly stimulate these receptors?
.
A) A patient who has directly inhaled ammonia through a health and safety failure
B) A patient having endotracheal intubation due to anaphylactic shock
C) A patient with an asthma attack
D) A pneumonia patient with profound alveolar consolidation
E) A patient with pneumothorax

Answer 20

D) A pneumonia patient with profound alveolar consolidation

J-fibres: Present on the walls of the alveoli and have close contact with the capillaries
.
Stimulated by pneumonia, congestive heart failure (CHF), pulmonary oedema as well as exposure to e.g. histamine

Question 21

Which is one cause of increased chest wall resistance?
.
A) Breathing low density gas
B) Increased airway radius
C) Reduced surfactant production
D) Reduced abdominal pressure
E) Pregnancy

Answer 21

E) Pregnancy

Question 22

Compliance is being measured in a patient. Normal lung compliance ranges from 0.1 – 0. 4L/cm H2O
.
Patient A: A 100 mL change in volume is caused by a 2 cmH20 change in pressure
.
Patient B: A 500 mL change in volume is caused by a 1 cmH20 change in pressure.
.
Which patient is most likely to have hyperinflation?

Answer 22

=patient B
.
Compliance is volume/pressure
Patient A - 0.1L/2 cmH2O= 0.05 L/cmH2O
Patient B - 0.5/1 cmH2O = 0.5 L/cmH2O
Emphysema has increased compliance – hence B – this is associated with increased TLC.

Question 23

A patient has a lower than expected FEV1 and elevated FEV1/FVC for their age. What condition (s) might underlie the spirometry results?
.
A) Asthma
B) Bronchiectasis
C) Asbestosis
D) Chronic bronchitis
E) Cystic fibrosis

Answer 23

C) Asbestosis

This FEV1/FVC trend is typical for restrictive lung diseases. Asbestosis is one such example but all others are obstructive states

Question 24

SAQ 10 marks

1) Identify and explain the clinical tests used to diagnose TB (5 marks)
.
2) Describe what you would observe in a positive result ( 5 marks)

Answer 24

1) Skin test, measure diameter of swelling – 1
B – Microbiological sampling, sputum analysis – 1
C – Blood test, interferon gamma etc. – white blood cells – 1
D – Molecular testing, NAAT – 1
E – Imaging – X-ra/CT thorax – 1
.
2) Positive results
A – 5mm or larger
B – Culture growth of mycobacterium tuberculosis
C – IFN-g release
D – Bacterium present
E – Inflammation of lungs – opacities in specific site

Question 25

SAQ 10 marks

1)Describe the anatomical features of pneumonia (5 marks)
.
2) Further explain possible outcomes of pneumonia (5 marks)

Answer 25

Lobar pneumonia is alveoli to alveoli (1) organisms rapidly access alveoli and spreads via alveolar pores (1). This pneumonia is common in adults with poor hygiene especially (1) Bronchopneumonia is present through the bronchi and alveoli (1). Colonise bronchi (1) It affects locally in the lobes (1) In young and elderly (1)
.
2) Fibrosis/scar tissue (1) Abscess formation (1) Death (1) Productive cough (1) destruction of connective tissue (1) Bacterimia (1)

Question 26

SAQ

Describe the pathogenesis of emphysema (3 marks)

Answer 26

any 3 of the following:
.
- Environmental toxins (cigarette smoke & other inhaled pollutants) stimulate release of inflammatory cells
- Neutrophils, macrophages and lymphocytes accumulate
- Neutrophils and macrophages release cytokines and proteases with breakdown ECM
- Emphysema is caused by the imbalance of proteases and anti-proteases resulting in lung parenchymal destruction
- Epithelial injury and ECM proteolysis due to presence of elastases, cytokines and oxidant

Question 27

SAQ

Compare & contrast COPD and Fibrosis with reference to:
.
i) the nature of the disease i.e., obstructive or restrictive (1 mark for each disease)
.
ii). the signs and symptoms (2 marks for each disease )
.
iii.) the major pathological changes involved (2 marks for each disease)

Answer 27

i) COPD obstructive; fibrosis restricitive
.
ii)COPD: CoughHyperresonant chestSputum productionCyanosis
.
fibrosis: CoughShortness of breathShallow breathingFinger clubbing
.
iii)COPD: Mucus gland hypertrophyMucus gland hyperplasiaMucus hypersecretion
.
fibrosis: Type 2 pneumocyte hyperplasiaexcess of ECM componentsthickened, stiff tissue
epithelial damage

Question 28

Respiratory biomarkers

Understand what a biomarker is and why they are needed
* Understand the different types of biomarker and sample options
* Be aware of some current respiratory biomarkers
* Understand what ‘Omics technologies are and what they add to the biomarker field
* Be aware of emerging technologies including cell free DNA

Question 29

SAQ

1. Explain what basic respiratory measurements/volume may be used to calculate the following lung volumes and/or capacities [6 marks]
   .
   (i) Inspiratory reserve volume (IRV)
   (ii) Vital capacity (VC)
   (iii) Functional residual volume (FRV)

Answer 29

(i) IRV = TLC – (TV, ERV and RV) or similar
(ii) VC= IRV +TV + ERV
(iii) FRV = ERV + RV (or TLC – IC + ERV)
2 marks each

Question 30

SAQ

(ii) What is the approximate value in ml for the residual volume in a healthy 70kg male? [1 mark]
.
(iii) Explain the effect of pulmonary fibrosis on the residual volume [3 marks]

Answer 30

ii) approx 1500 ml
(iii)Pulmonary fibrosis is a restrictive lung disease in which ability of lungs to expand for ventilation and gas exchange is reduced. As a consequence, all lung volumes are reduced including residual volume

Question 31

SAQ

(i) A 68 yr old man has noticed he is becoming breathless in comparison to his twin brother when walking on level ground to local shops. Explain the MRC score of breathlessness that would be assigned to this man [5 marks]
.
(ii) He is subsequently found to have been suffering from the effects of drug overdose and has CNS depression. With reference to the causes of respiratory failure, explain which type is he most likely to have? [5 marks]

Answer 31

i) MRC scale:
Grade 1 – Breathlessness when hurrying on the level or on a slight hill
Grade 2 – Breathlessness when walking with own age on level ground
Grade 3 – Has to stop because of breathlessness when walking on level ground at own pace
so, He has grade 2 breathlessness
(4 marks for scale, 1 for correct type.)
.
ii)Type I = hypoxia alone < 8kPa, Type II hypoxia and hypercapnia ( >6kPa). [1 marks]
.
Respiratory failure is caused by alveolar hypoventilation, shunts, diffusion deficit and VQ mismatch (+ brief description) [3 marks]
.
She most likely has type II respiratory failure as depression of the respiratory drive would reduced the ability to expel Co2 causing hypercapnia. [1 marks]

Question 32

SAQ

i) Describe the causes, pathology and classifications of pneumonia [6 marks]
.
(ii) Radiographs indicate that a lady with pneumonia has a large opaque area in the lower lobe of her right lung. Name 2 potential causes of opacity on x-ray and explain the physiological basis for breathlessness. [4 marks].

Answer 32

i) Lobar and bronchopneumonia. Microbiological basis to be included and pathogenesis to include inflammation and consolidation. A good answer will include the timeline (red and grey hepatization) and subsequent resolution
.
(ii) Could be any of the following: consolidation, pulmonary oedema, pleural effusions, carcinoma, pneumothorax, rib fracture, lung disease etc. (+ reasoning.)
.
1 mark for differential and 1 for associated reasoning

Question 33

SAQ

Describe, with the use of a diagram if necessary, the anatomy of the right lung under the following headings:
.
(i) Lobes [3 marks]
(ii) Surface marking [5 marks ]
(iii)Structures at the hilum [2 marks]

Answer 33

(i) Upper, middle and lower lobes; Oblique and horizontal fissures [3 marks]
.
(ii) The apex of the lung extends above the first rib into the root of the neck. The two lungs come close to one another at the level of the 2nd costal cartilage and then descends to the level of the 4th costal cartilage and further down till the 6th costal cartilage. It then deviates laterally to the level of the 8th rib at the mid axillary line and 10th thoracic vertebra posteriorly. [5 marks]
.
(iii) (From above downwards) Bronchus (eparterial), pulmonary artery, bronchus (hyparterial), pulmonary veins, lymphatics, autonomic nerves, bronchial arteries. [2 marks]

Question 34

SAQ

A woman with long term COPD is admitted to hospital. Her SaO2 on oxygen is 88%. Her blood gases are analysed.
.
(i) Explain, with reasoning, the nature/class of her respiratory failure & the acid-base disturbance most likely resulting from the condition injuries [6 marks].
.
(ii) Clearly state & explain whether each of his PaO2, PaCO2, pH and HCO3- results are likely to be increased or decreased [4 marks].

Answer 34

i) Definition of type I and type II failure [1 mark] and causes [2 marks]: needs to explain that this is most likely type II due to air trapping. Type II respiratory failure is most likely [1 mark]. Pathological destruction mechanisms is likely to cause difficulty in expiring carbon dioxide [1 mark] which would result in respiratory acidosis (most likely compensated) [1 mark].
.
(ii) The profile expected would be a high PaCO2 [1 mark] and a reduced from normal pH [1 mark] indicative of acidosis.
PaO2 is low as suggested by SaO2 [1 mark]
HCO3- is likely to be in high range due to renal compensation [1 mark]

Question 35

COVID by numbers

Relate exponential bacterial growth to graphs and equations
Use linear and logarithmic scales to display exponential growth
Estimate the generation doubling time

Question 36

respiratory pathogens

Recognise the demographics of respiratory infections & the differences between upper and lower respiratory tract infections
.
Describe the spectrum of microorganisms causing respiratory tract infection

Question 37

resp pathogens

Relate the features of respiratory pathogens to the pathogenesis of infections in the upper & lower respiratory tracts

Question 38

resp pathogen

Describe the processes involved in the laboratory diagnosis & identification of respiratory pathogens
.
Outline the treatment regimens available for respiratory infections

Question 39

lung function test

• To use peak flow rates using peak flow meters and to use dynamic respiratory manoeuvres (forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC))
  .
• To calculate predicted results and reference ranges for PEFR using adult reference equations and compare actual with predicted results.
  .
• To compare volume- time trends seen in response to simulated conditions (e.g., respiratory pathologies).
  .
• To compare flow volume loops from demonstrated normal with a variety of pathological presentations.

Question 40

resp pharmacology workshop

review the mechanism of action of common classes of drugs used in respiratory conditions including beta2 adrenergic agonists, corticosteroids, cys-leukotriene receptor antagonists, muscarinic antagonists.
.
review the adverse reactions associated with the common classes of drugs used in respiratory conditions and consider ways to reduce the likelihood of these adverse reactions occurring.
.
Describe the main types of inhalers and their pros and cons
.
Explain the effect of particle size on inhaled drug action.
.
Explain the advantages of using a spacer with an inhaler
.
Explain the appropriate use of nebulisers
Discuss the issues surrounding inhaler sustainability

Question 41

‘Pathology of pneumonia’

Describe the pathological features of acute pneumonia
Describe the causative agents, routes of infection and classifications of acute pneumonia
Describe the clinical symptoms, treatment and possible outcomes of acute pneumonia
Describe the causative agents of chronic pneumonia

Question 42

TB pathology

Describe the aetiology, risk factors and diagnosis of TB
Describe the signs and symptoms of TB
Describe granulomatous inflammation as a specific type of chronic inflammation
Describe the pathogenesis and sequelae of primary and secondary TB

Question 43

lung cancer

Describe the 4 main types of lung cancer, (Small cell carcinoma, squamous carcinoma, Adeno-carcinoma, Large cell carcinoma), in terms of: aetiology, pathology, staging, treatment & prognosis.
.
Distinguish small cell carcinoma from non-small cell carcinoma.
.
Outline the evidence linking smoking and lung cancer.

Question 44

Which one of the following statements is true of lung cancer?
.
a) Most are small cell in type
b) Approximately 25% of lung cancers are large cell anaplastic in histological type
c) 80% are due to smoking
d) Screening has proved beneficial

Question 45

Which one of the following is true regarding lung cancer?
.
a) Adenocarcinomas tend to grow quickly
b) 5% of patients with lung cancer present with, or develop complications of non-metastatic paraneoplastic syndromes
c) Syndrome of inappropriate antidiuretic hormone (SIADH) is associated with hypernatraemia
d) 80-90% of small cell carcinomas have spread beyond the thorax at the time of diagnosis

Question 46

Which one of the following statements is true of surgery for non-small cell lung cancer (NSCLC)?
.
a) Post-operative mortality rate is approximately 10%
b) About 30% of patients are suitable for resection at diagnosis
c) Pneumonectomy is the most commonly performed operation
d) Surgery offers the best chance of cure

Question 47

Which one of the following statements is true of small cell lung cancer (SCLC)?
.
a) Surgery is the most important treatment modality
b) Limited stage disease describes disease less than T2 N1 M0
c) Approximately 80% of patients respond to chemotherapy
d) Prophylactic cranial irradiation has been shown to prolong survival

Question 48

TB pathology

1. Mycobacterium tuberculosis is the main cause of TB. Discuss the other microorganisms that may cause TB
   .
2. Describe the methods of diagnosis for TB.
   .
3. Outline the stages of granulomatous inflammation.
   .
4. What is miliary tuberculosis and what is the route of dissemination?
   .
5. Explain why immunocompromised patients are at risk from TB? What are the likely outcomes of Primary and Secondary TB in an immunosuppressed patient?

Question 49

pneumonia pathology

1. Pneumonia is a form of acute inflammation. The 3 pathological changes in acute inflammation are dilation of blood vessels, increased vascular permeability and emigration and migration of neutrophils.
   What is the impact of these changes on the lung tissue in pneumonia? How are these linked to the symptoms experienced by the patient?
   .
2. Depending on the causative organism of pneumonia, different treatments would be prescribed.
   What empirical treatment is used? How would you identify the causative agent?
   .
3. Pneumonia can be classified anatomically as bronchopneumonia or lobar pneumonia. Explain these terms and what is the difference between them?
   .
4. Pneumonia can be acquired in a range of settings with each being associated with particular causative pathogens. Give some examples of Community-acquired and Hospital-acquired pathogens.
   .
5. What are the possible routes of infection for Community-acquired and Hospital-acquired pathogens?
   .
6. Explain why immunocompromised patients are at risk from pneumonia. What organisms are likely to underly pneumonia in this case?
   .
7. Explain the basis of aspiration pneumonia. Who is at risk and what organisms are the most likely causes?
   .
8. List the possible outcomes of pneumonia. Ensure you include resolution and understand what that means.

Question 50

surface anatomy

Demonstrate the surface landmarks of the thorax
Describe the surface markings of both the lungs
Describe the surface marking of the parietal pleura
Demonstrate the surface markings of the fissures in both lungs
Understand some common respiratory conditions with their signs and symptoms
Understand the concept of inspection, palpation, percussion, and auscultation in sequence during a methodical thoracic / respiratory examination

Question 51

Respiratory role in pH homeostasis & blood gas analysis

State the normal plasma pH range
Describe the factors involved in pH homeostasis
Appreciate the rationale for the relationship between blood plasma pH, [H+], PaCO2 and [HCO3-] and the relevance of the respiratory and renal systems to the carbonic acid-bicarbonate buffer system and pH control
Explain, with examples, why respiratory (and metabolic) acid/base disturbances can arise and the compensation and corrective mechanisms
Interpret blood arterial blood gas analysis data

Question 52

pH homeostasis & blood gas analysis

Which of the following is a likely causation of non-respiratory (i.e. metabolic) alkalosis?
.
Diarrhoea -
Diabetes mellitus -
Gastric suction -
Infection -
Pulmonary embolism

Answer 52

Gastric suction
.
non-respiratory (i.e. metabolic alkalosis) suggests a loss of acid or a gain
of alkali that is not caused by the respiratory system e.g. via gastric vomiting, gastric suction, diuretics or
excessive use of antacids. In this particular question, gastric suction is the most likely cause

Question 53

see Q1 in ‘MGEM2013 pH & blood gas analysis Qs’ powerpoint
.
more Qs at https://abg.ninja/abg

Question 54

lower resp tract anatomy practical

• Describe the bones, cartilages, and muscles forming the thoracic cage
• Explain the role of the intercostal muscles and the diaphragm during breathing, including their nerve supply
• Describe the trachea, the structure of the bronchial tree
• Demonstrate the different parts of the pleura, its reflections, nerve supply, the pleural cavity, and explain the effects of pleural injury and irritation
• Identify the lobes, fissures, and hila of the lungs
• Demonstrate the surface markings of the lungs and pleurae

Question 55

surfacee anatomy & imaging practical

• Describe the surface markings of both the lungs and pleurae
• Demonstrate the surface markings of the fissures in both the lungs
• Identify the major thoracic structures on the PA and lateral chest radiographs, and on the thoracic scans (MRI and CT).

Question 56

control of breathing

Describe the location(s) and the role of the neural control centres in initiating and automatically controlling ventilation
.
Describe the location, affecting stimuli and the means by which the peripheral and central chemoreceptors mediate their effect(s) on the rate and depth of breathing.
.
Describe why breathing can be voluntarily controlled.
.
Deduce the effect of altered pulmonary ventilation (e.g. hyperventilation, hypoventilation, breath-holding) on PaO2 and PaCO 2.
.
Describe influences on respiratory rhythm (e.g. different receptors)
.
Explain why ventilation and its control may be affected by chronic disease processes (e.g. obstructive lung disease, obstructive sleep apnoea syndrome).
.
Describe the neurogenic means by which lung receptors and reflexes control respiration e.g. stretch receptors, the Hering Breuer inspiratory reflex, ‘ J’ receptors, cough reflex, thermoreceptors etc.
.
Compare different breathing patterns, terminologies, approximate respiration rates and causes (Eupnea, Tachypnea, Bradypnea, Apnea, Hyperpnea, Hypopnea, Cheyne Stokes, Biot’s and Kaussmaul’s)

Answer 56

https://www.chegg.com/flashcards/control-of-breathing-1facebe8-fdfb-43cf-b7ff-fb392883b9d2/deck

Question 57

The lateral wall of nasal cavity

Answer 57

Ethmoid bone: Superior nasal concha, middle nasal concha and uncinate process
Perpendicular plate of palatine bone
Medial pterygoid plate of sphenoid bone
Medial surfaces of lacrimal and maxillary bones
Inferior nasal concha

Question 58

The floor of the nasal cavity comprise of?

Answer 58

soft tissues of external nose
palatine process of maxilla
horizontal plane of the palatine bone
.
all form the hard palate
.
smooth and concave
wider than roof

Question 59

The anterior and posterior plates of the roof

Answer 59

Anterior plate:
the Roof slopes inferior to the nostrils
formed by the nasal bone, frontal bone, alar cartilage and lateral processes septal cartilages.

posterior plate: roof slopes inferior to choana
formed by the vomer, sphenoid and palatine bone.

opening between the sphenoidal and spheno-ethomoidal recess

Question 60

The nasal vestibule features?

Answer 60

lined by skin
had hair follicle
small dilated space

Question 61

Respiratory region features?

Answer 61

largest of the nasal cavity
rich in Neurovascular supply
Lined by respiratory epithelium

Question 62

Olfactory region features?

Answer 62

Found on the Apex of the respiratory region on either side of nasal cavity
.
small
lined by olfactory epithelium
.
sense of smell (olfactory epithelium)

Question 63

Structures opening onto the lateral nasal wall?

Answer 63

Frontal sinuses
ethmoidal recess
Maxillary sinuses
nasalacrimal duct: inferior nasal meaters

Question 64

upper resp tract anatomy

Describe the structure, function, mucosal lining, & anatomical relations of Nasal cavities

Answer 64

nasal cavity:
Nasal vestibules
Olfactory regions -covered with olfactory epithelium
Respiratory regions
.
conchae & nasal cavities covered with a thick, vascular, glandular (goblet cells) mucosal layer with pseudostratified ciliated columnar epithelium (=respiratory epithelium)
.
anterior opening (=nares) are formed by 2 nostrils, nasal vestibules lie just inside of nares
.
posterior openings (=choanae) open into nasopharynx
.
floor of nasal cavity is formed by maxillary bone & palatine bone, which form the hard palate (=roof of oral cavity)
.
midline nasal septum made of ethmoid & vomer bone (posteriorly) & of septal cartilage (anteriorly)
.
roof is made of the frontal & nasal bones of skull (anteriorly), cribriform plate of the ethmoid bone (centrally) & the sphenoid bone of skull (posteriorly)
.
cribriform plate in olfactory region contains numerous small perforations that transmit olfactory nerves (CN I) (that conveys the sense of smell)
.
lateral walls are formed by several bones of the skull, by cartilage & soft tissues.
.
3 nasal conchae (curled shelves of bone – also called the ‘turbinates’) protrude from the lateral walls =superior, middle & inferior nasal conchae.
.
The conchae create 4 air channels/meatuses, which lie underneath each lip of bone (concha), and which are contained within the respiratory regions of nasal cavity
.
conchae & meatuses increase the surface area of contact between tissues of the lateral wall of the nasal cavity & the respired air. This improves the filtration, heating & humidification of the inspired air. Foreign material caught by the nasal hairs in the vestibule & mucous is usually swallowed.
The turbulent airflow created by the internal nasal anatomy also pushes inspired air & odorants to olfactory area (=cribriform plate)
.
Functions: ???need check
1) Warms & humidifies the inspired air
2) Removes pathogens & debris from the inspired air
3) Responsible for sense of smell
4) Drains & clears paranasal sinuses & lacrimal ducts

Question 65

upper resp tract anatomy

Describe the structure, function, mucosal lining, & anatomical relations of Paranasal air sinuses
.
- - their contents, nerve supply, & drainage.

Answer 65

paranasal air sinuses = air-filled spaces
.
Function:
Lighten the weight of the head,
humidify & warm the inhaled air,
increase the resonance of speech/voice,
serve as a crumple zone to protect the vital structures in the event of a facial trauma
.
mucosa of paranasal air sinuses is thinner, less vascular, & has fewer goblet cells than mucosa of nasalcavity. Like nasal cavities, they’re lined by pseudostratified ciliated columnar (=respiratory) epithelium
.
anatomically close to orbits, meninges, brain and thin bony walls of nasal sinuses –favour infection spread from paranasal air sinuses to these regions
.
=frontal sinuses supplied by ophthalmic (V1) division of CN V (=trigeminal nerve)
=ethmoidal & sphenoidal sinuses & nasal cavity supplied by both ophthalmic (V1) & maxillary (V2) divisions of CN V
=maxillary sinuses supplied solely by maxillary (V2) division of CN V
.
All the sinuses drain into nasal cavity assisted by gravity (except for the maxillary sinuses - making them more prone to infections – maxillary sinusitis).
When this drainage system is impaired, infections result in swollen mucosa, blocked drainage holes & subsequent pressure (and pain) on the nearby structures
.
sphenoid sinus & part of ethmoidal sinus drain into the sphenoethmoidal recess above superior concha
.
maxillary, frontal, & most of ethmoidal sinuses mainly drain into middle meatus via semilunar hiatus & ethmoid bulla???

Question 66

upper resp tract anatomy

Explain the patterns of pain referral from the paranasal air sinuses

Answer 66

Forehead pain & headache may result from frontal sinusitis due to compression/irritation of branches from the ophthalmic (V1) division of trigeminal nerve (CN V)
.
Dental pain may occur with acute maxillary sinusitis due to compression/irritation of branches from the maxillary (V2) division of trigeminal nerve (CN V)
.
sinusitis =inflammation of the lining of nasal cavity & sinuses). The infection may be viral/bacterial

Question 67

upper resp tract anatomy

Describe the structure & nerve supply of:
.
Pharynx – include Anatomy, muscles, nerve supply
Oropharynx
Nasopharynx
Laryngopharynx
.

Answer 67

pharynx= 12–14 cm long Musculo-membranous tube which extends from choanae (posterior openings of nasal cavity) to oesophagus at the level of cricoid cartilage (vertebral level C6)
.
divided into nasal, oral & laryngeal part
.
nasal cavities & middle ear (part of URT, via pharyngotympanic tube) open into nasopharynx, which can be closed by lifting of the soft palate (=floor of nasopharynx), e.g. during swallowing. nasopharynx contain adenoids/pharyngeal tonsils (=a lymphoid tissue)
.
nasopharynx becomes oropharynx at pharyngeal isthmus – which closes during swallowing
.
oral cavity open into oropharynx. oral cavity can be closed by depression of the soft palate (e.g. during nose breathing). Oropharynx contain Palatine & lingual tonsils. posterior tongue forms anterior surface of oropharynx
.
tip of epiglottis =start of laryngopharynx. laryngeal inlet opens into anterior laryngopharynx
.
external circular constrictors: Superior, Middle & Inferior constrictor, supplied by CN X vagus nerve
.
internal longitudinal elevators:
Salpingopharyngeus - supplied by CN X
Palatopharyngeus -CN X
Stylopharyngeus -CN IX =glossopharyngeal nerve
.
sensory nerve supply:
nasopharynx –CN IX + maxillary (V2) division of Trigeminal nerve (CN V)
oropharynx –Glossopharyngeal nerve (CN IX)
laryngopharynx –Glossopharyngeal & Vagus

Question 68

upper resp tract anatomy

Describe the Cartilages, muscles, nerve supply, vocal folds of the larynx

Answer 68

cricoid cartilage, Arytenoid Cartilages x2, thyroid cartilage, epiglottis, corniculate cartilages x2 & Cuneiform Cartilages x2
.
extends from the tongue (C3 vertebral level) - suspended from the hyoid bone down to the trachea (C6 vertebra)
.
It is a hollow tube formed by a series of 9 cartilages interconnected by ligaments and fibrous membranes
.
It moves up and down during swallowing under the action of a number of extrinsic muscles (i.e. muscles that originate from neighbouring structures and insert into the larynx)
.
Intrinsic muscles (have their origin & insertion within larynx) move the vocal folds & modify the laryngeal inlet:
cricothyroid muscle, supplied by superior laryngeal branch of Vagus
#Transverse & oblique arytenoids,
#Posterior crico-arytenoids
#vocalis
#Lateral crico-arytenoids
#Thyro-arytenoids
#means supplied by recurrent laryngeal branch of Vagus nerve
.
The only muscle which opens the glottis (by abducting the vocal folds) =posterior cricoarytenoids – if these are paralysed then asphyxiation/breathlessness can result!
.
pseudostratified ciliated columnar epithelium (=respiratory epi) lines the larynx.
.
vocal ligaments form the skeleton of true vocal folds (they extend from the vocal process of arytenoid cartilage to thyroid cartilage). They are covered with non-keratinized, stratified squamous epithelium (NOT the usual respiratory mucosa usually found in the larynx). This protects the tissue from the effects of mechanical stresses that act on the surfaces of vocal folds
.
true vocal folds are formed by the mucosa covering the underlying vocal ligaments. By stretching and relaxing vocal ligaments, true vocal folds can be abducted & adducted by moving intrinsic muscles of larynx.
.
Moving the vocal folds opens & closes the rima glottidis (rima=gap), to produce sounds & protect the airway

Question 69

lower resp tract anatomy

Describe the thoracic cage, its inlet, outlet, bones, cartilages,

& muscles forming the thoracic cage
.
Understand the role of intercostal muscles & diaphragm during breathing, including their nerve supply

Answer 69

Typical ribs (3rd - 9th ribs)
Upper border is smooth & lower border is sharp
have tubercle, neck (separates the head from the tubercle), angle, costal groove (at lower border of rib’s internal surface)
anterior end is continuous with its costal cartilage which link them to sternum directly/indirectly, posterior end (aka head of rib) articulates with vertebral column
.
Atypical ribs (1st, 2nd, 10th, 11th, 12th ribs)
1st rib: superior surface has scalene tubercle, which separates 2 smooth grooves: anterior groove for subclavian vein, posterior groove for subclavian artery. Head of rib has ONLY 1 articular facet/surface
.
1st & 2nd ribs =flat
.
10th rib ONLY 1 articular facet at head of rib
.
11&12th: has no tubercle/neck. Both ribs are short, have little curve & pointed anteriorly.
.
Ribs 1-7 = True ribs
Each articulate via a single costal cartilage directly to sternum
.
Ribs 8-10 = False ribs
Articulate indirectly to sternum via a shared costal cartilage of the above rib
.
Ribs 11&12 = Floating ribs
Do not articulate with sternum at all
.
sternum has sternal notch (T2 vertebra level) > manubrium> sternal angle (lower border of T4) >body > xiphoid process (T9/T10)
.
sternum clinical significance: it is where:
Tracheal bifurcation occurs (=Carina)
Aortic arch starts & ends
thoracic duct (where most lymph drain into) deviates from right to left
Pulmonary trunk divides into left & right pulmonary arteries
.
Diaphragm:
arises from lower ribs, xiphoid process & lumber vertebrae. All skeletal muscle fibres insert into central tendon
.
major role in respiration - Contracts (flattens) during inspiration increasing vertical diameter of thoracic cavity
.
3 major Openings in diaphragm allow structures to travel to/from the abdomen e.g., Inferior vena cava (T8 vertebral level), Oesophagus (T10) & Aorta (T12)
.
Innervation supplied by phrenic nerve (C3, C4, C5)
.
External intercostal muscles most active in inspiration, moves ribs superiorly & bend them more open, thus increasing anteroposterior & lateral diameter of thoracic cavity, to create a negative intra-thoracic pressure. –As anterior end of ribs is lower than posterior ends, when ribs are elevated, they move sternum upward & forward (increase anteroposterior dimension of thorax), opposite when ribs are depressed. As middle part of rib shafts are lower than ribs’ 2 ends, rib elevation =increase lateral dimension
.
Internal & innermost intercostal muscle move ribs inferiorly – help forced expiration (as quiet expiration is passive process)
.
All intercostal muscle supplied by intercostal nerves,(=anterior rami of spinal nerves T1-11). neurovascular bundle lies in the costal groove in lower border of superior rib. So to avoid damaging nerve/vessel, insertion of chest drain needle should be at upper border of lower rib
.
inlet =superior thoracic aperture borderd by body of vertebra T1 posteriorly, 1st rib (slope inferiorly) & manubrium anteriorly.
.
superior margin of manubrium =anterior border of superior thoracic aperture (approx the level of intervertebral disc between vertebrae T2 & T3). posterior border= T1 vertebral level
.
outlet/inferior thoracic aperture bordered by T12 vertebral body posteriorly, 12th rib & distal end of 11th rib posterolaterally, costal margin anterolaterally (=distal cartilaginous ends of 7-10th ribs) & xiphoid process anteriorly. diaphragm seals the inferior thoracic aperture

Question 70

lower resp tract anatomy

Describe the trachea, structure of the bronchial tree & the bronchopulmonary segmentation of lungs (including its blood supply)
.
Describe the different parts of pleura, its reflections, nerve supply, the pleural cavity, & explain the effects of pleural injury & irritation
.
Identify the lobes, fissures, & hila of the lungs & structures passing through the hila.
.
Explain the functional significance of bronchopulmonary segments (postural drainage & surgical section)

Question 71

lower resp tract anatomy

Describe the thoracic cage, its inlet, outlet, bones, cartilages, and muscles forming the thoracic cage
.
Understand the role of the intercostal muscles and the diaphragm during breathing, including their nerve supply
.
Describe the trachea, the structure of the bronchial tree and the bronchopulmonary segmentation of the lungs (including its blood supply)
.
Describe the different parts of the pleura, its reflections, nerve supply, the pleural cavity, and explain the effects of pleural injury and irritation
.
Identify the lobes, fissures, and hila of the lungs and structures passing through the hila.
.
Explain the functional significance of bronchopulmonary segments (postural drainage and surgical section)

Question 72

lower resp tract anatomy

Describe the thoracic cage, its inlet, outlet, bones, cartilages, and muscles forming the thoracic cage
.
Understand the role of the intercostal muscles and the diaphragm during breathing, including their nerve supply
.
Describe the trachea, the structure of the bronchial tree and the bronchopulmonary segmentation of the lungs (including its blood supply)
.
Describe the different parts of the pleura, its reflections, nerve supply, the pleural cavity, and explain the effects of pleural injury and irritation
.
Identify the lobes, fissures, and hila of the lungs and structures passing through the hila.
.
Explain the functional significance of bronchopulmonary segments (postural drainage and surgical section)

Question 73

lower resp tract anatomy

Describe the thoracic cage, its inlet, outlet, bones, cartilages, and muscles forming the thoracic cage
.
Understand the role of the intercostal muscles and the diaphragm during breathing, including their nerve supply
.
Describe the trachea, the structure of the bronchial tree and the bronchopulmonary segmentation of the lungs (including its blood supply)
.
Describe the different parts of the pleura, its reflections, nerve supply, the pleural cavity, and explain the effects of pleural injury and irritation
.
Identify the lobes, fissures, and hila of the lungs and structures passing through the hila.
.
Explain the functional significance of bronchopulmonary segments (postural drainage and surgical section)

Question 74

lower resp tract anatomy

Describe the thoracic cage, its inlet, outlet, bones, cartilages, and muscles forming the thoracic cage
.
Understand the role of the intercostal muscles and the diaphragm during breathing, including their nerve supply
.
Describe the trachea, the structure of the bronchial tree and the bronchopulmonary segmentation of the lungs (including its blood supply)
.
Describe the different parts of the pleura, its reflections, nerve supply, the pleural cavity, and explain the effects of pleural injury and irritation
.
Identify the lobes, fissures, and hila of the lungs and structures passing through the hila.
.
Explain the functional significance of bronchopulmonary segments (postural drainage and surgical section)

Question 75

clinical imaging of thorax

Have an understanding of the range of clinical imaging techniques available
.
Identify the main features and organs of the thorax on x-ray
.
Describe commonly used clinical imaging techniques and recognise images produced by them
.
Discuss the reasons for choosing a suitable imaging technique
.
Comment on likely considerations and suitability of a particular imaging technique/s for imaging any specific part/s of the respiratory tract.

Answer 75

X-ray: projection (Anterior-posterior or posterior-anterior are common)
rotation
penetration
Inspiration/Expiration
.
AP views make heart appear larger than it actually is.
.
x-ray check for ABCDE:
Airways -Trachea, endotracheal tube, etc.
Bones - Clavicles, ribs, sternum, thoracic vertebrae, etc.
Cardiac shadow
Diaphragm (Right hemidiaphragm slightly higher.
Everything else (wires, tubes, pacemaker, effusions, etc.)
.
Apices and hila of the lungs
Behind the heart
Costophrenic angles (CPA)
Diaphragm - Look below it
Soft tissues (breast, surgical emphysema)

Question 76

Applied respiratory physiology

a) Circulations - Compare and explain the physiological characteristics of the pulmonary and systemic circulations in terms of pressure, compliance and resistance
.
b) Compliance, specific compliance and elastance - Explain changes in these parameters as may occur in respiratory pathologies and relate these to calculated values

Question 77

In terms of physiology, why does pulmonary circulation have low pressure, low resistance & high compliance?

Answer 77

LOW PRESSURE (25/8 mmHg)
because it only needs to pump blood to the top of the lungs.
if it is High pressure, then following Starling forces, the fluid would flood the lungs.
.
LOW RESISTANCE
- only 1/10th of the resistance of the systemic circ.
arterioles have less smooth muscle, veins are wider & shorter & pulmonary vessel walls are thinner.
.

HIGHLY COMPLIANT
accommodates 5-6 L of blood (same as the systemic circulation)
Accommodates shifts of blood more quickly e.g. when a person shifts from a standing to a lying position

Question 78

In terms of physiology, why does systemic circulation have high pressure, high resistance & low compliance?

Answer 78

HIGH PRESSURE
B/c it needs to send blood to the brain even when standing & to the tip of an elevated fingertip.
.
HIGH RESISTANCE
because of increased smooth muscle in the arterioles & the meta-arterioles.
.

LOW COMPLIANCE
because of resistance offered by the arterioles and the meta-arterioles

Question 79

Airway resistance & NRDS

Explain types of respiratory resistance

Answer 79

static resistance – chest wall:
Force of movement of chest wall is opposite that of lun . Chest Wall has tendency to expand (pull out) but held by negative pleural pressure
.
Unopposed reaches 70% of TLC (resting position)
.
When thorax is intact, in equilibrium with the lungs, its resting level is Functional Residual Capacity (FRC)
.
static resistance – lungs
=Elastin & collagen Interwoven in lung parenchyma (1/3 of static resistance arising from lungs)
Tendency to oppose stretching
.
=Surface tension (2/3 of this resistance)
Small alveoli are unstable and have a greater tendency to collapse and empty its air into connected larger alveoli (i.e. atelectasis)
Reduction of ST forces allows interdependent/stability

dynamic resistance we need learn? intrapleural=pleural pressure?

Question 80

Airway resistance & NRDS

Describe the volume (V) and pressure (P) changes in the respiratory cycle & the PV relationship

Answer 80

normal pleural pressure at beginning of inspiration is about −5 cm H2O, which is the amount of suction required to hold the lungs open to their resting level.
.
During normal inspiration, expansion of chest cage pulls outward on the lungs with greater force & an increase in lung volume of ~0.5L (by ~1cm diaphragm movement) decrease intrapleural pressure to about −7.5/-8 cm H2O & decrease alveolar pressure to below atmospheric pressure, about −1 cm H2O, so gas flow into alveoli down the partial pressure gradient.
.
Expiration: lung volume reduce back to functional residual capacity (FRC) level, intrapleural pressure increase back to -5cm H2O, alveolar pressure increase back to above atmospheric pressure, gas flow out of alveoli down partial pressure gradient

Question 81

Airway resistance & NRDS

Describe the composition & secretion of surfactant
.
explain its physiological benefits

Answer 81

benefits:
3 times less transmural pressure is needed to expand lungs as surfactant lowers surface tension which tends to collapse alveoli (if airways leading from them are blocked), thereby reducing the work/effort required by respiratory muscles to expand lungs
.
Keeps alveoli dry
=It lowers the inwardly directed pressure which draws water into the alveoli
.
Maximises area for ventilation and perfusion
=ST of small alveoli are reduced more than larger alveoli as surfactant molecules crowd into the smaller space
.
Maintains ‘alveolar interdependence’
=Aided by fibrous tissue septal and septal walls between alveoli of different sizes which act as additional splints
.
surfactant secreted by type II pneumocyte (=alveolar epithelial cells), These cells are granular, containing lipid inclusions that are secreted in the surfactant into alveoli.
.
Surfactant is a complex mixture of several phospholipids, proteins & ions, most important components are phospholipid dipalmitoyl phosphatidylcholine, surfactant apoproteins & calcium ions . The dipalmitoyl phosphatidylcholine and several less important phospholipids are responsible for reducing surface tension. They can perform this function because part of the molecule dissolves while the remainder spreads over the surface of fluid lining alveoli. It reduce surface tension of alveolar fluid lining to ~1/12th to 1/2 of surface tension of pure water

Question 82

airway resistance

Which of the following is the most prevalent/abundant component in surfactant?
.
a.dipalmitoyl phosphatidylcholine
b.calcium
c.cholesterol
d.SP -B
e.phosphatidyl glycerol

Answer 82

dipalmitoyl phosphatidylcholine (DPPC) =a phospholipid
.
surfactant made of 80% phospholipid, 10% lipid & 10% surfactant proteins

Question 83

lung airway resistance

A pharmaceutical company is developing a novel therapy that reduces number of epithelial cells that are NOT synthetic for surfactant within alveoli.
.
Which type of Pneumocytes are targetted?

Answer 83

type 1 as surfactant is secreted by type2 pneumocytes

Question 84

Airway resistance & NRDS

Define neonatal respiratory distress syndrome
.
describe causations, pathogenesis, signs and symptoms & aim of treatment regimes

Answer 84

Defi: Increasing respiratory distress, commencing at, or shortly after birth and increasing in severity until progressive resolution occurs among survivors, usually around 2nd to 7th day.
.
Caused by deficiency of surfactant. contributing factor include
=Fetal head injury during birth
=Aspiration of blood or amniotic fluid
=Excessive sedation of mother during birth
=Maternal diabetes (excess insulin suppresses surfactant production)
=Cold stress
=Genetic disorders e.g. abnormalities in proteins B and C or transport proteins ABC transporter 3 [ABCA3]
.
symptoms:
Tachypnea (> 60 breaths/min)
Grunting
Nasal flaring
Intercostal recession
Cyanosis
Reduced entry of air
histology have Ground glass appearance, Lungs appear airless, Darkened and dense, show Fibrin, cell debris, erythroctyles, Neutrophils & macrophages, waxy layers of hyaline, Bleeding and vascular congestion & collapsed alveoli
.
pathogenesis:
immature & damaged Type II pneumocytes due to prematurity/risk factor/specific cause >alveoli collapse >uneven perfusion & hypoventilation >hypoxaemia & hypercapnia >acidosis >Pulmonary vasoconstriction & hypoperfusion> alveolar endothelial & epithelial damage >plasma leak into alveoli> Fibrin + necrotic cells =hyaline membrane >increased diffusion gradient> worse hypoxaemia & hypercapnia

.
treatment: aim to lower surface tension, increase compliance, reduce work of breathing
For babies: Synthetic surfactant therapy (endotracheal) & assisted ventilation & Supportive care e.g. thermoregulation, fluid management, nutrition
.
Pre-term mothers: i.v. betamethasone 26-28 wks gestation

Question 85

Airway resistance & NRDS

Describe pressure-volume curve, relate this to the work of breathing
.
explain influential factors & their consequences on the curves

Answer 85

V-P curve shows the capacity of the lungs to adapt to transpulmonary pressure changes.
.
gradient = compliance
.
work of breathing = the area in the loop (expiratory + inspiratory non-elastic resistance) + the hatched area (=elastic resistance).
.
If lack surfactant, surface tension not reduced, surface tension adds resistance so harder to stretch =reduced compliance
=larger pressure would only increase slightly lung volume =so graph would shift towards right

Question 86

Airway resistance & NRDS

Compare ‘compliance’ & ‘elastance’ in terms of definition, mathematical calculation, & relevance to the respiratory system

Answer 86

Compliance: Distensibility (stretch) of the lung i.e. the change in lung volume that occurs with each unit change in transpulmonary pressure (=difference between alveolar & intrapleural Pressures)
C=V/P
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For both lungs this is 200mL/cm H2O i.e. 1cmH2O change expands lung by 200 mL.
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Specific compliance is this corrected for volume at that time i.e. compliance/V
This standardizes compliance for different volumes
.
Elastance: Property of resisting deformation (resistance) or desire to return to original shape
E = 1/C

Question 87

Overview of respiratory pathologies

Describe the structure of respiratory system in the context of understanding lung disease

Answer 87

Conducting airways: nose, pharynx, larynx, trachea, bronchi, & bronchioles.
.
Respiratory airways: respiratory bronchioles, alveolar duct, alveolar sacs, & alveoli.
.
trachea>main bronchus>lobar bronchus>segmental bronchus>terminal bronchiole>respiratory bronchiole>alveolar duct>alveolar sac>alveoli
.
respiratory wall: Respiratory epithelium, basement membrane, vascular lamina, smooth muscle, glandular sub-mucosa (glands have mucous & serous parts), cartilage.

Question 88

Overview of respiratory pathologies

Describe the causes, clinical symptoms & underlying mechanisms of the major obstructive lung diseases

Answer 88

OBSTRUCTIVE: limitation of airflow
chronic bronchitis -
* causes: smoking & urban pollution
.
* symptoms: (definition) persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. & sputum production
.
* mechanism: Hypertrophy & hyperplasia of mucous glands/goblet cells in epithelium
-Hypersecretion of mucus
-hypertrophy of smooth muscle
- Inflammation – T cells, neutrophils & macrophages (no eosinophils – in contrast to asthma)

.
emphysema -
* causes: smoking, congenital anti-protease ‘α1-anti-trypsin’ deficiency
.
* symptoms: WITHOUT bronchitis - dyspnoea, obvious hyperventilation, prolonged expiration, tachypnoea & increased minute ventilation
Barrel chest due to use of accessory muscle
Prolonged onset >40 years
pursed lips breathing
decreased breath sounds
cachexia (appear abnormally slim, lose muscle, have no energy)
.
WITH bronchitis: dyspnoea less prominant, body retains CO2 – hypoxic & cyanotic
tend to be obese
.
* mechanism:
inhaled cigarette smoke & noxious particles/air pollutants (plus genetic predisposition), generate reactive oxygen species (ROS) - oxidative stress increasing apoptosis & senescence; inflammatory cells release chemotactic & growth factors & proinflammatory cytokines; Protease–Anti-protease imbalance, all lead to alveolar wall destruction.
.
ROS inactivate anti-proteases. Protease mediate damage of extracellular matrix. protease-anti-protease imbalance lead to increased neutrophil elastase. Small airways are normally held open by elastic recoil of lung parenchyma, and loss of elastic tissue in alveolar walls that surround respiratory bronchioles reduces radial traction, so causes respiratory bronchioles to collapse during expiration =functional obstruction with no mechanical obstruction.
.
Asthma
* cause: Immunologic or undefined cause. Extrinsic trigger like seasonal allergen; intrinsic trigger like infection, exercise, drugs (eg penicillin)
.
* symptoms: Episodic wheezing, cough, dyspnea, chest tightness
.
* mechanism:
-Intermittent & reversible airway obstruction
-Chronic bronchial inflammation with eosinophils
-Bronchial smooth muscle hypertrophy & hyper-reactivity
.
atopic asthma is associated with excessive Th2 helper cell activation. Th2 cell-produce cytokines that stimulate IgE production, eosinophils activation & mucus production. IgE coats submucosal mast cells, which on exposure to allergen release their granule contents & secrete cytokines and other mediators, causing early & late phase reactions.

• Early-phase: bronchoconstriction, increased mucus production & vasodilation. Bronchoconstriction is triggered by mediators released from mast cells, (eg, histamine, prostaglandin D2,) & by reflex neural pathways.
  .
• Late-phase: inflammation. Inflammatory mediators stimulate epithelial cells to produce chemokines that promote recruitment of Th2 cells, eosinophils, other leukocytes, thus amplifying an inflammatory reaction
  .
• Repeated bouts of inflammation lead to structural changes in the bronchial wall =airway remodeling: hypertrophy of bronchial smooth muscle & mucus glands, increased vascularity & deposition of subepithelial collagen
  .
  bronchiectasis:
• cause: Persistent/severe infections OR obstruction
  .
• symptoms: Cough, purulent sputum, fever
  .
• mechanism:
  obstruction or chronic infection, Either may be the initiator. E.g., obstruction caused by a foreign body impairs clearance of secretions, providing a favorable substrate for superimposed infection. The resultant inflammatory damage to bronchial wall & the accumulating exudate further distend airways, leading to irreversible dilataion. OR e.g. a persistent necrotizing infection in bronchi/bronchioles may lead to poor clearance of secretions, obstruction, inflammation with peribronchial fibrosis & traction on bronchi (=fibrotic tissue pulling on bronchi), cause bronchi dilatation

Question 89

Overview of respiratory pathologies

Describe the causes, clinical symptoms & underlying mechanisms of the major restrictive lung diseases

Answer 89

RESTRICTIVE:
Acute respiratory distress syndrome (ARDS):
* cause: pneumonia (35%–45%), sepsis (30%–35%), aspiration, trauma …
.
* symptoms: respiratory failure occurring within 1 week of a known clinical insult with bilateral opacities on chest imaging. severe case has rapid onset of life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy
.
* mechanism:
Under the influence of proinflammatory cytokines such as interleukins IL-8 and IL-1 and tumor necrosis factor (TNF) (released by pulmonary macrophages after acite lung injury), neutrophils are sequestered in the pulmonary microvasculature and then egress into the alveolar space, where they undergo activation. Activated neutrophils release leukotrienes, oxidants, proteases, and platelet-activating factor (PAF), which contribute to local tissue damage to endo- & epithelium, accumulation of oedema fluid, surfactant inactivation & hyaline memb formation. endothelium and epithelium damage causes vascular leakiness & loss of surfactant that make alveoli unable to expand. Subsequently, macrophage release fibrogenic cytokines such as transforming growth factor-β (TGF-β) & platelet-derived growth factor (PGDF) stimulate fibroblast growth and collagen deposition associated with the healing phase of injury.
.
Idiopathic Pulmonary Fibrosis (IPF):
* cause: idiopathic
* symptom: Persistent alveolitis, gradual onset of non-productive cough & progressive dyspnea, most patients have characteristic “dry” or “Velcrolike” crackles during inspiration. Cyanosis, cor pulmonale, peripheral edema may develop in later stages of disease
.
* mechanism:
result from repeated injury and defective repair of alveolar epithelium, often in a genetically predisposed individual
.
it’s hypothesized that abnormal epithelial repair at the sites of chronic injury and inflammation (macrophage recruit neutrophil which release ROS & proteases that damage type 1 pneumocyte) gives rise to exuberant fibroblastic or myofibroblastic proliferation,
Stimulated fibroblasts deposit collagen & ECM excessively for an extended time, leading to the characteristic fibroblastic foci
.
Pneumoconiosis
* causes:
.
* symptoms:
asbestosis: Progressively worsening dyspnea appears 10 to 20 years after exposure. It is usually accompanied by a cough and production of sputum. The disease may remain static or progress to congestive heart failure, cor pulmonale, and death. Pleural plaques are usually asymptomatic and are detected on radiographs as circumscribed densities.
Both lung carcinoma and malignant mesothelioma develop in workers exposed to asbestos. The risk for developing lung carcinoma is increased about 5-fold for asbestos workers
.
silicosis: fine nodularity in the upper zones of the lung on radiograph. Most patients do not develop shortness of breath until late in the course, after progressive massive fibrosis (PMF) is present. Many patients with PMF develop pulmonary hypertension and cor pulmonale as a result of chronic hypoxia–induced vasoconstriction and parenchymal destruction. The disease is slowly progressive, often impairing pulmonary function to such a degree that physical activity is severely limited
.
coal worker’s pneumocosis: usually is a benign disease that produces little decrement in lung function. If PMF develops, there is increasing pulmonary dysfunction, pulmonary hypertension, and cor pulmonale
.
* mechanism:
Silica, asbestos, and beryllium are more reactive than coal dust, resulting in fibrotic reactions at lower concentrations. Most inhaled dust is entrapped in mucus blanket & rapidly removed from lungs by ciliary movement. But, some particles become impacted at alveolar duct bifurcations, where macrophages accumulate & engulf trapped particulates. After macrophages’ phagocytosis, many particles activate inflammasome & induce production of the pro-inflammatory cytokine IL-1 & other factors, which initiates an inflammatory response that leads to fibroblast proliferation & collagen deposition. Some of the inhaled particles may reach the lymphatics either by direct drainage or within migrating macrophages, thereby in inflammasome and the subsequent release of inflammatory mediators by pulmonary macrophages, including IL-1, TNF, fibronectin, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokines.
.
silicosis: inhaled silica particles interact with epithelial cells and macrophages. cause activation of inflammasome & the subsequent release of inflammatory mediators by pulmonary macrophages, including IL-1, TNF, fibronectin, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokines.
.
asbestosis: after phagocytosed by macrophages, asbestos fibers activate inflammasome & damage phagolysosomal membranes, stimulating release of proinflammatory factors & fibrogenic mediators. In addition to cellular and fibrotic lung reactions, asbestos probably also functions as both a tumor initiator and a promoter

Question 90

Overview of respiratory pathologies

Describe the pathological features & diagnosis of obstructive & restrictive lung disease
.
differentiate between them

Answer 90

OBSTRUCTIVE: limitation of airflow
chronic bronchitis -
* luminalaccumulationofmucous forming plugs to block bronchiole
* gobletcellhyperplasia & metaplasia???,basementmembthickening, bronchial wall fibrosis, inflammatorycells indicating inflammation & narrowed lumen.
* bronchialwallhassquamousmetaplasiaofluminal epithelium&hyperplasiaofepithelium
.

emphysema -
* Destruction of alveolar walls without fibrosis - loss of gas exchange surface area, loss of elasticity cause difficulty exhaling
* Enlarged air spaces
* Number of alveolar capillaries diminishes
* Deformed terminal & respiratory bronchioles & loss of septa - Permanent dilation of respiratory bronchioles & alveoli
.

asthma - Airway remodelling:
* Excess mucus production by goblet cell & glandular hypertrophy
* Bronchial wall oedema due to inflammatory exudate: eosinophil & mast cell accumulation
* Smooth muscle hypertrophy and fibrosis
* Luminal occlusion caused by muscle constriction, thickening of airway wall, increased smooth muscle mass

.
bronchiectasis:
* Permanent dilation of main bronchi & bronchioles
* Airways then dilate, as surrounding scar tissue (fibrosis) contracts
* Secondary inflammatory changes lead to further destruction of airways

.
RESTRICTIVE: - reduced lung parenchyma expansion & total lung capacity
Acute respiratory distress syndrome (ARDS):
* Acute inflammation of alveoli, heavily involving neutrophils, rapidly damages capillaries & epithelium =** diffuse alveolar damage** (DAD)
* uncontrolled inflammation
* (Acute onset of dyspnea & hypoxemia due to) vascular leakiness & loss/inactivation of surfactant affecting gaseous exchange
* accumulation of oedema fluid & hyaline membrane formation

.
Idiopathic Pulmonary Fibrosis (IPF):
* Stimulated fibroblasts deposit collagen & ECM excessively for an extended time
* Patchy interstitial fibrosis that worsens with time, subpleural & basilar fibrosis, referred to as usual interstitial pneumonia (UIP)
* reticular abnormalities
* Fibroblastic foci – become more collagenous & less cellular
* Cause collapse of alveolar walls & formation of cystic spaces =honeycomb fibrosis

.
Pneumoconiosis
* Immune response stimulated by particles/macrophages travelling in lymphatics
* Lesions consist of pigmented/pale nodules of particle-laden macrophages & dense collagen
* compressed alveoli & congested capillary

• Silicosis - cleft-like spaces contain silica particles. Under microscope, silicotic nodule show hyalinized collagen fibers in whorled arrangement surrounding an amorphous center. The “whorled” appearance of collagen fibers is quite distinctive for silicosis. As disease progress, individual nodules may coalesce into hard, collagenous scars, with eventual progression to PMF. The intervening lung parenchyma may be compressed/overexpanded, a honeycomb pattern may develop. Fibrotic lesions also may occur in hilar lymph nodes & pleura
  .
• Asbestosis – Severe diffuse pulmonary interstitial fibrosis with disorganisation of lung architecture & numerous asbestos bodies visible (asbestos fibers coated with iron-containing proteinaceous material) & pleural plaques. In contrast with CWP & silicosis, asbestosis begins in lower lobes & subpleurally, spreading to middle & upper lobes of lungs as fibrosis progresses. Contraction of fibrous tissue distorts normal architecture, creating enlarged air spaces enclosed within thick fibrous walls; eventually, the affected regions become honeycombed. Simultaneously, fibrosis develops in visceral pleura, causing adhesions between lungs & chest wall. The scarring may trap & narrow pulmonary arteries and arterioles, causing pulmonary hypertension & cor pulmonale
  .
• coal worker’s pneumoconiosis (CWP):
  coal macules & larger coal nodules visible in simple CWP; severe CWP/Progressive Massive Fibrosis show coalescence/aggregation of coal nodules & generally develops over many years. It is characterized by multiple dark black scars larger than 2 cm consisting of dense collagen & pigment

Question 91

diagnosis of obstructive & restrictive lung disease?

restrictive FEV1/FVC ratio?

Answer 91

emphysema:
Pulmonary function tests reveal reduced FEV1 with normal/near-normal FVC. so FEV1 to FVC ratio is reduced
.
asthma
.
chronic bronchitis:
.
bronchiectasis:
diagnosis depends on appropriate history and radiographic demonstration of bronchial dilatation. It is not a primary disorder, as it always occurs secondary to persistent infection/obstruction caused by a variety of conditions
.
Idiopathic Pulmonary Fibrosis:
radiologic and histologic pattern of fibrosis is referred to as usual interstitial pneumonia (UIP), which is required for the diagnosis of IPF
.
Asbestosis :
marked by diffuse pulmonary interstitial fibrosis , characterized by the presence of asbestos bodies, which are seen as golden brown, fusiform or beaded rods with a translucent center

Question 92

resp failure & VQ mismatch

Describe alveolar-blood gas diffusion and partial pressures for O2 and CO2 exchange (in mmHg and/or kPa).
.
Describe factors that influence gas exchange in health (including exercise) and in disease states:
* Influential factors (Fick’s principle)
* Ventilation-perfusion VQ matching
.
Explain the effect of gravity on Ventilation and Perfusion and the VQ ratios from lung apex to base
.
Explain how VQ is controlled and the effect of increased and decreased VQ matching on partial pressures
.
Define Respiratory Failure, describe main causes and explain clinical examples arising from these causes