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Medicine 2 > RCM Week 2 (COPD) > Flashcards

RCM Week 2 (COPD) Flashcards

1
Q

What are the 2 types of chemoreceptors

A

Central chemoreceptors: (CCRs) found on the medulla- sensitive to changes in [H+] and pCO2

Peripheral chemoreceptors (PCRs) found within the aortic arch and carotid arteries - sensitive to changes in arterial pO2 and pH

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2
Q

Describe the structure of the central chemoreceptor

A

Blood vessel is surrounded by BBB (blood brain barrier) which is impermeable to H+ and HCO3- but permeable to CO2
- increase in pCO2 causes CO2 to diffuse out of the blood vessel
H+ ions are formed from the reaction

  • increase in [H+] in the ECF and CSF is detected by CCRs and leads to hyperventilation
  • hyperventilation decreases pCO2 in the blood and CSF
  • decrease in pCO2 = hypoventilation
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3
Q

Describe the structure of peripheral chemoreceptors

A

Found within the aortic arch and carotid arteries

  • decreased arterial O2- hyperventilation (stimulated when arterial pO2 falls below 13.3 kPa)
  • increased pCO2- not as important as the CCR response
  • fall in pH- detected by carotid and not aortic bodies
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4
Q

What is respiratory acidosis (due to hypoventilation)

A

Increase in CO2 which will then have an effect on the pCO2 in arterial blood
- leads to an increase in [H+] and then an acidic environment

This is responded to by the kidneys that excrete excess [H+] in the urine but also increase bicarbonate which acts as a buffer to correct imbalance

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5
Q

What is metabolic acidosis

A

A decrease in the ability of the kidneys to excrete H+ and reabsorb HCO3 (due to uncontrolled diabetes)
So an increase in H+, decrease in pH
This is resolved by hyperventilating to try and decrease the levels of CO2

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6
Q

What is metabolic alkalosis

A

Caused by vomiting or ingesting a base

- increase in bicarbonate ions, decrease in [H+] and increase in pH

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7
Q

What is the difference in terms of sensitivity of central chemoreceptors and peripheral chemoreceptors

A

Central chemoreceptors- are most sensitive to pCO2 changes- levels held to within 0.3 kPa

Peripheral chemoreceptors will detect rapid changes in pCO2 but are comparatively insensitive - levels held to within 1.3 kPa

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8
Q

What detects pO2 and why is it important

A

Peripheral chemoreceptors detect changes in pO2
PO2 levels have a wider control margin but PCRs are stimulated when pO2 levels drop below 13.3 kPa

PO2 levels are controlled to avoid hypoxia

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9
Q

What is the purpose of neural regulation of ventilation

A

Sets the rhythm and pattern of ventilation

Controls the respiratory muscles

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10
Q

What is the purpose of chemical regulation of ventilation

A

Detects central and peripheral arterial pCO2 and pH and peripheral pO2

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11
Q

Why is neural regulation faster than chemical regulation

A

Neural control is dependent on fast acting impulses to and from the CNS.
Chemical control responds to changes in partial pressure of CO2 / O2

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12
Q

What is respiratory depression

A

The rate and / or depth of respiration is insufficient to maintain adequate gas exchange in the lungs
Occurs as a result of effects on the medullary and pons respiratory centres

Some drug side effects eg benzodiazepines, opioids can cause respiratory depression - can be reversed by analeptics eg doxapram hydrochloride

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13
Q

What is the role of the dorsal respiratory group (DRG)

A

Fibres from DRG innervated the diaphragm and external intercostal muscles.

  • diaphragm contraction and thoracic cavity expansion causes inspiration
  • DRG neurons switch on for 2 seconds and switch off for 3 seconds causing a rhythmic pattern
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14
Q

What is the role of the ventral respiratory group (VRG)

A

Fibres from VRG innervated the abdominal muscles and internal intercostal muscles
- activity enhanced during forced expiration

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15
Q

What is the role of the pneumotaxic centre

A

Transmits signals to the DRG

  • role is to limit inspiration
  • ‘fine tunes’ breathing - sends inhibitory impulses to the DRG
  • limits the period of inspiration to 2 seconds
  • prevents over inflation of the lungs
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16
Q

What is the role of the apneustic centre

A

Responsible for prolonged inspiration gasps (apneusis)

  • prolongs DRG stimulation
  • not clear on involvement in normal human respiration
  • apneusis observed in severe brain injury
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17
Q

What is the role of the vagus nerve

A

Sends afferent information from the lungs to the DRG

- role is to prevent over inflation of the lungs by switching off inspiration

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18
Q

Summary of the functions of the different elements of the respiratory control system

A

DRG- inspiration
VRG- forced expiration
Pneumotaxic centre- switch off inspiration
Apneustic centre- prolongs DRG stimulation (inspiration)
Vagus nerve - switch off inspiration

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19
Q

What is the role of the cerebral cortex

A

Stimulates motor neurons of the inspiratory muscles
Bypasses the medullary centres when consciously controlling breathing eg breath holding or changing the depth of breathing

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20
Q

What is the role of the hypothalamus

A

Strong emotions, pain and changes in temperature can alter respiration rate and rhythm
- apnoea : suspension of breathing - can be induced by a germ pain or a decrease in temperature

Tachypnoea: rapid breathing- can be induced by excitation or an increase in temperature

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21
Q

What are stretch receptors

A

Located in smooth muscle of trachea and bronchi

Sensitive to lung expansion

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22
Q

What are respiratory reflexes

A

Juxtapulmonary aka J or C fibre receptors

  • lie in alveolar wall between the epithelium and endothelium - close to the pulmonary capillaries
  • stimulated by congestion, oedema, histamine
  • activation results in apnoea or rapid shallow breathing, bronchoconstirction and mucus secretion
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23
Q

What are irritant receptors

A

Located between epithelial cells

  • sensitive to irritant gases, smoke and dust
  • activation results in rapid shallow breathing cough, bronchoconstriction, mucus secretion and augmented breaths (gasps)
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24
Q

What does stimulation of different respiratory receptors affect

A

Stimulation of receptors in the bronchioles- airways constrict (asthma)

Stimulation of receptors in the trachea and bronchi - coughing

Stimulation of receptors in the nasal cavity - sneezing

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25
Q

What happens during exercise

A

Increase in pulmonary ventilation rate

At rest = 6 l/min
During exercise can reach 120 l/min

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26
Q

How do you calculate pulmonary ventilation rate

A

Freq / resp rate x tidal volume

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27
Q

What happens in initial stage o exercise ( rapid increase in ventilation )

A

Attributed to motor centre activity and afferent impulses from proprioceptors of the limbs, joints and muscles

Neural control- activates the respiratory centres in the brain

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28
Q

What adaptations happen during exercise

A
  • increased blood flow to muscles, increased cardiac output, increased oxygen consumption
  • decreased pH and increased temp, unloading O2 from blood into muscle
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29
Q

Effects of altitude on the body

A
  • hypoxia - reduction in barometric pressure
  • loss of appetite
  • changes in mental performance
  • insomnia
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30
Q

Role of peripheral chemoreceptors

A

Detect acute hypoxia and then try to increase breathing

As ventilation increases, PaCO2 falls and cerebrospinal fluid becomes alkaline and system is trapped :
Breathe more = die from alkalosis
Don’t breathe more = die from hypoxia

31
Q

Adaptations to high altitude

A

Mild hypoxia = decreased PO2, increased ventilation, decreased PCO2

Decreased PCO2= increased CSF pH (alkaline), increased HCO3-

Choroid plexus cells export HCO3- from CSF to correct pH
Hypoxic drive is reinstated and ventilation increases further

Breathing is controlled around lower PCO2, increased ventilation from hypoxic drive (over a couple of hours)

Over a couple of days the alkalinity of blood is corrected by excretion of HCO3- in urine

32
Q

Adaptations to high altitude (chronic exposure)

A

Oxygen carrying capacity of blood is increased with adaptations like 2,3 DPG and polycythaemia

Cardiac output is increased and directed to vital organs

Systemic acid-base imbalance is corrected

33
Q

Describe the increase in pressure when scuba diving

A

Scuba diving increase in pressure

At 33 feet (10.1 metres) pressure is exerted by weight from the atmosphere above sea level as well as pressure from the weight of the water so at 33 feet = 2 atm pressure = 200kPa (sea level- 101 kPa)

34
Q

Effects of diving exposure on the body

A

Gases physiologic at sea level can be harmful at depth

Oxygen partial pressure increases at depth- breathing air at a depth of 40m is equivalent to breathing 100% oxygen at seal level (hyperoxia)

Nitrogen is insoluble at sea level but soluble at depth

  • nitrogen narcosis or rupture of the deep during descent
  • decompression sickness during ascent (excruciating pain)
35
Q

Summary of lung function at depth

A

Increase in FVC- does the repeated exposure to breathing ‘dense’ gas lead to the training effect on the respiratory muscles

  • loss of lung function : is this due to continued exposure to increased levels of oxygen and nitrogen leading to hyperoxia and decompression stress

Effects on susceptible individuals eg asthma: inconclusive findings with some reporting significant deterioration in spirometry measurements and others reporting no differences

36
Q

What are the causes of breathlessness

A

Respiratory:

  • asthma: reversible
  • COPD
  • pneumonia
  • COVID 19
  • lung cancer
  • interstitial lung disease

Cardiovascular:

  • heart failure: pulmonary oedema
  • pulmonary embolism
  • AF

Others:

  • functional breathlessness eg due to obesity
  • anaemia : need for a full blood count
37
Q

What is the significance of different colours of sputum

A

Colour signifies WBC
Green shows an abundance of neutrophils
Patient knows what is normal for them eg if they have chronic lung disease and so should monitor any changes but ensure they are not constantly taking antibiotics as green sputum can be normal

38
Q

Causes of a cough

A
  • coryza- a cold
  • acute bronchitis
  • tracheitis - a dry rasping and painful cough which is often associated with a viral infection
  • pneumonia
  • COPD
  • asthma : wheezing and breathlessness, often a nocturnal cough (particularly in a child)
  • drug induced eg ACE inhibitors
39
Q

Any other conditions that have similar symptoms to COPD that would also be considered when diagnosing

A

Chronic lung disease
Heart failure
Asthma
Fibrosis

40
Q

How relevant is age to making a diagnosis of COPD

A

Be aware of COPD in patients over the age of 40 presenting with a relevant trigger eg smoking, occupational

41
Q

What is the difference between bronchiectasis and COPD

A

Bronchiectasis is a pathological situation that develops when the bronchi become like pockets in the lung - less functioning - cilia are damaged so sputum collects in pores in the lungs - higher chance of it becoming infected so patients have to be taught different ways to expel sputum eg going for a walk, postural drainage

42
Q

Alerting symptoms for COPD

A
  • cough >3 weeks
  • a history of smoking associated with haemoptysis (coughing up blood)
  • a change in ‘smokers cough’ is a serious alerting symptom
43
Q

Describe the types of wheezes that may be shown on examination

A

Polyphonic - multiple frequency of sounds - affects the bronchi of all different calibres and can be heard throughout the lung
Monophonic - one frequency, one tone - due to a narrowing of one specific bronchi can be due to a foreign body or a cancer

44
Q

What are normal O2 sats for a patient with COPD

A

Lower than 92% may be considered for oxygen therapy as long as they have stopped smoking

45
Q

For measurements of FVC and FEV1 at what point would you consider the % of the predicted value to be low

A

In COPD, peak flow is often low but stable unlike asthma where it fluctuates

Usually FEV1 below 80%, below 50% is severe and below 30% is very severe

46
Q

Why may a patient have stained fingers

A

Nicotine staining - smoker

47
Q

What is the difference between emphysema and chronic bronchitis

A

Emphysema is alveolar destruction- not directly detected on any lung function or chest X-ray it is detected on a CT scan

Bronchitis is a physiological diagnosis by nature of productive sputum for more than 3 months in 2 consecutive years - history based diagnosis

48
Q

Causes of COPD in patients that haven’t smoked

A

Household air pollution- particularly in low income countries where they cook over an open fire

Occupation- more exposure to gases/ pollution

Air pollution

49
Q

What is eGFR

A

Estimated glomerular filtration rate

The best test to measure level of kidney function and determine stage of kidney disease

50
Q

What vaccinations would be recommended for a patient with COPD

A

Influenza on an annual basis
One off pneumococcal
Covid vaccine when offered

51
Q

Are mucolytics given to every patient with COPD

A

Are of value to some patients with COPD: the ones that produce thick and tenacious phlegm (sticky, having to pull out)
Mucolytics make this more liquidy

52
Q

Is there evidence that e cigarettes can be harmful towards patients

A

Full of chemicals, not clean, fresh air

Likely in the majority to be better than cigarettes in terms of carcinogens

Should not be encouraged but could be used to help someone quit smoking - cuts down nicotine and tobacco - would still be encouraged to come off e cigarettes as can cause lung reaction, still contain nicotine and contain chemicals that we don’t know much about

53
Q

What are the cardiovascular adaptations to exercise

A

Myocardial contractile force

Cardiac acceleration

Peripheral vasoconstriction

Activation of sympathetic nervous system

54
Q

Why do skeletal muscle contract

A

Compresses blood vessels

Blood is translocated from peripheral vessels into heart and lungs

Increased cardiac output

55
Q

What happens in acute exposure of inadequate delivery of oxygen to body tissues

A

Acute hypoxia is detected by peripheral chemoreceptors which try to increase breathing

As ventilation increase, PaCO2 falls and cerebrospinal fluid (CSF) becomes alkaline

System is trapped because breathe more = die from alkalosis, don’t breathe more = die from hypoxia

56
Q

What happens in chronic exposure to inadequate delivery of oxygen to body tissues

A

Mild hypoxia
Choroid plexus cells export HCO3- from CSF as a pH correction mechanism

Hypoxia drive is reinstated and ventilation increases further

Hours P breathing is controlled around lower PCO2, ventilation from hypoxic drive
Days P alkalinity of blood is corrected by excretion of HCO3- in urine.

57
Q

What is boyles law

A

P u 1/V

Pressure is inversely proportional to volume at a constant temperature

58
Q

What happens in terms or respiration on descent

A

Body and equipment occupy a smaller volume (compress)

Compress air in lungs, gut, sinuses and middle ear

Valsalva manoeuvre

59
Q

What happens in terms of respiration on ascent

A

Body an equipment occupy a larger volume (expand)

Expand air in lungs, gut, sinuses and middle ear

Release air from buoyancy control device

60
Q

Respiratory consequences of diving - nitrogen

A

Air = 79% N2 which is poorly soluble at sea level pressure
Increased pressure in diving causes more N2 to dissolve in the body

Descent: N2 dissolves in Body
Nitrogen narcosis
Euphoria, drowsiness, weakness, clumsiness, unconsciousness

Ascent: already dissolves N2 comes out of solution and forms N2 gas bubbles
Decompression sickness
Excruciating pain, fatigue

61
Q

Consequences of space flight

A

Weightlessness is characterised by zero gravity
Puffy face and bird legs

Acute: motion sickness with nausea and vomiting
Chronic: - in blood volume, - in cardiac output, - in red blood cell mass, - in muscle strength
Loss of Ca2+ and PO43- from bones

62
Q

What happens on return to earth after space flight

A

Orthostatic hypotension - cardiovascular system not used to responding to gravity hence dizziness, fainting etc may be experienced

Due to the fact that baroreceptor reflexes (maintains blood pressure) are down-regulated due to lack of use in space

63
Q

What are the steps of cheyne- stokes

Occurs in individuals with CNS diseases, head trauma, intracranial pressure, heart failure

A

1) Over breathing = removal of excess CO2 from pulmonary blood and increased O2
2) takes several seconds for message on change in pulmonary blood to get to the brain and inhibit excess ventilation
3) person is overventilated for the extra few seconds
4) overventilated blood eventually gets to the respiratory centres causing their depression
5) opposite cycle commences resulting in CO2 increase and O2 decrease

64
Q

What is respiratory depression

A

The rate and / or depth of respiration is insufficient to maintain adequate gas exchange in the lungs

  • occurs as a result of the effects on the medullary and pons respiratory centres
  • some drug side effects can cause respiratory depression eg benzodiazepines, opiods)
  • respiratory depression reversed by analeptics eg doxapram hydrochloride
65
Q

What is the dorsal respiratory group

A

Fibres from DRG innervate the diaphragm and external intercostal muscles

Diaphragm contraction and thoracic cavity expansion causes inspiration

DRG neurons switch on for 2s and switch off for 3s causing a rhythmic pattern

66
Q

What is the ventral respiratory group

A

Fibres from VRG innervate the abdominal muscles and internal intercostal muscles
Activity enhanced during forced expiration

67
Q

What is the pneumotaxic center of the respiratory control system

A 
Transmits signals to the DRG 
Role is to limit inspiration 
Fine tunes breathing - sends inhibitory impulses to the DRG 
Limit the period of inspiration to 2s
Prevents over inflation of the lungs
68
Q

What is the apneustic centre of the respiratory control system

A

Responsible for prolonged inspiratory gasps (apneusis)
Prolongs DRG stimulation
Not clear on involvement in normal human respiration
Apneusis observed in severe brain injury

69
Q

What is the role of the cerebral cortex

A
  • stimulates motor neurons of the inspiratory muscles
  • bypasses the medullary centres when consciously controlling breathing eg breath holding
  • limited ability to breath hold- respiratory centres automatically reinitiate breathing when O2 conc in the blood reach critical levels
  • drowning victims eventually reinstate breathing with the result of water in the lungs
70
Q

What is the role of the hypothalamus

A

Strong emotions, pain and changes in temperature can alter the respiration rate and rhythm

  • apnoea (suspension of breathing) can be induced by anger, pain, or decrease in temperature
  • tachypnoea (rapid breathing) can be induced by excitation, or increase in temperature
71
Q

What are stretch receptors

A

Located in smooth muscle of trachea and bronchi
Sensitive to lung expansion
Prevent over inflating of the lungs

72
Q

What are irritant receptors

A

Located between epithelial cells
Sensitive to irritant gases, smoke and dust
Activation results in rapid shallow breathing, cough, bronchoconstriction, mucus secretion, augmented breaths

73
Q

What factors influence the rate and depth of breathing

A
  • pulmonary (and non pulmonary) irritant reflexes are stimulated by activation of receptors that repsond to irritants in the lungs eg accumulated mucus, inhaled smoke, dust, lint or noxious fumes
  • irritant receptors send signals to the respiratory centres via afferent fibres of the vagus nerve
  • stimulation of receptors in the bronchioles - airways constrict (asthma)
  • stimulation of receptors in the trachea and bronchi - coughing
  • stimulation of receptors in the nasal cavity - sneezing
74
Q

What do you need to include when counselling a patient for a drug

A 
What the medicine is for 
When to take 
How to take 
Dose
Frequency 
Key side effects 
What to do if miss a dose 
How long for treatment

Medicine 2 (16 decks)

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