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LSS 1 - Thorax anatomy, Respiratory and Circulatory system > RS Lecture 9 and 10 - Acid Base Regulation and Sensory Aspects of Respiratory Disease > Flashcards

RS Lecture 9 and 10 - Acid Base Regulation and Sensory Aspects of Respiratory Disease Flashcards

1
Q

What is alkalaemia?

A

Raised pH of blood

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2
Q

What is acidaemia?

A

Lowered pH of blood

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3
Q

What is alkalosis?

A

Describes circumstances that will decrease [H+] and increase pH

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4
Q

What is acidosis?

A

Described circumstances that will increase [H+] and decrease pH

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5
Q

What is the main equilibrium in the body?

A

H2O+CO2 H2CO3 H+ + HCO3-

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6
Q

What is the blood’s buffering capacity?

A

It is huge and reacts almost immediately to imbalances

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7
Q

What is the equation for pH and [H+]?

A

pH= –log10[H+] [H+]= 10^-pH

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8
Q

What are the 2 types of acids in the body?

A

Respiratory acid (CO2) and metabolic acid (pyruvic acid, etc)

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9
Q

What is the Henderson equation and the Henderson-Hasselbalch equation?

A
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10
Q

What can we tell from an arterial blood gas sample?

A

Changes in pH, PaCO2, PaO2, BE

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11
Q

What are the values for PaO2 in the blood?

A

>10kPa is normal, 8-10 mild hypoxaemia, 6-8 moderate hypoxaemia, and

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12
Q

What are the 2 compensatory mechanisms?

A

Changes in ventilation can stimulate a RAPID compensatory response to change CO2 elimination and thus alter pH. Changes in HCO3- and H+ retention/secretion in kidneys can stimulate a SLOW compensatory response to increase/decrease pH

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13
Q

How can you compensate acidosis/alkalosis?

A

Acidosis needs alkalosis. Alkalosis needs acidosis.

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14
Q

What are the 2 compensatory mechanisms for respiratory acidosis?

A

Acute: CO2 moves into RBC , to combine with H2O to from H+ and HCO3- which is transported via the AE1 transporter into the blood, where they join with the excess H+ to form conjugate acid, increasing pH Chronic: Increasing reabsorption of HCO3- in the nephron

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15
Q

How is metabolic alkalosis compensated for (graph)?

A
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16
Q

How is metabolic acidosis compensated for (graph)?

A
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17
Q

How is respiratory alkalosis compensated for (graph)?

A
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18
Q

How is respiratory acidosis compensated for (graph)?

A
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19
Q

What are the 4 basic disturbances and what do they cause?

A

Hypoventilation -> respiratory acidosis. Hyperventilation -> respiratory alkalosis. Diarrhoea -> metabolic acidosis. Vomiting -> metabolic alkalosis

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20
Q

How do you interpret ABG?

A

Type of imbalance (alkal/acidaemia); aetiology of imbalance (respiratory, metabolic or mixed); homeostatic compensation present (UC, PC, FC); oxygenation (hypoxaemia, normoxaemia, hyperoxaemia)

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21
Q

What are the normal values of [Hb], pH, PCO2, PO2, HCO3-, BE and standard BE?

A
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22
Q

How do you interpret blood gases? -> chart

A
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23
Q

Work out these acid-base problems:

A
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24
Q

What is the prevalence of cough, chest pain and shortness of breath as respiratory symptoms?

A

Cough -> 3rd most common complaint heard by GP. Chest pain -> most common pain for which medical attention is sought. SOB: 6-27% of general popn; 3% of visits to GP

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25
Q

What are some signs and symptoms that can be seen in respiratory diseases?

A

Symptoms: cough, chest pain, shortness of breath. Signs: hyperinflation of chest, dullness on percussion of chest wall, increased resp rate, reduced movement of chest wall

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26
Q

What is the physiologic/pathologic stimulus leading to conscious sensation pathway?

A

Sensory stimulus -> transducer (sensor) -> excitation of sensory nerve -> integration of CNS -> sensory impression (neurophysiology) => sensory impression -> perception -> evoked sensation (behavioural psychology)

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27
Q

What is a cough?

A

Crucial defense mechanism protecting the LRT from inhaled foreign material and excessive mucous secretion

28
Q

When does a cough occur?

A

Secondary to mucociliary clearance (usually), but is important in lung disease when mucociliary function is impaired and mucous production is increased

29
Q

What is the function of the expulsive phase of cough?

A

Generates high velocity of airflow, which is facilitated by bronchoconstriction and mucus secretion

30
Q

Where are cough receptors located and what are they?

A

Nerve profile - rapidly adapting irritant receptors; located within airway epithelium, most numerous on posterior wall of trachea -> present at main carina and branching points of large airways, less numerous in more distal airways, absent beyond bronchioles -> possibly in pharynx, external auditory meatus, eardrums, paranasal sinuses, diaphragm, stomach, pleura, pericardium

31
Q

What is the stimuli for cough receptors?

A

Laryngeal and tracheobronchial receptors respond to chemical and mechanical stimuli

32
Q

What are the 3 types of sensory receptors in the lung and airways?

A

Slowly adapting stretch receptors, rapidly adapting stretch receptors and C-fibres

33
Q

What are c-fibre receptors?

A

Free nerve endings -> small unmyelinated fibres

34
Q

Where are c-fibre receptors located?

A

Larynx, trachea, bronchi, lungs

35
Q

What stimulates C-fibres and what do they release in response?

A

Stimulates: chemical irritants, inflammatory mediators. Release: neuropeptide inflammatory mediators Substance P, neurokinin A, calcitonin gene related peptide

36
Q

Where are the rapidly adapting stretch receptors present and what are they?

A

Naso-pharynx, larynx, trachea, bronchi -> small myelinated nerve fibres

37
Q

What stimulates the rapidly adapting stretch receptors?

A

Mechanical, chemical irritant stimuli and inflammatory mediators

38
Q

Where are the slowly adapting stretch receptors present and what are they?

A

In airways smooth muscle, predominantly in trachea and main bronchi -> myelinated nerve fibres

39
Q

What stimulates the slowly adapting stretch receptors?

A

They are mechanoreceptors so respond to lung inflation

40
Q

What are the 2 types of receptors innervating the trachea and what do they react to?

A

Mechanoreceptors (mechanical displacement, citric acid) and Nociceptors (Capsaicin, bradykinin, citric acid, cinnamaldehyde)

41
Q

What are the afferent neural pathways for cough?

A

Stimulation of irritant receptors or cough receptor by mechanical or chemical stimuli

42
Q

What is the cough pathway?

A
43
Q

What are the mechanics of cough?

A

Inspiratory phase -> glottic closure -> expiratory phase (sound)

44
Q

How do the sounds of cough form?

A

2 phases with initial explosive phase that is the first cough sound, followed by an intermediate phase with decreasing sound -> additional 3rd phase called the voiced/glottal phase gives rise to second cough sound

45
Q

What are the common causes of cough?

A
46
Q

What is an acute cough caused by and what are some symptoms associated with it?

A

Caused by common cold - present for cough, post nasal drip, throat clearing, nasal blockage/discharge

47
Q

What is a chronic persistent cough caused by?

A

> 3wks -> asthma/eosinophilic related (25%), Gastro-oesophageal reflux (25%), rhinosinusitis (20%), chronic bronchitis (8%), bronchiectasis (5%), drugs (ACE inhibitor 1%), post-viral (3%), idiopathic (10%), others (3%)

48
Q

What is chronic cough?

A

Indication of increased cough reflex -> cough hypersensitivty syndrome -> irritation in the throat/upper chest, cough paroxysms difficult to control (not throat clearing)

49
Q

What triggers cough hypersensitivity syndrome to cough?

A

Deep breath, laughing, talking too much, vigorous exercise, smells, cigarette smoke, eating crumbs, cold air, lying flat

50
Q

What is plasticity of neural mechanisms?

A

Excitability of afferent nerves increased by chemical mediators, increase in receptor/VGC’s, NT increase

51
Q

What are the mechanisms of chronic cough?

A

x

52
Q

What are the current antitussive types?

A

Symptomatic suppressant therapies, disease-specific therapies

53
Q

What are some examples of symptomatic suppressant therapies for antitussives?

A

Central action: opiates -> dihydro/phol/codeine, dextromethorphan (dia/morphine). Peripheral action: eosinophil-associated -> inhaled corticosteroids; GORD -> H+ pump inhibitors, H2 antagonists; post-nasal drip -> topical steroids, antihistamines; bronchiectasis -> postural drainage, Ab

54
Q

How do we manage cough hypersensitivity syndrome?

A

As sensory neuropathic cough -> Speech pathology management: ^ voluntary control, decrease cough sensitivity/laryngeal irritation/laryngeal muscle contraction; Pharmacology -> amitryptiline, gabapentin, opiates

55
Q

What is the sensory input to the lungs, airway and chest wall?

A

Nose (CNV), pharynx (CNIX/X), larynx/lungs (CNX), chest wall (spinal nerves)

56
Q

How does pain sensation reach the brain?

A

NB: the nerves change sides in the dorsal horn (contralateral)

57
Q

How does touch sensation reach the brain?

A

NB: the nerves change sides in the medulla

58
Q

What are the different types of pain?

A

Visceral pain is difficult to localise, diffuse and referred to somatic structures. Somatic pain is like that from skin. Much less number of visceral afferents than somatic

59
Q

What can cause chest pain in the respiratory system?

A

Pleuropulmonary disorders: pleural inflammation, pneumothorax, malignancy. Tracheobronchitis -> infections, inhalation of irritants. Inflammation or trauma to chest wall -> Rib fracture, muscle injury, malignancy, herpes zoster.

60
Q

Where does diaphragmatic irritation refer to?

A

Shoulder tip

61
Q

What non-respiratory disorders can cause chest pain?

A

CVD: myocardial infarction, pericarditis, dissecting aneurysm, aortic valve disease. GID: oesophageal rupture, GORD, cholecystitis, pancreatitis. Psychiatric disorders: panic disorder, self-inflicted

62
Q

What is dyspnoea?

A

Shortness of breath, occurring at inappropriately low levels of exertion and limits exercise tolerance

63
Q

What is the clinical dyspnea scale?

A
64
Q

What is the modified Borg scale?

A
65
Q

What are the 3 types of breathlessness?

A

Air hunger, work/effort and tightness

66
Q

Which disorders present with dyspnoea?

A

Impaired pulm function (airflow obstruction, restriction of lung mechanics, extrathoracic pulmonary restriction, NM weakness, gas exchange abdnormalities); imparied CV function (Myocardial disease leading to HF, valvular/pericardial /pulm vascular/ congenital vascular disease); altered central ventilatory drive/perception (systemic/metabolic disease, metacidosis, anaemia)

67
Q

How do you treat dyspnoea?

A

Treat the cause, therapeutic options: add bronchodilators, drugs affecting brain, lung resection, pulmonary rehabilitation

LSS 1 - Thorax anatomy, Respiratory and Circulatory system (27 decks)

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