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Medicine YEAR 1 > Phase 1 - Week 8 (Respiratory System, Asthma), Phase 3 - Week 4 (Pneumothorax), Phase 3 - Week 5 (Spirometry, COPD) > Flashcards

Phase 1 - Week 8 (Respiratory System, Asthma), Phase 3 - Week 4 (Pneumothorax), Phase 3 - Week 5 (Spirometry, COPD) Flashcards

1
Q

List the functions of the respiratory tract

A
  1. Ventilation
  2. Gas exchange
  3. Blood pH
  4. Air preparation
  5. Vocalisation
  6. Olfaction
  7. Protection + defense
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2
Q

List the sections of the respiratory tract

A
  1. Nose/mouth
  2. Pharynx
  3. Larynx
  4. Trachea
  5. Primary bronchi
  6. Secondary (lobar) bronchi
  7. Tertiary (segmental) bronchi
  8. Conducting bronchioles
  9. Terminal bronchioles
  10. Respiratory bronchioles
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3
Q

Pharynx

A
  • Muscular tube lined with mucous membrane

- Joins nasal + oral cavities to oesophagus and larynx

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4
Q

List the parts of the pharynx

A
  1. Nasopharynx
  2. Oropharynx
  3. Laryngopharynx
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5
Q

Nasopharynx

A
  • Nasal cavity -> oropharynx
  • Separated from oral cavity by soft palate
  • Receives Eustachian tubes (auditory/pharngotypanic) from inner ear
  • Contains pharyngeal tonsils - protect against inhaled pathogens
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6
Q

Oropharynx

A
  • Between soft palate + upper border of epiglottis - posterior to oral cavity + tongue
  • Contains palatine, pharyngeal + lingual tonsils
  • Palatine = 2 masses of lymphatic tissue, posterior oral cavity between glossopalatine + pharyngopalatine arches
  • Pharyngeal = patch of lymphatic tissue in posterior wall of nasopharynx, most prominent in children, atrophies from 7 y/o onwards
  • Lingual = posterior surface of tongue
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7
Q

Laryngopharynx

A
  • Behind larynx

- Terminates to level of cricoid cartilage (becomes continuous w/ oesophagus)

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8
Q

Larynx

A

Cartilaginous, made of:

  • Thyroid cartilage
  • Cricoid cartilage
  • Epiglottis
  • Arytenoid cartilage
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9
Q

Trachea

A
  • Begins at C6, below cricoid cartilage of larynx
  • Descends through thorax
  • Divides at T4 into 2 principal bronchi
  • C-shaped tracheal cartilage rings, anteriorly united by fibroelastic membrane, posteriorly by trachealis muscle
  • Lined w/ psuedostratified columnar epithelium with goblet cells - ciliated to transport mucus + inhaled particles of lungs - swallowed + neutralised by stomach
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10
Q

Corina

A

Thick, incomplate cartilaginous ring - runs between 2 primary bronchi at bifurcation of trachea

  • Directs air into principal bronchi during respiration
  • Most sensitive area of the trachea for triggering the cough reflex
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11
Q

Primary bronchi

A
  • Begin at T4 - L and R bronchi emerge as division of trachea
  • Similar structure to trachea - incomplete rings of cartilage anteriorly united by fibroelastic membrane
  • Travel obliquely to enter each lung through hilum - divide into smaller branches
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12
Q

Describe the structural differences between the left and right bronchi

A

Left = vertical, shorter, wider

Right = horizontal, longer, narrower

Obstruction more likely in left bronchi

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13
Q

Secondary (lobar) bronchi

A
  • Branches of principal bronchi

- Left = 2, Right = 3 (1 per lobe)

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14
Q

Tertiary (segmental) bronchi

A
  • Each serves specific bronchopulmonary segment
  • Left = 8, Right =10
  • Cartilaginous plates - not c-shaped
  • Branch into bronchioles
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15
Q

Describe the general structure of bronchioles

A

Composed of fibroelastic membrane and smooth muscle, usually don’t contain cartilage

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16
Q

Terminal bronchioles

A
  • No cartilage
  • Mostly smooth muscle
  • Branch into respiratory bronchioles
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17
Q

Respiratory bronchioles

A
  • Branch into alveolar ducts, have alveoli directly attached to them
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18
Q

Describe the location of the lungs

A

In the thoracic cavity, occupying most of the space around the mediastinum

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19
Q

Describe the structure of the lobes of the lungs

A 
Left = 2 lobes, superior + inferior
Right = 3 lobes, superior, middle and inferior
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20
Q

Describe the fissures of the lungs

A

Fissures = narrow depressions which separate the lobes

Right = oblique and horizontal fissures

Left = Oblique fissure

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21
Q

Describe the pulmonary circulation

A

2 pulmonary arteries from the heart supply the lungs (1 per lung) with deoxygenated blood and 4 pulmonary veins (2 per lung) return oxygenated blood to the heart

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22
Q

Describe the blood supply to the lungs

A

Lung tissue is supplied with oxygenated blood via the bronchial arteries - direct branch of the aorta. Bronchial veins drain deoxygenated from the lungs. Left bronchial vein drains into the hemizygous vein, right bronchial vein drains into the azygous vein.

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23
Q

Hilum

A

Triangular structure of the medial surface of the lung - primary bronchi and neurovascular structures enter and leave the lung here

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24
Q

List the regions of the lungs

A
  • Apex = tip, protrudes above clavicle
  • Base = inferior concave surface, rests on diaphragm
  • Hilum
  • Cardiac impression s = concavity on ateroinferior + medial surfaces of each lung where heart rests - larger on left lung
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25
Q

Describe the structure of the pleura

A
  • Double sheet of thin serous membrane
  • Each is a closed sac with the lung invaginated into it
  • Creates 2 layers - continuous at the hilum
  1. Visceral
  2. Parietal
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26
Q

Which anatomical landmark indicates the bifurcation of the trachea into the left and right primary bronchi?

A

Bifurcation occurs at the level of the sternal angle

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27
Q

Describe the mucociliary escalator

A
  • Trachea is lined by ciliated pseudostratified columnar epithelium
    • has goblet cells which produce mucin
  • Inhaled particles and pathogens become trapped in the mucus, which is swept up the airways by cilia
  • Mucus and trapped particles/pathogens are then swallowed
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28
Q

Describe the innervation of the trachea

A

Sensory info from the recurrent laryngeal nerve

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29
Q

Describe the vascular supply to the trachea

A
  • Arterial supply from tracheal branches of inferior thyroid artery
  • Venous drainage via brachiocephalic, azygous + accessory hemizygous veins
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30
Q

Describe the innervation of the bronchi

A

Pulmonary branches of the vagus nerve (CN x)

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31
Q

Describe the vascular supply to the bronchi

A
  • Arterial supply = bronchial arteries

- Venous drainage = bronchial veins

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32
Q

Conducting bronchioles

A
  • Branch from tertiary bronchi
  • For transport/direction of air
  • Don’t have glands
  • Not involved in gas exchange
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33
Q

Describe the innervation of the lungs

A
  • Derived from pulmonary plexus

- Sympathetic, parasympathetic + visceral afferent fibres

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34
Q

Describe the parasympathetic innervation of the lungs and its effect

A

Derived from the vagus nerve, stimulates secretion from bronchial glands, contraction of bronchial smooth muscle + vasodilation of pulmonary vessels

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35
Q

Describe the sympathetic innervation of the lungs and its effect

A

Derived from sympathetic trunks, stimulates relaxation of bronchial smooth muscles and vasoconstriction of pulmonary vessels

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36
Q

Describe role of the visceral afferent innervation of the lungs

A

Conducts pain impulses to sensory ganglion of the vagus nerve

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37
Q

What are alveoli?

A
  • Tiny-thin walled sacs with rich blood supply

- Site of gas exchange - high surface area

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38
Q

Describe the structure of the alveolar walls

A
  • One cell thick, capillaries are also one cell thick (gases diffuse across 2 cells)
  • Internal surface covered in alveolar fluid - allows gases to dissolve for diffusion. Contains surfactant.
  • Contain macrophages that phagocytose foreign particles
  • Wall composed of type I and II alveolar cells surrounded by epithelial basement membrane
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39
Q

Composition and function of surfactant

A

Rich in phospholipids and proteins that decrease surface tension in alveoli, preventing collapse of thin alveoli walls which are prone to collapse. Prevents alveoli from sticking together with each breath by keeping surface between cells and air moist.

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40
Q

Type I alveolar cells

A
  • Broad, simple squamous epithelial cells
  • Majority of cells lining walls of alveoli
  • Function = lie in a thin, single layer which allows from diffusion of gases across respiratory membrane
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41
Q

Type II alveolar cells

A
  • Cuboidal-shaped cells that line remaining space on walls of alveoli
  • Fewer in number that type 1 alveolar cells
  • Function = repair alveolar wall after damage + secrete surfactant.
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42
Q

Alveolar basement membrane

A
  • Epithelial basement membrane, thin extracellular membrane surrounding alveolar wall
  • Basal lamina + fibrous reticular lamina
  • Function = anchors alveolar cells to surrounding connective tissue
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43
Q

Describe the function of the interstitial space

A
  • Minute gap between cells and tissues
  • Filled with interstitial fluid, bathes surrounding cells
  • Function = allows diffusion of gases to occur across respiratory membrane
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44
Q

What is a serous membrane?

A

Layer of mesothelial cells, supported by connective tissue

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45
Q

Pleural cavity

A
  • Potential space between 2 layers of the pleura

- Contains small volume of serous fluid

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46
Q

Describe the function of the fluid in the pleural cavity

A
  • Lubricates surfaces of plurae, allowing them to slide over each other without friction
  • Produces surface tension - pulling parietal + visceral pleura together - ensures that when the thorax expands the lung also expands, filling w/ air
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47
Q

Parietal pleura

A
  • Covers internal surface of thoracic cavity

- Thicker than visceral pleura

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48
Q

Visceral pleura

A
  • Covers outer surface of lungs

- Extends into interlobar fissures

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49
Q

Pleural recesses

A
  • Anteriorly and posteroinferiorly pleural cavity is not entirely filled by lungs - produces recesses
  • 2 recesses in each pleural cavity
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50
Q

List the pleural recesses present in each pleural cavity

A
  1. Costodiaphragmatic = between costal pleurae + diaphragmatic pleura
  2. Costomediastinal - between costal pleurae and mediastinal pleurae, behind sternum
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51
Q

Describe the neurovascular supply to the parietal pleura

A
  • Sensitive to pressure, pain and temperature
  • Produces well localised pain
  • Innervated by phrenic + intercostal nerves
  • Blood supply from intercostal arteries
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52
Q

Describe the neurovascular supply to the visceral pleura

A
  • Not sensitive t pain, temperature or touch
  • Sensory fibres only detect stretch
  • Receives autonomic innervation from pulmonary plexus (sympathetic trunk + vagus nerve)
  • Arterial supply via bronchial arteries (branches of descending aorta), also supply parenchyma of lungs
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53
Q

What is the cough reflex?

A

Unlearned, automatic reflex mechanism of lungs to get rid of noxious harmful substances (protective reflex) - expels foreign material from lungs

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54
Q

What are the requirements of the cough reflex?

A
  • Large volume of air to clear foreign material
  • Fast flow rate of air - generation of large pressure gradient between lungs + atmosphere
  • A stimulus to irritate the lining of the airway - mechanical or chemical
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55
Q

Describe the mechanism of the cough reflex

A
  1. Rapid deep inspiration - brought about by contraction of diaphragm + external intercostal muscles
  2. Closure of glottis (vocal folds) - simultaneously, relaxation of inspiratroy muscles, contraction of expiratory muscles (internal intercostal + abdominal muscles)
  3. High intra-thoracic pressure generate - sudden opening of vocal cords, rapid expulsion of unwanted foreign material
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56
Q

Explain how the cough reflex is triggered

A
  • Pulmonary irritant receptors that detect stimulus -rapidly acting pulmonary stretch receptors, found mainly in pharynx + trachea
  • Afferent pathway - branches of vagus nerve -> medulla oblongata in brainstem of CNS (respiratory centre)
  • Efferent pathway - several - phrenic nerves, spinal motor nerves travel to effector muscles, laryngeal muscles, abdominal muscles
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57
Q

Define asthma

A

Common chronic disease primarily affecting the small conducting airways of the lungs. Causes intermittent episodes of reversible airway obstruction - treatment = removal of trigger + treatment w/ medication. Airway inflammation, airway hypersensitivity, airway obstruction.

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58
Q

How does asthma cause obstruction in the airways

A
  • Smooth muscle spasm in walls of small bronchi/bronchioles
  • Oedema of mucosa of airways
  • Increased mucus secretion
  • Damage to epithelium
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59
Q

Describe the pathogenesis of obstruction due to asthma

A
  • Mediators of inflammation (e.g. histamine, prostaglandin, leukotrienes, enzymes) - cause bronchial hyperesponsiveness + airway obstruction resulting in asthma symptoms
  • Bronchoconstriction increases responsiveness of bronchial smooth muscle
  • Hypersecretion of mucus - plugging of airways
  • Mucosal oedema (accumulation of interstitial fluid) leading to narrowing o fairway lumen, extravasation (force fluid out) of plasma in submucosal tissues due to leakage from vessels contributes to muscosal oedema
  • Infiltration of bronchial mucosa by eosinophils, masts cells, lymphoid cells + macrophages
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60
Q

List the classifications of asthma

A
  1. Extrinsic asthma (atopic)

2. Intrinsic asthma

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61
Q

Extrinsic (atopic) asthma

A

Early onset asthma triggered by environmental factors. Patients usually predisposed - family history of allergic diseases. IgE levels high, immediate hypersensitivity to allergen.

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62
Q

Intrinsic asthma

A

Adult onset, associated with chronic bronchitis and other asthma triggers e.g. cold, exercise. IgE level normal, no family history of allergic disorders.

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63
Q

List the triggers/causes of asthma

A
  1. Environmental exposure to allergen
  2. Viral infections
  3. Cold air
  4. Emotion
  5. Irritant dusts, vapour + fumes
  6. Genetic factors
  7. Drugs
  8. Atmospheric pollution
  9. Exercise
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64
Q

Give examples of common allergens associated with asthma

A

Grass pollen, domestic pets

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65
Q

Gives examples of viral infections associated with asthma

A
  • Rhinovirus

- Parainfluenzal virus

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66
Q

Give examples of drugs which can trigger symptoms of asthma

A
  • NSAIDs
  • Beta-adrenoceptors
  • Blocking agents
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67
Q

Give examples of pollutants in the atmosphere associated with asthma

A

Sulphuric dioxide, ozone

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68
Q

Why can exercise trigger asthma symptoms?

A

Due to release of histamine, prostaglandins (PGs) and leukotrienes from mast cells

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69
Q

List the symptoms of asthma

A
  • Breathlessness
  • Chest tightness
  • Wheezing - whistling noise during breathing
  • Cough
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70
Q

List the criteria used for diagnosis of asthma

A
  1. Presence of risk factors - family history, allergen exposure, atopic history, nasal polyps
  2. Recent upper respiratory tract infection
  3. Dyspnoea - difficult, laboured breathing, worse with allergen exposure, cold air etc.
  4. Cough
  5. Expiratory wheezes
  6. Nasal polyposis
  7. Spirometry tests
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71
Q

List the drugs used to treat asthma

A
  1. Short acting beta 2 agonists e.g. sulbutamol
  2. Long acting beta 2 agonists - salmeterol
  3. Antimuscarinic bronchodilators e.g. corticosteroids
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72
Q

Explain how corticosteroids work to treat asthma

A

Decrease airway inflammation (decrease oedema and mucus secretion)

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73
Q

List the types of inhalers used to treat asthma

A
  1. Reliever inhaler (blue)

2. Preventer inhaler (brown)

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74
Q

Describe the use of reliever inhalers

A
  • SABA - quick relief
  • Doesn’t decrease inflammation, (doesn’t help long term) only for quick relief of symptoms
  • E.g. salbutamol
  • Given to everyone with asthma
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75
Q

Describe the use of preventer inhalers

A
  • Work over time to reduce inflammation + sensitivity of airways, decrease risk of attacks
  • Used regularly (1/2 times daily) to control asthma
  • Contains inhaled corticosteroids e.g. beclomethasone
  • Used alongside LABA
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76
Q

Describe the use of LABAs to treat asthma

A
  • Long acting beta 2 agonist - take longer to act, effects last up to 12 hours (2 times daily = full coverage) e.g. salmeterol
  • Always taken with preventer - if alone it may allow condition to worsen while masking symptoms, increases chance of sudden asthma attack
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77
Q

List the stages of asthma

A
  1. Intermittent
  2. Mild persistant
  3. Moderate persistant
  4. Severe persistant
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78
Q

Intermittent asthma

A
  • Symptoms e.g. wheezing come and go
  • Symptoms < 1/2 times per week, nighttime awakening <2 per month
  • No interference with normal activity/lung function
  • Inhaler use < 3 days per week
  • Treatment = SABA only
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79
Q

Mild persistant asthma

A
  • Symptoms >2 days per week, not daily, 3-4 nighttime awakenings per month
  • Inhaler use > 2 days per week, not daily, not more than 1 per day
  • Minor limitation on normal activity
  • Treatment = SABA, long acting steroids (blue and brown inhalers)
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80
Q

Moderate persistant asthma

A
  • Daily symptoms, nighttime awakenings > 1 per week
  • Daily inhaler use
  • Some limitation on normal activity, decreased lung function
  • Treatment = low-dose steroid, LABA
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81
Q

Severe persistant asthma

A
  • Symptoms througout the day and nighttime awakening may be every night
  • Attacks severely limit normal activity
  • SABA required several times per day
  • Lung function severely decreased
  • Treatment = high does inhaled steroids, LABA
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82
Q

List examples of electrical signalling

A
  1. Between nerve cells

2. Stimulation of cardiac cells

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83
Q

Describe the movement of electrical impulses along nerve cells

A

When nerve is stimulated, a wave of altered charge (depolarisation, action potential) sweeps along the membrane of the nerve axon. The mechanism for charge changes = sequential opening and closing of ion channels in axon membrane.

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84
Q

Describe how electrical signalling stimulates cardiac cells

A
  • In pacemaker cells - Purkinje fibres. Ion movements across membrane carry charge signals (like nerves)
  • In myocytes - charge transmitted through gap junctions
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85
Q

Describe the mechanism by which ion-channel linked receptors allow for signalling between cells

A
  • Receptor is an ion channel
  • Binding of ligand to receptor causes conformational change that opens ion channel
  • Ion moves through channel along concentration gradient - inhibits action potential formation (depolarisation)
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86
Q

Give an example of signalling through ion-channel linked receptors and explain its mechanism of action.

A

Acetylcholine at the neuromuscular junction:

  1. Acetylcholine released from motor neurone
  2. ACh binds to ion-channel receptor on muscle cell, opens sodium channel
  3. Sodium ion entry causes depolarisation of muscle cell membrane and muscle contraction
  4. Acetylcholinesterase enzyme and reuptake transporter switch off the signal
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87
Q

Give examples of G-protein coupled receptors

A

Adrenaline (hormone), serotonin (neurotransmitter)

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88
Q

Explain the mechanism of action of G-protein-coupled receptors

A
  • Ligand binding to extracellular domain causes conformational change in cytoplasmic domain
  • Conformational change allows G-protein to bind receptor and be activated
  • Activated G-protein activates downstream enzymes
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89
Q

What are:

a) First messengers
b) Second messengers

A

a) Ligand/hormones
b) Small molecules that transduce signal from cell surface to effector proteins that produce the cell’s response e.g. cAMP, DAG

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90
Q

What do the following second messengers do:

a) cAMP
b) Calcium ions
c) DAG

A

a) Activates protein kinase A
b) Activates calcium-dependent enzymes
c) Activates protein kinase C

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91
Q

Explain the effects of adrenaline and the GPCRs that adrenaline binds to to elicit these cell-specific responses

A
  1. Increased heart rate/force, Beta 1 adrenergic receptors in cardiac muscle cells
  2. Bronchodilation, vasodilation - increased blood supply to skeletal musce, Beta 2 adrenergic receptors in airway smooth muscle lining, vascular smooth muscle cells
  3. Vasoconstriction - reduced blood flow, Alpha 1 adrenergic receptors in vascular smooth muscle cells
  4. Vasoconstriction - reduced blood flow, Alpha 2 adrenergic receptors in vascular smooth muscle cells
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92
Q

List the methods of drug administration through parenteral injection sites

A
  1. Subcutaneous injection
  2. Intramuscular injection
  3. Intravenous injection
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93
Q

Discuss the advantages and disadvantages of intravenous drug administration

A

Advantages:

  • Rapid-immediate onset
  • Bypasses liver
  • Permits titration

Disadvantages:

  • Increased risk of adverse effects
  • Requires intravenous access
  • Infection
  • Pain
94
Q

Discuss the advantages and disadvantages of intramuscular drug administration

A
  • Drug injected into muscle mass
  • Absorption depends on blood flow

Advantages:

  • Bypasses liver
  • Rapid onset and shorter duration

Disadvantages:

  • Neurovascular damage
  • Bleeding e.g. anticoagulant therapy
  • Pain
  • Infection
  • Delayed absorption in shock
95
Q

Discuss the advantages and disadvantages of subcutaneous drug administration

A
  • Absorption depends on blood flow

Advantages:

  • Constant and slow absorption
  • Prolonged effect
  • Bypasses liver

Disadvantages:

  • Pain
  • Infection
  • Delayed absorption in shock
96
Q

Enteral administration of drugs

A

Oral (or rectal) administration

97
Q

Discuss the advantages and disadvantages of enteral administration of drugs

A

Advantages:

  • Convenient
  • Safest
  • Cheapest
  • Slower onset - prolonged but less potent action

Disadvantages:

  • Drug passes through liver
  • Absorption rate can be highly variable
  • Absorption influenced by stomach contents
  • Gastric acid interferes with absorption - some drugs can’t be given orally
  • Uncooperative patients may not take them
98
Q

Describe pulmonary routes of drug administration

A
  • Inhalation into the lungs

- Poor systemic absorption

99
Q

Describe topical routes of drug administration

A
  • Placing drug on surface with a mucous membrane
  • Sublingual - under tongue
  • Intranasal - powder/liquid absorbed through mucous membrane in the nose
  • Skin - skin patches or topical anaesthesia
100
Q

F (drug dosage)

A

Fraction of the administered dose of drug that reaches the systemic circulation

101
Q

List the factors that affect F

A
  1. Drug factors - molecular weight/ionisation
  2. Absorption - gastric pH/health of GI tract
  3. First pass metabolism (hepatic) - phenytoin may reduce F, grapefruit juice may increase F
102
Q

Value of F for IV drugs

A

F = 1 for IV drugs

103
Q

Apparent volume of distribution

A

Apparent volume into which a known amount of drug must be dispersed to give the measured plasma concentration - relates the plasma concentration to the total amount of drug in the body

104
Q

What affects the apparent volume of distribution

A
  • Plasma protein and tissue binding
  • Molecular weight
  • Lipid solubility
105
Q

What is the apparent volume of distribution used to determine

A
  • Loading dose amount

- Elimination half-life, dosage interval

106
Q

How is the loading dose of a drug calculated

A

Loading dose (mg) = Target Concentration (mg/L) x Volume (L)

107
Q

Clearance

A

Theoretical volume of plasma (blood etc.) ‘cleared’ of drug per unit time (e.g. ml/minute or L/hour)

108
Q

Half life

A

Time required for serum plasma concentration to decrease by half

109
Q

What determines half life

A

Determined by clearance and volume of distribution

110
Q

How many half-lives are required to clear a drug

A

4-5

111
Q

How is the maintenance dose calculated?

A

Rate in should equal rate out

112
Q

Steady state

A
  • Amount of drug administered is equal to the amount of drug eliminated within one dosing interval
  • Drugs with short half-life reach steady state rapidly
  • Drugs with long half-life can take days to reach steady state
113
Q

How long does it take to reach steady state?

A

4-5 half lives

114
Q

Pharmacokinetics

A

What the body does to the drug

115
Q

Pharmacodynamics

A

What the drug does to the body

116
Q

Organ-specific autoimmune diseases

A
  • Autoimmune attack on self antigens of given organ

- Causes damage to organ structure and function

117
Q

Non-organ specific (systemic) autoimmune diseases

A
  • Widespread self-antigens are targets for autoimmune attack

- Damage affects such structures as blood vessels, cell nuclei etc.

118
Q

Give examples of organ-specific autoimmune diseases

A
  • Type 1 diabetes mellitus
  • Multiple sclerosis
  • Grave’s disease
119
Q

Give examples of systemic autoimmune diseases

A
  • Rheumatoid arthritis

- Systemic lupus

120
Q

Primary immunodeficiency diseases

A

Deficiency is the cause of the disease. Primary immunodeficiencies are usually congenital, resulting from genetic defects in some component of the immune system

121
Q

Secondary immunodeficiency diseases

A

Deficiency is acquired as a result of other diseases or condition:

  • HIV infection
  • Malnutrition
  • Immunosuppression
122
Q

Definition of health

A

A state of complete physical, mental and social well-being and not merely the absence of disease or infirmity

123
Q

Outline the current main components of public health

A
  • Infectious diseases
  • Chemicals and poisons
  • Radiation
  • Emergency responses
  • Environmental health hazards
124
Q

Describe the cell types in the

a) Trachea
b) Bronchi
c) Bronchioles
d) Alveoli

A

a) Ciliated pseudostratified columnar epithelium, goblet cells
b) Ciliated pseudostratified columnar epithelium
c) Transitions from ciliated columnar epithelium to low cuboidal epithelium, club cells
d) Type 1 alveolar = simple squamous epithelial cells, type 2 alveolar = cuboidal-shaped cells, macrophages

125
Q

Describe inspiration and expiration in relaxed breathing

A

Inspiration is active, expiration is passive

126
Q

List the inspiratory muscles used in relaxed breathing

A
  1. Diaphragm - contracts to increase size of thoracic cavity, drawing air into the lungs
  2. External intercostal muscles - contract to increase size of thorax by drawing ribs upwards
127
Q

Describe the mechanism for expiration in relaxed breathing

A
  • Elastic recoil of chest wall and lungs
  • Diaphragm and external intercostal muscles relax, lung volume decreases
  • Pressure in lungs > pressure of atmosphere, air leaves lungs
128
Q

How is forced inspiration/expiration brought about?

A

Use of accessory inspiratory muscles and expiratory muscles

129
Q

What is the function of the accessory inspiratory muscles

A
  • Normally function to move arms/neck
  • During strenuous exercise are used to increase volume of thorax, reduces pressure in chest to allow flow of air from the atmosphere to the lungs
130
Q

List the accessory inspiratory muscles

A
  1. Sternocleidomastoid and scalene muscles - anterior neck, pull the chest up towards the head, increasing volume
  2. Pectoralis major/minor - connect anterior chest to upper arm, if arms are fixed in place contraction pulls chest forwards, increasing volume of chest
131
Q

List the expiratory muscles used in forced breathing

A
  1. Internal intercostal muscles - contract to pull ribs down, decrease chest volume
  2. Abdominal muscles - contract to pull ribs down, decrease chest volume
132
Q

Boyle’s Law

A

Volume of gas is inversely proportional to the pressure of the gas

133
Q

Explain how Boyle’s law can be used to explain inspiration

A

Lungs expand, volume increases, pressure decreases compared with atmospheric pressure, air flows in

134
Q

Explain how Boyle’s law can be used to explain expiration

A

Lungs shrink, volume decreases, pressure increases compared with atmospheric pressure, air flows out

135
Q

How is chemical control of breathing mediated?

A

Via central and peripheral chemoreceptors

136
Q

Chemoreceptors

A

Specialised sensory receptors which respond to chemical substances and generate a biological signal

137
Q

Central chemoreceptors

A

Collection of neurones near the ventrolateral surface of the medulla, close to exit of CN IX and X

138
Q

Describe the mechanism of action of central chemoreceptors

A
  • Sensitive to pH of surrounding cerebrospinal fluid (CSF)
  • CSF is separated from blood by blood-brain barrier (tight endothelial layer lining BVs of brain), impermeable to polar molecules, but carbon dioxide can diffuse across it
  • Stimulation of central chemoreceptors by fall in CSF pH causes increase in ventilation
139
Q

List the parts of the medulla involved in control of breathing

A
  1. Dorsal respiratory group (DRG)

2. Ventral respiratory group (VRG)

140
Q

Describe the function of the dorsal respiratory group

A
  • Functions in every respiratory cycle (quiet and forced)
  • Inspiratory centre discharges action potentials to innervate lower motor neurons to external intercostal muscles and the diaphragm
141
Q

Describe the function of the ventral respiratory group

A
  • Functions only in forced breathing
  • Expiratory centre produces action potentials to innervate lower motor neurons to accessory respiratory muscles for active expiration
142
Q

Where are peripheral chemoreceptors found?

A

Within the carotid and aortic bodies

143
Q

Where is the carotid body located?

A

At bifurcation of common carotid artery, just above carotid sinus

144
Q

Describe the innervation of the carotid body

A

Innervated by carotid sinus nerve, leading to glossopharyngeal nerve

145
Q

List the cells found in the carotid body

A
  1. Glomus cells (type I - responsible for chemoreception, has dense granules containing neurotransmitters and contact axons or the carotid sinus nerve
  2. Sheath cells (type II - support and protect glomus
146
Q

How do the chemoreceptors in the carotid body respond to low PO2/pH

A

Increase firing rate in carotid sinus nerve, therefore ventilation

147
Q

Aortic bodies

A
  • Distributed around aortic arch
  • Innervated by vagus
  • Less important than carotid body
148
Q

Dalton’s Law

A
  • Each gas in a mixture behaves as if no other gases were present
  • Total partial pressure pf a gas mixture can be determined by adding together the partial pressures of all the individual gases in the mixture
149
Q

Henry’s law

A
  • The quantity of a gas that will readily dissolve in a solution is proportional to the partial pressure of that gas and its solubility
  • Gas with high partial pressure and high solubility stays within solution for much longer than a comparable gas with a low partial pressure + solubility
150
Q

How can Henry’s law be applied to carbon dioxide and oxygen?

A

Carbon dioxide has a higher solubility in blood plasma compared with oxygen, therefore at the same partial pressure, more carbon dioxide will stay in the blood than oxygen

151
Q

Define external respiration

A

Exchange of oxygen and carbon dioxide between air in alveoli and blood in pulmonary circulation

152
Q

Describe the movement of oxygen and carbon dioxide in external respiration

A
  • Oxygen from air in alveoli to blood in pulmonary circulation
  • Carbon dioxide from blood in pulmonary circulation to air in alveoli
153
Q

How is the rate of diffusion of gases determined?

A

By the partial pressures of the gases - will always go from high partial pressure to low partial pressure

154
Q

Give the partial pressures of oxygen in

a) Alveoli
b) Capillaries

A

a) PO2 = 105 mmHg

b) PO2 = 40 mmHg

155
Q

Give the partial pressures of carbon dioxide in

a) Alveoli
b) Capillaries

A

a) PCO2 = 40 mmHg

b) PCO2 = 45 mmHg

156
Q

Define internal respiration

A

Exchange of oxygen and carbon dioxide between cells of the body and blood in systemic capillaries

157
Q

Describe the movement of oxygen and carbon dioxide in internal respiration

A
  • Oxygen from systemic capillaries to tissues

- Carbon dioxide from tissues to systemic capillaries

158
Q

Give the partial pressures of oxygen in

a) Tissues
b) Systemic capillaries

A

a) 40 mmHg

b) 100 mmHg

159
Q

Give the partial pressures of carbon dioxide in

a) Tissues
b) Systemic capillaries

A

a) 45 mmHg

b) 40 mmHg

160
Q

How is the majority of oxygen transported and why?

A

98.5% binds to haemoglobin as oxygen is not very water soluble

161
Q

Describe the structure of haemoglobin and its role in oxygen transport

A
  • Globular protein made of 2 alpha and 2 beta chains - 4 haem groups
  • Each haem group has one iron atom which binds to oxygen
  • When oxygen binds = oxyhaemoglobin
  • When oxygen dissociates = deoxyhaemoglobin
162
Q

List the factors effecting haemoglobin’s affinity for oxygen

A
  1. Partial pressure of oxygen
  2. Partial pressure of carbon dioxide
  3. Temperature
163
Q

How does the partial pressure of oxygen effect haemoglobin’s affinity for oxygen?

A
  • Saturation of haemoglobin, or number of oxygen molecules it is bound to is dependent on partial pressure of oxygen in blood
  • Oxygen binding causes conformational change that increases haem groups’ affinity for oxygen
  • Higher partial pressure of oxygen = higher affinity of haemoglobin for oxygen
164
Q

How does the partial pressure of carbon dioxide effect the affinity of haemoglobin for oxygen?

A
  • Increase in PCO2 creates more acidic environment and contributes to Bohr effect (haemoglobin’s oxygen affinity is inversely related to acidity and concentration of carbon dioxide)
  • CO2 can also bind to haemoglobin, reduces amount of O2 that can bind to it
  • Higher partial pressure of CO2 = lower affinity of haemoglobin for oxygen
165
Q

How does temperature effect the affinity of haemoglobin for oxygen?

A
  • Increased metabolism = increased production of heat
  • Reduces affinity of haemoglobin for O2 + promotes dissociation
  • Decrease in temperature = increase in haemoglobin affinity for O2
166
Q

Describe how carbon dioxide is transported in the body

A
  • Can be transported in several ways
  • Majority is as bicarbonate ions
  • Smaller percentage as carbaminohaemoglobin
  • Even smaller percentage in blood plasma
167
Q

Describe how carbon dioxide is transported as bicarbonate ions

A
  • Carbon dioxide moves out of tissues into RBCs and reacts with water to form carbonic acid
  • Carbonic acid dissociates into hydrogen and bicarbonate ions
  • Enzyme carbonic anhydrase speeds up process
  • As increasing amounts of CO2 enter blood, bicarbonate ions accumulate in RBCs
  • As concentration gradient is established, bicarbonate ions move out of RBC into blood plasma
  • To maintain electrical balance, as one bicarbonate ion moves into plasma, one negative chloride ion moves into RBC from plasma
168
Q

Define pneumothorax

A

Accumulation of air in pleural cavity, resulting in collapse of lung on affected side. Extent of collapse is dependent on amount of air present.

169
Q

List the types of pneumothorax

A
  1. Primary spontaneous pneumothorax
  2. Secondary pneumothorax
  3. Traumatic pneumothorax
  4. Latrogenic pneumothorax
  5. Catamenial pneumothorax
170
Q

Primary spontaneous pneumothorax

A

Pneumothorax occurring in healthy people (esp. tall, thin, 20-40 year old men)

171
Q

Secondary pneumothorax

A
  • Associated with underlying lung disease

- Consequences significantly greater, management more difficult

172
Q

Traumatic pneumothorax

A

Follows penetrating chest trauma e.g. stab wound, gunshot injury or fractured rib

173
Q

Latrogenic pneumothorax

A

Follows number of procedures e.g. mechanical ventilation and interventional procedures e.g. central line placement, lung biopsy and percutaneous liver biopsy

174
Q

Catamenial pneumothorax

A
  • At time of menstruation
  • Usually in R lung
  • Up to 24 hours before or within 72 hours from onset of menstruation
  • Thoracic endometriosis leading to necrotic holes in diaphragm allowed passage of air from genital tract (possible when cervical mucus plug is liquefied at time of menstruation)
175
Q

List the categories of patients at risk of developing a pneumothorax

A
  • Ventilated patients
  • Trauma patients
  • Resuscitation patients (CPR)
  • Lung disease, esp. acute asthma + COPD
  • Blocked, clamped or displaced chest drains
  • Patients receiving non-invasive ventilation
  • Patients undergoing hyperbaric oxygen treatment
176
Q

List the risk factors for developing a pneumothorax

A
  • Smoking
  • Tall - Marfan’s syndrome esp.
  • Not associated with onset during exercise
  • Women w/ endometriosis
  • Subpleural blebs and bullae
  • Underlying lung conditions - COPD, tuberculosis, sarcoidosis, cystic fibrosis, malignancy
  • Family history of the disease
177
Q

List the symptoms associated with a pneumothorax

A
  • Sudden onset of pain
  • Shortness of breath
  • Many have no symptoms
  • Patient looks distressed/is sweating
  • Cyanosis
  • Tachycardia
  • Hypotension
  • Decreased chest expansion on affected side
  • Deviated trachea away from side of collapse
  • Hyper-resonance on percussion
  • Reduced/absent breath sounds over affected area
178
Q

List the investigations which would be carried out to confirm diagnosis of a pneumothorax

A
  • Chest X-ray
  • Ultrasound
  • CT for uncertain/complex cases
  • Arterial blood gases show hypoxia
179
Q

Describe treatment of a pneumothorax

A
  • Oxygen
  • Emergency needle decompression
  • Needle aspiration/chest drain
  • Referral to chest physician
  • Smaller managed by observation
  • Intercostal tube drainage
  • Pleurodesis
  • Surgery
180
Q

Describe how emergency needle decompression is used to treat a pneumothorax

A
  • Large-bore needle inserted into pleural space through second/third anterior intercostal space over superior margin in anterior axillary line
  • Entry just above rib rather than below to reduce risk of hitting neurovascular bundle
  • Gush of air confirms diagnosis
181
Q

Explain the use of pleurodesis in the treatment of a pneumothorax

A
  • Pleural space is artifically obliterated
  • Mild irritant put into pleural space
  • Prevents risk of recurrent pneumothorax
182
Q

Mechanoreceptors

A
  • Provide feedback on mechanical status of lungs, chest wall and airways
  • Sensory receptors that detect changes in pressure, movement and touch
  • Activated by inflation of the lungs
  • Neural signals sent via vagus nerve to nucleus tractus solitarius (NTS) in brainstem
  • Ventilation is adjusted accordingly
183
Q

List the types of respiratory neurones found in the brainstem

A
  1. Inspiratory neurones = active during inspiration

2. Expiratory neurones = active during expiration

184
Q

Define spirometry

A

Series of tests used to measure lung function, determines airflow in and out of lungs

185
Q

Describe how spirometry is carried out

A
  • Patient breathes into a spirometer
  • Records volume of air breathed in and out and velocity of airflow
  • Full inspiration, hold breath for few seconds, full expiration
  • Can’t smoke an hour before, avoid alcohol, can’t eat a large meal, no restrictive clothing
186
Q

What is spirometry used for

A

To diagnose respiratory problems - COPD, asthma, restrictive lung disease and other disorders affecting lung function
- Monitor chronic lung conditions to check treatment is working

187
Q

List the values recorded during a spirometry test which are used to determine lung function

A
  • Tidal volume
  • Inspiratory reserve volume
  • Expiratory reserve volume
  • Residual volume
  • Inspiratory capacity
  • Functional residual capacity
  • Vital capacity
  • Total lung capacity
  • Forced expiratory volume in 1 second (FEV1)
  • Forced vital capacity (FVC)
  • Peak expiratory flow
188
Q

Tidal volume

A

Occurs during normal quiet breathing, 500mL moves in and out of lungs with each breath

189
Q

Inspiratory reserve volume

A

Volume of air that can be inspired beyond tidal volume

190
Q

Expiratory reserve volume

A

Volume of air that can be expired after tidal expiration

191
Q

Residual volume

A

Excess 1200ml that remains in the lungs to prevent atelectasis (partial/complete collapse of the lung)

192
Q

Inspiratory capacity

A

Total volume of air that can be inspired after tidal expiration

193
Q

Functional residual capacity

A

Volume of air in the lungs after tidal expiration

194
Q

Vital capacity

A

Total volume of exchangeable air

195
Q

Total lung capacity

A

Sum of all lung volumes, normal around 6L in males, 4L in females

196
Q

FEV1

A

Maximal volume of gas which can be expired from the lungs in the first second of forced expiration from full inspiration (effected by height, age and gender)

197
Q

FVC

A

Maximal volume of gas which can be expired from the lungs during forced expiration from full inspiration

198
Q

What value is calculated from spirometry tests to determine lung function?

A

FEV1/FVC ratio (%)

199
Q

FEV1/FVC ratio

A

Proportion of FVC which can be expelled during the first second of expiration, expressed as a percentage

200
Q

Peak expiratory flow

A

Maximum expiratory flow that can be sustained for a minimum of 10 miliseconds

201
Q

Describe the differences in FEV1/FVC ratio in

a) Restrictive diseases
b) Obstructive diseases

A

a) FEV1 and FVC are equally reduced, ratio remains the same

b) FEV1 is reduced, FVC is the same, ratio is reduced

202
Q

Describe the differences in the flow graph in:

a) Obstructive diseases
b) Restrictive diseases

A

a) Expiratory flow is reduced, inspiratory flow is the same

b) Expiratory and inspiratory flow are both reduced

203
Q

List pulmonary tests (other than spirometry) used to diagnose problems with lung function

A
  1. Plethysmography - measures lung volume

2. Diffusion capacity test - evaluates alveoli function

204
Q

Obstructive lung diseases

A

Obstruction of the airways, making it difficult to breathe. FEV1/FVC is low (<70%), e.g. asthma, COPD, cystic fibrosis

205
Q

Restrictive lung diseases

A

Restrict lung expansion, resulting in decreased lung volume. FEV1/FVC may be normal (75%) or high (90%). Pulmonary fibrosis (scarring of lung tissue), sarcoidosis (autoimmune diseases), scoliosis, neuromuscular disease

206
Q

List the factors which effect lung volume

A
  • Height
  • Altitude at which person lives
  • Level of exercise/activity
207
Q

COPD

A

Umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, refractory (non-reversible) asthma and some forms of brochiectasis. Characterised by increasing breathlessness. Irreversible damage, can only be slowed not halted. Caused by long-term exposure to toxic particles/gases (e.g. in smoking)

208
Q

Emphysema

A

Abnormal, permanent enlargement of airspaces distal to the terminal bronchiole. Alveoli break down, get bigger. Less effective gas exchange. Walls are stretched, less flexible, air trapped inside lungs (dead air). Means that diaphragm becomes shortened, unable to assist breathing

209
Q

Chronic bronchitis

A

Inflammation of the airways. Productive cough. Cilia are damaged, cough up mucus, more coughing, more irritation, more mucus production - airways are swollen and clogged. Also invasion of inflammatory cells. Obstruction and shortness of breath.

210
Q

List the symptoms of COPD

A
  • Shortness of breath
  • Frequent coughing (with or without sputum)
  • Increased breathlessness
  • Feeling tired, especially when exercising or doing daily activities
  • Wheezing
  • Tightness in chest
211
Q

Describe the pathogenesis of COPD

A
  • Increased number of mucus secreting goblet cells in bronchial mucosa
  • Immunological infiltration of the bronchial walls, predominantly CD8 killer cells
  • Epithelium layer may become ulcerated and squamous epithelium may replace columnar cells
  • Inflammation is followed by thickening and scarring of the walls which narrows small airways
  • Progresses with squamous cell metaplasia and fibrosis of bronchial walls
  • Leads to airflow limitation
212
Q

Pink puffers

A

Emphysema

  • Destruction of alveolar lung tissue/capillary bed, decreases the ability to oxygenate the blood
  • Hypoxemia (low oxygen)
  • Typically thin and often breathless
  • Have to work hard to maintain a normal PCO2
  • Appearance = Barrel-shaped/hyper-inflated chest, breathing through pursed lips
213
Q

Blue bloaters

A

Chronic bronchitis

  • Body tries to decrease ventilation and increase CO2
  • Develop (or tolerate) hypercapnia earlier -more severe hypoxemia than pink puffers
  • Develop oedema and secoandary polycythaemia (increased haemoglobin in the blood)
  • Appear breathless, bloated, plethoric and cyanosed
214
Q

How does smoking cause COPD

A
  • Causes inflammatory cells to produce excess of protease enzymes such as neutrophil elastase over anti-proteases, such as alpha 1-antitrypsin
  • Protease/anti-protease imbalance results in lung tissue damage and development of COPD
  • Alpha 1-antitrypsin is a proteinase inhibitor produced in the liver, secreted into blood - travels to lungs
  • In lungs it inhibits proteolytic enzymes e.g. neutrophil elastase - capable of destroying alveolar wall connective tissue
215
Q

Describe the complications which are common in COPD and how they are managed

A

Recurrent bad respiratory infections which sufferers struggle to fight off. Vaccinated/treated with antibiotics.

216
Q

Describe the diagnosis of COPD

A
  • Mild COPD - no signs/quiet wheezing
  • Severe COPD - rapid breathing, prolonged expiration
  • Poor chest expansion
  • Presence of risk factor (smoking)
  • Cough w/ sputum
  • Shortness of breath
  • FEV1/FVC ratio less that 70%
  • Hyperinflation may be seen on X-ray - low flattened diaphragm
  • Blood gases - normal at rest, desaturate on exercise
  • Advanced = hypoxemia, hypercapnia
217
Q

Describe the first step in the management of COPD

A

Smoking cessation - most useful measure is to persuade the patient to stop smoking. Even in advance COPD, this may slow down the rate of deterioration and prolong the time before disability and death occur

218
Q

List the pharmacological measures taken to manage COPD

A
  1. Bronchodilators
  2. Antimuscarinic drugs
  3. Xanthines
  4. Corticosteroids
  5. Mucolytic drugs
  6. Ventilatory support
219
Q

Explain how bronchodilators are used to manage COPD

A
  • Beta-adrenergic agonists e.g. salbutamol
  • Reduce breathlessness
  • Long acting beta 2 agonists should be used in severe airway limitation e.g. Salmeterol
220
Q

Explain how antimuscarinic drugs are used to manage COPD

A

Give more prolonged and greater bronchodilation e.g. tiotropium (long-acting) and ipratropium

221
Q

Explain how corticosteroids are used to manage COPD

A

E.g. prednisolone 30mg daily for 2 weeks. Always used in moderate/severe COPD. Lung function measurements should be taken before and after treatment - ideally FEV1 should increase by >15%. Combination of corticosteroid and long acting beta 2-agonist is recommended, which protects against decline in lung function, though it does not improve overall mortality

222
Q

Respiratory Acidosis

A

When ventilation < CO2 production, therefore low pH due to hypercapnia

223
Q

Hypercapnia

A

Condition of abnormally elevated carbon dioxide levels in the blood

224
Q

List the compensatory mechanisms of respiratory acidosis

A
  1. Chemorecptor relfex
  2. Haemoglobin
  3. Renal compensation
225
Q

Chemoreceptor reflex which corrects respiratory acidosis

A

Chemoreceptors monitor PCO2 of the plasma and the CSF and eliminate respiratory acidosis by increasing ventilation rate

226
Q

Describe how haemoglobin corrects respiratory acidosis

A

Binds and buffers H+ ions more effectively when PO2 is low. Increased H+ binding decreases the affinity of haemoglobin for O2, thus increasing O2 unloading in respiring tissues and decreasing the HbO2 saturation. AN increase in 2,3 BPG production by erythrocytes when HbO2 saturation is low also facilitates oxygen unloading and delivery.

227
Q

Describe renal compensation of respiratory acidosis

A

When H+ ion concentration is high, more hydrogen ions are filtered and secreted by the kidneys. This allows more HCO3 to be reabsorbed from the tubules.

228
Q

List the factors which contribute to the development of COPD

A
  • Smoking
  • Air pollution
  • Wood burning
  • Nutrition
  • Occupation
  • Socioeconomic status
  • Bacterial colonisation
  • Genetics
229
Q

List the factors which may contribute to exacerbations of COPD

A
  • Element of asthma
  • Bacterial colonisation
  • Aspergillus sensitisation
  • Hypoxia
  • Reflux
  • Underlyin bronchiectasis
230
Q

List the clinical signs of bronciectasis

A
  • Purulent daily sputum
  • 50% idiopathic
  • Recurrent infection
  • Crackles heard on exam

Medicine YEAR 1 (18 decks)

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