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Year 1 - semester 2 amy > respiratory > Flashcards

respiratory Flashcards

1
Q

coagulase pos vs neg bacteria

A

Coagulase positive
- S.aureus

Coagulase negative
- Coagulase Negative Staphylococcus (CNS)

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2
Q

staph aureus (including MRSA)

A

coag-pos

many virulent factors

causes

  • infections from boils to osteomyelitis
  • blood-stream infections
  • toxin illnesses
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3
Q

staphlococci

A

coag-neg

not as virulent

Lots of different species

infections in the presence of foreign body (e.g prosthetic joint).

Staph saprophyticus: cause of UTI

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4
Q

streptococcus

A

alpha haemolytic - green zone
eg - Str. pneumoniae

beta haemolytic - golden yellow zone
eg - Str. Pyogenes

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5
Q

Dalton’s law

A

gases in a mixture exert pressures that are independent of each other

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6
Q

Henry’s Law

A

the concentration of a dissolved gas is directly proportional to its partial pressure

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7
Q

oxygenated blood

A 
Po2 = 13.3kPa
[O2] = 200ml/L = 8.9mmol/L

1.5% is dissolved in plasma and 98.5% bound to haemoglobin

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8
Q

modulation of oxygen binding to haemoglobin

A

The bohr effect - H+/ph

the haldane effect - PCO2 reactignwith amino groups in deoxy-Hb > carbino-Hb (this has a lower O2 affinity)

binding of 2,3-bisphospoglycerate

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9
Q

2,3-bisphospoglycerate

A

present only in ethrocytes

conc - 4mmol/L

preferably binds to deoxy-Hb, 1 mol 2,3-BPG per Hb tetramer

lowers affinity of O2 to improve O2 delivery

foetal Hb has a lower affinity for it

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10
Q

effects of anaemia and CO poisoning

A

CO is a shorter curved shape

anaemia is a shorter S-shaped curve

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11
Q

dissolved Carbon Dioxide

A 
PCO2 = 5.3 kPa
[CO2] = 530 ml/L = 24 mmol/L

Of this,
7% is dissolved CO2
70% is hydrated to carbonic acid and bicarbonate
23% is combined as carbamino-haemoglobin

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12
Q

gas exchange in the alveoli

A

Gas exchange in the alveoli is so rapid that equilibrium is usually attained. If equilibrium is not reached, it is usually because of V/Q mismatch.

hypoxia more likely than hypercapnia as CO2 diffusion is 20x faster than O2

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13
Q

nitrogen

A 
Elemental nitrogen (N2) has no function in human metabolism.  
Its solubility in blood is low, at high pressure dissolves in blood and tissues, producing nitrogen narcosis (‘rapture of the deep’); 
return to normal pressure nitrogen emboli may form in capillaries - local ischaemia, bubbles within tissues (‘bends’).
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14
Q

haemaglobin structure

A

tetrameric protein with two types of subunit

molecular weight 64,500

HbA (normal adult) = a2b2 ; HbF (foetal) = a2y2

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15
Q

bicarbonate

A

carbonic anhydrase catalyses hydration of CO2 to carbonic acid

carbonic acid ionixes to bicarbonate

bicarbonate moves into plasma in exchange for CL- - THE “CHLORIDE SHIFT”

most CO2 is transported as bicarbonate in plasma

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16
Q

acetazolamide

A

inhibits carbonic anhydrase

used to be used as a diuretic (inhibits Na+ uptake in kidney)

now used to prevent altitude sickness - lowering ph of blood

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17
Q

elastic recoil definition

A

having the property of returning to the original shape after being distorted

to spring back

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18
Q

expiration - resting breath -

A

inspiratory muscle activity ceases - elastic recoil causes lungs to shrink (passive)

elastic recoil causes positive pressure in alveoli - air moves out towards mouth

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19
Q

mechanism of inspiration

A

inspiratory neural activity from brain

diaphragm and external intercostals contract and thoracic cage expands

pleural pressure < atmospheric P

air flows down conc grad. into alveoli

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20
Q

expiration - large/forced breath

A

internal intercostals and abdominal muscles contract

diaphragm moves up, ribs are depressed - reduce thoracic volume

alveolar pressure increases and air flows out of alveoli

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21
Q

Vt

A

tidal volume

volume of gas breathed out with each breath (litres)

normally 0.4-0.8 litres

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22
Q

f r

A

respiratory frequency

breaths per minutes

normally 12-15 breaths/min

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23
Q

(V)

A

minute ventilation = Vt * f r

amount of gas breathed in or out of lungs per minute litres/min

normally 5-8 litres/min

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24
Q

central neural control for breathing

A

cortex + upper pons
- removal = slow gasping breaths

pons
- removal = return to rhythmic breathing

medulla
- removal stops breathing

spinal cord

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25
Q

respiratory groups in brainstem

A

pontine RG
ventral RG
dorsal RG

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26
Q

things that change the basic breathing pattern

A

inhaled noxious substances
speech
sleep
exercise

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27
Q

feedback inputs to the resp rhythm generator

A

lung receptors (afferent nerve fibres carried in vagus)

  • slowly adapting rec
  • rapidly adapting rec
  • C-fibre endings

CHEMORECEPTORS

  • central chemorec
  • peripheral chemorec.
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28
Q

slowly adapting receptors (SARs)

A
  • also called stretch rec.
  • mechanorec. close to airway smooth muscle
  • stimulated by stretch of airway walls in insp.
  • help initiate exp. & prevent overinflation
  • initiate Hering-Breuer inflation reflex
  • afferent fibres = myelinated
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29
Q

rapidly adapting receptors (RARs)

A
  • also called irritant receptors
  • primarily mechanoreceptors responding to rapid lung inflation
  • respond to chemicals (eg histamine, smoke…)
  • RARa in trachea & large bronchus initiate cough, mucus prod. &
    bronchoconstriction
  • afferent fibres = myelinated
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30
Q

C-fibre endings

A
  • unmyelinated nerve fibres
  • in broncus - stimulated ny increased interstitial fluid (oedema) & inflammatory mediators (histamine, prostagladins, bradykinins)
  • pulmonary c-fibres
    (JUSTAPULMONARY CAPILLARTY RECEPTOR)
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31
Q

response to O2 & CO2

A

chemoreceptors
-peripheral
fast response to ;
arterial pO2, arterial pCO2, arterial h+

-central slow response to ;
arterial pCO2

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32
Q

blood brain barrier

A

pCO2 can’t cross over so is converted into H+ which is picked up by central chemoreceptors on surface of medulla which generates a medullary rhythm

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33
Q

breathing during sleep

A

Respiratory drive decreases (loss of wakefulness drive)
– reduction in metabolic rate
– reduced input from higher centres such as pons and cortex
• Loss of tonic neural drive to upper airway muscles

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34
Q

phasic upper airway activity

A

contraction of upper airway muscles

opening of upper airway

facilitates inward airflow

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35
Q

tonic upper airway activity

A

continuous background activity

tends to maintain patent airway

varies with state of alertness

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36
Q

obstructive sleep apnoea (OSA)

A

Common
• Fragments sleep causing daytime sleepiness
• Important cause of traffic accidents
• Risk factors: obesity, alcohol, nasal obstruction, anatomical anomalies

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37
Q

respiratory depressant drugs

A

anaesthetics
- almost all

analgesics
- opioids (morphine and its analogues)

sedatives (anti-anxiolytics, sleeping tablets)
- benzodiazapines (diazepam, temazepan, etc)

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38
Q

respiratory stimulant drugs

A

Primary action:
Doxapram

Secondary action:
B 2 - agonists (bronchodilators)

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39
Q

generation of basic rhythm

A
  • Discharge from the inspiratory neurones activates the respiratory muscles via spinal motor nerves, resulting in inspiration
  • Expiratory neurones fire and inhibit the inspiratory neurones. Nerve impulses to the inspiratory muscles stop and passive expiration occurs.
  • If forceful expiration is required, expiratory neurone activity also activates expiratory muscles to enhance expiration
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40
Q

lung defence mechansims

A

Mechanical
• Ciliated epithelium
• Mucus
• Cough

Immunological
• IgA & antimicrobials in mucus
• Resident alveolar macrophages & dendritic cells
• Innate / adaptive immune responses

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41
Q

what is the parenchyma

A

The parts of the lungs involved in gas transfer
including the alveoli, interstitium, blood vessels,
bronchi and bronchioles.

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42
Q

pneumonia

A

Greatest cause of deaths due to infection in the developed
world
• Eighth leading cause of death (2.3% of all deaths) in the United States
• 15% of all deaths of children under 5 yrs
• Caused by range of
pathogens • bacteria • viruses • fung

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43
Q

pneumonia categories

A
  • Community acquired
  • Hospital acquired
  • Health care associated
  • Aspiration associated
  • Immunocompromised host
  • Necrotising / abscess formation
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44
Q

community acquired pneumonia

A 
Streptococcal pneumoniae
• Haemophilus influenzae
• Moraxella catarrhalis
• Staphylococcus aureus
• Klebsiella pneumoniae / Pseudomonas aeurginosa
• Mycoplasma pneumoniae
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45
Q

hospital acquired / Healthcare associated pneumonia

A
  • Gram-negative rods, Enterobacteriaceae, Pseudomonas

* Staphylococcus aureus (usually methicillin-resistant)

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46
Q

aspiration pneumonia

A

• Anaerobic oral flora mixed with aerobic bacteria

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47
Q

pneumonia in immunocompromised host

A
  • Cytomegalovirus
  • Pneumocystis jiroveci (PCP)
  • Mycobacterium avium-intracellulare
  • Invasive aspergillosis
  • Invasive candidiasis
  • “Usual” bacterial, viral, and fungal organisms
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48
Q

necrotising / abscess formation pneumonia

A

• Anaerobes, S. aureus, Klebsiella, S. pyogenes

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49
Q

respones to infection -neutrophils

A 
Chemotaxis
• Degranulation
• Reactive oxygen species
• Extracellular traps
• Phagocytosis
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50
Q

response to infection - macrophages

A 
Cytokine &amp; chemokines
• Phagocytosis (bacteria &amp; dead
cells)
• Antimicrobial peptides
• Resolution
• Also involves T cells, dendritic
cells &amp; epithelial cells
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51
Q

clinical presentation of pneumonia

A 
Cough
• Sputum
• Pyrexia
• Pleuritic chest pain
• Haemoptysis
• Dyspnoea
• Hypoxia
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52
Q

bronchopneumonia

A 
Most common pattern
• Patchy consolidated areas of acute
suppurative inflammation
• Often elderly with risk factors
• Cancer, heart failure, renal failure, stroke,
COPD
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53
Q

lobar pneumonia

A

Rust coloured sputum
• S. pneumoniae
• consolidation of a large portion of a
lobe or of an entire lobe

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54
Q

complications of pneumonia

A 
Local
• Abscess formation
• Empyema
Systemic
• Sepsis
• ARDS
• Multi-organ failure
Not resolving?
• ?cancer
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55
Q

acute respiratory distress syndrome

A
  • Incidence 10-14/100,000/yr
  • Mortality rate ~40%

Clinical diagnosis
• Hypoxia (PaO2/FiO2 ≤ 300mmHg )
• Non-cardiogenic pulmonary oedema

Causes
• Direct – pneumonia, aspiration, hyperoxia, ventilation
• Indirect – sepsis, trauma, pancreatitis, acute hepatic
failure

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56
Q

bronchiectasis

A 
Definition
• The permanent dilatation of one
or more large bronchi
• Typically affects the 2nd to 8th order of segmental
bronchi.
• largest central airways more robust.
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57
Q

tuberculosis

A
  • Extremely common worldwide
  • 8.9 million new cases in 1995
  • 1.66 million die per annum of this disease
  • Much more common in developing world
 Predisposing factors
• Alcoholism
• Diabetes mellitus
• HIV / AIDS
• Some ethnic groups
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58
Q

primary TB

A

3-4 weeks

  • multiplies within alveolar macrophages (can’t kill)
  • bacterium resides in phagasomes & carried lymph nodes -> circulation

3-8 weeks

  • onset of cellular immunity & delayed hypersensitivity
  • activated lymphocytes further activate macrophages to kill
  • most primary infections arrested
  • few bacilli may survive dormant
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59
Q

progressive primary TB

A

Infection not arrested
• Minority
• Infants, children, immunocompromised

Tuberculous bronchopneumonia
• Infection spreads via bronchi
• Results in diffuse bronchopneumonia
• Well developed granulomas do not form

 Miliary Tuberculosis
• Infection spreads via blood-stream
• Organisms scanty
• Multiple organs
• lungs, liver, spleen, kidneys, meninges, brain
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60
Q

secondary tuberculosis

A 
Also termed ‘Post-primary’ TB
• Reactivation of old, often subclinical
infection
• Occurs in 5-10% of cases of primary
infection
• More damage due to hypersensitivity
• Apical region of lung
• Tubercles develop locally, enlarge and
merge
• Erode into bronchus and cavities develop
• May progress to tuberculous
bronchopneumonia
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61
Q

other causes of granulomatous pulmonary inflammation

A 
Other infection – fungi
• Sarcoidosis
• Rheumatoid arthritis
• Berrylosis
• Hypersensitivity pneumonitis
• Aspiration pneumonia
• Langerhans Cell Histiocytosis
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62
Q

asbestoes

A 
• Occupational lung disease
• Exposure in shipyards, building trade
• Several diseases
• Pleural plaques (benign)
• Asbestosis (progressive fibrosis)
  • Mesothelioma
  • Adenocarcinoma
  • Issues surrounding compensation for patient and
families
• Other occupational factors
    • Silica, coal dust, berrylium
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63
Q

hypersensitivity pneumonitis

A 
• Type III hypersensitivity
• Ab/Ag complex within the lung
• Various causative agents
- Farmer’s lung
- Pigeon fancier’s lung
- Mushroom picker’s lung
- Hot tub lung (!)
• Most resolve when agent of exposure removed but
can be chronic
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64
Q

complications of bronchiectasis

A 
Local
• Distal airway damage / loss and lung fibrosis
• Pneumonia
• Pulmonary abscess formation
• Haemoptysis
• Airway colonisation by aspergillus
• Aspergilloma
• Tumourlet formation

Physiological
complications
• Respiratory failure
• Cor pulmonale

  • Systemic complications
  • Metastatic abscess
  • Amyloid deposition
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65
Q

patterns of bronchiectasis

A 
Based on imaging
appearances
• Cylindrical
• Sacular
• Varicose
• Cystic
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66
Q

function of the chest wall

A

1st Respiration
2nd Protection
3rd Muscle Attachments

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67
Q

thoracic cavity

A

Divided into 3 major spaces
• Heart with coverings (pericardium - pericardial cavity) + the
major vessels
• Lungs with coverings (pleura - pleural cavities)

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68
Q

chest wall anatomy

A 
• Thoracic vertebrae
• Ribs
• Sternum - manubrium, body, xiphoid
process
•Intercostal spaces - intercostal muscles
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69
Q

features of a thoracic vertebrae

A
  • body
  • facets for articulation with ribs
  • facet for articulation with adjacent vertebra
  • transverse, inferior, spinous, superior processes
  • lamina
  • pedicle
  • vertebral foreamen
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70
Q

features of a rib

A

posterior -> anterior

  • head
  • neck
  • tubercle
  • angle
  • internal surface
  • costal groove
  • external surface
  • costal cartilage
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71
Q

sternocostal joints

A

true ribs - I-VII
false ribs - VIII-XII (articulate with sternum via costal cartilage of rib above)
floating ribs - XI-XII (the 2 at the bottom)

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72
Q

intercostal space

A
  • external and internal and innermost intercostal muscles
  • intercostal vein, artery and nerve
  • collateral branches of V, A & N
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73
Q

diaphragm openings

A

Inferior Vena Cava - T8
caval opening

• Oesophagus - T10
esophageal hiatus

• Aorta - T12
aortic hiatus

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74
Q

trachea

A

c-shaped hyaline cartilage rings
bifurcates into R & L main bronchus at TIV/TV
Carina - hook-shaped tracheal ring

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75
Q

bronchial trees - L & R

A 
Right main bronchus
Wider
Vertical
Shorter
Divides into 3

Left main bronchus
Long
More horizontal
Thin
Divides into 2
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76
Q

bronchial tree

A 
Trachea
Main bronchus (primary)
Lobar bronchi (3R, 2L) (secomndary)
Segmental bronchi (tertiary)
Conducting bronchioles
Respiratory bronchioles
Alveoli
Alveolar ducts
Alveolar sacs
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77
Q

alveoli

A
  • microscopic air cells
  • 150-300 million in adults
  • single layer epithelial & elastic fibres line the walls
  • surrounded by capillary network
  • coated with thin layer pulmonary surfactant to prevent collapse
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78
Q

lung lobes

A

right

  • superior
  • middle
  • inferior
  • oblique fissure
  • horizontal fissure

left

  • superior
  • inferior
  • oblique fissure
  • lingula
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79
Q

right medial surface lung

A

root structures

  • pulmonary arteries
  • pulmonary veins
  • bronchus

impressions

  • superior vena cava
  • inferior vena cava
  • oesophagus
  • azygos vein
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80
Q

hilum

A

where important structures enter / exit each lung

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81
Q

left medial surface lungs

A

smaller than right lung

root structure

  • P. arteries
  • P. veins
  • bronchus

impressions

  • heart
  • aortic arch
  • thoracic aorta
  • oesophagus
  • L. subclavian artery
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82
Q

lung development

A

During development the lung is pushed into the sac to form two layers:Visceral & Parietal pleura

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83
Q

costodiaphragmatic recess

A

Between costal pleura & diaphragmatic pleura

Clinically important

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84
Q

mediastinum

A

Separates the pleural cavities

Divided into two parts:
- Superior mediastinum
- Inferior mediastinum
Anterior
Middle
Posterior
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85
Q

contents of mediastinum

A 
Aorta
Heart
Azygous vein
Trachea
Main bronchi
Oesophagus
Vagus nerves
Phrenic nerves
Thoracic duct
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86
Q

innervation to pleura

A

Parietal pleura – somatic innervation

Costal pleura – intercostal nerves

Mediastinal pleura –
phrenic nerves

Diaphragmatic pleura

  • phrenic nerves to domes
  • Lower 5 intercostal nerves to periphery

Visceral pleura – autonomic innervation

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87
Q

innervation to mediastinum

A

Vagus nerve
Parasympathetic supply to all organs of thorax

Phrenic nerve
Motor & sensory to diaphragm

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88
Q

lungs - pleura

A

2 layers of pleura

parietal pleura

  • costal
  • mediastinal
  • diaphragmatic
  • cervical

visceral pleura

  • adhere to wall of lungs
  • covering surface of each lobe
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89
Q

therapeutic index

A

= toxic conc. / effective conc.

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90
Q

alexander fleming

A
  • observed fungal exudate killing staphylococci (1928)
  • unable to purify penicillin
  • later purified by Florey and Chain
  • 1st antibiotic in clinical use
  • used against gram positive bacteria
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91
Q

pharmacokinetics

A

The time course of events relating to how the body
handles the drug

 Includes absorption, distribution, metabolism,
protein-binding, excretion

 Measured by:
volume of distribution, Cmax, tmax, T1/2 : half life

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92
Q

pharmacodynamics

A

 Describes the interaction between the antibiotic
and the bacteria

 Includes bacteriocidal/ bacteriostatic activity,

 Minimum Inhibitory Concentration (MIC),
Minimum Bactericidal Concentration (MBC),

 Post antibiotic effect

 Time dependent killing

 Concentration
dependent killing

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93
Q

antibiotic classification

A 
 1. Effect on micro organism
-  bacteriostatic, bactericidial
 (2. Chemical structure)
 3. Target site
- cell wall
- cell membrane
- protein synthesis
- nucleic acid synthesis
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94
Q

cell wall synthesis inhibitirs

A

Earliest known antibiotics
• Still some of the safest antibiotics
• Selectively toxic to bacteria because there is no
cell-wall in mammalian cells
• Removal of cell-wall destroys bacterial
maintenance of osmotic pressure
• Usually bactericidal in action

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95
Q

cell wall synthesis inhibitors examples

A

beta-lactams
glycopeptides
eg vancomycin, teicoplanin

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96
Q

beta lactams

A
  • penicillins
  • cefalosporins
  • monobactums
  • carbapenems

 All possess a beta lactam ring
 Differ in the side chain attached to this
nucleus
 Target site is peptidoglycan which is present
only in bacteria

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97
Q

side effects of penicillin

A

 Relatively safe
 Hypersensitivity rash
 Avoid amoxicillin in patients with infectious
mononucleosis -‘glandular fever’ - EBV
 Anaphylaxis rare (0.004%) but can be fatal
 Excreted by the kidneys: reduce dose in renal
failure
 Diarrhoea – not uncommon

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98
Q

cefalsporins

A

 Mostly stable to staphylococcal betalactamase

 Much &laquo_space;than 10% cross allergy with penicillins

 So diverse – defy rigid classification

 Consider: oral cefalexin (UTI) AND
 iv cefuroxime,
 iv ceftriaxone/cefotaxime (sepsis, meningitis)
 iv ceftazidime (pseudomonas)
 Improved ßlactamase stability:
cefalexin < cefotaxime < ceftazidime
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99
Q

glycopeptides

A

 e.g vancomycin, teicoplanin
 Inhibit cell wall synthesis by binding to terminal
D-ala-D-ala of the peptide chain and prevents
incorporation of new sub units to the growing cell
wall.
 For Gram positives not Gram negatives
Important in MRSA infection
 Some nephro and ototoxicicity - check serum
levels
 IV for systemic infection (but oral for C. difficile
infection- not absorbed)

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100
Q

protein synthesis inhibitors

A 
 Aminoglycosides e.g gentamicin
 Tetracyclines
 Macrolides (erythromycin,
clarithromycin)
 Chloramphenicol (rarely used in the UK)
 Lincosamides
 Oxazolidones
 Fusidic acid
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101
Q

aminoglycosides

A 
 Low therapeutic index
 Very good v.s Gram negatives eg E. coli, Pseudomonas
aeruginosa (…and Mycobacteria..)
 Anti-Staphylococcal activity
 Not active against anaerobes
 Not absorbed orally
 Ototoxic and nephrotoxic
 Monitor serum levels during therapy
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102
Q

tetracyclines

A 
 Bacteriostatic
 Broad spectrum
 Intracellular bacteria e.g. chlamydia
 May cause diarrhoea, nausea
 Teeth discolouration, avoid in children,
pregnant &amp; lactating women
103
Q

macrolides

A

 Erythromycin; clarithromycin, azithromycin
 Usually bacteriostatic, bactericidal in high
concentrations
 Mainly narrow spectrum (mainly Gram positives
e.g. S.aureus, Group A streptococci)
 Suitable for penicillin allergic patients
 Intracellular bacteria e.g Legionella sp, chlamydia
 Erythromycin cheap

104
Q

side effects of macrolides

A

 Gastrointestinal upset common – less with
newer agents
 Thrombophlebitis when given intravenously
 ‘Newer’ macrolides have broader spectrum
- clarithromycin and azithromycin

105
Q

protein inhibitor synthesis inhibitors (cont)

A

 Lincosamides: clindamycin
 Gram positives esp Group A strep, anaerobes;
bacteriostatic, oral/iv; cheap, diarrhoea/colitis

 Oxazolidone: ‘Linezolid’:
Bacteriostatic; gram positives only;
VRE/MRSA, may cause pancytopaenia, neuritis
& neuropathy, oral/iv, costly!

106
Q

inhibitors of nucleic acid synthesis

A

 1) Synthesis of tetrahydrofolic acid
(THFA)
 2) Synthesis of RNA
 3) Synthesis of DNA

107
Q

1) THFA inhibitors

A

 Sulphonamides - structural analogues of
PABA (para-aminobenzoic acid)
 Trimothoprim – ‘folate’ antagonist – binds
dihydrofolate reductase – selectively toxic
to bacteria
Humans, unlike bacteria do not make folic
acid, must take in diet

108
Q

inhibitors of RNA synthesis

A

rifampicin
Inhibits RNA polymerase enzyme
 Used as part of combination treatment for
Mycobacterium tuberculosis + M. leprae.
 Also for severe Staphylococcus aureus infections
 Always in combination as resistance develops
easily on monotherapy
 Significant drug interactions (hepatic enzyme
inducer); colours secretions;
inactivates oral contraceptive pill

109
Q

inhibitors of dna synthesis - 1

A

QUINOLONES
 Useful– mainly: multi R GNB; UTI; typhoid
 Synthetic, well absorbed. IV/PO.
 Act by inhibiting DNA gyrase (Gram negatives)
and topoisomerase IV (Gram positives)
 Bactericidal

110
Q

DNA synthesis inhibitors - 2

A

Fluoroquinlones - Ciprofloxacin

  • Broad-spectrum
  • Low MICs
  • Rapidly bactericidal
  • Resistance can be slow to develop
111
Q

quinolones side effects

A

Neurotoxicity, confusion, fits
 Cartilage defects. Not used in pregnant
women and children
 Photosensitivity
 Association with C. difficile infection
 (Previously in lime-light for anthrax prophylaxis/ treatment;
now 1st choice for meningococcal
contacts prophylaxis)

112
Q

main route of administration

A 
 Parenteral (intravenous/intra muscular)
 Intraperitoneal
 Oral
 Rectal
 Topical often discouraged
113
Q

what are the factors that promote the success of antibiotic resistance

A 
1. Antibiotic Usage
• Too much antibiotic
• Too little antibiotic
2. Effective Genetic Mobility
• Plasmid Carriage
• Transposons
•Integrons
3. Efficient Resistance Mechanism
• Bacterial factors
114
Q

location of resistance genes

A

 Chromosome
 Plasmid
 Transposon
 Integron

115
Q

transposon

A

 “Jumping genes”
 Go between plasmid & chromosome
 Unable to replicate independently

116
Q

integron

A 
 Genetic element
 Usually resides on transposon
 Able to ‘poach’ resistant genes ie extracts
DNA segments and inserts into other DNA
segments
117
Q

main mechanisms of resistance

A

 1) Target site alteration
 2) Reduced access (efflux or impermeability)
 3) Drug inactivation
 4) Metabolic bypass

118
Q

what antibiotics are we trying to avoid

A 
Broad spectrum antibiotics
Ciprofloxacin and other quinolones
Cephalosporins
Clindamycin
Co-amoxiclav
119
Q

viral infectivity cycle - 1

A

Attachment/Adsorption
Penetration
Uncoating

120
Q

viral activity cycle - 2

A

Transcription
Synthesis of nucleic acid & proteins
Assembly
Release by rupture or budding – often results in cell death

121
Q

antivirals

A

Definition – inhibit viral replication
(most narrow spectrum, N.B. selective toxicity)

Virustatic – do not stop replication completely – this is done by immune system

Uses -Therapeutic/ Prophylactic
Population at risk, Immunocompromised (e.g. Cancer, Transplant & HIV)
Pregnant women, neonates

122
Q

viral DNA/RNA synthesis inhibitors

A

aciclovir (HSV & Herpes) zidovudine (HIV)

123
Q

viral protein synthesis inhibitors

A

ritonavir (HIV)

boceprevir (HCV)

124
Q

release of viral particles inhibition

A

oseltamavir (influenza)

125
Q

fungi - general

A

the eukaryotic fungal cell is more difficult to selectively inhibit than the prokaryotic bacterial cell.
Fungi have sterols in their cell membrane
-usual drug target site

126
Q

classes of antifungals

A

Polyenes
Azole group (Imidazole & Triazoles)
Echinocandins
Others

127
Q

principles of TB therapy

A

Always combination Rx (treatment)
Drugs “first” and “second” line
Choice of number and types of drugs based on history, previous treatment, source, geographical location…
Rx of TB undertaken by specialists only
(now increasing PCR diagnosis on specimens)

128
Q

causes of lung cancer

A 
• SMOKING (>95%)
– Passive smoking (effects difficult to quantify)
• Occupational exposures
– Uranium mining
– Asbestos exposure
• Environmental exposures
– Radon gas
• Genetic
– Li-Fraumeni Sydrome (mutated p53 gene)
129
Q

types of lung cancer

A 
• Squamous Carcinoma (30-40% and
decreasing)
• Adenocarcinoma (40-50% and increasing)
• Small cell carcinoma (20%)
• Others (5%)
– Carcinoid tumours
130
Q

squamous carcinoma

A
  • the tumour cells are showing squamous differentiation
  • keratin production or ‘prickles
  • common finding in smokers
  • reversible
131
Q

adenocarcinoma

A

Evidence of a glandular growth pattern or mucin production
• Central tumours may arise in a similar
manner to squamous carcinoma but premalignant states not really recognised
• Peripheral tumours now believed to arise
through a sequence of step-wise changes.

132
Q

small cell (undifferentiated) carcinoma

A

Very poorly differentiated carcinoma showing variable evidence of
neuroendocrine differentiation
aggressive tumour

133
Q

carcinoid / neuroendocrine

A

Typical (Classical) carcinoid
– < 2 mitoses per 2mm2
– No necrosis

• Atypical carcinoid
– > 2 but < 10 mitoses per 2mm2
– Focal necrosis (may be very focal commedo like)
– > 10 mitoses per 2mm2 with usually extensive necrosis
then classified with LCNEC

134
Q

symptoms and signs of lung cancer

A 
• Cough
• Dyspnoea
• Haemoptysis
• Weight loss
• Chest/shoulder pain
• Hoarseness
• Fatigue
• Slow to clear
pneumonia
• Finger clubbing
• Cervical
lymphadenopathy
• Liver, bone, brain
metastases
• Pleural effusion
135
Q

initial investigations - lung cancer

A 
• Radiology
– Chest x-ray
– CT scan
• Bloods
– High Ca
– Abnormal liver function tests
– Low serum Na
136
Q

immunohistochemistry - lung cancers

A 
Squamous markers
• CK5, CK14, p63, 34βE12
– Adenocarcinoma
• CK7, TTF1 (c. 70-80% of primary
lung tumours)
137
Q

behaviour of lung cancers

A 
• Intrapulmonary growth
– Obstructive pneumonia
– Lymphangitis carcinomatosis
• Invasion of adjacent structures
– Pleura (with associated effusion)
– Chest wall
– Mediastinum (SVC, phrenic nerve, recurrant laryngeal
nerve, atrium, aorta, oesophagus)
– Diaphragm
138
Q

staging lung cancer

A

Staging is assessing the extent of tumour growth
and spread
• Allows patients to be grouped together for
treatment schedules/trials
• Predictor of prognosis
• TNM system
– ‘T’ a measure of the growth of the primary tumour
– ‘N’ indication of the extent of local nodal disease
– ‘M’ presence or absence of distant metastases

139
Q

treatment for lung cancer

A 
Best supportive / palliative care
• Chemotherapy
• Radiotherapy
• Surgery
– around 15%
– Advanced disease at presentation
– Co-morbities eg emphysema, ischaemic heart
disease
140
Q

lung function after lung cancer operations

A

Lobectomy – early deficit with later recovery & little permanent loss in PFT (≤10%) & no decrease in exercise capacity.
Pneumonectomy – early permanent deficit 33% loss in PFT and 20% decrease in exercise capacity

141
Q

anatomical shunts

A

A small amount of arterial blood doesn’t come from the lung (Thebesian veins)
A small amount of blood goes through without seeing gas (bronchial circulation)

142
Q

Physiological shunts (decreaseV) and alveolar dead space (decreaseQ)

A

Not all lung units have the same ratio of ventilation (V) to blood flow (Q)
V/Q mismatch

143
Q

what decreases the partial pressure of O2 in blood

A

Hypoventilation so less oxygen to enter the blood
Hypoventilation allows less air to enter and leave the alveoli and have decreased alveolar oxygen
Decreased environmental oxygen e.g. altitude

144
Q

what can increase partial pressure of oxygen

A

Hyperventilation

Administration of oxygen

145
Q

increase in available PO2 in healthy state

A

Slight increase in haemoglobin saturation
Little change in oxygen content
At a normal PO2, blood carries nearly as much oxygen as it possibly can
Therefore increasing the PO2 has very little effect on the oxygen content
However in disease oxygen therapy is a key intervention

146
Q

ventilation to perfusion ratio

A

V/Q
If ventilation = perfusion then will get perfect gas exchange
In the lung naturally have V/Q mismatch with less blood and air going to the top of the lung

147
Q

normal V/Q mismatch

A

Less airflow and blood flow at the top of the lung but V>Q = increased V/Q
Middle of lung V/Q normal
Bottom of lung more ventilation and more blood flow but V

148
Q

increased V/Q ratio

A

Lots of ventilation to alveoli, not much blood
Alveoli and blood reach an equilibrium which is closer to air
PO2 is therefore higher
(and PCO2 is lower)

149
Q

decreased V/Q ratio

A

Less ventilation to alveoli, lots of blood
Alveoli and blood reach an equilibrium which is closer to venous blood
PO2 is therefore lower (and PCO2 is higher)

150
Q

physiological dead space

A

Anatomical dead space represents the conducting airways where no gas exchange takes place

Alveolar dead space represents areas of insufficient blood supply for gas exchange and is practically non-existent in healthy young but appears with age and disease

Physiological dead space = anatomical dead space + alveolar dead space

151
Q

quantifying V/Q mismatch

A

Calculate the expected alveolar PO2 (PAO2) using the alveolar gas equation
Compare with the measured arterial PO2 (PaO2)
If PAO2 = PaO2 then no mismatch

152
Q

quantifying A-a Gradient

A

Tells us the difference between alveolar and arterial oxygen level
Can help to diagnose the cause of hypoxaemia
High A-a gradient
Problem with gas diffusion
V/Q mismatch
Right to left shunt

153
Q

hypoventilation and CO2

A

During normal ventilation CO2 diffuses out of blood into alveolus following a partial pressure gradient

CO2 is mostly dissolved in blood rather than bound to haemoglobin

If there is lower ventilation then CO2 accumulates in the alveolar space meaning less can be removed from the blood

154
Q

arterial blood gases - WHAT IS MEASURED

A
  • PaO2
  • PaCO2
  • HCO3-
  • H+
155
Q

PaO2 low, CO2 normal

A

Type 1 respiratory failure

Probably has V/Q mismatch

156
Q

PaO2 low, CO2 high

A

Type 2 respiratory failure
Patient has ventilatory failure
(May well have V/Q mismatch too

157
Q

failure of ventilatory pump

A

Won’t breathe: control failure
Brain failure to command e.g. drug overdose
Sometimes in COPD

Can’t breathe: broken peripheral mechanism
Nerves not working e.g. phrenic nerve cut
Muscles not working e.g. muscular dystrophy
Chest can’t move e.g. severe scoliosis
Gas can’t get in and out e.g. asthma/COPD

158
Q

type 2 respiratory failure

A 
Decrease in PO2
Increase in PCO2
Common causes in hospital:
Severe COPD (can be acute or chronic)
Acute Severe Asthma
Pulmonary Oedema in acute Left Ventricular failure
Due to hypoventilation as main feature
159
Q

How do we treat type 2 respiratory failure

A

Give oxygen
Controlled in COPD patients with chronic respiratory failure

Treat the underlying cause to reverse hypoventilation e.g. bronchodilators for acute asthma or opiate antagonists for overdoses

Support ventilation
Non-invasive ventilation
Invasive ventilation

160
Q

what causes V/Q mismatch

A
  • Most lung diseases effecting the airways and parenchyma
  • Lung infection such as pneumonia
  • Bronchial narrowing such as asthma and COPD (although they can also progress to type 2 resp failure)
  • Interstitial lung disease
  • Acute lung injury
161
Q

V/Q mismatch in pneumonia

A

Creates a shunt leading to low PO2 because blood does not come into contact with adequate O2

162
Q

what happens to arterial CO2 in V/Q mismatch

A
  • Blood leaving areas of low V/Q ratio has
    • Low PaO2
    • High PaCO2
  • High PaCO2 stimulates ventilation
  • ‘Extra’ ventilation goes to areas of normal lung and areas with high V/Q ratio so get blood with low CO2
  • Blood from both areas mixes so overall CO2 is normal
163
Q

what happens to to arterial O2 in V/Q mismatch

A
  • Blood leaving areas of low V/Q ratio has
  • Low PaO2
  • High PaCO2
  • High PaCO2 stimulates ventilation
  • ‘Extra’ ventilation goes to areas of normal lung and areas with high V/Q ratio
  • But extra ventilation can’t push O2 content much higher than normal
  • Blood from both areas mixes but cannot overcome the low oxygen level
164
Q

treatment of pulmonary embolism

A

Oxygen in acute episode

Anticoagulation to stop further clot propagation

Thrombolysis in some cases where circulatory compromise

165
Q

asthma and respiratory failure

A

Hypoxaemia suggests significant asthma attack

Bronchospasm and mucous plugging causes ventilation defects and V/Q miss match

Type 2 resp failure develops when severe bronchospasm causes hypoventilation of alveoli or exhaustion

The patient needs oxygen to survive

Invasive ventilation may be required

166
Q

COPD and respiratory failure

A

COPD is a mixture of chronic airways inflammation and narrowing and emphysema

Problems with V/Q mismatch and hypoventilation

May present acutely with respiratory failure type 1 or type 2

May have chronic type 2 respiratory failure in advanced disease

Treat respiratory failure with oxygen but with caution in chronic type 2 respiratory failure

167
Q

oxygen therapy masks

A

Variable performance
Cheap and cheerful
Exact inspired O2 concentration not known

Fixed function
Constant, known inspired concentration

Reservoir mask
High inspired concentration of O2

168
Q

how do we treat respiratory failure

A
  • Give oxygen
  • This is a short term life saving measure
  • The fundamental problem is inadequate gas exchange
  • Improve gas exchange: treat underlying cause
  • In some cases mechanical ventilation is required
169
Q

why measure blood gases

A

To assess very sick patients
To diagnose respiratory failure
To diagnose metabolic problems

170
Q

quantifying O2 carriage

A

1 - Haemoglobin saturation
Because it’s very easy to do!
Assuming Hb is normal, it’s an accurate reflection of oxygen content

2- Arterial blood gases
More complicated and invasive
PaO2 reflects haemoglobin saturation but is a measure of the partial pressure of O2 in the blood

171
Q

how to measure haemoglobin saturation

A
  • Oxygenated haemoglobin is RED
  • Deoxygenated haemoglobin in BLUE
  • Using absorption spectroscopy, it is possible to estimate the degree of saturation of haemoglobin
  • SpO2, pulse oximetry
172
Q

how to measure ABG

A

Single arterial puncture technique

  • Radial artery
  • Femoral artery
  • Brachial artery

Measurement from in-dwelling arterial catheter or A-line
- Only really an option in HDU/ITU

173
Q

what does blood gas measure

A
  • PaO2
  • PaCO2
  • Hydrogen ion/pH
  • Bicarbonate
  • Some analysers may also measure electrolytes and Hb
  • Other forms of haemoglobin:
  • Carboxyhaemoglobin
174
Q

normal blood gas values

A

H+ 36-44 nmol/l

PO2 12-15 kPa

PCO2 4.4-6.1

HCO3 21-27.5

BE +2 to -2 mmol/l

175
Q

understanding O2 kPa

A

Partial pressure of oxygen in the air is 21 kPa

The total pressure in the atmosphere is 100 kPa

21% of the air is oxygen, therefore 21% of the total pressure is the partial pressure of oxygen

This depends on environment

176
Q

acidosis

A

H+ is increased by:

An increase in pCO2 (respiratory acidosis)

An increase in acid production or decrease in excretion (metabolic acidosis)

177
Q

acute vs chronic type 2 respiratory failure

A

Acute hypoventilation e.g. due to opiate toxicity leads to hypoxia, hypercapnia and acidosis

Chronic hypoventilation e.g. neuromuscular disease or severe COPD leads to hypoxia and hypercapnia but may not have acidosis due to compensation
- increased bicarbonate retention in kidney

178
Q

respiratory alkalosis

A 
Not usually associated with respiratory failure
Caused by hyperventilation
Have low PCO2 and low H+
PO2		14
PCO2		2.2
H+		32
HCO3		25
179
Q

metabolic problems

A

Excess acid production by the body e.g. lactic acidosis or diabetic ketoacidosis

Kussmal breathing is a classical clinical sign of acidosis as a compensatory mechanism to increase CO2 removal from the blood

Full compensation is difficult: need to treat the underlying cause of increased acid load e.g. treatment of DKA

180
Q

interpreting bicarbonate

A

Actual bicarbonate:
- Calculated with actual H+ and pCO2 values

Standard bicarbonate:

  • Calculated with actual H+ and a pCO2 of 5.3kPa (normal pCO2)
  • Standard bicarbonate is therefore only influenced by metabolic effects
181
Q

base excess

A

The amount of base needed to be removed from a litre of blood at a normal pCO2 in order to bring the H+ back to normal

Sounds complicated but it’s not:

  • It is calculated with a normal CO2, so it only looks at the metabolic component
  • Normal value is zero (-2 to 2 mmol/l)
  • A big negative value indicates a metabolic acidosis
  • A positive value seen in compensated respiratory acidosis
182
Q

anion gap

A

The anion gapis the difference between primary measured cations (Na+and K+) and the primary measuredanions (Cl-and HCO3-) in serum.

183
Q

causes of respiratory acidaemia

A
  • impaired gas exchange‐- Hyperventilation
  • Lung disease, COPD
    ‐Drugs (respiratory depression)
    ‐Muscle paralysis
184
Q

causes of respiratory alkalaemia

A

hyperventilation from -
‐Salicylate poisoning (aspirin)
‐Hysteria, anxiety
‐Cerebral diseases such as viral infection/head injury

185
Q

causes of metabolic acidaemia

A
  • acidic metabolic products
  • loss of HCO3
  • chronic diarrhea (bile salts)
  • increase buffering demand (eg keto/lactic acidaemia)
  • acid indigestion
186
Q

causes of metabolic alkalaemia

A
  • bicarbonate indigestion

‐ Severe vomiting (HCl loss)

187
Q

common causes of metabolic acidaemia (anion gap)

A 
methanol
ethylene glycol
salicylate
lactic acidaemia
alcoholic ketoacidosis
renal failure
diabetic ketoacidosis
188
Q

principle buffers in plasma

A

phosphate

  • buffers intracellular fluid
  • important urinary buffer

protein

  • present in large amounts
  • buffers intracellular fluid & plasma
  • haemoglobin buffers RBC

bicarbonate
- primary extracellular fluid buffer

ammonia
-allows excretion of H+ as NH4 in acidaemia

189
Q

acute bronchitis

A 
Inflammation of bronchi
• Often viral
• May be bacterial e.g. H influenzae
• May also involve larynx and trachea -
laryngotracheobronchitis
• Acute exacerbations of ‘chronic bronchitis’ are
common
190
Q

bronchiolitis

A
  • Inflammation of bronchioles
  • A feature of chronic bronchitis
  • Primary bronchiolitis
  • Usually in children
  • Respiratory syncytial virus (RSV)
  • Tachypnoea and dyspnoea
  • Rare types
  • Follicular bronchiolitis
  • Bronchiolitis obliterans
191
Q

diffuse obstructive airway disease

A 
• Reversible and intermittent OR Irreversible and
persistent
• Centred on bronchi and bronchioles
• Diffuse disease as many airways involved
• Pulmonary function tests ‘obstructive’
• Reduced vital capacity (VC)
• Reduced FEV1 / FVC ratio
• Reduced peak expiratory flow rate
192
Q

examples of diffuse obstructive airway disease

A
  • Several clinico-pathological entities
  • Chronic bronchitis
  • Emphysema
  • Asthma
  • (Bronchiectasis)

• Chronic obstructive pulmonary disease (COPD)
• Spectrum of co-existence of chronic bronchitis and
emphysema

193
Q

chronic bronchitis

A

Cough and sputum for 3 months in 2 consecutive
years
• Aetiology - pollution, smoking
• Clinical
• Middle-aged heavy smokers
• Recurrent low-grade bronchial infections (exacerbations)
• H. influenzae, S. pneumoniae, viruses
• Airway obstruction may be partially reversible

194
Q

progression of chronic bronhcitis - final outcome

A 
• Hypercapnia
• Hypoxia
• Pulmonary hypertension
•
‘Cor pulmonale’ - right ventricular failure

• ‘Blue bloater’

195
Q

pathology of chronic bronchitis

A
  • Respiratory bronchiolitis (<2mm diameter)
  • Can lead to centrilobular emphysema
  • Mucus hypersecretion
  • Mucous gland hypertrophy
  • Chronic bronchial inflammation
  • Squamous metaplasia, increased risk of malignancy
196
Q

emphysema

A

• Irreversible dilatation of alveolar spaces with
destruction of walls
• Associated with loss of surface area for gas
exchange

197
Q

centrilobular emphysema

A

Strongly associated with smoking
• Seen in some with pneumoconiosis, particularly
coal-workers
• Most commonly in upper lobes
• Respiratory bronchiolitis often present

198
Q

panlobular emphysema

A

• Usually lower lobes
• Lungs overdistended
• Associated with alpha-1-antitrypsin deficiency
• Markedly accelerated in smokers with this
disorder

199
Q

other forms of emphysema

A
  • Paraseptal
  • Distension adjacent to pleural surfaces
  • May be associated with scarring
  • Irregular
  • Associated with scarring
  • Overlap with paraseptal emphysema
  • Others
  • Bullous: distended areas >10mm
  • Interstitial
200
Q

clinical features of emphysema

A 
• Hyperventilation
• Normal pO2, pCO2
• ‘Pink puffer’
• Weight loss
• Right ventricular failure
• Often co-existing chronic bronchitis, in which case
clinical features are mixed
201
Q

asthma

A 
Reversible wheezy dyspnoea’
• Increased irritability of the bronchial tree with
paroxysmal airway narrowing
• Five aetiological categories
• Atopic
• Non-atopic
• Aspirin-induced
• Occupational
• Allergic bronchopulmonary aspergillosis (ABPA)
202
Q

atopic asthma

A

Associated with allergy
• Triggered by a variety of factors
• Dust, pollen, house dust mite etc etc
• Often associated with eczema and hay fever
• Bronchoconstriction mediated by a type I
hypersensitivity reaction

203
Q

non-atopic asthma

A
  • Associated with recurrent infections
  • Not immunologically mediated
  • Skin testing negative
204
Q

allergic bronchopulmonary aspergillosis

A

Specific allergic response to the spores of Aspergillus
fumigatus
• Mixed type I and type III hypersensitivity reaction
• Mucus plugs common
• Associated with bronchiectasis
• Not to be confused with an aspergilloma, which is a
fungal ball, usually colonising a pre-existing cavity in
the lung (often tuberculous)

205
Q

bronchiectasis - 2

A

• Permanent dilatation of bronchi and bronchioles
• Due to a combination of obstruction and inflammation
(usually infection)
• May be localised or diffuse, depending on cause
• Historically seen in patients with pulmonary
tuberculosis involving hilar lymph nodes
• Classically associated with childhood infections,
particularly measles and whooping cough
• Diffuse bronchiectasis seen in patients with cystic
fibrosis

206
Q

clinical features of bronchiectasis

A 
• Chronic cough productive of copious
sputum
• Finger clubbing
• Complications
• Spread of infection
• Pneumonia, Empyema, Septicaemia, Meningitis,
Metastatic abscesses e.g. brain
• Amyloidosis
• Respiratory failure
207
Q

the air travels down

A

Nasal Cavity
Pharynx
Larynx
Trachea

Bronchi
Bronchioles
Alveoli

208
Q

features of the nasal cavity

A

Conchae = turbinate

Meatus = passage or opening

209
Q

paranasal sinuses

A

frontal

ethmoidal

maxillary

sphenoidal

drain into nasal cavity

210
Q

nasal cavity- communicating structures

A

Pharyngotympanic tube– connects nasal cavity to the middle ear

Nasolacrimal duct (tear duct) – connects lacrimal sac to nasal cavity

211
Q

the pharynx

A

nasopharynx
oropharynx
laryngopharynx

soft palate “flutter valve”

212
Q

innervation of the pharynx

A

vagus nerve [X]

glossopharyngeal nerve [IX]

213
Q

the larynx - structure

A

Voice Box

Cartilaginous structures

  • hyaline cartilage
  • elastic fibrocartilage
214
Q

epiglottis

A

Closes over the entrance to the larynx to stop food/ liquid entering during swallowing

215
Q

histology of respiratory system

A

Most of the upper respiratory tract is covered in pseudostratified columnar ciliated epithelium (“respiratory epithelium”)

Goblet cells (G) – produce mucus to trap foreign particles

Cilia (C) - beat to transport mucus out of the respiratory system

216
Q

bronchiole histology

A 
<1mm lumen
Pseudostratified ciliated columnar epithelium  Ciliated columnar epithelium
NO glands
NO cartilage
Smooth muscle (M)
217
Q

what is an obstructive disorder

A
  • narrowing of airway
  • reduced inflow of gas
  • reduced inflation of alveoli
218
Q

factors affecting airway internal diameter

A
  • Increased mucus production
  • Anatomical features
  • Autonomic and Non-Adrenergic/Non-Cholinergic (NANC) systems
  • Inflammation
219
Q

autonomic and NANC Nervous systems

A

parasympathetic nerve (vagus)

  • acetyl choline
  • muscarinic receptors
  • constriction

the circulation

  • B2 adrenergic receptors
  • bronchodilation
220
Q

cystic fibrosis

A
  • autosomal recessive
  • mutation in CTFR gene - encodes it protein, a chloride and bicarbonate ion channel present on cell membrane
  • multi-system disease
  • median survival 47 yrs
221
Q

how to measure obstruction

A

peak flow
spirometry
lung volumes & flow

222
Q

airway resistance and flow calculation (calculates peak expiratory flow)

A

(upstream pressure - downstream pressure) / resistance

volume of gas per unit of time

223
Q

PEF in asthmatics

A

morning dips

224
Q

FEV1 & FVC

A

FEV1 - How much can the patient exhale in a given time, e.g. 1 second

FVC - How much they can exhale altogether

225
Q

Factors to consider when looking at FEV1:FVC ratio

A

We compare to predicted values based on age, sex and height

Predicted values are based on population of healthy individuals

if <0.7 suggests obstructive airway pathology

226
Q

Global Lung Initiative (GLI) lung function prediction

A

Global initiative set up in 2008 to standardize the predicted values for spirometry

Now adopted as gold standard in many countries

Online tool for data interpretation

227
Q

effect of mild/moderate obstruction on lung volumes

A

TLC remains in normal range

  • airway narrowing and collapse leads to gas trapping
  • RV increased above normal range
  • RV/TLC ratio increased above normal
228
Q

effects of severe airway obstruction on lung volumes

A

TLC increased above normal range due to destruction of lung tissue (emphysema)

VC decreased

  • extensive airway narrowing and collapse leading to gas trapping
  • RV substantially increased above normal range
  • RV/TLC ratio increased
229
Q

reversibility of spirometry

A

Used as a diagnostic test in Asthma e.g. following bronchodilator

Asthma reversible vs. COPD fixed airways obstruction

Can also use bronchial challenge agents (histamine) to induce bronchospasm and obstructive spirometry

230
Q

what is a restrictive disorder

A

A disorder in which prevents normal expansion of the lungs

231
Q

what causes lung restriction

A

Extra-pulmonary disease
i.e. visceral pleura, pleural space, chest wall including parietal pleura, bones, muscles, nerves

Intra-pulmonary disease
i.e. alveolar spaces

232
Q

extra-pulmonary restrictions

A
  1. Integrity of nerves to respiratory muscles
    e. g. high cervical dislocation
  2. Impaired neuromuscular junctions
    e. g. myasthenia gravis
  3. Impaired muscles
    e. g. muscular dystrophy
  4. Pleural thickening
    e. g. asbestos exposure
  5. Skeletal abnormalities
    e. g. scoliosis
233
Q

intra-pulmonary restrictions

A

diseases causing increased fibrous tissue in lung

  • silicosis in stonemason
  • asbestosis
  • drug-induced lung fibrosis
  • coal-worker pneumoconiosis
  • rheumatoid-lung
  • bird-fanciers lung
  • idiopathic pulmonary fibrosis
234
Q

how do fibrotic lung diseases cause restrictive disease

A
  1. Inflation pressure
  2. Compliance
  3. Elastic recoil
235
Q

elastic recoil pressure =

A

alveolar pressure minus pleural pressure

236
Q

pulmonary compliance

A

the ability of the lungs to stretch during a change in volume relative to an applied change in pressure (‘stretchability’)

237
Q

relationship between inflation pressure, compliance and elastic recoil

A

A lower compliance means greater inflation pressure required to inflate which means higher elastic recoil

238
Q

effects of a decreased compliance on inflation

A

increased fibrous tissue (more rigid)

decreased compliance (requires high pressure to inflate)

Increased elastic recoil (deflates easily)

239
Q

what casues increased compliance

A

Associated with an OBSTRUCTIVE defect, particularly emphysema

240
Q

effects of increased compliance on deflation

A 
decreased elastic tissue (more floppy)
increased compliance (inflates at low pressures)
decreased elastic recoil (difficult to deflate)
241
Q

alveolar features making them different from balloons

A
  1. Alveoli are moist

2. Alveoli are of different sizes

242
Q

alveoli being different size - effect

A

air moves from HIGH pressure area to LOW pressure area

SMALLER alveolus empties into LARGER alveolus

There is INSTABILITY of adjacent alveoli

243
Q

surfactant

A

produced by alveolar Type II cells

composed of lipids (90%, mainly phospholipids) and proteins (10%)

reduces surface tension

244
Q

well-expanded alveoli (inspiration) - surfactant

A

Surfactant spread evenly over alveolar surface but molecules spread out

Surfactant has little effect on surface tension (sT)

245
Q

deflated alveoli (expiration) - surfactant

A

Tightly packed surfactant molecules

Some surfactant molecules extruded from the surface

Surfactant significantly reduces surface tension (T) with accompanying lower pressure (P)

246
Q

pressure equation

A

P = (2 * sT) / radius

247
Q

respiratory distress syndrome of the newborn

A

caused by lack of surfactant

Surfactant first produced  210 days c.f. full term = 280 days (40 weeks)

low compliance
high inflation pressures
rapid shallow breathing - fatigue
hypoxaemia

248
Q

impaired surfactant contributes to what resp. disorders

A 
Adult respiratory distress syndrome (ARDS)
Pneumonia
Idiopathic pulmonary fibrosis
Lung transplant
			………etc
249
Q

spirometry and lung volumes in restriction

A

decreased….
spirometry
- FEV1
- FVC

Helium dilution

  • total lung capacity
  • vital capacity
  • residual volume
250
Q

gas transfer measurement

A

Gas transfer is a measure of the diffusing capacity of the lung.

It requires a measurement of GAS EXCHANGE and ALVEOLAR VOLUME

251
Q

measuring gas exchange

A

use CO - carbon monoxide

Rapidly taken up by haemoglobin with very high affinity
Not produced by the body
Non-toxic
Easy to measure

252
Q

measuring alveolar volume

A

use He - Helium

NOT TAKEN UP by haemoglobin
Not produced by the body
Non-toxic
Easy to measure

253
Q

what can you calculate using single breath method - CO

A

TLCO (mmol/min/kPa)
- total gas exchange capacity

VA
- alveolar volume

KCO
- efficiency of gas transfer per unit of lung

254
Q

TLCO and KCO - extra-pulmonary restrictive

A

TLCO low
-lungs are smaller

KCO high
-alveoli are normal and tightly packed with blood vessels

Year 1 - semester 2 amy (6 decks)

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