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Y1S2- Cardio, Resp, Loco > Respiratory > Flashcards

Respiratory Flashcards

1
Q

1 kPa=

A

7.5 mmHg

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2
Q

Dalton’s Law

A

gases in a mixture exert pressures that are independent of each other
Therefore: atmospheric pressure is the sum of the partial pressures of all of the gases in the atmosphere
Pat = PN2 + PO2 + PCO2 + PH2O + Pothers

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3
Q

Henry’s Law

A

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

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4
Q

what is gas exchange in the lungs driven by?

A

differences in partial pressure across the alveolar membrane: inspired air has higher PO2 and a lower PCO2 than the plasma

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5
Q

1 mol=

A

22400 ml of gas

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6
Q

equilibrium in gas exchange in alveoli

A
  • Gas exchange in the alveoli is so rapid that equilibrium is usually attained
  • If equilibrium is not reached, usually due to V/Q ratio
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7
Q

V/Q ratio

A

amount of air that reaches your alveoli divided by the amount of blood flow in the capillaries in your lungs

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8
Q

passive diffusion through biological membranes

A
  • Gases go through membranes by diffusion
  • The rate of permeation is proportional to the concentration difference
  • If concentrations are the same of each side of the membrane, there is no net movement (diffusion occurs at equal rates on each side)
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9
Q

what is P (permeation constant) dependant on?

A

membrane thickness, membrane area, diffusion constant and the partition coefficient

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10
Q

solubility of oxygen=

A

= 1.5% in free solution and rest is bound to haemoglobin

- Oxygen carrying capacity depends on the amount of haemoglobin

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11
Q

haemoglobin: structure, cooperativity and conformational states

A
  • Tetrameric protein
  • 2 types of subunits adult = alpha2beta2 (and foetal= alpha2gamma2)
  • Every molecule of Hb binds 4 O molecules
  • As one oxygen molecule binds, each subunit undergoes a conformational change by non-covalent inter-subunit bonds which makes it easier for other oxygen molecules to bind
  • 2 conformational states: oxy and deoxy- binding and release of O2 occurs over a relatively small range of oxygen concentrations
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12
Q

why can foetuses take oxygen from maternal blood?

A

foetal haemoglobin has higher oxygen affinity than adult haemoglobin so it can take oxygen from maternal blood to the foetus

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13
Q

factors which affect O2 affinity for haemoglobin:

A
  • conc. hydrogen ions
  • conc. carbon dioxide
  • temperature
  • carbon monoxide
  • 2,3 diphosphoglycerate
  • oxidation of iron in haemoglobin
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14
Q

H+ conc. effect on O2 affinity for haemoglobin:

A

The Bohr effect: as [H+] increases, affinity for oxygen decreases which favours oxygen release in metabolising tissue

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15
Q

CO2 conc. effect on O2 affinity for haemoglobin:

A

The Haldane effect- as [CO2] increases, the affinity for oxygen decreases as CO2 reacts with amino groups

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16
Q

temperature effect on O2 affinity for haemoglobin:

A

as temperature increases, affinity for O2 decreases (eg. O2 is released when temperature rises ie. In muscle)

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17
Q

2,3 diphosphoglycerate effect on O2 affinity for haemoglobin:

A

lowers O2 affinity

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18
Q

carbon monoxide effect on O2 affinity for haemoglobin:

A

binds to Hb with an affinity 200 times greater than oxygen- also affects affinity of remaining sites as affinity for oxygen is increases so oxygen is released poorly in metabolising tissue

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19
Q

Oxidation of iron in haemoglobin effect on O2 affinity for haemoglobin:

A
  • Oxidation of iron in haemoglobin to Fe3+ converts it to methemoglobin which does not bind oxygen- methemoglobin reductase reduces this back to Fe2+
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20
Q

carbon dioxide carriage in blood

A

Co2 is far more soluble than oxygen in blood but only a small proportion of CO2 is directly dissolved. Three mechanisms contribute to bulk of transport: bicarbonate- mediated transport, carbamino-mediated transport and dissolution.

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21
Q

60% of carbon dioxide transport is mediated by:

A

HCO3 through an equilibrium between plasma Co2 and carbonic acid (H2CO3), which is important in pH regulation.
carbonic anhydrase within the red blood cells quickly converts the carbon dioxide and water into carbonic acid, which immediately dissociates into bicarb ions and H+ ions. this reaction allows for the continued uptake of carbon dioxide into the blood down its concentration gradient.

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22
Q

30% of carbon dioxide transport is carried out by:

A

carbamino groups
The N-terminus of proteins contains a free NH2 group which can combine with CO+2 to produce a carbamino group. This reaction is readily reversible releasing CO2¬ if the pCO2 falls. Most carbamino groups are found on the peptide chains haemoglobin.

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23
Q

does deoxyhaemoglobin or oxyhaemoglobin have higher capacity for forming carbamino groups?

A

Deoxygenated haemoglobin has a higher capacity for forming carbamino groups than oxygenated haemoglobin.

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24
Q

10% of carbon dioxide transport

A

is transported dissolved in blood. The dissolved amount proportional as always to the partial pressure of the solution.

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25
Q

why is chorine important in bicarbonate mediated carbon dioxide transport?

A

Bicarbonate can diffuse out of cells but H+ cannot cross the erythrocyte membrane so Cl- transport into the cell is necessary to maintain charge neutrality across the membrane
In venous blood, more CO2 is present and therefore more intracellular Cl- is found.

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26
Q

elasticity of lungs and chest wall

A
  • The lungs and chest wall are elastic: lungs tend to recoil inwards and the chest wall resists being distorted inwards from its natural resting shape resulting in an outward force
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27
Q

inspiration process

A
  • Inspiratory muscles (diaphragm, external intercostals) contract and thoracic cage expands
  • Pleural pressure becomes more negative relative to atmospheric: this negative pressure is transmitted to the alveoli
  • Air flows into the lungs down the pressure gradient from mouth to alveoli and the lungs inflate
  • The incoming air holds the small intrathoracic airways wide open
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28
Q

resting breathing expiration process

A
  • Inspiratory muscle activity ceases and elastic recoil causes lungs to shrink- expiration is passive
  • Elastic recoil produces positive pressure in the alveoli
  • Air moves down pressure gradient from alveoli to mouth
  • Small intrathoracic airways tend to be compressed and narrowed by surrounding alveoli during expiration
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29
Q

Vt:

A

tidal volume, volume of gas breathed in or out of the lungs with each normal breath (litres)- normal resting value 0.4-0.8 litres

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30
Q

fR:

A

respiratory frequency, number of breaths per minute- normal resting values 12-15 breathes/ min

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31
Q

Ve:

A

minute ventilation; the amount of gas breathed in or out of the lungs per minute (litres/min)- normal resting value 5-8 l/min

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32
Q

large/ forced expirations process

A
  • Expiratory muscles (internal intercostals, abdominal muscles) contract depressing rubs, pushing diaphragm up, reducing thoracic volume and so increasing alveolar pressure and airflow
  • Maximum airflow limited by compression of small intrapulmonary airways by surrounding alveoli
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33
Q

what does the CNS control in breathing?

A

the rhythmical contraction and relaxation of the respiratory muscles (diaphragm, intercostals)

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34
Q

basic breathing rhythm is generated in the

A

medulla

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35
Q

removal of the upper part of the pons in animals results in

A

slow, gasping breathing, suggesting neurones in this area help to control breathing

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36
Q

Main areas of respiratory neurones in the medulla and pons:

A
  1. Ventral Respiratory Groups (VRG)
    ventrolateral side of the medulla, contains inspiratory and expiratory neurones
  2. Dorsal Respiratory Groups (DRG)
    In the floor of the 4th ventricle- predominantly inspiratory neurones, pacemaker of controlled breathing
  3. Pontine Respiratory Group (PRG)
    Bilateral areas in the upper pons, contains neurones that are active in both inspiratory and expiratory phases
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37
Q

functional model of generation of breathing 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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38
Q

reflux sensory information affecting breathing

A
  • sensory information originates in lungs
  • afferent fibres carried in vagus nerves (cranial X)
  • activation initiates expiration
  • sectioning the vagus nerves causes prolongation of inspiration (i.e. expiration is not commenced)
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39
Q

Rapidly Adapting (irritant) Receptors:

A
  • sub epithelial mechanoreceptors in the trachea and bronchi, stimulated by inhaled irritants or mechanical factors, such as smoke, dust and chemicals such as histamine
  • cause coughing, mucus production and bronchoconstriction
  • their afferent fibres are myelinated
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40
Q

Slowly Adapting (stretch) Receptors:

A
  • mechanoreceptors located close to airway smooth muscle, which are stimulated by stretching of airway walls during inspiration
  • help prevent over-inflation by initiating expiratory rhythms.
  • important role in the Hering-Bruer reflex (prolonged inspiration causes prolonged expiration). Afferent fibres are also myelinated
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41
Q

C fibres:

A
  • unmyelinated nerve endings stimulated by oedema and various inflammatory mediators such as histamine and bradykinin
  • cause rapid, shallow breathing and dyspnoea
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42
Q

Normoxia

A
  • O2 in normal range
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43
Q

Hypoxia

A
  • fall in O2 below normal (strictly speaking relates to O2 in a gas)
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44
Q

Hypoxaemia

A
  • fall in O2 below normal in blood
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45
Q

Hyperoxia

A
  • rise in O2 above normal
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46
Q

Normocapnia

A
  • CO2 in normal range
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47
Q

Hypercapnia

A
  • increase in CO2 above normal level
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48
Q

Hypocapnia

A
  • fall in CO2 below normal
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49
Q

sites of peripheral and central chemoreceptors

A

Central chemoreceptors on ventrolateral surface of medulla

Peripheral chemoreceptors in carotid bodies

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50
Q

peripheral chemoreceptors have a fast response to

A

arterial pO2, pCo2 and arterial [H+]

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51
Q

central chemoreceptors have a slow response to

A

respond indirectly and slowly to changes in arterial pCO2; CO2 crosses blood-brain barrier, produces [H+] ions which stimulate receptor cells

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52
Q

hypercapnia leads to

A

Linear increase in minute ventilation (Ve); this happens almost instantaneously when pCO2 rises above normal levels.
30% of the response caused by the peripheral chemoreceptors; fast response (2-4 sec)
70% caused by central chemoreceptors; slow response (4 min to reach maximum response)

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53
Q

minute ventilatory responses to hypercapnia

A
  • Increased by hypoxia: decreased by hyperoxia

- Interaction mediated at the peripheral chemoreceptors

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54
Q

hypocapnia leads to

A

little change in ventilation- dog leg of curve

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55
Q

hypoxia leads to

A

Curvilinear increase in ventilation.
There is little change in ventilation until pO2 has fallento about 8 kPa (60 mmHg), then a sharp increase. - mediated by peripheral chemoreceptors

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56
Q

hyperoxia leads to

A

small decrease in ventilation as tonic activity of chemoreceptors is switched off.

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57
Q

response to hypoxia

A
  • increased by hypercapnia

* interaction mediated at the peripheral chemoreceptors

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58
Q

Severe chronic airflow obstruction causing failure of normal chemoreceptor control of breathing

A
  • Lungs unable to excrete metabolic CO2 load
  • Chronic hypercapnia - desensitises central chemoreceptors
  • Patient becomes dependent on hypoxic drive to breathe
  • In this situation ONLY, giving high flow oxygen can dangerously suppress breathing- can lead to CO2 narcosis and death
  • Avoid by using controlled low-flow oxygen therapy in emergency situations in these patients only
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59
Q

altered control of breathing during sleep

A
  • Respiratory drive decreases (loss of wakefulness drive)
  • Partly related to reduction in metabolic rate partly due to reduced input form higher centres such as pons and cortex
  • Also- loss of tonic activity (state of continuous activity that exists in both the sympathetic and parasympathetic divisions) to upper airways
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60
Q

Consequence of loss of wakefulness drive:

A

patients with diminished capacity to ventilate (eg. muscle weakness, severe lung disease, neuropathy or spinal deformity) first develop respiratory failure (raised arterial CO2) during sleep

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61
Q

obstructive sleep apnea

A
  • some patients have narrowed upper airway due to structural difference (shape of jaw) or excess fat around the neck
  • during sleep, loss of upper airway tone allows upper airways to collapse
  • can cause cessation of breathing in excess of 1 minute
  • occurs in approx. 2% of population
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62
Q

drugs that depress breathing

A

almost all anaesthetics, opioids, benzodiazepines

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63
Q

drugs that stimulate breathing

A

doc-ram (now rarely used), beta 2 agonists

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64
Q

mechanical and immunological defences of the body

A

Mechanical: ciliated epithelium, mucus, cough
Immunological: IgA and antimicrobials in mucus, resident alveolar macrophages & dendritic cells, innate/ adaptive immune responses

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65
Q

parenchyma

A

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

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66
Q

microorganisms involved in community acquired pneumonia

A
  • Streptococcal pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Klebsiella pneumoniae/ Pseudomonas aeruginosa
  • Mycoplasma pneumoniae
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67
Q

microorganisms involved in hospital acquired pneumonia

A
  • Gram negative rods, Enterobacteriaceae, pseudomonas

* MRSA

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68
Q

microorganisms involved in aspiration acquired (oral/gastric contents in bronchial tree) pneumonia

A

• Anaerobic oral flora mixed with aerobic bacteria

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69
Q

microorganisms involved in immunocompromised host pneumonia

A
  • Cyclomegalovirus
  • Pneumocystis jiveroci (PCP)
  • Mycobacterium avium-intracellulare
  • Invasive aspergillosis
  • Invasive candidiasis
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70
Q

microorganisms involved in necrotising/ abscess formation pneumonia

A

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

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71
Q

clinical presentation of pneumonia

A
  • Cough
  • Sputum
  • Pyrexia
  • Pleuritic chest pain
  • Haemoptysis
  • Dyspnoea
  • Hypoxia
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72
Q

appearances of pneumonia

A
  1. Bronchopneumonia
    - Most common pattern
    - Patchy consolidated areas of acute supprative (pus) inflammation
    - Often elderly with risk factors- cancer, heart failure, renal failure, stroke, COPD
  2. Lobar pneumonia
    - Rust coloured sputum
    - S.pneumoniae
    - Consolidation of a large portion of a lobe or an entire lobe
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73
Q

local factors of pneumonia

A

Local Factors:

  • Loss or suppression of the cough reflex- drugs
  • Injury to the mucocilliary apparatus- viruses, gases
  • Accumulation of secretions- CF, obstruction (tumour)
  • Impaired alveolar macrophages function- alcohol, tobacco
  • Pulmonary congestion and oedema
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74
Q

complications of pneumonia

A

Local: abscess formation, parapneumonic effusion, empyema
Systemic: sepsis, ARDS, multi-organ failure
If not resolving, could be cancer?

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75
Q

acute respiratory distress syndrome (ARDS): definition, clinical diagnosis, causes

A
  • Respiratory failure characterised by rapid onset of widespread inflammation in the lungs
  • 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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76
Q

Bronchiectasis: definition and causes

A
  • Permanent dilation of one or more large bronchi
  • Typically affects the 2nd to 8th order of segmental bronchi- large central airways more robust

Causes:

  • Infection: mycobacterial
  • Hereditary: cystic fibrosis
  • Immunodeficiency
  • Chemical injury/aspiration
  • Idiopathic
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77
Q

cystic fibrosis

A
  • Autosomal recessive genetic disease
  • CFTR encodes its protein, a chloride and bicarbonate ion channel present on cell membranes
  • Difficult for patients to clear mucus
  • Multi-system disease affecting the GI tract, liver, reproductive system
  • death is principally related to airways inflammation and infection leading to respiratory failure, which occurs from childhood
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78
Q

tuberculosis risk factors

A
  • TB contact
  • Very young/elderly
  • Immunosuppression
  • Malnutrition/ alcoholism
  • Live or visit TB endemic countries
  • Health care worker
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79
Q

Primary TB: 3-4 weeks

A
  • Mycobacterium tuberculosis multiplies within alveolar macrophages (naïve, unable to kill)
  • Bacterium resides in phagosomes carried to regional lymph nodes from there to circulation
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80
Q

Primary TB: 3-8 weeks

A

3-8 weeks

  • Onset of cellular immunity & delayed hypersensitivity
  • Activated lymphocytes further activate macrophages to kill
  • Primary infection arrested in most immunocompetent people
  • Few bacilli may survive dormant
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81
Q

progressive primary TB

A
  • Infection may not be arrested in minority- infants, children, immunocompromised
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82
Q

tuberculous bronchopneumonia

A
  • Infection spreads via bronchi
  • Results in diffuse bronchopneumonia
  • Well-developed granulomas do not form
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83
Q

military TB

A
  • Infection spreads via bloodstream
  • Organisms scanty (small or insufficient in quantity)
  • Multiple organs- lungs, liver, spleen, kidneys, meninges, brain
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84
Q

Secondary TB (also called ‘post primary’ TB)

A
  • Reactivation of old, often subclinical infection
  • More damage due to hypersensitivity
    • Apical region of lung
    • Tubercles develop locally, enlarge and merge
    • Erode into bronchus and cavities develop
    • May progress into tuberculous bronchopneumonia
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85
Q

asbestos fibrosing lung disease

A

occupational lung disease, exposure in shipyards, building trade. Pleural plaques can lead to mesothelioma and adenocarcinoma.

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86
Q
  • Hypersensitivity pneumonitis (fibrosing lung disease)
A

Type 3 hypersensitivity reaction eg. pigeon fancier’s lung, mushroom lung, hot tub lung- normally resolve when agent is resolved but can be chronic

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87
Q

Usual interstitial pneumonitis-

A

fibrotic foci, mixed inflammatory infiltrate, excess alveolar macrophages
progressive scarring of both lungs

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88
Q

symptoms fo restrictive chronic lung disease

A

dyspnoea, tachypnoea, late stage cyanosis and inspiratory crepitation

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89
Q

causes of lung cancer

A
  • Smoking (>95%)
  • Occupational hazards- uranium mining, asbestos exposure
  • Environmental exposure- radon gas
  • Genetic- Li- Fraumeni Syndrome (mutated p53 gene)
  • ? viral infection- retroviral infection in sheep leads to lung adenocarcinomas
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90
Q

types of lung cancer

A
  • Squamous carcinoma
  • Adenocarcinoma
  • Small cell carcinoma
  • Other- carcinoid tumours
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91
Q

mechanisms of carcinogenesis

A
  • Oncogenes are mutated genes encoding growth- promoting proteins – these are overexpressed in neoplasia eg k-Ras, cylinD1
  • Oncosuppressor genes are mutated genes encoding growth-inhibitory proteins – decreased expression can result in neoplasia eg retinoblastoma gene (Rb)
  • Genes regulating apoptosis may also be mutated eg p53
  • Genes regulating DNA repair may be mutated
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92
Q

Classification & Clinical Significance of Carcinoid/ Neuroendocrine Tumours in the Lung

A 
-	Typical (classical) carcinoid
•	<2 mitoses per 2mm2
•	No necrosis
•	10-15%  have hilar nodal involvement
•	Feq eventually develop in distant sites
  • Atypical carcinoid
    • >2 but <10 per 2mm2
    • Focal necrosis (may be focal commedo like)
    • >10 mitoses per 2mm2 with usually extensive necrosis then classified with LCNEC
    • 40-50% have nodal metastases
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93
Q

Squamous metaplasia

A
  • Common finding in smokers
  • Airways become lined with squamous epithelium rather than normal respiratory epithelium
  • Reversible
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94
Q

Adenocarcinoma: arises, commonly invades & metastasises

associated with and diagnosis

A
  • Arise peripherally from mucous glands and the cells retain some of differentiation and mucus production
  • Commonly invade pleura and mediastinal lymph nodes
  • Commonly metastasise to brain and bones

Associated with: smoking, asbestos exposure, arises around scar tissue
- Distinguished using CT scans and other investigations to check for the primary as they are similar to secondary tumours

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95
Q

symptoms and signs of adenocarcinoma

A

Symptoms of Lung Cancer

  • Cough
  • Dyspnoea
  • Haemoptysis
  • Chest/shouder pain
  • Hoarseness
  • Fatigue

Signs of Lung Cancer

  • Slow to clear pneumonia
  • Finger clubbing
  • Cervical lymphadenopathy
  • Liver, bone, brain metastases
  • Pleural effusion
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96
Q

diagnosis of lung cancer

A 
Biopsies
-	Bronchial biopsies
-	CT guided lung biopsies
-	Biopsies of distant metastases eg. pleura, liver, lymph node
Cytology
-	Bronchial brushings and washings
-	Sputum
-	Pleural fluid aspiration
-	Fine needle aspirates of metastases
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97
Q

behaviour of lung cancer

A

Intrapulmonary growth

  • Obstructive pneumonia
  • Lymphangitis carcinomatosis

Invasion of adjacent structures: pleura, chest wall, mediastinum, diaphragm

Distant metastases via lymphatics and blood: hilar and mediastinal nodes, liver, bones, brain

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98
Q

lymphoid infiltration in lung carcinomas may be associated with

A

better outcomes

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99
Q

screening for lung cancer

A
  • Screening with LDCT (low dose CT) can detect early stage lung cancer
  • CXR/sputum cytology as screening has no effect on mortality
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100
Q

Process by which squamous cell carcinomas develop into necrotic masses

A
  • Secretes tumour angiogenesis factors which causes blood vessels to grow into the mass of tumour cells- allows rapid growth and size increase
  • If the tumour grows too large for its blood supply then the central area can become deprived of oxygen and nutrient leading to necrotic areas
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101
Q

options for lung cancer treatment

A
  • Resection- only 7-10% suitable, 5 year survival, 70%
  • Concurrent chemo-radiotherapy- 5 year survival, 30%
  • Palliative chemotherapy- overall survival benefit, few months
  • Palliative radiotherapy- symptom control
  • Best supporting care- symptom control
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102
Q

lung function after operations in lung cancer

A
  • Lobectomy- early deficit with later recovery, no decrease in exercise capacity & little permanent loss in PFT
  • Pneumonectomy- early permanent deficit, decrease in exercise capacity & PFT
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103
Q

groups of patients respond well to EGFR blocking therapy-

A

East Asian, adenocarcinoma, females, non-smokers

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104
Q

small cell lung cancer: characteristics, staging, prognosis

A
  • Very aggressive tumour
  • Early dissemination
  • Virtually all patients have metastatic spread at presentation

Staging
Limited Disease: restricted to one hemithorax ± ipsilateral nodes
Extensive disease: spread beyond one hemithorax

Prognosis

  • Sensitive to chemotherapy and radiotherapy
  • Long term survivors <5% of patients
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105
Q

Bacteriostatic-

A

stops bacteria from reproducing, while not necessarily killing them otherwise

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106
Q

Bactericidal-

A

kills bacteria, particularly preferred in serious infection

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107
Q

cell wall inhibitors function

A
  • 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
  • Bacitracin acts at Gram positive cell membrane
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108
Q

cell wall synthesis inhibitors examples

A
  • Beta- lactams
  • Glycopeptides eg. vancomycin
  • Fosfomycin
  • Bacitracin
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109
Q

beta lactase- structure and mechanism

A

examples: penicillins, cefalosporins, carbapenems, monobactams
- All possess a beta lactam ring
- Differ in side chains attached to this nucleus
- Target site is peptidoglycan which is present in only bacteria

Mechanism: act in the final step of cell wall synthesis by binding to enzymes responsible for cross linking of polysaccharide chains in the cell wall peptidoglycan (also known as transpeptidases or ‘penicillin binding proteins’)

110
Q

Cmax:

A

the maximum serum concentration that a drug achieves in a specified compartment or test area of the body after the drug has been administrated

111
Q

Tmax:

A

the term used to describe the time at which the Cmax is observed

112
Q

oral drugs characteristics

A

must be able to survive acidic conditions of the stomach

  • may do this either by resistance to acid destruction, or they may have functional groups added to form esters, which are then cleaved by acids to form functional antibiotics.
  • typically indirect; have to go around the body in the circulation to reach the site of infection.
  • easier and cheaper to administer
113
Q

what are different types of beta lactams used for?

A

penicillin: Group A step, meningococci
cefalosporin: broader spectrum, not enterococci (gram positive)
carbapenem= broad spectrum

114
Q

side effects of beta lactase

A
  • Hypersensitivity rash, allergy
  • Avoid amoxicillin in patients with mono- EBV
  • Rare: anaphylaxis but can be fatal
  • Excreted by kidneys: must reduce dose in renal failure
  • Diarrhoea- not uncommon
115
Q

beta lactamase stability

A

cefalexin< cefotaxime < ceftazidime

116
Q

glycopeptides- cell wall synthesis inhibitor

A
  • Eg. vancomycin
  • Inhibit cell wall synthesis by binding to terminal D-ala-D-ala of the peptide chain and prevents incorporation of new subunits to the growing cell wall
  • For gram positives not gram negatives- important in MRSA infection
  • nephron and toxicity- check levels
117
Q

protein synthesis inhibitors

A
  • Aminoglycosides eg. gentamicin
  • Tetracyclines
  • Macrolides (erythromycin, clarithromycin)
  • Chloramphenicol (rarely used in UK)
  • Lincosamides
  • Oxazolidones
  • Fusidic acid
118
Q

aminoglycoside- protein synthesis action, used for, side effects

A

eg. gentamicin
- Inhibit binding of 30S subunit to mRNA =protein synthesis inhibited
- Very good vs gram negatives eg. E.coli, Pseudomonas aeruginosa, Mycobacteria ect.
- Anti-staphylococcal activity
- broad spectrum
- Ototoxic and nephrotoxic
- Monitor serum levels during therapy

119
Q

tetracycline- protein synthesis inhibtion action, used for, side effects

A

action: Inhibit binding of tRNA= protein synthesis inhibited
- Bacteriostatic, Broad spectrum
- Intracellular bacteria eg. chlamydia

  • May cause diarrhoea, nausea
  • Teeth discolouration, avoid in children, pregnant & lactating women
120
Q

macrolides- protein synthesis action, used for, side effects

A
  • Erythromycin, clarithromycin
    action: Prevent peptidyl transferase from adding the growing peptide attached to tRNA to the next amino acid = protein synthesis inhibited

Narrow spectrum: Gram positive- S.aureus, Group A streptococci, legionella, chlamydia, pneumonia (atypical, in COPD exacerbations)
[newer have broader spectrum eg. clarithromycin]

SE: GI upset common
- Thrombophlebitis when given intravenously

121
Q

Lincosamides- protein synthesis inhibitors

A

eg. clindamycin
Bacteriostatic against gram positives(especially Group A streptococci) and anaerobes

action: bind to 50S subunit = protein synthesis inhibited

side effects: diarrhoea/ colitis

122
Q

THFA inhibitors nucleic acid action and examples

A

THFA inhibitor act on nucleic acid synthesis
Sulphonamides–structural analogues of PABA (para‐aminobenzoic acid)
Trimethoprim–‘folate’ antagonist, binds dihydrofolate reductase.
Individually these drugs are bacteriostatic, together they are bactericidal

123
Q

when should trimethoprim not be given?

A

in pregnancy

124
Q

cotrimoxazole

A

combined trimethoprim and sulphonamides

  • There is in vivo energy between the drugs- combined effect if greater than expected sum of activities- used in pneumocystis pneumonia
  • in UK trimethoprim is used for UTI but cotrimoxazole use increasing
125
Q

RNA synthesis inhibitors action:

A
  • Binds to DNA dependant RNA polymerase
  • Forms stable complex with beta subunit (encoded by rpoB gene mutates readily)
  • Inhibits intiation- not elongation
  • Usually bactericidal
126
Q

RNA synthesis inhibitors examples, use, SE

A

rifampcin
used for TB (in combination)
side effects: drug interactions: inactivates oral contraceptive, hepatitis, nausea, body fluids go orange

127
Q

DNA Synthesis Inhibitors- Quinolones action

A
  • Act by inhibiting DNA gyrase (gram negatives) and topoisomerase IV (gram positives) so DNA coiling inhibited
  • Bactericidal
128
Q

fluoroquinolone example, uses, side effects

A

Ciprofloxacin
- Broad spectrum
previously used for anthrax, now meningococcal contact prophylaxis, UTI, typhoid

side effects:

  • Neurotoxicity, confusion, fits
  • Cartilage defects, not used in pregnant women and children
  • Photosensitivity
  • Association with C.difficile
129
Q

broad spectrum antibiotics associated with C.diff (4Cs)

A

Co-amoxiclav
Clindamycin
Ciprofloxacin and other quinolones
Cephalosporins

130
Q

benefits of combination therapy

A

Delay emergence of resistance
Allow smaller doses of each agent (synergy)
Useful if awaiting laboratory results while patient is in severe sepsis
For example: trimethoprim and sulfonamide for pneumocystis pneumoniae

131
Q

cons for combination therapy

A

Worse side effects
Disturb normal gut flora, cause diarrhoea, thrush
Superinfection by resistant bacteria
Additive toxicity –for example, the use of vancomycin & gentamicin or quinolones & macrolides can cause QT prolongation and arrhythmias

132
Q

factors that promote antibiotic resistance

A
  1. Antibiotic Usage- too much or too little
  2. Effective Genetic Mobility- plasmid carriage, transposons, integrons
  3. Efficient Resistance Mechanism- bacterial factors
133
Q

action of resistance genes

A

chromosome, plasmid, transposon, integron

134
Q

mechanism of resistance- target site alteration

A

Target site alteration, e.g. bacterium modifies target site so affinity of drug for site is reduced, antibiotic cannot bind

135
Q

mechanism of resistance- reduced access

A

Reduced access e.g. antibiotic removed from bacterial cell, or bacteria no longer permeable to drug

136
Q

mechanism of resistance- drug inactivation

A

Inactivation of drug e.g. beta lactamases are enzymes produced by bacteria which deactivate the beta lactam ring in certain beta lactam antibiotics, such as penicillin. Clavulanic acid can be given with these antibiotics –it binds to beta lactamases and inactivates them, allowing the antibiotics to work

137
Q

mechanism of resistance- metabolic bypass and hyper production

A

Metabolic bypass through production of additional target so new drug‐resistant metabolic enzyme produced to bypass the inhibited metabolic stage
Hyper-production - overproduction of antibiotic target (titration) for secondary ‘additional’ targets

138
Q

intergrons

A
  • Gene capture and expression systems
  • Usually resides on transposon
  • Able to poach resistant genes ie. extract DNA segments and inserts into other DNA segments
139
Q

Resistance Control Strategies

A
  1. Conservation
    - Remove devices eg. urinary and central catheters
  2. Prudent use- discourage topical, date for stopping
  3. Surveillance
  4. Infection control eg. hand disinfectant
140
Q

oxygen requirement and carbon dioxide production at rest

A

Oxygen requirement at rest= 250ml/min

Carbon dioxide production at rest= 200ml/min

141
Q

gas transfer requirement of surface area between air (alveoli) and blood (capillaries)

A

there is extensive branching in both bronchial and arterial anatomy. Blood vessels branch more than bronchi so have bigger airspaces with smaller vessels.

Airways and vessels have thin walls. Large surface area of air in contact with blood.

142
Q

Equilibrium of Partial Pressure-

A

diffusion of oxygen down a partial pressure gradient

At equilibrium, partial pressure of gas in solution= partial pressure of gas above liquid

143
Q

oxygen and Hb dissociation

A
  • The affinity of binding O2 increases with each successively bound O2 molecule- allosteric effect
  • Once bound, a number of factors can alter ability of Hb to take up and liberate oxygens
  • Ultimately want Hb to take up O2 in the lung and liberate O2 at the tissues (muscles)
144
Q

oxygen content and partial pressure in capillary blood

A

Pulmonary arteries are pumping in deoxygenated blood into small vessels . Oxygen moves from the alveolus into the capillary blood until the partial pressure of the oxygen equilibrates.

145
Q

why is partial pressure of oxygen in mixed alveolar gas higher than that of arterial blood?

A

due to shunting- leads to PO2 being lower than expected

146
Q

anatomical shunts

A
  • Small amount of arterial blood doesn’t come from lung (Thebesian veins- drain heart muscle back into heart)
  • Small amount of blood goes through without seeing gas (bronchial circulation- arteries that oxygenate lung tissue)
147
Q

physiological shunts and alveolar dead space

A

Physiological shunts (lower V) and alveolar dead space (lower Q)
• Not all lung units have same ratio of ventilation to blood flow
• V/Q mismatch

148
Q

Factors that can decrease the partial pressure of oxygen in the blood:

A
  • Hypoventilation- less oxygen to enter the blood, less air enters and leaves the alveoli, decreased alveolar oxygen
  • Decreased environmental oxygen eg. altitude
149
Q

Factors that can increase the partial pressure of oxygen:

A
  • Hyperventilation- PO2 is higher but oxygen content isn’t that much higher
  • Administration of oxygen
150
Q

increase in available pO2 in healthy state leads to

A
  • Slight increase in Hb saturation
  • Little change in oxygen content
  • At a normal PO2, blood carried nearly as much oxygen as it possibly can so increasing PO2 has very little effect on oxygen content
151
Q

Ventilation to Perfusion Ratio (V/Q)

A
  • If ventilation= perfusion then perfect gas exchange

* In the lung, you naturally have V/Q mismatch with less blood and air going to the top of the lung

152
Q

normal V/Q mismatch in different parts of the lung

A

Top of Lung: less airflow and blood flow but V>Q= higher V/Q
Middle of lung: normal
Bottom of lung: more ventilation and more blood flow but V

153
Q

increased V/Q Ratio means that

A
  • Lots of ventilation to alveoli, not much blood
  • Alveoli and blood reach an equilibrium which is closer to air
  • The region of the lung with the high V/Q ratio has a higher PO2 (and a lower PCO2) than other regions
154
Q

decreased V/Q Ratio means that

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)
155
Q

Alveolar dead space=

A

areas of insufficient blood supply for gas exchange and appears with age and disease

156
Q

Anatomical dead space=

A

conducting airways where no gas exchange takes place

157
Q

Physiological dead space=

A

There are some areas of high and low V/Q ratios

PDS= anatomical dead space + alveolar dead space

158
Q

quantifying V/Q mismatch

A
  • Calculate expected alveolar PO2 (PAO2) using the alveolar gas equation
  • Compared with the measured arterial PO2 (PaO2)
  • If PAO2= PaO2 then no mismatch
159
Q

A-a gradient and reasons for a high A-a gradient

A

• Shows difference between alveolar and arterial oxygen level
• Can help to diagnose the cause of hypoxaemia
• High A-a gradient could be due to:
- Problem with gas diffusion
- V/Q mismatch
- Right to left shunt

160
Q

Arterial blood gases (ABG) are used to assess

A

hypoxaemia

161
Q

respiratory vs ventilatory failure

A

Respiratory failure- failure to oxygenate properly leading to hypoxaemia

Ventilatory failure- failure of the ventilatory pump mechanism leading to hypoxaemia

162
Q

Why do patients become hypoxic?

A
  • Hypoventilation
  • Ventilation perfusion (V/Q) mismatch (pathological vs. physiological)
  • Both
163
Q

hypoventilation leads to

A
  • Oxygen levels of down in hypoventilation
  • During normal ventilation CO2 diffused out of blood into alveolus following a partial pressure gradient
  • If there is lower ventilation, then CO2 accumulates in the alveolar space meaning less can be removed by blood
  • O2 decreases while CO2 increases
164
Q

if PaO2 lower than expected =

A

respiratory failure (PaO2< 8 kPa)

165
Q

causes of failure of the ventilatory pump

A

Won’t breathe: control failure
- Brain failure to command eg. drug overdose
- Sometimes in COPD
Can’t breathe: broken peripheral mechanism
- Nerves not working e.g phrenic nerve cut
- Muscles not working eg. muscular dystrophy
- Chest can’t move eg. severe scoliosis
- Gas can’t get in and out eg. asthma/COPD

166
Q

type 2 respiratory failure: definition, causes

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
167
Q

treatment of type 2 respiratory failure

A
  • Oxygen- controlled in COPD patients with chronic respiratory failure
  • Treat underlying cause to reverse hypoventilation eg. bronchodilators for acute asthma or opiate antagonists for overdoses
  • Support ventilation- invasive or non-invasive
168
Q

non invasive ventilation

A
  • Common treatment for COPD exacerbations with type 2 respiratory failure
  • Tight fitting mask, no need for sedation and incubation
  • Increased ventilation efficiency
  • Also useful in neuromuscular disease and thoracic wall disease
169
Q

causes of V/Q mismatch

A
  • Most lung disease effecting the airways and parenchyma
  • Lung infection such as pneumonia
  • Bronchial narrowing such as asthma and COPD (can also progress to Type 2 resp failure)
  • Interstitial lung disease
  • Acute lung injury
170
Q

creation of shunt due to pneumonia

A

Pneumonia causes inflammation and damage in the small airways and alveoli. This creates a shunt leading to low PO2 because blood does not come into contact with adequate O2.

171
Q

V/Q mismatch due to perfusion problems

A

Pulmonary embolism

  • Can range from small PTE (pulmonary thromboembolism) causing no problem with gas exchange to massive PE with hypoxia
  • Emboli effectively causes areas of dead space where there is ventilation but no perfusion causing hypoxia
172
Q

asthma and respiratory failure

A
  • Hypoxaemia suggests significant asthma attack
  • Bronchospasm and mucous plugging causes ventilation defects and V/Q mismatch
  • Type 2 resp failure develops when severe bronchospasm causes hypoventilation fo alveoli or exhaustion
  • Patient needs oxygen to survive, invasive ventilation may be required
173
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 both types of resp failure
  • May have chronic type 2 resp failure in advanced disease
  • Treat resp failure with oxygen but with caution in chronic type 2 resp failure
174
Q

oxygen therapy masks

A
  • Variable performance- cheap, exact inspired O2 concentration not known
  • Fixed function- constant, known inspired concentration
  • Reservoir mask- high inspired concentration of O2

Venturi Mask- pre mixed gases, accelerate gas through nozzle, controlled oxygen therapy, aim to supply oxygen at flow rate faster than the patient can breath

175
Q

how do we quantify oxygen carriage?

A
  1. Haemoglobin saturation
    - If Hb is normal, accurate reflection of oxygen content
    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
  2. Arterial blood gases
    - PaO2 reflects haemoglobin saturation but is a measure of the partial pressure of O2 in the blood
176
Q

How to measure ABG?

A
  • Single arterial puncture technique- radial/ femoral/ branchial artery
  • Measurement from in-dwelling arterial catheter of A-line (only an option in HDU/ITU)
177
Q

difference between PA and Pa

A 
PA= partial pressure in alveolus
Pa= partial pressure in arterial circulation
178
Q

Carbon Monoxide Poisoning

A
  • CO is produced form incomplete combustion of hydrocarbons
  • CO binds to haemoglobin (high affinity) in the place of oxygen to form carboxyhaemoglobin
  • Also interferes with mitochondrial respiration
  • Death by asphyxia
  • Treatment is high conc. Oxygen (to displace CO from haemoglobin)
179
Q

effects of ventilation on pCo2 and CO2 content

A
  • More ventilation= low pCO2 and content
  • Less ventilation= high pCO2 and content
  • Hypoventilation causes build-up of alveolar CO2 and therefore less is removed form blood
  • Increase in blood CO2 leads to acidosis
180
Q

blood gases in type 1 respiratory failure

A
  • low PaO2- blood not being oxygenated on passage through pneumonic lung
  • normal (or low) CO2
    caused by V/Q mismatch decreasing adequate gas exchange eg. pneumonia
  • Patient breathes faster so can get rid of excess CO2 but can’t increase O2
181
Q

blood gases in type 2 respiratory failure

A
  • low PaO2
  • high PaCO2- due to increased levels in alveolar space and less removed from blood
  • caused by hypoventilation
  • may be acute or chroncic
  • if acute, will have respiratory acidosis (high H+)
182
Q

H+ is increased by:

A

An increase in pCO2 (respiratory acidosis)

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

183
Q

Acute vs Chronic Type 2 Respiratory Failure- hypoventilation

A
  • Acute hypoventilation eg. due to opiate toxicity leads to hypoxia, hypercapnia and acidosis
  • Chronic hypoventilation eg. neuromuscular disease of severe COPD leads to hypoxia and hypercapnia but may not have acidosis due to compensation
184
Q

Compensation=

A

increased bicarbonate retention by the kidney compensates for acidosis

185
Q

Respiratory Alkalosis

A
  • Not usually associated with respiratory failure
  • Caused by hyperventilation
  • Have low PCO2 and low H+
186
Q

metabolic acidosis

A
  • Excess acid production by the body eg. lactic acidosis or diabetic ketoacidosis
  • Sign= kussmal breading as a compensatory mechanism to increase CO2 removal from blood
  • Full compensation is difficult: need ot treat the underlying cause of increased acid load eg. treat DKA
187
Q

causes of respiratory and metabolic acidosis

A 
Respiratory= if the pCO2 is high
Metabolic= if the standard bicarbonate is low, or the base excess has a more negative value than  -2mmol/l, e.g -3mmol/l
188
Q

Bicarbonate interpretation- increase and decrease

A
  • HCO3- is increased by an increase in pCO2

- decreased by an increase in acid production or decrease in excretion

189
Q

actual and standard 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

190
Q

base excess

A

BE= 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

  • Calculated with normal CO2 so it only looks at the metabolic component
  • Normal value: 0 (-2 to 2 mmol/l)
  • A big negative value indicates a metabolic acidosis
  • A big positive value is seen in compensated respiratory acidosis
191
Q

acute bronchitis

A
  • Inflammation of bronchi
  • Often viral, may be bacterial eg. H.influenzae
  • May also involve larynx and trachea- laryngeotracheobronchitis
  • Acute exacerbations of chronic bronchitis are common
192
Q

Bronchiolitis: definiton, types

A
  • Inflammation of bronchioles
  • A feature of chronic bronchitis
    Primary bronchiolitis:
    • Usually in children
    • Respiratory syncytial virus (RSV)
    • Tachypnoea and dysnpoea
  • Rare types: follicular bronchiolitis, Bronchiolitis obliterans
193
Q

Localised Airway Obstruction: causes, leads to

A
  • Airway obstruction can be due to:
    • Lesion outside the wall eg. large lymph node
    • Lesion in the wall eg. tumour
    • Lesion in the lumen eg. foreign body
  • Causes distal collapse or over inflation
  • May be distal, lipid or infective pneumonia
194
Q

Diffuse Obstructive Airways Disease

A
  • Reversible and intermittent or irreversible and persistent
  • Centred on bronchi and bronchioles
  • Diffuse disease as many airways involved
195
Q

Pulmonary function tests ‘obstructive’:

A

Reduced vital capacity (VC)
• Reduced FEV1/ FVC ratio
• Reducing peak expiratory flow rate

196
Q

COPD-

A

spectrum of co-existence of chronic bronchitis and emphysema

  • Increased mucous production
  • Destruction of alveoli and connective tissue leading to collapse of conducting airways
  • Smoking= main cause
  • Smokers have elastin degradation in the body also leading to small airway collapse
197
Q

chronic bronchitis: definition, aetiology, clinical presentation

A

Clinical definition- 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

198
Q

chronic bronchitis: pathology

A

Pathology

  • Respiratory bronchiolitis (<2mm diameter)
  • Can lead to centrilobular emphysema
  • Mucus hypersecretion- mucous gland hypertrophy
  • Chronic bronchial inflammation- squamous metaplasia, increased risk of malignancy
199
Q

progression of chronic bronchitis

A
  • Hypercapnia
  • Hypoxia
  • Pulmonary hypertension
  • Cor pulmonale- right ventricular failure
  • Blue bloater- overweight and cyanotic
200
Q

emphysema: definiton and clinical features

A

Anatomical Definition- irreversible dilatation of alveolar spaces with destruction of walls, associated with loss of surface area for gas exchange

Clinical Features

  • Hyperventilation
  • Normal pO2¬, pCO2
  • Pink puffer
  • Weight loss
  • Right ventricular failure
  • Often co-existing chronic bronchitis
201
Q

classifications of emphysema

A
  1. Centrilobular Emphysema
    - Associated with smoking, seen in some pneumoconiosis- particularly coal workers
    - Most commonly in upper lobes
    - Respiratory bronchiolitis often present
  2. Panlobular Emphysema
    - Associated with alpha-1- antitrypsin deficiency
    - Usually lower lobes
    - Lungs overdistended
    - Markedly accelerated in smokers with this disorder
  3. Paraseptal Emphysema
    - Distension adjacent to pleural surfaces
    - May be associated with scarring
  4. Irregular Emphysema
    - Overlap with paraseptal emphysema
    - Associated with scarring
  5. Others
    - Bullous: distended areas >10mm
    - Interstitial
202
Q

asthma definiton

A
  • Reversible wheezy dyspnoea

- Increased irritability of the bronchial tree with paroxysmal airway narrowing

203
Q

atopic asthma

A
  • Associated with allergy
  • Can be triggered by: dust, pollen, house dust mite ect.
  • Often includes eczema and hay fever
  • Bronchoconstriction mediated by a type I hypersensitivity reaction

The hypersensitivity reaction often leads to:

  • Bronchial obstruction with distal overinflation or collapse
  • Mucus plugging of bronchi
  • Bronchial inflammation
  • Mucous gland hypertrophy
  • Bronchial wall smooth muscle hypertrophy
  • Thickening of bronchial basement membranes
204
Q

Asthma can lead to sudden death due to

A

mucus plugging

205
Q

types of asthma

A
  1. Atopic Asthma
  2. Non-Atopic Asthma
    - Associated with recurrent infections
    - Not immunologically medicated
    - Skin testing negative
  3. Aspirin- induced Asthma
    - Associated with recurrent rhinitis, nasal polyps and urticaria
    - Mechanism of asthma unclear
  4. Occupational Asthma
    - Hypersensitivity to an inhaled allergen
    - May be non-specific in those with hyper-reactive airways
    - May be a specific allergic response
  5. Allergic bronchopulmonary aspergillosis (ABPA)
206
Q

Allergic bronchopulmonary aspergillosis (ABPA)

A
  • Specific allergic response to the spores of Aspergillus fumigatus
  • Mixed type I and III hypersensitivity reaction
  • Mucus plugs common
  • Associated with bronchiectasis
  • Not to be confused with an aspergilloma: fungal ball, usually colonising a pre-existing cavity in the lung (often tuberculosis)
207
Q

bronchietstasis: definiton, clinical feature and complications

A
  • Bronchial dilatation
  • Acute & chronic inflammation, fibrosis

Clinical Features

  • Chronic cough productive of copious sputum
  • Finger clubbing

Complications

  • Spread of infection- pneumonia, empyema (collection of pus in pleural cavity), septicaemia, menigitis, metastatic abscesses eg. brain
  • Amyloidosis
  • Respiratory failure
208
Q

similarities between asthma and COPD

A
  • Asthma usually due to atopic and allergen exposure whereas COPD is mainly due to smoking/ hydrocarbon exposure
  • Asthma is characterised by reversible airways obstruction and an early and late phase response to stimuli
209
Q

main effector cells of asthma and COPD

A
  • Asthma- eosinophil main effector cell

- COPD- neutrophil main effector cell, causes lung destruction

210
Q

obstructive lung diseases

A
  • asthma
  • COPD
  • Causing obstructive picture: bronchiectasis, cystic fibrosis- chronic destructive disorders that are associated with decreased lung function
211
Q

Factors affecting Airway Internal Diameter:

A
  • Increased mucus production- mucus normally sweeps along the airway, gel-like mucus sits above cilia with liquid between them
  • Anatomical features
  • Autonomic and non- adrenergic/ non cholinergic (NANC) systems
  • Inflammation causing obstruction- COPD, asthma, cystic fibrosis
212
Q

Autonomic and NANC Nervous Systems

A
  • The lung contains muscarinic receptors and stimulation of these causes bronchoconstriction- COPD drugs act at these receptors
  • The lung also contains beta-adrenergic receptors and stimulation of these causes bronchodilatation- salbutamol acts at this receptor
  • receptors often found on smooth muscle cells
213
Q

small decrease in airway radius=

A

big increase in resistance, decrease in airflow

214
Q

Peak Flow

A
  • Peak Expiratory Flow Rate (PEFR)
  • Measures maximum speed of expiration
  • Crude measurement of conducting air flow
  • Can aid in asthma diagnosis/management
  • Excellent bedside/patient based tool
  • (cheap + easy to use)
215
Q

Ratio of FEV1¬ to FVC

A
  • Useful to differentiate between obstruction and restriction
  • If ratio <0.7- then suggests obstructive airways pathology
  • In mild obstruction, biggest impact on FEV1
  • In severe obstruction, FVC can also be impacted
216
Q

effect of mild/moderate obstruction on lung volumes

A

RV increased due to gas trapping and FVC slightly reduced but TLC normal as don’t have bad emphysema.

217
Q

effect of severeobstruction on lung volumes

A

TLC increased as lung tissue destroyed and have emphysema. But due to loss of elastic recoil the effective FVC is decreased and the RV is massively increased

218
Q

Reversibility of Spirometry

A
  • Used as a diagnostic test in asthma eg. following bronchodilator
  • Give salbutamol and wait 15 minutes
  • Asthma reversible vs. COPD fixed airways obstruction
  • Can also use bronchial challenge agents (histamine) to induce bronchospasm and obstructive spirometry
219
Q

Restrictive Disorder-

A

a disorder which prevents normal expansion of the lungs

220
Q

Lung restriction can occur due to:

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
221
Q

Types of Extra-pulmonary Restriction

A
  1. Integrity of nerves to respiratory muscles eg. high cervical dislocation
  2. Impaired neuromuscular junctions eg. myasthenia gravis
  3. Impaired muscles eg. muscular dystrophy
  4. Pleural thickening eg. asbestos exposure
  5. Skeletal abnormalities eg. scoliosis
222
Q

Types of Intrapulmonary Restriction: diseases causing increased fibrous tissue in the lungs

A
  • Silicosis in a stonemason
  • Asbestosis
  • Drug induced lung fibrosis
  • Coal workers pneumoconiosis
  • Rheumatoid lung
  • Bird fanciers lung
  • Idiopathic pulmonary fibrosis
223
Q

Inflation Pressure-

A

pressure delivered to alveoli, pressure that can be generated by intercostal muscles and the diaphragm into the alveolar space

224
Q

Pulmonary Compliance-

A

the ability of the lungs to starch during a change in volume relative to an applied change in pressure (stretchability), fibrotic diseases can decrease pulmonary compliance

225
Q
  1. Elastic Recoil=
A

alveolar pressure – pleural pressure

226
Q

effect of decreased compliance (rigidity/scarring) on inflation

A
  • Less lung volume achieved for a certain pressure- high pressure required to inflate
  • increased elastic recoil (deflates easily)
227
Q

effect of increased compliance- more floppy (obstructive defect eg. emphysema)

A
  • Increased lung volume achieved for a certain pressure

- decreased elastic recoil (difficult to deflate)

228
Q

large radius=

A

less effect of surface tension.

229
Q

pressure inside alveoli according to Laplace’s Law for a sphere

A

Well inflated alveolus → large radius → relatively low alveolar pressure
Underinflated alveolus → small radius → relatively high alveolar pressure

230
Q

Alveoli are connected so:

A
  • Air moves from high pressure area to low pressure area
  • Smaller alveolus empties into larger alveolus
  • There is instability of adjacent alveoli- leads to respiratory failure
231
Q

surfactant function

A

(surface active agent) in the alveolar lining fluid prevents collapse and keeps alveoli stable. It equals out the surface tensions of alveoli of different sizes eliminating different alveolar pressures- equal pressures can be achieved and surface tension is reduced

232
Q

structure of surfactant

A
  • Made of alveolar Type II cells

- Composed of lipids (mostly phospholipids) and proteins

233
Q

surfactant molecule interactions

A
  • They can only exert their influence if they are close together and can interact
  • Water molecules between surfactant molecules prevent them from interacting
234
Q

surfactant mechanism of action on well expanded alveoli eg. inspiration

A
  • Surfactant spread evenly over alveolar surface but molecules spread out and separated by water molecules
  • Surfactant has little effect on surface tensions (sT)
235
Q

surfactant mechanism of action on deflated alveoli eg. expiration

A
  • Tightly packed surfactant molecules
  • Some surfactant molecules extruded from the surface
  • Surfactant significantly reduces sT with accompanying lower pressure
236
Q

cause of respiratory distress syndrome of the new-born

A

lack of surfactant.

Signs: low compliances, high inflation pressures, rapid shallow breathing → fatigue, hypoxaemia

237
Q

Primary surfactant deficiency

A

very rare in adult disease but it can contribute to the pathogenesis of: ARDS, pneumonia, idiopathic pulmonary fibrosis, lung transplant

238
Q

gas transfer measurement

A

Gas transfer is a measure of the diffusing capacity of the lung. It requires measurement of gas exchange and alveolar volume. Carbon monoxide (rapidly taken up by Hb) or Helium can be used in this measurement.

239
Q

Using the carbon monoxide gas transfer measurement, one can calculate:

A
  • TLCO (mmol/min/kPa)- total gas exchange capacity
  • VA- alveolar volume= number of contributing lung units
  • KCO- efficiency of gas transfer per unit of lung
240
Q

TLCO and KCO in normal , extrapulmonary and intrapulmonary disease

A

In a healthy person: TLCO and KCO will be normal

In extrapulmonary disease: TLCO is low (lungs are smaller) and KCO is high (alveoli are normal and tighly packed with blood vessels

In intrapulmonary disease: TLCO is low (lungs are smaller) and KCO is low (alveoli are abnormal)

241
Q

nasal cavity function

A
  • Nasal cavity warms, humidifies and cleans inspired air thereby protecting respiratory surface from dehydration, temperature changes and pathogens
242
Q

asthma rescue treatment

A

Hypoxia (poor gas exchange)
- Oxygen

Bronchoconstriction
- B2 agonists eg. salbutamol
• Bronchodilator that may rapidly reduce airway obstruction
• But not 100% specific so risk of activating b1 receptors in the heart (increased heart rate) and b2 receptors in the muscles (tremor)
• Inhaled medication preferred as reduces systemic effects

Airways Inflammation
- Corticosteroids eg. Prednisolone orally, hydrocortisone IV
• Used to stabilise severe attacks by reducing airway inflammation
• Effect takes a few hours to become apparent

243
Q

presentations of COPD

A
  • Chronic bronchitis: cough producing sputum most days for 3 months over 2 consecutive years
  • Emphysema: enlarged airspaces distal to terminal bronchioles
  • Bronchiolitis: fibrosis and inflammation of small airways
244
Q

signs of COPD

A
  • Resting RR >20 breaths/min
  • Accessory muscle use
  • Pursed lipped breathing
245
Q

Pharmacological and surgical management of COPD

A

Pharmacological:

  • Oxygen
  • Bronchodilators (e.g. b2 agonists, antimuscarinic, theophyllines)
  • Corticosteroids (prednisolones)
  • Antibiotics

Surgical
- Bullectomy (removal of bulla- dilated air space in parenchyma), transplant

246
Q

short and long acting b2 agonists

A

Short acting b2 agonists: salbutamol

Long acting: salmeterol

247
Q

salbutamol: actions, indications, AE

A

Main actions: act as an agonist at b2 receptors to increase cyclic AMP, smooth muscle relaxation and bronchodilatation
Indications:
- Low dose inhaled: as require or prophylactic
- High dose nebulised: asthma/COPD exacerbations
- Other uses: hyperkalaemia
Adverse effects: tremor, tachycardia & palpitations, hypokalaemia

248
Q

cholinergic receptors

A 
Cholinergic receptors (M1, M2, M3) are located in the airways
-	Acetylcholine is the neurotransmitter released from postganglionic neurones in the vagus nerve tending
249
Q

cholinergic receptor agonists and antagonists

A

Cholinergic agonists cause:
Smooth muscle to contract → airway narrowing
Submucosal glands to secrete mucus

Cholinergic antagonists cause:
Bronchodilatation
Reduced mucus production
Also inhibits PNS impulses by selectively blocking M2 receptors. Decreases spasms.

250
Q

short and long acting cholinergic antagonists

A

Short acting: ipratropium bromide

Long acting: tiotropium

251
Q

Anticholinergic Adverse Effects:

A

Reduced secretion = dry mouth, throat
Reduced SM contraction = urinary retention, constipation
Reduced vagal tone = headaches, nausea

252
Q

how can systemic adverse effects of respiratory drugs can be significantly reduced?

A

if they are inhaled into the lungs rather than administered by mouth

253
Q

anticholinergic indications

A

Indications: COPD, bronchial asthma, rhinitis (inflammation of inside of nose)

254
Q

drugs where monitoring plasma concentration is useful

A

theophylline, digoxin, phenytoin, gentamicin

255
Q

xanthines: actions, indications, AE

A

Main actions:

  • Phosphodiesterase inhibitor → increase cAMP → PKA activation, TNFa inhibitor and inhibition of leukotriene synthesis
  • Bronchodilation

Indications: mainly COPD, asthma rarely

Adverse Effects: tachycardia, palpitations, nausea

256
Q

xanthine drugs

A

oral: theophylline
IV: aminophylline

257
Q

Leukotriene antagonists e.g. monteleukast: action, indications, AE

A

Action: Reduces airway narrowing and mucous production usually caused by leukotrienes
Indications: treatment of exercise induced asthma, seasonal allergic rhinitis
AE: abdominal pain, thirst, headache, hyperkinesia, hypersensitivity (vasculitis), increased infection risk, muscle aches, liver damage

258
Q

different routes of corticosteroids

A

Inhaled: beclometasone
Oral: prednisolone
IV: hydrocortisone

259
Q

Mast Cell Stabilisers e.g. cromoglicate

A

Action: Stabilises mast cells and reduces release of histamine, prevents airway inflammation
Indications: prophylaxis of asthma, conjunctivitis, allergic rhinitis
Side effects: local irritation (cough), transient bronchospasm

260
Q

adverse effects of oxygen delivery

A
  • Respiratory depression in COPD because when hypoventilation and CO2 retention is prolonged the brain adjusts and is no longer sensitive to CO2 as a drive to breathe
  • Patients who then rely on hypoxia as the drive to breath may stop breathing if exposed to too much oxygen
261
Q

Drugs that cause bronchospasm

A
  • Beta-adrenoreceptor antagonists eg. propranolol, atenolol

- Non-steroidal anti-inflammatory drugs (NSAID)

262
Q

NSAID Induced Bronchospasm

A

Arachidonic acid released from phospholipids is a precursor to prostaglandins which cause inflammation. Blocking this pathway means that the arachidonic acid is push to the other pathway to produce leukotrienes → cause bronchospasm

263
Q

Drugs that supress respiration

A
  • Opioids eg. morphine

- Benzodiazepines eg. diazepam

264
Q

Drugs that cause interstitial lung disease (fibrosis)

A
  • Amiodarone
265
Q

pros and cons of inhalation as a route of administration

A

Advantage –delivers drug directly to the lung, minimises side effects to other parts of the body.
Disadvantage –difficulty in ‘timing’ of delivery of the drug, i.e. using an inhaler effectively, can end up depositing most of drug on back of throat rather than inhaling properly. Can use ‘spacers’ to increase ease of use of inhaler

266
Q

TB treatment

A

Rifampicin

  • Metabolised by liver, induces cytochrome p450
  • Discolours body fluids orange, rash, hepatitis

Isonazide
- Metabolised by liver, enzyme inhibitor
- Hepatitis, rash
Pyridoxine (Vitamin B6) when patients are given Isonazide
- To reduce peripheral neurological effects

Pyrazinamide

  • Metabolised by liver
  • Hepatitis, rash, arthralgia, gout

Ethambutol

  • Metabolised by kidneys, ½ dose if chronic renal failure
  • Retrobulbar neuritis
267
Q

TB course

A

all of RIPE typically for 2 months, then Rifampicin and Isoniazide for 4 more months

268
Q

HBsAg=

A

surface antigen of Hep B

269
Q

Cor pulmonale

A

describes structural changes to the right side of the heart due to pulmonary disease. The most frequent mechanism is pulmonary hypertension, which is in turn most commonly caused by COPD

270
Q

factors that cause right shift on O2 saturation curve

A

increase in:

  • temperature
  • [H+]
  • [CO2]
  • 2-3 DPG
271
Q

factors that cause left shift on O2 saturation curve

A

carbon monoxide

Y1S2- Cardio, Resp, Loco (3 decks)

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