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Year 1 - semester 2 amy > respiratory > Flashcards

respiratory Flashcards

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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
respiratory groups in brainstem
pontine RG ventral RG dorsal RG
26
things that change the basic breathing pattern
inhaled noxious substances speech sleep exercise
27
feedback inputs to the resp rhythm generator
lung receptors (afferent nerve fibres carried in vagus) - slowly adapting rec - rapidly adapting rec - C-fibre endings CHEMORECEPTORS - central chemorec - peripheral chemorec.
28
slowly adapting receptors (SARs)
- 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
29
rapidly adapting receptors (RARs)
- 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
30
C-fibre endings
- unmyelinated nerve fibres - in broncus - stimulated ny increased interstitial fluid (oedema) & inflammatory mediators (histamine, prostagladins, bradykinins) - pulmonary c-fibres (JUSTAPULMONARY CAPILLARTY RECEPTOR)
31
response to O2 & CO2
chemoreceptors -peripheral fast response to ; arterial pO2, arterial pCO2, arterial h+ -central slow response to ; arterial pCO2
32
blood brain barrier
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
33
breathing during sleep
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
34
phasic upper airway activity
contraction of upper airway muscles opening of upper airway facilitates inward airflow
35
tonic upper airway activity
continuous background activity tends to maintain patent airway varies with state of alertness
36
obstructive sleep apnoea (OSA)
Common • Fragments sleep causing daytime sleepiness • Important cause of traffic accidents • Risk factors: obesity, alcohol, nasal obstruction, anatomical anomalies
37
respiratory depressant drugs
anaesthetics - almost all analgesics - opioids (morphine and its analogues) sedatives (anti-anxiolytics, sleeping tablets) - benzodiazapines (diazepam, temazepan, etc)
38
respiratory stimulant drugs
Primary action: Doxapram Secondary action: B 2 - agonists (bronchodilators)
39
generation of basic rhythm
* 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
40
lung defence mechansims
Mechanical • Ciliated epithelium • Mucus • Cough Immunological • IgA & antimicrobials in mucus • Resident alveolar macrophages & dendritic cells • Innate / adaptive immune responses
41
what is the parenchyma
The parts of the lungs involved in gas transfer including the alveoli, interstitium, blood vessels, bronchi and bronchioles.
42
pneumonia
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
43
pneumonia categories
* Community acquired * Hospital acquired * Health care associated * Aspiration associated * Immunocompromised host * Necrotising / abscess formation
44
community acquired pneumonia
``` Streptococcal pneumoniae • Haemophilus influenzae • Moraxella catarrhalis • Staphylococcus aureus • Klebsiella pneumoniae / Pseudomonas aeurginosa • Mycoplasma pneumoniae ```
45
hospital acquired / Healthcare associated pneumonia
* Gram-negative rods, Enterobacteriaceae, Pseudomonas | * Staphylococcus aureus (usually methicillin-resistant)
46
aspiration pneumonia
• Anaerobic oral flora mixed with aerobic bacteria
47
pneumonia in immunocompromised host
* Cytomegalovirus * Pneumocystis jiroveci (PCP) * Mycobacterium avium-intracellulare * Invasive aspergillosis * Invasive candidiasis * “Usual” bacterial, viral, and fungal organisms
48
necrotising / abscess formation pneumonia
• Anaerobes, S. aureus, Klebsiella, S. pyogenes
49
respones to infection -neutrophils
``` Chemotaxis • Degranulation • Reactive oxygen species • Extracellular traps • Phagocytosis ```
50
response to infection - macrophages
``` Cytokine & chemokines • Phagocytosis (bacteria & dead cells) • Antimicrobial peptides • Resolution • Also involves T cells, dendritic cells & epithelial cells ```
51
clinical presentation of pneumonia
``` Cough • Sputum • Pyrexia • Pleuritic chest pain • Haemoptysis • Dyspnoea • Hypoxia ```
52
bronchopneumonia
``` Most common pattern • Patchy consolidated areas of acute suppurative inflammation • Often elderly with risk factors • Cancer, heart failure, renal failure, stroke, COPD ```
53
lobar pneumonia
Rust coloured sputum • S. pneumoniae • consolidation of a large portion of a lobe or of an entire lobe
54
complications of pneumonia
``` Local • Abscess formation • Empyema Systemic • Sepsis • ARDS • Multi-organ failure Not resolving? • ?cancer ```
55
acute respiratory distress syndrome
* 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
56
bronchiectasis
``` 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. ```
57
tuberculosis
* 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 ```
58
primary TB
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
59
progressive primary TB
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 ```
60
secondary tuberculosis
``` 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 ```
61
other causes of granulomatous pulmonary inflammation
``` Other infection – fungi • Sarcoidosis • Rheumatoid arthritis • Berrylosis • Hypersensitivity pneumonitis • Aspiration pneumonia • Langerhans Cell Histiocytosis ```
62
asbestoes
``` • 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 ```
63
hypersensitivity pneumonitis
``` • 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 ```
64
complications of bronchiectasis
``` 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
65
patterns of bronchiectasis
``` Based on imaging appearances • Cylindrical • Sacular • Varicose • Cystic ```
66
function of the chest wall
1st Respiration 2nd Protection 3rd Muscle Attachments
67
thoracic cavity
Divided into 3 major spaces • Heart with coverings (pericardium - pericardial cavity) + the major vessels • Lungs with coverings (pleura - pleural cavities)
68
chest wall anatomy
``` • Thoracic vertebrae • Ribs • Sternum - manubrium, body, xiphoid process •Intercostal spaces - intercostal muscles ```
69
features of a thoracic vertebrae
- body - facets for articulation with ribs - facet for articulation with adjacent vertebra - transverse, inferior, spinous, superior processes - lamina - pedicle - vertebral foreamen
70
features of a rib
posterior -> anterior - head - neck - tubercle - angle - internal surface - costal groove - external surface - costal cartilage
71
sternocostal joints
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)
72
intercostal space
- external and internal and innermost intercostal muscles - intercostal vein, artery and nerve - collateral branches of V, A & N
73
diaphragm openings
Inferior Vena Cava - T8 caval opening • Oesophagus - T10 esophageal hiatus • Aorta - T12 aortic hiatus
74
trachea
c-shaped hyaline cartilage rings bifurcates into R & L main bronchus at TIV/TV Carina - hook-shaped tracheal ring
75
bronchial trees - L & R
``` Right main bronchus Wider Vertical Shorter Divides into 3 ``` ``` Left main bronchus Long More horizontal Thin Divides into 2 ```
76
bronchial tree
``` Trachea Main bronchus (primary) Lobar bronchi (3R, 2L) (secomndary) Segmental bronchi (tertiary) Conducting bronchioles Respiratory bronchioles Alveoli Alveolar ducts Alveolar sacs ```
77
alveoli
- 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
78
lung lobes
right - superior - middle - inferior - oblique fissure - horizontal fissure left - superior - inferior - oblique fissure - lingula
79
right medial surface lung
root structures - pulmonary arteries - pulmonary veins - bronchus impressions - superior vena cava - inferior vena cava - oesophagus - azygos vein
80
hilum
where important structures enter / exit each lung
81
left medial surface lungs
smaller than right lung root structure - P. arteries - P. veins - bronchus impressions - heart - aortic arch - thoracic aorta - oesophagus - L. subclavian artery
82
lung development
During development the lung is pushed into the sac to form two layers:Visceral & Parietal pleura
83
costodiaphragmatic recess
Between costal pleura & diaphragmatic pleura | Clinically important
84
mediastinum
Separates the pleural cavities ``` Divided into two parts: - Superior mediastinum - Inferior mediastinum Anterior Middle Posterior ```
85
contents of mediastinum
``` Aorta Heart Azygous vein Trachea Main bronchi Oesophagus Vagus nerves Phrenic nerves Thoracic duct ```
86
innervation to pleura
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
87
innervation to mediastinum
Vagus nerve Parasympathetic supply to all organs of thorax Phrenic nerve Motor & sensory to diaphragm
88
lungs - pleura
2 layers of pleura parietal pleura - costal - mediastinal - diaphragmatic - cervical visceral pleura - adhere to wall of lungs - covering surface of each lobe
89
therapeutic index
= toxic conc. / effective conc.
90
alexander fleming
- 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
91
pharmacokinetics
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
92
pharmacodynamics
 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
93
antibiotic classification
```  1. Effect on micro organism - bacteriostatic, bactericidial  (2. Chemical structure)  3. Target site - cell wall - cell membrane - protein synthesis - nucleic acid synthesis ```
94
cell wall synthesis inhibitirs
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
95
cell wall synthesis inhibitors examples
beta-lactams glycopeptides eg vancomycin, teicoplanin
96
beta lactams
- 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
97
side effects of penicillin
 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
98
cefalsporins
 Mostly stable to staphylococcal betalactamase  Much << 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 ```
99
glycopeptides
 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)
100
protein synthesis inhibitors
```  Aminoglycosides e.g gentamicin  Tetracyclines  Macrolides (erythromycin, clarithromycin)  Chloramphenicol (rarely used in the UK)  Lincosamides  Oxazolidones  Fusidic acid ```
101
aminoglycosides
```  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 ```
102
tetracyclines
```  Bacteriostatic  Broad spectrum  Intracellular bacteria e.g. chlamydia  May cause diarrhoea, nausea  Teeth discolouration, avoid in children, pregnant & lactating women ```
103
macrolides
 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
side effects of macrolides
 Gastrointestinal upset common – less with newer agents  Thrombophlebitis when given intravenously  ‘Newer’ macrolides have broader spectrum - clarithromycin and azithromycin
105
protein inhibitor synthesis inhibitors (cont)
 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
inhibitors of nucleic acid synthesis
 1) Synthesis of tetrahydrofolic acid (THFA)  2) Synthesis of RNA  3) Synthesis of DNA
107
1) THFA inhibitors
 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
inhibitors of RNA synthesis
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
inhibitors of dna synthesis - 1
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
DNA synthesis inhibitors - 2
Fluoroquinlones - Ciprofloxacin * Broad-spectrum * Low MICs * Rapidly bactericidal * Resistance can be slow to develop
111
quinolones side effects
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
main route of administration
```  Parenteral (intravenous/intra muscular)  Intraperitoneal  Oral  Rectal  Topical often discouraged ```
113
what are the factors that promote the success of antibiotic resistance
``` 1. Antibiotic Usage • Too much antibiotic • Too little antibiotic 2. Effective Genetic Mobility • Plasmid Carriage • Transposons •Integrons 3. Efficient Resistance Mechanism • Bacterial factors ```
114
location of resistance genes
 Chromosome  Plasmid  Transposon  Integron
115
transposon
 “Jumping genes”  Go between plasmid & chromosome  Unable to replicate independently
116
integron
```  Genetic element  Usually resides on transposon  Able to ‘poach’ resistant genes ie extracts DNA segments and inserts into other DNA segments ```
117
main mechanisms of resistance
 1) Target site alteration  2) Reduced access (efflux or impermeability)  3) Drug inactivation  4) Metabolic bypass
118
what antibiotics are we trying to avoid
``` Broad spectrum antibiotics Ciprofloxacin and other quinolones Cephalosporins Clindamycin Co-amoxiclav ```
119
viral infectivity cycle - 1
Attachment/Adsorption Penetration Uncoating
120
viral activity cycle - 2
Transcription Synthesis of nucleic acid & proteins Assembly Release by rupture or budding – often results in cell death
121
antivirals
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
viral DNA/RNA synthesis inhibitors
aciclovir (HSV & Herpes) zidovudine (HIV)
123
viral protein synthesis inhibitors
ritonavir (HIV) | boceprevir (HCV)
124
release of viral particles inhibition
oseltamavir (influenza)
125
fungi - general
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
classes of antifungals
Polyenes Azole group (Imidazole & Triazoles) Echinocandins Others
127
principles of TB therapy
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
causes of lung cancer
``` • 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
types of lung cancer
``` • Squamous Carcinoma (30-40% and decreasing) • Adenocarcinoma (40-50% and increasing) • Small cell carcinoma (20%) • Others (5%) – Carcinoid tumours ```
130
squamous carcinoma
- the tumour cells are showing squamous differentiation - keratin production or ‘prickles - common finding in smokers - reversible
131
adenocarcinoma
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
small cell (undifferentiated) carcinoma
Very poorly differentiated carcinoma showing variable evidence of neuroendocrine differentiation aggressive tumour
133
carcinoid / neuroendocrine
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
symptoms and signs of lung cancer
``` • 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
initial investigations - lung cancer
``` • Radiology – Chest x-ray – CT scan • Bloods – High Ca – Abnormal liver function tests – Low serum Na ```
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immunohistochemistry - lung cancers
``` Squamous markers • CK5, CK14, p63, 34βE12 – Adenocarcinoma • CK7, TTF1 (c. 70-80% of primary lung tumours) ```
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behaviour of lung cancers
``` • 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 ```
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staging lung cancer
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
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treatment for lung cancer
``` Best supportive / palliative care • Chemotherapy • Radiotherapy • Surgery – around 15% – Advanced disease at presentation – Co-morbities eg emphysema, ischaemic heart disease ```
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lung function after lung cancer operations
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
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anatomical shunts
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)
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Physiological shunts (decreaseV) and alveolar dead space (decreaseQ)
Not all lung units have the same ratio of ventilation (V) to blood flow (Q) V/Q mismatch
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what decreases the partial pressure of O2 in blood
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
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what can increase partial pressure of oxygen
Hyperventilation | Administration of oxygen
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increase in available PO2 in healthy state
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
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ventilation to perfusion ratio
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
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normal V/Q mismatch
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
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increased V/Q ratio
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)
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decreased V/Q ratio
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)
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physiological dead space
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
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quantifying V/Q mismatch
Calculate the expected alveolar PO2 (PAO2) using the alveolar gas equation Compare with the measured arterial PO2 (PaO2) If PAO2 = PaO2 then no mismatch
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quantifying A-a Gradient
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
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hypoventilation and CO2
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
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arterial blood gases - WHAT IS MEASURED
- PaO2 - PaCO2 - HCO3- - H+
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PaO2 low, CO2 normal
Type 1 respiratory failure | Probably has V/Q mismatch
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PaO2 low, CO2 high
Type 2 respiratory failure Patient has ventilatory failure (May well have V/Q mismatch too
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failure of ventilatory pump
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
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type 2 respiratory failure
``` 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 ```
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How do we treat type 2 respiratory failure
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
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what causes V/Q mismatch
- 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
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V/Q mismatch in pneumonia
Creates a shunt leading to low PO2 because blood does not come into contact with adequate O2
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what happens to arterial CO2 in V/Q mismatch
- 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
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what happens to to arterial O2 in V/Q mismatch
- 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
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treatment of pulmonary embolism
Oxygen in acute episode Anticoagulation to stop further clot propagation Thrombolysis in some cases where circulatory compromise
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asthma and respiratory failure
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
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COPD and respiratory failure
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
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oxygen therapy masks
Variable performance Cheap and cheerful Exact inspired O2 concentration not known Fixed function Constant, known inspired concentration Reservoir mask High inspired concentration of O2
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how do we treat respiratory failure
- 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
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why measure blood gases
To assess very sick patients To diagnose respiratory failure To diagnose metabolic problems
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quantifying O2 carriage
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
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how to measure haemoglobin saturation
- 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
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how to measure ABG
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
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what does blood gas measure
- PaO2 - PaCO2 - Hydrogen ion/pH - Bicarbonate - Some analysers may also measure electrolytes and Hb - Other forms of haemoglobin: - Carboxyhaemoglobin
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normal blood gas values
H+ 36-44 nmol/l PO2 12-15 kPa PCO2 4.4-6.1 HCO3 21-27.5 BE +2 to -2 mmol/l
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understanding O2 kPa
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
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acidosis
H+ is increased by: An increase in pCO2 (respiratory acidosis) An increase in acid production or decrease in excretion (metabolic acidosis)
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acute vs chronic type 2 respiratory failure
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
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respiratory alkalosis
``` Not usually associated with respiratory failure Caused by hyperventilation Have low PCO2 and low H+ PO2 14 PCO2 2.2 H+ 32 HCO3 25 ```
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metabolic problems
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
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interpreting bicarbonate
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
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base excess
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
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anion gap
The anion gapis the difference between primary measured cations (Na+and K+) and the primary measuredanions (Cl-and HCO3-) in serum.
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causes of respiratory acidaemia
- impaired gas exchange‐- Hyperventilation - Lung disease, COPD ‐Drugs (respiratory depression) ‐Muscle paralysis
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causes of respiratory alkalaemia
hyperventilation from - ‐Salicylate poisoning (aspirin) ‐Hysteria, anxiety ‐Cerebral diseases such as viral infection/head injury
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causes of metabolic acidaemia
- acidic metabolic products - loss of HCO3 - chronic diarrhea (bile salts) - increase buffering demand (eg keto/lactic acidaemia) - acid indigestion
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causes of metabolic alkalaemia
- bicarbonate indigestion | ‐ Severe vomiting (HCl loss)
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common causes of metabolic acidaemia (anion gap)
``` methanol ethylene glycol salicylate lactic acidaemia alcoholic ketoacidosis renal failure diabetic ketoacidosis ```
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principle buffers in plasma
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
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acute bronchitis
``` 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 ```
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bronchiolitis
* 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
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diffuse obstructive airway disease
``` • 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 ```
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examples of diffuse obstructive airway disease
* Several clinico-pathological entities * Chronic bronchitis * Emphysema * Asthma * (Bronchiectasis) • Chronic obstructive pulmonary disease (COPD) • Spectrum of co-existence of chronic bronchitis and emphysema
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chronic bronchitis
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
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progression of chronic bronhcitis - final outcome
``` • Hypercapnia • Hypoxia • Pulmonary hypertension • ‘Cor pulmonale’ - right ventricular failure ``` • ‘Blue bloater’
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pathology of chronic bronchitis
* Respiratory bronchiolitis (<2mm diameter) * Can lead to centrilobular emphysema * Mucus hypersecretion * Mucous gland hypertrophy * Chronic bronchial inflammation * Squamous metaplasia, increased risk of malignancy
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emphysema
• Irreversible dilatation of alveolar spaces with destruction of walls • Associated with loss of surface area for gas exchange
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centrilobular emphysema
Strongly associated with smoking • Seen in some with pneumoconiosis, particularly coal-workers • Most commonly in upper lobes • Respiratory bronchiolitis often present
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panlobular emphysema
• Usually lower lobes • Lungs overdistended • Associated with alpha-1-antitrypsin deficiency • Markedly accelerated in smokers with this disorder
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other forms of emphysema
* 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
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clinical features of emphysema
``` • Hyperventilation • Normal pO2, pCO2 • ‘Pink puffer’ • Weight loss • Right ventricular failure • Often co-existing chronic bronchitis, in which case clinical features are mixed ```
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asthma
``` 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) ```
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atopic asthma
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
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non-atopic asthma
* Associated with recurrent infections * Not immunologically mediated * Skin testing negative
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allergic bronchopulmonary aspergillosis
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)
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bronchiectasis - 2
• 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
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clinical features of bronchiectasis
``` • Chronic cough productive of copious sputum • Finger clubbing • Complications • Spread of infection • Pneumonia, Empyema, Septicaemia, Meningitis, Metastatic abscesses e.g. brain • Amyloidosis • Respiratory failure ```
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the air travels down
Nasal Cavity Pharynx Larynx Trachea Bronchi Bronchioles Alveoli
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features of the nasal cavity
Conchae = turbinate Meatus = passage or opening
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paranasal sinuses
frontal ethmoidal maxillary sphenoidal drain into nasal cavity
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nasal cavity- communicating structures
Pharyngotympanic tube– connects nasal cavity to the middle ear Nasolacrimal duct (tear duct) – connects lacrimal sac to nasal cavity
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the pharynx
nasopharynx oropharynx laryngopharynx soft palate "flutter valve"
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innervation of the pharynx
vagus nerve [X] | glossopharyngeal nerve [IX]
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the larynx - structure
Voice Box Cartilaginous structures - hyaline cartilage - elastic fibrocartilage
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epiglottis
Closes over the entrance to the larynx to stop food/ liquid entering during swallowing
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histology of respiratory system
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
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bronchiole histology
``` <1mm lumen Pseudostratified ciliated columnar epithelium  Ciliated columnar epithelium NO glands NO cartilage Smooth muscle (M) ```
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what is an obstructive disorder
- narrowing of airway - reduced inflow of gas - reduced inflation of alveoli
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factors affecting airway internal diameter
- Increased mucus production - Anatomical features - Autonomic and Non-Adrenergic/Non-Cholinergic (NANC) systems - Inflammation
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autonomic and NANC Nervous systems
parasympathetic nerve (vagus) - acetyl choline - muscarinic receptors - constriction the circulation - B2 adrenergic receptors - bronchodilation
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cystic fibrosis
- 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
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how to measure obstruction
peak flow spirometry lung volumes & flow
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airway resistance and flow calculation (calculates peak expiratory flow)
(upstream pressure - downstream pressure) / resistance | volume of gas per unit of time
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PEF in asthmatics
morning dips
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FEV1 & FVC
FEV1 - How much can the patient exhale in a given time, e.g. 1 second FVC - How much they can exhale altogether
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Factors to consider when looking at FEV1:FVC ratio
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
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Global Lung Initiative (GLI) lung function prediction
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
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effect of mild/moderate obstruction on lung volumes
TLC remains in normal range - airway narrowing and collapse leads to gas trapping - RV increased above normal range - RV/TLC ratio increased above normal
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effects of severe airway obstruction on lung volumes
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
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reversibility of spirometry
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
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what is a restrictive disorder
A disorder in which prevents normal expansion of the lungs
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what causes lung restriction
Extra-pulmonary disease i.e. visceral pleura, pleural space, chest wall including parietal pleura, bones, muscles, nerves Intra-pulmonary disease i.e. alveolar spaces
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extra-pulmonary restrictions
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
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intra-pulmonary restrictions
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
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how do fibrotic lung diseases cause restrictive disease
1. Inflation pressure 2. Compliance 3. Elastic recoil
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elastic recoil pressure =
alveolar pressure minus pleural pressure
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pulmonary compliance
the ability of the lungs to stretch during a change in volume relative to an applied change in pressure (‘stretchability’)
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relationship between inflation pressure, compliance and elastic recoil
A lower compliance means greater inflation pressure required to inflate which means higher elastic recoil
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effects of a decreased compliance on inflation
increased fibrous tissue (more rigid) decreased compliance (requires high pressure to inflate) Increased elastic recoil (deflates easily)
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what casues increased compliance
Associated with an OBSTRUCTIVE defect, particularly emphysema
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effects of increased compliance on deflation
``` decreased elastic tissue (more floppy) increased compliance (inflates at low pressures) decreased elastic recoil (difficult to deflate) ```
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alveolar features making them different from balloons
1. Alveoli are moist | 2. Alveoli are of different sizes
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alveoli being different size - effect
air moves from HIGH pressure area to LOW pressure area SMALLER alveolus empties into LARGER alveolus There is INSTABILITY of adjacent alveoli
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surfactant
produced by alveolar Type II cells composed of lipids (90%, mainly phospholipids) and proteins (10%) reduces surface tension
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well-expanded alveoli (inspiration) - surfactant
Surfactant spread evenly over alveolar surface but molecules spread out Surfactant has little effect on surface tension (sT)
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deflated alveoli (expiration) - surfactant
Tightly packed surfactant molecules Some surfactant molecules extruded from the surface Surfactant significantly reduces surface tension (T) with accompanying lower pressure (P)
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pressure equation
P = (2 * sT) / radius
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respiratory distress syndrome of the newborn
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
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impaired surfactant contributes to what resp. disorders
``` Adult respiratory distress syndrome (ARDS) Pneumonia Idiopathic pulmonary fibrosis Lung transplant ………etc ```
249
spirometry and lung volumes in restriction
decreased.... spirometry - FEV1 - FVC Helium dilution - total lung capacity - vital capacity - residual volume
250
gas transfer measurement
Gas transfer is a measure of the diffusing capacity of the lung. It requires a measurement of GAS EXCHANGE and ALVEOLAR VOLUME
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measuring gas exchange
use CO - carbon monoxide Rapidly taken up by haemoglobin with very high affinity Not produced by the body Non-toxic Easy to measure
252
measuring alveolar volume
use He - Helium NOT TAKEN UP by haemoglobin Not produced by the body Non-toxic Easy to measure
253
what can you calculate using single breath method - CO
TLCO (mmol/min/kPa) - total gas exchange capacity VA - alveolar volume KCO - efficiency of gas transfer per unit of lung
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TLCO and KCO - extra-pulmonary restrictive
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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