PSP resp Flashcards

1
Q

process of inspiration into lungs

A

-external intercostals contract+pulls chest wall out and up-increases chest cavity volume
-diaphragm contracts+flattens-increases chest cavity volume
-accessory muscles: SCM(sternocleidomastoid, scalenes)
-increasing chest cavity volume decreases chest pressure;hence air moves in

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2
Q

process of expiration

A

-external intercostals+diaghragm relax (passive movement)

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3
Q

what is lung compliance

A

how easily the lungs stretch

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4
Q

what factors influence lung compliance

A

-elasticity(1/3)
-surface tension(2/3)

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5
Q

how does elasticity impact lung compliance

A

decrease compliance=more rigid=increase elastic recoil
-reduced lung expansion BUT increases recoil

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6
Q

how does surface tension impact lung compliance

A

surface tension resists expansion
-alveolar cells produce surfactant during gestation-
reduces surface tension to make lungs more compliant

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7
Q

what 2 factors influence ventilation

A

compliance and airway radius/resistance

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8
Q

what is airway radius/resistance influenced by

A

-bronchial tree
-autonomic NS control

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9
Q

how does the bronchial tree work on airway radius/resistance

A

flow=1/R
resistance=L/r^4 therefore 1/2 radius=16x resistance
resistance is greatest in medium sized bronchioles

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10
Q

how does autonomic NS impact ventilation

A

PSNS=bronchoconstriction
SNS=bronchodilation

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11
Q

how would an obstructive disease present on spirometry

A

FEV1 reduced more than FVC
-low FEV1/FVC

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12
Q

how would a restrictive diease present on spirometry

A

FEV1 and FVC reduced but FEV1:FVC ratio is normal or high

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13
Q

what is FEV1

A

forced expiratory volume in 1 second

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14
Q

what is FVC

A

total volume a person can forcefully exhale after maximum possible inspiration

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15
Q

how is VC(vital capacity) measured

A

IRV(inspiratory reserve volume)+TV(tidal volume)-ERV(expiratory reserve volume)

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16
Q

what is ficks law

A

A=area
D=diffusion constant(solubility of the gas in water
P1-P2=pressure difference

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17
Q

what does daltons law state

A

-total pressure is the sum of the partial pressures of the individual gases
-pressure is dependent on temperature and concentration
-partial pressure is proportional to the percentage of the gas in the mixture and the total pressure of the gas mixture

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18
Q

what does henrys law state

A

-concentration of gas in solution depends on atmospheric pressure
-amount of gas dissolved=solubilityxPP

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19
Q

factors affecting diffusion

A

-thin alveolar membrane=small distance to travel
-larger surface area for diffusion
-pressure difference across the membrane
-gas itself

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20
Q

what is the DLCO

A

a lung function test which shows how much CO is transferred from an inhaled gas mixture across the alveolar membrane to plasma

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21
Q

what is the normal DLCO reading

A

25mL/min/mmHg

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22
Q

ventilation-perfusion

A

for efficient effusion there must be a match between the perfusion of each area of the lung an the ventilation to that part of the lung-measured with V/Q ratio

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23
Q

normal V/Q ratio+meaning of high/low

A

-normal=0.8(4L/min air and 5/min blood)
-lower than 0.8=shunting(reduced ventilation) which may indicate pneumonia/asthma
-higher than 0.8=dead space(reduced perfusion) which may indicate a pulmonary embolism

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24
Q

where does most air go in the lung

A

more air goes to the base of the lung than the top

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25
why does more air go to the base of the lung rather than the top
alveloi at the base are squashed whereas those at the top are stretched open -those at the base contribute more to TV(amount of air that moves in or out of the lung with each respiratory cycle)
26
V/Q ratio maintenaince mechanisms
-capillary diameter=capillaries constrict if PO29partial pressure of O2) decreases, diverting blood to regions with higher PO2 -bronchiolar diameter= bronchioles respond to PCO2 of nearby alveoli; bronchioles dilate to increase PCO2 clearance
27
2 methods of O2 transport around the circulatory system
-bound to a Hb molecule(98.5%) -dissolved in plasma(only 0.3mL per Litre as it is not very soluble)
28
at 100mmHg arterial pressure, how much Hb is in a litre of blood
200mL
29
what is oxygen saturation
the percentage of Hb occupied by O2
30
what is the ICU point(hypoxic point)
60mmHg-gives a reading of 90 on oximeter
31
what is the O2 saturation percentage in the lungs and in circulation
-in the lungs it is 100% -as it circulates and is absorbed it drops to 75%
32
why is it important that bound oxygen % is 75mmHG
-means that there is enough leftover bound oxygen in case of a further drop e.g exercise -if pts have a reading of 90 on oximeter(60mmHg), any further drop in PO2 will result in a large decrease in )2 saturations
33
correlation between PO2 and % Hb that is bound
as PO2 decreases, so does the % of Hb that is bound to O2
34
what does it mean if the oxygen dissociation curve shifts right
for any partial pressure, less Hb will be bound(easier for O2 to dissociate from Hb)
35
what factors cause oxygen dissociation curve to shift right
-increased PCO2 -increased temp -decreased pH -increase in 2,3-DPG(diphosphoglycerate)
36
physical barrier of resp system
mucociliary transport
36
what does mucociliary transport involve
-epithelial cells form an epithelial barrier -goblet cells in the epithelial barrier secrete mucus -cilia beat in an assymetric rhythm and move the mucus along at 1cm/min =>defects in mucociliary transport can lead to recurrent resp infections
36
how is the medulla involved in control of ventilation(neuronal control)
The medulla generates the automatic rhythm that allows for breathing -the site for this is in the pre-Botzinger complex in the upper part of the VRG -pacemaker cells send neural signals to DRG which give rise to automatic firing
37
VRG in medulla involvement in neuronal control of ventilation
-pre botzinger complex in VRG sets out the pattern and sends to DRG, this is pacemaker control(regulation of unconscious breathing) -ventral respiratory group is inactive during normal respiration but upon sigals from carotid bodies, stretch receptors and chemo/mechanoreceptors(e.g during exercise), they cause more forceful exhalation(via innervating the INTERNAL intercostal muscles) -suppressed by opiates causing respiratory arrest
38
DRG in medulla involvement in neuronal control of ventilation
-acts as central control for breathing, gives rise to autonomic firing (dont need any signalling to do so) to signal the diaphragm (signals sent through C3,4,5)to cause inspiration (and external intercostals) -sends information to the VRG to modulate the rate of breathing
38
pons involvement in control of ventilation
-neurons from the pons can feed into the DRG and modulate the firing pattern
39
what are the 2 centres in the pons
-pneumotaxic -apneustic
40
what does the pneumotaxic area do in controlling ventilation
-rapidly halt firing and let muscles passively relax -sends inhibitory signals to the DRG
41
control centres for the pneumotaxic centre
-irritant receptors in lungs (Detect harmful substances like smoke or dust and trigger reflexes like coughing or rapid shallow breathing to protect the lungs) -stretch receptors in lungs (if expand too much, will cease inhalation) -higher brain centre (voluntary control of breathing) -pain/ emotional stimuli
42
apneustic centre in control of ventilation
-generate burst of action potentials for contraction -speeds up breathing
43
control centres for the apneustic centre
-peripheral chemoreceptors (aortic arch via vagus nerve) (carotid bodies via glossopharyngeal nerve) detecting low O2, high H+, high CO2) -stretch receptors in muscles and joints during exercise -central chemoreceptors detecting high CO2 -higher brain centre (cerebral cortex, voluntary) -pain/emotional stimuli
44
how does chemical control of ventilation work
-modulates breathing based on tissue/oxygen deands -feeds information to the DRG to increase breathing (when a high H+ is detected->meaning low O2 and high CO2) -detected by central and peripheral chemoreceptors
45
where are central chemoreceptors located
medulla
46
where are peripheral chemoreceptors located
carotid bodies and aortic arch
47
what do central chemoreceptors monitor
CO2 via H+concentrations
48
what do peripheral chemoreceptors monitor
monitors O2 (mainly pO2), CO2 and H+ (measures CO2 levels with H+ receptors too)
49
which chemoreceptors ( central or peripheral) have a slower speed but a greater effect
central chemoreceptors
50
how do pH receptors work for central chemoreceptors to be able to detect H+
​when CO2 levels are high, some CO2 enters the brain by passing the BBB, and then reacts with water to form carbonic acid and H+ ions
51
how do peripheral chemoreceptors work
- respond to decreases in PO2 and increases in PCO2 or H+->increases rate for inspiration and expiration by feeding into the DRG -receptors only fire when PO2=<60mHG (<90% O2 saturation) -can be activated in chronic respiratory disease or at high altitude
52
how does underwater drowning work
-person hyperventilates and low PCO2 (hypocapnia) - this lowers the trigger point that signals the brain to breathe -in a normal dive, the PCO2 levels usually rise and PO2 drops, until the PCO2 reaches a point that signals the body to breathe -hyperventilating before means PCO2 needs longer to reach that point as it starts lower, therefore PO2 continues to drop until hypoxic/ blackout
53
true ribs
-articulates with vertebrae and has individual costal cartilages =>1-7
54
false ribs
articulates with vertebrae through shared costal cartilages =>8-10
55
floating ribs
articulates only with vertebrae =>11-12
56
typical ribs
ribs 3-9
57
atypical ribs
1,2+ 10-12
58
what sits at the angle of loius (sternal angle)
-Rib 2 -Arch or Aorta -Tracheal Bifurcation -Pulmonary trunk -Ligamentum Arteriosum/ Left recurrent laryngeal nerve -Azygos vein -Nerves (cardiac plexus) -T4/5 + Thoracic duct ==>RATPLANT
59
external intercostals function
elevate ribs during forced respiration -E for elevate
60
external intercostals fibre direction
sexternal (hands in pockets)
61
external intercostals innervation
intercostal nerves
62
internal intercostals function
depress ribs during forced expiration
63
external intercostals fibre direction
chinternal direction of fibres (hands to chin)
64
external intercostals innervation
intercostal nerves
65
innermost intercostals function
depress ribs during forced expiration
66
innermost intercostals fibre direction
vertical
67
innermost intercostals innervation
intercostal nerves
68
diaphragm function and innervation
-assisting muscle of respiration - innervated by C3,4,5
69
where are there hiatuses
T8 T10 T12
70
T8 hiatus
-Vena cava hiatus -contains IVC+ right phrenic nerve
71
T10 hiatus
-oesophageal hiatus -oesophagus+ vagus nerve
72
T12 hiatus
-aortic hiatus -aorta+ thoracic duct
73
function of the thoracic cage
-helps protect internal organs -aids in resp by providing space, coordinating mvmnt and decreasing friction
74
what condition is caused by low lung elasticity
fibrosis
75
what condition is caused by too high lung elasticity
emphysema, therefore difficult to exhale
76
what segment of the mediastinum does the phrenic nerve innervate
anterior mediastinum
77
what innervates the anterior mediastinum
phrenic nerve
78
what innervates posterior mediastinum
vagus nerve
79
what segment of the mediastinum does the vagus nerve innervate
posterior mediastinum
80
how does the pulmonary artery sit in relation to the bronchus in the right lung hilum
anterior to the bronchus -RALS
81
how does the pulmonary artery sit in relation to the bronchus in the left lung hilum
superior to the bronchus
82
what is a normal carina angle
40-80 degrees
83
what is the carina
where the trachea bifurcates
84
what can be some causes of carina angle widening
-mediastinal tumours -lymph node enlargement -mass effects of lung lesions e.g lobar collapse
85
left vs right main bronchus shape
right main bronchus is wider, shorter and more vertical
86
why is it easier to aspirate stuff to the right lung compared to the left
because the right main bronchus is wider, shorter and more vertical
87
what do the main bronchi divide into
lobar/ secondary bronchi
88
how many lobar bronchi in the right lung
3 as there is one for each lung
89
what do secondary/lobar bronchi divide into
segmental/tertiary bronchi
90
what do the segmental/ tertiary bronchi do
supply bronchopulmonary segments and further divides into bronchioles
91
what is acute rhinosinusitis
<4wks of inflamm of nasal cavity and paranasal sinuses
92
what can acute thinosinusitis be caused by
viral or bacterial pathogens, or allergic->mainly viruses associated with the common cold
93
treatments for acute rhinosinusitis
-if inadequate response after 2-3 days>amoxicillin+clavulanate -if unable to use penicilins>cefuroxime/doxycycline
94
what is the physical innate barrier for the resp system
mucociliary transport
95
components of mucociliary transport
-epithelial cells -goblet cells -cilia
96
what do epithelial cells do in mucociliary transport
form an epithelial barrier
97
what do goblet cells do in mucociliary transport
secrete mucus N.B they are in the epithelial barrier
98
what does cilia do in mucociliary transport
-beat in an assymetric, coordinated wave like rhythm to move mucus along at 1cm/min
99
when can issues arise in the mucociliary transport in the body
-smokers as toxins from cigarettes can paralyze cilia -anaesthetics as they supress ciliary movement temporarily -CF as the viscosity of mucus changes -infections as they may damage cilia and cause them to be inflamed -immotile cilia syndrome
100
3 immune functions of respiratory epithelial cells
>recognition=express pattern recognition receptors (e.g TLRs , NODs) >recruitment=secrete chemokines+cytokines which recruit immune cells to the subepithelial layer and lamina propria >response=secrete antimicrobial compounds at the luminal surface (e.g defensins)
101
examples of how immune cells can regulate the epithelial barrier function
-IL-22 promotes epithelial cell proliferation+barrier integrity -ILC3+Th17 are immune cells in lamina propria/BALT that secrete IL-22
102
2 types of lung macrophages
-alveoli macrophage -interstitial macrophages
103
what do alveoli macrophages do
phagocytose inhaled particles
104
what do interstitial macrophages do
activate if epithelial barrier is reached
105
neutrophil recruitment in healthy lungs
neutrophils remain in blood vessels
106
neutrophil recruitment in infected lungs
neutrophils recruited and destroy microorganisms by phagocytosis, reactive oxygen species(ROS) and degranulation
107
neutrophil recruitment in lungs with pneumonia
ROS and granule contents from neutrophils causes pulmonary damage
108
macrophages role in innate immunity
they have PRRs that detect pathogens they then release cytokines and chemokines this attracts neutrophils and other immune cells blood vessels expand and become more permeable
109
definition of chronic rhinosinusitis
>12 wks of inflamm of nasal cavity and paranasal sinuses
110
causes of chronic rhinosinusitis
can be multifactorial->bacterial,allergic, CF, obstruction
111
general treatment of chronic rhinosinusitis
give corticosteroids for underlying infection and antibiotics if infection isnt self limiting and pus is seen with nasal endoscopy
112
Sx of rhinosinusitis
nasal congestion facial tenderness tooth pain fever cough discoloured discharge
113
choice of antibacterial for rhinosinusitis
Amoxicillin >add calculanate (b-lactam) if inadequate response within 48-72 hrs >can give alternatives e.g cefuroxime or doxycycline for ppl with penicillin allergy
114
why is amoxicillin used for rhinosinusitis
-first line for chronic, B-lactam inhibitor -broad spectrum -well tolerated
115
why is doxycycline preferrably not used for rhinosinusitis
many adverse effects e.g bone growth >contraindicated in children <8y/o, pregnancy >16 wks and hepatic impairment
116
is pharyngitis usually viral or bacterial
viral(70-90%)
117
common causes of bacterial pharyngitis
group A strep, gonorrhoea, H. influenzae
118
Sx of pharyngitis (tonsillitis)
-swollen tonsils -pus-filled lesions -tender cervical lymphadenopathy -fever -sore throat
119
what is the common bacterial pathogen for bacterial pharyngitis
strep pyogenes
120
treatment for bacterial pharyngitis
narrow spectrum penicillin e.g -phenoxymethylpenicillin -benzylpenicillin
121
why are antibacterial agents needed for bacterial pharyngitis
to avoid complications like rheumatic fever and heart disease
122
what is given to patients allergic to penicillin for bacterial pharyngitis
cephalexin or azithromycin
123
what is otitis media
middle ear infection
124
treatment for otitis media
-symptomatic treatment for pain and fever e.g paracetamol -Antibiotics e.g amoxicillin->give short course to increase compliance and reduce adverse effects e.g diarrhoea, vomiting or rash in children
125
describe bronchitis
inflammation of bronchus -usually self limiting and viral unless caused by influenza
126
what to give if bronchitis is caused by whooping cough
Macrolide(clarithromycin)
127
why is clarithromycin used
-reduces symptoms -prevents transmission if diagnosed <3wks after cough onset N.B is given as prophylaxis to infants <6 months, unvaccinated children, last month of pregnancy
128
what to give if bronchitis is caused by influenza
-usually self limiting but can use oseltamivir
129
what is pneumonia treated based on
severity
130
how to treat low severity pneumonia
-amoxicillin -if allergic, or atypical pathogen, use doxycycline or clarithromycin -combination therapy can inclue doxycycline with amoxicillin/cefuroxime
131
how is moderate severity pneumonia treated
benzylpenicillin with doxycycline/clarithromycin
132
how is high severity pneumonia treated
-usually in ICU with directed therapy or empirical broad spectrum
133
how is TB treated
RIPE -Rifampicin -Isoniazid -Pyrazinamide -Ethambutol
134
negatives of TB treatment
-Lots of adverse effects and drug interactions -major issues due to rifampicin inducing potentially being able to induce hepatotoxicity, so LFTs need to be monitored, and also may induce CYP450
135
main causes of common cold
-rhinovirus and coronavirus(50%)
136
causes of common cold
rhinovirus coronavirus adenovirus parainfluenza influenza
137
describe the common cold
-virus infects epithelial cells lining nasal passage and pharynx,causing destruction of epithelial layer (ciliated coumnar epithelium)
138
transmission of common cold
direct contact droplet inhalation
139
Sx of common old
rhinorrhoea sneezing sore throat headache malaise fever cough
140
what is malaise
feeling of discomfort
141
Tx of common cold
antihistamines, paracetamol, hydration
142
how does diptheria cause damage
multiplies locally without invading deeper tissue-> adheres to tissue of larynx and pharynx, killing tissue and making a false membrane from dead tissues
143
diptheria aetiology
toxin-producing strains of corynebacterium diptheria
144
diptheria Sx
-may pump toxins that can cause heart and liver damage -necrotic exudate(false membrane) that can block airways enlarged cervical lymph nodes also called 'bull-neck'
145
Tx of diptheria
-penicillins -anti toxin -monitor for respiratory obstruction->if there is i.e laryngeal diptheriae, emergency tracheostomy is needed
146
aetiology of glandular fever
Epstein-Barr virus (herpesviridae)
147
symptoms of glandular fever
fever anorexia swollen tonsils/ lymph nodes headache lethargy sore throat enlarged liver/spleen
148
transmission of glandular fever
via saliva e.g kissing
149
aetiology of acute laryngitis
viral causes
150
Sx of acute laryngitis
barking cough sore throat cold symptoms hoarseness
151
LRTIs list(10)
TB typical pneumonia atypical pneumonia viral pneumonia whooping cough influenza acute bronchitis acute BRONCHIOLITIS lung abscess empyema
152
whooping cough cause (organism)
bordetella pertussis
153
symptoms of whooping cough
-URTI symptoms -whoop -episodic coughing -vomiting
154
phases of whooping cough
>incubation phase(1-3wks)-incubation >catarrhal phase(1-2wks)-URTI symptoms, highly infectious >paroxysmal phase(2-4wks)-whoop, episodic cough, vomiting >covalescent phase-gradual recovery, less persistent
155
how to diagnose whooping cough
pre-nasal swab
156
Tx of whooping cough
macrolides like clarithromycin or azithromycin
157
aetiology of acute bronchiolitis
75% RSV 25% para/influenza virus, mycoplasma pnemonia
158
Sx of acute bronchiolitis
fever cold-like symptoms wheeze respiratory distress
159
Dx of acute bronchiolitis
nasopharyngeal aspirate
160
aetiology of acute bronchitis
-usually viral e.g rhino/corona/adenovirus,influeza -can be bacterial e.g mycoplasma pneumoniae
161
Sx of acute bronchitis
cough thick mucus
162
Dx of acute bronchitis
sputum culture
163
possible complications of acute bronchitis
can lead to secondary bacterial infection
164
difference between typical and atypical pneumonia
typical= fast, severe, productive cough atypical=slow, milder, dry cough
165
aetiology of typical pneumonia
everyone- S. pneumoniae elderly,COPD,alcoholics-H. pneumoniae, M catarrhalis, K.pneumoniae elderly, IVDUs-S. aureus CF-P.aeruginosa
166
Sx of typical pneumonia
-abrupt onset -fever -purulent sputum/cough -rapid RR -dyspnoea
167
Dx of typical pneumonia
x-ray (lobar) sputum/blood culture bronchoscopy
168
Tx of typical pneumonia
mild=amoxicillin, doxycycline moderate= benzylpenicillin+doxycycline severe=ceftriaxone/cefotaxime + azithromycin
169
aetiology of atypical pneumonia
mycoplasma chlamydophila
170
Sx of atypical pneumonia
fever dry cough constitutional symptoms
171
Dx of atypical pneumonia
X-ray (interstitial) serology
172