Respiratory Week 2 Flashcards
1
Q
below epiglottis - microbes?
A
generally sterile - small amounts of aspirated microbes
2
Q
defences that keep respiratory tract beyond epiglottis sterile
A
- physical defences - mucous, cilia
- alveolar macrophages
3
Q
what bacteria found in >50% healthy people
A
viridans streptococci
H.influenza Type B
4
Q
what bacteria found occasionally in healthy people
A
strept. pyogenes
5
Q
bacteria found in
A
enterobacteria
6
Q
most of bacteria in upper respiratory tract are aerobic or anaerobic
A
anaerobic
7
Q
does a respiratory syndrome have one cause?
A
no- each can be caused by different agents, and each agent can cause different sydnromes
8
Q
agent of common cold
A
rhinovirus
9
Q
agent of pharyngitis/tonsillitis (with nasal involvement)
A
adenovirus
10
Q
agent of pharyngitis/onsillitis (no nasal involvement)
A
strept. pyogenes
11
Q
agent of sinusitis
A
primary: viral
secondary: H influenzae
12
Q
agent of otitis media
A
pneumococci
13
Q
agent of epiglottitis
A
H influenzae type b
14
Q
agent of croup (LTB)
A
parainfluenza virus
15
Q
pathogenesis of common cold
A
- virus adheres to respiratory epithelial cells, adsorbed, replicates
- cell damage, necrosis of epithelial cells
- host defences activated
- low grade overgrowth of bacterial commensals
16
Q
when would you need a laboratory diagnosis of URTI if possible
A
pharyngitis/tonsillitis
epiglottitis
17
Q
when would you treat pharyngitis/tonsillitis or sinusitis
A
if bacterial
18
Q
when would you treat epiglottitis
A
always
19
Q
when would you treat otitis media
A
if
20
Q
acute bronchitis usually caused by
A
viral URTI
21
Q
acute exacerbation of chronic bronchitis usually caused by
A
pneumococci and/or H influenzae
22
Q
bronchiolitis usually caused by
A
RSV
23
Q
pneumonia caused by virus or bacteria
A
both
bacteria - typical and atypical
virus
24
Q
lung abscess caused by
A
mixed anaerobes
25
empyema caused by
staph. aureus
26
"typical" bacterial cause of community acquired pneumonia
strept. pneumonia
| H influenzae
27
"atypical" bacterial cause of community acquired pneumonia
mycoplasma pneumoniae
28
viral cause of CAP
influenza
29
fungi cause of CAP
pneumocystis jirovecii
30
when does pneumonia occur - what does it require
- defect in host defence
- microbe is highly virulent
- infective dose is large
31
usual route of infection causing pneumonia
microaspiration of UR microbiota
32
why do you need to make a specific diagnosis of pneumonia
appropriate antibiotic prescribing
| e.g. P aeruginosa - intrinsically resistant to normal antibiotics, need tailored ones
33
main way to make a clinical diagnosis of pneumonia
laboratory tests
34
clinical considerations when diagnosing pneumonia
- community or hospital acquired
- severity index
- underlying illness (AIDS, cystic fibrosis)
- occupation, trave
35
treatment of community-acquired pneumonia
best guess: pen G/amoxycillin + doxycycline/macrolide
36
two types of vaccines to prevent pneumonia
influenza, pneumococcal vaccine
37
what type of epithelium is respiratory epithelium
pseudostratified
38
types of cells that make up respiratory epithelium
-ciliated columnar cells
-goblet cells
-basal stem cells
-brush cells (only have microvilli)
-serous cells
-small granule cells
sensory cells to initiate coughing
39
structure of normal cilia
9+2 microtubular structure (axoneme)
40
how fast do cilia beat
10-15Hz
41
what do radial spokes do in cilia
hold microtubules in perfect circle
42
what is on microtubules in cilia
dynein arms
43
name of congenital cilia abnormality
Kartagener's syndrome
44
3 layers of trachea
mucosa
submucosa
adventita
45
mucosa of trachea =
respiratory epithelium + lamina propria
46
submucosa of trachea =
glands and connective tissue
47
what keeps tracheal surface moist
mucous and serous glands
48
submucosa of bronchi =
glands and smooth muscle
49
what defines bronchi to bronchiole separation
when cartilage gone = bronchiole
50
cell changes from bronchi to bronchioles
bronchi to bronchioles epithelium loses goblet and ciliated cells and gains Clara cells (ciliated cells extend further down than goblet cells)
51
what keeps bronchioles open
radial connective tissue
52
what do clara cells secrete
surfactant - to repel surface tension
53
what shape are clara cells, structural feature
columnar to cuboidal with short microvilli
54
what are terminal bronchioles
final level of conducting system, give rise to respiratory bronchioles
55
respiratory bronchiole leads to
first alveoli
56
epithelium of respiratory bronchiole
cuboidal to squamous, v thin
57
how wide is an alveoli, type of epithelium, wall contains many... , individual alveoli connected by
200um
simple squamous
wall contains pulmonary capillaries
individual alveoli connected by pores
58
what is between alveoli
| what does it contain
alveolar septum
| contains reticular fibres and elastin fibres
59
what does elastin in alveoli
keeps alveoli from collapsing
60
type I pneumocytes
forms majority of surface area of alveoli - forms alveolar simple squamous epithelium
-provides gas exchange surface
61
type II pneumocytes
more numerous than type I but only 5% of area
| -cuboidal cells, often in angle between alveoli
62
characteristics of type II pneumocytes
lamellar bodies - secrete surfactant
| short microvilli
63
turnover of type I and II pneumocytes
type I - must die and be replaced
| type II - can divide and give rise to new type I or II
64
blood-gas barrier consists of
```
surfactant
type I pneumocyte
basal lamina
connective tissue
basal lamina
endothelial cell
plasma
erythrocyte membrane
```
65
when intra-alveolar macrophages are "full" they..
migrate up the airways until they are carried off by ciliated cells
some end up in interalveolar septum loaded with particles
66
pleura is what type of epithelium
squamous
67
does visceral pleura contain lymphatics
yes
68
what do microvilli on surface of mesothelium epithelium of visceral pleura do
trap hyaluronic acid betwen visceral and parietal pleura (lubrication)
69
where do some lymphatics of lung drain
into pleural space - problem because pathway for metastatic cancer
70
alveolar-capillary membrane composed of
1 layer of surfactant
2 type 1 alveolar cell
3 basement membrane
4 vascular endothelium
71
why are alveoli ideally suited for gas exchange
large surface area and thinness
72
infection of lung parenchyma (alveolar membrane)
pneumonia
73
infection of airways
bronchitis
74
disruption of alveolar membrane
emphysema
75
what are the likely physiological effects of disrupting the AC membrane
1 abnormal gas exchange
2abonrmal lung mechanics
3 pulmonary vascular complications
76
PAO2 in alveoli
100mmHg
77
PACO2 in alveoli
40mmHg
78
is partial pressure of O in alveoli same as in capillaries
no - as blood goes past alveoli PAO2 will go down
79
what is rate of diffusion of a gas determined by
fick's law
V =(A*D*(P1-P2) )/T
A=surface area
P1-P2 = difference in partial pressures
T = thickness of membrane
D = constant
80
what diffuses more efficiently O or Co2
what are the consequences of this
CO2
dont see high levels of Co2 if diffusion impairment
81
reason for having elevated CO2
hypoventilation (inadequate alveolar ventilation)
82
possible reasons for having low O in blood
hypoventilation, abnormal gas exchange (V/Q mismatch, shunt, diffusion impairment) or low PiO2
83
time course of O diffusion
RBC in contact with alveolar membrane for 0.75s. Blood fully oxygenated in first 0.25s (rest of time no O taken up)
84
advantage of all O taken up in 0.25s
as need for CO increases, blood flows more quickly, time in contact with alveolar membrane shortens, but blood going past still fully oxygenated
85
in disease, what mechanism is cause of hypoxia at rest
usually V/Q mismatch
86
in disease, what mechanism is cause of hypoxia during exercise
diffusion impairment
87
can elevated CO2 be due to diffusion impairment
RARELY (only when alveolar membrane severely disrupted)
| usually lack of alveolar ventilation
88
what causes breathlessness in restrictive lung disease
stiff lungs so harder to breath in
89
what happens to FVC, FEV1 and FEV1/FVC in restrictive lung disease
lungs have reduced compliance so all lung volumes reduced
- reduced FVC
- reduced FEV1
- normal FEV1/FVC (b/c its a ratio)
90
what does compliance of lungs depend on
1 tissue composition
| 2 surface tension in alveoli (reduced by surfactant)
91
in pulmonary fibrosis (restrictive lung disease) what needs to change to ensure same change in air volume when you breathe
need much higher pressure
92
in general, how does the breathing change of someone with restrictive lung disease
rapid shallow breaths
93
what happens to maximum ventilation in restrictive lung disease
it reduces
94
if have high pH and low CO2, respiratory or metabolic alkalosis
respiratory (from hyperventilation) alkalosis
95
if high pH and CO2 NOT low
metabolic alkalosis
96
if low pH and high CO2
respiratory acidosis
97
if low pH but NOT high CO2
metabolic acidosis
98
work of breathing as opposed to elastic work of breathing
WOB - energy needed to overcome friction of air going through airways
elastic WOB - work to expand the lungs
99
pulmonary artery pressure (what number value)
25/8mmHg
100
capillary pressure (value)
12-8mmHg
101
does pulmonary artery pressure rise with exercise/increased CO? why
NO
because dilatation and recruitment of pulmonary vessels (capillary bed volume increases) - to accomodate increase in blood flow
102
when would there be an increase in pulmonary artery pressure?
in disease
103
why is systolic BP lower on inspiration than expiration
because there is pooling in lungs, so decreased venous return to LA, so decreased CO
104
pulses paradoxus
accentuation of normal decrease in systolic on inspiration - result of forceful use of respiratory muscles
105
two mechanisms of crepitations
1. pulmonous mechanism - air bubbling through fluid - on both inspiration and expiration
2. high pitched, at end of inspiration = sudden opening of alveoli that have collapsed on expiration (happens in people with stiff scarred lungs) (less common)
106
what is low CO2 a result of in acidosis
compensatory mechanism to metabolic acidosis
107
what are the factors that influence fluid movement across the pulmonary capillaries
hydrostatic pressure, oncotic pressure inside and outside capillaries
permeabilitiy
108
normal PaO2
25-100mmHg
109
normal CO2
38-42mmHg
110
normal HCO3-
22-28mmol/l
111
normal pH
7.35-7.42
112
acute respiratory distress syndrome (ARDS)
syndrome occurring after trauma, if multiple fractures - increases capillary permeability in lungs
113
where does fluid that normally leaks out of capillaries go
leaks into interstitial space, but not into alveoli - drained by lymphatics
114
how can fluid leak into alveoli in disease? what is cuase
more fluid than normal leaking into interstitium, enough pressure for fluid to move into alveoli
115
effects of pulmonary oedema on lung function
- decreased compliance
- decreased lung volumes
- increase airway resistance
- increased work of breathing (elastic and resistive)
116
initial changes in arterial blood gases and pH in pulmonary oedema, then what happens if v severe
- decreased PaO2
- decreased CO2
- increased pH
if severe, increase in PaCO2, decrease in pH
117
are capillary and alveolar membranes permeable to water ions and small molecules?
capillary endothelium YES
alveolar epithelium NO - actively pumps water from alveoli into interstitial spaces
118
rate lymphatics can pump out interstitial fluid from lungs
20mL/h
119
does interstitial oedema in lungs have functional effect on lungs?
no
120
two causes of pulmonary oedema
1. increased capillary hydrostatic pressure
| 2. increased capillary permeability (trauma, sepsis, toxins)
121
'sex-influenced' in regard to genetic disease
acts as different type of inheritance in men and women
| e.g. male pattern baldness - dominant trait for men, recessive for women
122
congenital
developmental errors apparent at birth
| DOESN'T MEAN GENETIC
123
what are disorders of mitochondrial inheritance
disorders of energy - poor growth and development
| disorders in energy-hungry tissues (CNS, ears, eyes)
124
are mitochondrial disorders passed through mother or father
mutations in mitochondrial genome - only mother
mutations in mitochondrial genes in nuclear genome - mother or father
125
tyrosinase
begins cascade of pigment pathways -
126
albinism - defect in what gene
tyrosinase (required to make ANY pigment)
127
e.g. of polygenic inheritance
skin colour
128
melanin
polymer of structures derived from tyrosine, involving tyrosinase
129
one or many genes involved in structure of collagen?
many
130
sequence of most collagens involves multiple repeats of what sequence
collagen mostly what aa
Gly-Pro-Ala
| mostly glycine, then proline and then alanine
131
osteogenesis imperfecta
glycine at particular position mutates to cysteine
disruption of collagen helix causes kink and interferes with strand alignment
many different levels of severity, 8 types
132
type of inheritance of osteogenesis imperfecta
autosomal dominant or recessive
133
ehlers danlos syndrome
caused by mutation in collagen or enzymes that process genes - causes hyperflexibility of tendons
134
inheritance of ehlers danlos syndrome
autosomal dominant
135
neurofibromatosis
small nerve ending tumours grow on skin, not lethal
136
marfan syndrome
disorder of connective tissue - long limbs and fingers and face
137
hereditary spherocytosis
change in shape of erythrocytes which are destroyed by spleen - anaemia
138
which single gene disorders do we test for prenatally
PKU
CF
galactosaemia
primary congenital hypothyroidism
139
inheritance of PKU
autosomal recessive
140
what is PKU
lack of phenylalanine hydroxyase
| phenylalanine accumulation, conversion to phenlypyruvate - builds up and damages brain
141
what clinically does CF cause
build up of mucous in lungs leading to repeated chest infections, malabsorption, mucous blockage in small intestine pancreatitis, CF related diabetes
142
CF defect in what
CF transmembrane conductance regulator - chloride channel
143
test for CF, detects all causes?
elevated immunoreactive trypsinogen (IRT)
| only detects 90% cases
144
what is primary congenital hypothyroidism
defect in thyroid hormone or thyroid gland itself not developed
145
what does primary congenital hypothyroidism cause if untreated
growth failure and permanent intellectual disability
146
diagnosis of primary congenital hypothyroidism
heel prick - high TSH or low thyroxine (T4)
147
why do we prenatally test for only certain things
because these things need early intervention
148
why dont we test for genes in prenatal testing of genetic diseases
because different mutations can cause the same syndrome
149
normal RR
12-20/min
150
normal minute ventilation
7L/min
151
normal TV
500mL (dead space 150mL)
152
normal PAO2
100mmHg
153
normal PACO2
40mmHg
154
what is asbestosis
form of diffuse interstitial lung disease (DILD) due to asbestos exposure
155
what pathologically occurs in asbestosis
progessive diffuse inflammation and fibrosis of lung parenchyma causing disruption and destruction of AC membrane
156
ascites
fluid in peritoneal cavity
157
if pulmonary pressure increases RV compensates by
| then what happens
- hypertrophy
- eventual dilation of ventricle
- incompetency of tricuspid valve
- regurgitation
158
in exercise, does anything happen to PAo2 and arteriole saturation?
no - gas exchange remains normal due to ventilation increase to cope
159
what is the effect of pulmonary hypertension on RA and systemic venous pressures
they increase
160
what is effect of increased systemic venous pressure on systemic capillary bed
if severe,
- peripheral oedema
- ascites
- pleural effusions
161
3 causes of increased pulmonary vascular resistance
- vasoconstriction
- obstruction (embolism e.g.)
- obliteration (emphysema, pulmonary fibrosis)
162
two results of right ventricle dilation and hypertrophy
- increase systemic venous pressure
| - poor cardiac output
163
in acidosis, why does bicarb go down
buffer systems attempts to limit change in pH
164
anion gap
clinical tool - usually measured anions are less that cations by 15
165
if metabolic acidosis due to loss of bicarb, what happens to anion gap
for every unit of bicarb lost, Cl is reabsorbed - so anion gap normal
166
if metabolic acidosis is due to new acid, what happens to anion gap
Cl stays the same, and bicarb consumed in buffering, so less anions than normal so bigger gap
167
body's compensation for respiratory acidosis, how long does it take
bicarb retention, days
168
compensation for metabolic acidosis
hyperventilation
169
acinus
respiratory bronchiole and alveoli
170
lobule
terminal bronchiole, respiratory bronciole and alveoli
171
obstructive and restrictive FEV1 and FVC
obstructive - decreased FEV1, normal FVC
restrictive normal FEV1, reduced FVC
172
3 branches of COPD
emphysema
chronic bronchitis
small airway disease (with some reversible bronchospasm)
173
what causes COPD
smoking
174
wat is emphysema
abnormal permanent enlargement of air spaces distal to terminal bronchiole, from destruction of alveolar wall without fibrosis
175
what is cronic bronchitis
persistent cough productive of sputum for at least 3 months in 2 consecutive years with no other cause
176
definition of asthma
increased responsiveness of airways to various stimuli leading to episodic bronchoconstriction which is at least partly reversible
177
two types of asthma
1. atopic/allergic - increased IgE, specific environmental allergens
2. non-allergic - normal IgE, non-specific triggers (more common)
178
asthma acute/immediate phase
-increased vascular permeability
increased mucous production
- bronchospasm
179
late phase response 4-8h
chemotaxis of eosinophils, mast cells, lymphocytes, macs - ongoing inflammation
- epithelial damage
180
do bronchodilators help in late phase astma
no
181
trigger of asthma (cellular)
release of mediators from mast cells
182
status asthmaticus
acute severe asthma not responding to bronchodilators
183
how does smoking cause emphysema
smoking upsets balance of proteases and anti-proteases - proteases digest our alveolar walls
184
how does emphysema cause airway obstruction
loss of elastic recoil - loss of supporting elastic tissue around small airways leads to collapse
185
cor pulmonale
abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels
186
what occurs in chronic bronchitis to the airways
- increased mucous production in larger airways
| - airway inflammation, scarring and narrowing in smaller airways
187
complications of chronic bronchitis
- superimposed infective exacerbations
- hypoxia, pulmonary hypertension, cor pulmonale
- squamous metaplasia, squamous dysplasia (premalignant)
188
location in airways of emphysema, chronic bronchitis and small airways disease
emphysema - alveoli
chronic bronchitis - large airways
small airways disease - small airways in-between
189
infective exacerbations of COPD
bacterial bronchitis, increased bronchospasm
190
clinical presentation of emphysema
O levels don't fall b/c breath harder, decreases CO2
191
clinical presentation of bronchitis
tolerate O2 decline - body lets levels fall (don't breathe harder)
get cor pulmonale
192
bronchiectasis
irreversible, abnormal dilation of bronchi/bronchioles
193
pathogenesis of bronchiectasis
severe destructive inflammation of airways
| loss of surrounding elastic tissue and msucle exeeds contraction of fibrous tissue
194
causes of bronchectasis
necrotising infections
195
idiopathic pulmonary fibrosis
histologic pattern is usual interstitial pneumonitis - interstitial inflammation, fibrosis , progression to end-stage lung disease
196
wat is usual interstitial pneumonitis
fibrosis and inflammation that appears to be of varying ages
