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MD1 > Respiratory Week 2 > Flashcards

Respiratory Week 2 Flashcards

1
Q

below epiglottis - microbes?

A

generally sterile - small amounts of aspirated microbes

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2
Q

defences that keep respiratory tract beyond epiglottis sterile

A
  • physical defences - mucous, cilia

- alveolar macrophages

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3
Q

what bacteria found in >50% healthy people

A

viridans streptococci

H.influenza Type B

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4
Q

what bacteria found occasionally in healthy people

A

strept. pyogenes

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5
Q

bacteria found in

A

enterobacteria

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6
Q

most of bacteria in upper respiratory tract are aerobic or anaerobic

A

anaerobic

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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

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8
Q

agent of common cold

A

rhinovirus

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9
Q

agent of pharyngitis/tonsillitis (with nasal involvement)

A

adenovirus

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10
Q

agent of pharyngitis/onsillitis (no nasal involvement)

A

strept. pyogenes

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11
Q

agent of sinusitis

A

primary: viral
secondary: H influenzae

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12
Q

agent of otitis media

A

pneumococci

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13
Q

agent of epiglottitis

A

H influenzae type b

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14
Q

agent of croup (LTB)

A

parainfluenza virus

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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
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16
Q

when would you need a laboratory diagnosis of URTI if possible

A

pharyngitis/tonsillitis

epiglottitis

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17
Q

when would you treat pharyngitis/tonsillitis or sinusitis

A

if bacterial

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18
Q

when would you treat epiglottitis

A

always

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19
Q

when would you treat otitis media

A

if

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20
Q

acute bronchitis usually caused by

A

viral URTI

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21
Q

acute exacerbation of chronic bronchitis usually caused by

A

pneumococci and/or H influenzae

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22
Q

bronchiolitis usually caused by

A

RSV

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23
Q

pneumonia caused by virus or bacteria

A

both
bacteria - typical and atypical
virus

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24
Q

lung abscess caused by

A

mixed anaerobes

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25
Q

empyema caused by

A

staph. aureus

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26
Q

“typical” bacterial cause of community acquired pneumonia

A

strept. pneumonia

H influenzae

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27
Q

“atypical” bacterial cause of community acquired pneumonia

A

mycoplasma pneumoniae

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28
Q

viral cause of CAP

A

influenza

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29
Q

fungi cause of CAP

A

pneumocystis jirovecii

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30
Q

when does pneumonia occur - what does it require

A
  • defect in host defence
  • microbe is highly virulent
  • infective dose is large
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31
Q

usual route of infection causing pneumonia

A

microaspiration of UR microbiota

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32
Q

why do you need to make a specific diagnosis of pneumonia

A

appropriate antibiotic prescribing

e.g. P aeruginosa - intrinsically resistant to normal antibiotics, need tailored ones

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33
Q

main way to make a clinical diagnosis of pneumonia

A

laboratory tests

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34
Q

clinical considerations when diagnosing pneumonia

A
  • community or hospital acquired
  • severity index
  • underlying illness (AIDS, cystic fibrosis)
  • occupation, trave
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35
Q

treatment of community-acquired pneumonia

A

best guess: pen G/amoxycillin + doxycycline/macrolide

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36
Q

two types of vaccines to prevent pneumonia

A

influenza, pneumococcal vaccine

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37
Q

what type of epithelium is respiratory epithelium

A

pseudostratified

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38
Q

types of cells that make up respiratory epithelium

A

-ciliated columnar cells
-goblet cells
-basal stem cells
-brush cells (only have microvilli)
-serous cells
-small granule cells
sensory cells to initiate coughing

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39
Q

structure of normal cilia

A

9+2 microtubular structure (axoneme)

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40
Q

how fast do cilia beat

A

10-15Hz

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41
Q

what do radial spokes do in cilia

A

hold microtubules in perfect circle

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42
Q

what is on microtubules in cilia

A

dynein arms

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43
Q

name of congenital cilia abnormality

A

Kartagener’s syndrome

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44
Q

3 layers of trachea

A

mucosa
submucosa
adventita

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45
Q

mucosa of trachea =

A

respiratory epithelium + lamina propria

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46
Q

submucosa of trachea =

A

glands and connective tissue

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47
Q

what keeps tracheal surface moist

A

mucous and serous glands

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48
Q

submucosa of bronchi =

A

glands and smooth muscle

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49
Q

what defines bronchi to bronchiole separation

A

when cartilage gone = bronchiole

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50
Q

cell changes from bronchi to bronchioles

A

bronchi to bronchioles epithelium loses goblet and ciliated cells and gains Clara cells (ciliated cells extend further down than goblet cells)

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51
Q

what keeps bronchioles open

A

radial connective tissue

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52
Q

what do clara cells secrete

A

surfactant - to repel surface tension

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53
Q

what shape are clara cells, structural feature

A

columnar to cuboidal with short microvilli

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54
Q

what are terminal bronchioles

A

final level of conducting system, give rise to respiratory bronchioles

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55
Q

respiratory bronchiole leads to

A

first alveoli

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56
Q

epithelium of respiratory bronchiole

A

cuboidal to squamous, v thin

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57
Q

how wide is an alveoli, type of epithelium, wall contains many… , individual alveoli connected by

A

200um
simple squamous
wall contains pulmonary capillaries
individual alveoli connected by pores

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58
Q

what is between alveoli

what does it contain

A

alveolar septum

contains reticular fibres and elastin fibres

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59
Q

what does elastin in alveoli

A

keeps alveoli from collapsing

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60
Q

type I pneumocytes

A

forms majority of surface area of alveoli - forms alveolar simple squamous epithelium
-provides gas exchange surface

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61
Q

type II pneumocytes

A

more numerous than type I but only 5% of area

-cuboidal cells, often in angle between alveoli

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62
Q

characteristics of type II pneumocytes

A

lamellar bodies - secrete surfactant

short microvilli

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63
Q

turnover of type I and II pneumocytes

A

type I - must die and be replaced

type II - can divide and give rise to new type I or II

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64
Q

blood-gas barrier consists of

A 
surfactant
type I pneumocyte
basal lamina
connective tissue
basal lamina
endothelial cell
plasma
erythrocyte membrane
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65
Q

when intra-alveolar macrophages are “full” they..

A

migrate up the airways until they are carried off by ciliated cells
some end up in interalveolar septum loaded with particles

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66
Q

pleura is what type of epithelium

A

squamous

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67
Q

does visceral pleura contain lymphatics

A

yes

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68
Q

what do microvilli on surface of mesothelium epithelium of visceral pleura do

A

trap hyaluronic acid betwen visceral and parietal pleura (lubrication)

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69
Q

where do some lymphatics of lung drain

A

into pleural space - problem because pathway for metastatic cancer

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70
Q

alveolar-capillary membrane composed of

A

1 layer of surfactant
2 type 1 alveolar cell
3 basement membrane
4 vascular endothelium

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71
Q

why are alveoli ideally suited for gas exchange

A

large surface area and thinness

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72
Q

infection of lung parenchyma (alveolar membrane)

A

pneumonia

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73
Q

infection of airways

A

bronchitis

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74
Q

disruption of alveolar membrane

A

emphysema

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75
Q

what are the likely physiological effects of disrupting the AC membrane

A

1 abnormal gas exchange
2abonrmal lung mechanics
3 pulmonary vascular complications

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76
Q

PAO2 in alveoli

A

100mmHg

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77
Q

PACO2 in alveoli

A

40mmHg

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78
Q

is partial pressure of O in alveoli same as in capillaries

A

no - as blood goes past alveoli PAO2 will go down

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79
Q

what is rate of diffusion of a gas determined by

A

fick’s law
V =(AD(P1-P2) )/T

A=surface area
P1-P2 = difference in partial pressures
T = thickness of membrane
D = constant

80
Q

what diffuses more efficiently O or Co2

what are the consequences of this

A

CO2

dont see high levels of Co2 if diffusion impairment

81
Q

reason for having elevated CO2

A

hypoventilation (inadequate alveolar ventilation)

82
Q

possible reasons for having low O in blood

A

hypoventilation, abnormal gas exchange (V/Q mismatch, shunt, diffusion impairment) or low PiO2

83
Q

time course of O diffusion

A

RBC in contact with alveolar membrane for 0.75s. Blood fully oxygenated in first 0.25s (rest of time no O taken up)

84
Q

advantage of all O taken up in 0.25s

A

as need for CO increases, blood flows more quickly, time in contact with alveolar membrane shortens, but blood going past still fully oxygenated

85
Q

in disease, what mechanism is cause of hypoxia at rest

A

usually V/Q mismatch

86
Q

in disease, what mechanism is cause of hypoxia during exercise

A

diffusion impairment

87
Q

can elevated CO2 be due to diffusion impairment

A

RARELY (only when alveolar membrane severely disrupted)

usually lack of alveolar ventilation

88
Q

what causes breathlessness in restrictive lung disease

A

stiff lungs so harder to breath in

89
Q

what happens to FVC, FEV1 and FEV1/FVC in restrictive lung disease

A

lungs have reduced compliance so all lung volumes reduced

  • reduced FVC
  • reduced FEV1
  • normal FEV1/FVC (b/c its a ratio)
90
Q

what does compliance of lungs depend on

A

1 tissue composition

2 surface tension in alveoli (reduced by surfactant)

91
Q

in pulmonary fibrosis (restrictive lung disease) what needs to change to ensure same change in air volume when you breathe

A

need much higher pressure

92
Q

in general, how does the breathing change of someone with restrictive lung disease

A

rapid shallow breaths

93
Q

what happens to maximum ventilation in restrictive lung disease

A

it reduces

94
Q

if have high pH and low CO2, respiratory or metabolic alkalosis

A

respiratory (from hyperventilation) alkalosis

95
Q

if high pH and CO2 NOT low

A

metabolic alkalosis

96
Q

if low pH and high CO2

A

respiratory acidosis

97
Q

if low pH but NOT high CO2

A

metabolic acidosis

98
Q

work of breathing as opposed to elastic work of breathing

A

WOB - energy needed to overcome friction of air going through airways

elastic WOB - work to expand the lungs

99
Q

pulmonary artery pressure (what number value)

A

25/8mmHg

100
Q

capillary pressure (value)

A

12-8mmHg

101
Q

does pulmonary artery pressure rise with exercise/increased CO? why

A

NO
because dilatation and recruitment of pulmonary vessels (capillary bed volume increases) - to accomodate increase in blood flow

102
Q

when would there be an increase in pulmonary artery pressure?

A

in disease

103
Q

why is systolic BP lower on inspiration than expiration

A

because there is pooling in lungs, so decreased venous return to LA, so decreased CO

104
Q

pulses paradoxus

A

accentuation of normal decrease in systolic on inspiration - result of forceful use of respiratory muscles

105
Q

two mechanisms of crepitations

A
  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
Q

what is low CO2 a result of in acidosis

A

compensatory mechanism to metabolic acidosis

107
Q

what are the factors that influence fluid movement across the pulmonary capillaries

A

hydrostatic pressure, oncotic pressure inside and outside capillaries
permeabilitiy

108
Q

normal PaO2

A

25-100mmHg

109
Q

normal CO2

A

38-42mmHg

110
Q

normal HCO3-

A

22-28mmol/l

111
Q

normal pH

A

7.35-7.42

112
Q

acute respiratory distress syndrome (ARDS)

A

syndrome occurring after trauma, if multiple fractures - increases capillary permeability in lungs

113
Q

where does fluid that normally leaks out of capillaries go

A

leaks into interstitial space, but not into alveoli - drained by lymphatics

114
Q

how can fluid leak into alveoli in disease? what is cuase

A

more fluid than normal leaking into interstitium, enough pressure for fluid to move into alveoli

115
Q

effects of pulmonary oedema on lung function

A
  • decreased compliance
  • decreased lung volumes
  • increase airway resistance
  • increased work of breathing (elastic and resistive)
116
Q

initial changes in arterial blood gases and pH in pulmonary oedema, then what happens if v severe

A
  • decreased PaO2
  • decreased CO2
  • increased pH

if severe, increase in PaCO2, decrease in pH

117
Q

are capillary and alveolar membranes permeable to water ions and small molecules?

A

capillary endothelium YES

alveolar epithelium NO - actively pumps water from alveoli into interstitial spaces

118
Q

rate lymphatics can pump out interstitial fluid from lungs

A

20mL/h

119
Q

does interstitial oedema in lungs have functional effect on lungs?

A

no

120
Q

two causes of pulmonary oedema

A
  1. increased capillary hydrostatic pressure

2. increased capillary permeability (trauma, sepsis, toxins)

121
Q

‘sex-influenced’ in regard to genetic disease

A

acts as different type of inheritance in men and women

e.g. male pattern baldness - dominant trait for men, recessive for women

122
Q

congenital

A

developmental errors apparent at birth

DOESN’T MEAN GENETIC

123
Q

what are disorders of mitochondrial inheritance

A

disorders of energy - poor growth and development

disorders in energy-hungry tissues (CNS, ears, eyes)

124
Q

are mitochondrial disorders passed through mother or father

A

mutations in mitochondrial genome - only mother

mutations in mitochondrial genes in nuclear genome - mother or father

125
Q

tyrosinase

A

begins cascade of pigment pathways -

126
Q

albinism - defect in what gene

A

tyrosinase (required to make ANY pigment)

127
Q

e.g. of polygenic inheritance

A

skin colour

128
Q

melanin

A

polymer of structures derived from tyrosine, involving tyrosinase

129
Q

one or many genes involved in structure of collagen?

A

many

130
Q

sequence of most collagens involves multiple repeats of what sequence
collagen mostly what aa

A

Gly-Pro-Ala

mostly glycine, then proline and then alanine

131
Q

osteogenesis imperfecta

A

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
Q

type of inheritance of osteogenesis imperfecta

A

autosomal dominant or recessive

133
Q

ehlers danlos syndrome

A

caused by mutation in collagen or enzymes that process genes - causes hyperflexibility of tendons

134
Q

inheritance of ehlers danlos syndrome

A

autosomal dominant

135
Q

neurofibromatosis

A

small nerve ending tumours grow on skin, not lethal

136
Q

marfan syndrome

A

disorder of connective tissue - long limbs and fingers and face

137
Q

hereditary spherocytosis

A

change in shape of erythrocytes which are destroyed by spleen - anaemia

138
Q

which single gene disorders do we test for prenatally

A

PKU
CF
galactosaemia
primary congenital hypothyroidism

139
Q

inheritance of PKU

A

autosomal recessive

140
Q

what is PKU

A

lack of phenylalanine hydroxyase

phenylalanine accumulation, conversion to phenlypyruvate - builds up and damages brain

141
Q

what clinically does CF cause

A

build up of mucous in lungs leading to repeated chest infections, malabsorption, mucous blockage in small intestine pancreatitis, CF related diabetes

142
Q

CF defect in what

A

CF transmembrane conductance regulator - chloride channel

143
Q

test for CF, detects all causes?

A

elevated immunoreactive trypsinogen (IRT)

only detects 90% cases

144
Q

what is primary congenital hypothyroidism

A

defect in thyroid hormone or thyroid gland itself not developed

145
Q

what does primary congenital hypothyroidism cause if untreated

A

growth failure and permanent intellectual disability

146
Q

diagnosis of primary congenital hypothyroidism

A

heel prick - high TSH or low thyroxine (T4)

147
Q

why do we prenatally test for only certain things

A

because these things need early intervention

148
Q

why dont we test for genes in prenatal testing of genetic diseases

A

because different mutations can cause the same syndrome

149
Q

normal RR

A

12-20/min

150
Q

normal minute ventilation

A

7L/min

151
Q

normal TV

A

500mL (dead space 150mL)

152
Q

normal PAO2

A

100mmHg

153
Q

normal PACO2

A

40mmHg

154
Q

what is asbestosis

A

form of diffuse interstitial lung disease (DILD) due to asbestos exposure

155
Q

what pathologically occurs in asbestosis

A

progessive diffuse inflammation and fibrosis of lung parenchyma causing disruption and destruction of AC membrane

156
Q

ascites

A

fluid in peritoneal cavity

157
Q

if pulmonary pressure increases RV compensates by

then what happens

A
  • hypertrophy
  • eventual dilation of ventricle
  • incompetency of tricuspid valve
  • regurgitation
158
Q

in exercise, does anything happen to PAo2 and arteriole saturation?

A

no - gas exchange remains normal due to ventilation increase to cope

159
Q

what is the effect of pulmonary hypertension on RA and systemic venous pressures

A

they increase

160
Q

what is effect of increased systemic venous pressure on systemic capillary bed

A

if severe,

  • peripheral oedema
  • ascites
  • pleural effusions
161
Q

3 causes of increased pulmonary vascular resistance

A
  • vasoconstriction
  • obstruction (embolism e.g.)
  • obliteration (emphysema, pulmonary fibrosis)
162
Q

two results of right ventricle dilation and hypertrophy

A
  • increase systemic venous pressure

- poor cardiac output

163
Q

in acidosis, why does bicarb go down

A

buffer systems attempts to limit change in pH

164
Q

anion gap

A

clinical tool - usually measured anions are less that cations by 15

165
Q

if metabolic acidosis due to loss of bicarb, what happens to anion gap

A

for every unit of bicarb lost, Cl is reabsorbed - so anion gap normal

166
Q

if metabolic acidosis is due to new acid, what happens to anion gap

A

Cl stays the same, and bicarb consumed in buffering, so less anions than normal so bigger gap

167
Q

body’s compensation for respiratory acidosis, how long does it take

A

bicarb retention, days

168
Q

compensation for metabolic acidosis

A

hyperventilation

169
Q

acinus

A

respiratory bronchiole and alveoli

170
Q

lobule

A

terminal bronchiole, respiratory bronciole and alveoli

171
Q

obstructive and restrictive FEV1 and FVC

A

obstructive - decreased FEV1, normal FVC

restrictive normal FEV1, reduced FVC

172
Q

3 branches of COPD

A

emphysema
chronic bronchitis
small airway disease (with some reversible bronchospasm)

173
Q

what causes COPD

A

smoking

174
Q

wat is emphysema

A

abnormal permanent enlargement of air spaces distal to terminal bronchiole, from destruction of alveolar wall without fibrosis

175
Q

what is cronic bronchitis

A

persistent cough productive of sputum for at least 3 months in 2 consecutive years with no other cause

176
Q

definition of asthma

A

increased responsiveness of airways to various stimuli leading to episodic bronchoconstriction which is at least partly reversible

177
Q

two types of asthma

A
  1. atopic/allergic - increased IgE, specific environmental allergens
  2. non-allergic - normal IgE, non-specific triggers (more common)
178
Q

asthma acute/immediate phase

A

-increased vascular permeability
increased mucous production
- bronchospasm

179
Q

late phase response 4-8h

A

chemotaxis of eosinophils, mast cells, lymphocytes, macs - ongoing inflammation
- epithelial damage

180
Q

do bronchodilators help in late phase astma

A

no

181
Q

trigger of asthma (cellular)

A

release of mediators from mast cells

182
Q

status asthmaticus

A

acute severe asthma not responding to bronchodilators

183
Q

how does smoking cause emphysema

A

smoking upsets balance of proteases and anti-proteases - proteases digest our alveolar walls

184
Q

how does emphysema cause airway obstruction

A

loss of elastic recoil - loss of supporting elastic tissue around small airways leads to collapse

185
Q

cor pulmonale

A

abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels

186
Q

what occurs in chronic bronchitis to the airways

A
  • increased mucous production in larger airways

- airway inflammation, scarring and narrowing in smaller airways

187
Q

complications of chronic bronchitis

A
  • superimposed infective exacerbations
  • hypoxia, pulmonary hypertension, cor pulmonale
  • squamous metaplasia, squamous dysplasia (premalignant)
188
Q

location in airways of emphysema, chronic bronchitis and small airways disease

A

emphysema - alveoli
chronic bronchitis - large airways
small airways disease - small airways in-between

189
Q

infective exacerbations of COPD

A

bacterial bronchitis, increased bronchospasm

190
Q

clinical presentation of emphysema

A

O levels don’t fall b/c breath harder, decreases CO2

191
Q

clinical presentation of bronchitis

A

tolerate O2 decline - body lets levels fall (don’t breathe harder)
get cor pulmonale

192
Q

bronchiectasis

A

irreversible, abnormal dilation of bronchi/bronchioles

193
Q

pathogenesis of bronchiectasis

A

severe destructive inflammation of airways

loss of surrounding elastic tissue and msucle exeeds contraction of fibrous tissue

194
Q

causes of bronchectasis

A

necrotising infections

195
Q

idiopathic pulmonary fibrosis

A

histologic pattern is usual interstitial pneumonitis - interstitial inflammation, fibrosis , progression to end-stage lung disease

196
Q

wat is usual interstitial pneumonitis

A

fibrosis and inflammation that appears to be of varying ages

MD1 (5 decks)

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