Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HDT 2.2 > respiratory system > Flashcards

respiratory system Flashcards

1
Q

what is the total pressure in atmospheric air?

A

Pn2+ Po2+ Pco2+Ph20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how would you calculate the partial pressure?

A

partial pressure= fractional conc. of gas x total pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what’s the PP at sea level?

A

PIO2 = 21% x 95kPa
= 20kPA

95 is the barometric pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why does the alveolus partial pressure drop?

A

blood in the alveolus removes oxygen from air so it drops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the conducting zone and respiratory zone and their functions?

A

conducting zone; movement of air to gas- exchanging regions
- trachea, bronchi, bronchioles, terminal bronchioles
respiratory zone; gas exchange
- respiratory bronchioles, alveolar ducts, alveolar sacs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does gas move through conducting zone?

A
  • bulk flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is total flow formula

A

speed x area

forward velocity of gas decreases- good for gas diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are goblet cells and how are they affected when damaged?

A

they secrete mucus
any ciliary arrest allows bacteria to invade
inflammation/asthma can increase viscosity of mucus
smokers are more susceptible to infections as nicotine paralyses cilia in the airway therefore bacteria can invade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the dead space and when does it occur?

A

it is a volume of gas within the respiratory system where no gas exchange takes place
occurs:
i. where there is no effective airflow
ii. where there is no blood flow/perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the anatomic dead space?

A

when no gas exchange takes place due to lack of alveoli
=150ml
affected by body size, age, drugs, postures

drugs e.g. bronchodilators, constrictors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the alveolar dead space?

A

when there is volume of alveoli in the respiratory zone with no or inadequate blood flow for gas exchange
= >5ml but increases in disease

inspired gas reaches alveolus but alveolus is ineffective in oxygenating venous blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the physiological dead space?

A

the anatomic dead space + alveolar dead space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is tidal volume?

A

vol of air breathed in and out in one breath

for about 70kg adult it is 500ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is respiratory frequency?

A

(f)- numbers of breaths per min

= 12 per min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the minute ventilation?

A

(minute volume) (VE)

= tidal volume x respiratory frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the dead space ventilation (Vd) and alveolar ventilation?

A

Vd= volume of dead space x frequency

Alveolar ventilation (Va)
= Ve - Vd
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can drug induced hypoventilation be caused?

A
  • alcohol
  • tranquilizers
  • opiates
  • sedatives
  • hypnotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what must the respiratory muscles do in order to breathe?

A
  1. must stretch the elastic components of the respiratory system
  2. and overcome resistance to flow

takes up 10% of the total body oxygen consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do the lungs and chest wall act when there is no air flow?

A

the lungs want to collapse inwards and the chest wall outwards
but they are held by cohesive action of liquid in the plural space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what kind of pressure does intrapleural fluid have?

A

has a negative pressure less than the Pb- atmospheric pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the volume of the lung at rest? how would you find lung and chest wall distending pressure at FRC?

A

at the end of expiration the lung has a volume called Functional Residual Capacity
Pb= 0
Palv= 0
Ppl= -0.5kPa

lung pressure= Pin-Pout = Palv-Ppl
= 0-(-0.5) = +0.5kPa
chest wall pressure= Pin - Pout = Ppl - Pb
= -0.5-0
= -0.5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how does air move in and out of the lungs?

A

it moves in and out as Palv will alternatively become bigger and then smaller than Pb
when Palv < Pb then inspiration will occur
and when Palv > Pb then expiration will occur
P alv changes when the thorax expands and lung volume changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is Boyles Law?

A

the pressure exerted by a constant number of gas molecules in a container is inversely proportional to the volume of the container
P inversely proportional to 1/V
as volume increases pressure decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are some inspiratory muscles? used for?

A

diaphragm, external intercostals, scalenes

used for quite breathing, coughing, exercising, vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how does the diaphragm act as an inspiratory muscle?

A
  • used in quite breathing
  • lengthens the thorax
    at rest; relaxed
    inspiration; it contracts allowing thoracic volume to increase
    expiration; relaxes, thoracic volume decreases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

during inspiration, what is the Palv and Pb?

A

they are identical
both are 0 at the start of the breath
Poutside = Pinside
no air flows in or out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the process of inspiration?

A
  1. thoracic cavity enlarges and cavity flattens
  2. due to pleural membranes, lungs move out with the thorax
  3. lungs expand and vol. increases
  4. alveolar pressure becomes less than pressure outside
    Pinside < Outside
    P alv = -0.1kPa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the process of expiration?

A
  1. chest wall moves inward
  2. volume of Thorax decreases and lungs recoil
  3. alveolar pressure becomes greater than pressure outside
  4. lungs momentarily squeeze the air in the lungs due to their elastic inward coil
    Palv= +0.1kPa
    so air flows out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is meant by elasticity and compliance?

A

elasticity- resistance of an object to deformation by an external force; resistant to stretch (E)

compliance- ability to stretch; 1/E (C)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the lung distending pressure during inspiration?

A

P dist= Palv-Ppl
= 0-(-1)kPa
= +1kPa
more positive os the lung is distended

chest wall expands
Palv= 0.1
Ppl= -1kPa
Pb= 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

if you have a greater outward distending pressure what does this mean for the lung vol.?

A

this means there will be a greater change in lung vol.
represented by the pressure-volume curve
lung expansion is proportional to distending pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what determines the compliance of the lungs?

A
  1. elastic properties of tissue; elastic connective tissue forces
    thick lung tissue decreases compliance
  2. surface tension at air-water interfaces within alveoli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is surface tension? how is it effected by surfactants?

A

a collapsing force
surfactant from type 2 cells decreases surface tension
- surfactants molecules have strong attraction for each other but low attraction for other molecules so reduce ST by accumulating at the surface
- they place themselves in between water molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how does surfactant presence affect compliance?

A

is there was no surfactant compliance would decrease and lung volume would decrease as pressure increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is the area-dependant effect of surfactant?

A
  • smaller radius alveoli
  • > density of surfactant
  • effective during deflation of lung and smaller alveoli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the factors that rate of airflow depends on?

A
  1. density and viscosity of gas
  2. driving pressure; difference of pressure at 2 points; depends of type of airflow as some airflows might need higher pressures
  3. types of airflow
  4. airway resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is laminar and turbulent flow?

A

laminar flow is when there is a slower velocity and small airways
turbulent flow is high velocity and reorganised flow due to a large radius of the airways; needs a higher driving pressure to move air to alveolus from mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what movement can cause airways radius to increase?

A

bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is transitional flow?

A

when there is both laminar and turbulent flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

resistance to airflow is due to what?

A
  1. friction between air and lung tissue
  2. friction between air and airways

need small resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

where does airway resistance from?

A

40-50% respiratory tract - airways with diameter >2mm
mouth breathing can reduce airflow resistance by bypassing upper airways
50-60% total airway resistance is in lower respiratory tract
most resistance is from the trachea and the bronchi but beyond terminal bronchioles the resistance is virtually zero

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how does resistance change with flow and viscosity?

A
  • if viscosity increases then resistance will increase also
  • the longer the length of the tube is, then the resistance to flow is higher
  • small radius changes have a larger effect on resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is resistance proportional to?

A

resistance is proportional to L x h / r4

resistance increases with 1/r4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

how does decreased airflow occur?

A

contraction of smooth muscle in the bronchioles -> decreased radius of airway -> increased resistance to airflow -> decreased airflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the difference in the airways for asthmatic lungs and normal lungs?

A

normal lungs have normal lining and normal amount of mucus; muscle is relaxed
asthmatic lungs have swollen lining and excess- the muscle tightens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are some long and short bronchodilators used for asthma patients?

A
  • anticholinergics
  • beta-receptor agonists
  • steroids
  • anti-inflammatory drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

why is upper and lower airway resistance important?

A 
Upper 
- intraluminal airway obstruction 
- aspiration of foreign objects 
- bronchospasms, mucus, oedema 
- obstruction by tongue 
Lower 
- COPD e.g asthma, bronchitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are the two ways to control airway resistance?

A
  1. autonomic control
  2. local chemical mediators
  3. decrease in CO2 in over-ventilated areas- bronchoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how do vagal fibres evoke bronchoconstriction?

A

the vagal preganglionic fibres will release ACh from their synaptic clefts and this will act on the muscarinic M3 receptors which cause bronchconstriction
airways constrict and airflow is reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what do sympathetic fibres innervation cause?

A

sympathetic fibres innervation of airways when circulating adrenaline it acts at B2 adrenoreceptors which then causes bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the role of local chemical mediators?

A

local chemical mediators are inflammatory substances
when the bronchi airways are constricted mast cells are activated and cause release of inflammatory substances such as histamine
histamine acts on the constricted bronchi causing vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the PO2 in inspired air and PO2 in alveoli?

A

inspired air= 20kPa

alveoli = 13 kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

why is there a lower PO2 in the lung than in the air?

A

oxygen is constantly entering pulmonary blood at 250ml/min from alveoli to meet metabolic demand
O2 is constantly removed from alveolus into blood to satisfy metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the PCO2 in inspired air and in the alveoli?

A

inspired air = 0

alveoli = 5kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

why is there more CO2 in the lung than in the air?

A

because CO2 produced by metabolism is constantly added from the blood into the alveolar air at 200ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is the PO2 of alveolar gas determined by?

A
  1. PO2 in the atmosphere air
  2. rate of replenishment of O2 by alveolar ventilation (VA)
    - > increased VA increases PAO2 and vice versa if VO2 is unchanged
  3. rate of removal of O2 by pulmonary capillary blood
    - > if VO2 increases, PAO2 decreases and vice versa if VA is unchanged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is PCO2 of alveolar gas determined by?

A

determined by:

  1. rate of metabolism if breathing unchanged
  2. alveolar ventilation; increased VA will decrease PACO2 and vice versa is VCO2 is unchanged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how does Va change with metabolism?

A
  • if metabolism doubles, Va doubles
  • if metabolism halves, Va halves

alveolar gases, blood gases and pH are kept relatively constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

how does disease occur?

A

when respiration, Va, cannot meet metabolic demand at rest severe or changes in demand

alveolar gases, blood gases and pH are abnormal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is the difference between hypoventilation and hyperventilation?

A

hypoventilation; alveolar ventilation doesn’t keep pace with CO2 production; PACO2 and PaCO2 increases
hyperventilation; alveolar ventilation is too great for the amount of CO2 being produced; PACO2 and PaCO2 decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is hypernoea?

A

it is when you are breathing deeper and more rapid than normal but increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

how do I know if my patient is hyperventilating?

A
  1. PaCO2 lower than normal
  2. dizziness -> low PaCO2 causes vasoconstriction of cerebral vessels and lack of O2 to brain
  3. Tetany- carpopoedal spasm, numbness and pins and needles

can measure CO2 levels and arterial gas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what is Tetany? how does it occur?

A

extracellular levels of Ca+, nervous system is more excitable as there is an increased permeability to Na+ ions and allows AP imitation to occur

there is a fall in PaCO2 which leads to membranes hyperexcitability; alters free levels of Ca+ and changes membranes excitability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is Fick’s law and what is it dependant on?

A

Fick’s law is diffusion through tissues and is dependant on

  1. surface area; can be changed in restrictive diseases
  2. thickness of the barrier; usually 0.5 micrometers
  3. partial pressure difference between two sides; large gradient for O2
  4. diffusion constant for that gas through that barrier; depends on gas, MW and solubility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

is CO2 or O2 more soluble?

A

CO2 is more soluble

lower Partial pressure needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

if a given lung unit is equally well ventilated and perfused with blood what is then optimised?

A
  • gas exchange
  • uptake of o2 from alveolar gas -> blood
  • elimination of CO2 from blood into alveolar gas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is the ventilation: perfusion ratio?

A

Va (V); 4 L/min
blood flow to lung (Q) = 5 litres/min

so ratio = V/Q = 4/5
= 0.8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what happens to V/Q ratio in an under ventilated/overperfused alveolus? how will lung adjust?

A

V>Q
there is no ventilation but O2 is being removed and CO2 is going into alveoli
blood returning to the heart from these alveolus is hypoxic and hypercapnic therefore V/Q = 0

hypoxic blood causes localised hypoxic vasconstriction so blood is diverted away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what happens to V/Q ratio in an over ventilated/under perfused alveolus? how does the lung adjust?

A

V>Q
this is alveolar dead space
there is no blood flow so Q is 0
so V/Q is infinity
no CO2 being added to alveolus and no O2 being extracted from blood
low PCO2 causes localised bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what forms are O2 carried in?

A
  • dissolved in plasma
  • combined with haemoglobin (Hb)

O2 has poor H20 solubility

71
Q

what is the total O2 content?

A

1L of arterial blood contain
3ml dissolved O2
197ml O2 bound to Hb

200ml total O2

72
Q

why isn’t haemoglobin a plasma protein?

A

if it were in plasma

  • viscosity would be high; increases resistance to flow
  • Hb would be lost by kidney; filtered in glomerulus
  • Hb could be attacked by enzymes
73
Q

what is the haemoglobin? how is oxyhaemoglobin?

A

4 x globin = polypeptide chains each containing 1 molecule of haem
4 x haem = has central atom of ferrous iron which can combine reversibly with 1 molecule of O2

oxyhaemoglobin is 1 molecule of Hb with 4 O2 molecules

74
Q

what are the theoretical value of O2 binding capacity?

A 
1g Hb can combine with 1.34ml O2 
each 100ml of blood has Hb = 15g 
O2 binding capacity = Hb x 1.34 
= 20.1 mlO2/dL 
proportional to heamocrit of the blood and increases/decreases with haemoglobin conc.
75
Q

what are the theoretical value of O2 binding capacity for an anaemic person?

A

10 x 1.34 = 13.4 ml O2/dL

76
Q

what is the saturation of Hb and how do you calculate it?

A

it is the % of Hb binding sites in the bloodstream occupied by oxygen

% saturation = ( O2 bound to Hb/O2 capacity) x 100
dependant on PO2
at 100% all team groups are occupied by O2

77
Q

what is the physiological significance of the O2 dissociation curve?

A

the curve is steepest at levels of PO2 that occur in tissues

this allows O2 to be readily given up without fall in PO2 and so a high diffusion gradient is maintained

78
Q

why is a left and right shift on the PO and % Hb saturation caused?

A 
left = a decrease in PCO2, decreased H+, decreased temp 
right = increase PCO2, increased H+, increased temp
79
Q

what causes the left and right shift of the Bohr’s effect?

A

left shift= higher affinity for O2 of haemoglobin and favours loading of O2 in the lung; decrease in CO2 and H+
right shift = lower haemoglobin affinity for O2 and give up more tissues to O2

80
Q

what are the forms CO2 is carried in?

A
  • dissolved in physical solution - 10%
  • bound to proteins as carb amino compounds - 30%
  • as bicarbonate (carbonic acid) - 60%
81
Q

why does the Haldane effect occur?

A
  1. deoxyhaemaglobin is better at mopping up H+
    so H+ from forming bicarbonate will be used in
    H+ + HbO2 H + Hb+
  2. deoxyHb has greater ability to bind to CO2 and form carb amino compounds
82
Q

why is the Haldane effect important?

A
  • as blood gives up O2 in tissue so capacity for CO2 carriage increases aiding transport back to lung
  • as oxygenation of Hb occurs in the lung blood gives up CO2 into the alveoli
83
Q

how is H+ buffered?

A 
1. plasma proteins 
H+ + R-NH2 -> R-NH3+
2. globin chain of Hb 
Hb + H+ -> HbH
3. carbonic acid-bicarbonate system 
H+ + HCO3- -> H2CO3 -> CO2 + H20
84
Q

how can H+ be buffered in solutions?

A

by adding an acid or an alkali :

  • blood
  • intracellular fluid
  • extracellular fluid
85
Q

what is the arterial pH?

A

7.40

86
Q

what is the Henderson - Hasselbach equation?

A

relates the pH of solution to

a) pKa of buffer system
b) ionised (A-) and unionised forms (HA)

H+ + A- HA

87
Q

what is metabolic acidosis?

A

loss of body acids leads to decrease in breathing and retention of CO2
if H+ rises, mass reaction pushed to left:

CO2 + H2O

88
Q

what is respiratory acidosis?

A

if CO2 decreases, mass reaction pushed to right
CO2 + H2O -> H2CO3 -> HCO3- + H+
HCO3- is reabsorbed by kidney and H+ is secreted by kidney

89
Q

what is the function of the respiratory system?

A
  • gas exchange and pH maintenance
  • need to monitor ECF and arterials chemical composition
  • if metabolism changed and no respiration change occurred the blood O2 would fall and CO2 would rise; hypoxic tissues and pH disturbances
90
Q

how is Va increased and how is this detected?

A

it is increased by:

  • low arterial PO2
  • high arterial PCO2
  • low arterial pH

detected by chemoreceptors:

  • > maintain homeostasis of PaO2, PaCO2 and pH
  • > assists in ensuring Va is appropriate to level of metabolism
91
Q

where are peripheral chemoreceptors found?

A

found in the aortic bodies and carotid bodies

carotid bodies are in the bifurcation of internal and external carotid arteries

92
Q

how do the carotid bodies work?

A

when there is high PO2, the K+ channel is open and so there is a fall in PO2

  1. PO2 falls and the K+ channel closes. Vm depolarises
  2. Ca2+ channels open
  3. Ca2+ influx triggers NT release
  4. sensory afferents signal to CNS
93
Q

what are the properties of carotid bodies?

A
  • low activity at normal PaO2
  • respond to PaO2 not O2 content
  • also respond to H+ derived from acids other than CO2
  • removal leads to decreases in ventilation during hypoxia
94
Q

what are aortic bodies?

A
  • less important
  • less vascular and have lower blood flow
  • dont respond to pH changes
  • respond to increase in PaCO2, fall in PaO2 and O2 content
  • innervated by vagus nerve
  • play a role in CV reflexes
95
Q

what is the response when hypoxia occurs?

A

the minute ventilation will start to increase when PaO2 < 8 kPa ; O2 level in blood when Hb sat decreases
when Hb sat drops carotid bodies will respond

96
Q

what are the properties of central chemoreceptors?

A
  • stimulated when arterial PCO2 increases
  • account for 60-80% of response to hypercapnia
  • insensitive to hypoxia
  • only slightly stimulated by increase in arterial acidity
  • separated from blood by BBB
97
Q

what stimulates the central chemoreceptor neurons?

A

the acidification of CSF and ECF

the CSF is a poor buffer so small changes in PaCO2 lead to CSF acidosis stimulating the chemoreceptors

98
Q

what is hypercapnia and what is the response when it occurs?

A

it is when you have high CO2
when it increases more than 1 kPa then it can double the Va
for the graph it has a steeper slope

99
Q

how do you calculate Ve?

A

Ve = Vt x Rf
minute ventilation = tidal volume x respiratory frequency

resonance allows right timing and requires less effort

100
Q

how do internal intercostal muscles and external obliques help with expiration?

A

external obliques will push air out of the lungs

both muscles help depress the ribs and shrink diameter of thoracic cavity

101
Q

what are the main areas of CNS involved with respiratory?

A

PONS ( pontine respiratory group PRG)

Medulla - medulla respiratory centre

102
Q

what are the medullary respiratory centres?

A
  1. dorsal respiratory group; neurons here mainly discharge AO, prior to or in inspiration; they project to the contralateral phrenic nerve to control the diaphragm
  2. ventral respiratory group ( VRG; inspiratory and expiratory)
  3. Botzinger complex; expiratory and important when breathing increases
  4. PreBotzinger complex; pivotal in rhythm generation
103
Q

where is the DRG? and what occurs at this location?

A

the DRG is in the Nucleus Tractus Solitarius (NTS)

NTS receives numerous responses and CV afferent inputs; integrates info from chemo and mechanoreceptor afferents related to breathing

104
Q

what neurones drive inspiration during quiet breathing?

A

DRG neurones and VRG neurones active
these inspiratory neurones project down to motor neurones in the C spinal cord and phrenic nerve activity increases and AP generation causes diaphragm to contract and inspiraton occurs

105
Q

what causes expiration?

A

in quiet breathing expiration is entirely passive
DRG and VRG neurones are inactive and so diaphragm relaxes and passive recoil
causing expiration to FRC

106
Q

what is responsible for the basic rhythm of breathing?

A

the cyclical electrical activity of DRG

107
Q

what happens when the demand for ventilation increases?

A

sensory information is transferred on dorsal surface of the medulla from the NTS
NTS sends signal and causes DRG and VRG neurones to be active
the VRG neurones project to neurones in T spinal cord and accessory inspiratory muscles contract causing forced inspiration
the DRG neurones cause diaphragm to contract harder and have more AP potential

108
Q

what happens when demand for ventilation increases (expiration)?

A

Botzinger complex will inhibit the DRG and VRG I neurones and will excite VRG E neurones
so the diaphragm relaxes and other inspiratory muscles relax
when the VRG E neurones are active this causes accessory expiratory muscles to contract -> more forceful expiration

109
Q

what happens when we have voluntary control of our breathing?

A

we take large breaths, we speak, hold our breaths or we hyperventilate
the signal is sent from the cerebral cortex direct to spinal cord bypassing the medullary centres

110
Q

what does the pontine group do?

A

it influences switching between inspiration and expiration

it also can inhibit DRG respiratory neurones to prevent inspiration

111
Q

what are the higher brain centres and what do they control?

A

the hypothalamus; control flight/fight and temperature
limbic system; emotion/pain and whether its excitatory or inhibitory
motor cortex:
-> limb receptors; increase in ventilation during exercise
-> exercise; central motor cortex activates and feed forward common to the DRG activating them to increase ventilation

112
Q

what’re some mechanoreceptors?

A
  1. lung and airways
  2. nose and upper airways
  3. joints and muscles
  4. arterial baroreceptors
113
Q

What are pulmonary stretch receptors?

A
  • they are myelinated sensory vagal fibres
  • stimulated by lung inflation; more tension in airways the greater the lung inflation
  • slowly adapting stretch receptors
  • these receptors are vagal nerve ending in smooth muscle of trachea and lower airways
114
Q

what are the type of activity patterns from PSRs?

A
  1. a receptor which continues to be active during expiration
    - highly excited during inspiration
  2. a receptor with phasic activity and high threshold
115
Q

what is the hering-breuer reflex

A

it is present during sleep
more powerful in babies
important in individuals with low lung compliance

116
Q

what is the central mechanisms with PSRs?

A

they inhibit and promote expiration

  • there is a vagal input from stretch receptors that send signal to NTS
  • NTS sends signal to PRG and DRG
117
Q

what are lung irritant receptors?

A

vagal nerve endings between epithelia of trachea and lower airways

  • stimulated by mechanical stimuli
  • stimulated by noxious gases, smoke, dust, cold air
  • rapidly- adapting receptors
118
Q

what do baroreceptors do?

A
  • increase in blood pressure leads to reflex hypoventilation or apnoea
  • decrease in BP leads to reflex hyperventilation
  • may be important in complex stimuli such as haemorrhage where numerous reflexes occur at once
119
Q

what are proprioreceptors?

A
  • muscle spindles in intercostal muscles
    they allow for increased force of inspiration and expiration if movement is needed
    sense stretch, tension and proprioception
    responsible for sensation of dyspnoea
120
Q

when smoke, irritants and oxidants enter why does bronchoconstriction occur?

A

to prevent any noxious substances getting down into lungs where it could affect delicate lung tissue
irritant receptors play a role in asthma induced bronchoconstriction

121
Q

what can irritant receptors do?

A

they can initiate augmented breaths

  • these occur naturally every few minutes; ‘sighs’
  • more frequent in small animals
  • reverse slow collapse of lung during quiet breathing
122
Q

what is the purpose of nasal mucosa?

A

they are trigeminal nerve endings

  • initiate sneeze and diving reflex
  • stimulated by mechanical and chemical irritants
  • stimulation of trigeminal receptors leads to diving reflex
123
Q

what is the role of the larynx and trachea?

A

vagal nerve endings

  • irritate cough
  • increase expiratory air flow velocity and help expel any irritants
124
Q

where are the C and J receptors?

A

the C receptors are in the bronchial walls and the J receptors are in the alveolar walls close to capillaries

they are both usually silent - stimulated by mechanical distortion and increase in interstitial fluid
- they evoke rapid shallow breathing or apnoea

125
Q

what is asthma?

A

asthma is characterised by paroxysmal and reversible obstruction of the airways
- it is increasingly understood as an inflammatory condition combined with bronchial hyper-responsiveness

126
Q

symptoms of asthma?

A
  • wheeze
  • chest tightness
  • cough
  • shortness of breath
127
Q

what are the types of asthma?

A
  1. extrinsic; associated with allergy to inhaled antigenic substances
  2. intrinsic; wheeze and breathlessness in the absence of an obvious allergen
  3. exercise-induced; within a few mins of exercise
  4. asthma combined with COPD
128
Q

what factors can cause asthma attacks?

A
  • cold symptoms
  • cold air
  • exercise
  • pollution
  • allergens
  • time of day
  • work
129
Q

what are the treatments of asthma?

A
  • prevention of exposure to allergens
  • reduction of bronchial inflammation
  • bronchi dilation
130
Q

what investigations can be done for asthma?

A
  • peak expiratory flow rate
  • spirometry
  • chest x-ray?
131
Q

what is COPD?

A

inflammatory lung disease that causes obstructed airflow from the lungs

  • link to smoking and dust
  • disease of smaller airways
132
Q

how would you calculate pack years?

A

pack years = (no. of cigarettes a day/20) x no of years of smoking

133
Q

what treatment would be given for COPD?

A
  • same as asthma

- antimuscarinics are more effective than B2 receptors

134
Q

what bronchodilators can be used for treatment of asthma? and COPD?

A
  • B2 agonists
  • muscarinic agonists
  • methylxanthines
135
Q

what kind of reliever medication can be given?

A
  • you can be given short acting b-adrenoreceptor agonist bronchodilators
  • salbutamol and terbutaline; selective b-agonists and have few b1-mediated side effects
  • side effects can be CV stimulation such as palpitations and tachycardia- given in high doses
136
Q

what are some long acting beta2-agonists?

A

formeterol and salmeterol are used via inhalation and only given in patients with asthma who regularly use inhaled corticosteroid

137
Q

what do muscarinic antagonists do for treatment of asthma? how may anticholinergic agents help?

A
  • muscarinic antagonists block the muscarinic receptors in the smooth muscle of the bronchi (M1, M2 and M3)
  • ipratropium has a slower onset of action but has a longer duration of action
  • anticholinergic agents can be used for patients with obstructive airway diseases
138
Q

what are methylxanthines?

A

e. g. theophylline
- has a narrow therapeutic index and its hepatic metabolism varies with individuals
- tis clearance can be affected by many factors
- should adjust dose to keep plasma levels within a window of 10-20mg/L

139
Q

what monitoring should be done for theophylline?

A

plasma levels should be measured 5 days after starting oral treatment
should be measured 3 days after changing the dose
after a MR preparation has been orally administered a blood sample should be taken 4-6 hours

140
Q

what can the side effects of theophylline be?

A
  • mild effects such as nausea and vomiting
  • CV effects like tachycardia
  • CNS effects such as tachycardia
141
Q

what is omalizumab? what’s it used for and how does it work?

A

it is an anti-IgE monoclonal antibodies

  • > used for treatment of sever persistent IgE-mediated asthma as add
  • > targets the high-affinity receptor binding site on IgE
142
Q

what three questions can be used for patients when inquiring about their asthma?

A
  1. have they had difficulty sleeping due to the asthma? in last month/week?
  2. have you had your usual symptoms such as cough, wheeze, chest tightness, during the day?
  3. has the asthma interfered with daily activities?
143
Q

how often should you review asthma treatment?

A

every three months
if you can you should step it down but consider the symptoms and severity of asthma
use lowest possible dose of inhaled corticosteroids to control asthma symptoms
when reducing steroids cut dose by 25-50% each time

144
Q

what is a corticosteroids?

A

corticosteroids are the drug of choice for long-term control in patients with any degree of persistent asthma
inhaled CS are long-term control in children and adults
- to be effective in controlling inflammation, GC are used regularly

145
Q

what is the effect of CS on the lungs?

A
  • doesn’t affect airways smooth muscle
  • can decrease inflammatory cascade
  • with regular use they reduce the hyper responsiveness of smooth muscle to bronchoconstrictor stimuli e.g. allergens or irritants
146
Q

what are the routes of admin for CS?

A

can use inhalation

e. g. beclometasone dipropionate, budesonide
- can combine with a long acting beta-2 agonist to help patients stability

orally or systemically

  • for severe asthma
  • doesn’t suppress hypothalamic-pituitary-adrenal cortex axis
147
Q

what are the pharmacokinetics of corticosteroids?

A
  • absorption of oral steroids is rapid
  • after 2-8 hours has a max biological effect
  • oral dosing is given in the morning
  • inhaled avoids systemic effects
148
Q

adverse effects of CS?

A
  • glaucoma
  • hypertension
  • peripheral edema
  • hypokalaemia
  • increased diabetes risk
  • increased appetite
  • osteoporosis
149
Q

why are inhaled CS better? what effects can it have and how can this be sorted?

A
  • have less systemic effects than oral
    however high doses of ICS can induce adrenal suppression and adrenal crisis and coma
  • consider giving a steroid card
  • oral candidiasis can occur; use a spacer device or rinsing mouth after dose inhalation helps
    -> can use anti fungal oral suspension or oral gel
150
Q

what is MoA for sodium cromoglycate and nedocromil? how are these drugs suited for asthma treatment?

A

inhibit mast cell degranulation and release of histamine
prophylaxis with sodium cromoglycate is less effective than ICS
dosing should three to four times daily; affects adherence and limits use
neither medication have any value in acute attack treatment

151
Q

what are other asthma treatment medication options?

A
  • leukotriene receptor antagonists
    e. g. montelukast and zafirlukast
  • they are products of 5-lipoxygenase pathway of arachidonic acid metabolism and part of inflammatory cascade
  • 5-lipoxygenase is found in mast cells, eosinophils, neutrophils and basophils
152
Q

what is Roflumilast?

A

it is an oral phosphodiesterase-4 inhibitor used to reduce exacerbations in patients with severe chronic bronchitis

  • reduces COPD inflammation
  • has side effects including nausea, vomiting headache and diarrhoea
153
Q

what are signs of COPD?

A

respiratory distress; breathlessness on exertion, tachypnoea
abnormal posture; leaning forward, arms rested to help breathing
drowsiness; flapping tremor and mental confusion

  • underweight
  • ankle oedema
  • cyanosis
  • downward displacement of liver
154
Q

how can stages of COPD be diagnosed with the severity of airflow obstruction by FEV1?

A

Stage 1; 80% or above
Stage 2; 50-79%
Stage 3; 30-49%
Stage 4; below 30%, very severe

155
Q

what classes of drugs can be used for COPD and asthma treatment?

A
  1. short-acting beta2-agonists e.g. salbutamol and terbutaline
  2. long-acting beta2-agonists e.g. salmeterol
  3. short acting antimuscarinics e.g. ipratropium
  4. long- acting antimuscarinics e.g. bromide, tiotropium
156
Q

best combination of ICS’s for asthma treatment?

A
  • short-acting beta2-agonists and long acting antimuscarinics
  • long-acting beta2-agonists and long acting antimuscarinics; reduces symptoms and FEV1
  • ICS and LABA -reduces exacerbations
  • LABA and LAMA and ICS - all rounder improvement
157
Q

what vaccinations and treatments might COPD patients need?

A

pneumococcal vaccinations and annual influenza vaccination

  • antivirals for influenza; zanamivir and oseltamivir
  • or oxygen therapy or physiotherapy
158
Q

how could you manage adult acute-asthma?

A
  1. can give supplementary oxygen to hypoxaemic patients with acute severe asthma to maintain SpO2
    - nebuliser can be given
  2. use beta2-agonist bronchodilators
    - use high dose inhaled B2- agonists as first line for acute asthma patients
    - nebuliser can be option for life-threatening acute asthma
  3. ipratopium bromide
    - nebulised ipratopium bromide to b2-agonist treatment
  4. steroid therapy
    - adequate doses e.g. prednisolone 40-50mg daily
159
Q

what is tuberculosis?

A 
infectious disease caused by myobacterium tuberculosis 
affects the lung 
can infect 
- CNS 
- lymph nodes
- miliary; whole body
160
Q

what is the pathogenesis of tuberculosis?

A
  • inhalation of mycobacteria
  • immune response is usually the macrophage system being activated
  • any mycobacteria that survived are proliferated within macrophages
  • cytokines are produced and this induces recruitment of monocytes, neutrophils etc
  • immune cells to site of infection stop mycobacteria proliferation and prevent its spread
  • eventually becomes late infection
161
Q

what is TB mode of action?

A

spread from person to person

  • through air
    e. .g coughing, sneezing or spit

not by:
- shaking someone’s hand
- sharing food
touching bed linens or toilet seats

162
Q

what is meant by latent TB?

A
  • lives but doesn’t grow in body
  • no symptoms occur
  • cannot spread
  • cant advance to the disease
163
Q

what is the screening or tests for latent and active Tb?

A 
latent 
- has a skin test or blood result 
- has normal chest x ray and -ve sputum smear 
- needs treatment to prevent TB 
active 
- has skin test or blood test 
- abnormal chest x ray or +ve sputum smear 
- needs treatment for TB
164
Q

risk factors for TB?

A
  • people who have had recent infections of TB
  • close contact with infected person
  • immigration of people from high rate TB countries
  • working at hospital
  • medical conditions that weaken immune system
165
Q

what are TB symptoms?

A
  • persistent cough > 3 weeks
  • phlegm
  • night sweats
  • weight loss
  • high temp
  • tiredness and fatigue
  • loss of appetite
  • swellings in neck
166
Q

what are symptoms of extra pulmonary TB outside the lungs?

A
  • persistently swollen glands
  • abdominal pain
  • pain and loss of movement
  • confusion
  • fits
  • a persistent headache
167
Q

how can you diagnose TB?

A
  • Mantoux test
  • laproscopy
  • urine and blood test
  • biopsy
  • lumbar puncture
  • CT scan, MRI
  • sputum test 3 deep cough sputum samples
168
Q

what is the Mantoux test?

A

used to diagnose TB

  • injects PPD into forearm skin
  • those with latent TB are sensitive to PPD and hard red bump will develop at the site of injection usually within 48 to 72 hours
  • a strong skin reaction suggests active TB
169
Q

what is the follow up for TB?

A

should be conducted routinely
patients should watch for symptoms of relapse
patients who had drug-resistant TB should have a follow up for 12 months after treatment

170
Q

when should you offer directly observed therapy?

A
  • do not adhere to treatment
  • have had previous TB treatment
  • history of homelessness or drug issues
  • are in prison or have been <5 years ago
  • in denial of the TB diagnosis
  • request this therapy
  • too ill to self-administer
171
Q

what medication should be given for CNS TB?

A

at the start of the anti-TB treatment regimen, offer people with active TB, dexamethasone or prednisolone at high dose initially
gradually withdraw over 4-8 weeks

172
Q

what medication should be given for extensively drug-resistant TB?

A
  • resistance to at least isoniazid and rifampicin, 1 injectable agent and 1 flurorquinoone
173
Q

what dosing regimens should be given for TB?

A

use fixed-dose combination tablets as part of treatment

  • dont offer this regimen of fewer than 3 times a week
  • offer a daily dosing schedule to people with active P TB
  • people with extra pulmonary TB should be considered for a daily dosing schedule
174
Q

how is MDR-TB formed?

A

is a form of TB caused by bacteria that dont respond to isoniazid and rifampicin, the most powerful first-line anti-TB drugs

it is treatable and curable with second line drugs

HDT 2.2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions