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Medicine Phase One > Cardio-Respiratory Week Five > Flashcards

Cardio-Respiratory Week Five Flashcards

1
Q

What are the characteristic of type one respiraoty failure?

A

PaCO2 is normal or low and PaO2 is low. Examples include pneumonia or pulmonary oedema.

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2
Q

What are the characteristic of type two respiraoty failure?

A

PaCO2 is elevated and PaO2 is low. Example is COPD.

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3
Q

Name examples of short beta-2 agonists

A

Salbutamol, terbutaline

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4
Q

Name examples of short anti-muscarinic drugs

A

Ipratropium

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5
Q

Name examples of long beta-2 agonists

A

Salmeterol, formoterol, indocaterol

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6
Q

Name examples of long anti-muscarinic drugs

A

Tiotropium, glycopyronium

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7
Q

What kind of drug i beclometasone dipropinate?

A

Corticosteroids

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8
Q

What is ventilation?

A

Amount of gas going into the alveoli

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9
Q

What is perfusion?

A

Amount of blood flow into the alveoli

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10
Q

Describe V and Q in zone one of the lung

A

There is decreased perfusion due to gravity which causes waster ventilation. There is larger alveoli caused by more negative intrapleural pressure.

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11
Q

Describe V and Q in zone three of the lung

A

There is continuous blood flow due to gravity and there are smaller alveoli.

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12
Q

Where is the control centre for respiration?

A

The medullary rhythmicity centre in the medulla

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13
Q

What is the role of the dorsal respiraoty group?

A

This has inspiratory neurons. This is mainly responsible for normal inspiration. It sends impulses to external costals and diaphragm to contract at regular intervals. When it stops, expiration will occur passively.

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14
Q

What is the role of the ventral respiraoty group?

A

This has inspiratory and expiratory neurons. This initiates normal inspiration and expiration when it is forced. This is mostly in forced breathing.

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15
Q

Describe the control of Quiet breathing

A

The activity in the DRG increases over a period for about 2 seconds and this stimulates inspiratory muslces. Over this period, inhalation occurs. After around 2 second, the DRG neurons become inactive. They remain quiet for the next 3 second to allow inspiratory muslces to relax. Passive exhalation will then occur.

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16
Q

Describe the control of Forced breathing

A

There is increased activity of the DRG and this stimulates neurons in the VRG. This activates the accessory muscles for inhalation. After each inhalation, active exhalation takes place as neurons of the expiratory centre stimulate appropriate accessory muslces.

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17
Q

What is the function of the Pneumotaxic centre?

A

Transmits inhibitory impulses to DRG that help turn off inspiratory neurons, limiting duration of inspiration

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18
Q

What is the function of the Apneustic centre?

A

This stimulates inspiratory neurons in the DRG and VRG. Over stimulation from the apneustic centre results in apneustic breathing which is characterized by long gasping inspiration interrupted by occasional expirations.

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19
Q

What is the function of peripheral chemoreceptors?

A

These are located in the aortic body and carotid body. They detect oxygen, carbon dioxide and pH.
A decrease in oxygen, decrease in pH or increase CO2 will cause more signals to be sent up to respiratory centre and caused an increase in respiraoty rate.

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20
Q

What can sometimes happen when PCO2 remain chronically elevated?

A

Chemoreceptors will adapt and reset their values. They will lose their sensitivity to CO2.

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21
Q

What is the function of central chemoreceptors?

A

These are located in the Ventrolateral surface of the medullar oblongata. They respond to pH and PCO2.

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22
Q

What gases can cross the blood-brain barrier and what is the significance of this?

A

Carbon dioxide can. It will react and from hydrogen ions and bicarbonate. There will be a decrease in pH and this will cause more inhalation.

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23
Q

What is the function of mechanoreceptors?

A

Smooth muscle of trachea, bronchi and bronchioles have stretch recepotrs on them. When the lung is inflated, they send signals via the Vagus nerve to limit inflation. The Vagus nerve sends signals to the apneustic centre and this becomes inhibited. As exhalation begins, the signals are stopped and hence inspiration will begin again.

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24
Q

What is the Hering-Breuer reflex?

A

Shortens exhalation when lung is deflated.

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25
Q

What is the function of irritation recepotrs?

A

Stimulation will causes hyperventilation, bronchospasm and this prevents harmful irritants entering the alveoli.

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26
Q

What are the three types of recepotrs involved in the cough reflex?

A

RARS, SARS and C-fibres (part of Vagus nerve)

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27
Q

What are the efferent nerve fibres that the Vagus nerve synapses with?

A

Phrenic, Spinomotor and recurrent laryngeal

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28
Q

What happens during the first stage of the cough reflex?

A

This is called the inspiratory phase. There is a big breath taken in and this causes stretching of the expiratory muslces and pressure in lung increases.

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29
Q

What happens during the second stage of the cough reflex?

A

This is the compression stage. The glottis opens and the expiratory muslces will contract. There will be a further increase in lung pressure.

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30
Q

What happens during the third stage of the cough reflex?

A

This is the expiratory phase. The glottis opens and air is pushed out due to high lung pressure.

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31
Q

What is the difference in acute and chronic respiraoty acidosis?

A

Acute: abrupt failure of ventilation
Chronic: PCO2 is elevated as alveolar ventilation is insufficient

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32
Q

Explain the acute compensations of respiratory acidosis

A

An increase in carbon dioxide will move its equilibrium to the right and cause an increase in hydrogen and bicarbonate. The hydrogen is buffered by proteins and phosphates, mainly by haemoglobin. The bicarbonate will be exchanged for chlorine and this will raise the pH slightly.

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33
Q

Explain the chronic compensations of respiratory acidosis

A

The response occurs because increased arterial pCO2 increases intracellular pCO2 in proximal tubular cells and this causes increased H+ secretion from the PCT cells into the tubular lumen.
This results in:
- increased HCO3 production which crosses the basolateral membrane and enters the circulation (so plasma [HCO3] increases.)
- increased Na+ reabsorption in exchange for H+ and less in exchange for Cl- (so plasma [Cl-] falls)
- increased ‘NH3’ production to ‘buffer’ the H+ in the tubular lumen (so urinary excretion of NH4Cl increases)

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34
Q

What will happen to breathing rates during respiraoty acidosis?

A

Increases

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35
Q

What does haemoglobin do in decreased oxygen and higher carbon dioxide (respiraoty acidosis)?

A

The increased hydrogen will decreases haemoglobins affinity for oxygen, thus increasing the unloading of oxygen into respiratory tissues.

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36
Q

What will 2,3-BPG do when there is reduced oxygen?

A

There will be an increase in 2,3-BPG production and it will bind to haemoglobin to allow oxygen to be unloading for delivery.

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37
Q

What is there an imbalance of in emphysema?

A

There is an imbalance of:

  • elastase and anti-elastase
  • oxidants and anti-oxidants
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38
Q

What is the function of elastin in the airways?

A

Elastin keeps the lumen open, particularly during exhalation. It prevents collapse

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39
Q

What affect does nicotine have on the body?

A

Chemoattractant for neutrophils. When neutrophils become activated, they will release their elastase.

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40
Q

Tobacco smoke contains ROS, what affects can be seen from this in emphysema?

A

This will activate NFK-B which is a transcription factor. This will cause activation of IL-8, LTB4 and TNF. This will attract more neutrophils.
ROS will also cause inactivation of antiproteases.

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41
Q

What is the difference between congenital and functional alpha-one antitrypsin deficiency?

A

Functional: ROS will cause inactivation of anti-proteases
Congenital: born with the deficiency

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42
Q

When macrophages come activated in emphysema what will they release?

A

MMPS (6/9) and elastase

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43
Q

Explain the process of air trapping, something that occurs in emphysema

A

As exhalation is very hard, the elastin that is usually there does not allow recoil, and hence the alveoli have to expand by force. The loss of elastin causes them to become narrower during inhalation. During exhalation, narrowing and absence of recoil means air is trapped.

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44
Q

Why does the area for gas exchange decrease in emphysema?

A

The septa, the thing that holds the alveoli together, is broken down

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45
Q

Why are sufferers of emphysema known as ‘pink puffers’?

A

People will experience dyspnoea due to diminished gas exchange. People will exhale slowly with pursed lips to increase the pressuring the airways and prevent them from collapsing. This type of breathing can also cause weight loss.

46
Q

What is hypoxic vasoconstriction?

A

An area of poor gas exchange will vasoconstrict in attempt to shunt blood to an area with better gas exchange. However, if there are too many areas of this, it can cause pulmonary hypertension. This leads to increased work of right side of the heart and can lead to it failing.

47
Q

What is centriacinar emphysema?

A

This is the most common type of emphysema. This only damaged the proximal and central areas of the acini. This usually affects the upper lobes and is due to smoking as the chemicals cant reach the distal ends.

48
Q

What is panacinar emphysema?

A

The entire acini is affected. Commonly this is associated with alpha-one antitrypsin deficiency and this usually affects the lower lobes and anterior margin.

49
Q

What is paraseptal emphysema?

A

This affects the distal ends and the respiraoty bronchi are normal. This usually affects the tissue present on the periphery of the lobule.

50
Q

What is irregular emphysema?

A

This is mainly seen in areas of scarring.

51
Q

What is respiraoty acini?

A

Respiratory portion of the lung

52
Q

What are the layers of the respiratory airway?

A

The ciliated Pseudostratified columnar epithelium and goblet cells, the basement membrane and connective tissue make up the mucosa layer (the basement membrane and connective issue make up the lamina propria).
There is layer of smooth muslce and connective tissue that make up the submucosa.
The bronchial glands live in the connective tissue layer of the submucosa.
In the bronchi, there is a layer of cartilage below the submucosa.

53
Q

What happens to the bronchial mucinous glands and goblet cells when exposed to irritants?

A

They go through hypertrophy and hyperplasia and cause an increase in mucous production.

54
Q

What is the Reid index and what is the significance in chronic bronchitis?

A

This is the thickness of glands to thickness of the wall. This is usually below 40% but will be over 4-% in chronic bronchitis.

55
Q

Why to people with chronic bronchitis get nicknamed ‘blue-bloaters’?

A

The mucous cause baked airflow and this causes hypercapnia. This causes lowered oxygen. The increase in carbon dioxide causes cyanosis and hence they appear blue.

56
Q

What is chronic bronchitis?

A

Chronic bronchitis is one type of COPD (chronic obstructive pulmonary disease). The inflamed bronchial tubes produce a lot of mucus. This leads to coughing and difficulty breathing.

57
Q

What is COPD?

A

Chronic obstructive pulmonary disease (COPD) is the name for a group of lung conditions that cause breathing difficulties.
It includes:
emphysema – damage to the air sacs in the lungs
chronic bronchitis – long-term inflammation of the airways

58
Q

Why are diagnosis tests for COPD done pre and post bronchodilation medication?

A

TO check is the condition is asthma as COPD is reversible but asthma is.

59
Q

What are some x-ray signs of COPD?

A
  • increase in anterior-posterior diameter
  • heart vertically orientated
  • depressed diaphragm due to hyper-inflated lungs
  • appear darker due to the air
  • increased lung-filled lucency
60
Q

Why may a barrel chest develop in COPD?

A

Due to air trapping an hyperinflation.

61
Q

What is car pulmonae?

A

Abnormal enlargement of the right side of the chest

62
Q

What will happen to RV and TLC during emphysema?

A

These will increase due to air spaces enlarging.

63
Q

What will happen to the FEV1/FV ration in COPD?

A

Both numbers will decrease and hence the ratio will decrease. It will be <70%

64
Q

How is prednisolone used in the treatment of COPD?

A

This can be taken 30mg daily for 2 weeks. Lung function will be taken before and after. It should increase by 15%.

65
Q

What are the role of M3 receptors on lungs?

A

These are activated by parasympathetic nerves and this causes phospholipase C to convert PIP to IP3. IP3 causes contraction. Anti-muscarinic drugs will block these. Examples include tiotropium and ipratropium.

66
Q

What is the tidal volume?

A

Volume of gas moved in and out during normal breathing

67
Q

What is the inspiratory reserve volume?

A

Maximum volume of gas inspired from the end of tidal-inspiration

68
Q

What is the inspiratory capacity?

A

Maximum volume of gas inspired from resting expiratory level

69
Q

What is the vital capacity?

A

Maximum volume of air expired after maximum inspiration

70
Q

What is the residual volume?

A

Volume of gas remaining in lung after maximum expiration

71
Q

What is the total lung capacity?

A

Volume of gas in lungs at the end of maximum inspiration

72
Q

What is the functional residual capacity?

A

Volume of lugs at end of normal respiraoty level

73
Q

What is the thoracic gas volume?

A

Volume of gas in entire thoracic cavity resting expiratory level

74
Q

What is the FEV1?

A

Volume of expired air in first second of maximum expiration.

75
Q

What is the normal FEV1/FVC ratio?

A

80%

76
Q

What is FEV1/FVC ration in obstructive diseases?

A

The FEV1 and FVC are reduced disproportionately. The FVS is normal or reduced and the FEV1 is reduced. Therefore the ratio is below 70%

77
Q

What is the spirometry curve in asthma?

A

The curve is smooth due to the airway obstruction being relatively constant

78
Q

What is the spirometry curve in COPD?

A

The cube will be kinked as lung will collapse during forced expiration

79
Q

What is the spirometry curve in restrictive lung disease?

A

The curve will be normal height but with a very steep gradient as the lung volume is diminished.

80
Q

What is FEV1/FVC ration in restrictive lung disease?

A

The FEV1 and FVC are reduced proportionality. As both numbers are reduced, the ratio will be normal

81
Q

What happens when V/Q is zero?

A

There is physiological shunt as there is perfusion but no ventilation

82
Q

What happens when V/Q is infinity?

A

The perfusion is low and there may be a dead space

83
Q

What is the V/Q ration in COPD and asthma?

A

It is low due to impaired gas exchange

84
Q

What are the tests for metabolic acidosis?

A

Low pH and low carbon dioxide

85
Q

What are the tests for metabolic alkalosis?

A

High pH and high carbon dioxide

86
Q

What are the tests for respiratory acidosis?

A

Low pH and high carbon dioxide

87
Q

What are the tests for respiraoty alkalosis?

A

High pH and low carbon dioxide

88
Q

What kind of diuretic is Bendroflumethaizide?

A

Thiazide: decrease sodium transport in early DCT

89
Q

What kind of diuretic is Furosemide?

A

Loop: decrease sodium transport out of thick ascending loop of Henle

90
Q

What kind of drug is atenolol?

A

Beta-one antagonist

91
Q

What kind of drug is sodium chromoglicate?

A

Mast cell stabilizer

92
Q

Omalizumab is a drug used in asthma. What is the mechanism of action?

A

This binds to IgA antibodies and prevents that from binding to mast cells

93
Q

What are some signs of asthma in the airway?

A
  • mucous plug
  • desquamation
  • hyperplasia
  • SM hyperplasia
  • thickened BM
  • granulocyte infiltration
94
Q

What is the difference between type one and two brittle astham,?

A

One: sustained chronic variability in PEFR
Two: unpredictable drops in PEFR

95
Q

What is Bronchiectasis?

A

There is permeant enlargement of parts of the airways in the lungs. There is a mucous build-up and this causes persistent cough and breathlessness. The lungs are more prone to infection.

96
Q

Describe lung compliance

A

This is the stretchiness of the alveoli. Initially it is quite difficult to start inflate (low compliance) but then it becomes easier. As alveoli get more full, it gets more difficult to inflate until it reaches the elastic limit, where it will deflate.

97
Q

What are the gas levels when V/Q > 1?

A

Low carbon dioxide

98
Q

What are the gas levels when V/Q < 1 ?

A

Low oxygen and normal carbon dioxide

99
Q

What nerve innervates the dorsal respiraoty group?

A

Phrenic

100
Q

What nerve innervates the ventral respiraoty group?

A

Contralateral and intercostal nerves

101
Q

What does the flat portion of the oxygen-dissociation curve show?

A

A drop in partial oxygen pressure does not have large effect on saturation

102
Q

What pressure of oxygen will allow little effect in changes when it is above this value?

A

60mmHg. Below this there is progressive hyperventilation.

103
Q

Where do hypercapnia responses originate?

A

Central chemoreceptors

104
Q

What does NTS stand for?

A

Nucleus Tractus Solitarius

105
Q

Where is the NTS?

A

Dorsal respiratory group

106
Q

What type of respiraoty failure if Asthma?

A

Type Two

107
Q

What is hypoxemia?

A

Low oxygen in the blood

108
Q

What is hypoxia?

A

Low oxygen reaching tissues

109
Q

Where is voluntary control of breathing regulated?

A

High cortical centres

110
Q

What is thrombocytopenia?

A

Low platelet count

111
Q

What is emphysema?

A

This is abnormal swelling or permeant enlargement of the lung alveoli, causing a loss of elastic recoil. The destruction of the septa causes the surface area to decrease and hence has exchange is less sufficient.

112
Q

What is the unit of measurement for the peak flow?

A

L/Min

Medicine Phase One (44 decks)

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