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RCR1 > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the functions of the respiratory system?

A

Gas exchange

Regulation of acid/base balance

Immune surveillance and Host defence

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2
Q

Asthma and COPD are an example of what kind of abnormal gas exchange?

A

Airway disorders

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3
Q

Emphysema is an example of what type of abnormal gas exchange?

A

Alveolar disorder

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4
Q

Asbestosis is and example of what type of respiratory disorder?

A

Fibrotic lung disease

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5
Q

What does nasal breathing do?

A

Filters air

Warms air

Humidifies air

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6
Q

How is Humidification in nasal breathing achieved?

A

Mucous galnds

Seromucous glands

Goblet cells

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7
Q

How is heating achieved in Nasal Breathing?

A

The use of a rich capillary network.

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8
Q

Three examples of disorders caused by abnormal mucosal defence?

A

Pneumonia

Lung abscesses

Bronchiectasis

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9
Q

What causes respiratory acidosis and alkalosis?

A

Acidosis - inadequate clearance of CO2

Alkalosis Hyperventilation leading to too little CO2

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10
Q

What is type 1 respiratory failure and Type 2?

A

Type 1 - Low PaO2 and normal or low PaCO2

Type 2 - Low PaO2 and high PaCO2

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11
Q

Where does type 2 respiratory failure normally occur?

A

COPD
Neuromuscular Disease
Primary and secondary abnormalities of ventilation control.

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12
Q

What is the equation for pressure?

A

N/unit area (m2)

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13
Q

What is the partial pressure of a gas?

A

The individual pressure that one gas exerts.

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14
Q

What does Daltons law state?

A

That the total pressure is equivalent to the sum of the partial pressures.

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15
Q

At equilibrium the partial pressure of a gas in solution is what to it in it’s gaseous state?

A

Equal.

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16
Q

What is henry’s law?

A

[gas] = partial pressure x solubility coefficient.

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17
Q

What are the normal values for the PaO2 and % Hb saturation of arterial blood and of mixed (venous) blood?

A

Arterial: 13.3 kPa, 97-98%

Venous: 5.3 kPa, 75%

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18
Q

IN what two forms is oxygen transported around the body?

A

dissolved in blood plasma

bound to Hb

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19
Q

Why is Haemoglobin so important?

A

Increases oxygen carriage capacity.

The body needs around 250ml/min of Oxygen, the [O] in the blood is only 3ml, if only dissolved Oxygen was present then this quota could not be reached.

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20
Q

How does oxygen get delivered to tissues?

A

Through diffusion, there is a massive diffusion gradient into mitochondria (their Po2 is only 0.1 kPa compared to arterial blood’s 13.3 kPa.

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21
Q

What is the structure of Haemoglobin?

A

Consists of 4 subunits, each subunit consists of a glob in chain (peptide) and a haem group.

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22
Q

1g of Hb binds how many ml’s of O2?

A

1.36

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23
Q

if 1g of Hb binds 1.36ml’s of O2, what is the O2 content (ml/l) of a person with an [Hb] of 15g/100ml?

A

204ml/l

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24
Q

What does anaemia result from?

A

A lack of Hb in the blood caused by:

Impaired production
Increased breakdown
Blood loss
Fluid Overflow - haemodilution.

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25
Q

What is anaemia?

A

A lack of Hb in the blood.

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26
Q

What are the different types go haemoglobin, what are they made up of and what is the percentage proportion of those types in the adult body?

A

Adult haemoglobin (HbA) (97%)

  • 2 alpha chains
  • 2 beta chains

HbA2 (2%)

  • 2 alpha chains
  • 2 delta chains

HbF (fetal haemoglobin) 1%

  • 2 alpha chains
  • 2 gamma chains
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27
Q

When does the switch from fetal haemoglobin to Adult Hb happen?

A

between 3-6 months of age.

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28
Q

What’s thalassaemia?

A

A defect in the synthesis of the globin chain of Hb.

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29
Q

What is sickle cell disease?

A

A defect in the structure of the globin chain of Hb

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30
Q

What are the two types of thalasseamia?

A

Alpha and Beta, Alpha affects only Major HbA, Beta affects all forms.

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31
Q

What is the genetic cause of sickle cell disease?

A

A specific mutation in the ß-chain.

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32
Q

What are the two forms of sickle cell disease and their symptoms?

A

Heterozygous Hb (carrier)

  • generally asymptomatic
  • anoxia can manifest in stress situations such as air travel
  • protection against malaria
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33
Q

What is the name of the process of O2 binding to Fe2+ in the porphyrin ring?

A

Oxygenation.

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34
Q

What does an Hb saturation of 50% mean?

The molecules are all half loaded with O2 or half the molecules are fully loaded?

A

Half of the molecules are fully loaded, half are not at all.

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35
Q

What is cooperative binging of O2?

A

The fact that once O2 has binded to Hb then it is much more likely to bind again.

This is why there are a negligible amount of half filled Hb molecules.

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36
Q

At what paO2 does Hb begin to desaturate?

A

About 8 kPa

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37
Q

What is the use of Hb not desaturating until about 8 kPa?

A

Means there is a large functional reserve of O2, if PaO2 should fall.

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38
Q

Do all tissues have the same O2 functional reserve? use the examples of the heart and Kidney.

A

No, The heart receives uses a lot of the O2 from the blood it receives and so has little functional reserve and to increase output blood flow must increase

The kidney receives a lot of blood, due to its excretory role and so has a very large functional reserve, as it does not use much of the O2

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39
Q

What are the three major factors that alter Hb affinity?

A

Temperature
The Bohr effect (H+) - pH
BPG

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40
Q

Will increased or decreased temperature increase the Hb affinity?

A

Decreased temp will increase Hb Affinity.

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41
Q

Will increased H+ increase or decrease the Hb affinity and O2 delivery? Why?

A

Increased H+ will decrease Hb affinity, as H+ stabilises Hb.

Decreased H+ will also increase O2 delivery because O2 at the site of the tissue is no longer bound to Hb and so will diffuse into that tissue.

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42
Q

Tissues in anaerobic respiration produce H+ and metabolically active tissues produce more Co=O2, why is this useful in terms of oxygen?

A

Both will make the blood more acidic and will increase O2 delivery.

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43
Q

What is the role of BPG in oxygen delivery? how is this accomplished?

A

At high altitude or in chronic hypoxia BPG levels increase, thus increasing the delivery of oxygen.

This is because BPG stabilises Deoxy-Hb (attaches between the two ß-chains), so this prevents binding of O2 to it.

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44
Q

BPG does not affect HbF why is this important?

A

Because The bobby needs a lower oxygen saturation, to take O2 from the Mother.

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45
Q

What is Methaemoglobin (MetHb) and how is it formed?

A

It is formed when O2 oxidises Fe2+ to Fe3+ and so it cannot bind O2

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46
Q

How can MetHb be formed?

A

Spontaneously

Side effects of drugs such as nitrates sulphonamides

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47
Q

How are levels of MetHb controlled within the body?

A

MetHb reductase (keeps MetHb levels at 1.5% of total Hb)

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48
Q

What happens when MetHb reductase is deficient? How can this be treated?

A

Can allow MetHb concentration to rise to levels up to 25%, Treated with reducing agents such as Vit. C and methylene blue.

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49
Q

What can happen to Hb if a patent has high blood plasma glucose, what does this mean?

A

Can form Glycosylated Hb (HbA1c) when glucose attaches to ß-chains, has no direct effect on oxygen carriage.

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50
Q

Levels over what percentage of HbA1c can be problematic?

A

Over 7.5%, normal is 4-6%

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51
Q

What is cyanosis and what causes it?

A

Inadequate oxygenation of the blood, caused by the blue colour of deoxy-Hb.

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52
Q

What are the two forms of Cyanosis?

A

Peripheral cyanosis: Poor tissue perfusion leading to increased O2 extraction from available blood (turning it Blue)

Central Cyanosis: Poor oxygenation of blood to the lungs.

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53
Q

Is Cyanosis more likely to be seen in patients with Polycythaemia (increased [Hb]) or in patients with Anaemia (decreased [Hb])

A

Polycythaemia

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54
Q

What is Carboxyhaemoglobin?

A

Hb bound to CO.

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55
Q

What would a Carboxyhaemoglobin % of 0.7, 5 and 60 mean?

A

0.7% - normal

5% - smoker

60% - loss of consciousness

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56
Q

average values of PCO2 for arterial and venous blood?

A

Arterial: 5.3 kPa

Venous: 6.1 kPa

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57
Q

What are the three forms that CO2 can be carried in the blood? What proportion is carried by each?

A

Dissolved CO2 - 10%

Carbamino compounds - 10%

Bicarbonate ions - 80%

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58
Q

How are Carbamino compounds formed?

What’s the most common?

A

Reactions of CO2 with Amine groups on proteins

Most common is caraminohaemoglobin, the Co2 binds to the globin chains not the Haem.

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59
Q

Where is bicarbonate formed? With what enzyme?

A

In erythrocytes using carbonic anhydrase

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60
Q

What is the Haldane effect?

A

The fact that Oxy-Hb is a stronger acid than Deoxy-Hb and so [H+] increases in the lungs when O2 is taken into Hb, this promotes the separation of bicarbonate into CO2 and H2O.

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61
Q

What’s Myoglobin?

A

Similar to Hb but found in muscle, is equivalent to one globin chain and one haem group.

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62
Q

What is the use of myoglobin?

A

Facilitates diffusion of O2 from plasma membrane to mitochondria (creates a larger concentration gradient)

Acts as a small store (one or two heartbeats)

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63
Q

What is caisson disease?

A

The bends. When the patient has gone under high pressure and N2 solubility has increased, at lower pressures the N2 escapes and this causes the symptoms of the condition.

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64
Q

How do you treat Caisson disease?

A

Re-pressureise and then gradually depressurise.

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65
Q

How much oxygen is consumed and carbon dioxide produced per minute?

A

250ml of O2 consumed

200ml of CO2 produced

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66
Q

What is the determining factor for ventilation, [CO2] or [O2] why?

A

[CO2] this is because CO2 controls the bodies acid-base balance, and if PaCO2 is okay then normal PaO2 is too.

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67
Q

What is PAO2 and PaO2?

A

PAO2 is alveolar partial pressure of O2

PaO2 is arterial Partial pressure of O2

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68
Q

What are the three lines of defence in the airway?

A

1st - Nose and nasal passages of upper airway warm, moisten and filter for pathogens.

2nd - mucociliary escalator.

3rd - White blood cells in CT of lung tissue

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69
Q

What is the dead space of the lungs?

A

The conducting zone of the lungs that does not take part in gas exchange

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70
Q

What is the functional residual capacity?

A

The volume of air left inside the lungs after a normal quiet expiration.

Expiratory reserve volume + residual vol

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71
Q

What is the vital capacity?

A

The total volume of gas it is possible to inhale or exhale with a single breath.

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72
Q

What is residual volume?

A

The volume of gas left in the lungs at the end of a maximum expiration.

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73
Q

How do you work out the minute volume?

A

Tidal vol. x Rate

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74
Q

What is the alveolar ventilation and how do you work it out?

A

The Alveolar Ventilation (VA) is the amount of air actually passing through the gas-exchanging parts of the lung a minute.

(Tidal volume - Dead Space) x rate/min

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75
Q

What is the respiratory quotient, and what can it be used to measure?

A

CO2 Production/O2 consumption

Measures what someone is metabolising, if someone were metabolising pure glucose it would be 1.

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76
Q

What is PiO2?

A

The air arriving in the alveoli.

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77
Q

How do you calculate PAO2? what can this be used to do?

A

PiO2 (19.9 - usually) - PACO2/R (rate of respiration).

Compared the PAO2 to the PaO@ and if they are different there is a gas exchange issue.

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78
Q

If the PaCO2 is low the patient is Hypo/Hyperventilating?

A

Hyperventilating.

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79
Q

If the alveolar ventilation doubles what happens to the PACO2?

A

Halves.

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80
Q

Why is the Arterial PCO2 such a good indicator of Alveolar PCO2?

A

Because CO2 is so soluble.

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81
Q

If the PAO2 and the PaO2 do not mismatch what is the most likely explanation?

A

A V/Q mismatch or shunt.

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82
Q

What four mechanism helps maximise ventilation/Perfusion (Q) matching?

A

Gravity ensures the bases of the lungs are better perfused

Because lungs hang in the chest the lower parts of the lungs are better ventilated

Oxygen in the lungs is a vasodilator

Areas of the lung that are better perfused have more CO2 which is a bronchodilator.

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83
Q

What is the difference in a V/Q mismatch and a shunt?

A

A V/Q mismatch is when there is reduced ventilation to part of the lung

A shunt is when pulmonary arterial blood reaches the systemic circulation without being exposed to ventilation.

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84
Q

In a ventilation perfusion mismatch the PaO2 will be reduced, how is it possible that the PaCO2 can remain normal?

A

Because the body can over-ventilate the parts of the lungs that are being perfused and will therefore release enough CO2, these areas already have a Hb of 100% so this is not possible for paO2.

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85
Q

How is it possible to diagnose a Ventilation perfusion mismatch (V/Q or shunt)?

A

If the PaO2 is reduced, but the PaCO2 is normal.

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86
Q

Will supplementary oxygen improve the situation of a V/Q mismatch or a Shunt?

A

It will improve the situation in a V/Q mismatch as this results from poor ventilation, however it will not help in a shunt because the blood passing through the shunt will not be affected.

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87
Q

If the PaCO2 is normal but the PaO2 is less than predicted what is the problem (ventilation or gas exchange) and a likely diagnosis?

A

Ventilation is fine, there is a gas exchange problem, e.g. pulmonary oedema.

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88
Q

If the PaCO2 is elevated and the PaO2 is normal what is the problem (ventilation or gas exchange) and a likely diagnosis?

A

gas exchange is fine, there is a ventilation issue, hypoventilation. e.g. respiratory depressant drug (e.g.morphine)

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89
Q

If the PaCO2 is elevated and the PaO2 is less than calculated, what is the problem (ventilation or gas exchange) and a likely diagnosis?

A

Hypoventilation and a gas exchange problem e.g. COPD

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90
Q

If the PaCO2 is reduced, but the PaO2 is normal what is the problem (ventilation or gas exchange) and a likely diagnosis?

A

No gas exchange issue, only hyperventilation e.g. panic attack.

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91
Q

The PaCO2 is reduced and so is the PaO2 what is the problem (ventilation or gas exchange) and a likely diagnosis?

A

Hyperventilation and gas exchange. e.g. asthma.

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92
Q

What muscles are used in inspiration and which in expiration?

A

Inspiration - Diaphragm, external intercostals and shoulder girdle muscles

Expiration - Internal intercostals and abdominal wall muscles

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93
Q

What three conditions require the expiratory muscles to actually be used?

A
  • To go below FRC
  • To achieve High pressures
  • To achieve high flow rates
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94
Q

What contributes to elastic recoil?

A

The elastic fibres of lung tissue

Surfactant in the alveoli

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95
Q

What contributes to the alveolar pressure?

A

The Pressure acting on the outside of the alveolus (pleural) and the pressure generated by the elastic recoil of the alveolus.

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96
Q

Explain the concept of flow limitation.

A

The fact that there is a maximal flow for each lung volume which cannot be exceeded. This occurs because the resistance to flow determines the air flow.

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97
Q

Why does airway collapse happen on forced expiration?

A

Happens as the pleural pressure becomes greatly positive, more so than the pressure at the critical closing point.

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98
Q

Why do pink puffers breath through pursed lips?

A

In order to raise airway pressure and avoid collapse.

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99
Q

What conditions might affect the capacity to inspire?

A

If lungs are abnormally stiff e.g. Fibrosis, pulmonary oedema.

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100
Q

What is orthopnoea?

A

Shortness of breath when supine, can occur in obese patients that struggle to depress the diaphragm.

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101
Q

What increases airway resistance?

A

Bronchoconstriction, swelling of the wall or airway by secretions.

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102
Q

In what situations is lung compliance increased and in what situations is it decreased?

A

Increased in emphysema as a result of elastin and also surface area which can lead to loss of surface tension.

Decreased in restrictive conditions such as asbestosis and fibrosis.

Decreased in left side heart failure as the pulmonary vessels are engorged with blood and there is pulmonary oedema.

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103
Q

What is surfactant mostly made up of?

A

Lipids.

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104
Q

What is the function of surfactant?

A

Allows alveoli to be expanded in inspiration and prevent alveolar collapse at expiration

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105
Q

What are the two types of receptors involved in controlling ventilation?

A
  1. Mechanoreceptors e.g. in limbs, chest wall and airways.
  2. Chemoreceptors e.g. Central chemoreceptors (in brain), Peripheral (aortic and carotid bodies - normal contribute little, but important in ‘hypoxic drive’)
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106
Q

What are the two types of lung diseases? examples?

A

Restrictive - decreased lung compliance (smaller lungs), e.g. tumours or fibrosis.

Obstructive - impaired airflow, especially during expiration, normally involving airway narrowing and or obstruction. e.g. Asthma, COPD.

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107
Q

What is emphysema? what causes it?

A

Enlargement of the airspaces distant to the terminal bronchiole. Due to breakdown of alveolar walls, normally due to excessive protease activity caused by smoking.

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108
Q

What is bronchitis?

A

Chronic over-production of mucus in the bronchial tree, with periods of infection.

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109
Q

What happens to the FEV1 and FVC in bronchitis and in emphysema?

A

Decreased FVC and FEV1 in emphysema and bronchitis

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110
Q

What is COPD?

A

Normally chronic lung disease has features of both emphysema and bronchitis and is categorised as COPD

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111
Q

How does H+ react with proteins?

A

Reacts with negative charges on proteins.

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112
Q

What is the normal arterial pH rang?

A

7.35-7.45

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113
Q

Difference in strong and weak acids?

A

Strong acids dissociate completely in solution.

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114
Q

What are buffers?

A

Weak acids or weak bases.

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115
Q

What are three physiological buffers in the human body?

A

Bicarbonate buffer (HCO3-)

Proteins (they can accept H+ due to -ve charges)

Phosphate buffer (important in urine) - H2PO4

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116
Q

How are acid product dealt with in the body?

A
  1. buffered by physiological buffers.

2. Eliminated via lungs and kidneys

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117
Q

Where are Co2 and metabolic acids eliminated

A

CO2 in the lungs

metabolic acids in the kidneys

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118
Q

What is carbonic anhydrase?

A

The enzyme that catalyses the bicarbonate buffer reaction

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119
Q

In relation to carbonic anhydrase what do RBC’s do in the body and then differently in the lungs?

A

In the body they take up CO2 and convert it to HCO3- and H+

In the lungs they take up HCO3- and H+ to convert to CO2

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120
Q

What does the kidney do to HCO3-?

A

Resorbs it in the proximal tubule

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121
Q

What will Increasing pH/CO2 do to the respiratory system?

A

will increase rate and depth and more CO2 will be expired – increasing pH

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122
Q

What do clinical acid-base machines measure, how do they measure [HCO3-]?

A

Measure PaCO2, PaO2 & pH (via an electrode), then the [HCO3-] is determined from the henderson-haselbach eq.

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123
Q

What are the measurements that determine respiratory acidosis and alkalosis?

A

PaCO2 > 6.1

PaCO2 < 4.8

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124
Q

What would a proportionate change in PaCO2 and HCO3- suggest, and what would a disproportionate one suggest?

A

Proportionate: A respiratory acid-base imbalance.

Disproportionate: Metabolic imbalance

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125
Q

What is base excess (BXS)?

A

The change in [HCO3-] produced only by the metabolic component of the acid/base balance.

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126
Q

Is the base excess positive or negative in metabolic acidosis?

A

Not enough bicarbonate so negative

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127
Q

Is the base excess positive or negative in respiratory acidosis?

A

effectively 0.

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128
Q

What is the standard bicarbonate?

A

It is an estimate of what the HCO3- would be if the PaCO2 was normal

provides the same info as Base excess.

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129
Q

What are the two ways in which we control our respiration?

A

Voluntary control - Cerebral cortex

Involuntary - Brainstem

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130
Q

Is normal expiration passive or active?

A

Passive.

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131
Q

What are the two medullary centres controlling ventilation? What does each do?

A

Dorsal respiratory group:
- causes inspiration, expiration occurs passively.

Ventral respiratory group:
- involved in inspiration and expiration when there is increased demand to breathe, e.g. in exercise.

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132
Q

What are the two types of neurones that are part of the dorsal respiratory group

A
  1. I alpha that are inhibited by lung inflation

2. I alpha excited by lung inflation

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133
Q

How does the ventral respiratory group work in an increased drive to breathe?

A

Uses accessory muscles for increased inspiration and abdominal muscles for forced expiration.

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134
Q

What is the role of the pons in ventilation?

A

Controls filling duration of the lungs and rate and depth of breathing.

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135
Q

What do the central chemoreceptors respond to?

A

Increased PaCO2 and decreased pH

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136
Q

What are the carotid and aortic bodies sensitive to?

A

Aortic have minimal role and are mostly sensitive to total O2 flow

Carotid bodies are only sensitive to PO2

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137
Q

If H+ ions cannot diffuse across the blood-brain barrier how are central chemoreceptors sensitive to H+?

A

Co2 indirectly influences the pH by increasing the number of H+ ions through bicarbonate.

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138
Q

What is the pentose phosphate pathway and how does it differ from glycolysis?

A

An alternative pathway (to glycolysis) of glucose metabolism; provides raw materials for cellular functions such as NADPH and pentose phosphates.

Does NOT produce ATP

Does NOT oxidise glucose completely

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139
Q

What is the Hexose monophosphate shunt?

A

The point of glycolysis (at Glc-6-phosphate) that the pentose-phosphate shunt can occur.

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140
Q

What are the two main stages of the pentose phosphate pathway?

What do the produce?

A

An irreversible redox stage
- NADPH and pentose phosphates

A reversible interconversion stage
- Excess pentose phosphates are converted into glycolytic intermediates.

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141
Q

What can the pentose phosphates be used for in the cell?

A

Production of DNA and RNA.

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142
Q

What happens in the redox stage of the Pentose Phosphate Pathway (PPP)?

What can then happen to the product?

A

First reaction produces 6-phosphogluconate, in a dehydrogenase reaction with the enzyme Glucose-6-Phosphate dehydrogenase.

Final reaction produces ribulose-5-phosphate, in a dehydrogenase reaction using the enzyme 6-phosphogluconate dehydrogenase.

Ribulose-5-phosphate can then be used for DNA/RNA synthesis, or put into the interconversion stage.

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143
Q

What determines whether the ribulose-5-phosphate produced from the redox stage of the PPP then gets used for DNA/RNA or goes into the interconversion stage?

A

The need for NADH over the need for DNA/RNA synthesis.

In dividing cells they need pentose phosphates to produce DNA/RNA

In non-dividing cells there is an increased need for NADH and so pentose phosphates can be put back into glycolysis.

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144
Q

What happens in the interconversion stage of the PPP?

A

Re-arrangement of carbon in three 5-Carbon ribulose-5-phosphates to produce:

Glyceraldehyde-3-Phosphate (3C)

and 2x fructose-6-phosphate (6C)

They are then fed back into glycolysis.

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145
Q

What is the difference in NADPH and NADH, and what is the advantage of having both in a cell?

A

The single phosphate has no effect on electron carrying ability, it serves to distinguish the two electron carriers. This is so that the cell can regulate both pathways independently and have access to both oxidising and reducing agents for two sets of reactions in a cell.

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146
Q

What is reduced glutathione (GSH), and how is NADPH relevant?

A

Reduced glutathione converts dangerous metabolites in the cell e.g. H2O2 to H2O

NADPH reduces GSSG to 2x GSH

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147
Q

What is Glucose-6-phosphate dehydrogenase (G6PD) deficiency? how does it confer protection to malaria?

A

X-linked recessive condition, mutating G6PD altering it’s structure/stability.

Malaria relies on a metabolite produced by G6PD

148
Q

What are the other biochemical effects of G6PD deficiency?

A

G6PD also regulates NADPH levels in the cell, so NADPH is reduced:

  • NADPH converts GSSG to GSH, which means if there is little GSH H2O2 cannot be converted to to H2O, if not reduced H2O2 will degrade rbc’s
149
Q

What do patients with G6PD present with?

A

Neonatal Jaundice

Haemolytic anaemia:
- Oxidative stress with no GSH can result in loss of Hb function, can result after oxidative drugs are administered e.g. aspirin, anti-malarial drugs.

150
Q

What reflex do the Nasal, Epipharangeal, Larangeal and Tracheal receptors all produce? What nerve enervates them?

A

Nasal - Sneeze (Trigeminal)

Epipharangeal - Aspiration (Glossopharangeal)

Larangeal - Cough (Vagus)

Tracheal - Cough (Vagus)

151
Q

What is tidal volume?

A

Volume of air inspired and expired during quiet breathing.

152
Q

What is the Inspiratory reserve volume?

A

The maximal volume of air that can be inhaled after a normal tidal volume inspiration.

153
Q

Expiratory reserve volume?

A

Maximum amount of air that can be exhaled from the resting expiatory level.

154
Q

Residual volume?

A

Volume of air remaining in the lungs at the end of maximum expiration.

155
Q

Vital capacity?

A

Volume of air that can be exhaled from the lungs after maximum inspiration

156
Q

What is FEV1 and FVC?

A

FEV1: Volume of air that can be exhaled in 1 second from full inflation.

FVC: Total volume of air that can be exhaled from full inflation.

157
Q

Examples of obstructive airway disorders?

A

COPD, Asthma.

158
Q

What characterises obstructive expiratory disorders?

A

Limitation in expiratory airflow.

Decreased FEV1 and FEV1/FVC ratio.

159
Q

What are restrictive airways disorders caused by?

A

Diminished lung volume, by alteration of lung tissue or other disease.

160
Q

What are restrictive airways disorders characterised by?

A

Low FVC and FEV₁

161
Q

How are lung volumes clinically measured?

A

Dilutional methods such as 100% oxygen or helium.

Body plethysmography

162
Q

How is pulmonary function clinically tested?

A

Blood gasses, cardiopulmonary exercise tests, metabolic measurements.

163
Q

What are Mucins?

A

A substance secreted by goblet cells and mucous glands in the upper respiratory tract that provides stickiness to the mucous and traps particles.

164
Q

What is the first line of defence against pathogens that reach the alveolar space?

A

Alveolar Macrophages

165
Q

What receptors are present on alveolar macrophages?

A

TLR (toll-like receptors)

PRR, Pattern recognition receptors.

166
Q

What are the primaryAPC of the respiratory system?

A

Dendritic cells

167
Q

What is IgA’s role in mucous defence?

A

inhibits:

bacterial adhesion
inflammatory effects of other immunoglobulins

Neutralises bacterial/viral toxins

168
Q

What is Bronchiectasis?

A

Permanent dilation of the Bronchi, generally accompanied by suppurative inflammation (sputum production)

169
Q

What are the two main heart sounds caused by?

A

The first ‘lub’ is the closure of the atrioventricular valves

The second is the closure of the aortic and pulmonary valves

170
Q

When is ventricular and atrial systole occurring in relation to the heart sounds?

A

Ventricular - in-between the first and second heart sounds

Atrial - just before the first sound

171
Q

What part of the ECG represents electrical event happening at atrial systole and which at ventricular systole?

A

Atrial - P wave

Ventricular - QRS

172
Q

What is isovolumic contraction?

A

Occurs in systole when the ventricular pressure rises but the ventricular volume is constant.

173
Q

What causes an early systolic murmur?

A

When the AV valves fail to close fully in atrial systole, or when aortic/pulmonary valves do not full open.

174
Q

What can cause an early diastolic murmur?

A

If the aortic or pulmonary valves fail to close fully in diastole.

175
Q

What are the 3rd and 4th heart sounds caused by?

A

Both are not always heard:

3rd: ‘sail flapping in the wind’ Due to rapid ventricular filling.
4th: Heard due to atrial systole, heard due to ischaemic heart disease or hypertension. Heard when a hypertrophied left atrium pumps into a stiffened left ventricle.

176
Q

Quick way to work out heart rate from an ECG?

A

Count the squares between two QRS complexes and divide by 300

177
Q

What are the two types of limb leads in an ECG?

A

Bipolar limb leads (I,II and III)

Unipolar limb leads (aVR, aVL and aVF)

178
Q

Apart from the Limb leads, what else is included on the ECG?

A

The 6 Chest leads

179
Q

What direction do all the limb leads travel?

A

I: RA to LA
II: RA to LL
III: LA to LL

aVR: (LA-LL) to RA
aVL: (RA-LL) to LA
aVF: (RA-LA) to LL

180
Q

What is idiopathic ventilation?

A

Sustained alveolar and arterial hypocapnia. during rest and exercise.

181
Q

Cause of idiopathic ventilation?

A

inappropriate cortical processing.

182
Q

What are some respiratory adaptations to training?

A

Pulmonary ventilation increases at maximal effort, by increasing strength of inspiratory muscles.

Pulmonary diffusion increases at maximal work rates

Slight increase in total lung capacity

Decreased respiratory rate and pulmonary ventilation at rest.

183
Q

Why is there less haematocrit in the capillaries?

A

To reduce resistance.

184
Q

What are the major features of cardiac muscle?

A

Striated
Branched
Intercalated discs

185
Q

Main mechanism of control of cardiac muscle?

A

Increased intracellular calcium to increase strength of contraction.

All positive inotropic drugs work this way

186
Q

Three ways in which Intracellular calcium concentrations are raised?

A

Enters the cell from the outside
Released from intracellular stores
Calcium mediated calcium release

187
Q

How are calcium level returned to resting in cardiac muscle cells? (3)

A

Active calcium extrusion (pump)
Active Na+/Ca2+ exchange
Active uptake into SR

188
Q

What is the cause of a stiff ventricle due to cardiac ischaemia?

A

Slowed uptake of calcium, causing a raised resting potential in cardiac muscle cells.

189
Q

Is the contractile mechanism in cardiac muscle the same or different to the mechanism in skeletal muscle?

A

the same.

190
Q

Phases of the ventricular action potential?

A

Phase 0 - Depolarisation due to sodium influx

Phase 1 - Initial depolarisation caused by potassium efflux

Phase 2 - Plateau caused by calcium influx and potassium efflux.

Phase 3 - actual depolarisation by potassium efflux

Phase 4 - resting potential

191
Q

how does hyperkalaemia cause cardiac arrest?

A

The membrane may not return to it’s normal resting value due to high K+ concentration and Na+ channels may not be fully reset, therefore dialling contraction.

192
Q

Two examples of positive inotropes and their mechanism of action?

A

Beta agonists (dobutamine): Speed Ca++ uptake into intracellular stores

Cardiac Glycosides (Digoxin): Inhibit Na+/K+ ATPase, increasing intracellular [Na+], thus decreasing Na/Ca exchange and increasing intracellular [Ca++]

193
Q

Two examples of negative inotropes, and their mechanism of action?

A

Calcium channel blockers: Guess.

Beta Blockers: Decrease Ca++ uptake into intracellular stores

194
Q

Factors which determine preload?

A 
Gravity
Thoracic pump
The muscle pump
Co-localisation
Venomotor tone
Blood volume
195
Q

How does gravity affect preload?

A

In the upright position the preload is increased form the SVC and decreased from the IVC.

196
Q

What is the thoracic pump and how does it affect preload?

A

On inspiration preload falls due to decreased thoracic pressure.

197
Q

What is co-localisation?

A

The fact veins are bound together with arteries and when the artery pulses the blood moves up the vein.

198
Q

What is venomotor tone, and how does it affect preload?

A

The fact some of the great veins have smooth muscle that is stimulated by a-1 receptors, making it contract increasing preload.

199
Q

Increased preload increases what?

A

Increased end diastolic volume, the same systolic volume and increased cardiac output

200
Q

Increased after load increases what?

A

Increased end diastolic volume but maintained stroke volume and cardiac output

201
Q

What is the molecular basis of increased force of contraction due to increased preload/afterload?

A

The actin and myosin strands are thought to be drawn closer together.

202
Q

What is an increase in contractility e.g. from an inotropic drug ?

A

An increase in the fore of contraction that does not result from increased stretch.

203
Q

Process of events that result after left ventricular ischaemia?

A

The right ventricle function better than the left

The right continues to pump blood to the lungs but it is ineffectively cleared by the left, and so pulmonary and left atrial bp rise.

Eventually ventricular balance will be restored as the left ventricle will move up it’s starling curve, at the cost of pulmonary congestion and possible oedema.

204
Q

What is orthopnoea?

A

Breathlessness when lying flat, commonly due to left side heart failure.

205
Q

What causes pain due to hypoxia?

A

Na+/K+ pump malfunction.

206
Q

Corneal arcus and xanthelasmata are commonly caused by what?

A

Hypercholesterolaemia

207
Q

Process of fat digestion and absorption in the small intestine?

A

Chyme (partially digested food) is mixed with Bile,
Pancreatic juice and Intestinal juice.

This is then emulsified, digested and absorbed.

208
Q

What is the function of pancreatic lipase?

A

It hydrolyses triglyceride contained within the fat droplet.

209
Q

Four main types of lipoprotein?

A

Chylomicron very large, formed in small intestine enterocytes.

VLDL - very low density lipoprotein - triglyceride rich and formed in the liver

LDL - Cholesterol rich formed by VLDL

HDL - Cholesterol rich (less than LDL’s) formed in the liver

210
Q

Functions of apolipoproteins?

A

The actual protein component of lipoproteins.

To solubilise the lipid particle

Maintain structural integrity

To confer specificity on the lipoprotein particle and therefore direct it’s metabolism.

211
Q

What is lipoprotein lipase?

A

Enzyme found on the surface of capillaries/hepatocytes that hydrolyses the TG to release fatty acids near the tissue.

212
Q

Where are renin, ACE and angiotensinogen produced?

A

Renin is produced by the kidneys

ACE is produced in the lungs

Angiotensinogen is continuously produced by the liver

213
Q

What does renin do to angiotensinogen and what does ACE then do?

A

Renin converts Angiotensinogen to Angiotensin I and then ACE converts Angiotensin I to II (the active form)

214
Q

What is the interaction between ACE and bradykinin?

A

Bradykinin is a vasodilator (in the lungs) ACE will break it down and so ACE inhibitors can affect this (can cause dry cough)

215
Q

Actions of Ang II?

A

Vasoconstriction
Aldosterone release
Increased sympathetic stimulation
Promotes Na+ retention

216
Q

What factors increase renin release?

A

Low arterial BP

Low Blood Volume

Altered sodium handling

217
Q

Factors that decrease renin release?

A

High arterial BP

Increased Blood Volume

Angiotensin II (negative feedback)

218
Q

What are the two Ang II receptors, and their features?

A

AT1 receptors

  • Mitogenic
  • Pro-fibrotic
  • Vasoconstriction & increased BP

AT2 receptors

  • Anti - mitogenic
  • Anti - fibrotic
  • Vasodilation & decreased BP
219
Q

How do AT1 receptors cause vasoconstriction?

A

Direct action on vascular smooth muscle

Release of ADH

potentiation of Sympathetic NS

220
Q

How do AT1 receptors act on the Sympathetic NS?

A

Act on peripheral nerve endings

  • potentiate noradrenaline release
  • block noradrenaline reuptake
  • increase noradrenaline synthesis

noradrenaline leads to vasoconstriction.

221
Q

How is aldosterone regulated and what does it do?

A

Regulated by Ang II

Aldosterone promotes water retention:

  • increases Na+ retention in kidney and gut
  • increases ADH secretion
  • potent dipsogen (promotes thirst)
222
Q

What are the actions of AT2 receptors?

A

Stimulates vasodilation

Increased activity of collagenases

Decrease growth factor expression

223
Q

What are the interactions of Ang II in heart failure?

A

Ang II can increase cardiac remodelling due profibrotic/mitotic effects

224
Q

What drugs block the RAAS system?

A

Beta-blockers

Renin inhibitors

ACE inhibitors

AT receptor antagonists

225
Q

Two types of exercise?

A

Static or dynamic

226
Q

Two different types of muscle?

A

Slow Twitch:

  • Dependent of oxidative phosphorylation, good blood supply

Fast Twitch:
IIa: oxidative
IIb: glycoloytic

  • Dependent on Creatine Phosphate
227
Q

In what three ways is an oxygen debt incurred after exercise begins?

A
  • Depletion of cellular ATP
  • Depletion of creatine phosphate
  • Build up of Lactic Acid
228
Q

How is oxygen repaid after oxygen debt is acquired?

A

Fast: Rephosphorylation of ATP/Creatine
Slow: Lactate converted back to glucose/glycogen
Very Slow: Increased metabolic rate following exercise

229
Q

Main physiological adaptations to exercise?

A

Increased HR
Increased SV
Decreased total peripheral resistance
Changes in distribution of blood flow

230
Q

How is heart rate and Stroke volume mediated by the body?

A

Heart rate increased by the Sympathetic Nervous System, and decreased by the parasympathetic

Stroke volume modulated by preload and contractility.

231
Q

What blood vessel mostly determines total peripheral resistance?

A

The arterioles

232
Q

What is metabolite induced vasodilation? What are some examples?

A

When increased metabolism increases the amount of metabolites including; CO2, H+, lactate, K+ and Adenosine. These induce vasodilation.

233
Q

Do arterial blood gasses change in response to exercise?

A

No

234
Q

What are the parts of the body that act to increase ventilation in exercise?

A

Higher centres in the brain, peripheral chemoreceptors, skeletal muscles (chemo and mechanoreceptors)

235
Q

What are the physiological changes to the lungs in exercise?

A

respiratory rate and ventilation increase.

236
Q

What are the changes to the baroreceptor response in exercise?

A

The brain alters the ‘set point’ of blood pressure and so blood pressure is perceived as being too low. So heart rate is increased to compensate.

237
Q

What is the limiting system to increase VO2 max?

A

Cardiovascular system

238
Q

Responses in the muscle to training?

A 
Muscle hypertrophy
Increased number of myofibrils
Increased mitochondrial enzymes
Increased ATP and Phospho-creatine
Increased glycogen
239
Q

Effects of training on Respiration?

A

Reduced ventilation at the same work rate.

240
Q

Main difference in the CV system’s response to static exercise?

A

There is no significant drop in peripheral resistance.

241
Q

What’s VO₂ max used to measure?

A

The functional capacity of the entire cardiopulmonary system.

242
Q

Reasons for termination of an exercise test?

A

Moderate to severe angina
dizziness or syncope
Subject wishes to stop

243
Q

What does it tell you if the murmur is long?

A

Possibly a septal defect.

244
Q

What is a wide pulse pressure and what does it mean?

A

A large gap between the systolic and diastolic blood pressures, represents a stiff aorta normally if the systolic is raised.

245
Q

What are the two theories on the auto regulation of blood pressure in tissues?

Which applies to the afferent arterioles?

A

Metabolic theory: improved blood flow increases metabolism and has vasoactive effects?

Myogenic theory: Smooth muscle constricts when stretched, via an increase in intracellular [Ca].

246
Q

What is Tubuloglomerular feedback?

A

When the fluid content is monitored in the DCT in the macular dense and there is feedback to the glomerulus and GFR is modified.

247
Q

If the Na+ and Cl- is too high in the DCT what changes will happen to the afferent arteriole?

A

Afferent constriction.

248
Q

What is the difference in the blood flow/O2 Consumption to the cortex and to the medulla?

A

The Cortex receives a lot of blood and has a relatively low O2 consumption

In the medulla each nephron is individually supplied by the vasa recta and so blood flow is low and O2 consumption is relatively high, leaving little residual capacity

249
Q

What are the two characteristics that determine whether a molecule will pass through the glomerular filter.

A

Charge (Negative will be repelled), Size

250
Q

What kind of things are not filtered into the PCT?

A

Cells and proteins

251
Q

What effect will afferent arteriole constriction have on Blood flow into the glomerulus, Glomerular pressure and GFR?

A

Decrease for all.

252
Q

Mediators of Afferent arteriole Vasoconstriction/dilation?

A

Constriction:

Sympathetic tone
Adenosine
Endothelin

Dilation:

NO
ANP
Prostaglandins

253
Q

What effect will Efferent arterial dilation have on Blood flow out of the glomerulus, Glomerular pressure and GFR?

A

Decrease Blood flow out

Increase Glomerular pressure and GFR

254
Q

What are the Mesangial cells in the glomerulus?

A

Cells that support the glomerular filter

Phagocytic and contractile.

255
Q

Contraction of Mesangial cells does what?

A

decreases surface area and decreases GFR

256
Q

What’s the textbook GFR?

A

125ml/min

257
Q

What’s compensatory SNGFR?

A

Increases in single nephron GFR, through hypertrophy of blood vessels and tubules, can maintain GFR following nephron loss.

258
Q

Definition for renal clearance?

A

Volume of plasma that is completely cleared of a marker per unit time

259
Q

What are the properties which mean a clearance marker can be use to measure GFR

A 
Freely filtered in the glomerulus 
Not secreted nor reabsorbed
non-toxic
Not metabolised in the kidney
No effect on GFR
260
Q

How do you work out the amount of marker excreted?

A

(Urine [marker] x vol) / Time

261
Q

How do calculate the amount of marker filtered?

A

GFR x Urine [marker]

262
Q

How do you calculate clearance of a marker, and GFR if it’s suitable?

A

(U x V / P x T)

263
Q

What are the markers usually used to measure GFR?

A

Inulin (gold standard)

Creatinine (routine) Urea

264
Q

Why is inulin not commonly used?

A

Too time consuming as it is not endogenous

265
Q

How is creatinine handled by the kidney?

A

Freely filtered
Not reabsorbed
Slightly secreted (about 10% discrepancy)

266
Q

What factors can affect [Creatinine]?

A

Muscle mass

Age

Gender

267
Q

How is Urea handled by the Kidneys?

A

Freely absorbed and not secreted

About 40% reabsorbed

268
Q

What factors affect [urea]?

A

Protein turnover

Hydration status (due to release of ADH)

269
Q

Why is the Urea:Creatinine Concentration useful?

A

Both should be equally affected by any change in GFR so if they change disproportionately there may be underlying problems (e.g. dehydration)

270
Q

To measure renal plasma flow what properties must a marker exhibit?

An example?

A

Freely filtered not reabsorbed

Must be mostly secreted

e.g. PAH (90% cleared)

271
Q

How do you calculate Renal Plasma flow?

A

UxV / PxT

272
Q

Two main types of nephron? What’s the difference?

A

Cortical Nephrons Glomeruli in outer cortex short loop of henle

Juxtamedullary nephrons Glomeruli near the boundary between Cortex/Medulla the loop of henle descends into the medulla.

273
Q

Main functions of the nephron?

A

Resorption of solutes

Secretion

Regulation of urine volume

274
Q

What is the mechanism of obligate reabsorption in the proximal convoluted tubule?

A

Na+ dependent active transport across the membrane.

275
Q

Why is glucose seen in uncontrolled diabetes?

A

When there is so much glucose in the plasma that the glucose transported in the PCT are saturated and have reached ‘renal threshold’

276
Q

If the GFR increases what will happen to the PCT resorption of Na+/K+?

A

doesn’t change this is because there is a set proportion absorbed independent on the amount

277
Q

How is Na+ reabsorbed in the PCT?

A

Actively with glucose/amino acids and also as an H+/Na+ anti-port

278
Q

In the proximal tubule what is the rate of bicarbonate reabsorption?

A

90%

279
Q

How is water reabsorbed in the PCT?

A

The amount of solutes being reabsorbed creates an osmotic gradient (where sodium flows water follows)

280
Q

How are Cl-, K+ and Urea reabsorbed in the PCT?

A

The reabsorption of Na+ and water causes a chemical gradient and a diffusion gradient is created.

281
Q

What things are secreted into the PCT and how does this occur?

A

Organic acids and bases, occurs through active transport.

282
Q

Very basic overview of what is permeable in the loop of henle?

A

Thin descending limb permeable to water and not Na+ or Cl-

Thin ascending permeable to Na+ and Cl-

Thick ascending limb actively pumps Na+ and Cl-

283
Q

What happens to Na+/K+ and Cl- in the thick ascending limb exactly?

A

Na+/K+/2Cl- active transport from the tubular epithelium to the epithelial cell

Na+ is pumped into medullary interstitium, Cl- diffuses into the medullary interstitium, K+ diffuses back into the tubule

284
Q

Detail on how the loop of henle functions.

A

The Na+ and Cl- efflux from the Thick ascending limb causes the interstitium to be hyperosmolar

Drawing water out of the descending limb, making the electrolytes inside more concentrated

Then when the fluid reaches the thin ascending limb it is permeable to Na+ and Cl- and they diffuse out.

then the Na+ and Cl- and K+ are actively pumped out of the thick ascending limb

285
Q

If the collecting duct is permeable to water where will it diffuse?

What hormone causes this?

A

Out of the collecting duct and into the hyperosmolar medulla

ADH

286
Q

Where is ADH made and secreted, due to what stimulus, in response to what receptors?

A

MAde in the soma of the hypothalamus neurones and transported to the pituitary. Secreted if the fluid increases in osmolarity.

Due to the osmoreceptors or from input from the medulla

287
Q

How does ADH increase permeability?

A

Inserts aquaporins in the collecting duct, they are water channels.

288
Q

What stimuli can cause ADH secretion?

A 
Increased osmotic pressure of plasma
Decreased Extracellular fluid
Pain, emotion, stress
Exercise
Nausea/vomiting
Angiotensin II
289
Q

What stimuli can decrease ADH secretion?

A

Decreased Osmotic pressure
Increased ECF volume
Drugs e.g. alcohol
ANP

290
Q

What are the different sensory inputs for water and salt regulation?

A

Osmoreceptors in hypothalamus

Low pressure receptors in the atria

High pressure baroreceptors in aortic arch and carotid sinus

Juxtaglomerular apparatus

291
Q

What stimuli cause thirst?

A

Increased plasma osmolarity

Decreased blood volume

During meals

292
Q

What is diabetes insipidus?

A

The inability to concentrate urine as a lack of ADH activity, either not secreted or nephron does not respond.

293
Q

Where is sodium reabsorption regulated?

A

Regulated in the distal nephron

Ascending loop of henle
Distal tubule
Early collecting duct

294
Q

What hormones control Na+ regulation?

A

Aldosterone

ANP

295
Q

How is Na+ reabsorbed in the DCT?

A

Through a Na+/Cl- co-transporter from lumen to cell

and through the Na+/K+ antiport from cell to interstitium

296
Q

Two major cell types in the collecting ducts?

A

Principle cells: Resorb Na+ and secrete K+

Intercalated cells: secrete H+, maintain acid/base balance

297
Q

What happens in the early collecting duct?

A

Na+ resorption by principle cells, Na+ leaves through water filled channels and is not linked to any other ion.

298
Q

What does aldosterone do, and how does aldosterone work?

A

Promotes Na+ retention and K+ excretion & H+

Priniciple cell:
Increases the amount of Na+ and K+ channels in the luminal membrane, also promotes Na+/K+ ATPase activity in the basolateral membrane

Intercalated cell:
Increase the Na+/H+ symporter

299
Q

Examples of aldosterone antagonists? what type of diuretic are they?

A

Spironolactone, they are potassium sparing diuretics.

300
Q

What factors affect aldosterone action?

A

High [PGE₂] inhibits Na+/K+ ATPase

it is produced by endothelia and ANP

301
Q

What are the main actions of Natriuretic peptides?

Examples?

A

Mostly oppose the actions of the RAAS pathway.

ANP - atrial natriuretic peptide
BNP - brain natriuretic peptide

302
Q

Problems with hypo/hyperkalaemia?

A

Hyper - membrane potential increased, particularly crucial in the heart, causing sudden cardiac death syndrome

Hypo - Membrane potential decreased, causing muscle weakness and arrhythmia

303
Q

Causes of hypokalaemia?

A

Alkalosis

V&D

Diuretics

Eating Clay

304
Q

Causes of hyperkalaemia

A

Acidosis

Strenuous exercise

Inadequate hormonal control

305
Q

how do you calculate excretion?

A

[Urine] x vol / time

306
Q

What plasma protein has the highest concentration in the plasma?

A

Albumin.

307
Q

How are proteins reabsorbed in the PCT?

A

Epithelial cells in the PCT engulf the proteins through endocytosis

308
Q

What are healthy reasons why proteins are found in the urine?

A

Protein release in the tubule

Glomerular leakage (where the amount of protein exceeds the reabsorption capacity)

309
Q

What is tubular proteinuria?

A

When tubule-intestinal disease impair tubular function so that the tubule cannot reabsorb protein and it appears in the urine

310
Q

What is Overflow proteinuria?

A

Excess production of small proteins which are filtered at too great a quantity to be reabsorbed in the PCT.

311
Q

What is Glomerular proteinuria?

A

Reflects an increase in the permeability of the glomerulus to protein. Capillaries or the basement membrane may be damaged.

312
Q

Common causes of Glomerular Proteinuria?

A

Hypertension/Diabetes

313
Q

What is Nephrotic syndrome?

A

Umbrella term for an increase in the glomerular permeability to proteins

Associated with Salt and water retention and Hypoalbuminaemia causing oedema.

314
Q

What is microalbuminuria?

A

Albumin excretion of >30mg but less than 150mg a day

First indicator of Diabetic nephropathy

315
Q

What does a dipstick test test for?

A

Will test for proteinuria and will give positive if the urine is alkaline

316
Q

What do you do if a dipstick test is positive?

A

24hour urine collections or a albumin/creatinine ratio

317
Q

What would you define as a lower UTI?

A

Infection of bladder or urethra

318
Q

What’s cystisis?

A

Inflammation of the lining of the bladder

319
Q

What would you define as an uncomplicated UTI?

A

No co-morbidity (healthy people)

320
Q

Whats pyuria?

A

Raised white cell count in the urine.

321
Q

What’s an upper UTI?

A

Pyelonephritis (kidney infection)

322
Q

Formula for CO and BP?

A

CO = SV x HR

BP = CO x TPR

323
Q

What is starlings law of the heart?

A

Ventricular filling is proportional to SV by the increased contractility of the myocytes.

324
Q

What are the cardiac responses to a fast haemorrhage?

A

Increased sympathetic drive manages to maintain stroke volume through increased contractility, but decreases left atrial pressure

325
Q

Other cardiovascular responses to haemorrhage?

A

Vasoconstriction, Venoconstriction.

326
Q

Where does sympathetic vasoconstriction occur in response to haemorrhage?

A

Skin, Kidneys, GI tract and skeletal muscle

327
Q

Physiological advantage to venoconstriction?

A

Raised central venous pressure

Increased preload

Increased SV and CO

328
Q

At what percentage blood loss in a haemorrhage would it become likely to be fatal?

A

Above 30%

329
Q

During haemorrhage what happens to the net movement of fluid in capillaries? What is this called?

A

There is net movement into the capillary, due to decreased capillary hydrostatic pressure, Internal transfusion.

330
Q

What ways does the body raise blood pressure to maintain perfusion?

A

Internal transfusion

Baroreceptor response

331
Q

How does the body replace the volume of blood in the long term?

A

Salt and water retention.

RAAS, ADH, and thirst

332
Q

What does ANP do?

A

Promotes Na+ and water excretion (not an appropriate response to haemorrhage)

333
Q

What is decompensated (irreversible) shock?

A

Shock following >30% blood loss and a 3 hour delay in replacing fluids.

there is prolonged vasoconstriction in some organs leading to failure, e.g. kidney and liver

334
Q

Examples of replacement fluids?

A

Blood

Crystalloids

Colloids

335
Q

How does Dextrose/Colloids/saline work as a replacement fluid?

A

Colloids cannot move from blood vessels and will expand the fluid in blood vessels

Saline can move to the ECM and expand it

Dextrose can move into cells and will expand the ICM

336
Q

General signs of shock?

A

Weakness

Lethargy

Tachycardia

Cyanosis

337
Q

Definition of renal failure?

A

A decrease in GFR resulting in increased [creatinine] and [urea]

338
Q

What are the names for acute and chronic renal failure?

A

AKI (acute kidney injury)

Chronic Kidney Disease

339
Q

Is AKI defined by GFR or urine flow or both?

A

Only by GFR, not defined by urine flow (although it may decrease)

340
Q

What is oliguria and anuria?

A

Oliguria is less than 400ml/day

Anuria is less than 50ml/day

341
Q

Clinical signs of AKI?

A

Decline in GFR

Often oliguria

Rise in plasma [urea] and [creatinine]

342
Q

What are the three classifications of AKI?

A

Prerenal: before the nephron

Intrarenal: in the nephron

Postrenal: after the nephron

343
Q

What could cause Prerenal kidney injury?

A

Inadequate perfusion of the glomerulus

e.g. renal artery stenosis

hypotension

heart failure

344
Q

What are some examples of drug induced prerenal injury?

A

NSAID drugs: block PGE2 induced dilation of afferent arteriole

ACE/AT1 receptor antagonists: Block constriction of efferent arteriole by Angiotensin II

345
Q

Causes of Intrarenal injury?

A

Acute tubular necrosis

Acute glomerulonephritis

endogenous or exogenous toxins

interstitial nephritis

346
Q

Two types of acute tubular necrosis?

A

Toxic

Ischaemic

347
Q

What happens in acute tubular ischaemia?

A

Occlusion or obstruction leads to ischaemia, which produces paradoxical vasoconstriction mediated by endothelins and involving Ca2+ and ROS

348
Q

A raised urea to creatinine ratio will often mean the condition is what type of AKI?

A

Pre-renal

349
Q

What are buffers?

A

Weak acids or bases

350
Q

What are the physiological buffers of the body?

A

Bicarbonate buffer

Proteins

Phosphate buffer

351
Q

Two types of acid produced in metabolism?

A

CO2 (blown off in lungs)

Metabolic acids taken away by the kidneys

352
Q

Examples of metabolic acids are produced by the body?

A

Sulphuric acid

Phosphoric acid

Lactic acid

Ketone Bodies

353
Q

What Reaction does carbonic anhydrase catalyse?

A

CO2 + H2O = H2CO3

354
Q

What roles do the kidneys play in the acid/base balance?

A

Reabsorbs filtered bicarbonate

Excretes excess acid

Generates new bicarbonate

355
Q

How does reabsorption of filtered bicarbonate occur in the PCT?

A

The Na from the HCO3- & Na+ gets pumped into the epithelium and the Na+ is replaced by H+ to make H2CO3.

This is then converted into H20 and CO2 by carbonic anhydrase. The CO2 diffuses back into the epithelium and can then be used to make H2CO3 again and be pumped out.

356
Q

How does excess acid excretion occur in the DCT?

A

In the distal nephron H2O and CO2 is also converted to H2CO3 where H+ is secreted into the lumen and HCO3 is secreted into the interstitium

357
Q

How is the excreted H+ in the urine buffered?

A

Phosphate

ammonia

358
Q

Does aldosterone cause secretion or reabsorption of H+?

A

secretion

359
Q

Four different types of acid/base disturbances in the body?

A

Respiratory acidosis

Respiratory alkalosis

Metabolic acidosis

Metabolic alkalosis

360
Q

Causes of metabolic acidosis?

A

Increased acid intake

Increased metabolic acid production

Increased GI loss of bicarbonate

Decreased acid excretion

361
Q

Causes of metabolic alkalosis?

A

Increased alkali intake

Increased loss of H+

Increased HCO3 generation in kidneys

362
Q

What does a proportionate change in PaCO2 and HCO3 suggest?

what does a disproportionate change suggest?

A

Proportionate: respiratory acid base imbalance

Disproportionate: metabolic imbalance

363
Q

What is the base excess a measure of?

A

The change in [HCO3-] produced solely by the metabolic component of an acid-base disturbance.

364
Q

If the base excess is positive what does it mean?

A

Metabolic alkalosis

365
Q

If the base excess is negative what does that mean?

A

Metabolic acidosis

366
Q

Increased anion gap represents what?

A

Metabolic acidosis

RCR1 (11 decks)

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