Brainscape's Knowledge GenomeTM

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


See full index

12. Respiratory > 5. Control of Breathing > Flashcards

5. Control of Breathing Flashcards

1
Q

What is hypoxia?

A

A fall in alveolar, and thus arterial pO2.

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

What is hypercapnia?

A

A rise in alveolar, thus arterial, CO2.

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

What is hypocapnia?

A

A fall in alveolar, thus arterial CO2.

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

What is hyperventilation?

A

Ventilation increases with no change in metabolism.

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

What is hypoventilation?

A

Ventilation decreases with no change in metabolism.

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

How are pCO2 and pH affected by hyperventilation?

A

pCO2 decreases, pH increases.

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

How are pCO2 and pH affected by hypoventilation?

A

pCO2 increases, pH decreases.

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

What is respiratory acidosis caused by?

A

Hypercapnia from hypoventialtion so pH falls below 7.0.

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

What is the risk with respiratory acidosis?

A

Enzymes can become lethally denatured.

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

What is respiratory alkalosis caused by?

A

Hypocapnia from hyperventilation so pH rises about 7.6.

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

What is the risk with respiratory alkalosis?

A

Free calcium concentration can fall enough to produce fatal tetany and nerves become hyper-excitable.

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

What is respiratory acidosis?

A

CO2 is produced more rapidly than it is removed by lungs, hypoventilation. Alveolar pCO2 rises, so dissolved [CO2] rises more than [HCO3-] and plasma pH drops.

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

What is compensated respiratory acidosis?

A

Respiratory acidosis persists and the kidneys respond to low pH by reducing excretion of HCO3- so the ratio of [CO2] to [HCO3-] is restored and thus the pH is restored.

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

What is respiratory alkalosis?

A

CO2 is removed from alveoli more rapidly than it is produced, hyperventilation. Alveolar pCO2 fall and the ratio of [CO2] to [HCO3-] is disturbed to raise pH.

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

What is compensated respiratory alkalosis?

A

Respiratory alkalosis persists so the kidneys respond to high pH by excreting HCO3-, the ratio of [CO2] to [HCO3-] is restored and therefore the pH is restored.

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

What is metabolic acidosis?

A

Metabolic production of acid displaces HCO3- from plasma as the acid is buffered, therefore the pH of blood falls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is compensated metabolic acidosis?

A

The ratio of [CO2] to [HCO3-] is restored to near normal by lowering pCO2 by increasing ventilation. This corrects the pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is metabolic alkalosis?

A

Plasma [HCO3-] rises, causing the pH of blood to rise.

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

Give an example of a cause of metabolic alkalosis.

A

Vomiting.

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

What is compensated metabolic alkalosis?

A

The ratio of [CO2] to [HCO3-] is restored by raising pCO2 by decreasing ventilation to correct pH.

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

What is falling arterial pO2 detected by?

A

Peripheral chemoreceptors in the carotid and aortic bodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do the peripheral chemoreceptors in the carotid and aortic bodies respond to?

A

Decrease in oxygen supply relative to their own small oxygen supply, so respond to large drops in O2.

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

What is the result of stimulation of the peripheral chemoreceptors?

A

Increases the tidal volume and rate of respiration, changes in circulation to direct more blood to the brain and kidneys, increased pumping of blood by the heart.

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

What are the peripheral chemoreceptors in the carotid and aortic bodies fairly insensitive to?

A

Changes in pCO2.

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

What detects changes in pCO2?

A

Central chemoreceptors in the medulla of the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do central chemoreceptors respond to a small rise in pCO2?

A

Increase ventilation.

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

How do central chemoreceptors respond to a small fall in pCO2?

A

Decrease ventilation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Summarise the negative feedback central control of breathing.

A

pCO2 rises, central chemoreceptors stimulate ventilation, more CO2 is blown off and pCO2 returns to normal and vice versa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What do central chemoreceptors respond to?

A

Changes in pH of cerebro-spinal fluid.

30
Q

How is cerebro-spinal fluid [HCO3-] controlled?

A

By choroid plexus cells.

31
Q

Why does [HCO3-] and [H+] in the cerebro-spinal fluid need separate controlling?

A

Because of blood brain barrier, HCO3- and H+ can’t cross the barrier but CO2 can so CSF pCO2 is determined by arterial pCO2.

32
Q

What determines the pH of the cerebro-spinal fluid?

A

The ratio of [HCO3-] to pCO2.

33
Q

What is the result of short term falls in pCO2 on CSF?

A

Increased pH as HCO3- is fixed.

34
Q

What is the result of short term rises in pCO2 on CSF?

A

Decreased pH as HCO3- is fixed.

35
Q

How can persisting changes of pCO2 in CSF be compensated for?

A

Via the choroid plexus cells that alter CSF [HCO3-].

36
Q

What is hypoxia?

A

A fall in alveolar, thus arterial pO2.

37
Q

How is respiratory failure defined numercially?

A

Arterial pO2 that falls below 8kPa when breathing air at sea level.

38
Q

What is type I respiratory failure?

A

Arterial hypoxia, accompanied by normal or low pCO2.

39
Q

What are the signs and symptoms of type I respiratory failure?

A

Breathlessness, exercise intolerance, central cyanosis.

40
Q

What is type II respiratory failure?

A

Arterial hypoxia, accompanied by an elevated pCO2.

41
Q

How can low pO2 in inspired air cause respiratory failure?

A

At high altitudes, everything else is normal except the air breathed in has less O2.

42
Q

How can hypoventilation cause respiratory failure?

A

Associated with increased pCO2. Neuromuscular problems, chest wall problems (mechanical), or hard to ventilate lungs lead to less air breathed in.

43
Q

How can diffusion impairments cause respiratory failure?

A

O2 diffuses much less readily than CO2 so type I. Structural changes (lung fibrosis), increased path length (oedema), or total area for diffusion reduced (emphysema) lead to diffusion impairment.

44
Q

What type of respiratory failure is ventilation perfusion mismatch?

A

Type I as pCO2 is low/normal.

45
Q

What can cause ventilation perfusion mismatch?

A

Reduced ventilation of some alveoli from lobar pneumonia, reduced perfusion of some alveoli from pulmonary embolism.

46
Q

What congenital heart defect could lead to respiratory failure?

A

Cyanotic heart diseases like tetralogy of Fallot causes abnormal right to left cardiac shunting.

47
Q

What will the blood gas results be for type I respiratory failure?

A

Increased respiratory rate, decreased pO2, normal CO2.

48
Q

What will the blood gas results be for type II respiratory failure?

A

Increased respiratory rate, decreased pO2, and increased CO2.

49
Q

What is asthma?

A

A chronic disorder characterised by airway wall inflammation and remodelling. It is a reversible airflow obstruction.

50
Q

What happens to the airways in asthma?

A

Thickened smooth muscle and basement membrane.

51
Q

What effect do asthma triggers have on the airways?

A

Cause smooth muscle contraction, which reduces airway radius and increases resistance so airflow is reduced.

52
Q

How many people in the UK receive treatment for asthma currently?

A

5.4 million people.

53
Q

How is asthma diagnosed?

A

Clinically. Look at the symptoms: wheeze, cough, breathlessness, chest tightness, variable airflow obstruction.

54
Q

What are the characteristics of a wheeze in asthma?

A

High pitched, expiratory sound. It originates in airways which have been narrowed by compression or obstruction. It has variable intensity and tone.

55
Q

What are the characteristics of a cough in asthma?

A

Often worse at night, exercise induced, dry cough.

56
Q

What brings on breathlessness in asthma?

A

Exercise.

57
Q

What does inspection of the chest in asthma show?

A

Chest may have hyper-expansion (Barrel chest), may have eczema or hay-fever.

58
Q

What will the percussion of asthmatic chest be?

A

Hyper-resonant.

59
Q

What will auscultation of asthmatic chest be?

A

Polyphonic wheeze.

60
Q

Which tests can assess the condition of a patient with suspected asthma?

A

Spirometry flow volume loop, allergy testing, chest X ray.

61
Q

How is spirometry used to assess potentially asthmatic patients?

A

Low PEFR, low FEV1/FEC ratio, >12% in FEV1 following salbutamol.

62
Q

How is allergy testing used to assess potential asthmatic patients?

A

Skin prick to aero-allergen and blood IgE levels to specific aero-allergens.

63
Q

Why are potentially asthmatic patients given chest X rays?

A

To exclude other diseases.

64
Q

What are the inflammatory results of asthma?

A

Mast cells are increased in asthma and release prostaglandins, histamine, etc. Eosinophils are found highly in the bronchial wall and secretions of asthmatics. Dendritic cells and lymphocytes are prevalent due to their roles in uptake, presentation, and destruction of foreign matter.

65
Q

How are the airways remodelled in asthmatic patients?

A

Epithelium is stressed and damaged so loses ciliated columnar cells. Basement membrane has deposits of collagens so thickens. Smooth muscle undergoes hyperplasia causing thickening of the muscle wall.

66
Q

What are the precipitating factors for asthmatic attacks?

A

Lack of treatment adherence, respiratory virus infections associated with the common cold, exposure to allergen of triggering drugs (e.g. NSAIDs).

67
Q

Why is education important with asthmatic patients?

A

Patients should be able to recognise their symptoms and use their medications timely, and appropriately.

68
Q

What are the primary preventions of asthma?

A

Stop smoking, fresh air, reduce exposure to allergens/ triggers, and weight loss.

69
Q

What is involved in pharmacological management of asthma?

A

B2-adrenoagonists and anti-inflammatory agents.

70
Q

How do B2-adrenoagonists work in asthma?

A

They are muscarinic antagonists so provide short term relief.

71
Q

What is an example of a B2-adrenoagonist used in asthma?

A

Salbutamol.

72
Q

How are anti-inflammatory agents used in asthma?

A

As preventer therapy.

12. Respiratory (10 decks)

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