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Respiratory System > Session 5 > Flashcards

Session 5 Flashcards

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1
Q

Define hypoxia.

A

Deficiency in the amount of oxygen reaching tissues.

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2
Q

Define hypocapnia.

A

Reduced carbon dioxide levels in the blood.

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3
Q

Define hypercapnia.

A

Increased carbon dioxide levels in the blood.

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4
Q

Define hyperventilation.

A

Increase in ventilation without a change in metabolism.

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5
Q

Define hypoventilation.

A

Decrease in ventilation without a change in metabolism.

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6
Q

What does hyperventilation cause?

A

Increase in pO2 and decrease in pCO2.

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7
Q

What does hypoventilation cause?

A

Decrease in pO2 and increase in pCO2.

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8
Q

What happens if pO2 rises without a change in pCO2?

A

pO2 is corrected physiologically which results in a reduction of pCO2, causing hypocapnia.

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9
Q

What is the normal range of values for blood pH?

A

7.35-7.45.

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10
Q

Briefly, what happens if blood pH becomes too low?

A

Enzymes begin to denature.

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11
Q

briefly, what happens if blood pH becomes too high?

A

Free calcium concentration drops causing tetany.

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12
Q

Describe the effect of hypoventilation on plasma pH.

A

Causes increased pCO2; hypercapnia causes reduced plasma pH; respiratory acidosis sets in.

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13
Q

Describe the effect of hyperventilation on plasma pH.

A

Causes decreased pCO2; hypocapnia causes increased plasma pH; respiratory alkalosis.

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14
Q

How are respiratory driven changes in plasma pH compensated?

A

By changing plasma bicarb concentration via the kidneys.

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15
Q

What causes metabolic acidosis?

A

Tissues produce more acid due to increased activity; acid reacts with bicarb in the plasma; [bicarb] decreases so pH falls; metabolic acidosis sets in.

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16
Q

How is metabolic acidosis compensated?

A

By increasing ventilation to reduce pCO2.

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17
Q

What innate barrier can cause metabolic alkalosis?

A

Vomiting as it causes increased plasma [bicarb].

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18
Q

How can metabolic alkalosis be compensated?

A

By decreasing ventilation.

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19
Q

Where are the sensors for respiratory control and what do they detect?

A

Pulmonary receptors detect stretch; joint and muscle receptors detect stretch and tension; central chemoreceptors in the brain medulla detect [H]; peripheral chemoreceptors in the carotid and aortic bodies detect [O2], [CO2] and [H].

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20
Q

Where is the control centre for respiration?

A

In the medulla of the brain.

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21
Q

What can the respiratory control centre affect to allow respiratory control?

A

Diaphragm; external intercostals and accessory muscles for inspiration; internal intercostals and abdominal muscles for expiration.

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22
Q

Which of the chemoreceptors involved i respiratory control are most sensitive to pCO2 changes?

A

Central chemoreceptors in the brain medulla.

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23
Q

Describe briefly how central chemoreceptors work.

A

Located in the brain ECF; respond to changes in CSF pH; CSF pH is controlled by the choroid plexus cells.

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24
Q

How is CSF pH determined?

A

By the ratio of [bicarb] to pCO2; CSF [bicarb] is fixed in the short term as it can’t penetrate the BBB; persisting changes in pH are corrected by the choroid plexus cells which change [bicarb].

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25
Describe how increased plasma pCO2 is detected by central chemoreceptors.
Increased plasma pCO2 drives CO2 across the BBB into the CSF; CSF [bicarb] is initially constant so CSF pH falls; chemoreceptors detect the decrease in pH.
26
What is the function of the choroid plexus?
Determines what pCO2 is associated with normal CSF pH so sets the control system to a particular pCO2.
27
Define hypoxaemic hypoxia.
Poor oxygenation in the lungs causing a low pO2 and low O2 sats.
28
Define anaemic hypoxia.
Hypoxia caused by insufficient Hb to carry O2.
29
What commonly causes anaemic hypoxia?
Anaemia or carbon monoxide poisoning.
30
Define stagnant hypoxia.
Hypoxia due to poor perfusion of tissues; may be local or global.
31
What are common causes of stagnant hypoxia?
Shock, peripheral vascular disease, etc.
32
Define cytotoxic hypoxia.
Hypoxia due to tissues being unable to utilise oxygen despite adequate oxygen delivery.
33
What is the normal range of blood oxygen saturation?
94-98%.
34
Below what oxygen saturation is tissue damage likely to occur?
Below 90%.
35
Define type 1 respiratory failure.
Low arterial pO2 and oxygen saturations but normal or low pCO2.
36
Define type 2 respiratory failure
Low arterial pO2 and oxygen saturations with elevated pCO2.
37
What is the underlying mechanism behind type 2 respiratory failure?
Failure of ventilation causing insufficient air to be moved in and out of the lungs.
38
What is the underlying mechanism behind type 1 respiratory failure?
Either poor diffusion across the alveolar membrane or ventilation-perfusion mismatching.
39
Give some common causes of type 2 respiratory failure.
Head injury, trauma, myasthenia gravis, flail rib segment, pneumothorax, PE, upper airway obstruction, severe acute asthma.
40
Give some common causes of chronic type 2 respiratory failure.
Myopathy, MND, kyphoscoliosis, lung fibrosis, late stage COPD.
41
What diffusion defects can cause respiratory failure?
Lung fibrosis, emphysema, etc.
42
Why does diffusion impairment usually cause type 1 respiratory failure?
Oxygen diffusion rate is less than CO2; O2 diffusion is impaired more easily; disease will affect oxygen but not CO2.
43
Why may pCO2 be lowered in type 2 respiratory failure?
Hypoxia stimulates peripheral chemoreceptors to increase ventilation so more CO2 will be removed and pCO2 falls.
44
What happens when ventilation perfusion ratio falls below 1?
pO2 falls and pCO2 rises; causes type 1 respiratory failure.
45
What causes V/Q mismatching?
Reduced ventilation to part of the lungs; reduced perfusion to part of the lungs.
46
How is respiratory failure managed?
Cause is treated. Oxygen therapy to improve hypoxia in type 1; type 2 may need ventilation due to hypercapnia.
47
How does hypoxia typically present?
Exercise intolerance; tachypnoea (seen as breathlessness); confusion (cerebral hypoxia); cyanosis.
48
What are the effects of chronic hypoxia?
Increased oxygen delivery: elevated Hb levels; increased 2-3-BPG levels. Hypoxic vasoconstriction of pulmonary arterioles causing: pulmonary hypertension; right heart failure; cor pulmonale.
49
What usually causes chronic hypercapnia?
COPD.
50
How is an increase in Hb levels brought about?
Kidneys increase erythropoietin secretion to stimulate erythropoiesis in bones, more RBCs are made so more Hb.
51
Which microbes are commensal in the upper respiratory tract?
Viridans streptococci, Neisseria spp., anaerobes, Candida sp.
52
What mechanisms does the respiratory tract have to defend against infection?
Muco-ciliary clearance; coughing; sneezing; respiratory mucosal immune system.
53
What usually causes upper respiratory tract infections?
Viruses such as rhinovirus or coronavirus, influenza, etc. May also be due to bacteria.
54
Give some examples of URT infections.
Rhinitis, pharyngitis, laryngitis, sinusitis, otitis media.
55
Give some examples of LRT infections.
Bronchitis, bronchiolitis, bronchiectasis, pneumonia, empyema, lung abcess.
56
What is bronchitis?
Inflammation of the medium sized airways (bronchi).
57
What are the common symptoms of acute bronchitis?
Cough, fever, more sputum, SOB.
58
What typically causes acute bronchitis?
Strep. pneumoniae, H. influenzae, M. catarrhalis.
59
How is acute bronchitis usually treated?
Chest physio and antibiotics.
60
What is pneumonia?
Inflammation of the lung alveoli due to infection.
61
How do pneumonia sufferers usually present?
Fever, cough, pleuritic chest pain, SOB, yellow sputum, malaise, nausea, vomiting.
62
How is pneumonia classified?
By clinical setting where it was acquired; presentation (acute/chronic); organism(bacterial, fungal, etc.); lung pathology (lobar, broncho-, interstitial, etc.).
63
What is pneumonitis?
Inflammation of the lung alveoli. May be with or without infection.
64
How may pneumonia appear histologically?
Fibrin rich exudate, neutrophil infiltration and macrophage infiltration in the affected tissues.
65
What are the risk factors for pneumonia?
Pre-existing lung disease, immunocompromisation, travel history, exposure to animals, ventilation.
66
What organisms usually cause community-acquired pneumonia?
Strep. pneumoniae, H. influenzae, M. catarrhalis, Staph. aureus, K. pneumoniae. Mainly first 2.
67
What may be found on examination of pneumonia sufferers?
Pyrexia, tachycardia, tachypnoea, cyanosis, dullness of percussion, bronchial breathing, auscultative crackles.
68
What investigations should be performed for pneumonia patients?
FBC, U&E, CRP, ABG, CXR, sputum sample, blood cultures, BAL fluid sample, nose and throat swabs.
69
How is pneumonia managed?
Do CURB-65 score, if 2 ?admit, if 2-5 manage as severe.
70
What factors are taken into account in a CURB-65 score?
Confusion, urea conc, resp rate, blood pressure, age (over 65).
71
What is the empiric therapy for CAP pneumonia?
Amoxicillin/doxycycline/erythromycin/clarithromycin if mild to moderate illness. Co-amoxiclav and clarithromycin/doxycycline if moderate to severe illness.
72
What complications may result from bacterial pneumonia?
Lung abscess, bronchiectasis, empyema.
73
How is Strep. pneumoniae pneumonia treated?
Penicillin or amoxicillin.
74
What samples are usually taken in hospital acquired pneumonia and why?
Bronchial lavage fluid samples so URT and LRT bacteria can be distinguished.
75
How is hospital acquired pneumonia typically treated?
Co-amoxiclav as first line, if fails or in ITU use tazobactam/pipperacilin/meropenem.
76
What is aspiration pneumonia?
Pneumonia caused by aspiration of exogenous material or endogenous secretions into the RT.
77
Who is at increased risk of aspiration pneumonia?
Patients with neurological dysphagia, epilepsy, alcoholics, drowning victims, nursing home residents, drug overdose patients.
78
How is aspiration pneumonia treated?
Co-amoxiclav.
79
What causes aspiration pneumonia?
Viridans streptococci and anaerobes in a mixed infection.
80
How is pneumonia prevented?
Immunization wit flu vaccine/pneumococcal vaccine, chemoprophylaxis for at risk groups, smoking advice.

Respiratory System (9 decks)

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