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Medicine Sem 2 > Case 1 > Flashcards

Case 1 Flashcards

1
Q

what percentage of air movement does diaphragmatic and external intercostal muscle contraction count for at rest?

A
  • diaphragmatic contraction accounts for 75% of the air movement in normal breathing at rest
  • contraction of external intercostal muscles accounts for 25% of volume of air in lungs at rest
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2
Q

contraction of the scalene muscles causes an increase in which diameter?

A

anteroposterior diameter

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3
Q

what happens in forced inspiration?

A
  • contraction of the accessory muscles assist the external intercostal muscle in elevating the ribs
  • these muscles increase the speed and amount of rib movement
  • the accessory muscles include: sternocleidomastoid, scalene muscles (anterior and medius), serratus anterior and pectoralis minor
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4
Q

what happens during inspiration?

A
  • root of the lungs descends and the level of the bifurcation of the trachea may be lowered by as much as two vertebrae
  • the bronchi elongate and dilate and the alveolar capillaries dilate, thus assisting the pulmonary circulation
  • air is drawn into the bronchial tree as a result of the posterior atmospheric pressure exerted through the upper part of the respiratory tract and the negative pressure on the outer surface of the lungs brought about by the increased volume of the thoracic cavity
  • with expansion of lungs, the elastic tissue in the bronchial walls and connective tissue are stretched
  • as the diaphragm descends, the costodiaphragmic recess of the pleural cavity opens and the expanding sharp lower edges of the lungs descend
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5
Q

why does elastic recoil of the lungs happen?

A
  • because of the elastic fibres in the connective tissue of the lungs and because of the surface tension of the film of fluid that lines the alveoli
  • as water molecules pull together, they also pull on the alveolar walls causing the alveoli to recoil and become smaller
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6
Q

what are the two factors that prevent the lungs from collapsing?

A
  • surfactant (reduce surface tension)

- interpleural pressure

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7
Q

what happens during forced expiration?

A
  1. the internal (and innermost) intercostal muscles and the transversus thoracis muscles depress the ribs and reduce the width and depth of the thoracic cavity
  2. the abdominal muscles:
    - external and internal oblique, transversus abdominis and rectus abdominis muscles can assist the internal intercostal muscles in exhalation by compressing the abdomen and forcing the diaphragm upwards
  3. forcible contraction of the muscles of the anterior abdominal wall
  4. quadratus lumborum also contracts to pull down the 12th rib
  5. serratus posterior inferior and the latissimus dorsi muscles also play a minor role
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8
Q

what happens in expiration?

A
  • roots of the lungs ascend
  • bifurcation of the trachea ascends
  • bronchi shorten and contract
  • elastic tissue of the lungs recoils and the lungs become reduced in size
  • diaphragm moves upwards
  • the lower margins of the lung shrink and rise
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9
Q

describe the voluntary and involuntary components of respiratory control

A

involuntary:

  • the involuntary respiratory centres regulate the activities of the respiratory muscles involved in quiet respiration
  • they control the respiratory volume by adjusting the frequency and depth of pulmonary ventilation

voluntary:
this reflects the activity in the cerebral cortex that affects either
- the output of the respiratory centres in the medulla oblongata and pons
- the motor neurons in the spinal cord that control respiratory muscles

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10
Q

what are the respiratory centres?

A

three pairs of nuclei (clusters of nerve cell bodies) in the medulla oblongata and pons

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11
Q

what are the respiratory centres of the medulla oblongata?

A
  1. dorsal respiratory group (DRG)

2. ventral respiratory group (VRG)

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12
Q

describe the DRG

  • where’s it located
  • what does it control
  • with which nerves
A
  • located in the dorsal portion of the medulla oblongata
  • DRG controls mostly inspiratory movements and their timing
  • it controls both quiet and forced inspiration

DRG’s inspiratory centre controls:

  • the phrenic nerve which innervates the diaphragm
  • the intercostal nerves which innervate the external intercostal muscles
  • nerves which innervate the accessory respiratory muscles involved in maximal inhalation (scalene muscles, sternocleidomastoid, serratus anterior and pectoralis minor)
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13
Q

describe the ventral respiratory group (VRG)

A
  • located in the ventrolateral part of the medulla
  • mainly causes forced expiration

VRG’s expiratory centre controls:

  • the intercostal nerves which innervate the internal (and innermost) intercostal muscles
  • nerves which innervate the accessory respiratory muscles involved in active exhalation (abdominal muscles mainly)

VRG’s inspiratory centre aids the DRG during forced inspiration - this centre controls:

  • nerves which innervate the accessory respiratory muscles involved maximal inhalation (scalene muscles, sternocleidomastoid, serratus anterior and pectoralis minor)
  • when the respiratory drive for increased pulmonary ventilation becomes greater than normal, respiratory signals spill over the VRG from the DRG
  • this activates the inspiratory centre of the VRG, allowing it to innervate the accessory respiratory muscles of forced inspiration
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14
Q

describe the inspiratory ‘ramp’ signals in normal respiration

A

the signals sent from the respiratory centres to the respiratory muscles occur in bursts of action potentials

1) The signals begin weakly and increase steadily in a ramp manner for about 2 seconds, providing the stimulation to the inspiratory muscles (inhalation occurs).
2) Then, the signals cease abruptly for approximately the next 3 seconds, which turns off the excitation of the diaphragm and allows elastic recoil of the lungs and the chest wall to cause expiration (passive exhalation occurs).
3) Next, the inspiratory signal begins again and this cycle repeats again, with expiration occurring in between.

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15
Q

what is the advantage of the ‘ramp’?

A

causes a steady increase in the volume of the lungs during inspiration, rather that inspiratory gasps

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16
Q

describe what happens to the ramps in deep breathing and faster breathing

A

Deep breathing:

  • the signals become stronger more quickly
  • the rate of increase of the ramp signal is faster

Faster breathing:

  • the signals start and cease earlier
  • the ramps are less than 2 seconds
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17
Q

what are the respiratory centres of the pons? and what do they do?

A

apneustic centres and penumotaxic centres of the pons adjust the output of DRG and VRG
- their activities regulate the respiratory rate and depth of respiration in response to stimuli or other centres in the brain

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18
Q

what are the stimuli or other centres in the brain that they respond to?

A

stimuli: impulses from receptors around the body are carried via the vagus or glossopharyngeal nerves to eh respiratory centres
other centres: these include hypothalamus or the cerebrum

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19
Q

describe apneustic centres

  • where’s it located
  • what does it do
  • what does it coordinate
  • how is it inhibited
A
  • located in the lower pons
  • provides continuous stimulation to the DRG, resulting in a long, deep inhalation
  • continuous stimulation builds the ramp signal during quiet inspiration
  • it coordinates transition between inhalation and exhalation
  • under normal conditions, after the 2 seconds, the apneustic centre is inhibited by the pneumotaxic centre on the same side
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20
Q

describe pneumotaxic centres

  • where
  • what does it do
  • what alters activity
A
  • located in the upper pons
  • this inhibits the aponeustic centre - it controls the ‘switch-off’ point of the ramp signal, thus limiting inspiration
  • centres in the hypothalamus and cerebrum can alter the activity of the pneumotaxic centres, as well as the respiratory rate and depth
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21
Q

the activities of the respiratory centres are modified by sensory information from several sources - what are these?
(respiratory reflexes)

A
  • chemoreceptor
  • baroreceptors: changes in blood pressure
  • stretch receptors: changes in volume of the lungs
  • irritating physical/chemical stimuli in the nasal cavity, larynx or bronchial tree
  • other sensations: pain, changes in body temperature and abnormal visceral sensations
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22
Q

what does excess carbon dioxide or excess hydrogen ions and oxygen act on?

A
  • Excess carbon dioxide or excess hydrogen ions in the blood mainly act directly on the respiratory centre itself, causing greatly increased strength of both the inspiratory and the expiratory motor signals to the respiratory muscles
  • Oxygen in contrast acts almost entirely on peripheral chemoreceptors located in the carotid and aortic bodies, and these in turn transmit appropriate nervous signals to the respiratory center for control of respiration
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23
Q

describe the direct chemical control of respiratory centre by H+ ions and CO2

A
  • A chemosensitive area is located bilaterally, lying beneath the ventral surface of the medulla.
  • This area is highly sensitive to changes in either blood PCO2 or hydrogen ion concentration, and it in turn excites the other portions of the respiratory centre.
  • Carbon dioxide has little direct effect in stimulating the neurons in the chemosensitive area.
  • Hydrogen ions have a direct effect in stimulating the neurons in the chemosensitive area.
  • However, hydrogen ions cannot pass through the blood-brain barrier.
  • Carbon dioxide can cross the blood-brain barrier.
  • Carbon dioxide crosses the barrier and reacts with the water of the tissues to form carbonic acid, which dissociates into hydrogen and bicarbonate ions; the hydrogen ions then have a direct stimulatory effect on the chemosensitive area in the brain.
  • Therefore, more hydrogen ions are released into the respiratory chemosensitive sensory area of the medulla when the blood carbon dioxide concentration increases than when the blood hydrogen ion concentration increases.
  • For this reason, respiratory centre activity is increased very strongly by changes in blood carbon dioxide.
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24
Q

explain the regulation of respiration during exercise and what causes it

A
  • In strenuous exercise the arterial PCO2, pH and PO2 remain almost exactly normal.
  • Therefore, the increased ventilation doesn’t occur as a result of alterations in the arterial PCO2, pH or PO2.
  • It is likely that most of the increase in respiration results from neurogenic signals transmitted directly into the brain stem respiratory centre at the same time that signals go to the body muscles to cause muscle contraction.
  • The onset of exercise, the alveolar ventilation increases instantaneously, without an initial increase in arterial Pco2. In fact, this increase in ventilation is usually great enough so that at first it actually decreases arterial Pco2 below normal. The presumed reason that the ventilation forges ahead of the build-up of blood carbon dioxide is that the brain provides an “anticipatory” stimulation of respiration at the onset of exercise, causing extra alveolar ventilation even before it is needed.
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25
Q

where are peripheral chemoreceptors located? and what are they important for?

A
  • Located outside the brain.
  • Important for detecting changes in oxygen levels in the blood.
  • Transmit nervous signals to the respiratory centres in the brain.
  • Carotid bodies: found in the carotid arteries. Their nerve fibres pass through the glossopharyngeal nerves and then to the dorsal respiratory area.
  • Aortic bodies: found in the arch of the aorta. Their nerve fibres pass through the vagi, also to the dorsal respiratory area.
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26
Q

which nerves do carotid bodies and aortic bodies send information through to the dorsal respiratory area?

A

Carotid bodies = glossopharyngeal nerves

Aortic bodies = vagi nerves (A and V look similar)

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27
Q

where are stretch receptors located?

A

Located in the muscular portions of the walls of the bronchi and bronchioles throughout the lungs

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28
Q

through which nerve do stretch receptors send information through and to where? and when?

A

through the vagus nerve into the dorsal respiratory group of neurons when the lungs become over stretched

  • when the lungs become over inflated, the stretch receptors activate an appropriate feedback response that ‘switches off’ the inspiratory ramp and thus stops further inspiration
  • Hering-Breuer inflation reflex - this reflex also increases the rate of respiration
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29
Q

local regulation of gas transport and alveolar function:

  • what happens when there’s a rising PCO2 in normal tissue
  • what happens in alveolar capillaries
  • what happens in bronchioles
A
  • The rising Pco2 relaxes smooth muscle in walls of arteries and capillaries, causing vasodilation and so increasing blood flow
  • In alveolar capillaries, blood is directed where Po2 is relatively high, this occurs because alveolar capillaries constrict when local Po2 is low
  • In bronchioles, oxygen is directed towards lobules where Pco2 is high, because these lobules are actively engaged in gas exchange - this occurs because smooth muscle in the bronchioles bronchodilate when Pco2 is high
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30
Q

what are causes of hypoxia?

A
  1. Inadequate oxygenation of the blood in the lungs because of extrinsic reasons
     - Deficiency of oxygen in the atmosphere
     - Hypoventilation (neuromuscular disorders)
  2. Pulmonary disease
     - Hypoventilation caused by increased airway resistance or decreased pulmonary compliance
     - Abnormal alveolar ventilation – perfusion ratio
     - Diminished respiratory membrane diffusion
  3. Venous-to-arterial shunts (“right-to-left cardiac shunts”) – allows blood to flow from the right heart to the left heart
  4. Inadequate oxygen transport to the tissues by the blood
     - Anaemia or abnormal haemoglobin
     - General circulatory deficiency
     - Localized circulatory deficiency (peripheral, cerebral, coronary vessels etc)
     - Tissue oedema
  5. Inadequate tissue capability of using oxygen
     - Poisoning of cellular oxidation enzymes (cyanide poisoning)
     - Diminished cellular metabolic capacity for using oxygen, because of toxicity, vitamin deficiency, or other factors
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31
Q

what causes cyanosis?

A
  • caused as a result of excessive amounts of deoxygenated haemoglobin in the skin blood vessels
  • this deoxygenated blood has an intense dark blue-purple colour that is transmitted through the skin
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32
Q

what is pleural pressure? and what is it normally?

A
  • the pressure of the ‘fluid’ in the pleural cavity

- normally it is slightly negative and becomes more negative during inspiration

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33
Q

when is the pressure in all parts of the respiratory tree equal to atmospheric pressure? and what is this considered to be?

A
  • when the glottis is open and no air is flowing into or out of the lungs
  • considered to be zero reference pressure in the airways - that is, 0 cmH2O
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34
Q

the slight negative pressure of -1 cmH2O is enough for what to happen?

A

enough to pull 0.5 litres of air into the lungs in the 2 seconds required for normal quiet inspiration

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35
Q

what does work of breathing depend on?

A
  • Tidal volume: increased tidal volume = more work done by the lungs
  • Respiratory frequency: increased frequency = more work done by the lungs
  • Lung compliance: increased compliance = less work done by the lungs
  • Airways resistance: increased resistance = more work done by the lungs
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36
Q

equation for airflow?

A

change in pressure/airways resistance

change in pressure = Palv - Patm

airways resistance is proportional to length/radius^4

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37
Q

how does length affect airway resistance?

A

the longer the airway, the greater the airways resistance

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38
Q

what is surfactant? what is it secreted by? and what’s it composed of?

A
  • This is a surface active agent in water, which means that it greatly reduces the surface tension of water.
  • It is secreted by special surfactant-secreting epithelial cells called type II alveolar epithelial cells, which constitute about 10% of the surface area of the alveoli.
  • Surfactant is a complex mixture of several phospholipids, proteins, and ions.
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39
Q

what is the clinical presentation of pneumothorax?

A
  • sudden onset of unilateral pleuritic pain
  • progressively increasing breathlessness
  • if the pneumothorax enlarges, the patient becomes more breathless and may develop pallor and tachycardia
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40
Q

what are the 4 types of pneumothorax?

A
  1. primary spontaneous pneumothorax
  2. secondary spontaneous pneumothorax
  3. traumatic pneumothorax
  4. tension pneumothorax
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41
Q

what is the most common type of pneumothorax?

A

primary spontaneous pneumothorax

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42
Q

primary spontaneous pneumothorax:

  • cause
  • what happens
  • whose usually affected
  • male to female ratio
  • outcome
  • risk factors
  • treatment
A
  • caused by rupture of a small subpleural emphysematous bulla or pulmonary bleb (usually apical)
  • thought to be due to congenital defects in the connective tissue
  • this is a weakness and out-pouching of the lung tissue, which can rupture
  • this introduces air into the pleural space, causing the lung to start collapsing
  • as the lung collapses, the hole formed by the ruptured bleb seals, preventing more air from entering the intrapleural cavity
  • tall, thin, young men (20-40 years) with no underlying disease usually affected
  • in patient over 40 years, the usual cause is underlying COPD
  • male: female ratio = 5:1
  • rarely causes significant physiological disturbance
  • at higher risk if already had one spontaneous pneumothorax
  • risk factor: smoking
  • treatment: pleurodesis (needle aspiration and chest drain) to fuse visceral and parietal pleura by medical (bleomycin/talc) or surgical (abrasion of pleural lining)
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43
Q

secondary spontaneous pneumothorax:

  • seriousness
  • cause
  • most at risk group
A
  • much more deadly
  • caused by respiratory diseases that damage lung structure: most commonly COPD and asthma, infective diseases (pneumonia), rarely inherited diseases
  • incidence increases with age and severity of underlying disease
  • usually occurs in males >55 years
  • ICU patients with lung disease are at a particular risk due to high presses (barotrauma) and alveolar distention (volutrauma) associated with mechanical ventilation
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44
Q

traumatic pneumothorax:

  • causes
  • what happens
  • flow of air
  • often associated with what
A
  • blunt or penetrating chest trauma
  • gas may enter the intrapleural space either from the atmosphere through a hole in the chest wall or from alveoli through a hole in the lung
  • flow of air is two way
  • therapeutic procedures such as line insertion or thoracic surgery are common causes
  • traumatic pneumothorax can usually be associated with haemothorax
45
Q

tension pneumothorax:

  • when most common
  • air flow
  • specific symptoms
  • treatment
A
  • most common during mechanical ventilation/following traumatic pneumothorax
  • flow of air is one way (from the lung into the pleural cavity) upon inspiration - the air from the atmosphere enters the pleural cavity (from the stab wound) down the pressure gradient
  • upon expiration, the air can’t escape from the pleural cavity and remains trapped there because the pleural pressure doesn’t increase above the atmospheric pressure
  • every inspiration results in a build-up of air and pressure
  • specific symptoms: cyanosis, severe breathlessness
  • treatment: needle aspiration and chest drain
46
Q

what is the most consistent clinical finding for pneumothorax?

A

a reduction in breath sounds on the affected side

47
Q

how does pneumothorax affect percussion?

A

note will be resonant

48
Q

how do you diagnose pneumothorax?

A
  • Examination of the chest with a stethoscope reveals decreased or absent breath sounds over the affected lung.
  • The diagnosis is confirmed by chest x-ray.
  • An x-ray can illustrate the collapse of the lung as extra black space, indicating the presence of air, will be seen in the x-ray around the lung.
  • In tension pneumothorax, the lung shrivels up away from the affected side and the mediastinum (trachea and other components) will shift towards the unaffected side – trachea displacement.
  • The combination of absent breath sounds and resonant percussion is diagnostic of pneumothorax.
49
Q

physical examinations for pneumothorax

A
  1. Inspection:
    - Patient looks distressed and is sweating.
    - Dyspnoea (SOB) may be apparent.
    - Cyanosis, depending on degree of respiratory inadequacy.
  2. Palpation:
    - Palpation may show affected side moves less than normal side. (air in intrapleural space allows ribcage to expand outwards)
  3. Percussion:
    - Affected side sounds hyperresonant (sound similar to percussion of puffed cheeks).
  4. Auscultation:
    - Breath sounds on the affected side are diminished.
    - This is because less gas enters the collapsed lung during inspiration, air in intrapleural space acts as a barrier to the transmission of sounds from lungs to the chest wall.
  5. Trachea displaced away from side of collapsed lung in tension pneumonia.
  6. Pulse Examination
    • Tachycardia common, pulse rate >135 beats per minute suggests tension pneumothorax.
    • Pulsus paradoxicus (slow pulse on inspiration) suggests severe pneumothorax
  7. Monitoring reveals hypotension and desaturation (less oxygen being carried in the blood)
50
Q

what to look at on an X-ray?

A 
A = airways 
B = breathing and bones 
C = cardiac 
D = diaphragm 
E = everything else
51
Q

what is the treatment for primary pneumothorax?

A 
small = observe 
moderate = aspirate 
complete = aspirate / chest drain
52
Q

what is the treatment for all other pneumothoraxes?

A

chest drain

53
Q

difference between treatment of tension pneumothorax and a small PSP?

A
  • a tension pneumothorax must be drained immediately

- a small PSP can be managed by observation using clinical assessment and chest X-ray

54
Q

what is a chest drain?

A

plastic tubing inserted into the intrapleural space through a small incision

55
Q

how does a chest drain work?

A
  • as pressure in intrapleural space becomes positive (during coughing/forced expiration), air passes along chest drain and out to the atmosphere through the underwater seal, pneumothorax is drained
  • bubbles appear in the underwater seal until the hole in the pleura has sealed
  • after the hole has healed, the water level will rise and fall slowly and the chest drain can be removed
56
Q

What is the primary ATLS survey?

A

Airway maintenance with cervical spine protection:

  • ensure airway is clear and patient can breathe
  • neck and cervical spine must be maintained in the neutral position to prevent secondary injuries to the spinal cord

Breathing and ventilation:

  • chest examination by inspection, palpation, percussion and auscultation
  • life-threatening injury like tension pneumothorax must be identified
Circulation with Haemorrhage Control:
- external bleeding must be controlled
- internal bleeding must be diagnosed
	
Disability and Neurologic status:
- neurological assessment is made
	
Exposure and Environment:
- patient should be completely undressed, usually by cutting off the garments
- privacy maintained
- cover the patient with warm blankets to prevent hypothermia
- intravenous fluids should be warmed and a warm environment maintained
57
Q

describe the secondary survey of ATLS

A
  • This begins when the primary survey is completed, resuscitation efforts are well established, and the vital signs are normalizing.
  • It is a head-to-toe evaluation of the trauma patient, including a complete history and physical examination, including the reassessment of all vital signs - each region of the body must be fully examined.
  • If at any time during the secondary survey the patient deteriorates, another primary survey is carried out as a potential life threat may be present.
  • The person should be removed from the hard spine board and placed on a firm mattress as soon as feasible, as the spine board can rapidly cause skin breakdown and pain while a firm mattress provides equivalent stability for potential spinal fractures.
58
Q

what are all preganglionic neurones?

A

cholinergic = acetylcholine

59
Q

what are the postganglionic neurones?

A

most of the sympathetic are adrenergic = norepinephrine

almost all parasympathetic are cholinergic = acetylcholine

60
Q

what receptors does acetylcholine mainly activate?

A
  1. Nicotinic receptors - found in the autonomic ganglia at the synapses between the preganglionic and postganglionic neurons of both the sympathetic and parasympathetic systems
  2. Muscarinic receptors - found on all effector cells that are stimulated by the postganglionic cholinergic neurons of the parasympathetic nervous system.
61
Q

what are the two major types of adrenergic receptors?

A
  1. Alpha receptors
    Alpha 1:
    - Found in the walls of blood vessels.
    - Upon activation, cause smooth muscle contraction.
    - Vasoconstriction and vasodilation are controlled by the SNS. Stimulation of SNS causes vasoconstriction - less stimulation of SNS causes vasodilation.

    Alpha 2:
    • Inhibits adenylate cyclase – decreasing cAMP formation.
      - Negative feedback for the release of norepinephrine from the presynaptic neuron.
      - Inhibition of insulin release and induction of glucagon release in the pancreas.
  2. Beta receptors
    - All beta receptors stimulate adenylate cyclase

Beta 1:
- Located mainly in the heart - Increase cardiac output

Beta 2:
- Found mainly in the lungs – Bronchodilation.

Beta 3:
- Located in fat cells - Lipolysis in adipose tissue.

62
Q

what type of receptors are alpha and beta?

A

they are both G-protein coupled receptors (intracellular messengers)

63
Q

do norepinephrine and epinephrine excite alpha or beta receptors?

A
  • norepinephrine excites mainly alpha receptors and beta receptors to a lesser extent
  • epinephrine excites both types of receptors equally
64
Q

what is a form of stress?

A

any condition, physical or emotional, that threatens homeostasis is a form of stress

65
Q

what are the stages of a stress response?

A
  1. the alarm phase
  2. the resistance phase
  3. the exhaustion phase
66
Q

what happens during the alarm phase?

- what is the dominant hormone

A
  • During the alarm phase, an immediate response to the stress occurs.
  • This response is directed by the sympathetic nervous system.
  • Activation of the SNS causes increased secretion of adrenaline.
  • Adrenaline is the dominant hormone of the alarm phase, and its secretion accompanies a generalized sympathetic activation.

In the alarm phase:

  1. Energy reserves are mobilized, mainly in the form of glucose
  2. The body prepares to deal with the stress-causing factor by “fight or flight” responses
67
Q

what are characteristics of the alarm phase?

A
  1. Increased mental alertness.
  2. Increased energy use by all cells, especially skeletal muscles.
  3. Mobilization of glycogen (Hepatocytes perform glycogenolysis) and lipid reserves (adipose tissue cells perform lipolysis).
  4. Changes in circulation, including increased blood flow to skeletal muscles and decreased blood flow to the skin, kidneys, and digestive organs.
  5. A drastic reduction in digestion and urine production.
  6. Increased sweat gland secretion.
  7. Increases in blood pressure, heart rate, respiratory rate and metabolic rate.
  • Although the effects of adrenaline are most apparent during the alarm phase, other hormones play supporting roles.
  • In this phase, there is increased production of adrenaline and noradrenaline so that both the alpha and beta adrenergic receptors are activated with better efficiency.
  • For example, the reduction of water losses resulting from ADH production and aldosterone secretion can be very important if the stress involves a loss of blood.
68
Q

describe the resistance phase

- what hormones involved

A
  • If a stress lasts longer than a few hours, the individual enters the resistance phase of the stress response.
  • Glucocorticoids (cortisol) are the dominant hormones of the resistance phase.
  • Growth Hormone, ADH and glucagon are also involved.
  • Energy demands in the resistance phase remain higher than normal.
  • Neural tissue has a high demand for energy, and neurons must have a reliable supply of glucose. If blood glucose concentrations fall too far, neural function deteriorates.
  • Glycogen reserves are adequate to maintain normal glucose concentrations during the alarm phase, but are nearly exhausted after several hours. Therefore, alternate energy sources are sought for in the resistance phase.
  1. Mobilization of remaining lipid and protein reserves:
    - The hypothalamus produces GHRH, stimulating the release of GH and glucocorticoids.
    o Adipose tissue responds to GH and glucocorticoids by releasing stored fatty acids.
    o Skeletal muscles respond to glucocorticoids by breaking down proteins and releasing amino acids into the bloodstream.
  2. Conservation of glucose for neural tissues:
    - Glucocorticoids (cortisol) and GH stimulate lipid metabolism in peripheral tissues.
    o Peripheral tissue (except neural) breaks down lipids to obtain energy.
    - Neural tissues do not alter their metabolic activities, however, and they continue to use glucose as an energy source.
  3. Elevation and stabilization of blood glucose concentrations:
    - As blood glucose levels decline, glucagon and glucocorticoids (cortisol) stimulate the liver to manufacture glucose from other carbohydrates (glycerol) and from amino acids provided by skeletal muscles.
  4. Conservation of salts and water, and the loss of K+and H+:
    - Blood volume is conserved through the actions of ADH and aldosterone.
    - As Na+ is conserved, K+ and H+ are lost.
69
Q

when does the resistance phase end?

A

- If starvation is the primary stress, the resistance phase ends when lipid reserves are exhausted and structural proteins become the primary energy source.
- If another factor is the cause, the resistance phase ends due to complications brought about by hormonal side effects.

70
Q

describe the exhaustion phase

A

• When the resistance phase ends, homeostatic regulation breaks down and the exhaustion phase begins.
• Unless corrective actions are taken almost immediately, the failure of one or more organ systems will prove fatal.
• Mineral imbalances contribute to the existing problems with major systems.
 - The production of aldosterone throughout the resistance phase results in a conservation of Na+ at the expense of K+.
 - As the body’s K+ content declines, a variety of cells—notably neurons and muscle fibers—begin to malfunction.
 - Although a single cause (such as heart failure) may be listed as the cause of death, the underlying problem is the inability to sustain the endocrine and metabolic adjustments of the resistance phase.

71
Q

when does stress occur?

A

when the perceived demands of a situation are appraised as exceeding a person’s perceived resources and ability to cope

72
Q

how do males and females cope with stress differently?

A
  • Males tend to respond to stress with increased levels of cortisol relating to ah higher chance of the fight-or-flight behavior in males. In females, they discovered that instead of increased cortisol levels, an increase in the activity of the limbic system was initiated.
  • Females’ increased limbic activity gave proof to the tend-and-befriend theory for female coping strategies and says that females are more likely to alleviate stressful situations by nurturing and running to acceptable social groups
73
Q

what is allostatic load?

A

Allostatic load is “the wear and tear on the body” that accumulates as an individual is exposed to repeated or chronic stress. It represents the physiological consequences of chronic exposure to fluctuating or heightened neural or neuroendocrine response that results from repeated or chronic stress.

74
Q

how is stress recovery linked with allostatic load?

A

The body’s physiological systems constantly fluctuate as the individual responds and recovers from stress – a state of allostasis – and that, as time progresses, recovery is less and less complete and the body is left increasingly depleted.

75
Q

describe the role of appraisal - Lazarus’s ‘model of stress’

A

• Lazarus argued that stress involved a transaction between the individual and their external world, and that a stress response was elicited if the individual appraised a potentially stressful event as actually being stressful.
• Lazarus’s “model of stress”:
 Described individuals as psychological beings who appraised the outside world, not simply passively responding to it.
 Lazarus defined two forms of appraisal: primary and secondary.
1. Primary appraisal:
 The individual initially appraises the event itself.
 There are four possible ways that the event can be appraised:
1) Irrelevant
2) Benign (gentle) and Positive
3) Harmful and a Threat
4) Harmful and a Challenge
2. Secondary appraisal:
 The individual evaluating the pros and cons of their different coping strategies.

• Therefore primary appraisal involves an appraisal of the outside world and secondary appraisal involves an appraisal of the individual themselves.
• The form of the primary and secondary appraisals determines whether the individual shows a stress response or not.
• This stress response can take different forms:
 Direct action
 Seeking information
 Doing nothing
 Developing a means of coping with the stress in terms of relaxation or defense mechanisms

  • Lazarus’s model of appraisal and the transaction between the individual and the environment indicated a novel way of looking at the stress response – the individual no longer passively responded to their external world, but interacted with it.
  • It is not an event itself that elicits stress, but the individual’s interpretation or appraisal of those events.
  • This appraisal can be modified by providing information or withholding information from the individual.
  • An event needs to be appraised as stressful before it can elicit a stress response.
  • It could be concluded from this that the nature of the event itself is irrelevant – it is all down to the individual’s own perception.
  • Multitasking seems to result in more stress than the chance to focus on fewer tasks at any one time. Therefore a single stressor which adds to a background of other stressors will be apprised as more stressful than when the same stressor occurs in isolation.
  • If a stressor can be predicted and controlled then it is usually appraised as less stressful than a more random uncontrollable event.
  • A feeling of being in control reduces the stress of an event and contributes to the process of primary appraisal.
76
Q

describe Cannon’s fight/flight response

A 
•	Acute: 
	Increased sympathetic activation
	Increased cognitive performance
	Increased muscular priming
	Increased immune functioning
•	Chronic: 
	Decreased immune functioning
	Decreased cognitive performance
	This eventually leads to exhaustion.
77
Q

what is lidocaine?

A
  • an anaesthetic (blocks sensation) with minor analgesic (pain killer) properties
  • class Ib drug
    - It has a fast onset.
    - It counters kinetics – it has little or no effect at slower heart rates, and more effects at faster heart rates
    - Shorten the action potential duration.
    - Decrease refractoriness.
78
Q

what are class I drugs?

A

- block voltage-sensitive (voltage-gated) sodium channels; this blockage causes a loss of sensation and eliminates the responsiveness of these cells to pain.
- bind to the sodium channels most strongly when they are in either the open or the refractory/inactive state, less strongly to channels in the resting state.
- their action therefore shows the property of ‘use dependence’ (i.e. the more frequently the channels are activated, the greater the degree of block produced).

79
Q

how can class I drugs be subdivided?

A
  • Ia: lengthen the action potential (bind to sodium channel in the open or inactive/refractory states (open state binding > refractory/inactive state binding))
    - Ib: shorten the action potential (bind to sodium channel in the open or inactive/refractory states (refractory/inactive state binding&raquo_space; open state binding))
    - Ic: no significant effect on the action potential (bind to sodium channel in the open state)
80
Q

what are the uses of lidocaine?

A
  • Given by intravenous infusion to treat and prevent ventricular dysrhythmias in the immediate aftermath of a myocardial infarction.
  • Also used as a local anaesthetic (analgesic) for minor surgery.
  • Widely used for local anaesthesia (analgesic) (for needle aspirations/ chest drains).
81
Q

what are side-effects of lidocaine?

A

Side-effects – drowsiness, disorientation, convulsions, bradycardia, decreased cardiac output, vasodilation.

82
Q

what are the major symptoms of post traumatic stress disorder?

A
  • Feeling numb to the world with a lack of interest in former activities and a sense of estrangement from others
  • Reliving the trauma repeatedly
  • Sleep disturbances
  • Difficulty concentrating
  • Over alertness
83
Q

describe the diagnosis of PTSD

- acute and chronic

A
  • Duration of symptoms = ≥1 month.
  • Clinically significant distress or impairment in functioning.
  • Acute = symptoms of 1 to 3 months.
  • Chronic = symptoms duration of 3 months or more.
  • Delayed onset = onset of symptoms at least 6 months after stressor
84
Q

what is the primary goal of CBT for PTSD?

A

to undergo some sustained emotional processing of the traumatic experiences

85
Q

what does CBT involve? what’s its aim?

A

exposure (relearning response):
- acclimatisation of anxiety through exposure to trauma related stimuli

anxiety management:
- learning how to cope

cognitive therapy:
- modification of thinking styles

  • CBT is a structured therapy that focuses on clearly identified and achievable treatment goals.
  • CBT for PTSD is designed to desensitise the person to the traumatic event.
  • CBT techniques are used to reprocess the feared event and improve their strategies to decrease the sense of threat.
  • The aim of CBT is to modify unhelpful and maladaptive beliefs and to generate more flexible, rational and adaptive beliefs.
  • CBT emphasizes that the way we think about situations (ourselves, others, our world, future) influences our mood and behaviours.
86
Q

what does behavioural therapy involve?

A

changing maladaptive behavioural responses (behaviours that inhibit a person’s ability to adjust to particular situations) and substituting them with new responses

87
Q

what is the Cochrane review? what does it investigate? and what’s the method?

A
  • Cochrane Review are systematic reviews of primary research in human health care and health policy, and are internationally recognised as the highest standard in evidence-based health care
  • They investigate the effects of interventions for prevention, treatment and rehabilitation – they also asses the accuracy of a diagnostic test for a given condition in a specific patient group and setting

Method:

  • Each systematic review addresses a clearly formulated question
  • All the existing primary research on a topic that meets certain criteria is searched for and collated
  • Its then assessed using stringent guidelines, to establish whether or not there is conclusive evidence about a specific treatment
  • The reviews are updated regularly, ensuring that treatment decisions can be based on the most up-to-date and reliable evidence
88
Q

equation for compliance?

A

compliance = pressure x change in volume

89
Q

what causes reduced compliance?

A
  • reduced surfactant

- pulmonary fibrosis

90
Q

how much air do you take in in each breath and how much gets to the alveolar space for gas exchange?

A

out of the 0.5L that you take in of air, only 0.35ml is getting into the alveolar space for gas exchange (0.15L is dead space)

91
Q

equation for pulmonary ventilation

A

pulmonary ventilation = tidal volume x respiratory rate

92
Q

what different cells are there in different locations in the respiratory airways?

A

Trachea – ciliated epithelium
Primary bronchus – basal cells (stem cells)
Secondary bronchus – basal cells
Tertiary bronchus – basal cells

Smaller bronchi
Bronchioles
Terminal bronchioles

Respiratory bronchioles 
Alveolar sacs (150 million) – alveolar type I & II
93
Q

what cells are there present as you go down the respiratory tract?

A
  • ciliated epithelium
  • basal cell
  • goblet cell
  • club cell
  • serous cell
  • brush cell
  • alveolar type I
  • alveolar type II
94
Q

what are the function of each of the cells?

A

Ciliated epithelium – protective barrier, mucociliary clearance
Basal cell – renew damaged cells
Goblet cell – mucus secretion
Club cell – production of surfactant (lubricant)
Serous cell – antibacterial secretions
Brush cell – unknown – at bifurcations
Alveolar type I – gas exchange
Alveolar type II (much thinner than club cells) – production of surfactant

95
Q

what is the function of surfactant at different parts of the airways?

A

Higher in airways – lubricant so airways don’t stick together
Lower in airways – reduces surface tension at the air-liquid interface – holds airspace open, because no cartilage there to do this

96
Q

what is the basic structure of the conducing airways?

A
  • Airway lumen
  • Ciliated epithelial cell
  • Basement membrane
  • Blood vessels
  • Mucous glands which channel into lumen
  • Bronchial smooth muscle – innervated
  • Cartilage
97
Q

what are the functions of the conducting airway epithelium?

A
  • Protection by secretion and movement of mucus by cilia towards the pharynx – mucociliary clearance (these epithelial cells don’t have receptors for pathogens to bind to, or the cilia gets in the way)
  • Physical barrier to pathogens – junctional components between cells (tight, adherens, desmosomes – keep epithelial cells together)
  • Production of regulatory and inflammatory mediators:
  • chemokines (e.g. IL-8 and IL-6) – attract inflammatory cells
  • cytokines (e.g. GM-CSF and TGF-B) – cell signalling
  • proteases (e.g. plasminogen activators, MMPs) – migration, degradation of ECM (extracellular matrix), growth factor activation
98
Q

what decreases and increases in tertiary bronchi?

A
  • Reduced cartilage, more smooth muscle (to control opening of airways)
  • Fewer goblet cells and submucosal glands
  • Increase in club cells producing surfactant
99
Q

what is and isn’t present in bronchioles?

A
  • Single layer of ciliated epithelium
  • No cartilage
  • Reduced smooth muscle
  • No goblet cells or submucosal glands
  • More club cells producing surfactant
100
Q

describe the alveoli - what is and isn’t present and inside them?

A
  • Alveoli – passive gas exchange with capillary network – 150 million
  • Collagen, elastic fibres and fibroblasts and macrophages present (not many in health) in septal junctions – matrix surrounding them – keeps alveoli in place (and tiny bit of small muscle to regulate airway tone)
  • Several alveoli grouped into lobules surrounded by connective tissue
  • In each alveolus you have one macrophage
101
Q

how does the sympathetic nervous system affect airflow?

A

Alpha -> constricts blood vessels – affect gas exchange

Beta2 agonists -> relaxes smooth muscle (increase airflow – more oxygen – heart can pump more (don’t get confused with relaxing blood vessels)

102
Q

what regulatory and inflammatory mediators of airflow are there?

A
  • Mast cell histamine – constriction
  • Arachidonic acid metabolites – constrict and dilate (e.g. prostaglandins, leukotrienes)
  • Cytokines – constrict and dilate, increase mucus
  • Hormones (e.g. adrenaline)
103
Q

what are the pathological changes in the asthmatic airway-remodelling?

A
  • Mucus hypersecretion
  • Denuded (stripped) epithelium
  • Goblet cell hyperplasia
  • Reticular thickening
  • Appearance of myofibroblasts
  • Smooth muscle cell hypertrophy
  • Angiogenesis
  • Plasma extravasation (escaping of blood into tissues)
104
Q

what is they key point about chronic stress?

A

chronic stress is maladaptive (stress does not respond to the environment – stress will stay with you even if you change environment)

105
Q

how does chronic stress lead to cardiovascular problems?

A

Chronic work stress – changes in physiology (increase blood pressure, increase heart rate) and behaviour which over time lead to damage to the cardiovascular system

Chronic stress -> atherosclerosis -> heart attack
Acute stress can go straight to atherosclerosis or heart attack

106
Q

what is the general adaptive syndrome?

A

What if flight or fight response is prolonged?

  • Alarm
  • recognising a stressor
  • Resistance
  • cope with or adapt to the stressor
  • Exhaustion
  • depletion of resources if stressor cannot be overcome
  • symptoms reappear
  • Physiological responses to stress – adaptive in the short term
  • However, prolonged activation of stress response systems damaging
  • depletion of resources and ill health
107
Q

what determines someone’s coping strategy?

A 
Emotional response to health threat
-	Fear 
-	Anxiety 
-	Depression 
Representation of health threat (illness beliefs)
-	Identity 
-	Cause 
-	Consequences
-	Timeline – e.g. short-term = alleviates stress 
-	Cure/control
108
Q

what are the two main groups of physiological changes from stress?

A
  1. Sympathetic activation
    - Triggers responses in the sympathetic nervous system
    - Results in production of adrenaline and noradrenaline which cause changes in blood pressure, heart rate, sweating and pupil dilation
    - Similar to fight or flight
    - Have an effect on a range of body tissues and can lead to changes in immune function
  2. Hypothalamic-pituitary-adrenal axis (HPA)
    - Results in increased levels of corticosteroids (cortisol)
    - Physiological changes such as the management of carbohydrate stores and inflammation
    - Background effect of stress, and cannot be detected by the individual
    - Similar to alarm, resistance, exhaustion approach as part of General Adaptation Syndrome
    - Raised levels of brain opioids beta endorphin and enkephalin following stress – lead to immune related problems

Medicine Sem 2 (10 decks)

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