Case 1 Sem 2 Flashcards
(119 cards)
1
Q
Muscles in the lungs
A
Control diameter of airways
2
Q
Air flows from
A
Region of high pressure to region of low pressure
3
Q
Inspiration
A
Pressure in elastic alveoli made low (lower than outside atmospheric pressure) by stretching them by reducing pressure around them by expanding chest wall thus increasing its volume, air sucked into lungs
4
Q
Expiration
A
Pressure in elastic alveoli increased (higher than atmospheric pressure outside) by decreasing size of chest thus decreasing its volume , compressing the gas in the lungs
5
Q
Quiet inspiration (eupnoea)
A
- Increase in vertical diameter: contraction of diaphragm flattens floor of thoracic cavity, increasing its volume and decreasing mitral solar pressure, drawing air into lungs. Diaphragm contractual accounts for 75% or air movement in normal breathing at rest
- Increase in transverse diameter: contraction of external intercostal muscles elevate ribs? Contributes to 25% of volume of air in lungs at rest
Ribs curve downward as well as forward around chest wall, resemble bucket handles. If ribs raised, transverse diameter of thoracic cavity increases - Increase in anteroposterior diameter: contraction of scalenei muscles causing first rib to be fixed. All ribs drawn together and raised toward first rib
Downward facing ribs raised at sternal ends, anteroposterior diameter of thoracic cavity increased, sternum thrust forward
6
Q
Forced inspiration
A
Maximum increase in thoracic cavity occurs
1. Contraction of accessory muscles assist external intercostal muscle in elevating the ribs
These muscles increase speed and amount of rib movement
7
Q
Accessory muscles
A
Sternocleidomastoid, scalenei muscles (anterior and medius), serratus anterior and pectoralis minor
8
Q
What happens in inspiration?
A
Root of lung descends, level of bifurcation of trachea may be lowered as much as two vertebrae
Bronchi elongate and dilate, alveolar capillaries dilate assisting pulmonary circulation
Air drawn into bronchial tree due to positive atmospheric pressure exerted through upper part of respiratory tract and negative pressure on outer surface of lungs due to increased capacity of thoracic cavity
With expansion of lungs, elastic tissue in bronchial walls and connective tissue stretched
As diaphragm descends, costadiaphragmic recess of pleural cavity opens, expanding sharp lower edges of lungs descend
9
Q
Quiet expiration
A
Passive
Elastic rebound/recoil of lungs: elastic fibres in connective tissue and surface tension of film fluid lining alveoli. As water molecules pull together, also pull on alveolar walls causing alveoli to recoil and become smaller
Muscles of inhalation relax, elastic components recoil returning the diaphragm and rib cage to original positions
10
Q
What prevents lungs from collapsing?
A
Surfactant (reduces surface tension) and interpleural pressure
11
Q
Forced expiration
A
Active
Internal and innermost intercostal muscles and transfers us thoracic muscles depress ribs and reduce width and depth of thoracic cavity
External and internal oblique, transverse abdominis and recuts abdominis muscles assist internal intercostal muscles in exhalation by compressing abdomen and forcing diaphragm upwards
Forcible contraction of muscles in anterior abdominal wall
Quadratics lumborum contracts to pull down 12th rib
Serratus posterior inferior and latissimus dorsi muscles play minor role
12
Q
Simple mechanism of expiration
A
Roots of lungs descend
Bifurcation of trachea ascends
Bronchi shorten and contract
Elastic tissue of lungs recoil and lungs reduce in size
Diaphragm,over upwards
Lower margins of lungs shrink and rise
13
Q
Involuntary respiratory control
A
Involuntary respiratory centres regulate activities of respiratory muscles in quiet inspiration
Control respiratory volume by adjusting frequency and depth of pulmonary ventilation
14
Q
Voluntary respiratory control
A
Reflects activity in cerebral cortex that effects either:
Output of respiratory centres in medulla oblong at a and pons
The motor neurone in spinal cord that control respiratory muscles
15
Q
Respiratory centres
A
Three pairs of nuclei (clusters of nerve cell bodies) in medulla oblongata and pons
16
Q
What do the respiratory rhythmicity centres do?
A
Set the basic pace for respiratory movements
17
Q
Dorsal Respiratory Group (DRG)
A
Respiratory centre
Located in dorsal portion of medulla oblongata
DRG controls Inspiratory movements and their timing
Controls both quiet and forced inspiration
18
Q
DRG controls
A
Phrenic nerve which innervates diaphragm
Intercostal nerves which innervation external intercostal muscles
Nerves which innervate accessory respiratory muscles involved maximal inhalation (scalenei muscles, sternocleidomastoid, serratus anterior and pec minor)
19
Q
Ventral respiratory group (VRG)
A
Respiratory centre
Located in ventrolateral part of medulla
VRG mainly causes forced expiration
20
Q
VRGs expiratory centre controls
A
Intercostal nerves which innervate internal intercostal muscles
Nerves which innervate accessory respiratory muscles involved in active exhalation (abdominal muscles)
21
Q
VRGs Inspiratory centre
A
Aids DRG during forced inspiration
Controls nerves which innervate accessory respiratory muscles involved maximal inhalation (scalenei muscles, sternocleidomatoid, serratus anterior and pec minor)
22
Q
When the respiratory drive for increased pulmonary ventilation becomes greater than normal….
A
Respiratory signals spill over into the VRG from DRG, activating inspiraroy ventre of VRG allowing it to innervate the accessory respiratory muscles of forced inspiration
23
Q
Signals sent from respiratory centres to respiratory muscles occur in
A
Bursts of action potentials
24
Q
Inspiratory ramp signal in normal respiration
A
Signals begin weakly and increase steadily in ramp manner for 2 seconds providing stimulation to inspiratory muscles (inhalation occurs)
Signals cease abruptly for 3 seconds which turns off excitation of diaphragm and allows elastic recoil of lungs and chest wall to cause expiration (passive exhalation occurs)
Inspiratory signal begins again and cycle repeats with expiration occurring in-between
Advantage: causes steady increase in volume of lungs during inspiration, rather than inspiratory gasps
25
Inspiratory ramp signal - deep breathing
Signals become stronger more quickly
Rate of increase of ramp signal is faster
26
Inspiratory ramp signal - faster breathing
Signals start and cease earlier
Ramos are less than 2 seconds
27
Respiratory centres of pons
Apneustic centres and pneumotaxic centres of pons adjust output of DRG and VRG
their activities regulate and depth of respiration in response to stimuli or other centres in brain
28
Stimuli
Impulses from receptors around the body carried via vagus or glossopharyngeal nerves to respiratory centres
29
Other centres
Hypothalamus (deviation in temp) or cerebrum
30
Apneustic centres
Located in lower pons
Provides continuous stimulation to DRG resulting in long deep inhalation
Continuous stimulation builds ramp signal during quiet inspiration
Coordinates transition between inhalation and exhalation
After 2 seconds and under normal conditions, Apneustic centre inhibited by pneumotaxic centre on same side
31
Pneumotaxic centres
Located in upper pons
Inhibits aponeutic centre. Controls switch off point of ramp signal limiting inspiration
Centres in hypothalamus and cerebrum alter activity of pneumotaxic centres as well as respiratory rate and depth
32
Respiratory reflexes
Activities of respiratory centres modified by sensory information
33
Chemoreceptors
Sensitive to PCO2, pH or PO2 of blood or cerebrospinal fluid
34
Baroreceptors
Blood pressure - carotid and aortic baroreceptors detect changes in blood pressure have small effect on respiration
Sudden rise in BP decreases rate of respiration and drop in BP increase respiratory rate
35
Stretch receptors (Hering-Breurer inflation Reflex)
Located in muscular portions of walls of bronchi and bronchioles throughout lungs, transmit signals through vagus nerve and into dorsal respiratory group of neurons when lungs are over stretched
When lungs overly inflated, stretch receptors activate feedback response that switches off inspiratory ramp stopping further inspiration
This reflex increases rate of respiration
36
Irritating physical/chemical stimuli
In nasal cavity, larynx or bronchial tree
37
Other senses (respiratory reflexes)
Pain, changes in body temp, abdominal visceral sensations
38
Chemical control of respiration/ central chemoreceptors
Excess carbon dioxide or excess hydrogen ions in blood act directly on respiratory centre causing increased strength of inspiratory and expiratory motor signals to respiratory muscles
Oxygen acts on peripheral chemoreceptors located in carotid and aortic bodies, in turn transmitting appropriate nervous signals to respiratory centre for control of respiration
39
Direct chemical control of respiratory centre
Chemisensitive area located bilaterally lying beneath ventral surface of medulla
Area is highly sensitive to changes in blood PCO2 or hydrogen ion conc in turn exciting other portions of respiratory centre
CO2 has little effect in stimulating neutrons in chemosensitive area
Hydrogen ions have direct effect in stimulating neutrons in chemosensitive area
Hydrogen ions cannot pass through blood brain barrier
CO2 can cross blood brain barrier
CO2 crosses barrier and reacts with water of tissues to form carbonic acid which dissociates into hydrogen and bicarbonate ions, hydrogen ions have direct stimulator effect on chemosensitive area in brain
More hydrogen ions are released into respiratory chemosensitive sensory area of medulla when blood CO2 conc increases than when blood hydrogen ion conc increases
Respiratory centre activity increased strongly by changes in blood CO2
40
Regulation of respiration during exercise
In strenuous exercise arterial PCO2, PH and PO2 remain normal
Increased ventilation doesn’t occur as a result of changes in arterial PCO2, pH or PO2
Likely that most of increase in respiration results from neurogenic signals transmitted directly into brain stem respiratory centre at same time that signals go to body muscles to cause muscle contraction
The onset of exercise, alveolar ventilation increases instantaneously without initial increase in arterial PCO2. Increase in ventilation great enough that it decreases arterial PCO2 below normal
41
Presumed reason that ventilation forges ahead of build up of blood CO2 is…
The brain provides anticipatory stimulation of respiration at onset of exercise causing extra alveolar ventilation before it is needed
42
Peripheral chemoreceptors
Located outside brain
Detects changes in oxygen levels in blood
Transmit nerve signals to respiratory centres in brain
Carotid bodies: found in carotid arteries. Nerve fibres pass through glossopharyngeal nerves and then to dorsal respiratory area
Aortic bodies: found in arch of aorta. Nerve fibres pass through vaginal so to dorsal respiratory area
43
Local regulation of gas transport and alveolar function
In normal tissues, if tissue becomes more active, PO2 falls and PCO2 rises
The change in partial pressure causes more oxygen to be delivered
The rising PCO2 relaxes smooth muscle in arteries and capillaries causing vasodilation and increasing blood flow
In alveolar capillaries, blood directed where PO2 is high, this occurs because alveolar capillaries constriction when PO2 is low
In bronchioles, oxygen directed towards lobules where PCO2 is high because these lobules are engaged in gas exchange (because smooth muscle in bronchioles bronchodilator when PCO2 is high)
44
Hypoxia
Lack of oxygen
45
Causes of hypoxia
1. Inadequate oxygenation of blood in lungs because of extrinsic reasons: deficiency of oxygen in 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)
4. Inadequate oxygen transport to tissues by blood: anaemia or abnormal haemoglobin, general circulatory deficiency, localised circulatory deficiency (peripheral, cerebral, coronary vessels), tissue oedema
5. Inadequate tissue capability of using oxygen: poisoning of cellular oxidation enzymes (cyanide poisoning), diminished cellular metabolic capacity for using oxygen, toxicity, vitamin deficiency, other factors
46
Effects of hypoxia
Acute: drowsiness, lassitude (lack of energy), mental and muscle fatigue, headache, nausea
Decreased mental proficiency, decreasing judgement, memory and performance of discrete motor movements
47
Cyanosis (hypoxia)
Blueness of skin
Caused by excessive amounts of deoxygenated haemoglobin in skin blood vessels (intense dark blue purple colour transmitted through skin)
48
Changes in pleural pressure anatomy
No attachments between lung and walls of chest cage, except where it is suspended at its hilum from mediastinum
Lung floats in thoracic cavity surrounded by pleural fluid that lubricates movement of lungs within cavity
Continuous suction of excess fluid into lymphatic channels maintains slight suction between visceral pleural surface of lung and parietal pleural surface of thoracic cavity
Therefore lungs held to thoracic wall by surface tension, but well lubricates and can slide freely as chest expands and contracts
49
Pleural pressure
Pressure of fluid in pleural cavity (space between visceral and partial plurae)
Normally has slightly negative pressure
Normal pleural pressure at beginning of inspiration = -5 cm of water (3.68mmHg). This is the amount of suction required to hold lungs open to their resting level
During normal inspiration, expansion of chest cage pulls outward on lungs with greater force and creates more negative pressure to around -7.5cm H2O (-5.5mmHg)
50
Alveolar pressure
Pressure of air inside lung alveoli
When the glottis is open and no air is flowing in and out of lungs, pressure in all parts are equal to atmospheric pressure which is zero reference pressure - 0cmH2O
To cause inward flow of air to alveoli during inspiration, pressure of alveoli must fall slightly below atmospheric pressure (below 0)
Second curve (alveolar pressure) demonstrates that during normal inspiration, alveolar pressure decreases to -1cm H2O
This light negative pressure is enough to pull 0.5 litres of air into lungs in 2 seconds recquired for normal quiet inspiration
During normal expiration, opposite pressures occur: alveolar pressure rises to 1+cm H2O, forces O.5 litre of inspired air out of lungs during 2-3 seconds on expiration
51
Transpulmonary pressure/ transpluerual pressure
Difference between alveolar pressure and pleural pressure
Also a measure of elastic forces in lungs that tend to collapse lungs at each instant of respiration (recoil pressure)
52
Work of breathing depends on:
Tidal volume: increased tidal volume = more work done by lungs
Respiratory frequency: increased frequency = more work done by lungs
Lung compliance: increased compliance = less work done by lungs
Airways resistance: increased resistance = more work done by lungs
53
Increased work of breathing leading to fatigue causes
Respiratory failure
54
Airways resistance
The longer the airway, the greater the airways resistance
The narrower the airway, the greater the airways resistance
55
Compliance
Indication of a lungs expandability, how easily lungs expand and contract
Lower compliance, greater force required to fill and empty lungs
Greater compliance, easier it is to fill and empty lungs
56
Factors affecting compliance
Elastic forces of lung tissue
Elastic forces caused by surface tension of fluid that lines inside walls of alveoli and lung spaces
57
Surfactant
Surface active agent in water, reduces surface tension of water
Secreted by epithelial cells (type 2 alveolar epithelial cells) - 10% surface area of alveoli
Phospholipids, proteins and ions
58
Dead space
Amount of fresh air reaching alveoli/ gas exchange areas of lung (alveolar ventilation) is less than amount of fresh air entering airways at mouth and nose (pulmonary ventilation)
Slow deep breathing gives more alveolar ventilation than fast breathing
59
Pneumothorax
Collection of air between visceral and parietal pleura causing a real rather than potential air space
60
Under normal conditions, pressure within intrapleural space is
Negative with respect to atmosphere and alveolar gas
61
If a connection is made between atmospheric pressure and pleural cavity
Gas flows into intrapleural space increasing its pressure to atmospheric
Lung partially collapses due to elastic recoil pressure
62
Clinical presentation of pneumothorax
Spontaneous pneumothorax- best pain and breathlessness
Sudden onset, localised to affected side, made worse on inspiration
Dyspnoea (laboured breathing) produced by difficulty to take a deep breath, also dependent on size of pneumothorax and presence of underlying lung disease
Reduction in breath sounds on affected side
Chest wall movement reduced
Percussion note resonant
63
How many types of pneumothorax
4
64
Primary spontaneous pneumothorax
Most common
Caused by rupture of small subpleural emphysematous bulla or pulmonary bleb (usually apical), due to congenital defects in connective tissue. This is a weakness and out pouching of lung tissue which can rupture, introducing air into pleural space causing lung collapse
As lung collapses, hole formed by ruptured bleb seals preventing more air entering intrapleural cavity
COPD can cause
Rarely causes physiological disturbance
People who have had spontaneous pneumothorax at risk of recurrence
65
Risk factors of primary spontaneous pneumothorax
Smoking, tall stature and presence of apical subpleural blebs
66
Treatments of primary spontaneous pneumothorax
Pleurodesis (needle apisration and chest drain) to fuse visceral and parietal pleura by medical (bleomycin/talc) or surgical (abrasion of pleural lining)
67
Secondary spontaneous pneumothorax
Deadly
Caused by respiratory diseases that damage lung structure (COPD, asthma, pneumonia etc)
Incidence increases with age
ICU patients with lung disease at risk due to high presses (barotrauma) and alveolar distention (volutrauma) associated with mechanical ventilation
Protective ventilation strategies using low pressure, limited volume ventilation reduce the risk
68
Traumatic pneumothorax
Blunt (road traffic accident), penetrating (stab wounds, fractured ribs), chest trauma
Gas may enter intrapleural space from atmosphere through hole in chest wall or from alveoli through hole in lung
Flow of air two way
Therapeutic procedures eg line insertion, thoracic surgery common causes
Usually associated with haemothorax
69
Haemothorax
Collection of blood in pleural cavity
70
Tension pneumothorax
Most common during mechanical ventilation/ following traumatic pneumothorax
Flow of air is one way (from lung into pleural cavity) upon inspiration.
Upon inspiration , air from atmosphere enters pleural cavity (from stab wound) down pressure gradient
Upon expiration, air can’t escape from pleural cavity and remains trapped because pleural pressure doesn’t increase above atmospheric pressure
Every inspiration results in build up of air and pressure (tension)
71
Mechanical ventilation
Form of life support
72
Symptoms of tension pneumothorax
Cyanosis, severe breathlessness
73
Treatment of tension pneumothorax
Needle aspiration and chest drain
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Diagnosis of pneumothorax
Examination with stethoscope: decreased/absent breath sounds over affected lung
Diagnosis confirmed by chest x ray
X ray illustrates collapse of lung as black space (air) around lung
Tension pneumothorax- lung shrivels up away from affected side and mediastinum will shift towards unaffected side (trachea displacement)
Combination of absent breath sounds and resonant percussion
75
Physical examinations pneumothorax
1. Inspection: distressed, sweating, dyspnoea, cyanosis
2. Palpation: affected side moves less than normal side (air in intrapleural space allows rib cage to expand outwards)
3. Percussion: affected side sounds hyperresonant
4. Auscultation: breath sounds on affected side diminished as less gas enters collapsed lung during inspiration, air in intrapleural space acts as barrier to transmission of sounds from lungs to chest wall
5. Trachea displaced away from side of collapsed lung in tension pneumothorax
6. Pulse Examination: tachycardia, pulse > 135 bpm (tension pneumothorax). Pulse paradoxicus (slow pulse on inspiration) suggests severe
7. Monitoring reveals hypotension and desaturation (less oxygen carried in blood)
76
Investigations pneumothorax
1. Chest X ray confirms diagnosis: clear line of visceral pleura with absence of peripheral lung markings beyond it, trachea and mediastinum deviated away from affected side, standard erect posterior anterior films usually adequate.
2. Arterial blood gases show hypoxia. More disturbed in SP - less reserve in presence of pre existing lung disease
3. CT scan not routinely used, but differentiates a large bulla from a pneumothorax, may detect localised pneumothoraces
77
Treatment of pneumothorax
Graded depending on degree of lung collapse
Tension pneumothorax drained immediately
Small PSP managed by observation hissing clinical assessment and chest x ray
PSP > 30% aspirated in second intercostal space in midclavicular line, using 15mL syringe connected to 3 way tap and underwater seal. Used to suck out as much air as possible. If patient coughs, this is achieved
SP and traumatic pneumothorax always requires hospital admission and intercostal chest drainage
78
Chest drain
Length of plastic tubing inserted into intrapleural space through small incision made under local anaesthetic between two ribs
Allows air to escape from intrapleural space so that underlying lung can reinflate
One way valve placed at end of drain so that CD removes air from intrapleural space rather than allowing more air to enter it (underwater seal)
Underwater seal consists of container of water with tube extending below surface of water
Gas passes from tube into atmosphere by bubbles in water, no gas can pass up the tube, water cast as a one way valve at end of tube
Pressure in intrapleural space is positive (coughing/ forced expiration), air passes along chest drain and out to atmosphere through underwater seal, pneumothorax is drained
Bubbles appear in underwater seal until hole in pleura has sealed
After hole healed, water level will rise and fall slowly and chest drain removed
Underwater seal collects blood and secretions that pass along chest drain
79
ATLS protocol
Advanced trauma life support - standard method for initial management of injured patients
Treat greatest threat to life first
Loss of airway will kill before inability to breathe, inability to breathe will kill before bleeding and loss of circulation
80
Primary survey
ABCDE
1. Airway maintenance and cervical spine protection: ensure airway is clear, patient can breathe, neck and cervical spine maintained in neutral position to prevent secondary injuries to spinal cord
2. Breathing and ventilation: chest examined by inspection, palpation, percussion and auscultation, life threatening injury identified
3. Circulation and haemorrhage control: external bleeding controlled, internal bleeding diagnosed
4. Disability and neurologic status: neurological assessment made
5. Exposure and environment: patient undressed, cutting off garments, privacy maintained, warm blankets prevent hypothermia, IV fluids warmed and warm environment maintained
81
Secondary survey
Once primary survey completed, resuscitation efforts established, vital signs normalising
Head to toe evaluation - complete history and physical examination inc reassessment of all vital signs (each region of body fully examined)
If at any time patient deteriorates, primary survey done again
Firm mattress, prevents spinal fractures
82
Autonomic nervous system subdivisions
Sympathetic
Parasympathetic
83
Sympathetic and parasympathetic nervous systems secrete
Acetylcholine (fibres are cholinergic)
Norepinephrine (fibres are adrenergic)
84
Preganglionic neurons are
Cholinergic
85
In postganglionic system, sympathetic and parasympathetic are
Sympathetic: adrenergic
Parasympathetic: cholinergic
86
Acetylcholine receptors
1. Nicotinic receptors - found in autonomic ganglia at synaoses between preganglionic and postganglionic neurons of both the sympathetic and parasympathetic systems
2. Muscarinic receptors - found on all effector cells that are stimulated by postganglionic cholinergic neurons of parasympathetic nervous system
87
2 types of adrenergic receptors
Alpha and Beta
88
Alpha receptors
1. Alpha 1: found in walls of blood vessels, activation causes smooth muscle contraction. Vasoconstriction and vasodilation are controlled by SNS. Stimulation of SNS causes vasoconstriction and less stimulation causes vasodilation
2. Alpha 2: inhibits adenylate cyclase, decreasing cAMP formation. Negative feedback for release of norepinephrine from presynaptic neuron. Inhibition of insulin release and induction of glucagon release in pancreas
89
Beta receptors
All beta receptors stimulate adenylate cyclase
Beta 1: in heart, increases cardiac output
Beta 2: in lungs, bronchodilation
Beta 3: in fat cells, lipolysis in adipose tissue
90
What type of receptors are alpha and beta?
G protein coupled receptors (Intracellular messengers)
91
Norepinephrine excites
Alpha
Beta to lesser extent
92
Epinephrine excites
Alpha and beta equally
93
Stress response
In some instances, almost all of sympathetic NS discharge (mass discharge). Happens when hypothalamus is activated by fright, fear, extreme pain
Sympathetic NS has small preganglionic nerves and long postganglionic nerves. Preganglionic in close proximity (thoracic and lumbar regions). Talk to each other. When SNS activated, preganglionic nerves activated simultaneously
Threatens homeostasis = stress
94
Phases of stress response
Alarm, resistance, exhaustion
95
Alarm phase
Immediate response to stress occurs directed by sympathetic nervous system
Activation of SNS increases secretion of adrenaline
Adrenaline is dominant
1.energy reserves mobilised (glucose)
2. Body prepares - fight or flight
Increased production of adrenaline and noradrenaline (both alpha and beta adrenergic receptors activated with efficiency)
96
Characteristics of alarm phase
Increased mental alertness
Increased energy used (partic skeletal cells)
Mobilisation of glycogen (hepatocytes perform glycogenolysis) and lipid reserves (adipose tissue cells perform lipolysis)
Changes in circulation, increased blood flow to skeletal muscles and decreased blood flow to skin, kidneys and digestive organs
Reduction in digestion and urine production
Increased sweat
Increases in BP, heart rate, resp rate and metabolic rate
97
Resistance phase
Stress longer than few hours
Glucocorticoids (cortisol) dominant, GH, ADH and glucagon also involved
Energy demands higher
Neural tissue has high demand for energy, must have supply of glucose. Glucocorticoids falls, neural function gone
Glycogen reserves exhausted after several hours
98
Endocrine secretions of resistance phase achieve four results
1. Mobilisation of remaining lipid and protein reserves: hypothalamus produces GHRH, releasing GH and glucocorticoids. Adipose tissue responds to GH and glucocorticoids by releasing stored fatty acids. Skeletal muscle responds to glucocorticoids by breaking down proteins and releasing amino acids into blood stream
2. Conservation of glucose for neural tissues: glucocorticoids (cortisol) and GH stimulate lipid metabolism in peripheral tissues. Peripheral tissue (except neural) breaks down lipids to obtain energy. Neural tissues don’t alter metabolic activities but continue to use glucose as energy source
3. Elevation and stabilisation of blood glucose concentrations: blood glucose levels decline, glucagon and glucocorticoids (cortisol) stimulate liver to manufacture glucose from other carbs (glycerol) and from amino acids provided by skeletal muscles
4. Conservation of salts and water through loss of potassium and hydrogen: blood volume conserved through ADH and aldosterone. As sodium conserved, postassium and hydrogen lost
99
Why can resistance phase not be maintained?
If starvation is primary stress, resistance phase ends when lipid reserves exhausted and structural proteins become primary energy source
If another factor, resistance phase needs due to complications brought about hormonal side effects
100
Side effects experienced due to hormones in resistance phase
1. Glucocorticoids (cortisol): anti inflammatory action slows wound healing and increases susceptibility to infection
2. Continued conservation of fluids under ADH and aldosterone stresses cardiovascular system by producing elevated blood volumes and higher than normal BP
3. Suprarenal cortex may be unable to continue producing glucocorticoids eliminating acceptable blood glucose conc
101
Exhaustion phase
When resistance phase ends, homeostatic regulation breaks down and exhaustion phase begins
Failure of one or more organs, fatal
102
Mineral imbalances in exhaustion phase
Production of aldosterone in resistance phase results in conservation of sodium at expense of potassium
As potassium declines - neurons and muscle fibres malfunction
103
What is PTSD?
Going through frightening and intense experiences beyond the level of normal suffering
Anxiety related condition
Long lasting effects
104
Symptoms of PTSD
Numbness to world and previous interests
Over alertness
Sleep disturbances
Reliving trauma repeatedly
105
Categories of PTSD
A: actual/threatened death, serious injury, threat to physical integrity
B: 1+ symptom of reliving trauma
C: 3+ symptoms of avoiding trauma stimuli, numbness
D: 2+ symptoms of persistent increased arousal
106
PTSD diagnosis
Symptoms for one or more months
Acute: 1-3 months after event
Chronic: 3 or more months after event
Delayed onset: 6 or more months after event
107
What is CBT?
Reprocess event, improve strategies to decrease sense of threat
Modification of thinking styles
Desensitise to traumatic event
108
What is Anaesthesia?
Loss of sensation
109
What is Analgesia?
Pain relief
110
2.Depolarisation phase of sodium channels
Sodium channels open, action potential beings when neurone depolarised by 20mV (now -40mV - threshold potential) rapidly increases to +40mV
111
3.Repolaristion phase of sodium channels
Sodium channels close, potassium channels open. Once peak positive value hit, rapidly repolarises returning to negative membrane potential
112
1.Resting state of sodium channels
-60mV, sodium and potassium channels are closed
113
4.Hyperpolarisation phase of sodium channels
(undershoot) sodium channels become inactive and potassium channels stay open, membrane potential often more negative than resting potential
114
5.Second resting phase
Membrane returns to resting state (-60mV)
115
Lazarus model of stress
Individuals are psychological beings who appraise the outside world, they don’t passively respond (interpretation of stressor), therefore the event needs to be appraised as stressful before it can illicit a stress response
116
Primary appraisal of stress
(Outside world)
Individual initially appraises event itself
Perceives it as irrelevant/ gentle/ harmful and challenge/ harmful and threat
117
Secondary appraisal of stress
Individual evaluates pros and cons of their coping strategies
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Cannons fight or flight response
Acute stress: increased cognitive function, immune response, muscle priming, sympathetic activation
Chronic: decreased cognitive function and immune response, eventually leading to exhaustion
119
Hans selyes general adaption syndrome (gas)
1. Alarm phase - shock (SNS activated, adrenaline/ epinephrine and cortisol increased) counter shock (homeostasis)
2. Resistance phase - adaption (PNS returns some functions back to normal, increases blood glucose, resp rate, BP and HP, cortisol and adrenaline levels remain elevated
3. Exhaustion phase - stressors continue beyond bodies capacity, resources used up, susceptible to death or disease
