Term
| What are adrogenic anabolic steroids? |
|
Definition
| synthetic substances related to male sex hormone |
|
|
Term
|
Definition
| actions that are those involved in the primary and secondary sexual characteristics |
|
|
Term
|
Definition
| actions consist of positive effects of testosterone in inhibiting urinary nitrogen loss and stimulating protein synthesis, especially in skeletal muscle |
|
|
Term
| Describe the synthesis equation for testosterone |
|
Definition
| Cholesterol -> androstenedione + 17beta-hydroxysteroid dehydrogenase in liver -> testosterone |
|
|
Term
| Where is testosterone formed? |
|
Definition
| Leydig cells of the testis and also in the adrenal cortex |
|
|
Term
| What is the adrenal cortex important in? |
|
Definition
females as well as males.
important for secondary sexual characteristics. |
|
|
Term
| Testosterone is _____ soluble |
|
Definition
|
|
Term
| Describe testosterones mode of action |
|
Definition
1. diffuses into cell
2. combines with testosterone binding protein and is transported to nucleus
3. interacts with hormone receptor elements and activates protein synthesis |
|
|
Term
| How do some steroids and testosterone differ? |
|
Definition
| steroids may also produce via cell surface receptors |
|
|
Term
| What are anabolic effects? |
|
Definition
| effects that promote muscle hypertrophy (increase in muscle cells) |
|
|
Term
| How so anabolic steroids and testosterone compare? |
|
Definition
| AS have greater effects than testosterone but will also have an unavoidable adronergic effect |
|
|
Term
| Why is isolated natural testosterone ineffective when taken orally |
|
Definition
| metabolised in the liver to inactive compounds |
|
|
Term
| Why is isolated natural testosterone ineffective when injected |
|
Definition
| gets into the blood and goes into the liver where it is broken down into inactive compounds |
|
|
Term
| What types of testosterone modifications are there? |
|
Definition
| Type A, Type B and Type C |
|
|
Term
| Describe a Type A testosterone modification |
|
Definition
| modified to be made suitable for depot injection |
|
|
Term
| Describe a Type B testosterone modification |
|
Definition
| addition of an alkyl group renders the structure orally inactive |
|
|
Term
| Describe a Type C testosterone modification |
|
Definition
| allows oral dosing and sometimes increased potency |
|
|
Term
| What is a depot injection? |
|
Definition
| an injection of a substance in a vehicle that tends to keep it at the site of injection so that absorption occurs over a prolonged period |
|
|
Term
| What are the clinical purposes of testosterone analogues? |
|
Definition
| replacement therapy in men and women |
|
|
Term
| Which circumstances call for testosterone replacement therapy in men? |
|
Definition
- stimulate a delayed puberty
- when testes have been removed (surgically or accidental), treatment throughout life is needed |
|
|
Term
| Which circumstances call for testosterone replacement therapy in women? |
|
Definition
- sexual infantilism (lack of sexual development) which would lead to lack of oestrdiol, progesterone and testosterone)
- restore libido in postmenopausal women
- gynaecological disorders (linked to adverse effects) |
|
|
Term
| How was testosterone analogues used before athletes? |
|
Definition
- used to inhibit loss of protein and aid muscle regeneration after surgery or disorders (DMD)
- used post WW2 to aid recovery of victims of concentration camp |
|
|
Term
| What other clinical uses are there for testosterone? |
|
Definition
- some (nandrolone and oxadrolone) are useful for treating AIDs
- stimulation of growth in prepubertal bodies
- can stimulate appetite and feeling of well being with terminal diseases |
|
|
Term
| What are the 3 types of administration regiments used by athletes? |
|
Definition
Cycling
Pyramiding
Stacking |
|
|
Term
| Describe cycling administration |
|
Definition
| period of administration followed by a period of abstinence (6-8 weeks) |
|
|
Term
| What are the benefits of cycling administration |
|
Definition
| reduces incident of side effects |
|
|
Term
| Who prefers cycling administration |
|
Definition
|
|
Term
| Describe pyramiding administration |
|
Definition
| variation in cycling where it is gradually built up in the cyle to a peak and then is gradually reduced |
|
|
Term
| What are the supposed benefits of pyramiding administration |
|
Definition
| thought to reduce the behavioural effects of coming of a drug |
|
|
Term
| Describe stacking administration |
|
Definition
| use of more than one anabolic at a time, usually anabolic and injecting in order to avoid plateauing |
|
|
Term
| Why are amateur 'gym pharmacologists' wrong |
|
Definition
| they use stacking as they believe it stimulates more receptor sites, however the number of intracellular testosterone steroid receptors are stable and all saturated under normal conditions |
|
|
Term
| What is hCG what what is it used for? |
|
Definition
| dosing of hCG follows abuse cycles in males to restimulate testosterone production |
|
|
Term
| What are the specific side effects in males and females |
|
Definition
heart disease
liver cancer
depression
anger and hostility
eating disorders
stunted height
beard
acne
risk of HIV |
|
|
Term
| What are the general side effects in men? |
|
Definition
-reduced spermatogensis or even azospermia (absence of motile sperm)
-testicular atrophy
-gynaecomastia: development of mammary tissue 'moobs' |
|
|
Term
| What are the general side effects in women? |
|
Definition
- facial hair
- hoarsing/deepening of the voice
- genital reconfiguration (enlarged clitoris) |
|
|
Term
| What are the 4 specific side effects |
|
Definition
cardiovacscular
salt and water retention
hypertension
ventricular function
liver/kidney carcinomas
tendon damage
diabetes |
|
|
Term
| Describe the cardiovascular effects of steroidal abuse |
|
Definition
|
|
Term
| What causes increased osmotic pressure? |
|
Definition
| salt water retention and hypertension |
|
|
Term
| Describe the ventricular function after steroidal abuse |
|
Definition
thickening of left ventricle
cardiac myopathy
hypertrophy |
|
|
Term
| How is steroidal abuse and cancer related? |
|
Definition
| hepatic tissue dies which causes liver/kidney carcinomas |
|
|
Term
| How are tendons affected from steroidal abuse |
|
Definition
tendon cannot keep up with muscle growth
anabolics inhibit collagen formation |
|
|
Term
| How is diabetes caused by steroidal abuse |
|
Definition
| Type II due to increased insulin resistance |
|
|
Term
| What are the long term effects of testesterone analogues |
|
Definition
- Addiction (hormone dependent disorder) including behavoural effects like depression and psychotic symptoms
- irreversible testicular atrophy
- irreversible masculination in females
- premature death |
|
|
Term
|
Definition
| the single acute build up of bodily exertion or muscular activity that requires an expenditure of energy above resting level and that, in most, but not all, causes results in voluntary movements |
|
|
Term
| Define exercise mode and how it is classified |
|
Definition
the type of activity or sport
classified by energy demand or type of muscle action |
|
|
Term
|
Definition
| a consistent or chronic progression of exercise sessions designed to improve physiological function for better health or sport performance |
|
|
Term
| What is needed in aerobic exercise? |
|
Definition
| the ability to deliver large amounts of o2 to the working muscles for prolonged periods of time, and for these muscles to be able to use this o2 to generate ATP |
|
|
Term
| What is the first of 3 stages of getting O2 from the atmosphere to ATP regeneration to muscle mitochondria? and what system does it involve? |
|
Definition
| O2 in air to O2 in arterial blood (respiratory system) |
|
|
Term
| What is the second of 3 stages of getting O2 from the atmosphere to ATP regeneration to muscle mitochondria? and what system does it involve? |
|
Definition
| O2 in arterial blood to O2 in the interstitial fluid surrounding the muscle fibres (cardiovascular system) |
|
|
Term
| What is the last of 3 stages of getting O2 from the atmosphere to ATP regeneration to muscle mitochondria? and what system does it involve? |
|
Definition
| O2 in ISF to ATP in the mitochondria (muscle characteristic) |
|
|
Term
| What tasks does aerobic exercise impose on the cardiovascular system? |
|
Definition
1. pulmonary blood flow must increase to enhance gaseous exchange in the lungs
2. blood flow through the working muscles must increase
3. a reasonably stable blood pressure must be maintained |
|
|
Term
| In the case of exercise, O2 consumption may increase to up to about __ times its resting level |
|
Definition
|
|
Term
| How is a 13-fold o2 consumption increased? |
|
Definition
1.5x increase in stroke volume
3x increase in heart rate
3x increase in arteriovenous o2 difference |
|
|
Term
| Describe the relationship increase with CO and O2 consumption |
|
Definition
|
|
Term
| In an untrained adult, CO can increase from around ___L.min-1 at rest to a maximum of ____L.min-1. A ___ fold increase |
|
Definition
|
|
Term
| How does heart rate change during exercise? |
|
Definition
linearlly
work rate up to a maximum of 180-200 beats min-1 in adults |
|
|
Term
| What causes an increase in heart rate? |
|
Definition
- decreased vagal (parasympathetic) inhibitors
- increased sympathetic stimulation of the pacemaker cells in the SAN
- sympathetic stimulation of the AVN speeds up AP conduction and shortens the AV delay |
|
|
Term
| A ___ fold increase in CO can result in a ___fold increase in muscle blood flow |
|
Definition
|
|
Term
| What causes vasodilation in the vascular beds of active muscle and what does it cause? |
|
Definition
mainly caused by metabolic autoregulation
decreases resistance and increases blood flow |
|
|
Term
| What is vasoconstriction in the vascular beds mediated by, and what does it do? |
|
Definition
sympathetic nerves
diverts a greater proportion of the CO to active muscles |
|
|
Term
| What is arterovenous difference? |
|
Definition
| the difference in the O2 content of the blood between the arterial blood and venous blood. |
|
|
Term
| What does the arterovenous difference reflect? |
|
Definition
| the amount of O2 (per litre blood) that is taken up in the lungs and liberated in the peripheral tissues (primarily skeletal muscle) |
|
|
Term
| What can an arterovenous difference be increased to and how? |
|
Definition
3-fold increase
very low venous O2 conc (rather than an increase in arterial O2 content) |
|
|
Term
| What is O2 transport from the lungs to mitochondria of active muscles also known as? |
|
Definition
the maximal attainable cardiac output
extracellular resistance to diffusion between the erythrocytes and muscle myoglobin |
|
|
Term
| What structural cardiac changes increase cardiac output? |
|
Definition
- ventricular wall increases in thickness
- ventricular cavities enlarge
- myocardial vascularity increases |
|
|
Term
| What do structural cardiac changes increasing cardiac output also cause to change? |
|
Definition
| increases in ventricular EDV and ejection fraction (ESV decreases) which lead to an increase in stroke volume |
|
|
Term
| What factors cause stroke volume to increase? |
|
Definition
1. more blood in the ventricle at the start of systole (increased EDV)
2. less blood remaining at the end of systole (decreased ESV)
3. therefore increased ejection fraction |
|
|
Term
| How do trained and untrained individuals's resting CO compare? |
|
Definition
| very similar however a trained athlete achieves this at lower heart rates (due to an increase in resting stroke volume) |
|
|
Term
| How does an athletes heart rate change? |
|
Definition
- maximum heart rate is not significantly altered as a result of training
- lower resting heart rate
- therefore a larger change can occur |
|
|
Term
| Athletes can achieve a maximum CO up to _x resting |
|
Definition
|
|
Term
| Which adaptations improve the diffusion of O2 from blood to muscle mitochondria? |
|
Definition
1. development of new capillaries
2. muscle mitochondria
3. muscle myoglobin |
|
|
Term
| How do development of new capillaries improve the diffusion of O2 from blood to muscle mitochondria? |
|
Definition
| within the skeletal muscle vascular beds reduce the average diffusion distance |
|
|
Term
| How do muscle mitochondria improve the diffusion of O2 from blood to muscle mitochondria? |
|
Definition
| increases in number, especially at sub-sarcolemmal sites close to capillaries |
|
|
Term
| How do muscle myoglobin improve the diffusion of O2 from blood to muscle mitochondria? |
|
Definition
|
|
Term
| How does endurance training change blood volume? |
|
Definition
| increases blood volume (more intense training causes greater effect) |
|
|
Term
| What causes the increase in blood volume from endurance training? |
|
Definition
initially caused by a result in increased plasma volume due to the osmotic effect of increased amount of plasma proteins, especially albumin
followed by increased RBCs |
|
|
Term
| How does this affect the haematocrit? |
|
Definition
| plasma volume increases more than total RBC mass which decreases haematocrit slightly |
|
|
Term
| What does a decreased haematocrit mean? |
|
Definition
- reduces blood viscosity
- which reduces resistance to flow
- enhances o2 delivery to active muscle |
|
|
Term
| Describe the mechanism of muscle myoglobin |
|
Definition
1. o2 enters muscle fibre and binds to myoglobin
2. myoglobin stores O2 and releases it into mitochondria when o2 availability decreases |
|
|
Term
| What are oxidative enzymes and their significance |
|
Definition
| oxidative enzymes (eg SDH and CT) are dramatically influenced by aerobic training |
|
|
Term
| How can ATP be generated? |
|
Definition
1. use of phosphocreatine (PCr) stores
2. anaerobic glycolysis
3. oxidative phosphorylation |
|
|
Term
| When does the creatine kinase reaction occur? |
|
Definition
| brief, intense bursts of muscular activity (eg 100m sprint) |
|
|
Term
| What do muscles rely on in the first few seconds of exercise? |
|
Definition
| muscles rely on existing ATP stores |
|
|
Term
| What do muscles rely on in the additional 10-20 seconds of exercise? |
|
Definition
| utilise phosphocreatine stores |
|
|
Term
| What occurs post exercise? |
|
Definition
| stores are rapidly re-synthesised post-exercise |
|
|
Term
| When does glycolysis occur? |
|
Definition
| peak levels of activity (>20s) |
|
|
Term
| What occurs in glycolysis? |
|
Definition
| pyruvic acid concerted into lactic acid |
|
|
Term
| What are the negatives in glycolysis? |
|
Definition
| inefficient and un-desireable pH |
|
|
Term
| When does oxidative phosphorylation occur? |
|
Definition
| sustained, moderate exercise (eg running a marathon) |
|
|
Term
| What occurs in oxidative phosphorylation? |
|
Definition
- glucose/glycogen are catabolised to pyruvic acid (glycolysis)
- pyruvic acid and rarely amino acids are metabolised in the mitochondria |
|
|
Term
| What are the benefits of oxidative phosphorylation? |
|
Definition
| high yield of ATP and sustainable |
|
|
Term
| What factors are used to classify skeletal muscle fibres? |
|
Definition
| contractile speeds and metabolic capacities |
|
|
Term
| What are the major classes of skeletal muscle fibres? |
|
Definition
slow oxidative fibres (type I)
fast oxidative fibres (type IIa)
flast glycolytic fibres (type IIX) |
|
|
Term
| What fibres do muscles contain? |
|
Definition
| muscles usually contain all 3 but in different proportions |
|
|
Term
|
Definition
| fatigue resistance, high endurance and low power. |
|
|
Term
| What are type of exercise are Type I fibres specialised for? |
|
Definition
| performance of repeated, relatively weak , contractions over prolonged period |
|
|
Term
| What are type of exercise are Type IIX fibres specialised for? |
|
Definition
specialised for delivering rapid, powerful contractions for brief periods.
quickly fatigues |
|
|
Term
|
Definition
contract rapidly (like Type IIX)
high oxidative capacity (like Type I)
Intermediate power output and fatigue resistance |
|
|
Term
| What is an individuals fibre composition determined by? |
|
Definition
|
|
Term
| How is pH related to fatigue? |
|
Definition
1. lactate produced by glycolysis
2. strong contractions cause blood vessels supplying glycotic fibres to be compressed
3. o2 delivery and lactate removal decreased
3. potentially leads to fatigue |
|
|
Term
| What is thought to cause fatigue in low-intensity exercise? |
|
Definition
1. lactate accumulation does not occur
2. oxidative fibres, thought to occur due to substrate depletion (glycogen in particular) |
|
|
Term
| What are the 6 laws of training? |
|
Definition
1. specificity principle
2. overload principle
3. progression principle
4. individually principle
5. principle of diminishing returns
6. principle of reversibility |
|
|
Term
| Describe the specificity principle |
|
Definition
| adaptation is specific to the muscles trained, the intensity of the exercise performed, the metabolic demands of the exercise and the joint angle trained |
|
|
Term
| Describe the overload principle |
|
Definition
| for training adaptations to occur, the muscle or physiological component being trained must be exercised at a level that it is not normally accustomed to. Muscle needs to be stimulated with a resistance of relatively high intensity. |
|
|
Term
| Describe the progression principle |
|
Definition
| in order to maintain the same absolute training stimulus, the resistance used continually needs to be modified |
|
|
Term
| Describe the individuality principle |
|
Definition
| people respond differently to the same training stimulus depending on pre-training status, genetic pre-disposition, gender and age |
|
|
Term
| Describe the principle of diminishing returns |
|
Definition
| performance gains are related to the training experience of the individual |
|
|
Term
| Describe the principle of reversibility |
|
Definition
| when the training stimulus is removed or reduced, the ability of the athlete to maintain performance at a particular level is also reduced |
|
|
Term
| What characteristic make for a good sprinter? |
|
Definition
1. large muscle mass (hypertrophy of the relevant muscle groups)
2. high proportion of fast-twitch (Type II) muscle fibres
3. rapid reaction time, highly developed balance and agility
4. high capacity for anaerobic respiration |
|
|
Term
| What training uses anaerobic training? |
|
Definition
|
|
Term
| Which training used more fast twitch fibres? and therefore which fibres undergo hypertrophy? |
|
Definition
anaerobic training
consequently Type IIa and Type IIX fibres undergo hypertrophy |
|
|
Term
| What does anaerobic training improve? |
|
Definition
| the muscles capacity to tolerate the H+ that accumulates due to lactic acid production |
|
|
Term
| How much does the buffer capacity increase by following 2 months of anaerobic training? |
|
Definition
|
|
Term
| What are the major intracellular buffers? |
|
Definition
phosphate
histidine-containing peptides (eg camosine)
proteins |
|
|
Term
| What happens to extracellular buffering? |
|
Definition
| it is enhances so H+ can leave muscle fibres at a faster rate |
|
|
Term
| What are the major extracellular buffers? |
|
Definition
| bicarbonate and blood proteins (albumin) and haemoglobin |
|
|
Term
| What are the 4 epithelial barriers? |
|
Definition
skin
linings of the lungs
linings of the GI system
linings of the kidney tubules |
|
|
Term
| When does a substance enter the internal environment? |
|
Definition
| when the substance crosses the epithelial barrier |
|
|
Term
| Define the internal environment |
|
Definition
| ISF because it constitutes the immediate environment of most the body's cells |
|
|
Term
|
Definition
| maintenance of the ISF's composition, temperature and volume |
|
|
Term
| Refine regulated variable |
|
Definition
| maintained within narrow limits (eg MAP) |
|
|
Term
|
Definition
| acute regulation of MAP around a set point of 95mmHg |
|
|
Term
| what does systematic vascular resistance (SVR) equal? |
|
Definition
| total peripheral volume (TPR) |
|
|
Term
| What follows an increase in blood volume? |
|
Definition
1. increase in venous pressure
2. increase in venous return to the heart
3. increase in EDV
4. increase in SV
5. therefore increase in CO
6. therefore increase in MAP
7. increase in urinary losses of sodium and water
8. decrease in plasma volume
9. decrease in blood volume |
|
|
Term
| How do you calculate cardiac output? |
|
Definition
| heart rate x stroke volume |
|
|
Term
| How do you calculate mean arterial pressure? |
|
Definition
| cardiac output x total peripheral resistance |
|
|
Term
| How are the long term changes in blood volume? |
|
Definition
- changes in the concentration of plasma proteins (primarily albumin) which affect the osmotic balance between plasma and ISF
- changes in the numbers of formed elements of blood (primarily RBCs) that are present. |
|
|
Term
|
Definition
bleeding or the abnormal flow of blood.
may be external or internal |
|
|
Term
|
Definition
| a critical condition brought about as a result of a sudden drop in blood flow around the body |
|
|
Term
| Describe the changes in MAP following a blood donation |
|
Definition
| loss of 10% of total blood volume is well tolerated, with little change in MAP |
|
|
Term
| Describe the changes in MAP following loss of over 10% of total blood volume (eg after haemorrhage) |
|
Definition
| significant loss leads to loss in MAP and recovery is not certain |
|
|
Term
| What are the compensatory mechanisms following a decline in MAP? |
|
Definition
- baroreceptor reflexes
- chemoreceptor reflexes
- cerebral ischaemia responses
- reabsorption of tissue fluids
- release of endogenous vasoconstrictor substances
- renal conservation of salt and water |
|
|
Term
| What is the general aim of the compensatory mechanisms following a decline in MAP? |
|
Definition
| increase CO and/or TPR and hence MAP |
|
|
Term
| Describe the baroreceptor reflex |
|
Definition
| decrease in MAP and pulse pressure result in decreased stimulation of the arterial baroreceptors located in the carotid sinuses and aortic arch |
|
|
Term
| What are the results of the baroreceptor reflex? |
|
Definition
Increase in sympathetic and decrease in parasympathetic nervous activity:
1. increase heart rate
2. increased myocardial contractility, leading to increased SV
3. venoconstriction, leading to increased venous pressure, EDV and SV
4. vasoconstriction (systematic arterioles, leading to increase TPR) |
|
|
Term
| Describe the chemoreceptor reflex |
|
Definition
| lower threshold for arterial baroreceptor stimulation (60mmHg) |
|
|
Term
| What are the primary effects of the chemoreceptor reflex? |
|
Definition
1. sympathetically-mediated vasoconstriction (increases TPR)
2. stimulation of the respiratory centre leading to increased rate and depth of breathing |
|
|
Term
| What are the benefits of the chemoreceptor reflex? |
|
Definition
- a reflex increase in heart rate (increases CO)
- increase in venous return (increases EDV and SV therefore CO) |
|
|
Term
| When does cerebral ischaemia occur? |
|
Definition
| When MAP < 40mmHg and the sympathoadrenal system is acitvated |
|
|
Term
| What are the results of cerebral ishaemia? |
|
Definition
1. intense vasoconstriction which further increases TPR
2. increases in myocardial contractility which increases SV therefore CO
BOTH INCREASE MAP |
|
|
Term
| What do severe degrees of cerebral ischaemia cause? |
|
Definition
- stimulation of vagal centres
- increased parasympathetic discharge
- bradycardia
- decreased CO
- decreased MAP |
|
|
Term
| What brings about decreased hydrostatic pressure in capillaries? |
|
Definition
1. decreased MAP
2. arteriolar vasocontriction
3. reduced venous pressure |
|
|
Term
| What does decreased hydrostatic pressure in capillaries promote? |
|
Definition
| NET reabsorption of ISF into the capillaries, increasing blood volume |
|
|
Term
| What occurs to the levels of circulating catecholamines when MAP <40mmHg? |
|
Definition
| they increase up to x50 resting levels, reinforcing the effects of sympathetic nervous activity |
|
|
Term
|
Definition
| potent vasoconstrictor and secreted by the posterior pituitory in response to haemorrhage |
|
|
Term
| What are the effects of this? |
|
Definition
increased TPR and therefore MAP.
Decreased renal perfusion leads to the secretion of renin (which leads to formation of angiontensin II, a very potent vasoconstrictor) |
|
|
Term
| Fluids and electrolytes are conserved in the kidney after several stimuli, these include: |
|
Definition
1. ADH which stimulates the reabsorption of water
2. increased renal sympathetic nerve activity reduces excretion of NaCl + H2O
3. decreased MAP decreases GFR therefore loses
4. angiotensin II stimulates aldosterone release which increases reabsorption |
|
|
Term
| What are the 5 decompensatory mechanisms |
|
Definition
1. cardiac failure
2. acidosis
3. CNS depression
4. aberrations in blood blotting
5. depression of MPS |
|
|
Term
| Describe how a decline in MAP causes cardiac failure |
|
Definition
| decreased MAP reduces coronary blood flow which depresses ventricular function therefore decreases CO and MAP |
|
|
Term
| What does decreased blood flow to peripheral tissues lead to? |
|
Definition
| an accumulation of vasodilator metabolites therefore decreased TPR and MAP |
|
|
Term
| How does decreased MAP lead to acidosis? |
|
Definition
- inadequate blood flow = inadequate o2 delivery
- increased production of anaerobic metabolites (eg lactic acid)
- impaired kidney function reduces H+ excretion
- depresses cardiac function |
|
|
Term
| How does decreased MAP lead to CNS depression? |
|
Definition
- cerebral ishaemia result in sympathetic stimulation of the heart and blood vessels
- depressed cardiovascular centre therefore reduced sympathetic activity (decreased MAP)
- endogenous opoids released |
|
|
Term
| How does decreased MAP lead to aberrations in blood clotting? |
|
Definition
1. Hyper-coagulability: platelets and leukocytes adhere to the vascular endothelium and clots develop
2. release of TXA2 from ischaemic tissues enhances the response |
|
|
Term
| Describe the mononuclear phagocytic system |
|
Definition
1. MPS becomes depressed
2. phagocytic activity of the MPS is modulated by an opsonic protein
3. opsonic activity in plasma decreases in shock
4. antibacterial and antitoxin defence mechanisms impaired
5. endotoxin has a vasodilatory effect therefore decreased TPR and MAP |
|
|
Term
|
Definition
| attraction of 2 masses, objects accelerate to Earth at 1g (9.8ms-2) and exists in orbit (eg 250 miles above Earth the gravitational field strength in 89% of that on Earth) |
|
|
Term
|
Definition
| free falling/seems weightless (1 x10-6g) |
|
|
Term
| What are the 4 physiological adaptations and prevention before going into space? |
|
Definition
Neurovestibular disturbances
Physiosocial effects
Immune dysregulation
Fluid redistribution |
|
|
Term
| Describe neurovestibular disturbances in space and what causes it |
|
Definition
space motion sickness occurs 1-2 days after arriving in space and on return to Earth
caused by neurovestibular and visual mismatch (can impair emergency function) |
|
|
Term
| What is the treatment for neurovestibular disturbances |
|
Definition
| time and anti-nausea medication |
|
|
Term
| What physiosocial effects do astronauts experience? |
|
Definition
- sleep deprivation due to acoustic noise
- disrupted circadian cycles
- isolation from family |
|
|
Term
| How are astronauts treated for the physiosocial effects they experience? |
|
Definition
- rigorous selection procedures
- sleeping medication |
|
|
Term
| How are astronauts immune systems disturbed? |
|
Definition
- immune response suppressed = viral/bacterial infections
- lymphocyte activity reduced
- decreased NK cells
- impaired cell mediated immunity
- high emotional/physical stress levels
- promotes reactivation of latent Herpes virus |
|
|
Term
| How are astronauts treated for immune dysregulation? |
|
Definition
|
|
Term
| Describe fluid redistribution astronauts undergo |
|
Definition
- fluid moves to the head (10% less in the legs)
- distension of vascular baroreceptors (carotid artery and aorta) reduce renin-angiotensin and cause release of ANP leading to increased water and salt retention and reduction in plasma volume |
|
|
Term
| What is the overall blood change? |
|
Definition
| overall blood volume and RBS decreased (10%) |
|
|
Term
| How does SV change during space flight |
|
Definition
|
|
Term
| What changes occur post flight? |
|
Definition
aerobic capacity is decreased post flight due to reduced SV
low blood pressure |
|
|
Term
| What are the treatments for fluid redistribution? |
|
Definition
- exercise during microgravity
- negative pressure suits for lower body fluid redistribution
- on return, isotonic fluids |
|
|
Term
| How do muscles change during space? |
|
Definition
| loss of muscle mass and strength (especially postural muscles) |
|
|
Term
| What is muscle change caused by? |
|
Definition
| absence of gravitational loading on bones and muscles which cause protein synthesis decreased and degradation increased |
|
|
Term
| What changes occur to the muscle fibres? |
|
Definition
reduction in muscle fibre size (atrophy)
Type I fibres shift to type II |
|
|
Term
| How are muscle effects treated? |
|
Definition
- 2hrs exercise a day (not that effective and consumes on board time and resources)
- dietary supplements with amino acids and electrical stimulation
- return to earth exercise programmes return muscle mass |
|
|
Term
| What are the effects on bone and how is this caused? |
|
Definition
| reduced bone density caused by higher co2 concentration which causes respiratory acidosis. bone broken down to use phosphate and bicarbonate for buffers. Also leads to calcium loss |
|
|
Term
| What other bone effects are there? |
|
Definition
PTH is decreased
Vit D is decreased in blood therefore increased risk of kidney stones due to elevated Ca2+ excretion |
|
|
Term
| How are bone effects treated? |
|
Definition
dietary supplements (Vit D and K)
resistance exercise |
|
|
Term
| What is our atmosphere defined as? |
|
Definition
| pressure exerted by the approximate 24 miles of air above us. 760mmHg. |
|
|
Term
|
Definition
|
|
Term
| __ of water (noncompressable) exerts the same pressure as __ miles of air (compressable). Each __ depth of water adds _ ATA of pressure |
|
Definition
|
|
Term
|
Definition
at a constant temperature, the volume of a gass is inversely proportional to the pressure to which it is exerted.
pressure 1 x volume 1 = pressure 2 x volume 2 |
|
|
Term
| What does Boyle's Law have a negative effect on in the body? |
|
Definition
| air spaces in the body eg sinuses/ears/lungs |
|
|
Term
|
Definition
| swimming underwater on a single breath. |
|
|
Term
| What is the arterial PO2 required for consciousness? |
|
Definition
|
|
Term
|
Definition
| the pressure exerted by a mixture of gases is equal to the sum of the partial pressures |
|
|
Term
| How does pressure change as divers descend? |
|
Definition
| pressure increases and partial pressure of O2 does so consciousness can be maintained. |
|
|
Term
| How does pressure change as divers ascend? |
|
Definition
| pressure drops and PO2 falls |
|
|
Term
| What is the mammalian diving reflex? |
|
Definition
| bradycardia (slowed heart rate) when face is immersed in water to conserve air |
|
|
Term
| How does ear pressure change during descent? |
|
Definition
| pressure on the outside of the eardrum increases and the eardrum is pushed inwards (very painful). This can cause the eardrum to rupture unless the diver equalises |
|
|
Term
| What is a mask squeeze and when is it used? |
|
Definition
pressure changes can suck/push on eyeballs causing damage.
diver equalises pressure by breathing into mask through the nose |
|
|
Term
| What happens to air spaces as depth increases? |
|
Definition
| volumes of air spaces (eg lungs) are decreased (Boyles Law) |
|
|
Term
| What are the effects of decreased air space volumes and how does the body oppose them? |
|
Definition
- lung squeeze could cause rupture of capillaries, internal bleeding and collapsed lung.
- blood shift from other parts of the body and flood the lungs to resist collapse
- blood is drawn from the peripheries to the vital organs |
|
|
Term
| What factors positively affect maximum breath hold time? |
|
Definition
- breathing movements
- diving response
- valsava
- swallowing
- larger lung volume
- respiratory isometric exercise
- central voluntary suppression of respiratory drive |
|
|
Term
| What factors negatively affect maximum breath hold time? |
|
Definition
- cold shock
- low O2
- high CO2
- chest wall afferents |
|
|
Term
| What is the started pressure in a SCUBA tank? |
|
Definition
|
|
Term
| What changes occurs at the first stage? |
|
Definition
| reduces pressure to 10 ATA above ambient |
|
|
Term
| What changes occurs at the second stage? |
|
Definition
| delivers air to diver at ambient pressure |
|
|
Term
|
Definition
| the weight of gas absorbed by a given weight of liquid with which it does not combine chemically is directly proportional to the partial pressure of gas above the liquid |
|
|
Term
| What does Henry's Law mean for divers? |
|
Definition
| The greater the pressure, the more gas dissolves in liquid, when pressure is reduced, gas will come out of solution. As they go down gas goes into tissue and vice versa. |
|
|
Term
| What are the problems associated with breathing gases at pressure? |
|
Definition
1. air embolism
2. nitrogen narcosis
3. decomposition sickness
4. oxygen toxicity |
|
|
Term
|
Definition
| excessive stretching of the alveolar membrane forces micro bubbles into the circulation, these aggregate and can lodge in the brain or other vital organs. |
|
|
Term
| What causes air embolism? |
|
Definition
when a diver ascends their lungs expand (Boyles Law)
unless the diver exhales during ascent, their lungs will be damaged |
|
|
Term
| What is spontaneous pneumothorax and intestinal emphysema? |
|
Definition
| excessive expansion can tear the alveoli causing lungs to collapse |
|
|
Term
| What is nitrogen narcosis? |
|
Definition
| nitrogen dissolves into blood and acts as a neural anaesthetic |
|
|
Term
| At what distance causes an intoxicating effect? |
|
Definition
20-30m
70m+ cause stupor and unconciousness |
|
|
Term
| What is nitrogen narcosis influenced by? |
|
Definition
| conditions (eg darkness, cold and nervousness) |
|
|
Term
| What does nitrogen do at depth? |
|
Definition
- at depth, nitrogen dissolves into the blood and tissues
- reaches equilibrium slowly in many tissues and dissolves more in fatty tissues and leave the body slowly |
|
|
Term
| What occurs regarding nitrogen upon ascent? |
|
Definition
| dissolved nitrogen comes out of solution and forms bubbles in body tissues and fluids |
|
|
Term
| What are the symptoms of decompression sickness? |
|
Definition
they appear 4-6 hours after dive (severe in minutes)
- dizziness, itchy skin, joint pain
- CNS bubbles : tension in brain and spinal cord
- lungs: asphyxia |
|
|
Term
| What is the treatment for decompression sickness? |
|
Definition
O2 therapy on site
decompression chambers |
|
|
Term
| What is the prevention for decompression sickness? |
|
Definition
decompression stops
time of stop determined by slowest tissue in terms of nitrogen elimination |
|
|
Term
|
Definition
- high o2 levels for sufficient time is toxic
- oxygen can be reduced to form free radicals
- high levels of free radicals damage cellular components and membranes |
|
|
Term
| How can O2 toxicity and nitrogen narcosis be reduced? |
|
Definition
by varying gas mixes
helium is the most common inert gas substituted for N2 in deep diving because it does not induce narcosis and is more easily rid from the body |
|
|
Term
| What are the issues with temperature and diving? |
|
Definition
| water conducts heat away from the body (hypothermia) |
|
|
Term
| What is used to solve thermal issues in diving? |
|
Definition
passive systems: wet/dry suits
active thermal protection: electrically heated suits and hot water suits |
|
|
Term
| What is saturation diving? |
|
Definition
-divers are hailed in steel chambers pressurised to the depth at which they are working (they do not decompress between dives)
-nitrogen in the air is replaced by helium
-end of working period the pressure is slowly brought back to 1 ATA |
|
|
Term
| What effects does cold air have on a body? |
|
Definition
1. peripheral cooling: incapacitation and cold injury
2. deep body cooling: hypothermia |
|
|
Term
|
Definition
body core temperature falls below 35 degrees C
classified as mild, moderate and severe |
|
|
Term
| What are the 3 major responses to a fall in body core temperature? |
|
Definition
1. increased heat production (shivering and non-shivering thermogenesis)
2. decreased heat loss (peripheral vasoconstriction)
3. behavioural responses (clothing, sheltering, huddling) |
|
|
Term
|
Definition
| the movement of air over the surface of the body increases the rate of heat loss via convection. Therefore increased wind speed increases risk. |
|
|
Term
| At what temperature does mild hypothermia occur? |
|
Definition
|
|
Term
| What are the body's responses to mild hypothermia? |
|
Definition
normal
- intense cold sensation
- peripheral vasoconstriction
- violent shivering |
|
|
Term
| What are the effects of the body's responses to mild hypothermia? |
|
Definition
- vasoconstriction reduced heat losses
- shivering increases heat production |
|
|
Term
| At what temperature does moderate hypothermia occur? |
|
Definition
|
|
Term
| What are the body's responses to moderate hypothermia? |
|
Definition
they begin to fail and spontaneous recovery becomes unlikely
- decreased shivering
- joints become stiff and muscles rigid
- progressive reduction in metabolism and VO2
- CNS cooling = dullness, irrational behaviour and unconsciousness
- cardiac cooling = decreasing heart rate and CO |
|
|
Term
| At what temperature does severe hypothermia occur? |
|
Definition
|
|
Term
| What are the effects of severe hypothermia? |
|
Definition
intensified moderate hypothermia
- heart rate continues to fall
- heart becomes irritable and prone to arrhythmias
- cooling and dehydration increase blood viscosity
- slow and shallow respiration
- ventricular fibrillation causes death (27degrees) |
|
|
Term
| Who would active rewarming be appropriate for? |
|
Definition
moderately cold (Tcore below 34)
shivering and fully concious |
|
|
Term
| How can active rewarming be carried out? |
|
Definition
supervised hot bath (40)
hot shower (less effective and can induce 'rewarming collapse' |
|
|
Term
| What are the advantages of active rewarming? |
|
Definition
- quickly, rapidly and restores feeling of well being (reduced stress)
- inhibits/reduced intensity of shivering therefore reduces heart workload |
|
|
Term
| Who would passive/assisted rewarming be appropriate for? |
|
Definition
severely hypothermic (Tcore below 34)
unconscious or semi-conscious |
|
|
Term
| How can passive/assisted rewarming be carried out? |
|
Definition
sleeping bag/blankets
insulated head
unconscious patients in the recovery position |
|
|
Term
| Why is passive/assisted rewarming used? |
|
Definition
slow rate of reawrming (0.5-1 degrees per hour)
reduces the risk of rewarming collapse |
|
|
Term
| When is extraneous heating used and how? |
|
Definition
- if shivering is absent and Tcore is near lethal level (below 30)
- hot water bottle or electric blanket |
|
|
Term
| When does frostbite occur and what happens? |
|
Definition
when the temperature of exposed peripheral tissues falls below -0.55 degrees c
tissue fluid may freeze |
|
|
Term
| Define mild and severe frostbite |
|
Definition
mild -> only skin
severe -> deep tissue (muscle, tendon, bone) |
|
|
Term
| What causes cell damage in frostbite? |
|
Definition
| mechanical action of ice crystals and from cell dehydration |
|
|
Term
| What effect does freezing have on small blood vessels? |
|
Definition
| causes the permeability of small blood vessels to increase, which causes a loss of fluid from the circulation into the ISF |
|
|
Term
| What happens to blood vessels upon thawing? |
|
Definition
- RBCs 'sludging' in microcirculation, which reduces/stops local blood flow
- leads to gangrene and possible loss of fingers, toes etc |
|
|
Term
| When does a Non-freezing cold injury (NFCI) occur? |
|
Definition
at tissue temperatures 17-(-0.55) degrees c last for a protracted period.
cold, wet feet lose heat very rapidly, inducing intense local vasoconstriction |
|
|
Term
| What are the effects of a Non-freezing cold injury (NFCI)? |
|
Definition
- local hypoxia
- accumulation of toxic metabolites
(both cause tissue death)
- blisters, ulcers and gangrene (may need amputation) |
|
|
Term
Thermal conductivity of water is ____ than that of air.
The rate of heat loss is ____ in water than in air. |
|
Definition
|
|
Term
| When does cold shock occur? |
|
Definition
| lasts for one minute after sudden immersion in cold water |
|
|
Term
| What are the 3 responses to cold shock? |
|
Definition
1) involuntary inspiratory gasp in response to rapid skin cooling
2) hyperventilation leads to loss of consciousness due to reduced cerebral blood flow
3) peripheral vasoconstriction leads to increased after load on the heart |
|
|
Term
| What are the main causes of death from cold shock? |
|
Definition
drowning
cardiac arrest
cardiac arrhythmias |
|
|
Term
| When does cold incapacitation occur? |
|
Definition
| 5-10 mins of being in cold water |
|
|
Term
| What are the body's responses to cold incapacitation? |
|
Definition
- vasoconstriction decreases blood flow to the extremities (thus allowing peripheries to cool) to protect the vital organs
- muscles and nerve fibres fail and movement is lost (drowning) |
|
|
Term
| How long does it take for an adult to become mildly hypothermic? |
|
Definition
| 30 mins immersed in cold water |
|
|
Term
| What factors affect survival rates? (5) |
|
Definition
1. subcutaneous fat levels
2. surface area to volume ratio
3. magnitude of shivering response
4. activity levels and posture
5. clothing (amount and type) |
|
|
Term
| What factors determine collapse? |
|
Definition
heightened senses
high stress hormones |
|
|
Term
| What are the effects of collapse? |
|
Definition
- mental relaxation and muscular relaxation
- decreasing the level of stress hormones
- decreased blood pressure
- cardiac function is significantly affected by victim handling and removal |
|
|
Term
| What are the rescue techniques of collapse? |
|
Definition
- horizontally/head down
- helicopter: head should be towards the front of aircraft
- rescue boat: head should be towards the stern |
|
|
Term
| What are the 3 human adaptations to cold? |
|
Definition
metabolic -> increased metabolic response to cold
insulative -> increased insulation
hypothermic -> greater fall in deep body temperature on exposure to cold |
|
|
Term
|
Definition
| condition in which the body or a region of the body is deprived of adequate oxygen supply (general or local) |
|
|
Term
| What is sea level atmospheric pressure |
|
Definition
|
|
Term
| When is aerobic performance affected? |
|
Definition
|
|
Term
| What is compromised at higher altitudes? |
|
Definition
| The gradient that drives gas exchange in the lungs due to lower pressure. This causes the blood to become less saturated and the body has to work harder to maintain delivery. |
|
|
Term
| What altitude is inhabitable? |
|
Definition
|
|
Term
| At what altitude is there an AMS risk? |
|
Definition
|
|
Term
| When should acclimation occur? |
|
Definition
| 1500-4000m (extreme risk) |
|
|
Term
| What should be avoided at all costs? |
|
Definition
|
|
Term
| How are hypoxia responses measured? |
|
Definition
oxyhaemoglobin (Hb02) saturation monitored
nearly 100% saturation at rest |
|
|
Term
|
Definition
| process in which an organism adjusts to a gradual change in its environment, allowing it to maintain performance across a range of environmental conditions |
|
|
Term
| What responses does one undergo under acclimatisation? |
|
Definition
- increase heart rate
- hyperventilation
- increased haemoglobin concentration
- increased capillary density |
|
|
Term
| Describe the factors for acclimatisation management? |
|
Definition
optimal altitude: 2000-2500m
>20 days
22 hours a day |
|
|
Term
| What are the health risks at altitude? |
|
Definition
acute mountain sickness (AMS)
high altitude cerebral oedema (HACE)
high altitude pulmonary oedema (HAPE) |
|
|
Term
| Where does AMS occur and who does it affect? |
|
Definition
>2500-3000m
unacclimatised athletes at low altitudes and people with dulled ventilatory response to altitude, however, no clear predictors |
|
|
Term
| What are the symptoms of AMS |
|
Definition
- rapid onset (3-96hours)
- severe headache, nausea, vomiting, fluid retention
- malaise, dyspnoea, rapid pulse, insomnia
- loss of appetite, indigestion, flatulence, constipation
- incapacitation for several days
- hypoxaemia and alkalosis implicated |
|
|
Term
|
Definition
- no treatment with aerobic training
- if symptoms persist, return to sea level
- rapid recovery with descent
- supplemental o2
- drug: acetazolamide |
|
|
Term
| How can all health risks with altitude be avoided? |
|
Definition
| slow rate of ascent 1300.day^-1 >3000m |
|
|
Term
| Where does HACE occur and who does it affect? |
|
Definition
> 4300m
athletes at low altitudes (>3000m) plus those who ascent too quickly |
|
|
Term
| What are the symptoms of HACE |
|
Definition
- rapid onset (12 hours)
- severe headache caused by severe head swelling, which is caused by fluid shifts and increased in cranial/spinal pressure
- ashen skin colour
- mental confusion by pulmonary oedema
- poor movement co-ordination
- often occurs in combination with HAPE |
|
|
Term
|
Definition
- treatment is essential, otherwise will result in death/coma
- immediate descent and return to sea level
- rapid recovery upon descent but complications may last > 1 week
- supplemental o2
- drug: dexmethasome (powerful anti-inflammatory) |
|
|
Term
| Where does HAPE occur and who does it affect? |
|
Definition
rapid ascent >2700m
can afflict athletes at low altitudes (>3000m) plus those who ascend too rapidly. Young active males in particular |
|
|
Term
| What are the symptoms of HAPE |
|
Definition
- rapid onset (12-96hours)
- accumulation of fluid in the lungs inhibits gas transfer
- caused by fluid shifts linked to hypobaria
- excessive, rapid breathing, tachycardia
- bluish skin colour (poor Hb saturation)
- coughing, spluttering, production of frothy sputum
- in combination with HACE |
|
|
Term
|
Definition
- immediate
- immediate descent to sea level
- portable 'Gamov' bag reduced altitude by 2000m
- drug: Nifidipine (vasodilator) |
|
|
Term
| Extreme heat strain danger... |
|
Definition
| heat/sun stroke highly likely |
|
|
Term
|
Definition
| sunstroke, muscle cramps and/or heat exhaustion likely |
|
|
Term
| Extreme heat strain caution... |
|
Definition
| sunstroke, muscle cramps and/or heat exhaustion |
|
|
Term
|
Definition
|
|
Term
|
Definition
| stored energy = metabolic heat produced - (+/-)mechanical work +/- radiation +/- convection +/- conduction +/- evaporation |
|
|
Term
| When is there a risk of cell denaturation? |
|
Definition
| when body temp is 42 degrees c |
|
|
Term
| What is the Critical internal temperature hypothesis? |
|
Definition
exercise in the heat is limited by a critical internal temperature. Homeostatic.
untrained > 38.7 DC
trained > 40DC |
|
|
Term
| What is the Central Governor Model? |
|
Definition
There is an anticipatory reduction in work intensity by:
- heat storage in the skin
- feed towards loop
- prevents critical internal temperature (>40DC)
- concious |
|
|
Term
| What is the maximal sweat rate? |
|
Definition
|
|
Term
| What is a marathon runners sweat rate? |
|
Definition
|
|
Term
| When is dehydration fatal and then critical? |
|
Definition
| about 10% is fatal and 5.5% is critical |
|
|
Term
| What effect does dehydration have on the heart? |
|
Definition
| Dehydration causes a decrease in plasma volume and therefore the heart need to work harder to achieve the same outcome. Cardiovascular drift is amplified. |
|
|
Term
| Consequently, how does dehydration impair cardiovascular systems? |
|
Definition
1. reduced plasma volume
2. reduced blood volume
3. reduced stroke volume, increased heart rate
4. skeletal muscle o2 demand remains constant: battle of metabolism and thermoregulation |
|
|
Term
| What are the effects of dehydration on the body? |
|
Definition
1. decreased skin blood flow
2. decreased sweating
3. increased body temperature
4. increased risk of heat illness and exhaustion |
|
|
Term
|
Definition
| brief fainting spell without significant rise in body temperature |
|
|
Term
|
Definition
| an inability to continue exercising |
|
|
Term
| What are the signs of heat exhaustion? |
|
Definition
- ineffective circulatory adjustments and reduced blood volume
- raised Tb
- no organ damage
- persistent sweating
- up to 7% loss in body mass |
|
|
Term
| What are the symptoms of heat exhaustion? |
|
Definition
- breathlessness and hyperventilation
- weak and rapid pulse
- dizziness and headache
- flushed skin
- nausea and irritability
- lethargy and general weakness |
|
|
Term
| What is the treatment for heat exhaustion? |
|
Definition
- cease exercising
- remove from heat source
- lie down
- control breathing/reduce panic
- rehydrate
- forced convective cooling |
|
|
Term
| Who is at risk of heat exhaustion? |
|
Definition
| trained and untrained sportspeople, especially unacclimatised atheletes |
|
|
Term
|
Definition
| failure of the thermoregulatory system resulting in significantly elevated Tb |
|
|
Term
| What are the signs of heat stroke? |
|
Definition
- medical emergency
- Tb raised significantly
- risk of organ damage
- sweating may or may not be present
- onset may be rapid |
|
|
Term
| What are the symptoms of heat stroke? |
|
Definition
- confusion
- dry skin (if sweating is absent)
- circulatory instability and/or thermoregulatory collapse
- vomiting/diarrhoea
- confusions/coma |
|
|
Term
| What is the treatment for heat stroke? |
|
Definition
- artificial sweat (spray casualty)
- consider water immersion
- deep body temperature monitored every 5 mins
- casualty should improve rapidly, if not evacuate to medical facility |
|
|
Term
| Who is at risk of heat stroke? |
|
Definition
|
|
Term
| What are the intervention techniques for heat exercise related issues? |
|
Definition
- pre/post exercise cooling (10km and 15km)
- acclimatisation
- maintain hydration status
- maintain electrolyte balance
- behavioural regulation: train at coolest times of day
- protective clothing |
|
|
Term
| What are the main types of carbohydrates? Give examples |
|
Definition
Complex -> starch and glycogen (polysaccharides)
Sucrose and lactose (disaccharides)
Fructose (monosaccharides) |
|
|
Term
| Describe enzymes used in carbohydrate digestion and where they are found |
|
Definition
Mouth: salivary amylase
Duodenum: pancreatic amylase
Enterocytes: brush border enzymes |
|
|
Term
| Which enzymes are used to break down di/tri/oligo-saccharides? |
|
Definition
|
|
Term
| What is the main site of carbohydrate digestion? |
|
Definition
intestine
the stomach is too acidic for amylase to work therefore there is no breakdown in the stomach |
|
|
Term
| How are carbohydrates absorbed? |
|
Definition
| monosaccharides are absorbed by facilitated diffusion and co-transport |
|
|
Term
| Name the 3 brush border enzymes |
|
Definition
|
|
Term
|
Definition
| splits maltese into 2 glucose molecules |
|
|
Term
|
Definition
| breaks disaccharide sucrose into glucose and fructose |
|
|
Term
|
Definition
| hydrolyses lactose into glucose and galactose |
|
|
Term
| What does it mean to be lactose intolerant? |
|
Definition
| person who lacks lactase and therefore lactose cannot be absorbed. Leads to diarrhoea and vomiting |
|
|
Term
| What is co-transport responsible for? |
|
Definition
| glucose and galactose uptake |
|
|
Term
| What is required for co-transport? |
|
Definition
- an Na+ and glucose molecule to bind to the carrier protein (SGLT) before entering the cell
- an Na+ concentration gradient achieved by basal lateral Na+-K+ pump which ejects Na+ out |
|
|
Term
| What is the role of GLUT-2? |
|
Definition
| moves glucose, galactose and fructose into the capillary via diffusion down the concentration gradient |
|
|
Term
| What is facilitated diffusion responsible for? |
|
Definition
| fructose uptake at brush border via GLUT-5 |
|
|
Term
| What is our source for proteins? |
|
Definition
1. ingested (polypeptide or larger)
2. cell breakdown (30-60%) |
|
|
Term
| What does the enzyme endopeptidase do? |
|
Definition
| splits polypeptides at interior bonds |
|
|
Term
| What does the enzyme exopeptidase do? |
|
Definition
| cleave terminal amino acids |
|
|
Term
| Where are proteins digested? |
|
Definition
there are peptidases present in the saliva
digestion begins in the stomach
pepsinogen is activated into pepsin when the stomach is below pH 4 (due to HCl release) |
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Term
| Where does the rest of protein digestion occur? |
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Definition
- duodenum (main site)
- enzymes secreted by the pancreas again, however, as inactive zymogens that become active in the small intestine |
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Term
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Definition
| an inactive enzyme precursor |
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Term
| Why are pancreatic enzymes not released in their active form? |
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Definition
| the pancreatic enzymes would begin to breakdown the cells that line the ducts from the pancreas to the small intestine |
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Term
| Describe the mechanism of protein digestion in the duodenum |
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Definition
1. pancreas secretes trypsinogen (inactive)
2. once they have reached the small intestine, the enterocytes secrete enterokinase
3. trypsinogen is activated into trypsin
4. trypsin activates further pancreatic peptidases |
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Term
| What are the products of protein digestion? |
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Definition
| free amino acids and bi/tripeptides |
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Term
| How are amino acids absorbed? |
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Definition
| transported via Na+ co-transport and then again across the basolateral membrane into capillary |
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Term
| How are peptides absorbed? |
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Definition
| transported via a H+ co-transport and broken down inside cell |
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Term
| How are small peptides absorbed? |
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Definition
| carried intact across the cell by transcytosis (involves vesicles) |
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Term
| What types of fat do we digest? |
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Definition
triglycerides (90%)
phospholipids
cholesterol |
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Term
| What enzymes are used to digest fat? |
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Definition
lingual lipase (mouth)
gastric lipase (secreted in the stomach)
pancreatic lipase (small intestine) |
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Term
| What is the aim of fat enzymes? |
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Definition
| our membranes are made of phospholipids, therefore free fatty acids can diffuse from the small intestine to the capillaries |
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Term
| Describe the fat digestion mechanism |
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Definition
1. bile salts are secreted by the liver (stored in the gall bladder)
2. bile salts act as a detergent and emulsify fat globules in duodenum
3. lipases work on triglycerides and release fatty acids
4. free fatty acids are absorbed across the apical membrane down their concentration gradient |
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Term
|
Definition
| one side in hydrophobic and one side is hydrophilic |
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Term
| How is the concentration gradient maintained? |
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Definition
| free fatty acids congregate to form a micelle |
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Term
| Describe how the concentration gradient is maintained |
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Definition
- fatty acids move to sER where they combine to form triglycerides
- triglycerides move to the golgi apparatus where they are packaged into cyclomicrons
- they leave via exocytosis and enter circulation via lacteals (lymphatic system) as they are too large for capillary walls |
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Term
| How is food intake regulated? |
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Definition
| peripheral satiety signals and peripheral hunger signals |
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Term
| What are peripheral satiety signals? |
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Definition
'anorexigenic': switch off hunger
originate in the gut and travel via vagus to nTS in brain stem |
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Term
| How do peripheral satiety signals work? |
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Definition
1) activation of stretch receptors (when stomach is full)
2) chemical content of gut
3) GI peptides/hormones released during eating
4) longterm signals: leptin and insulin |
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Term
| What are peripheral hunger signals? |
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Definition
orexigenic
arise from GI system
occur 2-4 hours after gastric emptying
eg Ghrelin and neuropeptide Y |
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Term
| What are the factors of food intake? |
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Definition
- energy content
- frequency
- amount |
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Term
| What are the factors of food expenditure? |
|
Definition
- resting metabolic rate
- thermal effect of food
- physical activity |
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Term
| How and where is long term body weight regulated? |
|
Definition
hypothalamus
senses nutrients in blood and integrates information from other food centres |
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Term
| How and where is appetite regulated? |
|
Definition
forebrain: cortico-limbic systems
- memory and learning
- reward
- choice
- modulated by lifestyle and environment |
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Term
| How and where is satiety regulated? |
|
Definition
1. hindbrain
- parasympathetic increases activity
- autonomic outflow and endocrine responses from pituitary
2. gut
- nutrient, hormones and vagal afferents
- nutrient signals, hormones and stored/released fuel
- modulated by ingestive behaviour |
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Term
| What is the gut brain axis? |
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Definition
| The gut–brain axis refers to the biochemical signaling taking place between the gastrointestinal tract and the nervous system |
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Term
| Describe what links the medulla and the gut |
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Definition
| In the medulla, there are dorsal motor vagal nucleus (DMV) which is where vagal efferents lead to the gut |
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Term
| What types of motor (post-ganglionic) neurones are there? |
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Definition
- cholinergic which increase motility and emptying
- NO which decrease motility and emptying |
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Term
| What can act on the vagal afferents that enter the medulla? |
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Definition
| distension of the gut or presence of GI hormones |
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|
Term
| Describe hypothalamic regulation |
|
Definition
multiple sub-nuclei within the hypothalamus that collectively control feeding/satiety
Periventicular (detection) -> medial (integration) -> lateral (outputs) |
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Term
| How is weight classified? |
|
Definition
BMI (kg/m^2)
underweight: under 18.5
normal: 18.5-25
overweight: 25-40 |
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|
Term
|
Definition
| 25% of the British population are obese. UK is the most obese in Europe |
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|
Term
| What are the major effects of obesity? |
|
Definition
- disability
- work absentism
- reduced productivity
- UK economy £50billion pa
- poor mental health/self esteem
- early death
- NHS £5.5billion pa
- reduce life expectancy by 9 years |
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Term
| How role do genetics play in the obesity epidemic? |
|
Definition
genetic basis about 25%
5% of child obesity is due to genetic mutation of MC4-R
modification in leptin (a hormonal signal from body fat to brain) |
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Term
| What are the other causes of the obesity epidemic? |
|
Definition
- food production and supply
- education
- macro-economy and wealth
- changing nature of work
- early life experience
- built environment and transport |
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Term
| What are the physiological consequences of obesity? |
|
Definition
1. increased o2 cost of exercise (more to carry around)
2. increased cardio-respiratory response to exercise
3. increased ventilatory work (chest strap of weight) |
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|
Term
| Explain increased cardio-respiratory response to exercise |
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Definition
- decreased maximum response to external exercise
- decreased cardiovascular reserve |
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Term
| Explain increased ventilatory work (chest strap) |
|
Definition
- decreased vital capacity and decreased fucntional residual capacity
-hypoxemia at rest
-pulmonary vascular resistance |
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|
Term
| Where does the majority of excess fat go? |
|
Definition
| around the abdominal organs |
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|
Term
| What are the pathophysiological consequences of obesity? |
|
Definition
1. musculoskeletal system
2. circulatory system
3. metabolic and endocrine systems
4. cancer
5. reproductive and urological problems
6. respiratory problems
7. GI and liver disease
8. psychological and social problems |
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Term
| Describe the effects obesity has on the musculoskeletal system |
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Definition
| stress on bones, joints, increased risk of arthritis and lower back pain |
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Term
| Describe the effects obesity has on the circulatory system |
|
Definition
risk of hypertension and strokes
reduced motility causes blood pools in veins (deep vein thrombosis)
blocked lungs capillaries |
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|
Term
| Describe the effects obesity has on the metabolic and endocrine system |
|
Definition
increased risk of type II diabetes
altered fat profile in blood |
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|
Term
| Describe the effects obesity has on reproductive and urological systems |
|
Definition
| stress incontinence and effects are passed onto children |
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Term
| Describe the effects obesity has on respiratory system |
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Definition
| 'fat neck' causes stopped breathing in sleep (deep apnosea) |
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|
Term
| Describe the effects obesity has on the GI and liver |
|
Definition
non-alcoholic fatty liver disease
reflux
gall stones |
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|
Term
| Describe the psychological and social effects of obesity |
|
Definition
stress
depression
social disadvantage |
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Term
| In starvation, how long do carbohydrate stores last? |
|
Definition
|
|
Term
| What follows depletion of carbohydrate stores? |
|
Definition
body fat is depleted
therefore increased release of free fatty acids (most tissues can use fat as an energy source - not the brain) |
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Term
|
Definition
| gluconeogenesis in the liver supplies the brain with glucose |
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|
Term
| What is the final energy store? |
|
Definition
hard to release proteins (eg enzymes in cells)
leads to cell death
50% of protein depletion = death (63 days) |
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|
Term
| What happens to the free fatty acids? |
|
Definition
free fatty acids are transported to the liver and converted into ketone bodies which causes:
- acetone in breath
- metabolic acidosis and increased ventilation |
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|
Term
| Starvation causes muscle atrophy, what are the effects of this? |
|
Definition
- decreased ability to work
- decreased respiratory function
- decreased HR, circulatory volume and CO |
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|
Term
| What are the 5 other effects of starvation? |
|
Definition
1. vitamin deficiencies (7-14 days)
2. increased ammonium excretion
3. risk of hypothermia
4. weak and apathetic
5. confusion and cognitive deficits |
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