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213- pharmacology > block B- systems physiology > Flashcards

block B- systems physiology Flashcards

1
Q

what is the autonomic nervous system?

A

its really important to regulate body function and agonists mediate functional responses via receptors (mostly GCPRs)

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2
Q

what direction do afferent neurons go?

A

from the peripheral nervous system towards the central nervous system

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3
Q

what dircetion do efferent neurons go?

A

towards the peripheral nervous system

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4
Q

what are the three types of peripheral nerves?

A

sensory, autonomic and somatic

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5
Q

what is the function of the sympathetic division?

A

its the emergency system in charge of fight or flight

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6
Q

what is the function of the parasympathetic division under non-stressful conditions?

A

it effects predominately during the times of ‘rest and repair’

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7
Q

what does the parasynthetic system do to the body?

A

it slows the heartbeat, promotes digestion and gland secretion

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8
Q

what are the receptors in the ANS?

A

they’re mostly G-protein coupled receptors which mediate the action of released transmitters

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9
Q

what are the 2 subgroups of ANS receptors?

A

acetylcholine and noradrenaline

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10
Q

what are the two types of acetylcholine receptors?

A

nicotinic and muscarinic

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11
Q

what do second messengers link in the ANS?

A

they link the functional outcomes important in the ANS-beta-1 receptors in the heart

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12
Q

what do beta-2 receptors do the airways via cAMP?

A

they cause relaxation

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13
Q

what do alpha-1 receptors in vascular smooth muscle do?

A

they cause contraction
- this could also be muscarinic M3 receptors in guinea pig ileum because receptors share signalling mechanisms
- these muscarinic receptors are found in the airways smooth muscle

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14
Q

what do different second messenger systems link receptors to different functional outcomes due to activation of receptors by?

A

agonists

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15
Q

what mediate the function of both the sympathetic and parasympathetic parts of the ANS?

A

receptors

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16
Q

what receptors are heterogenic and what are the two types of each?

A

alpha-Adrenoceptors
alpha-1 (postsynaptic at sympathetic neuroeffector synapses)
alpha-2 (presynaptic at sympathetic neuroeffector synapses)

beta-Adrenoceptors
beta-1 (heart, intestinal smooth muscle)
beta-2 (bronchial, vascular and uterine smooth muscle)

Acetylcholine receptors
nicotinic (in sympathetic and parasympathetic ganglia)
muscarinic (parasympathetic neuroeffector synapses)

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17
Q

what are sympathomimetrics?

A

theyre driugs that mimic the actions of noradrenaline and adrenaline

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18
Q

what do the 4 types of sympathomimetics do?

A

beta-2-agonists cause bronchial dilation and are used in the treatment of asthma
beta-1-agonists are sometimes used to stimulate the force of the heart contraction
alpha-1-agonists are used to treat blocked nose/ sinuses
alpha-2-agonists are centrally acting hypotensive drugs

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19
Q

what are the two types of selective adrenoceptor antagonists?

A

alpha-adrenoceptor antagonists - blockers for these receptors reduce arteriolar and venous tone
beta-adrenoceptor antagonists - blockers for these receptors reduce heart rate and force contraction of the heart with less effect on blood vessels and bronchioles

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20
Q

what are some of the uses of muscarenic receptor antagonists?

A

anti-pasmodics
mydratics
bronchodilators
bladder relaxants
antiemetic

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21
Q

why study the heart in pharmacology?

A

it keeps you alive and cardiovascular disease is one of the biggest health issues in the UK

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22
Q

what are the main functions of the cardiovascular system?

A

rapid transport of nutrients
removal of waste products of metabolism
hormonal control by transporting hromones to their target organs and by secreting its own hormones
temperature regulation by controlling heat distribution between the body core and the skin
host defense, transporting immune cells, antigens and other mediators

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23
Q

what are the walls of the heart called and what are they made up of?

A

they’re called the myocardium and are made of cardiac muscle

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24
Q

what is the endocardium?

A

inner surface of walls that is in contact with the blood

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25
Q

what is the epicardium?

A

its the inner lining of the pericardium which is continuous with the covering of the heart itself

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26
Q

what is the pericardium?

A

its where the heart is located within a fluid membranous sac

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27
Q

what are the two phases of the cardiac cycle?

A

the contractile phase (systole) and the relaxation, filling stage (diastole)

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28
Q

what changes occur in the heart during and following a single heart beat?

A

electrical and mechanical changes

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29
Q

what does the alternation between contranctiona nd relaxation produce?

A

it produces differences in pressure which push the blood into the heart chambers and the circulation

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30
Q

what are cardiac muscle cells joined together by?

A

gap junctions

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31
Q

what do gap junctions allow?

A

they allow for the spread of exitations from one cell to another and allow the cardiac muscle to act as a whole

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32
Q

what do the specialised cells in the myocarium make up? and what are they essential for?

A

they make up the conducting system and are essential for heart excitation

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33
Q

what blood vessels supply the myocardium with blood?

A

coronary arteries

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34
Q

what are the events leading up to cradiac contranction?

A

depolarisation of the plasma membrane
opening of voltage-sensitive Ca2+ ion channels
Ca2+ ions flow into the cell and Ca2+ release from sarcoplasmic reticulum
rise in cystolic Ca2+ concentration
CONTRACTION

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35
Q

what is the role of the sino-atrial node?

A

it acts as a pacemaker

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36
Q

how do the atrioventricular node, ventricular conducting fibres and ventircular myocardium spread electrical activity?

A

atrioventricular node- a tactical pause
ventricular myocardium - surface roads
ventricular conducting fibres - freeways

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37
Q

what is cardiac potential?

A

its an action potential - this is a transient depolarisation of the cell membrane and are initiated when the membrane is depolarised, they happen spontaneously and transmission is from adjacent myocytes through gap junctions

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38
Q

what are the two types of depolarising cells?

A

fast and slow

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39
Q

what are the two types of refractory periods?

A

absolute refractory period (ARP) ~250ms in myocytes
relative refractory period (RRP)

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40
Q

what is chronotropic control?

A

its changes in heart rate

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41
Q

how much does temperature affect pacemaker?

A

its estimated that heart rate increases by 10bpm for every degree C increase in temperature - this is why heart rate increases when a person has a fever

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42
Q

what system increases heart rate?

A

sympathetic fibres - noradrenaline -beta1 receptors increase the permeability of the nodal cell plasma membrane to Na+ and Ca2+

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43
Q

what system reduces heart rate?

A

parasympathetic- acetylcholine - M2 receptors increase permeability to K+ and decrease Na and Ca2+ permeability

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44
Q

how do you calculate cardiac output?

A

stroke volume x heart rate

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45
Q

what is stroke volume?

A

its the volume of blood pumped per contraction

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46
Q

what is end-diastolic volume (EDV)?

A

volume of blood in ventricle before contraction

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47
Q

how much of EDV (end-diastolic-volume) is usually pumped per contraction?

A

normally about 60% of the EDV is ejected on each contraction

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48
Q

how much is the normal SV?

A

70-140 ml

49
Q

at rest, what is CO in adults?

A

4-5L/min

50
Q

how much can the CO increase by during excersize?

A

4-8x during exercise

51
Q

what receptors are present in the heart?

A

main ones- beta-1-receptor (mostly the muscarenic M2 version)
others - beta-2
alpha-1
angiotensin II receptors
these all help to modify contractility/heart rate

52
Q

what 2 things combine to regulate BP?

A

the heart and blood vessels

53
Q

what is arterial blood pressure formed by?

A

given by cardiac output x total peripheral resistance

54
Q

what does total peripheral vascular resistance depend on?

A

blood viscosity and arteriolar radius (inversely related- higher the radius, the less resistance there is

55
Q

what is involved in the control of arteriolar radius?

A

sympathetic nerves- release noradrenaline to constric
symphathetic cholinergic- nerves (skeletal muscle) release acetylcholine and muscarenic (M3) to dilate the arteries
plasma adrenaline- beta2 to dilate
local controls- ↓PO2, ↑ PCO2 ↑K+ ↑ adenosine

56
Q

what is involved in the immediate regukation of arterial blood pressure?

A

baroreceptor reflex and chemoreceptor reflexes

57
Q

what is involved in the longer term (hormonal) controil of arterial blood pressure?

A

vasopressin (this is an anti-diuretic hormone)
angiotensin II
aldosterone
atrial natriuretic peptide (ANP)

58
Q

what facotors influence blood pressure?

A

ones that affect cardiac output of blood- ↑ stroke volume and ↑heart rate
ones that affect oerioheral resistance - ↑blood viscosity ↓ arteriolar diameter

59
Q

what are the names of some drugs that can either reduce heart rate/ stroke volume and reduce vascular constriction (ie reduce vascular resistance)

A

beta blockers
selective alpha 1 antagonists
ACE inhibitors

60
Q

what is respiration?

A

its ventilation, gas exchange air↔blood ↔ tissues in the blood
metabolism of oxygen within thebody

61
Q

what are the names of the branches, strating at the biggest and going down in size?

A

trachea
bronchi
bronchioles
terminal bronchioles
respiritory bronchioles
alviolar ducts
alveolar sacs

62
Q

how to calculate flow of lungs?

A

flow=change in pressure/ resistance
= (P alveoli - P atmosphere) /R

63
Q

what is partial pressure?

A

its the pressure of a gas in a mixture
proportional to concentratio so Po2 is the concentration of oxygen

64
Q

what are the 5 steps of gas exchange?

A
  1. ventilation - bulk flow exchange of air, 4L/min at alveoli
  2. diffusion of )2 and CO2 at lung capilaries driven by concentration gradients
  3. bulk flow transport of O2 and CO2 through circulation, cardiac output =5L/min
  4. diffusion of O2 and CO2 at tissues driven by concentration gradients
  5. end-point: the cells use O2 and produce CO2
65
Q

how much oxygen bound to haemoglobin is present in 5L of arterial blood?

A

15mL of physically dissolved O2, the remainder (985mL O2) is bound to haemoglobin
4x subunits = 4x globin-haeme

66
Q

what happens in the in and out breath in the diaphragm?

A

in breath- the diaphragm contracts and the external intercostal muscles pull the ribs up and out
out breath- the diaphragm relaxes and abdominal organs press upwards, lung elasticity recoils inwards

67
Q

what happens to the body during maximum respiration?

A

the sternum moves up and out
and the diaphragm contracts more

68
Q

what happens to the body in maximum expiration?

A

internal intercostal muscles pull ribs down and out
the abdominal muscles compress organs and force diaphragm higher

69
Q

what controls breathing?

A

diaphragm and intercostal muscles, controlled by motor neurons form medulla and is modulated by chemireceptors

70
Q

what are some pharmacology examples for adrenoreceptors?

A

beta-agonists - pulmonary smooth muscle relaxation e.g. salbutamol in asthma inhalers
alpha-agonsists- vascular smooth muscle contraction e.g. phenylephrine and psuedophrine in decongestants

71
Q

what does beclomethasone do?

A

its an asthma inhaler - glucotorcoid receptor agonist that inhibits pulmonary inflammation

72
Q

what does supplementary O2 do?

A

it increases driving force for O2 uptake

73
Q

what are deaths from opioids commonly from?

A

theyre commonly because these drugs decrease activity of neurons in medulla that drive breathing

74
Q

what happens in the body during carbon monoxide (CO) poisoning?

A

haemoglobon binds CO more readily than O2 and also looses co-operativity when it does

75
Q

what is the function of skeletal muscle?

A

movement

76
Q

what type of nerve cells control skeletal muscle cells?

A

controlled by somatic motor nerves

77
Q

what causes contraction in skeletal muscle cells?

A

an actin potential in the muscle which causes Ca2+ to rise, causing contraction

78
Q

how many cells makes up a skeletal muscle fibre?

A

1, they have multiple nuclei and hundreds of mictofibrils each

79
Q

why are skeletal muscles striated?

A

due to contractile filaments
the myosin are the thick layers and actin + trponin are the thin layers

80
Q

what is the role of transverse-t-tubule?

A
  • they’re responsible for transmitting electrical impulses deep into the muscle and facilitating coordinated contraction across the muscle
  • critical for excitation-contraction coupling, the process by which electrical stimulation triggers the release of calcium ions from the sarcoplasmic reticulum and subsequent muscle contraction.
81
Q

what is the role of sarcoplasmic reticulum?

A

its acts as a Ca2+ store

82
Q

what is the role of mitochondria in skeletal muscle?

A

O2 untilisation/ ATP production

83
Q

what happens at neuromuscular junctions when ACh is released?

A

it binds to nicotonic ACh-receptors, causing an Na+ influx, causing end-plate potential, causing action potential propagates

84
Q

what does myosin bind to drive contraction?

A

actin

85
Q

what are the stages of contraction when myosin binds actin?

A

the action potential propagates into T-tubules
voltage fates sensor activates ryanodine receptor on sarcoplasmic reticulum
then Ca2+ is released
Ca2+ binds to troponin to cause tropomyosin to move aside then myosin is able to bind troponin
ATP hydrolysis energiese myosin and the cycle of ATP binding, hydrolysis, ADP/Pi release drives like a ratchet

86
Q

what process energies myosin?

A

ATP hydrolysis

87
Q

what 3 processes does ATP hydrolysis drive in skeletal muscles?

A

cross-bridge cycling (myosin ATPase)
2. restoration of plasma-membrane ion gradients (Na+/K+-ATPase)
3. removal of Ca2+ from cytosol back into sarcoplastic reticulum (Ca2+-ATPase)

88
Q

how much can ATP consumption increase by during muscle contraction?

A

100x

89
Q

how is the skeletal muscle resupplied with ATP?

A
  1. phosphorylation of ADP by phosphocreatine
  2. mitochondrial oxidative phosphorylation (this needs oxygen)
  3. glycolysis - anerobic metabolism of glucose in the form of blood and catabolism of muscle glycogen
90
Q

what different levels of characteristics could different types of muscle fibres have? in this ive put 4 different types

A
  1. some contain- lots of mitochondria, lots of O2 binding myoglobin, lots of small blood vessels - these fibres look very red
  2. others contain- few mitochondria, lots of glycolytic enzymes, large glycogen stores- these muscle fibres look white
  3. some contain slower acting myosin ATPase- these are slow twitch fibres
  4. others contain very fact acting myosin ATPase - fast twitch fibres
91
Q

what are type II fibres?

A

fast-glycolytic fibres

92
Q

is a whole muscle unit made up of one muscle cell or many?

A

whole skeletal muscles are made up of many motor units, never just one type

93
Q

what is whole muscle tension?

A

its the sum of recruitment of motor units

94
Q

what are multiple muscle fibres of the same type innervated by?

A

theyre innervated by 1 motor neuron to make 1 motor unit

95
Q

what is the difference between 75% fast twitch and 25% slow twitch in terms of running?

A

75% fast twitch- sprinting
25% slow twitch - jogging

96
Q

what do motor nerves generate to allow myosin-actin cross-bridge cycling to contract muscle?

A

muscle action potental

97
Q

what does muscle contraction use up?

A

lots of ATPis used up by:
cycling Ca+/ Na+/ K+ pumping
restored from phosphocreatine
glycolysis (glucose from blood)
mitochondria from aerobic respiration

98
Q

what are the three types of muscle fibres?

A

I slow-oxidative
IIa fast-oxidative-glycolytic
IIb/x fast glycolytic

these all have different methods of ATP production/ myosin speed/ contraction speed and tiring

99
Q

what do NMJ blockers do?

A

they cause paralysis, some are used alongside anesthetics during surgery

100
Q

what happens during depolarisation caused by NMJ blockers?

A

ACh mimic but much slower hydrolysis, cause sustained contraction > paralysis e/g/ suxamethonium

101
Q

what happens during non-depolarising caused by NMJ blockers?

A

competitive inhibitors nAChR that block ACh binding and EPP formation

102
Q

what does botulinum toxin do?

A

it inhibits ACh release
flaccid paralysis, local muscle paralysis to treat excessive sweating - or facial wrinkle formation

103
Q

what does dantrolene do? and what type of drug is it?

A

its a direct-action on muscle excitation-contraction
it inhibits ryanodine receptor Ca2+ release
its sometimes used to treat muscle spasticity or malignant hyperthermia (RYR1 genetic mutation that can cause RyR Ca2+ release when exposed to some anesthetics or suxamethonium)

104
Q

what does excersize do to skeletal muscle?

A

excersize decreases muscle: ATP, phosphocreatine, O2

105
Q

how does the cardiovascular and respiratory systems respond to increased demands?

A

by supplying O2 from lungs to skeletal muscle via increased blood flow
thermo-regulation: increased peripheral blood flow and sweating

106
Q

what does low intensity aerobic exercise do to skeletal muscle?

A

increases mitochondria and increases capillaries

107
Q

what does endurance training do to the muscle fibres?

A

the fast-glycolytic fibres become fast-oxidative-glycolytic fibres (IIb>IIa)

107
Q

does does high intensity strength training do to the muscle fibres?

A

increased diemeter of fast twitch fibres (hypertrophy)
increased expression of glycolytic enzymes
greater synchronised expression of motor unit recruitment

108
Q

what does excersize do to cardiovascular and respiratory systems?

A
  • they need to supply oxygen from the lungs to the skeletal muscle via increased blood flow
  • they also need to control body temperature (thermoregulation) increasing peripheral blood flow and sweating
109
Q

what is the process of contracting skeletal muscles causing an increase in local blood flow in muscle?

A

contracting skeletal muscles
local chemical changes
dilates muscle arterioles
increase in local blood flow in muscles

110
Q

what changes do brain ‘exercise centres do’?

A

increase in parasympathetic output to heart
decrease in sympathetic output to heart, veins, abdominal arterioles and kidneys

111
Q

what changes in acute blood flow are there in different parts of the body compared to the brain blood flow?

A

brain - the same
heart - 3.5x
skeletal muscle - 12x
skin - 4.4x
kidneys - 0.6x less
gut - 2x less
total blood flow in the body - 3.5x

112
Q

what increases/decreases are there in sympathetic activity and parasympathetic systems?

A

sympathetic activity- increased
parasympathetic activity- decreased

113
Q

why must the venous return increase during exsercize?

A

to cope with decreased ventricular filling time

114
Q

what does exercise training do to the respiratory system?

A

breathing rate increases
blood O2 doesnt decrease
blood [H+] and CO2 only decrease at extremes

115
Q

what heappens to oxygen consumption during exersize?

A

it increases in proportion to exersize intensity up to a point of maximal O2 consumption - VO2 max

116
Q

what is VO2 max?

A

(arterial content - venous O2 content) x CO
increase up to about 25% with increase, long term exersize

117
Q

does increasing mitochondria levels affect VO2 max?

A

no it doesnt but it does increase endurance up to 300%

118
Q

what does an increase in stroke volume lead to?

A

heart remodelling
increase in skeletal muscle blood vessels
increased blood volume

213- pharmacology (5 decks)

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