Physiology Flashcards

1
Q

Which part of the brain is involved in thermoregulation?

A

Hypothalamus

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2
Q

Outline the composition of intracellular fluid

A

Cytoplasm: high in K+, low in Na+ and Cl-

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3
Q

Outline the composition of extracellular fluid

A

Interstitial fluid and plasma; Low K+, high Cl- and Na+

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4
Q

Define ‘osmolarity’

A

Number of osmoles of solute per litre of solution (Osm/L)

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5
Q

Define ‘osmolality’

A

Osmoles of solute per kg of solvent (Osm/kg)

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6
Q

Define ‘colloid’

A

Large molecular weight particles present in solution

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7
Q

What is the ‘Donnan effect’?

A

If cell doesn’t do anything to control osmolarity –> higher solutes inside –> water flow inwards –> lysis/rupture

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8
Q

Define ‘tonicity’

A

Actual effect of solution on living cell

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9
Q

What is tonicity influenced by?

A

By solutes which can’t cross membrane

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10
Q

Where is sodium absorbed in the kidney?

A

Distal convoluted tubule regulated by aldosterone

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11
Q

Where is water reabsorbed in the kidney?

A

Collecting duct, regulated by ADH

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12
Q

Describe ‘hyponatraemia’

A

Decrease in extracellular osmolarity as total body water increases and there is decrease in plasma electrolytes - often caused by overhydration

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13
Q

Describe ‘hypernatraemia’

A

Increase in extracellular osmolarity as total body water decreases so there is increase in plasma electrolytes, often due to dehydration

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14
Q

Define ‘buffer system’

A

Substances present in body fluids and limit pH change by ability to accept or donate hydrogen ions

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15
Q

Define ‘buffer’

A

Solution which can maintain a constant pH if solution is diluted or strong acids/bases added - consists of weak acid and it’s conjugated base, or weak base and it’s conjugate acid

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16
Q

Describe the phosphate buffer system (include equation)

A

Present in intracellular fluid (cytoplasm) only:

H+ + HPO42- H2PO4-

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17
Q

Describe the haemoglobin buffer system

A

Present in RBCs only:

H+ + Hb HHb

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18
Q

Describe amino acid buffers

A

Proteins accept or donate proton (present in ICF and ECF)

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19
Q

Describe the carbonic acid-bicarbonate buffer system (include equation)

A

Present in ECF:

CO2 + H2O H2CO3 H+ + HCO3-

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20
Q

Describe respiratory regulation of pH

A

Alter rate/depth of respiration to retain or eliminate CO2 –> changes are rapid

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21
Q

Describe renal regulation of pH

A

Excretion or conservation of bicarbonate/hydrogen ions –> changes are slow

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22
Q

What should serum pH be?

A

7.35-7.45

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23
Q

State the equation to calculate pH

A

pH = -log10[H+]

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24
Q

Define ‘acidemia’

A

pH less than 7.35

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25
Q

Define ‘alkalemia’

A

pH greater than 7.45

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26
Q

What can affect serum pH?

A

Bicarbonate rise/drop and CO2 rise/drop

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27
Q

What is the cause of respiratory acid-base disorders?

A

Abnormal respiratory function –> rise /fall in CO2 in ECF

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28
Q

What is the cause of metabolic acid-base disorders?

A

Generation of acids (organic or fixed) which affects concentration of bicarbonate ions in ECF

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29
Q

Explain how to interpret arterial blood gases

A
  1. Look at the pH to see if primary problem is acidosis or alkalosis
  2. Check the CO2 levels (respiratory indicator)
  3. Check the HCO3- (metabolic indicator)
  4. Decide which is the primary disorder (respiratory or metabolic); whichever is concurrent with the change in pH (carbon dioxide is acidic and bicarbonate is alkali)
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30
Q

Describe ‘paracrine signalling’

A

Molecules act locally and include neural communication systems

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31
Q

How does the Na+/K+ pump contribute to establish resting membrane potential?

A

3 Na+ ions in for 2 K+ out –> negative inside, positive outside

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32
Q

Describe voltage-sensitive Na+ channels

A

Activation gate: closed at rest, opens on depolarisation (fast)
Inactivation gate: open at rest and closes in response to depolarisation (close is slow)

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33
Q

Describe voltage-sensitive K+ channels

A

Closed at rest, open on depolarisation (slightly more slowly than Na+ activation gate) –> stays open throughout depolarisation

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34
Q

Describe a normal action potential curve

A

Resting (-70mV) –> depolarisation (Na+ activation gate opens, influx) –> threshold potential –> action potential –> repolarisation (Na+ activation gate closes, K+ channel opens) –> hyperpolarisation (K+ channel overshoots) –> Na+/K+ pump re-establishes resting membrane potential

35
Q

What is the ‘absolute refractory period’?

A

Cannot open voltage-gated Na+ channels regardless of size of stimulus

36
Q

What is the ‘relative refractory period’?

A

Difficulty in producing another action potential during hyperpolarisation

37
Q

Describe the mechanism of action of local anaesthetics

A

Bind to open voltage-gated sodium channels –> prevents them from responding by re-opening –> no action potentials generated

38
Q

Why do axons with greater diameter conduct faster?

A

Cytoplasmic resistance decreases with increased diameter

39
Q

Describe Aα axons

A

Motor neurones; thick myelin and large diameter –> fast conduction

40
Q

Describe Aβ axons

A

Mechanical touch/pressure receptors so thick myelin

41
Q

Describe Aδ axons

A

Pain receptor so thick myelin to allow sudden response

42
Q

Describe C axons

A

Slow pain receptor, thin diameter and no myelin (for things such as itch)

43
Q

What are the most common excitatory neurotransmitters in the nervous system?

A

Glutamate

44
Q

What are the most common inhibitory neurotransmitters in the nervous system?

A

GABA and glycine

45
Q

Describe how excitatory post-synaptic potentials are created

A

Glutamate-gated channels cause depolarisation on post-synaptic neurone

46
Q

Describe how inhibitory post-synaptic potentials are created

A

GABA/Glycine-gated channels cause net influx of Cl- –> hyperpolarisation

47
Q

What are axosecretory synapses?

A

Axon secretes directly into bloodstream

48
Q

What are axoaxonic synapses?

A

Axon terminal secretes into another axon

49
Q

What are axodendritic synapses?

A

Axon terminal ends on a dendritic spine

50
Q

What are axoextracellular synapses?

A

Axon with no connection secretes into ECF

51
Q

What are axosomatic synapses?

A

Axon terminal ends on soma

52
Q

What are axosynaptic synapses?

A

Axon terminal ends on another axon terminal

53
Q

What type of receptor binds Ach?

A

Nicotinic

54
Q

What does an ionotropic response involve?

A

Opening of ligand-gated ion channels (fast response)

55
Q

What does a metabotropic response involve?

A

Where a ligand activates a receptor which then activates G proteins –> effects enzymes

56
Q

Outline 3 ionotropic receptors

A

Nicotinic receptors, glutamate receptors, GABAa receptors

57
Q

Describe nicotinic receptors

A

Activated by binding of 2 ACh molecules causing Na+ to flow into post-synaptic cell

58
Q

Describe G protein-coupled receptors

A

7 transmembrane segments and involve: G-protein receptor, G-protein, enzyme and second messengers

59
Q

What are the 3 main types of second messenger?

A

Hydrophilic water-soluble, hydrophobic lipid-soluble, gases

60
Q

Name 4 sensory skin receptors

A

Pucinian corpuscle, Meissner corpuscles, Merkel cells and Ruffini endings

61
Q

What do Meissner corpuscles do?

A

Register light touch (rapidly adapting)

62
Q

What do Merkel cells do?

A

Register pressure texture (slow adapting)

63
Q

What do Pacinian corpuscles do?

A

Register vibration (rapidly adapting)

64
Q

What do Ruffiini endings do?

A

Register skin stretching (slow adapting)

65
Q

What do parasympathetic afferents detect?

A

Physiological information

66
Q

What do sympathetic afferents detect?

A

Pathophysiological information e.g. pain

67
Q

What are the parasympathetic cranial nerves?

A

Oculomotor, facial, glossopharyngeal and vagus (III, VII, IX, X)

68
Q

Where does the sympathetic nervous system run?

A

Thoracolumbar (T1-L2)

69
Q

How does the adrenal medulla act as a modified post-ganglionic cell?

A

From thoracic spinal cord, sympathetic preganglionic fibres project directly to adrenal medulla cells –> secrete adrenaline and noradrenaline into blood

70
Q

What is the myenteric plexus?

A

In small intestine between circular and longitudinal muscle layers –> controls motility

71
Q

What is the submucosal plexus?

A

In intestines: located between submucosa and circular muscle layer; controls secretion and muscle function of mucosae

72
Q

What nervous input goes to the enteric nervous system?

A

Extrinsic efferent information from vagal preganglionic fibres and sympathetic post-ganglionic fibres

73
Q

What do nicotinic receptors respond to?

A

ACh

74
Q

What do muscarinic receptors respond to?

A

ACh and Bethanechol

75
Q

What neurotransmitters are used in the autonomic nervous system?

A

ACh between pre and post-ganglionic, then noradrenaline/ACh at effector

76
Q

How are muscarinic receptors targeted clinically?

A

Antagonists: anti-secretory, anti-spasmodics ad bronchodilators
Agonists: stimulate gut and bladder function

77
Q

What neurotransmitter do adrenoreceptors respond to?

A

Noradrenaline

78
Q

What do alpha 1 adrenoreceptors do?

A

Agonist: vasoconstriction and inhibition of GI and bladder sphincters
Antagonist: vasodilation (treat hypertension)

79
Q

What do beta 1 adrenoreceptors do?

A

Agonist: increase HR and force
Antagonist: decrease HR (beta blockers)

80
Q

What do beta 2 adrenoreceptors do?

A

Agonist: bronchodilation and vasodilation
Antagonist: asthma

81
Q

What is the resting membrane potential?

A

-70mv

82
Q

What is the threshold potential?

A

-55mV

83
Q

What membrane potential does an action potential peak at?

A

+30mV

84
Q

What do all GPCRs respond to?

A

Noradrenaline