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Foundations of Clinical Science > Fluids, Dehydration and Pharmacology > Flashcards

Fluids, Dehydration and Pharmacology Flashcards

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1
Q

What is the body’s fluid requirements?

A

2-2.5L water per day (mostly gained via ingestion) need it because all chemical reactions occur in aqueous conditions

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2
Q

What are insensible losses?

A

Evaporation from respiratory tract and diffusion from skin (~700ml/day) EXCLUDING SOLUTE LOSS

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3
Q

What are sensible losses?

A

Sweat, faeces and urine INCLUDING SOLUTE LOSS

Sweat depends on climate/exercise, only a little from faeces and urine highly variable

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4
Q

60 40 20 rule

A

60% of body is water
40% (2/3) intracellular (ICF)
20% (1/3) extracellular (ECF) plasma + interstitial

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5
Q

What is ECF split into?

A

Plasma - fluid component of blood
Interstitial Fluid - fluid surrounding cells
Transcellular space - space between cells

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6
Q

What is the main cation of ECF?

A

Na+

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7
Q

What is the main cation of ICF?

A

K+ ‘bananas in the sea’

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8
Q

What 2 factors are key in fluid movement between compartments?

A

Osmosis

Starling’s principle of fluid exchange

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9
Q

Why does osmosis occur?

A

Water (solvent) moves down its concentration gradient across a semi permeable membrane from an area of LOW SOLUTE CONCENTRATION to HIGH SOLUTE CONCENTRATION

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10
Q

What is osmolality?

A

Number of dissolved solute molecules per kg of solvent (osmol/kg)

Normal plasma osmolality = 280-290 mOsmol due to extracellular NaCl

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11
Q

What is osmotic pressure?

A

Pressure generated by flow of water down concentration gradient across semi-permeable membrane (pressure needed to prevent movement of free water down gradient)

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12
Q

How do we measure the strength of osmotic potential?

A

USE OSMOLALITY: Number of molecules dissolved per kg solvent

1 mol of NaCl dissolved in 1 Kg:
molality = 1 mol/Kg
osmolality of 2 Osmol/Kg (splits into Na+ and Cl-, 2 particles)

1 mol of Glucose dissolved in 1 Kg:
molality = 1 mol/Kg
osmolality = 1 Osmol/Kg (it doesn’t split and remains 1 particle)

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13
Q

Describe the structure of a lipid molecule?

A

Hydrophilic head attracted to water

Hydrophobic tail repelled by water

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14
Q

What are the properties of a solute?

A

Concentration gradient
Size of solute
Lipid solubility

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15
Q

What are the properties of the plasma membrane?

A 
Membrane thickness/composition
Aqueous pores in the membrane
Carrier-mediated transport
Active transport mechanisms
Semi permeable- not a barrier to H2O
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16
Q

What is convection?

A

Movement down a PRESSURE GRADIENT (to move solutes and fluids over long distances) like blood flow from heart to vessels
Can be passive

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17
Q

What types of molecules can easily pass through membrane?

A

Small
Lipophilic
Hydrophobic
(eg. O2, CO2, urea, anaesthetics, glycerol)

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18
Q

What types of molecules cannot easily pass through membrane?

A

Large
Lipophobic
Hydrophilic
(eg. Electrolytes, glucose, amino acids, plasma proteins, therapeutic drugs)

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19
Q

What is simple diffusion?

A

No ATP required
Molecules move RANDOMLY from high to low concentration
Short distances
Lipid soluble substances

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20
Q

Why does simple diffusion only work for short distances?

A

Time taken (t) for one randomly moving molecule to move a net distance (x) in one specific direction increases with the distance squared

t = x2 / 2D

D = diffusion coefficient for molecule within the medium e.g. D for O2 in water vs. D for O2 in air are different

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21
Q

What is Fick’s Law?

A

Controls simple diffusion of solutes

Js = D A (delta C/x)

Js = mass per unit timr m/t, determined by 4 factors:

D= Diffusion coefficient of solute – Ease with which solute moves through solvent (e.g. through water, air, oil etc.)

A =Area (more area more solute movement)

DC / x =Concentration difference (C1-C2) across distance x termed concentration gradient(more gradient more movement)

Negative value : flowing ‘down’ a concentration gradient

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22
Q

What are the two types of passive transport?

A

Simple

Facilitated

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23
Q

What are the two types of active transport?

A

Primary PUMP MEDIATED needs direct ATP hydrolysis

Secondary CARRIER MEDIATED uses concentration gradient

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24
Q

What type of transport are endocytosis and exocytosis?

A

Active transport

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25
Q

Na/K ATPase and Ca ATPase are what kind of proteins? What is their function?

A

Carrier proteins that require energy (ATP) to transport ions Against a concentration gradient to control intracellular and extracellular electrolyte balance

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26
Q

How does facilitated diffusion work?

A

Initially primary active transport (energy use) creates concentration gradients, e.g. Na/K-ATPase

Co-transporters and Exchangers (carrier proteins) use these concentration gradients to transport solutes, e.g. glucose

Does not require energy (no ATP needed)

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27
Q

What 2 characteristics are associated with carrier mediated transport?

A

Specificity for a solute – e.g. GLUT transporter only carry glucose

Saturation of carrier limits solute transport – e.g. GLUT transporter numbers are finite and have a maximum capacity

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28
Q

How does glucose transport work in intestinal cells?

A

SECONDARY ACTIVE TRANSPORT: Carrier protein lets sodium ions move down their gradient, but simultaneously brings a glucose molecule up its gradient and into the cell (both going in same direction SYMPORT). The carrier protein uses the energy of the sodium gradient to drive the transport of glucose molecules.

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29
Q

What transporters are present in the intestine?

A

On epithelial membrane:
NA+/GLUCOSE TRANSPORTERS
CHLORIDE TRANSPORTERS

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30
Q

Why are Na+/glucose transporters important for fluid requirements?

A

Absorption of Na+/glucose facilitates water absorption across gut

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31
Q

Why are chloride transporters important for fluid requirements?

A

Secretion of chloride into gut lumen facilitates water secretion

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32
Q

What is the E.Coli effect?

A

Blocks sodium absorption and stimulates chloride secretion = diarrhoea

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33
Q

What is the mechanism by which glucose is transported across the intestinal epithelium?

A

Secondary active transport

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34
Q

What is molarity vs molality?

A 
Molarity = MOLES per VOLUME (Litres)
Molality = MOLES per WEIGHT (Kg)
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35
Q

What is osmolarity vs osmolality?

A 
Osmolarity = OSMOLS per VOLUME (Litres)
Osmolality = OSMOLS per WEIGHT (Kg)
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36
Q

What is tonicity?

A

Influence of a solution’s osmolality on cell size

Depends on membrane permeability of the solute - e.g. greater tonicity with NaCl (membrane impermeable ) vs. urea (membrane permeable)

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37
Q

What is Starling’s principle of fluid exchange?

A

Capillary blood pressure exerts HYDROSTATIC pressure (wants to squeeze fluid out)

Large molecules in blood (e.g. plasma proteins, albumin) exert an osmotic pressure across the capillary wall - ONCOTIC Pressure (wants to draw fluid back in)

LONG EXPLANATION
Capillary wall is a semi-permeable membrane
Allows low (e.g. glucose) but not high (e.g. proteins) molecular weight solutes through
Large molecules (e.g. plasma proteins, albumin) exert an osmotic pressure across the capillary wall: Termed Oncotic Pressure

Fluid movement depends on balance of hydrostatic (capillary blood pressure) andoncotic pressures across capillary wall

Generally produces filtration of fluid from capillaries to interstitial fluid, some reabsorbed due to oncotic pressure

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38
Q

What is an isotonic solution?

A

Isotonic conditions surrounding cells, same osmolality inside/outof cells e.g. iv 0.9% NaCl saline

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39
Q

What is a hypotonic solution?

A

Hypotonic conditions surrounding cells, less osmolality than inside cell eg. excessive NaCl loss, iv 0.45% NaCl saline

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40
Q

What is a hypertonic solution?

A

Hypertonic conditions surrounding cells,greater osmolality than inside of cell e.g. excess water loss, iv 3% NaCl saline

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41
Q

Where does water move in a hypertonic, isotonic and hypotonic solution?

A

Isotonic: no moevement of water between compartments
Hypertonic: water moves out of the cell ICF into ECF
Hypotonic: water moves into cell ICF

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42
Q

Besides filtration and reabsorption what maintains the interstitial volume?

A

Lymphatic system (makes sure not too much fluid in interstitial space, or lost from blood vessels)

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43
Q

What is lymphoedema?

A

Swelling in body tissues due to fluid not being taken up by lymphatic system

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44
Q

What solution has:

a) increased tonicity
b) decreased tonicity?

A

a) Hypertonic

b) Hypotonic

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45
Q

How do H2O and Na+ regulate fluid balance?

A

Changes in H2O / Na+ levels alter:

Changes in osmolality

Shift in H2O between extracellular and intracellular components

H2O and Na+ levels need to be highly regulated

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46
Q

What is the role of osmoreceptors in fluid balance?

A

in brain
sense Increase in osmolality
Release anti-diuretic hormone (ADH)
–> Increased H2O reabsorption in kidney

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47
Q

What is the role of filling receptors in fluid balance?

A

in heart
senses increase in blood volume
Release atrial natriuretic peptide (ANP)
Increased excretion of Na+/H2O from kidney

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48
Q

What is the function of the juxtaglomeruler apparatus?

A 
senses decrease in perfusion pressure/NaCl load
Increase release of Renin
Increase RAAS
Increase aldosterone
Increase Na+/H2O reabsorption
49
Q

Define dehydration

A

Lack of water or
Lack of water and salt or
Reduction of plasma volume

50
Q

Define water overload

A

Excessive water intake or
Excessive water reabsorption in the kidney
(e.g. excessive ADH levels)
or
Excessive water filtration in capillaries (e.g. expansion of interstitial volume, oedema)

51
Q

What is isonatremic dehydration?

A

Also called loss of isotonic fluid:

Loss of water and solutes in equal amount
(Normal levels of plasma Na and osmolality remain)

e.g. diarrhoea, vomiting

LOSS OF PLASMA VOLUME = LOWER BP

52
Q

What happens to fluid compartments and plasma osmolality in:

a) isotonic fluid loss
b) hypo-osmotic fluid loss
c) hyper-osmotic fluid loss?

A

a) ECF DECREASE, ICF NO CHANGE, plasma osmolality NO CHANGE
b) ECF DECREASE, ICF DECREASE, plasma osmolality INCREASE
c) ECF DECREASE, ICF INCREASE, plasma osmolality DECREASE

53
Q

How does the body compensante for isotonic fluid loss?

A

Decreased hydrostatic capillary blood pressure leads to movement of water (about 500 ml) from interstitial space into plasma via osmosis

HOWEVER Little change in plasma osmolality (lose both fluid and solutes)
No movement of fluid between intracellular and extracellular compartments

Need to replace fluid – 0.9% NaCl (isotonic) – expand extracellular volume

54
Q

Why is someone with isonatremic dehydration given 0.9% NaCl?

A

This is an isotonic solution, so has the same osmolality and wont move into ICF but will stay in ECF and expand it, increase blood volume and reduce symptoms

55
Q

What is loss of hyponatremic dehydration?

A

LOSS OF HYPER-OSMOTIC FLUID

More loss of NaCl relative to water (plasma hyponatremia remain) e.g. Addison’s disease – less aldosterone, excessive NaCl lossDiuretics - excessive Na loss

LOSS OF NACL AND DECREASED PLASMA OSMOLALITY

56
Q

What is loss of hypernatremic dehydration?

A

LOSS OF HYPO-OSMOTIC FLUID

Extreme water loss relative to Na loss (plasma hypernatremia remains) e.g. decreased water intake, excess sweating, insensible loss, fever

LOSS OF PLASMA VOLUME AND INCREASED PLASMA OSMOLALITY

57
Q

How does the body compensate for hyper-osmotic fluid loss?

A

Water moves from plasma to interstitial to intracellular, balance osmolality but – Cells Swell

Hyperosmotic agents - mannitol/hypertonic saline to shift fluid from intracellular into extracellular compartment

58
Q

How does the body compensate for hypo-osmotic fluid loss?

A

Water moves from interstitial space to plasma, increasing interstitial osmolality which draws water from intracellular space – Cells Shrink

Need to replace fluid – 0.9% NaCl (isotonic, will equilibrate osmolality over time)

59
Q

Right sided heart failure

A

Increased fluid retention in peripheral circulation

Build up of fluid in RS heart –> increased capillary pressure in peripheral side of body –> PERIPHERAL OEDEMA because of excess filtration that lymphatics cannot cope with

60
Q

Left sided heart failure

A

Increased fluid retention in pulmonary circulation

Build up of fluid on LS heart –> increasd pressure in pulmonary veins –> increased capillary pressure in lungs and increased filtration –> more fluid filtered into interstitial space in lungs –> PULMONARY OEDEMA preventing efficient gas exchange, very serious

61
Q

What is the impact of excessive fluid intake such as drinking or drugs like ecstasy (MDMA)?

A

increases ADH levels,excessive water reabsorption in kidneys, plus you drink more as you are hot

DECREASED plasma osmolality –> due to the excessive water intake and/or reabsorption by kidneys

COMPENSATION: water moves from extracellular to intracellular compartment due to osmosis – Cells Swell
Potentially very serious – enclosed cranium, cerebral oedema

62
Q

How to treat excessive fluid intake?

A

Hyperosmotic agents - mannitol/hypertonic saline to shift fluid from intracellular into extracellular compartment

Reverse cells swelling

63
Q

What are drugs?

A

Chemicals that produce biological effects

64
Q

What type of drug is aspirin?

A

NSAID (non-steroidal anti-inflammatory drug)

PHARMACODYNAMICS:
analgesic (painkiller)
anti-pyretic (reduces fever)
anti-inflammatory (reduces immune response)
in low doses reduces formation of blood clots

65
Q

What is the mechanism of action of aspirin?

A

Irreversible inhibition cyclooxygenase (COX) 1 & 2

Because COX cannot catalyse reaction producing PGs and thromboxane, aspirin prevents pain, inflammation, swelling and platelet aggregation (analgesic, anti-inflammatory, anti-pyretic, anti-platelet aggregation)

66
Q

What is the action of COX enzyme?

A

Catalyses conversion of arachidonic acid into prostaglandins (PGs) and thromboxanes

PGs can:
sensitise nerve endings- produce pain
dilate blood vessels redness
increase blood vessel permeability - swelling
reset body temp - fever
thromboxane = platelet aggregation (clot formation)

67
Q

What are the pharmacokinetics of aspirin?

A

ie how does drug enter body and what happens to it

Routes of administration – oral (other routes IV, IM, SC, inhalation)
Readily absorbed from stomach and intestine
Broken down in liver, some excreted unchanged- half-life of 4 hours in low doses
Excreted in urine – need kidney function
Important in deciding dose and how often administrated

68
Q

What are the clinical uses of aspirin?

A

Analgesia, e.g. headaches, toothache, dysmenorrhoea

Reduce fevers (makes you feel ill)

Acute and chronic inflammation, rheumatoid arthritis

To reduce platelet aggregation after myocardial infarction, many patients take aspirin for life

69
Q

What are the properties of the actions of drugs?

A
  1. Tissue selectivity (i.e., receptors located at specific tissues)
  2. Chemical selectivity (i.e., drugs have a specific structure → changes to structure = changes in action of drug).
  3. Amplification (i.e., small amounts of drug produces an action)
70
Q

What are some adverse effects of aspirin?

A

Gastrointestinal irritation and bleeding, might be severe in some individuals (side effect)

Tinnitus, vertigo, nausea and vomiting – high doses (side effect

Should be avoided in asthmatics – may stimulate attack (potential contraindication)

May cause Reye’s syndrome in children which can be fatal – do not give to young children (contraindication)

71
Q

What is a drug receptor?

A

A specific target molecule which a drug interacts with to produce a cellular response

It is not simply a binding site, it alters cell function

72
Q

What is an agonist?

A

A drug which binds to a receptor to produce a biological cellular response
e.g. adrenaline increases heart rate

73
Q

What is an antagonist?

A

A drug which binds to a receptor but does not produce a biological effect

Antagonists bind to receptors to prevent agonists producing effects e.g. Atenolol blocks adrenaline-mediated increases in heart rate
Atenolol is a beta-adrenoceptor blocker

74
Q

Do antagonists have efficacy?

A

No, while both agonists and antagonists have affinity for receptors, only agonists produce a cellular response (have efficacy)

75
Q

What are the reversible types of receptor binding?

A

Hydrogen, ionic bonding and van der waal’s forces

All relatively weak, reversible binding and dissociation of drug-receptor interactions

76
Q

What type of receptor bonding is irreversable?

A

Covalent bonding

Stable strong bonds, irreversible binding and poor dissociation

77
Q

What determines drug affinity?

A

Law of mass action: rate of reaction is deoendant on concentration of reactants involved

Agonist + Free Receptors –> Agnoist-Receptor complex
TOWARDS: Association rate
REVERSE: Dissociation rate

Low [A] - lots of Rfree - few AR interactions – reaction rate to right is limited
As we increase [A] - more AR interactions – reaction rate greatly increases
Reaches maximum as numbers of receptors is finite (There is a maximal number of AR interactions due to finite number of receptors)

78
Q

What is KA?

A

When 50% of receptors are free and 50% are bound to agonist = equilibrium constant of a drug (KA)

KA is the [A] at equilibrium, e.g. KA of 50 nM means that at this agonist concentration 50% of receptors will be occupied

Each drug has it own KA value

Smaller KA (e.g. 5 nM) means agonist has a greater AFFINITYfor a receptor than a drug with a higher KA value (e.g. 50 nM)

79
Q

What determines efficacy?

A

a) Threshold concentration
b) EC50 = effective concentration giving 50% biological response
Used to compare drug potency (determined by both affinity and efficacy)
c) Maximal concentration

These values are very important for determining drug dose

80
Q

What is efficacy vs affinity?

A

Affinity – occupancy, binding of drug to receptor

Efficacy – biological effect, e.g. increase in heart rate

81
Q

Affinity (KA) and Efficacy (EC50) of a drug are not equal- why?

A

Outcome - You do not need full occupancy to give a maximum response
Why? - Remember receptors amplify signals, so only a small number of drug-receptor interactions is needed to produce biological function

82
Q

What is a partial agonist?

A

Present at receptors because it has high affinity but less efficacy means:
Reduce withdrawal effects
Whilst reducing addictive ‘highs’

Heroin-induced highs (diamorphine, full agonist) are reduced is taken in presence of partial agonist

83
Q

What occurs in competitive antagonism?

A

Receptors bind either Agonist (A) or Antagonist (Ant) – not both at same time
A and Ant COMPETE FOR THE SAME BINDING SITE

A and Ant both bind reversibly
Reaction now dependent on two equilibrium constants, KA and Kant
If KAnt < KA, then Ant has greater affinity for Receptor than A
[A] must increase to overcome Ant binding to Receptor

84
Q

What happens to the curve in competitive antagonism?

A

In the presence of the Ant - effect of curve is shifted to night
Shift to right is linearly related to [Ant]
Linear part of curve is parallel
Same maximal response is obtained
If you increase [A] you will ‘out-compete’ antagonist
‘Surmountable’ antagonism

Examples - beta-blockers preventing the action of adrenaline on the heartor anti-histamines to present histamine-induced symptoms of hay fever

85
Q

What does non-surmountable antagonism do to the curve?

A

Reduce slope

Depress maximum

86
Q

What is non-competitive antagonism?

A

Antagonist binds to a different site to that of the agonist

e.g. ketamine (anaesthetic) blocking glutamate NMDA receptor in brain

87
Q

What is irreversible antagonism?

A

Antagonist binds irreversibly to either agonist- or non-agonist binding sites on the receptor through covalent bonds
Reduces number of receptors the agonist can bind to

e.g. aspirin – acetylates COX enzyme

88
Q

The ANS is split into SNS and PNS. What are the features of the SNS?

A 
“Fight or flight”
• Increased heart rate and 
contractility
• Increased BP
• Opening of airways
• Increased fuel deliver to muscles
• Increased sweating
• Pupil dilation
89
Q

The ANS is split into SNS and PNS. What are the features of the PNS?

A

– “Rest and digest”
• Slowing heart rate – Rest
• Accommodation of the eye (i.e., pupil constriction) –
Rest (newspaper reading)
• Bladder : micturition – Rest (time for a pee)
• GI tract motility/secretions – Time for eating /
digestion
• Metabolism – Insulin release, glucose uptake and
storage
• Bronchoconstriction – Rest, less O2 intake required

90
Q

What is an automatic ganglion?

A 
A collection of cell bodies outside of the CNS, which 
are stimulated (or inhibited) by neurotransmitters
91
Q

What is a neurotransmitter?

A

A chemical released from the end of a nerve fibre

92
Q

Whats the main difference between sympathetic and parasympathetic ganglia?

A

Parasympathetic:
• Long pre-ganglionic fibre → release acetylcholine
(Ach)
• Short post-ganglionic fibre → mainly release Ach

Sympathetic:
• Short pre-ganglionic fibre → release Ach
• Long post-ganglionic fibre → mainly release
noradrenaline (NA)

93
Q

What is the ENS?

A

ENTERIC nervous system controlling GI tract

94
Q

How is ANS involved in the heart?

A

Sino-atrial node cells – Regulates heart rate
Atrial-ventricular node cells – Regulates electrical conduction through heart
Cardiac myocytes – Regulates contractility of heart

95
Q

How is ANS involved in smooth muscle?

A

ANS contracts or relaxes smooth muscle cells which are present in in many tissues/organse.g. blood vessels, airways, intestine, bladder

96
Q

How does ANS affect gland cells?

A

ANS cause secretions from glandular cells e.g. release of saliva, sweat, gastric acid,insulin, glucagon

97
Q

How many nerons are involved in ANS conduction? What are they called?

A

2 efferent neurons arranged in series conducting electrical activity from CNS to peripheral tissues/organ

PRE-GANGLIONIC NERVE is neuron in CNS, goes to
POST GANGLIONIC NERVE which goes to peripheral organ

98
Q

What are utonomic ganglia?

A

Group of neuronal cell bodies lying outside CNS

99
Q

Why can pre-ganglionic nerves be controlled by higher functions?

A

Because they start in the CNS

100
Q

Where do the pre ganglionic nerves of the sympathetic system lie?

A

Thoracic and lumbar regions

101
Q

Where do the pre ganglionic nerves of the parasympathetic system lie?

A

Medulla and sacral regions

102
Q

Why are the pre ganglionic fibres of the sympathetic system short?

A

Sympathetic ganglia lie close to spinal cord so PRE ganglia short, POST ganglia long

103
Q

Why are pre ganglionic fibres in parasmpathetic system long?

A

Parasympathetic ganglia lie very close to the end organ so PRE ganglia long, POST ganglia short

104
Q

What neurotransmitter is used by parasympathetic nerves?

A

Acetylcholine

105
Q

What neurotransmitter is used by sympathetic nerves?

A

Noradrenaline

106
Q

What receptors does acetylcholine act on in post gangionic fibres of parasympathetic nerves?

A

Nicotinic receptors

107
Q

What receptors does acetylcholine at on in the peripheral end organ of parasympathetic nerves?

A

Muscarinic receptors

108
Q

What receptors does acetylcholine act on in post gangionic fibres of sympathetic nerves?

A

Nicotinic receptors

109
Q

What neurotransmiter is released by sympathetic post ganglionic fibres?

A

Noradrenaline

110
Q

What receptors does noradrenaline at on in the peripheral end organ of sympathetic nerves?

A

Alpha or beta adrenoreceptors

111
Q

What is the process of chemical transmission?

A
  1. Synthesis of neurotransmitter
  2. Storage of NT in vesicles
  3. Arrival of AP at synaptic terminal
  4. Terminal depolarises, activation of voltage-gated Ca2+ channels, Ca2+ influx
  5. Ca2+-dependent release of NT
  6. NT binds to receptor induces response
  7. Uptake/breakdown of NT
112
Q

What organs are only innervated by SNS?

A

sweat glands, kidney, blood vessels

113
Q

What organs are only innervated by parasympathetic?

A

pancreas, secretory cells of stomach, lungs (but airways contain beta adrenoreceptors, modulated by circulating adrenaline)

114
Q

What is an organ that both SNS and PNS innervate to produce the same effect?

A

salivary gland = increase secretions

115
Q

How does ANS respond to a decrease in blood pressure when standing up?

A

Drop in blood pressure –>
Change in baroreceptor activity (stretch receptors in aortic arch) –>
Change in firing of sensory afferent fibres to CNS
Sensory information processed by CNS –>
Signals are sent out via sympathetic nerves (efferent fibres) to the heart, blood vessels, kidney to increase in blood pressure

116
Q

All pre ganglionic nerves (SNS and PNS) release…

which acts at what receptors?

A

Acetylcholine

acts at nicotinic receptors

117
Q

What is the difference between SNS and PNS post ganglionic receptors?

A

PNS nerves release Ach which acts on muscarinic receptors

SNS nerves release NA which acts at alpha/beta adrenoreceptors

118
Q

What do SNS nerves release in sweat glands?

A

Ach which acts at muscarinic receptors

119
Q

Are post ganglionic fibres involved in innervation of adrenal glands?

A

No

stimulation of pre ganglionic sympathetic fibres releases 80% adrenaline and 20% noradrenaline from adrenal glands

Foundations of Clinical Science (4 decks)

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