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Physiology and Pharmacology Year 1 > Part As - 2007-2011 > Flashcards

Part As - 2007-2011 Flashcards

1
Q

Is the resting membrane of an excitable cell many times MORE/LESS permeable to sodium compared to potassium?

A

Less

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2
Q

Is the Na+/K+ ATPase pump necessary to restore the membrane potential to its resting value at the end of an action potential?

A

No

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3
Q

Increasing the external potassium concentration HYPERPOLARISES/DEPOLARISES the resting membrane potential of an excitable cell

A

Depolarises

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4
Q

Will the resting membrane potential of this excitable cell be the same as the potassium equilibrium potential (Ek)?

A

No

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5
Q

Cardiac dysrhythmia drug

A

beta-adrenoceptor antagonist

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6
Q

Nasal decongestant

A

alpha1-adrenoceptor agonist

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7
Q

Suppression of contractions during pregnancy

A

beta2-adrenoceptor agonist

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8
Q

Myasthenia gravis drug

A

cholinesterase inhibitor

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9
Q

Ophthalmic inspection

A

muscarinic receptor antagonist

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10
Q

A patient who has ingested an unknown drug presents with the following symptoms:
 increased salivation
 difficulty with breathing
 decreased heart rate
 hypotension
 abdominal colic
 pupillary constriction
From the list provided select: The class of drug that probably caused these effects

A

inhibitor of cholinesterase

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11
Q

A patient who has ingested an unknown drug presents with the following symptoms:
 increased salivation
 difficulty with breathing
 decreased heart rate
 hypotension
 abdominal colic
 pupillary constriction
From the list provided select: The main type of receptor involved

A

muscarinic receptors

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12
Q

A patient who has ingested an unknown drug presents with the following symptoms:
 increased salivation
 difficulty with breathing
 decreased heart rate
 hypotension
 abdominal colic
 pupillary constriction
From the list provided select: A drug class that might worsen the difficulty with breathing

A

beta2-adrenoceptor antagonist

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13
Q

A patient who has ingested an unknown drug presents with the following symptoms:
 increased salivation
 difficulty with breathing
 decreased heart rate
 hypotension
 abdominal colic
 pupillary constriction
From the list provided select: A drug class that might worsen the hypotension

A

alpha1-adrenoceptor antagonist

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14
Q

A patient who has ingested an unknown drug presents with the following symptoms:
 increased salivation
 difficulty with breathing
 decreased heart rate
 hypotension
 abdominal colic
 pupillary constriction
From the list provided select: A drug class that would block the symptoms

A

muscarinic receptor antagonist

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15
Q

The main neurotransmitter released from preganglionic parasympathetic neurones is

A

acetylcholine

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16
Q

The main action of this neurotransmitter on the postganglionic parasympathetic neurones is

A

excitation

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17
Q

Excitation is mediated by

A

nicotinic cholinergic receptors

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18
Q

The main neurotransmitter released from postganglionic parasympathetic neurones is

A

acetylcholine

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19
Q

Parasympathetic ACh acts on

A

muscarinic cholinergic receptors

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20
Q

Lidocaine

A

Na+ channel blocker

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21
Q

Propranolol

A

beta-adrenoceptor antagonist

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22
Q

Amiodarone

A

K+ channel blocker

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23
Q

Verapamil

A

Ca2+ channel blocker

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24
Q

Adenosine

A

Purinergic receptor agonist

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25
Q

From the following list select four factors that increase the velocity of conduction of an action potential in nerve fibres

A
  • decrease in external resistance
  • decrease in internal resistance
  • decrease in membrane capacitance
  • increase in membrane resistance
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26
Q

What is the velocity of conduction in A alpha nerve fibres?

A

100 m/sec

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27
Q

Select the membrane channel responsible for the inward current during the depolarising phase of the action potential in nerve fibres

A

voltage-gated Na+ channel

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28
Q

Name one drug that blocks Na+ channels

A

tetrodotoxin - TTX

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29
Q

Select which membrane channels are responsible for the repolarising phase of the action potential in nerve fibres

A

delayed rectifier K+

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30
Q

Name a drug that blocks K+ channels

A

tetraethylammonium - TEA

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31
Q

What accounts for the absolute refractory period that follows an action potential

A

voltage-gated Na+ channel

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32
Q

Ouabain acts on

A

Na+/K+ ATPase

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33
Q

Tetrodotoxin acts on

A

Voltage gated sodium channels

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34
Q

Tetraethyl ammonium ion acts on

A

Voltage gated potassium channels

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35
Q

cAMP acts on

A

Protein kinase A

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36
Q

Neostigmine acts on

A

Acetylcholinesterase

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37
Q

Therapeutic use of Beta 2 adrenoceptor agonist

A

Asthma

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38
Q

Therapeutic use of Cholinesterase inhibitors

A

Myasthenia gravis

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39
Q

Therapeutic use of inhibitor of angiotensin converting enzyme

A

Hypertension

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40
Q

Therapeutic use of Na+ channel blocker

A

Cardiac dysrhythmia

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41
Q

Therapeutic use of Inhibitor of H+/K+ ATPase

A

Peptic ulcer

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42
Q

Example of a non-depolarizing blocking agent at the neuromuscular junction

A

Tubocurarine

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43
Q

Example of an irreversible antagonist of a metabolic enzyme

A

Aspirin

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44
Q

Example of a stimulant at the autonomic ganglia

A

Nicotine

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45
Q

Example of a blocker of vesicular transport

A

Reserpine

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46
Q

Example of a a reversible competitive antagonist on gastro-intestinal smooth muscle

A

Atropine

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47
Q

Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: Muscarinic M2 receptor

A

cAMP fall

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48
Q

Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: Oxytocin receptor

A

IP3 rise

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49
Q

Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: β2-adrenoceptor

A

cAMP rise

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50
Q

Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: α1-adrenoceptor

A

IP3 rise

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51
Q

Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: Nitric oxide synthase

A

cGMP rise

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52
Q

Noradrenaline in peripheral sympathetic nerves is released from preganglionic sympathetic nerves

A

False

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53
Q

Noradrenaline in peripheral sympathetic nerves is synthesised from dopamine

A

True

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54
Q

noradrenaline in peripheral sympathetic nerve transport into presynaptic vesicles is proton-dependent

A

True

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55
Q

noradrenaline in peripheral sympathetic nerve action is terminated by transporters located both pre- and postsynaptically

A

True

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56
Q

noradrenaline in peripheral sympathetic nerves once released - its action is blocked by an inhibitor of tyrosine hydroxylase

A

False

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57
Q

Example of an acetylcholinesterase inhibitor

A

physostigmine

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58
Q

Does Cl- contribute to the downstroke of the action potential?

A

No

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59
Q

Which ion makes the greatest contribution to the resting membrane potential?

A

K+

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60
Q

Rigor Mortis is due to myoplasmic ATP depletion. This results in rigor because

A

myosin head remains attached to actin

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61
Q

Acts on a Nicotinic receptor

A

Alpha-bungarotoxin

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62
Q

Acts on an Epithelial sodium channel

A

Amiloride

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63
Q

Acts on Voltage-gated calcium channel

A

Nifedipine

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64
Q

What is a clinical use for an inhibitor of voltage gates Na+ channels?

A

local anaesthetic

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65
Q

Which type of ion channel underlies the upstroke of the action potential in smooth muscle?

A

Ca2+

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66
Q

State a molecule that can inhibit Ca2+ channels

A

verapamil

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67
Q

Example of an Alpha 1 receptor agonist

A

phenylephrine

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68
Q

Example of an Alpha 1 receptor antagonist

A

prazosin

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69
Q

Example of an Inhibitor of noradrenaline release

A

guanethidine

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70
Q

Example of an Uptake 1 inhibitor

A

Cocaine

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71
Q

Example of a Beta receptor agonist

A

isoprenaline

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72
Q

The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves competitive antagonism of Nicotinic receptors

A

False

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73
Q

The mechanism of action of depolarizing blockers at the vertebrate neuromuscular
junction involves inactivation of voltage gated sodium channels in muscle fibres

A

True

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74
Q

The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves stimulation of nicotinic receptors

A

True

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75
Q

The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves blockade of voltage gated calcium channels

A

False

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76
Q

The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves inhibition of acetylcholine release from motoneurones

A

False

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77
Q

What is the typical concentration of intracellular K+?

A

140 mM

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78
Q

What is the typical concentration of intracellular Na+?

A

15 mM

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79
Q

At rest, is the normal cell membrane more permeable to Na+ or K+?

A

more permeable to K+

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80
Q

What is the stoichiometry and direction of Na+ and K+ movements powered by the Na+/K+ ATPase in a resting cell?

A

3Na+ out and 2K+ in

81
Q

Myelination increases conduction velocity because it

A

Decreases membrane capacitance

82
Q

One mechanism that releases the ion from the endoplasmic (or sarcoplasmic) reticulum

A

IP3

83
Q

A calcium binding protein that mediates the effects of calcium

A

Calmodulin

84
Q

A calcium-activated enzyme that stimulates smooth muscle contraction

A

myosin light chain kinase (MLCK)

85
Q

Example of a ganglion blocker

A

trimetaphan

86
Q

Action potential conduction velocity in the largest myelinated nerve fibre is

A

120 m/s

87
Q

Myelination increases conduction velocity because it

A

permits saltatory conduction

88
Q

The sequence of nerve block by local anaesthetics is

A

pain first, then general sensory, then motor last

89
Q

A clinical use of a voltage-gated K+ channel blocker is

A

antidysrhythmic

90
Q

A depolarising blocker at the skeletal neuromuscular junction

A

suxamethonium

91
Q

A blocker of autonomic ganglia receptors

A

hexamethonium

92
Q

Sympathetic nerves innervate the motor endplate in skeletal muscle

A

False

93
Q

Parasympathetic nerves innervate the motor endplate in smooth muscle

A

False

94
Q

Smooth muscle of the gastrointestinal tract is directly innervated mainly by
sympathetic nerves

A

False

95
Q

Parasympathetic nerves contract bladder smooth muscle

A

True

96
Q

Insulin is a

A

tyrosine kinase receptor

97
Q

Noradrenaline in peripheral sympathetic nerves is released from preganglionic sympathetic nerves.

A

False

98
Q

Noradrenaline is synthesised outside the vesicle in nerve terminals and then transported into the vesicle

A

False

99
Q

Released NA acts on muscarinic M3 receptors in bladder smooth muscle

A

False

100
Q

Once released the action of NA is terminated by tyrosine hydroxylase

A

False

101
Q

NA, by action at beta1-adrenoceptors, increases cAMP levels in the heart

A

True

102
Q

Nicotinic ACh receptors are found in

A

parasympathetic ganglia

103
Q

Muscarinic ACh receptors are found in

A

endothelial cells

104
Q

Bradycardia is produced by acetylcholine action on

A

M2 muscarinic cardiac receptors

105
Q

The TWO main mechanisms underlying bradycardia are

A

a decrease in cAMP and potassium channel activation

106
Q

The upstroke of the action potential in cardiac pacemaker cells is due to

A

L type voltage-gated Ca2+ channels

107
Q

Hyperpolarisation is due to

A

voltage-gated K+ channels

108
Q

Regarding the rate of rise of the cardiac action potential, local anaesthetics will

A

decrease it

109
Q

Cortisol is produced in the

A

adrenal cortex

110
Q

The upstroke of the action potential in skeletal muscle is usually blocked by calcium channel blockers

A

False

111
Q

Skeletal muscle fibres have a well-defined t-tubule system

A

True

112
Q

Sarcomeres are poorly developed in skeletal muscle

A

False

113
Q

Troponin C binds calcium and initiates cross bridge cycling

A

True

114
Q

The endplate potential is initiated by the actions of acetylcholine released from somatic motor nerves acting at muscarinic M3 receptors

A

False

115
Q

An example of a primary active ion-transporter is

A

SERCA (sarcoplasmic endoplasmic reticular Ca2+- ATPase)

116
Q

An example of a secondary active ion transporter is

A

Na+ -glucose symporter

117
Q

The Na+ /K+ ATPase is directly inhibited by the drug

A

cardiac glycoside

118
Q

and (v) Na+ /K+ ATPase inhibition causes the following two effects

A

Fall of intracellular K+ and rise of intracellular Na+

119
Q

The typical equilibrium potential for K+ ions (EK) across the plasmalemma of a resting nerve cell (measured inside relative to outside; in mV) is

A

-90

120
Q

The typical equilibrium potential for Na+ ions (ENa) across the plasmalemma of a resting nerve cell (measured inside relative to outside; in mV) is

A

60

121
Q

Raising the extracellular K+ concentration bathing a nerve cell would

A

make Ek less negative (more positive)

122
Q

Reducing the extracellular concentration of Na+ ions would

A

Make ENa more negative (less positive)

123
Q

Noradrenaline released at a noradrenergic synapse is removed from the cleft by

A

Both presynaptic and postsynaptic reuptake

124
Q

Acetylcholine applied to the heart

A

Decreases atrial contractility

125
Q

Which of the following drugs is a Ca2+ channel antagonist that may be used for treatment of cardiac arrhythmias?

A

verapamil

126
Q

The major excitatory receptor on skeletal muscle

A

Nicotinic acetylcholine receptor

127
Q

The major mammalian presynaptic channel controlling transmitter release

A

Neuronal calcium channel

128
Q

Enzyme for breaking down acetylcholine

A

AChE

129
Q

Depolarizing NMJ blocker

A

Suxamethonium

130
Q

Non-depolarizing NMJ blocker

A

Tubocurarine

131
Q

Action potentials occur in most smooth muscles

A

True

132
Q

Intracellular cAMP generally contracts smooth muscle cells

A

False

133
Q

Smooth muscle contraction is generally faster than cardiac muscle

A

False

134
Q

Troponin C is the major calcium regulated protein in the control of smooth muscle contractility

A

False

135
Q

Neurotransmitters often evoke smooth muscle contraction by stimulating a rise in inositol trisphosphate (IP3)

A

True

136
Q

Catecholamine neurotransmitter example

A

Noradrenaline

137
Q

Thin filaments

A

Actin

138
Q

thick filaments

A

Myosin

139
Q

Where are calcium release channels located in skeletal muscle

A

Sarcoplasmic reticulum (SR)

140
Q

Where are nicotinic receptors on skeletal muscle located

A

Sarcolemma

141
Q

During contraction, which of the following remains constant in length?

A

I band

142
Q

The major adrenoceptor in ventricular muscle whose activation increases cardiac contractility

A

β1

143
Q

The adrenoceptor in liver cells whose activation leads to glycogenolysis

A

α1 and β2

144
Q

An adrenoceptor whose activation leads to vascular smooth muscle contraction

A

α1

145
Q

an adrenoceptor whose activation leads to vascular smooth muscle relaxation

A

β2

146
Q

a presynaptic adrenoceptor whose activation leads to decreased neurotransmitter release

A

α2

147
Q

A doubling of the intracellular Na+
ion concentration will … membrane
ion transport by Na+ /K+ ATPase proteins.

A

Stimulate

148
Q

A change of extracellular K+ ion concentration to 2.0 mM will … membrane ion transport by Na+ /K+ ATPase proteins.

A

Decrease

149
Q

A selective inhibitor of Na+ /K+ ATPase proteins is

A

Digoxin

150
Q

The Na+/K+ ATPase protein is

A

primary active ion transporter

151
Q

The depolarization phase (from point A-C) of an action potential is mediated by ionic current flow through

A

voltage-gated Na+ channels

152
Q

The initial (local) depolarization (immediately after point A) is mediated by

A

ligand-gated ion channels

153
Q

From region C to D the process primarily responsible is ionic current flow through

A

voltage-gated K+ channels

154
Q

Membrane potential at point E is more negative than point A due to

A

open K+ channels

155
Q

Local anaesthetics act directly on

A

voltage-gated Na+ channels

156
Q

Ionotropic receptors

A

are ligand gated ion channels

157
Q

Metabotropic receptors

A

are coupled downstream to G proteins

158
Q

Sympathetic nerves constrict blood vessels

A

by releasing noradrenaline that binds to α1 receptors

159
Q

Synaptic transmission at sympathetic autonomic ganglia is blocked by

A

a nicotinic antagonist

160
Q

Electrical coupling between adjacent cardiac myocytes is blocked by

A

a rise of intracellular [H+]

161
Q

Contraction in fast twitch skeletal muscle is caused by

A

an action potential propagating in the transverse tubules

162
Q

Skeletal muscle relaxation is mediated by

A

pumping of Ca2+ into the sarcoplasmic reticulum

163
Q

Myocardial contraction is

A

reduced by verapamil

164
Q

Contraction of vascular smooth muscle can typically be caused by

A

IP3 dependent release of sarcoplasmic reticular Ca2+

165
Q

Contraction of skeletal muscle fibres is triggered by activation of sarcolemmal

A

nicotinic receptors

166
Q

Beta adrenergic receptors are coupled to the G-protein

A

Gs

167
Q

Beta adrenergic receptors modulate the concentration of the second messenger

A

cyclic AMP

168
Q

Cyclic AMP levels can be decreased by the enzyme

A

phosphodiesterase

169
Q

Cyclic AMP activates

A

Protein kinase A

170
Q

Methylxanthines inhibit

A

phosphodiesterase

171
Q

The extracellular free concentration of Ca2+

A

1 mM

172
Q

The extracellular concentration of Na+

A

140 mM

173
Q

The intracellular concentration of Na+

A

15 mM

174
Q

The intracellular free concentration of Ca2+ is lower than extracellular free Ca2+ concentration by approximately

A

10,000 fold

175
Q

The intracellular concentration of K+ is

A

140 mM

176
Q

The primary barrier to ion diffusion across membranes is

A

the hydrophobic core

177
Q

The resting membrane potential is due to a flow of ions mainly through

A

K+ channels

178
Q

The Na+/K+ pump obtains energy from

A

ATP

179
Q

Acetylcholine is removed from the neuromuscular junction mainly by

A

hydrolysis

180
Q

At the nicotinic acetylcholine receptor, depolarizing neuromuscular blocking drugs are

A

agonists

181
Q

At the nicotinic acetylcholine receptor, common non-depolarizing neuromuscular blocking drugs are

A

competitive antagonists

182
Q

Non-depolarizing neuromuscular block can be reversed by

A

neostigmine

183
Q

The catecholamine neurotransmitters are synthesized from the amino acid

A

Tyrosine

184
Q

Activation of alpha1 adrenergic receptors would acutely

A

Increase blood pressure

185
Q

Airway smooth muscle can be relaxed by inhalation of a (an)

A

beta agonist

186
Q

Catecholamine neurotransmitters are removed from the synapse by

A

Reuptake

187
Q

Amphetamines act by

A

displacing catecholamines from secretory vesicles

188
Q

In cardiac muscle during a ventricular action potential the rapid depolarization is mediated by

A

Na+ influx

189
Q

In cardiac muscle during a ventricular action potential the plateau phase is mediated mainly by

A

Ca2+ influx

190
Q

During excitation-contraction coupling in cardiac cells, membrane depolarization is transduced into Ca2+ release from the sarcoplasmic reticulum by

A

Ca2+ induced Ca2+ release

191
Q

A stimulant at the autonomic ganglia

A

Nicotine

192
Q

A blocker of acetycholine uptake into vesicles

A

vesamicol

193
Q

A competitive antagonist of alpha1 adrenoceptors

A

prazosin

194
Q

Smooth muscle cells are electrically connected by gap junctions

A

True

195
Q

Smooth muscle cells have a well-defined t-tubule system

A

False

196
Q

Sarcomeres are poorly developed in smooth muscles

A

True

197
Q

Troponin C binds calcium and initiates cross bridge cycling

A

False

198
Q

Smooth muscle cells in blood vessels are usually innervated by the sympathetic and parasympathetic nervous systems

A

False

Physiology and Pharmacology Year 1 (2 decks)

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