Part As - 2007-2011 Flashcards
Is the resting membrane of an excitable cell many times MORE/LESS permeable to sodium compared to potassium?
Less
Is the Na+/K+ ATPase pump necessary to restore the membrane potential to its resting value at the end of an action potential?
No
Increasing the external potassium concentration HYPERPOLARISES/DEPOLARISES the resting membrane potential of an excitable cell
Depolarises
Will the resting membrane potential of this excitable cell be the same as the potassium equilibrium potential (Ek)?
No
Cardiac dysrhythmia drug
beta-adrenoceptor antagonist
Nasal decongestant
alpha1-adrenoceptor agonist
Suppression of contractions during pregnancy
beta2-adrenoceptor agonist
Myasthenia gravis drug
cholinesterase inhibitor
Ophthalmic inspection
muscarinic receptor antagonist
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
inhibitor of cholinesterase
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
muscarinic receptors
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
beta2-adrenoceptor antagonist
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
alpha1-adrenoceptor antagonist
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
muscarinic receptor antagonist
The main neurotransmitter released from preganglionic parasympathetic neurones is
acetylcholine
The main action of this neurotransmitter on the postganglionic parasympathetic neurones is
excitation
Excitation is mediated by
nicotinic cholinergic receptors
The main neurotransmitter released from postganglionic parasympathetic neurones is
acetylcholine
Parasympathetic ACh acts on
muscarinic cholinergic receptors
Lidocaine
Na+ channel blocker
Propranolol
beta-adrenoceptor antagonist
Amiodarone
K+ channel blocker
Verapamil
Ca2+ channel blocker
Adenosine
Purinergic receptor agonist
From the following list select four factors that increase the velocity of conduction of an action potential in nerve fibres
- decrease in external resistance
- decrease in internal resistance
- decrease in membrane capacitance
- increase in membrane resistance
What is the velocity of conduction in A alpha nerve fibres?
100 m/sec
Select the membrane channel responsible for the inward current during the depolarising phase of the action potential in nerve fibres
voltage-gated Na+ channel
Name one drug that blocks Na+ channels
tetrodotoxin - TTX
Select which membrane channels are responsible for the repolarising phase of the action potential in nerve fibres
delayed rectifier K+
Name a drug that blocks K+ channels
tetraethylammonium - TEA
What accounts for the absolute refractory period that follows an action potential
voltage-gated Na+ channel
Ouabain acts on
Na+/K+ ATPase
Tetrodotoxin acts on
Voltage gated sodium channels
Tetraethyl ammonium ion acts on
Voltage gated potassium channels
cAMP acts on
Protein kinase A
Neostigmine acts on
Acetylcholinesterase
Therapeutic use of Beta 2 adrenoceptor agonist
Asthma
Therapeutic use of Cholinesterase inhibitors
Myasthenia gravis
Therapeutic use of inhibitor of angiotensin converting enzyme
Hypertension
Therapeutic use of Na+ channel blocker
Cardiac dysrhythmia
Therapeutic use of Inhibitor of H+/K+ ATPase
Peptic ulcer
Example of a non-depolarizing blocking agent at the neuromuscular junction
Tubocurarine
Example of an irreversible antagonist of a metabolic enzyme
Aspirin
Example of a stimulant at the autonomic ganglia
Nicotine
Example of a blocker of vesicular transport
Reserpine
Example of a a reversible competitive antagonist on gastro-intestinal smooth muscle
Atropine
Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: Muscarinic M2 receptor
cAMP fall
Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: Oxytocin receptor
IP3 rise
Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: β2-adrenoceptor
cAMP rise
Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: α1-adrenoceptor
IP3 rise
Match from the drop-down list below the following receptors or enzymes to the principal second messenger response which they elicit: Nitric oxide synthase
cGMP rise
Noradrenaline in peripheral sympathetic nerves is released from preganglionic sympathetic nerves
False
Noradrenaline in peripheral sympathetic nerves is synthesised from dopamine
True
noradrenaline in peripheral sympathetic nerve transport into presynaptic vesicles is proton-dependent
True
noradrenaline in peripheral sympathetic nerve action is terminated by transporters located both pre- and postsynaptically
True
noradrenaline in peripheral sympathetic nerves once released - its action is blocked by an inhibitor of tyrosine hydroxylase
False
Example of an acetylcholinesterase inhibitor
physostigmine
Does Cl- contribute to the downstroke of the action potential?
No
Which ion makes the greatest contribution to the resting membrane potential?
K+
Rigor Mortis is due to myoplasmic ATP depletion. This results in rigor because
myosin head remains attached to actin
Acts on a Nicotinic receptor
Alpha-bungarotoxin
Acts on an Epithelial sodium channel
Amiloride
Acts on Voltage-gated calcium channel
Nifedipine
What is a clinical use for an inhibitor of voltage gates Na+ channels?
local anaesthetic
Which type of ion channel underlies the upstroke of the action potential in smooth muscle?
Ca2+
State a molecule that can inhibit Ca2+ channels
verapamil
Example of an Alpha 1 receptor agonist
phenylephrine
Example of an Alpha 1 receptor antagonist
prazosin
Example of an Inhibitor of noradrenaline release
guanethidine
Example of an Uptake 1 inhibitor
Cocaine
Example of a Beta receptor agonist
isoprenaline
The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves competitive antagonism of Nicotinic receptors
False
The mechanism of action of depolarizing blockers at the vertebrate neuromuscular
junction involves inactivation of voltage gated sodium channels in muscle fibres
True
The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves stimulation of nicotinic receptors
True
The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves blockade of voltage gated calcium channels
False
The mechanism of action of depolarizing blockers at the vertebrate neuromuscular junction involves inhibition of acetylcholine release from motoneurones
False
What is the typical concentration of intracellular K+?
140 mM
What is the typical concentration of intracellular Na+?
15 mM
At rest, is the normal cell membrane more permeable to Na+ or K+?
more permeable to K+
What is the stoichiometry and direction of Na+ and K+ movements powered by the Na+/K+ ATPase in a resting cell?
3Na+ out and 2K+ in
Myelination increases conduction velocity because it
Decreases membrane capacitance
One mechanism that releases the ion from the endoplasmic (or sarcoplasmic) reticulum
IP3
A calcium binding protein that mediates the effects of calcium
Calmodulin
A calcium-activated enzyme that stimulates smooth muscle contraction
myosin light chain kinase (MLCK)
Example of a ganglion blocker
trimetaphan
Action potential conduction velocity in the largest myelinated nerve fibre is
120 m/s
Myelination increases conduction velocity because it
permits saltatory conduction
The sequence of nerve block by local anaesthetics is
pain first, then general sensory, then motor last
A clinical use of a voltage-gated K+ channel blocker is
antidysrhythmic
A depolarising blocker at the skeletal neuromuscular junction
suxamethonium
A blocker of autonomic ganglia receptors
hexamethonium
Sympathetic nerves innervate the motor endplate in skeletal muscle
False
Parasympathetic nerves innervate the motor endplate in smooth muscle
False
Smooth muscle of the gastrointestinal tract is directly innervated mainly by
sympathetic nerves
False
Parasympathetic nerves contract bladder smooth muscle
True
Insulin is a
tyrosine kinase receptor
Noradrenaline in peripheral sympathetic nerves is released from preganglionic sympathetic nerves.
False
Noradrenaline is synthesised outside the vesicle in nerve terminals and then transported into the vesicle
False
Released NA acts on muscarinic M3 receptors in bladder smooth muscle
False
Once released the action of NA is terminated by tyrosine hydroxylase
False
NA, by action at beta1-adrenoceptors, increases cAMP levels in the heart
True
Nicotinic ACh receptors are found in
parasympathetic ganglia
Muscarinic ACh receptors are found in
endothelial cells
Bradycardia is produced by acetylcholine action on
M2 muscarinic cardiac receptors
The TWO main mechanisms underlying bradycardia are
a decrease in cAMP and potassium channel activation
The upstroke of the action potential in cardiac pacemaker cells is due to
L type voltage-gated Ca2+ channels
Hyperpolarisation is due to
voltage-gated K+ channels
Regarding the rate of rise of the cardiac action potential, local anaesthetics will
decrease it
Cortisol is produced in the
adrenal cortex
The upstroke of the action potential in skeletal muscle is usually blocked by calcium channel blockers
False
Skeletal muscle fibres have a well-defined t-tubule system
True
Sarcomeres are poorly developed in skeletal muscle
False
Troponin C binds calcium and initiates cross bridge cycling
True
The endplate potential is initiated by the actions of acetylcholine released from somatic motor nerves acting at muscarinic M3 receptors
False
An example of a primary active ion-transporter is
SERCA (sarcoplasmic endoplasmic reticular Ca2+- ATPase)
An example of a secondary active ion transporter is
Na+ -glucose symporter
The Na+ /K+ ATPase is directly inhibited by the drug
cardiac glycoside
and (v) Na+ /K+ ATPase inhibition causes the following two effects
Fall of intracellular K+ and rise of intracellular Na+
The typical equilibrium potential for K+ ions (EK) across the plasmalemma of a resting nerve cell (measured inside relative to outside; in mV) is
-90
The typical equilibrium potential for Na+ ions (ENa) across the plasmalemma of a resting nerve cell (measured inside relative to outside; in mV) is
60
Raising the extracellular K+ concentration bathing a nerve cell would
make Ek less negative (more positive)
Reducing the extracellular concentration of Na+ ions would
Make ENa more negative (less positive)
Noradrenaline released at a noradrenergic synapse is removed from the cleft by
Both presynaptic and postsynaptic reuptake
Acetylcholine applied to the heart
Decreases atrial contractility
Which of the following drugs is a Ca2+ channel antagonist that may be used for treatment of cardiac arrhythmias?
verapamil
The major excitatory receptor on skeletal muscle
Nicotinic acetylcholine receptor
The major mammalian presynaptic channel controlling transmitter release
Neuronal calcium channel
Enzyme for breaking down acetylcholine
AChE
Depolarizing NMJ blocker
Suxamethonium
Non-depolarizing NMJ blocker
Tubocurarine
Action potentials occur in most smooth muscles
True
Intracellular cAMP generally contracts smooth muscle cells
False
Smooth muscle contraction is generally faster than cardiac muscle
False
Troponin C is the major calcium regulated protein in the control of smooth muscle contractility
False
Neurotransmitters often evoke smooth muscle contraction by stimulating a rise in inositol trisphosphate (IP3)
True
Catecholamine neurotransmitter example
Noradrenaline
Thin filaments
Actin
thick filaments
Myosin
Where are calcium release channels located in skeletal muscle
Sarcoplasmic reticulum (SR)
Where are nicotinic receptors on skeletal muscle located
Sarcolemma
During contraction, which of the following remains constant in length?
I band
The major adrenoceptor in ventricular muscle whose activation increases cardiac contractility
β1
The adrenoceptor in liver cells whose activation leads to glycogenolysis
α1 and β2
An adrenoceptor whose activation leads to vascular smooth muscle contraction
α1
an adrenoceptor whose activation leads to vascular smooth muscle relaxation
β2
a presynaptic adrenoceptor whose activation leads to decreased neurotransmitter release
α2
A doubling of the intracellular Na+
ion concentration will … membrane
ion transport by Na+ /K+ ATPase proteins.
Stimulate
A change of extracellular K+ ion concentration to 2.0 mM will … membrane ion transport by Na+ /K+ ATPase proteins.
Decrease
A selective inhibitor of Na+ /K+ ATPase proteins is
Digoxin
The Na+/K+ ATPase protein is
primary active ion transporter
The depolarization phase (from point A-C) of an action potential is mediated by ionic current flow through
voltage-gated Na+ channels
The initial (local) depolarization (immediately after point A) is mediated by
ligand-gated ion channels
From region C to D the process primarily responsible is ionic current flow through
voltage-gated K+ channels
Membrane potential at point E is more negative than point A due to
open K+ channels
Local anaesthetics act directly on
voltage-gated Na+ channels
Ionotropic receptors
are ligand gated ion channels
Metabotropic receptors
are coupled downstream to G proteins
Sympathetic nerves constrict blood vessels
by releasing noradrenaline that binds to α1 receptors
Synaptic transmission at sympathetic autonomic ganglia is blocked by
a nicotinic antagonist
Electrical coupling between adjacent cardiac myocytes is blocked by
a rise of intracellular [H+]
Contraction in fast twitch skeletal muscle is caused by
an action potential propagating in the transverse tubules
Skeletal muscle relaxation is mediated by
pumping of Ca2+ into the sarcoplasmic reticulum
Myocardial contraction is
reduced by verapamil
Contraction of vascular smooth muscle can typically be caused by
IP3 dependent release of sarcoplasmic reticular Ca2+
Contraction of skeletal muscle fibres is triggered by activation of sarcolemmal
nicotinic receptors
Beta adrenergic receptors are coupled to the G-protein
Gs
Beta adrenergic receptors modulate the concentration of the second messenger
cyclic AMP
Cyclic AMP levels can be decreased by the enzyme
phosphodiesterase
Cyclic AMP activates
Protein kinase A
Methylxanthines inhibit
phosphodiesterase
The extracellular free concentration of Ca2+
1 mM
The extracellular concentration of Na+
140 mM
The intracellular concentration of Na+
15 mM
The intracellular free concentration of Ca2+ is lower than extracellular free Ca2+ concentration by approximately
10,000 fold
The intracellular concentration of K+ is
140 mM
The primary barrier to ion diffusion across membranes is
the hydrophobic core
The resting membrane potential is due to a flow of ions mainly through
K+ channels
The Na+/K+ pump obtains energy from
ATP
Acetylcholine is removed from the neuromuscular junction mainly by
hydrolysis
At the nicotinic acetylcholine receptor, depolarizing neuromuscular blocking drugs are
agonists
At the nicotinic acetylcholine receptor, common non-depolarizing neuromuscular blocking drugs are
competitive antagonists
Non-depolarizing neuromuscular block can be reversed by
neostigmine
The catecholamine neurotransmitters are synthesized from the amino acid
Tyrosine
Activation of alpha1 adrenergic receptors would acutely
Increase blood pressure
Airway smooth muscle can be relaxed by inhalation of a (an)
beta agonist
Catecholamine neurotransmitters are removed from the synapse by
Reuptake
Amphetamines act by
displacing catecholamines from secretory vesicles
In cardiac muscle during a ventricular action potential the rapid depolarization is mediated by
Na+ influx
In cardiac muscle during a ventricular action potential the plateau phase is mediated mainly by
Ca2+ influx
During excitation-contraction coupling in cardiac cells, membrane depolarization is transduced into Ca2+ release from the sarcoplasmic reticulum by
Ca2+ induced Ca2+ release
A stimulant at the autonomic ganglia
Nicotine
A blocker of acetycholine uptake into vesicles
vesamicol
A competitive antagonist of alpha1 adrenoceptors
prazosin
Smooth muscle cells are electrically connected by gap junctions
True
Smooth muscle cells have a well-defined t-tubule system
False
Sarcomeres are poorly developed in smooth muscles
True
Troponin C binds calcium and initiates cross bridge cycling
False
Smooth muscle cells in blood vessels are usually innervated by the sympathetic and parasympathetic nervous systems
False
