Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
90 Cards in this Set
- Front
- Back
What are the two signs of MS that can be elicited on clinical examination? |
Uhthoff’s sign |
|
What are the two investigations that should be done if MS is suspected? What is expected to be seen? |
MRI ➙ Lesions Lumbar puncture ➙ oligoclonal bands |
|
What investigation distinguishes MS from GBS? |
EMG leading to decreased conduction or conductivity speed in GBS and normal in MS |
|
Name 7 functions of Type A nerves |
Proprioceptor Motor Touch Pressure Muscle spindles Pain Temperature |
|
Name 1 function of Type B nerves |
Preganglionic |
|
Name two functions of Type C nerves
|
Pain Postganglionic |
|
Differentiate Type A, B and C nerves in terms of diameters and myelination |
Type A: large and highly myelinated Type B: medium and weakly myelinated Type C: small and not myelinated |
|
Two clinical features of upper/lower motor neurone lesions |
Upper: Reflex below the level of the lesion ➚ and spastic paralysis
|
|
How many ions and in what direction are transported by Na/K ATPase? |
3Na+ out of the cell and 2K+ into the cells |
|
Give the range of potentials in which voltage-gated sodium channels are in each of the three states. |
Open in [-50mV ➙ +40mV] Closed below -50mV Inactivated in [+40mV ➙ -70mV]. |
|
Name the four phases of AP |
Initiation
Upstroke RepolarisationRefractory period |
|
Name three stimuli that can cause the changes in cations permeability that initiates the AP |
Binding of neurotransmitter Heat Pressure |
|
What current is responsible for the upstroke in the AP? |
Sodium influx through voltage-gated sodium channels |
|
What current is responsible for the repolarisation in the AP? |
Potassium efflux through voltage-gated potassium channels |
|
Use-dependent mechanism of action of local anaesthetics |
Reversibly bind to open voltage-gated Na+ channels ⇒ Channels cannot return to closed state after inactivation ⇒ Action potential cannot propagate |
|
Name one local anaesthetics |
Lidocaine |
|
Name one side effect of local anaesthetics |
Nerve damage ⇒ prolonged numbness, feeling of pins and needles, respiratory depression |
|
Relate gap junction, connexons and connexins |
Gap junctions are made of 2 connexons each made of 6 connexins. |
|
Name two types of synapse |
Chemical and electrical |
|
Differentiate chemical and electrical synapse in terms of: speed of propagation, directionality, and possibility to integrate signals. |
Electrical: fast, bidirectional, no integration Chemical: slow, monodirectional, integration |
|
In which tissues are electrical synapses located? |
Smooth and cardiac muscles |
|
In which tissues are chemical synapses located? |
Skeletal muscles
|
|
What ion channel is responsible for the eventual exocytosis of the neurotransmitter at the presynaptic membrane? |
Voltage-gated calcium channels |
|
Name 6 categories (molecules) of neurotransmitters |
1) Amino acids 2) Monoamine 3) Opioids 4) Gas 5) Tachykinins 6) Secretins |
|
Name 5 monoamine neurotransmitters |
Catecholamines
Dopamine Histamine Serotonin Melatonin |
|
Name and differentiate two types of postsynaptic receptors |
Ionotropic: ligand-gated ion channels Metabotropic: receptor-coupled second messenger (e.g. G-protein) |
|
What transport protein is responsible for the recovery and maintenance of the resting potential after the undershoot of repolarisation in an AP? |
Na/K pumps |
|
Three fates of neurotransmitter after exocytosis |
(a) reuptake into presynaptic cell, (b) diffuse away from synaptic cleft, (c) undertake enzymatic breakdown |
|
How is ACh synthesised (reaction)? |
Acetyl-CoA + Choline ➙ Acetylcholine |
|
What enzyme catalyses synthesis of ACh? |
choline-O-acetyltransferase |
|
What proteins mediating the exocytosis of vesicles do Ca2+ bind in the presynaptic neurone? |
SNARE
|
|
What is the effect of botulinum on NMJ? |
Cleaves SNARE proteins ⇒ Release of ACh is blocked ⇒ Paralysis known as botulism (including respiratory failure) |
|
What series of events happens in the post-synaptic cell when ACh binds to nicotinic ACh receptors, leading to initiation of an action potential? |
Membrane conductance to Na+ and K+ ➚ ⇒ Depolarisation of the muscle fibres ⇒ End-plate potential (not yet an action potential, because the NMJ lacks voltage-gated channels) ⇒ Propagation of the end-plate potential by local circuit currents ⇒ Initiation of an action potential in the vicinity of the NMJ |
|
Mechanism of action of depolarising blockers |
Activates nicotinic ACh receptors ⇒ One action potential followed by sustained depolarisation ⇒ Paralysis |
|
Name one depolarising blockers |
Suxamethonium |
|
Mechanism of action of non-depolarising blockers |
Competitive antagonist of (binds to but does not activate) ACh receptors |
|
Name one non-depolarising blocker |
Tubocurarine |
|
Two side effects of depolarising blockers |
1) Initial spasms leading to post-operative muscle pain 2) Bradycardia |
|
One side effect of non-depolarising blockers |
Histamine release (contraindicated in asthmatics and allergies) |
|
How can effects of non-depolarising blockers be reversed? |
Inhibitors of acetylcholinesterase (e.g. eserine) |
|
Name 3 applications of cholinesterase inhibitors |
Diagnosis of myasthenia gravis Treatment of myasthenia gravis Reverse the effects of non-depolarizing blockers |
|
Name 3 side effects of cholinesterase inhibitors |
Bradycardia Hypotension Breathing problems (By activating PNS) |
|
Briefly outline the pathogenesis of myasthenia gravis |
1) Antibodies destroy AChR at the NMJ ⇒ Muscle weakness 2) Antibodies destroy MuSK ⇒ Muscle weakness |
|
Name one disease in which muscles get weaker and weaker as they are being used |
Myasthenia gravis |
|
Treatment of myasthenia gravis |
Cholinesterase inhibitors |
|
Two specific signs of MS |
1) Worsening of symptoms when temperature ➚ (Uhthoff’s sign) 2) Electrical sensation running down the back elicited by bending head forward (Lhermitte’s sign) |
|
What muscles are grouped into the category of striated muscles |
skeletal and cardiac |
|
Name the three levels of protection to the skeletal muscles |
|
|
What is the equivalent names for cytoplasm, membrane and endoplasmic reticulum for myocytes |
Myoplasm Sarcolemma Sarcoplasmic reticulum |
|
What structure in myocytes allow the depolarisation of the membrane to quickly penetrate to the interior of the cell |
T-tubules (invagination in the sarcolemma) |
|
What are myofilaments and myofibrils? |
Myofibrils are elongated contractile threads found in striated muscles. They are made of myofilaments (proteins)
Myofilaments < Myofibrils < Myofibre < Fascicle < Muscle |
|
Name the two types of myofilaments and their principal constituent |
Thin myofilament: made of actin Thick myofilament: made of myosin |
|
Besides actin, what other two key proteins do thin filaments contain? |
Troponin Tropomyosin |
|
What does troponin bind and at what sites do they bind them? |
Tropomyosin (T subunit) Actin (I subunit) Calcium (C subunit) |
|
What does tropomyosin bind? |
Actin and myosin |
|
Outline the lines and bands of sarcomeres |
|
|
In what region of the sarcomere do thin filaments attach |
Z-line (Think Zin filament) |
|
In what region of the sarcomere do thick filaments attach |
M-line |
|
What does the action potential triggers once it has reached the interior of the cells via T-tubule? |
Release of Ca2+ from sarcoplasmic reticulum through ryanodine receptors (RyRs) (that are Ca2+ channels coupled to the T-tubular system) to the myoplasm |
|
Why is intra-cellular calcium in the thin filaments important to trigger muscle contraction? |
Troponin C binds 4 Ca2+ ions causing conformational changes in tropomyosin which exposes binding sites and allows myosin and actin to interact to form cross-bridge cycling. |
|
What happens to intracellular calcium in thin filaments when the muscle relaxes? |
Ca2+ is pumped back into the the SR by Ca2+ ATPase |
|
Explain how motion of filaments against one another (thick against thin) is modulated by ATP |
1) ATP binds to myosin causing myosin head to dissociate from actin 2) Myosin hydrolyses ATP to ADP causing conformational change of the angle of myosin head 3) ADP (and Pi) released from myosin causing conformational change of the angle of myosin head |
|
Mechanism of rigour mortis |
After death, the absence of ATP causes muscle to remain contracted for 72 hours before protein degradation. |
|
How does frequency of stimuli change force of muscle contraction ? |
Train of stimuli leads to summation of tension as Ca2+ accumulate in cytoplasm. |
|
By what mechanism does training increases force of muscle contraction? |
Training increases cross-sectional area of myofibre but not their number. |
|
What are isometric and isotonic contraction? |
Isometric contraction: contraction of muscles without shortening Isotonic contraction: shortening of muscles against constant load |
|
How many calcium ions does troponin bind in muscles? |
Skeletal: 4 Cardiac: 3 |
|
What basic principle differentiates Type 1 from Type 2 muscle fibres? |
Type 1 are for long, resistant efforts |
|
Difference between Type 1 and Type 2 fibres in terms of colour, contraction speed and conduction velocity |
Type 1: Red, slow, slow Type 2: White, fast, fast |
|
Difference between Type 1 and Type 2 fibres in terms of metabolism, power and energy source |
Type 1: aerobic, weak, TAGs Type 2: anaerobic, powerful, ATC |
|
Define motor unit |
Group of muscle fibres (6 to 1000s) that a single lower motor neurone innervates |
|
Name two ways in which the body can achieve stronger muscle contraction |
Increasing frequency of action potentials or increasing the number of lower motor neurones recruited |
|
In what order are motor neurones recruited when contracting a muscle |
Size principle: First: Small neurones (Type 1) Second: Medium neurones (Type IIa) Third: Large neurones (Type IIb) |
|
Name two types of reflexes elicited in muscles |
Stretch reflex opposes a rapid increase in muscle length Golgi tendon reflex opposes an increase in muscle tension |
|
Name the two types of sensory nerves from muscles and what they are sensitive to |
Type Ia: absolute changes in muscle length and rate of changes Type II: absolute changes in muscle length only |
|
What are muscle spindles and what do they contain? |
Sensory receptors within the belly of a muscle containing Bag1, Bag2 and chain fibres |
|
What do nerves from the muscle spindles synapse with in the stretch reflex? |
α and γ motor neurones |
|
What do γ motor neurones do in the stretch reflex? |
Contract the fibres in the spindle itself so they remain aligned with the muscle |
|
What do α motor neurones do in the stretch reflex? |
Contract the muscle itself to activate the reflex |
|
Give a practical example of a Golgi tendon organ reflex |
Place a bowling ball on a stretch arm. Muscles of the arm contract to avoid overstretching the tendon |
|
Distinguish monosynaptic vs. polysynaptic reflex arches |
Mono: no interneurone involved Poly: 1 or several interneurones involved |
|
Differentiate neurogenic and myogenic smooth muscle |
Neurogenic: require nerve inputs Myogenic: spontaneous activity |
|
What functionally replaces troponin in smooth muscles? |
Myosin light chain kinase |
|
Compare smooth muscles and skeletal muscles in terms of number of nuclei, presence of T-tubules, and size of SR |
Skeletal: multinucleate, T-tubules, Large SR Smooth: mononucleate, no T-tubule, Small SR |
|
Where do thin filaments in smooth muscles insert? |
Dense bodies (not Z-line) |
|
Compare the actin:myosin ratio in smooth and skeletal muscles |
Skeletal: low Smooth: high (⇒ greater degree of contraction) |
|
Compare presence of gap junctions in smooth and skeletal muscles. Why is that important? |
Skeletal: No gap junction Smooth: gap junctions to allow coordinated contraction |
|
What two coupling processes may lead to contraction of smooth muscles? |
1) Excitation-contraction coupling 2) Pharmacomechanical coupling |
|
What is the role of Pharmacomechanical coupling in smooth muscles? |
Triggers contraction of smooth muscles even when membrane potential is at rest. |
|
How does the pharmarcomechanical coupling work? |
Ca2+ enters the smooth muscle cell by activation of ligand-gated Ca2+ channels or G protein coupled receptor and Ca2+ then activates myosin light chain kinase (MLCK) |