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MD2002 > FUNCTION > Flashcards

FUNCTION Flashcards

1
Q

Difference between alpha motoneurone and a motor neurone?

A

No difference

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2
Q

What makes up a motor unit?

A

A motoneurone and a muscle fibre

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3
Q

Name three things that make up the NMJ?

A

Axon terminals
Motor end plates on the muscle membrane
Schwann Cell sheaths

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4
Q

What neurotransmitter is released at the NMJ and what is it’s purpose?

A

ACh
To alter the permeability of the muscle fibre membrane to ion to cause a depolarisation of the membrane and activated voltage gated ion channels

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5
Q

What enzyme degrades ACh in the synaptic cleft?

A

Acetylcholinesterase

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6
Q

What binds to the nicotinic ach receptor and what happens on activation?

A

2 molecules of ACh bind to the receptor, opening the non-specific monovalent cation channel.
Both Na+ and K+ can pass freely through the channel. Na+ in, K+ out

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7
Q

What events take place at the motor end plate?

A
  1. Action potentials arriving at the axon terminal open voltage gated Ca2+ channels
  2. Influx of Ca2+
  3. Fusion of acetylcholine-containing vesicles (ACh) with the pre-synaptic membrane
  4. ACh diffusion across the 20nm synaptic cleft
  5. Nicotinic ACh receptors (nAChR) are chemically gated ion channels which permit monovalent cations to flow through
  6. Net entry of Na+ into end plate region causes depolarisation- end plate potential)
  7. Action potential triggered in muscle fibre membrane
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8
Q

What is the sarcolemma?

A

true cell membrane that encloses the muscle fibre

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9
Q

what is the sarcoplasm?

A

intracellular fluid that fills spaces between myofibrils

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10
Q

Myoblasts –> ??? –> MUSCLE FIBRE

A

MYOBLASTS–>… FUSE…–>MULTI-NUCLEATE MYOTUBES–>… DIFFERENTIATE… MYOCYTES–> MUSCLE FIBRES

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11
Q

what are the contractile proteins of the sarcomere?

A

Actin
myosin
tropomyosin
troponin complex

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12
Q

When a muscle contracts which zones/bands shorten and which stay the same?

A

Shorten: I band and H zone
Same: A band

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13
Q

What are t tubules?

A

A transverse tubule
is a deep invagination of the sarcolemma which allows depolarisation of the membrane to quickly penetrate to the interior of the cell.

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14
Q

What is a triad?

A

A triad is the structure formed by a T tubule with a sarcoplasmic reticulum (SR) on either side known as the terminal cisterna

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15
Q

What is a dihydropyridine receptor protein (DHPR)?

A

L-type voltage-gated calcium channel in the T-tubule membrane

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16
Q

Ryanodine receptor protein (RYR)?

A

calcium release channel in the SR

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17
Q

Dihydropyridines, what are they? e.g.?

A

Voltage-gated Ca2+ channel blocking drugs (e.g. Nifedipine)

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18
Q

SERCA, what does it stand for?

A

Sarcroplasmic Endoplasmic Reticulum Calcium ATPse

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19
Q

Role of Ca2+ATP-ase (SERCA)?

A
  • The increase in intracellular calcium concentration activates a Ca2+ATP-ase (calcium pump) in the SR membrane
  • Active transport of calcium from the cytoplasm into the SR (2 Ca2+ ions per molecule ATP hydrolysed)
  • [Ca2+] decreases to
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20
Q

What is the calsequestrin?

-

A

Stores calcium at high concentrations in the terminal cisternae to establish a concentration gradient from the SR to the cytoplasm
Allows the concentration gradient to be less steep so its not as difficult to pump calcium back into the SR
Binds 43 Ca2+ ions per molecule

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21
Q

What is the neurotransmitter of the sympathetic and parasympathetic control of cardiac muscle?

A

Sympathetic: nor adrenaline (increased HR)
Parasympathetic: ACh (slows HR)

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22
Q

What are the two types of smooth muscle?

A

unitary/visceral

multi-unitary

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23
Q

Describe unitary/visceral smooth muscle?

A

Sheets of electrically coupled cells which act in unison

Often is spontaneously active

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24
Q

Describe multi-unitary smooth muscle?

A

tissue made of discrete bundles of cells which are densely innervated and contract only in response to its innervation

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25
Q

give two examples of unitary and multi-unitary smooth muscle?

A

Unitary: gut and blood vessels

Multi-unitary: vas deferens, iris, piloerectors

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26
Q

what is the smooth muscle equivalent to z-discs?

A

Dense bodies connected to actin via intermediate filaments

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27
Q

Which is more energy efficient and acts for longer.. smooth or skeletal/cardiac muscle?

A

SMOOTH

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28
Q

Discuss the t-tubules in smooth muscle?

A

there aren’t any silly

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29
Q

What are the three sources of Ca in smooth muscle?

A
  1. Voltage dependent ion channels
  2. Ligand gated ion channels
  3. intracellular stores
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30
Q

What is the concentration change of Ca that initiates contraction?

A

10^-7 –> 10^-5

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31
Q

Describe the mechanism of intracellular Ca stores in smooth muscle

A
  1. Activation of the receptor by nt/hormone
  2. Change of activity of enzyme which triggers an intracellular process
  3. Phospholipase C is the enzyme. When activated it cleaves molecules in the membrane to create signalling molecules.
  4. This molecule is inositol triphosphate. This triggers the release of Ca from the SR vesicles (the intracellular stores)
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32
Q

Name the stages in contraction of smooth muscle?

A
  1. Initiated by calcium from ECF (extracellular fluid) or SR
  2. Calcium binds to calmodulin (instead of troponin as in skeletal muscle)
  3. Ca-calmodulin- MLCK (Myosin Light Chain Kinase) complex leads to phosphorylation of MLC
  4. MLC is part of myosin head
  5. Phosphorylated myosin head binds to actin and power stroke occurs automatically
  6. A second ATP is required to release myosin head from actin
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33
Q

Name the stages in relaxation of smooth muscle?

A
  1. Calcium concentration dips below a critical level due to being pumped out of the cell and into the SR
  2. Calcium is released from calmodulin
  3. MLCP (myosin light chain phosphatase) removes phosphate from the MLC causing detachment of the myosin head from the actin filament causing relaxation
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34
Q

What is metabolism?

A

Means by which organisms extract energy from their environment and use this to synthesise large molecules

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35
Q

A reaction can only occur spontaneously if the free energy change is…

A

NEGATIVE

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36
Q

What value is the rate of reaction dependent on?

A

The free energy of activation
Which is unrelated to ΔG. this is because the reaction rate depends on the energy hump that must be climbed for the reaction to occur

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37
Q

Why is glucose-6-P only produced in the cell is it going to be used in?

A

Because it cannot easily pass through cell membranes

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38
Q

Glyconeogenesis?

-

A

Meaning: formation of glucose from non-carbohydrate sources

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39
Q

why can’t the brain use fats as a metabolic source?

A

because of the blood brain barrier

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40
Q

Under conditions when muscle protein is being broken down, what happens to the amino acids?

A

many amino acids pass their amino group to pyruvate (transamination) to form alanine. The alanine enters the liver via blood where it is converted to pyruvate which is used to synthesise glucos

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41
Q

What is the main function of adipose tissue in metabolism?

A

Synthesise and store triglyercides (triacyl glycerols ) and release fatty acids and glycerol in times of need.

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42
Q

The key hormones involved in regulating metabolism are?

A
  • Insulin
  • Glucagon
  • Adrenaline (epinephrine) and nonadrenaline (norepinephrine)
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43
Q

what is type 1 diabetes?

A

An autoimmune condition in which beta-cell of the pancreas are destroyed

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44
Q

Tissues at risk of damage of diabetes?

A
  • Blood vessels (polyneuropathy)
  • Eyes (retinal blood vessels)
  • Kidneys (urine infection, scarring and swelling in glomeruli)
  • Cardiovascular disease (due to narrowing of blood vessels)
  • Ketone bodies cause acidosis which cannot be fully counteracted.
  • Dehydration with low blood pH can result in a coma
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45
Q

where does the citric acid cycle take place?

A

matrix of mitochondria

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46
Q

what molecules are given of in the citric acid cycle and how many?

A

3x NAD
1 x CO2
1 x GTP
1 x FADH2

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47
Q

How is the electrochemical gradient in the citric acid cycle generates?

A

Movement of electrons down the respiratory chain generates an H+ ion (pH) gradient across the inner mitochondrial membrane.

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48
Q

Why is the electrochemical gradient produced in the citric acid cycle useful for atp?

A

The resulting electrochemical gradient is used to drive ATP synthesis by the way of ATP synthase (H+-ATPase).
It uses the gradient as a source of energy

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49
Q

differences between skeletal and smooth muscle?

A

skeletal is under voluntary control
skeletal is multi mucleated
skeletal is striated hence it has a myofibrillar structure, smooth is not
skeletal muscle has t-tubules, smooth does not
Instead of z-discs (skeletal) there are the dense bodies connected to actin via intermediate filaments.in smooth muscle
Smooth muscle acts for longer than skeletal and cardiac muscle (creates longer last tension) and is more energy efficient

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50
Q

What is makes up a myosin molecule?

A
  • 2 identical subunits
  • 2 globular head regions
  • 2 long chain alpha helical regions
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51
Q

What is the composition of an actin molecule?

A
  • Constructed from individual G-actin molecules

- Two chains wound in an alpha helix (F-actin)

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52
Q

what is tropomyosin?

A

Threadlike protein lying in the groove of the actin helix which blocks the myosin binding sites

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53
Q

The Troponin Complex types? Name 3 types and their function

A
  • Troponin T (TnT): interacts with tropomyosin
  • Troponin I (TnI): inhibits myosin ATP-ase
  • Troponin C (TnC): calcium binding protein
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54
Q

what is Rigor Mortis?

A
  • Stiffening of skeletal muscles after death
  • Begins 3-4hrs after death
  • Maximum after 12 hours
  • Cause: the cells accumulate calcium. In the absence of ATP, cross bridges can bind to actin but the cross-linkage is irreversible. Thus step 3 (detachment) cannot occur
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55
Q

Additional Sources of ATP?

A
  • Creatine phosphate
  • Oxidative phosphorylation (aerobic)
  • Anaerobic glycolysis (absence of oxygen)
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56
Q

What are the different muscle fibre types and what activities are they best suited for?

A

Type I-endurance, marathon running
Type IIa- Sprinting, walking
Type IIb- Short-tern, intense/powerful exercise

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57
Q

Initially when recovering from exercise what are the levels of creatine phosphate, glycogen and lactate?

A

creatine phosphate = low
glycogen = low
lactate = low

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58
Q

PRESYNAPTIC BLOCKAGE How does it act by inhibiting ACh release?

A
  • Local and general inhalational anaesthetics interfere by…
    o As they block the voltage gated Na channels
    o So the action potential cannot be propagate down the nerve
  • Blocking voltage gated Ca channels (which stimulate the release of Ach) with inhibitors/competitors of Ca such as..
  • Exocytosis of Ach can be disrupted by the action of neurotoxins
    o Botulinum toxin (clostridium botulinum) ie botox
    o Beta-bungareotoxin
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59
Q

What is an agonist of nAChR? two examples

A

causes a positive event in a channel which mimics the action of ACh e.g. nicotine, suxamethonium

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60
Q

What is an antagonist of nAChR? two examples

A

opposes the action of ACh e.g. tubocurarine, atracurium

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61
Q

How do competitive antagonists work?

A

How it works:

  1. Prevents ACh binding to receptor by occupying site
  2. Decreases the motor end plate potential (EPP)
  3. Decreases depolarisation of the motor end plate region
  4. No activation of the muscle action potential
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62
Q

Depolarising blockers /Agonist of nAChR’s at the nmj, how do they work?

A

Not metabolised by ACh esterase
How it works:
1. Persistent depolarisation of the motor end plate
2. There is a prolonged EPP
3. Prolonged depolarisation of the muscle membrane
4. Membrane potential above the threshold for the resetting of the voltage-gated sodium channels
5. Sodium channels remain refractory
6. No more muscle action potentials generated

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63
Q

Phases of agonist blockage?

A

Can occur in two phases:
- PHASE 1
o Muscle fasciculations observed then blocked
o Repolarisation inhibited as K+ leaks from the cells leading to hyperkalemia
o Voltage –gated Na+ channels kept inactivated
- PHASE 2
o Prolonged exposure to drug
o “desensitisation blockage”
 Depolarisation cannot occur, even in absence of drug

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64
Q 
How are these nAchR blocking drugs metatbolised and eliminated?
Drug:
o	Atracurium
o	Mivacurium
o	Suxamethonium
o	Pancuronium
o	Vecuronium
o	Rocuronium
A 
Method:
-	Ester hydrolysis and Hofmann elimination
o	Atracurium
-	Plasma cholinesterases
o	Mivacurium
o	Suxamethonium
-	Hepatic metabolism
o	Pancuronium
o	Vecuronium
-	Unchanged in bile/urine
o	Rocuronium
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65
Q

What are the two cholinesterases?

A

Acetylcholinesterase

Plasma cholinesterase

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66
Q

how do anticholinesterase drugs interact with cholinesterases?

A

they inhibit them

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67
Q

Two clinical uses for using anticholinesterase?

A

Anaesthesia: Reverse non-depolarising muscle blockade as it prevents the degradation of ACh hence stimulates depolarising

In treatment of myasthenia gravis: Increase neuromuscular transmission

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68
Q 
Free nerve endings:
Detects?
Fibre type?
Skin type?
Rapid/slow Adapting?
High/low threshold?
A 
Detects: pain
Fibre: A (pain) and C (hot/cold burning ache)
Skin type: All
Slow adapting
High activation threshold
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69
Q

Merkel’s Disks:
Detects?
Fibre type?
Skin type?

A

Detects: Static touch and pressure
Fibre: A
Skin type: All

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70
Q 
Meissner's corpuscles
Detects?
Fibre type?
Skin type?
Rapid/slow Adapting?
High/low threshold?
A 
Detects: changes in touch and pressure
Fibre: A
Skin: Glabrous
Rapid acting
Low threshold
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71
Q 
Pacinian corpuscles
Detects?
Fibre type?
Skin type?
Rapid/slow Adapting?
High/low threshold?
A 
Detects: high frequency vibrations in the deep layers of the dermis (hands, feet and nipples)
Fibre: A
Skin: All
Rapidly acting
low threshold
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72
Q

Ruffini corpuscles
Detects?
Skin type?
Found in?

A

Detects: Skin stretch
Skin: All
Found in: Hands, fingers and soles of feet

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73
Q

Name the 5 different sensory receptors found in the skin?

A 
Free nerve endings
Meissners corpuscles
Ruffini corpuscles 
Merkel's Disks 
Pacinian corpuscles
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74
Q

Explain how the CNS tells the difference between pain receptor nerves from different regions ?

A
  1. The CNS reads the final destination of the nerve fibre. For example, information of a particular modality is always from a particular region.
  2. Modal information is also delivered to the CNS in a topographic fashion. i.e. pain from the leg is delivered to a particular part of the CNS which is different to the area when vibration signals form the leg are delivered.
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75
Q

What are APs initiates in sensory neurones?

A

The generator potential initiates impulses in sensory nerves.

The greater the generator potential, the faster the frequency of sensory nerve impulses. Hence a greater intensity of signal is produced.

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76
Q

What happens to the generator potential amplitude and the APs as you move away from the site of origin?

A

The amplitude of the generator potential decreases with distance from the site of origin BUT the action potentials they initiate are self-propagating.

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77
Q

Difference between generator potentials and postsynaptic potentials?

A

Although both trigger action potentials and are local in nature, generator potentials will last as long as the receptor is stimulated and the amplitude is determined directly by the intensity of the sensory stimulus (not by neurotransmitter concentration)

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78
Q

How is the location of a stimulus determined in relation to receptive fields?

A

Information sent from the area of overlap will be sent down both axons. Stimulations on the periphery of the receptive field don’t generate as strong an action potential as those in the centre.

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79
Q

Decrease in receptive field size = ……………. in linear discrimination

A

= increase in linear discrimination

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80
Q

What is shingles?

A

Herpes zoster virus causes chicken pox in children.
The virus can remain dormant in the dorsal root ganglion for many years in its retroviral form. If it becomes reactivated the virus travels along specific axons to the dermatomes innervated and produces shingles which is excruciating painful.

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81
Q

Sensory nerve: A-alpha
Velocity?
Diameter?
Function?

A

70-120m/s
12-20um
Proprioception and somatic motor

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82
Q

Sensory nerve: C
Velocity?
Diameter?
Function?

A

0.5-2m/s
0.1-2um
Postganglionic sympathetic, pressure, pain, hot/cold

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83
Q

Sensory nerve: A-beta
Velocity?
Diameter?
Function?

A

30-70m/s
5-12um
Touch and pressure

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84
Q

Sensory nerve: A-gamma
Velocity?
Diameter?
Function?

A

15-30m/s
3-6um
Motor to muscle spindles

85
Q

Sensory nerve: A-delta
Velocity?
Diameter?
Function?

A

12-30m/s
2-5um
Pain and temperature

86
Q

Sensory nerve: B
Velocity?
Diameter?
Function?

A

3-15m/s
1-3um
Preganglionic autonomic

87
Q

Name the scheme 2 fibre types, their origins and their scheme 1 equivalents

A

IA- muscle spindles (A-alpha)
IB- GTOs (A-alpha)
II- Muscle spindles, touch and pressure (A-gamma and A-beta)
III- Pain and temperature (A-delta, origin = function)
IV- Pain and other (C)

88
Q

Why are larger alpha-motor neurons harder to recruit?

A

Large alpha-motoneurones have a LOWER RESTING MEMBRANE POTENTIAL so it’s more hyperpolarised. Therefore it takes a greater number of EPSP’s to summate before it reaches the threshold

89
Q

Describe the role of Group IA sensory fibres in muscle reflexes. What do they sense? How do they sense it? Effect of excessive stretch in the spindle?

A

Group IA sensory fibre (afferent) form a spiral (annulospiral ending) wrapping around the intrafusal fibres. These sense any change in length of the intrafusal fibre. If the spindle is to stretch/contract a lot the Grp1A becomes less sensitive.

90
Q

What two sensory neuron types innervate intrafusal fibres?

A

Group IA (monitor rate of length change) and II (monitor total change in length)

91
Q

What is the function of the gamma motor neuron efferent?

A

This provides motor supply to the muscle spindles. When the muscle is almost completely contract, the spindle sensitivity is compromised. To prevent this the CNS activates the gamma motor neuron effects to adjust the length of the spindle by extending/shortening the contractile spindle ends.

92
Q

Reflexes are mediated by the muscle spindles which are found in the [Muscle/tendon]

A

Muscle

93
Q

How does voluntary contraction of the muscle occur without causing a change in the annulospiral fibres?

A

When a voluntary signal for muscular contraction leaves the spinal cord, it travels to both intrafusal (via Gamma MN’s) and extrafusal muscle fibres (via Alpha MN’s) causing both sets of fibres to contract.
With this method the spindle fibre ends shorten in concert with the extrafusal fibres, which keeps the central portion constant in length, so that the anulospiral sensory endings do not detect a change in muscle length

94
Q

What structures mediate stretch muscle reflexes?

A

Muscle spindles mediate monosynaptic and polysynaptic stretch reflexes

95
Q

‘bag’ type intrafusal fibres are not innervated by which type of sensory nerve fibres?

A

type II sensory nerve fibres

96
Q

What is the fibre type in GTO’s?

A

Type 1B sensory fibres

97
Q

What is the function of GTO’s? (2)

A

To monitor the tension in the muscle because they are in series with the muscle fibres
To compliment the information from muscle spindles in the CNS

98
Q

Skeletal muscle contraction is therefore a combination of which 3 forms of nervous control?

A
  1. Alpha MN mediated contraction (under the control of the CNS)
  2. Gamma MN medicated spindle fibre contraction enabling accurate feedback
  3. GTO mediated inhibitory feedback to the alpha MNs
99
Q

Rotatory nystagmus, what is it?

A

eye movements driven by moving visual images

100
Q

Post rotatory nystagmus, what is it?

A

eye movements driven by the movement of fluid in the semi-circular canals of the inner ear. This can be seen when your eyes continue flickers after being spun

101
Q

Where are nicotinic ACh receptors located?

A
  • Neuromuscular junction
  • Sympathetic and parasympathetic ganglia
  • CNS
102
Q

Where are muscarinic ACh receptors located?

A
  • Parasympathetic target organs
  • Sweat glands (sympathetic)
  • CNS
103
Q

Nicotinic ACh receptor can be differentiated by the agonist, Nicotine. This is not an agonist of muscarinic receptors.
What is the main agonist for nicotinic ACh receptors?

A

Nicotine

104
Q

What is the main agonist for muscarinic ACh receptor?.

A

Muscarine

105
Q

M1 muscarinic receptor: Functional response? Location? Cellular response?

A

Function: Gastric secretions
Location: autonomic ganglia, glands
Cellular response: increase IP3 and DAG

106
Q

M2 muscarinic receptor: Functional response? Location? Cellular response?

A

Function: Cardiac inhibition
Location: atria of heart
Cellular response: decrease in cAMP

107
Q

M3 muscarinic receptor: Functional response? Location? Cellular response?

A

Function: gastric + salivary secretions, GI smooth muscle contraction, ocular accommodation, vasodilation
Location: exocrine glands, smooth muscle and blood vessels
Cellular response: increase IP3 and DAG

108
Q

Name two non-selective agonists of muscarinic receptors?

A

pilocarpine and bethanechol

109
Q

What is the function of atropine? And name the other drugs that are similar to it?

A

Non-selective antagonist of muscarinic receptors
CNS effects
Uses- anticholinesterase poisoning, bradycardia and cardiac arrest
Similar drugs- Glycopyrronium, Hyoscine hydrobromide, hyoscine butylbromide, ipratropium, tropicamide

110
Q

What are the clinical problems of selectivity with using muscarinic antagonists?

A
  • Few differentiate between subtypes effectively
  • Muscarininc ACh receptors widespread = side effects
  • Control by route of administration and distibution.
111
Q

During surgery a patient becomes bradycardic as result of a muscle relaxant. What drug could be used to counteract it?

A

Suxemethonium causes bradycardia when blocking the muscarinic receptors as it is a parasympathetic agonist. Atropine can be used to counteract it.

112
Q

In a synapse release NA what molecules are involved in its uptake and degradation?

A

Uptake: alpha2 adrenoreceptors on presynaptic membrane
Degradation: MOA breakdown NA to metabolites when the concentration gets too high

113
Q

What are the 4 adrenoreceptor sub types?

A

Alpha 1 and 2

beta 1 and 2

114
Q

Alpha 1 adrenoreceptor subtype: location and functional response?

A

Location: CV, GI, Genitourinary
Response: Vasocontriction, Smooth muscle contraction

115
Q

Alpha 2 adrenoreceptor subtype: location and functional response?

A

Location: Neuronal
Response: decrease in transmitter release

116
Q

Beta 1 adrenoreceptor subtype: location and functional response?

A

Location: heart and kidneys
Response: increase cardiac rate and force, renin release

117
Q

Beta 2 adrenoreceptor subtype: location and functional response?

A

Location: lungs, smooth muscle, skeletal muscle
Response: Bronchodilation, relaxation of visceral smooth muscle, vasodilation

118
Q

What does trimeric mean? And name an example of a structure which is trimeric?

A

Composed of three different subunits. Alpha, beta and gamma

The G protein coupled to receptor in GPCR mechanism

119
Q

In GPCR mechanism, what does the initial binding of a ligand to the receptor cause?

A

It results in a conformational change of the receptor that causes the receptor the bind to the G-alpha protein. In doing so the GDP is displaced and GTP is bound.

120
Q

Why is GTP bound to G-alpha protein short lived?

A

GTP bound to G-alpha hydrolyses to GDP in seconds leading the re-association of G-alpha and G-betagamma and inactivation of the adenylate cyclase.

121
Q

Name 4 potential GPCR recetors?

A

Alpha 1/2 and beta 1/2 adrenergic receptors

122
Q

Several G protein (G-alpha) classes:

A
  • Gαs (or Gs) → stimulates adenylate cyclase, increases cAMP
  • Gi → inhibits adenylate cyclase, decreases cAMP
  • Gq → stimulates phospholipase C, PLC-β
123
Q

How does PKA activate gene expression?

A

A specific transcription factor, the cAMP Response Element Binding protein (CREB), binds to this sequence and activates transcription of downstream genes. When CREB is unphosporylated, it is inactive; only in its phosphorylated state does CREB activate transcription
I.e. ligand binding to a surface can induce gene expression

124
Q

What ischolera toxin? What is the risk of it? and What chemical acts in a reverse manner to it?

A

An oligomeric complex which after cleavage becomes active and enters intestinal epithelial cells to stimulate Gαs

The overstimulation of cAMP production results in a release of water and ions including Na+, K+, Cl- and HCO3- into the lumen of the small intestine. This leads to rapid fluid loss and dehydration.

Pertussis toxin acts in a reverse manner stimulating Gαi to inhibit cAMP production in lung epithelia.

125
Q

What two signalling molecules are liberated from PLC?

A

PLC liberates two signalling molecules from PIP2, inositol 1,4,5 triphospohate (IP3 ) and diacyglycerol (DAG)

126
Q

What is the connection between PLC and PKC (Protein Kinase C)?

A

When PLC liberates IP3 and DAG, the IP3 then goes onto release Ca2+ from the endoplasmic reticulum. This calcium then activates a PKC-DAG complex.

127
Q

Types of PKC? (hint: there’s 3, think Activation)

A
  1. Conventional: requires both DAG and Ca2+
  2. Novel: require DAG but not Ca2+
  3. Atypical: doesn’t require either
128
Q

Substrates of DAG-dependent-PKCs? (3)

A
  • Tumour suppressor p53 → prevents tumour formation
  • CaV 1.2 calcium channel → heart muscle contraction
  • IkB-alpha → apoptosis and immune functioning
129
Q

Describe the structure of a lipoprotein?

A

Core: contains hydrophobic lipids (triglycerides and cholesterol esters)
Coat: hydrophilic coat of polar substances (including phospholipids, associated proteins

130
Q

What are the 5 classes of lipoproteins?

A
  1. High density lipoproteins (HDL)
  2. Intermediate density lipoproteins (IDL)
  3. Low density lipoproteins (LDL)
  4. Very low density lipoproteins (VLDL)
  5. Chylomicrons
131
Q

Describe the role of lipoproteins in the transport of TG and cholesterol in the body

A
  1. Chylo microns transport TG (triacylglycerol) and cholesterol from the GI to tissues.
    - Split by lipoprotein lipase to release free fatty acids (FFAs)
    - FFAs taken up by muscle and adipose tissue
  2. Cholymicron remnants taken up in the liver
    - Cholesterol stored, oxidised to bile acids or released to VLDL
  3. VLDL transport cholesterol and newly synthesised TG to tissues
    - TGs removed from VLDL leaving LDL with a high cholesterol (taken up by cells or liver)
  4. HDL absorbs cholesterol from cell breakdown and transfer it to VLDL and LDL
132
Q

What is stenosis?

A

Stenosis: abnormal narrowing of a vessel in the body

133
Q

What is the ideal level of cholesterol in the blood?

A
134
Q

What are the 3 source of cholesterol in the body?

A

Cholesterol is derived from 3 sources:

  1. De Novo synthesis in liver
  2. Uptake from circulating LDLs
  3. Uptake of chylomicrons remnants.
135
Q

How does cholestryamine reduce cholesterol?

A
  1. Sequesters bile acids to prevent enterohepatic recirculation
  2. Reduce absorption of exogenous cholesterol
  3. Increase the metabolism of endogenous cholesterol into bile acids
  4. Increase the LDL receptor numbers in the liver resulting in their removal from the blood
136
Q

What is the action of ezetimibe?

A

Inhibit transport protein for cholesterol in the brush border of enterocytes in the duodenum

137
Q

What is the action of the fibrate drug group? Name 2 examples

A

Alter the levels of plasma lipoproteins by activating lipoprotein lipase which decreases conc of triglyceride in VLDL.
Clearance of LDL by the liver and production of HDL is also stimulated.
e.g. Fenofibrate, bezafibrate,

138
Q

What is the action of the statin drug group? Name 4 examples

A

Inhibit the synthesis of cholesterol by inhibiting the conversion of HMG-CoA to MVA (which produces cholesterol)
e.g. Simvastatin, pravastatin, atorvastatin, rosuvastatin

139
Q

What are the 3 clinical uses of fibrates?

A
  • Mixed dyslipidaemia (I.e. raised serum triglyceride as well as cholesterol)
  • In patients with low HDL and high risk of atheromatous disease (e.g. Type 2 diabetes)
  • Combined with other lipid-lowering drugs in patients with severe treatment resistant dyslipidaemia
140
Q

What is the mechanism of nicotinic acid as a cholesterol lowering drug?

A

Lowers VLDL production = decrease in LDL

Activates lipoproteins lipase

141
Q

What is another name for statins?

A

HMG-CoA reductase inhibitors

[HMG-CoA reductase is involved in the major rate limiting step in the production of cholesterol]

142
Q

What are the clinical uses for statins?

A

Secondary prevention of MI/stroke
Primary prevention of arterial disease for patients with high serum cholesterol
Atorvastatin lowers serum cholesterol in familial hypercholesterolaemia

143
Q

What is the main side effect of cholesterol lowering drugs?

A

GI disturbances

144
Q

What is bioavailability?

A

The fraction of unchanged drug that reaches the systemic circulation

145
Q

What are the 4 ways that small molecules cross the cell membrane?

A
  1. Diffusing directly through the lipid.
  2. Diffusing through aqueous pores
  3. Transmembrane carrier protein
  4. Pinocytosis
146
Q

How does the solubility of lipophilic drugs and hydrophilic drugs differ?

A

Hydrophilic drugs: Soluble in aqueous, polar media. e.g. cytosol, blood plasma, interstitial fluid
Lipophilic drug: soluble in fats and non-polar media. e.g. fats and the interior of the lipid bilayer

147
Q

What are the 2 main properties that affect drug absorption and distribution ?

A

Lipophilicity + Ionisation

148
Q

What is lipophilicity?

A

How easily a drug passes through the plasma membrane

149
Q

What ending to bisphosphonates have?

A

“dronate” e.g. alendronate, zoledronate

150
Q

What is a common plasma protein that drugs bind to?

A

Albumin

151
Q

What are the 4 main compartments that body water is split into?

A

Plasma water
Interstitial water
Intracellular water
Trans-cellular water

152
Q

What are the two phases of metabolism?

A

Phase I: Oxidation/reduction/hydrolysis reveals the reactive chemical group of the drug
Phase II:
Synthetic conjugative reactions produce hydrophilic inactive compounds

153
Q

Cytochrome P450 enzymes:
What are they?
Function?
Effect of drugs on activity?

A

What are they? Mixed function monoxygenases found in the liver
Function: Biosynthesis of bile acids, steroids and fatty acids + metabolisms of endogenous and exogenous substrates
Effect of drug of activity? Drugs can increase/decrease expression of p450 enzymes

154
Q

Describe the effect of depleted Glutathione levels in paracetamol metabolism?

A

the toxic metabolite (produced when CYP450 enzymes act of para) combines with hepatic proteins instead of glutathione. Leading to TOXICITY

155
Q

What is the effect of grapefruit juice on the metabolism of statins?

A

Simvastatins is metabolized by CYP3A4 in the gut wall and liver.
Grapefruit juice block the CYP3A4 by competition, hence raising levels of drug in circulation

156
Q

Name 3 non-depolarizing NMJ blockers?

A

Vecuronium, Atracurium and mivacurium

157
Q

What is the process of metabolism/elimination of:
Vecuronium?
Atracurium?
Mivacurium?

A

V- Liver. Eliminated via the urine and bile
A- Spontaneous degradation in plasma
M- Plasma cholinesterases

158
Q

Between which values does the therapeutic window lie?

A

The minimum effective concentration and the minimum toxic concentration
[Oral administration]

159
Q

What does “onset of action” represent?

A

The time between administration and plasma concentration reacting the therapeutic window
[Oral administration]

160
Q

What does “duration of action” represent?

A

Time duration at which the plasma concentration was within the therapeutic window
[Oral administration]

161
Q

What does Cmax and Tmax represent?

A

Cmax= peak plasma concentration
Tmax= Time to peak plasma concentration
[Oral administration]

162
Q

What does absorption half-life (t abs) represents?

A

Time taken to reach half the concentration

[Oral administration]

163
Q

What does “plasma clearance half life” represent?

A

Time taken from peak to the plasma concentration being below therapeutic window.
[Oral administration]

164
Q

What is Css?

A

Css= The concentration reaches when plasma drug conc. during IV infusion reaches a steady state. i.e. rate of input=rate of output

165
Q

What are the main objectives of NSAIDs?

A

Anti-inflammatory
Analgesic
Antipyretic (reduce fever)
All by inhibition of prostaglandins biosynthesis by direct action on cyclo-oxygenase enzymes

166
Q

What are the two main mechanism of action of NSAIDS in inhibiting cyclo-oxygenase (COX)?
And name one example of a drug for each mechanism

A

An irreversible, time dependent inhibition of the enzyme e.g. Aspirin
A rapid, reversible competitive inhibition of the enzyme e.g. Ibuprofen

167
Q

Arachidonic acid + COX enzymes –>

A

Prostaglandins

168
Q

What are the products of arachidonic acid metabolism?

A

PROSTAGLANDINS
Thromboxanes
Leukotrienes

169
Q

What are the two main cyclo-oxygenase enzymes?

A

COX-1: Constitutive, important in maintaining GIT integrity

COX-2: Inducible, involved in inflammatory response

170
Q

What are the actions of PGE2, PGI2 and PGD2?

A

Potent vasodilators
Synergise with other inflammatory mediators (e.g. histamine and bradykinin)
Potentiate histamine and bradykinin actions on post capillary venule permeability and pain sensory nerves

171
Q

List the 3 steps by when prostaglandins raise set point of hypothalamus thermostat?

A
  1. Bacterial endotoxins cause release of factors (e.g. interleukin 1) from macrophages
  2. Interleukin 1 causes generation of prostaglandins in the hypothalamus
  3. Prostaglandins increase the thermostat set point
172
Q

Why are inflamed regions painful?

A

Due to bradykinin and histamine release.
These activate nocioreceptive afferent nerve termination and register a painful stimulus.
The prostaglandins sensitise nocioreceptive nerves to these compounds.

173
Q

Name an example of an NSAID drug in the following groups:
Salicylates?
Propionic acid + fenamate?
Selective COX-2 inhibitors?

A

Salicylates: Aspirin
Propionic acids + fenamates: Ibuprofen, naproxen, mefanamic acid
Selective COX-2 inhibitors: Celecoxib

174
Q

Which NSAIDs provide short-term analgesia?

A

Aspirin, paracetamol, ibuprofen

175
Q

Which NSAIDs provide long term analgesia?

A

Naproxen, diclofenax

176
Q

Why is ibuprofen used when treating chronic inflammatory disorders?

A

As dosage must be high and ibuprofen has low incidence of side effects

177
Q

What are the different zones of the epiphyseal plate, from diaphysis to epiphysis?

A

Calcification
Hypertrophy
Proliferation
Resting

178
Q

Describe the difference in structure between cortical (compact) bone and cancellous (trabecular) bone?

A

Cortical is concentrically arranged lamellae in haversian systems
Cancellous is a meshwork of trabeculae with intercommunication spaces

179
Q

When a bone is “comminuted” what does that mean?

A

It is broken into fragments

180
Q

What is an avulsion fracture?

A

When a fragment of bone is separated from the main mass

181
Q

What is a buckled fracture?

A

When the ends are driven together

182
Q

What are the 3 phases of fracture healing?

A
  1. Reactive phase
  2. Reparative phase
  3. Remodelling phase
183
Q

What happens during the reactive phase of fracture healing?

A

Fibroblasts in the periosteum proliferate to from granulation tissue around the fracture site

184
Q

What happens during the reparative phase of fracture healing?

A

Callus formation: osteoclasts quickly form a woven bone to bridge the gap. This woven bone is weak as the collagen fibres are arranged irregularly.
Next lamellar bone is laid down, the collagen is organized in sheets to give strength and resilience

185
Q

What happens during the remodeling phase of fracture healing?

A

Remodelling by osteoclasts to restore bones original shape

186
Q

What are the causes of cancer? (2 main, 2 lesser)

A
    • Mutation in DNA resulting in production of abnormal cells with altered proliferation mechanisms
    • Changes in DNA caused by covalent mutations
  • Radiation (ionizing/UV)
  • Chemical carcinogens
187
Q

What characteristics do cancer cells exhibit that normal cells do not?

A

Uncontrolled proliferation
Invasiveness
Metastases

188
Q

What are the three main methods when treating established cancers?

A

Surgical excision, radiotherapy and chemotherapy

189
Q

What are the 4 groups of chemotherapy?

A

Alkyating agents
Plant derivatives
Metabolites
Cytotoxic antibodies

190
Q

What is the action of alkylating agents?

A

Intrastrand crosslinking of DNA which disrupts helix and prevents proliferation

191
Q

What is the mechanism of alkylating agents in chemotherapy?

A

Normally guanine residues in DNA exist in KETO TAUTOMER, this allows guanine to base pair with cytosine. When the guanine is alkylated the ENOL TAUTOMER is formed. This means that the modified guanine can mispair with thymine residues during DNA synthesis.
This change destabilizes the ring and triggers cell death by apoptosis

192
Q

What are the three major groups of alkylating agents?

A

Nitrogen mustards
Nitrosoureas
Platinum based compounds

193
Q

Name an example of a nitrogen mustard and how it is activated

A

Cyclophosphamide. Activated in the liver by p450 oxidases

194
Q

Name two examples of nitrosoureas and how they work as alkylating agents?

A

Lomustine and carmustine
As these drugs are lipid soluble they are able to cross the blood brain barrier so can be used to treat tumours of the brain and meninges

195
Q

Name one example of a platinum based compound and how it works as an alkylating agent?

A

Cisplatin
Contains Cl- which dissociate to leave behind a reactive complex. This reacts with water and then interacts with the DNA to cause cross linking, then local denaturation of the DNA chain

196
Q

Name an example of an antifolate and how it works

A

Methotrexate

Inhibit folic acid reductase hence DNA synthesis and cellular replication is inhibited

197
Q

Which chemotherapy drugs can cross the blood brain barrier?

A

The nitrosoureas (in alkylating agent group) e.g. carmustine, lomustine

198
Q

Name an example of an antipyrimidine and how it works as an antimetabolite?

A

Fluorouracil

It is converted into a fraudulent nucleotide (cytarabine instead of cytosine) which inhibits DNA polymerase

199
Q

Name 3 examples of antipurines and how they work?

A

Examples: Mercaptopurine, thioguanine, fludarabine
Mercaptopurine: Inhibits number of enzymes in the de novo synthesis of purines hence a fraudulent nucleotide is produced.
These inhibit DNA polymerase

200
Q

What are the 4 categories of cytotoxic antibodies?

A

Antracyclines (e.g. doxorubicin)
Dactinomycin
Bleomycin
Mitomycin

201
Q

What is Doxorubicin and how does it act in cancer treatment?

A

Main anticancer anthracycline antibiotic
It lowers the activity of topoisomerase II which is responsible for winding/unwinding DNA during replication of proliferating cells. This causes the process of replication to seize up

202
Q

How does dactinomycin act in chemotherapy?

A

This is a cytotoxic antibody. Interferes with the movement of DNA polymerase along the gene and prevents transcription

203
Q

How do bleomycins act as cytotoxic antibody in chemotherapy?

A

They degrade preformed DNA, causing chain fragmentation and the release of free bases

204
Q

How does mitomycin act as a cytotoxic antibody in chemotherapy?

A

Cross links and degrades DNA via free radicals

205
Q

What are the three drugs groups in the plant derivative family of chemotherapeutics

A

Vinco alkaloids
Taxanes
Camptothexins
Etoposide

206
Q

What is the main action of plant derivatives as chemotherapeutics?

A

Affect microtubule function and prevent mitotic spindle formation

207
Q

Name 5 drawbacks of chemotheraphy

A
  • Drugs target cell proliferation, not the more lethal properties of invasiveness and metastasis
  • Non-specific cell killers (rather than being aimed at the particular changes that make a cell malignant)
  • The development of resistance to anticancer drugs
  • Tumour stem cells persist
  • Patient compliance due to side effects
208
Q

Name 4 general approaches to cancer therapy

A
  1. Enhance immune response
  2. Kill/remove malignant cells
  3. Inactive components of the oncogene signaling pathway
  4. Restore function of tumour suppressor gene

MD2002 (7 decks)

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