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Medicine A100 > M&R > Flashcards

M&R Flashcards

1
Q

What is an amphipathic molecule?

A

Molecule that contains both hydrophilic and hydrophobic moieties

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2
Q

In what ways can lipid molecules move in a Lipid Bilayer?

A
  • Vibration
  • Rotation
  • Lateral Diffusion
  • Flip-flop
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3
Q

How are lipid bilayers formed in water?

A

Spontaneous - driven by the van der Walls between the hydrophobic tails

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4
Q

In which ways can membrane proteins move in a lipid bilayer?

A
  • Conformational change
  • Rotation
  • Lateral diffusion
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5
Q

How are peripheral membrane proteins bound to the surface of cells? How are they removed?

A
  • Bound by electrostatic + H-bonds

- Removed by changes in pH or ionic strength

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6
Q

How are Integral membrane proteins bound to cells? How are they removed?

A
  • Interact with the hydrophobic regions of lipid bilayer

- Removed with detergent or organic solvents which compete for non-polar interactions in the bilayer

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7
Q

Describe the Protein Secretion Pathway

A
  1. Free Ribosome initiates protein synthesis from mRNA
  2. Hydrophobic N-terminal is produced
  3. Recognised & bound by Signal Recognition Peptide (SRP)
  4. Protein synthesis stops
  5. GTP-bound SRP directs the ribosome to SRP receptors on ER
  6. SRP dissociates
  7. Protein synthesis continues and protein is fed into the ER via a pore called Peptide Translocation Complec
  8. Signal sequence is removed by signal peptidase, ribosome detaches
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8
Q

How does Cholesterol work?

A
  • Reduces phospholipid packing, increasing fluidity

- Reduces phospholipid chain motion, decreasing membrane fluidity

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9
Q

How is the Erythrocyte Cytoskeleton structured?

A

A network of Actin + Spectrin is attached to the membrane by Ankyrin. Attachment of integral membrane proteins to the cytoskeleton restricts lateral mobility of the membrane protein

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10
Q

What causes Hereditary Spherocytosis?

A

Decreased levels of Spectrin results in the rounding up + increased lysis of RBC’s

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11
Q

What causes Hereditary Elliptocytosis?

A

Spectrin molecules are unable to form stable heterotatramers which leads to fragile ellipsoid cells

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12
Q

What is the approximate composition of a biological membrane?

A

40% Lipid, 60% Protein, 1-10% Carbohydrates

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13
Q

How do Loop Diuretics work?

A

Block Na re-uptake in the thick ascending limb

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14
Q

Describe how transporters produce diarrhoea

A

CFTR is overly active once phosphorylated by Protein Kinase A, Cl is excessively transported into the lumen which causes water to follow

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15
Q

What is the resting membrane potential of Nerve cells?

A

-50mV to -70mV

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16
Q

What is the resting potential of Smooth Muscle cells?

A

-50mV

17
Q

What is the resting potential of Cardiac + Skeletal muscle cells?

A

-80mV to -90mV

18
Q

What is the Intracellular + Extracellular concentration of Na+?

A

Intra - 10mM

Extra - 145mM

19
Q

Whats the Intracellular + Extracellular concentration of K+?

A

Intra - 160mM

Extra - 4.5mM

20
Q

Whats the Intracellular + Extracellular concentration of Cl-?

A

Intra - 2mM

Extra - 114mM

21
Q

What happens in fast Synaptic Transmission?

A

The receptor protein is also an ion channel so binding of the transmitter causes the channel to open

22
Q

What happens in Slow Synaptic Transmission?

A

The receptor protein + ion channel are separate. They are connected by either G-proteins or intracellular messengers

23
Q

Describe an action potential

A
  1. Membrane is depolarised past threshold
  2. Voltage gated Na channels open causing Na influx + depolarisation of membrane
  3. Na channels are inactivated
  4. Voltage gated K channels are opened by depolarisation causing flux of K causing depolarisation of membrane
24
Q

What is the Absolute Refractory Period?

A

Nearly all Na channels are in the inactivated state + a second action potential can’t be stimulated no matter how large the stimulus

25
Q

What is the Relative Refractory Period?

A

Na channels are recovering from inactivation, a second action potential can be stimulated if the stimulus is large enough

26
Q

What is Accommodation?

A

During slow depolarisation a larger depolarisation is needed to stimulate an action potential due to more Na channels being inactivated

27
Q

Describe the action of local anaesthetics (Procaine)

A

Bind + block Na channels preventing action potential generation, block in nerve fibres in this order;
- Small Myelinated Axons
- Non-Myelinated Axons
- Large Myelinated Axons
Because of this they tend to affect sensory before motor neurones

28
Q

What factors effect the conduction velocity of an action potential?

A
  • Membrane resistance - Higher the resistance in the membrane the higher the potential difference across it
  • Axon Diameter - Higher the diameter the lower the cytoplasmic resistance
  • Membrane Capacitance (ability to store charge) - Membrane with a low capacitance will take less time to charge increasing conduction velocity
29
Q

How does Myelination effect conduction velocity?

A
  • Reduces Capacitance
  • Increases Membrane Resistance
  • Allows Saltatory Conduction
30
Q

What happens in Multiple Sclerosis?

A

Autoimmune disease where myelin is destroyed, leads to decreased conduction velocity, complete block or cases where only some action potentials are transmitted

31
Q

Describe the passage of an AP across a Synaptic junction

A
  1. AP arrives at pre-synaptic membrane opening voltage gated Ca channels causing influx of Ca
  2. Ca binds to Synaptotagmin leading to the formation of a snare complex
  3. Fusion pore is made from the snare complex + Ach is released
  4. Ach binds to Nicotinic Ach receptor on post-junctional membrane and produces an AP
32
Q

What is Myasthenia Gravis and how does it present?

A

Autoimmune disease which targets Nicotinic Ach receptors, this damages the post-synaptic membrane of skeletal muscles. Endplate potentials are reduced in amplitude leading to muscle weakness + fatigue. (Droopy eyelids area common sign) Treated with Ach-esterase inhibitors to increase time Ach is in cleft

33
Q

Describe the uptake of Cholesterol

A
  1. LDL’s bind to LDL-Receptors which are located over Cathrin coated pits
  2. When it binds the pit invaginates to produce a coated vesicle, these are then uncoated using ATP (as the pits form spontaneously) and fuse with Endosomes
  3. Endosomes have a low pH, at low pH LDL Receptor has a low affinity for the LDL + they dissociate. Endosome is also known as Compartment for the Uncoupling of Receptor + Ligand (CURL)
  4. Receptors bud off + are recycled back to the membrane
  5. Endosomes containing LDL fuse with lysosomes + Cholesterol is hydrolysed from the esters
34
Q

What are the main mutations causing Hypercholesterolaemia?

A
  1. Non-Functioning Receptor - Prevents binding + uptake of LDL’s
  2. Receptor Binding Normal - Deletion of C-terminal cytoplasmic domain, prevents interaction between receptor and Clathrin coat so receptors will be spread across membrane
  3. Receptor Deficiency
35
Q

Describe the uptake of Fe3+ ions by Transferrin

A
  1. Two Fe3+ ions bind to Apotransferrin to form Transferrin
  2. Transferrin binds to the Transferrin Receptor at neutral pH and is internalised
  3. When in low pH Endosome the Fe ions are released from Transferrin but Apotransferrin has a high affinity for the receptor at this pH
  4. Receptor-Apotransferrin complex is recycled out of the cell, at neutral pH they have a low affinity + dissociate
36
Q

Describe the uptake of Insulin

A
  1. Insulin binds to receptor causing a conformational change allowing it to be recognised by the Clathrin pit + is internalised
  2. In the endosome the Insulin + Receptor remain bound + complex is sent to lysosome for degradation
  3. The destruction of receptors reduces number on membrane desensitising the cell to continued presence of high Insulin
37
Q

Describe how G-Proteins interact with receptors

A
  1. α subunit binds to GTP causing it to dissociate from the βγ subunit
  2. Both α-GTP + βγ subunits interact with effectors
  3. GTPase hydrolyses GTP -> GDP, this increases the affinity for the α + βγ subunits + they reform their heterotrimer

Medicine A100 (6 decks)

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