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Medicine > M&R > Flashcards

M&R Flashcards

1
Q

What range of movement is available to proteins in bilayers?

A

Conformational change
Rotational
Lateral diffusion

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2
Q

How are peripheral proteins removed from the lipid bilayer?

A

Changes in pH or Ionic strength

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3
Q

How are integral proteins removed from the lipid bilayer?

A

Agents that compete for non-polar interactions, e.g. detergents

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4
Q

What is the structure of Cholesterol?

A

Hydrophilic polar head group
Rigid planar steroid ring structure
non polar hydrophobic hydrocarbon tail

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5
Q

What are the 3 main molecules that make up the cytoskeleton and how are they arranged?

A

Ankyrin anchors Spectrin to cell membrane, Actin molecules link Spectrin cells

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6
Q

What causes Hereditary Spherocytosis? What does it lead to?

A

Deficiency of Spectrin, erythrocytes round up and become less resistant to lysis during passage through capillaries.
Shortened RBC life leads to Haemolytic anaemia

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7
Q

What causes Hereditary Elliptocytosis? What does it lead to?

A

Defect in spectrin molecules means they can’t form end to end junctions so lattice cant form, results in fragile cells
Leads to Haemolytic anaemia

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8
Q

What does the Na+ K+ ATPase transporter do?

A

Pumps 3Na+ outwards + 2K+ inwards

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9
Q

What does the PMCA (Plasma Membrane Ca2+ATPase) do? Whats its primary role?

A

Pumps 1 H+ in and 1 Ca2+ out of the cell

Main role is to remove residual Ca2+ from the cell, its a high affinity but low capacity transporter

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10
Q

What does SERCA transporter do? Whats its primary role?

A

Pumps 1 H+ out of ER and 1 Ca2+ into ER

Main role is to remove residual Ca2+ from the cell, its a high affinity but low capacity transporter

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11
Q

What does the NCX (Sodium-Calcium exchange) do? Whats its primary role?

A

Pumps 3 Na+ into the cell and 1 Ca2+ out of the cell

Removes toxic levels of Ca2+ as its low affinity but high capacity transporter

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12
Q

What does the NHE (Sodium Hydrogen Exchange) do? Whats its primary role?

A

Pumps 1 Na+ in and 1 H+ out

Acid extrusion

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13
Q

How is Bicarbonate reabsorbed in the kidney?

A

Na/K Pump keeps the intracellular [Na+] low so NHE can pump H+ into the proximal tubule. H+ then ‘picks up’ Bicarbonate and brings it back into the cell

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14
Q

What is the function of Loop Diuretics? How does it work?

A

Anti-hypertensive drug
Blocks the Na/Cl/K exchanger in the thick ascending limb preventing the Na+ reuptake therefore increasing the amount of water excreted from kidney

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15
Q

Which gene is affected in Cystic Fibrosis? How does it effect transport in and out of the cell?

A

CFTR Gene
Faulty CFTR gene creates a faulty transporter, Cl isnt transported out of the cell so water doesn’t follow causing thick mucus

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16
Q

Which transporters lead to diarrhea?

A

Over activation of the CFTR gene by PKA leads to excessive Cl- being pumped into the lumen

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17
Q

What is fast synaptic transmission?

A

The receptor protein is also the ligand gated ion channel

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18
Q

What is slow synaptic transmission?

A

The receptor and the channel are separate proteins, the signal is passed between them either by;
Direct G-protein gating
Gating via intracellular messenger

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19
Q

What is Accommodation?

A

The longer a stimulus the larger the depolarisation needed to initiate an action potential. This is because Na+ channels become inactive in the time leading up to the threshold voltage being reached

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20
Q

What are the properties of a voltage-gated Na+ channel? Whats different about a K+ channel?

A
  • Main pore forming subunit is one peptide consisting of 4 homologous repeats. Each repeat has 6 transmembrane domains. One domain can sense voltage across the membrane
  • K+ channel is similar in structure but each repeat is a separate subunit
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21
Q

How do local anaesthetics work? (Procaine)

A

Act by binding to and blocking open Na+ channels preventing them from generating an action potential

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22
Q

Which 3 properties of an axon lead to a high conduction velocity?

A
  • High Membrane resistance (increased potential difference across membrane)
  • Larger axon diameter (lower cytoplasmic resistance)
  • Low membrane capacitance (ability to store charge)
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23
Q

Which cells myelinate the CNS and the PNS?

A 
CNS = Oligodendrocytes 
PNS = Schwann cells
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24
Q

What is Multiple Sclerosis?

A

Autoimmune attack against the myelin cells. Demyelination affects ability to conduct action potentials properly

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25
Q

Describe the release of Neurotransmitters

A
  • Ca2+ enters and binds to Synaptotagmin
  • Vesicle containing neurotransmitter is brought close to the membrane
  • Snare complex makes a fusion pore
  • Transmitter released from vesicle through the fusion pore into the synaptic cleft
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26
Q

Describe the binding of Neurotransmitters to receptors on the post synaptic membrane

A

Ach will bind to Nicotinic Ach Receptors (nAchR) on post synaptic membrane. nAchR has 2 binding sites so 2 Ach molecules must bind to produce conformation change to open the channel. When activated it allows 3Na+ in and 2K+ out depolarising the membrane. Ach is rapidly broken down by Ach esterase

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27
Q

What is Succinylcholine used for? How does it work?

A

Used in operations to induce paralysis.
Binds to nAchR + opens channels to maintain depolarisation, adjacent Na+ channels won’t open as they have become inactive so can’t product AP.
Sccinylcholine takes longer to break down than Ach

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28
Q

What is Myasthenia Gravis? Hows does it present?

A

Autoimmune disease targeting nAch receptors. Antibodies directed at nAchR’s lead to loss of function and receptor degredation.
End plate potentials are reduced in amplitude leading to muscle weakness + fatigue

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29
Q

What receptor on the side of the ER is responsible for Calcium Induced Calcium Release?

A

Ryanodine

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30
Q

What are the 4 common mechanisms for extracellular to intracellular signal transduction?

A
  1. Membrane bound receptor with integral ion channel
  2. Membrane bound receptor with integral enzyme activity (insulin receptor)
  3. G-Protein coupled receptors
  4. Intracellular receptor for hydrophobic ligands (testosterone, Cortisol, T3/T4)
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31
Q

What is Receptor Mediated Endocytosis?

A

Specific binding of molecules to cell surface receptors permits the selective uptake of substances into the cell

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32
Q

How is cholesterol taken up into the cell?

A
  1. LDL-receptors are located over Clarathin coated pits, when LDL binds the pit invaginates to form coated vesicles
  2. Vesicles are uncoated and fuse with endosomes (Compartment for the Uncoupling of Receptor and Ligand)
  3. CURL has pH of 5.5-6, this causes LDL-receptor to have low affinity for LDL so they dissociate
  4. Receptors bud off in vesicle and return to plasma membrane
  5. Endosome with LDL’s inside fuses to Lysosome so cholesterol can be hydrolysed from esters
33
Q

How is the coat structure of Clarathin coated pits formed and unformed?

A

Assembly of the coat is spontaneous

Disassembly of coat is carried out by ATP-dependant uncoating protein

34
Q

What 3 mutations can affect LDL-receptors?

A
  1. Receptor Deficiency
  2. Non-functional receptor (no binding of LDL)
  3. Loss of C-terminal which forms interaction with coated pit, means that LDL receptors are spread across cell
35
Q

Describe the uptake of Fe3+ ions by transferrin

A
  1. Two Fe3+ ions bind to apotransferrin forming transferrin in the circulation
  2. Transferrin binds to Transferrin receptor at neutral pH and is internalised
  3. In acidic endosome Fe3+ ions are released from transferrin, at this pH apotransferrin still binds to the receptor
  4. Ligand receptor complex is recycled back to plasma membrane, at neutral pH apotransferrin dissociated from receptor
36
Q

What does CURL stand for?

A

Compartment for Uncoupling of Receptor + Ligand

37
Q

Describe the uptake of Insulin into the cell. What does it lead to?

A
  1. Insulin receptors only congregate over clarathin coated pits when the agonist is bound
  2. In endosome the receptor remains bound to Insulin and complex is targeted to lysosomes for destruction
  3. This causes a reduction in the number of Insulin receptors which desensitises the cell to continued presence of insulin
38
Q

What is Transcytosis? What is an example of this?

A
  1. Some ligands that remain bound to their receptors can be transported across a cell
  2. Examples of this include maternal immunoglobulins to the foetus via the placenta
39
Q

Describe the action of GPCR’s

A
  1. GPCR receptor activates + interacts with G-protein
  2. GPCR-G protein interaction activates the g protein by exchanging GDP for GTP
  3. α-By complex dissociates into α-GTP and By subunits, both subunits can interact with effector proteins
  4. α-GTPase hydrolyses GTP -> GDP, this causes the a-GDP and By subunits to reform
40
Q

What leads to Retinitis Pigmentosa

A

Loss of function mutation to rhodopsin

41
Q

Describe the chain of events caused by Adenyl Cyclase

A
  1. The enzyme Hydrolyses cellular ATP to generate cyclic AMP
  2. cAMP interacts with cAMP-dependant protein kinase (PKA)
  3. PKA can then phosphorylate many other proteins in the cell
42
Q

What are the main effects on the body with the increased cellular levels of Adenyl Cyclase? Which G-proteins cause increase + decrease in levels?

A
  1. Increased Glycogenolysis + Gluconeogenesis
  2. Increased Lipolysis in adipose tissue
  3. Relaxation of smooth muscle
  4. Positive Chonotropic + Inotropic effect on heart
    - Increased by Gs, decreased by Gi
43
Q

Describe how Phospholipase C produces its response

A
  1. Phospholipase C hydrolyses PIP2 to generate two secondary messengers, IP3 + DAG
  2. IP3 binds to receptor inside the ER to allow Ca2+ release
  3. DAG interacts with PKC’s
44
Q

Which G-proteins are responsible for the increase in levels of Phospholipase C? What are the main actions of this signalling pathway?

A
  • Gq G-proteins increase levels
    1. Vascular, GI tract + airways smooth muscle contraction
    2. Mast cell degranulation
    3. Platelet aggregation
45
Q

How is chonotrpy in the heart regulated?

A
  1. Activation of M2-musclarinic increases the open probability of K+ channels which are controlled directly by αi-GTP subunit
  2. Increased membrane permeability hyperpolarises the cell which slows the intrinsic firing rate
46
Q

How is Ionotropy in the heart regulated?

A
  1. Activation of a1-adreonoceptors increases cAMP levels
  2. cAMP activates PKA
  3. PKA phosphorylates + activates VOCC and Ca2+ flows in
  4. αs-GTP can also interact directly with VOCC’s
  5. Increase in Ca2+ causes positive inotropic effect
47
Q

How is Neurotransmitter release reduced by opioids?

A
  1. μ-opioid receptors can be stimmulated to couple with with Gαi-proteins
  2. By-subunit interacts with VOCC’s to reduce the entry of Ca2+ through these channels
  3. Decrease in Ca2+ influx inhibits the release of neurotransmitter from pre-synaptic terminal
48
Q

What is Bmax and what does it give an indication of?

A

Maximum binding capacity, gives information on total number of receptors

49
Q

What is Kd? What does a low Kd indicate?

A

Concentration needed for 50% occupancy, A lower Kd value indicates higher affinity

50
Q

What is Emax?

A

Maximum response

51
Q

What is EC50? whats it a measure of?

A

Effective concentration that gives 50% of the maximum response, its a measure of potency

52
Q

Whats the difference between how Salbutamol and Salmeterol activate B2-adrenoceptors to to relax airways in asthma?

A

Salbutamol - Has greater affinity and selective efficacy for B2-adrenoceptors
Salmeterol - Greater affinity for B2-adrenoceptors but no selective efficacy

53
Q

What effect does having spare receptors have on reaching a full response?

A

Having more receptors reduces the percentage of receptors filled to produce a full response so it becomes more sensitive

54
Q

What are partial agonists?

A

Even with full receptor occupancy the agonist can’t produce a full response

55
Q

What is the clinical use of partial agonists?

A
  1. Buprenomorphine is a partial agonist with a higher affinity but lower efficacy than morphine
  2. Can be used for people that are addicted to Heroin as it is less likely to lead to respiritory depression as it’s a partial agonist
56
Q

What is Naloxone used for and how does it work?

A

Used to treat Heroin overdose

Its a high affinity competitive antagonist. High affinity means it will compete effectively with other opioids

57
Q

What are non reversible competitive antagonists? What is an example of one and what is it used for?

A
  1. Occurs when the antagonist dissociates slowly or not at all
  2. Phenooxybenzamine - Used in hypertensive episodes of phoechromocytoma (tumour of adrenal gland causing release of NA/adrenaline)
58
Q

What is a non-competitive antagonism?

A

The allosteric binding of an antagonist to a receptor (not at the ligand binding site)

59
Q

What is oral bioavailability?

A

The proportion of the drug given orally that reaches the circulation unchanged

60
Q

What is the Therapeutic ratio defined as?

A

Maximum tolerated dose / Minimum effective dose

61
Q

What is first pass Metabolism?

A

Drugs absorbed from the lumen of the ileum enter the hepatic portal vein and are transported directly to the liver. Liver contains lots of enzymes so drug is extensively metabolised during the first pass.

62
Q

What is the volume of distribution?

A

The theoretical volume into which the drug has distributed assuming this occurs instantaneously

63
Q

What are Object (Class I) and Precipitant (Class II) drugs?

A

-Object drugs are displaced from albumin binding sites raising the free levels of the Object drug
-Object drugs are used at a dose much lower than no. of albumin binding sites
Precipitant drugs are used at a dose higher than no. of albumin binding sites

64
Q

What is an example of Object and Precipitant drugs?

A

Object drug - Warfrarin

Precipitant drug- Sulphonamides, Aspirin, Phenytoin

65
Q

What are first order Kinetics?

A

Metabolism of these drugs is proportional to the drug concentration, gives a curved line when plotted against time

66
Q

What are zero order Kinetics?

A

The enzyme is saturated so the rate of decline is constant regardless of concentration, gives a straight line when plotted against time

67
Q

What is Dangerous about drugs with zero order kinetics?

A

Gives a therapeutic response that can suddenly escalate as elimination mechanisms become saturated

68
Q

Describe drug metabolism in the Liver

A

Phase I
1. Most drugs are unreactive (Pro-drugs), in phase I a reactive group is exposed on the parent molecule or added. Requires cytochrome P450 + NADPH.
Phase II
2. Reactive intermediate from Phase I is conjugated with a polar molecule to form a water soluble complex. Requires UDPGA.

69
Q

How is drug excretion in the Kidney controlled?

A
  • For weak acidic drugs (aspirin), Alkaline urine makes the drug ionised so stays in the lumen
  • For weak basic drugs (amphetamine) the opposite is true and acidic urine will increase output of drug
70
Q

Describe NA synthesis

A
  1. Tyrosine is converted to DOPA by Tyrosine Hydroxylase
  2. DOPA is converted to DOPA Decarboxylase to Dopamine
  3. Dopamine is converted to Noradrenaline by Dopamine B-hydroxylase
  4. Transported against concentration gradient into cell with H+
71
Q

What is Tachyphlaxis?

A

Excessive exposure to an agonist leading to reduced sensitivity

72
Q

What is Suprasensitivity?

A

Agonist deprivation or excessive exposure to an agonist leading to increased sensitivity

73
Q

What happens during opioid dependence?

A
  1. Repeated use leads to increase in number of receptors (Tachyphalaxis), receptors that have been bound once are less likely to form receptor-agonist complex, more opioids required to produce the same response
  2. On opioid withdrawal, secondary messenger activity falls and the patient perceives pain
74
Q

What happens with Phaeochromocytoma?

A
  1. Tumour of the adrenal medulla, causing intermittent increased secretion of catecholomines, adrenaline + noradrenaline
  2. Leads to intermittent signs of over sympathetic innervation (sweating, pallor, tremor, high BP)
  3. Adrenoceptors don’t downregulate and the intermittent release of catecholomines means tachyphylaxis does not occur
75
Q

What is used to treat Glaucoma? What does it stimulate? How does it work?

A

Pilocarpine - acts on all musclarinic receptors but used topically (so only M3)
Used to treat Glaucoma as it contracts the pupil + cilary muscle opening the trabecular network + increases fluid loss from the eye

76
Q

What is Salbutamol used to treat? Which receptors does it act on?

A

Treatment of Asthma attacks

Acts on B2 receptors so dilates the bronchi

77
Q

What is Adrenaline used for in a hospital setting? Which receptor does it stimulate?

A

At high concentration it stimulates α1 receptors to cause vasoconstriction to prolong the affects of local anaesthetics

78
Q

What is Propanolol used to treat? How does it do it?

A

Its a non-selective Beta adrenoceptor antagonist so reduces chronotropy + inotropy, therefore used to treat Hypertension

79
Q

What is Prazosin used to treat? How does it act?

A

Blocks α1-adrenoceptors, this stops vasoconstriction lowering TPR and lowering BP, used to treat Hypertension

Medicine (10 decks)

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