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ESA 2 > MR 6-9 > Flashcards

MR 6-9 Flashcards

0
Q

Difference between a receptor and acceptor

A

Receptors are functionally silent without agonist, acceptors are normally active and activity is effected by binding of ligands

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1
Q

Define a partial agonist

A

Cannot create a full response with maximal binding.

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2
Q

What are the differences between rectors and ligands

A

Kd< Km, so higher binding affinity of ligands to receptors -9 to -6 compared with -6 to -3
Ligand is unchanged at receptor but changed by active site.

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3
Q

What is the structure of a classical integral ion channel?

A

Consists of 5 subunits. Each subunit has 4 transmembrane domains, one of which forms the channel lining.

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4
Q

Typical structure of G protein coupled receptors?

A

7 transmembrane domains.

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5
Q

Describe membrane bound receptors with integral enzyme activity

A

Tyrosine kinase linked receptors autophosphorylate. This can then allosterically activate an enzyme or be recognised by a transducin protein which in turn activates an enzyme.

Also make be linked to guanylyl cyclase.

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6
Q

Describe intracellular receptors for hydrophobic ligands.

A

Ligand binds, and receptor dissociates from chaperone or heat shock protein and interacts with DNA control regions to regulate gene expression .

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7
Q

What is the difference between phagocytosis, pinocytosis and RME

A

Phagocytosis is in response to the binding of a ligand to a receptors, pseudopods are extended which also bind to ligands (normally attached to another cell) and engulf it.

Pinocytosis is a non specific invagination of particles from outside the cell- does not involve receptors.

RME involves invagination, brought about by spontaneous formation of vesicles by triskelions (May be pinocytosis also) of specific ly receptor dense areas/ coated pits. Bonding of ligand can trigger membrane coating. RME is the selective internalisation of molecules into the cell through binding to specific receptors.

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8
Q

What is the triskelion made out of?

A

3 Cathrin chains and 3 light chains

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9
Q

Describe uptake of cholesterol

A

Apoprotein b binds to LDL receptor
Endocytosed and fuses with CURL/ endo some.
Low pH so dissociation.
Receptor back to membrane (via golgi?) sequestered to specific region.
LDL goes to lysosome.

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10
Q

Give mutations effecting LDL receptor

A

Deficiency so not present.
Non functional so apoprotein cannot bind
Binding normal but cannot trigger coat.

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11
Q

Describe the uptake of fe3+

A

Free fe3+ binds to apotransferrin twice to form transferrin.
Binds to transferrin receptor.
Endocytosed and fuses with curl/ endosome.
Fe dissociates at pH but apotransferrin stays bound.
Receptor sent to membrane where apotransferrin dissociates.

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12
Q

Give an example of the passage of large molecules across cells

A

Transcytosis. Receptor and ligand (e.g. IgA (maternal immunoglobulins to foetus) Endocytosed and in vesicle receptor is cleaved so that IgA with part of receptor is released other side.

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13
Q

Insulin control of receptor number?

A

Insulin binds to receptor, conformational change so the receptor can be targeted to coated regions.
Insulin and receptor degraded.

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14
Q

Entry of membrane enveloped viruses

A

Enter via REM, in endosome, low pH is favorable and so the viruses fuse their membrane and their DNA is sent into cell.

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15
Q

How to G protein coupled receptors work?

A

Binding
GDP swapped for GTP on alpha subunit -(receptor acts as a guanine nucleotide exchange factor (GEF))
Alpha and beta/gamma subunits dissociate.
Subunits activate/inhibit other enzymes
Intrinsic GTPase dephosphorylates GTP to GDP and unit re associate with receptor.

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16
Q

Name 4 G proteins and their effectors

A

Gs - stimulates adenylyl cyclase
Gi - inhibits adenylyl clclase
Gq - stimulates phospholipases C to convert PIP2 to IP3 and DAG
Gt - stimulates cyclic GMP phosphodiesterase (light)

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17
Q

Name some toxins aimed at G protein cascades.

A

Pertussis toxin prevents the GDP/GTP exchange in Gi proteins.

Cholera prevents the GTPase in Gs so effect lasts longer.

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18
Q

Define efficacy

A

The ability of a drug, once bound to a receptor to cause a response after binding. Depends on its ability to activate the receptor once bound (intrinsic efficacy) and cellular factors. It is measured in relative terms not absolute.

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19
Q

What is IC50

A

The amount of inhibitor needed to give 50% inhibition.

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20
Q

Why is EC50 often less than KD

A

Because often binding less than 100% of receptors produces maximal response as there are spare receptors. This allows greater sensitivity.

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21
Q

Give a cause of drug tolerance/ tachyplaxis

A

Receptor number is not sufficient for a maximal response

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22
Q

Give an example of how a partial agonist can prevent a full response in the present of a full agonist.

A

Partial agonist must have higher affinity so that it out competes full agonist. E.g. Buprenorphine relieves the effects of morphine.

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23
Q

How does a competitive reversible antagonist effect the agonist concentration response curve?

A

Causes a parallel shift to the right (is surmountable)

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24
Q

How does a non-competitive reversible antagonist effect the agonist concentration response curve? (Same as competitive)

A

Shift curve to right but at higher concentrations there will no longer be a maximal response. Non surmountable

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25
Q

What is kB?

A

Kd (affinity) / 50%) when derived pharmacologically.

26
Q

Who is pharmaceutical process, pharmacokinetics, pharmacodynamics and what does this produce?

A

Pharmaceutical process is putting the drug into the patient.
Pharmacokinetics is what the body does to the drug
Pharmacodynamics is what the drug does to the body.
This produces a therapeutic effect.

27
Q

Describe the methods of administering drugs and what is first pass metabolism?

A

Enteral - sublingual, renal, oral
Parental - intramuscular, subcutaneous, intravenous, transdermal, inhalation

First pass metabolism is everything but oral as it bypasses the portal system from gut to liver.

28
Q

Define volume of distribution, how can it be calculated?

A

The theoretical volume in which a drug spreads into assuming it occurred instantaneously = amount given/ plasma concentration at time 0 (found by plotting a graph of plasm conc vs time and extrapolating backwards)

29
Q

Why might volume of distribution be higher?

A

More drug has gone into tissues than expected.

Hydrophobic drugs tend to have higher VOD.

30
Q

When might the fact that only free drug (not bound) can cause an affect be significant?

A

If more than 90% of drug is bound to albumin.
If low VOD
Drug has a low therapeutic index

31
Q

What are object (classI) drugs and precipitant (class II) drugs?

A

Object= given at a conc lower than the albumin concentration/ available binding sites.
Precipitant = given at a conc much higher than the albumin concentration/ available binding sites.
Therefore precipitant drugs can be given to increase free conc of object drugs.

32
Q

What is bio availability and how can it be measured/ calculated?.

A

Amount of drug that reaches the systemic circulation unchanged (not IV as all does).
Measured by amount (dependent on 1st pass metabolism and absorption) or rate (dependent on pharmacological factors and gut absorption.

To calculate, plot plasma conc vs time or a drug given orally vs IV. Bio- availability = AUC oral/ AUC IV x 100

33
Q

How is therapeutic ratio calculated?

A

LD50/ EC50
Minimal lethal dose/ maximal effective dose.
Larger the better (more room for error).

34
Q

What do NADPH cytochrome p450 reductase and cytochrome p459 do?

A

Hydrolysis in phase I. Have low substrate specificity and an affinity for lipid soluble drugs.
Liver microsomal enzymes. Inhibit able and inducible.

35
Q

What is first order and zero order drug elimination kinetics

A

First order = proportional to drug conc so a curve

Zero order = constant rate so straight line.

36
Q

Give some enducers of warfarin action and explain why

A

Alcohol - inhibits metabolism
Asprin, sulphonamides, phenytoin- displace from plasma proteins
Broad spectrum antibiotics - inhibit vit K synthesis by bacteria in gut
asprin - reduce platelet aggregation

37
Q

Name some inhibitors of warfarin

A

Rifampicin and barbiturates induce liver enzymes

38
Q

What is a loading dose?

A

High dose of drug so that it doesn’t take 5 half lives to reach a steady dose.

39
Q

How does urine secretion affect rate at which drug is excreted by kidneys?

A

Only free drug is removed. An acidic urine would mean that any alkali drug is ionised in the urine and so can’t be reabsorbed and vice versa from the lumen

40
Q

How does the kidneys remove drugs from the body?

A

Free drug is lost through the glomerular tuft.

Can be actively secreted though by the tubule.

41
Q

What might be a complication in renal disease?

A

t1/2 may increase if main elimination method is via kidneys. May alter protein binding or loading dose to alter concs in body. Maintainence dose - less needed.

42
Q

How do neutrophils get into the cytoplasm at the site of acute inflammation

A

Chemo taxis- follow gradient of chemoattractants (change membrane so it has pseudopods).
margination- move to blood vessel walls losing laminar flow
Rolling- sticks to vessel wall intermittently to receptors/ integrins
Adherence- sick more avidly
Emigration- enters tissue from blood stream through endothelium via relaxation of junctions and digestion of basement membrane.

43
Q

How do neutrophils phagocytose

A

Contact, recognition, initiation often helped by opsonisation (Fc and Cb3)

44
Q

How do neutrophils kill?

A 
ROS
O2 independent- 
Lysozyme & hydrolases
Bacterial permeability increasing protein (BPI)
Cationic proteins called defensins
45
Q

What is the purpose of fluid exudation?

A

Delivers proteins such as immunoglobulins, inflammatory mediators and fibrinogen.
Dilutes toxins
Increases lymphatic drainage so that microbes and antigens go to immune system

46
Q

Give some examples of pyrogens produced in acute inflammation

A

TNfa and IL-1

47
Q

What is leukocytosis?

A

Result of acute inflammation.
Increased leukocyte production- bacterial then neutrophils, viral them lymphocytes.
Il1 and TNFa increase rate from marrow.
Macrophages and T cells produce colony stimulating factors.

48
Q

Name some symptoms of acute phase response in acute inflammation

A

Shock, decreased apetite, raised pulse, altered sleep, changes is plasma proteins e.g. A1 antitripsin and fibrinogen

49
Q

Give some mechanisms for complete resolution after acute inflammation

A

Degredating proteins e.g. Plasmin
Drainage to lymphatics
Mediators have short half lives
Inhibitors bind

50
Q

What are the outcomes of acute inflammation

A

Resolution
Acute with chronic.
Chronic with fibrous repair
Death

51
Q

Describe some possible complications of acute inflammation

A

Swelling causing blockages e.g. Bile duct and intestine.
Exudation of fluid can cause compression/ cardiac tamponade.
Loss of fluid from burns
Pain and loss of function

52
Q

Give a few clinical examples of acute inflammation

A

Meningitis.
Lobar pneumonia - streptococcus pneumonia. Alveoli has exudate instead of area leading to hypoxaemia.
Abscesses
Blisters

53
Q

Discuss inherited disorders in acute inflammation

A

A1 antitrypsin deficiency - emphysema
Neutrophil defect numbers or function
Complement deficiencies.
Hereditary agiodema

54
Q

Describe synthesis and degredation of ACh.

A

Choline + acetylCoA –> acetylcholine + CoA (choline acetyltransferase CAT)

ACh –> acetate and choline acetylcholinesterase

55
Q

Synthesis and breakdown of NA?

A

Tyrosine, dopa, dopamine then noradrenaline. Tyrosine hydroxylase is the rate limiting step.
Broken down my monoamine oxidase (MOA) or COMT or remove via uptake 1/2.

56
Q

Give some classes drugs that affect ACh transmission and the disorders they treat.

A

Nicotinic antagonists e.g. Anaesthetics such as trimetaphan.
Nicotinic agonist

Not many muscurinic antagonists/ agonists but looking into allosteric binding due to poor selectivity but better when administered locally. Current antagonists e.g. Tolterodine to treat over active bladder. Agonists treat glaucoma and can stimulate bladder emptying.

57
Q

What is a varcosity?

A

Found on post ganglionic sympathetic and they synapse with effector cells.

58
Q

How is noradrenergic transmission terminated?

A

Uptake 1, high affinity Na/ NA symporter into varcosity.

Uptake 2- non neuronal, low affinity.

61
Q

Give an example of a selective B2 agonist and other adrenergic agonists.

A

Salbutamol - asthma.
A1 antagonists and B1 antagonists used in CVD probs e.g. Hypertension.
A1 blocker = doxazosin
B blocker e.g. Bisoprolol

65
Q

How is NA release modulated?

A

Binds to a2 adrenoceptor a on presynaptic membrane, By causes inhibition of VOCC, decreasing ca and neurotransmitter release.

66
Q

Name some pharmacological interventions in adrenergic transmission.

A

Indirectly- acting Sympathomimetoc drugs such as amphetamine are uptaken into vesicles containing NA and cause a slow leak of NA into the cytoplasm and out through the synaptic cleft.
Uptake 1 inhibitors e.g. Tricyclic antidepressants affect mainly CNS but can cause tachycardia.

67
Q

Describe what is meant by desensitivity (homologous vs heterologous), tolerance and suprasensitivity.

A

Homologous desensitisation- agonist at high conc decresses cell responsiveness to that agonist - e.g. PKa phosphorylates B2 adrenoceptor a with agonist bound.
Heterologous desensitisation- one agonist in high concentration decreases responsiveness to other agonists. E.g. Substances increase pKa/ cAMP increase phosphoryltion.
Desensitisation= tachyphylaxis (tolerance quickly and not dose dependant)
Suprasensitisation from antagonist or low agonist.
Tolerance can be from pharmcokinetics (body to drug e.g. Enducers enzyme) or pharmacodynamics (drug to body e.g. Desensitisation)
Tolerance

ESA 2 (9 decks)

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