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MCPHS MEDCHEM 1 E2
MCPHS - MedChem I Exam 2 (c)
| Question | Answer |
|---|---|
| Enzyme-Linked Domains? | E.C. = N-terminal & Intra-cellular = C-terminal cytosolic domain (gen. Enzymatic) |
| What do Enzyme-Linked Receptors do? | +/- phosates on proteins (cell signaling) |
| What does Phosate addition do? | causes large neg charge added to protein. Changes 3D structure & activity. Teversible (reg in time & space) |
| Enzyme-Linked Rcptr Reactions are? | Slower than GPCRs (min-Hrs) |
| What Functions do Enzyme-linked rcpts do? | cell metab., growth, differntiation.. |
| Four types for Enzyme-linked ? | Tyrosine Kinase, Tyrosine Phosphatase (removes phos.), Ser/Thr Kinase, Guanylyl Cyclases (conv. GTP to cGMP) |
| Two types of EZ-Linked Tyr Kinase? | (two ligands) Dimerized/Intrinsic Trans-PO4 (Growth Fxtrs, EGF, Insulin, BCR-ABl, Hormones) & Intracellular Domain Recruts (NTKs) possessing Kinase Activity ( Cytokines, Immune Cells - JAK Phos STAK that causes Gene Trans.) one ligand |
| Ez-Linked Tyr-Phosphatase? | Single, Signal mech (immune cells) Removes Phos. |
| Guanylyl Cyclase? | Ez-Linked, Smallest trans-membrane rcptr, B-Type Nat. Peptide, Particulate cGMP is Intrinsic |
| Guanylate Cyclase ? | cGMP by NO in cytosol (solu) |
| Intracellular rcptrs? | Reg Domain (where on gene attached), DNA Bind Domain (hsp 90 cover Zn fingers), Hinge Domain, Ligand Binding Domain (Which ligands will bind) |
| Cross Talk? | %of types of rcptrs present on cell determine net effect |
| PSD - 95? | Post Synaptic Density Protein has PDZ domains that link to trans-membrane receptors (example of how rcptrs don't fxn' alone) |
| Tubocurarine? | Antagonist on nACh receptor binds to rcptr |
| Nicotin? | Agonists on nACh rcptr |
| Affinithy? | small amt drug needed, low Kd |
| Efficacy ? | effecacy aka intrinsic activity (full or partical) ability to produce effect |
| Full Agonist? | Same efficacy but diff affinity (epi acts on alph1 incr. BP, Phenylephrine acts to produce equ. response ) |
| Phenylephrine is? | Specific Agonist (w/less affinity than epi) |
| Epinephrine? | Non-specific agonist |
| Partial Agonist? | Incr. Conc. does not produce Max Response even if max rcpts are occupied |
| Can partial agonist have same affinity? | yes, but less efficacious |
| Pilocarpine? | partial agonist on mAChR (less salvation than ACh) |
| Inverse Agonist ? | Opp to norm. response. 1) Allosteric Binding decrease Affinity for Agonist decreasing Response. 2)Spontaneously/Constitutively act. rcptr, Normally act. w/out ligand binding. Binding to a constitutive rcptr reduces response. |
| Constitutive 5-Ht rcptr? | no ligand = activated, leads to schizophrenia, Olanzapine binds = inactivates, antipsycohotic effect) |
| Antagonists? | Bock same site as endogenous ligand, but No Intrinsic activity/efficacy. |
| Phentolamine? | Antagonist blocks Epinephrine on alpha1 Increasing Systolic BP (only part of the story) |
| Phentolamine w/out Epi? | no real response |
| Epi in system before Phentolamine is administered? | decreases BP by blocking Epi (which is a complecated net result of what other rcptrs epi works on) |
| Epi after Phentolamine ? | Drop in BP |
| Two types of antagonists? | Competitive (reversible) & Non-competitive (binds tight or on to allosteric site) |
| Cimetidine ? | H2 Receptor Blocker (Competitive) |
| Propranolol? | Beta-adrenergic Receptor Blocker (Competitive) |
| What does cimetidine look like? | Histamine, so it blocks H2 receptor reducing acid secretion |
| What is an Irreversible antagonist? | Non-Competetive (binds to either allosteric or active site, but dissociation is slow to none) |
| Phenoxybenzmine? | irreversible antagonist strong bonds with alpha-adrenergic receptors |
| What does Penoxybenzamine block? | Norepinephrine |
| Tubocurarine? | Allosteric Binding Antagonist Non-Competitive blocking ACh stopping skeletal muscle contraction |
| tolerance is also called? | adaption |
| receptor activity is regulated by? | tolerance |
| angonists are ? | down regulated (desesitization) |
| antagonists are? | up-regulated (super-sensitivity) |
| what happens to receptors when morphine is administered for a long time? | adaption |
| reversible adaption? | can occur after a period of rest |
| rapidly developed tolerance is called? | tachyphylaxis |
| What is Heterologous desensitization? | sharing of effector that to receptor activations by different drugs cause both to be desensitzed |
| What else can cause decreased response? | decrease in recptr synthesis by inhibition of trans/translation recptr encoding gene by drug |
| Receptor Phosphorylation does what? | desensitization: Beta-adrenergic Rcptrs by B-ARK to Ser or Thr on C-terminal |
| What does Beta-arrestin do? | binds to phosphate groups to prevent g-protein interaction |
| What happens when agonist is removed from desensitized receptor? | B-arrestin dissociates and phos. is removed from G-Protein and now a response can be activated again |
| How does BARK do this? | conformational change of tail on C-terminal that blocks cytosolic binding site of G-Protein |
| How long does BARK Cycle take? | few min.s |
| What is another name for internalization? | recycling of receptors |
| How long does receptor sequenstration ? | sequestration cycle can take hours |
| What is CURL | Compartment of Uncoupling of Receptr and Ligand where receptor is recycleed while ligand *(agonist) is degraded |
| What is retro endo cytosis | some receptors and ligands are returned to cell surface |
| What is receptor degradation? | Sim. to Sequestration but receptors & ligands are degraded. leads to loss of receptor number. Cycle takes DAYs to be able to respond again. Problematic in Asthma Tx. |
| What are states of VGSC? | open, closed, closed -but unable to be activated |
| How fast are VGSC desensitized? | Rapidly Sec.s |
| Amphetamine releases catecholamines doing what? | Amphetamies deplete catecholaminess faster Exhausting Mediators |
| Degradation does what to drugs? | Drugs like Barb's & Etoh activate enzymes that degrade them |
| What is supersensitiveity? | Opp of Tolerance - Agonist causes a greater responce than normal |
| How does Supersensitiveity usually occur? | Antagonists for polonged exposure may cause upregulation of receptors and when the antagonist is removed the natural endogenous ligand may cuase a much greater responce |
| What must pts do when on propranolol for a prolonged period of time? | propranolol is a comptve blocking antagonist, so it must be tappered off, not stopped completely |
| What is Ser/Thr Kinases? | Dimerzied (two ligands) Ser/Thr Kinases (CA progression - TGF-Beta rcptrs & MAPK ) phosphoralates either ser or thr |
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