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130 Cards in this Set
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Local Anesthetic
a.) what channel is blocked? b.) effect on consciousness c.) receptors or enzymes involved? |
a.) Na channel is blocked (reversible)
b.) no loss of consciousness c.) none (that is an analgesic) |
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Difference between analgesic and local anesthetic?
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Analgesics involve receptor (opioid) or enzyme (cyclo-oxygenase) interaction
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Ideal local anesthetic characteristics: Acronym
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BAM-Os
Block on sensory neurons is reversible Action duration is sufficient Minimal effect on motor neurons Onset is rapid Systemic toxicity: none |
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BAM-Os
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Ideal characteristics of local anesthetics
Block on sensory motor neurons is reversible, duration of action is sufficient, minimal effect on motor neurons, onset is rapid, no systemic toxicity |
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What are the structural classes of local anesthetics? (2)
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1.) Tropane
2.) Isogramine |
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1.) What is the SAR group associated with tropane?
2.) what is tropane? |
1.) aminoalkyl ester
2.) tropane is a class of local anesthetics (isogramine is the other) |
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1.) What is the SAR group associated with isogramine alkaloid?
2.) what is isogramine alkaloid? 3.) what benefit does isogramine alkaloid have? |
1.) aminoalkyl amide
2.) isogramine alkaloid is a class of local anesthetics (tropane is the other) 3.) reversible amide = increased stability |
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What 4 SAR features make a local anesthetic?
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1.) lipophilic group
2.) ester or h-bonding group 3.) spacer between ester and amine 4.) ionizable amine |
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3 types of miscellaneous local anesthetics
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1.) aminoalkyl ether
2.) aminoalkyl phenylketone 3.) no ionizable amine: alcohol/ benzoic acid ester |
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1.) what SAR can only do pathway A?
2.) what SAR can only do pathway B? 3.) what SAR can only do pathway C? |
1.) quaternary amine
2.) no ionizable amine 3.) none |
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Pros and cons of alpha methyl
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Pro: increases stability and duration of action
Con: increases CNS toxicity |
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alkyl groups vs. aromatic groups: which increases ADR?
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alkyl groups will increase cholinergic activity
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How do ortho and para substituents affect drug efficacy? (3)
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1.) They increase binding through resonance.
2.) Can increase stability if benzylic methyls are in ortho poistion 3.) Ether substituent can increase hydrophobicity/ pathway B |
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How do you decrease local anesthetic activity?
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Add stuff between the aromatic ring and intermediate chain
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How do you increase anti-cholinergic activity in local anesthetics?
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Add stuff between the aromatic ring and intermediate chain
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What happens when you add stuff between the intermediate chain and aromatic ring of local anesthetics?
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Decreased anesthetic activity, increased anti-cholinergic activity
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General anesthetics
a.) what causes hepatotoxicity |
a.) halothane metabolites (acid halides, halogenated acid halides)
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General anesthetics
a.) what causes nephrotoxicity |
a.) if the halogen is Fluorine in an acid halide or halogenated acid halide
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Ideal characteristics of general anesthetics: acronym
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ASPIRIN-D
ADRs are absent Safe and non-toxic Potent enough to permit adequate O2 supply when mixed Inexpensive Relaxes skeletal muscles Induction and withdrawal is rapid and pleasant Non-flammable/ non-explosive Delivery device compatible with chemical |
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ASPIRIN-D
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Ideal characteristics of general anesthetics
Absence of ADRs Safe; non-toxic Potent enough to provide adequate O2 supply when mixed Induction and withdrawal is rapid and pleasant Relaxes skeletal muscle Inexpensive Non-flammable; non-explosive; non-reactive Delivery device is chemically compatibile |
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Primary MOA of sulfonylureas
a.) what b.) where c.) how |
Promotes insulin secretion from beta-cells by closing ATP-sensitive K channels (SUR1), which causes calcium channels to open. Calcium activates adenylate cyclase, which increases cAMP. cAMP and calcium contract the microtubule/ microfilament system, allowing calcium to be released.
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Sulfonylureas
a.) agent class b.) dependency to glucose |
a.) hypoglycemic agent
b.) MOA is independent of glucose levels |
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Secondary MOA of sulfonylureas (2)
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1.) inhibits hepatic glucagon secretion
2.) enhances insulin receptor sensitivity |
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First generation sulfonylurea
a.) SAR (3) |
arylsulfonylurea that ionized and has a para substituent that is small and lipophilic
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Second generation sulfonylurea
a.) different SAR and its purpose |
p-(betacarboxyamidoethyl) which increases binding to the ATP-sensitive K channels
also the arylsulfonylurea + ionization and para substituent |
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Sulfonylurea therapy failure
1.) primary failure - definition 2.) secondary failure - definition and examples |
1.) initially does not respond
2.) initially responds but then therapy fails. This can be either physiological or lifestyle based. a.) physiological: the beta-cells are exhausted and no more insulin is secreted, resulting in high glucose and less GLUT4 b.) lifestyle: patient has poor adherence and does not modify lifestyle like diet and exercise |
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Meglitinide
a.) MOA b.) similarity and differences between sulfonylurea |
a.) binds to SUR1 receptor and 2 other receptors on beta-cells that are different from sulfonylurea binding sites
b.) similar: hypoglycemic agent; difference: non-sulfonylurea, MOA, and DEPENDENT OF GLUCOSE LEVELS |
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What advantage does meglitinide have?
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Insulin secretion is dependent on glucose levels. Thus there is less chance for hypoglycemia because it will stop secreting insulin when glucose levels are low.
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What are the 2 primary MOAs of biguanides?
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a.) inhibits hepatic glucose production (decreases gluconeogenesis and increases glycolysis)
b.) increases GLUT4 |
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Biguanides
a.) agent b.) MOA |
a.) anti-hyperglycemic agent
b.) inhibits hepatic glucose production and increases GLUT4 |
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Minor MOA of biguanide
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activates AMPK which manages lipolysis (increased glucose uptake, decreased glucose production)
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What SAR contributes to biguanides specific ADR?
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The hydrophobic group causes lactic acidosis. The larger the hydrophobic group, the more likely it will get stuck in the mitochondrial membrane, which inhibits aerobic metabolism and accumulates lactic acid. You want small hydrophobic groups that overall still make the drug hydrophilic, like metformin, so that will decrease any lactic acidosis ADR
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Glitazones
a.) agent b.) MOA (2) |
a.) insulin sensitivity enhancer
b.) glitazones/ thiazolidinedione binds to PPAR gama, which activates the receptor to turn on DNA that increases GLUT4 biosynthesis. It also increases insulin receptor sensitivity so that when the insulin binds to the receptor, there is increased migration of GLUT4 to facilitate the transport of glucose into cells |
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Thiazolidinediones are also known as
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Thiazolidinediones = Glitazones
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What drug is involved with PPAR gamma?
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Glitazones. They bind to PPAR gamma to activate the receptor, which turns on the DNA gene that will increase GLUT4 biosynthesis
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What drug has a post-receptor effect after insulin is bound?
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Glitazones. When insulin is bound (in the presence of glitazones), there is increased migration of GLUT4
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alpha-glycosidase inhibitor
a.) MOA b.) SAR c.) ADR |
a.) inhibits alpha-glucosidase (intestine) or alpha-amylase (pancreas), which decreases carbohydrate degradation and thus decrease glucose absorption
b.) sugars, hydrophillic c.) bloating, diarrhea, flatulence, borborygmi |
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Which drug slows the rate of glucose absorption?
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alpha-glucosidase inhibitor
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Amylin
a.) what is it secreted with? When? where? b.) amylin activity in T1DM c.) amylin acitivity in T2DM d.) effect on plasma glucose? |
a.) co-secreted with insulin when glucose is high/ food intake; secreted from pancreatic beta cells
b.) zero c.) minimal d.) since it decrease gastric emptying, it will slow the time for it to be absorbed |
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The roles of amylin receptor agonists: acronym
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GGC
Glucagon secretion is suppressed Gastric emptying is decreased Caloric intake is reduced |
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GGC
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the roles of amylin
Gastric emptying is decreased Glucagon secretion is suppressed Caloric intake is decreased |
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How would you increase amylin stability?
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substitute some amino acids with proline. The proline causes a kink/ shape change in the peptide so that endogenous enzymes can't degrade it. This causes an increase in drug SOLUBILITY and drug STABILITY (via decreased drug-drug aggregation and decreased drug adhesion)
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GLP-1 agonist
a.) agent b.) where does it function? c.) MOA |
a.) hypoglycemic agent (glucose dependent) / incretin mimetic
b.) glucagon-like agent functions in the ileal brake to slow down upper GI motility when food is in the distal small intestine. |
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Which drugs are glucose-dependent? (2)
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1.) incretin mimetics/ GLP-1 agonists
2.) meglitinide |
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Incretin hormone
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gut hormone that stimulates insulin secretion in response to high glucose levels
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BIG-GF
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GLP-1 agonist/ incretin mimetic
Beta cell function and mass increased Insulin secretion increased in GLUCOSE-DEPENDENT manner Gastric emptying is decreased Glucagon and somatostatin secretion decreased Food intake is decreased (via NT in hypothalamus) |
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PPAR alpha vs gamma
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alpha affects lipid panel, gamma affect GLUT 4
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GLP-1
a.) synthesis and where (2) b.) degradation enzyme |
a.) Either post-translational modification of proglucagon to GLP-1 in the small intestine (GLP-1(7-36amide)) or post-translational modification of proglucagon to glucagon in the pancreas
b.) DPP-IV |
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What is the major form produced when proglucagon is cleaved in the small intestine?
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GLP-1 (7-36amide)
the other is GLP-1 (7-37) |
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GLP-1 (7-36amide)
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The major form produced when proglucagon is cleaved to GLP-1 in the small intestine (L cells)
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DPP
1.) What kind of protease is it? 2.) What amino acids does it cleave and where? 3.) what does it catalze? |
1.) Aminodipeptidase
2.) serine protease 3.) A two amino acid peptide containing alanine or proline in the second position of the N-terminus (amino dipeptidase) 4.) the degradation of GLP-1 |
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How to improve GLP-1 stability? (2)
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1.) inhibit DPP-IV
2.) change the GLP-1 peptide sequence to decrease proteolytic degradation (alanine to glycine), addition of a fatty acid (n-alpha-hexadecanoyl) |
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What is the limitation of GLP-1 agonists?
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Due to its effect on slowing GI motility, it will affect the absorption of drugs that need to be rapidly absorbed and are dependent on threshold concentrations for efficacy (antibiotics, contraceptives).
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The stages of anesthetic induction (4)
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1.) Analgesia
2.) Delirium (dentist) 3.) Surgical anesthesia (eye rolling, regular breathing, loss of many reflexes) 4.) Respiratory paralysis |
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Partition coefficient
a.) definition b.) what does a large P mean? c.) what does a small P mean? |
a.) Partition coefficient describes the solubility of the drug to the blood, which determines rate of induction an recovery; ratio of Blood:Gas
b.) Need a large amount of drug to saturate the blood before it can enter the CNS meaningfully. This is bad because it increases ADR and is SLOW in induction and recovery c.) Need a small amount of drug to saturate the blood and get to the CNS meaningfully. Thus, decreased ADRs and has FAST induction and withdrawal (ideal). |
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Pathway of general anesthetics
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1.) Inhale gas
2.) Goes to alveoli 3.) Saturates in blood 4.) Enters tissues and CNS |
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MAC
a.) definition b.) what does a high MAC mean? c.) what does a low MAC mean? |
a.) Minimum alveolar concentration: The volume percent concentration needed to cause immobility in 50% of middle aged patients. MAC is not potency, but it is related to potency. MAC can be additive.
b.) high MAC means you need a lot of drug to cause 50% of people to be immobile. It is a weak drug c.) low MAC means you need a tiny amount of drug to cause 50% immobility in people. It is a strong drug |
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MAC awake
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This is the concentration of drug needed to cause 50% of patients unable to respond correctly to verbal commands.
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Anesthetic emergence
a.) aka b.) MOA (2) |
a.) Recovery
b.) Exhalation or removal of drug from tissues; metabolic transformation |
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Meyer-Overton Theory
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The MOA of general anethetics: Its lipophilic character causes it to take up space in the membrane, which distorts Na channels directly (allosterically with K and Cl), which stops conduction, which inhibits depolarization
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General anesthetics
a.) definition b.) pathway |
a.) Meyer-Overton theory: General anesthetics are lipophilic and occupy space in the membrane. This occupation distorts the membrane so that Na channels are squeezed or distorted directly (allosterically with K and Cl), causing conductance to be interrupted and thus cannot depolarize
b.) pathway B |
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Pathway of general vs local anesthetics
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General: Pathway B
Local: Can be all 3, depending on the presence of an ionizable amine |
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Channels involved in general anesthetics
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Na - Direct
K and Cl - allosteric |
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What is ketamine?
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NMDA receptor antagonist
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What is halothane?
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NMDA receptor antagonist
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Which 2 drugs are NMDA receptor antagonists?
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Halothane and ketamine
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What does Isoflurane do? (2)
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1.) Decrease glutamate (excitatory aa) release and enhances its removal
2.) increase K conductance |
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Which drug gets rid of glutamate?
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Isoflurane
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Which general anesthetic increases K conductance?
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Isoflurane
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GLUT2 transporter
a.) location b.) MOA |
a.) pancreatic beta cells
b.) The glucose receptor that gets activated when glucose binds to pancreatic beta cells. GLUT2 facilitates glucose entry into the cell to cause insulin secretion |
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6 steps of insulin secretion
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*needs to have high plasma glucose
1.) glucose binds to beta cells on pancreas, which activates GLUT2, causing glucose to get into the beta cells 2.) once inside, glucose gets phosphorylated, which increases the ration of ATP:ADP 3.) increased ATP deactivates potassium channels and opens calcium channels, allowing Ca inside the cell 4.) calcium activates adenylate cyclase to increase cAMP 5.) cAMP and calcium cause contraction of microtubule/ microfilament 6.) insulin with secretory cells come in contact with the beta cell membrane and cause exocytosis |
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1.) When does the A chain become inactive?
2.) When can it retain its biological activity? |
1.) When you shorten the chain in anyway OR switch N-terminal glycine with D-alanine
2.) When you change N terminal glycine with L-alanine |
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1.) Up to which aa can B chain retain biological activity when cleaved? (2)
2.) How to increase potency? 3.) what else affects potency? |
1.) 6 cleaved off from the N-terminus, 3 cleaved off from the C-terminus
2.) delete 24-26 to increase potency 2x insulin 3.) addition of D-aa |
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What needs to be present in both A and B chain to retain biological activity?
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3 disulfide bonds. So don't get rid of the cysteine; methionine can be replaced
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Insulin receptor
a.) name + roles b.) MOA c.) essential feature |
a.) Glycoprotein alpha2beta2. alpha unit: binding; beta unit: enzymatic activity
b.) insulin binds to the alpha subunit, which activates tyrosine kinase, which phosphorylates the whole receptor and intracellular messengers c.) oligosaccharide on the alpha unit that is responsible for insulin recognition and signal transduction |
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What is the essential binding interaction sequence in B-chain insulin?
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B24-Phe; B25-Phe; B26-Tyr
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What is the MOA after insulin binds (8)
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1.) Insulin-receptor association
2.) Signal sent to stored vesicles (GLUT4) 3.) Transporter-vesicle translocation 4.) Binding of transporter-vesicle to cell membrane 5) Fusion of transporter-vesicle to cell membrane 6.) Glucose enters cell via transporter (GLUT4) 7.) Insulin dissociates from receptor 8.) Transporter-vesicle endocytosis |
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Hormone of fuel storage
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Insulin
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Hormone of fuel mobilization
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Glucagon
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Glucagon
a.) where is it secreted from? b.) what stimulates it? inhibits it? c.) aka hormone d.) MOA e,) indications |
a.) ALPHA pancreatic beta cells (unlike insulin from beta cells)
b.) stimulated by decreased plasma glucose. inhibited by high plasma glucose c.) hormone of fuel mobilization d.) glucagon binds to receptor, activates it, and catalyzes glycogenolysis e.) insulin induce hypoglycemia, beta-blocker overdose, GI smooth muscle relaxation for tumor visualization, diabetes development marker |
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alpha pancreatic beta cells
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glucagon
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somatostatin
a.) location b.) indication c.) MOA d.) small role in T2DM drug |
a.) pancreatic islet D cells
b.) sulfonylurea overdose c.) inhibits calcium entry into alpha and beta cells to inhibit the release of glucagon and insulin d.) somatostatin gets inhibited in GLP-1 agonists |
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What to take for SFU overdose?
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somatostatin
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SGLT1 transporters
a.) location b.) function |
a.) intestine
b.) renal glucose reabsorption |
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SGLT2 transporters
a.) location b.) function |
a.) kidney
b.) glucose reabsorption from glomerular filtrate |
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GLUT4 transporter
a.) location b.) MOA |
a.) adipose and muscle tissue
b.) when insulin binds to receptor, GLUT4 comes to the surface to allow glucose to enter the tissue |
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1.) what does a decrease in GLUT2 mean?
2.) what does a decrease in GLUT4 mean? |
1.) decreased GLUT2: decreased insulin secretion
2.) decreased GLUT4: decreased glucose entry into cell |
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What is the rate limiting step in insulin dissolution?
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Protamine sulfate dissociation from hexamer
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Protamine sulfate
a.) charge b.) MOA |
a.) positive charge
b.) wraps around the negatively charged insulin to increase dissociation time. this is an insulin stabilizer/ modifying protein |
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What is an insulin stabilizer? (3)
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1.) protamine sulfate
2.) polysorbate 3.) zinc |
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What is a modifying protein?
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protamine sulfate
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Polysorbate
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An insulin stabilizer that takes the place of zinc, causing no dimer formation, thus decreasing the dissociation step. This leads to a quicker onset and shorter duration
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m-cresol
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preservative
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preservatives (2)
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1.) m-cresol
2.) phenol |
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Speed of insulin based on insulin form: from quickest to slowest (4)
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insulin analogue > insulin form > crystalline > modified with pH 4
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Difference between short acting and rapid acting
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Rapid acting either has no zinc for hexamer formation or no proline to cause dimerization
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What makes insulin ultra long acting? (2)
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1.) Presence of lipophilic chain, which has a high affinity for albumin. The binding of albumin increases its dissociation time
2.) Presence of arginine. At a pH of 4, it is highly ionized. When put in a pH of 7.4, part of it becomes unionized, which forms a precipitate, thus increasing its dissociation time. It is either a binding or solubility issue. |
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Major ways insulin is degraded (2)
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1.) Insulin-specific protease in the cytosol
2.) Reductive cleavage of disulfide bonds via glutathione-insulin transhydrogenase |
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Oral-lyn: describe its value of delivery
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Oral-lyn is a buccal delievery system. It is valuable because it provides an alternative to injecting insulin. No pain, easy, quick delivery to the mouth
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Hypoglycemia definition
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An ADR where low glucose causes a fight or flight response. Increased norepinephrine and epinephrine, increased hepatic production. Causes increased heart rate, abnormal CNS problems (mental confusion, anxiety)
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Hypoglycemic unawareness
a.) definition b.) how to reverse it |
a.) the body gets used to hypoglycemia and the adrenergic response does not become noticeable until much lower (20-60 mg/dL)
b.) decrease the number of hypoglycemic episodes per unit time such as carrying lifesavers with you |
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Insulin resistance
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When antibodies to insulin form (usually when using beef-pork products) and cause a decrease in insulin receptor sensitivity
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Type B insulin resistance
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Insulin resistance (low receptor sensitivity) caused by H. pylori or macrophages in fat that cause inflammation
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Insulin degludec
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Insulin analog that is ultra long, lasting 1-2 day due to its multihexamer assembly. The hexamers first have to dissolve away from each other, then dissolve regularly.
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Which type of insulin is a multhexamer?
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Insulin degludec
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Amylin blackbox warning
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When used with insulin, can cause insulin-induced hypoglycemia. Decrease insulin dose when co-administering with amylin. Amylin by itself does not cause hypoglycemia
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Pancreatic alpha cells (2)
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1.) Where GLP-1 receptors are. Decreases glucagon and somatostatin secretion
2.) Where post-translational modification of proglucagon to glucagon takes place (other is in the small intestine L cells of proglucagon to GLP-1) |
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Location of proglucagon to GLP-1 cleavage
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Small intestine L cells.
This occurs post-translationally |
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Location of proglucagon to glucagon cleavage
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alpha pancreatic beta cells
This occurs post-translationally |
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Which T2DM enzyme is a serine protease?
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DPP (dipeptidyl peptidase)
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DPP IV inhibitor
a.) MOA b.) limitations |
a.) inhibits DPP serine protease enzyme, which inhibits the degradation of GLP-1, thus INDIRECT increase in insulin and INDIRECT decrease in hepatic glucose production
b.) dirty drug/ will degrade other enzymes; may not be able to achieve the right amount of GLP concentrations to control blood glucose (DPP IV inhibitor < GLP-1 agonists) |
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What are gliptans?
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DPP-IV inhibitors
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SAR of DPP-IV inhibitors (3)
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1.) basic group in the ala position except for pyrrolidine
2.) EWG on pyrrolidine or triazole 3.) amine-side chain-carbonyl peptide sequence |
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What are the basic groups of DPP IV inhibitors (3)
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1,) Pyrrolidine (not basic)
2.) 1,3,4 triazole 3.) piperidine |
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What 3 defects are addressed when a thiazolidinedione is added to DPP-IV therapy?
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1.) insulin resistance
2.) beta cell dysfunction 3.) alpha cell dysfunction |
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What are the GLP mediated effects of DPP-IV inhibitors?
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increased insulin secretion, decreased hepatic glucose production
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Which drug causes more glucose to be eliminated/ excreted?
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SLGT2 inhibitor
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SLGT2 inhibitor
a. SAR b.) MOA |
a.) glucose mimic
b.) fools SLGT2 transporter into thinking its glucose and inhibits it, causing more glucose to be eliminated |
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Dual PPAR receptor agonist
a.) receptors and roles |
1,) PPAR alpha: fibrates decrease TG and increase HDL
2.) PPAR gamma: increase GLUT4 biosynthesis |
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Glitazar - class
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PPAR alpha agonist
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PPAR alpha
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Fibrates: decrease TG and increase HDL. Helps manage the metabolic syndrome of T2DM
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PPAR gamma
a.) effect b.) drugs (2) |
a.) increase GLUT4 biosynthesis
b.) glitazones (thiazolidinedione), glitazar (dual PPAR receptor agonist) |
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How to get central control of blood glucose
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Use a D2 agonist
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D2 agonist MOA
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works to decrease hepatic glucose production
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Secondary complications of T2DM
a.) diseases (3) b.) pathophys c.) drug |
a.) neuropathy, nephropathy, retinopathy
b.) glucose is catalyzed by aldose reductase to form sorbitol. The metabolism from sorbitol to fructose is slow so sorbitol accumulates in the tissues. Sorbitol is hydrophilic and attracts water, which increases osmotic pressure, which is bad for cell functionality. c.) aldose reductase inhibitor |
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Aldose reductase inhibitors
a.) indication b.) MOA |
a.) treats secondary complications of T2DM
b.) Inhibits aldose reductase, the enzyme that catalyzes glucose to sorbitol. Thus decreased sorbitol, which means decreased osmotic pressure and no damge to cell function to cause secondary complications of T2DM |
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Protein Kinase C beta inhibitor
a.) indication b.) MOA |
a.) diabetic retinopathy
b.) inhibits beta1 and beta 2 isoforms of protein kinase c. this increases retinal flow and nerve conduction velocity |
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What to treat for diabetic retinopathy?
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PKC beta inhibitor
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which drug needs an A-S-C sequence?
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DPP IV inhibitors
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How to make chain B in insulin inactive? (3)
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1.) remove more than 3 aa from carboxy terminus
2.) remove more than 6 aa from amino terminus 3.) add more than 50% of D-aa to chain |
