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69 Cards in this Set
- Front
- Back
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Name 3 enteral routes of drug administration. (L1)
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Oral, Sublingual, Rectal
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Name 3 parenteral routes of drug administration. (L1)
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Intravenous, Subcutaneous, Intra-muscular
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Name 4 routes of drug administration that are neither enteral nor parenteral. (L1)
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Inhalation, Intra-nasal, Transdermal, Intrathecal
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What are the advantages and disadvantages of oral drug administration? (L1)
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Adv: convenient, safe, economical
Dis: GI irritation, destruction by enzymes, irregular absorption due to food or pH, cooperation of patient, first pass effect |
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what are advantages and disadvantages of sublingual drug administration? (L1)
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Adv: rapid, avoids first pass effect
Disadv: rapid |
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What is the First Pass Effect? (L1)
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Liver mediated metabolism of drugs administered orally/rectally before the drug enters the bloodstream
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What are advantages and disadvantages of rectal drug administration? (L1)
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Adv: can be used to avoid vomiting and part of first pass effect
Disadv: absorption can be irregular |
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What are advantages and disadvantages to intravenous drug administration? (L1)
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Adv: instant and accurate administration, drug effects can be titrated, potentially irritating solutions can be administered.
Disadv: toxicity danger due to instantaneous delivery, self injection difficult, loss of patent veins |
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What are advantages and disadvantages to subcutaneous drug administration? (L1)
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Adv: slow, constant absortion gives a sustained effect, can co-administer a vasoconstrictor further reducing rate of absorption, can be a solid pellet
Disadv: cannot use for irritating solutions, causes necrosis |
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What are advantages and disadvantages to intra-muscular drug administration? (L1)
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Adv: rapid absorption of aqueous drugs, slow constant absorption of drugs in oil based solutions (like vaccines)
Disadv: painful |
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Define bioavailability. (L1)
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The amount of drug absorbed that reaches circulation (expressed as a % or fraction). Takes into account absorption, metabolism before drug reaches bloodstream (incl first pass effect),and excretion.
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What is the bioavailability of a drug administered via IV? (L1)
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The bioavailability would = 1
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Define bioavailable dose. (L1)
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The amount of drug (absolute or normalized to body weight) that enters circulation
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Bioavailablility is affected by what 3 variables? (L1)
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1. Route of administration
2. Properties of drug (charge, size, in lipid/aqueous sol) 3. Physiology of the patient |
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What 2 ways can drugs cross cell membranes to get to site of action? (L1)
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1. Passive diffusion
2. Carrier mediated transport |
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Define passive diffusion. (L1)
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when the rate of flow across the membrane linearly increases with increased drug concentration. previously believed to be the predominant mechanism of drug delivery.
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How does lipid solubility and pH affect passive diffusion? (L1)
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If lipid soluble, the compounds diffusion is unaffected by size. If the drug is polar (hydrophilic/water soluble) then diffusion decreases as the size of the drug increases. pH will affect where in the GI tract passive diffusion of drugs can occur.
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Define carrier mediated transport. (L1)
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when the rate of flow across the cell membrane increases with increased drug concentration until all transporters are saturated.
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Where are weak acids best absorbed? (L1)
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In the stomach/beginning of the small intestine - will be more of uncharged form of the drug in an acidic environment
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Where are weak bases best absorbed? (L1)
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In the intestine
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What are factors affecting where absorption? (L1)
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1. drug solubility in aqueous solution
2. dissolution rate 3. surface area 4. circulation at site of absorption |
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Define Volume of Distribution (L1)
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the hypothetical volume of plasma a drug would distribute into if it only distributes in the plasma. It is different for every drug. Vd=Bioavailable dose/conc of drug in plasma. normalize to weight by dividing by wt in kgs
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What does a large volume of distribution indicate? (L1)
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A Vd greater than the total water space inticates the drug must accumulate in non-plasma compartments like fat or organs
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What does a small volume of distribution indicate? (L1)
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The drug is not distributing through plasma compartment. May be tightly bound to plasma proteins.
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What is the Volume of Distribution dependent on?
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1. The % cardiac output to organs
2. properties of the drug 3. barriers to bulk flow (BBB) |
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Define clearance. (L1)
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rate of drug elimination. The ability of the body to eliminate a drug by all routes - metabolism and excretion
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What are the major routes of drug excretion? (L1)
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Bile and urine
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What is the difference between drug elimination first order kinetics and zero order kinetics?
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First order kinetics - the same % of drug is eliminated during a given time period regardless of drug concentration
Zero order kinetics - the same amount of drug is eliminated during given time intervals instead of the same fraction of drug |
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What neurotransmitter is released from all preganglionic synapses? (L4)
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Acetylcholine
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What neurotransmitters are released from postganglionic synapses? (L4)
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Norepinephrine, Epinephrine, or Acetylcholine
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What neurotransmitter is releaset from sympathetic postganglionic fibers to smooth mm, cardiac cells, or gland cells? (L4)
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Norepinephrine
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What neurotransmitter is released from sympathetic postganglionic fiber to sweat glands? (L4)
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Acetylcholine
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What neurotransmitter is released from sympathetic postganglionic fibers to adrenal medula? (L4)
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Acetylcholine
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What neurotransmitter does the adrenal medulla release? (L4)
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Norepinephrine and epinephrine
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What neurotransmitter is released from parasympathetic postganglionic fibers to smooth mm, cardiac cells, or gland cells? (L4)
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Acetylcholine
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What are the catecholamine neurotransmitters? (L4)
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Dopamine
Norepinephrine Epinephrine |
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Where are catecholamines synthesized? (L4)
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Adrenergic nerve terminals
Adrenal Gland |
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What is the process of catecholamine synthesis at adrenergic nerve terminals? (L4)
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1. L-tyrosine is converted to dopa by tyrosine hydroxylase (*rate limiting step, occurs in cytoplasm)
2. dopa converted to dopamine by dopa decarboxylase (in cytoplasm) 3. dopamine converted to norepinephrine by dopamine B hydroxylase (*occurs in vesicles) |
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How is synthesis of catecholamines at adrenergic nerve terminals regulated? (L4)
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1. Excess norepinephrine in cytoplasm inhibits tyrosine hydroxylase (end produce inhibition)
2. Nerve activity (increased nerve firing leads to increased synthesis) |
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What is the process of epinephrine synthesis in the adrenal gland? (L4)
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Occurs in adrenal medulla
1. norepinephrine diffuses into cytoplasm of chromaffin cells from vesicles and is converted to epinephrine via Phenylethanolamine N Methyl transferase (PNMT) |
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How is dopamine transported into vesicles? (L4)
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by vesicular transmembrane transporter (VTT)
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Where is PNMT found? (L4)
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Only in adrenal medulla. Not found in nerve terminals
(PNMT converts NE to epi) |
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What is the fate of catecholamines after release? (L4)
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1. receptor binding and activation
2. autoinhibitory (binding to presynaptic autoreceptor) 3.reuptake into nerve terminal by plasma membrane transporter 4. reuptake into synaptic vesicles 5. transmitter metabolism by monoamine oxidase (MAO) or COMT |
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What is the major mechanism of catecholamine action termination? (L4)
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reuptake into nerve terminal by plasma membrane transporters - metabolism is too slow
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What is the function of monoamine oxidase? (L4)
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Degrades norepinephrine in cytoplasm - located in outer membrane of mitochondria in nerve terminals
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What is the function of COMT? (L4)
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degrades catecholamines in synaptic cleft of neurons in the liver. metabolites are excreted in urine
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Why isn't the inhibition of neurotransmitters at the adrenergic synapse via metabolism? (L4)
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It's too slow. Need to stop by reuptake using plasma membrane transporters
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What type of receptors to catecholamines bind to? (L4)
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G protein coupled receptors
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What are the different types of adrenergic G protein coupled receptors? (L4)
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alpha 1
alpha 2 beta 1-3 |
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A full agonist will have an intrinsic activity of...? (L4)
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1
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What is the EC50 used to measure? (L4)
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Compound potency - potency can only be used to describe FULL agonists or antagonists
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In which direction will a dose response curve shift if an antagonist is added? (L4)
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To the right. affects EC50/potency
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What is the rank order of potency for adrenergic alpha receptors? (L4)
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Epi is greater than or equal to Norepi, which is greater than Dopamine, which is much greater than iso
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What is the rank order of potency for adrenergic beta receptors? (L4)
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Iso is much greater than epi which is greater than or equal to Norepi, which is greater than Dopamine
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What are 4 factors that determine the actions of sympathetic amines? (L4)
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1. relative potency of the amine in the activation of alpha or beta receptors
2. proportion and density of receptor type and subtype in organ 3. autonomic tone of the organ 4. reflex (hemostatic adjustments) made by the organism in response to the amine |
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What tone predominates in blood vessels? what will happen if you add an alpha 1 antagonish? (L4)
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sympathetic. an alpha 1 antagonist will cause vasodilation bc already have Norepi mediated vasoconstrictive tone on vessels
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What happens to pulse rate, blood pressure, and peripheral resistance if you administer norepinephrine via IV? (L4)
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pulse rate - decreased
blood pressure - increased peripheral resistance - increased |
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What happens to pulse rate, blood pressure and peripheral resistance if you administer epinephrine via IV? (L4)
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pulse rate - increased
blood pressure - peripheral resistance - decreased |
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What happens to pulse rate, blood pressure and peripheral resistance if you administer isoproterenol via IV (L4)?
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pulse rate - increased
blood pressure - decreased peripheral resistance - decreased |
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How is the heart affected by alpha adrenergics? (L4)
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It is not.
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How is the heart affected by beta adrenergics? (L4)
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at SA node - cause increased heart rate (beta 1)
at AV node - cause increased conduction velocity (beta 1) at atria and ventricles - cause increased contraction (beta 1) |
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How are the blood vessels affected by alpha adrenergics? (L4)
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cause constriction of both cutaneous and skeletal mm blood vessels
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How are blood vessels affected by beta adrenergics? (L4)
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no effect on cutaneous blood vessels
dilation of skeletal mm blood vessels (Beta 2) |
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At low epinephrine concentrations, what receptors are primarily activated? (L4)
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Beta receptors
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At low epinephrine concentrations what is the effect on heart rate, force of contraction, and cardiac output?
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HR - increased (B1)
FC - increased (B1) CO - increased (B1) |
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At low epinephrine concentrations, what is the effect on systolic and diastolic pressure, vasodilation, vasoconstriction, peripheral resistance and vascular resistance?
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SP - increased (B1)
DP - decreased (B2) VD - increased (B2) PR - decreased (B2) VR - no change |
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What is the effect of high levels of epinephrine on heart rate, force of contraction, cardiac output, syst pressure, dyastolic pressure, overall blood pressure, vasodilation, vasoconstriction, peripheral resistance, and vascular resistance? (L4)
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HR - inc and then decreases
FC - stays same CO - inc and then decreases (B1) SP - increases (B1) DP - increases (A1) BP - inc and then dec (A1) VD - stays same VC - increases (A1) PR - increases (A1) VR - increases |
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What is the predominant tone in the heart? (L4)
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parasympathetic. the heart always has "brake" on to prevent it from beating too fast
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Which beta adrenergic receptors are present in the heart? which are present in blood vessels? (L4)
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Beta 1 receptors are in the heart
Beta 2 receptors are in the blood vessels |
