Anonymous
06-30-2004, 10:37 PM
21:13:00 [Lorena] ANS, cardio and renal
21:13:28 [Step_1] in that order?
21:13:29 [kokushubila] Ace , how are you doing ? Good I guess... I mean recovering ...
21:13:43 [kokushubila]
21:13:49 [acestep1] yes. thnx
21:13:55 [acestep1]
21:14:11 [acestep1] much better now . back to studying
21:14:22 [acestep1]
21:14:32 [kokushubila] Good for you!!! I am happy !
21:14:40 [acestep1] how abt u . how r u feeling
21:14:53 [acestep1] ya. thnx
21:15:00 [kokushubila] I am OK Thanks
21:15:27 [nne] lorena, take the lead...
21:15:46 [acestep1] ur welcoem . any time
21:15:48 Carlos_Viru enters this room
21:15:56 [acestep1]
21:15:59 [Lorena] ok
21:16:07 [Carlos_Viru] hi everybody
21:16:08 [acestep1] agree with nne
21:16:14 [jwls29] hi
21:16:25 [Lorena] Nn receptors, location
21:16:34 [Lorena] hi ccarlos
21:17:07 [Lorena] NN
21:17:37 [Carlos_Viru] hi lorena how are u?
21:17:43 [nne] what is NN?
21:17:49 [Lorena] very good thanks
21:17:53 amdoc123 enters this room
21:17:54 [Carlos_Viru] haven't talk to you in long time
21:18:03 [kokushubila] Sorry Lor what is NN
21:18:03 [Lorena] Nicotinic receptors
21:18:36 [Carlos_Viru] where's roxana?
21:18:41 [Step_1] nicotinic receptors located on cell bodies of ganglia of all parasymp and sympath nerves. also found in adrenal medulla
21:18:46 [Carlos_Viru] well what's the subject
21:19:02 [kokushubila] Ok , Preganglionic and neuromuscular junction
21:19:22 [Step_1] pharm, ans
21:19:32 [nne] AND IN SKELETAL END PLATES
21:19:34 [Lorena] N subtype N
21:20:08 [Step_1] we all miss rox, but she's busy taking a course and will be away from the chats for a while
21:20:11 [nne] ANS ganglia
21:20:12 [acestep1] no sk muscles is Nm
21:20:13 [jwls29] the neuromuscular junction would be N subtype M
21:20:23 [Carlos_Viru] ok
21:20:41 [Lorena] very good ...team work
21:20:49 [acestep1] oh ok when will she b back step1?
21:20:57 [acestep1]
21:21:28 [Step_1] i'm not sure, but i hope soon because she is a great contributor
21:21:34 [Lorena] where are the M receptors located?
21:21:59 [acestep1] yes agree
21:22:25 [jwls29] eye,lungs,gi, heart, bladder,blood vessels
21:22:31 [kokushubila] Cardiac and smooth muscle, gland cells , nerve terminals and sweat glands
21:22:35 [Step_1] organs innervated by postganglionic nerves and sweat glands
21:22:51 [jwls29] forgot the sweat glands
21:22:51 sanya enters this room
21:23:15 [Lorena] postganglionic of the PANS and sweat glands, very good
21:23:16 [Step_1] hi sanya
21:23:33 [Lorena] hi sanya
21:23:46 [kokushubila] Hello Snaya
21:23:54 [acestep1] hi sanya
21:23:58 [kokushubila] sorry , Snaya
21:23:59 [sanya] Hi everyone, I'm just going to be silent today coz' I haven't yet read Pharm properly but I just wanted to participate
21:24:22 [Lorena] subtype of M receptor inn heart? and in glands?
21:24:26 [acestep1] np
21:24:39 [Step_1] no prob
21:24:44 [acestep1] m2 in hrt
21:24:50 [sanya] Thanks!
21:24:56 [Step_1] m2
21:24:58 [jwls29] and glands
21:25:00 [acestep1] n m3 in gland- git ones
21:25:04 [jwls29] no
21:25:09 [jwls29] m1
21:25:22 [acestep1] oops imean m1
21:25:27 [Lorena] yes
21:25:36 [acestep1] agree with jwls
21:25:37 [jwls29] m1 glands, m2 heart
21:25:44 [Step_1] M1 is GI secretions, m2 is heart
21:25:54 [Lorena] the rest of organs basically have M3 receptors
21:27:01 [Lorena] what is the nerutransmitter that activates them?
21:27:34 [kokushubila] Ach
21:27:37 [jwls29] Ach
21:27:48 [acestep1] agree
21:27:49 [sanya] Ach
21:27:51 [Step_1] agree
21:27:58 [Lorena] yes
21:27:59 [nne] AGREE
21:28:53 [Step_1] which one of the Musc will cause increase adenlyl cyclase?
21:29:09 [acestep1] m2
21:29:20 [Step_1] oops i meant decrease
21:29:30 [Lorena] M2
21:29:49 [jwls29] m2 is decrease
21:29:52 [acestep1] np
21:30:10 [Step_1] yes, my will decrese adenylyl cyclase...good
21:30:36 [Step_1] how does M1 and M3 work in that sense?
21:30:46 [Lorena] none of the muscarinic causes decrease , instead what do they activate?
21:30:51 [acestep1] Gq
21:31:18 [Lorena] same question but presented differently ....
21:31:27 [sanya] IP3 mechanism
21:31:35 [jwls29] Gq coupled so will increase DAG and IP3, increasing calcium
21:31:36 [acestep1] ic
21:31:40 [Step_1] M1 and M3 work by Gq which will inc IP3 and DAG resulting in an increase in intracell Ca
21:31:45 [Step_1] very good
21:31:50 [Lorena] they activate phospholipase C (releasing IP3 & DAG)
21:33:25 [kokushubila] What is the MOA of Bethanechol in BPH?
21:34:08 [Step_1] facilitate voiding?
21:34:11 [Lorena] stim muscarinic receptors in bladder
21:34:23 [jwls29] agree
21:34:34 [acestep1] oh i thought in BPH alpha blkers were used
21:34:48 [acestep1] relaxes teh trigone?
21:35:07 [Lorena] M receptors are located in trigone and sphincter= relaxation
21:35:13 [acestep1] n causes voiding
21:35:28 [Lorena] alpha blockers are used too ace
21:35:32 [acestep1] agree with lorena
21:35:46 [acestep1] k thnx
21:35:52 [kokushubila] Yes Drs , agree
21:36:06 [Lorena] also detrusor contraction = allows urination
21:36:09 [acestep1]
21:36:22 [acestep1] yes v true
21:36:38 [Step_1] alpha blocker are the new drug of choice....the 3 sins for BPH (all end in -sin)
21:36:49 [acestep1] wow
21:36:58 [acestep1] step1 excellent
21:37:11 [acestep1] n finasteride takes time
21:37:16 [Step_1] mock question had patient with poisoning from organophosphates with musc symptoms and asked where the problem was occurring. choices were presynaptic, post synaptic, etc.
21:37:19 [Lorena] prazocin, terazocin, and...
21:37:29 [acestep1] n inh 1 aplha reducatse i think ?
21:38:15 [acestep1] i think synaptic cleft ?
21:38:15 [Step_1] prazosin, terazosin, and dozazosin
21:38:20 [Lorena] they form Ach E inhibitors so it is presynaptic?
21:38:51 [Step_1] now that i think about it, that was a mock question too with a pt with HTN who also had BPH
21:39:01 [acestep1] lol
21:39:13 [acestep1]
21:40:10 [Lorena] alpha 1 blockers for HTN + BPH...right? the sin family you said step
21:40:16 [Step_1] i think the ans is presynaptic cleft because Ach is being prevented from getting released
21:40:36 [Lorena] i think so too
21:40:48 [acestep1] hmm ic
21:41:04 [jwls29] i agree with lorena...wouldn't the drug for the pt with htn and bph be prazosin?
21:41:10 [sanya] Lorena isn't it post synaptic because the enyme AChesterase is inhibited not ACh so less degradation of Ach and more action of ACh on the post syn receptors, right?
21:41:18 [acestep1] i said synaptic slfet cuz ach esterase was being inh over there
21:41:20 [Step_1] yes lorena...the 3 sins. i dont even think you will need to memorize them b/c they're the only ones i think that end in -sin
21:41:42 [Lorena] doxa or prazo...terazocin is non selective and would have more side effects
21:41:42 [acestep1]
21:42:15 [acestep1] didnt get u lorena
21:42:40 [Step_1] non selective....i thought those were alpha 1 selective
21:42:56 [Lorena] but AchE is located presynaptic ...and thats what is inhibited ....
21:43:04 [acestep1] ya . me 2
21:43:16 [acestep1] ic
21:43:21 [acestep1] thnx
21:44:03 [Step_1] according to kap lan, the 3 sins in the sin family are alpha 1 selective and used for tx of HTN and BPH
21:44:04 [kokushubila] Yes alpha 1 selective
21:44:16 [Lorena] sorry
21:44:23 [Lorena] got mixed up....
21:44:39 [acestep1] k
21:44:41 [Lorena] yes, alpha 1 selective
21:44:56 [Step_1] while we're on the subject, which are the non-selctive alpha blockers
21:45:04 [kokushubila] The non selective is Phenoxybenzamine which is used for the treatment of Pheocromocytoma
21:45:22 [Lorena] phentolamine and phenoxybenzamine
21:45:33 [jwls29] agree
21:45:37 [acestep1] also phentolamine - diagnosis of it
21:45:45 [Step_1] yes lorena, very good....also jwls
21:46:14 [jwls29] pheochromocytoma
21:46:14 [kokushubila] Phenoxy-irreversible and Phento Reversible
21:46:18 [Lorena] thanks
21:47:00 [Step_1] the question gave a pt with pheochromocytoma who developed tachy. which drug should be given? propranolol, labetolol, atenolol?
21:47:01 [jwls29] and phento increases gastric secretion
21:47:39 [acestep1] propanolol
21:47:43 [Lorena] atenolol?
21:47:46 [jwls29] atenolol
21:47:48 [acestep1] ???????????
21:47:57 [jwls29] isn't atenolo cardioselective?
21:48:13 [Lorena] because it is B 1 selective
21:48:15 [Step_1] labetolol has alpha and beta activity, so that is the correct choice...i think. the others only block beta
21:48:19 [acestep1] or labetalol
21:48:13 [Lorena] because it is B 1 selective
21:48:15 [Step_1] labetolol has alpha and beta activity, so that is the correct choice...i think. the others only block beta
21:48:19 [acestep1] or labetalol
21:48:31 [acestep1] yes agree
21:48:39 [Lorena] thanks
21:48:57 [Step_1] labetolol and carbedilol and the beta blocks that have alpha activity
21:49:23 [acestep1] yes but step 1 one q plz
21:49:48 [Step_1] go ahead please
21:49:49 [acestep1] does carvedalol has only alpha 1 n b1 activity like labetalol
21:49:56 [acestep1] :0
21:50:09 [acestep1]
21:50:14 [acestep1] thnx
21:51:07 [acestep1] u there step1?
21:51:10 [Step_1] not sure, that wasnt one of the choices so maybe not. but i know it has both alpha and beta. labetolol would be the correct choice. let me look it up
21:51:34 [acestep1] k . thnx
21:51:42 [acestep1]
21:52:00 [acestep1] ok carvedalol is used in ?
21:52:08 [Lorena] LABEtaALol- LABEl of beta bloquer but also ALpha blocker
21:52:32 [kokushubila] I think propanol is the answer to step 1 Q
21:52:35 [Step_1] Carvedilol is a nonselective beta-adrenoreceptor antagonist and an alpha1-adrenoreceptor antagonist
21:53:13 [acestep1] k thnx a billion step1
21:53:14 [Lorena] why koku?
21:53:33 [Step_1] propranolol is contraindicated because you would have unopposed alpha 1 activity from the cats being released in pheochromocytoma
21:53:37 [acestep1]
21:54:13 [kokushubila] Ok , Thanks didnn't understood at first Thanks a lot
21:54:16 [Lorena]
21:54:16 [sanya] Carvedilol is one of the drugs lately used in CCF
21:54:43 [acestep1] yes . v gd sanya
21:54:53 [Step_1] thanks sanya....i was about to add that
21:54:59 [acestep1] also amlodipine
21:55:08 [sanya] thankyou
21:55:33 [acestep1]
21:56:14 [acestep1] ok doc for emergency tx of glucoma
21:56:22 [acestep1] ?
21:57:05 [Step_1] i think the new one is pilocarpine, but used to be acetazolamine....hopefully both are not choices
21:57:06 [Lorena] physostigmine.... pilocarpine?
21:57:14 [sanya] is it pilocarpine
21:57:28 [acestep1] hmm lippin says pilocarpine
21:57:32 [Step_1] or maybe even mannitol?
21:57:54 [acestep1] its the doc for both open n closed angle glucoma
21:58:06 [Lorena] mannitopl is a good choice too but i would guess pilocarpine since it is local acts faster?
21:58:20 [acestep1] yes ur right step1 i also remb mannitol being used for er raised iop
21:58:38 [acestep1] ya lippin says pilocarpine
21:58:50 [Step_1] so its pilocarpine?
21:59:09 [Lorena] what does pilocarpine do in teh eye?
21:59:16 [acestep1] yes
21:59:41 [acestep1] miosis n opening of teh trabecular meshawork
22:00:06 [acestep1] so tht aqeous humour is drained
22:00:10 [sanya] does it contract the trabecular meshwork opening canal of schlem
22:00:25 [Lorena] very good
22:00:27 [kokushubila] Causes Ciliary mx contraction, opening of trabecular meshwork and Increase in outflow of aqueos humor
22:00:56 [sanya] Ok then i'm wrong
22:02:33 [Step_1] a question showed a graph where bp increased after NE given. new drug given that didnt effect bp and then another that decreased bp and asked which 2 drugs given?
22:02:38 [acestep1] thnx
22:03:24 [acestep1] the one tht decs bp should b isoproterenol
22:03:30 [kokushubila] Looks like the same Q in Kap lan Bank
22:03:45 [Lorena] agree with ace
22:04:21 [Step_1] i think that one of the choices for 2nd drug was phentolamine or phenoxybenzamine, and the first was a beta 2 blocker. this was basically the famous epi reversal question, but asked about NE instead
22:05:24 [Lorena] thanks step
22:05:27 [acestep1] hmm
22:05:27 [Step_1] so the keys are to know that NE does not have B2 activity and that an alpha blocker will decrease bp if given after epi or NE
22:06:02 [acestep1] yes . v true . thnx :0
22:06:12 [acestep1]
22:06:14 [jwls29] thanks step
22:06:21 [Lorena]
22:06:59 [sanya] thanks step1
22:07:24 [Step_1] another question showed diagram of sympathetic nerve terminal and asked where in diagram does amphetamine work?
22:07:45 [Step_1] the problem was that i didnt see a mobile pool??
22:07:59 [Lorena] mobile pool
22:08:04 [Lorena] oh no
22:08:31 [jwls29] were u supposed to know where the mobile pool went without them drawing it in the diagram?
22:08:38 [Step_1] but there was an area that had a reversible arrows of NE...maybe that was the mobile pool?
22:08:58 [acestep1] ic
22:09:01 [Lorena] what other choices did they point at?
22:09:24 [Lorena] the arrows went out of the nerve ending?
22:09:39 [Step_1] i saw the mao thing and the ne being taken up, trosine converted to dopa, etc. they just kinda mixed things around i guess
22:10:44 [Lorena] MOA of reserpine?
22:11:04 [Step_1] the NE came in, then had reversible arrows while inside, but also had it being produced from tyrosine on the other end...now that i think about it...that was the mobile pool
22:12:17 [acestep1] i think its a neuronal blker
22:12:25 [Step_1] blockade of intragranular uptgake and reuptake for moa of resperine
22:12:52 [Lorena] RESERPINE : decreases the RESERves of NE by decreasing its granular uptake.
22:13:16 [jwls29] thanx, lorena
22:13:21 [Step_1] good one lorena
22:14:23 [Lorena] and guanethidine? MOA?
22:15:12 [Step_1] inhibits release of NE
22:15:30 [acestep1] prevents the release of ne
22:16:10 [Lorena] yes by preventing its release from the Granules
22:16:36 [Lorena] very good
22:16:50 [acestep1] thnx
22:17:24 [Step_1] btw, know the receptor and mechanisms of ANS very well....a few questions at least. you know the ones about beta 1 and 2 increase adenlyl cyclase and cAMP, etc. but they give the drug names that inervate those receptors rather than the receptors themselves
22:19:03 [kokushubila] Thanks for info step-1
22:19:03 [Step_1] another question described pt with glaucoma who got cycloplegia. what drug?
22:19:06 [Lorena] thank you step
22:19:39 [acestep1] atrpoine
22:19:53 [Lorena] it has to be muscarinic one
22:20:10 [acestep1] ic
22:20:11 [Step_1] nevermind....that was a q.bank question that i just remembered...sorry, but the ans was pilocarpine i think
22:20:14 [Lorena] muscarinic blocker i mean
22:20:26 [acestep1] k
22:20:34 [acestep1]
22:21:43 [Step_1] sorry, i should probably write these down instead so that i dont confuse you guys
22:21:58 [Step_1] they're just all coming back to me
22:21:58 [acestep1] np step1
22:21:58 [Lorena] diff between depolarizing and non depolarizing NMJ blockers?
22:22:16 [Lorena] noo step!! this is great because you make us think
22:22:49 [acestep1] yes . agree with lorena
22:23:00 [acestep1]
22:23:07 [jwls29] me too
22:23:44 [Step_1] ok, i'll try to think it thru first instead of typing while i'm thinking
22:24:10 [kokushubila] Step _1 you don't confuse us , in this way we learn a lot Thanks for the kindest heart
22:24:26 [acestep1] dont remb lorena abt depolarizing n nondepolaring agents
22:24:32 [Step_1] differences are fasiculations, flaccid paralysis and Ach will inc vs dec
22:24:45 [kokushubila] Sorry , I meant you are not confusing us
22:24:59 [acestep1]
22:25:15 [Lorena] yes step 1
22:25:28 [jwls29] nondep are antagonists and are reversible by AchE Inhibitors and and end in curium,curonium
22:25:54 [acestep1] k .
22:26:06 [Step_1] these remembered questions are from the study group mock exam
22:26:23 [acestep1]
22:26:28 [acestep1] k
22:26:42 [Lorena] nondepolarizing are competitive antagonists at NM receptors in contrast with depolarizing which are agonists but at the end both have the same result
22:26:53 [Lorena] very goog jwls
22:27:12 [jwls29] depolarizing are agonists and they induce fasiculations,flaccidity,and then paralysis and not reversible
22:27:33 [Lorena] excellent step, so nobody post the transcript, step 1 will after editing it
22:27:48 [jwls29] ok
22:27:58 [Step_1] which ones are contraindicated in glaucoma? depol or non depol?
22:29:06 [Step_1] succinylcholine, a non-competitive (depolarizing), is contraindicated in glaucoma because it produces inc intaocular press
22:29:41 [acestep1] k
22:29:42 [Lorena] thnx
22:29:56 [acestep1] hey guys i gtg now
22:30:12 [acestep1] ill see u guys next week
22:30:17 [Step_1] good chatting with you ace
22:30:21 [acestep1]
22:30:22 [Lorena] on saturday
22:30:33 [Lorena] take care ace , see you
22:30:37 [acestep1] same here step1
22:30:40 [kokushubila] why so early Ace? we will miss u
22:30:48 [acestep1] thnx lorena . u2
22:30:50 [kokushubila] Bye bye
22:30:55 [jwls29] see you
22:31:08 [acestep1] thnx koku .
22:31:10 [nne] bye
22:31:25 [kokushubila] U r welcome
22:31:28 [acestep1] have 2 finish some work
22:31:39 [acestep1]
22:31:45 [kokushubila] k
22:31:50 [acestep1] bye nne , jwls
22:31:54 [Lorena] betablockers with intrinsic sympathetic activity?
22:32:00 [acestep1] take care all of u
22:32:07 [jwls29] bye ace
22:32:10 [Lorena] bye
22:32:21 [acestep1] acebutalol n pindolol
22:32:26 [acestep1] byee
22:32:26 [sanya] bye ace!
22:32:36 [acestep1] bye sanya
22:32:37 [Step_1] ISA are acebutolol and pindolol
22:32:41 [Step_1] bye ace
22:32:48 [Lorena] yes ace
22:32:54 [kokushubila] Which Nm blocking drug is ci in burns and why?
22:33:11 [Step_1] dont give ISA drugs with Angina
22:34:00 [Step_1] succinyl choline i think
22:34:21 [Step_1] because of hyperkalemia
22:34:28 [Lorena] i dont know
22:35:13 [Step_1] is that right kokush or am i way off?
22:35:16 [Lorena] but succinilcholine is an agonist
22:36:14 [Step_1] i think that they block NMJ
22:36:15 [Lorena] Nm blocking would be the urium family.... i guess
22:36:17 [kokushubila] Succinyl may cause hyperkalaemia esp in pts with burn, spinal cord injury , peripehral nerve dysfunction or muscular dystrophy
22:37:53 [Lorena] i see, but it is an agonist, remember it causes fasciculation first and then paralysis for persistent depolarization...
22:37:55 [kokushubila] Hyperkalaemia due to prolonged therefore the muscles releases K+
22:38:25 [Lorena] god question koku
22:38:29 [Lorena] good
22:38:37 [kokushubila] Prolonged muscle depolarisation .Real Q in kap
22:39:09 [jwls29] very good question
22:39:38 [kokushubila] thanks
22:39:52 [Lorena] want to move to cardiac?
22:40:31 [jwls29] yes
22:40:33 [Step_1] yes. i have a mixed ans and cardio question to make transition easier...
22:40:38 [kokushubila] sure
22:40:44 [Step_1] which cardio selective beta blockers can cause an increase in lipids
22:41:24 [jwls29] propranolol?
22:41:53 [Step_1] atenolol and metoprolol cause an increase in lipids as side effects, so carful in hyperlipidemia
22:42:04 [jwls29] yikes
22:42:08 [Step_1] propranolol does also, but not cardioselective
22:42:10 [Lorena] propranolol too but is non selective
22:42:20 [jwls29] propranolol is not even cardio selective
22:42:24 [jwls29] realized it too late
22:42:49 [Step_1] no prob, but you knew the side effect which is important
22:42:55 [Lorena] np, we are here to learn
22:43:58 [Step_1] the other important one is not to give non select beta blocker in asthmatics because of B2 blocking activity can cause broncho constriction
22:45:16 [Lorena] what about in diabetics?
22:46:03 [Step_1] yes thats a big one too...also contraindicated
22:46:19 [Lorena] yes
22:46:37 [sanya] you do not give because it could mask the symptoms of hypoglycemia
22:46:41 [Step_1] because masks effects of hypoglycemia
22:46:59 [Step_1] i think that was a q.bank question
22:48:11 [Step_1] which drug, digozin or digitoxin, should be decreased in renal insufficiency?
22:49:06 [sanya] digoxin
22:49:29 [kokushubila] Digoxin
22:49:30 [Lorena]
22:49:58 [Step_1] digoxin is eliminated renal and digitoxin eliminated hepatic. so if renal is impaired, less eliminated and left longer in body to accummulate. risk of digoxin tox, so need to decrease dose. good job
22:50:25 [kokushubila] Is Digitoxin =Digoxin?
22:50:52 [Step_1] no, same class...different drug
22:51:19 [Step_1] what is its main use?
22:51:40 [kokushubila] k , on top of that hypokalaemia potentiate the Digoxin side effects
22:51:45 [jwls29] digitoxin has a longer half life,doesn't it?
22:51:50 [Lorena] CHF
22:52:18 [kokushubila] Yes Lor and atriall fibrillation
22:52:31 [Step_1] yes, main uses are CHF and particularly for Atrial fib...great
22:52:51 [Lorena] hypokalemia, hypomagnesemia and hypercalcemia increase its toxicity
22:53:07 [Step_1]>[jwls29] yes, much longer half life
22:53:19 [Lorena] what drugs increase its toxicity?
22:53:38 [kokushubila] Agree and also hypothyroidism, hypoxia
22:53:42 [sanya] quinidine, verapamil
22:54:01 [Lorena] thanks kokush
22:54:05 [sanya] also thiazides I think
22:54:12 [kokushubila] Diuretics? Loop n Thiazides
22:54:27 [sanya] amiodarone too.
22:54:29 [Step_1] any drugs that decrease potassium
22:54:36 [Lorena] diuretics that can cause hypokalemia or aklter electrolytes
22:54:55 [Step_1] the hypokalemia is very important for diabetics....why? what effect on insulin?
22:54:58 [kokushubila] yes agree
22:55:29 [Lorena] takes the glucose inside the cell?
22:55:44 [kokushubila] I think Insu has to do with muscle K+ not sure
22:56:17 [sanya] insulin actually pushes K into the cell its used in treating hyperkalemia
22:56:52 [Step_1] inc K will increase increase insulin and decrease glucose. dec K will dec insulin and inc glucose
22:57:00 [Lorena] thanks sanya
22:57:08 [kokushubila] Insu increases K+ uptake by the muscles
22:57:26 [Step_1] so a drug like digoxin will have what effect on a diabetic pt?
22:58:04 [sanya] can cause hyperkalemia, right
22:58:22 [kokushubila] Causes hyperglycaemia
22:58:38 [Step_1] digoxin will have hypokalema which will dec insulin and incr glucose, so you will need to incr insulin dose in diabetics... very good
22:59:10 [kokushubila] Thanks step 1
22:59:27 [Lorena] i am lost....then digoxin causes hypokalemia?
23:00:00 [sanya] I too can't understand why dig cause hypokalemia
23:01:01 [sanya] Digoxin toxicity is caused by hypokalemia but digoxin produces hyperkalemia this is what I have understood.
23:01:15 [Lorena] i understand that hypokalemia increases toxicity with digoxin...but does digoxin causes hypokalemia??
23:01:18 [Step_1] i think i'm reading my notes wrong...remember i took test today.....hypokalemia will increase dig tox and hyperkalemia wil decrease dig activity.....is that right
23:02:03 [Step_1] i think i am brain fried right now and mixing things up....its been a very long day
23:02:04 [Lorena] ok
23:02:10 [sanya] Digoxin inhibits Na-K pump so less K pumped into the cell so more is outside the cell and hence hyperkalemia
23:02:47 [Lorena] ok, i agree with that
23:03:30 [Step_1] oh, i see where i confused it. if given a drug like a diuretic and you have hypokalemia, what effect will you have on diabetic on digoxin?
23:03:31 [kokushubila] Yes agree with Sanya
23:03:43 [sanya] How was your test step1?
23:04:21 [kokushubila] OOh step 1 I am sorry , I can imagine how tired you are now !
23:04:27 [Step_1] it was long. as you can see, i'm not really myself right now
23:04:38 [Lorena] you are doing great step
23:04:47 [kokushubila] Again thanks for the kindest heart
23:05:15 [sanya] yes thankyou step1
23:05:33 [Step_1] i should probably just stay quietly in the background while i recover
23:06:20 [Lorena] your inputs are very good, lots of clinical scenarios which is the best for us
23:07:07 [jwls29] well folks, i'm leaving
23:07:15 [jwls29] i will try to make saturday's chat
23:07:16 [Lorena] side effects of amiodarone
23:07:21 [jwls29] have a good night
23:07:30 [jwls29] smurf skin
23:07:35 [Lorena] you too jws, see you
23:07:40 [Step_1] bye jwls
23:07:59 [kokushubila] bye J
23:07:59 [kokushubila] bye J
23:09:45 [hutals] please continue
23:10:19 [hutals] i'm learning alot
23:10:38 [Lorena] anybody? amiodarone side effects
23:10:42 [kokushubila] pulmonary fibrosis, corneal deposits, hepatoxicity
23:11:14 [Lorena] very good koku
23:12:03 [kokushubila] Skin deposits resuling in phtotodematitis, neurological effetcs,CVS (bradycardia,heart block), Hypo/hyperthyroidism
23:12:14 [Lorena] smurf skin, increased LDL
23:12:28 [Lorena] muscle weakness
23:12:51 [kokushubila] So remember to check PFTs,LFTs,TFTs when using Amiodorone
23:14:04 [kokushubila] Can anyone please explain the torsades de pointes I duno it
23:14:18 [Lorena] what does that stand for koku?
23:15:00 [Lorena] torsades de pointes is increase in QRS and QT intervals
23:15:23 [kokushubila] Ok , PFT =Pulmonary function test, LFT= Liver function tests, TFT =Lung Function test
23:15:45 [Lorena] caused by type Ia and III antiarrythmics
23:15:50 [Lorena] thank you koku
23:15:57 [kokushubila] TFT =Thyroid F. Test
23:16:13 [kokushubila] Sorry not Lung Lor , U r welcome
23:16:59 [Lorena] ok
23:17:05 [kokushubila] Thanks for Torsades , I understand now...
23:17:32 [Lorena] how to treat it?
23:18:13 [kokushubila] I have no idea Lor
23:18:57 [Lorena] correct hypomagnesemia, discontinue drugs that porlong QT interval and attemot to shrt action potential duration with drugs (isoproterenol)
23:19:32 [kokushubila] Ok Thanks
23:19:45 [Lorena] it is in k a pl an antiarrythmics (magnesium)
23:20:12 [kokushubila] Ok
23:21:01 [Lorena] this is a little dead now.....are you guys still there?
23:21:21 [kokushubila] Think we are only two here or
23:21:23 [Step_1] i'm silently observing
23:21:45 [Lorena] cinchonism...what is it?
23:21:48 [kokushubila] Ok
23:21:50 [hutals] i'm always quiet, but still here
23:22:15 [kokushubila] It's ok was just kidding...
23:22:27 [Lorena] good to know koku and i were feeling very lonely
23:23:36 [kokushubila] Cinchonism =headache and tinnitis
23:23:51 [Lorena] yes
23:24:10 [kokushubila] Caused by Quinidine
23:24:23 [Step_1] i'll be back in 5 mins
23:24:34 [Lorena] ocular dysfunction, GI ...yes quinidine or other malarial drugs
23:24:41 [kokushubila] k
23:25:15 [kokushubila] What drugs are used to treat supraventricular Tachycardia?
23:25:52 [Lorena] class IV ?
23:26:23 [kokushubila] Class II the B Blockers
23:26:57 [Lorena] ok
23:27:16 [Lorena] class IV is prophylaxis then
23:27:43 [kokushubila] Think so note sure...
23:28:11 [kokushubila] Hey Lor and others I think I have to go now
23:28:47 [kokushubila] Nice discussion , You helped me a lot -Didn't have to mood for reading today ...
23:29:15 [Lorena] i have to go too
23:29:24 [Lorena] thanks koku
23:29:37 [Lorena] see you on saturday
23:29:54 [Lorena] bye hutals bye guys!!!
23:30:18 [kokushubila] Yes definetly I will be here
23:30:29 [kokushubila] Bye bye have a nice Day in HAwaii
21:13:28 [Step_1] in that order?
21:13:29 [kokushubila] Ace , how are you doing ? Good I guess... I mean recovering ...
21:13:43 [kokushubila]
21:13:49 [acestep1] yes. thnx
21:13:55 [acestep1]
21:14:11 [acestep1] much better now . back to studying
21:14:22 [acestep1]
21:14:32 [kokushubila] Good for you!!! I am happy !
21:14:40 [acestep1] how abt u . how r u feeling
21:14:53 [acestep1] ya. thnx
21:15:00 [kokushubila] I am OK Thanks
21:15:27 [nne] lorena, take the lead...
21:15:46 [acestep1] ur welcoem . any time
21:15:48 Carlos_Viru enters this room
21:15:56 [acestep1]
21:15:59 [Lorena] ok
21:16:07 [Carlos_Viru] hi everybody
21:16:08 [acestep1] agree with nne
21:16:14 [jwls29] hi
21:16:25 [Lorena] Nn receptors, location
21:16:34 [Lorena] hi ccarlos
21:17:07 [Lorena] NN
21:17:37 [Carlos_Viru] hi lorena how are u?
21:17:43 [nne] what is NN?
21:17:49 [Lorena] very good thanks
21:17:53 amdoc123 enters this room
21:17:54 [Carlos_Viru] haven't talk to you in long time
21:18:03 [kokushubila] Sorry Lor what is NN
21:18:03 [Lorena] Nicotinic receptors
21:18:36 [Carlos_Viru] where's roxana?
21:18:41 [Step_1] nicotinic receptors located on cell bodies of ganglia of all parasymp and sympath nerves. also found in adrenal medulla
21:18:46 [Carlos_Viru] well what's the subject
21:19:02 [kokushubila] Ok , Preganglionic and neuromuscular junction
21:19:22 [Step_1] pharm, ans
21:19:32 [nne] AND IN SKELETAL END PLATES
21:19:34 [Lorena] N subtype N
21:20:08 [Step_1] we all miss rox, but she's busy taking a course and will be away from the chats for a while
21:20:11 [nne] ANS ganglia
21:20:12 [acestep1] no sk muscles is Nm
21:20:13 [jwls29] the neuromuscular junction would be N subtype M
21:20:23 [Carlos_Viru] ok
21:20:41 [Lorena] very good ...team work
21:20:49 [acestep1] oh ok when will she b back step1?
21:20:57 [acestep1]
21:21:28 [Step_1] i'm not sure, but i hope soon because she is a great contributor
21:21:34 [Lorena] where are the M receptors located?
21:21:59 [acestep1] yes agree
21:22:25 [jwls29] eye,lungs,gi, heart, bladder,blood vessels
21:22:31 [kokushubila] Cardiac and smooth muscle, gland cells , nerve terminals and sweat glands
21:22:35 [Step_1] organs innervated by postganglionic nerves and sweat glands
21:22:51 [jwls29] forgot the sweat glands
21:22:51 sanya enters this room
21:23:15 [Lorena] postganglionic of the PANS and sweat glands, very good
21:23:16 [Step_1] hi sanya
21:23:33 [Lorena] hi sanya
21:23:46 [kokushubila] Hello Snaya
21:23:54 [acestep1] hi sanya
21:23:58 [kokushubila] sorry , Snaya
21:23:59 [sanya] Hi everyone, I'm just going to be silent today coz' I haven't yet read Pharm properly but I just wanted to participate
21:24:22 [Lorena] subtype of M receptor inn heart? and in glands?
21:24:26 [acestep1] np
21:24:39 [Step_1] no prob
21:24:44 [acestep1] m2 in hrt
21:24:50 [sanya] Thanks!
21:24:56 [Step_1] m2
21:24:58 [jwls29] and glands
21:25:00 [acestep1] n m3 in gland- git ones
21:25:04 [jwls29] no
21:25:09 [jwls29] m1
21:25:22 [acestep1] oops imean m1
21:25:27 [Lorena] yes
21:25:36 [acestep1] agree with jwls
21:25:37 [jwls29] m1 glands, m2 heart
21:25:44 [Step_1] M1 is GI secretions, m2 is heart
21:25:54 [Lorena] the rest of organs basically have M3 receptors
21:27:01 [Lorena] what is the nerutransmitter that activates them?
21:27:34 [kokushubila] Ach
21:27:37 [jwls29] Ach
21:27:48 [acestep1] agree
21:27:49 [sanya] Ach
21:27:51 [Step_1] agree
21:27:58 [Lorena] yes
21:27:59 [nne] AGREE
21:28:53 [Step_1] which one of the Musc will cause increase adenlyl cyclase?
21:29:09 [acestep1] m2
21:29:20 [Step_1] oops i meant decrease
21:29:30 [Lorena] M2
21:29:49 [jwls29] m2 is decrease
21:29:52 [acestep1] np
21:30:10 [Step_1] yes, my will decrese adenylyl cyclase...good
21:30:36 [Step_1] how does M1 and M3 work in that sense?
21:30:46 [Lorena] none of the muscarinic causes decrease , instead what do they activate?
21:30:51 [acestep1] Gq
21:31:18 [Lorena] same question but presented differently ....
21:31:27 [sanya] IP3 mechanism
21:31:35 [jwls29] Gq coupled so will increase DAG and IP3, increasing calcium
21:31:36 [acestep1] ic
21:31:40 [Step_1] M1 and M3 work by Gq which will inc IP3 and DAG resulting in an increase in intracell Ca
21:31:45 [Step_1] very good
21:31:50 [Lorena] they activate phospholipase C (releasing IP3 & DAG)
21:33:25 [kokushubila] What is the MOA of Bethanechol in BPH?
21:34:08 [Step_1] facilitate voiding?
21:34:11 [Lorena] stim muscarinic receptors in bladder
21:34:23 [jwls29] agree
21:34:34 [acestep1] oh i thought in BPH alpha blkers were used
21:34:48 [acestep1] relaxes teh trigone?
21:35:07 [Lorena] M receptors are located in trigone and sphincter= relaxation
21:35:13 [acestep1] n causes voiding
21:35:28 [Lorena] alpha blockers are used too ace
21:35:32 [acestep1] agree with lorena
21:35:46 [acestep1] k thnx
21:35:52 [kokushubila] Yes Drs , agree
21:36:06 [Lorena] also detrusor contraction = allows urination
21:36:09 [acestep1]
21:36:22 [acestep1] yes v true
21:36:38 [Step_1] alpha blocker are the new drug of choice....the 3 sins for BPH (all end in -sin)
21:36:49 [acestep1] wow
21:36:58 [acestep1] step1 excellent
21:37:11 [acestep1] n finasteride takes time
21:37:16 [Step_1] mock question had patient with poisoning from organophosphates with musc symptoms and asked where the problem was occurring. choices were presynaptic, post synaptic, etc.
21:37:19 [Lorena] prazocin, terazocin, and...
21:37:29 [acestep1] n inh 1 aplha reducatse i think ?
21:38:15 [acestep1] i think synaptic cleft ?
21:38:15 [Step_1] prazosin, terazosin, and dozazosin
21:38:20 [Lorena] they form Ach E inhibitors so it is presynaptic?
21:38:51 [Step_1] now that i think about it, that was a mock question too with a pt with HTN who also had BPH
21:39:01 [acestep1] lol
21:39:13 [acestep1]
21:40:10 [Lorena] alpha 1 blockers for HTN + BPH...right? the sin family you said step
21:40:16 [Step_1] i think the ans is presynaptic cleft because Ach is being prevented from getting released
21:40:36 [Lorena] i think so too
21:40:48 [acestep1] hmm ic
21:41:04 [jwls29] i agree with lorena...wouldn't the drug for the pt with htn and bph be prazosin?
21:41:10 [sanya] Lorena isn't it post synaptic because the enyme AChesterase is inhibited not ACh so less degradation of Ach and more action of ACh on the post syn receptors, right?
21:41:18 [acestep1] i said synaptic slfet cuz ach esterase was being inh over there
21:41:20 [Step_1] yes lorena...the 3 sins. i dont even think you will need to memorize them b/c they're the only ones i think that end in -sin
21:41:42 [Lorena] doxa or prazo...terazocin is non selective and would have more side effects
21:41:42 [acestep1]
21:42:15 [acestep1] didnt get u lorena
21:42:40 [Step_1] non selective....i thought those were alpha 1 selective
21:42:56 [Lorena] but AchE is located presynaptic ...and thats what is inhibited ....
21:43:04 [acestep1] ya . me 2
21:43:16 [acestep1] ic
21:43:21 [acestep1] thnx
21:44:03 [Step_1] according to kap lan, the 3 sins in the sin family are alpha 1 selective and used for tx of HTN and BPH
21:44:04 [kokushubila] Yes alpha 1 selective
21:44:16 [Lorena] sorry
21:44:23 [Lorena] got mixed up....
21:44:39 [acestep1] k
21:44:41 [Lorena] yes, alpha 1 selective
21:44:56 [Step_1] while we're on the subject, which are the non-selctive alpha blockers
21:45:04 [kokushubila] The non selective is Phenoxybenzamine which is used for the treatment of Pheocromocytoma
21:45:22 [Lorena] phentolamine and phenoxybenzamine
21:45:33 [jwls29] agree
21:45:37 [acestep1] also phentolamine - diagnosis of it
21:45:45 [Step_1] yes lorena, very good....also jwls
21:46:14 [jwls29] pheochromocytoma
21:46:14 [kokushubila] Phenoxy-irreversible and Phento Reversible
21:46:18 [Lorena] thanks
21:47:00 [Step_1] the question gave a pt with pheochromocytoma who developed tachy. which drug should be given? propranolol, labetolol, atenolol?
21:47:01 [jwls29] and phento increases gastric secretion
21:47:39 [acestep1] propanolol
21:47:43 [Lorena] atenolol?
21:47:46 [jwls29] atenolol
21:47:48 [acestep1] ???????????
21:47:57 [jwls29] isn't atenolo cardioselective?
21:48:13 [Lorena] because it is B 1 selective
21:48:15 [Step_1] labetolol has alpha and beta activity, so that is the correct choice...i think. the others only block beta
21:48:19 [acestep1] or labetalol
21:48:13 [Lorena] because it is B 1 selective
21:48:15 [Step_1] labetolol has alpha and beta activity, so that is the correct choice...i think. the others only block beta
21:48:19 [acestep1] or labetalol
21:48:31 [acestep1] yes agree
21:48:39 [Lorena] thanks
21:48:57 [Step_1] labetolol and carbedilol and the beta blocks that have alpha activity
21:49:23 [acestep1] yes but step 1 one q plz
21:49:48 [Step_1] go ahead please
21:49:49 [acestep1] does carvedalol has only alpha 1 n b1 activity like labetalol
21:49:56 [acestep1] :0
21:50:09 [acestep1]
21:50:14 [acestep1] thnx
21:51:07 [acestep1] u there step1?
21:51:10 [Step_1] not sure, that wasnt one of the choices so maybe not. but i know it has both alpha and beta. labetolol would be the correct choice. let me look it up
21:51:34 [acestep1] k . thnx
21:51:42 [acestep1]
21:52:00 [acestep1] ok carvedalol is used in ?
21:52:08 [Lorena] LABEtaALol- LABEl of beta bloquer but also ALpha blocker
21:52:32 [kokushubila] I think propanol is the answer to step 1 Q
21:52:35 [Step_1] Carvedilol is a nonselective beta-adrenoreceptor antagonist and an alpha1-adrenoreceptor antagonist
21:53:13 [acestep1] k thnx a billion step1
21:53:14 [Lorena] why koku?
21:53:33 [Step_1] propranolol is contraindicated because you would have unopposed alpha 1 activity from the cats being released in pheochromocytoma
21:53:37 [acestep1]
21:54:13 [kokushubila] Ok , Thanks didnn't understood at first Thanks a lot
21:54:16 [Lorena]
21:54:16 [sanya] Carvedilol is one of the drugs lately used in CCF
21:54:43 [acestep1] yes . v gd sanya
21:54:53 [Step_1] thanks sanya....i was about to add that
21:54:59 [acestep1] also amlodipine
21:55:08 [sanya] thankyou
21:55:33 [acestep1]
21:56:14 [acestep1] ok doc for emergency tx of glucoma
21:56:22 [acestep1] ?
21:57:05 [Step_1] i think the new one is pilocarpine, but used to be acetazolamine....hopefully both are not choices
21:57:06 [Lorena] physostigmine.... pilocarpine?
21:57:14 [sanya] is it pilocarpine
21:57:28 [acestep1] hmm lippin says pilocarpine
21:57:32 [Step_1] or maybe even mannitol?
21:57:54 [acestep1] its the doc for both open n closed angle glucoma
21:58:06 [Lorena] mannitopl is a good choice too but i would guess pilocarpine since it is local acts faster?
21:58:20 [acestep1] yes ur right step1 i also remb mannitol being used for er raised iop
21:58:38 [acestep1] ya lippin says pilocarpine
21:58:50 [Step_1] so its pilocarpine?
21:59:09 [Lorena] what does pilocarpine do in teh eye?
21:59:16 [acestep1] yes
21:59:41 [acestep1] miosis n opening of teh trabecular meshawork
22:00:06 [acestep1] so tht aqeous humour is drained
22:00:10 [sanya] does it contract the trabecular meshwork opening canal of schlem
22:00:25 [Lorena] very good
22:00:27 [kokushubila] Causes Ciliary mx contraction, opening of trabecular meshwork and Increase in outflow of aqueos humor
22:00:56 [sanya] Ok then i'm wrong
22:02:33 [Step_1] a question showed a graph where bp increased after NE given. new drug given that didnt effect bp and then another that decreased bp and asked which 2 drugs given?
22:02:38 [acestep1] thnx
22:03:24 [acestep1] the one tht decs bp should b isoproterenol
22:03:30 [kokushubila] Looks like the same Q in Kap lan Bank
22:03:45 [Lorena] agree with ace
22:04:21 [Step_1] i think that one of the choices for 2nd drug was phentolamine or phenoxybenzamine, and the first was a beta 2 blocker. this was basically the famous epi reversal question, but asked about NE instead
22:05:24 [Lorena] thanks step
22:05:27 [acestep1] hmm
22:05:27 [Step_1] so the keys are to know that NE does not have B2 activity and that an alpha blocker will decrease bp if given after epi or NE
22:06:02 [acestep1] yes . v true . thnx :0
22:06:12 [acestep1]
22:06:14 [jwls29] thanks step
22:06:21 [Lorena]
22:06:59 [sanya] thanks step1
22:07:24 [Step_1] another question showed diagram of sympathetic nerve terminal and asked where in diagram does amphetamine work?
22:07:45 [Step_1] the problem was that i didnt see a mobile pool??
22:07:59 [Lorena] mobile pool
22:08:04 [Lorena] oh no
22:08:31 [jwls29] were u supposed to know where the mobile pool went without them drawing it in the diagram?
22:08:38 [Step_1] but there was an area that had a reversible arrows of NE...maybe that was the mobile pool?
22:08:58 [acestep1] ic
22:09:01 [Lorena] what other choices did they point at?
22:09:24 [Lorena] the arrows went out of the nerve ending?
22:09:39 [Step_1] i saw the mao thing and the ne being taken up, trosine converted to dopa, etc. they just kinda mixed things around i guess
22:10:44 [Lorena] MOA of reserpine?
22:11:04 [Step_1] the NE came in, then had reversible arrows while inside, but also had it being produced from tyrosine on the other end...now that i think about it...that was the mobile pool
22:12:17 [acestep1] i think its a neuronal blker
22:12:25 [Step_1] blockade of intragranular uptgake and reuptake for moa of resperine
22:12:52 [Lorena] RESERPINE : decreases the RESERves of NE by decreasing its granular uptake.
22:13:16 [jwls29] thanx, lorena
22:13:21 [Step_1] good one lorena
22:14:23 [Lorena] and guanethidine? MOA?
22:15:12 [Step_1] inhibits release of NE
22:15:30 [acestep1] prevents the release of ne
22:16:10 [Lorena] yes by preventing its release from the Granules
22:16:36 [Lorena] very good
22:16:50 [acestep1] thnx
22:17:24 [Step_1] btw, know the receptor and mechanisms of ANS very well....a few questions at least. you know the ones about beta 1 and 2 increase adenlyl cyclase and cAMP, etc. but they give the drug names that inervate those receptors rather than the receptors themselves
22:19:03 [kokushubila] Thanks for info step-1
22:19:03 [Step_1] another question described pt with glaucoma who got cycloplegia. what drug?
22:19:06 [Lorena] thank you step
22:19:39 [acestep1] atrpoine
22:19:53 [Lorena] it has to be muscarinic one
22:20:10 [acestep1] ic
22:20:11 [Step_1] nevermind....that was a q.bank question that i just remembered...sorry, but the ans was pilocarpine i think
22:20:14 [Lorena] muscarinic blocker i mean
22:20:26 [acestep1] k
22:20:34 [acestep1]
22:21:43 [Step_1] sorry, i should probably write these down instead so that i dont confuse you guys
22:21:58 [Step_1] they're just all coming back to me
22:21:58 [acestep1] np step1
22:21:58 [Lorena] diff between depolarizing and non depolarizing NMJ blockers?
22:22:16 [Lorena] noo step!! this is great because you make us think
22:22:49 [acestep1] yes . agree with lorena
22:23:00 [acestep1]
22:23:07 [jwls29] me too
22:23:44 [Step_1] ok, i'll try to think it thru first instead of typing while i'm thinking
22:24:10 [kokushubila] Step _1 you don't confuse us , in this way we learn a lot Thanks for the kindest heart
22:24:26 [acestep1] dont remb lorena abt depolarizing n nondepolaring agents
22:24:32 [Step_1] differences are fasiculations, flaccid paralysis and Ach will inc vs dec
22:24:45 [kokushubila] Sorry , I meant you are not confusing us
22:24:59 [acestep1]
22:25:15 [Lorena] yes step 1
22:25:28 [jwls29] nondep are antagonists and are reversible by AchE Inhibitors and and end in curium,curonium
22:25:54 [acestep1] k .
22:26:06 [Step_1] these remembered questions are from the study group mock exam
22:26:23 [acestep1]
22:26:28 [acestep1] k
22:26:42 [Lorena] nondepolarizing are competitive antagonists at NM receptors in contrast with depolarizing which are agonists but at the end both have the same result
22:26:53 [Lorena] very goog jwls
22:27:12 [jwls29] depolarizing are agonists and they induce fasiculations,flaccidity,and then paralysis and not reversible
22:27:33 [Lorena] excellent step, so nobody post the transcript, step 1 will after editing it
22:27:48 [jwls29] ok
22:27:58 [Step_1] which ones are contraindicated in glaucoma? depol or non depol?
22:29:06 [Step_1] succinylcholine, a non-competitive (depolarizing), is contraindicated in glaucoma because it produces inc intaocular press
22:29:41 [acestep1] k
22:29:42 [Lorena] thnx
22:29:56 [acestep1] hey guys i gtg now
22:30:12 [acestep1] ill see u guys next week
22:30:17 [Step_1] good chatting with you ace
22:30:21 [acestep1]
22:30:22 [Lorena] on saturday
22:30:33 [Lorena] take care ace , see you
22:30:37 [acestep1] same here step1
22:30:40 [kokushubila] why so early Ace? we will miss u
22:30:48 [acestep1] thnx lorena . u2
22:30:50 [kokushubila] Bye bye
22:30:55 [jwls29] see you
22:31:08 [acestep1] thnx koku .
22:31:10 [nne] bye
22:31:25 [kokushubila] U r welcome
22:31:28 [acestep1] have 2 finish some work
22:31:39 [acestep1]
22:31:45 [kokushubila] k
22:31:50 [acestep1] bye nne , jwls
22:31:54 [Lorena] betablockers with intrinsic sympathetic activity?
22:32:00 [acestep1] take care all of u
22:32:07 [jwls29] bye ace
22:32:10 [Lorena] bye
22:32:21 [acestep1] acebutalol n pindolol
22:32:26 [acestep1] byee
22:32:26 [sanya] bye ace!
22:32:36 [acestep1] bye sanya
22:32:37 [Step_1] ISA are acebutolol and pindolol
22:32:41 [Step_1] bye ace
22:32:48 [Lorena] yes ace
22:32:54 [kokushubila] Which Nm blocking drug is ci in burns and why?
22:33:11 [Step_1] dont give ISA drugs with Angina
22:34:00 [Step_1] succinyl choline i think
22:34:21 [Step_1] because of hyperkalemia
22:34:28 [Lorena] i dont know
22:35:13 [Step_1] is that right kokush or am i way off?
22:35:16 [Lorena] but succinilcholine is an agonist
22:36:14 [Step_1] i think that they block NMJ
22:36:15 [Lorena] Nm blocking would be the urium family.... i guess
22:36:17 [kokushubila] Succinyl may cause hyperkalaemia esp in pts with burn, spinal cord injury , peripehral nerve dysfunction or muscular dystrophy
22:37:53 [Lorena] i see, but it is an agonist, remember it causes fasciculation first and then paralysis for persistent depolarization...
22:37:55 [kokushubila] Hyperkalaemia due to prolonged therefore the muscles releases K+
22:38:25 [Lorena] god question koku
22:38:29 [Lorena] good
22:38:37 [kokushubila] Prolonged muscle depolarisation .Real Q in kap
22:39:09 [jwls29] very good question
22:39:38 [kokushubila] thanks
22:39:52 [Lorena] want to move to cardiac?
22:40:31 [jwls29] yes
22:40:33 [Step_1] yes. i have a mixed ans and cardio question to make transition easier...
22:40:38 [kokushubila] sure
22:40:44 [Step_1] which cardio selective beta blockers can cause an increase in lipids
22:41:24 [jwls29] propranolol?
22:41:53 [Step_1] atenolol and metoprolol cause an increase in lipids as side effects, so carful in hyperlipidemia
22:42:04 [jwls29] yikes
22:42:08 [Step_1] propranolol does also, but not cardioselective
22:42:10 [Lorena] propranolol too but is non selective
22:42:20 [jwls29] propranolol is not even cardio selective
22:42:24 [jwls29] realized it too late
22:42:49 [Step_1] no prob, but you knew the side effect which is important
22:42:55 [Lorena] np, we are here to learn
22:43:58 [Step_1] the other important one is not to give non select beta blocker in asthmatics because of B2 blocking activity can cause broncho constriction
22:45:16 [Lorena] what about in diabetics?
22:46:03 [Step_1] yes thats a big one too...also contraindicated
22:46:19 [Lorena] yes
22:46:37 [sanya] you do not give because it could mask the symptoms of hypoglycemia
22:46:41 [Step_1] because masks effects of hypoglycemia
22:46:59 [Step_1] i think that was a q.bank question
22:48:11 [Step_1] which drug, digozin or digitoxin, should be decreased in renal insufficiency?
22:49:06 [sanya] digoxin
22:49:29 [kokushubila] Digoxin
22:49:30 [Lorena]
22:49:58 [Step_1] digoxin is eliminated renal and digitoxin eliminated hepatic. so if renal is impaired, less eliminated and left longer in body to accummulate. risk of digoxin tox, so need to decrease dose. good job
22:50:25 [kokushubila] Is Digitoxin =Digoxin?
22:50:52 [Step_1] no, same class...different drug
22:51:19 [Step_1] what is its main use?
22:51:40 [kokushubila] k , on top of that hypokalaemia potentiate the Digoxin side effects
22:51:45 [jwls29] digitoxin has a longer half life,doesn't it?
22:51:50 [Lorena] CHF
22:52:18 [kokushubila] Yes Lor and atriall fibrillation
22:52:31 [Step_1] yes, main uses are CHF and particularly for Atrial fib...great
22:52:51 [Lorena] hypokalemia, hypomagnesemia and hypercalcemia increase its toxicity
22:53:07 [Step_1]>[jwls29] yes, much longer half life
22:53:19 [Lorena] what drugs increase its toxicity?
22:53:38 [kokushubila] Agree and also hypothyroidism, hypoxia
22:53:42 [sanya] quinidine, verapamil
22:54:01 [Lorena] thanks kokush
22:54:05 [sanya] also thiazides I think
22:54:12 [kokushubila] Diuretics? Loop n Thiazides
22:54:27 [sanya] amiodarone too.
22:54:29 [Step_1] any drugs that decrease potassium
22:54:36 [Lorena] diuretics that can cause hypokalemia or aklter electrolytes
22:54:55 [Step_1] the hypokalemia is very important for diabetics....why? what effect on insulin?
22:54:58 [kokushubila] yes agree
22:55:29 [Lorena] takes the glucose inside the cell?
22:55:44 [kokushubila] I think Insu has to do with muscle K+ not sure
22:56:17 [sanya] insulin actually pushes K into the cell its used in treating hyperkalemia
22:56:52 [Step_1] inc K will increase increase insulin and decrease glucose. dec K will dec insulin and inc glucose
22:57:00 [Lorena] thanks sanya
22:57:08 [kokushubila] Insu increases K+ uptake by the muscles
22:57:26 [Step_1] so a drug like digoxin will have what effect on a diabetic pt?
22:58:04 [sanya] can cause hyperkalemia, right
22:58:22 [kokushubila] Causes hyperglycaemia
22:58:38 [Step_1] digoxin will have hypokalema which will dec insulin and incr glucose, so you will need to incr insulin dose in diabetics... very good
22:59:10 [kokushubila] Thanks step 1
22:59:27 [Lorena] i am lost....then digoxin causes hypokalemia?
23:00:00 [sanya] I too can't understand why dig cause hypokalemia
23:01:01 [sanya] Digoxin toxicity is caused by hypokalemia but digoxin produces hyperkalemia this is what I have understood.
23:01:15 [Lorena] i understand that hypokalemia increases toxicity with digoxin...but does digoxin causes hypokalemia??
23:01:18 [Step_1] i think i'm reading my notes wrong...remember i took test today.....hypokalemia will increase dig tox and hyperkalemia wil decrease dig activity.....is that right
23:02:03 [Step_1] i think i am brain fried right now and mixing things up....its been a very long day
23:02:04 [Lorena] ok
23:02:10 [sanya] Digoxin inhibits Na-K pump so less K pumped into the cell so more is outside the cell and hence hyperkalemia
23:02:47 [Lorena] ok, i agree with that
23:03:30 [Step_1] oh, i see where i confused it. if given a drug like a diuretic and you have hypokalemia, what effect will you have on diabetic on digoxin?
23:03:31 [kokushubila] Yes agree with Sanya
23:03:43 [sanya] How was your test step1?
23:04:21 [kokushubila] OOh step 1 I am sorry , I can imagine how tired you are now !
23:04:27 [Step_1] it was long. as you can see, i'm not really myself right now
23:04:38 [Lorena] you are doing great step
23:04:47 [kokushubila] Again thanks for the kindest heart
23:05:15 [sanya] yes thankyou step1
23:05:33 [Step_1] i should probably just stay quietly in the background while i recover
23:06:20 [Lorena] your inputs are very good, lots of clinical scenarios which is the best for us
23:07:07 [jwls29] well folks, i'm leaving
23:07:15 [jwls29] i will try to make saturday's chat
23:07:16 [Lorena] side effects of amiodarone
23:07:21 [jwls29] have a good night
23:07:30 [jwls29] smurf skin
23:07:35 [Lorena] you too jws, see you
23:07:40 [Step_1] bye jwls
23:07:59 [kokushubila] bye J
23:07:59 [kokushubila] bye J
23:09:45 [hutals] please continue
23:10:19 [hutals] i'm learning alot
23:10:38 [Lorena] anybody? amiodarone side effects
23:10:42 [kokushubila] pulmonary fibrosis, corneal deposits, hepatoxicity
23:11:14 [Lorena] very good koku
23:12:03 [kokushubila] Skin deposits resuling in phtotodematitis, neurological effetcs,CVS (bradycardia,heart block), Hypo/hyperthyroidism
23:12:14 [Lorena] smurf skin, increased LDL
23:12:28 [Lorena] muscle weakness
23:12:51 [kokushubila] So remember to check PFTs,LFTs,TFTs when using Amiodorone
23:14:04 [kokushubila] Can anyone please explain the torsades de pointes I duno it
23:14:18 [Lorena] what does that stand for koku?
23:15:00 [Lorena] torsades de pointes is increase in QRS and QT intervals
23:15:23 [kokushubila] Ok , PFT =Pulmonary function test, LFT= Liver function tests, TFT =Lung Function test
23:15:45 [Lorena] caused by type Ia and III antiarrythmics
23:15:50 [Lorena] thank you koku
23:15:57 [kokushubila] TFT =Thyroid F. Test
23:16:13 [kokushubila] Sorry not Lung Lor , U r welcome
23:16:59 [Lorena] ok
23:17:05 [kokushubila] Thanks for Torsades , I understand now...
23:17:32 [Lorena] how to treat it?
23:18:13 [kokushubila] I have no idea Lor
23:18:57 [Lorena] correct hypomagnesemia, discontinue drugs that porlong QT interval and attemot to shrt action potential duration with drugs (isoproterenol)
23:19:32 [kokushubila] Ok Thanks
23:19:45 [Lorena] it is in k a pl an antiarrythmics (magnesium)
23:20:12 [kokushubila] Ok
23:21:01 [Lorena] this is a little dead now.....are you guys still there?
23:21:21 [kokushubila] Think we are only two here or
23:21:23 [Step_1] i'm silently observing
23:21:45 [Lorena] cinchonism...what is it?
23:21:48 [kokushubila] Ok
23:21:50 [hutals] i'm always quiet, but still here
23:22:15 [kokushubila] It's ok was just kidding...
23:22:27 [Lorena] good to know koku and i were feeling very lonely
23:23:36 [kokushubila] Cinchonism =headache and tinnitis
23:23:51 [Lorena] yes
23:24:10 [kokushubila] Caused by Quinidine
23:24:23 [Step_1] i'll be back in 5 mins
23:24:34 [Lorena] ocular dysfunction, GI ...yes quinidine or other malarial drugs
23:24:41 [kokushubila] k
23:25:15 [kokushubila] What drugs are used to treat supraventricular Tachycardia?
23:25:52 [Lorena] class IV ?
23:26:23 [kokushubila] Class II the B Blockers
23:26:57 [Lorena] ok
23:27:16 [Lorena] class IV is prophylaxis then
23:27:43 [kokushubila] Think so note sure...
23:28:11 [kokushubila] Hey Lor and others I think I have to go now
23:28:47 [kokushubila] Nice discussion , You helped me a lot -Didn't have to mood for reading today ...
23:29:15 [Lorena] i have to go too
23:29:24 [Lorena] thanks koku
23:29:37 [Lorena] see you on saturday
23:29:54 [Lorena] bye hutals bye guys!!!
23:30:18 [kokushubila] Yes definetly I will be here
23:30:29 [kokushubila] Bye bye have a nice Day in HAwaii