Chat transcript - Physiology (Renal, Acid base, GI)

[Anonymous]

21:15:38 [Step_1] Define filtration fraction.

21:15:46 [upman] change of color

21:16:02 [Hmmmmmm] upman good enuf

21:16:25 [Step_1] mangotango, might want to pick brighter color from rainbow on right

21:16:28 [hutals] GFR/ RPF

21:16:40 [mang0tang0] this ok?

21:16:54 [Hmmmmmm] wow too bright

21:17:23 [mang0tang0] now?

21:17:39 [Step_1] hutals is correct. FF = GFR/ RPF . good job!

21:17:43 [Hmmmmmm] try the colors on the left side of the rainbow

21:18:23 [Step_1] At what concentration is the transport mechanism for glucose saturated?

21:18:40 [upman] 180mg/dl?

21:18:51 [Hmmmmmm] 120?

21:19:23 [hutals] i think thats around 300

21:19:31 [mang0tang0] i remember it being pretty high something like 200

21:20:22 [Step_1] its 300 mg/dL. there is a diagram in kap lan that shows it pretty well. easy to remember once you see the diagram, so i will try to post it tomorrow

21:20:26 [upman] ...doesnt glucosuria begin at >180, which wd mean its saturated by then?

21:21:14 [Step_1] it is actually saturated at 375, but around 300 is when it begins to level off on graph

21:21:52 [Hmmmmmm] step 1 thats the rate or concetration?

21:21:59 [Step_1] thats a good point upman, never thought about that

21:22:35 [Step_1] concentration, not rate

21:23:18 dgrosen enters this room

21:23:28 [Step_1] actually, i'm wrong, it is rate on the graph, but the question has concentration of 300

21:23:33 [dgrosen] back

21:23:47 [Hmmmmmm] thanks, please dont mind if i just observe kinda confused here

21:24:24 [Step_1] my notes say that the glucose will appear in the urine before you reach the max concentration

21:25:02 [Hmmmmmm] oh ok

21:25:11 [Hmmmmmm] im seeign teh diagram rite now

21:25:18 [Hmmmmmm] page 308 in ka plan

21:25:53 [Step_1] yep, thats the one

21:26:02 [Step_1] How much of the ECF is interstitial fluid?

21:26:21 [mang0tang0] 2/3

21:26:31 [upman] yep

21:26:38 [Hmmmmmm] agree

21:26:43 [dgrosen] me too

21:27:28 [Hmmmmmm] what give the -ve charge to the glomerular membrane?

21:27:46 [Step_1] yes, everyone is correct

21:27:57 [mang0tang0] heparin

21:28:02 [Step_1] heparin

21:28:07 [Hmmmmmm] how does this help?

21:28:07 [mang0tang0] heparin in the BM

21:28:12 [hutals] heparin

21:28:16 [Hmmmmmm] yes rite!

21:28:30 [dgrosen] cool I did not know that one

21:28:47 [upman] thats a good pt

21:28:48 [Hmmmmmm] heparan sulfate

21:29:19 [Hmmmmmm] its useful i think to push away proteins

21:29:40 [mang0tang0] yea its heparan

21:30:12 [upman] is it the loss of that -ve charge that causes proteinuria, as in Neph S-

21:30:34 [upman] ..along w. teh podocyte thing

21:30:53 [dgrosen] and endothelial damage

21:31:00 [Hmmmmmm] yes

21:31:07 [dgrosen] and basal membrane disruption

21:31:14 [Hmmmmmm] or goodpasture's

21:31:32 [Hmmmmmm] what is clearance?

21:31:40 [dgrosen] huh

21:32:42 [Hmmmmmm] sorry clearance of subs. from kidney *what formula

21:33:30 [mang0tang0] urine conc x urine flow/plasma concentration

21:33:40 [Hmmmmmm] yeah

21:33:47 [Hmmmmmm] good

21:33:57 [hutals] in diabetic glomerulosclerosis, will you have increased or decrease GFR? why?

21:34:05 [dgrosen] UxV/P

21:34:18 [mang0tang0] decreased

21:34:45 [Hmmmmmm] less

21:35:12 [Step_1] i think the GFR would increase because the efferent would be narrow

21:35:37 kiranadi enters this room

21:35:45 [mang0tang0] wouldnt affernt b narrow too

21:35:47 [dgrosen] I am with Step !

21:36:24 [mang0tang0] but yea i guess the blood stays longer

21:36:33 [Step_1] i mean the lumen would be more narrow because of arteriosclerosis. the efferent hylanizes before the afferent for some reason

21:36:55 [Hmmmmmm] u get hyaline deposition therefore should be less GFR rite?

21:37:55 [dgrosen] if the eferent is narrow then the GFR decreases

21:38:16 [dgrosen] sorry increases

21:38:21 [Hmmmmmm] hutals answer please

21:38:30 hiwa enters this room

21:38:35 [hutals] filtration will increase because it stays in the kidney longer because can't get out through the narrow efferents as easily, so GFR should increase

21:39:13 [Hmmmmmm] hmmmm why doesnt the affrent narrow?

21:39:49 [hutals] the afferent does narrow, but not nearly as much or as soon as the efferents

21:40:01 [dgrosen] it will narrow later

21:40:26 [dgrosen] what will happen to the FF?

21:40:28 [hutals] treatment includes angiotensin 2 blockers or ace inhibitors. what effect would this have on the GFR in this pt?

21:40:49 [mang0tang0] what about the hydrostatic pressures affect on GFR

21:40:58 [Hmmmmmm] decrease GFR

21:41:07 drkittu enters this room

21:41:30 [upman] vasodilatation, so inc GFR?

21:41:31 [Step_1] giving either one of those drugs would cause dialation which would decrease the GFR

21:42:02 [Hmmmmmm] agree with step

21:42:15 [upman] ok i got it

21:42:20 [dgrosen] agree with step as well

21:42:49 [hutals] yes, step is right

21:43:04 [hiwa] ace mainly work on efferent , so dec hydrost. pressure and GFR

21:43:33 [Step_1] an increase in cap pressure increases GFR and a decrease in cap pressure will decrease GFR

21:44:15 [Hmmmmmm] i think u posted a picture on this today step 1

21:45:19 [Step_1] yes, that post explains it pretty well if you get the chance to read it

21:45:36 [hutals] T/F. Secondary active transport of amino acids is saturable.

21:45:52 [Hmmmmmm] where is angiotensin 1 activated to angiotension 2?

21:45:55 [Step_1] T

21:46:02 [hiwa] true

21:46:06 [Hmmmmmm] t

21:46:11 [hiwa] lung

21:46:14 [upman] lungs?

21:46:20 [hutals] yes, true

21:46:21 [Hmmmmmm] yes

21:46:23 [mang0tang0] in the lung

21:46:27 [Hmmmmmm] yes lungs

21:46:29 [Step_1] lungs

21:46:33 [drkittu] lungs, endothelium

21:47:22 [Step_1] a real question mentioned giving ace inhibitor and developing a cough. what was mech of getting cough?

21:47:58 [hutals] inc bradykinin

21:49:19 [dgrosen] bradykinin

21:49:40 [Step_1] angiotensin 1 is converted to angiotensin 2 by ACE (lungs), but ACE also inactivates bradykinin (vasodialator). so blocking ACE will also cause bradykinin to remain active which will cause things like cough

21:50:18 [Step_1] so what medication can you give as an alternative which would have similar effects without the cough?

21:50:44 [hutals] lorsartan

21:50:48 [dgrosen] enalapril

21:50:52 [upman] Ang 2 antagonist

21:50:57 [hiwa] Losartan,why in sarcoidosis there is inc ace activity

21:52:38 [Step_1] AT-1 receptor blockers will not effect the ACE part, so will not effect bradykinin getting inactivated. but it will have similar effects on other things. lorsartan is an example

21:53:43 [hutals] not sure about that one hiwa?

21:54:22 [hiwa] i dont have the answer either, anyone

21:54:26 [dgrosen] I dont think there is an answer to that one hiwa

21:54:39 [dgrosen] problably related to the formation of granulomas?

21:57:28 [hutals] What 3 layers form the glomerular filtration barrier?

21:57:45 [hiwa] I think the epithelioid cells in the granuloma secreting ace

21:58:13 [mang0tang0] i read somewhere that the epitheloid cells int he granuloma produces ACE

21:58:18 [Step_1] BM, endothelium, epithelium

21:58:52 [dgrosen] endoth, BM, epith

21:59:04 [hiwa] agree

21:59:15 [drkittu] agree

21:59:20 [mang0tang0] agree

21:59:55 [hiwa] what is the structure of the BM

22:00:29 [Step_1] heparan sulfate

22:00:48 [hutals] 1. Fenestrated capillary endothelium 2. Fused basement membrane with heparan sulfate 3. Epithelial layer consisting of podocyte foot processes

22:01:21 [hiwa] correct

22:02:15 [hutals] What actions does ADH have on the kidney?

22:02:38 [Step_1] Increase water permeability

22:02:45 [upman] ..prob a couple of trivial modifications to things mentnd above......BRS says that interstitial fluid is 3/4 of ECF (its ICF that is 2/3 of TBW)......and losartan is an at-2 receptor blocker

22:02:47 [hiwa] clear water retention in collecting duct

22:04:36 [drkittu] promotes water reabsoption in collecting duct

22:05:29 [Step_1] i agree with the 3/4....thats what i thought we answered?? oops. as far as lorsartan, i have it as a competitive AT-1 receptor blocker, which are found on vascular smooth muscle and in the adrenals

22:06:19 [hutals] -Increase water permeability of principle cells in collecting ducts -Increase urea absorption in CD -Increase Na/K/2Cl transporter in the thick ascending limb

22:06:57 [upman] lippincott 2 Ed p 187, says AT-2...is this outdated info?

22:07:34 [dgrosen] yes is an AT1 not 2

22:08:57 [hiwa] <a href=http://www.amazon.com/exec/obidos/ASIN/0071429484/qid%3D1085033910/sr%3D2-1/valuetheplace-20>FA</a> says AT2

22:09:31 [hiwa] what haappened to my post ?

22:10:00 [hiwa] <a href=http://www.amazon.com/exec/obidos/ASIN/0071429484/qid%3D1085033910/sr%3D2-1/valuetheplace-20>FA</a> says AT2 receptor

22:10:58 [dgrosen] Kap lan has it as AT1 Rc (-)

22:11:22 [dgrosen] producing VD and decrease in Aldosterone

22:11:43 [hiwa] the room is sensitive for the word F>A, says AT" recep

22:13:37 [hiwa] logically should be AT2 because AT2 is physiologically active

22:13:45 [Step_1] ok, after some digging, i found that there are different receptors for angiotensin 2, depending on location (vascular smooth muscle, adrenals, etc). there is the AT 1 recept and the AT 2 recept....both are for angiotensin 2, so dont mix the numbers up

22:14:09 [dgrosen] exactly

22:14:19 [hiwa] make sense, thanx

22:14:37 [dgrosen] losartan is a new angiotensin II receptor antagonist that inhibits AT1

22:14:41 [upman] ..thats cleared...thnx

22:14:54 [Step_1] angiotensin-II receptor antagonists interrupt the type 1*receptor subtype (AT1) of angiotensin II.

22:15:59 [hutals] thanks, now i see it

22:16:18 [hutals] What actions does AII have on the kidney?

22:16:25 [hiwa] ADH

22:16:56 [hiwa] ignore me

22:17:27 [hiwa] decrease GFR

22:17:55 [Step_1] it is a powerful vasoconstictor, so constricting the efferents will increase GFR

22:18:38 [upman] ...and the aldosterone effect

22:18:39 [hiwa] true Aii, not acei

22:19:16 [Step_1] yes, i agree. acei would decrease GFR and A2 will increase it

22:19:20 [hutals] -Contraction of efferent arteriole increasing GFR -Increased Na and HCO3 reabsorption in proximal tubule

22:19:47 [hutals] What are the 4 actions of angiotensin II?

22:20:08 [Step_1] vasoconstriction

22:20:23 [hiwa] hyperK

22:20:31 [Step_1] aldosterone release

22:20:38 [hiwa] opposit sorry

22:21:17 [Step_1] cant think of anything else. maybe increase ADH??

22:21:42 [Step_1] hiwa, it will cause hyperK

22:22:01 [Step_1] well the inhibitor will

22:22:21 [hutals] 1. Vasoconstriction 2. Release of aldo from adrenal cortex 3. Release of ADH from posterior pituitary 4. Stimulates hypothalamus to increase thirst

22:22:53 [Step_1] we should probably move on to another part of physio, any suggestions?

22:23:22 [Step_1] someone suggested acid base earlier?

22:23:28 [hiwa] good job, I am abit confused bet acei and ang 2

22:24:49 [Step_1] hiwa, if you look at a diagram (i'm a visual learner) of the pathway and see where ace and angiotensin work, it becomes much easier to see it. i will try to post something tomorrow for you

22:25:27 [hiwa] that is great thanx

22:25:49 [Step_1] what is the formula for anion gap?

22:26:39 [hutals] AG=Na-(Cl+HCO3)

22:27:33 [drkittu] AG=(Na+K)-(Cl+HCo3) as K+ negligible you can just write as hutal mentioned

22:27:46 [drkittu] sorry hutals

22:28:44 [Step_1] anion gap is basically the most common anions (Cl and HCO3) subtracted from the most common cation (Na), and an apparent AG is present which represents the unaccounted for anions not in the formula such as ....

22:28:58 [Step_1] albumin, phosphate, sulfate, lactate

22:29:50 [drkittu] What are the normal values for Anion Gap?

22:30:01 [drkittu] and units

22:30:50 [hiwa] 12 meq

22:31:15 [Step_1] 140 - (104 + 24) = 12 mEq/L +/- 4 (8-16)

22:31:47 [drkittu] Yes, its 8 to 16 mEq/L

22:31:50 [hutals] between 8 to 16 meq per L

22:32:18 [Step_1] what are some causes of increased AG met acidosis?

22:32:49 [upman] DKA?

22:32:58 [hutals] ketoacidosis, ethylene glycol poisoning

22:33:11 [hutals] salicylate intox

22:33:19 [hutals] lactic acidosis

22:33:21 [hiwa] renal failure

22:33:40 [drkittu] DKA, Uramia,

22:34:06 [drkittu] Salicylate, INH, Ethnol

22:35:01 [hutals] mneumonic is LA MUD PIE.....Lactic Acidosis, Aspirin, Methenol, Uremia/renal failure, Diabetic ketoacidosis, Polyethylene glycol, Inh, Ethylene glycol poison

22:35:38 [Step_1] yes, thats correct

22:35:48 [drkittu] Another mneumoni is MUDPILES

22:35:57 [drkittu] Methanol

22:36:00 [drkittu] Uremia

22:36:10 [drkittu] Dia Keto acidosis

22:36:18 [drkittu] Paraldehyde

22:36:23 [drkittu] INH

22:36:30 [drkittu] Lactic Acidosis

22:36:38 [Step_1] drkittu, can you pick a brighter color from the rainbow on the right, having trouble reading text

22:36:50 [drkittu] Ethanol, Ethylene Glycol

22:37:11 [drkittu] Salicylate

22:37:33 [Step_1] good mneumonics drkittu and hutals

22:37:34 [drkittu] Sure, thanks for letting me know

22:37:55 [upman] useful...thnx

22:38:34 [Step_1] thanks drkittu, much better color

22:38:49 [drkittu] No Problem

22:39:04 [hiwa] Failure to excrete NH4 and increase loss of HCO3 lead to normal anionic gap, ie kidney and GI causes, Other Metabolic reactions lead to inc AG

22:39:57 [Step_1] can someone explain what hyperchloremic normal AG met acidosis means and give example?

22:41:08 [hutals] diarrhea can give this i think because HCO3 is lost in stool, but replaced by Cl which maintains the normal AG

22:41:57 [hiwa] same with RTA

22:42:30 [Step_1] yes, anything that leads to a loss of HCO3 with an equal increase in Cl (hyperchloremic) will give a normal AG (between 8 and 16).

22:43:31 [hiwa] just to add this,because we dont have organic acids in the equation

22:44:18 [upman] how does the Cl increase?

22:44:59 [hiwa] because it replace HCO3 loss

22:45:22 [drkittu] http://www.fpnotebook.com/REN11.htm this link has some causes

22:47:12 [Step_1] good site, thanks

22:47:28 [drkittu] Not a proble

22:47:29 [drkittu] m

22:48:37 [Step_1] what is a cause of met alkalosis

22:49:08 [hutals] vomitting (bulemic)

22:49:10 [hiwa] repeated vomiting

22:49:47 [hutals] diuretics

22:50:45 [hutals] yes, also mineralocorticoid excess, primary aldosteronism

22:50:49 [hiwa] true,thiazide because hypok

22:51:02 [Step_1] both correct

22:51:24 [Step_1] what about resp alkalosis?

22:51:28 [hiwa] what about inc antacid use

22:51:35 [hutals] hypervent

22:51:52 [hiwa] aspirin

22:52:05 [hutals] high altitude

22:52:59 [Step_1] anxiety (hyperventilation), normal pregnancy, high alt, salicylates, endotoxins, cirrhosis

22:53:03 [hiwa] dec perfusion

22:53:06 [Step_1] good job

22:53:29 [Step_1] what about resp acidosis?

22:53:48 [hiwa] copd

22:54:13 [hutals] lung diseases like COPD, pneumonia, CF

22:54:27 [hiwa] anything dec ventilation

22:55:15 [Step_1] also anything that dec mudullary resp center like barbs, opiods (resp depression), CNS trauma

22:55:24 [drkittu] Resp center Depression

22:55:40 [drkittu] COPD/Asthma

22:55:54 [hiwa] pneum. is pathological shunting lead to dec perfusion I think cause resp alk

22:58:11 [Step_1] restrictive lung dz typically causes resp alk while things like COPD, cystic fibrosis, severe pneumonia, ARDS can cause resp acidosis

22:59:29 [hiwa] thnx step1 it is clear now

22:59:49 [Step_1] what can cause a mixed disorder?

23:00:01 [hutals] aspirin tox

23:01:13 [Step_1] yes, salicylate intoxication is a good example where you will see a mix of resp alkalosis and met acidosis

23:01:25 [hiwa] DKA

23:03:04 [Step_1] here is a high yield question. a pt comes to ER with asthma attack and has resp alkalosis at first, but now shows resp acidosis. what do you do next?

23:03:46 [hiwa] this means the asthma is sever

23:04:03 [hutals] asthma should give resp alkalosis because hyperventilating

23:04:43 [hiwa] yes but later they get exhausted and retain co2

23:05:23 [Step_1] the resp alkalosis is normally seen in mild to moderate asthma. if you ever see resp acidosis, the pt is tiring and must be intubated immediately

23:05:41 [hiwa] u have to treat this patient as acute sever asthma

23:05:58 [hiwa] yes intubation

23:06:00 [drkittu] intubate and give oxygen

23:06:39 [Step_1] that is pretty high yield because it really gives you a good understanding of acid base changes, why they occured, and how to manage. boards love it!

23:07:04 [hiwa] good q

23:07:25 [Step_1] we should probably move on to GI now since running out of time

23:07:46 [hutals] ok

23:07:56 [hiwa] better

23:09:00 [hutals] what type of cells release HCl?

23:09:20 [hiwa] parietal

23:09:38 [Step_1] parietal cells

23:09:59 freaha enters this room

23:10:05 [hutals] yep, parietal

23:10:16 [Step_1] hi freaha

23:10:21 [hiwa] what is the stimulant for its release

23:10:23 [hutals] hey freaha

23:10:36 [freaha] hi everyone

23:10:52 [hiwa] hi

23:11:12 [hutals] gastrin

23:11:13 [freaha] hows it going so far...we have lots of new people here...

23:11:34 nne enters this room

23:11:43 [Step_1] hi nne

23:11:52 [hutals] hey nne

23:11:57 [freaha] hi nne

23:12:11 [drkittu] hi freaha and nne

23:12:11 [hiwa] vagal stimulation

23:12:18 [Step_1] yes, its great to see both new and old faces

23:12:52 [hutals] Function of Intrinsic factor secreted in the stomach?

23:13:25 [Step_1] combines with vit B12

23:13:31 [nne] hi

23:13:42 [freaha] vit B12 transport thru the intestinal wall

23:14:02 [nne] hello everyone

23:14:11 [hutals] Binding protein required for vitamin B12 absorption (in terminal ileum)

23:14:34 [drkittu] B-12 transport

23:14:51 [hiwa] what other factors necessary for B12 absorption

23:15:13 upman enters this room

23:16:57 [hutals] not sure drkittu

23:16:58 upman exits from this room

23:17:15 upman enters this room

23:17:33 [upman] sorry guys....some computer probs

23:17:35 [hutals] having problems upman?

23:17:58 [hutals] thats ok, as long as you made it back

23:18:15 [Step_1] patient described having CF, what vit deficiency?

23:18:28 [Step_1] CF = cystic fibrosis

23:18:39 [hiwa] ADEK

23:19:00 [hutals] fat soluble adek

23:19:33 [Step_1] yes, patients with CF have trouble with fat soluble vits (ADEK)

23:19:55 [freaha] whts the reason...behind this????

23:19:57 [hutals] From what cells is bile secreted?

23:20:20 [hiwa] hepatocytes

23:20:55 [Step_1] i believe it has to do with pancreatic insufficiency and unable to produce the proper enzymes for proper breakdown

23:21:10 [drkittu] ADEK and B12 deficiency

23:21:15 [drkittu] in CF

23:21:40 [hiwa] Lipase deficiency

23:22:10 [hiwa] B12 cause R factor not released by Pancrease

23:22:12 [freaha] hmm

23:23:21 [Step_1] according to golijan, pancreatic malabsorption of fat and fat soluble vits in CF

23:23:56 [Step_1] hepatocytes for hutals question

23:24:15 [hutals] yep, hepatocytes

23:24:17 [drkittu] Agree

23:24:32 [hiwa] agree

23:24:52 [hutals] Four functions of H+ secreted in the stomach?

23:24:59 [freaha] i wont forget it now....

23:25:18 [Step_1] kills bacteria

23:25:43 [hiwa] pepsinogen--->pepsin

23:25:53 [freaha] pepsin function

23:26:15 [hiwa] irron metabolism

23:26:22 [Step_1] acidity required for pepsin

23:26:48 [hutals] -Kills bacteria -Breaks down food -Lowers pH to optimal range for pepsin function (conversion of pepsinoget) -Sterilizes chyme

23:27:11 [hutals] Four categories of drugs that inhibit/decrease secretion of gastric acid:

23:27:26 [freaha] wht abt iron metabolism??

23:28:03 [hiwa] acidity of the stomach help change of ferric to ferrous

23:28:15 ggg enters this room

23:28:32 [freaha] cool...

23:28:41 [hutals] yes, good catch, i agree

23:28:51 [Step_1] PPI's, H2 antagonists

23:28:56 [Step_1] hi ggg

23:29:15 [drkittu] Proton pump inhibitors

23:29:17 [freaha] hi ggg

23:29:24 [drkittu] H2 antagonists

23:29:49 [Step_1] misoprostol

23:30:09 [Step_1] can't think of a 4th

23:30:23 [hiwa] Atropin

23:30:24 [hutals] 1. Proton pump inhibitors (omeprazole) 2. H2 receptor antagonists (Rantidine, Cimetidine, Famotidine) 3. Anticholinergics 4. Prostaglandin receptor antagonists (Misoprostol)

23:30:43 [Step_1] ah yes, anticolinergics

23:31:17 [ggg] hi to every one

23:31:28 [hiwa] hi ggg

23:31:45 [hutals] hey ggg

23:31:59 [hutals] Exocrine secretion of zymogens by secretory acini is stimulated by what?

23:32:35 [Step_1] CCK??

23:32:58 [drkittu] cck

23:33:22 [hutals] -Acetylcholine -CCK

23:33:23 [hiwa] secretin

23:33:55 [hiwa] I think I am wrong

23:34:23 [hutals] How do you treat Pancreatic Insufficiency?

23:34:43 [hutals] thats ok, we're here to learn from each other

23:35:19 [hiwa] secretin only stimul HCO3

23:35:36 [Step_1] well, that describes the CF pt from earlier, so you will have fat malabsorption. i guess decrease fat intake

23:36:10 [hiwa] artificial Panc enzyme

23:36:24 [drkittu] Nutritional suppliments

23:36:39 [drkittu] Vitamins

23:36:43 [drkittu] ADEK

23:37:02 [hutals] the answer says -Limit fat intake -Monitor for signs of fat-soluble vitamin (A,D,E,K) deficiency, but i agree that artificial pancreatic enz can be given to

23:38:47 [hutals] they dont have a problem with availablitiy of ADEK, they just cant absorb it because no enzymes, so giving supplemental vits will probably further the symptoms unless an enz is given. its like giving milk to lactose intol pt

23:40:01 [hiwa] medium chain triglycerides also useful because doesnt need lipase for absorption

23:40:27 [Step_1] good point hiwa

23:40:39 [Step_1] since we're almost out of time and we covered most subjects of physio, does anyone want to go over anything specific from physio?

23:40:40 [hiwa] thanx

23:42:17 [drkittu] What's next week's topics?

23:43:03 [upman] ..can someone tell me the subject matter for each chat session.....i hv seen teh time table w/ the weekly subjects... but dont seem to see what shd be prepared for each specific chat session

23:43:06 [Step_1] for next week, we will meet on wed at 9 pm eastern to discuss micro (gen micro, and bacteria, fungi) and the remainder (parasites and viruses) on sat

23:43:40 [drkittu] Thank You

23:44:01 [Step_1] i'll try to post a breakdown of the subjects for the remainder of the schedule so we'll know ahead of time.

23:44:06 [hiwa] Y dont u make it earlier than 9

23:45:02 [upman] hey guys....its been v usefull....though i cdnt contribute much.......hope that will change the next time

23:45:11 [Step_1] the problem we have is that many people come late, but also the time is best for all the people worldwide. a little late for east coast of U.S., but a little early for those in India.....

23:45:32 [freaha] thank u step 1...and thank u all...good nite...see ya later

23:45:44 [drkittu] Good night folks

23:46:00 [upman] thanks a lot everybody....esp step_1

23:46:04 [hutals] upman, i was only an observer for past couple of months until just a couple of weeks ago, so dont worry. it will happen when you feel comfortable

23:46:06 [hiwa] I dont know if I can make it, coz it is almost 5 am here, ok I have to be with the majority, thanks and good nite

23:46:57 [upman] thnaks for the encouragement hutals....it helps

23:47:09 [Step_1] good night to all and thanks for the great chat. hope to see you all in next chat and study hard!

23:47:48 [hutals] good nite. bye