Anonymous
10-18-2004, 09:43 PM
20:07:50 [hutals] so we're starting with cell injury from goljans notes and then inflammation....right?
20:08:31 [hutals] what are some causes of hypoxemia?
20:08:40 [drymalik] ok
20:09:08 [Lorena] increase altitude
20:09:35 [drymalik] carbon mono oxide poisoning ,
20:09:46 [ninadnashua] respiratory acidosis, ventilation difusion perfusion problems
20:10:01 [Lorena] ops closed the window accidentally
20:10:14 [ninadnashua] methemoglobinemia
20:10:41 [ninadnashua] lalso left shift of oxygen curve
20:10:55 [hutals] the 4 causes of hypoxemia are resp acidosis, vent problems, perfussion problems and diffusion problems. increased altitude can cause resp acidosis....so that would be correct as well. CN poisoning i will need to check on
20:11:08 jwls29 enters this room
20:11:13 [Lorena] agree
20:11:17 [jwls29] hi all
20:11:27 BlakeH enters this room
20:11:39 [drymalik] ok
20:11:42 [ninadnashua] ya
20:11:46 [Lorena] hi jwls and blake
20:12:14 [BlakeH] hello all
20:12:14 [hutals] hypoxemia by definition has a decreased PaO2 and CO poisoning would have normal PaO2, so it would not cause hypoxemia
20:12:34 [hutals] hey jwls and blake
20:12:51 [drymalik] ahan thanks for correction
20:12:58 [Lorena] ok
20:13:25 [hutals] no prob....i thought it would cause it also, but had to look it up to make sure
20:13:34 zoya enters this room
20:14:01 [hutals] what causes right shifted oxygen curve?
20:14:10 [hutals] hey zoya
20:14:28 [zoya] hi
20:14:42 [drymalik] inc ph
20:14:46 [jwls29] hi zoya
20:14:55 [drymalik] inc 2-3 BP glycerate
20:14:57 [jwls29] increased 2,3 dpg
20:15:06 [jwls29] fever
20:15:07 [BlakeH] Increased co2
20:15:08 [Lorena] temperature, 23DPG
20:15:16 [ninadnashua] fever acidosis increase 2 3 dpg
20:15:21 [drymalik] yah temp too
20:15:23 [jwls29] decreased ph (acidosis)
20:15:34 [jwls29] high altitude
20:15:36 [drymalik] sory
20:15:36 [Lorena] inc CO2, decreased pH
20:15:59 [zoya] hi,jwls
20:16:19 [BlakeH] increased H+
20:16:23 [hutals] for right shift it has decreased affinity for O2 and readily releases the )2 into blood. think of excercising mucle.....dec pH from lactic acid and incr PCO2, inc 2,3 BPG from inc glycolysis, inc temp. also high altitude.....very good everyone
20:18:08 [Lorena] type of coagulation in sarcoidosis?
20:18:37 [ninadnashua] non caseating
20:18:50 [hutals] non caseating
20:19:01 [Lorena] yes, very good
20:19:50 [hutals] inhibitors of cytochrome oxidase? hint- mneumonic 3 C's
20:19:53 [BlakeH] point of no return in cell injury???
20:19:55 [Lorena] even if they form granulomas, it is not caseous -caseous is almost exclusively for mycobacterium
20:20:15 kiranadi enters this room
20:20:27 [Lorena] cyanide?
20:20:29 [jwls29] and systemic fungal infections
20:20:37 [kiranadi] hi
20:20:37 [ninadnashua] yes because they have lipids mycolic acid un cell wall
20:20:47 [BlakeH] cyanide is one
20:21:14 [jwls29] carbon monoxide
20:21:14 [hutals] Cytochrome oxidase inhibitors are Cyanide and Carbon monoxide
20:21:20 [kiranadi] why was the chat stopped in the middle?????????????/
20:21:37 [kiranadi] i'm sorry for interrupting
20:21:45 [hutals] hey kiranadi
20:21:45 [Lorena] what is the other C?
20:22:23 [kiranadi] hi hutals....saw ur post in another forum and joined here
20:22:28 [Lorena] hi kiran
20:22:43 [hutals] 3 C's are the first for Cyt ox, 2. Cyanide, 3. Carbon monoxide.....one is the cyt ox itself
20:22:55 [jwls29] you think maybe rizwana is lost?
20:23:03 [Lorena] ah ok thanks hutals
20:23:08 [ninadnashua] ya
20:23:10 [jwls29] no one else in the general chat room
20:23:16 [hutals] glad the post led u here
20:23:18 [kiranadi] hi lorena
20:23:36 [BlakeH] point of no return in cell injury???
20:23:36 [drymalik] what are the diagnostic features of sarcoidosis
20:23:45 [hutals] someone is in the gen chat....maybe lost??
20:23:52 [kiranadi] yes
20:24:02 [jwls29] disruption of cell wall
20:24:08 [jwls29] membrane i meant
20:24:17 [BlakeH] ACE+, bilateral pehillar lymph nodes( potato nodes)
20:24:23 crusher enters this room
20:24:41 [hutals] someone who came in late should try to get that person because the beginning of chat will be lost if i go to get rizwana
20:24:48 [Lorena] agree with jwls
20:25:02 [hutals] hey crusher
20:25:03 [crusher] hello all
20:25:05 [drymalik] wait me go
20:25:06 [jwls29] rizwana> rizwana hi are you looking for the path chat?
20:25:13 drymalik exits from this room
20:25:15 [jwls29] that didn't work
20:25:31 [jwls29] hi crusher
20:25:32 [Lorena] hi crush
20:25:44 [jwls29] brb
20:25:47 [ninadnashua] hi crush
20:26:05 [hutals] non caseating bilater hilar something also are buzz words for sarcoid...right?
20:26:06 [zoya] hi crusher
20:26:13 [crusher] hello everybody
20:26:34 [BlakeH] bilateral pehillar lymph nodes( potato nodes)
20:26:39 [ninadnashua] ya
20:26:48 [Lorena] thanks blake
20:26:51 acestep1 enters this room
20:27:04 [BlakeH] ok
20:27:16 [Lorena] hi ace
20:27:23 [hutals] i'm counting on multiple choice recognition to help me remember those types of words
20:27:28 [hutals] hey ace
20:27:50 drymalik enters this room
20:27:52 [BlakeH] changes seen in irreversible injury???
20:27:52 [acestep1] hi lor n hutals
20:28:10 [acestep1] how r u guys
20:28:17 [jwls29] disruption of cell membrane
20:28:26 [zoya] definitive dx requires biopsy demonstrating noncaseating granulomas
20:28:27 [Lorena] calcium , membrane damage
20:28:29 [jwls29] damage to mitochondria
20:28:41 [hutals] thanks for going to help rizwana drymalik
20:28:45 [jwls29] calcium influx
20:28:46 [Lorena] nuclear changes
20:29:07 [jwls29] nuclear changes
20:29:20 [jwls29] pyknosis
20:29:25 [drymalik] i left messege there but no reply from rizwana
20:29:25 [hutals] doing good ace, great to see you
20:29:26 [jwls29] karryorexis
20:29:33 [BlakeH] piknosys, karorrhexis, karyolysis are the nuclear changes
20:29:40 [jwls29] karyolysis
20:29:43 [Lorena] intreacellular enzymes leak
20:29:49 [acestep1] agree with jwls n lor n also lysozymal enzyme leakage
20:29:49 [hutals] no prob....at least we tried drymalik
20:29:53 [BlakeH] right
20:30:12 [drymalik] piknosys, karorrhexis, karyolysis are the nuclear changes arent they the nuclear changes in apoptosis?
20:30:28 [acestep1] is this colour ok ?
20:30:33 [BlakeH] can u change ur color acestep1]
20:30:43 [BlakeH] they are also seen in necrosis
20:31:01 [Lorena] in apoptosis the chromatin is condensed and fragmented -more organized
20:31:17 [acestep1] hmm i think in apoptosis u ahve muclear n cytoplasm condensation n then both break
20:31:26 [jwls29] form apoptotic bodies
20:31:40 [jwls29] from cellular memb blebs
20:31:49 [acestep1] agree with lor n jwls
20:32:07 [Lorena] and no inflamatory process ina poptosis
20:32:22 [jwls29] very important
20:32:43 [drymalik] ok so we discussed apoptosis too
20:32:45 [jwls29] examples of apoptosis?
20:32:55 [acestep1] agree . aslo its genetic n only 1 cell or a small # die
20:33:06 [drymalik] development of embryo
20:33:08 [hutals] an important point from earlier that i forgot to mention was that fever right shifts the curve to make O2 more available in blood to help fight infection. As docs, we always try to take away this natural defense mech by taking away the fever....golijan made a point about that and found it importan
20:33:11 [BlakeH] menstrual period
20:33:17 [acestep1] agree - dry
20:33:18 [Lorena] in embnryonic life ,
20:33:39 [jwls29] thanks hutals
20:33:47 [acestep1] viral inf
20:33:52 [BlakeH] thymus. mullerian duct. wolffian duct
20:34:05 [jwls29] yes
20:34:17 [acestep1] ty - hutals
20:34:25 [BlakeH] genes regulatin apoptosis????
20:34:34 [hutals] no prob
20:34:35 [drymalik] councilman bodies in viral hepatitis
20:34:37 [Lorena] thanks
20:34:42 [acestep1] yes
20:34:58 [Lorena] Rb, p53, bcl
20:35:16 [acestep1] when p53 leaks out n cytochrome c lost .
20:35:19 [BlakeH] right
20:35:22 [drymalik] and cystic fibrosis
20:35:38 [acestep1] agree with lor . aslo bax gene the youth gene
20:35:43 [jwls29] caspases set into motion cell death
20:35:48 [BlakeH] bcl2 inhibits apoptosis, overexpressed in follicular lymphoma
20:36:03 [jwls29] agree with blake
20:36:05 [acestep1] k
20:36:31 [Lorena] ok
20:36:40 [BlakeH] p53 facilitates apoptosis, seen in many tumors ( Li- Fraumeni Sx)
20:37:14 [hutals] did anyone mention psammoma bodies for example of pathologic role of apotosis
20:37:23 [Lorena] diference between dystrophic and metastatic calcification?
20:37:55 [jwls29] dystrophic is seen in tissue already damaged with a normal serum calcium and phosphorus
20:38:10 [Lorena] psamomma bodies are an example of dystrophic calcification seen in papillary tumors of the thyroid , ovaries and meningioma
20:38:15 [BlakeH] metastatic is due to high Ca and dystropic is calcificat in a previously damage tissue
20:38:18 [jwls29] metastatic is seen on normal tissue with high calcium and phosphorus
20:38:38 [Lorena] very good
20:39:12 [hutals] D-ystrophic is in D-amaged tissue and metastatic is in normal tissue
20:39:28 [Lorena] examples of dystrophic calcification?
20:39:43 [Lorena] M-etastatic is M-etabolic
20:39:56 [jwls29] atherosclerotic plaques,
20:39:57 calender enters this room
20:40:02 [BlakeH] valve calcification
20:40:10 [hutals] atherosclerosis, psammoma bodies
20:40:14 [jwls29] damaged cardiac valves
20:40:22 [ninadnashua] enzymatic fat necrosis
20:40:24 [acestep1] good one lor
20:40:32 [hutals] hey calendar
20:40:37 [drymalik] arthrosclerotic plaques
20:40:51 [Lorena] hi calender
20:40:52 [ninadnashua] cmcongenital cmv
20:41:03 [Lorena] good everyone
20:41:09 [jwls29] calcification in CMV
20:41:50 [hutals] what is the best screening test for iron disorders?
20:42:03 [jwls29] serum ferritin
20:42:05 tomilola enters this room
20:42:06 [ninadnashua] also tuberculous lesions
20:42:11 [BlakeH] vitamin deficit assoc wit squamous metaplasia???? examples????
20:42:27 [hutals] hey tomilola
20:42:31 [calender] hi Lorena
20:42:40 [jwls29] vit a, i think
20:42:42 [hutals] yes, serum ferritin is correct
20:42:43 [Lorena] vit a deficiency ?
20:42:53 [hutals] agree, vit a
20:43:04 [tomilola] ?
20:43:10 [BlakeH] right...examples???
20:43:49 [Lorena] glossitis
20:44:09 [acestep1] lung ca
20:44:15 [BlakeH] examples of squamous metaplasia???
20:44:16 tomilola exits from this room
20:44:17 tomilola exits from this room
20:44:30 [BlakeH] right
20:44:30 [ninadnashua] squamous epithelium in mainstem bronchus
20:44:50 [hutals] oxygen toxicity in newborn causes superoxide FR damage.....retrolental fibroplasia, leads to blindness in newborns....is that an example??
20:44:53 [acestep1] also i think in kidney
20:44:53 [BlakeH] squamous epithelium in cervix
20:44:56 [Lorena] oh ok
20:45:21 [acestep1] agree- hutals
20:46:28 [BlakeH] oxygen tox can lead to retrolental fibroplasia and to????
20:46:30 [hutals] bladder transitional epithelium in schistosomiasis
20:46:45 [jwls29] necrotizing enterocolitis
20:47:53 [zoya] hutal, what <a target=new HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=<a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A>&mode=books><a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A></A> notes/book are you guys following? sorry for th interruption .......cause i have <A HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Board%20Review%20Series&mode=books><A HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Board%20Review%20Series&mode=books>BRS</A></A> path........i was planning to get <a target=new HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=<a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A>&mode=books><a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A></A> ............but there are so many options ........i am a bit confused....again sorry for th interruption
20:48:19 [Lorena] oh my God
20:48:33 [BlakeH] lol
20:48:43 [zoya] opps....sorry
20:48:47 [Lorena] lol
20:48:50 [jwls29] blake is that right?
20:48:58 [hutals] zoya, try not to type words like b r s, golijan, , etc
20:49:08 [jwls29] necrotizing entercolitis and subarachanoid hemorrhage?
20:49:26 [BlakeH] haven heard of those
20:49:27 [zoya] ok.............soooooooooooooorrrrrrrrrrry
20:49:42 [BlakeH] alveolar damage =ARDS
20:49:43 [jwls29] that's in a premature infant
20:49:44 [Lorena] it sounds logic because of reperfusion injury
20:49:52 [jwls29] sorry mixing step 2 with step 1
20:49:52 [BlakeH] oh ok
20:49:54 [hutals] no prob....we've all done it before....and probably will again
20:50:04 [BlakeH] its true
20:50:30 [Lorena] thanks jwls
20:50:43 [jwls29] no prob
20:50:56 [BlakeH] greatest suceptibility to hypoxia????
20:51:05 [BlakeH] cell??
20:51:13 [Lorena] what is reperfusion injury?
20:51:41 [hutals] zoya, i think you're asking about which golijan notes we're using? i'm using his 500 pg lecture notes. some others might be using other things from him....they're all good and follow more or less the same concepts
20:51:49 [zoya] thanks
20:53:06 [hutals] atherosclerosis?
20:53:53 ash enters this room
20:54:03 [BlakeH] what cell has the greatest suceptibility to hypoxia???
20:54:05 [hutals] oh, i just saw the "cell" part of your question blake....nevermind my ans
20:54:20 [hutals] hey ash
20:54:26 [ash] hi all
20:54:31 [Lorena] neuron
20:54:35 [BlakeH] no prob
20:54:36 [jwls29] reperfusion injury is when there has been ischemiaand then blood flow is restored to the area
20:54:37 [hutals] red blood cell??
20:54:38 [Lorena] hi ash
20:54:45 [ash] sorry i am so late
20:54:59 [BlakeH] what neuronal cell???
20:55:02 [jwls29] there is too much oxygen in a tissue that was already deprived
20:55:32 [jwls29] hi ash
20:55:35 [hutals] nope....thinking out loud, but that can't be it because the RBCs dont require O2
20:55:36 [acestep1] purkinje
20:55:44 [Lorena] yes jwls because the sudden increase in oxygen causes increase in reactive oxygen species and catalase gets overwhelmed and cannot reduce all the oxygen
20:55:56 [ash] the tissue plasminogen activator will form toxic o2 radicals on reperfusion
20:55:57 [BlakeH] right acestep1
20:56:29 [acestep1] tpa will form free radicals?
20:56:38 [BlakeH] purkinje an hippocampus cells
20:56:56 [hutals] cyanosis not relieved by oxygen in a pt coming home from a camping trip in the Rocky mountains?
20:56:58 [Lorena] thanks ace and blake
20:57:25 [jwls29] nitrates
20:57:30 [acestep1] ur welcome. anytime lor
20:57:40 [jwls29] reducing agent
20:57:41 [ash] thats what i heard in golj a n audio
20:57:51 [acestep1] lymes d/s
20:57:58 [acestep1] ic
20:58:17 [hutals] methemoglobinemia is correct. the water in the mountains has nitrites that oxidize iron to ferric condition
20:58:45 [Lorena] ok
20:58:45 [hutals] nitrates is also correct ans
20:58:57 [ash] what is the similarity between mallory body and lewy body?
20:59:26 [BlakeH] ubiquination????
20:59:39 [ash] good blake
20:59:40 [hutals] what would be the treatment for the pt with methemoglobinemia
20:59:41 [hutals] ?
21:00:01 [ash] methylene blue and vit. c
21:00:05 [jwls29] methylene blue iv and ascorbic acid as an ancillary treatment
21:00:08 [BlakeH] methilene blue
21:00:32 [acestep1] dunno
21:00:33 [Lorena] cells that are degenerating
21:00:40 [hutals] IV meth blue is gold standard and ascorbic acid (vit C) as ancillary tx....great!
21:00:43 [Lorena] agre methylene blue
21:00:47 dr_yasir enters this room
21:00:53 [ash] what is the difference between mallory body and councilman body?
21:01:29 [hutals] why would a pt with HIV have methemoglobinemia?
21:01:38 [Lorena] Councilman's bodies: apoptotic bodies of hepatocellular origin seen in viral hepatitis
21:01:43 [hutals] hey dr yasir
21:01:49 [jwls29] mallory body is alcoholic, and councilman body is viral
21:01:49 [BlakeH] councilman seen in hepatocyte apoptosis mallory in alcohol
21:01:59 [Lorena] and mallory are in alcoholic hepatitis?
21:02:01 [ash] because of sulfamethoxazole for pneumocystis carinii
21:02:13 [jwls29] a pt with Hiv would have methb b/c of tmp/sx for pcp
21:02:59 [hutals] very good jwls.....you were paying attention to papi
21:03:04 [ash] their basic structure is also different.mallory bodies are keratin aggregates and councilman bodies are apoptotic cells
21:03:05 [hutals] and ash
21:03:39 [jwls29] lol...yes i was
21:03:56 [ash] DNA injury will stimulate which gene normally?
21:04:00 [BlakeH] wear and tear pigment seen in elderlies???
21:04:16 [jwls29] lipofuscin
21:04:19 [Lorena] lipofuscin
21:04:38 [ash] agree lipofuschin
21:04:45 [BlakeH] right
21:05:04 [acestep1] p53-ash
21:05:28 [ash] great acestep1.what does it do?
21:05:56 [acestep1] just remb stimulates apoptosis
21:06:10 [acestep1] ;0
21:06:14 [ash] good
21:06:14 [acestep1]
21:06:23 [dr_yasir] it will either cause repair and if cant b repaired then will cause apoptosis me thinks
21:06:31 [Lorena] the guardin of the genome, check for errors and if they cannot be repared stimulates apoptosis
21:06:33 [hutals] p53 supressor gene inhibits ....allows DNA repair in cell or cell undergoes apoptosis
21:06:38 [ash] right yasir
21:06:54 [acestep1] also i think lack of harmone cytokines will do the same
21:07:10 [ash] which is the gene of youth?
21:07:19 [acestep1] bax
21:07:25 [Lorena] bax
21:07:45 [BlakeH] bcl2????
21:07:57 [ash] what about bcl-2?
21:08:11 [ash] right blake
21:08:13 [hutals] real question had 18 yo in accident with an increase in CK of 1000x. What was the source of the CK?
21:08:19 [BlakeH] bcl2 inhibits apoptosis
21:08:24 [ash] muscle
21:08:27 [Lorena] bcl2 inhibits apoptosis
21:08:28 [jwls29] muscle damage
21:08:39 [Lorena] muscle
21:08:46 [acestep1] agree with lor n jwlz
21:08:46 [BlakeH] muscle , heart, brain
21:08:53 [dr_yasir] yess mucle i agre too
21:08:58 [BlakeH] muscle in this case
21:09:04 [dr_yasir] if its CK MB then its heart me thinks
21:09:28 [ash] agree with yasir
21:09:39 [Lorena] yes
21:09:40 [hutals] i agree that it was from muscle in this 18 yo since not likely to be from heart in such a young pt
21:10:03 [BlakeH] CCL4 poisoning????
21:10:31 [acestep1] liver damage?
21:10:33 [dr_yasir] i think liver ca
21:10:46 [jwls29] agree with liver
21:11:01 [BlakeH] right
21:11:01 [ash] ccl4 poisoning causes hepatic damage.dry cleaners .free radical damage
21:11:02 [hutals] agree, liver
21:11:16 [Lorena] ok
21:11:40 [hutals] what happens to other kidney if one is damaged or removed?
21:11:41 [BlakeH] girl with painful mass in breast after an accident????
21:11:58 [dr_yasir] and also kidney toxicity
21:11:58 [Lorena] fat necrosis
21:11:58 [jwls29] traumatic fat necrosis
21:12:01 [BlakeH] hypertrophy???
21:12:12 [jwls29] it hypertrophies
21:12:23 [hutals] yes, hypertrophy
21:12:26 [Lorena] agree
21:12:28 [BlakeH] right
21:12:36 [acestep1] agree - lor
21:12:46 sweta_med enters this room
21:13:05 [sweta_med] hi everyine
21:13:10 [hutals] first sign of tissue hypoxia in tissue?
21:13:11 [jwls29] hi sweta
21:13:13 [Lorena] hi sweta
21:13:17 [hutals] hey sweeta
21:13:25 [Lorena] swelling?
21:13:30 [sweta_med] i would just observe today
21:13:34 [BlakeH] what kind of necrosis is seen in immune mediated vascular damage?????
21:13:34 [acestep1] er swelling ?
21:13:35 [jwls29] cyanosis
21:13:52 [Lorena] fibrinoid
21:13:53 [ash] what will increase circulating absulute neutrophil count and what will decrease it?
21:14:03 [ash] fibrinoid
21:14:10 [BlakeH] right lor
21:14:11 [hutals] cell swelling because of inactivation of Na/K ATPase pump (water follows Na into cell)
21:14:11 [jwls29] fibrinoid necrosis,blake
21:14:18 [BlakeH] yes
21:14:24 [dr_yasir] acute infec
21:14:37 [Lorena] increase with corticoids
21:14:37 [dr_yasir] will inc
21:14:52 [ash] infection causes left shift
21:15:09 [ash] right lorena
21:15:16 [ash] and decrease?
21:15:19 [hutals] agree with lor
21:15:34 [hutals] alcohol gives neutropenia
21:16:02 [acestep1] agree
21:16:30 [ash] decrease is seen with endotoxins as they increase the production of adhesion molecules
21:16:41 [Lorena] agranulocytosis, drugs, .....
21:17:03 [Lorena] thanks ash
21:17:10 [acestep1] ic
21:17:42 [ash] you r welcome
21:17:51 [Lorena] what IL increases expression of adhesion molecules?
21:18:07 [ash] how is emigration possible by cancer cells?
21:18:15 [acestep1] il1
21:18:17 [hutals] IL 1
21:18:19 [Lorena] in organs with dual supply
21:18:23 [ash] 1
21:18:32 [ash] liver
21:18:33 [Lorena] cancer cells have collagenases
21:18:51 [dr_yasir] iL8
21:18:52 [ash] right lorena
21:19:12 [hutals] chemotaxis mediators?
21:19:16 [Lorena] like intestine can have hemorrhagic infarct
21:19:18 [ash] esp. type 4 collagenase
21:19:20 [BlakeH] right'
21:19:36 [jwls29] testicle can have hemorrhagic infarct
21:19:47 [BlakeH] bowel, lungtestes
21:19:57 [acestep1] il8, bact lysis prod, anaphylotoxins
21:20:10 [Lorena] chemotaxis: c5a, IL8
21:20:14 [ash] n-formyl methionine,ltb4,c5a,il-8,pdgf
21:20:29 [Lorena] leukotriene B4
21:20:34 [BlakeH] kid who umbilical cord doesnt fall???? what is the defect?????
21:20:50 [jwls29] adhesion molecule defect
21:20:55 [ash] chediac higashi
21:21:01 [Lorena] adhesion molecule defects for a mutation in adhesion molecules
21:21:03 [hutals] C5a, LTB4, bacterial products are the ones i have.....probably also the ones listed....good job
21:21:12 [acestep1] ok which drug inhibits lb4?
21:21:13 [BlakeH] right jwls
21:21:34 [ash] corticosteroids
21:21:44 [Lorena] zileuton?
21:21:47 [ash] by inhibiting phospholipase
21:21:55 [BlakeH] zileuton
21:22:00 [acestep1] colchicin as well
21:22:23 [acestep1] v gd all three - steriods, ziluten n colchicin
21:22:43 [Lorena] what about zafirlukast?
21:22:56 [BlakeH] what pathways links factor XII????
21:23:19 [hutals] zarfirlukast inhibits the receptor
21:23:28 [acestep1] agree tht 2- lor
21:23:37 [Lorena] yes good ace
21:23:51 [Lorena] good hutals
21:23:51 [dr_yasir] u pplz are not discussing pathology me think
21:23:53 [acestep1] thanks
21:24:43 [hutals] thats because golijans notes go beyond path and links all subjects together
21:25:13 [Lorena] the intrinsic one?
21:25:31 [ash] appendicitis is most similar to which necrosis?
21:25:37 [jwls29] agree with lore
21:25:54 [BlakeH] Factor XII links kinin ,coagulation , plasminogen and complement system
21:26:07 [BlakeH] licuefactive
21:26:10 [acestep1] gangrene
21:26:29 [acestep1] agree- blake
21:26:39 [Lorena] agree liquefactive
21:26:56 [jwls29] liquefactive
21:27:08 [ash] right .liquifactive
21:27:41 [ash] what happens to rbcs upon loss of isotonic fluid?i
21:28:35 [dr_yasir] nothing
21:28:39 [Lorena] no change
21:28:50 [jwls29] agree
21:29:37 [BlakeH] agree
21:29:37 [ash] come on guys there is a change and it is not in size.
21:29:57 [dr_yasir] dec in hematocrait ?
21:30:42 [ash] ok, rouleaux formation is the answer
21:30:51 [Lorena] hemoconcentration?
21:30:52 [dr_yasir] n what u are asking is physiology
21:31:15 [BlakeH] also seen in multiple mieloma due to viscosity
21:31:23 [Lorena] ok
21:31:27 [ash] yasir this is g o l j a n.
21:31:44 [ash] in the exam they will mix patho with physio
21:31:58 [ash] right blake
21:32:02 [Lorena] very good thanx
21:32:09 sweta_med enters this room
21:32:13 [dr_yasir] oh i am sory actualy i read <a target=new href=http://click.linksynergy.com/fs-bin/click?id=c97WUMRO5hY&offerid=47491.10002441&type=3&subid=0 ><a target=new href=http://click.linksynergy.com/fs-bin/click?id=c97WUMRO5hY&offerid=47491.10002441&type=3&subid=0 >Kaplan</a><IMG border=0 width=1 height=1 src=http://ad.linksynergy.com/fs-bin/show?id=c97WUMRO5hY&bids=47491.10002441&type=3&subid=0 ></a><IMG border=0 width=1 height=1 src=http://ad.linksynergy.com/fs-bin/show?id=c97WUMRO5hY&bids=47491.10002441&type=3&subid=0 > i dont have <a target=new HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=<a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A>&mode=books><a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A></A> i wont disturb u pplz any more
21:33:23 [dr_yasir] i am sory i pasted by mistake
21:33:49 [Lorena] what pathway do you evaluate with PT? and which one with PTT?
21:33:52 [hutals] yasir, you should try to get your hands on goljans notes. they are very comprhensive for most high yield subjects and integrates them all together....but the problem is that they dont concentrate on path
21:33:54 [dr_yasir] actualy i was serching for <a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A> and by mistake i psted here
21:34:11 [BlakeH] Prostaglandin that causes pain in inflammation, keeps the ductus arterious open and helps form the barrier in the stomach???
21:34:40 [hutals] yasir, try not to post words like golijan, first aid, etc or you will get a link instead
21:34:40 [Lorena] pGE
21:34:56 [hutals] extrinsic for PT and intrinsic for PTT
21:34:57 [dr_yasir] oh ok
21:35:06 [acestep1] n pgi2
21:35:12 [BlakeH] right Lor PGE2
21:35:13 [dr_yasir] i didnt knew i am sory
21:35:16 [Lorena] yes hutals
21:35:20 [acestep1] agree- hutals
21:35:45 [hutals] no prob yasir....we all type those by mistake
21:36:16 [hutals] i remember it as PeT and PiTT (pet and pittsburg)
21:36:38 [ash] thanks hutals
21:36:42 [Lorena] PGE2 also dilates aferent arteriole in kidney
21:36:50 Newone enters this room
21:36:56 [acestep1] agree with lor
21:37:02 [BlakeH] pettin a pittbull!!!
21:37:08 [hutals] hey newone
21:37:08 [acestep1] whta bt pge1
21:37:21 [hutals] good one blake
21:37:26 [acestep1] wht abt pge1 imean
21:37:28 [Newone] hello all
21:38:00 [jwls29] hello newone
21:38:03 [Lorena] hi newone
21:38:25 [Lorena] i dont remember PGE1 ace
21:38:40 [acestep1] np
21:38:43 [ash] pge2 is also natriuretic
21:38:49 [Lorena] is it protacyclin?
21:38:57 [ash] hi newone
21:39:05 [acestep1] i think pge1 mediates pain n causes abortion
21:39:27 [acestep1] prostacylcin-pgi2
21:39:37 [ash] leukoterine that is a vasodilator?
21:39:51 [BlakeH] renal tubular cells are what kind cells accordin to teir regeneration?????
21:40:08 [acestep1] ok misoprostol - analog of wht pg
21:40:18 [Lorena] PGI is prostacyclin and causes vasodilation and inhibits platelet agregation
21:40:28 [acestep1] lt r vasoconstrictors i think
21:40:40 [acestep1] agree - lor
21:40:55 [ash] ace-pgf2alpha????
21:40:59 [Lorena] PGF? the one that causes dysmenorrhea?
21:41:16 [acestep1] nono ash
21:41:24 [BlakeH] PGI is vasodilator and inhibits platelet aggregation
21:41:38 [acestep1] agree both f2 n e1
21:41:46 crusher enters this room
21:42:06 [hutals] PGE analog
21:42:17 [BlakeH] renal tubular cells are what kind of cells accordin to their regeneration?????
21:42:22 [Lorena] renal tubular cells are stable cells?
21:42:27 [acestep1] i think hutals is right- misoprostol
21:42:28 [ash] acemisoprostol+pg
21:42:30 [dr_yasir] mifoprostol
21:42:40 [BlakeH] right lor
21:42:45 [ash] sorry misprint
21:42:54 [acestep1] k
21:43:03 [acestep1] np
21:43:21 [Lorena] what is the only phase of the cell cycle that changes in length?
21:44:21 [ash] go
21:44:42 [Lorena] i meant the most variable
21:45:00 [BlakeH] S??
21:45:14 [Lorena] G1
21:45:32 [BlakeH] skeletal muscle cells is what kind of cell???
21:45:39 [BlakeH] thxs Lor
21:45:40 [acestep1] k
21:45:52 [Lorena] permanent
21:46:08 [acestep1] agree
21:46:27 [crusher] permanant
21:46:28 [BlakeH] also wit neurons and myocardial
21:46:44 [hutals] skeletal are permanent cells
21:46:49 [BlakeH] neuronal exception to that?????
21:47:11 [ash] microglia
21:47:25 [BlakeH] microglia are not neurons
21:47:47 [BlakeH] microglia are macrophages of CNS
21:48:22 [Lorena] thanks blak
21:48:48 [ash] thnx
21:48:56 [BlakeH] only neurons that divide are the ones in the olphatory epithelium
21:49:25 [ash] thnx blake
21:49:51 [acestep1] k
21:50:04 [BlakeH] composition of a granuloma?????
21:50:48 [hutals] pt gets recurrent infections to staph aureus, has a negative NBT test.....what diagnosis?
21:50:57 [crusher] epitheloid cells....giant cells
21:51:07 [Lorena] epithelioid cells,
21:51:15 [acestep1] cgd
21:51:22 [ash] macrophages-epitheloid cells,giant cells
21:51:24 [crusher] NAHPH oxidase def
21:51:25 [Lorena] CGD
21:51:31 [ash] cd8 t cells
21:51:47 [acestep1] agree epitheliod cells giant cells n fibroblast
21:52:06 [acestep1] epitheloid - diagnostic
21:52:18 [ash] if caseus then lipid debris in center
21:52:27 [Lorena] what is an epithelioid cell?
21:52:40 [hutals] yep, CGD deficiency or NADPH oxidase deficiency which will lead to an absent resp burst.....negative NBT test
21:52:42 [ash] macrophage
21:53:06 [acestep1] fused macro - multinucleated
21:53:14 sweta_med enters this room
21:53:17 [BlakeH] multiple macrophages joined together
21:53:22 [Lorena] yes ash
21:53:48 [Lorena] when epithelioid cells fuse then become a giant cell
21:54:06 [dr_yasir] multiple macrophages joined together are the giant cells
21:54:14 [hutals] which cells are prominent in acute inflammation? what about chronic inflammation?
21:54:19 [Lorena] epithelioid cell is a macrophage that has been stimulated by IFN gamma
21:54:21 [BlakeH] Langhans giant cells
21:54:47 [acestep1] agree- lor
21:54:54 [dr_yasir] epitheliod cells are the lymphocytes i think
21:54:55 [BlakeH] acute = neutrophils, mast cells
21:55:01 [Lorena] acute:neutrophils
21:55:05 [crusher] acute ..neutrophils...chronic machrohages
21:55:15 [BlakeH] chronic = mononuclear cells
21:55:23 [acestep1] agree- crusher
21:55:30 [hutals] neutrophils are key cells in acute inflammation and monocytes/macrophages are key cells in chronic inflammation.....very good
21:55:31 [Lorena] chronic: lymphocites (Th1)
21:56:25 [BlakeH] 5 causes of granulomatous inflammation???
21:56:31 [hutals] lymphocytes are primary inflammatory cell in what type of infections?
21:56:37 [Lorena] oh sorry lymphocytes Th1 is in retarded hypersensitivty
21:56:48 [jwls29] viral infections
21:57:06 [Lorena] viral
21:57:15 [crusher] yes viral infections
21:57:16 [acestep1] all i guess but mainly viral n fungal
21:57:38 [hutals] yes, lyphocytes in viral infections. also in type 4 hypersens and pertusis infections
21:58:12 [acestep1] k
21:58:41 [hutals] TB granuloma is one
21:59:05 [Lorena] sarcoidosis, chrons. disease
21:59:07 [acestep1] viral fungal autoimmune, slow growing bact, foriegn body- blake
21:59:26 [hutals] type 4 hypersensitivity is another one i think
21:59:28 [Lorena] fungal diseases
21:59:42 [acestep1] hey guys i gtg . illsee u guys tom . tc all of u
21:59:42 [BlakeH] infectious ( TB, cat scratch, trponema), foreign bodies,sarcoiosis
21:59:49 [BlakeH] right guys
21:59:58 [jwls29] bye ace
22:00:11 [Lorena] take care ace
22:00:11 [acestep1] bye jwls
22:00:25 [acestep1] bye lor
22:00:39 [ash] bye
22:00:42 [BlakeH] gotta go to guys
22:00:47 [BlakeH] a tomorrow
22:00:49 [hutals] are we done?
22:00:52 [BlakeH] c ya
22:01:02 [jwls29] bye blake
22:01:15 [hutals] ok, well thanks for chatting. c ya all tomorrow
22:01:28 [Lorena] i can stay longer
22:01:30 [ash] we havent touched the 3 rd chapter yet
22:01:40 [Lorena] if you have more q's
22:01:45 [ash] me too
22:01:47 [jwls29] i can stay longer too
22:02:07 [Lorena] cool lets continue then
22:02:15 [ash] lets wait for some more time
22:02:15 [hutals] oh, ok, i thought everyone was leaving....sorry
22:02:25 [ash] great
22:02:31 [dr_yasir] and i will watch u guys
22:03:24 [ash] what are dohle bodies?
22:03:24 [Lorena] important cofactors in collagen sx?
22:03:38 [ash] copper,vit.c
22:03:48 [dr_yasir] cu
22:03:49 [ash] and zinc
22:04:12 [Lorena] very good
22:05:05 [dr_yasir] vit c for hydoxilation and cu for collagen chain arrangement am i right?
22:05:12 [ash] what are dohle bodies?
22:05:19 [Lorena] what are they ash? dohle?
22:05:20 [dr_yasir] hydroxilation of proline residues
22:06:01 [Lorena] yes yasir
22:06:05 [ash] dohle bodies are gray cytoplasmic inclusions .they are dilated endoplasmic reticulum
22:06:30 [ash] copper is required for lysyl oxidase
22:06:43 [Lorena] in what disorder are they present?
22:06:48 [ash] type of collagen in keloid?
22:07:06 [Lorena] type III
22:07:14 [dr_yasir] yes u are rigth ash
22:07:52 [hutals] type3
22:08:10 [Lorena] where is lysil oxidase? RER?or extracellular space?
22:08:40 [hutals] what type of cancer is a keloid predisposed to?
22:08:58 [Lorena] squamous
22:08:58 [ash] right
22:09:31 [hutals] yes, squamous, particularly if due to third degree burns
22:09:40 [ash] lorena they are not in a disorder i know of.they are normally seen
22:09:56 [ash] in neutrophils
22:10:06 [Lorena] oh ok thanks ash
22:10:07 [hutals] is a keloid hyperplasia, hypertrophy, metaplasia, dysplasia?
22:11:05 [dr_yasir] its a hyperplastic scar tissue
22:11:18 [Lorena] hyperplasia?
22:11:19 [hutals] keloids are hypertrophic scar tissue......resembles a tumor and is often seen in african americans
22:11:40 [ash] in another book i have read they are depolymerised ribosomes
22:11:55 [hutals] i would have thought hyperplasia also, but golijan has it as hypertrophy??
22:12:35 [dr_yasir] in robin its writen hyperplastic me thinks
22:12:44 [Lorena] ok thanx
22:13:12 [hutals] maybe its a typo in golijans because it seems like it should be hypertrophy
22:13:23 [hutals] ooops i mean seems like hyperplasia
22:14:21 [Lorena] ok
22:14:39 [hutals] but that brings up another confusing misconception.....is BPH hypertropy or hyperplasia?
22:15:12 [ash] bph is hyperplasia as it is a glandular tissue
22:15:14 crusher enters this room
22:15:20 [dr_yasir] thats hypertrophy but its actualy hyperplasia
22:15:26 [Lorena] hyperplasia
22:15:46 [dr_yasir] its called hypertrophy but its hyperplasia
22:16:49 [hutals] i agree. i think the old timers used to think it was hypertrophy and the name stuck, but now it is known as hyperplasia....i think
22:17:26 [dr_yasir] yess i am sure abut it
22:17:32 sweta_med enters this room
22:17:36 [Lorena] what part of the nephron is more susceptible to hypoxia?
22:18:36 [dr_yasir] early convuluted ??
22:19:04 [ash] medullary
22:20:00 [ash] what will happen to the esr in iron deficiency anemia and sickle cell anemia?
22:20:01 [Lorena] the proximal tubule i think
22:20:37 [hutals] decreased esr
22:20:46 [hutals] in sickle cell anemia
22:21:00 [Lorena] ESR is decreased in sickle cell
22:21:32 [ash] what abt iron def?
22:22:21 [hutals] anemia enhances settling, so inc esr is my guess
22:22:29 [Lorena] increased in anemia
22:22:38 [dr_yasir] i think it dec ub iron def and inc in sickle
22:23:19 [ash] right hutals and lorena
22:23:56 [dr_yasir] ok
22:23:57 [ash] what cells contain weibel palade bodies and what do these bodies store?
22:24:51 [Lorena] contain vW factor
22:25:04 [ash] correct
22:25:15 [ash] and what cells?
22:25:20 [dr_yasir] in microcytic anemia its dec in ESR
22:25:24 [Lorena] they can be seen in angiosarcoma of the liver
22:25:45 [hutals] endothelial cells
22:25:51 [Lorena] they are endothelial cells
22:26:24 [ash] right
22:26:52 [hutals] i dont see how microcytic anemia would decrease the ESR?
22:27:03 [ash] where did you read it yasir?
22:27:25 [dr_yasir] A common cause of high ESR is anemia, especially if it is associated with changes in the shape of the red cells; however, some changes in red cell shape (such as sickle cells in sickle cell anemia) lower ESR
22:29:44 [dr_yasir] may b i have mistaken
22:29:52 [Lorena] ok folks, i have to go now
22:30:01 [dr_yasir] i will watch it later
22:30:03 [hutals] that is what we are saying.....sickle cell anemia lowers the ESR, but iron deficiency anemia will increase ESR.....am I reading that right?
22:30:36 [hutals] maybe I'm misunderstanding it
22:30:50 [Lorena] byeee
22:31:07 [ash] yasir has made a very good point here
22:31:12 [hutals] ok lorena, i will be going too. will you post the transcript?
22:31:18 [dr_yasir] bbye lorena
22:31:19 [ash] bye lorena
22:31:29 [dr_yasir] hutals
22:31:57 [hutals] nite lorena
22:31:58 [ash] i agree with yasir for microcytes it is decrease esr.
22:32:09 [ash] ok goodnite all.
22:32:21 [hutals] nite yasir, ash, and everyone else
22:32:49 [dr_yasir] no its inc in esr with microcytic
22:33:14 [dr_yasir] and dec in esr with sickle cell
22:34:46 [hutals] http://www.danielballarin.com/esr.htm
22:34:50 [dr_yasir] looks like every one off the net ???????
22:35:15 [hutals] that gives more info on the ESR and the causes of inc vs dec
22:36:07 [dr_yasir] thanks for the link hutals
22:36:34 [hutals] no prob. nite and c ya tomorrow
22:36:46 [jwls29] what is that link for
22:36:54 [jwls29] i'm sorry i was gone
22:37:18 [dr_yasir] ok u take care too hutals thanks
22:37:36 [hutals] the link is for further info on ESR since we were confused about what causes an increase vs a decrease jwls
22:37:54 [jwls29] thanks guys
22:38:00 [jwls29] i'm leaving now
22:38:05 [hutals] ok, bye
22:38:08 [jwls29] is someone going to post the transcript?
22:39:33 [jwls29] this was a very good chat. Let's keep it up...i'll see you all tomorrow
22:39:52 [dr_yasir] bye jwls
22:40:07 [jwls29] who is posting the transcript?
22:40:21 [hutals] i was hoping that lorena would post it, but i'll post it if she doesn't.
22:40:34 [dr_yasir] tell me how to post i will do it
22:40:40 [jwls29] ok...she's gone
22:40:47 [jwls29] i don't know how
22:40:55 [jwls29] goodnite
22:41:11 [hutals] yep, i was just checking to see if she posted it.....i dont see it so i will post it.....nite
20:08:31 [hutals] what are some causes of hypoxemia?
20:08:40 [drymalik] ok
20:09:08 [Lorena] increase altitude
20:09:35 [drymalik] carbon mono oxide poisoning ,
20:09:46 [ninadnashua] respiratory acidosis, ventilation difusion perfusion problems
20:10:01 [Lorena] ops closed the window accidentally
20:10:14 [ninadnashua] methemoglobinemia
20:10:41 [ninadnashua] lalso left shift of oxygen curve
20:10:55 [hutals] the 4 causes of hypoxemia are resp acidosis, vent problems, perfussion problems and diffusion problems. increased altitude can cause resp acidosis....so that would be correct as well. CN poisoning i will need to check on
20:11:08 jwls29 enters this room
20:11:13 [Lorena] agree
20:11:17 [jwls29] hi all
20:11:27 BlakeH enters this room
20:11:39 [drymalik] ok
20:11:42 [ninadnashua] ya
20:11:46 [Lorena] hi jwls and blake
20:12:14 [BlakeH] hello all
20:12:14 [hutals] hypoxemia by definition has a decreased PaO2 and CO poisoning would have normal PaO2, so it would not cause hypoxemia
20:12:34 [hutals] hey jwls and blake
20:12:51 [drymalik] ahan thanks for correction
20:12:58 [Lorena] ok
20:13:25 [hutals] no prob....i thought it would cause it also, but had to look it up to make sure
20:13:34 zoya enters this room
20:14:01 [hutals] what causes right shifted oxygen curve?
20:14:10 [hutals] hey zoya
20:14:28 [zoya] hi
20:14:42 [drymalik] inc ph
20:14:46 [jwls29] hi zoya
20:14:55 [drymalik] inc 2-3 BP glycerate
20:14:57 [jwls29] increased 2,3 dpg
20:15:06 [jwls29] fever
20:15:07 [BlakeH] Increased co2
20:15:08 [Lorena] temperature, 23DPG
20:15:16 [ninadnashua] fever acidosis increase 2 3 dpg
20:15:21 [drymalik] yah temp too
20:15:23 [jwls29] decreased ph (acidosis)
20:15:34 [jwls29] high altitude
20:15:36 [drymalik] sory
20:15:36 [Lorena] inc CO2, decreased pH
20:15:59 [zoya] hi,jwls
20:16:19 [BlakeH] increased H+
20:16:23 [hutals] for right shift it has decreased affinity for O2 and readily releases the )2 into blood. think of excercising mucle.....dec pH from lactic acid and incr PCO2, inc 2,3 BPG from inc glycolysis, inc temp. also high altitude.....very good everyone
20:18:08 [Lorena] type of coagulation in sarcoidosis?
20:18:37 [ninadnashua] non caseating
20:18:50 [hutals] non caseating
20:19:01 [Lorena] yes, very good
20:19:50 [hutals] inhibitors of cytochrome oxidase? hint- mneumonic 3 C's
20:19:53 [BlakeH] point of no return in cell injury???
20:19:55 [Lorena] even if they form granulomas, it is not caseous -caseous is almost exclusively for mycobacterium
20:20:15 kiranadi enters this room
20:20:27 [Lorena] cyanide?
20:20:29 [jwls29] and systemic fungal infections
20:20:37 [kiranadi] hi
20:20:37 [ninadnashua] yes because they have lipids mycolic acid un cell wall
20:20:47 [BlakeH] cyanide is one
20:21:14 [jwls29] carbon monoxide
20:21:14 [hutals] Cytochrome oxidase inhibitors are Cyanide and Carbon monoxide
20:21:20 [kiranadi] why was the chat stopped in the middle?????????????/
20:21:37 [kiranadi] i'm sorry for interrupting
20:21:45 [hutals] hey kiranadi
20:21:45 [Lorena] what is the other C?
20:22:23 [kiranadi] hi hutals....saw ur post in another forum and joined here
20:22:28 [Lorena] hi kiran
20:22:43 [hutals] 3 C's are the first for Cyt ox, 2. Cyanide, 3. Carbon monoxide.....one is the cyt ox itself
20:22:55 [jwls29] you think maybe rizwana is lost?
20:23:03 [Lorena] ah ok thanks hutals
20:23:08 [ninadnashua] ya
20:23:10 [jwls29] no one else in the general chat room
20:23:16 [hutals] glad the post led u here
20:23:18 [kiranadi] hi lorena
20:23:36 [BlakeH] point of no return in cell injury???
20:23:36 [drymalik] what are the diagnostic features of sarcoidosis
20:23:45 [hutals] someone is in the gen chat....maybe lost??
20:23:52 [kiranadi] yes
20:24:02 [jwls29] disruption of cell wall
20:24:08 [jwls29] membrane i meant
20:24:17 [BlakeH] ACE+, bilateral pehillar lymph nodes( potato nodes)
20:24:23 crusher enters this room
20:24:41 [hutals] someone who came in late should try to get that person because the beginning of chat will be lost if i go to get rizwana
20:24:48 [Lorena] agree with jwls
20:25:02 [hutals] hey crusher
20:25:03 [crusher] hello all
20:25:05 [drymalik] wait me go
20:25:06 [jwls29] rizwana> rizwana hi are you looking for the path chat?
20:25:13 drymalik exits from this room
20:25:15 [jwls29] that didn't work
20:25:31 [jwls29] hi crusher
20:25:32 [Lorena] hi crush
20:25:44 [jwls29] brb
20:25:47 [ninadnashua] hi crush
20:26:05 [hutals] non caseating bilater hilar something also are buzz words for sarcoid...right?
20:26:06 [zoya] hi crusher
20:26:13 [crusher] hello everybody
20:26:34 [BlakeH] bilateral pehillar lymph nodes( potato nodes)
20:26:39 [ninadnashua] ya
20:26:48 [Lorena] thanks blake
20:26:51 acestep1 enters this room
20:27:04 [BlakeH] ok
20:27:16 [Lorena] hi ace
20:27:23 [hutals] i'm counting on multiple choice recognition to help me remember those types of words
20:27:28 [hutals] hey ace
20:27:50 drymalik enters this room
20:27:52 [BlakeH] changes seen in irreversible injury???
20:27:52 [acestep1] hi lor n hutals
20:28:10 [acestep1] how r u guys
20:28:17 [jwls29] disruption of cell membrane
20:28:26 [zoya] definitive dx requires biopsy demonstrating noncaseating granulomas
20:28:27 [Lorena] calcium , membrane damage
20:28:29 [jwls29] damage to mitochondria
20:28:41 [hutals] thanks for going to help rizwana drymalik
20:28:45 [jwls29] calcium influx
20:28:46 [Lorena] nuclear changes
20:29:07 [jwls29] nuclear changes
20:29:20 [jwls29] pyknosis
20:29:25 [drymalik] i left messege there but no reply from rizwana
20:29:25 [hutals] doing good ace, great to see you
20:29:26 [jwls29] karryorexis
20:29:33 [BlakeH] piknosys, karorrhexis, karyolysis are the nuclear changes
20:29:40 [jwls29] karyolysis
20:29:43 [Lorena] intreacellular enzymes leak
20:29:49 [acestep1] agree with jwls n lor n also lysozymal enzyme leakage
20:29:49 [hutals] no prob....at least we tried drymalik
20:29:53 [BlakeH] right
20:30:12 [drymalik] piknosys, karorrhexis, karyolysis are the nuclear changes arent they the nuclear changes in apoptosis?
20:30:28 [acestep1] is this colour ok ?
20:30:33 [BlakeH] can u change ur color acestep1]
20:30:43 [BlakeH] they are also seen in necrosis
20:31:01 [Lorena] in apoptosis the chromatin is condensed and fragmented -more organized
20:31:17 [acestep1] hmm i think in apoptosis u ahve muclear n cytoplasm condensation n then both break
20:31:26 [jwls29] form apoptotic bodies
20:31:40 [jwls29] from cellular memb blebs
20:31:49 [acestep1] agree with lor n jwls
20:32:07 [Lorena] and no inflamatory process ina poptosis
20:32:22 [jwls29] very important
20:32:43 [drymalik] ok so we discussed apoptosis too
20:32:45 [jwls29] examples of apoptosis?
20:32:55 [acestep1] agree . aslo its genetic n only 1 cell or a small # die
20:33:06 [drymalik] development of embryo
20:33:08 [hutals] an important point from earlier that i forgot to mention was that fever right shifts the curve to make O2 more available in blood to help fight infection. As docs, we always try to take away this natural defense mech by taking away the fever....golijan made a point about that and found it importan
20:33:11 [BlakeH] menstrual period
20:33:17 [acestep1] agree - dry
20:33:18 [Lorena] in embnryonic life ,
20:33:39 [jwls29] thanks hutals
20:33:47 [acestep1] viral inf
20:33:52 [BlakeH] thymus. mullerian duct. wolffian duct
20:34:05 [jwls29] yes
20:34:17 [acestep1] ty - hutals
20:34:25 [BlakeH] genes regulatin apoptosis????
20:34:34 [hutals] no prob
20:34:35 [drymalik] councilman bodies in viral hepatitis
20:34:37 [Lorena] thanks
20:34:42 [acestep1] yes
20:34:58 [Lorena] Rb, p53, bcl
20:35:16 [acestep1] when p53 leaks out n cytochrome c lost .
20:35:19 [BlakeH] right
20:35:22 [drymalik] and cystic fibrosis
20:35:38 [acestep1] agree with lor . aslo bax gene the youth gene
20:35:43 [jwls29] caspases set into motion cell death
20:35:48 [BlakeH] bcl2 inhibits apoptosis, overexpressed in follicular lymphoma
20:36:03 [jwls29] agree with blake
20:36:05 [acestep1] k
20:36:31 [Lorena] ok
20:36:40 [BlakeH] p53 facilitates apoptosis, seen in many tumors ( Li- Fraumeni Sx)
20:37:14 [hutals] did anyone mention psammoma bodies for example of pathologic role of apotosis
20:37:23 [Lorena] diference between dystrophic and metastatic calcification?
20:37:55 [jwls29] dystrophic is seen in tissue already damaged with a normal serum calcium and phosphorus
20:38:10 [Lorena] psamomma bodies are an example of dystrophic calcification seen in papillary tumors of the thyroid , ovaries and meningioma
20:38:15 [BlakeH] metastatic is due to high Ca and dystropic is calcificat in a previously damage tissue
20:38:18 [jwls29] metastatic is seen on normal tissue with high calcium and phosphorus
20:38:38 [Lorena] very good
20:39:12 [hutals] D-ystrophic is in D-amaged tissue and metastatic is in normal tissue
20:39:28 [Lorena] examples of dystrophic calcification?
20:39:43 [Lorena] M-etastatic is M-etabolic
20:39:56 [jwls29] atherosclerotic plaques,
20:39:57 calender enters this room
20:40:02 [BlakeH] valve calcification
20:40:10 [hutals] atherosclerosis, psammoma bodies
20:40:14 [jwls29] damaged cardiac valves
20:40:22 [ninadnashua] enzymatic fat necrosis
20:40:24 [acestep1] good one lor
20:40:32 [hutals] hey calendar
20:40:37 [drymalik] arthrosclerotic plaques
20:40:51 [Lorena] hi calender
20:40:52 [ninadnashua] cmcongenital cmv
20:41:03 [Lorena] good everyone
20:41:09 [jwls29] calcification in CMV
20:41:50 [hutals] what is the best screening test for iron disorders?
20:42:03 [jwls29] serum ferritin
20:42:05 tomilola enters this room
20:42:06 [ninadnashua] also tuberculous lesions
20:42:11 [BlakeH] vitamin deficit assoc wit squamous metaplasia???? examples????
20:42:27 [hutals] hey tomilola
20:42:31 [calender] hi Lorena
20:42:40 [jwls29] vit a, i think
20:42:42 [hutals] yes, serum ferritin is correct
20:42:43 [Lorena] vit a deficiency ?
20:42:53 [hutals] agree, vit a
20:43:04 [tomilola] ?
20:43:10 [BlakeH] right...examples???
20:43:49 [Lorena] glossitis
20:44:09 [acestep1] lung ca
20:44:15 [BlakeH] examples of squamous metaplasia???
20:44:16 tomilola exits from this room
20:44:17 tomilola exits from this room
20:44:30 [BlakeH] right
20:44:30 [ninadnashua] squamous epithelium in mainstem bronchus
20:44:50 [hutals] oxygen toxicity in newborn causes superoxide FR damage.....retrolental fibroplasia, leads to blindness in newborns....is that an example??
20:44:53 [acestep1] also i think in kidney
20:44:53 [BlakeH] squamous epithelium in cervix
20:44:56 [Lorena] oh ok
20:45:21 [acestep1] agree- hutals
20:46:28 [BlakeH] oxygen tox can lead to retrolental fibroplasia and to????
20:46:30 [hutals] bladder transitional epithelium in schistosomiasis
20:46:45 [jwls29] necrotizing enterocolitis
20:47:53 [zoya] hutal, what <a target=new HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=<a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A>&mode=books><a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A></A> notes/book are you guys following? sorry for th interruption .......cause i have <A HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Board%20Review%20Series&mode=books><A HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Board%20Review%20Series&mode=books>BRS</A></A> path........i was planning to get <a target=new HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=<a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A>&mode=books><a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A></A> ............but there are so many options ........i am a bit confused....again sorry for th interruption
20:48:19 [Lorena] oh my God
20:48:33 [BlakeH] lol
20:48:43 [zoya] opps....sorry
20:48:47 [Lorena] lol
20:48:50 [jwls29] blake is that right?
20:48:58 [hutals] zoya, try not to type words like b r s, golijan, , etc
20:49:08 [jwls29] necrotizing entercolitis and subarachanoid hemorrhage?
20:49:26 [BlakeH] haven heard of those
20:49:27 [zoya] ok.............soooooooooooooorrrrrrrrrrry
20:49:42 [BlakeH] alveolar damage =ARDS
20:49:43 [jwls29] that's in a premature infant
20:49:44 [Lorena] it sounds logic because of reperfusion injury
20:49:52 [jwls29] sorry mixing step 2 with step 1
20:49:52 [BlakeH] oh ok
20:49:54 [hutals] no prob....we've all done it before....and probably will again
20:50:04 [BlakeH] its true
20:50:30 [Lorena] thanks jwls
20:50:43 [jwls29] no prob
20:50:56 [BlakeH] greatest suceptibility to hypoxia????
20:51:05 [BlakeH] cell??
20:51:13 [Lorena] what is reperfusion injury?
20:51:41 [hutals] zoya, i think you're asking about which golijan notes we're using? i'm using his 500 pg lecture notes. some others might be using other things from him....they're all good and follow more or less the same concepts
20:51:49 [zoya] thanks
20:53:06 [hutals] atherosclerosis?
20:53:53 ash enters this room
20:54:03 [BlakeH] what cell has the greatest suceptibility to hypoxia???
20:54:05 [hutals] oh, i just saw the "cell" part of your question blake....nevermind my ans
20:54:20 [hutals] hey ash
20:54:26 [ash] hi all
20:54:31 [Lorena] neuron
20:54:35 [BlakeH] no prob
20:54:36 [jwls29] reperfusion injury is when there has been ischemiaand then blood flow is restored to the area
20:54:37 [hutals] red blood cell??
20:54:38 [Lorena] hi ash
20:54:45 [ash] sorry i am so late
20:54:59 [BlakeH] what neuronal cell???
20:55:02 [jwls29] there is too much oxygen in a tissue that was already deprived
20:55:32 [jwls29] hi ash
20:55:35 [hutals] nope....thinking out loud, but that can't be it because the RBCs dont require O2
20:55:36 [acestep1] purkinje
20:55:44 [Lorena] yes jwls because the sudden increase in oxygen causes increase in reactive oxygen species and catalase gets overwhelmed and cannot reduce all the oxygen
20:55:56 [ash] the tissue plasminogen activator will form toxic o2 radicals on reperfusion
20:55:57 [BlakeH] right acestep1
20:56:29 [acestep1] tpa will form free radicals?
20:56:38 [BlakeH] purkinje an hippocampus cells
20:56:56 [hutals] cyanosis not relieved by oxygen in a pt coming home from a camping trip in the Rocky mountains?
20:56:58 [Lorena] thanks ace and blake
20:57:25 [jwls29] nitrates
20:57:30 [acestep1] ur welcome. anytime lor
20:57:40 [jwls29] reducing agent
20:57:41 [ash] thats what i heard in golj a n audio
20:57:51 [acestep1] lymes d/s
20:57:58 [acestep1] ic
20:58:17 [hutals] methemoglobinemia is correct. the water in the mountains has nitrites that oxidize iron to ferric condition
20:58:45 [Lorena] ok
20:58:45 [hutals] nitrates is also correct ans
20:58:57 [ash] what is the similarity between mallory body and lewy body?
20:59:26 [BlakeH] ubiquination????
20:59:39 [ash] good blake
20:59:40 [hutals] what would be the treatment for the pt with methemoglobinemia
20:59:41 [hutals] ?
21:00:01 [ash] methylene blue and vit. c
21:00:05 [jwls29] methylene blue iv and ascorbic acid as an ancillary treatment
21:00:08 [BlakeH] methilene blue
21:00:32 [acestep1] dunno
21:00:33 [Lorena] cells that are degenerating
21:00:40 [hutals] IV meth blue is gold standard and ascorbic acid (vit C) as ancillary tx....great!
21:00:43 [Lorena] agre methylene blue
21:00:47 dr_yasir enters this room
21:00:53 [ash] what is the difference between mallory body and councilman body?
21:01:29 [hutals] why would a pt with HIV have methemoglobinemia?
21:01:38 [Lorena] Councilman's bodies: apoptotic bodies of hepatocellular origin seen in viral hepatitis
21:01:43 [hutals] hey dr yasir
21:01:49 [jwls29] mallory body is alcoholic, and councilman body is viral
21:01:49 [BlakeH] councilman seen in hepatocyte apoptosis mallory in alcohol
21:01:59 [Lorena] and mallory are in alcoholic hepatitis?
21:02:01 [ash] because of sulfamethoxazole for pneumocystis carinii
21:02:13 [jwls29] a pt with Hiv would have methb b/c of tmp/sx for pcp
21:02:59 [hutals] very good jwls.....you were paying attention to papi
21:03:04 [ash] their basic structure is also different.mallory bodies are keratin aggregates and councilman bodies are apoptotic cells
21:03:05 [hutals] and ash
21:03:39 [jwls29] lol...yes i was
21:03:56 [ash] DNA injury will stimulate which gene normally?
21:04:00 [BlakeH] wear and tear pigment seen in elderlies???
21:04:16 [jwls29] lipofuscin
21:04:19 [Lorena] lipofuscin
21:04:38 [ash] agree lipofuschin
21:04:45 [BlakeH] right
21:05:04 [acestep1] p53-ash
21:05:28 [ash] great acestep1.what does it do?
21:05:56 [acestep1] just remb stimulates apoptosis
21:06:10 [acestep1] ;0
21:06:14 [ash] good
21:06:14 [acestep1]
21:06:23 [dr_yasir] it will either cause repair and if cant b repaired then will cause apoptosis me thinks
21:06:31 [Lorena] the guardin of the genome, check for errors and if they cannot be repared stimulates apoptosis
21:06:33 [hutals] p53 supressor gene inhibits ....allows DNA repair in cell or cell undergoes apoptosis
21:06:38 [ash] right yasir
21:06:54 [acestep1] also i think lack of harmone cytokines will do the same
21:07:10 [ash] which is the gene of youth?
21:07:19 [acestep1] bax
21:07:25 [Lorena] bax
21:07:45 [BlakeH] bcl2????
21:07:57 [ash] what about bcl-2?
21:08:11 [ash] right blake
21:08:13 [hutals] real question had 18 yo in accident with an increase in CK of 1000x. What was the source of the CK?
21:08:19 [BlakeH] bcl2 inhibits apoptosis
21:08:24 [ash] muscle
21:08:27 [Lorena] bcl2 inhibits apoptosis
21:08:28 [jwls29] muscle damage
21:08:39 [Lorena] muscle
21:08:46 [acestep1] agree with lor n jwlz
21:08:46 [BlakeH] muscle , heart, brain
21:08:53 [dr_yasir] yess mucle i agre too
21:08:58 [BlakeH] muscle in this case
21:09:04 [dr_yasir] if its CK MB then its heart me thinks
21:09:28 [ash] agree with yasir
21:09:39 [Lorena] yes
21:09:40 [hutals] i agree that it was from muscle in this 18 yo since not likely to be from heart in such a young pt
21:10:03 [BlakeH] CCL4 poisoning????
21:10:31 [acestep1] liver damage?
21:10:33 [dr_yasir] i think liver ca
21:10:46 [jwls29] agree with liver
21:11:01 [BlakeH] right
21:11:01 [ash] ccl4 poisoning causes hepatic damage.dry cleaners .free radical damage
21:11:02 [hutals] agree, liver
21:11:16 [Lorena] ok
21:11:40 [hutals] what happens to other kidney if one is damaged or removed?
21:11:41 [BlakeH] girl with painful mass in breast after an accident????
21:11:58 [dr_yasir] and also kidney toxicity
21:11:58 [Lorena] fat necrosis
21:11:58 [jwls29] traumatic fat necrosis
21:12:01 [BlakeH] hypertrophy???
21:12:12 [jwls29] it hypertrophies
21:12:23 [hutals] yes, hypertrophy
21:12:26 [Lorena] agree
21:12:28 [BlakeH] right
21:12:36 [acestep1] agree - lor
21:12:46 sweta_med enters this room
21:13:05 [sweta_med] hi everyine
21:13:10 [hutals] first sign of tissue hypoxia in tissue?
21:13:11 [jwls29] hi sweta
21:13:13 [Lorena] hi sweta
21:13:17 [hutals] hey sweeta
21:13:25 [Lorena] swelling?
21:13:30 [sweta_med] i would just observe today
21:13:34 [BlakeH] what kind of necrosis is seen in immune mediated vascular damage?????
21:13:34 [acestep1] er swelling ?
21:13:35 [jwls29] cyanosis
21:13:52 [Lorena] fibrinoid
21:13:53 [ash] what will increase circulating absulute neutrophil count and what will decrease it?
21:14:03 [ash] fibrinoid
21:14:10 [BlakeH] right lor
21:14:11 [hutals] cell swelling because of inactivation of Na/K ATPase pump (water follows Na into cell)
21:14:11 [jwls29] fibrinoid necrosis,blake
21:14:18 [BlakeH] yes
21:14:24 [dr_yasir] acute infec
21:14:37 [Lorena] increase with corticoids
21:14:37 [dr_yasir] will inc
21:14:52 [ash] infection causes left shift
21:15:09 [ash] right lorena
21:15:16 [ash] and decrease?
21:15:19 [hutals] agree with lor
21:15:34 [hutals] alcohol gives neutropenia
21:16:02 [acestep1] agree
21:16:30 [ash] decrease is seen with endotoxins as they increase the production of adhesion molecules
21:16:41 [Lorena] agranulocytosis, drugs, .....
21:17:03 [Lorena] thanks ash
21:17:10 [acestep1] ic
21:17:42 [ash] you r welcome
21:17:51 [Lorena] what IL increases expression of adhesion molecules?
21:18:07 [ash] how is emigration possible by cancer cells?
21:18:15 [acestep1] il1
21:18:17 [hutals] IL 1
21:18:19 [Lorena] in organs with dual supply
21:18:23 [ash] 1
21:18:32 [ash] liver
21:18:33 [Lorena] cancer cells have collagenases
21:18:51 [dr_yasir] iL8
21:18:52 [ash] right lorena
21:19:12 [hutals] chemotaxis mediators?
21:19:16 [Lorena] like intestine can have hemorrhagic infarct
21:19:18 [ash] esp. type 4 collagenase
21:19:20 [BlakeH] right'
21:19:36 [jwls29] testicle can have hemorrhagic infarct
21:19:47 [BlakeH] bowel, lungtestes
21:19:57 [acestep1] il8, bact lysis prod, anaphylotoxins
21:20:10 [Lorena] chemotaxis: c5a, IL8
21:20:14 [ash] n-formyl methionine,ltb4,c5a,il-8,pdgf
21:20:29 [Lorena] leukotriene B4
21:20:34 [BlakeH] kid who umbilical cord doesnt fall???? what is the defect?????
21:20:50 [jwls29] adhesion molecule defect
21:20:55 [ash] chediac higashi
21:21:01 [Lorena] adhesion molecule defects for a mutation in adhesion molecules
21:21:03 [hutals] C5a, LTB4, bacterial products are the ones i have.....probably also the ones listed....good job
21:21:12 [acestep1] ok which drug inhibits lb4?
21:21:13 [BlakeH] right jwls
21:21:34 [ash] corticosteroids
21:21:44 [Lorena] zileuton?
21:21:47 [ash] by inhibiting phospholipase
21:21:55 [BlakeH] zileuton
21:22:00 [acestep1] colchicin as well
21:22:23 [acestep1] v gd all three - steriods, ziluten n colchicin
21:22:43 [Lorena] what about zafirlukast?
21:22:56 [BlakeH] what pathways links factor XII????
21:23:19 [hutals] zarfirlukast inhibits the receptor
21:23:28 [acestep1] agree tht 2- lor
21:23:37 [Lorena] yes good ace
21:23:51 [Lorena] good hutals
21:23:51 [dr_yasir] u pplz are not discussing pathology me think
21:23:53 [acestep1] thanks
21:24:43 [hutals] thats because golijans notes go beyond path and links all subjects together
21:25:13 [Lorena] the intrinsic one?
21:25:31 [ash] appendicitis is most similar to which necrosis?
21:25:37 [jwls29] agree with lore
21:25:54 [BlakeH] Factor XII links kinin ,coagulation , plasminogen and complement system
21:26:07 [BlakeH] licuefactive
21:26:10 [acestep1] gangrene
21:26:29 [acestep1] agree- blake
21:26:39 [Lorena] agree liquefactive
21:26:56 [jwls29] liquefactive
21:27:08 [ash] right .liquifactive
21:27:41 [ash] what happens to rbcs upon loss of isotonic fluid?i
21:28:35 [dr_yasir] nothing
21:28:39 [Lorena] no change
21:28:50 [jwls29] agree
21:29:37 [BlakeH] agree
21:29:37 [ash] come on guys there is a change and it is not in size.
21:29:57 [dr_yasir] dec in hematocrait ?
21:30:42 [ash] ok, rouleaux formation is the answer
21:30:51 [Lorena] hemoconcentration?
21:30:52 [dr_yasir] n what u are asking is physiology
21:31:15 [BlakeH] also seen in multiple mieloma due to viscosity
21:31:23 [Lorena] ok
21:31:27 [ash] yasir this is g o l j a n.
21:31:44 [ash] in the exam they will mix patho with physio
21:31:58 [ash] right blake
21:32:02 [Lorena] very good thanx
21:32:09 sweta_med enters this room
21:32:13 [dr_yasir] oh i am sory actualy i read <a target=new href=http://click.linksynergy.com/fs-bin/click?id=c97WUMRO5hY&offerid=47491.10002441&type=3&subid=0 ><a target=new href=http://click.linksynergy.com/fs-bin/click?id=c97WUMRO5hY&offerid=47491.10002441&type=3&subid=0 >Kaplan</a><IMG border=0 width=1 height=1 src=http://ad.linksynergy.com/fs-bin/show?id=c97WUMRO5hY&bids=47491.10002441&type=3&subid=0 ></a><IMG border=0 width=1 height=1 src=http://ad.linksynergy.com/fs-bin/show?id=c97WUMRO5hY&bids=47491.10002441&type=3&subid=0 > i dont have <a target=new HREF=http://www.<a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon</A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=<a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A>&mode=books><a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A></A> i wont disturb u pplz any more
21:33:23 [dr_yasir] i am sory i pasted by mistake
21:33:49 [Lorena] what pathway do you evaluate with PT? and which one with PTT?
21:33:52 [hutals] yasir, you should try to get your hands on goljans notes. they are very comprhensive for most high yield subjects and integrates them all together....but the problem is that they dont concentrate on path
21:33:54 [dr_yasir] actualy i was serching for <a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan</A> and by mistake i psted here
21:34:11 [BlakeH] Prostaglandin that causes pain in inflammation, keeps the ductus arterious open and helps form the barrier in the stomach???
21:34:40 [hutals] yasir, try not to post words like golijan, first aid, etc or you will get a link instead
21:34:40 [Lorena] pGE
21:34:56 [hutals] extrinsic for PT and intrinsic for PTT
21:34:57 [dr_yasir] oh ok
21:35:06 [acestep1] n pgi2
21:35:12 [BlakeH] right Lor PGE2
21:35:13 [dr_yasir] i didnt knew i am sory
21:35:16 [Lorena] yes hutals
21:35:20 [acestep1] agree- hutals
21:35:45 [hutals] no prob yasir....we all type those by mistake
21:36:16 [hutals] i remember it as PeT and PiTT (pet and pittsburg)
21:36:38 [ash] thanks hutals
21:36:42 [Lorena] PGE2 also dilates aferent arteriole in kidney
21:36:50 Newone enters this room
21:36:56 [acestep1] agree with lor
21:37:02 [BlakeH] pettin a pittbull!!!
21:37:08 [hutals] hey newone
21:37:08 [acestep1] whta bt pge1
21:37:21 [hutals] good one blake
21:37:26 [acestep1] wht abt pge1 imean
21:37:28 [Newone] hello all
21:38:00 [jwls29] hello newone
21:38:03 [Lorena] hi newone
21:38:25 [Lorena] i dont remember PGE1 ace
21:38:40 [acestep1] np
21:38:43 [ash] pge2 is also natriuretic
21:38:49 [Lorena] is it protacyclin?
21:38:57 [ash] hi newone
21:39:05 [acestep1] i think pge1 mediates pain n causes abortion
21:39:27 [acestep1] prostacylcin-pgi2
21:39:37 [ash] leukoterine that is a vasodilator?
21:39:51 [BlakeH] renal tubular cells are what kind cells accordin to teir regeneration?????
21:40:08 [acestep1] ok misoprostol - analog of wht pg
21:40:18 [Lorena] PGI is prostacyclin and causes vasodilation and inhibits platelet agregation
21:40:28 [acestep1] lt r vasoconstrictors i think
21:40:40 [acestep1] agree - lor
21:40:55 [ash] ace-pgf2alpha????
21:40:59 [Lorena] PGF? the one that causes dysmenorrhea?
21:41:16 [acestep1] nono ash
21:41:24 [BlakeH] PGI is vasodilator and inhibits platelet aggregation
21:41:38 [acestep1] agree both f2 n e1
21:41:46 crusher enters this room
21:42:06 [hutals] PGE analog
21:42:17 [BlakeH] renal tubular cells are what kind of cells accordin to their regeneration?????
21:42:22 [Lorena] renal tubular cells are stable cells?
21:42:27 [acestep1] i think hutals is right- misoprostol
21:42:28 [ash] acemisoprostol+pg
21:42:30 [dr_yasir] mifoprostol
21:42:40 [BlakeH] right lor
21:42:45 [ash] sorry misprint
21:42:54 [acestep1] k
21:43:03 [acestep1] np
21:43:21 [Lorena] what is the only phase of the cell cycle that changes in length?
21:44:21 [ash] go
21:44:42 [Lorena] i meant the most variable
21:45:00 [BlakeH] S??
21:45:14 [Lorena] G1
21:45:32 [BlakeH] skeletal muscle cells is what kind of cell???
21:45:39 [BlakeH] thxs Lor
21:45:40 [acestep1] k
21:45:52 [Lorena] permanent
21:46:08 [acestep1] agree
21:46:27 [crusher] permanant
21:46:28 [BlakeH] also wit neurons and myocardial
21:46:44 [hutals] skeletal are permanent cells
21:46:49 [BlakeH] neuronal exception to that?????
21:47:11 [ash] microglia
21:47:25 [BlakeH] microglia are not neurons
21:47:47 [BlakeH] microglia are macrophages of CNS
21:48:22 [Lorena] thanks blak
21:48:48 [ash] thnx
21:48:56 [BlakeH] only neurons that divide are the ones in the olphatory epithelium
21:49:25 [ash] thnx blake
21:49:51 [acestep1] k
21:50:04 [BlakeH] composition of a granuloma?????
21:50:48 [hutals] pt gets recurrent infections to staph aureus, has a negative NBT test.....what diagnosis?
21:50:57 [crusher] epitheloid cells....giant cells
21:51:07 [Lorena] epithelioid cells,
21:51:15 [acestep1] cgd
21:51:22 [ash] macrophages-epitheloid cells,giant cells
21:51:24 [crusher] NAHPH oxidase def
21:51:25 [Lorena] CGD
21:51:31 [ash] cd8 t cells
21:51:47 [acestep1] agree epitheliod cells giant cells n fibroblast
21:52:06 [acestep1] epitheloid - diagnostic
21:52:18 [ash] if caseus then lipid debris in center
21:52:27 [Lorena] what is an epithelioid cell?
21:52:40 [hutals] yep, CGD deficiency or NADPH oxidase deficiency which will lead to an absent resp burst.....negative NBT test
21:52:42 [ash] macrophage
21:53:06 [acestep1] fused macro - multinucleated
21:53:14 sweta_med enters this room
21:53:17 [BlakeH] multiple macrophages joined together
21:53:22 [Lorena] yes ash
21:53:48 [Lorena] when epithelioid cells fuse then become a giant cell
21:54:06 [dr_yasir] multiple macrophages joined together are the giant cells
21:54:14 [hutals] which cells are prominent in acute inflammation? what about chronic inflammation?
21:54:19 [Lorena] epithelioid cell is a macrophage that has been stimulated by IFN gamma
21:54:21 [BlakeH] Langhans giant cells
21:54:47 [acestep1] agree- lor
21:54:54 [dr_yasir] epitheliod cells are the lymphocytes i think
21:54:55 [BlakeH] acute = neutrophils, mast cells
21:55:01 [Lorena] acute:neutrophils
21:55:05 [crusher] acute ..neutrophils...chronic machrohages
21:55:15 [BlakeH] chronic = mononuclear cells
21:55:23 [acestep1] agree- crusher
21:55:30 [hutals] neutrophils are key cells in acute inflammation and monocytes/macrophages are key cells in chronic inflammation.....very good
21:55:31 [Lorena] chronic: lymphocites (Th1)
21:56:25 [BlakeH] 5 causes of granulomatous inflammation???
21:56:31 [hutals] lymphocytes are primary inflammatory cell in what type of infections?
21:56:37 [Lorena] oh sorry lymphocytes Th1 is in retarded hypersensitivty
21:56:48 [jwls29] viral infections
21:57:06 [Lorena] viral
21:57:15 [crusher] yes viral infections
21:57:16 [acestep1] all i guess but mainly viral n fungal
21:57:38 [hutals] yes, lyphocytes in viral infections. also in type 4 hypersens and pertusis infections
21:58:12 [acestep1] k
21:58:41 [hutals] TB granuloma is one
21:59:05 [Lorena] sarcoidosis, chrons. disease
21:59:07 [acestep1] viral fungal autoimmune, slow growing bact, foriegn body- blake
21:59:26 [hutals] type 4 hypersensitivity is another one i think
21:59:28 [Lorena] fungal diseases
21:59:42 [acestep1] hey guys i gtg . illsee u guys tom . tc all of u
21:59:42 [BlakeH] infectious ( TB, cat scratch, trponema), foreign bodies,sarcoiosis
21:59:49 [BlakeH] right guys
21:59:58 [jwls29] bye ace
22:00:11 [Lorena] take care ace
22:00:11 [acestep1] bye jwls
22:00:25 [acestep1] bye lor
22:00:39 [ash] bye
22:00:42 [BlakeH] gotta go to guys
22:00:47 [BlakeH] a tomorrow
22:00:49 [hutals] are we done?
22:00:52 [BlakeH] c ya
22:01:02 [jwls29] bye blake
22:01:15 [hutals] ok, well thanks for chatting. c ya all tomorrow
22:01:28 [Lorena] i can stay longer
22:01:30 [ash] we havent touched the 3 rd chapter yet
22:01:40 [Lorena] if you have more q's
22:01:45 [ash] me too
22:01:47 [jwls29] i can stay longer too
22:02:07 [Lorena] cool lets continue then
22:02:15 [ash] lets wait for some more time
22:02:15 [hutals] oh, ok, i thought everyone was leaving....sorry
22:02:25 [ash] great
22:02:31 [dr_yasir] and i will watch u guys
22:03:24 [ash] what are dohle bodies?
22:03:24 [Lorena] important cofactors in collagen sx?
22:03:38 [ash] copper,vit.c
22:03:48 [dr_yasir] cu
22:03:49 [ash] and zinc
22:04:12 [Lorena] very good
22:05:05 [dr_yasir] vit c for hydoxilation and cu for collagen chain arrangement am i right?
22:05:12 [ash] what are dohle bodies?
22:05:19 [Lorena] what are they ash? dohle?
22:05:20 [dr_yasir] hydroxilation of proline residues
22:06:01 [Lorena] yes yasir
22:06:05 [ash] dohle bodies are gray cytoplasmic inclusions .they are dilated endoplasmic reticulum
22:06:30 [ash] copper is required for lysyl oxidase
22:06:43 [Lorena] in what disorder are they present?
22:06:48 [ash] type of collagen in keloid?
22:07:06 [Lorena] type III
22:07:14 [dr_yasir] yes u are rigth ash
22:07:52 [hutals] type3
22:08:10 [Lorena] where is lysil oxidase? RER?or extracellular space?
22:08:40 [hutals] what type of cancer is a keloid predisposed to?
22:08:58 [Lorena] squamous
22:08:58 [ash] right
22:09:31 [hutals] yes, squamous, particularly if due to third degree burns
22:09:40 [ash] lorena they are not in a disorder i know of.they are normally seen
22:09:56 [ash] in neutrophils
22:10:06 [Lorena] oh ok thanks ash
22:10:07 [hutals] is a keloid hyperplasia, hypertrophy, metaplasia, dysplasia?
22:11:05 [dr_yasir] its a hyperplastic scar tissue
22:11:18 [Lorena] hyperplasia?
22:11:19 [hutals] keloids are hypertrophic scar tissue......resembles a tumor and is often seen in african americans
22:11:40 [ash] in another book i have read they are depolymerised ribosomes
22:11:55 [hutals] i would have thought hyperplasia also, but golijan has it as hypertrophy??
22:12:35 [dr_yasir] in robin its writen hyperplastic me thinks
22:12:44 [Lorena] ok thanx
22:13:12 [hutals] maybe its a typo in golijans because it seems like it should be hypertrophy
22:13:23 [hutals] ooops i mean seems like hyperplasia
22:14:21 [Lorena] ok
22:14:39 [hutals] but that brings up another confusing misconception.....is BPH hypertropy or hyperplasia?
22:15:12 [ash] bph is hyperplasia as it is a glandular tissue
22:15:14 crusher enters this room
22:15:20 [dr_yasir] thats hypertrophy but its actualy hyperplasia
22:15:26 [Lorena] hyperplasia
22:15:46 [dr_yasir] its called hypertrophy but its hyperplasia
22:16:49 [hutals] i agree. i think the old timers used to think it was hypertrophy and the name stuck, but now it is known as hyperplasia....i think
22:17:26 [dr_yasir] yess i am sure abut it
22:17:32 sweta_med enters this room
22:17:36 [Lorena] what part of the nephron is more susceptible to hypoxia?
22:18:36 [dr_yasir] early convuluted ??
22:19:04 [ash] medullary
22:20:00 [ash] what will happen to the esr in iron deficiency anemia and sickle cell anemia?
22:20:01 [Lorena] the proximal tubule i think
22:20:37 [hutals] decreased esr
22:20:46 [hutals] in sickle cell anemia
22:21:00 [Lorena] ESR is decreased in sickle cell
22:21:32 [ash] what abt iron def?
22:22:21 [hutals] anemia enhances settling, so inc esr is my guess
22:22:29 [Lorena] increased in anemia
22:22:38 [dr_yasir] i think it dec ub iron def and inc in sickle
22:23:19 [ash] right hutals and lorena
22:23:56 [dr_yasir] ok
22:23:57 [ash] what cells contain weibel palade bodies and what do these bodies store?
22:24:51 [Lorena] contain vW factor
22:25:04 [ash] correct
22:25:15 [ash] and what cells?
22:25:20 [dr_yasir] in microcytic anemia its dec in ESR
22:25:24 [Lorena] they can be seen in angiosarcoma of the liver
22:25:45 [hutals] endothelial cells
22:25:51 [Lorena] they are endothelial cells
22:26:24 [ash] right
22:26:52 [hutals] i dont see how microcytic anemia would decrease the ESR?
22:27:03 [ash] where did you read it yasir?
22:27:25 [dr_yasir] A common cause of high ESR is anemia, especially if it is associated with changes in the shape of the red cells; however, some changes in red cell shape (such as sickle cells in sickle cell anemia) lower ESR
22:29:44 [dr_yasir] may b i have mistaken
22:29:52 [Lorena] ok folks, i have to go now
22:30:01 [dr_yasir] i will watch it later
22:30:03 [hutals] that is what we are saying.....sickle cell anemia lowers the ESR, but iron deficiency anemia will increase ESR.....am I reading that right?
22:30:36 [hutals] maybe I'm misunderstanding it
22:30:50 [Lorena] byeee
22:31:07 [ash] yasir has made a very good point here
22:31:12 [hutals] ok lorena, i will be going too. will you post the transcript?
22:31:18 [dr_yasir] bbye lorena
22:31:19 [ash] bye lorena
22:31:29 [dr_yasir] hutals
22:31:57 [hutals] nite lorena
22:31:58 [ash] i agree with yasir for microcytes it is decrease esr.
22:32:09 [ash] ok goodnite all.
22:32:21 [hutals] nite yasir, ash, and everyone else
22:32:49 [dr_yasir] no its inc in esr with microcytic
22:33:14 [dr_yasir] and dec in esr with sickle cell
22:34:46 [hutals] http://www.danielballarin.com/esr.htm
22:34:50 [dr_yasir] looks like every one off the net ???????
22:35:15 [hutals] that gives more info on the ESR and the causes of inc vs dec
22:36:07 [dr_yasir] thanks for the link hutals
22:36:34 [hutals] no prob. nite and c ya tomorrow
22:36:46 [jwls29] what is that link for
22:36:54 [jwls29] i'm sorry i was gone
22:37:18 [dr_yasir] ok u take care too hutals thanks
22:37:36 [hutals] the link is for further info on ESR since we were confused about what causes an increase vs a decrease jwls
22:37:54 [jwls29] thanks guys
22:38:00 [jwls29] i'm leaving now
22:38:05 [hutals] ok, bye
22:38:08 [jwls29] is someone going to post the transcript?
22:39:33 [jwls29] this was a very good chat. Let's keep it up...i'll see you all tomorrow
22:39:52 [dr_yasir] bye jwls
22:40:07 [jwls29] who is posting the transcript?
22:40:21 [hutals] i was hoping that lorena would post it, but i'll post it if she doesn't.
22:40:34 [dr_yasir] tell me how to post i will do it
22:40:40 [jwls29] ok...she's gone
22:40:47 [jwls29] i don't know how
22:40:55 [jwls29] goodnite
22:41:11 [hutals] yep, i was just checking to see if she posted it.....i dont see it so i will post it.....nite