Chat transcript - Goljans path (cell injury and inflammation

[Anonymous]

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& lt;/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 &lt;a target=new href=http://click.linksynergy.com/fs-bin/click?id=c97WUMRO5hY&offerid=47491.10002441&type=3 &subid=0 >&lt;a target=new href=http://click.linksynergy.com/fs-bin/click?id=c97WUMRO5hY&offerid=47491.10002441&type=3 &subid=0 >Kaplan&lt;/a><IMG border=0 width=1 height=1 src=http://ad.linksynergy.com/fs-bin/show?id=c97WUMRO5hY&bids=47491.10002441&type=3&sub id=0 >&lt;/a><IMG border=0 width=1 height=1 src=http://ad.linksynergy.com/fs-bin/show?id=c97WUMRO5hY&bids=47491.10002441&type=3&sub id=0 > i dont have &lt;a target=new HREF=http://www.&lt;a HREF=http://www.amazon.com/exec/obidos/redirect?tag=valuetheplace-20&path=subst/home/books.html>Amazon&lt;/A>.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=&lt;a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan&lt;/A>&mode=books>&lt;a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan&lt;/A>&lt;/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 &lt;a target=new HREF=http://www.amazon.com/exec/obidos/external-search?tag=valuetheplace-20&keyword=Goljan&mode=books>Goljan&lt;/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

[Anonymous]

Hi hutals
Thank u for posting the transcript. i wanted to join the chat yesterday, but i couldn't able to login. today i checked the transcript...and i had a small doubt.
u posted
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

increased altitude causes res acidosis. ...

.but in kaplan physio its given that increased altitude causes res alkolosis (hypoxemia....stimulate peripheral chemorecepters, inducing hyperventilation and it causes loss of CO2 and respiratory alkalosis. To compensate, the kidney loses bicarbonate and so metabolic acidosis.
please corect me if i am wrong. i always have the confusion with high altitude.)

thank u verymuch. hope i can login today.

[Anonymous]

yes, you're absolutely correct. i looked it up to verify and i agree with you completely. i guess i got mixed up on that.....thanks for pointing that out and hope to see you in the chat tonight.

[Anonymous]

thank u hutal. i tried to login today also but couldn't. i was there in chat or 2 days ...with ID .usmle12004. but now i ám not able to log in to chat and also cannot able to register with other ID. anyways thanks. please keep posting trancripts. that will help somany people like me. Thanks again.