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 What Goljan Says !!!  

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salam gik
keep up the good work nod i am following your post
jazak Allah


well well,u guyz are just amazing .1st timer and clearly hav my work cut out.good 2 be here.sure will start off maybe 2 days time.really happy.cheers


Gik I found another small little detail:

When you get to bone pathology, he says the most common B9 tumor of the cartilage/bone is Exostosis (osteochondroma) and then he says that the multiple form of it is Ollier's disease. When in fact Ollier's is the multiple form of Enchondromas.
Side note: Marfucci's is Ollier's + hemangiomas.

So basically, he's saying that Osteochondromas and Enchondromas are the same thing.wink

Keep it up man! We'll pass this test easy!grin

Edited by jorgefhoyos on Apr 25, 2009 - 2:07 PM


Welll nice to c ev one here.... m doing this UW... n could't fix my schedule rite now... will be updating it soon:

Painkiller --- thanx buddy

Mex ---- Either 1st timer or oldies ... this site is cool. take care

Jorge --- really happy to c all ur support... with in 2-3 i will fix this issue... n will be updating ASAP...

all the best ev one and keep rocking smiling facewinknodcool



is there any way you can send me or post here link to this goljan audio please....


I must say again,great work:d


Post 64: (Dated: May 20th - 2009)

So E.Murmur like Aortic stenoisis has crescendo decrescendo appearance.

Valves heard best:

Aortic valve = Rt second intercoastal space.
Pulmonic valve = Lt second intercoastal space
TCV = Lt parasternal border.
MV = Apex

That does't necessarily means thats where the valve is. Its just where the noise is heard.

Aortic stenosis: You have an Ejection type of murmur in systole. Heard best in the right second intercoastal space. Radiates into the carotids and the murmur intensity increases on expiration and you hear S4.

Pulmonic stenosis: Mainly on the left. Ejection type murmur. Increase on expiration.

Diastole: Stenosis murmurs; Mitral and triscupid valves are opening.

Mitral: Stenosis ---> problem in opening it. Left atrium has problem in opening the MV. This valve does't wanna open, and LA has to get it open to get blood in it ---> its gonna get pretty strong because it has an afterload to deal with ---> gets dilated and hypertrophied; Predisposes to Atrial fibrillation with stasis of blood, thrombus and all kind of things.

The left atrium has to force the blood into the ventricle in a milisecond ---> MV snaps open ---> all that blood that was built up behind ---> gushing in ---> mid diastolic rumble; So you have an opening snap followed by a rumbling sound.

In MS there is a problem in opening the valve ---> you are underfilling the LV ---> no hypertrophy at all since all the work done by LA.

The murmur gonna be heard at apex and will increase in intensity on expiration.

Regurgitation: Problem in closing the valve; in systole Mitral and tricuspids are closing. You certainly dont want the mitral, aortic and pulmonic valve to close on systole ---> you wanna make sure that the blood does't go back in to the atrium. So MV and TCV are closing in systole so if they are incompetent and they cant close properly ---> systole occurs ---> because the MV cant close properly and lets say 30 ml goes back into the LA and 50 ml goes out of the aorta ---> there is even more blood in the LA than normal now.

You just put 30 ml of stroke of the Stroke volume in it + its already been trying to fill up ---> you have excess blood there ---> volume overloaded.

Murmur: Since its the problem in closing the valve ---> gonna be "sheeeeeeewwwwwwwww" ---> as the blood all the way through systole is going through incompetent valve into the LA ---> so its pansystolic murmurs; More of a striaght line; Some times obliterating S1 and S2. (not cresendo decresendo)

So again Apical murmur, pansystolic, S3 and S4 heart sound because we have a problem with compliance as well as volume overload, increases in intensity on expiration.

You can figure out the TCR ---> pansystolic, S3 and S4, left parasternal border, increases in intensity on inspiration.

Scenario: IV drug abuser with fever, pansystolic murmur along the parasternal border, S3 and S4, accentuation of the neck veins. Dx? Ans- Infective endocarditis of TCV. Most common infection of IV drug abuser.

The Murmur and heart sounds increase on inspiration ---> Rt sided.

Changed Scenario: They said that the murmur intensity increased on expiration, it would have been infective endocarditis of MV.

Diastole: Closing of Aortic and pulmonic ---> what you just pump out does't comes back in.

Aortic Regurgitation: You have systole ---> the blood goes out ---> the valves should be closing properly but it does't ---> some blood will be trickling back ---> let say 80 cc went out initially and 30 cc of blood drift back in ---> at the begining of diastole you have volume overloaded chamber and frank starling gonna invalve ---> end diastolic volume gonna be 200 ml which is supposed to be 120 ml.

The murmur of AR is heard after the second heart sound because its not closing and the blood is dripping back in ---> makes a sound, high pitch diastolic blowing murmur right in second intercoastal space ---> increases in intensity on expiration, S3 and S4 heart sounds because its a volume overloaded chamber + all those bounding pulse.

The ant. leaflet of M.V ---> is actually one side of the outflow tract out into the aorta ---> the murmur called Austin flint murmur; When you have AR and you have austin flint murmur ---> you call you cardiac surgeon, thats the time to remove the valve because if you have that murmur then you are significantly dripping back in here, that valve has to be replaced.

Scenarios: Left and Right sided heart failure.

This is section through lungs ---> Lf
Liver ---> Rt
Paroxysmal nocturnal dyspnea ---> Rt

Left Heart Failure: Its forward failure or your left ventricle is failed. It has to push against and after load, it fails; it has to deal with an excess volume it fails; you have so many infarcts that the left ventricle no longer muscle and its fibrous tissue so the contractility is decreased.


Hello every one... wanna say thanks again for all ur support... M thinking about squezing this to my schedule in these days ... i will listen n write AMAP.

Jorge --- Where are you bro... hope u r doing great with studies... man come back its time to rock in the hall. N yeh ur explanations n mistake points worths a lot... al the best buddy.winksmiling facenodcoolrolling eyes

Dipen18 --- well wat u r asking is somethin which is not my territory ... If i get a link ... I will definitely send u... take care smiling facecoolnod

Chipden --- Chip I have to say again... THANKS a LOT... RIP grin

N e ways guys... take care n Juz Keep Rocking smiling facewinkgrincoolnodgrin


Post 65: (Dated: May 29 - 2009)

So that means that your EDV gonna increased because you cant get all the blood out or you cant push it out. With that pressure the volume gonna go back in to the LA and back into the Pulmonary Vessels ---> increase the hydrostatic pressure ---> Pulmonary Edema.

When you have chronic LHF ---> you have hemmorhage with alveolar macrophages that phagocytose the RBC ---> rusty colored sputum ---> you do cytology and see Heart failure cells, those are alveolar macrophages that have phagocytose the RBC and its broken down into hemosiderin.

LHF is the diagnosis of symptoms ---> "Doc 'm having trouble in breathing"
RHF is the diagnosis of signs ---> Since its the problem in the RT heart getting blood through the Pulmonary vessels to the left heart. So if it fails ---> blood builts behind it ---> its backward failure ---> hydrostatic pressure will increase in the venous circuit ---> you have neck vein distension; painful hepatomegaly called as Nutmeg liver because the increased pressures in the vena cava gonna be transmitted to the hepatic vein which empties into it and back into the liver into the central vein and you are gonna get the little dots all around it and looks like a Nutmeg.

Most common cause of the congested hepatomegaly is RHF. The increase in hydrostatic pressure also gonna produce pitting edema and possibility of even ascities.

So neck vein distension, hepatomegaly, pitting edema, ascities ---> all right heart failure.

When you lie down and go to sleep ---> you can reasorb upto about a litre fluid from interstitium goes into the venous side of circulation because there is no effective gravity any more ---> little bit of extra blood going into the right heart and into the left heart; if you have left heart failure ---> you have all that excess blood that was't there when you were standing up is now coming back and this left heart is having big time problem to get it out and you have more coming in ---> blood goes back into the lungs ---> windows goes up ---> paroxysmal nocturnal dyspnea.


gr8 post ....very very thnks for making sucha a post doing goljan and i can do revision from here ...thank you and good luck.


Post 66: (Dated: June 02 - 2009)

Eventually it settles down and you go to sleep this stincky thing happens again. If there is one pillow othropnea its not too bad but if you have to sit up ---> serious left heart failure.

You are imposing gravity. Just placing only one pillow decreases your venous return to the right side of your heart. You put two pillows that decreases even more. You sit up it decreases even more. So pillow orthopnea and PND are signs of LHF not right.

Rx of LHF or RHF ---> best non-pharmacological treatment ---> restrict water and salt.

The king of the Rx of heart failure: Its king because it decreases afterload and decreasespreload at the same time ---> ACE inhibitor ---> decreases preload (decrease in aldosterone, decreases salt and water reabsorbtion) and by blocking ATII you decreases vasoconstrictive effect on PRA so you decreasing the afterload.

Article: People that were on ACE-inhibitors and spironolactone did better than those who were on ACE-inhibitors alone. The reason to that was, aldosterone got elevated again even you are on ACE inhibitor so its not a permanent suppression. So giving aldosterone and ACE inhibitor increases prognosis.

High Output failure (HOF): In Endotoxic shock ---> PRA were dilated, C3a, C5a, Nitric oxide ---> increases venous return in the heart.

Poiseles Law: Viscosity over radius to the 4th power. So if you vasso dilate the PRA ---> decreased TPR ---> more blood comes back to the right heart, left heart has to deal with it ---> you run the risk of high output failure.

Beside septic shock another cause of vassodilatation is thiamine deficiency.

Since the problem in thiamine deficiency is ATP depletion ---> smooth mucle cells in the PRA need ATP ---> decreased ATP ---> vassodilation of the PRA ---> HOF.

Graves disease: Thyroid hormone increases synthesis of Beta receptors in the heart ---> increased in force of contraction ---> there is more blood, systolic pressure are higher ---> HOF.

AV-Fistulas: If you are stabbed in leg ---> develop AV-malformation ---> arterial blood bypassing microcirculation goes directly in the venous circulation ---> blood will be coming faster than normal ---> bruit over the mass, pulsatile, if you press the proximal portion of it the heart rate will slow (branham sign).

Fetal circulation: Baby is not exchanging blood with O2 in our lungs. The Pulmonary vessels in fetus look like they have P.Hyp ---> they are so thick that is extremely hard to get blood through the P.A into the left ventricle. Therefore you need PDA in order to get it out of there.

The O2 in fetus is coming from the chorionic villous dipping into the lake of blood which drives from mommy's spiral arterioles. Its not a good O2 source as lungs. So you need high affinity hemoglobin to able to get O2 ---> HbF which has high affinity for O2. The bad thing is that it does't wanna give it up. This produces tissue Hypoxia so EPO is released ---> 18 gm hemoglobin is present normaly. Newborns have polycythemia.

Therefore HbF has high affinity ---> you have more RBCs with more Hb in it.


Thanx Dr.Independant... take care n gud luk with ur revision. smiling face


gik84!! Plz help me with understanding Mitral Valve Prolapse:

I am confused with the click murmur associated with MVP and its going against my senses. Can somebody help me plz?

Gojan says that when preload is increased the murmur gets closer to S2 and when preload is decreased the murmur gets closer to S1.

To me it seems the otherway. When preload is increased that means EDV and EDP are increased. Meaning the prolapse will start earlier in systole and hence closer to S1. Likewise when the preload is decreased that means EDV and EDP are reduced. Meaning the prolapse will start delayed.

I am sure I am missing some mechanics somewhere. Please can somebody help me understand this?? May God bless you for that!


Hey Gik... This is the best post ever !!!

Thanks a lot !!!


wow... great posts here, i m starting my patho and this i think would be a high yield and great review immersing in this platform... wish u luck guys.


Post 67: (Dated: July 17 - 2009)

So the blood O2 goes through syncytiotrophoblast of chorionic villous ---> cytotrophoblast ---> myxomatous stroma of the chorionic villous ---> goes into the blood vessels of the chorionic villi ---> umbilical vein which has the highest O2 concentration ---> goes up to liver and there are 2 ways it can go ---> (1) In to hepatic sinusoids, and through hepatic vein and gets dumped into IVC or (2) They can select the ductus venosus and goes into right IVC, ---> Right side of the heart.

Picture this: Foramen ovale is opened. Oxygenated blood is coming up from IVC ---> right atrium ---> foramen ovale ---> left atrium ---> left ventricle ---> aorta.

The SVC blood goes through tricuspid valve ---> right ventricle ---> since pulmonary vessels are too thick, blood goes through the patent ductus arteriosus (kept opened by PGE2 made by placenta, a vasodilator) ---> Right-left-shunt ---> dumped into the aorta.

When the baby is born: baby breaths ---> pulmonary vessels gets opened in milli seconds ---> blood goes through them; Patent ductus begins functionally closing and eventually closes and forms the ligamentum arteriosum.

When the blood goes out the Aorta: it goes into 2 umbilical arteries; there is one umbilical vein. The vessels with the least amount of O2 are the umbilical arteries, where as the most O2 is in the umbilical vein.

If you have left-right-shunt and you have Oxygenated blood going into un-oxygenated blood ---> Step up of O2 saturation on the right side.

If you have right-left-shunt with unoxygenated blood going into left side ---> step down.

The O2 saturation of the blood on the right side of the heart, returning from the body is 75%.

The O2 saturation on the left side is 95%.

Slide ASD: Normally there is a membrane in this portion of the septum. Its not just all muscles going straight up there; Notice the close relationship of aortic valve leaflet in that septum.

The left ventricle is stronger then right ---> direction of shunt is left-right ---> Oxygenated blood dumped into the right ventricle ---> Step up; also its gonna pumped out of the pulmonary artery ---> step up. So you have step up of O2 in the right ventricle and pulmonary artery.

If this is not corrected: Since you are volume overloading the right side of the heart by all this blood coming over here ---> pulmonary arteries have to deal with more blood ???---> pulmonary hypertension ---> right ventricle having problem in contracting, get bads ---> hypertrophied ---> risk of reversal of shunt because the right ventricle could become stronger than left ventricle ---> eisenmenger syndrome ---> cyanosis (also called as cyanosis tardive).

Most of the VSD close spontaneously, some need to be patched.

Atrial septal defect: It is normal for the fetus to have patent foramen ovale, but its not normal once they are born. The flow of blood is from left to right as left is always stronger than the right ---> step up in R.A ---> goes from 75-85% ---> step up in R.V ---> step up in P.A.

Difference bw ASD vs VSD: Step up of O2 also in right atrium.

Since there is a volume overloading in the right side of the heart ---> risk for Eisenmenger syndrome.

Also there is a risk of paradoxical embolisation.

If there is a DVT in leg ---> embolized up, the pressures in the right side of the heart are increasing ---> patent foramen ovale ---> embolus goes into right atrium ---> left atrium ---> a venous clot in your arterial system.

Fetal alcohol syndrome: Most commonly has ASD associated with it. 2 out of 1000 kids with Fetal alcohol syndrome have ASD.

Patent ductus arteriosus: Normal in fetus but is't when they are born.

Slide: there is a connection bw aorta and the P.A; Aortic pressures are higher ---> Oxygenated blood goes from left and get dumped in to the PA before it goes into the lungs ---> step up in PA about 80%; Since there is an opening bw these, the blood switching back and forth persistently in diastole ---> pheeeeesshhhhh ooooo pheeeeesshhhhh ooooo pheeeeesshhhhh ooooo ---> machinery murmur ---> gonna hear bw the shoulder blades.

PDA: Left-right-shunt ---> volume overload at the Right side of the heart ---> P.HTN. The shunt will be directed like the fetal one. There will be unoxygenated blood dumping in to the aorta. Since the ductus empties distal to subclavian artery ---> babies gonna have pink on top and blue on the bottom because you are dumping unoxygenated blood below the subclavian artery (differential syanosis).


RX: Thanx for asking this question... as i will look about the details as well... I will PM u ASAP... take care. smiling face

Bro Ocano: thanx pal... it feels really good when u appreciate Pappi stuff.smiling facewinkcool

Fireonmyeyes: Thanx... good luck with ur patho. winknod

Well every one... take care and keep rocking ...RIP smiling facewinkgrincoolnodcool


keep going man


Post 68: (Dated: July 22 - 2009)

Congenital Rubella is associated with patent ductus.

PDA with out any other heart defects dependant on it ---> closed with indomethacin, a potent non-steroidal which inhibits PGE2 ---> PDA start to constrict on its own.

tetralogy of fallot: Most common cyanotic congenital heart disease.
1) Over riding Aorta
2) Membranous septal defect
3) Pulmonic stenosis below the valve.
4) R.V hypertrophy.

The degree of Pulmonic stenosis determines the cyanosis.

Not all babies with TOF have cyanosis. They are called Acyanotic-tetrology; The degree of P.Stenosis is't all that bad. When the right ventricle contracts, there would be lots of blood goes up in P.A and gets oxygenated and much less blood will go and get dumped into left ventricle ---> wont have cyanosis at birth.

In case of very severe stenosis: When right ventricle contracts, very little get up there and most of it will be shunted from right to left ---> step down of O2 in left ventricle may from 95-80% ---> cyanosis.

Cardioprotective groups of shunts: PDA and ASD

ASD: the blood will go from left-right ---> step up

PDA: From aorta-Pulmonary artery ---> some of unoxygenated blood also gets oxygenated ---> pulmonary vein is 95% oxygenated.

Its good to have a PDA and patent foramen ovale in TOF.

Abnormalities in right-left shunting: Polycythemia; risk for infective endocarditis, because you have shunt going from right side going into systemic circulation ---> risk for vegetations spreading to brain, and multiple cerebral abcesses any where they want.

All congenital heart diseases have risk for infective endocarditis.

Kartagener's syndrome ---> normal heart on the right side of chest.

Transposition of great vessels: Right atrium is still getting unoxygenated blood; left atrium still getting 95% O2 saturated blood from pulmonary vein; the problem is in the ventricles.

Right ventricle is being emptied by Aorta. Left ventricle is emptied by Pulmonary artery.

So the things thats transposed are venticles while atria are fine. Incompatible with life unless you have shunts.

Three shunts are working: Patent foramen ovale, septal defect and PDA.

Since 95% O2.sat in left atrium ---> thats going from left-right atrium---> step up of O2 in right atrium ---> step up in right ventricle ---> some of it, gonna go out the aorta, some of its gonna go in left ventricle.

Since left ventricle is being emptied by P.A ---> blood goes into lungs to get oxygenated.

The blood wont by 95% saturated but may be 80% ---> cyanosis in these patients.

Coarctation of aorta: Pre means before ductus; Post means after ductus.

Pre-ductal occurs in turner syndrome. Most common congenital disease in turners.

Post-ductal are't present at birth; Actually occurs any time in adult life. Its important to recognize because there is a surgically cause of HTN ???

Slide: We have stenosis over here in the aorta. Proximally there is a problem with getting blood through that, you will hear a systolic murmur there which probably be heard between the shoulder blades.

There will be lots of pressure build up proximally and this would dilate the proximal aorta ---> lots of pressure going up to those branched vessels like the subclavian and internal carotids; so the BP in upper extremities gonna be higher and certainly than the lower (limb). There is increased blood flow going into the brain right at the junction where the communicating branches hit the main branch of the cerebral vessels, we have no internal elastic lamina and no smooth muscles ---> its a weak area ---> all of us have potential for developing berry aneurysms and HTN will exacerbate it.

In APKD ---> 20-25% cases develope berry aneurysm; Also increase incidence in essential HTN, coarctation or any cause of HTN can produce the berry aneurysm.


Thanx khan ... take care smiling face

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