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MEDICINE OSCE - Part 1 — Transcript

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0:01Yeah.
0:03Okay. So I think uh this was a request
0:06that was told about medicine OSKIS where
0:09image based or uh clinical image based
0:12or clinical scenarios and all those
0:13things are going to be kept for exams
0:15possibly this times most of the exams uh
0:18in most of the centers have been done in
0:20this pattern itself. So some of the
0:24universities have kept realtime cases.
0:26Many of them have given case scenarios
0:28and quite a few of them have done oskis.
0:32So uh so here a new thing that we are
0:35doing I'm saying it's not that we have
0:36hard fast rules how oski has to be
0:38conducted actually oski has to be
0:40observed clinical scenario where you
0:42check it and you have a checklist which
0:43is given but then with this scenario
0:45where we do not have much interaction
0:47with the realtime s subjects so most of
0:50the clinical uh images are being used
0:53for oski and the assessment occurs based
0:55on that. So generally they would give
0:58you a image or they'll project an image
1:01of a case or a clay scenario will be
1:04given and then you'll have to be asked
1:06about the approach to that or they may
1:08give you an ECG or a X-ray or an image
1:11and based on that questions may be
1:13asked. So I've tried to incorporate as
1:17much as possible things that can be
1:19possibly asked. Uh and I think we'll
1:23begin. So as Krishna has mentioned let's
1:25keep it interactive. So whoever would
1:28want to answer uh could answer at any
1:32time there whenever the image comes and
1:34if you do not know anybody else can
1:36answer there's nothing wrong in uh
1:38there's nothing uh to lose here it's all
1:40going to be interactive there is a
1:42mistake I think we learn on how it is.
1:44So let's begin with the first image that
1:47I'm displaying here. So this would be a
1:50common image kept and generally they
1:53would ask questions based on this image
1:55and what are the findings that you're
1:57getting. So anyone can tell me what are
2:01you seeing on this image
2:06sir? Differential clubbing sir
2:08prominently lower limbs.
2:09Okay. So you're saying it's differential
2:11clubbing because there is involvement of
2:14the lower limbs and not involvement of
2:17the upper limbs. So what do you think is
2:19the diagnosis?
2:21What condition you get this pattern
2:25where the lower limbs are clubbed and
2:26the upper limbs are not club?
2:28PDA with the reversal sir.
2:30Okay. So you say it's PDA with reversal
2:32of shunt. But what would be the features
2:34be there along with the clubbing if
2:36there is a reversal of shunt
2:39sinosis? Yeah, you should have had
2:41sinosis also and generally once reversal
2:44occurs you would find central sinosis.
2:46So you do expect a lot of uh bluish
2:49tinge there but yes you this pattern
2:52actually you get it in PDA with reversal
2:54of sh is the sparad in PDA with reversal
2:58of sh why the upper limbs are spared
3:07yes
3:10why is the only lower limbs are clubbed
3:12or sinos and upper limbs pad in PDA with
3:14reverse option
3:17Subclavian artery arises before the
3:21connection between the patus artis
3:25blood supply that's the doctor's
3:27communication is after the left subclav
3:30that has been given. So after the left
3:32subclav that has been given that shunt
3:34is there existing after that. So the
3:36reversal will occur after that point. So
3:39the bloods that goes to the lower limb
3:42only gets deoxxygenated blood goes
3:45there. Whereas upper limb blood is
3:47normal. So possibly that's the reason
3:49for why this you get it. Okay. Can
3:51anyone tell me what are the common
3:53theories of clubbing? Whenever this is
3:55kept for you they would ask anything in
3:57related to clubbing. So can anyone tell
3:59me what are the theories of clubbing or
4:01what's the most accepted theory of
4:03clubbing at present? You have a large
4:05number of theories.
4:09platelet derived growth factor uh most
4:12accepted yes that's the most accepted
4:15one at present that's the platelet
4:17derived growth factor theory so platelet
4:19derived growth factor and because of
4:21that there is uh development of a canals
4:25under the uh subangal region there and
4:28that produces clubbing what grade of
4:30clubbing is this what grade of clubbing
4:33is this
4:34grade four grade four Grade three parrot
4:38baking.
4:39Grade three. Okay. Grade three parrot
4:41baking. How do you say it's grade four
4:43to say grade four?
4:44Hyper.
4:45What else should be there?
4:49Osteoarth. So, how do you check for
4:52that? How do you check for grade four
4:56or where do you look for grade four?
5:01Yes.
5:02Compression of the wrist joint and the
5:04ank and the elbow joint. You will be
5:06careful.
5:07Yeah, you will be testing or you'll be
5:10compressing at the distal end of long
5:11bones, the wrist as well as the lower
5:13limb. That's where you will be
5:16compressing and seeing the tenderness if
5:18it is there or not. Or you can take an
5:20image and see if there is a superior
5:22newborn formation. So this is clinically
5:24it looks like grade three clubbing. You
5:25have a parrot making appearance that's
5:27there. Okay. What are the common
5:29nonrespiratory non-cardiac causes of
5:32clubbing?
5:35Non-respiratory non-cardiac
5:37genetic
5:40ulcerative colitis.
5:42Yes. So inflammatory bowel disease.
5:44Correct.
5:44In bowel disease.
5:46Any other causes?
5:49Uh infert colonitis.
5:52G malignancy.
5:54Okay. Can Yeah.
5:56Carcinoma most commonly you can get it
5:59inital as you said. Familial clubbings
6:01could be there. Any neurological
6:03condition where you can get clubbing?
6:05Hemoplegia.
6:06Hemiplesia.
6:07Okay. Longstanding hemiplasia can
6:09produce more commonly in the upper limbs
6:12you can have clubbing.
6:15In patients with stringomalia
6:17seringomalia you can have clubbings in
6:19the upper limb. You get a classical
6:21finding in cingomalia also. So these are
6:23non respiratory non-cardiac. But most
6:25common causes are the respiratory and
6:27cardiac. So, so this is differential
6:31clubbing. Any doubts with clubbing?
6:33Anyone of you have?
6:36So, one of the most common clinical
6:38signs they ask you to demonstrate as
6:40well as they ask you about entire things
6:43about clubbing. Is clubbing reversible?
6:45Can clubbing reverse?
6:49Does it go back to normal?
6:53Yes sir.
6:54What conditions clubbing can reverse?
6:57Lung abapsis and empa.
6:59Yes. Whenever you have some sort of
7:02uh infective endocarditis is one common
7:04cause you should remember. Subaccute
7:07infective endocarditis if you're treated
7:08well the clubbing can go off or
7:11anyurative lung conditions like you have
7:13the lung absis. As we said if it is
7:15treated well possibly it can be
7:17reversed. Possibly it can be reversed.
7:20So
7:22uh why there is reversal of shunt in
7:24PDA?
7:26Anyone? Yes.
7:29Simple. It's for mild for ugre
7:34in pulmonary hypertension.
7:36Yeah. Okay. It can be development.
7:38Development of pulary hypertension. It's
7:40called isomeorization.
7:43Okay. Good.
7:46What age does PDA usually is mangorize
7:50of the three shant lesions ASD, VSD and
7:53PDA? Which is the one which is
7:56mangarizes the earliest?
8:01VST.
8:02Which condition are we like the volume
8:05overload is more for pressures?
8:10Of the three conditions which will occur
8:12the earliest?
8:14VSD sir.
8:15VSD I think sir.
8:17VSD or PDA? Which one?
8:19PDA. PDA sir.
8:22Generally PD is mangarizes the earliest
8:24followed by VSD. ASD may not is
8:27mangarize at all. ASD might remain like
8:29that for lifelong. ASD is mangers maybe
8:33after the age of 40. There is a general
8:36rule ruled by uh Sir Paul Wood. You
8:39heard of Sir Paulwood?
8:42Sir Paul would you have heard?
8:46Would you have heard would in what
8:49terminologies have you or what context
8:51have you heard would
8:55okay law
8:57okay your pulmonary artery pressure is
8:59measured in terms of wood's units isn't
9:02it so this is general rule they say
9:05though it's not written anywhere PDA
9:07will usually mangarize by the age of 16
9:11and BSD usually is mangarizes by the age
9:14of 28 and ASD D might is angorize much
9:18much later much later fourth decade okay
9:2140 and above so that's a general rule of
9:24is mangorization though it's not hard
9:25fast but as may not isomeorize at all
9:30can you tell anyone tell me what are the
9:32features that clinically will appear
9:34once is mangorization happens what are
9:36the features that would appear in the
9:38patient
9:39clubbing
9:41clubbing correct
9:43sinosis
9:44central sinosis correct
9:47Supposedly a patient with ASD is mangar
9:49what are the other features that will
9:51develop?
9:57Always remember this common things they
9:59ask you there are two sounds which come
10:05there are two murmurs which appear and
10:07two murmurss which disappear they say.
10:10So two sounds which appear once is
10:13meorization happens you know the right
10:14ventricle pressure is increased isn't it
10:16so what will happen the right sided
10:18sound what are the two rights sided
10:20sounds which appear you have the right
10:23ventricular S4 that will appear and the
10:26pulmonary ejection click not S3 S4 RV S4
10:31and pulmonary ejection click these are
10:34the two sounds that appear
10:37two murmurs will soften you know As
10:40usual in ASD there is flow across two
10:43valves isn't it the pulmonary valve and
10:46the triricuspid valve there are flow
10:48mmmers that are there so normally the
10:50mmmers that you get in ASD is there's no
10:52flow across the ASD the flow mas are
10:55across the pulmonary and triricuspid
10:56valve so what's the flow m across the
10:58triricuspid valve
11:04what type of mama you get when there is
11:06increased flow across the triricuspid
11:08valj sister
11:11triricuspid valve ejection no
11:13diastolic murmur
11:15mid diastolic murmur
11:16you get a mid diastolic murmur in the
11:18triricuspid area and in pulary area you
11:20get a ejection systolic as you said so
11:22normally whenever you have an ASD
11:25patient you normal without is
11:27mangorization these are the two mmers
11:29that you get you get an ejection
11:30systolic murmur in the pulmonary area
11:33and a mid diastolic murmur in the
11:37triricuspid area so what happens happens
11:39when isomeorization happen these two
11:41murmurs will soften and the opposite
11:43murmurs will come that is a triricuspid
11:46regurgitated MM a pans systolic murmur
11:49in the a triricuspid area and a uh mid
11:54early diastolic mmer of pulary
11:56regurgitation in the pulmonary area. So
11:58this is a simple rule all of you
12:00remember
12:01two sounds appear two mmas soften or
12:05disappear and two murmurs appear this is
12:07a rule for all mice mangorization but in
12:09adults when you get is ASD is the usual
12:11case that is skipped so they ask you
12:13about this so can anybody repeat what
12:15are the things that clinically happen
12:18Vijay
12:19I think you have written quite a lot of
12:21on chat you can repeat
12:23you can you can unmute yourself and
12:24answer Vijay
12:28Yes. Uh there are two murmurss that
12:30disappear. One is the flow murmurss on
12:33the right side disappear.
12:36Yes. What are those?
12:38The murmur of uh MDM disappears.
12:42MDM in dry cuspit area disappears and
12:47pulmonary
12:51uh ESM in the pulmonary area disappears.
12:54ation system disappears.
12:55Two mas which appear are
12:58pulmonary click appears and pulmonary
13:01click and RVs4 appears
13:04RVS4
13:05RVs4 appear. Two mummas which yeah two
13:08mas which appear
13:11are the pulmonary regurgitation and
13:12triricuspid regurgitation ma regation.
13:14Tricuspid regurgitation you get a
13:16panistolic mama and pulmonary
13:18regurgitation you get a early diastolic
13:21mama and clubbing and cyanosis will
13:23appear and JVP if you look for once
13:26isomeorization happens you get a becomes
13:29equivalent to Vwave.
13:31What about hard sounds?
13:32A become more prominent
13:34heart sounds. Yeah, I think he has
13:36written it in the chat there. ASD
13:39normally what's the hallmark of ASD
13:41oscultation wise the hallmark
13:44fixed wide s2 fixed wide to split
13:47wide split
13:49yes correct correct what happens to that
13:52once uh is mangorization happens what
13:55happens to the split
13:56it narrows or can become singled
13:59yes but always remember if you have to
14:01differentiate asd mangar vsd is and uh
14:06pdis mangar
14:09The first thing that you're going to
14:10look for is differential clubbing. If
14:11there is differential clubbing, it is
14:13PDA. So you don't have to think of
14:15anything. ASD and VD is manganger have
14:18pan digital clubbing and pan digital
14:20signs. Now how do you differentiate
14:22whether it is ASD is mangar or VSD is
14:25mangar is based on the uh split as you
14:28said in both as VSSD and PD mangar once
14:33pulmonary artery hypertension develops
14:35pulary hypertension develops the split
14:37becomes very very narrow but in ASD
14:41mangar however severe the pulary
14:43hypertension happens the split might
14:45narrow but it'll never be single it'll
14:48never be single so first thing look for
14:51differential cyanosis and if that is
14:53there it is PDA second oscultate on
14:56second heart sound if it is single and
14:58it's not there is no mobility there that
15:02means vsd is mangus that is what you'll
15:05have to think of so always remember the
15:07rule for oscultation for cardia is
15:09second heart second heart sound gives
15:12you everything in cardiology oscultation
15:15okay so just by this image only you can
15:17get a lot of questions so the same image
15:19can be kept for All of the candidates
15:21and the questions can be different. So
15:22you have to be prepared for that. Okay,
15:25we'll move on to the next one.
15:29Tell me about images.
15:40I'm not able to see your names. So
15:42anyone can
15:44call and tell. So dupetin contraure
15:48paroted swelling gynecomastia
15:50first
15:51contracture correct
15:54correct
15:56gynecomastia as you said correct what
16:00else
16:05yes
16:06flapp flapping tremor
16:07flapping tremors correct what is the
16:09next image to flapping tremors what is
16:10the next image showing
16:13this one
16:15Okay, Luc Nika is there. Okay, what's
16:17next one? Oridometer.
16:20This is the orchidometer. It goes by the
16:23name of
16:25Prada's orchidometer. Okay. And this
16:27one,
16:30the last one that you have here.
16:32KID formation.
16:33Koid formation.
16:34There is a koid there. Okay. There is a
16:36patient who has a koid is there.
16:39Nicholas pattern of a tattoo mark.
16:42Okay. Tattoo mark is there. Good. Then
16:44anything else? What is this
16:48good?
16:48What is this one?
16:50Spider navies.
16:51Spider.
16:52Okay, spider nei. You can make out some
16:54spider nei there. Okay, fine. So, what
16:57is the [clears throat]
16:57impression of the entire thing? These
16:59are all signs of
17:00liver cell.
17:01Liver cell failure. Okay. Liver cell
17:03failure. Okay. Which of these are signs
17:06of alcoholism?
17:09Paroted swimming.
17:11Yeah. Enlargement and dupitance. These
17:14are the first [clears throat] two images
17:15that you're seeing are signs of
17:17alcoholism. Alcoholism. Okay. Based on
17:20the last image, what else impression do
17:22you have? You have said these are all
17:23signs of liver cell failure. This
17:25patient you said there is a tattoo there
17:27and there is a kloid there. So any
17:29relevance?
17:33Yes.
17:34Any viral infection?
17:36Yes. Viral infections. Which viruses you
17:38suspect?
17:40Heb
17:41or hep or heeps. So it could be a
17:44postsurgical scar which has gone into a
17:46kiloid or there is a tattoo mark that's
17:48there which could have gone into the uh
17:50where the viruses could have come
17:52through a bottle. Okay. Can anyone tell
17:55me about this flapping tremor? If I ask
17:58you to discuss the flapping tremor, what
18:00is flapping tremor? What is the
18:02mechanism of flapping tremor?
18:09Basically a negative myioonis.
18:11Okay, it's a negative myocronus. Person
18:13is not able to maintain the sustained
18:15posture sir. So person is not able to
18:17maintain a sustained posture. What is
18:19that due to
18:21uh
18:21because of the uh
18:24because of suppression of the
18:27andus?
18:28Yeah. So suppression of the reticular
18:31activation system due to various causes
18:34in this patient. The cause is due to
18:36increase in the
18:40increase in the whatopathy.
18:42The ammonia isn't it?
18:43Ammonia.
18:44Ammonia is the one which is causing it.
18:47So it's a negative myioonis. Very
18:49important. Though the word we are using
18:50is flapping tremor. Why is it not a
18:53tremor?
18:55Because there is no rhythmic movement
18:57across the
18:58there is no rhythmical movement. If you
18:59see flapping tremor is only forwards. It
19:01goes forwards. Tremor has to be to and
19:04fro. Okay. So this is okay. Can you tell
19:06me some causes of flapping tremor other
19:09than hpatic and
19:13respirator? Correct. Respiratory failure
19:16specifically
19:18hyperapasia.
19:20Correct. CO2 naros. Correct.
19:22Chronic renal failure.
19:24Chronic failure. Very good. Yes. Uremia.
19:26Correct. Then
19:29cardiac failure also can cause. So all
19:30the organ major organ failures can
19:32produce this also drugs okay especially
19:37anti-epileptics that we give
19:40yeah phenitoine is known to cause this
19:42if you patients on long-term phentoine
19:46you can get this finding that could be
19:48seen that is rare in the patients with
19:51uh
19:53with the flapping tremors that could be
19:56there okay fine okay how do you uh
19:59diagnose knows gynecomastia.
20:02How do you clinically make out
20:04gynecomastia? Anyone?
20:08Palpation of this tissue is more than
20:11very important. It is not an inspector
20:13finding. It is palpation. Palpation
20:16only. You'll have to palpate a
20:17nodularity
20:19size maybe 4 cm some say or but it
20:22should be palpable. It's not a inspector
20:25find. Correct. Fine. Okay. Can anyone
20:28tell me some causes of gynecomastia
20:30other than cerosis of liver
20:34drug induced?
20:35Yes. Can you tell me some drugs? Name
20:37some drugs.
20:38Amiodoron. No. Omiodoron is not common.
20:43Siradine.
20:45Correct. Spyronolactone. Cementedine.
20:47Correct.
20:52Very good. Yes. INH. Very good.
20:56So these are the common drugs. INH is a
20:58common drug. Ketoonazole symmetro.
21:04Estrogen.
21:05Estrogen.
21:06Yeah. Estrogen can cause. Correct.
21:08Anti-androgens which we use for ca
21:10prostrate. Isn't it? That can also cause
21:13other than drugs any other causes where
21:15you can get gynecomastia.
21:18Yes. It could be due to Yes. Tumors.
21:21Correct. More importantly
21:23in males, young males,
21:25young males,
21:26puberty,
21:28puberty. Okay. Physiological
21:30physiological
21:32gynecomastia.
21:33Senile can be there. I mean saying a
21:35young male comes with a gynecomastia.
21:38What is the thing that you want to
21:39suspect? Not pubertal.
21:41Kleinfelters.
21:43Okay. Kleinfelters is possible. Very
21:45important is testicular tumors.
21:48Testicular tumors. You always have to
21:50examine the testice and see. So it could
21:52just be a finding there. Patient may not
21:54be noticing the testicular tumor that
21:56much but the gynecomastia might be a
21:58finding. So testicular tumor is one
22:00thing that you should always remember.
22:03Fine. So
22:06sir I have one question sir.
22:07Yes tell me
22:09sir why the dupet contraction and
22:11paroted swelling is specific for
22:12alcoholics can be seen in other
22:15conditions also. It can be seen but then
22:17if you see the list of cerosis now we
22:19are talking about cerosis in a patient
22:22with cerosis. If you find these two
22:26they are specific for alcoholic
22:28ethiology. Okay. The other causes of
22:31cerosis do not cause dipetrins and
22:33parotid that is what is the relation.
22:35Not that parotid enlarge parotin
22:37enlargement can occur due to anything
22:38like mums and other things but this
22:40combination if it is there's contraure
22:43parotid and sometimes they say the third
22:46finding is palariththema. Okay
22:49palarthema also has been described as
22:51seen more often in alcoholics. The
22:53dupitrance contraure is secondary to the
22:55fibrosis which occurs in alcoholics in
22:58every part of their body starting from
23:00their liver retroparonium in the plantar
23:04fasia in the penile fasia. You heard of
23:06a disease called as uh ponese disease.
23:10Now that's called as penile fasia. All
23:12of those are common with alcoholic
23:14patients. Okay. [snorts] All of them are
23:16common with alcoholic patient because
23:17fibrosis is more common. Parotid
23:20enlargement is secondary to the
23:21autonomic dysfunction that happens
23:23secondary to alcohol. So these two
23:25findings are not seen in the other
23:27causes of alcohol uh other causes of
23:29cerosis be it hepatitis B or a nash etc.
23:34All of them do not cause this find that
23:37is why that's told as specific for
23:39alcoholism.
23:41Okay. Uh and paroted enlargement need
23:44not mean cerosis of liver. Deportance
23:47contraction did not mean cerosis of
23:49liver. It may be just seen in alcoholics
23:51itself.
23:53Can you tell me some causes of
23:54dupitrance contraure? You told me it can
23:56be seen in other conditions. What are
23:57the conditions where you can get
23:58dupitrins?
24:00Hypothyroidism, macroaggali and
24:03idiopathy can be seen
24:04more commonly commonest cause that you
24:06you would see
24:07diabetes.
24:08Diabetes always remember diabetes.
24:10[clears throat] You have a condition
24:11called as diabetic kioarthropathy where
24:14you can get that. Okay. And people who
24:16are mechanical uh work they do
24:20especially
24:21or laborers who have uh working with
24:24vibrating instruments etc can happen.
24:26Okay. Fine.
24:29Any other doubts regarding this?
24:32So again based on these you can say the
24:34various complications the patient has.
24:37Okay. There is spider nei that's there.
24:39So possibly he has portal hypertension
24:41that's there and he has luconia that
24:44means there is hypoalamineia that's
24:46there and flapping tremors if it is
24:48there it means apatic enchilathy. So you
24:51can make out certain complications also
24:53of the patient.
24:56What's the most common cause of cerosis
24:58world over?
25:01Most common cause of cerosis.
25:06Most
25:07Yes.
25:09Nash.
25:10Yeah, Nash is coming up. But still for
25:12your exams, I think you should still
25:13maintain it as Nash is coming up. I
25:16agree with Nash. But for your exams, you
25:18should still say
25:20post viral. No, not alcoholic. Alcoholic
25:23has gone down a lot. Post viral. Okay.
25:25Post hepatitic is still
25:27Yeah. Hepatitis B, hepatitis C, that's
25:29still the nash has definitely come up.
25:31But uh I think for exams you can still
25:33maintain as postviral, followed by
25:35alcoholic and followed by nash. Okay.
25:41Can anyone tell me some noninvasive
25:44test that can detect nash?
25:47Shanjib.
25:48Fibro.
25:49Fibrocan.
25:50Fibro.
25:50Electrography.
25:51Electrography. Fibro scan. Yes. These
25:54are some non-invasive tests which are of
25:57late useful for the detection of uh your
26:00uh it can be detecting fibrosis even in
26:04cerosis also not only. Yes. USD can be
26:07mentioned sir.
26:09USG yeah USG is a good old test but then
26:12the scoring whatever based on the
26:14fibrosis now USG can tell you that there
26:17is shrunken liver etc. The fibrosis if
26:20they ask you I think it has to be told
26:21as a fibrocan or a elastograph
26:25ultrasound elastograph ultrasound only
26:28they use the same method but they use it
26:30with a uh reflection of the waves etc
26:33they calculate okay and please read
26:36about it there are certain scores that
26:38are there various blood markers like a
26:41sorry alt platelet count etc are all
26:45picked up and they make a score of it
26:46okay let's go on to the Next slide here.
26:49Yes.
26:52KF
26:53KF ring.
26:54This is a quesia fia ring. So what is
26:56your diagnosis?
26:57Wilson disease.
26:59Wilson's disease. Okay. Now can you tell
27:01me the differences between the KF ring
27:03and the arcus?
27:08Arcuselis
27:10appears with a gap from the limbbus
27:12whereas KF ring appears at the limbbus.
27:15Okay. So that's the first difference.
27:16Correct.
27:19And
27:20uh it arcus begins in the superior
27:24temporal region.
27:27Arcus does it begin like that?
27:30KF ring begins in the beginning.
27:32Always remember KF means the beginning
27:35it's in the upper part then the lower
27:37part then it comes to the sides. Okay.
27:39So whereas arcus comes through and
27:41through. Okay. That's the second
27:42difference. Correct.
27:44Then
27:46some more
27:49it is seen better in the lamp sir. KF
27:51rings.
27:52Yes. KF is seen better with the slit
27:53lamp whereas arcus can be seen on the
27:56Yes. Correct. Then
27:58reversible with the treatment.
28:00Yes. Correct. KF is reversible with
28:02treatment. Once we start them on
28:04chilating agents KF can reverse whereas
28:06arcus remains. Correct.
28:09Age sir younger and uh elders.
28:11Yeah that's correct. So age is also a
28:13very important feature and associated
28:15features isn't it? Wilson's can be
28:17associated with what features
28:22features
28:24neurological
28:26manifestations.
28:27Sometimes cerosis also can be there
28:29correct and sometimes they may not have
28:30anything only the kfring can be there
28:33and please remember kring is more often
28:35associated with neurological winssons
28:37rather than the hpatic Wilsons that
28:39could be there. Okay. uh whereas arcus
28:41is usually associated with what arcus
28:46aging
28:47aging aosclerosis
28:51that's one difference the color is also
28:53different
28:54in case color is yeah arcus is whitish
28:57this is golden brown golden brown okay
29:01so what are the conditions where you can
29:03get kring other than Wilson's disease
29:07foreign body corporate body position
29:11Power in body will it deposit all over?
29:13No,
29:14it won't be all over.
29:15Unilateral.
29:17Usually one side and one part only. It
29:19won't be full.
29:24Primary bilary cerosis any kind of
29:26longstanding obstructive joint.
29:28Whenever there is an obstruction okay
29:30chronic obstructive
29:32uh to the bilary tract that is there
29:35chronic obstruction. So primary bilary
29:37cerosis or sclerosing colangitis
29:40sometimes chronic active hepatitis these
29:42are the three important causes which
29:44they expect you to answer in the exam
29:46primary bilary cerosis primary sclerosin
29:48colangitis and uh chronic active
29:51hepatitis okay you could get this okay
29:54uh you can get the PF okay so how do you
29:58uh confirm the diagnosis of Wilson's
30:00what is the gold standard
30:03biopsy
30:05liver
30:08is the gold standard which we don't do
30:09often. What do we do?
30:11Urinary copper levels and ceroplasma
30:14levels.
30:14Urinary copper excretion as well as
30:18plasma ceroplasine levels. What happens
30:20to the ceroplasine? Increased or
30:22decreased?
30:24It reduces.
30:25Reduced. Okay. And then you have
30:26something called as a depensamine
30:28challenge. Anyone can tell me about
30:30dependencine challenge.
30:37Deepensamine challenge. What do you mean
30:39by that?
30:40Uh 500 mgram of pen penicellamine is
30:43given at the beginning of 24 hours and
30:45later on.
30:46Yeah. So you do a urinary you do the
30:48urinary test and then you give a
30:50challenge.
30:51You give a
30:53deep penisamine and then check the
30:55urinary copper again. So you make out
30:57whether the copper has been excreted in
30:59that. Sometimes the values may be in
31:00borderline then you'll have to do this.
31:03Okay fine. So I think that's about the
31:06KF ring. Again a very common thing
31:08that's asked for you
31:11even in your clinical vas that would be
31:13C. Okay.
31:16Yes.
31:19Anyone can describe this for me.
31:27Rheumatopy.
31:28Rheumatopathy.
31:30Okay. So, what are the things that you
31:31look at? What are the things that you're
31:33seeing?
31:36Swan neck. Correct.
31:38Hitchhikers.
31:39Second.
31:40Yeah. In the thumb, you can see the
31:41hitchhikers. Correct.
31:44Third image here.
31:47What is this?
31:48Alnar deviation.
31:50You have some sort of a uh Yeah. alnar
31:53plus some zed sort of deformity here
31:55it's going like this you can see the
31:57thumb is also gone into some sort of a
31:59zed there okay this image
32:02Alex wus
32:03Alex vgus what has happened to the other
32:05toes
32:07they've gone down isn't it it's called
32:09as hammer toes
32:11hammer toes what is this last one
32:15nodule
32:16okay there's a nodule there but what
32:18about the hand what is this called as
32:20intr wasting sir
32:23wasting correct but what is the sign
32:25called this
32:27looks like what
32:28I think in chat somebody has mentioned
32:31no
32:33yeah the deformities are agreed but what
32:34do you call this the uh these are seen
32:37like strings now
32:40piano
32:41piano doesn't have strings
32:43no no no
32:44piano doesn't have strings what are
32:45strings
32:47it's called as a bow string sign okay so
32:50okay so all these are features of uh
32:54rheumatoid arthritis which is erosive.
32:57What about the first image? Nobody told
32:58me about the first image.
33:02Last 28 score.
33:04Okay. So this is the uh okay the scoring
33:07system or the joints which are commonly
33:09involved in uh rheumatoid arthritis. So
33:12that is what you can see that okay so
33:14this is a deformed rheumatoid arthritis
33:16that you see. So already there are
33:18enough deformities. How do you
33:20differentiate u the deformities that you
33:23see in rheumatoid versus the deformities
33:25that you can get in SLE?
33:28Erosive.
33:29Okay. Erosive. You can take an image and
33:31see whether it's erosive. Any other can
33:34you get deformities in
33:37d
33:40uh dip will be spared in rheumatide.
33:43Okay. So DIP will be spared in
33:45rheumatide in SLE
33:48not commonly in all s not the basic
33:51thing is the deformities are correctable
33:55okay they are correctable they don't
33:57remain like this okay it gets corrected
34:00and there is no erosion that's very
34:01important very rarely you can get
34:03erosive arthritis in that is called as
34:09yes I think people have written in the
34:11chat it's called as jakud's arthritis is
34:13very rarely you can get erosive
34:16arthritis in SL. Okay. Fine. So why
34:19can't it be seriatic arthritis?
34:23How do you differentiate serorasis
34:24versus rheumatoid?
34:29History of sorasis or active sorasis.
34:32Okay. Stimulations will be there.
34:33DIP involvement.
34:35Yes. DIP involvement. Again, please
34:36remember in almost 30% of patients with
34:39seriatsis, the arthritis precedes the
34:42disease. It precedes the disease. It
34:44doesn't come skin involvement is not
34:46there. It is the DIP involvement which
34:49specifically rules out uh uh it rules
34:54out rheumatoid rheumatoid you don't get
34:55DIP involvement that is seen. Okay. A
34:58patient with rheumatoid arthritis comes
35:00with coarseness of voice.
35:04What do you think is the cause?
35:12Yes.
35:14Secondary to pulmonary hypertension.
35:16Sir,
35:17pulmonary hypertension. How does it
35:19produce horarsseness?
35:22Partner syndrome. You're saying
35:23syndrome.
35:24Very very far-fetched. Now, it has to
35:26cause ID and then the ID has to cause
35:29pulmonary hypertension. Something more
35:31commoner and simpler.
35:33Yes, I think somebody has put it in the
35:35chat. Vishnu Pria has written. Yes,
35:38joint involvement. Trickorit joint can
35:41get involved in case of rheumatoid.
35:43Okay, again it's a very rare thing.
35:46What's a commonest thing if somebody has
35:48rheumatoid arthritis and is on treatment
35:51and gets horarsseness and what could be
35:55there?
35:57It's imunosuppressed, isn't it? So what
35:59could be there? Steroids causing
36:02horarsseness. How does steroid cause
36:03horarsseness?
36:05Arjun we have written there as steroid
36:08causing horarsseness.
36:14Inhale steroids and all can cause but
36:17systemic steroids causing host. What can
36:19happen in the larynx? Opportunistic in
36:21tuberculosis. Please remember whenever
36:23they come with hostseness the first
36:25thing that we have to rule out is lenial
36:26tuberculosis. Second is creeknoid joint
36:29involvement and then as uh I think Vijay
36:33told it could be pulmonary artery
36:34hypertension. There could be other
36:35causes also. Always remember
36:37tuberculosis is very common when they
36:39are imunosuppressed especially with
36:41vitrix and steroids. Okay. A patient
36:43with rheumatoid arthritis comes with
36:45paraplegia or quadriplegia. What do you
36:48think is the cause?
36:52Involvement.
36:53Clantoaxial dislocation. The clentoxial
36:55dislocation that can occur there. Okay.
36:57Patient with rheumatoid comes with hip
37:00pain.
37:03Avascular necrosis.
37:04Avascular necrosis.
37:05Because of steroids.
37:06Because of steroids. Okay. Any other
37:09mechanism? Avascular necrosis. Correct.
37:12Because of steroids is correct. Any
37:14other mechanism? Avascular necrosis can
37:17happen
37:19in a patient with arthritis.
37:22Arthritis is one thing you should always
37:23remember. Correct? Because it could be
37:26uh due to imunosuppression there could
37:28be tuberculosis of the joint. One
37:30important thing osteoporosis secondary
37:33to steroid can be can you have avascular
37:36necrosis and rheumatoid itself?
37:41Can the vessels get affected because of
37:42rheumatoid arthritis?
37:46Yes, it can cause vasculitis.
37:48Vasculitis. So when they come with hip
37:50pain, you should always think of these
37:52possibilities. Always rule out
37:53tuberculosis of the hip, septic
37:55arthritis, osteoporotic fractures. But
37:57always remember avascular necrosis is a
38:00common complication of long-term
38:01steroids also.
38:04Okay, I think we'll move to the next
38:06one.
38:10Yes.
38:12Uh sir,
38:13yes.
38:17Icepack.
38:22So this is myiaastthenia
38:24seeing it that the there istosis and
38:28then the ice is placed on the eyes and
38:31then you find that there is an
38:32improvement of tossis that is there. So
38:34this is called as reversibletosis
38:37secondary to so how does the ice help?
38:39Why is the ice helping?
38:42What's the mechanism ice is helping?
38:48Yes
38:54inhibition.
38:56So
38:57same.
38:58Okay. So when the temperature decreases
39:01there is less yeah the estoline stresses
39:04will uh improve. There is an improvement
39:06because there's less depletion of that.
39:08There is no activity that's happening.
39:10So it's like rest with addition of cold
39:13that is there. So it improves better.
39:15Okay. So ocular myastthenia isn't it
39:18ocular myastia.
39:20What are the antibodies that you do for
39:22myastia gravis?
39:26Receptor antibodies.
39:31Correct. Then
39:35antimus. Yes. LRT4. That's a very
39:39important thing you have to remember
39:40because you have a major group of
39:42myastthenia what we call it as antibbody
39:44negative myastthenia gravis and for them
39:47these receptors these newer antibodies
39:50that have come up and they can be
39:52diagnosed based on that the uh treatment
39:55modalities is slightly different for
39:57each of them. Yeah, antistatic muscle is
39:59one group of the anti- uh same group of
40:03antibodies.
40:05How do you grade any uh scaling scale
40:08you know for myia
40:10any staging system for myastia?
40:20Anyone
40:22any scale you know of myastia
40:26scaling or grades based on which the
40:30treatment can be modified?
40:36Nobody
40:38sir.
40:41Yes. Our man's aerman man's grading
40:43system is there. Fine.
40:46What is the Can anybody tell me about
40:48the neurohysiological testing that we do
40:50for myastenna? What is the gold standard
40:53test?
40:57Repetitive nerve stimulation.
40:58Single fiber.
40:59Yeah, single fiber muscle
41:02electromyiography and the repetitive
41:03nerve stimulation test. So you get what
41:07sort of response in myastia?
41:10Decremental response.
41:11Decremental response. Very important. So
41:13decremental response.
41:14Response. Yes. Can you tell me the
41:16differences between myastia gravis and
41:18lambert eaten myia gravis? Can you tell
41:20me some profile differences
41:22there? It will be incremental response
41:24on the
41:25So one is your incremental response.
41:27Correct.
41:29Clinically the weakness worsens in the
41:31evening in case of my gravies and
41:33improves in case of lambertton syndrome.
41:37Okay that's okay that uh maybe it's
41:40textbook wise it's like that but
41:42clinically you may not get that pattern.
41:44Okay. As you said fatigability and
41:46worsening as the day progresses is more
41:48suggestive of myastthenia. Okay, that
41:51can be said as
41:53where is the problem with the myastia?
41:55Where is the problem in lambert?
41:59What is there? We have it against
42:01chestile receptor presinaptic one here
42:04and where there it is the post synaptic
42:08uh calcium channel calcium channel
42:12pre synaptic voltage gated calcium
42:14channels correct so that's one
42:16difference any other differences what is
42:19the malignancy that is associated with
42:21CA
42:22CA lung correct what's the malignancy
42:24associated with myastia
42:28so remember thyoma for myastthenia and
42:32or small cell carcinoma for this one.
42:34The other most important clinical
42:36difference I think somebody has already
42:37written that DTRs
42:40very important deep tendon reflexes are
42:43absent in Lambertton whereas in myastia
42:46however severe it is the reflexes are
42:48present. Why does that happen in
42:49Lambertton?
42:51Why is the reflexes absent?
42:59Yes.
43:01Why is reflex absent in lambertton?
43:04So please remember it's a paranoplastic
43:06manifestation. So there is associated
43:10neuropathy. Lambertton is not only
43:13[clears throat] neuromuscular junction,
43:14there is associated neuropathy also.
43:16That is why the reflexes are absent.
43:18Okay. Reflexes are absent. And as you
43:21said the EMG finding you told me there
43:22is a decremental, there is an
43:24incremental. And the other thing that
43:25you uh the treatment treatment ocular
43:28involvement is rare with lambertton
43:31whereas it is almost a rule with with
43:33myastinia gravis it is a rule whereas
43:35with lambertton it is not common the
43:38treatment how do you treat LMS it
43:40responds to only what drug
43:43uh
43:48it's a poor prognosis because it's
43:49already paranoplastic but which drug
43:51helps in lambert
43:56348
43:58I couldn't hear you.
44:02Yeah, diaminopyirin. Diaminopyodin may
44:05be beneficial whereas here your
44:07classical drugs would be beneficial in
44:09this case.
44:19Yes.
44:23What do you find buffalo moon faces
44:30it try
44:31with the buffalo hump obesity and moon
44:34faces. So these are the features of
44:36pushings
44:37cushings. So how do you approach a
44:40patient? So this is a patient whom you
44:42suspect to be having pushings. By far
44:44the most common cause of pushings is
44:46what?
44:48Most common cause?
44:52because of drugs. Correct. So how do you
44:55approach this patient?
44:58What is the way you will approach? You
45:01want to know that this is what is the
45:03thing? So what do you want to do for
45:05this?
45:06Dexamethasone suppression.
45:08Dexamethasone suppression straight. You
45:10want to do the suppression test only.
45:13You want to confirm 3 a.m. cortisol. 3
45:15a.m. cortisol early morning cortisol.
45:18Okay. Midnight or early morning not
45:20early morning yeah somewhere midnight
45:22cortisol is one thing because you could
45:24get pseudo cushing features isn't it
45:25pseudo cushing features can be that
45:27though you may not get this purplish try
45:29and all in that so you would do a
45:32cortisol so cortisol is the basic based
45:34on that then you will have to go on to
45:36rule out whether it's a Cushing syndrome
45:39or it's a Cushing disease whether it is
45:42what's the next thing you want to
45:43classify it as whether it is
45:46KCDS dependent
45:48Correct. You want to classify it as HTT
45:50dependent on non-dependent. So uh
45:53midnight cortisol is the one thing that
45:55you would want to do first and then you
45:57would want to uh perform the rest of the
46:00cortisols possibly. The earlier
46:02algorithm was to do a 24-hour urinary
46:05free cortisol. This no we don't do it.
46:07We just do a serum cortisol and see. But
46:10this is for if you want to follow a
46:12algorithm then we'll have to do this.
46:14That is the 24-hour urinary for your
46:15cortisol. If it is normal then it rules
46:17out pushings. If it is abnormal only
46:19then you'll perform go on to the ACT
46:22levels and based on that you can perform
46:24the high dose low dose etc. And then uh
46:28if you have uh localiz it to the
46:31particular organ you'll have to do the
46:32imaging of the particular point you may
46:34have to do a contrast CT you may have to
46:37do an MRI and then you may have to
46:38proceed. Okay. What are the
46:40complications of Cushing syndrome?
46:45Hypertension correct bruising
46:47hypertension it can cause hypertre
46:49chance of infection
46:50correct psychosis
46:52psychosis correct
46:53osteopitis
46:55osteoporitis yes diabetes malitis so
46:57these are important complications which
46:59can again hypertension always when you
47:01have a recent onset hypertension that's
47:03when you have to suspect what is medical
47:06adrenalctomy
47:08can you name some drugs which produce
47:11mitoapone
47:14correct
47:15Konazole.
47:16Ktoonazole. Correct.
47:18Some more
47:21gallium.
47:25What is that?
47:26Motain can be used.
47:28Motine. Mitoine. Correct. They told me
47:30metapone. Ketoonazoo. Correct
47:32sir. Octtoide. Sir. Octootide.
47:34Okay. Octootide can be used. But again
47:36remember octtoide is a short acting
47:37thing. So it's difficult to use that.
47:40Ainoglutamide can be used. So these are
47:43all the ways to give highdose ketoconol
47:45is uh again very importantly
47:47ketogonazole is used and abused for
47:50fungal infections. People are taking
47:51ketogonosol daily for years together.
47:54They finally end up in some sort of a
47:57sort of features in a clonic usage. It's
48:00coming up now
48:02because of that but it's a high dose not
48:04the routine dose which has been given
48:05for skin infections. Okay.
48:12Yes.
48:14Hyperyroid.
48:16Hyperyroidism. Correct.
48:17Okay. Are you right in saying
48:19hyperyroidism?
48:22Thyrotoxyosis.
48:26What's the difference between
48:27hypothyroidism and thyrotoxyosis?
48:30Thyrotoxyosis.
48:32Thyrotoxicosis is
48:34like increase in the thyroid increase in
48:36the thyroid hormone levels.
48:39Okay. thyroid hormone also it will
48:41include primary secondary
48:44whereas in hyperyroid secretion when you
48:47call
48:48very important hyperyroidism is
48:51increased secretion from the thyroid
48:54only when there is an increased
48:56secretion from the thyroid for example
48:58what's the example for hyperyroidism
49:02graves
49:04graves disease there is an antibbody
49:05which is stimulating and it is producing
49:07so thyroid itself is producing the
49:09hormone excessive. So it is
49:10hyperthyroidism. Whereas thyrotoxyosis
49:13is any condition where there is
49:14increased hormones in the blood. It can
49:17be secondary to hypothyroidism. It can
49:19be due to other causes like very common
49:21that we get is thyroiditis. Please
49:24remember Hashimoto's much commoner than
49:27Graves. Graves is an autoimmune disease.
49:29Uh we may not get it so often but
49:32Hashimoto's very very common. Okay. So
49:35it produces transient hypothyroidism
49:37because there is an inflammation of the
49:38gland and the hormones are secreted out.
49:41How hormones are released out or
49:43iatrogenic or a paranoplastic something
49:45like that. All of them are causes of
49:48hyperthyroid. They are causes
49:50thyrotoxyosis not hypothyroidism but
49:53based on these features you have the
49:54orbital that is very classical the
49:57diagnosis is graves disease isn't it?
50:00Graves disease. Okay. So what is the
50:02images showing?
50:08Okay. Proptosis. This is also showing
50:09proptosis. Yes. This is showing a
50:13nod. Nod.
50:16Yeah. Nodular go. Okay. By examining the
50:19goer. Can you differentiate whether it
50:21is a hyperthyroidism or hypothyroidism?
50:25By examining the goer. Can you tell?
50:31If there is a brewy then mostly it may
50:33be a correct.
50:34So you have to oscultate. If you
50:36oscultate on the thyroid and if you're
50:38able to hear a brewy there that means it
50:40is a vascularity increase. So it's a
50:43hyperyroid. So it's a very important
50:44sign that clinically you have to make
50:46out because majority of the thyroid
50:48enlargements we get goiters are
50:50generally u or hypothyroid. Hyperyroid
50:53is not so common compared to hypo. Hypo
50:56is a much commoner disease that you
50:57would encounter. Okay. So what is the
51:01test that you want to do for this
51:03patient? Investigation.
51:09Yes.
51:13[snorts]
51:14TSH.
51:15Okay. You would want to do the
51:16antibodies. What antibbody for graves?
51:19TSH receptor.
51:20TPO.
51:21AntiTPO.
51:23AntiTPO is basically for Hashimoto.
51:26Hashimoto.
51:26Hashimoto. TSH receptor antibodies what
51:30we do for
51:31Graves disease.
51:33So TSH receptor antibbody could be there
51:35and you have some other antibodies also
51:36that could be there. Okay. If I do a
51:38radiooding scan for this patient what
51:40will I get?
51:42Diffuse uptake.
51:44Diffuse uptake will be a hot
51:48cold warm
51:51hot sir.
51:52So it'll be a hot increased uptake will
51:54be there. So increased uptake. Okay. Do
51:56I require to do a FNAC or a biopsy of
51:59the thyroid?
52:01No sir.
52:02Okay. For this patient we don't require
52:03because there is telltale evidences of
52:06graves the ofthalmopathy as well as the
52:08pretibial mixadema. If that is there
52:11that becomes graves. But then if these
52:13two are not there supposedly you have no
52:15eye signs or you don't have pitbial
52:18mixedma and it's not an autoimmune
52:20antibodies plus minus then possibly
52:22we'll have to do a FNA and see if there
52:24is any malignancy that could be there
52:27that has to be ruled out in a patient.
52:29Okay. Okay. How do you treat this
52:32patient?
52:39Okay. So you will be starting them on
52:41antiyroid drugs. Okay.
52:42Again very important remember when it is
52:45hyperthyroidism you'll have to give
52:47antiyroid drugs. But for thyrotoxyosis
52:49without hyperyroidism
52:52we are not supposed to give antiyroid
52:54drug. Thyrotoxyosis without anti without
52:56hyperyroidism we're supposed to just do
52:59symptomatic treatment like beta blockers
53:02etc. Because if you give antiyroid drugs
53:04for a hashimotos what will happen?
53:07For a hashimotos I give neomarosol. What
53:09will happen
53:15initially during the thyrotoxic may then
53:18the patient will go into more
53:19hypothyroidism.
53:20Patient will go into overt
53:21hypothyroidism very
53:23in a few uh months weeks time. So you
53:27will be hastening that hypothyroidism by
53:28giving antiyroid drugs. So in acute
53:31phase unless the patient has severe
53:33features of hypothyroidism you do not
53:35have to give any anti-thyroid drugs for
53:38Hashimoto's you just have to give beta
53:40blockers and maybe you might have to
53:42give certain sometimes steroids may be
53:44needed so but antiyroid drugs should not
53:47be used so often
53:49again please read about the antiyroid
53:51drugs very common questions asked for
53:53you in your vivas about the drugs the
53:55dosage the side effects a granloytosis
53:58and how do you manage all those things.
54:00So
54:04yes,
54:09also you have to know about the other
54:10eye signs. Sometimes they ask you the
54:13eye signs of thyroid. Yes. What is this
54:14image showing?
54:16Gum hypertrophy.
54:17Hypertrophy.
54:18Gum hypertrophy or gum hypoglacia. Can
54:20you tell me some causes?
54:24Correct. Cycllosporin.
54:26Cycloporin. Correct. One more drug
54:30possibly the more common drug
54:32calcium channel block
54:33calcium channel block
54:34calcium channel blockers especially in
54:35nidepin.
54:36So these are three common drugs that
54:39produce gum hyperlasia. Okay. What are
54:41the other causes other than
54:43AML? Yes, AML is one thing that you have
54:46to think of. Whenever there is bleeding
54:47associated with gum hypoplasia, then
54:55females pregnancy can produce pregnancy
54:57itself can produce gum hypoplacia. You
55:00could have chronic gingivitis can
55:02produce the features or even jaw tumors
55:05but though it will not be so much
55:07regular it'll be localized to particular
55:09sites. Okay. What are the chronic side
55:12effects of phenitoine? When a patient
55:14with phenitoine has this, what else will
55:16he look for?
55:17Osteoporosis.
55:19Correct.
55:20Macroyic.
55:21Macroyic anemia.
55:22Good sir.
55:23Yes.
55:26Neurological neurological
55:29atexia, tremors.
55:31They can have tremors. They can have
55:32atexia. Sometimes uh they can have
55:35herutism
55:37they can have uh yeah nestagmas. Yeah.
55:39That's part of the uh cerebellar
55:41toxicity that could be there. So they
55:43could have that. So these are the
55:44problems that could be there. Okay. What
55:46is the difference between phenitoine and
55:49phosphenito?
55:56It is a pro drug of phenitoine sir. It
55:58can be given very quickly through IV but
56:01phenine has to be given slowly.
56:04Okay. So that's the main difference is
56:06the rapidity or how fast you can load.
56:09Phosphenitoine can be loaded within 15
56:11to 20 minutes. You can load the full
56:12dose whereas phenitoine you'll have to
56:15load it over 45 minutes to 1 hour. So
56:17that's a uh that's the main side effect
56:19that is there. Uh and as you said it's a
56:22pro drug. The side effect profile might
56:24be a little lesser than spanetine but
56:26the same so same side effects would
56:28occur with positine also.
56:31Again very common drugs that are asked
56:33for you in your vivas is anti-epileptic
56:35drugs. So you have to know the
56:37classification. You have to know the
56:38newer agents. Can anyone tell me some of
56:40the newer anti-epileptic drugs?
56:44Locos.
56:46Okay. Lacosomide
56:49then
56:55okay levator. Okay. can be still
56:58considered as newer though it's not very
57:00new
57:02sir
57:03okayetam yes zonomide zonomide is a
57:06little newer one glob
57:09okay so you have a few set of new drugs
57:13please read about levatory again it's
57:17the drug which everybody uses for
57:18everything now so you have to know how
57:21does levatoram act what's the mechanism
57:23of action
57:25levator
57:27sodium channel.
57:28Okay. Sodium channel. Sodium channel.
57:30Okay. Is it safe during what are the
57:31antiepileptics safe in pregnancy? Again,
57:33a very common question.
57:40Which are the anti-epileptics which can
57:42be safely given for eclamsia
57:46patients?
57:46Magnesium sulfate.
57:48Okay. Magnesium doesn't come into our
57:50medical classification of anti-epileptic
57:56lamoten and lem are safe for pregnancy.
58:00Always remember litam is absolutely
58:02safe. Lamatrogen is also safe.
58:04Lamotrogen is also safe and if it is
58:06nearing I mean all these drugs are
58:08unsafe because for the uh development of
58:12the fetus isn't it? So in the first and
58:14second trimester obviously first
58:15trimester it's definitely
58:17contraindicated during the later parts
58:19possibly the patient is already in the
58:20third trimester and you have no other
58:22drugs you can start all the other drugs
58:24also there is no problem for uh the
58:27fetus at least the fetus toxicity is not
58:29common with that
58:33we go on to the next one
58:36yesial
58:40candid oral candid Candidas
58:44what's the difference? What is the
58:45difference between the two?
58:47One is [snorts] oral candidas is
58:49oroparangial. One more is esophasial
58:53is organism is same
58:59what's the difference between supposedly
59:01I have a retroviral disease patient and
59:04I find these findings
59:07wh
59:08esophadial candidasis is age defining.
59:11Okay. So fine remember moment it crosses
59:13the fairings and goes below or beyond
59:16the fan it becomes systemic candidasis
59:18it becomes systemic candidasis if it is
59:21just oral or just fingial there doesn't
59:24become systemic candidasis again the
59:26duration of treatment varies duration of
59:29treatment is longer and oral candidasis
59:32can be used you can use topical
59:35applications that could be used for oral
59:37candidasis but for uh uh Esophasial
59:41candidasis you require the drugs you
59:44require to use the oral drugs that could
59:46be there. Okay. Again HIV please read
59:49about the AIDS defining illnesses and at
59:52what CD4 what AIDS defining illness
59:55comes. Okay. Can anyone tell me what are
59:58the AIDS defining conditions that can
1:00:00come when the CD4 count is less than 50?
1:00:05Mac CMV.
1:00:07Okay. Mac
1:00:09titogalo virus then
1:00:13PCP pneumonia
1:00:14PCP pneumonia occurs much early PCP is
1:00:17200 and below what else
1:00:21below 50
1:00:23primary CNS lymphoma
1:00:24primary CS
1:00:28yeah CMV and MAC is correct PMLE PMLE
1:00:32what is PMLE
1:00:35progressive multif focal
1:00:36progressive multif focal lucid to
1:00:37encphilopathy. So this also happens when
1:00:39the CD4 is less than 50. So you have to
1:00:42know that and you have to know the drugs
1:00:44that are used for the treatment of each
1:00:46uh prophylaxis and treatment of this.
1:00:52We'll go on to the next. I think we have
1:00:54finished very few. We will go a little
1:00:57fast.
1:00:59Yes. What is your
1:01:01diagnosis?
1:01:03What is this patient having? And what is
1:01:05your differential diagnosis?
1:01:18So it could be leptospirrosis. Any other
1:01:20different correct leptospirus is the
1:01:21first diagnosis. Any other condition you
1:01:24can think of where you can have jaundice
1:01:26and hemorrhage.
1:01:29It's a deep jaundice and hemorrhage.
1:01:30Agreed. Any other causes?
1:01:34is correct.
1:01:35Viral.
1:01:37Viral. Which viral will produce
1:01:39jaundice? Emmer is okay. Jaundice.
1:01:42CLD with coagalopathy.
1:01:44CLLD with cogalopathy. Okay. Jaundice is
1:01:47little less likely for CLD unless there
1:01:49is an obstructive element.
1:01:52Severe sepsis. Severe sepsis in a
1:01:54pregnant lady. In a pregnant lady you
1:01:57have the liver disease of the pregnancy
1:01:59which comes which can have that
1:02:01they can have this manifestations
1:02:03because of that. Okay. Okay. So what's
1:02:05the gold standard test for diagnosis of
1:02:07leptospirrosis?
1:02:12Microaggation.
1:02:13Matt Matt microaggation.
1:02:15Microaggation. Anything more specific?
1:02:18That's what we asked for.
1:02:21ELSA for IGM IG is
1:02:23okay. Elisa if you want a gold standard
1:02:25then it goes like that a serial rising
1:02:28okay the the in the initial phase and
1:02:31after the immune phase clears if you do
1:02:33two two times of aglutination and the
1:02:35titus rising that is more specific for
1:02:38that okay what any named criteria you
1:02:40know of leptospirrosis
1:02:44veins
1:02:44fins
1:02:45you have something called as a modified
1:02:46fins criteria which can be used for the
1:02:49diagnosis of leptospirrosis okay what is
1:02:51wheels disease
1:02:56hemorrhagic leptospiryosis.
1:02:58Okay. The severe form of leptospirrosis
1:03:00where you have a rohearagic part of
1:03:02leptopyrosis that is uh called as wheels
1:03:06disease that is there. How do you treat
1:03:08leptospirrosis?
1:03:14Drug of choice.
1:03:17Okay. So the drug of choice is
1:03:18crystalline pencil.
1:03:19Pencil is the drug. Toxicycling toxic.
1:03:22So please remember spyroites be it
1:03:24syphilis be it leptospirrosis or any
1:03:26other spyroet still they are sensitive
1:03:29to penicellin. So penicellin is the drug
1:03:32of choice. If not you can give
1:03:34doxycycline in milder cases. Now
1:03:36doxycycline is available as parental
1:03:38also. So that can be used. Septrioxone
1:03:41can be used but crystalline pencils is
1:03:43the drug of choice for leptospiryosis.
1:03:47What is the mode of spread of
1:03:49leptospirrosis?
1:03:56Contaminated water.
1:03:58Invasion of the bacteria.
1:04:00How does it enter inside?
1:04:06Correct. Through the abrasions.
1:04:07Cutaneous. Don't say it's oral. Don't
1:04:10say it is inhalational. It is through
1:04:12the skin. It has to enter through the
1:04:14skin. uh contaminated uh whatever rodent
1:04:18uh urine through that it enters the skin
1:04:20and then it that's how it goes about.
1:04:25Okay.
1:04:27Yes. [snorts]
1:04:29Anthrax.
1:04:31Anthrax. Okay. Anthrax. Why do you say
1:04:33it's anthrax?
1:04:35Black escar.
1:04:36Black estar. Okay. Blas exchar. Do you
1:04:39find anthrax so common?
1:04:41No sir.
1:04:42So what else? Which is scrub typus.
1:04:45Scrub typus.
1:04:46Yes. Scrub typhus. So scrub typhus is
1:04:49one condition where you can get this.
1:04:51You can get this. You can see multiple
1:04:53escars that you're seeing. Anthrax is
1:04:54where it was described for. But what you
1:04:56see is now scrub tyifus. Along with that
1:04:59you find certain hemorrhages, isn't it?
1:05:00You find this is some sort of a
1:05:03echyimosis more than pik and
1:05:05copyrightites. Some sort of an echimosis
1:05:07that is there. So what is the test that
1:05:10you want to do?
1:05:13What investigation you would want to
1:05:14ask?
1:05:17Whe
1:05:18Phelix
1:05:20wheel
1:05:22IGM scrub
1:05:23Elisa IGM IGM
1:05:25Elisa. Okay, you do have ELISA available
1:05:28now everywhere. So that is more
1:05:30specific. Will fix is wheelix is a
1:05:34glutination test. These have low
1:05:35specificities. Those sensitivities could
1:05:37be higher but uh the things is little
1:05:39less. Now you have IGM that is
1:05:41available. Okay. What's the drug of
1:05:42choice?
1:05:44Doxycyc.
1:05:45Doxycycline is a drug of choice. If it's
1:05:47a little complicated then you would add
1:05:49on
1:05:53oroxisol. Eithroyc. You would have added
1:05:56on eithroycing. That's there. Okay. What
1:05:58is this sign called as
1:06:02cigarette burn? It's called as a
1:06:05cigarette burn sign. Okay. How is it
1:06:08spread?
1:06:10Tick bite.
1:06:11Bite,
1:06:12bite of ticks. Okay, bite of ticks.
1:06:15And again very important it is the uh
1:06:18the these escars may not be seen on a uh
1:06:22area which is exposed. Usually you will
1:06:24have to examine the patients and
1:06:26especially the moist areas the groins
1:06:30the axilla such regions you'll have to
1:06:33examine for the escars. [snorts]
1:06:36Okay. So those were the initial set of
1:06:38clinical images. A few examples which I
1:06:40have given. The next set of images which
1:06:43next set of questions that we are going
1:06:44to discuss are uh a short history and
1:06:48then some clinical images that will be
1:06:49given. So here we have the first one
1:06:52that is the 36 year old male who has
1:06:54mild mental detardation and has
1:06:56recurrent seizures and an examination
1:06:58has these findings.
1:07:00Tuberous.
1:07:02Yeah. So this is the first finding that
1:07:03you're seeing here.
1:07:05What are you finding here?
1:07:06Adinoma sebace. Adma seation. You're
1:07:08finding adenoma sebaceium. So you have
1:07:10this adinoma in the area of the face.
1:07:13Adenoma sebaceium. Yes. What is this
1:07:16you're seeing?
1:07:16Subangual. Yeah.
1:07:18Yeah. Subangual fibramas.
1:07:21This is perangual not subangal. What is
1:07:23the other name for this?
1:07:28What is it also called as?
1:07:31Yeah, these are hematas only. These are
1:07:33called as Kenan's tumors. Okay. These
1:07:35are called as Kenan's tumors.
1:07:38Okay. And what is these
1:07:42shag patch?
1:07:44This is the shag green patch and the ash
1:07:46leaf macu. Okay. So the total diagnosis
1:07:48would be as you said.
1:07:51Yes.
1:07:55Yeah. Tuberous sclerosis. So tuberous
1:07:56sclerosis is your diagnosed.
1:07:59Okay. What are the uh
1:08:02what are the other names for this
1:08:04disease? What is it also called as?
1:08:05Tuboscleros is also called as
1:08:07born.
1:08:09Born disease. Okay. What is epiloa?
1:08:14Epilepsy.
1:08:15Huh? Epilepsy
1:08:17low acronym low IQ and
1:08:21adenoma.
1:08:22Adinoma seation. So adenoma seation. So
1:08:24this is one of the neuroccutaneous
1:08:26syndromes that you have. So this is one
1:08:28of the neuroccutaneous syndromes that
1:08:30you have. All right. [clears throat]
1:08:31Uh so can you tell me some more
1:08:33neuroccutaneous syndromes? Name some
1:08:36fibromyitosis. Okay.
1:08:39Sorry. Uh
1:08:42sturgeber syndrome. Good. Yes.
1:08:46Hypomelanosis of
1:08:48hypomelanosis of good.
1:08:50Attack
1:08:52atia. Correct.
1:08:57Some more
1:09:00one hippo syndrome. Yes, war hippolindo
1:09:03syndrome.
1:09:05Again a very common theory question for
1:09:07you. It's a usually a long question 15
1:09:10marks or 20 marks. They ask you
1:09:11neuroccutaneous syndromes and the
1:09:13clinical features. By far the most
1:09:15common that what we get clinically is
1:09:17neurop fibromyitosis type one and you do
1:09:20get ad tuberous sclerosis also and
1:09:23attackia especially in young children
1:09:25with cerebellar disease you do get that
1:09:27and sometimes you get stru also there
1:09:30are more than 23 neuroccutaneous
1:09:32syndromes okay at least some you should
1:09:35remember and you should know the what is
1:09:37the uh clinical manifestation of all
1:09:41these syndromes
1:09:44Okay, let's go on to the next scenario
1:09:47that you have here. So you have a
1:09:49retroviral disease patient who comes
1:09:51with fever worsening disna and the uh
1:09:55chest X-ray is showing these pattern can
1:09:58see that there are bilateral reticulo
1:10:01mild nodular changes and this is the
1:10:04staining that is used for the organism.
1:10:06So the diagnosis is
1:10:12yes. So pneumosyus zerowichi is the
1:10:15organism that is there. So it's a zea
1:10:17staining. What are the simple test that
1:10:19you can confirm this? Again the stain is
1:10:22not done everywhere. So we don't do it.
1:10:25Koh mount
1:10:27a mount may not pick it.
1:10:30Simple clinical test which helps you to
1:10:32suspect this.
1:10:35What do we do for COVID?
1:10:38Excise oxymetry. Always remember that
1:10:41whenever a patient with retroviral
1:10:43disease when you suspect uh if his CD4
1:10:46is less than 200 or 250 and below you do
1:10:49a exercise oximter what you're doing
1:10:51with COVID. So if you find excise
1:10:52desaturation your diagnosis of this is
1:10:55very very specific. If the saturation
1:10:57drops for more than four or four or less
1:11:01after a walking you can suspect it and
1:11:04then you can do the HRCT to confirm it
1:11:06because this organism staining may not
1:11:08be available everywhere you don't have
1:11:10to diagnose it you can straight start
1:11:12them on treatment so what is the
1:11:14treatment for this condition
1:11:18okay cotrimoxisole
1:11:20how much
1:11:20steroids
1:11:22how much of cotrimoxisol do you give for
1:11:24the treatment of PCP pneumonia
1:11:30Okay. Double strength tablet. Correct.
1:11:32How much dozing
1:11:37treatment is?
1:11:38BD BD is not treatment. Treatment when
1:11:41you're suspecting is eight tablets per
1:11:43day. Sorry, six tablets per day. That is
1:11:46222.
1:11:48Yeah. Two T.
1:11:49Two T is the treatment of choice. And
1:11:52suppose somebody is allergic to
1:11:55sulfa.
1:11:59Somebody's allergic to sulfa. What can
1:12:01you give? You can give clindomy.
1:12:04[clears throat]
1:12:04Clender is there. Okay. Clindomy can be
1:12:07used. But please remember cotryoxol is a
1:12:09good old good drug. It's a very cheap
1:12:13and available drug and sulfa allergy is
1:12:15not that common. So you can still use
1:12:17that. And if the patient has hypoxia,
1:12:20significant hypoxia, then you'll have to
1:12:23add on steroids. Okay, add on steroids.
1:12:27Okay. What are the uh opportunistic
1:12:32infections for which cotrimoxol works
1:12:36other than pneumosis?
1:12:39Cryptoporidiosis.
1:12:41Okay. Cryptoperidiosis.
1:12:47One more. GI
1:12:49isospora
1:12:51cryptosperidosis isospora
1:12:54toxopplasma
1:12:55any other opportunistic infection
1:12:58toxopplasma
1:12:59yeah toxopplasma is correct but then the
1:13:01drug for toxo is what actually drug for
1:13:03toxo is not sulfamethoxazone it is
1:13:09toxoplasm
1:13:10sulfine
1:13:12diosine sulfur dioine okay
1:13:14sulfine is not available so we use sulf
1:13:16for methoxisole.
1:13:18Uh so toxol is okay. Yes. And very
1:13:20common the commonest respirators.
1:13:23Yeah.is
1:13:24can candidasis corrimoxol will not help.
1:13:28Canidasis you require antifungal.
1:13:30Corrimoxol is an antibacterial. Uh the
1:13:33commonest respiratory infection they
1:13:35develop is any infection like pneumonia
1:13:37could be there. Any other bacterial
1:13:39pneumonia for which also combat
1:13:40trioxazole will work. Okay. Cotryoxole
1:13:43will work. That's why that's the most
1:13:45common. Okay.
1:13:48So that's the next scenario that we
1:13:49have.
1:13:53Uh a retroviral disease patient has come
1:13:56with these manifestation where there is
1:13:58a gradual progress defect and this is
1:14:01the MRI brain that's showing.
1:14:07So
1:14:09what is your diagnosis?
1:14:11EML.
1:14:12Okay. So this is the
1:14:14Okay. So you say it's toxo. Why do you
1:14:16say it's toxoplasmosis?
1:14:24Toxoplasmosis generally produces what?
1:14:27Ring enhancing leion.
1:14:29Generally you get ring enhancing leions.
1:14:30Rarely you get non-ring enhancing. So
1:14:32here it's not a ring enhancing leion at
1:14:34all. It's a diffused white matter
1:14:36disease that you're seeing here.
1:14:38Diffused white matter.
1:14:39Asymmetrical
1:14:40asymmetrical that is there. So your
1:14:42diagnosis is PMLE. So how do you confirm
1:14:46what is it PMLE due to
1:14:50JC virus?
1:14:51Yeah, it's JC virus. So you can do a CSF
1:14:54and do the JC virus or you can do a
1:14:57brain biopsy. What's the prognosis for
1:14:59PMLE?
1:15:04bad prognosis,
1:15:06bad prognosis is generally a very uh
1:15:08poor it's a downhill course that they
1:15:10develop once this develops.
1:15:12So this is the viral genome that's there
1:15:15and the JC virus it's one sort of a slow
1:15:20viral disease that's there one of them
1:15:22that can be seen
1:15:25okay what's the diagnosis
1:15:26multiple myoma
1:15:27multiple myoma
1:15:29multiple myoma
1:15:30any other differential diagnosis you
1:15:32want to give
1:15:33secondary
1:15:35hyperarid
1:15:36okay say it is secondaries okay anything
1:15:39else
1:15:41hyperarid
1:15:42Hyper pararathyroidism.
1:15:44Hyperarathyroidism would have been more
1:15:46finer. It won't be so big. Any other
1:15:50myoma secondary? Third one is
1:15:53LCH.
1:15:54LC.
1:15:56What is LCH?
1:16:01So these are the three differential
1:16:02diagnosis that you have. So if I want to
1:16:05confirm myoma, what do I do?
1:16:08Serum electrophorosis.
1:16:10Okay. Serum electrophorosis what is the
1:16:12gold standard test as of now for myoma
1:16:14what we do
1:16:15just electrophorosis
1:16:17plasma biopsy
1:16:19okay bone marrow is plus minus we don't
1:16:21have to do it in all we have to do the
1:16:24imixation
1:16:26and serum
1:16:27you want to know the type of
1:16:28iminoglobiline so you want to do a
1:16:31quantitative
1:16:32imoglobulin essay isn't it you do a
1:16:35quantitative you want to know what type
1:16:36of imoglobilin so that is the important
1:16:39thing that you lab.
1:16:41So you have to know about myoma. One of
1:16:43the commonest tumors that you see in
1:16:45elderly and it's very common. You should
1:16:47know about the diagnosis. Again you said
1:16:50bone marrow you do the plasma cells etc.
1:16:53And then the renal failure you can do
1:16:55the urine benzones protein all those
1:16:56things are there the skeletal survey
1:16:58that has to be done. And what is the
1:17:00drug of choice at present?
1:17:02Bismab
1:17:04is the drug of choice. The drugs which
1:17:07is available other than that other than
1:17:09the monoconal antibodies
1:17:13yeah steroids with yeah steroids with
1:17:16lenolum
1:17:18lenidomide so those were the available
1:17:20at present is the monoconal antibbody
1:17:22and what's the prognosis for myoma
1:17:28good prognosis
1:17:28yeah generally it's a very chronic
1:17:31diseases okay
1:17:34so good prognosis unless Unless the
1:17:36patient develops renal failure and
1:17:39cognitance.
1:17:40Okay.
1:17:43Yes.
1:17:45Okay. So you say this is pericardial
1:17:47effusion. Why do you say it's
1:17:48pericardial eusion?
1:17:53Appearance.
1:17:53Money bag appearance.
1:17:54So you have a cardomegali that's there.
1:17:56You have a gross cardomegali with
1:17:59stenciled hard borders. Isn't it?
1:18:00Stencil hard borders or as you said it's
1:18:03a money bag appearance. That's what you
1:18:05see there and the lung shadows are
1:18:07absolutely clear. So it's a gross
1:18:09cardomegali with stencile heart border.
1:18:12So you say it's pericardial eusion.
1:18:13Okay. Tell me some causes of pericardial
1:18:15eusion.
1:18:16Hypothyroidis.
1:18:18Okay.
1:18:18Tuberculosis.
1:18:19Tuberculosis. Correct.
1:18:21Malignancy. Correct. Then hypothyroidis.
1:18:26Yes. Hypothyroidism is correct.
1:18:30Urania. Connected tissue disorders.
1:18:32Correct.
1:18:36pericard.
1:18:38Okay, you could have it as a part of
1:18:40your
1:18:42generalized anosarka sort of features
1:18:44but then they would have plural eusion
1:18:46etc also. So most important and common
1:18:48ones that you have to rule out is
1:18:50thyroid. If there is fever, weight loss
1:18:52etc you may have to rule out
1:18:54tuberculosis and malignancy definitely
1:18:57uremia has to be ruled out. Uremia has
1:18:59to be ruled out. Okay. Any other signs
1:19:01of pericardial efficion you know of on
1:19:03X-ray
1:19:08if I take a lateral X-ray of this
1:19:10patient any sign I might get
1:19:18okay somebody's written on the chat it's
1:19:21called as a Oreo cookie sign okay
1:19:23because you'll have a paricardial fat
1:19:27and then there is the paricardium and
1:19:29then there is the fluid that you're
1:19:30seeing So it looks like the Oreo cookie
1:19:32two colors and one this one. So
1:19:35again whenever this X-ray is kept they
1:19:37would ask you you can do a pericardial
1:19:39tapping and send it for analysis. You if
1:19:42you suspect anything which is chronic
1:19:44then you might have to do a CT or an MRA
1:19:47and measure the thickness of the
1:19:48pericardium. That's basically for
1:19:50chronic constrictive paricarditis and
1:19:53then they'll ask you about constrictive
1:19:55pericarditis the clinical features etc.
1:20:04Yes.
1:20:08So again this X-ray also shows
1:20:10cardomegali.
1:20:11So the first thing always they ask you
1:20:13is how do you make out cardomegali?
1:20:16How do you clinically x-ray wise make
1:20:18out cardomegali? We saw it in the
1:20:20earlier x-ray also. See cardiothoracic
1:20:23ratio. Okay. So how do you measure the
1:20:25cardiothoracic ratio?
1:20:29Firstly we'll draw in the midline sirus.
1:20:34First we'll draw the midline line there
1:20:36and then we'll uh mark the horizontal
1:20:39maximum horizontal border of the heart.
1:20:41So always remember it is not a straight
1:20:43line we going to measure we going to
1:20:45measure the maximum on both
1:20:46maximum horizontal. So maximum on this
1:20:48side plus the maximum on this side. So
1:20:51total it out and then measure the trans
1:20:54thoracic isn't it? And how much should
1:20:56we eat? More than
1:20:5850%
1:21:00more than 50% on a PA view. And on an AP
1:21:04view normally you have cardomegali. On
1:21:06AP view, how much it should be to say
1:21:08cardomegali?
1:21:11PA view is 50. AP is
1:21:13more than 60.
1:21:14Yeah. More than 60. Ideally, it's more
1:21:16than 57%. 60%. Okay. So here we have
1:21:19cardomegali.
1:21:23Okay. You're seeing that there is a
1:21:24prosthetic valve. Anything else you're
1:21:27able to see?
1:21:29Why do you say it's a mital valve? Why
1:21:31not iotic valve?
1:21:33Left heart.
1:21:35Why is this val mital? Why not iotic?
1:21:39How do you deciper whether it's a mital
1:21:40or iotic valve? By looking at the val or
1:21:44the position of the valve.
1:21:47Yes, a you told position. How do you say
1:21:49that?
1:21:55You have to draw a line, isn't it? You
1:21:58draw a line from here, that is the right
1:22:01cardophrenic angle to the
1:22:05left. So you're drawing a line here like
1:22:07this. Okay, you're drawing a line from
1:22:09here to here. So if it is below that, it
1:22:13is mital. If it is above that line, it
1:22:16is iotic. Ideally, this line is drawn on
1:22:18a lateral view, not on a chest X-ray PA.
1:22:20It's to be drawn on the lateral U X-ray.
1:22:22But you can use the same corary here. If
1:22:25you draw a line here and if it is below
1:22:27it's mital and above it is iotic. So
1:22:29you're finding a metallic valve here. So
1:22:31metallic valve. So you know it's a mital
1:22:34valve. So what are the other features of
1:22:35mital valve disease you're seeing on
1:22:37this X-ray?
1:22:40Left atrial enlargement straight
1:22:42straightening of left heart on the left
1:22:45side.
1:22:46Okay. finding that there is a
1:22:47very very clearly left heart border is
1:22:50straightened. Okay. Are you able to see
1:22:52a double atrial shadow
1:22:55where is the double atal shadow seen
1:22:57left side or the right side?
1:22:59Right side.
1:23:00Right side. Right side.
1:23:01You can see the double density here. You
1:23:03can see one density here and one density
1:23:05here. So it's a double atal shadow. And
1:23:07very classically you can see this
1:23:09playing of karina.
1:23:11You can see the normal carina. This is
1:23:12the trachea and this is the bronchus.
1:23:14Normal subcarinal angle is how much?
1:23:18Obuse.
1:23:19Yeah, it's acute. Normally it is acute.
1:23:2165° is normal. Here you can see it is
1:23:23very nicely obtuse, isn't it? Obtuse.
1:23:27And what are these you're seeing here?
1:23:30What are these?
1:23:33Sternotomy.
1:23:34Yes. Sternotomy sutures. Correct.
1:23:36Sternotomy sutures. So this is a post
1:23:39valve replacement. Mital valve patient
1:23:42is post valve replacement and you see
1:23:44the pulmonary markings are also very
1:23:46much prominent. You can see that the
1:23:48upper lobe veins are very much
1:23:49prominent. You call it as sephilization
1:23:52of blood flow. So pulmonary hypertension
1:23:54is also there. Okay. So what are the
1:23:58drugs this patient should be on?
1:24:02Diuretics.
1:24:04Anticop.
1:24:05Diuretics. Correct. Then
1:24:07anticolent.
1:24:08Anticulants. Anticulants. Which
1:24:10anticogulant will you give this patient?
1:24:12Will you give him barferin? Will you
1:24:14give him
1:24:15diabet?
1:24:20Why not? Dabatan.
1:24:22Noak is not used in
1:24:25nonvular.
1:24:26Not preferred in valular hearts.
1:24:28Not preferred. Why?
1:24:34Why? Any idea why no is not preferred in
1:24:36valular heart disease? I mean a
1:24:38prosthetic valular heart disease for
1:24:41everything else you use noax
1:24:43we don't have much studies over it okay
1:24:46so we don't have much studies so I think
1:24:48eventually we will be able to use that
1:24:51also okay it's a much a longer process
1:24:54that you'd be there much longer you'll
1:24:56have to give whereas in case of DVT and
1:24:58all such conditions is a shorter
1:25:00duration possibly that's where it's been
1:25:02studied that's all and romatic heart
1:25:04disease is not so common in the west so
1:25:06they wouldn't get so sample size to do
1:25:08studies and prove that the nonvalular AF
1:25:12is where you use the uh non valvular AF
1:25:16is where it's used for okay then the
1:25:18other drugs for heart failure as you
1:25:19said uh diuretics uh beta blockers
1:25:24penicellin all those things and yeah
1:25:26plus or minus deoxin may be needed
1:25:30test.
1:25:36Yes,
1:25:40she's having pulmonary artery
1:25:41hypertension.
1:25:42Okay. So, you're saying it's pulmonary
1:25:43artery hypertension. Why do you say so?
1:25:46What are you seeing? Which makes you
1:25:48feel that?
1:25:50Sir, hilar prominence on the left.
1:25:52Hilar prominence more important. What is
1:25:53this? Which part of the pulmonary is
1:25:55this?
1:25:57This is the branch of the pulmonary,
1:25:59isn't it? Which branch is this?
1:26:03It's the
1:26:06descending branch, isn't it? Right
1:26:07descending branch of the pulmonary
1:26:08artery is very huge. Huge right
1:26:11descending pulmonary artery. Ascending
1:26:13is also huge. And you can see here there
1:26:15is a big pulmonary artery. Left
1:26:16pulmonary cornus is prominent. So she
1:26:19has pulmonary hypertension. Okay. So
1:26:21what is the cause for pulary artery
1:26:23hypertension? You think so young lady?
1:26:29in the chat. Mital stenosis, secondary
1:26:31mital stenosis.
1:26:32So it could be mital stenosis. It could
1:26:35be ASD with pulary artery hypertension.
1:26:38So is it mital stenosis or it is? How do
1:26:41I differentiate?
1:26:43Is
1:26:45if it is mital stenosis, which chamber
1:26:46should have got enlarged?
1:26:49Left atrium.
1:26:51Left atrium. Whereas ASD you do not have
1:26:53left atal enlargement. So is there
1:26:55evidence of left at enlargement? So what
1:26:57are the evidences of left atal
1:26:58enlargement on X-ray?
1:27:01Double
1:27:01straightening of left border
1:27:03double atrial sign
1:27:05correct. So double atal sign
1:27:06straightening of left heart border
1:27:08playing of karina these three things you
1:27:09should be able to see. So you can see
1:27:11here this the right heart border and
1:27:13left heart border you should know what
1:27:15are the structures that form. So the
1:27:17left heart border on the top what is the
1:27:19structure here right on top
1:27:23after that is the after that is
1:27:26pulmonary artery normally it's not so
1:27:28big normally it's small there followed
1:27:30by
1:27:31left atalage
1:27:33left ventricle okay left ventricle left
1:27:36atrial appendage comes somewhere between
1:27:38the pulmonary and the
1:27:40left ventricle so here is the left atal
1:27:42appendage which is empty so it is not
1:27:45there okay the right heart border is
1:27:47made up of what structure?
1:27:49Right ventricle.
1:27:51No, no, not right ventricle.
1:27:52Superior vina, right atrium and
1:27:55this is the right atrium. So right heart
1:27:57border is formed by the right atrium and
1:27:59a little part here could be the superior
1:28:01veneer. So here you're not finding any
1:28:03evidence of
1:28:05left atal enlargement. So this diagnosis
1:28:08most often is ASD ASD with pulary artery
1:28:13hypertension and you have
1:28:17pulmonary hypertension severe pulmonary
1:28:19hypertension so could be is
1:28:21mangorization. So what do you call this
1:28:23pattern as? I think in the chat they
1:28:24have already written the answer. This
1:28:26pattern is called as the jug handle
1:28:29pattern. Okay, it's called as a jug
1:28:31handle pattern. So this is the handle of
1:28:34the jug. This is the jug and this is the
1:28:36handle. So characteristic of pulmonary
1:28:39arterial hypotension with
1:28:40isometerization. Yes.
1:28:46Yes. So what are you finding?
1:28:53Lymphnopathy. Bilateral.
1:28:55Bilateral hilar lymphnopathy. So there
1:28:57is bilateral high lympadnopathy. What
1:28:59are the differential diagnosis?
1:29:01Saridosis. Tubercarosis. Number one.
1:29:04Correct. Then
1:29:05tub tuberculosis
1:29:06rarely tuberculosis. Correct. Then
1:29:09unfortunately
1:29:09lymphas
1:29:10lymphoma always remember sarcoid and
1:29:13lymphoma. Bilateral lymph nodes.
1:29:15Unilateral lymph node. The first cause
1:29:17would be
1:29:19tuberculosis followed by
1:29:23unilateral hilar
1:29:25malignant. Always remember bilateral is
1:29:28sarcoid and lymphoma and unilateral is
1:29:31TB and malignancy. You could get it in
1:29:34other conditions also. So if it is
1:29:36sarcidosis, this is classical of
1:29:38sarcidosis where you have this bilateral
1:29:40hilar lymph node and the paratrichial
1:29:43lymph node as well as the subcarina
1:29:45lymph node also gets involved. Okay,
1:29:47it's called as the galand sign or the
1:29:49one two three sign. So how do you
1:29:53confirm the diagnosis of saridosis? What
1:29:55investigations?
1:29:58Biopsy
1:30:00standard is biopsy converting
1:30:04enhancer scan.
1:30:05Gallium enhancing the gatalinium
1:30:07enhancing scan there. Biopsy is little
1:30:09difficult from the hila lymph nodes.
1:30:11Okay, if peripheral lymph nodes are
1:30:12there, you can do that. You can do the
1:30:15calcium levels, you can do the AC
1:30:16levels. Okay, those scan tell you
1:30:19gallium scan is diagnostic. And in
1:30:22sarcord, you generally have some lung
1:30:24shadows also. Okay, here it's not there
1:30:26that much.
1:30:29Yes.
1:30:31What are we finding here?
1:30:32Aspergillosis with
1:30:34Asperilosis.
1:30:38Which one?
1:30:39Or the chest X-ray both.
1:30:43X-ray air crescent.
1:30:45Okay. X-ray is showing the air crescent
1:30:46sign which is diagnostic of
1:30:49asparagulus. Fungal.
1:30:51Fungal bald.
1:30:52Aspergilloma. Please remember X-ray it
1:30:54is air crescent sinus aspergilloma
1:30:58whereas CT the air crescent or the
1:31:00hallow sign is diagnostic of
1:31:05is it aspergilloma or aspergillosis
1:31:11hall sign is suggestive of invasive
1:31:13aspergilosis. Okay. CT halos sign is
1:31:16suggestive of invasive aspergilosis
1:31:18whereas the uh x-ray air crescent sign
1:31:21is suggestive of aspergilloma
1:31:25aspergilloma.
1:31:26Okay. What are the other conditions
1:31:28where you can get this air crescent sign
1:31:30of monad? Air crescent sign of monad
1:31:33which is the other conditions you can
1:31:34see.
1:31:36And how do you differentiate? That's the
1:31:38question they ask when this x-ray is
1:31:40kept.
1:31:44Where else can you get this air crescent
1:31:45sign like this?
1:31:52Yes.
1:31:57You can get that air crescent sign if
1:31:59there is a hematoma in the cavity.
1:32:02So the patients who have a cavity have
1:32:04hemoptis and because of that they can
1:32:06have hematoma in the cavity. So how do
1:32:09you differentiate whether it is a fungus
1:32:11ball or it is a hematoma in the cavity?
1:32:18By changing the position x-ray.
1:32:21Yes. You check change the position. You
1:32:24take ideally you're supposed to take a
1:32:25X-ray in a trendenburg position. So
1:32:28fungus ball is a freely mobile. So it
1:32:31position changes whereas a hematoma
1:32:33always is fixed to the cavity. So the
1:32:36air crescent sign the position will not
1:32:38change in case of hematoma. So how do
1:32:41you treat fungus ball
1:32:45for aspiril is waronazole.
1:32:48Okay. So wariconazoo. If it is
1:32:50localized, you can subject the patient
1:32:52to surgical resection of that lung. If
1:32:54it is systemic, then you'll have to use
1:32:56drugs.
1:33:04Yes.
1:33:15Anyone?
1:33:15Upper mass. widening.
1:33:18So you're finding it as upper
1:33:20medastininal widening. Okay. So you find
1:33:22that there is an upper medastininal
1:33:23widening.
1:33:25So there's an upper part of the
1:33:27mediainum not the lower part. So what is
1:33:30the differential diagnosis?
1:33:31Thyoma.
1:33:33Okay. Thyoma that's one possible. Second
1:33:37thyroid mass.
1:33:38Thyroid. Yes. Thyroid. Correct. Then
1:33:43one more.
1:33:45Lymphoma. Lymphoma can occur. Lymphoma
1:33:48can occur anywhere. So lymphoma can
1:33:50occur anywhere.
1:33:53Terteratomomas. Terteratomomas can occur
1:33:55anywhere. So first of all you'll have to
1:33:58make out whether it is a anterior or a
1:34:00posterior mediastinum. How do you make
1:34:02out that
1:34:05anterior or posterior medastinum?
1:34:08You'll have to look at the lateral view
1:34:10and see where this shadow is. Anterior
1:34:12AP view we may not be able to make out.
1:34:14If it is posterior mediestinal then it
1:34:16could be a neurop fibroma also. So here
1:34:19if you see you can see the shadow which
1:34:22is extending from the chest it is going
1:34:24to the neck isn't it the shadow is
1:34:27starting from here and going crossing
1:34:29the clavicle the clavicle it is crossing
1:34:32and going up so this is what we call I
1:34:34think in the chat somebody has written
1:34:36about it
1:34:38yeah soothoracic sign it's a very
1:34:40specific sign of thyroid so thyroid is
1:34:44the only one which starts from the neck
1:34:45and goes down okay thyroid is the one
1:34:47which starts starts from the neck and
1:34:48goes down. So it's quite specific for
1:34:51that. But then you'll have to do a
1:34:53lateral or an imaging CT and can confirm
1:34:56this. Okay. So what is the clinical sign
1:34:59which is specific for a retrosteral
1:35:02viter?
1:35:02Peanut sign.
1:35:04What do you mean by pimbertton sign?
1:35:08Lifting both the both hands above the
1:35:11neck above the head will cause the
1:35:13congestion of the uh face.
1:35:16Okay. So lifting the hands above the
1:35:18neck the patient will become breathless
1:35:20sinos congestion of the face. That's a
1:35:22specific sign that could be there in
1:35:24case of retroal.
1:35:29Fine. Yes. This is the next one
1:35:35cavity with the fluid levels.
1:35:40So as you said this is a thick walled
1:35:42cavity. Where is it located?
1:35:47Lower zone.
1:35:47Yeah, lower zone.
1:35:50How do you say it is lower, upper or mid
1:35:52zone?
1:35:53First, posteriorly we have to the ribs
1:35:56about
1:35:57first about two is the
1:35:59posterior rib or the anterior end of the
1:36:00rib?
1:36:02Anterior.
1:36:03Okay. So, always remember it's the
1:36:04anterior end. You can see here this is
1:36:06the first rib coming down here. This is
1:36:08the second rib which is coming down
1:36:09here. So, this is the anterior end of
1:36:12the second rib. The posterior end of the
1:36:14second rib is here. The posterior end of
1:36:16the first rib is here. So the anterior
1:36:17end of the second rib, that's the first
1:36:19point you're going to take on both
1:36:21sides. So you draw a line connecting the
1:36:24anterior inferior end of the second rib.
1:36:27Then you're going to draw a line
1:36:28connecting the anterior inferior end of
1:36:30the fourth rib. So fourth rib is here.
1:36:33So anterior inferior end of the fourth
1:36:35rib. So this is upper zone. This is mid
1:36:37zone. This is lower zone. So this shadow
1:36:39is in the lower zone. So you have a
1:36:42thick walled cavity with air fluid
1:36:44level. So your diagnosis is lung absis.
1:36:46Okay. Fine. Any differentials? Any other
1:36:48differentials you want to give?
1:36:52Bull.
1:36:55Bula will not be like this. What else?
1:37:00Hydrated. Hydrated is possible. Correct.
1:37:02Anything else?
1:37:06You said lung abapsis. Hydrated.
1:37:09Necrotising pneumonia. Should have had
1:37:11pneumonia more. Okay. Possible breaking
1:37:14down pneumonia. Could it be
1:37:15tuberculosis?
1:37:20Healing tubercular cavities.
1:37:22Okay. Healed tubercular cavity.
1:37:24Longstanding tuberculosis. Healed
1:37:26tubercular with the secondary infection.
1:37:28Active tuberculosis generally produces a
1:37:30thinwalled cavity and usually in the
1:37:32upper lobe, not in the lower part. Okay.
1:37:36If you have multiple such shadows,
1:37:38multiple such shadows, small small
1:37:40shadows, air fil, what else can it do?
1:37:45Will be very thin.
1:37:48Infective connectis.
1:37:50Okay. Septic emble. Okay. Multiple
1:37:52absesses. Correct. Any other
1:37:53possibilities?
1:37:54Was veg nurse always remember connective
1:37:57tissue disorder. Vegers is one thing we
1:37:59should always remember. Sometimes fungal
1:38:01pneumonia also can.
1:38:04So what's a common organism? Lungapsis
1:38:13usually anorobic infection. So it could
1:38:15be klepsiala could be anorobic. So how
1:38:18do you treat?
1:38:22Okay. You want to give them good
1:38:24antibiotic coverage. More than that what
1:38:27else has to be done?
1:38:30ICD placement.
1:38:31ICD. Yeah. Why ICD?
1:38:37ICD where will you place inside the lung
1:38:42require a good chest. Yeah, you would
1:38:44require a good chest physiootherapy and
1:38:46postural drainage. Okay, a good chest
1:38:48physiootherapy and postural drainage is
1:38:50what is needed. A big cavity with the
1:38:53air fluid level maybe an ICD is
1:38:55indicated. Not for such small ones. So
1:38:57you will put the patient on. What is the
1:39:00posture you want to put this patient on
1:39:02for the training of this part?
1:39:04Left lateral.
1:39:06Anything more specific? Left lateral.
1:39:08Correct.
1:39:09Head and down.
1:39:12Head down. Head should be down. Left
1:39:14lateral and head down would be the ideal
1:39:16position that would be there. So if it
1:39:18does not heal, what is the investigation
1:39:20that you want to do? You're given good
1:39:22uh antibiotics. You made sure that the
1:39:26physotherapy is done. It does not heal
1:39:29still persistent. What is the
1:39:31investigation that you want to do?
1:39:35Or practically for all lung absesses,
1:39:37you're supposed to do that
1:39:38investigation.
1:39:39Yeah. AFB has to be ruled out. You have
1:39:41to rule out tuberculosis. Agreed.
1:39:43Anything else you want to rule out?
1:39:45Non-healing.
1:39:48Broncos. Correct.
1:39:49You want to rule out a obstruction. You
1:39:52want to rule out an obstruction there.
1:39:55Usually elderly persons it could be a
1:39:56tumor. In young patients it could be a
1:39:58foreign body. So you will do a
1:40:00broncoscopy and see there and uh you may
1:40:03have to do the biopsy if it is there or
1:40:06else at least a representative sample
1:40:07that can be taken from there.
1:40:10Okay. And even melidosis is one disease
1:40:14which can manifest meidosis. Have you
1:40:17heard of meidosis? What is the organism
1:40:19which produces
1:40:22soda? Okay. Especially in patients who
1:40:24are chronic kidney disease or chronic
1:40:27diabetics, you could get this mealosis
1:40:30also and that would not respond to your
1:40:32normal therapy. You might require to use
1:40:34specific antibiotics for that and
1:40:36antifungals also for that or different
1:40:38not for meosis. You'll require for that.
1:40:41Yes.
1:40:46Which side?
1:40:47Right sideing
1:40:49media to left side. So you say it's a
1:40:52right-sided pneumothorax
1:40:54tension.
1:40:56Right sided tension pneumothorax. Okay.
1:40:59Anybody with better
1:41:05rightsided tension is the diagnosis
1:41:08which is wrong.
1:41:10So left side with compensator hyper
1:41:13inflation of right side
1:41:15leftsided what?
1:41:18collapse or pneumonic [snorts]
1:41:20leftsided collapse. The diagnosis is
1:41:22leftsided collapse. Right side is fine
1:41:24there. Okay. It's the leftsided trachea
1:41:27shifted to the left side with a
1:41:28homogeneous opacity on the left side. So
1:41:32whenever you have a homogeneous opacity
1:41:34the differential diagnosis remains
1:41:37chlorusion collapse pneumonect.
1:41:40So these are the three differential
1:41:42diagnosis that remains. Trachea shifted
1:41:44to the same side
1:41:46your diagnosis is collapse or pneumon.
1:41:49Trachea shifted to the opposite side
1:41:51your diagnosis remains plural eusion.
1:41:54And if the trachea is central and you
1:41:55get a homogeneous shadow very rarely you
1:41:58could get it with a pneumonia
1:42:02or sometimes the plural fibrosis the
1:42:04trachea is. So here the trachea is
1:42:06shifted to the left side. There is a
1:42:08homogeneous white shadow obliterating
1:42:10the angle here. There is a collapse on
1:42:12the left side. Why are you seeing this
1:42:15black? Because this is white. There is
1:42:17or it's an over penetrated film. You can
1:42:19see that. That's why this looks black.
1:42:22Now, what is very strongly against
1:42:24pneumthorax
1:42:28to make the diagnosis of pneumthorax
1:42:30bronco markings
1:42:33markings that is one thing. The most
1:42:35important is you should be able to see
1:42:36the
1:42:38Yeah, you should be able to see the
1:42:40visceral plural line or the collapse
1:42:42margin as you say
1:42:43the lung border the collapse margin what
1:42:45we call it as a visceral plural line
1:42:47that has to be seen that's not seen
1:42:49here. So is it collapse or pneumonctomy?
1:42:52How do you differentiate it?
1:42:58How can you differentiate collapse or
1:42:59pneumontomy?
1:43:02History. Yes,
1:43:04you'll have to carefully look for the
1:43:06ribs. If pneumonctomy has been done,
1:43:09the ribs would have been cut. So if you
1:43:12are able to see some cut ribs, okay,
1:43:14then it's possibly pneumonctomy.
1:43:16Otherwise, it's collapse and collapse in
1:43:18an elderly person is always to be
1:43:20suspected as a malignancy. This patient
1:43:22would require a broncoscopy and further
1:43:28uh proceed.
1:43:35Okay.
1:43:37Bulging fissure signapse.
1:43:39Okay. So you're saying it's a bulging
1:43:41fissure. So what's your diagnosis?
1:43:44Right.
1:43:45Right.
1:43:48Cleella. Okay. Cleella pneumonia. So
1:43:50it's a homogeneous opacity you're seeing
1:43:52here. Trachea central and the fissure
1:43:55you're saying is bulging. So it could be
1:43:57klepsella.
1:43:58That is one diagnosis. Any other anybody
1:44:01else would want to say anything else? Is
1:44:03the fisher actually bulging or is it
1:44:06pulled up?
1:44:08You're seeing that the fisher has bulged
1:44:10here
1:44:11but then it is pulled up here. The
1:44:12fissure should normally should have been
1:44:14here
1:44:17right upper lo collapse because of a
1:44:19there is so you can see that the fissure
1:44:22has been pulled up fisher should have
1:44:23been at fourth rib here has been pulled
1:44:25up here but it is bulging in the medial
1:44:28side. So it's taking a shape of a
1:44:29reverse S reverse S
1:44:31reverse S
1:44:32collapsical
1:44:33okay reverse S golden's reverse S sign
1:44:36which is always a sign of malignancy
1:44:38because of the malignancy there is a
1:44:40collapse so the fissure has moved up
1:44:42here but medial part there is a tumor or
1:44:44a lymph node there which is com which is
1:44:46producing the bulge here so that is why
1:44:48it takes a reverse S sign or a golden's
1:44:51reverse S sign very specific of
1:44:53malignancy that you can
1:44:59So this is suggestive of malignancy.
1:45:01You'll have to do a CT scan and confirm
1:45:04the diagnosis.
1:45:12Yes.
1:45:18So it's not only X-rays that are going
1:45:19to be kept, HRCTs, CT films also are
1:45:22going to be kept for you. So what are
1:45:25you finding here?
1:45:26Empire.
1:45:28What is that?
1:45:34What are these airfield spaces?
1:45:37Ble.
1:45:38Okay. It could be ble. It is present all
1:45:40over.
1:45:41Pneum
1:45:43pneumato seals. Num seals should be in a
1:45:46condition where there is pneumonia. In
1:45:48the pneumonia here the rest of the lungs
1:45:51peripheral. Why is it not empyma?
1:45:55M5 simma
1:46:00the airfield space more in the plural
1:46:02base that is there bilateral it is
1:46:07why can't it be misma
1:46:13anyone
1:46:17markings are
1:46:19there are no markings here.
1:46:24Okay. So this is emphymatis boule. Okay.
1:46:26Bilateral emphymatis boule that you can
1:46:28see there. The differential diagnosis
1:46:31could be lung cysts could be pneumatil
1:46:34as you said. Okay. So those could be the
1:46:37differential diagnosis for this
1:46:38condition. So depends upon the patient's
1:46:40age. If it's a very young patient very
1:46:42child you're seeing then it could be a
1:46:44sequestration cyst bilateral. If it is
1:46:47within the background of a pneumonia
1:46:49then pneumoto seals otherwise it could
1:46:51be a emphymatis that you're seeing in
1:46:53the periphery. What are the
1:46:55complications the patient can develop?
1:46:58Spontaneous neotox spontaneous. The
1:47:01patient can develop pneumothorax because
1:47:03of this ruptured bullet.
1:47:09Yes.
1:47:10Cycos.
1:47:10Neuroscystic circus. Almost circles
1:47:13disseminated
1:47:15disseminated not only neuro it is
1:47:17disseminated you can see it is in the
1:47:18soft tissue here you can see this rice
1:47:21grain sort of pattern in the soft tissue
1:47:23you can see it in the brain also so
1:47:25what's organism
1:47:29sodium
1:47:30how how is it acquired
1:47:33from the consumption of uncy
1:47:39green leafy it could be vegetarians also
1:47:41can develop it it's not only the pork is
1:47:43because of this. Okay. So how do you
1:47:45manage this patient?
1:47:48Alpendazol under the steroid cover is
1:47:51given.
1:47:51I see if we have to give steroids also
1:47:54along with
1:47:55alendazole with steroids. Why not
1:47:58praquental? Why alendazole?
1:48:01For disseminated combination therapy can
1:48:03be given sir.
1:48:05But why don't we use why do you want to
1:48:07use alendazole for the tapeworm? The
1:48:09drug of choice is prraiquental.
1:48:11But steroids decreases the efficacy of
1:48:14praziquental sir.
1:48:15So that's the reason. What's the
1:48:17mechanism of action of praziquental?
1:48:21It cannot penetrate brain.
1:48:24It cannot penetrate the
1:48:27brain. No.
1:48:33Albendol with steroid is correct. Plus
1:48:36or minus antiepileptics in the patient
1:48:37is steroid. But why not praise?
1:48:45Why alendazole? Albent is not effective
1:48:47for tenia. We don't give it for tape.
1:48:50But why do you give it for neurosy
1:48:51purposes?
1:48:57Okay.
1:49:00Okay. So basically the mechanism of
1:49:03action of prraziquental is it paralyzes
1:49:06the worm and it is not a it is used for
1:49:10adult worms here. It is the larae that
1:49:13we are acting on. So we require a
1:49:15systemic helmental that we have and
1:49:18alendazol is the only one which we have
1:49:20at present along with ivormectin.
1:49:23Ivormectin a lot of studies have been
1:49:25done with ivormectin also. So
1:49:27combinations can be also used. Uh again
1:49:30the problem with the
1:49:33uh praziquentil it is not going to yeah
1:49:37it is not you written it in the chat yes
1:49:39it won't kill the worm it is just for
1:49:41deworming you have to use something to
1:49:43flush the worm out after that so here we
1:49:46require to circidal drugs which can make
1:49:50sure that it goes there and
1:49:53causes a cidal effect there so that is
1:49:56why alendurol we do not use brazquentil
1:49:58as such
1:50:00Again neurosis you're required to know
1:50:02the staging of neuroscysteosis also
1:50:05based on MRI we have the various stages
1:50:07of neurosy cycosis. Anyone can tell me
1:50:11vesicular
1:50:12collidal vicular nodular
1:50:14vicular nodular
1:50:15nodular
1:50:17degenerative.
1:50:18Yeah the last one calcified stage. So
1:50:20based on that
1:50:22if it is already in calcification stage
1:50:24we don't require to treat because it is
1:50:25going to remain like that. If it is in
1:50:28the earlier stages, we'll require to
1:50:29treat the uh patient.
1:50:34Any other doubts or clarification?
1:50:35Somebody was asking.
1:50:42No.
1:50:43So every patient will need
1:50:46sir.
1:50:47No. That's what it depends upon. See
1:50:49what do you want to achieve? If it is
1:50:51not involving the brain, if it is only
1:50:53in the subcutaneous plane, isn't it? my
1:50:55own nothing has to be done. It doesn't
1:50:57cause any problem. It'll calcify and
1:50:59remain there. But if it is there and
1:51:01multiple lesions are there in the brain
1:51:03and the patient has symptoms, there is a
1:51:05seizure etc. then we'll have to use the
1:51:08treatment. Okay.
1:51:09Okay.
1:51:10For non-neurological, we don't require
1:51:12to give.
1:51:15Yes. Again, a very common CT kept for
1:51:17you.
1:51:21Anybody
1:51:31fingering glove sign
1:51:32can describe what you're seeing.
1:51:36You can describe the finding and then
1:51:42finger and glove. Okay.
1:51:46Which finger are you talking about with
1:51:48this ones? These are the finger and
1:51:49glove.
1:51:52Finger and glove. Which condition?
1:51:56Broncticis.
1:51:58Yeah, bronchis. The finger and glove is
1:52:00bronchis or as you said the proximal
1:52:03bronchis. It would have been much
1:52:05bigger. What is this pattern? I don't
1:52:07know whether it's clear or not. You can
1:52:09see
1:52:10the train bud appearance.
1:52:11Yes, this is the tree bud appearance.
1:52:13Okay. Train bud appearance where you're
1:52:16seeing the branches here of the trees
1:52:17and then the buds arising from that.
1:52:19What is your diagnosis? Yes. Uh Vijay,
1:52:22you saidary tuberculosis.
1:52:24Tuberculosis.
1:52:26Okay. Okay. In adults it is considered
1:52:28as pulary tuberculosis but in children
1:52:31diagnosis for train is
1:52:34bronchulitis. Bronchulitis.
1:52:35Broncholitis. In children it is
1:52:37broncholitis could be tuberculosis also.
1:52:40But in adults this is considered as a
1:52:41pattern which is more specific for
1:52:43tuberculosis. So that is why this is a
1:52:45very common image that is kept for you
1:52:48in your exam. So based on this you can
1:52:51uh do the uh other test maybe you can do
1:52:55a B and then you can take a sample from
1:52:57there uh and then you can start the
1:53:00patient on antitubacla therapy. Again
1:53:03very common questions about
1:53:05antitubercular therapy. You have to know
1:53:07the regimens the drugs the resistance
1:53:10patterns and the newer drugs that are
1:53:12there. Can you tell me some of the newer
1:53:14drugs used for tuberculosis?
1:53:18And so
1:53:21the one which is
1:53:22the one which is available all over and
1:53:25is used everywhere is
1:53:30bacquin has been used thoroughly.
1:53:32Bedquilline is available everywhere
1:53:35and the other drugs like you have the
1:53:36proaminide or the daminade
1:53:39uh etc. The problems with bidakim what
1:53:42is the worry that we have with bidak
1:53:44cutie prolongation
1:53:45prolongation and arhythmias so that's
1:53:48there with others also
1:53:50so that's the problem with these newer
1:53:53drugs these are used for resistant
1:53:55organisms
1:54:07Yes.
1:54:23Yes. What is this pattern?
1:54:26Signatur.
1:54:28Where are the signatures?
1:54:30Multiple ground glass opacities.
1:54:33Crazy pavement pattern.
1:54:35Okay. Crazy
1:54:36proteinosis
1:54:38pulmonary elvela protein. This is a
1:54:40differential diagnosis possible. It's a
1:54:42crazy pavement pattern. You can see
1:54:43there are filling and there are open
1:54:45waves here. Signaturing would have been
1:54:48much bigger than this. This is a crazy
1:54:50pavement pattern. Okay. Crazy pavement
1:54:53pattern that is there. What condition?
1:54:55Co.
1:54:57Okay. CO is what we see now forever.
1:54:59Everything is COVID. No, where was it
1:55:01described for?
1:55:04Other than the normal CT everything else
1:55:06is CO now. So
1:55:10which type of ILD?
1:55:12UIP.
1:55:14Okay. Okay. Usual intestial pneumonia.
1:55:17It could be seen as you said in
1:55:19pulmonary al filling disorders like
1:55:21pulmonary al proteinosis. It was also
1:55:23described. Uh so this is the crazy
1:55:27payment appearance. It's classically
1:55:28seen in the intestial pneumonia and
1:55:30COVID is one of the intestial pneumonas
1:55:33uh that is there presently where you see
1:55:36a lot of patterns that could be seen
1:55:40again a very common CT image that is
1:55:42kept for you. Okay with co definitely
1:55:45similar things will become this is a jug
1:55:47handle which I showed you that time I
1:55:49think this slide came later. Okay. So
1:55:51this is a jug handle for ASD which I
1:55:53wanted to show. Yeah.
1:55:59Sering.
1:56:00Seringia. Why do you say so?
1:56:07Why are you saying it's
1:56:09okay? So there is a hyper intense lesion
1:56:12that you're seeing there in the central
1:56:14part of the chord, isn't it? Central
1:56:16part of the chord you're seeing there
1:56:18and it's extending downwards. Okay. So
1:56:23singomalia. So what are the clinical
1:56:25features that are classically seen in
1:56:27seringomia?
1:56:29Dissociated sensory.
1:56:30Okay. Dissociative sensory loss.
1:56:32Correct.
1:56:38Bladder.
1:56:38Which part of the which part of the
1:56:40limbs is which which part of the body
1:56:42will be involved in this patient?
1:56:43Upper limb. Cape like
1:56:44upper limbs isn't it? Upper cape like
1:56:46disturbance will be the cape like
1:56:49distribution of sensory loss. Not
1:56:51capike. Usually the upper limbs only you
1:56:53get suspended sensor loss. Above that is
1:56:55normal. Below that it is normal. Cape
1:56:57like if it is extending to the
1:57:00cape like where do you get
1:57:03if it extends upwards isn't it? If it uh
1:57:06extending upwards what do you call that
1:57:07as singing extending into the brain
1:57:09stem?
1:57:10Singing
1:57:12there. There you get the cape like
1:57:13pattern on the face that's there. Okay.
1:57:16So this is a central chord lesion. This
1:57:18is an exception for the central chord
1:57:20leion. Why is it called as an exception
1:57:22for the central cord leion?
1:57:24Sacral spar
1:57:26sacral sparing is
1:57:29that's not the reason why it is called
1:57:31as exception. It differs from other
1:57:33central cord leations in one very
1:57:36important feature.
1:57:39If there is a central cord leion what's
1:57:40the first clinical feature they come
1:57:43bladder involvement isn't it? bladder.
1:57:45So bladder involvement is classical of
1:57:47central cord leations early bladder but
1:57:50singomia does not have this bladder
1:57:53involvement at all. It does not have the
1:57:55bladder involvement at all. So that's an
1:57:57exception that is uh of a central cord
1:58:00lesion. What will be the findings you
1:58:02get in the hand in these patients?
1:58:04Man and barrel syndrome.
1:58:06What is that man in barrel?
1:58:09Patchy and variable sensory loss.
1:58:12Okay. In the hands what you'll get if I
1:58:14see his hands how will it be?
1:58:17There will be ulcers. Correct. Clawing
1:58:19very important. Wasting of the hands,
1:58:22ulcers, atrophy will be there. And
1:58:24sometimes it is swollen. The hands
1:58:26become swollen. What is that? Due to
1:58:29swelling because
1:58:32hands are swollen atrophy atrophy of the
1:58:34muscles. But there'll be something like
1:58:35a swelling due to the autonomic
1:58:38dysfunction that's there. Okay.
1:58:40Autonomic dysfunction that could be
1:58:41there. So the hands can be and you can
1:58:43as you said there will be ulcers that
1:58:45will be there and very characteristic
1:58:47features of small muscle wasting of the
1:58:49hand muscles that you get. Where else
1:58:52can you get this dissociative sensory
1:58:54loss other than singomalia? Where else
1:58:57can you get dissociative sensory loss or
1:59:00what we call it as a pseudo syringoic
1:59:03pattern?
1:59:05Amotropic lateral.
1:59:08Why amic patrolosis will have sensory
1:59:10problem? It'll never
1:59:14Yes.
1:59:15Posterior spinal.
1:59:17Okay. There was rare. The commonest
1:59:19cause you should supposed to say is
1:59:20leprosy.
1:59:22Leprosy. What sensations are lost?
1:59:26In a patient who has leprosy what
1:59:28sensations are lost?
1:59:29Pain and pain and temperature is lost.
1:59:32The posterior column is preserved. So
1:59:34that is where you get the pseudo
1:59:35singeromyic pattern. You can get it in
1:59:38other neuropathies also.
1:59:41Tangous disease.
1:59:43It's a very rare one. You can get in
1:59:45diabetes also. Sometimes only small
1:59:47fibers are involved. You can get them.
1:59:50Lateral medary syndrome. What do you
1:59:52have in lateral medary syndrome with
1:59:53sensory is gone.
1:59:57pain and temperature pain and
1:59:58temperature is gone again isn't it? The
2:00:00posterior column is preserved. So all
2:00:03these are examples for as you said the
2:00:05spinal cord you said the anterior spinal
2:00:07artery thrombosis or a posterior spinal
2:00:09artery. If it's anterior spinal artery
2:00:11only pain temperature goes if it is
2:00:13posterior spinal artery then it is pain
2:00:15and temperature is preserved isn't it?
2:00:16So all these are called as so-called
2:00:19pseudocyic patterns that you see
2:00:25multiple sclerosis.
2:00:27What is the finding? What is the finding
2:00:31perentricular vein?
2:00:33Okay, you can see that there is white
2:00:34matter. What do you call this lesions as
2:00:40they called as
2:00:41Dawson's fingers?
2:00:43No, Dawson's finger is the name. What do
2:00:44you call this white patches as? They're
2:00:46called as
2:00:51I can't hear you.
2:00:54They're called as plaques. They're
2:00:56called as plaques. They're called as
2:00:58plaques that is there here. So white
2:01:02matter involvement there. And you can
2:01:03classically see the uh Dawson's fingers
2:01:06that you see. Okay. What's the commonest
2:01:08pattern of multiple sclerosis?
2:01:12Remitting and relapsing.
2:01:13Okay. So relapsing remitting pattern is
2:01:16the commonest pattern that you have. So
2:01:19how do you confirm the diagnosis? Once
2:01:21you know it's multiple sclerosis, how do
2:01:22you confirm the diagnosis?
2:01:26MRA and CSF.
2:01:28M is done. So you do the CSF. What do
2:01:30you get? CSF.
2:01:32Oloconal bands. Oloclonal bands. You'll
2:01:35do it. Okay. What is uta?
2:01:40Hot and cold. Sensitivity to hot
2:01:42temperature.
2:01:44Okay. So the symptoms will worsen during
2:01:46the temperature that is there. Okay.
2:01:49What is lit sign?
2:01:51Shock. Electrical shock like
2:01:54okaying of the neck of the
2:01:57because of the compression of the what?
2:02:00Posterior columns.
2:02:02Posterior columns isn't it? Posterior
2:02:03columns. Again a very characteristic
2:02:05feature in multiple sclerosis. You can
2:02:07get also you get something as
2:02:10interuclear of themopleia can be there.
2:02:13Okay.
2:02:13How do you different how do you
2:02:15differentiate multiple sclerosis versus
2:02:20NMO neurom
2:02:22bilateral optic neuritis
2:02:24longitudinal extensive
2:02:26okay
2:02:26multiple scerosis
2:02:29extensive
2:02:30longitudinal extensive in case of NMO
2:02:32correct then
2:02:35policonal bands will be usually absent
2:02:38in NMO
2:02:38what is that present in NMO what is the
2:02:41test antimo Anti
2:02:44antagon antibbody.
2:02:46Okay. Anti-acquafferin 4in
2:02:49equaporin 4 antibbody will be positive
2:02:51in that. So that is what you will get in
2:02:54case of NMO. So again whenever this is
2:02:56kept you do get questions on this
2:02:59[snorts] and various patterns of
2:03:01multiple scerosis and how do they
2:03:03manifest and how do you diagnose and how
2:03:05do you treat all that things will be
2:03:07asked.
2:03:09I think we have crossed 4:00.
2:03:14Do we continue or shall we stop?
2:03:18Continue, sir.
2:03:19We'll continue.
2:03:21Okay, we'll continue for another half an
2:03:23hour. After that, what is this?
2:03:27Pets.
2:03:28Okay, pets. So, what are the common
2:03:31indications and what are you seeing in
2:03:32this first pet?
2:03:34This is a serial pet of a patient. What
2:03:36are you seeing in this perspect?
2:03:41And this is after treatment.
2:03:45What are you finding?
2:03:46Metastasis.
2:03:48What are these structures? What I've got
2:03:50multiple nodes but
2:03:52this is lymph nodes.
2:03:55Axillary lymph nodes. Neck lymph nodes.
2:03:57Not not the spine. The spine is anyhow
2:04:00that is in the second one. You can see
2:04:01in the first one what you're seeing is
2:04:03your uh lymph nodes. You can see those
2:04:06lymph nodes there. Multiple lymph nodes
2:04:08that are there which have got involved
2:04:11and in the natural part maybe all the
2:04:12lymph nodes have regressed or responded
2:04:17to treatment and what you're seeing is
2:04:18the marrow being hyper intense here is
2:04:21the area where you have your uh marrow
2:04:24that is seen in the second. So what's
2:04:26the possible diagnosis? Hodkins.
2:04:28Hodkins.
2:04:30What are the other indications where you
2:04:32do the pets?
2:04:35Favor of pyrexy of unknown origin.
2:04:37Correct. Pyrexy of unknown origin is one
2:04:39of the important indications. Correct.
2:04:42Malignancy to detect secondary
2:04:44metastasis.
2:04:45Metastasis you can use. Correct. Staging
2:04:48of malignancies. Lymphoma before the
2:04:50start of chemotherapy.
2:04:52Yes. Before and after the start of
2:04:54chemotherapy. Yes.
2:04:57Pyrexy of unknown origin. So these are
2:04:59the general conditions that we can do
2:05:01where you can do the PET CT. You could
2:05:03do it uh do we do such cities to find
2:05:06bleeding sources
2:05:14to find out sources of bleeding. If
2:05:15there is an unknown source of bleeding
2:05:18can we use PET for that?
2:05:22You know radial lababelled PET can be
2:05:24used. Okay. RBC labelled scans can be
2:05:26done not the actual PET scans you can do
2:05:29RBC label scan to find out especially
2:05:31obscure bleeds when you do not find a
2:05:33sight of bleed you can use that for that
2:05:36how does this work what's the principle
2:05:38of
2:05:405D 18
2:05:435D yeah fluorio glucose is there so
2:05:47taken up by metabolically
2:05:49okay so metabolically active sites would
2:05:52generally take up this and that's how we
2:05:53can make
2:06:02Yes,
2:06:09the patient has hematuria and this is
2:06:11the
2:06:15CT of the chest.
2:06:17Veus.
2:06:18Okay, it could be vaginous. If you find
2:06:20that there is a granuloma sort of thing.
2:06:22Anything else other than vagness? you
2:06:24want to consider
2:06:26anti-GB.
2:06:27Yeah, anti-GBM good posture. Good
2:06:30postures is one more thing that you'll
2:06:31have to look for. Okay, so these are the
2:06:34hepto sorry the pulmonary renal
2:06:37syndromes. Okay, pulmonary renal
2:06:39syndromes. It can be seen with
2:06:41infections, lepto, ha virus, uh
2:06:46septacmias. You can get this pulmonary
2:06:48renal syndromes. But it could be due to
2:06:50connective tissue disorders like good
2:06:51pastures, could be veggars, could be
2:06:54other vasculitis, microscopic
2:06:55polyangitis etc. can also produce this.
2:06:58Lupus also can have sometimes these
2:07:00manifestations. So these are the
2:07:01differential diagnosis. So what are the
2:07:03investigations that you want to do to
2:07:05confirm
2:07:11anti-uclear anticy
2:07:14okay can do the anchor correct
2:07:17for the good pastures
2:07:20imofllororoscopy
2:07:22okay you take a biopsy and do the imof
2:07:24fllororosense
2:07:26can do the C3 levels
2:07:29you can biopsy the lung you can do the
2:07:30kidney biopsy also Antigbium antibodies
2:07:33also can be tested. How do you treat
2:07:36good posture syndrome?
2:07:42Treatment of good posture syndrome.
2:07:48It requires stronger more than steroids.
2:07:50It requires imunosuppression and plasma.
2:07:54Plasma therapy. Very important. Plasma
2:07:57flex is what is needed for good posture
2:07:59syndrome. When the patient has immaturia
2:08:01and this one that means it's an active
2:08:02disease patient will require plasma
2:08:04therapy. What's the prognosis? Good
2:08:06pastures
2:08:09good bad
2:08:11bad
2:08:12bad prognosis bad prognosis despite of
2:08:15plasma exchange and others don't have
2:08:17that much of uh survival that is
2:08:24yes
2:08:26calcific pancreas.
2:08:28Okay. So why do you say it is pancreas?
2:08:30Why is it not a gallbladder
2:08:33or a renal stones
2:08:35lateral view?
2:08:38Okay, it's crossing the midline. So it's
2:08:41pancreas only. Nothing will cross unless
2:08:43you have a horseshoe kidney there which
2:08:45but horseshoe kidney is not usually on
2:08:47the top. It is usually the connection is
2:08:50at the bottom there. So it's a
2:08:51pancreatic calcification as you say.
2:08:55So you said this diagnosis is chronic
2:08:58chronic calcific pancreatitis. Any other
2:09:00differential diagnosis?
2:09:06Any other type of pancreatitis can have
2:09:08this
2:09:10very common in our part.
2:09:12Autoimmune.
2:09:13Autoimmune. No autoimmune
2:09:15fibro calculus.
2:09:17Yes. Tropical calc PCP that is tropical
2:09:19calcific pancreatitis which is very
2:09:22common in the belt. where you can get
2:09:24this calcifications. Yes. What are the
2:09:26problems with this?
2:09:30Diabetes.
2:09:31Diabetes. Correct. Then
2:09:33malabsorption.
2:09:35Malabsorption. Correct.
2:09:36Insufficiency.
2:09:38Anything more important?
2:09:41Malabsorption. Diabetes. Correct.
2:09:44The are prone to develop cancer.
2:09:46Pancreatic cancers.
2:09:47Cancers is very common. Pancreatic
2:09:49malignancy. You will have to keep on
2:09:51sending the markers. CA 1919 and keep
2:09:54looking at that frequently.
2:10:05Air under diaphragm.
2:10:06Air under diaphragm. Which diaphragm?
2:10:09Right or left?
2:10:12The right side or left side?
2:10:15So left side.
2:10:17Left side is normal.
2:10:20Left side is normal. Huh? You can have
2:10:22the pandic gas shadow there.
2:10:25It was air under. You should have had it
2:10:26on both sides.
2:10:27Fiseral edema in the right.
2:10:29You can see here there is a nice
2:10:32Yeah. What we call it as a phantom tumor
2:10:34as you said interlobar eusion. Isn't it
2:10:37interlobar eusion? What does it suggest?
2:10:42Or
2:10:44it suggest heart failure. It suggests
2:10:46heart failure. You can also see that
2:10:47there is blunting of both the
2:10:50costtopherrenic angles. So there is
2:10:51bilateral plural eusion interloion. You
2:10:54can see that the pulmonary venus
2:10:56prominence is there. So it indicates
2:10:58cardiogenic pulmonary edema. Why is it
2:11:00called as phantom tumor
2:11:03disappear of diuretics?
2:11:05So if you give a dose of diuretic then
2:11:07you repeat an X-ray the interloba
2:11:10fissure becomes normal. So that's why
2:11:12it's called as a phantom tumor. So
2:11:14moment you see a X-ray like this you
2:11:16have to uh think of uh cardiogenic and
2:11:20you have to rule out cardiac failure.
2:11:22Supposedly the cardiac failure is not
2:11:24there and I find an interlobar eusion
2:11:26like this. What is your diagnosis
2:11:35which is other diseases which can
2:11:37produce interlobar efficient
2:11:46supposedly this patient has a good
2:11:48right-sided effusion here till here and
2:11:51then there is an interloion also
2:11:54which is the cause for
2:11:59The most common in India plural eusion
2:12:03tuberculosis
2:12:04tuberculosis always remember
2:12:06tuberculosis can produce inter
2:12:08interloion also but that does not heal
2:12:11completely you will have a fibrosis that
2:12:13is remaining there that remains okay
2:12:15tuberculosis has to be ruled out once
2:12:17you ruled out cardiogenic pulbe
2:12:25Yes.
2:12:30Deep sulcus sign.
2:12:32What's your diagnosis?
2:12:43Yes. What's the diagnosis?
2:12:47Pneumorax.
2:12:48Right side pneumorax.
2:12:49Rightided tension pneumthorax. Isn't it?
2:12:52So tension pneumorax. Here we are
2:12:54finding air without vascular markings
2:12:57and then the media is shifted to the
2:12:59opposite side. The trachea is shifted to
2:13:01opposite side. The visceral plural line
2:13:03possibly is this is what is the visceral
2:13:05plural line. Not very clear but we
2:13:07should have seen the visceral plural
2:13:09line that will be seen here. So this
2:13:12looks like tension. What will be the
2:13:14clinical features of a patient with
2:13:16tension?
2:13:20Hypotension tachicardia
2:13:22hypotension. Yeah.
2:13:23Peggardia
2:13:24resonant on percussion.
2:13:28What else?
2:13:29Resonant and chest perussion.
2:13:31Okay. Hyper resonant note will be there.
2:13:35Okay. So how do you treat this patient?
2:13:39ICD placement.
2:13:41ICD will take ICD available we can put
2:13:46in second interostal space. Ideally
2:13:49early emergency you can do a needle
2:13:51thoracic costm in the second intercostal
2:13:53space and then follow it up with the
2:13:55intercostal drainage in the middle.
2:13:57Okay. What are the conditions where you
2:13:59can get recurring pneumothorax?
2:14:02Marin marins correct
2:14:05smoking.
2:14:07Okay. Smokers. Okay. Due to bullar
2:14:09ruptures okay bullar ruptures.
2:14:13Any other conditions?
2:14:16Recurrent pneumthorax
2:14:21lymphoma.
2:14:22Yeah. Lymphia plural fistula.
2:14:25Bronco plural fistula. What sort of
2:14:26pneumthorax does it produce?
2:14:29Does it produce neumorax or something
2:14:31more?
2:14:33There's a fistula. No. So it produces a
2:14:36hydronneumorax.
2:14:38Broncoal fistula is always hydronumorax.
2:14:41It remains like that. What is ketamine
2:14:44pneumorax?
2:14:48during menstrual cycle
2:14:48occurs in females during menstrual
2:14:50cycle.
2:14:50So during menstrual cycle so they can
2:14:52have that's also a cause of recurrent
2:14:54pneumthorax that could be there possibly
2:14:56secondary to endometriosis of the plura
2:14:59that is what has been taught for that.
2:15:04Okay.
2:15:11Yes. Absor
2:15:15how do you describe this shadow
2:15:18ring enhancing
2:15:19there is a ring enhancing leion which is
2:15:21located in the right possibly the
2:15:24temporal parietital cortex isn't so what
2:15:26is the differential diagnosis
2:15:30absess
2:15:31metastasis
2:15:33so absessoma
2:15:35toxoplasmosis
2:15:37malignancy
2:15:39then metastasis as you said correct Then
2:15:42CNS lymphoma.
2:15:44Okay. Primary CNS lymphoma. Then
2:15:47radiation necrosis.
2:15:49Okay. Rarely radiation necrosis. Okay.
2:15:52So how do you differentiate? I what is
2:15:53your first diagnosis based on this?
2:15:58So how do you know it's toxopplasma?
2:16:01What will be the classical location for
2:16:03toxopplasma?
2:16:09HIV patient could have all of them. Now
2:16:11it could be a lymphoma. It could be a
2:16:13toxopplasma. It could be a tuberculoma.
2:16:15So how do you make out that where is
2:16:18your
2:16:19There is no spage or roll of
2:16:24again remember the toxopplasma
2:16:26classically located at the junction of
2:16:29the
2:16:30white and gray matter. So it's very
2:16:32classically located at that point.
2:16:34Tuboclomas can be located anywhere.
2:16:36Tuboclomas can be located anywhere.
2:16:39And if there is a large amount of edema
2:16:41supposedly I see this lesion and
2:16:44surrounding that you have a large amount
2:16:45of edema what's the possibility
2:16:48absis
2:16:49it could be an absess but out of
2:16:51toxocculoma
2:16:53which has more of edema toxopplasma has
2:16:56a lot of edema
2:16:58okay even lymphoma primary CNS lymphoma
2:17:01or a tumor also can have edema but
2:17:03between tuberculosis and toxoplasma
2:17:06edema is out of proportion and sometimes
2:17:08it cross midline also midline also you
2:17:10might be able to see. So that is how you
2:17:14can make out the difference between
2:17:16toxoplasma and tuberculoma. So these are
2:17:18the differential diagnosis for ring
2:17:19enhancing lesion in the uh brain. This
2:17:22is uh a very common CT that is kept for
2:17:24you in your exam.
2:17:28Okay. So that's what I told you.
2:17:38Yes.
2:17:42Liver secondary.
2:17:43Liver.
2:17:44Liver secondaries.
2:17:45What could be the primaries?
2:17:48Most common.
2:17:50Colon.
2:17:51Yeah. Most common is GIT itself. That is
2:17:54the colon or the stomach is the most
2:17:55common. You could get primaries from
2:17:57other sites also. So always the
2:18:00primaries are the uh usually the GI
2:18:03primaries itself. As you said colon is
2:18:05the most common
2:18:06followed by the stomach followed by the
2:18:08pancreas then the breast and the lung.
2:18:11So by looking at the site of the primary
2:18:14sorry sight of the secondaries can you
2:18:16localize which side of the colon it's
2:18:18arising from?
2:18:25Yeah.
2:18:27By looking at the sight of the primary
2:18:31sorry sight of the secondaries can you
2:18:33make out which side of the colon right
2:18:34sided colon leftsided colon supposedly
2:18:37the left lobe of the liver is involved
2:18:39supposedly right side of the li lobe is
2:18:40involved
2:18:42can you make out
2:18:47anyone
2:18:53anyone
2:19:02So if you see the blood supply to the
2:19:04liver, how is the blood supply coming
2:19:05from? How does the primary reach the
2:19:09liver from?
2:19:11How does it reach?
2:19:15Portal vein
2:19:16has to come through the portal vein
2:19:17itself, isn't it?
2:19:18Yes.
2:19:18So how is the portal vein formed?
2:19:22[ __ ] and superior ment and superior
2:19:25mentric vein. Uh [ __ ] superior mentric
2:19:29vein drains which part?
2:19:33Which part of the bubble?
2:19:36Uh
2:19:37right side or left side?
2:19:40Superentric vein is
2:19:43left
2:19:44left.
2:19:45Left right. Huh?
2:19:49So pyramentric vein is right side or
2:19:51left side of the colon?
2:19:53Right side of the colon.
2:19:54Sure. The right side. I'm just hearing
2:19:56left here a lot. So right side. Okay.
2:19:59The left side goes through
2:20:02vein and then it goes through the
2:20:04splenic vein and then comes there.
2:20:06Correct. So that's how it is going. So
2:20:08what happens? There is something called
2:20:10as a lamelar blood flow. That means the
2:20:12blood goes in a stream like pattern
2:20:17after the portal vein is given. It
2:20:19divides into the right and left. Okay.
2:20:22The right goes to the right lobe of the
2:20:23liver. The left goes to the left lobe of
2:20:25the liver. So whatever is coming from
2:20:27the left side by name meaning the left
2:20:29side that is the splenic inferior
2:20:32mentric all coming towards from that
2:20:34side will differentially go to the left
2:20:37lobe. Whereas whatever is coming from
2:20:39the right side you understand right
2:20:41colon seeum etc will go through the
2:20:43superior mentric vein through the right
2:20:45side of the portal and go through the
2:20:47right epatic vein. So that is what we
2:20:50call it as a lamelar pattern of flow. So
2:20:54that is one of the reasons why they say
2:20:55your amibsis.
2:20:58Where is the amic clever absis more
2:21:00common
2:21:02posterior? Which
2:21:03side? Right or left? Right. Right side.
2:21:06Where is it coming from?
2:21:10Where is the source? It's the right
2:21:11side, isn't it? So seeum that's where
2:21:14it's coming from up. If supposedly the
2:21:16sigmoid colon is predominantly involved
2:21:17into some uh pathology be it ambibiais
2:21:21or be something else generally it will
2:21:23go onto the left lobe of the liver. So
2:21:27this is due to the lamelar flow blood in
2:21:30these uh sections that could be there.
2:21:36Okay,
2:21:38I think uh we will stop at this for
2:21:41today. We've already crossed time. We'll
2:21:44continue this
2:21:46because I think we've had
2:21:50quite a detailed discussion on things.
2:21:53Yes sir.
2:21:54We will continue this in maybe a next
2:21:57session in the next week itself. Okay.
2:22:00Yes sir. Any doubts or clarifications,
2:22:05you can either
2:22:07uh message me or maybe during the next
2:22:09session we can take it up.
2:22:16Yes sir.
2:22:17Okay.
2:22:19Thank you sir.
2:22:20Okay.
2:22:20Thank you so much sir. It was a
2:22:22comprehensive and completely covered
2:22:25like from
2:22:27clinical scenarios
2:22:29oski pattern. It was a complete revision
2:22:32of the enter medicine
2:22:34two and a half hours.
2:22:36We will try to cover the rest of it. I
2:22:38think still the ECGs etc. I have to
2:22:40still cover. Maybe in the next session I
2:22:42will let you know when we'll do that.
2:22:44Okay.
2:22:44Yes sir.
2:22:46Thank you.
2:22:46Thank you sir.
2:22:46Thank you so much sir.
2:22:48Thank you sir.
2:22:49Thank you so much sir. Thank you so much
2:22:51sir.
2:22:52Thank you.

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