Study group discussion: Most common site of intraperitoneal abscess

Which is the most common site of intraperitoneal abscess?

It's pelvic.

The reason being gravity, common sites are subphrenic, paracolic, pelvic and right iliac fossa.

Pelvic is most common due to pelvic position of appendix and fallopian tubes, and due to leakages from colorectal surgeries.

I had a MCQ asking me to choose between paracolic, subphrenic and pelvic and stuff as options for the most common site.

So in that case, what would be the answer?

Pelvic would be the most common site, according to my teachers.

What is the best way to get to a pelvic abscess sample?

Through rectum? They usually burst into rectum and resolve.

In women, from the umm what do you call it..
Pouch of Douglas!

Nice Ikan :)

I tried so hard to recall the name. Almost blanked out for a moment there!

In women vaginal drainage is done.. Through posterior fornix vaginl drainage in women.

And if the abscess is pointing in rectum, rectal drainage is done.

In males, you would pass a needle through the rectum

Laparotomy is almost never necessary and rectal drainage is preferred over suprapubic which risks exposing the general peritoneal cavity to infection.

Study group discussion: Heparin induced thrombocytopenia and leech therapy

What's Heparin induced thrombocytopenia??

Antibodies are formed in the blood platelets due to heparin in certain individuals. This causes widespread petechia.

You discontinue heparin and give something else in HIT.

Lepirudin
Bivalrudin
Argatroban

And now the cool part :D
The drug Lepirudin is derived from the salivary glands of LEECH!

I know!!!

Haha ain't this cool?

Leech.. Didn't know that!

In school, they used to say if a leech bites you, you die. I never found out the truth though.

Maybe cause it releases these substances in your system..And you are not able to clot inside?

My 12th standard books also mentioned about leech having anticoagulant properties....Now I find out that it's used to prepare drugs!

HIRUDIN is the substance that is secreted by the salivary glands of leech!

I just Googled can a leech bite kill you :D
I don't think they can kill you, they don't take enough blood in a fast amount of time unless you put a few 100,000 on your body and left them there for a while.

100, 000...That's a lot of leech!

Lol I think it was a hyperbole!

I don't remember exactly....but I had heard of alopecia being treated with leech.

How? :O

The leech would suck blood... So keeping them for just the right amount of time they would increase the blood supply... I'm not sure though.

Leech therapy is known to increase blood circulation, therefore when therapy is applied to thinning or bald areas, the increase of blood circulation helps enhance the concentration and delivery of nutrients that assist in making hair follicles strong, thereby assisting in the promotion of hair growth. People suffering alopecia caused by fungal infections or dandruff can also benefit through the antibacterial component in the leeches saliva, which helps combat fungal infections.

It's also used in arthritis :O

The FDA approved the use of leeches in the USA in 2004. In October 2005 the first American hospital 'Beth Israel Medical Center New York' offered Leech Therapy to treat Osteoarthritis of the knee.

Arthritis?! Woah.

Study group discussion: Heparin, warfarin and the anti-fibrinolytics

Name the drugs which inhibit fibrinolysis.

TACA! Tranexaemic acid, amino caproic acid.

Describe the mechanism of action of heparin.

Binds to anti thrombin 3, blocks factor 10.

Which coagulation factors does warfarin affect?

Vitamin K dependent ones: 10, 9, 7, 2, protein C.

Why there is a lag of 2 - 3 days for warfarin to act?

Study group discussion: Management of Parkinson's disease

50 year old male, has no expressions, walks to your office, slowly. He complains of tremor while watching television. He says he can do tasks without the trembling his hands. His fingers keep moving as if he is rolling a pill as he is talking to you. Which drug will you prescribe to relieve his tremor?

It is Parkinson's disease. Anticholinergics will be prescribed.

Why not L-dopa? With carbidopa?

Study group experience #9

What is the kussmaul's sign? Is it seen in cardiac tamponade?

Mitral stenosis auscultatory findings

AV blocks simplified

Enzymes checked through RBCs 

G6PD deficiency and Myoglobinuria

How to study pharmacology (Most requested post ever)

Short course chemotherapy

Pharmacological management of diabetes

Mechanism of atropine induced hyperthermia 

Lepra type 1 and type 2 reaction 

Types of hypersensitivity reactions  (A simple Q&A at the end!)

Studying physiology 

Single Breath Count test in Guillain Barre syndrome

It was my birthday this week (13th February, to be precise). One of the awesomites got to know through Google plus and everyone wished me on my birthday which made it really special. Thanks everyone!

Happy belated Valentine's day everyone! May we all love what we do and do what we love.

I'm unable to access tumblr fan mails and ask messages at the moment. Sorry for the delay! I'll be back on tumblr in mid March but I'll try posting the study group experiences as and when possible!

-IkaN

Study group discussion: AV blocks simplified

Tell me little bit about what do you know about AV Block?

They occur when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. There are 3 degrees which we can recognize.

First degree consists of prolongation of the PR interval on the ECG (>200 msec in adults and >160 msec in young children).

In second degree, we can find atrial impulses that fail to conduct to the ventricles. And variations like mobitz I and II.

And finally, third degree, where we get multiple P waves that don't conduct at all.

Tell me differences in type 1 and 2 mobitz?

Well, in type I there is a prolongation of the PR interval until it drops and doesnt conduct

And in type 2, there is a constant PR interval and then it drops (:

Poem:
If your R is far from P, then you have a 1st degree.
Longer, longer, longer, drop...Then you have a Wenckebach.
If your PS don't go through, then you have a Mobitz 2.
If your PS don't agree, then you have a 3rd degree.

What's the treatment? For all of them?

First and second degree (mobitz I) only require treatment if they are symptomatic.

Mobitz II and 3rd degree usually require temporary and/or permanent cardiac pacing.

This was fun, thanks for the drawings!

*the drawings of medcomic were shared on the group, you should check them out*

Review question:
Which of the following is not a feature of complete heart block on the ECG:
a) Constant RR interval
b) Constant PP interval
c) Constant PR interval
d) PP interval shorter than RR interval

Answer: C

How to study pharmacology

First, you need to get the concepts right. Speed read and get a big picture, then understand the little details.

I dived into minute things I didn’t understand right away.. Now that I look back, I think I should’ve been patient.
Anyway, lil doubts made great blog posts!
Example: Why is lidocaine preferred in patients with arrhythmias following myocardial infarction?

It’ll take time to get a hang of the names of various drugs.. If mnemonics work for you, you should try making em! Try to put mechanism in the mnemonic to make it simpler (That’s what I do!)
Here are some recent examples of how I make my pharmacology mnemonics -
Antifungal drugs with mechanisms
Antiparkinsonism drugs with mechanisms

There are certain drugs which are unique and that is why remembering mechanism of action or their pharmacological property becomes very difficult :/
I talk about how to remember them in this post --> http://medicowesome.blogspot.ae/2014/06/pharmacology-study-tip.html

I requested my study group awesomites to contribute their tips so that I can share them. Here are the suggestions, tips, tricks, life hacks they told us! :D

One awesome way is to make a self constructed table. Side by side drugs.. Uses. Side effects and specific points. Helps a lot.
- Great tip by Sakkan.

I had small classification charts put up all over my cupboard and wall! I Would revise them at night....Since I found classifications a bit volatile.
- The repetitive memorization trick was submitted by Priyanka. (I made flash cards for the same!)

One useful tip is whenever you see a sachet of drug.. Just read the contents and dosages.
- Awesome tip by Sakkan. (Wish I did that earlier!)

And try explaining uncles and aunties taking them what's going on :D
- I like how Sakkan said, "Try" explaining. (She says she gets a lot off oooo, aaa and even a couple of blank faces too!)

I always discussed pharmacology with my friends, and mostly, taught juniors. You get good karma + revision.
- Manisha (Good karma always helps!)

It is very volatile but this subject manages appear everywhere.. All subjects. Everywhere there are therapeutic drugs mentioned. Makes it really difficult to grab the essence if you don't do pharmacology.
- Sakkan's way of telling us take pharmacology seriously.

I drew small cartoons...Of concepts I found difficult to remember.
- Priyanka (Send us your cartoons soon, girl!)

Book recommendations by awesomites:

A very good book for pharmacology is Colored Atlas pharmacology. For retaining most of it. By thieme. A page of drug and a page of illustration. Very helpful.

And there's at a glance series. Exists for all subjects. Comprises cool diagrams, flowcharts and accompanied with a page of description. Pretty standard text in her very easy format.

Motsbys pharmacology memory note cards. If you like cartoons this little book is great. (It's very adorable.) I have to admit there are drawings which I dont really get. Thats why doing your own drawings also comes in handy :)

I wonder if all international students refer Katzung or whether they have local authors too.
I think Lippincott is the standard, internationally.
Lippincott is simple to understand- standard and interesting book to read.
A book very commonly referred to in India is KD Tripathi.
We have Farrukh Jabbar, here, in Pakistan.

That's all!

I'll keep updating the post, adding new tips and tricks, till then, stay awesome!

-IkaN

Study group discussion: Types of hypersensitivity reactions

*We were discussing lepra reactions when we diverted to hypersensitivity reactions the other day*

I can't remember the types.

Here's a life saver for your soul -  http://medicowesome.blogspot.ae/2012/03/hypersensitivity-types-mnemonic.html

Apparently there is type 5 and type 6 hypersensitivity reactions too.

5? What's type 6? Oh my god.

I had received a long fan mail on it a few days back:
We had a test about 4 days ago on hypersensitivity reaction type 5 and a lot of people left it blank because they thought it was a typo. Well, I later found out that it is the same as type 2 non cytotoxic (In fact, there is a type 6. Can you believe it? ). In situations like this, I always imagine there is a bored researcher sitting in a corner of his office, maybe eating a donut and taking a sip of milk from a beaker or conical flask, who thinks the best pass time activity is to screw around with the heads of medical students. So he gets his iPad, types a whole new ( and sometimes unnecessary) classification, sends it to a journal thus forcing medical students to add one more thing to that cramped up space called the head.

Hahahahha. The fanmail is hilarious. Made my day! :D

Myasthenia gravis? Which type of hypersensitivity reaction?

Myasthenia is type 2. So is Grave's.

Nope. It's Type 5.

Why?

Type 5 is an extension of 2.

It is because of it's blocking antibody, right? Or because it doesn't incite any inflammation?
In that case what would Graves be that antibody is stimulating?

Graves and gravis are caused due to effect of cellular functions. Graves - Increase in cellular functions. Gravis decrease in cellular functions.

"Instead of binding to cell surface components, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

Some clinical examples:

Graves' disease
Myasthenia gravis

The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically segregated into their own subcategory of Type 2."
- Source: Wikipedia

So type 5 includes autoimmunity, right?

Yes.

I didn't know they had classified it under autoimmunity now. Got it!

Type 6 is Antibody Dependent Cell Mediated Cytotoxicity.. The NK cell stuff.

They kill viruses laden cells and tumors.

Basically, any antibody that causes a effect besides inflammation due to binding to cell receptors is type 5.

Immunology comics on ADCC :D http://immense-immunology-insight.blogspot.ae/2013/10/functions-of-antibodies-simplified.html

Okay, review questions!
Name type of hypersensitivity!

Poison ivy reaction after 48 hours in a camping trip.

Type 4.

Correct!

A person who was given horse serum for something.

Type 3. Type 1 if he presents early!

Good job!

Person underwent a screening test for tuberculosis.
Type 4.

Excellent!

Person develops hemolysis after receiving penicillin.

Type 2.

Oh kid gets a bee sting.

Type 1.

Person with leprosy develops new lesions after starting drug therapy.

Type 3.

Awesome!

Hypersensitivity pneumonitis?

It is both type 3 as well as type 4.

Inhibitors of electron transport chain mnemonic

Inhibitors of electron transport chain mnemonic

Submissions: Vancomycin emotified

This was submitted to us by Priyanka Parekh. Thanks, girl!

Study group discussion: Mechanism of atropine induced hyperthermia

Even atropine high dose causes hyperthermia. But I don't know, the mechanism to it.

Atropine is because it inhibits sweating.

Children are especially susceptible.

Oh.

Study group discussion: Pharmacological management of diabetes

Review question time B)

Name the oral anti-diabetic drugs which increase release of insulin?

Sulphonyl urea.

One more!

Meglitinides such as repaglinide and nateglinide are prandial insulin releasers that stimulate rapid insulin secretion.

So which oral diabetic drugs will you give in a thin person and a overweight one? And why?

Overweight - Metformin
Thin - Sulphonylurea

Metformin decreases gluconeogenesis.

Sulfonylurea have weight gain as a side effect. Metformin have anorexia and weight loss as a side effect.

Which of the oral drugs class is cardiotoxic? Because of which many have been with drawn from the market.

Rosaglitazone.

Correct!

Name the sulfonylureas you know.

Chlorpropamide
Tolbutamide
Glipizide
Glimipiride
Gliclazide
Glyburide

Which of these is most likely to cause hypoglycemia?

All of them?

They all do. Right.. But one of them is most likely to do so.

Glibenclamide. It is the most potent.

Nice to meet glibenclamide :P

Which type of insulin do you give in ketoacidosis?

Intravenous.

Not which route, which type?

Regular.

Correct.

The lente rapid acting type is given.

Which is given in pregnancy?

Regular insulin? The same?

Correct.

Which of these oral drugs have nausea as the main side effect?

Nausea - Umm the alpha glycosidase inhibitor?

They cause hepatitis and flatulence.  So they are generally not preferred so much is what I read.

Nope. It's incretin mimetics. 40-50% patients taking incretin mimetics have nausea

Oh. I didn't know that.

An easy question - Which oral hypoglycemic drug causes lactic acidosis?

Metformin

Correct!

Which drug will you not use in renal failure? Why?

Metformin not used in renal. Same reason.

A patient has an attack of hypoglycemia while on a oral diabetic drug..He eats a spoonful of sugar. But even then he collapses and worsens. What went wrong?

Sugar needs to be metabolized @_@
^Random guesses!

Haha. No.

Must have taken complex carbohydrate. Need to use simpler ones like candy and all.

Yup. Sugar contains sucrose.

Hey I said the same thing.. Needs to be metabolized! T_T
I didn't use complex words :P

Haha! Not a convincing enough answer. But you on the right path.

Awww.
Examiner is strict!

It's okay. One point to R!

Hahaha.

Yay!

The sugar he ain't couldn't be broken down to simple sugars. Why?

He used an alpha glucosidase inhibitor! Acarbose!

Oooo that's interesting.

Correct.

Bang on!

Yaay!

He had to take glucose. Since he took sucrose (table sugar) it didn't help him.

Oh I lost the point now! :O
Nice question!

Haha we're equal now, R :P

Acarbose stops conversion to monosaccharides! So if he is on acarbose and takes a complex carbohydrate for increasing glucose levels, he won't be able to break it. Acarbose is a glucosidase that acts upon 1, 4 - alpha bonds which breaks down starch and disaccharides to glucose.
Sucrose is a disaccharide (table sugar) so yeah.

Easy question - what is the effect of insulin on potassium?

Hypokalemia.

Why is it clinically relevant in a patient with diabetic keto acidosis?

Need potassium supplementation along with insulin. Otherwise hypokalemia occurs. Causing cardiac and other emergency conditions.

Causes insulin causes the uptake of potassium by cells. Therefore, in hyperkalemia, the main line of management is giving insulin along with glucose.

Correct!

Why isn't bicarbonate preferred in patients with DKA?

Good question. I wonder about that answer too.

Tell us?

It causes cerebral edema.

Oh. If given in large doses?

Nope. Not dose related. Only in children though.

Can you explain?

Needed a research paper to back me up -

Adverse effects of bicarbonate therapy in DKA: In essence, possible mechanisms include initial cerebral vasoconstriction and reduced cerebral blood flow from acidosis and hypocapnia, cytotoxic edema, and cerebral injury, followed by cerebral hyperemia, reperfusion injury, and vasogenic edema, coupled with increased blood brain barrier permeability, during the rehydration phase of DKA. Several reports of sudden death following irreversible coma in children and young adults with DKA were published in the 1960s, including development of diabetes insipidus in some, with postmortem findings of CE and neuronal degeneration.

I'll send you the link.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224469/
Read: Clinical impact of bicarbonate therapy in DKA
The paper is huge, read that specific part.

Thanks!

Multiple system atrophy (Shy Drager syndrome) mnemonic

Multiple system atrophy with orthostatic hypotension is the current classification for a neurological disorder that was once called Shy-Drager syndrome. I'll be sharing a mnemonic for this syndrome today!

Imagine a guy who has urinary incontinence (That's why he is shy!). He puts (or parks) his dagger knife (drager) into his brain (Cerebellum, to be precise).

So the mnemonic goes:
SHy Parked his Drager into his Cerebellum.

S: System atrophy (Multiple system atrophy)
H: Hypotension
Y: Why is he shy? Urinary involvement (urgency/incontinence).
Also remember autonomic symptoms like constipation, sexual impotence, vision disturbances, difficulty breathing and swallowing, sleep disturbances, and decreased sweating.

Parked: Symptoms of Parkinson's disease such as slow movement, stiff muscles, and tremor.

Cerebellum: Cerebellar problems like coordination and speech.

That's all!
-IkaN

Study group discussion: Single Breath Count test in Guillain Barre syndrome

I was reading about Guillain Barre syndrome and came across single breath count test.

Does any one know what is it / how to perform it?

GBS can cause respiratory paralysis. So you do the breath count test to know the level of respiratory compromise. The exact mechanism.. I am not sure..But you ask the patient to take a breath and count as many numbers he can starting from one.

Is it done to measure inspiration or expiration? They say that inspiration is affected in GBS but I think counting is expiration.. So I am confused.

I haven't read much into it..Can't answer that with confidence.

I tried Googling. No satisfactory answers. Maybe someone else in the group knows!

SBC is measured by asking patients to take a deep breath and count as far as possible in their normal speaking voice without taking another breath. It's measure your fvc (forced volume capacity).
Normal values are 40 to 44.

If the patient can count to 10 on one breath they likely have a forced vital capacity of about 1000 ml, if they can count to 25 then the vital capacity can be estimated at about 2000 ml.

Normal fvc values are 3000 ml to 4000 ml.

FVC is sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume.

Meaning SBC value is not just for your inspiration or expiration. But the whole capacity of lung to perform either of the function.

Thank you so much!

Study group discussion: Lepra type 1 and type 2 reaction

Can somebody explain lepra reaction in leprosy?

When the bacteria is killed, it's toxins are released & these toxins exaggerate the lesions.. More painful more red etc..

Lepra reaction 1 and 2?

I know that Lepra reaction 1 is type 4 HR and Lepra reaction 2 is type 3 HR.

Yes, 1 is 4, 2 is 3. The sum should be 5, that was my mnemonic

Oh okay ! Thanks for clearing this!!

This is a good way of remembering! 4+1=5 & 2+3=5!

Mnemonic you have to sum up so that total comes out to be 5
So in Lepra 1 + 4 HR = 5
And Lepra 2 + 3 HR =5

It's similar to the Jarisch Herxheimer reaction in syphilis right?!

Yes, the antigens cause the reaction.

Sometimes it happens when the patient begins treatment and loses faith in the doctor because of the reaction!

Woah! Loses faith in doctor!

Yes, so you have to explain the patient well. Maybe inform about the possibility before hand.

Is ENL the same? Or the severe form of lepra reaction?
Type 2 is ENL.
What's the difference between type 2 and 1?

The 2 is a type 3 hypersensitivity. Meaning deposition of antigen-antibody complexes.

Type 4 reaction is a delayed hypersensitivity due to t- lymphocytes. Which is seen lepra reaction type 1.

Type 1 is mediated by Th1 cells and type 2 is mediated by Th2 cells

In lepra reaction type 1 - there is widespread new lesions all over the body, cause those  Ag-ab reactions get deposited everywhere.

In type 2, the existing lesions become more pronounced, more red.

There are other differences based on extent of nerve damage and blah blah..Which I don't remember!

Treatment?

Aspirin!

Treatment is aspirin, steroids and even an anti leprosy drug, I guess.

Chloroquine.

Thalidomide used to be ...Not used now, right? Thalidomide is completely discarded due to  phocomelia.

Oh no.. It is still used. But strictly avoided in pregnancy.

In which case?

Used in behcet disease, Multiple myeloma.

Thalidomide is used only for type 2 reaction, not type 1.

And which anti leprosy drug was it? Clofamizine?

Yes.

*the discussion went on types of hypersensitivity reactions, which will be continued in the next post!*

Study group discussion: G6PD deficiency and Myoglobinuria

If a person has presents with hemolysis after ingestion of flava beans and dapsone, when will you ask to get G6PD levels?

Study group discussion: Short course chemotherapy

What's short course chemotherapy?

Earlier Tb treatment was given for 1.5 to 2 years, Tb drugs have lots of side effects and patient adherence to such long treatment is not good either. So after various research WHO introduced short course chemotherapy treatment for Tb under the name of Dots which gives treatment for 6-8 months. Good patient adherence and compliance.

Study group discussion: Studying physiology

Could you share with me tips to study pre med subject? Like physiology perhaps?

Physiology is my major, I draw diagrams basically. Understanding the stimulus and response first, then learn the steps in the middle.

Yup, flow charts for physiology!

Physiology is easier when you start at the big picture then elaborate on each pathway.

And make lots of notes. Here's a link on that http://medicowesome.blogspot.ae/2014/12/how-to-make-concise-medical-notes.html

I used to draw a lot of flow charts in physiology..and Youtube, try subscribing to armando hasudungan or medcram..They have nice videos!

Study group discussion: Enzymes checked through RBCs

Why is LDH non specific for MI?

LDH is elevated in many other diseases too!!

There is a much more specific reason for it.

The LDH -2 isoform is present in RBC, any sort of slight hemolysis will increase it as well.

Oh that's why! Didn't have the faintest idea.

Great!! So LDH -2 Isoform is also the one for MI?

Nope it's LDH-1.

But no one gets the specific enzyme type. Too expensive I guess.

I guess electrophorectically you can't differentiate both. Maybe.

Which poisoning is checked through RBC?
Lead!
Basophilic strippling.

Yes, one more!

Cobalt.

Which other poison then?

OPP. Organophosphorous poisoning.

How?

You check the acetylcholinesterase levels in mature RBC.

Which vitamin levels can be checked through RBCs?
Hint: A vitamin that affects enzymes.

Transketolase, Vitamin B1 deficiency.

How does it affect the RBC the transketolase?

Umm it's just a level that can be checked through RBCs. I don't think they do it in clinical practice.

Study group discussion: Mitral stenosis auscultatory findings

What is the characteristic feature of mitral stenosis? In terms of murmur? And echo findings?

Opening snap.
Enlarged  left atria.
Mid diastolic murmur.
Left heart failure.. Left atrial enlargement.
Sam of mitral leaflet.

Also one more auscultatory finding.

Loud S1

Correct!

One more!

Pre systolic accentuation.

Yes!

Advanced stage S 1 goes soft.

What happens to this murmur in cases of atrial fibrillation?

Disappear.

What disappears?

Psa.

Correct. Now tell me why?

Because presystolic accentuation is due to contraction of the atria.

May be bcoz atria are in tremora!

Correct. The final phase of atrial contraction is absent in afib.

Which auscultatory finding indicates the severity of the disease?

Length of murmur. The longer, the more severe the disease.

Opening snap moves closer to s2 as the severity increases.

When I said OS S2 interval, the examiner wasn't convinced.
I checked..and then I read somewhere about the length of murmur. You see..As the level of stenosis increases..Blood takes a longer time to enter from atria to ventricles. Hence, the length of murmur.

Maybe it's not anymore. I read a research publication on it.. It's not OS A2 anymore. But let's not confuse exam going students :P

Haha. Could be the length of the murmur!
It could be our PG question :O

Here's the paper for those who are interested http://www.ncbi.nlm.nih.gov/pmc/articles/PMC487332/

Interesting.

Study group discussion: What is the kussmaul's sign? Is it seen in cardiac tamponade?

Kassmaul sign is never found in cardiac tamponade

i.e inspiratory rise in jvp is not present in cardiac tamponade

Kussmaul sign is present in cardiac tamponade. That's what was explained.

Bt kussmaul sign absent in cardiac tamponade.I will recheck my sources for the kussmaul sign
Okay i saw..increased jvp is present and it is common in cardiac tamponade

overall JVP rises bt inspiratory rise is nt dere
I had read somewhere

kussmaul's which is an inspiratory increase is also present..but it is more pathognomic sign of constrictive pericarditis. 
Hence, its not a sure sign of cardiac tamponade

We need harrison for this. Could you check?

On it B)

The table in Harrison says Kussmaul's sign is absent in tamponade. 

A positive Kussmaul sign (seebelow) is rare in cardiac tamponade. 
-Harrison

(***the table in harrison says it is absent, but the text says it is rare***)

So I guess we ain't wrong after all (:

Yaay!

during inspiration there is  RV enlargement to accommodate more blood and in cardiac tamponade it can’t dilate more due to the blood enveloping around it so it pushes the septum and dilates....dilatation causes decrease pressure of right atrium and hence decrease in JVP

I have read about the septum being pushed to the left

Ya septum is pushed to left

The abrupt x descent in jvp shows that  pressure is increased

Ya pushed to left

There are a couple of mcq's asked on the same topic many a times

In tamponade diastole filling affected so it is transmitted in jugular vein , and presence or absence of JVP is indicative of degree of tamponade severity
Pressure

Rapid 'Y' Decent Seen In Constrictive Pericarditis Is Called As Friedreich's sign

So the conclusion we can draw is, it might be present in cardiac tamponade but in rare cases. Kussmauls sign is more pathognomic of constrictive pericarditis and very non specific sign for cardiac tamponade.

Yes!