Study group discussion: Mifepristone

Major use of mifepristone in obstetrics gynaecology is?
A) ectopic pregnancy
B) molar pregnancy
C) fibroid uterus
D) threatened abortion

A??

Yes, it's A. Please explain.

Mifepristone is abortifacient. It causes abortion by blocking progesterone.

But what if the ectopic site is not in connection with the uterine lumen. How will it be aborted?

I guess progesterone level in required to maintain the implantation.. A decrease in progesterone will cause it ectopic pregnancy to abort from that place.

That's right.

Mifepristone is also sometimes used to end pregnancies when more than 49 days have passed since the woman's last menstrual period; as an emergency contraceptive after unprotected sexual intercourse ('morning-after pill'); to treat tumors of the brain, endometriosis (growth of uterus tissue outside the uterus), or fibroids (noncancerous tumors in the uterus); or to induce labor (to help start the birth process in a pregnant woman).

Rh incompatibility USMLE Step 2 CK doubt

If the patient is sensitized and is making Rh antibody, there is no point giving, Rhogam right?

Nope. It is only for prevention to Rh sensitisation. It's not the treatment.

I see!

So once she is sensitized, nothing can be done?

Nope.

So, say there is a mother who had a kid with hemolytic disease last pregnancy. Will I be giving her Rhogam next pregnancy?

No.

You monitor the Rh antibody levels (by titres using indirect antiglobulin test).

If >1:4 woman is considered sensitized.

If >1:16 do the spectrometric test by using fetal cells taken by amniocentesis (To monitor bilirubin levels!)

Bilirubin low: Repeat amniocentesis in 2-3 weeks.

Bilirubin high: Measure hematocrit of baby using percutaneous umbilical blood sampling.

If the baby is affected (Fetal hematocrit low), only treatment is to give blood transfusion to the baby in utero (Intrauterine transfusion) And delivery at 37 weeks. Or even earlier.

Ooh. I get it all now <3

Study group discussion: Drugs and conditions that enhance Digoxin toxicity and the mechanism behind it

I read some cool things today on the group!

Why is there an increased risk of toxicity with digoxin in hypokalemia, hypercalcemia and hypomagnesemia?

Answers:

Potassium and digoxin compete for the binding site so if there will be less of potassium more of digoxin gets the chance to bind leading to toxicity. The NaKATPase is the binding site.

Digoxin toxicity is aggravated by increased calcium cause more calcium accumulates intracellulary. This leads to increased contraction.

Calcium intracellularly also increases the generation of ectopic foci within contractile cells.

Magnesium is used as treatment in the treatment of toxicity.

Magnesium is the cofactor for the Na-k pump. Less magnesium..less functioning of the pump. Hence aggaravated toxicity!

Here's an additional fun concept:

Drug of choice for supraventricular tachycardia?

Answer: Verapamil.

So if you have SVT in digoxin toxicity.. Would you give verapamil?

Answer: No.

Why not?

Don't know? Let me approach the explanation in a way which helps you think better - What is the mechanism of excretion for digoxin?

Answer: Renal excretion.

Digitoxin is via hepatic.

Here's a mnemonic on renal / liver excretion of Digoxin / Digitoxin: http://medicowesome.blogspot.ae/2014/03/how-to-remember-digoxin-is-renally.html

So when digoxin enters the tubular cell, it is excreted into the lumen via p-gp receptors. Those are the same receptors responsible for multidrug resistant. In cases of anti-cancer agents and anti-malarials. You see, verapamil is one of the rare drugs that block p-gp. Hence, decreasing digoxin excretion, thus, precipitating it's toxicity.

*pgp refers to P Glycoprotein receptors

Verapamil for the same reason is used to reverse resistance to anticancer and anti-malarials. Pretty cool info, ain't it?

I just fell in love with the whole drama digoxin plays in your body :D

So what drug is used in SVT induced by digoxin then?

Answer: Beta blocker.

That's all for today!

I'm trying to edit the stugy group discussions in a more reader friendly format. Hope you like them!

-IkaN

Study group discussion: Food analogies in Medicine

Who likes oreo cookies? I came to know about the Oreo Cookie sign today!
It's seen on a chest x ray (lateral view) when there is a pericardial effusion!
The anterior most layer (the chocolate part!) is the epicardial fat.
The mid layer (the cream part...yumm!) Is the fluid.
And the posterior layer (again, the  chocolate part) is the pericardial fat!

Coffee bean sign seen in?
Sigmoid volvulus! Also called omega sign!

Name some terms that starts with strawberry referring some conditions in our body:
Strawberry cervix - Trichomonas vaginalis infection
Strawberry tongue - Kawasaki disease, scarlet fever.
Strawberry scrotum - multiple sebaceous cysts (They're actually calcified epidermal cysts aka calcinosis cutis)
Strawberry haemangioma!

Speaking of food analogies.. Let's catch em all!

Oat cell carcinoma - Small cell carcinoma of the lung.

Cafe au lait spots - Neurofibromatosis.

We had a chart in pathology department - 'Pathology restaurant'

Apple birefringence - Amyloidosis!

Apple peel sign - Intestinal atresia.

Bread and butter appearance -  Fibrinous pericarditis.

Bread crumbs appearance in complicated cataract!

Honeycomb appearance of lungs.
Interstitial fibrosis.
Also pneumocystis, not sure.

Honey comb appearance of liver too.
Which condition is honey comb liver seen?
Seen in actinomycosis infection of liver. Burkholderia is a gram - bacteria. The honeycomb liver is seen in burkholderia infection....Which causes abcess...It's a radiologic sign!
Woah.

There's nutmeg liver - right heart failure!

Onion skin appearance - Ewings sarcoma!

Another Onion skin appearence seen in?
It's seen in Hyperplastic arteriolosclerosis!

Swiss cheese appearance - Metropathica hemorrhagica.

Also swiss cheese pattern in multiple serpingenous ventricular septal defects in VSD.

What appareance is in caseous necrosis, tuberculosis granuloma?

Cheese like?

Yeah. Here in spain is called: Queso fresco!

Cheesy necrosis in tuberculosis!

Dry cheese appearance in candida growth.

Cottage cheese appearance is found in which pathology?
Histological finding of caseous necrosis e.g in tuberculosis.

Anchovy sauce - Amoebic liver abscess!

Salt pepper appearance in?
EBV.

Salt and pepper skull - Hyperparathyroidism.

Rice water stools - cholera!! :)

Currant jelly sputum in?
Klebsiella pneumonia

Currant jelly stools in?
Intussuception!

So this is obvious - Maple syrup urine in?
Maple syrup urine disease!

Blue berry muffin rash - Congenital rubella.

Mulberry molars - Late congenital syphilis.

Olive shaped mass - Hypertrophic pyloric stenosis.

I know about Peau de orange!
Breast carcinoma.
And why is that?
Blockage of cutaneous lymphatics due to infiltration.
Blockage of lymphatic causes accumulation in the third space so it swells and the point where ligament is attached to the skin becomes pitted. Just like the skin of orange which has many small pits.

What about orange eyes?
Orange eyes are seen in Leptospirosis.

Apple core sign is found in which disease?
Colon cancer
Oesophageal carcinoma
Also a sign of IBD, I think.

What disease have Chicken drumsticks like fingers?
Psoriatic arthritis.

Napkin ring appearance also in colon cancer.

Which disease had grapefruit appearance?
Hyadatidiform mole.

There's chocolate cyst of ovary - endometriosis.

And chocolate agar!

Updated on 28th February, 2015:
A sandwich sign (sometimes known as a hamburger sign) refers to a mesenteric +/- para-aortic nodal mass giving an appearance of a hamburger. Confluent lymphadenopathy on both sides of the mesenteric vessels gives rise to an appearance described as the sandwich sign. The sign is specific for mesenteric lymphoma (typically non-Hodgkin’s)

Sandwich vertebra - Osteoporosis!

Updated on 1st March, 2015:
IkaN, did you get salt and pepper retinopathy on your foodie blog?

Yes, EBV!

Okay, I read that as a part of rubella. Could you explain what exactly happens tho?

Salt-and-pepper fundus with diffuse pigmentary lesions can be the signature of a previous systemic infection that had ocular involvement. Examples include inactive chorioretinal scars secondary to Lyme disease, tuberculosis, syphilis, congenital rubella, toxoplasmosis and bartonellosis.

There's a salt and pepper appearance in skin too! Systemic sclerosis and scleroderma have salt and pepper skin.

I found another salt and pepper term! In osteitis fibrosa cystica, punched out lesions produce a salt and pepper appearance on radiography. Multiple myeloma as well!

Updated on 3rd March, 2015:
Potato tumor: Carotid body tumor
Coconut appearance: Hyatid cyst

Study group discussion: Fatal familial insomnia, harmful effects of working at night and sleeping during the day

By the way, I saw a video on a very bad disease the other day - Fatal familial insomnia. Caused by prions just like Creutzfeldt Jacob disease.

I know about the disease.. I can't imagine not being able to sleep!

Has a late onset and the patient or rather I say victim does within a few weeks.
It's genetic.. Thalamus, sleep centre is damaged!
Therefore no sleep!
It's progressive, one falls into coma and finally death!
They basically sleep to die!

You can live without sleep for 5 days to a week, I suppose.

I had heard in physiology too.. That mice die if they are awakened before REM sleep chronically.

Even humans have reduced life span if they sleep for less than 4 hrs chronically.

Yes, I had heard someone who survived 2 weeks. He slept for only 4 hours per day

Why would anyone do that to themselves?

Workaholics.
Medical students!
Perfectionists.
Preparing for exams xD
We awesomites!

I sleep more than I should #vacations :P

That is also harmful.

How? =(
I get rebound insomnia though.

Read it in some article.

Ah.

6 to 7 hrs optimum.

Work hard. Sleep tighter.

Btw are there any harmful effects of working at night and sleeping during the day chronically?
I don't know and someone wanted to know!

Something related to messing up the circadian cycle? Because we have a diurnal surge of hormones?

Since all hormones are secreted at night and not sleeping at night disturbs the proper hormonal process... That's the reason people who don't sleep at night are also fat...

So they'd grow fat, that's it?

Anti aging 2, remember?
Serotonin mostly secreted from 11 p.m to 2 a.m and sleep during these is essential!

I found what I was looking for: Symptoms much like jet lag are common in people who work nights or who perform shift work. Because these people's work schedules are at odds with powerful sleep-regulating cues like sunlight, they often become uncontrollably drowsy during work, and they may suffer insomnia or other problems when they try to sleep. Shift workers have an increased risk of heart problems, digestive disturbances, and emotional and mental problems, all of which may be related to their sleeping problems. The number and severity of workplace accidents also tend to increase during the night shift. Major industrial accidents attributed partly to errors made by fatigued night-shift workers include the Exxon Valdez oil spill and the Three Mile Island and Chernobyl nuclear power plant accidents. One study also found that medical interns working on the night shift are twice as likely as others to misinterpret hospital test records, which could endanger their patients. It may be possible to reduce shift-related fatigue by using bright lights in the workplace, minimizing shift changes, and taking scheduled naps.

IkaN, goodjob!

Makes sense.

Is there any treatment for insomnia, if it's familial?

I don't think there is a treatment.. Since your thalamus is damaged, no pharmacotherapy can help you.
It's like in the thalamic pain syndrome, no amount of pain killers can help you!

So true! :(

Somogyi effect and dawn phenomenon in diabetes

So I read a lot of interesting things today and I'm formulating questions based on it.

A person took too much insulin at night and went to sleep. He checks his morning blood sugar levels and it's elevated. Why?

It's because stress hormones were released while he was asleep which caused the hyperglycemia. (This is called Somogyi effect!)

Now, a person took his appropriate dose of insulin at night and went to sleep. He checks his morning blood sugar levels and it's elevated. What happened this time?

There is a normal hormone surge at 7 am (Growth hormone, cortisol, glucagon and epinephrine) which caused the hyperglycaemia. This is called dawn phenomenon.

How will you differentiate Somogyi effect from dawn phenomenon? Why is this clinically relevant?

I guess the person with Somogyi effect will have certain signs and symptoms related to hypoglycemia. For instance, night terrors. Right?

People with hypoglycemia don't wake up but have nightmares.

The 3 am glucose levels to be precise. It is low in Somogyi effect and maybe normal or high in dawn phenomenon. You'll decrease NPH insulin at night in the former and increase the NPH insulin dose in the latter. 

NPH is an intermediate acting insulin. NPH insulin is usually taken at night. Duration of action 7- 14 hours!

In Somogyi, the excess insulin caused hyperglycemia. So you'll decrease the dose.
And similarly, in dawn phenomenon, the inadequate dosing caused the hyperglycaemia, so you'll increase NPH insulin.

If you're under the impression that is inadequate insulin and if you increase the dose of insulin, you can put the patient into a hypoglycemic coma! This is why, recognising Somogyi effect is very important.

I didn't get the management.. How is the adequacy of insulin assessed? If a patient comes with morning hyperglycemia, will you order 3 am glucose levels?

Nope. That would be hectic too. You wanna decrease the dose and see if the patient improves. If the patient doesn't, it means it wasn't the dreaded Somogyi effect and it was just the regular dawn phenomenon, so you can go ahead and increase the dose.

You keep tailoring the dose to suit the patient. 

Study group discussion: Some virology review questions

Hey everyone! I have a major virology exam coming up, would you like to go over some review questions with me? :)

Yes!!!

Great! I'll start:

Yaay!

Heterophile antibodies are positive in which viral infection?

These are multiple choice questions, shall I write the choices?

No, write them only when we can't guess it.

Ok :)

EBV?

Yes!

Which test is positive and is used to diagnose when there is an EBV infection?

Infectious mononucleosis.. Presence of human anti sheep antibodies, I think.

Yes! The test has a specific name though, anyone know it?

Umm.. Monospot test?

Coombs test ??

Neither of those

Would you like the choices?

Okay

Paul-Bunnel Test
Coombs Test
Indirect IFA
Western Blot
ELISA

Paul Bunnell! I forgot that.. Thanks!
Ok, ready for a new question?

Yes!

Which test is used to determine the specific genotype of HPV?
Another question would be, what is the first test you used to check for the existence of an HPV infection?

First test is Pap smear. Correct!

We'll need choices for the genotype - I'm guessing PCR though.

Ok here are the choices:
Consensus PCR
Line Probe Assay
Western Blot
Pap Smear
Latex aglutination

Consensus PCR?

No, I initially thought that too.

I'd say the line probe.

It is LiPA!

Why is that?

It uses the reverse hybridization to id specific  hpv genotypes by detection of specific sequences in the l1 region of the HPV genome.

It is more specific than the PCR

I see.

While we're on the topic of HPV, what are the high risk genotypes? And the most common low risk genotypes?

High risk: 16, 18
Low risk: 4, 6, 11

16 and 18 is usually used in the vaccine as well!

This changes a lot from place to place though, my medical faculty is working on developing a vaccine specially for this area/country

Oh that's great.. I didn't know that thanks.

:) no problem!

You guys want some more questions?

Yes

What is the main cause of non-bacterial gastroenteritis epidemics?

Rotavirus

That is one the choices here, but it's actually not that

Ooh. It's the main cause in India!

Choices?

Rotavirus
Norovirus
Adenovirus
Enterovirus
Astrovirus

Rotavirus usually infects infants and younger children, if I'm not mistaken.

Yup. So it's something else in adults?

Adults aren't really effected, the one we're looking for can infect people from different ages.

It's actually Norovirus!

It is the leading cause of viral gastroenteritis in the world!

Never heard of it :O
Is it the same as Norwalk virus?

Yes! Norwalk virus is a species of this genus. It's responsible for almost 90% of viral gastroenteritis epidemics globally!

Woah. That's a lot.

Norovirus happens in outbreaks, and stays infectious for a long time on surfaces yes?

Yes, exactly.

It's a calcivirus! http://medicowesome.blogspot.in/2014/04/how-i-remember-that-norwalk-virus-is.html

Family : Calcivirus, Genus: Norovirus :)

I'm going to have to leave soon, would you like 1 or 2 more questions?

Yes!

Which one of the viruses listed below, has a non-segmented genome?

Orthomyxovirus
Reovirus
Coronavirus
Arenavirus
Bunyavirus

Coronavirus?

Correct!

Review question: Does anyone know the clinical significance of the segmented genome?

A segmented genome has evolutionary advantages! Like, reassortment!

Allows reassortment and thus new viral strains in mixing vessels. Eg avian influenza.

What is the cause of Roseola?

Human herpes virus 6 or 7

Correct!

Brilliante!

One last question before I leave for now? :)

Yep yep yep

What is the most common cause of bronchiolitis in newborns?

Oh oh I know this.

RSV

Respiratory synctitial virus.

Correct :)

That was good, thanks!

I love random review question sessions!

Do it more often!

I have to go now, my friends are coming over to study! This was great, talk to you soon!

I have hundreds of review questions for my exam! Great! Looking forward to it.

This review question session was held by Fidan :) Thanks!

Study tips: Anxiety for test day

This is my first time talking to anyone I follow on anywhere... Be it twitter or tumblr. I am not very involved in social media, but I guess I am a bystander.

I am messaging you because I am in a bit of a dilemma. I am writing my USMLE step 1 exam in 5 days. I have been studying for it, believe it or not, for 2 years.

In this time, I have been home, my parents looking after me after I had gone to a med school on the island. I suffer from text anxiety... So like in the middle of the exam my brain just gives up, I feel at loss of hope. I just get this overwhelming feeling of failure.

I have bought the exam twice now and my date is scheduled for the last day possible. My parents are just fed up and they want me to get moving with my life. I have inconveninced them.

I have written all the NBMEs and I have never got a score above 300. I study so hard, but I hate to memorize if that makes sense. I have watched all the Kaplan videos, all the DIT videos and I have completed both Q banks. I know everything, but when it comes to route memorization... I can't do it for some reason, because I have this fear of it even is going to stick. I don't know what to do and I hoped some wise words from you might help me. You have some awesome things to say and they helped me lurch back up on a low day. I am literally trying to fly the coop right now.

Hope I am not intruding with my story.

- Email from an awesomite

Hey!

I'm glad you chose to speak to me.

The USMLE step 1 exam is scary. And it gets scarier as it gets closer. I had scheduled it on the last day too! My mum needed to go abroad and I had inconvenienced her. I never scored above 300 either in my NBME. But I got a good score on my step.

I'm telling you this to assure you that this is normal. That many have gone through the feelings you're going through and have made it before you. That you're not alone. That there is always hope.

You made it through various exams as you got here. Let's do this and get done with it. You have studied and you can trust yourself in midst of self doubt. You can do this.

You shouldn't be afraid of consequences. You've given your best shot. You have worked hard. Be confident that it'll work out for you in the best possible way.

Now this is a personal belief - I believe that not all five fingers are the same. Everyone is unique. That you have your own limitations and strengths. So some will score better than you, some won't. Accept it.

Once you have done your preparations well and that there is not one more thing you could've done, you must not worry about the results. Everything happens for the best. There's a good reason behind why things don't work out the way we want to - we don't see it right now but it doesn't mean it's not there. So I'm content with the results even before they come out.

I also believe that scores don't matter. That you can do wonderful things with your life without the scores. Yes, a good score will help you feel good about yourself and open doors - but a fear of a bad score shouldn't fill you with despair. The little anxiety you get should help you work hard, not come in your way.

I understand your memorization dilemma. Remembering things comes to us with repetition whether we like it or not.

There's not much you can do 5 days before the exam. But if there are certain high yield facts that you know you have not memorized - You can store facts in your short term memory and then forget them forever. We are capable of it. So you can't memorize everything, but please do what you can!

On the exam day: Focus on the question. Don't let your mind wander - go into past disappointments or future failures. Stay there. Read the question. What's the best answer to this question? Hmm.. This is an interesting one. What could the answer to this be? What are they trying to tell me in this question? Oh I don't know about this - will read about it later. The hints they're giving me are awesome. Ooh. This is a tricky one! I likey! I love medicine and it's enough. I'm living my passion. I'm lucky to be here. And that positivity, I tell you, will pull you through and give you hope.

I'm glad the things I said helped you. I hope this does too.

You're not intruding, be free to message me whenever you like (:

I understand that you might not get the time to reply after reading this - so I'll hear from you after the step. All the very best to you. I'll pray that you do well.

Love,
IkaN

Study group discussion: Newer vaccines

Can anyone explain what newer vaccines mean? And which vaccines are included in this?

I think HPV is a newer vaccine.
The flu, hepatitis, rotavirus, pneumococcal & meningococcal are newer vaccines too... But this is in general stuff.
If you're looking for a definition, I don't know about that :/

Oh wait - I found a good link to newer vaccines.

These are 4 new vaccines added to the universal immunization programme (UIP) in India.
They are - Rotavirus, JE, injectable polio and rubella.

And here's more to it - If you're studying PSM in India :P

Vaccines against rotavirus, rubella and polio (injectable) will help the country meet its Millennium Development Goals 4 targets that include reducing child mortality by two-thirds by 2015, besides meeting meet global polio eradication targets. An adult vaccine against Japanese encephalitis will also be introduced in districts with high levels of the disease.

Okey. I was not sure if they were newly added or newly developed, that's why asked.

I think newly added - they had been developed long before, I suppose.

Yap same in our settings..They added rubella. And HPV for young females (Tanzania)

(India) What is the program called in your country, like is it UIP there too?

(Tanzania) Yap we use EPI.. Extended programme for immunization.

(India) We have that here too.. There's national, extended and universal.

(India) EPI was for six vaccine preventable diseases... Then it was updated to UIP with vaccination of mother with TT and vaccine spectrum for child was also extended. The one we use now is infact the UIP.

Nice. I didn't know the difference.

P.S. Thanks IkaN!

They give tetanus toxoid to preg mothers!?

Yep.

At first visit and I think two months later.

It's actually a viva question - When does immunization of the baby begin? The answer is in utero because tetanus given to the mum helps the baby before it's born.

Study group discussion: Why are they called false localizing signs?

This was discussed on our study group. I tried to explain it :D

Can anyone explain why bilateral grasp reflex and bilateral babinski sign are false localizing signs?

There are certain signs which makes you think lesion is at that level so you localize it there but the lesion may be at a different level. So you localized it falsely, just because of that sign. 

Study group discussion: Removal of antigens from RBC's

Did anybody know that we can remove A and B antigen? :O

From what kind of RBCs?

Didn't know!

Yes, I read a research while back. The idea was simple, the O group has no antigen naturally, so they thought about removing A and B antigen too.. They first used coffee beans to remove it but it required acidic pH that resulted in hemolysis, finally they found the glycosades in bettle to remove A and B..

Nice.

http://www.nature.com/nbt/journal/v25/n4/full/nbt1298.html
Link to a research using bacteria to remove ABO group.. :)

Study group discussion: Blood group doubts

Can a person with blood group
AB -ve be given A -ve and B -ve?

Yes.

AB blood group people are universal acceptors. Of course, you can give.

The problem of Rh negative is important when it is a woman. You can't give a Rh positive blood to an Rh negative female.

Is it because of any future pregnancies or something else?

The Rh negative woman will develop antibodies against Rh positive blood groups.

In successive pregnancy there's risk of erythroblastosis fetalis.

But isn't it also bad to give Rh + blood to anyone who is Rh -? I've heard you can't give positive blood to a negative male too.. Because of the tranfusion reaction following it na?

The important difference here is unlike the AB blood groups..
A patient who is of B blood group..He is missing the a antigen on the cell. Therefore, he has the a antibody in the plasma. But if the patient is Rh negative..He won't have the corresponding antibody.

And if that person is given rh+ blood won't their body produce anti D antibodies? Since D is an antigen?

A Rh negative person will only form antibodies when exposed to RBC which are Rh positive.

So even in males antibodies will be formed. And haemolysis and consequent reactions will be there?

Yes.

So it shouldn't be preferable to give Rh + blood to anyone who is Rh - regardless of gender.

Theoretically.

Yes! Therefore, we ask for previous blood transfusions.

But in cases of emergency. You first go for O negative blood. If not available.. Even of positive can be used.

So if we would have to do a list
1. O Rh negative
2. O Rh positive

But especially in cases of women.. You have to be super cautious not to use a positive blood group if she is a negative.

You have a patient with A rh- blood who is in need of urgent transfusion. And you have two possible donors: An O Rh -  person and a A Rh + person. Which one do you choose?

O negative.

You can't give positive to a negative person!

Yeah since its a universal donor. And the Rh is same.

But O negative blood is reserved for emergencies..So it depends on the availability. If you manage to get hole of the same group..like A+ for an A+ That one is preferred

You preserve O - cause in emergencies there is hardly any time for blood group testing

Fair enough.

Treat positive as an antigen. You don't wanna create unnecessary antibodies in anyone because it increases the risk of organ rejection in the future. So regardless of the sex, you wanna properly match the blood.

Also future blood transfusions can be an issue.. Due to undue antibodies.

If you have no choice which antigen is worse the Rh, or the blood group?

The blood group.

They will cause an immediate reaction which is fatal.

Okay thanks! :)

As I said antibodies to Rh are not preformed.. They take time to form.

Oh I wasn't aware of that distinction. Thanks again.

Got a question. Would the anti A and anti B in O group prove antigenic to the patient? Of course, if he is either B or A respectively or AB

You mean to ask If the antibodies against A and B of O donor, will effect A B and AB recipient?

Yes, exactly.

No, I guess..

But why?

I think they are not in a significant quantity.

Because they are not yet exposed to A and B antigen when they were in donor.

In contrast, if mismatch occurs, the patient's body will produce numerous antibodies against the donor blood.

If I were to guess, I'd say once they leave their own system (the donor) they lose ability to mature into active antibodies.

They are not really viable ones the blood is collected from the donor. However we still have minor cross matching for that.

We had a discussion on that before!

Here it is:
O negative blood group  http://medicowesome.blogspot.com/2015/02/study-group-discussion-o-negative-blood.html

Oh.

The discussion is good. Thanks!

Study group experience #11

Here's everything we learnt (50 posts pending though)

Multiple myeloma and tumor lysis syndrome (USMLE oriented case)

ACE inhibitors 

Calcium channel blockers 

Antihypertensives - Arteriolar, venous and arteriovenodilators

Teratogenic effects of warfarin

Induction of enzymes by barbiturates 
Fluoroquinolones

Tetracyclines

Sulfonamides, Trimethoprim Sulfamethoxazole and other sulfa drugs 

Anti-tubercular drugs 

Anti-viral drugs used in herpes 

JVP in pulmonary hypertension and tricuspid regurgitation 

Extra books for USMLE 

Physiology books 

Embryology and gestational trophoblastic disease 

Normal movements in brain dead patients

Preganglionic and postganglionic fibers 

Vitamin B12 deficiency

I don't have a lot to say this week. I hope you're having fun reading the discussions!

-IkaN

Study group discussion: Calcium channel blockers

Which calcium channel blockers are not given in CHF?

Verapamil

Diltiazem

Correct. And why?

Decrease contractility.

Correct. They are negative dromotropic and negative ionotropic.

So in which conditions do you give verapamil and diltiazim?

Hypertension?

It's not hypertension. For hypertension you use dipines.

CCB are class 4 antiarrhythmics. So they are used in arrhythmias of atrial origin.

Remember.. The dipines act predominantly on vessels.. Hence they are preferred in hypertension.

Verapamil and diltiazem on the other hand act equally on heart as well as vessels.

Unstable angina?

They are used in unstable angina correct!

Which type of calcium channels do CCB act?

L type

First choice drug in hypertensive crisis?

Na nitropruside

Correct Priyanka

Now tell me why?

Marked fall in BP in a few mins.

There is one more reason.

Equal arterial as well as venous dilator!

Brilliant!

Study group discussion: Antihypertensives - Arteriolar, venous and arteriovenodilators

Tell me the drugs which are:
a. Specific venodilators
b. Arteriodilators
c. Arteriovenodilators

Arteriolar- hydralazine and minoxidil.

Correct!

Venodilators - GTN?

Actually, that is a googly question. There are no specific venodilators. Nitrates dilate the veins more.. But they dilate arteries too.

Cool.

What about arteriovenous dilators?
There are three classes to them!

Na nitroprusside.

Correct! Sodium nitroprusside it is.

Plasma kinins.

And by using what you make the kinins available to act on your blood vessels? Cause normally they are degraded.

ACEIs

Bingo!

Which receptors are responsible for vasoconstriction?

The autonomic nervous system ones! The alpha 1 blockers are the third class.

Last question. Nitrates act on veins more than arteries. Tell me which drugs act on arteries more than veins?

The calcium channel blockers, of course.

Study group discussion: Induction of enzymes by barbiturates

Why do barbiturates lead to hypertrophy of smooth ER and why do we need to increase the dose?

Barbiturates are CYP450 oxidase inducers. This enzyme is produced by smooth ER.. So there will be hypertrophy.

Ok agreed. But how the person becomes tolerant to the drug?

It is because the hypertrophied smooth ER metabolises the drug more causing adaptation.

Study group discussion: Teratogenic effects of warfarin

Random review questions! 

A baby is found to have stippled epiphysis, microcephaly and optic atrophy. Which drug was the mother exposed to during pregnancy which resulted in the birth defect?

Alcohol?

Alcohol will cause microcephaly, not the other two findings.

Steroids in the first trimester?

Umm no. Steroids cause cleft palate and cataract.

Phenytoin?

Again, phenytoin will cause microcephaly, not the other two defects.

Hint: The woman said she had developed joint pain when she was young. She also had skin rash and breathlessness on activity. That's why, the doctor prescribed her monthly injections.

So she had acute rheumatic fever?

Yes, she did!

So rheumatic fever patients become breathless during pregnancy. Why?

Penicillin?

It's not penicillin that caused the defect. It was some other drug!

Tetracycline?

Nope. Tetracyclines cause discoloration of teeth. She wasn't on antibiotics.

She also said that she consumed oral tablets during pregnancy.

Heparin or warfarin!

Warfarin correct! Heparin ain't teratogenic.

She was on a blood thinner, because of mitral stenosis due to RHD, probably wasn't informed that her medication should be changed during pregnancy.

Oh and can any guess why the neonate developed the Optic atrophy?

Warfarin makes the fetus susceptible to intraventricular hemorrhage. That's why the optic atrophy!

It's been suggested that warfarin causes repeated intracerebral hemorrhages which causes Optic atrophy, microcephaly and mental retardation.

Here's another cool fact - warfarin in early trimesters cause nasal hypoplasia and stippled epiphyses, and if taken in later trimesters cause the CNS defects.

This is so cool.

The mechanism of the first trimester defects are - Warfarin blocks protein C and S.. Which is essential in bone formation of the baby. Hence, you get nasal hypoplasia and epiphysial problems.

(UPDATE: This syndrome caused by warfarin is NOT called contradi syndrome. It's similar to Conradi-Hünermann syndrome, a rare genetic disorder characterized by skeletal malformations, skin abnormalities, cataracts and short stature.)

I got a doubt - What monthly injections was the lady taking?

Well, she was taking rheumatic fever prophylaxis. Benzathine penicillin intramuscular injections to be precise!

Study group discussion: Preganglionic and postganglionic fibers

What is importance of preganglionic and postganglionic fibers in our CNS?

The length of them? It differs from the parasympathetic and sympathtic!

Neurotransmitters of postganglionic varies by parasympathetic and sympathetic.

Parasympathetic: Cholinergic such as acetylcholine.
Sympathetic: Adrenergic such as epinephrine and norepinephrine.

Yes, and preganglionic neurotransmitters of both sympathetic and parasympathetic is Acetylcholine.

Study group discussion: Vitamin B12 deficiency

Causes for vitamin b12 deficiency?

Tapeworm
Inflammatory bowel disease
Methotrexate
Vegetarian diet

What about an autoimmune diseases causing b12 deficiency?

Pernicious anemia! Deficiency of intrinsic factor!

Which chronic infection causes vitamin B12 deficiency?

H pylori?

Tell me how!

It cause gastritis?

Yes. It causes atrophic gastritis.

What is triad for sub acute combined degeneration of spinal cord?

It has a classical triad:
Absent knee and ankle jerk - lmn
Extensor plantar -umn
Areflexia

It's called combined because a combination of various tracts ate involved.

Study group discussion: Normal movements in brain dead patients

Something from what I learnt today!

So here's the scenario:
Patient is reported brain dead, the relative walks in and is shocked to see that the patient's toe is moving. So he goes back and gets mad at doctor. What went wrong here?

These movements are normal! A person with brain death can have spontaneous movements, these originate from peripheral nerves or spinal cord which are intact!

On the other hand the brain stem and cerebral reflexes like pupillary, oculocephalic, oculovestibular, corneal, gag etc will be absent.

Interesting!

Study group discussion: Embryology and gestational trophoblastic disease

I have a few questions on embryology!

At which stage does the embryo implant?

Isn't confabulations when you lie and believe it to be the truth

Blastocyst? 18-20 cell stage?

Yes!

When does the urine pregnancy test become positive? And why?

14 days?

Why 14 days?

HCG is secreted.. I don't know. The placenta starts forming?

The trophoblast invades the sinuses at day 12 so that's when beta HCG from the syncitiotrophoblast gets into the mother's blood in high amounts.

Okay! I didn't know this :D

*We had a confusion about when it gets in the blood vs when it comes in urine, so we Googled*

A urine home pregnancy test HPT usually becomes positive within a week or so after implantation, or around the time of your expected menstrual period. It becomes positive about 12-14 days days after ovulation and fertilization.

Implantation occurs at which day?

6 day!

So 6+7=13

That's when you'll get urine test positive!

Speaking of placenta, which Placental hormone is the cause of gestational diabetes?

HPL. Human placental lactogen.

Yes, HPL it is!

Which placental hormone correlates best with growth of placenta?

Human placental somatomammotropin.

If a patient is pregnant through IVF. Till when do you give progesterone and why?

8 weeks.

Cause it takes 8-12 wks for the placenta to completely take over the function of hormone production from ovaries.

Yes, placenta takes over progesterone production around 10 weeks!

Also serum HCG doubles up every 48 hours!

Yes, hCG doubles every 2 days

Clinical significance?

In Ectopic pregnancy, it fails to double.

Downs syndrome!

What if it's more?

In GTD, it increases.

Yep.

Snow storm apperance! It's seen in gestational trophoblastic disease on USG.

Yes, snow storm is in hydatidiform mole.

In my viva, I was asked how will you suspect GTD in a normal pregnancy, clinically?

Thyroid symptoms.
Excess vomiting.

Patient has no symptoms. She came in for a normal check up. Clinically, no tests.

Increased hCG.

You won't do hCG for everyone who comes in, right?

You will see grape like vesicles per vaginum. Excess vaginal bleeding.

No grapes visible. She is at 7 month gestation. Completely normal.

Think more basic, guys!

You are asking just signs, right?

I was asked how will you suspect hydatidiform mole CLINICALLY in a asymptomatic patient.

The uterus height does increase.
That's symphysio fundal height (SFH)

Correct!

And if you are lucky enough.. There is this boggy feeling to the uterus.

No palpable finding.. No fetal parts.
Yes!

Then you won't be able to asculate for a heart sound. That's what my examiner wanted to hear!

Study group discussion: Multiple myeloma and tumor lysis syndrome

Alright! Let's do review questions!

Patient has a high serum protein, normal albumin, rouleax formation on blood smear and monoclonal IgG spike. Urine analysis shows proteinuria. What do you think the patient has?

Multiple myeloma.

Correct!

What are the proteins on urinalysis called?

Bence jones proteins.

Patient develops bone pain. Why?

Lytic lesions!

Which factor causes the lesions?

Interleukin 2?
Umm. IL 2 causes proliferation of T cells.

It's IL 1 aka osteoclast activating factor

Oh.. OAF is right!

What is the characteristic appearance of plasma cell nucleus?

Cart wheel. Due to clumped chromatin.

Correct! Also a perinuclear halo!

What will you see on the xray skull in the patient?

Punched out lesions.

Will you do a bone scan to detect lytic lesions?

Nope.

Why no?

Ummm because the lesions will be visible right on X-ray so why use any more complex technique!

Not exactly but you're right!

Bone scan misses lytic lesions so you do a skeletal survey instead.

O woahhh!

Okay, so our patient now develops tingling numbness in the palm thumb, index and middle finger. What happened?

Hypocalcemia.. But in multiple myeloma hypercalcemia happens!

It's not related to calcium. That's why it's a trick question!

Seems like carpal tunnel due to some protein deposition!!??

On the right thinking process. Which protein?

Think, think, think! It's a basic pathology concept. Which protein will accumulate over time?

Amyloid!

Correct!

Patient developed amyloidosis due to light chains.

Patient now develops renal failure. Although there are a number of mechanisms for it which would be the two most likely cause of renal failure?

Amyloid
Hypercalcemia
And?

Amyloid isn't that common.

Why hypercalcemia will lead to renal failure?

Hint: Think more basic. What is going into the Kidneys?

Calcium :P

I gave you the labs of the patient in the question.

It's the proteins, guys! They'll block the tubules and cause RF.

Weren't we discussing the hypercalcemia leading to renal condition?

Oh that! Nephrocalcinosis.. Due to calcium!

Yeah that's why I was worried about sending calcium to kidney! :P

What will you do about the calcium? So that the patient won't go into renal failure? He has high calcium and is not responding to chemo. Calcium is 12 mg/dL

Fluids!

It won't bring the calcium levels down. Patient is still having calcium deposition in his kidneys!

We can use the bisphosphonates! Dronates?
Yes!

You'd give fluid and diuretics if he was having a hypercalcemic crisis

Yeah this is a chronic condition.

Why did our patient have rouleax formation on his blood smear?

Hyperviscosity?

Nope. That ain't the reason why the RBC's are sticking to each other!

ESR? That would lead to hyperviscosity syndrome.
Something to do with the changing shapes of RBC?

Nope.

Think more basic. What is in the blood of this patient?

Monoclonal antibodies!

Yes! Immunoglobulins coat the RBC and neutralize the ionic charge than normally repells em.

Nice!!

Is the rouleaux formation confined to these ig's only?...i mean what about any other ig?(if present, say)

Any immunoglobulins would cause rouleax formation! Usually it's IgG or IgA.

oes that mean rouleaux formation occurs whenever there are Ab's in blood?

I think only when they are present in excess such as in this state!!

Yes! In multiple myeloma, there are so many that it is effecting the RBC charge.

Ooh! Thanks guyz !

No but infections and inflammatory conditions also cause rouleax formation.. So I think it's reasonable to think that way!

Our patient now develops pneumococcal pneumonia. Why?

Although proteins are in excess they are not functional.

Exactly. They don't have clonality required to fight off infections!

This one has no thinking associated with it - what, if present in the patient, will be associated with a poor prognosis?

It's IL 6

Ohh!! So IL6 is associated with poor prognosis?

Yup. I donno why though. It's just a fact you should remember!

Patient is just diagnosed and is started on chemo, responding well and suddenly his creatinine levels start to spike. Calcium normal. No proteins in urine. What could be the cause?

Bence Jones protein not detected by dip stick?

Nope. No proteins in urine.

Tumour lysis.

Correct!

Wouldn't uric acid be detected in urine?

It would. Pathologist comes back to you and says he switched reports. Uric acid crystals were present in urine of your patient :P

How come creatinine is up? Creatinine would increase either due to excess muscle breakdown or renal failure!

That's because he went into renal failure due to urate nephrolithiasis. As in uric acid crystals caused obstructive nephropathy!

Which drug could've prevented this?

Allopurinol. Fluids.

Mechanism of action of Allopurinol.

Xanthine oxidase inhibitor.

What other ______ oxidase inhibitor do you know of?

Rasburicase.

Mechanism?

Urate oxidase inhibitor!

Chronic granulomatous disease - Catalase positive organisms mnemonic

CGD (chronic granulomatous disease)

Diagnosis: Negative Nitroblue tetrazolium reduction.

NADPH oxidase deficiency: Susceptible to Catalase+ organisms.

I had got this mnemonic on someone's (arghlblargh) tumblr but I can't seem to find it so I'll publish it here!

“The Recoiling Red Asp wasn’t Sorry towards the moaning Cat because it had Noheart.”

Recoiling  = E.coli
Red  = Serratia
Asp = Aspergillus
Sorry = S. Aureus
Moaning  = Pseudomonas
Cat = Catalase + organism
NoHeart = Nocardia

Study group discussion: Extra books for USMLE

Could someone suggest books to use for mle step 1? Everyday someone new tells me that the kaplan book is not good for a particular subject.

Haha

BRS + Kaplan for physiology
Road map to gross anatomy
Biochemistry Kaplan (Pretty good)
Goljan for pathology
Microbiology Kaplan (more than enough)
Pharmacology Kaplan
Behavioral Kaplan + BRS + a lot of resources online and it's never enough

What about the other subsections of anatomy?

Umm which subsections? Embryology and Histology isn't high yield.

Oh alright. Neuroanatomy?

That's a pain! There are these anki flashcards I found on neuro.. I'll send you guys the link when I'm home. Thanks!

Do all brain stem sections for step 1. Any image on neuro and you need to identify the tracts/structures!

Ah. Why don't you try clinical neuroanatomy made ridiculously simple? I have heard its a recommended book for USMLE Step 1.

Ridiculously simple series is good!

Neuroanatomy one is really short and nice.

I've read the neuroanatomy book too. It's good.

Related post:
Preparing for the USMLE Step 1 exam
I have no idea about USMLE Step 1
USMLE for Indian medical students

Study group discussion: Anti-viral drugs used in herpes

Name the DNA polymerase inhibitor antiviral drugs.
(Hint - Drugs used against herpes virus)

Acyclovir and related drugs too.

One more drug which is used in resistant cases of herpes.. It's foscarnet!

Which drug is used for herpes ophthalmicus?

The drug of choice for CMV retinitis - Ganciclovir.

Study group discussion: JVP in pulmonary hypertension and tricuspid regurgitation

One question...Giant "a" wave in JVP will be due to which of the two.. Pulmonary hypertension or tricuspid regurgitation?

I would go for pulmonary hypertension.. Because Tricuspid stenosis causes giant a waves whereas tricuspid regurgitation causes giant v waves. I'm not sure, correct me if I'm wrong. a wave is due to atrial contraction.

Ya that's what I think is right too... But I get to see different answer at different places. Ok... Pulmonary hypertension it is then!

What abnormal wave does the other cause then?

It's like all the blood is regurgitating into the atria when the ventricles are contracting.. So it'll cause a giant cv wave. The a wave should remain normal. I don't get why pulmonary hypertension should cause a giant A wave though.. I get that the back flow should hypertrophy the right atrium and right ventricle so maybe that's why!?

Study group discussion: Anti-tubercular drugs

Name the first line anti - tuberculosis drug which is a static drug?

Ethambutol.

Name the bactericidal drugs.

Bedaquiline.

Bedaquiline isn't approved in India yet! It's still undergoing trials, according to the TOI.

Woah.

HRZS.

Which of the HRZES drug has the best CNS penetration?

It's pyrazinamide.

Which of the drug doesn't penetrate the CNS?

It's the aminoglycoside.

Streptomycin!

Which of these drugs you don't prescribe in children? And why?

Ethambutol? Because kids can't tell you if they're going color blind

Correct.

Which of the drugs you don't give if the patient is receiving HIV drugs?

Rifampicin?

Right.

Instead of it which drug you give?

Rifabutin.

Why don't we give?

Rifampicin is a cytochrome enzyme inducer.

Hence, it will reduce the concentration of PI and NNRTI.

Which TB drug causes orange color tears? Can't recall!

Rifampicin.

Study group discussion: Sulfonamides, Trimethoprim Sulfamethoxazole and other sulfa drugs

One extra review question session for today!

Give one example of longest acting sulphonamides.

Sulfadoxine!

Which are the other drugs with a sulfa structure?

Diuretics - Loop, thiazide and also acetazolamide. Except ethacrynic acid.

So any more drugs?

Hint- one anti-leprosy, anti-hypertension, and another one anti-diabetic.

Dapsone.

Correct!

Umm Sulfonylureas.

The hint was in the name! Correct!

Which anti hypertensive though? :O

Diazoxide :)

Ahh!

Side effects of diazoxide?

Ahh..Steven Johnson syndrome?

I'm looking for the very unique side effect which helps in treating a tumor.

Diazoxide has an anti-insulin effect.. It's used in insulinomas.

Ooh.

And what's the unique side effect of Minoxidil?

Minoxidil was used as an antihypertensive, but it caused hair growth. So they used it topically for hair loss!

If the dose of sulfamethoxazole in cotrimoxazole is 100 mg. What is the dose of trimethoprim

It's always given in the ration of 1:5
One part trimethoprim to 5 parts sulfamethoxazole

Ohh so 20 mg trimethoprim

Yup.

What is fixed drug eruptions?

Every time you eat the drug..you get a specific skin reaction at the same place every single time.

Name the site of action of smx and tm. How do they produce the sequential blockade?

Folate synthase SMX and TMP DHFRase

Sulfo doesn't inhibit the enzyme..its not the main action

Prevents formation of dihydrofolate?  Folate synthase right?

No. It's an antimetabolite. Structure similar to PABA. It attaches itself in place of PABA ..hence the mechanism of action!

One last question. Name other drugs which inhibit dihydrofolate reductase ?

Methotrexate.

Hint-  anti- epileptic drugs and one anti malarial.

Oh yes. Anti malarial! Pyrimethamine!

Correct!

Is it phenytoin?

Yes!

That's why these drugs are not given in pregnancy!

I guessed because of the megaloblastic anemia side effect!

High chances of NTD due to folic acid deficiency.

Oh well IkaN..It's all inter related :)

Totally! Medicine <3

Nice session!

Study group discussion: Tetracyclines

Which are the broad spectrum antibiotics?

Chloramphenicol and tetracycline.

Which tetracycline causes cholestatic jaundice?

It's chlortetracycline.

Doxycycline is secreted in feces. So in which conditions it is preferred?

Renal comprise.

Exactly!

Which is the common side effect of all tetracyclines?

Photosensitivity :)

Which tetracycline is used in SIADH?

Demeclocycline is used in SIADH.

What happens when you give outdated tetracycline?

Fanconi's syndrome!

Study group discussion: Fluoroquinolones

Review questions please!

You are asking questions?

No, I was waiting from them! :)

Haha review questions then!

Which enzyme does fluoroquinolones inhibit in gram negative and gram positive bacteria?

DNA gyrase!

Umm specific types of it in both gram negative and gram positive bacteria.

Topoisomerase 2 in gram negative and topoisomerase 4 in gram positive.

What are the side effects of quinolones?

Tendon rupture, photo toxicity!

Can cause convulsion.. Because they are also GABA inhibitory.

Somnolence. You don't prescribe them to people who drive for the same reason.

QT prolongation.

Nausea, vomiting and taste disturbance.

Tendon rupture in elderly people taking steroids.

QT prolongation only in gemifloxacin, lomefloxacin, moxifloxacin and levofloxacin.

Why don't you give it in pregnant ladies and young children?

In children, it can cause some defects in bone/cartilage formation. So it'll cause bending of long bones and stuff.

Yup. It causes defect in collagen.. Articular rupture and tendonitis!

Okie moving on.. Name the respiratory fluoroquinolones.

There are four of them. They have been termed that because they can be given to patients suffering from COPD.

Gatifloxacin, gemifloxacin, levofloxacin, moxifloxacin.

Could you explain the concept of respiratory fluoroquinolones a lil bit more? It's a new concept to me.  sorry! Why can't you give the others to someone with COPD?

They are especially used for lower RTI and upper RTI.. Cause they inhibit anaerobic, gram positive, atypical as well as gram negative aerobes. The others do that too..but these are especially preferred for respiratory infections.

Study group experience #10

Tissues that are exclusively dependent on glucose for metabolism 

Vitamins (Antioxidants, Vitamin E and vitamins in egg) 

HNPCC (Lynch syndrome) and microsatellite instability 

Peutz Jegher's Syndrome 

Iron metabolism 

Management of Parkinson's disease (USMLE oriented case)

Gate control theory of pain 

QT prolongation 

Mechanism of pulsus paradoxus in severe acute bronchial asthma 

Sickle cell anemia

Heparin, warfarin and the anti-fibrinolytics

Aminoglycoside review questions and mnemonics 

Zidovudine 

Heparin induced thrombocytopenia and leech therapy 

Virchow's triad 

Mechanism of hypercoagulability in obesity and smoking 

Type 2 polyglandular syndrome 

Most common site of intraperitoneal abscess 

I love how when people are unable to answer questions, the person who asks gives hints, clues and mini questions to lead to the right answer. This creative thinking and understanding process is what I love most about the study group <3

How to join the study group

Study group discussion: Zidovudine

Review questions!

Full form of HAART?

Highly active anti retroviral therapy.

Which is more toxic.. Zidovudine or acyclovir? And why?

Zidovudine due to bone marrow suppression.

Yes! It causes BM suppression.

Actually, both of these drugs cause it..but zidovudine causes it at a much severe level.
Acyclovir and zidovudine have to be activated to their respective triphosphate. Zidovudine uses the host cell enzymes for this but acyclovir uses the viral enzyme FIRST and then the host cell enzyme. Hence in cases of zidovudine the toxicity is very high.

Wow what a concept!

The myelosuppression is so bad.. That you have to give blood transfusion and growth factors.

It effects the mitochondria of the cells too I guess.

AZT induces significant toxic effects in humans exposed to therapeutic doses...
Cytogenetic observations on H9-AZT cells showed an increase in chromosomal aberrations and nuclear fragmentation when compared with unexposed H9 cells...
The toxicities explored here suggest that the mechanisms of AZT induced cytotoxicity in bone marrow of the patients chronically exposed to the drug in vivo may involve both chromosomal and mitochondrial DNA damage.

Study group discussion: HNPCC (Lynch syndrome) and microsatellite instability

Just was mentioned in lecture: What is the cause of lynch syndrome (the specific cause)?

It's HNPCC. DNA mismatch repair affected.

Yes, a bit more specific! Which part of MMR?

I think it's micro satellite instability or MSH2.

Msh2 is one of them, correct!

MLH1 as well.

Mhmm. One more?

Donno any more T_T

Apparently MSH6 as well :)

Could you sum them all up? What is lynch syndrome..What are it's features?

Ovarian, Colon and Endometrial carcinoma are the features. You do the molecular talk!

Lynch syndrome (also known as HNPCC) increases the chance of colon cancer up to 80% along with increasing chances of other sorts of cancer.

It is caused by disruption of Mismatch Repair system due to mutations in 3 MMR factors : MSH2, MSH6, and MLH1

What about the microsatellite instability pathway? Which syndrome was that?

Oh I found out.. Microsatellite instability is found particularly in cells which are expressing mismatch repair defects. HNPCC is one of the of the most important syndromes where this happens. However its not an "exclusive feature" of MMR defects.

The microsatellite  instability is the evidence that the MMR isn't working properly and can't detect insertion-deletion loops that forms in the S phase. Googled and paraphrased.

Ah makes sense. Thanks!

Elaborate on the term microsatellite instability.

Umm it's kind of complex.. Usually you detect DNA by PCR, right?

Yup. You amplify the DNA!

So if while PCR, little microfragments of DNA split up which weren't there originally. They are called microsatellites. They were made during PCR. So if those are created, it means the fragment has microsatellite instability.

So these are abnormal?

They occur naturally.. But usually detected by MMR and dispatched if MMR doesn't work...
They will be present!

Yep!

Got it. Thanks!

Study group discussion: Peutz Jegher's Syndrome

What's Puetz jegher syndrome?

Hamartomatous polyp with pigmentation on lips.

Study link! http://medicowesome.blogspot.ae/2014/10/tumors-of-colon-and-of-polyposis.html

Another life problem solved! Haha thanks!

Lkb1 is involved in PJS. How?

Peutz Jegher's Syndrome mnemonic:
Remember the initial letters of the disease - PJS.
P: Pigmented oral mucosa
J: Jejunal polyps
S: STK 11 defect
Thank you  IkaN!

Oh nice. LKB1 kinase activity is lost due to somatic mutations. In Peutz Jegher's Syndrome, that is.

Study group discussion: Mechanism of pulsus paradoxus in severe acute bronchial asthma

Which one of the following does not cause pulsus paradoxus?

a. Severe aortic regurgitation
b. Cardiac tamponade
c. Constrictive pericarditis
d. Acute severe bronchial asthma

Study group discussion: Aminoglycoside adverse effects and mnemonics

1. Name the adverse effects of aminoglycosides.

Nephrotoxic
Ototoxic
Vestibulotoxic

And? (This one is most commonly forgotten)

Study group discussion: Iron metabolism

In which form is iron absorbed?

Fe2+
Ferrous!

In which form is it stored?

Ferritin!
Fe3+

Study link! http://medicowesome.blogspot.ae/2013/11/ferrous-vs-ferric-mnemonic.html

In which form does heme contain iron?
Ferrous

Remember..Heme is always in the ferrous form when free..And in the ferric form when bound. In heme..it is an exception.
Others ferritin, transferrin..it is always in ferric form

Ohh. Interesting!

Antidote for choice for acute iron overdose?

Desferoxamine?

Yup. Desferrioxamine is given IV.. It is for acute iron overload.

Which antidote is preferred for chronic iron overdose then?

Oral drug.. Deferiprone.
Desferoxamin SC.

Study group discussion: Sickle cell anemia

Name the three crisis of sickle cell anaemia.

Aplastic crisis
Vaso-occlusive crisis
Sequestration crisis

What causes aplastic crisis?
Parvovirus B19

*doubt discussion*
In sickle cell anemia what analgesic do we use? I've heard that morphine can cause vasoconstriction and that would make it worse, but I'm not sure that's true.

Yup, opiates are used.

One cause of death in sickle cell anemia is acute chest syndrome, if I give the patient morphine (that has a secondary coronary vasoconstrictor effect) that will kill the patient.

Correct.

Acute chest syndrome is due to occlusion of the pulmonary vessels.

The major issue hear is to given oxygen to the patient..Cause hypoxia aggravates the whole situation.

So I'm not supposed to worry about Myocardial Infarction?

Not that I've heard of.

Doesn't it cause CHF?

"The acute chest syndrome may mimic CHF however it is uncommon." Says the internet.

New drug for SCA. Read in Harrison. Azacytidine.

Mechanism of action of azacytidine?

Azacytidine increases HbF production and reduces anemia in sickle cell disease.

There's a drug which blocks gardos channel in RBC membrane. It's under trials too. It's the one I was talking about.

The mechanism is interesting because it prevents dehydration of the RBC.. That's the cause of sickling.

I like the sound of it - Gardos channel.

It's a potassium channel!

A greek god!

Me too.. It guards the RBC!

Gargoyle ..thats what my mind said.

Haha. They were guardians too!

Another interesting thing.. An anti fungal we use also blocks this channel in vitro!

Study group discussion: Electrolyte abnormalities that cause QT prolongation

Which electrolyte abnormalities lead to QT prolongation?