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!