Medicowesome

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!

Wednesday, February 18, 2015

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.

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.

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Friday, February 20, 2015

Thursday, February 19, 2015

Wednesday, February 18, 2015