Monday, September 26, 2016

Biophysical profile mnemonic and step 2 CK notes

Hello!

Here's a mnemonic for biophysical profile: BAT HAM
Breathing
Amniotic fluid volume
Tone
Heart rate Acceleration
Movements

Here's an overview of interpretations from the BPP score.

BPP 10/10
BPP 8/10 (Normal AFV)
No fetal indication for intervention.
Repeat weekly.

BPP 6/10 (Normal AFV)
Equivocal. Repeat test within 24 hours.

BPP 4/10 (Normal AFV)
Fetal lungs mature (>37 weeks), deliver.
Fetal lungs immature, betamethasone, repeat test within 24 hours.

General rule: If oligohydramnios, consider delivery.

BPP 8/10 (Decreased AFV)
BPP 6/10 (Decreased AFV)
Assess clinical scenario, consider delivery depending on gestational age, risk of fetal, maternal death, etc.

BPP 4/10 (Decreased AFV)
If >32 weeks, deliver.
If <32 weeks, observe.

BPP 2/10
BPP 0/10
Deliver regardless of gestational age.

That's all!
I wrote this down from a number of resources, including uptodate
-IkaN

Study group discussion: Rh incompatibility and ABO incompatibility

Here is some food for thought.

Think about which of the following scenario is worse:
1- Mom is O- and baby is O+ first pregnancy
2- Mom is O- and baby is O+ second pregnancy
3- Mom is O+ and baby is O+ second pregnancy
4- Mom is O+ and baby is A+ second pregnancy
5- Mom is O- and baby is A+ second pregnancy
6- Mom is O+ and baby is O- first pregnancy

Answer is 2
Rh incompatibility in second pregnancy. In presence of ABO incompatibility, Rh incompatibility, has lesser effect.

Detailed explanation:

The most common group O has anti A IgM, anti B IgM and anti AB IgG.
Group A has anti B IgM.
Group B has anti A IgM.
Group AB has no antibodies.

So if I was dumb enough to transfuse GroupyA blood to a group B guy there would be hemolysis. But what would be the mechanism for this?

The patient with group B would have anti A IgM. IgM is a very potent complement activator. IgM is very trigger itchy, it first shoots the cell and then asks questions. So this hemolysis is very fast.

Now coming to the Rh question, imagine there was a mom with O- group and baby with O+ group.

In first pregnancy, the mom is not exposed to the Rh antigen until delivery, so the 1st baby is safe. But there would be a mixture of baby and mom's blood.

Now imagine a weird person (Rh+ cell) walking through an airport, he would taken by the TSA (macrophage) for an "interrogation". So the macrophages do this interrogation (phagocytosis) in the dark corners of spleen and pick up info (antigens) about these weirdos. This info is passed to T cells and they issue warrants to B cells (IgG) for identifications of these guys and they are killed on site (IgG mediated destruction)

You can see that this will, obviously, take time time. When she gets pregnant with Rh incompatibile kid again, the IgG have been synthesized and they cross placenta and attack the baby RBC's. Voila - Hydrops fetalis.

Now imagine a mom who is O- and has a baby with A+ group. This time, at delivery, there is mixing of blood again!
But the mom has anti A IgM which is so fast like a ninja, kills of the majority of the cells before they go for their interrogation with macrophages in spleen... So ABO incompatibility actually protects against the Rh sensitization.

What's the clinical significance of Rh incompatibility?

Whenever you take care of a pregnant lady, you will confirm her blood group and if you suspect Rh incompatibility you would give her "Rh IgG" (standard dose) at 28 weeks, even though the fetal blood is not exposed to mom's immune system, this is done just in case - there might be a fall, injury etc and baby's blood may get into mom's circulation.

Why do you give Rh IgG when you want prevent the disease which is itself caused by IgG?

Rh IgG are heat treated and they cannot cross the placental barrier unlike normal IgG.

And finally, you give another dose of Rh IgG after delivery. But this time, you actually estimate the amount of fetal blood which is mixed with mom's blood by doing "Kleihauer betke test" and you give an appropriate dose.

Explained by DJ AweSpear.

Related posts:
Rh incompatibility
Hydrops fetalis
Blood group doubts
Removal of antigens from RBC's
Barts hemoglobin mnemonic

Sunday, September 25, 2016

Differentials of nodular lymphangitis

To make this post fun, I created hypothetical scenarios. This will help making a differential diagnosis =)

Scenario 1: Patient is a rose gardener.

Scenario 2: Patient is an aquarium cleaner.

Scenario 3: Patient is a vegetable labourer in a farm. Honey colored drainage is seen at the site of ulceration. It is followed by subcutaneous nodules draining the primary lesion.

Scenario 4: There was a painful chancre at the primary lesion. After 5 days, tender lymphadenitis developed.

Answers:

Scenario 1: Sporothrix schenckii

Scenario 2: Mycobacterium marinum

Scenario 3: Lymphocutaneous disease by nocardia brasiliensis.

Scenario 4: Tularemia

Reading material:
Sporotrichosis, often occurring in gardeners, remains the most recognized cause of nodular lymphangitis.
Injuries sustained in marine environments suggest Mycobacterium marinum infection.
An incubation time of 1 to 5 days, a painful chancre at the initial lesion site, and prominent tender lymphadenitis strongly implicate tularemia.
Frankly purulent discharge from the primary lesion is associated with some infections due to Francisella and Nocardia species.

That's all!

-IkaN

Karyotype seen in different disorders

Karyotype in:
Turners syndrome
Kallmanns syndrome
Klinefelters syndrome

Answers:
45 XO
46 XX
47 XXY

Thursday, September 22, 2016

Nocardia treatment mnemonic

Hello, peace keepers of the earth! =)

In today's post, I want to emphasise that the drug of choice for treatment of nocardia is TMP SMX. That's it!

Mnemonic: Since nocardia is associated with SULFur granules, use SULFonamides for treatment.

Another mnemonic: PANT
Penicillin for Aspergillosis
For Nocardia, use TMP SMX

Other drugs used for the treatment of nocardia: CARDIA!
Ceftriaxone
Amikacin
R
Doxycycline, Minocycline
Imipenem
Amoxicillin clavulanic acid

That's all!
Happy international day of peace everyone!
-IkaN

Monday, September 19, 2016

Hantavirus mnemonic

Remember H for Hantavirus infections.

Hantavirus infections are associated with high Hematocrit, pulmonary edema (Heart failure like lungs), Hemorrhagic fever and Hypotension.

They're transmitted through deer mice feces.

That's all!

-IkaN

Sunday, September 18, 2016

Antibiotics for Listeria monocytogenes infection

Mini Q&A for the day!

What is the drug of choice for Listeria monocytogenes meningitis?

Ampicillin.

What is the drug of choice for penicillin allergic patients?

TMP SMX for penicillin allergic patients.

What drugs do you use empirically for treatment of meningitis? When do you use ampicillin?

Ceftriaxone
Vancomycin
Add ampicillin for Listeria monocytogenes (Especially in elderly, neonate, immunocompromised.)

Ceftriaxone and cefotaxime

Why is cefotaxime preferred over ceftriaxone in neonates and patient with liver disease?

Ceftriaxone-induced biliary sludge is a solubility problem that occurs in patients receiving high-dose treatment (greater than or equal to 2 g).

The risk of developing ceftriaxone-associated biliary "pseudolithiasis" increases with increasing ceftriaxone dose and in patients with impaired gallbladder emptying.

Cefotaxime has renal excretion and therefore preferred over ceftriaxone.

Study group discussion: ACEI and bilateral renal artery stenosis

Angiotensin converting enzyme inhibitors (ACEI) are contraindicated in bilateral renal artery stenosis. Why?

In renal artery stenosis, renal perfusion is less and hence GFR is low. In such a case, nephrons adapt the filtration by causing efferent arteriolar constriction to maintain the pressure needed for filtration.
If ACEI is given, there is dilation of efferent arteriole and renal perfusion will again decrease further and GFR will become more low. Hence, contraindicated.

In bilateral renal stenosis, the effective renal blood flow is not significantly reduced but maintained at the cost of increasing the efferent artery tone. ACEI causes inhibition of angiotensin 2, leading to efferent artery vasodilation in glomerulus. This decreases intra glomerular pressure and filtration, resulting in renal  function detoriation.

Most commons of bacterial endocarditis

Q&A for the day!

Most common cause of bacterial endocarditis:

After tooth extraction -
Injection drug use -
Health care / catheter associated -
Originates from GI tract -
After genitourinary manipulation -

Answers:

After tooth extraction - Streptococcus viridans

Injection drug use - Staphylococcus aureus (Less common - Pseudomonas aeruginosa, Candida species)

Health care / catheter associated - S. aureus (Also Coagulase negative staphylococci CoNS)

Originates from GI tract - S. gallolyticus (Formerly known as Streptococcus bovis)

After genitourinary manipulation - Enterococci

That's all!
-IkaN

Saturday, September 17, 2016

Glasgow coma scale mnemonic

Hello!

This post is on the Glasgow Coma Scale (GCS)

An important MCQ they like asking is that if the patient doesn't respond to pain, doesn't open his eyes and doesn't talk - What is the GCS? You'll be tempted to mark zero. Remember, the lower limit of GCS is 3, not 0.

Thursday, September 15, 2016

Corticosteroid Side Effects Notes and Mnemonics

What a great day to study today!

In this post, I uploaded my notes on corticosteroids side effects mnemonics. 

Hope you find it helpful. 

That's all! 

-  शुभम् पाटीदार mbbs 013 बेच।

Tuesday, September 6, 2016

Authors diary: Teachers day

Thank you for all the teachers day wishes. They truly made me smile (=

I'm glad I could be of help to all of you.

Monday, September 5, 2016

Inheritance: Funny illustration

From the authors diary:

I created this image for Jason Compton. Last year, they did a play on Beta Blockers at RhinoFest and used one of my illustrations for it. Even though I couldn't attend it, I'm always glad to be a part of being a fun way of information spreading!

This year, they're doing a family (multi-generational) theme and educating about genetics, inherited traits, etc.

I created this fun image for them.

Parents "hand me down" their clothes (jeans) and genes! The blue and yellow DNA mix to form different shades of green in the children.

I hope you like this illustration and all the very best for your play! =)

-IkaN

Viva questions: CHF and checking edema

So I thought of writing a few posts on questions that were asked to me in my vivas. You may not be asked the same questions, but these are just for you to get an idea on how it goes (:

What is the difference between orthopnea and paroxysmal nocturnal dyspnoea?
Orthopnea is dyspnea in the recumbent position.
PND is acute shortness of breath and cough, usually occurring after 1-3 hours of sleep.
Orthopnea is relieved by sitting upright, PND persists even after assuming the upright position.

Where will you check for edema in a bed ridden patient?
In the sacral area or in the scrotum.
(In ambulatory patients, check in the ankles and pretibial region.)

That's all!
I'll keep updating as and when I remember =)
-IkaN

Step 2 CK: Diagnosis of aortic dissection

I'll keep this post short and point wise.

Best initial: Chest x-ray (CXR).
Shows widened mediastinum.

Friday, September 2, 2016

Localization of stroke based on clinical findings

Hello!

This post focuses on the localization of the lesion in stroke, re-written from Harrison.
I divide this post into "Important to know" and "Extra notes" which are optional to learn about.

What's a stroke?
A stroke, or cerebrovascular accident, is defined by this abrupt onset of a neurologic deficit that is attributable to a focal vascular cause. Causes of ischemic stroke here.

Stroke syndromes are divided into:
(1) large-vessel stroke within the anterior circulation,
(2) large vessel stroke within the posterior circulation
(3) small-vessel disease of either vascular bed.

During vivas, you'll mostly be asked to localize the lesion into anterior circulation (ACA vs MCA). They don't expect much, but you should at least know the divisions (anterior circulation vs posterior circulation), occlusion of which artery involves speech, monoparesis of a leg is seen in stroke involving which artery, etc. Just the basics.

How to remember ACA stroke findings

Hello!

This is how I remember that stroke in the anterior cerebral artery predominantly involves hemiparesis of contralateral leg and foot.

The A is between the legs!

Wednesday, August 31, 2016

Study group discussion: Red cell Distribution Width (RDW)

Let's discuss Red cell Distribution Width (RDW) today!

RDW represents variation in RBC size.
If the RDW is large, it says that the cells are different in sizes.
Analogy: If RDW is large, we know the RBCs are all unity in diversity. Like India :P
What's the clinical significance?

Study group discussion: Different sized spherocytes

The difference in size of spherocytes has significance. It is assessed manually, on peripheral smear examination.

What's the importance of assessing size difference of spherocytes?
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