McCune–Albright syndrome is suspected when two of the three following features are present:
Endocrine hyperfunction such as precocious puberty
Polyostotic fibrous dysplasia
Unilateral Café-au-lait spots
Here's a mnemonic :)
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
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
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 in:
Turners syndrome
Kallmanns syndrome
Klinefelters syndrome
Answers:
45 XO
46 XX or 46 XY
47 XXY
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
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.)
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.
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.
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
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!
- शुŕ¤ŕ¤®् पाटीदार mbbs 013 बेच।
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
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