Kleihauer–Betke test: KB test.
1) Why do we do this test?
- To calculate Fetal RBCs in blood. This helps us to measure amount of Anti-D required to neutralize it.
2) How do we do it?
- Basically, we are going to take blood sample and add acid to it and measure red blood cells under microscope.
3) How do you differentiate Fetal and Maternal blood?
- Fetal RBCs are acid resistant. Adding acid in the preparation leads to lysis of the Maternal RBCs.
4) What are important points regarding this test that should be kept in mind while solving MCQs?
- Do not confuse it with APT test. APT is done in Alkali and it is a Qualitative test. It helps in differentiating Maternal and Fetal blood only. On the other hand, in KB test (Also know as Acid dilution test), we use Acid and we quantify Fetal blood.
- Minimum dose even after KB test is 300 microgram.
5) How do we calculate amount of Anti-D required to neutralize Fetal RBCs?
- If 20 RBCs in HPF are seen, then it means 1 ml Fetal blood is in circulation.
-1 ml fetal blood requires 10 microgram of Anti-D for neutralization
6) What if they don't mention "Fetal RBCs" and instead, mention "Fetal blood" in the question?
- Here is a trick. Always remember, 1 ml Fetal blood has 0.5 ml Fetal RBCs.
Applied calculations:
Q1) A Multigravida with twin pregnancy has 20 ml Fetal RBCs. How much Anti-D will be required to neutralize it?
(Take a deep breath. You don't need to worry about twin pregnancy. All the important points are already covered in above segment)
- 20 ml Fetal RBCs = 40 ml Fetal blood.
- 1 ml Fetal blood = 10 micrograms Anti-D
Answer = 400 micrograms Anti-D
400 micrograms is the enough amount of blood given to neutralize 40 ml fetal blood or 20 ml Fetal RBCs.
(Done easily? Perfect ! Let's level up.
I want you to go through blog once again before heading down.)
Q2) This time patient comes with same clinical presentation but with 20 ml fetal blood.
- 1 ml fetal blood = 10 micrograms of the Anti-D
- 20 ml Fetal blood will require 200 micrograms Anti-D.
Perfect. We calculated correctly but my question is - Will you administer 200 micrograms Anti-D to the patient showing 20 ml Fetal blood to neutralize it?
Answer is big 'NO'.
Go back to bullet (4) point 2:
Minimum amount is still 300 micrograms after KB test. So you cannot administer 200 micrograms. You have to give 300 micrograms.
I hope this blog is better than my previous blogs. Any important points you have regarding KB test, do comment in comment box
That's it
-Demotional bloke
1. The respiratory rate of the retina is twice that of the brain.
2. The retina does not require insulin for glucose to enter the cells!
3. In the retina, glycolysis occurs despite having sufficient oxygen supply.
4. The retina is not just a sensory organ. Much of the image processing occurs at the retinal level itself.
-Sushrut
Hello everyone!
D-lactic acidosis is an unusual form of lactic acidosis.
Which patients develop D-lactic acidosis?
1. In patients with jejunoileal bypass, small bowel resection, or other causes of the short bowel syndrome.
2. Patient who receives or ingests a large amount of propylene glycol
3. Patients with diabetic ketoacidosis
In this post, I'm going to specifically talk about D-lactic acidosis in patients with small bowel syndrome.
How do patients with D-Lactic acidosis present?
Increased anion gap metabolic acidosis.
Neurologic findings of intermittent confusion, slurred speech, and ataxia.
Why does it happen in patients with small bowel syndrome?
Glucose and other carbohydrates are normally absorbed by the small bowel. If the small bowel is bypassed, removed, or diseased, then delivery of these substances to the colon increases.
Also, overgrowth of gram-positive anaerobes, such as Lactobacilli seen in small bowel syndrome contributes to lactic acidosis.
How is it metabolized?
D-lactate is not metabolized by L-lactate dehydrogenase, the enzyme that catalyzes the conversion of the physiologically occurring L-lactate into pyruvate. Thus, D-lactate is slowly metabolized in humans, accumulates in body fluids, and generates metabolic acidosis.
Diagnosis:
Laboratory studies show increased anion gap metabolic acidosis with normal plasma lactate levels, because the D-isomer is not measured by conventional laboratory assays for lactate. Diagnosis is confirmed by specifically measuring D-lactate.
Treatment:
Sodium bicarbonate if D-lactic acidosis and acidemia are severe.
Oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) can be used when D-lactic acidosis that decrease the number of D-lactate-producing organisms.
FYI: Although antimicrobials are sometimes helpful, they can occasionally precipitate D-lactic acidosis in susceptible subjects by causing an overgrowth of lactobacilli.
Low-carbohydrate diet (or the use of starch polymers rather than simple sugars) is also helpful because it diminishes carbohydrate delivery to the colon.
That's all!
-IkaN
-Fas ligand/ FasL/ CD95 ligand is a type 2 membrane protein belonging to the TNF superfamily and is found on lymphocytes.
-In the eye, it is expressed on Iris and corneal endothelial cells.
-In the rest of the body, it is expressed on the thymus, testes, and the brain.
-Liver and intestines express this only in periods of severe inflammatory process.
- Apoptosis of the T lymphocytes can be triggered by FasL. Loss of this mechanism is touted to be one of the causes of uveitis.
Mechanism by which it acts is believed to be the selective apoptosis of cells producing TNF or by IL2 activation of lymphocytes.
-Sushrut
This is a mechanism by which the eye wards off the secondary effector phase of the immune response arc.
Thus, the cell mediated immunity appears to function less effectively in the uvea compared to the rest of the body.
Possible mechanisms include-
1. Immunomodulatory cytokines produced by the ocular tissues.
2. Immunomodulatory neuropeptides produced by ocular nerves
3. Functionally unique APCs.
4. Compliment inhibitors
..and some other factors.
-Sushrut
The large spaces of choroid act as a sort of trap to organisms, especially fungi. Therefore most fungal lessons of the posterior segment begin as choroiditis.
Hello Awesomites!
I would like to highlight difference between these two terms. It is confusing.
1.Cholecystohepatic triangle:
Medial boundary- Common hepatic duct
Inferior boundary- Cystic duct
Superior boundary- Inferior edge of liver
2. Calot's triangle:
Medial boundary- Common hepatic duct
Inferior boundary- Cystic duct
Superior boundary- Cystic artery
Happy Studying!
Upasana Y. :)
It's interesting to note that the optic nerve, which is considered to be a purely sensory nerve has some efferent fibres, that is, fibres from the brain to the optic disc. The presumed role of these fibres is in dreams, where the brain sends impulses to the retina, image is generated and it is carried back to the brain via the afferent fibres.
-Sushrut
Some specific antigens when placed in the anterior chamber of the eye result in a suppression of cell mediated immunity, with a normal humoral component.
There is something known as the ' oculo splenic axis' , whereby the antigens travel via the trabecular meshwork and reach the spleen. In the spleen, they secrete MIP 2 which attracts the NK cells. The NK cells in turn secrete IL10 and TGF beta. The T cells in this environment become regulatory cells and suppress the cell mediated immunity. Production of IL2 is suppressed.
The eye is an immuno privileged organ, as it needs to be structurally maintained pristine to preserve it's light carrying capability. ACAID is a mechanism by which Nature attempts to limit unwanted inflammatory responses in the anterior chamber.
It has implications in intraocular tumors, autoimmune, and infectious immune responses.
-Sushrut
PS- The failure of ACAID in the mechanism of lens induced uveitis still remains unexplained!
"Are you ready for solo practice?"
My father read out the topic from a WhatsApp forward he had received.
I was drinking tea, with all the absent-mindedness of a resident who barely has the luxury to sit down and have said cup of tea.
I stared at my father aghast, wondering where this daunting question sprung from, till he elaborated that it was the topic of an essay competition.
As I read through the message myself I corrected him, "That’s not what it says! It's asking whether you're adequately trained for solo practice in the future."
"Your future is just a couple of years away. Will you be ready by then?" he asked.
"I don’t know about ready, but I’m sure I’ll be adequately trained," I answered.
He nodded and after a beat, leaned in and asked,
"But have you really thought about it yet?" ((And what makes you so sure? Have you really thought about it yet?))
That got me thinking indeed.
As a year old paediatrician, the most important lesson I learnt was how much there was to
learn. My days were spent working with any time off work spent catching up on missed sleep. I felt like I whizzed
through my first year, barely retaining any of the knowledge I was expected to glean as an intern. Being a houseman had felt like operating at spinal level, for the lack of there being a synaptic level
any lower than that. Perhaps I wasn't ready at all.
My face seemed to betray my thoughts as my father interrupted them. "Instead of lamenting over what you haven’t learnt," he asked kindly, as if reading my thoughts, "Why don’t you try and think about how much you have?"
Convinced that I had learnt nothing of value anyway, I decided to humour him nevertheless. I spoke about my housemanship month by month, about what each sick child and each hopeful parent had taught me. A resident doctor in a busy municipal hospital barely gets time for their own basic life needs like food, sleep, or even a bath (and needless to say, sleep always takes priority!). Most of what we learn is on the go. Nobody gets enough time to go back and read about the cases we've seen in the ward. Thankfully the vast number of cases and immense workload ensures that we at least know how to manage basic ailments that a child presents with.
However amidst putting orders, histories, and ensuring investigations for so many patients, we forget to learn about the little things - how to allay a parent's concerns about their child, how important the so called 'cosmetic' part of our practice is. Of course, all these concerns are still things that can be worked on if one can put their heart into it.
And yet, are we being adequately trained to do this for future solo practice? The answer, shockingly, is a resounding no.
Add to this, we're barely trained to make decisions by ourselves, especially when there are so many seniors waiting to teach us, guide us, and by extension, take responsibility for our actions. How is one supposed to adjust to suddenly being so independent?
In a tertiary care setting, we are used to sending out references left, right, and centre. We fail to learn the basics of anything that would result in us putting even one toe out of our own speciality and instead rely on the services of others, who are just a single written call away. It's very obvious that this is not going to be the case when one starts practising by oneself.
Another important thing that nobody teaches you in residency is how to ask for remuneration for our services. Being employees of the state or the corporation, we are used to working endlessly for a fixed salary being ddeposited in our accounts each month. As a result, we fail to realise our worth in monetary terms, there being a certain amount of guilt with each patient we charge. Maybe this is something we realise only after getting into private practice, where taking care of every patient is translated into putting food on our own plate. At this stage in life, while I hope I wouldn't underestimate and thus undercharge for my abilities, I really don't know what that would be like be like.
So, coming back to the question that started it all - no, I am not adequately trained for future solo practice. And no, I am not ready for it either. But two years down the line, I have hope for the former statement. And as for the latter? Well, I believe that at least that "I'm not ready." will transform into" I'm not ready...yet. But I'm willing to stick around till the day I am."
Written by Aditi
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| 1. The catheter itself is composed of (a) a tip for insertion into the vein, (b) wings for manual handling and securing the catheter with adhesives, (c) a valve to allow injection of drugs with a syringe also called a LUER lock-valve, (d) an end which allows connection to an intravenous infusion line, and capping in between uses. 2. The needle (partially retracted) which serves only as a guidewire for inserting the cannula. 3. The protection cap which is removed before use. (By courtesy of Wikipedia (https://en.wikipedia.org/wiki/Peripheral_venous_catheter) retrieved 7/5/2019) |
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| (Note that in some countries 26G could be of Purple colour) - Table by courtesy of Wikipedia (Retrieved 7/5/2019) - |
