Acute myocardial infarction (AMI), especially of the inferior left ventricular wall, is often associated with transient hypotension and sinus bradycardia.
Ever wondered... Why?
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