This post is on Denosumab!
MOA:
- Monoclonal antibody against the receptor activator of nuclear factor κB ligand (RANKL)
- Reduces bone resorption by inhibiting the development of osteoclasts
Route: SC
Dosing: Administered twice yearly
This post is written by Sweta Senthil.
I don't know why she targeted me to make this mnemonic but it makes sense to remember the complication of Quinsy.
So mnemonic is "OJAS Pee"
Edema of larynx
Jugular Vein Thrombosis
Abscess of Lung/Pneumonitis
Septicemia, Spontaneous hemorrhage
Parapharyngeal Abscess
That's it!
Most common answer would be the centre.
That however is not the case as the light rays pass undeviated right through the centre.
In fact, phakic IOLs have an opening right in the centre for aqueous to circulate.
The most important part is the pericentral area, as the refracted rays through this area get focussed on the macula.
-Sushrut
It is the motion of the eyeball during lid closure and is a reflex between the occulomotor and the facial nerves. There are 4 types-
1. Normal- Upward and outward movement of
the eyeball.
2. Inverse- Upward but inward movement.*
3. Reverse- Downward movement.*
4. Perverse- Lateral movement.
*Some authors opine that inverse is downward and outward while reverse is upward and inward.
The Bell's phenomenon is of importance in ptosis and lag ophthalmos surgeries .
-Sushrut
Traumatic optic neuropathy is a tough nut to crack. High dose steroids and surgical decompression were the empirical modes of management. There is an ongoing search to save the optic nerve in trauma.
The innate adaptive T cell response has been deemed to be protective in traumatic optic neuropathy. It supposedly acts against the self directed antigens in traumatic optic neuropathy. The response can be augmented or induced depending upon an individual.
Other modalities are monisialogangliosides, neurotropic growth factors, and gene transfer of anti inflammatory cytokines.
A new group of steroids, the 'lazaroids' (great name that!) or 21 amino steroids provide free radical binding capability inherent to the group sans the glucorticoid activity.
-Sushrut
ARV INTERVENTION
|
RISK OF HIV TRANSMISSION FROM MOTHER TO CHILD
|
NO ARV BREASTFEEDING +
|
30-45%
|
NO ARV BREASTFEEDING -
|
20-25%
|
3ARVS(ART) BREASTFEEDING +
|
2%
|
3ARVS(ART) BREASTFEEDING -
|
1%
|
TARGET POPULATION
|
ART REGIMEN
|
PREGNANT AND BREAST FEEDING WOMEN WITH HIV
BUT NOT ON ART
|
TDF+3TC+EFV
|
PREGNANT WOMEN AND BREAST FEEDING WOMEN WITH HIV AND RECIEVING ART
|
THE SAME ART REGIMEN MUST BE CONTINUED
|
NAME OF THE GROUP
|
BREAST FEEDING
|
BARRIER METHOD
|
ISOLATION
|
BCG VACCINATION
|
IAP
|
TO CONTINUE
|
COUGH HYGIENE
|
1.IF MOTHER ON TREATMENT -NOT REQUIRED
2.IF MOTHER HOSPITALIZED, NON-ADHERENT TO THERAPY,MDR-TB - ISOLATION REQUIRED
|
AT BIRTH
OR
EVEN WITH INH PROPHYLAXIS
|
DOTS
|
ONLY IF MOTHER IS SPUTUM NEGATIVE
|
FACE MASK
|
IF MOTHER HAS ACTIVE DISEASE,NON-COMPLIANT AND HAS RECIEVED ATT PRIOR TO DDELIVERY
|
POSTPONED
OR DONE
WITH INH RESISTANT OF BCG VACCINE
|
AAP
|
ONLY IF MOTHER IS ON ATT
|
FACE MASK
|
MDR -TB AND NON COMPLIANT
|
GIVE BCG IN THESE MDR TB MOTHER
|
WHO
|
TO CONTINUE
|
FACE MASK
|
MDR -TB
|
INH THERAPY COMPLETED THEN AFTER 2 WEEK OF COMPLETION BCG VACCINE GIVEN
|
AT ROOM TEMPERATURE
|
8-10 HOURS
|
IN A REFRIGERATOR
|
24 HOURS
|
IN A DEEP FREEZER (-20 degree)
|
3 MONTHS
|
Both have the same presentation of tight lid closure.
In dark, blepharospasm won't be completely abolished while photophobia would.
Anaesthetisation(topical) reduces greatly the blepharospasm but not photophobia.
-Sushrut
Following this are ascribed to Fuch
1. Fuch's heterochromic iridocyclitis
2. Fuch's corneal endothelial dystrophy
3. Gyrate atrophy of the choroid
4. Ciliary body adenoma
-Sushrut
In lipofuscinoses like Stargardt's, fundus flavimaculatus, and Best's disease spectrum, Vitamin A and related compounds are avoided as the metabolites of those is what causes the disease in the first place. Usually, Vitamin A is prescribed empirically by general ophthalmologists for degenerative diseases of the retina.
-Sushrut
1. Dry AMD is the most common form, but wet AMD is responsible for 90% of the cases of visual loss.
2. Type 1 choroidal neovascular membrane is 'occult' and type 2 is 'classic'. This might be counter intuitive to remember.
3. In the genome, except for chromosome nos 7,11,13,21, and the Y chromosomes, all the other harbour genetic loci for AMD!
4. Hypermetropic eyes are at a greater risk of AMD. This, again is counterintuitive as myopic eyes are usually more prone to degenerative conditions.
5.Another, (sort of) counter intuitive fact is that 'hard' drusens do not lead to macular degeneration while 'soft' drusens precede macular degeneration.
6.Beta carotene, a treatment modality for AMD increases the risk of carcinoma of the lung in smokers as well as non smokers. Zinc causes genitourinary complications- UTIs, prostatic hyperplasia, and in women,stress incontinence. Also, zinc is ineffective in the prevention of advanced AMD. These results are from the two RCTs- AREDS 1 and 2 .
-Sushrut
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