Thursday, November 30, 2017

Guidelines for treatment of drug-susceptible tuberculosis 2017 UPDATE

Hello Awesomites :D

This is to inform you the updated guidelines.
I was overwhelmed with the data in the book. I tried to simplify it.

1.The name given to this scheme is "99 DOTS"
99 means that 99% benefits should reach to all the people who are enrolled under this programme.

2.INTRODUCTION OF FDC (fixed dose combination)
 (Please make a correction in the following diagram :- ETHAMBUTOL=275mg)

4.Information technology is incorporated to monitor the adherence of patient to treatment regimen.
by toll free no. 

I hope it helped. 
(Edit1:- 99DOTS

-Upasana Y. :)

Tuesday, November 28, 2017

USMLE Step 3 CCS: Asthma exacerbation

Orders to remember!

Pulse oximetery (every 1-2 hours to access response)
Physical examination
Albuterol nebulizer
Intravenous methylprednisone
Peak flow (every 1-2 hours to access response)
EKG (is this cardiac?)
CXR (to find out cause of asthma excerbation - infection)
CBC (to find out cause of asthma excerbation - infection)

Other stuff:
Cardiac monitor
Head elevation
Ipratropium for severe exacerbations
NSS 0.9%
Discharge on oral prednisone for 5-7 days

- Use inhaled short-acting beta agonists early and frequently, and consider concomitant use of ipratropium for severe exacerbations
- Start systemic glucocorticoids if there is not an immediate and marked response to the inhaled short-acting beta agonists
- Make frequent (every one to two hours) objective assessments of the response to therapy until definite, sustained improvement is documented


Wednesday, November 22, 2017

Mapelson circuits in anaesthesia mnemonic


So I've faced a lot of problems trying to remember the various Mapelson semiopen circuits for inhalational anaesthesia and sadly they have been asked in exams so I tried to identify them using these simple points.

Firstly, remember, the circuits are semi open so part of the gases will be exhaled and part of them will be re inhaled.

Basic parts of any circuit are
-an inlet for fresh gases
-an outlet valve for exhalation
-the patient end
-the distal end usually with a bag to control rise and fall of the chest.

1) Mapelson A
The only circuit where fresh gases come in from the distal end. The exhaling valve is near the patient. It is suitable for spontaneous ventilation so rate of flow of gases = minute volume.

2) Mapelson B
Remember, B for both. So both inlet and outlet are together at the patient end. Otherwise it's the same as A.

3) Mapelson type C
C for closed and C for corrugationless. It's a closed circuit and the only one which has no corrugations.

4) Mapelson D
It is the exact opposite of A. Inlet for fresh gases is near the pt, outlet is far away. It is suitable for controlled ventilation.

5)Mapelson E
This is a valveless circuit and also has no bag (the only one without a bag). Since the arrangement is in the form of a T, it is also called Ayre's T piece.

6) Mapelson F
It is the same as E, valveless, but it has a bag to control the rise and fall of chest. It is mainly used in infants and neonates.

Fresh gases distally ➡A
Inlet outlet both together➡B
No corrugation➡C
Opposite of A➡D
No exhaling valve ➡ E and F
No bag ➡ E
Same as E but with bag ➡F

Submitted by Aditi

Sunday, November 12, 2017

DD of white membrane over tonsil

DD of white membrane over tonsil -

M- Membranous tonsillitis
A - Aphthous ulcers
L -  Leukocytosis
A -  Agranulocytosis

V - Vincent Angina
I   - Infectious mononucleosis
T  - Traumatic ulcers

D- Diphtheria
C - Candidia infection

Thank you :)
~Pratheek Prabhu

Sunday, November 5, 2017

Steroid Hormone synthesis pathway (Clinical aspect)

Hello Awesomites :D

I was reviewing the corticosteroid synthesis pathway and its applied.
Let us begin. :))
Adrenal gland consist of two parts :-
Adrenal dysfunction includes hyperfunction / hypofunction of medulla and cortex.

A) HYPERFUNCTION - pheochromocytoma

A)HYPERFUNCTION -Conn's disease
                                      -Cushing's syndrome (Primary tumors)
                                                                          (excess ACTH -pituitary hypersecretion,ECTOPIC)
B)HYPOFUNCTION -ACTH deficiency (Iatrogenic , pituitary insufficiency)

C)CONGENITAL ADRENAL HYPERPLASIA (from partial enzyme deficiencies due to mutation in genes)

Clinical features of CAH :-

-Sodium wasting (hyponatremia+dehydration+shock)
 (early presentation)
-increased potassium
-increased ACTH
In female , virlization.
In male, No symptom, increased size and pigmentation of penis.

Q. What is the difference between 21-hydroxylase deficiency and 11beta hydroxylase deficiency ?
Ans. In 21-hydroxylase deficiency, hypotension occurs due to salt wasting.
Accumulation of 11-deoxycorticosterone as a result of 11 beta hydroxylase deficiency leads to "HYPERTENSION".

Q.Most common form of CAH is due to mutation or deletion of which gene?
Ans. CYP21A resulting in 21-HYDROXYLASE DEFICIENCY .

Q.Which Enzyme deficiency showing virlization in females?
Ans. -21 hydroxylase
        -3beta HSD
       -11 Beta hydroxylase.

Q. Two hypertensive form of CAH.
Ans. 11beta hydroxylase and 17hydroxylase deficiency.

Other points :
- Females with 17-hydroxylase deficiency appear phenotypically female at birth but do not develop breasts and mensturate in adolescent because of INADEQUATE ESTRADIOL PRODUCTION(17 hydroPregnenolone is also a precursor of estrogen). They may present with hypertension.
-CAH is a type of enzyme deficiency. So it can be partial or complete .There is a severity spectrum.
More severe form shows salt wasting.
Milder form shows "NON CLASSICAL TYPE of CAH".


  • 17hydropregnenolone with or without ACTH test
  • CYP21A2 panel,sequencing,deletion
  • Carrier screening test (Preconception test)
  • Karyotyping ( In case of ambiguity of sex)
  • Hormones and electrolytes
  • Counsel the parents.
  • Protect from Adrenal insufficiency ( Give mineralocorticoid and glucocorticoid)
  • Avoid salt wasting crisis during illness,stress,etc. ( Increase dose of glucocorticoid,Give IV fluids and sodium and dextrose)
  • Surgery ,sex assignment.
(Note :- There are two more variants of CAH 1. Lipoid CAH 
2.POR deficiency ( P450 oxidoreductase enzyme deficiency) - also involved in both sterol and steroid synthesis pathway).

Study hard.
-Upasana Y. :)

Friday, November 3, 2017

Sequels of corneal ulcer perforation

Sequels of corneal ulcer perforation :

S- Subluxation of lens
I -  Iris prolapse
L-  Leucoma
I -  Intraocular haemorrhage
C- Corneal fistula
A-  Adherent Leucoma

P- Phthisis bulbi
A- Anterior synechiae
P- Purulent infection
A- Anterior Staphyloma

Thank you :)

~Pratheek Prabhu

Complications of corneal ulcer

Complications of corneal ulcer - "DEPICT"

D- Descemetocele
E- Ectatic cicatrix ( Keratectasia )
P- Perforation
I - Inflammatory glaucoma 
C- Corneal scarring
T-  Toxic iridocyclitis

Thank you :)

~ Pratheek Prabhu

DD of neonatal cloudy cornea

Differential diagnosis of neonatal cloudy cornea - "STUMPED"

T-Tear in Descemet's membrane
M-Metabolic condition
P-Posterior corneal defect
E- Endothelial dystrophy

Thank you :)

~Pratheek Prabhu

Wednesday, November 1, 2017

MELD score mnemonic

Hello everyone!

Model for End-Stage Liver Disease (MELD) The Model for End-Stage Liver Disease (MELD) is a reliable measure of mortality risk in patients with end-stage liver disease. It is used as a disease severity index to help prioritize allocation of organs for transplant.

MELD uses the patient's values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. Sodium was recently added to improve predictive value.

Desmosomes and its disorders

Hello friends,
This post is about the importance of desmosomes in various dermatological conditions.

Desmosomes are present in stratum spinosum of epidermis.  They are calcium channel dependent adhesion molecules (cadherins)  and hence form intercellular connections.

Desmosomes are seen all through the epidermis, but are obvious as spines in spinous layer.

They have many constituents. Important transmembranous  parts are:
•Desmoglein (DSG)
•Desmocollin (DSC).

Now we will focus on Desmoglein (DSG) .
•DSG-3 is present mainly in basal layer of epidermis and strongly seen in mucosae.
•DSG-1 is present in superficial epidermis and is not seen in mucosae.

Clinical importance:
* If DSG-3 is damaged --->
   early, severe mucosal involvement.
   Lower level of damage to epidermis.
* If DSG-1 is damaged --->
    No mucosal involvement.
    Superficial epidermal damage.

° If IgG antibody is formed against DSG-3, then the resulting disease is known as Pemphigus vulgaris.
° If IgG antibody is formed against DSG-1, then the resulting disease is known as Pemphigus foliaceous.

A mnemonic to remember DSG-3 for basal layer and mucosal involvement :

Thanks for reading