Mapelson circuits in anaesthesia mnemonic

Hey!

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.

Summary:

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

Side effects of carbamazepine mnemonic

carbAMAZEpine AMAZES me :P

Here's a mnemonic!

DD of white membrane over tonsil

DD of white membrane over tonsil -
" MALA VIT DC"

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

Medicare mnemonic for USMLE

Hello!

Here is how I remember medicare plans - A B C and D

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 :-
1. MEDULLA
2.CORTEX
Adrenal dysfunction includes hyperfunction / hypofunction of medulla and cortex.
1. MEDULLA

A) HYPERFUNCTION - pheochromocytoma
                                        -Neuroblastoma
2.CORTEX

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 :-

1.DUE TO DECREASED ALDOSTERONE :-
-Sodium wasting (hyponatremia+dehydration+shock)
 (early presentation)
-increased potassium
-acidosis
2.DUE TO DECREASED CORTISOL:-
-Hypoglycemia
-increased ACTH
3.DUE TO INCREASED TESTOSTERONE :-
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".

Diagnosis:-

• 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

Treatment:-

• 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. :)

Sequels of corneal ulcer perforation

Sequels of corneal ulcer perforation :
"SILICA PAPA"

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"

S-Sclerocornea
T-Tear in Descemet's membrane
U-Ulcer
M-Metabolic condition
P-Posterior corneal defect
E- Endothelial dystrophy
D-Dermoid

Thank you :)

~Pratheek Prabhu

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.

Basics:
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
Madhuri.

Neonatal Resuscitation Tray

Hello :D

The tray consist of the following :-
1.Long cuff surgical gloves.
2.Stethoscope
3.Mucous extractor/ suction apparatus - (yankauer suction tube)
4.Suction catheter (6,8,10 Fr= French)
5. Facemask  size 0 and 1
6. Self inflating bag with reservoir , flow inflating bag or T-peice device
7. Laryngoscope with STRAIGHT BLADE (0 and 1 size)  (keep spare bulb and batteries)
8. Endotracheal tube (2,2.5,3,3.5,4 mm ID=internal diameter)
9. Stylet
10. Nasogastric tube (6,8 Fr= French)
11. Disposable syringes ( 1,2 and 10 ml)
12. IV cannula
13. Adhesive tapes and scissors
14. Umblical vessel catheters
15. Pediatric reflex Hammer
16. Drugs (Rarely indicated)
 -Adrenaline (1:10,000)
-Naloxone
-Sodium bicarbonate
-Calcium gluconate (not a routine resuscitation drug)
-Potassium chloride (I have seen in my tray!)

So What is in your tray ? :P
Go and find out it in your NICU.
Do share it below in the comment section.

-Upasana Y. :)

Swine flu categories

Hello!

Here's a post on the categories of Patients with Swine flu.
The categories are A, B1, B2 & C.

Category A:

Mild fever plus Cough, Sore throat, Headache, Body ache, Diarrhoea, Vomitting.

Action in Category A:

No Testing for H1N1
No Temiflu
Only daily observation for symptoms

Category B1:

Category A symptoms plus high grade fever, severe sore throat.

Action in Category B1:

No Testing for H1N1
Tab Temiflu as per dose
Home isolation
Avoid public places

Category B2:

Category A symptoms plus high risk conditions such as
Child< 5 yrs
Age > 65 yrs
Pregnancy
Chronic disease
Diabetes
On long term treatment with steroids

Action in category B2:

Tab Temiflu as per dose
Home Isolation
No H1N1 Testing

Category C:

Category B symptoms plus
Chest pain
Breathlessness
Blood in cough
Blue nails
Worsening of underlying disease

Action in category C:

Tab Temiflu as per dose
H1N1 Testing
Hospitalization isolation

~Pratheek Prabhu

Electrocardiogram

P wave

• Positive wave
• Shape is up rounded deflection
• Cause: Depolarisation of atrial musculature.
• Duration: 0.1 sec
• Intensity: 0.1-0.12 mV
• Represents functional activity of atria.

Clinical Aspects:

1. Mitral stenosis: left atrium is hypertrophied and P wave is larger and prolonged.
2. Tricuspid stenosis: Right atrium is hypertrophied and P wave is taller but there is no change (normal) duration.
3. Atrial fibrillation: P wave disappears and is replaced by fine irregular oscillations.
4. Ectopic Pacemaker: (reverse) The impulses are sent from AV node to SA node.

QRS COMPLEX

• Q wave is often absent.
• Cause: Ventricular Depolarisation.
• Duration: 0.08 sec ( less than P wave)
• Intensity: 0.1 mV to 0.2 mV ( amplitude is more)
• R wave is 1 mV
• S wave is 0.4 mV
• Total Intensity is 1.5 mV to 1.6 mV

Clinical Aspects

1. Deep Q wave: more than 0.2 mV. This is seen Myocardial Infarction.
2. Tall R wave: more than 0.1 mV. This is seen in ventricular hypertrophy.
3. Low Voltage QRS Complex:  This is related to hormones and pericardial fluid. Hypothyroidism and Pericardial fluid around the heart.
4. QRS COMPLEX: Prolonged in bundle branch block.

T wave

• Cause: Ventricular Repolarization.
• It’s positive wave because the direction of Ventricular repolarization is opposite to depolarization.
• Duration: 0.27
• Intensity: 0.3 mV

Clinical Aspects

1. Flattened T wave: old age.
2. Height increases: during exercise.
3. Inverted T wave: this is seen in myocardial infarction.
4. Tall and peaked T wave:  Hyperkalaemia.

U wave

• Positive round wave
• Repolarization of papillary muscled
• Duration: 0.08 sec
• Intensity: 0.2 mV
• Rarely seen
• Prominent in hypokalaemia.

P R interval

• Onset of P wave to onset of QRS complex (PQ interval)
• Represents AV conduction time.
• Duration: 0.12 to 0.21 sec

Clinical Aspects

1. Prolonged PR interval: AV conduction block.

J Point

• The meeting point of QRS complex with ST segment.
• It represents the end of Depolarisation and beginning of repolarization.
• At this point, no current flows around heart.

I hope this helped you :))  Have a good day!