Sunday, November 12, 2017

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

Friday, November 10, 2017

Medicare mnemonic for USMLE

Hello!

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

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 :-
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. :)

Friday, November 3, 2017

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

Thursday, November 2, 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.

Wednesday, November 1, 2017

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.

Sunday, October 29, 2017

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. :)



Thursday, October 26, 2017

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

Sunday, October 22, 2017

Electrocardiogram


File:Ecg.png - Wikimedia Commons

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!

Saturday, October 21, 2017

Lesions of visual pathway

Visual pathway starting from retina consists of optic nerve , optic chiasma , optic tracts , lateral geniculate bodies , optic radiations and the visual cortex .
Courtesy :- Comprehensive Ophthalmology 6th edition ; AK Khurana ; Pg.314


Sl . no
Site of lesion
Type of lesion
1
Optic nerve
Complete blindness on ipsilateral side
2
Anterior Chiasma
Junctional scotoma
3
Central chiasma
Bitemporal hemianopia
4
Lateral chiasma
Binasal hemianopia
5
Optic tracts / LBG
Incongruous homonymous hemianopia
6
Part of optic radiations in temporal lobe
Superior quadrant hemianopia (pie in sky )
7
Part of optic radiations in parietal lobe
Inferior quadrant hemianopia (pie on floor )
8
Optic radiations
Complete homonymous hemianopia
9
Visual cortex sparing macula
Congruous homonymous hemianopia
10
Visual cortex , only macula
Congruous homonymous macular defect
11
Bilateral Visual cortex , only macula
Bilateral homonymous macular defect


`~ Pratheek Prabhu

Pneumococcal vaccines mnemonic for the USMLE

Hey!

So we already have a wonderful post written about these vaccines here.

I am just here to share the mnemonic! :)

Mentzer index mnemonic

Hello everyone!

Monday, October 16, 2017

Na-K ATPase and Donnan effect

Hello Awesomemites :D

In Previous post, I gave an overview on Gibbs Donnan equilibrium.
This is to clear the doubt that Could animal cells attain Gibbs Donnan equilibrium?

Animal cells could never attain equilibrium. Plasma membrane can't sustain hydrostatic pressure gradient without evolution of some means of avoiding Gibbs-Donnan equilibrium.
Why do we need some new means? Because we couldn't afford to have "Protein free cell or no protein containing cell".
So,
Na-K ATPase counteract Gibbs Donnan equilibration.
The bottom line effect of this is to make cell effectively impermeable to NaCl. Gibbs Donnan equilibrium do not reached and cell does not swell inspite of the presence of protein ion.
Hope you got it.
-Upasana Y. :)

Donnan Effect

Hello Awesomemites :D

I was reviewing my 1st year physiology notes then I found this topic.
Let us begin. :D

We know that ions move across the membrane depending on 2 gradients :-
1. Concentration gradient (No. Of ions)
2. Electrical gradient (Charge of ions)

 The net movement of ion  is decided by the Electrochemical gradient.

I will do some calculations below. Caution point is when I will talk about electrical neutrality, I consider charge of ions.

Donnan Effect  ON DISTRIBUTION OF IONS has three effects:-
1. Because of charged proteins in cells, there are more osmotically active particles in cells than outside.
So what does it means? Animal cells do not have cell wall. Osmosis would make them swell and eventually rupture.

How to prevent this?
This implies need for evolution of pump (Na-K ATPase) to maintain osmotic equilibrium between cells and interstitial fluid across cell membrane.

2. At equilibrium the distribution of the permanent ions across the membrane is assymetric, an ELECTRICAL difference exists across the membrane.

What does it means?
K+ moves along its concentration gradient (as it is free to move)  lead to electrical disequilibrium.

This disequilibrium influence K+ to move continuously. Chloride also move it's side to equilibrate with charge.

Eventually ion concentration would stabilise (in diagram 64=64)  and individual solute concentration would not change over time (means 6 Na+ 4 Cl- 10 K+ 3 prot4- inside)
Gibbs Donnan force are responsible for development of a membrane charge due to passive process.

3.Because there are more proteins in plasma than in interstitial fluid,there is Donnan effect on ion movement across the capillary wall.

What do you mean by Donnan equilibrium?





Have a great day.
-Upasana Y. :)



Sunday, October 15, 2017

Neuroendocrine tumours of the Stomach



Neuroendocrine tumours of the stomach are uncommon tumours with a benign behaviour usually- hence known commonly as "Carcinoids"

They are diagnosed by the usual histomorphology of small organoid nests or clusters of cells with salt pepper or stippled nuclear chromatin and synaptophysin or chromogranin positivity.

We divide them into 4 types

1. One develops in the background of reactive gastrin secreting cell hyperplasia in cases of pernicious anemia

2. The second type is a part of Zollinger Ellison syndrome

3. The third is independent of any syndromic association or association with pernicious anemia

4. The fourth type is classified based on the histomorphology- "Neuroendocrine Carcinoma"- showing mitosis, nuclear pleomorphism, hyperchromasia

The closest differential could be Gastrc Lymphoma-
1. Lymphomas would not usually have an organoid pattern, tend to grow sparing the crypts and tend to form lymphoepithelial clusters
2. They would not have synaptophysin or chromogranin positivity
3. They would stain for the relevant lymphoid markers according to the cell of their origin- B or T cell type.
4. Hormone or S. Gastrin levels would be useful

Friday, October 13, 2017

House MD - Neurocysticerosis

Well, the post is from Author's diary. So read it when you are free.

Story time.

"Roll no 33, tell me how is Neurocysticerocis formed?" Asked our microbiology professor and ordered me-roll no 34 to be ready with my answer for the same. This happened during my preliminary viva. Microbiology was my last viva. This was my last moment with vivas, after this, awaited the exotic diwali vacations!! ( Rather PLs)

Roll no 33 started answering the question. However, she was wrong. Sir interrupted her and said, "I need the mechanism, not life-cycle! ".

He turned towards me and asked the same.Till this time I was in a delusion that neurocysticerocis is formed because larvae get an access to systemic circulation and end up infecting the brain!!
I was more than wrong! I got a deduction in my marks obviously.

Nevertheless, I was happy with "The End of viva".
Well, I tried to find out the mechanism of neurocysticerocis in my free time but I was not able to find it in any of the books.

So, vivas were over and I was free. I started watching the remaining episodes of "House MD. After coming home, I realized that I forgot to install the remaining episodes of House MD :(

I had season 1, so I preferred re-watching it.
Season 1 - Episode 1 - Pilot.

Guess what!!!!?
I found my viva answer of neurocysticerocis in my favourite series. Dude how can I miss this?!

So House explain's neurocysticerocis as follows:

"In a typical case, if you don't cook pork well enough, you digest live tapeworm larvae. They have  got these little hooks, they grab on your bowel, live,  grow up and reproduce.Tapeworm can produce 20,000-30,000 eggs which go out in excretion but not all of them. Unlike the larvae, eggs can pass through the walls of intestine and enter the circulation. Obviously, blood goes everywhere. As long as, it's healthy, your immune system doesn't even know it’s existence. The worm builds a wall, uses its  secretions to shut down immune system and control fluid flow. It’s really very beautiful. As it dies, this parasite loses it's ability to control the immune system. Immune system wakes up, starts attacking the worm and everything starts swelling up."

After this episode I realized I am a big moron and I haven't watched House MD with my utmost dedication. So, I am
re-watching it now :D

Everybody lies!!

Good - bye!

--Demotional bloke.

Thursday, October 12, 2017

Quick Facts - Swimming associated Diseases.

Hello everybody!
Let's swim through microbiology today and review some swimming related diseases.

Swimming pool conjunctivitis -
Caused by : Adenovirus 3,7 and 14 (tends to occur in children's swimming camps)
                      Chlamydia Trachomatis.

Swimming pool Granuloma -
Caused by Mycobacterium Marinum.

Swimmer's Itch -
Caused by Schistosoma Mansoni.

Swimmer's Ear - Pseudomonas.

Swimming in contaminated water can also cause Primary Amoebic Meningoencephalitis by Naegleria Fowleri which is a free living ameba.

If you come across more eponymous swimming diseases do share.

Let's learn Together!
-Medha.

BRCA1 vs BRCA2 gene mutations and associated chromosomes (mnemonic)


BRCA1 gene mutation is located on choromosome 17 while BRCA2 gene mutation is located on chromosome 13, how to remember that?

BRCA2 :
- 1 and 3 in number 13 if joined together, they look like a breast 1+3 =>13
- this reminds me of its association with breast cancer.

BRCA1 is really famous:
-Another Famous mutation is P53 gene mutation which causes LI Fraumeni syndrome.
-Flip IL in LI Fraumeni and you get the number 17.
-Asssociate LI Fraumeni (p53) and  BRCA1 together since both are very famous => both are due to chromosome 17 mutations.

and that's it :)

-Murad

Wednesday, October 11, 2017

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