Monday, October 16, 2017

Donnan Effect

Hello Awesomites :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

Tuesday, October 10, 2017

Quick Facts - Fried Egg Appearance!

Hello everybody!
So the next time you make your own fried egg add some medicine to it!
Here is a list of certain characteristic fried egg appearances that you may Come across:
Mycoplasma Pneumoniae colonies show fried egg colonies on Eaton agar.
Oligodendroglioma cells show a fried egg appearance.
Hairy cell leukemia cells on bone marrow biopsy.
Seminoma and Dysgerminoma  cells on light microscopy.
Parietal cells of the stomach due to acidophilic cytoplasm & large central nuclei also resemble fried egg appearance.
Plasma cells in MULTIPLE MYELOMA
Malassezia furfur 
They also show fried egg appearance on sabourauds dextrose agar with olive oli overlay.

Let's learn Together!
Medha.

Quick Facts - Human Herpes Virus 6!

Hello everyone!

Here are some quick important facts for the Human herpes Virus 6 (HHV-6)

HHV-6 affects T cells binds to CD46.

It has two variants 6A and 6B

The 6B variant causes 6th disease  (easy to remember HHV-6 causes 6th disease)
also called as Roseola infantum or exanthema subitum in children.

Roseola infantum -The disease is characterized by high grade fever wherein Febrile seizures can be seen.
After the defervescence the Rash classically appears.
One important finding is Nagayama spots which are small reddish papular lesion seen on the soft palate.

In Older age grp causes Infectious Mononucleosis like disease.

If you have more facts on it, Do share!

-Let's Learn Together!
Medha

USMLE Step 3: CCS Inflammatory bowel disease checklist

These are just my notes / checklist from the UW case 3. This post will not make sense to you if you are not preparing for CCS.

How to remember Sulfasalazine is associated with low sperm count

Hello!

I keep forgetting that sulfasalzine is the IBD drug associated with oligospermia... Sooo mnemonic.

Sunday, October 8, 2017

High tHcy associated with mortality from acute stroke!

Hey Awesomites

Various prospective studies in the past years have concluded that high levels of total Homocysteine ( tHcy ) are an independent risk factor for increased mortality from ischemic stroke, after adjustment of confounding factors!

This association is only significant in the large vessel atherosclerosis stroke subtype, and is relatively not significant in small vessel occlusion subtype.

The question that now arises is - Do elevated plasma tHcy levels cause more serious strokes or is it that more serious strokes result in higher tHcy levels?

Studies have found that elevated tHcy levels induce oxidative injury to vascular endothelial cells and impair the production of NO, thus increasing the arterial pressure and risk of stroke.
Also, tHcy enhances platelet adhesion to endothelial cells, promotes the growth of vascular smooth muscles, and is associated with higher levels of prothrombotic factors such as Beta- thromboglobulin, tissue plasminogen activator, and factor VII C.

Whether the more serious strokes increase  levels of tHcy and the changes in the levels before and after the acute episode needs further studies for clarification.

Note : High tHcy is not a cause of stroke and is not associated with stroke severity. Patients in the highest tHcy quartile ( >18.6 umol/L ) with Acute ischemic stroke  in large vessels of brain are in increased risk of Long - term mortality.

Therapy to control and lower tHcy levels with vitamin B supplements has been shown to reduce the risk of stroke and other acute cardiovascular events.
Metabolic B12 deficiency is present in 30% of vascular patients over the age of 70 years, while higher doses of B12 are required in elderly people than younger ones.
However, renal function tests should be done before starting the supplementation because high doses of cyanocobalamine increase cyanide levels in patients with renal impairment ( GFR <50 ml/min ).

Source  )
That's all
- Jaskunwar Singh

Saturday, October 7, 2017

Heme Synthesis Mnemonic

Hello Everyone!

Lets discuss heme synthesis today.  Here's the Pathway:


That's all,
Thankyou
 -Chai

Post - intubation Cardiac Arrest : possible mechanisms

Hey Awesomites

Early post - intubation Cardiac Arrest ( within 10 minutes ) is a serious major complication of emergency intratracheal intubation associated with high in - hospital mortality, and occurs with approximately 2% frequency in the ED.

Various retrospective and case- control studies have been well designed to establish the connection and factors associated in the causation. One of the studies by Heffner et al. found that a higher pre - intubation shock index ( PISI ), that is defined as heart rate divided by systolic BP, and a higher weight of the patient are independently associated with post - intubation CA.

Systolic hypotension ( BP less than 90 mmHg ) is independently associated with post - intubation CA.

Emergency intubation can cause hypotension potentially as a consequence of actual intubation acting as a sympatholytic stimulus, mechanical ventilation ( positive pressure ventilation with subsequent fall in venous return ), and/ or the induction agents used.

Also important to note is that the association between pre - intubation hypotension and post - intubation progressive decline in BP and subsequently pulseless electrical activity arrest raises the question of whether treatment of hypotension before intubating by fluid resuscitation and vasopressors can decrease the rate of post - intubation CA.

That's all
- Jaskunwar Singh