Tuberculosis mnemonics

Hello!

Today's post is all about TB! :D

So many names to remember :/

Enterobius vermicularis notes & mnemonics

Enterobius vermicularis notes

Here are my notes for Enterobius vermicularis. Uploading so you guys can refer to them (:

GI Hormones: Zollinger Ellison Syndrome

Hi everyone ! So this is the 2nd post in  the series of the hormones of the GIT. 

Last post we discussed about the functions of the hormone Gastric.  This post we look at its applied aspects. And that's majorly looking into the Zollinger Ellison Syndrome. 

Hope you like it. ::)

⛔ZOLLINGER ELLISON SYNDROME⛔

■Etiology: sporadic or Associated with MEN1 SYNDROME (Multiple Endocrine Neoplasia syndrome)

■TRIAD : Tumor + Hypergastrinemia + Peptic ulcerations. 

↪Tumor. = Gastrinoma. 50% gastrinomas are malignant.                                                       ○MC Site is the duodenum
○(☆MC site for PUD in general is also duodenum. So it only makes sense that for the mucosa to ulcerate there must be a local gastrin supply available ).

○2nd MC site for gastrinoma = Pancreas. Originally the tumor was defined as a non Beta cell Pancreatic tumor. 😨. Now its been realised the duodenum was the culprit all along.
○PUD and Hypergastrinemia. = due to increased gastrin secretion by the tumor, gastrin exerts an increase in the acid secretion + its trophic action on gastric mucosa. This causes erosions of gastric mucosa as well as causes hypertrophy of it (paradox). Thus we get a Hypertrophic Gastropathy + PUD.

↪S/S:
○Abdominal pain is the MC symptom . Can mimic PUD.
○2nd MC symptom is Diarrhea.
May be associated with mucosal damage due to acid leading to villous atrophy (excessive acid of stomach. Pancreatic/intestinal alkalinity may be unable to counteract. Pancreatic secretions may be compromised due to tumor)
○Heartburn
○GI bleed -- hematemesis, melena. Due to ulcer-hemorrhage. 

↪Inv:
○S.gastrin levels - >100. IOC for screening
○May follow up a positive result with gastric acid function tests
○Somatostatin receptor scintigraphy.
○Evaluate for Liver /LN mmets
○S.Calcium -- associated with MEN1.

↪Rx :
○PPI. Symptomatic treatment achieved with OMEPRAZOLE and friends.
○Can use Octreotide - Somatostatin analogue. It's a generalised inhibitor of pretty much all hormones.
○Surgical Rx of tumor advised to avoid mets

☆☆☆☆☆MEN1 --> Hyper parathyroidism , pituitary tumors ,Pancreatic tumors.
(Mnemonic : All MEN like 3 things - Pus*y, Pus*y, Pus*y. = parathyroid, pituitary, pancreas) ; 

Autosomal Dominant. cause men are dominant, lol. ¤¤ 

The next post is going to be about the only  other member in the Gastrin family -CCK PZ. 

So don't fail it to check it out. ;;) 

Bye till then. :* :D

GI Hormones: Gastrin

Hi everyone, so this is my first post in the series of GI hormones!

There are 2 families of GI hormones -

1. Gastrin family (Gastrin , CCK)

2. Secretin family (Secretin, glucagon, VIP, GIP)

Others - Motilin, Peptide YY, Substance P, Ghrelin, Guanylin

In this post, I'll be talking about one of the members of the gastrin family, gastrin itself! :D


⛔⛔GASTRIN⛔⛔

I. Produced by: 

■ G cells - enteroendocrine cells located in antral gastric mucosa.

II. Physiology of secretion:     

■ Acts via CCK-B receptor

■ Progastrin is cleaved to form 3 different residues :G 14, 17,34.

■ Sulfated and carboxylated forms also exist.

■ Amidated form is more stable.

■ G17 is principal form w.r.t. GI actions.

■ G34 has longer t1/2 than others.

■ Inactivated in SI, kidneys

III. Functions: 

■ Stimulates Gastric acid and Pepsin secretion

■ Trophic action - stimulates growth of mucosa of Gut.

IV. Regulation:

A. Factors that increase secretion of gastrin: 

■ Luminal:

- Amino Acids (Aromatic) in stomach 

- Distension

Because the job of this hormone is to bring about protein breakdown via pepsin and increase pH of the stomach, Hence it is released in response to protein and other contents entering the stomach. Tells the stomach it's time to do its job!

■ Neural:

- Vagal discharge as it secretes GRP at the postganglionic fibres.

Both sympathetic and parasympathetic fibres in gut are stimulatory (dual ANS stimulation).. What can we do about it?

■ Bloodborne:

- Epinephrine

- Ca2+

Calcium is a universal stimulant of motility and exocytosis from glands; epinephrine = dual ans stimultion.

Factors that decrease secretion of gastrin:

■ Luminal:

- Acid

- Somatostatin

Acid tells the G cell to shut up. There's enough acidity. No need for stomach to yap.

Somatostatin keeps all other hormones in check!

■ Bloodborne:

- Secretin family (Secretin, VIP, GIP, glucagon) (archnemesis)

Applied aspects of Gastrin:
■ Normal S. Gastrin levels = upto 100pg/ml
■ Hypergastrinemia:
- Pathological Increase (eg. Gastrin secreting tumor)
- Compensatory Increase (eg. Pernicious Anemia i.e. Type A Gastritis; due to destruction of    acid secreting cells compensation with increased  gastrin.)
■ Hypogastrinemia:
- Antral loss eg. Antrectomy, Achlorhydria.
- H pylori associated ulcers/gastritis may show hypogastrinemia, but association is not very clearly established. 

My next post will be on Zollinger Ellison Syndrome.  Excited? :D I know I am 😎

Hope you guys like it. 

~ A. P. Burkholderia

Strongyloides Stercaralis Notes And Mnemonics

Hey everyone!
These are microbiology  notes made by me =) Hope it helps you ☺

"Inception"- a real thing!

Hello!

Remember the movie, "Inception" starring Leonardo DiCaprio??? Loved it.. right? :D
OK. Let me recall it for you.. Leo's character interferes with other's dreams to implant new ideas in their minds. It was a trippy plot premise. But, not entirely a Sci-Fi!!!

So, now what if I say we could do 'inception' without the subject being aware of what is being learned... "Yes, it is possible in reality now", the scientists say.

Normal AST, ALT and ALP values mnemonic

Continuing the normal values mnemonic posts :D

Today's post is on liver enzymes!

Normal SGOT, SGPT and ALP values!

Immunization schedule notes and chart

Hello!
So in these notes, I write about type of vaccine, strain used for vaccine prepration, diluent, content, dose, route, site of vaccination,strength,  protective efficacy, protective duration, contraindications, complications, age limit and storage of vaccines and special points used in the Indian immunization schedule.

It's a nice summary for those studying pediatrics, preventive and social medicine, pharmacology, microbiology and medicine. 

Stay Awesome ☺

Step 2 CK: Interventions that lower mortality in STEMI and ACS

Hello!

For Step 2 CK, remembering things that lower mortality is essential. Here's a mnemonic for interventions that lower mortality in STEMI (ST elevation MI), NSTEMI (Non ST elevation MI) and UA (Unstable angina).

Gastrointestinal Stromal Tumors Mnemonic

Hi everyone !
So here is a post about a few important points on GIST I figured can be remembered in an easier way if you love the letter "C" ! G does look like a C :D

Uses of somatostatin and bromocriptine notes & mnemonics

Hey everyone!
These are pharmacology notes made by me =)

Olympics 2016 and the Zika

Hey Awesomites!!!

You all know the Olympics and Paralympics are on their way in August and September. Excited, aren't you? Woohhooooo! :D

Its taking place in Rio de Janeiro, Brazil this year. So if any of you or your known really plan to travel to Brazil for the Olympics and the Paralympics... You have to know about the current situation of Zika virus out there. Brazil, along with many surrounding countries of America, are experiencing an Outbreak of Zika Virus.

Forensic toxicology notes part - 3

These are my toxicology notes. Hope it helps you!

Forensic toxicology notes part - 2

These are my toxicology notes. Hope it helps you.☺

Instructions for new authors: How to post through blogger app

If you wanna be an independent author at Medicowesome, here's what you need to do:

Email me at medicowesome@gmail.com asking that you want to write for Medicowesome. I'll say yaay! Of course, yes! :D

Make a blogger account (blogger.com) using your Gmail account.

Send me your gmail address. I will send you an author invitation, you must accept it within 24 hours.

Forensic Toxicology notes part - 1

These are my toxicology notes. Hope  it helps you! 

Alkaptonuria notes and mnemonic

Today, Hari sent me his notes on Alkaptonuria.

Alkaptorr makes him think of helicopter! And he imagines a black ox sitting in it!

Alkaptonuria mnemonic

Diuretics and antidiuretics notes

Diuretics and anti-diurectics notes by Shubham. Isn't he plain awesome for sending his notes to us?

Treatment of acne mnemonic

Hello!

Here's a short post on acne.

Antimicrobials for treatment of acne mnemonic: ABCDE
Azelaic acid
Benzoyl peroxide
Clindamycin
Dapsone
Erythromycin

GnRH agonists, GnRH antagonists, uses and mnemonic

Hey guys!

Here are a few more notes by the one and only, Shubham Patidar! This time on dopamine, prolactin and GnRH :D

Potter Sequence

A sequence is where a single initial aberration leads to a series of anomalies in the body. The best example of a sequence is 'Potter Sequence'.

Conditions like renal agenesis, maternal hypertension lead to oligohydramnios. The amniotic fluid plays a role in the lung development in the second half of pregnancy & so, there is a higher incidence of pulmonary hypoplasia in such foetuses which is the main cause of their death.

Oligohydramnios leads to direct pressure of the uterine wall on the developing foetus leading to flattened nose, recessed chin & low set ears. This is Potter sequence- sequence here because the initial aberration- oligohydramnios leads to & explains all the changes occurring later.

Happy Sunday!

Metronidazole notes and mnemonic

These amazing notes on Metronidazole were written by Shubham Patidar!

Biotin deficiency mnemonic

Hello!

Here's an interesting case of vitamin deficiency you should read.

Biotin deficiency is rare. Nice to know for exams though. Soooo.. I made a mnemonic. Biotin reminds me of the comic character, Tin Tin!

Biotin mnemonic

Study group discussion: A case of vitamin deficiency

Here's a vignette that I found on USMLE forums:

A 20-year-old male patient is admitted to the hospital 6 months ago following a motorcycle accident resulting in a severe closed head injury. The man has experienced recurrent fungal skin infections resistant to treatment for 1 month and severe vomiting over the last 2 days. Review of the patient's records shows he was well before the injury. He now suffers severe permanent cognitive impairment and requires continuous high-dose phenytoin therapy to manage chronic debilitating tonic-clonic seizures. The patient is resting comfortably in no apparent distress. He is unable to converse coherently. Vital signs are normal. Physical exam is striking for nearly total alopecia. A periorofacial erythematous macular rash is present along with severe seborrheic dermatitis and several truncal ringlike lesions consistent with tinea corpus infection.

Select the most likely vitamin deficiency.

Answer Choices:

A. Vitamin A deficiency

B. Vitamin B12 deficiency

C. Vitamin C deficiency

D. Vitamin D deficiency

E. Vitamin E deficiency

F. Thiamine deficiency

G. Pyridoxine deficiency

H. Folate deficiency

I. Biotin deficiency

Order of decision making

Ideally, a doctor discusses the available options of treatment with the patient, the patient makes a decision and informed consent is obtained.

However, this may not be possible on every occasion and it is the physician's responsibility to ensure that a decision is made that would be what the patient would have wanted (if the patient does not have the capacity to make the decision himself/herself).

Apoptosis genes mnemonic

Hello all :)

So we basically have bcl 2 , bcl XL, mcl-1, Bax, bak, bcl -xs genes which influence apoptosis.

Now let's imagine a cell committing suicide which is apoptosis.

Dysphagia

Hi everyone!

So, here's what I found interesting today!

Dysphagia is awareness of something sticking in the throat or retrosternally during swallowing.

Whereas, odynophagia is pain as food or drink descends the esophagus. It almost always implies an infection of esophagus e.g.candida esophagus in HIV patients.

Remember, dysphagia often has a significant cause which can be malignant and almost always needs investigation!

Can there be different patterns of dysphagia?
Yes.
It can be more for solids than liquids.
When it is rapidly progressive, look out for a malignant cause! When it's fairly less rapid in progression, suspect a benign stricture (rarely an esophageal pouch)!

Or, it can be more for liquids than solids.
This usually is the case in neurogenic dysphagia and can be sometimes associated with aspiration or coughing.

That's all!
- Rippie

Cronkhite Canada syndrome

Cronkhite Canada syndrome

Cyanosis

So, I found a few interesting things about cyanosis.

Cyanosis is bluish discolouration of skin and mucous membranes.

Reason?
It occurs when amount of reduced Hemoglobin is more than 4g/dl. (Harrison's, 19E)
Even small amounts of methemoglobin (1.5g/dl) and sulphmethemoglobin (0.5g/dl) can evoke cyanosis!
(Just remember, bigger the name lesser the amount required :P)

Types?
Central and Peripheral cyanosis

What happens in both of them?
Central cyanosis has either i) low arterial oxygen saturation or ii) abnormal Hemoglobin derivatives so skin as well as mucous membranes are involved!

Peripheral cyanosis is due to either i)increased oxygen extraction or ii)reduced amount of blood reaching periphery (simply, vasoconstriction [so you may find cold skin] or reduced cardiac output =D) so only skin is involved.

Where to check for cyanosis?
Lips, nail beds, ears and malar eminences.

Fun facts:

1. Cyanosis in heart failure can be mixed i.e. Central plus peripheral

2. "Differential cyanosis" is when lower limbs are cyanosed and NOT the upper limbs! It happened when there's a Patent Ductus Arteriosus (PDA) with Reversal of shunt!

3. So can cyanosis of only upper limbs happen? Yeah, if there's a PDA with Reversal of shunt with Transposition of great vessels!

Most interesting one:
4. In PDA with reversal of shunt with Pre-ductal coarctation of aorta all limbs except for Right Upper Limb can be cyanosed! If you're wondering why, then the answer is that if the coarctation is before the origin of left Subclavian Artery you may find its blood supply being hampered and so the cyanosis of left upper limb. Both the lower limbs get its blood supply from arteries after the level of coarctation, so it's invariably going to be cyanosed!

Quite a lot, right?
That's all!

-Rippie

Evolution, transposons, retrotransposons.

We all like to think mutation as a random occurrence, an occurrence only due to chance which is mostly harmful and may be evolutionary significant once in a blue moon.
There are actually, contrary evidences to all that. Evidences which will force us to rethink all our notions and accept Jean Baptiste Lamarck as our hero(yeah the Giraffe-neck guy).

How,do you ask? Well, we'll have to begin by learning what 'junk' DNA is. Junk DNA (better call it noncoding DNA) is a vast amount of nucleic acid lying unused in the nucleus. Actually, only 3% of the 'normal' DNA codes at a given time. Rest of it lies unused.

With me still here? Great. Now, we come to 'jumping genes' or 'transposons'. What initially was considered as a rigid blueprint, the DNA is so not like it. In fact, its a dynamic entity. Genes moving here and there, cutting,copying, and  pasting themselves within the strands.
These frisky genes are the transposons. In experiments conducted by Barbara MC Clintock, it was discovered that when corn plants were subjected to environmental stresses, the genes arranged themselves so as to confer them with a survival benefit. Yes, a sort of intentional mutation was done by the plant itself!
Later, in experiments conducted by Harvard researcher John Cairns on certain lactophobic strains of E coli, where the bacteria were deprived of all the nutrition except for lactose, it was observed that those bugs lost their milk fear rather readily, quicker than mere chance would have allowed to mess with their genetics.
Lamarck doesn't sound too stupid now, does he?!

And now, coming to the most interesting part, does all this magic occur in us, as well? Hell yeah. And wait till I mention the name of the partner in crime - Retroviruses.Yep.You read that right.
These are the viruses which can penetrate the Weissman barrier - a barrier which prevents traits acquired by the parent's somatic cells to pass to the germ cells.The idea is to prevent harmful acquired traits like radiation induced DNA damage from passing to the offspring.

Coming to viruses again,we all know how they work their charm. Using the host machinery and then in the process, sometimes ending up as a part of our own DNA- the junk DNA about which I wrote earlier.Today,it is a known fact that at least 8% of our DNA can be traced back to retroviruses. With this vast noncoding (junk) DNA, the space to play for the jumping genes opens up many folds, and hence a higher number of permutations and combinations become available for an acceptable mutation to occur.

Now what the hell are 'retrotransposons' in the title? Well, a subtype of jumping genes. Normal transposons work by cutting and pasting within the genome, while these retrotransposons are copy pasters.
But more interestingly, their work resembles very, very close to retroviruses. A retrotransposon initially copies itself on an RNA strand, travels,and uses reverse transcriptase to paste itself into a new location on the DNA strand. Does this mean retrotransposons are descended from retroviruses?! You bet!

This has led many to theorize that viruses have actually accelerated human evolution by endowing us with acres of junk DNA and retrotransposons, while we continued to provide them a warm, cozy environ. 
Some thought innit?

LDL Cholesterol- The 'bad' turns good

Hello!

Since long back, the low-density lipoproteins have been linked to high rates of cardiovascular disease and mortality! But is it really so?

USMLE STEP 1: Psychiatry: Malingering and Factitious disorders.

Hey there..! Hello..

 So whenever you come across a clinical vignette in which the patient comes with UNEXPLAINED symptoms or complaints and doesn't seem to have an actual illness, but is either faking it or creating it, the patient is either MALINGERING or has a FACTITIOUS DISORDER.

Alzheimer's due to infections?

Hey awesomites!!!
Could Alzheimers' stem from infections?

Stress and epilepsy

For epilepsy patients Stress and anxiety exacerbate the condition by increasing the frequency and severity of attacks!!

MAC prophylaxis mnemonic

Bonjour!

Mycobacterium avium complex infections need to be prevented in patients with AIDS if their CD4 cell counts are less than 50/microL.

Clinical and radiological features of rickets mnemonic

Hello!

So I had created this video long back but just realized I never uploaded it on the blog. Here it is! :)

Study group discussion: White jaundice

Can anyone explain about what is white jaundice?

I think it refers to cholestasis syndrome (obstruction of bile outflow)

Jaundice (Increased conjugated bilirubin)
Acholia (Pale stools, thus "white jaundice")
Choluria (Dark urine)
May have generalized pruritus (Due to cholesterol)

Here's what someone else wrote:

White Jaundice is not a separate disease, it is a very old term for jaundice.

Jaundice is a condition in which bilirubin, which is a yellow coloured pigment, accumulates in the body and causes the skin to turn bright yellow. In severe cases, the skin can appear brown.

To confirm that someone is jaundiced, and not just dark-skinned, the whites of the eyes are examined, yellow colouration here is a clear sign of jaundice, hence the old expression "white jaundice".

Migraines linked to Vitamin D deficiency

Hey awesomites!

A new study suggests that migraine attacks are linked to vitamin deficiencies.

The question is - 'Could supplements be the key to fight such attacks?'

Vitamin D in Type - 2 Diabetes Mellitus

Hey awesomites!

Vitamin  D has an important role in overcoming insulin resistance in type 2 diabetes. Here's how...