Mnemonico diagnostico : SLE revised 2012 diagnostic criteria

Hey Awesomites

SLICC classification criteria for Systemic Lupus Eryhtematosus mnemonic :

Step 2 CK: Which Pneumococcal Vaccine to administer & when?

FENO in asthma: routine clinical testing

Hey Awesomites

One of the additional tests for determining the present status of airways in asthmatics is the measurement of Fraction of Nitric Oxide in Expired air (FENO).

The levels of Nitric oxide are elevated in the presence of inflammation in the airways, that is eosinophilic in nature.

In children <12 years, normal FENO is usually less than 36 ppb. However, in case of allergic inflammation of airways, the levels rise to >50 ppb.

Note that FENO is not diagnostic, but a test for independent prediction of exacerbations in asthmatic patients and is now done routinely in clinical practice, as approved by US- FDA.

Thats all
- Jaskunwar Singh

Cryptococcus neoformans notes and mnemonics

Hello!

This post is on cryptococcus neoformans.

Chronic granulomatous disease mnemonic

Chronic granulomatous disease mnemonic

CGD - GRANULES!
G - chronic Granulomatous disease
R - Rhodamine (Dihydrorhodamine abnormal flow cytometry)
R - ROS, Respiratory burst decreased
A - Abscess / Granulomas
N - Nitroblue tetrazolium dye test
N - NADPH oxidase defective

Catalase positive organisms mnemonic: CATALASE!
Candida
Aspergillus
Tuberculosis
Listeria
Staphylococcus aureus
Serratia
pSeudomonas
E coli

That's all!

-IkaN

Hypersensitivity types mnemonics

Hypersensitivity types are:

Difference between polysaccharide vaccines and conjugated vaccines

Polysaccharides are strings of sugars. Some bacteria, such as Streptococcus pneumoniae and Neisseria meningitidis, have large amounts of polysaccharide on their surface, which encapsulate the bacteria. The polysaccharide capsules protect the bacteria from the host’s immune system and can make the bacteria more virulent. 

Polysaccharide vaccines are poorly immunogenic. They produce low affinity antibodies (which do not bind well to the antigen) and, because they do not elicit T-cell responses, immune memory does not develop. 

The new generation conjugate vaccines contain carrier proteins that are chemically attached to the polysaccharide antigens. Attaching relatively non-immunogenic polysaccharides to the highly immunogenic carrier proteins means that by activating a T-cell response, conjugate vaccines induce both high-affinity antibodies against the polysaccharide, and immune memory.

So in conclusion:

Polysaccharide vaccine - T cell independent B cell response

Conjugate vaccine -  Carrier proteins - T cell dependent B cell response

Mnemonic:
CT (Like a CT scan?)
ConjugaTe has a T cell response

That's all! 

-IkaN 

Brutons disease (X linked agammaglobulinemia) mnemonic

Hello! 

Guess who made a new video?

Fish oil for treatment of asthma

Hello

Asthma is a chronic, exaggerated and allergic inflammatory response in the respiratory airways to certain allergens that vary according to seasons.

Omega- 3 fatty acids in high- quality fish oils and other products reduce the inflammation by regulating B- cell function. IgE production is reduced, which otherwise acts to cause asthma symptoms and allergic reactions in patients with mild form of asthma.

The fatty acids are used up by the cells in the lining of respiratory passages to produce hormones that tend to "turn- off" certain factors responsible for attracting white blood cells to the site of inflammation such as leukotrienes, interleukins, and other cytokines.

However, these oils are less effective in severe forms of the disease and in the majority of patients taking corticosteroids.

According to a study, prenatal exposure to fish oils (mainly in third trimester) reduces the risk of wheeze and asthma in children.


Thats all
- Jaskunwar Singh

Why does cyanotic heart disease predispose to brain abscess?

Ever wondered why cyanotic heart disease predisposes to brain abscesses?

Immunohistochemistry and cytogenetics for leukemias: Part 2

Here's part 2! On Chronic myeloid, chronic lympoid and MDS!

Immunohistochemistry and cytogenetics for Non Hodgkins Lymphoma

Hello!

Immunohistochemistry and cytogenetics for leukemias: Part 1

Hello!

Psoriatic arthritis mnemonic

A simple one: PSORIATIC

P- Pencil-in-cup deformity

Pencil-in-cup deformity

S- Sausage-like digits

O- Onycholysis and Onychodystrophy

R- Rheumatoid factor negative

I- Ivory phalanx (increased bone density)

A- Arthritis multilans

T- Telescopic fingers

I- Itchy skin

C- Cold weather (more severe)

Thats all

- Jaskunwar Singh

Basics of Immunoglobulin G

Hey  readers!! ,So I have started with immunoglobulin section where I will be putting facts about a single immunoglobulin ,so today it is IgG!.

Immunoglobulin G or IgG occupies about 80% of serum antibodies.! .It's normal concentration is about 8-16mg/ml.They are created and release by plasma B cells .
There are two unique facts about IgG
1)It's catabolism.
2)Suppression of homologus antibody synthesis by a feedback process.

What's unique in catabolism?.
Well we can say body has complete control over the catabolism and to make it simpler let's say body and IgG both acts opposite to each other !.(Just a saying :p,Infact we know IgG works for body).For example In some diseases like chronic malaria ,kala azar or myeloma IgG level rises and as we know body has complete control and it acts against it So, IgG synthesis its gonna catabolised it rapidly !
Conversely,In hypogammaglobulinemia IgG given for treatment is metabolised slowly.

Suppression of homologus antibody synthesis
IgG has another unique property of suppressing the antibody synthesis which looks like it or performs similar kind of functions or simply homologus antibody.
Now let's say IgG is quite insecure about its true but dominating love -"Body". It doesn't want any competition so it kicks away all the antibodies which looks like it or perform similar function like him
(Such a insecure antibody it is  !)and this unique property is utilised in the Iso-immunisation of a women by administration of anti-Rh(D) IgG during delivery.

Well some more characteristics of our hero IgG is
It's the only maternal immunoglobulin that is transported across placenta and provides "Natural passive immunity"in new born (Not present in infants )

It has 4 subclasses due to presence of gamma 1,gamma 2 , gamma 3 and gamma 4 chains .

IgG1=65%
IgG2=23% (By the way 23 is also half life of IgG)
IgG3=8%
IgG4=4%

Here are functions of IgG molecule

Multiple sclerosis mnemonic

Hey awesomites!

Presenting to you the first post of 2017 :)

Multiple sclerosis clinical features mnemonic:

DONALD TRUMP

D- Demyelinating disease

O- Optic neuritis

N- Neuromyelitis optica

A- Autoimmune aetiology

L- Leg pain

D- Depression

T- Triad of Charcot

R- Relapsing and remitting type (most common)

U- Uhthoff's phenomenon

M- McDonald's criteria (diagnostic)

P- P100 latency of nerves (delayed)

Thats all

- Jaskunwar Singh

An AIDS patient with abnormal CT scan

Hey! Here's a case kinda thingy that I made up.

An HIV positive male presents with loss of recent memory and left sided paralysis. A CT scan is done. What are the differentials based on the CT findings given below?

1. Multiple ring enhancing lesions
2. Single, periventricular ring enhancing lesion
3. Cerebral atrophy with secondary ventricular involvement
4. Multiple non enhancing white matter lesions

Answers given below
.
.
.
.
.

1. Multiple ring enhancing lesions - Toxoplasmosis. TMP SMX for prevention!

2. Single, periventricular ring enhancing lesion - CNS lymphoma. Usually, positive for EBV.

3. Cerebral atrophy with secondary ventricular involvement - AIDS dementia complex. Though paralysis would not be a feature. Only defects in short term memory and executive function is seen.

4. Multiple non enhancing white matter lesions - Demyelination of subcortical white matter suggestive of progressive multifocal leukoencephalopathy is caused by JC virus.

That's all!
-IkaN

Pentavalent vaccines

Hey Awesomites!

Let's discuss something about the pentavalent vaccines and what advantage they have in the immunization of newborns..

Rheumatoid arthritis mnemonic

Hello!

Here's an old mnemonic on some of the clinical features of Rheumatoid arthritis.
Well, the name itself tells it.. RHEUMATOID ;p

R- Respiratory distress (Interstitial lung disease, bronchiolitis, pleural effusion)
H- Haematological manifestations (anemias, thrombocytosis, neutropenia)
E- Extra- articular RA (ExRA)
U- Urinary tract infections (mainly drug- induced)
M- Median nerve compression/ Morning stiffness
A- Amyloidosis
T- Tenosynovitis and bursitis
O- Ocular manifestations (Keratoconjunctivitis sicca, scleritis, episcleritis)
I- Immunologic manifestations (Sjogren's, Felty's and Caplan's syndrome)
D- Deformities (boutonniere, swan- neck, button- hole)

Thats all :)

- Jaskunwar Singh

Study group discussion: Rh incompatibility and ABO incompatibility

Here is some food for thought.

Think about which of the following scenario is worse:
1- Mom is O- and baby is O+ first pregnancy
2- Mom is O- and baby is O+ second pregnancy
3- Mom is O+ and baby is O+ second pregnancy
4- Mom is O+ and baby is A+ second pregnancy
5- Mom is O- and baby is A+ second pregnancy
6- Mom is O+ and baby is O- first pregnancy

Answer is 2
Rh incompatibility in second pregnancy. In presence of ABO incompatibility, Rh incompatibility, has lesser effect.

Detailed explanation:

The most common group O has anti A IgM, anti B IgM and anti AB IgG.
Group A has anti B IgM.
Group B has anti A IgM.
Group AB has no antibodies.

So if I was dumb enough to transfuse GroupyA blood to a group B guy there would be hemolysis. But what would be the mechanism for this?

The patient with group B would have anti A IgM. IgM is a very potent complement activator. IgM is very trigger itchy, it first shoots the cell and then asks questions. So this hemolysis is very fast.

Now coming to the Rh question, imagine there was a mom with O- group and baby with O+ group.

In first pregnancy, the mom is not exposed to the Rh antigen until delivery, so the 1st baby is safe. But there would be a mixture of baby and mom's blood.

Now imagine a weird person (Rh+ cell) walking through an airport, he would taken by the TSA (macrophage) for an "interrogation". So the macrophages do this interrogation (phagocytosis) in the dark corners of spleen and pick up info (antigens) about these weirdos. This info is passed to T cells and they issue warrants to B cells (IgG) for identifications of these guys and they are killed on site (IgG mediated destruction)

You can see that this will, obviously, take time time. When she gets pregnant with Rh incompatibile kid again, the IgG have been synthesized and they cross placenta and attack the baby RBC's. Voila - Hydrops fetalis.

Now imagine a mom who is O- and has a baby with A+ group. This time, at delivery, there is mixing of blood again!
But the mom has anti A IgM which is so fast like a ninja, kills of the majority of the cells before they go for their interrogation with macrophages in spleen... So ABO incompatibility actually protects against the Rh sensitization.

What's the clinical significance of Rh incompatibility?

Whenever you take care of a pregnant lady, you will confirm her blood group and if you suspect Rh incompatibility you would give her "Rh IgG" (standard dose) at 28 weeks, even though the fetal blood is not exposed to mom's immune system, this is done just in case - there might be a fall, injury etc and baby's blood may get into mom's circulation.

Why do you give Rh IgG when you want prevent the disease which is itself caused by IgG?

Rh IgG are heat treated and they cannot cross the placental barrier unlike normal IgG.

And finally, you give another dose of Rh IgG after delivery. But this time, you actually estimate the amount of fetal blood which is mixed with mom's blood by doing "Kleihauer betke test" and you give an appropriate dose.

Explained by DJ AweSpear.

Related posts:
Rh incompatibility
Hydrops fetalis
Blood group doubts
Removal of antigens from RBC's
Barts hemoglobin mnemonic