Cortisol and eosinophils

Today, I forgot the relationship between cortisol and esosinophils. Completely screwed up a practice question because I couldn't remember it.

Now I made a mnemonic to remember this :D

Mnemonic: In hypERcortisolism, Eosinophils Reduce.

Why do corticosteroids cause eosionopenia? Why does hypocortisolism cause an increase in eosinophil count?

Fact of the day : Biopsy for atypical hyperplasia and risk of breast cancer

Hello

Women who have had breast biopsies in the recent past, that showed atypical hyperplasia, are at increased risk of breast cancer in the future. This is because of the changes in the breast that prompted the biopsies and not the biopsy itself, according to the Gail model of breast cancer risk assessment.

Moreover, high breast density (due to high fat diet and obesity) - individualised and as a modifiable risk factor itself, in combination with proliferative benign breast disease, increase the risk of cancer, but is relatively uncommon.

Source: http://jnci.oxfordjournals.org/content/105/14/1043.full.pdf

Thats all
- Jaskunwar Singh

Acute Kidney Injury due to Anticancer drugs

Hey guys, there are multiple causes of acute kidney injury in a cancer patient, namely sepsis, metastasis, tumor lysis syndrome, etc. But there is another reason which we often overlook, which is drug-induced.

1. Thrombotic microangiopathy: Associated with agents targeting vascular endothelial growth factor(VEGF), eg., Ranibizumab, Bevacizumab. These drugs also block the angiogenesis in the glomerular vasculature, such that the injured endothelium isn't replaced, leading to multiple foci of platelet aggregations just like in TTP and HUS.

2. Focal segmental glomerulosclerosis: Associated with tyrosine kinase inhibitors are the most common and are frequently associated with acute kidney injury.

3. Acute Interstitial Nephritis:
The checkpoint inhibitors ipilimumab, nivolumab, and pembrolizumab activate host T cells to enhance tumor killing by preventing tumor ligand binding to cytotoxic T-lymphocyte antigen 4 and programmed death 1 receptors, which deactivate T cells. However, this effect causes loss of self-tolerance (and perhaps tolerance to other drugs), leading to various forms of autoimmune injury, including acute interstitial nephritis, which is associated with moderate-to-advanced-stage acute kidney injury.

That's all!

-VM

Melanoma marker mnemonic

The immunohistological marker for melanoma is HMB 45.

You can remember it by remembering the gorilla named 'Harambe' (HaraMBe) of Cincinnati zoo who was in the news as he unfortunately had to be put down because a child entered his enclosure.

You can correlate melanoma's black pigment with that of Harambe's black fur.

That's​ all!

- Sushrut Dongargaonkar

Paraneoplastic Dermatoses - Bazex Syndrome.

Hello everybody,

So to continue our series on cutaneous manifestations of internal malignancies
Let's quickly learn about Bazex Syndrome.

Bazex syndrome — acrokeratosis
paraneoplastica is a paraneoplastic phenomenon associated with squamous cell carcinoma of the upper digestive tract.

Presents more commonly in Males and over the age of 40.

Presentation: Erythematous to violaceous psoriasiform plaques predominantly located in acral areas (especially the fingers, toes, nose, and helices).

Nail dystrophy, palmoplantar keratoderma, and alopecia are common.

In most patients, manifestations of Bazex syndrome precede the diagnosis of malignancy or the malignancy is diagnosed concurrently.

The lesions of Bazex syndrome are usually resistant to targeted therapies, but treatment of the neoplasm usually leads to resolution of the cutaneous findings, although not always.

Let's learn together!
-Medha!

Trastuzumab notes + mnemonic

Trastuzumab (Herceptin) is a humanized monoclonal antibody directed against the extracellular domain of the tyrosine kinase receptor HER2.

Fact of the day: Ferritin is an inflammatory disease marker

Ferritin is an acute phase reactant.

Serum ferritin arises from damaged cells, and is thus a marker of cellular damage.

Facts and Fallacies: Vitamin D link to cancer

Hey Awesomites

Vitamin D has been shown beneficial for a variety of disorders and diseases. Recent studies now suggest that those deficient in vitamin D are at a  higher risk of developing cancer compared to those with adequate levels.

Fanconis anemia mnemonic

Hello!

Here's a post on Fanconis anemia!

Fact of the day: Factors that are lost in stored blood

Hello awesomites !

What happens to blood that is stored in blood bank ?

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!

H. pylori infection : Facts and Fallacies

Here are some interesting facts about cytotoxin- associated gene A (CagA)- positive strains of H. pylori and its role in esophageal and gastric carcinoma.

- Chronic Helicobacter pylori infection results in lower gastric acid secretion by inducing atrophic gastritis, thus hinting to have an inverse association with EC.
- H. pylori infection reduces ghrelin synthesis due to loss of P/D1 cells in the fundus and body of stomach which decreases gastrointestinal motility and induces delay in gastric emptying, thus increasing the risk of GERD.
- Also the CagA positive strains induce fluctuations in the levels of somatostatin, gastrin, dopamine and other essential hormones, which might cause increased reflux symptoms and metaplastic changes in chronic cases.
- Upregulation of proinflammatory cytokines and impaired TNF-alpha levels might play a role in pathogenesis of esophageal and gastric carcinoma. Extragastric diseases such as Colorectal polyps, nonalcoholic fatty liver disease, dental caries, coronary heart disease, the parkinson's disease, and iron deficiency anemia are also associated with H pylori infection through multiple signaling pathways.

Inspite of much evidence, there have been arguments and debates on the underlying mechanisms in causing esophageal carcinoma. A meta- analytic study, on the other hand has recently concluded that CagA- positive strains of H. pylori have a protective role in EAC while there is no such clear association with ESCC.

Thats all
- Jaskunwar Singh

Acute Post-hemorrhagic anemia

Hey Awesomites

Today I am gonna talk about the Anemias of blood loss, particularly the acute cases of posthemorrhagic anemia.

The Basics- Anaemia

Hey Awesomites

"Anaemia is defined as a decrease in the level of haemoglobin due to loss of a significant amount of red blood cells which decreases the oxygen- transporting capacity of blood."

Immunohemolytic anemias part-2

Hello readers, here is the continuation of the previous topic, Immunohemolytic anemias. Today we will discuss the next two types, its more like winter special.

B) Cold agglutinin type-  Cold agglutinin derives their name from the fact that they show maximal activity at temperature lower than normal body temperature.
It is present in low titres in healthy individuals.
Physiological cold agglutinin develops naturally after birth as a result of change in expression of Red cell antigens and reacts maximally at 4°C.
While pathological cold agglutinin maximally reacts at around 28-31° C and tend to occur at very low titres.

Mnemonic is "Cold MILL"
C     -  Complement mediated hemolysis. 
         
M    -  IgM is the causative antibodies

  I     -  Cold agglutinin antibodies appear  
           transiently following Infections 
            [Mycoplasma pneumoniae, EBV,
            HIV, influenza virus, CMV]
          - I antigen is the most common
              target
           
L     - Chronic cold agglutinin AIHA is
          associated with Lymphoid 
           neoplasm
          (esp B cell neoplasm), leukemias     
           like CLL

Mechanism- IgM binds to red cell where the temperature may fall below 30°C. It agglutinates red cells, and fixes complement rapidly. As blood recirculates and warms, IgM is released,but sufficient deposition of complements leads to phagocytosis of affected red cells in spleen, liver, bone marrow.

Clinical presentation- Exerts their pathological effects either via hemolysis and red cell destruction in RE system predominantly liver or by vaso occlusion due to agglutination.
-Mild anemia, purplish discoloration of fingers, toes, earlobes [ Acrocyanosis],  mild hepatospleenomegaly,
Raynaud phenomenon in peripheral cold exposed parts.

C) Cold hemolysin type -
Also known as paroxysmal cold hemoglobinuria.
It's a rare fatal disorder causing intravascular hemolysis and hemoglobinuria when auto antibodies binds to P blood group antigens in cool, peripheral regions of body.

Paroxysmal Cold HemoGlobinuria:
P- P blood group antigens
C- Complement mediated lysis occurs.

    IgGs auto antibodies binds to red cell in  
    cool peripheral regions, Complement
    mediated lysis occurs when affected
    red cell recirculates to warm regions,
    because complement cascade 
    functions
    more efficiently at 37°C

H- Hemoglobinuria
G - Auto antibodies belong to class IgG

Symptoms of the patients aggravates on exposure to cold.

Winter is coming, we know what's coming with it.
Stay warm :)

Immunohemolytic anemias part-1

Hello awesomites!
This is my very first post, so am starting with my favorite subject Hematology.
Today's post is about Immunohemolytic anemias, commonly ignored type of anemia

Also referred as Autoimmune hemolytic anemias(AIHA)
Where antibodies are responsible for premature destruction of red blood cell.
Types- warm antibody type
            - cold agglutinin type
            - cold hemolysin type

Warm antibody type  -  It is the most common type of AIHA.
you can remember it by mnemonic
" WARM GRILLED "
W - Warm because, antibodies are active  
       at 37°C
A -  Associated with other Autoimmune        
       disorders ( secondary causes like 
       SLE)
R - Red cell hemolysis is mainly
      extravascular
M- Moderate spleenomegaly due to
       hyperplasia of splenic phagocytes      

G- Ig G class - most common causative
      antibodies ( IgA sometimes too)

R- Rh blood group antigens are the main
      target 
I- 50% primary cases are  Idiopathic
       Secondary causes can be

L- Lymphoid neoplasm

ED-  Exposure to Drugs.
Examples - penicillin, cephalosporins, quinidine, methyl dopa etc

Mechanism - A) Antigenic drugs-
Drugs such as penicillin binds to red cell membrane and they are recognized by the antidrug antibody. The antibody either recognizes the drug and bind to it or both drug and membrane protein,ultimately results in hemolysis.

B) Tolerance breaking drugs- In drugs such as methyl dopa, antibodies are formed against red cell antigens particularly Rh antigens.

Stay awesome✌️

Top 10 series: Methotrexate

Hello!
Here are top 10 facts about methotrexate!

LAP score

Leukocyte Alkaline Phosphatase score is used to differentiate a reactive process from chronic myelogenous leukemia. Here I  just mention the conditions with high and low LAP score (not a mnemonic this time :p )

High lap score:
- Neutrophilia ( as in bacterial infections)
- Polycythemia vera (neoplasm of bone marrow)
- Blast phase of XML
- Hodgkin's disease
- Leukemoid reactions
- in newborns, children and pregnancy.

Low lap score:
- Chronic Myelogenous leukaemia (chronic phase)
- Paroxysmal nocturnal hemoglobinuria
- Hereditary hypophosphatasia


That's all
Happy Medicowesome :)

- Jaskunwar Singh