Comprehensive review of pathology

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Dermatopathology textbook for pathologists and dermatology residents.
Link to get it provided above!!

Book is still the second best seller book in Pathology on amazon...

Second edition of "Comprehensive review of Pathology" is now the second best seller book in Pathology on amazon within two days of its launch..

Introducing second edition of Comprehensive review of Pathology.
Book will be available from 20th May onwards. Book covers all chapters of pathology in 2000 mcqs along with recent aiims and neet pg mcqs and explanations.
Book will be available on amazon and on selected book stores after 20 May 2019 or can be ordered from the publisher directly.
Dr Sonam Kumar Pruthi

2018 edition available now on https://www.amazon.in/dp/8184452047

Pattern of distribution of mcqs

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This page provides you an update of interesting Pathology topics, important points which you can learn, without opening a text book.
Beautifully crafted by Dr Alekh Verma, SR, Pathology, NDMC medical college and Hindu rao hospital, New Delhi

Pathlogos Hey there I am Dr. Alekh Verma.
This page was created to discuss the "Why's" and "How's" in Pathology along with some random fun facts in pathology ,
Feel free to ask any questions.

Thanks

Good Morning.
Yesterday, I was seeing DNB secondary Pathology Question papers, I found them very tough, a lot of molecular genetics questions were being asked
When a normal post graduate resident, have no exposure to molecular genetics, I wonder why the examiners keep on asking such questions, which look handsome only to read, but no one can memorize them, as they are not widely practiced, but unfortunately, this is our medical education system, which hinders a lot and hence, we are a lot behind than the practices followed in west, not in terms of knowledge, but in way of availability and utilization of resources

Today, I will pen down here, molecular genetics in breast cancers, recently followed criteria, because it is used presently for treatment protocol, so any physician or pathologist should be thorough with this criteria.
It is complex in all the books, you read, but I am trying to simplify it for better understanding.

Molecular sub-types of Invasive breast cancers:

1. ER (estrogen receptor)-positive, HER- negative (also termed “luminal,”):
Most common form of invasive breast cancer and is divided as:

a) Low proliferation category (40-55% of cancers):
Most common in older women & men
Most commonly diagnosed on mammography
Cured by surgery and has the lowest incidence of recurrence
Metastasis to bone (most commonly) can be seen rarely
Responds well to hormonal therapy
Shows incomplete response to chemotherapy
Examples (microscopy): Well to moderately differentiated mucinous, papillary, cribriform, and lobular carcinomas
(Pneumonic: CLuMP)

b) High proliferation (10% of cancers):
Most common type of breast carcinoma associated with BRCA2 germline mutations
10% patients responds well to chemotherapy
Includes poorly differentiated lobular carcinoma

2) HER2-positive (20% of cancers):
Second most common molecular subtype of invasive breast cancer
Can be ER +ve or ER-ve, more common in young women
Familial breast cancer patients show germline TP53 mutations (Li-Fraumeni syndrome) mutations and are positive for both ER and HER2
Trastuzumab (Herceptin), inhibits HER2 and is used for its treatment
Examples: Poorly differentiated cancers. E.g. apocrine cancers & micro papillary cancers

3) ER-negative, HER2-negative tumors (“basal-like” triple negative carcinoma; 15% of cancers):
More common in young premenopausal women
Carcinomas arising in women with BRCA1 mutations
Metastasis occurs early to bone, viscera & brain
Examples: Poorly differentiated cancers e.g. squamous cell, spindle cell, medullary, adenoid cystic, metaplastic carcinomas
(Pneumonic: MMASS)

Well, this is tough, I have not yet, discussed, the methods to interpret it and the scoring systems or FISH implications, for this entity, but as a medicine individual, this much knowledge will be handful for practice.
It is based on recent advances and recent followed criteria for its diagnosis and treatment
Thank you.. Hope you learnt something new from it.
Will come up soon, with something new. Till than enjoy reading.. Bye..

Hi, everyone on the page.
I am starting from today, conceptual discussion of pathology facts, which will make you help understand the subject a bit easy. I will try to do it on regular basis from now on.

Today I am going to start with difficult topic of "Complications of diabetes", what is responsible for the changes, which are seen in patients on long standing diabetes, Type I & II and how cell injury is brought about??
Important points to learn about this topic are:
1. In Diabetes, there are macrovascular and microvascular complications, are seen, which you must be well aware off. All this is happening because of the endothelial damage.
Now, how, this endothelial cell damage is brought about ???
2. Most important mechanisms responsible are:
a) Production of Advanced glycation end (AGE)products
b) Activation of protein kinase C and
c) Oxidative stress and disturbances in polyol pathways
How are all these bringing the damage?
1. AGE products in Diabetic patients combines with its receptor and forms R (receptor)AGE.
AGE-RAGE complex in turn activates TGF β (increased basement membrane production),VEGF (implicated in angiogenesis) and increased proliferation of vascular smooth muscle cells
All these will initiate end organ damage, in simpler terms: microangopathy, retinoapthy, nephropathy, glomerular damage, vessel wall damage, to name a few!!
2. Activation of protein Kinase C: stimulates the production of VEGF, TGF-β by the vascular endothelium, resulting in addition to the injury brought about by AGE-RAGE complex.
How is this protein kinase C (PKC) activated?
This activation of PKC is brought by increased production of Diacyl glycerol (DAG), which in turn is produced because of hyperglycemia.
3. Oxidative Stress and Disturbances in Polyol Pathways:
See the interesting sequences of the things happening under this subheading:
a) In Diabetic patients, glucose is metabolized to sorbitol by aldose reductase (and further sorbitol is reduced to fructose)
b) Aldol reductase enzyme, uses NADPH as a cofactor
If, you would have understood the cell injury chapter, when you read it, your concept about the Oxidative stress and ROS, must be clear, I hope so!!
c) NADPH is also required by enzyme glutathione reductase in a reaction that regenerates reduced glutathione (GSH)
(You must be thorough with ROS , how it damages a cell and how a normal cell counteracts its damage, which is explained well in chapter 2 robbins!!)
d) Now because of less NADPH, there will be more :"reduced GSH"
e) Increased "Reduced GSH" levels, results in increased cellular susceptibility to ROS (“oxidative stress”)
f) Thus, now in diabetes, affected cell will suffer injury from these ROS
g) Also, Sorbitol, produced from glucose, can show accumulation in the lens, resulting in cataract formation

This is how initiation of diabetic macrovascular (myocardial infarction, stroke, and lower extremity ischemia) and microvascular (diabetic retinopathy, nephropathy, and neuropathy) complications are brought about
Mechanism:: ENDOTHELIAL CELL DAMAGE.

Hope you would have understand the complex mechanism of Diabetic complications, which I have tried to explain in a simple language

If any doubts, you can post it here. Will try to clear them
Bye for now!! Read well..

Will come up soon again, with something new and important in concept building!!

Few important book stores Pan-India where book is available

The question asked in AIIMS Nov 2015, raised doubts in many minds, lets try to solve it..
Q) Not specific for iron metabolism:
a) DMT-1
b) Hepcidin
c) Ferroportin
d) Ferritin
Important points to remember:
1. Divalent metal transporter-1 (DMT1), ferroportin (FPN1), and transferrin receptors (Tfrs) in association with ferroxidases such as duodenal cytochrome B, ceruloplamin (Cp) and heme carrier protein (HCP1), are involved in the cellular membrane transportation of iron (Robbins)
2. Hepcidin acts as a key regulator of iron metabolism (Robbins)
3. Extracellular ferritin can function as an iron carrier to provide iron to cells (Pubmed article::Iron metabolism: current facts and future directions)
4. Which means all four options are correct, as they are important for iron transfer to the cells
5. Hence, answer should be None of the above
6. But, if we have to choose one option, d) Ferritin is the one to mark, as it is the storage form of iron, and least important in iron transfer and metabolism...For details..refer Q 202 & Q 68 of ch. 28 of the book..