laboratory

term

http://www.alere.com/EN_US/products/alere-inratio-2-pt-inr-monitoring-system-poc-test/index.jsp

 http://www.medtechzone.com/data/sero/ANA.php







(Source: Flickr / shindodo)





moxielicious:

ABSTRACT Molecular mimicry has been proposed
as a pathogenetic mechanism for autoimmune disease,
as well as a probe useful in uncovering its etiologic
agents. The hypothesis is based in part on the
abundant epidemiological, clinical, and experimental
evidence of an association of infectious agents with
autoimmune disease and observed cross-reactivity of
immune reagents with host ‘self’ antigens and microbial
determinants. For our purpose, molecular mimicry
is defined as similar structures shared by molecules
from dissimilar genes or by their protein
products. Either the molecules’ linear amino acid sequences
or their conformational fits may be shared,
even though their origins are as separate as, for example,
a virus and a normal host–self determinant.
An immune response against the determinant shared
by the host and virus can evoke a tissue-specific immune
response that is presumably capable of eliciting
cell and tissue destruction. The probable mechanism
is generation of cytotoxic cross-reactive effector lymphocytes
or antibodies that recognize specific determinants
on target cells. The induction of cross-reactivity
does not require a replicating agent, and
immune-mediated injury can occur after the immunogen
has been removed—a hit-and-run event.
Hence, the viral or microbial infection that initiates
the autoimmune phenomenon may not be present by
the time overt disease develops. By a complementary
mechanism, the microbe can induce cellular injury
and release self antigens, which generate immune responses
that cross-react with additional but genetically
distinct self antigens. In both scenarios, analysis
of the T cells or antibodies specifically engaged in
the autoimmune response and disease provides a fingerprint
for uncovering the initiating infectious
agent.—Oldstone, M. B. A. Molecular mimicry and
immune-mediated diseases. FASEB J. 12, 1255–1265

Full Research paper here

(Source: turbulentmoxie)


The Pathology Student website

laboratorysciencereview:

Pathology student

This website has helped me a lot. I tend to get bogged down in the literature and end up taking notes on EVERYTHING which means my notes end up being as long as the chapters themselves.

However, the author of The Pathology Student really breaks stuff down to the bare essentials- very helpful in studying for board exams (or just cramming for a final). You can get a free “The Top Ten Anemias” book, and also a really awesome hemostasis book for $13.

I would HIGHLY recommend both. Even if they don’t teach you something new, they are good review materials, the hemostasis book gives good mnemonic devices for remembering stuff about the coagulation cascade, standard tests, and hemostatic disorders.

Via Laboratory Science Review


jtotheizzoe:

We were all undifferentiated, once.

(via Biocomicals)


Thrombus vs. embolus

insane-in-the-meninges:

An embolus is a blood clot that forms away from the site of occlusion and then results in a vascular occlusion.

A thrombus is a blood clot that forms at the site of vascular occlusion.

Via Insane in the Meninges
RN Charli: ITP - Idiopathic thrombocytopenia Purpura

itsjustcharli:

DEFINITION

ITP refers to an abnormally low platelet count in the blood, from an unknown cause (however most commonly due to an autoimmune response).

CAUSE

Most commonly, ITP is caused by an autoimmune response which results in the destruction of platelets, particularly in the spleen.

SIGNS AND SYMPTOMS

- Spontaneous bruising (Purpura)
- A rash-like appearance on the skin caused by tiny bruises (petechiae)
- Nose bleeds
- Bleeding gums
- Abnormal menstruation
- Haematomas/blood blisters in the mouth
- Excessive bleeding from cuts and grazes

TREATMENT

Steroids, such as dexamethasone and prednisone, are used to suppress the immune system and therefore prevent destruction of platelets. IV Ig may be used to increase platelet count and decrease bleeding risk in the short term (eg. Before surgery). Thrombopoietin may be used to increase platelet counts in the longer term. A splenectomy may be considered to reduce the destruction rate of the platelets.

Platelet transfusions are not generally given as the body is likely to destroy them. They may be given in emergency situations to prevent excessive bleeding.

CAUSE

Most commonly, ITP is caused by an autoimmune response which results in the destruction of platelets, particularly in the spleen.

SIGNS AND…

Via RN Charli


statlab:

Anon left asks about this in rapid succession, so I guess that is my cue to talk about megaloblastic anemia, haha.

Megaloblastic anemia is a non-hemolytic anemia, usually attributed to either B12 deficiency (impaired absorption because of a gastrectomy, pernicious anemia, inflammation, or transcobalamin deficiency) or Folate deficiency (dietary, drug related impairment of use, loss though kidney). Both are cofactors in DNA synthesis, especially of thymidine. The result is nuclear cytoplasmic asynchrony wherein the nucleus matures slower than the cytoplasm, and you can see all the cells are a little off looking as a result.

In your smear, you won’t see much in the way of retics, but there will be extensive hypersegmentation of neutrophils, large platelets, huge macrocytes/macroovalocytes, tear cells, schistocytes, pancytopenia, and howell-jolly bodies. A few giant bands and metamyelocytes much sneak into the circulation too. Things are generally just. Big.

The bone marrow will have very distinct megaloblastic changees. The myeloid:erythroid ratio will be decreased but the marrow is almost always hypercellular. Very early erythroid precursors predominate over late precursors because of ineffective erythropoiesis. In contrast to the comically large myeloid precursors, megakaryocytes are small and hypolobated because they have so much DNA they are affected the most by impaired synthesis. 

(Source: )


Via The Stat Lab

Creative Ethers: Antibiotic-resistant Bacteria

creativeethers:

Antibiotic-resistant Bacteria

Announcements about breakthroughs in medicine are always on the news nowadays. Pharmaceutical companies have found new ways to tackle cancer, diabetes and quite a hefty list of other chronic conditions that plague humanity. However, we are facing a growing problem that has slowly become increasingly neglected decade after decade. With huge incentives for pharmaceutical companies to deliver products that need to be taken for extended periods of time, if not always, as well as cost a premium, there is a dwindling interest in the research of new antibiotics.

Antibiotics are no longer a lucrative pursuit for most pharmaceutical companies for several reasons: they are prescribed for very short periods of time, doctors have become much more frugal in prescribing them in order to prevent the cultivation of antibiotic-resistant bacteria and they become obsolete once resistance develops. The money that drug companies could make on a new antibiotic is only a fraction of a fraction of what they could make on a new drug that prevents heart disease or increases longevity.

The present issue is that antibiotic-resistant bacteria cases grow larger and more dangerous with every passing year. New strains of antibiotic-resistant bacteria are found worldwide every year. An enzyme that makes bacteria resistant called New Delhi metallo-beta-lactamase 1(NDM-1), first found in 2008, has caused worldwide concern. A better known resistant bacteria called Methicillin-resistant Staphylococcus aureus (MRSA) is also a dominant issue today. In 2005, the CDC reported that MRSA was responsible for 19,000 deaths in the United States alone, killing more than AIDS does. The latest grave issue is a completely resistant form of tuberculosis. Gonorrhea, a previously easily treated infection since WWII, has now become almost totally drug resistant. These infections, which all could have been easily cured a few decades ago with a simple course of antibiotics, are now proving to be incredibly lethal. Such epidemics should not exist in the 21st century.

Extensive misuse of antibiotics over the past 60 years, as well as the growing use of antibiotic and other anti-microbial chemicals in our food and environment, have played a big role in cultivating these lethal strains. While doctors have grown more prudent with prescribing antibiotics to patients, this alone will not fix the problem when the chicken we eat and the cows that give us milk are given antibiotics regularly in order to maximize commercial yield by preventing illness. The FDA has already begun cracking down on the use of antibiotics in livestock this year, but more still needs to be done. While all this will decrease the likelihood that new strains will emerge, it will not do anything about the ones currently present.

It is necessary for an aggressive approach to be taken against new bacterial strains by funneling more energy and money into researching new and novel antibiotics. Government-funded research, as well as financial incentives, needs to be presented to pharmaceutical companies in order to counter the decline of effective treatment against bacterial infections. Unnecessary deaths are occurring when infections that could be easily cured with new antibiotics are given carte blanche.

This is not to say that the work that pharmaceutical companies are doing today is meaningless. The discoveries and progress they are making against diseases like cancer, AIDS and cardiovascular diseases are astounding. However, they have neglected the crucial importance of fighting bacterial infections. This has created an unnecessary, everyday danger to all individuals in society.  Hopefully, change will be made soon.

Via Creative Ethers


doortoreality:

This puts things into perspective doesn’t it?… O_o

(Source: healthy-cravings)



scientificillustration:

Escherichia coli

“This illustration shows a cross-section of a small portion of an Escherichia coli cell. The cell wall, with two concentric membranes studded with transmembrane proteins, is shown in green. A large flagellar motor crosses the entire wall, turning the flagellum that extends upwards from the surface. The cytoplasmic area is colored blue and purple. The large purple molecules are ribosomes and the small, L-shaped maroon molecules are tRNA, and the white strands are mRNA. Enzymes are shown in blue. The nucleoid region is shown in yellow and orange, with the long DNA circle shown in yellow, wrapped around HU protein (bacterial nucleosomes). In the center of the nucleoid region shown here, you might find a replication fork, with DNA polymerase (in red-orange) replicating new DNA.”

© David S. Goodsell 1999. 



mylifeasamedstudent:

Occasionally, my mind can’t take being serious and writing copious amounts of text, so instead I leave you with the first in a two part series of why they should never have let me pass pre-clinical years.

(Yes, this is what I tried to pass off as studying. Yes, I did almost fail that exam.)


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