This is a medical logbook.
Serving the Tumblr community with fresh medical info, anecdotes and answers.

It is maintained by:
Arturo C.
and
Heber R.

16th January 2012

Photo reblogged from Catch for Us the Foxes with 3,095 notes


“it was trapped between two lungs”

“it was trapped between two lungs”

Source: audiocolour

4th January 2012

Photo reblogged from Under The Microscope with 47 notes

micro-scopic:

Thyroid, Human (H&E stain)

micro-scopic:

Thyroid, Human (H&E stain)

15th December 2011

Photo with 7 notes

An unidentified fungi - picked from bread mold.
Some of these can cause disease, specially if you have immune-issues (as in AIDS).

An unidentified fungi - picked from bread mold.

Some of these can cause disease, specially if you have immune-issues (as in AIDS).

Tagged: micologymedicine

15th December 2011

Photo with 34 notes

From left to right: T. saginata, Ascaris lumbricoides and Fasciola hepatica.
Some of the many parasites that can live inside us - some causing disease.

From left to right: T. saginata, Ascaris lumbricoides and Fasciola hepatica.

Some of the many parasites that can live inside us - some causing disease.

Tagged: parasitologymedicine

8th December 2011

Photo reblogged from Medical School with 71 notes

medicalschool:

Woven bone is the primitive bone first laid down during fracture repair  or new bone formation. It consists of a higher percentage of osteocytes  than normal. The gross structure is highly disorganized and thus much  weaker. It is eventually replaced by concentrically organized lamellar  bone with much lower proportions of osteocytes. The histology slide  shown demonstrates woven bone arising directly from surrounding  mesenchymal tissue.

medicalschool:

Woven bone is the primitive bone first laid down during fracture repair or new bone formation. It consists of a higher percentage of osteocytes than normal. The gross structure is highly disorganized and thus much weaker. It is eventually replaced by concentrically organized lamellar bone with much lower proportions of osteocytes. The histology slide shown demonstrates woven bone arising directly from surrounding mesenchymal tissue.

30th November 2011

Photo reblogged from Biomedical Ephemera, or: A Frog for Your Boils with 45 notes

biomedicalephemera:

Taenia solium, 1-10
1-3. Eggs and embryos of Taenia solium
4. Cysticercus cellulosae in the flesh
5. The same, six weeks after feeding a pig with Taenia solium
6. The same, in the retina of a human eye
Taenia mediocanellata, 11-16
Echinococcus scolicipariens, 17-19
On Animal and Vegetable Parasites of the Human Body. Translated by Edwin Lankester,1857. 

biomedicalephemera:

Taenia solium, 1-10

1-3. Eggs and embryos of Taenia solium

4. Cysticercus cellulosae in the flesh

5. The same, six weeks after feeding a pig with Taenia solium

6. The same, in the retina of a human eye

Taenia mediocanellata, 11-16

Echinococcus scolicipariens, 17-19

On Animal and Vegetable Parasites of the Human Body. Translated by Edwin Lankester,1857.
 

22nd March 2011

Photo reblogged from White Coat with 68 notes

white-coat:

And then there’s Loa Loa, who is much like guinea worm but has a nice affinity for your conjunctiva. Transmitted by a host of different fleas, people who experience Loa Loa come to the doctor complaining of seeing something move in their eye.

white-coat:

And then there’s Loa Loa, who is much like guinea worm but has a nice affinity for your conjunctiva. Transmitted by a host of different fleas, people who experience Loa Loa come to the doctor complaining of seeing something move in their eye.

18th March 2011

Photo reblogged from articulo mortis with 81 notes

25th February 2011

Photo reblogged from Medical State of Mind with 6,337 notes

Dissection of neck next friday. I’m anxious…

Dissection of neck next friday. I’m anxious…

Tagged: heber

20th February 2011

Photo with 34 notes

Ataxia Telangiectasia
So we were studying the different ways our DNA can mutate and, pretty much, kill us. One of them is the ionizing rays (viz. X-rays, gamma-rays, cosmic rays) which induce big changes in our chromosome structure, including deletions, duplications, inversions and translocations of our DNA. Other of them, non-ionizing rays which is basically UV rays may not change that much our DNA, but it may be absorbed by many of our molecules on our DNA altering them.
What happens if son ionizing radiation comes and alters the DNA that produces the ATM protein? Well, we get Ataxia Telangiectasia. The Ataxia Telangiectasia Mutated (ATM) protein avoids, indeed, this disease. The gene located in the chromosome 11 in q23 produces ATM, which regulates many other proteins, which are pretty important for our body: protein p53, CHK2, H2AX which are tumor suppressors.
In overview, the absence or malfunctioning of ATM alters the normal apoptosis of cells, the normal mitotic division and the DNA repairs processes. Then, what happens next? Well, Ataxia Telangiectasia “attacks” primarly the cerebellum, making it smaller and thus reducing coordination of movements. That sign is called Ataxia. Then it goes to our vessels and makes them bigger, specially the ones in the whites of the eyes, cheeks and nose, this is called Telangiectasia, which isn’t dangerous at all, those vessels won’t hurt and won’t burst.
Besides from these: people with A-T may develop cancer and tumors pretty easily. That’s why they should never be exposed to x-rays, only if it is crucially needed. Pulmonary cancer or infections, lymphomas and leukemia are the mayor cause of death among the people with A-T.

Ataxia Telangiectasia

So we were studying the different ways our DNA can mutate and, pretty much, kill us. One of them is the ionizing rays (viz. X-rays, gamma-rays, cosmic rays) which induce big changes in our chromosome structure, including deletions, duplications, inversions and translocations of our DNA. Other of them, non-ionizing rays which is basically UV rays may not change that much our DNA, but it may be absorbed by many of our molecules on our DNA altering them.

What happens if son ionizing radiation comes and alters the DNA that produces the ATM protein? Well, we get Ataxia Telangiectasia. The Ataxia Telangiectasia Mutated (ATM) protein avoids, indeed, this disease. The gene located in the chromosome 11 in q23 produces ATM, which regulates many other proteins, which are pretty important for our body: protein p53, CHK2, H2AX which are tumor suppressors.

In overview, the absence or malfunctioning of ATM alters the normal apoptosis of cells, the normal mitotic division and the DNA repairs processes. Then, what happens next? Well, Ataxia Telangiectasia “attacks” primarly the cerebellum, making it smaller and thus reducing coordination of movements. That sign is called Ataxia. Then it goes to our vessels and makes them bigger, specially the ones in the whites of the eyes, cheeks and nose, this is called Telangiectasia, which isn’t dangerous at all, those vessels won’t hurt and won’t burst.

Besides from these: people with A-T may develop cancer and tumors pretty easily. That’s why they should never be exposed to x-rays, only if it is crucially needed. Pulmonary cancer or infections, lymphomas and leukemia are the mayor cause of death among the people with A-T.

Tagged: diseaseshebermedicineadnmutations

5th February 2011

Video with 11 notes

I’ve been thinking a lot about my medical specialty after the med school and this is one of the processes that move my inner self. I actually can’t lecture or hold a class about this right now! But it’s one of the topics that I’m widely exited about in my medical career.

Tagged: arturo

Source: youtube.com

5th February 2011

Photo with 56 notes

Duchenne Muscular Dystrophy
It has been a week since med-school began. First semester seems to be saturated with information of many classes, but in one of them, Biochemistry, we studied one interesting disease that’s related to the cell structure.
Duchenne Muscular Dystrophy (DMD) was the topic to study and then talk about in the classroom. It is an X-chromosome-recessive-related disease where a mutation in one of the genes (actually, the biggest one) causes our cells to stop producing dystrophin which has an important role in our body.
This protein, dystrophin, is the link between the cell’s cytoskeleton and the cell membrane (sarcolemma) in the muscle cells. It gives a strong structure in the cell to undergo the stress of movement.
What would happen if we don’t have it? The cell membrane loses stability and may leak it’s contents, or other fluids like water may enter and burst the mitochondria. In any of the cases, the muscle cell dies and is replaced with adipose cells or fiber cells, thus, removing the functionality of a muscle.
DMD is progressive. It gets worst every day. Since it is a X-recessive-related disease, women only carries the bad gene and men suffer the pathology. Children from 3 years old and on start to develop muscle weakness, they’ll show what’s called the “Gower’s sign”; later, from 6 to 7 years old the child will hardly walk, needing a chair-wheel sometimes, then, from 12 years and on will need it always and may encounter cardiovascular, respiratory and digestive problems because the muscles in those systems may stop working. No coughing, because of the weak diaphragm will cause a pneumonia; a weak heart may cause a mind’s activity loss, and finally, it is expected to live until the 20s.
Isn’t it amazing how a simple malfunction in the cell, the loss of a protein, causes all of that?

Duchenne Muscular Dystrophy

It has been a week since med-school began. First semester seems to be saturated with information of many classes, but in one of them, Biochemistry, we studied one interesting disease that’s related to the cell structure.

Duchenne Muscular Dystrophy (DMD) was the topic to study and then talk about in the classroom. It is an X-chromosome-recessive-related disease where a mutation in one of the genes (actually, the biggest one) causes our cells to stop producing dystrophin which has an important role in our body.

This protein, dystrophin, is the link between the cell’s cytoskeleton and the cell membrane (sarcolemma) in the muscle cells. It gives a strong structure in the cell to undergo the stress of movement.

What would happen if we don’t have it? The cell membrane loses stability and may leak it’s contents, or other fluids like water may enter and burst the mitochondria. In any of the cases, the muscle cell dies and is replaced with adipose cells or fiber cells, thus, removing the functionality of a muscle.

DMD is progressive. It gets worst every day. Since it is a X-recessive-related disease, women only carries the bad gene and men suffer the pathology. Children from 3 years old and on start to develop muscle weakness, they’ll show what’s called the “Gower’s sign”; later, from 6 to 7 years old the child will hardly walk, needing a chair-wheel sometimes, then, from 12 years and on will need it always and may encounter cardiovascular, respiratory and digestive problems because the muscles in those systems may stop working. No coughing, because of the weak diaphragm will cause a pneumonia; a weak heart may cause a mind’s activity loss, and finally, it is expected to live until the 20s.

Isn’t it amazing how a simple malfunction in the cell, the loss of a protein, causes all of that?

Tagged: dmddiseasesduchennemedicineheber

28th January 2011

Photo reblogged from Medical State of Mind with 73 notes

medicalstate:

Ascaris lumbricoides.
This did not sit well during  lecture. This is a parasite, specifically a kind of intestinal helminth.  You can get this parasite inside of you by ingesting contaminated foods  laced with its eggs. The larvae hatch from the eggs in your small  intestine and then proceed to enter your blood stream to reach the  lungs, where they grow in the alveoli. When matured, they move up the  bronchus, causing coughing and swallowing of the larvae where they  eventually mature into adults in your large intestine.
The adults  can get up to 20-30cm in length. For most people this infection is  asymptomatic, but if there is large numbers of matured ascaris in your  colon, you can get obstruction and that can get nasty really fast. Just imagine a plumbing pipe clogged with lots and lots of hair. With that last description and the above imagery, I may have ruined spaghetti for you forever.

Interesting. How come something can grow that big… and we don’t notice anything about it? Even parasites have evolved to success in survival. And a extra tip: avoid eating on poor hygienic places to avoid this kind of infection and parasites.

medicalstate:

Ascaris lumbricoides.

This did not sit well during lecture. This is a parasite, specifically a kind of intestinal helminth. You can get this parasite inside of you by ingesting contaminated foods laced with its eggs. The larvae hatch from the eggs in your small intestine and then proceed to enter your blood stream to reach the lungs, where they grow in the alveoli. When matured, they move up the bronchus, causing coughing and swallowing of the larvae where they eventually mature into adults in your large intestine.

The adults can get up to 20-30cm in length. For most people this infection is asymptomatic, but if there is large numbers of matured ascaris in your colon, you can get obstruction and that can get nasty really fast. Just imagine a plumbing pipe clogged with lots and lots of hair. With that last description and the above imagery, I may have ruined spaghetti for you forever.

Interesting. How come something can grow that big… and we don’t notice anything about it? Even parasites have evolved to success in survival. And a extra tip: avoid eating on poor hygienic places to avoid this kind of infection and parasites.

Tagged: heberdiseases

20th January 2011

Photo reblogged from White Coat with 19 notes

white-coat:

Flexor Withdrawl Reflex - classic example of a spinal reflex. what does that mean? your brain is not required for the body to sense injury and pull your hand away.

white-coat:

Flexor Withdrawl Reflex - classic example of a spinal reflex. what does that mean? your brain is not required for the body to sense injury and pull your hand away.

Tagged: human bodyheber

10th January 2011

Link

White Coat: So you wanna go to med school →

Lately I’ve been receiving a lot of inquiries about advice for getting into med school. Really, it boils down to the same generic advice everyone gives, but I’ll shed some light on the admissions process from my experience.

1.) Take school seriously. You don’t need a 4.0 to go to medical school….

The conditions to enter a med-school in México aren’t very different from the US. There are very good schools and there are the not so much. Even the later ones are saturated of applicants (basically the private small ones), and speaking of the good ones, the spots are extremely low.

Your resources to be accepted in any medical school in México are three:

  • High-school final grade.
  • Results in the admission test (varies between universities, not like in the US that has an almost universal SAT)
  • Extra-help (like money, important people and other non-legit ways to get in) 

If you’re missing one of these, your chances of getting in are reduced quite a bit. But it’s not impossible, anyway; if you effort enough to get high grades in high-school, maybe you won’t need a high score in the admission test or extra-help at all. 

Now, if you have enough money to enter a private university like the UVM or ITESM, go ahead, the selection processes for those universities aren’t as hard as the ones in public universities. 

The link above has more information, useful even for mexicans. Furthermore, I’d like to add something up:

Don’t get dismayed if you fail once, or twice, or even thrice. If your dream is to be a doctor, by whatever your reasons are, don’t give up, don’t change your mind if you don’t want to. It’s hard to get in, it’s hard to get out. But at the end, everything will be worthwhile, even in the middle of your second year in med-school: all the knowledge you’re getting has a tremendous value.

Tagged: medhebermexicomedicina