Diary of a medical scientist

microaerophilic:

so… uh, I think I found your problem.

patient with a white count of around 140,000/uL. normal range is about 4500-11,000/uL… our cutoff for a critical value is 40,000/uL so this is pretty high.

possibly a case of chronic lymphocytic leukemia since there weren’t any immature cells that I noticed, but 95% lymphocytes and several smudge cells (the purple amorphous blobs without any blue cytoplasm).

usmlenotes:

Deep-vein-thrombosis-mnemonic!

usmlenotes:

Deep-vein-thrombosis-mnemonic!

ah-thenah:

Thrombotic Thrombocytopenic Purpura

Thrombotic Thrombocytopenic Purpura (TTP) is a rare blood disorder characterized by clotting in small blood vessels of the body (thromboses), resulting in a low platelet count. In its full-blown form, the disease consists of the pentad of microangiopathic hemolytic anemia, thrombocytopenic purpura, neurologic abnormalities, fever, and renal disease.”

Image 1: Peripheral smear from a patient with thrombotic thrombocytopenic purpura: Red blood cells are fragmented and appear as schistocytes. Certain schistocytes have the appearance of helmet cells (H). Spheroidal cells often are present (S). Occasional nucleated erythroid precursors may be present.

Image 2: A small platelet-fibrin thrombus is seen in a glomerular capillary above the arrow. This occurred in a patient with thrombotic thrombocytopenic purpura (TTP). This rare coagulopathy mainly affects kidneys, heart, and brain with small arteriolar thrombi. Acute renal failure can occur. The classic pentad of fever, acute renal failure, neurologic changes, thrombocytopenia, and microangiopathic hemolytic anemia is often present.

Sources: [x] [x]

mynotes4usmle:

WARFARIN-INDUCED SKIN NECROSIS
Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of its development.[3]:122 Heparin-induced necrosis can develop both at sites of localinjection and - when infused intravenously - in a widespread pattern.[3]:123
In warfarin’s initial stages of action, inhibition of protein C and Factor VII is stronger than inhibition of the other vitamin K-dependent coagulation factors II, IX and X. This results from the fact that these proteins have different half-lives: 1.5 to six hours for factor VII and eight hours for protein C, versus one day for factor IX, two days for factor X and two to five days for factor II. The larger the initial dose of vitamin K-antagonist, the more pronounced these differences are. This coagulation factor imbalance leads to paradoxical activation of coagulation, resulting in a hypercoagulable state and thrombosis. The blood clots interrupt the blood supply to the skin, causing necrosis. Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels, it can lead to massive thrombosis with necrosis and gangrene of limbs.
Notably, the prothrombin time (or international normalized ratio, INR) used to test the effect of coumarins is highly dependent on factor VII, which explains why patients can have a therapeutic INR (indicating good anticoagulant effect) but still be in a hypercoagulable state.[1]
In one third of cases, warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C. The condition is related to purpura fulminans, a complication in infants with sepsis (blood stream infection) which also involves skin necrosis. These infants often have protein C deficiency as well. There have also been cases in patients with other deficiency, including protein S deficiency,[6][7] activated protein C resistance (Factor V Leiden)[8] and antithrombin III deficiency.[9]
Although the above theory is the most commonly accepted theory, others believe that it is a hypersensitivity reaction or a direct toxic effect.[1]

mynotes4usmle:

WARFARIN-INDUCED SKIN NECROSIS

Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of its development.[3]:122 Heparin-induced necrosis can develop both at sites of localinjection and - when infused intravenously - in a widespread pattern.[3]:123

In warfarin’s initial stages of action, inhibition of protein C and Factor VII is stronger than inhibition of the other vitamin K-dependent coagulation factors IIIX and X. This results from the fact that these proteins have different half-lives: 1.5 to six hours for factor VII and eight hours for protein C, versus one day for factor IX, two days for factor X and two to five days for factor II. The larger the initial dose of vitamin K-antagonist, the more pronounced these differences are. This coagulation factor imbalance leads to paradoxical activation of coagulation, resulting in a hypercoagulable state and thrombosis. The blood clots interrupt the blood supply to the skin, causing necrosis. Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels, it can lead to massive thrombosis with necrosis and gangrene of limbs.

Notably, the prothrombin time (or international normalized ratio, INR) used to test the effect of coumarins is highly dependent on factor VII, which explains why patients can have a therapeutic INR (indicating good anticoagulant effect) but still be in a hypercoagulable state.[1]

In one third of cases, warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C. The condition is related to purpura fulminans, a complication in infants with sepsis (blood stream infection) which also involves skin necrosis. These infants often have protein C deficiency as well. There have also been cases in patients with other deficiency, including protein S deficiency,[6][7] activated protein C resistance (Factor V Leiden)[8] and antithrombin III deficiency.[9]

Although the above theory is the most commonly accepted theory, others believe that it is a hypersensitivity reaction or a direct toxic effect.[1]

Hi! I'm currently studying medical science in australia and i was wondering what's it like working in the hospital laboratory? did you have to do an honours degree because I was told that a bachelor degree is not enough to get a job because in australia a medical scientist occupation is not very stable due to lack of government funding. I intend to get into medicine so research is my backup. nice to meet you by the way!

Hi!
I’m not sure of the system in place in Australian hospitals, but in Ireland you would need an honours degree which has been accredited by the Academy of Medical Laboratory Science. You also need to have completed clinical rotations in an approved hospital before you can work as a medical scientist in a hospital. It’s important to note that you don’t need to do the rotations to work in industrial laboratories, though. The placement in a hospital is only needed if you plan on working on human diagnostic specimens.
I’m sorry if that’s not helpful, it’s just the way it worked out here for me. I must say that I love working where I do. I have been working in a histopathology lab now for almost 2 years and it has been far from boring. There is always something to learn - even people in their late 50s are still doing courses and progressing their careers! Some are even doing histodissection :)

If you want to ask anything else, feel free. I hope my personal experience has helped in some way!

How do lactose intolerant people while they are babies drink mothers milk ?
Anonymous

Lactose intolerance usually occurs after a baby has been weaned from breast milk to solid food, so it’s usually not a problem. It’s caused by a lack of lactase persistence alleles in their lactase gene. There is, however, a very small population with a condition called congenital lactase deficiency, where they are born without the ability to metabolise lactose in milk. They would not be able to consume the mother’s milk without the typical symptoms of lactose intolerance.

neurosciencestuff:

The anatomy of fear: Understanding the biological underpinnings of anxiety, phobias and PTSD 
Fear in a mouse brain looks much the same as fear in a human brain.
When a frightening stimulus is encountered, the thalamus shoots a message to the amygdala — the primitive part of the brain — even before it informs the parts responsible for higher cognition. The amygdala then goes into its hard-wired fight-or-flight response, triggering a host of predictable symptoms, including racing heart, heavy breathing, startle response, and sweating.
The similarities of fear response in the brains of mice and men have allowed scientists to understand the neural circuitry and molecular processes of fear and fear behaviors perhaps better than any other response. That understanding has spurred breakthroughs in treatments for psychiatric disorders that are underpinned by fear.
Anxiety disorders are one of the most common mental illnesses in the country, with nearly one-third of Americans experiencing symptoms at least once during their lives. There are generalized anxiety disorders and fear-related disorders, which include panic disorders, phobias, and post-traumatic stress disorder (PTSD).  
Emory psychiatrist and researcher Kerry Ressler is on the front lines of fear-disorder research. In his lab at Yerkes National Primate Research Center, he studies the molecular and cellular mechanisms of fear learning and extinction in mouse models. At Grady Memorial Hospital, he investigates the psychology, genetics, and biology of PTSD. And through the Grady Trauma Project, he works to draw attention to the problem of inner city intergenerational violence.
"If you look at Kerry’s work, it can seem like it’s all over the place — he’s got so many studies going on, and he collaborates with so many other scientists," says Barbara Rothbaum, associate vice chair of clinical research in psychiatry and director of the Trauma and Anxiety Recovery Program at Emory. "But they are all pieces to the same puzzle. All his work, from molecular to clinical to policy, fits together and starts telling a story." A Howard Hughes Medical Institute investigator, Ressler was recently elected to the Institute of Medicine — one of the highest honors in the fields of health and medicine. He was named a member of a new national PTSD consortium led by Draper Laboratory. And he recently appeared on the Charlie Rose show’s brain series.
Panic attacks seem to tie the fear-related disorders together, he explained on Charlie Rose. Everyone experiences fear, which evolved as a survival mechanism, but it only rises to a clinical level when people are unable to function normally in the face of it. For instance, PTSD includes not only intrusive thoughts, memories, nightmares, and startle responses, but also the concept of avoidance, which may extend to other areas of the individual’s life.
"There’s a patient I’ve seen who was attacked in a dark alley," Ressler shared on the show. "Initially it just felt dangerous to go out at night, but after a while she grew afraid of men and couldn’t go to that part of town. Then she couldn’t leave her house, and finally, her bedroom. The world got more and more dangerous."

neurosciencestuff:

The anatomy of fear: Understanding the biological underpinnings of anxiety, phobias and PTSD

Fear in a mouse brain looks much the same as fear in a human brain.

When a frightening stimulus is encountered, the thalamus shoots a message to the amygdala — the primitive part of the brain — even before it informs the parts responsible for higher cognition. The amygdala then goes into its hard-wired fight-or-flight response, triggering a host of predictable symptoms, including racing heart, heavy breathing, startle response, and sweating.

The similarities of fear response in the brains of mice and men have allowed scientists to understand the neural circuitry and molecular processes of fear and fear behaviors perhaps better than any other response. That understanding has spurred breakthroughs in treatments for psychiatric disorders that are underpinned by fear.

Anxiety disorders are one of the most common mental illnesses in the country, with nearly one-third of Americans experiencing symptoms at least once during their lives. There are generalized anxiety disorders and fear-related disorders, which include panic disorders, phobias, and post-traumatic stress disorder (PTSD).  

Emory psychiatrist and researcher Kerry Ressler is on the front lines of fear-disorder research. In his lab at Yerkes National Primate Research Center, he studies the molecular and cellular mechanisms of fear learning and extinction in mouse models. At Grady Memorial Hospital, he investigates the psychology, genetics, and biology of PTSD. And through the Grady Trauma Project, he works to draw attention to the problem of inner city intergenerational violence.

"If you look at Kerry’s work, it can seem like it’s all over the place — he’s got so many studies going on, and he collaborates with so many other scientists," says Barbara Rothbaum, associate vice chair of clinical research in psychiatry and director of the Trauma and Anxiety Recovery Program at Emory. "But they are all pieces to the same puzzle. All his work, from molecular to clinical to policy, fits together and starts telling a story." A Howard Hughes Medical Institute investigator, Ressler was recently elected to the Institute of Medicine — one of the highest honors in the fields of health and medicine. He was named a member of a new national PTSD consortium led by Draper Laboratory. And he recently appeared on the Charlie Rose show’s brain series.

Panic attacks seem to tie the fear-related disorders together, he explained on Charlie Rose. Everyone experiences fear, which evolved as a survival mechanism, but it only rises to a clinical level when people are unable to function normally in the face of it. For instance, PTSD includes not only intrusive thoughts, memories, nightmares, and startle responses, but also the concept of avoidance, which may extend to other areas of the individual’s life.

"There’s a patient I’ve seen who was attacked in a dark alley," Ressler shared on the show. "Initially it just felt dangerous to go out at night, but after a while she grew afraid of men and couldn’t go to that part of town. Then she couldn’t leave her house, and finally, her bedroom. The world got more and more dangerous."