A 2nd year RN who just started work in the ED. This blog is nursing info, humor, healthcare, and medical science related. Some images and stories may be graphic and/or hilarious.

Background Illustrations provided by: http://edison.rutgers.edu/
Reblogged from starsaremymuse  9,787 notes
sixpenceee:

Schizophrenia: patients usually have less brain tissue
Major Depression: scans show less brain activity in depressed brain
Alzheimer’s: brain tissue significantly shrinks, hippocampus is usually the first region to go
ADHD: less brain activity in the frontal cortex (area associated with decision making) 
OCD: high brain activity 
Post Traumatic Stress Disorder (PTSD): hippocampal volume reduction (area involved in memory) and increased activation of the amygdala (area involved in emotional responses) 

sixpenceee:

  • Schizophrenia: patients usually have less brain tissue
  • Major Depression: scans show less brain activity in depressed brain
  • Alzheimer’s: brain tissue significantly shrinks, hippocampus is usually the first region to go
  • ADHD: less brain activity in the frontal cortex (area associated with decision making) 
  • OCD: high brain activity 
  • Post Traumatic Stress Disorder (PTSD): hippocampal volume reduction (area involved in memory) and increased activation of the amygdala (area involved in emotional responses) 
Reblogged from medresearch  55 notes
medresearch:

Metabolic Enzyme Stops Progression of Most Common Type of Kidney Cancer
"In an analysis of small molecules called metabolites used by the body to make fuel in normal and cancerous cells in human kidney tissue, a research team from the Perelman School of Medicine at the University of Pennsylvania identified an enzyme key to applying the brakes on tumor growth. The team found that an enzyme called FBP1 – essential for regulating metabolism – binds to a transcription factor in the nucleus of certain kidney cells and restrains energy production in the cell body. What’s more, they determined that this enzyme is missing from all kidney tumor tissue analyzed. These tumor cells without FBP1 produce energy at a much faster rate than their non-cancer cell counterparts. When FBP1 is working properly, out-of-control cell growth is kept in check.”
Funding:This work was supported by the Howard Hughes Medical Institute, and the National Cancer Institute (CA104838).
Read more

medresearch:

Metabolic Enzyme Stops Progression of Most Common Type of Kidney Cancer

"In an analysis of small molecules called metabolites used by the body to make fuel in normal and cancerous cells in human kidney tissue, a research team from the Perelman School of Medicine at the University of Pennsylvania identified an enzyme key to applying the brakes on tumor growth. The team found that an enzyme called FBP1 – essential for regulating metabolism – binds to a transcription factor in the nucleus of certain kidney cells and restrains energy production in the cell body. What’s more, they determined that this enzyme is missing from all kidney tumor tissue analyzed. These tumor cells without FBP1 produce energy at a much faster rate than their non-cancer cell counterparts. When FBP1 is working properly, out-of-control cell growth is kept in check.”

Funding:This work was supported by the Howard Hughes Medical Institute, and the National Cancer Institute (CA104838).

Read more

Reblogged from scienceyoucanlove  223 notes
jewsee-medicalstudent:

Sofosbuvir is now totally free in Italy.
Sofosbuvir is a drug used to treat Hepatitis C infection and it is effective in 90 percent of patients. It inhibits the RNA polymerase that the hepatitis C virus (HCV) uses to replicate its RNA. 
Its price was quoted in various media sources as $84,000 to $168,000 for a course of treatment in the U.S. and £35,000 for 12 weeks in the UK.
Sofosbuvir is, from today, totally free in Italy for patients with most critical conditions (cirrhosis of the liver or post transplantation).

jewsee-medicalstudent:

Sofosbuvir is now totally free in Italy.

Sofosbuvir is a drug used to treat Hepatitis C infection and it is effective in 90 percent of patients. It inhibits the RNA polymerase that the hepatitis C virus (HCV) uses to replicate its RNA.

Its price was quoted in various media sources as $84,000 to $168,000 for a course of treatment in the U.S. and £35,000 for 12 weeks in the UK.

Sofosbuvir is, from today, totally free in Italy for patients with most critical conditions (cirrhosis of the liver or post transplantation).

Reblogged from nurseeyeroll  13 notes
Hi Nurse Eye Roll! So I just graduated in May and passed my boards in the beginning of July. Now I'm looking for a job and feel like I've applied EVERYWHERE with no response. Any recommendations for the meantime as I am steadily losing faith? Thanks, Laura

nurseeyeroll:

Hi there!  I recommend reading a post I did about a year ago when someone else was having the same delimma.  Unfortunately, it’s kind of common now.  Let me know if this answers your question!

http://www.nurseeyeroll.com/new-grads-2/i-graduated-now-what/

Reblogged from cacajao  169 notes
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]