Silly stories, words, and images in the life of a medical student and her friends


Photo

Jul 28, 2014
@ 8:45 am
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518 notes

erratic-emedicine:

erratic-emedicine:

This diagram shows how the mechanics of the heart co-ordinate with the heart sounds and the ECG (EKG).
By keeping this diagram in mind, it can make identifying murmurs much easier, by taking the pulse whilst auscultating.  
The pulse represents the maximum arterial pressure, which as you can see in the diagram occurs in between heart sounds 1 and 2. Once you have identified which heart sound is which, you can more easily identify systole, and diastole, and describe with greater accuracy the nature of a murmur if present. 


Murmur Murmur
Here’s some causes of murmur patterns:
Ejection Systolic Murmurs

AorticStenosis - Ejection systolic murmur, radiates to carotids (In Aortic Sclerosis, there is no carotid radiation)
Pulmonary Stenosis  - Ejection systolic murmur which radiates to back/left scapula (may obscure second heart sound)
Atrial Septal Defect - sounds like pulmonary stenosis
Hypertrophic Cardiomyopathy - Harsh Ejection systolic murmur, palpable

Pansystolic Murmurs

Mitral Regurgitation - Best heard at apex, radiates to axilla
Tricuspid Regurgitation - Best heard at left lower sternal edge (tricuspid region) 
Ventricular Septal Defect - Best heard at left sternal edge

Early Diastolic Murmurs

Aortic Regurgitation - best heart at left sternal edge, in expiration, with patient leaning forward
(Rarely) Pulmonary Regurgitation

Mid-Diastolic Murmurs

Usually Mitral Stenosis - Best heard with Bell of stethescope at apex, with patient rolled to left
Rarely Tricuspid stenosis - sounds simliar to Mitral Stenosis

Continuous Murmur - referred to as a ‘machinery murmur’, although I don’t think anyone knows what machine it sounds like.

Patent Ductus Arteriosus - rare in adults. Best heard over upper left sternal border, radiates to back/left scapula

erratic-emedicine:

erratic-emedicine:

This diagram shows how the mechanics of the heart co-ordinate with the heart sounds and the ECG (EKG).

By keeping this diagram in mind, it can make identifying murmurs much easier, by taking the pulse whilst auscultating.  

The pulse represents the maximum arterial pressure, which as you can see in the diagram occurs in between heart sounds 1 and 2. Once you have identified which heart sound is which, you can more easily identify systole, and diastole, and describe with greater accuracy the nature of a murmur if present. 

Murmur Murmur

Here’s some causes of murmur patterns:

Ejection Systolic Murmurs

AorticStenosis - Ejection systolic murmur, radiates to carotids (In Aortic Sclerosis, there is no carotid radiation)

Pulmonary Stenosis  - Ejection systolic murmur which radiates to back/left scapula (may obscure second heart sound)

Atrial Septal Defect - sounds like pulmonary stenosis

Hypertrophic Cardiomyopathy - Harsh Ejection systolic murmur, palpable

Pansystolic Murmurs

Mitral Regurgitation - Best heard at apex, radiates to axilla

Tricuspid Regurgitation - Best heard at left lower sternal edge (tricuspid region) 

Ventricular Septal Defect - Best heard at left sternal edge

Early Diastolic Murmurs

Aortic Regurgitation - best heart at left sternal edge, in expiration, with patient leaning forward

(Rarely) Pulmonary Regurgitation

Mid-Diastolic Murmurs

Usually Mitral Stenosis - Best heard with Bell of stethescope at apex, with patient rolled to left

Rarely Tricuspid stenosis - sounds simliar to Mitral Stenosis

Continuous Murmur - referred to as a ‘machinery murmur’, although I don’t think anyone knows what machine it sounds like.

Patent Ductus Arteriosus - rare in adults. Best heard over upper left sternal border, radiates to back/left scapula

(via md-admissions)


Quote

Jul 28, 2014
@ 7:30 am
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79,305 notes

Growth is painful. Change is painful.But nothing is as painful as staying stuck somewhere you don’t belong.

— Mandy Hale


Photo

Jul 28, 2014
@ 6:15 am
Permalink
276 notes

i-heart-histo:

How to construct a blood vessel!
Making sense of the histology of arteries and veins
Source:
If you like words, the full post about How to classify blood vessels (including this image) visit the ihearthisto.com post here
Or you can just sit back, watch and realize that you just learned about the tunics of a vessel. That’s histology folks!
Have fun,
i♡histo

i-heart-histo:

How to construct a blood vessel!

Making sense of the histology of arteries and veins

Source:

If you like words, the full post about How to classify blood vessels (including this image) visit the ihearthisto.com post here

Or you can just sit back, watch and realize that you just learned about the tunics of a vessel. That’s histology folks!

Have fun,

i♡histo

(via mymedlife)


Text

Jul 27, 2014
@ 11:31 am
Permalink
9 notes

Anonymous said: How realistic is grey's anatomy??

I never watched it but according to everyone to everyone in my class who has watched it? Not realistic at all. But if you like it, just enjoy it as fiction! There’s nothing wrong with that :)


Text

Jul 27, 2014
@ 8:45 am
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98 notes

protestthebeero said: So, I've wanted to be a doctor for a few years now, but I haven't been in school. I'm going back (community college) in the fall and I somehow got a job in an oncology lab... and it's hard. It's really fucking hard, and it's frustrating, and I'm surrounded by MDs and PhD students who know a ton about microbiology and onocology and I can barely get my PCR to work right. The medical field isn't all this intimidating, is it? I've been thinking about OB/Gyn as a career, fyi.

It is absolutely hard, and anyone who judges you has no idea what kind of guts and determination it takes to pick up after being away from school to work towards med school!

The medical field will always be somewhat intimidating. It is a place where there are no idiots, everyone sets the highest standards for themselves, and we all demand excellence. I’m a fourth year, and I thought there would be a day I’d stop feeling dumb. But you know what? I still feel a little dumb every day. My internal medicine attending told me that even now, she feels humbled by the practice of medicine. OB/Gyn is definitely a field where professionals are hard on themselves, because they know that their decisions impact two patients (mom and baby), not just one.

However, there are two ways of looking at it:

  1. You decide “being around smart people, being wrong, learning forever? That sucks. I don’t want this. I want to feel good at something, is that so wrong?!” You then refuse to look dumb or make mistakes. By doing that, you never learn and grow.
  2. You decide “feeling dumb sucks, but I have to forgive myself, too. Everyone is at a different stage of learning! I won’t shy away from the areas that I’m not good at! I’m going to get better!” It’s a much harder path to take, but you will grow and become a stronger person and professional.

You can’t get your PCR to work right currently, but you know what? I know that you’ll be able to with a little time, some help, and determination! Get those MDs and PhD students to share their knowledge with you. I bet they’ll even learn when you ask them questions! Those who scoff at your or don’t teach? Pity them, for they have forgotten what’s most important: to never stop learning!

You can do it!

md-a


Chat

Jul 27, 2014
@ 7:30 am
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13,167 notes

Interviewer: Do you think that rock music could push people to take drugs?

David Bowie: I'll go the other way on that. If I had a fan of mine who got through university and became a doctor, would I also get the credit for that please?


Photo

Jul 27, 2014
@ 6:15 am
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175 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]

(via fyeahmedlab)


Video

Jul 26, 2014
@ 8:45 am
Permalink
217 notes

corporisfabrica:

Annotated radiographs of the hands of an adult (above) and a child (below)

From childhood, the bones of the hand undergo major development. Note the changes in position and size among the bones of the wrist as well as the joining of the phalanges to their proximal epipheses (seen below as dark, narrow bands adjacent to each bone in the fingers of the five-year-old).

See if you can spot something unusual in one of the radiographs…

Illustration from Cunningham’s Manual of Practical Anatomy, 7th Edition (1920) 


Text

Jul 26, 2014
@ 7:30 am
Permalink
50 notes

cranquis:

thunderandballoons:

Everything Dr. Cranquis said in the H&P podcast made my insides go warm and fuzzy. Go listen to it for elaborate theories on pillow forts, humor in medicine and the medblr community. 

Look! The old Dean of PMTH speaks!

(via confessions-of-a-redhead)


Text

Jul 26, 2014
@ 6:15 am
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14 notes

hyperkangaroo said: Do you think I could get away with wearing a bowtie and suspenders - both bright red, contrasting with a gray pant-suit - to a medical school interview?

I attempted something similar with a Firefly-themed outfit for a Bacc/MD program when I was in college. As one enthusiastic geek to another, I must advise against it. You can TOTALLY do it once you get into med school, and you’ll probably get some appreciative nods!

But during the interview, the school wants to know that you’re a rock of reliability, composure, and thoughtfulness. So put on your best formal suit set, and save your “Doctor’s” attire when you celebrate ;)

Best,

md-a