Medical Seraph

[medicowesome]

Skin cancer mnemonics

Here are some memory aids that I use :) Pearls are found at the bottom (base) of the ocean. Pearly appearance is characteristic of basal cell carcinoma. Marjolins becomes Malignant in Malformed skin. Marjolin’s ulcer is squamous cell carcinoma in previously traumatized, chronically inflamed, or scarred skin. You can see them in: Chronic wounds Burn injuries Venous ulcers Ulcers from osteomyelitis Post radiotherapy scars. That’s all! -IkaN

[medical-seraph]

#amwriting

[medical-seraph]

Surprisingly good.

[jayparkinsonmd]

There are two healthcare systems in America, I call them The Last 5% and The First 95%.

The Last 5%

It’s characterized by expensive daily drugs, highly specific tests, detailed imaging, super-specialized specialists, robots, massive hospital campuses, and every expensive thing but the kitchen sink. It’s the world’s best. It’s powered by specialists and big hospital buildings. And when people talk about the US healthcare system being the world’s best, it’s because of this “Last 5%” System. It’s life-changing when everything goes right. It’ll cost you an arm and a leg, but it can sometimes work miracles, if your definition of miracle is maintaining a beating heart. It’s also highly unsafe, risky, and prone to complications, hospital-acquired infections, and disconnected care. But that’s not something The Last 5% likes to think about. I call it The Last 5% because it’s solving the last 5% of human health problems. Remember, 80% of your lifetime medical costs are spent in the last 6 months of your life. It’s treating people, mostly adults, at the end of their life, after an unhealthy lifestyle from an unhealthy culture and environment has done a number on their bodies. Any problem where you’re trying to solve the last 5% of the problem is ungodly expensive and can only get more expensive.

The First 95%

It’s vaccines, clean water, short-term antibiotics, quick fixes, healthy food, exercise, education, and environments. It’s powered by neighborhood primary care doctors in small practices, farmers markets, bike paths, relationships with family and friends, and anything else that helps you get to the last 5% of your life. Health insurance companies are terrible at impacting this System for the better. But for an idea of how they could, see how the largest health insurance “company” in America has agreed to pay for removing lead in Flint. Compared to The Last 5%, there’s not a lot of money to be made here. That’s why the medical component of this sort of looks and feels like the DMV. It’s also not really connected to the Last 5% System. But it’s 95% of the solution. It helps you live a wonderful life throughout your life. And that’s what matters. That’s why all I want to do with my life is fix 95% of the problem.

[medical-seraph]

Where's the lesion? MNEMONIC

Parkison Disease: Dopaminergic neurons of Substancia Nigra; Direct & Indirect pathways ("PARKING the BLACK car")

Huntington Disease: GABAergic neurons of neostriatum; Indirect pathway ("HUNTING is my NEW hobbie")

Wilson Disease: Copper accumulation in liver, eyes, brain, especially putamen; Indirect pathway ("a WILSON le gustan las PUTAS")

Hemiballism: contralateral subthalamic nucleus; Indirect pathway ("a BULLET was fired in the SUBWAY")

Tourette Syndrome: Indirect pathway

[wnq-writers]

To swim against the tide of my own thoughts is the hardest battle I fight.

afkwrites (via wnq-writers)

[medicowesome]

Medicowesome: Step 2 CK: Anterior and posterior urethral injuries and mnemonic

Today was a fun study day, I also read about rupture of the bladder dome. A full bladder and a blow to the abdomen during a motor vehicle accident can cause intraperitoneal bladder rupture. One of the sites I was reading this on wrote, "Always empty your bladder before going on a drive." lol :P

What are the pats of the male urethra?

Why is the membranous urethra so susceptible to injury?

In which conditions does anterior urethral injury occur?

What is contradicted in suspected urethral injury?

So many questions, click for the answers :D

[austinkleon]

Being a writer is like having homework every night for the rest of your life.

Lawrence Kasdan (via austinkleon)

[thoughts-memories]

[ikwt]

[md-admissions]

Spent morning de-escalating an angry son, comforting a very crying-prone patient, pushing away the creepy romantic advances of another patient, trying to elicit a medical history out of a man in alcohol withdrawal, and attempting to persuade urology to be primary on a patient whose only issue is a scrotal abscess.

And people wonder why I just want to sit in silence and be left alone to decompress when I go home.

[doctorkintsugi]

the talk

I’m on nights in the ED, and last night was an intense shift. 

My first patient of the evening was a woman who was sent to the ED by her PCP for an indicentally-discovered WBC count of over 200, with 8% blasts (immature cells). That, non-medblrs, is very high, and she came in the door already understanding that she almost certainly had leukemia. I sat down with her and explained the next steps, and gave her The Talk that I have started to routinely give to people with new, serious diagnoses. The Talk goes roughly like this:

“A lot of things are about to happen in a pretty short amount of time. There will be a lot of people helping to take care of you. It might feel invasive and overwhelming, but I want you to know that you are the driver. If you are confused, ask questions. If something is happening that you don’t like, you can tell us to stop. This is your body and you always get to decide what happens to it. As doctors we sometimes get swept up in treating your disease, and I apologize in advance if you ever feel like we’ve forgotten about the rest of you, but please feel free to remind us. We are experts in medicine, but you are the expert on you.”

I then placed her first IV. It felt like I was firing the starting pistol at a race that this woman really didn’t want to have to run. 

Unfortunately, she wasn’t the last person to get The Talk last night. The second person came in with abdominal pain, something we see often in the ED. While this patient wasn’t feeling all that sick, his story worried me, and on exam he had a large palpable mass in his abdomen. As soon as my hands touched the mass I could envision his CT scan in my mind. We ordered the test, and the actual scan looked worse than what I had imagined. There was really nothing that could look like this except for a widely metastatic cancer. 

It was a very busy night, and my (awesome) attending was running all over the place. I offered to go tell the patient the bad news, imagining that she would probably want to be there for that conversation. But she just thanked me, and off I went. 

I’ve had serious conversations with patients and families, sometimes unsupervised. I had not, however, actually delivered this kind of news before. Of course it was somewhat hedged; cancer is diagnosed by biopsy, not by imaging. But it would have been impossibly dishonest not to tell them that all of the testing we were about to recommend was a cancer workup.

They were fairly stoic about it, which probably made it easier on me, though it made me worry at first that I wasn’t being clear. They asked good questions. They wanted to see the CT scan, so I went over it with them. I gave them The Talk, and they seemed to appreciate it. We wanted to admit him, but they decided to go home and plan further diagnostics as an outpatient, and I felt like The Talk had worked. He wanted to go home, so he did. 

I spent the rest of the night sewing and splinting, which is the beauty of emergency medicine: the heavy shit is mixed in with easy, fun, satisfying fixes. But I honestly really love the hard stuff. I love the type of healing that starts – and often ends – with words. 

[doctorofwhut]

This is an amazing Talk and I’m going to have to steal it for future use. 

[cranquis]

Just give me an address to send the royalties every time I use your Talk with future patients – that’s TERRIFIC. (Great post, too!)

[mynotes4usmle]

ANTIBIOTICS CHEAT SHEET :)

Also, REMEMBER!!!!

* Sulfonamides compete for albumin with:

Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies

Warfarin: increases toxicity: bleeding

* Beta-lactamase (penicinillase) Suceptible:

Natural Penicillins (G, V, F, K)

Aminopenicillins (Amoxicillin, Ampicillin)

Antipseudomonal Penicillins (Ticarcillin, Piperacillin)

* Beta-lactamase (penicinillase) Resistant:

Oxacillin, Nafcillin, Dicloxacillin

3°G, 4°G Cephalosporins

Carbapenems 

Monobactams

Beta-lactamase inhibitors

* Penicillins enhanced with:

Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)

Aminoglycosides (against enterococcus and psedomonas)

* Aminoglycosides enhanced with Aztreonam

* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)

* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)

* Both inhibited by Probenecid during tubular secretion.

* 2°G Cephalosporines: none cross BBB except Cefuroxime

* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.

* Cephalosporines are "LAME“ bc they  do not cover this organisms 

L  isteria monocytogenes

A  typicals (Mycoplasma, Chlamydia)

M RSA (except Ceftaroline, 5°G)

E  nterococci

* Disulfiram-like effect: Cefotetan & Cefoperazone (mnemonic)

* Cefoperanzone: all the exceptions!!!

All 3°G cephalosporins cross the BBB except Cefoperazone.

All cephalosporins are renal cleared, except Cefoperazone.

Disulfiram-like effect

* Against Pseudomonas:

3°G Cef taz idime (taz taz taz taz)

4°G Cefepime, Cefpirome (not available in the USA)

Antipseudomonal penicillins

Aminoglycosides (synergy with beta-lactams)

Aztreonam (pseudomonal sepsis)

* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.

* Covers VRSA: Linezolid, Dalfopristin/Quinupristin

* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.

* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)

* Phototoxicity: Q ue S T  ion?

Q uinolones

Sulfonamides

T etracyclines

* p450 inhibitors: Cloramphenicol, Macrolides (except Azithromycin), Sulfonamides

* Macrolides SE: Motilin stimulation, QT prolongation, reversible deafness, eosinophilia, cholestatic hepatitis

* Bactericidal: beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), aminoglycosides, fluorquinolones, metronidazole.

* Baceriostatic: tetracyclins, streptogramins, chloramphenicol, lincosamides, oxazolidonones, macrolides, sulfonamides, DHFR inhibitors.

* Pseudomembranous colitis: Ampicillin, Amoxicillin, Clindamycin, Lincomycin.

* QT prolongation: macrolides, sometimes fluoroquinolones

[kneelpraylove]

Im reblogging this with hope that when i get into med school i can finally interpret it

[mynotes4usmle]

And I’m reblogging it to remind you that you will get into med school and you will learn all of this 😁

[md-admissions]

Shittest day of intern year (with a couple bright spots)

-got sick with a viral URI and walked around febrile and sniffly all day at work -got my period and couldn’t even leave to get a pad, I didn’t have coins to buy one, and basically I had to make a complex layered paper towel thing to deal all day -cramps and bloating all day -it turns out that the intern I am subbing in for is absolutely not coming back this month and I am not going back to ID this year -she does not have a family or medical emergency, which the Chiefs blatantly lied about when they spoke to me -and she’s actually delaying her paperwork pending to finalize her return to work so she’s been essentially on vacation for two months (because she’s an idiot and she puts her hikes and travels out of state on Facebook) -causing multiple people to be pulled from rotations to cover for her BUT I am the only person to be pulled for a complete rotation for her -my abstract edits are due tonight but… -my blue apron delivery was sent to my neighbor’s apartment and he’s coming home “late tonight”

So I am hungry, sick, tired, stressed, angry, sad, bloated, cramping, and exhausted.

The only bright spots are: -I’m off tomorrow -two patients thanked me today for being a good doctor -I approached one of the program directors who has arranged for me to be on an ID rotation early on in 2nd year -my team is really sweet and the med students are really good

Finally, anyone who is compelled to respond with some trite bullshit like “it’s not that bad, I’ve had worse” and “so many people are less fortunate than you be grateful” guess what this list isn’t about you. I’m a human being who happens to be in a profession that is simultaneously both overly maligned and glorified, who had a bad day, and have no trouble this evening eviscerating you with the written word. So shut the fuck up and move along.

[drveebs]

If you don’t have a beer or twelve, imma have to start drinking FOR you.

[md-admissions]

Don’t worry, thoughtful friend. This hot toddy is currently more bourbon than anything else.

[md-admissions]

So I feel like my motivation to be a doctor isn't 'enough'. I haven't "always wanted to be a doctor" or been "dreaming about it since I was a kid". I just decided, in my third year of college and realizing I didn't like the direction I was going, that hey.... Being a doctor IS what I want to do....I'd be good at it and I'd like it. But I kind of feel like i'm... Idk fake?? That my motivation isn't justified somehow idk

Hi there, anon!

Maybe you haven’t wanted to be a doctor since you were a fetus. You haven’t personally saved thousands of lives with some kind of dangerous and sexy volunteer work in between raising guide dog puppies and getting A++++s on every class you’ve ever taken. 

So what?

Do not judge your ambition by comparing it to those around you. Lord, I didn’t want to be a physician until junior/senior year of undergrad. Some people don’t realize until they’re in their 30s or 40s. Others have to delay their dream because of financial reasons, children, family tragedy. 

But that doesn’t make anyone’s aspiration less valid.

You want to do medicine? Do medicine! Your reasons are your own, and they are valid.

[medical-seraph]

Post 13: A Spore-forming Gram positive Rod: Bacillus anthracis

Gram positive.

They are Spore-forming, so they can live in various kinds of conditions. The spore is located at the center of the rod bacteria. The bacteria have clear cut edges and they are big in size.

Aerobes.

On culture they have “Medusa Head” appearance (see pic).

Bacillus anthracis is the causative agent of Anthrax. That’s why it is a potential item for bioterrorism.

This disease is found in herbivore animals such as goats, sheep, and cows, and it is found in humans as well. It is a highly infectious and highly fatal disease. Usually, it comes in the form of either skin ulcers (cutaneous anthrax) or a fatal pneumonia (pulmonary anthrax).

Human is the accidental host (there is no human to human transimission).

Trasmission happens by three ways: (1) Contact transmission which is the most common, but causes skin ulcers with least mortality. (2) Inhalation of contaminated dust causing what’s known as “Woolsorter’s Disease” with mortality rate of 95%! (3) Ingestion which is the least common way and simply causes hemorrhagic diarrhea.

It has two important virulence factors:

1- Poly-D-glutamic acid capsule which is anti-phagocytic – thus phagocytes can’t properly dispose the bacteria 2- Anthrax toxin being made up of three proteins: protective antigen (PA), edema factor (EF), and lethal factor (LF). PA does the binding and EF acts an adenylyl cyclase that will increase cAMP thus causing release ions outside thus edema. Whereas, LF is cytotoxic and it allows the bacteria to quickly kill the host.

Acquiring the spores is essential to cause disease. 12 to 36 hours after that, a simple papule is noticed. This papule quickly becomes a vesicle and then a pustule; which will become necrotic. When it becomes necrotic, it starts spreading, so you can notice erythema (redness), induration (hardening), and increase in vascularization. What is seen is a Gelatinous Edema with an increased vascular permeability; which has the appearance of a burnt skin! So we call it a Black Eschar (eschar is the crust that forms on the skin after a burn) – Remember, there is no burning here! It is just an infection. All of this will progress to hemorrhage (bleeding), sepsis, and ultimately death.

The bacteria in the lesions are very invasive.

In Woolsorter’s disease, they are found in the alveoli, and they travel to the mediastinal lymph nodes, and cause “Hemorragic Mediastinitis” 

[medicowesome]

To remember about SVT, all you need to remember is the cause and you know the symptoms and treatment!

SVT occurs due to accessory conduction pathway through the AV node.

A - ABCD

Adenosine

Beta blockers

Calcium channel blockers

Digoxin

V - Vagal maneuvers

Valsalva

Ice immersion

Carotid massage

SVT: Start Vagal Treatment - - > If fails, use pharmacotherapy (ABCD drugs)

The P in Pvst reminds us that it presents with Palpitations in a hemodynamically stable patient (HR: 160-180/min)

*PVST: Paroxysmal supraventricular tachycardia

Interesting fact: In an asthmatic patient with SVT, you can’t give adenosine or beta blockers. The drug of choice in an asthmatic patient is therefore, diltiazem (A calcium channel blocker)

That’s all!

-IkaN