I need that vitamin M.D.!

MEDBLR! F21 || Filipino MedStudent. 🇵🇭 🏳️‍🌈 Y1 🏁 Mental Health is a priority! Community Medicine! Terrified 24/7 but it's fine I guess.

[md-admissions]

I was wondering if you could elaborate on the biases toward patients with opioid addiction and what you think we should do better. I see a lot of infective endocarditis patients, and it's frustrating and sad and I know I'm guilty of biases.

@runner-kat, this is an EXCELLENT question. 

Let me make one thing clear: I am no saint. I did not come out of life or medical training aware or ‘woke’ about this issue. I learned, as my hero and inspiration for this blog, Anthony Bourdain did when he acknowledged his contribution to toxic masculine kitchen culture: by fucking up, listening to people who knew better than me (patients themselves, social workers, addiction psychiatrists, my attendings, residents), changing my ways, and continuing to learn. If I can change, you can, too. 

I think there are two very major, pervasive biases I see across disciplines and healthcare professions that can also be easily remedied. 

Common bias #1: Language What we do: “This is a 28 year old heroin addict” “This is a 32 year old IV drug user” “This is a 48 year old opioid abuser”

Addict, user, and abuser are words with blatant value judgement behind them. It changes the way we think about the patient before we even see them. It hurts our patients, too. We as physician know better, we know that illness does not make a patient more or less valuable as a person. 

We KNOW that addiction is a physiologic illness. It’s not “all in your head” or “weak will” or “poor upbringing”. One that comes with stigma, its symptoms manifest as behaviors, its side effects and endpoints catastrophic to patients, families, children, and communities. One of the saddest things I heard in the past year was when a twenty four year old with terrible septic arthritis told me, “I’m a drug abuser. I don’t deserve this surgery, you guys should just leave me to die.”  It told me how little she thought of herself and how hopeless she felt. It told me that someone who claimed they loved her said that to her. That’s fucked up. Use instead: “This is a 28 year old with heroin use disorder” “This is a 32 year old person who injects drugs” “This is a 48 year old person with opioid use disorder” This is non-judgmental language that succinctly addresses the medical illness of the patient at hand. Disorder, of course, in the medical sense, and not the colloquial sense. Common bias #2: Patients with a history of or current usage of opioids do not provide learning value.What we do: Residents. Attendings. Med students. Raise your hand if you’ve ever heard or said: “Ugh, another opioid user you’re going to learn nothing” or “I prioritize teaching on my service, so you’re not gonna get the annoying stuff like placements or drug users.”

I’ve said all those things before. I’m not proud of it. I don’t say shit like that anymore. And I educate residents to not say that, either. 

There is teaching and learning value so long as you look. But why do we say shit like this? Because we’re burnt out and patients with opioid use disorders need a LOT of multidisciplinary services, time, and help we often cannot give as a lone med student or resident. Their suffering and sometimes their behavior forces us to confront things about ourselves, our healthcare system, our society that we’d rather look away from. These patients can also often press our buttons and stir up emotions that we’d rather not feel and can test our compassion. 

Let me offer some suggestions for teaching points for both teachers and learners:

-Ask your patients about the first time they injected or took more pills or fentanyl patches. The stories will break your heart. The number of patients I’ve met who were given an injection against their will? Too many. Patients who took pills because they felt their life and future was going nowhere? Too many as well. -Learning about injection habits and learning how to educate people on safer injection habits if they’re not ready to stop to prevent life-threatening infections is seriously interesting and lifesaving medical education. Maybe I’ll do a post someday soon.-Learning about medication-assisted treatment (MAT) to help patients ready to stop using opioids. Interesting and educational from a pharmacologic perspective, physiologic, and medically. Attendings out there, find out if you can get certified to provide MAT! I’m in the process of certifying!-**Framing injection drug use as a medical condition with its own focused review of systems, questions, physical exam, and work-up. Ask about fevers, night sweats, systemic symptoms. Injection methods: you must ask because it will address where infection lies on your differential and what else you need to work-up. Ask about prior methods the patient has tried to stop injecting. Have they tried quitting cold turkey, tried methadone, suboxone, vivitrol, etc. What were those experiences like? What have they heard? Would they like to try? Looking for back pain (potentially a concern for an epidural abscess or vertebral osteomyelitis), a good MSK exam for septic arthritis or muscle abscesses, murmurs for endocarditis, etc. Work-up for transmissible diseases like HIV, Hep C, blood cultures for bacterial or fungal bloodstream infections. Do I have your interest yet?

Obviously there’s more to do. But I think if medicine as a whole could do just these two things, we’ll be doing a whole lot better.

Fantastic question, thank you!!

md-a

[cranquis]

I learned a lot here.

[biomedicool]

Pregnancy - physiology

Hormones

hCG - human chorionic gonadotropin - present in blood and urine, produced by blastocyst and placenta

Low levels of hCG could mean miscarriage, ectopic pregnancy, miscalculation of dates

High levels = molar pregnancy (cells that normally form a baby dysfunction and form cysts instead), multiple pregnancy (twins etc), miscalculation of dates

Progesterone increases fat deposition in early weeks and stimulates appetite

Increased oestrogen from corpus luteum promotes mammary gland development (breasts enlarge)

And inhibits ovulation via negative feedback [OES decreases GnRH release by hypothalamus –> linhibition of FHS and LH –> no ovulation]

Relaxin (secreted by corpus luteum) softens connective tissue in preparation for labour - not specific, all joints can be affected

Peaks in early and late pregnancy

Physical changes

Blood pressure

As early as 4 weeks into pregnancy 

plasma volume increase

caused by the affects of oestrogen and progesterone on the kidneys

OES and Prg cause vasodilation 

less resistance = less pressure

Heart rate increases by 25% to compensate

stroke volume increases 

increased overall cardiac output by 50% in third trimester

Direct action of enlarged uterus:

compresses the descending aorta and inferior vena cava 

decreased venous return - less blood in means less blood out, less blood in ventricle –> reduced pressure on walls –> reduced force to exit –> reduced placental perfusion

increased aortic pressure

increased heart rate

[shouldn’t sleep on back for this reason]

Outcomes:

Fall in blood pressure (can cause collapse if serious)

Can cause foetal hypoxia even without mother symptoms

Haematological changes

red cell mass increase by 20% (renal - increased erythropoietin production in response to detection of blood oxygenation and sodium/water balance)

Plasma volume increases more than RBC count does, causing the impression of decreased haemoglobin (anaemia)

Increased tendency to clot (hypercoagulable)

due to increase in clotting factors and plasma fibrinogen

platelet production increase (however count drops due to increase in activity and consumption) - function remains normal]

WBC count may increase due to an increase in granulocytes

Respiratory changes

Increased chest diameter, diaphragmatic expression and elevation

dyspnoea common (difficulty breathing)

breathing becomes more costal (mouth) than abdominal 

mainly mediated by progesterone levels (cause bronchial and smooth muscle relaxation and hypersensitivity to CO2)

Changes to the urinary system

cardiac output increase –> increase in renal plasma flow and glomerular filtration

increase in urea, creatinine, urate and biocarbonate clearance 

with progesterone, renin and aldosterone up water retention increases

can lead to urinary stasis and increased risk of UTI

Any drugs given that are excreted renally must be given in much higher quantities consequently

Gastrointestinal changes

Appetite increase + cravings 

Gastric reflux sphincter relaxation (increased indigestion, also due to increased intra-gastric pressure (expanding uterus)) 

gallbladder dilated 

GI motility decreased and transit time slower 

albumin and protein decrease 

cholesterol twice normal value

Muskuloskeletal 

Calcium reuptake into bloodstream results in mild decalcification of bones 

relaxin softens joints (pubic symphysis + alters gait (waddling))

abdominal muscles stretch to elastic limit 

stretch marks (stria gravidarum) caused by rupture of elastic fibres and small blood vessels 

Reproductive changes

Massive increase in mass

Placenta growth (nutrition, excretion, immunity, endocrine) 

Parental blood supply 

[wayfaringmd]

Wayfaring! Any thoughts on the current coronavirua?

I think the media publicity is way overblown for something that is essentially a cold for most people and if they would do daily updates on the hospitalization and death toll from the flu every year like they are for coronavirus maybe people would take it more seriously.

[drdessertfox]

[cranquis]

[wodneswynn-deactivated-deactiva]

Tag urself I'm Tiddy Skittles

[vaapadataru]

@undercovermindflayer

[eliksniapologist]

Breast mints is my new fucking favorite term for my estrogen

[vaapadataru]

Femme&M’s also has a nice ring to it.

[dnd-apothecary]

honestly I am crying over the whole list but I love tit tacs and femme&ms, and antiboyotics. But the real kicker for me is Notorious HRT lololol

[jaubaius]

Vampire and werewolf dating

[runcibility]

OP I CAN’T BELIEVE YOU DIDN’T CREDIT THIS, BECAUSE THERE IS SO MUCH MORE!

This is an ongoing series by @sarahseeandersen called “Fangs” - it’s absolutely worth following and keeping up with!

https://tapas.io/episode/1559785

[cottoncandyinsides]

Sharing the credited version!

[inficetegodwottery]

[phuntasm]

[beingdreeyore]

A few of you have asked how it went today. I’ve paused before responding because I want my response to be clear in my brain. I want to be objective. 

In a word? Actually, give me two. If I had to use two words to describe it, I’d call it a FUCKING CLUSTERFUCK.

But that wouldn’t be ladylike, so instead let’s just use one word and say that it was a little disappointing. 

The appointment was a psychiatric evaluation. A few years ago I saw a psychiatrist when my anxiety was raging during the pesky med school OSCEs, and it was exactly the same. Same questions, same pace, same focus. 

That made it tough.

We did a full run-through of my childhood. We had a great discussion about the mental health issues and challenges my mother has faced my entire life. We talked about how I am in relationships. He was clued on enough to decipher from the letter from my clinical psychologist that I had at one stage met the borderline criteria and that I’d done DBT (though she didn’t use those words. Intentionally). We talked about whether I met the criteria now (I don’t) and how I cope with struggles in life (really fucking well actually). We talked about those drenching Effexor sweats and how much sweeter life is without them.

We talked about what friends I have. We talked about my relationship breakdown. We talked about how I coped last time I was in the dark place. We talked about what I’m doing now to cope and survive in amongst this perfect storm. I cried at intervals through all of this. I told him I was a crier. I didn’t apologise for it. I’m sick of apologising for who I am. 

What we didn’t talk about was bullying or the fact that I have been assessed as a competent and safe intern. When I tried to raise this I was told that that’s not what we were there for. Of course that made me cry more. Once again I didn’t have a voice, I was just that crying chick with the bipolar mother who abandoned her. The chick who cries when the surgical fellow bullies her. What a basket case. Insane till she proves her sanity, just look at her mother!

He tried to comfort me, to tell me that it wasn’t his job to assess whether I’d been bullied, but more whether I could handle such adverse events in life. I asked him if there was a single thing in my history that would suggest I couldn’t. I asked him if crying was now a sign of not coping or whether sometimes it was nothing more than an appropriate response to a shit moment in time. I asked him when the response to bullying had been to demand the victims be strong enough to handle it, rather than the perpetrators be held accountable. 

It felt so goddam unfair. It felt like being on trial. He told me that he couldn’t tell me what the outcome would be, but from his experience in similar situations people had been instructed to see a psychiatrist regularly and the psychiatrist would report back to the board. Which feels a lot like being punished. He told me he saw nothing that would be career-limiting. I asked him why I would need to see a psychiatrist in the future then; even if I’d had cancer but I didn’t have it now, it wouldn’t be common for me to check in with my oncologist monthly. If I was safe, if I was managing well, if my responses were appropriate, then why was I required to see a medical specialist for a condition I didn’t have?

I’m hoping that this is my interpretation only because right now I’m raw and my skin is on fire. I’m hoping that once the tears settle I will see things more positively. But I don’t have much hope. The tears have been falling for hours. 

Before I left I asked him if his impression of me was that I wasn’t looking after my health. He said that no, he didn’t think that was the case. He wouldn’t say more, other than that he thought I knew exactly how to best handle challenges in a way that worked for me. 

So the likely outcome, as per the psychiatrist, is that I will have to be continually evaluated throughout my medical career, whilst the person who has a well-documented history of bullying interns escapes without even a mark against his name. This is medicine, where anyone can accuse you of anything and you’re guilty till proven innocent. Unless that thing is bullying, in which case carry on, business as usual. So bully as you like. Scream, yell, throw papers at interns, but whatever you do, don’t cry. Anything but cry. In medicine, crying is the only punishable offence. 

[flyonthewallmedstudent]

I think the wounds are still fresh from what’s happened to you. Don’t over think it, just vent and give it time. 

I don’t think there’s anything in wrong in having ongoing mental health support which is what they’re providing. I don’t think it’s punishment at all if there’s nothing limiting your career progression. If you don’t have a choice about it, then try to see the lighter side. It’s 100% your own time with a professional to talk about the shitty things about this career. And there are a lot of shitty things we’d all like to unburden ourselves with. 

I saw a clinical psychologist sporadically, once on the prompting of a consultant on team after a particularly bad week (3 codes, 2 patients unexpectedly during 2, a registrar who’d gone awol and needing to looking after mine and their interns). I wish I had stuck it out, but I never did. essentially I never put in the work that would have been for myself (as apart from all the other stuff I do for my job). May haunt me later. 

Don’t dwell on the bullies, they’ll get what’s coming to them later. 

It’s harder to deal with in intern year, as so many things are still fresh and new. it gets easier with time - you learn better ways of not just coping but helping the system deal with it. It’s completely unfair, but it’s hard to get away from bullying in this career. But you do the best you can and then try to move past it and focus on being happy. 

[rhokotela]

My patient today is in for a palliative modified radical mastectomy for stage four breast ca (Mets to lung, liver and spine).

She’s 34 with two kids, 8 and 13. Spent all morning getting to know her and her husband. They’re so lovely.

She’s being re-discussed as a candidate for surgery since we found disease in her other breast today on exam. Poor response to neo adjuvant chemo.

BRACA negative. No family history. No risk factors.

[rhokotela]

Surgery denied by oncology team, even though surgeons were happy to cut.

She had a mixed response to eight rounds of NACT as per re-staging CT - regression of liver mets and pulmonary mets and a clinical response of the primary tumor and lymph nodes. Progression of thoracic, lumbar and 1st rib mets as well as new suspicious nodules in the contralateral breast.

They phoned her and her husband to drive the hour in to the hospital for a face to face meeting to deliver the bad news.

[captain-flint]

Oscar and his greying manbun 😩👌

[tiktokarchive]

Doctor: [singing to oneself]: Tka tka tooh, do do do do do do, de do do do do do beow beow beow beow beow beow buh nuh, bah dah buh buh buh buh, hey!

Someone else: Hey!

Doctor: What?

[quilavastudy]

Do any fellow doctors or other healthcare professionals have any tips on how to ‘switch off’ and stop worrying about work when you get home, because this has been an issue for me recently!

[camilleinbluejeans]

During FY1, I used to walk to and from work. 

I used to give myself the entirety of my journey home (usually about 15 minutes) to overthink and work through how the day had gone, with the understanding that I was not allowed to do it at home.

I basically forced myself to only think work thoughts at work, and home thoughts at home. If I ever had the odd stressful patient-associated thought pop into my head at home, I would consciously dismiss it by telling myself, “I did my best. Someone else is there. I can do more tomorrow.”

It definitely helped.

I’d recommend talking to people too- sometimes I’d call my best friend from medical school if I knew she was on a similar shift pattern as me- and have a bit of a debrief that way. Either way, it’s fine to let the thoughts come, just carry on working on dismissing them. 

You’ll get there, you’re doing amazingly!

[quilavastudy]

Thank you so much <3

[sometimeswegetlonely]

My friends and I have a group chat.

Being able to send each other a message saying “x happened, I did y, should I have done something else” or “someone just asked me to do z and it seems unnecessary but they won’t explain, what am I missing” is really helpful.

I especially like being able to send stuff at night. There’s something about sending thoughts into a void that is cathartic.

[moonbeam-llama]

I don’t have the same kind of “I’m home, not at work” as folks with shifts do (I’m always on call, and can be contacted at any hour 24/7 unless I’m on vacation and someone is covering for me) but wind-down and self care are quite important for this situation! I have a routine. The drive home is to wallow, think over everything I’ve done, etc. When I’m home, that’s it. Unless there are extenuating circumstances, work does not come home with me, and I literally wash it off when i come in - a shower or just my face and arms, depending on what I was doing. I put on clean clothes or pajamas. Then I drink a big glass of water and have a meal. I know a lot of folks who meditate, or get frequent bodywork, do a few minutes of yoga, or have a special playlist for the commute home.

[problemedic]

I lived with other FY1s in hospital accommodation in FY1 and we would meet up and debrief every couple of days. Then the practice persisted into FY2, we’re now scattered but we keep a “debrief” WhatsApp group

[flyonthewallmedstudent]

There’s a lot of good stuff in here, in the re-blog’s and comments. 

1. It gets easier with time. It’s always harder in your first year out. What you’re feeling is completely normal and clearly we all go through it. 

Things roll off your back as you get more exposure and experience. Medicine is so repetitive in some ways, it will be like deja vu sometimes. 

As you gain more confidence, you’re able to worry less. 

I used to call the ward or the after hours guy from time to time to ask them to do something or chase something I forgot. I rarely do that now. 

Most of the time, I can go home and know I’ve done everything I could but that came with a lot of hard lessons, experiences, made my small mistakes. I didn’t learn to be thorough overnight, that took time. 

2. Can the nagging feeling wait? If you forget something or are concerned, how urgent is it? you can easily prioritize in your mind, okay, tomorrow first thing I or my interns/FY1′s need to do these things. 

3. I write things down. 

I keep a notebook and use that as my “handover” document for myself. I never lose track of what I need to remember etc. They’re really short entries, they did start off long in my PGY2 year. 

It also serves as a journal, if there’s cool cases for presentations later, I have it go back to. 

4. Ventilating on tough cases/patients or patient families with colleagues.

I still get bad days from time to time, or instances where I go - I wish things had gone differently or that I had done something different. 

That’s where group chats help with your work friends - particularly if they’re the same level and work at the same hospital. It’s hard to find time to socialize with chaotic rosters, I could be on nights and my friends will be on regular shifts. But everyone is always attached to their phones.

Coffees with the team also always helps. Never say no to coffee if someone on the team offers it, particularly someone senior. It’s important bonding time and if you have a tough time one day, you have that foundation formed already with your registrars or consultants. Putting it out there as I know some interns or FY1′s do turn it down - but don’t!

5. As mentioned in the other comments - exercise and hobbies all go a long way with clearing your mind. 

6. Studying, heh, probably the last thing anyone will think of. Read up on the patient case after work, but don’t dwell on it. It makes it easier when you study for the MRCP or other exams later. You also make yourself feel a bit better. 

7. Change of environment.  Walk around the mall, go to the movies, get pampered at a fancy coffee shop. 

[kitchenism]

I want mental health to be so normalised that little children can tell their parents if they’re feeling mentally ill just like they would if they had a stomach ache or a fever.

I want mental health to be so normalised that school lets you go home after a panic attack episode like they do if you sustain an injury.

I want mental health to be so normalised that when someone’s in recovery the people around them ask for progress reports and send get well soon cards just like they would for any other sort of recovery.

I want mental health to be normalised because every mental health disorder is just as frightening, just as damaging as a life threatening injury and we pass people by every day who are so unwell in this sense but who don’t receive a fraction of the care they deserve just because mental health is unseen.

[resuscitationist]

#Repost @medicaltalks ・・・ ⚠️ This teen is lucky to be alive after he was stabbed through the neck by a needlefish!

This injury occurred when a needlefish jumped out of the water and pierced the neck of a boat passenger!

The teen was fishing with his parents at the time in Buton waters, South East Sulawesi on Saturday, January 18, and it is believed the needlefish “flew in their direction” impaling itself in the unsuspecting teen’s neck narrowly missing life-giving arteries and blood vessels.

Photographs show the fish’s snout pierced all the way through the patient’s neck from right under his chin through to under the back of his skull.

Luckily the teen was rushed to a hospital before being transferred to a larger hospital to undergo a delicate surgical procedure. Five doctors including three surgeons and two anaesthetists helped to removed the impaled fish from the patient’s neck.

The chief surgeon told local media the team had to be very careful due to large vessels being in close range of the injured site. It took two hours to perform the procedure.

He is now recovering, with doctors monitoring his condition over the next few days in case of infection.

Needlefish are adept jumpers, carnivorous in habit, and distinguished by long, slender jaws equipped with sharp teeth.

They can make short jumps out of the water traveling at up to 60 km/h (37 mph) and often leap over the decks of shallow boats rather than going around.

The largest needlefish ever recorded measured about 1.2 m (4 feet) long! (at Ocean Reef Club) https://www.instagram.com/p/B7ozWijhasb/?igshid=12prrtz4e2wbe

[docresa]

[learntheheart]

From the LearnTheHeart.com Cardiology Blog

So you are on the wards rounding and happen to have one of those cardiology attendings that gets some evil pleasure out of asking questions randomly to students (commonly known as “pimping”). I have seen some attendings get upset if students don’t know the correct answer and basically will send them to the library, tell them to look it up, then come back when they are smarter!

As a medical student, you MUST get these questions right if you are looking to get into a competitive residency/fellowship or just want to avoid embarrassment in front of your peers. Here is a list of the top 50 pimp questions that you may get on a cardiology rotation…know them and impress everyone! Want to really knock everyone’s socks off? I included some “Bonus” tidbits that are interesting and most people don’t know and links for those gunners who want to read more. 

I have organized all of this into general cardiology pimps, physical exam pimps and ECG pimps. This is a lot to know, but should prepare you well!

General Cardiology Pimps

1. What are the toxicities of amiodarone?

I dare you to look your attending in the eye with a serious face and say “BITCH” if asked this question! It is probably not wise to do this unless you are sure they have a good sense of humor. Remember the mnemonic BITCH to recall the issues with amiodarone

Bradycardia/Blue man syndrome Interstitial lung disease Thyroid (hyperthyroid OR hypothyroid) Corneal/Cutaneous Hepatic/Hypotension

Another way to remember is “Check PFTs, TFTs and LFTs” for pulmonary, thyroid and liver function tests. But really the only monitoring that is done is a TSH level every 6 months as routine PFTs and LFTs are not recommended.

2. What are the causes of atrial fibrillation?

Remember PIRATES for the causes of atrial fibrillation. This is quite a comprehensive list:

Pulmonary embolism, Pulmonary disease, Post-operative Ischemic heart disease, Idiopathic (“lone atrial fibrillation”), IV central line (irritating the right atrium) Rheumatic valvular disease (mitral stenosis or regurgitation) Anemia, alcohol (“holiday heart”), Age, Autonomic tone (vagal atrial fibrillation) Thyroid disease (hyperthyroidism) Elevated blood pressure (hypertension), Electrocution Sleep apnea, Sepsis, Surgery

3. What are the different types of shock and their treatment?

This picture summarizes it all:

4. What are the causes of congestive heart failure (CHF) exacerbations?

You will very likely get this one. Congestive heart failure (CHF) is the #1 cause of hospital admission in the US. Whenever a patient comes in with volume overload from CHF, you must always as the question “Why did this patient’s heart failure get worse”. Here are the reasons from most common to least:

1. Medication non-compliance (not taking diuretics or other medications) 2. Fluid/sodium restriction non-compliance 3. Acute worsening of cardiac output:

Arrhythmia

Ischemia or acute coronary syndrome

Worsening/Progression of cardiomyopathy/valve disease

5. Which medications for systolic congestive heart failure reduce mortality?

Easy…beta-blockers, ACE inhibitors or ARBs, and spironolactone. If ACE inhibitor and ARB intolerant, then the combination of hydralazine and nitrates are used and reduce mortality, especially in African Americans. Note that digoxin and diuretics DO NOT reduce mortality! They are for symptom relief and to prevent heart failure hospitalization only. The gunners can review Heart Failure here.

6. Which beta-blockers are FDA approved to treat systolic congestive heart failure?

Not all beta-blockers have clinical trials to support their use in systolic heart failure. Use these three:

Carvedilol (Coreg) Bisoprolol Metoprolol succinate (Toprol) and NOT metoprolol tartrate (Lopressor)

Atenolol, propranolol and the other beta-blockers SHOULD NOT be used in systolic heart failure.

7. What is the most common cause of right heart failure?

Left heart failure! When anything causes left heart failure (ischemia, valve disease, cardiomyopathy etc…), the LV pressure increases and transmits back to the lungs causing pulmonary hypertension. This then strains the right heart and eventually causes right heart failure. Know the difference between signs/symptoms of left versus right heart failure.

8. A patient comes in with chest pain, what are the 4 life-threatening causes that should be exclude?

Acute coronary syndrome Pulmonary embolism Aortic dissection Esophageal rupture (Boerhaave’s syndrome)

9. What are the signs/symptoms and issues with digoxin toxicity?

This is a good one:

Nausea/Vomiting/Abdominal pain

Weakness/dizziness

Symptoms of arrhythmia

Altered mental status

Vision changes (yellow vision or “Xanthopsia”)

Digoxin causes EVERY arrhythmia EXCEPT rapidly conducted atrial rhythms (atrial fibrillation or flutter with a rapid ventricular rate). The classic ECG has the “reverse check” sign:

The two pathognomonic rhythms in digoxin toxicity are atrial tachycardia with 2:1 block and bidirectional ventricular tachycardia. 

Atrial Tachycardia with 2:1 AV Block ECG Example 1

Atrial Tachycardia with 2:1 AV Block ECG Example 2

Bidirectional Ventricular Tachycardia ECG Example

Reverse with digibind if:

Evidence of end-organ damage (altered mental status, shock liver etc…)

Life threatening arrhythmia

Potassium level > 5.5

Digoxin CAUSES hyperkalemia, but is potentiated by hypokalemia (also hypocalcemia)

Wow…thats a lot to know.

BONUS: The “Stone Heart” theory. Digoxin toxicity can cause hyperkalemia. Recall that the treatment for hyperkalemia causing ECG changes is usually intravenous calcium administration. In the setting of digoxin toxicity and hyperkalemia, giving IV calcium may be potentially fatal. The massive influx of calcium into myocytes after the IV calcium is given has been theorized to induce a non-contractile state and has been termed “Stone Heart” (recall the end-point effect of digoxin’s actions is to open calcium channels increasing influx into cells).

BONUS BONUS: Vincent Van Gogh (the artist) was toxic on digoxin (he used the flower foxglove for a seizure disorder) and this is why he painted everything yellow before he reportedly commited suicide. Check out this painting of his:

10. What are the FIVE life-threatening complications of aortic dissection?

Coronary dissection, usually the right coronary artery (RCA) causing inferior ST elevation MI

Carotid dissection causing stroke

Aortic rupture

Cardiac tamponade from rupture into pericardium

Acute aortic valve regurgitation causing cardiogenic shock

11. Which atrial fibrillation patients can we use only aspirin (ASA) for and who needs full anticoagulation to prevent stroke?

Use the CHA2DS2 Vasc Score:

If 0-1 points then aspirin 81 mg - 325 mg If > 2 points then full anticoagulation (warfarin, dabigatran, rivaroxiban, apixiban)

Congestive heart failure Hypertension Age ( > 65 = 1 point, > 75 = 2 points) Diabetes Stroke/TIA (2 points) Vascular disease (peripheral arterial disease, previous MI, aneurysm aortic atheroma)

NOTE: Female gender is also included in this scoring system = 1 point!

12. What are the different properties of beta-blockers and name specific drugs?

Cardioselectivity: All beta-blockers act upon both beta-1 and beta-2 receptors. The “Cardioselective” beta-blockers act upon beta-1 receptors much more than the beta-2 receptors. For this reason, the cardioselective  beta-blockers are safer to use in patients with asthma or reactive airway diseases.

Lipid solubility: Beta-blockers that are lipid soluble, such as propranolol or metoprolol, can cross the blood-brain barrier easily. These medications are commonly used for migraine headaches, stage fright and panic attacks for these reasons.

Intrinsic sympathomimetic activity (ISA): Beta-blockers with ISA only partially antagonize while actually causing a small degree of activation of the beta receptors. So they will have some beta-blocking effects, but not to the degree of beta-blockers without ISA. These are commonly used in younger patients or in athletes where heart rates need to elevate (allowing overall increased cardiopulmonary effort) in order to compete in sports. Examples include pindolol and acebutolol.

Membrane stabilization: Stabilizing membranes decreases the propagation of action potentials. This is also the mechanism that local anesthetics work (lidocaine). Class I antiarrhythmic drugs possess this characteristic as well. The importance of this is not clear in clinical medicine in regards to beta-blockers. Perhaps this is partially an explanation for propranolol treating migraine headaches.

13. What are the side effects and other issues with ACE inhibitors?

Just remember the mneumonic “CAPTOPRIL”

Cough Angioedema Potassium excess Taste changes Orthostatic hypotension Pregnancy contraindication/Pressure drop (hypotension) Renal failure/Rash Indomethacin inhibition Leukopenia (rare)

14. What class of antiarrhythmic drug is ______ in?

Remember what drug is in what class was hard for me, even in fellowship! Now that I use them all the time I can remember them. Just keep going over them and eventually they will stick. A more detailed review of antiarrhythmic drugs is here.

Class IA: “Queen Amy Proclaims Diso’s Pyramid” = Quinidine, Amiodarone, Procainamide, Disopyrimide

Class IB: Lidocaine, mexiletine

Class IC: Flecainde, propafenone

Class II: Beta-blockers

Class III: Sotalol, amiodarone (yes…again), dronedarone, dofeilide

Class IV: Calcium channel blockers (diltiazem, verapamil)

Class V: Mechanism unknown

15. How do you diagnose and treat cardiac tamponade?

Beck’s triad: Hypotension, muffled heart sounds, elevated neck veins Pulsus paradoxus: Abnormal if > 12 mmHg. Review how to measure here. Water Bottle Heart: Chest x-ray finding - heart shaped like a canteen

Cardiac tamponade is a CLINICAL diagnosis, not an echocardiographic one, but an echo will show a pericardial effusion and if the right ventricle is collapsing in diastole, then tamponade is thought to be present (right ventricle is lowest pressure chamber, so collapses first. Pressure is lower in diastole than systole).

Treat with IV fluids to increase preload and prevent right ventricular collapse. Pericardiocentesis is therapeutic.

BONUS: DO NOT rely on analysis of pericardial fluid like we to pleural fluid after thoracentesis of ascites after paracentesis as the whole “transudate or exudate” thing is not validated here.

16. What is the classic triad of symptoms in aortic stenosis?

Angina, Syncope and Dyspnea (from heart failure) is the classic triad.

BONUS: Back in the day aortic valve replacement was not available, so they watched people with severe aortic stenosis to see how long they live. A classic pimp question is mortality based on that triad of symptoms if the aortic valve is not replaced. Average life expectancy is:

Dyspnea = 2 years Syncope = 3 years Angina = 5 years

This pic shows it all:

17. What is the most common cause of mitral valve stenosis?

By far the most common cause is rheumatic heart valve disease. Gunners read on mitral stenosis here.

BONUS: Mitral stenosis is in the differential diagnosis of hemoptysis which can occur due to rupture of a bronchial vein (they call this “pulmonary apoplexy”).

18. What are the indications for aortic valve replacement (AVR) in aortic stenosis and aortic regurgitation?

For either aortic regurgitation or stenosis, aortic valve replacement is indicated when symptoms occur or if the left ventricular systolic function declines, but there is one more tricky one for aortic regurgitation. AVR is indicated even if the left ventricular ejection fraction is normal when the end systolic dimension increases to > 55 mm or end diastolic dimension to > 75 mm on echocardiography.

19. What are the causes of mitral valve regurgitation?

Mitral regurgitation is either organic (actual valve apparatus problem) or functional (dilation of the annulus).

  20. What is the treatment for coronary vasospasm?

DO NOT give beta-blockers!!! So they say this causes “unopposed” agonism at alpha receptors since the circulating catecholamines can’t act on the beta-receptors if a beta-blocker is given. The catecholamines decide to go to the alpha receptors and stimulate them which can worsen vasospasm. Use a non-dihydropyridine calcium channel blocker (i.e. amlodipine). Maybe the two beta-blockers that also block alpha receptors are OK (carvedilol and labetalol), but who knows…there is no data on this.

BONUS: Coronary vasospasm can occur with cocaine intoxication, so the same above principle applies (don’t use beta-blockers).

21. Which statin lowers the LDL the most? Which has fewest side-effects?

Rosuvastatin lowers LDL the most. Pravastatin fewest side-effects and safest in liver disease. Probably not much more to know but for the gunners here is a HMG CoA Reductase inhibitor review.

22. What are the mechanical complications of myocardial infarction?

Acute ventricular septal defect (VSD) Acute mitral regurgitation (MR) Left ventricular free wall rupture

For the gunners read about more complications of MI in the STEMI review.

23. What is the most common cause of aortic valve stenosis in a patient over the age of 70? Under the age of 70?

Over the age of 70 = senile calcific aortic stenosis Under the age of 70 = bicuspid aortic valve

24. In a patient with unstable angina or a non-ST elevation MI (NSTEMI), when should an early invasive strategy be used?

Invasive coronary angiography (an “early invasive” approach) in unstable angina or non-ST elevation MI is indicated when:

1. Increased cardiac biomarkers (troponin, CK-MB) 2. New ST segment depression 3. Signs or symptoms of congestive heart failure (rales on examination, hypoxia with pulmonary edema on chest x-ray) 4. Hemodynamic instability 5. Sustained ventricular tachycardia or ventricular fibrillation 6. Recent coronary intervention within 6 months 7. Prior coronary artery bypass grafting 8. High TIMI risk score 9. Reduced left ventricular systolic function (EF < 40%) 10. Recurrent angina at rest or with low level activity 11. High risk findings from non-invasive testing

25. What are the absolute and relative contraindications to thrombolytics?

Absolute contraindications to thrombolytic therapy include:

1. Prior intracranial hemorrhage 2. Ischemic stroke within 3 months 3. Known cerebrovascular abnormality such as aneurysm or arteriovenous malformation 4. Known malignant intracranial tumor 5. Significant closed head trauma or facial trauma within 3 months

Relative contraindications to thrombolytic therapy include:

1. Uncontrolled hypertension (blood pressure > 180/110) either currently or in the past 2. Intracranial abnormality not listed as absolute contraindication (i.e. benign intracranial tumor). 3. Ischemic stroke > 3 months prior 4. Bleeding within 2-4 weeks (excluded menses) 5. Traumatic or prolonged cardiopulmonary resuscitation (CPR) 6. Major surgery within 3 weeks 7. Pregnancy 8. Current use of anticoagulants 9. Non-compressible vascular puncture 10. Dementia

26. What are the indications for valve replacement in patients with endocarditis?

Congestive heart failure from valvular regurgitation

Failure of antibiotic therapy to successfully suppress the infection or infection with difficult to treat organisms (fungal, Pseudomonas, Brucella, drug-resistant organisms)

Valvular annular abscess

Peripheral embolism of vegetation

Size of vegetation > 1.0 cm

27. What are the common causes of endocarditis?

Streptococcal viridins, Staph aureus, and Enterococcus are the leading three.

BONUS: If Streptococcus bovis endocarditis is associated with colon cancer.

BONUS BONUS: Know the culture negative causes of endocarditis (vegetation on the valve but no organism growing in blood cultures). These are known as the “HACEK” organisms:

Haemophilus aphrophilus Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae

28. What are the secondary causes of hypertension?

Remember “ABCDEF”

Apnea (obstructive sleep apnea), Acromegaly, Accuracy (incorrect measurement) Birth control, Bad kidney Coarctation of the aorta, Cushing’s syndrome, Conn’s syndrome, Catecholamines Drugs (alcohol, nasal decongestants, estrogens) Endocrine disorders, Erythropoietin Fibromuscular dysplasia

BONUS: The most common cause of difficult to control hypertension is uncontrolled obstructive sleep apena followed by renal artery stenosis.

29. Which cardiac biomarker elevates first? Which stays elevated the longest?

Myoglobin elevates first (30 minutes), then troponin and creatine kinase (CK). Troponin stays high for 7-10 days, but CK for only 3-4 days.

30. What are the three types of cardiomyopathy?

Dilated cardiomyopathy: This results in left ventricular systolic dysfunction and clinical manifestations of congestive heart failure. Etiologies include viral, alcoholic, idiopathic, familial and other rare causes. 

Hypertrophic cardiomyopathy: Also known as hypertrophic obstructive cardiomyopathy (HOCM), this results in abnormal hypertrophic changes most commonly in the interventricular septum  with pathologic “myocardial disarray”. HOCM is familial in about 50% of cases and transmitted in an autosomal dominant fashion. HOCM can result in clinic heart failure, life-threatening arrhythmias, mitral regurgitation and sudden cardiac death.

Restrictive cardiomyopathy: This results in heart failure related to severe diastolic dysfunction. Causes include amyloid heart disease, infiltrative disorders, and familial.

Physical Examination Pimps

31. Take a listen to his heart, do you hear the S4 heart sound?

NO YOU DON’T!!! The patient is in atrial fibrillation and CAN’T have an S4 heart sound! Recall that an S4 happens when the atrium contracts into a non-compliant left ventricle causing the blood to forcefully strike the left ventricle creating the sound. Patients with atrial fibrillation DO NOT have any atrial contraction and are not able to have an S4 heart sound. Don’t let your attending trick you…

32. What causes an S3 heart sound versus an S4 heart sound?

An S3 heart sound, a.k.a. the ventricular gallop can be present in systolic heart failure, but can also be there in normal healthy hearts. The S4 heart sound is almost always pathologic and can occur in the setting of diastolic heart failure and/or myocardial ischemia.

33. How severe is the aortic stenosis on exam?

There are only 3 ways to tell  how severe the aortic stenosis is on physical exam:

1. Timing of the murmur peak (late in systole = severe) 2. The intensity of the S2 heart sound (soft or absent = severe) 3. Pulsus Parvus et Tardus (carotid upstroke weak and late)

34. What are the three causes of a holosystolic murmur?

Mitral regurgitation, tricuspid regurgitation, ventricular septal defect.

BONUS: The “Galliveridin” phenomenon in aortic stenosis is when the murmur radiates to the apex and can sound holosystolic mimicking mitral regurgitation. Handgrip maneuvers or transient arterial occlusion will increase mitral regurgitation and not the aortic stenosis murmur. Gunners read an aortic stenosis review here.

35. Describe the murmur of aortic regurgitation.

Early diastolic decrescendo. If an actual valve problem caused the aortic regurgitation (i.e. endocarditis), then the murmur is at the left lower sternal border BUT if it is from dilation of the aorta (i.e. ascending aortic aneurysm as occurs in Marfan’s), then the murmur is at the aortic listening post which is the right upper sternal border. Tricky.

BONUS: The murmur is best heard with the patient leaning forward at end-expiration.

BONUS BONUS: When the aortic regurgitation is severe the murmur is quite short in early diastole since sooooo much blood leaks back into the left ventricle that the pressure between the aorta and the LV equalize quickly. Conversely, if mild it takes quite some time for the pressure to equalize so the murmur is longer (see pic)

36. What is the Austin-Flint murmur?

This is when the aortic regurgitation get strikes the anterior leaflet of the mitral valve in diastole forcing it partially closed. This kind of creates a mitral stenosis-like picture and a “diastolic rumble” at the cardiac apex called the Austin-Flint murmur.

37. What are some of the peripheral signs of aortic regurgitation?

Reel off all of these and people will be staring with their mouths wide open:

Corrigan’s pulse: A rapid and forceful distension of the arterial pulse with a quick collapse. De Musset’s sign: Bobbing of the head with each heartbeat (like a bird walking). Muller’s sign: Visible pulsations of the uvula. Quincke’s sign: Capillary pulsations seen on light compression of the nail bed. Traube’s sign: Systolic and diastolic sounds heard over the femoral artery (“pistol shots”). Duroziez’s sign: Gradual pressure over the femoral artery leads to a systolic and diastolic bruit. Hill’s sign: Popliteal systolic blood pressure exceeding brachial systolic blood pressure by 60 mmHg or greater (most sensitive sign for aortic regurgitation). Shelly’s sign: Pulsation of the cervix. Rosenbach’s sign: Hepatic pulsations. Becker’s sign: Visible pulsation of the retinal arterioles. Gerhardt’s sign (aka Sailer’s sign): Pulsation of the spleen in the presence of splenomegaly. Mayne’s sign: A decrease in diastolic blood pressure of 15 mmHg when the arm is held above the head (very non-specific). Landolfi’s sign: Systolic contraction and diastolic dilation of the pupil.

38. What maneuver makes the murmur of hypertrophic obstructive cardiomyopathy (HOCM) louder?

Valsalva decreases left ventricular filling. In HOCM this allows the very thick interventricular septum to buldge more into the left ventricular cavity causing more of a left ventricular outflow tract obstruction, thus making the murmur louder. Much different than the murmur of aortic stenosis (see pic).

39. What murmur gets louder with inspiration?

Tricuspid regurgitation does. This is called “Carvallo’s sign”. Pulmonic regurgitation can sometimes as well.

BONUS: Severe tricuspid regurgitation causes large “V waves” in the jugular venous pulsations from blood leaking back from the right ventricle into the internal jugular during systole. Also look for a pulsatile liver.

ECG Pimps

First of all, you need to know the basics, like how to diagnose a left and right bundle branch block, chamber enlargements, axis, heart rate, myocardial infarctions etc… read the ECG Review here. Below are some of the specific ECG pimp questions that I have run into.

40. What is the most common ECG findings of pulmonary embolus?

Everyone wants to reflexively say “S1Q3T3” and if you do, then you are wrong. It is sinus tachycardia. The S1Q3T3 pattern is the classic finding (see pic below), but sinus tachycardia is more common.

BONUS: The S1Q3T3 pattern is not just for pulmonary embolism, but for anything that causes acute right heart strain (can occur in COPD or asthma exacerbations, respiratory failure etc…) and it is also called the McGinn-White sign.

41. Can you diagnose a myocardial infarction on ECG if there is a left bundle branch block (LBBB)?

Whoooo hoooo! You are ready for this one! You know that traditionally the answer is no, ischemia is not readily detected if a left bundle branch block (LBBB) is present, but there are some means to do this. The Sgarbossa criteria, Chapman’s sign, Caberera’s sign and also by examining the T waves in lead V5 and V6. Know these and you will look like a superstar!

Sgarbossa criteria: This is a point scoring system.

1. ST elevation > 1 mm and in the same direction (concordant) with the QRS complex. 5 points

2. ST depression > 1 mm in leads V1, V2, or V3. 3 points

3. ST elevation > 5 mm and in the opposite direction (discordant) with the QRS. 2 points

A score of 3 points is required to diagnose an acute myocardial infarction. Criteria #3 is under debate as to its usefulness, so basically you need to have either criteria 1 or criteria 2. Below is an image of ST elevation in V5 and V6 with a LBBB:

Chapman’s sign: A notch in the upslope of the R wave in lead I, aVL or V6. This has a low sensitivity, but a specificity of about 90%. See Chapman sign ECG here.

Cabrera’s sign: Notching at 40 milliseconds in the upslope of the S wave in lead V3 and V4. This has a poor sensitivity of 27% for myocardial infarction. See Cabrera’s sign ECG here.

T waves in V5 and V6: If upright in these leads when a left bundle branch block is present, then ischemia is more likely present, although sensitivity is low for this finding.

42. What are the causes of AV dissociation on ECG?

Ventricular tachycardia (VT) and complete heart block (3rd degree AV block)

Here is AV dissociation from VT:

Here is AV dissociation in complete heart block:

BONUS: When AV dissociation is present, this causes the atria to contract at the same time as the ventricle when the P wave falls on top of the QRS complex. Thus, the atrium is contracting against a closed mitral/tricuspid valve. This makes blood forcefully go backwards causing intermittent “cannon A waves” in the jugular venous waveform.

BONUS BONUS: That huge stretch of the atrium during AV dissociation due to the above mentioned atrial contraction against closed valves causes release of ANP (atrial natriuretic peptide) which causes diuresis and thus polyuria! Yes…polyuria can be a symptom of complete heart block! BAAAMMM!!! Not too many people know this and it will certainly impress.

43. What are the ECG changes of hyperkalemia and what can you give to resolve them?

Peaked T waves is the answer most people are looking for. The QRS complex can widen in a non-specific pattern (not left or right bundle) a.k.a. a “non-specific intraventricular conduction delay”. Eventually

44. The patient has 2:1 AV block - How can you tell if it is 2nd degree type I or 2nd degree type II AV block?

First quick rule: If the PR interval of the conducted beat is prolonged AND the QRS complex is narrow, then it is most likely second degree type I AV nodal block (Wenckebach). Alternatively, if the PR interval is normal and the QRS duration is prolonged, then it is most likely second degree type II AV block and a pacemaker is probably warranted.

Less quick rule: Exercise the patient. Walk them in the hall or on a treadmill. If it is 2nd degree type I, the heart rate will increase and you will see prolonging PR intervals until a beat is dropped. If it is 2nd degree type II, then nothing will happen. You can also give atropine or do a carotid massage and see what happens.

Here is a pic of 2:1 AV block:

45. What is a _____ wave on the ECG?

Detla wave = Wolff-Parkinson White (short PR interval that is slurred into the QRS complex)

Osborne wave (a.k.a. J wave) = Classically hypothermia, but also hypercalcemia

U wave = hypokalemia

Epsilon wave = Arrhythmogenic right ventricular dysplasia (ARVD) which is RARE

46. What are the causes of ST elevation on ECG besides acute MI?

ECG Causes of ST segment elevation: ELEVATION

Electrolyte abnormalities Left bundle branch block Aneurysm of left ventricle Ventricular hypertrophy Arrhythmia disease (Brugada syndrome, ventricular tachycardia) Takotsubo/Treatment (iatrogenic pericarditis) Injury (myocardial infarction or cardiac contusion) Osborne waves (hypothermia or hypocalcemia) Non-atherosclerotic (vasospasm or Prinzmetal’s angina)

47. What are the ECG findings of a posterior MI?

You better know anterior and inferior MI ECG changes. The posterior MI ECG findings are a bit more tricky:

ST segment depression (not elevation) in the septal and anterior precordial leads (V1 to V4). This occurs since these ECG leads will see the MI backwards (since the leads are placed anteriorly, but the myocardial injury is posterior).

The ratio of the R wave to the S wave in leads V1 or V2 is > 1.

ST elevation in the posterior leads of a posterior ECG (leads V7 to V9). Suspicion for a posterior MI must remain high, especially if inferior ST elevation is also present.

ST elevation in the inferior leads (II, III, and aVF) may be seen if an inferior MI is also present

48. What are the three irregularly irregular rhythms on ECG?

The three irregularly irregular rhythms are atrial fibrillation, atrial flutter with VARIABLE conduction and multifocal atrial tachycardia (MAT)

49. What are the causes of a prolonged QT interval?

Electrolyte abnormalities (hypokalemia, hypocalcemia, hypomagnesemia)

Medications (quinolones, macrolides, haloperidol, class IA and class III antiarrhymics)

Genetic long QT syndromes

Myocardial ischemia 

BONUS: Patients with a prolonged QT interval are at risk for Torsades de Points or polymorphic ventricular tachycardia (see pic). Treat with IV magnesium.

50.  How can you distinguish the ECG findings of pericarditis from myocardial infarction or early repolarization?

The ST elevation that occurs in pericarditis is “diffuse” meaning in every lead. Acute MI frequently has “reciprocal” ST depression and less commonly PR segment depression as is present in pericarditis.

BONUS: Another cause of PR depression is “atrial infarction”.

Any other pimp questions you have run into that you think we should know?

Leave a comment on the LearnTheHeart.com blog article “Top 50 Cardiology Pimp Questions”

[mdintraining]

I’m pretty sure I’m not the only one who has trouble remembering developmental milestones. I put these together, but can’t take credit for any of the photography. Hope someone finds them helpful!

[movioletta]

Dear medical Publishers, a book containing 700 pages is hardly a “pocket guide”, thanks for coming to my Ted talk. 

[ihearthisto]

The Seamless Gut by i♡histo

Each region of your digestive tract is histologically different.

Specialized in its own unique way to impart a specific function. When the different regions of these tubes work together they function as a seamless system that protects, absorbs and secretes. Ensuring that we digest the products we ingest, remove the nutrients that we need and dispose of those that we don’t.

Students of histology frequently meditate on the differences between these regions in an attempt to correlate structure with function and categorize regions based on appearance.

The seamless gut tube demonstrates these differences in a single image allowing junior histologists to compare and marvel in the functional specializations of each region.

1. Esophagus

The non-keratinized stratified squamous epithelium provides protection against the abrasive forces encountered as the food bolus is transmitted toward the stomach. 

Note the epithelium has a thin layer of smooth muscle underneath it called the muscularis mucosa. The presence of this tells you that you are observing esophagus and not another region of non-keratinized stratified epithelium in the body (e.g. anal canal or some regions of the oral cavity like the cheek)

The muscularis externa is composed of a unique smooth and skeletal muscle mix (in the middle 1/3rd). The upper 1/3rd it is all skeletal muscle. The lower 1/3rd it is all smooth muscle.

2. Stomach

This is the fundus of the stomach (the cardia and pylorus have a different appearance). 

The large folds of mucosa and submucosa are rugae, which allow the stomach to distend as it fills with food.

The glandular epithelium is composed of gastric pits opening into deep gastric glands. These contain numerous cells each with their own role to play in the digestion process through secretion of either hydrochloric acid (parietal cells), pepsinogen (chief cells), mucus (surface/neck mucous cells) or hormones (enteroendocrine cells).

3. Duodenum

The start of the small intestine! The mucosa becomes heavily folded to form villi, finger-like projections that increase the surface area across which absorption can occur.

Each simple columnar epithelial cell also has a highly folded apical membrane forming microvilli, which further increases the surface area for absorption.

You can always identify duodenum from other regions of small intestine because of its distinctive Brunner’s glands in the submucosa. These release a bicarbonate rich secretion into the duodenal lumen to neutralize the acidic contents released from the stomach and helping prevent duodenal ulcer. The pancreatic enzymes that are released here (trypsin and chymotrypsin) also work best at a more neutral pH…so that’s a bonus!

4. Jejunum

Villi, microvilli and plicae circulares (circular folds of the mucosa) are evident in the jejunum. It lacks any submucosal features which makes it easy to distinguish from other regions of the small intestine - duodenum and ileum.

5. Ileum

The final section of the small intestine also contains villi and epithelial cells with microvilli.

Large lymphoid aggregates known as Peyer’s patches reside in the submucosa, breach into the lamina propria. Peyer’s patches are a distinctive feature of the ileum and you will never confuse it for other regions of the small intestine if you look out for them.

6. Appendix

Similar to the appendix at first glance, the appendix contains lymphoid nodules. However these completely surround the organ (instead of forming patches). If you look closely you will also see that this vestigial region of gut tube has no villi or microvilli (which is a feature of the small intestine). Instead its mucosa contains deep crypts of Lieberkuhn lined by goblet cells that secrete mucus, like in the colon…

7. Colon

Distinctive because of its large crypts of Lieberkuhn lined by goblet cells that produce large volumes of mucus. The mucus facilitates the passage of feces which become increasingly dry as more water is absorbed from them as they pass through the large intestine.

The muscularis externa has a distinctive arrangement in the colon also. The outer longitudinal layer of muscle no longer forms a sheet of smooth muscle around the tube, but is organized into three thin, evenly spaced bands called teniae coli.

If you are a student of histology. Look for these features and you will be able to identify any region of the digestive tract. Guaranteed.

i♡histo