What’s the relationship between aneurysm, thrombosis, and stenosis?

I got this really great question from one of my students, and it got me thinking about how important it is to have really clear definitions of pathologic conditions. These three conditions – aneurysm, thrombosis, and stenosis – are totally different things. And yet they can sometimes co-occur, or one can cause another – so it can become confusing!

I thought I’d share the question and my answer here, because I’m sure there are other students who are having trouble understanding these disorders.

Here’s the question:

I was reviewing the Blood Vessel Pathology lecture notes from this past week and was having a bit of trouble differentiating between aneurysm, thrombosis and stenosis. I’ve written what I believe to be the differences, but would you mind giving me some feedback on if this is correct?

“An aneurysm is when a clot occurs, widening the blood vessel to unhealthy proportions due to high blood pressure and or atherosclerosis, and it may rupture with no warning signs, leading to internal bleeding. The difference between aneurysm and thrombosis is that aneurysm causes damage to the lining wall of the blood vessel. Thrombosis is clotting of a blood vessel without damage to the walls. Stenosis is narrowing of the artery to cause clotting, and it comes with the warning sign of severe chest pain.”

Great question!! You’re on the right track – but there are some things in your statement that aren’t quite right – so I’ll give you my definitions and then comment on what you wrote.

Aneurysm

An aneurysm is an abnormal widening (or dilation, or outpouching) of a blood vessel. It’s focal in nature, which means that it’s just in one place; you can point to where it is (it’s not like the entire vessel is just a little bit wider). Here’s an image of a normal vessel and a vessel with an aneurysm:

Aneurysms can be caused by lots of things (like trauma and atherosclerosis), or they can be congenital. Sometimes aneurysms just sit there and never cause any problems. But sometimes they get larger and larger, and the vessel wall weakens to the point where it eventually ruptures.

Thrombosis

A thrombosis (or thrombus) is an abnormal blood clot. It’s not just a normal little blood clot formed to repair a hole in a vessel – it’s a blood clot that’s been made when it isn’t needed. The most common place for a thrombus is in the deep veins of the legs – but you can form a thrombus anywhere in the body.

It’s not good to have a thrombus for a few reasons:

  • If it’s big enough, the thrombus can block blood flow through the vessel, and the tissues fed by that vessel can be damaged or even die as a result.
  • Thrombi can weaken and damage the vessel wall, leading to other problems (like aneurysms, or even rupture of the vessel if it gets weak enough).

Here’s a related term: embolus. An embolus is a blood clot that’s floating in the blood (maybe it broke off from a thrombus in the leg, or maybe it formed on its own somewhere). The point is that it is mobile, and it’s going to move with the blood until it gets to a vessel that’s too small for it to pass through, and it will lodge there. If the embolus is tiny, you may not notice anything clinically. But if the embolus is big enough to block off an important vessel (say, one of the vessels in the brain), that means that the tissue fed by that blood vessel won’t get blood, and it will die.

Stenosis

Stenosis just means “narrowing.” It can be used to describe abnormal narrowing of lots of different structures in the body (like heart valves and the spine). When a blood vessel is stenotic, that means its lumen is smaller than normal.

There are many possible causes of stenosis in vessels. Here are some common ones: atherosclerosis (formation of plaques that take up space and narrow the lumen), thrombosis (formation of an abnormal clot that takes up space within the vessel lumen), and vasculitis (inflammation of the vessel).

Like the other abnormalities we talked about above, stenosis can be asymptomatic if it is mild. But if a vessel is very stenotic (for example, if the vessel lumen is only 20% of its normal diameter), that can impair blood flow enough to cause serious problems to the tissue downstream. This is particularly a problem if the vessel feeds the heart or the brain; in these places, restriction of blood flow can cause severe symptoms (or even death).

Why these things are confusing

These three conditions are distinct and separate entities – but they can occur together, and they can also occur sequentially – and this can be confusing. For example, if you have a thrombus in a vessel, that can weaken the vessel wall enough to cause an aneurysm. Or you can have a thrombus that simply sits there and takes up space in the vessel lumen, causing stenosis of the vessel.

So the best way to approach this is to make sure you understand what each of these disorders is – and then once you have that down, you can go on to learn about what causes them and what they can lead to.

Back to the statement part of the question – my comments are in blue.

An aneurysm is when a clot occurs, widening the blood vessel to unhealthy proportions due to high blood pressure and or atherosclerosis, and it may rupture with no warning signs, leading to internal bleeding. You’re correct in saying that an aneurysm is a widening of a blood vessel that may be caused by high blood pressure or atherosclerosis, and that it may rupture. And it’s true that aneurysms can be caused by abnormal blood clots (thrombosis) – but just to clarify – not all aneurysms are caused by clots. The main point is that an aneurysm is an abnormal widening of a blood vessel – and there are many potential causes. The difference between aneurysm and thrombosis is that aneurysm causes damage to the lining wall of the blood vessel. Thrombosis is clotting of a blood vessel without damage to the walls. No; the difference between aneurysm and thrombosis is that an aneurysm is an abnormal dilation/widening of a blood vessel, whereas a thrombosis is a blood clot that forms within a blood vessel. Both aneurysms and thromboses can damage the vessel wall. Stenosis is narrowing of the artery Yes! to cause clotting Not exactly. Stenosis is just the narrowing of a vessel lumen; it doesn’t necessarily cause the formation of a blood clot. However, thrombosis (abnormal clotting) can lead to stenosis (narrowing of the vessel lumen)! This is where you have to be really strict about your definitions, otherwise it gets confusing! and it comes with the warning sign of severe chest pain Sometimes! If the stenotic vessel is one that supplies the heart, and if the stenosis is moderately severe (meaning that the lumen is narrowed enough to decrease the amount of blood that can flow through the vessel), then the patient will experience chest pain (because there’s less blood flow to the heart than usual). This is a warning sign – it tells you that the tissue isn’t getting quite enough blood flow, and you better go see a cardiologist and get those vessels looked at. However, if the stenosis is really severe (like if the lumen is only 10% of its normal diameter), then almost no blood is getting through, and that may be enough to actually cause tissue death (myocardial infarction, or heart attack). In this case, the chest pain the patient experiences isn’t just a warning sign – it’s a sign that the tissue is actually dying right now.

Does pyknosis occur in necrosis or apoptosis?

Q. Would a pyknotic cell be a form of necrosis or apoptosis? Or am I totally off base here?

A. No you’re totally not off base – that’s a really good question!!

We typically use the word “pyknosis” to mean one of the three nuclear patterns seen in necrotic cells…but pyknosis can also occur in apoptosis! I’ll explain a bit more.

When cells undergo necrosis, they show a lot of different morphologic abnormalities. Overall, necrotic cells appear enlarged and more eosinophilic, and their nuclei look abnormal due to breakdown of DNA. There are three specific patterns of nuclear change in necrosis, which are:

  • Pyknosis (the nucleus shrinks and becomes dark blue/black)
  • Karyorrhexis (the nucleus breaks apart, or fragments, like a cookie crumbling into bits)
  • Karyolysis (the nucleus just fades away)

Here’s a nice diagram I found (I modified it a bit from the original) showing these changes:
When cells undergo apoptosis, they also show a lot of different morphologic features. Overall, apoptotic cells appear shrunken, with really dense, dark, eosinophilic cytoplasm, and the chromatin in the nucleus aggregates into a dense mass which can fragment. Here’s a photo from Robbins showing an apoptotic cell:

The word “pyknosis” isn’t typically used when describing an apoptotic cell – but Robbins does say that pyknosis can be a feature of apoptotic cells, so there you go.

So…the bottom line is that pyknosis is a nuclear change in which the nucleus shrinks and becomes dark blue/black. Typically, we associate the word “pyknosis” with necrotic cells – but apoptotic cells can show pyknosis too.

How to study diseases

If you want to be precise, the word pathology means “the study (logos) of pain (pathos).” And it’s true, in a way, because a lot of the things we discuss in pathology involve some sort of pain. Not to mention the pain of studying pathology itself, but we won’t get into that, since this is a pain-free space.

What we really study in pathology isn’t pain, exactly, but disease. So if you’re starting out in a pathology course – or even if you’re halfway through – it’s not a bad idea to come up with a little plan of attack for studying diseases.

Why use a plan when learning new diseases?

Because it reduces your cognitive load. You have to hold and process information in your working memory before you can put it in your long-term memory. And your working memory has limited space! So if you approach every disease a different way, and just try to memorize everything, you won’t actually get that information into your long-term memory – and obviously, that’s important for passing exams.

But if you have a little mental template that you use for each disease, that organizes the information into smaller, meaningful chunks that WILL stay in your working memory. Also, if you do that for every disease, it lets your brain relax a bit, because your brain likes categories and consistency.

Here’s a good plan.

Here is a disease plan that works well for pathology because it’s simple, straightforward, and widely applicable. It breaks information down into four categories:

  1. Etiology (cause)
  2. Pathogenesis (mechanism)
  3. Morphology (gross and microscopic appearance)
  4. Clinical manifestations (signs and symptoms)

Can I see an example?

But of course! Let’s take a look at how this would work for a particular disease: squamous cell carcinoma of the lung.

  1. Etiology: smoking
  2. Pathogenesis: The epithelium of the lung passes through several stages – including dysplasia and carcinoma in situ – before developing into invasive carcinoma. Each stage is characterized by different and new genetic abnormalities within the epithelial cells.
  3. Morphology: squamous cell carcinoma cells are large, with abundant cytoplasm and intercellular bridges.
  4. Clinical manifestations: persistent cough and weight loss.

There you go! Obviously you’d want to flesh out these categories a bit more – but this would be a good start.

One last piece of advice

One more nice thing about this plan is that it helps you avoid the “can’t see the forest for the trees” problem so common when you’re first learning about a disease. This plagued me during medical school. I’d learn so much about tiny details that I couldn’t zoom out and give you a big picture. It’s better to start with the big picture and then add in details later.

Your brain will say “Thank you for reducing my cognitive load! I’m so happy!”

Is Factor V Leiden a Mendelian Disorder?

Here is a great question I got from a student about the genetics of Factor V Leiden.

Q. Factor V Leiden is autosomal dominant – but it doesn’t seem to follow Mendel’s laws. Would you say it shows incomplete dominance?

A. This is such a good question! Factor V Leiden is an autosomal dominant disease – and you’re right: it does NOT follow Mendelian laws. However, the non-Mendelian pattern it follows is not incomplete dominance, but incomplete penetrance.

First, here’s why Factor V Leiden is a non-Mendelian disorder.

Factor V Leiden is an autosomal dominant disease. If it followed Mendel’s laws, everyone who inherited ether one or two copies of the Factor V Leiden gene (which is the dominant gene) would display the same phenotype (in this case, they’d all have the same exact amount of abnormal clot formation). But that’s not how it works in this disease.

Patients with factor V Leiden have an increased risk of developing abnormal clots. But not everyone with an FVL gene (or even with two FVL genes) develops a clot! Some do, and some don’t. So the phenotype is not the same in everyone with the FVL gene.

So how would you describe this non-Mendelian weirdness?

This weird phenomenon is called incomplete penetrance.

In Mendel’s experiments, his dominant alleles showed complete penetrance. In other words, every plant with a genotype containing a dominant allele (or two!) always displayed the same phenotype.

But in real life, that’s not always the case – sometimes penetrance is not complete, and factor V Leiden is a good example. As we mentioned above, the factor V Leiden gene confers an increased risk of abnormal clotting – but that’s all it is, just a risk, not a certainty. So some patients with the FVL gene display the disease phenotype, and some do not.

Incomplete dominance is also a non-Mendelian pattern of gene expression – but it’s different than incomplete penetrance.

In Mendelian dominance, there are two alleles and two phenotypes. In the left image below, the two phenotypes are purple and white flower colors – and as long as you have at least one dominant allele (in this case, P), you’ll get a purple flower.

In incomplete dominance, there are two alleles and three phenotypes. In the right image below, the phenotypes are red, white, and pink flower colors. If you are homozygous for either the R or the W allele, you’ll get a red or a white flower. But if you have both the R and the W allele, you’ll get a “blend” of the two other phenotypes – a pink flower!

 

 

Mendelian dominance

 

Incomplete dominance

 

Snapdragons actually display this incomplete dominance pattern! Good thing Mendel happened to use sweet peas in his experiments.

 

 

What exactly does “storiform” mean?

Do you know what a “storiform” pattern is? Yeah, neither did I when I was a medical student. However, that term did get thrown around in pathology lectures a lot, without any description or definition. There are lots of terms like this – so I’m gonna just go ahead and create a new category called:

Words Pathologists Use In Lecture As If You Know What They Mean.

I think it’s important to pause and define these terms, because otherwise this is what happens: given the sheer volume of stuff you’re supposed to learn, and the minimal amount of time you have to accomplish this task, you’re not going to look up every word you have a nagging doubt about. You’re going to infer the meaning from whatever was said in lecture, and wind up with a fuzzy and probably incorrect definition. And then someone will ask you about it on rounds, and it will be frustrating.

SO. We’ll start with “storiform” today – and I’ll keep adding posts about terms in this category as I run across them. Please email me if you find a word like this! Then we’ll wind up with a nice glossary of these formerly-unexplained terms, and you’ll look like the star you are when one of these terms comes up on rounds.

First, a little Latin

Storiform comes from the Latin storea (woven mat) and formis (form, or pattern) – so technically, storiform means “having the pattern of a woven mat.” When we use “storiform” in pathology, though, it has a more specific meaning. It refers to a tumor pattern consisting of spindle cells in a pinwheel-shaped arrangement (radiating out from a central core).

What does it look like?

Sooo…what does a pinwheel-shaped arrangement of spindle cells look like under the microscope? Let’s try looking at an un-marked slide first, just to see if you can find pinwheels on your own. Here’s an image (below, right) of a skin lesion called dermatofibrosarcoma protuberans (DFSP), which is known for its storiform pattern. Take a look and see if you can find areas where the tumor cells are arranged in a pinwheel-shaped fashion. Then scroll down to see a labeled image.

Ready to see the labeled image? Okay, scroll down….

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Keep going…

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Here’s the same image, faded out a bit so you can see the pinwheel-shaped areas outlined in black:

Okay, they’re not perfectly symmetrical pinwheels, but they do look pinwheel-ish, with tumor cells radiating out from a central core region.

One last thing, now that we’ve got the pinwheels down…if you go back and look at the unmarked image again, you might be able to imagine that the cells are arranged like a woven mat, like the Latin term suggests.

I hope you feel comfortable with “storiform” now. That’s one less undefined term!

How do gallstones form?

There are two types of gallstones: cholesterol stones and pigment stones. If you didn’t know anything about gallstones, you’d guess (rightly so) that cholesterol stones are made up of cholesterol. And you’d also probably guess that you get cholesterol stones when there’s too much cholesterol around. But how, exactly? And pigment stones – what are those made of? Pigment?

Turns out there are very good explanations for all of these questions. Let’s take a look.

Cholesterol gallstones

Cholesterol gallstones contain – not surprisingly – cholesterol. And they arise when there’s more cholesterol around than the gallbladder can handle. But what does this actually mean?

A tiny bit of basic science here. Under normal conditions, cholesterol is soluble in bile because it binds to bile salts (which are water-soluble) and lecithins (which are water-insoluble). These guys both act like detergents, and cholesterol is dispersed within the bile, and everything’s cool.

But what happens if there’s too much cholesterol around? If the concentration of cholesterol exceeds the solubilizing capacity of bile, then cholesterol will nucleate into solid cholesterol crystals, which can over time get big enough to form stones.

Pigment gallstones

These stones are made of unconjugated bilirubin (mixed with calcium salts). They’re called pigment gallstones because they’re dark brown to black in color (compared to cholesterol stones, which are usually pale yellowish-greenish in color).

The two main conditions in which you see pigment stones are chronic hemolytic anemia and infection of the biliary tract. Why would these conditions lead to an accumulation of unconjugated bilirubin in the bile? In order to answer that, let’s quickly review bilirubin metabolism in the bile itself.

Normally, the liver conjugates bilirubin and dumps it into the bile. So the bile contains just conjugated bilirubin, then, right? Wrong! About 1% of the bilirubin in bile undergoes deconjugation while it’s still in the biliary tree (betcha didn’t know that!). Bile is then dumped into the gut, where bacterial-glucuronidases convert most of the remaining conjugated bilirubin into its unconjugated form.

Back to the causes of pigmented stones. If you have an infection in the biliary tree, and the infectious agent makes glucuronidase, then you’ll end up deconjugating more bilirubin than normal…and over time, that unconjugated bilirubin can accumulate and form stones.

The other main cause of pigmented stones is chronic hemolysis. If you’re busting open lots of red cells, all that heme gets transformed into bilirubin, which the liver conjugates and dumps into the bile. So the bile contains a lot more bilirubin than usual. Most of that bilirubin remains conjugated – but around 1% is turned into unconjugated bilirubin right there in the biliary tree. If you’re making a lot more bilirubin than normal, that 1% is significant – and over time, that excess of unconjugated bilirubin can be enough to lead to pigment stones.

Name that organism!

Can you identify this organism?

Wow, I got lots of good feedback on the last post I did with a “name that bug” theme – so I’m going to do more! I like learning this way – especially when there’s no one around to judge you. Unknown conferences during pathology residency could be pretty brutal…but we’re all friends here – so if you don’t get the answer right, it’s not a problem – it’s just an opportunity to learn something new. How nice.

Okay. Start by taking a look at this image – maybe you’ll know right away what it is, and maybe you won’t. If you want more hints, just scroll down a little and keep reading.  The answer is at the bottom – so don’t scroll way down until you’re ready.

How do you get it?

Our mystery organism makes its home in soil. It particularly likes damp soil that’s rich with decomposing stuff (like wood and leaves). In the US, it’s seen mostly in central eastern and southeastern states (if you draw a line from the western border of Minnesota down to the eastern border of Texas, this organism doesn’t really like to live west of that line). It’s seen in Canada too.

What are the symptoms?

This organism typically just affects the lungs – but some patients do develop disseminated disease. Very rarely, the organism directly infects the skin, and just causes problems there. Most patients present with abrupt-onset productive cough, fever, chills, and chest pain. It may resolve on its own, or hang around and become chronic.

What does it look like?

The main thing you see under the microscope with this organism is suppurative (pus-filled) granulomas. Macrophages aren’t so great at killing this organism – so neutrophils come to the rescue (they’re the main cellular constituent of pus).

The organism itself is a round, with a thick (some say “double-contoured” but our photo doesn’t show that) cell wall, and – here’s the kicker – broad-based budding. In a histologic section, like this one (which is stained with PAS, by the way), you can see nice big nuclei in each round organism.

The cells in green circles are neutrophils (you can tell by their “busy” nuclei that look like Mickey Mouse ears); the yellow arrow points to the thick cell wall, the red arrows point to the nuclei, and the red oval points out the broad-based budding between two organisms.

Okay. Ready for the answer? Scroll down…

 

 

Keep going!

 

 

 

 

 

 

 

This organism is Blastomyces dermatitidis! Normally, I’d link the image itself – but in this case, I didn’t want you to accidentally see the answer…so here’s the link.

Here’s a recap of the main things to remember about Blastomyces and blastomycosis:

  • Lives in decomposing soil
  • Ohio and Mississippi river valleys
  • Usually just causes pneumonia, but can become disseminated
  • Rarely, localized to skin (which is probably why it got the name dermatitidis)
  • Suppurative granulomas
  • Large, round, thick-walled organisms with broad-based budding

Finally, as an aside, I remember when we were learning this in med school, we put a capital “B” by the organism, because it’s Blastomyces (obviously), and:

  • It’s pretty big
  • It shows broad-based budding
  • When it buds, it kind of looks like a capital B if you use your imagination.

 

Name that organism!

Can you identify this organism?

Start by taking a look at the image – and if you need more hints (it’s okay if you do!), keep reading. The answer is at the bottom – so don’t scroll down until you’re ready.

How do you get it?

Let’s start by talking about the places you’re most likely to encounter our mystery organism. This little guy likes to hang out in contaminated dust or soil. The most common means of contamination is through bird or bat droppings (yuck). The organism is acquired by inhalation – so spelunkers (who might breathe in soil with bat poopy) and construction workers (who might breathe in dust with bird poopy) are at increased risk.

Endemic areas in the US include the Ohio and Mississippi rivers. Outside the US, this organism is endemic in the Caribbean – but it’s also found in a bunch of other places (Mexico, Central and South America, eastern/southern Europe, Africa, eastern Asia, and Australia). I hate these long lists, btw. I mean, you might as well memorize the places this organism is NOT found. In these situations, it’s best to just memorize the endemic places first, and then if there’s room in your head later, you can stick in the other places.

What are the symptoms?

This organism can produce several different clinical patterns of disease, including:

  • Focal, self-limiting lung lesions with mild or no symptoms
  • Chronic, progressive lung disease with cough, fever, and night sweats
  • Disseminated disease

Although disease can occur in immunocompetent patients, it’s more common (and more severe) in patients who are immunocompromised.

What does it look like?

The main histologic abnormality this organism causes is granulomas. Non-immunocompromised patients get caseating granulomas which tend to undergo calcification after a while. Immunocompromised patients can’t really form nice granulomas, especially if they have diminished T cell function (because you need working T cells to make granulomas). So in these patients, you’ll just see clumps of organism-containing phagocytic cells here and there.

The organism itself is a cute little guy – emphasis on little. In fact, it’s so tiny that you really have to go on high power to see it. It’s usually seen in macrophages (weird place to hang out, unless you have a death wish). It’s spherical in shape, and its walls are thin.

Here’s a labeled image so you can see what’s going on. The red circles all show macrophages stuffed with varying numbers of organisms and/or cut in varying planes of section. What you’re really seeing is the cytoplasm of these macrophages (it’s often hard to see macrophage nuclei, especially when they’re so stuffed). There are TONS of organisms, but I’ll just point out one really good one (red arrow) to sear into your brain for future reference.

Okay. Ready for the answer? Scroll down…

 

 

Keep going!

 

 

 

 

 

 

 

This organism is Histoplasma capsulatum! Normally, I’d link the image itself – but in this case, I didn’t want you to accidentally see the answer…so here’s the link. The CDC has a lot of great images, by the way, if you’re ever looking for one for a presentation.

Here’s a recap of the main things to remember about Histoplasma and histoplasmosis:

  • Inhalation of dirt with bird/bat poopy
  • Ohio and Mississippi rivers, Caribbean
  • Asymptomatic, or chronic lung disease, or disseminated disease
  • Worse in immunocompromised patients
  • Cute, tiny, round organisms in macrophages

 

What does megaloblastic mean?

Here are a few great questions about megaloblastic anemia I received by email.

Megaloblastic vs. macrocytic

Q. Do I have to say “megaloblastic macrocytic” anemia? Aren’t megaloblastic and macrocytic the same thing?

A. Macrocytic refers to the size of the mature red cells in the blood. It means that the red cells are big. Normal is 80-100 femtoliters. If the red cells are over 100, they’re macrocytic; if they’re under 80, they’re microcytic.

Megaloblastic refers to the weird morphologic changes (immature nucleus, mature cytoplasm, large overall size) you see in red cell precursors (and, to some extent in neutrophil precursors), in patients who are B12 deficient. So the term is really referring to the cells in the bone marrow, not mature, circulating red cells. However, you can also see changes in the blood that indicate megaloblastic anemia, the most common of which is hypersegmented neutrophils (like the one above).

So the terms are not equivalent.

That being said, you don’t need to say both terms if you have a megaloblastic anemia, because all megaloblastic anemias are also macrocytic. You just say “megaloblastic anemia.”

Conversely, if you just say “macrocytic anemia,” that doesn’t say anything about whether there are megloblastic changes present or not! It just says: there’s an anemia, and the red cells are big.

Non-megaloblastic anemia

Q. What really is non-megaloblastic anemia? Because my lectures have mentioned it but I’m not sure what it really is.

A. Non-megaloblastic anemia just means an anemia without megaloblastic changes – and technically, that encompasses every single anemia except megaloblastic anemia! But really, when people say non-megaloblastic anemia, they’re usually referring to a macrocytic anemia (one in which the red cells are large, over 100 femtoliters) without megaloblastic changes (funny looking red cells). This type of anemia can be seen in liver failure and in myelodysplasia.

Pernicious anemia and megaloblastic anemia

Q. I don’t understand the difference between pernicious anemia and megaloblastic anemia. Pernicious anemia is just a deficiency in intrinsic factor that helps with absorption of B12…so patients have low B12 levels. But how is that different from megaloblastic anemia?

A. The best way to think about these two terms is: pernicious anemia is one cause of megaloblastic anemia.

Megaloblastic anemia is a type of anemia in which you get weird morphologic changes (megaloblasts, hypersegmented neutrophils, oval macrocytes) due to a lack of B12 and/or folate. There are lots of things that can cause a lack of B12 and/or folate…so when you see a case of megaloblastic anemia, you have to investigate to find out what the cause is.

Pernicious anemia (in which patients can’t absorb B12 due to a lack of intrinsic factor) is one cause. Another cause is folate-depleting drugs (like chemotherapy drugs); another is dietary deficiency.

It’s kind of confusing because they put the term “anemia” in pernicious anemia – so it makes it sound like pernicious anemia is a category in and of itself. It’s not – it just falls under the heading of megaloblastic anemia.

 

 

 

 

 

 

Blood cookies!

I’ve been really busy teaching this fall, so I haven’t been posting nearly as much as I’d like. I will be back to normal (ha) soon – but until then, I thought I’d share what we did in class yesterday. We’ve been learning about hematopathology (my favorite) – so I made cookies depicting some of the diseases we covered.

It’s super geeky, but I’m okay with that. It’s really fun to combine path knowledge with something that’s actually creative and pretty. And it’s sort of educational for my class…at the very least, they get a well-deserved break from the HOURS of lecture they have to sit through. Here are the end results (with a few high-yield things about each cell).

Sickle cells

Sickle cells are seen, of course, in sickle cell anemia. They’re abnormally shaped because when sickle hemoglobin deoxygenates, it polymerizes, contorting the red cell into a sickle shape.

Reed-Sternberg cell

Reed-Sternberg cells are the malignant cells in Hodgkin lymphoma. They’re gigantic, and typically they have two nuclei with prominent nucleoli, giving the cell an “owl’s-eye” appearance.

Neutrophil with Döhle body

In some cases of bacterial infection, neutrophils develop little blue cytoplasmic inclusions, called Döhle bodies, which are chunks of revved-up rough endoplasmic reticulum.

Butt cell

No, I didn’t make this up! Follicular lymphoma is made up, in part, of small cleaved cells – and when these get out into the blood, their nuclei totally look like butts. Adorable.

Faggot cell

Faggot cells contain TONS of Auer rods (faggot means bundle of sticks). They’re pathognomonic of acute promyelocytic leukemia, which has a t(15;17) that you should stick in your head somewhere.

Blast with Auer rod

Auer rods are only seen in malignant myeloblasts. So if you see one, you know you’re dealing with acute myeloid leukemia. Not all AMLs have Auer rods, though – so the absence of Auer rods doesn’t rule out AML.

Platelets

These could be normal platelets…but since we’re talking about diseases, let’s say they’re platelets from essential thrombocythemia, which is one of the four chronic myeloproliferative disorders (it’s the one in which the blood has an extremely high platelet count).