Megaloblastic anemia and macrocytosis
Q. I’m confused how in megablastic anemia, cells become macrocytic due to immature nuclei when RBCs don’t have nuclei! Is it referring to the erythroblast precursors before the nuclei are lost?
Q. I’m confused how in megablastic anemia, cells become macrocytic due to immature nuclei when RBCs don’t have nuclei! Is it referring to the erythroblast precursors before the nuclei are lost?
Q. I have a question about von Willebrand Factor – where is it stored? All that I can gather is that it’s stored in ‘Weibel-Palade bodies’, but where are they? (more…)
I received a bunch of great questions from a student in my pathology course, and thought I’d share them with you. I think reading about things in in question/answer format helps the material stick in your head. These particular questions are about congenital heart defects.
Q. Can VSD and PDA also lead to the same pulmonary problems as ASD since they are all left to right shunts?
A. Yes! Any left-to-right shunt, if it is big enough, can eventually put enough pressure on the right side of the circulation that the lungs respond by constricting vessels and laying down fibrotic tissue, leading to pulmonary hypertension. Eventually, if pressures on the right side exceed those on the left, the shunt reverses, becoming a right-to-left shunt.
Q. What is the effect/outcome of the overriding aorta in Tetralogy of Fallot?
A. The main problem in Tetralogy of Fallot is the pulmonary outflow obstruction – that really determines the extent and severity of the clinical picture. The overriding aorta doesn’t contribute much. It does allow unoxygenated blood to flow directly into the aorta, which doesn’t help matters. There already is a ventricular septal defect, which allows mixing of blood, so the overriding aorta would just exacerbate that mixing, making it even easier for blood to bypass the lungs and go straight to the peripheral circulation. Which manifests as cyanosis.
Q. Can you surgically repair transposition of the great arteries?
A. Yes. Patients with TGA usually have some sort of shunt as well (like a VSD) – and depending on the degree of shunting, they may be fairly stable for a little while. However, most of the time, the transposition is repaired surgically within weeks of birth.
Q. Is mitral valve prolapse an insufficiency since it cannot close properly?
A. Yes – that’s exactly right. Insufficiency means the valve can’t close properly; stenosis means it can’t open properly. In mitral valve prolapse, the leaflets are floppy, and they don’t come together like they should, so during diastole, blood regurgitates into the left atrium.
Here’s a very good question about the diagnostic use of the bleeding time.
Q. I’m currently studying heme for boards and came across a practice questions that used platelet count, bleeding time, PT and PTT values to differentiate between certain diseases/problems. I was just wondering how in both Vitamin K deficiency and liver disease you can get an increase in PT and PTT but the bleeding time doesn’t change…I guess I figured that bleeding time would have to increase. Can you explain this to me?
A. Yeah, that does sound weird, you’d think the bleeding time would change – but actually, the bleeding time is only a measure of platelet function. It really has nothing to do with coagulation!
I kind of think of it like this: the platelet plug is the first thing to form, and that is enough to stop the bleeding from the incision made at the beginning of the test. The coagulation cascade happens next, and the status of that won’t be apparent in the bleeding time results. The patient might have some more bleeding later if their coagulation system is really screwed up…but the bleeding time assay will be done by then. In reality, it probably happens a little more concurrently than that (platelet plug is followed very closely by fibrin formation – the two probably even overlap a bit), but I think it’s a good way to remember the concept.
The same reasoning fits with the way that people with coagulation factor disorders bleed (as opposed to patients with platelet disorders). People with platelet abnormalities tend to bleed spontaneously into mucous membranes without much provocation (probably because they’re having a hard time forming that initial platelet plug) whereas patients with coagulation factor abnormalities, like hemophilia, tend to have deep, severe bleeds that happen after some time has elapsed (because they form the initial platelet plug okay, but they can’t seal it up with fibrin very well, so they end up bleeding later on).
Here’s an example of a common question students have in the beginning of a medical school or dental school pathology course.
Unfortunately, students often feel like they “should” know the answers to certain questions – so they don’t ask. Don’t fall into this trap! You never need to feel embarrassed about asking a question; everyone has things they don’t know – even professors. That’s why you’re taking the class – to learn!
On to the question.
Q. What is the main difference between a neutrophil and a monocyte? This is what I understand:
PMNs:
fight bacteria and fungi (but they are different than NK cells–right?)
act as antigen presenting cells
phagocytic
are generally the first to arrive; part of the acute inflammatory response
Monocytes:
act as antigen presenting cells
can secrete cytokines and attract inflammatory cells like fibroblasts, etc.
phagocytic
bigger role in chronic inflammation
A. Broadly, the similarities are: neutrophils and monocytes are both phagocytes, and they both work to fight infections. But moncytes can turn into macrophages (when they get into tissues), which are very good at eating things, as well as presenting antigens. Neutrophils eat, but don’t present, antigens. One of the big differences, too, you already mentioned: neutrophils are the first to come in during an inflammatory process. Lymphocytes come next, then monocytes/macrophages come in to mop up the mess.
One note: neutrophils are phagocytes, but not antigen presenting cells. Another note: You are right, neutrophils are different than NK cells. NK (natural killer) cells are specialized lymphocytes which have functions different than those of neutrophils and monocytes.
Also: neutrophils look different than monocytes/macrophages. Neutrophils have a “busy” nucleus (that’s why they are called “polymorphonuclear” leukocytes), with several lobes. You can see one at 2 o’clock in the above photo. They also have granules, both primary (azurophilic) and secondary (fawn-colored). Monocytes have a horseshoe-shaped nucleus, with dishwater-gray cytoplasm and a few tiny granules. See the lower left corner in the above photo.
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