#so it’s not like he had 3 clots. he likely had a large DVT that migrated

[ravisdivorceddads]

Me, a doctor, tryna have a good time watching 9-1-1: 🥰

*chimney saying “it doesn’t make sense to shock him he’s in full cardiac arrest!”*

Me: 🫠🫠🫠🫠🫠🫠🫠

[mcatmemoranda]

Going through questions:

The most common pediatric leukemia is acute lymphoblastic leukemia (ALL). T cell or B cell ALL can occur. In T cell ALL, mediastinal masses occur.

Non-Hodgkin lymphoma causes B symptoms (weight loss, night sweats). Epstein Barr virus infects B cells and is associated with NHL. HIV infection is associated with NHL.

Multiple myeloma - plasma cell cancer-> monoclonal immunoglobulin (M-spike); presents with osteolytic lesions. Radiolucent bone lesions will be seen. Metastatic prostate cancer causes blastic bone lesions.

Bleeding time tells you about platelet defects. Von Willebrand disease-> prolonged bleeding time and PTT. vWF is needed for platelet adhesion and it is needed to stabilize factor 8. So No vWF-> no platelet adhesion (causing increased bleeding time) and unstable factor 8 (which is part of the intrinsic pathway, so increased PTT). I remembered that Von Willebrand's disease is the most common heritable bleeding disorder, which is why I got the question right. But now the increased bleeding time and PTT going with it make sense. It's AD.

Blood loss, not decreased nutritional intake, is the cause of iron deficiency anemia to rule out first in post-menopausal women. It could be an occult GI bleed.

LMWH binds to factor Xa and prevents it from converting prothrombin to thrombin. Unfractionated heparin can bind to factor Xa and to thrombin. So LMWH (e.g. enoxaparin) doesn't bind thrombin like unfractionated heparin does. LMWH is like heparin, but has fewer molecules than heparin.

Pyruvate kinase converts PEP to pyruvate in glycolysis. Pyruvate kinase deficiency-> hemolysis. Pts with pyruvate kinase deficiency have splenomegaly because cells in red pulp have more damaged RBCs to filter out.

I didn't know what a minor red blood cell antigen was. It's an antigen on the RBC that may not be screened for, thus a week later, pts have a reaction to it in delayed hemolytic transfusion reactions. He didn't mention this one in OnlineMedEd. The pt was initally exposed to the minor RBC antigen and developed memory B cells. The next time the pt is exposed, the B cells release antibodies (anamnestic response). Delayed hemolytic transfusion reaction occurs more than 24 hours after transfusion. Anamnestic response = delayed response

G6PD deficiency is X-linked recessive. I knew that's what the pt had in a question, but I forgot it's inheritance pattern. D: Heinz bodies are the hemoglobin that got damaged by oxidative stress because G6PD wasn't around to help regenerate the NADPH that is needed to make reduced glutathione, which prevents oxidative damage.

Herditary spherocytosis has AD inheritance pattern.

Schistocytes = hemlet cells. Thes occur in microangiopathic hemolytic anemia and in pts who have had heart valve surgery, which damages the RBCs. Artificial heart valves can damages RBCs-> schistocytes on blood smear. HUS, TTP, and DIC cause fibrin stands in small blood vessels-> schistocytes.

LMWH (e.g. enoxaparin) can be given for DVT in pregnant women. I remembered that heparin doesn't cross the placenta. But it is renally cleared, so if you have renal insufficiency (creatinine clearance less than 30 mL/min), then LMWH is contraindicated and you can give unfractionated heparin instead.

Azathioprine is a prodrug of 6-mercaptopurine. It gets metabolized by HGPRT into active 6-thioguanine, which is a purine analogue that disrupts DNA synthesis and thus prevents cell proliferation. 6MP is inactivated by xanthine oxidase and TPMT. Xanthine oxidase is inhibited by allopurinol and febuxostat. Some people have genetic deficiency of TPMT. If neither xanthine oxidase nor TPMT can inactivate 6MP, more of the 6MP gets converted to active 6-TG-> toxicity and increased immunosuppression. So some pts get genetic testing for TPMT before starting azathioprine and some pts need to avoid being on 6MP and allopurinol or febuxostat simultaneously.

Sickle cell is autosomal recessive, so you need 2 bad alleles to have it. If each parent is a carrier, then 1/4 kids will have it and 24 kids will be carriers. 1/4 kids will be normal. Glutamic acid (polar) is replaced by valine (non-polar) in sickle cell anemia. A point mutation in one of the codons for beta globin causes this substitution. This causes HbS.

One of my classmates mentioned rasburicase to me last year and I know it was between two answers in this question, but I chose the wrong one. D: It makes uric acid more soluble. In tumor lysis syndrome, more cells are being lysed by the chemotherapy. Since cells have high levels of K+ and phosphate, this can lead to hyperkalemia and hyperphosphatemia. Also, more protein needs to be broken down. Therefore, there's more purine catabolism. And purines end up as uric acid, which can precipitate in the kidneys and cause kidney injury. Rasburicase turns uric acid into allantoin, which is more soluble than uric acid and can be eliminated in the urine. Yeah, I remember my friend telling me that rasburicase is in certain animals. Rasburicase is recombinant urate oxidase. Animals have urate oxidase, but humans don't. So rasburicase turns uric acid into soluble allantoin, which is eliminated in urine. Allopurinol prevents formation of uric acid; it looks like purine and prevents xanthine oxidase from breaking down hypoxanthine. Febuxostat inhibits xanthine oxidase and has fewer adverse effects than allopurinol.

I didn't know heat stroke causes increased procoagulants. But it does and that leads to DIC due to increased coagulation factors; then you get increased fibrinolysis to get rid of the clots that form. Because the platelets and clotting factors all get used up, pts will bleed.

Multiple Myeloma = B cells become plasma cells that make a ton of useless immunoglobulin light chains. Treated with bortezomib, which causes increased apoptosis of plasma cells. Multiple myeloma causes lytic bone lesions, anemia, AKI, fatigue, constipation, weight loss. Myeloma kidney = light chain casts. Tons of kappa and lambda light chains being filtered by the kidney combine with Tam-Horsfall proteins (pretty sure I never heard of that) and cause casts that damage the tubules-> AKI. 24 hour rine protein is elevated.

Myeloma cells makes RANKL and destroy osteoprotegerin, which cause more activation of osteoclasts, hence the lytic bone lestions. I already reviewed RANK and RANKL and I know it pretty well. Glad I posted about it before. Multiple myeloma cells also release IL-3, IL-7, and Wnt pathway inhibitors, which inhibit osteoblasts.

I knew that this baby in this question had dactylitis, which occurs in sickle cell anemia, but I didn't understand what they were asking. If you have sickle cell, the sickled RBCs get destroyed, releasing hemoglobin. Hemoglobin is toxic and needs to be bound to haptoglobin. So the haptoglobin leven in the baby would be abnormal (decreased) because it would be all bound up by the Hgb coming from the hemolysis of the sickled RBCs. It had mentioned the baby's brother dying from an infection and I wasn't sure how that was related. It was because the brother also had sickle cell and therefore he probably had autosplenectomy due to the sickle cell. No spleen leaves you susceptible to encapsulated bugs like strep pneumo and the brother died from strep pneumo sepsis.

Hepcidin is an inflammatory mediator and it also decreases absorption of iron. So in anemia of chronic disease, hepcidin plays a role.

I knew this pt had beta thalassemia minor, I just didn't know what initiates it. It's a problem with mRNA. You see target cells and hypchromic, microcytic RBCs on blood smear. Pts have increased HbA2 (2 alpha chains and 2 delta chains; an alternate form of adult Hgb because they lack beta globin chains) and sometimes increased fetal Hgb (2 alpha chains and 2 gamma chains). If you try to treat these pts with iron, it doesn't do anything because they aren't iron deficient. Beta thalassemia is due to mutations that affect the transcription of mRNA for beta globin. Usually, there's messed up splicing of pre-mRNA or premature translation termination.

In obstructive sleep apnea, the kidney doesn't get enough oxygen, so it releases erythropoitein-> polycythemia (increased hematocrit).

Chemotherapy Induced Nausea and Vomiting (CINV) can be treated with 5HT3 receptor antagonists (ondansetron) and neurokinin-1 receptor antagonists (aprepitant). Early CINV is due to release of serotonin from enterochromaffin cells in the intestine that are damaged by the chemo. This leads to stimulation of 5HT3 vagal fibers-> vomiting reflex. Delayed CINV is due to substance P in the blood and CSF-> substance P binds neurokinin-1 receptor in the nucleus tractus solitarius and area postrema-> vomiting. Aprepitant can block the neurokinin-1 receptors and is therefore used for delayed CINV.

Low oxygen level leads to sickling of HgbS. High acid or dehydration also trigger the cycling. 2,3-BPG stabilizes the taut form of Hgb, which also would cause sickling. Low 2,3-BPG would increase Hgb's affinity for oxygen and thus decrease sickling. So high oxygen, high pH, and low levels of 2,3-BPG would prevent sickling. The opposite causes sickling. That's why pts with sickle cell anemia can't do as much strenuous activity--their HgbS starts sickling when they have less oxygen, more acid (from working muscles), and more need to unload oxygen to tissues (facilitated by 2,3-BPG) during exercise.

Fetal Hgb has replacement of histidine (positively charged amino acid) for serine, which is less positively charged. This prevents 2,3-BPG from binding for fetal hemoglobin, thus fetal hemoglobin has higher affinity for oxygen than adult hemoglobin. This helps baby take O2 from mom's hemoglobin in utero.

AML = Acute Myloid Leukemia = blasts (large nuclei, little cytoplasm) with Auer rods (rods seen in the blasts; not present in acute lymphoblastic leukemia, so look closeley to see if there are Auer rods--if there are, it's AML). Pts have pancytopenia. More than 20% myeloblasts in bone marrow. Chronic myelogenous leukemia = more mature cells.

Fluorescence In-Situ Hybridization (FISH) = cytogenetic test; finds deletions, translocations, and chromosome duplications in cells. FISH probes = ssDNA; they're added to the cell and combind with complementary DNA. FISH is more sensitive than karyotype.

Abixaban is a direct factor Xa inhibitor. It prevents conversion of factor II (prothrombin) to factor IIa (thrombin). I got the question wrong and so did 58% of respondents. It doesn't prevent conversion of factor X to Xa--it prevents factor Xa from converting prothrombin to thrombin. Wow. -_-

You need mitochondria to make heme. The precursors for RBCs have nuclei and mitochondria. After a certain division, they lose their nuclei, then they lose the mitochondria. So if they're at the point where they lack mitochondria, they can't make heme. Heme is made in the liver and in the erythrocyte precursors in the bone marrow.

Polycythemia can be relative (due to dehydration or diuresis), in which case plasma volume is decreased, but RBC mass, SaO2, and EPO levels are normal. Primary polycythemia = polycythemia vera; increased plasma volume, increased RBC mass, normal SaO2, and decreased EPO level. Secondary polycythemia can be physiologic or inappropriate. Physiologic = due to hypoxia; normal plasma volume, increased RBC mass, decreased SaO2, increased EPO level. Inappropriate = tumor that make EPO; normal plasma volume; increased RBC mass, normal SaO2, and increased EPO level.

Polycythemia vera = myeloproliferative disease of hematopoietic stem cells (HSC); mutation of JAK2 wherein valine is replaced with phenylalanine-> HSC are more sensitive to growth factor (EPO and thrombopoeitin, growth factors that stimulate erythrocyte and thrombocyte production). Pts can have itching after they shower due to release of histamine from basophils; plethora (red face), splenomegaly. Dx with low serum EPO and bone marrow study that shows the JAK2 mutation. Tx: phlebotomy.

I got confused about hepcidin. I know how it works and made a post about it before. I thought it came from the intestinal cells, but it doesn't. It comes from the liver and it can affect intestinal cells by preventing the absorption of iron from the gut. Hepatic parenchymal cells secrete hepcidin, which controls the storage and release of iron from other cells. Hepcidin is high when there's already enough serum iron. Hepcidin is also an acute phase reactant and is elevated during inflammation. Increased erythropoiesis and low oxygen lower hepcidin levels. Ferroportin-1 allows iron to come in on the basolateral side (the side of the intestinal cell that faces the blood) of intestinal cells. Ferroportin-1 is also located on macrophages. High serum iron or inflammation causes hepcidin to increase and hepcidin causes breakdown of ferroportin-1, preventing iron from coming into the blood. On the apical surface of intestinal cells (the side facing the gut lumen) is Divalent Metal Transporter-1 (DMT-1), which allows Fe2+ to be absorbed from the small intestine into the intestinal cell. Inside the enterocyte, the iron is either maintained inside ferritin, or it goes through ferroportin-1 into the blood, where transferrin binds to it and carries it to whatever cells have transferrin receptors, which allow the iron to be taken into said cell.

Nephrotic syndrome = loss of protein in urine; can lose anticoagulation factors, like antithrombin III in the urine-> hypercoagulable state-> renal vein thrombosis. Renal vein thrombosis-> hematuria, flank pain, increased LDH. So nephrotic syndrome is a hypercoagulable state.

Heparin is found in mast cells. LMWH enhances the effect of antithrombin III and inhibits factor Xa. Unfractionated heparin not only inhibits factor Xa, it also inhibits thrombin.

Ugh! There was a question about cancer and I knew breast cancer was more common in women but also knew that lung cancer has higher mortality. Most common cancers (by incidence) in women are breast, lung, and colorectal cancer. Breast cancer is more common in women, but not as deadly as lung cancer.

[yourcycleyourfood]

What you need to know about blood clots + family history going on the pill #followerstory

Alrighty so this all happened during 2015, before my senior year of high school. 

My period was EXTREMELY irregular, as in 3 months no flow, then a whole month of non-stop visit. 

A rather simple solution was to get onto birth control pills because of the side effect of regularity. 

My mom had no problems with it so I was in the clear. 

I get on the pill and have a great time. Regular cycle, weight loss, clearer skin, just felt happy and healthy. 

Fast forward about 6 months. 

I’m outside cleaning my rabbit cages and get out of breath frequently and have to go inside to the air conditioner like every 5 minutes. 

A 20 minute job turned into an hour and a half. (Mind you, I live in Texas and heat + humidity is no joke). 

Don’t think much of it, probably just an off day. 

A week later we go on a 2 week trip to the beach that had been planned for a while.

Everything is fine and dandy until I start having bad symptoms. 

Out of breathe, can’t take deep breathes without pain, pain in back and butt/thigh area, almost passing out from lack of oxygen, sleeping/laying down a lot, heart rate 160 while resting, blood pressure at 200/140, etc. 

Can’t even walk up 10 tiny steps without almost blacking out. 

At this point some of you may already know what’s going on, I did not. 

I was terrified. 

Anyway, I get through the trip without passing out or anything. 

The symptoms have faded and im not to worried about it anymore. 

Fast forward a week. 

We are watching the new King Tut series starring Avan Jogia when I start feeling a pain that felt like my sciatic nerve.

Over an hour I can FEEL the pain growing and elongating down my butt and up. 

We have a long running history in our family of such problems so we gloss over it and I get some pain pills we have lying around. 

Over the next few days the pain actively gets worse and worse. 

It’s to the point where I don’t even want to walk. 

Finally I decide it’s time to go to the doctor and see what the hell is going on with my nerve; at this point it should have subsided. 

The next day My mom and I walk into the clinic. 

Actually, it’s more like she walked and I hobbled while leaning on her. 

I couldn’t walk whatsoever. I was wearing short shorts and a t shirt, but I was sweating profusely. My shirt and hair were soaked with sweat. 

By the time they take my vitals I am pretty much bawling at the pain. 

We sit in the room waiting for the Dr when I feel the sensation of my leg going cold. I look down, and lo and behold, My leg is purple. 

I stand up and sit down trying to see what happens. 

When I’m up, color returns, when I sit, purple. 

The Dr walks in and IMMEDIATELY knows somethings up. 

I show her my leg, tell her all the symptoms I’ve had over the past month or two. 

She asks me to sit on the table so she can check out my leg. 

They both had to support me over to it. 

As soon as I finally get up, I feel like things are getting milky in my head. 

Tunnel vision/red and black dots, cotton in my ears, and I feel my equilibrium thrown off. 

As im falling to the side, I say “Im going to faint”. 

Things get hazy after that but the Dr lays me down and I come back to my senses slightly. 

She calls the hospital and talks to a specialist. The other Dr says I need to get to the hospital ER immediately. 

Everyone at this point knows what’s going on accept for me. 

My mom calls a family friend and we get driven to the ER. 

We are met at the door and get vitals rechecked, everything. 

Also I should mention that my heart rate was ridiculously high as well as my blood pressure. 

We wait until the Dr comes in and let’s us know what will be happening.

I have to get an ultrasound of my leg. 

If you’ve never had an ultrasound, they put a lot of pressure on wherever they are checking to see what’s going on. 

It was excruciating how hard she would press on my leg, and when I would think she was done, she wasn’t. 

Finally I’m let out and we are waiting for results. 

I get IVs in my arm for fluids and what not since they figured I would have a longer stay. 

In the end, it turns out that I had a 15 inch long blood clot in my abdominal and femoral artery. A DVT. 

They rush me to get checked in and to see specialists and bla bla…this is ridiculously long already so I’m gonna condense the rest. 

I am placed into the ICU and am pumped full of blood thinners, such as TPA and heparin. 

At the same time. They get me onto the table and go into my leg to scrape out the blood clot as much as possible. 

They take me out and within a time frame of 4 hours after the “surgery” I had no thinners in my system. 

No-one believed me when I told them I was still in pain until I told my mom that I would rather be dead. 

Finally they did another ultrasound, and lucky me, I had a NEW clot. 18 inches long this time. 

The Drs were baffled. 

My family was in tears. 

I was crying. 

They stuck me back in that table and went back to work. 

I was in the hospital for 2 weeks. 

I had CT scans, ultrasounds, xrays, needles upon needles upon needles stuck into me. 

I had a quarter size clot in my lung, as well as some others. 

To get to the lung, the clot had to pass through my heart. 

I was black and purple and blue up and down my arms. 

I lost 20 lbs while laying down basically 24/7 cuz I was not eating. 

I saw people come and go, was passed nurse to nurse and had 10 doctors checking on me. 

Later on I found out that my dad’s side of the family have a blood clotting factor called Prothrombin Factor 2, which was a large contributing factor that mixed with the pills to cause the clot. 

People in the rooms beside me were dying. I was sure I would be the next. 

But thanks to my being young, and the doctors and nurses and their medicines, I was able to go to My first day of senior year, while still learning how to walk and have mobility in my leg again. T

he fact that I am alive and without any problems other than feeling when the weather or pressure change is incredible. 

Honestly, it is a miracle. I could go on and on with this story but then it would be redundant and ridiculously long. 

But, The one good thing that came out of it is my period is now regular 😌.

TL;DR: Went on birth control, lots of symptoms, had 15 inch blood clot, later reclotted to 18 inches, hospital 2 weeks, nearly died pretty much every day for a month and a half. Turns out I had Prothrombin Factor 2

Moral of the story: ALWAYS know your family history before going on any type of medicine, especially the pill. ALWAYS.

by @germex

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