Decoding Blood: Hematocrit, White Cells, and Hemostasis

Drew Bennett

Now, here's the deal. Take a tube of blood and spin it in a centrifuge, and it sorts itself into layers. On top you get straw colored plasma, about 55 percent of the volume. On the bottom you get the formed elements, the cells, at about 45 percent. And squeezed in between is a thin pale line called the buffy coat. That's your white cells and platelets, and together they're one percent or less of the whole sample.

Lizzie Stevens

And the heavy red layer on the bottom is what gives us the hematocrit, right? The percentage of the blood volume that's red cells.

Drew Bennett

Exactly. Rough reference numbers are about 37 to 48 percent for adult females and 42 to 52 percent for adult males. Your lab prints its own reference range, so go by that, but those numbers give you a feel. There's also a handy rule of thumb: the hematocrit is roughly three times the hemoglobin value. If a hemoglobin is 14, you'd expect a hematocrit around 42. If those two numbers don't roughly agree, that's worth a second look.

Lizzie Stevens

I love that one for sanity checking. Now, there's a classic exam trap in here. Plasma is not the same thing as serum. Plasma is the clear liquid matrix, and it's mostly water, about 92 percent, plus albumin, globulins, fibrinogen, electrolytes, nutrients, hormones, and gases. Serum is plasma minus the clotting proteins. That's why blood is classified as a connective tissue. It has cells, and it has a liquid matrix, and the matrix is plasma.

Drew Bennett

So when you look at a CBC, you're really asking four questions. Can this patient carry oxygen? Can this patient fight infection? Can this patient stop bleeding? And later we'll get to the fourth one, can this patient safely receive blood? The big idea is red cells carry, white cells defend, platelets plug, and plasma transports.

Lizzie Stevens

Let's start with the carrying. A red blood cell, an erythrocyte, is basically an oxygen delivery truck. It's shaped like a biconcave disc, a saucer with a dent on both sides, and that gives it a large surface area for oxygen and carbon dioxide to diffuse through. It's also flexible, so it can fold and squeeze through tiny capillaries and spring back. And a mature red cell has no nucleus, which means it can't replicate. Everything inside is packed with hemoglobin.

Drew Bennett

Hemoglobin is the red pigment, and more than a third of the inside of the cell is filled with it. Break the word down. Globin is the protein part, four ribbon like chains. Heme is the iron containing part attached to each chain. Each heme grabs one oxygen molecule, so one hemoglobin molecule carries four oxygens and becomes oxyhemoglobin. Each red cell holds 200 to 300 million hemoglobin molecules. And here's a detail people miss: carbon dioxide doesn't ride on the heme. It binds to the globin.

Lizzie Stevens

Which means how much oxygen the blood can carry depends on two things, how many red cells you have and how much hemoglobin is in them. So when a patient is anemic, short of breath, pale, tired, that's the chain of thinking. Fewer carriers, less oxygen delivered.

Drew Bennett

So who decides how many carriers to make? The kidneys. Picture a patient who moves to high altitude, where the atmospheric oxygen is lower. The kidneys detect the falling oxygen and secrete a hormone called erythropoietin, EPO. Think of EPO as the message, we need more oxygen carriers. It tells the red bone marrow to make new erythrocytes, and the marrow releases immature ones called reticulocytes, which mature into red cells in one to two days.

Lizzie Stevens

And it's a negative feedback loop. Once the oxygen level rises back up, the kidneys make less EPO and red cell production calms down. So at altitude, you'd expect more EPO, more red cell production, and more reticulocytes in the blood. And a neutrophil count wouldn't change just because of altitude. That's a favorite test question.

Drew Bennett

Now, red cells live about 120 days. Then macrophages in the liver and spleen eat the worn out ones. The globin gets broken down into amino acids that the body reuses. The heme splits into iron and bilirubin. The iron goes back to build new hemoglobin, and the bilirubin is excreted into the intestines as part of bile.

Lizzie Stevens

The nursing connection is when too many cells are destroyed. That's hemolysis. The body can't handle that much bilirubin, so it spills into the tissues, and you see a yellow tint in the skin and the sclera, the whites of the eyes. That's jaundice. And I always think of newborns when I say that, but it applies to anyone with excessive red cell destruction.

Drew Bennett

One more number, because it's strange. An adult makes about 200 billion red cells, 400 billion platelets, and 20 billion white cells every single day. The red bone marrow does the heavy lifting, in the ends of long bones and flat bones like the sternum, skull, vertebrae, and pelvis. Lymphatic tissue in the spleen, lymph nodes, and thymus adds lymphocytes to the mix.

Lizzie Stevens

Okay, white cells, the defenders. There are five types, and the mnemonic is Never Let Monkeys Eat Bananas. Neutrophils, lymphocytes, monocytes, eosinophils, basophils, in order from most common to least common. Roughly, neutrophils are 60 to 70 percent, lymphocytes 20 to 25, monocytes 3 to 8, eosinophils 2 to 4, and basophils half a percent to one percent.

Drew Bennett

They split into two groups based on what you see under a stained microscope. Granulocytes have obvious granules and a multilobed nucleus. That's the neutrophils, eosinophils, and basophils. Agranulocytes have few or no granules, and that's the lymphocytes and monocytes. Every white cell has a nucleus, which is a nice contrast with the red cells.

Lizzie Stevens

Neutrophils are your first responders to acute bacterial infection. They roam the body, eat bacteria, and when they die in large numbers, they make pus. Eosinophils go after parasites and help dial down allergic reactions. Basophils carry histamine, which dilates vessels and makes capillaries leakier, and heparin, an anticoagulant that keeps clots from forming where they shouldn't.

Drew Bennett

Then the agranulocytes. Monocytes circulate briefly, then move into tissue and turn into macrophages, the big eaters and cleanup crew, and they also show antigens to lymphocytes. And lymphocytes are the stars of specific immunity. B cells, T cells, and natural killer cells. We'll come back to them in a bit.

Lizzie Stevens

So how do we use this on a CBC? A total white count is usually about 5,000 to 10,000 per microliter. Above 10,000 is leukocytosis, and that points toward infection, stress, inflammation, or leukemia. Below 5,000 is leukopenia, which can come from bone marrow depression, severe viral infection, or chemotherapy. The rule from the slides is simple: any white cell abnormality, start thinking infection, inflammation, or immune response.

Drew Bennett

And then there's the shift to the left. That's when the differential shows lots of immature neutrophils, called bands, compared with mature ones. It tells you the marrow is pushing cells out faster than it can finish them, which fits with a serious acute bacterial infection.

Lizzie Stevens

Now platelets. Platelets are thrombocytes, but they're not really cells. They're fragments broken off the edges of giant marrow cells called megakaryocytes. They live about seven days, and a normal count is roughly 150,000 to 400,000 per microliter. Below 150,000 is thrombocytopenia, and that patient bleeds easily. Think petechiae, bruising, nosebleeds. Above 400,000 is thrombocytosis, and now the worry is clotting.

Drew Bennett

The job of platelets is hemostasis, stopping bleeding, and the slides give you three words to hold onto. Clamp, plug, seal. Step one, vascular spasm. When a vessel is cut, the smooth muscle in its wall spasms and slows the blood flow. That's the clamp.

Lizzie Stevens

Step two, the plug. The cut exposes collagen fibers, and that rough spot turns passing platelets sticky. They stick to the wall and to each other, and they release chemicals that constrict the vessel more and call in even more platelets. That's a temporary seal, but it's not stable.

Drew Bennett

Step three, coagulation. That's a cascade of clotting factors. The extrinsic pathway starts from damage outside the blood, in the injured tissue. The intrinsic pathway starts inside the blood, like platelets touching collagen. The extrinsic one reaches factor X in a single reaction, and the intrinsic one takes four. After that, both join a common pathway that makes prothrombin activator. That turns prothrombin into thrombin, and thrombin turns soluble fibrinogen into insoluble fibrin.

Lizzie Stevens

If you remember one thing, fibrin makes the mesh. It's a sticky web that traps red cells and platelets and stabilizes the clot. And a clot works well on smaller vessels, but clotting alone might not stop a hemorrhage from a large vessel. Then, once the vessel heals, platelets in the clot contract and pull the edges together, and a protein called plasmin dissolves the fibrin. That's fibrinolysis, the clot cleanup crew.

Drew Bennett

And the body works to prevent clots where we don't want them. Smooth endothelium keeps platelets from sticking. Normal blood flow dilutes thrombin. And basophils and mast cells secrete heparin, which blocks thrombin. But when blood pools in the legs, say from prolonged sitting or lying down, thrombin can build up. A clot sitting inside a vessel is a thrombus. If a piece breaks off and travels, it's an embolus. Thrombus stays, embolus travels.

Lizzie Stevens

And a classic one is a clot traveling to the pulmonary circulation, a pulmonary embolism, which blocks perfusion to the lung. So as nurses, we think, how do we promote circulation? Moving patients, getting them up, all of that.

Drew Bennett

That brings us to the fourth question from the CBC, can this patient safely receive blood? Every red cell carries antigens on its surface, and the ABO system has two: A and B. Type A has the A antigen. Type B has the B antigen. Type AB has both. Type O has neither. And here's the rule: antigens live on the red cell, antibodies live in the plasma.

Lizzie Stevens

And the plasma carries antibodies against the antigens you don't have. Type A has anti B. Type B has anti A. Type AB has no antibodies at all, so it's the universal recipient. Type O has both anti A and anti B, but no antigens for anyone to attack, so it's the universal donor for red cells.

Drew Bennett

Now picture the wrong blood going in. The recipient's antibodies recognize the donor's antigens and attack. The red cells clump together, that's agglutination, and then they burst, that's hemolysis. The clumps block vessels and cut off oxygen, and the free hemoglobin can block tubules in the kidney, leading to renal failure and possibly death. That's a transfusion reaction.

Lizzie Stevens

And then there's Rh. Rh positive means the Rh antigen is present, Rh negative means it's absent. Unlike ABO, an Rh negative person doesn't naturally have anti Rh antibodies. They develop them after being exposed to Rh positive blood. And that matters a lot in obstetrics. Say an Rh negative mother carries an Rh positive baby. The first pregnancy usually goes fine because maternal and fetal blood don't normally mix. But at delivery or miscarriage, fetal blood often mixes with the mother's, and she makes anti Rh antibodies.

Drew Bennett

Then in a later pregnancy with another Rh positive baby, those antibodies can cross the placenta, even though the red cells can't. They attack the fetal red cells, and the baby develops a severe anemia called erythroblastosis fetalis. The prevention is Rh immune globulin, often called RhoGAM, given at about 28 weeks and within 72 hours after delivery, so the mother never gets sensitized in the first place.

Lizzie Stevens

Antigens and antibodies are the perfect bridge to immunity. The big idea for this chapter is drain it, filter it, fight it, remember it. And it starts with plumbing. Every day, fluid leaves the capillaries and enters the tissues. The capillaries take back about 85 percent, which leaves about 15 percent behind. Over a day, that adds up to as much as 4 liters, enough to cause massive swelling and even death if nothing cleaned it up.

Drew Bennett

The lymphatic system cleans it up. Fluid enters tiny blind ended lymphatic vessels through gaps between overlapping cells. Lymphatic vessels have thin walls and valves, like veins, and the fluid moves in only one direction, away from the tissues. It's not a circuit like blood, it's a one way return trip. Tissue, lymphatic vessel, lymph node, larger vessel, duct, subclavian vein. Movement comes from rhythmic contraction of the vessels, skeletal muscle, and the pressure changes of breathing.

Lizzie Stevens

Two collecting ducts finish the job. The right lymphatic duct drains the upper right quadrant into the right subclavian vein. The thoracic duct drains everything else into the left subclavian. Right gets a little, thoracic gets a lot. Also, specialized lymphatic vessels in the small intestine absorb dietary fats and fat soluble vitamins. So the three jobs are fluid balance, fat absorption, and immunity.

Drew Bennett

Now the organs. Primary lymphatic organs are where lymphocytes develop and learn, and that's the red bone marrow and the thymus. Secondary organs are where mature lymphocytes get activated, and that's the lymph nodes and spleen. And the must know pairing is T cells and thymus, B cells and bone marrow. Both start as stem cells in the marrow, but T cells leave early and finish their schooling in the thymus. B cells stay in the marrow until they're mature.

Lizzie Stevens

I like calling the thymus T cell University. It sits in the mediastinum, and young T cells are protected there from antigens in the blood while they learn to tell self from foreign. Once they pass, they're called immunocompetent and get released. The thymus grows through childhood, then begins shrinking around age 14, with fat and fibrous tissue replacing it. Fewer new T cells could be part of why older adults get more infections.

Drew Bennett

Lymph nodes are the filtering stations. You've got over 600 of them, shaped like beans. Lymph comes in through several afferent vessels, and flows slowly through sinuses lined with macrophages. Compartments called cortical nodules are full of lymphocytes, and the germinal centers release more lymphocytes when there's an infection. Then the filtered lymph leaves through a single efferent vessel.

Lizzie Stevens

And that's why nodes swell. When antigens show up, the lymphocytes multiply and the node enlarges, which is lymphadenopathy. A fast stretch of the capsule makes it painful. Most of the time, it's an infection in the area the node drains. Swollen suboccipital nodes suggest a scalp or head infection, for instance. But the consistency matters. Soft nodes suggest infection or inflammation. Very firm, rubbery nodes suggest lymphoma. Stony hard nodes typically suggest metastatic cancer. So an enlarged node is not automatically cancer, but it's always something to report.

Drew Bennett

The easy distinction is lymph nodes filter lymph, the spleen filters blood. The spleen is about the size of a fist, the largest lymphatic organ, in the left upper abdomen. White pulp is packed with lymphocytes and screens the blood for antigens. Red pulp is full of blood filled sinuses and macrophages that remove worn out red cells. It also stores 20 to 30 percent of the body's platelets, and it makes red cells in the fetus.

Lizzie Stevens

Then there's immune tissue sitting where the outside world gets in. That's mucosa associated lymphatic tissue, MALT, in the respiratory, digestive, urinary, and reproductive tracts. The biggest collections are the tonsils, Peyer's patches, and the appendix. There are three sets of tonsils: the pharyngeal tonsil, which is the adenoids, the palatine tonsils, and the lingual tonsils. The palatine ones are the largest and the most likely to get infected.

Drew Bennett

Peyer's patches are in the small intestine, monitoring bacterial populations and alerting lymphocytes when a harmful one invades. And the appendix is packed with lymphocytes. People used to call it useless, but recent research suggests it may serve as a reservoir for beneficial gut bacteria.

Lizzie Stevens

So now the three lines of defense: block, blast, remember. The first line is the external barriers, skin with its acid mantle, and mucous membranes, with lysozyme in mucus, tears, and saliva. Keep them out. The second line is nonspecific, also called innate, meaning present from birth. It's fast and broad, but it has no specific memory. The third line is specific immunity, and it's slower at first but it remembers.

Drew Bennett

The second line has a lot of tools. Start with phagocytes, the Pac Man cells. Find the germ, engulf it, digest it, dispose of the remains. The main ones are neutrophils, which roam, and macrophages, which sit in strategic places like the lung alveoli, liver, bone, and spleen. Chemicals from injured cells call neutrophils to the scene, that's chemotaxis, and they squeeze out between capillary cells, that's diapedesis.

Lizzie Stevens

Then the antimicrobial proteins. Interferons are released by a virus infected cell to warn its neighbors, who start making enzymes that would block the virus if it got in. The complement system is more than 20 proteins circulating inactive. Once triggered, they work in a cascade, coat pathogens so phagocytes can find them, boost inflammation, and finally punch ring shaped holes in bacteria so that fluid rushes in and the bacterium bursts. And natural killer cells are lymphocytes that destroy virus infected cells, cancer cells, and foreign cells.

Drew Bennett

Inflammation is where you've seen all of this in real life. Injured cells release histamine. That causes vasodilation and makes capillaries leaky. Blood and fluid rush in, and you get redness, heat, swelling, and pain. Fibrinogen leaks out and forms a clot that walls off the area. Neutrophils arrive and eat pathogens, and they release cytokines to call in more help. Macrophages clean up the dead cells. And all those dead phagocytes and debris pile up as pus. If pus collects in a tissue cavity, that's an abscess.

Lizzie Stevens

Fever fits right in. Neutrophils and macrophages release a pyrogen, the hypothalamus makes prostaglandin E, and that resets the temperature set point. Now the body thinks 98.6 is freezing, so it shivers and constricts skin vessels, and the patient has chills and cold, clammy skin. When the infection is controlled, the set point returns to normal, and the body sweats and dilates skin vessels, so the skin looks warm and flushed. And fever isn't the enemy. It boosts interferon activity and slows the reproduction of bacteria and viruses.

Drew Bennett

Third line, specific immunity, has two arms. Cellular, or cell mediated, immunity is T cells, and it handles problems inside cells, like infected cells, abnormal cells, and foreign cells. Humoral immunity is B cells and antibodies, and it handles problems outside cells. Both start when an antigen presenting cell, like a macrophage, swallows an antigen and displays pieces of it on its surface. A T cell spots it, binds, and gets activated.

Lizzie Stevens

The T cell then clones itself, and the slides give you three jobs. Cytotoxic T cells are the assassins that kill infected cells directly. Helper T cells are the coach, releasing interleukins that attract neutrophils, natural killer cells, and macrophages, and they stimulate T and B cell production. Memory T cells are the historian, ready for the next exposure. Helper T cells also help B cells with the humoral arm.

Drew Bennett

B cells, once activated, clone as well. Some become antibody secreting cells and some become memory cells. Antibodies, or immunoglobulins, are Y shaped proteins, and the tips fit one specific antigen like a key in a lock. Humoral immunity doesn't kill directly. It marks the pathogen for later destruction. And the brief adds that IgG is the most abundant and crosses the placenta, IgA shows up in breast milk, saliva, and tears, and IgE is the one tied to allergies.

Lizzie Stevens

On allergy, the first exposure makes IgE, which binds to mast cells, and the person is now sensitized. Later, the allergen links two or more of those antibodies, and the mast cells release histamine, and you get runny nose, watery eyes, hives. The severe, whole body version is anaphylaxis. And autoimmune disease is the opposite problem, when the immune system can't tell self from foreign and attacks the body's own tissue. It's more common in women, and there are more than 100 of them, like lupus, Graves' disease, and ulcerative colitis.

Drew Bennett

Last piece, the types of immunity. Just ask, who made the antibodies? If I made them, it's active. If someone else made them, it's passive. Natural active is getting infected and recovering. Artificial active is a vaccine. Natural passive is mom to baby, through the placenta or breast milk. Artificial passive is injected antibodies, like for rabies. Active lasts a long time because you form memory. Passive lasts only a few months, since your own body didn't build memory.

Lizzie Stevens

Now for a switch of gears. Reproduction is one of those chapters where anatomy and endocrine finally collide, and the framework is make it, move it, meet it, maintain it. Make the gametes, move them through the tract, give sperm and egg somewhere to meet, and use hormones to keep the cycle going.

Drew Bennett

Start with the vocabulary. The primary sex organs, the gonads, are the testes and ovaries, and they make gametes and sex hormones. Sperm is the male gamete, the ovum is the female gamete. Everything else is a secondary sex organ, there for transport, fertilization, and development. And both sexes run on the same hormone chain. The hypothalamus releases GnRH, and that tells the anterior pituitary to release FSH and LH.

Lizzie Stevens

The testes hang in the scrotum, and that's on purpose. Sperm production needs a temperature a couple of degrees cooler than core body temperature. The cremaster muscle surrounds the spermatic cord and testis, and in cold weather it contracts to pull the testes closer to the body for warmth. Inside, each testis is divided into over 200 lobules, and each lobule holds one to three coiled seminiferous tubules.

Drew Bennett

Two cells to know. Sertoli cells live in the tubule walls and support developing sperm. They supply nutrients, remove waste, and secrete inhibin. Leydig cells sit between the tubules, and they make testosterone. The hook is Leydig, let's make testosterone, Sertoli, support sperm. So if a question asks where testosterone is produced, it's the interstitial cells, not the seminiferous tubules.

Lizzie Stevens

And then the sperm highway. Seminiferous tubules make the sperm. Next is the rete testis, where they partially mature, then the efferent ductules, then the epididymis, where sperm mature and are stored in the tail for 40 to 60 days. After that, if they aren't ejaculated, they disintegrate and are reabsorbed. Then the vas deferens carries them up through the spermatic cord, over the ureter, and behind the bladder. Seminiferous tubules make, epididymis matures and stores, vas deferens moves.

Drew Bennett

The vas deferens joins the seminal vesicle to form the ejaculatory duct. That passes through the prostate and empties into the urethra, and the sperm exit. On the way, three glands add fluid. Seminal vesicles contribute the most, about 60 to 65 percent of semen, a thick yellowish fluid with fructose to feed the sperm. The prostate adds about 30 percent, a thin, milky, alkaline fluid that protects and supports sperm and helps motility. The bulbourethral, or Cowper's, glands add about 5 percent, a clear fluid that lubricates the urethra and neutralizes leftover acidic urine.

Lizzie Stevens

The alkalinity matters, because sperm become immobile in acid, and the vagina is acidic. Semen also turns sticky and jelly like right after ejaculation, which helps it cling to the vaginal and cervical walls instead of draining out. One ejaculation is 2 to 5 milliliters, with 40 to 100 million sperm, according to the slides. And the penis has three cylinders of erectile tissue, the paired corpus cavernosa and the smaller corpus spongiosum around the urethra, which fill with blood during arousal.

Drew Bennett

Spermatogenesis, and the slide literally says please do not stress. The details are spermatogonia, primary spermatocytes, secondary spermatocytes, spermatids, then mature sperm. What matters is that the starting cell has 46 chromosomes, meiosis cuts that in half, and the sperm ends up with 23. Mitosis is same, meiosis is half. Then a sperm has three parts. The head holds the DNA and an acrosome cap with enzymes to penetrate the egg. The midpiece is packed with mitochondria for energy. The tail is a whip like flagellum for movement. Head is information, middle is energy, tail is movement.

Lizzie Stevens

Now my side of the hospital. The ovaries are about the size and shape of almonds, one on each side of the uterus, and they make ova and the hormones estrogen and progesterone. The fallopian tubes carry the ovum toward the uterus. The fimbriae, those finger like projections, sweep across the ovary to catch the ovulated egg, because the tube isn't physically attached to the ovary. The middle section, the ampulla, is the usual site of fertilization. Cilia help move the egg along.

Drew Bennett

And if the fertilized egg implants in the tube instead of the uterus, that's an ectopic pregnancy. So the tube anatomy isn't trivia, it's a safety issue.

Lizzie Stevens

The uterus has three regions. The fundus is the top, the curved upper portion. The body is the middle. The cervix is the bottom, and the cervical canal links the uterus to the vagina. Glands in the canal make thick mucus, and around ovulation it thins so sperm can get through. The wall has three layers. Perimetrium is the outer layer, think perimeter. Myometrium is the thick smooth muscle, and it's the part that contracts in labor, when oxytocin gets called. And endometrium is the inner lining, where the embryo implants.

Drew Bennett

The endometrium has two layers of its own. The stratum functionalis thickens every month and sloughs off in menstruation. The stratum basalis underneath stays put, attaches the endometrium to the myometrium, and helps the functional layer regenerate. And the vagina is a muscular tube about 3 inches long that receives the penis and sperm, serves as the menstrual outlet, and is the birth canal. The vulva is the external structures, the mons pubis, labia majora and minora, clitoris, and the vestibule with the urethral and vaginal openings. Vulva is not vagina. The Bartholin's glands on either side of the vaginal opening and the Skene's glands near the urinary meatus add moisture and lubrication.

Lizzie Stevens

The breasts have 15 to 20 lobules, each with clusters of tiny sacs called acini that make milk. Small ducts merge into a lactiferous duct for each lobe, which widens into a lactiferous sinus before opening at the nipple, and the pigmented areola surrounds it. Two hormones to keep straight: prolactin means produce, oxytocin means out. Prolactin makes the milk, oxytocin ejects it.

Drew Bennett

Now the part that scares everybody, the female cycle. The slide's advice is do not memorize four random hormones. Follow what's happening to the egg and the uterus. The cycle averages 28 days but can range from 20 to 45. There are two cycles running at once. The ovarian cycle is about the ovary and is run by FSH and LH. The menstrual cycle is about the uterus and is run by estrogen and progesterone.

Lizzie Stevens

Ovarian cycle, step one. Low estrogen and progesterone at the end of the last cycle tell the hypothalamus to release GnRH, which tells the pituitary to release FSH and LH. FSH, follicle stimulating hormone, wakes up several follicles. Only one makes it to maturity, the graafian follicle, and as it grows it makes estrogen. FSH means follicle.

Drew Bennett

Around the midpoint, estrogen peaks, and that triggers a sudden spike in LH. That LH surge makes the follicle rupture and release the ovum. LH launches the egg. The fimbriae catch it. Then the leftover follicle becomes the corpus luteum, which marks the luteal phase, and it makes large amounts of progesterone and a little estrogen. Progesterone is pro gestation. It keeps the lining thick and vascular.

Lizzie Stevens

And all that progesterone and estrogen also tell the pituitary to quiet down on FSH and LH, so no other follicle develops. If there's no fertilization, the corpus luteum degenerates into a scar called the corpus albicans. Hormone levels plummet, the lining loses its support, and menstruation starts. With the hormone brake released, FSH starts rising again, and we do the whole thing over.

Drew Bennett

Meanwhile the uterus goes through its own phases. Menstrual phase, day one is the first day of bleeding, lasting 3 to 5 days as the functional layer sheds. Proliferative phase, starting about day 6, estrogen rebuilds the lining and grows blood vessels. Ovulation. Then the secretory phase, where progesterone makes the endometrium a nutritious bed about 5 to 6 millimeters thick. And if there's no pregnancy, progesterone falls, the vessels feeding the lining spasm, the tissue becomes ischemic and necrotic, and it sloughs off.

Lizzie Stevens

So the short version, which I'd put on a sticky note, is FSH, follicle, estrogen, LH surge, ovulation, corpus luteum, progesterone. Estrogen establishes the lining, progesterone protects it. If you know where the egg is going and what the hormones are trying to accomplish, you don't have to memorize reproduction as a giant list. Follow the gamete and follow the hormones.