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In people with psoriasis, the immune system essentially becomes confused and overreacts, even though there is no real danger. T-cells become overactive and mistakenly attack healthy skin cells. These T-cells release cytokines which are chemical messengers that tell the body to make more skin cells and call in other immune cells. This creates inflammation and causes the skin to grow and divide much faster than normal (about every 3-4 days instead of the usual 28-30 days). Because the body can't get rid of the old skin cells quickly enough, they pile up on the surface of the skin which leads to the red, scaly patches in psoriasis, which are often itchy, dry, and sometimes painful.

This relates to our exam topics because it directly involves both the blood and the immune system. T-cells (which psoriasis is driven by) are a key part of the adaptive immune system that we learned about. Psoriasis is an example of how autoimmune diseases develop (when the immune system wrongly targets the body's own tissues instead of harmful invaders).

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Congenital Afibrinogenemia is a genetic disorder in which the patient does not have fibrinogen. There is a similar condition called hypofibrinogenemia in which the patient has limited fibrinogen. As we learned in class, fibrinogen is turned into fibrin during the coagulation cascade. Fibrin acts as glue and is used to bind elements together to form a solid mass which stops bleeding (coagulation). Symptoms of this condition point to the body's inability to stop the bleeding, such as easily bruising, nose bleeds that are hard to stop, or heavy bleeding after injury or surgery. Most people are able to live with this condition unless the bleeding is in the brain. One treatment option that is implemented before surgery is RiaSTAP, which gives the patient fibrinogen. In class, we learned that antibodies are formed against anything the body does not recognize. This can present a problem in patients with Congenital Afibrinogenemia taking RiaSTAP as the body does not recognize fibrinogen.

Congenital Afibrinogenemia Information | Mount Sinai - New York. 2023 Feb 2. Mount Sinai Health System. [accessed 2025 Apr 9]. https://www.mountsinai.org/health-library/diseases-conditions/congenital-afibrinogenemia.

RIASTAP. 2022 Mar 7. Food and Drug Administration. [accessed 2025 Apr 10]. https://www.fda.gov/vaccines-blood-biologics/approved-blood-products/riastap.

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Celiac disease is a condition where a person’s body reacts badly to gluten which is a protein found in wheat, barley, and rye. When someone with celiac disease eats gluten their immune system will mistakenly attack the lining of the small intestine (especially the villi - finger like and helps absorb nutrients from food). When these villi are damaged the body can’t absorb important nutrients properly. This can lead to problems like stomach pain, diarrhea, weight loss, and feeling tired. This condition relates to what we are learning in class because it involves the adaptive immune system. It specifically involves the topic of T cells that react to gluten as if it was a harmful pathogen. The inflammation and tissue damage in the small intestine are part of the inflammatory response we learned about with cytokines and immune cells like macrophages and T cells. Also since we haven’t learned about immune memory yet in class, I did a little more research on it. Basically, once the body has reacted to gluten it remembers it using “memory T cells” and “memory B cells”. This means that the next time gluten is eaten (no matter the amount) the immune system reacts faster and stronger which is why it is a chronic condition.

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Caused by genetic and environmental factors, Graves' disease is when the immune system makes an antibody to one part of the cells in the thyroid gland. This is an autoimmune disease that can lead to other diseases like lymphoid hyperplasia and potentially thyroid lymphoma. With Graves' disease, your immune system attacks your thyroid gland, causing it to make more thyroid hormones than your body needs as a defense. As a result, many of your body's functions speed up because of the overactivity of hormone production. The immune system produces antibodies that bind to the thyroid gland, causing it to overproduce thyroid hormone and leading to hyperthyroidism by mistakenly reacting to the excess hormones as something dangerous to the body. Hyperthyroidism also increases the body's sensitivity to adrenic hormones (like adrenaline), which can cause symptoms like nervousness, anxiety, and tremors. Other symptoms of Graves’ Disease can be irritability, the enlarged thyroid gland, skin having the texture of an orange peel, bulging eyes, etc.

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In type 1 diabetes, an autoimmune disease, the body's immune system unintentionally targets and kills the beta cells in the pancreas that produce insulin. A hormone called insulin transports glucose from the bloodstream into the body's cells, where it is converted into energy. People with Type 1 diabetes have little to no insulin production, which prevents glucose from entering cells and causes it to accumulate in the bloodstream. This results in hyperglycemia, or elevated blood sugar levels. The body starts using fat and muscle as fuel when glucose isn't available, which can lead to various health issues or even death if treatment isn't received. This autoimmune disorder affects the adaptive immune system. T cells, which are crucial parts of the immune response, mistakenly perceive beta cells as dangerous and destroy them. The function of T cells, their ability to identify diseases, and their ability to tell the difference between the body's own cells and external invaders are all related to what we have been studying. An autoimmune reaction against the pancreas results from the failure of this identification mechanism in Type 1 diabetes.

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Glucose-6-Phosphate Dehydrogenase, also known as G6PD, is an enzyme that plays a crucial role in protecting red blood cells from oxidative damage(unstable molecules on cells and tissues). Your erythrocytes are constantly exposed to different harmful oxidative factors. The G6PD enzyme helps produce NADPH which maintains glutathione and neutralizes free radicals(Ex: H₂O₂). People who have G6PD Deficiency (such as myself) have a hard time handling oxidative stress well. This leads to damage to the RBCs cell membranes which overtime causes your cells to essentially break apart. Your reticulocyte count is essentially higher and this is your bone marrow trying to compensate for the broken RBCs. This is an anemia known as hemolytic anemia(hemolysis). Your body struggles to replace these broken RBCs which leads to your hemoglobin levels being lowered, constant fatigue(shortness of breath), rapid heart rate, and other symptoms. Most patients are usually asymptomatic. If symptoms do show and continue over time, your spleen and kidney become involved which can cause severe back pain(speaking from experience), and your urine will naturally be darker. If my case ever becomes life threatening, a blood transfusion is necessary. The donor must have normal G6PD levels and the erythrocytes are separated from the plasma so that I can only get the packed red blood cells.

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Malaria is a disease that is transmitted by a bite of an Anopheles mosquito. This disease is caused by a Plasmodium parasite and once in the body it effects your red blood cells (erythrocytes) after it grows/matures in your liver. This is such a deadly disease because when it is inside of your red blood cells it multiplies and causes the cell to burst. Patients diagnosed with Malaria tend to have symptoms like fever, anemia, or inflammation. On a physiological level this disease impacts the circulatory system and blood which is also relevant to our class content. In class we discussed erythrocytes and how their job is to transport oxygen to tissues. Malaria ruptures these red blood cells which is why the transportation of oxygen to the tissues decreases and causes anemia or tissue hypoxia. Also, after a red blood cell is ruptured there is leftover debris which can trigger an immune response and cause inflammation. People infected with Malaria can have issues with Hemostasis and blood flow because the disease can cause red blood cells to clump which will cause obstructions in the capillaries and cause disruptions with tissue perfusion.

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Mast Cell Activation Syndrome is a condition affecting mast cells which are part of the immune system. They are  similar to white blood cells in the sense that they protect the body by releasing mediators in response to injury or allergens to help promote inflammation and healing. However, this condition occurs when these cells become too active and release too many inflammatory substances like histamines and other chemicals. In a normal person, mast cells releasing these chemicals at the right time when they sense an issue occurring. In a person exhibiting MCAS, these cells activate too often or at the wrong times and this leads to widespread inflammation. Symptoms of MCAS include flushing, rapid heartbeat, low blood pressure, difficulty breathing, digestive problems brain fog, headaches, fatigue, and skin rashes. These symptoms are the physiological result of the disruption of normal tissue due to the excessive release of chemicals from mast cells.

This disorder relates to the lymphatic and immune system lecture from class because it is involved with irate immunity and inflammatory mediators. Mast cells are part of the immune system and release histamine and cytokines, which were covered when we talked about inflammatory response. It also connects to immunity because this disorder may come from the body forming exaggerated responses to harmless antigens. MCAS shows an example of how immune dysregulation can lead to effects harming the body. This disorder highlights the importance of the bodies need to maintaining immune homeostasis to protecting against overreaction because it could then have the opposite effect of what the immune system is trying to accomplish and cause itself cellular injury.

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Systemic Lupus Erythematosus is a disease where the body’s immune system attacks healthy tissue and organs that they mistake for bad which causes severe inflammation and damage to the body. The symptoms of this disease can vary in every person and patients can have “flare ups” – as my mom who has lupus calls it. Some of these symptoms include fatigue, joint pain and swelling, skin rashes, fever, hair loss, and sensitivity to sunlight. Since this disease is “systemic” it attacks multiple organs and these symptoms reflect that. This connects to class content because with this disease the body produces autoantibodies which mistakenly attacks healthy tissues. Antibodies are produced by the immune system in order to recognize and eliminate foreign bodies whereas autoantibodies are also produced by the immune system but attack the healthy tissues. There are two main autoantibodies associated with the disease, anti-dsDNA and anti-Sm, which both target the body's DNA and RNA.

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Von Willebrand Disease (vWD) is a genetic disorder where the blood doesn’t clot properly because of a problem with a protein called von Willebrand factor (vWF). This protein helps platelets stick to broken blood vessels and also protects another clotting protein, factor VIII. Without enough working vWF, it’s harder for clots to form, so people with vWD may bruise easily, have frequent nosebleeds, or bleed for a long time after injuries.

This condition connects to what we’ve learned in class about hemostasis and blood clotting. Clot formation depends on platelets and plasma proteins like vWF.

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Guillain-Barré Syndrome (GBS) is an autoimmune disorder in which the body’s immune system attacks the peripheral nervous system. This condition is often triggered by a prior infection or even vaccines such as the flu vaccine that causes immune cross-reactivity. Meaning that the immune system mistakenly identifies similar proteins in different substances as being identical. Antibodies target components of myelin or axon membranes, leading to demyelination and/or axon damage. This disrupts saltatory conduction along motor and sensory neurons, resulting in muscle weakness, numbness, and even paralysis. In some cases, the autonomic nervous system is also affected, causing irregular heart rate or blood pressure.

This condition is directly related to our current class content. First, it shows how demyelination impairs signal transmission. Second, it connects to the immune system and how immune cells like T cells and macrophages can invade nerve tissues. Studying GBS reinforces our understanding of how peripheral nerves and their coverings (Schwann cells/myelin) are essential for voluntary movement and sensory function.

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Inflammatory bowel disease is a chronic disease of the gastrointenstial system. It causes severe stomach pains and cramps, as well as diarrhea and bloody stool. It can be controlled with medication, but never fully goes away. There are two types of IBDs: Crohn’s disease and Ulcerative Colitis. Crohn’s disease is inflammation of any part of the GI tract. Ulcerative Colitis is inflammation of the colon and rectum only.  IBD happens when the immune system attacks healthy tissue in the GI tract. This realates to our class because it has to do with the immune system attacking healthy tissue. The immune system recongnizes the normal gut flora as pathogens, so it attacks them, which also causes inflammation in the gut. When this happens, an immune response is signaled again. This causes the release of cytokines which further causes inflammation of the gut. This cycle of inflammation caused by the immune system attacking healthy tissue which signals an immune response that causes more inflammation is what makes this disease chronic. It is a never ending cycle.

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Acute lymphocytic leukemia is a cancer of the blood and bone marrow that occurs when DNA mutations arise in bone marrow cells, which ultimately affects the production of white blood cells. We have learned in class that all blood cells, red and white, originate from hematopoietic stem cells found in bone marrow, which then differentiate into specialized blood cells. The presence of cancerous cells in the bone marrow disrupts normal cell production and differentiation, which then leads to a significantly weakened immune system and improper clotting mechanisms (thrombocytopenia; excessive bruising) due to a lack of platelets, which are also produced by bone marrow. Additionally, the decreased production of red blood cells can lead to anemia, meaning not enough oxygen is circulating through the body, which can lead to fatigue and shortness of breath. Symptoms of acute lymphocytic leukemia include enlarged lymph nodes, bruising, fever, bone pain, bleeding from the gums, and frequent infections. It is also the most common form of childhood cancer with treatments including chemotherapy and drug therapy targeted at killing cancerous cells.

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Burkitt lymphoma is a highly aggressive cancer of the lymphatic system that originates in B-cells—key components of your immune system responsible for producing antibodies. Its triggered by a genetic mutation in which a segment of one chromosome switches with another, relocating the MYC gene—a gene that deal with cell growth and division—which is also next to a highly active region of B-cell DNA.

This abnormal positioning causes the overexpression of MYC, leading to uncontrolled B-cell proliferation and the development of cancer. The B-cells infiltrate lymphoid tissues such as the lymph nodes, spleen, and MALT, forming tumors in areas like the jaw, abdomen, or central nervous system.

This growth impairs the adaptive immune system, diminishing the body’s ability to respond effectively to pathogens that were not already eliminated by the innate immune system.

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Hemophilia is a genetic disorder that disables or impairs the ability to clot blood. Symptoms that individuals with hematoma typically experience include: excessive/prolonged and unexplained bleeding, large deep bruises, and more.

Physiologically, this is caused due to lack of or impairment of clotting factors VIII(hemophilia A) or IX( hemophilia B)

Those with hemophilia A experience absence of factor VII, which is a cofactor to vWF. These are the molecules typically released by the endothelial cells, and would typically bind to platelets to make a platelet plug but cannot effectively due to the lack of the activating coagulation factors.With hemophilia B, factor IX is deficient, which activates X and is necessary for fibrin to be produced.

My explanation of the physiological differences between the two types of hemophilia are relevant to the class content because both impact different events of the coagulation cascade. Specifically it covers beginning events of platelet plug formation and coagulation.

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Hodgkin’s Lymphoma is a type of cancer that affects the lymphatic system. It develops from B-Lymphocytes, also known a B-cells. B-cells come from the bone marrow and then concentrate mainly in the lymph nodes and spleen and are vital for immune function. B-cell have receptors on their surface that recognize antigens from bacteria, viruses, or any foreign substance. The b-cell will then engulf the antigen and present it to a helper t-cell. Then the b-cells multiple into plasma cells which produce antibodies against the foreign substance. Hodgkin’s Lymphoma triggers the B-cells to go through abnormal changes and create Hodgkin and Reed-Sternberg cell. These cells look visibly different from b-cells and multiple uncontrollably.  It causes swollen lymph nodes and triggers and suppresses the immune systems causing lots of problems and inflammation. The condition relates to the class because it disrupts the production of B-cells and triggers the immune systems causing impairments for its normal functions.

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This is a photo showing protests in response to the AIDS crisis, or more specifically, the lack of medical and governmental support for it. Stigma against LGBTQIA+ caused extreme delays to vaccinations, research, and medical care for a disease that was killing many. If you want to go into the medical field, I highly recommend educating yourself on this (or the tuskegee syphilis study or the difference in mortality rates between black and white women in labor in America), because the medical discrimination was so apparent in this case, and its important to stay educated in order to undo past (and present) wrongdoings.

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AIDS - Acquired Immune Deficiency Syndrome

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AIDS - Acquired Immune Deficiency Syndrome

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AIDS is an immune system disease caused by HIV, human immunodeficiency virus. There are two main types of HIV, HIV-1 and HIV-2, and both can lead to AIDS. Both types of HIV destroy T-cells until the body is unable to fight off any kind of illness. In class, we learned that T-cells allow for cell-mediated immunity that allow a response to infected cells, whether that’s in the form of a foreign cell, a cancer cell, or a pathogen. T cells can recognize an antigen and interact with it to remove it. HIV infects helper T cells and causes a significant drop in the white blood cell count. HIV initially causes flu-like symptoms, and then is asymptomatic. If HIV remains undiagnosed for long enough, it can progress into AIDS. AIDS is when the helper T cells drop low enough that the sick individual can now present with illnesses that aren’t seen in healthy individuals, and it can cause extreme weight loss, tiredness, fevers, and skin discoloration.

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SCID is a rare genetic disorder in which babies are born with little to no immune system. The disease, also colloquially referred to "bubble boy disease", prohibits the baby from being able to produce T cells, leaving B cells non-functional, thus meaning there is essentially no immune system. Those who have SCID are at constant risk of developing pneumonia, thrush, chronic diarrhea, and a variety of other invasive infections.

It is hard to deduce certain symptoms as babies won't show specific symptoms outside of having an infection, so the condition will basically be undetectable until the baby develops an infection or illness. The most notable/detectable problem would be failure to thrive. There are over 15 variations of SCID, however the most frequently diagnosed variation is caused by a defect on a baby's X chromosome. Meaning only biological males are affected, however biological females are carriers of the disorder. To diagnose SCID, a baby will have to undergo a blood test and in some cases genetic testing as well.

To treat this disorder, babies will commonly have a stem cell transplant performed, some may need chemotherapy, and for some even gene therapy. Devastatingly, if not caught early enough, babies are not likely to live beyond a year.

This disorder relates directly to course information in that those with the disorder do not have much of the immune function we spoke about. There are no T-cells to kill foreign pathogens, and there are no B-cells to bind to antigens. With neither of these cells there would be no adaptive immunity

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Rheumatoid arthritis is an autoimmune disorder where the immune system attacks the synovial lining of joints, leading to inflammation, pain, and stiffness. This condition causes the body's immune cells to target healthy tissues in the joints, which is responsible for lubricating the joints. This results in chronic inflammation, which can eventually lead to joint destruction, deformities, and loss of function. Over time, the inflammation affects cartilage and bone, which can further contribute to joint damage. It can be treated by medication, physical therapy, and surgery. This condition relates to the class because it involves key immune system processes, including the role of T-cells and cytokines in inflammation, which are directly linked to autoimmune disorders. In RA, cytokines such as tumor necrosis factor (TNF) and interleukins (ILs) are elevated, contributing to the inflammatory response.

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Vitamin D is an essential vitamin that your body uses for normal bone development and maintenance. It also plays a role in the nervous system, musculoskeletal system, and immune system. Vitamin D deficiency simply means that your body does not have enough vitamin and this can primarily trigger issues with your bones and muscles. Vitamin D plays an important role in maintaining the balance of calcium in your blood. With lower levels of Vitamin D, if you do not absorb as much calcium or phosphorus in your intestines it could lead to hypocalcemia (low blood calcium levels) which ultimately leads to hyperparathyroidism (overactive parathyroid glands that attempt to keep your blood calcium levels normal). These two conditions, if left untreated, and cause muscle weakness, cramps, fatigue, and depression. It relates to this class because it has a big affect on the blood and causing the inability to clot properly. Vitamin D deficiency is associated with an increased risk of venous thromboembolism and might have an anticoagulant effect. Without the ability to clot, your body will lose more blood than necessary upon bleeding.

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Sickle cell disease is a genetic disorder that affects the body's ability to produce normal hemoglobin, the protein in red blood cells that carries oxygen. People with this condition have an abnormal form called hemoglobin S, due to a mutation in the HBB gene. When this hemoglobin loses oxygen, it sticks to itself and forms long chains, which cause red blood cells to become rigid and they have a crescent shape. These cells are less flexible and tend to stick together, leading to blockages in small blood vessels. This reduces blood flow and oxygen delivery to tissues, causing pain and potential organ damage. This relates to class content because we have talked about the blood, and red blood cells function to carry oxygen to tissues. The cells involved in sickle cell carry oxygen less efficiently, which can affect tissue function. Additionally, sickled cells have a much shorter lifespan than normal red blood cells, leading to anemia because the body cannot produce new cells quickly enough. The spleen, which helps fight infection related to the immune system we have talked about in class, often becomes damaged early on, making individuals with sickle cell disease more vulnerable to serious bacterial infections.

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Vasculitis is characterized by an inflammation of blood vessels, most often in response to an immune attack. The immune system identifies blood vessels as foreign, at random, and launches an attack. The reason why the immune system attacks these vessels is still unknown but often times vasculitis is attributed to other conditions like heart problems, cancer, or the use of certain medications. The direct mechanism of immune defense can come from a variety of responses, most often including neutrophil activation, antibody-mediated attack, cytokine release, involvement of t-cells and macrophages, and immune complex formation. The immune attack triggers inflammation in the affected vessel, causing the walls to thicken. This can be damaging as the thickened walls add more resistance to blood flow, meaning that less of the oxygen and nutrients transported by blood are able to get to their target organs. Ultimate consequences of vasculitis include major organ damage like kidney, liver, or lung failure. Chronic vasculitis is also responsible for increasing the likelihood of an aneurism due to the way in which this condition weakens important vessels.

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Babesiosis is an infection primarily transmitted through ticks, which affects your blood. However, incorrect blood transfusions can transmit it, but not person to person. The parasite invades and destroys red blood cells. With fewer red blood cells, there is a shortage of oxygen-carrying capacity. This lack of oxygen in the blood can cause dizziness and fatigue. On a larger scale, it can cause organ damage and low blood pressure. This infection relates to our class because we learned how the structure and function of red blood cells are perfect for carrying oxygen. We know that oxygen attaches to the hemoglobin in the red blood cells. Since this infection kills red blood cells, it answers the question: “What happens when oxygen doesn’t have a carrier?” Lack of oxygen in the blood can become a serious issue and its very interesting to know why that is.

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Kostmann Syndrome, or SCN, is a rare disease characterized by severe neutropenia, or lack of mature neutrophils - which are the leukocytes responsible for fighting bacterial infections. In patients with SCN, they are unable to produce enough neutrophils because of a gene malfunction causing their bone marrow to produce inadequate and or defective neutrophils. This not only leads to higher susceptibility to bacterial infections, but can also lead to leukemia. SCN is a failure in production of granulocytes in hematopoiesis, which is directly related to class content because without granulopoiesis, the immune system is unable to function properly. Neutrophils are also key players in the innate immune response, they are on the first-line of defense, and without them, innate immunity is compromised. Overall, Kostmann Syndrome is linked directly to our class content because of its real life demonstration of how when there is a defect in hematopoiesis it can compromise the immune system to a high degree, and in SCN specifically, neutropenia can compromise innate immunity.

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Bernard Soulier syndrome is an inherited condition resulting in abnormal platelets. People with Bernard Soulier are both larger than normal platelets, but also lower in number. People with Bernard Soulier Syndrome present with excesses bruising and bleeding. This is because the body has trouble with blood clotting. People with Bernard Soulier have a mutation to the Gp1b complex, which sticks out off of the surface of platelets. The Gp1b complex, in combination with the von Willebrand factor is responsible with beginning the clotting process. When the Gp1b complex is abnormal and cannot bind to the von Willebrand factor, then blood clotting cannot begin efficiently. This is why people that have Bernard Soulier are advised to stay away from things like contact sports where bleeding may be common. The location of the Gp1b complex on the membrane of the platelet is what contributes to the large size, but low number of platelets.

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T-cell Lymphoma is a type of non-Hodgkin lymphoma that leads to uncontrollable clonal expansion of abnormal T cells. Normally, T cells develop in the thymus and undergo positive and negative selection to ensure that only functional T cells, non autoreactive enter circulation. At the physiological level, it can disrupt the immune system by immune dysregulation since malignant t cells might not function the right way. infiltration of the malignant cells into lymph nodes, spleen, bone marrow, leading to organ dysfunction. Also cytokine release by abnormal t cells can cause symptoms like fever, night sweats, etc. In class we learned T cells that are autoreactive die and get destroyed but in lymphoma they survive and can expand. In class we learned that the immune system can destroy and kill abnormal or potential cancer cells. It is carried out by cytotoxic cells, natural killer cells, and dendritic cells. But in T-cell lymphoma they are the cancerous cells and develop ways to avoid being detected and killed by the immune system so they can replicated easily.

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Hairy Cell Leukemia is a chronic type of blood cancer that effects lymphocytes. The bone marrow over produces B leukocytes that build up in the marrow, spleen and bloodstream. This buildup crowds up blood cell production, not leaving room for other cells such as RBCs, platelets and other healthy WBCs. It causes extreme susceptibility to infections due to the deficit in health WBCs, swollen lymph nodes and lower abdominal pain. In addition, anemia is a common symptom. This relates to class content as we observe the importance of proper blood cell production and the effects of a condition that inhibits that system. The immune system is compromised due to unhealthy white blood cells spreading in the blood and inhibiting the effectiveness of the lymphatic system. The effectiveness is largely disrupted from the system being basically clogged with pathogens (bad WBCs).