Biochemistry Exam 3: Hemostasis & Clotting

Heparin is an anticoagulant that helps with fibrinolysis, preventing blood clots by binding to antithrombin, increasing its action against thrombin and factor Xa. This decreases blood clotting ability.

Warfarin is a vitamin K antagonist. It doesn't directly affect blood but acts on liver cells that synthesize clotting factors, slowing down their production. This indirectly slows down blood clotting.

Fibrinolysis is the breakdown of blood clots, both existing ones and those formed during wound healing. It's essential to prevent excessive clotting.

A test of primary hemostasis that measures the time it takes for blood vessel constriction and platelet plug formation to stop bleeding. It does not allow clot formation, so only focuses on the initial stages of blood clotting.

Evaluates the intrinsic pathway of coagulation, testing factors XII, XI, IX, VIII, X, V, II, prothrombin, and fibrinogen. It's used to monitor heparin therapy.

Evaluates the extrinsic pathway of coagulation, testing factors VII, X, V, II, and fibrinogen. It's commonly used to assess blood clotting.

International Normalized Ratio (INR) is a standardized measure of prothrombin time (PT), used to monitor warfarin therapy. 1 is normal clotting, 2 is twice the normal clotting time.

Aspirin inhibits platelet aggregation, preventing them from sticking together and contributing to blood clot formation.

Addison's disease is another name for primary adrenal insufficiency, a condition where the adrenal glands don't produce enough cortisol and aldosterone.

Addison's disease symptoms include muscle weakness and fatigue, weight loss and decreased appetite, darkening of skin (hyperpigmentation), low blood pressure, fainting, salt craving, and low blood sugar (hypoglycemia).

Glucocorticoids decrease the activity of phospholipase A2 (PLA2), an enzyme involved in the first step of eicosanoid synthesis.

Thromboxane, produced by platelets, promotes platelet aggregation, which is the clumping together of platelets to form a clot.

Aspirin irreversibly inhibits cyclo-oxygenase (COX), an enzyme involved in the synthesis of prostaglandins and thromboxane.

Collagen's unique features include a triple-helical structure, the presence of hydroxyproline and hydroxylysine, cross-linking for strength, and heterogeneity with 28 different types fulfilling specific roles.

Vitamin C is required for the post-translational modifications of prolines and lysines, which are crucial for forming stable collagen triple helices.

Collagen is a glycoprotein, and glycosylation can influence its immunogenicity, which has implications for autoimmune diseases.

Calcium plays vital roles as a messenger within cells (signal transduction) and as a structural component in bone and teeth. It is also essential for various cellular processes like muscle contraction, neurotransmitter release, and T-cell activation.

Bone plays a dynamic role in calcium homeostasis by releasing calcium when blood levels are low (through osteoclast activity) and storing calcium when levels are high (through osteoblast activity).

The gastrointestinal tract absorbs calcium from food, a process regulated by vitamin D and parathyroid hormone (PTH).

Small, non-nucleated cells that circulate in the blood in an inactive form. They are essential for blood clotting.

Platelets become activated when they encounter a damaged blood vessel, such as a cut or tear. They bind to exposed collagen and other factors, triggering a cascade of events that ultimately lead to clotting.

The kidneys maintain calcium balance by reabsorbing calcium back into the bloodstream and excreting excess phosphate, both influenced by PTH.

PTH increases blood calcium levels by stimulating bone resorption, enhancing calcium absorption in the gut, and promoting calcium reabsorption by the kidneys.

TXA2 is a potent platelet activator that causes vasoconstriction and promotes platelet aggregation. It works by binding to receptors on platelets and triggering a signaling cascade.

PGI2 is a powerful inhibitor of platelet aggregation. It works by binding to receptors on platelets and triggering a signaling cascade that reduces the release of calcium, preventing platelet activation.

Vitamin D promotes calcium absorption in the gut, aiding in maintaining calcium levels within a healthy range.

Calcitonin acts to lower blood calcium levels by inhibiting bone resorption (osteoclast activity), promoting calcium deposition in bone.

The first step in blood clotting is the formation of a platelet plug. This occurs when platelets aggregate at the site of injury, forming a temporary seal.

Osteoporosis, a condition of weakened bones, also affects teeth. Osteoclasts, the cells responsible for bone breakdown, can lead to jaw degradation, gum atrophy, and more porous tooth structure.

Fibrinogen is a protein that binds to activated platelets and helps them stick together, strengthening the platelet plug. It acts as a bridge between platelets.

The coagulation cascade is a complex series of enzymatic reactions that ultimately leads to the formation of a fibrin clot. This is the final step in blood clotting.

Hemostasis (blood clotting) involves three main steps: vasoconstriction, platelet plug formation, and coagulation cascade. These steps work together to stop bleeding and repair damaged blood vessels.

Lead poisoning disrupts heme synthesis in various ways. It displaces iron in ferrochelatase, affecting the final step of heme production. Additionally, lead inhibits δ-aminolevulinate dehydratase, causing a buildup of δ-aminolevulinate, a neurotoxin.

Iron, essential for heme synthesis, is absorbed inefficiently in the intestine. It's transported in the blood bound to transferrin, which delivers it to cells via specific receptors. Free iron is toxic, so levels are tightly controlled.

Iron is stored within cells as ferritin, particularly in the liver. Hepcidin, a hormone secreted by the liver, regulates iron uptake by controlling ferroportin, a protein involved in iron release from intestinal cells. High hepcidin = low iron uptake, and vice versa.

Iron deficiency leads to anemia, characterized by a lack of red blood cells and hemoglobin. Iron overload, on the other hand, can cause damage to organs due to excessive iron accumulation.

When red blood cells break down, heme is converted to bilirubin in macrophages. Bilirubin, a yellow pigment, is then transported to the liver for excretion. An accumulation of bilirubin in the blood results in jaundice.

Heme can be recycled within a cell but not between cells. This recycling process involves the breakdown of hemoglobin and the reuse of iron for new heme synthesis.

Porphyrias are a group of genetic disorders characterized by defects in heme synthesis. This leads to the accumulation of porphyrin precursors, which can cause various symptoms like photosensitivity, abdominal pain, and neurological dysfunction.

There is no known mechanism for active excretion of iron from the body. Iron is mostly recycled, and any excess is stored primarily in the liver and spleen.

The main salivary enzymes are amylase, lysozyme, lactoferrin, and immunoglobulins.

Salivary amylase breaks down ingested starch into simpler sugars, primarily maltose.

Lysozyme is an enzyme that breaks down the cell walls of bacteria, helping to protect against infections.

Lactoferrin binds to iron, preventing bacteria from using it for growth, thus inhibiting their multiplication.

The main immunoglobulins in saliva are IgA and IgG. IgA is the most important, protecting against pathogens in the oral cavity.

Dental enamel is the hardest structure in the body, composed mainly of hydroxyapatite.

Hydroxyapatite in enamel is maintained by constant ion exchange via fluids percolating through the enamel's micropores.

Acidity below pH 5.5 causes demineralization of enamel, dissolving hydroxyapatite and weakening the enamel.