Topic 9: Chpt 16 and chpt 24 Flashcards

1
Q

What is blood, and what is its primary function?

A

Blood is a connective tissue composed of cellular elements suspended in plasma. It is the circulating portion of the extracellular compartment, responsible for carrying material from one part of the body to another.

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2
Q

What is plasma, and what percentage of blood does it make up?

A

Plasma is the fluid matrix of blood, making up about 60% of the blood volume. It is composed of water (92%), proteins (7%), and dissolved organic molecules, ions, trace elements, and gases (1%).

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3
Q

How is total blood volume calculated for a 70-kg man and a 58-kg woman?

A

A 70-kg man has about 5 liters of blood (7% of body weight), with 2 liters of blood cells and 3 liters of plasma. A 58-kg woman has about 4 liters of total blood volume.

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4
Q

What is the composition of plasma, and how does it compare to interstitial fluid?

A

Plasma is composed of water (92%), proteins (7%), and dissolved organic molecules, ions, trace elements, and gases (1%). It is identical to interstitial fluid except for the presence of plasma proteins.

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5
Q

What are the main proteins found in plasma, and what percentage do they constitute?

A

The main proteins in plasma are albumins (60%), globulins, clotting protein fibrinogen, and iron-transporting protein transferrin, making up more than 90% of all plasma proteins.

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6
Q

Where are most plasma proteins produced, and what are immunoglobulins?

A

Most plasma proteins are made by the liver and secreted into the blood. Immunoglobulins (antibodies) are a type of globulin synthesized and secreted by specialized blood cells.

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7
Q

How do plasma proteins affect osmotic pressure and fluid balance in the body?

A

The presence of proteins in the plasma increases the osmotic pressure of the blood, pulling water from the interstitial fluid into the capillaries and offsetting filtration out of the capillaries created by blood pressure.

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8
Q

What are the functions of plasma proteins?

A

Plasma proteins participate in blood clotting, defense against foreign invaders, and act as carriers for steroid hormones, cholesterol, drugs, and certain ions. Some plasma proteins also act as hormones or extracellular enzymes.

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9
Q

What makes up the remaining 1% of plasma’s composition?

A

The remaining 1% of plasma is composed of dissolved organic molecules (amino acids, glucose, lipids, nitrogenous wastes), ions (Na+, K+, Cl-, H+, Ca2+, HCO3-), trace elements, vitamins, dissolved oxygen (O2), and carbon dioxide (CO2).

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10
Q

What is the role of albumins in the plasma?

A

Albumins are the most prevalent plasma proteins, making up about 60% of the total. They help maintain osmotic pressure and act as carriers for various substances in the blood.

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11
Q

How do plasma proteins contribute to the body’s defense mechanisms?

A

Plasma proteins, including immunoglobulins (antibodies), play a crucial role in the body’s defense against foreign invaders by participating in the immune response.

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12
Q

What role do plasma proteins play in blood clotting?

A

Plasma proteins such as fibrinogen are essential for blood clotting, helping to prevent excessive bleeding and promote wound healing.

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13
Q

How do plasma proteins function as carriers?

A

Plasma proteins carry steroid hormones, cholesterol, drugs, and certain ions (such as iron) through the blood, aiding in their transport and distribution throughout the body.

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14
Q

In what ways can plasma proteins act beyond transport and defense?

A

Some plasma proteins act as hormones, regulating various physiological processes, and as extracellular enzymes, catalyzing biochemical reactions outside cells.

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15
Q

What are the three main cellular elements found in blood?

A

The three main cellular elements in blood are red blood cells (RBCs or erythrocytes), white blood cells (WBCs or leukocytes), and platelets (thrombocytes).

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16
Q

What are red blood cells and their primary function?

A

Red blood cells (RBCs or erythrocytes) transport oxygen from the lungs to tissues and carbon dioxide from tissues to the lungs. They lose their nuclei by the time they enter the bloodstream.

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17
Q

What are platelets, and what is their role in the body?

A

Platelets (thrombocytes) are cell fragments that split off from megakaryocytes. They lack a nucleus and play a key role in coagulation, which is the process of blood clot formation to prevent blood loss in damaged vessels.

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18
Q

What are white blood cells, and what is their primary function?

A

White blood cells (WBCs or leukocytes) are fully functional cells that play a key role in the body’s immune responses, defending against foreign invaders such as parasites, bacteria, and viruses. Their work is usually carried out in the tissues rather than in the circulatory system.

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19
Q

How many types of mature white blood cells are there, and what are they?

A

There are five types of mature white blood cells: lymphocytes, monocytes, neutrophils, eosinophils, and basophils.

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20
Q

What do monocytes become when they enter tissues, and what are tissue basophils called?

A

Monocytes develop into macrophages when they enter tissues. Tissue basophils are called mast cells.

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21
Q

How are white blood cells grouped based on their characteristics?

A

White blood cells can be grouped as follows:

  • Phagocytes (neutrophils, monocytes, macrophages) which can engulf and ingest foreign particles.
  • Immunocytes (lymphocytes) responsible for specific immune responses.
  • Granulocytes (basophils, eosinophils, neutrophils) which contain cytoplasmic inclusions giving them a granular appearance.
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22
Q

What are phagocytes, and which cells are included in this group?

A

Phagocytes are cells that can engulf and ingest foreign particles such as bacteria. This group includes neutrophils, monocytes, and macrophages.

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23
Q

What are immunocytes, and which cells are included in this group?

A

Immunocytes are responsible for specific immune responses directed against invaders. This group includes lymphocytes.

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24
Q

What are granulocytes, and which cells are included in this group?

A

Granulocytes contain cytoplasmic inclusions that give them a granular appearance. This group includes basophils, eosinophils, and neutrophils.

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25
Q

Where do all blood cells originate from?

A

All blood cells are descendants of a single precursor cell type known as the pluripotent hematopoietic stem cell, primarily found in bone marrow.

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26
Q

What is the role of pluripotent hematopoietic stem cells?

A

Pluripotent hematopoietic stem cells can develop into many different cell types. They first become uncommitted stem cells, then progenitor cells, which are committed to developing into specific cell types.

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27
Q

Into what types of cells do progenitor cells differentiate?

A

Progenitor cells differentiate into red blood cells, lymphocytes, other white blood cells, and megakaryocytes, the parent cells of platelets.

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28
Q

How common are uncommitted stem cells in the bone marrow?

A

Uncommitted stem cells are rare, making up about one out of every 100,000 cells in the bone marrow.

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29
Q

What is umbilical cord blood, and why is it significant?

A

Umbilical cord blood, collected at birth, is a rich source of hematopoietic stem cells used for transplants in patients with hematological diseases like leukemia.

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29
Q

How are uncommitted hematopoietic stem cells used in medical treatments?

A

These stem cells are isolated and grown to replace those killed by cancer chemotherapy. They can be obtained from bone marrow, peripheral blood, or umbilical cord blood.

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30
Q

What is hematopoiesis?

A

Hematopoiesis is the synthesis of blood cells, beginning early in embryonic development and continuing throughout life.

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31
Q

When and where does hematopoiesis begin in fetal development?

A

In the third week of fetal development, specialized cells in the yolk sac form clusters that become the endothelial lining of blood vessels and blood cells.

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32
Q

How does the site of blood cell production change during development?

A

Blood cell production spreads from the yolk sac to the liver, spleen, and bone marrow. By birth, the liver and spleen no longer produce blood cells.

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33
Q

Where does hematopoiesis occur in adults?

A

In adults, hematopoiesis occurs in the pelvis, spine, ribs, cranium, and proximal ends of long bones.

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34
Q

What is the difference between red and yellow marrow?

A

Active bone marrow is red due to hemoglobin, while inactive marrow is yellow because of adipocytes (fat cells).

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35
Q

Can inactive marrow resume blood cell production?

A

Yes, the liver, spleen, and inactive (yellow) marrow can resume blood cell production in times of need.

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36
Q

What percentage of developing cells in active marrow are red blood cells vs. white blood cells?

A

About 25% of the developing cells are red blood cells, while 75% are destined to become white blood cells.

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37
Q

Why must white blood cells be replaced more frequently than red blood cells?

A

White blood cells have a shorter lifespan than red blood cells. For example, neutrophils have a 6-hour half-life, and the body must produce over 100 million neutrophils daily. Red blood cells live for nearly four months in circulation.

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38
Q

What controls the production and development of blood cells?

A

The production and development of blood cells are controlled by cytokines, which are peptides or proteins released from one cell that affect the growth or activity of another cell.

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39
Q

How are newly discovered cytokines often named?

A

Newly discovered cytokines are often called factors, with modifiers that describe their actions, such as growth factor, differentiating factor, and trophic factor.

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40
Q

What are colony-stimulating factors (CSFs), and what is their role in hematopoiesis?

A

Colony-stimulating factors (CSFs) are cytokines made by endothelial cells, marrow fibroblasts, and leukocytes. They stimulate the growth of leukocyte colonies in culture and regulate leukocyte production and development (leukopoiesis).

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41
Q

What do CSFs induce in stem cells?

A

CSFs induce both cell division (mitosis) and cell maturation in stem cells. Mature leukocytes lose their ability to undergo mitosis.

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42
Q

How do existing white blood cells influence leukopoiesis?

A

Existing white blood cells help regulate the production of new leukocytes, allowing development to be specific and tailored to the body’s needs.

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43
Q

What are some examples of how differential white cell counts are used in diagnosis?

A

A high total number of leukocytes with increased neutrophils typically indicates a bacterial infection. A high, normal, or low white cell count with an increased percentage of lymphocytes often indicates a viral infection.

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44
Q

How do cytokines affect the production of leukocytes during infections?

A

During infections, cytokines released by active leukocytes stimulate the production of additional leukocytes. For bacterial infections, this increases neutrophils and monocytes. For viral infections, it often increases lymphocytes.

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45
Q

What is the significance of understanding leukopoiesis for treating diseases?

A

Understanding leukopoiesis helps develop treatments for diseases characterized by abnormal leukocyte levels, such as leukemias (excess leukocytes) and neutropenias (deficient leukocytes).

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46
Q

What was the historical significance of thrombopoietin (TPO)?

A

TPO was first described in 1958, and its gene was cloned in 1994. Genetically engineered TPO was used to stimulate platelet production in patients with thrombocytopenia, though the first TPO drugs had to be recalled due to adverse side effects. Newer TPO agonists are now in clinical use.

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47
Q

What is thrombopoietin (TPO), and what is its function?

A

Thrombopoietin (TPO) is a glycoprotein that regulates the growth and maturation of megakaryocytes, the parent cells of platelets. It is primarily produced in the liver.

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48
Q

What is erythropoietin (EPO), and how does it function in erythropoiesis?

A

Erythropoietin (EPO) is a glycoprotein that controls red blood cell production (erythropoiesis). It is produced mainly in the kidneys in response to hypoxia (low oxygen levels in tissues).

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49
Q

How does hypoxia influence erythropoietin (EPO) production?

A

Hypoxia stimulates the production of hypoxia-inducible factor 1 (HIF-1), which activates the EPO gene to increase EPO synthesis, promoting red blood cell production.

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50
Q

What was the progression of scientific discovery and clinical use of erythropoietin (EPO)?

A

The existence of EPO was suggested in the 1950s, purified two decades later, and its gene identified nine years after that. EPO was then produced by recombinant DNA technology for clinical use, benefiting patients undergoing chemotherapy.

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51
Q

What concerns have been raised about erythropoiesis-stimulating agents?

A

In 2007, the FDA issued new dosing instructions and warnings about the increased risk of blood clots in patients taking higher doses of erythropoiesis-stimulating agents.

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52
Q

What roles do interleukins play in hematopoiesis and the immune system?

A

Interleukins, such as IL-3, are cytokines released by white blood cells to act on other white blood cells, playing crucial roles in hematopoiesis and the immune system.

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53
Q

How are interleukins named, and what is an example of their function?

A

Interleukins are numbered once their amino acid sequences are identified, such as interleukin-3 (IL-3). They are important in immune responses and hematopoiesis.

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54
Q

What is the most abundant cell type in blood and how many are there per microliter?

A

Erythrocytes, or red blood cells, are the most abundant cell type in blood, with about 5 million per microliter. This is compared to 4,000-11,000 leukocytes and 150,000-450,000 platelets per microliter.

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55
Q

What are the primary functions of red blood cells?

A

The primary functions of red blood cells are to facilitate oxygen transport from the lungs to cells and carbon dioxide transport from cells to the lungs.

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56
Q

How is the ratio of red blood cells to plasma clinically indicated?

A

The ratio is indicated by the hematocrit, which is expressed as a percentage of total blood volume.

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57
Q

How is hematocrit determined?

A

Hematocrit is determined by drawing a blood sample into a capillary tube, centrifuging it, and measuring the column of packed red cells as a percentage of the total sample volume.

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58
Q

What is the normal range of hematocrit for men and women?

A

The normal range of hematocrit is 40-54% for men and 37-47% for women.

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59
Q

Why is the hematocrit test valuable?

A

The hematocrit test provides a rapid and inexpensive way to estimate a person’s red cell count and can be collected by simply sticking a finger.

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60
Q

How do red blood cells mature in the bone marrow?

A

In the bone marrow, committed progenitor cells differentiate into large, nucleated erythroblasts. As erythroblasts mature, the nucleus condenses, the cell shrinks, and the nucleus is pinched off and phagocytized by bone marrow macrophages. Other organelles break down, and the final immature cell, called a reticulocyte, enters circulation and matures into an erythrocyte in about 24 hours.

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61
Q

Describe the structure of mature red blood cells.

A

Mature red blood cells are biconcave disks, shaped like jelly doughnuts with the filling squeezed out. They are membranous bags filled with enzymes and hemoglobin, lacking a nucleus and mitochondria.

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62
Q

How do red blood cells generate ATP?

A

Without mitochondria, red blood cells rely on glycolysis as their primary source of ATP.

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63
Q

Why do red blood cells become more fragile as they age?

A

Red blood cells cannot make new enzymes or renew membrane components due to the lack of a nucleus and endoplasmic reticulum, leading to a loss of membrane flexibility and increased fragility.

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64
Q

What allows red blood cells to change shape as they pass through capillaries?

A

The flexibility of red blood cells is due to a complex cytoskeleton composed of filaments linked to transmembrane attachment proteins.

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65
Q

What are the morphological changes in red blood cells indicative of disease?

A

Red blood cells can become spherical in spherocytosis, crescent-shaped in sickle cell anemia, abnormally small (microcytic) in iron-deficiency anemia, and pale (hypochromic) due to lack of hemoglobin

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66
Q

What is hemoglobin, and what is its role?

A

Hemoglobin is the main component of red blood cells, responsible for oxygen transport. It is a large, complex protein with four globular protein chains, each wrapped around an iron-containing heme group.

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67
Q

What are the different isoforms of globin proteins in hemoglobin?

A

The most common isoforms are alpha, beta, gamma, and delta. Adult hemoglobin (HbA) typically has two alpha chains and two beta chains, while a small portion has two alpha chains and two delta chains (HbA2).

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68
Q

What is the composition of each heme group in hemoglobin?

A

Each heme group consists of a carbon-hydrogen-nitrogen porphyrin ring with an iron atom in the center. About 70% of the body’s iron is found in these heme groups.

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69
Q

Why is dietary iron important for hemoglobin synthesis?

A

Hemoglobin synthesis requires an adequate supply of iron, which is primarily obtained from red meat, beans, spinach, and iron-fortified bread.

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70
Q

How is iron absorbed and transported in the body?

A

Iron is absorbed in the small intestine by active transport, binds to the carrier protein transferrin, and is transported in the blood. The bone marrow uses iron to make the heme group of hemoglobin for developing red blood cells.

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71
Q

Where is excess iron stored in the body?

A

Excess iron is stored mostly in the liver inside a protein molecule called ferritin, which can release soluble iron when needed for hemoglobin synthesis.

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72
Q

What are the symptoms and consequences of iron toxicity?

A

Initial symptoms of iron toxicity include gastrointestinal pain, cramping, and internal bleeding. Severe consequences can include liver failure, which can be fatal.

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73
Q

How long do red blood cells live in circulation, and what happens to them as they age?

A

Red blood cells live for about 120 ± 20 days. As they age, they become increasingly fragile and may rupture in narrow capillaries or be engulfed by macrophages in the spleen.

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74
Q

What happens to the components of destroyed red blood cells?

A

Amino acids from hemoglobin’s globin chains are recycled into new proteins, and some iron from heme groups is reused for new heme groups. The spleen and liver convert heme remnants into bilirubin, which is processed by the liver.

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75
Q

How is bilirubin processed and excreted?

A

Bilirubin is carried by plasma albumin to the liver, metabolized, and incorporated into bile. Bile is secreted into the digestive tract, and bilirubin metabolites are excreted in feces. Some metabolites are filtered by the kidneys and contribute to the yellow color of urine.

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76
Q

What is jaundice, and what causes it?

A

Jaundice is a condition where elevated bilirubin levels cause yellowing of the skin and eyes. It can result from rapid breakdown of fetal hemoglobin in newborns or liver disease preventing bilirubin processing.

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77
Q

Why are newborns particularly susceptible to bilirubin toxicity?

A

Newborns are susceptible because their fetal hemoglobin is being broken down and replaced with adult hemoglobin, leading to elevated bilirubin levels.

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78
Q

What is anemia, and what are common symptoms?

A

Anemia is a condition where hemoglobin content is too low, leading to insufficient oxygen transport. Symptoms include tiredness and weakness, especially during exercise.

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79
Q

What are hemolytic anemias, and what causes them?

A

Hemolytic anemias occur when red blood cell destruction exceeds production. They are often hereditary, with fragile cells due to defective or deficient cytoskeletal proteins. They can also be acquired diseases.

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80
Q

What is hereditary spherocytosis?

A

Hereditary spherocytosis is a defect where the erythrocyte cytoskeleton does not link properly, making cells spherical instead of biconcave. These cells rupture easily and cannot withstand osmotic changes.

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81
Q

What is sickle cell disease, and what causes the sickle shape of red blood cells?

A

Sickle cell disease is a genetic defect where valine replaces glutamate in hemoglobin’s beta chain. This abnormal hemoglobin (HbS) crystallizes upon oxygen release, causing cells to sickle and block blood flow, leading to tissue damage and pain from hypoxia.

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82
Q

How is sickle cell disease treated?

A

One treatment involves hydroxyurea, which inhibits DNA synthesis and induces production of fetal hemoglobin (HbF), preventing HbS crystallization and sickling. Research is also exploring bone marrow transplants and gene therapy as potential cures.

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83
Q

What causes iron-deficiency anemia, and what are its characteristics?

A

Iron-deficiency anemia occurs when iron loss exceeds intake, slowing hemoglobin synthesis. It results in low red blood cell count or low hemoglobin content, causing smaller (microcytic) and paler (hypochromic) red blood cells.

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84
Q

Why are women who menstruate more likely to suffer from iron-deficiency anemia?

A

Menstruating women are more likely to suffer from iron-deficiency anemia due to iron loss in menstrual blood.

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85
Q

What is polycythemia vera, and what are its effects?

A

Polycythemia vera is a stem cell dysfunction producing too many blood cells, causing high hematocrit levels (60-70%). This increases blood viscosity, making it more resistant to flow through the circulatory system.

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86
Q

What happens to hematocrit levels when an athlete overhydrates?

A

Overhydration temporarily decreases hematocrit due to increased plasma volume. Correcting the volume overload restores normal hematocrit levels.

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86
Q

What is relative polycythemia, and what causes it?

A

Relative polycythemia occurs when red blood cell count is normal, but hematocrit is elevated due to low plasma volume, such as in dehydration.

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87
Q

What are common causes of jaundice in newborns and adults?

A

In newborns, jaundice is caused by the breakdown of fetal hemoglobin and replacement with adult hemoglobin. In adults, it is commonly caused by liver disease preventing bilirubin processing and excretion.

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88
Q

What is the role of the spleen in red blood cell turnover?

A

The spleen filters and engulfs old and fragile red blood cells, breaking them down and recycling components like amino acids and iron.

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89
Q

How is bile related to bilirubin, and what is its function in the body?

A

Bile, produced in the liver, contains metabolized bilirubin. It is secreted into the digestive tract to aid in digestion and excretion of bilirubin metabolites through feces.

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90
Q

How can sickle cell disease impact blood flow and oxygen delivery?

A

Sickle-shaped cells can block blood flow in small vessels, causing hypoxia, tissue damage, and pain. This obstruction prevents adequate oxygen delivery to tissues.

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91
Q

What are the potential consequences of untreated iron-deficiency anemia?

A

Untreated iron-deficiency anemia can lead to severe fatigue, weakness, and compromised immune function due to inadequate oxygen transport to tissues.

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92
Q

What are the symptoms and treatment options for polycythemia vera?

A

Symptoms include increased blood viscosity and resistance to flow. Treatment may involve phlebotomy, medications to reduce blood cell production, and managing symptoms to prevent complications.

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93
Q

What diagnostic tests are used to identify anemia and other red blood cell disorders?

A

Diagnostic tests include complete blood counts (CBC), hematocrit measurements, and examining red blood cell morphology and hemoglobin content.

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94
Q

What happens to red blood cells in hypertonic and hypotonic media?

A

In hypertonic media, red blood cells shrink and develop a spiky surface. In hypotonic media, they swell and form a sphere without membrane disruption.

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95
Q

What does the morphology of red blood cells indicate?

A

The morphology of red blood cells can provide clues to the presence of diseases, such as spherocytosis (spherical shape), sickle cell anemia (sickle shape), and iron-deficiency anemia (microcytic and hypochromic cells).

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96
Q

How is hemoglobin structured, and what are its components?

A

Hemoglobin is a large, complex protein with four globular protein chains, each wrapped around an iron-containing heme group. It has several isoforms, including alpha, beta, gamma, and delta chains.

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97
Q

What are the dietary sources of iron, and how is iron absorbed?

A

Dietary sources of iron include red meat, beans, spinach, and iron-fortified bread. Iron is absorbed in the small intestine by active transport.

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98
Q

How is iron transported and stored in the body?

A

Iron is transported in the blood by the carrier protein transferrin. Excess iron is stored in the liver within a protein molecule called ferritin.

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99
Q

How does hydroxyurea treat sickle cell disease?

A

Hydroxyurea inhibits DNA synthesis and induces the production of fetal hemoglobin (HbF), which prevents HbS crystallization and red blood cell sickling.

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100
Q

What are some acquired causes of hemolytic anemia?

A

Acquired causes of hemolytic anemia include immune reactions, infections, drugs, and exposure to toxic chemicals. These factors can lead to increased destruction of red blood cells.

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101
Q

What is the role of albumin in bilirubin transport?

A

Albumin binds to bilirubin in the plasma and transports it to the liver for processing and excretion in bile.

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102
Q

What is mean corpuscular volume (MCV), and what does it indicate?

A

Mean corpuscular volume (MCV) is the size of red blood cells. It can be abnormally large or small in certain diseases, indicating the presence of conditions such as iron-deficiency anemia (microcytic cells).

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103
Q

How do macrophages in the spleen contribute to red blood cell turnover?

A

Macrophages in the spleen engulf old and fragile red blood cells, breaking them down and recycling their components such as amino acids and iron.

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104
Q

What is hyperbilirubinemia, and how does it manifest?

A

Hyperbilirubinemia is elevated bilirubin levels in the blood, causing jaundice, which results in yellowing of the skin and eyes.

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105
Q

How does bilirubin contribute to the color of urine and feces?

A

Bilirubin metabolites are filtered from the blood by the kidneys, contributing to the yellow color of urine. It is also incorporated into bile and excreted in feces, contributing to their color.

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106
Q

What is the role of scavenging macrophages in red blood cell turnover?

A

Scavenging macrophages in the spleen engulf and digest old red blood cells, recycling their components like amino acids and iron.

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107
Q

How are platelets produced, and what is their origin?

A

Platelets are cell fragments produced in the bone marrow from huge cells called megakaryocytes. Megakaryocytes develop their large size by undergoing DNA replication up to seven times without nuclear or cytoplasmic division, resulting in a polyploid cell with a lobed nucleus.

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108
Q

How do megakaryocytes contribute to platelet formation?

A

The outer edges of megakaryocytes extend through the endothelium into the lumen of marrow blood sinuses, where the cytoplasmic extensions fragment into disk-like platelets.

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109
Q

What are the characteristics and components of platelets?

A

Platelets are smaller than red blood cells, colorless, and lack a nucleus. Their cytoplasm contains mitochondria, smooth endoplasmic reticulum, and numerous membrane-bound vesicles called granules, which are filled with a variety of cytokines and growth factors.

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110
Q

How many types of granules are found in platelets, and what do they contain?

A

There are at least three different types of granules in platelets. One type of granule contains more than 280 different proteins, including VEGF (promotes angiogenesis) and matrix metalloproteinases (MMPs).

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111
Q

What is the lifespan of platelets, and what are their primary roles?

A

Platelets have a typical lifespan of about 10 days. They are best known for their role in helping stop blood loss but also act as immune cells and mediators of the inflammatory response.

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112
Q

How do platelets contribute to the immune system and inflammation?

A

Platelets help the immune system fight infectious diseases such as malaria and may contribute to the inflammatory process of atherosclerosis.

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113
Q

What is Platelet-Rich Plasma (PRP) therapy, and what is its intended benefit?

A

PRP therapy involves using the growth factors and cytokines inside platelet granules to promote healing of tendons and ligaments, which have minimal blood supply and heal slowly. The therapy gained popularity after Tiger Woods used it for knee surgery recovery.

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114
Q

Describe the size and color of platelets and their life span.

A

Platelets are smaller than red blood cells, colorless, and have a typical lifespan of about 10 days.

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115
Q

What types of proteins are found in the granules of platelets?

A

The granules in platelets contain more than 280 different proteins, including VEGF (which promotes angiogenesis) and matrix metalloproteinases (MMPs).

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116
Q

How do megakaryocytes become polyploid?

A

Megakaryocytes become polyploid by undergoing DNA replication up to seven times without nuclear or cytoplasmic division.

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117
Q

What role do platelets play in the inflammatory response?

A

Platelets act as immune cells and mediators of the inflammatory response, helping the immune system fight infections like malaria and contributing to the inflammatory process of atherosclerosis.

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118
Q

What is the role of megakaryocytes’ lobed nuclei?

A

The lobed nuclei result from megakaryocytes undergoing DNA replication up to seven times without nuclear or cytoplasmic division, creating a polyploid cell with multiple copies of its DNA.

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119
Q

Describe the cytoplasmic extensions of megakaryocytes.

A

The cytoplasmic extensions of megakaryocytes extend through the endothelium into marrow blood sinuses and fragment into disk-like platelets.

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120
Q

What is the theory behind PRP therapy for tendons and ligaments?

A

The theory behind PRP therapy is that growth factors and cytokines inside platelet granules will promote healing in tendons and ligaments, which have minimal blood supply and are notoriously slow to heal.

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121
Q

How do platelets contribute to the body’s response to infectious diseases?

A

Platelets help the immune system fight infectious diseases such as malaria, acting as immune cells and mediators of the inflammatory response.

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122
Q

Why is it challenging for the body to repair a damaged blood vessel while maintaining blood flow?

A

The body must plug holes in damaged blood vessels without blocking the vessel entirely, as cells downstream need oxygen and nutrients. The repair “patch” must also withstand blood pressure to avoid being blown out.

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123
Q

What are the first steps taken by the body to stop blood loss from a damaged vessel?

A

The body first decreases pressure in the vessel to create a secure mechanical seal in the form of a blood clot. Once the clot is in place and blood loss has stopped, the body’s repair mechanisms take over, dissolving the clot and clearing debris.

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124
Q

Define hemostasis and its importance.

A

Hemostasis (from haima, blood + stasis, stoppage) is the process of keeping blood within a damaged blood vessel. It is crucial to prevent excessive blood loss and maintain circulatory system integrity.

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125
Q

What is the opposite of hemostasis?

A

The opposite of hemostasis is hemorrhage (from -rrhagia, abnormal flow), which is the uncontrolled flow of blood from a damaged vessel.

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126
Q

What are the three major steps of hemostasis?

A

The three major steps of hemostasis are: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) coagulation, the formation of a clot that seals the hole until tissues are repaired.

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127
Q

Describe the first step of hemostasis.

A

The first step is immediate constriction of damaged vessels (vasoconstriction) to decrease blood flow and pressure within the vessel temporarily. This can be aided by applying pressure to a bleeding wound.

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128
Q

What causes vasoconstriction during hemostasis?

A

Vasoconstriction is caused by paracrine molecules released from the endothelium of the damaged vessel.

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129
Q

What happens during the second step of hemostasis?

A

The second step involves the mechanical blockage of the hole by a loose platelet plug. Platelet adhesion occurs, where platelets stick to exposed collagen, become activated, release cytokines, and aggregate to form a plug.

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130
Q

How do platelets become activated, and what role do they play in hemostasis?

A

Platelets become activated by adhering to exposed collagen in the damaged area. Activated platelets release cytokines that reinforce vasoconstriction and activate more platelets, forming a loose platelet plug.78

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131
Q

What is an example of a positive feedback loop in hemostasis?

A

Platelets activating more platelets is an example of a positive feedback loop.

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132
Q

Describe the third step of hemostasis.

A

The third step is the formation of a fibrin protein mesh that stabilizes the platelet plug to form a clot. This involves a series of enzymatic reactions known as the coagulation cascade.

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133
Q

What is the coagulation cascade, and what is its end product?

A

The coagulation cascade is a series of enzymatic reactions that result in the formation of fibrin, a protein that stabilizes the platelet plug to form a clot.

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134
Q

How do exposed collagen and tissue factor contribute to hemostasis?

A

Exposed collagen and tissue factor initiate the formation of a fibrin protein mesh by triggering the coagulation cascade.

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135
Q

What role does fibrin play in hemostasis?

A

Fibrin stabilizes the platelet plug to form a stable clot that seals the hole in the damaged vessel.

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136
Q

What happens as the damaged vessel repairs itself?

A

As the damaged vessel repairs itself, the clot retracts, and fibrin is slowly dissolved by the enzyme plasmin. Scavenger leukocytes ingest and destroy the debris.

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137
Q

What is the role of plasmin in hemostasis?

A

Plasmin slowly dissolves the fibrin in the clot, aiding in clot retraction and removal as the wound heals.

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138
Q

Why is it important to maintain the proper balance during hemostasis?

A

Proper balance is crucial because too little hemostasis can lead to excessive bleeding, while too much can create a thrombus, a blood clot that can block the vessel and stop blood flow.

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139
Q

What is a thrombus, and why is it dangerous?

A

A thrombus is a blood clot that adheres to the undamaged wall of a blood vessel. A large thrombus can block the vessel’s lumen, stopping blood flow, which can be dangerous.

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140
Q

What happens when a blood vessel wall is first damaged?

A

When a blood vessel wall is damaged, exposed collagen and chemicals from endothelial cells activate platelets. Normally, the endothelium separates collagenous matrix fibers from circulating blood, but damage exposes the collagen, causing platelets to adhere.

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141
Q

How do platelets adhere to collagen, and what helps them?

A

Platelets adhere to collagen with the help of integrins, which are membrane receptor proteins linked to the cytoskeleton. Binding activates platelets, causing them to release contents of their intracellular granules.

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142
Q

What substances do activated platelets release?

A

Activated platelets release serotonin (5-hydroxytryptamine), ADP, and platelet-activating factor (PAF). PAF sets up a positive feedback loop by activating more platelets and initiating pathways that convert platelet membrane phospholipids into thromboxane A2.

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143
Q

What are the roles of serotonin and thromboxane A2 in hemostasis?

A

Serotonin and thromboxane A2 are vasoconstrictors. They also contribute to platelet aggregation, along with ADP and PAF, leading to the formation of a growing platelet plug that seals the damaged vessel wall.

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144
Q

What prevents the platelet plug from spreading beyond the injury site?

A

Platelets do not adhere to normal endothelium. Intact vascular endothelial cells convert their membrane lipids into prostacyclin, an eicosanoid that blocks platelet adhesion and aggregation. Nitric oxide released by normal endothelium also inhibits platelet adhesion.

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145
Q

How does the combination of platelet attraction and repulsion create a localized response?

A

Platelet attraction to the injury site and repulsion from the normal vessel wall create a localized response that limits the platelet plug to the area of damage.

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146
Q

What is coagulation, and how does it convert a platelet plug into a clot?

A

Coagulation is the process by which fluid blood forms a gelatinous clot. It involves two pathways (intrinsic and extrinsic) that merge into one, leading to the creation of thrombin, which converts fibrinogen into insoluble fibrin polymers that stabilize the platelet plug.

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147
Q

Describe the intrinsic pathway of coagulation.

A

The intrinsic pathway, also known as the contact activation pathway, begins when damage to tissue exposes collagen. Collagen activates factor XII, starting the cascade. This pathway uses proteins already present in the plasma.

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148
Q

Describe the extrinsic pathway of coagulation.

A

The extrinsic pathway, also called the cell injury pathway or tissue factor pathway, starts when damaged tissues expose tissue factor (factor III). Tissue factor activates factor VII, initiating the extrinsic pathway.

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149
Q

What happens when the intrinsic and extrinsic pathways of coagulation converge?

A

The two pathways converge at the common pathway to create thrombin, the enzyme that converts fibrinogen into insoluble fibrin polymers. These fibrin fibers become part of the clot.

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150
Q

How was coagulation initially regarded, and what is the current understanding?

A

Coagulation was initially regarded as a simple cascade, with each enzyme converting an inactive precursor into an active enzyme. Current understanding shows that it is a complex network with interactions between intrinsic and extrinsic pathways, sustained by positive feedback loops

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151
Q

What is the final step of coagulation?

A

The final step of coagulation is the conversion of fibrinogen into fibrin, catalyzed by thrombin. Fibrin fibers weave through the platelet plug and trap red blood cells within their mesh, stabilizing the clot.

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152
Q

How is the clot stabilized?

A

Active factor XIII converts fibrin into a cross-linked polymer, stabilizing the clot.

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153
Q

What happens to the clot as the damaged vessel wall repairs itself?

A

As the damaged vessel wall repairs itself, the clot disintegrates when fibrin is broken into fragments by the enzyme plasmin.

154
Q

What is plasmin, and how is it formed?

A

Plasmin is an enzyme that breaks down fibrin. It is formed from its inactive precursor plasminogen, which is part of the clot. Thrombin and tissue plasminogen activator (tPA) convert plasminogen into plasmin.

155
Q

What is fibrinolysis?

A

Fibrinolysis is the process by which plasmin breaks down fibrin, leading to the disintegration of the clot.

156
Q

Why can the number of factors involved in coagulation be confusing?

A

The large number of factors involved in coagulation and the fact that a single factor may have many different names can be confusing. Factors are numbered according to the order of discovery, not the order in which they participate in the coagulation cascade.

157
Q

What role does thrombin play in coagulation and fibrinolysis?

A

Thrombin converts fibrinogen into fibrin during coagulation and works with tissue plasminogen activator (tPA) to convert plasminogen into plasmin during fibrinolysis.

158
Q

What are the roles of serotonin, ADP, and PAF in platelet plug formation?

A

Serotonin, ADP, and PAF released by activated platelets contribute to vasoconstriction and platelet aggregation, which help form the growing platelet plug that seals the damaged vessel wall.

159
Q

How do nitric oxide and prostacyclin released by intact endothelium affect platelets?

A

Nitric oxide and prostacyclin released by intact endothelium inhibit platelets from adhering to the normal vessel wall, preventing the platelet plug from spreading beyond the injury site.

160
Q

What mechanisms limit the extent of blood clotting within a vessel?

A

Two mechanisms limit blood clotting: (1) inhibition of platelet adhesion and (2) inhibition of the coagulation cascade and fibrin production. Factors such as prostacyclin and plasma in the blood vessel endothelium restrict the platelet plug to the area of damage.

161
Q

What role do anticoagulants play in the body, and how do they work?

A

Anticoagulants prevent coagulation by blocking one or more reactions in the coagulation cascade. The body produces heparin and antithrombin III, which block active factors IX, X, XI, and XII. Protein C inhibits clotting factors V and VIII.

162
Q

How have discoveries about coagulation and fibrinolysis influenced medical treatments?

A

Discoveries about coagulation and fibrinolysis have led to treatments for diseases like heart attacks. Fibrinolytic drugs such as streptokinase and tissue plasminogen activator (tPA) dissolve clots, while antiplatelet agents prevent further clot formation.

163
Q

How do antiplatelet agents work, and what is an example of one?

A

Antiplatelet agents prevent platelet adhesion to collagen and platelet plug formation. Acetylsalicylic acid (aspirin) inhibits COX enzymes, preventing the synthesis of thromboxane A2 and blocking platelet aggregation.

164
Q

Why might people at risk of developing blood clots take aspirin?

A

People at risk of developing blood clots may take aspirin to prevent clots from forming by blocking platelet aggregation. Aspirin does not make the blood less viscous but inhibits COX enzymes to prevent thromboxane A2 synthesis.

165
Q

What is the role of anticoagulant drugs like warfarin?

A

Warfarin, a coumarin anticoagulant, blocks the action of vitamin K, a cofactor in synthesizing clotting factors II (thrombin), VII, IX, and X. It is prescribed for people at risk of forming clots that could block critical vessels.

166
Q

How does EGTA function as an anticoagulant in blood samples?

A

EGTA removes free Ca2+ from plasma, an essential clotting factor. Without Ca2+, coagulation cannot occur. However, in the living body, plasma Ca2+ levels do not decrease to levels that interfere with coagulation.

167
Q

What is hemophilia, and what are its common symptoms?

A

Hemophilia is a group of diseases where a factor in the coagulation cascade is defective or lacking. Symptoms include easy bruising, spontaneous bleeding, and bleeding into joints and muscles. Severe cases may result in fatal brain bleeding.

168
Q

What is hemophilia A, and how common is it?

A

Hemophilia A is a deficiency in clotting factor VIII, the most common form of hemophilia, occurring in about 80% of all cases. It is a recessive sex-linked trait usually affecting males.

169
Q

What is the role of calcium in the coagulation process?

A

Calcium is an essential clotting factor required for the coagulation process. In its absence, as in the presence of EGTA in blood samples, coagulation cannot occur.

170
Q

What is the clinical significance of aspirin in heart attack treatment?

A

Aspirin is given routinely as emergency treatment for suspected heart attacks because it prevents platelet plug formation by inhibiting COX enzymes, thereby reducing the risk of further clotting.

171
Q

How do heparin and antithrombin III work together?

A

Heparin and antithrombin III work together to block active factors IX, X, XI, and XII, thereby preventing coagulation.

172
Q

What is the importance of protein C in coagulation inhibition?

A

Protein C is an anticoagulant that inhibits clotting factors V and VIII, playing a crucial role in preventing excessive clot formation.

173
Q

What effect do endothelial cells have on coagulation?

A

Endothelial cells release chemicals known as anticoagulants, such as heparin and antithrombin III, which block reactions in the coagulation cascade, preventing excessive clotting.

174
Q

What is psychoneuroimmunology?

A

Psychoneuroimmunology is the study of the interaction between the immune system, the nervous system, and the endocrine system.

175
Q

How do commensal bacteria in the gut play a role in metabolism?

A

Commensal bacteria permitted by the immune system to live inside the gut play an important role in metabolism by aiding digestion and contributing to immune function.

176
Q

How does inflammation relate to the immune system and disease states?

A

Inflammation created by the immune system is a factor in many disease states, such as atherosclerosis, and is a response to infection or injury.

177
Q

How can the brain affect the immune system?

A

The brain can assist or derail the immune system depending on our psychological state, influencing immune responses positively or negatively.

178
Q

What are the primary functions of the immune system?

A

The immune system’s primary functions are to protect the body from damage by distinguishing self from nonself, including pathogens and defective cells.

179
Q

What are the body’s first lines of defense against external pathogens?

A

Physical, chemical, and mechanical barriers, such as skin, tears, mucus, and stomach acid, are the body’s first lines of defense against external pathogens.

180
Q

What are the four basic steps of the internal immune response?

A

The four steps are: 1) detection and identification of the pathogen, 2) communication with other immune cells, 3) recruitment and coordination of the response, and 4) destruction or suppression of the pathogen.

181
Q

What are immunogens and antigens?

A

Immunogens are substances that trigger the body’s immune response. Antigens are immunogens that react with products of the immune response.

182
Q

What is the difference between the innate and adaptive immune responses?

A

Innate immunity is the body’s immediate, non-specific response present from birth. Adaptive immunity is a specific response that takes days to weeks to develop and includes memory cells for faster responses upon reexposure.

183
Q

What are the key features of innate immunity?

A

Innate immunity is present from birth, responds immediately to pathogens, and is not specific to any one pathogen. It includes inflammation and phagocytosis by leukocytes.

184
Q

What is the role of phagocytes in the innate immune response?

A

Phagocytes identify pathogens, ingest them via phagocytosis, and digest them. Some phagocytes display bits of digested pathogens on their surface to attract cells involved in the adaptive immune response.

185
Q

What are antigen-presenting cells (APCs)?

A

APCs are cells that display bits of digested pathogen on their surface to attract and activate cells involved in the adaptive immune response.

186
Q

What characterizes adaptive immunity?

A

Adaptive immunity is specific to particular invaders, involves memory cells for faster response upon reexposure, and includes cell-mediated and antibody-mediated immunity.

187
Q

What is cell-mediated immunity?

A

Cell-mediated immunity requires contact-dependent signaling between an immune cell and receptors on its target cell.

188
Q

What is antibody-mediated (humoral) immunity?

A

Antibody-mediated immunity uses antibodies secreted by immune cells to bind to and disable foreign substances or make them more visible to immune cells.

189
Q

How do the innate and adaptive immune responses interact?

A

The innate response is rapid and non-specific, while the adaptive response is slower and specific. They are interconnected parts of a single process, with the adaptive response reinforcing and amplifying the innate response.

190
Q

Why can’t some pathogens be completely destroyed by the immune system?

A

Some pathogens, such as the tuberculosis bacterium, the malaria parasite, and herpes viruses, hide inside cells and can only be suppressed by the immune system rather than destroyed.

191
Q

What are the three major functions of the immune system?

A

The immune system: 1) recognizes and removes abnormal self cells, 2) removes dead or damaged cells, and 3) protects the body from disease-causing pathogens.

192
Q

What types of microorganisms act as pathogens?

A

Pathogens include bacteria, viruses, fungi, and one-celled protozoans. Larger pathogens include multicellular parasites.

193
Q

Why is the immune system considered the least anatomically identifiable system of the body?

A

The immune system is integrated into the tissues of other organs, such as the skin and gastrointestinal tract, making it less anatomically identifiable.

194
Q

What are the two anatomical components of the immune system?

A

The immune system’s two anatomical components are lymphoid tissues and the cells responsible for the immune response.

195
Q

Where is the immune system positioned in the body, and why?

A

The immune system is positioned where pathogens are most likely to enter the body, such as the mucous membranes of the oral cavity.

196
Q

What are the primary lymphoid tissues and their functions?

A

The primary lymphoid tissues are the thymus gland and the bone marrow, where cells involved in the immune response form and mature.

197
Q

What are the secondary lymphoid tissues, and how are they divided?

A

Secondary lymphoid tissues are sites where mature immune cells interact with pathogens and initiate a response. They are divided into encapsulated tissues (spleen and lymph nodes) and unencapsulated diffuse lymphoid tissues.

198
Q

What are the encapsulated lymphoid tissues, and what is their function?

A

Encapsulated lymphoid tissues, including the spleen and lymph nodes, have fibrous collagenous capsule walls and monitor the extracellular compartment for foreign invaders

199
Q

How do the spleen and lymph nodes contribute to immune function?

A

The spleen traps and removes aging red blood cells, while lymph nodes capture pathogens from the lymphatic circulation to prevent their spread.

200
Q

How does lymphatic circulation work, and what is its role in the immune system?

A

Blood pressure creates net fluid flow out of capillaries into the interstitial space. This fluid is picked up by lymph capillaries and passes through lymph nodes, where immune cells capture pathogens.

201
Q

What causes lymph nodes to become swollen during an infection?

A

Swollen lymph nodes result from active immune cells collecting in the nodes to fight infection.

202
Q

What are unencapsulated diffuse lymphoid tissues, and where are they found?

A

Unencapsulated diffuse lymphoid tissues are aggregations of immune cells found in the skin, tonsils, and mucosal surfaces exposed to the external environment.

203
Q

What is mucosa-associated lymphoid tissue (MALT)?

A

MALT includes immune cells associated with mucosal surfaces, such as the gut-associated lymphoid tissue (GALT) and lymphoid tissues in the respiratory, urinary, and reproductive tracts.

204
Q

Why is the GALT considered the body’s largest immune organ by some authorities?

A

Due to the large surface area of the digestive tract epithelium, the GALT is considered by some authorities to be the body’s largest immune organ.

205
Q

What are leukocytes, and what is their primary function?

A

Leukocytes, or white blood cells, are the primary cells responsible for immune responses and can function both within and outside the blood vessels.

206
Q

How numerous are leukocytes compared to red blood cells in the blood?

A

One microliter of whole blood contains about 5 million red blood cells but only about 7,000 leukocytes.

207
Q

How do leukocytes function extravascularly?

A

Leukocytes leave the capillaries to function outside the vessels, with some living in tissues for months and others for only hours or days.

208
Q

What are the six basic types of leukocytes?

A

The six basic types of leukocytes are basophils (and mast cells), eosinophils, neutrophils, monocytes (and macrophages), dendritic cells, and lymphocytes (and plasma cells).

209
Q

Which leukocytes are typically not found in the blood?

A

Dendritic cells and mast cells are not usually found in the blood.

210
Q

How can leukocytes be distinguished from one another in stained tissue samples?

A

Leukocytes can be distinguished by the shape and size of their nucleus, the staining characteristics of the cytoplasm, cytoplasmic inclusions, and the regularity of the cell border.

211
Q

What are granulocytes, and which cells are included in this group?

A

Granulocytes are white blood cells with cytoplasmic granules. They include basophils, eosinophils, and neutrophils.

212
Q

How are the names of granulocytes determined?

A

The names of granulocytes are determined by the staining properties of their granules. Basophil granules stain dark blue, eosinophil granules stain dark pink, and neutrophil granules do not stain darkly.

213
Q

What is degranulation?

A

Degranulation is the process by which activated granulocytes release their granule contents by exocytosis

214
Q

What are phagocytes, and which cells are included in this group?

A

Phagocytes are leukocytes that ingest material from the extracellular fluid using large vesicles. They include neutrophils, macrophages, and dendritic cells.

215
Q

What are antigen-presenting cells (APCs), and which cells are included in this group?

A

APCs are cells that display bits of antigen on their surface to signal other immune cells. The primary APCs are macrophages and dendritic cells.

216
Q

Where are basophils and mast cells found, and what is their function?

A

Basophils are rare in circulation and found in blood smears by their large, dark blue granules. Mast cells are found in the connective tissue of skin, lungs, and the gastrointestinal tract. Both release chemicals that contribute to inflammation and the innate immune response.

217
Q

Where are eosinophils found, and what is their function?

A

Eosinophils are found in the digestive tract, lungs, urinary and genital epithelia, and skin. They defend against parasitic invaders and participate in allergic reactions by releasing toxic enzymes and oxidative substances.

218
Q

What are the characteristics and functions of neutrophils?

A

Neutrophils are phagocytic cells that ingest and kill 5-20 bacteria during their short life span of 1-2 days. They are the most abundant white blood cells and release cytokines, including fever-causing pyrogens and chemical mediators of inflammation.

219
Q

What are monocytes, and what do they differentiate into?

A

Monocytes are precursor cells of tissue macrophages. They are not very common in the blood and spend about eight hours in transit from the bone marrow to tissues, where they differentiate into macrophages.

220
Q

What are the functions of macrophages?

A

Macrophages are primary scavengers in tissues, ingesting up to 100 bacteria during their life span. They also remove larger particles, such as old red blood cells and dead neutrophils.

221
Q

What are some specialized macrophages, and where are they found?

A

Specialized macrophages include histiocytes (skin), Kupffer cells (liver), osteoclasts (bone), microglia (brain), and reticuloendothelial cells (spleen).

222
Q

What is the mononuclear phagocyte system?

A

The mononuclear phagocyte system refers to macrophages in tissues and their parent monocytes circulating in the blood.

223
Q

What are dendritic cells, and what is their function?

A

Dendritic cells are macrophage relatives with long, thin processes. They are found in the skin (Langerhans cells) and various organs. They link innate and adaptive immune responses by displaying bits of foreign antigen.

224
Q

What are lymphocytes, and what is their role in the immune system?

A

Lymphocytes and their derivative plasma cells mediate the specific adaptive immune response. They constitute 20-35% of all white blood cells and are primarily found in lymphoid tissues.

225
Q

Where do all white blood cells begin their development?

A

All white blood cells begin their development, or hematopoiesis, in the bone marrow under the influence of cytokines called colony-stimulating factors and interleukins.

226
Q

What are the two primary lymphocyte precursor cells, and where do they mature? What is the third category of lymphocytes, and where do they develop?

A

-T lymphocytes (T cells) migrate from the bone marrow to the thymus gland to mature, while B lymphocytes (B cells) remain in the bone marrow to mature.
-The third category of lymphocytes is Natural Killer (NK) cells, which are thought to develop in the bone marrow as well as in other tissues.

227
Q

What are antibodies also known as, and what is their role?

A

Antibodies are also known as immunoglobulins, which are globular proteins that participate in the adaptive immune response.

228
Q

What roles do T lymphocytes and NK cells play in the immune system?

A

T lymphocytes and NK cells play important roles in defense against intracellular pathogens, such as viruses.

229
Q

What are lymphocytes, and how do they differ on a microscopic and molecular level?

A

Lymphocytes are the primary effector cells for the antigen-specific responses of adaptive immunity. Microscopically, all lymphocytes look alike, but at the molecular level, they can be distinguished by their membrane receptors.

230
Q

What is a lymphocyte clone, and why is it important?

A

A lymphocyte clone is a group of lymphocytes that bind a particular antigen. It is important because the immune system keeps only a few cells of each clone on hand, which can quickly reproduce if a matching pathogen appears.

231
Q

What is self-tolerance, and when does it begin?

A

Self-tolerance is the lack of immune response by lymphocytes to the body’s own cells. It begins during embryonic development.

232
Q

How is the specificity of lymphocyte clones determined?

A

The specificity of lymphocyte clones resides in the proteins that become cell surface receptors or antibodies, formed by rearranging the sequence of amino acids in receptor proteins into millions of combinations during development.

233
Q

What happens to lymphocytes that develop with receptor proteins recognizing self-antigens?

A

Lymphocytes with receptor proteins that recognize self-antigens are targeted for destruction by apoptosis in a process called clonal deletion, preventing autoimmune responses.

234
Q

What is the hygiene hypothesis?

A

The hygiene hypothesis proposes that challenging the immune system early in life strengthens it, suggesting that a too-clean environment weakens the immune system, potentially leading to autoimmune and allergic diseases.

235
Q

What alternative hypothesis has been proposed regarding the increase in autoimmune and allergic diseases?

A

An alternative hypothesis suggests that it is not the lack of exposure to microbes but the lack of diversity in the human microbiome that contributes to a weakened immune system and the increase in autoimmune and allergic diseases.

236
Q

What roles do molecules play in the innate immune response?

A

Molecules in the innate immune response are involved in detection, identification, communication, recruitment, coordination, and attack on invaders through membrane receptors and signal molecules like cytokines and antibodies

237
Q

What are chemotaxins and opsonins?

A

Chemotaxins are signal molecules that attract leukocytes to infection sites, while opsonins are molecules that coat foreign particles to make them more visible for phagocytic leukocytes.

238
Q

How do cytokines function as pyrogens?

A

Some cytokines act as pyrogens by raising body temperature through altering the hypothalamic setpoint.

239
Q

What is the role of acute-phase proteins in the immune response?

A

Acute-phase proteins, produced mainly by the liver during the acute phase of an immune response, include opsonins, enzyme inhibitors, and C-reactive protein (CRP). They help coat pathogens, prevent tissue damage, and indicate inflammation or disease.

240
Q

What is C-reactive protein (CRP) and its significance in chronic diseases?

A

CRP is an acute-phase protein that acts as an opsonin. Elevated levels of CRP are associated with chronic inflammatory diseases like rheumatoid arthritis and increased risk of coronary heart disease.

241
Q

What is the role of histamine in the inflammatory response?

A

Histamine, found in mast cells and basophils, initiates the inflammatory response by dilating blood vessels and making capillaries leaky, allowing leukocytes and plasma proteins to enter the injury site, causing edema (swelling).

242
Q

What are complement proteins, and what is the complement cascade?

A

Complement proteins are a group of over 25 plasma and cell membrane proteins that, when activated, form a complement cascade similar to the blood coagulation cascade. The cascade involves opsonization, leukocyte attraction, mast cell degranulation, and formation of the membrane attack complex.

243
Q

What is the membrane attack complex, and how does it function?

A

The membrane attack complex is formed by lipid-soluble proteins that insert into the membranes of pathogens and virus-infected cells, creating giant pores that allow water and ions to enter, causing the cells to swell and lyse.

244
Q

What happens during the acute phase following an injury or pathogen invasion?

A

During the acute phase, the body increases the concentration of various plasma proteins, including acute-phase proteins, to aid in the immune response.

245
Q

How does histamine increase blood flow to an injury site?

A

Histamine increases blood flow to an injury site by dilating blood vessels and opening pores in capillaries, allowing plasma proteins and leukocytes to enter the interstitial space.

246
Q

How does the complement cascade help in fighting infections?

A

The complement cascade helps fight infections by acting as opsonins, attracting leukocytes, causing mast cell degranulation, and forming the membrane attack complex that lyses pathogen cells.

247
Q

What is the role of antigen presentation in adaptive immunity?

A

Antigen presentation is required for immune cells to recognize and respond to pathogens. It involves the presentation of pathogen antigens to immune cells by membrane proteins known as major histocompatibility complexes (MHC).

248
Q

What are the three groups of molecules that participate in antigen presentation?

A

The three groups of molecules are MHC (major histocompatibility complexes), B lymphocyte receptors, and T lymphocyte receptors.

249
Q

What are major histocompatibility complexes (MHC), and where are they found?

A

MHCs are membrane protein complexes encoded by specific genes. MHC class I molecules are found on every nucleated cell, while MHC class II molecules are found primarily on antigen-presenting cells (APCs), including macrophages and dendritic cells.

250
Q

How do MHC proteins function in antigen presentation?

A

MHC proteins combine with peptide fragments of antigens that have been digested within the cell. The MHC-antigen complex is inserted into the cell membrane so that the antigen is visible on the extracellular surface and can interact with T-cell immune receptors.

251
Q

What is the significance of MHC variability among individuals?

A

MHC proteins vary from person to person due to the huge number of potential MHC variants inherited from parents. This variability is why tissues cannot be transplanted without establishing compatibility and why MHCs play a role in rejecting foreign tissue.

252
Q

What are the antigen-recognition molecules of B and T lymphocytes?

A

B lymphocytes make antibodies that bind antigens and make them more visible to the immune system. T lymphocytes have antigen-specific membrane proteins known as T cell receptors that bind only to MHC-antigen complexes on antigen-presenting cells.

253
Q

What are antibodies, and what is their primary role?

A

Antibodies, also known as immunoglobulins, are proteins that bind to antigens. They help the immune system react to specific antigens but are not toxic themselves and cannot destroy antigens directly.

254
Q

Describe the structure of a basic antibody molecule.

A

A basic antibody molecule has four polypeptide chains linked into a Y shape. The arms contain antigen-binding sites, while the stem, or Fc region, determines the antibody class. Each arm, or Fab region, consists of one light chain and one heavy chain.

255
Q

What determines the specificity of an antibody?

A

The variability in the light and heavy chains of the antibody determines its specificity. Each B lymphocyte clone produces a unique antibody.

256
Q

What are the five general classes of antibodies (immunoglobulins)?

A

The five general classes are IgG, IgA, IgE, IgM, and IgD.

257
Q

What are the characteristics and functions of IgG antibodies?

A

IgGs make up 75% of plasma antibody in adults, some cross the placental membrane to give infants immunity, and some activate complement.

258
Q

What are the characteristics and functions of IgA antibodies?

A

IgAs are found in external secretions such as saliva, tears, mucus, and breast milk. They bind to pathogens and flag them for phagocytosis if they reach the internal environment.

259
Q

What are the characteristics and functions of IgE antibodies?

A

IgEs target parasites and are associated with allergic responses. When mast cell receptors bind with IgEs and antigen, mast cells degranulate and release chemical mediators like histamine.

260
Q

What are the characteristics and functions of IgM antibodies?

A

IgMs are associated with early immune responses to pathogens, strongly activate complement, and react to antigens on red blood cells. They are made up of five Y-shaped antibody molecules

261
Q

What are the characteristics and functions of IgD antibodies?

A

IgD antibodies appear as receptors on the surface of B lymphocytes and help activate B cells.

262
Q

What are the polymeric forms of immunoglobulins, and which classes have them?

A

IgM is made up of five Y-shaped antibody molecules, and IgA can have from one to four antibody molecules.

263
Q

What are common multicellular parasites that affect humans?

A

Common multicellular parasites include hookworms and tapeworms.

264
Q

What are two examples of pathogens that are introduced into the body by biting insects?

A

The malaria protozoan and the Zika virus are examples of pathogens introduced by biting insects.

265
Q

How do bacteria and viruses differ structurally?

A

Bacteria are cells with a cell membrane and usually a cell wall. Some have an additional protective capsule. Viruses are not cells; they consist of nucleic acid (DNA or RNA) enclosed in a protein coat called a capsid, and some have an envelope of phospholipid and protein from the host cell membrane.

266
Q

How do bacteria and viruses differ in terms of living conditions and reproduction?

A

Bacteria can survive and reproduce outside a host with the required nutrients, temperature, and pH. Viruses must use the intracellular machinery of a host cell to replicate.

267
Q

How do bacteria and viruses differ in susceptibility to drugs?

A

Most bacteria can be killed by antibiotics that destroy them or inhibit their growth. Viruses cannot be killed by antibiotics; they require antiviral drugs that target specific stages of viral replication.

268
Q

Describe the replication cycle of a virus.

A

The replication cycle of a virus begins when it invades the host cell. The virus’s nucleic acid takes over the host cell’s resources to make new virus particles. Some viruses kill the host cell, others replicate sporadically, and some incorporate their DNA into the host cell DNA.

269
Q

What are oncogenic viruses, and provide an example?

A

Oncogenic viruses are viruses that cause cancer. An example is the human immunodeficiency virus (HIV).

270
Q

How do some viruses incorporate their DNA into the host cell DNA?

A

Some viruses, like HIV and oncogenic viruses, incorporate their DNA into the host cell DNA, allowing them to persist and potentially cause long-term effects such as cancer.

271
Q

What are the two lines of defense in the human body?

A

The two lines of defense are physical and chemical barriers (such as skin) that keep pathogens out, and the internal immune response that takes over if barriers fail, beginning with the nonspecific innate responses followed by the adaptive response.

272
Q

: What are some examples of physical barriers in the body?

A

Physical barriers include the skin, protective mucous linings of the gastrointestinal and genitourinary tracts, and the ciliated epithelium of the respiratory tract.

273
Q

Why are the digestive and respiratory systems particularly vulnerable to microbial invasion?

A

They have extensive areas of thin epithelium in direct contact with the external environment.

274
Q

How does the female reproductive tract protect against pathogens?

A

The opening to the uterus is normally sealed by a plug of mucus that keeps bacteria in the vagina from ascending into the uterine cavity.

275
Q

What role do secretions and mechanical removal play in the body’s first line of defense?

A

Secretions from exocrine glands and mechanical removal of pathogens assist physical barriers. For example, mucus in the respiratory system traps inhaled particles, which are then expelled or swallowed.

276
Q

What is lysozyme, and where is it found?

A

Lysozyme is an enzyme with antibacterial activity found in respiratory tract secretions, saliva, and tears. It attacks cell wall components of unencapsulated bacteria.

277
Q

What happens when pathogens trigger the innate immune response?

A

The innate immune response either clears the infection or contains it until the adaptive immune response is active.

278
Q

What are pathogen-associated molecular patterns (PAMPs)?

A

PAMPs are classes of molecules unique to microorganisms that are recognized by leukocyte pattern recognition receptors (PRRs) to activate immune responses.

279
Q

What are chemotaxins?

A

Chemotaxins are chemical signals that attract leukocytes to areas of infection or injury.

280
Q

What are danger-associated molecular patterns (DAMPs)?

A

DAMPs are endogenous danger signals from tissue injury that indicate a location needing defense.

281
Q

What are the primary phagocytic cells in the innate immune response?

A

Tissue macrophages and neutrophils are the primary phagocytic cells responsible for initial defense.

282
Q

What is extravasation?

A

Extravasation is the process by which circulating leukocytes leave the blood by squeezing through pores in the capillary endothelium to reach an infection site.

283
Q

What is pus, and how is it formed?

A

Pus is a thick, whitish to greenish substance formed from a collection of living and dead neutrophils and macrophages, tissue fluid, cell debris, and other remnants of the immune process.

284
Q

What is phagocytosis, and which cells are primarily involved?

A

Phagocytosis is the engulfing and ingestion of targets by phagocytes, primarily neutrophils, macrophages, and dendritic cells.

285
Q

How do phagocytes recognize and ingest foreign particles?

A

Phagocyte receptors recognize various foreign particles, binding to pathogen-associated molecular patterns (PAMPs) on the pathogen surface, leading to engulfment and ingestion.

286
Q

What are phagosomes and how do they function?

A

Phagosomes are cytoplasmic vesicles containing ingested particles. They fuse with lysosomes, which contain enzymes and oxidizing agents that digest organic pathogens.

287
Q

How do certain bacteria evade recognition by phagocytes?

A

Some bacteria have evolved a polysaccharide capsule that masks their surface markers from the host immune system, making them harder to recognize by phagocytes.

288
Q

What are natural killer (NK) cells, and what is their role?

A

NK cells are a class of lymphocytes that participate in the innate response against viral infections by recognizing and inducing virus-infected cells to undergo apoptosis.

289
Q

How do NK cells target virus-infected cells?

A

NK cells target virus-infected cells by looking for cells with low concentrations of MHC class I proteins on their surface, as some viruses block MHC synthesis to avoid detection.

290
Q

What are the three important roles of inflammation in fighting infection?

A
  1. Attracting immune cells and chemical mediators to the site, 2. Producing a physical barrier to retard the spread of infection, 3. Promoting tissue repair once the infection is under control.
291
Q

What are the four classic signs of inflammation?

A

Redness (rubor), heat (calor), swelling (tumor), and pain (dolor).

292
Q

What causes the classic signs of inflammation?

A

Activated immune cells release cytokines that attract additional immune cells, increase capillary permeability, and cause fever.

293
Q

What are interferons, and what is their function?

A

Interferons are antiviral cytokines secreted by NK cells that promote the synthesis of antiviral proteins and interfere with viral replication.

294
Q

What is the role of antigen-presenting cells (APCs) in bridging innate and adaptive immunity?

A

APCs, such as macrophages and dendritic cells, digest pathogens and present antigen peptides on their surface with MHC class II proteins to activate lymphocytes for the adaptive response.

295
Q

How do adaptive immune responses differ from innate immune responses?

A

Adaptive immune responses are antigen-specific, recognizing and reacting to particular foreign substances. They overlap with innate immunity and enhance the inflammatory response.

296
Q

What is clonal expansion?

A

Clonal expansion is the process by which a specific clone of lymphocytes divides and creates additional cells in response to an antigen, ensuring sufficient cells to fight off the invader.

297
Q

What are the two types of cells formed during clonal expansion?

A

Effector cells, which carry out the immediate response and die within a few days, and memory cells, which are long-lived and continue reproducing themselves for a quicker secondary response.

298
Q

What are the three main types of lymphocytes?

A

B lymphocytes, T lymphocytes, and natural killer (NK) cells.

299
Q

What is the function of activated B lymphocytes?

A

Activated B lymphocytes develop into plasma cells that secrete antibodies.

300
Q

What is the function of activated T lymphocytes?

A

Activated T lymphocytes attack and destroy virus-infected cells and help regulate other immune cells.

301
Q

What is the function of NK cells in the immune response?

A

NK cells attack and destroy virus-infected cells as part of the innate immune response.

302
Q

What triggers the primary immune response in B lymphocytes?

A

The initial exposure of a naïve lymphocyte clone to its antigen, leading to antigen binding to B cell receptors and activation of the lymphocytes.

303
Q

What are plasma cells, and what is their role?

A

Plasma cells are differentiated effector B cells that synthesize and secrete antibody molecules to create humoral immunity.

304
Q

What is the difference between the primary and secondary immune responses?

A

The primary immune response is slower and lower in magnitude because the body has not encountered the antigen previously. The secondary immune response is quicker and larger due to the presence of memory B cells from the first exposure.

305
Q

What is the role of long-lived plasma cells (LLPC) in the immune response?

A

LLPCs remain in the bone marrow, secreting low levels of antibodies to provide continued immunity after the primary immune response.

306
Q

How does clonal expansion enhance the secondary immune response?

A

Memory B cells enhance clonal expansion during the secondary response, resulting in faster and higher antibody production.

307
Q

What is the role of cytokines in the inflammatory and adaptive immune responses?

A

Cytokines released during inflammation attract lymphocytes, which release additional cytokines to enhance the inflammatory response and regulate immune cells

308
Q

What is an antibody-antigen complex, and what does it facilitate?

A

An antibody-antigen complex is formed when an antibody binds to an antigen. It facilitates the recognition and destruction of antigens by the immune system.

309
Q

How do antibodies inactivate bacterial toxins?

A

Antibodies bind to and inactivate toxins produced by bacteria, preventing them from killing host cells.

310
Q

What is an example of natural immunity involving antibodies and bacterial toxins?

A

Natural immunity to diphtheria occurs when the host produces antibodies that disable the toxin produced by Corynebacterium diphtheria.

311
Q

What is the role of antibodies as opsonins?

A

Antibodies act as opsonins by tagging the immune complex for destruction, allowing phagocytes to recognize and engulf the tagged pathogens.

312
Q

How do antibodies trigger degranulation of immune cells?

A

The combination of antigen, antibody, and cell receptors triggers degranulation, releasing chemicals stored in mast cells, NK cells, and eosinophils.

313
Q

What is antibody-dependent cell-mediated cytotoxicity?

A

It is the process where NK cells degranulate and destroy antibody-tagged pathogens.

314
Q

How do antibodies activate complement proteins?

A

Antibodies activate complement proteins, which assist with the innate response, including mast cell degranulation.

315
Q

How do antibodies activate B lymphocytes?

A

Antigen binds to B cell receptors, activating B cells to differentiate into plasma cells and memory cells.

316
Q

What is passive immunity, and how can it be acquired?

A

-Passive immunity occurs when antibodies made by another organism are acquired. It can be through the transfer from mother to fetus or by injections containing antibodies.
-Travelers may receive injections of gamma globulin, providing passive immunity for about three months.

317
Q

What is active immunity, and how can it occur?

A

Active immunity occurs when the body produces its own antibodies after exposure to a pathogen, either naturally or artificially through vaccinations.

318
Q

How do vaccinations work to provide active immunity?

A

Vaccinations contain altered pathogens that trigger the creation of memory cells specific to the pathogen, allowing for a rapid secondary immune response upon future exposure.

319
Q

What is the role of cytotoxic T lymphocytes (T cells)?

A

Cytotoxic T cells defend against intracellular pathogens by attacking and destroying cells displaying MHC-I-antigen complexes.

320
Q

How do cytotoxic T cells kill their targets?

A

They release perforin and granzymes, inducing apoptosis, or activate Fas, a death receptor on the target cell.

321
Q

What is the role of helper T (TH) cells?

A

Helper T cells bind to immune cells displaying foreign antigen in MHC-II complexes and secrete cytokines to influence other immune cells.

322
Q

How does HIV affect helper T cells?

A

HIV infects and destroys helper T cells, compromising the host’s immune response.

323
Q

What is the function of regulatory T cells (Tregs)?

A

Regulatory T cells suppress excessive immune responses by binding to MHC-II complexes and preventing overactive immune reactions.

324
Q

What are the two pathways of the immune response and how do they work together?

A

The innate response starts first and is reinforced by the more specific adaptive response. These pathways are interconnected, requiring cooperation and communication to respond to different immune challenges.

325
Q

What role does the complement system play in bacterial invasion?

A

The complement system activates due to bacterial antigens, enhancing phagocytosis, promoting inflammation through histamine release, attracting leukocytes, and lysing unencapsulated bacteria by forming membrane attack complexes.

326
Q

How do phagocytes respond to bacterial invasion?

A

Macrophages ingest unencapsulated bacteria immediately, while encapsulated bacteria require opsonins to coat the capsule before phagocytes can recognize and ingest them.

327
Q

How does the adaptive immune response enhance the innate response during bacterial invasion?

A

Antibodies act as opsonins, neutralize bacterial toxins, and activate naïve B cells to produce more antibodies and memory B cells if the infection is new.

328
Q

What is the role of the coagulation cascade in bacterial invasion?

A

If blood vessels are damaged, platelets and coagulation proteins minimize damage, and growth factors and cytokines control repair after bacteria are removed.

329
Q

What are the initial responses to a viral infection?

A

The innate immune responses and antibodies attempt to control the virus during its extracellular phase, similar to bacterial infection.

330
Q

How do cytotoxic T lymphocytes and NK cells defend against intracellular viruses?

A

They recognize infected host cells and destroy them, preventing viral replication.

331
Q

How do antibodies play a role in the early stages of a viral infection?

A

Antibodies coat viral particles, making them targets for antigen-presenting cells, and prevent viruses from entering target cells.

332
Q

What happens when macrophages ingest viruses?

A

They insert viral antigen fragments into MHC-II molecules on their membranes, secrete cytokines to initiate inflammation, and produce interferon-a to prevent viral replication.

333
Q

How do helper T cells contribute to the immune response against viruses?

A

Helper T cells bind to viral antigens on macrophage MHC-II molecules, secrete cytokines to stimulate B lymphocytes and cytotoxic T cells, and help activate memory B cells.

334
Q

What triggers the activation of memory B lymphocytes during a viral infection?

A

A second exposure to the virus activates memory B cells, promoting plasma cell development and additional antibody production.

335
Q

How do cytotoxic T cells kill virus-infected host cells?

A

They use viral antigen-MHC-I complexes to recognize infected cells, secrete perforin to create pores in the host cell membrane, and deliver granzymes that induce apoptosis.

336
Q

How do NK cells recognize and kill virally infected cells?

A

NK cells recognize cells lacking MHC-I complexes, caused by some viruses withdrawing these receptors, and kill them similarly to cytotoxic T cells.

337
Q

What is an allergy, and what triggers an allergic response?

A

An allergy is an inflammatory immune response to a nonpathogenic antigen called an allergen. Allergens can be any exogenous molecule, and the immune response is inappropriate as if the allergen were a more threatening pathogen.

338
Q

What are the two types of hypersensitivity reactions, and how do they differ?

A

Immediate hypersensitivity reactions are mediated by antibodies and occur within minutes of exposure to allergens. Delayed hypersensitivity reactions are mediated by helper T cells and macrophages and may take several days to develop.

339
Q

What happens during the sensitization phase of an immediate hypersensitivity reaction to an allergen like pollen?

A

The allergen is ingested and processed by an antigen-presenting cell, which activates a helper T cell. The helper T cell then activates B lymphocytes that produce IgE antibodies, which bind to mast cells.

340
Q

What occurs upon reexposure to an allergen in an immediate hypersensitivity reaction?

A

The allergen binds to IgE on mast cells, triggering the release of histamine, cytokines, and other mediators that cause allergic symptoms.

341
Q

What are the common symptoms of an allergic reaction caused by histamine release?

A

Symptoms include edema in the nasal passages leading to a stuffy nose, localized reactions near the site of allergen entry, and systemic reactions such as total body rashes.

342
Q

What is anaphylaxis, and how can it be treated?

A

Anaphylaxis is a severe IgE-mediated allergic reaction that causes widespread vasodilation, circulatory collapse, and bronchoconstriction. It can be treated promptly with injectable epinephrine to prevent death.

343
Q

How does the immune system respond to a viral infection initially?

A

The innate immune response and preexisting antibodies attempt to control the viral invasion during the early extracellular phase.

344
Q

How do cytotoxic T lymphocytes and NK cells respond to intracellular viruses?

A

Cytotoxic T cells recognize and destroy infected host cells displaying MHC-I-antigen complexes, while NK cells target cells lacking MHC-I complexes.

345
Q

What role do helper T cells play in the immune response to viruses?

A

Helper T cells bind to viral antigens on macrophage MHC-II molecules, secrete cytokines to stimulate B lymphocytes and cytotoxic T cells, and help activate memory B cells.

346
Q

What is the process of clonal expansion in adaptive immunity?

A

Clonal expansion occurs when naïve lymphocytes are exposed to an antigen, causing them to divide and create additional effector and memory cells for a stronger and faster secondary immune response.

347
Q

How do antibodies enhance the immune response during a viral infection?

A

Antibodies act as opsonins, coat viral particles, prevent viruses from entering target cells, and neutralize viral particles in the extracellular fluid.

348
Q

What triggers the immune response in an allergic reaction to pollen?

A

Upon reexposure to pollen, the allergen binds to IgE on mast cells, triggering the release of histamine and other mediators that cause allergic symptoms.

349
Q

How do memory cells contribute to a faster and stronger immune response upon reexposure to an antigen?

A

Memory cells “remember” their prior exposure to the antigen and rapidly activate upon reexposure, producing more effector cells and antibodies for a quicker and larger immune response.

350
Q

How do allergens differ from pathogens in their effect on the immune system?

A

Allergens are nonpathogenic antigens that trigger an inappropriate immune response, whereas pathogens are disease-causing agents that the immune system targets to protect the body.

351
Q

What is the role of IgE antibodies in allergic reactions?

A

IgE antibodies bind to mast cells and, upon reexposure to the allergen, trigger the release of histamine and other mediators causing allergic symptoms.

352
Q

How does the body prevent widespread clotting from occurring during an immune response?

A

Endothelial cells release anticoagulants like heparin and antithrombin III, which block reactions in the coagulation cascade to prevent excessive clotting.

353
Q

What are MHC proteins, and why are they important in tissue transplantation?

A

MHC proteins, also known as human leukocyte antigens (HLA), are primary tissue antigens that determine whether donated tissue is recognized as foreign by the recipient’s immune system. Compatibility of MHC proteins between donor and recipient increases the likelihood of successful tissue transplantation.

354
Q

What are the two types of rejection that can occur in tissue transplantation?

A

The two types of rejection are graft versus host, where donor tissue attacks the recipient’s body, and host versus graft, where the recipient’s immune system attacks the donated tissue.

355
Q

What types of immune cells are primarily responsible for the acute rejection of solid tissue grafts?

A

T cells are primarily responsible for the acute rejection of solid tissue grafts. Incompatible matches trigger antibody production and activate cytotoxic T cells and T helper cells.

356
Q

Why do red blood cells (RBCs) lack MHC protein markers, and what antigens are important for blood transfusions?

A

RBCs lack MHC protein markers found on nucleated cells. The important antigens for blood transfusions are the ABO blood group antigens and the Rh antigens.

357
Q

How are the ABO blood groups determined?

A

The ABO blood groups are determined by combinations of two glycoprotein antigens (A and B) on the red blood cell membrane. Each person inherits two alleles (A, B, or O), resulting in four blood types: A, B, AB, and O.

358
Q

What antibodies are present in the plasma for each ABO blood type?

A

Type A: anti-B antibodies
Type B: anti-A antibodies
Type AB: no anti-A or anti-B antibodies
Type O: both anti-A and anti-B antibodies

359
Q

What occurs during a transfusion of incompatible blood, such as type O receiving type A blood?

A

The recipient’s anti-A antibodies bind to the transfused type A red blood cells, causing agglutination and activation of the complement system. This leads to hemolysis and the release of hemoglobin, which can cause acute renal failure.

360
Q

What are Rh blood groups, and why are they significant in maternal-fetal interactions?

A

Rh blood groups include at least 49 different antigens, with the D antigen being most significant. An Rh-negative mother with an Rh-positive fetus can produce anti-D antibodies that may attack the fetus’s red blood cells, causing hemolytic disease of the newborn (HDN).

361
Q

How does Rh D incompatibility occur, and what are the consequences for the fetus?

A

Rh D incompatibility occurs when an Rh-negative mother is exposed to Rh D antigen from an Rh-positive fetus, leading to the production of anti-D antibodies. These antibodies can cross the placenta and destroy fetal red blood cells, causing hemolytic disease of the newborn (HDN).

362
Q

How do ABO blood group antigens affect blood transfusions?

A

ABO blood group antigens determine compatibility in blood transfusions. Incompatible transfusions result in immune reactions, including agglutination and hemolysis, leading to potential renal failure.

363
Q

What are the implications of the presence of anti-A and anti-B antibodies in individuals with different ABO blood types?

A

The presence of anti-A and anti-B antibodies in individuals with different ABO blood types ensures that only compatible blood types are used for transfusions to prevent adverse immune reactions.

364
Q

What is the significance of the complement system in the context of incompatible blood transfusions?

A

The complement system is activated during incompatible blood transfusions, leading to the formation of membrane attack complexes that cause hemolysis of the transfused red blood cells and potential renal failure.

365
Q

How do treatments for Rh D incompatibility work to prevent hemolytic disease of the newborn (HDN)?

A

Treatments for Rh D incompatibility involve administering manufactured antibodies that bind to the Rh D antigen or the mother’s anti-D antibodies, thereby preventing the immune-mediated destruction of the fetus’s red blood cells.

366
Q

What are the roles of cytotoxic T cells and helper T cells in the rejection of solid tissue grafts?

A

Cytotoxic T cells directly attack and destroy the graft cells, while helper T cells assist in the immune response by activating other immune cells, contributing to the rejection of the graft.

367
Q

What is the relationship between MHC proteins and tissue transplantation success?

A

The success of tissue transplantation is higher when donor and recipient share similar MHC proteins, as it reduces the likelihood of the recipient’s immune system recognizing the tissue as foreign and rejecting it.

368
Q

How do ABO and Rh blood group antigens differ in their impact on blood transfusions and maternal-fetal interactions?

A

ABO blood group antigens impact compatibility in blood transfusions, while Rh blood group antigens, particularly the D antigen, play a significant role in maternal-fetal interactions, with Rh incompatibility leading to hemolytic disease of the newborn (HDN).

369
Q

How does the absence of MHC protein markers on red blood cells (RBCs) influence immune responses to blood transfusions?

A

The absence of MHC protein markers on RBCs means that immune responses to blood transfusions are primarily based on ABO and Rh blood group antigens, rather than the more complex MHC markers found on nucleated cells

370
Q

What is the role of the complement system in blood transfusion reactions, and how does it contribute to the severity of these reactions?

A

The complement system is activated during blood transfusion reactions, leading to the formation of membrane attack complexes that cause hemolysis of the transfused cells, contributing to the severity of the reactions, including potential renal failure.

371
Q

What are the three categories of immune system pathologies?

A

The three categories are: incorrect responses (autoimmune diseases), overactive responses (allergies and hypersensitivity), and lack of response (immunodeficiency diseases).

372
Q

What occurs during an incorrect immune response?

A

An incorrect immune response happens when mechanisms for distinguishing self from nonself fail, leading to the immune system attacking the body’s normal cells, resulting in autoimmune diseases.

373
Q

What are overactive immune responses, and what conditions do they cause?

A

Overactive immune responses occur when the immune system creates a response out of proportion to the threat posed by an antigen, leading to allergies and hypersensitivity reactions, which can be life-threatening in extreme cases.

374
Q

What are immunodeficiency diseases? What are examples of acquired immunodeficiencies?

A

-Immunodeficiency diseases arise when some component of the immune system fails to work properly. They include primary immunodeficiencies (genetically inherited) and acquired immunodeficiencies (resulting from infections or therapies).
-Examples include acquired immunodeficiency syndrome (AIDS) caused by the human immunodeficiency virus (HIV) and immunodeficiencies arising as a side effect of drug or radiation therapies used to treat cancer.

375
Q

How do autoimmune diseases result from self-tolerance failure? What triggers autoimmune diseases, and what is one example?

A

-When self-tolerance fails, the body makes antibodies against its own components through T cell-activated B lymphocytes, leading to autoimmune diseases specific to particular organs or tissue types.
-Autoimmune diseases often begin in association with an infection, potentially triggered by foreign antigens similar to human antigens. One example is type 1 diabetes mellitus, where islet cell antibodies destroy pancreatic beta cells.

376
Q

What is Graves’ disease, and how does it involve autoimmunity?

A

Graves’ disease is an autoimmune condition where the body makes thyroid-stimulating immunoglobulins that mimic thyroid-stimulating hormone, causing the thyroid gland to oversecrete hormone.

377
Q

What is the immune surveillance hypothesis?

A

The immune surveillance hypothesis proposes that the immune system detects and destroys abnormal cells, such as cancer cells, before they can spread.

378
Q

What is neuroimmunomodulation?

A

Neuroimmunomodulation, or psychoimmunology, is the study of brain-immune interactions, examining how emotions and mental states can affect immune function.

379
Q

Describe the experiment involving mice, chemical suppressants, and camphor odor.

A

Mice conditioned with a chemical that suppressed lymphocyte activity and camphor odor showed suppressed immune cell activity when later exposed only to camphor odor, illustrating the mind-body link.

380
Q

What three systems share common signal molecules and receptors?

A

The immune, nervous, and endocrine systems share common signal molecules and receptors, such as hormones, neurotransmitters, and cytokines.

381
Q

How can hormones and neuropeptides alter immune function?

A

Increased cortisol levels due to stress decrease antibody production, lymphocyte proliferation, and NK cell activity. Substance P induces degranulation of mast cells, and sympathetic innervation of bone marrow increases antibody synthesis and cytotoxic T cell production

382
Q

How do cytokines from the immune system affect neuroendocrine function?

A

Cytokines like interleukin-1 can induce stress responses in the CNS, and immune cell-secreted ACTH can activate the cortisol pathway, showing the bidirectional communication between the systems.

383
Q

Summarize the model of interaction among the nervous, endocrine, and immune systems.

A

These systems are linked through bidirectional communication using cytokines, hormones, and neuropeptides, with autonomic neurons and CNS neuropeptides linking the brain to the immune system, and immune cells secreting hormones influencing both systems.

384
Q

How do acute and chronic stress differ in their impact on the body? How can laughter impact the immune system?

A

-Acute stress triggers the rapid fight-or-flight response, while chronic stress elevates adrenal cortisol levels, suppressing immune response.
-Studies suggest that laughter can enhance immune cell activity, supporting the old saying that laughter is the best medicine.