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Published byAnnis Fleming Modified over 7 years ago
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Veins returning blood Veins have large radii and low resistance. Walls are thin, not elastic Most blood volume is in veins
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Veins Valves prevent engorgement and backflow
Sympathetic NS constricts veins to increase venous return Skeletal muscles also help return
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Baroreceptor reflex Baroreceptors detect fluctuations in blood pressure and send info to medulla Signals go to ANS Baroreceptors
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Response to low pressure
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Problems with vessels Hemorrhage Why do aneurysms form?
Hypertension, inflammation, arteriosclerosis, genetics… Aneurysm
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Blood pressure problems
Hypertension – Blood pressure over 140/90 Baroreceptors can adjust to higher BP High BP puts stresses on vessels, elasticity (atherosclerosis, strokes) and stresses on heart (heart attacks), kidneys
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Blood pressure problems
Treatments for hypertension: Low salt diet, reduce stress, increase exercise ACE inhibitors (reduce blood volume) Alpha, beta blockers (reduce sympathetic effects) Calcium blockers (reduce cardiac contractions)
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Blood pressure problems
Circulatory shock – blood pressure drops too low to serve tissues. From weak heart, blood loss, dilation from allergic response Body compensates w/sympathetic signals, fluid shifts
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Components of blood Plasma
Blood cells: erythrocytes leukocytes (WBC), and platelets Hematocrit is the % of blood occupied by RBC. (RBC)
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What is plasma? Ions: mostly Na+ and Cl-.
Gasses, waste, nutrients, hormones Plasma proteins: Albumins establish an osmotic gradient, carry some hormones Globulins (alpha, beta, gamma) transport molecules, serve as antibodies Fibrinogen - blood clotting
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RBCs RBCs have no nuclei, ribosomes, or organelles
Packed with hemoglobin “Doughnut-like” shape
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Hemoglobin Heme - contains iron and binds with one molecule of O2
Globin - 4 protein chains Turns bright red when combined with oxygen CO2, CO, H+ can also bind
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RBCs replenished every second
Spleen removes old RBCs, RBCs last about 4 months RBCs are produced in bone marrow from pluripotent stem cells (2 M/sec)
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Kidney controls RBC production
Kidney is sensitive to anemia and releases erythropoietin
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Blood doping Banned in competitive sports:
Erythropoietin (EPO) can be synthesized and injected to enhance endurance An athlete’s own blood can be stored and reinjected to boost RBC’s Hematocrit can detect
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Causes of anemia? Anemia – O2 to tissues is low
Due to RBC, erythropoiesis, or hemoglobin “Pernicious anemia” – lack of B12 results in low RBC production Aplastic anemia – bone marrow production
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How the body repairs itself
Initial response: vascular spasm - reduces blood flow through the vessel platelet plug - Aggregation of platelets. Platelets attach to areas with exposed collagen These processes are stimulated by ADP
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Platelets Platelets are cell fragments that are functional for 10 days
Reduce blood loss (maintain hemostasis) Platelets and a RBC
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Positive feedback at injury site
Initial stimulus is exposed collagen Repair is contained to site of injury 3 Platelets ADP Inhibits platelet aggregation Inhibits platelet aggregation Prostacyclin and nitric oxide Prostacyclin and nitric oxide 2 4 5 Vessel wall Normal endothelium Plug Normal endothelium 1 Injury site
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How the body repairs itself
Stopping blood loss: Fibrinogen (plasma protein) is converted into fibrin (thread-like protein). This conversion is catalyzed by thrombin Fibrin threads trap RBCs, forming a clot
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How the body repairs itself
Stopping blood loss: Fibrinogen (plasma protein) is converted into fibrin (thread-like protein). This conversion is catalyzed by thrombin Fibrin threads trap RBCs, forming a clot Thrombin is formed from inactive prothrombin in plasma
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The clotting cascade...! Clotting cascade is a series of reactions activating enzymes in a series... final conversion is fibrinogen into fibrin
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Vessel damage Exposed collagen Cascade is initiated when a platelet plug is present or from exposed collagen. Platelet aggregation Hageman factor Activation of next thrombin PF3 Clotting cascade Activation of thrombin Formation of fibrin meshwork Damaged vessel is sealed
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Clots are temporary Fibroblasts form scar tissue for vessel repair.
The clot is dissolved slowly by the enzyme plasmin (breaks down fibrin). Plasmin is activated by the clotting cascade Phagocytic WBC remove the products of clot breakdown
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Ok, but what is pus? Well, pus comes from infected wounds and consists of phagocytes, dead tissue and bacteria.
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End of exam 3 material (estimated)
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White blood cells There are five kinds of WBCs
WBCs defend against pathogens, cancer and clean up debris
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Introduction to the WBCs
Granulocytes Eosinophils - attack parasitic worms Basophils - make and store histamine and heparin Neutrophils - phagocytes, 1st to respond to infection Monocytes - settle in tissue and become macrophages Lymphocytes - B and T cells of specific immune response Neutrophil Eosinophil Monocyte Lymphocyte Basophil
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Production of WBCs Produced from pluripotent stem cells in bone marrow
Lymphocytes made in lymph tissue during adulthood Two-thirds of the leukocytes in the blood are granulocytes, mainly neutrophils
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Immune system Body must resist disease in order to function
Defends against pathogens, identifies and destroys abnormal cells. The primary pathogens are bacteria and viruses.
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Nonspecific immunity vs. Adaptive immunity
Nonspecific responses work immediately - 1st line of defense. Neutrophils, macrophages, inflammation, MAC attack Adaptive immunity specifically targets certain pathogens to which the body has been exposed B and T lymphocytes, antibodies
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Nonspecific response: inflammation
Redness and warmth Blood flow due to vasodilation Swelling Increased capillary permeability Pain Nociceptors stimulated by fluid pressure inflamed knee
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Inflammation : the beginning
First response involves cells already in nearby tissue: macrophages and mast cells Macrophages ‘eat’ bacteria Triggered by infection, mast cells secrete histamine, causing vasodilation Fibrin walls off infection Guided by chemotaxins, neutrophils and monocytes go to the area Mast cells in tissue
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How do phagocytes know what to eat?
Bacteria get labeled for destruction by opsonins Opsonins are made from complement cascade, helper T cells, antibodies Bacteria acquire opsonins, getting labeled for macrophage to engulf it
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Phagocytes also send signals
They present antigens to helper T-cells to induce a specific response They ‘wear what they eat’
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plasma proteins (including opsonins and chemotaxins) histamine Phagocytes: stimulate histamine release, trigger clotting cascade, release pyrogen which causes fever, induce more WBC
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Review
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What do those plasma proteins do?
Some are clotting proteins..clotting cascade! Some are antibodies! (discussed later) Some are part of the complement system! (discussed now…)
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Nonspecific response : Complement system
Complement = cascade of plasma proteins Cascade activated by molecules on surface of bacteria or antibodies Complement proteins are opsonins, chemotaxins or form MAC attack MAC
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Complement has the potential to be very damaging to host tissues
Bacterial wall has holes from membrane attack complex Complement has the potential to be very damaging to host tissues
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Nonspecific response: What about viral infections?
Infected cells release interferon Cause neighboring cells to produce virus-fighting enzymes Attracts natural killer cells Host Interferon Nasty virus
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Adaptive immune response
Also fights viral and bacterial infections but uses B and T lymphocytes found in lymph Pathogens have particular antigens, which induce a specific response from B and T cells. Only cells with the antigen are attacked.
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B cell response B lymphocytes respond to bacteria and toxins
An antigen stimulates some specific B cells to become plasma cells and produce antibodies Contact with antigen can occur via macrophages
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B cell response How antibodies work Once labeled, bacteria killed by:
antigen bacteria Once labeled, bacteria killed by: MAC attack Phagocytosis Killer cells binding site for this specific antigen Labels cell to be killed
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Result of labeling
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