Card Set Information

2011-05-04 09:36:51

Show Answers:

  1. Characteristics of endocrine glands
    DuctlessSecrete hormones (chemical signals) into the blood. Target organs have SPECIFIC hormone receptors
  2. List the major endocrine glands.
    Hypothalamus, pituitary, adrenal gland, thyroid gland, parathyroid gland, pancreatic islets, etc
  3. Describe nonpolar hormones and give examples
    • Nonpolar hormones must be transported by carrier proteins in plasma, but can diffuse directly through the plasma membrane. Receptors for nonpolar hormones are located inside cells.
    • Examples include: steroids (cortisol, testosterone, estrogen, progresterone) produced by adrenal cortex/gonads and thyroid hormones produced by the thyroid gland.
  4. Describe polar hormones and give examples
    • Polar hormones dissolve in plasma, but cannot diffuse through the plasma membrane. Receptors for polar hormones are located in the plasma membrane of cells, and they act through second messengers.
    • Examples include epinephrine (adrenaline) produced by the adrenal medulla and polypeptides, proteins, and glycoproteins (most hormones) produced by the hypothalamus, pituitary, pancreas, and parathyroid.
  5. Describe the hypothalamic control of the anterior pituitary
    Hypothalamus secretes releasing hormones (RH) and inhibiting hormones (IH) to the hypothalamo-hypophyseal portal system. This controls anterior pituitary hormone secretion/inhibition.
  6. Describe 3 different RHs and their functions
    • Corticotropin-releasing hormone (CRH) stimulates ACTH (adrenal corticotrophic hormone)
    • Thyrotropin-releasing hormone (TRH) stimulates TSH (thyroid stimulating hormone) secretion
    • Gonadotropic-releasing hormone (GnRH) stimulates FSH (follicle stimulating hormone) and LH (luteinizing hormone)
  7. Describe the hypothalamic control of the posterior pituitary
    Neurosecretory neurons in the hypothalamus produce two different peptide hormones (ADH and Oxytocin) which then transported and stored in the posterior pituitary. They are released from the posterior pituitary when the neurons undergo an AP.
  8. ADH effects in detail
    (AKA Vasopressin) increases water retention by the kidneys, decreases urine volume (opposite of diuresis), constricts blood vessles
  9. Oxytocin effects in detail
    Uterine contraction during childbirth (labor) and milk letdown during breastfeeding
  10. Describe the structure of the pituitary (including embryological origins) and alternate names.
    • Hypophysis – extends from the inferior surface of the hypothalamus, linked to hypothalamus by infundibulum
    • Posterior lobe (neurohypophysis) is a downgrowth from the brain
    • Anterior lobe (adenohypophysis) is derived from oral epithelium
  11. What type of hormones (general) does the anterior pituitary secrete, and which cells secrete them?
    Different cell types secrete 6 peptide (polar) hormones
  12. List the hormones secreted by the anterior pituitary, their functions, and their releasing hormone (if applicable).
    • TSH (Thyroid stimulating hormone) – activates thyroid gland, increases thyroid hormones, increases size of thyroid gland, stimulated by TRH
    • ACTH (Adrenocorticotrophic hormone) – activates adrenal cortex to release cortisol, stimulated by CRH [usually in times of stress]
    • GH (Growth hormone) – stimulates growth, protein synthesis, fat breakdown, increases blood glucose levels [works at epiphysial plate]
    • Prolactin – breast development and milk production during pregnancy
    • LH (Lutenizing hormone)
    • FSH (Follicle stimulating hormone) – females: regulates ovaries (egg) and female sex hormones (estrogen and progesterone), males: regulates testes (sperm) and male sex hormones (testosterone), stimulated by GnRH
  13. What are the gonadotropins?
    LH and FSH
  14. How do the hypothalamus and pituitary regulate the hormone levels of the body (general)?
    • Hormone receptors are located in the hypothalamus and pituitary (in addition to target organs)
    • These receptors allow homeostasis of hormone levels (thereby hormone effects) through alteration of RH/IH concentration, sensitivity, etc
  15. Describe the pituitary-gonad axis’s negative feedback loop.
    • GnRH (hypothalamus) stimulates FSH and LH secretion (anterior pituitary)
    • FSH and LH stimulate sex steroid secretion (gonads)
    • Sex steroids act on hypothalamus (inhibit GnRH secretion) and anterior pituitary (inhibit sensitivity to GnRH)
    • Less stimulation of the gonads causes decreased secretion of sex steroids
  16. Describe the anatomy of the adrenal gland and basic function.
    • Located above each Kidney
    • Contains two distinct tissues; medulla (inner) and cortex (outer)
    • Releases hormones in response to stress
  17. Name the medullary hormone of the adrenal gland. What causes its secretion? Describe its function and characteristics.
    • Epinephrine (adrenaline) release is stimulated by pre-ganglionic sympathetic nerve fibers which innervate the adrenal medulla
    • It is sympathomimetic to norepinephrine (activates the same receptors in the same manner).
    • Increases the effects of the sympathetic system (fight/flight) and increases glucose levels in blood
  18. What is epinephrine’s method of action?
    • Polar hormone (cannot diffuse into cell) requires receptors in the membrane.
    • Binds to G-Protein-linked receptor in cell membrane
    • G-Protein sub-unit activates Adenalate Cyclase which produces the second messenger cAMP
    • cAMP activates various protein kinases which activate/deactivate various enzymes, producing varied effects between cells
  19. Name the corticosteroids. What causes their secretion? Describe their functions and characteristics.
    • Aldosterone and Cortisol (hydrocortisone) are secreted in response to stress (CRH and ACTH)
    • Aldosterone [mineralocorticoids] - increases K+ exretion and Na+ retention by kidneys (regulation of blood pressure/K+ homeostasis)
    • Cortisol [glucocorticoids] - elevates blood glucose, amino acids, and fatty acid levels. Also suppresses inflammation and the immune system
  20. What is Corticosteroid method of action?
    • Nonpolar hormone (can diffuse into cell)
    • Binds directly to protein receptors in cytoplasm or nucleus
    • Receptor binds to gene regulatory proteins in the nucleus, stimulates transcription of that gene (protein expression)
  21. Describe the negative feedback of glucocorticoids.
    • (cortisol) – CRH (hypothalamus) stimulates ACTH secretion (anterior pituitary)
    • ACTH stimulates cortisol secretion (adrenal cortex)
    • Cortisol inhibits CRH and ACTH secretion (hypothalamus and anterior pituitary)
  22. Describe the anatomy of the thyroid gland.
    • Located in the thyroid cartilage, and consisting mainly of thyroid follicles (“water balloons” that trap Iodine)
    • Follicular cells (surround the colloid) and colloid (fluid within the follicles)
  23. How is thyroid hormone synthesized?
    • Iodine accumulates in colloid (fluid) in follicles and combines with protein resulting in thyroglobulin
    • Thyroglobulin is converted to thyroid hormone in the follicular cells
  24. Describe the effects of thyroid hormone.
    • Thyroid hormone targets general body tissues and increases BMR and body heat production
    • It is required for the growth and maturation of the CNS
  25. What is thyroid hormone’s method of action?
    • (nonpolar) – transported by carrier protein in blood
    • Passes directly through cell membrane
    • Binds to nuclear receptor (in nucleus)
    • Stimulates expression of gene (protein production)
  26. Describe the negative feedback of the thyroid hormone.
    • TRH (hypothalamus) stimulates TSH secretion (anterior pituitary)
    • TSH stimulates thyroid hormone AND growth of thyroid
    • Thyroid hormone inhibits TSH secretion (anterior pituitary)
  27. Causes of goiter w/ descriptions.
    • Inadequate Iodine in diet leads to insufficient thyroid hormone (hypothyroidism), hypothalamic pituitary axis responds by increasing TSH secretion, stimulates excessive growth the of the thyroid
    • Grave’s disease (autoimmune disease) antibodies mimic effects of TSH, stimulate growth of the thyroid and overproduction of thyroid hormone (hyperthyroidism)
  28. Describe the anatomy of the parathyroid glands and their function (including hormone function).
    • 4 small organs located on the posterior surface of the thyroid cartilage.
    • Detect low Ca2+ levels, secrete parathyroid hormone (PTH)
    • PTH increases blood Ca2+ level by increasing osteoclast activity, inhibiting Ca2+ secretion by kidneys, and increasing Ca2+ uptake by intestines
  29. Describe the negative feedback of PTH.
    Parathyroid detects blood Ca2+, so there is no brain involvement. When Ca2+ levels reach the set point PTH is secreted in smaller amounts (parathyroid)
  30. Describe the anatomy and function of the pancreas.
    • Both endocrine (blood glucose levels) and exocrine (digestive) functions
    • Endocrine cells located in islets of Langerhans
    • Alpha cells – secrete glucagon
    • Beta cells – secrete insulin
  31. Describe insulin functions and effects.
    • Beta cells detect high blood glucose and secrete insulin
    • Insulin increases glucose uptake by muscle, liver, and fat
    • increases glucose transporters in plasma membrane (via exoctyosis), promotes removal of glucose from blood (facilitated diffusion), and lowers blood glucose levels
    • Promotes conversion of glucose into triglyceride storage in adipose tissue, conversion of glucose to glycogen in skeletal muscle and the liver.
  32. Describe insulin/glucagon regulation.
    • Blood glucose level is the major factor controlling insulin/glucagon secretion.
    • Maintenance of blood glucose at homeostatic levels via negative feedback (islets of Langerhans)
  33. Describe glucagon functions and effects.
    • Alpha cells detect low blood glucose and secrete glucagon
    • Increases blood glucose (promotes breakdown of glycogen to glucose, production of glucose from amino acids, promotes breakdown of fat/production of ketone bodies)
    • ketone bodies are a byproduct of fatty acid breakdown. Ketone bodies can be used for fuel by heart and brain when glucose is low, but can also lower pH, be secreted in urine, etc
  34. Describe Diabetes mellitus (general) and its symptoms.
    • Insulin deficiency or reduced insulin sensitivity.
    • Cells do not take up glucose which results in hyperglycemia (high blood glucose)
    • This can lead to dehydration from loss of excess water from urination, which can result in blood volume and pressure problems
    • Can lead to starvation when the body can’t use the glucose and glucose is lost in the urine, resulting in the breakdown of fats and formation of ketone bodies
  35. Describe Type 1 Diabetes
    • (juvenile onset) – degeneration of beta cells in pancreas (autoimmune disease)
    • No insulin made by body
    • Must receive insulin shots
  36. Describe Type 2 Diabetes
    • (adult onset) – cells resistant to the effects of insulin
    • Often associated with obesity
    • May be controlled by diet and exercise
  37. What separates muscle tissue from other tissue types and what are its functions?
    • Specifically designed to contract and generate mechanical force.
    • Functions include locomotion and external movements, internal movements (digestion, circulation, etc), and heat generation (side product)
  38. What are the three types of muscle and where can they be found?
    Skeletal (attached to skeleton), smooth (found in walls of hollow visceral organs), cardiac (heart)
  39. Skeletal muscle details (general)
    • Connected to skeleton via tendons
    • Bends the skeleton at joints
    • Arranged in antagonistic pairs (contraction of agonist causes stretching of antagonist)
  40. Describe myofibers.
    • Muscle cells/fibers – elongated, multinucleated cells arranged parallel to one another and grouped in fascicles (bundles) by CT.
    • Sarcolemma = cell membrane of a myofiber
  41. Describe the bands of skeletal muscle and what they comprise.
    • A band – (dark band) – runs the length of the thick filaments, includes thin overlap
    • H zone – (light area at the center of the A band) – thick filaments with no thin overlap
    • I band – (light band) – thin filaments with no thick overlap (across 2 sarcomeres)
    • Z disc – (thin dark lines at center of I band) – point of attachment for thin filaments, separates sarcomeres
  42. Describe myofibrils
    • Long bundles of myofilaments (actin [thin] and myosin [thick]) within muscle fibers.
    • Myofilaments arranged in sarcomeres.
  43. What is a sarcomere?
    Repeating units of myofilaments along myofibrils
  44. Describe a sarcomere.
    • Length of a sarcomere is from Z disc to Z disc
    • Thick filaments at the center, with thin filaments on both ends ( attached to the Z line)
    • ½ I band at either end (only thin myofilaments)
    • A band at midsection (thick and thin filaments)
    • H zone at center (only thick filaments, no thin overlap)
  45. What is a twitch?
    • The contraction and relaxation of a motor fiber in response to an action potential
    • An AP always elicits a twitch in a motor unit (no threshold)
  46. Describe summation of a twitch.
    • Arrival of a 2nd AP before a muscle fiber relaxes causes more cross bridges to form and more tension to be generated
    • When a muscle is stimulated multiple times in rapid succession the strength of contraction increases
  47. How can whole-muscle contraction strength be modified?
    The strength of a whole-muscle contraction can be modified by altering the number of motor units involved. (motor unit recruitment)
  48. Describe incomplete tetanus and complete tetanus and what happens in the body
    • Incomplete tetanus – muscle stimulation at high enough rate so that the muscle does not fully relax between contractions
    • Complete tetanus – muscle stimulation at high enough rate so that no muscle relaxation occurs (steady state of tension, maximum tension)
    • In the body complete tetanus is avoided by activating different motor units in rapid succession to generate a sustained contraction
  49. Isometric contraction vs isotonic contraction.
    • Isometric contraction – muscle does not shorten (force generated by the contraction is equal to or less than the load applied)
    • Isotonic contraction – muscle shortens (force generated by the contraction exceeds the load applied)
  50. Describe the sliding filament mechanism. What happens to the bands?
    • Thick filaments are stationary, thin filaments slide past the thick filaments and increase overlap (length of filaments do not change, sarcomere shortens)
    • A band is unchanged, I band shortens, H band shortens
  51. Describe the thick myofilament structure in the sarcomere.
    • Bundles of myosin proteins (intertwining tails and globular heads that project outward towards thin filaments)
    • Myosin heads (cross-bridges) contain actin binding sites and an ATPase
  52. Describe the thin myofilament structure in the sarcomere.
    • Two twisted strands of actin molecules
    • Actin – molecules in polymer chain, contains myosin binding site
    • Tropomyosin – wraps around actin, covers myosin binding sites on the actin filaments
    • Troponin – Ca2+ binding protein, holds tropomyosin in place until Ca2+ is present
  53. Describe crossbridge cycling.
    • The myosin head binds to actin (ATP required)
    • Power stroke – globular head bends toward center of sarcomere, thin filaments pulled inward
    • Cross bridge link broken, head “unbends” (ATP required to unbind crossbridge)
    • Myosin binds to next actin molecule on thin filament and repeats process
    • sarcomere shortens
  54. Describe the length tension relationship. What is optimal? What happens if shortened? Elongated?
    • Normal resting length (sarcomere length ~2.0 μm) generates the maximum amount of tension (maximum cross-bridges formed)
    • If muscle length increases (sarcomere length >2.2 μm) tension is reduced as overlap between thick and thin filaments decreases
    • If muscle length decreases (sarcomere length <2.0 μm) tension is reduces as thin filaments from opposite ends of the sarcomere collide
  55. Describe how a crossbridge is formed. (starting with AP)
    • APs induce the release of Ca2+ into the sarcoplasm
    • Ca2+ binds to troponin on the thin filament, causing a conformational change
    • Tropomyosin shift away from the myosin bind sites (conformational change)
    • Myosin can now bind to actin
  56. What is the sarcoplasmic reticulum? Describe its structure and functions.
    • Network of smooth endoplasmic reticulum around each myofibril (bundles of myofilaments)
    • At rest Ca2+ pumps (Ca2+ATPase) move Ca2+ from the sarcoplasm to the sarcoplasmic reticulum, keeping sarcoplasmic Ca2+ levels low
    • The Sarcoplasmic reticulum contains voltage-gated Ca2+ ion channels
    • Basic function of SR – to store Ca2+ during resting periods and release Ca2+ to stimulate contraction
  57. What are T-tubules? Describe their structure and functions.
    • Extensions of the sarcolemma that continue to the interior of the muscle fiber and extend around each myofibril. (appear as dimples on the surface of the sarcolemma)
    • Carries an AP into the muscle fiber, opening voltage-gated Ca2+ channels in SR
  58. Describe neural activation of muscle contraction (excitation only).
    • AP travels down SMN axon to axon terminal (NMJ) inducing the exocytosis of ACh
    • ACh binds to nicotinic AChR at the motor end plate and opens ion channels
    • Na+ diffuses into cell (via nicotinic AChR) and induces an AP in the sarcolemma of muscle fibers
  59. How do botox and curare affect the neural activation of muscle contraction?
    • Botox blocks the exocytosis of ACh at the SMN
    • Curare blocks the Nicotinic AChR on the motor end plate
  60. What is excitation-contraction coupling? Describe it.
    • The events that link muscle excitation (AP) to contraction (crossbridge cycling)
    • AP from NMJ propagates down the sarcolemma
    • Transverse tubules conduct AP into the cell’s interior
    • Voltage gated Ca2+ channels open in the sarcoplasmic reticulum
    • Ca2+ is released into the sarcoplasm
    • Ca2+ binds to troponin
    • Troponin moves tropomyosin away from myosin binding sites
    • Crossbridge cycling occurs (muscle contracts)
  61. What occurs during muscle relaxation?
    • NMJ stops firing, muscle APs stop, voltage-gated Ca2+ channels in SR close.
    • Ca2+ is pumped back in to the SR via active transport (ATP required)
    • Troponin releases Ca2+, tropomyosin re-covers myosin binding site of the actin molecules and cross-bridge cycling is halted
    • The cell elastically recoils to its resting length
  62. What muscle activities require energy? What are the available sources of energy to the muscle (in order of use)?
    • Muscle contraction (cross-bridge cycling), muscle relaxation (Ca2+ pump), and the SMN’s Na+/K+ ATPase
    • Muscles can use cytosolic ATP [small amount], phosphocreatine (creatine phosphate), aerobic respiration, or anaerobic respiration (fermentation).
  63. Describe how a muscle uses phosphocreatine for energy and describe its additional characteristics.
    • ATP in the muscle is limited, and used up after only a few contractions
    • Phosphocreatine is the muscle’s way of storing high-energy phosphate bonds, which it can use to quickly regenerate ATP from ADP
    • There is a limited storage of phosphocreatine in the cells
  64. Describe how a muscle uses aerobic respiration for energy and describe its additional characteristics + what type of exercise? Source of energy?
    • Aerobic respiration occurs in mitochondria, and requires O2 to form ATP
    • Fatty acids contain a large amount of energy, but require O2 for release.
    • Fatty acids are the primary nutrient source during light/moderate exercise
    • The body’s maximum O2 uptake (thereby delivery to muscles) determines a person’s maximum level of aerobic activity
  65. Describe how a muscle uses anaerobic respiration for energy and describe its additional characteristics + what type of exercise? Source of energy?
    • Anaerobic respiration is the result of glycolysis and lactate fermentation and does not require O2 to form ATP
    • It is a breakdown of glucose (which is stored as glycogen in muscle cells)
    • It generates ATP quickly (faster than aerobic respiration) but is less effective than aerobic respiration (only 2ATP/glucose)
    • It is used during intense exercise (when the O2 supply cannot keep up with demand)
    • Lactate (lactic acid) is produced resulting in muscle soreness and fatigue
  66. What are ketone bodies?
    Ketone bodies are a byproduct of fatty acid breakdown. Ketone bodies can be used for fuel by heart and brain when glucose is low, but can also lower pH, be secreted in urine, etc
  67. Describe passive force of a muscle.
    • Elastic elements connect myofilaments to sarcomere (resulting in recoil)
    • When muscles are stretched a tension is generated (regardless of muscle activity) due to this property.
  68. Describe active force of a muscle.
    Directly related to length of sarcomere (optimal range) and being activated.
  69. What is muscle fatigue?
    • The inability to maintain tension due to previous contractive activity
    • ATP stores are used up, glycogen is used up, ion concentrations are disrupted, and there are high lactic acid levels
  70. What is oxygen debt?
    • Increased O2 consumption (breathing) after excersize
    • Restores myoglobin and hemoglobin O2 content, metabolizes lacate
  71. What changes occur to skeletal muscle with regular sustained exercise?
    • An increase in the number and size of mitochondira
    • An increase in the number of blood capillaries supplying muscles (resulting in an increase of O2, nutrients, and more effective waste removal)
    • An increase in the amount of myoglobin in muscle tissue
    • An increase in the size of muscle fibers (results from weight training, not aerobic exercise) [size increase is a result of more myofibrils (actin/myosin) not a change in the number of myofibers
  72. Describe cardiac muscle characteristics
    • Branched, striated cells connected end to end (contain sarcomeres)
    • The basic mechanisms of contraction are similar to skeletal muscle
  73. How does cardiac muscle excitation differ from skeletal muscles?
    • Myocardial cells are linked end to end by intercalated disks which contain gap junctions
    • This enables APs to travel from one cell directly to the next, causing the myocardium to contract as a single unit
    • Specialized myocardial cells (pacemaker cells) generate spontaneous APs that cause the heart to contract a certain frequency (no NMJs)
    • Autonomic input does not cause contraction, but does influence rate/force of contraction
  74. Describe smooth muscle characteristics
    • Found in the walls of hollow visceral organs
    • Contains small tapered fibers
    • Lacks striations (contractile proteins not arranged within myofibrils)
    • Has poorly developed SR
  75. How are the contractile proteins of smooth muscle arranged? What properties does this provide?
    • Contractile proteins are arranged in a fish-net network with long, thin filaments attatched to the plasma membrane of dense bodies. (dense bodies ~ Z disks)
    • This allows the muscle to contract even when greatly stretched (bladder)
  76. Describe smooth muscle excitation-contraction coupling.
    • Depolarization of the sarcolemma opens V-gated Ca2+ channels
    • Ca2+ enters the cell from the extracellular fluid (NOT the SR)
  77. Difference between smooth muscle contractions and skeletal muscle contractions?
    • Smooth muscle generates slow, sustained contractions
    • Skeletal muscle generates fast, easily fatigued contractions
  78. What is ascites?
    • Accumulation of liquid in the peritoneal cavity (result of liver failure)
    • Lack of albumin from the liver causes a change in the blood’s tonicity and water diffuses out of blood, into peritoneal cavity
  79. What are the basic elements of the cardiovascular system and their basic functions?
    • Blood (transport medium) – consists of cells and fluid
    • Heart (pump) – drives the circulation of blood
    • Blood vessels – tubing that conducts blood to its destination
  80. What is the function of blood? Approximate volume in the body? Tonicity? pH?
    • Transport medium for gases, nutrients, wastes, hormones, ions, cells, etc
    • Volume of ~5L
    • Tonicity of ~300 mOsm (.3 Osm)
    • pH of ~7.35-7.45
  81. What elements compose blood (including % volume)?
    • Plasma (~55% of blood volume) – the fluid portion of blood
    • Formed elements (~45% of blood volume) – cells and fragments
  82. What is serum?
    Plasma fluid lacking clotting proteins (typical source of antibodies)
  83. What is a buffy coat?
    A layer of WBCs and platelets that appears after a centrifuge of blood.
  84. Describe plasma in detail (including any sub-units in plasma).
    • 90% water – dissolved materials (ions, gases, nutrients, etc) the fluid medium for transport of blood cells and plasma proteins
    • 7-9% proteins
    • albumin - maintains osmotic pressure of blood
    • α & β globulins – carrier proteins for lipids (amphipathic molecules)
    • gamma globulins – antibodies
    • other proteins – hormones, fibrinogen, etc
  85. What cells make up the formed elements?
    • Erythrocytes – red blood cells
    • Leukocytes – white blood cells
    • Thrombocytes – blood platelets
  86. Describe erythrocyte structure and function.
    • Thin, biconcave disc-shaped cells (7.5 μm diameter) that lack nuclei and mitochondria and contain many molecules of hemoglobin
    • Transport respiratory gases (mainly O2) on hemoglobin
  87. What is erythropoesis? Where does it occur? What stimulates it? How much per day?
    • Erythrocyte production occurs in myeloid tissue (bone marrow) and creates ~200 billion RBCs per day
    • Stimulated by Erythropoetin (a hormone) secreted by the kidneys in response to decreasing O2 concentration in blood
  88. What is the “life expectancy” of RBCs? Why? Where does their “demise” occur?
    • RBCs last only 120 days after release into the blood stream due to their lack of nuclei and mitochondria
    • Old cells are engulfed by phagocytic cells in the spleen, liver, and bone marrow
  89. Describe hemoglobin structure, its properties, and its related disorders.
    • A protein made of 4 heme subunits (quaternary structure), it contains iron and reversibly binds O2 and CO2
    • Hemoglobin changes color when bound to O2 (bound = bright red, unbound = dark maroon)
    • Cyanosis (light blue/grey lips and finger nails) is a result of inadequate O2 levels
    • Anemia is an inadequate RBC count in the blood (or amount of hemoglobin)
  90. Describe leukocyte functions, and list the leukocytes by category.
    • Immunity: defense against harmful foreign invaders or abnormal cells
    • Functions: destroy pathogens (bacteria, viruses, protozoans, and worms), destroy cancer cells, remove dead/injured cells (wound healing)
    • Granular: neutrophils, eosinophils, basophils
    • Agranular: lymphocytes, monocytes
  91. Leuokcyte descriptions and functions in detail.
    • Neutrophils: Show very little stain. Phagoctyes (devour pathogens and dead cells), are able to leave blood vessels and enter CT
    • Eosinophils: Show pink/orange under stain. Attacks parasites
    • Basophils: Show dark stains that obscure nucleus. Produce histamine, promoting allergic reactions
    • Lymphoctyes: part of the lymphatic system, functions in immune responses
    • Monocytes: Circulating phagocytes, differentiate into “wandering macrophages” in tissues outside of blood
  92. Describe platelet origins, details, and functions.
    • Platelets are cell fragments from megakaryocytes in bone marrow
    • Last 5-9 days in circulation
    • Important in forming clots to stop bleeding when blood vessels are damaged (platelets attach to collagen and form a platelet plug, fibrin is formed (from fibrinogen) to reinforce the clot)
  93. Describe blood typing (basic)
    • Cells have markers on their surfaces that identify them as part of your body, foreign markers act as antigens and evoke an immunological defense mechanism)
    • Erythrocytes have relatively few markers (ABO blood types and Rh factor (antigen))
  94. Describe the heart (very generally)
    A hollow, muscular organ located in the center of the thoracic cavity (mediastinum) which pumps constantly (at variable rates).
  95. Describe the two blood circuits (very generally) and their functions.
    • Pulmonary circuit: heart (right) -> lungs -> heart (left). Exchanges gas with the atmosphere (releases CO2, picks up O2)
    • Systemic circuit: heart (left) -> organs -> heart (right). Exchanges gas with body tissues (releases O2, picks up CO2)
  96. Describe the chambers of the heart and their basic functions.
    4 chambers: L/R atria receive blood from veins, L/R ventricles pump blood into arteries
  97. Describe the interventricular septum, its function, and differences between the two sides it creates
    • The interventricular septum divides the heart into 2 parallel pumps with different chemistries and different pressures
    • The right side pumps deoxygenated blood at low pressure (low resistance)
    • The left side pumps oxygenated blood at high pressure (high resistance)
    • The flow between sides remains equal (flow = pressure / resistance)
  98. Describe the two different types of valves found in the heart, their locations, names, functions and structures
    • Atrioventricular valves [right (tricuspid) and left (bicuspid / mitral)] allow blood to flow from the atrium to the ventricle ONLY (1 way valve). Chordae tendinae attached to papillary muscles prevents valves from everting during ventricular contraction.
    • Semilunar valves [pulmonary (left) and aortic (right)] are located at the openings of the arteries that leave the ventricles and prevent blackflow of blood during ventricular relaxations.
  99. Describe the flow of blood through the heart (in depth, separated by circuit).
    • Pulmonary circuit: Deoxygenated blood enters the right atrium from the vena cava -> right AV valve -> right ventricle -> pulmonary semilunar valve -> pulmonary trunk and arteries -> lungs -> pulmonary veins
    • Systemic circuit: Oxygenated blood enters left atrium through pulmonary veins -> left AV valve -> left ventricle -> aortic semilunar valve -> aorta -> tissues -> veins
  100. Describe the cardiac cycle and list its phases (no description).
    • The contraction (systole) and relaxation (diastole) of the heart’s ventricles (simultaneous)
    • 1. Isovolumetric contraction [systole]
    • 2. Ejection [systole]
    • 3. Isovolumetric relaxation [diastole]
    • 4. Rapid filling [diastole]
    • 5. Atrial contraction [diastole]
  101. Describe isovolumetric contraction.
    • [systole] beginning of ventricle contraction, no blood ejected
    • semilunar valves closed for the duration
    • when ventricle pressure rises above atrial pressure (~0 mmHg) AV valves shut
  102. Describe ejection in cardiac cycle.
    • [systole] blood flows out of ventricles into arteries
    • Pressure in ventricles exceeds pressure in arteries, semilunar valve opens
    • blood flows into arteries, causing ventricular pressure to fall
    • AV valve closed for the duration
    • pressure forces the semilunar valves open and blood is ejected from the ventricle
  103. Describe isovolumetric relaxation in cardiac cycle.
    • [diastole] beginning of ventricle relaxation, no blood ejected/filled
    • Pressure in ventricle drops below arterial pressure, semilunar valve closes (prevents backflow of blood)
    • No change in ventricular volume
    • AV valve closed for duration
  104. Describe rapid filling in cardiac cycle.
    • [diastole] blood flows out of atrium into ventricle
    • Pressure in ventricles falls below atrial pressure, AV valve opens
    • Blood flows from atrium into ventricles
    • Semilunar valve closed for duration
  105. Describe atrial contraction in cardiac cycle.
    • [diastole] – small atrial contraction before ventricle contraction
    • Small atrial contraction pushes final amount of blood into ventricles just prior to ventricle contraction (creates EDV)
  106. Approximate amount of time for diastole and systole in cardiac cycle
    • Diastole ~.5s
    • Systole ~.3s
  107. What is EDV?
    End diastolic volume – the amount of blood in the ventricles at the end of diastole (nearly full)
  108. What is ESV?
    End systolic volume – the amount of blood in the ventricles at the end of systole (nearly empty)
  109. What is SV?
    Stroke volume – the amount of blood ejected by the ventricles (EDV – ESV)
  110. Describe the sounds of the heart, and what causes them.
    • Lub (first sound) – closing of the AV valves at the start of systole
    • Dub (second sound) – closing of the semilunar valves at the start of diastole
  111. Describe the structures involved in cardiac excitation, their location, and their function.
    • Sinoatrial (SA) node (right atrium near superior vena cava) – pacemaker of the heart, site where APs are first generated
    • Atrioventricular (AV) node (bottom/middle right atrium to interventricular septum) – delays conduction to ventricles
    • Atriolventricular bundle (bundle of His) (interventricular septum, splits into two) – conducts signals through the interventricular septum
    • Purkinje fibers (middle apex of heart up sides of heart) – conducts signals up lateral walls of ventricle
  112. Describe the path of cardiac excitation
    • SA node cells undergo spontaneous pacemaker potentials which creates APs
    • APs conducted through the atrial network
    • Atrial fibers activated (atrial contraction)
    • APs excite AV node which delays AP (allows completion of atrial contraction)
    • APs of AV node travel down AV bundle to apex of heart
    • Signals conducted to Purkinje fibers throughout ventricle (ventricular contraction)
    • Contraction from Apex upward to accommodate “pumping” to ateries located at top of heart
  113. What are pacemaker cells? How do they generate APs?
    • Modified cardiac muscle cells that spontaneously produce pacemaker potentials
    • Pacemaker potentials are spontaneous depolarizations during diastole that lead to the APs for contraction. They begin again almost immediately after pacemaker cell repolarization.
  114. When does the myocardial AP occur? How does it differ from a neural AP? Describe it.
    • The myocardial AP is triggered when myocardial cells receive the AP originally generated by the SA node
    • Myocardial APs have a prolonged duration when compared to the neural “spike” AP, and have involvement of 3 V-gated ion channels rather than just 2.
    • Na VG channels are opened to begin AP, Na+ flows in causing depolarization
    • The 200-300msec plateu phase is caused by a slow Ca2+ influx which combats the slow K+ output from K+ leak channels
    • Repolarization occurs by the delayed opening of VG K+ channels (and closing of Ca2+)
    • The prolonged refractory period ensures a pumping action without the possibility of summation (allows relaxation)
  115. What is an ECG? What does it measure?
    Electrocardiogram – recording electrodes on extremities allow a recording of the electrical activity of the heart (not contraction)
  116. What are the various “waves” of an ECG? describe them.
    • P wave (initial hill) – depolarization in atria just before contraction
    • QRS complex (small valley, large spike, deeper valley) – depolarization of ventricles just before contraction (beginning of systole), also includes atrial repolarization (not shown on ECG)
    • T wave (final hill followed by nothing until next P wave) – repolarization of ventricles (beginning of diastole)
  117. What measurements can be taken with an ECG, how can they be used?
    Waveform shapes, time intervals, segments,etc can be used to diagnose cardiac pathologies
  118. Name various arrhythmias and give details about them
    • Bradycardia – abnormally slow heartbeat (<60bpm)
    • Tachycardia – abnormally fast heartbeat (>100bpm)
    • Flutter – extremely rapid, but coordinate heartbeat (200-300bpm)
    • Fibrillation – different cells product APs and contract and different times (uncoordinated pumping). Defibrillator shocks the heart, putting the entire myocardium into a refractory period (“resetting” the heart)
  119. What are blood vessels? Describe the different types in order of blood flow.
    • Tubes that conduct blood through the body
    • Elastic arteries -> muscular arteries -> arterioles -> capillaries -> venules -> veins
  120. What is blood pressure, and why is it produced? Describe its functions and characteristics as it flows through the body.
    • The force exerted on blood vessel walls by blood, produced by heart contractions.
    • Blood pressure is the major driving force for the flow of blood through the blood vessels.
    • Blood pressure decreases as blood moves farther from the heart
    • Blood pressure is a function of cardiac output and Total Peripheral Resistance
    • (Flow = Pressure/Resistance AKA Pressure = Flow x Resistance)
  121. What does systolic blood pressure measure?
    Pressure of blood in the arteries during ventricular systole
  122. What does diastolic blood pressure measure?
    Pressure of blood in the arteries during ventricular diastole
  123. What is pulse pressure?
    The difference between systolic and diastolic pressure
  124. What is Mean Arterial Pressure? How is it calculated? Why is it important?
    • (MAP) is the average blood pressure throughout the cardiac cycle
    • It is not a simple mean, because systole and diastole have different lengths (.3msec vs. .5msec)
    • This measurement is the most functionally relevant to blood movement in the body
  125. How is blood pressure measured using BP Cuff and stethoscope? Describe the process.
    • Place cuff, pump pressure to ~160 mmHg (higher than BP)
    • Gradually release pressure until you hear the first sound [first Kortkoff sound] caused by ventricular systole forcing a small amount of blood under the cuff
    • Continue to release, there will be continued sounds during ventricular systole
    • Release until no sounds occur [final Korotkoff sound] caused by cuff pressure being equal to ventricular diastole pressure
  126. What is essential hypertension? What risks come with it? What therapeutic methods can help it? What medicines (and what do the medicines do)?
    • BP greater than 140/90 without known cause
    • Increased risk of atherosclerosis, heart attack, and stroke
    • Stop smoking, lose weight, lower salt intake
    • Diuretics (decrease blood volume), α-blockers and β-blockers (adrenergic receptor blockers), Ca2+ blockers (prevent Ca2+ channels in blood vessel smooth muscle from opening, prevent contraction), ACE inhibitors (prevent angiotensin I -> angiotensin II) and ARB (block angiotensin II binding sites)
  127. Describe elastic arteries in detail.
    • Large vessels receiving blood from the heart.
    • Rapid transport of blood (large radius, high pressure)
    • Pressure reservoirs (walls expand upon systole, recoil during diastole)
    • Maintain blood flow during ventricular diastole
  128. Describe arterioles in detail.
    • Small arteries
    • Provide greatest resistance to blood flow (caused by friction to flow of blood from small radius)
  129. What is the relationship between resistance and radius? How is this used by the body?
    • Resistance is inversely proportional to a change in the radius^4
    • Radius is used to control blood flow to different organs by sympathetic control (no parasympathetic control) of the smooth muscle in the arteriole wall.
  130. What happens to blood pressure as it reaches the arterioles and capillaries? Why?
    • [P=FR] – Blood pressure falls dramatically
    • An increase in total cross-sectional area decreases the flow which makes up for the increase in resistance caused by the smaller radius
  131. Describe capillaries in detail.
    • Very thin vessels which have enormous quantities in the body
    • Walls consist of a single endothelial cell layer
    • Site of material exchange between blood and interstitial fluid
  132. Properties of capillaries that promote diffusion?
    • Short diffusion distance (thin capillary walls, narrow diameter)
    • High surface area (extensive branching – close to ALL cells)
    • Slow blood flow (increases time for exchange to occur)
  133. What is stroke volume? What is it dependant on (and how?)
    • (SV) amount of blood ejected by ventricles per beat
    • Depends on EDV [direct], contractility [direct], and TPR [indirect]
    • Frank-Starling Law
    • External influences (sympathoadrenal system increases contractility and heart rate)
  134. What does the Frank-Starling Law state?
    • Increased EDV causes increased contractility and increased SV
    • Volume in must equal volume out, amount of contraction is dependent on how “full” the chamber is (how stretched the sarcomeres are)
  135. What is the formula for cardiac output? Each part has what units? What effects each part (excite/inhibit)?
    • Cardiac output [volume/min] = heart rate [beats/min] x stroke volume [volume/beat]
    • [Cardiac rate] parasympathetic nerves (decrease), sympathetic nerves (increase)
    • [Stroke volume] TPR (decrease), EDV (increase), contraction strength (increase, contraction strength increased by stretch and sympathetic nerves)
  136. What is Total Peripheral resistance? What affects resistance?
    • Total blood flow resistance the left ventricle must overcome
    • Direct: Vessel length and blood viscosity
    • Indirect: radius^4 <- very powerful in changing resistance
  137. What is EDV dependant on? What is EDV important for?
    • Dependant on venous return
    • Important to stroke volume
  138. What are the influences on venous return? Why are they important?
    • Skeletal muscle pump – skeletal muscle moving blood through the veins, against gravity
    • Breathing pump – diaphragm moving blood through the veins, against gravity
    • One-way venous valves – prevent blood from flowing backward in veins
    • Without these measures blood pooling will occur in veins.
  139. Describe the baroreceptor reflex and its pathway.
    • (Short term blood pressure regulation)
    • The baroreceptor reflex regulates heart rate and blood pressure [negative feedback loop]
    • Baroreceptors detect blood pressure (located in the aortic arch and carotid sinuses)
    • Baroreceptors send signals to the reticular formation in the medulla
    • In response: the sympathetic system causes increased heart rate and blood pressure or the parasympathetic system causes decreased heart rate and blood pressure
  140. Describe orthostatic hypotension and its causes.
    • Feeling faint upon standing up as a result of the baroreceptor reflex latent period (a few seconds)
    • Caused by lowered blood pressure when standing after laying down (increased gravity requires increased contraction of the heart) which results in decreased blood flow to the brain
  141. Describe the effects of blood volume on blood pressure. Describe its regulation.
    • (Long term blood pressure regulation)
    • Increased blood volume causes increased stroke volume
    • Increased stroke volume causes increased cardiac output
    • Mean Arterial Pressure = cardiac output x total peripheral resistance
    • Therefore: increased blood volume causes increased MAP [BP]
    • Excretion of urine by the kidneys is the major way the body regulates blood volume (ADH, aldosterone)
  142. Describe capillary filtration and absorption in detail.
    • Filtration: movement of fluid and solutes from capillary to interstitial fluid (driven by hydrostatic pressure AKA BP)
    • Absorption: diffusion of fluid and solutes from interstitial fluid to capillary (driven by osmotic pressure)
    • Proteins do not leave the capillaries (think albumin) and create the osmotic pressure that drives reabsorption of fluid.
  143. What is lymphatic drainage?
    The volume of fluid that is filtered out by capillaries but not reabsorbed (~4L/day) which needs to be returned to blood.
  144. Describe the lymphatic system and give its characteristics.
    • Lymph capillaries take up interstitial fluid (lymph)
    • One way flow (unlike circular blood flow)
    • Cells, bacteria, and debri are also taken up (these may be too large for blood capillaries)
    • Lymph flows through lymph nodes (immune defense cleans/filters the lymph)
    • Clean lymph flows back into bloodstream at the subclavian veins
    • The lymph system prevents edema
  145. What is edema? What can cause it? What is the severe case of edema called? What causes it?
    • Excessive fluid accumulation caused by failure of lymph drainage (eg. Removal of lymph nodes)
    • Elephantiasis is caused by parasites that block lymph flow
  146. What are the two major steps of the kidneys producing urine?
    • Filtration of blood by glomeruli (180L/day)
    • Reabsorption of useful solutes (99% of water reabsorbed, ~1.5 L excreted in urine/day)
  147. How is kidney reabsorption regulated by hormones (basic)? How does this affect BP?
    • ADH from posterior pituitary increased water reabsorption
    • Aldosterone from adrenal cortex increases reabsorption of Na+, Cl-, water / increases K+ excretion
    • Increased absorption of water increases blood volume, raising BP.
  148. How is blood volume related to blood pressure?
    Increased blood volume results in increased blood pressure
  149. Describe ADH’s role in the regulation of blood volume.
    • Secreted by posterior pituitary in response to increased blood osmolarity (low blood volume and/or increased solute concentration) (eg dehydration or salt ingestion)
    • Increases water retention by the kidneys (increases blood volume)
    • Acts by “telling” cells in the kidney to insert additional aquaporins (for water retention)
  150. Describe Aldoesterone’s role in the regulation of blood volume.
    • Secreted by adrenal cortex in response to low blood pressure and low blood flow to kidneys
    • Increases reabsorption of both salt (and water) by the kidneys (prevents reduction of blood volume even if salt levels are low)
    • Low NaCl -> Low OsM -> increased urine -> decreased blood volume -> decreased blood pressure [it prevents this from happening]
  151. How do the kidney’s stimulate aldosterone secretion? Describe the process.
    • Through the renin –angiotensin-aldosterone system
    • 1 – Kidney cells detect low blood pressure
    • 2 – cells in the juxtaglomerular apparatus of kidney tubules secrete renin (an enzyme) into the blood
    • 3 – Renin converts angiotensinogen (already in the blood) to angiotensin I
    • 4 – ACE (angiotensin converting enzyme) converts angiotensin I into angiotensin II as it circulates in the blood
    • 5 – angiotensin II stimulates aldosterone secretion and vasoconstriction of arterioles
  152. Describe the regulation of blood flow to the heart and skeletal muscles (intrinsic and extrinsic)
    • Intrinsic control: increased blood flow to areas with an increased metabolism (eg skel muscle). Blood vessels dilate, and hyperemia (localized increase in blood flow) occurs
    • Extrinsic control: sympathetic activation and adrenaline (increase in HR and SV). Parasympathetic activation (decrease in HR and SV).
  153. What are the short-term cardiovascular changes that occur with exercise?
    • Blood flow increases dramatically to the heart and skeletal muscles, yielding an increased cardiac output [due increased heart rate, stroke volume, sympathetic input, and Frank-Starling law]
    • Intrinsic metabolic vasodilation in skeletal muscles and heart (increased blood delivery to muscles, active hyperemia)
    • Sympathetic nerve-induced vasoconstriction in the viscera and skin
  154. What changes occur to blood flow (% of total and L/min) during excersize? How does total cardiac output change?
    • % changes: GI – decreased, heart – equal, kidneys – decreased, bone – decreased, brain – decreased, skin – decreased, skeletal muscle – dramatic increase
    • L/min: GI – equal, heart – increased, kidneys – decreased, bone – decreased, brain – equal, skin – decreased, skeletal muscle – dramatically increased
    • Total cardiac output from 5L/min resting to 25L/min active
  155. How does cutaneous blood flow vary with temperature?
    • Vasodilation in response to high body temperature
    • vasoconstriction in response to low body temperature
    • Sympathetic control of vascular smooth muscle [no parasympathetic], hypothalamic control of autonomic nervous system
  156. Describe the blood flow to the brain, and how it is maintained.
    • Autoregulation maintains constant blood FLOW to the brain (F = P/R)
    • Brain needs constant flow due to enclosure in skull (can’t expand)
    • increased blood pressure (increased flow) causes vasoconstriction (decreased flow)
    • Decreased blood pressure (decreased flow) causes vasodilation (increased flow)
    • Active hyperemia causes increased blood flow to brain regions with increased activity (eg. Visual stimulation will direct flow to occipital lobe) (seen with fMRI and PET scans)