LEC 1 Exam.txt

  1. (SG1.1) Name the four chambers of the heart:
    • left and right atria, or receiving chambers
    • left and right ventricles, or major pumping chambers
  2. (SG1.2) Characteristics and functions of the Atria:
      • Left and right atria are thin-walled pumps, which take blood input from veins: pulmonary (oxygen-rich to the left) and vena cava’s and coronary sinus (oxygen-poor to the right)
      • 20% of this blood is "pumped" into the ventricles, while 80% flows due to gravity.
      • Walls (myocardia thickness) of Atria are thinner than either ventricle.
  3. (SG1.3) Characteristics and functions of the Ventricles:
      • All heart valves except the bicuspid, have three flaps.
      • Left and right ventricles are major (left) systemic and (right) pulmonary pumping chambers
      • Walls of the left ventricle being significantly thicker than the right because of the distance the left has to pump through.
      • The left ventricle receives blood through the mitral or bicuspid valve and outputs it to the aorta via the aortic semilunar valve.
      • Right ventricle receives blood through the tricuspid valve and outputs it to the pulmonary trunk via the pulmonary semilunar valve.
      • BP at Aorta: 100-120 mm Hg, and at Right Atrium: 0 mm Hg.
  4. (SG2.1) Morphology of RBC?
      • About 7.5 µm in diameter
      • Biconcave - very large surface area to volume
      • No nucleus, ribosomes or mitochondria
      • Males: 4.5-6.3 million RBC / mm³, Females: 4.2-5.5 million RBC / mm³
      • One-third of the cell volume is the red protein pigment: hemoglobin which is a protein.
      • Hemoglobin has a higher attraction to CO versus O2.
      • Hematocrit is the % of whole blood that is RBC: Males about 45%, Females about 42%.
      • Hematocrit would be high with diarrhea or vomiting, and low if you drank a lot of water.

      • Can fit through capillaries often smaller in diameter than 7.5 µm
      • Flexibility through stretchable fibers of protein spectrin
      • Circulating life: 105-120 days
      • Each RBC has 200-300 million molecules of hemoglobin and 95% of the dry weight of each cell
  5. (SG2.2) Physiology of RBC?
      • Each hemoglobin molecule is made up of 4 globin protein chains, each with a "red pigment" heme group with one iron atom.
      • Each of 4 iron atoms can combine with an oxygen molecule to form a reversible reactant oxyhemoglobin.
      • Each globin can form a reversible reactant with carbon dioxide to for carbaminohemoglobin.
      • RBCs contain enzyme carbonic anhydrase (CA), which is a catalyst to join carbon dioxide and water to form carbonic acid. This then dissociates to bicarbonate ions and hydrogen ions, which diffuse out of the RBC to be excreted or used to buffer the bloods pH.
  6. (SG2.3) Relate anemia to hemoglobin content
    Normal men have 14-16 g of hemoglobin per 100 ml of blood (this is because of the stimulating effect on erythropoiesis by testosterone, the primary adrogen: male sex characteristic), while women have 12-14 g. Anyone with less than 10g/100ml is diagnosed as having anemia.
  7. (SG3.1) Erythropoiesis?
      • All formed blood elements, including RBCs, which is what erythropoiesis is about, are generated from adult blood-forming stem cells known as hematopoietic stem cells, which are called hemocytoblasts.
      • Maturation from these nucleated cells begins in the red bone marrow.
      • The differentiated daughter cell created via mitosis for erythrocytes is the proerythroblast.
      • Development states progress until the cell no longer has a nucleus and is called a reticulocyte.
      • The complete process takes about 4 days.
      • RBC are created at a rate of 200 billion per day to replace worn out/damaged RBCs.
      • from kidneys stimulates erythropoiesis when there is a low partial pressure, i.e. you are acclimating to the mountains.
  8. (SG4.1) Characteristics of the outermost layer of the heart.
      • Be carefull! The outermost layer of the heart is the epicarium, a layer of simple squamous epithelial cells underlain by loose connestive tissue.
      • Fibrous Pericardium and parietal layer of the serous pericerdium are considered by Titi to be "coverings of the heart"
      • The parietal layer is attached to the diaphragm and to the major blood vessels exiting the top of the heart.
  9. (SG4.2) Layers of the Heart from outside to inside...
    • Fibrous Pericardium
    • Parietal layer of the serous pericardium
    • Pericardial space filled with 10-15 ml of pericardial or serous fluid
    • Epicardium or visceral layer of the serous pericardium
    • Fatty connective tissue with coronary vessels
    • Myocardium
    • Endocardium covering beamlike protrusions of the myocardium called trabeculae carneae
  10. (SG4.3) Characteristics of Fibrous pericardium
      • Tough
      • Loose fitting
      • Inelastic
      • Not attached to the heart, only to blood vessels exiting the heart and the diaphragm.
  11. (SG4.4) Function of the Serous pericardium
    Consisting of the Parietal layer, attached to the fibrous pericardium, and the Visceral layer or Epicardium and the very important lubricating fluid in between them, they provide an environment wherein the heart can easily move with no danger from friction.
  12. (SG4.5) Characteristics of the Endocardium
      • Delicate layer of endothelium - simple squamous cells.
      • Lines the heart and all of the blood vessels.
      • Covers muscular projections of myocardium called trabeculae carneae or "fleshy beams", which help to add force to the inward contraction of the heart wall.
      • Inward folds of endocardium make of the flaps or cusps of the heart valves.
  13. (SG5.1) Wall layers of blood vessels. Contrast with capillaries.
    Tunica Intima
    • Lining endothelial cells
    Tunica Media
    • Elastic fibers
    • Smooth muscle cells
    • Arteries thicker than veins
    • Missing in capillaries
    Tunica Externa (a.k.a. Tunica ADVENTITIA)
    • Collagen fibers
    • Arteries thicker than veins
    • Missing in capillaries
    Capillaries have only an endothelial cell lining surrounded by a basement membrane.
  14. (SG5.2) Name and describe the types of Capillaries
    • Continuous
      • Has "Pinocytic vesicles", which can transport substances rapidly.
      • Has many "fenestrations" or pores.
      • Many intercellular clefts (large gaps or openings), and an incomplete or missing basement membrane.
    • There are more than a billion capillaries in the body.
    • The concentrations of capillaries are greatest in this order:
      1. Lungs
      2. Kidneys
      3. Skin
  15. (SG6.1) Normal pattern of impulse conduction through the heart:
      1. Sinoatrial (SA) node - alone or with influence from sympathetic/parasympathetic
      2. Three internodal bundles, including an interatrial bundle to the left atrium
      3. Atrioventricular (AV) node - impulse SLOWS here to allow complete contraction of both atria
      4. AV bundle (bundle of His)
      5. Left and right AV bundle branches (septum)
      6. Subendocardial branches (Purkinje fibers) to lateral walls. Note: these start at the apex of the heart.
  16. (SG6.2) Four structures make up the core of the electrical conduction system of the heart:
      1. Sinoatrial (SA) node
      2. Atrioventricular (AV) node
      3. AV bundle (bundle of His)
      4. Subendocardial branches (Purkinje fibers)
      Less than 1% of all myocardial tissue is made up of the above four conductive tissues, which means that 99% of the myocardium is contractile tissue.
  17. (SG7.1) Blood Flow beginning with return of deoxygenated blood?
      1. Returns to Right Atrium via the superior and inferior Vena Cava, as well as the Coronary Sinus.
      2. The thin wall between the laft and righrt atrium is the fossa ovalis - open during fetal development.
      3. SVC: Arms, head and Upper Torso
      4. IVC: Legs, Abdomin and Pelvis
      5. Through AV Tricuspid Valve to Right Ventricle.
      6. Out the Pulmonary Semilunar Valve to the Pulmonary Trunk.
      7. To Lungs or Pulmonary Circuit.
      8. Returns to Left Atrium via the Left and Right Pulmonary veins.
      9. Through AV Mitral or Bicuspid Valve to Left Ventricle.
      10. Out the Aortic Semilunar Valve to the Ascending Aorta.
      11. To Body or Systemic Circuit.
  18. (SG7.2) What is Anastomosis?
    The junction formed by a vein or artery splitting into two or joining from two to one.
  19. (SG8.1) Numbers of blood types and their relevance to emergency situations.
      • In addition to Antigens A, B and Rh (or D), there are nearly two dozen additional blood antigens that vary from person to person.
      • Only the A, B and Rh antigens require a "match" in a time-critical transfusion situation. When transfusions are planned, more antigens are types for a match.
      • Agglutination is a clumpping of RBCs associated with transfusion issues. It is NOT Clotting.
      • Agglutination does progress to Hemolysis, or rupturing of the RBCs.
  20. (SG8.2) Define the ABO blood types and explain the "universal" donor and recipient label in terms of antigens and antibodies.
      • There are four blood groups from ABO: A, B, AB, and O.
      • A and B refer the named antigens (agglutinogens) on the RBCs: A has A antigens, B has B, AB has both, and O has neither.
      • If a person has antibodies in their plasma, they will not have the antibodies against their own antigens. For example, if a person has A antigens, they will have anti-B antibodies, and they will definitely not have anti-A antibodies.
      • The antigens on the donors RBCs and the antibodies in the recipient’s plasma are the critical factors for donation and they define the universal donor and recipient.
      • Since type O blood has neither A or B antigens on its RBCs, it can be given in an emergency to any ABO typed recipient. This is because whatever antibodies the recipient may have, there are no antigens in the donor blood to react with.
      • To understand the universal recipient, consider that the AB recipient cannot have any anti-A or anti-B antibodies, so blood from ANY donor cannot be attacked by the antibodies of the recipient since they have NONE.
  21. (SG8.3) How is the Rh antigen different from the AB antigens?
      • Not having the "Rh" specifically the D antigen on RBCs is pretty rare, about 1% for all 'races', except European.
      • Unlike A and B where for example, an A type will have anti-B antibodies, an Rh- type will not "normally" contain anti-Rh antibodies.
      • The only way that they get there is getting a transfusion with Rh+ blood or pregnancy with a Rh+ fetus and no prenatal treatment with RhoGAM.
      • Failing prenatal treatment and a subsequent pregnancy of another Rh+ fetus, it may develop erythroblastosis fetalis, a condition where the mother's anti-Rh antibodies enter the baby through the placenta and agglutinate the Rh+ RBCs.
  22. (SG9.1) Know the valves of the heart and their pathologies.
    The right pulmonary semilunar and tricuspid valves can suffer from the problems below, but it is probably a greater issue for the left heart valves.

    Stenosed Valves
    • Valves that are narrower than normal, slowing blood flow through the heart. This can be caused by calcific nodules as on the cusps of the mitral valve. It can also be caused by rheumatic fever which can cause stenosis or other deformities of the valves, chordae tendineae, and myocardia.
    Mitral Valve Prolapse
    • It has a genetic basis, but can result from rheumatic fever. The prolapse condition (generally less serious than a valve stenosis.) results in the flap extending back into the left atrium causing incompetence (leaking). Though 1 in 20 have the condition, in most cases, it is asymptomatic.
    Aortic Regurgitation
    • The leaking of ejected blood back into the left ventricle causes a volume overload on the left ventricle with subsequent hypertrophy and dilation. The left ventricle tries to overcome the increased load by increasing its contractions (Starling's Law), but this can lead to stress that ultimately results in a myocardial ischemia, i.e. decreased blood supply to the heart.
  23. (SG10.1) Nervous System Division Review:
    • Somatic - under your control
      • Somatic Sensory - afferent
      • Somatic Motor = efferent
      Autonomic - NOT under your control
      • Visceral Sensory - afferent
      • Sympathetic - efferent - "Fight or Flight"
      • Parasympathetic - efferent - "Rest and Repair"
  24. (SG10.2) Neurological factors that affect heart rate
    Ratio of sympathetic and parasympathetic nerve impulses (autonomic) conducted to the SA node.

    • sympathetic (fight/flight)
      1. Through: distal end of cardiac nerve
      2. Action: stimulatory
      3. Mode: release of norepinephrine
      Parasympathetic (rest/repair)
      1. Through: chiefly by vagus nerve
      2. Action: inhibitory
      3. Mode: release of acetylcholine
  25. (SG10.3) Describe anatomy of cardiac pressoreflexes
    Baroreceptors in the aortic arch and carotid sinuses send signals to the cardioregulatory centers of the medulla oblongata via the Vagus (cranial nerve X) and Nerve of Hering (branch of cranial nerve IX) respectively.

    A negative feedback loop there sends control impulses via ratio of sympathetic and parasympathetic action.

    These are "carotid sinus reflex" and "aortic reflex" feedback loops.
  26. (SG11.1) Name the 5 phases of a complete cardiac cycle
    • Titi’s "Chronological Order":
      1. Passive ventricular filling
      2. Atrial systole - NOT Included by Titi (~130 mm)
      3. Isovolumetric ventricular contraction
      4. Ejection: 120 mm Hg on left, and 25 mm Hg on right, SV = ~70 mm
      5. Isovolumetric ventricular relaxation
      6. reserve Volume = ESV = ~60 mm
  27. (SG12.1) Resting cardiac output in ml/min?
  28. (SG12.2) How do CO (cardiac output) and PR (peripheral resistance) affect arterial BP?
    Pressure increases in direct relationship with increases in volume, so as CO increases, volume will increase, and as PR (in the arterioles) increases, the amount of blood leaving the arteries is REDUCED, thus increasing the volume REMAINING inside, and increasing arterial BP.

    Blood Volume is also a factor that affects BP.
  29. (SG12.3) What is Cardiac Output and the factors that influence it?
    • Cardiac Output is the Stroke Volume (SV) times the Heart Rate (HR). Therefore, anything that affects either SV or HR can affect CO.
    • Factors affecting HR:
      • Longer myocardial fibers at the beginning of ventricular contract -> stronger contraction -> ↑SV -> ↑CO.
      • Stress and exercise can trigger both of the following:
        1. Sympathetic nerve released norepenephrin -> stronger contraction...
        2. Adrenal medulla released epinephrine into blood -> stronger contraction...
      • Factors that affect HR, and therefore CO, are the negative feedback loop from the Autonomic cardiac control via Carotid Sinus Reflex and Aortic Reflex.
      • Emotions, exercise, hormones, blood temperature, pain, nicotine, caffeine, drugs, electrolytes and stimulation of various exterocepters (skin sense of pain, temperature and bodily movement) can affect HR.
      • Anxiety, fear, anger -> ↑HR; Grief -> ↓HR
      • Exercise normally accelerates the HR, but the mechanism is not clearly understood.
      • Sudden intense stimulation of pain receptors in visceral structures such as gall bladder, ureters or intestines can slow the HR to such an extent that fainting may result.
    • Factors affecting SV:
      • Preload (from Starling)
      • Contractility
      • Afterload - Anything that increases Arterial BP, e.g. peripheral resistance
  30. (SG13.1) Define CO (cardiac output) in terms of volume/minute
    = SV (stroke volume)

        in (volume/beat)

    X HR (heart rate)

        in (beats/minute)

    This volume of blood is also known as the "systolic discharge".
  31. (SG14.1) What did Starling find and how does it relate to Starling's law of the heart?
    English physiologists Ernest Starling, expanding earlier work of Otto Frank (Frank-Starling), found that, within limits, i.e. normal conditions, the longer or more stretched myocardial fibers are at the beginning of a contraction, the stronger that contraction will be.

    What influences how stretched these muscle fibers get is directly related to how much venous blood is returned to the ventricles, or venous return. The effect is that under normal conditions, the heart will pump out the amount of blood that is returned to it.
  32. (SG14.2) What physiological factors affect the strength of a heartbeat besides Starling's law?
      • norepinephrine (NE) released by sympathetic fibers in the cardiac nerve
      • Epinephrine released into the blood by the adrenal medulla
      • Thyroxin
      • Digitalis
      ... can all increased the strength of contraction or contractility, of the heart
  33. (SG15.1) Factors that contribute to Venous Return to the heart
      • The reservoir function of the veins which occurs whenever BP drops and the elasticity of the veins adapts to maintain pressure and return flow to the heart.
      • Gravity can be a factor for a person sitting or standing still. They will have a tendency for blood to reservoir in the legs, which is called the orthostatis "standing upright" effect.
      • Venous Pumps are of two basic types:
      • Respirations cause a change in pressure gradient between the thoracic and abdominal cavities from the action of the diaphragm. "Increased respiration and increased circulation go hand in hand."
      • Skeletal muscle contractions serve as booster pumps for the heart, and like respiratory affect on venous pressure, rely on the one-way valves in veins that prevent backflow.
      • Total Blood Volume, or the more blood you have, the more that is returned. The quickest way to increase (or decrease) total volume is through water added to or taken out of the plasma.
  34. (SG16.1) Compare/contrast blood pressure with pulse pressure.
    Blood Pressure is measure by two numbers: the maximum hydraulic pressure exerted during a left ventricle systole, and the minimum pressure observed during diastole. Pulse Pressure is the difference between systole and diastole. Pulse pressure characteristically increases with arteriosclerosis, mainly because systolic pressure increases more than diastolic pressure.
  35. (SG17.1) Anatomy and Physiology of Lymphocytes?
      • 6-9 µm in diameter; spherical shape; round (single-lobed) nucleus; smallest lymphocytes have scant cytoplasm.
      • Agranulocyte
      • Humoral defense-secretes antibodies; involved in immune system response and regulation; T-lymphocytes directly attack an infected or cancerous cell; B-lymphocytes produce antibodies against specific antigens.
      • 20-25% of WBC; typ 25%; Days to years
      • Formation: 1) Hemocytoblasts, 2) Lymphoblast, 3) Lymphocyte
  36. (SG17.2) Anatomy and Physiology of Basophils?
      • 11-14 µm in diameter; spherical shape; generally two-lobed nucleus; large purple-staining cytoplasmic granules
      • Granulocyte
      • Secretes heparin (anticoagulant) and histamine (important in inflammatory response)
      • 0.5-1% of WBC; typ 1%; Hours to 3 Days
      • Formation: 1) Hemocytoblasts, 2) Myeloblast,... 6) Basophils
  37. (SG17.3) Anatomy and Physiology of Eosinophils?
      • 10-12 µm in diameter; spherical shape; generally two-lobed nucleus; large, orange-red-staining cytoplasmic granules.
      • Granulocyte
      • Cellular defense-phagocytosis of large pathogenic microorganisms, such as protozoa and parasitic worms; releases anti-inflammatory substances in allergic reactions.
      • 2-5% of WBC; typ 3%; 10-12 Days
      • Formation: 1) Hemocytoblasts, 2) Myeloblast,... 6) Eosinophils
  38. (SG17.4) Anatomy and Physiology of platelets?
      • 2-5 µm in diameter; irregularly shaped fragments; cytoplasm contains very small, pink-staining granules. Colorless per Titi.
      • Releases clot-activating i.e. hemostatsis substances and helps in formation of actual blood clot by forming platelet "plugs".
      • Together with WBCs, they make up the "buffy coat" seen in centrifuged blood.
      • 140,000-340,000 per cubic mm and less than 0.1% of the formed elements
      • 7-10 Days
      • Formation: 1) Hemocytoblasts, 2) Megakaryoblast, 3) Megakaryocyte,... 5) Platelets
  39. (SG17.5) Anatomy and Physiology of leukocytes?
      • White Blood Cells
      • Together with platelets, they make up the "buffy coat" seen in centrifuged blood.
      • All WBC = 5000-9000 per cubic mm or less than 0.1% of the formed elements.
      • Less than 5000 / mm³ is Leukopenia.
      • More than 9000 / mm³ is Leukocitosis.
      • As a group they are defensive with specialties including: phagocytosis, antibody formation, secretion of heparin (anticoagulant), and histamine (important in inflammatory response).
  40. (SG17.6) Anatomy and Physiology of agranulocytes?
      • WBC that lack large granules in their cytoplasm.
      • Lymphocytes and Monocytes
  41. (SG17.7) Anatomy and Physiology of megakaryocytes?
      • Third step in formation of Platelets.
      • Formation of platelets, a.k.a. thrombocytes, is referred to as thrombopoiesis. It begins with stimulation of precursor cells called Megakaryoblast, and is controlled by the hormone thrombopoietin.
      • Mature Megakaryocytes are huge cells (20 to100 µm) with large nuclei contain as many as 20 lobes.
      • Mature megakaryocytes are largely confined to red bone marrow though some are located in the lungs and, to a lesser extent, the spleen.
      • Between 2000 and more than 3000 platelets are released when the irregular cytoplasmic membrane surrounding the mature megakaryocyte ruptures.
      • The resulting platelets have a limiting plasma membrane but, like RBCs, no nucleus.
  42. (SG17.8) Anatomy and Physiology of monocytes?
      • 12-17 µm in diameter (largest of WBC); spherical shape; nucleus generally kidney-bean or horseshoe shaped with convoluted surface; ample cytoplasm often "steel blue" in color.
      • Agranulocyte
      • Capable of migrating out of the blood to enter tissue spaces as a macrophage-an aggressive phagocytic cell capable of ingesting bacteria, cellular debris, and cancerous cells.
      • 3-8% of WBC; typ 6%; Months
      • Formation: 1) Hemocytoblasts, 2) Monoblast, 3) Monocyte
  43. (SG17.9) Anatomy and Physiology of neutrophils?
      • 12-15 µm in diameter; spherical shape; multilobed nucleus; small, pink-purple-staining cytoplasmic granules.
      • Granulocyte
      • Cellular defense-phagocytosis of small pathogenic microorganisms.
      • ; typ 65%; Hours to 3 Days
      • Formation: 1) Hemocytoblasts, 2) Myeloblast,... 6) Neutrophils
  44. (SG17.10) Anatomy and Physiology of granulocytes?
      • WBC that contain large granules in their cytoplasm.
      • Basophils, Eosinophils, and Neutrophils
  45. (SG18.1) Characteristics of Anaphylactic shock?
      • Results from an acute allergic reaction called anaphylaxis. Anaphylaxis causes the same kind of blood vessel dilation characteristic of neurogenic shock.
      • "Experienced" nurses will have cortizone on hand... Connie says only in a treatment room with potent drugs - steroids (cortizone) AND antihistamines.
  46. (SG18.2) Characteristics of Cardiogenic shock?
      • Results from any type of heart failure, such as that after severe myocardial infarction (heart attack), or heart infections, and other heart conditions. Because the heart can no longer pump blood effectively, blood flow to the tissues of the body decreases or stops.
  47. (SG18.3) Characteristics of Hypovolemic shock?
      • Results from the loss of blood volume in the blood vessels (hypovolemia means "low blood volume").
      • Reduced blood volume results in low blood pressure and reduced flow of blood to tissues. Hemorrhage is a common cause of blood volume loss leading to hypovolemic shock. Hypovolemia can also be caused by loss of interstitial fluid, causing a drain of blood plasma out of the vessels and into the tissue spaces. Loss of interstitial fluid is common in chronic diarrhea or vomiting, dehydration, intestinal blockage, severe or extensive burns, and other conditions.
  48. (SG18.4) Characteristics of Septic shock?
      • Results from complications of septicemia, a condition in which infectious agents release toxins into blood. The toxins often dilate blood vessels, thereby causing shock. The situation is usually made worse by the damaging effects of the toxins on tissues combined with the increased cell activity caused by the accompanying fever. One type of septic shock is toxic shock syndrome (TSS), which usually results from staphylococcal infections that begin in the vagina of menstruating women and spread to the blood.
  49. (SG18.5) Characteristics of Neurogenic shock?
      • If sympathetic stimulation is disrupted by an injury to the spinal cord or medulla, depressive drugs; emotional stress, or some other factor, blood vessels dilate significantly. Widespread vasodilation reduces blood pressure, thus reducing blood flow.
      • Results from widespread dilation of blood vessels caused by an imbalance in autonomic stimulation of smooth muscle in vessel walls. It is also sometimes called vasodilatory shock. You may recall from Chapter 14 that autonomic effectors such as smooth muscle tissues are controlled by a balance of stimulation from the sympathetic and parasympathetic divisions of the autonomic nervous system. Normally, sympathetic stimulation maintains the muscle tone that keeps blood vessels at their usual diameter.
  50. (SG19.1) How is hypertension related to atherosclerosis?
      • There is a direct relationship between age and high blood pressure or hypertension (HTN), the "Silent Killer".
      • As age advances the blood vessels become less compliant AND there is a higher incidence of atherosclerosis - plaque buildup. These factors prevent the vessels from dilating to increase volume so as to maintain homeostatic BP.
      • Artheriosclerosis is a complication of arteriosclerosis.
  51. (SG19.2) Arteriosclerosis versus Atherosclerosis
      • Arteriosclerosis is characterized by thickening of arterial walls that eventually progresses to hardening as calcium deposits form.
      • The thickening and calcification reduce the flow blood to the tissues. If blood slows in peripheral tissues such as hands, lower legs, or feet, the condition is often referred to as peripheral vascular disease and the result is ischemia.
      • There are several types of arteriosclerosis, but perhaps the most well known is atherosclerosis, described earlier as the blockage of arteries by lipids and other matter.
      • Eventually, the fatty deposits in the arterial walls become fibrous and perhaps calcified-resulting in sclerosis (hardening).
      • High blood levels of triglycerides and cholesterol, which may be caused by a high-fat and high-cholesterol diet, smoking, and a genetic predisposition, are associated with atherosclerosis.
      • In general, arteriosclerosis develops with advanced age, diabetes, high-fat and high-cholesterol diets, hypertension (high blood pressure), and smoking.
      • Arteriosclerosis can be treated by drugs called vasodilators, that trigger the smooth muscles of the arterial walls to relax, thus causing the arteries to dilate (widen).
      • Some cases of atherosclerosis are treated by mechanically opening the affected area.
  52. (SG20.1) Define Pernicious Anemia:
      • Results from a dietary deficiency of vitamin B12. Vitamin B12 is used in the formation of new RBCs in the bone marrow. In many cases, pernicious anemia results from the failure of the stomach lining to produce intrinsic factor-the substance that allows vitamin B12 to be absorbed. Pernicious anemia can be fatal if not successfully treated. One method of treatment involves intramuscular injections of vitamin B12.
  53. (SG20.2) Define Hemolytic Anemia:
      • Result from inherited blood disorders characterized by abnormal types of hemoglobin.
      • The term hemolytic means "relating to blood breakage", where RBCs become distorted and easily broken, i.e. lysed.
      • Sickle Cell Anemia and Thalassemia are examples.
  54. (SG20.3) Define Aplastic Anemia:
      • Although idiopathic (unknown causes) forms of the disease occur, most cases result from destruction of bone marrow by drugs, toxic chemicals, or radiation. Less commonly, aplastic anemia results from bone marrow destruction by cancer. Because tissues that produce other formed elements are also affected, aplastic anemia is usually accompanied by a decreased number of WBCs and platelets. Bone marrow transplants have been successful in treating some cases of aplastic anemia.
  55. (SG20.4) Define Iron-Deficiency Anemia:
      • In addition to dietary, it can result from inadequate uptake or absorption.
      • The amount and quality of hemoglobin within RBCs are just as important as the number of RBCs. In hemoglobin disorders, RBCs are sometimes classified as hyperchromic (abnormally high hemoglobin content) or hypochromic (abnormally low hemoglobin content). Iron (Fe) is a critical component of the hemoglobin molecule, forming the central core of each heme group. Without adequate iron in the diet, the body cannot manufacture enough hemoglobin. The result is iron deficiency anemia - a worldwide medical problem. Although the body carefully protects its iron reserves, they may be depleted through hemorrhage, increased requirements such as wound healing or pregnancy, or low intake. Unfortunately, iron deficiency is the most common nutritional deficiency in the world. The tragic result is that an estimated 10% of the population in some developed countries and up to 50% in developing countries suffers from iron deficiency anemia.
  56. (SG20.5) Define Hemorrhagic Anemia?
      • Anemia induced by acute (injury resulting in hemorrhage) or chronic blood loss, as from bleeding ulcers.
  57. (SG21.1) Show basic understanding of Murmur:
      • Murmurs are abnormal heart sounds that are produced as a result of turbulent blood flow that is sufficient to produce audible noise.
      • Murmurs may also be the result of various problems, such as narrowing or leaking of valves, or the presence of abnormal passages through which blood flows in or near the heart.
  58. (SG21.2) Show basic understanding of Bradycardia:
      • In the context of adult medicine, is the resting heart rate of under 60 beats per minute, though it is seldom symptomatic until the rate drops below 50 beat/min.
      • It may cause cardiac arrest in some patients, because those with bradycardia may not be pumping enough oxygen to their heart.
      • It sometimes results in fainting, shortness of breath, and if severe enough, death.
      • Trained athletes or young healthy individuals may also have a slow resting heart rate (e.g. professional cyclist Miguel Indurain had a resting heart rate of 28 beats per minute).
      • Resting bradycardia is often considered normal if the individual has no other symptoms such as fatigue, weakness, dizziness, lightheadedness, fainting, chest discomfort, palpitations or shortness of breath associated with it.
  59. (SG21.3) Show basic understanding of Vasoconstriction:
      • Angiospasm - decrease in vessel lumen via smooth muscle in vessel wall.
      • Narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, particularly the large arteries, small arterioles and veins.
      • The process is particularly important in staunching hemorrhage and acute blood loss. When blood vessels constrict, the flow of blood is restricted or decreased, thus, retaining body heat or increasing vascular resistance.
      • Cutaneously, this makes the skin turn paler because less blood reaches the surface, reducing the radiation of heat.
      • On a larger level, vasoconstriction is one mechanism by which the body regulates and maintains mean arterial pressure.
      • Substances causing vasoconstriction are called vasoconstrictors or vasopressors.
      • Many vasoconstrictors also cause pupil dilation.
      • Medications that cause vasoconstriction include antihistamines, decongestants and stimulants used to treat ADHD.
  60. (SG21.4) Show basic understanding of Blood Pressure:
      • It is different from Pulse Pressure, BUT the two are derived from the same data.
  61. (SG21.5) Show basic understanding of Stenosis:
      • An abnormal narrowing in a blood vessel or other tubular organ or structure.
      • Stenosis of the vascular type are often associated with unusual blood sounds resulting from turbulent flow over the narrowed blood vessel.
  62. (SG21.6) Show basic understanding of Dysrhythmia:
      • Also known as arrhythmia - is a term for any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. The heart beat may be too fast or too slow, and may be regular or irregular.
      • These palpitations have also been known to be caused by atrial/ventricular fibrillation, wire faults, and other technical or mechanical issues in cardiac pacemakers/defibrillators.
      • Still others may not be associated with any symptoms at all, but may predispose the patient to potentially life threatening stroke or embolism.
      • Some arrhythmias are very minor and can be regarded as normal variants. In fact, most people will on occasion feel their heart skip a beat, or give an occasional extra strong beat; neither of these is usually a cause for alarm.
  63. (SG21.7) Show basic understanding of Ischemia:
      • A restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, thrombosis or embolism).
  64. (SG21.8) Show basic understanding of Vasodilation:
      • Widening of blood vessels resulting from relaxation of smooth muscle cells within the vessel walls, particularly in the large arteries, smaller arterioles and large veins.
      • When vessels dilate, the flow of blood is increased due to a decrease in vascular resistance. Therefore, dilation of arterial blood vessels (mainly arterioles) leads to a decrease in blood pressure.
      • The response may be intrinsic (due to local processes in the surrounding tissue) or extrinsic (due to hormones or the nervous system).
      • The response may either be localized to a specific organ (depending on the metabolic needs of a particular tissue, as during strenuous exercise), or systemic (seen throughout the entire systemic circulation).
  65. (SG21.9) Show basic understanding of Diastole:
      • Diastole is the period of time when the heart fills with blood after systole (contraction). Ballistics accurately describes diastole as recoil opposed to coil or systole.
      • Ventricular diastole is the period during which the ventricles are relaxing, while atrial diastole is the period during which the atria are relaxing.
  66. (SG21.10) Show basic understanding of Angina pectoris:
      • Temporary and reversible heart ischemia.
      • Commonly known as angina, is severe chest pain due to ischemia (a lack of blood, hence a lack of oxygen supply) of the heart muscle.
      • Generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels).
      • Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries.
      • There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle (i.e., there can be severe pain with little or no risk of a heart attack, and a heart attack can occur without pain).
  67. (SG21.11) Show basic understanding of Myocardial infarction:
      • Commonly known as a heart attack, is the interruption of blood supply to a part of the heart, causing heart cells to die.
      • This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery.
      • The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).
  68. (SG21.12) Show basic understanding of Tachycardia:
      • Persistent HR over 100.
      • A heart rate that exceeds the normal range for a resting heart rate (heart rate in an inactive or sleeping individual). It can be dangerous depending on the speed and type of rhythm.
      • When the heart beats excessively rapidly, the heart pumps less efficiently and provides less blood flow to the rest of the body, including the heart itself.
      • The increased heart rate also leads to increased work and oxygen demand by the heart, which can lead to rate related ischemia.
  69. (SG21.13) Show basic understanding of Embolism...
      • ... is the event of lodging of an embolus [any detached, itinerant intravascular mass (solid, liquid or gaseous)] into a narrow capillary vessel of an arterial bed which causes a blockage (vascular occlusion) in a distant part of the body.
  70. (SG21.14) Show basic understanding of Fibrillation:
      • There are two major classes of cardiac fibrillation: atrial fibrillation and ventricular fibrillation.
      • Atrial fibrillation occurs commonly in mitral stenosis, rheumatic heart disease, and infarction of the atrial myocardium. It can be treated with digoxin or by cardioversion - the application of carefully timed electrical shocks to restore normal rhythm.
      • Ventricular fibrillation is rapidly fatal if not reversed by defibrillation. No electrical impulse is given off in this form of dysrhythmia.
      • Fibrillation may sometimes be used after heart surgery to stop the heart from beating while any minor leaks are stitched up.
  71. (SG21.15) Show basic understanding of Heart block:
      • A heart block is a disease in the electrical system of the heart.
      • This is as opposed to coronary artery disease, which is disease of the blood vessels of the heart. While coronary artery disease can cause angina (chest pain) or myocardial infarction (heart attack), heart block can cause lightheadedness, syncope (fainting), and palpitations.
      • A heart block can be a blockage at any level of the electrical conduction system of the heart, e.g. SA nodal blocks, AV nodal blocks, infra-Hisian blocks (named after the bundle of His), etc.
  72. Other "Infarction" sites?
    Lung and intestinal, as well as cardiac.
  73. (SG21.16) Show basic understanding of Ectopic focus:
      • Pacemaker cells in the SA Node posses an intrinsic rhythm, that is they themselves initiate impulses at regular rhythms without stimulation of nerve impulses from the brain.
      • An ectopic pacemaker or ectopic focus is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the human heart.
      • Acute occurrence is usually non-life threatening, but chronic occurrence can progress into tachycardia, bradycardia or ventricular fibrillation.
      • In a normal heart beat rhythm, the SA node usually suppresses the ectopic pacemaker activity due to the higher impulse rate of the SA node. However, in the instance of either a malfunctioning SA node or an ectopic foci bearing an intrinsic rate superior to SA node rate, ectopic pacemaker activity may rule over the heart rhythm.
  74. (SG22.1) Main steps of hemostasis and the factors that influence the process:
      • Complex process which causes the bleeding process to stop. It refers to the process of keeping blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage).
      • A secondary function of clotting is to prevent infection, i.e. to trap and bind bacteria to prevent an infection.
      Major Steps:
      1. Vascular spasm or contraction via smooth muscle of the vessel wall to restrict flow.
      2. Platelet Plug Formation
        1. PF3 from platelet's exposure to tissue factor plus calcium and other clotting factors facilitate the formation of Prothrombin activator.
        2. Prothrombin activated via Prothrombin activator yields Thrombin.
        3. Fibrinogen activated via Thrombin yields Fibrin.
        4. Fibrin (or Blood) Clot with trapped RBCs results in Coagulation.
  75. Electrocardiogram, written and spoken
    • written - ECG
    • spoken - EKG
  76. Intrinsic SA (Sinoatrial) rate in BPM
  77. Abnormal ectopic pacemaker rates
    If the SA node fails for any reason and AV (Atrioventricular) node takes over:

        40-60 BPM
  78. Sarcolemma?
    Plasma membrane of a striated muscle cell (including cardiac)
  79. Syncytium (sin-SISH-ee-em)
    Meaning "joined cells", the connections of individual heart muscle cells via intercalated disks results in a continuous and electrically coupled impulse of myocardial tissue.

    NOTE: Heart muscle "cannot summate to produce tetanus and thus does not fatigue".
  80. Depolarization of the atria causes what ECG wave?
  81. Repolarization of the atria and depolarization of the ventricles causes what ECG wave?
  82. Repolarization of the ventricles causes what ECG wave?
  83. Describe the ECG U wave, if present
    Sometimes, an additional U wave may be seen in the electrocardiogram. The U wave, when visible, appears as a tiny "hump" at the end of the T wave. The U wave results from late repolarization of Subendocardial branches (Purkinje fibers) in the papillary muscle of the ventricular myocardium. If not too big, U waves are usually considered to be normal. Sometimes, however, U waves can be a sign of hypokalemia (low blood potassium) or too much digoxin (a heart medication).
  84. At what ECG wave does the first heart sound (LUBB) appear?
    Starts at R and ends just past S
  85. At what ECG wave does the second heart sound (DUBB) appear?
    Starts at the end of T
  86. What causes the LUBB heart sound?
    • The first or systolic sound
    • is a contraction of the ventricles and vibrations from the closing of the Atrioventricular or cuspid valves.
    • It is longer and lower than the DUBB sound.
  87. What causes the DUBB heart sound?
      • The second or diastolic sound
      • is caused by vibrations from the closing semilunar valves.
      • It is shorter and sharper than the LUBB sound.
  88. What do abnormal heart sounds mean, e.g. a murmur?
    Any deviation from the normal is an indication of an improperly functioning valve. A "swishing" sound may mean an incomplete closing of the value (valvular insufficiency) or a stenosis (constriction or narrowing).
  89. What is the pressure called that is needed for blood to flow through tissue and what does it mean?
    Perfusion pressure, which means "flow through"
  90. How are blood volume and arterial pressure related?
    Pressure increases with increases in volume and vice versa.
  91. Two factors that affect arterial blood volume?
    Cardiac output and peripheral resistance.
  92. Relate, i.e. increases/decreases: SV, HR, CO, arterial blood volume (ABV), and BP
    As SV or HR change, so to do CO, ABV and BP tend in the same direction.

    The reason for tend is because the book wanted to point out that the relationship only works if there are no other changes in a conflicting direction.
  93. Formula for EF% (ejection fraction)...
    SV (stroke volume)

    / EDV (end diastolic volume)

    X 100
  94. Name the four tissue types and what type is blood
    Epithelial, connective, muscle and nervous.

    Blood is CONNECTIVE
  95. Compare viscosity of blood to water.
    Blood is 5X ticker than water because of the inclusion of formed elements.
  96. Components of blood plasma?
      • ~55% (46-63%) of whole blood.
      • Plasma is non living.
      • 91% water
      • 7% plasma proteins
        • Albumins 57%
        • Globulins 38%
        • Fibrinogen 4%
        • Prothrombin 1%
        • 1% other solutes
          • enzymes, ions nutrients, waste products, and gasses
  97. Components of blood formed elements?
    (counts are per cubic millimeter)

    • ~45% (37-54%) is living cells (55% plasma)
      • 99.9% RBC, 4.2-6.2 million erythrocytes
      • <0.1%, 5000-9000 leukocytes 700X less than RBC
      • <0.1%, 140-340k platelets 70X less than WBC
  98. Components of WBC?

    • Neutrophils
      • Multi-lobed, Pink-Purple Granulocyte
      • 60-70%
      • Cellular defense; phagocytosis of small pathogensLymphocytes
        • Smallest WBC; Scant cytoplasm
        • 20-25%
        • Humoral (fluid) defense; Immune System response & regulation; Antibodies; T- attack infected or cancerous cells; B- produce antibodies.Monocytes
          • Largest WBC; Horseshoe Nucleus
          • 3-8%
          • Migrating Macophage: Bacteria, cellular Debris; Cancerous cellsEosinophils
            • Two-lobed; Orange-Red Granulocyte
            • 2-4%
            • Vellular defense; Eats Protozoa & Parasitic Worms; Antiinflammatory for Allergic reactionsBasophils
              • Two-lobed; Purple Granulocytes
              • 0.5-1%
              • Anticoagulant: Heperin; Inflammatory response: Histamine
  99. Name the three parts of the cardiovascular system.
      1. Heart
      2. Blood vessels
      3. Blood
  100. What is a typical Ejection Fraction for healthy adults?
    55% or more
  101. Formation of Blood Cells
    • Hemocytoblasts
      • 2) Myeloblast,... 6) Neutrophils
      • 2) Lymphoblast, 3) Lymphocyte
      • 2) Monoblast, 3) Monocyte
      • 2) Myeloblast,... 6) Eosinophils
      • 2) Myeloblast,... 6) Basophils
      • 2) Megakaryoblast, 3) Megakaryocyte,... 5) Platelets
      • 2)Proerythroblast, 5) Reticulocyte (no nucleus), 6) Erythrocytes
Card Set
LEC 1 Exam.txt