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A&P ch. 9,10,17,18
muscle tissue, muscle ID, blood, heart
| Question | Answer |
|---|---|
| The functional unit of contraction in a skeletal muscle fiber is the - | sarcomere |
| "Cross bridges" that link between the thick and thin filaments are formed by the _________ | globular head of thick filaments |
| Area of the sarcomere with overlapping thick and thin filaments | A band |
| Acetylcholinesterase | Enzyme released into neuromuscular junction to break down acetylcholine |
| The thin myofilaments of skeletal muscle are composed chiefly of __ | actin |
| Oxygen storage molecules in skeletal muscle | myoglobin |
| Type of contraction represented by a single stimulus/contraction/relaxation sequence | twitch |
| Rodlike contractile elements within a muscle fiber containing myofilaments | myofibril |
| Cross bridges | myosin heads |
| Area in the center of the A band containing only thick filaments | H zone |
| blood | fluid connective tissue composed of plasma and formed elements |
| formed elements | Erythrocytes (red blood cells, or RBCs) Leukocytes (white blood cells, or WBCs) Platelets |
| Hemacrit | formed elements Percent of blood volume that is RBCs 47% ± 5% for males 42% ± 5% for females |
| Blood characteristics | Sticky, opaque fluid Color scarlet to dark red pH 7.35–7.45 38 degrees C ~8% of body weight Average volume: 5–6 L for males, and 4–5 L for females |
| Functions of blood | Distribution Regulation Protection |
| Distribution (function of blood) | distributes: O2 and nutrients to body cells Metabolic wastes for elimination Hormones transport |
| Regulation (function of blood) | regulates: Body temperature Normal pH using buffers Adequate fluid volume |
| Protection (function of blood) | protects against: Blood loss clot formation Infection Antibodies Complement proteins WBCs defense |
| Blood plasma | 90% water Proteins are mostly produced by the liver 60% albumin – Abundant - osmotic pressure 36% globulins - antibodies 4% fibrinogen – clotting |
| Formed elements info | Only WBCs are complete cells RBCs have no nuclei or organelles Platelets are cell fragments Most formed elements survive in the bloodstream for only a few days Most blood cells originate in bone marrow and do not divide |
| Erythrocytes (RBC) | Biconcave discs Anucleate no organelles Filled with hemoglobin (Hb) Are the major factor contributing to blood viscosity |
| Erythrocytes (RBC) structure | Structural characteristics contribute to gas transport Biconcave shape—huge surface area relative to volume >97% hemoglobin (not counting water) No mitochondria; ATP production is anaerobic; no O2 is used in generation of ATP |
| Function of Erythrocytes | RBCs are dedicated to respiratory gas transport Hemoglobin binds reversibly with O2 structure: Protein globin: two alpha and two beta chains Heme pigment bonded to each globin chain |
| Erythrocytes O2 transport info | Iron atom in each heme can bind to one O2 molecule Each Hb molecule can transport four O2 |
| Composition of blood plasma | nutrients: carbs, glucose, amino acids respiratory gasses: 02 and CO2 Electrolytes: Na+, Ca+, K+, Cl, HCO3 by products of metabolism: urea and creatinine hormones |
| 02 loading in the lungs | Produces oxyhemoglobin (ruby red) |
| O2 unloading in tissue | Produces deoxyhemoglobin or reduced hemoglobin (dark red) |
| CO2 loading in tissues | Produces carbaminohemoglobin (carries 20% of CO2 in the blood) |
| Hematopoiesis (hemopoiesis): | blood cell formation Occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur |
| Hemocytoblasts (hematopoietic stem cells) | Give rise to all formed elements Hormones and growth factors push the cell toward a specific pathway of blood cell development |
| Where do new blood cells go? | they enter blood sinusoids |
| What do reticulocytes become? | become mature erythrocytes |
| phases in development of RBCs | Ribosome synthesis Hemoglobin accumulation Ejection of the nucleus and formation of reticulocytes |
| Erythropoiesis: | red blood cell production A hemocytoblast -> proerythroblast -> early erythroblasts |
| regulation of Erythropoiesis: | Too few RBCs leads to tissue -> hypoxia Too many RBCs ->increases blood viscosity Balance between RBC production and destruction depends on Hormonal controls supplies of iron, amino acids, and B vitamins |
| causes of hypoxia | Reduces RBC numbers Hemorrhage Increased RBC destruction Insufficient hemoglobin (e.g., iron deficiency) Reduced availability of O2 (e.g., high altitudes) |
| Hormonal Control: Erythropoietin (EPO) (REGULATION OF ERYTHROPOIESIS) | Direct stimulus for erythropoiesis Released by the kidneys in response to hypoxia |
| Dietary requirements for Erythropoiesis: | Iron Stored in Hb (65%), the liver, spleen, and bone marrow Stored in cells as ferritin and hemosiderin Transported loosely bound to the protein transferrin Vitamin B12 and folic acid —necessary for DNA synthesis for cell division |
| Dietary requirements for Erythropoiesis (Nutrients) | Nutrients—amino acids, lipids, and carbohydrates |
| Fate and destruction of Erythrocytes | Life span: 100–120 days Old RBCs become fragile, and Hb begins to degenerate Macrophages engulf dying RBCs in the spleen |
| Anemia | blood has abnormally low O2-carrying capacity A sign rather than a disease itself Blood O2 levels cannot support normal metabolism Accompanied by fatigue, paleness, shortness of breath, and chills |
| Polycythemia: | excess of RBCs that increase blood viscosity |
| Causes of Anemia: Insufficient erythrocytes | Hemorrhagic anemia: acute or chronic loss of blood Hemolytic anemia: RBCs rupture prematurely Aplastic anemia: destruction or inhibition of red bone marrow |
| Causes of Anemia: Abnormal Hemoglobin | Thalassemias Absent or faulty globin chain RBCs are thin, delicate, and deficient in hemoglobin Sickle-cell anemia Defective gene codes for abnormal hemoglobin (HbS) Causes RBCs to become sickle shaped in low-oxygen situations |
| Causes of Anemia: Low Hemoglobin Content | Iron-deficiency anemia Secondary result of hemorrhagic anemia or Inadequate intake of iron-containing foods or Impaired iron absorption Pernicious anemia low B12 Lack of intrinsic factor needed for absorption of B12 |
| Breakdown of Erythrocytes: STEP 1 | Iron -> stored as ferratin and hemosiderin -> released into blood as transferrin |
| Breakdown of Erythrocytes: STEP 2 | transferrin is degraded to a yellow pigment called bilirubin |
| Breakdown of Erythrocytes: STEP 3 | The liver secretes bilirubin into the intestines as bile |
| Breakdown of Erythrocytes: STEP 4 | The intestines metabolize Bile into urobilinogen |
| Breakdown of Erythrocytes: STEP 5 | urobilinogen leaves the body in feces, in a pigment called stercobilin |
| Microscopic Anatomy of Cardiac Muscle | Cardiac muscle cells - striated, short, fat, branched, and interconnected Connective tissue matrix (endomysium) connects to the fibrous skeleton T tubules are wide but less numerous SR is simpler than in skeletal muscle Numerous large mitochondria |
| Intercalated discs | junctions between cells anchor cardiac cells Desmosomes prevent cells from separating during contraction Gap junctions allow ions to pass; electrically couple adjacent cells |
| What do intercalated discs do? | Intercalated discs anchor cardiac cells together and allow free passage of ions |
| How does heart muscle behave? | Heart muscle behaves as a functional syncytium – cells are electrically coupled by gap junctions, the myocardium acts as a single coordinated unit. |
| Cardiac Muscle Contraction breakdown | -1% is autorhythmic or special ability to depolarize spontaneously – pacemaker cells of the heart - 99% is contractile muscle fibers – responsible for pumping activity |
| Cardiac Muscle contraction | Is stimulated by nerves and is self-excitable -> automaticity or autorhymicity Contracts as a unit Has a long (250 ms) absolute refractory perio |
| Pacemaker potential | This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is never a flat line. |
| Depolarization | The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+ influx through Ca2+ channels. |
| Repolarization | due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage. |
| Plateau phase | due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because few K+ channels are open. |
| Intrinsic Conduction System: Autorhythmic cells | Initiate action potentials Have spontaneously changing membrane potential or unstable resting potentials called pacemaker potentials Use calcium influx (rather than sodium) for rising phase of the action potential |
| Sequence of Excitation (1) | Sinoatrial (SA) node (pacemaker) Generates impulses about 75 times/minute (sinus rhythm) Depolarizes faster than any other part of the myocardium |
| Sequence of Excitation (2) | Atrioventricular (AV) node Smaller diameter fibers; fewer gap junctions Delays impulses approximately 0.1 second Depolarizes 50 times per minute in absence of SA node input |
| Sequence of Excitation (3) | AV bundle - Connect the atria to the ventricles |
| Sequence of Excitation (4) | Right and left bundle branches - Two pathways in the interventricular septum that carry the impulses toward the apex of the heart |
| Sequence of Excitation (5) | Purkinje fibers - Complete the pathway into the apex and ventricular walls - AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input |
| Tachycardia | A rapid heart rate, usually defined as greater than 100 beats per minute |
| Bradycardia | A slow heart rate, usually defined as less than 60 beats per minute |
| Fibrillation | rapid, irregular contractions; useless for pumping blood |
| Arrhythmias | irregular heart rhythms |
| What modifies the heartbeat? | the Autonomic Nervous System (ANS) |
| Where are cardiac centers located? | medulla oblongata |
| Cardioinhibitory center | inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves |
| Cardioacceleratory center | innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons |
| vagus nerve | decreases heart rate |
| sympathetic cardiac nerves | increases heart rate and force of contraction |
| ECG/EKG | a composite of all the action potentials generated by nodal and contractile cells at a given time |
| P wave: | - depolarization of SA node - atrial contraction |
| QRS complex | - ventricular depolarization - ventricular contraction |
| T wave | - ventricular repolarization - ventricular relaxation |
| Heart sounds | Two sounds (lub-dup) associated with closing of heart valves - 1st sound: AV valves closing and signifies beginning of systole - 2nd sound: when SL valves close at the beginning of ventricular diastole |
| Heart Murmur | abnormal heart sounds most often indicative of valve problems |
| Cardiac cycle | Blood flow through heart during one complete heartbeat: -atrial systole and diastole followed by ventricular systole and diastole |
| systole | contraction -Blood is ejected from atria and ventricle -Atrial contraction -Ventricular contraction |
| systole | -relaxation -Blood flow to the atria and ventricles -Atrial filling -Ventricular filling |
| Cardiac cycle phases | Phase 1 – Ventricular Filling Phase 2 – Atrial Contraction Phase 3 – Isovolumetric Contraction Phase 4 – Ventricular Ejection Phase 5 – Isovolumetirc Relaxation |
| Ventricular Filling | Atrial – relaxed Ventricles – relaxed Valves: AV valves – open SL valves – closed Blood flows from: SVC, IVC ->Right Atrium Pulmonary veins -> Left Atrium Atria -> ventricles |
| Atrial Systole | Atria – contraction or depolarization ECG Wave – P wave Ventricles – diastole Valves: AV valves – open SL valves – closed Blood flows from: Right Atrium -> Right Ventricle Left Atrium -> Left Ventricle |
| End diastolic volume (EDV): | Volume of blood in the ventricles after the atrial contraction |
| Ventricular systole | Ventricular contraction - begins Atria relaxing ventricular pressure > Atrial pressure ECG – QRS wave |
| Isovolumetric Contraction | Ventricle contracting with no change in the volume Atrial relaxing Ventricles: systole V. pressure > A. pressure Closing of AV 1st Heart sound ->LUB SL valve – closed |
| Ventricular Ejection | V. pressure > Aortic or Pulmonary artery pressure SL valves open Blood ejected to aorta and pulmonary trunk |
| Ventricular Isovolumetric Relaxation | Ventricles relaxing No change in the volume of the ventricle Valves: AV valves – closed SL valves – closing SL valve closing 2nd Heart Sound Dub sound ECG - T wave |
| End Systolic Volume (ESV) | Volume of blood in the ventricles after the ejection |
| stroke volume | the volume of blood ejected from the heart in one beat (b-a) |
| The plateau portion of the action potential in contractile cardiac muscle cells is due to: | influx of calcium ions |
| Cardiac Output | Volume of blood pumped by each ventricle in one minute CO = heart rate (HR) x stroke volume (SV) HR = number of beats per minute SV = volume of blood pumped out by a ventricle with each beat |
| The stimulus for the heart’s rhythmic contractions comes from | a pacemaker potential |
Created by:
davisobr
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