Anatomy and Physiology Lab - The Endocrine System

Anatomy & Physiology Lab Exam 1 Study Guide The Endocrine System: Production and Stimulation of Hormones: 1. TRH: hypothalamus releases thyrotropin-releasing hormone 2. TSH: anterior pituitary releases and produces thyroid-stimulating hormone - Stimulates the thyroid to produce Thyroxine 3. Thyroxine: controls metabolic rate (measures Oxygen uptake which gets converted to mL of O2 per Kg per Hour ● Thyroid hormone levels are low, so they secrete more TRH and TSH, which stimulates the thyroid to make more hormones. ● Thyroid hormone levels are too high, so they secrete less TRH and TSH, which reduces hormone production by the thyroid. Negative Feedback Example: ● The stimulus is the decrease in T3 and T4 concentrations in the blood/low body temperature. The hypothalamus releases Thyroid Releasing Hormone and the Anterior Pituitary releases TSH. The thyroid gland follicles release T3 and T4 so that homeostasis can be restored. ● Insulin lowers blood glucose when levels are too high and glucagon raises blood glucose when levels are low. Rat Questions: ml of o2 per kg per hour 1. Which rat had the fastest basal metabolic rate (BMR)? - The normal rat. 2. What will occur metabolically with a rat that has had its thyroid gland removed? - The BMR would decrease. 3. What happens to the metabolic rate of a rat with no thyroid gland when thyroxine is injected into the rat? - The BMR would increase. 4. If an animal had been thyroidectomized, what hormone(s) would be missing in its blood? - Thyroxine and Calcitonin 5. What was the effect of TSH injections on the normal rat’s BMR? - The metabolic rate went up and the baseline was a lot lower. 6. What was the effect of PTU injections on the normal rat’s BMR? - It slowed the metabolic rate, compared to the normal baseline. PTU inhibits the production of thyroxine. 7. An injection of TSH to an otherwise normal animal will cause… - Goister development Insulin & Glucose: - Both produced by the pancreas (which maintains homeostatic blood glucose levels) Insulin decreases blood glucose ❏ Released by the beta cells in the pancreas in response to rising glucose in the bloodstream (hyperglycemia) - Glucagon increases blood glucose levels due to the breakdown of glycogen and the release of glucose into the bloodstream ❏ Released by Alpha cells to stop blood sugar levels dropping too low (hypoglycemia) ❏ Glucose is stored in the liver and bloodstream. ➔ Normal fasting blood glucose: less than 110 mg/dl Diabetes: ● Type 1: pancreas doesn’t produce enough Insulin (juvenile diabetes) ● Type 2: body cells don’t respond to insulin (triggered by obesity) Prediabetes or Borderline Impairment: 110-126 mg/dl Diabetes: 126 or above mg/dl ➔ Gestational Diabetes: diagnosed during pregnancy, can start when the mother’s body is unable to make & use all the insulin it needs for pregnancy How do you determine Blood Glucose Levels using the Standard Curve? - You measure optical density & read the curve to determine glucose levels. The percentage of glucose taken during a meal & storing it as glycogen? - 75% A male patient has had successive fasting plasma glucose reading of 115, 110, and 122 mg/dl. The healthcare provider will inform him that: - He appears to have impairment or borderline impairment of insulin-mediated glucose uptake by his cells Hematocrit & Hemoglobin: Hematocrit: percentage of Erythrocytes (Red Blood Cells) in a sample of whole blood - Normal Hematocrit for Males: 42-52% - Normal Hematocrit for Females: 37-47% ➔ Anemia causes: low or depressed hematocrit from hyperthyroidism, cirrhosis, etc. ➔ Polycythemia causes: high hematocrit from living at high altitudes & congestive heart failure Hemoglobin: a protein found in red blood cells which is necessary for the transport of oxygen from the lungs to the cells of the body. - Normal Hemoglobin for Males: 13.5-18 g/100ml - Normal Hemoglobin for Females: 12-18 g/100ml ➔ Higher in males due to more muscle & more oxygen transport. Testosterone controls muscle & bone development increasing red blood cell creation. ➔ Causes of Low Hemoglobin levels: aplastic anemia, sickle cell, iron deficiency 4 Basic Blood Types: A, B, AB, O Blood Cells: Neutrophils: Most Numerous, Multilobed (3-6), Nucleus Eosinophils: bright red, course (large), 2 distinct nuclei, kill worms (too large to be phagocytosed) Basophils: Least Numerous, course, dark purple, blank granules, releases (inflammatory chemical), attracts other WBCs to the area Lymphocytes: large, dark purple nucleus 90% of the volume of the cell, moon cytoplasm, almost perfectly round histamine crescent-shaped Monocytes: large, dark purple nucleus which is kidney-shaped , biggest white blood cell, undergoes phagocytosis Erythrocytes: - Red Blood Cells - Anucleate (no nucleus) - 45% is normal - Biconcave disc: when the microscope light is turned up too far, it washes out the middle of erythrocytes, looks like a donut Blood Typing: 4 Types: A, B, AB, O - Antigens: Blood Groups - Antibodies: Agglutinins or preformed antibodies that act against the red blood cells carrying ABO antigens NOT present on the person’s own type - Agglutination: 2 Types determine which type the person inherits of ABO group 1. Type A 2. Type B - Rh-Positive vs. Rh-negative: There are 52 named Rh agglutinogens each of which is called an Rh factor. Only 5 of these, the C, D, E, c, and e antigens are fairly common. If you are Rh-Positive, you carry the D antigen , and those that don’t will be Rh-negative. Identification of the Heart: Systemic & Pulmonary System ● ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ Structures To Know: Right atrium Left atrium Right ventricle Left ventricle Bicuspid (Mitral) (Inside Heart) Tricuspid valves (Inside Heart) Pulmonary and Aortic semilunar valves Pulmonary trunk Pulmonary arteries Superior and Inferior vena cava Aorta Coronary artery (Superficial) Interventricular septum Auricles (Superficial) Blood Flow Pathways: ● Pulmonary Circuit: Lung Circuit ➔ Carries DEOXYGENATED blood away from the heart, TO THE LUNGS ➔ 1. Right Atrium (deoxygenated blood) => 2. Right Ventricle => 3. OUT Ventricle UP to the Pulmonary Arteries & 4. OUT to the Lungs ➔ Returns: OXYGENATED blood back to the heart FROM THE LUNGS ● Systemic Circuit: Rest of the Body ➔ Carries OXYGENATED blood away from the heart, TO THE REST OF THE BODY ➔ 1. Left Atrium (oxygenated blood) => 2. Left Ventricle => 3. UP and OUT Aorta to the rest of the body ➔ Returns: DEOXYGENATED blood back to the heart (vena cavae) ★ Right Side of Heart: carries deoxygenated blood ★ Left Side of Heart: carries oxygenated blood Refractory Period of Cardiac Muscle: - Dramatically longer than Skeletal Muscle - Prevents tetanus from occurring & ensures each contraction is followed by enough time to allow the heart chambers to refill with blood before the next contraction Wave Summation: - The second contraction happens before the muscle is able to relax Tetanus: - So many stimuli you can’t tell them all apart (doesn’t happen in cardiac muscle) Autonomic Nervous System Effects on Heart Sympathetic Nervous System: - Cardiac Nerve releases Norepinephrine/Epinephrine (upregulatory) - Increases heart rate and force of contraction Parasympathetic Nervous System: more effective - Vagus Nerve releases Ach (downregulatory) - Decreases heart rate but doesn’t affect the force of contraction Vagal Stimulation: - Excessive vagal stimulation slows down the heart to the point where it will stop beating Vagal Escape: - Resumption of the heart rhythm (result of sympathetic reflexes or initiation of the heart beat by the purkinje fibers) Chemical Modifiers: Norepinephrine and Epinephrine: bind to B1 adrenergic receptors in the SA Node - This opens the Na and Ca channels thus increasing the rate of depolarization & heart rate Acetylcholine: opens the K+ channcels & closes the Na and Ca channels - Decreasing rate of depolarization & heart rate Adrenergic: chemical modifiers that inhibit, mimic, or enhance the action of norepinephrine and epinephrine Cholinergic: modifiers that inhibit, mimic, or enhance the action of ach Agonist: modifier has the same effect as the neurotransmitter Antagonist: modifier has the opposite effect as the neurotrasmitter Atropine, Digitalis, Pilocarpine - All of these chemicals are derived from plants. Atropine - mimics the action of the Sympathetic Nervous system’s effect on the heart rate. It is an acetylcholine antagonist and increases the rate of depolarization and the heart rate ■ Digitalis and Pilocarpine - are acetylcholine agonists ■ Digitalis - is given to patients with weakened hearts. It slows down the heart rate, giving the ventricles more time to fill with blood while at the same increasing the force of contraction and stroke volume. ■