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Endocrinology (1-6-99) Comp Boards Adjusting – 20 stations – need to pass 14 of them (70%) (with at least a 70% at each of these 14 stations) - Dr. Mannello’s stuff gets added in here - Net of ~ 24 stations - Called “Criteria Referenced Grading” Written – “Norm Referenced Grading” (curved) - typically, you’re in the bottom 5% of your class if you fail this - but – possible for no one to fail x-ray – “Norm Referenced Grading” also can still go into clinic if you fail the written or the x-ray part (but not both) but not if you fail the gym part Dr. Sanders’ E-mail address: [email protected] Endocrine systems - all patients have them - ex – endo thyroid Graves’ disease What do chiros need to know about endocrinology? - the ability to recognize signs and symptoms and correlate them to etiologies clinical reasoning (to reach a Dx from a bunch of patient data) we do – collection of clinical data - which tests to do, interpretation - your clinical knowledge base is important doctors spend most of their time collecting data and evaluating it (the actual adjusting doesn’t take very long) - develop your own style of clinical reasoning and modify it as you go along hypertension – can miss this in patients if you don’t take their BP hypoglycemia – a pathophysiologic condition - you need to take a patient’s blood glucose to see this symptoms may be the result of hypertension or hypoglycemia (or not!) find out the symptoms and determine what’s causing them, then do something about them increased thyroid levels increased HR (why?) increased bowel movements Cushing’s Disease – increased cortisol level – pituitary problem Cushing’s Syndrome – increased cortisol level – adrenal problem - similar symptoms, except some Cushing’s Disease patients are hyperpigmented (a differentiating feature) (elbows, knees, heels, hands, nose, chin, etc.) Cushing’s Disease – pituitary tumor ACTH adrenal increased cortisol Also increased melanin and melatonin in melanocytes When ACTH is produced from precursor molecules (PROMC), you also get melanocyte stimulating hormone and beta___ due to post-translational modification Course 5-6 quizzes (15-20Q each) (recognition-based) 1st quiz in approximately 2 weeks over Ch. 199 (10 pages) if miss a quiz, the make-up is fill-in-the-blank or essay (with Dr. Wilkerson) He prefers that you not take notes in class – listen and pay attention - all of his slides are on a web site (and in the library – reserved) (can download and print them) Endocrinology (1-20-99) Hormones: distinct chemical messengers that transmit information from one cell to another to coordinate homeostatic adaptations, growth, development, and reproduction endocrine system: used to talk in terms of a signal used to believe problems were due to either too much or too little hormone (problem – this model doesn’t work on everyone) diabetes mellitus – some people have too much insulin diabetes insipidus – some people have too much ADH hormones = effectors that bring about the effect Q – what causes decreased hormone levels? Hormones act in distinct locations But – some other biologically active substances do this also Hormone receptors are also important If they are not there, the hormone can’t work Not related to the endocrine system Made by protein synthesis, so protein synthesis problems can affect the endocrine system hormone – from the Greek word meaning “excite” or “set in motion”. 1 hormone can have multiple actions (ex – testosterone) 1 action can have several hormones (ex – glucose metabolism) testosterone – males have more red blood cells than females due to increased synthesis of erythropoietin Different actions are due not to different mechanisms but to differences in target cell response. Glucose Maintenance Insulin – protects against hyperglycemia via hepatic glucose production and enhanced glucose uptake glucagon – primary – protects against hypoglycemia } stimulate epinephrine – backup - protects against hypoglycemia } glucose norepinephrine – backup - protects against hypoglycemia } production cortisol – backup - protects against hypoglycemia } (in liver) thyroxine – stimulates appetite There is a wide range of interaction of hormones. Peptide Hormones vs. Steroid Hormones Differ in structure and mode of action (how they do what they do) Ex – shot in the head = manner of death Mode of death = hypoxia Injection in liver: mode = liver damage The mode depends on the type of cells being stimulated. Peptide Hormones Complex peptides: Intermediate peptides: Small peptides: Dipeptides: Single amino acids: Steroid Hormones Intact steroid nucleus: Broken steroid nucleus: LH, HCG insulin, glucagon TRH thyroxine histamine, serotonin adrenal hormones Vitamin D Last 20 years: learned a lot about the endocrine system 1) Peptide vs. Steroid Present in small amounts Didn’t even know they existed before 1965 (technology wasn’t good enough to detect them) ex: grams: mg: ug: ng: pg: fg: albumin, hemoglobin glucose, cholesterol T4, cortisol, GH T3 ACTH endorphins before 1965, they couldn’t detect anything smaller than 100 ug (had to use indirect methods to know they were there) radioimmunoassay: Rosalind Yallow (Nobel prize for it) endorphins human chorionic gonadotrophin is tiny! 2) Hormone activity has to be controlled Need to know how this is done Can’t just control the effects by the concentration of the hormone Transport: Need an intact vascular system or hormones can’t get to where they’re going Solubility (peptides are water-soluble, steroids are not water-soluble) Steroids have to be altered by transport proteins to be water-soluble (also see this with lipids and cholesterol) Lipid transport: Uses the protein part of a lipoprotein (the apoprotein) If not enough transport proteins, there are backup modes of transport General transport proteins: Specific transport proteins: albumin, prealbumin thyroxine binding globulin Cortisol binding globulin To find what’s in serum, separate them Use electrophoresis to separate proteins (by size and by net charge) Ex – Bence-Jones protein in urine Look for a ‘myeloma spike’ (M-spike) electrophoresis: use an agar gel put a drop of serum on it and let it dry for a few minutes put it in an aqueous medium (pH = 8.6) (the pH of 8.6 gives most proteins a negative charge) run a current through the gel for X minutes/hours stain the gel get different bands at different distances 5 major bands in serum (alpha-1, alpha-2, beta, gamma, ??) prealbumin goes in the opposite direction from the rest of the bands prealbumin is an isovariant of albumin (not much different functionally) preformed antibodies (gamma globulins) help you ward off infections how to measure the amounts densitometry – measures the density of the color of the band shine a light through the band record the transmission or absorption get ‘tracings’ (of peaks for the different band wavelengths) multiple myeloma has an ‘M-spike’ for Bence-Jones proteins Specific transport proteins are not exclusive in that a specific hormone can also be transported by a general transport protein. Feedback relationships a distinguishing feature of the endocrine system the classic model is the hypothalamic-pituitary-thyroid axis interdependence of glands is involved Feedback relationships (cont) The hypothalamus releases TRH, which acts on the pituitary, causing it to release TSH, which acts on the thyroid, causing it to release T3 and T4, which act on the target cell, the hypothalamus, and the pituitary. T3 and T4 feed back to the hypothalamus and the pituitary. High levels of T3 and T4 shut off (inhibit) TRH production. Note: If you inhibit an inhibitor, you get stimulation. ex – As thyroid hormones decrease (T3 and T4 decrease), there is less inhibition of the hypothalamus, so the TRH levels increase, and so on. thyroid hormone – very potent - a 10% increase can cause a very rapid heart rate but – you generally don’t get much fluctuation in the heart rate even though the thyroid hormone fluctuates, due to other mechanisms that help control hormone activity. (It’s not just based on hormone concentration.) The same treatment won’t work on all Pts since the problem could be in different parts of the loop/pathway. ex – pituitary tumor – secondary to increased TSH thyroid tumor - primary hypothalamus tumor – tertiary primary vs. secondary vs. tertiary tumors they all look the same clinically, they just have different causes TRH TSH TH A indeterminate decreased increased primary B decreased increased increased secondary C greatly increased greatly increased increased tertiary TRH – primary – indeterminate – the increased TH tends to decrease TRH but - the decreased TSH tends to increase TRH