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48 Cards in this Set
- Front
- Back
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type of hormonal communication that sends hormones into blood stream
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hemocrine
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secretion into blood stream to affect distant tissue
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hemocrine
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hormone affects the same cell
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autocrine
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hormone affects neighboring cell
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paracrine
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affect via gap junction
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paracrine: intercrine
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affects via cell receptor on neighbor
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juxtacrine (paracrine) ie: osteoblast and osteoclasts
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hormone via synaptic and nonsynaptic affect
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neurocrine (non-synaptic refers to a neuron releasing directly into the blood stream)
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hormone taken up by a cell and modifed in to a new hormone and binds to a receptor inside the cell
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(ie: T4--> T3) intracrine
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influence of the effect of hormones: pattern of secretion
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there is always a basal tone/level of hormone (is there a stimulation or inhibition to affect the level?) secreted in a pattern or rhythm (ie: circadian pattern)
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hormone interactions
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synergistic, antagonistic,permissive
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messenger molecule secreted into lumen of ductal system (i.e. GI,
respiratory, urogenital). |
solinocrine
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regulation of release
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nerve activation, environmental, hormonal, feedback
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name the regulation: metabolic or osmotic changes
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environemental (internal)
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name the regulation: manipulation, stretch
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nerve activation
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what regulates the hormonal stimulation
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hypothalamus and pituitary glands
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KNOW THE Hypo-pit axis!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
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****
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free standing endocrine gland example
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pancrease secreting insulin, insulin affects the targe organ (muscle or adipose tissue) and changes in glucose levels will alter the release of insulin from the pancreas (insert diagram)
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what are the factors that affect the activity of hormones
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Synthesis
Storage Secretion Chemical properties (stability, solubility…) Elimination Receptors (affinity, number, distribution….) Second messengers |
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classes of hormones
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peptide (polypeptide), lipid derivatives, aa derivatives
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cleaved from precursor protiens and stored for later use
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peptide hormones
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what makes peptide hormones stable in serum
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glycosylation of the hormone
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percursor proteins of peptide hormones have several active peptides..... how does this affect the symptoms in a pt
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if two peptides are made from the same precursor protein, you may have two different symptoms or levels of hormones
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short half lives, water soluble, no usualy protein bound, eliminated by Serum proteases
Receptor mediated endocytosis followed by lysosomal degradation Kidney/liver excretion |
peptide hormones
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where do steriod hormones come from
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LDL receptor, Scavenger receptor, lipid droplets (insert diagram)
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will the amount of exogenous cholesterol affect the level of steroids?
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not really because of the many pathways to give cholesterol
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21 alpha hydroxylase step in steroid synthesis
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progesterone to deoxycortisterone
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what is the common start off all steriods
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cholesterol
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knowing how steriods are created, how can one block in the process affect other hormones
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things get shunted
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what is the synthesis of calcitriol
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*** need more info
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hydrophobic, bound to plasma proteins, long half lives, metabolized by the liver to soluble forms that are excreted (glucuronidation, sulfonation)
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steroid hormone properties
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Hydrophobic/lipophilic
Bound to plasma proteins Long half lives (days, T4 longer than T3) Peripheral metabolism through deiodination Metabolized to active or inactive forms Some inactivation through glucuronidation, sulfonation |
thryoid hormones (aa derivatives)
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Synthesized from essential fatty acids
Parallel pathways for w-3 and w-6 A key step is the release of fatty acids from membrane lipids through hydrolysis Arachidonic acid is the most common precursor (released by phospholipase A2 or phospholipase C) |
eicosanoids
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how to measure levels of hormones
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Immunoassays---
Radioimmunoassay (RIA) Immunoradiometric assay (IRMA) Enzyme linked assay (ELISA/EIA) Type of assay done depends on the lab Results between labs can vary greatly making it difficult to compare/standardize Immunochemiluminometric assay (ICMA) Immunofluorescence assays GC- MS or LC- MS/MS--- Generally more accurate |
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Peptides, amines and eicosanoids typically signal through cell surface receptors
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GPCRs:
Melanocortins, glucagon, catecholamines and serotonin, eicosanoids, TSH, LH, FSH, PTH, TRH… Receptor kinases: GH, insulin, prolactin… Guanylyl cyclase: ANP |
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desensitization processes
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uncoupling of G-proteins after ligand binding, endocytosis, mod by other proteins, altered expression, one hormone can affect its out activity
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hydrophobic hormones go where
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into the cell and into the nucleus
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what hormone is regulated by co-repressors and co-activators
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steriod and aa derivatives (thyroid hormones)
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defects of hormones
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abnormal hormonal activity, neoplasm, iatrogenic
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endocrine hypofunction
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Primary endocrine organ failure – genetic; acquired
agenesis genetic defect in hormone biosynthetic pathway (CAH) destruction (autoimmune; infection) deficiency in precursor (iodine) Production of abnormal hormone Secondary organ failure (hypogonadal due to hypopituitarism |
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endocrine hyperfunction
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Primary (tumor – parathyroid adenoma; autoimmune – Grave’s)
Secondary (ACTH pituitary adenoma; ectopic production - cancer) |
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Abnormality in hormone metabolism
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(abnormal glycosylation of TSH)
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Abnormality in hormone transport
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defect in thyroid binding globulin; liver disease
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Abnormality in receptor binding and / or signal transduction
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(type II diabetes mellitus)
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cholcalciferol (D3)--> 25 hydroxyvitamin D --> 1,25 dihydroxyvitamin D: what are the enzymes that convert at each step
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25-hydroxylase in liver and 1-alpha-hydroxylase (in kidney)
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where is vitamin D made
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in the liver and the kidney (two steps)
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what is calcitriol
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vitamin D (steroid)
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how is food vs. sun exposure different when making vitamin D
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ergocalciferol (D2) comes from food and calciferol (D3) comes from the sun exposure
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when you measure the level of hormones, what is important
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if they are counts for bound or unbound
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