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Intro to endocrine
Clinical Medicine II
| Question | Answer |
|---|---|
| Function of the endocrine system | sex differential, reproduction, growth and development, metabolic fxns, emergency responses |
| How does the endocrine system | tight control of certain electrolytes, narrow limits, works w/ nervous sys, stress to response, hierarchy (chart) |
| What are catacholimines | epi and norepi |
| Fxn of catacholamines | flight or fight, ↑ HR, vasoconstriction, ↑ blood sugar ↑ATP |
| Fxn of corticoids | BP control |
| What are characteristics of chemical Messengers | secreted by endocrine glands, transported thru blood, target tissues, regulatory effects |
| Paracrine glands | secretions affects neighboring cells |
| Exocrine | externally excreted |
| What is the thyroid cascade | TRH→TSH→TH |
| Functions of hormones | alter rate of synthesis, alter biological acivity: EPI and Glucagon, Alter cell permeability of membranes |
| What is an enzyme cascade important | has exponentially exaggerated effects, w/o enzyme pathways very slow! |
| Fxns of insulin | alter permeability of cell membranes, ion flux, transport processes, membrane potential |
| Three main types of hormones | peptide/protein, amines, steroids |
| What are some other hormone-like proteins | vitamin A & D, neurotransmitters and neuropeptides, prostaglandins, growth factors, interferons, pheromones, chemotactic agents |
| Characteristics of peptide hormones | proteins, glycoproteins, oligopeptides, polypeptides, fast-acting, short T1/2 |
| How does synthesis occur for peptide hormones | we make it once cells are stimulated |
| What does C-peptide do | measure of insulin production |
| Will type 1 and 2 diabetes pt’s have a high c-peptide | type 1: low, type 2: high |
| Pancreas hormones | insulin, glucagon, somatostatin |
| Alimentary hormones | gastrin, secretin, ghrelin, CCK |
| Pit hormones | oxytocin, ADH, ACTH, TSH, GH, prolactin, LH, FSH |
| What is an amine hormone | tyrosine derived |
| 5 amine hormones | T4, T3, Epi, norepi, dopamine |
| What is T4, and T3 | T4: thyroxine, T3: Triodothyronine |
| Is T3, T4 fast or slow hormones | SLOW-acting, acting at the nuclear level, T4 T1/2: 7 days T3: 1 day |
| When would we use dopamine | acute HOTN, and parkinson’s |
| Fxn of dopamine | |
| Fight/ Flight response online | |
| What are catecholamines like | fast acting w/ short T1/2, emergent responses, |
| Characteristics of amine hormones | derivatives ofsingle aa, fast and slow acting |
| Types of steroid hormones | glucocorticoids: cortisol, mineralcorticoids: aldosterone, Estrogens, progestins, androgens, 1,25 dihydroxy-vit D3 |
| Characteristics of steroid hormones | steroid/cholesterol derivatives, nuclear response, lipophilic (need protein carriers), slow-acting→steady state |
| What are water-soluble hormones | peptides, proteins, amino acids (unbound) |
| Lipid-soluble hormones | steroids, carrier, free hormones |
| Receptor location and fxn for peptide hormones | PH: proteins, peptides, and amine hormones, bind to receptor w/ lock and key mechanism on cell surface |
| Receptor location and fxn for steroid homrones | both steroid, T3 and T4 act on cytoplasmic and nuclear receptors, can concentrate in the tissues or cells |
| How do water-soluble hormones work | bind to cell surface, lock-key, receptor on cell transports hormone’s message into cell |
| Do all cells work all over the body | some like insulin, others no like TSH |
| What are the 4 types of surface receptors | G-protines, receptor tyrosine kinase, cytokine, receptors, serine kinase receptors (Don’t NTK) |
| How do lipid soluble hormones work | bind to lipid soluble receptors in cells, transported into cell and nucleus which stimulates transcription, allow hormone to concentrate in specific tissue or cells |
| Fxns of insulin | promotes fat synthesis, inhibits breakdown of fat, helps glucose into the cells |
| How and why are receptors down-regulated | d/t too much hormone around, cell engulf receptors into cell→↓ cell surface receptors |
| When does this commonly occur | type 2 DM and insulin resistance d/t ↓ # receptors |
| Why do we want to have a steady state glucose in DM | to ↓ a floods of insulin and fluctuation |
| MOA of steroid hormones | hormone transported into nucleus (no surface receptor), initiates transcription of enzyme or protein causing cellular effects |
| What is the fxn of the 2nd messenger in the cell | phosphorylation of proteins (some makes proteins active, some inactive) |
| How are hormone secretion regulated | response to internal and external stimuli of the CNS, mediated by hypo-pit axis, controlled by –FB mechanisms |
| What is negative feedback | release hormone, substance released from target tissues, exerts bio effect, product of this turns off the synthesis of hormone up stream |
| -FB for Target Tissue regulation | substance released from target tissue regulates hormone eg: glucagon stimulates gluconeagensis at liver, liver releases glucose, which turns off glucagon |
| What is + FB | release of hormone promotes further hormone stimulation: oxytocin |
| 3 patterns and examples of hormone secretion | continuous: T4, Intermittent: Circadian-Gonadotropins and cortisol, cyclic- estrogen, progesterone, LH, FSH, Fluctuating: in response to ext stimuli-insulin, glucagon, aldosterone, ADH, PTH |
| What is released from hypothalamus for thyroid | TRH, acts on ant pit to release TSH, which goes to thyroid hormone in thyroid gland |
| What happens if we don’t have idodine in our body | can’t make thyroid hormone, TSH is high d/t –FB |
| What is a target tissue regulation of – FB | glucagon stimulates gluconeagenis at liver, liver releases glucose, which turns off glucagon |
| What is –FB hormone product regulation | ex: low Ca++→↑PTH→↑ ca++ absorbtion at GI and bone reabsorption→↑SCa++→↓PTH |
| Major functions of glands in the body | know em |
| Functions of the pancreas | alpha: secrete glucagon, beta cells: insulin, D cells: somatostatin |
| d/o of pancreas | DM or pancreatic cell tumors |
| what pancreas dz’s can cause dm | severe pancreatitis, and cystic fibrosis of the pancreas |
| Loss of libido, ED, amenorrhea, ↓ testosterone can result from | Tumor in ant pit causing ↓ LH and FSH |
| What causes marked wasting of the body | panhypopituitarinsm |
| What causes growth retardation, hypoglycemia, anemia | Autoimmune against TSH, post pit tumor |
| What causes ↑ sympth stimulation, goiter, ↑ metabolic rate, heat intolerance | ↑TSH production |
| causes of endocrine dysfunction with hyperfunction | neoplasms, autoimmune, itrogenic, infectious/inflammatory, activating receptors mutations |
| causes of resistance | receptor mutations, signaling pathway mutations, post-receptor defects (type 2 DM) |
| causes of hypofxn | autoimmune, iatrogenic (thyroid), infx/inflame, hormone mutations (GH), enzyme defects, nut. Def, hemorrhage of glands, |
| Common symptoms of endocrine d/os | body size/shape, metabolic effects: fatigue, weakness, local effects, reproduction/sexual, skin |
| How do we test for endocrine fxn | Hormone assays: ELISA or RIA (must remember patterns of secretion, Cyclic, Circadian |
| Whathormones usually remain at steady state | T4, T3 |
| When would we use 24hr urine sample for hormone tests | cortisol or catecholamines |
| Example for testing hypofxn | challenge oral glucose tolerance test |
| Example for testing hyperfxn | dexamethasone in Cushing’s syndrome dx: SHOULD turn off ACTH by –FB and ↓ cortisol, if no change in production: cushing’s |
| What do we do if we suspect adrenal insuff | cortisol level, stimulation test, recheck 30-60min later |
| Tx for endocrine dysfx | hormone replacement, suppression vs. surgery, sxs control |
| What does the pineal gland secrete | melatonin |
| Hormones of the adrenal medulla | epi and norepi |
| Hormones of the adrenal cortex | mineralcorticoids, glucocorticoids |
| Ant pit hormones | GH, prolactin, TSH, ACTH, FSH, LH |
| Post pit hormones | Oxytocin, ADH |
| Pancreas hormones | a: glucagon b: insulin c: somatostatin |
| Thyroid gland hormone | T3, T4, calcitonin (↓ serum Ca++) |
Created by:
becker15
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