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Altered Hormonal and Metabolic Regulation exam review note.docx

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Dalhousie University
NURS 2090
Heather Helpard

Altered Hormonal and Metabolic Regulation Review Metabolic regulation= homeostatic+ feedback (mostly negative) Characteristics of Hormones 1. Control: synthesis and release are controlled by tissues/organs (i.e. hypothalamus-pituitary axis) 2. Feedback: negative/positive 3. Patterns of secretion, metabolism, elimination 4. Receptor binding: must locate and attach to target 5. Action: Effects on target cells, tissues, organs Control Mechanisms (* memorize hormone name and function) Negative feedback mechanism example (TRH TSH  ; control of temperature Note: ovarian hyperstimulus syndrome: When doctors use the fertility drugs used to stimulate your ovaries, you will to produce more eggs in order to increase the fertility possibility. However, this clinical action might interrupt and impair the negative feedback mechanism. The over stimulating of ovaries will cause the enlargement, inflammation of ovaries; altered fluid balance and possible organ failure. Intervention: need to monitor blood work (especially LH/FSH level) regularly. Positive feedback loop example (oxytocin during labor and delivery) ----positive feedback is usually specific, less common If positive feedback loop interrupted, might cause the difficulty deliver birth (it’s a very dangerous situation). Stress Response (2 mechanisms: neurological and hormonal) 1- Neurologic mechanisms:  ANS: “Fight or Flight”, sympathetic (↑ HR, BP, RR, pupil dilation, sweating)  Cerebral Cortex: cognitive actions  Limbic system: emotional activities and stimulates RAS  Thalamus: sensory input (vision, etc)  Hypothalamus: releases hormones to initiate neuroendrocrine response, acts on 
 ANS  RAS (reticular activating system): increase alertness and muscle tension, helps 
 stim ANS. 2- Hormonal mechanisms: (4 hormones involved)  CRH (hypo) → ACTH (anterior) → Cortisol (adrenals) 
 : increase metabolism, regulate blood glucose and anti- inflammatory effects.  Catecholamines {epinephrine, norepinephrine, dopamine} (trigger by sympathetic nervous system) → (adrenal glands): induce a neurologic response (fight or flight) to receptive organs General Adaptation Syndrome: (3 Stages) describe neuroendocrine response and corresponding physiologic changes that initiated by a stressor 1. Alarm stage: Fight/Flight   Catecholamines and cortisol are released in response to stimulation of sympathetic nervous system, hypothalamic-pituitary axis 
 and adrenal glands.   Prepare body for short and mild stress   Suppresses certain hormones: GH, thyroid, reproductive (to conserve energy)   Activates certain hormones: ADH (maintain BP) 2. Adaptation stage: resistance   Cortisol levels decrease through neg. Feedback   Cortisol helpful in the beginning but “bad” for long term, lead to exhaustion of inflammatory and immune response, excessive loss of body protein and tissue breakdown, and glucose intolerance (lots of problems)   Suppression of GH, thyroid and reproductive cause long term problems, and ADH 
 leads to HTN and fluid retention 3. Exhaustion stage: depletion of energy and poor health. Body no longer responds. Altered Hormone Function 1- Impairment of endocrine gland: damage to HP axis or glands (3 consequences for HP axis damage) a. Hypopituitarism: decreased secretion of one or more pituitary hormones b. Hyperpituitarism: excess hormone secretion c. Panhypopituitarism: decrease in pituitary hormones  Because pituitary involve in LOT kinds of hormone secretion, damage to pituitary gland can cause a huge problem. (first thing to check) 2- Lack of/excessive hormone synthesis (relate to endocrine glands; can be impaired for lot of reasons, such as autoimmune destruction, degeneration, infection, inflammation, neoplastic, hypoxia…) 3- Impaired receptor binding- (4 possibilities) a. Decrease receptor number b. less sensitive to hormone(for example, Type 2 diabetes & insulin resistant) c. presence of antibodies (BLOCK the way) d. presence of tumor cell (colonizing to unaffected cell via receptor activity) Warning sign: same amount of certain circulating hormone level didn’t elicit a proper cellular response, or much less response than normal 4- Impaired feedback mechanisms- could be caused by ectopic 
 hormones that come from tumors, drug or inflammatory mediators. 5- Impaired cell response to hormones (ex. Allergy response) 6- Damage to metabolism and elimination mechanism General Manifestations of Altered Hormone Function  Variable depending upon the specific hormone and activity of the target tissue  Common excesses or deficits can be detected in relation to: 1- Growth 2- Reproductive function 3- Metabolism and energy level Detecting Altered Hormone Function  History and physical examination  Laboratory: serum or urine hormone levels and hormone suppression or stimulation 
 tests (detect honone response) a. pregnancy= HcG b. electrolytes (if kidney issues with ADH)  Imaging studies: CT or MRI for enlarged glands/tumors  Genetic testing 
 (mainly check for receptor mutation) Treating Altered Hormone Function  Dependent upon cause  Hormone excesses o Remove tumor secreting ectopic hormone o Remove part or all of endocrine gland o Medications that block effects  Hormone deficits o Medications that stimulate release or replace hormone Clinical Module Syndrome of Inappropriate Antidiuretic Hormone (SIADH) *Decreased sodium level in blood and concentrated urine Pathophysiology:  Excess production and release of ADH  Most common cause: ectopic secretion (tumor)  ADH promotes excessive water retention where it accumulates intracellularly and 
 promotes altered cell function  Eventually sodium is diluted from extracellular space  Result: hypotonic hyponatremia (in clinical look for hyponatremia symptoms; CNS changes) 
 Clinical Manifestations:  Decreased urine output (concentrated like with dehydration)
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