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NURS 2090 (20)
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Altered Hormonal and Metabolic Regulation.docx

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Department
Nursing
Course
NURS 2090
Professor
Heather Helpard
Semester
Fall

Description
Altered Hormonal and Metabolic Regulation 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 Stress Response 1. Neurologic mechanisms: 1. ANS: Fight or Flight (↑ HR, BP, RR, pupil dilation, sweating) 2. Cerebral Cortex: cognitive actions 3. Limbic system: emotional activities and stimulates RAS 4. Thalamus: sensory input (vision, etc) 5. Hypothalamus: releases hormones to initiate neuroendrocrine response, acts on ANS 6. RAS (reticular activating system): increase alertness and muscle tension, helps stim ANS. 2. Hormonal mechanisms: 1. CRH (hypo) →ACTH (anterior) → Cortisol (adrenals) which is used to increase metabolism, regulate BG and anti-inflammatory effects. 2. Catecholamines (sympathetic nervous system) → adrenal glands Which induce a neurologic response to receptive organs (fight or flight) GeneralAdaptation Syndrome: 1. Alarm stage:  Catecholamines and cortisol are released in response to stim of SYPM, HP axis and adrenal glands. (fight or flight)  Prepare body for short and mild stress  Suppresses certain hormones: GH, thyroid, reproductive (to conserve energy)  Activates certain hormones: ADH (maintain BP) 2. Resistance stage:  Cortisol levels decrease through neg. Feedback  Cortisol helpful in the beginning but detrimental long term  Suppression of GH, thyroid and reproductive cause long term probs, and ADH leads to HTN and fluid retention 3. Exhaustion stage: depletion of energy and poor health. Body no longer responds. Short Term Cortisol Long Term Cortisol Energy creation: ↑metabolism by Exhaustion of inflammatory and immune breaking down proteins, releasing lipids, responses increasing glucose Excessive loss of body proteins and break down of tissues Glucose intolerance- diabetes Altered Hormone Function 1. Impairment of endocrine gland: damage to HP axis or glands Hypopituitarism: decreased secretion of one or more pituitary hormones Panhypopituitarism: decrease in pituitary hormones 2. Lack of/excessive hormone synthesis 3. Impaired receptor binding- less sensitive to hormone, (if you ↑weight, you need more hormone, ∆ you need to lose weight) 4. Impaired feedback mechanisms- thermostat not working, could be caused by ectopic hormones that come from tumors or inflammatory mediators. 5. Impaired cell response to hormones General Manifestations ofAltered 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 DetectingAltered Hormone Function  History and physical examination  Laboratory: serum or urine hormone levels and hormone suppression or stimulation tests  pregnancy= HcG  electrolytes (if kidney issues withADH)  Imaging studies: CT for enlarged glands/tumors  Genetic testing TreatingAltered Hormone Function  Dependent upon cause  Hormone excesses 1. Remove tumor secreting ectopic hormone 2. Remove part or all of endocrine gland 3. Medications that block effects  Hormone deficits 1. Medications that stimulate release or replace hormone Syndrome of InappropriateAntidiuretic Hormone (SIADH) Pathophysiology:  Excess production and release ofADH  Most common cause: ectopic secretion (cancer cells)  ADH promotes excessive water retention where it accumulates intracellularly and promotes altered cell function  Eventually sodium is diluted from extracellular space  Result: hypotonic hyponatremia (∆ look for hyponatremia symptoms; CNS changes) Clinical Manifestations:  Decreased urine output (concentrated like with dehydration)  Severity of symptoms dependent upon serum sodium levels 1. Anorexia, nausea, vomiting, 2. Headache, Irritability, disorientation (dehydration) 3. Muscle cramps, weakness (any time Na/K imbalance you get this) 4. Psychosis, seizures, coma Diagnostic Criteria  Hyponatremia (serum sodium <135 mEq/L)  Hypotonicity (plasma osmolality <280 mOsm/kg)  Decreased urine volume  Highly concentrated urine with a high sodium content Treatment  Remove cause (i.e. tumor in the posterior pituitary)  Water restriction (↓ edema)  Isotonic or hypertonic IV fluid replacement  Pharmacologic treatment (if due to a receptor) Diabetes Insipidus Pathophysiology:  InsufficientADH; inability to concentrate or retain water  Causes: (usually after surgery near hypothalamus, most common cause) 1. InsufficientADH production 2. Inadequate kidney response toADH 3. Water intoxication Clinical Manifestations:  Polyuria: Large volumes of urine  Excessive thirst  Hypernatremia/ Hyperosmolality  Shock/ death Diagnostic Criteria  History and physical examination (recent surgery/trauma)  Laboratory tests 1. Serum osmolality- look for low Na because extra fluid dilutes it! 2. ADH levels 3. Urine specific gravity Treatment  Treat cause  Hydration  Pharmacologic treatment Serum Na Serum OSM Urine OSM SIADH ↓ ↓ ↑ Dehydration ↑ ↑ ↑ DI ↑ ↑ ↓ Look at the urine! If it looks concentrated, then look for SIADH or Dehydration. If it is dilute, maybe it is DI!After you see irregularities with the urine, examine the Serum Na. (opposite Urine OSM/Serum Na indicates a problem) Too muchADH= edema, so you will have dilute Na, seen with SIADH Pt. LackingADH= getting rid of too much urine and becomes dehydrated, seen with DI Hyperthyroidism **Graves Disease is a type of Hyperthyroidism TRH → TSH → thyroid hormones (T3 active form/T4) Pathophysiology:  Condition of excess thyroid hormone due to 1. Excess stimulation of thyroid gland 2. Excess production of TSH  Medications can induce it also  Graves disease is most common form of hyperthyroidism 1. Autoimmune; IgG binds to TSH receptors (stimulates thyrotoxicosis) 2. Cause unknown Clinical Manifestations:  Goiter  Excess metabolic rate 1. Weight loss, Diarrhea 2. Agitation, restlessness, tremors, palpitations, tachycardia, weakness 3. Heat intolerance, s
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