Endocrine System Notes PDF

Endocrinefystem Neg Feedback regulates hormones Hormones Steroid acts in cell Peptide acts on cell Surface Amine fatty acid derivative hypothalamus C...

Endocrinefystem Neg Feedback regulates hormones Hormones Steroid acts in cell Peptide acts on cell Surface Amine fatty acid derivative hypothalamus Controls re lease of hormones in pituitary CRH TRH GnRH GnRH somatostatin thyroid gland makes Tz Ty also calcitonin iodine thyroid hormone TRH from hypothalamus controls release of TSH TSH from anterior pituitary controls release of thyroid hormone Thyroid gland hypothalamus THR thyrotropin releasing hormone anterior 5 TSH pituitary 73 Ty thyroid gland  T3 more potent than Ty calcitonin responds to cal ÉÉm level a calcium deposition in bone Functions Thyroid gland of reg growth development energy metabolism electrolyte balance with Primary something wrong thyroid gland Selundary 5 issue w function usually happens in pituitary gland Tertiary impacts hypothalamus Myxedema severe hypothyroidism bradycardia edema hypothermia weight gain enlarged tongue loma disorientation seizure Chronic hypothyroidism serum cholesterol disease support of cardiac coronary artery function resp function Hypothyroidism Hashimoto's disease  Health do not Teaching change brand of med w out doc Hyperthyroidis nervousness flushed skin rapid pulse weight loss poor heat toleration systolic BP bulging eyes exophthalmos hyperplasia overgrowth of lens Goiter Hashimoto's infiltration of white blood cells due to overstimulation from Grave's enlarged auto antibodies Exophthalmos common in Grave's disease Fibroblast muscle target eye turn into adipose tissue Thyroid storm uncontrolled hyperthyroidism stressors or radioactive iodine tx triggered by major Symptoms 38.5 any laudia 130bmpl agitation anxiety tremors restless confused psychotic systolic hypertension seizure coma collab care bodytemp hypothermia blanket mattress dified 02 be of 02 A Ihug iodine output of Removal of the parathyroidglands may result in hyponatremia  hyperactivity of Hyperthyroidism thyroid gland hormones sympathetic nervous system metabolic rate T hrt rate stroke causes flight or fight volume myocardial contractility and BP w out Thyrotoxicosis can occur hyperthyroidism but weight due Pt has appetite high needs to energy amiodavone antiarrhythmic heavy or hypo iodinated can develop hyper thyrodism Grave's hyper thyroidism TSH that bind to makes antibodies or dies enlarged gland hypertrophy diagnostic testing hyperthyroidism radioiodine uptake blood work thyroid ultrasound  I g p radioio line and surgery meds methim azole the PTU inhibit Propyl thiouracil hormones synthesis of thyroid but do not inactivate circulating thyroid hormone iodine a Kiodine inhibit synthesis release Beta blockers tontrol adrenergil signs and symptoms myocardial O2 demand destruction of Radioiodine progressive thyroid in special circumstances surgerysonly considerations Nursing vital monitor signs rate BP a temp watch for th in hrt watch for tremors heat intolerance irritability emotional changes monitor Blood cell count liver panels bilirubin transaminases including monitor blood glulose a ele Holytes Watch for iodine toxicity Hypothyroidism deficiency of thyroid hormones congenital hypothyroidism preventable w neonatal screening tx cause most common is chronic autoimmune thyroiditis or Hashimoto disease is loused by Selveton hypothyroidism OF TRH from hypothalamus or secretion of TSH from anterior pituitary gland  metabolic rate venergy glycosaminoglya build up in cells causing edim myxedema no pitting slow onset vague no specific hypo levels TSH in blood are Diagnostic elevated levels are Primary Tz Ty Ty norma Subclinical elevated TSH Tz med levo thyroxine in older adults use cautiously diabetes w cardio disease hypertension opposes the effects of levothyroxine of hyperglycemia insulin risk  Ty low if circulating levels of Tz are T of TSH release Thyroid hormones are high inhibited TSH Thyrotoxic crisis heightened response that sites in catecholamine receptor SNS effect intensifies blockers myocardia reduce meds beta oxygen demands thionamide block thyroid Sythesis PTY iodine block hormone release radio contrast glucocorticoids or iodinated Conversion of T4 73 and reduce promote vasomotor stability  Disease Chronic Pulmonary COPD cause airflow obstruction chronic bronchitis emphysema Patho physiology and Airflow limit is progressive associated w abnormal inflammatory response occurs inflamm response airways lung parechyma throughout vasculature and pulmonary of airway Star tissue and narrowing inflammatory response Chronic Bronchitis for 3 mths Cough Sputum in 2 consecutive yrs secretion and inflammation hyper to infect more susceptible resp mucus secreting glands and  globlet cells increase funct redued bronchial ciliary wall thicker mucus plugs airways works harder for 02 Risk factors occupational exposure airpollution sin Alpha 1 antitryp genetic 3 primary symptoms tough sputum dyspnea on exertion FEVI FVC rato assessment cannot force exhalation Pt below 701 therapy Pharmatologic bronino dilators tortilosteroids dangerous long term  I Bullectomy lung volume surgery lung transplant antitussive good to get sleep collab problems to apse of Atelectasis partial lungs of total Colapse Pneumothorax air fills space btwn lung king Ribs manodiattos outicosteroid B berfore C admin proper Emphysema Pink puffers distention of air space beyond bronchioles destruction of alveoli areolar surface dead space impaired O2 diffusion pulmonary cap bed pulmonary vascular  resistance artery pressure hypoxemia results pulmonary artery pressure cause right sided heart may failure Chronis inflammation Panulobular Centrilobular Both types PLE y impairs gas exchange Effg CLE Change in destroy resp bronchiole alveolar lobule duct aveolus peripheral aveoli space enlarged air loss change in dyspnea weight chest ventilation perfusion hyper expanded Hypoxemia 02 hyperraphia S hrt  RI e failure resp Asthma causeses hyper responsiveness mucosal edema and mucus production Allergy is the strongest predisposing factor most tommon chronic disease of childhood  Pathophysiology Clininal manifestations audible wheeze on expiration resp dyspnea hypoxemia cynosis Ploughing of muscles tachycardia use accessory LOC SOB lead to can Longer resp Cycle then cardiac Lab assessment allergy response ABGS elevated levels serum eosinophil IgE FUC forced vital capacity FEV Forced is volume PEF Peak expiratory flow Meds for asthma Quirk relief Long acting brothodialators corticosteroids one Beta Adrenergic agonist relax hide rot snogths inflammation Anticholinergic ium bromide reduce vagal tone of the airway Peak flow monitoring have moderate or severe asthma worsening symptoms environmental or unexplained response occupational exposures  Status Asthmaticus does not respond to lonvential therpy can progress quickly to asphyxiation most common scenario severe broncho spasm w mucus plugging leading to asphyxia epinephrine can lause rebound effect 4 24hr5