Endocrine System Medical Notes PDF

ENDOCRINE SYSTEM MEDICAL SURGICAL NURSING ​ Secretes hormones -​ Hormones are natural chemicals that target specific tissues -​ Use blood as a mode of transportation ​ Complex network of “ductless” glan...

ENDOCRINE SYSTEM MEDICAL SURGICAL NURSING ​ Secretes hormones -​ Hormones are natural chemicals that target specific tissues -​ Use blood as a mode of transportation ​ Complex network of “ductless” glands and organs ​ Uses hormones to control & coordinate your body’s metabolism, energy level, reproductive, growth and development, response to injury, stress, and mood. ​ Functions​ - Metabolism​ - Growth​ - Fluid and electrolyte imbalance​ - Reproductive processes​ - Sleep and wake cycles HORMONE - RECEPTOR ACTION Lock and Key Hormone Receptor Binding -​ problem occurs when there is problem with the hormone or tissue FEEDBACK CONTROL MECHANISM -​ depends on the body’s need A.​ Negative -​ for homeostasis [stability] -​ self regulation -​ stabilizing B.​ Positive -​ ex. oxytocin -​ release of hormone initiates actions that lead to an additional release of that hormone. BANOEY, KC HOPE U. 1  TRANS: Module 1 → Decreased Blood Volume → Decreased Blood Pressure → Infarction = NECROSIS PITUITARY GLAND ​ master gland 3.​ PITUITARY APOPLEXY ​ aka hypophysis ​ > Adenoma + Bleeding → outgrows blood supply → compression of PATHOPHYSIOLOGY blood vessels of the PG → Decreased DIRECT Vascular Supply → Decreased Function = > Hypothalamus → Posterior Pituitary Gland → DECREASED HORMONES neurophysins → neurological projections >Hormones COMPLICATIONS 1.​ ADH [antidiuretic hormone] ANTERIOR PG -​ vasopressin 1.​ GROWTH FAILURE -​ water-sodium retention 2.​ Oxytocin -​ love hormone > Decreased GH → Liver [Decreased IGF-1] -​ childbirth, breastfeeding = DWARFISM > Diagnostics: INDIRECT -​ Obtain IGF-1 > Hypothalamus → median eminence → blood -​ GH Stimulation test [arginine] vessel via hypophyseal portal system → Anterior -​ CT Scan, MRI, Angiography Pituitary Gland [adenohypophysis] > Interventions: > Hormones and Trophic Cells: -​ HGH at night 1.​ Growth Hormone: Somatotroph 2.​ Thyroid Stimulating Hormone: Thyrotroph 2.​ HYPOGONADISM 3.​ Prolactin: Lactotroph 4.​ Adrenocorticotropic Hormone: Corticotroph > Assessment: 5.​ Luteinizing Hormone: Gonadotroph 1.​ Female:​ 6.​ Follicle-Stimulating Hormone: - Amenorrhea 7.​ Melanocyte- Stimulating Hormone: - Anovulation​ Melanotroph - Low Estrogen levels​ - Breast Atrophy​ - Loss of bone density​ HYPOPITUITARISM - Decreased axillary & pubic hair > Pituitary gland does not produce normal - Decreased libido amounts of all the hormone 2.​ Male:​ > Low GTPALFM- AO - Decreased Facial hair - Decreased Ejaculate Volume​ CAUSES - Reduced Muscle mass​ 1.​ PITUITARY COMPRESSION - Decreased body hair​ > Macroadenoma [>10mm] - Decreased libido​ → destruction of PG → Loss of function = - impotence DECREASED HORMONES → compression of neural chiasma = > Diagnostics BILATERAL HEMIANOPIA -​ Obtain FSH/LH & sex hormone -​ CT Scan 2.​ PITUITARY DESTRUCTION -​ MRI > Sheehan Syndrome [ PP Hemorrhage]= DIC -​ Angiography NAME 2  TRANS: Module 1 > Interventions: b.​ Nephrogenic [drug related]​ 1.​ Female: - Problem in the kidney -​ hormone replacement 1.​ Lithium Carbonate [0.6-1.2] [combination: estrogen + 2.​ Hypokalemia progesterone] 3.​ Hypercalcemia -​ Complication: > destroy vasopressin & hypertension aquaporin → doesn’t allow deep vein thrombosis kidney to accept ADH 2.​ Male: > Diagnostics: -​ Sex Steroid therapy with ​ Obtain Serum Na androgens ​ Water Deprivation Test -​ require high doses ​ Obtain Osmolarity -​ Side Effects:​ ​ Obtain DDAVP Gynecomastia ​ CT Scan Acne​ ​ MRI Baldness​ > Treatment Prostate Enlargement ​ Desmopressin: synthetic form of vasopressin ​ Aqueous Vasopressin: short term 3.​ LACTATION FAILURE therapy -​ inability to produce breast milk after giving birth PANHYPOPITUITARISM 4.​ HYPOTHYROIDISM > Simmonds Disease or Pituitary Cachexia -​ TG can’t produce enough thyroid hormone > decrease in all the hormones of the APG [GTPALFM] 5.​ ADRENAL INSUFFICIENCY CAUSES -​ AG can’t produce enough cortisol 1.​ Pituitary Damage 2.​ Pituitary Compression POSTERIOR PG 3.​ Sheehan’s Syndrome 1.​ DIABETES INSIPIDUS HYPERPITUITARISM -​ water loss problem caused by either an ADH > Overactive Pituitary Gland deficiency or an inability of the kidneys to > Increase in 1 or all of its hormones respond to ADH > Classifications: CAUSES a.​ Neurogenic​ 1.​ Tumors​ - primary, secondary​ - microadenoma [ Increased ADH​ ANTERIOR > receptor: vasopressin 2 [kidneys]​ > Increased ADH → Increased Vasopressin 2 → 1.​ ACROMEGALY Increased aquaporins → affecting tubules → blood ​ = Increased H20 in blood causes serum osmolarity​ > Increased GH = OSA​ → urine = Decreased H20 causes increase in urine > adults​ osmolarity​ > Diagnostics:​ → Na = HYPONATREMIA [dilutional hyponatremia]​ ​ - Obtain IGF-1​ > Causes: ​ - CT Scan​ A.​ Conditions leading to hypoxia​ ​ - MRI​ - intracranial Dse ​ - OGTT​ - Drugs: SSRI, Carbamazepine, TCI > Interventions:​ B.​ Ectopic ADH Production​ ​ a. Dopamine Agonists​ > cancer cells express neural antigens ​ - Bromocriptine​ that cause the body to produce ​ - Cabergoline​ antibodies that cross-react with ​ - Pergolide​ neural tissue ​ b. Somastation & GH Receptor Blocker​ ​ - Octreotide​ ​ - Pegvisomant​ ​ c. Radiation Therapy​ ​ d. Hypophysectomy​ ​ e. Craniotomy​ 2.​ HYPERPROLACTINEMIA ​ > increase in prolactin ​ >Assessments:​ ​ - loss of secondary sexual characteristics​ ​ - decreased gonadotropin levels​ ​ - galactorrhea​ ​ - Increased body fat​ ​ - increased serum PRL levels​ ​ > Diagnostics:​ ​ - obtain PRL level​ ​ - CT Scan​ ​ - MRI​ ​ > Intervention​ ​ - Cabergoline or Bromocriptine​ ​ - Transphenoidal resection of adenoma POSTERIOR 1.​ SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION [SIADH] > body makes too much ADH NAME 4  TRANS: Module 1 COMPLICATIONS PARATHYROID GLAND ​ 2 pair of small, oval shaped glands 1.​ TETANY ​ Located next to the thyroid gland lobes in the neck Decreased PTH = Decreased Ca ​ Pea-sized [3-4mm] > Low Ca → Na influx in the neurons → ​ Produce Parathyroid Hormone neuronal depolarization → Increased action potential/ neurotransmitters → Increased nerve excitability HYPOPARATHYROIDISM a.​ Facial nerve= Chvostek Sign > Under drive of the parathyroid gland b.​ Brachial nerve= Trousseau Sign c.​ Seizures= Possible perioral paresthesia CAUSES [ twitching inside the mouth] 1.​ Iatrogenic- Parathyroid Destruction > Hospital acquired a.​ thyroidectomy 2. TORSADES DE POINTES b.​ parathyroidectomy > Twisting of the Points 2.​ Idiopathic- Autoimmune > Prolonged QT interval >Unknown cause [can lead to V.Fib, then sudden a.​ Autoimmune Polyglandular Syndrome cardiac arrest, lastly, death] [APS] → due to dysfunction in the AIRE CARDIAC ACTION POTENTIAL [Autoimmune Regulator] gene → Phase 4- resting potential attacks parathyroid gland → Phase 0- rapid depolarization Increased PTH Phase 3- plateau phase [longest phase] S/Sx: Mucocutaneous Candidiasis Phase 2- rapid repolarization Adrenal Failure Phase 1- rapid depolarization Hypoparathyroidism SITES OF ABSORPTION OF CALCIUM APS is a rare disease that occurs when the 1.​ Osteoclasts: Bones to Blood body’s immune system attacks multiple 2.​ Kidney → Distal Convoluted Tubule [DCT] → glands Blood 3.​ Kidney → Proximal Convoluted Tube [PCT] → 3.​ Absent Parathyroid Gland Vitamin D to its active form >DiGeorge Syndrome 4.​ Vitamin D [ transporter of Ca] → small > Due to the absence of the 3rd and 4rth intestine [ jejunum, ileus] pharyngeal pouches > Pharyngeal Pouches PSEUDOHYPOPARATHYROIDISM -​ due to lack of chromosome 22 -​ responsible for the formation of > Albright Hereditary Osteodystrophy structures like the thymus, palatine > Problems in the receptor sites tonsils & parathyroid glands. > PTH Resistance S/Sx: CATCH 22 > Autosomal Dominant [Maternal Side] Cardiac Defects > S/Sx: Short Stature Anomalous Face Brachydactyly Thymus hypoplasia- risk for infection Developmental problems Cleft Palate Hypoparathyroidism NAME 5  TRANS: Module 1 PSEUDOPSEUDOHYPOPARATHYROIDISM HYPERPARATHYROIDISM > Autosomal Dominant [Paternal side] > Overdrive of the parathyroid gland > no PTH resistance CAUSE > Normal PTH & Ca Levels > S/Sx: Short Stature 1.​ Adenoma Brachydactyly > Benign tumor that gained capacity to Developmental problems secrete hormone [PTH] 2.​ Multiple Neoplasia Type 1 ASSESSMENT > Hyperplasia of the parathyroid gland 1.​ Obtain Patient info about: > Enlargement of the PTG → Increased PTH ​ Any head or neck surgery, head or a.​ Adenoma of the Pituitary gland, neck radiation therapy [check for Pancreas, Parathyroid Gland scar] b.​ Medullary Thyroid Cancer ​ Hx of serious neck injury Pheochromocytoma- adrenal ​ Presence of tingling and numbness medulla around the mouth, hands and feet Parathyroid Gland ​ Presence of muscle cramps and TYPES hand & feet spasm 2.​ Assess for Hypocalcemia Signs and PRIMARY symptoms a.​ Bone [osteoclasts] → Increased Ca bone to ​ Irritability or psychosis blood = hypercalcemia ​ Tetany b.​ DCT → Increased Ca → blood = ​ bands/pits encircling the crowns of Hypercalcemia teeth c.​ PCT → Increased Vit. D activation → Increased Ca in Small intestine → blood = DIAGNOSTICS Hypercalcemia 1.​ Serum Electrolyte Tests > Vit. D, PTH, Ca SECONDARY 2.​ CT Scan > Occurs when the body produces more PTH in 3.​ Urine Cyclic Adenosine Monophosphate response to low Ca levels [CAMP] levels > Can be caused by Vit. D deficiency or renal failure a.​ Vit. D Deficiency INTERVENTIONS PCT → Low Vit. D Activation → Low Ca → 1.​ Medical Management Low Ca in Small intestine → Low Ca in Blood a.​ IV calcium gluconate = Hypocalcemia b.​ PTH replacement b.​ CKD c.​ Oral Vit. D ​ Increased PO4 bind to Ca → Low Ca 2.​ Nursing Intervention = hypocalcemia a.​ Teaching about the drug regimen ​ Vit. D not activated → Low Ca and interventions to reduce anxiety absorption = Hypocalcemia b.​ Teaching client to eat foods high in calcium but low in phosphorus Decreased Ca triggers production of PTH by c.​ Reiterate that hypocalcemia therapy negative feedback. is lifelong d.​ Medical Bracelet alert TERTIARY e.​ Monitor and manage seizure > Characterized by excessive PTH secretion after f.​ Monitor neuromuscular function long standing secondary hyperparathyroidism g.​ Tracheostomy @ bedside NAME 6  TRANS: Module 1 > Usually affects people with chronic kidney disease 6. PSYCHIATRIC OVERTONES who are on dialysis. a.​ ESRD/ESKD > Increased Ca → Decreased neuronal excitability Low Ca trigger PTG [hyperplasia] = Increased → Decreased neuron firing = depressed & confused PTH patients Bone Resorptive Process = Increased Ca PO4 = not excreted 7. CONSTIPATION > Increased Ca → Low Smooth muscle contraction → decreased Peristalsis = constipation > Increase fiber and oral fluid intake ASSESSMENT 1.​ Obtain patient info about: ​ Bone Fractures ​ Weight loss COMPLICATIONS ​ Arthritis 1.​ NEPHROLITHIASIS ​ Hx of Kidney stones 2.​ Assess for: > Increased Ca excreted by kidney combines w/ ​ Bone deformities oxalates = Calcium oxalate stones ​ GI manifestations [ ANorexia, N/V, > UTI, Hematuria Epigastric pain] ​ Fatigue and lethargy 2. PATHOLOGICAL FRACTURES ​ Lab values > Massive resorptive process → Increased Ca bones DIAGNOSTICS to blood → osteopenia/ osteoporosis = Pathological 1.​ Serum Electrolyte Levels fractures 2.​ Serum PTH and Urine CAMP levels 3.​ CT Scan 3. PANCREATITIS 4.​ X-ray showing Ca deposits, renal stones or bone problems > Increased Ca → activate pancreatic enzymes → Inflammation → epigastric pain INTERVENTIONS 1.​ Nonsurgical 4. NEPHROGENIC DIABETES INSIPIDUS a.​ calcitonin b.​ plicamycin > Increased Ca → Decreased ADH → Decreased V2 c.​ IV saline → Urine d.​ gallium [ganite] > Polyuria, Polydipsia, Dehydration 2.​ Surgical a.​ Parathyroidectomy 5. BRADYCARDIA [removal of one or more parathyroid > Increased Ca → Low QT interval → risk for glands] bradycardia 3.​ Nursing management > Monitor VS a.​ Evaluate VS, cardiac rate & rhythm, ECG monitoring b.​ I & O monitoring c.​ close monitoring of serum Ca levels NAME 7  TRANS: Module 1 d.​ Diet modification: low Ca and Vit. D -​ severe physical and mental [post op: high Ca, fat and retardation due to iodine carbohydrates] deficiency e.​ Strain urine [calculi] -​ short stature, developmental f.​ Injury prevention delays THYROID GLAND 2.​ Destruction of Follicular Cells PRIMARY ​ butterfly shaped organ in the neck [ Increased TSH, Decreased T3T4 ] ​ located just under the skin a.​ Autoimmune Diseases [Painless] ​ connected in the middle [isthmus] ¬ body attacks own tissues → ​ 2 inches [5cm] in size immune reaction → destruction of TG ​ fight or flight response → Low T3T4 ​ Produce T3 [Triiodothyronine] T4 [Thyroxine] ​ HASHIMOTO’S DISEASE hormone > Permanent > Enlarged and inflamed FUNCTIONS underactive thyroid 1.​ Regulate the body’s metabolic rate > Chronic autoimmune 2.​ Growth and development thyroiditis [anti-TPO; anti-TGB] 3.​ Plays a role in controlling heart, muscle and > HLA [D3&D4] mutation → digestive function, brain development and alteration to immune function bone maintenance → underproduction of T3T4 *HLA: Human Leukocyte PATHOPHYSIOLOGY Antigen Hypothalamus produces TRH → Anterior Pituitary Gland produces TSH → follicular cells → ​ TRANSIENT HYPOTHYROIDISM Thyroglobulin binds with Iodine via TPO → Thyroid > Postpartum Hypothyroidism gland produces T3T4 > Occurs postpartum [ Rare and often temporary Follicular cells: structural and functional cells of the > Anti-TPO thyroid gland > TG can regenerate & TPO: Thyroid peroxidase self-limiting Thyroglobulin + Iodine: structural framework of T3T4 ​ RIEDEL’S THYROIDITIS HYPOTHYROIDISM > Riedel Struma, Ligneous > Under drive of the thyroid gland Struma, Chronic Invasive > aka Underactive thyroid Fibrous Thyroiditis > Low T3T4 > Problem with IgG4 antibodies CAUSES > Fibroblast production → 1.​ Iodine Deficiency increase in fibrous tissues → > Iodine is a mineral that helps the thyroid replace N tissues w/in the TG gland produce hormones that regulate → Low T3T4 metabolism, digestion, and HR → Too low > Compression Effects: iodine → thyroid gland can’t produce -​ RLN: hoarseness of enough hormones = Hypothyroidism voice a.​ Cretinism -​ Trachea: stridor NAME 8  TRANS: Module 1 -​ Esophagus: dysphagia 2.​ METABOLIC DYSFUNCTION > Low T3T4 → Low ATP → Low Na & K Pump b.​ Infection [Painful] Activity → Low metabolic rate ¬ De Quervain’s Thyroiditis -​ [catabolic] → unconverted glucose, ¬ aka Subacute Granulomatous fats = WEIGHT GAIN Thyroiditis -​ low heat generation → decreased ¬ due to upper viral respiratory body temperature = COLD infection INTOLERANCE ¬ signs and symptoms of infection ¬ inflammation → damages follicular 3.​ NEUROLOGIC DYSFUNCTION cells → direct injury to TG → Low T3T4 > Total body energy expenditure can slow down c.​ Iatrogenic > Low T3T4 → Low Metabolic Rate → Brain ¬ Hospital acquired or surgery [Efferent nerves] → Decreased Neuron ¬ removal of TG due to cancer/ excitability → Depression, lethargy, Severe hyperthyroidism → T3T4 not Fatigue, Decreased DTR produced DTR ¬ Wolff-chaikoff Effect +0 = Absent -​ temporary physiological +1 = Diminished response that occurs when +2 = Normal the TG is exposed to high +3 = Hyperactive levels of iodine +4 = Hyperactive + Clonus -​ High Iodine → negative feedback → Low T3T4 4.​ CARDIOVASCULAR DYSFUNCTION production > Low T3T4 → Low Beta 1 receptor sensitivity -​ Causes → Low HR and Contractility = Bradycardia > Chronic intake of → Decreased dilation → Constriction → amiodarone Increased SVR = Increased BP > Radioactive iodine therapy ​ > Beta 1 [dilation of the heart] is affected by T3T4; lowers HR and contraction ​ SECONDARY > Low T3T4 → Decreased LDL Receptor ​ [ Decreased TSH, Decreased T3T4] expressed a.​ Pituitary Adenoma → LDL not transported from bloodstream to Compress the Pituitary gland liver → hyperlipidemia = ATHEROSCLEROSIS thyrotrophs → disrupt blood flow of hypothalamus and PG → damage 5.​ REPRODUCTIVE DYSFUNCTION PG normal cells > Low T3T4 → triggers APG → Increased PRL b.​ Sheehan’s syndrome → Estrogen + Progesterone = Menstrual Pituitary defect, hypovolemic shock, Dysfunction [amenorrhea, menorrhea, ischemic necrosis → damage the PG Infertility, Decreased Libido → Failure to produce enough TSH > PRL can interfere with the ovaries ability to produce estrogen CLINICAL MANIFESTATIONS 1.​ GOITER 6.​ GASTROINTESTINAL DYSFUNCTION > describe any enlarged thyroid gland > Low T3T4 → Low smooth muscle > constant low T3T4 undergo replication → contractility → decreased peristalsis = hypertrophy of TG → Enlargement = GOITER CONSTIPATION NAME 9  TRANS: Module 1 7.​ INTEGUMENTARY DYSFUNCTION ​ Levothyroxine [Levo T, Synthroid] > Low T3T4 → Increased TRH & TSH → -synthetic form of T4 production of fibroblast → GAG -long acting; less potent [glycosaminoglycans] → edema = Pretibial ​ Liotrix [Thyrolar] Myxedema [main], periorbital edema, CTS -synthetic form of T3 SUMMARY -short acting Low T3: Metabolism & GI tract -more potent -​ Weight gain ​ *both are given before Meals in the morning -​ Constipation ​ *not to be given with laxatives Low T4: Heat, Energy production 2.​ Laxatives for constipation -​ Cold Intolerance 3.​ Encourage moisturizer use for dry skin -​ Shivering, Dry 4.​ Encourage to exercise regularly -​ Brittle nails & hair SNS HYPERTHYROIDISM -​ Lethargic > Overdrive of the thyroid gland -​ Decreased HR CAUSE COMPLICATIONS PRIMARY > Increased T3T4, Decreased TRH & TSH MYXEDEMA COMA/ MYXEDEMA CRISIS 1.​ Graves Disease [Autoimmune] > TSH-R mimicry in the TG → TSI [Thyroid > Severe form of Hypothyroidism Stimulating immunoglobulin → Increased T3T4 > Life threatening > occur when there is Low T3T4 + Metabolic stress 2.​ Toxic Adenoma ​ Metabolic stress: [surgery, infection, > 1 adenoma hypothermia, non-compliance to > it produces to much thyroid hormone = maintenance-levothyroxine] Increased T3T4 increases metabolic demand > can lead to encephalopathy → confusion 3.​ Toxic Multinodular Goiter → difficulty being aroused = COMA > enlarged thyroid with multiple nodules > decreased HR & contractility + increased producing too much thyroid hormone SVR → Acute Heart Failure 4.​ Jod-Basedow Phenomenon DIAGNOSTICS > aka Iodine-induced hyperthyroidism 1.​ Thyroid Function Test > High Iodine Causes 2.​ Pituitary MRI -​ chronic use of amiodarone 3.​ Anti-TPO/ Thyroid Gland Antibodies -​ radioactive iodine therapy -​ Pathological response ASSESSMENT ​ > results to Increased T3T4 1.​ Check the patients ​ Weight SECONDARY ​ Appetite > Increased T3T4, TRH & TSH ​ Fluid intake 1.​ Pituitary Microadenoma 2.​ Monitor response to medication > secretes TSH causing hyperthyroidism due 3.​ Check laboratory results to assess thyroid to stimulation of TG to produce excess hormone levels thyroid hormones TREATMENT CLINICAL MANIFESTATION 1.​ Hormone replacement therapy NAME 10  TRANS: Module 1 1.​ GOITER KOCHER’S SIGN = Thyroid store; ”staring > occur only in secondary hyperthyroidism look”, “Frightening Eyes” > High T3T4 → Increased TRH & TSH → replication → Hypertrophy COMPLICATIONS 2.​ METABOLIC DYSFUNCTION THYROID STORM > High T3T4 → Na & K pump → ATP usage → Increased metabolic activity → macronutrients to smaller units = WEIGHT Severe form of hyperthyroidism LOSS Abrupt onset and being left untreated is → heat generation → increased body temp fatal = HEAT INTOLERANCE [Sweaty, Diaphoretic] Increased T3T4 + Metabolic stress > Increased HR Contractility & Decreased 3.​ NEUROLOGIC DYSFUNCTION Vasodilation → Decreased Afterload → SVR > High T3T4 → Increased BMR → Increased → Increased Cardiac Output = HEART neuronal excitability = Irritability, Insomnia, FAILURE Anxiety, Agitation Manifestations ​ High Fever 4.​ CARDIOVASCULAR DYSFUNCTION ​ Extreme Tachycardia > High T3T4 → Increased Beta 1 ​ Exaggerated S/Sx of Hyperthyroidism → Increased contractility ​ Delirium → High HR → Tachycardia → Increased ​ Psychosis Dilation & Constriction = VASOPLEGIA/ ​ Coma VASODILATED DIAGNOSTICS 5.​ REPRODUCTIVE DYSFUNCTION 1.​ Thyroid Function Test > High T3T4 → Increase Thyroxine-binding 2.​ Pituitary MRI Globulin → S → Menstrual irregularities, 3.​ CT Scan Decreased Libido, Infertility 4.​ T3T4 levels INTERVENTIONS 6.​ GASTROINTESTINAL High T3T4 → Increased Small muscle 1.​ Antithyroid Medications contraction → Increased Peristalsis → -​ inhibits synthesis or secretion of T3T4 DIARRHEA -​ Propylthiouracil [PTU] -​ Methimazole [Tapazole] 7.​ INTEGUMENTARY -​ block extrathyroidal conversion of > High T3T4 → Increased TSH → Activate T3T4 TSH-R -​ Thioamides & Decreased WBC = → Fibroblast → GAG → Edema → Pretibial Agranulocytosis Myxedema 2.​ Surgical → Adipose Tissue [eye] → Swelling → Eye -​ THYROIDECTOMY: protrusion = EXOPHTHALMOS > removal of a part or lobe of TG VON GRAEFE’S SIGN = Lid lag 3.​ Radioactive Iodine Therapy JOFFROY’S SIGN = Lack of wrinkling in -​ destroys over productive thyroid cells forehead -​ tasteless, colorless radioiodine DALRYMPLE’S SIGN = Lid retraction -​ starts within several weeks -​ second dose if 1st dose unsuccessful NAME 11  TRANS: Module 1 ADRENAL GLAND ADDISON’S DISEASE > aka Adrenal Insufficiency ​ aka Suprarenal glands > decrease in all of the hormones ​ small, triangular-shaped ​ located on top of kidney CAUSE 1.​ AUTOIMMUNE FUNCTIONS > Autoimmune Polyglandular Disease [APS] 1.​ Hormone Production -​ can cause adrenal insufficiency by 2.​ Stress response destroying the adrenal cortex 3.​ Blood sugar > body attacks itself → antibodies [21 4.​ Salt and water balance hydroxylase antibodies] → multiple layers of 5.​ Sex Development AG → Decrease function of AG → Decreased hormones 3 ZONES 1.​ Zona Glomerulosa 2.​ ADRENAL INFECTION > Mineralocorticoids → Aldosterone > TB [Mycobacterium Tuberculosis] → lung > Aldosterone is responsible for: infection → blood stream [miliary -​ Na & H20 reabsorption tuberculosis] → Adrenal Gland → Decreased -​ K excretion Function → Decreased secretion of -​ H+ excretion Hormones > TB can destroy the AG 2.​ Zona Fasciculata > It can cause caseous necrosis, fibrosis, > Glucocorticoids → Cortisols calcification, and tuberculosis granuloma. > Cortisol is responsible for -​ Stress response 3.​ ADRENAL HEMORRHAGE -​ Sugar > aka Waterhouse-Friderichsen Syndrome -​ Immune Suppression [WFS] or Hemorrhagic Adrenalitis -​ Protein Breakdown > bleeding into the glands -​ Calcium Management > Meningococcemia [neisseria meningitidis] → bilateral bleeding → Decreased function 3.​ Zona Reticularis → Decreased hormone secretion > Androgens → Secondary characteristic > S/Sx: > Mustache, breasts, etc. -​ Rash -​ Fever 4.​ Adrenal Cortex​ -​ Sepsis > GMA -​ Stiff neck 5.​ Adrenal Medulla 4.​ ADRENAL METASTASIS > Adrenaline; Noradrenaline > Cancer has spread to the AG from other parts of the body 6.​ Other Hormones > Tumor → Infiltrate organs → AG → > Adrenal Decrease function → Decreased hormone secretion > Common Sites of Metastasis: -​ Adrenal Gland -​ Bone -​ Liver -​ Lungs NAME 12  TRANS: Module 1 5.​ PITUITARY SUPPRESSION > Secondary 3.​ CARDIOVASCULAR DYSFUNCTION > Exogenous source of steroids in the blood > Decreased cortisol → decreased AI → can cause the AG to reduce or stop Decreased Vasoconstriction → Systemic production of cortisol, and go into sleep-like Vascular resistance state → Vasodilation → VASOPLEGIA → Shock > Exogenous Corticosteroids → body detects → Decreased SVR → DECREASED BP enough/ increased cortisol → Negative feedback → Hypothalamus won’t produce > Types of shock: CRH + APG won’t produce ACTH → a.​ Hypovolemic Hypotrophy of AG → disruption/ = Decreased blood volume non-compliance/ abrupt discontinuation of b.​ Cardiogenic exogenous steroid → Increased Demand, = Heart problem Decreased supply → Decreased Hormone c.​ Distributive secretion = Widespread Vasodilation [blood vessels] CLINICAL MANIFESTATION d.​ Neurogenic 1.​ NEUROLOGICAL DYSFUNCTION = Brain [ Hypo, Brady, Brady] > Cortisol = SNS activity ​ > Decreased Aldosterone > Decreased cortisol → Decreased SNS → Decreased Na & H20 Reabsorption = activity → Decreased fight/flight response = HYPONATREMIA [Tall Peak T waves, Flattened fatigue, drowsiness, lethargy → confusion, P wave, Widened QRS, ST Depression] difficult to arouse, coma → Decreased K excretion = HYPERKALEMIA → Decreased H+ excretion = ACIDOSIS a.​ Adrenal Crisis: > Decreased GMA + stress → 4.​ RENAL DYSFUNCTION Multiplied S/Sx > Manifestations such as Hypotension, > S/Sx Hyponatremia, Hyperkalemia and Acidosis -​ Lightheadedness/ Dizziness -​ Weakness 5.​ INTEGUMENTARY DYSFUNCTION -​ Sweating > Decreased Cortisol → Increased CRH & -​ Abd Pain ACTH → POMC → Increased A-melanocyte -​ N/V R-1 → Melanin = BRONZE SKIN -​ Loss of consciousness > Low Cortisol → Low ATP = MUSCLE 2.​ METABOLIC DYSFUNCTION WEAKNESS > CORTISOL is a -​ Counter regulatory hormone ASSESSMENT -​ glucose homeostasis ​ Manifestation for Hypoglycemia -​ Pathways: -​ Low blood glucose a.​ Glycogenolysis: breakdown of -​ Sweating glycogen = Glucose -​ Headaches b.​ Gluconeogenesis: Synthesis of -​ Tachycardia Glucose from NON-CARB -​ Tremors sources to GLUCOSE > Decreased Cortisol → Decreased function of pathway = DECREASED BLOOD SUGAR LEVELS NAME 13  TRANS: Module 1 ​ Manifestations of Hypovolemia 2.​ ENDOGENOUS -​ Postural Hypotension > usually due to tumor in the AG or PG -​ Dehydration > Tumor in the PG/AG → Increased ACTH & GMA = Increase in Hormone Production ​ Cardiac Problems from Hyperkalemia -​ Dysrhythmias -​ T-wave changes ECTOPIC ACTH PRODUCTION > non-pituitary tumor produces and releases ACTH ​ Muscle Weakness resulting to Hypercortisolism ​ Electrolyte Abnormalities > Small Cell Lung Cancer → Paraneoplastic ​ Areas of Increased Pigmentation Syndrome ​ Decreased alertness, Forgetfulness, Confusion CUSHING’S DISEASE DIAGNOSTICS > a type of cushing syndrome 1.​ Medical Hx and Physical Exam > Benign tumor in the PG that secretes too much 2.​ Blood & Urine Test ACTH that triggers increased cortisol secretion from -​ measure adrenal hormone and ACTH the AG. 3.​ ACTH Stimulation Test CLINICAL MANIFESTATIONS -​ measure cortisol in blood before and after synthetic ACTH 1.​ GLUCOCORTICOSTEROIDS 4.​ Imaging Test a.​ Increased Cortisol → trigger lipolysis → -​ X-ray, MRI, UTZ redistribution of fats → axial skeleton= -​ MOONFACE INTERVENTIONS -​ TRUNCAL OBESITY 1.​ Replacement Therapy -​ BUFFALO HUMP a.​ Hydrocortisone -​ for corticosteroid deficiency b.​ Increased Cortisol → Increased b.​ Fludrocortisone Immunity suppression = -​ for Aldosterone deficiency -​ INCREASED RISK FOR INFECTION​ 2.​ Nursing Management a.​ Weigh patients daily c.​ Increased Cortisol → Increased b.​ Monitor VS Protein Breakdown [proteolysis] → c.​ Check for Dysrhythmias decreased collagen = d.​ Monitor Glucose levels -​ EASY BRUISING e.​ Monitor Lab Values -​ STRIAE “PURPLE” -​ WEAKNESS -​ STRETCH MARKS​ CUSHING’S SYNDROME d.​ Increased Cortisol → Decreased > increase in all of the hormones Calcium → Osteopenia → Osteoporosis = CAUSE -​ PATHOLOGICAL FRACTURE​ 1.​ EXOGENOUS > due to side effects of medications taken to e.​ Increased Cortisol → Increased Stress treat other conditions -​ avoid stress f.​ Increased Cortisol → Increased Glucose NAME 14  TRANS: Module 1 -​ HYPERGLYCEMIA​ 2.​ Surgery -Adrenalectomy g.​ Increased Cortisol → Increased SNS 3.​ Radiation Therapy activity → agitated, insomnia 4.​ Medications -​ PSYCHOSIS -​ Ketoconazole -​ Mitotane [Lysodren] 2.​ MINERALOCORTICOIDS -​ Osilodrostat [Isturisa] Increased Aldosterone -​ Levoketoconazole [Recorlev] a.​ Increased Na & H20 reabsorption -​ Metyrapone [Metopirone] = HYPERNATREMIA 5.​ Nursing Management b.​ Increased K excretion​ a.​ monitor sugar = HYPOKALEMIA b.​ avoid crowded places and infection c.​ Increased H+ Excretion c.​ avoid stress = ALKALOSIS d.​ Increase protein, calcium, Vit. D, Potassium 3.​ ANDROGEN e.​ Decrease sodium, fluid intake Increased Androgens restriction = Increased Secondary Characteristics f.​ therapeutic communication a.​ Masculinization : HIRSUTISM g.​ Post op: WOF ADDISONS b.​ Feminization: GYNECOMASTIA 4.​ OTHERS a.​ BRONZE SKIN DEXAMETHASONE -​ low dose -​ stimulant for the Hypothalamus & APG DIAGNOSTICS 1.​ Serum PTH and Urinary Free Cortisol [UFC] Test: -​ measure amount of cortisol in urine for 24hrs 2.​ Late Night Salivary Control [LNSC] Test -​ measure cortisol level in the saliva in the late evening 3.​ Dexamethasone Suppression Test -​ determines if body is producing too much cortisol 4.​ ACTH level -​ Measure ACTH in blood or urine 5.​ Scalp-Hair Cortisol/ Cortisone Analysis -​ Evaluate long term exposure to glucocorticoids 6.​ CT Scan 7.​ MRI INTERVENTIONS 1.​ Reducing Glucocorticoid use PANCREAS NAME 15  TRANS: Module 1 ​ dual system [Endo and GI] > Increased Blood Glucose → use of ATP → ​ large tadpole-shaped gland Increased Catabolic State → Increased ​ located on deep in the abdomen, tucked Appetite behind the stomach ​ Hormones: COMPLICATION a.​ Insulin: ​ - transfer glucose from blood to cells​ DIABETIC KETOACIDOSIS [DKA] - lowers glucose​ > A life threatening problem that affects people with - from beta cells​ Diabetes. > more than 250 mg/dL b.​ Glucagon:​ > Decreased/ No insulin → alternative pathways to - store glucose in the liver for usage​ produce ATP → unused carbohydrates → use - increase glucose​ proteins and lipids → lipolysis → Acetyl CoA → NO - from alpha cells Krebs Cycle → alternative → KETONE BODIES produces: FUNCTIONS a.​ FRUITY ODORS 1.​ Produce enzymes for protein digestion b.​ CO2 = KUSSMAUL'S RESPIRATION 2.​ Makes hormone: INSULIN c.​ increased protons → Acidosis + HCO3 = METABOLIC ACIDOSIS DIABETES MELLITUS A chronic metabolic disease that occurs when the INTERVENTION body doesn’t produce enough insulin or use it 1.​ Insulin Injections or Insulin Pump properly. This results in High levels of blood sugar or 2.​ Pancreas Transplant Hyperglycemia. 3.​ Islet Cell Transplant 4.​ Frequent Blood Sugar Test DM 1 5.​ Carbohydrate Counting > Juvenile > aka Brittle DM, Labile DM DM 2 > Late onset > Autoimmune > aka Syndrome X, Insulin Resistance Syndrome, Dysmetabolic Syndrome CAUSE > > 80 years old UNKNOWN > Lifestyle > Autoimmune → Anti-GAD [Glutamic-Acid Decarboxylase] → destruction of beta cells of Islet of CAUSE/ RISK FACTORS Langerhans = DM 1 METABOLIC SYNDROME 1.​ Abdominal Obesity CLINICAL MANIFESTATIONS 2.​ High Blood Pressure 1.​ POLYDIPSIA >130/80 mmHg > increased blood glucose → Increased 3.​ Impaired Fasting Blood Glucose hyperosmolar → osmo receptors [H] → Thirst > 110 mg/dL response 4.​ High Triglyceride level 2.​ POLYURIA > 150 mg/dL > Increased blood glucose → osmotic 5.​ Low HDL molecule → Urine [H20]=POLYURIA; < 40 mg/dL [women] → glucose in Urine = GLYCOSURIA < 50 mg/dL [men] 3.​ POLYPHAGIA 6.​ High Waist Circumference 3 of the risk factors can indicate possible DM2 NAME 16  TRANS: Module 1 1.​ A1C Test CLINICAL MANIFESTATIONS -​ average plasma blood glucose for 1.​ POLYDIPSIA the past 2-3 mos. > increased blood glucose → Increased -​ > than or equal to 6.5 % hyperosmolar → osmo receptors [H] → Thirst response 2.​ Fasting Plasma Glucose 2.​ POLYURIA -​ > than or equal to 126 mg/dL > Increased blood glucose → osmotic molecule → Urine [H20]=POLYURIA; 3.​ Random Plasma Glucose Test → glucose in Urine = GLYCOSURIA -​ > than or equal to 200 mg/dL 3.​ POLYPHAGIA > Increased Blood Glucose → use of ATP → 4.​ Oral Glucose Tolerance Test Increased Catabolic State → Increased -​ 2 hrs test Appetite -​ checks before and after 2 hrs -​ tells how the body process sugar COMPLICATION -​ > than or equal to 200 mg/dL HYPERGLYCEMIC HYPEROSMOLAR GENERAL INTERVENTION NONKETOTIC SYNDROME [HHNS] > A life threatening problem that involves extremely Keep Healthy Weight through a healthy diet and high blood sugar [glucose] exercise plan. > decreased sensitivity/ resistance to insulin receptors A.​ Nursing Management > can utilize carbohydrates to generate ATP 1.​ Collaborate with patient > No ketone Bodies 2.​ Consistency in timing and food > High Osmolarity amount > 600 mg/dL 3.​ Dietary Guidelines > can lead to ENCEPHALOPATHY a.​ Carbohydrates: 45% [min. 130g/day] OHA: Oral Hypoglycemic Agent = METFORMIN b.​ Proteins: 15% c.​ Fats: 20-30% INTERVENTION 4.​ Encourage Regular Exercise 1.​ Lifestyle Changes 2.​ Monitor Blood Sugar 3.​ Intake of Oral Diabetes drugs, Insulin or Both GENERAL ASSESSMENT 1.​ Elevated Blood Glucose 2.​ Positive for Urinary Ketones 3.​ Abd Pain, N/V 4.​ Dehydration -​ Poor Skin turgor -​ Dry mucous membranes -​ Hemoconcentration -​ Dark & Strong-smelling urine GENERAL DIAGNOSTICS NAME 17  TRANS: Module 1 15.​ The nurse is reviewing the laboratory results of a 45 yr UNIT TEST old client who reports extreme lethargy. Based on the laboratory result [increased TSH, Decreased T3 and 1.​ Which of the following outcomes indicates that the T4], which clinical manifestations would the nurse not interventions for a client with diabetes insipidus has expect? been effective? -​ Warm, moist skin -​ Fluid intake is less than 2500 ml/day 16.​ A client who has undergone a subtotal thyroidectomy 2.​ The nurse caring for a patient who is receiving is subject to complications in the first 48 hrs after desmopressin acetate. Which is a priority evaluation surgery. The nurse should obtain and keep at the while caring for this patient? bedside equipment to -​ Urine output and serum sodium -​ Perform a tracheostomy 3.​ A client is admitted to the ICU after he suffered a 17.​ The nurse notes that the mustache dressing applied on traumatic brain injury. After more than 24hrs, the a client after a hypophysectomy through the client's urine output suddenly rises above 300 ml/hr. transsphenoidal approach has a clear exudate with a Which laboratory findings would support the suspicion pale, yellow-colored ring at the edge of the drainage. of diabetes insipidus? What should the nurse do next? -​ Below normal urine osmolality level, above -​ Report the finding to physician normal serum osmolality level 18.​ A child demonstrated sudden onset of thyrotoxicosis. 4.​ A client has suspected alterations in antidiuretic The nurse anticipates that besides antithyroid therapy, hormone function. Which diagnostic test does the the child is likely also to receive which type of drugs? nurse anticipate will be requested for this patient? -​ Beta-adrenergic blocker -​ Cranial computed Tomography 19.​ Serum concentrations of thyroid hormone and thyroid 5.​ The ICU nurse is caring for a postoperative stimulating hormone are tests ordered for the client transsphenoidal hypophysectomy patient. Which data with primary hypothyroidism. Which of the following would warrant immediate intervention? laboratory values are indicative of the condition? -​ The client has an output of 2500 mL since -​ Decreased thyroid hormone concentrations surgery and an intake of 1000mL and elevated TSH 6.​ A client is admitted for treatment of the syndrome of 20.​ Propylthiouracil (PTU) is prescribed for a client with inappropriate antidiuretic hormone. Which nursing Graves disease to decrease circulating thyroid intervention is appropriate? hormone. The nurse should not teach the client to -​ Restricting fluid immediately report which of the following signs and 7.​ A client with syndrome of inappropriate antidiuretic symptoms? hormone is admitted with a serum sodium level of 118 -​ Increased urine output mEq/L. Which of the following order of the physician 21.​ The nurse is caring for a post-parathyroidectomy client. should be prioritized? The nurse finds the client anxious, with tingling around -​ Administer infusion of 150mL of 3% NaCl the mouth and muscle twitching in the right arm. Which over 3 hrs is the most important for the nurse to implement? 8.​ The client is diagnosed with SIADH. Which -​ Obtain a serum calcium level interventions should the nurse implement? 22.​ A client is suspected of having hyperparathyroidism. -​ Assess for nausea and vomiting and weigh Which intervention would the nurse include in the care daily plan? 9.​ A nurse cares for a client with suspected SIADH with -​ Fractures serum sodium level of 120 mEq/L. Which of the 23.​ A nurse is caring for a client diagnosed with following is a priority nursing interventions? hypoparathyroidism. Which intervention would the -​ Restrict the client’s fluid intake to 600mL/day nurse include in the care plan? 10.​ A client is diagnosed with overdrive of pituitary -​ Instruct about thyroid replacement therapy function. Which clinical manifestations should the 24.​ A nurse is caring for a client with laboratory results nurse expect? noting extremely low calcium levels. The nurse would -​ Protrusion of the lower jaw expect further assessment findings? 11.​ The nurse is caring for a client with suspected Grave’s -​ Positive trousseau’s sign disease. Which assessment findings require immediate 25.​ A nurse is caring for a client after parathyroidectomy. action? Which of the following assessments requires -​ Agitation and Confusion immediate intervention? 12.​ A client is suspected of having Graves disease. Which -​ Laryngeal stridor symptom is not expected to be present in this client? 26.​ A client with hyperparathyroidism is receiving -​ Bradycardia calcitonin. Which of the outcomes has the highest 13.​ The nurse is caring for a client who just had a total priority regarding this medication? parathyroidectomy. What assessment should the nurse -​ Reaching normal serum calcium levels address first? 27.​ A nurse is monitoring a client following a -​ Noisy Breathing thyroidectomy. Which of the following signs likely 14.​ The nurse is caring for a 65 yr old client admitted to the indicates presence of hypocalcemia? emergency department for altered mental status -​ Tingling sensation around the mouth secondary to hypothyroidism. The client denies intake 28.​ A nurse is collecting data on a client with of medications for several months. Initial assessment hyperparathyroidism. Which of the following questions includes: T-35, BP- 90/50, HR-50, RR-10, SpO2- 83. would support the diagnosis? Which action is priority? -​ Do you feel any pain in your joints -​ Prepare for endotracheal intubation NAME 18  TRANS: Module 1 29.​ A client suddenly exhibits Torsades de Pointes. The concerned about which client’s risk for metabolic nurse knows which of these is true about this syndrome? arrhythmia? -​ 55 year old woman with waist circumference -​ It can be short-lived and self- limited without of 38 inches, HDL of 49, and fasting blood any treatment, but it can lead to V.Fib if not glucose of 118 corrected and treated. 43.​ The nurse is teaching a group of clients diagnosed with 30.​ A patient is recovering from parathyroidectomy. The DM. Which lesson regarding foot care should not be patient starts to complain of numbness in the mouth, included? face, fingers. Which of the following findings warrants -​ rub feet vigorously with a towel after bathing immediate attention? to ensure dryness -​ Calcium levels: 6mg/dL 44.​ Upon initial admission fo a client, the nurse notices a 31.​ The nurse assesses a client with Cushing Syndrome. fruity odor to the breath, Kausmaul’s respirations, and Which clinical manifestations should the nurse not lethargy. The glucose level is 700 mg/dL, positive expect? ketones in the urine and the family member states they -​ Hyponatremia have not been able to afford the insulin. Which results 32.​ A client is recently admitted with signs and symptoms would the nurse expect on the ABG’s? suggesting Cushings Syndrome. When evaluating -​ pH 7.25, CO2 36, HCO3 18 laboratory results, which of them would support the 45.​ A client with diabetic ketoacidosis had repeat ABG diagnosis of Cushing’s syndrome? drawn 24 hours after initiation of a RI intravenous -​ Increased serum cortisol level infusions. The results are: pH-7.30, PaCO2-29, 33.​ A client with addison’s disease experesses concerns PaO2-95, O2 sat 99%, HCO3-20 and Base excess 1.2. about adding extra salts to meals. The nurse should The nurse would interpret the results to be which explain that the added salt is necessary for which acid-base imbalance? reason? -​ Metabolic acidosis -​ The lack of sufficient aldosterone means 46.​ A client with type 1 DM is admitted to the emergency sodium is lost in the urine; therefore, department. Which of the following respiratory patterns additional salt is necessary for replacement requires immediate action? 34.​ A client who underwent adrenal gland radiation therapy -​ Deep, rapid respirations with long expirations for a benign tumor is receiving fludrocortisone acetate 47.​ Which of the following conditions is the most significant for mineralocorticoid and glucocorticoid replacement. risk factor for the development of type 2 DM? What is a priority nursing concern for this client? -​ Obesity -​ Risk for fluid overload 48.​ You are caring for a client of a newly diagnosed 35.​ The nurse is assessing a client suspected for Cushing diabetic patient who is preparing to go home. His wife Syndrome. Which of the following findings support this is not so familiar with his diagnosis, so she asked you diagnosis? the primary difference between Type 1 and type 2 -​ Bruising diabetes. Your appropriate response is? 36.​ The nurse is assessing a client suspected for adrenal -​ Type 1 diabetes is always insulin dependent insufficiency. Which of the following findings supports while type 2 DM is not this diagnosis? 49.​ The nurse provides information to a client with DM who -​ Hypotension is taking insulin about the manifestations of 37.​ A nurse is caring for a patient with Cushing syndrome hypoglycemia. Which of the following manifestations with BP of 160/100. Which adrenal hormone is altered should the nurse not include in the information? in this patient? -​ Lightheadedness, Polyuria -​ Glucocorticoid or Mineralocorticoid 50.​ A client with type 2 DM is being discharged from the 38.​ A client presents to the emergency department hospital after an occurence of hyperglycemic exhibiting signs of Adrenal crisis. Which of the hyperosmolar state. The nurse develops a discharge following interventions must be done first? teaching plan for the client and identifies which as a -​ Administer IV bolus of PNSS as ordered priority? 39.​ The nurse notes hirsutism, moon face, truncal obesity -​ Monitoring for signs and symptoms of and abdominal striae upon assessment with a patient dehydration diagnosed with addison's disease who takes daily oral corticosteroids. Which order of the physician should the nurse anticipate? -​ Obtain serum ACTH level 40.​ A nurse is caring for a patient exhibiting signs and symptoms of fluid volume excess, hypernatremia and hypokalemia. The nurse knows that these symptoms most likely correlate to dysfunction of which part of the adrenal gland? -​ Zona Glomerulosa 41.​ The nurse is planning a client care conference with the parents of a 3 year old with newly diagnosed type 1 DM. What is the priority outcome for the caregivers? -​ Knowing how to keep blood sugar stable 42.​ The nurse is conducting a health-screening clinic at an industrial work site. The nurse should be most NAME 19