Understanding Endocrine System Disorders: Key Concepts and

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South College**We aren't endorsed by this school

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PATHO 3113

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Nursing

Date

Dec 11, 2024

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Uploaded by BrigadierAtom12909

Chapter 16 study guideDestiny DanielSouth collegeFall 2024CHAPTER 16Endocrine System Disorders1. (p. 403) See Fig. 16.1 of the text.A.Pituitary gland, B.Pineal gland, C.Four parathyroid glands on posterior thyroid, D.Thyroid gland,E.thymusF.Adrenal glandG.pancreasH.KidneyI.Ovary in female, J.Testis in male2. (p.403) Hormones are chemical messengers and can be classified by:Action:control or hormone levels, i.e., blood calcium levelsSource:endocrine organ, i.e., adrenal glandChemical structure:amino acid derivatives or steroids3. (p. 403) negative feedback4. (p. 404) an excessive amount of hormone or a hormonal deficit5. (P. 406) Radioimmunoassay and immunochemical assaysDIABETES MELLITUS6. (p. 407, Table 16.2) Familial history (type 1) obesity, advancing age (type 2)7. (p. 407, Table 16.2)Type 1:genetic factor (family history); autoimmune destruction of pancreatic beta cellsType 2:familial, lifestyle, and environmental factors, especially obesity8. (pp.407-408) An insulin deficit leads to the following sequence of events and can be categorized into the initial stage and progressive effects:Initial stage:decreased transportation and use of glucosehyperglycemiaglucosuriapolyuria with loss of fluid and electrolytesfluid loss through the urine and high blood glucose levels dehydrationpolydipsia due to dehydrationlack of nutrients entering the cells, stimulating appetite and leading to polyphagiaProgressive effects:catabolism of fats and proteins due to lack of glucose in cells; resulting in ketosis as metabolites accumulate ketoacidosis

ketonuriaglomerular filtration drops, resulting in decompensated metabolic acidosis9. (p. 411, Fig. 16.4) The lack of glucose in cells results in catabolism of fats, leading to excessive buildup of fattyacids and their metabolites, ketone (ketoacids).10. (p. 412, Table 16.3) Warning signs include:polyuria:hyperglycemia results in excess glucose in the urine as renal tubular reabsorption capacity is exceeded; the glucose in the filtrate exerts osmotic pressure, increasing the volume of urine producedpolydipsia:fluid and electrolyte loss due to glucosuria results in dehydration and stimulation of the thirst response (hypothalamus)polyphagia:lack of nutrients in cells stimulates appetiteweight loss: particularly with type 1, due to fat catabolism 11.(p.408) Diagnosis is established from the following: fasting blood glucose level, glucose tolerance test, and glycosylated hemoglobin test.12.(p. 408) Dietary modifications include dieting to reduce weight or maintain optimum weight:adding more complex carbohydrates, getting adequate protein, and taking in low saturated fats and fiber to reduce cholesterol levels.Having minimal intake of simple and refined sugars and balancing and reducing food intake to match insulin availability, metabolic needs, and activity level.13.(p. 409) Oral hypoglycemics act in a number of different ways to lower blood sugar; some stimulate beta cells to release more insulin, others reduce insulin resistance of cells and hepatic glucose production, and another type increases cell sensitivity to insulin.14.(p. 409)hypoglycemiagastrointestinal vomitingdisturbances; anorexia, nausea,anemiapruritus (itching)liver and kidney damagemetallic taste (with metformin)15.(p. 409) The various forms of insulin differ in onset of action, peak insulin levels, and duration of action.16.(p. 409) Insulin can be administered by subcutaneous injections, continuous subcutaneous infusion ("insulin pump", or inhalation, which was just approved by the U.S. Food and Drug Administration (FDA).17.(pp. 409-410, Fig. 16.3) Factors that could precipitate a hypoglycemic or insulin reaction include increased physical exercise, skipping a meal or fasting, delayed or inadequate food intake, insulin overdose (too much insulin), and nutritional and/or fluid and electrolyte imbalances due to nausea and vomiting.18.(p. 409) Verify that patients have eaten and taken appropriate medications.Schedule appointments that do not unduly delay meals, 19.See (p. 412) Table 16.4.20.(p. 413) Diabetic neuropathy is a disorder of peripheral nerves that produces impaired sensation, numbness,tingling, weakness, and muscle wasting. It results from ischemia and altered metabolic process. Degenerative changes occur in both unmyelinated and myelinated fibers. There is a risk of tissue trauma and infection.Autonomic nerve degeneration leads to bladder incontinence, impotence, diarrhea, and impaired vasomotor reflexes. Vascular impairment decreases tissue resistance and slows healing; sensory impairment means that an individual may not realize that he has injured himself and therefore does not implement appropriate measures.21.(p. 413) Risk of infection is greatly increased when vascular and sensory impairment coexist.22.(p. 414)tuberculosisinfections in the feet and handsfungal infectionsurinary tract infectionsperiodontal disease

23.(pp. 408 412) There may be delayed healing because of decreased circulation to the injured site due to both macroangiopathy and microangiopathy. Individuals are more prone to infections, which will further delay healing.24.(p. 415 and Chapter 22) diabetes that develops during pregnancy and usually ends with the delivery of the infant25.(pp. 410-411; Figs. 16.3 and 16.4) see chart below:Hypoglycemic ShockKetoacidosisOther namesInsulin shockInsulin reactionDiabetic comaCauseHypoglycemiaHyperglycemiaPrecipitating factorsIncreased physical exerciseSkipping a meal or fastingDelayed or inadequate food intakeInsulin overdose-too much insulinNutritional and/or fluid and electrolyte imbalances due to nausea and vomitingExcessive food and/or alcohol intakeinadequate insulin-skipped or delayedIncreased requirement for insulin: infection, stress, glucocorticoidsSpeed of onsetRapidSlowManifestationsApprehensive, headachePale, cold, diaphoretic, "clammy"Hungry, thirstyAppears intoxicated: unexpected behavior,slurred speech, incoherent, disoriented, staggering gaitDifficulty problem solvingMuscle twitching, tremorsSeizuresPermanent brain damageDeathIncreased hunger and thirstPolyuriaFatigue, confusionNausea and vomitingSigns of dehydration: flushed, warm, dry skin and mucous membranesAcetone breathTachycardia and lowered blood pressureRapid, deep breathing Loss of consciousnessEmergency treatmentGlucose in rapidly absorbed forminsulinFluid and electrolyte replacementSodium bicarbonateSpeed of response to emergency treatmentRapidSlowPreventionNever interfere with normal mealtimes of diabeticNever tell diabetic to fast without seeking medical consultHave available a ready source of glucoseCareful observation for warning signsNever tell a diabetic not to take medication without medical consultCareful observation for warning signs26. (p. 407)Type 1 (IDDM)Type 2 (NIDDM)Percentage of individuals with DM20%80%Age at onsetPreadolescentOlder than 30Speed of onset of symptomsAcuteInsidiousFamily historyyesVery strongBody buildThinobese

Presence of autoantibodiesyesnoInsulin receptor defectsnoyesSeverity of manifestationsAcuteMildStability (i.e., maintenance of normal blood glucose)More difficultMore stableFrequency of complicationsFrequentLess commonOccurrence of ketoacidosisFrequentLess commonFrequency of hypoglycemiaFrequentLess commonTreatment with insulinalwaysLess commonTreatment with oral hypoglycemics NoFrequentPARATHYROID DISORDERS27. (pp. 415-416)oHypoparathyroidism:congenital lack of parathyroid glands, following surgery or radiation in the neck region, or as a result of autoimmune diseaseoHyperparathyroidism: adenoma, hyperplasia, secondary to renal failure28. (p. 417, Fig. 16.10) hypoparathyroidism leads to hypocalcemia, which affects nerve and muscle func-tion. It can lead to weak cardiac muscle contractions but increased excitability of nerves, leading to spontaneous contractions of skeletal muscle: twitching and29. (pp. 416-417; Fig. 16.10, p. 417) hypoparathyroidism causes hypercalcemia, which leads to forceful cardiac contractions; osteoporosis due to excess bone demineralization; and increased predisposition to kidney stones.ACROMEGALY30.(p. 422) excess growth hormone secretions from a pituitary adenoma in the adult31.(p. 419, Fig. 16.12) Manifestations include:•bones that become broader and heavier•soft tissues that grow, resulting in enlarged hands and feet•a thicker skull•changes in facial featuresComplications include:•nerve and blood vessel compression in the skull•carpal tunnel syndrome•arthritis•diabetes•hypertension and cardiovascular diseaseANTIDIURETIC HORMONE32.(pp. 418 422) Diabetes insipidus is due to insufficient antidiuretic hormone (ADH; also known as vasopres-sin) release—no sugar in urine, diabetes mellitus is caused by a lack or insufficient release of insulin or insulin resistance sugar in urine.THYROID DISORDERS33.(pp. 420-421, Figs. 16.13 and 16.14) A goiter is an enlargement of the thyroid gland that is often visible on the neck; it is caused by hypothyroidism (endemic goiter) and hyperthyroidism (toxic goiter).34.(p. 420, Table 16.5)HyperthyroidismHypothyroidismFormsGraves' diseaseAdult: myxedemaInfant: cretinismEtiologyAutoimmune: thyroid-stimulating antibodiesCongenital:

Adenoma: thyroid or pituitaryToxic goiter• Thyroid agenesis or dysgenesis• Lower TSH or I, and T4Adult:• Autoimmune (Hashimoto's disease)• Surgical removal• DrugsSerum T, and I, levelsHighLowMetabolic rateHighLowNervous system effectsRestlessness, anxiety, irritabilityInsomniaTremorsImpaired concentrationChild: severe mental retardationDecreased reflexesFatigue, sluggishnessHeadacheSlow intellectual functionsComaCardiovascular effectsTachycardiaPalpitations, arrhythmiasIncreased blood pressureCardiomegalySevere: angina pectoris, myocardial infarctionBradycardiaDecreased CODecreased blood pressureHyperthyroidismHyperventilationHypoventilationRespiratory effectsSkeletal effectsDyspneaIncreased resorptionAdvanced bone ageRetarded bone age"Stubby hands"Muscular effectsOsteoporosisIncreased tone leading to tremors and twitchingDiarrheaDecreased tone and reflexesMuscle weaknessDecreased peristalsis leading to constipation, flatulence, and abdominal distentionSkin and hairIncreased sweatingFlushed warm skinSoft nailsThin, silky hairPale; yellowish hueCoolDry and roughHair brittle and coarseAlopeciaLoss of lateral third of eyebrowsTemperature toleranceIncreased body temperatureHeat intoleranceDecreased body temperatureCold intoleranceEyesExophthalmosDecreased blinking and eye movements"Lid lag"PuffyBody weightDecreased with increased appetiteIncreased with decreased appetitePresence of goiterWith Graves' diseaseWith endemic goiterTreatmentAntithyroid agentsRadioactive iodineThyroidectomyReplacement therapyADRENAL DISORDERS35. (pp. 423-425, Figs. 16.16 to 16.18; Table 16.6)Cushing's SyndromeAddison's DiseaseEtiologyAdrenal tumorGlucocorticoids therapyPituitary tumorParaneoplastic syndromeAutoimmune destructionProlonged treatment with corticosteroids Infections: tuberculosis, fungi, cancerPhysical appearanceRound "moon face"Thinning of skinPurple striaeHyperpigmentation of skin, particularly in creases-also buccal mucosa and tongue "bronzing"

EcchymosesCervical or supraclavicular fat pads-"buffalo hump"HirsutismAlopeciaProtruding abdomenCushing's SyndromeFluid and electrolytesIncreased Nat and CIDecreased K+Increased HCO3 and decreased H+Water retention resulting in edemaAddison's DiseaseDecreased Na* and CI-Increased K*Increased H and decreasedHCO3Blood pressureIncreasedDehydrationBlood sugarIncreasedDecreasedMusculoskeletal effectsAtrophyOsteoporosisNormal or decreasedWeaknessInflammatory responseDecreasedDecreasedImmune responseDecreasedDecreasedResponse to stressDecreasedDecreasedTreatmentSurgeryPalliative treatment: diuretics, antihypertensives, hypoglycemics or insulin antibiotics, etc.Replacement therapy36. (pp. 422-423) Excessive glucocorticoids depress both inflammation and immunity, thereby impairing normal defenses. Antibacterial drugs are prescribed in an effort to prevent infection.MULTIPLE ENDOCRINE NEOPLASIA TYPE I37. MENI causes tumors to develop in the parathyroid glands, the pituitary gland, the pancreas as well as sites in the digestive tract such as the stomach and the duo-denum. MENI can also cause benign tumors in other endocrine glands as well as other tissues including the adrenal glands, the lungs, the meninges and the skin.Multiple tumors will often appear in different tissues at the same time.CONSOLIDATION38. (p. 427)i. thyroid (T3 and T4) hypersecretion ii, growth hormone hypersecretion as a child iii. hyposecretion of thyroid hormones T3 and T4 as an adultiv. hyposecretion of ADHV. growth hormone hypersecretion as an adult vi. hypersecretion of glucocorticoids vii. hyposecretion of growth hormone viii. hyposecretion of insulin ix. hyposecretion of mineralocorticoids, glucocorticoids, and androgensx. hyposecretion of thyroid hormones as a child39. (p. 427)i. diabetes mellitus, Cushing's, acromegaly ii. hyperthyroidismiii. diabetes mellitus, Addison's, Cushing's iv. hypothyroidismv. Cushing's hyperthyroidism, hyperparathyroid-ismvi. cretinism (hypothyroidism as child) vii. hyperparathyroidism vili. Addison's, hypothyroidism ix. hypothyroidism-cretinism, hyposecretion ofgrowth hormone

x. Addison'sxi. diabetes mellitus type 1, hyperthyroidism-Graves', hypothyroidism-Hashimoto's inappropriate ADH syndrome, hypothyroid-ism—myxedema, Cushing's hyperthyroidism-Graves'xiv. hypothyroidism xv. Cushing's xvi. Cushing's, hypothyroidism xvii.Addison's, Cushing's, hyperthyroidismxviii. diabetes mellitus, inappropriate ADH syn-drome, hyperthyroidism, Cushing's xix. diabetes mellitus, hyperthyroidism xx. hyperthyroidism (Graves'), hypothyroidism(endemic)xxi.acromegaly xxii. hyperthyroidismxxili. inappropriate ADH syndrome, Addison's xxiv. hypoparathyroidism