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Individuals Individuals Experiencing Experiencing
Endocrine Endocrine DisordersDisordersNURS 2016NURS 2016
Glands That Control Glands That Control Endocrine RegulationEndocrine Regulation
HypothalamusHypothalamus PinealPineal PituitaryPituitary ThyroidThyroid ParathyroidParathyroid ThymusThymus AdrenalAdrenal Islets of LangerhornIslets of Langerhorn Ovaries/TestesOvaries/Testes
Figure 42-2 The pituitary gland, the relationship of the brain to pituitary action, and the hormones secreted by the anterior pituitary and the posterior pituitary.
Thyroid GlandThyroid Gland Produces thyroxin (T4) and Produces thyroxin (T4) and
triiodothyronine (T3) and calcitonintriiodothyronine (T3) and calcitonin Release of thyroid hormones (T3 and Release of thyroid hormones (T3 and
T4) controlled by thyroid stimulating T4) controlled by thyroid stimulating hormone (TSH) secreted by pituitaryhormone (TSH) secreted by pituitary
T3 and T4 control cellular metabolismT3 and T4 control cellular metabolism TSH normal is 0.6-5.2 mg/LTSH normal is 0.6-5.2 mg/L Goiter: enlarged thyroid glandGoiter: enlarged thyroid gland
Hypothyroidism CMHypothyroidism CM
MildMild ModerateModerate SevereSevere
BradycardiaBradycardia HypothermicHypothermic Extreme Extreme fatiguefatigue
Hair lossHair loss Brittle nailsBrittle nails Dry skinDry skin
Numb fingersNumb fingers Menstral Menstral disturb.disturb.
Weight gainWeight gain
Skin becomes Skin becomes thickthick
Mask-like Mask-like faceface
Mental Mental processes processes subduedsubdued
Slowed Slowed speechspeech
Hypothyroidism Hypothyroidism TreatmentTreatment
Medications:Medications: Levothyroxin Levothyroxin Single dose in AMSingle dose in AM Not IVNot IV Therapeutic effect is not immediateTherapeutic effect is not immediate
HyperthyroidismHyperthyroidism
AKA: Grave’s diseaseAKA: Grave’s disease Excess secretion Excess secretion of thyroid hormonesof thyroid hormones
Clinical ManifestationsClinical Manifestations
MildMild ModerateModerate SevereSevere
NervousnessNervousness IrritableIrritable PalpitationsPalpitations
TachycardiaTachycardia AmenorreheaAmenorrehea Poor heat Poor heat toler.toler.
Excess Excess perspirationsperspirations
Flushed skinFlushed skin ExophthalmosExophthalmos
Increased Increased appetiteappetite
Decreased Decreased weightweight
Fatigue/Fatigue/weaknessweakness
Hyperthyroidism Hyperthyroidism TreatmentTreatment
3 main Treatments:3 main Treatments:
2 Pharmacological & 1 surgical2 Pharmacological & 1 surgical Radioactive iodine treatment: destroys Radioactive iodine treatment: destroys
overactive thyroid cellsoveractive thyroid cells 70-85% patients cured with one dose70-85% patients cured with one dose High incidence of hypothyroidismHigh incidence of hypothyroidism Fear of radioactive componentFear of radioactive component
Anti thyroid meds Propacil,TapazoleAnti thyroid meds Propacil,Tapazole Surgical removalSurgical removal
HyperthyroidismHyperthyroidism NCPNCP
Maintain nutritional statusMaintain nutritional status
Enhance coping measuresEnhance coping measures
Improve self esteemImprove self esteem
Maintain normal body Maintain normal body temperaturetemperature
Monitor for complications –Monitor for complications –recurrent hyperthyroidism, recurrent hyperthyroidism, permanent hypothyroidismpermanent hypothyroidism
Promote /teach self care Promote /teach self care
Acute PancreatitisAcute Pancreatitis
Inflammation of the pancreasInflammation of the pancreas Range from a relatively mild, self-Range from a relatively mild, self-
limiting disorder to a rapidly fatal limiting disorder to a rapidly fatal diseasedisease
AutodigestionAutodigestion CausesCauses Mortality is highMortality is high
Clinical ManifestationsClinical Manifestations Severe abdominal painSevere abdominal pain Acute illnessAcute illness Abdominal guardingAbdominal guarding EcchymosisEcchymosis Nausea & vomitingNausea & vomiting HypotensionHypotension Acute renal failureAcute renal failure TachycardiaTachycardia Respiratory distressRespiratory distress Abnormal blood gas valueAbnormal blood gas value Fever,Fever, JaundiceJaundice
AssessmentAssessment
Presence & character of painPresence & character of pain Serum amylase & lipase are 3x Serum amylase & lipase are 3x
higher higher Nutritional fluid status & hxNutritional fluid status & hx History of GI problemsHistory of GI problems Respiratory statusRespiratory status Abdominal pain, tenderness & Abdominal pain, tenderness &
guardingguarding
Nursing DiagnosesNursing Diagnoses
Pain & discomfortPain & discomfort Imbalanced nutritionImbalanced nutrition Ineffective breathing patternIneffective breathing pattern Impaired skin integrityImpaired skin integrity
GoalGoal
Nursing InterventionsNursing Interventions Relieving Pain & discomfortRelieving Pain & discomfort
Administer Demerol as orderedAdminister Demerol as ordered Improving nutritional statusImproving nutritional status
NPO, NG tube, IV fluidNPO, NG tube, IV fluid Providing wound careProviding wound care Improving respiratory functionImproving respiratory function Monitoring complicationsMonitoring complications
Fluid & electrolyte disturbanceFluid & electrolyte disturbance Pancreatic NecrosisPancreatic Necrosis Shock & multiple organ failureShock & multiple organ failure
Chronic PancreatitisChronic Pancreatitis
Progressive anatomic & functional Progressive anatomic & functional destruction of the pancreasdestruction of the pancreas
Mechanical obstruction of the Mechanical obstruction of the pancreatic & common bile ducts and pancreatic & common bile ducts and duodenumduodenum
Inflammation & destruction of the Inflammation & destruction of the secreting cells of the pancreassecreting cells of the pancreas
Clinical ManifestationsClinical Manifestations Severe upper abdominal & back painSevere upper abdominal & back pain Risk of addiction to opiatesRisk of addiction to opiates Weight lossWeight loss Altered digestionAltered digestion Calcification of the pancreasCalcification of the pancreas
Management…depends on Management…depends on causecause
Treatment directed towards Treatment directed towards Prevent acute attackPrevent acute attack Relieving painRelieving pain Managing endocrine and exocrine Managing endocrine and exocrine
inefficiencyinefficiency
Hepatic EncephalopathyHepatic Encephalopathy Profound liver failureProfound liver failure Accumulation of ammonia and other toxins Accumulation of ammonia and other toxins Hepatic comaHepatic coma
Clinical ManifestationsClinical Manifestations Mental changesMental changes Motor disturbancesMotor disturbances AsterixisAsterixis Hand writing becomes difficultHand writing becomes difficult Constructional apraxiaConstructional apraxia Reflexes disappear & extremeties become Reflexes disappear & extremeties become
flaccidflaccid
Hepatic EncephalopathyHepatic Encephalopathy
Diagnosis:Diagnosis: EEG shows slowing brain wavesEEG shows slowing brain waves
Treatment:Treatment: Lactulose reduces serum ammonia Lactulose reduces serum ammonia
(watch for watery stools)(watch for watery stools) Vital signs, hand writing monitoring, Vital signs, hand writing monitoring,
hydrationhydration
Principles of ManagementPrinciples of Management
An Overview of HepatitisAn Overview of Hepatitis
Inflammation of the liver caused by a Inflammation of the liver caused by a virusvirus
Clinical Manifestations:Clinical Manifestations: JaundiceJaundice Liver tenderness Liver tenderness
Hepatic CirrhosisHepatic Cirrhosis
Chronic, progressive disease with Chronic, progressive disease with widespred fibrosis and nodule widespred fibrosis and nodule formationformation
Normal flow of blood, bile, and Normal flow of blood, bile, and hepatic metabolites is altered by hepatic metabolites is altered by fibrosis and changes in the fibrosis and changes in the hepatocytes, bile ductules, vascular hepatocytes, bile ductules, vascular channels, and reticular cellschannels, and reticular cells
Hepatic Encephalopathy, Hepatic Encephalopathy, Hepatitis, & CirrhosisHepatitis, & Cirrhosis
Chronic disorders and nurses treat Chronic disorders and nurses treat them as suchthem as such
Treatment:Treatment: control ascites, bleeding esophageal control ascites, bleeding esophageal
varices, infectionvarices, infection proper nutrition, support, rest, proper nutrition, support, rest,
corticosteriods may maximize liver functioncorticosteriods may maximize liver function no alcoholno alcohol avoid infectionavoid infection
Clinical Manifestations Clinical Manifestations Hepatic CirrhosisHepatic Cirrhosis
Intermittent jaundiceIntermittent jaundice FeverFever AnorexiaAnorexia Muscle wastingMuscle wasting DiarrheaDiarrhea Depleted platelet countDepleted platelet count FatigueFatigue
Advanced detoriation Advanced detoriation AscitesAscites VarciesVarcies EncephalopathyEncephalopathy Liver atrophyLiver atrophy
DiabetesDiabetes
Diabetes InsipidusDiabetes Insipidus Diabetes MellitusDiabetes Mellitus
type I (IDDM)type I (IDDM) type II (NIDDM)type II (NIDDM)
Gestational DiabetesGestational Diabetes Diabetic KetoacidosisDiabetic Ketoacidosis Diabetic ComaDiabetic Coma Diabetic NeuropathyDiabetic Neuropathy
Diabetes InsipidusDiabetes Insipidus
Due to decreased secretion of ADH Due to decreased secretion of ADH (usually from pituitary surgery)(usually from pituitary surgery)
Polyuria (9L/day)Polyuria (9L/day) Watch for dehydrationWatch for dehydration Transient in natureTransient in nature
DiabetesInsipidusDiabetesInsipidus Medical managementMedical management
To replace ADHTo replace ADH To ensure adeq fluid replacementTo ensure adeq fluid replacement
Pharmacological treatmentPharmacological treatment Desmopressin - sprayDesmopressin - spray IM form of ADHIM form of ADH
Nursing ManagementNursing Management SupportSupport TeachingTeaching Medical braceletMedical bracelet
Diabetes MellitusDiabetes Mellitus
Type I (Insulin Dependent Diabetes Type I (Insulin Dependent Diabetes Mellitus)Mellitus)
Causes:Causes: Genetic component (however many type Genetic component (however many type
I diabetics have no known relatives with I diabetics have no known relatives with diabetes)diabetes)
Viruses may destroy beta cellsViruses may destroy beta cells Unknown in most casesUnknown in most cases
Type IType I
Islet of Langerhans (more specifically the Islet of Langerhans (more specifically the beta cells within) cannot produce enough beta cells within) cannot produce enough or any insulin to combat glucose levels or any insulin to combat glucose levels within the bodywithin the body
Consequently, glucose levels riseConsequently, glucose levels rise Stress can trigger increased glucose Stress can trigger increased glucose
responseresponse Individuals become dependent on Individuals become dependent on
exogenous insulin administration to exogenous insulin administration to survivesurvive
Type IIType II
Type II (Non-insulin Dependent Type II (Non-insulin Dependent Diabetes Mellitus)Diabetes Mellitus)
Causes:Causes: no known genetic componentno known genetic component obesityobesity
Type IIType II
Beta cells are unable to respond to Beta cells are unable to respond to hyperglycemia hyperglycemia
This causes the beta cells to become This causes the beta cells to become less efficient with timeless efficient with time
This process is reversible with This process is reversible with normalization of glucose levelsnormalization of glucose levels
Some individuals have a resistance to Some individuals have a resistance to insulin that may trigger NIDDM as insulin that may trigger NIDDM as wellwell
Clinical ManifestationsClinical Manifestations Type I Type II
Polyuria Most times Sometimes
Polydipsia Most times Sometimes
Polyphagia Most times Sometimes
Weight Loss Most times Never
Blurred Vision Sometimes Most times
Asymptomatic Never Most times
Gestational DiabetesGestational Diabetes
Usually develops in 2nd or 3rd Usually develops in 2nd or 3rd trimestertrimester
After delivery, glucose tolerance in After delivery, glucose tolerance in most clients returns to normalmost clients returns to normal
However, type II diabetes develops in However, type II diabetes develops in 40-60% of women with GDM within 5-40-60% of women with GDM within 5-15 years15 years
Most GDM require insulin Most GDM require insulin adminstrationadminstration
Diabetic KetoacidosisDiabetic Ketoacidosis A little patho:A little patho:
hyperglycemia occurs due to glucose cannot be hyperglycemia occurs due to glucose cannot be transported to cells because of lack of insulintransported to cells because of lack of insulin
the liver starts to convert glycogen back to glucose the liver starts to convert glycogen back to glucose and increases synthesis of glucoseand increases synthesis of glucose
unfortunately the complicates mattersunfortunately the complicates matters fatty acids are mobilized from adipose tissue and fatty acids are mobilized from adipose tissue and
the liver starts to produce ketonesthe liver starts to produce ketones ketones are excreted in the urine and accumulate ketones are excreted in the urine and accumulate
in the bloodin the blood metabolic acidosis occurs from the increased acid metabolic acidosis occurs from the increased acid
due to rising ketonesdue to rising ketones
Diabetic KetoacidosisDiabetic Ketoacidosis
A medical emergencyA medical emergency Sometimes brought on by stress, Sometimes brought on by stress,
surgery, pregnancy, puberty, infectionsurgery, pregnancy, puberty, infection #1 cause: diabetic not taking his/her #1 cause: diabetic not taking his/her
insulin (fed up or non-compliance)insulin (fed up or non-compliance) S & S:S & S:
ketosisketosis dehydrationdehydration electrolyte and acid-base imbalanceelectrolyte and acid-base imbalance
DK ManagementDK Management
Medical ManagementMedical Management Txmt for hyperglycemiaTxmt for hyperglycemia Correct dehydration, electrolyte loss, Correct dehydration, electrolyte loss,
acidosisacidosis
Nursing ManagementNursing Management Monitor for s/s hypokalemiaMonitor for s/s hypokalemia Monitor lab work for electrolytesMonitor lab work for electrolytes Monitor urine outputMonitor urine output
Diabetic ComaDiabetic Coma Bicarbonate buffering system fails to compensate for Bicarbonate buffering system fails to compensate for
ketosis ketosis Respirations increase in rate and depth (Kussmaul’s Respirations increase in rate and depth (Kussmaul’s
respirations) & breath has fruity or acetone odourrespirations) & breath has fruity or acetone odour Renal system attempts to excrete ketones which leads Renal system attempts to excrete ketones which leads
to hemoconcentrationto hemoconcentration Hemoconcentration impedes blood circulation & leads Hemoconcentration impedes blood circulation & leads
to tissue anoxia & lactic acid productionto tissue anoxia & lactic acid production The rise in lactic acid production further acidifies blood The rise in lactic acid production further acidifies blood
pHpH Rising ketones eventually overwhelms the body’s Rising ketones eventually overwhelms the body’s
defenses against the acid & the body succumbs to comadefenses against the acid & the body succumbs to coma
Diabetic NeuropathyDiabetic Neuropathy
Neuropathy
Trauma
Ulceration
Faulty Healing
Gangrene
Other chronic Other chronic complicationscomplications
macrovascular complications:macrovascular complications: coronary artery diseasecoronary artery disease cerebrovascular diseasecerebrovascular disease hyptertensionhyptertension peripheral vascular diseaseperipheral vascular disease
infectionsinfections nephropathynephropathy retinopathyretinopathy
Diabetic Neuropathy Diabetic Neuropathy ManagementManagement
Overall goal is to:Overall goal is to: regulate blood glucose levelsregulate blood glucose levels prevent acute and chronic complicationsprevent acute and chronic complications
Proper management consists of:Proper management consists of: physical activityphysical activity dietdiet perhaps medicationsperhaps medications
Education is a key element in diabetes Education is a key element in diabetes controlcontrol
MedicationsMedications
Oral:Oral: First generation:First generation:
Orinase, TolinaseOrinase, Tolinase Second generation:Second generation:
Glucotrol, Diabeta (Glyburide)Glucotrol, Diabeta (Glyburide) Third generation:Third generation:
Metformin, AcarboseMetformin, Acarbose
MedicationsMedications
Insulin:Insulin: Short Acting:Short Acting:
Humulog, RegularHumulog, Regular Intermediate Acting:Intermediate Acting:
NPH, Lente, 30/70NPH, Lente, 30/70 Long Acting:Long Acting:
UltralenteUltralente
Insulin ActionInsulin Action
Action Name Colour Onset Peak Duration
Short Humulog Clear Immediate 0.5-1.5 hr 2-4 hr
Intermediate
NPH Cloudy 2-4 hr 4-10 hr 10-16 hr
Long Ultralente Cloudy 6-10 hr None 18-20 hr