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