medical

1. PITUITARY
DISORDERS
&
ADRENAL TUMORS
SUBMITTED TO
 Anita ma’am
 Faculty of C.O.N
VMMC &
Safdarjung hospital
SUBMITTED BY
 Sirsha De
 Bsc(h)nursing 2nd
year
 Enroll no.
 04750306618

2. Pituitary gland is referred to as the
master gland because of the
influence it has on secretions of
hormones by other endocrine
gland.

7. CAUSES OF DISORDER OF
PITUITARY GLAND
Mainly of 2 reasons:
 Hyperactivity
 Hypoactivity

9. HYPERPITUITARISM
(HYPERACTIVITY)
 Having anoveractive pituitary gland is called hyperpituitarism.
 Mostcommonlycausedbynoncancerous tumors.
 This causes glandtosecrete toomuchofcertain kinds of
hormonesrelated to growth,reproduction andmetabolism.
DISORDERS CAUSED :
 Gigantism
 Acromegaly
 Acromegalic gigantism
 Cushing syndrome

10. GIGANTISM

11.  Pituitary glandsecretesgrowthhormone,whichis responsible
for overallgrowthanddevelopmentof humanbodyduring
childhood.
 Whentoomuchgrowthhormoneis secretedthat augmentsthe
growthof muscle,bonesandconnectivetissuein childhoodor
adolescencebeforetheendof thepuberty,thisconditionis
calledGigantism.
 Theresult is anincreasein heightandformationofadditional
soft tissues.
Characterizedby:
• Excessgrowthof body(sometimesmoreintrunkandlimbs).
• Averageheightis approximately7-8feet.

12. ETIOLOGY
Inmost of thecases,noncancerous pituitary glandtumor is
caused duetogigantism.
 McCune-Albright syndromeis adisorder that causes
unusual growth of bone tissues, gland irregularities and
patches of light andbrownskin.

13.  Carneycomplexisararehereditaryconditionwhichis
characterised bymultiple benigntumorsmostoften
affecting heart,skin andendocrinesystemand
abnormalities inskinpigmentationresultinginspotty
appearancetotheskinof affectedareas.

14.  MultipleEndocrineNeoplasiaType1is alsoa
hereditary condition whichcausetumorsin the
pancreas,parathyroidglandsandpituitarygland.
 Neurofibrinomatosisisahereditary diseasethat
causestumorsinnervoussystem.

15. CLINICAL FEATURES
Childwill bemuchtaller thanotherchildrenofthesameage.Partsofbodymaybe
visiblybigger thanothers.
1. Largehandandfeet
2. Thicktoesandfingers
3. Abulgingjawandforehead
4. Improperfacial features
5. Childrensufferingfromgigantismmayshowlargeheads,lipsortongue.
6. Somemayexperiencevisionproblems, headachesandnauseafromtumors.
7. Onsetofpubertyin childrenmaybedelayed.
8. Irregularitiesinmenstrual cycle
9. Deafness
Thesymptomsofgigantismdependonthesizeofpituitaryglandtumors.

16. DIAGNOSTIC EVALUATION
 Historycollection
 CTscan
 MRI scan(to rule out pituitarytumor)
 Oral GlucoseT
oleranceT
est (to rule out hyperglycemia)
 Bloodtest (to rule out growthhormonelevel,highprolactin
level, increaseininsulinlevel&growthfactors)

17. MANAGEMENT
 Gigantism requires early detection &strongtreatmenttoprevent
excessproductionof growthhormoneandto improvelife
expectancy.
 Surgeriesinclude-
⚫ TransfenoidalAdenomectomy
⚫ Hypophysectomy
Surgeryis thefirst line oftreatmentwith theobjective of removing
thetumorto minimize growthhormonelevels &reducethe
pressureonthenerves.
 Radiation Therapyis anotheroptionif surgerycannotbe
implemented. Radiationtherapycantakeseveral years.
 ½of the clientsgetcontrolled growthhormonein 5-10years.

18. ACROMEGALY

19. Acromegaly is achronicmetabolic disorder in whichthereis a
secretionoftoomuchgrowthhormone&thebodytissues
graduallyenlarge.
ETIOLOGY:
 Pituitary tumors Benign tumor,adenoma of pituitary gland
 Non Pituitary tumors Benign or cancerous tumor of the
other part of body such as lungs,pancreas,adrenal
glands.
 Excessgrowthhormone&growthhormonereleasingfactorsinthe
bloodlevels results in changes in theappearance &functions ofthe
body.

20. SYMPTOMS
 Handswelling,sausage likefingers
 Increaseinshoesize
 Diaphoresis
 Thickening of thefacial features
 Increaseprominence in jaw&forehead
 Thickened skin
 Swelling of tongue
 Arthritis
 Sleepapnoea
 Headache
 Partial loss of vision
 Pain,numbness,tingling weaknessin hands&wrists
 Increased thirst nurination,hyperglycemi,heart failure etc

21. CONTINUED:
• Thyroid, parathyroid andadrenal glands showshyperactivity.
• Hyperglycemia andglycosuria
• Hypertension
• Headache
• Visual disturbance-BITEMPORAL HEMIANOPIA

22. DIAGNOSTIC EVALUATION
 Historycollection
 Physical examination
 CTscan,MRI scanof head,chest,abdomen, pelvis,adrenal gland &
ovaries.
MANAGEMENT:
 Goalof treatment is torelieve &reverse thesymptomsof acromegaly.
 Surgical treatment is the1st line treatment
⚫ TRANSPHENOIDALHYPOPHYSECTOMY
Transsphenoidal meansthrough the sphenoid sinus. This is the air sinus
(cavity) at the back of your nose. Weremove the pituitary tumour through
thenose.Hypophysectomy referstothepituitary gland.

24.  RADIATION THERAPY: Isanoptiontoreducethesizeofthe
tumor&hencereducetheproduction of growthhormone.
Radiationtherapyfocusesonhighintensityradiationatpituitarytumorto
destroytheabnormal cells.
 Givenin2forms: External beam&stereotactic
 DRUG THERAPY:
⚫ Somatostatinanalogs: reduce growthhormonerelease
⚫ Dopamine agonist: prevents thereleaseof growthhormone
⚫ Growthhormonereceptor antagonist: blocks theeffectofgrowth
hormoneeg,Pegvisomant

26. HYPOPITUITARISM(HYPOACTIVI
TY)
 Hypopituitarism(pituitary insufficiency) is ararecondition in
whichyour pituitaryglanddoesn’t makeenough of certain
hormones.
 Canbecauseddue topituitary tumorswhich when increases
its size maycompressanddamagepituitary tissues, interfering
withhormoneproduction.
 DISORDERS CAUSED:
• Dwarfism
• Acromicria
• Simmond’s disease

27. DWARFISM
It is anendocrine disorder resulting fromhyposecretion of growth
hormoneduring critical developmental period in children.

28. TYPES OF DWARFISM
1. Proportionate
2. Disproportionate
⚫ Short limb
⚫ Short trunk
3. Asymmetry

29. CAUSE OF DWARFISM
 Reduction inthegrowthhormonein
infancy or early childhood.
 Occurs becauseof following reasons:
 Tumorofpituitarygland,whichcompress&
destroysthenormal cell secreting growth
hormone
 Defof GHRHbyhypothalamus
 Defof somatomedinC
 Atrophyor degenerationof acidophilliccells
intheanterior pituitary
 Lesionof anterior pituitaryduetoinfectionor
injury resultsinhyposecretion of growth
hormone
 Geneticdisorder
 Hereditary

30. SIGNS AND SYMPTOMS
 Stunted skeletal growth
 Maximumheight approximately 3feet
 Headbecomesslightly larger inrelationtobody
 Mental activityisnormal without anydeformity
 Reproductive systemis notaffected dueto lack ofgrowth
hormonebutin Panhypopituitarism puberty is notobtained due
tolack of gonadotrophic hormone.

32. DIABETESINSIPIDUS
 Diabetes insipidus is adisorder oftheposterior lobe ofthepituitary gland
characterized byadeficiency ofADHorvasopressin.
 Greatthirst,polydipsia &large volumeof dilute urine characterize the
disorder.

33. TYPES OF DIABETES INSIPIDUS
1. Central diabetesinsipidus
2. Nephrogenicdiabetesinsipidus
3. Psychogenic diabetesinsipidus
4. Gestational diabetesinsipidus

34. CAUSES
 Central diabetesinsipidus:
⚫ Headtraumaor surgery
⚫ Pituitary or hypothalamictumor
⚫ Intracerebral occlusionor infection
 Nephrogenicdiabetesinsipidus:
⚫ Systemicdiseaseinvolvingkidney:-
⚫ Multiplemyeloma
⚫ Sicklecell anemia
⚫ Polycystickidneydiseases
⚫ Pyelonephritis
⚫ Medicationsuchaslithium

35. PATHOPHYSIOLOGY
 Central diabetesinsipidus:
⚫ Lossofvasopressinproducingcells
⚫ CausingdeficienciesinADHsynthesis
⚫ DeficiencyinADH,resultingin aninability to conservewater
⚫ Leadingtoextremepolyuria& poiydipsia
 Nephrogenicdiabetesinsipidus:
⚫ Depressionof aldosteronereleaseorinability of nephrons torespondto
ADH,causingextremepolyuriaandpolydipsia.

36. SIGNS AND SYMPTOMS
 Polyuria with urineoutputof 5to15Ldaily.
 Polydipsia,especially adesire for coolfluids.
 Markeddehydration,asevidencedbydrymucous
membrane,dryskin&weightloss.
 Anorexia&epigastricfullness
 Nocturia &relatedfatigue from interrupted sleep.

37. DIAGNOSTIC TEST RESULTS
 Highserumosmolarity,usually above300mosmol/kg of water.
 Lowurineosmolarity
,usually50to200mosmol/kgof water.
 Lowurine–specificgravityof lessthan1.005.
Management:theobjectiveof therapyare:
1
. T
oreplaceADH,which is usually alongtermtherapeutic
programme.
2
. T
oensureadequatefluidreplacement
3
. T
oidentify&correct theunderlyingcause.

38. TREATMENT:
 ReplacementofvasopressintherapywithintranasalorI.V
DDA
VPC(desmopressin acetate).
 Correction ofdehydration andelectrolyteimbalance.
 Thiazolediuretic increaserenal water reabsorption
 Restriction of salt &proteinintake.
NURSING MANAGEMENT: Thenurse reviews thepatient history&
physical assessment.
 Thenurseis responsible toeducate thepatient, family &other caregivers
about follow upcare,prevention of complication &emergencymeasures.
 Thenurseshould demonstrate andmaketheclient understand about his
medical condition.

39. SIADH-SYNDROME OF
INAPPROPRIATE ANTI DIURETIC
HORMONE
 SIADH,isadisorderof impaired waterexcretion
causedbytheinability to suppress secretionsordue
toexcessivesecretions&actionsof anti diuretic
hormone.
 If water intakeexceedthereducedurineoutput i.e
concurine,theensuringwaterretentionleadstothe
development of hyponatremia.
 MostcommoncauseofHypoosmolarEuvolemic
Hyponatremia.

40. ETIOLOGY
1. Neoplasms
2. Carcinomas of lung,duodenum,ovary,bladder,ureter,any
other neoplasms.
3. Thymoma
4. Mesothelioma
5. Bronchial adenoma
6. Carcinoid gangliocytoma
7. Ewing’scarcinoma

41. PATHOPHYSIOLOGY

43. DRUGS
1
. V
asopressinor demopressin
2. Chloropropamide
3
. Oxytocinhighdose
4. Vineristine
5. Carbamazepine
6. Nicotinephenothiazines
7. Cyclophosphamide
8. Serotonin reuptakeinhibitor ,etc.

44. INVESTIGATION TESTS FOR
DIAGNOSIS OF SIADH
1. SerumNa+,KClandbicarbonate
2. Plasmaosmolarity
3. Urinesodium
4. Urineosmolarity
5. Serumcreatinine
6. Bloodureanitrogen
7. Bloodglucose
8. Serumuricacid
9. Serumcortisol
10. Thyroidstimulatinghormone

45. MANAGEMENT
 Fluidrestriction:
Is amainstay of therapy in mostpatient with SIADH,with asuggested
goal,intake ofless than800ml/ day.
Theassociated-vewaterbalanceinitially raisestheserumNaconc
towards normal&withmaintenance therapy in chronic SIADH,prevents
further reduction inserumsodium.
 Intravenous saline:
Symptomaticor resistant=Hyponatremia in patient with SIADHoften
requires theadministration of NaCl.

46. NURSING MANAGEMENT
 Closemonitoringof fluidintake&output
 Dailyweight checkup
 Urineandbloodinvestigationstobemeasuredonregular
basis,inorder toindicateanyrisk for theclient.
 Supportive measuresandexplanationof procedureand
treatment will assist thepatient inmanagingthisdisorder.

47. ADRENALGLAND

48. INTRODUCTION
 Eachpersonhas2adrenal gland,oneattached to
superior part of eachkidney
.
 Eachadrenalglandis,in reality,two endocrineglands
with separateindependent function.
 Adrenal glandconsist of 2parts:
1. Adrenalmedulla
2. Adrenalcortex

49.  Adrenalmedulla: Presentat thecentreof thegland,
secretedcatecholamines andtheouterportion of gland.
 Adrenalcortex: it secretessteroid hormones.Thesecretion
ofhormonefromtheadrenal cortex is regulatedbythe
hypothalamus-pituitary –adrenal axis.
Hypothalamus secretescorticotrophinreleasing
hormone(CRH),which stimulates thepituitary glandto
secreteACTH,which in turn stimulates theadrenal cortex to
glucocorticoid hormones(cortisol).
Increasedlevel of adrenal hormone inhibit theproductionof
CRH&ACTH.
This systemisanexampleof –vefeedbackmechanism.

50. ANATOMICAL STRUCTURE OF
ADRENAL GLAND
 Right adrenal glandistriangular inshape
 Left adrenal glandiscrescent inshape.
 Left adrenal gland is moreelongated thanright &lie inmoresuperior position
thantheright one.
 3TYPESOFSTEROIDHORMONEPRODUCEDBYADRENALCORTEX
ARE:-
1. Glucocorticoids
2. Mineralocorticoid
3. Sexhormones
 ADRENALCORTEXISDIVIDEDINTO3ZONES:-
1. Zonaglomerulosa
2. Zonafasciculata
3. Zonareticularsis

51. ADRENAL GLAND TUMORS
Dividedintotumorsarisingfromadrenal glandcortex &
arisingfrommedulla:-
 Adrenal cortex:-
1. Cushingsyndrome
2. Primary hyperaldosteronism(Conn’s disease)
3. Adrenal carcinoma
 Adrenal medulla:-
1. Pheochromocytoma
2. Neuroblastoma

52. CUSHINGSYNDROME

53.  Hypersecretion of cortisolcausedbyendogenous production
of corticosteroids isknown asCushing’s syndrome.
 ThemostcommoncauseisACTHdependentcushing
syndrome,resultingfrompituitary adenomathatsecrete
excessiveamount ofACTH.
 Adrenocortical carcinoma&bilateral macronodularhyperplasia
representrarecauseof hypercorticolism.
CLINICALSYMPTOMS:-
Atypical patient ischaracterizedby
⚫ Afacial plethora
⚫ ABuffalohump
⚫ Amoonface

54. CLINICAL FEATURES OF CUSHING
SYNDROME
 W
eight gain/central obesity
 Diabetes
 Hirusitism
 Hypertension
 Skinchanges(abdominalstriae)
 Muscleweakness
 Menstrual irregularity
 Depression
 Osteoporosis
 Hypokalemia

55. DIAGNOSIS
 Biochemical test
 Radiological investigation
NURSING MANAGEMENT
 Decreaseriskof injury
 Decreasing risk of infection
 Preparing thepatient for allergy test.
 Encouragingrest&activity
 Promotingskinintegrity
 Improvingbodyimage

56. PRIMARY HYPERALDOSTERONISM
(CONN’S DISEASE)
 Primary aldosteronism (PA), also known as primary
hyperaldosteronism or Conn's syndrome, refers to the excess
production of the hormone aldosterone from the adrenal glands, resulting
in low renin levels.[1] This abnormality is caused by hyperplasia or tumors.
Many suffer from fatigue, potassium deficiency and high blood
pressure which may cause poor vision, confusion or headaches.

57. Primaryhyperaldosteronism(PHA)is definedbyhypertension,
hypokalemia&hypersecretionof aldosterone.
 InPHA,plasma reninactivity is suppressed.
 Amongpateients with hypertension theincidenceof
hypokalemia.
 PHAis approximately 2%recent studies haverevealed that
upto12%ofhypertension patient havePHA,with normal
potassiumlevels.
CAUSESOFPHA:-
1. Aldosteroneproducingadencema.
2. Bilateraladrenalhyperplasia(ideopathic
hyperaldosteronism)
3. Aldosterone-producingadrenocortical carcinoma.

58. CLINICAL FEATURES
1. Most patient arebetween30-50yearsof agewith female
predominance.
2. Apartfromhypertension &hypokalemia,patient complains
of nonspecificsymptoms.
3. Headache,muscleweakness,cramps,polyuria,intermittent
paralysis,polydipsia &nocturia.
DIAGNOSIS
 Assessment of potassiumlevels
 Antihypertensive&diuretic therapy
 Oncebiochemical diagnosisisconfirmed,MRI or CTscan
canbeperformed.

59. ADRENOCORTICALCARCINOMA

60.  Adrenocorticalcarcinomaisararemalignancywitha
incidenceof 1-2casesper10lakhspopulationperyear.
 Avariablebut generally poor prognosis.
 Aslight femalepredominanceisobserved(1:5:1)
 1st peakin childhood &asecondbetween4th or5thdecade.

61. PATHOLOGY
1. Criteriafor malignancy aretumor size,thepresence
of necrosisor haemorrhage&microscopic features
suchascapsular or vascular invasion.
2. Theseshould beassessedin termsof microscopic
diagnosticscore.
3. Additional informationis providedby immunohisto
chemistry.
4. Macroscopic features commonly multinodularity &
hexogenous structure.

62. DIAGNOSIS
1. Dexamethasonesuppressiontest
2
. MRI &CTscan
3
. MRI angiography
4
. WHOclassification-
1. Tumor <5cm(stage1)
2. >5cm(stage2)
3. Locallyinvasivetumor(stage 3)
4. Tumor withdistant metastasis (stage4)
TREA
TMENT
⚫ Completetumor resection
⚫ Laproscopicadrenalectomy
⚫ Adjuvant radiotherapy

64. PHEOCHROMOCYTOMA

65.  Atumor beginswhenhealthycellschange&growout of
control formingamass.
 Atumor canbecancerousor benign.
 Acanceroustumor ismalignant, measuringit cangrow&
spreadtoother partsof body
.
 Abenigntumor meansthetumor cangrowbut will not
spread.
 Theadrenal glandtumor cansometimes producetoo
much ofhormone,Whenit does,thetumoris
called”functioning tumor”.
 It iscatecholamines-secretingneoplasmsassociatedwith
hypertension of chromaffin cellsofadrenal medulla.

66. ETIOLOGY
 Medullary thyroidcarcinoma
 Parathyroidhyperplasia
 Emotional &physical stress
 General factor
Increasedor decreased
secretionof hormone.

68. CLINICAL FEATURES
 Hypertension
 Posturalhypotension,thisresultsfromvolumecontraction
 W
eight loss
 Pallor
 Fever
 Tremor
 Neurofibromas
 Patchesof cutaneouspigmentation
 T
achyarrhythmias
 Pulmonaryoedema
 Cardiomyopathy

69. LABORATORY SIGNS
 Hyperglycemia
 Hypercalcaemia
 Erythrocytosis
5’H’s SYMPTOMS
1. Hypertension
2. Headache
3. Hyperhidrosis
4. Hypermetabolism
5. Hyperglycemic
Classically,pheochromocytoma showsSwisscheese
configuration.

70. NURSING MANAGEMENT
 Educatingpatient about self care
⚫ During preoperative&postoperativephasesof care ,the nurse
educatethe patient aboutfollow upmonitoringto ensurethat
pheochromocytomadoesnot reactivate.
 Nurseprovideverbal &writteninstructionsabout
⚫ Theprocedurefor collecting 24hrs urine specimento monitor
urinefor catecholamineslevel.
 Continuingcare
⚫ Thepatient is scheduled for periodic follow up appointments to
observefor return of normal bloodpressure&plasmafor urine
levelsof catecholamines.

71. TREATMENT
1. Laparoscopic resection is nowaroutine treatment
for pheochromocytoma.
2. If thetumor islarger than8-10cmor radiological
signsof malignancy aredetectedanapproach
shouldbeco

73. SUMMARY
 The presentation includes the
Pituitary disorders
⚫ Gigantism
⚫ Acromegaly
⚫ Dwarfism
⚫ Diabetes insipidus
⚫ SIADH
Adrenal tumors
⚫ Cushing syndrome
⚫ Primary hyperaldosteronism
⚫ Adrenocortical carcinoma
⚫ Pheochromocytoma
Their causes,clinical features,diagnosis,treatment and
management have also been covered.

74. BIBLIOGRAPHY
 Brunner’s & Suddharth’s text
book of MEDICAL SURGICAL
NURSING 13th edition.
 https://www.endocrinweb.com
 https://www.cancer.org.com
 www.slideshare.com