1.
Disorders of the Endocrine system

2.
Review Of Anatomy/Physiology Of The Endocrine Glands
 The endocrine system is made up of glands and the hormones they secrete.
 Although the endocrine glands are the primary hormone producers, the brain, heart, lungs, liver, skin, thymus,
gastrointestinal mucosa, and placenta also produce and release hormones.

3.
 The primary endocrine glands are the pituitary (the master gland), pineal, thyroid,
parathyroid, islets of Langerhans, adrenals, ovaries in the female and testes in the male.
 The function of the endocrine system is the production and regulation of chemical
substances called hormones.
 A hormone is a chemical transmitter. It is released in small amounts from glands,
and is transported in the bloodstream to target organs or other cells.
 Hormones are chemical messengers, transferring information and instructions
from one set of cells to another.

4.
 Hormones regulate growth, development, mood, tissue function, metabolism, and sexual function.
 Hyposecretion or hypersecretion of any hormone can be harmful to the body.
 Controlling the production of hormones can treat many hormonal disorders in the body.

5.
The endocrine system and nervous system work together to help maintain homeostasis… balance.
The hypothalamus is a collection of specialized cells located in the brain, and is the primary link between the
two systems.
It produces chemicals that either stimulate or suppress hormone secretions of the pituitary gland.

6.
Anterior Pituitary Gland
● Growth Hormone (GH)- affects growth of skeletal muscles
and bones
● Prolactin (PRL)- stimulates milk production after pregnancy
● Gonadotropic- regulates hormone activity of sex organs
● Also effects adrenal cortex and thyroid hormone release

7.
Posterior Pituitary
● Oxytocin- helps during pregnancy
● Antidiuretic hormone (ADH)- inhibits urine
production
● Alcohol inhibits ADH causing increased
output of urine

8.
Growth Hormone (GH):Essential for the growth and development of bones,
muscles, and other organs. It also enhances protein synthesis, decreases the
use of glucose, and promotes fat destruction.
Over secretion of growth hormone:
Giantism in childhood Acromegaly in adults (with large bones of face,
hands and feet ).
Under secretion of growth hormone:
Dwarfism in childhood

9.
Adrenocorticotropin (ACTH): Essential for the growth of the adrenal cortex.
Thyroid-Stimulating Hormone (TSH):Essential for the growth and development of the
thyroid gland.

10.
Follicle-Stimulating Hormone (FSH):is a gonadotropic
hormone.
It stimulates the growth ovarian follicles in the female and
the production of sperm in the male.

11.
Luteinizing Hormone(LH):is a gonadotropic hormone
stimulating the development of corpus luteum in the female
ovarian follicles and the production of testosterone in the
male.
Prolactin (PRL):stimulates the development and growth of
the mammary glands and milk production during
pregnancy.

12.
Melanocyte-stimulating hormone (MSH): regulates skin
pigmentation and promotes the deposit of melanine in the
skin after exposure to sunlight.

13.
Antidiuretic Hormone (ADH): stimulates the reabsorption of water by the
renal tubules.
Hyposecretion of this hormone can result in diabetes insipidus.
Oxytocin: stimulates the uterus to contract during labor, delivery, and
parturition.
A synthetic version of this hormone, used to induce labor, is called Pitocin.
It also stimulates the mammary glands to release milk.

14.
The islets of Langerhans are small clusters of cells located in the
pancreas.
Langerhans. Alpha cells facilitate the breakdown of glycogen to
glucose. This elevates the blood sugar.
Beta cells secrete the hormone insulin, which is essential for the
maintenance of normal blood sugar levels. Inadequate levels result in
diabetes mellitus.

15.
Assessment
24
History
Changes in energy level
T
olerance to heat or cold
Weight
Fat and fluid distribution,
Secondary sexual characteristics
Sexual dysfunction
Memory
Concentration
Sleep patterns
Mood

16.
History…
The healthhistoryinformation should include:
1. The severityofthesechanges
2. The lengthoftimethepatienthas experienced
thesechanges
3. The wayinwhichthesechangeshave
affectedthepatient’
s abilityto carryout ALD
4. The effectofthechangeson thepatient’
s self-perception
25

17.
Physical Exam
• Vitalsigns
• Visualhead-to-toeassessment
• T
actileexamination
• Appearanceoffacialhairinwomen
• “moonface,”
• “buffalohump,”
• Exophthalmos
26

18.
Physical Exam …
• Edema
• Thinning of theskin
• Obesity of the trunk
• Thinness of theextremities
• Increasedsize of the feet and hands
• Elevated/Decaresed blood pressure
• Behavioral changes such as agitation, nervousness, a flat affect,
or a lack of concern about personal appearance

19.
Endocrine-related Problems
28
1. Overproduction of ahormone
2. Underproduction of ahormone
3. Nonfunctional receptors that cause target cells to become
insensitiveto hormones

20.
Disorders of the islets of Langerhans
The pancreatic islets also called “islets of Langerhans” or island
of Langerhans are the regions of the pancreas that contain its
endocrine (i.e., hormone producing) cells.
The most common islet cell the Beta cell. Insulin is the major
hormone in the regulation of carbohydrates, fat, and protein
metabolism.

21.
Cont.…
There are three main types of cells in the pancreatic islets.
 (alpha) 20 % cells that secrete “glucagon”.
 (beta) 75% cells that secrete “insulin”.
 (delta) 5% cells that secrete “somatostatin”.

22.
INSULIN
A hormone produced in the pancreas by the islets of Langerhans,
which regulates the amount of glucose in the blood.
 The lack of insulin causes a form of diabetes mellitus.
The main function of insulin is to lower blood levels of absorbed
nutrients when they rise above normal.

23.
GLUCAGON
A hormone formed in the pancreas which promotes the breakdown of glycogen
to glucose in the liver and assist insulin in regulating blood glucose in the
normal range.
1.Gluconeogenesis:The synthesis of glucose from noncarbohydrate
source ( such as amino acids & glycerol)
2.Glycogenolysis:Glycogen breakdown releases glucose when it is
needed.

24.
SOMATOSTATIN
SOMATOSTATIN (GHRIH) Also known as growth inhibiting
hormone.
The effect of this hormone, also produced by the hypothalamus, is
to inhibit the secretion of both insulin and glucagon.

25.
Diabetes mellitus
Diabetes mellitus is characterized by chronic hyperglycemia due to
inadequate insulin secretion and/or the effectiveness of endogenous
insulin (insulin resistance).
Diabetes mellitus is a contributing factor to development of
cardiovascular disease, hypertension, kidney disease, neuropathy,
retinopathy, peripheral vascular disease and stroke as individuals
age.

26.
Cont.…
Type 1 diabetes mellitus is an autoimmune dysfunction
involving the destruction of beta cells, which produce insulin in
the islets of Langerhans of the pancreas.
Immune system cells and antibodies are present in circulation
and may also be started by certain genetic tissue types or viral
infections.

27.
Cont…
Type 1 diabetes mellitus usually occurs at a young age, and there
are no successful interventions to prevent the disease.
Type 2 diabetes mellitus is a progressive condition due to
increasing inability of cells to respond to insulin (insulin
resistance) and decreased production of insulin by the beta cells.
It often occurs later in a client’s life due to obesity, inactivity, and
heredity.

28.
Risk Factors
 Family history of diabetes
 Obesity (BMI > 27 k/m2)
 Race
 Age ≥ 45 years
 Previously identifiedimpaired fasting glucose or impaired glucose
tolerance
 Hypertension (≥ 140/90mmhg)
 HDL cholesterol level≤ 35 mg/dL(0.9mmol/l) and /ortriglyceride levelof
≥ 250mg/dL (2.8 mmol/L)
 History of gestational diabetes or delivery ofbabies over 9lbs (4 Kg)

29.
DM Classification
1. Type1 diabetes(previouslyreferredto as insulindependent
diabetes(IDD)
2. Type2 diabetes (previouslyreferredto as non-insulindependent
diabetes(NIDD)
3. Gestationaldiabetes
4. Diabetes mellitusassociatedwith other conditions or syndrome

30.
Type 1 Diabetes (T1D)
T1Discharacterizedbydestructionofthe pancreaticbetascells
Factorscontributingtobetacelldestruction:
 Genetic(common)
 Immunologic
 Environmental(e.g.,viral)

31.
Type 2 Diabetes (T2D)
 Accountsforapproximately90to95%ofcases
 Results from decreased sensitivity of tissues to insulin (called insulin resistance) &
impairedβ-cellfunctioningresultingindecreasedinsulinproduction
 MostpeoplewithT2Dareobeseadults>40yrsofage
 Obesity appears to play a major role in T2Dby down regulating insulinreceptors in
skeletal muscleandfat cells
 Peripheralinsulinresistance
 Stimulatesincreasedinsulinproductionasacompensatory response,whichmay
alsopredisposethepatienttoweight gain.

32.
Cont.…
 The exact mechanisms that lead to insulin resistance and impaired insulin secretion in
T2Dareunknown,althoughgeneticfactorsarethoughttoplayarole
 Prevalenceofdiabetesincreaseswithage, withabout half ofcasesinpeopleolderthan55
 Despite the impaired insulin secretion that is characteristic of T2D, there is enough
endogenousinsulinpresent, topreventlipolysisandproductionof ketenebodies
Therefore,diabeticketoacidosis(DKA)doesnottypicallyoccurinT2D

33.
SIGNS AND SYMPTOM
⚫ Hallmarksymptomsof all typesof DMarethe3Ps:
• Polyuria
• Polydipsia
• Polyphagia

34.
SIGNS AND SYMPTOM
Type I:
• Fast onset because no insulin is being produced
• Increased appetite (polyphagia) because cells are starved for energy
• Increased thirst (polydipsia) from the body attempting to rid itself of glucose
• Increased urination (polyuria) from the body attempting to rid itself of glucose
• Weight loss since glucose is unable to enter cells
• Frequent infections as bacteria feeds on the excess glucose
• Delayed healing because elevated glucose levels in the blood hinders healing
process

35.
Cont.…
Type II:
Slow onset because some insulin is being produced
Increased thirst (polydipsia) from the body attempting to rid itself of
glucose
Increased urination (polyuria) from the body attempting to rid itself of
glucose
infection as bacteria feeds on the excess glucose
Delayed healing because elevated glucose levels in the blood hinder the
healing process

36.
Diagnosis
47
• History- personal,family,symptoms
• Physicalexamination
• Neurology examination
• Lab tests

37.
cont.…
52
⚫ Serumglucose
⚫ Serumacetone(ketones)
⚫ Electrolytes
⚫ Arterialbloodgases(ABGs)
⚫ CBC
⚫ RFT

38.
Dx …
BloodT
ests
A.FastingBloodglucose(IBG)test
⚫ Mostaccuratewhenthetestisperformedonbloodobtainedinthemorningbyvein-puncture
⚫ Theclientshouldbefastingforatleast8hours(W
aterispermitted)
BGL (mg/dL) Indication
≤99 Normal
100 to 120 Pre-diabetic (impaired fasting
glucose)
126 and above Diabetes
* Confirmed by repeating the test on a different day

39.
Dx …
B.OralglucoseT
oleranceT
est(OGTT)
◦ Most sensitive test for the of diabetes
◦ Lessconvenient thanFBGtest
◦ Performedinthemorningafter 10-12hourfast
BGL (mg/dL): After 2hrs Indication
139 and below Normal
140 to 199 Pre-diabetic (impaired glucose tolerance)
200 and above Diabetes*
* Confirmed by repeating the test on a different day

40.
Dx …
C.RandomplasmaGlucoseT
est(RPG)
⚫ RPGlevelof200mg/dLplusthe3Psandunexplainedweightlossindicatesdiabetes
D.GlycosylatedHemoglobinassays(HbAsc)
⚫ HbAscisthebestindicatoroftheaverageBGLinthelast 120days
⚫ NormalrangeofHbA1cinadultsis4%-6%
⚫ Levelsover8%indicatespoordiabeticcontrol
E.Electrolytes,BUNandserumcreatinine

41.
Criteria for the of DM (especiallyT2D)
I. Symptomsofdiabetespluscasual BGL≥200mg/dL
Theclassicsymptomsofdiabetesincludethe3Ps
II. Fasting plasmaglucose≥126mg/dL(7.0mmol/L)
Fastingisdefinedasnocaloricintakeforatleast 8
hours
III. 2-hourpostloadglucose≥200mg/dL(11.1mmol)duringanoral
glucosetolerancetest.Thetestshouldbeperformedusinga
glucoseloadcontainingtheequivalent of75gglucosedissolvedin
water

42.
Diabetes Management
The main goal of diabetes treatment is to
normalize insulin activity and blood
glucose levels to reduce the development
of vascular and neuropathic complications.
There are five components of diabetes
management which are equally important

43.
Objective of treatment
 Relieve symptoms
 Prevent acute hyperglycemic complications
 Prevent chronic complications of diabetes
 Prevent treatment-related hypoglycemia
 Achieve and maintain appropriate glycemic targets
Ensure weight reduction in overweight and obese individuals

44.
1. Nutritional therapy

45.
1. Nutritional therapy
57
 Nutrition, meal planning, and weight control are the foundation of diabetes
management
 Thegoals of nutritional managementinclude:
• Providingall theessentialfoodconstituents necessary for optimal
nutrition
• Meeting energy needs
• Achieving and maintaining reasonable weight
• Preventingwidedailyfluctuations inbloodglucose levels
• Decreasing serum lipid levels, if elevated

46.
 For obese diabetic patients (especially with T2D) weight loss is the key
to treatment
 Ingeneral - overweight is considered to be a BMI of 25-29
 Obesity is defined as 20%above a BMI equalto or greater than 30
 Theuse of fiber diets:
 Soluble (legumes, fruits)
 Insoluble (whole grain breads and serials) plays a role in lowering
total cholesterol and low density lipoprotein cholesterol in the blood
58

47.
2.Exercises
Exercise is extremely important in managing diabetes because
it lowers the BGL by:
Increasing the up take of glucose by body mussels and
Improving insulin utilization

48.
Cont.…
Exerciserecommendations
 People with diabetes should exercise at the same time (preferably
whenbloodglucoselevelsareat their peak) andinthesameamount
eachday
 Aslow,gradualincreasein theexerciseperiodis encouraged
 Formanypatients, walking isasafeand beneficial formof
exercise.

49.
Whocanexercise(ADARecommendations)Thosewith;
A.Bloodglucose lessthan250 mg/dl
B. Nosymptomsof retinopathy
C. Noneuropathy
D.NoNephropathy
E. Nocardiovascular problemssuchasangina, embolism,or aneurysm
F. Noother condition that makesexercise inadvisable

50.
Generalprecautionsforexercisein Diabetes
Avoid exercise during periods of poor metabolic control
Inspect feet daily after exercise
Avoid exercise in extreme cold or heat
Use proper foot wear and if appropriate, other protective equipment

51.
3. Monitoring Glucose levels and ketones
Blood glucose monitoring is a cornerstone of diabetes
management, and self-monitoring of blood glucose (SMBG)
levels has dramatically altered diabetes care.

52.
4. Pharmacologic Therapy
 Includestreatmentwithinsulinor oral anti-diabeticagents
 Decisions in drug treatment should be based primarily on the
typeof diabetes andthegoals for glycoliccontrol.

53.
InsulinTherapyandPreparations
⚫ Because the body losses the ability to produce insulin in T1D, exogenous insulin must be
administeredforlife.
⚫ InT2D,insulinmaybenecessary:
 Onalongtermbasistocontrolglucoselevelsifdiet andoralagentsfail
 ForsomepatientsinwhomT2Disusuallycontrolled bydietaloneorbydietandoral
agentspatientsmay requireinsulintemporaryduring:
 Infection
 Pregnancy
 Surgery, or
 Someotherstress-full events.

54.
Cont.…
Insulinaction
The main action of insulin is to stimulate carbohydrate metabolism by
increasing the movement of glucose and other monosaccharide in to the cells
of muscle, fat, andliver.
Once insulin binds with receptors on the cell membrane, glucose can move
intothecell,promotingcellularmetabolismandenergyproduction.

55.
Cont.…
Anumberof insulinpreparationsareavailableTheyvaryaccordingtothree
(3)main characteristics:
1. Timecourseofaction,
2. Species(source)and
3. Manufacturer

56.
Suggested insulin injection site

57.
 Insulin regimen in type 1 Diabetes Mellitus
 1. Conventional insulin therapy-describes simpler non-
physiologic insulin regimens, such as single daily injections, or
two injections per day (including a combination of regular or
short-acting and NPH insulin)
 2. Intensive insulin therapy-describes treatment with three or
more injections per day or with continuous insulin infusion with
an insulin pump.

58.
 Intensive insulin therapy requires: - Monitoring blood sugar before
breakfast (fasting), before lunch, before dinner & before bed.
 Counting and recording carbohydrates.
 Adjusting insulin doses in response to given glucose patterns. -
Coordinating diet, exercise, and insulin therapy.
 Responding appropriately to hypoglycemia

59.
 Designing insulin therapy
Total insulin dose per day Initiation, 0.2 to 0.4 units/kg/day
Maintenance – highly variable roughly 0.6 to 0.7 units/kg/day
Regimen options-with NPH and regular insulin (commonly available in
Ethiopian setting)
1. NPH twice daily injection – before breakfast and at bed time and
Regular Insulin twice daily injection-before breakfast and before dinner
2. 70/30 (70% NPH & 30% regular) twice daily injection-before
breakfast and before dinner
3. NPH twice daily injections – before breakfast and before bedtime

60.
ADVERSE REACTIONS Of INSULIN
Thetwomajoradversereactionsseenwithinsulinadministrationare:
1.Hypoglycemia, occurswhen:
 Thepatient eatstoolittlefood
 Theinsulindoseisincorrectlymeasuredandisgreaterthanthatprescribed
 Thepatient drasticallyincreasesphysical activity
2.Hyperglycemia, occurswhen:
 Thepatient eatstoomuchfood
 T
oolittleor noinsulinisgiven
 Thepatientexperiencesemotionalstressinfection,surgery,
pregnancy
, or anacuteillness

61.
Complications of InsulinTherapy
77
1. Local allergicreactions
Rx- antihistamine1hourbeforetheinjection
2. Systemicallergicreactions Rx- desensitization
3. Insulinlipdystrophy
LipoatrophyandLipohypertrophy
Mgt-Rotationof injectionsites

62.
Complications of InsulinTherapy…
4. InsulinResistance
• Mostcommonlyoccursbecauseof obesity
, whichcanbeovercomebyweight
loss
• Clinicallydefinedasadailyinsulin requirementof200unitsor
more
Rx
• Moreconcentratedinsulinpreparation, suchas U500
• Occasionally
, prednisonetoblocktheproduction of antibodies

63.
OralAnti-diabeticAgents
 May be effective for patients who have T2D that cannot
be treated by diet and exercise alone
 Cannot be used during pregnancy
 May also be used with insulin in the management of
some patients withT2D
 Use with insulin may decrease the insulin dosage in
some individuals

64.
Cont.…
Metformin –
the first line medicine for initiation of therapy
if intolerant to metformin or have a contraindication to it,
sulfonylureas can be the initial treatment medicine.
 Metformin, 500mg, P.O.daily with meals. Titrate dose slowly
depending on blood glucose

65.
Cont.…
Glibenclamide, 2.5mg-5mg, P.O.daily 30 minutes before
breakfast.
Titrate dose slowly depending on HbA1c and/or fasting
blood glucose levels to 15mg daily.
 When 7.5mg per day is needed, divide the total daily
dose into 2, with the larger dose in the morning.
 Avoid in the elderly and patients with renal impairment.

66.
5.Patient Education
🢅 Nutrition
🢅 Medication effects and side effects
🢅 Exercise
🢅 Disease progression
🢅 Prevention strategies:blood glucose monitoring
techniques,and medication adjustment
🢅 T
eaching survival skills
Basic definitions of insulin
T
reatment modalities
Recognition,treatment,and prevention of acute complications
🢅 Preventive measures of long term complications

67.
Pt educationCont’d…
Teaching patients to self administer insulin
🢅Storing insulin
🢅Selecting syringes
🢅Preparing the injection mixing insulins
🢅With drawing insulin
🢅Selecting and rotating the injection site
🢅Preparing the skin.Alcohol is not recommended for
cleansing
🢅Inserting the needle
🢅Aspiration is generally not recommended

68.
Acute Complications of Diabetes
There are three major acute complications of diabetes
related to short-term imbalances in bloodglucose levels:
a. Hypoglycemia
b. Diabeticketoacidosis/ DKA, and
c. Hyperglycemichyperosmolarnon-ketotic syndrome/HHNS,
which is also called hyperglycemic hyperosmolar syndrome
or state

69.
1.Hypoglycemia (Insulin Reactions)
⚫ OccurswhentheBGLsfallsto<50to60mg/dL(2.7to 3.3mmol/L)
Causes
⚫ T
oo much insulin or OHAs
⚫ T
oo little food
⚫ Excessive physical activity
Often occurs before meals, especially if meals are
delayed or snacks are omitted

70.
Hypoglycemia Clinical manifestations
i. Mildhypoglycemia
Stimulationof sympathetic nervous
systemresultingina surgeof
epinephrine and norepinephrine
 Inturnresultsin:
Sweating
Tremor
Tachycardia
Palpitation
Nervousness
Hunger
TheC/Msarebecause of:
1. Adrenergic
stimulation
2. Effect of hypoglycemiaon
CNS

71.
Hypoglycemia C/Ms Cont’d
ii. Moderatehypoglycemia
• DropinBGLdeprives thebraincellsof neededfuel for functioning
• Signsof impairedfunctionof theCNSmayinclude:
 Inability toconcentrate
 Headache,Light headiness,
 Confusion, Memoryloses,
 Slurredspeech,
 Double vision
 Drowsiness,
 Numbnessof thelips anN
do
v
e
tm
ob
ne
r
g1
6
u,2
e0
1
5
Adrenergic symptom:
Sweating
Tremor
Tachycardia
Palpitation
Nervousness
+

72.
Hypoglycemia C/Ms Cont’d
iii. Sever hypoglycemia
Resultsin:
ImpairedCNSfunctions
Disorientedbehavior
Seizures,
Difficultyarousingfromsleep, and
Lossof consciousness

73.
Management
By:Fikadu B.JU 95
A.Immediatetreatmentwithcarbohydrate
 Theusual recommendation isfor 15gof afast-acting
concentratedsourceofcarbohydratesuchasthe following,
givenorally:
A. Threeor four commercially prepared glucosetablets
B. 100-150ml of fruit juiceor regular soda
C. 6to10hardcandies
D. 2to3teaspoons of sugar or honey
NursingAlert: To prevent sharp increase in BGL, it is not necessary to
add sugar to juice, even if it is labeled as unsweetened juice: the fruit
sugarin juicecontainsenough carbohydrateto raisethe BGL

74.
Management
Immediatetreatmentwithcarbohydrate…
• TheBGLshouldberetested in 15minutesandretreatedif it isless
than70to75mg/dL(3.8 to4mmol/L)
• If thesymptomspersistforlongerthan10to15minutesafterinitial
treatment, thetreatmentis repeated
• Oncethesymptomsresolve,asnackcontainingproteinandstarch
(eg,milk orcheeseandbananas/crackers) isrecommendedunless
thepatientplanstoeataregular meal or snackwithin30to60
minutes

75.
Management
Immediatetreatment withcarbohydrate…
B.InitiatingEmergencyMeasures
Glucagoninjection:
Hasanonsetof 8to 10minutes, andits action lasts12to27minutes
Foradults whoareunconsciousandcannotswallow,aninjectionof
glucagon1mgcanbeadministered either subcutaneouslyor
intramuscularly
Afterinjection of glucagon,thepatient maytakeaslongas20
minutesto regainconsciousness

76.
Management
Immediatetreatmentwithcarbohydrate…
Aconcentratedsourceof carbohydrate:
• Shouldbegiventothepatientonawakeningto preventrecurrenceof
hypoglycemiafollowedbyasnack
• 50%/40%Dextroseinwater (D50W/D40W)
• 🗸
Forpatientswhoareunconsciousorcannot swallow
• 🗸
25to50mLof 50%/40%dextroseinwater may beadministeredIV
• 🗸Theeffectisusuallyseenwithinminutes

77.
C.ProvidingPatientEducation
 Consistentpatternofeating,administeringinsulin,and exercising
 Between-mealandbedtimesnacksmaybeneededtocounteractthemaximuminsulineffect
 Thepatient should cover the time of peakactivity of insulin byeating asnackandbytaking
additionalfoodwhenphysical activityisincreased
 Routinebloodglucosetests to anticipate change insulinrequirementsandtoadjust the
dosage

78.
 T
oprevent unexpected hypoglycemia all patients treated with insulin should
wearanidentification braceletortagstatingthat theyhavediabetes
 Symptomsofhypoglycemia
 Patientswithdiabetes,especially thosereceiving insulin,learntocarrysomeformof
simplesugarwith themat all times
 Advisingtorefrainfromeatinghigh-calorie,high-fat dessert foods(eg,cookies,
cakes, icecream)totreat hypoglycemiabecausetheirhighfatcontentmayslow
theabsorptionoftheglucoseandresolutionofthe hypoglycemicsymptoms

79.
Diabetic Ketoacidosis (DKA)
Definition
• DKA is a metabolic derangement in T1D that is
caused by an absence or markedly inadequate
amount of insulin
• Insulin deficiency results in disorders in the
metabolism of carbohydrate,protein, and fat

80.
DKA Causes:
84
Threemaincauses:
1. Decreased or misseddoseor deficiencyof insulin
causedby:
An insufficient dosageof insulin prescribed
An insufficient insulin being administered bythepatient
Patient error in drawing upor injecting insulin
Intentional skipping of insulin doses
Equipment problems
2.Illnessor infection
3. Undiagnosedanduntreateddiabetes

81.
DKA Causes …
 Illnessesandinfections areassociatedwith insulin resistance
 Inresponsetophysical(andemotional)stressors, thereis anincrease
in thelevel of “stress”hormones:
 Glucagon,
 Epinephrine, norepinephrine,
 Cortisol, and
 Growthhormone
Thesehormonespromoteglucose productionbytheliver and
interferewith glucoseutilizationby muscleandfat tissue

82.
DKA: Pathophysiology
Thethreemainclinical featuresofDKAare:
1. Hyperglycemia
2. Dehydrationandelectrolyteloss
3. Acidosis

83.
DKA: Diagnosis
 BGLs may vary from 250 to 800mg /dL
 Serum Bicarbonate 0-15mq/L
 PH 6.8-7.3
 PaCO2 10-30mmHg – Respiratory
compensation
 Increased creatinine
 Increased BUN
 Increased hematocrite

84.
DKA: Prevention
 If DKA is related to illness,teach the patient about
“Sick day” rules for managing their diabetes when ill
 Assess diabetic self management skills including blood
glucose testing and insulin administration
 If insulin dose is intentionally altered, psychological
counseling is recommended for patients and family
members

85.
DKA: Medical Management
T
reatment Goals:
1. T
reating hyperglycemia
2.Correcting dehydration
3. Maintaining electrolyte balance
4.Reversing acidosis

86.
HHNS
Is ametabolic disorderofT2Dresulting fromarelativeeffective
insulin deficiency (i.e., Insulin resistance) initiatedbyaninter-
currentillness that raises the demandfor insulin,associated with
polyuria andseverdehydration.
 Occurs most often in older people (50 to 70 years of age) who
havenoknownhistoryof diabetesor who havetype2diabetes

87.
Hyperosmolalityandhyperglycemiaarepredominant
The patient’s persistent hyperglycemia causes osmotic diuresis,
resulting in losses of waterandelectrolytes.
 BecauseofwatershiftsfromICFspacetoECFspace thepatientmay
presentwithneurologicabnormalities suchas:
Somnolence, coma,
Seizures,
Hemiparesis, and
Aphasia

88.
HHNS: Precipitating factors
i. Acute illness (e.g.pneumonia,stroke)
ii. Medications that exacerbate BGL (e.g.
thiazides)
iii. T
reatments such as dialysis

89.
H HNS: Diagnosis
History
Physical Examination
Lab test
BGL 600 to 1200mg/dL
Electrolytes
BUN
CBC- RBCs
Serum osmolality >350 mosm/kg
ABG analysis – PH normal

90.
HHNS: Medical Management
TheoverallapproachtothetreatmentofHHNSis
similartothat of DKA:
Fluidreplacement,
Correctionof electrolyteimbalances, and
Insulinadministration

91.
Comparison of DKA and HHNS
Characteristics DKA HHNS
Patients most
commonly
Can occur in type 1 or type 2
diabetes; more common in type 1
diabetes
Can occur in type 1 or type 2
diabetes; more common in type 2
diabetes,
especially elderly patients with
type 2 diabetes
Precipitating event Omission of insulin; physiologic
stress (infection, surgery, CVA, MI)
Physiologic stress (infection,
surgery, CVA, MI)
Onset Rapid (<24 h) Slower (over several days)
Blood glucose levels Usually >250 mg/dL (>13.9 mmol/L) Usually >600 mg/dL (>33.3 mmol/L)
Arterial pH level <7.3 Normal
Serum and urine
ketones
Present Absent
Serum osmolality 300–350 mOsm/L >350 mOsm/L
Plasma bicarbonate
level
<15 mEq/L Normal
BUN and creatinine
levels
Elevated Elevated
Mortality rate <5% 10–40%

92.
Long term of dm complication
 assigment

93.
Disorders of the thyroid gland
 It is a butterfly-shaped organ
 Located in the lower neck, anterior to the trachea
 Consists of two lateral lobes connected by an isthmus
 Is about 5 cmlong and 3 cmwide and weighs about 30 g
 Hasvery high blood flow:
 About 5 mL/min per gram of thyroid tissue (150ml/min)
Approximately five times the blood flow to the liver
Highmetabolic activity of thethyroidgland

94.
Synthesis of thyroid hormones (T3 &T4)
 T3+T4= Iodine molecule + tyrosine (amino acid)
The major use of iodine in the body is by the thyroid gland, and the
major derangement in iodinedeficiencyis alteration of thyroid function.

95.
Function ofThyroid Hormone
A.Theprimary functionof thyroid hormoneisto control cellular
metabolicactivity
 T4
Relativelyweak hormone
Maintainsbody metabolisminasteadystate
 T3
Is about fivetimes as potent asT4
Has amore rapid metabolicaction
B.Influencecellreplicationandare important inbrain development.
C. Necessary for normal growth.

96.
Cont.….
Metabolism
⚫ The complex of physical and chemical processes occurring
within a living cell or organism that are necessary for the
maintenance of life.
⚫ Catabolism is the set of metabolic pathways that
breaks down molecules into smaller units that are either
oxidized to release energy
, or used in other anabolic
reactions
⚫ Anabolism is the set of metabolic pathways that
construct molecules from smaller units

97.
Definition of terms
Euthyroid:state of normalthyroid hormoneproduction
Thyroid storm: severe life-threatening hyperthyroidism
precipitated by stress; characterized by high fever,
extreme tachycardia, andalteredmental state
Thyrotoxicosis: condition produced by excessive endogenous or
exogenousthyroid hormone

98.
SpecificDisorders of theThyroid Gland
Goiter
Hyperthyroidism
Hypothyroidism

99.
Goiter
 A lack of iodine in the patient’s diet (endemic, simple goiter) causes the
thyroid gland to become enlarged.
 The thyroid gland can also become enlarged by ingesting large amounts of
goitrogenic drugs or goitrogenic foods that decrease production of
thyroxine, such as strawberries, cabbage, peanuts, peas, peaches, and
spinach.
 A simple goiter is not caused by inflammation or neoplasm.

100.
SIGNS AND SYMPTOMS
 Difficulty in swallowing (dysphagia) due to a large thyroid pressing on
the esophagus
 Enlarged thyroid gland
 Respiratory distress from the large gland, causing pressure on the trachea
 A tight feeling in the throat from a large gland
 Coughing

101.
TREATMENT
 If increased TSH, administer hormone replacement with
levothyroxine (T4), desiccated thyroid, or liothyronine (T3).
 If the thyroid gland is overactive, then administer small
doses of Lugol’s solution or potassium iodide solution.
 If the simple goiter cannot be reduced through medication,
then a thyroidectomy is performed during which all or part of
the thyroid is removed.

102.
NURSING INTERVENTION
 Avoid goitrogenic foods or drugs in sporadic goiter since they make thyroid
hormone production.
 Use iodized salt to prevent and treat endemic goiter, since the thyroid needs
iodine to make thyroid hormone.
 Explain to patient:
 The need for life-long thyroid replacement after thyroidectomy and
radioactive iodine.
 The need for intermittent lab work to monitor the thyroid.
 Visits to the primary care practitioner to monitor size of thyroid gland.

103.
Hyperthyroidism
 There is an overproduction of T3 and T4 by the thyroid gland that can
be caused by an autoimmune disease where the body’s immune system
attacks the thyroid gland.
 Other causes can be a benign tumor (adenomas) resulting in an
enlarged thyroid gland (goiter) or an overproduction of TSH by the
pituitary gland, caused by a pituitary tumor.

104.
 The thyroid gland produces three hormones: thyroxine (T4),
triiodothyronine (T3), and thyrocalcitonin (calcitonin). Secretion of T3
and T4 is regulated by the anterior pituitary gland through a negative
feedback mechanism.
 When serum T3 and T4 levels decrease, thyroid-stimulating hormone
(TSH) is released by the anterior pituitary.
 This stimulates the thyroid gland to secrete more hormones until normal
levels are reached.

105.
Cont.….
 T3 and T4 affect all body systems by regulating overall body metabolism,
energy production, and fluid and electrolyte balance, and controlling
tissue use of fats, proteins, and carbohydrates.
 Calcitonin inhibits mobilization of calcium from bone and reduces blood
calcium levels.
 Hyperthyroidism is a clinical syndrome caused by excessive circulating
thyroid hormones.
 Because thyroid activity affects all body systems, excessive thyroid
hormone exaggerates normal body functions and produces a
hypermetabolic state.

106.
Risk Factors
 Causes of hyperthyroidism
■ Graves’ disease is the most common cause. Autoimmune
antibodies result in hypersecretion of thyroid hormones.
■ Toxic nodular goiter, a less common form of hyperthyroidism, is
caused by overproduction of thyroid hormone due to the
presence of thyroid nodules.
■ Exogenous hyperthyroidism is caused by excessive dosages of
thyroid hormone.

107.
SIGNS AND SYMPTOMS
 Enlarged thyroid gland (goiter) caused by tumor
 Protrusion of the eyeballs (exophthalmos) due to lymphocytic infiltration
which pushes out the eyeball
 Sweating (diaphoresis); excess thyroid hormone raises the metabolic rate
 Increased appetite due to increased metabolism
 Nervousness due to high levels of thyroid hormone
 Weight loss due to increased metabolism
 Menstrual changes due to elevated levels of thyroid hormone

108.
Laboratory Tests
Serum TSH test – Decreased in the presence of Graves’
disease (may be elevated in secondary or tertiary
hyperthyroidism)
 Free thyroxine index (FTI) and T3 – Elevated in the
presence of disease
 Thyrotropin-releasing hormone (TRH) stimulation test –
Failure of expected rise in TSH

109.
TREATMENT
 For mild cases and for young patients, administer antithyroid medication
such as propylthiouracil and methimazole to block synthesis of T3 and T4.
 For Graves’ disease and for patients 50 years of age or older, radioactive
iodine therapy is used to decrease production of thyroid hormones.
Administer Lugo's solution, SSKI, or potassium iodide.
 For severe cases where the size of the thyroid gland interferes with
swallowing or breathing, the thyroid gland is surgically reduced in size or
removed.

110.
Cont.…
 Administer beta blockers such as propranolol until hyperthyroidism
diminishes to decrease sympathetic activity and control tachycardia,
tremors, and anxiety.

111.
NURSING INTERVENTION
 Monitor vital signs.
 Provide cool environment.
 Protect the patient’s eyes with dark glasses and artificial tears if the
patient has exophthalmos.
 Provide a diet high in carbohydrates, protein, calories, vitamins, and
minerals.
 Monitor for laryngeal edema following surgery (hoarseness or inability to
clearly speak).
 Keep oxygen, suction, and a tracheotomy set near bed in case the neck
swells and breathing is impaired.

112.
 Keep calcium gluconate near the patient’s bed following surgery.
 This is the treatment for tetany and is used to maintain the serum calcium
level in normal range.
 Place the patient in a semi-Fowler’s position to decrease tension on the
neck following surgery.
 Support the patient’s head and neck with pillows.
 Monitor for muscle spasms and tremors (tetany) caused by manipulation of
the parathyroid glands during surgery.
 Check drainage and hemorrhage from incision line; red flags are frank
hemorrhage and purulent, foul smelling drainage.
 Monitor for signs of hypocalcemia (tingling of hands and fingers).
 The treatment is IV calcium, administered quickly.

113.
 Check for Trousseau’s sign (inflate blood pressure cuff on the arm and
muscles contract).
 Check for Chvostek’s sign (tapping of the facial nerve causes twitching
of the facial muscles).
 Both this sign and Trousseau’s sign are positive when the parathyroid
glands have been manipulated during thyroid surgery, in which case
they secrete too much phosphorus and not enough calcium.
 Since muscles, i.e. the heart, need calcium for work, a low calcium level
may cause muscle spasms which are easily detected by Chvostek’s sign
and Trousseau’s sign.

114.
Complication
 Hemorrhage at the incision site due to a released surgical tie, excessive
coughing, or movement.
 Thyroid Storm/Crisis ;-Thyroid storm/crisis results from a sudden
surge of large amounts of thyroid hormones into the bloodstream,
causing an even greater increase in body metabolism.
 Airway Obstruction;-Hemorrhage, tracheal collapse, tracheal mucus
accumulation, laryngeal edema, and vocal cord paralysis can cause
respiratory obstruction, with sudden stridor and restlessness.
 Hypocalcemia and Tetany;-Damage to parathyroid gland causes
hypocalcemia and tetany

115.
Hypothyroidism
Hypothyroidism is a condition in which there is an inadequate
amount of circulating thyroid hormones triiodothyronine (T3 )
and thyroxine (T4 ), causing a decrease in metabolic rate that
affects all body systems.

116.
Classifications of hypothyroidism by etiology
 Primary – Primary hypothyroidism stems from dysfunction of the thyroid gland. This is the
most common type of hypothyroidism and is caused by disease (autoimmune thyroiditis –
Hashimoto’s disease) or loss of the thyroid gland (iodine deficiency, radioactive iodine
treatment, surgical removal of the gland).
 Secondary – Secondary hypothyroidism is caused by failure of the anterior pituitary gland to
stimulate the thyroid gland or failure of the target tissues to respond to the thyroid hormones
(pituitary tumors).
 Tertiary – Tertiary hypothyroidism is caused by failure of the hypothalamus to produce thyroid-
releasing factor.

117.
Hypothyroidism is also classified by age of onset
 Cretinism – Cretinism is a state of severe hypothyroidism found in infants.
 Juvenile hypothyroidism – Juvenile hypothyroidism is most often caused
by chronic autoimmune thyroiditis and affects the growth and sexual
maturation of the child.
 Adult hypothyroidism;-Because older adult clients who have
hypothyroidism may have manifestations that mimic the aging
process, hypothyroidism is often undiagnosed in older adult clients,
which can lead to potentially serious adverse effects from
medications (sedatives, opiates, anesthetics).

118.
Risk Factors
 The disorder is most prevalent in women, with the incidence rising
significantly in people who are 30 to 60 years of age.
 Many individuals who have mild hypothyroidism are frequently undiagnosed,
but(intraoperative hypotension, cardiac complications following surgery).
 Use of medications (lithium [Lithobid], amiodarone [Cordarone])
 Inadequate intake of iodine

119.
SIGNS AND SYMPTOMS
 Fatigue due to slow metabolism
 Hypothermia due to slow metabolism
 Brittle nails due to low levels of thyroid hormone, which helps
growth and development
 Thick dry hair from lack of thyroid hormone
 Dry skin from lack of thyroid hormone
 Menstruation changes due to diminished levels of thyroid hormone
 Slow cognitive function due to slow metabolism
 Weight gain, low levels of thyroid hormone causes fatigue,
sluggishness

120.
Diagnostic Procedures
 Skull x-ray, computed tomography scan, and magnetic resonance
imaging
☐ These procedures can locate pituitary or hypothalamic lesions that
may be the underlying cause of hypothyroidism.
 ECG
☐ Sinus bradycardia, flat or inverted T waves, and ST deviations

121.
TREATMENT
Replacement hormone; levothyroxine is the treatment of
choice.
Serum measurements of T3 and T4 will need to be performed
after 6 to 8 weeks to determine if the patient is taking the
correct dose.
The patient needs to be aware that this is a lifetime
replacement.

122.
NURSING INTERVENTION
 Monitor vital signs.
 Provide a warm environment.
 Low-calorie diet.
 Increase fluids and fiber to prevent constipation.
 Take thyroid replacement hormone each morning to avoid insomnia.
 Monitor for signs of thyrotoxicosis (an increase in T3): nausea, vomiting,
diarrhea, sweating, tachycardia.
 Explain to the patient:
Side effects of thyroid hormone replacement.
Review the signs of hyperthyroidism and hypothyroidism.
Have patient contact health care provider if signs change.

123.
Complications
Myxedema;-
 Myxedema is a life-threatening condition that occurs when hypothyroidism is
untreated or when a stressor (such as infection, heart failure, stroke, or
surgery) affects an individual who has hypothyroidism.
 Clients who have been taking levothyroxine and suddenly stop the medication
are also at risk.

124.
Clinical Manifestations
 Significantly depressed respirations (hypoxia, hypercapnia)
 Decreased cardiac output
 Worsening cerebral hypoxia
 Lethargy, stupor, coma
 Hypothermia
 Bradycardia, hypotension
 Hyponatremia

125.
Nursing Actions
Maintain airway patency with ventilatory support if
necessary.
Provide continuous ECG monitoring.
Monitor ABGs to detect hypoxia, hypercapnia, respiratory
acidosis.
Warm the client with blankets.
Monitor the client’s body temperature until stable

126.
 Replace thyroid hormone by administering large doses of levothyroxine
(Synthroid) IV bolus.
 Monitor vital signs because rapid correction of hypothyroidism can
cause adverse cardiac effects.
 Monitor intake and output, and daily weights. With treatment, urine
output should increase, and body weight should decrease; failure to do
so should be reported to the provider.
 Treat hypoglycemia with glucose.
 Administer corticosteroids.
 Check for possible sources of infection (blood, sputum, urine) that may
have precipitated the coma. Treat any underlying illness.

127.
Disorders of the parathyroid glands

128.
Hypoparathyroidism
 Hypoparathyroidism is diminished functioning of the parathyroid glands
leading to low levels of PTH, which causes hypocalcemia.
 The primary cause of hypoparathyroidism is destruction of the glands by
an autoimmune cause.
 Occasionally the gland(s) may be accidentally removed during
thyroidectomy

129.
SIGNS AND SYMPTOMS
Tetany (muscle irritability) due to abnormal levels of calcium
Tingling of periorbital area, hands, and feet from abnormal
calcium levels
Lethargy due to low levels of parathyroid hormone
Cataract development
Convulsions due to acute low calcium levels

130.
INTERPRETING TEST RESULTS
 Decreased serum calcium due to low levels of PTH.
 Increased serum phosphate due to low levels of PTH.
 Decreased serum PTH from diminished secretion from the
parathyroid glands.
 Decreased urinary calcium from diminished PTH.
 Positive Chvostek’s sign due to decreased calcium levels.
 Positive Trousseau’s sign due to decreased calcium levels.

131.
TREATMENT
 Administer calcium gluconate by slow IV drip for acute hypocalcemia
 Oral calcium—calcium gluconate, lactate, carbonate (Os-Cal).
 Large doses of vitamin D (calciferol) to help absorption of calcium.
 Aluminum hydroxide gel (Amphogel) or aluminum carbonate gel; basic
(Basaljel) to decrease phosphate levels.
 Keep tracheostomy set and injectable calcium gluconate at bedside for
impaired respiration from swelling as well as for emergency
administration of calcium.

132.
NURSING INTERVENTION
 Monitor patients condition
 If the parathyroids were damaged during thyroid surgery:
• Administer calcium to maintain the serum levels in a low normal range.
• Testing should be done every 3 months.

133.
Hyperparathyroidism
Overactivity of the parathyroid glands caused by a tumor
produces too much PTH, resulting in hypercalcemia and
hypophosphatemia.
Excess calcium is reabsorbed by the kidneys and may result in
kidney stones; however, malfunction in the feedback mechanism
prevents detection of excessive calcium levels in the blood,
thereby failing to adjust the secretion of PTH.
Parathyroid tumors are usually benign.

134.
SIGNS AND SYMPTOMS
Asymptomatic
Increased serum calcium level
Bone pain or fracture as a result of excreting calcium from bone
 Kidney stones
 Frequent urination as a result of increased calcium in the urine
(hypercalciuria)

135.
INTERPRETING TEST RESULTS
Increased serum calcium.
Increased serum PTH.
Decreased serum phosphate.
Increased urine calcium.
Presence of parathyroid tumor shows on ultrasound.
Fine needle biopsy of the parathyroid tumor.

136.
TREATMENT
Surgical removal of the parathyroid tumor.
Administer bisphosphonates to lower serum calcium by
increasing calcium absorption in the bone.
 IV normal saline to dilute serum calcium.
Diuretic such as furosemide to excrete excess calcium in
the urine.

137.
NURSING INTERVENTION
 Monitor intake and output.
 Monitor for fluid overload.
 Monitor electrolyte balance.
 Give the patient acid-ash juices such as cranberry juice.
 Strain urine for kidney stones.
 Place the patient on a low-calcium and high-phosphorus diet.
 Explain to patient:
 Avoid over-the-counter calcium supplements.
 Maintain daily activities.

138.
Disorders of the pituitary gland

139.
HYPOPITUTARISM
 Hypopituitarism is an underactive pituitary gland
that results in deficiency of one or more pituitary
hormones.
 This may result from disorders involving the
pituitary gland, hypothalamus or surrounding
structures.
 If there is decreased secretion of most pituitary
hormones, the term panhypopituitarism is used.

140.
ETIOLOGY
 Disease of the pituitary gland itself, such as
pituitary tumors (adenomas)
 Destruction of the pituitary gland by trauma
or vascular lesion or brain surgery.
 Radiation therapy to the head and neck area.

141.
Contd…
 Infections: cerebral-bscess, meningitis, encephalitis,
 Ischaemia and infarction
 Autoimmune inflammation (hypophysitis)
 Congenital malformations of the pituitary gland

142.
CLINICAL FEATURES
• The clinical features depends upon type of hormone
deficiency.
Type of
hormone
Symptoms
LowACTH Decrease production of cortisol by the
adrenal glands which causes symptoms
related to adrenal insufficiency.
Low growth
hormone
Failure of growth in children causing
short height (dwarfism) and undue
tiredness and weakness in adults.

143.
Type of
hormone
Symptoms
Low LH &
FSH
In Men: decrease in libido, impotence &
impaired fertility due to a decreased ability
to produce testosterone.
In Female: irregular or absent menstrual
periods leading to infertility.
Low thyroid
hormone
Undue tiredness, weight gain,
constipation, dry skin and feeling
colder than usual.

144.
Types of hormone Symptoms
Lack ofADH From the posterior part of
the pituitary gland results in
the passing of uncontrolled
large amounts of urine and
causes severe thirst.
Prolactin deficiency Low levels can lead to a
woman inability to produce
breast milk after childbirth.

145.
DIAGNOSTIC EVALUATION
 Health history and clinical manifestation
 Change in physical appearance
 Blood test
 Radioimmunoassay

146.
DEFICIENCY HORMONE
THERAPY
DOSE
TRH L-thyroxine 0.1 – 0.15 mg /day
LH In female: Cyclical
estrogen therapy with
Ethinyl oestradiol
20 – 30 μg for 3 weeks

147.
DEFICIENCY HORMONE
THERAPY
DOSE
LH &FSH Progesterone (medroxy
progesteroneAcetate)
In male: Teststerone
5mg/day from day 14-21
Of menstrual cycle
250-300mg IM every2-4
weeks
GH Biosynthetic 24U/m2/week
SC

148.
SURGICAL MANAGEMENT
Transsphenoidal surgery:
• Removal of the tumor by an operation
through the nose and the sphenoidal sinuses.

149.
Contd
…
 Craniotomy: Tumor is removed by opening
the skull.

150.
DWARFISIM
• Dwarfism is when an individual is short in stature
resulting from a medical condition caused by problems
that arise in the pituitary gland in which the growth of the
individual is very slowed or delayed.

151.
CAUSES
 The most common causes are achondroplasia
is a bone-growth disorder
 Turner syndrome
 Growth hormone deficiency and
 Poor nutrition.

152.
SIGN & SYMPTOMS
 Short stature
 Delayed puberty
 Symptomatic hypoglycemia in 10% cases
 Delayed eruption of secondary teeth in
children

153.
TREATMENT
 Hormone therapy
• Growth hormone deficiency is treated with injections of a
synthetic version of the hormone.
 Surgical treatment:
• Inserting metal staples into ends of long bones where growth
occurs (growth plates) in order to correct the direction in which
bones are growing.

154.
Disease conditions caused by hypopituitarism:
 Dwarfism
 Dibetes Insipidus
 Addisson’s disease
 Hypothyroidism

155.
DIABETES INSIPIDUS
 It is a disorder of the posterior lobe of the
pituitary gland characterized by a deficiency of
antidiuretic hormone (ADH), or vasopressin.
 Great thirst (polydipsia) and large volumes of
dilute urine characterize the disorder.

156.
CAUSES
 Head trauma
 Brain tumor
 Surgical ablation or irradiation of the pituitary
gland
 Infections of the central nervous system
 Failure of the renal tubules to respond to ADH

157.
CLINICAL FEATURES
 Excessive thirst
• May be intense or uncontrollable
• Involves craving for water
 Excessive urine volume

158.
DIAGNOSIS
 Urine analysis
 Monitoring urine output
 Water deprivation test
 Hypertonic saline test
 MRI

159.
TREATMENT
The objectives of therapy are:
 To replace ADH (which is usually a long-term
therapeutic program).
 To ensure adequate fluid replacement.
 To identify and correct the underlying
intracranial pathology.

160.
Contd…
1. Fluid replacement
2. Central diabetes insipidus may be controlled
with vasopressin (desmopressin, DDAVP). It
can be taken as either an injection, a nasal
spray, or tablets.

161.
COMPLICATIONS
 Dehydration:  Electrolyte imbalance
• Dry skin and mucus • Fatigue, lethargy
• Fever & Rapid heart rate • Headache
• Sunken eyes
• Unintentional weight loss
• Irritability
• Muscles pain

162.
Syndrome of inappropriate antidiuretic hormone
(SIADH)
SIADH is caused by too much ADH being secreted by the
posterior pituitary gland.
ADH is responsible for controlling the amount of water
reabsorbed by the kidney; it prevents the loss of too much fluid.
 When too much water is detected, ADH production or secretion
is halted.

163.
SIADH may be caused by damage to the hypothalamus or
pituitary, inflammation of the brain, some medications
such as selective serotonin receptor inhibitors (SSRIs),
carbamazepine, cyclophosphamides, and chlorpropamide.
Certain cancers, especially lung, may produce ADH.

164.
SIGNS AND SYMPTOMS
Headaches due to hyponatremia
Nausea and vomiting due to hyponatremia
Confusion due to hyponatremia
Personality changes due to hyponatremia

165.
INTERPRETING TEST RESULTS
Hyponatremia (low serum sodium) due to the
dilution
Treatment
Administer saline IV to replenish sodium.
Treat underlying cause.

166.
NURSING INTERVENTION
Monitor electrolytes to determine sodium levels.
Restrict fluid because excess fluid dilutes sodium levels.
Weigh the patient daily using the same scale, at same
time of day with similar clothing.
Monitor intake and output.

167.
HYPERPITUTARISM
 Hyperpituitarism is the primary
hypersecretion of pituitary hormones.
 It typically results from a pituitary adenoma.
 There are usually three hormones that are
over secreted due to pituitary adenoma are
prolactin, adrenocorticotropic
hormone (ACTH) and growth hormone (GH).

168.
Contd…
 Some of the common disorders as a result of
hypersecretion of piutitary glands are as
follows:
 Excess prolactin: Prolactinoma.
 Excess ACTH: Cushing’s disease.
 Excess GH: Gigantism and Acromegaly.

169.
ETIOLOGY
 Pituitary tumor
 Inherited condition known as multiple
endocrine neoplasia type 1

170.
CLINICAL FEATURES
 Headache
 Visual field loss
or Double vision
 Excessive sweating
 Hoarseness
 Milk secretion
from breast
 Sleep apnea
 Joint pain and limitation
of motion
 Muscle weakness

171.
Difference between Gigantism & Acromegaly
179
Gigantism
 Start in infancy and growth is
continuous.
 Onset before puberty.
 Excessive growth 8-
9feet,enlargement of organs
heart, liver, spleen.
Acromegaly
 Starts at age 20-50yrs and
growth is slow.
 Onset after puberty.
 Increase in size of hands, feet,
lower jaw, skin becomes thick
and coarse.

172.
DIAGNOSIS
 Physical examination
 Laboratory investigations
 Radiological imaging studies

173.
TREATMENT
Medication:
Drugs may be used to shrink large tumors before
surgery or in cases where surgery is not an option.
Medication to reduce prolactin levels is usually the
preferred treatment for patients with a prolactinoma.

174.
Cond…
Bromocriptine and Cabergoline are
dopamine agonists (drugs that behave like
dopamine) and can shrink prolactinomas and return
secretions of prolactin to normal levels.
Acromegaly may be treated with Somastatin analogs
(octreotide) to lower growth hormone levels and
shrink tumors.

175.
Contd…
Radiation:
Used to treat patients who cannot undergo
after
surgery or for residual tumor tissue
surgery and do not respond to medication.
There are two approaches to radiation:
 Conventional
 Stereotactic therapies

176.
Contd…
Conventional radiation therapy
• It is administered in small doses over a period
of 4 to 6 weeks.
• One drawback is that radiation treatments can
damage normal tissue surrounding the tumor.

177.
Contd…
Stereotactic therapy
• It provides a high-dose beam of radiation
targeted at the tumor.
• It may be completed in one session, resulting
in less damage to surrounding tissue.

178.
Note
• Most patients that undergo radiation treatment require
hormone replacement therapy due to a gradual decline in
the secretion of other pituitary hormones.

179.
Contd…
3. Surgery:
 Trans-sphenoidal Adenectomy
 Hypophysectomy

180.
Nursing Intervention
 Help to accept altered body image that is irreversible.
 Assist family to understand what client is experiencing.
 Help to recognize that the need for medical supervision will be life-
long.
 Help to understand the basis for the change in sexual functioning.

181.
Contd…
 Provide psychological and emotional support.
 Perform range of motion exercise to assure joint mobility.
 Monitor for hyperglycemia and cardiovascular problems
(hypertension, angina, CHF) and modify care accordingly

182.
Contd…
 Teach self-care after a hypophysectomy.
 Encourage to follow the established medical regimen, particularly
hormone replacement
 Limit stressful situations.
 Protect self from infection.