NCMB316 LECTURE: Prelim Week

05
Endocrine System and Pituitary Disorders
Bachelor of Science in Nursing 3YB
Professor: Dr. Potenciana A. Maroma
ENDOCRINE SYSTEM AND PITUITARY DISORDERS • Hypo-secretion:
- Composed of ductless glands that releases hormones - Absence of milk during lactation
directly into the bloodstream • ACTH (Adrenocorticotropic Hormone)
- Hypothalamus control most of the endocrinal activity of - Stimulates adrenal cortex to secrete the adrenal
the pituitary gland hormones cortisol and aldosterone
- Secretes RELEASING HORMONES: GHRH, CRH, TRH, - Hyper-secretion:
GnRH, PRH o Cushing’s Syndrome
• Pituitary Gland (Hypophysis) - Divided into 2 lobes: - Hypo-secretion:
- Anterior Pituitary (Adenohypophysis) o Addison’s Disease
o 70% of the gland - TSH (Thyroid Stimulating Hormone)
o Found in the sella turcica, a depression in the o Stimulates the thyroid gland to secrete T3 and T4
sphenoid bone at the base of the brain - Hyper-secretion:
o Secretions: GH, PRL, ACTH, TSH, LH, FSH, o Hyperthyroidism
MSH - Hypo-secretion:
- Posterior Pituitary (Neurohypophysis) - Hypothyroidism
o Stores & secretes ADH & Oxytocin produced by - Gonadotropin (FSH/ LH)
the hypothalamus • Affect growth, maturity and functioning of primary and
secondary sex characteristics
• They influence the gonads (ovaries and testes) to
secrete gonadal hormones- estrogen, progesterone,
testosterone
• Hyper-secretion:
o precocious puberty
• Hypo-secretion
o Males: impotence,  production of spermatozoa
o Females: no ovulation, no menstruation,
infertility
- MSH (Melanocyte Stimulating Hormone)
• Stimulates the skin melanocytes to produce the
pigment melanin
• Hypersecretion:
o Bronze appearance of the skin
(hyperpigmentation)
• Hyposecretion:
-
Disorders are generally grouped into:
o Albinism (hypopigmentation)
o HYPER - when the gland secretes excessive
- ADH (Antidiuretic Hormone / Vasopressin)
hormones
o HYPO - when the gland does not secrete enough • causes the renal retention of water (not affecting
hormones sodium) in the renal tubules
- Hyper and Hypo can be classified as: • It can also cause vasoconstriction; “vasopressin”
o PRIMARY - when the Gland itself is the problem • Hyper-secretion:
o SECONDARY - when the problem is the pituitary or o SIADH - excessive retention of water by the renal
the hypothalamus tubules:
- Growth hormone (Somatotropin) • Hypo-secretion:
o Growth of body tissues and bone o DI - inability of the renal tubules to retain water
• Hyper-secretion: o Diagnostic Test: Water deprivation test
- GIGANTISM (children) • Oxytocin
- ACROMEGALY (adults) o released during childbirth to cause uterine
- Hypo-secretion of GH: Dwarfism contraction
• Prolactin (Mammotropic/ Lactotropic Hormone) o responsible for the “let-down” reflex of milk
- Mammary tissue growth and lactation. ejection
• Hypersecretion:
- Galactorrhea (abnormal breast-milk production)
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 316 LECTURE: WK5 – ENDOCRINE SYSTEM AND PITUITARY DISORDERS

Pituitary Gland Disorders - Pharmacotherapy

Hyperpituitarism
- Chronic, progressive hyper-function of the anterior
pituitary resulting in oversecretion of one or more of the
anterior pituitary hormones
- Etiologic factors:
o Tumor and hyperplasia (Benign pituitary
adenoma, hyperplasia of pituitary tissue)
o Prolactinomas (prolactin-secreting tumors)
account for 60 to 80% of all pituitary tumors
- GH-producing adenomas
Assessment Findings
• Acromegaly
- gradual, marked enlargement of the bones of the face,
jaw, hands and feet. There can be diaphoresis,
hyperglycemia, oily skin and hirsutism
• Gigantism
- proportional overgrowth of all body tissues with
remarkable height
• Neurologic manifestations
- Headache
- Somnolence, Behavioral changes, seizures
- Signs and symptoms of increased ICP
- Disturbance in appetite, sleep, temperature
regulation and emotional balance due to
hypothalamic involvement
- Visual disturbances due to the compression of the
optic chiasm above the pituitary gland:
- Hemianopsia or scotomas or blindness
- SCOTOMA “blindspot in vision”
Diagnostic Tests
• skull x-ray, CT scan, MRI (tumor or pituitary enlargement)
• Plasma GH levels determination: increased
• Adult male-.4-10ng/ml
• Female-1-14ng/ml
• Child- 10-50ng/ml
Medical Management
- Surgery
o Removal of pituitary gland
o Transphenoidal hypophysectomy
- Radiation
o Bromocriptine (Parlodel) is used to treat
- amenorrhea, a condition in which the
menstrual period does not occur;
- infertility (inability to get pregnant) in women
- abnormal discharge of milk from the breast
- Hypogonadism
- Parkinson's disease
- inhibit the synthesis of GH & prolactin
Nursing Management: Surgery
Pre-operatively: Health Teaching
- explain to the patient that this surgery will remove the
tumor from the pituitary gland
- A nasal catheter and nasal packing are expected in the
nasal cavity for a day
- Indwelling catheter will be inserted (to monitor UO) –
Diabetes Insipidus can be a complication of the surgery
- Review all patient’s medication regimen and provide
routine pre-op care
Post-operatively:
- Strictly keep the patient on BED rest for 24° and
encourage ambulation on day 2
- position the patient fowler’s to avoid tension on the
suture line and to avoid increased intracranial pressure
- Remind the patient NOT to sneeze, forcefully cough, bend
over and blow the nose for several days to avoid disturbing
the suture lines
- Mild analgesic can be given for headache
- Anticipate the patient to manifest signs and symptoms of
DI after surgery
- Be alert for  thirst and  UO w/ low SG
- Replace fluids and administer IV vasopressin as
ordered. DI should resolve in 72°
- Report outputs above 900 ml / 2 hours or
specific gravity below 1.004 (D. Insipidus)
- Arrange for a visual field testing because progressive
visual field defects may indicate bleeding
- Be alert for potential leakage of CSF from the operative
site
- If rhinorrhea is present, test the discharge for glucose and
if positive, report to the physician of the CSF leakage
Nursing Management
- Provide emotional support to help patient cope with an
altered body image
- Perform range of motion exercises to promote maximum
joint mobility and prevent injury due to muscle weakness
- Keep skin dry and avoid using oily lotion
- Provide safety measures because pituitary tumor can
cause visual disturbances. Approach the patient to the
unaffected side if he has hemianopsia.
- Deal with the mood swings appropriately
- Home teaching include: emphasizing that hormone
replacement is needed lifetime, wear an ID, have regular
follow-up
• Home care instruction
- Explain the need to take the medication as prescribed
- Report progressive visual changes, excessive urination

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 316 LECTURE: WK5 – ENDOCRINE SYSTEM AND PITUITARY DISORDERS

- Advise patient NOT to brush the teeth for 2 weeks to

avoid injury to the suture lines
- Find alternative measures for oral care like mouthwash
Hypopituitarism
- Hypo-function of pituitary gland causing deficiencies in
both the pituitary hormones and the hormones of the
target glands
- Clinical Manifestation:
o Observed when 75% of the pituitary gland is
dysfunctional
o Metabolic dysfunction
o Sexual immaturity
o Growth retardation
o Hypo-function of pituitary gland causing
deficiencies in both the pituitary hormones and the
hormones of the target glands
o Observed when 75% of the pituitary gland is
dysfunctional
o Metabolic dysfunction
o Sexual immaturity
o Growth retardation
• Causes:
o Trauma
o Tumor
o Vascular lesion
o Surgery / radiation of pituitary gland
o Congenital
Assessment Findings
• Hemianopsia / headache (if due to tumor)
• Weight loss, emaciation
• Varying signs of hormonal disturbances depending on
which hormones are being under-secreted
- menstrual dysfunction
- hypometabolism
- adrenal insufficiency
- growth retardation
Diagnostic Tests
• Skull x-ray, CT scan, MRI (reveal pituitary tumor)
• Blood examination:
•  plasma hormone levels (depending on specific hormones
under-secreted)
Collaborative Management
- specific treatment depends on cause
o Tumor: surgical removal or irradiation of the
gland
o Regardless of cause, treatment will include
replacement of deficient hormones (HRT):
- Corticosteroids
- Thyroid hormone
- Sex hormones, gonadotropins

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 NCMB316 LECTURE:
Diabetes Mellitus
Bachelor of Science in Nursing 3YB
Professor: Dr. Potenciana A. Maroma
DIABETES MELLITUS
Pancreas
- Islets of Langerhans (containing beta cells, which produce
insulin. While alpha cells secrete glucagon)
• Alpha cells
- Glucagon –  glucose levels (it function with
gluconeogenesis)
- Pag mababa ang blood sugar, glucagon will be released
by alpha cells and it will raise glucose levels.
• Beta cells
- Insulin -  glucose levels by:
o Transcellular membrane transport of glucose
o Inhibits breakdown of fats & CHON
- Requires Na+ for transport of CHON
- Requires K+ for production
• Delta cells
- Somatostatin – inhibits action of growth hormone
Diabetes Mellitus
- A chronic metabolic disease characterized by
hyperglycemia due to disorder of carbohydrate, fat and
protein metabolism.
- Once u have it, sayo na yan lifetime (sanaol ung DM hindi
ka na iniiwan, pero ung jowa d lifetime hays)
J.A.K.E 1 of 6
Midterm Week
07
- Predisposing Factors:
• Heredity – strongly associated with Type II DM
• Obesity – Adipose tissues are resistant to insulin,
therefore glucose uptake by the cells is poor
• Stress – Stimulates secretion of epinephrine, nor-
epinephrine, glucocorticoids  increased serum
carbohydrates
• Viral infection – increase risk to autoimmune disorders
• Autoimmune Disorders – more associated with Type I
DM
• Multigravida Women with large babies
Types of Diabetes Mellitus
1) Type I
2) Type II
3) Gestational Diabetes
4) Diabetes associated with other conditions or syndromes
- Pancreatic disease, Cushing’s syndrome
- Use of certain drugs:
o Steroids
o Thiazide diuretics
o Oral contraceptives
Type I (IDDM) Insulin Dependent Diabetes Mellitus
- Juvenile – onset, Brittle DM, Unstable DM
- Onset is less than 30 years
- Common in children or in non-obese adults
- NO insulin production (there is destruction on pancreas,
therefore there’s no insulin production at all)
- Prone for DKA (Diabetic Ketone Acidosis, because there is
absolute deficiency of insulin, the body will burn protein
and fat reserves) DKA develops when your body doesn't
have enough insulin to allow blood sugar into your cells for
use as energy. Instead, your liver breaks down fat for fuel, a
process that produces acids called ketones.
- Management:
• Diet
• Exercise
• Insulin lifetime
Type II (NIDDM) Non-Insulin Dependent Diabetes Mellitus
- Maturity – onset, Stable DM, Ketosis – resistant DM
- Onset is 40 years
- Common in obese adults
- Inadequate insulin production or cells do not respond to
insulin. (Meron pero konti lng)
- Prone for HHNKS (Hyperosmolar Hyperglycemic
Nonketotic Syndrome – high BP) mataas ang bp pero hindi
necessarily mataas ang ketone bodies because there is
still circulating insulin.
- Pwede rin sila magkaroon ng DKA, pero bihira lng.
Magkakaroon lng sila kapag may severely stress.
 316 LECTURE: WK7 – DIABETES MELLITUS

- Management:
• Diet
• Exercise
• OHA (Oral Hypoglycaemic Agents), Insulin in
STRESSFUL situation
Pathophysiology

- Pag kumain or nag ingest ng food ang patient dito na

papasok yung functioning ng mga absorption ng mga
nutrients galing sa food
- Isa ang pancreas sa mag se secrete ng mga chemicals at
yung isa doon is beta cells na nag p produce ng insulin.
- Ang insulin mag bi bind yan sa mga receptor nya para ma
decrease yung dami ng glucose sa katawan or ma balance
- Once na mag malfunction ang pancreas or magka problem
ang organ either hindi sya magpo produce ng insulin or
yung mga receptor is hindi mag fu function leading to
glucose will stay in the blood and result as diabetes either
type 1 or 2.
- Hyperglycemia: 3P’s
1) Polyuria
2) Polydipsia
3) Polyphagia

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 316 LECTURE: WK7 – DIABETES MELLITUS
- Ketones act as CNS depressants and may decrease brain
pH leading to coma.
Protein metabolism
- Due to increased blood viscosity
• Sluggish circulation
• Proliferation of microorganisms
- Infections, Periodontal, UTI, Vasculitis, Cellulitis,
Vaginitis, Furuncles, Carbuncles, Retarded Wound
Healing
- MUST: thoroughly inspect your feet daily and keep
them clean and dry
Complications
• Macroangiopathy (malalaking blood vessels)
- Brain – Cerebrovascular accident
- Heart – Myocardial infarction
- Peripheral arteries – Peripheral vascular disease
• Microangiopathy (maliliit na blood vessels)
- Kindeys – Renal failure due to nephropathy
- Eyes – Cataract due to retinopathy
• Neuropathy
- Spinal Cord/ ANS
- Peripheral neuropathy – Involves damage to the PNS,
Affect movement, sensation, and bodily functions
(numbness/ tingling)
- Paralysis
- Gastroparesis (delayed gastric emptying)
- Neurogenic bladder (bladder does not empty properly)
- Decreased Libido, impotence.
Diagnostic Test
• Random Blood Sugar (RBS)
- Blood specimen is drawn without preplanning.
(Kinukuhanan ng dugo agad ang pasyente without
preplanning)
- ≥ 200mg/dl + symptoms is suggestive of DM
• Fasting Blood Sugar (FBS)
- Blood specimen after 8 hours of fasting
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- Normal (70-100 mg/dl), pre-diabetes (101 but < 126mg/
dl)
- DM – > 126 mg/dl
• Postprandial Blood Sugar
- Blood sample is taken 2 hrs after a high CHO meal
- No DM (70-140mg/dl), prediabetes (≥140 but <200
mg/dl)
• Oral Glucose Tolerance Test (OGTT)
- Diet high in CHO is eaten for 3 days.
- Client then fast for 8 hours. A baseline blood sample is
drawn & a urine specimen is collected.
- An oral glucose solution is given, and time of ingestion
recorded.
- Blood is drawn at 30 minutes & 1, 2, and 3 hours after
the ingestion of glucose solution. Urine is collected.
o No DM (glucose returns to normal in 2-3 hours &
urine is negative for glucose)
o DM (blood glucose returns to normal slowly; urine is
positive for glucose)
• Glycosylated hemoglobin (HbA1c)
- Single sample of venous blood is withdrawn.
- The amount of glucose stored by the hemoglobin is
elevated above 7% in the newly diagnosed client with
DM, in one who is noncompliant, or in one who is
inadequately treated.
- HbA1c is something that's made when the glucose
(sugar) in your body sticks to your red blood cells. Your
body can't use the sugar properly, so more of it sticks to
your blood cells and builds up in your blood.
Management
• Diet
- Low caloric diet specially if obese
- Diet should be in proportion.
o 20% CHON
o 30% Fats
o 50% CHO
• Consume complex CHO and HIGH fiber diet.
- inhibits glucose absorption in the intestines.
• Exercise
- This should be regularly
- Increases CHO uptake by the cells.
- Decreases insulin requirements.
- Maintains ideal body weight, serum carbohydrates &
serum lipids.
- Guidelines:
o Allow additional sources of CHO like snacks during
exercises.
 316 LECTURE: WK7 – DIABETES MELLITUS

o Exercise is done 1-2hours after eating to prevent • Thiazolidinediones

hypoglycemia. • Meglitinides
o Exercise must be regular pattern rather than
sporadic to maintain stable serum carbohydrate Nursing Responsibilities in Insulin Therapy
levels. • Route: Subcutaneous
- Slow absorption, less painful, 90° (thin) 45° obese
Medications clients, no need to aspirate, do not massage site of
Insulin injection
- Used for Type I diabetes - IV insulin: given in emergency cases (DKA)
- Used in Type II diabetes (client in stressful situation or • Administer insulin at room temperature
hospitalized) - Cold insulin can cause lipodystrophy.
- Insulin preparations can consist of a mixture of: o Lipoatrophy – loss of subcutaneous fat usually
• beef and pork insulin caused by the utilization of animal insulin.
• Pure beef o Lipohypertrophy – development of fibrofatty masses,
• Pure pork usually caused by repeated use of injection site.
• Human insulin - purest insulin and has the lowest • Store vial of insulin in current use at Room
incidence of hypersensitivity Temperature
- Human insulin is recommended for: - Insulin can be stored at RT for 1 month
• All newly diagnosed Type I diabetics - Other vials should be refrigerated
• Type II diabetics who need short-term insulin therapy - In use – at room temperature
• Pregnant client - Not in use – in refrigerator
• Diabetic clients with insulin allergy or severe insulin • Rotate the site of injection
resistance - To prevent lipodystrophy
Insulin Onset Peak Duration
- Lipodystrophy inhibits insulin absorption
• Gently roll vial in between the palms to redistribute
Rapid acting (clear) insulin particles
5 30 mins
- Lispro (Humalog) 2 to 4 hrs • DO NOT Shake
minutes - 1hr
- Aspart (Novalog) - bubbles make it difficult to aspirate exact amount
Short acting (clear) • Observe for side effects of insulin therapy
Regular (Humulin R) 30 min 2 t0 4 - Localized: Induration or Redness, Swelling, Lesion at
6 to 8 hrs
(Novolin R) (Iletin II to 1 hr hrs the site, Lipodystrophy
regular) - Generalized:
Intermediate (cloudy)
o Edema – due to sudden resolution of hyperglycemia
- NPH
1-2 hrs 6 -12 hrs 18 to 24 hrs o Hypoglycemia
1-2 hrs 8 -12 hrs 18 to 24 hrs o Somogyi phenomenon
- Humulin N
1-2 hrs 8 -12 hrs 18 to 28 hrs
Lente, Humulin L

Long acting 5 to 8 14 to 20
30 to 36 hrs
- Ultralente hrs hrs
rs
Glargine (Lantus) UK UK

Oral Hypoglycemic Agents (OHA) Insulin Therapy: Insulin Pumps

- for Type II - a computerized device that delivers insulin to patients
- Sulfonylureas automatically throughout the day
- Nonsufonylureas - Dosage instruction are entered into the pump small
• Biguanides computer and the appropriate amount of insulin is then
injected into the body in a calculated controlled manner
• Alpha-glucosidase inhibitors
- closely mimic normal pancreatic functioning
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 316 LECTURE: WK7 – DIABETES MELLITUS

- It contain a 3 ml syringe attached to a long (42-inch), OHA

narrow-lumen tube with a needle or Teflon catheter at the - Stress importance of taking the drug regularly
end - Avoid alcohol intake while on medication
- The needle or Teflon catheter is inserted into the • Sulfonylureas can precipitate extreme vomiting if given
subcutaneous tissue (usually on the abdomen) and with alcohol
secured with tape or a transparent dressing
- The needle or catheter is changed at least every 3 days General Nursing Interventions
- The pump is worn either on a belt or in a pocket • Monitor urine sugar and acetone (freshly voided specimen)
- The pump uses only regular insulin • Perform finger sticks to monitor blood glucose levels as
- Insulin can be administered via the basal rate (usually 0.5- ordered (more accurate than urine tests)
2.0 units/hr) and by a bolus dose (which is activated by a • Observe for signs of hypo and hyperglycemia
series of button pushes) prior to each meal • Provide meticulous skin care and prevent injury
• Maintain intake and output; weigh daily
Management • Provide emotional support; assist client in adapting to
Sulfonylureas “insulin releasers” change in life-style and body image
- Stimulate the beta cells to secrete more insulin.
• Observe for chronic complications and plan care
- Increases the ability of insulin cell receptors to bind insulin.
accordingly
- SE: weight gain, hypoglycemia, secondary failure of
• Provide client teaching and discharge planning concerning:
pancreas due to overstimulation
- Disease process
• Tolbutamide (Orinase) - Diet
• Acetohexamide (Dymelor) - Insulin - insulin at RT, gently roll vial between palms of
• Tolazamide (Tolinase) hands, Draw up insulin using sterile technique, If mixing
• Chlorpropamide (Diabenese) insulin, draw up clear insulin before cloudy insulin
• Glipizide (Glucotrol) • Provide many opportunities for return demonstration for
• Glyburide (micronase, Glynase) proper and correct insulin administration
• Glimepiride (Amaryl) • Perform good oral hygiene and have regular dental exams
Nonsulfonylureas • Regular checkup every 3 mos
• Biguanides • Have regular eye exams
o Metformin (Glucophage) • Care for the diabetics under stress
- Help tissues use available insulin more efficiently - Do not omit insulin or oral hypoglycemic agents if taking
- “insulin sensitizers” antibiotics since infection causes increased blood
- SE: Stomach upset, flatulence, diarrhea sugar
- no weight gain, no hypoglycemia unlike
sulfonylureas Hypoglycemia
- it will increase the sensitivity of insulin receptors. - Causes: Overdose of insulin, omission of meals, Strenuous
• Alpha-glucosidase inhibitors exercise, G.I. upset (N&V)
o Miglitol (Glyset), Acarbose (Precose) - Sign and symptoms:
- Alpha-glucosidase is an intestinal enzyme that • Shaking
breaks down carbohydrates into glucose, when this • Sweating
enzyme is inhibited, the process of forming glucose
• Anxious
is slowed and glucose is absorbed more slowly from
• Dizziness
the small intestine.
• Hunger
- Taken 15 minutes before meal.
- It will decrease the absorption of glucose in the • Fast heartbeat
small intestine. • Impaired vision
• Thiazolidinediones (TZDs) • Weakness, fatigue
o Rosiglitazone (Avandia), Pioglitazone (Actos) • Headache
- Help tissues use available insulin more efficiently. • Irritable
- “insulin sensitizers” - Assessment: <60 mg/dl
- SE: weight gain, edema & liver damage (kaya - Management: Simple Sugars p.o.
imonitor ang SGPT – Serum Glutamic Pyruvic • 3-4 oz regular soft-drink
Transaminase, a blood test performed to measure • 8 oz fruit juice
the enzyme created in the liver called Alanine • 5-7 pcs lifesaver’s candies
Transaminase (ALT). • 3-4 pcs hard candies
• Meglitinides • 1 tbsp sugar
o Repaglinide (Prandin) • 5 ml pure honey/ karo syrup
- An “insulin releaser” • 10-15 gm CHO
- SE: same as with sulfonylureas

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 316 LECTURE: WK7 – DIABETES MELLITUS

• D50 W 20-50 ml IV push ( if unconscious) or 1 mg • BUN, Creatinine, Hematocrit are elevated (due to
glucagon dehydration)
• Monitor BS (blood sugar) • Serum sodium decreased, potassium (elevated due to
the acidosis)
Hyperglycemia • ABGs: metabolic acidosis with compensatory
- Causes: Stress (infection, surgery), Overeating, under dose respiratory alkalosis
of insulin • Metabolic acidosis compatible with hyperkalemia
- Sign and symptoms: - Management:
• Extreme thirst • Maintain a patent airway.
• Frequent urination • Maintain F&E balance.
• Dry skin • Administer IV therapy as ordered.
• hunger o Normal saline (0.9% NaCl), then hypotonic (0.45%
• Blurred vision NaCl) sodium chloride
• Drowsiness o When blood sugar drops to 250 mg/dl, may add 5%
• Nausea dextrose to IV
- Assessment: o Potassium will be added when the urine output is
• 3P’s (polyphagia if insulin is absent) adequate.
• Warm flushed dry skin, Soft eyeballs • Observe for fluid and electrolyte imbalances, especially
• Tachycardia, N&V, Abdominal pain fluid overload, hypokalemia & hyperkalemia
• Kussmaul’s breathing, Fruity odor of breath • Administer insulin as ordered.
• Urine (+) glucose & Ketones o ONLY Regular insulin is given IV (drip or push) and/or
• Altered LOC subcutaneously (SC).
- Management: o If given IV drip, give with small amounts of albumin
• Patent airway since insulin adheres to IV tubing
o Monitor blood glucose levels frequently.
• O2 therapy
• Check urine output every hour
• NSS + regular insulin IV
• Monitor vital signs
• D10W once glucose reaches 250 mg/dl level
• Assist client with self-care
• KCI / Slow IV drip, once urine output is adequate
• Provide care for the unconscious client if in a coma
• Monitor blood sugar
• Discuss with client the reasons ketosis developed and
Diabetic Ketoacidosis (DKA) provide additional diabetic teaching if indicated
- Acute complication of DM characterized by:
Hyperosmolar Hyperglycemic Nonketotic Syndrome
• Hyperglycemia
(HHNKS)
• Accumulation of ketones in the body; causes metabolic
- A complication of DM characterized by:
acidosis
• Hyperglycemia
• Frequently occurs in DM Type I (IDDM)
- Precipitating factors: • Hyperosmolar state without ketosis
- Occurs in Type II DM
• Undiagnosed diabetes
- Precipitating factors are:
• Neglect of treatment
• Undiagnosed diabetes
• Infection, cardiovascular disorder
• Infections, major burns, other stress
• Other physical or emotional stress
• certain medications (Dilantin, Thiazide diuretics)
- Assessment Findings:
• Dialysis, Hyper-alimentation, pancreatic disease
• 3 P’s
- Assessment Findings:
• N&V, abdominal pain
• Similar to ketoacidosis but without Kussmaul
• Warm, dry, flushed skin
respirations and acetone breath
• Dry mucous membranes; soft eyeballs
- Laboratory tests:
• Kussmaul’s respirations or tachypnea; acetone breath
• Blood glucose level extremely elevated
or fruity breath
• BUN, creatinine, Hct elevated (due to dehydration)
• Altered LOC, Hypotension
• Urine positive for glucose
• Tachycardia - Nursing interventions:
• Sobrang taas ng blood sugar, mataas ang osmotic
• Treatment and nursing care is similar to DKA, excluding
pressure, ihi ng ihi ang pasyente kaya magkakaroon ng
measures to treat ketosis and metabolic acidosis
severe dehydration, metabolic acidosis – cns
depressant
- Diagnostic Test:
• Serum glucose (up to 600 mg/dL) and ketones elevated
(positive urine ketones)
J.A.K.E 6 of 6
 NCMB316 LECTURE: Midterm Week

08
DI, SIADH, and Thyroid Disorders
Bachelor of Science in Nursing 3YB
Professor: Dr. Potenciana A. Maroma
DI, SIADH, AND THYROID DISORDERS ADH Feedback Loop
SIADH
Brain Regulation
- Disorder of sodium and water balance is a common
complication following neurosurgery.
- Neuroscience patients must be continually assessed and
monitored for their response to therapy.
- Early detection is critical to the protection and integrity of
the brain.
Normal Brain Regulation
1) TBW accounts for 60% of body weight
- 20% ECF
- 40% ICF
2) Fluid shifts can occur depending on concentrations of
solutes in ICF and ECF
3) Na and K are principal determinants in fluid shifts
4) Osmolarity: amount of solute in fluid (urine, blood)
- Normal Serum Osmolarity: 270-295 mOsm/L
5) Serum Osmo above 295 mOsm/L = water deficit
- Concentration is too great OR
- Water concentration is too little
6) Serum Osmo below 270 mOsm/L = water excess
- Amount of particles or solute is too small in proportion
to the amount of water OR Syndrome of Inappropriate Antidiuretic Hormone
- Too much water for the amount of solute • SIADH: Persistent abnormally high (inappropriate) levels of
ADH in the absence of stimuli with normal renal function
To maintain plasma or serum osmo within range, free - No longer regulated by plasma osmo and volume
water intake and excretion must balance - Imbalance of fluid and electrolytes
• Antidiuretic Hormone (ADH): balances Na and water in • Feedback system is impaired and posterior pituitary
body and controls water conservation continues to release ADH
• Changes in pressure of ECF triggers release of ADH from • Renal tubules continue to reabsorb free water regardless
pituitary gland of the serum osmolality
• Release is coordinated with activity of the thirst center- • Excessive activity of the neurohypophyseal system r/t brain
regulates intake disease
• ADH binds with receptor sites of the collecting duct in Risk Factors
kidney resulting in increased free-water resorption • Post-Operative with pituitary surgery
• ADH causes vasoconstriction • Acute head injury
- Presence of ADH- renal tubule permeability to water is • Pulmonary infections (Pneumonia)
increased and water is reabsorbed • Nervous system infections (meningitis)
- Absence of ADH- renal tubule permeability to water is Conditions
decreased – renal excretion to fluids • Fluid status with accurate I&O
• Plasma osmolality = Primary regulatory mechanism for the • Confusion
release of ADH • Dyspnea
• Receptors in the brain are sensitive to changes in • Headache
osmolality
• Fatigue
• Receptors that trigger thirst mechanism are close to those
• Weakness
that control ADH release
• Change in LOC
• Serum osmo greater than 295 mOsm/L triggers thirst
• Lethargy
• Vomiting
• Muscle weakness and cramping
• Muscle twitching
• Seizures
J.A.K.E 1 of 6
 316 LECTURE: WK8 – DI, SIADH, AND THYROID DISORDERS

Laboratory Diagnosis Pathophysiology of DI

Serum Sodium Less than 135 mEq/L • Central/Neurogenic
- Inadequate secretion of ADH due to loss or malfunction
Urine Sodium Greater than 20 mEq/L of neurosecretory neurons that make up the posterior
pituitary.
Urine Osmolality Higher than serum
- Vasopressin Sensitive
Serum Osmolality Less than 275 mOsm/L • Nephrogenic
- Inadequate response by the kidneys to ADH.
BUN/Creat WNL - A disorder of renal tubular function resulting in the
inability to respond to ADH in absorption of water.
Urine Specific Gravity Greater than 1.005
- Vasopressin Resistant
Adrenal/threshold WNL • Dipsogenic
- Suppression of ADH secondary a defect or damage to
Serum Potassium Less than 3.5 mEq/L the thirst mechanism located in the hypothalamus
Treatment resulting in increased fluid intake or psychogenic
• Correct underlying cause causes
• Fluid restriction 500-1000 ml/day Clinical Sign
• Severe hyponatremia: 3% NSS may be given • Dehydration! Excessive loss of water from body tissue and
• Lasix may be given (watch K level) imbalance of essential electrolytes (Na, K, Cl)
Nursing Management • Polydipsia (excessive thirst)
• Frequent Neuro assessment: Mental status and LOC • Polyuria (excessive amount of urine)
• Pulmonary assessment: s/s fluid overload • Low specific gravity (1.001 to 1.005)
• Cardiac assessment: Dysrhythmias and BP abnormalities • Serum hyperosmolality and hypernatremia
• Monitor for seizure activity: Seizure precautions Causes
• Accurate I&O • Head Trauma
• Daily Weights: Same time each day, same scale, same • Post-operative (hypophysectomy, pituitary tumor)
clothes • Brain Tumors
• Oral hygiene • CNS Infection (meningitis, abcess)
• Reduce stress, pain, discomfort • Increased ICP
Correlation of Decreasing Sodium Levels and Symptoms • Idiopathic
Serum Sodium Level Symptoms • ICH
• Stroke
Normal concentration, no • Hypoxia
145-135 mEq/L
symptoms • Medications (Dilantin, clonidine, alcohol)
• Damage to hypothalamus or posterior pituitary
135-120 mEq/L Generally no changes
Investigate the following for DI
HA, apathy, lethargy, weakness, • Unquenchable thirst
120-110 mEq/L disorientation, thirst, fatigue, • Polydipsia
seizures • Polyuria (hourly urine output > 200 mls)
• Unexplained weight loss
Confusion, hostility, lethargy,
• Urinary frequency
110-100 mEq/L N/V, abdominal cramps, muscle
twitching • Dry skin/poor skin turgor
• Tachycardia and hypotension
Delirium, convulsions, coma, • Inability to respond to the increased thirst stimulus and
100-95 mEq/L hypothermia, areflexia, Cheyne- compensate for the excessive polyuria
Stokes respirations, death • Hypernatremia that becomes severe and is manifested by-
confusion, irritability, stupor, coma and neuromuscular
Diabetes Insipidus (DI) hyperactivity progressing to seizures.
- Disordered regulation of water balance due to impaired • Unconscious/intubated
urinary concentrating ability secondary to inadequate Labs and Diagnostics
secretion of ADH or resistance to ADH. • Serum calcium
- Four Types of DI: • Glucose
1) Central/Neurogenic (CDI) • Creatinine
2) Nephrogenic (NDI) • Potassium
3) Dipsogenic • Urea level
4) Gestational • The following may also be indicated:
- 24hr urine collection to quantitative polyuria
J.A.K.E 2 of 6
 316 LECTURE: WK8 – DI, SIADH, AND THYROID DISORDERS

- CT/MRI - rule out pituitary causes, metastases, Nursing Management

hemorrhage, neuronal damage, cerebral tumors. • Hourly Neuro Checks
- Radioimmunoassy: to measure circulating ADH • Frequent Vital Signs
concentrations • Evaluate for s/s of hypovolemic shock
Lab Value Result • Strict I&O
• Rehydrate for symptoms of extreme thirst
Serum Sodium Above 145 mEq/L • Measure and record weight using the same scales at the
Serum Osmolality Above 290 mOsm/kg same time and with the patient wearing the same clothing
• Assess mucous membranes and skin turgor and monitor
Urine Specific Gravity of the Below 1.005 for symptoms of dehydration
first morning voiding • Provide rest
• Safety measures to prevent injury secondary to dizziness
Urine Sodium Above 145 mEq/L
and fatigue
Urine Osmolality Below 300 mOsm/L • Alert the health care team of problems of urinary frequency
Diagnosis of DI should be considered in any person producing and extreme thirst that interferes with sleep and activities.
large volumes of dilute urine
Water Deprivation Test SIADH vs DI Lab Values
- After baseline measurement of: weight, ADH, plasma Finding SIADH DI
sodium, and urine/plasma osmolality, the patient is
deprived of fluids under strict medical supervision Less than 200 mls Greater than
Urine Output
- Frequent (q2h) monitoring of plasma and urine osmolality x 2hrs 250 mls x 2hrs
follows. Below 135 mEq/L Above 145
- The test is generally terminated when plasma osmolality is Serum Sodium
mEq/L
>295 mOsm/kg or the patient loses ≥3.5% of initial body
weight. Urine Sodium Below 25-30 mEq/L Decreased
- DI is confirmed if the plasma osmolality is >295 mOsm/kg
Urine Above 900 Below 400
and the urine osmolality is <500 mOsm/kg.
Osmolality mOsm/kg mOsm/kg
Nephrogenic DI vs Neurogenic DI
• DDAVP Challenge Plasma Below 275 Above 295
- Check urine osmolality 1-2hrs after 1mcg SQ DDAVP Osmolality mOsm/L mOsm/L
- If little or no change: likely NDI or dipsogenic DI
- If significant increase in urine osmolality, likely CDI Blood Pressure Normotension Hypotension
• 5 units vasopressin IV Fluid Status No Dehydration Dehydration
- Measure osmolality
- A significant increase (>50%) in urine osmolality after Confusion, Seizures, coma
Neuro
administration of ADH is indicative of CDI delirium, coma
Symptoms
Treatment with low Na
Correct the underlying cause and maintain adequate fluid
replacement. Complications to treatments of DI and SIADH
• DI Therapy varies with the degree and type of DI present or • Cerebral Edema!
suspected. • Central Pontine Myelinolysis: brain cell dysfunction caused
• IVF may be necessary to correct hypernatremia; avoid by destruction of the myelin sheath covering nerve cells in
rapid replacement brainstem
• Free water restriction • Na levels rise too fast or corrected too quickly
• After assessing fluid status and serum sodium level, treat • s/s: (not necessarily immediate)
both dehydration and hypernatremia - Acute paralysis
• For chronic neurogenic DI- require hormonal replacement - Dysphagia
therapy: DDAVP (nasal vasopressin) - Dysarthria
• Consultation with an endocrinologist is strongly Most Important Nursing Intervention for DI and SIADH
recommended • Frequent Labs
Removal of the underlying cause/offending drug - We have severe electrolyte abnormalities
• DDAVP usually ineffective - Careful not to correct too quickly!!
• Thiazide diuretic (HCTZ) is first line treatment - Na should not rise more than 0.5mEq/L/hr and 10
• Adequate hydration mmol/L/24 hrs
• Low-sodium diet + thiazide diuretics to induce mild sodium • Frequent neuro assessment
depletion. - The nurse can pick up abnormal behavior and signs and
• Indomethacin may also be useful to reduce urine volume. symptoms first. Note any changes from baseline

J.A.K.E 3 of 6
 316 LECTURE: WK8 – DI, SIADH, AND THYROID DISORDERS

Thyroid Gland Disorder • Goiter

- Secretes the following hormones - Enlargement of the thyroid gland associated with
• T3 (Triidothyronine) hyperthyroidism, hypothyroidism or euthyroidism
 Metabolism and growth - A hyperthyroid goiter is called toxic goiter
• T4 (Thyroxine, tetraiodothyronine)
 Catabolism and body heat production Hyperthyroidism (Thyrotoxicosis)
• Thyrocalcitonin • Grave’s Disorder
 regulates serum Ca++ levels • Basedow’s Disorder
 bring down the blood Ca++ level • Exophthalmic Goiter
Diagnostic Tests • Diffuse Toxic Goiter
• T3/ T4 levels - Common in female, below 40 y/o
-  level: hyperthyroidism - Causes:
-  level: hypothyroidism • Severe emotional stress
• PBI (Protein-bound Iodine) • Autoimmune Disorder
- Preparation: No foods, drugs, test dyes with iodine 7-10 • Thyroid inflammation
days before the test
• RAIU (Radioactive Iodine Uptake)
- Tracer dose of I131 is used P.O. & at 2°, 6°, and 24° 
exposure to scintillation camera is done
- No foods, drugs, test dyes with iodine 7-10 days before
the test, temporarily discontinue contraceptive pills
(these may metabolic rate)
- Result:
o  iodine uptake: hyperthyroidism
o  iodine uptake: hypothyroidism

Hyperthyroidism: Key concepts

• Thyroid Scan
- Radioisotope Iodine is injected IV
- Exposure to scintillation camera
• FNB (Fine Needle Biopsy)
- Cytology (detection of malignant cells)
• BMR (Basal Metabolic Rate)
- Measures O2 consumption at the lowest cellular activity
- Oxygen uptake is measured as an indirect
measurement of metabolic rate
- increased utilization O2 (hyperthyroid)
• Reflex Testing (Kinemometry)
- Tendon of Achilles Reflex (TAR)
- What are the hormones produced by the thyroid gland?
• T3
• T4
• Calcitonin
- 3 BASIC CONCEPTS:
•  T3 =  metabolic rate
•  T4 =  body heat production
•  Thyrocalcitonin =  calcium
Assessment Findings
• Restlessness, nervousness, irritability, agitation, fine
tremors, tachycardia, hypertension, voracious appetite to
eat, weight loss, diaphoresis, diarrhea, heat intolerance,
amenorrhea, fine silky hair, pliable nails
• Exophthalmos
- Due to accumulation of fluids, mucopolysaccharides at
the fat-pads behind the eyeballs
- It can lead to corneal ulceration,
• Von Graefe’s sign (LID LAG)
- Long and deep palpebral fissure is still evident when
one looks down
• Jeffrey’s sign – Forehead remains smooth when one looks
up
• Dalyrimple’s sign (Thyroid stare)
- Bright-eyed stare, infrequent blinking
• Dermopathy
- Warm, flushed sweaty skin
- Thickened hyper-pigmented skin at the pretibial area

J.A.K.E 4 of 6
 316 LECTURE: WK8 – DI, SIADH, AND THYROID DISORDERS

Management o ECG – Heart failure/ cardiac damage results from HPN/

• Rest (non-stimulating cool environment)
• Diet
- HIGH Calorie, HIGH protein; vitamin and mineral
supplement
- Increased fluid intake (if with diarrhea)
- Replace F&E losses
- Avoid stimulants like coffee, tea and nicotine
• Promote safety
• Protect the eyes
- Artificial tears at regular intervals
- Wear dark sunglasses when going out under the sun
Management: Pharmacotherapy
• ß-blockers: Propranolol
• Ca++ channel blockers
- These drugs are given to control tachycardia and HPN
• Iodides: Lugol’s solution
- SSKI (Saturated Solution of Potassium Iodide)
- Are given to inhibit release of thyroid hormone
- Mix with fruit juice with ice or glass of water to improve
its palatability
- Provide drinking straw to prevent permanent staining of
teeth
- Side effects: Allergic reaction, Increased salivation,
colds
• Thioamides
- PTU (Propylthiouracil) & Tapazole (Methimazole)
- These are given to inhibit synthesis of thyroid hormones
- Side effects of PTU
o AGRANULOCYTOSIS / NEUTROPENIA This is
manifested by unexplained Fever, Sore throat, Skin
rashes
o The nurse must elicit these symptoms and if present,
the physician must be alerte
• Paracetamol for fever
- Aspirin must be avoided because it can displace the
T3/T4 from the albumin in the plasma causing increased
manifestations
• Dexamethasone
- inhibit the action of thyroid hormones
- Steroids are given to prevent the conversion of T4 to T3 in
the peripheral tissues
• Radiation therapy (Iodine)
- Need isolation for few days; body secretions are
radioactive contaminated
- NOT recommended in pregnant women because of
potential teratogenic effects. Pregnancy should be
delayed for 6 months after therapy
Surgery
• Subtotal Thyroidectomy- Usually about 5/6 of the gland is
removed
• Pre-op Care
o Promote euthyroid state
- Control of thyroid disturbance
- Stable VS
o Administer Iodides as ordered – To reduce the size &
vascularity of thyroid gland, thereby prevent post-op
hemorrhage and thyroid crisis
tachycardia
o Position : Semi-fowler’s with head, neck & shoulder
erect
o Prevent Hemorrhage: ice collar over the neck
o Keep tracheostomy set available for the first 48° post-
op
o Ask the patient to speak every hour (to assess for
recurrent laryngeal nerve damage)
o Keep Ca++ gluconate readily available – Tetany occurs if
hypocalcemia is present. This may be secondary to the
accidental removal of the parathyroid gland
o Monitor Body Temperature: hyperthermia is an initial
sign of thyroid crisis
o Monitor BP (hypertension may be a manifestation of
thyroid storm)
o assess for Trousseau’s sign (hypocalcemia)
o Steam inhalation to soothe irritated airways
o Advise to support neck with interlaced fingers when
getting up from bed
o Observe for signs and symptoms of potential
complications
- Hemorrhage
- Airway obstruction
- Tetany
- Recurrent laryngeal nerve damage
- Thyroid crisis / storm / thyrotoxicosis
- Myxedema
• Client Teaching
o ROM exercises of the neck 3 to 4 days after discharge
o Massage incision site with cocoa butter lotion to
minimize scarring
o Regular follow – up care
Thyroid crisis/ storm
- Sudden, life-threatening exacerbation of hyperthyroidism/
thyrotoxicosis
- Causes: Stress, Infection, Unprepared thyroid surgery
Assessment
• Initial sign: Elevated temperature
• Tachycardia
• Dysrhythmias
• Tremors, apprehension, restlessness
• Delirium, psychotic state, coma
• Elevated BP
Management
• Monitor the following every hour
- Temperature
- Intake and output
- Neurologic status
- Cardiovascular status
• Administer increasing doses of oral PTU
- (200 to 300 mg q 6 hrs) as ordered, following a loading
dose of 800 to 1,200 mg. p.o as ordered
• Administer iodide preparation as ordered
• Administer dexamethasone to help inhibit the release of
thyroid hormone

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 316 LECTURE: WK8 – DI, SIADH, AND THYROID DISORDERS

• Administer propranolol to control hypertension and • Increased sensitivity to sedatives, narcotics, and
tachycardia anesthetics
• Implement measures to lower fever
- cooling devices
- cold baths
- acetaminophen (avoid aspirin)
• Administer oxygen as needed
• Maintain quiet, calm, cool, private environment until crisis
is over

Hypothyroidism
- results from deficiency of thyroid hormones

- What are the hormones produced by the thyroid gland?

• T3
• T4
• Calcitonin
- 3 BASIC CONCEPTS:
•  T3 =  metabolic rate
•  T4 =  body heat production
•  Thyrocalcitonin =  calcium Management
- Causes • Monitor vital signs
• Autoimmune – Hashimoto’s disease or chronic • Be alert for signs and symptoms of cardiovascular
lymphocytic thyroiditis - an autoimmune disorder in disorders
which your immune system inappropriately attacks your • Monitor the weight daily
thyroid gland causing an inflammation • Diet: LOW Calorie, High fiber (constipation)
• after surgery (thyroidectomy) • Provide warm environment during cold climate
• after radiation therapy (radioactive iodine) Pharmacotherapy
• antithyroid drugs • Thyroid hormonal replacement
Assessment - Proloid (Thyroglobulin)
• Slowed physical, mental reactions, apathy - Synthroid (Levothyroxine)
• Dull, expressionless, mask-like face - Dessicated Thyroid Extract
• Anorexia - Cytomel (Liothyronine)
• Obesity o Before administration, the nurse should monitor BP
• Bradycardia & PR
• Hyperlipidemia & atherosclerosis o Start with low dose and gradually increase
• Cold intolerance, subnormal temperature Myxedema Coma
• Constipation - Extreme, severe stage of hypothyroidism, in which the
• Coarse, dry, sparse hair client is hypothermic and unconscious
• Brittle nails - Management includes:
• Irregular menstruation (menorrhagia, amenorrhea) • IV thyroid hormones
• Husky, hoarse voice • Correction of hypothermia
• Extreme fatigue • Maintenance of vital function
• Slow speech • Treat precipitating factors
• Enlarged tongue

J.A.K.E 6 of 6
 NCMB316 LECTURE:
Adrenal and Parathyroid Gland Disorders
Bachelor of Science in Nursing 3YB
Professor: Dr. Potenciana A. Maroma
ADRENAL AND PARATHYROID GLAND DISORDERS
Adrenal Gland Diseases
- Adrenal gland – also known as suprarenal gland, small
triangular shapes gland located on the top of the both
kidneys. 4-5 grams in weight.
- Consists of:
• Zona glomerulosa is the outermost region of the adrenal
cortex and is the only zone of the adrenal gland that
contains the enzyme aldosterone synthase (CYP11B2).
• Zona fasciculata, the middle zone of the adrenal cortex
secretes glucocorticoids which are important for
carbohydrate, protein and lipid metabolism. (Regulates
blood sugar)
• Zona reticularis produces androgens (sex hormones)
Addison’s Disease
- Hypofunction of the adrenal cortex resulting to a
decreased secretion of the
• Mineralocorticoids
• Glucocorticoids
• Sex hormones
- Causes:
• Idiopathic atrophy of the adrenal cortex possibly due to
an autoimmune process
• Destruction of the gland secondary to tuberculosis or
fungal infection
J.A.K.E 1 of 5
Midterm Week
09
• Tumor (not secreting adequate hormone –
hypopituitarism)
- Key Concept: Know the functions of the hormones and
you will know the signs & symptoms.
- Mineralocorticoids (Aldosterone)
• Promotes Na & H2O reabsorption & K+ excretion.
- Glucocorticoids (Cortisol)
• Affects CHO, CHON, Fat metabolism.
- Body’s response to STRESS
• Emotion stability
• Immune Function
- Sex Hormones
• Major source of androgen in women
Assessment
• Fatigue, muscle weakness
• Anorexia, N&V, abdominal pain, weight loss
• Frequent hypoglycemic reactions
• Hypotension, weak pulse
• Bronze like pigmentation of the skin
- Due to MSH (Melanocyte-stimulating hormone) 2° to
loss of adrenal-hypothalamic-pituitary feedback system
• Decreased capacity to deal with stress.
 316 LECTURE: WK9 – ADRENAL AND PARATHYROID GLAND DISORDERS

Diagnostic Tests • Affects CHO, CHON, Fat metabolism

• Low cortisol levels • Body’s response to STRESS
• Hyponatremia • Emotion stability
• Hypovolemia • Immune Function
• Hyperkalemia - Sex Hormones
• Acidosis • Major source of androgen in women
• Hypoglycemia Assessment Findings
Nursing Intervention • Muscle weakness, fatigue
• Administer HRT as ordered. (kung kulang ng hormone, edi • Obese trunk with thin arms and legs, muscle wasting
bigyan ng hormone, HRT – Hormonal Replacement (pendulous abdomen)
Therapy) • Irritability, depression, frequent mood swings
- Glucocorticoids (Cortisone, Hydrocortisone) – simulate • Moon face, buffalo hump
diurnal rhythm of cortisol release, give 2/3 of dose in • Purple striae on trunk, acne, thin skin
early morning and 1/3 of dose in afternoon. • Signs of masculinization in women; menstrual dysfunction,
- Mineralocorticoids (Fludrocortisone acetate) decreased libido
• Monitor VS • Osteoporosis, decreased resistance to infection
• Decrease stress in the environment. • Hypertension, edema
• Provide rest periods; prevent fatigue. Diagnostic test
• Prevent exposure to infection. • cortisol levels
• Monitor I&O, weigh daily. • slight hypernatremia
• Provide proper nutrition in small, frequent feedings of diet • hypokalemia
high in Sugar (carbohydrate), Salt (sodium) and Protein • hyperglycemia
• Provide client teaching and D/C planning concerning: When cushing’s is suspected, a blood sample will be
- Use of prescribed medications for lifelong replacement taken for laboratory analysis.
therapy; never omit medications. 1) ACTH- 7.2- 52 pg/ml
- Need to avoid stress, trauma, and infections, and to 2) Plasma cortisol - 10-20mcg/dl
notify physician if these occur as medication dosage - It decreases in the evening- during early phase of
may need to be adjusted sleep
- Stress management techniques 3) Dexamethasone suppression test (Confirmatory test)
- Diet modification - Measures the response of adrenal glands to ACTH.
- Use of salt tablets (if prescribed) or ingestion of salty Dexamethasone 1mg is given oral at 11pm.
foods (potato chips) if experiencing increased sweating. - Plasma cortisol is obtained at 8am…>50% reduction in
- Importance of alternating regular exercise with rest plasma cortisol
periods, avoidance of strenuous exercise especially in 4) MRI/ CT scan
hot weather Medical Management
• Emergency condition: Addisonian crisis is a life- • Mitotane- [Lysodren] to decrease production of
threatening situation that results in low blood pressure, glucocorticoids
low blood levels of sugar and high blood levels of
• Korlym [Mifepristone]- Cortisol Receptor blocker
potassium. (circulatory failure or shock, it could be cause
• Ketoconazole
by a sudden withdrawal of corticosteroids on patient who
• Metyrapone [Metopirone]
has having high dose of corticosteroids)
Cushing Syndrome • Insulin
- Hyperfunction of the adrenal cortex resulting to an Nursing Intervention
excessive secretion of the: • Maintain muscle tone (Provide ROM exercises, assist with
• Mineralocorticoids ambulation) there is instability because of muscle
• Glucocorticoids weakness
• Sex hormones • Prevent accidents or falls and provide adequate rest
- Causes: • Protect client from exposure to infection
• Overproduction of ACTH- hyperpituitarism • Maintain skin integrity.
• Benign or malignant tumors • Provide meticulous skin care.
• Prolonged corticosteroids therapy • Prevent tearing of skin: use paper tape if necessary.
• Exogenous • Minimize stress in the environment
- Key Concept: Know the functions of the hormones and • Monitor VS: observe for hypertension, edema
you will know the signs & symptoms • Measure I&O and daily weights
- Mineralocorticoids (Aldosterone) • Provide diet that is:
• Promotes Na & H2O reabsorption & K+ excretion - low in calories and sodium
- Glucocorticoids (Cortisol) - high in protein, K+, Ca++

J.A.K.E 2 of 5
 316 LECTURE: WK9 – ADRENAL AND PARATHYROID GLAND DISORDERS
- vitamin supplements
• Monitor urine for glucose and acetone; administer insulin if
ordered
• Provide psychological support and acceptance.
• Prepare client for hypophysectomy or radiation if condition
is caused by a pituitary tumor.
• Prepare client for an adrenalectomy if condition is caused
by an adrenal tumor or hyperplasia.
• Provide client teaching D/C planning concerning:
- Diet modifications
- Importance of adequate rest
- Need to avoid stress and infection
- Change in medication regimen (alternate day therapy or
reduced dosage) if cause of the condition is prolonged
corticosteroid therapy.
Conn’s Syndrome (Hyperaldosteronism)
- Excessive aldosterone secretion from the adrenal cortex
- Seen more frequently in women (30-50 y/o)
- Cause by a tumor or hyperplasia of adrenal gland
- Key Concept: Mineralocorticoids (Aldosterone) –
Promotes Na+ & H2O reabsorption & K+ excretion
Assessment findings
• Headache
• Hypertension
• Muscle weakness
• Polyuria, polydipsia
• Metabolic alkalosis
• Cardiac arrhythmias (due to hypokalemia)
Diagnostic tests
•  Serum K +
• Alkalosis
• Urinary aldosterone levels elevated
Laboratory Test
• Plasma aldosterone- in supine position with normal
sodium diet
• 2-9 ng/dl or 55-250 pmol/L, with upright /standing position
or seated for at least 2hrs is 2-5x supine value
• Urine aldosterone - 14-56 nmol/24 hrs
Nursing Interventions
• Monitor VS, I&O, daily weigh
• Maintain sodium restriction as ordered
• Administer spironolactone (Aldactone) and potassium
supplements as ordered
• Prepare the client for an adrenalectomy if indicated
• Provide client teaching and discharge planning concerning:
- Use and side effects of medication if the client is being
maintained on spironolactone therapy
- Signs of symptoms of hypo/ hyperaldosteronism
- Need for frequent blood pressure checks and follow-up
care
Pheochromocytoma
- A condition of hyper-functioning tumor of the adrenal
medulla resulting to excessive secretion of epinephrine &
norepinephrine
- Occurs most commonly between ages 25-50, hereditary in
some cases
J.A.K.E 3 of 5
Assessment findings
• Severe headache, apprehension, palpitations, profuse
sweating, nausea
• Hypertension, tachycardia, vomiting, hyperglycemia,
dilation of pupils, cold extremities
Diagnostic tests
• Increased plasma levels of catecholamines
• Elevated blood sugar
• Glycosuria
• Elevated urinary catecholamines and urinary
vanillylmandelic acid (VMA) levels
• Presence of tumor on x-ray
Laboratory Test
• Serum epinephrine – 0-140 pg/ml [764.3 pmol/L
• Norepinephrine – 70- 1700pg/ml or 413.8- 10048.7pmol/L
• Catecholamine test uses a sample of blood or urine to
measure levels of some adrenal hormones.
• Normetanephrine – 18- 111 pg/ml
• Metanephrine – 12-60 pg/ml
• Urine catecholamines – 14-110mcg/24 hrs
• VMA – Vanillyl Mandelic Acid is produced in the liver and
is a major product of epinephrine and norepinephrine
metabolism which is excreted in the urine.
- Preparation: No food and fluid with coffee, tea, cocoa,
chocolate for 48 hours before the test
- Normal level 2-7 mg/24 hours
Nursing interventions
• Monitor vital signs, especially blood pressure.
• Administer medications as ordered to control hypertension.
• Promote rest; decrease stressful stimuli.
• Monitor urine tests for glucose and acetone
• Provide high-calorie, well-balanced diet; avoid stimulants
such as coffee, tea.
• Provide care for the client with an adrenalectomy as
ordered; observe post adrenalectomy client carefully for
shock due to drastic drop in catecholamine level.
• Provide client teaching and discharge planning: same as
for adrenalectomy.
Parathyroid Gland
- Produces parathyroid hormone (PTH) or parathormone
which regulates calcium and phosphorous balance.
• Hyperparathyroidism – Hypercalcemia
• Hypoparathyroidism – Hypocalcemia
 316 LECTURE: WK9 – ADRENAL AND PARATHYROID GLAND DISORDERS

Hyperparathyroidism • Increased alkaline phosphatase levels

- Characterized by excessive secretion of the PTH
- Causes:
• parathyroid adenoma
• congenital hyperparathyroidism
• multiple endocrine neo plasia- a group of disorders that
affect the body’s network of hormones producing
glands
• Secondary hyperparathyroidism can occur due to
o rickets (softening of the bone)
o vitamin D deficiency
o chronic renal failure
o phenytoin and laxative abuse
Pathophysiology
Assessment
• CNS – psychomotor and personality disturbances, loss of
memory, depression, psychosis, confusion, disorientation,
stupor and coma
• GI – abdominal pain, anorexia, nausea, vomiting,
dyspepsia and constipation
• Neuromuscular – fatigue, marked muscle weakness and
atrophy
• Renal – nephrolithiasis, renal insufficiency
• Skeletal – chronic lower back pain, fractures, bone
tenderness and joint pain
• Vision impairment – scleritis/ red eye keratopathy,
asymptomatic conjunctival
• Calcification and conjunctivitis
Diagnostic test
• Increased serum calcium, with decreased level of
phosphate
• X-rays will show diffuse demineralization of bones, bone
cysts, erosions
• Elevated urine and serum calcium
• UTZ, MRI
• Normal Values
- PTH- 10-55 pg/ml
- Serum Calcium- 8.6- 10 mg/dl
- Serum phosphate- 2.5-4.5 mg/dl
- Alkaline phosphatase- 44- 147 IU/L
Medical Management
• Surgery to remove the adenoma
• Increased fluids to force diuresis
• Dietary restrictions of calcium
• Medications – Furosemide and ethacrynic acid, oral
calcitonin, oral potassium phosphate
Nursing Interventions
- Record I&O accurately
- Strain all urine to check for stones
- Monitor electrolyte levels (Na+, K+, Mg++)
- Be alert for pulmonary edema if IVF therapy is initiated
- Prevent injury due to fracture: Provide a safe environment
to ensure against complications related to potential
osteoporosis and joint and bone pain
- Monitor for cardiac arrhythmias and decreased cardiac
output
- Increase fluids, 2-3 L, cranberry juice
- Encourage mobility
Hypoparathyroidism
- Deficiency of PTH, that leads to hypocalcemia and
produces neuromuscular symptoms ranging from
paresthesia to tetany
- Causes:
• Congenital absence, autoimmune disease
• Removal of the parathyroid glands
• Post-thyroidectomy
• Massive thyroid radiation therapy
Clinical Manifestations
• Positive Chvostek’s and Trousseau’s sign
• Tetany, paresthesia
• INCREASED neuromuscular irritability,  DTR
• Psychosis
• Dysphagia, abdominal pain
• Arrhythmias, bronchospasm, laryngospasm
• Cataracts
• Hair loss, brittle nails, dry skin
• Weakened tooth enamel
Diagnostic Test
- PTH
- serum calcium
- serum phosphate
- X-ray reveals increased bone density
- ECG- prolonged QT intervals and QRS complex and ST
segment changes
Medical Management
• Therapy includes vitamin D supplements, and
supplemental calcium like Calcium Citrate, Caltrate Plus,

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 316 LECTURE: WK9 – ADRENAL AND PARATHYROID GLAND DISORDERS

Calcium carbonate, given with meals bec. It requires

stomach acid to dissolve and absorb it.
- Life-threatening hypocalcemia is managed by IV
calcium gluconate to raise calcium levels.
• Sedatives and anti-convulsant are used to prevent seizures
Nursing interventions
• Maintain a patent IV line & keep calcium gluconate 10%
solution available
• Administer prescribed sedatives, anticonvulsants &
calcium gluconate (slow IV)
• Institute seizure precaution
• Keep a tracheostomy set and endotracheal tube available
• Watch out for cardiac arrhythmias and decreased cardiac
output
• Encourage to take high calcium and low phosphate diet
early in the disease process
• Creams and lotions can be used to sooth dry skin

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