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Primary
Problem in the target gland; autonomous
Secondary
Problem in the pituitary
Tertiary
Problem in the hypothalamus
ANTERIOR PITUITARY
DISORDERS
HYPERPITUITARISM
May be due to overactivity of gland
or the result of an adenoma
Characterized by:
Excessive serum concentration
of pituitary hormones (GH, ACTH, PRL)
Morphologic and functional changes
in the anterior pituitary
GROWTH HORMONE
HYPERSECRETION
Gigantism Acromegaly
Prior to closure After closure
of the epiphyses; of the epiphyses;
proportional growth disproportional
growth
HYPERPITUITARISM:
CLINICAL MANIFESTATIONS
Arthritis
Chest: barrel-shaped
Rough facial features
Odd sensations: hands and feet
Muscle weakness & fatigue
Enlargement of organs
Growth of coarse hair
Amenorrhea; breast milk production
Loss of vision; headaches
Impotence; increased perspiration
Snoring
HYPERPITUITARISM:
CLINICAL MANIFESTATIONS
HYPERPITUITARISM:
MANAGEMENT
Medication Radiation
Bromocriptine- Indicated for larger
Cabergoline tumors
(dopamine agonists)
GH hypersecretion Surgery
and prolactinoma Trans-sphenoidal
hypophysectomy
Ocreotide
(somatostatin)
GH hypersecretion
TRANS-SPHENOIDAL
HYPOPHYSECTOMY
Post-surgery nursing care
Semi- to high- Fowler’s position
Protect from infection and stressful situations
Hormone replacement
Constant neurologic checks
MIOW to check for DI
WOF CSF leak
Encourage deep-breathing, but not coughing
Institute measures to prevent constipation
[straining increases ICP]
HYPOPITUITARISM
Causes
Infections / Inflammatory disorders
Autoimmune diseases
Congenital absence
Tumor
Surgery / Radiation therapy
HYPOPITUITARISM
Simmonds' disease Sheehan’s syndrome
[Panhypopituitarism]
[Post-partum
Complete absence
pituitary necrosis]
of pituitary hormones
Cachexia: A complication
most prominent feature of delivery
Follows destruction Results from severe
of the pituitary blood loss and
by surgery, infection, hypovolemia
injury, or a tumor Pituitary ischemia
HYPOPITUITARISM:
CLINICAL MANIFESTATIONS
Medication Radiation
Hormonal substitution Indicated for larger
[maybe for life] tumors
Corticosteroids Surgery
Levothyroxine Trans-sphenoidal
Androgen / Estrogen hypophysectomy
Growth hormone
POSTERIOR PITUITARY
DISORDERS
DIABETES INSIPIDUS
Characterized by massive polyuria
due to either lack of ADH or renal insensitivity
Central DI
Due to a deficiency in ADH production
Nephrogenic DI
Due to a defect in the kidney tubules
that interferes with water absorption
Polyuria is unresponsive to ADH,
which is secreted normally.
DIABETES INSIPIDUS:
DIAGNOSTICS
Nephrogenic DI:
Indomethacin-
-hydrochlorothiazide
-desmopressin
-amiloride
Clofibrate, chlorpropamide
SYNDROME OF INAPPROPRIATE ADH
Disorder due to excessive ADH release
Clinical Manifestations
Serum TSH
Single best screening test [high sensitivity]
0.38 – 6.15 mcU/mL
If TSH is normal, fT4 should be normal.
Screening required beginning 35 years,
then q 5 years thereafter
Also used for monitoring thyroid hormone
replacement therapy
THYROID FUNCTION TESTS
Serum fT4
A direct measurement of free
thyroxine,
the only metabolic fraction of T4
0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L)
Used to confirm an abnormal TSH
THYROID FUNCTION TESTS
Nursing Implications
Determine whether the patient has taken
medications or agents that contain iodine
[antiseptics, multivitamins, cough syrup, amiodarone]
because these may alter the test results.
Assess for allergy to iodine or shellfish.
For scans, tell patient that radiation is only
minimal.
HYPERTHYROIDISM
Causes
Grave’s disease (autoimmune)
Initial manifestation of thyroiditis
TSH-screening pituitary tumor
Toxic adenoma
Factitious thyrotoxicosis
Amiodarone therapy
HYPERTHYROIDISM:
CLINICAL MANIFESTATIONS
GI hypermotility
Rapid weight loss
Apprehension
[tremors, tachycardia, palpitations]
Volume deficit; voracious appetite
Exophthalmos; erratic menses
Systolic BP elevated; sweating
Iodine deficiency
Autoimmune Oncologic
Developmental Drugs
Dietary Iatrogenic
Non-thyroidal
Endocrine
HYPOTHYROIDISM
Causes
Chronic autoimmune [Hashimoto’s]
thyroiditis
Hypothalamic failure to produce TRH
Pituitary failure to produce TSH
Inborn errors of TH synthesis
Thyroidectomy / Radiation therapy
Anti-thyroid therapy
Iodine deficiency
HYPOTHYROIDISM
Classified according to the time of life in which it occurs
Cretinism
In infants and young children
Lymphocytic thyroiditis
Appears after 6 years of age
and peaks during adolescence; self-limiting
Hypothyroidism without myxedema
Mild thyroid failure in older children and adults
Hypothyroidism with myxedema
Severe thyroid failure in older individuals
HYPOTHYROIDISM:
CLINICAL MANIFESTATIONS
Hypotension
Precipitating Factors
Bradycardia
Acute illness
Hypothermia
Rapid withdrawal
of thyroid medication
Hyponatremia
Anesthesia / Surgery
Hypoglycemia
Respiratory failure
Hypothermia
Comause
Opioid
HYPOTHYROIDISM:
MANAGEMENT
Prevention
Prophylactic iodine supplements to decrease
the incidence of iodine-deficient goiter
Symptomatic cases
Hormonal replacement
Levothyroxine (Synthroid)
Liothyronine (Cytomel)
Liotrix (Thyrolar)
Dosage increased q 2-3 weeks
especially in elderly patients
HYPOTHYROIDISM:
MANAGEMENT
Constipation
Apathy
Lordosis
Cardiac dysrhythmias
Upset GIT
Low energylevels
Increased BP
PTH
Calcium
Alkaline phospatase
PO4
HYPERPARATHYROIDISM:
MANAGEMENT
Dyspnea; dysrhythmias
Extremities: tingling
Fotophobia
Increased bone density
Chvostek sign; cramps
Irritability
Trousseau sign; tetany
PTH
Calcium
Alkaline phospatase
PO4
HYPERTHYROIDISM:
MANAGEMENT
IV Ca chloride or gluconate [emergency treatment]
DOC post-thyroidectomy
Oral Ca salts (Ca carbonate or gluconate)
Vitamin D supplementation
Increase intestinal Ca absorption
Dihydrotachysterol, ergocalciferol
Trousseau’s &
E levated serum PO4; low
Chvostek’s
T
Caingling
2+
Alkalosis; Arrhythmias
Narrowing of airway
Irritability
Cramps
HYPOPARATHYROIDISM
C
ALCIUM
ARE
GLUCONATE
Release
cathecholamines
Epinephrine
Norephinephrine
Released during
“fight or flight”
situations
(sympathetic effect)
PHEOCHROMOCYTOMA
Adrenal tumor
Heredity
PHEOCHROMOCYTOMA
Headache
Anxiety
Nausea
Eye disturbances
Severe hypertension
PHEOCHROMOCYTOMA
BP
HR
Diaphoresis
BMR
VMA
Glucose
PHEOCHROMOCYTOMA
Adrenalectomy
Steroid treatment
Antihypertensive and
antidysrhythmic
nitroprusside (Nipride)
propranolol (Inderal)
phentolamine (Regitine)
PHEOCHROMOCYTOMA
MBP / MIO
Fluid replacements
Decrease environmental stimulation
Maintenance doses of steroids
Follow-up check up
24-hour urine specimens
[VMA and catecholamine studies]
Avoid: coffee, chocolate, beer, wine, citrus
fruit, bananas, and vanilla 24h before
test
ADDISON'S DISEASE
ADRENAL CORTEX HORMONES
Glucocorticoids
Cortisol, corticosterone
Increase blood glucose levels by
increasing rate of gluconeogenesis
Increase protein catabolism
Increase mobilization of fatty acids
Promote sodium and water retention
Anti-inflammatory effect
Aid the body in coping with stress
ADRENAL CORTEX HORMONES
Mineralocorticoids
Aldosterone, Corticosterone,
Deoxycorticosterone
Regulate fluid and electrolyte balance
Stimulate reabsorption of sodium, chloride
and water
Stimulate potassium excretion
Underthe control of Renin-Angiotensin-
Aldosterone system (RAAS)
ADRENAL CORTEX HORMONES
Sex hormones
Androgens, Estrogens
Influences the development of
sexual characteristics
ADDISON'S DISEASE
Hyposecretion of adrenocortical
hormones
Idiopathic atrophy
ADDISON'S DISEASE
Weakness
Excess stress
A/N/V/D
K & ACTH elevation; Low Na,
BP, cortisol, glucose
ADDISON'S DISEASE
Replacement of hormones
Hydrocortisone; Fludrocortisone
PNSS (0.9 NaCl)
Dextrose
Diet:
High-CHO & CHON
Low potassium, high sodium
ADDISON'S DISEASE
Adrenal hyperplasia /
tumor
Cushing’s disease
Tumor-secreting ACTH
Hypothalamic
Buffalo hump
Unusual behavior (depression, personality
changes, fatigability)
Facial features (moonface, hirsutism in
women)
Fat (truncal obesity)
ACTH and cortisol in blood
elevated;
Loss of muscle mass
Overextended skin (abdominal
striae with easy bruisability)
Hypertension, hyperglycemia,
hypernatremia
Urinary cortisol elevated
Menstrual irregularities
Porosity of bones
(osteoporosis)
CUSHING’S SYNDROME
CUSHING'S SYNDROME
Hypophysectomy or irradiation
Adrenalectomy
CUSHING'S SYNDROME
Cyproheptadine (Periactin)
Metyrapone
Mitotane (Lysodren)
Aminoglutethamide (Cytadren)
Potassium supplements
High-CHON; Low Na
CUSHING'S SYNDROME
MVS, MIOW, MBP, MBG
Electrolyte levels: Na & K
Urine specimens
[LOW 17- hydroxycorticosteroids & 17-
ketosteroids]
Physical appearance
Changes in coping & sexuality
[verbalization]
Stress reduction
DIABETES MELLITUS
DIABETES MELLITUS
Pancreatectomy, Cushing's
syndrome, drugs
DIABETES MELLITUS
Hyperglycemia
Glucosuria
Polyuria
Gluconeogenesis
DIABETES MELLITUS
Complications
Microvascular
Retinopathy & Renal failure
Macrovascular
CV and PVD
Peripheral neuropathy
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healing
Normal Impaired DM
Diet
complex CHO [50% to 60%]
water-soluble fiber
oat, bran, peas, beans, pectin-rich
FV
CHON [12% to 20%]
60 and 85 g
CHOO [<30%]
70 to 90 g/day / MUFA
DIABETES MELLITUS
Somogyi effect
Epinephrine & Glucagon
Glycogenolysis
[iatrogenically-induced hyperglycemia]
Lowering insulin dosage at night
MBG
DIABETES MELLITUS
Insulin pump
1) Basal doses of regular insulin delivered
every few minutes bolus doses delivered
pc
Biguanides
Reduces hepatic production of glucose
by inhibiting glycogenolysis
Decrease the intestinal absorption of
glucose and improving lipid profile
Agents:
Phenformin
Metformin (Glucophage, Glucophage XR)
Buformin
ORAL HYPOGLYCEMICS
Alpha-glucosidase inhibitors
Inhibits alpha-glucosidase enzymes in
the small intestine and alpha
amylase in the pancreas
Decreases rate of complex
carbohydrate metabolism resulting
to a reduced rate postprandially
Agents:
Acarbose (Precose, Gluconase, Glucobay)
Miglitol (Glyset)
ORAL HYPOGLYCEMICS
Thiazolidinediones
Enhances insulin action at the cell and post-
receptor site and decreasing insulin
resistance
Agents:
Pioglitazone (Actos)
Rosiglitazone (Avandia)
Rosiglitazone + Metformin
(Avandamet)
DIABETES MELLITUS
Reflects
effectiveness of
treatment
< 7.5% (good control)
7.6% - 8.9% (fair control)
> 9% (poor control)
DIABETES MELLITUS
Administer insulin
sterile technique
rotating injection sites
dosage / types / strengths / peak
CHO source
Avoid:
Avoid tight shoes; smoking;
heat
DIABETES MELLITUS
hypoglycemia
Headache
Nervousness
Diaphoresis
Rapid, thready pulse
Slurred speech
THE CLIENT IS TIRED!
Tremors
achycardia Hypoglycemia: <50 mg/dL
Irritability Causes:
Restlessnes
Overtreated hyperglycemia
Increased exercise
sxcessive hunger β-blockers
E xcitability Gastric paresis
Alcohol intake
Headache 20-30 gm
Inability to concentrate carbohydrate
Mood swings
Irritability
Glucagon 1 mg
Slurred speech SQ/IM
Severe:
Rx:
Seizures
Unconsciousnes 25 gm D dextrose IV
50
s
Disorientation Glucagon 1 mg IM/IV
DIABETES MELLITUS
diabetic coma
Restlessness
Hot, dry, flushed skin
Thirst
Rapid pulse
Nausea
Fruity odor to breath
Ketoacidosis
Urinary changes
Rx:
Sunken eyeballs Regular insulin drip
Skin is warm & 0.9% or 0.45% NSS
flushed 1:1 [100U:100cc]
Membranes are dry Nursing care:
Check glucose
Arrhythmias
250-300 mg/dL
Upset GI system [q30-60mins]
Low BP 250 mg/dL
Saline solution DC the drip
NON
Ketosis is absent
Electrolyte imbalance [K+
decrease]
Thirst
Obtundation
Treat with regular insulin
drip
Initiate diet
Correct hyperglycemia
Normal creatinine?
Erythrocyte sedimentation rate [ESR: 0-20
mm/hr]
Poor glycemic control
Hemodialysis
Restrict: Na+, CHON, K+, weight
Output & input (MIO)
No symptoms
Reduced O2 in the eye
Elevated sugar & BP
Tension is high in the retina
Increased lens opacity
NO eyesight
Annual eye exam [every 6-12
months]
MAJOR DISORDERS
OF THE ENDOCRINE
SYSTEM
THANK YOU!